The Merck Veterinary Manual, 11th Edition
Author: The Merck Veterinary Manual-John Wiley; Sons (2016)
Date: 2020-01-13T09:07:41+00:00
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THE MERCK

VETERINARY

MANUAL

ELEVENTH EDITION

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Dedicated to all veterinarians and their colleagues in animal health worldwide.

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THE MERCK

VETERINARY

MANUAL

ELEVENTH EDITION

Editor-in-Chief: Susan E. Aiello, DVM, ELS

Executive Editor: Michael A. Moses

Editorial Board

Dana G. Allen, DVM, MSc, DACVIM

Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM

Andrew Dart, BVSc, PhD, DACVS, DECVS

Peter R. Davies, BVSc, PhD

Katherine E. Quesenberry, DVM, DABVP (Avian Practice) Philip T. Reeves, BVSc, PhD, FACVSc

Jagdev M. Sharma, BVSc, MS, PhD

Published by

MERCK & CO., INC.

KENILWORTH, NJ, USA

2016

Editorial and Production Staff

Editor-in-Chief: Susan E. Aiello, DVM, ELS

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Executive Editor: Michael A. Moses

Publisher: Melissa Adams

Partnership Manager: Michael Wisniewski

Subsidiary Rights Coordinator: Sheryl Olinsky-Borg

Sales and Service Specialist: Leta S. Bracy

Associate Director, Merck Digital Publications: Michael DeFerrari Library of Congress Control Number: 2016905370

ISBN-13: 978-0911910612

ISSN Number: 0076-6542

Copyright© 2016 by MERCK & CO., INC.

All rights reserved. No part of this book may be reproduced or used in any form or by any means, electronic or mechanical, including photocopying, or by any information storage and retrieval system, without permission in writing from the Publisher. Address inquiries to Merck Publishing Group, P.O. Box 2000, RY34A-426, Rahway, NJ 07065

Printed in the USA

Designer: Jerilyn Bockorick, Cenveo® Publisher Services Composition by Cenveo® Publisher Services

Fort Washington, Pennsylvania

Printed and bound at RR Donnelley

Crawfordsville, Indiana

THE MERCK VETERINARY MANUAL

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Previous Editions

First Edition

1955

Second Edition

1961

Third Edition

1967

Fourth Edition

1973

Fifth Edition

1979

Sixth Edition

1986

Seventh Edition

1991

Eighth Edition

1998

Ninth Edition

2005

Tenth Edition

2010

Foreign Language Editions

Chinese

China Agriculture Press, Beijing

Croatian/Slovakian

Komora Vetarinarnich Lekarov, Brno

French

Editions d'Apres, Paris

Italian

Cristiano Giraldi Editore, Bologne

Japanese

Gakusosha, Tokyo

Portuguese

Editora Roca, Sao Paulo

Spanish

Editorial Oceano, Barcelona

OTHER

MERCK BOOKS

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The Merck Index

First Edition, 1889

The Merck Manual of Diagnosis and Therapy

First Edition, 1899

The Merck Manual of Medical Information'

Home Edition

First Edition, 1977

The Merck Manual of Health and Aging

First Edition, 2004

The Merck/Merial Manual for Pet Health

First Edition, 2007

The Merck Manual of Patient Symptoms

First Edition, 2008

The Merck Manual Go-To Home Guide for Symptoms

First Edition, 2013

Merck books are published as a service to the scientific community and the public.

FOREWORD

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Merck & Co., Inc., has a long history of providing medical information to both human and animal health care professionals. For more than 60 years, the Merck Veterinary Manual (MVM) has provided veterinarians and other animal health professionals with concise and authoritative information on diseases and management of food-producing, c9mpanion, laboratory, and exotic animals. The 11th edition carries on this proud tradition.

This new edition has been completely updated and revised to continue to address the many diverse aspects of veterinary medicine. The first half of the book covers all body systems, including discussions of disease etiology, diagnosis, treatment, control, and prevention. The second half addresses special topics, including behavior, clinical pathology, management and nutrition, pharmacology, toxicology, and poultry medicine.

Although the contents of the book have expanded with each edition, the MVM remains true to its original objective: a concise, easy-to-use, comprehensive reference that covers the diversity of species and animal diseases worldwide. Coverage is straightforward and practical, with explicit recommendations given for treatment whenever possible. The succinct discussions also serve to give readers a strong foundation for seeking out and understanding more detailed information available elsewhere.

The MVM covers all the basics, but it is also often relied on for areas not commonly encountered in the daily routine of most animal health professionals. This is no more evident than in the growing responsibility of veterinarians to society, in which general practitioners and specialists alike must vigilantly embrace their role in the international movement of animals, maintaining a safe food supply, and minimizing the spread of infectious animal disease and zoonotic agents. In this vein, a new section is dedicated to public health, covering public health functions and agencies, epidemiologic principles, disease outbreak investigations, food safety, and an extensive table of zoonoses.

Other significant new information has been added on heart disease, diagnostic imaging, emergency medicine, wound management, and pharmacology, including drug resistance. The emerging area of aquaculture is reflected in new chapters on aquaculture, aquatic systems, and aquarium fish. Veterinary responsibilities under the new Veterinary Feed Directive rule are also summarized. Additional timely new topics have been added throughout, covering subjecl.s as diverse as backyard poultry, equine arboviral encephalomyelitis, neonatal management, smoke inhalation, rhodococcosis, scorpion bites, spider flies, xylitol toxicity, toxicologic hazards in the workplace, and the human-animal bond and service animals. And as medical knowledge of exotic and laboratory animals continues to increase, so does the MVM's coverage of pet birds, rabbits, reptiles, rodents, fish, and other nontraditional species.

The contents of the MVM are available online and as an app for handheld devices, providing enhanced capability to quickly access needed information. Digital versions are updated more frequently and include thousands of additional images and other multimedia offerings.

As always, we are deeply grateful to the authors and reviewers who have contributed to the current and past editions of the MVM. The 11th edition of the MVM is an extensive collaboration of the MVM Editorial Board and nearly 400 veterinary experts from academia, government, research organizations, and specialty practices, representing more than 20 countries worldwide. It is only through their dedication to animal health and their efforts and willingness to share their time and expertise that the MVM
is possible.

vii
viii

FOREWORD

Acknowledgment and thanks are also due to the following individuals for their assistance in the 11th edition of the MVM: Jennifer A. Doyle for business operations and technical troubleshooting, Lisa P. Glinski for index entry coding and other critical tasks, Jean L. Perry for general project administrative support, and Michelle A. Steigerwald for image processing. Appreciation is also expressed to Robert S. Porter, MD, for his manage

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ment support.

Lastly, there is nothing more rewarding than hearing directly from our readers. Please continue to share your many thoughts, experiences, and stories about the MVM so that the book and its legacy can continue to improve, evolve, and endure.

SusanE. Aiello, DVM, ELS, Editor-in-Chief

MiclwelA. Moses, Executive Editor

GUIDE FOR READERS

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• The Contents shows the title of each section of the Merck Veterinary Manual (MVM) and the corresponding thumb tab abbreviation.

• Each section has its own Table of Contents that lists chapter and subchapter titles in that section.

• Many cross-reference page numbers are found throughout the text to enable the reader to quickly find discussions of related material elsewhere in the book.

• A number of abbreviations and symbols used routinely throughout the text are listed beginning on p xiii. Other abbreviations used in the text are defined at their first use.

• Generic ( nonproprietary) names of drugs are used in most instances.

• Running heads on left-hand pages correspond to the chapter title of the text appearing at the top of that page. Running heads on right-hand pages correspond to the chapter title of the text appearing at the bottom of that page. In other words, running heads are used as in a standard dictionary.

• The Index is the best way to locate specific discussions of a disease, condition, or syndrome for which the name is known.

• The first half of the MVM is arranged into anatomic systems, and specific conditions are located in the system that is primarily affected. Conditions that may affect more than one system are covered in the section Generalized Conditions (GEN). The second half of the MVM covers special topics or disciplines.

• The authors, reviewers, editors, and publisher have made extensive efforts to ensure that treatments, drugs, dosage regimens, and withdrawal times are accurate and conform to the standards accepted at the time of publication. However, constant changes in information resulting from continuing research and clinical experience, reasonable differences in opinions among authorities, unique aspects of individual clinical situations, and the possibility of human error in preparing such an extensive text require that the reader exercise individual judgment when making a clinical decision and, if necessary, consult and compare information from other sources. In particular, the reader is advised to check the product information currently provided by the manufacturer of each drug before prescribing or administering it, especially if the drug is unfamiliar or is used infrequently.

Many of the drug dosages given are considered extra-label usages, which require a valid veterinarian-client-patient relationship. Veterinarians should also be familiar and comply with the regulations set forth by the Veterinary Feed Directive.

ix

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CONTENTS

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Foreword
vii

Guide for Readers
ix

Abbreviations and Symbols
xiii

Editorial Board
xv

Contributors
xvii

CIR

Circulatory System

DIG

Digestive System

147

EE

Eye and Ear

487

END

Endocrine System

537

GEN

Generalized Conditions

585

IMM

Immune System

811

ITG
lntegumentary System

833

MET

Metabolic Disorders

983

MUS

Musculoskeletal System

1031

NER

Nervous System

1207

REP

Reproductive System

1321

RES

Respiratory System

1409

URN

Urinary System

1493

BEH

Behavior

1533

CPP

Clinical Pathology and Procedures

1583

EMG

Emergency Medicine and Critical Care

1657

EXL

Exotic and Laboratory Animals

1731

MGN Management and Nutrition

2061

PBH

Public Health

2389

PHM

Pharmacology

2485

POU

Poultry

2775

TOX

Toxicology

2945

REF

Reference Guides

3173

IND

Index

3187
xi

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ABBREVIATIONS AND SYMBOLS

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ad li b
as much as desired

IM
intramuscular(ly)

ADP
adenosine diphosphate
in.

inch(es)

ALT
alanine aminotransferase

IP
intraperitoneal(ly)

AST
aspartate aminotransferase
ru
international unit(s)

ATP
adenosine triphosphate

IV
intravenous(ly)

bid
twice a day
kcal
kilocalorie( s)

bpm
beats per minute
kg
kilogram(s)

BUN
blood urea nitrogen

L

Jiter(s)

Celsius (Centigrade)

LOH
lactate dehydrogenase
cal
calorie(s)

lb
pound(s)

CBC(s) complete blood count(s)

m
meter(s)

CDC

Centers for Disease Control

M
molar
and Prevention

Meal
megacalorie( s)

CFU
colony-forming unit
mcg
microgram
c m
centimeter( s)

ME
metabolizable energy

CNS
central nervous system
m Eq
milliequivalent( s)

CK
creatine kinase (CPK, creatine
mg
milligram( s)

phosphokinase)

min
minute(s)

CSF
cerebrospinal fluid
mL
milliliter( s)

CT
computed tomography
mm
millimeter( s)

cu
cubic
mo
month(s)

DIC
disseminated intravascular
coagulation
mol
mole(s)

dL
deciliter( s)

m Osm
milliosmole( s)

DNA
deoxyribonucleic acid
run
nanometer( s)

ECG
electrocardiogram

MRI
magnetic resonance imaging
eg
for example

NRC

National Research Council

ELISA enzyme-linked immunosorbent

NSAID(s) nonsteroidal anti-
assay
inflammatory drugcs)

EPA

Environmental Protection

OIE

Office International des

Agency

Epizooties

EPG
eggs per gram ( of feces)

oz
ounce(s)

et se q
and the following one(s)

p/pp
page/pages

EU

European Union

PCR
polymerase chain reaction

F

Fahrenheit

PCV
packed cell volume

FDA

Food and Drug Administration
pH
negative logarithm of hydrogen
fl.

femtoliter(s)

ion activity
ft
foot, feet

PO
per os, orally
g
gram(s)

ppb
part( s) per billion
gal.

gallon(s)

ppm
part( s) per million

GI
gastrointestinal
qid
four times a day

GnRH
gonadotropin-releasing
qsad
quantity sufficient to make
hormone

RBC(s) red blood cell(s)

H&E
hematoxylin and eosin

RNA
ribonucleic acid

Hg b
hemoglobin

SC
subcutaneous(ly)

hr
hour(s)

sec
second(s)

i e
that is

SI units International System of Units
lg
immunoglobulin (with class

SPF
specific pathogen free
following: A, D, E, G, or M)

sq
square

IL
interleukin
tbsp
tablespoon( s)

xiii
xiv

ABBREVIATIONS AND SYMBOLS

TDN
total digestible nutrients

(}(
alpha
tid
three times a day

�
beta
tsp
teaspoon(s)

6
delta
u
unit(s)

E
epsilon

UK

United Kingdom

"{
gamma

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USDA

United States Department of

A
lambda

Agriculture
µ
micro, mu

USA

United States of America

K
kappa

USSR

Union of Soviet Socialist

(T
sigma

Republics (former)

WBC(s) white blood cell(s)

wk
week(s)

wt
weight
yr
year(s)

EDITORIAL BOARD

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Dana G. Allen, DVM, MSc, DACVIM

Professor Emeritus, Ontario Veterinary College, University of Guelph, Ontario, Canada

Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM

Dean, College of Veterinary Medicine, University of Illinois at Urbana

Champaign, Urbana, IL

Andrew Dart, BVSc, PhD, DACVS, DECVS

Director, Research and Clinical Trials Unit, and Registered Equine Surgical Specialist, University of Sydney, NSW, Australia

Peter R. Davies, BVSc, PhD

Allen D. Leman Chair in Swine Health and Productivity, Department of Veterinary Population Medicine, University of Minnesota, St. Paul, MN

Katherine E. Quesenberry, DVM, MPH, DABVP (Avian) Avian and Exotic Pet Service, The Animal Medical Center, New York, NY

Philip T. Reeves, BVSc, PhD, FACVSc

Principal Scientist, Australian Pesticides and Veterinary Medicines Authority, Symonston, Australia

Jagdev M. Shatma, BVSc, MS, PhD

Research Professor, The Biodesign Institute, Visiting Professor, School of Life Sciences, Arizona State University, Tempe, AZ; Professor and Endowed Chair ifl Avian Health Emeritus, University of Minnesota, St.

Paul, MN
xv

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CONTRIBUTORS

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Tahseen Abdul-Aziz, BVMS, MS, PhD,

Glen W. Almond, DVM, PhD

DACPV

Professor, Swine Health and Production

Veterinary Pathologist, Rollins Animal

Management, North Carolina State Univer

Disease Diagnostic Laboratory, North
sity, Raleigh, NC

Carolina Department of Agriculture and

Consumer Services, Raleigh, NC

Postpartum Dysgalactia Syndrome and

Mastitis in Sows

Avian Encephalomyelitis; Botulism;

Listeriosis

Gary C. Althouse, BS, MS, DVM, PhD,

DACT

Stephen B. Adams, DVM, MS, DACVS

Professor of Reproduction. and Swine

Professor of Surgery, Department of

Health; Marion Dilley and David George

Veterinary Clinical Sciences, School of

Jones Endowed Chair in Animal Repro

Veterinary Medicine, Purdue University,
duction, Department of Clinical Studies,

West Lafayette, IN

New Bolton Center, University of Pennsylvania, Kennett Square, PA Arthroscopy; Lameness in Horses: Introduction; Musculoskeletal System: Intro

Management of Reproduction: Pigs
duction; The Lameness Examination

Claire B. Andreasen, DVM, PhD, DACVP

Andrew J. Allen, DVM, PhD, DACVIM

Associate Dean for Academic and Student

Assistant Professor, Department of Veteri

Affairs and Professor, College of Veterinary
nary Clinical Sciences, Washington State

Medicine, Iowa State University, Ames, IA

University, Pullman, WA

Staphylococcosis

Disorders of Calcium Metabolism: Partu

Frank M. Andrews, DVM, MS, DACVIM
rient Paresis in Cows; Metabolic Disor

(Large Animal)

ders: Introduction; Transport Tetany in

Louisiana Veterinary Medical Association

Ruminants.

Equine Committee Professor and Director,

Equine Health Studies Program, Depart

Dana G. Allen, DVM, MSc, DACVIM
ment of Veterinary Clinical Sciences,

Professor Emeritus, Ontario Veterinary

School of Veterinary Medicine, Louisiana

College, University of Guelph, Ontario,

State University, Baton Rouge, LA

Canada

Gastrointestinal Ulcers in Large Ani

Congenital and Inherited Anomalies;
mals: Gastrointestinal Ulcers in Horses

Systemic Pharmacotherapeutics of the

Cardiovascular System: Drugs Acting on

John A. Angelos, DVM, PhD, DACVIM
the Blood

Associate Professor, Department of Medicine and Epidemiology; Livestock Medicine Kelly E. Allen, MS, PhD
and Surgery, School of Veterinary Medicine,

Lecturer, Department of Veterinary

University of California, Davis, CA

Pathobiology, Center for Veterinary Health

Sciences, Oklahoma State University,

Infectious Keratoconjunctivitis

Stillwater, OK

David A. Ashford, DVM, MPH, DSc

Blood Parasites: Old World Hepatozo

Attache, US Department of Agriculture,
onosis and American Canine Hepatozo

Office of Agricultural Affairs, Port au
onosis

Prince, Haiti

Foot-and-Mouth Disease

Sandra Allweiler, DVM, DACVA

Assistant Professor, Department of

Clarke Atkins, DVM, DACVIM

Clinical Sciences, College of Veterinary

Jane Lewis Seaks Distinguished Professor,

Medicine and Biomedical Sciences,

Professor Emeritus, College of Veterinary

Colorado State University, Fort

Medicine, North Carolina State University,

Collins, CO

Raleigh, NC

Pain Assessment and Management

Heartworm Disease
xvii
xviii

CONTRIBUTORS

Rick Atwell, BVSc, PhD, FACVSc

Daniela Bedenice, DVM, DACVIM,

Honorary Professor, School of Veterinary

DACVECC

Science, University of Queensland, Bris

Assistant Professor, Department of Clinibane, Queensland, Australia cal Sciences, Cummings School of Vet

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Tick Paralysis
erinary Medicine, Tufts University, North

Grafton, MA

David G. Baker, DVM, MS, PhD,

Hypoxic lschemic Encepha.lopathy; Man

DACLAM
agement of the Neonate: Large Animals;

Director and Professor, Division of Labo

Sepsis in Foals
ratory Animal Medicine, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA

Sylvia J. Bedford-Guaus, DVM, PhD,

DACT

Eye-worm Disease

Animal Reproduction Consultant, Barcelona, Spain

Lora R. Ballweber, MS, DVM

Professor, Clinical Parasitology, College

Breeding Soundness Examination of the
of Veterinary Medicine and Biomedical

Male

Sciences, Colorado State University, Fort

Collins, CO

James K. Belknap, DVM, PhD, DACVS

Fluke Infections in Ruminants; Gastro

Professor of Equine Surgery, Department
intestinal Parasites of Pigs; Lungw01m
of Veterinary Clinical Sciences, College

Infection
of Veterinary Medicine, The Ohio State

University, Columbus, OH

Alejandro Banda, DVM, MSc, PhD,

Lameness in Horses: Disorders of the Foot

DACPV, DACVM

Associate Clinical Professor of Avian

Virology, Poultry Research and Diag

William G. Bickert, PhD

Professor Emeritus, Biosystems and
nostic Laboratory, College of Veterinary

Agricultural Engineering, Michigan State

Medicine, Mississippi State University,

University, East Lansing,

Mississippi State, MS

Ml

Duck Viral Enteritis

Ventilation

Gad Baneth, DVM, PhD, DECVCP

Rob Bildfell, DVM, MSc, DACVP

Professor, Koret School of Veterinary

Professor, Department of Biomedical

Medicine, Hebrew University, Rehovot,

Sciences, College of Veterinary

Israel

Medicine, Oregon State University,

Corvallis, OR

Leishmaniosis

Collection and Submission of Laboratory

Lisa G. Barber, DVM

Samples; Pyrrolizidine Alkaloidosis

Assistant Professor, Department of Clinical Sciences, Cummings School of Vet

Patrick Joseph Blackall, BSc, PhD
erinary Medicine, Tufts University, North

Principal Research Fellow, Queensland

Grafton, MA

Alliance for Agriculture and Food Itmo

Antineoplastic Agents
vation, The University of Queensland,

Brisbane, Queensland, Australia

George M. Barrington, DVM, PhD,

Infectious Coryza

DACVIM

Professor, Food Animal Medicine and

Surgery, College of Veterinary Medicine,

Barry R. Blakley, DVM, PhD

Washington State University, Pullman, WA

Professor, Department of Veterinary

Biomedical Sciences, Western

Congenital Erythropoietic Porphyria;

College of Veterinary Medicine,

Photosensitization

University of Saskatchewan, Saskatoon,

Canada

Robert B. Beckstead, PhD

Associate Professor, Department of

Copper Poisoning; Fluoride Poisoning;

Poultry Science, University of Georgia,

Lead Poisoning; Mercury Poisoning;

Athens, GA

Metaldehyde Poisoning; Molybdenum

Poisoning; Quercus Poisoning; S01·ghum

Hexamitiasis; Histomoniasis

Poisoning

CONTRIBUTORS
xix

Shauna L. Blois, DVM, DVSc, DACVIM

Scott A. Brown, VMD, PhD, DACVIM

Assistant Professor, Clinical Studies,

Josiah Meigs Distinguished Professor and

Ontario Veterinary College, University of

Head, Department of Small Animal Medi

Guelph, Ontario, Canada
cine and Surgery, College of Veterinary

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Diseases of the Stomach and Intestines in Medicine, University of Georgia, Athens, SmaU Animals: Gastrointestinal Neopla

GA
sia, Gastrointestinal Ulcers, Helicobacter

Infectious Diseases of the Urinary

Infections

System in SmaU Animals; Noninfectious

Diseases of the Urinary System in Small

Dawn Merton Boothe, DVM, PhD

Animals

Professor, Department of Anatomy, Physiology, and Pharmacology, College of Veterinary Cecil F. Brownie, DVM, PhD, DABVT, Medicine, Auburn University, Auburn, AL

DABFE,DABFM,FACFEI

Antibacterial Agents; Antifungal Agents;

Professor Emeritus, College of Veterinary

Antiviral Agents; Chemotherapeutics

Medicine, North Carolina State University,

Introduction; Pharmacology Introduction Raleigh, NC

Poisonous Mushrooms; Poisonous Plants

Manuel Borca, DVM, PhD

Research Microbiologist, Foreign

Animal Disease Research, USDA,

Glenn F. Browning, BVSc, DVCS, PhD

Orient Point, NY

Professor in Veterinary Microbiology,

Asia-Pacific Centre for Animal Health,

Classical Swine Fever

Faculty of Veterinary Science, The

University of Melbourne, Werribee,

Jane C. Boswell, MA, VetMB, CertVA,

Victoria, Australia

CertES (Orth), DECVS, MRCVS

Infectious Bronchitis

The Liphook Equine Hospital, Liphook,

Hampshire, UK

David Bruyette, DVM, DACVIM

Lameness in Horses: Disorders of the Stifle, Medical Director, VCA West Los Angeles Disorders of the Tarsus and Metatarsus

Animal Hospital, Los Angeles, CA

The Adrenal Glands; The Pancreas

Joan S. Bowen, DVM

Bowen Mobile Veterinary Practice,

Wellington, CO

Marie S. Bulgin, DVM, MBA, DACVM

Emerita, Caine Veterinary Teaching Cen

Health-Management Interaction: Goats;
ter, University ofldaho, Caldwell, ID

Lameness in Goats

Health-Management Interaction: Sheep;

Perle E. Boyer, DVM

Lameness in Sheep; Scrapie

Lecturer, North Carolina State University,

Raleigh, NC

Kristine E. Burgess, DVM, DACVIM

(Oncology)

Postpartum Dysgalactia Syndrome and

Assistant Professor, Department of Clini

Mastitis in Sows
cal Sciences, Cummings School of Veterinary Medicine, Tufts University, North R. Keith Bramwell, BS, MS, PhD

Grafton,MA

Extension Poultry Specialist, Cooperative

Extension Service, and Associate Profes

Antineoplastic Agents
sor, Department of Poultry Science, University of Arkansas, Fayetteville, AR

Amanda Burling, DVM

Maddie's Shelter Medicine Program, Col

Artificial Insemination (Poultry)

lege of Veterinary Medicine, University of

Florida, Gainesville, FL

Matthew T. Brokken, DVM, DACVS

Clinical Assistant Professor, Department

Feline Leukemia Virus and Related
of Veterinary Clinical Sciences, College

Diseases
of Veterinary Medicine, The Ohio State

University, Columbus, OH

Raymond Cahill-Morasco, MS, DVM

Lameness in Horses: Disorders of the

SeaPort Veterinary Hospital, Gloucester,

Carpus and Metacarpus, Disorders of the MA Fetlock and Pastern

Zinc Toxicosis
xx

CONTRIBUTORS

Robert J. Callan, DVM, MS, PhD,

Jens Peter Christensen, DVM, PhD

DACVIM

Associate Professor, Department of

Professor, Department of Clinical Sci

Veterinary Disease Biology, Faculty of
ences, College of Veterinary Medicine

Life Sciences, University of Copenhagen,
and Biomedical Sciences, Colorado State

Denmark

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University, Fort Collins, CO

Fowl Cholera; Riemerella anatipestifer

Bluetongue; Congenital and Inherited

Infection

Anomalies: Border Disease; Malignant Catarrhal Fever; Sporadic Bovine Edwin Claer ebout, DVM, PhD, DEVPC

Ence'J)halomyelitis

Professor, Department of Virology,

Parasitology and Immunology, Faculty of

John Campbell, DVM, DVSc

Veterinary Medicine, Ghent University,

Professor, Large Animal Clinical Sciences,

Merelbeke, Belgium

Western College of Veterinary Medicine,

University of Saskatchewan, Saskatoon,

Anthelmintics

Saskatchewan, Canada

Peter Clegg, MA, Vet MB, DECVS,

Respiratory Diseases of Cattle

PhD,MRCVS

Professor of Equine Surgery, Veterinary

Wayne W. Carmichael, PhD

Teaching Hospital, School of Veterinary

Professor of Aquatic Biologyffoxicology,

Sciences, University of Liverpool,

Wright State University, Dayton, OH

Neston, UK

Algal Poisoning

Lameness in Horses: Disorders of the

Back and Pelvis, Disorders of the Hip

James W. Carpenter, MS, DVM,

DACZM

Johann (Hans) F. Co etzee , BVSc,

Professor, Zoological Medicine, Depart

CertCHP, PhD, DACVCP
ment of Clinical Sciences, College of Veter

Department of Veterinary Diagnostic and
inary Medicine, Kansas State University,

Production Animal Medicine, College of

Manhattan, KS

Veterinary Medicine, Iowa State Univer

Hedgehogs
sity, Ames, IA

Systemic Pharmacotherapeutics of the

Phillip D. Carter, BVSc, MVS

Ruminant Digestive System

Queensland Department of Agriculture,

Fisheries and Forestry, Tick Fever Centre,

Stephen R. Collett, BSc, BVSc,

Wacol, Queensland, Australia

MMedVet

Blood Parasites: Babesiosis

Clinical Associate Professor, Department
of Population Health, College of Veterinary

Samuel C. Cartner, DVM, PhD,

Medicine, University of Georgia, Athens,

DA CLAM

GA

Assistant Vice President for Animal

Biosecurity; Sudden Death Syndrome of

Research Services and Director, Animal

Broiler Chickens

Resources Program, University of Alabama, Birmingham, AL

Michael T. Collins, DVM, PhD, DACVM

Euthanasia

Professor of Microbiology, Department of

Pathobiological Sciences, School of Vet

Chr istopher K. Cebra, VMD, MA, MS,
erinary Medicine, University of Wisconsin,

DACVIM

Madison, WI

Professor, Large Animal Medicine, College

Paratuberculosis
of Veterinary Medicine, Oregon State

University, Corvallis, OR

Peter D. Constable, BVSc (Hons), MS,

He'J)atic Lipidosis: Pregnancy Toxemia

PhD,DACVIM
in Cows

Dean, College of Veterinary Medicine,

University of Illinois, Urbana, IL

Sharon A. Center, BS, DVM, DACVIM

Professor, Department of Clinical Sci

Abdominal Fat Necrosis; Acute Intes
ences, College of Veterinary Medicine,
tinal Obstructions in Large Animals;

Cornell University, Ithaca, NY

Bovine Secondary Recumbency; Coccidiosis; Cryptosporidiosis; Diseases of He'J)atic Disease in Small Animals
the Abomasum; Disorders of Potassium

CONTRIBUTORS
xxi

Metabolism; Diseases of the Ruminant

Gary L Cromwell, PhD

Forestomach: Bloat in Ruminants, Grain

Professor, Department of Animal and

Overload, Simple Indigestion, Traumatic

Food Sciences, University of Kentucky,

Reticuloperitonitis, Vagal Indigestion

Lexington, KY

Syndrome; Infectious Diseases of the Uri

VetBooks.ir
nary System in Large Animals: Bovine

Iron Toxicity in Newborn Pigs; Nutri

Cystitis and Pyelone'J)hritis
tion: Pigs

Rhian B. Cope, BVSC, PhD, DABT,

Suzanne M. Cunningham, DVM,

ERT,FACTRA

DACVIM (Cardiology)

Toxicology Section, Office of Scientific

Assistant Professor of Cardiology, Depart

Evaluation, Therapeutic Goods Adminisment of Clinical Sciences, Cummings tration of Australia, Symonston, Australian School of Veterinary Medicine, Tufts Capital Territory, Australia

University, North Grafton, MA

Cyanide Poisoning; Smoke Inhalation;

Cardiovascular System Introduction;

Toxicologic Hazards in the Workplace

Thrombosis, Embolism, and Aneurysm

Robert W. Coppock, DVM, MS, PhD,

Andrew Dart, BVSc, PhD, DACVS,

DABVT,DABT

DECVS

President and CEO, Robert W. Coppock,

Director of the Research and Clinical

DVM, Toxicologist and Associate Ltd.,

Training Unit, Faculty of Veterinary Sci

Vegreville, Alberta, Canada
ence, The University of Sydney, New South

Wales, Australia

Persistent Halogenated Aromatic Poisoning

Congenital and Inherited Anomalies

Susan M. Cotter, DVM, DACVIM

Autumn P. Davidson, DVM, MS, DACVIM

(Small Animal, Oncology)

Clinical Professor, School of Veterinary

Distinguished Professor of Clinical Sci

Medicine, University of California, Davis, CA
ences Emerita, Cummings School of Veterinary Medicine, Tufts University, North Management of Re'J)roduction: Small

Grafton, MA

Animals; Management of the Neonate:

Small Animals; Re'J)roductive Diseases of

Blood Groups and Blood Transfusions;
the Male Small Animal

Hematopoietic System Introduction;

Hemostatic Disorders

Peter R- Davies, BVSc, PhD

Professor, Swine Health and Production,

Laurent L. Couetil, DVM, PhD,

Department of Veterinary Population

DACVIM (Large Animal)

Medicine, College of Veterinary Medicine,

Professor, Department of Veterinary Clini

University of Minnesota, St. Paul, MN
cal Sciences, College of Veterinary Medicine, Purdue University, West Lafayette, IN Exudative Epidermitis; Parakeratosis; Pityriasis Rosea in Pigs; Swine Vesicular

Pulmonary Emphysema

Disease; Vesicular Exanthema of Swine

Kate E. Creevy, DVM, MS, DACVIM

Sherrill Davison, VMD, MS, MBA,

Associate Professor of Internal Medicine,

DACPV

Department of Small Animal Medicine and

Associate Professor, Laboratory of Avian

Surgery, College of Veterinary Medicine,

Medicine and Pathology, School of Veteri

University of Georgia, Athens, GA
nary Medicine, University of Pennsylvania,

Canine Distemper; Canine Herpesviral

Kennett Square, PA

Infection; Infectious Canine He'J)atitis

Salmonelloses (Poultry)

Rocio Crespo, DVM, MSc, DVSc,

Scott A. Dee, DVM, MS, PhD

DACPV

Director of Research, Pipestone Applied

Associate Professor and Director,

Research, Pipestone Veterinary Services,

Avian Health and Food Safety Laboratory,

Pipestone, MN

Washington Animal Disease Diagnostic

Laboratory, Washington State University,

Infectious Diseases of the Uri:nary System

Pullman, WA
in Large Animals: Porcine Cystitis

Pyelonephritis Complex; Porcine Repro

Miscellaneous Conditions of Poultry:

ductive and Respiratory Syndrome;

Urate De'J)osition (Gout)

Pseudorabies; Respiratory Diseases of Pigs
xxii

CONTRIBUTORS

Alice Defarges, DVM, MSc, DACVIM

Systemic Pharmacotherapeutics of the

Assistant Professor in Internal Medicine,

Monogastric Digestive System; Systemic

Department of Clinical Studies, Ontario

Pharmacotherapeutics of the Muscular

Veterinary College, University of Guelph,

System; Systemic Pha1macotherapeutics

Ontario, Canada
of the Respiratory System; Systemic Phar

VetBooks.ir

Diseases of the Stomach and Intestines in macotherapeutics of the Urinary System Small Animals: Colitis in Small Animals,

Constipation and Obstipation in Small

Michael W. Dryden, DVM, PhD, DACVM

Animals, Inflammatory Bowel Disease in University Distinguished Professor of Small Animals

Veterinary Parasitology, Diagnostic

Medicine/Pathobiology, College of

Sagi Denenberg, DVM, DACVB,

Veterinary Medicine, Kansas State

DECAWBM (Behaviour), MACVSc

University, Manhattan, KS

(Behaviour)

Ectoparasiticides: Ectoparasiticides

North Toronto Veterinary Behaviour Spe

Used in Small Animals; Fleas and Flea
cialty Clinic, Thornhill, Ontario, Canada

Allergy Dermatitis; Mange: Mange in

Normal Social Behavior and Behavioral

Dogs and Cats

Problems of Domestic Animals

J.P. Dubey, MVSc, PhD

R. Page Dinsmore, DVM

Microbiologist, Animal Parasitic Dis

Associate Professor, Department of Clinieases Laboratory, Beltsville Agricultural cal Sciences, College of Veterinary Medi

Research Center, USDA, Beltsville, MD
cine and Biomedical Sciences, Colorado

State University, Fort Collins, CO

Toxoplasmosis

Health-Management Interaction: Dairy

Rebecca S. Duerr, DVM, MPVM, PhD

Cattle

Staff Veterinarian, International Bird Rescue Research Center, Cordelia, CA Stephen J. Divers, BVetMed, DZooMed,

DACZM, DECZM (Herpetology),

Management of the Neonate: Care

FR CVS
of Orphaned Native Birds and

Professor of Zoological Medicine, Depart

Mammals
ment of Small Animal Medicine and

Surgery, College of Veterinary M,edicine,

John Dunn, DVM, PhD

University of Georgia, Athens, GA

Veterinary Medical Officer, Avian Disease
and Oncology Laboratory, USDA-ARS,

Reptiles

East Lansing, MI

Thomas J. Divers, DVM, DACVIM,

Neoplasms (Poultry)

DACVECC

Professor of Medicine, Department of

Jack Easley, DVM, MS, DABVP

Clinical Sciences, College of Veterinary

(Equine)

Medicine, Cornell University, Ithaca, NY

Equine Veterinary Practice, LLC,

Leptospirosis: Horses, Ruminants,

Shelbyville, KY

Swine; Noninfectious Diseases of the

Dentistry: Dentistry in Large Animals

Urinary System in Large Animals

Scott H. Edwards, BSc, BVMS, PhD,

Thomas M. Donnelly, BVSc, DVP,

MANZCVSc

DACLAM,DABVP(ECM)

Senior Lecturer, Veterinary Pharmacology,

The Kenneth S. Warren Institute, Ossining,

Charles Sturt University, Wagga Wagga,

NY; Adjunct Associate Professor, Cum

New South Wales, Australia
mings School of Veterinary Medicine, Tufts

University, North Grafton, MA

Anti-injl,ammat01y Agents

Rodents

Steve M. Ensley, DVM, PhD

Patricia M. Dowling, DVM, MSc,

Veterinary Toxicologist, Veterinary

DACVIM, DACVCP

Diagnostic and Production Animal

Professor, Veterinary Clinical Pharma

Medicine, College of Veterinary
cology, Western College of Veterinary

Medicine, Iowa State University,

Medicine, University of Saskatchewan,

Ames,IA

Saskatoon, Canada

Toxicology Introduction

CONTRIBUTORS
xxiii

Ronald J. Erskine, DVM, PhD

Mark T. Fox, BVetMed, PhD, DEVPC,

Professor, Large Animal Clinical Sciences,

FHEA,MRCVS

College of Veterinary Medicine, Michigan

Professor of Veterinary Parasitology,

State University, East Lansing, MI

Department of Pathology and Pathogen

VetBooks.ir

Mastitis in Large Animals

Biology, The Royal Veterinary College,

University of London, UK

Paul Ettestad, DVM, MS

Gastrointestinal Parasites of Ruminants

State Public Health Veterinarian, Epidemiology and Response Division, New Mexico Ruth Francis-Floyd, DVM, MS, DACZM

Department of Health, Santa Fe, NM

Professor, Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Plague

University of F1orida, Gainesville, FL

Timothy M. Fan, DVM, PhD, DACVIM

Aquaculture; Aquarium Fishes; Aquatic

Associate Professor, Department of Veteri

Systems
nary Clinical Medicine, College of Veterinary

Medicine, University of Illinois, Urbana, IL

Robert M. Friendship, DVM, MSc,

DAB VP

Canine Lymphoma

Professor, Department of Population Medicine, Ontario Veterinary College, Univer

Susan E. Fielder, DVM, MS, DACVP
sity of Guelph, Ontario, Canada

(Clinical Pathology)

Clinical Assistant Professor, Department

Gastrointestinal Ulcers in Large Ani
of Pathobiology, Center for Veterinary
mals: Gastric Ulcers in Pigs; Health

Health Sciences, Oklahoma State Univer

Management Interaction: Pigs
sity, Stillwater, OK

Laurie J. Gage, DVM, DACZM

Reference Guides

Big Cat and Marine Mammal Specialist,

USDA APHIS Animal Care, Center for

Scott D. Fitzgerald, DVM, PhD,

Animal Welfare, Napa, CA

DACVP, DACPV

Management of the Neonate: Care of

Professor, Department of Pathobiology

Orphaned Native Birds and Mammals
and Diagnostic Investigation, College of

Veterinary Medicine, Michigan State Uni

Maricarmen Garcia, PhD
versity, East Lansing, MI

Associate Professor, Poultry Diagnostic

Congenital and Inherited Anomalies
and Research Center, Department of Popu
of the Urinary System; West Nile Virus
lation and Health, University of Georgia,

Infection in Poultry

Athens, GA

Infectious Laryngotracheitis

Sherrill A. Fleming, DVM, DACVIM,

DAB VP

Tam Garland, DVM, PhD, DABVT

Associate Professor, Food and Animal

Veterinary Medical Diagnostic Laboratory,

Medicine, College of Veterinary Medicine,

Texas A&M University, College Station, TX

Mississippi State University, Mississippi

State, MS

Arsenic Poisoning; Gossypol Poisoning

Pasteurellosis of Sheep and Goats

Jack M. Gaskin, DVM, PhD, DACVM

Associate Professor Emeritus, Department

Janet E. Foley, DVM, PhD
of Infectious Disease and Pathology, Col

Professor, Department of Medicine and
lege of Veterinary Medicine, University of

Epidemiology; Co-Director, Center for

F1orida, Gainesville, FL

Vector-Borne Disease, School of Veterinary

Medicine, University of California, Davis, CA Encephalomyocarditis Virus Infection Tularemia

Kirk N. Gelatt, VMD, DACVO

Emeritus Distinguished Professor, Depart

Jonathan H. Foreman, DVM, MS,
ment of Small Animal Clinical Sciences,

DACVIM (Large Animal)

College of Veterinary Medicine, University

Associate Dean, Professor, College of
of F1orida, Gainesville, FL

Veterinary Medicine, University of Illinois,

Urbana, IL

Neoplasia of the Eye and Associated

Structures; Ophthalmic Emergencies;

Hepatic Disease in Large Animals

Ophthalmology
xxiv

CONTRIBUTORS

Richard W. Gerhold, DVM, MS, PhD

Louis Norman Gotthelf, DVM

Department of Biomedical and Diagnostic

Animal Hospital of Montgomery; Mont

Sciences, College of Veterinary Medicine,
gomery Pet Skin and Ear Clinic, Montgom

University of Tennessee, Knoxville, TN
ery, AL

Coccidiosis (Poultry); Cryptosporidiosis

Tumors of the Ear Canal

VetBooks.ir

(Poultry); Trichomonosis

Marcelo Gottschalk, DVM, PhD

E. Paul J. Gibbs, BVSc, PhD, FRCVS

Professor, College of Veterinary Medicine,

Professor Emeritus, College of Veterinary

University of Montreal, St-Hyacinthe,

Medicine, University of Florida, Gaines

Quebec, Canada
ville, FL

Streptococcal Injections in Pigs

Pox Diseases

Gregory F. Grauer, DVM, MS, DACVIM

Thomas W. G. Gibson, BSc, BEd, DVM,

Professor and Jarvis Chair of Small Animal

DVSc, DACVS

Internal Medicine, Department of Clinical

Assistant Professor of Small Animal

Sciences, College of Veterinary Medicine,

Surgery, Department of Clinical Studies,

Kansas State University, Manhattan, KS

Ontario Veterinary College, University of

Guelph, Ontario, Canada

Ethylene Glycol Toxicity

Diseases of the Stomach and Intestines in

Deborah S. Greco, DVM, PhD, DACVIM

Small Animals: Gastric Dilation and Vol

Senior Research Scientist, Nestle Purina
vulus in Small Animals, Gastrointestinal

PetCare, New York, NY

Obstruction in Small Animals

The Pituitary Gland

Robert 0. Gilbert, BVSc, MMedVet,

Paul R. Greenough, FRCVS

DACT,MRCVS

Professor Emeritus of Veterinary Surgery,

Professor, Reproductive Medicine, Depart

Western College of Veterinary Medicine,
ment of Clinical Sciences, College of

University of Saskatchewan, Saskatoon,

Veterinary Medicine, Cornell University,

Canada

Ithaca, NY

Lameness in Cattle

Metritis in Large Animals; Retained Fetal

Membranes in Large Animals; Systemic

Tara L. Grinnage-Pulley, DVM, PhD

Pharmacotherapeutics of the Re-pro-

Adjunct Lecturer and Postdoctoral
ductive System; Uterine Prolapse and

Research Fellow, Department of Epidemi

Eversion; Vaginal and Cervical Prolapse;
ology, College of Public Health, University

Vulvitis and Vaginitis in Large Animals
of Iowa, Iowa City, IA

Sabine Gilch, PhD

Blood Parasites: Trypanosomiasis

Assistant Professor, Veterinary Medicine,

University of Calgary, Alberta, Canada

Walter Gruenberg, DMV, MS, PhD,

DECAR, DECBHM

Chronic Wasting Disease

Assistant Professor, Department of

Farm Animal Health, Utrecht University,

Eric Gonder, DVM, MS, PhD, DACPV

Utrecht, The Netherlands

Veterinarian, Butterball LLC, Goldsboro,

NC; Adjunct Professor, Department of

Colisepticemia; Disorders of Phosphorus

Population Health and Pathobiology,

Metabolism; Dystrophies Associated with

College of Veterinary Medicine, North

Calcium, Phosphorus, and Vitamin D;

Carolina State University, Raleigh, NC

Hepatic Lipidosis: Fatty Liver Disease of

Cattle; Intestinal Diseases in Ruminants;

Miscellaneous Conditions of Poultry:

Salmonellosis

Pendulous Crop

P. K. Gupta, PhD, Post Doc (USA),

Sonya G. Gordon, DVM, DVSc,

PGDCA, MSc VM & AH BVSc, FNA

DACVIM (Cardiology)

VSc, FASc, AW, FST, FAEB, FACVT

Associate Professor, Department of Small

(USA), Gold Medalist

Animal Clinical Sciences, Texas A&M

Editor-in-Chief, Toxicology International,

University, College Station, TX

Bareilly-lndia

Systemic Pharmacotherapeutics of the

Herbicide Poisoning; Pentachlorophenol

Cardiovascular System

Poisoning

CONTRIBUTORS
xxv

Ramesh C. Gupta, DVM, MVSc, PhD,

R. Reid Hanson, DVM, DACVS,

DABT, FACT, FACN, FATS

DACVECC

Professor and Head, Toxicology Depart

Professor of Equine Surgery, Department
ment, Breathitt Veterinary Center, Murray
of Clinical Sciences, College of Veterinary

State University, Hopkinsville, KY

Medicine, Auburn University, Auburn, AL

VetBooks.ir

Insecticide and Acaricide (Organic)

Congenital and Inherited Anomalies

Toxicity
of the Musculoskeletal System; Equine

Emergency Medicine: Thermal Injuries

James S. Guy, DVM, PhD

Professor, Department of Population

Joseph Harari, MS, DVM, DACVS

Health and Pathobiology, College of

Veterinary Surgeon, Veterinary Surgical

Veterinary Medicine, North Carolina State

Specialists, Spokane, WA

University, Raleigh, NC

Arthropathies and Related Disorders

Coronaviral Enteritis of Turkeys; Viral
in Small Animals; Lameness in Small

Encephalitides

Animals; Myopathies in Small Animals;

Osteopathies in Small Animals

Sharon M. Gwaltney-Brant, DVM, PhD,

DABVT,DABT

Billy M. Hargis, DVM, PhD

Toxicology Consultant, Veterinary Infor

Professor and Director, JKS Poultry Health
mation Network and Adjunct Faculty,

Research Laboratory, University of Arkan

College of Veterinary Medicine, University
sas; Tyson Sustainable Poultry Health
of Illinois, Urbana, IL

Chair, Department of Poultry Science,

Food Hazards; Household Hazards;

University of Arkansas, Fayetteville, AR

Snakebite; Toad Poisoning

Miscellaneous Conditions of Poultry:

Ascites Syndrome; Necrotic Enteritis;

Carlton L. Gyles, DVM, PhD

Spontaneous Cardiomyopathy of Turkeys

Professor Emeritus, Department of

Pathobiology, Ontario Veterinary College,

University of Guelph, Ontario, Canada

D. L. Hank Harris, DVM, PhD

Professor, Department of Animal Science,

Edema Disease

Iowa State University, Ames, IA

Caroline N. Hahn, DVM, MSc, PhD,

Intestinal Diseases in Pigs

DECEIM,DECVN,MRCVS

Senior Lecturer in Veterinary Clinical

Lynette A. Hart, PhD

Neuroscience, Royal (Dick) School of Vet

Professor, Population Health and Reproerinary Studies, University of Edinburgh, duction, School of Veterinary Medicine,

Midlothian, UK

University of California, Davis, CA

Dysautonomia

The Human-Animal Bond

Edward J. Hall, MA, VetMB, PhD,

Joe Hauptman, DVM, MS, DACVS

DECVIM-CA

Professor of Surgery, College of Veterinary

Professor of Small Animal Internal Medi

Medicine, Michigan State University, East
cine, Department of Clinical Veterinary

Lansing, MI

Science, University of Bristol, Bristol, UK

Diaphragmatic Hernia

Diseases of the Stomach and Intestines in

Small Animals: Malabsorption Syndromes

Jan F. Hawkins, DVM, DACVS
in Small Animals

Associate Professor, Veterinary Clinical

Sciences, School of Veterinary Medicine,

Jean A. Hall, DVM, PhD, DACVIM

Purdue University, West Lafayette, IN

Professor, Department of Biomedical

Diseases of the Esophagus in Large

Sciences, College of Veterinary Medicine,

Animals; Diseases of the Mouth in

Oregon State University, Corvallis, OR

Large Animals; Pharyngeal Paralysis;

Disorders of Calcium Metabolism: Puer

Pharyngitis
peral Hypocalcemia in Small Animals

Marcus J. Head, BVetMed, MRCVS

Jeffery 0. Hall, DVM, PhD, DABVT

Senior Associate, Rossdales Equine Hospi

Professor and Head of Diagnostic Toxicoltal and Diagnostic Centre, Newmarket, UK
ogy, Utah State University, Logan, UT

Lameness in Horses: Disorders of the

Selenium To:ricosis

Shoulder and Elbow
xxvi

CONTRIBUTORS

J. Jill Heatley, DVM, MS, DACZM,

Frederic J. Hoerr, DVM, PhD, DACVP,

DABVP (Avian)

DACPV

Associate Professor, Zoological Medicine,

Pathologist, Veterinary Diagnostic Pathol

College of Veterinary Medicine, Texas
ogy, LLC, Fort Valley, VA

VetBooks.ir

A&M University, College Station, TX

Aspergillosis; Miscellaneous Conditions of

Vaccination of Exotic Mammals

Poultry: Breast Blisters, Breast Buttons,

Cannibalism; Mycotoxicoses (Poultry)

Charles M. Hendrix, DVM, PhD

Professor, Department of Pathobiology,

Timothy N. Holt, DVM

College of Veterinary Medicine, Auburn

Associate Professor, Clinical Sciences,

University, Auburn, AL

Livestock Medicine and Surgery, College

CNS Diseases Caused by Helminths and
of Veterinary Medicine and Biomedical

Arthropods; Diagnostic Procedures for

Sciences, Colorado State University, Fort
the Private Practice Laboratory: Parasi

Collins, CO
tology; Flies; Venomous Arthropods

Bovine High-Mountain Disease

Thomas H. Herdt, DVM, MS, DACVN,

Sharman M. Hoppes, DVM, ABVP

DACVIM

(Avian)

Professor, Department of Large Animal

Clinical Associate Professor, Zoological

Clinical Sciences and Diagnostic Center

Medicine, Department of Veterinary Small
for Population and Animal Health, College

Animal Clinical Sciences, Texas A&M
of Veterinary Medicine, Michigan State

University, College Station, TX

University, East Lansing, Ml

Pet Birds

Ketosis in Cattle; Nutrition: DainJ Cattle Michael J. Huerkamp, DVM, DACLAM

Laurie Hess, DVM, DABVP

Director, Division of Animal Resources;

Veterinary Center for Birds & Exotics,

Professor, Pathology and Laboratory Medi

Bedford Hills, NY
cine, Emory University, Atlanta, GA

Sugar Gliders

Laboratory Animals

Michael Hess, DMV

Martin E. Hugh-Jones, VetMB, MPH,

Clinic for Poultry and Fish Medicine,
fhD,MRCVS

Department for Farm Animals and

Professor Emeritus, School of Veterinary

Veterinary Public Health, Urµversity of

Medicine, Louisiana State University,

Veterinary Medicine, Vienna, Austria

Baton Rouge, LA

Avian Spirochetosis; Miscellaneous

Anthrax

Conditions of Poultry: Fluke Infections

Staci Hutsell, DVM

Hugh Hildebrandt, DVM

Resident, Maddie's Shelter Medicine

Medford Veterinary Clinic, Medford, WI

Program, College of Veterinary Medicine,

Mink

University of Florida, Gainesville, FL

Feline Infectious Peritonitis

W. Mark Hilton, DVM, DABVP

Clinical Associate Professor, Veterinary

Basil 0. Ikede, BVetMed, DVM, PhD,

Clinical Sciences, School of Veterinary Med

FCVSN
icine, Purdue University, West Lafayette, IN

Retired Professor and Chair, Department

Health-Management Interaction: Beef
of Pathology and Microbiology, Atlantic

Cattle; Nutrition: Beef Cattle

Veterinary College, University of Prince

Edward Island, Charlottetown, Prince

Edward Island, Canada

Katrin Hinrichs, DVM, PhD, DACT

Professor and Patsy Link Chair in Mare

Bovine Petechial Fever

Reproduction, Department of Veterinary

Physiology and Pharmacology, College

Peter G. G. Jackson, MA, BVM&S,
of Veterinary Medicine and Biomedical

DVM&S, FRCVS

Sciences, Texas A&M University, College

St. Edmund's College, University of

Station, TX

Cambridge, Cambridge, UK

Cloning of Domestic Animals

Prolonged Gestation in Cattle and Sheep

CONTRIBUTORS
xxvii

Daral J. Jackwood, PhD

Peter D. Kirkland, BVSc, PhD

Professor, Department of Veterinary

Senior Principal Research Scientist,

Preventive Medicine, Ohio Agricultural

Officer-in-Charge, Virology Laboratory,

Research and Development Center, The

Elizabeth Macarthur Agricultural

Ohio State University, Wooster, OH

Institute, Menangle, New South Wales,

VetBooks.ir

_Infectious Bursal Disease

Australia

Congenital and Inherited Anomalies:

Mark W. Jackwood, PhD

Akabane Virus Infection

Professor, Department of Population

Health, College of Veterinary Medicine,

Mark D. Kittleson, DVM, PhD,

University of Georgia, Athens, GA

DACVIM (Cardiology)

BordeteUosis

Professor Emeritus, School of Veterinary

Medicine, University of California,

Davis, CA

Eugene D. Janzen, DVM, MVS

Professor, Production Animal Health,

Heart Disease and Heart Failure

Faculty of Veterinary Medicine, University
of Calgary, Alberta, Canada

Kirk C. Klasing, BS, MS, PhD

Histophilosis; Lightning Stroke and

Professor of Animal Biology, Department

Electrocution; Trichomoniasis
of Animal Science, University of California, Davis, CA LaRue W. Johnson, DVM, PhD

Nutrition and Management: Nutritional

Professor Emeritus, College of

Requirements of Poultri.J

Veterinary Medicine and Biomedical

Sciences, Colorado State University,

Thomas R. Klei, PhD

Fort Collins, CO

Boyd Professor and Associate Dean for

Llamas and Alpacas

Research and Advanced Studies, School
of Veterinary Medicine and Louisiana

Agricultural Experiment Station, Louisiana

Richard C. Jones, BSc, PhD, DSc,

State University, Baton Rouge, LA

FRCPath

Emeritus Professor, School of Veterinary

Gastrointestinal Parasites of Horses;

Science, University of Liverpool, Leahurst, Helminths of the Skin Neston, Wirral, UK

Malabsorption Syndrome; Viral Arthritis

Nick J. Knowles, MPhil

Head of Molecular Epidemiology Section,

Vesicular Disease Reference Laboratory,

Maureen H. Kemp, BVMS, MVM, PhD,

The Pirbright Institute, Woking, Surrey, UK

DCHP,MRCVS

Wern Veterinary Surgeons, Wales, UK

Teschovirus Encephalomyelitis

Laryngeal Disorders

Alexandre Kreiss, BVSc, PhD

Research Fellow, Menzies Research Insti

Robert J. Kemppainen, DVM, PhD
tute Tasmania, University of Tasmania,

Professor, Department of Anatomy,

Australia

Physiology & Pharmacology, College of

Veterinary Medicine, Auburn University,

Tasmanian Devils

Aubum,AL

Endocrine System Introduction; Neuro

Janice E. Kritchevsky, VMD, MS,
endocrine Tissue Tumors

DACVIM

Professor, Large Animal Medicine, Department of Veterinary Clinical Sciences, Safdar A. Khan, DVM, MS, PhD,

School of Veterinary Medicine, Purdue

DABVf

University, West Lafayette, IN

Director of Toxicology Research, ASPCA

Animal Poison Control Center, Urbana,

Equine Metabolic Syndrome;

Illinois

The Pituitary Gland: Hirsutism

Associated with Adenomas of the

Rodenticide Poisoning; Strychnine

Pars Intermedia; The Thyroid Gland:

Poisoning; Toxicities from Human

Non-neoplastic Enlargement of the

Drugs

Thyroid Gland

:xviii

CONTRIBUTORS
tomas G. Ksiazek, DVM, PhD

D. Bruce Lawhorn, DVM, MS
ofessor, Department of Pathology, Univer

Relief Veterinarian; Veterinary Informa

Y of Texas Medical Branch, Galveston, TX
tion Network Swine Consultant, College
imean-Congo Hemorrhagic Fever;

Station, TX

,pah Virus Infection

Potbellied Pigs

VetBooks.ir
ed F. Kuehn, DVM, MS, DACVIM

Andrea S. Lear, DVM

!Ction Chief, Internal Medicine, Michigan

Clinical Instructor, Department of Large

!terinary Specialists, Southfield, MI

Animal Clinical Sciences, College of

3spiratory Diseases of Small Animals;

Veterinary Medicine, The University of

3spiratory System Introduction

Tennessee, Knoxville, TN
iahesh C. Kumar, BVSc, MS, PhD,

Bluetongue; Congenital and Inherited

ACPV

Anomalies: Border Disease; Malig
onsultant, Poultry Health & Food Safety,
nant Catarrhal Fever; Sporadic Bovine
t. Cloud, MN

Encephalomyelitis
issecting Aneurysm in Turkeys

Margie D. Lee, DVM, PhD

Professor of Population Health, Poultry
iina Yu-Hsin Kung, PhD, MSc, BVSc,

Diagnostic and Research Center, College

,VM
of Veterinary Me(iicine, University of Georrincipal Veterinary Epidemiologist, gia, Athens, GA

.nimal Biosecurity and Welfare Program,
lepartment of Agriculture, Fisheries

Avian Campylobacter Infection
nd Forestry, Biosecurity Queensland,

!ueensland, Australia

Steven Leeson, PhD

Professor Emeritus, University of Guelph,
lendra Virus Infection

Ontario, Canada
ifichelle A. Kutzler, DVM, PhD, DACT

Fatty Liver Hemorrhagic Syndrome;
lanfield Professor of Companion Animal

Nutrition and Management: Nutritional
ndustries, Department of Animal and

Deficiencies in Poultry
langeland Sciences, Oregon State Univer

;ity, Corvallis, OR

MichaelL.Levin,PhD

"Janine Transmissible Venereal Tumor;

Medical Entomology Laboratory Director,
kfammary Tumors; Prostatic Diseases

Rickettsial Zoonoses Branch, Centers for

Disease Control and Prevention, Atlanta, GA

�atalie A. Kwit, DVM, MPH

Ticks
ri'oot-and-Mouth Disease

Julie K. Levy, DVM, PhD, DACVIM

Gary M. Landsberg, BSc, DVM,

Department of Small Animal Clinical Sci

MRCVS,DACVB,DECAWBM
ences, College of Veterinary Medicine, and

Veterinary Behaviourist, North Toronto

Director, Maddie's Shelter Medicine Pro

Veterinary Behaviour Specialty Clinic,
gram, University of F1orida, Gainesville, FL

Thomhill,Ontario,Canada

Feline Infectious Peritonitis; Feline

Behavioral Medicine Introduction;

Leukemia Virus and Related Diseases

Normal Social Behavior and Behavioral

Problems of Domestic Animals

Michel Levy, DVM, DACVIM

Thomas J. Lane, BS, DVM

Professor, Department of Veterinary Clini

Professor Emeritus, University of Florida,
cal and Diagnostic Sciences, University of

Gainesville, FL

Calgary, Alberta, Canada

Health-Management Interaction: Horses

Polioencephalomalacia

Jimmy C. Lattimer, DVM, MS, DACVR, Alicja E. Lew-Tabor, BSc (Hons), PhD

DACVRO

Principal Research Fellow, Queensland

Associate Professor (Radiology and Radia

Alliance for Agriculture & Food Innovation Oncology), Veterinary Medicine and tion, The University of Queensland,

Surgery, College of Veterinary Medicine,

Brisbane, Queensland, Australia

University of Missouri, Columbia, MO

Blood Parasites: Anaplasmosis; Enteric

Diagnostic Imaging; Radiation Therapy

Campylobacteriosis

CONTRIBUTORS
xxix

David H. Ley, DVM, PhD

Ingrid Lorenz, DMV, DMVH, DECBHM

Professor, Department of Population

Lecturer in Bovine Medicine, School of

Health and Pathobiology, College of

Agriculture, Food Science and Veterinary

Veterinary Medicine, North Carolina State

Medicine, University College Dublin, Ireland

VetBooks.ir

University, Raleigh, NC

Diseases of the Ruminant Forestomach:

Mycoplasmosis

Ruminal Drinking, Ruminal Parakerato
sis, Subacute Ruminal Acidosis

HuiChu Lin, DVM, MS, DACVAA

Professor, Large Animal Anesthesia,

Jodie Low Choy, BVSc, BVMS, IVAS

Department of Clinical Sciences, College

Cert
of Veterinary Medicine, Auburn University, Menzies School of Health Research; Auburn,AL

University Avenue Veterinary Hospital,

Malignant Hyperthermia

Durack, Northern Territory, Australia

Melioidosis

Dana Lindemann, DVM

Resident, Illinois Zoological and Aquatic

Katharine F. Lunn, BVMS, MS, PhD,

Animal Residency Program, Wildlife

MRCVS, DACVIM

Epidemiology Laboratory, College of

Associate Professor, Department of

Veterinary Medicine, University of Illinois

Clinical Sciences, College of Veterinary
at Urbana-Champaign, IL

Medicine, North Carolina State University,

Raleigh, NC

Hedgehogs

Fever of Unknown Origin; Leptospirosis

Andrew Linklater, DVM, DACVECC

Clinical Instructor, Lakeshore Veterinary

Robert J. MacKay, BVSc, PhD

Specialists, Glendale, WI

Professor, Large Animal Medicine, Department of Large Animal Clinical Sciences, Emergency Medicine Introduction;

College of Veterinary Medicine, University

Evaluation and Initial Treatment
of Florida, Gainesville, FL
of the Emergency Patient; Fluid

Therapy; Monitoring the Critically

Equine Protozoal Myeloencephalitis
m Animal; Specific Diagnostics and

Therapy

Charles Mackenzie, BVSc, PhD, ACVM,

AO

Jeanne Lofstedt, BVSc, MS, DACVIM

Professor, Department of Pathobiology

(Large Animal)

and Diagnostic Investigation, Michigan

Professor of Large Animal Internal

State University, East Lansing, MI

Medicine, Department of Health

Besnoitiosis

Management, Atlantic Veterinary College,

University of Prince Edward Island,

Kenneth S. Macklin, MSc, PhD

Charlottetown, Prince Edward Island,

Associate Professor, Department of Poul

Canada
try Science, Auburn University, Auburn,

Caprine Arthritis and Encephalitis

AL

Helminthiasis

Maureen T. Long, DVM, PhD,

DACVIM

John E. Madigan, DVM, MS

Associate Professor, Department of Infec

Distinguished Professor, Department of
tious Diseases and Pathology, College of

Medicine and Epidemiology, School of Vet

Veterinary Medicine, University of Florida,
erinary Medicine, University of California,

Gainesville, FL

Davis, CA

Equine Arboviral Encephalomyelitis;

Equine Granulocytic Ehrlichiosis

Meningitis, Encephalitis, and Encephalomyelitis

Richard A. Mansmann, VMD, PhD

(Hon), DACVIM (Large Animal)

Michael R. Loomis, DVM, MA,

Equine Podiatry & Rehabilitation Practice;

DACZM

Clinical Professor Emeritus, College of

Qhief Veterinarian, North Carolina Zoologi

Veterinary Medicine, North Carolina State
cal Park, Asheboro, NC

University, Raleigh, NC

Zoo Animals

?repurchase Examination of Horses
xxx

CONTRIBUTORS

Steven L. Marks, BVSc, MS, MRCVS,

Mushtaq A. Memon, BVSc, PhD, DACT

DACVIM

Theriogenologist, Department of Vet

Clinical Professor of Emergency and Intererinary Clinical Sciences, College of nal Medicine; Associate Dean and Director Veterinary Medicine, Washington State VetBooks.ir
of Veterinary Medical Services, College of

University, Pullman, WA

Veterinary Medicine, North Carolina State

University, Raleigh, NC

Reproductive Diseases of the Female

Small Animal

Anemia; Health-Management Interaction: Small Animats Paula I. Menzies, DVM, MPVM,

DECS-RHM

Bret D. Marsh, DVM

Professor, Ruminant Health Management

Indiana State Veterinarian, Indiana

Group, Department of Population Medi

State Board of Animal Health, Indiacine, Ontario Veterinary College, Univernapolis, IN
sity of Guelph, Ontario, Canada

?repurchase Examination of Ruminants Disorders of Calcium Metabolism: Parturiand Swine ent Paresis in Sheep and Goats; Hepatic

Lipidosis: Pregnancy Toxemia in Ewes and

Does; Management of Reproduction: Sheep;

Joerg Mayer, DMV, MSc, DABVP

Posthitis and Vulvitis in Sheep and Goats

(ECM), DECZM (Small Mammal)

Associate Professor of Zoological and

Sandra R. Merchant, DVM, DACVD

Exotic Animal Medicine, Department of

Professor of Dermatology, Department

Small Animal Medicine & Surgery, College
of Veterinary Clinical Sciences, School
of Veterinary Medicine, University of Georof Veterinary Medicine, Louisiana State gia, Athens, GA

University, Baton Rouge, LA

Rabbits

Dermatophytosis

Milton M. McAllister, DVM, PhD,

Joanne B. Messick, VMD, PhD, DACVP

DACVP

Associate Professor of Veterinary Clinical

Associate Professor, School of Animal

Pathology, Department of Comparative
and Veterinary Sciences, University of

Pathobiology, College of Veterinary Medi

Adelaide, Roseworthy, South Australia,
cine, Purdue University, West Lafayette, IN

Australia

Blood Parasites: Hemotropic Mycopuismas

Neosporosis

Samia A. Metwally, DVM, PhD

Senior Animal Health Officer (Virologist),

C. Wayne Mcilwraith, BVSc, PhD, DSc,

AGAH, AGA Division, Food and Agricul

FRCVS, DACVS, DACVSMR
ture Organization of the United Nations,

Department of Clinical Sciences, Oollege

Rome, Italy
of Veterinary Medicine and Biomedical

Sciences, Colorado State University, Fort

Nairobi Sheep Disease

Collins, CO

Patti J. Miller, DVM, PhD

Arthropathies in Large Animats; Lame

Veterinary Medical Officer, Exotic and
ness in Horses: Tendinitis

Emerging Avian Viral Diseases Research,

USDA Agricultural Research Service,

Thomas St. C. McKenna, DVM, PhD

Athens, GA

Assistant Director for New England,

Newcastle Disease and Other Paramyxo

Surveillance, Preparedness and Response
virus Infections: Newcastle Disease

Services, District 1, USDA, APHIS, Veterinary Services, Sutton, MA Kelly D. Mitchell, BSc, DVM, DVSc,

African Horse Sickness

DACVIM

Toronto Veterinary Emergency Clinic,

Scarborough, Ontario, Canada

Jennifer H. McQuiston, DVM, MS

Epidemiology Team Leader, Rickettsial

Diseases of the Stomach and Intestines

Zoonoses Branch, Centers for Disease
in Small Animats: Canine Parvovirus,

Control and Prevention, Atlanta, GA

Feline Enteric Coronavirus, Gastritis in

SmaUAnimats, Hemorrhagic Gastroen

Rickettsial Diseases
teritis in Small Animats

CONTRIBUTORS
xxxi

Harry W. Momont, DVM, PhD, DACT

Derek A. Mosier, DVM, PhD, DACVP

Clinical Associate Professor, Department of

Professor, Department of Diagnostic

Medical Sciences, School of Veterinary Medi

Medicine/Pathology, College of Vetericine, University of W1Sconsin, Madison, WI nary Medicine, Kansas State University,

VetBooks.ir

Reproductive System Introduction

Manhattan, KS

Hemorrhagic Septicemia

Donald R. Monke, DVM, MBA

Vice President, Production Operations,

Select Sires, Inc., Plain City, Ohio

Amelia S. Munsterman, DVM, MS,

DACVS, DACVECC

Seminal Vesiculitis in Bulls

Clinical Instructor, Equine Emergency and

Critical Care, College of Veterinary Medi

James N. Moore, DVM, PhD
cine, Auburn University, Auburn, AL

Distinguished Research Professor, Department of Large Animal Medicine, College Equine Emergency Medicine; Fatigue
of Veterinary Medicine, University of
and Exercise

Georgia, Athens, GA

Colic in Horses

Jeffrey Musser, DVM, PhD

Clinical Associate Professor, Department
of Veterinary Pathobiology, College of Vet

Gaston A. More, MV, DVM
erinary Medicine, Texas A&M University,

Facultad de Ciencias Veterinarias, Labo

College Station, TX
ratorio de Inmunoparasitologia, Universidad Nacional de La Plata, Buenos Aires, Vaccination of Exotic Mammals

Argentina

Sarcocystosis

Sofie Muylle, DVM, PhD

Faculty of Veterinary Medicine, Depart

Karen A. Moriello, DVM, DACVD
ment of Morphology, Ghent University,

Professor of Dermatology, Department of

Salisburylaan, Merelbeke, Belgium

Medical Sciences, School of Veterinary Medi

Dental Development
cine, University of W1Sconsin, Madison, WI

Acantlwsis Nigricans; Atopic Dermatitis; Dusty W. Nagy, DVM, MS, PhD, DACVIM

Congenital and Inherited Anomalies of
the Integumentary System; Cuterebra

Associate Teaching Professor, Department

Infestation in Small Animals; Dermaof Veterinary Medicine & Surgery, College of Veterinary Medicine, University of Mistophilosis; Hygroma; Integumentary System Introduction; Interdigital F'urunsouri, Columbia, MO
culosis; Otitis Externa; Otitis Media a.nd

Bovine Leukosis

Interna; Pyoderma

Teresa Y. Morishita, DVM, MPVM, MS,

T. Mark Neer, DVM, DACVIM

PhD,DACPV

Professor and Hospital Director, Center

Professor of Poultry Medicine & Food Safefor Veterinary Health Sciences, Oklahoma ty, College of Veterinary Medicine, Western

State University, Stillwater, OK

University of Health Sciences, Pomona, CA

Demyelinating Disorders; Motion Sickness

Enterococcosis; Streptococcosis

Robin A. J. Nicholas, MSc, PhD,

James K. Morrisey, DVM, DABVP

FRCPath

(Avian)

Animal Health and Veterinary Laboratories

Service Chief, Companion Exotic Animal

Agency, Addlestone, Surrey, UK

Medicine Service, Department of Clinical

Sciences, College of Veterinary Medicine,

Contagious Agalactia

Cornell University, Ithaca, NY

Ferrets

Paul Nicoletti, DVM, MS, DACVPM

Deceased

W. Ivan Morrison, PhD, BVMS

Professor Emeritus, College of Veterinary

Professor, The Roslin Institute, Royal

Medicine, University of Florida, Gaines

(Dick) School of Veterinary Studies, Univille, FL
versity of Edinburgh, Scotland, UK

Brucellosis in Dogs; Brucellosis in Large

Blood Parasites: Theileriasis

Animals
xxxii

CONTRIBUTORS

Michelle Nie Raghnaill, PhD

Chris Oura, BVetMed, MSc, PhD, MRCVS

Research Fellow, National Academy of

Senior Lecturer in Veterinary Virology,

Science, Canberra, Australia

School of Veterinary Medicine, University
of the West Indies, Champ Fleurs, Trinidad

Pharmacology Introduction: Dosage

VetBooks.ir

Forms and Delivery Systems, Drug

African Swine Fever

Action and Pharmacodynamics, Nanotechnology

Rebecca A. Packer, MS, DVM, DACVIM

(Neurology)

Joeke Nijboer, PhD

Assistant Professor, Neurology/Neurosur

Nutritionist, Rotterdam Zoo, Rotterdam,
gery, Department of Veterinary Clinical

The Netherlands

Sciences, and Department of Basic Medical Sciences, School of Veterinary Medi

Nutrition: Exotic and Zoo Animals
cine, Purdue University, West Lafayette, IN

Donald L. Noah, DVM, MPH, DACVPM

Congenital and Inherited Anomalies of

Associate Professor, Public Health, Col
the Nervous System
lege of Veterinary Medicine, Midwestern

University, Glendale, AZ

Terri Parrott, DVM

Veterinarian, St. Charles Veterinary Hospital,

Public Health Primer

Davenport, FL

Lisa K. Nolan, DVM, PhD

Nonhuman Primates

Dr. Stephen G. Juelsgaard Dean, College of Sharon Patton, MS, PhD

Veterinary Medicine, Iowa State University,

Professor, Department of Comparative

Ames,IA

Medicine, College of Veterinary Medicine,

Colibacillosis

University of Tennessee, Knoxville, TN

Amebiasis; Giardiasis

Kenneth Opengart, MS, DVM, PhD,

DACPV

Susan L. Payne, PhD

Vice President, Live Operations, Keystone

Associate Professor, Veterinary Pathobiology,

Foods, Huntsville, AL

Texas A&M University, College St.ation, TX

Gangrenous Dermatitis

Vaccines and Immunotherapy

Tanja Opriessnig, DMV, PhD

Lisa K. Pearson, DVM, MS, PhD, DACT

The Roslin Institute, University of

Clinical Instructor, Comparative Therio

Edinburgh, Scotland, UK;; Professor,
genology, Department of Veterinary Clinical

Department of Veterinary Diagnostic and

Sciences, College of Veterinary Medicine,

Production Animal Medicine, Iowa State

Washington State University, Pullman, WA

University, Ames, IA

Congenital and Inherited Anomalies of

Erysipelothrix rhusiopathiae Jnfection
the Digestive System

Stephanie R. Ostrowski, DVM, MPVM,

Angela Pelzel-McCluskey, DVM

DACVPM

National Epidemiologist for Equine Dis

Associate Professor, Department of Pathoeases, USDA, APHIS Veterinary Services, biology, College of Veterinary Medicine,

Fort Collins, CO

Auburn University, Auburn, AL

Vesicular Stomatitis

Public Health Primer

Maurice B. Pensaert, DVM, MS, PhD

Emeritus Professor of Animal Virology,

Gary D. Osweiler, DVM, MS, PhD

Faculty of Veterinary Medicine, Ghent

Professor Emeritus, Veterinary Diagnostic

University, Merelbeke, Belgium
and Production Animal Medicine, College
of Veterinary Medicine, Iowa State Univer

Porcine Hemagglutinating Encephalo
sity, Ames, IA
myelitis

Coal-Tar Products Poisoning; Mycotoxi

Andrew S. Peregrine, BVMS, PhD,
coses; Petroleum Product Poisoning

DVM, DEVPC, DACVM

Associate Professor, Department of

Raul E. Otalora, DVM

Pathobiology, Ontario Veterinary College,

Production ManagerNeterinarian, Quail

University of Guelph, Ontario, Canada

International, Inc., Greensboro, GA

Gastrointestinal Parasites of Small

Ulcerative Enteritis

Animals

CONTRIBUTORS
xxxiii

Donald Peter, DVM, MS, DACT

Karen W. Post , DVM, MS, DACVM

Veterinarian/Owner, Frontier Genetics,

Director of Laboratories, Veterinary

Hermiston, OR

Bacteriologist, North Carolina Veterinary

Diagnostic Laboratory System; Consumer

Bovine Genital Campylobacteriosis;

Services, Rollins Animal Disease, Diagnos

VetBooks.ir

Equine Coital Exanthema
tic Laboratory, Raleigh, NC

Christine Petersen, DVM, PhD

Diagnostic Procedures for the Private

Associate Professor, Department of

Practice Laboratory: Clinical Microbiol

Epidemiology, University of Iowa, Iowa
ogy

City, IA

David G. Pugh, DVM, MS, MAg, DACT,

Blood Parasites: Trypanosomiasis

DACVN,DACVM

Department of Pathobiology, College of

Mark E. Peterson, DVM, DACVIM

Veterinary Medicine, Auburn University,

Director of Endocrinology and Nuclear

Aubum,AL

Medicine, Animal Endocrine Clinic, New

York, NY

Nutrition: Goats; Nutrition: Sheep

The Parathyroid Glands and Disorders of

Sarah L. Ralston, VMD, PhD, DACVN

Calcium Metabolism; The Thyroid Gland:

Professor, Department of Animal Sciences,

Hyperthyroidism, Hypothyroidism

School of Environmental and Biological

Sciences, Rutgers University, New Bruns

Barb ara D. Petty, DVM
wick, NJ

North Florida Aquatic Veterinary Services, Nutrition: Horses Fort White, FL

John F. Randolph, DVM, DACVIM

Aquarium Fishes

Professor, Department of Clinical Sciences, College of Veterinary Medicine, James R. Philips, PhD

Cornell University, Ithaca, NY

Associate Professor of Science, Math/

Science Division, Babson College, Babson

Erythrocytosis and Polycythemia

Park, MA

Silke Rautenschlein, DVM, PhD

Air Sac Mite; Ectoparasites of Poultry

Professor, Clinic for Poultry, University of

Veterinary Medicine, Hannover, Germany

Carlos R. F. Pinto, MedVet, PhD,

DACT

Avian Metapneumovirus

Associate Professor, Theriogenology Section, Department of Veterinary Clinical Willie M. Reed, DVM, PhD, DACVP,

Sciences, School of Veterinary Medicine,

DACPV

Louisiana State University, Baton Rouge,

Dean, College of Veterinary Medicine,

LA

Purdue University, West Lafayette, IN

Quail Bronchitis; Turkey Viral Hepatitis

Embryo Transfer in Farm Animals

Philip T. Reeves , BVSc (Hons), PhD,

P aul J. Plummer, DVM, PhD, DACVIM

FA NZCVS

(Large Anim al), DECSRHM

Chief Regulatory Scientist, Veterinary

Department of Veterinary Diagnostic and

Medicines and Nanotechnology, Austra

Production Animal Medicine, College of
lian Pesticides and Veterinary Medicines

Veterinary Medicine, Iowa State Univer

Authority, Canberra, Australia
sity, Ames, IA

Phannacology Introduction: Chemical

Coxiellosis

&sidues in Food and Fiber; Dosage Fonns
and Delivery Systems, Drug Action and

Robert E. Porter, DVM, PhD, DACVP,

Phannacodynamics, Nanotechnology

DACPV

Clinical Professor, Veterinary Popula

Mason V. Reichard, PhD
tion Medicine, College of Veterinary

Associate Professor, Department of Veteri

Medicine, University of Minnesota,
nary Pathobiology, Center for Veterinary

St. Paul, MN

Health Sciences, Oklahoma State University, Stillwater, OK

Perirenal Hemon·hage Syndrome of Turkeys; Poisonings (Poultry) Cattle Grubs; Mange in Large Animals
xxxiv

CONTRIBUTORS

Hugh W. Reid, MBE, BVM&S, DT VM,

Guillermo R. Risatti, MV, MS, PhD

PhD,MRCVS

Associate Professor, Department of Patho

Moredun Research Institute, Pentlands,
biology and Veterinary Science, University

Science Park, Penicuik, UK
of Connecticut, Storrs, CT

VetBooks.ir

Louping nz

Classical Swine Fever

Douglas J. Reinemann, PhD

Narda G. Robinson, DO, DVM, MS

Professor and Chair, Department of

College of Veterinary Medicine and Bio

Biological Systems Engineering, College of logical Sciences, Colorado State Univer

Agricultural and Life Sciences, University
sity, Fort Collins, CO
of Wisconsin, Madison, WI

Complementary and Alternative Veteri

Stray Voltage in Animal Housing
nary Medicine

Christopher D. Reinhardt, BS, MS,

Kursten V. Roderick, DVM

PhD

Cardiology Resident, Cummings School

Assistant Professor and Extension
of Veterinary Medicine, Tufts University,

Feedlot Specialist, Animal Sciences

North Grafton, MA
and Industry, Kansas State University,

Cardiovascular System Introduction;

Manhattan, KS

Thrombosis, Embolism, and Aneurysm

Growth Promotants and Production

Enhancers

Camille Roesch, PhD

Nanosafety Pharmacist Consultant, Aus

Petra Reinhold, DVM, PhD
tralian Pesticides and Veterinary Medi

Friedrich-Loeffler-Institute, Federal
cines Authority, Symonston, Australia

Research Institute for Animal Health, Jena, Pharmaco'logy Introduction: Dosage Germany

Forms and Delivery Systems, Drug

Chlamydiosis

Action and Phmmacodynamics, Nanotechnology

Alexander M. Reiter, DT, DMv, DAVDC,

DEVDC

Peter Rolls, BVSc, MVS

Chief, Dentistry and Oral Surgery Service,

Veterinary Officer, Tick Fever Centre,

Ryan Veterinary Hospital, School.of Veteri

Department of Agriculture, Fisheries and
nary Medicine, University of Pennsylvania, Forestry, Biosecurity Queensland, Waco!, Philadelphia, !'A

Queensland, Australia

Dentistry: Dentistry in Small Animals;

Blood Parasites: Babesiosis

Diseases of the Mouth in Small Animals

Juan E. Romano, DVM, MS, PhD,

DACT

Marcio Garcio Ribeiro, DVM, PhD

Associate Professor, Department of Large

Professor, Infectious Diseases of Domes

Animal Clinical Sciences, College of Vettic Animals, Department of Veterinary erinary Medicine, Texas A&M University,

Hygiene and Public Health, School of

College Station, T_X

Veterinary Medicine and Animal Sciences,

Siio Paulo State University - UNESP, Botu

Hormonal Control of Estrus
catu, Siio Paulo, Brazil

A. Gregorio Rosales, DVM, MS, PhD,

Nocardiosis; Rhodococcosis

DACPV

Vice President of Veterinary Services,

Franklin Riet-Correa, PhD

Aviagen Inc., Huntsville, AL

Professor, Veterinary Hospital, Federal

University of Campina Grande, Patos,

Disorders of the Reproductive System

Paraiba, Brazil

(Poultry)

Cattle Grubs: Lechiguana

Stanley I. Rubin, DVM, MS, DACVIM

Clinical Professor, Department of

Yasuko Rikihisa, PhD

Veterinary Clinical Medicine, College of

Professor, Veterinary Biosciences, The

Veterinary Medicine, University of Illinois,

Ohio State University, Columbus, OH

Urbana, IL

Rickettsial Diseases: Salmon Poisoning

Digestive System Introduction; Diseases

Disease and Elokomin Fluke Fever
of the Rectum and Anus

CONTRIBUTORS
xxxv

Pamela L. Ruegg, DVM, MPVM

Charles M. Scanlan, DVM, PhD

Professor, Department of Dairy Science,

Professor, Department of Veterinary

College of Agricultural and Life Sciences,

Pathobiology, College of Veterinary Medi

University of Wisconsin, Madison, WI
cine and Biomedical Sciences, Texas A&M

Udder Diseases

University, College Station, TX

VetBooks.ir

Meat Inspection

Charles E. Rupprecht, VMD, MS, PhD

Director, LYSSA LLC, Lawrenceville, GA

Karel A. Schat, DVM, PhD

Rabie-s

Professor, Department of Microbiology
and Immunology, College of Veterinary

Bonnie R. Rush, DVM, MS, DACVIM

Medicine, Cornell University, Ithaca, NY

Professor, Equine Internal Medicine, Col

Chicken Anemia Virus Injection
lege of Veterinary Medicine, Kansas State

University, Manhattan, KS

Mary M. Schell, DVM, DABVT, DABT

Respiratory Diseases of Horses

Senior Toxicologist, ASPCA Animal Poison

Control Center, Urbana, Illinois

Y. M. Saif, DVM, PhD

Professor Emeritus, Food Animal Health

Rodenticide Poisoning

Research Program, The Ohio State University, Wooster, OH

David G. Schmitz, DVM, MS, DACVIM

(Large Animal)

Rotaviral Injections in Chickens, Turkeys,

Visiting Associate Professor, Depart-
and Pheasants
ment of Veterinary Large Animal Clinical

Sciences, College of Veterinary Medicine,

Jeremiah T. Saliki, DVM, PhD, DACVM

Texas A&M University, College Station, TX

Professor and Director, Athens Veterinary

Diagnostic Laboratory, University of

Cantharidin Poisoning

Georgia, Athens, GA

Thomas Schubert, DVM, DACVIM,

Peste des Petits Ruminants; Rinderpest

DABVP

Jean E. Sander, DVM, MAM, DACPV

Clinical Professor and Chief of Neurology

Dean, Center for Veterinary Health Sciences,

Service, Small Animal Clinical Sciences,

Oklahoma State University, Stillwater, OK

College of Veterinary Medicine, University
of Florida, Gainesville, FL

Candidiasis; Disposal of Carcasses and

Disinfection of Premises; Omphalitis

Facial Paralysis; Limb Paralysis; Nervous

System Introduction

Sherry Lynn Sanderson, BS, DVM,

PhD, DACVIM, DACVN

James Schumacher, DVM, MS

Associate Professor, Physiology and Phar

Professor, Large Animal Clinical Sciences,
macology, College of Veterinary Medicine,

College of Veterinary Medicine, University

University of Georgia, Athens, GA
of Tennessee, Knoxville, TN

Nutrition: Small Animals; Urinary

Lameness in Horses: Regional

System Introduction

Anesthesia

Yuko Sato, DVM, MS, DACPV

John Schumacher, DVM, MS

Assistant Professor, Veterinary Diagnostic

Professor, Department of Clinical Sci

& Production Animal Medicine, Poultry
ences, College of Veterinary Medicine,

Extension and Diagnostics, Iowa State

Auburn University, Auburn, AL

University, Ames, IA

Lameness in Horses: Regional

Backyard Poultry

Anesthesia

Ashley B. Saunders, DVM, DACVIM

Philip R. Scott, BVM&S, MPhil, DVM&S,

(Cardiology)

DSHP, DECBHM, FHEA, FRCVS

Associate Professor of Cardiology, Depart

Veterinary Clinical Sciences, University of
ment of Small Animal Clinical Sciences,

Edinburgh, Midlothian, UK

College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, Aspiration Pneumonia; Contagious

College Station, TX

Ecthyma; Listeriosis; Mycotic Pneumonia; Respiratory Diseases of Sheep Systemic Pharmacotherapeutics of the
and Goats; Ulcerative Dermatosis of

Cardiovascular System

Sheep
xxxvi

CONTRIBUTORS

Joaquim Segales, DVM, PhD, DECVP,

H. L. Shivaprasad, BVSc, MS, PhD,

DECPHM

DACPV

Facultat de Veterinaria, Departament de

Professor, California Animal Health and

Sanitat i d'Anatomia Animals and Centre

Food Safety Laboratory System, University
de Recerca en Sanitat Animals, Universitat

VetBooks.ir
of California, Tulare, CA

Autonoma de Barcelona, Bellaterra,

Barcelona, Spain

Hemon-hagic Enteritis/Marble Spleen

Disease

Gliisser's Disease; Porcine Circovirus

Diseases

Wayne Simpson, MSc (Microbiology),

BHort Sc, DHort

Patricia L. Sertich, MS, VMD, DACT

Scientist, Endophyte Mycology, Forage

Associate Professor-Clinician Educator,

Improvement Section, AgResearch Lim

Department of Clinical Studies, New
ited, Palmerston North, New Zealand

Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Ryegrass Toxicity

Square, PA

Management of Reproduction: Horses

Annette N. Smith, DVM, MS, DACVIM

Professor, Department of Clinical Sci

Torsten Seuberlich, DMV
ences, College of Veterinary Medicine,

Professor, NeuroCentre, Division of

Auburn University, Auburn, AL

Neurological Sciences, OIE Reference

Neopi,asia of the Nervous System; Paraneo

Laboratories for BSE and Scrapie; Vet
p/,astic Disorders of the Nervous System
suisse Faculty, Department of Clinical

Research and Veterinary Public Health,

Geof W. Smith, DVM, PhD

University of Berne, Berne, Switzer

Associate Professor of Ruminant Mediland
cine, Department of Population Health

Bovine Spongiform Encephalopa.thy
and Pathobiology, College of Veterinary

Medicine, North Carolina State University,

A. S. Shakespeare, BSc (Eng) (Natal),

Raleigh, NC

BVSc (Hons) (Pret), MMedVet (Med)

Actinobacillosis; Actinomycosis

(Pret)

Onderstepoort Veterinary Faculty, Univer

Joan A. Smyth, PhD
sity of Pretoria, South Africa

Director, Connecticut Veterinary Medi

Heartwater
cal Diagnostic Laboratory, Department
of Pathobiology and Veterinary Science,

Linda Shell, DVM, DACVIM (Neurol

University of Connecticut, Storrs, CT
ogy)

Egg Drop Syndrome '76

Professor, Small Animal Internal Medicine, Ross University School of Veterinary Victoria Smyth, PhD

Medicine, Basseterre, Saint Kitts and

Senior Scientific Officer for Avian Virology,

Nevis

Veterinary Sciences Division, Agri-Food

Systemic Pharmacotherapeutics of the
and Biosciences Institute, Belfast, UK

Nervous System

Avian Nephritis Viral Infections

Clifford F. Shipley, DVM, DACT

Arthur M. Spickett, BSc (Hons)

Clinical Associate Professor, Agricultural

Zoology

Animal Care and Use Program and Col

Parasites, Vectors and Vector-borne
lege of Veterinary Medicine, University of

Diseases Programme, ARC-Onderstepoort

Illinois, Urbana, IL

Veterinary Institute, South Africa

Management of Reproduction: Goats

Sweating Sickness

Michael Shipstone, BVSc, FACVSc,

Anna Rovid Spickler, DVM, PhD

DACVD

Veterinary Specialist, Center for Food

Queensland Veterinary Specialists, Bris

Security and Public Health, College of
bane, Queensland, Australia

Veterinary Medicine, Iowa State Univer

Systemic Pharmacotherapeutics of the
sity, Ames, IA

Integumentary System

Zoonoses

CONTRIBUTORS
xxxvii

Sharon J. Spier, DVM, PhD, DACVIM

Jamie Lynn Stewart, DVM

Professor, Department of Medicine and

Department of Veterinary Clinical

Epidemiology, School of Veterinary Medi

Medicine, College of Veterinary Medicine.

cine, University of California, Davis, CA

University of Illinois, Urbana, IL

Disorders of Ca!,eium Metabolism: Hypo

Management of Reproduction: Goats

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ca/.cemic Tetany in Horses; Lymphadenitis and Lymphangitis: Corynebacterium Bruce Stewart-Brown, DVM, DACPV
pseudotuberculosis Infection of Horses

Senior Vice President of Food Safety, Qm
and Cattle
ity, and Live Operations, Perdue Farms,

Salisbury, MD

Richard A. Squires , B VSc (Hons), PhD,

DVR, DACVIM, DECVIM-CA, GCert Ed,

Nutrition and Management Poultry:

MR CVS

Feeding and Management Practices

Head of Veterinary Clinical Sciences,

School of Veterinary and Biomedical Sci

Roger W. Stitch, MS, PhD
ences, James Cook University, Townsville,

Professor of Parasitology, Department of

Australia

Veterinary Pathobiology, College of Veterinary Medicine, University of Missouri, Feline Panleukopenia

Columbia, MO

Ectoparasiticides: Ectoparasiticides

Henry R. Stiimpfli, DVM, DMV, DACVIM

Professor, Large Animal Medicine,

Used in Large Animals

Department of Clinical Studies, Ontario

Veterinary College, University of Guelph,

Michael K. Stoskopf, DVM, PhD, DACZ!

Ontario, Canada

Professor of Wildlife and Aquatic Health,

Director of the Environmental Medicine

Clostridial Diseases

Consortium, College of Veterinary Medicine

North Carolina State University, Raleigh, N(

Jonathan Statham, MA, VetMB, DCHP,

Marine Mammals

MR CVS

Veterinarian, Bishopton Veterinary Group,

North Yorkshire, UK

George M. Strain , PhD

Professor of Neuroscience, Comparative

Cystic Ovary Disease; Management of

Biomedical Sciences, School of Veterina!J

Reproduction: Cattle

Medicine, Louisiana State University,

Baton Rouge, LA

Bryan L. Stegelmeier, DVM, PhD,

Deafness

DACVP

Veterinary Pathologist, Poisonous Plant

Reinhard K. Straubinger, DMVH, PhD

Research Laboratory, USDA-ARS, Logan, UT Professor and Head for Bacteriology and Bracken Fern Poisoning; Sweet Clover

Mycology, Institute for Infectious Dis

Poisoning
eases and Zoonoses, Faculty of Veterinar:

Medicine, Ludwig-Maximilians University

Jorg M. Steiner, DMV, PhD, DACVIM,

Munich, Germany

DECVIM-CA, AGAF

Lyme Borreliosis

Associate Professor and Director, Gastrointestinal Laboratory, Department of Bert E. Stromberg , PhD

Small Animal Clinical Sciences, College

Professor, Veterinary and Biomedical
of Veterinary Medicine and Biomedical

Sciences, College of Veterinary Medicine,

Sciences, Texas A&M University, College

University of Minnesota, St. Paul, MN

Station, TX

Infectious Diseases of the Urinary

The Exocrine Pancreas

System in Large Animals: Swine Kidney

Worm Infection; Trichinellosis

Allison J. Stewart , B VSC (Hons), MS,

DACVIM (Large Animal), DACVECC

David E. Swayne , DVM, PhD, DACVP,

Professor of Equine Internal Medicine,

DACP V

Department of Clinical Sciences, College

Laboratory Director, USDA-ARS, Southeas1
of Veterinary Medicine, Auburn University,

Poultry Research Laboratory, Athens, GA

Aubum,AL

Avian Influenza; Newcastle Disease and

Disorders of Magnesium Metabolism;

Other Paramyxovirus Infections: Other

Intestinal Diseases in Horses and Foals

Avian Paramyxovirus Infections
xxxviii CONTRIBUTORS

Thomas W. Swerczek, DVM, PhD
erinary Medicine, University of California,

Professor, Department of Veterinary Sci

Davis, CA
ence, University of Kentucky, Lexington, KY

Equine Recurrent Uveitis

T'yzzer Disease

Larry J. Thompson, DVM, PhD, DABVT

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Jane E. Sykes, BVSc (Hons), PhD,

Senior Research Scientist, Nestle Purina

DACVIM

PetCare, St. Louis, MO

Professor of Small Animal Medicine,

Department of Medicine and Epidemi

Nitrate and Nitrite Poisoning; Nonpro
ology, School of Veterinary Medicine,
tein Nitrogen Poisoning; Salt Toxicity

University of California, Davis, CA

Peter N. Thompson, BVSc, MMv, PhD

Chlamydial Conjunctivitis

Professor of Veterinary Epidemiology,

Faculty of Veterinary Science, University

Joseph Taboada, DVM, DACVIM
of Pretoria, South Africa

Professor and Associate Dean, Office of

Student and Academic Affairs, School

Rift Valley Fever; Wesselsbron Disease
of Veterinary Medicine, Louisiana State

University, Baton Rouge, LA

Ahmed Tibary, DMV, PhD, DACT

Professor, Comparative Theriogenol-

Fungal lrifections
ogy, Department of Veterinary Clinical

Sciences, College of Veterinary Medicine,

Jaime L. Tarigo, DVM, PhD, DACVP

Washington State University, Pullman, WA

Assistant Professor, Veterinary Clinical

Pathology, University of Georgia, Athens, GA Abortion in Large Animals; Congenital and Inherited Anomalies of the Repro

Blood Parasites: Cytauxzoonosis
ductive System

Marcel Taverne, PhD

John F. Timoney, MVB, PhD, Dsc,

Emeritus Professor of Fretal and Perinatal

MR CVS

Biology, Department of Farm Animal Health,

Keeneland Chair of Infectious Diseases,

Faculty of Veterinary Medicine, Utrecht

Gluck Equine Research Center, Depart

University, Utrecht, The Netherlands
ment of Veterinary Science, University of

Kentucky, Lexington, KY

Pseudopregnancy in Goats

Glanders

Charles 0. Thoen, DVM, PhD

Professor, Veterinary Microbiology and

Peter J. Timoney, MVB (Hons), MS,

Preventive Medicine, College of Veterinary

PhD,FRCVS

Medicine, Iowa State University, Ames, IA

Professor; Frederick Van Lennep Chair in

Equine Veterinary Science, Gluck Equine

Tuberculosis and other Mycobacterial

Research Center, University of Kentucky,
lrifections; Tuberqulosis in Poultry

Lexington, KY

Jennifer E. Thomas, DVM

Equine Irifectious Anemia; Equine Viral

Post-Doc Fellow, Department of Veteri

Arteritis
nary Pathobiology, Center for Veterinary

Health Sciences, Oklahoma State Univer

Ian Tizard, BVMS, PhD, DACVM
sity, Stillwater, OK

University Distinguished Professor of

Immunology; Director, Richard M. Schubot

Lice; Mange in Large Animals

Exotic Bird Health Center, Department of

William B. Thomas, DVM, MS, DACVIM Veterinary Pathobiology, College of Veteri

(Neurology)

nary Medicine and Biomedical Sciences,

Professor, Neurology and Neurosurgery,

Texas A&M University, College Station, TX

Department of Small Animal Clinical Sci

Amyloidoses; Immunologic Diseases; The
ences, University of Tennessee, Knoxville,

Biology of the Immune System; Vaccines

TN
and Immunotherapy

Diseases of the Peripheral Nerves and

Sheila M. F. Torres, DVM, MS, PhD,

Neuromuscular Junction; Diseases of the

DACVD

Spinal Column and Cord

Associate Professor, Dermatology, College

Sara M. Thomasy, DVM, PhD, DACVO
of Veterinary Medicine, University of Min

Vision Researcher, Department of Surgical
nesota, St. Paul, MN
and Radiological Sciences, School of Vet-

Diseases of the Pinna

CONTRIBUTORS
xxxix

Jerry L. Torrison, DVM, PhD, DACVPM Arnaud J. Van Wettere, DVM, MS, PhD, Swine Veterinarian, Zinpro Corporation;

DACVP

Adjunct Professor, College of Veterinary

Assistant Professor of Veterinary

Medicine, University of Minnesota,

Pathology, Utah Veterinary Diagnostic

St. Paul, MN

Laboratory, Utah State University,

VetBooks.ir

Lameness in Pigs

Logan, UT

Avian Chlamydiosis; Bloodborne Organ

Sandra P. Tou, DVM, DACVIM
isms; Disorders of the Skeletal System

Assistant Clinical Professor of Cardiology,

(Poultry); Myopathies (Poultry)

Department of Clinical Sciences, College
of Veterinary Medicine, North Carolina

Jozef Vercruysse, DVM

State University, Raleigh, NC

Professor, Faculty of Veterinary Medicine,

Congenital and Inherited Anomalies of

Ghent University, Merelbeke, Belgium
the Cardiovascular System

Anthelmintics; Blood Parasites: Shistosomiasis

Josie L. Traub-Dargatz, DVM, MS,

DACVIM

Alice E. Villalobos, DVM, DPNAP

Professor of Equine Medicine, Depart

Director, Animal Oncology Consultation
ment of Clinical Sciences, College of

Service; Director, Pawspice, Hermosa

Veterinary Medicine and Biomedical

Beach, CA

Sciences, Colorado State University, Fort

Tumors of the Skin and Soft Tissues

Collins, CO

Vesicular Stomatitis

Pedro Villegas, DVM, MS, PhD,

DACVM,DACPV

Robert Tremblay, DVM, DVSc, DACVIM

Professor Emeritus, Department of

Bovine/Equine Specialist, Boehringer

Population Health, College of Veterinary
lngelheim (Canada) Ltd, Burlington,

Medicine, Poultry Diagnostic & Research

Ontario, Canada

Center, University of Georgia, Athens, GA

Management and Nut1·ition Introduction

Inclusion Body Hepatitis/Hydropericardium Syndrome Deoki N. Tripathy, DVM, MS, PhD,

DACVM,DACPV

Patricia S. Wakenell, DVM, PhD,

Professor Emeritus, Department of Veteri

DACVP
nary Pathobiology, College of Veterinary

Head, Avian Diagnostics, Animal Disease

Medicine, University of Illinois, Urbana, IL

Diagnostic Laboratory; Associate Professor, Department of Comparative Patho

Fowlpox
biology, School of Veterinary Medicine,

Purdue University, West Lafayette, IN

Thomas N. Tully, Jr., BS, DVM, MS,

Backyard Poultry; Erysipelas

DABVP (Avian), DECZM (Avian)

Professor, Zoological Medicine, School

Peter J. Walker, BSc, PhD, DSc
of Veterinary Medicine, Louisiana State

CSIRO Biosecurity, Australian Animal

University, Baton Rouge, LA

Health Laboratory, Victoria, Australia

Ratites

Bovine Ephemeral Fever

Tracy A. Turner, DVM, MS

Patricia Walters, VMD, DACVIM,

Anoka Equine Veterinary Services, Elk

DACVECC

River, MN

New England Animal Medical Center, West

Lameness in Horses: Imaging

Bridgewater, MA

Techniques

Diseases of the Esophagus in Small

Animals

Stephanie J. Valberg, DVM, PhD,

DACVIM, ACVSMR

Kevin Washburn, DVM

Professor, Department of Veterinary Popu

Professor, Large Animal Clinical Sciences,
lation Medicine, University of Minnesota

College of Veterinary Medicine, Texas

Equine Center, St. Paul, MN

A&M University, College Station, TX

Myopathies in Horses; Myopathies in

Lymphadenilis and Lymphangitis: Gase

Ruminants and Pigs
ous Lymphadenitis
xi

CONTRIBUTORS

Nick Whelan, BVSc, MVSc, MACVSc,

Thomas Wittek, Univ.-Prof. Dr.med.

DACVCP, DACVO
vet., DECBHM

Animal Eye Clinic of Waterloo Region,

University Clinic for Ruminants, Universi

Cambridge, Ontario, Canada
ty of Veterinary Medicine, Vienna, Austria

VetBooks.ir

Systemic Pharmacotherapeutics of

Malassimilation Syndromes in Large
the Eye

Animals; Peritonitis

Brent R. Whitaker, MS, DVM

Zerai Woldehiwet, DVM, PhD, DAgric,

Vice President of Biological Programs,

MR CVS

National Aquarium, Baltimore, MD

Professor, Institute of Infection and Global

Amphibians

Health and School of Veterinary Science,

University of Liverpool, Wirral, UK

Thevor J. Whitbread, BSc, BVSc,

Tick Pyemia; Tickborne Fever

MRCVS, DECVP

Pathologist, Abbey Veterinary Services,

Devon, UK

R. Darren Wood, DVM, DVSc, DACVP

Associate Professor, Department of

Diagnostic Procedures for the Private

Pathobiology, Ontario Veterinary College,

Practice Laboratory: Clinical Biochem

University of Guelph, Ontario, Canada
ist1y, Clinical Hematology, Cytology,

Serology, Urinalysis

Leukocyte Disorders

Stephen D. White, DVM, DACVD

Peter R. Woolcock, BSc, MSc, PhD

Professor and Chief of Service,

Professor, Clinical Diagnostic Virology,

Dermatology, Department of Medicine

California Animal Health and Food Safety
and Epidemiology, School of Veterinary

Laboratory System, School of Veterinary

Medicine, University of California,

Medicine, University of California, Davis,

Davis, CA

CA

Eosinophilic Granuloma Complex; Food

Duck Viral Hepatitis

Allergy; Miscellaneous Systemic Dermatoses; Nasal Dermatoses of Dogs; Saddle Mariko Yamamoto, PhD

Sores; Seborrhea; Urticaria

Department of Population Health and

Reproduction, School of Veterinary Medi

Chris Whitton, BVSc, FANZCVS, PhD
cine, University of California, Davis, CA

Associate Professor, Equine Centre, Uni

The Human-Animal Bond
versity of Melbourne, Victoria, Australia

Lameness in Horses: Developmental

Roy P. E. Yanong, VMD

Orthopedic Disease

Associate Professor and Extension Veterinarian, Tropical Aquaculture Laboratory, Mark L. Wickstrom, DVM, MS, PhD

Fisheries and Aquatic Sciences Program,

Associate Professor, Department

School of Forest Resources and Conservaof Veterinary Biomedical Sciences, tion, Institute of Food and Agricultural Sci

Western College of Veterinary Medicine,
ences, University of Florida, Gainesville, FL

University of Saskatchewan, Saskatoon,

Canada

Aquaculture

Antiseptics and Disinfectants

Laszlo Zsak, DVM, PhD

Research Leader, USDA-Agricultural

Kevin P. Wrnkler, DVM, DACVS

Research Center, South Atlantic Area,

Surgeon, Georgia Veterinary Specialists,

Southeast Poultry Research Laboratory,

Atlanta, GA

Athens, GA

Wound Management

Goose Parvovirus Infection

CIRCULATORY SYSTEM

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THE BLOOD AND LYMPHATICS

HEMATOPOIETIC SYSTEM INTRODUCTION 4

Red Blood Cells 4

White Blood Cells 5

Platelets 7

ANEMIA 7

Regenerative Anemias 9

Blood Loss Anemia 9

Hemolytic Anemia 10

Nonregenerative Anemias 12

Nutritional Deficiencies 12

Anemia of Chronic Disease 13

Renal Disease 13

Primary Bone Marrow Diseases 13

BLOOD GROUPS AND BLOOD TRANSFUSIONS 15

Blood Typing 16

Crossmatching 16

Blood Transfusions 17

Blood Substitutes 18

BLOOD PARASITES 18

Anaplasmosis 18

Babesiosis 21

Cytauxzoonosis · 23

Equine Granulocytic Ehrlichiosis 697 (GEN)

Hemotropic Mycoplasmas 26

Feline Infectious Anemia 28

Old World Hepatozoonosis and American Canine Hepatozoonosis 29

Rickettsial Diseases 803 (GEN)

Schistosomiasis 31

Theileriases 33

East Coast Fever 34

Tropical Theileriosis 35

Other Theileriases of Cattle 35

Ovine and Caprine Theileriases 35

Equine Theileriasis 35

Trypanosomiasis 35

Tsetse-transmitted Trypanosomiasis 35

Surra 38

Dourine 38

Chagas' Disease 38

Nonpathogenic Trypanosomes 40

2

CIRCULATORY SYSTEM

BOVINE LEUKOSIS 743 (GEN)

CANINE LYMPHOMA 40

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EQUINE INFECTIOUS ANEMIA 699 (GEN)

ERYTHROCYTOSIS AND POLYC YTHEMIA 43

FELINE LEUKEMIA VIRUS AND RELATED DISEASES 790 (GEN) HEMOSTATIC DISORDERS 44

Coagulation Disorders 46

Platelet Disorders 46

Vascular Disorders 50

Coagulation Protein Disorders 51

Pathologic Thrombosis 54

LEUKOCYTE DISORDERS 56

Physiology of Leukocytes 56

Blood Vascular System 56

Granulocytes 56

Monocytes 57

Lymphocytes 57

Leukogram Abnormalities 57

Specific Interpretive Leukogram Responses 59

LYMPHADENITIS AND LYMPHANGITIS 63

Caseous Lymphadenitis of Sheep and Goats 63

Corynebacterium pseudo tuberculosis Infection of Horses and Cattle 66

Epizootic Lymphangitis 639 (GEN)

Melioidos.is 661 (GEN)

Strangles 1453 (RES)

Streptococcus porcinus Infection of Pigs 734 (GEN) THE HEART AND VESSELS

CARDIOVASCULAR SYSTEM INTRODUCTION 67

Abnormalities of the Cardiovascular System 70

Common Endpoints of Heart Disease 73

Heart Failure, Congestive Heart Failure, and the Failing Heart 73

Diagnosis of Cardiovascular Disease 73

Principles of Therapy 7 4

Common Therapeutic Agents 75

CONGENITAL AND INHERITED ANOMALIES 76

Outflow Tract Obstructions 78

Aortic Stenosis 78

Pulmonic Stenosis 78

Coarctation of the Aorta 79

Left-to-Right Shunts 79

Patent Ductus Arteriosus 79

CIRCULATORY SYSTEM

3

Ventricular Septal Defects 81

Atrial Septal Defects 82

Right-to-Left Shunts 83

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Tetralogy of Fallot 83

Other Cyanotic Heart Diseases 84

Conditions of the Atrioventricular Valves 84

Mitral Valve Dysplasia 84

Tricuspid Valve Dysplasia 84

Mitral Valve Stenosis 85

Vascular Ring Anomalies 85

Persistent Right �ortic Arch 85

Miscellaneous Congenital Cardiac Abnormalities 86

HEART DISEASE AND HEART FAILURE 87

Diagnosis 87

History and Signalrnent 87

Physical Examination 87

Radiography 91

Electrocardiography 92

Echocardiography 98

Cardiac Catheterization 99

Heart Failure 99

Systolic Dysfunction 99

Diastolic Dysfunction 100

Compensatory Mechanisms 100

Cardiac Biomarkers 101

Clinical Manifestations 101

Management 103

Specific Cardiac Diseases 112

MyxornatousAVValve Degeneration 112

Valvular Blood Cysts or Hematomas 115

Cardiomyopathies 115

Myocarditis 119

Other Causes of Myocardial Failure 120

Infective Endocarditis 121

Pericardial Disease 122

Systemic and Pulmonary Hypertension 125

Arterial Thromboembolism 126

HEARTWORM DISEASE 127

BOVINE HIGH-MOUNTAIN DISEASE 137

THROMBOSIS, EMBOLISM, AND ANEURYSM 141

4

HEMATOPOIETIC SYSTEM INTRODUCTION

HEMATOPOIETIC SYSTEM INTRODUCTION

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Blood supplies cells with water, electromost species, the kidney is both the sensor lytes, nutrients, and hormones and removes
organ and the major site of erythropoietin
waste products. The cellular elements
production, so chronic renal failure is
supply oxygen (RBCs), protect against
associated with anemia. Erythropoietin
foreign organisms and antigens (WBCs),
acts on the marrow in concert with other
and initiate coagulation (platelets). Because
humoral mediators to increase the number
of the diversity of the hematopoietic system, of stem cells entering RBC production, to its diseases are best discussed from a
shorten maturation time, and to cause early
functional perspective. Function may be
release of reticulocytes. Other factors that
classified as either normal responses to
affect erythropoiesis are the supply of
abnormal situations ( eg, leukocytosis and
nutrients (eg, iron, folate, or vitamin B12)

left shift in response to inflammation) or
and cell-cell interactions between erythroid
primary abnormalities of the hematopoietic
precursors, lymphoid cells, and other
system ( eg, pancytopenia from marrow
components of the hematopoietic microenfailure). Furthermore, abnormalities may be vironment. Factors that may suppress quantitative (ie, too many or too few cells)

erythropoiesis include chronic debilitating
or qualitative (ie, abnormalities in function).

diseases and endocrine disorders (such as
hypothyroidism or hyperestrogenism ).

RED BLOOD CELLS

1\vo mechanisms exist for removal
of senescent RBCs; both conserve the

The function of RBCs is to carry oxygen to
principal constituents of the cell for reuse.

the tissues at pressures sufficient to permit

Removal of aged RBCs normally occurs by
its rapid diffusion. This is accomplished
phagocytosis by the fixed macrophages of the
through the following mechanisms: a carrier spleen. As the RBC ages it may change molecule, hemoglobin (Hgb ); a vehicle
antigenically,acquiring senescent antigens

(RBC) capable of bringing the intact Hgb to
and losing its flexibility due to impaired ATP
the cellular level; and a metabolism geared
production. Both of these changes increase
to protect both the RBC and the Hgb from
the risk that the cell will become trapped in
damage. Interference with synthesis or
the spleen and removed by macrophages.

release of Hgb, production or survival of

After phagocytosis and subsequent

RBCs, or metabolism causes disease.

disruption of the cell membrane, Hgb is

Hgb is a complex molecule, formed of
converted to heme and globin. Iron is
four heme units attached to four globins
released from the heme ni.oiety and either

(two a and two f3 globins ). Iron is added in
stored in the macrophage as ferritin or
the last step by the ferrochelatase enzyme.

hemosiderin or released into the circulation

Interference with the normal production
for transport back to the marrow. The
of heme or globin leads to anemia. Causes
remaining heme is converted to bilirubin,
include copper or iron deficiency and lead
which is released by the macrophages into
poisoning. Hemoglobinopathies such as
the systemic circulation, where it complexes
thalassemias and sickle cell anemia,
with albumin far transport to the hepatoimportant genetic diseases of people, have cytes; there, it is cor\jugated and excreted into
not been seen in other animals. In these
the bile. In extravascular hemolytic anemias,
diseases, the production of globins ( a or f3

RBCs have a shortened life span, and the
or both) does not balance heme production,
same mechanisms occur at an increased rate.

and the Hgb is not functional. The only

Approximately 1 % of normal aging RBCs
known hemoglobinopathy of animals is
are hemolyzed in the circulation, and free
porphyria. Although described in several

Hgb is released. This is quickly converted
species, it is most important as a cause of
to Hgb dimers that bind to haptoglobin and
photosensitivity in cattle (seep 976).

are transported to the liver, where they are

Red cell mass, and thus oxygen-carrying
metabolized in the same manner as products
capacity, remains constant over time in
from RBCs removed by phagocytosis. In
healthy animals. Mature RBCs have a finite
intravascular hemolytic anemia, more
life span; their production and destruction

RBCs are destroyed in the circulation
must be carefully balanced, or disease ensues.

(hemoglobinemia) than can be bound to

Erythropoiesis is regulated by erythropoihaptoglobin. The excess Hgb and, etin, which increases in the presence of
therefore, iron are excreted in the urine
hypoxia and regulates RBC production. In

(hemoglobinuria).

HEMATOPOIETIC SYSTEM INTRODUCTION

5

The principal metabolic pathway of RBC

WHITE BLOOD CELLS
is glycolysis, and the main energy source in
most species is glucose. Glucose enters the

Phagocytes: The principal function of

RBC by an insulin-independent mechanism,
phagocytes is to defend against invading
and most is metabolized to produce ATP
microorganisms by ingesting and destroying

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and reduced nicotinamide adenine
them, thus contributing to cellular
dinucleotide (NADH). The energy of ATP is
inflammatory responses. There are two
used to maintain RBC membrane pumps so
types of phagocytes: mononuclear
as to preseive shape and flexibility. The
phagocytes and granulocytes. Mononuclear
reducing potential of the NADH is utilized
phagocytes arise primarily from the marrow
via the methemoglobin reductase pathway
and are released into the blood as monoto maintain the iron in Hgb in its reduced cytes. They may circulate for hours to a few
form (Fe2•).

days before entering the tissues and

The glucose not used in glycolysis is
differentiating to become macrophages.

metabolized via a second pathway, the

Granulocytes have a segmented nucleus
hexose monophosphate (HMP) shunt. No
and are classified according to their staining
energy is produced via the HMP shunt; its
characteristics as neutrophils, eosinophils,
principal effect is to maintain reducing
or basophils. Neutrophils circulate for only
potential in the form of reduced nicotinaa few hours before travelling to the tissues.

mide adenine dinucleotide phosphate

Five distinct stages in the process of

(NADPH). In conjunction with the
phagocytosis have been identified: 1)

glutathione reductase/peroxidase system,
attraction of phagocytes ( chemotaxis)

NADPH maintains the sulfhydryl groups
to microorganisms, antigen-antibody
of globin in their reduced state.

complexes, and other mediators of

Some disorders are the direct result of
inflammation; 2) attachment to the
abnormal RBC metabolism and interference organism; 3) ingestion; 4) fusion of cell with glycolysis. Inherited deficiency of
lysosomes with ingested microorganisms
pyruvate kinase, a key glycolytic enzyme,
and bacterial killing; and 5) digestion. In
causes ATP deficiency, which leads to
addition, many phagocytes have other
reduced RBC life span and hemolytic
specialized functions. Monocytes form
anemia. Excessive oxidant stress may
a link to the specific immune system by
overload the protective HMP shunt or
processing antigen for presentation to
methemoglobin reductase pathways,
lymphocytes and by producing substances
causing Heinz body hemolysis or methemosuch as interleukin-!, which initiates fever globin formation, respectively. Hemolytic
and lymphocyte activation and stimulates
anemia caused by a drug, such as acetaminearly hematopoietic progenitors.

ophen in cats, is an example of this

Eosinophils, while having a role as
mechanism. (See also ANEMIA, p 7.)

phagocytes, also have more specific

A decreased RBC mass (anemia) may
functions that include providing a defense
be caused by blood loss, hemolysis, or
against metazoan parasites and modulating
decreased production. In acute blood loss
the inflammatory process. They respond
anemia, RBCs are lost, but mortality is
chemotactically to histamine, immune
usually related to loss of circulating
complexes, and eosinophil chemotactic
volume rather than to loss of RBC. Iron is
factor of anaphylaxis, a substance released
the limiting factor in chronic blood loss.

by degranulating mast cells. Basophils are

Hemolysis may be caused by toxins,
not true phagocytes but contain large
infectious agents, congenital abnormaliamounts of histamine and other mediators of ties, or antibodies directed against RBC
inflammation. Eosinophilia and basophilia
membrane antigens. Decreased RBC
may be seen in response to systemic allergic
production may result from primary
reactions and invasion of tissues by parasites.

marrow diseases ( eg, aplastic anemia,

As with the RBCs, the production and
hematopoietic malignancy, or myelofibrocirculating numbers of phagocytes are sis) or from other causes such as renal
tightly regulated and controlled by various
failure, drugs, toxins, or antibodies
humoral factors, including colony-stimulating
directed against RBC precursors.

factors and interleukins. Unlike the RBCs,

Malignancy of RBCs or their precursors
which remain circulating in the blood, the
may be acute (eg, erythroleukemia) or
phagocytes use this compartment as a
chronic (eg, polycythemia vera). Animals
pathway to the tissues. Consequently, the
with erythroleukemia are anemic despite
number of phagocytes in the blood reflects
having a marrow filled with tubriblasts,
circumstances in the tissues ( eg, inflammawhereas those with polycythemia vera tion) as well as the proliferative function
have erythrocytosis.

of the bone marrow. The sensitivity with

6

HEMATOPOIETIC SYSTEM INTRODUCTION
which phagocytes reflect these conditions
lated B cell produces a clone of plasma cells,
varies from species to species. Abnormal
all producing the same specific antibody.

response, such as neutropenia from marrow

Antibody molecules (immunoglobulins)

failure, infections, drugs, or toxins, is likely fall into several classes, each with its own to result in secondary bacterial infections.

functional characteristics. For example, lgA

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Some cases of "idiopathic" neutropenia in
is the principal antibody of respiratory and
dogs may have an immune-mediated cause. intestinal secretions, IgM is the first antibody Finally, phagocyte precursors may undergo produced in response to a newly recognized malignant transformation, which results in
antigen, IgG is the principal antibody of the
acute or chronic myelogenous leukemia.

circulating blood, and IgE is the principal
antibody involved in allergic reactions.

Lymphocytes: Lymphocytes are

Antibodies perform their function by
responsible for both humoral and cellular
combining with the specific antigens
immunity. Cells of the two branches of the that stimulated their production. Antigenimmune system cannot be differentiated antibody complexes may be chemotactic
morphologically, but they differ in their
for phagocytes, or they may activate
dynamics of production and circulation.

complement, a process that produces both

Lymphocyte production in mammals
cell lysis and substances chemotactic for
originates in the bone marrow. Some of
neutrophils and macrophages. In this
the lymphocytes destined to be involved
manner, the humoral immune system is
in cellular immunity migrate to the thymus related to, and interacts with, the nonspeand differentiate further under the cific immune system.

influence of thymic hormones. These

The humoral immune system also is
become T cells and are responsible for a
related to both the nonspecific immune
variety of helper or cytotoxic immunosystem and the cellular immune system logic functions. Most circulating lymphoin other ways. Both "helper" (CD4) and cytes are T cells, but T cells are also

"cytotoxic" (CDS) T-cell classes have
present in the spleen and lymph nodes.

been described. Helper T cells recognize

The B cells migrate directly to organs
processed antigen and activate the humoral
without undergoing modification in the
immune response. Cytotoxic T cells, after
thymus and are responsible for humoral
sensitization by antigen, are effector cells,
immunity (antibody production).

which are especially important in antiviral

Thus, lymphoid organs have populations
immunity. Natural killer cells, which are a
of both B and T lymphocytes. In the lymph
class of lymphocyte distinct from T cells
nodes, follicular centers are primarily B
and B cells, destroy foreign cells ( eg,
cells, and parafollicular zones are primarily
neoplastic cells) even without prior

T cells. In the spleen, most of the lymphosensitization. Antigen processing by cytes of the red pulp are B cells, whereas
macrophages precedes recognition of an
those of the periarteriolar lymphoid sheaths antigen by lymphocytes. These complex are T cells. Close association ofT cells and
processes are involved in routine surveil

B cells within lymphoid organs is essential
lance against neoplastic cells and recognito immune function.

•
tion of "self."

Lymphocyte function in the cellular

Lymphocyte response in disease may be
immune system features both afferent
appropriate (activation of the immune

(receptor) and efferent (effector) composystem) or inappropriate (immune-mediated nents. Long-lived T cells of the peripheral
disease and lymphoproliferative malignanblood are the receptors. In response to cies). (See also THE BIOLOGYOFTilE IMMUNE
antigens to which they have been previously

SYSTEM, p 811.) Immune-mediated disease
sensitized, they leave the circulation and
results from failure of the immune system to
undergo blast transformation to form
recognize host tissues as self. For example,
activated T cells, which in turn cause other
in immune-mediated hemolytic anemia,

T cells to undergo blast transformation, both
antibodies are produced against the host's
locally and systemically. Stimulated T cells
own RBCs. Another inappropriate response
produce lymphokines with a wide range of
of the immune system is allergy. In allergic
activities, such as attraction and activation of individuals, IgE antibodies to allergens are neutrophils, macrophages, and lymphocytes. bound to the surface of basophils and mast The humoral immune system is comcells. When exposure to the allergen occurs, posed ofB cells that produce antibodies of
antigen-antibody complexes are formed, and
several classes. When sensitized B cells
degranulation of the mast cells and basophils
encounter antigen, they divide and
releases vasoactive amines. Reaction to this
differentiate into plasma cells that produce
may be mild ( as in urticaria or atopy) or
antibody. Therefore, each initially stimu-
life-threatening ( as in anaphylaxis ).

ANEMIA

7

Lymphocytosis occurs in some species,

Platelet disorders are either quantitative
especially the cat, as a response to

(thrornbocytopenia or thrombocytosis) or
epinephrine secretion. Atypical lymphoqualitative (thrombocytopathy). Thrombocytes may be seen in the blood in response cytopenia is one of the most common
to antigenic stimulation ( eg, vaccination).

bleeding disorders of animals. In general,

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Persistent lymphocytosis in cattle infected
platelet counts must fall to <30,000/µL
with bovine leukemia virus is a benign
before the risk of hemorrhage increases.

polyclonal increase in lymphocyte numbers. Consumption,destruction,or sequestration Lymphoproliferative malignancies include
of platelets causes thrornbocytopenia
lymphomas and acute lymphoblastic and
associated with increased production by the
chronic lymphocytic leukemias. Lymphopebone marrow. Consumptive thrombocytopenia may occur most commonly as a nia occurs with massive hemorrhage or with
response to glucocorticoid secretion.

disseminated intravascular coagulation,
secondary to a variety of diseases. Destruc

PLATELETS
tion occurs in immune-mediated thrombocytopenia, in which platelets become coated Platelets form the initial hemostatic plug
with antiplatelet antibodies and are removed
whenever hemorrhage occurs. They also
from the circulation by the fixed phagocyte
are the source of phospholipid, which is
system. Excessive sequestration of platelets
needed for the interaction of coagulation
by an enlarged spleen (hypersplenism) may
factors to form a fibrin clot. Platelets are
occur in conditions such as myeloproliferaproduced in the bone marrow from tive diseases.

megakaryocytes, under the influence of

Decreased production of platelets in the
thrombopoietin. Platelet production begins
marrow may be caused by drugs, toxins,
with invagination of the megakaryocyte cell
or by primary marrow disorders such
membrane and the formation of cytoplasas aplasia, fibrosis, or hematopoietic mic channels and islands. The cytoplasmic
malignancy. In primary marrow disorders,
islands produce platelets by fragmentation
more than one hematopoietic cell line is
from the megakaryocyte.

often decreased, resulting in pancytopenia.

Mature circulating platelets are packed

Thrombocytosis is rare and often
with dense granules containing ATP,
idiopathic. It may be associated with
adenosine diphosphate (ADP), and calcium,
primary marrow disease such as in
as well as serotonin, lysosomes, glycogen,
megakaryocytic leukemia. It is often
mitochondria, and an intracellular canalicuassociated with chronic blood loss and lar system. The mitochondria and glycogen
iron deficiency because of increased
are involved in energy production, and the
platelet production in the marrow
canalicular system serves both as a transport reacting to continued consumption and system for granule components and as a
loss.

source of phospholipid, which is found in

Thrombocytopathies comprise a poorly
high concentration in the membrane lining
defined group of diseases in which platelet
of the canals.

numbers are normal but their function is

When vessel walls are damaged, collagen
impaired. Von Willebrand disease is
and tissue factor are exposed, and circulatcharacterized primarily by a defect in ing platelets adhere via von Willebrand factor platelet adhesion to the endothelium. The and undergo a change in shape with the
platelets themselves are normal. Other
accompanying release of ADP. Local platelet
hereditary disorders of platelet function
aggregation is stimulated by ADP, with the
have been described but are relatively rare.

ultimate formation of the primary platelet

Probably the most common platelet
plug. The local accumulation of fibrin and
function defect is the irreversible inhibition
platelets is known as a hernostatic plug. The
of thromboxane (which is necessary for
fibrin clot that then forms is consolidated by
platelet aggregation) caused by aspirin
the action of platelet contractile proteins.

administration.

ANEMIA

Anemia is defined as an absolute decrease

PCV. It can develop from loss, destruction,
in the red cell mass as measured by RBC
or lack of production of RBCs. Anemia is
count, hemoglobin concentration, and/or
classified as regenerative or nonregenerative.

8

ANEMIA

With regenerative anemia, the bone marrow calculated by automated cell counters responds appropriately to the decreased red calibrated for the species in question. RBC
cell mass by increasing RBC production and size is expressed by the mean corpuscular releasing reticulocytes. With nonregeneravolume (MCV) in femtoliters and can reflect tive anemia, the bone marrow responds
the degree of regeneration. Macrocytosis

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inadequately to the increased need for

(an increase in the MCV) usually correlates

RBCs. Anemia caused by hemorrhage or
with a regenerative anemia Macrocytosis
hemolysis is typically regenerative. Anemia
can be a heritable condition in Poodles
caused by decreased erythropoietin or an
without anemia and may be seen in anemic
abnormality in the bone marrow is
cats infected with feline leukemia virus.

nonregenerative.

Microcytosis (a decrease in the MCV) is the
hallmark of iron-deficiency anemia The

Clinical Findings: Clinical signs in
hemoglobin concentration of each RBC,
anemic animals depend on the degree of
measured in g/dL, is defined as the mean
anemia, the duration ( acute or chronic), and corpuscular hemoglobin concentration the underlying cause. Acute anemia can

(MCHC). Terms used for description
result in shock and even death if more than
of abnormalities with MCHC include
a third of the blood volun1e is lost rapidly
normochromia and hypochromia Abnorand not replaced. In acute blood loss, the malities in RBC morphology, such as
animal usually presents with tachycardia,
basophilic stippling, can indicate lead
pale mucous membranes, bounding or weak intoxication. Heinz body formation indicates peripheral pulses, and hypotension. The
oxidative iltjury to the RBCs, secondary to
cause of the blood loss may be overt, eg,
toxin exposure ( see TABLE 1 ). Cats are more traun1a. If no evidence of external bleeding
susceptible to Heinz body formation than
is found, a source of internal or occult blood other species, and cats without anemia can loss must be sought, eg, a ruptured splenic
have a small number of Heinz bodies. The
tunlor, other neoplasia, coagulopathy, GI
presence of schistocytes or spherocytes
ulceration, or parasites. If hemolysis is
may also help identify the pathophysiology
present, the animal may be icteric. Animals
associated with the cause of anemia.

with chronic anemia have had time to

The reticulocyte count is usually reported
accommodate, and their clinical presentaas a percent of the RBC mass. This value tion is usually more indolent with vague
should be corrected for the degree of anemia
signs of lethargy, weakness, and anorexia.

to evaluate the degree of regeneration. An

These animals may have sinlilar physical
absolute reticulocyte count (measured by
examination findings such as pale mucous

RBCs/µL x reticulocyte percentage) of
membranes and weak peripheral pulses.

>50,000/µL in cats or >60,000/µL in dogs is

The lack of expected clinical signs may alert considered regenerative. To correct the the clinician to the time frame involved.

percent reticulocytes, the formula ( see

Splenomegaly, abdominal distention, and/or below) can be applied. A corrected heart murmur may be present, depending
reticulocyte percent > 1 % indicates
on the underlying C<J:use of anemia
regeneration in dogs and cats. After acute
blood loss or hemolytic crisis, reticulocyto

Diagnosis: A complete history is an
sis usually takes 3-4 days to become evident.

important part of the evaluation of an

A serum chemistry panel and urinalysis
anemic animal. Questions might include
evaluate organ function. If GI blood loss is
duration of clinical signs, history of
suspected, an examination of the feces for
exposure to toxins ( eg, rodenticides, heavy
occult blood and parasites can be useful.

metals, toxic plants), drug treatments,

Radiographs can help identify occult
vaccinations, travel history, and any prior
disease, such as a penny (zinc toxicity) in
illnesses.

the stomach of a puppy with hemolytic

A CBC, including a platelet and a
anemia. Bruising or bleeding may be signs of
reticulocyte count, will provide information
a coagulopathy and indicate the need for a
on the severity of anemia and degree of
coagulation profile. Presence of petechiae or
bone marrow response, and also allow for
ecchymotic hemorrhage suggest significant
evaluation of other cell lines. A blood smear
thrombocytopenia or thrombocytopathy. If
should be evaluated for abnormalities in
hemolytic disease is suspected, blood can be

RBC morphology or size and for RBC
evaluated for autoagglutination, or a direct
parasites. The RBC indices (measures of

Coombs' test might be indicated. A test for
size and hemoglobin concentration) are
autoagglutination can be done by placing a

.

.

PCV of the patient
corrected ret1culocyte % = ( observed ret1culocyte %) x - -

-�-- -

--- normal PCV for that species

ANEMIA

9
lr�:1111 TOXIC CAUSES OF ANEMIA

Pathogenic

Plants,

Toxins,

Heavy

Mechanism

Drugs

Foods

Chemicals

Metals

Oxidation

Acetaminophen, benzocaine,

Fava beans,

Crude oil,

Copper,

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dapsone, nitrofurans,
oak, onions, naphthalene zinc
prirnaquine, propofol,
propylene
quinacrine
glycol, red
maple

Blood loss

Aspirin, naproxen

Bracken fem, Dicoumarol
sweet clover

Inunune-

Cephalosporins, levamisole,

Pirimicarb
mediated
penicillin, propylthiouracil,
hemolysis
sulfonamides

Hemolysis

Fenbendazole, heparin
lndole

Lead,
selenium

Decreased

Amphotericin, azidothymi-

Bracken fem Benzene,

Lead
marrow
dine, cephalosporins,
trichloro
production
chloramphenicol, estrogen,
ethylene
fenbendazole, griseofulvin,
meclofenamic acid, pheno-
barbital, phenothiazine,
phenylbutazone, propylthio-
uracil, quinidine, recombinant
human erythropoietin, sulfona-
mides, thiacetarsamide
drop of saline on a slide with a fresh drop of

M:E ratio is always interpreted in light of a
the animal's blood; the slide should be gently recent CBC, because changes in the ratio rotated to mix the drops together, then
could also be due to suppression of one cell
evaluated grossly and microscopically for
line compared with the other.

macro- and microagglutination. If autoagglutination is present, there is no need to REGENERATIVE ANEMIAS
perform a Coombs' test. Serology or PCR for
infectious agents such as feline leukemia

BLOOD LOSS ANEMIA
virus, Ehrlichia, equine infectious anemia
virus, and Babesia may also help define the Acute blood loss can lead to shock and even
cause of anemia (see TABLE 2).

death if >30%--40% of blood is lost and the

Bone marrow evaluation by aspiration
hypovolemia that develops is not treated
and/or biopsy (seep 14) is indicated in
aggressively with IV fluids or compatible
any animal with an unexplained, nonblood (seep 17), or both. Causes of acute regenerative anemia. If the CBC reveals a
loss can be known ( eg, trauma, surgery) or
decrease in more than one cell line, possibly
occult. Coagulopathies, bleeding tumors,
indicating hypoplastic marrow, a biopsy
gastric ulceration, and external or internal
would be indicated along with an aspirate.

parasites should be excluded as causes. GI

Biopsies and aspirates are complementary:

parasites, such as Haemonchus in ruminants
biopsies are better to evaluate the
and hookworms in dogs, can lead to severe
architecture and degree of cellularity of
blood loss, especially in young animals.

the marrow, and aspirates allow for better

Low-grade, chronic blood loss eventually
evaluation of cellular morphology. Aspirates results in iron-deficiency anemia, although also allow for an evaluation of orderly
some degree of reticulocytosis may persist
maturation of the red and white blood cell
even after iron stores become depleted. The
lines, the ratio of myeloid to erythroid
hallmark of an iron-deficiency anemia is
precursors (M:E ratio), and the number of
microcytic, hypochromic anemia. This
platelet precursors. Iron stores can also be
chronic blood loss can be due to some type
evaluated by Prussian blue staining. An M:E
of parasitism in young animals ( eg, fleas, lice,
ratio of< 1 indicates that red cell production
intestinal parasitism), but in older animals,
is greater than white cell production; with
bleeding from GI ulcers or tumors is more
an M:E ratio > 1, the opposite is likely. The
common.

10

ANEMIA
l�lllll INFECTIOUS CAUSES OF ANEMIA

Infectious Agent

Species Affected

Hemolytic

Marrow Affected

BACTERIA

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Clostridium

Cattle, sheep

Yes

No
perfringens A

Clostridium

Cattle, she�p

Yes

No
haemolyticum

Leptospira

Cattle, pigs, sheep

Yes

No
interrogans

Mycoplasma spp

Cats

±

Rarely

H aemobartonella

Cattle, cats

±

No
spp

VIRUSES

Equine infectious

Horses

±

Rarely
anemia virus

Feline leukemia

Cats

±

Yes
virus

Feline immuno-

Cats

No

Yes
deficiency virus

RICKETISIA

Mycoplasma spp

Cattle, goats, llamas,

Yes

No
pigs, sheep•

(piglets only)

Anaplasma spp

Cattle, goats, sheep

Yes

No

Ehrlichia spp

Dogs

Yes

Yes

PROTOZOA

Babesiaspp

Cattle, cats, dogs,

Yes

No
horses, sheep

Theileria sppb

Cattle, goats, sheep

±

No

Cytaua:zoon spp

Cats

No

Yes

Trypanosoma spp

Cattle, horses, pigs

Yes

No

Sarcocystis cruzi

Cattle

Yes

No
a In adults, only clinically relevant in splenectomized or ciitically ill animals.

b Pathogenic species of Theileria are found in Africa, the Mediterranean, the Middle East, Asia, and Europe. Species found in North America are nonpathogenic.

HEMOLYTIC ANEMIA
immune mediated (6001<>-75%), although
toxins, RBC trauma, infections, and RBC

Hemolytic anemias are typically regeneramembrane defects can also cause hemolysis.

tive and result from lysis of RBCs in either
the intra- or extravascular space. Intravascu

Immune-mediated Hemolytic
lar hemolysis results in hemoglobinemia and Anemia: Immune-mediated hemolytic hemoglobinuria, whereas extravascular
anemia (IMHA, see p 826) can be primary
hemolysis does not. Both types of hemolysis
or secondary to neoplasia, infectious
can result in icterus. In dogs, the most
agents, drugs, or vaccinations. In IMHA, the
common cause of hemolytic anemia is
immune system no longer recognizes RBCs

ANEMIA

11
as self and develops antibodies to circulatwith or without clopidogrel 1-2 mg/kg/day) ing RBCs, leading to RBC destruction by
if the platelet count is >40,000/µL. The dosing
macrophages and complement. In some
range for heparin is wide and variable, and
cases, antibodies am directed against RBC
dosage also depends on whether fracprecmsors in the marrow, resulting in tionated or unfractionated heparin is used.

nonregenerative anemia Animals with

Heparin therapy can be monitored using

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IMHA are usually icteric, sometimes febrile,
activated partial thromboplastin time
and may have splenomegaly. Hematologic

(A.PTT) or antifactor Xa concentrations
hallmarks of IMHA are regenerative anemia,

(low-molecular-weight heparin).

hyperbilirubinemia, spherocytosis,

Mortality rates for IMHA range from
autoagglutination, or a positive Coombs'

200/o-75%, depending on the severity of
test.

clinical signs. Negative prognostic

Another methodology to evaluate dogs
indicators may include a rapid drop in PCV,
for anti-RBC antibodies is flow cytometry.

high bilirubin concentration, moderate to

Flow cytometry allows for detection and
marked leukocytosis (28,000 to >40,000
quantitation of red cell surface-bound IgG
cells/µL), increased BUN, petechiae,
and IgM. Flow cytometry was found to be
intravascular hemolysis, autoagglutination,

88o/o-1000A, specific for diagnosing dogs with
disseminated intravascular coagulation,
anti-RBC antibodies. One report suggests
and thromboembolic complications.

using flow cytometry to assess response to

Moderate to marked leukocytosis has
treatment for dogs, because there is a
been reported to be associated with tissue
decrease in surface anti-RBC antibodies
necrosis, most likely secondary to tissue
before reticulocytosis or increase in RBC
hypoxia or thromboembolic disease.

count. Flow cytometry may not be readily

Referral to tertiary care facilities may
available to all veterinary hospitals.

improve survival.

Animals with IMHA can show mild,
indolent signs or be in an acute crisis. It is

Alloimmune Hemolysis: Neonatal
important to tailor treatment to the anin1al's isoerythrolysis (NI) is an immune-mediated signs, including treating any underlying
hemolytic disease seen in newborn horses,
infections. Transfusion with packed RBCs
mules, cattle, pigs, cats, and rarely dogs.

is usually required. The goal of therapy is to

NI is caused by ingestion of maternal
stop the destruction of RBCs by treating
colostrum containing antibodies to one of
with immunosuppressive drugs; supportive
the neonate's blood group antigens. The
care is also a priority. Prednisone or
maternal antibodies develop to specific
prednisolone at a dosage of 1-2 mg/kg,
foreign blood group antigens dW'ing
bid, is considered first-line therapy, with
previous pregnancies, unmatched
azathioprine at 2 mg/kg/day ( azathioprine
transfusions, and from Babesia and
is contraindicated in cats and may be

Anaplasma vaccinations in cattle. Cats replaced by chlorambucil) or cyclosporine
are unique in that blood type B cats have
at 5-10 mg/kg/day considered as a possible
natW'ally occurring anti-A antibodies
second agent. In one study, low-dose
without prior exposme, and their kittens
aspirin at 0.5 mg/kg/day improved survival
that are type A develop hemolysis after
times in dogs treated with azathioprine and
nW"Sing. In horses, the antigens usually
prednisone. The veterinary literatme is
involved are A, C, and Q; NI is most
ambiguous on choice of second agent or
commonly seen in Thoroughbreds and
when to introduce a second agent. Other
mules. Neonates with NI are normal at birth
immunosuppressive agents that have
but develop severe hemolytic anemia within
been used include mycophenolate and

2-3 days and become weak and icteric.

leflunomide.

Diagnosis is confim1ed by screening

In the acute hemolytic crisis, drugs such
maternal serum, plasma, or.colostrun1
as cyclosp01ine ( 10 mg/kg/day, initially) or
against the paternal or neonatal RBCs.

human intravenous immunoglobin (MG,

Treatment consists of stopping any

0.5-1.5 g/kg as a single dose) may also have
colostrum while giving supportive care with
benefit because of rapid onset of action.

transfusions. If necessary, neonates can be

Pulmonary thromboembolism is a risk
transfused with triple-washed maternal
in dogs with IMHA. These dogs are often

RBCs. NI can be avoided by withholding
hypercoagulable, which can be documented maternal colostrum and giving colostrum with thromboelastography. Dogs docufrom a maternal somce free of the mented to be in a hypercoagulable state
antibodies. The newborn's RBCs can be
should be anticoagulated with heparin,
mixed with maternal serum to look for
which may be used in combination with
agglutination before the newborn is allowed
antiplatelet therapy (aspirin 0.5 mg/kg/day
to receive maternal colostrum.

12

ANEMIA

Microangiopathic Hemolysis: Microenzymes lead to shortened RBC life span angiopathic hemolysis is caused by RBC
and regenerative anemia In dogs with
damage secondary to turbulent flow
phosphofructokinase deficiency, the
through abnormal vessels. In dogs, it can
hemolytic crises are set off by alkalosis
be seen secondary to severe heartworm
secondary to excessive excitement or

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infection, vascular tumors (hemangiosar exercise. If such situations are minimized, coma ), splenic torsions, and disseminated
these dogs may have a normal life
intravascular coagulation; in other species,
expectancy. There is no treatment for
causes include hemolytic uremic syndrome
pyruvate kinase deficiency, and affected
in calves, equine infectious anemia, African
dogs will have a shortened life span due to
swine fever, and chronic classical swine
myelofibrosis and osteosclerosis of the
fever. Schistocytes are common in blood
bone marrow. Affected cats will have
smears from these animals. Treatment
chronic intermittent hemolytic anemia,
involves correction of the underlying
which is sometimes helped by splenectomy
disease process.

and steroids. Unlike dogs, cats have not
been reported to develop osteosclerosis.

Metabolic Causes of Hemolysis:

A hereditary hemoglobinopathy, porphyria

Hypophosphatemia ( see p 1000) causes

(seep 986), leads to build-up of porphyrins postparturient hemoglobinuria and
in the body and has been described in cattle,
hemolysis in cattle, sheep, and goats. It can
cats, and pigs. It is most prevalent in
occur 2-6 wk after parturition. Hypophos

Holstein cattle and can lead to a hemolytic
phatemia with secondary hemolysis is seen
crisis. Affected calves fail to thrive and are
in dogs and cats secondary to diabetes
photosensitive. Diagnosis is made by
mellitus, hepatic lipidosis, and refeeding
finding increased levels of porphyrins in
syndrome. Treatment with either oral or IV
bone marrow, urine, or plasma. Teeth of
phosphorus is indicated, depending on the
affected animals fluoresce under ultraviolet
degree of hypophosphatemia Cattle that
light.

drink too much water ( water intoxication)

are at risk of developing hemolysis
secondary to hypotonic plasma This is seen

NONREGENERATIVE ANEMIAS
in calves 2-10 mo old and causes respira

NUTRITIONAL DEFICIENCIES
tory distress and hemoglobinuria Clinical
signs can progress to convulsions and

Nutritional deficiency anemias develop
coma. Hemolytic anemia, hyponatremia
when micronutrients needed for RBC
and hypochloremia, decreased serum
formation are not present in adequate
osmolality, and low urine specific gravity
amounts. Anemia develops gradually and
in a calf would support the diagnosis of
may initially be regenerative but ultimately
water intoxication. Treatment consists of
becomes nonregenerative. Starvation
hypertonic fluids (2.5% saline) and diuretics
causes anemia by a combination of vitamin

( eg, mannitol).

and mineral deficiencies as well as a
negative energy and protein balance.

Toxins: Toxins and drugs can-cause

Deficiencies most likely to cause anemia are
anemia by many mechanisms. Those
iron, copper, cobalamin (812), B6, riboflavin,
implicated most frequently in animals and
niacin, vitamin E, and vitamin C (important
their pathogenic mechanisms are listed ( see
only in primates and guinea pigs).

TABLE 1).

Iron deficiency is the most common
deficiency seen in dogs and piglets but

Infections: Many infectious agentsoccurs less commonly in horses, cats, bacterial, viral, rickettsial, and protozoaland ruminants. Iron deficiency is rarely can cause anemia by direct damage to RBCs,
nutritional in origin-it most commonly
leading to hemolysis, or by direct effects
occurs secondary to blood loss (seep 9).

on precursors in the bone marrow

Young animals have minimal iron stores,

( see TABLE 2).

and milk contains very little iron. This can
be especially important for piglets that

Heritable Diseases: Several heritable
grow rapidly and are often raised indoors

RBC disorders cause anemia. Pyruvate
with no access to iron. Oral iron supplekinase deficiencies are seen in Basenjis, mentation is indicated as treatment for iron

Beagles, West Highland White Teniers,
deficiency; any source of blood loss must

Cairn Teniers, and other breeds, as well as
be elin1inated.

Abyssinian and Somali cats. Phosphofruc

Copper deficiency can develop in
tokinase deficiency occurs in English
ruminants fed forage grown in copper

Springer Spaniels. Deficiencies in these
deficient soil. Copper is necessary for the

ANEMIA

13
metabolism of iron. Copper deficiency may
anemia), after which the dosage is
occur secondary to high dietary molybdedecreased. Animals receiving recombinant num or sulfate in cattle and can develop in
human erythropoietin require supplemental
pigs fed whey diets. Low blood copper
iron to support RBC production. (See also
concentrations or low copper concentra

HEMATINICS, p 2540.) Darbepoeitin also has

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tions in liver biopsies ( more definitive) are
been found to be valuable in management
diagnostic. Treatment is oral or injectable
of anemia associated with chronic kidney
copper supplementation.

disease.

B vitamin deficiencies are rare. Certain
drugs (anticonvulsants, drugs that inter

PRIMARY BONE MARROW
fere with folate metabolism) have been

DISEASES
associated with development of folate
or cobalamin deficiency, leading to a

Primary bone marrow disease or failure
normocytic, normochromic, nonregenerafrom any cause can lead to nonregenerative tive anemia. Cobalamin malabsorption has
anemia and pancytopenia. With diffuse
been reported in Giant Schnauzers (their
marrow involvement, granulocytes are
enterocytes are unable to absorb cobalaaffected first, followed by platelets and min ). These dogs respond to parenteral
finally RBCs.

supplementation with cobalamin. Rumi

Aplastic anemia has been reported in
nants also develop a secondary cobalamin
dogs, cats, ruminants, horses, and pigs with
deficiency when grazing on cobalt-deficient
pancytopenia and a hypoplastic marrow,
pasture. Treatment with oral cobalt or
replaced by fat. Most cases are idiopathic,
parenteral cobalamin is indicated.

but reported causes include infection (feline
leukemia virus, Ehrlichia, parvovirus),

ANEMIA OF CHRONIC DISEASE
drug therapy (methimazole, chemotherapeutic agents, antibiotics [trimethoprim

Anemia of chronic disease can be characte1°
sulfa, chloramphemicol], fenbendazole),
ized as mild to moderate, nonregenerative,
toxin ingestion (estrogen), and total body
normochromic, and normocytic. It is the
irradiation ( see TABLES 1 and 2). There may most common fonn of anemia seen in
also be an immune-mediated component
animals. The anemia can be secondary
to this disease. Diagnosis is confirmed by
to chronic inflammation or infection,
bone marrow aspiration and core biopsy.

neoplasia, liver disease, hyper- or hypoad

Treatment consists of eliminating the
renocorticism, or hypothyroidism. The
underlying cause and providing supportive
anemia is mediated by cytokines produced
measures such as broad-spectrum
by inflammatory cells, which lead to
antibiotics and transfusions. lmmunosupdecreases in iron availability, RBC survival, pressive agents such as prednisone,
and the marrow's ability to regenerate.

cyclosporine, mycophenolate, or azathi<r

Treatment should be directed at the
prine may be considered. Recombinant
underlying disease and often results in
human erythropoietin and granulocyte
resolution of the anemia The anemia may
colony-stimulating factor (5 mcg/kg/day,
be reduced by treatment with recombinant

PO) can be used until the marrow recovers.

human erythropoietin, but the risk of
if the disease is idiopathic or if marrow
antibody formation to endogenous
recovery is unlikely ( eg, phenylbutazone
erythropoietin may outweigh benefit.

toxicity in dogs), bone marrow transplanta

Darbepoetin appears to have less impact
tion is beneficial if a suitable donor is
to induce reactive antibodies.

available (investigational and limited
availability).

RENAL DISEASE
in pure red cell aplasia (PRCA), only
the erythroid line is affected. It is character

Chronic renal disease is a common cause
ized by a nonregenerative anemia with
of nonregenerative anemia in animals.

severe depletion of red cell precursors in

Erythropoietin is normally produced by the
the bone marrow. It has been reported
peritubular endothelial cells in the renal
in dogs and cats and may be primary or
cortex. Animals with renal disease produce
secondary. Primary cases are most
less erythropoietin, leading to anemia
commonly immune mediated and may

Recombinant human erythropoietin
respond to immunosuppressive therapy.

( 44-132 U/kg, three times/wk, with most

Supportive care, including transfusion, may
animals starting at 88 U/kg) has been used
be indicated when anemia is severe. Feline
for treatment. PCV is monitored weekly
leukemia-positive cats can have PRCA.

until the desired improvement is reached

Recombinant human erythropoietin has

(this will vary with the initial degree of
been reported to cause PRCA in dogs and

14

ANEMIA
horses. Discontinuation of therapy may
underlying cause but usually consists of
eventually lead to RBC recovery in some
immunosuppressive therapy.

animals.

Primary leukemias are uncommon to
rare in domestic species but have been

Bone Marrow Aspiration and

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reported in dogs, cats, cattle, goats, sheep,

Biopsy: Bone marrow aspiration and
pigs, and horses. Retroviruses are a cause in
biopsy are techniques used to evaluate the
some cattle, cats, primates, and chickens.

bone marrow in domestic animal species.

Leukemias can develop in myeloid or

The basic technique involves introducing
lymphoid cell lines and are further classified a hollow needle into the bone marrow to as acute or chronic. Most affected animals
obtain a sample for evaluation. Bone
have nonregenerative anemia, neutropenia,
marrow aspiration provides a sample for
and thrombocytopenia, with circulating
cytologic evaluation, and bone marrow
blasts usually present. Acute leukemias,
biopsy provides a sample for histopathocharacterized by infiltration of the marrow logic evaluation.

with blasts, generally respond poorly to

Specific clinical indications to evaluate
chemotherapy. In animals that do respond,
bone marrow include but are not limited to
remission times are usually short. In acute
investigation of nonregenerative anemia,
lymphoblastic leukemia in dogs, the
thrombocytopenia, leukopenia, bicytoperesponse rate to chemotherapy is -300/o, nia, pancytopenia, abnormal circulating
with a median survival of 4 mo. Acute
cells of any type, monoclonal gammopathy,
myeloblastic leukemias are less common
suspected osteomyelitis, suspected bone
and even less responsive to treatment than
neoplasia, infectious disease affecting the
acute lymphoblastic leukemia. In acute
bone, and clinical staging of neoplastic
leukemias, the cell lineage is often difficult
processes such as lymphoma and mast
to identify morphologically, so cytochemicell disease.

cal stains or immunologic evaluation of cell

The conventional anatomic sites used for
surface markers may be necessary for
bone marrow aspiration include the iliac
definitive diagnosis. Chronic leukemias,
crest, the trochanteric fossa of the femur,
characterized by an overproduction of one
the tibial crest, and the greater tubercle of
hematopoietic cell line, are less likely to
the humerus. Some clinicians have also
cause anemia and more responsive to
used the rib (costochondraljunction) or
treatment.

stemabrae. The humerus is the most

Myelodysplasia ( myelodysplastic
common site for bone marrow biopsy.

syndrome, MDS) is considered a preleuke

For bone marrow aspiration, cats and
mic syndrome characterized by ineffective
dogs generally require sedation, although
hematopoiesis, resulting in a nonregenerasome cats may require general anesthesia.

tive anemia or other cytopenias. MDS has

General anesthesia is required for bone
been described in dogs, cats, and people.

marrow biopsy. The animal is positioned

The disease can be primary or secondary
in lateral recumbency when using the
and is commonly seen in cats with feline
trochanteric fossa or the greater tubercle,
leukemia. Primary syndromes prnbably
and in sternal recumbency when using the
arise from mutations in stem cells.

iliac crest. The area to be accessed is shaved

Secondary syndromes are caused by other
and aseptically prepared. The site, including
neoplasia or drug therapy. Some cats and
the periosteum, is infiltrated with local anesdogs respond to treatment with recombithetic. A# l l scalpel blade is ilien used to nant human erythropoietin and prednisone.

make a stab incision through the skin.

Supportive care with transfusions may be

The equipment used for these procedures
helpful. Survival is variable because MDS
may differ slightly. Most bone marrow
can progress to leukemia; many animals
aspiration needles ( eg, Rosenthal, Illinois)

are euthanized or die of sepsis, bleeding,
are very similar and have a removable stylet.

or anemia.

With the stylet in place, the needle is

Myelofibrosis causes bone marrow
advanced with a back and forth screw-like
failure secondary to replacement of normal
motion until the needle is well seated in the
marrow elements with fibrous tissue. It has
bone. The stylet is then removed, and a
been seen in dogs, cats, people, and goats. It
syringe (6-12 mL) attached for aspiration.

can be a primary disorder or secondary to

If the animal feels any discomfort, this is
malignancies, immune-mediated hemolytic
when it will occur. Only a small sample is
anemia, whole body irradiation, and
required, ie, enough to fill the syringe
congenital anemias ( eg, pyruvate kinase
hub, which should be put onto slides for
deficiency). Diagnosis can be made by bone
cytologic evaluation. The needle can then
marrow biopsy. Treatment varies with the
be removed.

BLOOD GROUPS AND BLOOD TRANSFUSIONS

15

Bone marrow biopsy generally requires a
core sample for histopathology, the needle

Jamshidi needle, which is rigid and hollow
is advanced further (about 1/,\ in.) into the
with a stylet. The Jamshidi needle has a cutmarrow and twisted in one direction. The ting edge at its end, designed to obtain a
needle is then moved in a wide, circular
core marrow sample ( although it can also
motion to try to dislodge a core sample.

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be used to obtain a bone marrow aspirate).

The needle is removed by twisting in

The needle is driven into the bone with a
the opposite direction in which it was

·back and forth, screw-like motion. Once
advanced. A blunt stylet is then passed
the needle is well seated, the cap is
retrograde to remove the core san1ple. The
unscrewed and the stylet removed. An
core can be gently rolled onto a slide for
aspirate can be obtained similar to the
cytology and then placed into formalin for
technique described above. To obtain a
histopathology.

BLOOD GROUPS AND BLOOD

TRANSFUSIONS

Blood groups are determined by genetically
occurring" isoantibodies, not induced by
controlled, polymorphic, antigenic
transfusion or pregnancy, may be present in
components of the RBC membrane. The
variable but detectable titers. For example,
allelic products of a particular genetic locus

Group B cats have naturally occurring
are classified as a blood group system.

anti-A antibody. Also, circulating antibodies

Some of these systems are highly complex,
to animal blood group antigens may be
with many alleles defined at a locus; others
induced by transfusion. With random blood
consist of a single defined antigen. Blood
transfusions in dogs, there is a 30o/o-4()0A,
group systems, in general, are independent
chance of sensitization of the recipient,
of each other, and their inheritance
primarily to blood group antigen DEA 1,
conforms to Mendelian dominance. For
but risk is also present for development of
polymorphic blood group systems, an
antibody to any other antigen lacked by
animal usually inherits one allele from each
the recipient. In horses, transplacental
parent and thus expresses no more than
inununization of the mare by an incompattwo blood group antigens of a system. An ible fetal antigen inherited from the sire ma,y
exception is in cattle, in which m.ultiple
occur. Inununization also may result when
alleles, or "phenogroups," are inherited.

some homologous blood products are used

Normally, an individual does not have
as vaccines ( eg, anaplasmosis in cattle). In
antibodies against any of the antigens
dogs, prior pregnancy does not result in
present on its own or against other blood
sensitization of the bitch to foreign blood
group antigens of that species' systems
group antigens.

unless they have been induced by transfu

The number of major recognized blood
sion, pregnancy, or immunization. In some
group systems ( see TABLE 3) varies among
species (people, sheep, cattle, pigs, horses,
domestic species, with cattle being the most
cats, and dogs), so-£alled "naturally
complex and cats the simplest. Animal

IH=iiii MAJOR BLOOD GROUPS OF CLINICAL INTEREST

Species

Blood Group

Canine

DEA 1.1 and 7

Feline

A,B,mic

Equine

A, C,Q

Bovine

B,J

Ovine

B,R

16

BLOOD GROUPS AND BLOOD TRANSFUSIONS
blood groups are typed to aid in the
animal receiving a transfusion might be
matching of donors and recipients and,
exposed to some antigens that are not
especially in horses, to identify breeding
present on its RBCs.

pairs potentially at risk of causing hemolytic disease in their offspring. Because CROSSMATCHING
expression of blood group antigens is

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genetically controlled and the modes of

Previously sensitized recipients or those
inheritance are understood, these systems
with naturally occurring antibodies can be
also have been used to substantiate
detected by crossmatching, which is done
pedigrees in cattle and horses; however,
to preclude administration of incompatible
in most cases, DNA testing has replaced
blood. In the USA, >99%of cats are of blood
blood typing for paternity testing.

group A, so the risk of incompatible
transfusion is low. However, certain breeds,

BLOOD TYPING
including Abyssinian, Birman, British

Shorthair, Devon Rex, Himalayan, Persian,

Antisera used to identify blood groups

Scottish Fold, and Somali, have a higher

( typing reagents) usually are produced as
frequency of blood group B. Any incompatisoimmune sera Their in vitro serologic ible transfusion in cats results in rapid
characteristics vary with the species. Many
destruction of transfused cells, so typing
reagents are hemagglutinins; others are
and crossmatching should be done before
hemolytic and require complement to
any transfusion. The mic antigen is present complete the serologic reaction, such as
in some cats, and naturally occurring
in cattle (because RBCs do not readily
antibodies are present in cats that lack the
agglutinate) and horses (because REC
mic antigen. For that reason, crossmatching rouleaux are a problem). Other typing
should be performed for cats before the first
reagents, neither hemagglutinating nor
transfusion, even if they will receive A or B
hemolytic, combine with REC antigens in
matched blood.

an "incomplete" reaction because they lack The direct crossmatch procedure, with
additional combining sites to agglutinate
appropriate controls, is effective for all
other RBCs; addition of species-specific
species. The major crossmatch detects
antiglobulin is required for agglutination.

antibodies already present in recipient

The diversity of blood groups in animals
plasma that could cause a hemolytic
and the lack of commercially available
reaction when donor RBCs are transfused;
blood-typing reagents to all antigens make
it will not detect the potential for sensitizacomplete typing difficult but should not tion to develop. Anticoagulant ( calcium
preclude the clinical use of transfusions. In
disodium edetate or citrate) is added to
horses and dogs, the blood group antigens
blood samples from donor and recipient;
most commonly implicated in transfusion
the donor RBCs are washed 3 times with
incompatibilities are known; by selecting

0.9"Ai saline, and a 4% REC suspension in
donor animals that lack these groups, or
saline is made from the washed cells. The
that match the recipient, the risk of
major crossmatch consists of combining
sensitization of the re�ipient to the most
equal volumes (0.1 mL) of the donor REC
important antigens can be minimized. For
suspension and recipient plasma. The
dogs and cats, commercially available,
control tube contains recipient RBCs
point-of-care testing for major antigens is
and recipient plasma The samples are
available in either gel or card testing kits.

incubated, centrifuged, and evaluated for

Reagents are available for only some
hemolysis or agglutination. Hemolysis is
antigens, generally those that are most
evaluated by comparing the color of the
likely to sensitize a recipient, or those for
supernatant in the test sample with that of
which naturally occurring antibodies,
the control sample. Each sample is then
primarily in cats, might be present. For
gently shaken until all cells in the "button"

example, dogs have more than 12 blood
at the bottom of the tube have returned to
group systems but generally are typed for
suspension. Again, the degree of cell
only one (DEA 1.1). An additional blood
clumping of the test sample is compared
group antigen ( dal) was discovered when
with that of the control sample. The test is
a dal-negative, previously transfused
negative, or compatible, when the plasma is

Dalmatian reacted to many potential
clear and the RBCs are readily suspended.

donors, and only a few Dalmatians were

A positive, or incompatible, test can have
found to be compatible. It is a common
hemolysis or hemagglutination or both. All
antigen in most dogs but is lacking in some
tests judged macroscopically to be negative

Dalmatians. Because multiple blood group
for hemagglutination should be confirmed
antigens are present, it is likely that an
microscopically at low power. Some newer

BLOOD GROUPS AND BLOOD TRANSFUSIONS

17
crossmatching systems that use a gel

For example, a 25-kg dog has a total blood
technique are becoming available. This is
volume of -2,000 mL; with a PCV of 15%, the
particularly important in horses, because

RBC volume is 300 mL; if the PCV is to be
their RBCs tend to form rouleaux.

increased to 20%, that equals an RBC

The minor crossmatch is the reverse of
volume of 400 mL. Therefore, 100 mL of

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the major crossmatch, ie, recipient cells are

RBCs or 200 mL of whole blood ( with PCV
combined with donor plasma. The minor
of 500A,) would be required to increase the
crossmatch is important only in species
recipient's PCV to the desired level. These
such as cats with clinically significant
calculations assume no ongoing losses of
naturally occurring isoantibodies or if the

RBCs through hemorrhage or hemolysis.

donor has been previously transfused or, in

Obviously, the post-transfusion PCV is the
horses, those with previous pregnancies.

most important measure of adequacy of red
cell dose. No more than 20% of a donor

BLOOD TRANSFUSIONS
animal's blood should be collected at one
time.

Frequently, the need for blood transfusions

Collection, storage, and transfusion
is acute, as in acute hemolysis or hemorof blood must be done aseptically. The rhage; transfusions are also appropriate in
anticoagulant of choice is citrate phosphate
treatment of acute or chronic anemias.

dextrose adenine (CPDA-1). Commercial

Animals with hemostatic disorders often
blood bags containing the appropriate
require repeated transfusions of whole
amount of anticoagulant for a "unit" (500
blood, red cells, plasma, or platelets. Blood
mL) are available. Heparin should not be
transfusions must be given with care,
used as an anticoagulant, because it has a
because they have the potential to furtl1er
longer half-life in the recipient and causes
compromise the recipient.

platelet activation; also, heparinized blood

Whole blood frequently is not the ideal
cannot be stored.

product to be administered. If the need is to

Blood collected in CPDA-1 with added
replace the oxygen-carrying capability of

RBC preservation or nutrient solutions may
the blood, then packed RBCs are more
be safely stored at 4 °C for 4 wk. If the blood
appropriate; if replacement of circulatory
will not be used immediately, the plasma
volume is needed, crystalloid or colloid
can be removed and stored frozen for later
solutions may be used, with packed RBCs
use as a source of coagulation factors or
added as needed. Platelet numbers rise
albunlin for acute reversible hypoalbunlinerapidly after hemorrhage, so replacement is rnia Plasma must be frozen at -20° to -30°C
rarely needed. Plasma proteins equilibrate
within 6 hr of collection to assure that levels
from the interstitial space, so plasma is not
of factor VIII are adequate and will remain
needed except in massive hemorrhage (> l
so for 1 yr. Chronic hypoproteinemia is not
blood volume in 24 hr). Animals that require
helped by plasma, because the fotal body
coagulation factors benefit most from
deficit of albumin is so large that it could not
administration of fresh-frozen plasma or
be improved by the small amount contained
cryoprecipitate if the need is specifically
in plasma. Colloid solutions such as
for factor VIII, von Willebrand factor, or
hetastarch are more effective for treatment
fibrinogen. Platelet-rich plasma or platelet
of hypoalbunlinemia. Human albumin has
concentrates may be of value in thrombobeen used in dogs; however, the risk of cytopenia, although immune-mediated
sensitization and allergic reactions is
thrombocytopenia usually does not respond significant.

to administration of platelets because they
are removed rapidly by the spleen.

Risks of Transfusion: The most serious

The decision to transfuse RBCs is
risk of transfusion is acute hemolysis.

determined by clinical signs, not by any

Fortunately, this is rare in domestic animals.

pre-selected PCV. Animals with acute

Dogs rarely have clinically significant
anemia show signs of weakness, tachycarpreformed antibodies, so only those that dia, and tachypnea at a higher PCV than
have received repeated transfusions are at
animals with chronic anemia. The amount
risk. The niost common hemolytic reacofRBCs required to relieve clinical signs tion in dogs that have received multiple
will generally increase the PCV above 200A
transfusions is delayed hemolysis, seen

Domestic animals have blood volumes of
clinically as shortened survival of trans7%-goA, of their body weight; cats have fused RBCs and a positive Coombs' test.

a slightly lower volume of -6.5%. By

Even crossmatch-compatible RBCs given
determining the recipient's blood volume
to horses or cattle survive only 2-4 days.

and knowing the animal's PCV, the required

N onirnrnune causes of hemolysis include
replacement RBC volume can be calculated. improper collection or separation of blood,

18

BLOOD GROUPS AND BLOOD TRANSFUSIONS
freezing or overwanning of RBCs, and
produce in large quantities, be nonantigenic,
infusing under pressure through a small
and persist in the circulation at least long
needle.

enough for resuscitation.

Other complications include sepsis from

One hemoglobin-based oxygen carrier of
contaminated blood, hypocalcemia from
bovine origin is currently licensed for use in

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too much citrate, and hypervolemia
dogs. The hemoglobin is collected asepti

( especially in animals with preexisting heart cally, filtered to remove all red cell stromal disease or in very small animals). Urticaria,
elements, and polymerized to allow the
fever, or vomiting are seen occasionally.

product to persist in the circulation for a

Transfusions can also spread disease from
half-life of -36 hr. This product has been
donor to recipient, such as RBC parasites
shown to carry and deliver oxygen

( eg, Mycoplasma in cats or Babesia in efficiently, can be used in1mediately without
dogs) and viruses ( eg, retroviruses in cats,
need for typing or crossmatching, and has a
horses, or cattle). Other diseases, such as

3-yr shelf life at room temperature. Because
those caused by rickettsia or other bacteria,
the strncture of the hemoglobin molecule is
can also be spread if the donor is bacteresimilar between species, bovine hemoglobin mic. Donors should be tested periodically
is mininlally antigenic. Although currently
for infectious diseases that are prevalent
licensed for use only in dogs, it has been used
locally. F1ea and tick prevention is also
in cats, horses, llan1as, birds, and people. Its
important to prevent vector-borne
colloidal effects are especially useful in
infections in donors.

resuscitation after trauma with acute blood
loss. Because t.he cost of hemoglobin
solution is often higher, and duration of

BLOOD SUBSTITUTES
effect is shorter than that of blood, the
main value of hemoglobin is in emergency

(Hemoglobin-based oxygen carrier
situations when blood is not inunediately
solutions)

available. Volume overload is a potential risk

Because of problems associated with
if hemoglobin is given too rapidly. Another
finding compatible donors and disease
concern with hemoglobin solutions is that
transmission by transfusion, the search for
nitric oxide is scavenged and removed by the
a red cell substitute has been ongoing for
product. This paradoxically might cause

>50 yr. An ideal substitute would can-y and
vasoconstriction and decrease oxygen
deliver oxygen like red cells, be easy to
delivery to ischemic tissues.

BLOOD PARASITES

ANAPLASMOSIS

(fom1erly E bovis), and A platys (fom1erly E platys), all of which invade blood cells

Anaplasmosis, formerly known as gall
other tllan erythrocytes of tlleir respective
sickness, traditionally refers to a disease of
manunalian hosts. Bovine anaplasmosis is of
ruminants caused by obligate intraerythroeconomic significance in tile cattle industry.

cytic bacteria of the order Rickettsiales,
family Anaplasmataceae, genusAna

Etiology and Pathogenesis: Clinical
plasma. Cattle, sheep, goats, buffalo, and
bovine anaplasmosis is usually caused by
some wild ruminants can be infected with

A ma.rginale. AnA marginale with an
the erythrocyticAnaplasma. Anaplasmosis
appendage has been called A caudatum,
occurs in tropical and subtropical regions
but it is not considered to be a separate
worldwide ( -40°N to 32°S), including South
species. Cattle are also infected with A
and Central Anlerica, the USA, southern
centrale, which generally results in mild

Europe, Africa, Asia, and Australia.

disease. A ovis may cause mild to severe

TheAnaplasma genus also includes A
disease in sheep, deer, and goats. A
plwgocylophilum ( compiled from species
phagocytophilum has recently been
previously known as Ehrlichia. phagocy
reported to infect cattle; however, natural
tophila, E equi, and hw11an granulocytic
infection is rare and it does not cause
ehrlichiosis agent, see p 803), A bovis clinical disease.

BLOOD PARASITES

19

Transmission and Epidemiology: Up
dose and typically ranges from 15-36 days
to 17 different tick vector species (including

( although it may be as long as 100 days).

Dermacentor, Rhipicephalus, !rodes,

After the prepatent period, peracute

Hyalomma, andAigas) have been reported (most severe but rare), acute, or chronic to transmitAnaplasma spp. Not all of these
anaplasmosis may follow. Rickettsemia

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are likely significant vectors in the field, and
approximately doubles every 24 hr during
it has been shown that strains of A
the exponential growth phase. Generally,
maiginale also coevolve with particular

10%-300!& of erythrocytes are infected at
tick strains. Rhipicephalus (Boophilus)

peak rickettsemia, although this figure may
spp are major vectors in Australia and
be as high as 65%. RBC count, PCV, and

Africa, and Dermacent.or spp have been
hemoglobin values are all severely reduced.

incriminated as the main vectors in the

Macrocytic anemia with circulating

USA. After feeding on an infected animal,
reticulocytes may be present late in the
intrastadial or trans-stadia! transmission
disease.

may occur. Transovarial transmission may

Animals with peracute infections
also occur, although this is rare, even in the
succumb within a few hours of the onset of
single-host Rhipicephalus spp. A replicaclinical signs. Acutely infected animals lose tive cycle occurs in the infected tick.

condition rapidly. Milk production falls.

Mechanical transmission via biting

Inappetence, loss of coordination,
dipterans occurs in some regions. Transplabreathlessness when exerted, and a rapid cental transmission has been reported and
bounding pulse are usually evident in the
is usually associated with acute infection of
late stages. The urine may be brown but, in
the darn in the second or third trimester of
contrast to babesiosis, hemoglobinuria does
gestation. Anaplasmosis may also be spread
not occur. A transient febrile response, with
through the use of contaminated needles or
the body temperature rarely exceeding
dehoming or other surgical instruments.

l06°F ( 41 °C) occurs at about the tin1e of

There is a strong correlation between age
peak rickettsemia Mucous membranes
of cattle and severity of disease. Calves are
appear pale and then yellow. Pregnant cows
much more resistant to disease (although
may abort. Surviving cattle convalesce over
not infection) than older cattle. This
several weeks, during which hematologic
resistance is not due to colostral antibody
paran1eters gradually return to norn1al.

from immune darns. In endemic areas

Bos indicus breeds of cattle appear to
where cattle first become infected with
possess a greater resistance to A marginale

A ma.rginale early in life, losses due to
infection thanB taunts breeds, but
anaplasmosis are minimal. After recovery
variation of resistance of individuals within
from the acute phase of infection, cattle
breeds of both species occurs. Differences
remain chronically infected carriers but
in virulence between A naplasma strains
are generally immune to further clinical
and the level and duration of the rickettdisease. However, these chronically semia also play a role in severity of clinical
infected cattle may relapse to anaplasmosis
manifestations.

when immunosuppressed ( eg, by cortico

Lesions: Lesions are typical of those
steroids), when infected with other
found in animals with anemia due to
pathogens, or after splenectomy. Carriers
erythrophagocytosis. The carcasses of cattle
serve as a reservoir for further transmission. tl1at die from anaplasmosis are generally Serious losses occur when mature cattle
markedly anemic and jaundiced. Blood is
with no previous exposure are moved into
thin and watery. The spleen is characteristiendemic areas or under endemically cally enlarged and soft, with prominent
unstable situations when transmission rates
follicles. The liver may be mottled and
are insufficient to ensure that all cattle are
yellow-orange. The gallbladder is often
infected before reaching the more
distended and contains thick brown or green
susceptible adult age.

bile. Hepatic and mediastinal lymph nodes
appear brown. There are serous effusions in

Clinical Findings: In animals < 1 yr old
body cavities, pulmonary edema, petechial
anaplasmosis is usually subclinical, in
hemorrhages in the epi- and endocardium,
yearlings and 2-yr-olds it is moderately
and often evidence of severe GI stasis.

severe, and in older cattle it is severe and

Widespread phagocytosis of erythrocytes is
often fatal. Anaplasmosis is characterized
evident on microscopic examination of the
by progressive anemia due to extra vascular
reticuloendothelial organs. A significant
destruction of infected and uninfected
proportion of erythrocytes are usually found
erythrocytes. The prepatent period of A
to be parasitized after death due to acute
maiginale is directly related to the infective infection.

20

BLOOD PARASITES

Diagnosis: A marginale, together with day for up to 10 days and then decreases.

the hemoprotozoaBabesia bovis and B

Severe anemia can persist for weeks after
bigemina, are the causative agents of tick
parasites cannot be detected in blood
fever in cattle. These three species have
smears.

similar geographic distributions, except that

Chronically infected carriers may be

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anaplasmosis occurs in the absence of babeidentified with a fair degree of accuracy by siosis in the USA. Microscopic examination
serologic testing using the msp5 ELISA,
of Giemsa-stained thin and thick blood films complement fixation, or card agglutination is critical to distinguish anaplasmosis from
tests. Nucleic acid-based detection
babesiosis ( see p 21) and other conditions methods are most useful, because species
that result in anemia and jaundice, such as
and strain differentiation tests may not
leptospirosis ( see p 646) and theileriosis detect carrier levels.

( see p 33). Blood in anticoagulant should

At necropsy, thin blood films of liver,
also be obtained for hematologic testing.

kidney, spleen, lungs, and peripheral blood

In Giemsa-stained thin blood films,
should be prepared for microscopic

Anaplasma spp appear as dense, homogeexamination.

neously staining blue-purple inclusions

0.3-1 µm in diameter. A marginale

Treatment, Control, and Prevention:

inclusions are usually located toward the

Tetracycline antibiotics and imidocarb are
margin of the infected erythrocyte, whereas
currently used for treatment. Cattle may be

A centrale inclusion bodies are located
sterilized by treatment with these drugs and
more centrally. A caudatum cannot be
remain immune to severe anaplasmosis
distinguished from A marginale using
subsequently for at least 8 mo.

Giemsa-stained blood films. Special staining

Prompt administration of tetracycline
techniques are used to identify this species
drugs (tetracycline, chlortetracycline,
based on observation of characteristic
oxytetracycline, rolitetracycline, doxycyappendages associated with the bacteria. A
cline, minocycline) in the early stages of
caudatum has been reported only in North
acute disease ( eg, PCV > 15%) usually

America and could possibly be a morphoensures survival. A commonly used logic form of A marginale and not a
treatment consists of a single IM irtjection of
separate species. Inclusion bodies contain
long-acting oxytetracycline at a dosage of 20

1-8 initial bodies 0.3-0.4 µm in diameter,
mg/kg. Blood transfusion to partially restore
which are the individual rickettsiae. The
the PCV greatly improves the survival rate
percentage of infected erythrocytes varies
of more severely affected cattle. The carrier
with the stage and severity of disease;.

state may be eliminated by administration
maximum rickettsemias in excess of 50%
of a long-acting oxytetracycline preparation
can occur with A marginale. Microscopi

(20 mg/kg, IM, at least two irtjections with a
cally, the infection ·becomes visible 2-6 wk

1-wk interval). Withholding periods for
after transmission. During the course of
tetracyclines apply in most countries.

infection, the rickettsemia can double each

Ir\jection into the neck muscle rather than
the rump is preferred.

lmidocarb is also highly efficacious
against A marginale as a single irtjection

(as the d.ihydrochloride salt at 1.5 mg/kg, SC,
or as imidocarb dipropionate at 3 mg/kg).

Elimination of the carrier state requires the
use of higher repeated doses of imidocarb

( eg, 5 mg/kg, IM or SC, two irtjections of the
d.ihydrochloride salt 2 wk apart). lmidocarb
is a suspected carcinogen with long
withholding periods and is not approved
for use in the USA or Europe.

In South Africa, Australia, Israel, and

South America, infection with live A

Anaplasma marginale in bovine blood,
centrale ( originating from South Africa) is Wright-Giemsa, 1 OOx oil immersion.

used as a vaccine to provide cattle with

Intracellular organisms appear as basophilic,
s
partial protection against the disease
pherical inclusions generally located near
the margin of erythrocytes. Echinocytes
caused by A marginale. A centrale (single
are frequently present. Courtesy of Ms. Sue dose) vaccine produces severe reactions in

Anderson, Tick Fever Centre, Wacol,.Oueensland,
a small proportion of cattle. In the USA,

Australia.

where live vaccines cannot be used,

BLOOD PARASITES

21
vaccines comprising nonliving A marginale

In Rhipicephalus spp ticks, the blood
purified from infected bovine erythrocytes
stages of the parasite are ingested during
and adjuvant have been used in the past but
engorgement and undergo sexual and
may not currently be available. Inununity
asexual multiplication in the replete female,
generated by using multidose killed vaccine
infecting eggs and subsequent parasitic

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protects cattle from severe disease on
stages. Transmission to the host occurs
subsequent infection, but cattle can still be
when larvae (in the case of B bovis) or
susceptible to challenge with heterologous
nymphs and adults (in the case of B
strains of A marginale. Instances of
bigemina) feed. The percentage of larvae
isoerythrolysis in suckling calves have
infected can vary from 0-500A, or higher,
occurred due to prior vaccination of dams
depending mainly on the level of parawith preparations that contained bovine sitemia of the host at the time the female
erythrocytic material. Long-lasting
ticks engorge. Under field conditions, the
immunity against A marginale is conferred
rate of tick transmission is generally higher
by preimmunization with live rickettsia,
for B bigemina than for B bovis.

combined with the use of chemotherapy

In endemic areas, three features are
to control severe reactions. The use of
important in detemtlning the risk of clinical
attenuated strains of A marginale as a live disease: 1) calves have a degree of immunity
vaccine has been reported, with instances

( related both to colostral-derived antibodies
of severe reactions also occurring. A
and to age-specific factors) that persists
marginale grown in tick cell cultw·es are
for -6 mo, 2) animals that recover from
being investigated as an alternative live

Babesia infections are generally immune
vaccine source. Subunit vaccines to confor their commercial life ( 4 yr), and 3) the trol bovine anaplasmosis are also under
susceptibility of cattle breeds to ticks and
investigation. In some areas, sustained strin Babesia infections varies; eg, Bos indicus gent control or elimination of the arthropod
cattle tend to be more resistant to ticks and
vectors may be a viable control strategy;
the effects of B bovis and B bigemina.

however, in other areas immunization is
infection than Bos taurus--derived breeds.

recommended.

At high levels of tick transmission, virtually
all calves become infected withBabesia by

BABESIOSIS

6 mo of age, show few if any clinical signs,
and subsequently become immune. This

Babesiosis is caused by intraerythrocytic
situation can be upset by either a natural
protozoan parasites of the genus Babesia.

( eg, climatic) or artificial ( eg, acaricide

Transmitted by ticks, babesiosis affects a
treatment or changing breed composition of
wide range of domestic and wild animals
herd) reduction in tick numbers to levels
and occasionally people. Although the
such that tick transmission of Babe:;ia to
major economic impact of babesiosis is
calves is insufficient to ensure all are
on the cattle industry, infections in other
infected during this critical early period.

domestic animals, including horses, sheep,

Other circumstances that can lead to
goats, pigs, and dogs, assume varying
clinical outbreaks include the introduction
degrees of importance throughout the
of susceptible cattle to endemic areas and
world.

the incursion of Babesia-infected ticks into Two important species in cattle-previously tick-free areas. Strain variation

B bigemina and B bovis-are widespread in immunity has been demonstrated but is
in tropical and subtropical areas and are the
probably not of practical significance in the
focus of this discussion. However, because
field.

there are many common features of the
diseases caused by differentBabesia, much

Clinical Findings and Pathogenesis:

of this information can be applied to other

B bovis is a much more virulent organism species.

than B bigemina. With most strains of B
bigemina, the pathogenic effects relate

Transmission and Epidemiology: The
more directly to erythrocyte destruction.

main vectors of B bigemina and B bovis are With virulent strains of B bovis, a hypoten
l-hostRhipicephalus (Boophilus) spp
sive shock syndrome, combined with
ticks, in which transmission occurs
generalized nonspecific inflammation,
transovarially. Although the parasites can
coagulation disturbances, and erythrocytic
be readily transmitted experimentally by
stasis in capillaries, contribute to the
blood inoculation, mechanical transmission
pathogenesis.

by insects or during surgical procedures has

The acute disease generally runs a course
no practical significance. Intrauterine
of -1 wk. The first sign is fever (frequently
infection has also been reported but is rare.

2!106°F [41 °C]), which persists throughout,

22

BLOOD PARASITES
and is accompanied later by inappetence,
and differentiating isolates have also been
increased respiratory rate, muscle tremors,
described. A procedure that may occasionanemia, jaundice, and weight loss; hemoally be justified to confirm infection in globinemia and hemoglobinuria occur in
suspected carrier aninlals is the subinothe final stages. CNS involvement due to culation of blood ( -500 mL) into a fully

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adhesion of parasitized erythrocytes in
susceptible aninlal, preferably a splenectobrain capillaries can occur with B bovis mized calf, and subsequent monitoring of
infections. Either constipation or diarrhea
the recipient for infection.

may be present. Late-term pregnant cows
may abort, and temporary infertility due

Treatment and Control: A vaiiety of
to transient fever may be seen in bulls.

drugs have been used to treat babesiosis in

Animals that recover from the acute
the past, but only dinlinazene aceturate and
disease remain infected for a number of
inlidocarb dipropionate are still in common
years with B bovis and for a few months in
use. These drugs are not available in all
the case of B bigemina .. No clinical signs endemic countries, or their use may be
are apparent during this carrier state.

restricted. Manufacturers' recommenda

Lesions: Lesions (particularly with
tions for use should be followed. For treating

B bovis) include an enlarged and friable
cattle, dinlinazene is given lM at 3.5 mg/kg.

spleen; a swollen liver with an enlarged

For treatment, inlidocarb is given SC at 1.2
gallbladder containing thick granular bile;
mg/kg. At a dosage of 3 mg/kg, inlidocarb
congested, dark-colored kidneys; and
provides protection from babesiosis for
generalized anemia and jaw1dice. Most

-4 wk and will also eliminateB bov'i.s and
clinical cases of B bigemina have

B bigemina from carrier ailimals.

hemoglobinuria, but this is not invariably

Suppmtive treatment is advisable,
the case with B bovis. Other organs,
paiticularly in valuable aninlals, and may
including the brain and heart, may show
include the use of anti-infla!llffiatory drugs,
congestion or petechiae.

cmticosteroids, and fluid therapy. Blood
transfusions may be life-saving in very
anemic aninlals.

Diagnosis: Clinically, babesiosis can be

Vaccination using live, attenuated strains
confused with other conditions that cause
of the parasites has been used successfully
fever, anemia, hemolysis, jaundice, or red
in a number of countries, including
urine. Therefore, confirmation of diagnosis

Argentina, Australia, Brazil, Israel, South
by microscopic examination of Giemsa

Africa, and Uruguay. The vaccine is
stained blood or organ smears is essenti�.

provided in either a chilled or frozen form.

From the live aninlal, thick and thin blood

One vaccination produces adequate
smears should be prepared, preferably from
immunity for the commercial life of the
capillaries in the ear or tail tip.

aninlal; however, vaccine breakdowns

Smears of heart muscle, kidney, liver,
have been reported. Several recombinant
lung, brain, and from a blood vessel in an
antigens have been shown experimentally
extremity ( eg, lower leg) should be taken
to induce some immunity, but commercial
at necropsy.

vaccines are not yet available.

Microscopically, the species of Babesia

Although controlling or complete eradiinvolved can be determined morphologication of the tick vector can break the cally, but expe1tise is required, especially in
transmission cycle, this a�proach is rarely

B bovis infections in which few organisms
feasible in the longte1m and can lead to
are present. B bovis is small, with the paralarge, susceptible populations in endemic sites in paired form at an obtuse angle to
areas with consequent risk of outbreaks of
each other and measuring -1-1.5 x 0.5-1 µm.

disease in naive aninlals.

B bigemina is larger (3-3.5 x 1-1.5 µm),
with paired parasites at an acute angle to

Zoonotic Risk: A number of cases of
each other. Single fom1s of both parasites
human babesiosis have been reported. The
are also commonly seen.

rodent parasite B microti and the cattle

A number of serologic tests have been
parasite B divergens are the most
described for detection of antibodies to
commonly implicated species in North

Babesia in carrier aninlals. The most

America and Europe, respectively.

commonly used are the indirect fluorescent

However, B duncani, B venatorum,
antibody test and ELISA. A commercially

B conradae, and some less well-defined
produced ELISA for B bigemina is
species have also been incrinlinated. The
available. PCR and real-time PCR assays
reservoir hosts and vectors of some of these
capable of detecting extremely low
species are not necessaiily known with any
parasitemias, as occur in carrier aninlals,
certainty. Human Babesia infections are

BLOOD PARASITES

23
acquired via bites from infected ticks or

These include B can is, B vogeli, and B
through contaminated blood from an
rossi. B canis is transmitted by Derma
infected transfusion donor. Cases reported
centor reticularis in Europe, B vogeli by in splenectomized or otherwise immuno

Rhipicephaliis sanguineus in tropical
compromised individuals are often fatal.

and subtropical countries, andB rossi by

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Haemaphysalis leachi in South Africa.

Consequences of Babesia infection vary

Other Important Babesia of
from a mild, transient illness to acute

Domestic Animals
disease that rapidly results in death.

More than 100 species of Babesia have been

B gibsoni is the other important Babesia isolated from domestic animals and wildlife. of dogs and is a much smaller parasite. It The following are indicative of those
has a more limited distribution and
affecting domestic animals, but the list is
characteristically causes a chronic disease
far from complete.

with progressive, severe anemia that is not
readily treated with normal babesiacides.

Cattle: B divergens and B major are two Illness of varying severity due to B felis in temperate-zone species with features
domestic cats has mostly been reported in
comparable to those of B bovis and B
southern Africa. Sporadic cases associated
bigemina, respectively. B divergens is a with other Babesia species have been
small, pathogenic Babesia of considerable
reported elsewhere. An unusual feature of
importance in the British Isles and

B felis is its lack of response to the normal northwest Europe, whereas B major is a
babesiacides. However, primaquine
large Babesia of lower pathogenicity. B
phosphate (0.5 mg/kg, IM, twice with a
divergens is transmitted by Ixodes ricinus, 24-hr interval) is reported to be effective.

and B major by Haemaphysalis punctata.

CYTAUXZOONOSIS

Horses: Equine babesiosis is caused by

Theileria (formerly Babesia) equi or B

Cytauxzoonosis is an emerging, life-threat
caballi. T equi is a small parasite and is
ening infectious disease of domestic cats
more pathogenic than B caballi. T equi was

(Felis catus) caused by the tick-transmitted reclassified as a Theileria ( see p 33) in protozoan parasite Cytauxzoonfelis.

1998. Equine babesiosis is found in Africa,

Cytauxzoon spp are apicomplexan

Europe, Asia, South and Central America,
parasites within the family Theileriidae
and the southern USA. It is transmitted by
along with their closest relatives of
ticks of the generaRhipicephalus,

Theileria spp. C felis is transmitted to Dermacentor, and Hyalomma. Intrauterine domestic cats by the lone star tick infection, particularly with T equi, is also (Amblyomma americanum ). The natural
relatively common.

host for C Jelis is the bobcat (Lynx rujus ); reservoir hosts of the parasite include
bobcats and domestic cats that survive

Sheep and Goats: Although small
infection.

ruminants can be infected by several

Since the discovery of feline cytauxzospecies of Babesia, the two most important onosis in Missouri in the mid-1970s, the
species are B ovis and B motasi, transmitdistribution of C Jelis has been expanding.

ted by Rhipicephalus bursa and Haema

C felis has been reported in domestic cats
physalis spp, respectively. Infection is of in Missouri, Arkansas, Florida, Georgia,
importance in the Middle East, southern

Louisiana, Mississippi, Oklahoma, Texas,

Europe, and some African and Asian

Kentucky, Kansas, Tennessee, North
countries.

Carolina, South Carolina, Nebraska, Iowa,
and Virginia. Anecdotal reports of C Jelis

Pigs: B trautmanni has been recorded as infection in domestic cats in additional
causing severe disease in pigs. This parasite
states include Alabama, southern Illinois,
has been reported from Europe and Africa.

and Ohio.

Another species, B perroncitoi, is of similar pathogenicity but apparently has a limited

Aberrant and Natural Hosts: The
distribution in the areas mentioned above.

domestic cat has been considered an

The vectors of these Babesia have not been
aberrant or dead-end host of C Jelis given
clarified, althoughRhipicephalus spp have
the acute and fatal course of disease;
been shown to transmit B t:rautmanni.

however, there are reports of domestic cats
surviving natural infection with and without

Dogs and Cats: Babesia species have treatment. As a natural host, the bobcat typibeen reported in dogs from most regions.

cally experiences subclinical infection,

24

BLOOD PARASITES
followed by a chronic parasitemia. Rare

Schizont-infected WBCs are the principal
cases of fatal cytauxzoonosis in bobcats
cause of disease and death; they are found
have been reported. Cytauxzoonosis has
predominantly lining and often occluding
been reported in several other wild felids in
blood vessels. These "parasitic thrombi"

the USA and other countries, with both fatal
result in ischemia and tissue necrosis.

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and nonfatal outcomes. Infection has been

Schizont-infected WBCs then rupture and
reported in cougars, panthers, and tigers in
release piroplasms ( merozoites ), which
the USA, in addition to two suspected but
infect RBCs. The piroplasms in RBCs are
unconfirmed cases in cheetahs. C felis
fairly innocuous, with parasitemias ranging
infections of wild felids reported in other
from 1 o/er-4% on average; however, higher
countries include lions, jaguars, pumas,
parasitemias (ie, >100/o) have been
ocelots, and little spotted cats. In the early
docun1ented. During acute infection,

1980s, interspecies transmission of Cfelis
detection of merozoite-infected RBCs is
was investigated to identify additional
variable and has been correlated with
potential natural and aberrant hosts among
an increase in body temperature and a

91 wildlife, laboratory, and domestic farm
decrease in leukocytes. Without treatment,
animals. Bobcats and domestic cats were
survivors typically remain chronically
the only anin1als confirmed to be susceptiparasitemic, and at least one cat has been ble to C felis.

shown experimentally to be solidly inlmune
to subsequent infections. Chronic para

Transmission and Risk Factors: Cfelis sitemia has been established via inoculation is transmitted by the lone star tick, A am.er
with merozoite-infected RBCs. These
icanum.. Cytauxzoonosis is typically
chronically parasitemic cats clid not develop
diagnosed during April through September,
overt clinical disease but were not immune
which correlates with climate-dependent
to subsequent challenge with infection of
seasonal tick activity. Cats living near
sporozoites/schizonts, suggesting that the
heavily wooded, low-density residential
schizogenous tissue phase is required to
areas pa.tticularly close to natural or
establish inlmunity in domestic cats.

unmanaged habitats where both ticks and
bobcats may be in close proximity are at

Clinical Findings and Lesions: Onset of
highest risk of infection. Experimental
clinical signs for cats infected with C felis
infections have been induced with
usually occurs 5-14 days ( -10 on average)

parenteral injection of tissue homogenates
after infection by tick transmission.

(SC, IP, and IV) from acutely infected cats.

Nonspecific signs such as depression,

However, infection was not induced when
lethargy, and anorexia are the most
these tissues were administered intragas

· common presenting problems. Pyrexia and
trically or when noninfected cats were
dehydration are the most conm10n findings
housed together with infected cats in the
on physical examination; body temperaabsence of arthropod vectors, suggesting ture, which increases gradually, can be as
that oral and "cat-to-cat" transmission
high as 106°F ( 41 °C). Other findings include
does not occur. One recent study failed
icterus, lymphadenomegaly, and hepatoto document perinatal transmissi6n of splenomegaly. In extremis, cats are often

C felis from 2 chronically infected dams to hypothermic, dyspneic, and vocalize as if

14 healthy kittens, suggesting that vertical
in pain. Without treatment, death typically
transmission may not occur commonly, if
occurs within 2-3 days after peak in
at all.

temperature. At necropsy, splehomegaly,
hepatomegaly, enlarged lymph nodes, and

Life Cycle and Pathogenesis: After
renal edema are usually seen. The lungs
transmission from the tick into the cat,
show extensive edema and congestion with

C felis undergoes two major stages:

petechial hemorrhage on serosal surfaces
schizogony and merogony. First, sporozoand throughout the interstitium. There is ites infect WBCs (mononuclear phagoprogressive venous distention, especially cytes) and undergo schizogony (asexual
of the mesenteric and renal veins and the
reproduction) to form schizonts.

posterior vena cava. Hydropericardium is

Schizont-infected WBCs have been
often seen with petechial hemorrhage of
detected -12 days after experimental
the epicardium.

infection and increase in size from 15 µm

When first described, mortality of C felis
to up to 250 µm in diameter. They are most
infection was reported to be nearly 1000/o. A
commonly detected in lymph node, spleen, study of C felis in northwestern Arka.tlSas liver, lung, and bone marrow but have
and northeastern Oklahoma indicated
been documented in many organs and are
survival of natural infection in 18 cats with
occasionally seen on blood smears.

and without treatment; these cats seemed

BLOOD PARASITES

25

"less sick" initially, did not have temperaclumps at low power. In the absence of tures > 106°F ( 41 °C), and never became hypodetection of RBC piroplasms or schizonts thennic. Similar sporadic reports in other
on blood smear, a rapid diagnosis should
areas exist. Some hypotheses for swvival in
be pursued by perfomting fine-needle
these cats have included the following:

aspiration of a peripheral lymph node,

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l) an atypical route of infection, 2) innate
spleen, or liver to identify schizonts
inununity in certain cats, 3) increased
cytologically. These phagocytes are 15-250
detection of carriers, 4) decreased virulence
µm in dian1eter and contain an ovoid
with strain attenuation or occurrence of a
nucleus with a distinctive, prominent, large,
new strain, 5) dose of infectious inoculum,
dark nucleolus. The cytoplasm is often
and 6) tinting and type of treatment.

greatly distended, with numerous small
deeply basophilic particles representing

Diagnosis: The most common abnordeveloping merozoites.

malities on the CBC in animals with
ln the absence of these observations, a
cytauxzoonosis include leukopenia with
diagnostic PCR test with greater sensitivity
toxic neutrophils and thrombocytopenia
and specificity than nticroscopy can be
with a normocytic, normochromic anemia
done. This test is recommended in suspect
seen at later stages. The most common
cases in which the parasite is not observed,
biochemical abnormalities are hyperbiliruas well as to confinn identification of binemia and hypoalbuminemia but may
piroplasms or schizonts.

vary depending on organ systems affected
by parasitic thrombosis and ischemia with

Treatment and Control: Historically,
tissue necrosis. Other, less consistently
attempts to treat cytauxzoonosis with a
detected abnormalities include increased
variety of anti.parasitic drugs (parvaquone,
liver enzyme concentrations and azotemia. buparvaquone, trimethoprim/sulfadiazine, Rapid diagnosis requires microscopic
sodium thiacetarsan1ide) have been met
observation of piroplasms or schizonts.

with little success. ln one study, five of six

Observation of piroplasms on blood
cats and one additional cat were successsmears is variable; they are seen in fully treated with dintinazene aceturate (not
association with increasing body
approved in the USA) and imidocarb
temperature and typically become
di propionate (2 mg/kg, lM, two injections
apparent approximately 1-3 days before

3-7 days apart), respectively.

death. There are anecdotal reports of a

The most consistent successful treatment
higher level of sensitivity when blood is
in a large case se1ies resulted in survival of
collected from smaller vessels ( eg, ear vein 64% of cats given a combination of prick) to prepare blood smears. On a
atovaquone (15 mg/kg, PO, ti.ct for 10 days)

well-prepared, well-stained (Wrightand azithromycin ( 10 mg/kg/day, PO, for 10

Giemsa, Giemsa, Romanowsky most
days) and supportive care. Atovaquone is a
commonly) blood smear, when detectable,
ubiquinone analogue that binds cytochrome
merozoites may be seen ranging from
b. In one study of C felis-i.nfected cats

1 o/o-4% on average, with extremely high
treated with atovaquone and azithromycin,
percentages (ie, > 10%) reported in some
a C Jet-is cytochrome b subtype ( cytb l) was cases. They are pleomorphic and may be
identified that was associated with
round, oval, anaplasmoid, bipolar (bi.nucleincreased survival in the cats infected with ated), or rod-shaped; however, the round
this subtype compared with other subtypes.

and oval piroplasm fom1s are most

Future development of a rapid means to
commonly seen. The round forms are
identify the cytb l C felis subtype in infected 1-2.2 µm in dian1eter, whereas oval fom1s
cats may help better predict the likelihood
are 0.8-1 µm x 1.5-2 µm. They are pale
of survival with treatment.

centrally and contain a small, magenta,

Supportive care, including rv fluid
round to crescent-shaped nucleus on one
therapy and heparin (100-200 U/kg, SC, tid)

side. Once the parasitemia is -0.5%,
should be instituted in all cases. Nutritional

Maltese cross and paired piriforms may be
support via an esophageal or nasoesophaseen. Smears must be examined carefully geal feeding tube is recommended, which
to exclude Mycoplasma haemofelis,
also facilitates administration of oral

Howell-Jolly bodies, stain precipitate,
medications ( eg, atovaquone and azithroand water artifact.

mycin). Oxygen therapy and blood

The schizont tissue stage precedes the
transfusions should be administered when
formation of the RBC phase. Occasionally,
necessary. Anti-i.nflanunatory drugs may be
schizonts may be seen in peripheral blood
warranted in cases with W1relenting fever;
smears, particularly at the feathered edge,
however, the use of NSAlDs is contraindiand may be ntistaken for large platelet cated in cats with azotemia or dehydration.

26

BLOOD PARASITES

Once a diagnosis is achieved and treatand formerly classified as rickettsial ments have begun, minimal stress and
organisms are now understood to be more
handling are recommended. Recovery,
closely related to the order Mycoplasincluding resolution of fever, is often slow matales. This affiliation is based on their
and may take as long as 5---7 days. Cats that
lack of a cell wall, use of the codon UGA to

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survive have a complete clinical recovery,
encode tryptophan, and 168 rRNA gene
including resolution of hematologic and
sequences. Although the reassignment of
biochemical abnormalities within 2-3 wk.

Eperythrozoon and Haemobartonella to Some survivors remain persistently
the genusMycoplasma is still under debate,
infected with piroplasms and may
referral to this genus has been embraced,
represent a reservoir of infection. In
and they are commonly referred to as
one study, dose-intense diaminazene
hemotropic mycoplasmas or hemoplasmas.

diaceturate ( 4 mg/kg/day, IM, for 5

Several of these previously described red
consecutive days) failed to reduce the
cell parasites, now also having supporting
severity of parasitemia in cats chronically
genetic data, have been renamed Myco
infected with C Jelis and resulted in
plasma, whereas newly described
adverse drug reactions.

hemoplasmas are given the designation

"Candidatus." The hemoplasmas infect a Prevention: Routine application of a tick
wide variety of vertebrates throughout the
preventive is recommended to prevent
world, including several reports of human
cytauxzoonosis; however, disease has
infection. They share similar characteristics
occurred in cats despite this treatment. In
and morphologic features such as rod,
one study, a tick-repellent collar for cats
coccoid, and ring-shaped structures found
containing imidacloprid 100/<Vflumethrin
individually or in chains on the red cell and

4.5% prevented A americanum ticks from
gram-negative staining because of the lack
attaching, feeding, and transmitting C Jelis
of a cell wall; none of the hemoplasmas
in 10 cats infested with infected ticks after
have been cultured outside their hosts. It
application of the collar. In the same study,
is well established that the hemoplasmas
ticks attached and fed on 10 of 10 control
attach to the surface of the red cell but may
cats not treated with a collar, and 9 of the
under certain conditions penetrate this host

10 control cats were infected with C felis.

cell.

Exclusion of cats from areas likely to be

Several hemoplasmas are of veterinary
infested with the tick vector (ie, indoor
importance (see TABLE 4). These organisms only) is still considered the best method
vary in their ability to cause clinically
of prevention.

significant hemolytic anemia, but infected
animals may remain carriers despite
antibiotic therapy. Parasitemia may

HEMOTROPIC MYCOPLASMAS
reemerge if the animal is stressed or
irnmunocompromised. Once an initial

(Hemoplasmas)

infection is controlled, either naturally

Eperythrocytic parasites prJNiously known
or after antibiotic treatment, protective
as Haemobartonella and Eperythrozoon
immunity develops against repeat

IM=i!ii HEMOPLASMAS OF VETERINARY IMPORTANCE

Species

Hemoplasma

Dogs

Mycoplasma haemocanis (formerly Haemobartonella canis)

"Candidatus Mycoplasma haematoparvum"

Cats

Mycoplasma haemofelis (formerly Haemobartonella felis)

"Candidatus Mycoplasma haemominutum"

"Candidatus Mycoplasma turicensis"

Pigs

Mycoplasma suis (formerly Eperythrozoon suis) Mycoplasma parzrum (formerly Eperythrozoon parvum) Cattle

Mycoplasma wenyonii (formerly Eperythrozoon wenyonii) Sheep and goats

Mycoplasma ovis (formerly Eperythrozoon ovis) Llamas and alpacas "Candidatus Mycoplasma haemolamae"

BLOOD PARASITES

27

M haemofelis infection; how long this
can cause a severe hemolytic anemia in
immunity will last and whether this
young crias. The prevalence of chronic
applies to other hemoplasma infections
infection in sheep, pigs, and kennel-raised
is unknown.

dogs is high, and outbreaks of acute
disease have been reported in animals

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Transmission: Hemoplasmas may be
during research studies. Whether the
transmitted by transfer of infected blood
infection is chronic or acute, it may affect

(blood transfusion or use of contaminated
experimental results and lead to misinterneedles, surgical instruments, herd or pretation of data.

flock management equipment) or via

The hemolysis caused by hemoplasma
arthropod vectors such as lice, flies, ticks,
infections is typically extravascular and
and mosquitoes. Vertical transmission
results in a regenerative anemia. Erythrofrom mother to offspring has been cyte agglutination may be present, and
reported in cats, swine, and camelids.

Coombs' test results are often positive in

Direct transmission associated with
cats infected with M haemofelis. Splenecfighting is suspected in cats and supported tomized dogs with acute hemolysis due to
by studies reporting presence of hemo

M haemocanis may have agglutination,
plasma DNA in saliva, on gingiva, and on
spherocytosis, and a positive Coombs' test.

claw beds of infected cats.

Hypoglycemia secondary to glucose
consumption by the bacteria has been

Clinical Findings: Hemoplasmas are
reported in heavily parasitized pigs, sheep,
capable of causing a hem(')lytic anemia,
llamas, and calves; however, rapid bacterial
but the severity varies greatly. In general,
glycolysis in vitro may also cause artifactuasymptomatic infections tend to occur in ally decreased blood glucose concentrahealthy adult animals, and more severe tions.

acute anemias are associated with
splenectomy, immunocompromise,

Diagnosis: Historically, diagnosis has
concurrent diseases ( such as feline
been made based on detection of organisms
leukemia virus or feline immunodeficiency
on routine Wright-stained blood smears, on
virus in cats), or coinfection with multiple
which they appear as small (0.5-3 µm),
hemoplasma species. The main exception
basophilic, round, rod, or ring-shaped
is M haemofelis, which causes acute
structures present on erythrocytes
hemolytic anemia in healthy cats. The
individually or in chains, or sometimes seen
anemia may be severe and occasionally
free in the background. However, parafatal. Typical clinical signs include lethargy, sitemia in chronic infections can be cyclic,
anorexia, and fever, with splenomegaly and
and organisms can disappear from
icterus occurring less often.

circulation in as little as 2 hr. In addition,

M haemocanis causes ac;ute hemolysis
hemoplasmas dissociate from erythrocytes
in dogs that are splenectomized, but
and die after a variable amount of time in
infections are usually asymptomatic in

EDTA, hampering detection of organisms
healthy dogs. M suis causes hemolytic
in aged samples. Recent development of
anemia accompanied by icterus in neosensitive PCR assays capable of discriminatnatal pigs, feeder pigs, and pregnant sows.

ing between various hemoplasmas has

Chronic infection is associated with poor
greatly enhanced diagnosis of these
growth rates, decreased conception rates,
parasites and has led to identification
reproductive failure, and decreased milk
of several new Mycoplasma species.

production. M wenyonii infection in cattle
is usually asymptomatic, but a syndrome

Treatment and Control: For acute
of mammary gland and hind.limb edema,
infections, tetracyclines ( doxycycline,
decreased milk production, fever, and
oxytetracycline) have been the mainstay of
lymphadenopathy has been described in
treatment; enrofloxacin and marbofloxacin
young, nonanemic, primiparous heifers.

have also been effective against M haemo

Infection in young bulls has been reported
felis. Glucocorticoids may be useful to
to cause scrotal and hind.limb edema.

decrease erythrophagocytosis in cases

M ovis infection in sheep and goats is often of severe hemolysis; some animals may asymptomatic, but hemolytic anemia can
require blood transfusion. Treated animals
occur in young animals, especially those
remain carriers and may experience
with heavy intestinal worm burdens.

periodic clinical relapses. Blood donors

Chronic infection may result in poor
should be screened using PCR-based DNA
weight gain, exercise intolerance,
assays to prevent transmission to transfudecreased wool production, and mild sion recipients. Iatrogenic transmission can
anemia. Hemoplasma infection in camelids
be avoided by using properly sterilized

28

BLOOD PARASITES
needles and equipment. Control of
may remain chronically infected despite
arthropod vectors is recommended, as
normal or near normal PCV values. It has
is minimizing stress in herd and flock
been suggested that recrudescence of anemia
situations.

may occur when these chronically infected
cats are subject to debilitating disease, stress,

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Zoonotic Risk: Hemoplasma infections
or immunosuppressive therapies.

are usually species specific, except for M

Any anemic cat, especially an anemia
ovis, which infects both sheep and goats,
showing evidence of regeneration
and "Candidatus M haemolamae," which (polychromasia and/or reticulocytosis ),
infects both llamas and alpacas. There are
may be suspected of having FIA. The
reports of human eperythrozoonosis from
severity of clinical signs correlates with the

Inner Mongolia, China, but supporting
rapidity of onset of anemia. Clinical findings
evidence is not compelling. However, there
include weakness, pallor of the mucous
have been rare reports of hemoplasma
membranes, tachypnea, tachycardia, and
infections in immunocompromised people
occasionally collapse. Acutely ill cats may
in which molecular methods were used for
be febrile, and moribund cats may be
confinnation. One report documented an
hypothermic. Other physical examination

HIV-positive human patient coinfected with
abnormalities may include cardiac

Bartonella henselae and a hemoplasma
murmurs, splenomegaly, and icterus. In
genetically similar to M haemofelis. This
chronic or slowly developing cases, there
individual owned five cats and had multiple
may be normal or subnormal body
scratch and bite wounds. All five cats were
temperature, weakness, depression,

PCR positive for Bartonella spp and two
and weight loss or emaciation.

were positive for M haemofelis, suggesting

Expected laboratory abnormalities
the possibility ofzoonotic transmission. The include a moderate to marked regenerative coinfection of a veterinarian in Texas with
anemia, increased numbers of nucleated

B henselae andM ovis also has been

RBCs, polychromasia, anisocytosis,
reported.

Howell-Jolly bodies, and an increased
reticulocyte count. Coombs' tests can

Feline Infectious Anemia
become positive 7-14 days after organisms
appear in the blood and remain positive

(Hemoplasmosis)

throughout the acute phase, reverting to

In cats, hemotropic mycoplasmosis can
negative in chronically infected carrier
produce a disease called feline infectious
cats.

anemia (FIA), previously known as .

Laboratory confinnation has traditionhemobartonellosis. Most cases are in ally been based on identification of
outdoor, male cats .. M haemofelis (previorganisms in the peripheral blood using ously the Ohio strain, or large form, of
light microscopy, although M haemofelis

Haemobartonellafelis) is the most
is visible <50% of the time in acutely
pathogenic organism causing FIA, and it
infected cats. Some laboratories offer
can cause hemolytic anemia in immuno

PCR assays that are considerably more
competent cats. "Candidatus M haemo
sensitive and specific than blood-smear
minulum" (previously the California strain, evaluation. Detection of M haemofel-is via
or small form, of H felis) is the most

PCR is more significant than detection of
common hemoplasma in cat populations
other hemoplasma species ("Candidatus
worldwide, but it has not been clearly

M turicensis" and "Candidatus M
associated with disease in immunocompe
haemominutum"), which are not as
tent cats. "Candidatus M turicensis" has strongly associated with anemia.

never been seen on blood smears, and its

Without treatment, one third of acutely
pathogenicity is not well understood. Both
ill cats may die. Treatment involves both

Candidatus species may be capable of
supportive therapies, such as oxygen and
inducing anemia in cats with underlying
blood transfusions, and specific therapy
immunosuppressive disease, such as feline
with doxycycline (10 mg/kg/day, PO, for
leukemia virus infection.

a minimum of2 wk). Because of the

In the case of M haemofelis infection, an
potential for esophagitis and esophageal
incubation period of 2--30 days is followed by
strictures, administration of doxycycline
anemia, with some cats developing cyclical
hyclate preparations should be followed
changes in PCV that coincide with the
by administration of a bolus of several
appearance of large nun1bers of organisms
milliliters of water. Enrofloxacin (5 mg/
on blood smears. In untreated cats, this acute
kg/day, PO) is a suitable alternative to
phase lasts for 3--4 wk, after which some cats
doxycycline. Treatment of PCR-positive,

BLOOD PARASITES

29
healthy cats is currently not recomsporulated oocysts. It is unknown at present mended, because no regimen has yet been whether a similar path of infection may identified that completely eliminates the
occur in H canis infections, although
organism. The use of immunosuppressive
monozoic cyst stages have been reported
dosages of glucocorticoids to suppress
in the spleen of both experimentally and

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immune-mediated RBC injury is contronaturally infected dogs. It is possible that versial but may be used in cats that do not
canids may serve as both transport and
respond to antimicrobial therapy alone,
definitive hosts of H canis.

or when primary immune-mediated

In much of the world (India, Africa,
hemolytic anemia is a possible cause.

southeast Asia, the Middle East, southern

Europe, and islands in the Pacific and Indian

Oceans), dogs with hepatozoonosis usually

OLD WORLD HEPATOZOO OSIS
have subclinical infections or only mild

AND AMERICAN CANINE
clinical signs. In these areas, imrnunosup

HEPATOZOONOSIS
pression caused by concurrent disease or
other factors appears to play an important

Etiology, Epidemiology, and Trans
role in the manifestation of significant
mission: Old World hepatozoonosis is a
clinical signs. In the USA, imrnunosupprestickbome disease of wild and domestic sion or concurrent disease does not appear
carnivores caused by the protozoa! agent
necessary to induce the more severe clinical

Hepatozoon canis. It is unclear whether
signs typically seen with ACH.

infections in wild and domestic Felidae are

ACH is an emerging disease that has
caused by H can is or by another species of primarily spread north and east from the

Hepatozoon. This organism is transmitted

Gulf Coast of Texas, where it was originally
by the brown dog tick, Rhipicephalus
detected in 1978. The distribution of this
sanguineus. In the late 1990s, unique
parasite parallels the distribution of the Gulf
features of the clinical presentation in North Coast tick. Most cases in the USA have been American dogs suggested that a different
diagnosed in Texas (primarily along the
strain or species of Hepatozoon might

Gulf Coast), Oklahoma, and Louisiana;
be responsible for the disease in North
numerous cases have been reported from

America than in other parts of the world; in

Alabama, and cases have been seen as far

1997, this suspicion was confirmed based on east as Tennessee, Georgia, and Florida parasite morphology, tissue tropism, and

Sporadic cases have been reported from
pathogenesis. The disease in North America
such disparate geographic locations as
is caused by H americanum, which is

California, Washington, and Vermont; it is
transmitted by the Gulf Coast tick,
assumed these dogs were relocated from

Amblyomma maculatum, rather than by
enzootic areas, because the Gulf Cqast tick
the brown dog tick. Accordingly, the disease has not become established in such distant in North America is now recognized as a
locations. H americanum may be present
separate entity, American canine hepatoin Central and South America, as is A zoonosis (ACH). Genetic and antigenic
maculatum, but to date, no autochthonous
differences now documented between the
transmission of H americanum has been

North American and Old World organisms
reported from these regions. A ovale has
further support their classification as
been identified as a vector for H canis in
distinct species.

South America It was previously thought

The mode of transmission of hepatothatH can is did not infect canids in Nmth zoonosis is not typical in the classical sense

America, despite the presence of R
of a tickbome disease; like other species in
sanguineus, but molecular evidence has
the genus, H canis and H americanum
recently emerged that suggests otherwise.

infections occur when an infected tick, the

Still, ACH remains the more severe and
definitive host, is ingested by the dog ( or
more common form of hepatozoonosis
other vertebrate intermediate host).

in the New World.

Sporozoites released from the mature

In general, imrnunocompetent dogs
oocysts in the tick's hemocoel enter the
appear to tolerate infection with H can is
vertebrate host via the gut. Dogs can also
very well. Although life-threatening
acquire ACH by eating paratenic (transport)

infections have been reported, clinical signs
hosts that contain cystozoites, a resting
associated withH canis infection are most
stage of H americanum encysted in their
often subclinical to mild. However, H
tissues. Experimentally, cystozoite-engen
americanum causes severe clinical signs
dered infection results in the same disease
in most dogs, with death often occurring
manifestations seen in dogs that ingest
within 1-2 yr without supportive therapies.

30

BLOOD PARASITES

Clinical Findings: The tissue phases of
finding rare gamonts in peripheral blood
the hepatozoonosis organism, especially
leukocytes (using Romanowsky-type
those of H americanum, induce pyogranustains) or identifying pathognomonic "onion lomatous inflammation, which results in
skin" cysts or pyogranulomas in stained

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clinical signs. These signs, which may be
sections of biopsied muscle san1ple. Muscle
intem1ittent, include fever, depression,
biopsy, although invasive, is considered the
weight loss, poor body condition, muscle
gold-standard method for diagnosing ACH,
atrophy, soreness, stiffness, and weakness;
because parasite and parasite-induced
mucopurulent ocular discharge is common,
lesions are often extensively distributed
and bloody diarrhea occurs occasionally.

tlu·oughout muscle tissue ( especially in

Surprisingly, many dogs maintain a nom1al
areas with observable atrophy). However, in
appetite if food is placed directly in front of
some dogs, multiple or sequential biopsies
them, but they often will not move to eat,
may be necessary to detect the organism.

apparently owing to intense pain. Severe

Unlike in H americanum infections,
hyperesthesia or pain over the paraspinal
parasitemia in dogs with clinical H can is region is a common finding on physical
infection is often quite high, and a diagnosis
exanlination; cervical,joint, or generalized
can readily be achieved by microscopic
pain is also seen. Hyperesthesia, presumexamination of stained blood fibns to ably due to severe inflammation within
visualize parasite-containing leukocytes.

muscle and sometinles along bone,

The most common abnom1ality on bloodmanifests as stiffness and reluctance to work in dogs infected with H can is is move, as well as cervical and/or truncal
anemia. Serum chemistry abnormalities
tigidity. Fever, which may fluctuate with the
may be sinlilar to those seen in dogs with
waxing and waning of clinical signs, ranges

ACH. Hepatitis, pneumonia, and glomerulofrom 102. 7°-l06°F (39.3°-41 °C) and is nephritis associated with H can is meronts unresponsive to antibiotics. Longterm
have been repmted postmortem in some
sequelae include glomerulonephritis and
anin1als with extremely high parasitemia.

amyloidosis. H ca.nis tissue stages reside Although experimental serologic assays
within bone marrow, lymph nodes, and
have been developed to detect both H
spleen. Unlike in dogs with ACH, dogs
americanum and H canis infections, none infected with H can is typically do not
is available commercially. PCR methods
appear painful at presentation; in dogs with
developed to detect circulating H epatozoon overt disease, nonspecific symptoms
are available through several different
including fever, lethargy, and depression
institutions (including Auburn University
may be seen.

and North Carolina State University),
although they may lack sensitivity in

Diagnosis: In dogs with ACH, the most

H americanum infections because of
consistent laboratory abnormality is a
typically low levels of parasitemia. These
neutrophilic leukocytosis, with counts
molecular tests have led to the realization
ranging from 20,000-200,000 cellsl�tL. This
that classical hepatozoonosis caused by H
is typically a pron0tmced, ma,.ture neutro
canis is more common in North America
philia, although a left shift may be present.

than previously known. Moreover,

A mild to moderate normocytic, nonnorecognized variation in an 18S rDNA chromic, nonregenerative anemia is also
sequence from infected clogs has raised new
common. The platelet count is typically
questions about canine hepatozoonosis. It
normal to high. Mildly increased alkaline
may be that still more species ( or strains)

phosphatase, hypoalbuminemia, and
that vary in pathogenicity and/or life cycle
increased CK may also be seen. Although
patterns will be found to cause disease in
profound hypoglycemia has been reported,
dogs.

this finding is thought to be an in vitro
sampling artifact that results from increased Treatment: Hepatozoonosis is generally metabolism of glucose by the overly
considered a lifelong infection in dogs. No
abundant leukocytes. On radiographs,
known therapeutic regimen completely
periosteal reactions may be seen involving
clears the body of the organism. In the past,
any bone, including the skull and ve1tebrae.

treatment of ACH has been frustrating,

These periosteal reactions resemble those
because most dogs showed only temporary
of hypertrophic osteoarthropathy, except
in1provement with frequent relapses within
that lesions tend to be proxin1al rather than

3-6 mo and death within 2 yr of diagnosis.

distal with ACH, often markedly obvious in

Remission of clinical signs can usually be
long bones. The physiologic basis of tl1e
achieved through a 14-day course of
bone lesions has not been determined.

combination therapy, referred to as TCP,

Definitive diagnosis of ACH is made by
which consists of trimethoprim-sulfadiazine

BLOOD PARASITES

31

(15 mg/kg, PO, bid), clindamycin (10 mg/kg,

However, high prevalence rates of

PO, tid), and pyrirnetharnine (0.25 mg/kg/
subclinical infections cause significant
day, PO). Unfortunately, remission with this
losses due to longtenn effects on growth
therapy has often been short-lived, and dogs
and productivity and increased susceptibil

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frequently relapse witllin 2-6 mo. However,
ity to other parasitic or bacterial diseases.

an adjunctive treatment using decoquinate

Schistosomes are members of the genus
has been useful. Decoquinate does not

Schistosoma, family Schistosomatidae.

resolve active clinical disease but may

Adult worms are obligate parasites of the
prevent clinical relapses; it is given after
vascular system of vertebrates. Schistoresolution of clinical signs as an adjunct to somes are dioecious. The mature female

TCP therapy. The reconunended dosage of
is more slender than the male and
decoquinate is 10-20 mg/kg, PO, bid
normally is carried in a ventral groove, the
continuously for 2 yr. The advent of TCP
gynaecophoric canal, that is formed by
combination therapy followed by daily
ventrally flexed lateral outgrowths of the
decoquinate therapy has resulted in marked
male body.

improvement in the prognosis for dogs with

Of the 19 species reported to naturally

ACH. NSAIDs may be the best treatment for
infect animals, S-all parasites of rumicontrol of fever and pain, especially during nants-have received particular attention,
the first few days of TCP therapy. Glucocormainly because of their recognized ticoid administration should be avoided
veterinary significance: S mattheei, S bovis,
because, although steroids may provide

S curassoni, S spinda.le, S indicum,
temporary relief, longterm use can

S nasale, S incognitum, and S japonicum.

exacerbate the disease.

S mattheei is found in southeastern Af1ica, H canis infections are treated with
from the Cape Province in South Afiica
i.rnidocarb dipropionate, twice montluy, at
northward to Tanzania and Zambia S bovis

5-6 mg/kg, SC, until the parasite is no longer
is found in the Mediterranean region and
evident in blood smears for 2-3 consecutive

Middle East, and is common in northern,
months. Prognosis often depends on the
western, and eastern Africa ( except Egypt)

degree of parasitemia; dogs with low
extending southward to Central Angola,
parasitemia typically respond well to
southern Congo, and possibly northern
treatment, whereas those with high

Zambia. S curassoni has been found in
parasitemia may not, especially if afflicted
runlinants in Senegal, Mauritania, Mali,
by concurrent illness.

Niger, and Nigeria. S spindale has been

Preventing access to ticks and discouragrecorded from India, Sri Lanka, Indonesia, ing predation are the most effective fonns

Malaysia, Thailand, and Vietnan1. The
of control for hepatozoonosis. Predation
distribution of S indicum appears confined
presents a dual 1isk for acquiring ACH:

to the Indian subcontinent. S nasale is
prey captured/ingested by dogs could have
found in India, Sri Lanka, Bangladesh, and
infected ticks on their coats that would

Myanmar. S incognitum has been reported
provide a source of sporozoites; additionfrom India, Thailand, and Indonesia. S
ally, the prey could contain cystozoites
japonicum is endemic in several countries

( at least in the case of H americanum)

of the Far East. Some of these species are
that are also infectious. Additionally, dogs
known to interact in areas where they
diagnosed with hepatozoonosis should not
coexist, and instances of interspecific
be bred because transplacental transmishybridization have been reported, eg, the sion of H can is has been documented,
cattle parasites S bovis and S curassoni.

and although vertical transmission of

Novel molecular tools have also provided

H americanum has not been reported,
evidence for the natural hybridization
the possibility should not be disregarded.

between S haematobium, a parasite of

There is no known zoonotic 1isk with
people, and S mattheei, S bovis, and
hepatozoonosis.

S curassoni. The hybridization between
human and run1inant schistosomes is of
particular interest, because for this to occur,

SCHISTOSOMIASIS
host switching must have taken place of

S mattheei, S bovis, or S curasson·i into Schistosomiasis is a common parasitic
people or of S haematobium into domestic
infection in cattle and rarely in other
livestock.

domestic animals in Africa and Asia.

To differentiate the differentSchisto

Although schistosomes may act as
soma spp, egg morphology ( size, shape) can important pathogens under rare conditions
be used. The species can also be differentifavoring intensive transmission, most ated through such taxonomic features as
infections in endemic areas are subclinical.

morphologic (adult worms), life-cycle, or

32

BLOOD PARASITES
behavioral characteristics; chromosomes;
may be recognized in the short term, high
host specificity; or enzyme and DNA
prevalence rates of chronic schistosome
studies.

infections cause significant losses on a
herd basis. These losses are due to less

Life Cycle, Transmission, and
easily recognizable effects on growth

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Epidemiology: Schistosomes live in the
and productivity, as well as increased
mesenteric and hepatic veins of the host
susceptibility to other parasitic and

( except for S nasale, which lives in the
bacterial diseases.

nasal veins), where they feed on blood and

Occasional outbreaks of clinical
produce eggs with a characteristic terminal
intestinal schistosomiasis due to
or lateral spine. Eggs passed in the feces

S mattheei, S bovis, or S spindale have must be deposited in water if they are to
been reported. They are usually restricted
hatch and release miracidia, which invade
to young livestock and adult animals
suitable water snails and develop through
undergoing relatively heavy primary
primary and secondary sporocysts to
infections under conditions of intensive
become cercariae. When fully mature, the
transmission. The disease is charactecercariae leave the snail and swim freely in rized by diarrhea, weight loss, anemia,
the water, where they remain viable for
hypoalbuminemia, hyperglobulinemia,
several hours. Ruminants are usually
and severe eosinophilia that develop after
infected with cercariae by penetration
the onset of egg excretion. Severely
of the skin, although infection may be
affected animals deteriorate rapidly
acquired orally while animals are drinking.

and usually die within a few months of

During penetration, cercariae develop into
infection, while those less heavily infected
schistosomula, which are transported via
develop chronic disease with growth
the lymph and blood to their predilection
retardation.

sites. The prepatent period varies

In the intestinal and hepatic forms, adult
according to the species but is generally
flukes are found in the portal, mesenteric,

45-70days.

and intestinal submucosal and subserosal

The occurrence of cattle schistosomes
veins. However, the main pathologic
within their range is discontinuous,
effects are associated with the eggs. In the
depending on the presence of intermediate
intestinal form, passage of eggs through
snail hosts, their level of infection, and the
the gut wall causes the lesions, while in the
frequency of water contacts. In areas where
hepatic form, granulomas form around
conditions are favorable, prevalence rates
eggs trapped in the tissues. Other hepatic
of infections in cattle may be 40%--- 700/o anp
changes include medial hypertrophy and
commonly higher.

hyperplasia of the portal veins, develop

The increased host range of the hybrid
ment of lymphoid nodules and follicles
parasites and changes in host distribution
throughout the organ, and periportal
seen in Africa may have a direct impact on
fibrosis in more chronic cases. Extensive
transmission of these schistosomes. Laboragranuloma formation also is seen in the tory hybrids have been observed to acquire
intestine. In severe cases, numerous areas
enhanced characteristics such as infectivity,
of petechiation and diffuse hemorrhage are
fecundity, and growth rates.

seen in the mucosa, and large quantities of

There is strong evidence that acquired
discolored blood may be found in the
immunity to schistosome infection in cattle intestinal lumen. Frequep.tly, the paraexists. This immunity mainly acts through sitized blood vessels are dilated and
suppression of worm fecundity. Examinatortuous. Vascular lesions also may be tion of naturally infected animals has
found in the lungs, pancreas, and bladder
shown that partial protection against
of heavily infected animals.

reinfection also occurs, and acquired resis

The hybridization events reported
tance to schistosomes is of major
between animal and human schistosomes
importance in the regulation of infection
may result in phenotypic characteristics
intensity in the field.

that influence pathology (and drug
sensitivity).

Nasal schistosomiasis is associated

Clinical Findings and Lesions: In
with cauliflower-like growths on the nasal
the great majority of cases, visceral
mucosa, causing partial obstruction of the
schistosomiasis in endemic areas is
nasal cavity and snoring sounds when
subclinical and characterized by a high
breathing. Hemorrhagic and/or mucopuruprevalence of low to moderate worm lent nasal discharge is a common feature.

burdens in the cattle population.

Adult flukes are found in the blood vessels

Although few or no overt clinical signs
of the nasal mucosa, but again, the main

BLOOD PARASITES

33
pathogenic effects are associated with the
methods, or their removal by mechanical
eggs, which cause abscesses in the mucosa.

barriers or snail traps. Ecologic measures

The abscesses rupture and release eggs and
against the snails that aim to render their
pus into the nasal cavity, which eventually
habitat unsuitable for survival, such as
leads to extensive fibrosis. In addition, large
drainage, removal of water weeds, and

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granulomatous growths are common on
increased water flow, have also proved
the nasal mucosa and occlude the nasal
valuable. These measures not only help
passages and cause dyspnea.

reduce the transmission of schistosomiasis
but also help control other parasitic

Diagnosis: Because signs and history
trematodes such as Fasciola gigantica and
alone are insufficient to distinguish visceral
paramphistomes, which also have water
schistosomiasis from other debilitating
snails as intermediate hosts and frequently
diseases, diagnosis should be confirmed by
are found in the same localities as
the presence and identification of eggs in
schistosomes.

the feces of the infected animal. At
necropsy, macroscopic examination of the

THEILERIASES
mesenteric veins for the presence of adult
worms or microscopic examination of

Theileriases are a group of tickbome
scrapings of the intestinal mucosa or of
diseases caused by Theileria spp. A large
crushed liver tissue (both for eggs) may
number of Theileria spp are found in
prove easier.

domestic and wild animals in tick-infested

Eggs of S bovis, S curassoni, and S
areas of the Old World. The most important
mattheei are spindle-shaped. Because of
species affecting cattle are T parva and
the interspecific hybridization between

T annulata, which cause widespread death

S bovis and S curassoni and the natural in tropical and subtropical areas of the Old
hybridization between S haematobium and

World. T lestoquardi, T luwenshuni, and

S mattheei, S bovis, and S curassoni, eggs T uilenbergi are important causes of
of intermediate morphology may be seen.

mortality in sheep.

The eggs of S spindale are more elongated

Both Theileria andBabesia are members
and flattened on one side, and those of
of the suborder Piroplasmorina. Although

S nasale are boomerang-shaped. The oval

Babesia are primarily parasites of RBCs,
eggs of S japonicum are relatively small,

The"ileria use, successively, WBCs and with a rudimentary spine.

RBCs for completion of their life cycle in

Very low fecal egg excretion is commonly
mammalian hosts. The infective sporozoite
seen in chronic infections; therefore, it may
stage of the parasite is transmitted in the
be preferred to use quantitative miracidial
saliva of infected ticks as they feed.

hatching techniques which, in addition to

Sporozoites invade leukocytes and, within
being more sensitive, also provide
a few days, develop to schizonts. In the
information on the viability of the eggs
most pathogenic species of Theileria
excreted in the feces.

( eg, T parva and T annulata ), parasite multiplication occurs predominantly within

Treatment and Control: Praziquantel
the host WBCs, whereas less pathogenic

(25 mg/kg) is highly effective, although two
species multiply mainly in RBCs. Developtreatments 3-5 wk apart may be required.

ment of the schizont stage of pathogenic

However, for practical and economic

Theileria causes the host WBC to divide; at reasons, schistosomiasis in domestic stock
each cell division, the parasite also divides.

is rarely treated. Only in China, where

Thus, the parasitized cell population
infected livestock constitute important
expands and, through migration, becomes
reservoirs of human infection, have mass
disseminated throughout the lymphoid
treatments with praziquantel been practiced system. Later in the infection, some of the widely.

schizonts undergo merogony, releasing

The most effective way to control cattle
merozoites that infect RBCs, giving rise to
schistosomiasis in endemic areas is to
piroplasms. Uptake of piroplasm-infected
prevent contact between the animals and

RBCs by vector ticks feeding on infected
the parasite by fencing of dangerous waters
animals is the prelude to a complex cycle
and supplying clean water. Unfortunately,
of development, culminating in transmisthis is not always possible in parts of the sion of infection by ticks feeding in their
world where nomadic conditions of
next instar (trans-stadia! transmission).

management prevail. Other methods of

There is no transovarial transmission as
control include destruction of the snail
occurs in Babesia. Occurrence of disease
intermediate host population at transmisis limited to the geographic distribution sion sites, either by chemical or biologic
of the appropriate tick vectors. In some

34

BLOOD PARASITES
endemic areas, indigenous cattle have a
needle aspirates from lymph nodes contain
degree of innate resistance. Mortality in
multinuclear schizonts. Anorexia develops,
such stock is relatively low, but introduced
and the animal rapidly loses condition;
cattle are particularly vulnerable. Unlike
lacrimation and nasal discharge may occur.

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in babesiosis, in theileriasis there is no

Terminally, dyspnea is common. Just before
evidence of increased resistance in calves
death, a sharp decrease in body temperature

<6mo old.

is usual, and pulmonary exudate pours from
the nostrils. Death usually occurs 18-24 days
after infection. The most striking postmor

East Coast Fever
tem lesions are lymph node enlargement and

East Coast fever, an acute disease of cattle,
massive pulmonary edema and hyperemia.

is usually characterized by high fever,

Hemorrhages are common on the serosal
swelling of the lymph nodes, dyspnea, and
and mucosal surfaces of many organs,
high mortality. Caused by Theileria parva,
sometimes together with obvious areas of
and transmitted by the tick vector
necrosis in the lymph nodes and thymus.

Rhipicephalus appendiculatus, it is a

Anemia is not a major diagnostic sign ( as it
serious problem in east and southern Africa. is in babesiosis) because there is minimal division of the parasites in RBCs, and thus

Etiology and Transmission: The African no massive destruction of them.

buffalo (Syncerus ca.ff er) is an important Animals that recover are immune to
wildlife reservoir of T parva, but infection is subsequent challenge with the same strains asymptomatic in buffalo. Tparva transmitbut may be susceptible to some heteroloted by ticks from either cattle or buffalo gous strains. Most recovered or immunized
cause severe disease in cattle, but buffaloanimals remain carriers of the infection.

derived parasites differentiate poorly to
merozoites in cattle and generally are not
transmitted by ticks. Hence, buffalo T parva Treatment and Control: Treatment are maintained as a separate population.

with parvaquone and its derivative

Buffalo T parva were previously considered buparvaquone is highly effective when a separate subspecies (T parva lawrencei),
administered in the early stages of clinical
but DNA typing indicate that the cattle and
disease but is less effective in the advanced
buffalo parasites are a single species.

stages, in which there is extensive destruc

T parva is usually highly pathogenic, causing tion of lymphoid and hematopoietic tissues.

high levels of mortality, although some less
hmnunization of cattle against T parva
pathogenic isolates have been identified.

using an infection-and-treatment procedure
is practical and continues to gain acceptance

Pathogenesis, Clinical Findings, and
in some regions. The components for this

Diagnosis: T parva sporozoites are
procedure are a cryopreserved sporozoite
iitjected into cattle by infected vector ticks.

stabilate of the appropriate strain( s) of

An occult phase of 5---10 days follows before

Theileri,a derived from infected ticks and a infected lymphocytes can be d�tected in
single dose of long-acting oxytetracycline

Giemsa-stained smears of cells aspirated
given simultaneously; although oxytetracyfrom the local draining lymph node.

cline has little therapeutic effect when

Subsequently, the number of parasitized
administered after development of disease,
cells increases rapidly throughout the
it inhibits development of the parasite when
lymphoid system, and from about day 14
given at the outset of infection. Cattle should
onward, cells undergoing merogony are
be immunized 3--4 wk before being allowed
observed. This is associated with wideon infected pasture. Parasitized bovine cells spread lymphocytolysis, marked lymphoid
containing the schizont stage of T parva and depletion, and leukopenia. Piroplasms in

T annulata can be cultivated in vitro as

RBCs infected by the resultant merozoites
continuously growing cell lines. ln the case
assume various forms, but typically they are
of T annulata, cattle can be infected with a small and rod-shaped or oval.

few thousand cultured cells. Attenuated

Clinical signs vary according to the level
strains produced by serial passage of such
of challenge, and they range from inapparcultures form the basis of live vaccines used ent or mild to severe and fatal. Typically,
in several countries, including Israel, Iran,
fever occurs 7-10 days after parasites are
lndia, and the former USSR.

introduced by feeding ticks, continues
lncidence of East Coast fever can be
throughout the course of infection, and may
reduced by rigid tick control, but this is not
be> 106°F ( 41 °C). Lymph node swelling
feasible in many areas because of cost and
becomes pronounced and generalized.

the high frequency of acaricidal treatment

Lymphoblasts in Giemsa-stained smears of
required.

BLOOD PARASITES

35

Tropical Theileriosis

Africa Mortality can approach 100%.

Theileria annulata, the causal agent of

Schizonts can readily be demonstrated in
tropical theileriosis, is widely distributed in

Giemsa-stained smears of needle biopsies
north Africa, the Mediterranean coastal
from swollen superficial lymph nodes.

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area, the Middle East, India, the former

Recently, two species of Theileria

USSR, and Asia. It is transmitted by several

T luwenshuni and T uilenbergi hav� been species of ticks of the genusHyalomma.

identified as the causal agents of a severe

T annulata can cause mortality of up to
disease in sheep in China These species are

9()0A,, but strains vary in their pathogenicity.

morphologically indistinguishable and

The kinetics of infection and the main
cause sinlilar disease but can be distinclinical findings are similar to those guished by DNA typing methods. They are
produced by T parva, but unlike in East
transmitted by ticks of the genus Haema

Coast fever, anemia is often a feature of the
physalis. Schizonts are detected in a range disease. Characteristic signs include fever
of tISsues, but later and in smaller numbers
and swollen superficial lymph nodes. If the
than in other pathogenic Theileria spp.

disease progresses, cattle rapidly lose

Prroplasms are consistently detected in
condition. The schizonts and piroplasms are RBCs. Morbidity and mortality rates of up to morphologically similar to those of T parva.

65% (T luwenshuni) and 75% (T uilenbergi) Animals that recover from infection are
have been seen in susceptible animals
immune to subsequent challenge. Treatintroduced into endemic areas. Affected ment and control are as described for East
aninlals show sustained fever and anemia

Coast fever (seep 34).

Several other nonpathogenic Theileria
spp ( eg, T ovis) are also widely distributed.

Piroplasms of these species are polymorphic.

Other Theileriases of Cattle

The Theileria oriental is group, consisting Equine Theileriasis
of the closely related parasites T orientalis

T buffeli, and T sergenti, has a worldwide Babesia equi was reclassified as T equi in distiibution. These parasites are transmit1998, based on DNA analysis and other ted by ticks of the genusHaemaphysalis.

biologic data ( see p 21).

The piroplasms are larger than those of T
parva and T annulata, and they multiply TRYPANOSOMIASIS
principally by intraerythrocytic division.

Mortality, particularly in indigenous cattle

Tsetse-transmitted Trypanosomiasis
is rare, but infection can sometin1es result'

in progressive chronic anemia.

This group of diseases caused by protozoa

T mutans and T vel'ifera are found in of the genus Trypanosoma affects all

Africa, where they are transmitted by ticks
domesticated aninlals. The major veterinary
of the genusAmblyomma. Multiplication ocspecies are T congolense, T vivax, T brucei curs mainly by intraerythrocytic division.

brucei, and T simiae. T brucei rhodesiense The piroplasms are morphologically indistinand T brucei gambiense are zoonotic, with guishable from those of T orientalis and T
people as the predominant host. For the
taurotragi ( an African parasite of eland and aninlals mainly affected by these tsetsecattle), but the parasites can be differentitransmitted trypanosomes and the ated by serologic tests such as indirect
geographic areas where tsetse-transmitted
fluorescent antibody and by DNA typing.

trypanosomiasis occurs, see TABLE 5.

Some strains of T mu tans are pathogenic as Cattle, sheep, and goats are infected in
well. In addition, concurrent infection may
order of importance, by T congolense
add to the pathogenicity of T parva.

T viva:i:, �d T brucei brucei. In pigs,'

T simiae 1s the most important. In dogs

Ovine and Caprine Theileriases
and cats, T brucei is probably the most
important. It is difficult to assign an order of

Theileria lestoquardi (formerly T hirci) unportance for horses and camels. T vivax
causes a disease in sheep and goats similar
is found outside tsetse-infested areas of
to that produced in cattle by T annulata
sub-Sailaran Africa, carried mechanically
with which it is closely related. T lesto-
by biting flies.

quardi is transmitted by ticks of the genus The trypanosomes that cause tsetse

Hyalomma. The limited available epidemio

�ansmitted trypanosomiasis (sleeping
logic data indicate that T lestoquardi has a sickness) m people, T brucei rhodesiense
more restricted geographic distribution than and T brucei gambiense, closely resemble that of T annulata, being particularly

T brucei brucei, and suitable precautions
prevalent in the Middle East and northeast
should be taken when working with such

36

BLOOD PARASITES

IM=iiii TSETSE-TRANSMITIED TRYPANOSOMES Major Geographic

Trypanosoma spp Animals Mainly Affected Distribution

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T congolense

Cattle, sheep, goats, dogs, pigs,

South and eastern Africa
camels, horses, most wild animals

Tvivax

Cattle, sheep, goats, can1els,

Africa, Central and South
horses, various wild animals

America, West Indies•

T brucei brucei

All domestic and various wild

South and eastern Africa
animals; most severe in dogs,
horses, cats

T brucei r/wdesiense Cattle, wild hooved stock, people South and eastern Africa T bruce-i garnbiense

Cattle, sheep, goats, people

West and central Africa,
including Uganda

Tsimiae

Domestic and wild pigs, horses,

South and eastern Africa
camels

" In non-tsetse ru-eas, transmission is by biting flies.

isolates. Domestic animals act as reservoirs
requires only that blood containing infectious
of human infections.

trypanosomes be transferred by bite from
one anin1al to another.

Transmission and Epidemiology:

Pathogenesis: Infected tsetse inoculate

Most tsetse transmission is cyclic and
metacyclic trypanosomes into the skin of
begins when blood from a trypanosomeanimals, where the trypanosomes reside for infected animal is ingested by the fly. The
a few days and cause localized inftanimation
trypanosome alters its surface coat,

(chancres). They enter the lymph and lymph
multiplies in the fly, then alters its surface
nodes, then the bloodstream, where they
coat again, and becomes infective. T
divide rapidly by binary fission. In T
brucei spp migrate within the tsetse from
congolense infection, the organisms attach
the gut and eventually to the salivary
to endothelial cells and localize in
glands; the cycle for T CO'YIJ!Olense stops at capillaries and small blood vessels. T brucei
the hypopharynx, and the salivary glands
species and T vivax invade tissues and are not invaded; the entire cycle for T
cause tissue damage in several organs.

vivax occurs in the proboscis. Therefore, The inlmune response is vigorous, and
the location within the tsetse can be useful
immune complexes cause inflammation,
in identifying the parasite species. The
which contributes to fever and other signs
animal-infective form in the tsetse salivary
and lesions of the disease. Antibodies
gland is referred to as the metacyclic form.

against the surface-coat glycoproteins kill

The life cycle in the tsetse may be as short
the trypanosomes. However, trypanosomes
as 1 wk with T v-iva.:x; or extend to a few
have a large family of genes that code for
weeks for T b·1ucei spp.

vaiiable surface-coat glycoproteins that a.re

Tsetse flies (genus Glossina) a.re
switched in response to the antibody
restricted to Africa from about latitude l5°N
response, evading inlmunity. This ai1tigenic
to 29°8. The three ma.in species inhabit
variation results in persistence of the
relatively distinct environments: G
organism. Antigenic vaiiation has prevented
rnorsitans usually is found in savanna
development of a protective vaccine and
cow1try, G palpal-is prefers areas a.row1d
permits reinfections when animals a.re
rivers and lakes, and G fusca. lives in high exposed to a new antigenic type.

forest areas. All three species transmit trypanosomes, and all feed on various mammals. Clinical Findings and Lesions: Sever

Mechanical o-ansm.ission can occur
ity of disease varies with species and age
through tsetse or other biting flies. In the case of the animal infected and the species of of T v'ivax, Tabanus spp and other biting flies trypanosome involved. The incubation seem to be the p1imary mechanical vectors
period is usually 1-4 wk. The primary
outside tsetse-endemic areas, as in Central
clinical signs a.re intermittent fever,
and South Amelica Mechanical transmission anemia, and weight loss. Cattle usually

BLOOD PARASITES

37
have a chronic course with high mortality,
suitable for herd and area screening than for
especially if there is poor nutrition or other individual diagnosis. Rapid agglutination stress factors. Ruminants may gradually
tests to detect circulating trypanosome
recover if the number of infected tsetse
species-specific antigens in peripheral
flies is low; however, stress results in
blood are available for both individual and

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relapse.

herd diagnosis, although their reliability

Necropsy findings vary and are nonsperemains varied. Molecular techniques for cific. In acute, fatal cases, extensive
trypanosome detection and differentiation
petechiation of the serosal membranes,
have been developed, but they are not
especially in the peritoneal cavity, may
generally available for routine field use.

occur. Also, the lymph nodes and spleen are
usually swollen. In chronic cases, swollen

Treatment and Control: Several drugs
lymph nodes, serous atrophy of fat, and
can be used for treatment (see TABLE 6).

anemia are seen.

Most have a narrow therapeutic index,
which makes administration of the correct

Diagnosis: A presumptive diagnosis is
dose essential. Drug resistance occurs and
based on fincling an anemic animal in poor
should be considered in refractory cases.

condition in an endemic area. Confirmation

Control can be exercised at several levels,
depends on demonstrating trypanosomes in
including eradication of tsetse flies and use
stained blood smears or wet mounts. The
of prophylactic drugs. Tsetse flies can be
most sensitive rapid method is to examine a
partially controlled by frequent spraying and
wet mount of the buffy coat area of a PCV
dipping of ani.nlals, aerial and ground
tube after centrifugation, looking for motile
spraying of insecticides on fly-breeding
parasites. Other infections that cause
a.i·eas, use of insecticide-in1preg.nated
anemia and weight loss, such as babesiosis,
screens and ta.t·gets, bush clearing, a.i1d other
anaplasmosis, theile1iosis, and haemonchohabitat removal methods. The Sterile Insect sis, should be excluded by exan1ining a

Technique (SIT) has been used with success
stained blood smear.

in Zanzibar and may be used in other

Va.iious serologic tests measw·e antibody
area-wide control operations after suppresto trypanosomes, but their use is more sion of tsetse populations by insecticides.

DRUGS COMMONLY USED FOR TRYPANOSOMIASIS IN DOMESTIC

ANIMALS

Drug

Animal

Trypanosoma

Main Action

Diminazene

Cattle
viva:.r, congolense,

Curative
aceturate
brucei

Homidium

Cattle
vivax, congolense,

Curative, some
bromide
brucei
prophylactic activity

Homidiun1

Equids
v'ivax

Curative, some
bromide
prophylactic activity

Homidium

Equicls
vivax

Curative, some
chloride
prophylactic activity

Isometamidium

Cattle
viva:x·, congolense

Curative and
chloride
prophylactic

Quinapyra.inine

Horses, ca.inels,
vivax, congolense,

Curative
sulfate
pigs, dogs
brucei, evansi,
equiperdum, simiae

Quinapyra.inine

Horses, ca.inels,
vivax, congolense,

Prophylactic
dimethylsulfate
pigs, clogs
brucei, evansi,
equiperdum, simiae

Sura.inin

Horses, camels,
brucei, evansi

Curative, some
clogs
prophylactic activity

Melarsomine

Cain els
evansi

Curative
clichlorhydrate

38

BLOOD PARASITES
of the tsetse-transmitted trypanosomes

(seep 35).

Dourine

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Dourine is a chronic venereal disease of
horses that is transmitted during coitus and
caused by T eqil'iperdum. The disease is
recognized on the Meclite1Tanean coast of

Africa and in the Middle East, southern

Africa, and South America; distribution is
probably wider.

Signs may develop over weeks or months.

Trypanosoma vivax, blood smear of a cow.

Early signs include mucopurulent discharge

Courtesy of Dr. Corrie Brown.

from the urethra in stallions and from the
vagina in mares, followed by gross edema of
the genitalia Later, characteristic plaques

There is renewed international interest in

2-10 cm in diameter appear on the skin, and
large-scale tsetse eradication through the
the horse becomes progressively emaci

Pan African Tsetse and Trypanosomiasis
ated. Mortality in untreated cases is

Eradication Campaign (PATTEC) supported

50%-700!.i.

by the African Union. Animals can be given

Demonstration of trypanosomes from
drngs prophylactically in areas with a high
urethral or vaginal discharges, skin plaques,
population of trypanosome-infected tsetse.

or peripheral blood is difficult m1less the

Drng resistance must be carefully monitored
material is centrifuged. Infected horses can
by frequent blood exanlinations for
be detected with the complement fixation
trypanosomes in treated animals.

test but only in areas where T evansi or T

Several breeds of cattle and water buffalo
brucei are not found because they have
have been identified that have innate
common antigens. An ELlSA test may
resistance to trypanosomiasis and could
become available for diagnosis.

play a valuable role in reducing the in1pact

In endemic areas, horses may be treated
of the disease in these areas. However,

(see TABLE 6). When eradication is reqtlirecl, restStance may be lost because of poor
st1ict control of breeding and elimination of
nutrition or heavy tsetse challenge.

stray horses has been successful. Alterna

Control is ideally achieved by combining
tively, infected horses may be identified
methods to reduce the tsetse challenge and
using the complement fixation test;
by enhancing host re.sistance with
euthanasia is mandatory.

prophylactic drngs.

Chagas' Disease

Surra

(Trypanosoma cruzi infection)

(Trypanosoma evansi infection)

Chagas' disease, or American trypanoso

Smrn is usually transmitted by other biting
miasis, is a zoonotic, vectorborne disease
flies that are found within and outside tsetse transmitted by triatomine bugs and caused fly areas. It occurs in North Africa, the
by T cruzi. All mammals are considered Middle East, Asia, the Far East, and Central
susceptible to infection; with infection
and South America. The distribution of T
demonstrated in > 100 man1malian species.

evansi in Africa extends into the tsetse

Avian species are not susceptible. The
areas, where differentiation from T brucei disease is best recognized in clogs and
is difficult. It is essentially a disease of
people, with clogs serving as a major
camels and horses, but all domestic animals
domestic reservoir. Domestic pigs and
are susceptible. The disease can be fatal,
cats can also be infected, but their rote as
particularly in camels, horses, and dogs.

reservoirs for hU111an infection is limited.

T evansi in other animals appears to be Wildlife reservoirs include opossU111s,
nonpathogenic, and these animals serve
am1adillos, raccoons, woodrats, and
as reservoirs of infection.

nonh U111an primates.

Transmission is primarily by biting flies,
probably resulting from interrnpted

Transmission and Epidemiology:

feedings. A few wild animals are susceptible

Chagas' disease is endemic in 21 countries
to infection and may serve as reservoirs.

of South America, Central America, and

Pathogenesis, clinical findings, lesions,

Mexico, and is increasingly reported in the
diagnosis, and treatment are sin1ilar to those southern USA. Chagas' was once confined

BLOOD PARASITES

39
to the Americas, but human and animal
at the site of parasitic entry. Dogs may also
migration has resulted in distribution to
present with regional or generalized

Europe, where it is an emerging disease of
lymphadenopathy, anorexia, lethargy,

Spain, Switzerland, France, Italy, Germany,
vomiting, diarrhea, and hepatomegaly or
and England. Seropositivity in dogs in

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splenomegaly. Rarely, acute clinical myocarendemic regions can vary from 5o/o-9ZO/o.

ditis is seen. Parasitemia peaks 2-3 wk after

In some areas such as Venezuela, the
infection and dissipates after the first month
seropositivity of dogs is sinillar to that
as the organism moves to predominantly
of people, whereas in other areas, such as
tissue-borne disease.

Can1peche, Mexico, seropositivity can be

The latent phase can last for months to
higher in dogs than people.

years. Chronic disease symptoms can

The nocturnal and hematophagous
include generalized weakness or sudden
triatomine insects of the 1hatoma,
death. Symptomatic dogs commonly present

Rlwdnius, andPanstrongylus genera serve with right-side congestive heart failure. This as vectors for T cruzi. Common nan1es
can progress to myocarditis, with arrhytllinclude the "kissing bug," "assassin bug,"

mias and bilateral cardiac dilation.

"cone-nosed bug," "vinchuca," "chinche,"

Histologic exan1ination of cardiac muscle
and "barbeiro." There are > 130 species of may contain uruuptured pseudocysts
triatomines in the Americas, and most are
without inflanunation or contain ruptured
considered competent vectors. Insects take
pseudocysts with lymphocytic, monocytic,
an infected blood meal ingesting extraceland/or neutrophilic inflanmrntion. Death lular T cruzi trypomastigotes. These
secondary to heart fai!W'e is conunon.

differentiate in the midgut to epirnastigotes
and divide. Epirnastigotes travel to the

Diagnosis: Diagnosis of Chagas' disease
hindgut, where they differentiate back into
can be made by visualization of the
rnetacyclic trypomastigotes. Infective
organism, detection of DNA, or antibody
metacyclic trypornastigotes are shed in
detection. Parasitemia during the acute
insect feces. In insectivorous animals,
phase allows for detection on a microscopy
including dogs, conswnption of infected
of a routine peripheral blood smear.

bugs or materials contaminated with

Although san1ples can be tested for T cruzi
infected triatomine feces is a major mode

DNA by PCR or cultured, these diagnostic
of transmission. The opossum (Didelphis
tests are uncommon in tl1e field. On Giemsa
species) is a wlique host for Tcruzi,
stain, T cruzi is an extracellular, C-shaped because the parasite can complete its entire
protozoan with a single flagellum.

life cycle without the need for a vector.

Antibody testing is of primary i.J.npmtance

T cruzi maturation occurs in the anal
during the chronic phase. Whole blood,
odoriferous glands, and infective trypomasplasma, or serum can be submitted. Testing tigotes can be shed in feces or urine and
methodologies include immunochromoingested. Additional methods of transmisgraphic "dipstick," i.J.nmunofluorescent sion include transplacentally or via blood
antibody, or ELISA. Notably, cross-reaction
transfusions and organ transplant.

with antibodies to Leishmania species,
another tryponsomatid, can occur. Because

Pathogenesis: Once metacyclic
of cross-reactivity of serologic tests, testing
t1ypomastigotes enter the bloodstream, they
with at least two different methodologies or
actively invade many cell types, exiting the
antigens is recommended. Additionally,
parasitophorous vacuole and becoming
cardiac tissue in the chronic phase can be
nonflagellated amastigotes. Intracellular
analyzed by PCR for T cruzi DNA or by
amastigotes divide every 15-18 hr for 5--6
i.J.nmunohistochemical analysis for
days. T cruzi transforms back into
amastigotes.

trypomastigotes and lyses the cell. Released
trypomastigotes invade new cells. T cruzi

Treatment and Control: Benznidazole
has a tropism for cardiac and smooth muscle is the drug of choice for treatment, but but can be fmmd in nwnerous other tissues.

nifurti.J.nox can also be used. In dogs,
benznidazole is administered at 5-10 mg/kg/

Clinical Findings and Lesions: Chagas'

day, PO, for 2 mo. In the USA, both of these
disease is divided into acute and chronic
drugs lack FDA approval, and their use
phases, with the chronic phase further
requi.J.'es permission from the CDC as
subdivided into latent and symptomatic
investigational protocols. Symptomatic
chronic disease. Incubation ranges from
treatment for heart failure and arrhythmias

5-42 days before acute disease. Acute
is also recommended.

infections may be asymptomatic or consist

No vaccine is available; thus, control
of nonspecific febrile illness with a chancre
focuses on preventing disease transmission.

40

BLOOD PARASITES

Vector control methods include pesticide
peripheral blood from cattle on every
application to eliminate triatomine vectors
continent. infection with similar trypanoand decreasing vector attraction to somes also has been detected in domestic
dwellings at night by turning off outdoor
and wild buffalo and various other wild

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lighting. Breeding of positive bitches is
ungulates. ln the few areas studied,
discouraged. Screening of blood donors
transmission is by contamination after a
is recommended. To avoid iatrogenic
cycle of development in species of tabanid
transmission, disinfection with 100/o bleach
flies. Although most parasitemias are
or 700/o ethanol is suggested for contamisubpatent, the trypanosomes may be seen nated surfaces. Dead infected insects
in a blood smear being examined for
can remain a source of infective T cruzi
pathogenic protozoa or in a hemocytometer
for up to 6 days at 10°C or up to 2 mo at
chamber. Pathogenicity has never been

26°-30°C.

proved experimentally.

T metophagium of sheep also has a
worldwide distribution.and is transmitted

Nonpathogenic Trypanosomes
by the sheep ked. T theodori, reported in

T'rypanosoma theileri or markedly similar
goats, may be a synonym for the same
trypanosomes have been detected in
trypanosome.

CANINE t.YMPHOMA

Canine lymphoma is a disease term
dysfunction. With the completion 'Of the dog
comprising a heterogeneous group of
genome, it is anticipated that genome-wide
malignancies with varying biologic
association studies will identify specific
aggressiveness derived from the uncongenetic and chromosomal signatures trolled and pathologic clonal expansion
involved in the pathogenesis of lymphoma
of lymphoid cells of either B- or T-cell
immunophenotype. Although neoplastic

Clinical Findings: Canine lymphoma is a
transformation of lymphocytes is not
heterogeneous cancer, with variable clinical
restricted to specific anatomic compartsigns, responses to therapy, and swvival ments, canine lymphoma most commonly
times. The heterogeneity associated with
involves organized primary and secondary
canine lymphoma is influenced in part by
lymphoid tissues, includingJ;he bone
several tumor and host factors, including
marrow, thymus, lyn1ph nodes, and spleen.

anatomic involvement, extent of disease,
ln addition to these lymphoid-rich organs,
morphologic subtype, host constitution, and
extranodal sites affected by lymphoma
immunocompetence. ln dogs, the most
include the skin, intestinal tract, liver, eye,
common clinical variants of lymphoma are

CNS, and bone. Lymphoma is reported to be
high-grade T- or B-cell variants, and four
the most common hematopoietic neoplasm
conventionally recognized anatomic
in dogs, with an incidence reported to
forms of lymphoma have been described:

approach 0.1 % in susceptible dogs. Despite
multicentric, alimentary, mediastinal, and
the prevalence of malignant lymphoma, the
extranodal (renal, CNS, cutaneous, ocular,
underlying causes for its development
bone, etc). Multicentric lymphoma is by
remain poorly characterized; however,
far the most common anatomic form,
advanced genetic studies have revealed
accounting for -800/o-85% of all diagnosed
that canine lymphoma can be molecularly
cases. The most common and overt clinical
distinguished and categorized into discrete
manifestation of multicentric lymphoma is
groups that correlate with biologic
the rapid and nonpainful development of
aggressiveness. Hypothesized causes
generalized lymphadenopathy. ln addition
include retroviral infection with Epsteinto peripheral lymphadenopathy, most Barr virus-like viruses, environmental
affected dogs will have malignant lymphocontamination with phenoxyacetic acid cytes that are detectable by sensitive
herbicides, magnetic field exposure,
diagnostic tests, including flow cytometry
chromosomal abnormalities, and immune
or PCR for antigen receptor rearrangement

CANINE LYMPHOMA

41

(PARR) that involve internal organs,
extranodal sites may include respiratory
including the spleen, liver, bone marrow,
distress (lungs), renal failure (kidneys),
and other extranodal sites. In dogs with
blindness (eyes), seizures (CNS), and
significant tumor burden, systemic
skeletal pain or pathologic fracture (bone).

constitutional signs, including profound

Although high-grade lyn1phoma of either

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lethargy, weakness, fever, anorexia,

B- or T-{;ell origin is most commonly
and dehydration, may become
diagnosed in dogs, low-grade or indolent
evident.

lymphoma is a recently desc1ibed molecular

Alimentary lymphoma accounts for <100/o
variant of canine lymphoma and comprises
of all canine lymphomas. Dogs with focal
up to 30% of all lymphoma diagnoses. Like
intestinal lesions may exhibit clinical signs
high-grade lymphoma, indolent lymphoma
consistent with partial or complete luminal
consists of several histopathologic subtypes,
obstruction ( eg, vomiting, constipation,
including marginal zone, follicular, mantle
abdominal pain). With diffuse involvement
cell, and T-zone lymphoma. Collectively,
of the intestinal tract, dogs with alimentary
indolent lymphomas are slowly progressive,
lymphoma may show significant and
and dogs often remain asyn1ptomatic for a
debilitating GI signs, including anorexia,
prolonged time regardless of therapy.

vomiting, diarrhea, hypoproteinemia, and
weight loss secondary to malabsorption and

Lesions: Commonly, peripheral and
maldigestion.

various internal lymph nodes are 3--10

Exclusive involvement of the cranial
times normal size (multicentric form) and
mediastinum with lymphoma comprises
nonpainful on digital palpation. Affected
only a small fraction of diagnosed cases;
nodes are freely movable, finn, and
however, sternal lymph node enlargement
gray-tan; they bulge on cut surface and
is frequently observed in dogs with
have no co1tical-medullary demarcation.

multicentric disease. Mediastinal lym

Fi·equently, there is hepatosplenornegaly
phoma is typically characterized by
with either diffuse enlargement or multiple,
enlargement of the cranial mediastinal
pale nodules of variable size disseminated
lymph nodes, thymus, or both. Mediastinal
in the parenchyma. In the alimentary form,
lymphoma arising from the thymus is
any part of the GI tract or mesenteric lymph
predominantly comprised of high-grade
nodes may be affected. Involvement of the
malignant T lymphocytes, and with
bone marrow, CNS, kidney, heart, tonsils,
advanced disease, clinical signs may
pancreas, and eyes can be seen but is less
include respiratory distress associated with common.

pleural fluid accumulation, direct compression of adjacent lung lobes, or caval Diagnosis: The definitive diagnosis of
syndrome. In addition to respiratory signs,
lymphoma is often uncomplicated a.I\d
some dogs with mediastinal lymphoma may can be obtained by either cytologic or have primary polyuria with secondary
histopathologic evaluation of the affected
polydipsia resulting from humoral hyperorgan system. Fine-needle aspiration of calcemia of malignancy, a paraneoplastic
enlarged peripheral lymph nodes or
syndrome seen in 10%--40% of dogs with
affected visceral organs usually provides
lymphoma. Confinnation of humoral
specimens of adequate cellular content and
hypercalcemia of malignancy can be
detail to make a definitive diagnosis.

documented through the measurment of

Cytologically, lymph node or tissue
ionized calcium, parathyroid hormone, and
aspirates may identify a monomorphic
parathyroid ho1mone-related peptide
population of lymphoid cells, either of large
within circulating blood.

(lymphoblastic ), intermediate, or small size.

The clinical signs associated with various

Despite the ease of diagnosis, conventional
high-grade extranodal lymphomas (which
cytology is limited for differentiating or
may involve the skin, lungs, kidneys, eyes,
categorizing the heterogeneous spectrum of

CNS, etc) are often variable and dictated by
lymphomas with regard to morphologic
the organs infiltrated. The most common
subtype ( diffuse versus follicular, cleaved
extranodal form of lymphoma-involves the
versus noncleaved) and histologic grade
skin, referred to as cutaneous lymphoma.

(lligh versus low). Specialized cytology

Cutaneous lymphoma ( epitheliotropic and
utilizing lineage-specific antibodies can
nonepitheliotropic) may appear as solitary,
differentiate between B-and T-{;ell
raised, ulcerative nodules or generalized,
lymphomas and can provide some
diffuse, scaly lesions. Involvement of
information regarding prognosis based on
peripheral lymph nodes and mucocutaneimmunophenotype. However, because of ous junctions is frequent. Clinical signs
the inherent limitations associated with
associated with lymphoma involving other
cytology, histopathologic tissue evaluation

42

CANINE LYMPHOMA
remains the gold standard for the diag

Although systemic chemotherapy
nosis of lymphoma, providing additional
remains the cornerstone to treat highmorphologic infom1ation required for grade lymphoma, the idea that both
definitive classification, as well as guiding
induction and maintenance phases of
therapeutic decisions.

chemotherapy are necessary to achieve

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In rare situations when cytology or
durable remission times has changed.

histopathology fails to confirm the

Shorter and more dose-intense chemodiagnosis of lymphoma, more advanced therapy protocols (eg, Madison Wisconsin
molecular techniques are available for
protocol) without maintenance provide
definitive diagnosis, including flow
disease-free intervals and survival times
cytometry for specific cell surface markers
equivalent to protocols that include
called cluster of differentiation (CD)

chronic maintenance therapy. Additionantigens and PCR for PARR. The use of ally, the use of half-body radiation in

PCR allows for the amplification of DNA
replacement of maintenance chemothersequences that confirms or denies the presapy has been demonstrated to be safe ence of lymphocytes of either clonal,
and clinically efficacious, providing
oligoclonal, or polyclonal origin. Because
another option to achieve durable
most neoplastic outgrowths result from
remission times without the need for
the clonal expansion of one malignantly
chronic chemotherapy. For select cases,
transformed cell, PCR techniques can
autologous canine bone man-ow transdifferentiate lymphocyte expansion as a plant after systemic chemotherapy and
consequence of cancer (lymphoma) versus whole-body radiation can afford some inflammation (reactive or hyperplastic
dogs extended, progression-free intervals
lymphocytosis). Although PCR techniques
and survival times.

are highly sensitive, the methodology

Despite the favorable outcomes
should be reserved for cases in which
expected in treating high-grade multicenconventional cytology and histopathology tric lymphoma, the successful manageprove nondiagnostic, or when results are ment of other anatomic forms of lymdiscordant with clinical signs and disease phoma is often more difficult and less
progression.

rewarding. Alimentary lymphoma, if focal,
can be treated effectively witl1 surgical

Treatment: Treatment of high-grade,
resection and combination chemotherapy.

multicentric ca.nine lymphoma with

However, with diffuse involvement of the
aggressive, multi-agent chemotherapy
intestinal tract, low constitutional reserve,
protocols is often rewarding, with >90% of
severe malabsorption of nutrients, and
all dogs achieving complete reduction of
loss of proteins often result in poor
tumor burden, termed complete remission.

clinical responses and short survival times

The most common chemotherapeutic

(ie, <3 mo). The use of combination
agents used in combination protocols are
chemotherapy with or without palliative
vincristine, doxorubicin, cyclophospharadiation therapy can afford dogs with mide, L-asparaginase, and prednisone.

mediastinal lymphoma considerable

Individual treatment protocols vary witl1
improvement in survival times and qualityrespect to dosage, frequency, and duration of-life scores. Lymphoma involving other
of treatment; advantages and disadvantages
extranodal sites (such as the skin) can be
of each treatment protocol can be found
managed with either single-agent oral
in medical oncology textbooks. With
lomustine or combination systemic
combination chemotherapy, tl1e expected
chemotherapies ( eg, CHOP); however,
survival time for dogs witl1 B-cell lymphoma
the development of refractory and
is -12 mo, whereas for dogs with T-cell
progressive disease is common and
lymphoma, expected survival times are
ultimately life limiting.

often in tl1e range of 6 mo. Altl1ough

Clinical prognosis for dogs diagnosed
in1111unophenotype (B- versus T-cell)

with low-grade, indolent lymphoma tends to
provides a general guideline for treatment
be good. The institution of low-intensity oral
prognosis, multiple factors (tun1or and host) chemotherapy protocols ( chloran1bucil and contribute to tl1e overall response duration
prednisone) often provides prolonged
and survival time of dogs diagnosed with
survival times (>2 yr), and in specific dogs
lymphoma. Dogs tl1at do not respond to
with localized and low-grade disease ( eg,
traditional combination chemotherapy or
splenic involvement), splenectomy can be
tl1at relapse may achieve disease remission,
an effective and durable treatment option
added survival times, or both witl1 t11e use
witl1out tl1e necessity of adjuvant chemoof various rescue protocols (eg, lomustine, therapy administration. (See ai,so TREATMENT

MOPP, ADIC, DMAC).

Ol'CANINE LYMPHOMA, p 40.)

ERYTHROCYTOSIS AND POLYCYTHEMIA

43

ERYTHROCYTOSIS AND POLYCYTHEMIA

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Erythrocytosis is a relative or absolute
hyperactivity or in cats with hyperthyroid

· increase in the number of circulating
ism or acromegaly is insufficient to cause

RBCs, resulting in a PCV increased above
clinical signs.

reference ranges. Polycythemia is
frequently used synonymously with

Clinical Findings: Clinical signs of
erythrocytosis; however, polycythemia may
absolute erythrocytosis include red mucous
imply leukocytosis and thrombocytosis, as
membranes, bleeding tendencies, polyulia,
well as erythrocytosis.

polydipsia, and neurologic disturbances

(ataxia, weakness, seizures, blindness,

Relative Erythrocytosis: Relative
behavioral change). On retinal exanlination,
erythrocytosis is an increase in RBC
dilated, tortuous vessels may be visualized.

numbers without an increase in total RBC

These collective clinical features are
mass. Usually, this is caused by loss of
attributed to hyperviscosity from tile
plasma volume with resultant hemoconincreased RBC mass.

centration, as seen in severe dehydration
attributable to vomiting and diarrhea.

Diagnosis: The dehydralion ai1d

Alternatively, a mild, transient f01m of
hemoconcentration of relative erythrocytorelative erythrocytosis unassociated with sis may be identified by clinical findings ( dry
clinical signs may develop in dogs when fear mucous membranes, loss of skin turgor), or excitement causes splenic contraction
laboratory vaiiables (hyperproteinemia,
with release ofRBCs into the circulation.

prerenal azotemia), and response to
rehydration. Excitable dogs with mild

Absolute Erythrocytosis: Absolute
erythrocytosis attributed to splenic
e1ythrocytosis, defined as increased RBC
contraction usually have nonnal PCV on
numbers because of increased RBC mass,
subsequent blood samples collected less
develops from primary or secondary causes. stressfully. Sighthounds ( eg, Greyhounds) Primary erythrocytosis (polycythemia
normally have mild erythrocytosis
vera) is a myeloproliferative disease of
compared witll standard canine reference
unlrnown cause that has been reported
ranges.

in dogs, cats, cattle, and horses. RBC

Witll absolute erythrocytosis, senun EPO
production is dran1atically increased, while
detem1inations have been recommended to
serum erytlu-opoietin (EPO) activity
differentiate primaiy from secondary
typically is low or low-nonnal. Secondary
causes. Unfortunately, considerable overlap
erythrocytosis, in contrast, generally
exists in EPO activity ainong nonnal
develops from excessive production of
animals, animals with primary erythrocyto

EPO. If EPO is secreted because of systemic sis, and animals with secondary erythrocyhypoxia, then the resultant erythrocytosis is tosis. Furthermore, cm-rent availability of an appropriate compensatory response.

validated EPO assays for companion

This may be seen with severe pulmonaiy
anin1als is limited. Routine examination of
disease or heart anomalies resulting in
bone ma.ITow is not useful to distinguish
right-to-left shunting with blood bypassing
primary from secondary erythrocytosis
the lungs ( eg, reversed patent ductus
because both conditions show erythroid
arteriosus, tetralogy ofFallot). IfEPO
hyperplasia. As a result, primary erythrocyproduction increases without systemic tosis usually is diagnosed by elinlinating
hypoxia, then the response is inappropliate.

secondary causes.

EPO-secreting tumors of the kidneys or

To investigate types of secondaiy
other organs, or non-neoplastic renal
erytlu-ocytosis, assessment of tissue
disorders resulting in local hypoxia with
oxygenation may be helpful. Aiteiial blood

EPO production, may cause inapprop1iate
p02 <80 mmHg and pulse oximetry oxygen
erythrocytosis. Another type of secondaiy
saturation <90%-95% are consistent witll tile
erythrocytosis, called endocrinopathyhypoxemia and tissue hypoxia of appropriate associated erythrocytosis, results from
secondaiy erytlu-ocytosis. Exanlination of
hom1ones other than EPO ( eg, cortisol,
heart and lungs by auscultation, radiographs,
androgen, thyroxine, growth hormone)

electrocardiography, and echocardiography
that stimulate erythropoiesis. The mild
may reveal tile underlying problem. Selective
erythrocytosis in dogs with adrenocortical
angiography or contrast echoaortography

44

ERYTHROCYTOSIS AND POLYCYTHEMIA
may be needed to confirm right-to-left
been advocated in affected dogs and cats.

cardiac shunting. If systemic hypoxia is not

RBC, WBC, and platelet counts should be
present, then locating the potential source of
monitored during hydroxyurea treatment.

inappropriate EPO production is facilitated

For inappropriate secondary erythrocy by physical and neurologic examinations, tosis, EPO-secreting tumors should be

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abdominal ultrasonography, IV urography,
managed with surgery, chemotherapy, or
and CT or MRI.

radiation therapy. Phlebotomy to normalize
the PCV helps reduce hyperviscosity.

Treatment: For relative erythrocytosis

For appropriate secondary erythrocydue to dehydration, therapy consists of tosis, the underlying problem should be
rehydration with IV fluids and treating the
addressed. If corrective treatment of that
underlying cause.

disease process is not feasible, clinical signs

For polycythemia vera, treatment initially associated with hyperviscosity may be consists of phlebotomy (5--20 mIJkg to
alleviated by judicious phlebotomy (5--10
reduce the PCV to -500/o-60%) with
mllkg) and hydroxyurea therapy. However,
simultaneous fluid replacement. Periodic
because this type of erythrocytosis is a
phlebotomy with or without administration
compensatory response to hypoxia, the
of hydroxyurea (30 mg/kg/day, PO, for 7-10

PCV should be maintained at values
days, then 15 mg/kg/day, PO, titrated) has
above normal reference ranges.

,HEMOSTATIC DISORDERS.

Effective hemostasis depends on an

Physiologic Understanding of
adequate number of functional platelets,

Hemostasis
an adequate concentration and activity
of plasma coagulation and fibrinolytic

A cell-based model of hemostasis has been
proteins, and a normally responsive blood
introduced that explains physiologic
vasculature. The diagnosis, treatment, and
hemostasis through a complex process in
monitoring of hypo- �d hypercoagulable
which the interacti'on of vascular tone,
animals is difficult with regard to both
blood flow, endothelial cells, platelets,
progression of disease and monitoring
leukocytes, coagulation factors, and
blood component and/or anticoagulation
fibrinolytic factors and their cofactors and
therapy. Citrated plasma samples are often inhibitors result in balanced hemostasis and used in veterinary medicin� to determine
formation of a clot at the ir\jured site. This
fibrinogen concentration, activated partial
dynamic model involves cellular regulation
thromboplastin time (APTT), prothrombin of coagulation in three phases: initiation, time (PT), and o-dimer or fibrinogen
amplification, and propagation.

degradation product (FDP) concentration.

TF-bearing cells initiat-e hemostasis. TF

The introduction of the cell-based, tissue
is a transm�mbrane glycoprotein receptor
factor (TF)/Factor VII-dependent model of found in extravascular tissues, including hemostasis has increased understanding of organ capsules and the adventitia of blood the complex biochemistry of physiologic
vessel walls. It is constitutively expressed
hemostasis, leading to reevaluation of the
on fibroblasts and, on cellular activation, on
traditional understanding of physiologic
vascular smooth muscle cells, monocytes,
hemostasis divided into the intrinsic
and neutrophils. The TF-bearing cells and
and extrinsic pathways of coagulation.

platelet surfaces act as the main cellular

Although citrated plasma contains many
surfaces for assembly of the procoagulant
of the factors involved in coagulation,
complexes. Any vessel ir\jury leads to TF
whole blood contains both the soluble
exposure. Factor VII binding to TF results in
factors and intravascular cells active in
activation to Factor VIia. Factor VIia bound
physiolo$ic and pathologic hemostasis,
to TF on the cell surface activates Factor IX
incorporating TF and phospholipidto Factor IXa and Factor X to Factor Xa.

bearing cells, such as platelets and

Initially, the formed Factor Xa is limited to
leukocytes.

the TF-bearing cell, because Factor Xa that

HEMOSTATIC DISORDERS

45
diffuses away from the cell is rapidly
hemostatic disorders. Primary hemostasis
inhibited by TF pathway inhibitor (TFPI) or
is accomplished by interaction of platelets
antithrombin.

with exposed subendothelial surfaces.

Together with formed Factor Va, Factor

Simultaneously, plasma coagulation

Xa is assembled into the prothrombinase
proteins are activated in a sequential

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complex on the surface of the TF-bearing
cascade that depends on the phospholipid
cell. An initial small amount of thrombin
provided by the activated platelets and
close to the cell independent of the
calcium ions from plasma to form a stable
presence of platelets is generated and is
clot ( secondary hemostasis ). Circumresponsible for activation of platelets, stances that activate platelets and the
release of Factor V from the platelets,
coagulation proteins also activate plasma
activation of Factor V, activation of Factor
fibrinolytic proteins, which ensure

VIII and release of Factor VIII from von
localization of the clot and its timely

Willebrand factor, and activation of Factor
dissolution.

XI. Platelets also are activated by other

Hemostatic capabilities are traditionally
mechanisms, including vessel wall collagen
assessed by tests of primary hemostasis
and von Willebrand factor, leading to

(platelet count and buccal mucosal bleeding
adhesion and aggregation at the injured site.

time) and secondary hemostasis through

As an essential part of the platelet
plasma-based assays designed to further
activation process, the procoagulant
localize defects, such as the APTT (intrinsic
phospholipid phosphatidylserine becomes
and common pathway) and PT ( extrinsic
available. The initially generated Factor IXa
and common pathway). The fibrinolytic
binds to the activated platelet surfaces,
system is traditionally evaluated with
promoting formation of the "tenase"

measurements of degradation products
complex; this results in major Factor
such as FOP and o-dirner, and endogenous

Xa fonnation and amplification of the
anticoagulant ability has been evaluated
coagulation process. The formed Factor IXa
through antithrombin, protein C, and
diffuses to the platelets, because it is not
protein S. Additional specialized individual
inhibited by TFPI and is inhibited slowly
coagulation factor tests can further localize
by antithrombin. The formed Factor Xa
congenital defects. Thus, plasma-based
complexes with Factor Va on the activated
coagulation screening tests can help
platelet surface, fonning the "prothrombiidentify the defective or deficient coagulanase" complex that leads to cleavage of tion protein. Although this traditional
prothrombin and to the major subsequent
approach makes it possible to effectively
burst of thrombin responsible for cleaving
and systematically localize the cause of
fib1inogen and fonning the hemostatic plug.

bleeding, it may be difficult from a clinical

Additional Factor IXa is supplied by Factor
perspective to evaluate general hemostatic

Xla on the platelet surface. Factor Xla
capability and to predict or monitor the
activates the antifibrinolytic pathway.

effect of anticoagulant or procoagulant

The second wave of thrombin activates
treatment. This may partially be because
plasmin, thereby initiating fibrinolysis. This
plasma-based tests of the secondary and
keeps the clot controlled at the site of injury. fibrinolytic systems target specific elements To control fibrinolysis, the antifibrinolytic
of the hemostatic system, thus potentially
pathway is activated by thrombin activaignoring other factors that may contribute tion of thrombin-activatable fibrinolysis
significantly to overall hemostatic
inhibitor (TAFI). TAFI slows the fibrinolytic
capability in acquired disorders. Another
process by inhibiting plasmin activity; this
plausible reason is the low sensitivity of
prevents premature clot lysis and allows

APTT and PT; usually, activity of a
clot propagation. The balance of fibrin
coagulation protein must be <300/o and
formation and fibrinolysis regulates the size
sometimes < 10% of normal before an
and quality of the fibrin plug and localizes it
abnormality is detected.

to the site of injury. The quality of the clot

Tests for increased risk or tendency
has a significant impact on how effectively
toward thrombosis are generally available
it provides hemostasis.

only through some academic and research
laboratories. Measurement of antithrombin

Clinical Approach to Hemostasis
activity is being offered by increasing
numbers of laboratories. Tests for

Although the traditional division between
measurement of activities of plasminogen,
primary and secondary hemostasis is not
protein C, a
biologically accurate, it is still a useful

2-antiplasmin, tissue plasminogen activator, and plasminogen activator diagnostic approach to hemostasis in
inhibitor have been established in some
animals with acquired or hereditary
domestic animals.

46

HEMOSTATIC DISORDERS

Assessment of Hemostatic Function
plasma components of coagulation with the
in Whole Blood
cellular components. TEG is perfom1ed on
unstabilized fresh whole blood within 4-6

Because whole blood contains all the
min of taking the blood sample. This is
intravascular factors and cells involved in
generally not practical in a routine clinical

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physiologic and pathologic hemostasis,
incorporating TF and phospholipid-bearing
setting, and using citrated stabilized whole
blood (with recalcification immediately
cells, whole blood assays may provide a
before analysis) has been proposed to
more accurate reflection of in vivo
increase the time span from sampling to
hemostasis than traditional plasma-based
hemostasis assays. However, few whole
analysis. A TF-activated TEG assay on
citrated whole blood has been validated in
blood assays to assess both primary and
secondary hemostasis have been used in
dogs and shown to have a low analytical
veterinary studies to date.

variation and good correlation to clinical
signs of bleeding compared with many traditional plasma-based coagulation assays.

PFA-100: The platelet function analyzer,

TEG is the first modality available to

PFA-100, is a method for quantitative,
clinicians that can evaluate hypercoagusimple, and rapid in vitro assessment of lability. It is especially useful in dogs with
primary platelet-related hemostasis at high
disseminated intravascular coagulation,
shear stress. The test requires a small
volume (0.8 mL) of citrated whole blood,
neoplasia, sepsis, and parvoviral infection,
and to evaluate platelet dysfunction in dogs
which is drawn under vacuun1 through a

200-µm diameter stainless steel capillary
with hypothennia. TEG analysis is a valuable
aid in the diagnostic evaluation of animals
and a 150-µm diameter aperture in a
nitrocellulose membrane coated with
with abnormal hemostasis and a supplement
to traditional coagulation tests such as PT,
collagen and epinephrine (CEPI) or
collagen and ADP (CADP). In response to

APTT, o-dirner, and fibrinogen assays.

the high shear rates and the agonists, a
platelet aggregate forms that blocks blood

COAGULATION DISORDERS
flow through the aperture; the time taken to
occlude the aperture is reported as the

Bleeding diatheses may be caused by
closure time. Prolonged closure times with
congenital or acquired defects in the
only the CEPI cartridge are seen with mild
vasculature, platelets, or the coagulation
proteins. Congenital or acquired defects
inherited platelet function disorders ( eg,
storage pool disorders) and with asp!fin
or deficiencies of platelets usually manifest
as superficial petechial and ecchyrnotic
ingestion, while prolonged closure times
with both CEPI and CADP cartridges are
hemorrhages ( especially of mucous
seen with more severe inherited platelet
membranes), epistaxis, melena, or
dysfunctions and with von WJ..llebrand
prolonged bleeding at irtjection and incision
disease. The PFA-100 also has the ability to
sites, whereas congenital or acquired
monitor response to treatment with both
deficiencies in coagulation proteins usually
manifest clinically as delayed deep tissue
desmopressin acetate and glycoprotein

Ilb/llla antagonists. The quality of blood
hemorrhage, hematoma formation, and
bleeding into joints and body cavities.

bank platelet concentrates for transfusion
can be evaluated, as well as response to

Pathologic thrombosis may occur
platelet transfusion. The PFA-100 is a good
because of primary or inherited disorders of
anticoagulant protein factors or because of
screening method to detect platelet function
defects. It also has been evaluated in many
secondary or acquired disorders. Collectively, these conditions are called hypercoother studies for its use in assessing drug effects or for evaluation of overall primary
agulable states. Systemic syndromes, s':'ch
as disseminated intravascular coagulation,
hemostasis in various clinical disorders or
that enhance platelet responsiveness to
during surgical procedures.

agonists and alter the balance between
anticoagulant and procoagulant protein

Thromboelastography (TEG): TEG
factors or that increase the reactivity of
allows for rapid assessment of hemostatic
endothelium are more common in animals
function in whole blood. It evaluates all of
than inherited disorders.

the steps in hemostasis, including initiation,
amplification, and propagation, as well as

PLATELET DISORDERS
fibrinolysis, including the interaction of
platelets and leukocytes with the proteins

Disorders of platelets can be divided into
of the coagulation cascade. Thus, TEG
acquired or congenital thrombocytopenias
combines evaluation of the traditional
and acquired or congenital functional

HEMOSTATIC DISORDERS

47
disorders (thrombocytopathias), with

All affected lambs died within 48 hr of birth.

acquired thrombocytopenia being the most

Thrombocytopenia was seen in whole
common.

blood, and platelets were markedly
decreased on blood smears. The presence

VetBooks.ir

Congenital Thrombocytopenia
of antibodies directed against platelets was
suspected because the cows from which

Hereditary Macrothrombocytopenia
colostrum was obtained had been used in a
in Cavalier King Charles Spaniels:

previous experiment in which they had been

This benign, inherited giant platelet
immunized against sheep blood.

disorder affects -500;6 of dogs in the breed. It
is characterized by thrombocytopenia with
macrothrombocytes in 300;6 of cases and

Acquired Thrombocytopenia
variable platelet aggregation in response to

Acquired thrombocytopenias are reported
adenosine diphosphate, depending on the
frequently in dogs and cats, less often in
platelet count. No correlation has been
horses, and rarely in other species.

found between macrothrombocytopenia

Numerous causes have been identified,
and age, gender, neuter status, coat color,
most involving immunologic or direct
weight, or heart murmur status. The
destruction of platelets.

disorder is detected by a routine CBC.

Affected dogs have normal coagulation

Primary Immune-mediated Thrombo
protein activity.

cytopenia: This condition ( also called
idiopathic thrombocytopenia or idiopathic

Cyclic Hematopoiesis in Gray Collie
thrombocytopenic purpura is character

Dogs: This autosomal recessive disorder
ized by immune-mediated destruction of
is characterized by 12-day cycles of
either circulating platelets or, less
cytopenia. All marrow stem cells are
commonly, marrow megakaryocytes. It has
affected, but neutrophils are most affected
been seen in dogs, horses, and rarely cats.

because of their short half-life ( usually <24

Clinical signs include petechiae of the
hr). Mild to severe thrombocytopenia can
gingivae or skin and ecchymosis, melena,
be seen, and excessive bleeding is a
or epistaxis. Platelet concentration is
potential complication. The disorder is fatal; usually <50,000/µL and often <10,000/µL
affected dogs usually die from fulminating
at the time of diagnosis. Evaluation of
infections before 6 mo of age. Even dogs
megakaryocytes (by bone marrow
that receive intensive antibiotic therapy
aspiration) helps determine whether
usually die by 3 yr of age with amyloidosis
circulating platelets or marrow megakaryo

( see p 592) secondary to chronic antigenic cytes are targeted by antibody. A test for
stimulation from recurrent infections. Treatplatelet factor 3 released from damaged ment with recombinant granulocyte
platelets has been unreliable or not readily
colony-stimulating factor has been
available commercially. A megakaryocyte
temporarily successful in alleviating the
immunofluorescence assay that detects
neutropenic cycles until antibodies are
antibodies on megakaryocytes has been
produced against the noncanine proteins.

done, but an adequate bone marrow
aspiration sample must be obtained. A

Fetal and Neonatal Alloimmune
direct test for the presence of antiplatelet

Thrombocytopenia: This disorder
antibodies-an ELISA that detects
occurs when maternal antibodies are
platelet-bound antibodies-has been
produced against a paternal antigen on fetal reported to have good sensitivity (94%) but platelets. It has been reported in a 1-day-old
is not highly specific for primary imrnune

Quarter horse foal. Immunoglobulins bound mediated thrombocytopenia. A negative to the foal's platelets were identified in the
test result likely excludes primary
mare's plasma, serum, and milk by indirect
immune-mediated thrombocytopenia as
assays. The immunoglobulins were further
the cause of thrombocytopenia; however,
shown to recognize platelets from the foal's
a positive test result could indicate either
full brother, born l year earlier. This
primary immune-mediated thrombocytopediagnosis should be considered for foals nia or secondary immune-mediated
with severe thrombocytopenia when other
thrombocytopenia ( eg, thrombocytopenia
causes can be excluded.

associated with autoimmune hemolytic

A group of lambs artificially reared and
anemia, lymphoproliferative diseases,
fed bovine colostrum had prolonged
systemic lupus erythematosus).

bleeding from puncture wounds from ear

Affected animals should be kept at rest,
tag placement, subcutaneous bruising,
and treatment is based on administration of
weakness, and pale mucous membranes.

corticosteroids, starting at a high dose and

48

HEMOSTATIC DISORDERS
then tapering (as in the treatment of IMMUNEtory mechanisms cause increased platelet MEDIATED 1-IEMOLITIC ANEMIA, p 10). Transfuconsumption and decreased platelet sion with fresh whole blood should be
survival. However, bleeding tendencies
performed in animals with a PCV < 15%;
without thrombocytopenia occasionally
however, whole blood transfusion to
exist. Altered platelet function due to an

VetBooks.ir
replenish platelets is often futile with
acquired membrane defect has been
regard to normalization of primary
associated with hyperglobulinemia.

hemostasis, because the platelets are

Vasculitis also may contribute to the
removed from circulation within a couple
hemostatic disorder.

of hours. Splenectomy should be reserved
as a treatment for animals that have

Vaccine-induced Thrombocytopenia:

recurrent episodes of thrombocytopenia.

Dogs vaccinated repeatedly with modified

Vincristine has been used to enhance the
live adenovirus and paramyxovirus
release of platelets from marrow megakaryvaccines may develop thrombocytopenia ocytes. It also coats platelets and has a

3--10 days after repeat vaccination. The
cytotoxic effect on macrophages that
thrombocytopenia is usually transient and
ingest coated platelets. A single dose of
may be sufficiently mild that a bleeding
vincristine at the time corticosteroids are
tendency will not be evident unless
started shortens the time to recovery of the
superimposed on another platelet or
platelet count.

coagulation disorder. Studies have failed
to confirm an association between recent

Rickettsial Diseases: Anaplasma platys, vaccination and development of idiopathic A phagoC?.Jtophilum, or Ehrlichia canis thrombocytopenic purpura; however, it
infections cause mild to severe thrombocymight still occur rarely.

topenia in dogs. A platys infection ( see p 803) usually is characterized by mild,

Drug-induced Thrombocytopenia:

often cyclic thrombocytopenia in the acute

Thrombocytopenia associated with
stages of disease. Chronic infections often
administration of certain drugs has been
have constant mild to moderate thrombocyreported in dogs, cats, and horses. One topenia Morula (single to multiple, round to
mechanism is marrow suppression of
oval basophilic inclusions) can sometimes
megakaryocytes or generalized marrow
be identified in platelets of infected dogs.

stem cell suppression (after administration

The thrombocytopenia is seldom severe
of estrogen, chloramphenicol, phenylbutaenough to result in clinical bleeding zone, diphenylhydantoin, and sulfonatendencies. Ticks are the likely vectors.

mides). Another mechanism is increased

E canis infections are characterized by
platelet destruction and consumption
variable alterations in total WBC count, PCV,

( after administration of sulfisoxazole,
and platelet count. In acute infections, there
aspirin, diphenylhydantoin, acetaminois usually thrombocytopenia and possibly phen, ristocetin, levamisole, methicillin,
anemia or leukopenia In chronic infections,
and penicillin). Drug reactions are
there may or may not be thrombocytopenia
idiosyncratic and therefore unpredictable.

or anemia; however, there is often leukocy

Platelets usually return to normal shortly
tosis and sometimes hyperglobulinemia
after the drug is discontinued. Drug

( monoclonal or polyclonal). Infected dogs
induced bone marrow suppression may
may have epistaxis, melena, gingival
be prolonged. The chemotherapy drug
bleeding, retinal hemorrhage, hematoma
lomustine has sometimes caused proformation, and prolonged bleeding after longed thrombocytopenia that persists
venipuncture or surgery.

after the drug is stopped.

A phagocytophilum infection has been
documented in a wide variety of domestic

Other: Quantitative platelet disorders
and wild animals. It is characterized by
have been reported in liver disease with or
fever, lethargy, and a reluctance to move.

without coagulation protein deficiencies. In

Changes in blood parameters include
two studies of cats with thrombocytopenia,
thrombocytopenia and lymphopenia

29%--5096 had infectious diseases, including
accompanied by increased serum alkaline
feline leukemia, feline infectious peritonitis,
phosphatase and hypoalbuminemia.

panleukopenia, or toxoplasmosis. The
mechanism of thrombocytopenia has not

Neoplasia: Hemangiosarcoma, lymbeen identified in many cases. Feline phoma, and adenocarcinoma may be
leukemia virus replicates and accumulates
associated with consumptive thrombocytoin megakaryocytes and platelets; aplasia or penia due to disseminated intravascular
hypoplasia of marrow stem cells, immune
coagulation. Immunologic and inflamma-
destruction of infected platelets, or

HEMOSTATIC DISORDERS

49
extra vascular sequestration of platelets
pattern of inheritance, homozygosity is
within lymphoid tissues may cont.Iibute
usually fatal, and heterozygosity results in
to thrombocytopenia in this disease.

asymptomatic carriers. ln the more common
inheritance pattern of autosomal dominant

VetBooks.ir

Congenital Platelet Function
with incomplete penetrance, homozygotes

Disorders
and heterozygotes can have variable bleeding
tendencies. Affected aninlals may have

Congenital disorders of platelet function
gingival bleeding, epistaxis, and hematuria
affect platelet adhesion, aggregation, or

Some puppies may bleed excessively only
secretion. They can be either intrinsic or
after injection, venipuncture, or surgery, such
extrinsic to platelets. Testing of intrinsic
as tail docking, ear cropping, and dewclaw
platelet function requires careful handling
removal.

of samples and specialized equipment that
vWF circulates as a complex with
is not routinely available in diagnostic
coagulation Factor VIII (also called Factor
laboratories; therefore, the incidence of

VIII-coagulant) and mediates platelet
intrinsic functional defects in platelets
adhesion to subendothelial surfaces-the
is not known accurately. However, if a
first step in clot formation. Defective or
bleeding disorder ( especially mucosal
deficient vWF mimics disorders caused by
bleeding or superficial petechiation) exists
thrombocytopenia or intrinsic platelet
in an animal that has not received any
defects. Von Willebrand disease should be
medication and that has norn1al coagulation suspected in animals with clinical signs of screening test results, platelet concentraa bleeding disorder that have normal tion, and von Willebrand factor concentraresults on coagulation screening tests tion, then an intrinsic platelet defect should

(APTT and PT) and adequate platelet
be suspected.

concentrations, long buccal mucosa

There is no specific treat.Inent for any of
bleeding time, and prolonged platelet
the intrinsic platelet function disorders. In
function analysis closure times. Quantitainstances of severe hemorrhaging, fresh, tive tests of vWF are diagnostic. Diagnosis
platelet-rich plasma can be administered.

is confirmed by identifying low vWF

Whole blood may be administered if the
concentration in plasma or via DNA
affected animal is anemic.

screening. Occasionally, affected animals
may have decreased Factor VIII-coagulant

Von Willebrand Disease: This disorder,
and therefore have prolonged APTT and
caused by a defective or deficient von
activated clotting time (ACT). Drugs

Wille brand factor ( vWF, also called Factor
known to interfere with normal platelet

VIII-related antigen), is the most common
function should be avoided in animals
inherited bleeding disorder in dogs (reported
with suspected disease. Transfusion-of
in nearly all breeds and in !Tlixed breeds). It
cryoprecipitate, fresh plasma, or fresh
has also been reported in cats, rabbits, cattle,
whole blood effectively alleviates a
horses, and pigs. It is relatively frequent
bleeding episode. 'fype 1 von Willebrand

(10%-700/o prevalence) in several breeds of
disease may respond to treatment with
dogs: Doberman Pinschers, German
desmopressin acetate, which causes

Shepherds, Golden Retrievers, Miniature

Weibel-Palade release (high-molecular

Schnauzers, Pembroke Welsh Corgis,
weight multimers) from the endothelium

Shetland Sheepdogs, Basset Hounds,
through an unknown method of action.

Scottish Terriers, Standard Poodles, and

Desmopressin may also be used in these

Standard Manchester Terriers. Canine von
dogs before surgery to minimize bleeding

Wtllebrand disease is classified into three
complications.

subtypes based on clinical severity, plasma

Concomitant hemostatic abnormalities
vWF concentration, and vWF multimer
may exacerbate von Willebrand disease.

composition. 'fype 1 is the most common

Hypothyroidism ( see p 553) previously had
form and is characterized by mild to
been thought to be associated with von
moderate clinical signs, low vWF concentra

Willebrand disease; both conditions are
tion, and a normal multimer distribution.

prevalent in many of the same breeds of

'fype 2 is characterized by moderate to severe
dogs, eg, Doberman Pinschers and Golden
clinical signs, low vWF concentration, and a

Retrievers. In one study, administration of
loss of high-molecular-weight multimers.

thyroid supplementation to hypothyroid

'fype 3, seen most often in Shetland
dogs without deficiency of vWF did not

Sheepdogs and Scottish Terriers, is a severe
increase vWF activity; in fact, in most of
disorder characterized by total absence of
the tested dogs, vWF activity actually
vWF. Two modes of inheritance are known.

decreased. Therefore, administration

In the less common autosomal recessive
of levothyroxine as a treat.Inent of von

50

HEMOSTATIC DISORDERS

Willebrand disease cannot be recom

(30%-80% of all platelets), bizarre, giant
mended and may even exacerbate the
platelets are seen on blood smears. Due to a
disease.

decreased synthesis of either glycoprotein

Ilb or IIIa, the membrane receptor

Chediak-Higashi Syndrome: This
glycoprotein Ilb-IIIa is reduced or lacking

VetBooks.ir
autosomal recessive disorder is characteron the surface of platelets. All affected ized by abnom1al granule formation in
anin1als to date have had a defect in lib
leukocytes, melanocytes, and platelets (see
synthesis.

p 59). The defect appears to be in micro

Blood from affected aninlals does not
tubule fom1ation; therefore, granules,
have normal clot retraction, and the
which are abnormally large but reduced in
platelets do not aggregate normally after
number, are evident in numerous types of
stimulation with adenosine diphosphate,
cells. Diluted coat color results from the
collagen, or thrombin.

defect in the melanocytes. Leukocytes may
have decreased functional ability to
phagocytize and kill organisms (an

Acquired Platelet Function
inconsistent finding in aninlals), and

Disorders
platelets have decreased aggregation and

Dogs with immune-mediated thrombocytorelease reactions. Platelets are almost penia also may have an acquired platelet
devoid of dense granules and have markedly functional defect. Dogs can have excessive decreased storage quantities of adenosine
bleeding tendencies without severely
diphosphate and serotonin. Prolonged
decreased platelet concentrations. In clogs
bleeding in affected blue smoke Persian
with immune-mediated thrombocytopenia,
cats occurs after venipuncture or surgery.

abnom1al platelet function in addition to

The syndrome has been diagnosed in mink,
decreased platelet concentration may
cattle, and beige mice with similar bleeding
contribute to their bleeding tendency.

tendencies.

Several diseases have been associated
with acquired platelet function disorders.

Canine Thrombopathia: This disorder

Hyperglobulinemia associated with multiple
has been described in Basset Hounds.

myeloma induces a platelet membrane

Affected dogs have epistaxis, petechiation,
defect resulting in impaired hemostatic
and gingival bleeding. Results of studies
function. ln uremia associated with any
suggest that inheritance is autosomal with
form of renal disease, platelet adhesion and
variable penetrance. Platelets have
aggregation are decreased.

abnormal fibrinogen receptor exposure and

Numerous drugs can impair platelet
in1paired dense granule release. Basset
function. Drugs reported to block platelet

Hounds with mucosa! bleeding and
receptor binding or to change platelet
petechiation and normal concentrations of
membrane charge or pem1eability include
platelets and vWF should be suspected of
furosemide, penicillin, carbenicillin,
having thrombopathia. Specific diagnosis of
liclocaine, phentolamine, and chlorpromathis disorder requires specialized platelet zine. Drugs that inhibit transduction of
function testing. Results of the clot
messages received at the platelet surface
retraction test are usually normal.

include caffeine, theophylline, dipyridamole, and papavarine. Drugs that inhibit Bovine Thrombopathia: This autosoexecution of platelet re�ponses (aggregamally inherited platelet function defect is tion, secretion, or thrornboxane producseen in Simrnental cattle. Bleeding can be tion) include aspirin, indomethacin,
mild to severe in affected cattle and is
acetanlinophen, phenylbutazone, ticlopiexacerbated by trauma or surgery. Platelets dine, pentobarbital, and sulfinpyrazone.

have in1paired aggregation responses.

Clinical bleeding problems may not be

Bovine viral diarrhea virus ( see p 1436)

caused by drug-induced in1pairment of
may cause thrombocytopenia in cattle.

platelet function unless another disorder
associated with a hernostatic defect is also

Glanzmann Thrombasthenia:

present.

This autosomally transmitted disorder,
previously thrombasthenic thrombopathia,
has been diagnosed in Otterhounds and

VASCULAR DISORDERS

Great Pyrenees dogs, and in Thoroughbredcross, Quarter horse, and Oldenburg filly Congenital Vascular Disorders
horses. Affected animals have prolonged

Cutaneous asthenia (Ehlers-Danlos
bleeding tin1es and fom1 hematomas at
syndrome, rubber puppy disease) is caused
sites of venipuncture or irtjury. Nun1erous
by a defect in the maturation of type I

HEMOSTATIC DISORDERS

51
collagen. This causes weak structural
usually done, that a bleeding tendency
support of blood vessels and can result in
may become apparent.

hematoma formation and easy bruising. The

Most of the congenital coagulation
disorder has been reported in dogs, cats,
protein disorders reported in domestic

VetBooks.ir
mink, horses, cattle, sheep, and people but
animals are deficiencies or abnormalities
is rare in domestic animals. The most
of a single factor.

striking clinical abnormality is loose,

Congenital afibrinogenemia (Factor I
hyperextensible skin that tears easily.

deficiency) has been reported in a family

No treatment is available.

of Saanen dairy goats but not in dogs or
cats. Hypofibrinogenemia, accompanied

Acquired Vascular Disorders
by severe bleeding, has been reported in

Saint Bernards and Vizslas and in one

Several diseases cause severe, often
mixed-breed dog; the ACT, AP'IT, PT, and
generalized vasculitis and are characterized
thrombin time (TT) were prolonged.

by bleeding disorders.

Dysfibrinogenemia has been reported in

Rocky Mountain spotted fever (see
an inbred family of Russian Wolfhounds
p 806) is caused by Rickettsia rickettsii,

(Borzois). The ACT, AP'IT, PT, and TT were
which is transmitted by the ticks Derma
prolonged, but fibrinogen was present by
centor variabilis and D andersoni. The quantitative testing. Affected dogs had mild
rickettsial organisms invade endothelial
bleeding episodes with epistaxis and
cells and cause cellular death with
lameness, but trauma or surgery resulted in
resultant perivascular edema and
life-threatening bleeding. IV administration
hemorrhage. Variable degrees of coagulaof fresh-frozen plasma or cryoprecipitate is tion cascade activation can occur along
the best treatment to stop the bleeding.

with thrombocytopenia. Infected dogs may

Factor II (prothrombin) disorders are
have epistaxis, petechial and ecchymotic
rare. Boxer dogs have been reported to have
hemorrhages, hematuria, melena, or retinal abnonnally functioning prothrombin but hemorrhages. In severely affected dogs,
normal concentrations; the defect was
disseminated intra vascular coagulation
inherited as an autosomal recessive trait.

may occur.

A disorder of Factor II has been reported

Canine herpesvirus generally affects
in English Cocker Spaniels; clinical signs
puppies 7 -21 days old. Generalized
in affected puppies ( epistaxis and gingival
necrotizing vasculitis is accompanied by
bleeding) decrease with age, and adults
perivascular hemorrhage. The disease is
bruise easily or have dermatitis. In affected
usually rapidly fatal, and most puppies die
puppies, TT is normal, while ACT, APTI',
within 24 hr after showing signs.

and PT are prolonged. Treatment is by transfusion of fresh-frozen plasma or fresh whole COAGULATION PROTEIN
blood if RBCs are needed.

DISORDERS

Factor VII deficiency has been reported
in Beagles, English Bulldogs, Alaskan

Congenital Coagulation Protein

Malamutes, Alaskan Klee Kai, Miniature

Schnauzers, Boxers, and mixed-breed dogs.

Disorders

It is inherited in an autosomal pattern with

In a severe deficiency or functional defect
incomplete dominance. Usually, it is not
of coagulation proteins, clinical signs
associated with spontaneous clinical
appear at an early age. Marked reductions in bleeding, but affected dogs may have activity of coagulation proteins essential to
bruising or prolonged bleeding after
hemostasis are usually fatal. Animals may
surgery. Prolonged postpartum hemorrhagbe stillborn if there is < l % of normal activity ing has been reported. Factor VII deficiency
or die shortly after birth owing to massive
is most often diagnosed coincidentally
hemorrhage. Insufficient production of
when coagulation screening tests are
coagulation proteins or limited access to
performed; the PT is prolonged, while
vitamin K by the immature neonatal liver

AP1T and other test results are normal.

may exacerbate a coagulation defect. If

Factor VIII deficiency (hemophilia A)

activity of any particular coagulation
is the most common inherited bleeding
protein is 5%-100/o of normal, the neonate
disorder in dogs and cats; it has also been
may survive, but signs usually appear before reported in several breeds of horses, 6 mo of age. It is during this time, when
including Arabians, Standardbreds, Quarter
numerous routine procedures ( eg,
horses, and Thoroughbreds. There is an
vaccination, declawing, tail docking,

X -linked pattern of inheritance, so usually
dewclaw removal, ear cropping, and
females are asymptomatic carriers and
castration or ovariohysterectomy) are
males are affected. Rarely, in highly inbred

52

HEMOSTATIC DISORDERS
families, a carrier female mated with an
prolonged bleeding after tail docking or
affected male can produce affected female
dewclaw removal can occur. Some animals
offspring.

are asymptomatic until trauma or surgery.

In affected puppies, prolonged bleeding is The ACT and APTT are prolonged. Carrier seen from the umbilical vessels after birth;
animals with 400/o-60% of normal Factor IX

VetBooks.ir
from the gingiva during tooth eruption; and
activity are usually asymptomatic, and
after surgery such as tail docking, dewclaw
results of coagulation screening tests are
removal, or ear cropping. Hemarthrosis
normal. Treatment requires transfusion
accompanied by intermittent lameness,
with fresh-frozen plasma (10 mIJkg), bid,
spontaneous hematoma formation, and
until bleeding resolves. Often, internal
hemorrhagic body cavity effusions also are
hemorrhage into the abdomen, thorax,
common clinical findings in dogs with <5%

CNS, or between muscle fascia! planes
of normal Factor VIII activity. Animals with
occurs and may be undetected until a

5o/o-100Ai of normal activity often do not
crisis.

bleed spontaneously but exhibit prolonged

Factor X deficiency has been reported
bleeding after trauma or surgery. Affected
in a single family of American Cocker
cats and sometimes small dogs may show

Spaniels and a mixed-breed dog. In the
prolonged bleeding after surgery or trauma
former, the inheritance pattern was
but rarely bleed spontaneously, probably
autosomal dominant with variable
because of their agility and light weight.

penetrance. Homozygotes usually die early

Affected animals usually have very low
in life or are stillborn because of massive
concentrations of Factor VIII ( <10%) and
internal hemorrhage. Heterozygotes have
prolonged ACT and A.PIT. Von Willebrand
mild to severe bleeding problems. The ACT,
factor (Factor VIII-related antigen)

A.PIT, and PT are usually prolonged when
concentrations are normal or greater than
animals have <30% normal activity of Factor
normal. Carrier animals have intermediate

X. Transfusions with fresh or fresh-frozen
concentrations of Factor VIII ( 40o/o-600Ai),
plasma are required to control hemorrhage.

and results of coagulation screening tests

Factor XI deficiency has been
are usually normal. Care should be taken in
recognized in Kerry Blue Terriers, a female
diagnosis if animals are <6 mo old because

English Springer Spaniel, a Great Pyrenees
of possible low production of coagulation
dog, Weirnaraners, and Holstein cattle.

factors by an immature liver. Usually, results Mild deficiencies usually go undetected.

of coagulation screening tests are normal in

In severe deficiencies with Factor XI at
carrier animals.

30o/o-400Ai or less of normal activity, mild

Treatment of bleeding diatheses requires
prolonged bleeding may occur after trauma
repeated transfusions of cryoprecipitate or
or surgery. Bleeding tendencies usually are
fresh-frozen plasma ( 10 mVkg) 2-3 times/
not immediate but delayed for 3-4 days.

day until bleeding has been controlled.

The ACT and A.PIT are usually prolonged.

Fresh-frozen plasma or cryoprecipitate is

Transfusion with fresh-frozen plasma (10
preferable to whole blood because of the
mIJkg) is sufficient to stop the bleeding for
possible sensitization of the anin1al to RBC
up to 3 days. Inheritance is autosomal, but
antigens with repeated transfusions.

it has not been determined whether the

Factor IX deficiency (hemophilia B)

gene is dominant or recessive. A single
is diagnosed less often than Factor VIII
case involving an adult cat with epistaxis
deficiency. It has been reported in several
and diagnosed with.systemic lupus
breeds of purebred dogs, a mixed-breed
erythematosus was attributed to the
dog, Himalayan cats, a family of Siamesepresence of a circulating inhibitor against cross cats, and a family of British

Factor XI.

Short-haired cats. The defect is X-linked

Factor XII (Hageman) deficiency
with carrier females and affected males,
has been reported in German Shorthaired
although affected females can be seen in

Pointers, Standard Poodles, a family of
closely inbred families. Clinical presenta

Miniature Poodles, and in cats. Affected
tion is similar to that of animals with
animals do not have clinical bleeding

Factor VIII deficiency. Animals with
problems. The deficiency is usually
extremely low Factor IX activity ( <l %)

diagnosed coincidentally when coagulation
usually die at birth or shortly thereafter.

screening tests are performed and the A.PIT

Animals with 5o/o-10% of normal Factor IX
is prolonged. People with Factor XII
activity may spontaneously form hematodeficiency do not have bleeding problems mas, hemarthroses, hemorrhagic body
but are predisposed to thrombosis or
cavity effusions, or organ hemorrhage.

infections, which is attributed to the normal

Gingival bleeding during tooth eruption or
role of Factor XII in fibrinolysis and

HEMOSTATIC DISORDERS

53
complement activation. Tendencies for

Vitamin K Deficiency: Vitamin K is
thrombosis or infection have not been
solubilized in mixed micelles before passive
reported in animals. Factor XII deficiency
diffusion across the brush border. Fat
has been found to coexist with von
malabsorption associated with inadequate

Willebrand disease in a dog and with

VetBooks.ir
an1ounts of bile salts ( eg, biliary obstruc

Factor IX deficiency in a cat, but bleeding
tion), lymphangiectasia, or severe villous
tendencies were not exacerbated. Factor
atrophy may result in vitamin deficiency and

XII is not present in the plasma of birds,
coagulopathy owing to the lack of
marine mammals, and reptiles, with no
production of the functional vitamin Kuntoward effects.

dependent Factors II, Vil,

Deficiency of Factors II, VII, IX, and

IX, and X.

X has been described in Devon Rex cats that In
experienced bleeding, most commonly after
gestion of Anticoagulant Rodenticides: Ingestion of certain rodenticides by surgery. The bleeding can be controlled by
dogs and cats causes a coagulopathy owing
vitamin K administration, and some of these to the lack of production of functional cats appear to overcome the bleeding
vitamin K-dependent factors (seep 3165).

tendency as adults.

Inactive precursor coagulation Factors II,

Prekallikrein deficiency has been

Vil,
reported in Poodles, a family of miniature

IX, and X are still produced by the liver,
but -y-carboxylation of the inactive
horses, and a family of Belgian horses.

precursors does not occur, because the

Clinical bleeding problems are not usually
rodenticide inhibits the epoxide-reductase
apparent. One horse bled excessively after
enzyme required for recycling of active
castration. The diagnosis is usually made
vitamin K. There are two general classes of
coincidentally when coagulation screening
anticoagulant rodenticides: the coumruin
tests are performed. The ACT and APTT are
compounds (warfarin, coumafuryl,
usually prolonged.

brodifacoum, and bromadiolone) and the

Poor clot strength in Greyhounds has
indanedione compounds ( diphacinone,
been found to cause delayed postoperative
pindone, valone, and chlorophacinone).

bleeding. An abnormal maximum amplitude The anticoagulant rodenticides are further is obse1ved on TEG in these dogs. Epsilon
divided into first- and second-generation
aminocaproic acid is effective to prevent or
based on their toxicity and half-life. In
stop bleeding in affected dogs.

general, the half-life of the coumarins (up
to 55 hr) is much shorter than that of the

Acquired Coagulation Protein
indanedione compounds (15-20 days).

Various concurrently administered drugs

Disorders
and coexisting disease may exacerbate the

Liver Disease: Most coagulation protoxicity of the ingested anticoagulant.

teins are produced primarily in the liver.

Affected animals may have hematoma

Therefore, liver disease characterized
formation ( especially over pressure points)

by necrosis, inflammation, neoplasia, or
and bruising of superficial and deep tissues.

cirrhosis often is associated with decreased

Often, the animals do not bleed within the
production of coagulation proteins,
first 24 hr after ingestion of the toxin. The
anticoagulants, and fibrinolytic proteins.

APTT, PT, and ACT are usually prolonged.

Because the various coagulation proteins

Factor Vil has the shortest half-life of the
have a relatively short half-life ( 4 hr to 2
vitamin K-dependent coagulation proteins;
days), mild to marked deficiencies can
therefore, the PT is often abnormal before
result in secondary to severe hepatopathies. other tests and can be used to monitor The APTT and/or PT are prolonged in
response to treatment. With acute ingestion,

50%-85% of dogs with severe liver disease,
emetics, absorbents, and cathartics ru·e used
meaning that the factor activity is <30% of
to mininlize absorption. Vitamin K therapy
normal. Nevertheless, <2% actually develop
is often initiated even in asymptomatic
hemorrhage and, when bleeding does occur, animals. Vitamin K" 2.5-5 mg/kg, SC, it is usually associated with concurrent
divided between several utjection sites, is
disease. Coagulation tests are often
recommended for initial treatment of
performed before liver biopsy.

coumarin toxicity, followed by 1.25-2.5

Severe hepatic diseases can also lead to
mg/kg, PO, bid for 4-6 days if the ingestion
disseminated intravascular coagulation.

is thought to be minimal. PT should be

Fibrinogen, an acute phase reactant, and
measured 48 hr after temlination of
von Willebrand factor, which is produced
treatment, and if prolonged, treatment
extrahepatically, can be increased in liver
should be continued for another 14 days. If
disease.

the initial PT is normal, another PT should

54

HEMOSTATIC DISORDERS
be perfom1ed in 48 hr. If that test is nom1al,

In veterinary medicine, the laboratory
treatment can be discontinued. Dosages of
diagnosis of DIC is not standardized and
vitanlin K, as high as 5 mg/kg, PO, for 3-6
the hemostatic function tests used are not
wk may be required for treatment of
consistent, but DIC is often diagnosed based

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indanedione toxicity; however, these high
on three or more abnormal hemostatic
dosages should be administered cautiously,
parameters such as APTT, PT, fibrinogen,
because Heinz body anemia has been
o-din1er, platelet count, and RBC morpholreported in dogs given 4 mg/kg for 5 days.

ogy, along with predisposing disease, which

IV adnlinistration of vitanlin K, is not
is a sensitive but unspecific approach.

recommended, because anaphylactic

Postmortem fibrinolysis makes necropsy
reactions can result. Administration of
an insensitive diagnostic criterion.

vitamin K3 is not useful.

Therapy is often empirically directed at
correcting the imbalance in the hemostatic

Disseminated lntravascular Coagula
system while treating the underlying disease
tion (DIC): DIC is not a primary disease
aggressively. Administration of balanced
but occurs secondary to numerous
electrolyte solutions and plasma expanders
underlying diseases, such as bacterial, viral,
to maintain effective circulating volun1e is
rickettsial, protozoal, or parasitic diseases;
in1perative. The response to treatment with
heat stroke; bums; neoplasia; or severe
fresh-frozen plasma and heparin is
trauma The underlying disease causes an
unpredictable, and their use is controversial.

uncontrolled systemic inf!anllllatory
response characterized by massive
activation and consumption of coagulation

PATHOLOGIC THROMBOSIS
proteins, endogenous inhibitors, fibrinolytic
proteins, and platelets.

Primary or Inherited Anticoagulant

In the initial stage of DIC, the animal is

Disorders
hypercoagulable because of circulating

Congenital deficiency of any anticoagulant
inflanm1atory mediators that cause
protein has not been recognized in domestic
activation of hemostasis through increased animals. If such a condition exists in animals, exposure of TF and inhibitor consumption.

it is probably incompatible with life.

With time, consumption of coagulation
factors, if not compensated by increased
production, may lead to a hypocoagulable

Secondary or Acquired Procoagulant
state with overt clinical symptoms.

Disorders

Because of the progressive nature of

The presence of hypercoagulability is

DIC, the clinical findings vary considerably
difficult to assess ante mortem in dogs, and
and range from no overt signs of disease,
the importance of hypercoagulability and
accompanied by no or perhaps only
thromboembolic disease has not been well
subtle changes in traditional hemostasis
defined in veterinary medicine. Thromboparameters (APTT, PT, o-dimer, fibrinogen, elastography (TEG, seep 46) enables
and platelet count), to clinical signs of
global assessment of hemostatic function in
organ failure, associated with microvaswhole blood; advantages of TEG include the cular thrombosis in vital organs, finally
evaluation of the viscoelastic properties of
culminating in overt bleeding symptoms.

the developing blood clot (including clot

The latter presentation is traditionally
formation, kinetics, strength, stability, and
thought of as the characteristic DIC
resolution) and immediate detection of
patient, in which there are also pronounced hyper- and hypocoagulable states.

alterations in hemostasis parameters and a

Certain diseases in animals have been
drop in the platelet count.

associated with increased risk of thrombo

Thromboelastography can differentiate
sis. Cats witl1 cardiomyopathy, more
the stage of DIC in dogs. Dogs diagnosed in
co1lll1only the dilated form but also the
the hypercoagulable stage have a much bethypertrophic and restrictive forms, can ter chance of survival than dogs diagnosed
develop large thromboemboli in the aorta or
in the hypocoagulable stage. This is likely
brachial artery. Thrombosis has been seen
because of early and aggressive intervenin dogs with protein-losing nephropathies, tion through supportive and/or anti thromhyperadrenocorticism, neoplasia, chronic botic therapy while the underlying disease
hypothyroidism accompanied by atherois treated. Aggressive treatment likely sclerosis, and instances of autoimmune
minimizes thromboembolic complications
hemolytic anemia. Thrombi and thromboand delays or even prevents progression to emboli have been seen in horses with
overt signs.

systemic inflanm1atory diseases ( such as

HEMOSTATIC DISORDERS

55
colic, laminitis, or equine ehrlichial colitis)

by altering platelet responsiveness to
and in instances of prolonged jugular
agonists.

catheter placement and infusion of drugs

Horses with colic associated with
that irritate the vasculature.

endotoxernia have decreased plasminogen

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Neoplasia is a risk factor for hypercoaguactivity and protein C antigen concentralability and likely associated complications, tion. These horses have increased
such as thromboembolic disease. Many of
mortality and 1isk of thrombus formation.

the cells and proteins involved in maintain

Laminitis is thought to be the end result of
ing hemostasis are also involved in the
several diverse systemic disorders.

processes of cancer growth, invasion,

Micro thrombi in the vasculature of the
metastasis, and angiogenesis. Deep venous
hoof lamina have been identified in the
thrombosis is a significant clinical complicaearly stages of laminitis. One theory is tion in human cancer patients, but whether
that endotoxin has direct effects on the
this is true in dogs with cancer is unknown.

vasculature and activates contact factors

In protein-losing nephropathies ( eg,
in the coagulation cascade. Ischemia of
glomerulopathies, nephrotic syndrome,
the lan1ina secondary to edema, vascular
renal amyloidosis), a deficiency of
compression, and possible blood shunting
antithrombin has been well documented.

at the level of the coronet also damage

Antithrombin has a molecular weight of
endothelium. When circulation is

57,000 kilodaltons (kD), which is similar
reestablished, reperfusion injury results,
in size to albumin (60,000 kD); therefore,
and the exposed subendothelial collagen
glomerular lesions sufficient to result in
promotes thrombosis.

albumin loss also result in loss of antithrom

The most appropriate treatment of an
bin. Other abnormalities identified in renal
animal with thrombi or thromboemboli
disease include increased responsiveness of is diagnosis and management of the platelets to agonists, increased procoaguunderlying disease process, along with lant activities, and decreased antiplasmin
good supportive care. Maintenance of
activity. Cun-ently, the cause of thrombosis
adequate tissue perfusion is critical.

is thought to be multifactorial.

Dissolution of clots and prevention of clot

Hypercholesterolernia has been
recurrence by administration of anticoassociated with increased risk of thromboagulants (eg, heparin and coumarin) has embolism. It is hypothesized that endothehad mixed success. Heparin facilitates the lial and platelet membrane phospholipid
action of antithrombin, but to be effective,
concentrations are altered, which leads to
adequate antithrombin must be present.

danrnged vasculature and increased platelet

In dogs with protein-losing nephropathies
responsiveness to agonists, respectively.

or in horses with endotoxemia, plasma

Increased production of thromboxane via
transfusion may be necessary before
the cyclooxygenase pathway in platelets
heparin therapy is effective. Coumarin
has been seen. Diseases characterized by
has been most useful for control or
hypercholesterolemia include hyperadrenoprevention, rather than for treatment.

corticism, diabetes mellitus, nephrotic

Fibrinolytic compounds have been
syndrome, hypothyroidism, and pancreatiadministered to animals to enhance tis. All have been associated with increased
dissolution of clots. Tissue plasminogen
risk of thrombus formation, often pulmoactivator (TPA) has more fibrin specificity nary thrombosis.

than does streptokinase or urokinase and,

Cats with cardiomyopathy have increased therefore, provides more localized risk of thromboembolism. Endomyocardial
fibrinolytic effects (although not totally).

lesions and turbulent blood flow through

The main deterrent to use of TPA is its
the heart chambers and valves secondary to
high cost. One study of cats with aortic
altered myocardial functioning are thought
thrombosis treated with TPA found a
to initiate thrombus formation. Specific
risk of reperfusion injury after the clot
deficiencies of anticoagulant or fibrinolytic
dissolved. Streptokinase is more available
proteins have not been seen. Interestingly,
and less expensive, but the therapeutic
antithrombin is markedly increased but
dose is difficult to determine. Many
does not provide protective benefits. Cats
animals have naturally occurring
with cardiac disease secondary to
antibodies to streptokinase as a result
hyperthyroidism are often treated with
of previous streptococcal infections.

drugs ( eg, propranolol, atenolol, or

Administration of streptokinase must be
diltiazem) that abate clinical signs of
sufficient to neutralize all antibodies but
cardiac dysfunction. These drugs appear to
not produce a systemic fibrinolytic state
protect against increased risk of thrombosis
with resultant bleeding diathesis.

56

LEUKOCYTE DISORDERS

LEUKOCYTE DISORDERS

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Leukocytes, or WBCs, in the blood of healthy appreciably because of movement of cells mammals include segmented neutrophils,
and/or fluid from one pool to the other as a
band neutrophils, lymphocytes, monocytes,
result of a change in equilibrium. In most
eosinophils, and basophils. Abnormal
species, WBCs are roughly equally
leukocytes include neutrophils less mature
distributed between the two pools. Cats
than bands ( eg, metamyelocytes, myelohave a greater distribution of leukocytes cytes, progranulocytes ), blast cells of any
within the marginal pool. WBCs in the
hematopoietic lineage, mast cells, and other
circulating pool can be increased by certain
neoplastic cells. WBCs vary in their site of
mechanisms: epinephrine can redistribute
production, their duration of circulation, and WBCs from the marginal pool to the the stimuli that affect their release into and
circulating pool, and corticosteroids can
migration out of the vascular system.

inhibit neutrophil endothelial adherence

Differences in leukocyte physiology account
and tissue migration.

for species differences in normal blood cell
concentrations and their responses in

Granulocytes
disease.

The leukogram, a component of the

Granulocytes include neutrophils,

CBC, is an organized tabulation of the total
eosinophils, and basophils, all of which
nucleated cell concentration, along with
are produced in the bone marrow from a
the concentrations of specific WBC types
common stem cell. Granulopoiesis is the
present in the sample, also known as the
term used to describe production of these
differential. Knowledge of species-specific
cells. The proliferative ( or mitotic) stages

WBC physiology and the influence of disease of development consist of myeloblasts, processes form the basis for interpreting
promyelocytes, and myelocytes. Promyeloabnormalities of the leukogram into cytes have azurophilic primary granules
diagnostic information. Most leukogram

Oysosomes) that become inapparent in later
interpretations define a process rather than
stages. The storage ( or maturation) pool
a specific diagnosis. Processes generally fall
consists of metamyelocytes, band
into four groups: 1) transient physiologic
neutrophils, and segmented neutrophils
responses that alter vascular hemodynamthat are functionally mature. Specific ics; 2) inflammatory, infectious, and
granules, which define final cell types, are
immunologic responses; 3) bone marrow
first produced at the myelocyte stage. Cell
responses to i..ajury; and 4) hematopoietic
types are recognized by characteristic
cell neoplasia. (See ai,so
granule staining affinity, eg, basophilic

WHITE BLOOD CELIS,
p 1612.)

granules for basophils, eosinophilic
granules for eosinophils, and neutral or
nonstaining granules for neutrophils.

PHYSIOLOGY OF LEUKOCYTES

The population of segmented and band
neutrophils in the bone marrow can be

Blood Vascular System
substantial in some species and is referred

The blood vascular system is conceptually
to as the marrow granulocyte reserve.

divided into two compartments: the central
pool and the marginal pool. The marginal

Neutrophils: In blood, neutrophils
pool consists of the microcirculation at the
typically are mature (segmented), with
capillary-tissue interface. The central pool
occasional more immature band forms.

consists of larger vessels. Blood samples

Neutrophils from bone marrow enter the
taken by venipuncture are inherently most
blood, where they remain for an average of
representative of the central pool. F1ow

8 hr. They tend to adhere to the microcircurate, fluid movement to the extravascular latory endothelium and then unidirectionspace, and selective WBC adhesion to ally enter tissues, where they may
endothelium are factors that may contribute participate in host defense. Given the short to marked differences in cell concentration
lifespan of neutrophils in blood, maintein the two pools. Furthermore, these pools nance of blood neutrophil concentration
are in hemodynamic equilibrium with each
depends on a relatively high, steady delivery
other and the extravascular space.

from bone marrow. This balance may

Therefore, WBC concentration may change
change dramatically when there is either

LEUKOCYTE DISORDERS

57
increased tissue demand associated with
and macrophages are a major source of
the development of an inflammatory
colony-stimulating factors and cytokines
process or a stem-cell i.Jtjury that reduces
that regulate inflammatory responses, and
the marrow production rate. During
they function as antigen-processing cells.

initiation of an inflammatory lesion, local
mononuclear cell release of specific

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Lymphocytes
stimulating factors rapidly stimulates bone
marrow to release neutrophil reserve and

Lymphocytes originate from a bone marrow
accelerate granulopoiesis. When the tissue
stem cell and mature in lymph nodes,
demand is intense, marrow production and
spleen, and other subepithelial lymphoid
release may accelerate dramatically,
tissues. Mature lymphocytes consist of two
resulting in a left shift and toxic changes
major subpopulations, B cells and T cells.

(seep 57).

B cells (for bone marrow or bursa
equivalent) are potential precursors of

Eosinophils: Eosinophils function in paraplasma cells that produce antibodies for site killing and also contain enzymes that
humoral immunity. T cells (for thymus)

modulate products of mast cells released in
engage in cellular immunity ( eg, histocomresponse to antigen-IgE receptor mast cell patibility and delayed-type hypersensitivdegranulation in allergic disease. For ity). Lymphocytes in tissue may return to
example, histamine released by mast cells is
the vascular system and recirculate. Some
modulated by histaminase in eosinophils.

lymphocytes are very long-lived compared

Eosinophilia is primarily induced by allergic
with other WBC types.

inflammatory responses and tissue invading
parasitic infestations. Less commonly,

LEUKOGRAM ABNORMALITIES
neoplasia may be associated with paraneoplastic induction of eosinophilia. Localized Abnom1alities of the leukogram include
eosinophilic tissue lesions do not necessarquantitative or numerical concentration ily produce a peripheral eosinophilia, eg, the abnormalities and WBC morphologic eosinophilic granuloma dermatopathies
abnormalities.

and oral lesions of cats. Eosinopenia is a
component of corticosteroid-induced

Numerical Abnormalities: WBC

(stress) leukograms.

concentration values are interpreted by
comparison with species-specific reference

Basophils: Basophils are rare in all
values. Interpretations should be made only
common domestic animals. Basophil
by considering the absolute numbers. For
granules contain histamine, heparin, and
reference values for total WBC and
sulfated mucopolysaccharides; understanddifferential WBC concentrations in absolute ing of their function is limited. As a result,
numbers for common domestic species, see
there is no clear interpretation for

TABLE 6, p 3176. The total WBC concentra basophilia. Basophilia is uncommon but tion is more variable and often higher in
may accompany eosinophilia, and it is the
neonates than in adults. Age-related
latter that is interpreted. Although blood
reference values should be used to evaluate
basophils and tissue mast cells have similar
leukograms in young animals, especially
enzymatic contents, basophils do not
species in which lymphocytes are more
become mast cells. They appear to arise
numerous ( and neutrophils less numerous)

from separate marrow stem cells .

in adults, such as runlinants. Generally,
differential WBC patterns of adults are

Monocytes
reached at about the age of sexual maturity.

Abnormality in the total WBC concentra

Monocytes are formed in the bone marrow
tion is useful only to alert the clinician to
from monoblasts and then develop to
look for and interpret abnormalities in the
promonocytes and finally mature monocell distributions in the differential. When cytes. Monocytes enter the peripheral blood the total WBC is abnormal, one or more for -24-36 hr and exit into tissues to mature
distributional abnormalities in the
into tissue macrophages. Monocytes and
differential are likely. When the total WBC is
macrophages perform phagocytosis of
normal, there still may be one or more distriorganisms and cellular debris at sites of butional abnormalities in the differential.

inflammation or tissue i.Jtjury. They may

As a result, evaluation of the differential
form multinucleated giant cells, particularly
absolute values is the most important
in response to foreign bodies or complex
component of the leukogram.

organisms that elicit granuloma formation,

Leukocytosis is an increase in the total
such asMycobacterium spp. Monocytes

WBC concentration, whereas leukopenia is

58

LEUKOCYTE DISORDERS
a decrease in the total WBC concentration.

indicate a leukemoid response are> 70,000/

Changes in the concentrations of specific
µL (70 x 1Q9fL) for dogs, >50,000/µL (50 x
leukocyte types are more in1portant for

1Q9fL) for cats, >30,000/µL (30 x 109/L) for clinical interpretation purposes.

horses, and >20,000/µL (20 x 1Q9fL) for

Neutrophilia or neutrophilic leukocytosis
ruminants.

is an increase in neutrophil concentration.

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Lymphocytosis is an increase in lymphocyte

Morphologic Abnormalities: Abnorconcentration. Monocytosis is an increase malities of morphology may be associated
in monocyte concentration. Eosinophilia
with either acquired or inherited disease.

refers to an increase in eosinophil

Toxic changes are identified only in
concentration, and basophilia to an increase neutrophils. The term originates from in basophil concentration. Metarubricytosis
historical observation that certain cell
is an increase in nucleated RBCs (nRBCs) in features were associated with general, blood. Mastocytosis is an increase in mast
usually overwhelming, toxic states, such
cells in blood.

as systemic bacterial infections and

Decreases in concentration of a cell type
severe, acute inflammatory lesions. The
are indicated by the suffix "penia." This tem1 is misleading in that it implies neutrois applied only to cell types in which a phil injury. The cells are not injured and
decrease is possible. It does not apply to cell have normal function. Toxic change is best types for which the concentration may be 0,
defined as a set of morphologic changes
such as monocytes, basophils, nRBCs, and
observed on the blood smear that occur as
any other abnormal cell type. Hence,
a result of accelerated marrow production
neutropenia is a decrease in neutrophil
of neutrophils. The accelerated producconcentration, lymphopenia is a decrease in tion is in response to relatively severe lymphocyte concentration, and eosinopenia
inflammatory states that maximally
is a decrease in eosinophil concentration.

stimulate the bone marrow. Morphologic

Cytopenia is a nonspecific term indicating a
changes include (in order of frequency)

decrease in cell concentration(s), but the
diffuse cytoplasmic basophilia, Dahle
cell type is not specified. Pancytopenia
bodies, and fine cytoplasmic vacuolation.

indicates all cell types are decreased, often

More rare changes include increased
to a severe degree.

prominence of cytoplasmic azurophilic

Terms used to describe or qualify
granules, cellular gigantism, and binucleaabnormalities most often associated with tion. Toxic change is almost always
inflan1matory responses include various left
associated with the concurrent presence
shifts and leukemoid response. A left shift is
of a left shift. It is graded as mild,
an increase in concentration of immature,

I)loderate, or severe by subjective
nonsegmented neutrophils, typically bands,
evaluation of the more common changes
but may also include metamyelocytes or
noted on examination of a blood smear.

even more immature forms. A regenerative

Dahle bodies, blue-gray cytoplasmic
left shift describes leukocytosis characterinclusions, are aggregates of endoplasmic ized by the combination of neutrophilia and
reticulum. They are unique in that they
a left shift. In this situation, the segmented
may be found in clinically healthy cats and
neutrophils will be greater in concefltration
therefore are not interpreted as toxic
than bands and less mature forms. A
change in this species unless accompanied
degenerative left shift describes a neutroby other features.

phil pattern characterized by normal to

Reactive lymphocytes have increased,
decreased total neutrophil concentration,
distinctly basophilic cytoplasm and may
but with a left shift in which the concentrahave irregular or clefted nuclei. They may tion of bands and less mature forms is
vary considerably in diameter. They have
greater than segmented neutrophils. This is
condensed chromatin and therefore are not
an indication of maximal release from bone
blasts. They are interpreted as immunologimarrow in response to inflan1mation and cally stimulated B cells.

signifies the presence of an acute, severe

Granular lymphocytes have condensed
lesion. A leukemoid response describes
chromatin and increased pale blue-gray
a marked neutrophilia of a magnitude
cytoplasm that contains several small pink
sufficient to indicate chronicity of an
or azurophilic granules. The nucleus may be
inflan1matory response and corresponding
round to clefted. These are large granular
substantial increase in granulopoiesis in the
lymphocytes and may be either natural
bone marrow. The magnitude is also such
killer (NK) lymphocytes or T lymphocytes.

that myeloproliferative disease becomes a

Blast cells are usually an indication of
diagnostic consideration. Guidelines for
hematopoietic cell neoplasia if they are
neutrophilic leukocytosis considered to
reproducible or present in large numbers.

LEUKOCYTE DISORDERS

59

Their lineage may be tentatively identified

Hypersegmentation is an increased
by morphologic criteria, but flow cytometric degree of nuclear segmentation resulting analysis is required to definitively identify
in multiple lobes connected by nuclear
lineage.

filaments. It is a nonspecific indication of

Many of the following morphologic
increased time in circulation and is normal

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changes are uncommon.

aging of the cell. This may be seen with

Chediak-lligashi syndrome (see
stress leukograms or corticosteroid
p 50) described in Persian cats, people,
administration.

·mmk, foxes, Hereford and Brangus cattle,

Leukocyte agglutination may occur
mice, and killer whales is an autosomal
with either neutrophils or lymphocytes. This
recessive defect involving lysosomal
is seen on low magnification as aggregates
granules. There is hyperfusion of granules
of 5-15 tightly clumped leukocytes. Avid
resulting in large, eosinophilic cytoplasmic
agglutination may result in a markedly false
inclusions. Susceptibility to bacterial
low total WBC concentration on some cell
infections is increased, as is the tendency
counting instruments. This is likely due to
to bleed because of both neutrophil and
the presence of a naturally occurring cold
platelet function abnormalities. Partial
agglutinin that is operative only in vitro at
oculocutaneous albinism due to abnormal
laboratory temperature. There is no known
melanin granule formation may occur.

clinical significance.

The mucopolysaccharidoses are a

Infectious disease inclusions are
group of lysosomal storage disorders in
occasionally recognized. Canine distemper
which there is a defect in degradation of
inclusions may be seen in neutrophils,
glycosaminoglycans. Both neutrophils and
monocytes, and lymphocytes, as well as
lymphocytes may contain accumulated
in newly produced erythrocytes. The
mucopolysaccharide product in the form
ehrlichioses of various animal species and
of purple or metachromatic intracytoplascanine hepatozoonosis may have cytoplasmic granules. Lymphocytes may also be mic inclusions of respective organisms of
vacuolated. These disorders are associthese tickbome diseases.

ated with a variety of systemic clinical
abnormalities and are seen in dogs and
cats.

Specific Interpretative Leukogram

Another group of lysosomal storage

Responses
disorders recognized in dogs and cats may

The abnormal leukogram is typically
result in cytoplasmic vacuoles predomiinterpreted into one of several responses, nantly in lymphocytes and occasionally in
each of which may consist of one or more
neutrophils. These disorders include
abnormalities in the differential. Some may
gangliosidoses, cx-mannosidosis, Niemann
also be associated with concurrent changes

Pick disease variants, acid-lipase deficiency,
in erythrocytes and platelets. Important
and fucosidosis. Most of these disorders
species differences in leukogram responses
result in severe, progressive neurologic
are described below.

disorders resulting from accumulated
product in neuronal tissue.

Corticosteroid-induced or Stress

Locoweed toxicity is regarded as an

Response: In this very common leukocyte
acquired form of lysosomal storage defect in
response, endogenous steroid release from
large animals. It is due to toxic principle from
stress or treatment with exogenous
the plant that inhibits one or more enzymes
corticosteroids results in a leukogram with
of oligosaccharide metabolism. This may
multiple changes. Lymphopenia is the most
result in vacuolation in lymphocytes.

consistent change, and mature neutrophilia

. Pelger-Huet anomaly is a nuclear
is usually present. Monocytosis and
hyposegmentation defect of granulocytes
eosinopenia are expected changes in dogs
in people, cats, rabbits, horses, and dogs
but are more variable in other species.

that are heterozygous for the anomaly.

Neutrophiliais due to decreased adherence

Neutrophils have normal function but a near to the vascular endothelium, which inhibits absence of segmented nuclear morphology.

margination and increases circulating time.

Most or all of the neutrophils appear as

As a result, neutrophils may also become
bands and metamyelocytes and may appear
hypersegmented. There may also be
as a marked left shift in an otherwise normal
increased marrow release of neutrophils.

leukogram. Eosinophils and basophils, if

Lymphocytes become redistributed to
present, also exhibit nuclear hyposegmentalymphoid tissues instead of remaining in tion. Affected heterozygote animals are
circulation. This response may be misinterclinically normal; the homozygous preted as inflanlffiation, but a left shift is not
inheritance of the trait is lethal.

usually present.

60

LEUKOCYTE DISORDERS

Excitement or Epinephrine Re
still stimulates maximal marrow production.

sponse: Leukocytosis may occur as

Examples of closed cavity processes are
a result of exercise or excitement; this
pyometra in dogs and traumatic reticuloperiresponse is mediated by increased tonitis (hardware disease) in cattle. In these
epinephrine concentration and may
conditions, the magnitude of the total WBC

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be thought of as a transient physiologic
concentration, consisting of neutrophilia,
response. Epinephrine flushes cells from the may be as high as 100,000/µL (100 x 109/L) marginal to the central pool. The effect may
of blood in dogs.

double the total WBC concentration within

Extreme neutrophilia, exceeding upper
minutes. In addition, splenic contraction
limits usually seen in inflammation, may be
releases WBCs and RBCs into the peripheral associated with leukemia, Hepatozoon circulation. The leukocytosis is usually due
canis infections, and rarely other neoto a mature neutrophilia without a left shift.

plasms that produce colony-stimulating

Lyrnphocytosis may be present, especially in factors.

young horses or cats. The effect in cats is

In contrast, cattle and most other
often recognized as a prominent lyrnphocyruminants have a relatively low reserve tosis--as much as two times the upper
of bone marrow neutrophils and a lower
reference value. The excitement response
capacity for accelerating granulopoiesis.

is relatively uncommon in dogs.

This is reflected in the relatively low
neutrophil concentration in normal
ruminant blood. As a result, acute inflamma

Inflammatory Response: The
tion in cows is characterized by neutropenia
concentration of neutrophils in blood in
that can be profound. Therefore, neutroperesponse to inflammatory disease is highly nia in cattle does not reveal the degree of
variable and dynamic. It is best viewed as a
inflammatory severity. After several days,
balance between tissue demand and bone
the bone marrow response may establish a
marrow production at all phases of the
return of blood neutrophils in modest
response. There are important species
concentration, characterized by a marked
differences in this balance that are related
left shift and toxic changes. Chronic, closed
to bone marrow storage reserve and
cavity inflammatory lesions are associated
proliferative capacity.

with magnitudes of neutrophilia that rarely

At the beginning of an inflammatory
exceed 25,000/µL of blood. Cats and horses
process, the bone marrow responds by
are intermediate in these responses, with
delivery of its reserve of late-stage maturing
cats being more like dogs and horses being
neutrophils, including band cells. If
more like cattle. Pigs have an inflammatory
consumption exceeds marrow delivery
leukograrn similar to that of dogs.

during this acute stage, neutropenia with a

Bovine leukocyte adhesion deficiency
prominent left shift will develop. In dogs
is a lethal, autosomal recessive disorder of
and cats, this is an indication of severity of

Holstein cattle. It is associated with marked
the inflammatory lesion.

neutrophilia; the neutrophils have a

Subsequently, it takes 2-4 days for the
deficiency of the glycoproteins (integrins)

marrow to accelerate neutrophil production that are essential for normal leukocyte by increased stem-<:ell entry and-expansion
adherence and emigration from the
of proliferative stages that feed the
vasculature. Recurrent bacterial infections,
maturation stages and amplify neutrophil
persistent neutrophilia ( often > 100,000/µL
delivery to blood. In dogs, the acute stage of

[100 x 109/L]), lyrnphocytosis, and death
the inflammatory response is usually charac

( usually between 2 wk and 8 ino of age) are
terized by mild to moderate neutrophilia,
characteristic. Calves often are stunted and
with the left shift being somewhat proporhave recurrent pneumonia, ulcerative tional to severity of demand.

stomatitis, enteritis, and periodontitis.

After a few days, accelerated bone marrow On examination of tissues, there are few production adds to the picture. Neutrophilia
neutrophils, except within vessel lurnens,
may increase along with left shift and toxic
because they persist in the circulation and
changes. As the process becomes chronic,
have impaired entry into the tissues. Testing
the balance between increased marrow
is available to detect carriers. A similar
output and consumption may favor the
defect has also been reported in some Irish
development of even higher magnitudes of

Setter dogs.

neutrophilia The most chronic form, present

Neutropenia may develop because of
for weeks or even months, is described as a
excessive tissue demand for neutrophils or

"closed cavity" inflammatory process. The
reduced granulopoiesis. It may be seen
lesion becomes somewhat walled off and
with overwhelming bacterial infections,
therefore consumes fewer neutrophils, yet it
especially gram-negative septicemia or

LEUKOCYTE DISORDERS

61
endotoxemia, in all species. Immunelymphopenia in cortjunction with an mediated destruction of neutrophils is
inflammatory neutrophil response (left
diagnosed by exclusion of other consumpshift). The neutrophil response to inflammative processes. Stem-cell iltjury may occur tion overrides and may be additive to the
from many causes such as certain viral
corticosteroid influence on neutrophils.

infections ( see TABLE 7), chemical iltjury, and VetBooks.ir
idiosyncratic drug reactions, eg, sulfona

Lymphocytosis: Mild lymphocytosis and
mides, penicillins, cephalosporins, and
reactive lymphocytes may occur after
chloramphenicol in cats. These reactions
vaccination. Modest lymphocytosis, in the
typically affect all bone marrow cell lines but range of 7,000-20,000/µL (7-20 x 109/L), are recognized initially as neutropenia
should prompt consideration of a possible
because of the relatively short lifespan of
physiologic excitement response, particuthis cell type.

larly in cats. lf that is excluded, then a

Neutropenia is seen in the now rare cyclic
lymphoproliferative disorder should be
hematopoiesis syndrome of gray Collie
considered. lf examination of lymphocyte
dogs, also known as canine cyclic neutropemorphology reveals prolymphocytes and/or nia It is an inherited, autosomal recessive
blast cells, then lymphocytic leukemia is the
disease characterized by a profound periodic working interpretation. lf the cells are all neutropenia, associated overwhelming
small with normal appearing chromatin, then
recurrent bacterial infections, bleeding, and
chronic lymphocytic leukemia is a consideracoat color dilution. The defect is due to a tion requiring further evaluation. Chronic
mutation in a protein that may regulate
ehrlichiosis may result in lymphocytosis of
neutrophil elastase activity. Neutrophil matuthis magnitude in dogs. At higher concentraration is arrested at regular intervals of 11-14 tions, the lymphocytosis may be regarded as days; the peripheral blood neutropenia lasts
conclusive evidence of leukemia

3--4 days and is followed by neutrophilia All

Persistent lymphocytosis in cattle is
other hematopoietic cells, including
defined by lymphocyte concentrations
lymphocytes, also have cyclic production
consistently> 7,500/µL (7.5 x 109/L). It is
that is minimally evident because of the
due to a B-cell proliferation that occurs in a
relatively long circulation time of other cell
subset of animals infected with bovine leuketypes. Affected puppies often die at birth or mia virus (BLV). Affected cattle are usually
during the first week and rarely live > 1 yr.

asymptomatic. The finding of persistent

Surviving dogs may be stunted and weak
lymphocytosis is regarded as a positive
and develop serious recurrent bacterial
indication of BLV infection in the individual.

infections during periods of neutropenia

A smaller subset of BLY-infected cattle,

Monocytosis may be seen in the
either with or without lymphocytosis, may
inflammatory pattern at any stage of its
progress to develop lymphoma or lymphoprogression. Monocytosis is more likely, cytic leukemia
and tends to be of greater magnitude,
when the process becomes chronic.

Lymphopenia: Lymphopenia is a
common leukogram abnormality most

Combined Corticosteroid-induced
commonly associated with endogenous
and Inflammatory Response: Inflam

(stress) or exogenous corticosteroid
matory disease processes commonly induce administration. The most likely cause is a concurrent endogenous corticosteroid
steroid-induced apoptosis of lymphocytes.

response, recognized by the presence of

Lymphopenia also rarely occurs due to
iih•D VIRAL INFECTIONS THAT MAY CAUSE TRANSIENT NEUTROPENIA Species

Infection

Dogs

Parvovirus, canine distemper ( acute phase)

Cats

Panleukopenia (parvovirus), feline leukemia virus

Horses

Equine influenza, equine viral arteritis (acute phase), equine herpesvirus

Cattle

Bovine viral diarrhea virus

Pigs

Classical swine fever virus, African swine fever virus

62

LEUKOCYTE DISORDERS
other causes, such as extravasation of

Hypereosinophilic syndrome has been
lymph ( eg, lymphangiectasia, chylous
reported in cats, dogs, and ferrets. This
effusion), some viral infections with tropism poorly understood syndrome is characterfor rapidly dividing cells ( eg, parvoviral ized by consistent marked eosinophilia and
infections), and hereditary immunodefieosinophil tissue infiltration with associated VetBooks.ir
ciency disease ( eg, combined immunodefiorgan dysfunction. Decreased concentraciency disease of Arabian foals).

tion of these cell types in blood has no
pathologic relevance.

Stem-cell Injury and Pancytopenia:

A number of factors may cause reversible or

Prominent Metarubricytosis: Although
irreversible stem-cell injury. These injuries
typically absent, metarubricytes occasionmay affect erythrocyte, platelet, lymphocyte, ally become a major component of the total and/or granulocyte production. Because of
nucleated cell count. The magnitude may be
short circulating lifespan, neutropenia is

10%-50% of the nucleated cell population or
often the first abnormality seen. When
more, with absolute numbers reaching
chronic or irreversible, these injuries result

5,000-10,000/µL (5-10 x 109/L). This may
in decreases in all three major blood cell
occur rarely in early phases of an intense
lines, with the hemogram demonstrating
regenerative response to anemia It may
leukopenia, nonregenerative anemia, and
also be associated with endothelial injury
thrombocytopenia General causes include

( eg, heat stroke) resulting in abnormal

1) overdoses of radiation and antineoplastic
release rate of nRBCs from marrow. Most
drugs, 2) drug or plant toxicities ( eg,
nRBCs will be counted as lymphocytes on
estrogen toxicity in dogs, bracken fem
cell counters with differential capability.

toxicity in cattle, phenylbutazone toxicity in

This may result in a preliminary result of
species other than horses), 3) hematopoietic
lymphocytosis being corrected later only
cell neoplasia involving bone marrow
by examiI\ation of the blood smear.

(myelophthisis), and 4) viral infections that
irtjure rapidly dividing cells and may cause

Hematopoietic Cell Neoplasia and
transient neutropenia ( see TABLE 7).

Leukemia: Most cases of hematopoietic
cell neoplasia of either lymphocytic or bone

Eosinophilia and Basophilia: Eosinomarrow origin will have some abnormal cells philia, or the combination of eosinophilia
in blood. Sometimes, neoplastic cells are
and basophilia, prompts the consideration
present in low numbers and are detected
of the following processes: allergic-based
only by scanning the blood smear under low
inflammation, parasitic infestation,
magnification. Finding abnormal hematopoisubepithelial (skin, respiratory, GI) etic precursor cells in blood in small numbers
inflammation that is likely allergic in
prompts investigation of bone marrow and/
nature, and less cpmmonly, paraneoplastic
or other hematopoietic tissues (such as the
induction. Eosinophilia is seen in most dogs
spleen) for possible neoplastic disease.

with heartworm disease and may be seen in

The opposite extreme is marked
dogs and cats with flea infestation.

leukocytosis with a predominance of the
abnormal (neoplastic) cell population. In
this situation, the blood sample is diagnostic
for leukemia. If poorly differentiated, the
cells are classified as blasts, with possible
cell lineage determined based on morphologic appearance. If well differentiated, the cell lineage is usually more clear, because
the cells are mature.

Lymphocytic leukemias are more
common in domestic animals than are
myeloproliferative disorders (ie, leukemias
of granulocytes, erythrocytes, or platelets).

Myelodysplasia is a term used to describe
peripheral blood cytopenias, a hyperplastic
response in bone marrow, and dysplastic
features in developing cells. This can occur
with a toxic insult to the bone marrow but

Leukemia, canine blood smear; note several
may also indicate a preleukemic phase, and
atypical large cells of hematopoietic origin
serial hemograms should be monitored.

with convoluted nuclei. Courtesy of Dr. Darren

A distinction is often made between an

Wood.

"acute" or "chronic" leukemia The terms

LYMPHADENITIS AND LYMPHANGITIS

63
are more in reference to the clinical course
large numbers of well-differentiated cells
of the disease rather than the duration of the in circulation and lack cytopenias.

tumor. An acute leukemia of leukocytes

Considerable progress is being made in
often causes systemic signs of illness and a
the use of monoclonal antibody labeling and
poor short-term prognosis. These animals
flow cytometric analysis to better establish
have variable numbers of poorly differenticell lineage, particularly when the morphol

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ated blast cells in circulation, as well as
ogy is equivocal. This is particularly useful
cytopenias in other cell lines. In contrast,
for poorly differentiated leukemias, in
a chronic leukemia of leukocytes often
which morphology alone is unreliable. The
causes few to no clinical signs,,may be
distinction between well-differentiated or
discovered incidentally, and can have a long
chronic myelogenous leukemia and extreme
clinical course. These animals usually have
neutrophilic leukocytosis can be difficult.

•

LYMPHADENITIS AND1 LY1MPHANGITIS

CASEOUS LYMPHADENms OF

Etiology and Pathogenesis: C pseudo

SHEEP AND GOATS
tuberculosis is a gram-positive, facultative, intracellular coccobacillus. Two biotypes

Caseous lymphadenitis (CL) is a chronic,
have been identified based on the ability of
contagious disease caused by the bacterium the bacteria to reduce nitrate: a nitrate

Corynebacterium pseudo tuberculosis.

negative group that infects sheep and goats,

Although prevalence of CL varies by region
and a nitrate-positive group that infects
and cpuntry, it is found worldwide and is
horses. Isolates from cattle are a heterogeof major concern for small ruminant neous group. All strains produce an
prodµcers in North America. The disease
exotoxin called phospholipase D that
is characterized by abscess formation in
enhances dissemination of the bacteria by
or near major peripheral lymph.nodes
damaging endothelial cells and increasing

( external form) or within internal organs
vascular permeability. The bacterium has a
and lymph nodes (internal form). Although
second virulence factor which is an external
both the external and internal forms of CL
lipid coat that provides protection from
occur in sheep and goats, the external forn1
hydrolytic enzymes in host phagocytes.

is more common in goats, and the internal

Replication of bacteria occurs in the
form is more common in sheep. Economic
phagocytes, which then rupture and release
losses from CL include death, condemnabacteria. The ongoing process of bacterial tion and trim of infected carc,isses, hide and replication, followed by attraction and wool loss, loss of sales for breeding animals, subsequent death of inflammatory cells, and premature culling of affected animals
forms the characteristic abscesses
from the herd or flock Once established on
associated with CL.

a farm or region (endemic), it is primarily

To establish infection, C pseudotubercu
maintained by contanlination of the
losis must penetrate skin or mucous
environment with active draining lesions,
membranes. The most common site of entry
animals with the internal form of the disease is the skin after an injury that may result that contanlinate the environment through
from shearing, tagging, tail docking,
nasal discharge or coughing, the ability of
castration, or other environmental hazards
the bacteria to survive harsh environmental
resulting in skin trauma Contact with
conditions, and lack of strict biosecurity
purulent material draining from open, active
necessary to reduce th� number and preyent lesions most commonly serves as the source introduction of new cases. Although CL is
of bacteria through these breaches in the
typically considere<j. a disease of sheep and
skin. Although less common, entry across
goats, it also occurs more sporadically in
mucous membranes from inhalation or
horses,cattle,camelids,swine,wild
ingestion of the bacteria also serves as a
ruminants, fowl, and people. Because of its
means of infection.

zoonotic potential, care should be taken

Once the bacteria have entered the body,
when handling infected animals or purulent
they move to the lymph nodes via the
exudate from active, draining lesions.

regional draining lymphatic system.

64

LYMPHADENITIS AND LYMPHANGITIS

Internally, the bacteria establish infection

Diagnosis: The presence of an external
not only in the lymph nodes but also in the
abscess on a small ruminant is highly
viscera. The incubation period varies from
suggestive of CL, especially in locations of

1 to 3 mo, culminating in development of
peripheral lyn1ph nodes. However, definitive
encapsulated abscesses. C pseudotubercu
diagnosis is only by bacteriologic culture of
losis is hardy in the environment and can
purulent material from an intact abscess.

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survive on fomites such as bedding and

Although other pyogenic organisms such as
wood for 2 mo and in soil for 8 mo. The

Trueperella pyogenes (formerly Arcanobac
presence of organic material, shade, and
terium pyogenes ), Staphylococcus aureus, moisture favor and enhance survival.

Pasteurella multocida, and anaerobes such
as F'usobacterium necrophorum can cause

Clinical Findings: The hallmark clinical
abscessation, affected animals should be
finding in cases of external CL is the
kept isolated pending culture results.

development of abscesses in the region of

Animals with visceral abscesses pose a
peripheral lymph nodes. Common sites of
greater diagnostic challenge. Radiography
development include the submandibular,
and ultrasonography can be useful to detect
parotid, prescapular, and prefemoral nodes.

internal lesions. Culture of a transtracheal

Less commonly, abscessation of suprarnarnaspirate obtained from an animal with mary or inguinal lymph nodes occurs, in
pneumonia can help detemline whether CL
addition to an occasional ectopic location
is the cause. Excluding other causes of
along the lymphatic chain. If left untreated,
chronic weight loss and ill thrift in the face
these lesions eventually mature into open
of proper nutrition and good appetite such
draining abscesses. The purulent material
as Johne's disease, parasitism, and poor
from these lesions has no odor and varies
dentition further raise suspicion.

in consistency from soft and pasty ( more

In the absence of accessible abscesses for
common in goats) to thick and caseous
bacterial culture, definitive diagnosis of

( more common in sheep). Once natural
active cases of CL is challenging. Although
draining occurs, the skin lesion heals with
many diagnostic tools are available, results
scarring. Recurrence is common, which
of these tests must be interpreted with
can be months later. CL should be highly
caution and with consideration of herd or
suspected in a sheep or goat with abscessaflock history, the presence or absence of tion in these reg.ions. Although other
active infection with.in the herd or flock, and
bacte1ia may also cause abscessation in
vaccination status. A synergistic hemolysin
these locations (and in other animals),
inhibition (SHI) test that detects antibodies
because of the ramifications of the presence
to the phosphol.ipase D exotox.in is available
of this disease within a herd or flock, these
at f\lany diagnostic laboratories. Positive
cases should be handled as CL until proved
titers indicate past resolved infections,
otherwise.

recent exposure, recent vaccination, or

The internal form of CL most commonly
active lesions or their development. Titers
presents as chronic weight loss and failure
of 1 :256 or higher have been correlated in
to thrive. The presence of other clinical
past studies with the presence of active,
signs depends on the organs of involvement, developing abscesses; however, in a recent which may include any of the major organ
systems. Lung abscessation is a common
site of visceral involvement in internal CL;
therefore, signs of chronic ill thrift with
cough, purulent nasal discharge, fever, and
tachypnea with increased Jung sounds
may be noted. The internal form is more
common in sheep and has been termed
the "th.in ewe syndrome."

The incidence of abscesses and development of clinical disease with either the external or internal form increases with age.

Lesions: In sheep, abscesses often
have the classically described laminated

"onion-1ing" appearance in cross section,
with concentric fibrous layers separated by
inspissated caseous exudate. In goats, the

Caseous lymphadenitis lesions, external
abscesses are Jess organized, and the
form, submandibular lymph node in a goat.

exudate is usually soft and pasty.

Courtesy of Dr. Kevin Washburn.

LYMPHADENITIS AND LYMPHANGITIS

65
study, a high titer was poorly correlated
recently, intralesional antimicrobial therapy
with presence or development of abscesses
has been investigated. However, use of
over an 18-mo period. When the status of an
any antimicrobial for treatment of CL is
animal with a positive titer is in doubt, the
extra-label; therefore, strict adherence to
titer should be repeated in 2-4 wk. If the
published guidelines on withdrawal times
titer is rising and clinical signs of abscesses
and an established veterinarian-client

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are noted, tl1en CL can be assumed to be the
patient relationship are mandatory.

cause. False-negative results can occur if

Longterm administration of procaine
testing is done in the first 2 wk after
penicillin G and rifampin has been
exposure before the animal has seroefficacious in some cases. Penicillin alone, converted. Also, animals with chronic,
although efficacious in vitro, is unlikely to
walled-off abscesses can have a false-negaeffectively penetrate the capsule of tive result. Colostral titers usually disappear
developed abscesses, as are many, if not
by 3-6 mo of age, so serologic testing of
most, of the water-soluble or moderately
lambs or kids <6 mo old should be
lipid-soluble antimicrobials. However, recent
interpreted with caution.

studies have shown that administration of
one dose of tulathromycin at 2.5 mg/kg,

Treatment and Control: Once a
either SC directly into the abscess cavity, or
diagnosis of CL has been established,
two doses at 2.5 mg/kg, administered at the
owner education stressing the persistent,
same time, one SC and one intralesionally,
recurrent nature of the disease is necescan resolve the lesions without lancing the sary. The most practical approach for
abscess. Further, effective concentrations
conunercial animals infected with CL is to
of tulathromycin can be achieved within
cull them from the herd or flock. However,
walled-off abscesses caused by C pseudo tu
animals with draining abscesses should not
berculosis after a single dose at 2.5 mg/kg, be sent through sale barns until draining

SC. The highly lipid-soluble property of
has ceased and the wound has healed.

tulathromycin may be particularly helpful in

Treatment of individual animals should be
cases of internal CL, when abscesses are not
undertaken with the understanding that CL
accessible for other forn1s of treatment.

is not considered a "curable" disease.

Despite the efficacy of intralesional and

Animals with genetic or emotional value
parenteral administration of tulathromycin
are treated mainly for aesthetic reasons
in many cases, recurrence remains a
and to limit their infectivity to the rest of
problem. Therefore, use of these drugs
the herd or flock. Treatment options have
cannot be considered curative but rather an
included lancing and draining, surgical
acceptable alternative to manage cases of
excision, formalin injection of lesions,

CL when culling from the herd or flock is
systemic antibiotics, and intralesional
not an acceptable-option for the owner.

antibiotics.

Because of the nature of the causative

If external abscesses are lanced and
organism, common means of exposure,
drained, the cavity should be lavaged with
chronicity of the disease, and difficulty in
dilute iodine solution and the animal
completely eliminating the organism from
isolated in an area that can be disinfected
individual anin1als, control of CL revolves
until the lesion stops draining and heals.

around strict biosecurity measures. The

Drained purulent material should be
overriding goals of any control program are
carefully collected and disposed of. Dilute
to eliminate the disease from the herd or
bleach and chlorhexidine solutions are
flock and to reduce the number of new
effective disinfectants of hard surfaces
cases either from the spread of disease
and fomites, but the presence of organic
or introduction to the farm.

material on these surfaces inactivates

Ideally, animals identified as infected
them and drastically reduces or prohibits
should immediately be culled. If immediate
effectiveness. Intact accessible abscesses
removal is not possible, infected animals
can be surgically removed; however, this
should be isolated from the rest of the herd
option is more expensive, and undetected
or flock. Diligence in this practice will
abscesses are often present and continue to
eventually result in decreased prevalence
develop. Recurrence rates with either
as animals that develop active cases are
lancing or surgical removal are high.

identified and removed, and given there

The practice of injecting abscesses with
are no new animals incubating the disease
formalin should be strongly discouraged,
introduced to the premises.

because the FDA has zero tolerance for

When elimination through culling is not a
extra-label use of a potent carcinogen in
viable option for tl1e owner, control of CL is
food-producing animals. The efficacy of
challenging at best. Dividing the herds or
systemic antimicrobial therapy and, more
flocks into "clean" and "infected" groups

66

LYMPHADENITIS AND LYMPHANGITIS
and eliminating older and less genetically
months later. Purchasing animals from
valuable animals over time is one control
sources with unknown histories is
strategy.

hazardous to maintaining a "clean" herd or Lambs and kids from infected dams can
flock Newly arrived animals should be
be raised on pasteurized colostrum and milk examined thoroughly for signs of CL such as away from infected animals. However, the
abscesses or scars near peripheral lymph

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internal form of CL and animals incubating
nodes. They should remain isolated from
the disease can maintain infection within
the rest of the herd or flock until their
the "asymptomatic clean" group and limit
serologic status is determined, and only
the success of this approach.

animals that are seronegative with no

Commercial CL vaccines are currently
evidence of present or past CL lesions
licensed for use in sheep and goats. These
should be allowed to enter the herd or flock
vaccines should only be used in the species
they are labeled for, because adverse
reactions have been reported in goats given

CORYNEBACTERIUM
vaccine labeled for sheep. Rigidly adhering
to vaccination schedules according to the

PSEUDOTUBERCULOSIS
manufacturer's labeling can help reduce the

INFECTION OF HORSES AND
prevalence and incidence of CL within

CATTLE
herds or flocks. However, it is important to
emphasize that efficacy of these vaccines is

(Pigeon fever, Dry land distemper)

not 1000/o, and vaccination will not clear

1n horses, Corynebacterium pseudotuber0
infected animals. Vaccination of young
culosis causes ulcerative lymphangitis (an
replacement stock should be considered,
infection of the lower limbs) and chronic
and older infected animals should be
abscesses in the pectoral region and ventral
gradually culled as economics allow. Once
abdomen. It is one of the most common and
the disease is at a low prevalence rate,
economically important infectious diseases
vaccination should be stopped and all
of horses in California and Texas and is
seropositive unvaccinated animals culled.

increasing in prevalence in other western

1n "clean" herds or flocks that have no
and Midwestern states of the USA. In cattle,
history of CL, vaccination is not recomthe bacteria most commonly cause mended.

cutaneous excoriated granulomas. Large,

The risks of disease transmission among
ulcerative skin lesions resembling infected
animals should be recognized when
granulation tissue and lymphangitis may
shearing or dipping, and management
occur in 2o/o-5% of cows. Location on the
practices should be adjusted accordingly.

animal is variable but is often associated

Animals with noted lesions should be shorn
with skin trauma. Healing often occurs
last, and clipper blades disinfected between
without treatment or with limited topical
animals. Shearers should recognize the
treatment in 2-4 wk Abortion and mastitis
hazards associated with contact with
may also occur. Rarely, visceral involvement
purulent material and the possibility of
has been reported.

acting as mechanical vectors, either on
clothing or via equipment, for spread of the..

Pathogenesis and Clinical Findings:

bacteria to new animals. Further, dipping

The onset of ulcerative lymphangitis in
tank solutions should be kept as fresh as
horses is variable and usually manifests as
possible, because C pseudotuberculosis
painful inflammation, nodules, and ulcers,
can survive within them and serve as a
especially in the region of the lower limb,
source of infection of freshly shorn sheep
or lameness and edematous swelling can
that have skin abrasions.

extend up the entire limb. The exudate is

Owners should remove hazardous items
odorless, thick, tan, and blood tinged.

(barbed wire, exposed nails, rough feeders)

Usually, only one leg is involved. If the
from the environment to decrease ir\jury
animal is not treated aggressively with
and potential CL transmission from the
antimicrobials, lesions and swelling usually
presence of bacteria on these fomites.

progress and become chronic with

One of the most common ways CL can be
relapses.

introduced into a previously "clean" herd or 1n the southwestern USA, C pseudo tuber
flock, or reintroduced to one in which CL
culosis infection in horses is seasonal, with has been reduced or eliminated, is through
a peak incidence in summer and fall.

the addition of replacement stock Often,

Infection results in abscessation of the
animals from other farms that are asymptopectoral region or ventral abdominal region matic on apival are incubating the disease
with secondary dissemination to internal
and then manifest infection weeks to
organs. Clinical signs include diffuse or

CARDIOVASCULAR SYSTEM INTRODUCTION

67
localized swellings, ventral pitting edema,
abscesses causing lameness, particularly
ventral midline dermatitis, lameness,
in the tiiceps musculature. Transtracheal
draining abscesses or tracts, fever, weight
aspirates are required to confirm pneumoloss, and depression. Leukocytosis and nia caused by C pseudo tuberculosis.

neutrophilia may be present. A marked or

Serologic testing with the synergistic hemolprolonged fever, anorexia, or weight loss ysis inhibition test, which detects IgG to the

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indicates untoward sequelae such as deep
phospholipase D exotoxin, is a useful
or recurring abscesses, internal abscessaadjunct for diagnosis of internal infection tion, or _systemic infection with abortion.

in the absence of external infection.

Abscesses can be large, up to 20 cm in
diameter before rupturing, and take weeks

Treatment: Lymphangitis and internal
to months to resolve. Weight loss, colic,
infection should be treated with longterm
splinted abdomen, or lethargy may be signs
antimicrobials (1 mo duration or as directed
of internal abscesses. Dermatitis lesions are by follow-up ultrasonography). The painful and mildly pruritic with alopecia,
organism is susceptible to most commonly
exudation, crusting, and ulceration.

administered antimicrobials; however,

The bacteria enter via skin wounds by
antimicrobial treatment of uncomplicated
arthropod vectors such as stable flies, horn
external abscesses may prolong the disease
flies, and house flies, or by contact with
by delaying abscess maturation. External
contaminated fomites or soil.

abscess swellings are treated with hot packs,
poultices, or hydrotherapy until they rupture

Diagnosis: Isolation of C pseudotu
or are drained surgically. Abscesses are
berculosis from lesions is necessary for
lanced and flushed with dilute antiseptic
confirmation. In all forms of lymphangitis
solutions. Deep abscesses in the triceps or
in horses, samples for culture include
quadriceps region require ultrasonography
aspirates of abscesses, swabs of purulent
to guide placement of an indwelling drain.

exudate beneath crusts associated with

Phenylbutazone relieves pain and swelling.

folliculitis, and punch biopsies. Differential

General supportive and nursing care is
diagnoses include pyoderma, abscesses,
indicated.

lymphangitis from other bacteria ( eg,

If treatment is successful, the swelling

Staphylococcus aureus, Rhodococcus equi, gradually recedes over days or weeks.

Streptococcus spp, or Dermatophilus spp ), Internal infection has a 300/er-40% mortality
dermatophytosis, sporotrichosis, equine
rate, even with appropriate treatment.

cryptococcosis, North American blastomy

Severe or untreated lymphangitis cases
cosis, and onchocerciasis.

often become chronic, and fibrosis and

Abdominal ultrasonography is useful for
induration of the leg occur. Isolation of
detection of internal infection of the liver,
infected horses, fly control, and good
spleen, or kidneys. Ultrasonography is also
sanitation are recommended for prevenuseful for detection and drainage of deep tion.

CARDIOVASCULAR SYSTEM INTRODUCTION

The cardiovascular system comprises the

Slightly > 100.tf, of all domestic animals
heart, the veins, and the arteries. The
examined by a veterinarian have some form
atrioventiicular (mitral and tricuspid) and
of cardiovascular disease. Similar to many
semilunar ( aortic and pulmonic) valves keep chronic diseases of other organ systems, blood flowing in one direction through the
cardiovascular diseases generally do not
heart, and valves in large veins keep blood
resolve but progress and become more
flowing back toward the heart. The rate and
limiting over time, which may ultimately lead
force of contraction of the heart and the
to death. Evaluation of the heart is perdegree of constiiction or dilatation of blood formed via assessment of heart sounds and
vessels are determined by the autonomic
murmurs, arterial pulses, degree of jugular
nervous system and hormones produced
vein distention, strength and location of the
either by the heart and blood vessels (ie,
apex beat, electrocardiography, radiography,
paracrine or autocrine) or at a distance from cardiac biomarkers, echocardiography, and the heart and blood vessels (ie, endocrine).

other advanced imaging techniques.

68

CARDIOVASCULAR SYSTEM INTRODUCTION

Heart Rate and the
following mechanism. When high-pressure

Electrocardiogram
arterial baroreceptors in the aortic and
carotid sinuses detect increases in blood

The heart beats because of a wave of
pressure, they send increased afferent
depolarization that originates in the
volleys to the medulla oblongata, which
sinoatrial (SA) node at the juncture of the
increases vagal efferents to the SA node and

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cranial vena cava and the right atrium. At
causes the heart rate to decrease. In heart
rest the SA node discharges -30 times/min
failure, the baroreceptors (laden with
in h�rses, > 120 times/min in cats (typically

Na+fK+-ATPase) become fatigued, which

180--220 times/min in a hospital setting), and
reduces the afferent signals to the medulla

60--120 times/min in dogs, depending on
oblongata. This results in less vagal efferent
their size. In general, the larger the species,
signaling. Thus, dogs in CHF have a
the slower the rate of SA node discharge
decrease in heart rate variability and
and the slower the heart rate. Birds can
frequently present with an underlying sinus
have a resting heart rate of -115--130
tachycardia.

beats/min, with active heart rates up to 670

Once the wave of depolarization reaches
beats/min, depending on size and species.

the atrioventricular

Hummingbirds can have an active heart
i(AV) node, the speed
of conduction is slowed through the nodal
rate of> 1,200 beats/min.

tissue, giving the atria time to contract

The rate of SA nodal discharge increand eject more blood into the ventricles, ases when norepinephrine is released
allowing for atrioventricular synchrony.

from the sympathetic nerves and binds to

The depolarization then travels rapidly to
the 13 ,-adrenoreceptors on the SA node.

the subendocardium of the ventricles and

This cardioacceleration may be blocked
to the ventricular septum. From these
by !3-adrenergic blocking agents ( eg,
points, it travels slowly through the
propranolol, atenolol, metoprolol,
ventricular myocardium, producing the
esmolol, carvedilol). The rate of SA nodal

QRS complex of the ECG with subsequent
discharge decreases when acetylcholine
ventricular contraction. The delay between
released by the parasympathetic (vagus)

the electrical activity visualized on ECG
nerves binds to the cholinergic receptors
and mechanical function accounts for
on the SA node. This vagally mediated
transmission of impulses, which allows
cardiodeceleration may be blocked by a
contraction of myocytes to occur in
parasympatholytic (vagolytic) compound
synchrony. Under rare conditions, there

(eg, atropine, glycopyrrolate). When the
may be depolarization without contraction;

SA node discharges and the wave of
this is called electromechanical
depolarization traverses the atria, the
dissociation.

P wave of the ECG is produced. Subse

The interval on an ECG between the
quently, the atria contract, ejecting a
onset of the P wave and the onset of the
small volume of remaining blood into

QRS complex is termed the PQ or PR
the respective ventricles (atrial kick).

interval. It is a measure of the time it takes

In quiet, healthy dogs, the variation of
for the electrical wave of depolarization
the heart rate with respiration is termed
respiratory sinus arrhythmia
to begin at the SA node and reach the

(RSA); it
ventricles (lastly traversing the AV node).

results from decreased vagal activity during

Factors that speed or slow the rate of
inspiration and increased vagal activity
discharge of the SA node (chronotropy)

during expiration. Therefore, vagolytic
also speed or slow conduction through the
compounds, as well as excitement, pain,

AV node (dromotropy). Thus, as the heatt
fever, and congestive heart failure (CHF),
rate increases, the PR interval shortens;
usually abolish or diminish RSA. Heart rate
when heart rate slows, the PR interval
variability synchronized with respirations is
lengthens.

a good indicator of cardiac health. It is rare

The T wave of the ECG represents
to find an animal that has active CHF with
repolarization of the ventricles. It is

RSA; however, comorbid conditions that
affected by electrolyte imbalance ( eg,
increase vagal activity ( such as primary
hypo- or hyperkalemia, hypo- or hypercalrespiratory or neurologic disease) may cemia ), myocardial injury, or ventricular
cause RSA to persist.

enlargement. Repolarization of the atria

Heart rate is also inversely related to

(Ta wave) is rarely seen, because it occurs
systemic arterial blood pressure. When
during the much larger QRS complex.

blood pressure increases, heart rate

Occasionally, it can be seen with AV nodal
decreases; when blood pressure decreases,
disease (AV block) or in horses with slow
heart rate increases. This relation is known
heart rates, appearing as a "hammock" after as the Marey reflex and occurs by the
the P wave.

CARDIOVASCULAR SYSTEM INTRODUCTION

69

Force of Ventricular Contraction

The amount of oxygen delivered to

The force with which the ventricles contract the h�art depends on how well the lungs is determined by many factors, including
function, how much Hgb is present to carry
the end-diastolic volume (preload), which is the oxygen, and how much blood carrying the volume of blood within the ventricles
the Hgb flows through the heart muscle via

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just before they begin to contract, and

�e coronary arteries. If pulmonary function
myocardial contractility (inotropy), which

IS normal and there is sufficient Hgb,

1s the rate of cycling of the microscopic
coronary blood flow will determine how
contractile units of the myocardium.

much oxygen is delivered to the myocar

The preload is determined by the
dium Coronary blood flow is determined by

_.

difference in end-diastolic pressure
the difference m mean pressure between
between the ventricle and the pleural space
the aorta (normally 100 mmHg) and the
divided by the stiffness of the ventricular
right atrium ( normally 5 mmHg), into which
myocardium. The end-diastolic pressure of
coronary blood empties. Because coronary
the ventricle is determined by the ratio of
flow 1s greatest during diastole, slower heart
blood volume and the compliance of the
rates ( which preferentially increase
myocardium. Preload is regulated
diastolic interval) are associated with
predominantly by low-pressure volume
improved myocardial oxygen delivery.

receptors in the heart and large veins.

The amount of oxygen consumed by the

When these receptors are stimulated by an
heart 1s termed myocardial oxygen
increase in blood volume or by distention of
consumption. It is determined, princithe structures the receptors occupy, the pally, by wall tension and heart rate. Wall
body responds by making more urine and by tension is expressed by the law of LaPlace dilating the veins-an attempt to decrease
in which tension increases with increases '

blood volume and lower the pressures in the in pressure or dian1eter of the ventricle veins responsible for venous distention. An
and tension decreases with increases i�
increase in end-diastolic volume (preload)

wall thickness of the ventricle. Tension
stretches the ventricular wall, resulting in
increases with conditions that increase
a more forceful contraction as per the
afterload (pressure), such as pulmonic

Frank-Starling mechanism, or Starling's law stenosis, subaortic stenosis, systemic or of the heart. Stretching of receptors in the
pulmonary hypertension, or preload
atria and ventricles causes them to release

(volume), including mitral valve insuffinatriuretic proteins: brain natriuretic ciency, left-to-right shunting defects, and
peptide (BNP) primarily from the ventricles
dilated cardiomyopathy. In the absence of
and atrial natriuretic peptide (ANP) from
a stenotic lesion, afterload is determined
the atria. These peptides are natriuretic
by the relative stiffness of the arteries
relax smooth muscle, and in general oppose and by the degree of constriction of the vasopressin and angiotensin IL A correlaarterioles. The tone of vascular smooth tion between BNP and NT-proBNP levels
muscle depends on many factors some of
and degree of stretch of the heart has been
which constrict the muscle (eg, a'drenergic
identified in dogs.

agomsts, angiotensin II, vasopressin

Myocardial contractility is determined by
endothelin) and some of which rel� the
the availability of ATP and calcium, which
muscle_ ( eg, norepinephrine, atriopeptin,
allows myosin-actin cross-bridging to occur. bradykmm, adenosine, nitric oxide).

The rate of liberation of energy from ATP

Afterload is often increased in heart
is determined, in part, by the amount of
failure, and therapy is often directed at
norepinep!1fine binding to (3 -adrenergic
decreasing it.

1
receptors m the myocardium. One of the

Increases in heart rate result in increasing
most important factors in heart failure is
myocardial oxygen consumption while
the down-regulation ( decreased number)

decreasing time for diastole when coronary
of myocardial 13,-receptors.

blood flow is greatest. The combination can
set the stage for an imbalance in myocardial

Oxygen and the Myocardium
oxygen demand and supply, leading to
myocardial ischemia. Cardiac failure is

Oxygen is essential for the production of
characte1ized by an increase in sympathetic
energy that permits all body functions. The
tone and relative increases in heart rate· the
amount of oxygen available for production
ultimate impact is an inefficient myocalof this energy is termed the tissue oxygen d1um that can result in deleterious
content. The myocardial oxygen content is
remodeling.

a b'.11ance between how much oxygen is

Oxygen is responsible for the production
delivered to the heart minus how much
of the vast majority of ATP, which fuels
oxygen is consumed by the heart.

both contraction and relaxation of the

70

CARDIOVASCULAR SYSTEM INTRODUCTION
myocardiwn. Calciwn must rapidly be
output, it is reasonable that ventricular
released by intracellular stores (sarcoplasmic function might be improved by decreasing reticulwn) via calciwn-induced calciwn
vascular resistance. Decreasing afterload
release to allow for excitation-<:ontraction

( arterial vasodilation) is one therapeutic
coupling, while equally rapid removal of
goal in heart failure therapy.

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calciwn back into the sarcoplasmic reticulwn
is necessary for relaxation. Both processes of
calciwn cycling are energy dependent.

ABNORMALITIES OF THE

In heart failure and cardiomyopathy,

CARDIOVASCULAR SYSTEM
inappropriate handling of calcium may
result in arrhythmogenesis and may also be

The following mechanisms can result in
the most important factor that leads to both
abnormalities of the cardiovascular system:

reduced force of contraction and reduced
l) the cardiac valves fail to close or open
rate of relaxation (ie, reduced systolic as
properly ( valvular disease); 2) the heart
well as diastolic function).

muscle pumps inefficiently or relaxes
inadequately (myocardial disease); 3) the
heart beats too slowly, too rapidly, or

Hindrance to Blood Flow
irregularly (arrhythmia); 4) the systemic

Blood flow from the heart, tem1ed cardiac
vessels offer too great an interference to
output, is via both the left and right
blood flow (vascular disease); 5) there may
ventricles. Cardiac output is detem1ined
be abnormal communications between
by the heart rate and ventricular stroke
chambers of the left side and right side of
volume. Blood flows through the systemic
the heart ( cardiac shunts) or between the
arterial (left ventricular) or puln10nary
systemic and pulmonary circulations
arterial (right ventricular) trees and is

( extracardiac shunts); 6) there is too little or
critical to satisfactory function of the heart
too much blood compared with the ability
and consequent perfusion of organs with
oft.he blood vessels to store that blood; and
adequate quantities of blood and the

7) there is parasitism of t.he cardiovascular oxygen it contains. Most (>90%) of the
system ( eg, heartworm disease). Cardiac
hindrance to blood flow is from the degree
diseases can be either congenital defects
of constriction of the arterioles, tem1ed
or acquired. The diseases of greatest
vascular resistance; however, some
importance, because of their prevalence,
interference is from the stiffness of the
are mitral regurgitation in dogs, hyperportion of the great arteries closest to trophic cardiomyopathy in cats, dilated
the ventricles, termed impedance. The
cardiomyopathy (DCM) in dogs, arrhythmoventricles eject a stroke volwne into the genic right ventricular cardiomyopathy in
proximal portion of the great arteries,

Boxers, and heartworm disease.

which expand to accommodate the stroke
volume; when the ventricles are relaxed,

Valvular Disease: Inadequate closure
the distended great arteries recoil and keep

(coaptation) of valves leads to regurgitation
blood moving through the arterioles into

(back flow of blood), which occurs most
the capillaries. The amtic and pulmonic
commonly as mitral regurgitation, or mitral
valves close and prevent the stroke volwne
and tricuspid regurgitation ( concurrent
from returning to the ventricle that ejected
tricuspid regurgitation occurs in -30% of
it. Systemic vascular resistance is the
cases with mitral regurgitation). Regurgitaopposing blood flow that must be overcome tion through the mitral and/or tricuspid to push blood through the peripheral
valves due to myxomatous degeneration of
circulation and is calculated by:

the valve leaflets constitutes > 75% of all

( mean arterial pressure - mean venous
heart disease in dogs. As blood regurgitates pressure)/cardiac output
through either set of AV valves, a typical
holosystolic murmur is heard between the

Pulmonary vascular resistance is
first and second heart sounds. A mid-syssimilarly calculated and is increased in tolic click, secondary to mitral valve
cases of pulmonary vascular obstruction
prolapse, may precede development of a
or pulmonary hypertension.

murmur in the early stages of disease. When

One of the most important features of
blood regurgitates through the mitral or
heart failure that leads to morbidity is
tricuspid valves, an excessive amount of
increased resistance of arterial, arteriolar,
blood moves back and forth between the
and venous smooth muscle because of
ventricle and atriwn. Thus, with mitral
increased angiotensin II, vasopressin, and
regurgitation, it is common to see dilation of
endothelin. Tf the left ventricle is unable to the left atrium and left ventricle. The degree
eject a nom1al stroke volwne or cardiac
of left atrial enlargement, documented by

CARDIOVASCULAR SYSTEM INTRODUCTION

71
either radiography or echocardiography,
correlates with the severity of the stenosis,
may predict disease severity. Mitra! or
which can be estimated by spectral
tricuspid regurgitation is most common in

Doppler echocardiography. Medications
older small-breed dogs and older horses

(�-blockers) or interventional procedures
that have valve leaflets thickened by

(balloon valvuloplasty) may be recommyxomatous degeneration (infiltration with mended in cases of severe subaortic or VetBooks.ir
glycosarninoglycans ). Mitra! regw·gitation
pulrnonic stenosis, respectively.

occurs more often in Cavalier King Charles

Spaniels, and at a younger age, than in any

Myocardial Disease: Impaired force
other breed; however, there is not a
of contraction is termed reduced systolic
significant difference in the time frame
function (pump failure), which occurs most
of progression to onset of CHF.

commonly with DCM-primary DCM in

Aortic regurgitation occurs most often
large-breed dogs, DCM-phenotype with
in older horses due to calcification or

Boxer cardiomyopathy, and in cats that are
noninflammatory degeneration of the
typically either taurine deficient or in the
aortic valve. It may also develop secondend-stages of other types of cardiomyopaary to aortic endocarditis (infection of the thy and in longstanding rnitral regurgitation.

valve leaflets), most often in large-breed

When this occurs, the cardiac muscle is said
dogs. The left ventricle and atrium can
to be in a reduced inotropic state, or to have
become dilated due to the aortic regurgitareduced contractile function. In large-breed tion, but this is proportional to the degree
dogs, this is usually termed idiopathic DCM,
of regurgitation. The murmur produced by because the origin is unknown.

blood regurgitating from the aorta into the

Impaired ventricular relaxation is
left ventricle is always a diastolic murmur,
termed reduced diastolic function, which
heard immediately after the second heart
occurs most commonly when the cardiac
sound. In horses, the murmur of aortic
muscle suffers oxygen debt and the
regurgitation can be described as
consequent lack of energy to fuel

"blowing" due to the regurgitant blood
relaxation. Diastolic dysfunction is seen in
flow, or as "buzzing" due to the aortic
most cardiac diseases as they progress to
leaflets vibrating as the blood flows past.

heart failure. The ventricular myocardium

The buzzing murmur is almost always
also relaxes poorly in hypertrophic
associated with a relatively small amount
cardiomyopathy (ie, when the muscle is
of regurgitant flow.

too thick), or with pericardia! disease

Inadequate opening of valves is termed
when either the thickened pericardium or
stenosis. Pulrnonic stenosis is most
fluid contained within the pericardia! sac
prevalent, valvular aortic stenosis is
interferes with relaxation. Hypertrophic
uncommon, and rnitral or tJ.icuspid stenosis
cardiomyopathy is most common in cats.

is rare. However, subaortic stenosis,

Probably >85% of cats with heart disease
produced by a fibrous or fibromuscular
have hypertrophic cardiomyopathy. A
band of tissue just beneath the aortic valves, smaller number of cats will have so-called is prevalent, especially in certain breeds ( eg, restrictive cardiomyopathy, in which the Newfoundlands, Golden RetJ.ievers, Boxers, heart fills poorly because the walls are Rottweilers, and German Shepherds). If a
stiffer than normal, unclassified cardiovalve opens inadequately, a greater pressure myopathy, or valvular disease. Pericardia!

must be generated to maintain the normal
disease is most common in older,
volume of blood flowing through it. The
large-breed dogs with tumors bleeding
ventricle responsible for pun1ping blood
into the pericardia! sac (eg, hemangiosarthrough the stenotic valve concentrically coma or chernodectorna).

hypertrophies (thickens) proportionally to
the degree of tightness of the stenosis. The

Arrhythmias: Any cardiac rhythm falling
systolic ejection quality murmurs produced
outside the nonnal sinus rhythm is te1med
by pulrnonic or subaortic stenosis are heard
an arrhythmia. An arrhytlunia that is too
between the first and second heait sound;
fast, too slow, or too trTegular can result in
typically, they are shorter in dw·ation than
reduced cardiac output, thereby causing
the holosystolic murmur of mitral
clinical signs that could include exercise
regurgitation and are heard best over the
intolerance, syncope, or exacerbation of
left heart base and thoracic inlet ( subaortic

CHF. The most conunon arrhythmias are
stenosis). In general, the louder the murmur, atrial fibrillation (seen commonly in horses the greater the stenosis, although the
and giant-breed dogs, or in any size dog with
severity of stenosis is not always predicted
advanced cardiac disease and severe left
by the intensity of the murmur. The velocity
atrial enlargement), ventJ.icuJai· premature
of blood flowing through a stenos is
depolarizations (seen most commonly in

72

CARDIOVASCULAR SYSTEM INTRODUCTION

Boxers and Doberman Pinschers), sick
inhibitors and amlodipine, are a mainstay
sinus syndrome (seen mainly in aged
of antiliypertensive therapy.

Miniature Schnauzers), persistent atrial
standstill ( seen in Labrador Retrievers and

Cardiac Shunts: Abnormal communica

English Springer Spaniels), and third-degree tions between the left and right side of the AV block.

circulation are termed cardiovascular shunts.

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In atrial fibrillation, depolarization of the

These take the form of (in decreasing
atria is not coordinated, stinmlation of the
prevalence) patent ductus arteriosus

AV node is frequent but random, and the

(between the aorta and pulmonary trunk),
heart rate is rapid and irregular. Ventricular
ventricular septa! defect (between the left
premature contractions (also called
and right ventricles), or atrial septa! defect
ventricular premature beats or depolariza

(between the left and right atria). When blood
tions) arise from irritated regions of the
crosses these defects from the left side to the
ventricles. Such irritations commonly result
right side, which is most common, these
from chronic stretch of the fibers, as well as
defects are termed left-to-right shunts. They
from oxygen debt or drug effects. A single
result in overcirculation of the lungs and
premature beat does not typically cause
dilatation of the cardiac chambers required to
clinical signs and can be relatively benign,
pwnp or to carry the shunted blood. Chronic
but premature beats may evolve into short
dilatation ultimately leads to myocardial
paroxysms (bursts) or long runs (ventricufailure. See also CONGENITAL AND INHERITED
lar tachycardia) that lead to hemodynarnic

ANOMALIES OF THE CARDIOVASCULAR SYSTEM, p 76.

impairment and syncope, or even to a

Tetralogy of Fallot �see p 83) is a
complete loss of coordination of ventricular
complex congenital anomaly that consists
activity (ventricular fibrillation) and sudden
of a hypoplastic right ventricular outflow
death. Ventricular tachycardia commonly
tract and/or pulmonary trunk, an aorta that
occurs in Dobennan Pinschers with DCM
overrides the interventricular septwn
and in Boxers with arrhythmogenic right

(therefore arising from both ventricles),
ventricular cardiomyopathy (previously
ventricular septa! defect, and right
termed Boxer cardiomyopathy) and
ventricular hypertrophy. Poorly oxygenated
warrants immediate treatment with
blood enters the systemic circulation
antiarrhythrnics. With either sick sinus

( right-to-left shunt) and produces a bluish
syndrome (ie, transient arrest of discharge
tinge ( cyanosis) to the mucous membranes
of the SA node alternating with periods of
and increased nwnbers of RBCs (polytachycardia) or complete heart block (in cythernia). Tetralogy of Fallot is the most
which no atrial depolarization enters the
common form of a right-to-left shunt,
ventricles), the ventricular rate is excepalthough any large atrial or ventricular tionally slow and may lead to hemodynarnic
septa! defect can result in right-to-left
impaim1ent (low cardiac output failure,
shunting (Eisenmenger physiology)

hypoperfusion, hypoxernia), exercise
secondary to pulmonary hypertension
intolerance, syncope, or sudden death.

from chronic pulmonary overcirculation.

A pacemaker is indicated in all dogs with

Right-to-left shunting patent ductus
persistent high-grade AV block or persistent
art.eriosus is also seen infrequently and
atrial standstill and in dogs that are •
typically results from persistent pulmonary
symptomatic for sick sinus syndrome.

hypertension from birth. Any cardiac or
extracardiac shunt can also originate as a

Vascular Disease: Interference to blood
left-to-right shunt and reverse in direction
flow through systemic arterioles (systemic
if the pressure within the pulmonary
hypertension) is mo
circulation or right heart becomes greater

'st common in aging
animals with impaired renal function ( dogs
than the pressure in the aorta or left heart.

and cats), hyperadrenocorticism (dogs),
or hyperthyroidism (cats). The exact

Heartworm Disease: Heartwom1
underlying cause is usually unknown, but
disease (seep 127) is seen predominantly
suspected causes include sodiw11 retention
in dogs but also in cats and is transmitted
and plasma volume expansion, hyperaldovia mosquitoes. In heartworm disease, adult steronism, increased sympathetic tone, and
heaitworms in the pulmonary vessels and
possibly increased angiotensin II. Regardthe pulmonary arte1ial changes they induce less of the cause, a loss in arteriolar
impede flow through the lungs. Severe,
compliance may persist even with adequate
persistent pulmonary hypertension may
treatment of the associated clinical
result in right ventricular hypertrophy,
condition. Arterial vasodilators, such as
increased right-side filling pressure, and
angiotensin-converting enzyme (ACE)

eventual development of right-side CHF

CARDIOVASCULAR SYSTEM INTRODUCTION

73

( cor pulmonale ). The disease progresses at
contractility and to identify myocardial
a varying rate in dogs but usually lasts <2 yr
failure. Almost any animal with heart
in cats. Both species may develop syncope
disease leading to chamber enlargement or
or cor pulmonale from pulmonary
increased wall thickness has a degree of
hypertension or may develop pulmonary
myocardial failure on the cellular level, but
thromboembolism from in situ thrombus
such animals may remain compensated

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formation or adult worm death. Antigenic
without clinical signs of heart failure for a
stimulation from the heartworms may also
prolonged time.

cause changes in the lungs, resulting in

Low output heart failure and CHF (see
eosinophilic pneumonitis. The death of
p 87) are clinical syndromes in which an
adult worms secondary to adulticide
animal manifests signs referable to a
therapy always results.in some degree of
complex interaction between a failing heart
pulmonary thromboembolism. Strict cage
and the blood vessels. In low output heart
rest is necessary in the month after
failure, cardiac output is insufficient to
adulticide therapy, and pretreatment with
perluse organs with enough oxygenated
doxycycline and ivermectin to kill
blood for the organs to function properly

Wolbachia organisms before adulticide
either at rest or during periods of exertion.

treatment may also mitigate the pulmonary

In CHF, blood dams up in or around
pathology resulting from won11 death.

organs-usually the lungs but occasionally
in the systemic organs-and causes the

Common Endpoints of Heart
congested organs to function abnormally,

Disease
become edematous, or both. The functional
classification of heart failure is expressed

Signs associated with any of the above
when, during graded exercise, the animal
diseases are due either to inadequate organ
shows signs ( eg, dyspnea, cough, collapse)

perlusion ( eg, exercise intolerance,
due to the heart disease. There are several
weakness, syncope, azotemia) or to blood
classifications of hea.it failure, the most
damming up in organs in which the venous
recent and perhaps most practical of which
effluent is emptied inadequately ( eg,
is based on the course of heart disease
pulmonary edema, ascites, pitting edema,
expressed in four basic stages (A, B l, 82,
other effusions). An animal showing signs

C, D) described in the ACVIM Consensus
due to relative inadequacy of the cardiovas

Statement on canine chronic valvular heart
cular system to deliver enough blood t0
disease.

sustain normal function is said to be in low
output, or forward heart failure. An animal
showing signs caused by blood damming up

DIAGNOSIS OF
in poorly drained organs is said to be in

CARDIOVASCULAR DISEASE

CHF. When inadequate amounts of oxygen
are present in systemic arterial blood and

Diagnosis of ca.i·diovascular disease is based
there is too much unoxygenated Hgb, the
on history and signalment, physical
mucous membranes appear cyanotic and
exanlination ( eg, inspection, auscultation,
polycythemia may develop.

palpation), cardiac biomarkers (NT

Animals with heart failure may deterioproBNP, BNP, ANP, troponin I), radiography, rate gradually, due most often to pulmonary
electrocardiography, and echocardiography.

edema, or they may die suddenly, due to

Clear images must be obtained for
arrhythmias, chordal rupture, or left atrial
radiography, electrocardiography, and
tear.

echocardiography, or accurate, valid
interpretation will not be possible. Most

Heart Failure, Congestive Heart
cardiovascula.i· diseases ( eg, mitral

Failure, and the Failing Heart
regurgitation, dilated cardiomyopathy) ca.11
be highly suspected based on the results of

Systolic myocardial failure is described as
physical exanlination and radiography.

reduced myocardial contractile function,

Electrocardiography is specific for
characterized by a reduced force of
diagnosis of rhythm disturbances ( eg, atrial
contraction from any given preload. More
fibrillation, sick sinus syndrome). Echocarobjectively, a failing heart can be described diography is excellent to confuw tentative
as one with a reduced rate of liberation of
diagnoses, assess severity of valvular
energy from the breakdown of ATP, or with
regurgitations and stenotic lesions, evaluate
a reduced velocity of fiber shortening when
chamber enlargement and quantify systolic
the heart contracts during the imaginary
and diastolic myocardial function,
situation of contracting against no load. It
characterize the form of cardiomyopathy in
is difficult to directly measure myocardial
cats, detect cardiac tumors or pericardia!

74

CARDIOVASCULAR SYSTEM INTRODUCTION
disease, diagnose pulmonary hypertension
the absence of skeletal muscle disease or
or heartworm caval syndrome, and identify
obesity; 8) the mucous membranes are
congenital cardiac defects. Thoracic
acutely cyanotic in the absence of primary
radiographs are the best diagnostic tool to
pulmonary disease.

evaluate the lungs for evidence of active

Echocardiography is more effective than

CHF Heartwonn disease is diagnosed best
radiography, which is more effective than

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by detecting antigens of mature, female
electrocardiography, to detect enlargement
heartworms circulating in the blood (dogs).

of chainbers of the heart and great vessels.

In cats, diagnosis of heartwonn disease may In general, the degree of cha111ber enlargeentail heartworm antigen and antibody ment parallels disease severity. The degree
testing, supplemented by thoracic
of pulmonary infiltrates detected radioradiographs and echocardiography.

graphically, or the degree of impairment of

Many heart diseases have specific breed
left ventricular wall motion or thinning of
prevalences. Any older Cavalier King
the left ventricular walls, may predict the

Charles Spaniel with a cough, labored
severity of heart failure. Unfortunately, the
breathing, and exercise intolerance should
correlation between hemodyna111ic or
be suspected to have left-side CHF due to
echocardiographic measurements and
mitral regurgitation; however, chronic
either signs or likeliliood of death is not
obstructive pulmonary disease with fibrosis
always good. There appears to be a better
may produce nearly identical signs and
correlation between increase in heart and
thoracic radiographs; echocardiography
respiratory rates a11d exercise incapacity to
and NT-proBNP testing may be needed to
severity of heart disease. NT-pro BNP testing
differentiate. Any middle-aged, depressed,
may also help in the prognostication of
coughing, exercise-intolerant Doberman
heart disease and heart failure.

Pinscher with a rapid, irregular heart rate

Diagnosis of specific cardiovascular
likely has dilated cardiomyopathy. Any
diseases are discussed in their respective
middle-aged to older Miniature Schnauzer
chapters.

with fainting likely has sick sinus syndrome.

Any Boxer who faints intem1ittently should

PRINCIPLES OF THERAPY
be suspected to have arrhythmogenic 1ight
ventricular cardiomyopathy; however,

See a.lso SYSTEMIC Pl·IARMACOTHERAPEln-lCS OP

Boxers can also develop neurocardiogenic

THE CARDIOVASCULAR SYSTEM, p 2525.

syncope or sick sinus syndrome, and Holter

Although therapy is disease-specific,
monitoring may be needed to diagnose the
there are some general goals of therapy for
underlying cause of syncope and to
heart disease: 1) Chronic stretch on
formulate the best treatment plan. A
myocardial fibers should be minimized,
middle-aged cat with labored breathing
because chronic stretch injures and iITitates
and reluctance to lie down probably has
fibers, causes them to consume excess
myocardial disease ( most coh1I11only
quantities of oxygen, and leads to their
hypertrophic cardiomyopathy), whereas an
death and replacement by fibrous connecolder cat with weight loss and behavioral tive tissue (remodeling). 2) Edema fluid
changes is likely to have hyperthyroidism,
should be removed because it makes the
which can result in systemic hypertension
lungs wet, heavy, and stiff and causes
and exacerbate cardiac disease.

ventilation-perfusion inequalities, impairs

Heart disease should be considered if any
oxygen diffusion, a11d fatigues muscles of
of the following are identified on physical
ventilation. 3) Cardiac output should be
examination: 1) the heait rate is rapid, slow,
improved, and the ainount of regurgitation
or irregnlar ( and not due to respiratory

( most often mitral regurgitation) decreased.

sinus arrhythmia); 2) respiratory sinus

Improved cardiac output enhances blood
arrhythmia is absent even when the animal
flow to important organs, a11d reducing
is at rest (this also occurs due to pain, fever,
rnitral regurgitation decreases stretch ai1d
or excitement); 3) more than two heart
reduces pressures in the left atlium and
sounds are heard ( eg, producing a "gallop"

pulmonary veins, thus reducing pulmonaiy
rhythm) in any animal but a horse (most
capillary pressure and edema formation. 4)

common in cats with cardiomyopathy); 4) a

Heait rate and rhythn1 should be regulated.

loud murmur is heard; 5) heart sounds are

A heait beating too slowly fails to eject
muffled in the absence of obesity (may
enough blood, whereas a heart beating too
indicate pericai·dial or pleural effusion);
rapidly does not have time to fill adequately

6) arterial pulsations are rapid, feeble, or
and consumes too much oxygen at a time
irregular with more heart beats tha11 aiterial
when there is too little coronary blood
pulsations (pulse deficits); 7) the a11imal
flow. A heart beating too irregularly may
faints or has reduced exercise tolerance in
deteliorate into ventlicular fibrillation and

CARDIOVASCULAR SYSTEM INTRODUCTION

75
sudden death. 5) Oxygenation of the blood
dogs with heart failure. Aldactazide, a
should be improved. Inadequate oxygenacombination diuretic consisting of tion leads to inadequate energy to fuel both
spironolactone and hydrochlorothiazide,
contraction and relaxation of the myocarmay be used in cases of refractory CHF
dium. Inadequate oxygenation of the

Renal values should be monitored closely
myocardium may also lead to myocardial
because of the risk of worsening azotemia

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fibrosis and arrhytlunia. 6) The likelihood of
and renal failure with aldactazide therapy.

thromboembolism should be minimized.

Amiloride and triamterene are also

Cats with hypertrophic cardiomyopathy
potassium-sparing diuretics; however, these
may shed emboli from the enlarged left
drugs are not typically used in veterinary
atrium, which may block major arterial
medicine.

branches and lead to ischemia and death.

Digitalis glycosides exert their effects by

7) Mature heartwom1s and microfilariae
inhibiting membrane Na•JK•-ATPase. This
should be killed. Mature heartworms may
increases intracellular sodium, which
initiate severe changes in the pulmonary
activates the sodium-calcium pump that
arteries that ultimately impede blood flow
increases intracellular calcium. Digoxin
through the lungs.

increases the force of myocardial contrac

The ultimate goals of therapy for
tion (to a minor degree), slows the heart
cardiovascular disease are achieved when
rate, and improves baroreceptor function.

treatment resolves the presenting clinical

Digoxin has a narrow therapeutic index;
signs, the respiratory and heart rates are not
thus, serum levels should be monitored, and
increased at rest, and quality of life is good
animals should be watched for signs of
for both pet and owner.

toxicosis (vomiting, diarrhea, inappetance,
arrhythmogenesis ).

Enalapril, benazepril, lisinopril, and

Common Therapeut.ic Agents
ran1ipril are ACE inhibitors commonly

Furosemide is a loop diuretic that decreases used in heart failure management in dogs.

resorption of sodiun1, chloride, and

They are all equally effective at blocking
potassium in the thick ascending lin1b of the
the conversion of angiotensin I to
loop of Henle. It is also a venodilator when
angiotensin II. They minimize remodeling
used IV. It is the most important and
of both blood vessels and myocardium.

effective means to remove edema fluid from

They are part of the mainstay treatment
animals with heart failure and frequently is
regimen for advanced cardiac disease and
lifesaving in the sho1t term. Diuresis with
heart failure.

furosemide may be augmented by using

Arnrinone and milrinone, analogues of
thiazide diuretics ( eg, hydrochlorothiazide ).

theophylline that deactivate other forms of

Thiazides suppress resorption of sodiun1
phosphodiesterase, are potent IV inodilaand water at the distal renal tubules. When tors. That is, they are both positive
using a loop diuretic and a diuretic that
inotropes and vasodilators. However, they
works at the distal tubules, the ability of
have been associated with worse outcomes
the kidneys to conse1ve water is reduced
in people with CHF and are not commonly
dramatically, so dehydration and hypokaused. Pin10bendan, a calciun1-sensitizing lemia may develop. This may be signaled by
agent and phosphodiesterase inllibitor, is
worsening azotemia, and renal values must
another inodilator shown to improve the
be monitored closely in animals on multiple
quality of life and in1prove Slllvival in dogs
diuretics. Torsemide is a loop diuretic that is with CHF Pimobendan is not approved for 10 times more potent than furosemide; it is
use in cats but may be beneficial in cats with
reserved for refractory CHF or in cases of
heart failure (that do not have evidence of
suspected diuretic resistance to furosemide. outflow tract obstruction). Sildenafil is a Spironolactone is a potassium-sparing
potent phosphodiesterase inhibitor used
diuretic that blocks the effects of aldosteto treat moderate to severe pulmonary rone. Like thiazides, it exerts its effect
hypertension in dogs. Sildenafil has been
principally at the distal convoluted tubule.

shown to improve exercise intolerance and

Although spironolactone effectively
quality of life in people and dogs with
maintains potassium levels, data suggest
pulmonary hypertension via pulmonary
that it does not induce a significant diuretic
arterial vasodilation. There may also be
effect. However, spironolactone minimizes
additional beneficial effects on vascular
remodeling of both blood vessels and the
remodeling and cardiac function.

heart, and like angiotensin-converting

Both procainamide and quinidine, class
enzyme (ACE) inhibitors and 13-blockers,

IA antiarrhythmics used fom1erly to manage
has been shown to decrease symptoms and
ventricular arrhythmias, have been
to prolong the lives of people and perhaps
superseded by the class III antiarrhythmics

76

CARDIOVASCULAR SYSTEM INTRODUCTION
sotalol and arniodarone, and the class IB

Atropine and glycopyrrolate block the
antiarrhythmic mexiletine for treatment of
effects of the vagus nerve on the SA node.

malignant ventricular arrhythmias. Sotalol

Because the vagus nerve slows discharge of
is used to treat both supraventricular and
the SA node and heart rate, these compounds
ventricular tachyarrhythmias, and it is
speed heart rate and may be useful when the
particularly effective in treatment of Boxers
heart beats too slowly. Nitroglycerin is a

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with arrhythmogenic right ventricular
venodilator usually applied in a paste fonn
dysplasia, either alone or in combination
to the skin inside the earflap or the mucous
with mexiletine. Amiodarone is useful to
membranes; venodilation causes blood to
manage all forms of arrhythmias, including
pool in the dilated peripheral veins and
ventricular arrhythmias, and rate control or
splanchnic organs, decreasing left ventricuconversion of atrial fibrillation. Increased lar preload and pulmonary edema Sodium
liver enzymes and hepatotoxicity are
nitroprusside is another nitrate that is a
potential adverse effects of arniodarone;
veno- and arterial dilator. Nitroprusside can
thus, liver enzymes and serum amiodarone
be administered IV to treat acute fulminant
levels should be monitored periodically

CHF. These two medications should never be
throughout therapy. Lidocaine, a class
given simultaneously. Aspirin, clopidogrel,

IB antiarrhythmic, is used only IV for
dalteparin, enoxaparin, and coumadin are
emergency ventricular arrhythmias such
antithrombotics that may prevent thromboas sustained ventricular tachycardia or embolism in cats with cardiomyopathy.

R-on-T morphology.

Rivaroxaban is an oral factor Xa inhibitor

Atenolol, propranolol, and metoprolol
that may prove useful for thromboprophyare oral �-blockers, and esmolol is an IV
laxis in cats and dogs, although further

�-blocker, that slow the heart rate, suppress
studies are needed to evaluate its dosing and
arrhythmias, and up-regulate adrenergic
safety. Taurine and L-carnitine are anlino
receptors. Carvedilol is a �- and
acids used to prevent dilated cardiomyopacx-adrenergic blocker that scavenges thy in cats and in a limited number of dogs,
oxygen-free radicals. Like ACE inhibitors
respectively. Melarsomine is used to kill
and spironolactone, carvedilol has been
mature heartwonns; ivermectin, milbemyshown to both prolong life and decrease cin, and selarnectin are used to kill microsymptoms in people with heart failure; filariae. Doxycycline should be administered
however, �-blockers are not generally
to target Wolbachia, an intracellular bacteria advised for use in animals with active CHF.

that has a symbiotic relationship with

�-blockers are often used to treat dogs with
heartworms.

subaortic stenosis, and for dynamic outflow

Pimobendan and ACE inhibitors have
obstruction in cats with hypertrophic
been proved to be safe and effective to treat
cardiomyopathy.

dogs with heart failure. Furosemide and

Diltiazem is a calcium-channel blocker
digoxin are approved but without data
used to slow ventricular rate in animals
proving either safety or efficacy. Use of
with atrial fibrillation or supraventricular
other agents to manage heart failure or
tachycardia. It is also used occasionally in
rhythm disturbances is based on anecdotal
cats with hypertrophic cardiomyopathy
evidence or unblinded,uncontrolled reports
and outflow tract obstruction.

and clinical experience.

CONGENITAL AND INHERITED ANOMALIES

OF THE CARDIOVASCULAR SYSTEM

Congenital anomalies of the cardiovascular
only for the effects they produce but also for
system are defects that are present at birth
their potential to be transmitted to offspring
and can occur as a result of genetic, environthrough breeding and thus affect an entire mental, infectious, toxicologic, pharmaceubreeding population. In addition to tical, nutritional, or other factors or a
congenital heart defects, many other
combination of factors. For several defects,
cardiovascular disorders have been shown,
an inherited basis is suspected based on
or are suspected, to have a genetic basis.

breed predilections and breeding studies.

Diseases such as hypertrophic cardiomy

Congenital heart defects are significant not
opathy, dilated cardiomyopathy, and

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM

77
degenerative valvular disease of small
use of Doppler echocardiography has
breeds of dogs may have a significant
supplanted the use of invasive cardiac
heritable component.

catheterization studies in the evaluation of

In dogs, the prevalence of congenital
most cardiac defects. Once the diagnosis
heart disease is estimated at <l %. In
has been made and severity determined,

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multiple large studies of congenital heart
treatment options can be developed and a
disease in dogs, the three most common
prognosis given.

defects are aortic stenosis, puln10nic

The clinical significance of congenital
stenosis, and patent ductus arteriosus
heart disease depends on the particular

(PDA). Less common defects include
defect and its severity. Mildly affected
ventricular septa! defect, atrial septa!

animals may exhibit no ill effects and live a
defect, mitral valve dysplasia, tricuspid
normal life span. Defects causing significant
valve dysplasia, tetralogy of Fallot, cor
circulatory derangement will likely cause
triatriaturn, and persistent right aortic arch.

neonatal death. Such defects, many

However, because of regional differences,
incompatible with life, also cause fetal
the most common congenital cardiac
death and reduced litter size. Medical or
defects in dogs in the USA vary from those
surgical management is most likely to
reported in the UK and may likely differ
benefit animals with congenital cardiac
from those in Europe and other regions.

defects of moderate or greater severity.

In cats, the prevalence of congenital heart Left-to-right shunting PDA is one notable disease has been estimated to be 0.2%-- 1 %
exception in which surgical correction is
and includes atrioventricular (AV) septa!

indicated in nearly all affected animals.

defects (including ventricular septa! defect,
atrial septa! defect, and endocardial cushion
defects), AV valve dysplasia, endocardial

Pathophysiology: Congenital heart
fibroelastosis, PDA, aortic stenosis, and
defects produce signs of cardiac failure
tetralogy of Fallot.

through a variety of pathophysiologic

The most common defects in other
mechanisms. Defects such as pulmonic
species are as follows: cattle--ventricular
stenosis and subaortic stenosis cause
septa! defect, ectopic heart, and ventricular
ventricular outflow obstruction and may
hypoplasia; sheep-ventricular septa!

result in right- and left-side failure, respecdefect; pigs-tricuspid valve dysplasia, tively. Outflow obstruction also leads to
atrial septa! defect, and subaortic stenosis;
concentric hypertrophy of the respective
horses-ventricular septa! defect, PDA,
ventricle, increasing the risk of ischerniatetralogy of Fallot, and tricuspid atresia.

induced arrhythmias and sudden death. PDA

Arabian horses have a relatively higher
and septa! defects are examples of abnormal
incidence of congenital defects than other
communications between the systemic and
breeds; a variety of defects have been
pulmonary circulatory systems and typically
reported for this breed.

result in left-to-right shunting of blood. The
recirculation of blood through the pulmonary

Detection, Diagnosis, and Clinical
circulation and into the left-side chambers

Significance: The early detection of a
often precipitates signs of left-side CHF ( eg,
congenital heart defect is critical for several
pulmonary edema, cough, fatigue). Larger
reasons. Certain defects are surgically
defects typically result in a greater degree of
correctable, and treatment should be
volume overcirculation to the left-side
performed before the onset of congestive
chambers. PDA is a possible exception, with
heart failure (CHF) or.irreversible cardiac
very large defects sometimes contributing to
damage; recently purchased animals may be
pulmonary hypertension and right-to-left
returned to avoid economic loss; pets with
shunting ( see p 83), also called a reversed congenital heart defects are likely to die

PDA. Animals with right-to-left shunting
prematurely, causing emotional distress;
defects (tetralogy of Fallot, reversed PDA)

and animals purchased for performance
may develop right heart failure but more
have limited potential and will likely be
often have clinical signs associated with
unsatisfactory. Early detection also
polycythernia ( see p 43), which develops
prevents incorporation of genetic defects
subsequent to renal perfusion with
into breeding lines.

deoxygenated blood. This results in an

The evaluation of most animals with a
increase in erythropoietin production by the
congenital cardiac defect usually consists of kidneys and consequent polycythernia a physical examination, electrocardiography, radiography, and echocardiography.

Innocent Murmurs: It is impera-

This allows for a definitive diagnosis and an
tive to appreciate that the presence of a
assessment of the severity of the defect. The
heart murmur in a young animal is not

78

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM
pathognomonic for a congenital heart
an ejection-type systolic munnur heard best
defect. Many young animals will have a
at the aortic valve area. The intensity of the
low-grade systolic munnur ( often grade
munnur correlates fairly well with the

IWI or less) that is the result of mild
degree of stenosis and may increase as
turbulence and is not associated with a
animals mature, reflecting progressive
congenital heart defect. These munnurs
stenosis. Puppies without detectable

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usually disappear by 6 mo of age in dogs
munnurs should not be considered free of
and cats. Innocent munnurs are heard in
disease until they reach maturity ( -1 yr of
the absence of any other demonstrable
age). In moderate to severe cases, femoral
evidence of cardiovascular disease. Highpulse strength is diminished. Electrocargrade systolic munnurs (grade IV/VI or diography may show left ventricular
greater) and diastolic munnurs are indicaenlargement (tall R waves in lead II) and tive of cardiac disease and should prompt
ventricular premature complexes that may
further investigation.

increase in frequency with exercise. Holter
monitoring is indicated in syncopal animals

OUTFLOW TRACT
or in animals with severe disease to define
the presence of any arrhythmias, assess

OBSTRUCTIONS
arrhythmia severity, and help determine the
risk of sudden death. A recheck Holter

This group of congenital cardiac defects
monitor may be considered after initiation
includes aortic stenosis, pulmonic stenosis,
of antiarrhythmic therapy to assess efficacy.

and coarctation of the aorta. All involve

Radiographically, there is variable left
obstruction to either right or left ventricular
ventricular enlargement and poststenotic
outflow.

dilatation of the aorta. Doppler echocardiography can generally provide a definitive AORTIC STENOSIS
diagnosis of aortic stenosis and exclude
other cardiac abnormalities. A visible

Aortic stenosis impedes normal left
subaortic ridge or ring may be visible, and
ventricular emptying and is caused by a
the velocity of systolic blood flow through
narrowing at one of three locations:

the defect determines the severity of the

1) below the aortic valve ( subvalvular or
stenosis. Dogs with more significant
subaortic), 2) at the aortic valve (valvular),
stenosis may show left ventricular
or 3) above the aortic valve (supravalvular).

concentric hypertrophy and hyperechoic

The most common form of aortic stenosis
areas within the myocardium consistent
in dogs is subaortic stenosis, caused by
with myocardial ischemia and fibrosis.

fibrous nodules or a ridge or ring of fibrous

Treatment options include medical
tissue within the left ventricular outflow
management, balloon valvuloplasty, and
tract just below the aortic valve. Subaortic
open surgical correction. Medical managestenosis is generally seen in large-br.eed ment generally consists of the use of a
dogs. Predisposed breeds include Boxers,

13 -blocker ( eg, atenolol) for its potential

Golden Retrievers, Rottweilers, German
to decrease myocardial oxygen demand,

Shepherds, and Newfoundlands.

prolong diastole, and reduce left ventricular
wall stress. Antiarrhythmic therapy is

Pathophysiology: Aortic stenosis induces indicated in dogs with significant ventriculeft ventricular concentric hypertrophy, the lar ectopy. Balloon valvuloplasty, although
degree of which depends on the severity of
potentially effective short term, is unlikely
the stenosis. In severe cases, left ventricular
to offer consistent longterm benefits. Open
output may be decreased, especially during
surgical resection is costly, limited to
exercise. The major ramification of left
facilities offering cardiopulmonary bypass,
ventricular hypertrophy is the risk of
and associated with higher morbidity/
myocardial ischemia secondary to inademortality. Mildly affected animals comquate perlusion. Myocardial ischemia is monly require no treatment, and the
a major factor in the development of
prognosis can be fair to good in animals
life-threatening ventricular arrhythmias.

very mildly affected. Affected animals
should not be bred.

Clinical Findings and Treatment: Clinical signs do not consistently parallel the severity of stenosis. Inadequate output can

PULMONIC STENOSIS
result in lethargy, exercise intolerance, and

Pulmonic stenosis is common in dogs and
syncope. Animals with no history of illness
infrequent in cats. It results in obstruction
may die suddenly, with the defect first
to right ventricular outflow due, in most
detected at necropsy. Affected animals have
cases, to dysplasia of the pulmonic valve

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM

79
cusps. Although the valvular form is most
severity of disease and determine the need
common, stenosis can also occur in the
for intervention. Animals with moderate or
subvalvular region (infundibulum) or in the
severe pulmonic stenosis can benefit from
supravalvular area. Breed predilections for
balloon valvuloplasty or surgical intervenvalvular pulmonic stenosis include English tion (valvulotomy, patch grafting, partial

Bulldogs, Boxers, Beagles, Boykin Spaniels,
valvulectomy, or conduits). Balloon

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and terriers. Supravalvula:r pulmonic
valvuloplasty is a minimally invasive and
stenosis is uncommon and may be most
highly effective treatment option. Some
often seen in Giant Schnauzers.

animals are medically managed with a

[:I-blocker ( eg, atenolol) alone or in

Pathophysiology: The right ventricle
conjunction with balloon valvuloplasty.

must generate increased pressure during

Congestive heart failure should be
systole to overcome the stenosis, which
medically managed if present. Similarly, the
in moderate to severe cases can lead to
presence of supraventricular or ventricular
dramatic right ventricular concentric
arrhythmias warrants therapy with the
hypertrophy and dilatation. As the right
appropriate antiarrhythmic drug( s ).

ventricle hypertrophies, ventricular
compliance diminishes, leading to increased
right atrial pressure and venous congestion.

COARCTATION OF THE AORTA

The turbulent jet of blood flow across the

This rare condition of dogs and cats
stenosis deforms the wall of the main
involves narrowing of the aorta distal to the
pulmonary artery; resulting in a poststenotic
subclavian artery, typically in the area of the
dilatation. In severe cases, right-side
ductus arteriosus. Similar to other stenotic
congestive failure may be noted. Concurrent
lesions, this leads to increased pressure
tricuspid valve dysplasia is sometimes noted
proximal to the narrowing, resulting in
in animals with pulmonic stenosis.

concentric hypertrophy of the left ventricle.

Anomalous coronary artery development

Other uncommon congenital abnormalities
has been documented in some affected
of the aorta include tubular hypoplasia of
animals with pulmonic stenosis such as
the ascending aorta and aortic interruption.

English Bulldogs and Boxers. Most

Surgical correction has been reported.

commonly, the left main coronary artery
originates from the right coronary artery and
encircles the right ventricular outflow tract.

LEFT-TO-RIGHT SHUNTS

Clinical Findings and Treatment:

PATENT DUCTUS ARTERIOSUS

Affected animals may have a history of
exercise intolerance and failure to thrive.

In fetal life, blood entering the right heart

Right-side CHF may be present and is
largely bypasses the nonfunctional lungs
characterized by ascites or peripheral
through either the foramen ovale or the
edema. A prominent ejection-type systolic
ductus arteriosus. The ductus arteriosus
murmur is present and heard best at the
effectively shunts blood from the pulmopulmonic valve area (left base). A correnary artery into the descending aorta sponding precordial thrill may be present.

(right-to-left shunt). At birth, several factors

Jugular distention and pulsations may also
mediate closure of the ductus to separate
be present. Electrocardiography will
the systemic and pulmonary circulatory
demonstrate evidence of right ventricular
systems. Inflation of the lungs and
enlargement ( deep S waves in lead II) in
remodeling of the fetal pulmonary
many cases. Radiographic abnormalities
vasculature allows the pulmonary
include right ventricular enlargement,
circulation to change from a high-pressure,
dilatation of the main pulmonary artery, and
high-resistance system to a low-pressure,
diminished pulmonary perfusion. Echocarlow-resistance system. Closure of the diography is indicated to obtain a definitive
ductus occurs shortly after birth, leading to
diagnosis and may demonstrate right
formation of the ligamentum arteriosum.

ventricular hypertrophy and dilatation,
thickened and relatively immobile pulmonic Pathophysiology: Persistence or patenvalve cusps, and turbulent blood flow cy of the ductus with an otherwise normal
across the stenosis. In a few cases,
systemic and pulmonary circulatory system
supravalvular or discrete subvalvular
results in significant shunting of blood from
stenosis can be noted. Pulmonic insuffithe descending aorta to the pulmonary ciency can sometimes be seen in dogs with
artery (left to right). Because systolic and
pulmonic stenosis. The velocity of blood
diastolic aortic pressures normally exceed
flow across the stenosis is used to assess the pulmonary artery pressures, shunting is

80

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM
continuous throughout the cardiac cycle.

Jar premature complexes. Radiographic

The result is a continuous murmur and
abnormalities depend on the size of the
volume overload of the pulmonary arteries
ductus and may demonstrate left atrial and
and veins, left atrium, and left ventricle.

left ventricular enlargement, prominent

Left atrial and left ventricular dilatation
pulmonary vessels, aortic and pulmonic
may result in cardiac arrhythmias. Diastolic aneurysmal dilatations ( ductal bump), and VetBooks.ir
flow ( also called diastolic run-off) through
variable degrees of pulmonary edema.

the ductus leads to a decrease in diastolic

Echocardiography is v.aluable in excluding
and mean systemic blood pressures. The
concurrent congenital cardiac defects, as
widened difference between systolic and
well as documenting presence of the PDA.

diastolic pressures creates an increased

Continuous turbulence in the main
pulse pressure and bounding femoral
pulmonary artery is characteristic of a
pulses. Chronic volume overload and
left-to-right shunting PDA. Left ventricular
dilatation of the left-side cardiac chambers
and left atrial dilatation are typically noted,
usually result in development of left-side
and mild mitral regurgitation may be

CHF in most untreated cases within the
present secondary to annular dilation.

first 1 - 2 years of life. Animals with a small

Because of the high risk of CHF early in
ductus and minimal shunting may reach
life for animals with a PDA, closure is
adulthood, although most affected dogs
generally recommended. There are two
have evidence of volume overload even at
major treatment options for PDA closure:

a young age. In some animals with a large
interventional transcatheter occlusion and

PDA, increased pulmonary blood flow may
surgical ligation. Catheter-based occlusion
induce pulmonary vasoconstriction and
is minimally invasive and typically involves
development of pulmonary hypertension.

placement of an occlusion device through

In cases of severe pulmonary hypertena peripheral vessel (most commonly the sion in which pulmonary pressures el{ceed
femoral artery). The Amplatz canine ductal
systemic pressures, blood flow through the
occluder is used most often and is highly
ductus can reverse and result in right-to-left successful with minimal complications.

shunting. This "reverse PDA'' causes disap

The use of other occlusion devices such as
pearance of the classic machinery murmur

Gianturco coils and vascular plugs has also
and results in caudal hypoxemia Delivery
been described. The major limitations to a
of O!(ygenated blood to the head and
transcatheter approach are ductal size and
neck results in pink mucous membranes
patient size. Surgical ligation of the ductus
cranially, while delivery of hypoxemic
is also usually curative and considered
blood caudally results in cyanotic mucous
most often for small dogs and cats. If
membranes caudally (vulva and prepuce).

present, CHF should be medically managed

Differential cyanosis is a characteristic exbefore anesthesia and surgery are amination finding in animals with reverse
performed.

PDA. In addition, perfusion of the kidneys

In animals with a reverse PDA, there is
with deol{ygenated blood causes excessive
usually a history of lethargy, exercise
release of erythropoietin and subsequent
intolerance, and collapse that relates to
polycythemia.

severe pulmonary hypertension and venous
admixture. Careful examination may reveal
differential cyanosis. The second heart

Clinical Findings and Treatment:

sound may be split, and there may be a soft

In animals with a left-to -right PDA, a
diastolic murmur of pulmonic insufficiency.

prominent, continuous, machinery-like

A continuous murmur is not present, and
murmur is present. The murmur is usually
femoral pulses are not bounding. The
loudest at the left base of the heart and is
finding of polycythemia in a young animal
often associated with a precordial thrill. In
with the above clinical signs should prompt
some cases, the ductus remains open for
further diagnostic evaluation of the heart.

several days after birth, so a continuous

Electrocardiography demonstrates severe
murmur may be detected during examinaright ventricular enlargement and occation of the neonate. Femoral pulses are sional arrhythmias. In reverse PDA, right
typically bounding. Most young animals do
ventricular enlargement and aneurysmal
not demonstrate clinical signs. Those with a
dilatation of the descending aorta can be
large shunt and older animals often have
noted on radiographs. Echocardiography is
signs of left-side CHF Electrocardiography
indicated in these cases and will demonfrequently demonstrates tall R waves in lead strate abnormalities associated with II, indicative of left ventricular enlargement.

pulmonary hypertension (right ventricular

A spectrum of cardiac arrhythmias may also
dilatation and hypertrophy, septa! flattening,
be seen, including both atrial and ventricu-
pulmonary artery dilatation). Contrast

CONGENITAL AND INHERITED ANOMALIES OF THE CAR[)IOVASCULAR SYSTEM

81
echocardiography using agitated saline can
pressures and a normal pressure gradient.

be used to confinn the diagnosis. After the

Significant shunting through the pulmonary
injection of agitated saline into a peripheral
arteries can induce vasoconstriction and
vein, microbubbles will pe seen within the
pulmonary hypertension. As resistance
right heart, pulmonary artery, and abdomirises, the shunt may reverse and result in nal aorta, suggesting a right-to-left shunt
right-to-left shunting of blood, cyanosis, ·and

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between the pulmonary artery and the
polycythemia. The reversal of shunt flow
aorta. Occlusion or ligation of the ductus is'

(right-to-left) through a septa! defect as a
contrainc(icated with reverse PDA, because
consequence of pulmonary hypertension
this results in an increase in pulmonary
is referred to as Eisenmenger syndrome,
hypertension (by causing an increase in
flow through the pulmonary arteries), right

Clinical Findings and Treatment: Cliniheart failure, and death. Therapy in these cal findings depend on the severity of the
cases involves medical management of
defect and the shunt direction. A small,
pulmonary hypertension and control of
restrictive defect usually causes minimal
polycythemia through periodic phlebotomy.

or no signs. Larger defects may result in

Longterm prognosis is poor.

left-side CHF. Cattle are prone to developing
signs of right-side failure. The development

VENTRICUlAR SEPTAL DEFECTS
of Eisenmenger syndrome is indicated by
cyan0sis, fatigue, and exercise intolerance.

Ventricular septa! defects are most

Most animals with a restrictive ventricular
commonly located in the perimembranous
septa! defect have a loud holosystolic
portion of the septum, high in the ventricumurmur heard best over the right thorax lar septum immediately beneath the right
that may be accompanied by a palpable
and noncoronary aortic valve cusps on
thrill. This murmur is often absent or faint
the left and just below the cranioseptal
when a very large defect is present 0r when
tricuspid valve commissure on the right.

shunting is right to left. On occasion, aortic

They vary in size and hemodynamic
valvular insufficiency develops secondarily,
significance. Doubly comrnittedjuxtabecause the defect may disrupt aortic valve arterial septa! defects (located beneath
apposition. In these cases, a concurrent
the aortic valve on the left and beneath the
diastolic murmur may be present, and the
pulmonic valve on the right} and muscular
combination systoliddiastolic murmur
septa! defects·(located at any site along

("to-and-fro" murmur) may be mistaken as the muscular septum) may also be seen.

that of a PDA. Thoracic radiographs can·

Ventricular septa! defects may be seen with
demonstrate generalized cardiomegaly with
other congenital cardiac anomalies. This
overcirculation of the pulmonary vessels.

defect is heritable in miniature swine.

The defect can usually be visualized by
echocardiography, although small defects

Pathophysiology: Shunting of blood
may be missed. Doppler echocardiography
from the left ventricle into the right
can often confinn the presence of a shunt.

ventricle or right ventricular outflowtract

Therapy depends on use of the animal,
occur,s in most animals because of the
severity of clinical signs, and direction of
pressure gradient between the two
the shunt. Animals with small ventricular
ventricles. The magnitude of the shunt
septa! defects do not typically require
depends on the size .of the defect, the ratio
therapy ancl have a good longterm prognosis
of pulmonary to systemic vascular
if significant aortic insufficiency is' not
resistance, and tihe Felative compliance of
presert. Animals with a moderate to severe
the two ventricles. Blood shunted into.the
ventricular i;;eptal defect and secondary
right.ventriele is recirculated,through
volume overload to the left heart more·
the pulmonary vessels and left cardiac
commonly develop clinical signs, and
chambers, which causes dilatation of these
treat;ment should be considered. Surgical'

structures. The right ventricle qiay dilate
closure of the' defect requires cardiopulmoas well, especially in animals with large nary bypass and is often limited by expense
ventricular septa! defects ( which are rare).

and,availability. Percutaneous transcathC;!ter

Small defects limit the volume of shunted
closure can be considered for muscular
blood and minimize hemodynamic effects,
septa! defects and involves placement of an
whereas large defects usually result in
occluder or coil. Pulmonary artery banding
severe circulatory derangements and
to increase right ventricclar outflow tract
clinical signs. Most ventricular septa!

resistance, and thus decniase left-to-right
defects are restrictive, in which the· degree
shunting, can be consiclered. Medi(:ally, the·
of shunting is small, all@wing the left and
use of drugs to reduce systemic vascular
right ventricles to maintain normal
resistance ( eg, vasodilators) may help to

82

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM
decrease the degree of left-to-right shunting.

septum, near the AV junction, and are often

With right-to-left shunting, surgical closure
a component of AV septa! (AV canal)

of the defect is generally contraindicated.

defects. Sinus venosus defects are most

Phlebotomy to relieve the effects of
often located at the junction of the right
polycythemia or use of hydroxyurea may
atrium and cranial vena cava.

be considered to relieve clinical signs;

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however, the prognosis is poor to guarded.

Pathophysiology: In most cases, blood

Animals diagnosed with a ventricular septa!

shunts from the left atrium to the right
defect should not be bred; the defect has
atrium, causing a volume overload of the
been demonstrated to be heritable in at
right-sided chambers. The magnitude of
least one breed (English Springer Spaniels).

shunting depends on the size of the defect,
the ratio of pulmonary to systemic vascular

ATRIAL SEPTAL DEFECTS
resistance, and the relative compliance of
the two ventricles. Excessive blood flow

A communication between the atria may be
through the right-side chambers results in
the result of a patent foramen ovate or a true their dilation and hypertrophy. Pulmonary atrial septa! defect. During fetal life, the
vasoconstriction and development of
foramen ovate, a flapped oval opening of the pulmonary hypertension may occur as a interatrial septum, allows shunting of blood
consequence of excessive pulmonary blood
from the right atrium to the left atrium to
flow and may precipitate right-side CHF In
bypass the nonfunctional lungs. This
conditions associated with high 1ight atiial
flapped oval opening develops between two
pressure (eg, pulmonic stenosis), shunting
septa that make up the interatrial septum:

may occur from right-to-left across a patent
the septum primum and septum secundum.

foramen ovate or atrial septa! defect,

At birth, the drop in right atrial pressure and
potentially resulting in cyanosis and
rise in left atrial pressure cause the foramen
polycythemia.

ovate to close and shunting to cease.

Increased right atrial pressure may prevent

Clinical Findings and Treatment: Signs
closure of the foramen ovate and lead to
of right heart failure ( eg, ascites, jugular
persistent shunting through a patent
venous distention) may be present. A soft
foramen ovate. This does not represent a
ejection-type systolic murmur is usually
true atrial septa! defect, because the septa
present over the pulmonic valve area,
have formed nom1ally. A true atrial septa!

reflecting increased blood flow through the
defect is an opening or hole within the
pulmonic valve. Blood flow through the
interatrial septum, which allows blood to
defect itself does not produce a murmur due
shunt from the atrium with the greater
to the low velocity of shunt flow. Prolonged
pressure. Septum secundum defects occur
ejection time of the right ventricle may
high in the interatrial septum, near the
result in a split second heart sound.

foramen ovate, and are the most common

Electrocardiography may reveal evidence of
type. Septum primum defects are located in
right ventricular or right atrial enlargement
the most apical portion of the interatrial

( right axis shift, deep S waves, tall P waves).

Right bunclle-branch block and arrhythmias
can also be noted. Radiographically, there
are variable degrees of right ventricular
enlargement and prominence to the
pulmonary vessels indicating pulmonary
overcirculation. Echocacdiography is
indicated and demonstrates varying
degrees of right atrial and right ventricular
dilatation, as well as identification of the
defect as a loss of echogenicity at the
interatrial septum. The normal loss of
echogenicity of the fossa ovate ( artifactual
drop out) should not be interpreted as an
atrial septa! defect. Doppler evaluation
confirms shunting through the defect and

Echocardiographic image of a secundumincreased ejection velocities across the ty
pulmonic valve. Surgical correction may
pe atrial septal defect (ASD) in a dog.

RA = right atrium, LA = left atrium, RV = right
be attempted but is associated with high
ventricle, LV = left ventricle. Courtesy of Dr.

expense and mortality. Animals with small

Sandra Tou.

or medium-sized septum secundum defects

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM

83
can tolerate the defects well, and many of

(resulting in fatigue, shortness of breath)

these defects are noted as an incidental
and generalized cyanosis (resulting in
finding in older animals. Larger defects,
polycythemia and weakness) caused by the
such as noted with septum prim um defects
mixing of deoxygenated blood from the
or endocardial cushion defects, are more
right ventricle with oxygenated blood from
likely to cause right-side CHF. The
the left ventricle. Because of venous

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prognosis is guarded to poor in these cases,
admixture, the kidneys release erythropoialthough many dogs show no clinical signs etin, resulting in polycythemia (see p 43).

for years. For dogs with large defects and

The increased blood viscosity associated
significant volume overload, surgical or
with polycythemia can lead to sludging
interventional correction is possible.

of blood and poor capillary perfusion.

Surgical closure of the defect requires

Consequences of polycythemia include
cardiopulmonary bypass and is often
ocular changes, bleeding diathesis, and
limited by expense and availability.

neurologic abnonnalities (ataxia,

Transcatheter closure using a septa!

seizures).

occluder has been reported for secundum
and muscular defects.

Clinical Findings and Treatment:

Typical historical features include stunted
growth, exercise intolerance, cyanosis,

RIGHT-TO-LEFT SHUNTS
collapse, and seizures. A precordial thrill
may be felt in the area of the puhnonic
valve, and in most cases, a murmur of

TETRALOGY OF FALLOT
pulmonic stenosis is present. The intensity
of the murmur is attenuated when severe

Tetralogy of Fallot is the most common
polycythemia is present, and in some
defect that produces cyanosis. It results from affected animals, a cardiac murmur is not a combination of four components:

present. Electrocardiographically, a pattern
pulmonic stenosis, large ventricular septa!

of right ventricular enlargement is usually
defect, right ventricular hypertrophy, and
seen ( deep S waves in lead II, right axis
dextropositioning ( overriding) of the aorta
shift), and arrhythmias are infrequent.

A single conotruncal malformation ( cranially Radiographs demonstrate variable right displaced formation of the upper portion of
heart enlargement and undersized
the inte1ventricular septun1) is believed to
pulmonary vessels. Echocardiography
result in narrowing of the right ventricular
confirms the diagnosis. Overriding
outflow tract (pulmonic stenosis ), overriding ( rightward displacement) of the aortic root, of the aorta, and the ventricular septa!

right ventricular hypertrophy, and a
defect. The tight ventricular concentric
ventricular septa! defect are evident. The
hypertrophy is simply a consequence of the
left-side.chambers may be small as a result
pulmonic stenosis. The pulmonic stenosis
of decreased pulmonary venous return.

may be valvular, infundibular, or both.

Routine contrast echocardiography

Breeds predisposed to tetralogy of Fallot
demonstrates right-to-left shunting at the
include Keeshonds, English Bulldogs, and
level of the ventricular septa! defect. Flow

Wrrehaired Fox Terriers. The trait is
through the defect can also be detected by
inherited in Keeshonds and presumably in

Doppler echocardiography.

other breeds. This defect has been recog[3-adrenergic blockade has been used to nized in other breeds of dogs and in cats.

reduce the dynamic component of right
ventricular outflow obstruction and to

Pathophysiology: The hemodynamic
attenuate [3-adrenergic-mediated decreases
consequences of tetralogy of Fallot depend
in systemic vascular resistance. Increases in
primarily on the severity of the pulmonic
systemic vascular resistance lower the
stenosis, the size of the ventricular septa!

magnitude of shunting. Polycythemia
defect (which is typically large and
should be controlled by periodic phlebotnonrestrictive), and the ratio of pulmonary omy to resolve clinical signs of polyto systemic vascular resistance. The cythemia. The prognosis is guarded, but
direction and magnitude of the shunt
animals with mild to moderate shunting
through the septa! defect depends in large
may reach adulthood.

part on the relative resistances to flow

Treatment options include surgical and
between the pulmonic circulation
medical management. Corrective surgery has

( obstructed by the pulmonic stenosis) and
been reported in dogs but is _rarely performed.

the systemic circulation. Consequences

Palliative surgical techniques to relieve
include reduced pulmonary blood flow
clinical signs associated with tetralogy of

84

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM

Fallot are also rarely perlormed and include

Clinical Findings and Treatment: Clinitechniques to produce systemic to pulmonary cal signs correlate with the severity of the anastomoses such as a modified Blalockdefect. Affected animals may display signs Taussig shunt These procedures increase
of left-side CHF A holosystolic murmur of
blood flow to the lungs to reduce signs of
mitral regurgitation is prominent at the left
pulmonary hypoperlusion and systemic
cardiac apex. A diastolic heart sound (gallop

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hypoxia In some cases, reducing pulmonic
rhythm) is present in some cases. Affected
stenosis is palliative. Surgical valvuloplasty
animals may have a precordial thrill over the
or balloon valvuloplasty of the pulmonic
left cardiac apex. Electrocardiography may
stenosis are also options.

demonstrate atrial arrhythmias ( atrial
premature complexes, atrial fibrillation),

OTHER CYANOTIC HEART
especially in severely affected animals with

DISEASES
left atrial dilatation. There may also be
evidence of both left atrial (widened P

PDA, ventricular septal defect, and atrial
waves) and left ventricular enlargement.

septal defect with Eisenmenger syndrome

Thoracic radiographs may demonstrate
are described previously. Other cyanotic
severe left atrial enlargement. Left
heart diseases, including truncus arteriosus,
ventricular enlargement and pulmonary
ventricular septal defect with pulmonary
venous congestion can also be noted.

atresia, double-outlet right ventricle, and

Echocardiography demonstrates malforma

D-transposition of the great arteries, are
tion of the mitral valve complex (fused
rare in dogs and cats.

chordae tendineae and thickened, immobile
valve leaflets, abnormal appearance to the
papillary muscles) and left atrial and ventric

CONDITIONS OF THE
ular dilatation. Doppler echocardiography
demonstrates severe mitral regurgitation.

ATRIOVENTRICULAR VALVES

Evidence of mitral stenosis can be identified
on the echocardiogram (seep 85).

MITRAL VALVE DYSPLASIA

Prognosis for animals with clinical signs
and severe disease is poor. Mildly affected

Congenital malformation of the mitral
animals may remain free of clinical signs for
valve complex (mitral valve dysplasia) is
several years. Animals with CHF should be
a common congenital cardiac defect in
treated medically. For therapy of progrescats. Canine breeds predisposed are Bull sive left-side CHF, see MANAGEMENT Ot' HEART

Terriers, German Shepherds, and Great

FAILURE, p 103 .

Danes. Mitra! valve dysplasia results in
mitral insufficiency and systolic regurgita

TRICUSPID VALVE DYSPLASIA
tion of blood into the left atrium. Any
component of the mitral valve complex

Congenital malformation of the tricuspid

(valve leaflets, chordae tendineae,
valve complex is seen in dogs and cats.

papillary muscles) may be malformed,

Breeds predisposed are Labrador Retrievers
and often more than one component is
and German Shepherds. Tricuspid dysplasia
defective.

results in tricuspid insufficiency and
systolic regurgitation of blood into the right

Pathophysiology: Malformation of the
atrium. Rarely, tricuspid valve stenosis can
mitral valve complex results in significant
be noted. Chordae tendineae are com_monly
valvular insufficiency. Chronic mitral
shortened or absent, and tricuspid valve
regurgitation leads to volume overload of
leaflets may be thickened or adhered to the
the left heart, which results in dilatation of
ventricular or interventricular septal wall.

the left ventricle and atrium. Severe mitral

Other concurrent congenital anomalies
regurgitation can subsequently result in
such as mitral valve dysplasia, septal
pulmonary venous congestion and left-side
defects, subaortic stenosis, or pulmonic

CHF Dilatation of the left-side chambers
stenosis may be present. In Ebstein
predisposes affected animals to arrhythanomaly, a variant of tricuspid dysplasia, mias. When mitral regurgitation is severe,
the tricuspid valve is displaced toward the
cardiac output decreases and signs of poor
cardiac apex.

cardiac output may occur ( weakness,
syncope). In some cases, malformation of

Pathophysiology: Malformation of the
the mitral valve complex causes a degree
tricuspid valve results in significant valvular
of valvular stenosis as well as insufficiency
insufficiency. Chronic tricuspid regurgitation

(seep 85).

leads to volume overload of the right heart,

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM

85
dilating the right ventricle and atrium.

widened P waves (indicating left atrial

Pulmonary blood flow may be decreased,
enlargement) and supraventricular
resulting in fatigue and tachypnea As the
arrhythmias. Echocardiography provides a
pressure in the right atrium increases,
definitive diagnosis. Doming of the mitral
venous return is impaired, causing signs of
valve leaflets toward the left ventricle
right heart failure ( ascites, jugular venous
during diastole, left atrial enlargement,

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distention, and possibly pleural effusion).

and thickening of the mitral valve leaflets
can be noted. Doppler echocardiography

Clinic�I Findings and Treatment: Clinidemonstrates turbulent diastolic flow cal signs correlate with the severity of the
across the mitral valve, beginning at the
defect. Affected animals may display signs
mitral valve and extending into the left
of right-side CHF. A holosystolic murmur of
ventricle. A pressure gradient is docutricuspid regurgitation is prominent at the mented between the left atrium and left
right cardiac apex. Atrial arrhythmias,
ventricle in early diastole.

especially paroxysmal atrial tachycardia,

Medical management of animals with
are common. Electrocardiography and
mitral valve stenosis involves use of
radiography typically demonstrate right
diuretics and dietary sodium restriction.

ventricular and right atrial enlargement.

Excessive diuresis should be avoided,

The caudal vena cava may be significantly
because this can reduce cardiac output
enlarged. Echocardiography demonstrates
severely. Surgical or interventional therapy
malformation of the hicuspid valve and
options include closed commisurotomy ( disvarying degrees of right atrial and ventricuruption of the stenosis without the use of lar dilatation. Doppler echocardiography
bypass), open commisurotomy, mitral valve
demonstrates tricuspid regurgitation.

replacement, and balloon valvuloplasty.

Prognosis for animals with clinical signs is
highly dependent on the severity of disease
and the degree of tricuspid regurgitation.

VASCULAR RING ANOMALIES

For dogs with right heart failure, CHF
therapy and periodic abdominocentesis may

Pairs of embryonic aortic arches exist
be needed to control peritoneal effusion.

during early fetal development and
subsequently give rise to the carotid arteries

MITRAL VALVE STENOSIS

(third arches), the aortic arch (left fourth
arch), and the pulmonary arteries and

Mitra! valve stenosis is a narrowing of the
ductus arteriosus (sixth arches). The other
mitral valve orifice caused by abnormalities
aortic arches regress, although the first
of the mitral valve, resulting in obstruction
aortic arches also become part of the
to left ventricular inflow. This congenital
maxillary arteries. Congenital defects may
abnormality is rare in dogs and cats and can
arise if development or dissolution of the
occur together with other congenital
aortic arches is disrupted. Multiple vascular
defects such as subaortic stenosis, mitral
ring anomalies have been reported in dogs,
valve dysplasia, and pulmonic stenosis.

including persistent right aortic arch,
double aortic arch, left aortic arch with right

Pathophysiology: The disease results in
ligamentum arteriosum, and retroesophaincreased resistance to left atrial outflow, geal subclavian arteries.

creating a pressure gradient between the
left atrium and left ventricle. This leads to

PERSISTENT RIGHT AORTIC ARCH
left atrial enlargement and increases in
pulmonary venous and capillary wedge

Persistent right aortic arch is the most
pressures. Pulmonary edema can develop
common vascular ring anomaly in dogs
as a consequence, and syncope occurs in

(German Shepherds and Irish Setters in
some cases.

particular) and has also been reported in
cattle, horses, and cats. The right aortic

Clinical Findings and Treatment: Miarch fails to regress normally, resulting in tra! stenosis can result in a diastolic heart
entrapment of the esophagus and trachea at
murmur that is typically low-grade (l-IINI).

the level of the heart base. The structures

If concurrent mitral valve dysplasia is
are encircled by the persistent arch on the
present, a systolic murmur with maximum
right, by the ligamentum arteriosum on the
intensity at the left cardiac apex may be
left and dorsally, and by the base of the
heard. Radiographs demonstrate varying
heart ventrally. The esophagus is typically
degrees of left atrial enlargement and
compressed, leading to the most common
pulmonary edema in animals with left-side
clinical sign of regurgitation ( often noted

CHF. Electrocardiography may demonstrate at weaning). Aspiration pneumonia is

86

CONGENITAL AND INHERITED ANOMALIES OF THE CARDIOVASCULAR SYSTEM
common in affected animals. Surgery is
effusion, or both. Surgical resection and
recommended to transect the ligamentum
balloon dilation of the membrane using a
arteriosum to free the esophagus from
surgical approach have been reported.

entrapment. Radiographically, right-ward

Cor triatriatum dexter is a rare defect of
deviation of the trachea on dorsoventral or
dogs. It is caused by persistence of the right
ventrodorsal view is highly sensitive and
valve of the sinus venosus. The remaining

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specific for the diagnosis of persistent right
fibrous membrane partitions the right
aortic arch. CT can confirm the diagnosis
atrium into two subchambers; the cranial
before surgery and assist surgical planning.

vena cava and tricuspid valve are associated
with the low-pressure subchamber (true

MISCELLANEOUS
right atrium), whereas the caudal vena cava
and coronary sinus are typically associated

CONGENITAL CARDIAC
with the high-pressure subchamber. The

ABNORMALITIES
membrane may contain one or more
perforations, or be imperforate. The degree

Peritoneopericardial diaphragmatic
of blood flow between the subchambers
hernia is the most common congenital
determines the severity of disease. Dogs
pericardial disease in dogs and cats. It
with more severe septation often present
results from abnormal development of the
with right heart failure (typically ascites).

dorsolateral septum transversum or from

Surgical resection and transcatheter
failure of the lateral pleuroperitoneal folds
balloon dilation of the membrane are
and the ventromedial pars stemalis to unite.

treatment options. CHF should be medically

The result is herniation of abdominal viscera managed before surgery.

into the pericardial sac. The liver is the most

Double chamber right ventricle is an
commonly herniated organ, followed by
unconunon defect in which an anomalous
the small intestine, spleen, and stomach.

muscle bundle divides the right ventricle

Clinical signs are highly variable, with many
into two chambers. The muscle bundle leads
animals remaining asymptomatic and the
to obstruction of the right ventricular
defect being discovered on postmortem
outflow tract, creating a high-pressure
examination. Thoracic radiographs can
proximal subchamber (receiving inflow
demonstrate lack of a visible diaphragmatic
through the tricuspid valve) and a lowborder and small-intestinal loops or liver pressure distal subchamber distal to the
crossing the diaphragm into the pericardial
obstruction. Increased pressure in the
sac. The suspicion of peritoneopericardial
proximal subchamber leads to left atrial
diaphragmatic hernia is heightened when
dilatation and subsequent right heart failure.

abdominal organs are seen adjacent to the

A systolic ejection murmur is often evident
heart on echocardiogram. A contrast
on auscultation. Definitive therapy requires
radiographic examination using oral barium
open-heart surgery to resect the muscle
may also identify small.intestinal loops or
bundles, which requires cardiopulmonary
stomach in the pericardial sac. CT can
bypass. Balloon valvuloplasty has not
usually confirm the diagnosis before
proved to be a successful treatment option.

surgery. In animals with respiratory signs or

Anomalous pulmonary venous
signs relatable to organ entra12ment, the
connection is a congenital abnormality in
hernia should be surgically reduced.

which varying numbers of pulmonary veins

Cor triatriatum sinister and dexter

(from one to all) attach to the right atrium
result from a fibrous membrane dividing
or a systemic vein.

the left or right atrium, respectively. Cor

Endocardial cushion defects (AV canal
triatriatum sinister is a rare defect of cats. It
defects, persistent AV ostium, AV septal
occurs when the common pulmonary vein
defects) involve abnormalities of endocarfails to regress normally; as a result, a fibrous dial cushion development and can produce membrane persists within the left atrium,
septum primum defects, AV valve abnordividing the left atrium into two subchammalities, and ventricular septal defects.

bers. There are commonly one or more

Dextrocardia, positioning of the heart
perforations in the separating membrane,
in the right hemithorax, can be seen as a
allowing communication between the two
congenital cardiac defect and by itselfis
portions of the atrium. The proximal,
typically benign. It can also be seen in
high-pressure subchan1ber receives
combination with situs inversus (an
pulmonary venous return, while the distal,
abnormal orientation of the organs of the
low-pressure subchamber is adjacent to the
body). The combination of these defects
mitral valve and contains the left auricular
is typically noted in animals with other
appendage. Affected cats can present in left
concurrent abnormalities such as sinusitis,
heart failure, with pulmonary edema, pleural bronchitis, and bronchiectasis.

HEART DISEASE AND HEART FAILURE

87-

HEART DISEASE AND HEART FAILURE

Heart disease is defined as any functional,

History and Signalment

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structural, or electrical abnormality of the
heart. It encompasses a wide range of

For animals with suspected heart disease,
abnormalities, including congenital
the signalment (age, breed, sex) helps
abnormalities ( see p 76) as well as
formulate a differential diagnosis list.

anatomic and physiologic disorders of

The signalment influences the relative
varying causes. Heart disease can be
importance of possible heart diseases ( eg,
classified by various characteristics,
endocarditis is rare in cats and small dogs
including whether the disease was present
but more common in cows and large dogs)

at birth or not ( eg, congenital or acquired),
as well as many specific abnormalities ( eg,
cause ( eg, infectious, degenerative, genetic
breed predispositions for certain congenital
or heritable), duration ( eg, chronic or
defects, dilated cardiomyopathy (DCM),
acute), clinical status ( eg, left heart failure,
myxomatous valve degeneration, etc).

right heart failure, or biventricular failure),

Animals presenting with heart disease
by anatomic malformation ( eg, ventricular
may have no clinical signs or have a history
septal defect), or by electrical disturbance
of tachypnea, dyspnea, abdominal distention

( eg, atrial fibrillation, ventricular premature

( ascites ), subcutaneous edema, wealrness,
complexes).

syncope (fainting), cyanosis, exercise

Heart failure is usually the end result of
intolerance, or weight loss. A few historical
severe, overwhelming systolic and/or
findings are more species specific, including
diastolic cardiac dysfunction that most
peripheral or ventral (subcutaneous) edema
commonly results in the formation of edema in horses and cattle. Cats rarely cough with or effusion ( eg, pulmonary edema, pleural
heart failure and more commonly present
effusion, ascites) severe enough to cause
with a history of tachypnealdyspnea ( which
clinical signs ( eg, tachypnea, dyspnea,
may be subtle and go unnoticed by the
abdominal distension). It may also produce
owner) and anorexia. In dogs, coughing can
signs referable to poor perfusion (low
occur due to pulmonary edema, but many
cardiac output). This most commonly
more dogs that cough do so because of lung
happens in late-stage chronic heart failure;
disease ( eg, chronic bronchitis), so extreme
rarely, it may be due to acute heart failure
care must be taken when evaluating dogs

( eg, ruptured chorda tendineae ). The most

( especially older, small-breed dogs) with a
common abnormalities in systole that lead
cough and a heart murmur because most are
to heart failure are decreased contractility
not in heart failure.

(eg, dilated cardiomyopathy), severe
valvular regurgitation ( eg, mitral regurgita

Physical Examination
tion), and left-to-right shunting cardiac

A complete physical examination should be
defects ( eg, ventricular septal defect, patent
performed on any animal being evaluated
ductus arteriosus ). Myocardial fibrosis is
for heart disease or that presents with signs
the most common abnormality that causes
that could be attributable to heart disease.

severe diastolic dysfunction, as seen in cats

The cardiac physical examination should
with hypertrophic cardiomyopathy. Heart
start with auscultation of the heart.

disease can be present without ever leading

Auscultation should be done in as quiet of
to heart failure. Heart failure, however, can
an environment as possible. In all cats, small
occur only if severe heart disease is present.

dogs, and small mammals, a pediatric
stethoscope should be used and only the
diaphragm of the stethoscope needs to be

DIAGNOSIS OF HEART DISEASE
used, because heart sounds, including
gallop sounds, in animals this size are not

The diagnosis of heart disease typically
low enough in frequency to require the bell.

involves evaluating the signalment, history,

In large dogs and large animals, the bell
and physical examination findings, as well
should also be used. In general, the left apex
as results of diagnostic tests such as
beat should first be located by palpation,
radiography, electrocardiography, and
then the head of the stethoscope placed
echocardiography. Rarely, more specialized
over it (mitral area). The stethoscope head
tests such as cardiac catheterization, C1�
then should be inched forward and upward

MRI, or nuclear studies are necessary.

to the left base (pulmonic and aortic area).

88

HEART DISEASE AND HEART FAILURE

In any young animal, care should also be
sounds in goats, sheep, and pigs; however,
taken to place the stethoscope head farther
only S and S are believed to be audible in
forward (left axillary region) to listen for a

1

2
these species.

continuous murmur (patent ductus
arteriosus). Then the right apical region

Three-Heart-Sound Rhythms (Gallop
should be ausculted. In a young animal

Heart Sounds and Systolic Clicks): A

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suspected of having congenital heart
gallop heart sound (rhythm) is the presence
disease, the right base and along the neck
of S, and S2 accompanied by an interceding
should also be ausculted.

sound or sounds in diastole (between S2 and

In addition to auscultation of the thorax,

S,) that is either an accentuated third heart
palpation of the ventral thorax should be
sound (Sa) or fourth heart sound (S,.), or
performed to assess for the presence of a
both. These are classified as protodiastolic
thrill ( vibration created by turbulent blood

(Sa), presystolic (S
flow that can be palpated with the

4), or sununation gallop
heart sounds (fusion of Sa and S,
fingertips) and alterations in intensity or

1). The most
common gallop heart sound noted in dogs is
location of the apex beat. Concurrent
a result of an accentuated Sa and typically
auscultation and palpation of the pulse
occurs secondary to a normal quantity of
should also be performed to identify pulse
blood "dumping" into a stiff left ventricle deficits (premature beats, atrial fibrillation)

( eg, DCM), or a massive amount of blood
and to assess the strength and character of

"dun1ping" into a normal left ventricle in the systemic arterial pulse. Pulmonary
early diastole ( eg, mitral regurgitation and
auscultation should be performed (see
patent ductus arteriosis ). An S.1 gallop heait
below). Mucous membrane color and refill
sound is caused by atrial contraction
time should be assessed but are often
pushing blood into a stiff left ventricle.

nonnal even in animals with severe heart

In cats with cardiomyopathy, especially
failure. Cyanosis may be present if the
hypertrophic cardiomyopathy, the left
animal is severely hypoxemic. Limbs should ventricle is stiff, so both third and fourth be examined for the presence of edema, and heart sounds can be heard. However, the abdomen should be assessed for
because the heart rate commonly exceeds
presence of ascites (palpation and

160-180 bpm in cats in an exainination
ballottement ). The jugular veins should be
room, it is usually impossible via auscultaexamined with the animal in a standing or tion to determine whether the gallop sound
sitting position for presence of abnormal
is due to an S
distention and pulsation. A normal jugular

3 or S4 gallop; often, it is a
summation of the two.

vein will be distended and may pulsate

Gallop rhythms are not the only
when an animal is laterally recumbent.

three-heart-sound rhythms that can be

. ausculted. Systolic clicks also occur in

Heart Sounds: Heart sounds are
dogs and cats and are much more common
generated by the rapid acceleration and
than gallop rhythms in dogs. A systolic
deceleration of blood and secondary
click is a short, sharp sound that occurs
vibrations in the cardiohemic system and
during mid to late systole. In dogs, they
are associated with valve closure. Four
occur mostly in middle-aged to older
heart sounds can potentially be ausculted.

small-breed dogs and are thought to be

The first heart sound (S1) is associated with
evidence of early myxomatous AV valve
closure of the atrioventricular ( mitral and
degeneration causing mitral valve prolapse
tricuspid) valves, and the second heart

(as they are in people). A systolic murmur
sound (S
may or may not also be present. Although

2) with closure of the semilunar

( aortic and pulmonic) valves. The third
systolic clicks are reasonably easy to
heart sound (Sa) occurs in early diastole
distinguish from a gallop sound in a dog
and is a result of the ventricles vibrating at

(they are usually relatively loud and high
the frequency heard at the time of rapid
pitched whereas a gallop sound is soft and
cessation of ventricular filling, and the
low-pitched), they often sound identical to
fourth heart sound (S
a gallop sound in a cat. Thoracic radio4) is in late diastole and associated with atrial systole ( atrial
graphs can be used to help make the
contraction). All four sounds can be
distinction between the two. In cats, gallop
heard in a healthy horse. In healthy cattle,
sounds are heard only in those with severe
typically only S, and S2 are audible, although heart disease. Systolic clicks are usually S or S can sometimes be heard. IV fluid
heard in cats with an otherwise normal

3

4
administration in cattle can be used to
heart. So if the heart is not enlai·ged, the
accentuate Sa and/or S
sound is more likely a systolic click.

4. In dogs, cats, and
ferrets, S1 and S2 are the only heart sounds

Systolic clicks usually are single but may
normally audible. Less is known about heart be multiple and can vary in intensity ( even

HEART DISEASE AND HEART FAILURE

89
completely disappearing) depending on
pulmonic stenosis or subaortic stenosis ).

cardiac loading conditions. Rarely, a three

A classic regurgitant systolic murmur
heart-sound rhythm can be caused by a
demonstrates a constant intensity
bigeminal rhythm.

throughout systole and is commonly

Splitting of S, or 5
caused by mitral or tricuspid regurgitation

2: Splitting of S1 is
caused by discordant closure of the mitral

( eg, myxomatous degeneration of the

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and tricuspid valves, which can occur when
mitral valve) or a ventricular septa! defect.

there is asynchronous contraction of the

However, these murmurs may also change
ventricles as in left or right bundle-branch
intensity during systole. Diastolic murmurs
block, cardiac pacing, and ectopic
are typically decrescendo ( decreasing in
premature ventricular beats. Splitting of 8
intensity through diastole) and usually the

1
can also occur in healthy, large-breed dogs
result of aortic insufficiency (such as that
and in large animals. Delayed closure of the
caused by aortic valve infective endocardipulmonic valve (in relation to the aortic tis in dogs or degenerative disease in
valve) results in splitting ofS
horses). In horses, the murmur of aortic

2• Splitting ofS2
can be a normal finding in horses during
insufficiency is most commonly musical,
respiration. Abnormal splitting of 8
although "musical" in this context is a

2 has
been associated with pulmonary hypertentechnical term (single frequency). They sion, as in pulmonary emphysema of horses
may sound like a dive-bomber or grunting.

and severe heartworm disease in dogs.

A continuous murmur is most commonly

Other possible causes include a large atrial
the result of patent ductus arteriosus and
septa! defect, right bundle-branch block, or
occurs throughout systole and diastole. A
premature ventricular ectopic beats of left
continuous murmur varies in intensity over
ventricular origin. Delayed closure of the
time, typically being most intense at the end
aortic valve (paradoxical splitting of 8
of ventricular ejection (second heart

2)

might be heard with left bundle-branch
sound) and then decreasing in intensity
block or premature ventricular ectopic
through diastole. A to-and-fro murmur
beats of right ventricular origin. A split
describes a murmur that occurs both in
second heart sound is a subtle finding that
systole and in diastole ( eg, in an animal
usually must be heard several times before
with subaortic stenosis and aortic
it can be appreciated.

insufficiency).

In horses, early systolic and diastolic
murmurs can be noted in the absence of

Heart Murmurs: Heart murmurs are
heart disease or anemia. The point of
audible vibrations (sound) emanating from
maximal intensity is typically located over
the heart or major blood vessels. The vast
the left heart base. A short, high-pitched,
majority are due to turbulent blood flow
squeaking, early diastolic cardiac murmur is
brought on by high velocity blood flow that
sometimes heard in healthy, young horses.

produces a mixed-frequency murmur. Much

Often, a systolic heart murmur is heard in a
less commonly, they are due to vibrations of
cat without cardiac disease. Some of these
cardiac structures such as part of a valve
systolic murmurs are due to an increase in
leaflet or chordal structure that produces
right outflow tract flow velocity ( dynamic
a single frequency (musical) murmur.

right ventricular outflow tract obstruction).

Murmurs are typically defined relative to

Innocent cardiac murmurs are also
tin1ing (systole, diastole, continuous),
sometimes noted in immature cats and dogs
intensity (grade I-VI), and location (eg, left

( <3 mo old) and may be the result of a
apex, left base) but can also be characterrelative increase in stroke volume (stroke ized by frequency (pitch), quality (eg,
volume/aortic cross-sectional area).

musical), and configuration (eg, crescendo

Heart murmur intensity is classified as
decrescendo ).

follows: Grade I -
the lowest intensity

A systolic murmur is classically
murmur that can be heard, typically
described as either ejection ( crescendodetected only while auscultation is decrescendo) or regurgitant (holosystolic,
perfom1ed in a quiet room; Grade II-a faint
plateau). However, making this distinction
murmur, easily audible, and restricted to a
is often difficult, even for an experienced
localized area; Grade III-a murmur
examiner, especially when the heart rate is
immediately audible when auscultation
fast. Ejection-quality systolic murmurs
begins; Grade IV-a loud murmur
typically demonstrate the greatest intensity
immediately heard at the beginning of
during mid-systole and appear diamondauscultation but not accompanied by a shaped on phonocardiography. They are
thrill; Grade V -
a very loud murmur with a
most commonly produced by stenotic
palpable thrill; and Grade VI-an extremely
lesions at the semilunar valves ( eg,
loud murmur with a thrill and that can be

90

HEART DISEASE AND HEART FAILURE
heard when the stethoscope is just removed A pulse deficit is an absent pulse despite from the chest wall.

auscultation of a heart beat and is thus
detected during simultaneous auscultation

Arrhythmias: Arrhythmias are abnormaliand pulse palpation. This often occurs as ties of the rate, regularity, or site of cardiac
the result of a premature beat that occurs so
impulse formation and are noted during
early that the ventricles are unable to fill

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auscultation. Other terms such as dysrhythsufficiently, resulting in a reduced stroke mia and ectopic rhythm are also used to
volume that produces either a weak pulse or
describe arrhythmias. The presence of a
no pulse. Atrial fibrillation also produces
cardiac arrhythmia does not necessarily
pulse deficits as well as alternating pulse
indicate the presence of heart disease; some strength.

arrhythmias are normal, such as sinus

Dogs with severe subaortic stenosis may
arrhythmia in a dog and second-degree AV
have a pulse pressure that slowly increases
block in a horse; many cardiac arrhythmias
during ventricular systole and reaches a
are clinically insignificant and require no
peak pressure late in systole called pulsus
specific therapy. Some arrhythmias,
parvus et tardus. Pulsus paradoxus is a
however, may cause severe clinical signs,
decrease in pulse pressure during inspirasuch as syncope, or lead to sudden death.

tion and an increase in pulse pressure

Numerous systemic disorders may be
during expiration. This is a normal
associated with abnormal cardiac rhythms.

occurrence in animals, but it is too subtle to

(For discussion of specific arrhythmias, see
observe on physical examination. Animals
p 94.) Common auscultatory findings in
with cardiac t.amponade (severe pericardia!

animals with an arrhythmia are a rate that is
effusion), however, demonstrate an
too slow (bradycardia), a rate that is too fast exaggeration of this finding, so it becomes (tachycardia), premature beats (a beat is
detectable. Pulsus alternans is an alternatheard too early), an irregular rhythm, and ing strong and weak pulse while the animal
pauses in the rhythm. Whenever an
is in sinus rhythm; it can be noted (albeit
abnormal rhythm is heard, an ECG should
rarely) in animals with severe ( usually
be performed.

terminal) myocardial failure or tachyarrhythmias. Pulsus bigeminus is an Pulses: The arterial pulse is the rhythmic
alternating strong and weak pulse caused by
expansion of an artery that can be digitally
an arrhythmia such as ventricular bigeminy.

palpated ( or visualized) during physical

The weaker pulse ( during the ventricular
examination. Physiologically, the pulse
premature contraction) typically follows
pressure is the systolic pressure minus the
a shorter time interval than the stronger
diastolic pressure. The arterial pulse can be
pulse.

felt best in several different locations. For

Jugular venous pulsation can be noted
example, in dogs and cats, the arterial pulse
in normal animals but typically does
is typically palpated at the femqral artery. In
not extend beyond the thoracic inlet.

horses, the facial artery is usually used. To
feel the maximum pulse, an examiner must

Respiratory Sounds: Pulmonary edema
first occlude the artery with his or her
may develop as a result of congestive heart
fingers and then gradually decrease the
failure (CHF). Animals with pulmonary
digital pressure until the maximum pulse is
edema will be hyperpneic (increased rate
felt. A weak pulse ( a reduction in pulse
and depth of respiration) and may be
pressure) is usually caused by a decrease in
dyspneic. The increased depth of respirasystolic pressure and can be noted with tion may increase bronchovesicular sounds.

decreased stroke volume in animals in heart Fine, and less commonly, coarse crackles failure, hypovolemic shock, or cardiac
might be ausculted in animals with
t.amponade, as well as with subaortic
pulmonary edema, but fine crackles are
stenosis. However, a weak pulse can also be
usually heard only at the end of a deep
felt in a healthy animal if the artery is not
inspiration. Coarse crackles in dogs are
palpated appropriately or in an obese or
most commonly heard with chronic
heavily muscled animal. A bounding pulse
bronchitis. Pulmonary edema is often silent

( an increase in pulse pressure) is usually

(no auscultatory abnormality). Respiratory
caused primarily by a reduced diastolic
sounds may be absent in animals with
pressure and can be noted with aortic
pleural effusion, especially ventrally.

insufficiency and patent ductus arteriosus.

However, the pulse in a thin, athletic dog

Ascites: Abdominal distention may occur
may also feel stronger than expected. The
as a result of gas, soft tissue, or fluid
pulse felt with mitral regurgitation is often
accumulation. Animals with right heart
normal but at times may be termed "brisk"

failure ( eg, due to severe heartworm

HEART DISEASE AND HEART FAILURE

91
disease, severe tricuspid valve dysplasia,
obtain an accurate assessment of size and
cardiac tamponade) can develop ascites.

shape. In deep-chested breeds, even severe

Because there are many causes of ascites, it
cardiomegaly can look normal on the lateral
is important to evaluate the jugular veins in
view and, because the heart sits more
every case in which ascites is present. If
upright in the chest, can also mask its
right heart failure is the cause of the ascites,
presence on the DV view ( eg, in Doberman

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the jugular veins may be distended (but

Pinschers with DCM). Obesity also interferes
often are not in dogs and cats) by the
with accurate reading of cardiac size by the
increase in right atrial pressure. If the
presence of intrapericardial fat or by pushing
juguiar veins are not distended in a dog or
the diaphragm forward, reducing the size of
cat with ascites, a hepatojugular reflux test
the thoracic space and pushing the heart into
should be performed. To do this, one person
the cranial and narrower aspect of the
examines the jugular veins with the animal
thoracic cavity. Because of the marked
standing or sitting, while another places
variation in chest conformation, the changes
firm and steady pressure on the abdomen.

seen between inspiration and expiration,

In a dog or cat in right heart failure, the
and the changes seen between systole and
jugular veins should distend well up the
diastole, only relatively dramatic changes in
neck with this maneuver. If ascites is
overall cardiac size can be identified in most
present without jugular venous distension
dogs. Consequently, conditions such as
and with a negative hepatojugular reflux
mild generalized cardiomegaly cannot be
test, then extracardiac causes of the ascites
identified on thoracic radiographs. The one
should be considered.

chamber where mild, moderate, and severe
enlargement can be relatively accurately

Synchronous Diaphragmatic Flutter:

identified is the left atrium. Finding

The diaphragm may contract synchronously enlargement of specific cardiac chambers with the heart to produce loud thumping
and great vessels makes the presence of
noises on auscultation and usually visible
heart disease more likely and may also
contraction in the flank area The syndrome
provide clues as to the specific disease
results from stimulation of the phrenic
present.

nerve by atrial depolarization and occurs

Cardiogenic pulmonary edema is a
primarily when there is a marked electrolyte common finding in animals with CHF and or acid-base imbalance, particularly with
may be associated with pulmonary venous
hypocalcemia It is most common in horses
congestion. However, the identification of
and dogs. It is seen most commonly in dogs
pulmonary edema is often difficult and may
in association with hypocalcemia and
not be possible in some dogs and even some
electrolyte disturbances induced by GI
cats. Cardiogenic pulmonary edema in dogs
disease. Similarly, in horses it is seen with
is typically found in the caudodorsal aspects
hypocalcemia and in endurance horses that
of the lungs. In many cases, this region has
are dehydrated and electrolyte depleted.

an interstitial density that is enhanced by
age and by expiration, giving a false

Radiography
impression that pulmonary edema is
present or masking the presence of

Thoracic radiographs frequently provide
pulmonary edema Digital radiography
valuable information in the assessment of
units, especially if not set up perfectly (to
animals with or suspected of having heart
match analog units), have made the
disease. However, thoracic radiography is
diagnosis even harder in many cases. In
rarely performed in horses or cows to
animals with chronic left heart failure, the
evaluate heart disease because of the
left atrium is usually severely and always at
animal's large size and body conformation,
least moderately enlarged. In acute heart
which reduces the quality of the images. In
failure ( eg, chorda tendineae rupture), the
dogs, in which numerous different body
left atrium may not be enlarged. Pleural
types must be dealt with, chest conformation effusion can usually be readily identified must always be assessed before attempting
radiographically. In most species, this is
to evaluate cardiac size. On the lateral view,
seen with right or biventricular heart failure.

dogs can be normal, shallow-chested, or

However, in cats it is seen most commonly
deep-chested. On the dorsoventral (DV) or
with left heart failure. Resolution of these
ventrodorsal (VD) views, they can be
abnormalities on subsequent thoracic
normal, narrow-chested, or barrel-chested.

radiographs can be used as one indication

Many small breeds of dogs are shallowof efficacy of therapy. The presence of chested. This makes the cardiac silhouette
pulmonary edema or pleural effusion does
appear to be enlarged on the lateral view and
not definitively confirm a cardiogenic origin
often necessitates relying on the DV view to
or exclude another origin.

92

HEART DISEASE AND HEART FAILURE

Overall cardiac size can be assessed
enlargement. Tall R waves in leads that have
using the vertebral heart scale or score. This the positive electrode on the left and/or is most commonly done using the lateral
caudal aspect of the body (leads I, II, a VF,
projection. The maximal diameter of the

CV6LL, and CV6LU) are evidence of left
cardiac silhouette from cranial to caudal is
ventricular enlargement. Deep S waves
measured, as well as the distance from the
in the same leads in which the positive

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carina to the apex of the cardiac silhouette
electrode is on the left side of the heart

( dorsal to ventral). These lengths are added
or the presence of a right-axis deviation
together and measured in terms of thoracic
suggest right ventricular enlargement. Wide
vertebral bodies, so they are normalized for

QRS complexes can be seen in animals with
the size of the animal. The vertebral bodies
either right or left ventricular enlargement;
are measured from the fourth thoracic
however, they can also be due to conduction
vertebra caudally. The normal range is
disturbances ( see p 93). The ECG is very

8.5-10.5 vertebral bodies in dogs and 6.9-8.1 insensitive at identifying mild to moderate in cats. In many cases, it is more important
changes in chamber size and unacceptably
to try to accurately assess the size of the left
insensitive for detecting severe enlargeatrium than the overall size of the cardiac ment. Although false-positive findings are
silhouette.

less frequent than false-negative findings,
they do occur. Consequently, the accuracy is
unacceptable, especially when compared

Electrocardiography
with echocardiography and even with

Electrocardiography is the recording of
thoracic radiography.

cardiac electrical activity from the body
surface (surface ECG). It should primarily

Sinus Rhythm and Sinus Node
be used to identify cardiac arrhythmias. It

Abnormalities: The sinus node initiates
can also identify conduction disturbances
depolarization of the rest of the heart in a
that do not alter rhythm and has been used
healthy animal, sets the normal rate and
to identify chamber enlargement in dogs
rhythm, and is called the normal pacemaker
and cats. However, its inaccuracy in
of the heart. It functions as the pacemaker
identifying chamber enlargement and the
because it is automatic ( depolarizes on its
advent of diagnostic ultrasound have
own) and does so at a rate faster than the
diminished this role. As opposed to small
other automatic sites in the heart (AV node
animals in which the Purkinje fibers
and Purkinje fibers). Normal sinus rhythm
penetrate only - 1hof the way into the
is regular and originates at the sinus node,
myocardium, Purkinje fibers in horses and
indicated on the ECG by a P wave that
cattle penetrate throughout the myocarprecedes each normal QRS complex. The dium, resulting in "burst" depolarization
rate at which the sinus node fires varies
of the ventricles and reduced waveform
tremendously from species to species and
production and complexes on the surface
situation to situation. For example, a

ECG. Consequently, there is no relationship
healthy horse can have a heart rate of 30
between complex height on a surface ECG
bpm at rest and 250 bpm during maxin1al
and chamber enlargement. The most comexercise. Sin1ilarly, a healthy dog can have a mon ECG lead used in large animals is a
heart rate in the teens when asleep and �250
base-apex that produces large deflections
bpm during maximal exercise. A healthy cat
and is used for rhythm analysis. ECGs
can have a heart rate of 240 bpm at rest in an
should be used only to characterize an
examination room.

arrhythmia in an animal with an ausculta

Sinus bradycardia is a regular sinus
tory arrhythmia and to monitor rhythm
rhythm that is slower than expected for that
during anesthesia; they should never be
species and for the situation the animal is in.

used as screening tools, as they are in

Sinus bradycardia may be noted in animals
human medicine (primarily for changes
overdosed with anesthesia or agents that
secondary to coronary artery disease).

can result in increased vagal tone (primary
or secondary) or reduced sympathetic

Waveform Abnormalities: Chamber
tone (eg, xylazine, 13-adrenergic blocker),
enlargement can be indicated by waveform
hypothermic animals, hypothyroid animals,
abnormalities in dogs and cats, but these
animals with sick sinus syndrome, or in
abnormalities are commonly absent when
animals with increased vagal tone secondthere is chamber enlargement and are someary to systemic disease ( such as respiratory, times present when the heart is normal. In
neurologic, ocular, GI, or urinary tract
lead II in dogs and cats, wide or notched
disease). Treatment for sinus bradycardia is

P waves suggest left atrial enlargement,
typically not needed unless clinical signs
whereas tall P waves suggest right atrial
associated with the bradycardia, such as

HEART DISEASE AND HEART FAILURE

. 93
exercise intolerance, weakness, or collapse,
disease, or both. This is usually due to some
are noted. In dogs and cats, atropine (0.04
form of sick sinus syndrome ( see below).

mg,'kg, IV, IM, or SC) may be considered for

Atrial standstill is characterized as the
treatment of bradycardia. The initiating
complete absence of P waves on the ECG
cause should also be corrected.

and occurs as a result of the atria being

Sinus tachycardia is the finding of a
unable to be depolarized from the SA node

VetBooks.ir
regular sinus rhythm at a rate faster than
discharge. This occurs either because the
normal but generally appropriate for the
atrial myocardium is functionally unable
situation the animal is in ( eg, stress,
to be depolarized ( usually due to hyperexercise, heart failure). If the rate is kalernia), or because it has been destroyed
inappropriately high ( eg, 200 bpm in an
by a cardiomyopathy or myocarditis
otherwise healthy dog at rest at home),

(persistent atrial standstill). In hyperanother form of tachycardia ( eg, atrial or kalernia, the sinus node continues to
ventricular) should be considered. Causes
depolarize, and the electrical tracts from the
include stress (resulting in high sympathetic sinus node to the AV node (intemodal tracts) drive), exercise, hyperthyroidism, fever,
continue to function, so the sinus node
pain, hypovolemia, cardiac tarnponade,
controls the rate ( albeit at a slower rate).

heart failure, or administration of agents

With persistent atrial standstill, the sinus
that can increase the rate of sinus node
node is destroyed, so the animal usually has
discharge (eg, catecholamines). Treatment
an AV nodal Gunctional) escape rhythm with
involves resolving the underlying cause.

a heart rate in the 40-65 bpm range ( dog).

Sinus arrhythmia occurs as a result of

Sick sinus syndrome is a constellation
irregular discharge of the sinus node most
of abnormalities, including ECG changes
commonly associated with the respiratory

( sinus arrest, junctional or ventricular
cycle. The site of impulse formation remains escape complexes, and possibly supraventhe sinus node; however, the frequency of tricular tachycardia) and possible weakness
the discharge varies. Sinus arrhythmia is a
or syncope from the bradycardia ( usual)

normal finding in dogs and horses; it is
or tachycardia (rare). With this clinical
abnormal in cats in the hospital setting,
syndrome, the principal problem either lies
although it appears to be more common in
within the SA node or perinodal tissue, or is
cats in their home environment. Respiratory due to increased vagal tone, or both. In sinus arrhythmia is characterized by an
some instances, other portions of the
increase in heart rate with inspiration and a
specialized conduction tissue of the
decrease with expiration. In dogs, sinus
myocardium, including the AV node, can
arrhythmia can also be seen that is not in
also be affected. Therefore, evidence for AV
sync with respiration. The variation in heart
block may also be seen (see below). This
rate is associated with variation in the
condition is commonly noted in geriatric
intensity of vagal tone. It is abolished
dogs, including Miniature Schnauzers and
by reduced vagal tone resulting from

American Cocker Spaniels. Medical therapy
excitement, exercise, or administration of
consisting of parasyrnpatholytics ( eg,
vagolytic drugs such as atropine. It may be
propantheline bromide, 0.25----0.5 mg,'kg, PO,
associated with a wandering pacemaker,
bid-tid) or syrnpathominletics ( eg, extendedwhich is characterized on the ECG by taller release theophylline, 10 mg,'kg, PO, bid;

P waves during faster rates and smaller P
terbutaline, 0.14 mg,'kg, PO, bid-tid in dogs)

waves during slower rates.

to increase heart rate can be tried, but these

Sinoatrial (SA) block occurs when the
are often ineffective or are effective for only
impulse from the SA node fails to be
a relatively short time or with unacceptable
conducted through the surrounding tissue
adverse effects. These drugs may also
to the atria and ventricles. Thus, no P waves
worsen supraventricula.r tachyarrhythrnias
or QRS complexes are noted on the ECG,
that can occur with sick sinus syndrome.

and the P-P interval surrounding the break

The most effective treatment for the
in sinus rhytlun is an exact multiple of the
bradycardia is pacemaker implantation.

normal P -P interval. This is often difficult to
diagnose in dogs because sinus arrhythmia

AV Conduction Disturbances: Atriois common, resulting in a variable nom1al ventricular (AV) block refers to alteration

P-P interval.

of impulse conduction through the AV

Sinus arrest (sinoatrial arrest, sinus
node from the atria to the ventricles. In
pause) is the absence of P waves on the
first-degree AV block (prolonged conduc

ECG for a short period (typically accepted
tion), the conduction time is increased and is
as a pause exceeding twice the normal
recognized on an ECG as an increased PR

P-P interval). Sinus arrest is caused by
interval. This is clinically silent. In secondexcessive vagal tone, inllerent sinus node degree AV block (intermittent conduction),

94

HEART DISEASE AND HEART FAILURE
occasional impulses fail to be conducted

The significance of the AV block varies by
through the AV node, bundle of His, or both
species. Both first- and second-degree AV
bundle branches and is characterized by
block may be present without outward
occasional P waves not followed by QRS
evidence of cardiac disease. First-degree AV
complexes. During the block, there is no
block may result from excessive vagal tone

S, or 82 and no arterial pulse. In horses, the
and usually is not significant in dogs or

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sound associated with atrial contraction
horses unless other evidence of heart

(84) is commonly heard, and the occurrence
disease or pathologic cause of increased
of 8 not followed by other heart sounds is
vagal tone ( eg, CNS or pulmonary disease)

4
diagnostic for second-degree heart block.

or AV nodal disease is present. In all species,

84 may also be audible in dogs with
second-degree AV block may be indicative of
second-degree AV block, but this is much
heart disease. However, in horses, Mobitz
less common. When the PR intervals
type I is common and is a normal physiologic
preceding the dropped beat progressively
response resulting from increased vagal
lengthen, the condition is known as Mobitz
tone. Mobitz type II second-, high-grade
type I second-degree AV block or Wencksecond-, and third-degree (complete) AV
ebach phenomenon. This is usually due to
blocks are always abnom1al in all species.

high vagal tone and is the most common type

Second- and third-degree AV blocks may
of second-degree AV block seen in horses
be caused by fibrosis, neoplasia, or ir\jury to
and puppies. No treatment is indicated. If the
the AV node, or by hypoxia, increased vagal

PR intervals do not change, the condition is
tone, or electrolyte abnormalities. The ideal
known as a Mobitz type II second-degree AV
treatment would be to correct the underlyblock. Again, no treatment is indicated, but ing cause, although this is not usually
closer swveillance may be warranted to see
possible. High-grade second-degree AV
whether the block progresses to a more
block and third-degree AV block can cause
severe form. A third type of second-degree
exercise intolerance or, more commonly,

AV block, high-grade second-degree AV
weakness, collapse, and syncope. Oral
block, refers to the situation when the block
therapy with extended-release theophylline
occurs with every other beat (2: 1 [ie, two P

(10 mgtkg, PO, bid), terbutaline (0.14 mgtkg,
waves for every QRS complex]) or more (3: 1, PO, bid-tid in dogs), or propantheline 4:1, etc). High-grade second-degree AV block bromide (0.2fr.-0.5 mgtkg, PO, bid-tid) may is distinguished from third-degree AV block
occasionally be useful in animals with
by identifying an association between the
second-degree AV block, but more

QRS complexes and the P wave preceding
aggressive therapy (pacemaker implantaeach one ( same PR interval for each). Dogs tion) is usually indicated in symptomatic
with high-grade second-degree AV block can

( eg, syncopal) anin1als. Third-degree heart
have signs the same as dogs with thirdblock is usually associated with irreversible degree AV block ( eg, syncope) and are also
lesions; the only effective treatment in dogs
at increased risk of sudden death.

is pacemaker implantation. Dogs with

In third-degree AV or complete heart
third-degree AV block are at risk of sudden
block, none of the impulses is conducted
death and so should have a pacemaker
from the atria to the ventricles. The atrial
in1planted regardless of clinical signs. In
rhythm (P waves) occurs more rapidly and
cats, third-degree AV block often produces
independently from the ventricular rhythm
no clinical signs and so requires no therapy.

(QRS complexes; a form of AV dissocia

However, problems can arise if it is not
tion), which originates from subsidiary
identified before anesthesia, and some cats
pacemakers (AV node or Purkinje fibers in
will faint and thus require pacemaker
the ventricles; nodal and ventricular escape inlplantation. Third-degree AV block is rare beats, respectively). The heart and pulse
in horses and other species. Pacemakers
rates are usually regular but slow and
have been inlplanted successfully in species
generally unresponsive to factors or
other than dogs and cats but has rarely been
agents that usually increase heart rate
done.

(eg, exercise, excitement, atropine). The
difference in timing between atrial and

Common Tachyarrhythmias: Tachyventricular contractions results in variation arrhythmias can be divided into supravenin ventricular filling and consequent tricular and ventricular based on their site
variation in intensity of S, (bruit de canon)

of origin. Supraventricular premature
and possibly arterial pulse pressure.

complexes are premature complexes (as

Periodically, the atria contract when the
seen on an ECG) that originate from ectopic
ventricle is in systole, which results in a

( nonautomatic) sites above the ventricles
pulsation in the jugular vein ( cannon A

( eg, atrial myocardium and AV node). They
wave).

may also be called atiial or nodal premature

HEART DISEASE AND HEART FAILURE

95
complexes/depolarizations/contractions/
node because of its nom1al long refractory
beats. Possible sites for ectopic depolarizapetiod, so the ventricular rate is slower than tions include the SA node (rare), atrial
the atrial rate.

myocardium (very common), and AV node

In dogs and cats, atrial fibrillation is

(AV junction). Electrocardiographically,
an even more rapid (>600-700 atrial
supra ventricular premature complexes are
depolarizations/min) atrial rhythm that
identified by a QRS complex that usually
results in a slower (in the 80-300 bpm range

VetBooks.ir
appears relatively normal but occurs earlier
in dogs) and always irregular ventricular
than the next expected normal QRS
rhythm. As in atrial flutter, the AV node is
complex. Variable P wave morphologies
bombarded by frequent atrial depolarizamay be noted before or after the supraventions. The AV node acts as a filter, allowing tricular premature complex or may be
only some of the depolarizations to reach
hidden in the preceding sinus complex or
the ventricles but always in an irregular
within the premature complex. Supravenfashion. In dogs and cats, atrial fibrillation is tricular premature complexes are most
characterized on the ECG by a supravencommonly a result of atrial enlargement or tricular ( normal-appearing QRS complexes)

disease, stress, or other causes of increased
and an irregular vent1icular rhythm that is
sympathetic tone. Supraventricular
most commonly fast. Once those charactertachycardia (SVT) is a series of supravenistics are identified, the next thing to look tricular premature complexes occurring
for is the absence of P waves and an
consecutively. It may be short (nonsusundulating baseline that can appear almost tained) or occur for prolonged periods
flat (fine) or very rough (coarse). The

( called sustained when >30 sec). SVT most
irregular rhythm results in variation in the
commonly ranges in rate from 200-350 bpm
diastolic filling period of the ventricles,
in dogs. At rates closer to 200 bpm, it may be
resulting in variability in stroke volwne and
indistinguishable from sinus tachycardia on
thus variability in pulse character, including
a surface ECG. Vagal maneuvers ( ocular
pulse deficits. This also causes variation in
pressure, carotid sinus massage), precordial the intensity of the heart sounds, especially blow ( chest thump), and IV drug administrathe second heart sound, creating a heart tion (eg, diltiazem) often "break" an SVT
that sounds like "tennis shoes in a dryer"

into sinus rhythm and either do not change
on auscultation in dogs. In dogs, atrial
or more gradually slow a sinus tachycardia.

fibrillation is most commonly associated

Diltiazem (0.5--4 mg/kg, PO, tid) is the most
with underlying cardiac disease. The
common drug used to treat SVT long-tenn,
notable exception occw-s in some giant dog
but it can also be used IV to break the SVT
breeds, such as Irish Wolfhounds, Scottish
into sinus rhythm (0.25 mg/kg, IV bolus

Deerhounds, Great Danes, and others, in
administered over 2 min, followed 15 min
which the rhythm can develop with an
later by up to 0.35 mg/kg, IV bolus adminisotherwise normal heart (so-called lone tered over 2 min, if needed). Digoxin and
or primary atrial fibrillation). Lone atrial

[3-blockers are also used. An accessory
fibrillation is the most common form seen
pathway (bypass tract) is a congenital
in horses ( see below). All cats in atrial
abnormality that forms an electrical connecfibrillation have severe underlying heart tion between an atJiurn and a ventricle
disease.

outside the normal connection (AV node/

The goal of treatment of atrial fibrillation
bundle of His). These pathways have been
in most dogs and all cats is control of the
recognized in dogs and cats and may result
ventricular rate, ie, the frequency with
in supraventricular tachycardia ( eg,
which QRS complexes are generated from
orthodrornic reciprocating tachycardia).

the fibrillatory depolarization waves. Rate

Treatment may include radiofrequency
control is usually accomplished with
catheter (heat) ablation of the bypass tract
digoxin alone, diltiazem alone, or a
or, more commonly, oral medications such
combination of the two. Diltiazem alone is
as procainamide, sotalol, or diltiazem.

generally more effective then digoxin alone,

Atrial flutter is a rare arrhythmia that
and the combination is generally more
often progresses to atrial fibrillation. It is
effective than either alone. A [3-blocker,
most commonly caused by a reentrant loop
such as atenolol, may also be used but never
within the atria and is classically characterin combination with diltiazem. These drugs ized on the ECG by a "saw-toothed" baseline prolong the refractory period of the AV node with relatively nom1al QRS complexes that
and slow AV nodal conduction, resulting in
can appear in a regular or irregular rhythm.

fewer atrial depolarizations crossing the AV

The atrial rate of discharge is very rapid
node to the ventricles. Arniodarone has also

(>400 bpm). Only intennittent atrial
been used to control the ventricular·
in1pulses are conducted through the AV
response rate, but its adverse effects

96

HEART DISEASE AND HEART FAILURE

(hepatic and thyroid toxicities) limit its use
toxicity is more likely to develop. Horses
to second-line therapy in animals refractory
with atrial fibrillation can also be successto the digoxin and diltiazem/atenolol fully converted to sinus rhythm electrically
protocol. In rare instances, electrical

( cardioversion). This requires the careful
cardioversion ( defibrillation of the·heart
placement of electrode catheters in a
that is synced to the ECG to prevent causing pulmonary artery and the right atrium (via VetBooks.ir
ventricular fibrillation) is used to convert
the jugular vein) of an awake horse followed
atrial fibrillation to sinus rhythm. This is
by anesthesia and then delivery of electrical
generally more rational in a dog with lone
shocks of increasing intensity through the
atrial fibrillation but has also been done in
catheters. This method is very successful
dogs with severe cardiac disease. In those
but is time-consuming and expensive. Most
instances, sinus rhythm commonly reverts
horses can return to successful racing
back to atrial fibrillation within weeks to
performance after conversion. However,
months, necessitating reconversion or
some will revert to atrial fibrillation over
rate control. Cardioversion is frequently
time. Conversion to sinus rhythm is not
combined with arniodarone administration
indicated in horses with severe underlying
in an attempt to prolong the time until
cardiac disease, because tl1e likelihood of
reversion to atrial fibrillation.

conversion, or maintenance of sinus rhythm

In runtinants, atrial fibrillation is usually
if converted, is very low.

paroxysmal and associated with GI tract

Ventricular premature complexes arise
disorders (eg, vagal indigestion), but it also
from a site within the ventricular myocarmay be persistent and occur as a sequela dium or specialized conduction system. On
of cor pulrnonale or with other cardiac
the ECG , the QRS complex usually appears
diseases.

wide and is followed by a large T wave that

In horses, atrial fibrillation can usually
is opposite in polarity to the QRS complex.

be diagnosed by identifying an undulating

This produces a large, bizalTe complex
baseline. It most often occurs in the absence when compared with nom1ally sinus-driven of underlying cardiac disease (primary or

QRS complexes, occurs earlier than the
lone atrial fibrillation) and is associated
next expected sinus-driven QRS complex
with the normally high vagal tone found

(ie, premature), and does not have an
in horses that most likely have some
associated preceding P wave, although
predisposition for the arrhythmia However, unassociated P waves going at a slower it may also occur secondary to cardiac
rate (AV dissociation) may be seen. Most
disease such as mitral insufficiency, aortic
commonly, these complexes occur from
insufficiency, myocarditis, pericarditis, or
noncardiac causes such as anesthesia, age,
untreated congenital cardiac defects. The
electrolyte abnormalities, acute toxicities,
resting heart rate is usually within the
neoplasia ( eg, splenic hemangiosarcoma in
normal range when there is no underlying
dogs), gastric distention ( eg, gastric dilation
cardiac disease, whereas it is typically
and volvulus syndrome in dogs), or trauma.

increased with underlying disease; this may

They may also be associated with ventricuhelp identify the cause of the arrhythmia on lar myocardial diseases such as DCM,
physical examination. Most horses with
arrhythmogenic right ventricular cardioprimary atrial fibrillation exhibit no clinical myopathy (Boxer eardiomyopathy), and
signs at rest or with moderate exercise or
myocanlitis.

work; however, more strenuous exercise

Ventricular tachycardia is tl1e occurrence
or work may result in evidence of reduced
of three or more sequential ventricular
cardiac output. This can be seen in
premature complexes. These can again be
racehorses who are evaluated for a sudden
nonsustained or sustained (>30 sec). They
reduction in race performance. In this
can also be divided into slower, benign
setting, the clinical signs could also be due
ventricular tachycardias and faster,
to paroxysmal atrial fibrillation, which can
malignant ones. A slower, benign ventricube identified only during the exercise lar tachycardia is called an accelerated
period. In horses with primary atrial
idioventricular rhythm (AIVR) and is
fibrillation, conversion to sinus rhythm with
commonly seen in dogs in the intensive
quinidine at a dosage of22 mg/kg, PO, every
care unit secondary to systemic ( often

2 hr until conversion, is still the treatment of intra-abdominal) disease or trauma. It is choice. The success rate for conversion is
characterized on the ECG by the presence
greatest in horses with atrial fib1illation of
of a ventricular tachycardia that is relatively
shorter duration. The chance for success is
slow (usually <200 bpm). Sinus rhythm may
considered excellent if the duration is <4
be interspersed with the AIVR, with one
mo and relatively good if >4 mo, although
rhythm taking control of the rhythm
conversion may take longer and quinidine
whenever it is slightly faster than the other.

HEART DISEASE AND HEART FAllURE

97

Fusion beats (hybrid sinus beat and
ventricular premature complexes, atrial and
premature ventricular contraction [PVC])

ventricular tachycardia) or to slow the
can also be seen. This arrhytlunia does
ventricular rate in animals with atrial flutter
not result in sudden death and usually
or fibrillation. Many of these drugs are being
dissipates on its own within 48-72 hr.

supplanted by automatic implantable

As such, it only needs to be treated ( eg,
defibrillators in human medicine, so the

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lidocaine) if it is causing hemodynamic
manufacture of these drugs is waning. Some
instability.

of the antiarrhythmics have negative

Malignant ventricular tachycardia is
inotropic effects, with the potential to
most commonly found in dogs with severe
worsen active CHF. This is most likely to
underlying cardiac disease, usually either a
occur with the use of J3 -blockers in the
cardiomyopathy ( eg, DCM or arrhythmotreatment of supraventricular tachyarrhythgenic right ventricular cardiomyopathy) mias and with sotalol.

or severe semilunar valve stenosis ( eg,

Atrial fibrillation is one of the most
subaortic stenosis, pulmonic stenosis).

commonly treated tachyarrhytlunias; it is

Malignant ventricular tachycardia
imperative to decrease the ventricular rate
predisposes the animal to sudden death
to s160 bpm if the rate is faster than that in
due to the tachycardia degenerating into
the clinic. In experimental situations, pacing
ventricular fibrillation. Frequently, this
the heart of a dog at a rate ;;:180 bpm results
arrhythmia is not identified, so the first
in myocardial failure severe enough to cause
clinical sign seen is sudden death. Some

CHF within weeks. Consequently, leaving
dogs ( especially Boxers and Doberman
the rate this high will cause further cardiac

Pinschers) will experience syncope as
disease and decompensation. There are no
the result of a very fast ( often >400 bpm)

firm data to suggest that keeping the heart
ventricular tachycardia that spontaneously
rate even lower than 160 bpm is beneficial in
reverts back to sinus rhythm within seconds dogs. Diltiazem (0.5--2 mg/kg, PO, tid) or a (must last >6 sec and usually lasts no more
combination of diltiazem and digoxin are
than 1 min) of its onset. Sotalol or a
generally the preferred methods of
combination of atenolol and mexiletine
controlling the ventricular rate in dogs with
effectively controls the arrhythmia in
atrial fibrillation. A low dose of a J3-blocker,

Boxers and usually stops the syncope and
such as atenolol (0.25 mg/kg, PO, bid), may
presumably prevents sudden death.

also be used instead of diltiazem, but its use

J3-blockers are frequently administered to
is uncommon. (See a/,so ANTIARRHYTIIMJCS, dogs with severe subaortic stenosis and to
p 2535.)

some with severe pulmonic stenosis in an

Ventricular tachycardia can degenerate
attempt to prevent sudden death. Proof of
into ventricular fibrillation and cause
efficacy is lacking. Sotalol may be a more
sudden death. Fast ventricular tachycardia
logical choice. Ventricular tachycardia must

(>250 bpm) and ventricular tachycardia in
be distinguished from ventricular escape
animals with severe underly.mg cardiac
rhythm, as seen with third-degree AV block,
disease, such as subaortic stenosis, DCM,
and from idioventricular rhythm, a terminal
and arrhythmogenic right ventricular
ventricular escape rhythm. A ventricular
cardiomyopathy ([ARVC] Boxers), are
escape rhythm is a slow rhythm (2�0
most vulnerable to dying suddenly from
bpm) that occurs because higher pacemakventricular tachycardia. In Boxers with ers (SA and AV nodes) have failed. Sup

ARVC, sotalol (0.5--3 mg/kg, PO, bid;
pression of a ventricular escape rhythm by
most commonly 80 mg/dog, PO, bid)

drug therapy ( eg, lidocaine) results in
or a combination of mexiletine
cessation of all cardiac electrical activity

(5--8 mg/kg, PO, tid) and atenolol

(ie, death).

(0.5--1 mg/kg, PO, bid) can effectively

Ventricular fibrillation is a result of
reduce or, more commonly, stop the
microreentrant circuits within the
syncope ( usually due to a ventricular
ventricular myocardium, resulting in the
tachycardia firing at a rate of >400 bpm)

absence of effective ventricular contracseen in these dogs. It also obviously tions; thus, it is a terminal rhythm. The only
decreases the incidence of sudden death
effective treatment is electrical defibrillaand so commonly results in years of tion.

survival. A minority of Boxers with ARVC
develop true DCM and are also prone to

Antiarrhythmics: A detailed discussion
sudden death. Doberman Pinschers with
of antiarrhytlunic therapy is covered

DCM also commonly die suddenly due to
elsewhere (seep 2535). Most antiarrhythmic ventricular tachycardia. In these instances, drugs are administered to suppress ectopic
the negative inotropic effects of sotalol can
premature depolarizations ( eg, atrial and
either push a dog into heart failure or make

98

HEART DISEASE AND HEART FAILURE
existing heart failure worse. Consequently,
and motion of valves and visualization of
if sotalol is to be used in either of these
congenital abnormalities ranging from a
patient populations, the dose must be
defect in the interventricular septum to
started low and titrated upward carefully,
a stenotic pulmonary valve. Blood flow
with pimobendan administered concurvelocity is also commonly measured, and rently. Mexiletine can also be used alone
turbulent blood flow is identified using

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but, at least in theory, is not as effective at

Doppler echocardiography. Pressure
preventing sudden death. Amiodarone
gradients, blood flow volumes, and several

(12-15 mg/kg/day, PO, for 2 wk [loading
indices of cardiac function can be calcudose J followed by 5--7 mg/kg/day, PO) is lated. Echocardiography can also identify
probably more efficacious at preventing
changes in myocardial tissue texture
sudden death than mexiletine but has many
indicative of ischemia and fibrosis and
more adverse effects. Doberman Pinschers
delineate masses, valvular vegetations,
appear to be particularly susceptible to the
pericardia! effusion, and many other
hepatotoxic effects of the drug.

features previously verifiable only with

Animals with chronic bradyarrhythmias as cardiac catheterization or at necropsy.

seen with AV block (high-grade second or

There are four main types of echocardiogthird degree) or sick sinus syndrome most raphy: three-dimensional, two-dimensional,
commonly present with weakness, episodic

M-mode ( one-dimensional), and Doppler.

weakness/collapse, and syncope. Pacemaker Two-dimensional echocardiography implantation is the treatment of choice. If
provides a wedge-shaped, two-dimensional
pacemaker implantation is not a viable
image of the heart in real-time. Several
option, anticholinergics, phosphodiesterase
standard long-axis and short-axis views

(PDE) inhibitors, or sympathomimetics may
obtained from standard imaging windows
be administered. Propantheline is a mild
on the thorax have been developed for dogs,
anticholinergic dosed at 0.25--0.5 mg/kg, PO,
cats, horses, and cows. M-mode echocardibid-tid. The parenteral formulation of ography is produced by a one-dimensional
atropine may be administered PO but must
beam of ultrasound that penetrates the
be diluted 10: 1 with com syrup at a dosage
heart, providing an "ice-pick view" over
of0.04 mg/kg, PO, tid-qid. Adverse effects
time. The tissue interfaces that are
include mydriasis, dry mucous membranes,
encountered by the beam are then plotted
tachycardia, and GI stasis. Theophylline is
on a screen. This mode of evaluation has
a nonselective PDE inhibitor with modest
been typically used to measure chamber
positive chronotropic effects. Extendeddimensions, wall thickness, valve motion, release tablets or capsules can be given at
and great vessel dimensions but, as frame

10 mg/kg, PO, bid. Ifno adverse effects are
rate of two-dimensional echocardiography
seen and the desired clinical effect is not
has improved, this mode has lost some of its
achieved, the dosage in dogs can be
usefulness. Three-dimensional echocardiincreased to 15 mg/kg, PO, bid, while ography is the newest modality and is still in
monitoring for adverse effects, and in cats to
its infancy. Doppler echocardiography uses

20 mg/kg, PO, every 24-48 hr. Adverse effects the principle of changing frequency of the may include restlessness, excitability,
ultrasonic beam after it contacts a moving
tachycardia, or GI upset. Terbutaline is a
structure ( eg, RBCs, cardiac wall) to

13-agonist that has more polent positive
measure velocity. Doppler echocardiograchronotropic effects but with similar adverse phy is further divided into spectral (pulsed effects to those seen with theophylline. It is
and continuous wave), color flow, and
dosed to effect at 1 .25--5 mg/dog (not per kg),
tissue Doppler echocardiography. Color

PO, tid, and 0.625 mg/cat, PO, bid. Attempts
flow Doppler echocardiography is a form
to overcome clinically significant bradyarof pulsed Doppler echocardiography prone rhythmias with oral therapy are often
to aliasing when high velocity flow is
unrewarding, although overall clinical signs
encountered, allowing high velocity (and
may improve in some animals.

therefore turbulent) flow in the heart and
great vessels to be detected. Continuous

Echocardiography
wave Doppler is used to quantitate high
velocity flow and thus used to calculate

Echocardiography, the use of diagnostic
pressure gradients, most commonly across
medical ultrasound to evaluate the heart
the regions of valves, using the modified
and proximal great vessels, complements

Bernoulli equation ( 4 x velocity2). Tissue
other diagnostic procedures by quantifying

Doppler imaging is used to measure the
chamber dimensions, wall thicknesses, and
lower velocity motion of cardiac structures,
the dynamic events of the cardiac cycle; it
most commonly ventriculai· walls, in an
also allows visualization of the anatomy
attempt to quantitate regional myocardial

HEART DISEASE AND HEART FAILURE

99
function. Variations include measuring
occurred, cardiogenic shock may predomistrain and strain rate.

nate, but even in this situation, acute
chordal rupture is the most common cause

Cardiac Catheterization
of acute heart failure in animals and results

Cardiac catheterization involves the
in an increased left atrial pressure and thus
placement of catheters into cardiac
pulmonary edema.

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chambers and surrounding great vessels to

Initial changes in cardiac chamber
measure pressure, inject contrast agents,
dimension (volume) or wall thickness that
and place devices. The latter is commonly
occur are best understood in relation to
termed interventional cardiology. Indicapreload (the tension imposed by venous tions include diagnostic evaluation ( eg,
return on the ventricular walls at end-diaswhen other diagnostic tests are insufficient tole) and afterload (the tension imposed on
to identify specific cardiac abnormalities or
the ventricular walls at end-systole).

are unable to identify the severity of a

Alterations in preload or afterload may be
lesion), presurgical evaluation ( eg, to help
caused by structural cardiac abnormalities,
diagnose constrictive pericarditis before
systemic compensatory mechanisms, or
surgery), therapeutic intervention, and
both. Volume overload states, such as those
clinical research. Diagnostic and presurgithat occur with chronic valvular disease/
cal cardiac catheterization, however, have
valvular insufficiencies, patent ductus
largely been replaced by echocardiography.

arteriosus, atrial or ventricular septa!

Currently, most cardiac catheterizations are defects, peripheral left-to-right shunts, interventional procedures to address
anemia, or hyperthyroidism, cause an
cardiac defects (eg, closure of a patent
increase in preload that leads to ventricular
ductus arteriosus).

growth and chamber enlargement

( euphemistically called dilation) via
eccentric myocyte hypertrophy. Pressure

HEART FAILURE
overload states, such as those that occur

Heart failure is a clinical syndrome that
with pulmonary or systemic hypertension,
occurs secondary to severe, overwhelming
and pulmonic or aortic stenosis, cause an
cardiac disease. It occurs because the heart
increase in after load ( systolic intraventricuis no longer able to maintain normal venous/ lar pressure) that leads to ventricular wall capillary pressures, cardiac output, and/or
thickening via concentric hypertrophy.

systemic blood pressure. It is most

Neither volume nor pressure overload is
commonly caused by a chronic disease that
synonymous with heart failure; either state
results in a severe decrease in myocardial
may result in heart failure, depending on the
contractility, severe regurgitation or
severity of the overload and the degree of
shunting, or severe diastolic dysfunction.

compensation.

However, it is common to have all three
abnormalities present simultaneously (but

Systolic Dysfunction
with one predominating). By far, the most

Systolic function is a broad classification
common clinical manifestations seen with
of cardiac function that encompasses all
heart failure are directly due to edema and
of the entities in systole that are capable
effusion ( congestive or backward heart
of altering blood flow into the aorta. It
failure). Much less commonly, animals
includes (but is not limited to) heart rate,
present because of signs referable to a
myocardial contractility, preload, afterload,
decrease in cardiac output (forward heart
hypertrophy (volume and pressure
failure). Very rarely, they present in
overload), leaks, and shunts. Diseases that
cardiogenic shock (low blood pressure due
alter.systolic cardiac function can become
to decreased cardiac output). This occurs
severe enough to overwhelm the ability of
because the cardiovascular system operates the cardiovascular system to compensate under a system of priorities. Its three
for the systolic dysfunction (primarily renal
primary functions are to maintain a normal
sodium and water retention, leading to
blood pressure and normal cardiac output,
hypervolemia, leading to increased venous
both at a normal venous/capillary pressure.

return to the heart, leading to increased

When the system is overwhelmed, it allows
stretch on the myocardium, leading to
venous/capillary pressure to increase first
myocardial growth and a larger left

( and so allows edema or effusion to form)

ventricular chamber [ eccentric or volume
and then allows cardiac output to fall. Only
overload hypertrophy]) and thus cause
after cardiac output has fallen remarkably
heart failure. The most common disease
does cardiogenic shock occur. In acute
that alters systolic function is mitral
heart failure, before any compensation has
regurgitation. Here, in systole, a portion of

100

HEART DISEASE AND HEART FAILURE
the blood flow that should be ejected into
more so by the myocardial fibrosis that
the aorta is ejected backward through the
builds up over time when severe disease is
mitral valve from the left ventricle into the
present. Restrictive cardiomyopathy is
left atrium. When the regurgitation is mild
another classic example of diastolic

( <500/o of the blood flow goes backward) to
dysfunction, but it is much less common.

moderate (50%---75% goes backward), the

Diastolic dysfunction also occurs in

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left ventricle is able to compensate for the
pericardia] diseases that cause cardiac
leak by growing larger (volume overload
compression (pericardia] effusion,
hypertrophy) and increasing the total stroke constrictive pericarditis ). With pericardia]

volume it ejects. When regurgitation is
disease, right heart failure ( eg, ascites)

severe(> 75% backward flow), the
predominates because systemic ( eg,
compensatory mechanisms may become
hepatic) capillaries leak more easily (leak
overwhelmed, resulting in an increase in left profusely at a pressure of 10 mmHg) than atrial pressure and so pulmonary edema
pulmonary capillaries (which can generally

The classic example of systolic dysfunction
withstand a pressure up to 20 mmHg
is dilated cardiomyopathy (DCM), in which
without leaking).

an inherent myocardial disease results

CHF may also occur if a tumor or other
in a decrease in myocardial contractility
anatomic obstrnction impedes venous

(myocardial failure). The decrease in
return to one or both atria. Pericardial
myocardial contractility results in an
disease or �ffusion leading to decreased
increase in the end-systolic diameter/
ventricular filling may also be thought of as
volume of the left ventricular chamber
an extracardiac cause of CHF Iatrogenic

(muscle is weaker and cannot contract
volume overload (ie, aggressive IV fluid
down as far in systole) and a decrease in
therapy) can lead to edema formation in
myocardial contraction (the an10unt of wall the absence of primary heart disease.

motion [shortening fraction or fractional
shortening] seen on an echocardiogram).

Compensatory Mechanisms

Again, the left ventricle grows larger to
compensate for this disease, but when the

Systemic blood pressure and blood flow
myocardial failure is severe, compensation

( and thus oxygen delivery to peripheral
can no longer maintain a normal diastolic
tissues and organs) is under strict neuroenpressure in the left ventricle (kidneys docrine control. Compensatory mechacontinue to retain sodium and water) and nisms act rapidly to correct any decreases
this increased pressure backs up into the
in blood flow and/or pressure. Acute
left atrium, pulmonary veins, and pulmocompensatory mechanisms, such as nary capillaries, creating pulmonary
increased sympathetic tone, are generally
edema.

short-lived and useful only for situations
that demand an acute change in cardiac
function (eg, hypovolemia). Chronic

Diastolic Dysfunction
mechanisms of cardiac compensation

Diastole can be roughly divided into early
generally take over within days of the onset
myocardial relaxation and late filling that
of a cardiac disease and are viable for years.

is altered primarily by compliance

They are responsible for the heart's ability

(!/stiffness). Most ventricular diastolic
to compensate for chronic disease. These
dysfunction severe enough to cause heart
remarkable mechanisms allow for an
failure is due to myocardial fibrosis, thus
animal to compensate for mild, then
due to a decrease in ventricular compliance
moderate, and then even severe disease,

(an increase in stiffness). When a ventricle
often for years. Only at the very end of a
is less compliant or stiffer than normal, for
chronic disease do they contribute to the
any given volume of blood that fills the
formation of heart failure and require
chamber in diastole, the pressure is higher.

medical intervention.

This increase in diastolic pressure (when

When a decline in stroke volume occurs
the AV valves are open) is transmitted back
secondary to cardiac dysfunction, cardiac
up into the atrium, veins, and capillary beds
output decreases. The acute response is an
behind the affected ventricle, resulting in
increase in sympathetic tone leading to
transudation of fluid and signs referable to
peripheral vasoconstriction, increased
edema or effusion. The classic example of a
heart rate, and increased cardiac contractildisease that primarily causes heart failure ity that serve to restore cardiac output and
due to diastolic dysfunction is hypertrophic
maintain systemic blood pressure. This
cardiomyopathy. Diastolic function is
effect fades within days as events such
compromised to some degree by the
as i3-receptor down-regulation occur.

thickening of the myocardium itself but

Chronically, the renin-angiotensin-aldoste-

HEART DISEASE AND HEART FAILURE·

101
rone system (RAAS) is activated. Activation
concentric or pressure overload hypertrois initiated by events such as decreased phy. In this situation, sarcomeres again
renal perfusion, leading to decreased
replicate within cardiac myocytes but in
sodium delivery to the macula densa
parallel ( side by side), to grow a wider

(which interacts with thejuxtaglomerular
myocyte and a thicker ventricular wall.

apparatus). The juxtaglomerular cells

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release renin, which converts angiotensinogen (synthesized in the liver) to angiotensin Cardiac Biomarkers

I. Angiotensin-converting enzyme (ACE)

A biomarker is a measurable characteristic
converts angiotensin I to angiotensin II,
that reflects the severity or presence of
chiefly in the lungs. A separate tissue RAAS
some disease state. Blood pressure,
exists in the brain, vascular, and myocardial
cholesterol, garnrna-glutamyl transferase,
tissues, which can generate angiotensin II
and BUN are all biomarkers. Studies in dogs
independently of the renal, or systemic,
and cats have shown that increased blood

RAAS.

concentrations of BNP ( most commonly

Angiotensin II has widespread effects,

N-terminal pro-B-type natriuretic peptide
including stimulation of aldosterone

[NT-proBNP]), ANP, and endothelin-1 are
synthesis and release from the adrenal
indicators of cardiac disease.that increase
glands, increased thirst via stimulation
proportionately with progressive cardiac
of antidiuretic hormone (ADH) release,
disease and CHF Cardiac troponin I ( cTnl),
increased norepinephrine and endothelin
which is released after cardiomyocyte.

release, and stimulation of cardiac
death, has also been evaluated as a
hypertrophy. Aldosterone forces the renal
biomarker for cardiac disease but found
distal tubules to retain sodium and water.

to be less sensitive than those mentioned

This, plus the effect of ADH, causes an
above. ANP, BNP, and cTnl have also been
increase in circulating blood volume. The
evaluated as screening tools for occult DCM
increased blood volume leads to an increase (before onset of CHF) in dogs. Increased in venous return to the affected ventricle.

levels of BNP were found to be highly

This chronic increase in preload stimulates
sensitive for the detection of occult DCM,
the myocytes to add in new sarcomeres
whereas ANP and cTnl were relatively less

(contractile elements), leading to the
sensitive. NT-proBNP is cleaved from BNP
growth of longer myocytes. This creates
in equal amounts in response to increased
a larger ventricle (larger chamber with
cardiac filling pressures ( myocardial
normal wall thickness (volume overload
stretch) and ischemia, and its greater
or eccentric hypertrophy]).

stability-and longer half-life make it more

In response to these compensatory
suitable for use as a diagnostic biomarker.

mechanisms, counter-regulatory systems

Several studies have demonstrated the
are in place such as the release of atrial
usefulness of NT-proBNP in differentiating
natriuretic peptide (ANP) from the atria,
between cardiac and primary respiratory
and B-type natriuretic peptide (BNP) from
causes of dyspnea in dogs and cats. A rapid
the atria and ventricles. ANP and BNP are
assay is available for this use in cats.

released in response to stretch of the atrial

Biomarkers such as NT-proBNP and
anp ventricular chambers. Both hormones
troponin I should never be evaluated in
setve to increase natriuresis (with
isolation, because they are not lOOOAi
subsequent diuresis) a.pd decrease
accurate. Instead, they should be used in
systemic vascular resistance, thus
concert with other diagnostic modalities.

countering the effects of the RAAS.

The effects of ANP and BNP are greatly
outweighed by those of the RAAS and

Clinical Manifestations
other systems in animals with chronic

The hemodynamic changes that occur in
disease. Again, this is beneficial up until
heart failure are relatively limited, as are
the end, when the RAAS continues to force
the clinical syndromes resulting from these
sodium and water retention despite the
changes. Much depends on the location(s)

presence of edema and effusion.

of cardiac chamber failure, as well as on

In situations when the heart must deal
species differences.

with higher than normal systolic intraventricular pressures ( eg, subaortic stenosis, Left Heart Failure: The pulmonary
p�onic stenosis, systemic arterial
veins drain into the left atrium. Left atrial
hypertension), the affected ventricle must
pressure increases as left heart diseases
contract aga,inst a greater force. Much like
worsen ( eg, from regurgitant blood flow and
skeletal muscle when it is forced to lift a
increased circulating blood volume). An
heavier weight, cardiac muscle undergoes
increase in left atrial pressure is transmitted

102

HEART DISEASE AND HEARTFAILURE
to the pulmonary veins and to the pulmoin1proves once pulmonary edema is treated.

nary capillaries. Pulmonary capillary

In some, it is associated with coughing and
hydrostatic pressure continues to increase,
is most likely a vagally mediated event (tranpromoting the transudation of fluid out sient asystole ). The syncope is frightening
of the capillaries and first into the lung
to the owner, but sudden death is rare
interstitium and then into the alveoli as the
unless associated with DCM or subaortic
pressure increase becomes more severe.

stenosis.

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Simply put, pulmonary edema develops and

The diagnosis of congestive left heait
becomes worse as heart failure progresses.

failure ( cardiogenic pulmonary edema) in

In animals, this first causes tachypnea and
dogs is classically made radiographically.

then dyspnea Most owners do not notice

However, the inability to take a radiograph
the tachypnea and so do not seek veterinary
during a deep inspiration is a diagnostic
attention until dyspnea is present. This
obstacle. Consequently, the caudodorsal
often makes it look like the onset of the
lung fields on a lateral radiograph, where
heart failure was acute, when, in fact, it was
cardiogenic pulmonary edema is usually
chronic.

identified, often have an interstitial density

Some dogs and a few cats and horses will
that is either mistaken for pulmonary
cough with cardiogenic pulmonary edema.

edema or hides pulmonary edema This is

Cough is a much more common manifestaexacerbated in older dogs. Most dogs with tion of primary lung disease in all species.

severe pulmonary edema can be identified

Coughing is always present in dogs with
radiographically, but those with mild to
chronic bronchitis. One manifestation of
moderate edema are often problematic. In
chronic bronchitis is airway collapse
these dogs, it is often beneficial to send tl1e

(tracheomalacia and bronchomalacia) on
dog home (if it is stable) to have the owner
radiographs. Bronchomalacia appears to be
count the dog's sleeping respiratory rate
evidence of chronic bronchitis in dogs.

(SRR). The owner must be taught how to

When the left atriun1 is enlarged, a collapsed count respiratory (breathing) rate and then left mainstem bronchus can often be seen
count the rate preferably while the dog is
above the left atrium, because the large left
sound asleep and in a cool environment. A
atrium highlights this finding. It does not
normal dog has an SRR <30 breaths/min, so
appear that the large left atrium actually
a rate greater than that is abnormally high
compresses this bronchus.

(ie, the dog has tachypnea). All dogs with

Animals with heart failure may also be
pulmonary edema have an increased SRR
exercise intolerant due to lower than

(are tachypneic). However, dogs with
normal cardiac output during exercise
respiratory disease/failure can also have
and/or hypoxemia, which is caused by
an increased SRR. Therefore, once an
pulmonary edema or pleural effusion. This
increased SRR is docun1ented, the dog
is a rare presenting complaint in cats,
should be started on furosemide at a dosage
because they usually do not exercise. The
of at least 2 mg/kg, PO, bid. If the SRR
same is true for many dogs. In dogs, most
decreases, then the diagnosis of left heart
true exercise intolerance (fatigue with
marked tachypnea or dyspnea) is due to
respiratory failure rather than heart failure.

However, most "exercise intolerlmce" ends
up being due to something else and is not
true exercise intolerance. Instead, it is
frequently an unwillingness to exercise
because of other conditions, such as
orthopedic disease or obesity. A dog that is
truly exercise intolerant looks and sounds

"out of breath." A severe decrease in cardiac output results in cold extremities (paws,
ears) and can lead to total body hypothe1°
mia, especially in cats. Although syncope

(transient loss of consciousness due to a
transient decrease in cerebral metabolic
substrate, most commonly oxygen) is not
a sign of or directly due to heart failure, it
may also be noted in dogs in heart failure,

Lateral radiograph of a dog with cardiogenic
especially in small-breed dogs with chronic
pulmonary edema due to severe mitral
valvular disease. In many instances, the
regurgitation. Note the large body of the
left atrium almost touching the spine.

cause is unknown. However, syncope often

Courtesy of Dr. Mark D. Kittleson.

HEART DISEASE AND HEART FAILURE

103
failure is confirmed. The same can be done
addressed. These are accomplished through
in cats for both puhnonary edema and
reducing preload and/or afterload ( diuretics
pleural effusion. All healthy cats have an
and vasodilators ), improving cardiac

SRR <40 breaths/min, with most <30
performance (positive inotropes, positive
breaths/min. Once the diagnosis is
lusitropes, antiarrhythmics), and using
established, the owner should continue
neurohormonal modulators (ACE
to count the SRR daily and titrate the
inhibitors, and potentially (3 -blockers,

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furosemide dosage to keep the SRR within
aldosterone antagonists, and angiotensin
the normal range. In dogs thought to be in

II receptor blockers).

an impending stage of heart failure (large
left atrium but no pulmonary edema), the

Diuretics: The loop diuretics are the owner can also be instructed to count the
single most effective agents used to

SRR daily to weekly in an attempt to identify decrease circulating blood volume and heait failure at an early stage. Owners
reduce signs referable to edema and
should also always be instructed to keep a
effusion in animals in heart failure. They act
log and bring it with them at each recheck.

via inhibition of the Na+ IK + /2 CJ- co trans

In cats, left heart failure also commonly
porter in the thick ascending loop of Henle.

manifests as pleural effusion. The visceral

This leads to increased renal sodiun1 and
pleural veins (veins on the surface of the
chloride excretion, with subsequent free
lung) drain into the left heart rather than the
water loss. Furosemide is the most widely
right heart. This also occurs in people and
used loop diuretic. When administered IV, it
dogs. The exact reason for this phenomalso directly reduces pulmonary capillary enon is not fully understood. The pleural
wedge pressure (before onset of dturesis)

effusion may be a modified transudate,
via local prostaglandin synthesis, which has
pseudochylous, or chylous in cats with left
a vasodilatory effect. The onset of action
heart failure. A small volume of pericardia!

after IV administration is 5 min, with effects
effusion can also be seen in cats with heart
peaking at 30 min and lasting -2 hr. The
failure and is generally of no hemodynai11ic
onset of action after oral administration is
consequence (pericai·diocentesis is not

60 min, with peak effects seen at 1-2 hr and
required). Cats also often stop eating and
lasting -6 hr.

may stop drinking when in heart failure.

Emergency therapy of puhnonary edema
often requires high doses of IV or IM

Right Heart Failure: The right atrium
furosemide ( 4-8 mg/kg for dogs; 2-4 mg/kg
receives systemic ai1d cardiac venous and
for cats), repeated at 60-to 120-min
lymphatic drainage via the cranial and
intervals until clinical signs, usually
caudal vena cavae and the coronary sinus.

referable to pulmonary edema (ie,

Right atrial pressure increases as right heart
tachypnea, dyspnea), are controlled.

disease worsens due to diseases such as

Because of the concern for dehydration,
tricuspid valve insufficiency and pulmonary
azotemia, and significant electrolyte
hypertension. Clinical manifestations of
disturbances with overzealous furosemide
right heart failure include jugular venous
administration, tape1ing to a lower dosage
distention, hepatomegaly, pleural effusion,
as soon as the respiratory rate decreases is
pericardia! effusion, ascites, and peripheral
mandatory. Once the pulmonary edema is
edema. Dogs and cats are more likely to
controlled, the dosage that keeps the
develop ascites (although 1ight heart failure
sleeping respiratory rate (SRR) normal is
is uncommon in cats). Horses and cows
recommended. Mild to moderate prerenal
more commonly develop subcutaileous
azotemia and electrolyte and acid-base
edema ventrally. In dogs and cats,jugular
disturbances (hyponatremia, hypokalemia,
venous distention may not be evident
and a hypochloremic metabolic alkalosis)

without inte1vention. A hepatojugular
are common and are generally well
reflux test is often useful (seep 91).

tolerated, so can be safely ignored (albeit
monitored carefully) as long as the animal is
eating and drinking. Oral doses used to man

Management
age chronic CHF may vary significantly
between animals; in theory the lowest

Management of heart failure is primaiily
possible dosage should be used, but care
directed at controlling clinical signs related
must be exercised, again via monitoring
to the presence of organ edema and cavity

SRR, not to lower the dosage too far. In
effusion ( eg, pulmonai-y edema, pleural or
dogs, CHF is often initially controlled at
pericardia! effusion, and ascites ). In some
dosages of 1-2 mg/kg, bid; cats are more
anin1als, decreased cardiac output, and
sensitive to the development of adverse
even cardiogenic shock, need to be
effects and generally require lower dosages

104

HEART DISEASE AND HEART FAILURE

(0.5---2 mg/kg every 12-24 hr). The maximal
in management of refractory heart failure in
dosage in dogs is generally 4 mg/kg, PO, tid.

which furosemide resistance has been

In cats, it may be closer to 2 mg/kg, PO, tid,
documented or when furosemide is not
but dosages as high as 4 mg/kg, tid, may
tolerated. The starting dosage is approxibe required. Use of furosemide or other mately one-tenth that of the current
diuretics as sole therapy in long-term
furosemide dose (take total daily cmrent

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management of CHF increases RAAS
dose of furosemide, multiply times 0.1, and
activation; thus, combination with an ACE
divide that dose bid). Most commonly that
inhibitor is generally recommended.

translates into a dosage of 0.1-0.3 mg/kg,

Furosemide resistance, typically defined
bid. However, dosages as high as 1 mg/kg,
by persistent signs of heart failure despite
bid, have been used in a few dogs with
dosages of 4 mg/kg, PO, tid, often develops
ascites but only using careful upward
in advanced cases of CHF. There are many
titration.

causes of diuretic resistance, including

Thiazide diuretics ( eg, hydrochlorothiremarkably severe cardiac disease, azide, chlorothiazide) decrease sodimn
decreased delivery of the drug to the
resorption via inhibition of the Na+/Clnephron (low cardiac output), activation of cotransporter in the distal convoluted
the RAAS (which counteracts the effects of
tubule. This results in increased sodiun1
ditrresis), and hypertrophy of the distal
and water delivery to the collecting ducts
convoluted tubular cells with consequent
and subsequent increased hydrogen and
increases in ion transport in this region of
potassium excretion. Although the thiazides
the nephron. GI edema secondary to right
are relatively weak diuretics, they do exert a

CHF may decrease absorption of orally
synergistic effect when administered with
administered diuretics and contribute to
loop diuretics and can cause profound
diuretic resistance. Animals with resistance
electrolyte abnonnalities (particularly
to chronic high doses of oral furosemide
hypokalemia) and dehydration when used
may thus have an improved diuretic
in combination if not used judiciously.

response from parenteral ( eg, SC)

Hydrochlorothiazide is more commonly
administration of the drug or from addition
used, with a recommended dosage of 1-4
of other diuretic agents ("diuretic stackmg/kg, PO, 1-2 times/day. It is also used as a ing"). In other cases, switching to torsemide
combination product with the potassium

(see below) may be the best option.

spaiing diuretic spironolactone (see below), Adverse effects seen with furosemide
which may be dosed at l-4 mg/kg, PO, 1-2
administration are generally related to dehytimes/day. Many animals do not tolerate dration from volume depletion, reduced
dosages at the higher end of this range, and
cardiac output and glomerular filtration
the lowest effective dosage should be used.

rate (GFR), and electrolyte and acid-base

Chlorothiazide is dosed at 20-40 mg/kg, PO,
abnormalities. Less common adverse

1-2 times/day. Thiazide diuretics are
effects include .vomiting, pancreatitis, and
generally reserved for those cases in which
idiosyncratic deafness with rapid IV
resistance to furosemide has developed.

administration. Anin1als with preexisting

Potassium-sparing diuretics are the
renal disease are more likely to develop
weakest of the diuretic class, exhibiting
adverse effects, and furosemide therapy
little to sometimes undetectable diuretic
should be reduced or temporarily witheffect at standard dosages, especially when drawn accordingly. Renal values should be
used alone in healthy dogs. Although they
monitored frequently when starting diuretic
may produce more diuresis in a dog in heart
therapy ( on initiation and at least 1 wk later) failure, they should never be relied on to and should be reassessed at least every 3----6
produce diuresis in an a.Jlimal in heart
mo during chronic administration. Some
failure. They should also never be used to
animals may remain mild to moderately
replace a loop diuretic; they are used only as
azotemic (usually with a greater increase in
adjunctive (add-on) agents. Drugs in this

BUN than in creatinine ), which is generally
class include the aldosterone inhibitors
tolerated provided they are eating and
spironolactone and eplerenone and those
drinking adequately.

that block sodium resorption at the distal

Torsemide is a newer loop diuretic that
tubules, trian1terene and ainiloride.

has better and more consistent bioavailabil

Spironolactone is currently the only one
ity (better and more consistent GI
used clinically in veterinary medicine. A
absorption), has a longer duration of action
large-scale clinical trial in people with heart

( can be administered less frequently), and is failure in the 1990s demonstrated significant more potent ( requires a lower dose) than
improvement in morbidity and mortality in
furosemide in dogs. Although there is less
patients with myocardial infarction
experience with this agent, it can be useful
administered spironolactone versus

HEART DISEASE AND HEART FAILURE

·105
placebo, in addition to standard heart
to myxomatous mitral valve degeneration,
failure,ther3111t-J! was subsequently shown
a study in Beagles with mild, naturally
that the beneficial effect was all due to
occurring mitral regurgitation demonstrated
spironolactone's antifibrotic effects in the
increased valvular lesions in dogs treated
myocardium, not its diuretic properties.

with pirnobendan compared with dogs

Only one discredited study from Emope
treated with benazepril. Preclinical studies

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has suggested benefit in dogs in heart
by the manufacturer suggest the san1e tiling
failure. In theory, spironolactone may be
might occur in healtlly dogs. A clinical study
of benefit in dogs with DCM, because
is nearing completion that looks at
myocardial fibrosis is·a component of
pimobendan vs placebo in small dogs with
this disease. It is unlikely that myocardial
mitral regurgitation before onset of heart
fibrosis and diastolic dysfunction are
failure to determine whetller it prolongs the
important components of the pathophysioltime to onset of heait failure. A study in ogy of primary mitral regurgitation. In one

Doberman Pinschers with DCM but no heart
study, spironolactone had no benefit in cats
failure suggested tllat low-dose pirnobendan
with hypertrophic cardiomyopathy before
administration may prolong the time until
tl1e onset of heart fail me, another disease
the onset of heart failure or sudden death.

with myocardial fibrosis. Eplerenone has

Neither of these disparate endpoints was
demonstrated a myocardial protective
statistically significant on its own, but the
effect in dogs with experin1entally induced
combined endpoint was.

myocardial infarction and heart failure.

The combination of increased inotropy

Spironolactone is used by many
with mild afterload reduction results in
veterinary cardiologists for its theoretical
improved cardiac output and reduced
benefits. It may be beneficial in some dogs
cardiac filling (diastolic) pressures in dogs
with refractory ascites or in those in which
in heart failure due to either rnitral
clinically significant hypokalemia has
regurgitation or DCM. Clinical in1provedeveloped. It is dosed at 1-3 mg/kg, PO, ments seen with pirnobendan may include

1-2 times/day.

improved quality of life, improved clinical
scores, and a longer survival time. It is not

Positive lnotropes: Pimobendan is a
unusual for a dog to improve clinically more
novel inodilator (inotropic drug and
than expected, and it is theorized that tile
vasodilator) approved by the FDA in 2007
drug may also have nonspecific phosphodifor use in dogs witll CHF related to atrioesterase-inhibiting properties (possibly ventricular valve insufficiency or DCM.

sinlilar to those of caffeine). Consequently,

It is classified as a calcium sensitizer and
the clinical improvement seen may not
a phosphodiesterase (PDE) ill inhibitor.

always be because of improvement in heart

The parent compound (pimobendan) is
failure. No studies to date have investigated
responsible for the calcium sensitization,
the effects of combining pirnobendan witll
while an active metabolite ( desmethylpian ACE inhibitor, but most ve�rinary mobendan) is a PDE III inhibitor (-100
cardiologists feel tllat tl1is combination may
times more potent tllan pimobendan).

confer additional clinical benefits. The

Pimobendan sensitizes cardiomyocyte
inotropic effect of pimobendan is significontractile proteins ( mostly tropo.nin C) cantly greater than tllat seen with digoxin,
to calcium, and desmethylpirnobendan
and pimobendan has supplanted digoxin for
increases cyclic AMP and calciun1 cycling
inotropic support in CHF in dogs.

within the cell. Myocardial oxygen

Pirnobendan effectively decreases
consumption is increased, as for any
calculated pulmonary artery systolic
positive inotropic agent, in healthy dogs.

pressure (tricuspid regurgitantjet velocity)

Vasodilation occurs via vascular PDE III
in dogs witll pulmonary hypertension
inhibition, leading to endothelial smooth
secondary to mitral regurgitation. Whetller
muscle relaxation and calcium efflux.

this decrease is due to tile expected

Vasodilation includes coronary artery
decrease in left atrial pressure, pulmonary
vasodilation, which leads to increased
arterial vasodilation, or both, is unknown.

coronary blood flow and increased

There are no studies that have shown tllat
myocardial oxygen delivery. Additional
pin10bendan is beneficial in dogs witll
beneficial effects may include improved
pulmonary hypertension due to causes
myocardial relaxation, anti-inflan1matory
other than left heait failure.

and anticytokine effects, and neurohumoral

There is ongoing debate regarding the use
modulation.

of pimobendan in cats. Pirnobendan is not

Pirnobendan is not approved for use
approved for use in cats, and tile package
in dogs before tile onset or heart failure.

insert states that it is contraindicated in cats

Witll regard to mitral regurgitation due
with hypertrophic cardiomyopatlly,

106

HEART DISEASE AND HEART FAILURE
although several studies have suggested
vascular resistance, although oc-adrenergic
that the drug is safe in cats, even those
stimulation ( as occurs with dopanline at
with hypertrophic cardiomyopathy, when
higher doses) can lead to vasoconstriction.

administered at the same dosage as in dogs.

Dobutarnine is administered IV as a

However, a pharrnacokinetic study showed
continuous-rate infusion at 2.5--20 mcg/kg/
that the serum concentration of pimobendan min diluted in 5% dextrose. Dosages > 15

VetBooks.ir
in cats given a canine dose results in a
mcg/kg/min are rarely required and can be
serum pimobendan concentration 10 times
associated with increased tachyarrhyththat seen in dogs. Cardiac pathology is mias. Starting at a lower dosage with
found in dogs administered 3--5 times the
uptitration every 15--30 min as required
recommended dose. It is unlikely any
is recommended. Concurrent ECG
species that experienced a similar calcium
monitoring is strongly recommended,
sensitization effect as dogs could swvive
and if arrhythmias worsen, the dosage
a dose 10 times the recommended dose,
of dobutarnine should be reduced or
which suggests that cats are somehow very
dobutarnine should be discontinued.

different. This requires more investigation

Because dobutarnine increases conduction
before rational recommendations can be
through the AV node, additional caution is
made with regard to using pimobendan in
advised in atrial fibrillation. Dobutarnine
cats. However, anecdotally and in one
may preferentially increase myocardial
retrospective study, pimobendan has been
flow, as compared with dopamine, which
used in cats with CHF from any cause and
tends to increase renal and mesenteric
has been beneficial clinically. Consequently, flow. Dobutarnine also tends to cause less if a cat is no longer responding to conventachycardia than dopamine. Dopanline is tional heart failure drug therapy, pimobendan administered as a continuous-rate infusion ( 1.25 mg/kg/cat, bid) may be tried.

at 2-8 mcg/kg/min; higher dosages ( > 10

Pimobendan is dosed at 0.2-0.3 mg/kg,
mcg/kg/min) are associated with vasocon

PO, bid, in dogs. With progression of heart
striction and tachycardia. Gradual
failure, many veterinary cardiologists
uptitration is recommended, as with
increase the dosing frequency in dogs to tid
dobutarnine. Both dopanline and dobuor double the dose. Adverse effects are rare tamine may cause GI upset. These agents
and generally seen at high dosages but may
are less commonly used in cats, although
include GI upset (anorexia, diarrhea). There the same general treatment strategy may is no clinical evidence supporting a
be followed, but starting at more conservasignificant increase in arrhythmias in tive infusion doses (-1 mcg/kg/min) for
animals treated with pimobendan; although
both dobutan1ine and dopamine.

some studies demonstrated such a trend,

The bipyridine compounds (rnilrinone,
others refuted this. There clearly was noarnrinone, or inamrinone) are PDE Ill inhibiincrease in the incidence of sudden death in tors. Inhibition of PDE Ill reduces the
the aforementioned study of Dobem1an
degradation of cAMP, with subsequent

Pinschers with subclinical DCM.

effects sinlilar to those seen with syrnpatho

The sympathomimetic amines ( eg,
rnimetic anlines. These agents are generally
dobutarnine, dopamine) improve contractilreserved for animals with severe refractory ity and cardiac output via l3.adrenergic
myocardial failure, because their use is
agonist effects and can be valuable in the
associated with a higher level of mortality
acute management of cardiogenic shock
than that seen with the syrnpathornimetic
or CHF secondary to myocardial failure.

anlines. Because of lack of dependence on

Stimulation of the membrane-bound 13

13-receptor stimulation, PDE III inhibitors
receptor activates adenyl cyclase, leading to are unaffected by 13-receptor downregulathe production of cAMP and subsequent tion or uncoupling that may occur with
phosphorylation of membrane-bound
progressive cardiac disease and may be
calcium channels on both the sarcolemma
useful in clinical situations when benefits of

(myocyte membrane) and sarcoplasrnic
syrnpathornimetic therapy are less than
reticulum. These cellular actions increase
expected. Additionally, vascular PDE III
myocardial contractility and relaxation, as
inhibition and lack of oc-adrenergic
well as oxygen consumption. Effects on ion
stimulation results in vasodilation. Adverse
channels in cardiac pacemaker cells and
effects noted with PDE III inhibitors include
conduction fibers lead to decreased
tachycardia, tachyarrhythmias, thrombocydepolarization threshold, increased heart topenia, GI upset, and hypotension at higher
rate, and increased conduction velocity, all
dosages. Amrinone is dosed at 1-3 mg/kg,
of which predispose to cardiac arrhythmias. IV, or as a constant-rate infusion at I 0-80

In the peripheral vasculature, mixed 131 and
mcg/kg/min. Milrinone is dosed at 30--300

132 stimulation has a negligible effect on
mcg/kg (loading dose), followed by 1-10

HEART DISEASE AND HEART FAILURE

107 .

mcg/kg/min constant-rate infusion ( start
discontinued (usually for at least 1-2
low and titrate).

days) and the dosage subsequently
reduced by at least 50%.

Cardiac Glycosides: The digitalis
glycosides ( eg, digoxin ) are relatively

Angiotensin-Converting Enzyme
weak positive inotropes (inhibit sodium

(ACE) Inhibitors: ACE inhibitors

VetBooks.ir
potassium ATPase pumps on cell surlace
competitively inhibit ACE, which converts
membrane) that increase vagal tone to
angiotensin I to angiotensin IL This blunts
the heart (primarily to supraventricular
the increase in systemic vascular resistregions), have a narrow therapeutic range, ance, hypertrophy, and aldosterone release
and are associated with significantly more
caused by angiotensin II. ACE inhibitors
adverse effects than pimobendan when
are mild balanced vasodilators. They may
administered in doses that produce toxicity.

reduce systemic vascular resistance up

Digitoxin is no longer commercially
to 25%, improving cardiac output and
available. Although used infrequently for its
reducing regurgitant fraction in mitral
inotropic effects since the introduction of
regurgitation, although these effects are
pimobendan, digoxin still plays an
rarely clinically apparent. Additional
important role in cardiac disease, particubenefits include a reduction in left larly in atrial fibrillation or supraventricular
ventricular filling pressure and thus
tachycardia with concurrent CHF, because
pulmonary edema. It is thought that the
it is the only available pharmacologic agent
beneficial effects of ACE inhibitors are
that slows AV nodal conduction without
primarily due to neurohormonal modulaconcurrent negative inotropic effects. (For tion, in addition to hemodynarnic benefits.

a complete discussion, seep 2529.)

Studies in dogs with CHF have demon

Rapid (IV) digitalization commonly
strated improved clinical scores when
results in toxicity and is not recommended.

an ACE inhibitor was added to standard

Digoxin may be administered at a conservatherapy ( diuretics with or without digitalis tive starting dosage of 0.003--0.005 mg/kg,
glycoside), although those benefits have

PO, bid. Adequate serum concentration is
generally been mild and apparent only for
not achieved until the second day of
short times. lrnprovements have generally
administration, and a serum digoxin
been more apparent in dogs with DCM than
concentration should be checked 4-7 days
in those with myxomatous mitral valve
after initiation of therapy, � hr after the
degeneration. A trend toward prolonged
last dose is given. The therapeutic serum
survival has been seen in some studies.

concentration is in the range of 0.5-2 ng/mL.

ln general, veterinary cardiologists agree

There is no added benefit to a higher serum
that an ACE inhibitor is indicated in dogs
concentration within that range, so trying to with CHF. The benefit of ACE inhibitor keep it in the lower end of the range is
therapy before the onset of CHF is more
recommended. Dosage adjustments should
controversial, although two prospective
be based on the animal's serum digoxin
studies and one retrospective study have
concentration and clinical response. If
shown no benefit in dogs with mitral
digoxin is used in cats, it may be started at
regurgitation due to myxomatous mitral
one-fourth of a 0.125-mg tablet every third
valve degeneration. One retrospective study
day for cats <5 kg and every other day for
has suggested mild benefit in Doberman
cats >5 kg. Some larger cats may ultimately

Pinschers with DCM. Studies of ACE
tolerate doses as high as one-fourth of a
inhibition in cats are limited, and none has

0.125-mg tablet daily. An alcohol-based
shown a true statistical benefit of ACE
elixir form is available, although cats
inhibition beyond what is gained from
generally dislike the taste.

standard diuretic therapy in cats with CHF.

Adverse effects are increasingly likely

These studies had low patient numbers,
at higher serum concentrations and
however, and most cardiologists do
generally occur in order of GI ( anorexia,
prescribe an ACE inhibitor in addition to
vomiting), cardiac (bradycardia, AV block, appropriate background therapy for cats premature ventricular contractions), and
with CHF. No benefit has been shown in

CNS derangements. Because of its ability
delaying the progression of occult
to slow electrical conduction as well as
hypertrophic cardiomyopathy.

increase intracellular calcium, digoxin can

The primary serious adverse effect of
cause almost any cardiac arrhythmia, and

ACE inhibition is related to excessive
it is contraindicated in cases of AV block,
efferent glomerular arteriolar vasodilation
significant bradycardia, and rapid
due to an acute decrease in plasma
ventricular tachycardia. If adverse effects
angiotensin II concentration, resulting in
are noted, the drug should be temporarily
a functional azotemia due to a reduced

108

HEART DISEASE AND HEART FAILURE
glomerular filtration rate (GFR). This is
constant-rate infusion. The major adverse
relatively rare but can happen in any anin1al
effect is systemic hypotension ( with or
given an ACE inhibitor. There are no known
without weakness, tachycardia, or
predictors in cats or dogs. Anorexia,
vomiting); thus, concurrent blood pressure
vomiting, and lethargy (uremia) may occur,
monit01ing is reconm1ended. However, its
so owners should be warned to watch for
duration of effect is very sh01t (1-2 n1in) so

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these clinical signs. Renal function tests
if problems arise, they dissipate rapidly

(BUN, creatinine) should be measured
once the infusion is stopped. Sodiwn
before starting an ACE inhibitor and again
nitroprusside is diluted in 5% dextrose and

3--7 days later. Many clinicians wait until a
can be started at 1-3 mcglkg/min, with
dog is hemodynamically stable before
careful uptitration every 5--10 min to desired
starting an ACE inhibitor. Although cough is
effect, or staited at 5 mcglkg/min and the
a common adverse effect of ACE inhibitor
anin1al and/or blood pressure more
therapy in people, this is not seen in dogs
cai·efully monitored. A dosage of 5--10
and cats.

mcglkg/min is usually sufficient to control

Enalapril is the only approved ACE inhibiclinical signs, and rarely is > 10 mcg/kg/n1in tor in the USA for dogs with CHF lt is
required. Prolonged administration(> 16 lu-)

generally dosed at 0.5 mg/kg, PO, bid. ACE
increases the risk of cyanide toxicity (see
inhibitors are "all-or-nothing" drugs, so
the package inse1t).

giving a lower or less frequent dose

If nitroprusside U1erapy is unavailable
probably produces no effect. Long-tem1
or undesired, nitroglycerin ointment and
dosing in cats is recommended at 0.5 mg/kg/
isosorbide dinitrate ( venodilation only)

day (most commonly 2.5 mg/cat), PO. ACE
might be tried, but neiU1er is usually
inhibitors are not emergency drugs. Clinical
clinically beneficial. However, they are
benefits, if any, are not commonly seen
extremely unlikely to produce harm.

before 2-3 wk. Renal values should be moni

Nitroglycerin is absorbed transcutai1eously
tored periodically ( at least every 6 mo)

by the person administering the drug, so
while on long-term ACE inhibitor therapy.

gloves must be worn dwing administration.

Other ACE inhibitors used for treatment

It is applied at-';.\ in. per 5 kg ( dogs and
of heart failure include benazepril (0.25-0.5
cats) eve1y 6-8 hr on a hairless region such
mg/kg/clay, PO), captopril (0.5--2 mg/kg, PO,
as the ilmer pinna or inguinal region. The
tid), and lisinop1il (0.5 mg/kg, PO, 1-2 times/
latter may be preferable il1 anin1als with
day). Unlike enalapril and other ACE
poor peripheral perfusion, in which the
inhibitors that are renally excreted,
pinnae and extremities may be cool to the
benazepril undergoes significant hepatobiltouch. The drug should be wiped or cleaned iary elin1ination ( as much as 5()0A, in dogs and off after 8-12 hr or before the next close is 85% in cats). This does not appear to 'reduce
given. Isosorbide dilutrate is almost never
the incidence of functional azotemia.

used. In U1e one study designed to look for

Whether benazepril is safer in anin1als
benefits in dogs in heart failure, none was
with renal insufficiency is unknown.

identified when isosorbide was adnunisterecl at 0.2-1 mg/kg, PO, tid. Another study Vasodilators: Vasodilators exe1t a
showed acute benefit in dogs with mitral
positive effect in CHF through dilating
regurgitation when isosorbide was
systemic arterioles (reduce resistance to
adnunistered at 5 mg/kg ( effect lasted 4 hr)

blood flow) or systemic venodilation. The
and 10 mg/kg ( effect lasted 11 hr). The
nitrates (sodiw11 nitroprusside, nitroglyclargest pill size is 40 mg. Tolerance to erin ointment, isosorbicle dinitrate) act via
nitrates has been de111onstrated il1 mai1y
the common end pathway of increased
experilnental canme models.

nitric oxide production, with subsequent

Hydralazine is a potent systemic
activation of cyclic guanosine monophosarte1iolai· vasodilator typically reserved for phate ( cGMP) and endothelial smootJ1
dogs with mitral regurgitation due to
muscle relaxation. Sodiwn nitroprusside
myxomatous mitral valve degeneration that

( administered IV) is a potent mixed
are refractory to conventional therapy, or in
vasoclilator, acting on both the arterial
acute CHF when nitropmsside is unavailand venous systems. The combination of able. Its presumed mechanism of action is
sodiun1 nitroprusside with dobutan1ine may
via production of vasodilatory prostaglanbe especially useful in cases with cardiodins. Hydralazine may reduce systenuc genic shock and severe pulmonary edema.

vascular resistance up to 500A,, This

Although sodium nitroprusside dramatireduction in resistance results in the left cally and acutely reduces preload and
ventricle pwnping more blood flow f01warcl
afterload, its use is limited by the need for
through U1e systenuc vasculature and less
close monitoring and administration as a
blood flow backward Uu·ough the mitral

HEART DISEASE AND HEART FAILURE

109
valve into the left atJiurn. This decreases left

Gingival hyperplasia can occur in clogs
atrial and pulmonary capillary pressures,
adnunisterecl ainloclipine, which often
reducing development of pulmonary edema. necessitates discontinuation of the drug.

Approximately 300A, of dogs vomit when

Phosphodiesterase type 5 (PDE 5)

receiving hydralazine; the drug generally
inhibitors ( eg, silclenafll, taclalafil) ai·e used needs to be discontinued when this
to relax the smooth muscle in pulmonaiy

VetBooks.ir
happens. The recommended starting dosage aiterioles. Their mechaiusm of action is in a dog in ctu·onic heait failure is 0.5 mg/kg,
somewhat sin1.ilai· to that seen with nitrates,

PO, bid, if the animal is already on an ACE
with a common increase in the second
inhibitor, and 1 mg/kg, PO, bid, if not, with
messenger cGMP PDE 5 inhlbitors are used
gradual ( every 1-3 clays) uptitration to
in the treatJnent of moderate to severe
effect, as high as 3 mg/kg, PO, bid. The drug
pulmonaiy aiterial hypertension. Studies in
is effective within 30 min, peaks in 1 -3 hr,
clogs have demonstrated modest clinical
and maintains that peak for 11-13 hr. In a
improvement (reduction or cessation of
clog in acute, severe heait failure, a dosage
syncope, in1provecl tight heait failure) with
of2 mg/kg, PO, can be aclministerecl.

usually minimal improvement in pulmonary

Hyclralazine is an "all-or-nothing" drug, so aitery pressures, at least at lower dosages
the primary clai1ger is in giving too low of a

(eg, 1 mg/kg, PO, bid-tic!). Anecdotally,
close and producing no beneficial effect.

PDE 5 inhibitors seem to provide the most

Approxin1ately 900A, of clogs respond to a
notable clinical benefit to anin1als with
dosage of 2 mg/kg. A small percentage of
syncope secondary to pulmonary hypertenthose clogs become weak for -12 hr and sion. Anecdotal success has also been
then recover. In a clog with chronic heait
rep01tecl in clogs with right-to-left shunting
failure clue to mitral regurgitation, a good
cardiac defects in which the shw1t is clue
target would be a decrease in systolic blood
to the increase in pulmonaiy vascular
pressure of 10-15 nunHg, but given the
resistance. Adverse effects are unconunon
inaccuracy of blood pressure measurement
but may include GI upset and hypotensivein clogs this type of documentation may not relatecl effects ( especially when combined
be feasible. Other evidence that the close
with niti·ates, which is contraindicated). A
being given is adequate is the presence of
major drawback regai·cling clinical use of
bright reel mucous membranes and a

PDE 5 inlubitors is expense, particulai·ly in
decrease in munnur intensity. In cats,
larger animals. Fake (85% in one study)

hyclralazine can be given at a starting dose
silclenafil is commonly sold online. Silclenafil
of2.5 mg/cat, PO, bid.

is administered at 1-3 mg/kg, PO, bid-tic! in

Amlodipine is a calcium channel
clogs, and at 1 mg/kg, PO, tic! in cats.

blocker with only peripheral vascular

Taclalafll is administered at 1 mg/kg, PO,
effects (no cardiac effects) and moderate
once to twice daily in clogs.

to marked vasodilatory effects on systemic
arterioles. Its actions are very similar to

�-Adrenergic Blockers: In people with
those of hyclralazine ( decreased mitral
myocardial failure ( eg, DCM), 13-blocker
regurgitation and pulmonary edema) but
administration, with a very low starting
without the adverse effects of vomiting
close titrated upward over months, results
and tachycardia. Amloclipine has a

(seenu.ngly paradoxically) in an improverelatively slow onset of action, so its ment in myocardial function. To elate, all
effects take 1-2 days to be noticeable. It is
attempts to replicate this phenomenon in
typically reserved for aiumals refractory to
client-owned dogs have failed. Dogs with
conventional heait failure drug therapy or
experimentally induced heait failure have
for those with moderate to severe systemic shown measurable in1provements in cardiac hype1tension. Adverse effects are
perfonnance after aclnunistration of
generally related to hypotension and are
metoprolol, but these were models of
unconunon when uptitration is clone
ischenuc cardiomyopathy, wluch is a rare
gradually. In clogs, therapy is initiated at 0.3 cause of DCM in dogs. Large clogs (>20 kg) mg/kg/clay, PO, and uptitratecl every 2-3
with experimentally induced 111.itral
clays to a maximal dosage of 1 mg/kg/clay
regurgitation also have had lesser decreases

(if needed). In cats, therapy is generally
in contractility over time when adminisstaited at 0.625 mg/clay (14 of a 2.5-mg tered atenolol when compared with
tablet) and gradually uptitratecl to effect,
placebo.

up to as much as 1.25 mg, bid, in some

[3-Blockers are conunonly administered
cases. Because ainlodipine reduces the
to cats with hypertrophic cardiomyopathy,
ainount of regurgitation, it may also
pri.mai·iiy to reduce systolic anterior motion
effectively slow the progression of mitral
of the mitral valve. However, evidence
regurgitation to heait failure in clogs.

that this results in clinical improvement,

110

HEART DISEASE AND HEART FAILURE
biochemical improvement, or prolonged
in which cardiac cachexia is present,
stuvival is lacking. Atenolol (6.25--12.5 mg,'cat, because lower sodium foods are often less PO, bid) is the 13-blocker most commonly
palatable. In general, maintaining adequate
used in cats. There are limited and
caloric intake is more important than
preliminary data associating the use
sodium restriction.

of atenolol in cats with hypertrophic

Supplementation with n-3 fatty acids

VetBooks.ir
cardiomyopathy and CHF with a shorter
has shown multiple benefits in people with
swvival, and consideration might be given

CHF, and a study in dogs suggests antito dosage reduction or withdrawal if CHF
arrhythrnic benefits as well. These fatty
develops.

acids may reduce circulating inflan1matory
cytokine levels and seem to improve

Nutritional Considerations: Important
appetite in some dogs with cardiac
metabolic changes may occur in animals
cachexia. Daily doses of eicosapentaenoic
with heart failure. Upregulatfon of the RAAS acid at 40 mg,'kg and docosahexaenoic acid leads to increased plasma volume, largely
at 25 mg,'kg can be tlied.

mediated by increased sodium retention.

Taurine supplementation is indicated

Increased production of inflan1matory
in animals with docw,1ented taurine
cytokines such as tumor necrosis factor
deficiency and DCM. The incidence of
and interleukin 1 may promote increased

DCM has declined dramatically in cats
metabolic demand and contribute to
since taurine deficiency was identified as
anorexia, thus worsening "cardiac
a primary cause in the late 1980s. Taurine
cachexia." Studies in people and a study in
deficiency is still documented in some cats
dogs have shown that patients with CHF
with DCM fed noncon1mercial diets
who lost weight dwing the course of these

( especially chicken, dog food, and
studies had a poorer prognosis. In some
vegetarian diets) and rarely a commercial
patients, nutrient deficiencies (taurine,
cat food diet. Supplementation at 250 mg,
carnitine) have been shown to cause DCM.

PO, bid, can be started in cats while

Decreased levels of circulating fatty acids
awaiting results of plasma and whole blood
have been documented in people and dogs
taurine concentrations. Dogs are able to
with heart failure. The overall nutlitional
synthesize more endogenous taurine than
goals in the management of animals with
cats and do not have an obligatory loss in
heart failure should therefore include
bile, so deficiency is less common in this
supplying adequate calories, modulating the species. However, American Cocker production of proinflanirnatory cytokines,

Spaniels with DCM urlifomlly have a low
managing sodiw,1 balance, and supplementplasma taurine concentration and respond ing nutrients that may be deficient.

to taurine or taurine and carnitine

The idea that sodium restriction
supplementation. Newfow,dlands are
reduces circulating plasma volw11e and
relatively predisposed to taurine deficiency,
preload is well established. However,
especially when fed lan1b and rice or
sodium restriction is known to activate the
high-fiber, low-protein/taurine diets. Rarely,

RAAS, and there is continued debate as to
other breeds ( mostly breeds not usually
the role of sodi urn restriction in animals,
thought of as being predisposed to
especially those with asymptomatic cardiac
developing DCM) with DCM will be taurine
disease or mild to moderate CHF. In
deficient/responsive. Whole blood and
contrast, moderate to severe sodium
plasma taurine concenti·ations should be
restriction may be indicated in animals with
obtained in any dog ::,uspected of having a
severe CHF, especially in those refractory to
taurine-deficient cardiomyopathy, and
drug therapy. It is also important to cow,sel
supplementation can be started at 500-1,000
owners to avoid foods and treats with high
mg, PO, bid-tid, while awaiting results.

sodiw,1 content, because an acutely high

Clinical improvement occurs within weeks
sodiw,1 load (as can be seen in animals
of starting taurine supplementation in cats
fed hw,1an snacks or table foods) may
or dogs with DCM due to taurine deficiency.

precipitate CHF in animals with compen

Echocardiographic improvement takes
sated heart disease. For animals in mild to
longer (2-3 mo).

moderate heart failure (ISACHC Class II),

L-Carnitine plays an important role in
moderate sodium restriction (50--80 mg,'100
fatty acid metabolism and energy produckcal) may be tried if the dog or cat will tion. Cami tine deficiency has been
readily eat such a diet. In animals with
documented in one family of Boxers and
severe refractory CHF, more aggressive
myocardial carnitine deficiency is common
sodium restliction ( <50 mg,'100 kcal) may
in dogs with DCM, but it is most likely that
be tried. This becomes even more of a
this deficiency is a result of cardiomyopatherapeutic challenge with some animals thy, not the cause, in these dogs. Carnitine

HEART DISEASE AND HEART FAILURE

111
has been supplemented in other breeds with treatment in animals with respiratory DCM but with little success. Diagnosis of
distress due to a significant volume of
carnitine deficiency is difficult and requires
effusion. However, caution again should
an endomyocardial biopsy. Supplementabe taken in paiticularly stressed animals, tion is also expensive, and given our limited
which may require pretreatment with
knowledge of the role carnitine plays in
oxygen and light sedation. Diuretic therapy

VetBooks.ir
canine cardiomyopathy, supplementation is
is ineffective at acutely resolving a large
not routinely recommended. Nevertheless,
volume of pleural effusion.

supplementation can be offered at 50-100
mg/kg, PO, bid-tid, to dogs with DCM.

Abdominocentesis: Ascites may

Coenzyme Q10 is involved with
produce abdominal discomfort and worsen
mitochondrial energy production and
dyspnea by reducing available lung capacity
possesses general antioxidant properties.

in animals in right heait failure. Abdomino

Anecdotal benefits of supplementation in
centesis should be performed at the time of
people and dogs with DCM have been
initial diagnosis of right heart failure if the
reported, but weU-controUed studies are
ascites is severe. In animals with recurrent
lacking, and reports are conflicting.

ascites refractory to diuretic therapy,

Consequently, there is no known benefit.

abdominocentesis may be performed every

The dosage in dogs is 30-90 mg, PO, bid.

1-4 wk to improve patient comfort and
quality of life. Every attempt should be

Oxygen Therapy: The presence of
made to remove aU or as much fluid as
pulmonary edema in animals with CHF
possible on each visit to prolong the time
increases the alveolar-arterial diffusion
between repeat abdominocenteses. This
distance for oxygen to pulmonary
does not result in hypoalbwninemia. Fluid
capillaries and disturbs ventilation/
can be removed manually using eitl1er a
perfusion matching. Supplemental oxygen
fenestrated catheter and large syringe or
administration increases the alveolar-artea suction device.

rial diffusion gradient and thus increases
arterial oxygen content. Oxygen may be

Ancillary Therapy: Bronchodilators
administered via oxygen cage, flow-by

(theophyUine, terbutaline) are generally
method (least preferred), nasal cannula, or
reserved for animals with chronic ai.!way
oxygen coUar ( constructed by covering the
disease, which is common in older
ventral 50%--75% of an Elizabethan coUar
smaU-breed dogs. Caution should be taken
with plastic wrap and taping oxygen tubing
in animals with CHF, especiaUy with
along the ventral aspect of the coUar ). The
tachyaii:hythmias, because of the sympaoxygen cage is least stressful for the animal thomimetic effects of these agents. In dogs
but is expensive, because high flows of
with cardiovascular disease and syncope,
oxygen are required to achieve therapeutic
theophyUine has been used with some
concentrations (>40%inspired oxygen). The success for its positive chronotropic effects.

oxygen coUar has the potential to achieve a

Dosages of theophyUine and terbutaline are
very high concentration of inspired oxygen
as previously described under treatment of

( as much as 800Ai) but may require light
bradyarrhythmias (see above).

sedation to increase patient tolerance.

Cough suppressants generaUy should
not be used if a cough is truly due to

Thoracocentesis: Pleural effusion
cardiogenic pulmonary edema. Instead,
decreases the available area for alveolar
they are reserved for dogs with chronic
ventilation and aiterial oxygenation. Pleural bronchitis and ai.!way coUapse (malacia) effusion should always be excluded as the
and, even tl1en, generaUy reserved for dogs
cause of dyspnea in animals in heart failure,
not responsive to a corticosteroid and/or
especiaUy cats. This is best accomplished
doxycycline with or without theophylline.

using ultrasound. If ultrasound is unavail

It is common for dogs with CHF to have
able, radiographs can be taken, but extreme concomitant chronic bronchitis. Conm1on care must be taken to avoid stressing tl1e
antitussive agents used for dogs with
animal (especiaUy cats), because stress in a
cardiac disease include butorphanol at
dyspneic animal often results in death. If

0.05-0.3 mg/kg, PO, tid-qid, or hydrocoradiographs carmot be taken, a diagnostic done at 0.22 mg/kg, PO, bid-tid.

thoracocentesis should be done. This can

Anxiolytic therapy may be used for
often be done in cats in the examination
some animals with severe respiratory
room using a butterfly catheter with the cat
distress secondary to CHF. Morphine has
in sternal recumbency. Iffluid is present,
traditionaUy been reconunended to aUeviate
as much as possible should be removed.

anxiety in dogs with acute CHF because of

Thoracocentesis is the most effective
its concurrent sedative and venodilating

112

HEART DISEASE AND HEART FAILURE

(and thus preload reducing) properties, but
borders of tl1e valve. Tllis condition is most
it also can produce respiratory depression,
common in older horses. It causes aortic
which can be catastrophic. The dosage of
regurgitation, wllich is heard as a diastolic
morphine in dogs is 0.1-0.25 mg/kg, SC.

mum1ur on the left side. The murmur is

It may also cause nausea or vomiting.

often "musical," meaning it has one

Morphine is generally avoided in cats,
frequency ca.used by tl1e valve st11.1ctures

VetBooks.ir
because it may induce agitation and
vibrating at the frequency heard. The
dysphmia. Butorphanol is a partial opiate
murmur may be high-pitched and sound
agonist/antagonist with minimal cardiovastruly musical, or it may be low-pitched and cular effects. A sedative dosage of 0.2--0.5
sound like a grunt or a dive bomber. The
mg/kg administered IM or IV can be used in
murmur is often loud, but the aortic
cats and dogs. Butorphanol may also be
regurgitation is usually mild. Clinical signs
combined with a benzodiazepine (mida

( eg, heait failure) a.re usually not seen,
zolam or diazepam), with the latter also
because severe a.mtic regurgitation is
dosed at 0.2-0.5 mg/kg, IM or IV. Phenothiaw1conunon.

zine tranquilizers ( eg, acepromazine) may

Insufficiency of an AV valve results in
be used to alleviate severe anxiety and have
turbulent, systolic (ie, during vent1iculai·
the potential added benefit of producing
contraction) flow through the affected valve
mild systemic arteriolar dilation; however,
from a ventlicle into an atrium. This
they should be used cautiously in animals
regurgitation results in a.ti increase in
with severe hemodynamic compromise or
volwne within tl1e atrium and thus to an
systemic hypotension. A low dosage of
increase in a.tlial chatnber size. When

0.01--0.1 mg/kg, IM or IV, can be used.

regurgitation is severe, a.tlial pressure may
also increase. If the mitral valve is affected,
the increased left ati·ial pressure results in

SPECIFIC CARDIAC DISEASES
increased pulmonaiy capillat)' pressures
and, if the increase is high enough (ie, >20

Myxomatous AV Valve
mmHg), in cai·diogenic pulmonat)' edema

Degeneration

(ie, left heart failure). If the bicuspid valve is

(Degenerative AV valvular disease,
affected, severe regurgitation can result in

Endocardiosis)

an increased systemic venous pressure and
signs of right heart failure (most conunonly

Myxomatous degeneration is a process of
ascites in dogs). The constant, high-velocity,
the fibrous layer of an AV valve breaking
regurgitantjet of blood through the affected
down to cause mitral valve prolapse
mitral valve physically datnages the

(hooding) and the spongifom1 layer
endoca.rdium of the left a.mum, resulting
proliferating to cause nodular thickening of . grossly in jet lesions. In cases with severe the cardiac valve leaflets, most severely at
regurgitation, the chronic increase in left
their tips. Myxomatous degeneration
atrial size and pressure can also result in left
commonly affects the mitral and tricuspid
atlial rupture and a.cute cardiac tatnponade,
valves in dogs. Chordae tendineae are also
often resulting in death.

affected by the degenerative process,

Pathophysiologically, the body compenmaking tl1em prone to rupture. J'he exact sates for valvular regurgitation ptirna.rily by
cause is unknown, but in Cavalier King
renal sodium and water retention, causing

Charles Spaniels and Dachshunds it is an
an increase in blood volwne and in venous
inl1erited trait. Myxomatous degenerative
return to the heart. This results in an
valve disease is the most common cardiac
enlargement in ventricular chan1ber size
disease in dogs and accounts for -75% of
and a left ventricle capable of ejecting a
cardiovascular disease in tllis species; -600/o
larger total stroke volume with each beat.

of affected dogs have only the mitral valve

That way, even though some percentage of
affected, 300/o have lesions in both the
blood flow is going backward into the left
tlicuspid and mitral valves, and 10% have
a.tliwn, a normal or neai· normal ai11ow1t can
only tricuspid valve disease. In dogs, tl1e
be (i\jected forwai·d into the aorta. Multiple
disease is age- and breed-related, with older, mechanisms exist for sodiun1 and water small-breed dogs demonstrating a m uch
retention, but the renin-angiotensinlligher incidence. Horses and ca.ts a.re also aldosterone system (RAAS, seep 100) is
affected by tllis disease ( most commonly
one of the most active and best studied.

affecting the nlitral valve leaflets); however,

Renin release by tl1ejuxtaglomerula.r
it is uncommon in tl1ese species. In horses,
apparatus in the kidneys cleaves angioa degenerative valve disease can also affect tensinogen into angiotensin I, and
the aortic valve cusps and consists of
angiotensin-conve1ting enzynie then cleaves
valvular nodules or fibrous bands at tl1e free
angiotensin I into ai1giotensin II. One of the

HEART DISEASE AND HEART FAILURE

113
main effects of angiotensin II is to stimulate
when heart failure is controlled. Sudden
aldosterone release by the adrenal glands.

death is rare but may occur secondary to

Aldosterone stimulates the cells in the distal left atrial ruptw·e or rupture of a p1irnary renal tubules to bring sodiwn back into the
mitral valve chord. Physical examination
vascular space, and water follows the
findings in animals that have developed left
sodiwn. The increase in blood volwne and
heart failure are primarily referable to the

VetBooks.ir
venous return to the heart places clu·onic
increased respiratory rate at1d effort. So.me
stretch on cardiac myocytes, resulting in
dogs may have respiratory crackles and
sarcomere replication within the myocytes
wheezes; however, these are much more
and growth of longer myocytes. This allows
conunon and more obvious in dogs with
the affected ventricle to develop a larger
chronic bronchitis, and many dogs with
chamber (ie, eccentric or volwne overload
pulmonaiy edema have no demonstrable
hypertrophy). This is the primary compenabnormal pulmonary sounds. If tricuspid satory mechanism for valvular regurgitavalve degeneration is significant, signs of tion. It is highly efficient and allows the
right heait failure may be noted ( eg, ascites,
heart to compensate not only for a valvular
jugular distention/pulses).

leak for years but also for an extreme

A CBC, sen.1111 chemistry profile, and
an10unt of regurgitation. For example, a
minalysis ai·e usually within norn1al limits.

small dog can completely compensate for

Left atrial enlai·gement is the chai·acteristic
regurgitation in which as much as 75% of the finding on thoracic radiographs of an animal blood flow from the left ventricle goes into
with myxomatous degeneration of the
the left atrium, while only 25% goes forward
mitral valve, and the size of the left atriwn
into the aorta
correlates directly with the severity of the

Activation of the RAAS and other
regm·gitation in small dogs. Other changes
compensatory mechanisms are commonly
include enlargement of the left ventricle
seen as dysfunctional and increases of
and pulmonary veins. As left heart failure
various neurohormones as detrin1ental,
develops, increased interstitial density to
because ove1t increases are often seen
the pulmonary parenchyn1a occurs, and as
in dogs that are in heart failure when
severity increases, an alveolai· pattern with
compensatory mechanisms are overair bronchogran1S (ie, severe pulmonary whelmed. However, these mechanisms are
edema) appeai·s. In dogs, these changes are
detrimental for only a few months at the end classically seen in the caudodorsal lung stage of U1e disease.

fields ai1d may be more prominent on the

Only -30% of dogs with mitral regurgitaright side. In older dogs, it is common to tion ever develop left heart failure. In dogs,
have an increased interstitial density in the
there are no clinical signs in the early and
lungs and to have radiographs taken at or
middle stages of the disease, altl1ough a
near end-expiration. This conunonly creates
systolic rnum1ur (grade I-VI) is heard with
the illusion of pulmonary edema and
maximal intensity at the left apex. The heart therefore the .misdiagnosis of left heart mtmnur intensity often does not correlate
failure. This can be avoided by rememberwith disease severity, although most soft ing that for a dog to be in chronic left heart
mummrs are heard in dogs with mild mitral
failure, the regurgitation must be severe and
regurgitation. Some dogs may also develop
overwhelming so the left atriwn is usually
a systolic click before developing a heart
severely enlarged. The exception to this rule
murmur. A systolic click is heard as a
is in dogs with acute heart failw·e due to a
three-heait-sound rhythm and may be
ruptured chord and a left atriun1 that is not
mistaken for a gallop sound (rhythm). A
severely e11Iai·ged. If the respiratory rate in
tlu·ee-heart-sound rhytlun in a middle-aged
the exainination room is nom1al ( <30
to older small-breed dog is al.most always a
breaths/min), the dog caruiot be in left heart
systolic click rather than a gallop sound. A
failm·e. If there is doubt regai·ding the
gallop som1d may be heard in a dog with
diagnosis of pulmonary edema in a dog Ulat
severe mitral regurgitation but is usually
is not in c1itical condition, it is usually best
difficult to auscult because of the loud heart to send the dog home and have the owner murmur also present. When the mitral
count the dog's respiratory rate when it is
regurgitation becomes severe and
sound asleep in a cool environment. If
overwhelming, left heart failure (pulmopulmonary edema is present, the sleeping nary edema) becomes evident, producing
respiratory rate (SRR) will always be
increases in respiratory rate (tachypnea)

increased. If the rate is increased, the dog
and effort (dyspnea), and cough. Syncope
should be administered furosemicle at a
may also occur. Although syncope is not a
dosage of at least 2 mg/kg, PO, bid. If the
sign of heart failure, it may be present when

SRR then decreases, the diagnosis of left
heart failure is evident ai1d may inlprove
heart failure can be made. In cats, the

114

HEART DISEASE AND HEART FAILURE
radiographic pattern is more diverse and
available. It might be useful for differentiatoften is not caudodorsal. A heavy interstitial ing dogs with chronic lung disease from
to alveolar pattern in the accessory lung
dogs in chronic left heart failure, but this
lobe on a lateral view is one of the more
can often be accomplished with less
common findings. Cats in left heart failure
expense and greater accuracy by having the
also commonly have pleural effusion.

owner count the dog's SRR and doing a

VetBooks.ir

Echocardiography demonstrates
furosemide response test if the rate is
thickened and irregular valve leaflets of
increased. NT-pro BNP often decreases after
normal to increased echogenicity. Chordae
successful treatment of left heart failure but
tendineae may be ruptured, causing the AV
frequently does not decrease to a value
leaflets to flail (ie, leaflet tips to protrude)

within the normal range. Predicting which
into the atrium during ventricular contracdogs with mitral regurgitation will go into tion. Mitral valve prolapse (hooding), in
heart failure is difficult. As populations,
which the body of a leaflet (not the tip)

dogs with a larger left ventiicular diastolic
protrudes into the left atrium in systole, may dimension, larger left atrial size, and a also be present. The size of the left atrium
higher NT-proBNP are at greater risk of
increases in direct correlation with the
developing heart failure, but translating that
severity of the mitral regurgitation in small
to an individual dog is often fraught with
dogs. Left ventricular chamber enlargement
error. The same is true for predicting

(ie, eccentric or volun1e overload hypertrocardiac death (ie, from heart failure or phy) also occurs in correlation to disease
sudden death) from severe mitral regurgitaseverity. In small dogs, left ventricular tion. Higher dosages of furosemide are
myocardial contractility or function is often
required in dogs with more severe heart
normal as evidenced by a normal end-sysfailure, so higher furosemide dosages tolic dian1eter or volume. The increase in
predict decreased survival.

end-diastolic diameter coupled with the

Studies in dogs with degenerative mitral
normal end-systolic diameter results in the
valve disease that are not yet in heart failure
left ventricular fractional shortening (ie, the
have failed to convincingly demonstrate a
amount of contraction [not contractility])

reduction in time to onset of CHF with use
being increased. Myocardial contractility is
of ACE inhibitors. Thus, treatI11ent in
decreased in some small dogs and many
small-breed dogs should be reserved for
large dogs at the onset of heart failure and
dogs with clinical signs of heart failure, ie,
may become decreased in small dogs when
those demonstrating cardiogenic pulmobeing treated for heart failure.

nary edema on thoracic radiographs and

Electrocardiographically, animals with
resting/sleeping tachypnea in the absence of
mild to moderate degenerative valve disease other severe pulmonary disease. Treatment have a normal sinus arrhythmia or norn1al
of CHF includes administration of a diuretic
sinus rhythm. When CHF develops, the

( almost always furosemide) and an ACE
increase in sympathetic tone often results in inhibitor as adjunctive therapy. Cardiogenic loss of sinus arrhythmia and usually in an
pulmonary edema should not be treated
increase in heart rate (ie, sinus tachycarwith an ACE inhibitor alone. Pimobendan dia). Left atrial enlargement promotes the

(0.25-0.3 mg/kg, bid) is also indicated in
development of atrial arrhythmias such as
dogs in heart failure. Spironolactone might
atrial premature complexes and atrial
have chronic, long-term benefits in dogs
fibrillation. Ventricular tachyarrhythrnias
with heart failure due to myxomatous
are uncommon. There may be evidence
mitral valve degeneration, but there is no
of left atrial enlargement (P mitrale or
convincing evidence of this in. dogs with
widened P waves) and left ventricular
mitral regurgitation, and it should not be
enlargement (tall and widened R waves) on
relied on to produce clinically relevant
an ECG, but these changes are unreliable
diuresis. Dogs refractory to administraindicators of chamber enlargement.

tion of a maxinial dosage of furosemide

Measurement of the plasma or serun1

( 4 mg/kg, tid) can be treated with several
concentration of NT-proBNP may be useful
additional drugs or a change in strategy. The
in dogs with mitral regurgitation. It is
pirnobendan dosage can be increased to tid,
usually not increased in dogs with mild
or the bid dosage can be doubled. Amlodimitral regurgitation, may be increased in pine and hydralazine decrease the an1ount
some dogs with moderate to severe mitral
of regurgitation and improve perfusion and
regurgitation, and is increased in most dogs
can be very effective. A thiazide diuretic
with left heart failure secondary to mitral
combined with furosemide is another
regurgitation. It would be most useful in
effective means of treating dogs with
dogs presented with severe tachypnea/dysprefractory heart failure, but care must be nea if a rapid assay (bedside test) were
taken to not produce clinically relevant

HEART DISEASE AND HEART FAILURE

115
dehydration and hypokalemia. Torsemide
dysfunction, these are more correctly
may be used to replace furosemide.

identified as secondary myocardial

Torsemide is more bioavailable (better
diseases or with a descriptive term
absorbed) and has a longer and more
preceding the term cardiomyopathy
consistent half-life. The starting dose is

(eg, taurine-responsive dilated cardiodetem1ined by multiplying the total daily myopathy).

VetBooks.ir
dose of furosemide by 0.1 and dividing that
dose bid. Care must be taken to have the

Dilated Cardiomyopathy (DCM): This
owner closely monitor the SRR when this is
disease is characterized by the progressive
done. If the SRR increases, the dose of
loss of myocyte nwnber and/or fw1ction and
torsemide must be increased promptly.

a decrease in cardiac contractility. Several

Surgical treatment of mitral regurgitation
forms of secondary DCM exist ( eg, taurine
is routine in human medicine and most
deficiency in cats, doxorubicin-or
commonly consists of mitral valve repair.

parvovirus-induced in dogs). In some

Successful mitral valve repair has also been

Doberman Pinschers (primarily those in tile
accomplished in dogs, but the only currently USA), tile disease is caused by a mutation truly successful program is in Japan.

in tile gene that encodes for pyruvate

Replacement of the mitral valve with a
dehydrogenase kinase 4 (PDK4), an enzyme
prosthetic valve is almost uniformly
in mitochondria required for ATP producw1successful.

tion. A small percentage of Boxers with

Abnormal arrhythmias such as atrial
arrhythmogenic right ventricular cardiofibrillation or other severe and sustained myopathy (see below) develop DCM. These
supraventricular arrhythmias, if present,
dogs have a mutation in the gene tllat
should eitller be resolved or tl1e rate
encodes for striatin, a desmosomal protein.

controlled witll digitalis glycosides and

DCM has a protracted subclinical phase
diltiazem or a 13-blocker ( eg, atenolol) to
in dogs, with clinical signs evident for a
prevent tachycardia-induced myocardial
relatively short time. During tile subclinical
failure. Optimal tllerapy should be planned
phase, compensatory mechanisms,
for each stage of disease. ln acute and severe primarily volume overload or eccentric CHF, oxygen and aggressive parenteral
hypertrophy, maintain normal hemodynamfurosemide administration are warranted.

ics. As cardiac contractile function is

Nitroprusside can also be beneficial.

progressively lost, cardiac output, and so

Some affected dogs can live for> 1 yr witl1 renal blood flow, decreases and tllen is appropriate therapy. However, survival time normalized again as renal sodiwn and water is highly variable, and no firm estimates
retention increase blood volWTie and
should be provided. If a dog has been
venous return and the affected ventricle is
treated for left heart failure for >2 yr, tile
stimulated to grow larger. The increased
diagnosis should be reassessed.

activation of the sympathetic nervous
system and tile RAAS, after years of initial

Valvular Blood Cysts or Hematomas
benefit, cause deleterious effects during the

These benign valvular lesions are present in
late phases of the disease (seep 100).

as many as 75% of calves <3 wk of age. They

Excessive stimulation of the myocardiWTI
are most commonly located on tile AV valves. by the sympathetic nervous system may stimulate ventricular arrhythmias and
myocyte deatll, while excessive activation

Cardiomyopathies
of the RAAS causes vasoconstriction and

Cardiomyopathy is defined as any disease
continued retention of sodiwn and water
involving primarily and predominantly the in the presence of edema/effusion.

heart muscle. Most of the cardiomyopa

DCM is most prevalent in dogs and is
thies of animals are idiopathic diseases
especially prevalent in certain breeds. It
that are not the result of any systemic or
most commonly affects large-breed dogs
other primary cardiac disease. In several
and far less commonly small-breed dogs
instances, a mutational cause has been

( witl1 a few exceptions such as American
identified. In others, a genetic cause has

Cocker Spaniels, Springer Spaniels, and
been identified. In animals (primarily

English Cocker Spaniels). Doberman
dogs and cats), they are classified as

Pinschers, Boxers, Great Danes, German
dilated cardiomyopathy, hypertrophic

Shepherds, Irish Wolfhounds, Scottish
cardiomyopathy, arrhythmogenic right

Deerhounds, Newfoundlands, Saint
ventricular cardiomyopathy, and

Bernards, and Labrador Retrievers, among
restrictive or unclassified cardiomyopaother large-breed dogs, are particularly at thy. If a disease process has been
risk. ln Portuguese Water Dogs, a juvenile
identified as the cause of myocardial
form of tile disease is seen. The disease is

116

HEART DISEASE AND HEART FAILURE
typically seen in middle-aged to older dogs;
is present, pulmonaiy edema is more
males are either affected more frequently or
conunonly evident in a large dog than it is in
more severely than females. The incidence
a small dog with mitral regurgitation, and
in cats has decreased dramaticalJy since the
the left atrium is moderately to markedly
discovery in 1987 that taurine deficiency
enlarged. Echocardiography is the best test
was responsible for most cases (taurineto definitively diagnose DCM. In dogs with VetBooks.ir
responsive DCM). Since then, taurine has
severe DCM that are in heart failure, there
been added to alJ conunercial cat foods.

is a dran1atic decrease in left ventricular

Most cases today are not taurine responsive
fractional shortening caused by an increase
and reflect primary ( or idiopathic) disease,
in left ventiicular end-systolic diameter.

although the disease is seen occasionalJy

Cai·diac chambers, especialJy the left atriun1
in cats fed noncommercial diets ( eg,
and left ventricle, are dilated. Mitra!

vegetarian, baby food, home-cooked food).

insufficiency typically develops as

Dobennan Pinschers typicalJy develop
progressive left ventricular chan1ber
concurrent and progressive ventricular
dilation results in separation of the valve
arrhythmias along with progressive systolic
leaflets. Abnonnal ECG findings may
dysfunction. Syncope and sudden death
include ventricular premature complexes
occur in as many as 20"A, of Doberman
and ventricular tachycardia ( especialJy in

Pinschers, and signs of left heart failure

Doberman Pinschers and Boxers), and
eventualJy develop. Most Doberman
atrial fibrillation (especialJy giant breeds).

Pinschers demonstrate evidence of

There may be electrocai·diographic
myocardial failure at the time syncopal
evidence of left atrial enlargement (P
episodes are noted. In other breeds, such as
nutrale or widened P waves) and left

Great Danes and Newfoundlands, sudden
ventticular enlargement (talJ and wide R
death and collapse are far less likely. Signs
waves). The occurrence of ventricular
of left heait failure, including tachypnea
premature complexes on a routine ECG in
and clyspnea clue to pulmonary edema,
a presumed healthy Dobermai.1 Pinscher
weakness, and exercise intolerance often
is highly suggestive of DCM.

predominate, but signs of right heart failure

The objectives of therapy ai·e to lessen

( ascites) may also be present. Pleural
edema/effusion formation ( eg, with
effusion may be present, most conunonly in
diuretics), in1prove contractility (eg, with
dogs with both left and right heart failure.

pimobendan), and reduce adverse effects

Ascites was noted in 35% of Newfoundlands
of angiotensin II and 0U1er neurohonnonal
with DCM in one study. Cats witl1 DCM
changes ( eg, witl1 an ACE inhibitor).

typicalJy present with severe respiratory

Taurine-responsive myocardial failure
signs clue to puln10nary edema and/or
occurs in some breeds, paiticularly
pleural effusion, and clirucal signs are often·

American Cocker Spaniels, and anecdotalJy
rapidly progressive and refractory to
in a few Golden Retrievers, Dalmatians,
therapy.

Welsh Corgis, Tibetan Teniers, and other

A soft systolic heart munnur, best heard
breeds. In many of these breeds, taurine
at the left cardiac apex, is often present. A
deficiency can be diagnosed by low plasma
galJop sound may also be present but is
or whole blood concentrations. Response to
subtle and usualJy identified in.clogs only by
taurine supplementation (which may take
an experienced exanliner. It is often more

2-4 mo) can be dran1atic and may obviate
obvious in cats. The femoral pulse may be
the need for other cardiac medications.

weak, and an arrhythmia with associated

Carnitine-responsive cardiomyopathy,
pulse deficits may be noted. The arrhythmia
although reported, is almost a nonentity.

is most commonly ventricular ectopy ( eg,

Coenzyme Q10 supplementation is an
premature ventricular contractions,
unproven and, many say, irrational
ventriculai· tachycardia) in Doberman
approach to tl1e disease. Adnunistration of

Pinschers and Boxers, and atrial fib1illation
fish oil might reduce tile severity of cai·diac
in giant-breed dogs. Ascites, tachypnea,
cachexia in aninlals with DCM.

dyspnea, or cough may also be noted,

CHF, which may be severe, should be
depending on the type of heait failure that
treated as discussed elsewhere (seep 99).

develops.

As severe pulmonary edema resolves,

Blood work may demonstrate prerenal
furosenude can be administered orally, with
azotemia (increased BUN, creatinine).

oxygen continued until clirucal signs are

Thoracic radiographs typicalJy demonstrate
controlled. Pimobendan and an ACE
moderate to marked cardiomegaly.

inhibitor ( eg, enalapril, benazepril) should

However, this finding may be masked by
be started. Pin10bendan may be indicated in
chest conformation ( eg, a deep chest in a

Dobem1an Pinschers with DCM before tl1e

Dobennan Pinscher). If left heart failure
onset of heart fa.ii ure. Antiarrhyth.mic

HEART DISEASE AND HEART FAILURE

117
therapy is frequently indicated, especially
occur. The diagnosis is based on the nmnber
for Doberman Pinschers with severe
of premature ventricula.i· complexes (PVCs)

ventricular arrhythmias. Holter monitoring
on a Holter monitor(> 100-300 PVCs in 24 hr
is the ideal method to evaluate both the
is generally considered diagnostic of ARVC
severity of an arrhytJ1mia and therapeutic
in this breed). The QRS complexes of the
efficacy. Mexiletine (5--10 mg/kg, tid) may

PVCs are most commonly upright in the

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be useful in animals with ventricular
leads where the QRS complex is usually
arrhythmias and concmTent hea.it failme,
upright, meaning they originate from the
because negative inotropy is less than with
right ventricle. The hea.it looks nom1al on
sotalol (1-3 mg/kg, bid); however, sotalol
thoracic radiographs and an echocardiocan be used if therapy is initiated with a gra.in in most Boxers with ARVC, although
low dose carefully titrated upwa.i·d and if
some will develop a true DCM and go into
pirnobendan is used concurrently.

hea.tt failure. Boxers presented for syncope

Amiodarone may be a more effective drug
without DCM are treated with sotalol
than mexiletine to prevent sudden death in

(1-3 mg/kg, PO, bid) or a combination

Doberman Pinschers, but its use is
of mexiletine (5--10 mg/kg, PO, tid) and
associated with a relatively high incidence
atenolol (12.5--25 mg/dog, PO, bid). Dogs
of hepatotoxicity in this breed.

refractory to sotalol may have mexiletine

The prognosis is grave for cats with DCM
added. In Boxers with ARVC that do not

(not tamine responsive), with a median
have DCM, tl1e prognosis is often good, and
smvival time of 2 wk Cats that a.i·e tamine
many live for several years on antia.t-rhytbresponsive also have an initial high risk of mic therapy. The longtem1 prognosis for
death. However, cats that smvive long
dogs with DCM that are in hea.tt failure is
enough for tamine to become effective (2-3
poor. Most live only several months.

wk) have an excellent prognosis, because

In cats, the disease usually ma.ttifests as
the disease is completely reversible. Dogs
right ventricular and atrial enla.i·gement and
that are tamine responsive also have a fair
right hea.tt failure, usually along with some
to good prognosis once signs of CHF abate.

supravent1icular a.i1d ventricular tachyar

The short-term prognosis for other dogs
rhythmias. Dyspnea and tachypnea due to
with DCM depends primarily on the severity pleural effusion, ascites, and nonspecific of the hea.tt fail me on presentation.

clinical signs such as a.i1orexia and lethargy

Longterm prognosis is poor, with smvival
a.i·e repo1ted in affected cats. Treatment is
tin1e measmed in months. The prognosis is
sintilar to that of DCM. Longtenn prognosis
poor in most Doberman Pinschers: in the
is generally poor.

past, -25% died within 2 wk of presenting
with hea.tt fail me, and 65% died within 8 wk.

Hypertrophic Cardiomyopathy:

Pimobendan apparently prolongs smvival,

Hypertrophic cardiomyopathy (HCM) is
sometimes dran1atically (months). The
characterized by primary concentric left
prognosis in other breeds is better but
ventricula.i· hypertrophy (ie, thick walls J
remains guarded; 75% die within 6 mo of
resulting from an inherent myocardial
diagnosis. As expected, dogs with severe
disorder rather than pressure overload
hea.tt fail me, particularly left heart failure,

(such as caused by aortic stenosis),
have a worse prognosis than those with
hormonal stimulation (such as hyperthymilder signs or signs of right hea.tt failure roidism or acromegaly ), infiltration of the
at presentation.

myocardium ( eg, lymphoma), or other
noncardiac disease. It is primarily seen in

Arrhythmogenic Right Ventricular
domestic cats and rarely in small dogs. It

Cardlomyopathy: Arrhythrnogenic right
has also been reported in cattle. Papillary
ventricular cardiomyopathy (ARVC) is seen
muscle enlargement is a consistent feature
almost exclusively in Boxers and is also
of the disease in cats. In people, HCM is
known as Boxer cardiomyopathy. It is ra.i·ely caused by mutations in a nmnber of seen in cats. ARVC is characterized by a
sarcomeric genes. Mutations in one
fatty or fibrofatty infiltrate of the right
sarcomeric gene, the cardiac myosin
ventricular myocardium. In Boxers, the
binding C gene, have been identified in
most common ma.ttifestation of the disease

Maine Coon and Ragdoll cats. These
is syncope caused by a very fast (>400 bpm)

mutations are thought to result in the
nonsustained ventricular tachycardia. It
production of dysfunctional sarcomeres
takes 6--8 sec of no blood flow to the brain
within myocytes. The myocardimn then
to result in unconsciousness, so the
produces new sarcomeres to help the
tachycardia must last for that long for
dysfunctional ones, resulting in hypertrophy
syncope to occur and then must stop
that may be ntild to severe. Severe
spontaneously for sudden death not to
hypertrophy is often accompanied by

118

HEART DISEASE AND HEARTFAILURE
cellular necrosis and resultant replacement
develop HCM earlier ( often before I yr of
fibrosis ( myocardial scarring).

age) and often develop a more severe form

Increased fibrosis coupled with severe
of the disease.

wall thickening results in a stiffer than

Many affected cats have no clinical signs,
normal left ventricle in diastole, which
especially those with mild to moderate

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increases diastolic pressure for any given
disease. Cats that develop severe disease
diastolic volume. The increased pressure is
may also have no clinical signs but will
transmitted backward into the left atrium in
usually go on to develop left heart failure,
diastole, resulting in left atrial enlargement
systemic thromboembolism, or sudden
and, if severe enough, in left heart failure.

death. Cats in heart failure have signs of

Left heart failure manifests as pulmonary
tachypnea and dyspnea secondary to
edema and pleural effusion in cats.

pulmonary edema or pleural effusion.

Myocardial contractility is nom1al, but left

Owners frequently do not note tachypnea
ventricular end-systolic dian1eter is usually
and so do not present the cat for exanlinaless than normal and may become zero tion until dyspnea, often marked, is present.

( end-systolic cavity obliteration) due to

Cats with systemic tlrromboembolism most
the increased wall thickness resulting in
commonly have an acute onset of hindlinlb
a decrease in systolic wall stress (ie,
pru·esis/paralysis coupled with acute pain,
afterload). Severe left at1ial enlargement
pulselessness, and poikilothermia. Cough
can develop, which causes blood flow to
is uncommon in cats with herut failure.

stagnate. This can lead to the fon11ation of

Physical exanlination frequently
a left atrial thrombus and the potential
demonstrates abnormal heart sounds,
for systemic thromboembolism.

including a soft to prominent systolic

A cranial displacement of the anterior
cardiac murmur and/or a gallop sound. The
mitral valve leaflet during ventricular
mun11ur is often dynru11ic, increasing in
systole, a phenomenon termed systolic
intensity with excitement and decreasing as
anterior motion of the mitral valve, is a
the cat relaxes. A murmur is not present in
common finding in cats with HCM and is
at least one-third of cats with HCM.

due to marked enlargement of the papillary

Increased respiratory sounds may suggest
muscles that drag the mitral valve leaflet
pulmonary edema, and decreased respirainto the left vent1iculru· outflow tract in tory sounds may indicate pleural effusion,
systole. This phenomenon produces two
but auscultation of the lungs is often normal.

turbulent jets-one of dyn8lll.ic subaortic

The femoral pulse may be normal or weak,
stenosis and the other of mitral regurgitaor absent if distal aortic thromboembolism tion. Systolic anterior motion is the most
has developed. Radiographically, there may
common cause of a heart murmur in a cat
be pronounced left atrial enlargement,
with HCM. Gross pathology includes
especially in a cat in left heart failure, and
increased cardiac weight (>20 g), increased
variable left ventricular enlargement. The
left ventricular wall thickness, papillary
cardiac silliouette can appear relatively
muscle hypertrophy, and often left atrial
normal even in the presence of moderate to
enlargement. The myocardium often
severe left ventricular hypertrophy if the left
contracts after death (ie, unde.cgoes rigor),
atriun1 is not enlarged. Echocardiography
so the postmortem diagnosis ofHCM often
allows confirmation of the diagnosis and
crumot be made based on left ventricular
assessment of additional therapy needed
wall thickness alone.

( eg, anticoagulants may be more beneficial

HCM is the most common primary heart
in cats with severe left atria:! enlargement).

disease diagnosed in cats, but it is rare in

Left ventricular wall thickening (<!6 mm;
dogs. It is fru11.ilial in many breeds of cats,
generalized or regional), along with
including Persians, Sphynx, Norwegian
papillary muscle hypertrophy are noted.

Forest Cats, Bengals, Turkish Vans, and

Systolic anterior motion of the mitral valve

American and British Shorthairs. As in
may be present. ECG abnormalities may

Maine Coons and Ragdolls, the mode of
include supraventriculru· premature
inheritance is thought to be autosomal
complexes, ventricular premature
dominant. The disease is seen in cats from
complexes, and ventricular tachycardia.

3 mo to 17 yr of age, although most cats are

With severe atrial enlargement, atrial
middle aged at presentation. It is not
fibrillation may rarely develop. An electrical
present at birth but develops over time.

axis deviation may be present. However,

Penetrance is often <lOO"Ai. Male and female many cats with HCM have a normal ECG.

cats are equally predisposed, but males tend The plasma concentration of NT-pro BNP is to develop more severe disease at an earlier
often increased in cats with severe disease
age. In Maine Coon and Ragdoll cats, cats
and particularly in those in heart failure (see
that are homozygous for the mutation often
p 101).

HEART DISEASE AND HEART FAILURE

119

Treatment is directed at controlling signs

However, because that diagnosis cannot
of CHF, improving diastolic function, and
be made using standard two-dimensional
reducing the incidence of systemic
echocardiography, it is better to tem1 this
thromboembolism. Furosemide (2---4 mg/kg,
type of disease unclassified cardiomyopathy

IV or IM, as needed) administration and oxyunless diastolic dysfunction can be gen are needed when acute CHF is present.

documented, usually by using tissue

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For chronic heart failure, furosemide and an Doppler imaging echocardiography.

ACE inhibitor, eg, enalapril (0.5 mg/kg/day,

Restrictive cardiomyopathy is characterized

PO), are indicated. For cats not in heart
by a stiff, noncompliant left ventricle,
failure, no drug strategy has been shown to
usually due to increased collagen (ie, scar)

alter the natural history of the disease.

formation in the left ventricle. The

Diltiazem (7.5 mg, PO, tid), a calcium
increased stiffness increases diastolic
channel blocker, may improve diastolic
pressure for any given diastolic volume.

function, but its effects are generally

As in hypertrophic cardiomyopathy, this
negligible and its use has diminished. Use of
results in an increase in left atrial size and
f3-blockers such as atenolol (6.25-12.5 mg,
left heart failure. ln some cats that have

PO, 1-2 times/day) may also be considered,
obvious endomyocardial thickening or
but proof of benefit is lacking. People
partial cavity obliteration, the diagnosis of
with HCM have shown improvement in
restrictive cardiomyopathy can be readily
exercise-induced angina and dyspnea, and
made using two-dimensional echocardiogexercise intolerance when given f3-blockers. raphy. A left atrial thrombus may be evident.

Cats rarely exert themselves, so those

Systolic function is usually preserved. Color
indications do not apply. However, a
flow Doppler echocardiography may
f3-blocker does reduce systolic anterior
demonstrate mitral regurgitation.

motion of the mitral valve and should be

Clinical signs of and treatment for heart
considered when this abnormality is severe
failure are sinlilar to those for HCM (see

(pressure gradient across the dynanlic
p 117); however, prognosis seems to be
subaortic stenosis is >80 mrnHg). ACE
worse, especially in cats with CHF. The
inhibitors have no apparent beneficial effect cause of restrictive/unclassified cardiobefore the onset of heart failure.

myopathy is unknown.

Prevention of left atrial thrombus
formation and systemic thromboembolism
is often a goal. Clopidogrel (18. 75 mg/day/

Myocarditis
cat) is the only drug shown to decrease the

Myocarditis is a focal or diffuse inflammaincidence of systemic thromboembolism tion of the myocardium with myocyte
in cats. Warfarin (0.2-0.5 mg/day, PO) is
degeneration and/or necrosis. Myocarditis
probably ineffective and produces bleeding
is rare in companion animals, although
in some cats. Aspirin (80 mg, PO, every third there are numerous causes, including day) is also believed to be ineffective.

several viruses and bacteria. Canine

Clopidogrel plus aspirin is a conunon
parvovirus (seep 373), encephalomyotherapeutic strategy in people. A lowcarditis virus (seep 718), and equine molecular-weight heparin such as enoxapainfectious anemia virus (seep 699) can rin (1 mg/kg, bid) might be efficacious but is
cause myocarditis. Myocardial degeneraexpensive and must be adnlinistered tion is seen in lambs, calves, and foals with
parenterally.

white muscle disease and in pigs with

The prognosis for cats with HCM is highly mulberry heart disease or hepatosis variable. Many mildly affected cats have a
dietetica. Streptococcus spp are the most
good longterm prognosis. Cats in CHF have
common cause of bacterial myocarditis in
a poor prognosis, with a median survival
horses. Salmonella, Clostridium, equine
time of 3 mo. However, as many as 20% of
influenza, Borrelia bU1;gdorferi, and
cats with CHF might survive for a more
strongylosis are other recognized causes.

prolonged period.

Mineral deficiencies ( eg, iron, selenium,
copper) can also result in myocardial

Restrictive/Unclassified Cardiomy
degeneration ( not myocarditis ). Deficien
opathy: A Jess common form of cardiocies of vitamin E or selenium may cause myopathy in cats is characterized by a
myocardial necrosis. Cardiac toxins include
relatively normal-appearing left ventricle
ionophore antibiotics such as monensin and
with left atrial enlargement. Although it
salinomycin, cantharidin (blister beetle
is logical to believe that these cats have
toxicosis, seep 3157), Cryptostegia
diastolic dysfunction, many do not. Those
grandijlora (rubber vine), and Eupato
that do have diastolic dysfunction have
rium rugosum (white snakeroot). These
some form of restrictive cardiomyopathy.

diseases cause typical signs of CHF. ln

120

HEART DISEASE AND HEART FAILURE
horses, signs of right heart failure are
anhythmias. There are no reports of DCM
corru11on and include ventral edema,
due to these organisms in dogs or cats.

ascites, venous congestion, and jugular
pulsations. A heart murmur of rnitral or

Other Causes of Myocardial Failure
tricuspicl regurgilation is usually audible as
well as an irregular rhythm. Atrial fiblilla

In addition to the diseases listed below,

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tion is common, and ventJ.icular or atrial
histophilosis in cattle (seep 754) can result premature complexes may also be seen.

in myocardial infarcts and abscesses.

Echocardiography reveals chan1ber dilation
and poor contraction with essentially

Persistent Atrial Standstill: A form of
nom1al valves. Neutrophilic leukocytosis
cardiomyopathy resulting in destruction of
and hyperfiblinogenernia are common.

the atJ.·ial myocardium (that may also affect

Cardiac isoenzyrnes (CK, troponin, and
the ventricular myocardium) has been
lactate dehyclrogenase) are often increased.

reported in dogs. Affected breeds include

TreatJ.nent should be aimed at improving

English Sp linger Spaniels, Old English
cardiac contractility, relieving congestion,

Sheepdogs, Shill Tzus, Gem1an Sh01thai.red
and reducing vasoconstJ.iction. Pimobendan

Pointers, and mixed-breed clogs. The
and digoxin are used most commonly to
clisease has also been repmted in some cats
in1prove cont:ractility. Furosemide is
with concmTent cardiomyopathy. Initially,
indicated to control signs of pulmonary
atrial myocardial destruction leading to
edema. C01ticosteroids are often used
atJ.ial standstill and an AV nodal escape
when cardiac isoenzymes are increased
rhythm is noted. Mitra! regurgitation that
and a viral infection is deemed unlikely.

may be severe is often seen at this stage.

Eventually, myocardial failure may ensue.

Chagas' Myocarditis: Trypanosoma

Clinical signs are similar to those in aninlals
cruzi, a flagellate protozoa, causes Chagas'

with DCM, with right or left heart failure
disease (seep 38). Acutely, ECG
being noted. Pacemaker implantation may
abnormalities such as first-, second-, or
improve heart rate and cardiac output.

third-<legree AV block; right bundle-branch

Other tJ.·eatJ.nent aims to relieve signs of
block; sinus tachycardia; and depressed R

CHF This treatment typically is ultimately
wave amplitude are noted. There are usually lUll'ewarding, sinillar to treatment results in no echocardiographic abnom1alities dming
other anin1als with myocarclial failure.

the acute phase; however, sudden death is
a concern. An asymptomatic latent phase

Doxorubicin-induced Myocardial
then develops for 27-120 days in dogs,

Failure: Doxorubicin is a common
followed by a chronic stage demonstrating
chemotherapeutic agent that causes
systolic dysfunction indistinguishable from
well-recognized ca.rdiotoxicity. Cardiotoxic

DCM. TreatJ.nent for the chronic phase is
ity tends to be close dependent, but rare
as for DCM but is typically ineffective at
patients show toxicity at far lower dosages
controlling signs of progressive myocardial
than others. Abnormalities include isolated
failure. The disease is most commonly
ventJ.icular premature complexes (which
identified in southern states (eg, Texas) but
develop in 80% of clogs administered 80 mg/
may be spreading.

m2/day for 2 days or 25 mg!m2/wk for 4-11
wk) and periods of ventricular tachycardia..

Tickborne Myocarditis: Lyme disease

Myocardial failure may also develop and

(seep 659) is caused by the spirochete Bo1°
has been documented in lOOOA, of dogs
relia burgd01feri; infection might result in expelimentally administered 25 mg/m2/wk
myocardial disease. In people, it causes a
for 20 wk. (Sudden death and heart failure
usually reversible thi.rd-<legree AV block.

were noted in 65% of dogs after administra

Animals developing myocardial disease
tion of-17 wk of therapy.) The cardiotoxic
secondary to Lyme infection may, at least in
effects are irreversible. Severe cardiotoxictheory, have ECG abnormalities such as ity is rare with current chemotherapeutic
ventJ.icular arrhythmias or conduction
protocols but depends on how aggressive
disturbances such as first-, second-, or
the chemotherapeutic protocol is.

transient third-degree AV block. However, a
recent study failed to identify evidence of

Endocardial Fibroelastosis: Endocarany tickborne organism in a group of dogs dial fibroelastosis,a disease of unknown
presented for third-degree AV block. Two
cause, is characterized by diffuse thickening
dogs with severe ventJ.icular tachyarrhythof the left atJ.ial, left ventJ.icular, and/or mias with a high antibody titer to Ana
mitral valve endocardium. It is a rare ca.use
plasma phagocytophilum required
of myocardial failure in young dogs and
prednisone and azathioprine to control the
cats. Affected animals are usually <6 mo old

HEART DISEASE AND HEART FAILURE

121
and present with clinical signs of left heart

In contrast, the tricuspid valve is the most
failure. Breeds reported include Labrador
commonly affected valve in cattle. Wective

Retrievers, Great Danes, English Bulldogs,
endocarditis is rare in cats, and there are no

Springer Spaniels, Boxers, Pit Bulls, and
breed predilections. In dogs, middle-aged,

Siamese and Burmese cats (in which the
large-breed dogs are predisposed; <l()OA, of
disease is believed to be inherited).

dogs diagnosed with infective endocarditis

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Echocardiography demonstrates dilation
weigh <15 kg. Most affected dogs are >4 yr
of the left ventricular and atrial chambers,
old, and males ai·e more commonly affected
decreased left ventricular fractional
than females. Dogs with subaortic stenosis
shortening due to an increased left
are at greater risk of developing infective
ventricular end-systolic diameter, and
endocai·ditis.

possibly diffuse endocardial thickening.

Wected thrombi released from the

Clinical signs, treatment, and prognosis
infected aortic or rnitral valves enter the
are similar to those of DCM.

systemic circulation and can embolize other
organs and limbs; therefore, infective

Duchenne Cardiomyopathy:

endocarditis can produce a wide spectrum

Duchenne cardiomyopathy is an inherited,
of clinical signs, including primary

X-linked neuromuscular disorder reported
cardiovascular effects or signs related to the
in dogs, particularly Golden Retrievers. A
nervous system, GI tract, urogenital system,
sin1i.lar disease called X-linked muscular
or joints. A chronic, intermittent or
dystrophy has been reported in Irish
continuous fever is usually present. Shifting

Teniers, Samoyeds, and Rottweilers. These
leg latneness may be reported, and weight
diseases may result in myocardial as well as
loss and lethargy are frequently present.

neuromuscular disease. ECG abnom1alities

Acute to subacute mitral or aortic valve
include deep and narrow Q waves, a
regurgitation can result in left heart failure
shortened PR interval, sinus atTest, and

(ie, pulmonary edema) and clinical signs of
ventricular tachyarrhythmias. Echocardiogtachypnea, dyspnea, and cough. If the raphy may demonstrate focal hyperechoic
tricuspid valve is affected, ascites and
lesions affecting primarily the left ventricujugular pulsations may be present. Mastitis lai· and papillary muscle myocardium. This
and decreased n1i.lk production can be
usually develops by 6-7 mo of age, with the
noted in affected cattle. Hematruia and
lesions decreasing in size throughout the
pyuria may also be noted. A cardiac murmur
next 2 yr. The lesions result from calcificais present in most cases; the exact type tion and fibrosis. In aninlals that survive,
depends on the valve involved. When the
myocardial failure may develop.

aortic valve is affected, a low-intensity
diastolic heatt mum1ur is present, with

Infective Endocarditis
maximal intensity over the left cai·diac base.

A soft systolic heart murmur caused by

Wection of the endocardium typically
increased stroke vol rune may also be noted.

involves one of the cardiac valves, although

In this instance, the arterial pulse is
mural endocarditis may occur. Endothelial
bounding (ie, increased pulse pressure) due
damage is a predisposing factor for infective to diastolic run-off and increased stroke endocarditis to develop, although in dogs it
volume. Mitra! valve endocai·ditis results in
is most common for endocarditis to form on
a heart murmur similar to that ca.used by
a normal valve. When the endothelium is
degenerative valve disease-a low- to
partially eroded and underlying collagen
high-intensity systolic heart murmur heard
exposed, platelets adhere and produce a
best over the left cardiac apex.

microthrombus. Immune deficiency may

Bacteria most often isolated from
also be a predisposing factor. Bloodbome
affected dogs and ca.ts include Streptococ
bacteria may become enmeshed in this
cus, Staphylococcus, Klebsiella spp, and
thrombic lattice, resulting in a localized

Escherichia coli, although a host of other
infection that causes a progressive
bacterial species may be involved.

destruction of the valve and results in

Bartonella is also a recognized cause of
valvular insufficiency. Vegetative lesions are
aortic valve infective endocarditis in clogs.

the most common finding on cai·diac valves

In people, 600/o-800Ai of patients with
and can create valvular stenosis ( eg, aortic
infective endocarditis have a predisposing
stenosis) but more commonly produce
cardiac lesion that facilitates bacterial
valvular insufficiency. In dogs, horses, and
attachment. In clogs, however, infection
cats, the aortic and rnitral valves are most
appears to develop conunonly in those
commonly affected. The tricuspid valve
with no evidence of valve abnormalities.

is rarely affected, and pulrnonic valve

Streptococcus and Actinobacillus spp ai·e infective endocarditis is exceedingly rare.

the most conunon isolates in horses, and

122

HEART DISEASE AND HEART FAILURE

Trueperella pyogenes is most commonly
infection is mild and limited to one of the AV
cultured from cattle.

valves. Controlling heart failure requires tile

A CBC often shows a neutrophilic
use of diuretics such as furosemide, an ACE
leukocytosis. Active infection may be
inhibitor, and when myocardial failure is
associated with the presence of band
present, pimobendan. Initially in dogs,

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neutrophils, and chronic infection with a
parenteral antibiotics are indicated for
monocytosis (900A, of cases in one series).

1-2 wk (which may be cost prohibitive),

Anemia of chronic disease is frequently
followed by oral antibiotics for at least
present. Serum analysis abnormalities

� wk. Initial broad-spectrum bactericidal
reflect organ involvement secondary to
antibiotics (a combination of ampicillin plus
infective emboli and may include increases
gentamicin or enrofloxacin, or cephalotllin
in liver enzymes, BUN, and creatinine. In
plus gentamicin) should be used and
animals that develop immune complex
changed, if needed, based on antibiotic
glomerulonephritis, significant urinary
sensitivity studies. Renal function should be
protein loss and hypoalburninemia may
monitored when gentamicin is used,
develop. Blood cultures with antibiotic
because it is nephrotoxic. The prognosis is
sensitivity should be obtained in affected
poor in most dogs. Those tllat respond to
animals. It is preferable to draw two or three therapy often require longterm medications blood samples, each 1-2 hr apart, in a 24-hr
for heart failure ( eg, diuretics, vasodilators,
period. Strict aseptic technique is required.

pin10bendan) and frequent reevaluations. In

However, blood culture results are
large animals, rifan1pin (5 mg/kg, PO, bid),
frequently negative ( and are positive in
togetller witll anotller broad-spectrunl
other types of septicemia) and cannot be
antibiotic, has been demonstrated to
used alone to make the diagnosis of
improve short-term outlook. Aspirin (100
endocarditis.

mg/kg/day in ruminants and 17 mg/kg every

Radiography may demonstrate cardiac
other day in horses) or heparin (30 U/kg, SC,
chamber enlargement, depending on the
bid in ruminants and horses) may prevent
location and degree of insufficiency of the
further thrombus and vegetative growth in
involved valve. lf the ao1tic or mitral valve is
large animals.

severely affected, there will be left atrial and

Antibiotic prophylaxis is indicated in
left ventiicular chan1ber dilation. Evidence
dogs witll subaoltic stenosis when any type
of left heart failure may be seen as an
of procedure that can result in significant
increase in interstitial density or, in severe
bacteremia is perfonned. Routine antibiotic

CHF, an alveolar pattern in the pulmonary
prophylaxis for dental procedures is not
parenchy:ma. lf the tricuspid or pulrnonic
warranted with oilier types of cardiac
valve is affected, right-side chamber
disease and especially not in dogs witll
enlargement is expected. Echocardiography my:xomatous mitral valve degeneration, is tl1e diagnostic test of choice, because
because tllere is no evidence these dogs are
blood cultures are positive in only 500/o-900Ai
at increased risk of infective endocarditis.

of dogs. The affected valve is usually easily
detected-the involved area is hyperechoic

(bright), thickened, and often vegetative (ie,

Pericardia! Disease
looks like a cauliflower). The vegetative

Pericardial disease most commonly causes
lesion may oscillate. Erosive lesions may
an accumulation of fluid witllin the
predominate in some animals. Doppler
pericardia! sac (ie, pericardia! effusion).

echocardiography will confirm insufficiency This accumulation can be acute or chronic, of the valve, and chan1ber enlargement on
but chronic is much more common in
the side of the affected valve is expected
veterinary medicine. When tile fluid
when significant insufficiency is present.

accun1ulation is severe enough to markedly

Electrocardiography may demonstrate
increase tile intrapericardial pressure,
atrial and ventricular premature complexes.

cardiac tamponade occurs. Acute cardiac

Infrequently, other arrhythmias such as
tamponade ( eg, due to left atrial rupture
atrial fibrillation or conduction disturor tlloracic traun1a) primarily results in bances are found.

decreased cardiac filling and an abrupt

Therapy is directed at controlling clinidecrease in cardiac output. Chronic cardiac cal signs of CHF, resolving any significant
tamponade primarily increases the diastolic
arrhythmias, sterilizing the lesion, and
intraventricular pressures. This causes
eliminating tile spread of infection. The
signs of CHF. Right-side diastolic-and so
heart failure may be severe and intractable
systemic venous and capillary pressure-if tile aortic valve is significantly involved; only have to increase from a nom1al of 5
tile prognosis is grave in tllese cases. The
mmHg to 10-15 mmHg to produce signs
prognosis is much more favorable when
of right heart failure, whereas left-side

HEART DISEASE AND HEART FAILURE

123
pressures must increase from a nom1al
emia may be seen in horses witl1 s_eptic
of <10 mmHg to >20 mmHg to produce left
pericarditis and effusion. In horses witl1
heart failure. Thus, signs of right heart
suspected septic pericarditis, culture and
failure predominate.

sensitivity of tl1e fluid should be performed.

Pericardia! effusion is a relatively

In septic pericarditis, tl1ere will be a large

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common form of acquired cardiovascular
number of neutrophils, witl1 some being
diseases in dogs, is uncommon in cattle,
degenerate. Protein content of tl1e fluid will
and is rare in horses and cats. In dogs, cases be high, and bacteria may be seen. Cytologic involving middle-aged, predominantly
features of idiopathic pericardia! effusion
male, large breeds are most frequent.

in horses are variable, with neutrophils,

Idiopathic pericarditis and cardiac
eosinophils, and macrophages present
neoplasia are tl1e most common causes of
in variable nun1bers. Cytologic evaluation
pericardia! effusion in dogs. Hemangiosarof tl1e pericardia! fluid usually does not coma and heart base Lumors ( chemodecprovide a definitive cause for the pericardia]

toma, ectopic thyroid carcinoma) are the
effusion in dogs unless an infection is
most frequently seen cardiac neoplasms.

present, which is uncommon. Rarely a

Mesotl1elioma is a less common form of
tumor (most commonly a hemangiosarpericardia! neoplasia. Using echocardiogracoma) will acutely bleed, producing an phy, hemangiosarcoma is most frequently
effusion witl1 a PCV similar to that of blood.

identified on the tight auricle, in tl1e right

Radiographs often show an increase in

AV groove, and in the right atrial chamber
the size of the cardiac silhouette, which
in dogs. Heart base tumors usually are
often takes on a rounded (globoid)

identified between the aorta and main
appearance. However, tl1is classic
pulmonary artery. In cats, the most
appearance is not always present. If tl1e
common cardiac neoplasia is lymphoma,
cause is a cardiac tumor, especially a heart
but tl1e most common cause of mild
base tumor, tl1e cardiac silhouette may have
pericardia! effusion is heart failure. Most
a bulge at tl1e top of tl1e heart cranial to tl1e
cases of pericardia! effusion in cats are not
carina or at tl1e region of the cranial waist if
severe enough to cause cardiac tamponade.

no or only slight effusion is present. The

Less common causes of pericardia! effusion caudal vena cava may be dilated if cardiac in dogs are infections ( eg, coccidioidomy tamponade is present. Pleural effusion cosis ), trauma, left atrial rupture, and CHF
may also be present, more commonly if

Cattle most often develop pericardia!

mesotl1elioma is tl1e cause of tl1e pericardia]

effusion secondary to traumatic reticuloeffusion. The ECG in most cases shows pericarditis ( see p 230) or cardiac neoplasia normal sinus rhythm to sinus tachycardia.

(lymphoma). Lymphoma in cattle can also
result in valvular insufficiencies. In horses,
septic pericarditis and idiopathic pericarditis are most commonly reported.

The severity of clinical signs depends on
tl1e rate of pericardiaJ fluid accumulation.

In dogs, ascites is by far tl1e most common
clinical manifestation. Collapse and
vomiting may be seen. The femoral pulse
may be weak or decrease on inspiration and
increase on expiration (pulses pa.radoxus ).

In horses, tl1ere is often a history of
respiratory tract infection, fever, anorexia,
and depression. Physical examination
findings, in addition to abdominal distention, include generalized weakness, jugular venous distention, muffled heart sounds,
and occasionally a pericardia! friction rub.

With slow development of pericardia! fluid,
tl1e pericardia! sac is able to stretch or
enlarge, and clinical signs of right heart
failure may not develop until severe
pericardia] effusion is present.

CBC, serum chemistry profile, and
urinalysis results are usually nonnaJ.

Mild anemia, neutrophilic leukocytosis,

Severe pericardia! effusion in a dog,
dorsoventral projection. Courtesy of Dr. Mark D.

hyperfibrinogenemia, and hyperprotein-

Kittleson.

124

HEART DISEASE AND HEART FAILURE

Occasional atrial premature and ventricular
pe1icardial effusion by echocardiography is
complexes may occur. The height of the R
advisable before perfornling pericardiocenwave is often decreased ( <l m V in dogs), tesis.

and there may be a pattern of alternating

Parenteral fluids may be given inunedivariation in R wave amplitude, referred to as ately before and after pericardiocentesis.

electrical alternans, when there is a large

Corticosteroids have not been shown to be

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amount of effusion present. This results
beneficial in idiopathic pericarditis (benign
from the swinging motion of the heart
pericardia! effusion) in dogs, although they
within the fluid-filled pericardia! sac.

have been used witl1 success in horses. Most

Echocardiography is the most sensitive and
tumors that cause neoplastic effusion do
specific test for detection of pericardia!

not respond well to chemotherapy. A heart
effusion. A tumor can be visualized in most
base twnor can be surgically debulked, but
cases of neoplastic effusion. When cardiac
only by a highly skilled surgeon. Rarely, a
tamponade is present, the walls of the right
hemangiosarcoma can be surgically
atriun1 and right ventricle may collapse in
removed if it is confined to tl1e right auricle
systole or diastole.

and no metastatic disease is present.

Aninlals with cardiac tan1ponade require

Chemotherapy ( eg, aclriamycin) might be
mechanical drainage of the pericardia!

beneficial in some dogs with hemangiosarspace (pericardiocentesis) using a catheter.

coma, although swvival times are generally

Medical therapy is typically ineffective at
measured in montl1s.

reducing pericardia! effusion. Diuretics are

When idiopathic pericarditis is suspected
contraindicated in acute cardiac tamponade (ie, no mass visible by echocardiography), because they decrease blood volwne and
the owner should be instructed to carefully
cause a fwther decrease in cardiac output.

monitor tl1e animal for any signs of

Pericardiocentesis in dogs and cats is done
recurrence. Should this occur, a repeat
by placement of a catheter through the
pericardiocentesis is indicated. A subtotal
chest wall on the right side, just above the
pericardectomy is generally recommended
costochondraljunction at the fourth to fifth
after the third pericarcliocentesis. Heait
intercostal space. Echocardiography can be
base twnors only rarely metastasize in
used to guide catheter placement at the
dogs, although they can grow to be quite
point where the pe1icardial sac is closest to
large and may compromise function of
the thoracic wall and most distended with
surrounding structures. If recurrent
fluid, but it is not necessary. Fenestrating
pericardia! effusion secondary to a heart
the catheter helps prevent blockage. A
base tun1or is diagnosed, subtotal
syiinge or extension set with stopcock and
pe1icai·dectomy should be considered.

syiinge (preferred) is attached to.the

A dog can survive as long as 2 yr after
catheter. The system must be closed to air
successful subtotal pericai·dectomy. The
at all times once the chest wall has been
prognosis for right atrial hemangiosarcoma
penetrated, to avoid creating a pnewnothois poor to grave. Many clogs have metastasis rax. The catheter is passed directly toward
or micrometastasis (most conunonly to the
the heart while gently aspirating. When the
lungs and not visible on radiographs) at the
pericardia! sac is entered, fluid ( usually
time of diagnosis.

quite bloody) flows freely into the syiinge.

Constrictive and constrictive/effusive

The catheter should be carefully advanced
pericai·ditis is rare and primaiily seen in
over the needle into the pericardia! sac. The
dogs. It is thought to be an end result of
fluid should be placed either in a glass tube
chronic idiopatllie peticarditis. A clog with
or in a tube containing thrombin to cause
constlictive pericarditis usually presents
clotting if blood from the heart is aspirated;
witl1 ascites, no munnw·, normal heart
if it does clot, the catheter should be
sounds, normal cai·diac silhouette on
removed from the cardiac chamber it is
thoracic radiographs, a positive hepatojuguin. As much fluid as possible should be lar reflux test, and distended hepatic veins
removed from the sac and a sample
on ultrasound. Diagnosis cai1 be difficult
submitted for analysis. When perfomling
and may require cardiac catheterization.

pericardiocentesis in horses, the left fifth

Treatment is surgical. With constrictive/
intercostal space should be used to avoid
effusive pericarditis, there is still a fluid
the atria, coronary arteries, and right
layer between the pericardia! sac and the
ventricle. Pericardia! lavage, with or
surface of the heait, so surgical removal of
without antibiotics, is often performed in
the pericai·cliwn is relatively easy. With
horses after peticardiocentesis. Pericardioconstrictive pericarditis, the pericardium centesis is relatively easy to perfon11 in
and epicarditllll are fused into one fibrous
clogs, and serious complications are rare.

layer tl1at must be painstakingly removed

However, confirming the presence of
surgically.

HEART DISEASE AND HEART FAILURE

125

Systemic and Pulmonary
pressure, blood pressure measurements

Hypertension
should be done only in dogs and cats that
have a disease that causes hype1tension or

Systemic hypertension is an increase in
that have a clinical problem referable to
systemic arte1ial blood pressure. There are
systemic hypertension ( eg, detached

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two major types of systemic hypertension.

retina). Blood pressure measurement is not

Essential hypertension, which is idiopathic
a screening tool in veterinary medicine as it

(prin1ary) hypertension, is rare ( essentially
is in human medicine, except in patient
nonexistent) in dogs and cats but common
populations that have a disease that causes
in people. Secondary hypertension results
systemic hypertension ( eg, dogs with renal
from a specific underlying disease. In dogs,
failure should be screened for systemic
the most common cause of hype1tension is
hypertension). Even in an animal with a
renal disease/failure; in cats, the most
disease that causes hypertension that has
common causes are renal disease/failure
an increased blood pressure measurement,
and hype1thyroidism. Hyperadrenocortidocumenting end-organ damage ( eg, cism, diabetes mellitus, and pheochromopresence of hype1tensive retinopathy) is cytoma are other causes of systemic
recommended before instituting therapy.

hypertension in dogs.

Dogs and cats with severe systemic

The diagnosis of systemic hypertension
hypertension often have no clinical signs.

is made by measurement of systemic blood

Acute blindness is the most common
pressure. The most accurate assessment
clinical sign. Retinal lesions ( eg, retinal
method is direct measurement via arterial
hemorrhage, retinal detachment, arterial
puncture, which is impractical in most
tortuosity, focal or diffuse retinal edema)

instances. The next most accurate method
were found in 80% of hypertensive cats in

(although still often inaccurate) is indirect
one study. Blood tests may demonstrate
measurement using a Doppler probe to
abnormalities consistent with the cause of
assess blood flow in an artery (typically the
hypertension (eg, increased T levels in
superficial palmar arterial branch of the

4
hyperthyroid cats, increased BUN and
radial artery) distal to pressure cuff
creatinine in animals with renal failure).

placement (typically on the forelimb). Cuff

Treatment should be initiated in animals
width should be 300Ai of the circunuerence
with consistently measurable hypertenof the forelimb in cats and 40% of the sion that are documented to have an
forelimb circunuerence in dogs. Shaving
underlying cause such as renal disease/
the hair just proximal to the palmar
failure and evidence of end-organ dan1age.

metacarpal pad for application of the

Systemic hypertension in cats and dogs

Doppler probe allows for more accurate
appears to be due to constriction of
results. The hind.limb can also be used, in
systemic arterioles, because only potent
which case the superficial plantar arterial
systemic arteriolar dilators are reasonably
branch of the caudal tibial artery is
effective to decrease systemic blood
assessed. The disadvantage of Doppler
pressure to a clinically significant degree.

blood pressure measurement is that

The treatment for cats is an1lodipine
only systolic blood pressure is reliably

(0.625-1.25 mg/day, PO). Other drugs, such
measured. Other methods to measure
as enalapril, diltiazem, 13-blockers ( eg,
systemic blood pressure, such as the
atenolol), and diuretics (eg, furosemide)

oscillometric method, are even less
are generally ineffective. In dogs,
accurate than the Doppler method,
amlodipine (0.2-1 mg/kg/day) and
especially in small dogs and cats. Although
hydralazine ( 1-3 mg/kg, bid) are the only
indirect blood pressure measurement is
consistently effective drugs. Some
less accurate than direct assessment, it can
clinicians have had success with prazosin
detect acute trends in blood pressure

(1-4 mg [total dose], PO, 1-2 times/day) in
during anesthesia. In conscious animals,
dogs. Phenoxybenzamine (0.25-2 mg/kg,
normal values vary with patient stress;

PO, bid) is expensive but can also be
values higher than expected for a healthy
effective in dogs. It is most often used in
animal often are caused by the stress of
dogs with a pheochromocytoma but can
examination. With certain exceptions,
also be effective in dogs with systemic
systolic pressures > 180 mmHg are likely to
hypertension due to other causes.

be truly increased in an animal that appears

Pulmonary hypertension is increased
calm, and values >200 mmHg should be
blood pressure in the pulmonary arterial
strongly considered evidence of systemic
circulation. Possible causes include
hypertension. Because of the inaccuracy of
increased pulmonary blood flow ( eg,
noninvasive blood pressure measurement
ventricular septa! defect, patent ductus
and the influence that stress has on blood
arteriosus ), increased pulmonary vascular

126

HEART DISEASE AND HEART FAILURE
resistance due to decreased overall
of ascites. Exercise tolerance may be
cross-sectional area of the pulmonary
improved. There is limited experience with
vascular bed ( such as caused by pulmonary
tadalafil (1 mg/kg, PO, 1 -2 times/day) but, in
arterial wall hypertrophy, pulmonary
theory, it should have the same effects.

thromboembolism, and pulmonary

Pimobendan reduces pulmonary aitery
vasoconstriction), or both. Primary
pressure in dogs with pulmonary hyperten

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pulmonary hypertension is rare in any
sion secondary to left heart failure. The best
species other than people. In cattle, the
chance for a successful longterm outcome
most common cause is hypoxia-induced
is when the underlying disease can be
pulmonary vasoconstriction caused by high
identified and treated, but this is rare.

altitude (seep 137). Chronic ingestion of
locoweed (Oxytropis andAstragalus spp)

or chronic pulmonary disease caused by

Arterial Thromboembolism
bronchopneumonia or lungwom1 infesta

Overt intravascular thrombus formation
tion can also result in pulmonary hypertenis rare with heart failure in most species sion severe enough to result in right heart
other than domestic cats and people. Cats
failure. In horses, pulmonary hypertension
frequently fom1 a thrombus in a severely
may occur secondary to left heart failure.

enlarged left atriun1, most commonly in the

In dogs, pulmonary hypertension most
left amide. This thrombus then commonly
commonly occurs secondary to heartwonn
breaks loose and flows into the systemic
disease, pulmonary thromboembolism,
circulation. Although this occurs most
severe hypoxemia due to primary pulmocommonly in a cat with a large left atrium nary disease, and left heart failure.

due to cardiomyopathy, it can also occur

Clinical signs are typically those of right
without left atrial enlargement, sometimes
heart failure ( ascites, exercise intolerance)

even happening in an otherwise healthy cat.

and episodic collapse or syncope, usually

In a cat with severe left atrial enlargement,
after exercise or excitement. Physical
it is assumed that the primary reason the
examination findings may include evidence
thrombus develops is because of blood flow
of ascites in dogs and ventral edema in
stasis. Red cells aggregate when blood flow
cattle and horses along with jugular vein
decreases below a critical velocity. When
distention and pulsation. Definitive
the left atriun1 enlarges, blood flow velocity
diagnosis requires direct measurement
decreases (assrnning no mitral regurgitaof pulmonary arterial pressure ( rarely tion). The area of lowest velocity is the left
performed), or estimation of pulmonary
aUiicle. In some cats, red cell aggregation
pressures by Doppler echocardiography
can be visualized as so-called spontaneous

(via measuring the velocity of a tricuspid or
contrast or "smoke" within tl1e left atrium.

pulmonary regurgitantjet). Echocardiogra

In a few cats, both a thrombus and
phy may demonstrate flattening of the
spontaneous contrast can be noted.

interventricular septum in systole, right

However, in most cats, the thrombus has
ventricular chamber dilatation and/or free
already become an embolus by the time an
wall thickening, and right atrial enlargeechocardiogram is done.

ment. Treatment is typically unrewarding,

The site the thrornboernbolus lodges
and the prognosis is often poor, depending
once it has broken loose from its site of
on the cause. In heartworm disease,
attachment in the left atrium depends on
successful clearance of adult worms from
the size of the ttu·ombus and blood flow
the pulmonary arterial vasculature often
patterns. A very small thrombus can gain
results in a reduction in pulmonary artery
entrance to a coronary artery and cause
pressure and resolution of right heart
myocardial infarction. A mid-sized
failure. Dogs with a right-to-left shunting
thrombus can exit into a branch corning off

PDA can live for several years despite
the aorta, such as the brachiocephalic trunk
severe pulmonary hypertension if their

(and then most commonly to the right
polycythemia is adequately controlled.

subclavian) or an intestinal branch. Most of

Sildenafil ( 1-3 mg/kg, bid-tid), a phosphothese thrombi, however, are large and so diesterase V inhibitor, is probably the most
cannot exit off any branch of the aorta and
effective drug to lower pulmonary artery
end up at the tenninal aorta. Here, they
pressure and improve clinical signs in dogs
occlude aortic flow and release vasoactive
with pulmonary hypertension, but it is
amines that shut down collateral circulaexpensive. It is primarily warranted in tion. Consequently, they cause acute
dogs with clinical signs due to pulmonary
cessation of blood flow to the hindlimbs.

hypertension, most commonly syncope

This results in pulselessness (no femoral
and right heart failure. In these patient
pulse), pallor (pale or purple foot pads),
populations, sildenafil often will reduce or
poikilothennia ( decreased rectal temperastop syncope and allow easier control ture and cold hindlimbs ), and initially

HEAR1WORM DISEASE

127
extreme pain. The gastrocnemius muscles
some of these cats have residual problems
are often very finn. The cat can often move

(eg, dry gangrene). Numerous treatments,
the legs above the stifles, and the tail is
including surgery, thrombolytic agents,
commonly unaffected. In some cats, only
and rheolytic thrombectomy, have been
one hindlimb is affected.

tried but are largely unsuccessful when

Diagnosis is most commonly based
compared with waiting for the thromboem

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on clinical signs, physical examination
bolus to lyse on its own. Euthanasia is
findings, and Doppler blood flow readings
common. Clopidogrel (18.75 mg/day/cat)

ofthe hindlimbs. Ultrasound can also be
has been shown to be effective at preventused to identify the thromboembolus.

ing recurrence of these events in cats and

Misdiagnosis of neurologic abnormalities
so is assumed to be effective at preventing
as an arterial thromboembolus in cats is
first occunence also; however, it is, by no
common. In some cats, the clot will lyse on
means, lOOOA, effective. Aspirin is believed
its own over time (1-72 hours). However,
to be ineffective.

HEARTWORM DISEASE

(Dirofilarosis, Dirofilariasis)

Heartworm (HW) disease is caused by the
reported in ferrets or cats, but male cats
filarial organism, Dirofilaria immitis. At have been reported to be more susceptible
least 70 species of mosquitoes can serve as
than females. Indoor and outdoor ferrets
intermediate hosts; Aedes, Anopheles, and
and cats can be infected. Other infections in

Culex are the most common genera acting
cats, such as those caused by the feline
as vectors. Patent infections are possible in
leukemia virus or feline immunodeficiency
numerous wild and companion animal
virus, are not predisposing factors.

species. Wild animal reservoirs include
wolves, coyotes, foxes, California gray

Life Cycle: Mosquito vector species
seals, sea lions, and raccoons. In companion acquire microfilariae (a neonatal larval animals, HW infection is diagnosed
stage) while feeding on an infected host.

primarily in dogs and less commonly in cats

Once ingested by the mosquito, microand ferrets. HW disease has been reported filariae develop into the first larval stage
in most countries with temperate,

(L
semitropical, or tropical climates, including

1). They then actively molt into the
second larval stage (Lz) and again to the
the USA, Canada, Australia, Latin America,
infective third stage (L
and southern Europe. In companion

3) within the
mosquito in -1-4 wk, depending on
anin1als, infection risk is greatest in dogs
environmental temperatures. This
and cats housed outdoors. Although any
development phase requires the shortest
dog or cat, indoor or outdoor, is capable
time (10-14 days) when the average
of being infected, most infections are
ambient temperature is >81 °F (27°C) and
diagnosed in medium- to large-sized, 3-
the relative humidity is 80%. When mature,
to 8-yr-old dogs living outside.

the infective larvae migrate to the labium

Wected mosquitoes are capable of
of the mosquito. As the mosquito feeds, the
transmitting HW infections to people, but
infective larvae erupt through the tip of the
there are no reports of such infections
labium with a small amount of hemolymph
becoming patent. Maturation of the
onto the host's skin. The larvae migrate
infective larvae may progress to the point
into the bite wound, beginning the
where they reach the lungs, become
intramammalian phase of the life cycle.

encapsulated, and die. The dead larvae

A typica1Aedes mosquito is capable of
precipitate granulomatous reactions called
surviving the complete development of

"coin lesions," which are visible with
only small numbers of HW larvae, usually
thoracic radiographs and significant

<10 larvae per mosquito.

because they mimic lung cancer.

In canids and other susceptible hosts,

HW infection rates in other companion
infective larvae CL:i) molt into a fourth stage
animals such as ferrets and cats tend to

(L.

parallel those in dogs in the same geo

1) in 3-12 days. After remaining in the
subcutaneous tissue, abdomen, and thorax
graphic region. No age predilection has been for -2 mo, L. 1 undergo their final molt at day

128

HEARTWORM DISEASE

50---70 into young adults, aniving in the heart cells, including infiltration of high nwnbers and pulmonary arteries -70-120 days after
of eosinophils. Live w01ms seem to have an
initial infection. Only 2.5-4 cm in length
inununosuppressive effect; however, the
on anival, wonns rapidly grow in the
presence of dead wom1s lea.els to more
pulmonary vasculature to adult wom1s
severe vascular reactions and subsequent

(males -15 cm long, females -25 cm). When
lung pathology, even in areas of the lw1g not

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juvenile heartwonns first reach the lungs,
directly contacting the dead heartwonns.

blood flow forces them into the more distal

Longterm infections, clue to all of the factors
small pulmonary arteries of the caudal lung
noted (ie, clirect i!Titation, wonn death, and
lobes; as the parasites grow, they occupy
immune response) result in clu-onic lesions
larger and larger pulmonary arteries,
and subsequent sca.i·ring. Active clogs tend
moving into the right ventricle and a.triun1
to more often develop pulmona.i-y hypertenwhen the w01m burden is high. Gravid sion than inactive clogs for any given worm
females produce microfila.riae as early as
burden. Frequent exertion increases

6 mo after infection but more typically at
pulmonary arterial pathology and pulmo7-9 mo after infection.

nary artery resistance (with resultant

Microfila.ria.e are detectable in most
pulmonary hypertension) and thereby may
infected canids ( -80%) not receiving
precipitate overt clinical signs, inclucling
macrolide prophylaxis and occasionally in
congestive heart failure (CHF). High wonn
those dogs placed on macrolide preventives
burdens a.i·e most often the result of
when a HW infection was already present.

infections acquired from nwnerous

The number of circulating microfila.riae
mosquito exposures. High exposures in
does not c01relate well to the adult female
young, naive clogs in temperate climates

HW burden. Adult worms typically live 3-5
can result in severe infections, possibly
yr, whereas microfilariae may survive for up
precipitating vena cava. syndrome the year
to 2 yr in the dog, while awaiting anival of a
after. l.n general, because of the worm size
mosquito intennedia.te host.

and smaller dimensions of the pulmona.i-y

Most dogs a.re highly susceptible to HW
vascula.ture, small dogs do not tolerate
infection, and most ( an average of 56%)

infections a.i1cl treatment as well as la.i·ge
experimentally administered infective
clogs.

larvae (L3) develop into adults. Ferrets and

The role of the enclosymbiotic bacteria.

cats a.re susceptible hosts, but the rate of

Wolbachia pipiens, which live intra.celluinfective larvae developing into adults is larly within the fila.ricl parasite, is still being
low ( an average of 6% in cats and 4()0A, in
cletenninecl. However, these bacteria have
ferrets). In ca.ts, the adult burden is often
been implicated as playing a role in the
only one to three worms. It appears that
pathogenesis of fila.rial cliseases, possibly
early death of juvenile wonns on arrival at
through enclotoxin production. Fwtherthe pulmonary vasculature is largely responmore, studies have demonstrated that a sible for the heartwonn-assotiatecl
primary swface protein of Wolbachia
respiratory disease (HARD) syndrome in

(WSP) induces a specific IgG response in
ca.ts. HARD does not require maturation
hosts infected by D immitis. For veterinarof heartw01ms but is due to the body's ians, the most irnpo1tant aspect of
response to the clying/clea.cl hea.itwom1s.

Wolbachia is its symbiotic relation with D

When maturation does occur, adult wonn
immitis. This ba.cteriwn is necessary for
survival in cats is typically not longer than
nonnal maturation, reproduction, and

2 -3 yr. In all anin1als capable of being
infectivity of the heartwonn. If Wolbachia
infected, abe1Tant larval migration may
a.re eradicated, the heartwom1 gradually
occur, resulting in pa.i·asitic lesions in the
dies, after first becon1ing sterile. This can be

CNS, systemic arterial system, and in
accomplished with cloxycycline therapy.

visceral and subcutaneous sites.

HW-associa.tecl inflanunatory mediators
that induce immune responses in the lungs

Pathogenesis: The severity of cardiopuland kidneys ( eg, immune complex monary pathology in clogs is cletem1inecl by
glomernJonephritis) ca.use vasoconstriction
wonn numbers, host immune response,
and possibly bronchoconstriction. Leakage
duration of infection, and host activity
of plasma and inflammatory mediators
level. Live adult heartwonns ca.use direct
from small vessels and ca.pilla.iies causes
mechanical trawna, and other suspected
pa.renchyrnal lung inflanm1ation and mild,
factors ( eg, antigens and excretions) a.re
nonca.i·diogenic edema fonna.tion.

thought to directly irritate or to stimulate

Pulmonary arte1-y clisease compromises
the hosts' inunune system to damage vessel
vascular compliance, and this, with reduced
intima, lea.ding to proliferative enclarteritis
ability to adequately vasoclilate, results in
and perivascula.r cuffing with inflammatory
increased flow velocity, especially with

HEARTWORM DISEASE

129
exe1tion, and resultant shear stresses
present with cough, hemoptysis, weight
further danrnge the endotheliwn. The
loss, lethargy, exercise intolerance,
process of endothelial damage, vascular
dyspnea, heartfailW'e (ascites), and
dysfunction, increased flow velocity, and
radiographic findings suggestive of HW
local ischemia is a vicious cycle. Inflan1m a disease (large main puhnonary artery and tion with ischemia can result in itTeversible
lobar pulmonruy arteries, tmncated and

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interstitial fibrosis.

tortuous pulmonary arteries, pulmonruy

Pulmonary arterial pathology in cats and
infiltrate, and hilru· lymphaclenopathy).

ferrets is similar to that in dogs, although

Class IV includes dogs with caval syndrome.

the small arteries develop more severe

Dogs 5-7 YT old are at higher risk of having a
muscular hypertrophy. Despite this,
heavy worm burden, presumably because of
pulmonary hypertension with CHF is less
increased time of exposW'e ru1cl for disease
common in cats than in dogs or fetTets.

development. Other concuJTent health

Arterial thrombi, thromboemboli, and living
factors ( eg, concuJTent cru·diopuhnonruy or
or dead wonns become lodged within
other organ system disease) affect risk
pulmonary arteries or arterioles, resulting in assessment. The degree to which exercise complete or partial obstrnction. In cats,
can be rest1icted dming the recove1y period
parenchymal changes associated with dead
is anotl1er important consideration.

herutworms differ from those observed in

Infected cats may be asymptomatic or
dogs and feITets. Rather than type I alveolar
exhibit intennittent coughing, dyspnea,
cell damage, as found in dogs, cats develop
heart failme, vomiting, lethru·gy, anorexia, or
type II alveolar cell hyperplasia, which can
weight loss. When evident, signs usually
act as a significant barrier to oxygenation.

develop dW'ing two phases of tl1e HW life

Most significantly, because of restricted
cycle: 1) the rurival of juvenile worms in the
pulmonruy vasculru· capacity and subsepuhnonruy vasculatme -3-4 mo after quent pathology, ferrets ru1cl cats are more
infection, and 2) death of adult heartworms.

likely thru1 clogs to die as a result of HW

The eru·ly signs ru·e associated with an acute
infection.

vasculru· and pru·enchymal inflrunmatory
response to the newly ruriving yow1g worms

Clinical Findings: In dogs, infection is
ru1d the subsequent death of many or all of
ideally identified by serologic testing before
tl1esejuveniles. This initial phase is often
onset of clinical signs; however, at the
misdiagnosed as asthma or allergic
earliest, HW antigenemia and microbronchitis. Howeve1� this is now considered filaremia do not appear until -5 and 6.5 mo
to be part of HARD. Antigen tests in such
after infection, respectively. When dogs do
cats are negative (measmed antigens ru·e
not receive preventive medication and are
associated with matme female wonns)

not appropriately tested, infection and
dtuing the early eosinophilic pnewnonitis
disease progress undetected. Clinical signs
synclrome, although antibody tests typically
of HW infection, such as coughing, exercise
are positive. Although not yet well
intolerance, unthriftiness, dyspnea,
characterized, it is believed that clinical
cyanosis, hemoptysis, syncope, epistaxis,
signs often resolve and may not reappear for
and ascites (1ight-side CHF) may develop.

months. HARD has been postulated to

The frequency and severity of clinical signs
contribute to longterm lung damage. Cats
correlate to lung pathology and level of
harboring matme wonns may exhibit
animal activity. Signs are often not observed
intennittent vomiting, lethargy, coughing, or
in sedentary dogs, even though the worm
episodic dyspnea. Deat:11 of even one adult
bW'den may be relatively high. Infected dogs heartworm cru1 lead to acute respiratory experiencing a clrrunatic increase in activity,
clistress and shock, which may be fatal and
such as dW'ing hunting seasons, may develappears to be the consequence of pulmonary op overt clinical signs. Likewise, worn1
thrombosis and/or anaphylactic-like shock.

death and thromboemboli precipitate

Ferrets, more so than cats, mimic canine
clinical signs.

HW infection in tenns of clinical signs. The

A dog may be classified as low- or
lru·ge parasite:host body weight ratio dictates
high-1isk for developing clinical signs, based that fe1Tets ( and cats) develop clinical signs on assessment of potential wonn bW'clen,
with relatively small wo1m bmdens. Ferrets
the health and age of the clog, and its
with HW disease may demonstrate one or
lifestyle. There is also a more complex
more of the following: weight loss, fatigue,
classification system in which dogs are
rapid ru1d/or labored breathing, herut
classified from I to IV, based on severity of
mw1.nm, distended and pulsatilejugulru·
signs. Class I dogs are minimally affected
veins, cough, grey and cold mucous
clinically. Class II dogs exhibit cough. Class
membranes, ascites, plemal effusion,

III clogs ru·e severely affected and variably
fainting, ru1d sudden death. See TABLE 8.

130

HEAR1WORM DISEASE

DIAGNOSTIC TESTS, CLINICAL SIGNS, AND TREATMENT FOR

HEARTWORMS IN DOGS, CATS, AND FERRETS

Diagnosis (Test Utility)

Thoracic

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Host

Microfilaria

Ag or Ab Test

Radio graphs

Echocardiography

Dog

****

***** (Ag)

***MPA, PA,

**

RHE, PTE, PIE

Cat

*

** (Ag)

**PA, PIE

****

**** (Ab)

Ferret

*

*** (Ag)

*RH

***
armidacloprid-moxidectin is the only approved microftlaricide.

* = rarely useful; **=somewhat useful;*** = moderately useful; **** = often useful;

***** = excellent test; Ag = antigen; Ab = antibody; MPA = main pulmonary artery enlargement; PA = pulmonary a,tery enlargement; PTE = pulmonary thrombus/thromboembolus; PIE = pulmonary inflltrate with eosinophils; RH = right heart enlargement; NA= not applicable Adapted from McCall, JW. Clin Tech Small Anim Pract. 1998;13(2): 112.

Diagnosis: The antigen detection test is

The terminology for HW antigen tests has
the prefeITed diagnostic method for routine
cha.11ged, with tl1e word negative being
screening of asymptomatic dogs or when
replaced by "below detectable limits" to
seeking verification of a suspected HW
w1derscore the possibility of HW-infected
infection. Antigen testing is the most
pets being a.11tigen negative a.11d that a
sensitive and specific diagnostic method
negative test may become positive as
available to veterinary practitioners. Even
worms mature.

in areas where the prevalence of HW

The level of a.11tigenemia is directly
infection is high, -20%.of infected dogs are
related to the nwnber of mature female
not microfilaremic, which diminishes the
worms present. Most dogs harboring more
utility of screening by testing for microtha.11 two adult female worms will test filaiiae. This figure is even higher for dogs
positive with most available tests. For
infected with adult heartworms and that
low-burden suspects, commercial
are consistently administered monthly
laboratory-based microwell titer tests are
macrolide prophylaxis, because tllis kills
the most sensitive. There is, however, no
microfilariae and induces embryo stasis in
test that ca.11 determine worm burden.

mature female dirofilatiae.

Testing for microfilatiae may be useful as

Tinting of antigen testing is critical. A
a.11 adjunctive test in suspect cases that
pre-detection period must be considered,
have negative a.11tigen test results.

because these tests detect only adult, female

In dogs, echocardiography is relatively
worms. This takes into account the time
unimportant as a diagnostic tool. Visualizafrom exposure to seroconversion to a tion of worms in the right heart a.11d vena
positive antigen test. A reasonable interval is cava is associated with high-burden 7 mo after last possible exposure. There is
infection with or without caval syndrome.

no value in testing a dog for antigen or micro

Severe, chronic pulmonary hypertension
filatiae before -7 mo of age. To ensure that a
causes right ventiicular hypertrophy, septa!

previously acquired infection does not exist
flattening, underloading of the left heart,
in these young dogs, they should be tested
a.11d high-velocity tlicuspid a.11d pulmonic

6--7 mo after beginning HW prophylaxis. For
regurgitation. The ECG of infected dogs is
dogs > 7 mo old, testing should be performed
usually normal. However, right ventlicular
when preventive therapy is started and 7-12
hypertrophy patterns are seen when there is
mo later. Subsequently, annual a.11tigen
severe, chronic pulmonary hypertension,
detection tests ai·e recommended.

often associated with overt or impending

HEARTWORM DISEASE

131

DI AGNOSTIC TESTS, CLINICA L SIGNS, AND TREATMENT FOR

HEARTWORMS IN DOGS, CATS, AND FERRETS (continued) Treatment

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Clinical Signs

Prevention

Adults

Microfilariae

Respiratory, weight

Ivermectin,

Melarsomine,

Moxidectin•,
loss, exercise
milbemycin,
doxycycline,
ivermectin +
intolerance
selamectin,
symptomatic
doxycycline,
moxidectin
treatment
milbemycin

Respiratory,

Ivermectin,

Symptomatic

NA
vomiting, sudden
milbemycin,
treatment, worm
death
selamectin,
extraction
moxidectin

Heart failure,

Topical

Symptomatic

NA
respiratory, sudden
imidacloprid-
treatment,
death
moxidectin
moxidectin?

right-side CHF ( ascites ). Cardiac rhythm
ity is useful in making a clinical diagnosis
disturbances are usually absent or mild, but
of HW disease in cats, and it certainly
atrial fibrillation is an occasional complicaidentifies cats at risk. False-positive results tion in dogs.

from cross-reactivity with other parasites

The diagnosis of HW disease in cats is
have not been seen. A negative antibody test
based on historical and physical findings,
indicates 2:90% probability of the absence
index of suspicion, thoracic radiographs,
of mature infection. Microfilariae are rarely
echocardiography, and serologic test
detected by modified Knott's tests ( <lOOAi)

results. Cats may develop a positive antigen
in cats. Annual screening of cats is not
test 7---S mo after LJ inoculation. However,
necessary but may yield information for
antigen tests alone are considered too
concerned cat owners. For this purpose, the
unreliable (insensitive, missing 25%--50% of
antibody test is preferred in that it detects
mature infections) as the initial screening
cats with heartwom1s and those at risk. The
test for cats. This occurs with unisex ( all
antigen test is not appropriate for screening
male) infections, infections with insufficient in cats because of its low sensitivity.

numbers of mature females to be detectable,

In cats, worms can often be imaged using
and in cats with HARD. Cats with HARD
echocardiography. This is because of the
may remain antigen negative if no adults
relative sizes of the heartwom1(s) and the
develop, in all-male infections, or when only
right heart and pulmonary arterial system of
one adult female matw·es. These cats can
cats. Heartwom1S, particularly the females,
also be only temporarily negative if tested
are long enough to occupy the pulmonary
before detectable antigenemia develops.

arteries as well as the right heart, where

The antigen test is strongly recommended in they can be easily imaged. Parallel cats in which HW infection is suspected.

hyperechoic lines, produced by the HW

Antibodies to heartworms, produced by
cuticle, may be seen in the right heart and

900,6 of infected cats, often appear by 2--3 mo pulmonary arteries. Echocardiography is after LJ infection and are generally present
more important in cats than in dogs because
by 5 mo. However, antibodies can persist for of the increased difficulty of diagnosis in several months after wom1 death. Also,
cats (low antigen test sensitivity and low
antibodies induced by larvae can persist in
antibody test specificity for mature
aborted infections and after macrolide
infection) and the relatively high sensitivity
prophylaxis has been instituted, killing the
of the test in experienced hands.

early larval stages. Thus, a positive antibody

In addition to special diagnostic tests in
test indicates infection by HW larval stages,
cats and dogs, a CBC, chemistry profile,
and possibly HARD, but not necessarily of a
urinalysis, and particularly thoracic
mature infection. In cortjunction with other
radiographs are indicated. Laboratory
provocative findings, antibody seropositiv-
data are often normal. Eosinophilia and

132

HEARTWORM DISEASE
basophilia alone or together may occur in
results may occur, especially in species that
dirofi.lariasis. Eosinophilia is most often
harbor lower worm burdens ( cats and
seen at the tin1e that stage 5 (yonng adult)

feJTets). Furthem1ore, although microfilaria
larvae arrive in the pulmonary arteries.

testing is only rarely helpful, adult worms can

Subsequently, eosinophil cotmts vary
often be seen with echocardiography and
but are usually high in dogs witll in1mnnenonselective angiography.

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mediated occult infections, especially if
eosinophilic pneumonitis develops ( <l()OA,

Treatment in Dogs: The extent of the
of total infections).

preadulticide evaluation varies, depending

Hyperglobulinemia due to antigenic
on tl1e clinical status of the dog, the
stimulation may be present in dogs and
likelihood of coexisting diseases that may
cats. Hypoalbwninemia in dogs can be
affect the outcome of treatment, the owner's
associated with proteinuria in severe
ability to restrict the dog's exercise, and
in1mw1e-complex glomerulonephritis or
cost considerations. Clinical laboratory data
witl1 severe emaciation/cardiac cachexia.

should be collected selectively to comple

Serwn ALT and alkaline phosphatase are
ment infonnation obtained from a thorough
occasionally increased but do not con-elate
histmy, physical exanlination, antigen test,
well with abnom1al liver function, efficacy of and tl1oracic radiography.

adulticide treatment, or 1isk of drug toxicity.

Two impmtant vaiiables known to

Urinalysis may reveal proteinmia that can
directly influence tl1e probability of
be quantitated by a urine protein:creatinine
thromboembolic complications after
ratio. Occasionally, severe glomeruloneadulticide treatment ai1d the outcome of pluitis can lead to hypoalbmninernia and
treatment are tl1e extent of concurrent
nephrotic syndrome. Dogs with hypoalbupulmonary vascular disease and the cun-ent minemia, secondary to glomemlar disease,
worm burden. Assessment of cardiopulmoalso lose antithrombin ill and are at risk of nary status is indispensable for evaluating a
thromboembolic disease. Hemoglobinmia is
dog's prognosis. Pulmonary thromboemassociated with caval syndrome and occurs bolic complications after adulticide
when RBCs are lysed in tl1e circulation.

treatment are most likely to occur in heavily

In dogs, thoracic radiography provides the
infected dogs already exhibiting clinical and
most irLfom1ation on disease severity and is a
radiographic signs of severe pulmonary
necessary screening tool to assess the clinical vascular disease, especially when severe status of dogs with dirofilariasis, particularly
pulmonaiy hypertension and CHF are
when syn1ptomatic. High-risk irLfections are
present.

characterized by a large main pulmonary

Before adulticide therapy, HW-infected
artery segment and dilated, tortuous caudal
dogs are assessed and rated for risk of
lobar pulmonary arteries. Right ventticular
postadulticide thromboembolism. Dogs can
enlargement may also be seen and, along with be categorized as follows: 1) low risk of enlarged pulmonary arteries, is indicative of
thromboembolic complications, light wom1
pulmonary hypertension. With pulmonary
burden, ai1d no evidence of parenchyn1al
thromboembolism and pulmonary infiltrate
and/or pulmonaiy vascular lesions; or
with eosinophils (pneumonitis ), ill-defined

2) high risk of thromboembolic complicaparenchyrnal infiltrates sun-otu1d.the caudal tions. Dogs in tl1e low-risk category would
lobar arteries, typically most severe in the
ideally fulfill the following conditions: no
right caudal lobe.

clinical signs, nom1al thoracic radiographs, a

In cats, cardiac changes and pulmonary
low level of circulating antigen or a negative
hypertension are less common. In -500A, of
antigen test with circulating rnicrofilariae,
infected cats, caudal lobar arteries are
no wom1s visualized by echocardiography,
larger than the con-esponding vein and> 1.6
no concU1Tent disease, and with owners
times the dian1eter of the ninth 1ib at tl1e
capable of completely restricting exercise.

nintl1 intercostal space. Patchy parenchy

The low-risk group would also include dogs
mal infiltrates may also be present in cats
having previously tu1dergone adulticidal
with respiratory signs. The main pulmotherapy but that remain antigen positive.

nary artery segment usually is not visible

Dogs with near-normal thoracic radiographs
because of its relatively midline location.

may develop severe thromboembolic

In fen-ets, the diagnosis is less readily made disease, occurring most often when exercise with thoracic radiographs, because only the
is not restricted. Dogs at high risk of
right ventricle tends to be enlarged. However,
thromboembolic complications include
the commercial antigen tests have detected
those with signs related to HW irLfection

HW antigen experimentally, as early as 5 mo

(eg, coughing, dyspnea, ascites), abnormal
after irLfection, and have been shown to be
thoracic radiographs, high level of
effective in clinical situations. False-negative
circulating antigen, worms visualized by

HEARTWORM DISEASE

133
echocardiography, concurrent disease, and
resultant wom1 death, the second and third
little or no possibility that the owners will
i.r\jections can be withl1eld indefinitely.

restrict exercise.

Dogs with high worm burdens are at

The only approved heaitwom1 adulticide
risk of severe respiratory complications.

is melarsomine dihydrochloride, which is

Because only -500A, of heai'tworms are
variably effective against mature (adult) and destroyed after the fu'St injection, the in1mature heartwonns of both sexes, with
cumulative impact of wom1 emboli on

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male worms being more susceptible.

severely diseased pulrnonai-y arteries and

Melarsomine is given at 2.5 mg/kg, deep
lungs is reduced. F\ui;hermore, if serious

IM in the belly of the epaxial (lumbar)

tlu-omboembolism develops, the second
musculature in the area of the third to fifth
two-dose part of tl1e regimen can be
lmnbar vertebrae, using a 22-gauge needle
delayed, allowing the lungs to heal from the

(1 in. long for dogs <10 kg or 1.5 in. for dogs
fu'St insult. Lastly, this approach destroys a

> 10 kg). Pressure at the i.r\jection site is
higher percentage of adult heartwo1ms than
applied and maintained for 5 min to prevent
the standard two-dose protocol. For the
drug migration. Approximately one-third
utility and advisability of various therapeuof dogs will exhibit local pain, swelling, tic protocols, see TABLE 9.

soreness with movement, or ste1ile

Doxycycline has become an important
abscessation at the if\iection site. Local
part of treatment of HW infection in dogs.

fibrosis is not tmcommon (and is the reason

Through its negative action on Wolbachia,
for targeting the belly of the epaxial
it provides benefits to the canid host and
musculature). In standard use, the
works to the detriment of D immitis.

procedure is repeated on the opposite side

Doxycycline is indicated in preadulticide

24 hr later for dogs at low risk of treatment
therapy (at 10 mg/kg, bid, for 30 days) in
complications. However, to reduce the

HW-infected dogs. It is given in conjuncdanger of tlu-omboembolism, a two-phase tion with ivermectin at the preventive

(also termed "split-dose" or "tlu-ee-dose"

dosage (6-12 mcg/kg/mo). This combinamethod) treatment is highly recommended tion reduces the severity of lung if\iury
for at-risk dogs and, indeed, for all patients,
after adulticidal therapy, probably tlu·ough

LU1less cost considerations prohibit this
reducing the an1ount of Wolbachia antigen
approach. Using this protocol, a single
and the proteins released from the HW
i.rtjection of melarsomine is given, followed
uterus as the bacteria die and the uterus
by two i.rtjections 24 hr apart, after an
degenerates. Doxycycline at this dosage
interval of at least 30 days. The American
hastens worm death when the "slow-kill"

Heaitwom1 Society recommends this
approach is used, thereby presumably
three-dose alternative regimen, regardless
reducing the negative impact of worms on
of the stage of disease or risk category.

the host. Doxycycline v.'ith ivermectin also

Exercise restriction is essential once
clears the host of microfilariae. Therefore,
treatment is started to minimize the risk of
in dogs undergoing slow-kill treatment,
pulmonary thromboembolism due to dead
this combination decreases risk of
and dying adult worms.

macrolide resistance, which is a concern

An approach to adulticidal therapy in
in the slow-kill method using ivermectin
which preventive is started at time of
alone. Doxycycline is advocated in
diagnosis is doxycycline (10 mg/kg, bid for
treating dogs with HW infection regardless

30 days) and monthly HW preventive, at the
of severity classification or protocol.

standard preventive dosage. After 2 mo,

The An1erican Heartworm Society
adulticidal i.r\jections (melarsomine at
recommends administration of prophylac2.5 mg/kg, IM) are initiated, as the dog's tic doses of macrolides for 2 mo before
condition allows. Daily corticosteroids,
administration of melarsomine, with the
using a tapering dosage, may also be
first dose given concurrently with the first
administered dming this period to reduce
dose of doxycycline (day 1) and a second
pulmonary inflai11matory lesions from dying
dose given after the end of the doxycycli.ne
wonns and from melarsomine. Although
treatment ( day 30). A third dose is then
exercise is minimized from the day of
given concurrently with the first dose of
diagnosis, cage rest must be enforced from
melarsomine (clay 60). Macrolide administl1e day of each initial if\iection for 4-6 wk.

tration is continued monthly thereafter at
l£ the dog's condition allows, melat'Somine
tl1e preventive dosage. The rationale for
i.rtjections are repeated in 1 mo (2 i.r\jections
tltis approach is to eliminate susceptible

24 hr apait), with tl1e san1e regimen of
migrating D immilis larvae and to allow
prescribed exercise restriction. If, after
nonsusceptible 2-4 mo old larvae to age to
the first i.r\jection, the dog has suffered
a point at which they are more susceptible
significant pulmonary dan1age from the
to melarsomine. This approach of a 2-mo

134

HEARTWORM DISEASE

IHNIII GUIDE TO CHOOSING HEARTWORM THERAPEUTIC PROTOCOL

Protocol

Advantages

Disadvantages

Utilitya

Split dose
f efficacy, ! risk Cost $$$$; exercise

Appropriate for

(3 ir\jections),
of PTE, safety
restriction for 2 mo
all; best approach
melarsomine and
of phased worm
for severe HW

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doxycycline;
kill, no
disease
thoracic radio-
resistance
graphs, CBC, UA,
concern
chemistry panel,
coagulation profile

2 Standard dose

! cost, ! risk of Cost $$$; f risk of

Appropriate

(2 ir\jections),

PTE (vs

PTE (vs split dose);
when financial
melarsomine and
standard dose), ! kill efficacy (vs split constraints and doxycycline;
exercise
dose)

mild to moderate
thoracic radio-
restriction only

HWdisease
graphs, CBC, UA,

1 mo,no
chemistry panel,
resistance
coagulation profile
concern

3 Standard dose

! cost; exercise Cost $$; f risk of PTE

Appropriate

(2 ir\jections),
restriction only (vs standard dose);
when financial
melarsomine
l mo,no

! kill efficacy ( vs split constraints and
resistance
dose); cage rest
mild HW disease
concern, easier imperative
for shelters

4 Slow kill with

! cost, no

Cost $; f risk of

Appropriate only
ivermectin,
ir\jections, no
resistance, not
when severe
doxycycline
hospitalization, approved by AHS,
financial or other
shorter

-12-mo course, lung
constraints
treatment
disease progression,
duration than
time of HW death
slow kill
unknown

5 Slow kill with

Inexpensive; no f risk of resistance,

Should be
ivern1ectin
il\jections

30-mo course, lung
avoided
disease progression,
time of HW death
unknown

•None of these is appropriate for initial management of caval syndrome but may be used to complete therapy after wom1 removal.

UA = urinalysis; JYJ'E = pulmonary thromboembolism; AHS = American Heaitwom1 Society; $ = relative cost
pretreatment with macrolides has become

Dogs with 1ight-side CHF should be
less compelling with the recent knowledge
treated with furosemide (1-2 mg/kg, bid),
that doxycycline kills developing larvae
an ru1giotensin-converting enzyme (ACE)

CI-'3>L. >young adults) when administered
inhibitor such as enalapril (0.5 mg/kg/day,

1
at 10 mg/kg, bid, for 30 days, thereby
increased to 0.5 mg/kg, bid, after 1 wk
closing the gap during which developing
pending renal function test results),
lruvae are not susceptible to melarsomine
moderate dietary sodiun1 restriction, and
treatment.

abdominal paracentesis, as needed.

High-risk dogs should be stabilized

The inodilator, pinlobendan, is also
before melarsomine administration.

indicated at 0.25 mg/kg, bid, to suppmt

Stabilizing treatment includes cage
myocardial function and reduce cardiac
confinement, oxygen, corticosteroids,
work. Sildenafil can be used initially at
and possibly heparm (75-100 U/kg, SC,
l mg/kg, ti.ct, as a pulmonru-y vasodilator.

tid) for 1 wk before the alternative (split

Caution is warranted with this and other
dosage) melarsomine treatment
vasodilators to avoid the adverse effect
protocol.

of systemic hypotension.

HEARTWORM DISEASE

135

After melarsomine irtjection(s), exercise
the right atrium and orifice of the t:ricuspid
must be severely restricted for 4---6 wk to
valve is typically necessary to save the life of
mininlize puh11onary thromboembolic
the dog. This may be accomplished by using
complications. Adverse effects of melarlight sedation, local anesthesia, and either a sonline are otherwise linlited to local
rigid or flexible alligator forceps, or an
inflammation, cough, brief low-grade fever,
intravascular retrieval snare, introduced

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and salivation. Hepatic and renal toxicity
preferentially via the right external jugular
are seldom, if ever, seen.

vein. With fluoroscopic guidance, if available,

Laboratory findings associated with
the instrun1ent should continue to be passed
adulticidal therapy may include an
until wom1S can no longer be retrieved.

inflan1matory leukogram, thrombocytopeli11mediately after a successful operation, the nia, and prolonged activated clotting time or clinical signs should lessen or disappear.

prothrombin time. A postiajection increase

F1uid therapy may be necessary in critically
in senun CK may be noted. Local or
ill, hypovolenlic dogs to restore hemodydisseminated intravascular coagulopathy nanlic and renal function. After full recovery
may occur when platelet counts are
from surgery, adulticidal therapy is

<100,000/iiL. Treatment for severe
unde1taken to elinlinate remaining wom1S.

thromboembolism should include oxygen,

Particular care should be taken if many
cage confinement, a corticosteroid at an
wom1S are still visible echocardiographically.

anti-inflan1matory dosage ( eg, prednisone
at 1 mg/kg/day, PO), and low-dose heparin

Microfilaricide Treatment: At specific

(75--100 U/kg, SC, tid) for several days to 1
preventive dosages, the macrolide
wk. Severe lung injury is likely present if,
preventive drugs are effective microfilariafter 24 lu· of oxygen therapy, no improvecides, although not approved by the FDA for ment is noted and partial pressures of
this purpose. Adverse reactions may occur
oxygen remain <70 mrnHg.

in dogs with high nlicrofilarial counts

The standard melarsonline protocol

(>40,000/µL), depending on the type of

(two-dose, 24-hr treatment regimen) kills
macrolide given. However, the nlicrofilarial
most adult worms, clearing 500Ar--85% of
count is usually lower, and mild adverse
dogs. Antigen testing should be performed
reactions occur in -10% of dogs. Most

8---12 mo after the third dose of the splitadverse reactions are linlited to brief dose (alternative) protocol. If a positive test
salivation and defecation, occurring within
result is obtained at this time, consideration
hours and lasting up to several hours. Dogs,
can be given to abbreviated retreatment
especially small dogs ( <10 kg), with high

(two irtjections, 24 hr apart). A "slow-kill"

nlicrofilariae counts (>40,000/µL) may
approach with ivermectin (0.6 mcg/kg,
develop tachycardia, tachypnea, pale
every 2 wk for 6 mo) can be substituted for
mucous membranes, lethargy, retching,
repeated melarsomine irtjection but should
diarrhea, and even shock. Treatment
definitely be preceded by 30 days of
includes an IV balanced electrolyte solution
doxycycline therapy (10 mg/kg, bid) because and a soluble corticosteroid. Recovery is this mininlizes the reaction to dead and
usually rapid when treatment is adnlinisdying wom1s, enhances the kill rate to -1 yr tered quickly. Microfilarial counts are not

( vs 2.5 yr with ivem1ectin alone) versus the
routinely performed, and thus severe
standard slow-kill approach, and is thought
reactions are seldom expected. Treatment
to decrease the risk of resistance (see
specifically targeting circulating nlicrofilarabove). The standard "slow-kill" approach iae has historically been undertaken 3-4 wk
with ivem1ectin alone is against the
after adulticide administration. More
current recon1mendations of the American
con1monly, nlicrofilariae are eventually

Heartworm Society. Longterm use of
eliminated, even from dogs not treated
macrolides, rather than melarsomine, to kill
with adulticide, after several months of
adult worms allows pulmonary pathology to
treatment with prophylactic doses of the
progress during the lengthy period in which
macrocyclic lactones. The current practice
worms are dying and being processed.

is to start a macrocyclic lactone for

Cava! syndrome results from wom1S
prevention and nlicrofilarial eradication
nligrating retrograde to the right atrium and
at the time of diagnosis. Although all
great veins and is usually the result of a
macrocyclic lactones have nlicrofilaricidal
precipitous fall in cardiac output, as nlight
activity and are the safest and most effective
occur with pulmonary thrombosis. Severe
drugs available, this characteristic varies
pulmonary hypertension is then complicated
within this dn1g group. Only the combinaby worm-induced tricuspid valve leakage, tion topical product containing inlidaclohemolysis, and damage to liver and kidneys.

prid and moxidectin is FDA approved as a

In caval syndrome, removal of wom1S from
nlicrofilaricide. Livestock preparations of

136

HEARTWORM DISEASE
these chugs should not be used to achieve
is given at the san1e dosage and frequency
higher doses for the purpose of obtaining
as in dogs. Moxidectin and imidacloprid
more rapid results. Perfonnance of a micro

( combination) is approved by tl1e FDA for
filaria test is recommended at the time of
use in ferrets to prevent HW infection and
diagnosis and 1-3 mo after microfilaricidal
to prevent and treat flea infestations.

therapy has begun.

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Prevention: Heartwonn infection is

Treatment in Cats: There is currently
generally completely preventable with
no satisfactory treatment approach for
macrolicle prophylaxis. Year-round
heartworm infection in cats. lnfection often
prevention is advised. Preventive therapy in
is lethal. Thus, all cats in regions endemic
dogs is recommended beginning at 6-8 wk
for canine HW disease should receive drug
of age. No testing is necessary at this age,
prophylaxis. The lifespan of adult heartbecause the presence of mat1.u-e female wonns in cats has traditionally been
heartworms is required to produce a positive
thought to be 2 yr, so spontaneous recovery
heartwom1 test (antigen or microfilaria).

is possible. Cats may remain asymptomatic,

When prophylaxis is started after 7 mo of
experience episodic vomiting and/or
age, an antigen test and a test for presence of
episodic dyspnea (resembling asthma), may
microfilariae is recommended, followed by
die suddenly from pulmonary tl1romboemanother antigen test 6-7 mo late1: This series bolism or an anaphylactoid reaction, or
of tests will help to avoid urmecessary delay
rarely, develop CHF
in detecting subclinical infections, as well as

Because there is no safe or approved
potential confusion concerning effectiveadulticide for cats, many are managed ness of the preventive progran1, because it
conservatively with restricted activity and
cannot be detennined until the second test
corticosteroid therapy, such as preclnisowhether infection existed before beginning lone (1-2 mg/kg, PO, every 24-48 hr).

chemoprophylaxis.

Steroids reduce the severity of vomiting and

Fom1ulations of the macrolide prevenrespiratory signs. The hope is that episodes tives ivem1ectin, milbemyci.n oxime,
of pulmonary complications will not prove
moxiclectin, and selamectin are safe and
fatal as the worms die. Barring consecutive,
effective, as prescribed, for all breeds of
additional infection, 25%-50% of cats may
dogs. Currently marketed products have
survive with this approach. Serial antigen
additional chemicals and parasite spectra,
and antibody testing ( at intervals of 6-12
including GI and ectoparasites: ivennectin
mo) can be used to monitor status. Although (hookwom1S ), ivermectin/pyrantel pan10ate tl1ere are no supportive data, adininistration

(hookwonns and row1dwom1S), ivem1ectin/
of doxycycline (10 mg/kg, bid for 30 days)

pyrantel pamoate/praziquantel (hookworms,
and ivermectin (24 mcg/kg/mo) to an
roundworms, and tapewonns), milbemycin/
infected cat could be theorized to cause
lufenuron (hookworms, rotmdwonns,
worm degradation and contracture, thereby
whipwonns, and ste1ilizes fleas), rnilbernylessening the potential for catastrophic cin/lufenuron/praziquantel (hookworms,
consequences when the worms die. Of
roundworms, whipwom1s, tapeworms, and
course, the macrocyclic lactone would also
sterilizes fleas), selan1ectin (fleas, ticks, ear
protect the cat from a new infection, if more
mites, sarcoptic mites), moxidectin
exposure is encountered.

ir\jectable (hookwom1s), moxidectin/

Surgical retrieval of wonns from tl1e right
inudacloprid (roundwonns, hookwom1s,
atrium, right ventricle, and vena cavae via
whipwonns, adult fleas, microfilariae ),
jugular venotomy can be attempted in cats
rnilbemycin/spinosad (hookwonns,
with high wonn burdens detected by
roundwom1s, whipwom1s, fleas).

echoca.rdiography. An endoscopic basket,

At the approved dosage, nillbemycin kills
snare, or horsehair brush can also be
nucrofilariae quickly, and in the face of high
advanced via the right jugular vein under
nucrofilarial concentrations a shock reaction
fluoroscopy. Cats in CHF have been cured
may occur. Thus, milbemycin should not be
by wom1 removal.

adi11inistered without close monitoring
and/or prophylactic pretreatment (steroids

Treatment in Ferrets: Treatmentin ferrets and/or antilustarnine) as a preventive in is, likewise, difficult, because there is no
clogs with high nwnbers of rnicrofilariae.

approved agent for this purpose. Adulticidal

HW prevention is also recommended for
therapies (thiacetarsemide and melarsornine) all cats in endemic regions, regardless of have resulted in -500A, mortality in ferrets.

housing status, because of the potential

Moxidectin (ir\jectable and topical fonnulafor severe consequences with infection.

tions) has been widely thought to be

Performing microfilaria testing in cats before
adulticidal for heartwom1S in ferrets and
starting preventive tl1erapy is not required,

BOVINE HIGH-MOUNTAIN DISEASE

137
because cats have small microfilarial
preventive dosage for ferrets is the same
nwnbers and the presence of microfilaria is
as that for dogs (not cats).

typically transient. Ivermectin for cats is safe

Sporadic resistance of heartworms to
and effective at 24 mcglkg, PO, once monthly. the macrocyclic preventive class has been At this dosage, the formulation is also
recognized since 2013. All the current
effective againstAncylostoma t11baeforrne
molecules used to prevent heartworm
and A brazilien.se. Preventive treatment
disease have been implicated. However,

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should be started in kittens at 6 wk of age
some fornrnlations appear to be more
and continued lifelong. There is cun-ently no
effective against resistant isolates than
milbemycin product marketed for use in cats
others. There have been isolates from six
in the USA.

dogs with varying degrees of resistance.

Formulations of selamectin and a

There is little evidence of spread out of the
combination of imidacloprid/moxidectin

Mississippi Delta region, where resistance
are labeled for both dogs and cats.

was first recognized. It is important to

Selamectin is administered topically at a
realize that the current preventives are
monthly dosage of -6 mg/kg and also kills
effective in the vast majority of cases
adult fleas and prevents flea eggs from
and should not be abandoned. Emphasis
hatching for 1 mo. It also is indicated for
should be placed on owner compliance
treatment and control of Otodectes cynotis
and year-round preventive therapy, as well
in dogs and cats, sarcoptic mange,
as on alternative methods of HW preven

Derrnacentor variabilis infestations in
tion, including topical and oral mosquito
dogs,Ancylostoma t1ibaeforrne, and
repellants, indoor/screened housing,

Toxocara cati in cats. A topical combined
especially at night, and mosquito abateformulation of imidacloprid and moxidectin ment programs. The role of slow-kill
administered at dosages of 10 mg/kg for
macrolide adulticidal therapy has been
i.rnidacloprid and 1 mg/kg for moxidectin is
questioned in the development of resistance
also effective against HW infection and flea
and should be avoided. If such therapy is
infestations. Although all currently
unavoidable, it should absolutely be
marketed preventives are likely effective in
accompanied by 30 days of doxycycline
ferrets, only in1idacloprid with moxidectin
treatment at the outset, with assurance
is approved by the FDA. Importantly, the
that microfilariae are eradicated.

BOVINE HIGH-MOUNTAIN DISEASE

("Brisket" disease, Big brisket, Dropsy, High-altitude disease, Pulmonar.y hypertension, Congestive right heart failure)

Bovine high-mountain disease (BHMD) is
arterioles, resulting in pulmonary hypertencharacterized by a noncontagious swelling sion and subsequent right ventricular (RV)

of edematous fluid in the ventral parasternal hypertrophy. Without intervention to reduce muscles (brisket region), the ventral aspect
the hypoxia-induced pulmonary hypertenof tl1e body including the abdomen, and the sion, the disease will eventually progress to
submandibular region in cattle raised in

RV congestive/dilato1y cardiac failure.

high-altitude regions (>5,000 ft [ 1,524 ml) in

Rarely, similar lesions have been described
the western USA most commonly and
in severely stressed and parasitized sheep
substantially affecting Colorado, Wyoming,
and deer. Etiologically similar hypoxia

New Mexico, and Utall. It also affects cattle
related heait failure has also been described
in mountainous ranges of the world, most
in chickens in the Andes Mountains and in
commonly at elevations >6,500 ft (1,981 m)

people living at extreme elevations. The
in western Canada and South America.

incidence in cattle on high mountain

BHMD affects cattle of all ages and breeds,
pastures averages 3o/c,-5% with variations
but not necessarily equally.

from 0.5%-100/o but has been as much as 65%

BHMD is a result of pulmonary arterial
in a genetically susceptible calf crop. A 25%
hypertension induced by pulmonary
calf loss is not uncommon in the high
hypoxia occurring at high altitude.

elevations of Colorado and Wyoming.

Hypoxia-induced pulmonary arterial

Although most commonly associated
vasoconstriction and arterial hyperplasia
with altitude, other genetic, physiologic,
reduce the dian1eter of the pulmonary
environmental, and toxic factors play

138

BOVINE HIGH-MOUNTAIN DISEASE
important roles in disease development and
inhe1ited. In addition to underlying genetic
progression. Any pulmonary disease, acute
predisposition, altered chemoreceptor
or chronic, that hinders pulmonary function
activity or myocardial metabolism may
can result in a hypoxic condition sinlilar to
also play a role. Acute viral or bacterial
altitude-induced BHMD.

respiratory disease can exacerbate
puln1onary hypoxia of high altitude,

Etiology: Although many factors may
resulting in a rapid onset of RV failure.

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contribute to the incidence of BMHD, the

Various ra11ge plants, both browse a11d
pathogenesis is directly related to the
non-browse types, have been associated
hypoxic condition that results from high
with increased incidence of BHMD, but only
altitude. Pulmonary vascular shunting is a
locoweed has been experimentally shown
nom1al physiologic response to hypoxic
to induce the disease. When consumed by
conditions and is seen in all animals. Strong
cattle at lligh elevation, locoweed ( certain
responses are seen in cattle, horses, and

Oxytropis a11dAstmgalus spp that contain
pigs, whereas people, dogs, guinea pigs, and
the alkaloid swainsonine) markedly increase
llamas are Jess responsive. These findings
the prevalence a11d severity of CHF, which
and the high incidence of disease in cattle
develops relatively quickly (within 1-2 wk)

indicate they are uniquely susceptible. The
with a11 incidence as high as 1000/o. Swainsovasoconstriction mechanism of shunting is nine, the toxin in locoweed, is excreted in
a way to divert unoxygenated blood to
nlilk, thereby predisposing nursing calves
oxygen-rich regions of the ltmgs (dorsal
to developing CHF Locoweed-poisoned
aspect) and away from poorly oxygenated
cows often abort, a11d rna11y develop severe
regions (ventral aspect). Exaggerated
hydrops amnii in addition to showing signs
shunting in response to hypoxia, the
ofBHMD. Locoweed poisoning directly
anatonlic pattern of the bovine lobulated
contributes to increased pulmonary vascular
lung, and the small lung-size/body -weight
resistaJlce a11d hypertension; inummohistoratio all contribute to a severe loss of chenlistry a11d electron nlicroscopy studies
functional pulmonary capacity.

have shown that poisoning causes severe

Pulmonary vascular shunting is initially
swelling a11d cytoplasnlic vacuolation of
mediated through pulmonary aiteriole
pulmonai-y intravasculai· macrophages a11d
const1iction in the acute stages of hypoxia.

endothelial cells. TI1e rnyocardiun1 also is

Vascular hypertrophy and tllickening of the
compronlised by locoweed, seen as extensive
medial layers of the pulmonary aiterioles
vacuolation of the myocardial interstitial

(medial hypertrophy) and adventitial
cells. Finally, swainsonine has systenlic
tissues occurs with chronic hypoxic
endocrine a11d pai·acrine effects due to
exposure (>3 wk). Vascular remodeling
altered glycoprotein metabolism, which may
leading to loss of peripheral pulmonary
also contribute to the pathogenesis ofBHMD.

aiteries also contributes to increased
pulmonary resistance. This combination

Clinical Findings: The clinical changes of
of events causes significant pulmonary

RV CHF of high-mountain disease usually
hypertension, which leads to a progression
develop slowly over several weeks,
of cardiac pathology: RV hypertrophy,
commonly within the first 34 wk after
followed by RV dilation, and finally right
cattle are moved from lower to higher
congestive heait failure (CHF).

elevations. This 34 wk period may be an

This pathogenesis of exaggerated
average time, but clinical signs a11d death
vasoconstrictive shunting, aiterial medial
from pulmonary hypertension a11d right
and adventitial hypertrophy, and vascular

CHF have been seen within 24 hr after
obliteration resulting in pulmonary
altitude exposure a11d have aiso been seen
hypertension appears to be characteristic
in animals that have lived in higher
of some cattle and is highly heritable. Some
elevations for years. In those areas in North
cattle appear to be more naturally resistant

America where cattle spend summer and
to tllis process, both on an individual and
fall grazing at high altitudes a11d return to
breed basis. There is marked individual and
lower elevations later in the fall, the disease
interspecies variability in hypoxia-induced
is usually mailifest in late summer a11d early
increases in pulmonary vascular resistance.

fall a11d seems to be associated with

The role of genetics in BHMD is supported
weather and environmental conditions as
by high familial incidence with mai·ked
seen in high elevations with cold nights a11d
variation in susceptibility between
hot days. Pulmonary hypertension and right
individual animals, breeds, and other

CHF seem to follow respiratory disease
species of animals. There is strong evidence
seen with these san1e climatic influences. In
that the susceptibility of cattle Lo hypoxiaareas where cattle live year round at high induced pulmonary hypertension is
altitudes, the disease incidence is greatest in

BOVINE HIGH-MOUNTAIN DISEASE

139
late fall, winter, or early spring. Periods of
based on clinical findings related to CHF in
severe cold or other envirorunental stress
cattle kept at high altitudes. Body tempera

( eg, pregnancy, change in nutrition) appear
ture and CBC are generally nonnal unless
to precipitate the onset of signs. Affected
there is other underlying inflanunatory
animals initially appear depressed and
pathology. Recent studies in elevations
reluctant to move. As the syndrome pro

�9,000 ft (2, 743 m) found body temperatures
gresses, subacute edema develops in the
in calves experiencing pulmonary

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brisket region and extends cranially to the
hypertension to be increased (>104°F
intermandibular space and caudally to the

[40°C]). This is hypothesized to be
ventral abdominal wall. Pleural effusion and secondary to an increased metabolic ascites are usually abundant. Marked
demand and tachypneic response to the
distention and pulsation of the jugular veins
hypoxic condition. Thoracic auscultation
are usually prominent. Appetite may be
may reveal a decreased intensity of breath
decreased. Profuse diarrhea may develop as sounds in the ventral thorax and muffled a result of intestinal venous hypertension.

heart sounds if pleural effusion is present.

Respiration is labored, and animals may

The heart and respiratory rates are
appear cyanotic. As the disease progresses,
generally increased, and a systolic cardiac
affected cattle become more reluctant to
murmur may be auscultated if RV enlargemove and may become recwnbent. With ment has resulted in right atrioventricular
forced exertion, severely affected animals
or pulrnonic valve insufficiency. In end-stage
may collapse and die. In the terminal stages, CHF, a gallop rhythm is often detected.

the animal is often anorexic, recwnbent,

Although jugular distention is a characterisand unable to rise. To the rancher and cattletic clinical sign, an abnormal jugular pulse men, an animal experiencing "brisket
may or may not be seen. The common
disease" is most often characterized by
clinical pathologic changes are increases
severe brisket and abdominal edema and
in hepatic enzymes, particularly AST and
swelling, jugular enlargement and pulsation, L-iditol dehydrogenase. Clinically affected bulging eyes, exophthalmos (secondary to
animals may be azotemic because of
venous congestion), ventral abdominal
decreased renal perfusion secondary to
distention (ascites), bloating, recwnbency
heart failure and dehydration/hypovolemia.

or inability to travel with the herd, and

BHMD should be differentiated from other
profuse diarrhea.

causes of CHF, including pericarditis,
traumatic reticulopericarditis, cardiac

Lesions: Generalized edema is especially
severe in the ventral subcutaneous tissues,
lymphosarcoma, valvular endocarditis, viral
skeletal musculature, perirenal tissues,
or bacterial myocarditis, cardiomyopathy
mesentery, and wall of the GI tract. Ascites,

( nutritional, hereditary, or idiopathic),
hydrothorax, and hydropericardiwn are
pulmonary arterial obstruction from embolic
consistent findings. Fluid characteristics
pnewnonia, or clu-onic hypoxia and cor
include low cellularity and low to nom1al
pulmonale due to other primary pulmonary.

protein, consistent with a transudate
disease. Btisket edema may not always be
secondary to cardiac failure. The liver
present in animals with peracute RV CHF; this
lesions, due to chronic passive congestion,
can result in BHMD in calves being mistaken
vary from an early "nutmeg" appearance to
for acute viral or bacterial pnewnonia
severe lobular and vascular fibrosis. The
lungs may have varying degrees of

Treatment and Control: Affected
atelectasis, interstitial emphysema, edema,
animals should be moved to a lower altitude
and pnewnonia. The heart has marked RV
with minin1al restraint, stress, and excitehypertrophy and dilatation; the cardiac apex ment. General supportive therapy, including is displaced to the left, making the enlarged
diuretics, thoracocentesis, antibiotics,
heart appear round. The right atriwn is often and appetite stirnulators such as vitamin 2-3 times larger than the left and is flaccid.

B complex, may be beneficial. Thoracocen

Pulmonary arterial thrombosis is a frequent
tesis is the single treatment that most
finding. Microscopically, there is hypertrodramatically improves an affected animal's phy of the media of small arteries and
chance of survival. At high elevations, use
arterioles in the lungs. Acute rupture of the
of oxygen or a hyperbaric chamber may be
pulmonary artery (aneurysm) secondary to
considered for valuable animals. Because
the severe pulmonary hypertension is often
the disease may recur, affected animals
seen as a reason for acute death without
should not be returned to high altitudes.

clinical signs of RV CHF.

Affected cattle should not be retained for
breeding because of heritability. Treatment

Diagnosis: There is no definitive diagof concurrent diseases, including respiranostic test for BHMD. A diagnosis may be tory/cardiac disease, GI disease, parasitism,

140

BOVINE HIGH-MOUNTAIN DISEASE
and plant toxicosis, should be addressed.

cattle, it appears that no one breed is

Because locoweed poisoning has been
resistant to the effects of high-altitude
directly linked to the development of CHF in
hypoxia, although some breeds, and
cattle, the exposure of susceptible animals to pedigrees within breeds, appear to be more locoweed should be minimized by ensuring
naturally resistant. It is not unusual to see a
that animals have a good selection of forages. difference in PAP measurements between VetBooks.ir

Animals should be moved to pastures free of
heifers and bulls because of husbandry
locoweed as soon as poisoning is recognized
practices. Bulls are often pushed nutritionto prevent severe and irreversible damage.

ally for faster growth and muscling, which

Treatment of BHMD can be expensive
may affect pulmonary function and give rise
and unrewarding, so prevention is preferred.

to pulmonary hypertension. Pregnant cattle

Genetic selection through the use of
have been noted to have a higher PAP
pulmonary arterial pressure (PAP) measuremeasurement than nonpregnant cattle. The ments to select cattle resistant to the effects
age of the animal at the time of PAP testing
of hypoxia is a more effective way to control
should always be considered, because there

BHMD. Identifying animals highly susceptiis greater variation and less predictability in ble to the effects of altitude hypoxia (those
cattle s l yr old. Testing aninlals at �16 mo of
with high PAP measurements) and eliminatage appears to be the most consistent and ing them from the breeding pool are practical
accurate at predicting susceptibility to
methods to reduce the prevalence of BHMD
puln1onary hypertension induced by high
in a herd. The PAP measurement procedure
altitude. Any concurrent illness, especially
involves passing flexible polyethylene
respiratory disease, or any cause of
catheter tubing (1.19 mm internal dian1eter x
temporary or pennanent puhnonary hypoxia

1. 7 mm external dian1eter) through a
can influence the PAP measurement.

large-bore needle (12 or 13 gauge, 3.5 in.)

Some cattle appear to be prone to
inserted into the jugular vein. The catheter is
developing right CHF, whereas others live at
advanced through the jugular vein to the right high altitude with a documented increased atriwn, into the right ventricle, and then into

PAP and never have a clinical problem.

the puhnonary artery.

Even though these animals may not develop

At altitudes of 5,000-7,000 ft (1,524-2,133
clinical BHMD, they can pass the genetic
m ), a normal mean PAP measurement should
predisposition to their offspring. This
be 34--41 mmHg. ln cattle displaying signs of
variable expression of clinical disease and
pulmonary artery hypertension, the PAP can
the variable penetrance of the gene makes
rangefrom 48-213rnrnHg. The PAP and the

PAP testing challenging at all elevations

RV pressure may be norn1al to subnonnal
and becomes an even greater concern at
in cattle with end-stage right CHF because
elevations <5,000 ft (1,524 m) where the
of the failing myocardiwn. Cattle with .

hypoxic conditions needed to stimulate a
ventJicular septa! or atrial septa! defects often pulmonary response are not sufficient. PAP
have mean systolic and diastolic measuremeasurements taken at low elevations ments in the hundreds. Any aninlal with a PAP ( <5,000 ft [1,524 ml) should not be used as a measurement >48 mmHg is considered at risk positive selection tool but only to identify of developing BHMD and may be a potential
animals highly susceptible to hypoxic condigenetic carrier and should l)Ot be maintained tions and hypertensive even at elevations
or used in breeding progranis at high altitude.

<5,000 ft (1,524 m). Cattle moved from low

These aninlals should also be auscultated for
elevations to high elevations should remain
cardiac mwmurs and evaluated for possible
at the altitude for �3 wk before PAP testing.

congenital cardiac defects. In general, cattle

Future advancements in the research of

>1 yr old that have a PAP <41 mmHg at an
pulmonary hypertension in cattle are
elevation >5,000 feet (1,524 m) are likely to
concentrating on identifying DNA markers
maintain an acceptable PAP at high altitude
for recognition of genetic caniers of
and setve as good breeding stock for herds at
pulmonary hyperresponders to hypoxic
high elevation. PAP measurements between
conditions. Other areas of interest and

41 and 49 rnrnHg are difficult to interpret
research are being directed at and
consistently; these animals should be used
addressing the alarming increase in
with caution at high elevation.

incidence of RV CHF at lower elevations as

Multiple factors contribute to the variation seen in heavy feedlot cattle at elevations of PAP in cattle, including breed, gender,
s4,000 ft (1,219 m). These fat cattle at this
age, body condition, concurrent illness,
elevation seem to have the san1e postmorenvironmental conditions, elevation, and tem lesions as those seen at higher
genetics. Based on tests of >300,000 head of
elevations.

THROMBOSIS, EMBOLISM, AND ANEURYSM

141

THROMBOSIS, EMBOLISM,

AND ANEURYSM

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A thrombus is an aggregation of platelets
also occw· ar1d may contribute to metastaand fibrin that may fom1 when certain sis. Systemic arterial thromboembolism is
conditions exist. Historically, these have
more important in cats, whereas dogs and
included some combination ofVirchow's
lar·ge anin1als appear to develop in situ artetriad such as blood stasis (reduced flow), rial thrombosis more commonly. Thromboendothelial if\iury, and/or an existing sis of limb arteries causing lameness and
hypercoagulable state. A thrombus can
gangrene has been reported in adult horses
develop in a cardiac chamber and be
and foals. This occurs secondary to
attached (mural) or less likely free floating
hypercoagulation and systemic inflarnma

(ball), or can originate in situ within a
tion (eg, septicemia in foals).

blood vessel where it can cause a partial or

An aneurysm is a vascular· dilation
complete obstruction. The tlu-ombus can
caused by weakening of the twlica media
be classified based on its location and the
of blood vessels. The weakness might be
clinical signs it produces ( eg, jugular venous primary or caused by degenerative or thrombosis in large aninrnls associated with
inflarnmatory changes progressing from ar1
prolonged venous catheterization,
intimal lesion. False anew-ysms (pseudopulmonary arterial thromboembolism anew-ysms) are caused by damage to all
associated with heartworm disease in
t11ree layers of the arterial wall and result in
dogs).

extravascular accwnulation of blood.

All or part of a thrombus may break off

Disruption of the endotl1eliun1 associated
and be carried through the bloodstream as
with a true aneUI-ysm can cause formation
an embolus tl1at lodges distally at a point
of a thrombus with subsequent embolizawhere the size of the embolus exceeds the tion; thus, aneurysms, thrombi, at1d emboli
vascular dian1eter. Poor irtjection or
may be recognized sinmltaneously.

catheterization techniques along witl1

Aneurysms are rare in domestic animal
inferior catheter material can result in
species, altl1ough they have been reported
vascular thrombosis. However, clinically
in dogs, cats, horses, primates, and turkeys.

significant vascular thrombosis is more
commonly seen in animals with underlying

Clinical Findings and Diagnosis: Acute
diseases that result in a hypercoagulable
onset of dyspnea is often associated witl1
state, such as systemic inflammation,
pulmonary thromboembolism, although
endotoxemia, neoplasia, or antithrombin
some animals may develop hemoptysis; tl1e
deficiency. lf left untreated or uncontrolled,
latter is most associated with pulmonary
systemic tlu-ombosis can result in hemorarterial disease such as that resulting from rhagic diathesis or disseminated intravascuheartworm infection (seep 127). Septic lar coagulation (DIC), a life-threatening
cardiac thrombi are associated wiili
disorder of hemostasis with deposition
endocarditis; nonseptic cardiac tJu·ombi are
of microthrombi and conswnption of
associated witl1 myocardial disease (most
coagulation factors that results in concurcommonly in cats), or rarely with cardiac or rent hemoffhage.

pulmonary neoplasia. Infarction witllin the

Thrombus fotmation can occw· in both
genitourinary system can present with
large and small arteries and veins. Horses
hematuria, abdominal pain, and splinting.

and cattle are more likely to develop venous

Splanchnic infar·ction usually results in
tlu-ombi, whereas in dogs ar1d cats, arte1ial
abdonlinal pain, with vomiting seen in small
tlu·ombi appear· to be more clinically
anin1als.

in1portant. Arterial thrombosis or emboliza

Aneurysms cause no clinical signs
tion results in ischemia of the tissues
w1less hemoffhage occurs or an associated
supplied by the infarcted vessel ( eg, cats
tlu-ombus develops. Except for dissecting
with car·diac disease and subsequent arterial anern-ysm in turkeys (seep 2787), aortic or thromboembolism). Emboli from infective
sinus ofValsalva rupture in horses with
conditions such as endocar·ditis are
sudden deaili, hemoffhage associated wiili
classified as septic (bacteria contained in
guttmal pouch mycosis in horses ( see
ilie embolus). Septic emboli can result in
p 1463), or pulmonary arterial aneurysm in
bacterial dissemination and infection of
cattle, spontaneous aneurysmaJ hemordistal capillary beds. Neoplastic emboli can rhage is rar·e, and clinical signs usually

142

THROMBOSIS, EMBOLISM, AND ANEURYSM
relate to thrombosis. An aneurysm of the

Horses: Cranial vena cava thrombosis
abdominal aorta and its branches in large
may result from extension of ajugular
animals may be palpated rectally as a fixed
thrombus. Jugular vein thrombosis in
firm swelling with a rough, irregular swface
horses is often associated with phlebitis
that pulsates with the heart beat. Fremitus
following catheterization or extravasation
may be present. In excess thrombus
of iJ\iected material and will cause swelling,

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fom1ation, the pulse may be delayed distally
heat, and pain of the affected area. Bilateral
and have a slow rate of rise in pressure, or it
jugular vein thrombosis can cause edema
may be absent. Other helpful diagnostic
and swelling of the head and neck,
modalities include ultrasonography and
mimicking cranial caval thrombosis.

angiography.

Ultrasonographic examination of the
affected vein can detennine the extent of

Cattle: Thrombosis of the caudal vena
the thrombus and degree of occlusion.

cava occurs in association with hepatic

Doppler ultrasound is a more sophisticated
abscessation and vascular erosion of
method to detemiine blood flow and vessel
the abscess. Embolic pneumonia with
patency. If a catheter-associated tlu·ombosecondary pulmonary abscessation, phlebitis is suspected, blood culture and
thromboembolism, and puhnonary arterial
catheter-tip culture can be perfom1ed.

aneurysms are common sequelae. Affected

Horses with colitis and other GI disorders
anin1als may present with coughing,
are at increased risk of developing jugular
tachypnea, dyspnea, and abnormal lung
thrombosis; ruminants are much less prone
sounds. Aneurysms in pulmonary arteries
to jugular thrombosis than horses. Caudal
that contain septic emboli may rupture and
vena cava-like syndrome has been
cause intrapulmonary hemorrhage, or
described in a Quarter horse with respirapulmonary abscesses may erode into tory signs. Hepatic abscesses, caudal vena
bronchi and result in hemorrhage into the
cava thrombosis, pulmonary thromboemboairways. The sequelae to these disorders lism, and embolic pneumonia were
may include epistaxis, hemoptysis, and
identified at necropsy.

death. Clinical pathologic data usually

Migrating Strongylus 'IYlllga1is larvae
support a diagnosis of vena caval syndrome

(seep 316) can cause arteritis with
but are not specific. Increased fibrinogen,
development of thrombi and verminous
anemia, and in cases with an active abscess
aneurysms in the aorta, cranial mesenteric,
process, increased liver enzymes may be
or iliac artery. In some horses, emboli
seen. Pulmonary arterial embolism and
develop and partially or completely occlude
embolic pneumonia are also frequent
terminal branches of the mesenteric
complications of tricuspid or pulmonic
arteries. Affected intestinal segments show
valvular endocarditis in cattle, but

. changes ranging from ischemia to
aneurysms rarely develop. Intermittent
hemorrhagic infarction. Clinical signs are
fever and anorexia due to bacteremia at
those of colic, constipation, or diarrhea. The
times of embolic showering are often
colic usually is recurrent, and attacks may
present, and the animal typically has a
be severe and prolonged. Newer anthelminhistory of a chronic active infection ( eg, foot tics and in1proved therapeutic regin1ens abscess, reticular abscess) as well as
have resulted in verminous arteritis
chronic weight loss with poor body
becoming an unconunon disorder.

condition score. Most cases of right heart

Tiu·ombosis with or without aneurysm
endocarditis in cattle are bacterial and are
of the tenninal aorta and proximal iliac
commonly associated with a cardiac
arteries produces a characteristic syndrome
murmur, with a point of maximal intensity
in horses. Although associated with
over the tricuspid valve. Echocardiography
parasitism, other causes are possible.

and blood cultures help identify right heart

Affected horses appear normal at rest;
vegetative lesions and the causative
however, graded exercise results in an
bacterial agent, respectively. Thrombosis
increasing severity of weakness of the
of the cranial vena cava in cattle produces
hindlin1bs with unilateral or bilateral
bilateral jugular engorgement; edema of the
lameness, muscle tremor, and sweating.

head, submandibular area, and brisket; and

Severely affected animals may show signs
pronounced oral mucosa! hyperemia.

of exercise intolerance, weakness, and

However, similar clinical signs are seen with atypical lameness that resolves after a sho1t right-side congestive heart failure, which
rest. Subnormal temperature of the affected
could be a sequela of tricuspid valve
limbs may be detectable, along with
endocarditis. Significant lingual, pharyndecreased or absent arterial pulsations and geal, or laryngeal edema may develop and
delayed and diminished capillary filling.

result in dysphagia and dyspnea.

Rectal palpation may show variation in

THROMBOSIS, EMBOLISM, AND ANEURYSM

143
pulse amplitude of the internal or external
atrial enlargement, including other
iliac aiteries ( or both) and asymmetric
cardiomyopathies, hyperthyroidism, or
vasculature. In severe cases, the hindquarcongenital heait disease, can predispose to ter muscles atrophy, and lameness may
aiterial thromboembolism. Intracavitaiy
become evident with only mild exercise.

thrombi typically form in the dilated left

Complete embolic or thrombotic occlusion
atrium where stagnant flow exists or, less
of the distal aorta may produce acute
commonly, within abnormal ai·eas in the left

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bilateral hindlimb paralysis and recumventricle. Although the condition is poorly bency in horses. Affected animals are
understood, these cats most likely possess
anxious, appear painful, and rapidly go into
some degree of concurrent hypercoagulabilshock. The hindlimbs are cold, and rectal ity, because all cats with cardiomyopathy do
palpation reveals an absence of pulsation in
not develop cardiogenic embolism. Portions
either iliac aitery. 'Iransrectal ultrasound
of these intracavitary tlu·ombi can break
can help determine bloodflow in the aorta
off and fom1 emboli that infarct aitelial
and iliac aiteries.

branches, most commonly the aortic

Aneurysm of the aortic root has been
trifurcation (saddle emboli). Clinical signs
reported in horses, commonly noted at the
include pain and paresis or lower motor
right aottic sinus with or without concurneuron pai·alysis of the hindlirnbs. The rent endocarditis. Similar to those in people, aitelial pulse ( either femoral or pedal) is aneurysms of the sinuses of Valsalva in
reduced to absent in the affected limbs,
horses can be congenital or acquired.

which are cooler than normal and have firm,

Rupture of an aortic aneurysm typically
swollen gastrocnemius muscle bellies.

leads to sudden death, a scenario most

These clinical signs can be unilateral,
commonly seen in breeding stallions during
bilateral, or bilateral but asyrnmetiic.

live cover.

Emboli may also infarct other aiterial
beds, including the right forelimb, renal,

Dogs and Cats: In dogs, and less
splanchnic, cerebral, or myocardial
commonly in cats, heartworm disease may
circulation. Decompensation of the
lead to pulmonary aiterial thromboembounderlying myocai·dial disease is not lism that commonly results in dyspnea and
unconm10n and may result in congestive
tachypnea. Affected animals are often
heait failure (puhnonary edema or pleural
reportedly healthy until sudden onset of
effusion). Ischemia and necrosis of infai·cted
coughing, hemoptysis, respiratory distress,
pelvic lin1b musculature results in increases
or sudden death. Clinical signs most
in serum CK and AST, and subsequent
commonly develop in the weeks after
reperfusion of affected muscles cw result in
treatment with adulticide; however,
life-threatening hyperkalemia and acidosis.

pulmonary thromboembolism may also

Echocardiography is the imaging modality of
develop from spontaneous worn1 death, or
choice to assess cai·diac structure, function,
pulmonary thrombosis can fonn in situ
and presence of an intracardiac thrombus,
secondaiy to pulmonary endothelial
whereas chest radiographs are used to
damage. Chest radiographs in affected
diagnose left-side congestive heait failure.

animals may be nom1al or show underperfu

Nucleai· perfusion studies, using the
sion of the affected lung lobe, interstitial to
unbound radioisotope 99mTc cw give
alveolar infiltrates, or pleural effusion.

sensitive information regarding the degree

Arterial blood-gas analysis typically
of perfusion of the hindlin1bs and areas that
demonstrates hypoxemia with a normal or
may require ai11putation in select cases,
low level of CO, in the blood. Ventilation/
although this is rarely done.

perfusion scanning with radionuclide

Systemic hypertension in cats and patent
labeled macroaggregated albUTilin and gases ductus aiteriosis, aortic coarctation, or pulmonary CT angiography can confinn
degenerative processes, and infections in
the diagnosis. Other diseases associated
dogs have been associated with aortic
with puhnonary thromboembolism in dogs
aneurysms.

and cats include protein-losing nephropathy

Cranial vena caval thrombosis and
or enteropathy, hyperadrenocorticism,
subsequent chylothorax and acute
immune-mediated hemolytic anemia, and
respiratory distress has been reported in
neoplasia.

dogs and cats with tra.I1Svenous pacemakers

In cats, cardiogenic embolism ( aiterial
and other indwellingjugulai· devices/
thromboembolism) is a devastating
catheters. Successful treatment of caval
complication of cardiac disease. Although
tllrombosis in affected animals has been
hypertrophic cardiomyopathy is the most
described using a combination of anticoagucommon type of cardiac disease in cats ( see lwts, thrombolytics, and balloon venop 117), any condition that results in left plasty.

144

THROMBOSIS, EMBOLISM, AND ANEURYSM

Treatment: Treatment of endocarditis
with conservative medical therapy. More
includes longtem1 antibiotics (several
aggressive therapy aimed at dissolution of
weeks to months) and in some cases
the thrombus through thrombolytic drugs or
intermittent administration of a.ntipyretic,
rheolytic i.nte1vention may result in inlproved
anti-inilan1matory, or anti thrombotic drugs.

short-term functional outcome, but survival

Antibiotic choice should be based on
is no better tl1an that from conse1vative

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culture and sensitivity results obtained from tl1erapy and, in some cases, may actually be blood cultures. The prognosis for recovery
worse. Conse1vative tl1erapy usually consists
is poor to guarded at best, and persistent
of initial pain management (hyclromorphone,
debilitating cardiac disease is common even 0.1 mg/kg, SC, IM, or IV every 4-6 hr; or if the active infection can be controlled.

buprenorphine HCl, 0.01--0.03 mg/kg, SC, IM,

Treatment of venous tluombosis in
or IV, every 6--8 lu) and anticoagulant therapy
horses and cattle is usually limited to

(heparin, 250-300 U/kg with first dose IV if
supportive care, including hydrotherapy of
anin1al is in shock, followed by administraaccessible veins, anti-inflammatory agents, tion SC, tid-qid; or daltepaiin 150-170 lU/kg,
and systemic antimicrobials to control

SC, bid-tid). The activated parbal tlu·ornbosecondary sepsis. Surgical removal of plastin time can be used to monitor heparin
thrombosedjugular veins has been
tl1erapy, with a goal of 1.5-1. 7 x the
pe1fonned successfully in horses, but
pretreatment value. The use of antiplatelet
unless both veins are severely affected,
therapy ( clopidogrel, 75 mg, PO, once on
inil.anunation will resolve with medical
admission, then 18. 75 mg/day, PO) should be
treatment, and fom1ation of collaterals will
considered to ftuther reduce the thrombotic
usually result in sufficient venous circulapotential; in addition, it may have a beneficial tion. Thrombosis of the cranial or caudal
effect on collateral circulation. Tlu·ombolytic
vena cava results in more severe clinical
therapy, although not routinely recomsigns and requires more aggressive therapy, mended, could include streptoki.nase (90,000
which could include thrombolytic drugs
ill/cat, IV over 20 min, followed by 45,000 ill
and/or intravascular/surgical removal
as a continuous infosion for 2-24 lu ),
followed by aggressive anticoagulation.

recombinant tissue-type plasminogen

Response to anticoagulation therapy alone
activator (tPA, 0.25-1 mg/kg/lu; IV, up to a
is generally inadequate.

total dose of 1-10 mg/kg), or urokinase (4,400

Measures to minimize trauma to, and
ill/kg, IV over 10 min, then 4,400 ill/kg/hr for
bacterial contamination of, veins remain the 12 hr). These drugs promote thrombolysis by best means to prevent venous thrombosis.

conve1ting plasminogen to plasmin, which

Extreme care should be taken when placing
subsequently breaks down fibrin strands.

catheters or giving IV injections. The

Streptokinase is considered a nonspecific
effectiveness of antiplatelet therapy (aspirin activator of plasminogen, because it activates 0.5-5 mg/kg/day or clopidogrel 1 -3 mg/kg/
circulating fibrin as well as fibrin contained
day), anticoagulant therapy (unfractionated
within thrombi/emboli, which can lead to a
heparin, 40--80 IU/kg, SC, bid-tid, or
systemic proteolytic state and bleeding.

low-molecular-weight heparin [ enoxaparin

Although urokinase and tPA are more
at I mg/kg, SC, bid, or dalteparin at 150-200
fibrin-specific tl1an streptokinase, bleeding

IU, SC, bid]) to facilitate intrinsic: thrombus
can also be seen with these agents. Moreover,
resolution is unknown but should at least
all of tl1ese agents are prohibitively expensive
prevent further thrombus fom1ation.

ai1d difficult to obtain. The use of antiplatelet

In horses, aneurysms due to Strongylus
agents such as clopidogrel has been shown
vulgaris rarely rupture; the chief concern is to hasten thrombus dissolution and reduce
thromboembolism of intestinal vasculature
acute aiteri.al retluornbosis in experimental
with subsequent colic. Generally, the
studies and human clinical trials, respecaiterial wall is sufficiently involved that tively. However, an in vitro feline study did
tlu·ombus removal is inlpracbcal. Antibactenot identify a significant difference in rial treatment and anthelrnintics to kill the
tluornbolysis rates. It is not known whether
migrating larvae are of considerable value.

these results can be applied to tl1e natural

The most rational approach to cranial
clinical clisease. Thrornbolytic therapy
mesenteri.c and aortic-iliac thrombosis in
appeai-s to have tl1e best response in cats
horses is prevention and control of
witl1 acute onset of clinical signs ai1d
strongylosis (seep 316).

incomplete or unilateral infarcbon. However,

Acute management of aortic emboli in
these cats may respond sinlilai·ly well to
cats CaJl be approached in several ways.

conservative therapy, without the 1isk of

More than 50% of cats that swvive a
reperfusion i.!1iury or expense of tl1ese agents.

cardioembolic event will regain some

Although a severe complete infarction is
function of the hincllimbs over 4-6 wk
more likely to develop reperfusion i.!1iury

THROMBOSIS, EMBOLISM, AND ANEURYSM

145
with thrombolytic therapy, these cats are
anti thrombotic for carclioembolic
also less likely to recover with conse1vative
prevention in cats.

therapy alone. The reported survival rates for

The low-moleculai0weight hepa1ins
initial aortic infarction events are similar

(LMWHs) are smaller in size than UIUracwhether conservative (35%-3996) or thrombotionated heparm but maintain the ability to lytic (33%) therapy is used. Cats with single
inhibit factor Xa, with a greatly reduced

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limb infarction do much better (68"/e>-93%)

inhibition of Ila. The reduced anti-Ila
than cats with bilateral hindlimb infarction
activity translates into a negligible effect on

(15o/e>-36%) regardless of therapy used.

the activated paitial tliromboplastin time,

Aspirin (25 mglkg, PO, every 48-72 hr; or 5
but measurement of anti-Xa activity can be
mg,'cat, PO, every 48-72 hr) has historically
used to monitor closing efficacy. Enoxaparin
been the most widely used preventive

(1-1.5 mg/kg, SC, once or twice daily) ai1d
therapy for cardioembolic disease in cats.

daltepai'in (150-170 IU/kg, SC, bicl-tid ) have

Altl1ough aspirin appears relatively safe in
both been used in cats. These drugs have
cats (up to 20"A,GI aclve1se effects) and is
been well tolerated with only rare bleeding
inexpensive unless compounding is done, the
repo1ted, but objective clinical studies
antiplatelet efficacy of aspi.Jin in cats has
evaluating their efficacy have not been
been called into question, and CUITently there
perfonned. These agents have been
is no evidence that aspirin prevents first-time
frequently combi.J1ecl with clopiclogrel in
or recun·ent cardioembolism. Clopidogrel
an attempt to provide a more complete
may be a more effective antiplatelet drug in
ai1tithrombotic effect. This protocol
this species.

appears to be well tolerated, altl1ough some

Clopiclogrel (18.75 mg,'cat/clay, PO)

minor bleeding has been seen. Reported
inhibits botl1 primary and secondary platelet
recurrence rates for cats receivi.J1g some
aggregation. These effects are more potent
fo1m of antithrombotic prevention ai·e
than tl1ose induced by aspirin. Clopidogrel
l 7o/e>-75%, with a 1-yr recurrence rate of
also inlpai.Js the platelet-release reaction,

25o/e>-50%. Long-tenn median survival times
decreasing the release of pro-aggregating
after an initial cardioembolic event have
and vasoconstrictive agents. Adve1se effects
ranged from 51-376 days. Although these
are rare but can include vomiting in up to
nll1llbe1s may seem daunting, many of these
l()OA, of cats; this appears to be an1elioratecl
cats can do well. lf owners ai·e willing to
by giving the drug witl1 food. A combination
treat, they should be encouraged to give
protocol of aspi.Jin and clopidogrel has been
cats 24-72 hr of supportive care before
used previously. Although this protocol has
decidi.J1g on euthanasia, UIUess severe
not been studied objectively, it seems to
infarction, severe CHF, or reperfusion injury
be well tolerated despite a theoretical
are present.

increased risk of bleeding. A multicenter,

Arterial thrombosis in clogs is most
randomized, prospective study revealed that commonly associated with protein-losing clopidogrel was associated witl1 a signifinephropathy and neoplasia, though cantly prolonged survival tin1e compared
idiopathic thrombosis is also seen. There is
with aspi.J'in in cats tl1at presented with
very little cli.Jlical experience with aiterial
cardiogenic aiterial thromboembolism. The
thromboembolism in dogs, but thrombotime to recun-ence of arte1ial thromboembolytic therapy using streptokmase, urokilism or deatl1 in the clopidogrel group was nase, and tPA have been reported in isolated

>365 days versus 192 days in tl1e aspi.Jin
cases with vai"iable success. There are no
group.

clinical trials evaluating the efficacy of

Warfai·i..11 (0.25-0.5 mg,'day/cat, PO) has
anti.thrombotic therapy for prevention of
also been used for prevention of primary or
arterial thromboembolism in dogs, but
secondary cai·dioemboli. Dosing is adjusted
dosing protocols for aspi.Jin (0.5-5 mg/kg,
to prolong the prothrombin tinle to 1.5-1. 7 x PO, once or twice daily), clopidogrel (1-3
the pretreatment value. Because warfarin
mglkg,'day, PO), wai'farin (0.1-0.22 mg/kg,'

decreases the anticoagulant proteins C and
day, PO), dalteparm (150 IU/kg, SC,bid-tid),

S before reduction in factors II, VII, IX, and
enoxaparin ( 1-1.5 mg/kg, SC, once or twice

X, joint treatment with heparin is recomdaily), and rivaroxaban (0.5-1 mglkg,'day, mended for the first 5-7 clays of warfarin

PO) have been reported.

therapy. Problems with wai'farin therapy

Treatment reconunendations for
include large inter- and intra-individual
pulrnonaiy embolism in dogs are sinlilai· to
variability, difficult dosing because of tablet
those for cardioembolic disease in cats.

size, and bleedmg, i.J1cluding fatal hem01°

Aspi.J'in (0.5 mglkg,'clay, PO) has inlproved
rhage. Because of these lin1itations and lack
survival in dogs with in1mtme-mediatcd
of objective clinical data demonstrating
hemolytic anemia when added to standard
efficacy, warfarin is not a fust-line
inlmunosuppressive therapy.

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DIGESTIVE SYSTEM

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INTRODUCTION 154

Function 154

Pathophysiology 155

Clinical Findings of GI Disease 156

Examination of the GI Tract 157

Infectious Diseases 158

Noninfectious Diseases 161

Principles of Therapy 161

CONGENITAL AND INHERITED ANOMALIES 162

Mouth 162

Teeth 164

Cysts and Sinuses of the Head and Neck 165

Esophagus 166

Hernias 166

Stomach 167

Small and Large Intestine 168

Liver 169

DENTAL DEVEL OPMENT 171

Estimation of Age by Examination of the Teeth 171

DENTISTRY 175

Large Animals 1 75

Congenital and Developmental Anomalies 176

Abnormal Tooth Eruption 177

Irregular Wear of the Dentition 177

Periodontal Disease 177

Dental Caries 178

Small Animals 1 78

Periodontal Disease 1 78

Endodontic Disease 180

Tooth Resorption 181

Developmental Abnormalities 182

Dentofacial Trauma 185

Dental Caries 185

PHARYNGEAL PARALYSIS 186

DISEASES OF THE RECTUM AND ANUS 187

Anal Sac Disease 187

Perianal Fistula 187

Perianal Tumors 188

Perinea! Hernia 188

Rectal and Anorectal Strictures 189

148

DIGESTIVE SYSTEM

Rectal Neoplasms 189

Rectal Polyps 189 Rectal

Prolapse 189 Rectal Tears

190

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BACTERIAL DISEASES

ENTERIC CAMPYLOBACTERIOSIS 191

SALMONELLOSIS 195

TYZZER DISEASE 199

PROTOZOAL DISEASES

AMEBIASIS 202

COCCIDIOSIS 203

Cattle

205

Sheep

206

Goats 207

Pigs 208

Cats and Dogs 208

CRYPTOSPORIDIOSIS 209

GIARDIASIS 211

LARGE ANIMALS

DISEASES OF THE MOUTH 213 DISEASES

OF THE ESOPHAGUS 215

Obstruction (Choke) 215

Strictures 217 Neoplasia 21 �

GASTROINTESTINAL ULCERS 218

Horses 218

Pigs 219

DISEASES OF THE RUMINANT FORESTOMACH 221

Simple Indigestion 221

Grain Overload 222

Subacute Ruminal Acidosis 225 Bloat

227

Traumatic Reticuloperitonitis 230 Vagal

Indigestion Syndrome 233 Ruminal

Drinking 236

Ruminal Parakeratosis 237

DISEASES OF THE ABOMASUM 238

Left or Right Displaced Abomasum and Abomasal Volvulus 238

DIGESTIVE SYSTEM

149

Abomasal Ulcers 241

Dietary Abomasal Impaction 244

ACUTE INTESTINAL OBSTRUCTIONS 245

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COLIC IN HORSES 248

Diseases Associated with Colic by Anatomic Location 258

Stomach 258

Small Intestine 258

Cecum and Large Intestine 262

INTESTINAL DISEASES IN RUMINANTS 266

Cattle 266

Bovine Viral Diarrhea and Mucosal Disease Complex 267

Jejunal Hemorrhage Syndrome 270

Winter Dysentery 271

Other Intestinal Diseases of Cattle 272

Sheep and Goats 273

Watery Mouth Disease in Lambs 27 4

Diarrhea in Neonatal Ruminants 275

INTESTINAL DISEASES IN HORSES AND FOALS 281

Diarrheal Disease in Horses 281

Salmonellosis 281

Potomac Horse Fever 283

Clostridia-associated Enterocolitis 285

Colitis-X 286

Coronavirus 287

Parasitism 287

Sand Enterocolopathy 287

Recurrent Diarrhea 288

Infiltrative Colonic Disease 288

Miscellaneous Causes of Diarrhea 288

Diarrheal Disease in Foals 289

Weight Loss and Hypoproteinemia 291

Gastrointestinal Neoplasia 291

Inflammatory Bowel Disease 291

NSAID Toxicosis 292

Small-intestinal Fibrosis 293

INTESTINAL DISEASES IN PIGS 293

Clostridium difficile Enteritis 293

Clostridium perfringens Type A Enteritis 295

Clostridium perfringens Type C Enteritis 295

Edema Disease 296

Enteric Colibacillosis 296

Hemorrhagic Bowel Syndrome 296

Intestinal Salmonellosis 296

Intestinal Spirochetosis 297

Parasitism 298

Porcine Epidemic Diarrhea 298

150

DIGESTIVE SYSTEM

Porcine Proliferative Enteritis 299

Rectal Strictures 300

Rotaviral Enteritis 301

Swine Dysentery 301

Transmissible Gastroenteritis 302

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Other Intestinal Viruses of Pigs 303

GASTROINTESTINAL PARASITES OF RUMINANTS 303

Cattle 308

Haemonchus, Ostertagia, and Trichostrongylus spp 308

Cooperia spp 310

Bunostomum sp 310

Strongyloides sp 310

Nematodirus spp 310

Toxocara sp 311

Oesophagostomum sp 311

Chabertia sp 311

Trichuris spp 312

Tapeworms 312

Sheep and Goats 312

Haemonchus, Ostertagia, and Trichostrongylus spp 312

Intestinal Trichostrongylosis 313

Bunostomum and Gaigeria spp 313

Nematodirus spp 313

Oesophagostomum sp 313

Chabertia sp 314

Strongyloides sp 314

Trichuris spp 314

Tapeworms 314

GASTROINTESTINAL PARASITES OF HORSES 315

Gasterophilus spp 315

Habronema spp 315

Oxyuris sp 316 .

Parascaris sp 316

Large Strongyles 316

Small Strongyles 317

Strongyloides sp 319

Tapeworms 319

Trichostrongylus sp 319

GASTROINTESTINAL PARASITES OF PIGS 320

Ascaris suum 320
lv1acracanthorhynchussp 321

Oesophagostomum spp 322

Stomach Worms 322

Strongyloides sp 323

Trichuris sp 323

DIGESTIVE SYSTEM

151

FLUKE INFECTIONS IN RUMINANTS 324

Fasciola hepatica 324

Fasciola gigantica 326

Fascioloides magna 327

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Dicrocoelium dendriticum 327

Eurytrema spp 328

Paramphistomes 328

HEPATIC DISEASE 329

Acute Hepatitis 338

Idiopathic Acute Hepatic Disease 338

Acute Hepatic Necrosis in Cattle 339

Fatty Liver Disease of Cattle 1018 (MET)

Infectious Hepatitis and Hepatic Abscesses 340

'Iyzzer Disease 340

Cholangiohepatitis 340

Equine Rhinopneumonitis 341

Infectious Necrotic Hepatitis 341

Bacillary Hemoglobinuria 341

Hepatic Abscesses 341

Hepatotoxins 341

Chemical and Drug-related Causes of Toxic Hepatopathy 342
lVlycotoxicoses 342

Blue-green Algae Intoxication 343

Hepatotoxic Plants 343

Cholelithiasis, Choledocholithiasis, and Hepatolithiasis 344

Chronic Active Hepatitis 345

Hyperlipemia and Hepatic Lipidosis 346

Hepatic Neoplasia 348
lVliscellaneous Hepatic Disorders 349

Cholangitis 349

Hepatic Failure in Foals 349

Biliary Atresia 349

Hemochromatosis 349

Right Hepatic Lobe Atrophy in Horses 350

Hepatic Lobe Torsion 350

Hepatic Amyloidosis 350

Congenital Hepatic Fibrosis 350

Primary Hyperammonemia of Adult Horses 350

Portosystemic Shunts 351

Hyperammonemia oflVlorgan Weanlings 351

Hyperbilirubinemia Syndromes 351

Gilbert Syndrome 351

Dubin-Johnson Syndrome 351

Liver Abscesses in Cattle 352

MALASSIMILATION SYNDROMES 353

ABDOMINAL FAT NECROSIS 360

152

DIGESTIVE SYSTEM

SMALL ANIMALS

DISEASES OF THE MOUTH 361

Oral Inflammatory and Ulcerative Disease 361

Feline Stomatitis 362

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Canine Stomatitis 363

Eosinophilic Granuloma Complex 971 (1TG)

Lip Fold Dermatitis and Cheilitis 364

Mycotic Stomatitis 364

Acute Necrotizing Ulcerative Gingivitis 364

Glossitis 365

Soft-tissue Trauma 365

Papillomas 366

Oral Tumors 366

Salivary Disorders 367

Ptyalism 367

Salivary Mucocele 368

Salivary Fistula 368

Salivary Gland Tumors 368

Sialadenitis 369

Sialadenosis 369

Necrotizing Sialometaplasia 369

Xerostomia 369

DISEASES OF THE ESOPHAGUS 370

Cricopharyngeal Achalasia 370

Dilatation of the Esophagus 370

Esophageal Dysmotility 371

Esophageal Strictures 371

Esophagitis 372

Esophageal Foreign Bodies 372

Esophageal Diverticula 373

Bronchoesophageal Fistula 373

DISEASES OF THE STOMACH AND INTESTINES 373

Canine Parvovirus 373

Colitis 377

Constipation and Obstipation 380

Feline Enteric Coronavirus 383

Gastric Dilation and Volvulus 384

Gastritis 386

Gastrointestinal Neoplasia 388

Gastrointestinal Obstruction 390

Gastrointestinal Ulcers 393

Helicobacter Infection 394

Hemorrhagic Gastroenteritis 396

Inflammatory Bowel Disease 397

Malabsorption Syndromes 400

DIGESTIVE SYSTEM

153

THE EXOCRINE PANCREAS 407

Pancreatitis 407

Exocrine Pancreatic Insufficiency 409

Pancreatic Neoplasms 411

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Pancreatic Abscesses 412

Pancreatic Pseudocyst 412

GASTROINTESTINAL PARASITES 412

Spirocerca lupi 412

Physaloptera spp 413

Ollulanus sp 413

Strongyloides sp 414

Roundworms 415

Hookworms 416

Whipworms 421

Acanthocephalans 421

Oncicola sp 421

Macracanthorhynchus sp 421

Tapeworms 421

Flukes 426

Intestinal Flukes 426

Hepatic Flukes 427

HEPATIC DISEASE 429

Laboratory Analyses and Imaging 430

Hematology 430

Coagulation Tests 430

Enzyme Activity 430

Other Serum Biochemical Measures 434

Hepatic Function Tests 436

Imaging 437

Cholecystocentesis 438

Liver Cytology 438

Liver Biopsy 438

Pathologic Changes in Bile 439

Nutrition 439

Diseases of the Liver 442

Fulrninant Hepatic Failure 442

Hepatic Encephalopathy 443

Portal Hypertension and Ascites 445

Portosysternic Vascular Malformations 446

Acquired Portosystemic Shunts 450

Other Hepatic Vascular Disorders 450

Hepatic Arteriovenous Malformation 450

Hepatic Vein Outflow Obstruction 451

Hepatotoxins 451

Infectious Diseases of the Liver 453

Feline Hepatic Lipidosis 456

154

DIGESTIVE SYSTEM

Biliary Cirrhosis 459

Canine Cholangiohepatitis 459

Canine Chronic Hepatitis 460

Copper-associated Hepatopathy 460

Idiopathic Chronic Hepatitis 462

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Breed-specific Chronic Hepatitis 464

Lobular Dissecting Hepatitis 466

Canine Vacuolar Hepatopathy 467

Metabolic Diseases Affecting the Liver 468

Hepatocutaneous Syndrome 468

Nodular Hyperplasia 469

Hepatic Neoplasia 469

Miscellaneous Liver Diseases 4 72

Glycogen Storage Disease 472

Hepatic Amyloidosis 4 72

Diseases of the Gallbladder and Extrahepatic Biliary System 4 73

Cholecystitis 4 73

Canine Gallbladder Mucocele 475

Other Disorders of the Gallbladder 4 77

Other Disorders of the Bile Ducts 4 77

Extrahepatic Bile Duct Obstruction 478

Cholelithiasis 479

Biliary Tree Rupture and Bile Peritonitis 480

Feline Cholangitis/Cholangiohepatitis Syndrome 481

Hepatobiliary Fluke Infection 484

DIGESTIVE SYSTEM INTRODUCTION

The digestive tract includes the oral cavity

Function
and associated organs (lips, teeth, tongue,
and salivary glands), the esophagus, the

The prin1ary functions of the GI tract
forestomachs (reticulum, rumen, omasum)

include prehension of feed and water;
of ruminants and the true stomach in all
mastication, ensalivation, and swallo�g
species, the small intestine, the liver, the
of feed; digestion of feed and ab_sorpt10n
exocrine pancreas, the large intestine, and
of nutrients; maintenance of tlwd and
the rectum and anus. Gut-associated
electrolyte balance; and evacuation of
lymphoid tissue (tonsils, ?eyer's patches,
waste products. There are four primary
diffuse lymphoid tissue) is distributed along
functions-digestion, absorption, motility,
the GI tract. The peritoneum covers the
and evacuation-and, correspondingly,
abdominal viscera and is involved in many
fow· primary modes of dysfunction.

GI diseases. Fundamental efforts to manage

Normal GI tract motility involves

GI disorders should always be directed
peristalsis, muscle activity that moves
toward localizing disease to a particular
ingesta from the esophagus to the rectum;
segment and determining a cause. A rational segmentation movements, which chum and therapeutic plan can then be fom1ulated.

mix the ingesta; and segmental resistance
and sphincter tone, which retard aboral

DIGESTIVE SYSTEM INTRODUCTION

155
progression of gut contents. In ruminants,
the intestinal wall. Contraction of the gut
these movements are of major importance
causes pain by direct and reflex distention
in normal forestomach function.

of neighboring segments. Spasm, an
exaggerated segmenting contraction

Pathophysiology
of one section of intestine, results in
distention of the immediately anterior

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Abnormal motor function usually manifests
segment when a peristaltic wave arrives.

as decreased motility. Segmental resistance

Other factors that may cause abdominal
is usually reduced, and transit rate
pain include edema and failure of local
increases. Motility depends on stimulation
blood supply, eg, in local embolism or
via the sympathetic and parasympathetic
twisting of the mesentery.

nervous systems (and thus on the activity

Specific diseases cause diaiThea by
of the central and peripheral parts of these
varied and characteristic mechanisms, the
systems) and on the GI musculature and its
recognition of which is useful in understandintrinsic nerve plexuses. Debility, accompaing, diagnosing, and managing GI diseases.

nied by weakness of the musculature, acute

The major mechanisms of diaJThea are
peritonitis, and hypokalernia, produces
increased penneability, hypersecretion, and
atony of the gut wall (paralytic ileus). The
osmosis. Disorders of motility are often
intestines distend with fluid and gas, and
secondary. In healthy animals, water and
fecal output is reduced. In addition, chronic
electrolytes continuously tra11Sfer across
stasis of the small intestine may predispose
the intestinal mucosa. Secretions (from
to abnom1al proliferation of microflora.

blood to gut) and absorptions (from gut to

Such bacterial overgrowth may cause
blood) occur simultaneously. In clinically
malabsorption by injuring mucosal cells, by
healthy anin1als, absorption exceeds
competing for nut1ients, and by deconjugatsecretion, ie, there is net absorption.

ing bile salts and hydroxylating fatty acids.

Inflan1mation in the intestines can be

Vomiting is a neural reflex act that results
accompanied by an increase in "pore size"

in ejection of food and fluid from the
in the mucosa, pe1mitting increased flow
stomach through the oral cavity. It is always
through the membrane ("leak") down the
associated with antecedent events such as
pressure gradient from blood to the
premonition, nausea, salivation, or
intestinal lwnen. If the ainount exuded
shivering and is accompanied by repeated
exceeds the absorptive capacity of the
contractions of the abdominal muscles.

intestines, diaJThea results. The size of the

Regurgitation is characterized by passive,
material that leaks through the mucosa
retrograde reflux of previously swallowed
varies, depending on the magnitude of the
material from the esophagus, stomach, or
increase in pore size. Large increases in pore
rumen. In diseases of the esophagus,
size permit exudation of plasma protein,
swallowed material may not reach the
resulting in protein-losing enteropathies ( eg,
stomach.

lymphangiectasia in dogs, paratuberculosis

One of the major consequences of
in cattle, nematode infections). Greater
subnormal motility is distention with fluid
increases in pore size result in the loss of
and gas. Much of the accumulated fluid is

RBCs, producing hemorrhagic diaJThea ( eg,
saliva and gastric and intestinal juices
hemorrhagic gastroenteritis, parvovirus
secreted during nonnal digestion. Disteninfection, severe hookwom1 infection).

tion causes pain and reflex spasm of

Hypersecretion is a net intestinal loss of
adjoining gut segments. It also stin1ulates fluid and electrolytes that is independent
further secretion of fluid into the lwnen of
of changes in permeability, absorptive
the gut, which exacerbates the condition.

capacity, or exogenously generated osmotic

When the distention exceeds a critical point, gradients. Enterotoxic colibacillosis is a11
the ability of the musculature of the wall to
exan1ple of dian·heal disease due to
respond dinlinishes, the initial pain
intestinal hypersecretion; enterotoxigenic
disappears, and paralytic ileus develops

Escherichia coli produce enterotoxin that
in which all GI muscle tone is lost.

stin1ulates the crypt epitheliwn to secrete

Dehydration, acid-base and electrolyte
fluid beyond the absorptive capacity of
imbalance, and circulatory failure are major
the intestines. The villi, along with their
consequences of GI distention. Accumulation digestive and absorptive capabilities, of gut fluids stimulates additional secretion
remain intact. The fluid secreted is isotonic,
of fluids and electrolytes in the anterior
alkaline, and free of exudates. The intact
segments of the intestine, which can worsen
villi are beneficial because a fluid ( administhe abnormalities and lead to shock.

tered PO) that contains glucose, ainino

Abdominal pain associated with GI
acids, and sodium is absorbed, even with
disease usually is caused by stretching of
hypersecretion.

156

DIGESTIVE SYSTEM INTRODUCTION

Osmotic diarrhea is seen when inadare antimicrobial or that drastically alter equate absorption results in a collection of
the pH of rumen contents.

solutes in the gut lumen, which cause water
to be retained by their osmotic activity. It
develops in any condition that results in

Clinical Findings of GI Disease
nutrient malabsorption or maldigestion or

Signs of GI disease include excessive

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when an animal ingests a large amount of
salivation, dian·hea, constipation or scant
osmotically active substances that are not
feces, vomiting, regurgitation, GI tract
absorbed, eg, an overeating puppy.

hemorrhage, abdominal pain and distention,

Malabsorption (seep 353 and seep 373) tenesmus, shock and dehydration, and
is failure of digestion and absorption due
suboptimal performance. The location and
to some defect in the villous digestive and
nature of the lesions that cause malfunction
absorptive cells, which are mature cells
often can be determined by recognition and
that cover the villi. Several epitheliotropic
analysis of the clinical findings. In addition,
viruses directly infect and destroy the
abnormalities of prehension, mastication,
villous absorptive epithelial cells or their
and swallowing usually are associated with
precursors, eg, coronavirus, transmissible
diseases of the oral mucosa, teeth, mandible
gastroenteritis virus of piglets, and rotavirus
or other bony structures of the head,
of calves. Feline panleukopenia virus and
pharynx, or esophagus. Vomiting is most
canine parvovirus destroy tl1e crypt
common in single-stomached animals
epithelium, which results in failure of
and usually is due to gastroente1itis or
renewal of villous absorptive cells and
nonalin1entary disease ( eg, uremia,
collapse of the villi; regeneration is a longer
pyometra, endocrine disease). The vomitus
process after parvoviral infection than after
in a dog or cat with a bleeding lesion (gast1ic
viral infections of villous tip epithelium (eg,
ulcer or neoplasm) may contain frank blood
coronavirus, rotavirus ). Intestinal malabor have the appearance of coffee grounds.

sorption also may be caused by any defect

Horses and rabbits do not vomit. Regurgitathat impairs absorptive capacity, such as tion may signify disease of the oropharynx
diffuse inflan1rnatory disorders ( eg,
or esophagus and is not accompanied by the
lymphocytic-plasmacytic enteritis,
premonitory signs seen with vomiting.

eosinophilic enteritis) or neoplasia ( eg,

Large-volume, fluid diarrhea usually is
lymphosarcoma).

associated with hypersecretion (eg, in

Other examples of malabsorption include
enterotoxigenic colibacillosis in newborn
defects of pancreatic secretion that result in
calves) or with malabsorptive (osmotic)

maldigestion. Rarely, because of failure to
effects. Blood and fibrinous casts in the
digest lactose (which, in large amounts,
feces indicate a hemorrhagic, fibrinohas a hyperosmotic effect), neonatal fann necrotic enteritis of the small or large
animals or pups may have diarrhea while
intestine, eg, bovine viral diarrhea,
they are being fed milk Reduced secretion
coccidiosis, salmonellosis, or swine
of digestive enzymes at the surface of
dysentery. Black, tarry feces (melena)

villous tip cells is characteristic of
indicate hemorrhage in the stomach
epitheliotropic viral infections recognized
or upper part of the small intestine.

in farm anin1als.

•

Tenesmus of GI origin usually is associ

The ability of the GI tract to digest
ated with inflammatory disease of the
food depends on its motor and secretory
rectum and anus.

functions and, in herbivores, on the activity

Small amounts of soft feres may indicate
of the microflora of the forestomachs of
a partial obstruction of the intestines.

ruminants, or of the cecum and colon of

Abdominal distention can result from
horses and pigs. The flora of ruminants can
accumulation of gas, fluid, or ingesta, usually
digest cellulose; ferment carbohydrates to
due to hypomotility (functional obstruction,
volatile fatty acids; and convert nitrogadynamic paralytic ileus) or to a physical enous substances to an1monia, amino
obstruction ( eg, foreign body or intussuscepacids, and protein. In certain circumtion). Distention may, of course, result from stances, the activity of the flora can be
something as direct as overeating. A "ping"

suppressed to the point that digestion
heard during auscultation and percussion of
becomes abnormal or ceases. Incorrect
the abdomen indicates a gas-filled viscus. A
diet, prolonged starvation or inappetence,
sudden onset of severe abdominal distention
and hyperacidity (as occurs in engorgein an adult run1inant usually is due to ruminal ment on grain) all impair microbial
tympany. Ballottement and succussion may
digestion. The bacteria, yeast.s, and
reveal fluid-splasl1ing sounds when t11e
protozoa also may be adversely affected
run1en or bowel is filled with fluid. Varying
by the oral administration of drugs that
degrees of dehydration and acid-base and

DIGESTIVE SYSTEM INTRODUCTION

157
electrolyte imbalance, which may lead to
differential diagnoses and determines the
shock, are seen when large quantities of fluid
direction of further investigation. However,
are Jost ( eg, in diarrhea or sequestered in
the clinician should appreciate that in some
intestinal obstruction) or in gastJ.ic or
instances the disorder can involve the
abomasal volvulus.

entire bowel, with one set of localizing

Abdominal pain is due to stretching or
signs overshadowing the other.

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inflammation of the serosal surfaces of

The clinical and laboratory techniques
abdominal viscera or the peritonewn; it may
and their applications include the following:

be acute or subacute, and its manifestation

1) visual inspection of the oral cavity and of
varies among species. In horses, acute
the con tom of the abdomen for distention
abdominal pain is conunon (seep 248).

or contraction; 2) palpation through the

Subacute pain is more common in cattle and
abdominal wall or per rectwn to evaluate
is characterized by reluctance to move and
shape, size, and position of abdominal
by grunting with each respiration or deep
viscera; 3) abdominal percussion to detect
palpation of the abdomen. Abdominal pain

"pings," which suggest gas-filled viscera; in dogs and cats may be acute or subacute

4) auscultation to deteffiline the intensity,
and is characterized by whining, meowing,
frequency, and dmation of GI movements,
and abnormal postmes ( eg, outstretched
as well as fluid-splashing soW1ds associated
forelin1bs, the stemwn on the floor, and the
with fluid-filled stomachs and intestines and
hindlirnbs raised). Abdominal pain may be
fluid-rushing sounds associated with
difficult to localize to a particular viscus or
diarrheal disease; 5) succussion to reveal
organ within the abdomen.

fluid-splashing sounds; 6) ballottement to
evaluate density and size of abdominal
organs by their movement away from and

Examination of the GI Tract
back to the abdominal wall; and 7) gross

A complete, accmate history and routine
examination of feces to assess bulk, conclinical examination can often detem1ine sistency, color, and presence of mucus,
the diagnosis. In outbreaks of GI tract
blood, or undigested food particles.

disease in farm animals, the history and

Microscopic studies include exanlination
epidemiologic findings are of prime
for parasites. Cytology of a rectal or colonic
importance. In small aninlals, travel history
mucosal smear stained with new methylene
or other details such as recent adoption
blue or Wright stain for fecal leukocytes is
from a shelter or recent kenneling or
useful to detect inflanunatory bowel disease
exposme to other animals in dog parks
or the presence of intracellular fungal organmight give clinical suspicion to certain isms in the case of infection with Histo
infectious diseases. If the history and
plasma capsulatum. The following may be epidemiologic and clinical findings are
useful (or necessary): 1) bacterial cult.me
consistent with GI disease, the lesion should and virus isolation; 2) endoscopy to be localized within the system, and the type
visualize the mucosa! surface of the
of lesion and its cause detennined.

esophagus, stomach, duodenwn, colon,

The abnom1ality may sometin1es be
and rectwn; 3) abdominocentesis to collect
localized to the large or small intestine by
fluid from distended viscera or from the
history, physical examination, and fecal
peritoneal cavity for examination; 4)

characteristics (see TABLE 1). The distincradiography ( contrast) to diagnose tion is important because it narrows the
obstructive disease; 5) abdominal ultra-

DIFFERENTIATION OF SMALL-INTESTINAL FROM LARGE-INTESTINAL

DIARRHEA

Clinical Sign

Small Intestine

Large Intestine

Frequency of defecation

Nom1al or slightly increased

Very frequent

Fecal volume

Normal to increased

Decreased

Urgency

Absent

Usually present

Tenesmus

Absent

Usually present

Mucus in feces

Usually absent

Frequent

Blood in feces

Dark black (melena)

Red (fresh)

Weight loss

May be present

Rare

158

DIGESTIVE SYSTEM INTRODUCTION
sonography to evaluate the wall thiclmess of pancreas-specific lipase, which are sensitive the stomach and intestines and to detect
and specific markers for the diagnosis of
abdominal masses, intussusceptions, and
pancreatitis; laparotomy and biopsy may be
mesente1ic lymphadenopathy in small
indicated in cases in which the diagnosis is
animals, and to investigate abdominal
not clear or in which surgical correction
disorders in horses and cows; 6) biopsy
may be required.

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(endoscopic, laparoscopic, ultrasoundguided, surgical) to obtain samples for INFECTIOUS DISEASES
microscopic examination (samples of
intestines and liver are useful to diagnose

The GI tract is subject to infection by many
chronic enteritis and liver disease); and 7)

pathogens, which are a major cause of
tests for digestion and absorption to
economic loss due to illness, suboptin1al
estimate and differentiate malabsorption
performance, and death ( see TABLE 2).

and maldigestion. Common absorption tests These infections spread by direct contact or include the measurement of the serun1
the fecal-oral route. Many of the pathogens
concentrations of cobalarnin (vitamin B,2)

are part of the normal intestinal flora, and
and folate. In addition, in small animals, an
disease develops only after a stressful event,
increased serun1 folate concentration in
eg, salmonellosis in horses after transportacoajunction with a decreased cobalanli.n tion, extended anesthesia, or surgery. The
is consistent with antibiotic-responsive
intestinal flora becomes established within
diarrhea Exoc1ine pancreatic ftmction can
a few hours after birth, which emphasizes
be evaluated by the detem1ination of serun1
the importance of the early ingestion of
trypsin-like immunoreactivity and by
colostrum to provide protection against
measurement of serum canine and feline
septicemia and il1testinal infection.

COMMON PATHOGENS OF THE GASTROINTESTINAL

TRACT

Pathogen

Cattle, Sheep, and Goats

Pigs

Vil1.1ses

Bovine viral diarrhea,

Transmissible gastroenteritis,
rotavirus, coronavirus,
porcine circovirus type II,
rinderpest, malignant catarrhal porcine epidemic diarrhea fever, bluetongue, footvirus, rotavirus, foot-andand-rnouth disease mouth disease, vesicular
stornatitis, vesicular exanthema

Rickettsiae

Bacteria

Enterotoxigenic Escherichia

Enterotoxigenic E coli,
coli, Scrlmonella spp, Myco

Salmonella spp, Brachyspira
bacte,ium paratube1·c1.llosis,
hyodysente,iae, Clost1idium

F'usobacte,-ium necrnphorum, pe,:f,ingens types B and C, Clost1-idium pe,:f,ingrns

Lawsonia intracellulmis,

(types B, C, and D), Actinoba

Clostridiwn dijficile
cillus lignieresii, Yersinia
rnte,·ocolitica, Campylobacte,·
jejuni

Protozoa

Eimeria spp, Cryptosp01-idi

Eimeria spp, Isospora s1.tis
um spp

Fungi

Candida spp (cattle)

Candidaspp

Algae

Prototheca spp

Prototheca spp

Parasites (helminths) See GASTROINTESTINAL PARASITES

See GASTROI TESTINAL PARASITES

OF RUMINANTS, p 303.

OF PIGS, p 320.

DIGESTIVE SYSTEM INTRODUCTION

159

Definitive etiologic diagnosis of

(eg, canine parvovirus, salmonellosis,
infectious disease of the GI tract depends
cryptosporidiosis ).

on demonstrating the pathogen in the
tract or in the feces of the affected animal.

Overview of Gastrointestinal

In herd epidemics, such as an outbreak

Parasitism
of acute undifferentiated diarrhea in

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newborn calves or piglets, the best

The GI tract may be inhabited by many
opportunity to establish a diagnosis is
species of parasites. Their cycles may be
in the earliest stage of the disease by
direct, in which eggs and larvae are passed
selecting untreated animals and submitin the feces and stadia! development occurs ting them for necropsy and detailed
to the infective stage, which is then ingested
microbiologic examination of the
by the final host. Alternatively, the inrn1ature
intestinal flora. When selective necropsy
stages may be ingested by an intern1ediate
is not an option, a series of carefully
host (usually an invertebrate) in which
collected daily fecal samples should be
further development occurs, and infection
submitted to a diagnostic laboratory with
is acquired when the intern1ediate host
a request for special culture techniques,
or free-living stage shed by that host is
depending on the infectious disease
ingested by the final host. Sometimes, there
suspected. Molecular technologies,
is no development in the intermediate host,
including ELISA and PCR, have been
in which case it is known as a transp01t or
developed to demonstrate the presence
paratenic host, depending on whether the
of viral, bacterial, or protozoa! proteins
laivae are encapsulated or in the tissues.

or nucleic acids within the feces, which

Clinical parasitism depends on the number
can provide a definitive diagnosis
and pathogenicity of the pai·asites, which

COMMON PATHOGENS OF THE GASTROINTESTINAL

TRACT (continued)

Horses

Dogs and Cats

Rotavirus, vesicular stomatitis, coronavirus Canine parvovirus, canine coronavirus, feline panleukopenia virus, feline enteric
corona virus, canine and feline rotaviruses, canine and feline astroviruses Neorickettsia risticii (Potomac horse fever Neorickettsia helminlhoeca (salmon

[ equine monocytic ehrlichiosis])

poisoning in dogs)

Enterotoxigenic E coli, Salmonella spp,

Salmonella spp, Yersinia enterocolilica, Rhodococcus equi, Aclinobacillus equuli,

Campylobacter jejuni, Clostridium spp,

Clostridium perfringens types Band C,

Clostridium piliforme, Mycobacter·ium

Clostridium difficile, Lawsonia intracel
spp, Shigella spp, adherent invasive
lulmis

E coli, Bra.chyspira spp

Eimeria spp, C?-yptosporidium spp

Isospora spp, Sarcocystis spp, Besnoitia spp, Hammondia sp, Toxoplasma sp,

Giardia sp, Tritrichomonas spp,

Enlamoeba hislolylica, Balanlidium
coli, Cryptosporidium spp, Neospora sp Aspergillus fumigatus

Hisloplasma capsulalum, Aspergillus
spp, Candida albicans, phycomycetes

Protolheca spp

Prototheca spp

See GASTROINTESTINAL PARASITES

See GASTROINTESTI AL PARASITES

OF HORSES, p 315.

OF SMALL ANIMALS, p 412.

160

DIGESTIVE SYSTEM INTRODUCTION
depend on the biotic potential of the
in pet animals. Control by vaccination is
parasites or, when appropriate, their
limited to lungwonns; vaccine for cattle is
intem1ediate host and the clin1ate and
available in several European countries, and
management practices. In the host,
vaccine for sheep is available in pruts of
resistance, age, nutrition, and concomitant
eastern Europe and in the Middle East.

disease also influence the course of

To estimate parasite load, seep 1620.

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parasitic infection. The economic in1portance of subclinical parasitism in farm Treatment of Infectious Diseases
animals is also determined by the above
factors, and it is well established that lightly

Antimicrobial agents ru·e used for the
parasitized animals that show no clinical
treatment of bacterial diseases, and
evidence of disease perfonn less efficiently
ru1thelmintics for parasitic diseases. There
in the feedlot, dairy, or finishing house.

is no specific therapy for treatment of viral

Feed conversion in light to moderate
diseases. Antin1icrobials are commonly
parasitism is adversely affected and is
given PO daily for several days until
primarily due to reduced appetite and poor
recovery is appru·ent, but tl1ere is little
use of absorbed protein and energy. Carcass objective evidence of efficacy. There is quality and size also are reduced, which
evidence tlrnt overdosage or prolonged oral
further reduce financial returns. Endoparatreatment may be detrin1ental ( eg, bacte1ial sites of companion animals can cause
overgrowth, villous atrophy). Parenteral
severe disease or unthrift.iness and are
administration of antimicrobials is
aesthetically undesirable. Furthermore,
indicated when septicemia is apparent or
some of these parasites also infect people.

may occur. The choice of antimicrobial

Because parasitism is easily confused
agent depends on the suspected disease,
with other debilitating conditions, diagnosis
previous results, and cost. In herd
depends heavily on the seasonal character
epidemics, antimicrobials may be added to
of parasitic infection; previous farm history;
the feed or water supplies at tl1erapeutic
and exan1ination of feces for evidence of
levels for several days, followed by
oocysts, worm eggs, or lruvae. Increased
preventive levels for an extended period,
serum pepsinogen levels can support the
depending on the infection pressure in the
diagnosis of some abomasal infections, as
population. The feed and water supplies of
can increased serun1 liver enzymes for liver
in-contact animals also may be medicated in
fluke infection. ELISA are being used, and
ru1 attempt to prevent new cases from
other serologic (including monoclonal
developing. (See also SYSl"EMIC PIIARMACOantibody) techniques are under develop

TIIERAPEUTICS Of THE DIGESl'IVE SYSl"EM, p 2544.) ment; serodiagnosis will likely be used more
frequently as the specificity of the tests

Control of Infectious Diseases
improves. These tests should be_patticulru·ly Effective control of the conunon infec-useful in companion animals hru·boring
tious diseases of the GI tract depends on
parasites incriminated in zoonoses.

practicing good sat1itation and hygiene,

Advances in epidemiology (particulru·ly
developing and maintaining nonspecific
regarding factors affecting seasonal
resistance in the anin1al, and in certain cases,
development of the free-living stages and
providing specific inununity by vaccinating
their survival), coupled with the discovery
tl1e pregnant dat11 or susceptible animal.

of highly efficient broad-spectrun1

Effective sat1itation and hygiene is
anthelrnintics, have made successful
achieved primarily by providing adequate
treatment and control of GI pru·asites both
space for animals and by regular cleaning of
possible and practical. Response to therapy
pens and efficient removal of manure from
is usually rapid, ru1d single treatments
tl1e inunediate environment. Development
usually suffice unless reinfection occurs
and maintenance of nonspecific resistance
or the lesions are patticularly severe.

depends on the genetic selection of animals

Preventive control in large animals is
that have a reasonable degree of inherent
generally achieved by integrating grassland
resistance and on the provision of adequate
management with the use of anthelmintics.

nutrition and housing, which minin1izes

Improved methods of administering
stress and allows the animals to grow and
anthelmintics ( eg, the pour-on method or
behave nom1ally. The development of
sustained or pulsed-release devices) have
infected but clinically healthy animals,
also helped. Strategies to prevent parasitism which can shed patl10gens for weeks or and related production losses are prut of
months, is a major problem with some infecany modem herd-health, flock, or stud tious diseases of the GI tract, eg, salrnonelprogran1. Similar preventive progrruns are losis. Ideally, these canier animals should
equally important in controlling parasitism
be identified by n1icrobiologic means and

DIGESTIVE SYSTEM INTRODUCTION

161
isolated from the rest of the herd until free

Elimination of tl1e primary cause may
of the infection or culled.

involve antinucrobials, coccidiostats,

Certain diseases ( eg, enterotoxigenic
antifungal agents, anthelmintics, antidotes
colibacillosis in calves and piglets) can be
for poisons, or surgical correction of
controlled by vaccination of the pregnant
displacements.

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dam several weeks before parturition. This

Correction of excessive or depressed
method depends on achieving a protective
motility appears rational, but often the
level of antibodies in the colostrum. There
nature and degree of abnormal motility ai·e
are exceptions but, in most cases, systemic
uncertain; in addition, available drugs may
immunity provides little protection against
not give consistent results. There is little
the infectious enteritides; effective
clinical evidence to recommend the routine
immunity against GI disease depends on
use of anticholinergic or opioid drugs to
stimulation of local intestinal immunity
slow intestinal transit. Slowing intestinal
after the neonatal period. During the neonatransit may be counterproductive to the tal period, protection can be provided
defense mechanism of diarrhea, which acts
through the local action of maternally
to evacuate harmful organisms and their
derived antibodies. For exan1ple, secretory
toxins. In general, anticholinergic drugs

IgA progressively increases in sow's milk
probably are justified only for short-term
from the time of farrowing until weaning,
symptomatic relief of pain and tenesmus
which provides the piglet with daily
associated with inflan1matory diseases of
protection during the nursing period.

the colon and rectum. In some disorders of
gastric or colonic motility, prokinetic drugs

NONINFECTIOUS DISEASES

( eg, metoclopramide, erythromycin) may be
useful.

The major causes of noninfectious disease

Replacement of fluid and electrolytes is
of the GI tract include dietary overload or
necessary when dehydration and electroindigestible feeds, chemical or physical lyte and acid-base imbalance occur as in
agents, obstruction of the stomach and
diarrhea, persistent vomiting, intestinal
intestines caused by tl1e ingestion of foreign
obstruction, or torsion of the stomach(s), in
bodies or by any physical displacement or
which large ainou.nts of fluid and electroinjury to the GI tract that interferes with lytes are sequestered.

the flow of ingesta, enzyme deficiencies,

Relief of distention medically by stomach
abnormalities of the mucosa tl1at interfere
tube (as in bloat in ruminants) or surgically
with normal function ( eg, gastric ulcers,

( as in acute intestinal obstruction, or in
intlan1matory bowel disease, villous atrophy, torsion of the abomasun1 in ruminants or of neoplasms), and congenital defects. GI
the stomach in monogastric anin1als) may
manifestations such as vomiting and
be required. The GI tract may become
dianhea may develop secondary to systemic distended with gas, fluid, or ingesta at any or metabolic diseases such as uremia, liver
level due to physical or functional
disease, and hypoadrenocorticism. The
obstruction.

causes are uncertain in several diseases,

Relief of abdominal pain by administraincluding abomasal ulcers in cattle, gastric tion of analgesics should be done when
ulcers in pigs and foals, gastric torsion in
the pain is reflexly affecting other body
dogs, and acute intestinal obstruction and
systems ( eg, cardiovascular collapse) or
displacement of the abomasum in cattle.

when it is causing the a11imal to injure

In noninfectious diseases of the GI tract,
itself because of rolling, kicking, or
usually only a single anin1al is affected at
throwing itself. Animals treated with
one time; exceptions are diseases associated analgesics must be monitored regularly with excessive feed intake or poisons, in
to ensure that the relief of pain does not
which herd outbreaks are common.

provide a false sense of security; the
lesion may be progressively worsening

PRINCIPLES OF THERAPY
while the a11imal is under the influence
of the analgesic.

See also SYSTEMIC PI-IARMACOTHERAPEUTICS

Reconstitution of ruminal flora should be

OF THE DIGESTIVE SYSTEM, p 2544, and
done in situations in which the ruminal flora

THE RUMINANT DIGESTIVE SYSTEM, p 2561.

may be seriously depleted ( eg, in prolonged

Although eliminating the cause of the
anorexia or acute indigestion). Transfau.nadisease is the primary objective, the major tion ( ruminal fluid transfer; see p 2562)

part of treatment is supportive and
involves oral administration of ruminal
symptomatic, aimed at relieving pain,
contents from a healthy anin1al that
correcting abnormalities, and allowing
contains rumen bacteria and protozoa
healing to occur.

and volatile fatty acids.

162

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM

CONGENITAL AND INHERITED ANOMALIES

OF THE DIGESTIVE SYSTEM

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MOUTH

Texel sheep with cleft lip. Teratogens and
nutritional causes during pregnancy include

Congenital Oronasal Fistulas (Cleft
high levels of vitainin A in the diet,

Palate and Cleft Lip): Congenital oronaadministration of g1iseofulvin, folic acid sal fistulas are the result of failure of fusion
deficiency, and ingestion of toxic plants.

of the palatine shelves during gestation

In cattle, ingestion of lupine during days

( which occurs at 25--28 days of gestation in

40-100 of gestation results in arthrygryposis
dogs). Clefts can be either of the primary
and cleft palate, due to the effects of
palate (involving the lip and incisive bone)

anagyrine found in Lupi nus sericeus and
causing cleft lip (harelip), or of the

L caudatus. Ingestion of poison hemlock
secondary palate (involving the hard and

(Conium maculatum), which contains the
soft palate) causing cleft palate. The
toxic principle coniine, results in sinlilar
conditions can occur singly or together. In
signs in both cattle and goats, whereas
dogs, CT studies have shown association
ingestion of Veratrum californicum in
of cleft palate with other craniofacial
sheep, goats, and cattle all result in cleft
abnom1alities, including hypoplastic
lip and/or palate in the fetus.

tyrnpanic bullae, hypoplastic nasal

For puppies and kittens in which
turbinates, and maxillary malocclusions,
euthanasia is not elected, medical
mostly of the incisors. Neurologic
management is required until surgical
exanlination should be performed in
options are explored. Animals are fed via
affected animals, because concurrent
orogastric intubation until dry food can be
hydrocephalus has also been described.

tolerated. Water can be offered by overhead

Animals are typically diagnosed at, or
dispenser. A custom-molded palate guard
shortly after, birth by oral examination, by
has been described in experimental settings
observation of dysphagia or milk from the
to allow adult dogs to eat and drink
nares after nursing, and/or by respiratory
nom1ally. Aspiration pneumonia should
compromise and aspiration pnewnonia.

be quickly identified and treated. Surgical

Many affected neonates are euthanized or
correction is recommended after at least
die early in life.

12 wk of age, although some studies have

Cleft palate and cleft lip have been
shown higher success when performed at
described in most domesticated animal

>20 wk, or as adults. Surgical correction has
species, including dogs, cats, runlinants,
a high failure rate because of continued
horses, and can1elids. In dogs, brachycegrowth of puppies or kittens postoperaphalic breeds are overrepresented, with up tively, the size of the patient, and irritation
to 300Ai risk factor. Other breeds with higher
of the surgery site by the tongue and feed
incidence include Beagles, Cocker Spaniels,
mate1ial. Surgical techniques depend on the

Dachshunds, German Shepherds, Labrador
location and size of the cleft defect. For

Retrievers, Schnauzers, Old Spanish
secondary palate defects, sliding mucoperi

Pointers, and Shetland Sheepdogs. The
osteal flaps or overlapping flaps are most
most conunonly affected cat breed is the
commonly used.

Sian1ese. Etiologies include genetic,

Extensive involvement of the soft palate
teratogenic, and nutritional causes. Modes
carries a poor prognosis, even with surgical
of inheritance are monogenic autosomal
intervention. Surgical repair should be
recessive or incomplete dominant in several
attempted only after ethical questions have
breeds. In Btittany Spaniels, Pyrenean
been addressed, and the affected animal

Shepherds, Beagles, Old Spanish Pointers,
should be surgically sterilized or removed
and Boxers, it is believed to be an autosofrom breeding stock to prevent reproducing mal recessive trait, whereas in Bulldogs
the anomaly in future offsp1ing.

(French and English) and Shill Tzus, an
autosomal dominant with incomplete

Occlusal Anomalies: Occlusal abnorpenetrance mode of inheritance is malities due to abnom1al lengths of the
suspected. Autosomal recessive inheritance
maxilla and mandible are common in
patterns are seen in Angus cattle with
animals. Brachygnathia, also called
arthrogryposis multiplex, in Charolais cattle overbite, overshot, overjet, short lower jaw, with cleft palate and arthrogryposis, and in
or parrot mouth in horses, is manifest when

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM

163
the mandible is shorter than the maxilla.

can result in "bulldog calves," with severe It can be found, with varying severity and
skeletal malformation and craniofacial
incidence, in all species of animals and is
dysplasia that has the appearance of
diagnosed by oral examination. In Red
prognathism.

Angus cattle, it is inherited in a recessive
manner through a deletion mutation on

Tongue Anomalies: Ankyloglossia,

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chromosome 4, which results in stillborn
also called "tongue-tie," is a disorder of calves with osteopetrosis (seep 1044),

Anatolian Shepherd dogs characterized
brachygnathism, and impacted molars. In
by a short, thickened lingual frenulum that

Simrnental cattle, brachygnathlsm can be
inhibits nonnal movements of the tongue.

seen in calves as an autosomal recessive

By unknown mechanism, the normal fetal
trait, or in combination with trisomy 17,
apoptosis of the cranial 2/3 of the frenulun1
a lethal condition. A lethal, autosomal
does not occur. Clinically, the tongue
recessive disorder of Merino sheep results
appears notched or with a "W" shape.

in brachygnathlsm, cardiomegaly, and renal

Animals may experience dysphagia;
hypoplasia. Brachygnathlsm is conunon in
difficulty suckling, ch-inking, or licking;
horses, due to either a lengthened maxilla or trouble vocalizing; and impedence of shortened mandible. Modes of inhe1itance
panting and therefore thennoregulation.

are unknown. It may occur in utero due to

Frenuloplasty is corrective. Breeding of
treatment of the mare with griseofulvin.

affected anin1als is not reconunended.

Most horses do not experience dysphagia;

Microglossia is a congenital defect
however, cheek teeth malocclusions are
characterized by missing or underdevelconunon, and regular dental care is oped lateral and rostral thin portions of the
required. Correction can be attempted in
tongue that result in prehensile and motility
foals via surgical placement of tension
disturbances. It is often referred to as "bird
band wires around the maxillary incisors
tongue" in dogs and may be a component
to inhibit maxillary growth.

of the fading puppy syndrome, because

In small animals, mild fonns may be of no
affected puppies have difficulty nursing and
clinical significance; however, more severe
swallowing and can aspirate or quickly
forms may result in trauma to the hard
become dehydrated. In cattle, excessive
palate or the restriction of nonnal
salivation has been seen. Even with supmandibular growth secondary to erupting portive dietary meastu-es, the prognosis
adult mandibular canine teeth. Treatment
is poor.

varies from none to various orthodontic or

Macroglossia, or large tongue, has been
endodontic procedures, depending on
described in association with nasopharynseverity. The mandibular canine teeth are geal dysgenesis in Dachshunds. It has also
often removed or a crown reduction
been seen in double-muscled cattle breeds,
procedure performed, with concurrent
such as the Belgian Blue, and can inhibit
pulpotomy or root canal. Intervention early
nursing of calves.

in life is reconunended and improves both

Epitheliogenesis imperfecta is a
short- and longtem1 outcomes.

disorder of the skin in which the epithelium

Prognathia, also called undershot,
is absent, revealing the dermis. Commonly
underjet, or monkey or sow mouth in
affected areas include the limbs, back, and
horses, is identified when the mandible is
oral mucosa and tongue. It is inherited by
longer than the maxilla. It is diagnosed by
a simple recessive manner and is well
oral examination. In brachycephalic dogs
described in cattle and horses, particularly
and Persian cats, it is considered a nonnal

Saddlebreds. Euthanasia is typically
breed characteristic. In horses, it is more
elected.

commonly seen in miniature and Arabian
breeds. The degree of severity is variable

Tight-lip Syndrome of Chinese
and may not require treatment. In severe

Shar-Pei: A small or absent lower anterior
cases in foals, surgical placement of tension
lip vestibule is a congenital defect of some
band wires can allow for continued

Shar-Pei dogs. The lower lip covers the
maxillary growth. The most severe
mandibular incisors and canines, disrupting
consequences are the result of malocclunormal occlusion, inhibiting mandibular sions. Affected foals may have difficulty
growth, and leading to the dog biting on the
nursing, and older anin1als may experience
lip (which presents welfare issues). In
difficulty grazing. Cheek teeth maloccluextreme cases, the mandibular incisors sions should be addressed with regular
become lingually directed. Surgical
dental care.

correction by chelioplasty has been

Chondrodysplasia, a sin1ple dominant
described using several different mucosal
trait of Dexter cattle, is a lethal defect that
flap techniques. Any animals that have

164

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM
undergone surgical correction should not
the horse, manifest as headshaking,
be presented for conformation showing and
inappetence, quidding, and training issues.

should not be bred.

Caps can be extracted if they are loose, if
the contralateral cap has al.ready been shed,

TEETH
or if there is space between the cap and the
pern1anent tooth below.

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Abnormal Number: Deviation from the

Retained deciduous teeth are common
dental formula has been seen in several
in dogs and secondary to the failure of the
species. Complete lack of development of
pe1iodontal ligament to detach from the
teeth, or anodontia, is rare. Hypodontia
deciduous tooth, with the permanent canine
or oligodontia has been described as
teeth erupting rostrally. One study showed
inherited by a recessive manner in Kerry
highest incidence in dogs <2 yr old, with

Blue Terriers and associated with X -linked
small breeds overrepresented, particularly
hypohidrotic ectodennal dysplasia in other

Toy Poodles. Retention may cause
breeds. Most cases appear to affect the
permanent tooth displacement, which can
premolars. Hyperdontia, also called
result in malocclusion or food entrapment
polyodontia or supernumerary teeth, is seen and subsequent periodontal disease.

most often in the permanent teeth and can

Therefore, retained deciduous teeth should
affect the incisors, premolars, or molars.

be removed as soon as possible, taking care

Presw11ably, these teeth arise from
not to dan1age the underlying pem1anent
overproliferation of the dental lamina
tooth bud.

during development. Supernwnerary teeth
tend to cause crowding and malocclusions,

Abnormalities in Position, Shape, and
which can cause dysphagia, dental disease,

Direction: Displacement or rotation of
and discomfort. In horses, supernumerary
teeth has been described in many species.

incisors are typically not extracted and are

In horses, the cheek teeth are affected
managed with regular reduction. For
more commonly than the incisors, with the
supernwnerary cheek teeth, diastema and
permanent teeth most often affected rather
sinusitis due to oromaxillary sinus fistula
than the deciduous teeth. Most displaceforn1ation are possible sequelae. Teeth are ments are due to crowding during eruption.

either extracted or reduced often to prevent

Sequelae include malocclusion, uneven
complications.

wear and development of sharp points, and
diastema witl1 associated feed packing.

Irregularities of Shedding: Retention

Treatment includes regular floating of
of the deciduous teeth in horses is conunon.

unopposed surfaces, or extraction if severe.

The incisors tend to retain rostrally to the

Diastema can be addressed by mechanical
pennanent incisors; however, radiographs ·
widening. In dogs, rotation has been
will help to discern their identity. Incisors
described conunonly in brachycephalic
retained in other orientations can result
and large breeds, with the first mandibular
in malocclusion and/or displacement of
premolar or upper third premolar often
permanent incisors. Retained cheek teeth
affected. Abnormally located or directed
are called "caps," which are typically shed teeth can result in malocclusions or affect
as the permanent tooth erupts underneath
the positioning of adjacent teeth. Extraction
them. Loose caps can cause discomfort to
can be perforn1ed in severely affected
anin1als; many cases are considered
incidental findings.

Enamel Lesions: Enamel hypoplasia,
hypomineralization, or dysplasia is seen in
both large and small anin1als. Conu11on
causes are pyrexia, trawna, malnutrition,
toxicosis ( eg, fluorosis in cattle), congenital
disorders (eg, epitheliogenesis irnpe1fecta
in Saddlebred foals), and infections (eg,
distemper virus in dogs or bovine viral
diarrhea virus in calves) that affect
ameloblast and odontoblast activity.

Lesions vary, depending on the severity and
duration of the insult, from pitted enan1el to
the absence of enamel with incomplete

Retained deciduous incisors in a horse.

tooth development. Affected teeth are

Courtesy of Dr. Gordon Baker.

prone to plaque and tartar accumulation

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM

165
and subsequent bacterial penetration and
try for presence of thyroglobulin. These
formation of caries. In small animals, resin
cysts arise from the thyroglossal duct,
restoration has been used to cover defects,
which in the embryo is present from the
although diligent dental hygiene and home
base of the tongue to the eventual location
care is critical to reduce the incidence of
of the thyroid and which is normally absent

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complications. Enamel may also develop
by birth. The cyst is solitary and usually
discoloration. In small animals, administralocated on ventral midline, although a case tion of tetracyclines to pregnant females
of a mediastinal thyroglossal duct cyst with
or to puppies <6 mo old may result in a
ectopic thyroid tissue was reported in a cat
permanent brownish yellow discoloration
and a case of subepiglottic thyroglossal
of the teeth. In ruminants, the enan1el of
duct cyst was reported in a dog. It is
some teeth may demonstrate flecks of
hypothesized that subepiglottic cysts in
varying color. The condition is thought to
horses are also of thyroglossal duct origin
have a genetic etiology but generally is of no
and may be associated with epiglottic
clinical significance; however, some believe
entrapment. In Damascus goats, thyroglosaffected teeth may be prone to more rapid sal duct cysts are heritable by an unknown
wearing.

genetic mechanism. Aspiration of the cyst
for measurement of thyroxine has not been
reliably diagnostic. Surgical resection is

CYSTS AND SINUSES OF THE
curative.

HEAD AND NECK

In horses, congenital cystic lesions of the
esophagus are typically of two types:

Congenital cysts, sinuses, orfistulae of the
intramural inclusion cysts and esophabranchial arch apparatus or thyrnglossal geal duplication cysts. Both have been
duct have been reported in horses, dogs,
described in yearling horses that presented
cats, and ruminants, yet are very rare. These
for recurrent choke, dysphagia, and
structures arise from persistent embryoaspiration pneumonia. Both occur in the logic pharyngeal pouches, arches, or clefts,
ceIVical esophagus and result in compresor the thyroglossal duct. Animals typically sion of the esophageal lumen and its
present with nonpainful, fluid-filled masses
function. Diagnosis is aided by inrnging,
in the ceIVical region. Clinical signs are
including video endoscopy, contrast
typically due to the space-occupying mass
radiography, and ultrasonography.

and include dyspnea, respiratory stridor,

Described treatments include surgical
intemlittent esophageal obstruction, and
resection and marsupialization with
coughing. Aninlals may present later in life;
sclerotherapy. Complications after excision
it is not known why a cyst may suddenly
have included left laryngeal hemiplegia and
enlarge but may be associated with
esophageal fistula formation. Histologically,
respiratory infection. Diagnostic imaging
esophageal duplication cysts include aJayer
includes radiography, ultrasonography,
of muscle, whereas inclusion cysts contain
video endoscopy, and contrast CT to
only keratinized squamous epithelium.

detemline whether there is communication

Heterotopic polyodontia, or teeth
with the pharynx. Branchial cysts (also
outside the dental arcade, includes both
called lateral ceIVical cysts) in horses are
dentigerous cysts, which have been
typically seen on the right side, although a
described in most domestic animal species,
bilateral case has been reported. Surgical
and the ear teeth, or temporal teratoma,
excision is curative, although complications
of horses. Dentigerous cysts contain all
include right laryngeal hemiplegia, seroma
or part of at least one tooth (including the
formation, and pneumonia. Alternatively,
crown). The cysts are lined by epitheliwn
some horses have been treated with
and often cause facial swelling or draining
marsupialization and iodine sclerotherapy
tracts, if fistulated. In horses, dentigerous
with good results. In dogs and cats, few
cysts are often seen in association with the
complications have been noted. Embryowolf teeth or canine teeth of mares; in dogs, logic origin of branchial cysts has been
commonly of the brachycephalic breeds,
mostly of the third pharyngeal pouch,
with the mandibular first premolars; and in
although anatomic location has also
sheep, with the mandibular incisors. They
suggested origin of the fourth and sixth
may be bilateral.

pouches in some cases.

Surgical removal of the cyst( s) is

Thyroglossal duct cysts appear similar
required, with definitive diagnosis based on
in appearance to branchial cysts; differensubsequent histopathologic exan1ination.

tiation is often made histologically by

Curettage of extremely large cysts with
demonstration of thyroid follicles
compromise of tile mandible may require
containing colloid or immunohistochemis-
bone grafts.

166

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM

ESOPHAGUS
esophageal sphincter achalasia is
considered to be a component of a more

Clinically significant esophageal disorders
generalized esophageal motor disturbance
generally manifest themselves as swallow

(ie, megaesophagus) and no longer a
ing dysfunction and regurgitation,
distinct entity.

especially when puppies or kittens are

Diagnosis of an esophageal disorder is

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weaned and begin to eat solid food. These
generally based on cha.i·acte1istic clinical
disorders, found predominantly in small
signs (eg, regurgitation, ptyalism, dysphaanimals, can be classified as congenital gia, aspiration pnewnonia) and contrast
megaesophagus, vascular ring entrapment
imaging. Radiography may identify a
anomalies, and achalasia. Congenital
distended, gas-filled esophagus, or
megaesophagus is thought to result from
fluoroscopy may identify alterations in
developmental anomalies in esophageal
esophageal peristalsis and swallowing.

neuromuscular innervation that controls

Diagnosis of the specific underlying etiology
dilation and peristalsis. In dogs, incidence is
may require further testing, such as
increased in Chinese Sha.i�Pei, Fox Terriers,
endoscopy, endocrine function testing, and

German Shepherds, Great Danes, Irish
elimination of myasthenia gravis. Treatment

Setters, Labrador Retrievers, Miniature
is directed at the prima.iy etiology. Some

Schnauzers, and Newfoundlands. In Fox
mildly affected animals may in1prove over

Teniers, it is an autosomal recessive trait,
time; however, in general the prognosis is
whereas in Miniature Schnauzers, it is
poor. Aspiration pnew11onia is a frequent
autosomal dominant. It is also seen in
and often lethal complication. Frequent,

Sian1ese cats and Friesian horses. Megaelevated feedings of small quantities of a esophagus may also be a component of a
highly digestible, soft diet may be helpful.

more diffuse congenital neuropathy, such as For horses, feeding a mash at chest height congenital myasthenia gravis. A laryngeal
or full-time pasture grazing have been
paralysis-polyneuropathy complex tl1at
suggested. Owner compliance is essential
often includes megaesophagus has been
for successful management. Surgical
reported in Dalmatians and Pyrenees
correction of vascular ring anomalies had

Mountain Dogs. Seconda.iy megaesophagus
an overall survival rate of 7'2:'lo in dogs in one may develop in association with hypoadstudy, whereas all horses and can1elids died renocorticism, neoplasia, or GI or
or were euthanized in others. In dogs, only
neuromuscular disorders. Vascular ring

30% were free of clinical signs after surgery.

anomalies occur due to errors in develop

Persistent clinical signs included regurgitament of the third, fourth, or sixth aortic arch tion and aspiration pnewnonia. Dietary
and result in entrapment of the thoracic
modification is often required for life.

esophagus and trachea, which lead to the

Esophageal diverticula may involve
clinical signs. They have been described in
t11e cervical esophagus just cranial to the
dogs, cats, horses, cattle, and camelids. The
thoracic inlet or be epiphrenic Oust cranial
most common anomaly is persistent right
to the diaphragm). Small diverticula may
aortic arch, but aberrant right and left
not cause any clinical signs. In more severe
subclavian arteries, right ligamentwn
cases, clinical signs may include impaction,
arteriosum, and double aortie arch have
esophagitis, and rarely rupture and
also been reported. In dogs, Boston Terriers, pyotl1orax. Treatment (if necessa.iy) is by German Shepherds, and Irish Setters have
surgical resection. Esophageal diverticulae
higher breed incidences. In cats, a report
just cranial to the thoracic inlet may be
associated persistent right aortic arch with
seen in English Bulldogs due to thoracic
axial skeletal abnonnalities. Advanced
shortening and external compression of the
imaging, including 3-D CT, is useful for
esophagus by other thoracic strnctures.

diagnosis of specific anomalies and surgical
planning. Cricopharyngeal achalasia is a

HERNIAS
failure of the upper esophageal sphincter

(specifically, the cricopharyngeal muscle)

A trne hernia is defined as having a hernia
to relax during swallowing, thereby
ring, sac, and contents. Hernias of the
preventing the nmmal passage of a food
abdominal wall are common in all domestic
bolus from the caudal pha.iynx to the cranial species and include umbilical hernias and esophagus. Cocker and Springer Spaniels
inguinal or scrotal hernias. Hernias may be
appear to be at increased risk. Treatment
direct (through a rent in the body wall) or
of congenital achalasia is c1icopharyngeal
indirect (through an already existing ring,
myectomy. Acquired achalasia is treated by
such as the inguinal ring or umbilical ring).

addressing the inciting cause and imple

Congenital hernias tend to be indirect,
menting dietary management. Lower
although direct, traumatic hernias may arise

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM

167
during dystocia or obstetrical manipulalethargy, and weight loss. In cattle, tions. Umbilical hernias vary in size and
herniation of the reticulum into the thorax
may contain only fat or omen turn, or in
has been described, with a right-side
more severe cases, intestinal loops. In dogs,
diaphragmatic defect. Clinical signs include

Weimaraners, Pekingese, Basenjis, and
anorexia, scant manure, tympani, and

Airedale Terriers are overrepresented. In
decreased or no rnmination. Diagnosis is by

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many cases, umbilical hernia is seen in dogs
radiography or ultrasonography. Perito
with concurrent cryptorchidisrn. Hereditary
neopericardial hernias ai·e defined as an
etiology is suspected but not proved. In
embryologic defect in the failure of fusion
cattle, the Holstein Friesian breed is overof the septum tratIBverswn dwing represented. Diagnosis in all animals is by diaphragn1atic development, allowing
observation of the hernia sac, palpation,
conunwucation between the abdominal
ultrasonography, and possibly radiographs.

cavity and pericardia] sac. Weimaraners and

Surgical closure of the body wall defect is domestic long-haired cats were overrepreindicated in most cases to reduce risk of sented in one study. Clinical signs reflect the
future intestinal incarceration.

contents of the hernia, which may include

Inguinal or scrotal hernias are
omen tum, liver, gallbladder, or small
common in pigs, horses (paiticularly draft
intestinal loops, and include car·diac
breeds and waimbloods ), and many breeds
tat11ponade, dyspnea, tachypnea, exercise
of dogs and are suspected to be hereditary.

intolerance, coughing, vomiting, and GI

Inguinal hernias can occur in bitches ai1d
obstrnction. In many cases, the diagnosis
may involve the uterns. Clinical signs vary
was an incidental finding during imaging
from nonpainful inguinal or scrotal swelling
or celiotomy for other reasons. Other
to acute colic in horses or vomiting in dogs,
congenital defects were found in many
paiticularly if the small intestine is
cases, including umbilical hernia, cryptorstrangulated. In horses, palpation per chidism, cleft palate, po1tosystemic shunt,
rectum can diagnose intestinal loops in the
and sternal or vertebral abnonnalities.

vaginal ring, which can be gently removed

Animals with clinical signs were treated
to provide relief before transport to a
with surgical herniorrhaphy, whereas
surgical facility. Any devitalized bowel is
animals with no clinical signs tended to be
resected via midline celiotomy. In stallions,
closely monitored. Hiatal hernias occur
testis-sparing laparoscopic closure of the
tJu·ough the esophageal hiatus and ar·e
inguinal rings has been perfonned in both
classified into four types. 'fype I, the sliding
standing ai1d recumbent horses with good
hernia, is the most common in small animals
outcome and subsequent fertility. In foals
and is characterized by intennittent
and calves, medical management through
displacement of the lower esophageal
reduction of the hernia and placement of a
sphincter and gastric fund us into the
figure-eight bandage has been successful in
thoracic cavity. 'fype II is less conunon
some cases. Hernias that do not spontaneand involves only the displacement of·
ously resolve ear·ly in life should be
the gast1ic fundus. Brachycephalic breeds
surgically corrected to prevent later
are overrepresented, with a hereditary
complications.

nature suspected in Shar-Pei. Clinical signs

Hernias between the abdominal ai1d
include dysphagia, regurgitation, vomiting,
thoracic cavities that involve the diaphragm
ptyalism, and esophagitis due to decreased
are of several types and can be congenital or function of the lower esophageal sphincter.

acquired (traumatic) in origin. Congenital

Diagnosis is by radiography or fluoroscopy;
pleuroperitoneal hernias have been
however, the intermittent nature can make
described in small animals, horses, and
diagnosis challenging. Medical treatment of
calves. In horses, a specific type of hernia,
esophagitis is required. Surgical correction
a retrostemal or Morgani hernia, has been
is by combination of hiatal plication,
described in which a hernial sac protrudes
esophagopexy, and left-side gastropexy.

into the thorax in the left dorsal tendinous
portion of the diaphragm. The sac is
chai·acte1ized by a pleural covering and a

STOMACH
peritoneal lining. In described cases, the
presenting complaint was colic, and the

Besides hiatal hernia, the most common
diagnosis was made during exploratory
abnonnality involving the stomach with a
celiotomy. Defects can be surgically
suspected he1itable etiology is pyloric
repaired using mesh products to reduce risk stenosis, which affects brachycephalic dog of recurrence. The hernial sac is usually left
breeds (Boxers, Boston Terriers, English
in situ. In cases of direct herniation, clinical

Bulldogs) and Sian1ese cats. Pyloric
signs include dyspnea, exercise intolerance,
stenosis or pyloric muscular hypertrophy

168

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM
results from muscular thickening of the
hypoallergenic diet trials and inununosuppyloric sphincter, which obstrncts pyloric pressive therapy directed at IBD ancVor
outflow. Clinical signs reflect delayed
glomeruloneph.ritis, prognosis is poor.

gastric emptying and usually manifest as

Gluten-sensitive enteropathy has
vomiting of food several hours after a meal
been shown to be inherited by an autosomal
but may also include poor weight gain,
recessive marmer in Irish Setters. However,

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aspiration pneumonia, depression, and
the pathogenesis in dogs appears to be
dehydration. Diagnosis is aided by contrast
different than that of celiac disease in
imaging and endoscopy, which is often
people. One case has also been described
combined with biopsy to exclude neoplasia.

in a horse. The wheat sensitivity is both

Sw-gical treatment is recommended to
confirmed and treated th.rough use of
relieve the obstrnction. Medical treatment
gluten-free diets.

of esophagi tis, acid-base abnonnalities, and

Baser\jis have been diagnosed as carriers
dehydration should be instituted before
of a severe fonn of lymphocytic-plasmacytic
sw-gery.

enteritis called Basenji enteropathy,

Abomasal emptying defect of sheep
although the mode of inheritance is not
is a dysautonomia characterized by
known. The stomach may also be affected.

functional obstruction of the pyloric

Clinical signs include diarrhea and weight
sphincter, possibly due to neurotoxicity
loss, with hyperglobulinemia. Diagnosis is
of the celicomesenteric ganglia. It is well
based on histopathologic examination of
described in Suffolk sheep with few cases

GI biopsies, usually obtained through
reported in Han1pshire, Dorset, and Texel
endoscopy. Treatment trials with in1munobreeds. The etiology is unknown; it may suppressive drngs and hypoallergenic diets
be hereditary or that certain genotypes
are usually unsuccessful unless aggressively
predispose to the condition. Pedigree
initiated early in the disease.

analysis of affected flocks does not show a
l.vmphangiectasia is a malformation of
simple inheritance pattern. Clinical signs
the intestinal lymphatic system that results
include weight loss, anorexia, depression,
in a protein-losing enteropathy that may be
dyspnea, decreased rnmen motility, and
congenital or acquired, with a 500A, incidence
progressive distention of the right ventral
in Norwegian Lundehunds in the USA.

abdomen. Even with abomasotomy, the

Other affected breeds include Yorkshire
prognosis is poor to grave.

Terriers, Maltese, Rottweilers, and Shar-Pei.

Lymph vessels become dilated, secreting

SMALL AND LARGE INTESTINE
lymph into the intestines, which results in
hypoproteinemia, lymphopenia, and

Maldigestion or malabsorption disorders
lipogranulomatous inflammation of
usually manifest as chronic, persistent GI
surrounding tissues. It is diagnosed through
signs, including vomiting, weight loss,
exclusion of other protein-losing diseases
small- ancVor large-intestinal diarrhea, or a
and confinned by histopathology of the
combination of the above. There are many
small-intestinal wall. Most affected animals
potential etiologies, both heritable and
respond to a combination of dietary
acquired, and most are associated with
manipulation and anti-inflanunatory doses
inflanm1atory bowel disease (IBD).

of glucoco1ticoids. Diets should contain

Congenital conditions may have specific
minimal fat, be energy dense, and easily
breed predilections.

digestible. Although remission of clinical

Soft-coated Wheaten Terriers have a high
signs may be achieved, the longterm
incidence of protein-losing enteropathy
outcome is usually poor.·

(PLE), which may be seen alone or in

Exocrine pancreatic insufficiency
association with protein-losing nephrop

(EPI) has a higher incidence in German
athy (PLN). Although the mode of

Shepherds and Rough Collies, although it
inheritance is not clear, the etiopathogenhas been diagnosed in many breeds. Disease esis of PL is likely different than that of
is due to pancreatic acinar atrophy, which is

PLE, due to podocytopathy. Dogs with PLE
due to immune-mediated destrnction and
have both food hypersensitivities and IBD,
infiltration of lymphocytes. In Gennan
although the pathogenesis is not clear.

Shepherds and Pembroke Welsh Corgis,

The demonstration of increased fecal
genome-wide association studies have
o.1-protease inhibitor concentrations can
identified several major histocompatibility
help confinn abnormal protein loss through
complex haplotypes associated with EPI in
the intestinal tract, although this is more
affected animals, suggesting a complex
useful as a screening test in animals <3 yr
mode of inheritance. The lack of pancreatic
old. A definitive diagnosis is based on
enzymes results in an osmotic diarrhea, in
intestinal and renal histopathology. Despite
which steatorrhea is a prominent featw-e.

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM

169

Affected animals either fail to gain weight
absence of an anal opening. It is rare in dogs
or, if EPI is acquired later in life, show a
but has been reported in several breeds,
dramatic weight loss. Diagnosis is through
including Toy Pooclles and Boston Terriers,
measurement of sernm trypsin-like
with an increased incidence in females.

in1munoreactivity; validated tests are

ConcwTent rectovaginal fistula may occur.

available for both dogs and cats. Treat

Euthanasia is recommended in large

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ment involves exogenous replacement of
animals. In small animals, postoperative
pancreatic enzymes and use of highly
fecal incontinence may be a complication
digestible diets.

of surgical intervention.

Granulomatous colitis, previously

Segmental aplasia of the rectum
called histiocytic ulcerative colitis, has been

(rectal atresia) is seen when the rectwn
diagnosed in Boxers and French Bulldogs,
terminates in a blind pouch before reaching
with sporadic cases in a few other breeds.

the anus. Surgical correction is difficult

The disease is characterized by granulomabecause the location of the temlinal section tous inflammation of the colonic mucosa in
varies, and iatroge1lic damage to nerves in
association with infection with adherent
the area may occur.

and invasive Esche1ichia coli. An auto

Enteric duplications are very rare,
somal recessive defect in the inu11 une
witl1 only a few cases described in several
system that predisposes to E coli infection species, and may include the colon or
is suspected. Clinical signs arise in animals
rectun1. Duplications may communicate

<4 yr old and include diarrhea, hematochewith the lwnen of the patent tract or be zia, tenesmus, and weight loss. Diagnosis
separate (duplication cyst). Affected
is by histologic exanlination of colonic
anin1als may be diagnosed by identification
mucosa! biopsies. Successful renlission
of an abdominal mass, or tl1ey may show
has been achieved in animals treated with

GI signs. Diagnosis is by ultrasonography
enrofloxacin; however, treatment has been
or contrast CT. Correction is via surgical
unsuccessful in cases in which the E coli
removal of the duplication, although some
was resistant to fluoroquinolones.

cases have multiple concurrent abdonlinal
lleocolonic agangliosis, or overo lethal
developmental anomalies that preclude
white syndrome, occurs in white foals with
complete surgical correction.

blue eyes produced by Overo-Overo

Rectourethral fistula has been
matings. The condition is fatal. It is due to
reported primarily in English Bulldogs and
mutation in the endothelin B receptor and is
is diagnosed cliilically as simultaneous
inherited in an autosomal recessive manner.

urination from both the urogenital and anal

Although the foals appear nom1al at birth,
orifices along with a llistory of chronic
they rapidly develop signs of colic and
urinary tract infections. Diagnosis is via
meconiwn impaction due to hypoinnervacystow-etlu·oscopy with concWTent tion of the intestinal tract, which causes
colorectal infusion of contrast material,
lack of motility. Diagnosis can be confirmed
or by contrast CT. Sw-gical correction.is
at necropsy by the lack of ganglia in the
cw-ative.

colon. Adult Overo horses can be screened

Rectovaginal fistula is a fistulous tract
for genetic status before breeding to reduce
that connects the vagina and rectum and
incidence. Congenital atresias of either the
usually is seen in conjunction witl1
small- or large-intestinal tracts have been
imperforate anus. Passage of feces through
described in most domesticated animal
the vulva is suggestive. Diagnosis may be
species. Atresia coli has been reported in
confumed by bariun1 enema, which outlines
several foals of differing breeds. Atresia
the extension of the defect into the vagina,
ilei in Swedish Highland cattle, and atresia or video endoscopy. Identification of the
jejunae in Jersey cattle are likely due to
fistula, surgical correction, and reestablishautosomal recessive inheritance. These ment of the nonnal anatomic structures are
conditions are invariably fatal. Aggressive
imperative. Prognosis is usually guarded.

manipulation of the bovine conceptus by

Complications are common and include
transrectal palpation early in gestation
fecal and urinary incontinence.

( <45 days) has been implicated as a cause,

Urinary and fecal incontinence is often
although a reduction in incidence through
seen in Manx cats as a sequela of heritable
selective breeding indicates a potential
spi.J1a bifida.

genetic predisposition as well.

Atresia ani results when the dorsal

LIVER
membrane separating the rectun1 and anus
fails to rnpture. Cllilical signs are apparent

Portosystemic shunts (PSSs) are the
at birth and include tenesmus, abdominal
most common congenital liver anomaly
pain and distention, retention of feces, and

(seep 446). PSSs typically involve single

170

CONGENITAL AND INHERITED ANOMALIES OF THE DIGESTIVE SYSTEM
extra-hepatic or intrahepatic vessels,

PSSs. Dogs that progress to clinical
with extrahepatic shunts more common
disease are treated medically as described
in toy breeds (Yorkshire Terriers, Cairn
for PSSs. Because there is no macroscopic

Terriers, Havanese, Maltese, Pugs, and
shunting vessel, surgery is not a therapeu

Miniature Schnauzers), and intrahepatic
tic option.

shunts more common in large breeds

Copper-associated hepatopathy

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(Irish Wolfhounds, Labrador and Golden
results either from a metabolic derange

Retrievers, Australian Cattle Dogs, and
ment of hepatic copper storage or

Old English Sheepdogs). They have also
secondary to hepatobiliary disease (mostly
been reported in Himalayan and Persian
cholestatic disease). In Bedlington Terriers
cats. Commonly, extrahepatic shunts
it has been identified as an autosomal
occur between the portal vein or its
recessive disorder, whereas in other breeds
branches, and the caudal vena cava or
that have been identified as susceptible
azygous vein, whereas intrahepatic

(Dalmatians, Skye Terriers, West Highland
shunts may be due to failure of closure

White Terriers, and Dobennan Pinschers)

of the ductus venosus or connections
no genetic basis has been identified.

between the portal vein branches and

Primary copper toxicosis is very rare in
hepatic veins. Clinical signs generally
cats. Affected animals may be asymptomanifest as neurologic disturbances matic or show acute signs of hepatobiliary

(hepatic encephalopathy) and are usually
disease, including vomiting, anorexia,
seen in young animals. Cats may show
depression, hemolytic anemia, and icterus.

ptyalism. In the later stages, GI signs

Older, chronically affected animals may

(including vomiting, anorexia, and
show progressive end-stage liver disease.

diarrhea) as well as ascites may develop

Treatment is based on dietary reduction of
secondary to portal hypertension. Other
copper and either treatment with zinc salts
concurrent clinical findings may include
to prevent GI absorption of copper in
renomegaly and urate urolithiasis.

asymptomatic animals, or copper chelators

Laboratory tests may show increased
to reduce copper in animals with clinical
liver enzymes and erythrocytic microsigns. Because copper chelators are not cytosis. Abdominal ultrasonography
without adverse effects, treatment should
is reported to be 100% sensitive for
be closely monitored.

intrahepatic PSSs (although some

Congenital hepatic cysts or congeniwhat less for extrahepatic PSSs), but tal hepatic fibrosis is seen in both
sensitivity depends on the skill of the

Persian and Persian-cross cats as an
ultrasonographer. Definitive diagnosis
autosomal dominant trait and in the Swiss
via positive-contrast portography can

Freiberger horse (also called the Franchesidentify shunt location and whether the Montagnes horse) as an autosomal
shunt is single or multiple. This procerecessive trait that can be traced back to dure also allows assessment of feasibility
one stallion. Both are features of a larger,
for surgical correction. Multiple shunts
polycystic organ syndrome that affects the
have a poor prognosis, because they
kidneys, liver, and/or pancreas. Clinical
are often secondary to an underlying,
signs in cats may not be apparent or
progressive hepatic parenchymal disease
manifest as chronic renal insufficiency.

( eg, cirrhosis).

In horses, affected foals present in the

Hepatoportal microvascular
first year of life witl1 weight loss, jaundice,
dysplasia is an intrahepatic circulatory
hepatic encephalopathy, abdominal
disorder that results in the shunting of
distention, fever, and colic signs. A repo1t
portal blood to the systemic circulation
of dogs with congenital hepatic fibrosis
yet no discernible large vessel shunt is
described ascites, vomiting, seizures, and
identified. The disorder has been classified
portal hypertension but did not draw
as a vaiiation of primary hypoplasia of the
inferences on heritability.

portal vein, which results in noncirrhotic

Primary or idiopathic hyperlipidemias
portal hypertension. The syndrome is well
of dogs and cats have been reported.

defined in Cairn Terriers and Yorkshire Te1°

Miniature Schnauzers have a high prevariers, although it has also been reported in lence of hypertriglyceridemia, up to 33%

Maltese, Dachshw1ds, Toy and Miniature
of animals in one study, with or witl10ut

Poodles, Bichon Frise, Pekingese, Shih
concurrent hypercholesterolemia and

Tzus, Norfolk and Norwich Terriers,
chylomicronemia. There was an effect

Tibetan Spaniels, Havanese, and Lhasa
of age, with higher prevalence in older

Apsos. Animals may be asymptomatic or
animals, and a genetic basis is suspected.

show clinical signs similar to those of

Hypercholesterolemia has been reported

DENTAL DEVELOPMENT

171
in Briards, Rough Collies, Shetland
treatment is aimed at the inciting disease

Sheepdogs, Dobennan Pinschers, and
as well as dietary modifications.

Rottweilers. Also in dogs, a syndrome of

In cats, familial hyperlipidemia due to
idiopathic hyperchylomicronemia has
hyperchylomicronemia has been identified
been reported, with hypertriglyceridemia
as due to an autosomal recessive defect
and nonnal semm cholesterol. Clinical
in lipoprotein lipase. Secondary to this

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signs may be absent or may include
disorder, cutaneous and systemic xanthom a vomiting, diarrhea, pancreatitis, lipemia tosis have been described, with deposition
retinalis, seizures, peripheral neuropathies,
oflipid-laden macrophages in the dermis,
and abdominal pain. Hyperlipidemias also
usually around the head and ears. Peripheral
occur secondary to other diseases,
neuropathy may develop secondary to nerve
including hypothyroidism, diabetes
compression by the xanthomas, paiticularly
mellitus, and hyperadrenocorticism, and
on the limbs and paws.

DENTAL DEVELOPMENT

All domestic animals have a diphyodont

Horses: The most appropriate teeth to
dentition, ie, a deciduous and a permaestimate age in horses are tl1e (lower) nent set of teeth. The morphology as well
incisors. It must be emphasized, however,
as the dental fonnula (see TABLE 3) of that dental appearances are subject to
mammalian teeth, however, are variable
individual and breed variations and to
and closely related to the animal's
differences in environmental conditions.

alimentation.

The deciduous incisors are smaller than the

Identification of teeth was fonnerly
pe1manent ones, and the surfaces of their
based on an anatomic system in which
crowns are whiter and have several small
incisors were designated as I, canines as C, longitudinal ridges and grooves. Emption premolars as P, and molars as M. Veteritimes are listed in TABLE 4. Pennanent incisors nary dentists now most often use the
are larger and more rectangular in shape.

modified Triadan system, which assigns

Their crown surfaces are largely covered
a 3-digit number to a specific tooth.

with cement and have a yellowish appear

The animal's head is divided into four
ance. The upper incisors have two distinct
quadrants, with the upper right quadrant
longitudinal grooves on their labial surface,
labeled " l " and the remaining quadrants while the lower incisors have only one.

numbered in a counterclockwise

Equine incisor teeth develop certain
direction. Numbers 1-4 are used to
wear-related macroscopic features
identify the quadrant for pennanent teeth,
traditionally used to estimate age. The
and 5-8 are used for the temporary
dental star consists of yellowish brown
dentition. The second and third digits idensecondai,r dentin tl1at fills up the pulp cavity tify the specific tooth number; eg, in
and appears at the occlusal surface as the
horses, the left lower second premolar
tooth wears. Its shape and position, as well
is tooth "306" and the last molar on the
as the appearance of the "white spot" in its right mandible is "411."

center, are related to age. The shape, size,
and time of disappearance of both the
infundibula or "cups" (funnel-like infoldings ESTIMATION OF AGE BY
in the occlusaJ surface) and the "marks"

EXAMINATION OF THE TEETH

( enan1el infundibular bottoms) are
additional but more variable indicators

In horses, which have a hypsodont
of age. Progressive dental wear causes an
dentition, age can be estimated by the
alteration of the occlusal shape of the
eruption tin1es and general appearance of
incisors. The occlusal surfaces of recently
the (lower incisor) teeth. In other species
empted incisors are elliptical, but with age
with brachydont incisors, such as cattle and
they subsequently become trapezoid, round,
dogs, age detennination is less accurate and
and then triangular, with the apex toward
is mostly based on dental eruption times.

the lingual side. The curvature of the dental

172

DENTAL DEVELOPMENT
ltM•il DENTAL FORMULAS

Deciduous

Permanent

3 0 3

Horse

(

2 Di

)

-Dc-Dp- = 24

2(If ct Pf Mf) = 36(-44)"b

3 0 3

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Cow<'

0 0 3

Sheep

(

2

)

Di-Dc-Dp- = 20

3 I 3

2(1� C� Pf Mf) = 32

Goat

3 I 3

Pig

(

2

)

Di-Dc-Dp- = 28

3 I 3

3 I 3

Dog

(

2

)

Di-Dc-Dp- = 28

2(1� ct Pi M�) = 42

3 I 3

3 I 3

Cat

(

2

)

Di-Dc-Dp- = 26

3 I 2
a The canine teeth are usually regressed or absent in mares.

b Small premolars 1 (wolf teeth) are often present, especially in the upper jaw.

c The canine tooth of domestic ruminants has commonly been counted as a fourth incisor.

arch fom1ed by the lower incisive tables is
also age related. In young horses this arch
is semicircular, whereas in older horses it
forms a. straight line. Additionally, the arch
fom1ed by the incisors of the opposingjaws

(as they meet) changes as the teeth advance
from their alveoli and undergo attrition. In
young horses, the upper and lower incisors
a.re positioned in a straight line. With
increasing age, the angle between upper and
lower incisors becomes more acute. The

Galvayne's groove and the "7-yea.r hook,"

which have traditionally been used as age
indicators, a.re va.rjable, inconsistent, and
thus of little value for age determination in
horses. The more useful signs are arranged
chronologically in the following list:

Birth to 5 yr: See TABLE 4.

5 yr: The comers a.re erupting. Dental
star in the central incisors.

6 yr: Dental star in the middle incisors.

Cups gone from the central incisors.

7 yr: Dental star in the comers.

8 yr: The central incisors a.re trapezoidal
and have a white spot in the dental star.

9 yr: The middle incisors a.re trapezoidal
and have a white spot in the dental star.

10 yr: Cups gone from the middle
incisors. Marks on the central incisors a.re

Top: occlusal view on lower incisors of a

6-yr-old mare. Dental stars are visible on 11 and
oval-triangular.

12 (arrows); cups are present as large elliptical

11 yr: White spot in the dental star on
info/dings (arrowheads). Occlusal surfaces of
the comers. Both the central and middle
the incisors are oval, and curvature of the
incisors have a lingual apex. The comers
dental arch is semicircular. Bottom: occlusal
a.re triangular with a labial apex.

view on the lower incisors of a 12-yr-old mare.

12 yr: Cups gone from all lower incisors.

In the center of the dental stars, a white spot is

14 yr: Marks on the central and middle
clearly visible (arrows). Cups have become
incisors are small and round.

smaller and more shallow. Occlusal surfaces
are more triangular. Courtesy of Dr. Sofie Muylle.

DENTAL DEVELOPMENT

173
ltlllll ERUPTION OF THE TEETH• Sheep

Horse

Cow
and Goat Pig

Dog

Cat

Dil

0-1 wk

Before birth 0-1 wk

3--4 wk

4-5wk

2-3wk

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Di2

4-6wk

Before bilth l-2wk

2-3mo

4-5wk

3--4wk

Di3

6---9mo

0-1 wk

2-3wk

Before

3--4 wk

3--4 wk
bilth

I 1

2Y2yr

2yr
l-1Y2yr

12-15mo 4mo

4-7mo

12

3Y2yr

2Y2yr
rn-2yr

16---20mo 4V2mo

4-7mo

13

4Y2yr

3Y2yr

2-2Y2yr'

8-lOmo

5mo

4-7mo

De

Does not

0-2wk

3--4 wk

Before

3--4 wk

3--4wk
erupt
birth
c

4-5yr

3\."2--4 yr

2\."2--4 yr"

6---lOmo

5-6mo

4-7mo

Dp2

0-2wk

0-3wk

0--4 wk

4-6wk

4-6wk

5-6wk

( upper only)

Dp3

0-2wk

0-3wk

0--4wk

1Y2mo

4-6wk

5-6wk

Dp4

0-2wk

0 -3wk

0--4 wk
l-5wk

4-6wk

5-6wk

Pl

5-6mo

5mo

4-5mo

(wolf tooth)

P2

2V2yr

2 -2Y2yr
l \&-2 yr

12-15 mo

5-6mo

4-7mo

(upper only)

P3

3yr

2-2Y2yr
l\&-2 yr

12-15mo

5-6mo 4-7mo

P4

4yr

2\&-3 yr
l\/2-2 yr

12-15mo 5-6mo 4-7mo

Ml

9-12 mo

5-6mo

3-6mod

4-6mo

4-5mo

4-7mo

M2

2yr
l-1Y2yr

9-12mo

8-12mo

5-6mo

M3

4yr

2-2\12yr
l\&-2 yr

18-20mo

6---7 mo
a Average data, subject to considerable variation
b 2 yr in goats
c 2V2-3 yr in goats
ct 3-4 mo in sheep

18 yr: Marks disappear from the central

6-7 yr: Central incisors a.re leveled and
incisors.

neck is visible.

20 yr: Marks are gone from the middle

8 yr: Middle incisors are leveled and neck
incisors and the comers.

is visible.

9-10 yr: Comers are leveled and neck is
visible.

Cattle: Emption times of incisors are the

As cattle continue to age, the teeth wear
most reliable feature for age determination
shorter and more neck becomes visible;
in cattle (see TABLE 4). Although breedthey loosen in the sockets and eventually related, eruption dates are more reliable for
drop out.

estilnation of age than signs of wear,
because macroscopic age-related dental
features are scarce ( dental stars) or absent

Dogs: The following data were found

( cups and marks) and because rate of wear
reliable in -90"Ai of large dogs. There is
is largely influenced by nutrition.

more variation in small dogs ( especially

Birth to 5 yr: See TABLE 4.

toy breeds) and in dogs with undershot

5 yr: All incisors in wear. Occlusal surface or overshot jaws. Even, or level, bites of the central incisors beginning to level.

usually result in excessive wear.

174

DENTAL DEVELOPMENT

/"' '

',
incisors 1 '

6-year-old

�"' ·r·:1 ::::::--,.,._ molars

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. / pren:i
canine
vestibular infundibulum
tooth
aspect ,.L \

10-year-old

�
profile

\
l-
r rieck ;� \_ Deciduous incisor

�
infundibulwn
peripheral /

. ..:::._.

enamel-

/ ,,____ Ga.lvayne's
dentin--- �central

·
groove
enamel
canine tooth
secondary/
dentin

7-8-9 and

11-year-olcl
pulp/

-

�
cavity

/ '•".;

�·
hook
incisors
j

Lower

Lower
molars
premolars

Dentition of the horse. Illustration by Dr. Gheorghe Constantinescu.

_/

-r"'

.J

11: r2�t

7
sectorial (

-=
carnassia.l) -

• �1{ �
tooth
t '::

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mo•=

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., 1

-�

I

\,

\

,�rn,•=<\

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r1

.

# lower
first
camne ---- -�

J

-
l \ �,�. sectoria.l
molar
tooth

·J, ·�
v'v tooth
incisors

Dentition of the dog. Illustration by Dr. Gheorghe Constantinescu.

DENTISTRY

175

1 Yi yr: Cusps worn off lower central

6 yr: Cusps worn off lower comers.

incisors.

Canines worn blunt. Lower canine shows

1 Yi-2 Yi yr: Cusps worn off lower middle
impression of upper comer.

incisors.

7 yr: Occlusal smface of lower central

31h yr: Cusps worn off upper central
incisor becomes elliptical with the long axis
incisors.

sagittal.

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4Yi yr: Cusps worn off upper middle

8 yr: Occlusal surface of lower central
incisors.

incisor is inclined forward.

5 yr: Cusps of lower comers slightly

10 yr: Lower middle and upper central
worn. Occlusal surface of lower central and
incisors have elliptical occlusal surfaces.

middle incisors is rectangular. Slight wear
of canines.

DENTISTRY

LARGE ANIMALS

Of the common domestic large animals,
horses generally require the most dental care.

Most large animals are herbivores, and

In the swine industry, removal or amputation
efficient dental function is the key to food
of deciduous canine teeth in piglets and tusk
intake and to the maintenance of normal
amputation in breeding boars may be part of
body condition. The variations in anatomic
routine management. In New World camelids
structure, dental formula, and emption

(llamas, etc), blunting the fighting teeth (ie,
schedule for deciduous and pennanent
the upper single incisor and canine and the
teeth is fundan1ental veterinary knowledge
lower canine teeth) is done to reduce the
and should be reviewed before perfom1ing
danger and consequences of fighting. (See
dentistry on any species (see TABLE 3).

also LLAMAS AND ALPACAS, p 1844, for additional The deciduous and permanent dental
information on dental care.) Exotic species
formula of cows, sheep, and goats are
may also have various dental conditions, eg,
similar. All rmninants lack upper incisor
in1pacted tusks in young elephants or
teeth, with the mandibular brachydont
maxillary dental periostitis and actinomyco

(short-crowned) incisors meeting with a
sis in wallabies and kangaroos.

maxillary comified dental pad. In many
herbivore species, the forces of almost
continuous grazing or rnn1ination leads

Signs of Dental Disease
to dental attrition. Dental crown wear

Dental disease (eg, broken teeth, periodonhas been matched by the development of tal disease, irregular dental arcade wear) is hypsodont (long-crowned) teeth with the
a common underlying cause of unthrifticontinuous emption of the reserve crown.

ness, loss of condition, or poor breeding or

The dental arcades in the horse consist of
nursing perfonnance. The classic signs of
at least nine teeth (three incisors separated
dental disease in horses include difficulty
by a diastema [ the interdental space], three
or slowness in feeding and a reluctance
premolars, and three molars) in each
to drink cold water. During the chewing
quadrant of the mouth. These hypsodont
process, the horse may stop for a few
teeth have regular serrations that expose
moments and then start again. Sometimes,
sharp enan1el edges for shredding and
the head is held to one side as if the horse
cmshing cellulose material. At the same
were in pain. Occasionally, the horse may
tin1e, the brittle nature of the enan1el of the
quid, ie, it may pick up its food, fom1 it
tooth is protected by the surrounding dentin into a bolus but drop the bolus from the and peripheral cementun1. In the nom1al
mouth after it has been partially chewed.

course of masticating forage, the rate of

Occasionally, the semi-chewed mass of
tooth emption is matched by the rate of
feed may become packed between the
occlusal crown wear. Adult male horses
teeth and the cheek or become lodged in
have large pem1anent canine teeth situated
the esophagus, leading to choke. To avoid
in the interdental space. These are absent or
using a painful tooth or a sore mouth, tl1e
very small in mares (sexual din1orphism).

horse may bolt its food and subsequently

176

DENTISTRY
suffer indigestion, choke, or colic. There
grain may require twice yearly oral
may be a lack of desire to eat hard grain
exanuna.tions and dental prophylaxis.

accompanied by uncrushed grain in the

The objective of dental prophylaxis is to
feces. Other signs of dental disease in
remove sharp enamel edges of cheek teetl1
horses include excessive salivation and
that might be ca.using soft-tissue irritation
blood-tinged mucus in the mouth,
and any occlusal surface elongations. This

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accompanied by the fetid breath of
odontoplasty procedure is often referred to
dental decay. Extensive dental decay
as "floating" the teeth. By maintaining the and accompanying periostitis and root
normal occlusal surface, development of
abscessation may lead to empyema of
irregulruities of wear on the dental arcades is
the paranasal sinuses and intermittent
inhibited. Dental prophylaxis can usually be
unilateral nasal discharge. There may
done with simple restraint a.11d/or the use of
be facial or mandibular swelling and
sedatives and a.11algesics. Power equipment
development of mandibular fistulas from
is now being used more frequently tl1an
apical infections of the lower cheek teeth.

handheld rasps to grind, balance, a.t1d realign

Horses may be reluctant to take the bit,
the occlusal surfaces oftl1e incisors and
shake their head when being ridden, or
cheek teeth. Motorized dental instruments
resist training techniques because of
should be used carefully to a.void thermal
irregularly worn cheek teeth and sharp
and pressure trauma to dentin and pulp.

edges on the maxillary cheek teeth and

This means using low-speed grinders
accompanying buccal mucosa laceration.

(6,000--12,000 rpm) with short contact times,

The presence of small upper first premolar
light pressure, and intennittent water

"wolf' teeth in horses may or may not be
irrigation, while removing no more than
associated with resistance to the bit.

3-5 nun of occlusal swface every 3-6 mo.

Sharp edges on wolf teeth have been

Dental Examination
incriminated as a cause of bit resistance

In most cases, history, age, and clinical
in horses. These small teeth, located just
signs are correlated. A thorough physical
rostral to the upper cheek tooth row, ru·e
examination should always be pe1fonned,
often extracted in performance horses. This
followed by a detailed and thorough oral and
procedure can be done in the standing,
dental examination. In most large animals,
sedated horse with the aid of local infutra.including horses, this may involve the use of tion anesthesia.. The gingival attachment to
sedation; certain anin1als may require general the tooth is elevated, and a dental luxator or anesthesia A thorough oral exan1ination is
elevator is used to loosen the tooth. A small
facilitated by 1insing the mouth with warm
extraction forceps can grasp the crown and
water and illuminating the oral cavity witj:l
pull the tooth from its socket. Minimal
a b1ight headlamp while using an oral
aftercare or diet and work restriction are
speculum. Most mouth speculurns designed
required for socket healing.

for horses or ponies can be modified by

Most dental procedures can be perreplacing the upper incisor plate with a flat formed on the standing, sedated horse with
padded gum plate for use in ruminants. A
or without regional anesthesia, but some
dental mirror or endoscopic camera greatly
major dental procedures ( eg, repulsions
increases tl1e quality of oral examination.

and fracture repairs) usually require

The oral dental examination is often aided
general anesthesia.. Radiographic evaluaby radiography or other advanced inlaging tion and protection of the airway from
such as CT, scintigraphy, or MRI.

debris ru·e necessary in most cases. Some
decayed teeth can be extracted per os using

Routine Dental Prophylaxis and
molar separators, extraction forceps, and
elevators. However, in some cases, surgical

Extractions
exposure and tooth repulsion or sectioning

Routine dental prophylaxis consisting of
and elevation is preferred. Tooth preservaa complete oral dental examination and tion by root end resection and endodontic
odontoplasty of sharp enamel points is
therapy has demonstrated that extraction is
important in the health ca.re of horses.

not required in all cases of dental decay in

Enamel edges should be removed twice
horses.

yearly during the establishment of the
pem1anent dentition and thereafter as

CONGENITAL AND
frequently as needed, depending on the

DEVELOPMENTAL ANOMALIES
management of the horse. Horses that graze
on free range or grass usually require a

In horses, the most commonly diagnosed
yearly dental prophylaxis; horses that are
oral congenital defonnity is pa.tTot mouth
stall confined and essentially fed hay and

( class 2 malocclusion), in which the maxilla

DENTISTRY

177
is relatively longer than the mandible. In

IRREGULAR WEAR OF THE
early embryonic development, the first

DENTITION
branchial arch extends as a solid hyaline
cartilaginous rod surrounded by a fibrocel

Except for pigs, most large animals have
lular capsule from the temporal region to the an intermandibular space that is narrower midline of the fused mandibular processes.

than the intermaxillary space; ie, they are

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If the first branchial arch fails to close
anisognathic. In horses, this, together with
properly in the equine fetus, tooth germ can
limited natural movement of the mandible,
displace and result in the formation of a
results in the development of enamel points
dentigerous cyst in the temporal region and
on the buccal edges of the upper arcades
a draining tract from the rostral pinna of
and on the lingual edges of the lower
the ear. In equids and cattle, many anomalies arcades. In cattle and sheep, because the of dental development may result from
temporomandibular joint affords greater
exposure to teratogenic toxins. However,
lateral movement of the mandible, such
underlying genetic factors should always be
irregularities do not develop as frequently.

considered.

Extreme fonns of disease, however, are

Dental irregularities accompany systemic
seen in all species and may be influenced
fluorosis in both cattle and sheep. In the
by other skeletal defonnities of the face or
milder f01ms of fluorosis, only the dentition
accompanying infections ( eg, Actinomyces
may be involved. In extreme fluorosis ( eg,
sp ). Gross shear mouth may result, with

40 ppm in the diet for several years), other
exaggerated obliquity of the molar tables. It
skeletal abnormalities may be seen
may be seen in older horses, and treatment

(phalanx fracture). (See also FLUORIDE
is usually unsatisfactory. Dental care should

POISONING, p 3075.)

be supplemented by special diets.

Supernumerary teeth (polyodontia) are

Enamel points are best treated by regular
seen occasionally. In both horses and cattle,
dental equilibration in horses (ie, floating).

double rows of incisor teeth or extra cheek

This should be done twice annually while
teeth may be seen. Missing teeth ( oligodonthe pem1anent dentition is developing; at tia) in a dental arcade is less common and
the san1e time, retained caps should be
can be developmental or secondary to
removed if they cause oral ulceration or
traun1a or previous tooth removal.

discomfort.

Treatment is detem1ined on a case-by-case

Wave mouth, step mouth, and rostral and
basis and may require extraction or frequent caudal hooks are dental overgrowths caused crown reduction of the unopposed teeth.

by uneven wear of the teetl1 and are the result

See also CONGENITAL AND INHERITED ANOMALIES of local pain, dent.al or jaw malalignment, or OF THE TEETH, p 164.

missing or dan1aged teeth. In time, this can
lead to abnom1al spaces fom1ing between
the teeth ( diastema), which have been shown

ABNORMAL TOOTH ERUPTION
to cause feed entrapment and secondary
gun1 and socket disease (ie, periodontitis).

Shedding deciduous teeth can be a source

Such conditions are best prevented by
of oral irritation in horses that are 2-5 yr
regular, routine dental prophylaxis. Once
old. Deciduous tooth caps can become
dent.al wear abnormalities are severe, results
loosened, displaced, or fractured, leading
of dent.al procedures are usually incomplete.

to problems with mastication and biting.

Although occlusal surfaces may be realigned,

Abnom1al eruption of permanent teeth is
dent.al care needs to be supplemented by
commonly a sequela of mandibular or
special dietary regimens.

maxillary trauma, eg, incisor avulsion
fractures in cattle and horses in which the

PERIODONTAL DISEASE
developing dental bud of the permanent
tooth is dan1aged by the fracture itself or

In all animals, a degree of inflanunatory
by the repair process. In horses, delayed
change occurs during the eruption of both
eruption or impaction of cheek teeth is a
the deciduous and permanent teetl1.

conunon cause of periapical infection.

However, if malocclusion occurs, severe

This particularly affects the second and
periodontal disease is inevitable. In horses,
third cheek tooth (premolar 3 [Triadan
this is a common sequela of diastema

07s J and premolar 4 [Triadan OSs]) in both
formation, oral traun1a, dental fractures,
the upper and lower arcades and is a
and impactions, and it is usually accompasequela of dental overcrowding. Medial nied by irregular wear.

displacement of the third cheek tooth is

In sheep, periodont.al disease of tl1e
another form of abnormal eruption due to
mandibular rostral teeth (incisors) is often
overcrowding.

referred to as broken mouth. Sometimes,

178

DENTISTRY
the viability of grazing sheep is affected
in horses can be corrected by grinding and
dramatically. The productive life of many
realigning the arcades every 6-12 mo.

frum-fed sheep is often 2 yr longer than that

Because of such complications, surgical
of range-fed animals. Little can be done to
techniques that preserve the teeth should be
alter the progress of this disease, although
considered, at least for horses. The age of
dental prophylaxis and restoration of
the animal and the specifics of local disease

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occlusal regularity of the incisor teeth has
should be considered before contemplating
been recommended. This can be done by use
root-end resection and endodontic therapy
of a dental grinder or a fine-bladed tooth float. in large animals.

DENTAL CARIES

SMALL ANIMALS

Infection may be introduced into the pulp
chamber of the teeth by various routes, eg,

PERIODONTAL DISEASE
hematogenous (a.nachoretic pulpitis),
periodontal, or from direct crown insult. In

Periodontal disease is infection and
horses, hypoplasia of the cementum in the
inflammation of the periodontium (the
enamel lakes (i.nfundibulae) of the upper
tissues that surround and suppo1t the
cheek teeth may predispose to infundibuteeth) due to plaque bacteria and the host's lar caries and subsequent pulpitis and
response to the bacterial insult. Gingivitis
apical osteitis. Depending on the site of the is common in dogs and cats and refers to infected tooth, there may be accompanying inflammation of the gingiva in response signs of maxillary sinusitis, local cellulitis,
to plaque antigen. Periodontitis is a more
periostitis, alveolar periodontitis, and
severe disease that involves inflammation
fistula formation. The pathologic features
of the periodontal ligament and alveolar
of dental decay are nonspecific. Consebone, eventually ca.using loss of attachquently, the cause of the apical infection ment (periodontal pocketing, gingival
in a draining mandibular dental fistula in
recession, bone resorption). Periodontitis
a horse or llama may be obscure. Many
is much more common in certain dog and
animals are not examined until the
cat breeds, but it can affect any individual.

infection is advanced, and tooth fractures
may well be secondary rather than primary.

Etiology and Pathogenesis: The oral

It has been suggested that, in some species
cavity supports a rich bacterial microflora.,

( eg, the horse), the initiating feature of
much of which thrives in plaque on tooth
the establishment of apical osteitis and
swfaces. Bacte,ial plaque on the crown
pulpitis is abnormal eruption and dental
surface of a tooth constantly presents antigen
impaction. The cause of apical osteitis in
to tl1e marginal gingiva., stin1ulating an
cattle and New World can1elids may be
inflammatory response and resulting in
similarly influenced.

gingivitis. The bacte1ia in plaque are predomi

When dental decay is advanced, extraction nantly nonmotile, gram-positive aerobes, of the affected tooth is recommended. In
including Staphywcoccus spp and Strepto
horses, this usually has been achieved by
coccus spp, but many others are also present.

surgical exposure offhe decayed tooth and

Although this microbiota does stimulate an
then repulsion into the mouth. Recent
in1mune response, tl1e bacteria in an
experience has shown that oral extraction
otl1erwise healthy mouth exist in relative
is possible, with careful technique, sedation,
corru11ensal hrumony witl1 the host. They may
and nerve blocks, tlrns avoiding serious
even be beneficial by helping to limit the
complications associated with repulsion
numbers of periodontopa.thogenic bacteria
and the use of general anesthesia After
lf the plaque becomes very tluck because of
exodontia., the socket should be cleaned
poor oral hygiene and oxygen within the
carefully to remove all fragments of diseased
plaque is depleted, the bacterial population
bone and tooth. Dental acrylics, dental
can become more pathogenic, with a higher
waxes, and wound packs should be used to
percentage of nonmotile, gram-negative
ensure that the socket can heal properly by
anaerobic rods. The bacteria. foill1d in the
protecting it from food material. After dental
presence of teetl1 with periodontal disease
extractions, the adjacent teeth gradually
include Bacleroides fragilis, Peplostreplo
move to close the gap in the dental arcade.

cocc1.ts, Porphyromonas g1.tlae, Porphy

However, this process is never complete,
romonas salivosa, Porphyromonas
and the occluding arcade will fom1 a step
denticanis, Prevolella inlennedia,
elongation opposite the missing teeth and

11·eponema spp, Bacteroides splanchnicus, hooks at the ends of the opposing arcades
and many others. Interestingly, some of the

(both rostral and caudal). Such irregularities
common hwnan periodontopa.thogens such

DENTISTRY

179
as Haemophilus (formerly Actinobacillus) extends under the crown of a multirooted
actinomycetemcomiw:ns are notably absent
tooth, through and through from one side
in animals. Subgi.ngival plaque (plaque on the
of the furcation out the other.

tooth surface below the gingival margin) is

A stage O mobility up to 0.2 mm is
also conunonly inhabited by these more
physiologic. A stage 1 mobility is present
pe1iodontopathogenic species of bacteria
when tooth mobility is increased in any

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Periodontitis is caused by the host's response direction other than axial over a di.stance of to subgingival plaque. Inflammatory

>0.2 mm and up to 0.5 mm. A stage 2 mobility
mediators produced by the host directly
is present when tooth mobility is increased
result in bone and tissue damage around the
in any direction other than axial over a
root. The bacteria themselves and their
distance of >0.5 mm and up to l l1Ul1. A stage
metabolic products also contribute to the

3 mobility is present when tooth mobility is
bone damage. Development of periodontitis
increased in any direction other than axial
is also affected by other intrinsic ( eg,
over a distance > 1 nm1 or any axial
genetics, tooth crowding, thin alveolar bone,
movement.

age) and extrinsic ( eg, diet, stress, concurrent disease, oral hygiene) factors.

Treatment: Removal of the bacterial

Clinical Findings and Lesions: Pe1ioplaque on the tooth surfaces is of utmost dontal disease is classified in stages. In
importance. This can reverse gingivitis,
teeth with healthy periodontal tissues,
retwni..ng the gingiva to a healthy, uninflan1ed
no gingivitis or periodontitis is evident.

state. This is achieved through professional

Stage 1: There is gingivitis only, without
dental cleaning (scaling and polishing) with
attachment loss; the height and architecture power and hand instruments under general of the alveolar margin are nonnal.

anesthesia Dental cleaning on an awake

Stage 2: There is early periodontitis with
animal in1proves the cosmetic appearance

<25% of attachment loss or, at most, there is
of tl1e tooth crowns but does not improve
a stage 1 furcation involvement in multiperiodontal health. The owner might falsely rooted teeth (see below). There are early
believe the condition has been treated, while
radiographic signs of periodontitis. The loss
periodontal disease continues to tllrive. lf
of periodontal attachment is <25% as
the gingivitis does not resolve, further examimeasured by probing of the clinical nation should be performed to identify
attachment level or by radiographic
additional complicating conditions such as
detenni..nation of the distance of the alveolar persistent subgingival plaque and calculus or margin from the cementoenameljunction
the presence of predisposing factor( s ). Some
relative to the length of the root.

less common causes of gingivitis, including

Stage 3: There is moderate periodontitis,
systemic disease ( eg, uremic stomatitis ),
with 25o/�A, of attachment loss as measured autoi..nunune disease,juvenile gingivitis, etc, by probing of the clinical attachment level or
may require more than only plaque removal.

by radiographic detenni..nation of the di.stance

Periodontitis requires more aggressive
of the alveolar margin from the cementoperiodontal treatment. Root scaling enan1eljunction relative to the length of the

(removing plaque and calculus on exposed
root, or there is a stage 2 furcation involveroot surfaces) and planing (smoothing the ment in multirooted teeth ( see below).

root surfaces by removing textural

Stage 4: There is advanced periodontitis,
irregularities and diseased cementuni) are
with >50% of attachment loss as measured by performed, followed by gingival curettage probing of the clinical attachment level or by
that removes the infected and inflamed inside
radiographic detenni..nation of the distance
layer of a periodontal pocket. Shallow
of the alveolar margin from the cementoperiodontal pockets are treated in a closed enameljunction relative to the length of the
fashion, but pockets >6 l1Ul1 deep require
root, or there is a stage 3 furcation involveopen surgery ( creation of a periodontal flap) ment in multirooted teeth ( see below).

to expose the root surface and alveolar bone

A stage 1 furcation involvement exists
for adequate treatment (root scaling,'planing
when a periodontal probe extends less than
and alveoloplasty). The connective tissue
halfway under the crown in any direction of
side of the flap needs to be debrided before
a multirooted tooth with attachment loss. A
wound closure to avoid contact of infected
stage 2 furcation involvement exists when
and inflamed granulation tissue with the
a periodontal probe extends greater than
planed root sU!faces. Local placement of a
halfway under the crown of a multirooted
gel contai..ni..ng antibiotics ( eg, doxycycline)

tootl1 with attachment loss but not through
into cleaned periodontal pockets may be
and through. A stage 3 furcation involvehelpful. Extraction is often the best treatment ment exists when a periodontal probe
for teeth with increased mobility that have a

180

DENTISTRY
guarded to poor prognosis. Periodontitis is
include ingredients that help decrease oral
not as readily reversible as gingivitis. Lost
bacteria or slow plaque mineralization.

bone may be augmented by use of bone grafts

Products that slow or prevent tl1e
or bone graft substitutes. Barrier membranes
attachment of pellicle or the adhesion of
should be placed between the bone defect
pioneering plaque bacteria may provide
and gingival tissues to achieve guided tissue
some benefit The Veterinary Oral Health

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regeneration. Maxillary canine teeth with

Council website (www.vohc.org) provides
pockets on their palatal side that have
further infonnation about products that
already progressed to fom1 an oronasal
meet certain requirements for plaque
fistula require extraction and oronasal fistula
and/or calculus control.

repair. Deep infrabony defects in multirooted

Prevention of periodontitis is more
teeth with bone loss that undermines a
complicated. Regular oral hygiene to remove
furcation can infect the pulp through a
supragingival plaque provides some
furcation canal, resulting in secondary
protection to help prevent development of
endodontic disease. Similarly, ifperiodontitis
subgingival plaque a.t1d to minimize the
has progressed apically and reached the apex
number of periodontopathogens in the
of the root of a tooth, seconda.ty endodontic
mouth. More in1porta.t1tly, predisposing
disease will develop. Saving such teeth also
factors should be identified a.t1d removed.

requires endodontic therapy ( see below), and Severe crowding Ca.t1 be relieved through the prognosis is detemlined by the extent of
selective extractions, predisposing a.t1atomy
periodontal disease.

ca.t1 be modified, diabetes or renal failure Ca.t1

Teeth that have become mobile because
be treated a.t1d controlled, a.t1d inappropriate
of loss of attachment should be extracted.

behaviors or parafunctional habits that

They can sometin1es be saved through
da.tnage the tissues ca.t1 be addressed.

major periodontal surgery procedures, but
disease will recur without drastic changes

ENDODONTIC DISEASE
in home oral hygiene. Extraction allows the
tissues to heal. A pet dog or cat ca.t1 function

Etiology and Pathogenesis: Endodontic
perfectly fine without teeth.

disease occurs when the dental pulp

( odontoblasts, fibroblasts, undifferentiated

Prevention: Prevention of gingivitis is
mesenchymal cells, blood vessels, a.t1d
the same as its treatment: plaque removal
nerves in the center of the tooth) becomes
and control. Plaque is a typical biofilm,
infected a.t1d/or infla.t11ed. The pulp is
composed of many microorga.ttisms that
protected from bacteria by tl1e in1pervious
differ from their planktonic forms. In a
ena.tnel covering the dentin of the crown.

biofilrn, microorga.ttisms are more resistant

Da.tnage to the ena.tnel, either through
to antibiotics, disinfectants, and antibactetrauma or from a developmental abnormalrial agents. However, biofilms are easily a.t1d ity that allows bacteria to reach the pulp,
effectively removed mecha.ttically with a
will result in pulpitis a.t1d possibly pulp
toothbrush. Even large accumulations of
necrosis. Blunt traun1a ca.t1 also il\iure the
supragingival plaque are easily removed by
pulp beyond its ability to heal. A tooth with
toothbrushing. The teeth should be brushed
direct exposure of the pulp at a fracture site
daily to remove plaque a.t1d prevent calculus requires endodontic treatment or extraction.

(tartar) accun1ulation. Some dogs a.t1d cats

Teeth are fractured from external trauma
may not allow regular toothbrushing, so the

( eg, catching rocks, automobile impacts,
plaque should be removed by wiping with
aggressive play) or from biting on inapproa gauze pad at least every second or third priate objects ( eg, real bones regardless of
day. Only the outside Oabial a.t1d buccal)

the state of processing, hooves, a.t1tlers, hard
surfaces of the teetl1 may be approachable
nylon toys, rocks, fences, or cages). An
for brushing in most dogs a.t1d cats. Plaque
infla.tned or dead pulp releases inf!a.t1U11atory
that remains on the tooth surface for >3
mediators into tl1e periradicular tissues
days mineralizes to form calculus that

(through furcation ea.t1als into the periodonca.tmot be removed by brushing. Although tal liga.tnent at the furcation of a multirooted
calculus gives the appeara.t1ce of unhealthy
tooth, through lateral ca.i1als into the
teeth, its contribution to periodontal
periodontal liga.t11ent at the mid-root level,
disease is minor.

a.t1d through apical fora.tllina into the

Texture of the diet, toys, a.t1d treats can
periapical tissues). The tissues surrounding
affect the self-clea.t1sing mecha.ttisms of the
the apex of a tootl1 develop a periapical
teeth. Firm, fibrous items that allow tooth
gra.t1uloma, cyst, or abscess.

penetration ca.t1 wipe plaque from the tooth
surfaces during chewing. In addition to

Clinical Findings and Lesions: A
texture, some diets are fom1ulated to
discolored tooth (pinkish, purple, or gray) is

DENTISTRY

181
evidence of previous trauma and hemor

Treatment: Teeth with iffeversible
rhage from the pulp into the dentinal
pulpitis or pulp necrosis require either
tubules. An inflamed pulp can heal after a
endodontic treatment (root canal therapy)

minor if\iury. However, more severe trauma
or extraction. Except in very young anin1als,
will cause iffeversible pulpitis, eventually
one of these options is indicated for every

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leading to pulp necrosis. Because dental
tooth in which a fracture has exposed the
pulp has no collateral circulation, if\iuries
pulp chamber. Canine teeth in dogs and
heal less readily, and extravasated blood
ca.ts and ca.rnassial teeth ( maxillary fourth
remains in the dentin, where it deteriorates
premolars and mandibular first molars) in
rather than being removed. The most
dogs are considered strategic teeth. Root
obvious indication of endodontic disease is
canal therapy of these teeth is much more
a fractured tooth with exposure of the pulp
comfo1table for the anin1al than extraction;
chan1ber. The exposed pulp bleeds for only
it also allows continued function. Military,
a short time. After the initial irtjury, it may
police, and assistance dogs may require
appear as a red dot at the site of the
fabrication and placement of a full or partial
exposure if the pulp remains vital, or as a prosthodontic crown.

black hole if it becomes necrotic. Either way,
treatment is required. Drainage is most
commonly tJu·ough the fracture site.

TOOTH RESORPTION

However, a periapical abscess can occur if
the site becomes occluded. The skin ventral

(Resorptive lesion, Cervical lesion, Neck
to the medial canthus of the eye is a common lesion, Feline odontoclastic resorption site for swelling and pwulent drainage from
lesion)

a fistula due to an endodontically diseased

Resorption of tooth structure occurs
maxillary fourth premolar. This can also
through the action of odontoclasts--cells
cause an intraoral red draining fistula near
virtually identical to osteoclasts. It can occur
the rnucocutaneous junction adjacent to the
on the external or internal tooth surface
tooth. An abscessed maxillary canine tooth

( external or internal resorption). Odontoin dogs can cause swelling along the side clast activity can be stimulated by inflammaof the nose; in cats, the swelling is often tion, pressure from adjacent stmctures,
in1.mediately rostral to the eye. Veterinary
orthodontic tootl1 movement, as a result of
patients often do not give an indication of
normal processes such as exfolia.tion of
discomfort, even for conditions that cause
deciduous teeth, or in the absence of these
severe orofacial pain in people.

processes (idiopathic). This idiopathic tooth

On a radiograph of a tooth with a
resorption occurs sporadically in many
periapical granuloma or cyst, the typical
species (including people), but it is most
lesion presents as a periapical lucency, ie,
frequently seen in domestic cats.

an irregular circular lesion with decreased
radiopacity around a root tip. A tooth with

Etiology and Pathogenesis: Tootl1
an acute peria.pical abscess (painful
resorption in ca.ts begins witl1 a. loss of the
accumulation of pus around the apex of
nonnal periodontal ligament architecture
a nonvital tooth) may not show distinct
and focal dan1age to the cementum that
radiographic signs. Throughout life, the
covers the root surface. Microscopic areas
pulp produces dentin on the inside surface
of root resorption often repair w1eventfully
of the pulp cavity, resulting in a constantly
in ca.ts. Tooth resorption from any cause
decreasing cross-sectional width of the pulp
occurs tJu·ough the action of odontoclasts
chamber in the crown and root canal in the
tl1at remove tooth structure, creating a
root of the tooth. A necrotic pulp discontinresorptive lacuna. In many but not all ues its norn1al dentin production, and thus
lesions, concomitant osteoblast and
it falls behind that of a normally maturing
cementoblastic activity replaces the lost
tooth adjacent to it or on the contralateral
tooth witl1 bone or cementwn. If repair does
side. Conversely, an inflamed pulp produces
not occur, the resorption progresses into
dentin at an accelerated rate. If there is
dentin and extends coronally into the crown
generalized pulpitis, the effect can be an
of tl1e tootl1 where it undeffi1ines the enamel
apparent accelerated aging of the entire
to cause clinically apparent defects on the
tooth with an a.bnonnally nan-ow root canal
tootl1 surface ( at the "neck" of the tootl1 ).

space and pulp chamber. Generally, when

Inflan1.111a.tion from periodontitis is known to
evaluating a tooth with endodontic and/or
ca.use external resorption and is most likely
peria.pical disease, the focus should be on
responsible for tooth resorption in areas of
structural defects at its crown and root
periodontal disease. However, the etiology
apex, the width of its pulp cavity, and the
of idiopathic tooth resorption affecting
appearance of the peria.pical tissues.

multiple (possibly all) teetl1 in ca.ts has not

182

DENTISTRY
yet been proved. Excessive intake of dietary
the tooth surface. Internal resorption may
vitamin D has been hypothesized as one
sometimes appear as pinkish discoloration
possible cause among many others.

of the crown but usually is only identifiable
radiographically as round to oval-shaped

Clinical Findings and Lesions: The cliniareas of decreased radiopacity.

cal appearance of tooth resorption greatly

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varies. In cats, the mandibular third pre

Treatment and Prevention: Most teeth
molar (the first cheek tooth) is often the first
affected with resorptive lesions should be
tooth affected. In dogs, premolar and molar
extracted. Surgical crown an1putation with
teeth are most commonly involved. Small
intentional retention of already resorbing
lesions on the enamel of the tooth crown
dental tissues can be performed on teeth
usually begin somewhere on the root
that are radiographically confirmed to be
surface but can progress coronally and then
type 2 lesions in the absence of periodontiappear at the gingival margin as inflamed tis, endodontic disease, and stornatitis (see
granulation tissue filling a defect. The
p 361). Oral hygiene prevents inflan1IT1atory
margin of the defect has a sharp ledge of
lesions caused by marginal periodontitis,
enamel. At this stage, tl1e visible part of the
and root canal therapy or extraction of
lesion is small, with most of tl1e defect
endodontically involved teeth prevents
affecting the roots. Tooth resorption is
resorption caused by apical pe1iodontitis.

characterized by severity (stage) and

Idiopathic lesions cannot be prevented,
radiographic appearance (type).

because their etiology is unknown.

Stage l lesions affect the cementum or
cementum and enamel but have not yet
progressed into the dentin.

DEVELOPMENTAL

Stage 2 lesions affect the dentin but have

ABNORMALITIES
not yet progressed into the pulp cavity.

Stage 3 lesions affect the pulp cavity, but

Proper growth and development of the oral
most of the tooth retains its integrity.

cavity depends on a series of events that

Stage 4 lesions have significant crown or
must occur nom1ally and in the proper
root damage, with most of the tooth having
sequence. Genetic abnormalities or traun1a
lost its integrity.

tllat affects eitller the developing tissues or

Stage 5 lesions have renmants of dental
the timing of their development can cause
hard tissue visible only as irTegular radiopacabnormalities. Defects that decrease ities, and gingival covering is complete.

comfort, healtll, or function require

Lesions are categorized radiographically
treatment; those that result in only an
as type 1 when a focal or multifocal
estlletic problem do not. Common develop-

.

radiolucency is present in the tooth with
mental problems include persistent
otherwise nom1al radiopacity and normal
deciduous teeth, unerupted teeth, malfonned
periodontal ligament space (infl=atory
teeth, malocclusion, and malformed jaws.

resorption), type 2 when there is narrowing
or disappearance of the periodontal

Persistent Deciduous Teeth
ligament space ( dentoalveolar ankylosis)

Deciduous teetll of kittens and puppies are
in at least some areas and decreasM
designed to function in a small mouth (fewer
radiopacity of part of the tooth ( replacein nwnber and smaller in size) and for a ment resorption, moth-eaten "ghost" roots), temporary period. Dental trauma during this
or type 3 when features of both type 1 and
time of energetic oral exploration is often
type 2 are present in the same tooth.

compensated for by the exfoliation of tlle

Tooth resorption lesions exposed to the
dan1aged teeth as the permanent teetll erupt.

oral cavity may cause discomfort. Lesions

The pem1anent teeth are larger and more
limited to root surfaces only are unlikely to
numerous, erupting as tlle jaws lengthen to
cause discomfort or other clinical signs
accommodate tllem.

unless they are associated with resorption

Exfoliation of deciduous teeth is a
of bone adjacent to the tooth resorption ( eg,
complex process, part of which involves
resorption caused by painful inflan1IT1ation
pressure exerted by the crown of the
from periodontal or endodontic disease).

subjacent permanent tooth against the root
of the deciduous tooth. If tlle permanent

Diagnosis: Marginal gingivitis of individual tootll does not erupt in the correct position, teeth in the absence of periodontitis may
the deciduous tooth may remain fumly in
indicate an early subgingival lesion. Lesions
position. This may be due to hypodontia
w1der the gi.ngival margin can be identified
witl1 no succedaneous permanent tooth, a
by sharp dental exploration. Larger lesions
genetically malpositioned permanent tooth
are identified by their typical appearance on
bud, or traumatic displacement of the tooth

DENTISTRY

183
bud. Persistence of a deciduous tooth in
a variation of normal. But in most anin1als,
areas of wide tooth spacing may not cause a
an edentulous area where there should be
problem. However, if the deciduous tooth
a tooth is an indication for radiography.

causes crowding with the pem1anent tooth

An unerupted tooth is easily identified.

( often the case with canine teeth in dogs),

Embedded refers to an unerupted tooth
then the area is predisposed to periodontitis.

covered in bone, the eruption of which is

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Additionally, the displaced permanent tooth
compromised by lack of eruptive force.

can itself result in traumatic occlusion that

Impacted refers to an unerupted or partially
requires treatment. Timing of deciduous
erupted tooth, the eruption of which is
tooth exfoliation and permanent tooth
prevented by contact with a physical barrier.

replacement are genetically determined. In

Teeth that are incompletely erupted with a
rare cases, trauma during tooth development persistent gingival covering can be treated can cause displacement of a tooth bud that
with operculectomy ( a form of gingivectomy)

affects exfoliation.

to sculpt the tissue to a nom1al architecture.

Most commonly, two canine teeth ( one

Individual teeth that are completely
deciduous and one permanent) are present
unerupted after maturity may remain quiet
at the same time. The permanent maxillary
and require only monitoring. However, they
canine tooth erupts mesial ("rostral") to the can also fom1 dentigerous cysts that can
deciduous one, giving the appearance of a
destroy large areas of the jaws. Mandibular
wider and more blunt canine tooth rostral
first premolars are significantly predisposed
to a narrower one with a sharper cusp. The
to cyst formation, particularly in brachycepermanent mandibular canine tooth erupts phalic breeds. For that reason, any missing
lingual ("medial") to the deciduous one,
mandibular first premolar should always be
giving the appearance of a wider and more
radiographed; any that are discovered should
blunt canine tooth toward the tongue next
be removed or closely monitored with
to a narrower one with a sharper cusp
periodic radiographs. Other unerupted teeth
positioned toward the lip. In the premolar
should be removed if they cause a problem.

area, it is common to see a deciduous tooth Surgical removal of deeply tmerupted
in an area with no sinmltaneous pem1anent
mandibular canine teeth can be challenging.

tooth. A smaller than normal premolar

Animals with unerupted teeth should not
should be radiographed for evaluation of
be bred unless it is known the condition was
its anatomy and root structure to detercaused by traun1a.

mine whether it is a deciduous tooth.

A deciduous tooth should be extracted

Malformed Teeth
when it remains firmly attached (no
mobility) after its successor permanent

Any interruption during tooth formation can
tooth has erupted. Persistent deciduous
result in a deformed tooth. The insult can be
teeth that do not have a permanent tooth
traun1atic, metabolic, infectious, or rarely
replacement may be left in place if the roots
genetic. Insults to epitheliogenesis ( eg,
are strong. However, radiographs should be
parvovirus, distemper virus, high fever) that
taken to verify there are no embedded or
occur during amelogenesis causes enamel
impacted permanent teeth at the site and
hypoplasia or hypomineralization. Insults
that the roots are not being resorbed.

to dentin formation can cause defo1med

Because most persistent deciduous teeth
or missing roots.

are genetic, pets with this problem should

Enamel abnormalities can be regional,
not be bred unless the condition is known
with circumferential lines of missing enamel
to have been caused by trauma.

( rough surface with staining), or generalized
with complete loss of enamel. Radicular

Unerupted Teeth
dysgenesis can present witl1 relatively
normal appearing crowns that are mobile.

Tooth eruption is genetically programmed.

The lack of roots is readily identified on

Some breeds, particularly small breeds ( eg,
radiographs. An interesting individual tooth

Maltese), are predisposed to delayed or
abnormality that appears to be genetic is
incomplete eruption. Some brachycephalic
convergent roots of the mandibular first
breeds are predisposed to malpositioned
molar. This anomaly less commonly affects
first premolar teeth that remain unerupted
other teeth. The crown may appear normal,
because of their abnormal position. Trauma
or it may have a small developmental groove
can also move a tooth bud into a position
on the buccal surface extending from the
in which it is unable to erupt because of
gingival margin. On a radiograph, the roots
in1pact against another structure.

converge apically instead of having their

In some breeds (particularly the terrier
normal divergent position. The crown
breeds), missing premolars are considered
sometimes appears too large in relation to

1 84

DENTISTRY
the size of the roots. The convergence causes

Jar mesioclusion ( class 3 malocclusion) or
the floor of the pulp chamber to arch dorsally
mandibular distoclusion ( class 2 maloccluinto the main pulp chamber, giving it the sion). The latter problem often causes
radiographic appearance of a "dens-in-dente" traumatic occlusion when the mandibular or dens invaginatus. These teeth conunonly
canine teeth impact against the most rostral
have a communication from the periodontal
hard palate. Linguoversion of the mandibu

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ligament to the pulp chamber in the furcation lar canines often accompanies this problem, area, resulting in an extremely high rate of
because they can be directed palatally as
endodontic disease. Many other individual
they erupt along the palatal surface of
tooth anomalies are seen occasionally, such
the maxillary canines. Individual tooth
as supernumerary teeth, twinning and fusion
malposition ( dental malocclusion or class l
of teeth, supernumerary roots, and ''peg"

malocclusion) can also be genetic, such as
teeth (short cylindrical teeth).

mesioversion of the canine teeth (ie, "lance

Enamel hypoplasia or hypomineralization
projection") in Dachshunds and Shetland
is treated with early dentin sealant to prevent Sheepdogs.

bacterial ingress to the pulp. Composite

During the deciduous dentition period,
resin veneers can also protect the softer
interceptive 01thodontics can be performed
dentin from abrasion and provide a smooth
by selectively extracting deciduous teeth. If
surface on which plaque is less able to fom1,
there is dental interlock, then extracting
but they will eventually wear or chip. Root
locked teeth can allow the jaws to grow to
dysgenesis carries a poor longterm
their genetic potential. Deciduous rostral
prognosis. The teeth can be maintained for
crossbite can be treated by extraction of the
years with strict oral care and avoidance of
deciduous maxillary incisors. This not only
any dental trauma or overuse. Individual
relieves the interlock but also encourages
anomalous teeth should be evaluated for
tl1e permanent incisors to erupt in a more
associated pathology; many cause no
labial angle (they normally erupt on tl1e
problem and do not require treatment.

palatal side of the deciduous incisors) to

Malfonned teeth are the result of trauma,
help correct the malocclusion. Likewise,
infections, or genetics. Routine caution and
deciduous mandibular distoclusion can be
care during tooth development prevents
treated by exti·action of the deciduous
most of them.

mandibular canine teeth. Again, tltls not
only relieves the dental interlock but also

Malocclusion and Malformed Jaws
encourages the permanent mandibular
canine teeth to erupt in a more labial angle

Malocclusion is nearly always genetic;

(they no1mally erupt on the lingual side of
however, trauma during development can
the deciduous canines) to help correct the
interfere with n01mal growth. Maxillary
malocclusion. Whenever deciduous teetl1
length is easier to manipulate than mandibuare extracted, touching the tooth bud of the lar length through selective breeding. As a
developing pem1anent teeth must be
result, a preference for longer faces and
avoided so as not to damage the enamel
noses inadvertently selects for mandibular
organs or developing enamel. This damage
distocclusion (ie, overbite, or lower jaw
can cause brown spots on tl1e crowns of
appears shorter than upper jaw), -whereas
permanent teeth due to focal enamel
selecting for a "blockier" head or shorter defects. Instruments should not be inse1ted
nose results in mandibular mesioclusion (ie,
on the palatal side of deciduous maxillary
underbite, or lower jaw appears longer than
incisors or on the lingual side of deciduous
upper jaw). The upper and lower jaws
mandibular canines. Even with proper
develop at different rates, making the timing
technique, enamel damage can occur,
of tooth eruption critical. lf thejaws have an
because the enamel epithelium can be
abnom1al relationship to each other at tl1e
tugged as tl1e deciduous tooth is extracted
time the permanent teeth gain enough height
from the alveolus.

to occlude, then the dentition is locked into

Mandibular mesioclusion in the
the abnonnal position. If this occurs
pennanent dentition is considered normal
unilaterally, it can allow continued jaw
for many brachycephalic breeds and does
lengthening on one side while arresting it on
not require treatinent unless it results in
the other side, resulting in a mismatch of the
trawnatic occlusion. If the mandibular
central incisor midlines (ie, asymrnetiic
canines impact against tl1e palatal aspect of
skeletal malocclusion such as "wry" bite).

the third or second maxillary incisors, then

The most common maxillary-mandibular
extraction of the maxillary incisors in
discrepancy is a ho1izontal symmetric
contact will create a wide diastema into
skeletal malocclusion, resulting in mandibu-
which the canine tooth can fit, resolving the

DENTISTRY

185
problem. The rostral crossbite (ie, maxillary
idine solution every 2 days helps decrease
incisors positioned lingual to the mandibuoral bacteria during healing.

lar incisors) rarely causes discomfort or

Maxillary fractures can be stabilized witil
health problems. In contrast, mandibular
wire and sutures. Mandibular fractures can
distoclusion often requires orthodontic or
be more challenging; when possible, tl1ey can
surgical intervention. Canine teeth can be
be repaired witil interdental wiring and an

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moved into a nontraumatic (not always
intraoral splint made of bis-acryl composite
normal) position that is comfortable and
resin. Other options include tape muzzling,
functional. Alternatively, the tooth can be
cerclage wiring, interarch splinting, intrashortened and the pulp treated with vital osseus wiring, external skeletal fixation,
pulp therapy. This approach requires sterile
or miniplates. Preserving nonnal occlusion
technique to avoid introduction of infection
is important. With rigid stabilization, tile
into the pulp and followup radiographs
pet can usually readily eat soft food until
throughout life to monitor the need for
the appliance is removed in 6----8 wk.

definitive endodontic treatment.

Caudal mandibular body fractures in the

Only animals with a normal, healthy
area of or caudal to diseased molars requiring
occlusion should be bred.

extraction are much more problematic
because of the lack of teetil on botil sides of

DENTOFACIAL TRAUMA
the fracture and tile thinner bone caudal to
the body of tile mandible. Plates can be used,

Teeth and jaws play a prominent role in the
but tile prognosis is guarded. Interarch
interaction of animals with their environsplinting (ie, between tile upper dental arch to ment. This predisposes them to traumatic
tile lower dental arch) can be successful, but
i.ajury, most commonly fights with otl1er
tilere is a risk of aspiration while tile splint is
aninlals, automobile impacts, getting caught
in place if the aninlal vomits. A feeding tube is
on fences, or falling onto hard surfaces.

used until tl1e splint is removed.

Mandibles can also suffer spontaneous
pathologic fractures due to severe periodontitis around tl1e mandibular first molars or DENTAL CARIES
to neoplasia

A fractured tooth with a red or black spot

Dental caries, or bacterial infections of the
in the center of an irregular crown surface
teeth, are common in people, uncommon
indicates pulp exposure. A missing tooth
in dogs, and essentially nonexistent in cats.

after trauma might be avulsed or may be

This may be related to the fact that human
fractured with retained root fragments,
saliva is more acidic, human teeth contain
which can be detennined radiographically.

many pits and fissures, and the human diet

Fractured mandibles cause acute maloccluis rich in highly refined carbohydrates. The sion and inability to eat. The midline of the
saliva of dogs and cats is more alkaline
mandible is usually displaced toward the side than that of people, their teeth contain of the fracture. The mouth may be held open,
fewer pits and fissures, and their diet is
particularly in bilateral mandibular fractures.

less rich in carbohydrates. Furthermore,

Fractured teetil are treated as described
cariogenic bacteria are less common in the
above (seep 181). Avulsed teeth can be
mouths of dogs and cats than in those of
replaced if treated promptly (wiiliin hours).

people. The initial lesion of ca.ii es is acidic

The owner should in1mediately place the
demineralization of the enamel. This is
tootil in a tooth transport mediun1 or milk,
accomplished by cariogenic bacteria that
witl10ut touching the root. The alveolus and
ferment sugar, thus releasing acids onto
root surface should be gently flushed witil
the tooth surface.

lactated Ringer's solution to remove dirt, and

In dogs, caries usually occurs on the
then the tooth placed into the alveolus and
occlusal surfaces of molar teeth. It has the
stabilized for 1 mo with interdental wiring.

appearance of a brown to black cavitated

Rigid stabilization with acrylic or composite
lesion with a soft surface into which a sharp
is less ideal for the periodontal ligament
explorer tip can penetrate and "stick."

repair because it encourages ankylosis, but it

The carious tootil structure must be
may be a good idea to protect against abuse
removed using a dental bur until healthy
of the recently replaced tootil. Root canal
dentin is reached. A radiograph should be
tilerapy is done when tile fixator is removed.

taken to determine whether tile infection

Soft-tissue trauma is repaired using
has spread to the pulp, in which case the
primary closure with absorbable sutures.

tooth also requires root canal therapy. The

Oral soft tissues are vascular and heal
missing tooth structure is tl1en restored
quickly. Oral flushes with dilute chlorhex-
using either composite or amalgam.

186

DENTISTRY

Dogs that have had dental caries are
any medications used. Therefore, only
predisposed to additional lesions; topical
small amounts should be placed on the
treatment with a stannous fluoride
occlusal surfaces of the teeth. Fluoride
product every 2 wk may help prevent
can cause gastritis, and it can be
future caries in these animals. Because
nephrotoxic if significant amounts are

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dogs do not expectorate, they swallow
ingested.

PHARYNGEAL PARALYSIS

Pharyngeal paralysis may be the result
tracheostomy before any clinical diagnostic
of a central or peripheral nervous system
techniques can be performed.

disorder or may develop secondary to severe
local disease that may cause collapse,
obstruction, or malfunction of the pharynx.

Diagnosis: The history and clinical signs

Of the CNS disorders, rabies ( see p 1302) is are usually indicative of pharyngeal
the most important of the viral causes of
paralysis. A baseline CBC and biochemistry
encephalomyelitis, although perhaps not the
profile should be perfom1ed. Affected
most frequent. CNS intoxication, lead
animals typically may be hemoconcentrated,
poisoning, cranial trauma, intracranial
have electrolyte and acid-base disturbances,
abscessation, and neoplasia may also result
and may exhibit prerenal azotemia. Serology,
in pharyngeal paralysis in many species.

skull radiographs, thoracic radiographs to

Peripheral causes of pharyngeal paralysis
evaluate for aspiration pneumonia,
include pharyngeal trauma and abnormaliendoscopy, ultrasonography, CT, and MRI (if ties of the pharyngeal adnexa, particularly
available) are all valuable aids to deteffiline
involving the guttural pouch of horses.

whether the underlying cause is central or

Disorders of the guttural pouch resulting in
peripheral. The use of CT and MRI has
pharyngeal paralysis include guttural pouch
particular value in evaluating CNS causes
mycosis, guttural pouch empyema, guttural
of pharyngeal paralysis in small animals.

pouch neoplasia, and osteoarthropathy of

Animals suspected of having rabies should
the temporohyoidjoint. Equine protozoal
be handled appropriately (seep 1302).

myeloencephalitis (seep 1309) can also
cause pharyngeal paralysis iu some horses.

Treatment: Treatment protocols for

The degree of pharyngeal paralysis ranges
pharyngeal paralysis vary depending on
from complete to incomplete, depending on
the underlying cause. Treatment generally
whether the abnormality is unilateral or
includes the administration of antimicrobial
bilateral or central versus peripher�.

and anti-inflanm1atory medications. Because

Unilateral lesions may result in partial
of the inability to swallow normally, IV
pharyngeal malfunction. For exan1ple,
administration is preferred. Animals with
horses with guttural pouch disease may be
hemoconcentration should be administered
able to swallow but may still develop clinical

IV fluids. lf the animal is unable to eat without
signs of dysphagia ( eg, nasal discharge of
aspiration, extraoral or parenteral nutrition
food or water, coughing).

should be strongly considered. Extraoral
alimentation with pharyngostomy, esopha

Clinical Findings and Lesions: Clinical
gostomy, or nasogastric tubes or temporary
signs of pharyngeal paralysis include
rumenostomy in ruminants can be an
dysphagia with oral or nasal discharge of
economical and effective way to provide
food, water, or saliva Other clinical signs
nutritional support. Other treatments include
include coughing, dyspnea, ptyalism, or bruxlocal therapy for pharyngeal abscesses.

ism. Affected animals are at risk of inhalation

The prognosis for pharyngeal paralysis
pneumonia, dehydration, and cardiovascular
varies with the instigating cause. The
and respiratory shock. Affected animals
prognosis for pharyngeal abscessation
frequently have one or more signs, including
can be favorable, whereas the prognosis
pyrexia, coughing, retching, and signs
for guttural pouch disease can be guarded.

compatible with esophageal obstruction.

If affected animals do not improve after

Severely affected animals may die or should

4-6 wk of symptomatic therapy, the
be considered for euthanasia. Animals with
prognosis is poor and euthanasia should
dyspnea may require an emergency
be considered.

DISEASES OF THE RECTUM AND ANUS

187

DISEASES OF THE RECTUM AND ANUS

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ANAL SAC DISEASE
disease. In the case of a suspected tumor,
the diagnosis should be confirmed by biopsy.

Anal sac disease is the most common disease

Regional and systemic metastasis should be
entity of the anal region in dogs. Small
evaluated, and serun1 calciun1 measured.

breeds are predisposed; large or giant breeds
are rarely affected. In cats, the most conunon Treatment: In1pacted anal sacs should be form of anal sac disease is impaction.

gently, manually expressed. A softening or
cerun1inolytic agent or saline can be infused

Etiology and Pathogenesis: Anal sacs
into the sac if tl1e contents are too dry to
may become impacted, infected, abscessed,
express effectively. Infected sacs should be
or neoplastic. Failure of the sacs to express
cleaned with antiseptic, followed by local and
during defecation, poor muscle tone in
systemic antibiotic therapy. Hot compresses,
obese dogs, and generalized seborrhea
applied every 8-12 hr for 15---20 min each, are

(which produces glandular hypersecretion)

beneficial for abscesses. Repeated weekly
lead to retention of sac contents. Such
flushings combined with infusion of a
retention may predispose to bacterial
steroid-antibiotic ointment may be needed.

overgrowth, infection, and inflanm1ation.

Adding supplemental fiber to the diet may
increase fecal bulk, facilitating anal sac

Clinical Findings and Lesions: Signs are compression and emptying. lf medical related to pain and discomfort associated
treatment is ineffective, or if neoplasia is
with sitting. Scooting, licking, biting at the
present, surgical excision of the sac is
anal area, and painful defecation with
indicated. The closed technique for excision
tenesmus may be noted. Induration,
is preferred and has the lowest complication
abscesses, and fistulous tracts are common.

rate. However, fecal incontinence, a conm1on

In in1paction, hard masses are palpable in
complication of anal sac surgery, may result
the area of the sacs; the sacs are packed
from damage to the caudal rectal branch of
with a thick, pasty, brown secretion, which
the pudendal neive and may be complete if
can be expressed as a thin ribbon only with
dan1age is bilateral. Chronic fistula formation
a large an1ount of pressure. When the sacs
may be seen when sac removal is incomplete
are infected or abscessed, severe pain and
or when the sac ruptures. Scar formation in
often discoloration of the area are present.

the external anal sphincter may result from

Fistulous tracts lead from abscessed sacs
surgical trauma and result in tenesmus. (See
and rupture through the skin; these must be
also APOCRINE GLAND TUMORS OF ANAL SAC ORIGIN, differentiated from perianal fistulas. Anal
p 950.)

sac neoplasms are usually nonpainful and
are associated with perineal edema,
erythema, induration, or fistula fom1ation.

PERIANAL FISTULA

Apocrine gland adenocarcinomas of the

Perianal fistula is characterized by chronic,
anal sac are typically seen in older female
purulent, malodorous, ulcerating, sinus
dogs. These dogs may be presented for
tracts in the perianal tissues. It is most
signs secondary to hypercalcemia, such as
conunon in Gennan Shepherds and is also
polyuria and polydipsia, or for problems
seen in Setters and Rettievers. Dogs > 7 y.r
related to the perineal mass.

old are at higher risk.

Diagnosis of impaction, infection, or
abscessation is confinned by digital rectal

Etiology and Pathogenesis: The cause
exan1ination, at which tin1e the sacs can be
is unknown, although many theories have
expressed. Microscopic exan1ination of the
been proposed. Contan1ination of the hair
contents from infected sacs reveals large
follicles and glands of the anal area by fecal
numbers of polyrnorphonuclear leukocytes
material and anal sac secretions may result in
and bacteria. A tumor should be suspected
necrosis, ulceration, and chronic inflanm1 a

(anal sac apocrine adenocarcinoma) in anal
tion of the perianal skin and tissues. Affected
sacs that are firm, enlarged, and nonexpressanimals may be predisposed to generalized ible even with irrigation. Ultrasonographic
skin problems. Hypothy.roidism, an
exan1ination may be useful to detem1ine
inm1tmologic defect, or an immunewhether a firm, nonexpressible anal sac is mediated component may conttibute to
due to infection/abscessation or neoplastic
susceptibility. The likelihood of contan1ina-

188

DISEASES OF THE RECTUM AND ANUS
tion is greater in dogs with a broad-based
reduce dyschezia. Perianal cleansing and
tail; deep anal folds may cause feces to be
antibiotics may reduce inflanunation.

retained within rectal glands and play a
major role. The draining tracts are lined with

PERIANAL TUMORS
chronic inflanunatory tissue and often

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extend to the lumen of the rectum and anus.

See HEPATOID GLAND TUMORS, p 951, and Wection may spread to deeper structures

APOCRINE GLAND TUMORS OF ANAL SAC ORIGIN,
involving the external anal sphincter and,
p950.

therefore, should be treated promptly.

PERINEAL HERNIA

Clinical Findings: In dogs, signs include

Perinea! hernia is a lateral protrusion of a
attitude change, tenesmus, dyschezia,
peritoneally lined hernial sac between the
anorexia, lethargy, dianhea, and attempts to levator ani and either the external anal bite and lick the anal area. Signs in cats are
sphincter muscle or tl1e coccygeus muscle.

similar to those in dogs but may include

Incidence in intact 6- to 8-yr-old male dogs is
matting of fur and sitting in the litter box.

disproportionately high, and Welsh Corgis,

Boston Terriers, Boxers, Collies, Kelpies and

Treatment: Histolically, management of

Kelpie crosses, Dachshunds and Dachshund
perianal fistulae was frustrating for both
crosses, Old English Sheepdogs, and
veterinarians and pet owners. Surgical

Pekingese are at higher risk.

therapy traditionally included anal
sacculectomy, in addition to destroying tl1e

Etiology and Pathogenesis: Many
diseased tissues. Surgical techniques
factors are involved, including breed
included excision, debridement, fulguration, predisposition, hormonal in1balance, and cryosurgery. Amputation of the tail at
prostatic disease, chronic constipation, and
its base was once advocated alone or
weakness of the pelvic diaphragm due to
acljunctively with other therapy. Surgery
chronic straining. The higher incidence
is now only recommended for fistulae
among sexually intact males is evidence that
resistant to medical therapy. Sequelae of
hormonal influences probably play a primary
surgery include fecal incontinence, rectal
role. Prostatic hypertrophy attributed to
stricture, and recurrence.

sex-horn1one imbalance has been strongly

Cyclosporine has been an effective
implicated. Both estrogens and androgens
treatment at a dosage of5-10 mg/kg, bid for
have been cited as causative agents.

10-20 wk and then for an additional 4 wk

Clinical Findings and Diagnosis:

after all fistulae appear to be healed.

Conunon signs include constipation and

Concurrent administration of ketoconazole
obstipation, tenesmus, and dyschezia.

(8 mg/kg/day) allows the dosage (and cost)

Strangulia and urinary obstruction may
of cyclosporine therapy to be reduced
develop secondary to retroflexion of the

(1-3.5 mg/kg/day). Prompt treatment is
bladder and prostate. Visceral strangulation
recommended early in the course of the
may be seen. A perinea! swelling ventrolatdisease to reduce the likelihood of eral to the anus is evident. Herniation may
recurrence. However, some dogs are
be bilateral, but two-thirds are unilateral
intolerant of ketoconazole. Cyclosporine
and >80% of these are on the right side.

at a dosage of 5 mg/kg/day can effectively

The mass is soft and fluctua(lt and may be
decrease the severity of lesions. In one
reduced digitally. A firm, painful swelling
study, the combination of cyclosporine
may be compatible with retropulsion of tl1e
therapy for 12 wk followed by surgical
bladder and prostate. Detemunation of
excision of any remaining draining tracts,
contents is often made by rectal exan1inaalong with cryptectomy and anal sacculection and perinea! centesis (to detern1ine tomy, successfully resolved disease with
whether urine is present). More than 90% of
minimal recutTence. Topical tacrolirnus
perinea! hernias contain a rectal deviation,

(0.1% ointment applied once to twice daily)

which is a sacculation of the rectum into the
in combination with a tapering course of
hernial sac, where the layers of the rectal
prednisone (2 mg/kg/day for 2 wk, l mg/kg/
wall remain intact.

day for 4 wk, and then 1 mg/kg every 2 days
for 10 wk) with metronidazole (10 mg/kg,

Treatment: Perinea! hernia is rarely an
bid for 2 wk) and a novel-protein diet has
emergency, except when the bladder has
also been found to be effective in some
strangulated and the animal is unable to
dogs. Other aspects of medical manageulinate. If cathetelization carmot be clone, ment include the use of fecal softeners to
the urine should be removed by cystocente-

DISEASES OF THE RECTUM AND ANUS

189
sis and an attempt made to reduce the

RECTAL POLYPS
hernia. An indwelling urinary catheter may
be necessary to ensw-e w-ethral patency and

Rectal adenomatous polyps are an infrequent,
prevent recurrence of obstruction.

usually benign disease, primarily of small

Surgical correction is always indicated, and animals. The larger the polyp, the greater VetBooks.ir
concurrent castration to reduce recurrence is
the potential for malignancy. Signs include
recommended. The prognosis is guarded
tenesmus, hematocllezia, and diarrhea
because of the high incidence of recurrence

The polyp is usually palpable per rectum

(100/<>--46%) and postoperative complications
and bleeds easily with surface ulceration.

such as infection, rectocutaneous fistula, anal

Periodically, the polyp may prolapse through
sac fistula, ischiatic and pudenda] nerve
the anal orifice. Surgical excision is usually
entrapment, and rectal prolapse.

followed by rapid clinical recovery and
lengthy survival time. New polyps may

RECTAL AND ANORECTAL
develop after surgery. A biopsy should always

STRICTURES
be submitted for histopathologic diagnosis.

Strictures are a narrowing of the lumen due

RECTAL PROLAPSE
to cicatricial tissue. Injury may result from
foreign bodies or trauma ( eg, bite wounds,

In rectal prolapse, one or more layers of
accidents) or as a complication of
the rectun1 protmde through the anus due
inflammatory disease ( eg, pe1ianal fistula
to persistent tenesmus associated with
disease, histoplasmosis, inflan1I11atory
intestinal, anorectal, or urogenital disease.

bowel disease, anal sacculitis ).

Prolapse may be classified as incomplete,

Neoplasia, enlarged prostate, and scar
in which only the rectal mucosa is everted,
tissue after perianal fistula or anal sac
or complete, in which all rectal layers are
abscess may all predispose to extraluminal
protruded.

constriction. In small animals, anorectal
stricture is more con1I11on than rectal

Etiology: Rectal prolapse is common in
strictures, but neither is frequent. Strictures
young animals in association with severe
are more common in German Shepherds,
diarrhea and tenesmus. Causal factors

Beagles, and Poodles.

include severe enteritis, endoparasitism,

Rectal stricture in cattle may result from
disorders of the rectun1 (eg, foreign bodies,
trauma, neoplasia, or fat necrosis in1pinging
lacerations, diverticula, or sacculation),
on or within the lun1en, or from defects
neoplasia of the recttun or distal colon,
associated with rectal and vaginal stricurolithiasis, w-ettu·aJ obstruction, cystitis, tures. Rectal strictures in pigs are seen
dystocia, colitis, and prostatic disease.

secondary to enterocolitis, after repair of

Perineal hernia, or other intermption of
rectal prolapse, and as a sequela of
normal innervation of the external anal
ulcerative proctitis induced by salmonellae.

sphincter, may also produce prolapse.

Treatment in small aninlals includes general

Aninlals of any age, breed, or sex may be
anesthesia followed by balloon dilation of
affected. Rectal prolapse is probably the
the stricture, combined with intralesional
most con1I11on GI problem in pigs due to
injections of long-acting corticosteroids
diarrhea or weakness of the rectal support

(triamcinolone). Treatment in large aninlals
tissue within the pelvis. In cattle, it may be
may include resection of the strictw-ed area
associated with coccidiosis, rabies, or
or rectal pull-through.

vaginal or uterine prolapse; occasionally,
excessive "riding" and associated traumatic RECTAL NEOPLASMS
injury may be causative in young bulls. It is
common in sheep with short tail docking

Malignant rectal neoplasms are usually
and especially in feedlot lambs, in which
adenocarcinomas in dogs and lymphosarhigh-concentrate rations may be causative.

comas in cats. Adenocarcinomas are slow

The use of estrogens as growth promotants,
growing and infiltrative. Local or systemic
or accidental exposure to estrogenic fungal
metastasis may develop before tenesmus,
toxins, may also predispose large aninlals to
dyschezia, hematochezia, or diarrhea is
rectal prolapse.

seen. Sw-gery is the treatment of choice for
adenocarcinomas, but it may be unreward

Clinical Findings, Lesions, and
ing because metastasis has usually occurred Diagnosis: An elongated, cylindrical mass before the diagnosis. Cats and dogs with
protmding through the anal orifice is usually
rectal lymphosarcoma are treated medically diagnostic. However, it must be differentiwith antineoplastic drugs.

ated from prolapsed ileocolic intussuscep-

190

DISEASES OF THE RECTUM AND ANUS
tion by passing a probe, blunt instrument, or

In general, the prolapse may be salvaged
finger between the prolapsed mass and the
by conservative measures, unless obvious
inner rectal wall. In rectal prolapse, the
deep necrosis or trauma to the tissue exists,
instrument cannot be inserted because
or the everted tissue is firm, indurated, and
of the presence of a fomix.

cannot be reduced. Under these circum

Ulceration, inflammation, and congestion
stances, submucosal resection or amputa

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of the rectal mucosa is common. Early,
tion should be considered. Amputation of
there is a short, non ulcerated, inflamed
the rectun1 should be reserved for severe
segment; later, the mucosa! surface darkens
cases. Complete amputation has a higher
and may become congested and necrotic.

incidence of rectal stricture formation,
especially in swine. A prolapse ring, syringe

Treatment: In all animals, identifying
case, or plastic tubing may be used as an
and eliminating the cause of prolapse is
alternative to surgical amputation in pigs
of primary importance.

and sheep. Postoperatively, the animal

In small animals, treatment includes
should receive antibiotics. Fecal softeners
prompt replacement of viable prolapsed
may be used in horses. Usually, it is not
tissue to its proper anatomic location, or
economically feasible to repair rectal
amputation if the segment is necrotic. Small
prolapses in lan1bs ready for market.

or incomplete prolapses can be manually
reduced under anesthesia by using a finger

RECTAL TEARS
or bougie. Warm saline lavage and
lubrication with a water-soluble gel should

A separation, rent, or tear in the rectal
be applied to the prolapsed tissue before
or anal mucosa is seen as a result of a
reduction. Alternatively, hypertonic sugar
laceration inflicted within the lumen.

solution (500A, dextrose or 7()0A, mannitol)

Foreign bodies ( eg, sharp bones, needles,
applied topically may be used to relieve
and other rough material) have been
edematous mucosa. The placement of a
implicated. Bite wounds and, in large
loose, anal purse-string suture for 5-7 days
animals, trauma from rectal palpation are
is indicated. Straining may be prevented by
common causes. The tear may involve only
applying a topical anesthetic (1% dibucaine
the superficial layers of the rectum (partial
ointment) or by administering a narcotic
tear) or penetrate all layers ( complete tear).

epidural injection before or after reduction
or correction. Postoperatively, a moistened

Clinical Findings and Diagnosis:

diet and a fecal softener ( eg, dioctyl sodium

Constipation and reluctance to defecate
sulfosuccinate) are reconunended. Diarrhea are usually attributed to pain. Diagnosis after surgery may require treatment.

is based on tenesmus and hemorrhage,

When questionable viability of tissue
perinea! discoloration, and inspection of the
prohibits manual reduction, rectal resection rectun1 and anus; fresh blood found on a and anastomosis are required. When rectal
glove or on feces after rectal examination is
tissue is viable but not amenable to manual
good evidence of a rectal tear. Edema may
reduction, celiotomy followed by colopexy
be present when the injury has persisted.

is indicated to prevent recurrence. As in

The integrity of the external anal sphincter
medical management, epidul'lll anesthesia
should be evaluated carefully.

may be used to reduce straining.

In large animals, caudal epidural

Treatment: In all species, treatment
anesthesia is suggested to reduce straining,
should be initiated immediately. The
facilitate repositioning of the prolapse, and
anorectal area should be cleaned thorpernlit surgical manipulations. Reduction oughly and systemic broa d -spectrun1
and retention with a purse-string suture is
antibiotics administered. IV fluids and
recommended. The suture should be loose
flunixin meglunline may be given to prevent
enough to leave a one-finger opening into
or treat septic and endotoxic shock. In small
the rectum in pigs and sheep, and slightly
animals, lacerations should be debrided and
larger in cattle and horses. Rectal prolapse
may be sutured through the anal orifice, via
in mares, if neglected, can lead to prolapse
laparotomy, or through a combination of
of the small colon. The blood supply to the
both depending on the location and degree
small colon is easily disrupted. Replaceof the tear. Antibiotics and fecal softeners ment of a rectal prolapse with prolapse of
should be administered postoperatively.

the small colon followed by p'urse-string

In cattle and horses, accidental perforasuture of the anus has a poor prognosis.

tion during rectal exanlination necessitates

More aggressive treatment of the prolapse
inunediate treatment to reduce the risk of
is dictated by the condition of the rectum.

peritonitis and death. Exploration through-

ENTERIC CAMPYLOBACTERIOSIS

191
out the abdomen should be slow, deliberate,

Grade I tears may be treated conservaand smooth. The temptation to use the tively with broad-spectrum antibiotics and IV
fingertips excessively or to push the arm
fluids. F1unixin meglumine may be given to
through a region of resistance must be
prevent or treat endotoxic shock. Mineral
avoided. Rectal tears in horses have been
oil is given via stomach tube to soften feces,
classified according to the tissue layers
and the diet should consist of pasture grasses

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penetrated. Grade I tears involve the mucosa or alfalfa Grade II and ill teaJS require or submucosa. Grade II tears involve rupture inunediate and more extensive surgery. A of the muscular layers only. Grade ill tears
consultation with a specialist is suggested
involve mucosa, submucosa, and muscular
inunediately after diagnosis. Grade IV tears
layers, including teaJS that extend into the
carry a grave prognosis; they should be
mesorectum. Grade IV tears involve
repaired only if small and if treatment is
perforation of all layers of the rectum and
instituted before the pe1itoneal cavity is
extension into the pe1itoneal cavity.

grossly contaminated.

ENTERIC CAMPYLOBACTERIOSIS

Campylobacter spp are spiral, microaero

C jejuni subsp jejuni ( enteritis and bic, gram-negative bacteria that cause
abortion), C coli, C mucosalis (porcine
gastroenteritis in people and animals.

enteritis), C upsaliensis, C helveticus

Several Campylobacter spp are zoonotic.

(companion pet enteritis), C hyointesti

Many domestic animals develop acute
nalis subsp hyointestinalis (porcine and gastroenteritis after ingestion of Campylo
bovine enteritis), C sputorum (abortions in
bacter spp, including dogs, cats, calves,
sheep), and Cfetus subspfetus (isolated
sheep, pigs, ferrets, mink, monkeys, and
from intestinal tracts of sheep and cattle,
several species of laboratory animals.

sporadic abortions). Certain species such as

(See also BOVINE GENITAL CAMPYLOBACTERIOSIS, C jejiini, C hyointestinalis, and C fetus p 1347, AVIAN CAMPYLOBACTER INFECTION, p 2806, possess closely related subspecies with
and ZOONOTIC DISEASES, p 2419.) Infection with different disease foci. Initially, Arcobacter C jejuni is one of the most common causes
spp were considered to be aerotolerant
of gastroenteritis in people worldwide and
campylobacters and are implicated in.

is the most extensively studied Campylo
reproductive disorders, mastitis, gastric
bacter species.

ulcers, and/or diatThea in livestock,
including A cryaerophilus (previously

Etiology: Campylobacter spp are spiral C cryaerophila ), A skirrowii, A thereius, or curved rods that exhibit a characteristic
and A butzleri.

corkscrew darting motility, mediated by a
single polar flagellum. These are slow

Transmission and Epidemiology:

growing, with a generation time of -90 min,

Transmission is food- or waterborne or via
fastidious, and require enriched medium
fecal-oral spread. Animals serve as reservoir
and microaerobic conditions with increased hosts for Campylobacter spp infections in C02 (3o/er-15% 02, 3"/er-lOOAi C02, 85% N2) for both animals and people throughout the
growth.

world. The predominant ecologic niche for

The family Can1pylobacteraceae consists

Campylobacter spp is the GI tract of a wide of three genera, including Campylobacter
variety of domesticated and wild verteand Arcobacter associated with animal and brates, and zoonotic transmission from
human diseases. Certain species are present animals to people in meat of animal origin, commensally in animals as suspected
especially chicken, is a food safety issue.

reservoiJS for human infections. The

Campylobacter spp are also commonly
them10philic Campylobacter spp, C jejuni, isolated from free-living birds, including
or C coli have the highest prevalence and
migratory birds and waterfowl, crows, gulls,
disease impact. Campylobacter species
and domestic pigeons, which can contanlicausing diseases in livestock include nate environments of grazing animals. Wild

192

ENTERIC CAMPYLOBACTERIOSIS
rodents and insects such as flies have also
are considered a significant source of the
been reported to harbor and transmit
bacte1iun1 for the hun1an population.

C jejuni. Fecal contamination of the

Diarrhea is usually acute but can be
environment provides a ubiquitous source
recurrent. Diarrhea lasting 515 days is the
of these organisms under appropriate
most common clinical sign in dogs <6 mo
conditions for their survival. Campylobac
old. It may be watery to bloody with mucus

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ter spp can persist for long periods in feces, and is sometimes bile-stained. Occasionally,
milk, water, and urine, especially at
the diarrhea becomes chronic and may be
temperatures close to 4°C. In adverse
accompanied by fever and increased WBC
conditions, C jejuni jejuni converts to a
count. Cats <6 mo old commonly have
viable nonculturable form that can be
diarrhea, which may be bloody. Some
reactivated when ingested.

infected cats show no signs. Additionally,

Human foods documented as contami

C jejuni jejuni has been isolated in the
nated with Campylobacter include chicken, profuse and odorless hemorrhagic vaginal turkey, beef, pork, fish, and milk. Domestidischarge from late-pregnancy abortions in cated poultry are the most significant
dogs.

reservoir of C jejuni jejuni for people,

In cattle and sheep, Campylobacter
causing 500/o-700/o of cases; chicken meat is
spp can cause enteritis and abortion,
the number one source. Dogs and cats are
including C jejuni jejuni, C fetus subsp
commonly infected sinillar to their owners
fetus, C hyointestinalis subsp hyointesti
when they ingest undercooked poultry.

nalis, and C sputorum (abortions in sheep). However, in studies that compared

Pathogenesis: Bacterial motility, mucus

C jejuni prevalence in healthy cattle and
colonization, toxin production, attachment,
in cattle considered "sick" because of
internalization, and translocation are among diarrhea, the frequency of Campylobacter the processes associated with C jejuni
spp was not significantly different. Beef
jejuni virulence. Infection begins with
and dairy cattle can have significant levels
ingestion of C jejuni jejuni in contamiof Campylobacter, with prevalences of nated foods or water. Gastric acid provides

2.5o/o-600/o. In a number of studies, cattle
a barrier, and the bacteria must reach the
checked at slaughter harbored Campylo
small and large intestines to multiply; C
bacter in gallbladders, large and small
jejuni invades both epithelial cells and
intestines, and liver. Fecal shed in cattle
cells within the lamina propria.

leads to contamination of milk and beef.

Campylobacters can contribute to colitis

Clinical Findings: Abdominal pain, fever,
in weaning aged pigs. Swine commonly
diarrhea, blood in feces, and inflammatory
carry C coli and C jejuni jejuni as cells in feces demonstrate the inflammatory · intestinal commensals, and studies in the nature of the infection. Natural infections

USA, Netherlands, Great Britain, and
with C jejuni jejuni resulting in enteritis Germany show that more than half of
have been reported in juvenile macaques,
commercially raised pigs excrete the
weaning-age ferrets, dogs, cats, and swine.

organisms. C coli strains comprise most

Chickens, rodents, fetTets, primates,
isolates from pigs, causing first watery,
rabbits, and pigs have been inoculated
then inflammatory diarrheal disease. Pigs
experimentally by various routes with
have anorexia, fever, and diarrhea for 1-5

C jej1mi and subsequently developed
days followed by remission of clinical
enteritis. Clinical reports describe primary
signs but continue to shed C jejuni jejuni
infections with systemic spread, infection
in the feces. C hyointestinalis hyointesti
with mucosa] disease, infection without
nalis and C mucosalis are also implicated disease but with short-tenn bacterial
as causes of enteritis in pigs. Concurrent
persistence, and infection with resistance
infections with viruses, other bacteria ( eg,
and no bacterial persistence. These reports

Escherichia coli), and parasites increase
support the idea that C jejuni jejuni
the disease and pathology caused by
produces a spectrum of disease scenarios,

Campylobacter spp in swine. C hyointes
depending on the immune status of the host, tinalis subsp lawsonii has been isolated bacterial virulence, gene expression, and
from pig stomachs; however, this
other factors.

subspecies has not been implicated in

C jejuni jejuni, C coli, C jejuni,
disease.

C upsaliensis, and C helveticus are the Birds, including intensively farmed

Campylobacter spp that have been
poultry, appear to have a higher infection
associated with intestinal disease in
rate and carriage of Campylobacter spp,
companion animals. C jejuni jejuni
especially C jejuni jejuni, than other
causes diarrhea in dogs and cats, which
aninlals. In broilers, the organism may

ENTERIC CAMPYLOBACTERIOSIS

193
colonize the palatine lymphoid tissues
significantly enlarged. Infection with
and the crop, leading to extremely rapid
particular strains of C jejuni produces
transmission through communal water
bloody exudates with mucus. Histopathotroughs and standard fecal-oral spread.

logic features include a marked inflrunma

However, the organism has been isolated
tion of the lan1ina prop1ia, dominated by
from the small intestines of clinically ill
neutrophilic polymorphonucleru· cells and

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birds, especially psittacines (pruTots) and
mononucleru· cells that sometimes extend
passerifmms (finches ru1d canaries), with
into submucosa. Immune cells such as
hepatitis, lethru·gy, loss of appetite, weight
plasma cells, macrophages, and monon uloss, ru1d yellow diruThea. Mortality may be clear cells have been found in smaller
high. Campylobacler spp have also been
numbers in the lan1ina propria. Damage to,
isolated from free-living birds, including
sloughing of, and ulceration of the epithelial
migratory birds and waterfowl, crows, gulls,
surface and edema have also been seen in
and domestic pigeons; however, disease due most infected species. In pigs and mice, to C jejuni jejuni, for exrunple in naturally d3111age to ilie epithelial sUiface is
infected birds, is rare.

associated wiili tl1e presence of C jejuni at Crunpylobacter GI disease has been
tl1e basolateral surface of the epithelium,
reported in exotic pets ( eg, ferrets, mink,
in paracellular junctions of the epitheliUI11,
primates, h3111sters, guinea pigs, mice, and
and in erosive and ulcerative lesions of the
rats). Although clinical signs vary in these
epithelium; there is often a mucopurulent
species, they generally include mucoid,
neutrophilic exudate with sloughed and
watery, bile-streaked diaIThea ( sometimes
lysed epithelial cells and erosive or
with blood), anorexia, vomiting, and fever.

ulcerative lesions where C jejuni is

Prolonged infections ru·e possible but
associated with the basolateral aspect
unconunon; most infections are self-limiting
of sloughing villous tip cells in the colon.

with mild signs.

Crypt abscesses and dan1age to the crypt

The following species have been isolated
epithelium ru·e also conu11on finclings.

from birds, shellfish, reptiles, mru-ine
mrunmals, and livestock not known to be

Diagnosis: Campylobacter spp can be associated with disease symptoms:

found in both healthy and diaITheic animals;

C avium, C hyoinleslinalis lawsonii,
thus, clinical signs and postmortem findings

C fetus subsp tesludinum, C canadensis, depend on the species and the host animal

C peloridis, C insulaenigrae, C subanl
and its age. Diagnosis of enteric crunpylo
arcticus, C volucris, and C ureolylicus bacteriosis relies on isolation of the

(previously Bacteroides ureolylicus ).

causative agent using selective media under

Several of these are implicated in human
microaerophilic conditions. Fresh fecal
diseases.

srunples should be collected and trans

Arcobacter spp infecting animals include
ported to the laboratory preferably on the

A cryaerophilus (livestock abortion), A
san1e day and within at least 2 days for
bulzleri (livestock diarrhea, bovine and
processing. If transport to the laboratory is
porcine abortions),A skirrowii (sheep
delayed, transport media and storage at 4°C
diaIThea, livestock abortions), ru1d A
produce the best results. Can1pylobacters
thereius (porcine abortion). Disease status
are very sensitive to environmental
is unknown, although these species have
conditions, including dehydration,
been isolated from food animals: A
atmosphe1ic oxygen, sllillight, and
cibarious (chicken meat, piggery effluent),
increased temperature. Organisms are thin

A trophiarnm (fattening pigs), and A suis (0.2-0.8 µm x 0.3-5 µm), grain-negative,

(pork meat). Approximately 11 additional
motile, curved rods. The cells ru·e S-shaped

Arcobacter spp found in shellfish, sewage,
or curved but ru·e occasionally long (8 µm)

seawater, sediments, and salt marsh plants
spiral rods. They exhibit a typical spiraling
are not known to cause diseases in animals
motility. In UIUavorable growth conditions,
or people.

spiral rods UI1dergo a degenerate conversion to coccoid forms. Crunpylobacters can Lesions: C jejuni can stably colonize the be quickly outgrown by contan1inating
small and large intestines, although most
microbes during prolonged transport to the
animals show cecal and colonic lesions with laboratory, and isolation of pure colonies typhlocolitis. In swine and mice, gross
for downstre3111 testing cru1 be difficult.

lesions observed in C jejuni enteritis

Filtration using 0.45 µm filters can help
include enlarged and fluid-filled ceca and
because crunpylobacters will pass through.

proxin1al colons with thickened walls.

Enrichment is required for most clinical

Lymph nodes (ileocecocolic and mesensampling unless material can be transteric) draining infected sites become ported to the laboratory immediately.

194

ENTERIC CAMPYLOBACTERIOSIS

When samples are collected in swabs, the
associated with human and animal diarrhea
use of commercially available transport
and with animal abortions. Arcobacters are
tubes containing medium, such as Amies,
usually not therrnophilic but can be
is recommended. The medium can be
confused with the nontherrnophilic
plain agar or charcoal-based. Several

Campylobacter spp if aerotolerance is
transport media have been described for
confirmed using standardized suspensions

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transport of fecal specimens, including
of organisms. Although most cases of

Cary-Blair, modified Cary-Blair, modified
human enteritis are attributed to C jejuni

Stuart medium, Campy thioglycolate
jejuni, C coli, C lmi, and C upsaliensis, it medium, alkaline peptone water, and
has been suggested that the importance of
semisolid motility test medium. Other
other species also associated with GI illness
media are recommended for the isolation
may be significantly underdiagnosed as a
of campylobacters associated with
consequence of inappropriate isolation and
reproductive losses.

identification methods.

Campylobacter spp do not ferment

Immunodiagnosis (ELISA) is unsuitable
carbohydrates, and other biochemical
to diagnose intestinal Campylobacter
characteristics are thus used to identify
infections.

different species. Them10philic/therrnotol

PCR-based methods effectively identify
erant Campylobacter spp, including
infection, especially if cultivation is difficult

C jejuni jejuni, C coli, C upsaliensis,
or if the sample has been somewhat

C lari, C mucosalis, C sputorum,
mishandled. However, a positive test is not

C hyointestinalis, and C helveticus grow sufficient evidence to determine causation
best at 42°C, although they are capable of
and must be considered in conjunction with
growth at 37°C. C fetus do not grow or grow clinical signs.

poorly at 42°C. Alternatively, this species
grows well at 25°C, whereas the therrnophilic campylobacters do not ( except Treatment and Control: Clindamycin,

C miicosalis, which can grow at 42° and
gentarnicin, tetracyclines, erythromycin,

25°C, weak growth for C hyointestinalis at
cephalosporins (eg, cephalothin), and

25°C). C jejuni is differentiated on its ability fluoroquinolones (eg, nalidixic acid) are to hydrolyze hippurate, and C upsaliensis
effective against C jejuni, C helveticus,
has negative or weak catalase production
and C upsaliensis. C fetus, C hyointesti
and is differentiated from other campylo
nalis, C mucosalis, and C sputorum are bacters because of its sensitivity to nalidixic usually resistant to the fluoroquinolones acid. C helveticus is also catalase negative yet sensitive to cephalosporins. C coli are but can be difficult to differentiate
sensitive to fluoroquinolones but resistant
biochemically from c upsaliensis relying
to cephalosporins. Susceptibilities to
on distinctive colony morphologies.

penicillins and trimethoprirn are variable

Differentiation of subspecies can be
across Campylobacter spp. Resistance to
necessary for identification of significant
the fluoroquinolones, tetracycline, kanamypathogens. C jejimi subsp jejuni is the cin, and some other antibiotics has been
main cause of enteritis, whereas C jejuni
documented among the Campylobacter
subsp doylei has beerl isolated only
spp, mediated by both chromosomal and
from enteritis cases of children and not
plasmid mechanisms. Culture-dependent
animals. They can be differentiated by
diagnosis can provide isolates for
the ability of C jejuni doylei to reduce
antibiotic sensitivity testing. However,
nitrate. Similarly, C hyointestinalis subsp some animals remain colonized and hyointestinalis can cause bovine and
become persistent shedders despite
porcine enteritis; however, C hyointesti
antibiotic therapy. If the goal of treat
nalis subsp lawsonii has been isolated ment is to decrease the risk of zoonotic
from the porcine stomach, but it is not
transmission to a susceptible household
known to cause disease. The subspecies
member, antibiotic treatment alone may
can be differentiated by testing the
be inadequate. Control involves treatment,
intolerance of C hyointestinalis
removal to a clean environment, and
lawsonii to 1.5% bile and/or 0.1%
prospective fecal testing to ascertain
potassium permanganate.

shedding status; even so, low infective

Arcobacter spp (previously known as
doses and the ubiquitous distribution of
aerotolerant campylobacters) can also be
the organism pose significant challenges.

SALMONELLOSIS

·195

SALMON ELLOSIS

Salmonella, a rod-shaped gram-negative
p 289, and INTESTINAL SALMONELLOSIS, p 296).

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bacterium belonging to the family Entero

Adult cattle, sheep, and horses commonly
bacteriaceae, is the causative agent of
develop acute enteritis, and chronic
salmonellosis. Salmonellosis in warmenteritis may develop in growing pigs and blooded vertebrates is in most cases
occasionally in cattle ( see also the chapters associated with serovars of Salmonella
on intestinal diseases in each of the major
enterica. The most common type of
domestic species, p 266, et seq). Pregnant
infection is the carrier state, in which
animals may abort. The clinically nonnal
infected animals carry the pathogen for a
carrier animal is a serious problem in all
variable period of time without showing any
host species. Salmonellosis is seen
clinical signs. Clinical disease is characterinfrequently in dogs and cats and is ized by two major syndromes: a systemic
characterized by acute diarrhea with
septicemia ( also termed as typhoid) and an
or without septicemia.

enteritis. Other less common clinical presentations include abortion, arthritis, respira

Etiology and Pathogenesis: Salmoneltory disease, necrosis of extremities, and losis has been recognized in all parts of the
meningitis.

world but is most prevalent in regions witl1

Only a few serotypes produce clinical
intensive animal husbandry. Although this
salmonellosis in healthy animals and
facultative intracellular patl10gen is
typically have a narrow range of host
primarily an intestinal bacterium, it is
species, a phenomenon tern1ed serovar-host commonly found in an environment subject specificity. Salmonella enterica serovar
to fecal contamination. Feces of infected

Typhi (S Typhi) and S Paratyphi produce animals can contan1inate feed and water,
typhoid in people, S Gallinarum produces a milk, fresh and processed meats from
similar disease in poultry, S Abortusovis in abattoirs, plant and animal products used
sheep, S Choleraesuis in pigs, S Dublin in as fertilizers or feedstuffs, pasture and
cattle, etc.

rangeland, and many inert materials. The

The remaining serovars ( serotypes)

organisms may survive for months in wet,
rarely produce clinical systemic disease
wann areas such as in feeder pig barns and
in healthy, adult, nonpregnant animals.

poultry houses or in water dugouts, but they

However, they colonize in the gut of many
survive < 1 wk in composted cattle manure.

species of animals, enter the human food

Rodents and wild birds are also sources of
chain, and produce gastroenteritis in people
infection for domestic anin1als . .Pelleting of

(food poisoning). S Typhimurium and S
feeds reduces the level of contamination by

Enteritidis are the most frequent causes of
salmonellae largely as a result of the heat
enteritis in people (nontyphoidal salmoneltreatment involved.

Josis) but are also able to produce typical

Although many other Salmonella spp
typhoid infections in mice; hence, the basis
may cause enteric disease, the more
of pathogenicity is unclear. Strains from this
common ones (to some extent varying
latter group may also produce more severe
according to geographic location) in each
disease, with systemic involvement
species are as follows: cattle-S 'lyphimuresembling typhoid in very young animals if rium, S Dublin, and S Newport; sheep and they have received insufficient protective
goats-S Typhimurium, S Dublin,
antibody from their darn or when they are

S Abortusovis, S Anatum, and S Monteviparticularly susceptible, eg, as a result of old deo; pigs-S 'lyphimurium and S Choleraeage, disease, or pregnancy. The host species suis; horses-S Typhimuriun1, S Anatum,
from which a serotype is characteristically

S Newport, S Enteritidis, and Salmonella isolated is not necessarily the only species
serovar Illa 18:z4:Zz3; and poultry-S Ente1°
that can act as a host; thus, epidemiologic
itidis, S 'lyphimuriwn, S Gallinarun1, and factors are in1portant in detern1ining

SPullorum.

prevalence.

Although tl1eir resulting clinical patterns

Young calves, piglets, Jambs, and foals
are not distinct, different species of
may develop both the enteritis and
salmonellae do tend to differ in their
septicemic form (see DlARRHEA IN NEONATAL
epidemiology. Plasmid profile and

RUMINANTS, p 275, DlARRflEAL DISEASE IN FOALS, drug-resistance patterns are sometimes

196

SALMONELLOSIS
useful markers for epidemiologic studies.

intermittently shed the organism in tl1e

The prevalence of infection va.iies among
feces.

host species and countries and is much

Calves rarely become carriers but
higher than the incidence of clinical disease, virtually all adults do for variable periodswhich in food animals is commonly up to 10 wk in sheep and cattle and up to
precipitated by stressful situations such as

14 mo in horses. Adult cattle infected with

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sudden deprivation of feed, transportation,

S Dublin may excrete the organism for drought, crowding, parturition, surgery, and
yea.i-s. Infection may also persist in lymph
administration of certain drngs, including
nodes or tonsils, with no salmonellae in the
oral antibiotics. Greater susceptibility in the
feces. Latent ca.i-iiers may begin shedding
very young may be the result of high gastric
the organism or even develop clinical
pH, absence of a stable intestinal flora, and
disease under stress. A passive canier
limited immunity.

acquires infection from the envirnnment but

The usual route of infection in ente1itis
is not invaded, so that if removed from the
is fecal-oral, although infection through
environment, it ceases to be a carrier.

the upper respiratory tract and the
conjunctiva have also been reported. After

Epidemiology: In cattle, STyphimwiun1
ingestion, the organism colonizes the
is commonly associated with outbreaks of
digestive tract and invades and multiplies
enteritis in calves <2 mo old, whereas
in enterocytes and tonsillar lymphoid

S Dublin has been associated with the same tissue. Penetration of bacteria into the
condition in older calves and adult cattle.

lan1ina propria contributes to gut dan1age

In calves a.i1d lambs, S Dublin is usually
and diarrhea. The complex process
endemic on a particular fa.i111, whereas
involves attachment through fimbrial

S Typhimuriurn is frequently associated
appendages and the injection by the
with introduction of calves from infected
attached Salmonella organisms into
farms and may cause sporadic explosive
epithelial cells of proteins, which induce
outbreaks. Subclinical infection with
changes in the actin cytoskeleton that
occasional herd outbreaks may be seen
induce membrane ruffling at the cell
in adult cattle. Stressors that precipitate
surface. This entraps the Salmonella
clinical disease include deprivation of feed
bacteria and results in fluid secretion
and water, minin1al levels of nutrition, long
and their ingestion by the cell. The
transport times, calving and antibiotic
cellular infection results in activation of
prophylaxis, and mixing and crowding in
a host alarm process through signalling
feedlots.

molecules as a result of the detection of

Outbreaks of septicemic salrnonellosis in
bacterial surface proteins, which in tum
pigs a.i·e ra.i·e and usually can be traced to a
induces a strong inflammatory response
purchased, infected pig. Purchase of feeder
that generally is able to restrict the
pigs from Salmonella-free herds and use of
bacteria to the intestine .. Some serotypes
the "all-in/all-out" policy in finishing units also become localized in the reproductive
minimize exposure. Increasing use of
tract. Serotypes that are able to cause
extensive outdoor rearing increases tl1e risk
typhoid can modulate the initial host
of exposure to environmental sources of
response and suppress the intlftnunatory
infection. Passerines, gulls, and pigeons can
response. Cell destruction follows, a.i1d the
present a direct source of infection or a
bacteria are ingested by phagocytic cells
source of conta.inination of feed and water.

such as macrophages and neutrophils.

Most cases in adult horses develop after

Although neutrophils are generally able to
the stress of surgery or tra.J1Sport related to
kill Salmonella, the bacteria can survive
sales yards and deprivation of feed and
and multiply within macrophages, which
water followed by overfeeding at their
represent the main host cell type during
destination. Mares may be inapparent
infection.

shedders and shed the bacteria at paituri

As infection progresses, a true septicemia
tion, infecting newborn foals. Septicemic
may follow, with subsequent localization in
salmonellosis may occur in foals, which
brain and meninges, pregnant uterus,joints
may be endemic, or there may be outbreaks.

and distal aspects of the linlbs, and tips of

(See INTESTINAL DISEASES IN HORSES AND FOALS, the ears and tails, which can result,
p 281.)

respectively, in meningoencephalitis,

Ma.i1y dogs and cats a.i·e asymptomatic
abortion, osteitis, and dry gangrene of
ca.i-iiers of salmonellae. Clinical disease is
the feet, tail, or ears. The organism also
uncommon, but when it is seen, it is often
frequently localizes in the gallbladder and
associated with hospitalization, another
mesenteric lymph nodes, and survivors
infection or debilitating condition in adults,

SALMONELLOSIS

197
or exposure to large numbers of the

, sow·ce of infection. Several rodent species
bacteria in puppies and kittens, in which

( eg, guinea pigs, hamsters, rats, and mice)

enteritis may be common.

and rabbits are susceptible. Rodents
conunonly act as a source of infection on

Clinical Findings: Infection with
farms where the disease is endemic. Pet
localization of the pathogen in tonsils or the
turtles were once a common source of

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GI tract that is not associated with clinical
infection in people that has been virtually
disease is a common fom1 of salmonellosis
eliminated by the cwtailment of conune1�
termed as the carrier state. Canier animals
cial trafficking.

are clu·onically infected and may shed
salmonellae intermittently into the

Diagnosis: Diagnosis of salmonellosis
environment. Carrier animals can develop
depends on clinical signs and isolation of
clinical disease whenever the immune
the pathogen from feces, blood, or tissues
function is compromised or concurrent
of affected animals. The presence of
infection with another pathogen occurs.

organisms may also be sought in feed,

Enteritis with septicemia is the usual
water supplies, and feces from wild
syndrome in newborn calves, lambs, foals,
rodents and birds that may inhabit rearing
fowl, and piglets, and outbreaks may occur
premises to determine the source of the
in pigs up to 6 mo old. When systemic
organism. Bacteria are usually identified
disease occurs with enteritis as a result of
by a range of biochemical tests. Identificainsufficient inununity, illness may be acute, tion to serotype may be done, followed
with depression, fever (105° -107°F
by further subdivision on the basis of

[40.5°--4l.5°Cl), and death in 24--48 hr.

susceptibility to selected bacteriophages

Nervous signs and pneumonia may be seen

(phage typing).

in calves and pigs. Mortality may reach

Serologic tests are available and are

1000/o, depending on the host genetic
increasingly used as a diagnostic tool in
background and strain virulence.

salmonellae surveillance and control

Acute enteritis without extensive
programs. These tests are normally
systemic involvement is more conunon in
developed to identify a limited spectrum
adults as well as in young animals �l wk
of salmonellae serovars and serogroups.

old. Initially, there is fever (105°-l07°F

Serologic tests are difficult to interpret in

[40.5°--4l.5°Cl), followed by severe wate1y
individual animals, because a seropositive
dian·hea, sometimes dysentery, and often
animal may no longer be infected. Furthertenesmus. In a herd outbreak, several hours more, specificity issues mean that in may lapse before the onset of diarrhea, at
countries with low infection prevalence,
which time the fever may disappear. The
many positive results are false-positive.

feces, which vary considerably in

The clinical syndromes usually are
consistency, may have a putrid odor and
characteristic but must be differentiated
contain mucus, fibrinous casts, shreds of
from several sin1ilar diseases in each
mucous membrane, and in some cases,
species as follows: cattle-diarrhea due
blood. Rectal examination causes severe
to enterotoxigenic Escherichia coli, dysendiscomfort and tenesmus. Milk production tery due to verotoxigenic E coli, coccidioften declines precipitously in dairy cows.

osis, cryptosporidiosis, the alimentary tract

Abdominal pain is common and may be
form of infectious bovine rhinotracheitis,
severe (colic) in horses. Mortality is
bovine viral diarrhea, hemorrhagic enteritis
variable but may reach 1000/o depending on
due to Clostridium pe1fringens types B
strain virulence. A marked leukopen.ia and
and C, arsenic poisoning, secondary
neutropenia are characteristic of the acute
copper deficiency (molybdenosis), winter
disease in horses. ln dogs and cats, clinical
dysentery, paratuberculosis, ostertagiosis,
disease takes the form of acute diarrhea
and dietetic dian·hea; sheep-enteric
with septicemia and is seen occasionally in
colibacillosis, septicemia due to Haemo
puppies and kittens or in adults stressed by
philus sp or pasteurellae, and coccidiosis; concurrent disease. Pneumonia may be
pigs-enteric colibacillosis and Clostrid
evident. When the enteritis becomes more
ium difficile of newborn pigs and
chronic, abortion may occur in pregnant
weanlings, swine dysentery (Bra.chyspira
dogs, cats, cattle, horses, and sheep, and
hyodysenteriae), campylobacteriosis, and
live progeny may have enteritis as well.

the septicemias of growing pigs (which

Conjunctivitis is sometimes seen in
include erysipelas, Lawsonia intracellula
affected cats.

ris, classical swine fever, and pasteurello

Fur-bearing and zoo carnivores may be
sis); horses-septicemia ( due to E coli,
affected. Contaminated feed is often the

Actinobacillus equuli, or streptococci);

198

SALMONELLOSIS
poultry-colifonn enteritis and Yersinia
different bacte1ia. Resistance to quino
pseudo tuberculosis.

lones is mutational, but random muta

Lesions: Lesions are most severe in the
tions may be selected by antibiotic use
lower ileum, cecum, and spiral colon and
and may be transferred by bacteriophages.

vary from shortening of villi with loss of the

Treatment should be continued daily for
epitheliwn to complete loss of intestinal
up to6days.

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architecture. There is infiltration of the

If oral medication is chosen, it should be
lan1ina propria with neutrophils and later
given in drinking water and not mixed into
with macrophages, and thrombi may be
solid feed, because affected aninlals are
seen in capillaries in this region. Hemorthirsty due to dehydration and their appetite rhage and fibrin strands are usually seen,

1s generally poor. Fluid therapy to correct
and there may be a fibrinonecrotic crust on
acid-base imbalance and dehydration may
the surface of the intestinal mucosa. Culture be necessary. Calves, adult cattle, and techniques that involve suppression of fecal
horses need large quantities of fluids. Antibi

E coli are usually necessary, and several
otics such as ampicillin or cephalosporins
daily fecal cultures may be necessary to
lead to lysis of the bacteria with release
isolate the organism. A nonselective
of endotoxin, and NSAIDs or flunixin
enrichment stage may be required for san1-
meglunline may be used to reduce the
ples in which bacteria may be present in
effects of endotoxemia.

low numbers, as in foodstuffs. This may be

The intestinal form is difficult to treat
followed by enrichment in selective broth
effectively in all species. Although clinical
and plating for colonies_ on a variety of

�ure may be .achieved, bacteriologic cure
selective agars that suppress other enteric

1s difficult, either because the organisms
bacteria likely to be present in the gut.

become established in the biliary system

Blood cultures in septicemic aninlals may
and are intennittently shed into the
be rewarding but are costly.

intestinal lumen, or because the animals
are reinfected from the environment at a

Treatment: Early treatment is essential
time when their normal gut flora which is
for septicemic salmonellosis, but there is
inhibitory to colonization by pathogens, is
controversy regarding the use of antimidepleted by antibiotic therapy. A concern crobial agents for intestinal salmonellosis.

with m1tin1icrobial therapy is that it may

Oral antibiotics may be ineffective and
increase the risk of creating carrier animals·
may deleteriously alter the intestinal
in people and other aninlal species
microflora, thereby interfering with
antimicrobial therapy prolongs th� period
competitive antagonism and prolonging
after clinical recovery during which the
sheddmg of the organism. There is also
pathogen can be retrieved from the GI tract.

concern that antibiotic-resistant strains of
salmonellae selected by oral antibiotics

Control and Prevention: Carrier
may subsequently infect people. By
aninlals and contaminated feedstuffs and
suppressing antibiotic-sensitive compoenvironment are major problems. Drain nents of the nonnal flora, antibiotics may
swabs or milk filters may be cultured to
also promote transfer of antibiotic
monitor the salmonellae status of a herd.

resistance from resistant !';trains of E coli

Th.e principles of control include prevention
to B_almonella. Use of chemotherapeutic
of mtroduction and limitation of spread
ant1b10t1cs for growth stimulation has been within a herd. In many countries and in the banned in many countries for this reason.

EU, government-backed programs have

Broad-spectrum antibiotics adminisbeen introduced to control and reduce tered systemically are indicated for
levels of infection in food aninlals
treatment of septicemia. Initial antimicroespecially poultry and pigs.

bial therapy should be based on knowledge

Prevention of Introduction: Every effort
of the drug resistance pattern of the
must be made to prevent introduction of a
organisms previously found in the area.

carrier; ideally, animals should be pur

Nosocomial infections may involve highly
chased directly only from farms known to
drug-resistant organisms. Trimethoprimbe free of the disease and should be isolated sulfonamide combinations may be
for �l wk while their health status is
effective. Alternatives are ampicillin
monitored. Ensuring that feed supplies are
fluoroquinolones, or third-generatio�
free of salmonellae depends on the integrity
cephalosporins. Resistance to ampicillin
of the source. Some countries also test for
trimethoprim, sulfonamide, tetracycline�,
contamination of and regulate importation
and ammoglycos1des 1s generally plasmid
and home production of feedstuffs and feed
mediated and transfers readily between
components.

TYZZER DISEASE

199

Limitation of Spread Within a Herd:

induce a lower level of protection. In

In an outbreak of salmonellosis, the
several studies, live attenuated Salmonella
following procedures should be implevaccines in pigs, cattle, and chickens mented: 1) Carrier animals should be
stimulated a strong cell-mediated immune
identified and either culled or isolated and
response and protected animals against
treated vigorously. Treated animals must
both systemic disease and intestinal
be rechecked several times before there
colonization. A live attenuated S Cholerae

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can be confidence they are not carriers.

suis vaccine licensed for use in swine

2) The prophylactic use of antibiotics in
appears to effectively reduce colonization
feed or water supplies may be considered
of tissues and protect pigs from disease

(the hazards are mentioned earlier).

after challenge with virulent organisms

3) Movement of animals around the farm
and under field conditions. This vaccine
should be restricted to limit infection to
also protected calves against experimental
the smallest group. Random mixing of
challenge with S Dublin and serogroup C l animals should be avoided. 4) Feed and
salmonellae after intranasal or SC
water supplies must be protected from
administration. A live S Gallinarum
fecal contamination. 5) Contan1inated
vaccine has been shown to be effective not
buildings must be vigorously cleaned and
only againstS Gallinarum (fowl typhoid)

disinfected. 6) Contaminated material
but also in significantly reducing the
must be disposed of carefully. 7) All
infection of laying hens challenged with
persons should be aware of the hazards of

S Enteritidis.

working with infected animals and the
importance of personal hygiene. A strict

Zoonotic Risk: Infections with
farm management program should be

Salmonella in food-producing animals
introduced. 8) Use of a vaccine should be
present a serious public health concern,
considered, particularly in an outbreak
because food products of animal origin
involving pregnant cattle, pigs, or laying
are considered to be a significant source
poultry. Commercial killed bacterins or
of human infection. Most common
autogenous bacterins may be used. Live
sources of infection are eggs and related
attenuated vaccines show considerable
products, and meat from poultry and
promise, but few are available commerother food animal species (seep 2865).

cially (see below). 9) Stresses should be

Milk and dairy products have also been
minimized.

associated with outbreaks of salmonellosis in people. In addition, contamination

Salmonella Vaccines: Salmonellae of fruit and vegetables by infected water
are facultative intracellular bacteria, and
may also be a source of infection. In
a live vaccine is therefore expected to be

Europe, S Enteritidis and S Typhimurium, necessary for optimal immune protection
and in the USA, S Typhimurium are the against disease; however, there is some
most prevalent serovars associated with
evidence that inactivated bacterins can
human disease.

TYZZER DISEASE

Tyzzer disease is an enterohepatic
cottontail rabbit, coyote, gray fox, lesser
syndrome of a wide range of anin1als ( see
panda, snow leopard, raccoon, marsupials,
p 1948) and is seen worldwide. Tyzzer
and white-tailed deer.

disease was first desc1ibed in mice in 1917.

The disease p1irnaiily affects young,

Several years later, it was reported in
well-nourished animals, especially those fed
laboratory rabbits and then in other small
high-protein diets, during periods of stress.

laboratory mammals, including guinea pigs,

Some species appeai· resistant unless
hamsters, gerbils, and rats. It is a highly fatal stressed or imrnunosuppressed, whereas disease of young foals. The disease is rare in
others appear to be susceptible without
other domestic animals, including dogs,
inununosuppression. Dietary factors,
cats, and calves. It has been reported in a
including excessive nitrogenous diets fed to
variety of wildlife, including m'uskrats,
laboratory animals and to nursing mares,

200

TYZZER DISEASE
seemingly may cause immunosuppression
the epithelial ai1d smooth muscle cells of
and may predispose susceptible animals to
the intestines, hepatocytes, ai1d cardiac
the disease. Other irnrnunosuppressive
myocytes. Stress factors such as capture,
agents and drugs and some antibacterials,
overcrowding, shipping, and poor sanitation
especially sulfonanudes, may also
appear to be predisposing. Sulfonanude
predispose animals to the disease.

administration predisposes rabbits to the

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Under laboratory conditions, stress is
disease. Mortality is highest at weaning age
created by i.mmunosuppressive drugs or
in rabbits. The disease in foals occurs most
other factors that can be easily identified.

often between 1 ai1d 6 wk of age, with most

With many experiments, stress may be
cases occurring between 1 and 2 wk of age.

involved as part of the protocol, and when

In some species, the disease has been
the disease develops, it is devastating.

identified concurrently with other diseases,
eg, feline infectious peritonitis in cats,

Etiology and Pathogenesis: The
distemper and mycotic pneumonia in dogs,
disease is caused by Clostridium pili
and cryptosporidial ai1d coronaviral
f01me, a motile, spore-fonning, rod-shaped, enteritis in calves.

flagellated, obligate, intracellular bacterium.

The disease in foals is more common

It does not grow in cell-free media but can
during the spring when nursing mares are
be cultured in the yolk sac of chick embryos
exposed to lush, high-protein pastures. The
or tissue culture cells. The vegetative phase
increase in the availability of nutJ.ients from
is very labile; spores may srnvive in soiled
pasture forages and supplemental diets may
bedding at room temperature for> 1 yr and
encourage the overgrowth of C piliforme in
are resistant to heating up to 60°C for 30
the gut of nursing mares; tlus seemingly
min, or e:Kposure to 700,.i, ethanol, 3% cresol,
predisposes neonatal foals to the disease

4% chlorhexidine, and 0.037% formaldewhen they ai·e exposed to massive nwnbers hyde; however, they are sensitive to 0.4%
of the bacteriwn after consunung the feces
peracetic acid, 0.015% sodiun1 hypochlorite,
of their dan1s soon after birth as a mecha-

1 % iodophor, and 5% phenol.

11ism to establish tl1eir normal intestinal

C piliforme appears to be common in the
flora. The in1mature gut is likely more
environment, but because it is difficult to
penneable to pathogens like C piliforme.

culture, very little knowledge has been

The disease in young foals primaiily
accun1ulated on the epidenuology,
affects the liver, where it induces a massive
pathogenesis, and inununity. Wection most
multi focal necrosis and hepatitis, and foals
likely results from oral exposure to spores
die of acute liver failure. In contrast, in
from the environment. The feces of infected
other aiumals, which generally are older
and carrier animals are the prin1ary source
when infected, the bacteriwn affects the
of spores that contanunate the environintestinal tract and to a lesser extent the ment.

liver and heart.

C pilif01me infections we often

Older foals up to 6 wk of age become
subclinical or asymptomatic but may be
more resistant to the disease as the gut
severe in many animal species. There may
becomes more mature and in1mune facbe differences in susceptibility within tors may be involved. The disease is not
aiurnal species. B lymphocytes, T lymphorecognized in older foals and adults, but cytes, and natural killer cells may play a role they carry tl1e bacteriun1 in their gut.

in mediating strain susceptibility. Seroanaly

Immune factors appear to be involved
sis using monoclonal antibody-based
with the disease in horses, because many
competitive inhlbition ELISA suggests that
adults have antibodies for C piliforme yet

Tyzzer disease may be relatively common in
do not develop Tyzzer disease. Only young
horses, which are susceptible to at least two
foals up to 6 wk old develop lesions. The
distinct strains.

disease is more common in foals when

Some isolates of C piliforme produce
young nursing mares are introduced to a
toxins, whereas others do not. The role of
farm where the disease is endemic and is
these toxins in the pathogenesis of infection
less common in suckling foals on older
is unknown, but the toxic isolates are
mares; this suggests that older mares are
generally more virulent than nontoxic
immune to the disease and may be secreting
isolates. The toxigenic strains appear more

C pilifo1me antibodies in the colostrwn
likely to induce hepatic lesions in mice,
that protects young foals.

whereas the nontoxigenic strains do not.

The primary site of infection is the lower
intestinal tract with subsequent dissemina

Clinical Findings: The disease often
tion via the blood or lymphatics to the liver
affects apparently healthy, fast-growing
and heart. The bacterium has an affinity for
foals without previously observed clinical

TYZZER DISEASE

201
signs. The incubation period in experimenand colon of rabbits, patchy areas of tally infected foals is 4-7 days after oral
necrosis extend as deep as tl1e muscularis
exposure to bacterial spores. Most foals are
extema with associated mucosa! and
found in a coma or dead. Clinical signs, if
submucosal infiltrates of neutrophils.

seen, are of short duration, from a few hours Organisms may be found within the to up to 2 days. Signs are variable but may
epitheliwn, muscularis mucosa, and

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include depression, anorexia, pyrexia,
muscularis externa of the affected intestine.

jaundice, diarrhea, and recun1bency.

When cardiac lesions are present, they

Terminally, there are convulsions and coma. consist of foci of fiber fragmentation, Clinical signs vary between animal species.

vacuolation, loss of cross-striations, and

Laboratory animals may be found dead at
mininlal inflammatory cell infiltration.

the start of an outbreak. As the disease
progresses, animals may show depression,

Diagnosis: Serology of the blood and

1uffled coat, and varying degrees of wate1y

PCR assay of tl1e feces of suspect infected
diarrhea.

animals may be used clinically to test for

Clinicopathologic tests are of little value

C pilifoime. However, clinical signs in
in laboratory animals, because they die so
addition to the commonly available
rapidly. In foals, the serum enzymes sorbitol diagnostic methods must be interpreted dehydrogenase, AST, alkaline phosphatase,
together for a preswnptive clinical
lactate dehydrogenase, and -y-glutamyldiagnosis.

transferase are increased. There is also

In postmortem specimens, a diagnosis is
hyperbilirubinemia, leukopenia, hemoconbased on demonstration of organisms in centration, and terminally profound
tissue sections with special stains. C pili
hypoglycemia.

forme stains poorly with H&E and Gram

Lesions: Characteristic lesions are seen
stains. With Giemsa stain, tl1e bacillus stains
in the liver, myocardiun1, and intestinal
well in the liver and intestinal epitl1eliun1 and
tract. In the liver, white, gray, or yellowish
in smears of infected organs but poorly in
foci of necrosis, 2 mm in diameter, are few
smooth muscles and cardiac muscle cells.

to disseminated. The hepatic necrosis is

The Warthin-Starry or Levaditi silver stains
most marked and disseminated in foals
are preferable to other stains, because tl1e
in which the multiple necrotic foci with
bacillus stains well in the cytoplasm of
slightly depressed hemorrhagic centers
all infected cells. In addition to special
appear to infect almost every hepatic lobule. histochemical stains, tl1e PCR assay can be In addition, there is marked hepatomegaly,
used to detect C piliforme gene sequences
and the hepatic lymph nodes are edematous in liver tissues from infected animals.

and hyperplastic. In rabbits, severe lesions
develop in the intestines and heart. The

Treatment and Control: Little is known
terminal ilewn, cecwn, and proximal colon
about the effectiveness of antibiotics for
are diffusely reddened. Diffuse ("painttreatment. Some antibiotics are known to brush") hemorrhage is frequently seen on
aggravate the disease. C piliforme is
the serosa of the cecun1. Patchy areas of
sensitive to tetracycline and pattially
mucosa! necrosis are present in the cecun1
sensitive to streptomycin, erythromycin,
and colon, together with marked edema of
penicillin, at1d chlortetracycline. It is resistatlt the wall of the cecum. Mesenteric lymph
to sulfonatnides and cllloramphenicol.

nodes may be enlarged and edematous.

In neonatal foals, the disease seems to be

White streaks in the myocardiun1 may be
neai·ly lO()OA, fatal, altl10ugh it is likely that
present, especially near the apex. Intestinal
older foals less severely affected may
and heart lesions are generally milder or
survive. Once the disease is present on a
absent in other animal species.

fa.tin, it may be seen sporadically year after

Microscopically, there are nwnerous
year. Animals suspected of being infected
widespread multifocal areas of necrosis and have been treated IV initially with 5()0A, hepatitis. In foals, the hepatic lesions are
dextrose, followed by lOOA, dextrose, other
more pronounced than in otl1er animals.

fluid therapy, and antibiotics. Most foals

Often the necrotic foci are so nwnerous that respond dramatically to the dextrose two or more coalesce. The hepatocytes in
therapy but relapse into a coma and die
the center of the necrotic foci are destroyed
in a few homs. A few preswnptive cases
and replaced by a mixture of mononuclear
of'Iyzzer disease in foals have been treated
cells, neutrophils, and red blood cells. The
successfully by intensive administration of
causative bacteria are found in a crisscross

IV dextrose, sodiwn bicarbonate, potassiwn
pattern in viable hepatocytes at the
chloride, penicillin, and sulfamethoxazoleperiphery of the necrotic foci. In the- cecwn trin1ethoprim.

202

TYZZER DISEASE

Because the disease in foals is sporadic
and nitrate in the diet that may induce
and not highly contagious, specific
immunosuppression in neonatal foals,
preventive measures are usually not
may lessen the incidence of the disease.

indicated. In areas where endospores are

In general, factors that cause stress and
present in the environment, many foals may
immunosuppression should also be
be exposed; however, only a few that are
reduced. When the disease is seen in a

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inununosuppressed become acutely
colony of laboratory animals, treatment is
affected. On premises where the disease is
not recommended because it prolongs the
prevalent, overfeeding of mares, especially
disease and possibly produces carrier
with high-protein diets seemingly predisanimals. It is best to destroy all animals in pose neonatal foals. Reducing the nitrogthe colony, decontaminate the environment, enous dietary compounds, including protein and restock with disease-free animals.

AMEBIASIS

(Amebiosis)

Arnebiasis is an acute or chronic colitis,
show weight loss, anorexia, tenesmus, and
characterized by persistent diarrhea or
chronic diarrhea or dysentery, which may
dysentery, that is prevalent in tropical and
be continual or intem1ittent. In addition to
subtropical areas worldwide. Its prevathe colon and cecwn, a.rnebae may invade lence has declined in the USA over the
perianal skin, genitalia, liver, brain, lungs,
past several decades, but the disease is
kidneys, and other organs. Signs may resemstill impo1tant in many tropical areas, ble those of other colonic diseases ( eg,
particularly in times of disasters. It is comtrichwiasis, balantidiasis). Invasive mon in people and nonhuman primates,
arnebiasis is exacerbated by in1munosometimes seen in dogs and cats, and rare suppression.

in other mammals. Several species of
arnebae are found in man1mals, but the
only known pathogen is Entamoeba

Diagnosis: Definitive diagnosis depends
histolytica. People are the natural host
on finding£ histolytica trophozoites or
for this species and the usual source of
cysts in feces. Trophozoites are best seen in
infection for domestic animals. Mammals
direct saline smears or in stained sections of
become infected by ingesting food or
affected colonic tissue. These parasites are
water contan1inated with feces containing
difficult to find, because many anin1als with
infective cysts. E dispq,r is a noninvasive, extra.intestinal arnebiasis have no concurnonpathogenic arneba that is molecularly rent intestinal infection. Colonoscopy with
distinct but morphologically indistinscraping or biopsy of ulcerations is more guishable from the pathogenic species
effective than fecal examination in

E histolytica. E invadens of reptiles is
diagnosing amebic colitis. In intestinal
also morphologically identical to E
infections, repeated examinations may be
histolytica, but it is not transmissible
necessary, because parasites may be passed
to mammals.

periodically in the feces.

Trophozoites range in size from 10 to 60 µm
but usually are >20 µmin dian1eter, have a

Clinical Findings: E histolytica is a single vesicular nucleus ( usually with a
pathogen with variable virulence. It lives in
central karyosome ), are motile, and may
the I w11en of the large intestine and cecwn
contain ingested RBCs. Feces should be
and may produce no obvious clinical signs,
examined promptly, because the trophozoor it may invade the intestinal mucosa and ites die quickly once outside the body. Fecal
produce mild to severe, ulcerative,
leukocytes may be mistaken for amebae, so
hemorrhagic colitis. In acute disease,
fixed and stained fecal smears (iodine,
fulminating dysentery may develop, which
tlichrome, iron hematoxylin, or periodic
may be fatal, progress to clu·onicity, or
acid-Schiff reaction) may be necessary for
resolve spontaneously. Chronic cases may
identification.

COCCIDIOSIS

203

Cysts range from 10 to 20 µm in diameter;
dazole (10-25 mg/kg, PO, bid for 1 wk) or
the usual size is 12-15 µm. Mature cysts
furazolidone (2-4 mg/kg, PO, tid for 1 wk)

have four nuclei, whereas immature cysts
has been suggested. Dogs may continue to
may have one or two. In primates, the cysts
shed trophozoites after therapy. Treatment
may be recovered and identified on zinc
recommendations for people are available
sulfate flotations or in fixed and stained
from the CDC Web site. For asymptomatic

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preparations (iodine, trichrome, or iron
infections in people, the CDC lists
hematoxylin); however, E histolytica cysts
iodoquinol, paromomycin, or diloxanide
are seldom, if ever, excreted by dogs or cats.

furoate (not conunercially available in the

An ELISA-based antigen test, available for

USA) as drugs of choice, and for symptodiagnosis in people, may also aid diagnosis matic intestinal disease or extraintestinal
in other mammals. lmmw10staining may
infections in people ( eg, hepatic abscess),
also be useful.

the drugs of choice are metronidazole or
tinidazole, inunediately followed by

Treatment: Scant information on
treatment with iodoquinol, paromomycin,
treatment in anin1als is available. Metroni-
or diloxanide furoate.

COCCIDIOSIS

Coccidiosis is usually an acute invasion
prevalent under conditions of poor
and destruction of intestinal mucosa by
nutrition, poor sanitation, or overcrowding,
protozoa of the generaEimeria or
or after the stresses of weaning, shipping,

Jsospora. Clinical signs include diarrhea,
sudden changes of feed, or severe weather.

fever, inappetence, weight loss, emaciation,

In general, for most species of farm
and in extreme cases, death. However,
animals, the infection rate is high and rate of
many infections are subclinical. Coccidiosis
clinical disease is low (5%---10%), although
is an economically important disease of
up to 80% of animals in a high-risk group
cattle, sheep, goats, pigs, poultry (see
may show clinical signs. Most animals
p 2791), and also rabbits, in which the liver
acquire Eimeria or Jsospora infections of as well as the intestine can be affected (see
varying severity when between 1 mo and
p 1952). In dogs, cats, and horses, coccidil yr old. Older animals usually are resistant osis is less often diagnosed but can result
to clinical disease but may have sporadic
in clinical illness. Other genera, of both
inapparent infections. Clinically healthy,
hosts and protozoa, can be involved (see
mature animals can be sources of infection

CRYPTOSPORIOIOSIS, p 209, SARCOCYSTOSIS,
to young, susceptible animals.

p 1058, and TOXOPLASMOSIS, p 685).

Etiology and Epidemiology: Eimeria

Pathogenesis: Wection results from
and I sospora typically require only one host ingestion of infective oocysts. Oocysts enter in which to complete their life cycles. Some
the environment in the feces of an infected
species of Isospora have facultative
host, but oocysts of Eimeria and Isospora intem1ediate (paratenic or transfer) hosts,
are unsporulated and therefore not infective
and a new genus nan1e, Cystoisospora, has
when passed in the feces. Under favorable
been proposed for these species of
conditions of oxygen, humidity, and

Isospora. Coccidia are host-specific, and
temperature, oocysts sporulate and become
there is no cross-inunWlity between species
infective in several days. During sporulaof coccidia.

tion, the amorphous protoplasm develops

Coccidiosis is seen Wliversally, most
into small bodies (sporozoites) within
conunonly in young animals housed or
secondary cysts ( sporocysts) in the oocyst.

confined in small areas contan1inated with

In Eimeria spp, the sporulated oocyst has
oocysts. Coccidia are opportWlistic
four sporocysts, each containing two
pathogens; if pathogenic, their virulence
sporozoites; in Isospora. spp, the sporulated may be influenced by various stressors.

oocyst has two sporocysts, each containing

Therefore, clinical coccidiosis is most
four sporozoites.

204

COCCIDIOSIS

When the sporulated oocyst is ingested
infective oocysts ingested, stage of the
by a susceptible animal, the sporozoites
infection, age and inlrnune status of the
escape from the oocyst, invade the
aninlal, prior exposw-e, consistency of the
intestinal mucosa or epithelial cells in other
fecal sample (free water content), and
locations, and develop intracellularly into
method of examination. Therefore, the
multinucleate schizonts (also called
results of fecal exan1inations must be

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meronts). Each nucleus develops into an
related to clinical signs and intestinal
infective body called a merozoite; merozolesions (gross and microscopic). Furtherites enter new cells and repeat the process.

more, the species must be detem1ined to

After a variable number of asexual
be pathogenic in that host. The finding of
generations, merozoites develop into either
numerous oocysts of a nonpathogenic
macrogametocytes (females) or microgaspecies concw-rent with diarrhea does metocytes (males). These produce a single
not constitute a diagnosis of clinical
macrogamete or a number of microgan1etes
coccidiosis.

in a host cell. After being fertilized by a
microgamete, the macrogamete develops

Treatment: The life cycles of Eimeria and into an oocyst. The oocysts have resistant

Isospora are self-limiting and end spontanewalls and are discharged unsporulated in ously within a few weeks unless reinfection
the feces. Oocysts do not survive well at
occurs. Prompt medication may slow or
temperatw-es below -30°C or above 40°C;
inhibit development of stages resulting from
within this temperatw-e range, oocysts may
reinfection and, thus, can sho1ten the length
survive ;,, 1 yr.

of illness, reduce discharge of oocysts,

Of the nurnerous species of Eimeria or alleviate hemorrhage and diarrhea, and

I sospora that can infect a particular host, lessen the likelihood of secondary infections
not all are pathogenic. Concw-rent
and death. Sick animals should be isolated
infections with two or more species, some
and treated individually whenever possible
of which may not nom1ally be considered
to ensure delivery of therapeutic drug levels
pathogenic, also influence clinical disease.

and to prevent exposure of other aninlals.

Within pathogenic species, strains may vary

However, the efficacy of treatment for
in virulence.

clinical coccidiosis has not been demonstrated for any drug, although it is widely Clinical Findings: Clinical signs of
accepted that treatment is effective against
coccidiosis are due to destruction of the
reinfection and should therefore facilitate
intestinal epitheliun1 and, frequently, the
recovery.

underlying connective tissue of the mucosa.

Most coccidiostats have a depressant effect

This may be accompanied by hemorrhage
on the early, first-stage schizonts and are
into the lumen of the intestine, catarrhal
therefore more appropriately used for control
inilan1mation, and diarrhea. Signs may
instead of treatment. Soluble sulfonamides
include discharge of blood or tissue,
are conunonly administered orally to calves
tenesmus, and dehydration. Serum protein
with clinical coccidiosis and are perceived to
and electrolyte concentrations (typically
be more effective than intestinal sulfonanlide
hyponatremia) may be appreciably altered,
fom1ulations (boluses). Amproliw11 is also
but changes in Hgb or PCV are seen only in
administered orally to calves, sheep, and
severely affected aninlals.

goats with clinical coccidiosis. Preventive
treatment of healthy exposed aninlals as a

Diagnosis: Oocysts can be identified in
safeguard against additional morbidity is an
feces by salt or sugar flotation methods.

inlp01tant consideration when treating

Finding appreciable nun1bers of oocysts of
individual animals with clinical signs. The
pathogenic species in tl1e feces is diagnostic

FDA is changing the marketing status of

(>100,000 oocysts/g of feces in severe
drugs, such as the sulfonamides that are used
outbreaks), but because diarrhea may
in human medicine, from over-the-counter to
precede the heavy output of oocysts by

(veterinary) prescliption for water medica1-2 days and may continue after the oocyst tion or Veterinary Feed Directive (VFD) for
discharge has returned to low levels, it is not
feed medication. Drugs, such as the
always possible to find oocysts in a single
ionophores, that are not used in human
fecal sample; multiple fecal examinations of
medicine will continue to have an ove1�theone animal or single fecal examinations of counter marketing status.

animals housed in the same environment
may be required. The munber of oocysts

Prevention: Prevention is based on
present in feces is influenced by the
linliting the intake of sporulated oocysts
genetically detemlined reproductive
by young animals so that an infection is
potential of the species, the number of
established to induce in1munity but not

COCCIDIOSIS 205
clinical signs. Good feeding practices and
considered part of the neonatal diarrhea
good management, including sanitation,
complex in calves.

contiibute to this goal. Neonates should

The most typical syndrome of coccidiosis
receive colostnun. Young, susceptible
is chronic or subclinical disease in groups of
animals should be kept in clean, dry
growing animals. Calves may appear
quarters. Feeding and watering devices
unthrifty and have fecal-stained perinea!

should be clean and must be protected from
areas. In light infections, cattle appeai·

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fecal contamination; this usually means
healthy a.t1d oocysts are present in normally
feed is placed in troughs above the ground
fmrned feces, but feed efficiency is reduced.

and positioned so that it is difficult for fecal

The most characteristic sign of clinical
contan1ination of feed to occur. Stresses
coccidiosis is watery feces, with little or

(eg, weaning, sudden changes in feed, and
no blood, and animals show only slight
shipping) should be minimized.

discomfort for a few days. Severe infections

Preventive administration of coccidioare rare. Severely affected cattle develop stats is recommended when animals under
thin, bloody diarrhea that may continue for
vaiious management regimens can be

> 1 wk, or thin feces with streaks or clots of
predictably expected to develop coccidioblood, shreds of epithelium, and mucus.

sis. In virtually all cases, Eimeria spp are They may develop a fever; become anorectic,
implicated. Decoquinate and ionophorous
depressed, and dehydrated; and lose weight.

antibiotics ai·e widely used for this purpose

Tenesmus is common because the most
in young run1inants. Continuous low-level
severe enteritis is confined to the large
feeding of decoquinate, lasalocid, monenintestine, although pathogenic coccidia of sin, or amproliurn during the first month of
cattle ca11 damage the mucosa of the lower
feedlot confinement has been reported to
small intestine, cecum, and colon. DLUing the
have preventive value. Ionophorous
acute period, some calves die; others die
antibiotics and amprolium have been
later from secondary complications ( eg,
reported to be effective in goat kids, as have
pneun10nia). Calves that survive severe
sulfonan1ides and an1prolimn in pigs.

illness can lose significant weight that is not
quickly regained or can remain perma11ently
stLU1ted. Calves with concurrent enteric

COCCIDIOSIS OF CATTLE
infections ( eg, Giardia) may be more
severely affected thai1 calves with coccidia

Twelve Eimeria spp have been identified in
infections alone. In adclition, management
the feces of cattle worldwide, but only three
factors, such as weather, housing, feeding

(E zuernii, E bovis, and E auburnensis) practices, a.t1d how at1irnals are grouped, are
are most often associated with clinical
importa.t1t in detennining the expression
disease. The other Eimeria spp have been
of clinical coccidiosis in cattle.

shown experimentally to be mildly or

Nervous signs ( eg, musculai· tremors,
moderately pathogenic but ai·e not
hyperesthesia, clonic-tonic convulsions.

considered important pathogens.

with ventroflexion of the head a.t1d neck,

Coccidiosis is commonly a disease of
nystagmus) a.t1d a high mortality rate
young cattle (1-2 mo to 1 yr) and usually is

(800/c,-900/o) are seen in some calves with
sporadic dLUing the wet seasons of the year.

acute clinical coccidiosis. Outbreaks of this

"Sununer coccidiosis" and "winter coccidio

"nervous form" are seen most commonly
sis" in range cattle probably result from
during, or after, severely cold weather in
severe weather stress and crowding around a midwinter in Canada and the northern USA; limited water somce, which concentrates the there are no reports of the "nervous form"

hosts and parasites within a restlicted area.

outside this geographic location. Affected

Although particulai·ly severe epidemics have
calves may die <24 hr after the onset of
been reported in feedlot cattle dLUing
dysentery a.t1d nervous signs, or tl1ey may
extremely cold weather, cattle confined
live for several days, commonly in a laterally
to feedlots are susceptible to coccidiosis
recumbent position with a mild degree of
throughout the yeai·. Outbreaks usually occm opisthotonos. Nervous signs have not been within the first month of confinement. Cows
reported in experin1ental clinical coccidimay contribute to environmental contaminaosis in calves, which suggests that the tion of E bovis oocysts through a petiparturinervous signs may be unrelated to the ent increase in fecal oocy�t counts. Time to
dysentery or, indeed, even to coccidiosis.

onset of dian·hea after infection is 16--23 days

Diagnosis of coccidiosis is by finding
for E bovis and E zuernii and 3-4 days for oocysts on fecal flotation or direct smear or

E alabamensis; clinical disease due to
by the McMaster technique. Qua11titative
coccidiosis does not typically occm in the
oocyst counts on individual rectal samples
first 3 wk of life. Coccidiosis is therefore not
from at least five calves in a pen are helpful

206

COCCIDIOSIS
to confirm coccidiosis as a cause of clinical
presence of appropriate feed bunks, or
disease. Differential diagnoses include
use of chemotherapeutics, to control the
salmonellosis, bovine viral diarrhea,
numbers of oocysts ingested by the aninlals
malnutrition, toxins, or other intestinal
while effective inununity develops.

parasites.

Coccidiostats are used to control naturally

Coccidiosis is a self-limiting disease, and
occurring coccidiosis. The ideal coccidiostat

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spontaneous recovery without specific
suppresses the full development of the life
treatment is conunon when the multiplicacycle of the coccidia, allows inunwlity to tion stage of the coccidia has passed.

develop, and does not interfere with

Drugs that can be used for therapy of
production performance. Sulfonanlides in
clinically affected animals include
the feed at 25-35 mg/kg for �15 days are effecsulfaquinoxaline (6 mg/lb/day for 3-5 days) tive to control coccidiosis in calves.

and amprolium (10 mg/kg/day for 5 days).

Monensin is an effective coccidiostat and

Sulfaquinoxaline is particularly useful for
growth promotant in calves. Postweaning
weaned calves that develop bloody diarrhea
coccidiosis in beef calves has been controlled
after arrival at a feedlot. For prevention,
using monensin administered via intralw1liamprolium (5 mg/kg/day for 21 days), nal continuous-release devices. Lasalocid is
decoquinate (22. 7 mg/45 kg/day for 28 days)

related to monensin and is also an effective
and lasalocid (1 mg/kg/day to a maximw11 of coccidiostat for rwninants. Mixing lasalocid 360 mg/head/day), or monensin (100-360
in the milk replacer of calves beginning at
mg/head/day) can be used. The major

2-4 days of age is an effective way to control
benefits of coccidiostats are through
coccidiosis. Lasalocid is also effective as a
improved feed efficiency and rate of gain.

coccidiostat when fed free-choice in salt at a
ln an outbreak, clinically affected animals
level of 0. 75% of the total salt mixture. A level
should be isolated and given supportive oral
of 1 mg/kg is the most effective and rapid
and parenteral fluid therapy as necessary.

and is recommended when outbreaks of

The population density of the affected pens
coccidiosis are inuninent. Decoquinate in
should be reduced. All feed and water
the feed at 0.5--1 mg/kg suppressed oocyst
supplies should be high enough off the
production in experimentally induced
ground to avoid fecal contamination. Mass
coccidiosis of calves. Decoquinate is most
medication of the feed and water supplies
effective in preventing coccidial infections
may be indicated in an attempt to prevent
when fed continually in dry feed at 0.5 mg/kg.

new cases and to mininlize the effects of

Monensin, lasalocid, and decoquinate at the
an epidemic. Cattle with coccidiosis and
manufacturer's reconunended levels are
ne1vous signs should be brought indoors,
equally effective. Toltrazuril administered at
kept well-bedded and warm, and given fluid

15 mg/kg as a single oral dose, 14 days after
therapy orally and parenterally. However,
anin1als are moved into group housing,
the case fatality rate of calves with
effectively prevents diaIThea due to
coccidiosis and nervous signs is high despite
coccidiosis. DiclazUiil (5 mg/kg) is being
intensive supportive therapy. Parenteral
investigated as an oral anticoccidial in calves.

sulfonanlide therapy may be indicated to

Control of infection should include
control development of secondary bacterial
changes in management factors that
enteritis or pneumonia, which nwy be seen
contribute to development of clinical
in calves with coccidiosis during very cold
disease. lnadequate housing and ventilation
weather. Corticosteroids are contraindishould be coITected, feeding practices cated, because they increase shedding of
adopted that avoid fecal contamination of
oocysts and have induced clinical disease
feed, calves grouped by size, and an "all-in/
in subclinically infected calves.

all-out" method of calf movement from pen

Coccidiosis has been difficult to control
to pen adopted.

reliably. Overcrowding of aninlals should be
avoided while they develop an inunwlity to

COCCIDIOSIS OF SHEEP
the coccidial species in the envirorunent.

Calving grounds should be well drained and
lnfection with Eimeria is one of the most
kept as dry as possible. All measures that
economically important diseases of sheep.

minimize fecal contamination of hair coats

Historically, some Eimeria spp were
and fleece should be practiced regularly.

thought to be infectious and transnlissible

Feed and water troughs should be high
between sheep and goats, but the parasites
enough to avoid heavy fecal contamination.

are now considered host-specific. The

Control of coccidiosis in feeder calves
names of some species of goat coccidia
brought into a crowded feedlot depends
are still eIToneously applied to species
on management of population density,
of sinlilar appearance found in sheep.

COCCIDIOSIS

207

E crandallis and E ovinoidalis (nina

•once at-6-8 wk of age (most common) or
kohlyakimovae) are pathogens of lambs
twice ( at 3-4 wk of age and again 3 wk later).

(usually l-6mo old);E ovina appears to be

Sulfaquinoxaline in drinking water at 0.015%
somewhat less pathogenic. Older sheep
concentration for 3-5 days may be used to
serve as sources of infection for the young.

treat affected lambs. In groups of lambs at

All other Eirneria of sheep are essentially pasture, frequent rotation of pastures for
non pathogenic, even when large numbers
parasite control also helps control coccidial

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of oocysts are present in feces.

infection. However, when lambs are

Signs include dian·hea (sometimes
exposed to infection early in life as a result
containing blood or mucus), dehydration,
of infection from the ewe and a contamifever, inappetence, weight loss, anemia, nated lambing ground, a solid inlmunity
wool breaking, and death. The ileum, cecum,
usually develops and problems are seen only
and upper colon are usually most affected
when the stocking density is extremely high.

and may be thickened, edematous, and
inflamed; sometimes, there is mucosa!

COCCIDIOSIS OF GOATS
hemonhage. Thick, white, opaque patches
containing large numbers of E ovina oocysts Numerous species of Eimeria, are found in may develop in the small intestine. Because
goats in No1th America and elsewhere. The
oocysts are prevalent in feces of sheep of all

Eimeria spp are host specific and are not
ages, coccidiosis cannot be diagnosed based
transmitted from sheep to goats.

solely on finding oocysts. Peak oocyst counts

E arloingi, E christenseni, and E ovinoi
of> 100,000/g of feces have been reported in
dalis are highly pathogenic in kids. Clinical 8- to 12-wk-old Jambs that appeared healthy.

signs include diarrhea with or without

However, diarrhea with oocyst counts of a
mucus or blood, dehydration, emaciation,
pathogenic species of >20,000/g is characterweakness, anorexia, and death. Some goats istic of coccidiosis in sheep. Immune
are actually constipated and die acutely
complex glomerulonephritis has also been
without diarrhea. Usually, stages and
attributed to coccidiosis. F1y strike and
lesions are confined to the small intestine,
secondary bacterial enteric infections
which may appear congested, hemonhagic,
may accompany coccidiosis in lan1bs.

or ulcerated, and have scattered pale,

Lambs 1-6 mo old in Jan1bing pens,
yellow to white macroscopic plaques in the
intensive grazing areas, and feedlots are at
mucosa. Histologically, villous epitheliun1 is
greatest risk as a result of shipping, ration
sloughed, and inflanlffiatory cells are seen
change, crowding stress, severe weather,
in the Jan1ina propria and submucosa. In
and contamination of the environment with
addition, there have been several reports of
oocysts from ewes or other Jambs. Because
hepatobiliary coccidiosis with liver failure
occurrence of coccidiosis under these
in dairy goats. Diagnosis of intestinal
management systems often becomes so
coccidiosis is based on finding oocysts of
predictable, coccidiostats should be
the pathogenic species in diarrheal feces,
administered prophylactically for 28 consecuusually at tens of thousands to millions per tive days beginning a few days after lambs are gram of feces. It is not unusual to find introduced into the environment. A conoocyst counts as high as 70,000/g of feces in centrated ration containing monensin at
kids without overt disease, but weight gain

15 g/tonne can be fed to ewes from 4 wk
may be affected.

before lambing until weaning, and to Jambs

Angora and dairy goats, raised under
from 4--20 wk of age. The toxic level of
different management practices, may have
monensin for Jambs is 4 mg/kg. Lasalocid
sinlilar patterns of exposure of kids. Just

(15-70 mg/head/day, depending on body wt)

after parturition, nursery pens and surroundmay be effective. A combination of monensin ing areas may be heavily contanlinated with
and lasalocid at 22 and 100 mg/kg of diet,
oocysts from does. Resistance to infection
respectively, is an effective prophylactic
is decreasedjust after shipping, changing
against naturally occurring coccidiosis in
rations, introducing new anin1als, or mixing
early weaned Jambs under feedlot conditions. young with older aninlals. Coccidiostats can Treatment of affected sheep once
be administered to a herd immediately after
coccidiosis has been diagnosed is not
diagnosis or as a preventive in predictable
effective, but seve1ity can be reduced if
situations such as those mentioned above.

treatment is begun early. A single treatment

Diagnosis and treatment are sinlilar to
of toltrazuril (20 mg/kg) can significantly
those for cattle and sheep. Sulfadirnidine at
reduce the oocyst output in naturally

55 g/tonne is also effective for control of
infected Jan1bs for -3 wk after administracoccidiosis in goats. In nonlactating goats, tion. Diclazuril (1 mg/kg) is an effective oral
adding monensin to the feed at 18 g/tonne
anticoccidial in lambs and is administered
is preventive.

208 COCCIDIOSIS

COCCIDIOSIS OF PIGS
proper cleaning, disinfection, at1d steatn
cleatling of the fatrnwing housing.

Eight species of Eimeria and one of Isospora A.mprolium (25% feed grade) at the rate infect pigs in Notth America. Piglets 5---15
of 10 kg/tonne of sows' feed statted 1 wk
days old are characteristically infected with
before fatTowing at1d continued until ilie
only I suis, which produces enteritis and
piglets are 3 wk of age has been recom

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diarrhea. These agents must be differentiated
mended, but the results at·e unsatisfactory.

from viruses, bacte1ia, and helminths that

A single dose of toltt·azmil (20 mg/kg, PO)

also cause scours in neonatal pigs.

decreased oocyst excretion, ilie incidence

I suis is prevalent in neonatal pigs.

of diatThea, at1d weight gain impairment in
lnfection is charactetized by a watery or
piglets with experimentally induced
greasy diatThea, usually yellowish to white
coccidiosis. Diclazuril (5 mg/kg) is being
and foul smelling. Piglets may appear weak,
investigated as at1 oral at1ticoccidial in
dehydrated, and undersized; weight gains are
piglets.

depressed, and sometimes piglets die. A
conttibuting factor to mortality is that piglets
become covered with diatTheic feces and stay COCCIDIOSIS OF CATS AND DOGS
damp. Oocysts at·e usually shed in the feces
and can be identified by their size, shape, and

Mat1y species of coccidia infect tl1e intessporulation chat·actetistics; however, in tinal tract of cats at1d dogs. All species
peracute infections, diagnosis must be based
appear to be host-specific. Cats have
on finding stages of the pat-a.site in impression
species of I sospora, Besnoitia, Toxo
smears or histologic sections of the small
plasma, Hammondia, at1d Sa1·coC'lJStis.

intestine, because pigs can die before oocysts

Dogs have species of Isospora, Hammon
are formed. In severely affected piglets,
dia, at1d Sarcocystis. Neiilier dogs nor cats histologic lesions confined to thejejunw11
have Eimeria.

at1d ilewn at·e chat-acte1ized by villous

Hammondia has an obligatory two-host
att·ophy, blunting of villi, focal ulceration,
life cycle wiili cats or dogs as final hosts at1d
at1d fibtinonecrotic entetitis with parasite
rodents or ruminat1ts as intetmediate hosts,
stages in epithelial cells.

respectively. Hammondia oocysts are

Preventive control by feeding anticoccidiindistinguishable from iliose of Toxoplasma als to sows from 2 wk before fan·owing
at1d Besnoitia but are nonpathogenic in
through lactation or to neonatal pigs from
either host. (See also BESNOJTIOSJS, p 597, birth to weaning has been reported;

SARCOCYSTOSI , p 1058, and TOXOPLASMOSJS,
however, effectiveness of the latter has not
p 685.)

been confirmed. Although the sow is a

The most common coccidia of cats at1d
logical source of infection for piglets, this·
dogs at·e Isospora. Some Isospora spp of cats has not been well docwnented. Thorough
at1d dogs can facultatively infect other
removal of feces and disinfection of
mat1u11als and produce in various orgat1S an
fatTowing facilities between litters greatly
encysted fom1 iliat is infective for the cat or
decreases infection. Piglets iliat recover
dog. Two species infect cats: Ifelis at1d
from infection at·e highly resistant to

I rivolta; both cat1 be identified easily by reinfection.

oocyst size at1d shape. Al.most every cat

Aliliough less commonly associated with
eventually becomes infected with 1 felis.

clinical coccidiosis, E debliecki, E neode

Four species infect dogs: I canis, I ohioenbliecki, E scabra, and E spinosa have been sis, I burrowsi, at1d I neorivolta. In dogs, fom1d in pigs -1-3 mo old with diarrhea.

only 1 canis ca11 be identified by tl1e oocyst Illness may last 7-10 days, wiili pigs
structure; ilie oilier three Isospora overlap in remaining untluifty.

din1ensions and cat1 be differentiated only by

Treattnent of coccidiosis may include
endogenous developmental characteristics.

sulfamethazine in drinking water. The

Clinical coccidiosis, although not
control of coccidiosis in newborn piglets
common, has been repotted in kittens at1d
infected with I suis has been mu-eliable.

puppies. In kittens, it is seen ptirnarily

The use of coccidiostats in ilie feed of ilie
during weatling stress. The most conunon
sow for several days or a few weeks before
clinical signs in severe cases at·e diatThea
and after fat-rowing has been recommended

(sometimes bloody), weight loss, at1d
at1d used in ilie field, but the results are
dehydration. Usually, coccidiosis is
vat"iable. A.mprolimn at1d monensin are
associated with oilier infectious agents,
ineffective for prevention of expetirnental
in1munosuppression, or stress.

coccidiosis in piglets. A control progratn

Treattnent may be unnecessary in cats,
designed to decrease ilie mu-nber of oocysts
because they usually spontaneously
has been reconunended at1d consists of
eliminate the infection. In clinically affected

CRYPTOSPORIDIOSIS

209
cats, trimethoprim-sulfonamide

2--3 wk thereafter) can be used. Sanitation

(30-60 mg/kg/day for 6 days) can be used.

is important, especially in catte1ies and

In kennel conditions when the need for
kennels, or where large numbers of animals
prophylaxis might be predicted, arnprolium
are housed. Feces should be removed
is said to be effective, although it is not
frequently. Fecal contamination of feed and
approved for use in dogs. In severe cases,
water should be prevented. Runs, cages, and

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in addition to supportive fluid therapy,
utensils should be disinfected daily. Raw
sulfonamides such as sulfadimethoxine
meat should not be fed. Insect control

(50 mg/kg the first day and 25 mg/kg/day for
should be established.

CRYPTOSPORIDIOSIS

Cryptosporidiosis is recognized worldwide,
organism does not appear to be an in1portant
primarily in neonatal calves but also in
enteric pathogen in pigs, although it may
lambs, kids, foals, and piglets. Cryptocontribute to postweaning malabsorptive sporidia cause varying degrees of natw·ally
diarrhea. Cryptosporidial infection in foals
occw1.ing diarrhea in neonatal farm
appears less prevalent and is seen at a later
animals. The parasites commonly act in
age than in rwninants, with excretion rates
conceit with otl1er enteropathogens to
peaking at 5--8 wk old. Wection is not
produce intestinal injury and diarrhea
usually detected in yearlings or adults. Most
studies indicate that cryptosporidiosis is not

Etiology and Epidemiology: There are
a common disease in foals; infections in
cwTently 19 species and 40 genotypes of
immw10competent foals are usually subclini

Clyptosporidium. C hominis (fom1erly
cal. Persistent clinical infections are seen in

C parvum type I) is a specific hwnan

Arabian foals with inherited combined
pathogen. C parvum (formerly C parvum inm1unodeficiency. Cryptosporidiosis is also
type II) is zoonotic and infective to many
recorded in young deer and can be a cause of
animals, including people and calves. Four
diarrhea in artificially reared orphans.

cryptosporidial species have been isolated
from cattle ( C parvum, C andersoni,

Transmission: The source of crypto

C bovis, and C ryanae). C andersoni spo1idial infection is oocysts that are fully
infects the abomaswn of older cattle;
sporulated and infective when excreted in

C bovis and C ryanae are cattle adapted the feces. Large numbers are excreted

( cattle are the major host). C parvum is during the patent period, resulting in heavy
a common cause of calf diarrhea, and
environmental contamination. Transmiscryptosporidial oocysts have been detected sion may occur directly from calf to calf,
in the feces of 7(J'/o of 1- to 3-wk-old dairy
indirectly via fomite or hwnan transmission,
calves. Wection can be detected as early as
from contamination in the envi.rorunent, or

5 days of age, with the greatest proportion
by fecal contamination of tl1e feed or water
of calves excreting organisms between days supply. A periparturient rise in the excretion 9 and 14. Many reports associate infection in of oocysts may occur in ewes. C parvwn is calves with diarrhea occurring at 5--15 days
not host-specific, and infection from other
of age.

species ( eg, rodents, fann cats) via

C parirum is also a common enteric
contamination of feed is also possible.

infection in young lambs and goats. Diarrhea

Oocysts are resistant to most disinfeccan result from a monoinfection but more tants and can survive for several months
commonly is associated with mixed
in cool and moist conditions. Oocyst
infections. Wection can be associated with
infectivity can be destroyed by ammonia,
severe outbreaks of diarrhea, with high case
fonnalin, freeze-drying, and exposure to
fatality rates in lan1bs 4--10 days old and in
temperatures <32°F (0°C) or> 149°F (65°C).

goat kids 5--21 days old. Cryptosporidial

Ammoniwn hydroxide, hydrogen peroxide,
infection in pigs is seen over a wider age
chlorine dioxide, 10% fom1ol saline, and 5%
range than in ruminants and has been seen
anm1onia are effective in destroying oocyst
in pigs from 1 wk old through market age.

infectivity. Wectivity in calf feces is

Most infections are asymptomatic, and the
reduced after 1-4 days of drying.

210

CRYPTOSPORIDIOSIS

Concun·ent infections with other enteric
feeder withholds milk and feeds only
pathogens, especially rotavirus and
electrolyte solutions durmg the episode
coronavirus, are common, and epidemiologic of diarrhea. The persistent nature of the studies suggest that dianhea is more severe
diarrhea leads to a marked energy deficit in
in mixed infections. Imrnunocompromised
these circwnstances, and the calves die of
animals are more susceptible to clinical
inanition at 3---4 wk old.

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disease than itmnunocompetent anit11als, but
the relationship between disease and failure

Lesions: Calves with persistent diarrhea
of passive transfer of colostral itmnunoglobhave villous atrophy in the small intestine.

ulins is not clear. Age-related resistance,

Histologically, large nwnbers of the parasite
uru·elated to prior exposure, is seen in lambs
are embedded in the microvilli of the
but not calves. Wection results in production absorptive enterocytes. ln low-grade of parasite-specific antibody, but both
itlfections, only a few parasites are present,
cell-mediated and hwnoral antibody are
with no apparent histologic changes in the
important in protection, as well as local
it1testine. The villi are shorter than nmmal,
antibody in the gut of the neonate.

with crypt hyperplasia and a mixed

Case fatality rates ill cryptosporidiosis
inflanmiatory cell mfiltrate.

are generally low unless complicated by
other factors ( eg, concurrent infections,

Diagnosis: Diagnosis is based on
energy deficits from itiadequate illtake of
detection of oocysts by examination of fecal
colostrwn and milk, chilling from adverse
smears with Ziehl-Neelsen stams, fecal
weather conditions).

flotation techniques, ELISA, fluorescentlabeled antibodies, a rapid inununochromatographic test, and PCR. Sheather's flotation Pathogenesis: The life cycle of Crypto
sedimentation stamillg is the most sensitive
sporidium consists of six major developmen

(830Ai) and specific (99"A,) of these techtal events. After ingestion of the oocyst, there niques, with a relatively low cost per test.

is excystation (release of infective sporozo

This technique requires centrifuging a fecal
ites), merogony (asexual multiplication),
sample ill Sheather's solution, aspirating the
gametogony (gan1ete fonnation), fertilizatop layer and dilutillg the fluid in phosphate tion, oocyst wall fom1ation, and sporogony
buffer salille, centrifugillg, and placillg the

(sporozoite formation). Oocysts of Crypto
sediment on the slide and perfonning a
sporidium spp can sporulate within host
modified Ziehl-Neelsen technique to look
cells and are infective when passed in the
for cryptosporidial oocysts. It has been
feces. Wection persists until the host's
suggested that if the dianhea is caused by
inm1une response eliminates the parasite. In
cryptosporidia, there should be 105-107
natural and experimentally produced cases in oocysts/mL of feces. The oocysts are small calves, cryptosporidia are most numerous in

(5----6 mm in diameter) and relatively nonthe lower part of the small intestine and less refractile. They are difficult to detect by
common in the cecwn and colon. Prepatent
nonnal light microscopy but are readily
periods are 2---7 days in calves and 2---5 days in
detected by phase-contrast microscopy.

lambs. Oocysts are usually passed in the feces
of calves for 3---12 days.

Treatment: There are no currently
licensed therapeutics available in the USA

Clinical Findings: Calves with cryptofor C parvum infection in food anin1als.

sporidiosis usually have a mild to moderate

Anecdotal reports of success with
diarrhea that persists for several days
extra-label use of variC'luS compounds have
regardless of treatment. The age at onset is
not been replicated in controlled trials.

later, and the duration of dian·hea tends to

Experimental treatments have for the most
be a few days longer than are seen in the
part been toxic or ineffective. Halofugillone
dianheas caused by rotavirus, coronavirus,
is reported to markedly reduce oocyst
or enterotoxigenic Escherichia coli. Feces
output in experimentally Wected lambs
are yellow or pale, watery, and contam
and natw·ally and experimentally Wected
mucus. The persistent dian·hea may result
calves; therapy was also reported to prevent
in marked weight loss and emaciation. In
diarrhea. Paromomycill sulfate (100 mg/kg/
most cases, the diarrhea is self-limiting after day, PO, for 11 days from the second day of several days. Varying degrees of apathy,
age) proved successful ill preventing natural
anorexia, and dehydration are present. Only
disease in a controlled clinical field trial ill
rarely do severe dehydration, weakness,
goat kids.

and collapse occur, in contrast to findings in

Affected calves should be suppo1ted
other causes of acute diarrhea in neonatal
with fluids and electrolytes, both orally and
calves. Case fatality rates can be high in
parenterally, as necessary until recovery
herds with cryptosporidiosis when the calf
occurs. Cows' whole milk should be given

GIARDIASIS

211
in small quantities several times daily (tt:>
period of oocyst excretion in experimentally
the full level of requirement) to optimize
infected calves. Protection is not related to
digestion and to minimize weight loss.

circulating levels of specific antibody but

Several days of intensive care and feeding
requires a high titer of C par1YUm antibody in may be required before recovery is
the gut lun1en for prolonged periods. Many
apparent. Parenteral nutrition may be
research groups have attempted to develop

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considered for valuable calves.

effective vaccines against cryptosporidia.

Unfortunately, to date, vaccinations have

Control: The disease is difficult to control.

not been effective.

Reducing the number of oocysts ingested
may reduce the severity of infection and
allow inummit;y to develop. Calves should be

Zoonotic Risk: Infections in domestic
born in a clean environment, and adequate
animals may be a reservoir for infection
amounts of colostrum should be fed at an
of susceptible people. C hominis and
early age. Calves should be kept separate

C parvum are considered to be relatively
without calf-to-calf contact for at least the
common nonviral causes of self-limiting
first 2 wk of life, with strict hygiene at
diarrhea in immunocompetent people,
feeding. Diarrheic calves should be isolated
particularly children. In immunocomprofrom healthy calves during the course of the mised people, clinical disease may be
diarrhea and for several days after recovery.

severe. The infection is transmitted

Great ca.re must be taken to avoid mechanipredominantly from person to person,
cal transmission of infection. Calf-rearing but direct infection from animals and
houses should be vacated and cleaned out on waterborne infection from contamination a regular basis; an "all-in/all-out" manageof surface water and drinking water by ment system, with thorough cleaning and
domestic or wild animal feces can also be
several weeks of drying between batches of
important. Animal handlers on a calf farm
calves, should be used. Rats, mice, and flies
can be at high risk of diarrhea due to
should be controlled when possible, and
cryptosporidiosis transmitted from
rodents and pets should not have access to
infected calves. Immunocompromised
calf grain and milk feed storage areas.

people should be restricted from access

Hyperimmune bovine colostrum can
to young animals and possibly from access
reduce the severity of diaffhea and the
to fam1s.

GIARDIASIS

(Giardosis, Lambliasis, Lambliosis)

Giardiasis is a chronic, intestinal protozoal
group from various warm-blooded animals.

infection seen worldwide in most domestic

There are at least four species in this
and wild mammals, many birds, and
third group, including G ardeae and
people. Infection is common in dogs, cats,

G psittaci from birds, G micro ti from ruminants, and pigs. Giardia spp have
muskrats and voles, and G duodenalis
been reported in 0.44%--39% of fecal

(also known as G intestinalis and
samples from pet and shelter dogs and cats, G lamblia ), a species complex with a wide 1 %--53% in small ruminants, 9%--73% in
mammalian host range infecting people
cattle, 1 %--38% in pigs, and 0.5%--20% in
and domestic animals. Molecular charhorses, with higher rates of infection in acterization has shown that G duodenalis
younger animals. Farm prevalences in
is in fact a species complex, comprising
production animals vary between ()OA, and
seven assemblages (A to G), some of which
l 00%, with the highest prevalence in
have distinct host preferences ( eg,
younger animals. The cumulative inciassemblage CID in dogs, assemblage F in dence on a farm where Giardia has been
cats) or a limited host range ( eg, assemdiagnosed is lOOOA, in cattle and goats blage E in hoofed livestock), whereas
and nearly lOOOA, in sheep.

others infect a wide range of anin1als,

Three major morphologic groups have
including people (assemblage A and B).

been described: G muris from mice,

There is increasing evidence that some

G agilis from amphibians, and a third
assemblages (A and B) that infect domestic

212

GIARDIASIS
animals can also infect people, although

Clinical Findings and Lesions:

transmission patterns are not totally

Giardia infections in dogs and cats may
understood. Dogs have mainly assembe inapparent or may produce weight loss blages C and D, cats have assemblages Al
and chronic diarrhea or steato1Thea, which
and F, and people are infected with
can be continual or intermittent, particuassemblages A2 and B; however, some larly in puppies and kittens. Feces usually

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studies have identified human assemblages are soft, poorly formed, pale, malodorous, of Giardia in canine fecal samples.

contain mucus, and appear fatty. Watery
diarrhea is unusual in uncomplicated

Cycle and Transmission: Flagellate
cases, and blood is usually not present in
protozoa (trophozoites) of the genus
feces. Occasionally, vomiting occurs.

Giardia inhabit the mucosa! surfaces of

Giardiasis must be differentiated from
the small intestine, where they attach to
other causes of nutrient malassimilation
the brush border, absorb nutrients, and

( eg, exocrine pancreatic insufficiency [ see
multiply by binary fission. They usually
p 409) and intestinal malabsorption [see
live in the proximal portion of the small
p 400)). Clinical laboratory findings
intestine. 'Irophozoites encyst in the small
usually are normal.

or large intestine, and the newly fonned

In calves, and to a lesser extent in other
cysts pass in the feces. There are no
production animals, giardiasis cai1 result in
intracellular stages. The prepatent period
diarrhea that does not respond to antibiotic
is generally 3-10 days. Cyst shedding may
or coccidiostatic treabnent. The excretion
be continual over several days and weeks
of pasty to fluid feces with a mucoid
but is often intermittent, especially in the
appearance may indicate giardiasis,
chronic phase of infection. The cyst is the
especially when the diarrhea occurs in
infective stage and can survive for several
young aninlals (1-6 mo old). Experimental
weeks in the environment, whereas
infection of goat kids, lainbs, and calves
trophozoites cannot.

resulted in a decreased feed efficiency and

'Iransrnission occms by the fecal-oral
subsequently a decreased weight gain.

route, either by direct contact with an

Gross intestinal lesions are seldom
infected host or through a contaminated
evident, although microscopic lesions,
environment. Characteristics that facilitate
consisting of villous atrophy and cuboidal
infection include the high excretion of cysts
enterocytes, may be present.

by infected animals and the low dose needed
for infection. Giardia cysts are infectious immediately after excretion and are very

Diagnosis: The motile, piriform
resistant, resulting in a gradual increase u:i
trophozoites (12-18 x 7-10 µm) are
environmental infection pressme. High
occasionally seen in saline smears of
humidity facilitates survival of cysts in the
loose or watery feces. They should not
environment, and ovei·crowding favors
be confused with yeast or with trichomotransmission.

nads, which have a single rather than
double nucleus, an undulating membrane,

Pathogenesis: Giardia infections cause and no concave ventral surface. The oval
an increase in epithelial permeability,
cysts (9-15 x 7-10 µm) can be detected in
increased numbers of intraepithelial
feces concentrated by the centrifugationlymphocytes, and activation ofT lymphoflotation technique using zinc sulfate cytes. 'Irophozoite toxins and T-cell

(specific gravity 1.18). S9diun1 chloride,
activation initiate a diffuse shortening of
sucrose, or sodium nitrate flotation media
brush border microvilli and decreased
may be too hypertonic and distort the
activity of the small-intestinal brush border
cysts. Staining cysts with iodine aids
enzymes, especially lipase, some proteases,
identification. Because Giardia cysts are
and dissachaiidases. The diffuse rnicrovillus
excreted intermittently, several fecal
shortening leads to a decrease in overall
exaininations should be performed if
absorptive area in the small intestine and an
giardiasis is suspected (eg, three samples
impaired intake of water, electrolytes, and
collected throughout 3-5 days). Giardia
nutrients. The combined effect of this
may be underdiagnosed, because the cysts
decreased resorption ai1d the brush border
are intermittently shed.

enzyme deficiencies results in malabsorptive

For the detection of parasite antigen,
diarrhea and lower weight gain. The reduced
immunofluorescence assays and ELISA are
activity of lipase and the increased produccommercially available. An in-house ELISA tion of mucin by goblet cells may explain the
available for use in dogs and cats is a useful
steatorrhea and mucous diarrhea that has
tool for clinical diagnosis, particularly when
been described in Giardia-infected hosts.

coupled with a centrifugal flotation

DISEASES OF THE MOUTH IN LARGE ANIMALS

213
examination of feces. It is best to test
be to treat first with fenbendazole for 5-10
symptomatic animals with a combination of
days or to administer both fenbendazole and
a direct saline smear of feces, fecal flotation
metronidazole together for 5 days, being sure
with centrifugation, and a sensitive, specific
to bathe the dogs to remove cysts. lf clinical

ELISA optimized for use in the animal being
disease still persists and cyst shedding
tested ( eg, ELISA for dogs and cats).

continues, the combination therapy should

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be extended for another 10 days.

Treatment: No drugs are approved for

Currently, no drug is licensed for the
treatment of gia.rdiasis in dogs and cats in the treatment of giardiasis in ruminants.

USA Fenbendazole (50 mg/kg/day for 5-10

Fenbendazole and albendazole
days) effectively .removes Giardia cysts

(5-20 mg/kg/day for 3 days) significantly
from the feces of dogs; no adverse effects are reduce the peak and duration of cyst

.reported, and it is safe for pregnant and
excretion and result in a clinical benefit in
lactating animals. This dosage is approved to
treated calves. Paromomycin (50-75 mg/kg,
treat. Giardia infections in dogs in Europe.

PO, for 5 days) was found to be highly

Fenbendazole is not approved in cats but
efficacious in calves.

may reduce clinical signs and cyst shedding

Oral fenbendazole may be an option for
at 50 mg/kg/day for 5 days. Albendazole is
treatment in some birds.

effective at 25 mg/kg, bid for 4 days in dogs
and for 5 days in cats but should not be used

Control: Giardia cysts are immediately in these species, because it has Jed to bone
infective when passed in the feces and
mar.row suppression and is not approved for
swvive in the environment. Cysts are a
use in these species. A combination of
source of infection and reinfection for
praziquantel (5.4-7 mg/kg), pyranlel
animals, particularly those in crowded

(26.8-35.2 mg/kg), and febantel (26.8--35.2
conditions ( eg, kennels, catteries, or
mg/kg) also effectively decreases cyst
intensive rearing systems for production aniexcretion in infected dogs when adminismals). Feces should be removed as soon as tered for 3 days. A synergistic effect. between
possible ( at least daily) and disposed of with
pyrantel and febantel was demonstrated in
municipal waste. Wected dogs and cats
an animal model, suggesting that the
should be bathed to remove cysts from the
combination product may be preferred over
hair coat. Prompt and frequent removal of
febantel alone.

feces limits environ.mental contamination,

Metronidazole ( extra-label at 25 mg/kg,
as does subsequent disinfection. Cysts are
bid for 5 days) is -65% effective in eliminatinactivated by most quaternary ammonium ing Giardia spp from infected dogs but may
compounds, steam, and boiling water.

be associated with acute development of

To increase the efficacy of disinfectants,
anorexia and vomiting, which may
solutions should be left for 5-20 min before
occasionally progress to pronounced
being rinsed off contaminated surfaces.

generalized ataxia and vertical positional

Disinfection of grass yards or runs is
nystag.mus. Metronidazole may be ad.minisimpossible, and these areas should be tered to cats at 10--25 mg/kg, bid for 5 days.

considered contan1ina.ted for at least a

Metronidazole benzoate is perhaps better
month after infected dogs last had access.

tolerated by cats. Safety concerns limit the

Cysts are susceptible to desiccation, and
use of metronidazole in dogs and cats. A
areas should be allowed to ·dry thoroughly
possible treatment strategy for dogs would
after cleaning.

DISEASES OF THE MOUTH

IN LARGE ANIMALS

LIP LACERATIONS
nied by mandibular or incisive bone
fractures with or without dental fractures

Wounds of the lips and cheeks occur
and tooth a.vulsions. These occur when a
frequently in horses. The most common
horse grasps objects with its mouth and
ca.use is external trauma or secondary to
then pulls back when startled. Lip
the use of inappropriate bits or restraint
lacerations witl1out bone or teetl1 involvedevices. Lip lacerations may be accornpa-ment can be sutw·ed, usually witl1 a good

214

DISEASES OF THE MOUTH IN LARGE ANIMALS
result. Healing is rapid because of the good
the mouth and cause hard, thickened,
blood supply to the head. Lacerations left
tumorous plaques that may not be detected
to heal by second intention can result in
until well advanced. Verrucose, fibroblastic,
orocutaneous fistula, which may require
and sessile or flat forms of equine sarcoid
resection and primaty wound closure.

can involve the mouth and lips.

Rarely, skin grafts or mucosa! flaps are

Carbon dioxide laser removal of oral

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required to manage orocutaneous fistula.

and lip melanomas should be considered.

Complete removal of oral and lip melanomas is not necessaiy for a successful GLOSSOPLEGIA
outcome. In addition, some horses may
respond to oral cin1etidine therapy. Surgical

G lossoplegia, or paralysis of the tongue,
resection of sai·coids can be performed
is uncommon. Causes in horses include
successfully with the carbon dioxide laser.

incorrect placement of obstetric snares

Along with laser resection, intratumoral
in neonates during forced extraction,
administration of cisplatin can be considstrangles, upper respiratory tract infections, ered to lessen the chances for recurrence.

meningitis, botulism, encephalomyelitis,

Cryosurgery is another acceptable method
leukoencephalomalacia, equine protozoa!

of treatment. Squamous cell carcinoma can
encephalomyelitis, and cerebral abscessabe difficult to treat because of its invasive tion. Any condition that damages the
nature. Surgical debulking with the carbon
hypoglossal nerve ( cranial nerve XII), which dioxide laser followed by intratwnoral is the major motor nerve to the muscles of
injection of cisplatin can be effective in
the tongue, can result in glossoplegia.

select cases. Regardless of treatment, the

Neonates with glossoplegia must be
prognosis for complete resolution of oral
monitored carefully to ensure they are able
squamous cell carcinoma is guarded to
to eat. If necessaiy in affected foals, a
poor. (See also TUMORS OF THE SKIN AND son
nasogastric tube should be placed for

TISSUES, p 942.)

administration of colostrum or IV plasma
administered to prevent failure of passive

SLAFRAMINE TOXICOSIS
transfer. Foals unable to maintain hydration
may require IV fluid therapy and anti-inflatn

Causes of slaframine toxicosis include the
matory medication ( eg, phenylbutazone,
ingestion of forages, particularly clovers,
flunixin meglumine, or dexan1ethasone ).

infected with the fungusRhizoctonia

Prophylaxis against gastric ulceration is
leguminicola, which produces the toxic
also indicated. If the condition persists for
alkaloid slafran1ine. Profuse ptyalism is

> 10 days after birth, the prognosis for
often the only clinical sign. Affected animals
regaining normal function is guarded.

have no evidence of oral ulceration or other

Inflammatory diseases and trawna may also
oral lesions. Ptyalism resolves once the
result in transient glossoplegia. Occasionanimal is removed from the affected forage.

ally, horses undergoing prolonged dental

The differential diagnoses for large animals
procedures involving excessive traction

(particularly ruminants) include blueon the tongue can develop temporaiy tongue, vesiculat· stomatitis, vesicular
glossoplegia. The prognosis gf glossoexanthema, and foot-and-mouth disease.

plegia depends on the horse's response
to treatment for the primaiy condition.

In cattle, glossoplegia may accompany
severe actinobacillosis (seep 589). There
may be complete paralysis of the tongue
accompanied by necrosis of the tip. Such
conditions are occasionally seen in outbreaks in feedlot cattle and may follow a bout of viral stomatitis.

NEOPLASIA

Neoplasia of the mouth and lips other than
viral papillomas are uncommon and include
melanomas, sarcoids, and squatnous cell
carcinoma. In gray horses, melanomas may

An extensive sarcoid involving the lower lip
develop and infiltrate the commissures of
of a horse. Courtesy of Dr. Jan Hawkins.

DISEASES OF THE ESOPHAGUS IN LARGE ANIMALS

215

STOMATITIS
catarrhal fever, and bovine viral diarrhea.

Epidemic diseases such as bluetongue in

Stomatitis is a clinical sign of many diseases
ruminants, swine vesicular disease, and
in large animals. Oral trauma or contact with
vesicular stomatitis in horses must be
chemical irritants ( eg, horses that lick at their differentiated from other forms of acute legs after having been blistered with caustic
noninfectious or contagious stomatitis.

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agents) may result in transient stomatitis.

Traumatic irtjury from the ingestion of the
awns of barley, foxtail, porcupine grass, and

PAPILLAR STOMATITIS
spear grass, as well as feeding on plants

Viral papillomas are found around the lips
infested with hairy caterpillars, also will
and mouths of young animals, particularly
result in stomatitis in horses and cattle.

in cattle from 1 mo to 2 yr old. In some

Clinical signs commonly associated with
herds, the rate of occurrence may be lOOOA,.

acute active stomatitis include ptyalism,

The lesions are characteristically white to
dysphagia, or resistance to oral examinapink, raised, and appear proliferative.

tion. Oral examination is facilitated by

Most papillomas resolve spontaneously.

sedation, after which the mouth can be

However, in some cases, the lesions may
examined carefully with the aid of a mouth
coalesce to form cosmetically unacceptable
speculum and a light source. Ulcers should
masses, and owners may request therapy.

be visually and digitally evaluated to

Surgical removal of larger masses can
determine whether embedded foreign
be cosmetically acceptable and lessen
material ( eg, grass awns) is present. If the
recovery tin1e. Small masses can also be
etiology is ingestion of foreign material,
manually debrided or crushed to stin1ulate
changing the quality and quantity of the hay
the in1mune system. Other therapies,
or removing the anin1al from a pasture with
including cryosurgery and the use of
grass awns may effect recovery.

autologous vaccines, may also be effective.

Differential diagnoses include actinobac

Most papillomas eventually disappear if
illosis, foot-and -mouth disease, malignant
given tin1e.

DISEASES OF THE ESOPHAGUS

IN LARGE ANIMALS

ESOPHAGEAL OBSTRUCTION
the neck. Affected horses may continue to
eat or drink, worsening the clinical signs.

(Choke)

In cattle, clinical signs include free-gas

Esophageal obstruction (choke) occurs
bloat, ptyalism, or nasal discharge of food
when the esophagus is obstructed by food
and water. Ruminants may be bloated and
or foreign objects. It is the most common
in distress or recumbent, or there may be
esophageal disease in large animals. Horses
protrusion of the tongue, extension of the
most commonly obstruct on grain, beet
head, bruxism, and ptyalism. Acute and
pulp, or hay. Esophageal obstruction can
complete esophageal obstruction is an
also occur after recovery from standing
emergency because it prohibits eructation
chemical restraint or general anesthesia.

of rurninal gases, and free-gas bloat

Cattle tend to obstruct on a single solid
develops. Severe free-gas bloat may result
object, eg, apples, beets, potatoes, turnips,
in asphyxia, because the expanding rumen
com stalks, or ears of com.

puts pressure on the diaphragm and
reduces venous return of blood to the
heart.

Clinical Findings: In horses, clinical signs associated with esophageal obstruction include nasal discharge of feed material Diagnosis: The clinical signs of esophaor saliva, dysphagia, coughing, or ptyalism.

geal obstruction are usually diagnostic.

The horse may appear anxious and/or

Physical examination findings compatible
appear to "retch" by stretching and arching with esophageal obstruction include nasal

216

DISEASES OF THE ESOPHAGUS IN LARGE ANIMALS
discharge of feed material and water,
positioned in lateral recumbency and
bruxism, ptyalism, and palpable enlargeorotracheally intubated. Again, the head ment of the esophagus; in some instances,
must be positioned lower than the torso to
foreign objects lodged in the cervical
prevent water passing into the lungs. A
esophagus may be located via palpation.

cuffed endotracheal tube (18-22111111) is

Subcutaneous emphysema, cervical
inserted into the esophagus as far as

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cellulitis, and fever may be associated with
possible or to the level of the esophageal
esophageal rupture. The inability to pass a
obstruction, and the cuff inflated. A
stomach (ruminants) or nasogastric tube
nasogastric tube is inserted through the

(horses) can also confinn the diagnosis.

endotracheal tube, and the esophagus is

An endoscopic examination helps
lavaged as previously described. Again,
localize the site of esophageal obstruction,
resolution of obstruction should be contype of obstructing material, and extent of firmed with endoscopy or passage of the
esophageal ulceration. Because of the risk
nasogastric tube into the stomach. An
of aspiration pneumonia, the respiratory
esophagotomy to resolve esophageal
tract should be evaluated carefulJy,
obstruction is rarely required.

including auscultation of the heart and

Aii clu-onic cases of esophageal
lungs and thoracic radiography. In
obstruction should be evaluated endoscopicomplicated or chronic cases, a CBC and cally after successful resolution. These
serum biochemistry profile should be
horses frequently have esophageal
perfonned. CBC abno1malities include
ulceration that can be circunlferential.

leukocytosis, left shift, toxic neutrophils,

Severe mucosa! ulceration can result in
and hyperfibrinogenemia. Biochemical
esophageal stricture and repeat obstruction.

abno1malities include hyponatremia,

Endoscopy is also useful to exclude
hypochloremia, and hypokalemia secondesophageal diverticula, which can ary to excessive loss of saliva.

predispose to esophageal obstruction.

Esophageal diverticula can also be
diagnosed with contrast esophagograms.

Treatment: In horses, many cases of

Horses without mucosa! ulceration
esophageal obstruction may resolve
should be fed water-soaked, complete
spontaneously if feed and water are
pelleted feed for at least 7 -14 days to
withheld. Spontaneous resolution can be
minimize the likelihood of repeat esophaaided by rv administration of sedatives geal obstruction. Horses with mucosa!

(such as xylazine and detomidine).

ulceration should be fed this diet for 60

Oxytocin (0.11-0.22 mg/kg, fV) has proved
days, after which follow-up endoscopy
useful to relax esophageal smooth muscle.

should be performed to evaluate whether

To ensure that the esophageal obstruction
mucosa! ulceration has resolved and
has resolved completely, all horses with
esophageal stricture has occurred. Horses
suspected obstruction should have a
with chronic mucosa! ulceration with
nasogastric tube passed into the stomach
strictw·e may require surgical management.

or an endoscopic examination.

Aspiration pneumonia should be managed

Waiting >4-6 hr before passing a
with rv or oral antimicrobials and antinasogastric tube is not reco1111�ended inflan1IT1atory drugs. Con1IT1only used
because of the risk of esophageal mucosa!

antimicrobials include potassium or
ulceration and aspiration pneumonia.

procaine penicillin G (22,000 U/kg, rv

Horses that do not respond to conservative

[potassium] or IM [procaine], bid-qid),
management (withdrawal of feed and water, trimethoprim sulfamethoxazole rv sedation or oxytocin) should be initially

(30 mg/kg, PO, bid), and gentamicin sulfate
treated with esophageal lavage as follows:

(6.6 mg/kg/day, rv or IM). Metronidazole

After rv sedation, a nasogastric tube is

(15 mg/kg, PO, qid) is useful for management
inserted to the level of the obstruction.

of anaerobic infections. The most common

Water is delivered to the obstruction site
anti-inflan1IT1atory drugs used are phenylwith a stomach pump, and the tube is slowly butazone (2.2-4.4 mg/kg, PO or rv, bid) and inserted and withdrawn to lavage the
flunixin meglwnine (l.l mg/kg, rv, bid).

esophagus. The head must be lower than

In cattle, esophageal obstruction
the torso to minimize aspiration of water
accompanied by ruminal tyrnpany is an
into the lungs. Lavage via nasogastric tube
emergency, and if clinical signs of distress
is successful in at least 900/o of cases.

indicate, the bloat (seep 227) must be

For horses unresponsive to standing
relieved by trocarization tlu-ough the left
esophageal lavage, general anesthesia
sub lumbar fossa. Once tyrnpany has been
should be considered, with the horse
relieved, solid objects (eg, potatoes) may

DISEASES OF THE ESOPHAGUS IN LARGE ANIMALS

217
often be massaged free or spontaneously
and a contrast esophagogram can be useful
dislodge as their outer surfaces are softened diagnostic tools. Once the site of esophageal by saliva. Caution should be used if any
stricture is identified, some cases of muscular
attempt is made to push an offending object
stricture can be resolved with esophageal
down the esophagus using a probang;
myotomy or removal of fibrous connective
esophageal rupture and fatal septic
tissue surrounding the esophagus.

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mediastinitis may result.

Esophageal obstruction in ruminants
can be managed with standing esophageal

ESOPHAGEAL STRICTURES
lavage via orogastric tube or while under
general anesthesia (seep 215). Large

Idiopathic esophageal strictures can occur
foreign bodies can often be pushed into the
in foals. Initial diagnosis based on clinical
rumen without further problems. Rare cases signs may be delayed because of other more of esophageal obstruction with foreign
frequent causes of dysphagia, including
bodies may be treated with esophagotomy.

idiopathic dorsal displacement of the soft
palate or nasal reflux of milk, cleft palate,
or pharyngeal cysts. All cases of nasal

Complications of Esophageal
discharge of milk in foals should be

Obstruction
evaluated with endoscopy. Esophageal
ln horses and cattle, aspiration pnewnonia
stricture in older horses or ruminants

(seep 1417) and septic pleuropneun10nia
typically results from mucosa! ulceration
may be complications of esophageal
secondary to esophageal obstruction.

obstruction, especially in chronic cases.

Appropriate treatment depends on whether

Chronic esophageal obstruction (>24 hr)

the stricture is mucosal or mural (involving
may be associated with pressure necrosis of the muscular wall). Mucosa! stJictures can the esophageal mucosa due to prolonged
be treated conservatively with dietary
contact with the foreign body. Circwnferenmanagement (seep 215), bougienage with tial mucosa! dan1age may contribute to
a cuffed endotracheal tube, or surgery.

esophageal stricture.

Mural st1ictures are best managed with

An often fatal complication of chronic
esophageal myotomy. Surgical treatinent of
esophageal obstruction is esophageal
mucosal strictures may involve esophagotrupture. Cervical esophageal rupture can omy through the strictured area with
lead to localized cervical cellulitis or septic
insertion of a nasogastric tube, resulting in a
mediastinitis or pleuropneumonia.

traction diverticulum, mucosal resection

Intrathoracic esophageal rupture is
and anastomosis, or full-thickness
typically fatal. Cervical esophageal rupture
esophageal resection and anastomosis.

can be managed by local drainage, wound
lavage, and insertion of a nasogastric tube
into the rupture site. A traction diverticulwn ESOPHAGEAL NEOPLASIA is allowed to form, and the nasogastric tube
is removed. Esophageal rupture managed

The most common neoplasia of the
with extraoral alimentation rarely results
esophagus in horses is squamous cell
in esophageal stricture. ln cases of septic
carcinoma, which carries a guarded
mediastinitis or pleuropneumonia,
prognosis. Focal neoplastic masses can be
euthanasia should be considered because
managed with esophageal resection and
of the difficulty in successfully resolving
anastomosis. Unfortunately, most cases of
the bacterial infection.

squamous cell carcinoma are not amenable
to surgery, and euthanasia should be
considered.

Esophageal Obstruction Secondary

In ruminants, bovine viral papillomas

(
to Extraesophageal Disease
ie, warts) occasionally develop in the
cranial esophagus and pharynx and, in the

Cervical and prethoracic trauma may result
presence of other agents, may result in
in periesophageal or esophageal fibrosis
development of esophageal carcinoma. ln
involving the muscular layer. This can result
some areas of the world ( eg, Scotland and
in esophageal stiicture and intemlittent or

South America), such disease may follow
recurrent esophageal obstruction. ln some
ingestion of natural bracken fem toxins.

cases, there is no external evidence of

There is also a causal relationship between
cervical or prethoracic trauma ln cases
such bracken fem tun1ors and bladder
of suspected extraesophageal trauma,
cancers in cattle. (See also BRACKEN FERN
endoscopic exanlination of the esophagus

POISONING, p 3089.)

218

GASTROINTESTINAL ULCERS IN LARGE ANIMALS

GASTROINTESTINAL ULCERS

IN LARGE ANIMALS

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Gastric ulcers are important in adult horses,
repeated direct insult from ultra-low pH
foals, and pigs. Abomasal ulcers (seep 241) fluid normally found in the glandular region
in mature cattle and calves appear to be
of the stomach. Pressure increases inside
increasing in in1portance.

the abdomen (associated with exercise),
collapsing the stomach and forcing the acid

GASTRIC ULCERS IN HORSES
gastric contents upward. The more fluid

(and highly acidic) contents of the lower

(Equine
stomach come in contact with the
gastric ulcer syndrome)

nonglandular squamous mucosa, causing

Gastric ulcers ( equine gastric ulcer
inflanm1ation and, potentially, erosions to
syndrome [EGUS]) are conunon in horses
varying degrees.

and foals. This syndrome is most closely

The causes of ulcers in the glandular
associated with horses involved in
mucosa of the stomach are less well
performance disciplines; changes in
defined. Use of nonselective NSAIDs are
housing or social interaction; and illness.

known to reduce blood flow to the GI tract,

Prevalence in urunedicated racehorses in
causing decreased production of the
active training is at least 900Ai, whereas that
mucobica.rbonate matrix by the gastric
in non-racing performance disciplines
glandular mucosa and resulting in
exceeds 600A Neonatal foals are at
ulceration. This is not a consistent finding,
significant risk for development of
however. Additionally, attempts have been
perforating peptic ulcers until they are
made to isolate and/or correlate evidence
several weeks old, because their gastric
of Helicobacter spp organisms from the
mucosa is not developed to full thickness
stomach of horses with and without
at birth. Although spontaneous healing of
gastritis and ulcers. Results of these studies
peptic ulcer lesions has been noted, if the
have been equivocal or negative, and the
horse is maintained in the circumstances
role of this organism in glandular equine
inciting EGUS, the lesions are unlikely to
gastric ulcers has not been determined.

heal without medical intervention.

EGUS describes a spectrum of inflanuna

Clinical Findings: Most foals with gastric
tory and disruptive mucosal pathophysiol-.

ulcers do not exhibit clinical signs. Clinical
ogy affecting tissues of the distal esophagus, signs become apparent when the ulceration stomach, and entrance µito the duodenum.

is widespread or severe. The classic clinical

Endoscopic surveys indicate that -800Ai of
signs for gastric ulcers in foals include
these lesions are found in the nonglandular
diarrhea, bruxism, poor nursing, dorsal
squamous mucosa of the stomach,
recumbency, and ptyalism. These signs are
especially on the lesser curvature just
vague and not specific for gastric ulcers. In
proxin1al to the margo plicatus. However,
fact, ptyalism is a sign of esophagitis, which
significant portions of the squamous
in most foals is secondary to gastric outflow
mucosa along the greater curvature and up
obstruction and gastroesophageal reflux.

into the fundus may also be involved, along

Other causes, including esophageal
with lesions in the antrum or pylorus.

obstruction and Candida infection, should

Duodenal ulceration in adult horses and
be considered. Importantly, when a foal
foals is considered part of EGUS and,
exhibits clinical signs, the ulcers are severe
hence, a peptic ( acid-induced) disorder.

and should be diagnosed and treated

Duodenal ulceration, perforation, and
immediately. Sudden gastric perforation
stricture can occur, and it is not known
without prior signs occurs sporadically in
whether these problems develop solely as a
foals.

result of enteritis ( duodenitis) or whether

Adult horses with ulcers display
peptic factors have a role. However, once a
nonspecific signs, including abdominal
stricture occurs, gastric and esophageal
discomfort (colic), poor appetite, mild
ulcers are often present and severe,
weight loss, poor body condition, and
secondary to delayed gastric emptying.

attitude changes. Horses with severe
abdominal pain or colic may have gastric

Etiology: Ulcers in the nonglandular
ulcers, but they are unlikely to be the
squamous mucosa are associated with
primary cause of the abdominal pain. No

GASTROINTESTINAL ULCERS IN LARGE ANIMALS

219
strong correlation between the extent of
are the primary treatment objectives.

ulceration and the severity of clinical signs

Studies have examined the use of surfacehas been seen.

coating agents, antacids, histamine type-2

Complications related to gastric ulcers
receptor antagonists (ranitidine and
are most frequent and severe in foals and
cin1etidine), and the proton pwnp inhibitor
include perforation, delayed gastric
omeprazole in a carrier designed to aid

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emptying, gastroesophageal reflux and
passage through the acid stomach into the
esophagitis, and megaesophagus secondary
small intestine for absorption. Sucralfate
to chronic gastroesophageal reflux. Ulcers
binds to the gastric glandular mucosa and
in the proximal duodenum or at the pylorus
may promote healing there, although
can cause fibrosis and st1icture. Duodenal
studies using sucralfate have not shown it to
and pyloric stricture can lead to delayed
be efficacious in the treatment of gastric
gastric emptying in foals and adult horses. In ulcers in horses or foals. Thus, its use in rare cases, severe gastric ulceration causes
horses is questionable. Antacids have yet to
fibrosis and contracture of the stomach.

be proved effective in either healing or
preventing gastric ulcers. They must be

Diagnosis: Neither clinical signs nor
administered in relatively high volumes
clinicopathologic laboratory tests are
every 2 hr to neutralize stomach acid.

specific for gastric ulcers, and an abnormal

Ranitidine (6.6 mg/kg, PO, tid) has been
ity in a laboratory test does not preclude
shown to be effective in healing gastric
the possibility that another disorder may
ulcers when horses were removed from
be present. Gastric ulcers can develop
training. Studies have not shown cimetidine
secondary to stress due to problems in
to be effective. Omeprazole is the only
many organ systems or as a result of
medication approved by the FDA for
hospitalization or stall confinement.

treatment ( 4 mg/kg/day, PO) or prevention

Endoscopy and visualization of the ulcers

( 1 mg/kg/day, PO) of gastric ulcers in
in an empty stomach is the only definitive
horses, and it has been shown to allow
method of diagnosis. Endoscopes with light
gastiic ulcers to heal in horses that continue
sources that can be varied in wavelength
their nonnal training.

may be used to more easily visualize
inflammatory stages of this disease before
breaching of the epithelium by outright

GASTRIC ULCERS IN PIGS
ulceration. A presumptive diagnosis can be
reasonably made from significant reduction

Ulcers affect the pars esophagea in pigs and
in clinical signs after several days of
cause sporadic cases of acute gastric
treatment with a medication known to be
hemorrhage, resulting in death or slow
effective in raising gastric pH and allowing
growth due to chronic ulceration.

healing of gastric mucosa.

Etiology: Ulcers result when the

Treatment: Suppression of gastric acidity
unprotected stratified squamous epitheand maintenance of a pH between 4 and 5
lium of the pars esophagea is subjected to
insult from the mixtw-e of acid, bile, and
digestive enzymes present in the distal
region of the stomach. The mucosa that
surrounds the esophageal opening is not
protected by mucus and therefore relies on
maintenance of a pH gradient between the
proximal and distal regions of the pig
stomach. Many risk factors are associated
with the development of ulcers, most of
which are associated with an increa5e in
fluidity of the stomach contents. The most
irnpo1tant of these factors relate to feed,
particularly the use of finely ground feed

( <700 microns average particle size).

Consumption of finely ground pelleted
feed results in rapid stomach transit time
and fluid stomach content. Other
important factors tend to be associated
with disruption in feed intake, eg, an

Gastric ulcers on endoscopy in a foal. Courtesy
outbreak of respiratory disease, hot
of Dr. Thomas Lane.

weather, or management errors that lead

220

GASTROINTESTINAL ULCERS IN LARGE ANIMALS
to empty feeders. Dismption in feed intake
in a rectangular area of white, glistening,
results again in fluid stomach contents and
nonglandular, squan10us epitheliwn. In a
lack of a physical barrier between the
pig that has died suddenly from a gastric
acidic distal contents and the sensitive
ulcer, it is common to find a crater �2.5-5 cm
pars esophageal region. It is possible that
in diameter encompassing the entrance of
factors that cause increased acid
the esophagus. The crater appears as a

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production may influence the prevalence
cream or gray, punched-out area and may
and severity of ulcers, but in general there
contain blood clots or debris. In acute
is little evidence that hyperacidity is a
hemorrhage, the stomach and upper small
primary cause. Similarly, Helicobacter-like
intestine contain dark blood. Earlier lesions
organisms can often be identified w1der
are characterized by hyperkeratosis and
the mucus on the surface of the glandular
parakeratosis of the squan1ous epitheliw11
mucosa of the distal stomach, but evidence in the area of the esophageal opening into that these bacteria are a cause of ulcer
the stomach. It is asswned that the
development in the pars esophagea is
thickening of the epiU1elial surface is a
lacking, and epidemiologic studies
defense against insult. Cracks and erosions
showing an association are inconsistent.

can occur, particularly near the pars

The presence of the bacteria in the
esophageal border. A deep erosion may
glandular region and the lesion in the pars
result in acute and severe blood loss even
esophagea is difficult to explain from a
while most of the surface of the pars
biological standpoint.

esophagea remains intact. The healed ulcer
appears as a stellate scar. Erosion and

Clinical Findings: Sudden death
healing may occm over and over. Severe
usually involving only a small number
scarring can create stenosis of the
of pigs in a grower-finisher barn is a
esophageal opening.

common presentation, but higher
numbers can occur sporadically and are

Diagnosis: Appearance in a pen of one
usually associated with a triggering event
or two listless, anorectic pigs that show
such as feed disruption. Death is caused
weight loss, anemia, dark feces, and
by acute hemorrhage from the ulcer into
sometimes dyspnea is suggestive of gastric
the stomach, so the carcass appears
ulceration, as is the sudden death of an
notably pale but generally in good body
apparently healthy pig. Differential
condition. If bleeding is less severe, the
diagnoses include hemorrhagic bowel
clinical signs are those associated with
syndrome, porcine proliferative enteropaanemia, such as paleness; if bleeding is thy (Lawsonia intracellularis infection),
prolonged, the pig will become weak, lose porcine circovims-associated disease, body condition, and grow slower than its
and swine dysentery. Gross lesions at
pen-mates. Scant amounts of black tarry
necropsy are usually sufficient to confirm
feces indicating digested blood may be
a diagnosis of gastric ulceration. Abattoir
noted. Vomiting may be seen but diarrhea
examination has been used to evaluate
is generally not present, which helps to
the prevalence of stomach lesions but
differentiate gastric ulceration from other must be interpreted with caution. Pigs conditions. Other causes of blood loss or
are generally held without feed before
anemia need to be excluded. The most
shipping and may be held overnight at the
common age group to show clinical signs
packing plant before slaughter, and dming
are pigs 2-6 mo old, as well as sows. Most
this time ulcers can form or become more
pigs reared in modern confinement
severe. On an inaividual animal basis,
systems develop lesions in the pars
possibly for a valuable breeding boar or
esophagea. Lesions can both develop and
a pet, an endoscopic exan1ination could
heal quickly. This makes it difficult to
readily identify a gastric ulcer.

determine whether erosions of the pars
esophageal mucosa cause slow growth
rate if blood loss is minimal and anemia is Treatment and Prevention: No econot present. Scarring can occur and, if nomically feasible treatments are currently
severe, can result in narrowing of the
available for commercial swine. For pet pigs
esophageal-gastric opening. Clinical signs or very valuable breeding animals, protonof esophageal stenosis include regurgitapwnp inhibitors have been shown to reduce tion of a meal shortly after consumption
gastric acidity and allow mucosa! healing.

and loss of body condition.

For commercial swine production, weak,
pale pigs in poor body condition should be

Lesions: Gastric ulcers in pigs involve
euthanized, and milder cases might respond
the mucosa near tl1e esophageal opening
to palliative care. Placing tl1e affected pig in a

DISEASES OF THE RUMINANT FORESTOMACH . 221
hospital pen and initially coaxing it tb eat
diseases are important to prevent gastric
using a highly palatable feed, and possibly
ulcer deaths. Attention to feed milling
administering analgesics, can be attempted.

practices has a major impact on reducing

Early marketing of affected pigs should be
ulcers. Feed produced using a roller mill is
considered.

regarded to be less ulcerogenic than feed

Preventing, or reducing the incidence of
made with a hammer mill. Fine particle size

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gastric ulcers should focus on maintaining
is associated with more likelihood of ulcers
good feed intake, including management
but is also associated with improved feed
steps such as ensuring feeders do not run
efficiency, so economic considerations must
out of feed, sufficient feeder space is
be understood before a drastic change in
available, and mixing of pigs is minimized.

particle size is recommended. In general,

During hot weather, it is important to make
a coarse feed that will protect pigs from
the pigs as comfortable as possible using
stomach lesions may not be an acceptable
cooling methods such as water spraying or
solution because of the added feed cost, but
high ventilation rates. Vaccination and other in an outbreak situation a short-term feed steps to minimize respiratory and systemic
change may be necessary.

DISEASES OF THE RUMINANT

FOR ESTO MACH

SIMPLE INDIGESTION
ruminal pH due to forestomach hypomotility and putrefaction of ingested feed. It can (Mild dietary indigestion)

also result from accumulation of excessive

Simple indigestion is a minor disturbance
quantities of relatively indigestible feed that
in ruminant GI function that occurs most
may physically impair rumen function.

commonly in cattle and rarely in sheep and

Multiple animals are usually simultaneously
goats. Simple indigestion is a diagnosis
affected because sin1ple indigestion has a
of exclusion and is typically related to an
nutritional basis, although the severity of
abrupt change in the quality or quantity
the clinical signs can vary among animals.

of the diet.

Clinical Findings: Clinical signs depend

Etiology: Almost any dietary factor that
on the type of animal affected·and cause of
can alter the intraruminal environment can
the disorder. Overfeeding of silage causes
cause simple indigestion. The disease is
anorexia and a moderate drop in milk
common in hand-fed dairy and beef cattle
production in dairy cattle. The rumen is
because of variability in the quality and
usually full, finn, and doughy; primary
quantity of their feed. Dairy cattle may
contractions are decreased in rate or
suddenly eat excessive quantities of highly
absent, but secondary contractions may
palatable feeds such as com or grass silage;
be present although usually decreased in
beef cattle may eat excessive quantities
strength. Temperature, pulse, and respir a of relatively indigestible, poor-quality tion are nom1al. The feces are normal to
roughage during winter. During drought,
finn in consistency but reduced in an10unt.

cattle and sheep may be forced to eat large

Recovery usually is spontaneous within
quantities of poor-quality straw, bedding, or

24--48 hr.

grain. Simple indigestion can result from

Simple indigestion due to excessive
suddenly changing the feed, using spoiled or feeding of grain results in anorexia and frozen feeds, introducing urea to a ration,
ruminal hypomotility to atony (stasis).

turning cattle onto a lush cereal grain

The rumen is not necessarily full and may
pasture, or introducing feedlot cattle to
contain excessive fluid. The feces are
a high-level grain ration.

usually soft to watery and foul smelling.

Simple indigestion is usually associated

The mechanism for diarrhea formation is
with a sudden change in the pH of the
uncertain but is most likely due to increased
ruminal contents, such as a decrease in
luminal osmolality as a result of the rapid
ruminal pH due to rapid fermentation of
degradation of ingested carbohydrates.

ingested carbohydrates or an increase in

The affected animal is bright and alert and

222

DISEASES OF THE RUMINANT FORESTOMACH
usually begins to eat within 24 hr. A more

GRAIN OVERLOAD
severe digestive upset due to excessive
feeding of grain is described as grain

(Lactic acidosis, Carbohydrate engorgement,
overload (see below).

Rumenitis)

Diagnosis:

Grain overload is an acute disease of

A diagnosis of simple
ruminants that is characterized by run1en

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indigestion is based on a history of an
hypomotility to atony, dehydration,
abrupt change in the nature or amount of
acidemia, diarrhea, depression, incoordinathe diet, multiple animals being affected, tion, collapse, and in severe cases, death.

and most importantly the exclusion of other
causes offorestomach dysfunction. The
diagnosis is confirmed by collection and

Etiology and Pathogenesis: The
examination of run1inal fluid, which may
disease is most conunon in cattle that
have an abnormal pH ( <6 or> 7), decrease
accidentally gain access to large quantities
in the numbers and size of protozoa, or
of readily digestible carbohydrates,
prolonged methylene blue reduction time
particularly grain. Grain overload also is

(a measure of bacterial metabolic activity).

common in feedlot cattle when they are

The systemic reaction and painful
introduced to heavy grain diets too quickly.

responses to deep palpation of the xiphoid

Wheat, barley, and corn are the most readily
in traumatic reticuloperitonitis are not seen.

digestible grains; oats are less digestible.

The history and the absence of ketonuria

Less common causes include engorgement
help eliminate clinical ketosis from
with apples, grapes, bread, batter's dough,
consideration. The possibility ofleft
sugar beets, potatoes, mangels, or sour wet
displaced abomasum usually can be
brewer's grain that was incompletely
eliminated by sinmltaneous percussion
fermented in the brewery. The amount of
and auscultation.

feed required to produce acute illness

Vagal indigestion, abomasal volvulus, and
depends on the kind of grain, previous
cecocolic volvulus become more readily
experience of the animal with that grain,
detectable as they progress. Grain overload
the nutritional status and condition of the
is differentiated from simple indigestion by
animal, and the nature of the ruminal
its greater severity and the pronounced fall
microflora. Adult cattle accustomed to
in the pH of the rumen contents to <5.5.

heavy grain diets may consume 30-45 lb

( 15-20 kg) of grain and develop only

Treatment: Treatment is aimed at
moderate illness, whereas others may
correcting the suspected dietary factors.

become acutely ill and die after eating

Spontaneous recovery is usual when

20 lb (10 kg) of grain.

animals are fed a typical ruminant diet.

Ingestion of toxic an10unts of highly

Administration of -20 L of warm water
fermentable carbohydrates is followed
or saline via a stomach tube, followed by
within 2--o hr by a change in the microbial
vigorous kneading of the run1en, may help
population in the rumen. The number of
restore rumen function in adult cattle.

gram-positive bacteria (such as Stre'J)to

Magnesium hydroxide PO may be useful
coccus bovis) increases markedly, which
when excessive amounts of grain have been
results in the production oflarge quantities
ingested, but magnesium hydroxide should
oflactic acid. The run1en pH falls to �5,
only be administered to cattle documented
which destroys protozoa, cellulolytic
to have low rwninal pH ( <6); otherwise,
organisms, and lactate-utilizing organisms,
excessive forestomach and systemic
and impairs rumen· motility. The low pH
alkalinization can result. Purported
allows the lactobacilli to utilize the
rumenatorics ( eg, nux vomica, ginger, tartar
carbohydrate and to produce excessive
emetic, parasympathomimetics) are not
quantities oflactic acid. The superimposirecommended as ancillary treatments. Iftoo tion oflactic acid and its salts, L-lactate and much urea ( see p 3043) or protein has been o-lactate, on the existing solutes in the
ingested, vinegar (acetic acid) may be
run1en liquid causes osmotic pressure to
administered PO to return rumen pH to the
rise substantially, which results in the
normal range. If the number or activity of
movement of excessive quantities of fluid
rwninal microbes is reduced, administrainto the rwnen, causing fluid rwninal tion of 4--8 L of rwninal fluid from a healthy
contents and dehydration.

cow will help. (See also RUMINAL FLUID

The low run1inal pH causes a chemical

TRANSFER, p 2562.) Oral or intravenous
rwnenitis, and the absorption of lactate,
electrolyte solutions may be needed to
particularly o-lactate, results in lactic
correct electrolyte and acid-base abnonnaliacidosis and acidemia. In addition to ties, particularly in dehydrated cattle.

metabolic ( strong ion) acidosis and

DISEASES OF THE RUMINANT FORESTOMACH

223
dehydration, the pathophysiologic
elicit fluid-splashing sounds in the nunen.

consequences are hemoconcentration,

The contents of the rumen, as palpated
cardiovascular collapse, renal failure,
through the left paralwnbai· fossa, may
muscular wealrness, shock, and death.

feel firm and doughy in cattle that were

Animals that survive may develop mycotic
previously on a roughage diet and have
rumenitis in several days and hepatic
conswned a large amount of grain. In cattle
abscesses several weeks or months later.

that have become ill on smaller ainounts of

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They may have evidence of ruminal
grain, the rumen will feel not necessarily
epithelial damage at slaughter. The
full, but rather resilient because of the
relationship between grain overload and
excessive fluid. Severely affected animals
chronic laminitis in cattle is unclear.

stagger and may bump into objects; their
palpebral reflex is sluggish or absent, and
the pupillaiy light reflex is usually present

Clinical Findings: Carbohydrate
but slower than normal. The extent of
engorgement results in conditions ranging
depression of the palpebral reflex is
from simple indigestion (seep 221) to a
associated with the plasma o-lactate
rapidly fatal acidemia and strong ion
concentration and provides a useful clinical

(metabolic) acidosis. The interval between
method to categorize severity of lactic
overeating and onset of signs is shorter with
acidosis and monitor response to treatment.

ground feed than with whole grain, and

Affected anin1als commonly lie quietly,
severity increases with the amount eaten.

often with the head turned into the flank,

A few hours after engorgement, the only
and their response to any stimulus is much
detectable abnormality may be an enlarged
decreased so that they resemble cases of
run1en and possibly some abdominal pain
parturient paresis.

(manifest by belly kicking or treading of the

Acute laminitis may be present and is
hindlimbs). In the mild form, the run1en
most common in those animals not severely
movements are reduced but not entirely
affected; chronic laminitis may develop
absent, the cattle are anorectic but bright
weeks or months later. Anuria is a conlll1on
and alert, and diarrhea is common. The
finding in acute cases, and diuresis after
animals usually begin eating again 3--4 days
fluid therapy is a good prognostic sign.

later without any specific treatment.

Death may occur in 24-72 tu·, and rapid

Within 24--48 hr of the onset of severe
development of acute signs, paiticularly
overload, some animals will be recumbent,
recumbency, indicates a need for aggressive
some will be staggering, and others will be
treatment. A decrease in heart rate, increase
standing quietly; all will be completely off
in temperature, return of rwni.nal movefeed. lnlll1ediately after consuming large ment, and passage of large amounts of soft
quantities of dry grain, cattle may gorge
feces ai·e more favorable signs. However,
themselves on water, but once ill they
some animals appear to improve temporarusually do not drink at all.

ily but become severely ill agai�3--4 days

Body temperature is usually below
later, probably because of severe bacterial
nom1al, 98°-101 °F (36.5° -38.5°C); howand fungal rumenitis; death from acute, ever, in animals exposed to the stm in hot
diffuse peritonitis usually follows in
weather, it may be increased to 106°F

2---3 days. In pregnant cattle that survive the

(41 °C). Respirations tend to be shallow
severe form of the disease, abortion may
and rapid, up to 60---90/min. The heart rate
occur 10--14 days later.

usually is increased in accordance with
severity of the acidemia; the prognosis is
poor for cattle with heait rates> 120 bpm.

Diagnosis: The diagnosis is usually

Diarrhea is conm1on and usually profuse
obvious if the history is available and
and malodorous. The feces are soft to liquid, multiple animals are affected. The diagnosis yellow or tan, and have an obvious
can be confirmed by the clinical findings, a
sweet-sour odor. The feces frequently
low rwninal pH ( <5.5 in cattle unaccuscontain undigested kernels of the feed that tomed to a high grain diet), and exanlination
has induced the overload. In mild cases,
of the microflora of the rnmen for presence
dehydration equals 4%--6% body wt, but
of live protozoa. When only one animal is
losses may reach 10°/<r-12% in severe cases.

involved and there is no history of engorge

In severe grain overload, the primary
ment, the diagnosis is less obvious, but the
contractions of the rumen are completely
clinical signs-a static rumen with gurgling
absent, although the gurgling sounds of gas
fluid sounds, diarrhea, ataxia, and a normal
rising through the large quantity of fluid are
temperature--are chai·acteristic. Rumen
usually audible on auscultation. Ballottefluid at1alysis in these atlin1als is required to ment and auscultation of the left flank may
confim1 the diagnosis of grain overload.

224

DISEASES OF THE RUMINANT FORESTOMACH

Although paiturient paresis (seep 988)

Treatment: For all cattle suspected of
may resemble rumen overload, diarrhea and having eaten large quantities of concentrate, dehydration are not typical, the intensity of
it is believed that restricting water intake for
heai"t sounds is reduced, and the response
the first 18---24 hr is helpful, although this has
to calciw11 ii.jection is usually dramatic.

not been proved. If overload is serious,

Peracute coliform mastitis and acute diffuse slaughter for salvage should be considered; VetBooks.ir
peritonitis may also resemble overload, but
in feeders nearing the end of their feeding
usually a careful exatllination will reveal the
period, it may well be the most economic
cause of the toxemia.

choice. Mortality is high in severely affected

To avoid an increase in pH on exposure
anin1als unless aggressive therapeutic
to air, the pH of rw11en fluid obtained by
measures are started early. In such animals,
ororuminal stomach tube or ruminal
removal of rumen contents and replacement
pai·acentesis should be checked promptly.

with ingesta taken from healthy anin1als is

Normally, the pH in cattle on roughage is
necessary. In anin1als still standing,

6-7; in those on a high grain diet, 5.5-6.

rumenotomy is preferred to rw11en lavage,

Values <5.5 are strongly suggestive of grain
because anin1als may aspirate during the
overload, and a rumen pH <5 indicates
lavage procedure and only rw11enotomy
severe acidemia and metabolic acidosis.

ensures that all ingested grain has been

Wide-range (2-11) pH indicator paper is
removed. Rumen lavage may be accomsuitable for field use. Rw11inal fluid should plished with a large stomach tube if
also be examined microscopically if access
sufficient water is available. A lai·ge-bore
to a laboratory is available; fluid from
tube (2.5 cm inside diai11eter, 3 m long)

affected cattle will have decreased numshould be used, and enough water added to bers of protozoa (particulai·ly large and
clistend tl1e left paralw11bar fossa; gravity
medium-sized protozoa). In grain overload,
flow is then allowed to empty out what it
a Gram stain of rw11inal fluid will reveal a
will. Repeating tl1is 15-20 times achieves the
change from predominantly gram-negative
same results (and requires about as much
bacteria ( nom1al) to predominantly
time) as using run1enotomy to empty and
gram-positive bacteria, with a concomitant
wash out the run1en with a siphon.

loss in bacterial diversity.

Emptying the rumen should be followed

Increased blood o-lactate and L-lactate
by rumen inoculation (seep 2561) and, if
and inorgattic phosphate concentrations,
not accomplished before signs of severe
mild hypocalcemia, and reduced urinary pH
illness are evident, by rigorous fluid therapy
are also seen, but it is seldom necessary to
to correct the metabolic acidosis and
check such values to make a firm diagnosis.

dehydration and to restore renal function.

The diagnostic problem is to properly

Initially, over a period of -30 min, 5%
assess which aiumals require vigorous
sodiun1 bicarbonate solution should be
therapy ( or slaughter), which require
given IV (5 Il450 kg). During the next 6-12 hr,
supportive therapy, which have only a mild
a balanced electrolyte solution, or a
indigestion that will correct itself if water

1.3% solution of sodiWll bicarbonate in
and grain intake are restricted and hay and
saline, may be given IV, up to as much as
exercise ai·e provided, and which need

60 Il450 kg body wt. Urination should
nothing beyond their routine c11Ie and
resw11e during tlus period. Usually, it is
ration. In an outbreak of overload involving
wmecessary and even undesirable to also
several anin1als, it is necessary to identify
adnunister antacids PO ( or intrarWllinally),
those anin1als that need tl1e most intensive
particularly if IV sodium bicarbonate has
therapy and those that will recover with
been administered. Procaine penicillin G
n1inin1al medical therapy.

(22,000 U/kg/day) should be administered

If the cattle are found while still eating, it

IM to all affected animals for at least 5 days
is possible that some of the group will fall
to minimize development of bacterial
into each category, and close monitoring is
rwnenitis and liver abscesses. Thian1ine
necessary to minin1ize losses. Cattle found
should also be administered IM to facilitate
while engorging or shortly thereafter should metabolism of L-lactate via pyrnvate and be allowed no more concentrate but plenty
oxidative phosphorylation; attimals with
of good hay for up to 24 hr and should be
grain overload also have low concentraforced to walk periodically. Cattle that tions of thiai11ine in rumen fluid because of
appear normal at the end of the first day are
increased production of tl1ian1inase by
probably in good health, although if even
ruminal bacteria. There is no effective
one is ill, all should be monitored closely for
preventive treatment for mycotic rw11enitis.

48 hr. Most of those that have eaten enough

Emptying the rumen is wmecessary in
concentrate to be affected seriously show
less severe cases. In these cattle, magnesiw11
signs witlun 6-8 hr.

hydroxide (500 g/450 kg body wt) should be

DISEASES OF THE RUMINANT FORESTOMACH

225
added to warm water, pumped into the
in rapidly fermentable carbohydrates and/or
rumen, and mixed therein via kneading the
deficient in physically active fiber. Subacute
flank. This may be all that is necessary if the
ruminal acidosis is most conm1only defined
rumen pH is >5 and the anin1al is still
as repeatedly occurring prolonged pe1iods
standing and reasonably alert several hours
of depression of the ruminal pH to values
after the engorgement. A heart rate of 70--85
between 5.6 and 5.2. The low ruminal pH
bpm, weak ruminal contractions, nonnal
is ca.used by excessive accwnulation

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body temperature, and especially willingof volatile fa.tty acids (VFAs) without ness to eat are additional reassurances that
persistent lactic acid accwnulation and is
this therapy will suffice. If any question
restored to normal by the a.ninlal's own
remains, additional fluids should be given.

physiologic responses.

During the convalescent period, which may

The ability of the rumen to rapidly absorb
last 2-4 days, good-quality hay and no grain
organic acids contributes greatly to the
should be given, and the grain then
stability of ruminal pH. It is rarely difficult
reintroduced gradually. If good appetite
for peripheral tissues to utilize VFAs already
returns within 3 days, the prognosis is good.

absorbed from the rumen; however,

However, if treatment was not started early
absorption of these VFAs from the run1en
enough to prevent acidification of the
can be an important bottleneck.

ruminal contents, and mycotic infection

Rwninal VFAs are absorbed passively
of the rumen wall ensues, relapse is likely
across the rumen wall. This passive
within 3-5 days and the prognosis is grave.

absorption is enhanced by finger-like
papillae, which project away from the

Prevention: Accidental access to
rwnen wall and provide massive surface
concentrates for which cattle have
area for absorption. Ruminal papillae
developed an appetite, in quantities to
increase in length when cattle are fed
which they are unaccustomed, should be
higher-grain diets; this presumably
a.voided. Feedlot cattle should be introincreases ruminal surface area and duced gradually to concentrate rations over
absorptive ca.pa.city, which protects the
a period of 2---3 wk, beginning with a mixture
a.ninla.l from acid a.ccunmlation in the
of ,::;5()0A, concentrate in the milled feed
run1en. Dairy cows are especially at risk in
containing roughage.

the transition period, because the rnrninal
mucosa needs several weeks to a.cljust to
high-grain diets, and in peak lactation, when

SUBACUTE RUMINAL ACIDOSIS
high levels of easily fermentable carbohydrates are fed to avoid excessive negative (Chronic ruminal acidosis, Subclinical ruminal
energy balance.

acidosis)

One mechanism by which affected

Ruminant a.ninlals are adapted to digest and
animals resolve ruminal acidosis and return
metabolize predominantly forage diets;
ruminal pH to normal is by selecting long
however, growth rates and milk production
forage particles, either by choosing to
are increased substantially when ruminants
preferentially consume long dry hay or by
consume high-grain diets. One consequence
sorting a mixed ration in favor of longer
of feeding excessive a.mounts of rapidly
forage particles. Another mechanism is by
fermentable carbohydrates in conjunction
reducing overall feed intake. Depressed
with inadequate fiber to runlinants is
dry-matter intake becomes especially
subacute ruminal acidosis, which is
evident if ruminal pH falls below -5.5.

characterized by periods of low ruminal pH

Intake depression may be mediated by
that resolve without treatment and is rarely
pH receptors and/or osmola.lity receptors
diagnosed. Da.ity cows, feedlot cattle, and
in the rumen. Inflammation of the ruminal
feedlot sheep are at risk of developing this
epitheliwn ( rwnenitis) could ca.use pa.in and
condition.

also contribute to intake depression during subacute ruminal acidosis.

Absorption ofVFA inherently increases as

Etiology and Pathophysiology: Rumiruminal pH drops. These acids are absorbed nal pH fluctuates considerably during a
only in tl1e protonated state. Because they

24--hr pe1iod (typically between 0.5--1 pH
have a pK,. of -4.8, the proportion of these
units) and is determined by the dynan1ic
acids that is protonated increases dramatibalance between the intake of fermentable cally as ruminal pH decreases below 5.5.

carbohydrates, buffering ca.pa.city of the

Lactate levels in the ruminal fluid of cattle
run1en, and rate of acid absorption from
with suba.cute ruminal acidosis, if measured,
the rumen. In general, subacute rwninal
are usually not increased; however, the
acidosis is ca.used by ingestion of diets high
pathogenesis of excessive lactate produc-

226

DISEASES OF THE RUMINANT FORESTOMACH
tion in the rumen is well described. Ruminal
may cause liver abscesses, which may
carbohydrate fermentation shifts to lactate
eventually lead to peritonitis around the
production at lower ruminal pH ( mostly due
site of the abscess.

to Streptococcus bovis proliferating and

Caudal vena cava syndrome is caused
shifting to lactate instead ofVFA producby the release of septic emboli from liver tion); this can offset gains from VFA
abscesses; tl1is septic material then travels

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absorption. Ruminal lactate production is
via the caudal vena cava to the lungs. These
undesirable, because lactate has a much
bacteria proliferate in lw1g tissue and may
lower pl{,. than VFAs (3.9 vs. 4.8). For
ultimately invade pulmonary vessels, causing
example, lactate is 5.2 times less protonated
them to ruptw-e. This is observed clinically as
than VFAs at pH 5. As a result, lactate stays
hemoptysis and even peracute deaths due to
in the rumen longer and contributes to the
massive pulmonary hemorrhage.

downward spiral in rurninal pH.

Subacute rurninal acidosis has tradition

Additional adaptive responses are
ally been associated with claw horn lesions,
invoked if lactate production begins.

assumed to be caused by subacute larninitis.

Lactate-utilizing bacteria, such as Mega

However, this pathophysiologic mechanism
sphaera etsdenii and Selenomonas
has not been experirnentally characterized
ruminantium, begin to proliferate. These
or reproduced. In recent years, alternative
beneficial bacteria convert lactate to other
explanations for the development of claw

VFAs, which are then easily protonated and
horn lesions have been suggested.

absorbed. However, the turnover time of
lactate utilizers is much slower than that of

Clinical Findings: The main clinical signs
lactate synthesizers. Thus, this mechanism
attributed to subacute rurninal acidosis are
may not be invoked quickly enough to fully
reduced or cyclic feed intake, decreased
stabilize rurninal pH. Periods of very high
milk production, reduced fat, poor body
rurninal pH, as during feed deprivation, may
condition score despite adequate feed
inhibit populations of lactate utilizers
intake, and unexplained diarrhea. High rates

(which are sensitive to higher rwninal pH)

of culling or unexplained deaths may be
and leave them more susceptible to severe
noted in the herd. Sporadic cases of caudal
ruminal acidosis.

vena cava syndrome may also be seen. The

Besides disrupting microbial balance,
clinical signs are delayed and insidious.

feed deprivation causes cattle to overeat

Actual episodes of low mrninal pH are not
when feed is reintroduced. This creates a
identified; in fact, by the tirne an animal is
double effect in lowering rw11inal pH.

observed to be off-feed, its rw11inal pH has

Cycles of feed deprivation followed by
probably been restored to normal. Diarrhea
overconsun1ption greatly increase the risk
may follow periods of low run1inal pH;
of subacute rw11inal acidosis.

however, this finding is inconsistent and

Low rurninal pH during subacute ruminal
may be related to other dietary factors as
acidosis also reduces the number of species
well.

of bacteria in the rumen, although the
metabolic activity of tl1e bacteria that

Diagnosis: Subacute rw11inal acidosis is
remain is very high. Protozoa! populations
diagnosed on a group rather than individual
are particularly limited at lo..yer rwni.nal pH;
basis. Measw-ement of pH in the rurninal
the absence of ciliated protozoa in rw11inal
fluid of a representative portion of
fluid is often obse1ved during bouts of
apparently healthy animals in a group has
subacute rw11inal acidosis. When fewer
been used to help make the diagnosis of
species of bacteria and protozoa are
subacute rurninal acidosis in dairy herds.

present, the rwni.nal microflora are less

Animal selection should be from higheststable and less able to maintain normal risk groups: cows between -15--30 days in
rurninal pH during periods of sudden dietary milk in component-fed herds and cows change. Thus, periods of subacute rurninal
between -50-150 days in milk in herds
acidosis leave anirnals more susceptible to
fed total mixed rations. Run1inal fluid is
future episodes of rw11inal acidosis.

collected by rumenocentesis, and its pH is

The pathophysiologic consequences
detennined on a pH meter. Twelve or more
of ru111inal acidosis have mainly been
animals are typically sampled at -2-4 hr
described in feedlot cattle and in cattle
after a grain feeding (in component-fed
surviving acute ruminal acidosis. Low
herds) or 6--10 hr after the first daily feeding
run1inal pH may lead to run1enitis, erosion,
of a total mixed ration. If >25% of the
and ulceration of the run1inal epithelium.

animals tested have a run1inal pH <5.5, then

Once the run1inal epithelium is inflamed,
the group is considered to be at high risk of
bacteria may colonize the papillae and leak
subacute run1inal acidosis. This type of diaginto the portal circulation. These bacteria nostic tool should be used in coajunction

DISEASES OF THE RUMINANT FORESTOMACH

227
with other factors such as ration evaluation,
delay their conswnption until later in the
evaluation of management practices, and
day or cause them to be refused completely.

identification of health problems on a herd

Sorting can be prevented by providing
basis.

long-fiber particles less than -5 cm in

Milk fat depression is a poor and
length, by having adequate ( -500h--55%)

insensitive indicator of subacute ruminal
moisture in the mixed ration, and by

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acidosis in dairy herds.

including ingredients such as liquid
molasses that help ration ingredients stick
together.

Treatment and Prevention: Because

Runlinant diets should also be formulated
subacute ruminal acidosis is not detected
to provide adequate buffering. This can be
at the time of depressed ruminal pH, there
accomplished by feedstuff selection and/or
is no specific treatment for it. Secondary
by addition of dietary buffers such as
conditions may be treated as needed.

sodiwn bicarbonate or potassiun1

The key to prevention of subacute
carbonate. The dietary cation-anion
ruminal acidosis is allowing for ruminal
difference (DCAD) is used to quantify the
adaption to high-grain diets, as well as
buffeting capacity of a diet; diets for
limiting intake of readily fermentable
aninlals at high risk of runlinal acidosis
carbohydrates. This requires both good diet
should be fonnulated to provide a DCAD of
formulation (proper balance of fiber and

>250 mEq/kg of diet dry matter, using the
nonfiber carbohydrates) and excellent feed
fonnula (Na+ K)- (CI+ S) to calculate
bunk management. Animals consunling

DCAD.

well-formulated diets remain at high risk of

Supplementing the diet with direct-fed
this condition if they tend to eat large meals
microbials that enhance lactate utilization
because of excessive competition for bunk
in the rumen may reduce the risk of
space or after periods of feed deprivation.

subacute rwninal acidosis. Yeasts,

Field recommendations to feed
propionobacteria, lactobacilli, and
component-fed concentrates to dairy cattle
enterococci have been used for this
during the first 3 wk of lactation are usually
purpose. Ionophore ( eg, monensin sodium)

excessive. Feeding excessive quantities of
supplementation may also reduce the risk
concentrate and insufficient forage results
by selectively inhibiting run1inal lactate
in a fiber-deficient ration likely to cause
producers and by reducing meal size.

subacute runlinal acidosis. The same
situation may be seen during the last few
days before parturition if the ration is fed in

BLOAT
separate components; as dry-matter intake
drops before calving, dry cows preferen

(Ruminal tympany)

tially consun1e concentrates instead of

Bloat is an overdistention of the rwnenoforage and develop acidosis.

reticulwn with the gases of fermentati,,on,

Subacute ruminal acidosis may also be
either in the form of a persistent foan1
caused by errors in delivery of the rations
mixed with the rwninal contents, called
or by formulation of rations that contain
prin1ary or frothy bloat, or in the form of
excessive a.mounts of rapidly fermentable
free gas separated from the ingesta, called
carbohydrates or a deficiency of fiber.

secondary or free-gas bloat. It is predomi

Recommendations for the fiber content of
nantly a disorder of cattle but may also
dairy rations are available in the National
be seen in sheep. The susceptibility of

Research Council report, Nutrient Require
individual cattle to bloat varies and is
ments of Dairy Cattle (seep 2250). Drygenetically determined.

matter content errors in total mixed

Death rates as high as 200Ai are recorded in
rations are commonly related to a lack
cattle grazing bloat-prone pasture, and in
of adjustment for changes in moisture
pastoral areas, the annual mortality rate
content of forages.

from bloat in dairy cows may approach l %.

Including Jong-fiber particles in the diet

There is also economic loss from depressed
reduces the risk of subacute rwninal
milk production in nonfatal cases and from
acidosis by encow·aging saliva production
suboptimal use of bloat-prone pastures.

during chewing and by increasing rwnina

Bloat can be a significant cause of mortality
tion after feeding. The provision of adequate in feedlot cattle.

long-fiber particles reduces the risk of
ruminal acidosis but cannot elinlinate it. If a

Etiology and Pathogenesis: In
total mixed ration is fed, it is in1portant that
primary ruminal tympany, or frothy
the long-fiber particles not be easily sorted
bloat, the cause is entrapment of the
away from the rest of the diet; this could
nom1al gases of fennentation in a stable

228

DISEASES OF THE RUMINANT FORESTOMACH
foam. Coalescence of the small gas bubbles
can a low roughage intake. Feedlot bloat
is inhibited, and intraruminal pressure
is most common in cattle that have been
increases because ernctation cannot occur.

on a grain diet for 1-2 mo. This timing may

Several factors, both animal and plant,
be due to the increase in the level of grain
influence the formation of a stable foam.

feeding or to the time it takes for the

Soluble leaf proteins, saponins, and
slime-producing lllll1en bacteria to

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hemicelluloses are believed to be the
proliferate to la.i·ge enough numbers.

primary foanting agents and to form a

In secondary ruminal tympany, or
monomolecular layer around gas run1en
free-gas bloat, physical obstrnction of
bubbles that has its greatest stability at
ernctation is caused by esophageal
about pH 6. Salivary mucin is antifoan1ing,
obstrnction due to a foreign body ( eg,
but saliva production is reduced with
potatoes, apples, turnips, kiwifruit),
succulent forages. Bloat-producing pastures stenosis, or pressure from enJa.i·gement are more rapidly digested and may release a
outside the esophagus (as from lyrnphadgreater amount of small chloroplast enopathy or sporadic juvenile thymic
particles that trap gas bubbles and prevent
lymphoma). Inteiference with esophageal
their coalescence. The inunediate effect of
groove function in vagal indigestion and
feeding is probably to supply nutrients for a
diaphragmatic hernia may cause chronic
burst of microbial fennentation. However,
lllll1inal tyrnpany. This also occurs in
the major factor that determines whether
tetanus. Tun1ors and other lesions, such as
bloat will occur is the nature of the nnninal
those caused by infection with Actinomy
contents. Protein content and rates of
ces bovis, of the esophageal groove or the
digestion and nuninal passage reflect the
reticular wall are less common causes of
forage's potential for causing bloat. Over a
obstrnctive bloat. There also may be

24-hr period, the bloat-causing forage and
inteiference with the nerve pathways
unknown animal factors combine to
involved in the ernctation reflex. Lesions of
maintain an increased concentration of
the wall of the reticulum (which contains
small feed pa.iticles and enhance the
tension receptors and receptors that
susceptibility to bloat.

discriminate between gas, foam, and liquid)

Bloat is most common in animals grazing
may interrupt the normal reflex essential for
legun1e or legume-dontinant pastures,
escape of gas from the lllll1en.

particula.i·ly alfalfa, ladino, and red and

Ruminal tyrnpany also can be seconda.iy
white clovers, but also is seen with grazing
to the acute onset of run1inal atony that
of young green cereal crops, rape, kale,
occurs in anaphylaxis and in grain overload;
turnips, and legume vegetable crops.

this causes a decrease in =en pH and

Legmne forages such as alfalfa and clover
possibly an esophagitis and nunenitis that
have a higher percentage of protein and a.i·e
can inteifere with ernctation. Runtinal
digested more quickly. Other legumes, such
tyrnpany also develops with hypocalcernia.

as sainfoin, crown vetch, milk vetch,

Chronic runtinal tyrnpany is relatively
fenugreek, and birdsfoot trefoil, a.i·e high in
frequent in calves up to 6 mo old without
protein but do not cause bloat, probably
appa.i·ent cause; this fonn usually resolves
because they contain condensed tannins,
spontaneously.

which precipitate proteip and are digested

Unusual postures, particularly lateral
more slowly than alfalfa or clover.

reclU11bency, are conrn10nly associated with

Legmninous bloat is most common
secondary tympany. Rlll11inants may die of
when cattle are placed on lush pastures,
bloat if they become accidentally cast in
particularly those dominated by rapidly
dorsal recumbency Qr other restrictive
growing leguminous plants in the vegetative
positions in handling facilities, crowded
and early bud stages, but can also be seen
tra.t1Sportation vehicles, or irrigation ditches.

when high-quality hay is fed.

Frothy bloat also is seen in feedlot cattle,

Clinical Findings: Bloat is a common
and less commonly in dairy cattle, on
cause of sudden death. Cattle not observed
high-grain diets. The cause of the foa.in in
closely, such as pastured and feedlot cattle
feedlot bloat is uncertain but is thought to
and dry dairy cattle, usually are found dead.

be either the production of insoluble slin1e

In lactating dairy cattle, which are observed
by certain species of rnmen bacteria in
regularly, bloat conunonly begins within
cattle fed high-carbohydrate diets or the

1 hr after being turned onto a bloat-producentrapment of the gases of fennentation by ing pasture. Bloat may develop on the first
the fine pa.iticle size of ground feed. Fine
day after being placed on the pasture but
particulate matter, such as in finely ground
more co11U110nly develops on the second or
grain, can markedly affect foam stability, as
third day.

DISEASES OF THE RUMINANT FOR ESTO MACH

229

In primary pasture bloat, the rumen
for the cow. Recovery is usually uneventful,
becomes obviously distended suddenly, and
with only occasional minor complications.

the left flank may be so distended that the

A trocar and cannula may be used for
contour of the paralumbar fossa protrudes
emergency relief, although the standardabove the vertebral column; the entire sized instrument is not large enough to
abdomen is enlarged. As the bloat proallow the viscous, stable foam in peracute VetBooks.ir
gresses, the skin over the left flank becomes
cases to escape quickly enough. A larger
progressively more taut and, in severe cases, bore instmment (2.5 cm in diameter) is cannot be "tented." Dyspnea and grunting
necessary, but an incision through the skin
are marked and are accompanied by mouth
must be made before it can be inserted
breathing, protrusion of the tongue,
through the muscle layers and into the
extension of the head, and frequent
rumen. If the cannula fails to reduce the
urination. Rumen motility does not decrease bloat and the anin1al's life is threatened, until bloat is severe. If the tympany
an emergency run1enotomy should be
continues to worsen, the animal will
perfom1ed. If the cannula provides some
collapse and die. Death may occur within 1
relief, an antifoarning agent can be
hr after grazing began but is more common
administered through the cannula, which

-3-4 hr after onset of clinical signs. In a
can remain in place until the animal has
group of affected cattle, there are usually
returned to normal, usually within several
several with clinical bloat and some with
hours.

mild to moderate abdominal distention.

When the anin1al's life is not immediately

In secondary bloat, the excess gas is
threatened, passing a stomach tube of the
usually free on top of the solid and fluid
largest bore possible is recommended. A
mminal contents, although frothy bloat may
few attempts should be made to clear the
be seen in vagal indigestion when there is
tube by blowing at1d moving it back and
increased rwninal activity. Secondary bloat
forth in an attempt to find large pockets of
is seen sporadically. There is tympanic
run1en gas that can be released. In frothy
resonance over the dorsal abdomen left of
bloat, it may be in1possible to reduce the
the midline. Free gas produces a higher
pressure with the tube, and an antifoaming
pitched ping on percussion than frothy
agent should be administered while the tube
bloat. The distention of the rumen can be
is in place. If the bloat is not relieved quickly
detected on rectal examination. In free-gas
by the antifoaming agent, the animal must
bloat, the passage of a stomach tube or
be observed cai·efully for the next hour to
trocarization releases large quantities of
determine whether the treatment has been
gas and alleviates distention.

successful or whether at1 alternative

Lesions: Necropsy findings are charactherapy is necessaiy.

teristic. Congestion and hemorrhage of

A variety of antifoa111ing agents are
the lymph nodes of the head and neck,
effective, including vegetable oils ( eg,
epicardium, and upper respiratory tract are
peanut, com, soybean) and mineral oils
marked. The lungs are compressed, and

(paraffins), at doses of 250-500 mL. Dioctyl
intrabronchial hemorrhage may be present.

sodium sulfosuccinate, a surfactant, is

The ce1vical esophagus is congested and
commonly incorporated into one of the
hemorrhagic, but the thoracic portion of the
above oils and sold as a proprietary anti bloat
esopha..,"lls is pale and blanched-the
remedy, which is effective if administered
demarcation known as the "bloat line" of
early. Poloxalene (25--50 g, PO) is effective in
the esophagus. The rumen is distended, but
treating legume bloat but not feedlot bloat.

the contents usually are much less frothy

Placement of a rumen fistula provides
than before death. The liver is pale because
short-term relief for cases of free-gas bloat
of expulsion of blood from the organ.

associated with external obstruction of the
esophagus.

Diagnosis: Usually, the clinical diagnosis
of frothy bloat is obvious. The causes of

Control and Prevention: Prevention of
secondary bloat must be ascertained by
pasture bloat can be difficult. Management
clinical examination to dete1mine the cause
practices used to reduce the risk of bloat
of the failure of emctation.

include feeding hay, particularly orchard
grass, before turning cattle on pasture,
maintaining grass dominance in the sward,

Treatment: In life-threatening cases, an
or using sttip grazing to restrict intake, with
emergency rumenotomy may be necessaiy;
movement of anin1als to a new strip in the
it is accompanied by an explosive release of
afternoon, not the early morning. Hay must
rwninal contents and, thus, marked relief
constitute at least one-third of the diet to

230

DISEASES OF THE RUMINANT FORESTOMACH
effectively reduce risk of bloat. Feeding hay
are available commerciaJJy. The addition of
or strip grazing may be reliable when the
legun1es with high condensed tannins to the
pasture is only moderately dangerous, but
pasture seeding mix ( lOOAisain.foin) can
these methods are less reliable when the
reduce the 1isk of bloat where there is sttip
pasture is in the pre-bloom stage and the
grazing, as can the feeding of sain.foin
bloat potential is high. Mature pastures are
pellets.

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less likely to cause bloat than immature or

To prevent feedlot bloat, rations should
rapidly growing pastures.

contain �10-15% cut or chopped roughage

The only satisfactory method available
mixed into the complete feed. Preferably,
to prevent pasture bloating is continual
the roughage should be a cereal, grain straw,
administration of an antifoarning agent
grass hay, or equivalent. Grains should be
during the risk petiod. This is widely
rolled or cracked, not finely ground.

practiced in grassland countries such as

Pelleted rations made from finely ground

Australia and New Zealand. The most
grain should be avoided. The addition of
reliable method is drenching twice daily ( eg, tallow (3%--5% of the total ration) may be at milking times) with an antifoaming agent.

successful occasionaJJy, but it was not

Spraying the agent onto the pasture is
effective in contt·olled ttials. The nonionic
equally effective, provided the animals have
swfactants, such as poloxalene, have been
access only to treated pasture. This method
ineffective in preventing feedlot bloat, but
is ideal for strip grazing but not when
the ionophore lasalocid is effective in
grazing is uncontrolled. The antifoan1ing
control.

agent can be added to the feed or water or
incorporated into feed blocks, but success
with this meU10d depends on adequate

TRAUMATIC
individual intake. The agent can be

RETICULOPERITONITIS

"painted" on the flanks of the animals, from which it is licked during the day, but anin1als

(Hardware disease, Traumatic gastritis)

that do not lick will be unprotected.

Traw11atic reticuloperitonitis develops

Available anti.foaming agents include oils
as a consequence of perforation of the
and fats and synthetic nonionic surfactants.

reticulwn. It is important as a differential

Oils and fats are given at 60--120 mllhead/
diagnosis of other diseases marked by stasis
day; doses up to 240 mL are indicated during of the GI tract, because it causes similar dangerous periods. Poloxalene, a synthetic
signs. Trawnatic reticuloperitonitis is most
polymer, is a highly effective non.ionic
common in mature dairy cattle, occasionsurfactant that can be given at 10--20 glhead/ ally seen in beef cattle, and rarely reported day and up to 40 glhead/day in high-risk
in other flU11i.nan ts.

situations. It is safe and economical to use

Cattle commonly ingest foreign objects,
and is administered daily through the
because they do not disc1iminate against
susceptible period by adding to water, feed
metal mate1ials in feed and do not
grain mixtures, or molasses. Pluronic agents completely masticate feed before swaJJowfacilitate the solubilization of wate1°insoluing. The disease is common when green blc factors that contribute to formation of
chop, silage, and hay are made from fields
a.stable foam. A pluronic detergent.(Alfathat contain old rusting fences or baling sure®) and a water-soluble mixture of
wire, or when pastures are on areas or sites
alcohol ethoxylate and pluronic detergents
where buildings have recently been

(Blocare 4511) also are effective but are
constructed, burned, or tom down. The
not approved by the FDA. Ionophores
grain ration may also be a source because
effectively prevent bloat, and a sustainedof accidental addition of metal·.

release capsule administered into the nm1en
and releasing 300 mg of monensin daily for a Etiology: Swallowed metallic objects, 100-day period protects against pasture
such as nails or pieces of wire, faJJ directly
bloat and improves milk production on
into the reticulwn or pass into the nun en
bloat-prone pastures.

and are subsequently carried over the

The ultinlate aim in control is developruminoreticular fold into the cranioventral ment of a pasture that permits high
part of the reticulwn by rwninal contracproduction, while keeping incidence of tions. The reticulo-omasal orifice is elevated
bloat low. The use of pastures of clover and
above the floor, which tends to retain heavy
grasses in equal amounts comes closest to
objects in the reticulum, and tl1e honeyachieving this goal. Bloat potential varies comb-like reticular mucosa traps sharp
between cultivars of alfalfa, and low-risk
objects. Contractions of tl1e reticultm1

LIRD (low initial rate of digestion) cul ti vars promote penett·ation of U1e waJJ by the

DISEASES OF THE RUMINANT FORESTOMACH

231
foreign object. Compression of the
cow exhibits an arched back; an anxious

1wninoreticulum by the uterns in late
expression; a reluctance to move; and an
pregnancy and straining during parturition
uneasy, careful gait. Forced sudden
increase the likelihood of an initial
movements as well as defecating, urinating,
penetration of the reticulum and may also
lying down, getting up, ai1d stepping over
disrnpt adhesions caused by an earlier
batTiers may be accompanied by groaning.

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penetration.

A grw1t may be elicited by applying pressure

Pe1foration of the wall of the reticulum
to the xiphoid or by finnJy pinching the
allows leakage of ingesta and bacteria,
withers, which causes extension of the
which contaminates the peritoneal cavity.

tl1orax and lower abdomen. The grunt can

The resulting peritonitis is generally
be detected by placing a stethoscope over
localized and frequently results in
the trachea and applying pressure or
adhesions. Less conm1only, a more severe
pinching the withers at the end of an
diffuse peritonitis develops. The object can
inspiration. Tremor of the triceps and
penetrate the diaphragm and enter the
abduction of the elbow may be seen.

thoracic cavity ( causing pleuritis and

In chronic cases, feed intake and fecal
sometimes pulmonary abscessation) and
output a.re reduced, and milk production
the pe1icardial sac ( causing pericarditis,
remains low. Signs of cranial abdominal
sometimes followed by myocarditis ).

pain become less a.ppai·ent, and the rectal

Occasionally, tl1e liver or spleen may be
temperature usually retwns to nonnal as
pierced and become infected, resulting in
the a.cute inflan1mation subsides and
abscessation, or septicemia can develop.

pe1itoneal contatnina.tion is walled off.

Some cattle develop vagal indigestion

Clinical Findings: The initial penetration
syndrome (seep 233) because of the
of the reticulwn is characterized by the
adhesions that fom1 after foreign body
sudden onset of nuninoreticular atony and
perforation, particularly those on the
a sharp fall in milk production. Fecal output
ventromedial reticulum.

is decreased. The rectal temperature is

Cows wit.11 plewitis or pericarditis due
often mildly increased. The heart rate is
to foreign body perforation usually ai·e
nom1al or slightly increased, and respiration depressed, tachycardic (>90 bpm), and is usually shallow and rapid. Initially, tl1e
pyrexic (104°F [40°C]). Pleuritis is manifest
reticulai· groove
atJium ruminis
heait
reticulum
dorsal sac
ventJ"al sac
of the rumen of the rnmen

The relationship between the reticulum, diaphragm, and heart and pericardium in large ruminants. Illustration by Dr. Gheorghe Constantinescu.

232

DISEASES OF THE RUMINANT FORESTOMACH
by fast, shallow respiration; muffled lung
whether peritonitis is present, particularly
sounds; and possibly pleuritic friction rubs.

the concentration of o-dimer and the

Thoracentesis may yield several liters of
neutrophil percentage in the peritoneal
septic fluid. Traumatic pericarditis is most
fluid. However, the peritonitis frequently
commonly characterized by muffled heart
becomes walled off, and in these cases
sounds; however, early in the disease
peritoneal fluid may be within the reference

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process pericardia! fiiction rubs or gas and
range unless obtained from within the
fluid splashing sounds (washing machine
lesion. The presence of a magnet in the
murmur) can be heard on auscultation.

reticulun1 can be determined by movement

Jugular vein distention and congestive heart of a magnetic compass in the region of the failure with marked submandibular and
cranioventral abdomen; the presence of a
brisket edema is a frequent sequela of
magnet in the reticulum makes traumatic
traw11atic reticuloperica.rditis. Prognosis is
reticuloperitonitis very unlikely unless the
grave with these complications. Penetration
penetrating object is not magnetic.

th.rough the pericardium into the myocat0

Ultrasonography of the ventral abdomen
dium usually results in extensive hemo1ůsing a 3-MHz transducer is the most rhage into the pericardia! sac or ventricular
accurate way to diagnose localized
arrhythmias and sudden death.

pe1itonitis near the reticulum and characterize the reticulru· contraction frequency. It Diagnosis: This can be based on history
rru·ely identifies the presence of a penetrat

(when available) and clinical findings if the
ing object. Ultrasonography of the heart and
cow is exatnined when signs initially
thorax is ve1y useful in the diagnosis of
appear. Without an accurate history and
pleuritis and pericarditis as a sequelae
when the condition has been present for
of traumatic reticuloperitonitis and has
several days or longer, diagnosis is more
replaced radiography in the diagnosis of
difficult. Other causes of peritonitis, parreticuloperitonitis.

ticularly perforated abomasal ulcers, can be

Lateral radiographs of the cranioventral
difficult to distinguish from traumatic
abdomen can detect metallic material in the
reticuloperitonitis. Differential diagnoses
reticulun1 but should be taken only after
should include conditions that can produce
oral administration of a magnet. To
variable or nonspecific GI signs, eg,
detennine whether the reticulwn is
indigestion, lymphosarcoma, or intestinal
currently perforated, the foreign body
obstruction. Abomasal displacement or
must be visible beyond tl1e border of the
volvulus should be excluded by simultanereticulum, unattached to the magnet in the ous auscultation and percussion. Pleuritis
reticulum, or positioned off the floor of the
or pericarditis of nontrawnatic origin
reticulum. A depression in the cranioventral
produces signs similar to those associated
aspect of the reticulum or identification of
with foreign body pe1foration.

an abscess (by gas accumulation outside a

Although not always necessary,
viscus), soft-tissue masses, or a fluid line in
laborato1y tests may be helpful. In many
the cranial abdomen are also reliable
cases, there is a neutrophilia with a left shift. radiographic findings of penetration.

Plasrna fibrinogen concentrations may be

Portable radiographic units cannot
increased, and serun1 haptoglobin, runyloid
penetrate the reticulru· area of standing

A, and total plasma protein concentrations
adult cattle, and the cow may need to be
may be markedly increased. Severely
transported to where there is equipment
affected cattle may have coagulation
with sufficient power. The cow should not
abnormalities, as evidenced by prolonged
be placed in dorsal recurnbency to obtain
prothrombin time, th.rombin time, and
radiographs, because such manipulation
activated partial th.romboplastin time. The
places stress on adhesions and may lead to
acid-base status at1d serum electrolyte
a localized peritonitis becoming a diffuse
levels are typically normal, because
peritonitis due to gravitational spread of
abomasal and small-intestinal absorption
infection.

can remain normal. However, mru·ked

Electronic metal detectors Catl identify
hypokalemic, hypochloremic metabolic
metal in the reticulun1 but do not distinguish
alkalosis can be seen, presumably because
between perforating and non perforating
adynrunic ileus from peritonitis can affect
foreign bodies.

abomasal and GI motility and resorption
of abomasal secretions. The metabolic

Treatment: Treatment of the typical case
alkalosis can be created or exacerbated by
seen early in its course may be surgical or
treatment with alkalinizing agents such as
medical. Eitl1er approach improves the
magnesiun1 hydroxide used as a laxative.

chances of recove1y from -600A, in untreated

Peritoneal fluid analysis can help dete1mine
cases to 800/<r-90%. Surge1y involves

DISEASES OF THE RUMINANT FORESTOMACH

233
rumenotomy with manual removal of the
the ventral vagus nerve. Vagal indigestion
object(s) from the reticulum; if an abscess
syndrome is seen most commonly in cattle
is adhered to the reticulum, it should be
but has been reported in sheep.

aspirated (to confinn it is an abscess) and
then drained into the reticulum. Antimicro

Etiology and Pathogenesis: Diseases
bials should be administered perioperathat result in inju1y, inflai11mation, or VetBooks.ir
tively. Medical treatment involves adminispressure on the vagus nerve can result in tration of antimicrobials to control the
clinical signs of vagal indigestion syndrome.

peritonitis and a magnet to prevent

However, vagal nerve datnage is not present
recunence. Because of the mixed bactein most cases of vagus indigestion, and tl1e rial flora in the lesion, a broad-spectrum
most common cause is traumatic reticuloantimicrobial agent such as ox.ytetracycline peritonitis (seep 230). Conditions resulting

(16 mg/kg/day, IV) should be used. Penicillin in mechanical obstruction of the cai·dia or (22,000 IU/kg, IM, once to twice daily) is
reticulo-omasal orifice ( eg, papillomas or
widely used and effective in many cases
ingested placenta) can also result in vagal
despite its limited spectrum. Affected cows
indigestion if ruminoreticular distention is
should be confined for 1-2 wk; placing them present and the condition is subacute to on an inclined plane ( elevated in front) is
chronic.

believed by some to limit further penetra

Historically, tl1ere were four types of
tion of the foreign object, but supporting
vagal indigestion described based on the
studies are lacking. Supportive tl1erapy,
purported site of the functional obstruction.

such as oral or occasionally IV fluids and SC

Type I was failure of eructation or free-gas
calcium borogluconate or calciwn
bloat, type II was a failure of omasal
gluconate, should be administered as
transport, type m was secondary abomasal
needed. Rumen inoculation ( 4---8 L of
impaction, ai1d type IV was indigestion of
ruminal fluid from a healthy donor) is
late gestation. Types I and IV are rai·e, and
beneficial in some cases witl1 prolonged
this categorization system has minimal clininuninal stasis and loss of normal flora.

cal relevai1ce.

More advanced cases, those with obvious

Type I vagal indigestion, or failw·e of
secondaiy complications, or those that do
eructation, results in free-gas bloat and has
not respond to initial medical or surgical
been attributed to inflanunatory lesions in
therapy should be evaluated from an
the vicinity of the vagus nerve, such as
economic perspective; if the cow is of
localized peritonitis, adhesions ( usually
limited value, slaughter should be considafter an episode of traumatic reticuloperitoered if the carcass is likely to pass nitis), or chronic pnew11onia with ante1ior
inspection.

mediastinitis. Other potential causes for
type I vagal indigestion include pharyngeal

Prevention: Preventive measures include
trauma, which affects a more proximal pait
avoiding the use of baling wire, passing feed
of tl1e vagus nerve, ai1d esophageal
over magnets to remove metallic objects,
compression by abscesses or neoplasia,
keeping cattle away from sites of new
such as lymphosarcoma. Vagal indigestion
construction, and completely removing old
can develop in cattle after abomasal
buildings and fences. Additionally, bar
volvulus without abomasal impaction.

magnets may be administered PO,

These cases would preswnably fall into the
preferably after fasting for 18--24 hr. Usually, catego1y of type I vagal indigestion with the magnet remains in the reticulum and
dainage to the vagal nerve near the
holds ai1y fenomagnetic objects on its
reticulun1 ai1d omasum.

surface. There is good evidence that giving

Type II vagal indigestion, more conectly
magnets to all herd replacement heifers and
termed failw·e of omasal transport,
bulls at -1 yr of age minimizes the incidence
develops as a result of any condition that
of traumatic reticuloperitonitis.

prevents ingesta from passing ilirough the
omasal canal into the abomasum. Adhesions and abscesses ( reticular or single liver VAGAL INDIGESTION SYNDROME abscesses) are tl1e most conm10n cause of (Chronic indigestion)

failure of omasal transport and are usually
located on the right or medial wall of the

Vagal indigestion syndrome is chai·acterized
reticulum neai· tl1e route of the vagus nerve.

by the gradual development of abdominal

Reticular abscesses and adhesions are
distention secondaiy to rurnenoreticulai·
almost invaiiably the result of traumatic
distention. The distention was originally
reticuloperitonitis. Mechanical obstruction
thought to be the result of lesions affecting
of the omasal canal by ingested material ( eg,

234

DISEASES OF THE RUMINANT FORE STOMACH
plastic bags, rope, placenta) or masses ( eg,
that mirror the movements of the hyperaclymphosarcoma, squamous cell carcinoma, tive rumen. However, rumen contraction
granulomas, or papillomas) can also cause
sounds are not audible because the contents
chronic mminoreticular distention due to
have become frothy due to the prolonged
failure of omasal transport.

contractions and failw-e of the rumen to

Type III vagal indigestion is a secondary
empty.

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abomasal impaction. Primary abomasal

Temperature and respiratory rate are
impaction develops due to feeding of dry,
usually normal; however, these can be
course roughage, such as straw, in a
increased depending on the cause.

chopped or ground fom1 with restricted

Braclycardia is present in 25%-40% of cases
access to water and usually during
and is clue to decreased feed intake rather
extremely cold temperatw-es (seep 244).

than a direct stimulation of the vagus nerve.

Secondary abomasal impaction is seen most Tachycardia develops as the disease commonly after an episode of traumatic
progresses and cattle become dehydrated.

reticuloperitonitis or occasionally as a

Over tin1e, the animal develops a rough hair
sequela of abomasal volvulus. Mechanical
coat, loses condition, and becomes weak (in
fixation of the reticulrun to the ventral
some cases to the point of recumbency),
abdominal floor in cows with reticuloperitowith marked clinical signs of dehydration.

nitis interferes with the normal sieving

On rectal palpation, the rumen is
action of the reticulum, with passage of
distended with gas or froth that occupies
large fiber particles (>2 mm long) into the
the entire left abdomen, pushing the left
abomasum. The abomasum has difficulty
kidney to the right of the midline. The
in emptying the larger particles of food
ventral sac of the rumen is enlarged and
because of the increased viscosity, and they
palpable to the right of the midline (the
accumulate in the abomasum, resulting in
characteristic "L-shaped" rrunen). It is
abomasal impaction.

impo1tant to recognize that diagnosis of

Type IV vagal indigestion, or partial
vagal indigestion syndrome requires the
forestomach obstruction, is poorly defined.

presence of a markedly increased rumino

It typically develops in cattle during
reticular volume. Palpation of the lower
gestation and is more appropriately tennecl
half of the right side of the abdomen below
indigestion of late gestation. The condition
the costochondraljunction may detect
is thought to be related to the enlarging
an in1pactecl abomasum that feels doughy.

uterus shifting the abomasum to a more

Hematologic findings vary. The PCV can
cranial position, which inhibits normal
be increased because of dehydration or
abomasal emptying.

decreased because of bone marrow
depression ( anemia of chronic disease).

Clinical Findings: The clinical signs vary

The WBC may be normal, increased, or
to some extent with the location of the
decreased. If an inflan1lllatory condition
obstruction. In all cases, there Is a gradual such as peritonitis is present, the neutrophil
development ( over days to weeks) of
to lyn1phocyte ratio is typically reversed,
abdominal distention secondary to
and a neutrophilia may be present.

ruminoreticular distention. Distention of

Lyrnphocytosis can be seen with vagal
the dorsal and ventral sacs of the rumen
indigestion due to lyrnphosarcoma.

results in an "L-shaped" rumen on rectal

Leukopenia may be present with diffuse
exanlination. Left dorsal and left and right
peritonitis. Increased serum globulin and
ventral distention of the abdomen causes a
total protein can be seen with abscesses.

"papple" (pear plus apple) shape as viewed Metabolic status is normal, or metabolic
from behind.

alkalosis may be present. The serum

Cattle with vagal indigestion syndrome
chloride concentration varies with the site
have a diminished appetite, which typically
of the obstruction. It is usually normal if the
improves temporarily if distention is
lesion is proxin1al to the abomasum. A low
relieved. Milk production gradually
serum chloride concentration is consistent
decreases, fecal output is reduced, and the
with reflux of chloride from the abomasum
rumen develops a "splashy" fluid consisinto the nU11en (internal vomiting) and tency. The feces are characteristically very
obstruction at the level of the abomasum
scant and sticky and may contain longer

(type III). Metabolic alkalosis is typically
than nonnal particles. The strength of
present if serum chloride is decreased.

rumen contractions is decreased; however,

Rwnen chloride concentration is increased
rumen motility is often increased (3-4
in type III vagal indigestion and provides a
contractions/min). It is commonly possible
useful method to differentiate type II from
to see movements of the left abdominal wall
type III vagal indigestion. The serum

DISEASES OF THE RUMINANT FORESTOMACH

235
potassium concentration is usually low due
motility. Stin1ulation of low-threshold
to decreased potassium intake in the feed.

tension receptors in the reticulw11 occurs

Serum calcium concentration is often
under normal circumstances and causes
moderately decreased because of ongoing
reflex reticuloruminal contractions.

mHk production, but it is rarely low enough

However, severe distention causes
to cause recumbency. Serum urea and
stimulation of high-threshold receptors

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creatinine concentrations increase with
that have the opposite effect and inhibit
dehydration due to prerenal azotemia.

contractions.

Suppo1tive or symptomatic therapy

Diagnosis: Diagnosis is based on the
should be provided in all cases, which
presence of subacute to clu·onic ruminoretypically involves correcting dehydration ticular and abdominal distention. Because
as well as calciwn and electrolyte deficits,
vagal indigestion is by definition a subacute
commonly with oral fluids and electrolytes.

to chronic disease, this diagnosis should not

Severely dehydrated animals and those with
be made in cattle that have not been sick for
longstanding disease require IV fluids. Fresh
at least several days, which excludes acute
water and nom1al feed should be avaHable.

rumen tympany and acute frothy bloat.

Transfaunation at surgery or via oroesopha

Other causes of abdominal distention, such
geal intubation may help reestablish nom1al
as ascites and uterine enlargement, are
nunen flora in cattle with chronic anorexia.

included in the differential diagnosis and

Antimicrobials (procaine penicillin or
can almost invariably be excluded by rectal
oxytetracycline) should be given if the
palpation because of the absence of
underlying cause is infectious or if a rumen
ruminoreticular distention. Occasional
fistula is created.

cases of longstanding obstruction of the

Treatment of type I vagal indigestion
cecum or small intestine can cause severe

(failure of eructation) also typically involves ruminoreticular and abdominal distention;
creating a rwnen fistula to allow free gas to
however, palpable cecal or small-intestinal
escape. If surgery is not economically
distention is also palpable rectally. In
feasible and the underlying cause of vagal
addition, the rumen is distended but not
indigestion has been identified and treated,

L-shaped, and a characteristic ping is
a rumen trocar can be placed temporarily.

present in the case of cecocolic volvulus.

Such trocars are commercially avaHable

Diagnosing the specific cause of vagal
and must be secure and self-retaining to
indigestion is more difficult but is important
prevent potentially fatal leakage of rumen
because of differences in treatment and
contents into the peritoneal cavity. The
prognosis. Physical examination, rectal
trocar should not be removed for at least 2
examination, CBC, blood acid-base
wk to allow fim1 adhesions to fom1 between
detem1ination, and serum biochemical
the rumen and body wall.

values are often useful. Peritoneal fluid

The prognosis for animals with type I
analysis can support the diagnosis of
vagal indigestion is usually favorable. After
peritonitis if total protein or nucleated cells
creation of a rumen fistula, the signs of
are increased. Lateral radiographs of the
vagal indigestion resolve in nearly all cases.

reticulum should be taken to identify an

However, anin1als with chronic respiratory
opaque linear .foreign body ( eg, wire) or
disease or pharyngeal trauma may not
reticular abscess. Ultrasonography of the
recover from the underlying condition.

cranioventral abdomen can indicate the

Leakage of ingesta from fistulas can cause
presence of focal peritonitis and the
off-flavored milk. Peritonitis can develop
reticular contraction rate. Definitive
from leakage around the fistula or after
diagnosis often requires exploratory
rumenotomy; however, this should not
surgery (left paralumbar fossa laparotomy
happen with good surgical teclutique.

and rumenotomy).

Type II vagal indigestion (faHure of
omasal transport) rarely responds to sup

Treatment and Prognosis: If the value
portive or symptomatic therapy without
of the anin1aljustifies treatment, surgery
surgical intervention. Left paralumbar fossa
is almost always needed to identify and
laparotomy and rwnenotomy can be used
potentially correct the underlying cause.

to identify adhesions in the vicinity of the

Medical management alone is usually
reticulum, reticular or hepatic abscesses, or
ineffective. A left paralun1bar fossa
obstrnction of the omasal canal. Removal of
laparotomy and rumenotomy provides the
foreign bodies, wires, and some masses at
opportunity for definitive treatment in some
surgery and lancing of perireticular
cases. Emptying the rumen at the time of
abscesses into the reticulum affords a fair to
surge1y may help restore nom1al rumen
good prognosis. A diagnosis of lymphosar-

236

DISEASES OF THE RUMINANT FORESTOMACH
coma at surgery wan·ants a grave prognosis.

of late gestation), and some cows have

Reticular abscesses identified at surgery
in1proved with this treatment; however,
should be cautiously drained into the
because type IV vagal indigestion is a poorly
reticulum, and antibiotics given for 10-14
defined condition, the prognosis is always
days. Reportedly, 83% of cattle with reticular guarded. A more specific prognosis is based abscesses respond favorably to treatment.

on response to therapy and identification of

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Identification of adhesions in the vicinity
a specific lesion at exploratory celiotomy
of the reticulum warrants a fair to good
and nunenotomy.

prognosis witl1 surgery, antibiotic therapy,
and appropriate supportive treatment.

Prevention: The most common cause of

Hepatic abscesses must be drained by a
vagal indigestion syndrome is traumatic
second surgery. Large-bore carumlas placed
reticuloperitonitis, which causes adhesions
through the body wall, through the
and abscesses that interfere with both
adhesions, and into the abscess will drain
reticular motility and the appropriate
the purulent material. However, recurrence
stratification of feed particles for passage
is more of a problem with hepatic abscesses
through the abomasum. Therefore,
than with reticular abscesses.

prevention of traumatic reticuloperitonitis

Animals witl1 type III vagal indigestion
is important. Good management practices

(secondary abomasal impaction) diagnosed
may prevent some cases of vagal indigestion
without surgery usually do not receive
associated with chronic pneumonia. Early
fwther treatment because of the poor
diagnosis of abomasal volvulus, with
prognosis, particularly if there is a history of same-day surgical correction, may prevent traumatic reticuloperitonitis or abomasal
some cases.

volvulus. If the diagnosis is made at surgery
or if the abomasal impaction is thought to

RUMINAL DRINKING
be dietary, dioctyl sodium sulfosuccinate
can be infused directly into the abomasum

"Rwninal drinking" is caused by failure of via the reticulo-omasal orifice after
the reticular groove reflex, and it results in
emptying the rumen. A nasogastric tube
nuninal acidosis in calves on a liquid diet.

can be passed into tl1e abomasum via the

The disorder presents as primary chronic
reticulo-omasal orifice at surgery and left
disease ( rurninal drinking syndrome) in veal
in place for continued treatment (3---4 L of
calves, and in its acute fonn as a complicamineral oil daily for 3-5 days). If possible, tion secondary to different neonatal
impacted material should be removed
diseases, most con11110nly neonatal
manually tl1rough the reticulo-omasal
diarrhea It has also been described in
mifice. Other lesions, such as abscesses in
artificially fed lambs.

the medial wall of the reticulwn, should be

The reticular groove is a muscular
identified and drained. Abomasotomy and
structure extending from the cardia to the
removal of abomasal contents, using a right
reticulo-omasal orifice. Its correct closure
paracostal approach with the cow in left
is a precondition for the direct passage of
lateral recumbency, can be performed as
ingested milk or milk replacer into the
a last resort. However, recurrence of the
abomasum. When the reticular groove
in1paction is common. Pyloric oj:Jstruction
partially or completely fails to close, milk
in cattle is rare and is most often due to
spills into the reticulorumen and is
a foreign body obstructing the lumen.

fennented to short-chain fatty acids and/or

Pyloromyotomy is almost never effective
lactic acid. The subsequent drop in the pH
in resolving abomasal impactions.

of the ruminal contents to values that

Type III vagal indigestion has a poor
occasionally fall below 4 leads to variable
prognosis regardless of the cause or the
degrees of inflanunation of the mucosa of
treatment. However, cattle with mild to
the forestomachs and the abomasum. In
moderate primary abomasal impactions
chronic cases, hyperkeratosis or parakera
will respond to therapy, although severely
tosis of the ruminal mucosa can lead to
affected anin1als will not (seep 244 ). Cattle impaim1ent of nuninal motility with chronic
with secondary impactions due to traumatic or recurrent tympany. Additionally, atrophy reticuloperitonitis or as a sequela of
of the intestinal villi and a decrease in brush abomasal volvulus seldom recover. Animals
border enzyme activity with maldigestion
with foreign bodies (eg, trichobezoars)

and malabsorption have been seen.

obstructing the pylorus have a good

Systemic consequences of acute ruminal
prognosis if the obstruction is removed.

drinking are mainly due to absorption of

Therapeutic induction of parturition has
organic acids from the digestive tract. In
been recommended for treatment of cattle
particular, the L- and D-isomers of lactic acid
with type IV vagal indigestion (indigestion
may lead to metabolic acidosis with the

DISEASES OF THE RUMINANT FORESTOMACH

237
accumulation of o-lactate because of an
spontaneously from mminal drinking after
absence of a specific enzyme for its
adequate treatment, and the condition will
metabolism in mammals. This accumulation in general remain unrecognized. In calves of o-lactate has recently been found to be
that were force-fed or that do not respond to
responsible for clinical signs such as
treatment as expected, mminal drinking

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depression, ataxia, and general weakness.

should be considered, and an exainination

Primary dysfunction of the reticular groove of the nuninal fluid perfonned. Removal of occurs as a result of stressful situations
the contents and lavage witl1 warm water

(prolonged transpott, grouping, change in
via stomach tube may be beneficial,
feeding techniques), especially in bucket-fed
especially after prolonged force-feeding.

veal calves. Clinical signs usually appear

Prophylaxis ofmminal &inking consists of
some weeks after the anival of the calves at
early treatment of diseased calves, adequate
the fattening units and are cha.racte1ized by
feeding techniques, and minimizing stress in
inappetence, depression, poor growth, hair
pmchased calves.

loss, recurrent tympany, ventral abdominal
clistention, and passing of clay-like feces.

Fluid-splashing sounds can be heard on

RUMINAL PARAKERATOSIS
succussion of the left flank. Recovery of
fennented mminal contents via stomach tube Run1inal parakeratosis is a disease of cattle is diagnostic. In these advanced, chronic
and sheep characterized by hardening and
cases the prognosis is poor. If the disease is
enlargement of the papillae of the mmen.

detected early enough, feeding small vohunes It is most conunon in anin1als fed a highof milk from a nipple-bottle or bucket may be concentrate ration dming the finishing
successful. Additionally, the closure of the
period. It also is seen in cattle fed rations
reticular groove can be triggered by allowing
of heat-treated alfalfa pellets, as well as in
the calf to suck a finger before the milk feed is calves with prolonged mminal acidosis due offered.

to mminal drinking. It does not appear to

Acute mminal acidosis secondary to
be related to the feeding of antibiotics or
other disorders is most commonly seen in
protein concentrates. Incidence in a group
calves with neonatal diarrhea but occurs
may be as high as 400,1,. The lesions are
also in other painful or weakening diseases.

tl1ought to be caused by the lowered pH and

In these cases, the clinical picture is usually
the increased concentration of volatile fatty
dominated by the underlying disease. In
acids (VFAs) in the rum.i.nal fluid, and do not
cases of severe mmenitis, calves may
usually develop in cattle fed unprocessed
exhibit teeth grinding, arching of the back,
whole grain ( on which anin1als gain weight
and slight abdominal distention. Forceas readily). This may be related to the higher feeding of inappetent or primarily anorectic · pH ai1d higher concentration of acetic acid calves can also cause rwninal acidosis or
than tl1ose of the longer chain VFAs in the
worsen the situation by providing substrate
mminal contents.

for fwther fermentation.

Many of the papillae are enlai·ged ai1d

The prognosis for secondary mminal
hai·de.ned, and several may adhere together
drinking depends mainly on the success of
to form bunclles. The papillae of the anterior
treatment of the underlying disease. Calves
ventral sac are conunonly affected. In cattle,
with metabolic acidosis and dehydration
the roof of tl1e dorsal sac may show multiple
due to neonatal diarrhea usually recover
foci ( each 2-3 cm2) of parakeratosis. In
sheep, abnom1al papillae may be visible
and palpable through the wall of tl1e intact
nunen. Affected papillae contain excessive
layers of keratinized epithelial cells,
particles of food, and bacteria. The mmens
of affected cattle are difficult to clean in
tl1e preparation of tripe. The abnormal
epithelium, by interfering with absorption,
may reduce efficiency of feed utilization and
rate of gain, although there is little evidence
to support this theory.

Run1inal parakeratosis may be prevented
by finishing animals on rations that contain
unground ingredients in the proportion of

Severe rumenitis in a 10-day-old calf after a

1 pa.it roughage to 3 parts concentrate. The
prolonged course of ruminal drinking. Courtesy
necessity ai1d economics of prevention are
of Dr. Ingrid Lorenz.

not well defined.

238

DISEASES OF THE ABO MAS UM

DISEASES OF THE ABOMASUM

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Abomasal disorders include left displaced
predisposition is correlated with milk yield,
abomasum (LDA), 1ight displaced abomaindicating that current selection practices sum (RDA), abomasal volvulus (AV),
for milk production are increasing the
abomasal ulceration, and impaction.

incidence of abomasal displacement.

Displacement or volvulus is seen most

Hypomotility is also related to ingestion
commonly in dairy cows but can also be seen of high-concentrate, low-roughage diets, in dairy bulls and calves. Except for AV,
which reduce abomasal motility through a
abomasal displacement is rare in beef cattle
poorly defined mechanism that may involve
and essentially undiagnosed in small
hyperinsulinemia or increased concentraruminants. Abomasal ulcers are seen in dairy tions of volatile fatty acids. One of the
and beef cattle and in calves and lambs; they
mechanisms of excessive gas accun1ulation
are rarely diagnosed in small ruminants.

in cattle with abomasal displacement is

Impactions can be primary, which. is most
reticulum-mediated inflow of ruminal gas
frequent in beef cattle, or secondary, which
into the abomasum that is hypomotile. In
develop most often in dairy cows as a forn1
addition, high-concentrate diets result in
of vagal indigestion. Impactions may have a
increased gas production in the abomasum
hereditary basis in some black-faced sheep.

(mostly carbon dioxide, methane, and
nitrogen). Finally, subclinical and clinical
ketosis increase the risk of abomasal

LEFT OR RIGHT DISPLACED
displacement through an unknown

ABOMASUM AND ABOMASAL
mechanism that may be associated with

VOLVULUS
decreased rumen fill.

Approximately 800/o of displacements are

Because the abomasum is suspended
seen within 1 mo of parturition; however,
loosely by the greater omentum and lesser
they can be seen at any time. LDA is much
omentum, it can be moved from its normal
more common than RDA (30 LDA to 1 RDA);
position on the right ventral part of the
cases of AV are also more common than RDA
abdomen to the left or right side (LDA,

(10 LDA to 1 AV). AV is preceded by RDA.

RDA), or it can rotate on its mesenteric axis
while displaced to the right and lateral to

Pathogenesis: In LDA, as a result of
the liver (AV). The abomasum can shift
abomasal hypomotility and gas production,
from its normal position to left displacethe partially gas-distended abomasun1
ment or to right displacement over a
becomes displaced upward along the left
relatively short period. AV can develop
abdominal wall lateral to the rumen. The
rapidly or slowly from an uncorrected RDA.

fund us and greater curvature of tl1e
abomasum are primarily displaced, which in

Etiology: Although LDA, RDA, and AV
turn causes displacement of the pylorus and

(previously incorrectly referred to as right
duodenum. The omasun1, reticulum, and
torsion of the abomasum) are often
liver are also rotated to varying degrees.

considered separately, there is evidence of

The abornasal obstruction is pa.itial, and
a common underlying etiology; they may
although the segment contains some gas
be different manifestations of the same or
and fluid, a certain a.J11ount can still escape,
a similar disease process.

and the distention rarely becomes severe.

The etiology is multifactmial, although

Because there is rnininlal interference with
abomasal hypomotility and dysfunction of
blood supply unless the gas distention is
the intrinsic nervous system are thought to
marked, the effects of displacement are
play an important role in development of
entirely due to interference with digestion
displacement or volvulus. Important
and passage of ingesta, which lead to
contributing factors include abomasal
decreased appetite and dehydration.

hypomotility associated with hypocalcemia

A mild metabolic alkalosis with
and possibly hypokalemia, as well as
hypoch.lorernia and hypokalemia are
concurrent diseases (mastitis, metritis)

common. The hypoch.lorernic metabolic
associated wilh endoloxernia and
alkalosis is due to abomasal hypomotility,
decreased rumen fill, periparturient
continued secretion of hydrochloric acid
changes in the position of intra-abdominal
into the abomasum, and the partial
organs, and genetic predisposition,
abomasal outflow obstruction, with
particularly in deep-bodied cows. Genetic
sequestration of chloride in the abomasum

DISEASES OF THE ABOMASUM

239
and reflux into the rumen. Hypokalemia is

The most important diagnostic physical
due to decreased intake of feeds high in
finding is a ping on simultaneous auscultapotassium, sequestration of potassium in tion and percussion of the abdomen, which
the abomasum, and dehydration. Secondary
should be performed in the area marked by a
ketosis is common and may be complicated
line from the tuber coxae to the point of the
by development of hepatic lipidosis (fatty
elbow, and from the elbow toward the stifle.

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liver disease; seep 1018).

The ping ( detected dmi.ng sin1ultaneous

In RDA, hypomotility, gas production,
percussion and auscultation) characteristic
and displacement of the partially gas-filled
of an LDA is most commonly located in an
abomasum occur as in LDA. Mild hypokaarea between ribs 9 and 13 in the middle to lemic, hypochloremic, metabolic alkalosis
upper third of the left abdomen; however,
develops as well. After this dilatation
the ping can be more ventral or more caudal,
phase, rotation of the abomasum on its
or both. Pings associated with a nunen gas
mesenteric axis leads to volvulus and local
cap are usually more dorsal, less resonant,
circulatory in1painnent and ischemia
and extend more caudally through the left

(hemorrhagic strangulating obstruction).

paralun1ba.r fossa. Rectal examination can

The volvulus is usually in a counterclockconfirm a gas-filled rumen or an extremely wise direction when viewed from the rear
empty rumen that con-elates with the rumen
and the right side of the animal. The
ping in these cases. Pings associated with
omasum is displaced medially and can be
pnewnoperitoneum typically are less
involved in the volvulus with occlusion
resonant, present on both sides of the
of its blood supply (called an omasalabdomen, and are inconsistent in location on abomasal volvulus) and displacement of
repeated evaluation. Frequently, secondary
the liver and reticulun1. In rare cases, the
ketosis develops, and ketones are present in
reticulum can be involved ( called a
the Uli.ne or milk. Ketosis that develops in
reticular-omasal-abomasal volvulus).

association with abomasal displacement

A large quantity of chloride-rich fluid (up
responds only transiently to treatment and
to 50 L) accun1ulates in the abomasum, and
recurs (versus in primary ketosis, which
hypochloremic, hypokalemic metabolic
develops early in lactation in high-producing
alkalosis develops. The blood supply to the
cows and responds to therapy permanently
abomasun1, and often the omasw11 and
if instituted early). (See also KETOSIS IN CA11'LE, proximal duodenum, is compromised,
p 1024.)

eventually resulting in ischemic necrosis of

The ping associated with RDA also is
the abomasum and proximal duodenum as
most commonly located in the area between
well as dehydration and circulatory failure.

ribs 10 and 13 on the right abdomen. Dif

As circulatory failure progresses, a
ferentiation between various causes of a
metabolic acidosis due to hyper-L-lacta right-side ping can be difficult in some cases, temia and azotemia can become superalthough a ping cranial to rib 10 usually imposed on the preexisting metabolic
indicates the presence of AV because tl1e
alkalosis.

liver is displaced medially by the distended
viscus. A small, right-side ping underlying

Clinical Findings: The typical history of
ribs 12 or 13 and extending as far fo1ward as
abomasal displacement includes anorexia
rib 10 is common in cows with fw1ctional

(most commonly a lack of appetite for grain
ileus from a number of causes. This ping
with a decreased or normal appetite for
is most often associated with gas in the
roughage) and decreased milk production
ascending colon and resolves with

( usually significant but not as dramatic as
correction of the underlying condition.

with traumatic reticuloperitonitis or other

Cecal dilatation and rotation are charactercauses of peritonitis). In AV, anorexia is ized by a right-side ping. The ping extends
complete, milk production is more
through the dorsal paralumbar fossa in cecal
markedly and progressively reduced, and
dilatation and usually is located more
clinical deterioration is rapid. In abomasal
caudally (well into the paralun1bar fossa)

displacement, temperature, heart rate, and
in cecal rotation than the ping of RDA.

respiratory rate are usually nonnal. The

Palpation per rectum is helpful in differentcaudal part of the rib cage on the side of the iating an RDA from cecal dilatation or
displacement may appear "sprung."

rotation. Other right-side pings are produced

Hydration appears subjectively normal with
by pneumoperitonewn or gas in the rectun1,
displacements except in some chronic
descending colon, duodenum, or uterus.

cases. Rumen motility may be normal but

Spontaneous fluid splashing or gas
often is reduced in frequency and strength
tinkling sounds may be heard on auscultaof contraction. Feces are usually reduced in tion of the area of the ping or on simultanequantity and more fluid than normal.

ous ballottement and auscultation of the

240

DISEASES OF THE ABOMASUM
rumen

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----:-8:1-;JHH---superficial wall of
greater omentum
reticulum --------

'

/
abomasum

A

1 I
abomasum
lesser
reticulum
omenttm1

�r---�'{--llr-l.--greater
omentwn

A) Normal topography of left abdominal viscera, cow. B) Left displacement of abomasum.

Illustration by Dr. Gheorghe Constantinescu. Adapted, with permission, from Delahunta and Habel, Applied

Veterinary Anatomy, W.B. Saunders, 1986.

abdomen (succussion). The characteristic
the abomasurn is usually palpable per
rectal examination findings with LDA
rectwn. Without therapy, the animal often
include a medially displaced rumen and
becomes recumbent within 48-72 hr after
left kidney. The abomasurn is rarely
developing volvulus. Death occurs from
palpable in LDA and only occasionally in
shock and dehydration and is sudden if the

RDA.

ischemic abomasurn ruptures.

The clinical signs associated with
abomasal volvulus are more severe than

Diagnosis: For displacement or
with simple displacements because of the
volvulus, diagnosis is based on the
vascular compromise. However, an early
presence of the characteristic ping on
abomasal volvulus can be difficult to
simultaneous auscultation and percussion
distinguish from an RDA except by the
and exclusion of other causes of left- or
presence of a right-side ping cranial to rib
right-side pings. Ultrasonography may

10 (indicating medial displacement of the
be helpful in confirming a diagnosis of
liver by the abomasal volvulus) and the

LDA, RDA, or AV, but it cannot reliably
anatomic position identified at surgery. In
differentiate RDA from AV. Recent
contrast to cases of displacement, an
parturition, partial anorexia, and
anin1al with AV has tachycardia propordecreased milk production suggest tional to the severity of the condition. The
displacement. A ketosis that is only
area of the ping is usually larger ( extending
temporarily responsive to treatment is
as far forward as rib 8), and the amount of
consistent with abomasal displacement,
succussible fluid is greater. The anin1al is
which may be intermittent. The typical
more depressed, and signs of weakness,
signs on physical examination (in addition
toxemia, and dehydration develop as the
to the ping), rectal examination, and
disease progresses. The caudal extent of
laboratory evaluation also support the

DISEASESOFTHE ABOMASUM

241
diagnosis. Melena or signs of peritonitis
infection. However, administration of an

(eg, fever, tachycardia, localized abdomiantin'licrobial for a nonantimicrobial effect nal pain, pneumoperitoneum) with an LDA
should not be promoted.

may indicate a bleeding or perforated

In simple displacement, fluid and
abomasal ulcer, respectively. In cattle
electrolyte abnom1alities correct spontanewith AV, blood L-lactate concentrations ously with access to water and a salt block.

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�2 mmol/L indicate a positive outcome

Providing electrolyte water (60 g sodium
with surgical correction, whereas cattle
chloride and 30 g potassium chloride in 19 L
with blood L-lactate concentrations
of water) via stomach tube is helpful in

�6 mmol/L have a high probability of a
cases of longer duration. Anin1als witl1
negative outcome.

significant dehydration and metabolic
derangement require IV tl1erapy, typically

Treatment: Open (surgical) and closed
administered as hype1tonic saline

(percutaneous) techniques can be used to

(7.2% NaCl, 5 mUkg, IV over 5 min).

correct abomasal displacements. Rolling a

Occasionally, animals with abomasal
cow through a 180° arc after casting her
displacement or volvulus have at1ial
on her right side corrects most LDAs;
fibrillation, tl1ought to be of metabolic origin
however, recurrence is very likely. LDA
and primarily due to concunent hypokacan be corrected surgically using right len'lia and metabolic alkalosis. Correction of
flank pyloric omentopexy, right paramedthe displacement or volvulus almost always ian abomasopexy, left paralumbar
results in correction of the atrial fibrillation
abomasopexy, combined left flank and
withrn 5 days.

right paramedian laparoscopy (two-step

Aggressive treatment of ketosis plays an
procedure), or left flank laparoscopy
impo1tant role in successful treatment of

( one-step procedure). Blind suture
abomasal displacement, because most of
techniques (toggle-pin fixation or the "big
tl1e cattle tl1at die after surgical correction
needle" [blind-stitch] method), performed
ofLDA and RDA do so from the metabolic
in the right paramedian area, are
consequences of prolonged anorexia.

percutaneous methods for correction of

The prognosis after correction of simple

LDA; however, the exact location of the

LDA or RDA is good, witl1 survival rates of
suture is not known. Potentially fatal

95%. AV has a variable and less favorable
complications can develop after blind
prognosis ( average survival rate of 700A,);
suture techniques, and the reported
a high heart rate, moderate to severe
success rate is less than that of surgical
dehydration, a longer period of illness, a
correction by right flank pyloric omenlarge quantity of fluid in the abomastm1, topexy. With toggle-pin fixation, the pH
increased blood or plasma L-lactate
can be checked to confirm that the pin is
concentration, and the presence of
in the abomasum, which reduces the likeliomasal-abomasal or reticulo-omasalhood of attaching rumen, small intestine, abomasal volvulus are associated with
or omen tum to the body wall rather than
a poorer prognosis.

the abomasum. RDA and AV are corrected
surgically (using right paralumbar fossa

Prevention: The incidence of abomasal
omentopexy) when economically feasible.

displacements can be decreased by

The right paran1edian abomasopexy
ensuring a rapid increase in rumen volume
should be used only to correct RDA and
after calving, feeding a total mixed ration

AV in cattle unable to stand.

ratl1er than feeding grain twice daily ("slug

Ancillary treatment of animals witl1
feeding"), avoiding rapid dietary changes,
abomasal displacement include treating any maintaining adequate roughage in the diet, concurrent disease ( eg, metritis, mastitis,
avoiding postpartmient hypocalcemia, and
ketosis). Calcium borogluconate or calcium minrntizing and promptly treating concurgluconate SC or calcium gels PO help rent disease and ketosis.

restore nom1al abomasal motility in many
cases. Administration of erytiu·omycin

ABOMASAL ULCERS

( 10 mg/kg, IM) at tl1e time of surgery
increases abomasal emptying rate and milk

Abomasal ulcers affect mature cattle
production in the in1mediate postoperative
and calves and have several different
period. Because surgical con-ection of
manifestations.

abomasal displacement or volvulus is
frequently done on the farm, tl1e prokinetic

Etiology and Pathogenesis: Except for
effect of erythromycin suggests that it
lymphosarcoma of the abomasum and tl1e
might be prefen-ed if antimicrobials are
erosions of the abomasal mucosa that
administered to control intraoperative
develop in viral diseases such as bovine

242

DISEASES OF THE ABOMASUM
viral diarrhea and bovine malignant
stasis, generalized abdominal pain with a
catarrhal fever, the causes of abomasal
reluctance to move and an audible grunt or
ulceration are not well understood. Many
groan with each breath, weakness, and
different causes have been suggested.

dehydration. Melena may not be present in

Although abomasal ulcers can be seen any
peracute cases, because it takes at least 8
time during lactation, they are common in
hr for abomasal blood to be detected in the

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high-producing, mature dairy cows within
feces. As the condition progresses, body
the first 6 wk after parturition. The most
temperature drops, and the animal
likely cause is prolonged inappetence,
becomes recumbent and dies within 6-8 hr.

which results in sustained periods of low

In general, bleeding ulcers do not
abomasal pH; hence, the adage "no acid, no
perforate, and perforating ulcers do not
ulcer."

bleed into the GI tract sufficiently to

Abomasal ulcers may also arise in associproduce melena. However, hemorrhage and ation with lymphosarcoma, abomasal
perforation are seen together occasionally,
disorders ( displacement or volvulus ),
usually in cases that are chronic or
or increased luminal pressure causing
associated with abomasal displacement.

ischemia of abomasal mucosa; they may

Calves with abomasal ulceration and
also appear to be unrelated to other disease.

hairballs may have a distended gas- and

Abomasal ulcers are very conunon in
fluid-filled abomasurn that is palpable
mil k -fed calves after they have consumed
behind the right costal arch. Deep palpation
milk or milk replacer for 4--12 wk. Most of
may reveal abdominal pain associated with
these ulcers are subclinical and nonhemorlocal peritonitis due to a perforated ulcer. In rhagic. Occasionally, milk-fed calves <2 wk
calves, perforating ulcers are more common
old are affected by acute, hemorrhagic
than bleeding ulcers.

abomasal ulcers that may perforate and
cause rapid death. Well-nourished suckling

Lesions: Ulceration is most conunon in
beef calves, 2-4 mo old, may be affected by
the fundic region in adult cattle and in the
acute abomasal ulcers. Abomasal trichopyloric antrurn in milk-fed calves. The single bezoars are common in these calves but
or multiple ulcers measure from a few
do not appear to increase risk of ulcer
millimeters to 5 cm in diameter. The
formation.

affected artery is usually visible after
ingesta and necrotic tissue are removed

Clinical Findings: The syndrome varies,
from a bleeding ulcerated area. Most cases
of perforation are walled off by the
depending on whether ulceration is
omenturn, which forms a cavity 12-15 cm in
complicated by hemorrhage or perforation
diameter that contains degenerated blood
and by the severity of such hemorrhage or
and necrotic debris. Material from this
peritonitis.

cavity may infiltrate widely through the

A system of classification is based on
the depth of penetration or the degree of
omental fat. Adhesions may fonn between
hemorrhage or peritonitis caused by the
the ulcer and surrounding organs or the
ulcer: Type I is an erosion or ulcer without
abdominal wall.

hemorrhage, Type II is hemorrhagic, Type

III is perforated with acute localized -

Diagnosis: In cases with only slight
peritonitis, Type IV is perforated with acute
bleeding and mild clinical signs, diagnosis
diffuse peritonitis, and Type Vis perforated
of abomasal ulcer is difficult and may
with peritonitis within the omental bursa.

require repeated fecal evaluations for

There may be only a single ulcer or many
occult blood. Other conditions that can
acute and chronic ulcers.

cause partial anorexia and decreased milk

Cattle with bleeding abomasal ulcers
production should be excluded by physical
may be asymptomatic except for intermitexamination and laboratory tests, tent occult blood in the feces, or they can
including abdominocentesis. In cases with
die acutely from massive hemorrhage.

melena, the diagnosis can be based on

Common clinical signs include mild
physical examination alone. The PCV can
abdominal pain, bruxism, sudden onset of
help to determine the degree of hemoranorexia, tachycardia (90-100 bpm), and rhage, although it takes at least 4 hr after
fecal occult blood or melena that may be
an acute hemorrhage before the PCV
intermittent. Signs of blood loss are seen
decreases. An occult blood test of the feces
with major hemorrhage and may include
can confirm melena. Other conditions that
tachycardia (100-140 bpm), pale mucous
result in blood in the feces should be
membranes, weak pulse, cool extremities,
eliminated. Blood from portions of tl1e GI
shallow breaths, tachypnea, and melena.

tract distal to the abomasum reacts on

More severe signs include acute rumen
fecal occult blood tests; it is usually bright

DISEASES OF THE ABOMASUM

243
red if from the large intestine or raspberry48 hr) is indicated for perforating ulcers.

colored if from the small intestine. Animals

Antacids effectively increase abomasal pH in
with abomasal lymphosarcoma can have
milk-fed calves when adnlinistered at 4- to
a bleeding syndrome similar to that

6-hr intervals in a manner that induces
associated with abomasal ulcers but do not
esophageal groove closure; however, their
respond to therapy. Occasionally, oral,
efficacy is extremely questionable in adult

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pharyngeal, and laryngeal lesions bleed,
ruminants because of dilution by the large
and the swallowed blood appears in the
rumen volume. H2-receptor antagonists
feces. Similarly, pulmonary abscesses that
effectively increase abomasal pH in nlilk-fed
fom1 as a sequela of rumenitis by embolizacalves; however, the oral dosages required tion to the lungs and liver can erode blood
for cimetidine (100 mg/kg, tid) and ranitidine
vessels and result in hemoptysis; if the

(50 mg/kg, tid) are high, making treatment
blood is swallowed, this can also result in
expensive. Proton pump inhibitors, such as
melena. Fecal occult blood may also be due omeprazole (2 mg/kg, IV) effectively increase to AV or rarely to bloodsucking helminths.

lunlinal pH, but again treatment is expensive.

Diagnosis of perforating abomasal ulcers is The efficacy of oral omeprazole ( 4 mg/kg) in based on physical exanlination and excluding adult ruminants is unknown, but it has some other causes of peritonitis. Abomasal
efficacy in milk-fed calves. Because NSAIDs
ulceration with perforation and local
can contribute to ulceration, their use is
peritonitis may be indistinguishable from
contraindicated. The prognosis for localized
chronic traumatic reticulope1itonitis ( see
peritonitis associated with perforating
p 230). A magnet in the reticulum ( conabomasal ulcers is good with medical firmed by use of a compass) or an accurate
tl1erapy and dietary alteration. Recovery
history of having given the cow a magnet
generally takes 1-2 wk, and animals fully
before the onset of signs decreases the
recovered for 1 -2 wk generally do not experilikelihood of traumatic reticuloperitonitis.

ence recwTence. Surgery is indicated for

Reticular radiographs may confu111 or
perforating abomasal ulcers only when the
exclude the presence of radiopaque foreign
abomasum is displaced; however, significant
bodies in the reticulum. In some cases, tl1ere
abdonlinal contamination can occur in the
is a neutrophilia, possibly with a left shift.

process of breaking down adhesions and

Evaluation of peritoneal fluid will confirm
resecting or oversewing the ulcer.

peritonitis if total protein or D -dimer

Aninlals with diffuse peritonitis after
concentration and nucleated cell count are
perforation of an abomasal ulcer rarely
increased. Intracellular bacteria or degene1°
respond to therapy, and the prognosis is
ate neutrophils are rarely seen because, in
grave. Treatment consists of rapid and
most cases, the infection is rapidly walled off.

continued IV fluid therapy (based on the

The diagnosis of diffuse peritonitis due to
current metabolic status) and IV broadperforation is based on physical exanlination spectrum antibiotics. The few aninlals that
and excluding other causes. Rupture of a
recover from diffuse peritonitis usually have
distended viscus, such as can occur with AV
massive abdominal adhesions.

or cecal rotation, produces similar signs.

For bleeding ulcers, blood transfusions and

Regardless of the cause of diffuse peritonitis,
fluid therapy may be necessary in addition to
the prognosis is grave because of overwhelmdietary management, stall confinement, and ing infection and cardiovascular deterioraoral antacids. If hemorrhage is acute, the tion. There is neutrophilia with a marked left

PCV may not reflect the severity because
shift and hemoconcentration. Abdominal
equilibration between intravascular and
fluid is usually readily obtainable in large
extravascular fluid after blood loss takes at
quantities, and the protein level is increased;
least4 hr. Generally, a blood transfusion is
the nucleated cell count may be increased, or
required whenever weakness and lethargy
it may be nom1al due to dilution or utilization. are present; a decision regarding transfusion should be based on clinical signs rather than

Treatment: Most cases of abomasal ulcers

PCV. Cross-matching is not usually necessary;
are undiagnosed and therefore untreated.

a single transfusion of 4--6 L of blood is

Occasionally, a presumptive diagnosis is
required. Some cattle require more than one
made and medical treatment instituted. The
transfusion over tile course of several days.

most important treatment is to get the anin1al Complete recovery usually takes 1 -2 wk. The to eat, because food is an excellent buffer
prognosis is good if weakness and lethargy
and continual flow of forestomach contents
have not developed before treatment is started.

(pH 6.0--7.0) into the abomasum helps
increase abomasal pH. Broad-spectrum

Prevention: Animals should be encow0
antinlicrobial therapy (given for ;:,5 days or
aged to keep eating to avoid prolonged
until the rectal temperature is normal for
periods of i.nappetence and low abomasal pH.

244

DISEASES OF THE ABOMASUM

DIETARY ABOMASAL IMPACTION
finely ground feed. The pH of the ruminal
fluid is usually normal (6.5-7). Protozoa!

Impaction of the abomasum develops in
activity in the run1en ranges from n01mal to
pregnant beef cows during cold winter
a marked reduction in numbers and activity
months when cattle have decreased water

(assessed microscopically under low
intake and are fed poor-{luality roughage.

power). The impacted abomasum is usually

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Impaction also has been seen in feedlot cattle in the right lower quadrant on the floor of fed a variety of mixed rations containing
the abdomen. Deep palpation and strong
chopped or ground roughage (straw, hay)

percussion of the right flank may indicate
and cereal grains and in late-pregnancy dairy
the presence of a large, fum mass (impacted
cows on similar feeds. Impaction of the
abomasum) and elicit a grunt ( as is common
pyl01ic antrun1 is an underdiagnosed
in acute traumatic reticuloperitonitis),
condition in dairy cows in early lactation.

probably because of distention of the
abomasum and stretching of its serosa.

Etiology and Pathogenesis: The cause

Severely affected cattle die 3-6 days after
of dietary abomasal impaction is unlrnown
the onset of signs. The abomaswn ruptures
but considered to be consun1ption of excess
in some cases, and death from acute, diffuse
roughage low in both digestible protein and
peritonitis and shock occurs precipitously
energy. Impaction with sand can occur if
in a few hours. In sar1d impaction, there is
cattle are fed hay or silage on sandy soils, or
considerable weight loss, chronic diarrhea
root crops that are sandy or dirty. Outbreaks with sand in the feces, wealrness, recun1-may affect up to 15% of all pregnant cattle
bency, and death in a few weeks.

on individual farms when the an1bient

Metabolic alkalosis, hypochlorernia,
temperature drops to -14 °F ( -26°C) or
hypokalemia, and hernoconcentration are
lower for several days. The cause in
common, as ar·e total and differential WBC
postparturient dairy cows is probably
counts within tl1e normal range. At necropsy,
related to abomasal hypomotility.

the abomasum is commonly enlarged ( up to

The pathogenesis is unlrnown but is

8 times normal size) and inlpacted with dry
related to diet. Once the abomasum
run1en-like contents. The omasum may be
becomes impacted, subacute obstruction
sin1ilarly enlarged ar1d in1pacted. The run1en
of the upper GI tract develops. Ions of
is grossly enlarged ar1d filled with di-y
hydrogen and chloride are continually
contents or fluid. The GI tract beyond the
secreted into the abomasum in spite of the
pylorus is characteristically empty and has
in1paction, and atony and alkalosis with
a dry appearar1ce. Varying degrees of
hypochloremia result. Varying degrees of
dehydration ar1d emaciation are also present.

dehydration develop, because fluids are not

If the abomasun1 has ruptured, lesions of
moving beyond the abomaswn into the
acute diffuse peritonitis are present. In dairy
duodenum for absorption. Sequestration of
cattle in early lactation, typically only the
potassium ions in the abbmasum results
pyloric ar1trum is impacted.

in hypokalemia. Dehydration, alkalosis,
electrolyte imbalance, and progressive

Diagnosis: Clinical diagnosis of dietary
starvation are seen. Impaction of the
abomasal impaction is based on the
abomasun1 may be severe eno11gh to cause
nutritional history, clinical evidence of
irreversible abomasal atony.

in1paction, ar1d laboratory results. The
disease must be differentiated from

Clinical Findings and Lesions: Comsecondary abomasal impaction as a plete anorexia, scant feces, moderate
f01m of vagal indigestion.

distention of the abdomen, weight loss,

In1paction of the abomasum as a
and wealrness are usually the initial signs
complication of traumatic reticuloperitoniof dietary abomasal impaction. Body tis usually is seen in late pregnar1cy, ar1d
temperatw·e is usually normal but may be
commonly only in one arlirnal. A mild fever
subnomlai during cold weather. A mucoid
may or may not be present, ar1d there may
nasal discharge tends to collect at the
be a grunt on deep palpation of the xiphoid.

external nares and on the muzzle; the

The run1en is enlarged and may be hypem10-
muzzle is usually dry and cracked, caused
tile (early) or atonic (late). In mar1y cases, it
by both the failure of the animal to lick its
is in1possible to distinguish between the two
nostrils and the effects of dehydration.

causes of impacted abomasum, ar1d a right

The heart rate may be increased, and mild
flar1k laparotomy may be necessary to
dehydration is common.

explore the abdomen for peritoneal lesions.

Most often, the run1en is static and
distended with d1-y contents, but it may

Treatment: The challenge is to recognize
contain excess fluid if the cow has been fed
the cases of dietary abomasal impaction

ACUTE INTESTINAL OBSTRUCTIONS IN LARGE ANIMALS

245
that will respond to treatment and those
mineral oil directly into tl1e abomasurn
that will not, ie, to determine those animals
through the reticulo-omasal orifice in an
that should be slaughtered inunediately
attempt to soften and promote evacuation
for salvage. Cows that are weak, have a
of the abomasal contents. Cattle with
severely impacted abomasum, and have a
secondary impactions tllat develop as a

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marked t.achycardia (100-120 bpm) are
sequela of traumatic reticulope1;tonitis or
poor treatment risks. Medical treatment

AV usually show signs of vagal indigestion,
usually requires a confirmed diagnosis via
and abomasal impaction may be diagnosed
right-side laparotomy. ln cows that are
at the time of exploratory surgery.

treated, the met.abolic alkalosis, hypochlo

The induction of pa.r.turition using
remia, hypokalemia, and dehydration
dexa.r.nethasone (20 mg, IM) may be
should be corrected. Lubricants can be
indicated in affected cattle within 2 wk of
used in an attempt to move the impacted
tem1 and in which the response to treatment
material; it is necessary to empty the
for a few days has been unsuccessful.

abomasum surgically only in cattle with

Partrn;tion may assist recovery because of
severe impaction. Balanced electrolyte solua reduction in intra-abdominal volun1e. For tions are infused IV continuously for up to
sand impaction, affected cattle should be

72 hr at a daily rate of80-120 mI.Jkg. Some
moved off the sandy soil and fed good hay
cows respond well to this therapy and begin and a grass mixture cont.aining molasses rnminating and passing feces in 48 hr.

and minerals. Severely affected cattle

Mineral oil should be administered at 4 U
should be treated with mineral oil ( 4 Uday
day for 3 days. Additionally, dioctyl sodium
for3 days).

sulfosuccinate (DSS) can be irtjected once
into the abomasum during standing right

Prevention and Control: Prevention of
flank laparotomy at 60-100 mL of a 25%
dieta.r.-y abornasal impaction is possible by
solution for a 1,000-lb ( 4 50-kg) animal. This
providing the necessary nutrient requiredose rate should not be administered PO
ments for wintering pregnant beef cattle.

because DSS kills rumen protozoa. A

When low-quality roughage is used, it
beneficial response cannot be expected in
should be analyzed for crude protein and

<24 hr; in cattle that respond, in1provement
digestible energy. Based on the analysis,
is usually seen by the end of day 3 after
grain is usually added to the ration to meet
treatment begins. Erythromycin (10 mg/kg,
energy and protein requirements.

IM, once to twice daily) can be administered

The nutrient requirements of beef cattle
as a prokinetic in cattle that do not improve

( see p 2248) are guidelines for use under after surgery, provided that mineral oil has
average conditions; higher nutrient levels
been administered and physical obstrncthan those indicated may be necessary, tions were not identified at surgery.

particularly during periods of severe cold

Surgery may be considered, but results
stress. Adequate fresh drinking water
are often unsuccessful, probably because of should be supplied at all times; the practice abomasal atony, which appears to worsen
of forcing wintering cows to obt.ain their
after surgery. An alternative may be a
water requirements by eating snow while
rnrnenotomy to empty the rumen and infuse on low-quality roughage is hazardous.

ACUTE INTESTINAL OBSTRUCTIONS

IN LARGE ANIMALS

Intestinal obstrnctions a.r.·e seen in all large

Obstructions intem.1pt the flow of ingest.a
aninlal species but a.r.·e most common in
and can be mechanical or functional in
horses. Cattle are the most commonly
nature. Mechanical intestinal obstructions are
affected rnminants; diagnosis in sheep and
cha.r.-acterized as being lwninal or extraltunigoats is rare, except for intestinal volvulus nal. Extralunlinal obstructions include
in lan1bs. Other than inguinal hernias,
hemorrhagic strangulating obstructions in
intestinal obstructions are infrequently
animals with volvulus of tl1e GI tract, or
recognized in pigs.

simple extralu.111.inal compression in animals

246

ACUTE INTESTINAL OBSTRUCTIONS IN LARGE ANIMALS
with an expanding abdominal mass such as
are most often the sequela of parasite
lymphosarcoma or fat necrosis. Functional
migration or abdominal surgery; however,
obstmctions have no gross abno1mality but
most adhesions are clinically silent.

are characterized by a generalized hypomotil

Pedunculated lipomas are common in older
ity or ileus. In general, fw1ctional obstructions horses. Ileocecal, cecocecal, cecocolic, and VetBooks.ir
occur more often than mechanical obstrucsmall-intestinal intussusceptions also are tions, and they are commonly identified in
seen. Lymphosarcoma and other abdominal
horses after abdominal surgery.

neoplasms as well as abdominal abscesses
can cause intestinal obstruction.

Etiology and Pathogenesis: The

In cattle, specific causes of intestinal
inciting cause of a fwlctional intestinal
obstruction include volvulus of the
obstmction often is not detennined.

duodenal sigmoid flexure; intussusception

Functional obstmctions are associated with
of the jejunum and ileum; volvulus of the
altered intestinal motility, often due to
jejunoileal flange of the small intestine;
dietary or management factors, phytovolvulus at the root of the mesentery; bezoars, parasite infection, enteritis,
luniinal occlusion of the jejunum due to a
peritonitis, or electrolyte abnonnalities.

blood clot secondary to hemorrhagic

Mechanical obstructions (physical blockage jejunitis; obstruction of the small intestine of ingesta) occur due to abnormalities in the or spiral colon due to phytobezoars; bowel lumen, in the wall, or outside the
cecocolic volvulus; and atresia coli, recti,
tract. Mechanical obstructions include
and ani. lntussusceptions are thought to be
congenital obstmctions (atresia jejuni, coli,
the result of irregular peristaltic movements
recti, and ani in calves; atresia ani in lambs
related to enteritis, intestinal parasitism,
and pigs) that result in the lack of passage
dietary disorders, and mural masses.

of feces since birth.

Altered intestinal motility due to ingestion

In horses, transient fwlctional obstrucof a rapidly fennentable substrate may tions are common, as are feed in1pactions,
cause intestinal volvulus. Obstructions of
which usually involve the pelvic flexure
the small intestine can develop due to a
of the left colon. Parasite infection or
variety of fibrous bands ( eg, adhesions,

Inigration, dental abnonnalities, and dietary
parovarian bands, falciform ligament,
or management factors are often implicated
spermatic cord retraction into the abdomen
in the development of fwlctional obstrucafter surgical castration), mural thickening tion. ln1pactions and other luniinal

( eg, intestinal adenocarcinoma), extramural
obstructions can result from coarse feeds,
masses ( eg, lymphosarcoma, fat necrosis,
reduced water intake, enteroliths, or
abdominal abscesses), herniation ( omental,
ingested foreign material. Sites of impaction. inguinal, or umbilical), or hemorrhagic other than the pelvic flexure are the small
jejunitis (which results in lurninal blood
colon, transverse colon, tjght dorsal colon,
clots and obstruction). Adhesions and
cecum, and ileum. Other causes of intestinal abdominal abscesses can fo1m subsequent obstruction in horses are volvulus (twist on
to peritonitis, intraperitoneal injections, or
the mesenteric axis), torsion (twist along
previous abdominal surgery. Decreased
the long axis of the bowel), displacement of
motility caused by accumulation of volatile
the ascending Oarge) colon, andvolvulus of
fatty acids, possibly related to high-concenpart or all of the small intestine. Altered trate rations or an abmpt increase in the
motility and possibly strenuous exercise
concentrate:forage ratio, have been
and rolling may be initiating causes.

suggested as causes of cecocolic volvulus

Broodmares may be predisposed to
in cattle. They also are associated with
volvulus, torsion, or displacement of the
advanced pregnancy and ileus from
ascending colon during gestation and
concurrent disease. Atresia coli develops
shortly after parturition. Obstruction occurs most commonly in Holstein-Friesian calves either due to incarceration of the intestine
secondary to in utero ischemia of the

( usually small) by herniation through the
developing spiral colon.

inguinal canal, diaphragm, mesenteric
defects, umbilicus, or epiploic foramen; or

Clinical Findings and Diagnosis:

because of fibrous bands ( adhesions,

Intestinal obstruction in horses generally
mesodiverticular bands, or stalks of
manifests as abdominal pain, which is
pedunculated lipomas). Standardbred
termed colic (seep 248). ln cattle, signs of
stallions and colts develop inguinal and
abdominal pain include treading of the
scrotal hernias more commonly than other
hindlimbs, stretching, restlessness, and
breeds. Diaphragmatic hernias and
kicking at the abdomen; rolling and
mesenteric defects may be congenital or
bellowing are rarely seen. The signs of
traumatically induced. Adhesions in horses
intestinal obstruction in cattle are generally

ACUTE INTESTINAL OBSTRUCTIONS IN LARGE ANIMALS

247
more subtle than in horses and are usually
color of the mucous membranes, prolonged
referable to small-intestinal distention,
capillary refill time, and dehydration, are
tension on the intestinal mesentery (by the
most commonly associated with hemorweight of distended bowel), or vascular rhagic strangulating obstructions such as
impairment. Signs of pain are relatively
volvulus of the jejW1al-ileal flange of the
consistent but often transient with
small intestine. Volvulus of the jejW1al-ileal

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intussusceptions and are seen in some cases flange and volvulus at the root of the of cecocolic volvulus. Cattle with volvulus
mesentery are characterized by acute onset
of the small intestine at tl1e root of the
and rapid cardiovascular deterioration. This
mesentery are severely affected.

is in contrast with cecocolic volvulus or

Usually, cattle with intestinal obstruction
intussusception, which can continue for
are anorectic and pass few or no feces, and
several days in cattle.

milk production in lactating cows drops

Metabolic derangements range from
suddenly. The feces that are passed may be
hypokalemic, hypochloremic metabolic
covered with mucus, or mixed or coated
alkalosis in longstanding small-intestinal
with blood. Thick, raspberry-colored blood
and duodenal obstructions to severe
mixed with scant feces is characteristic
metabolic acidosis with hemorrhagic
of small-intestinal bleeding, particularly
strangulating obstructions. Usually, tl1ere
that associated with intussusception or
are no metabolic derangements in mild
hemorrhagicjejunitis. Blood from the colon
functional obstructions and early (simple)

or rectum is generally brighter red. Melena
mechanical obstructions, particularly if a
is typical of abomasal bleeding. Calves with
relatively distal part of the intestinal tract
atresia coli are healthy at birth but have
is involved. Hypocalcemia can develop,
progressive abdominal distention and
presumably due to decreased calcium
decreased appetite during the first few days
absorption from the duodenum.

of life. (See also CONGENITAL AND INHERITED

Peritoneal fluid changes reflect the

ANOMALIES OF' THE DIGESTIVE SYSTEM, p 162.)

degree of peritonitis and may aid in the

Abdominal distention, usually with a
diagnosis in both cattle and horses,
ping on simultaneous auscultation and
although results are more variable in cattle.

percussion, in the upper right caudal

Hemorrhagic strangulating obstructions are
abdominal quadrant occurs with cecocolic
characterized by an increase in the total
volvulus. Cecal dilatation does not produce
protein concentration and nucleated cell
abdominal distention, but a ping is generally
coW1ts of peritoneal fluid due to extravasapresent in the caudal dorsal paralumbar tion through the bowel wall. Neutrophils
fossa. In cecocolic volvulus, one or more
become degenerative, and intracellular
large, distended loops of large intestine are
gram-positive and gran1-negative bacteria
identified on palpation per rectum. Rumen
are seen in peritoneal fluid as the integrity
hypomotility is usually present, and
of the bowel wall is lost. Plant material irl
metabolic and cardiovascular derangement
the peritoneal cavity is indicative of bowel
tend to be mild except in cecocolic volvulus
rupture or inadvertent enterocentesis.

of long duration.

Peritoneal fluid analysis is normal with

Abdominal distention in the lower right
most simple mechanical and functional
abdominal quadrant is sometimes seen with
obstructions. When neoplasms are present
small-intestinal distention. Distended loops
and causing an extralW11inal obstruction,
of bowel may be palpable on rectal
neoplastic cells are sometimes identified
exanlination, and fluid may be heard on
in peritoneal fluid.

simultaneous ballottement and auscultation
of the right side of the abdomen. Small areas Treatment: Treatment of intestinal of tympanic resonance may be heard on
obstruction in horses is covered elsewhere
simultaneous auscultation and percussion.

( see p 253). Treatment of functional

Intussusceptions and fibrous bands that
intestinal obstruction in cattle is generally
cause small-intestinal obstruction can be
symptomatic and supportive after
palpated per rectum in -25% of cases.

identifying and eliminating the inciting

Ultrasonographic exanlination of the
cause ( eg, hypocalcemia, hypokalemia,
abdomen via the right paralwnbar fossa or
excessive grain intake) and allowing time
per rectum may help identify the presence
for normal intestinal motility to return.

of small-intestinal distention, ileus, and

If present, dehydration and electrolyte
an increased pe1itoneal fluid volume.

imbalances should be corrected by

Occasionally, ultrasonography can identify
appropriate fluid therapy (PO or IV).

an intussusception.

Lactating cows often benefit from calcium

ProfoW1d changes in cardiovascular
chloride gels administered orally or calcium
paran1eters, such as tachycardia, abnormal
borogluconate or calcium gluconate

248

ACUTE INTESTINAL OBSTRUCTIONS IN LARGE ANIMALS
administered SC, and oral potassium
obstructions, but early surgical intervention
ch101ide (120-240 g twice at 12-hr intervals). can in1prove the prognosis.

Secondary ketosis should be treated if

In cattle, 700/er-800/o of those with cecocolic
present. Erythromycin (10 mg/kg, IM, bid) is volvulus sUIVive, although 10% of cases the most effective pharrnacologic method to recur. For cows with small-intestinal increase abomasal emptying rate in cattle
obstruction amenable to resection and

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(and presumably increasing intestinal
anastomosis, 300/o-400/o sUIVive and lead a
motility), but studies documenting efficacy
productive life. For cows with volvulus of
in functional intestinal obstruction are
the jejunal-ileal flange of the small intestine
lacking. Pro kinetics should not be
or at the root of the mesentery, -500/o sUIVive
administered to cattle with a mechanical
if surgical correction is performed within a
obstruction because of the increased risk of
few hours of onset. Less than 300/o of calves
intestinal rupture proximal to the obstrucwith atresia coli survive to adulthood.

tion. The prognosis with most functional

Surgical correction of atresia coli is not
obstructions is good with appropriate
recommended in Holstein-Friesian calves
supportive therapy, particularly if the
because the condition is probably inhe1ited
inciting cause is identified and eliminated.

in this breed, although vascular damage

Mechanical obstructions almost always
secondary to amniotic vesicle palpation in
require surgery. Antimicrobial therapy
the first 6 wk of embryonic development
should be started preoperatively;
can also lead to intestinal ischemia and
supportive therapy, such as fluids,
atresia in calves.

electrolytes, and calcium, should be
administered as needed.

Prevention: Prevention of all, or even

Horses that require exploratory
most, cases of intestinal obstruction is
laparotomy to correct an intestinal
not possible. However, abrupt changes in
obstruction have an overall longtem1
feeding and management; inadequate water
swvival rate of 500Ai. The survival rate
intake; parasite infection; dental abnormaliis lower for horses with hemorrhagic ties; and access to coarse feeds, highly
strangulating obstructions and small-intesfermentable feedstuffs, and foreign material tinal lesions than for horses with simple
should be avoided or corrected.

COLIC IN HORSES

In its strictest definition, the tenn "colic"

that is located on the left side of the
means abdominal pain. Throughout the
abdomen beneath the rib cage. The junction
years, it has become a broad tenn for a
of the distal esophagus and the cardia is a
variety of conditions that cause a horse to
functional 1-way valve, permitting gas and
exhibit clinical signs of abdominal pain.

fluid to move into the stomach but not out.

Consequently, it is used to refer to

Consequently, conditions that in1pede the
conditions of widely varying etiologies and
normal aboral movement of gas and fluid
severity. To understand these etiologies,
through the small intestine may result in
make a diagnosis, and initiate appropriate
severe dilation and rupture of the stomach.

treatments, veterinarians must first

Because of its position, the stomach is
appreciate the clinically relevant aspects
difficult to visualize with radiography or
of equine GI anatomy, the physiologic
ultrasonography in large adult horses. The
processes involved in movement of ingesta
smaller size of the foal, however, permits
and fluid along the GI tract, and the extreme
assessment of gastric emptying by contrast
sensitivity of the horse to the deleterious
radiography.

effects of the structural components of the

The small intestine comprises the
bacteria that reside witllin the lumen of the
duodenum,jejunum, and ilewn, with the
intestine.

latter joining the cecwn at a distinct ileocecal
junction. The duodenum is positioned

GI Anatomy
primarily dorsally on the horse's right side,

The horse is a monogastric anin1al, with a
where it is suspended from the dorsal body
relatively small stomach ( capacity 8-10 L)

wall by a short mesentery of 8-5 cm.

COLIC IN HORSES

249

Consequently, the duodenum is not involved
the junction between the left ventral colon
in small-intestinal displacements involving
and pelvic fle:>nrre is the most common
the mesentery (volvulus). At the base of the
location for impactions.

cecum in the right paralumbar fossa region,

The diameter of tl1e dorsal colon is largest
the duodenwn turns toward the midline. It is
either at its diaphragmatic flexure or in tl1e
at this point that the duodenum, if distended
right dorsal colon. There are no saccula

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with gas or fluid ( eg, in horses with proximal
tions in eitiler the left or right pottion of the
enteritis), can be felt on rectal examination.

dorsal colon. The right dorsal colon is

As tl1e small intestine reaches the dorsal
closely attached to the right ventral colon
midline, it turns anteriorly, its mesentery
by a short intercolic fold and to the body
lengthens, and it becomes known as the
wall by a tough, common mesente1ic
jejunum. The characteristic long mesentery
attachment with the base of the cecwn. In
allows loops of the jejunum to rest on the
contrast, neither the left ventral nor left
contents of the ventral portion of the
dorsal colons are attached directly to tl1e
abdomen. The jejunum is -65 ft (19.5 m)

body wall, allowing these portions of the
long; its length, coupled with its long
colon to become displaced or twisted.

mesentery, allow it to be involved in

Ingesta moves from the large right dorsal
small-intestinal volvulus and incarcerations.

colon into the sho1t transverse colon, which

At the end of the jejunum, tl1e wall of the
has a diameter of -10 cm and is fixed firmly
intestine becomes more muscular, the
to the most dorsal aspect of tile abdonlinal
lun1en is narrowed, and an additional
cavity by a strong, short, fibrous mesentery.

mesente1ic attachment becomes apparent.

The transverse colon is located cranial to

The last 18 in. (45 cm) of the small intestine,
the cranial mesenteric artery. Finally, the
the ileun1, joins the cecum at its dorsal
ingesta enters the sacculated descending
medial aspect. This junction is identified by
colon, which is 10-12 ft (3-3.6 m) long.

the attachment of the ileocecal fold from
the ileun1 to the dorsal band of the cecun1.

Blood Supply to the GI Tract

This ileocecal fold is used as a landmark to
locate the ileum during abdominal surgery.

The celiac and cranial mesenteric arte1ies

From the ileum, the ingesta enters the

(branches of tile abdominal a01ta) supply
cecum, a large, blind-ended fermentation
blood to the GI tract. The celiac artery
vat situated primarily on the horse's right
supplies arterial blood to the stomach,
side, extending from the region of the
pancreas, liver, spleen, and the first portion
paralumbar fossa to the xiphoid cartilage
of the duodenun1. The cranial mesente1ic
on ventral midline. The cecwn is 4-5 ft
artery supplies arterial blood to the

(1.2-1.5 m) long and can hold 27-30 Lof
remaining portion of tile duodenum; to all of
feed and fluid. Under tl1e influence of the
the jejunun1, ileum, cecum, large colon, and
cecal musculature, the ingesta in the cecum
transverse colon; and to the first portion of
is massaged, mixed with microorganisms
the descencling colon. Because tile larg!!

capable of digesting cellulose, and
colon is attached to the body wall only in tile
eventually passed through the cecocolic
region near tile cranial mesenteric aitery,
opening into the 1ight ventral colon. The
tile blood supplying all portions of the colon
attachment of the cecum to the dorsal body
must traverse the entire length of tile colon.

wall is wide, thus mininlizing the likelihood

The pelvic flexure receives its blood supply
the cecum can become displaced or twisted
from two branches of tl1e cranial mesenteric
on its own.

artery; one branch supplies tile right and left

The right ventral colon is divided into
dorsal colons before reaching the pelvic
sacculations that help mix and retain plant
flexure, and the oilier branch supplies tl1e
fibers until tiley are digested. It is positioned right and left ventral colons before reaching on the ventral aspect of the abdomen,
the pelvic flexure. Thus, volvulus of the
extending from the flank region to the rib
large colon near the junction of the colon
cage. The ventral colon then turns toward
and cecum may impede the flow of blood to
tile left, beconling the sternal flexure and
the entire left colon.

tl1en the left ventral colon. The left ventral

The major branches of the cranial
colon, which also is large and sacculated,
mesenteric artery can be damaged by the
passes caudally to tile left flank area. Near
migrating forn1s of Strongylus vulgaris
the pelvic region, the dian1eter of the colon

(seep 316).

decreases markedly, and the colon folds
back on itself. This region, called the

Natural Openings in the Abdomen
pelvic flexure, is tl1e initial portion of the

There are several natural openings or
unsacculated left dorsal colon. Presumably
spaces within the abdominal cavity that can
because of the abrupt decrease in diameter,
be important in conditions causing colic.

250

COLIC IN HORSES
transverse colon

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ileum
right ventral colon
apex of cecum

Left medial view of cecum and right colon, horse. Illustration by Dr. Gheorghe Constantinescu.

The inguinal canal provides an opening
the feed particles in the ingesta and then
through which intestine might pass and
initiates the appropriate motility pattern.

become trapped. Although inguinal hernias

If the ingesta has been digested sufficiently,
are conm1on in young foals, they rarely
it is moved in a norn1ograde ilirection; if
cause clinical problems; the situation is
additional digestion is necessary, the ingesta
considerably different in stallions. Similarly,
is moved in a retrograde direction to retain
if the ventral abdominal wall fails to forn1
it in the ventral colon. This theory has been
properly around the umbilicus, an opening
proposed to help account for the common
remains and the potential exists for
clinical occurrence of obstruction at or near
intestinal problems to develop secondary to
the pelvic flexure.

an umbilical hernia The epiploic foramen, a
natural opening between the portal vein, the
caudal vena cava, and the caudate lobe of

Clinical f"mamgs
the liver, can be the site of intestinal

Numerous clinical signs are associated with
incarcerations. Finally, there is a natural
colic. The most common include pawing
space between the dorsal aspect of the
repeatedly with a front foot, looking back at
spleen and the left kidney. This space is
the flank region, curling the upper lip and
bounded by the renosplenic ligament, a
arching the neck, repeatedly raising a rear
strong band of tissue that connects the
leg or kicking at the abdomen, lying down,
dorsomedial aspect of the spleen with the
rolling from side to side, sweating,
fibrous capsule of the left kidney. This
stretching out as if to urinate, straining to
ligament provides a "shelf' over which
defecate, distention of the abdomen, loss of
large colon can be displaced.

appetite, depression, and·decreased number
of bowel movements. It is uncommon for a

Co onic Motility Patterns
horse with colic to exhibit all of these signs.

Normograde peristalsis in the left ventral

Although they are reliable indicators of
colon moves ingesta toward the left dorsal
abdominal pain, the particular signs do not
colon, and the muscles in the wall of the left
inilicate which portion of the GI tract is
dorsal colon contract to move the ingesta
involved or whether surgery will be needed.

toward the diaphragmatic flei.'ure. There is
evidence, however, that the muscles in the

Diagnosis
left ventral colon contract in a retrograde

A diagnosis can be made and appropriate
fashion, from the pelvic flexure region
treatment begun only after thoroughly
toward the sternal flexure. Furthermore,
exan1ining the horse, considering the
these contractions appear to originate from
history of any previous problems or
a pacemaker region in the pelvic flexure. It
treatments, determining which part of the
has been hypothesized that this pacemaker
intestinal tract is involved, and identifying
senses either the size or the consistency of
the cause of the particular episode of colic.

COLIC IN HORSES

251
intercolic fold
pelvic flexure
left dorsal colon
small
neck of the colon
intestine

\
transverse
ampu� V

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colon

!1
of the

:-

I \

� \\
cecum

1�·'I
diaphragmatic

/
flexure

'> I
body�/'·, ,I/}'

�.

right ventral colon

The large intestine of the horse. Illustration by Dr. Gheorghe Constantinescu.

In most instances, colic develops for one of
the intestinal lining (ulceration), and
four reasons: 1) The wall of the intestine is

"w1explained colic." In general, horses with stretched excessively by either gas, fluid, or
strangulating obstructions and complete
ingesta. This stimulates the stretch-sensitive obstructions require emergency abdominal nerve endings located within the intestinal
surgery, whereas horses with the other
wall, and pain impulses are transmitted to
types of disease can be treated medically.

the brain. 2) Pain develops due to excessive

The history of the present colic episode
tension on the mesentery, as might occur
and previous episodes, if any, must be
with an intestinal displacement. 3) Ischemia
considered to determine whether the horse
develops, most often as a result of
has had repeated or similar problems or
incarceration or severe twisting of the
whether this episode is an isolated event.

intestine. 4) Inflammation develops and

The duration of the present episode, the rate
may involve either the entire intestinal wall
of deterioration of the horse's cardiovascu

(enteritis) or the covering of the intestine
lar status, the severity of pain, whether feces

(peritonitis). Under such circumstances,
have been passed, and the response to any
proinflan1matory mediators in the wall of
treatments are important pieces of
the intestine decrease the threshold for
information. It is also critical to determine
painful stinmli.

the horse's dewom1ing history (schedule,

The list of possible conditions that cause
treatment dates, drugs used), when the teeth
colic is long, and it is reasonable first to
were floated last, if any changes in feed or
determine the most likely type of disease
water supply or amount have occurred,
and begin appropriate treatments and then
whether or not the horse is a "cribber," and to make a more specific diagnosis, if
whether the horse was at rest or exercising
possible. The general types of disease that
when the colic episode started.

cause colic include excessive gas in the

The physical examination should include
intestinal lumen (flatulent colic), sin1ple
assessment of the cardiopulmonary and GI
obstruction of the intestinal lumen,
systems. The oral mucous membranes
obstruction of both the intestinal lumen and
should be evaluated for color, moistness,
the blood supply to the intestine (strangulatand capillary refill time. The mucous ing obstruction), interruption of the blood
membranes may become cyanotic or pale in
supply to the intestine alone (nonstrangulathorses with acute cardiovascular comproing infarction), inflan1111ation of the intestine mise and eventually hyperemic or muddy as (enteritis), inflanrn1ation of the lining of the
peripheral vasodiJation develops later in
abdominal cavity (peritonitis), erosion of
shock. The capillary refill time (normal-1.5

252

COLIC IN HORSES
sec) may be shortened early but usually
dorsal to the base of the cecwn on the right
becomes prolonged as vascular stasis
side of the abdomen, and distended loops of

(venous pooling) develops. The memjejunum can be identified in the middle of branes become dry as the horse becomes
the abdomen.

dehydrated. The heait rate increases due to

A san1ple of peritoneal fluid ( obtained
pain, hemoconcentration, and hypotension;
via paracentesis performed aseptically

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therefore, higher heart rates have been
on rnidline) often reflects the degree of
associated with more severe intestinal
intestinal damage. The color, cell count and
problems (strangulating obstruction).

differential, and total protein concentration

However, it is important to note that not all
should be evaluated. Nonna] peritoneal
conditions requiring surgery are accompafluid is clear to yellow, contains <5,000
nied by a high heart rate.

WBCs/µL (most of which ai·e mononuclear

An in1portant aspect of the physical
cells), and <2.5 g of protein/clL.

exanlination is the response to passing a

The age of the horse is impo1tant,
nasogastric tube. Because horses can
because a number of age-related conditions
neither regurgitate nor vomit, adynarnic
cause colic. The more common of these
ileus, obstructions involving the small
include the following: in foals-atresia coli,
intestine, or distention of the stomach with
meconiun1 retention, urope1itoneum, and
gas or fluid may result in gastric rupture.

gastroduodenal ulcers; in yearlings-as

Passing a stomach tube may, therefore, save
carid impaction; in the young-small-intesthe horse's life and assist in diagnosis of tinal intussusception, nonstrangulating
these conditions. If fluid reflux occurs, the
infarction, ai1cl foreign body obstruction;
volume and color of the fluid should be
in the middle-aged-cecal impaction,
noted. In healthy horses, it is common to
enteroliths, and large-colon volvulus; and
retrieve <l L of fluid from the stomach.

in the aged-pedunculated lipoma and

The abdomen and thorax should be
mesocolic rnpture.

auscultated and the abdomen percussed.

Ultrasonographic evaluation of the

The abdomen should be auscultated over
abdomen may help differentiate between
several areas ( cecum on the right, small
diseases that can be treated medically and
intestine high on the left, colon lower on
those that require surgery. The technique
both the right and left). Intestinal sounds
also can be applied transrectally to clarify
associated with episodes of pain may
findings noted on rectal palpation. In foals,
indicate an intralurninal obstruction ( eg,
echoes from the large colon and small
impaction, enterolith). Gas sounds may
intestine are commonly identified from
indicate ileus or distention of a viscus. Fluid
the ventral abdominal wall, whereas only
sounds may indicate impending diai.Th�a
large-colon echoes are usually seen in adult
associated with colitis. A complete lack of
horses. The large colon cai1 be identified by
sounds is usually associated with adynan1ic
its sacculated appearance. The duodenum
ileus or ischemia. Percussion helps identify
cai1 be identified in the tenth intercostal
a grossly distended segment of intestine
space and traced around the caudal aspect

( cecum on right, colon on left) that may
of the right kidney. The jejunum is rai·ely
need to be trocarized. The respiratory
identified during trai1sabdorninal ultrasonorate may be increased due"to fever, pain, graphic exan1ination of normal adult horses,
acidosis, or an underlying respiratory
whereas the thick-walled ileum can be
problem. Diaphragmatic hernia is also a
identified by transrectal examination.

possible cause of colic.

The most common abn01malities

The most definitive part of the examinaidentified by ultrasonography include tion is the rectal examination. The veterinaringuinal hernia, renosplenic entrapment of ian should develop a consistent method of
the lai·ge colon, sai1d colic, intussusception,
palpating for the following: aorta, cranial
enterocolitis, 1ight dorsal colitis, ai1d
mesenteric artery, cecal base and ventral
pe1itoni tis. Stallions with inguinal hernia
cecal band, bladder, peritoneal surface,
have incarcerated intestine on the affected
inguinal rings in stallions and geldings or the side; it is possible to identify the intestine ovaries and uterus in mai·es, pelvic flexure,
and to obtain irtforrnation concerning the
spleen, and left kidney. The intestine should
thickness of its wall as well as the presence
be palpated for size, consistency of contents or lack of peristalsis. In horses with (gas, fluid, or impacted ingesta), distention,
renosplenic entrapment of the large colon,
edematous walls, and pain on palpation. In
the tail of the spleen or the left kidney
healthy horses, the small intestine cannot
cannot be in1aged, or the gas-filled large
be palpated; with small-intestinal obstruccolon is present in the caudodorsal aspect of tion, strangulating obstruction, or enteritis,
the abdomen in the region of the renosplenic
the distended duodenum can be palpated
space. Horses with sai1cl colic have granular

COLIC IN HORSES

253
hyperechoic echoes originating from the

In these instances, the cause of colic is
affected portion of the colon. The characterpresumed to be spasm of intestinal muscle istic finding in horses with intussusception
or excessive gas in a portion of the intestine.

is the "bull's eye" appearance of the affected If, however, the pain is due to an intestinal
portion of the small intestine. Very often the
twist or displacement, some of the stronger
intestine proximal to the intussusception is
analgesics may mask the clinical signs that

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distended, and the strangulated portion is
would be useful in making a diagnosis.

thickened. Horses with enterocolitis

For these reasons, a thorough physical
frequently have evidence of hyperperistalsis, exanlination should be completed before any thickened areas of the bowel wall, and fluid
medications are given. However, because
distention of the intestine. In contrast,
horses with severe colic or pain may hurt
horses with right dorsal colitis commonly
themselves and become dangerous to people
have marked thickening of the wall of the
nearby, analgesics often must be given first.

right dorsal colon. In horses with peritonitis, Additionally, many horses with less severe the peritoneal fluid may be anechoic, or
problems may need pain relief until the other
there may be evidence of flocculent material treatments have time to be effective. An and fibrin between serosal surfaces of the
analgesic that has tl1e fewest adverse effects
viscera.

and causes the least alteration in the horse's
attitude should be selected.

Treatment

Medications used commonly for
abdominal pain are NSAIDs that reduce the

Horses with colic may need either medical
production of prostaglandins. When these
or surgical treatments. Almost all require
drugs are used as recommended, their toxic
some form of medical treatment, but only
effects on the kidneys and GI tract occur
those with certain mechanical obstructions
infrequently. Clinical experience suggests
of the intestine need surgery. TI1e type of
that flunixin megluniine may mask the early
medical treatment is determined by the
signs of conditions that require surgery and,
cause of colic and the severity of the
therefore, must be used carefully in horses
disease. In some instances, the horse may
with colic.

be treated medically first and the response

The most commonly used sedative for
evaluated; this is particularly appropriate
colic is xylazine, an a,-agonist. Within a few
if the horse is mildly painful and the
minutes after administration, the horse
cardiovascular system is functioning
stands quietly and is less responsive to pain.

normally. Ultrasonography can be used to

Unfortunately, the effects of xylazine are
evaluate the effectiveness of nonsurgical
short-lived, and it inhibits intestinal
treatment. If necessary, surgery can be used
muscular activity; it also decreases cardiac
for diagnosis as well as treatment.

output and thus reduces blood flow to the

If evidence of intestinal obstruction with
tissues. Detomidine, a more potent
dry ingesta is found on rectal exanlination, a a
primary aim of treatment is to rehydrate and

2-agonist that is much longer acting, is used
successfully in sinillar circun1stances.

evacuate the intestinal contents. If the horse

Of the narcotic analgesics, butorphanol
is severely painful and has clinical signs
is used most often in horses with colic.

indicating loss of fluid from the bloodstream Butorphanol has few adverse effects on the (high heart rate, prolonged capillary refill

GI tract or heart. However, when given in
time, and discoloration of the mucous
large doses, narcotics can cause excitemembranes), the initial aims of treatment ment, and the horse may become unstable.

are to relieve pain, restore tissue perfusion,

Butorphanol is frequently combined with an
and correct any abnormalities in the
a,-agonist to produce a more prolonged
composition of the blood and body fluids
period of analgesia.

(see TABLE 5). If damage to the intestinal wall Although pain relief usually is provided

( as a result of either severe inflammation or
by analgesics, tl1ere are other important
a displacement or strangulating obstrucways to reduce the degree of pain. For tion) is suspected, steps should be taken
example, passing a nasogastric tube (also
to prevent or counteract the ill effects of
an important part of the diagnostic
bacterial endotoxins that cross the damaged evaluation) may remove any fluid that has intestinal wall and enter the bloodstrean1.

accumulated in the stomach because of an

Finally, if there is evidence the colic episode obstruction of the small intestine. The is caused by parasites, one aim of treatment
removal of this fluid not only relieves pain
is to eliminate the parasites.

from gastric distention but also prevents
rupture of the stomach.

Pain Relief: In most cases of colic, pain is Horses with displacement of the colon
mild, and analgesia is all that is needed.

over the renosplenic ligament (ie, left dorsal

254

COLIC IN HORSES
displacement of the colon) may benefit from the degree of hemoconcentration and administration of phenylephrine. This drug
whether concentrations of electrolytes
is given to contract the spleen and often is
m·e abnom1al are critical for accurate
followed by light exercise on a lunge line in
treatment of horses with severe colic. The
an effort to dislodge the entrapped colon. It
balance of body fluids can be reestablished

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is important to note that this treatment may
by administering IV fluids formulated to
cause fatal hemorrhage due to hypertension
replenish the deficient electrolyte(s). In
in horses > 15 yr old.

most instances, however, fluid therapy
must be started before laboratory results

Fluid Therapy: Many horses with colic
are available, particularly when the horse
benefit from fluid therapy to prevent
is showing clinical signs of circulatory
dehydration and maintain blood supply to
shock.

the kidneys and other vital organs. The

When IV fluids are needed but the clinical
fluids may be given either through the
signs are mild to moderate, the horse is
nasogastric tube or IV, depending on the
usually given 8-10 L of a sterile replacement
particular intestinal problem (see TABLE 5).

fluid that contains electrolytes in concentra

Horses with strangulating obstruction or
tions similar to those that normally exist in
enteritis must be given fluids IV, because
the blood. This volmne is adn1inistered
absorption of fluids from the diseased
throughout 1-2 hr, and the horse is
intestine is in1paired and fluid may be
reevaluated to determine whether
secreted into the lumen of the intestine. The
additional fluids m·e needed. Horses in
latter mechanism causes a buildup of fluid
circulatory shock require much larger
in the intestine, which must be removed
volumes of IV fluids, given as rapidly as
from the stomach through a nasogastric
possible; as much as 20 L in 1 hr may be
tube. This abnormal movement of body
needed to reestablish tissue perfusion. In
fluids into the intestine contributes to the
severe cases, hypertonic saline (7% NaCl)

development of circulatory shock, which is
may be given to rapidly increase plasma
often the ultimate cause of death.

volume. Depending on the cause of colic, IV

In healthy horses, most of the fluid in the
fluids may be needed for several days until
intestinal tract is reabsorbed in the cecum
intestinal function has returned, electrolyte
and colons. In fact, -95% of the fluid that
concentrations m·e balanced, and the horse
normally enters the lun1en of the large
can maintain its fluid needs by drinking.

intestine is returned to the bloodstream.

Under such circumstances, the daily IV fluid

Therefore, horses with intestinal obstrucrequirements may range from 30 to 100 L.

tions near the pelvic flexure usually require

Fluids are sometimes given through the
relatively small amounts of IV fluids,
nasogastric tube as part of the treatment of
whereas horses with small-intestinal
in1pactions of the colon. Many clinicians
obstrnctions need extremely large
believe the san1e result can be accomamounts.

plished by giving large volumes offluids

The volun1e and type of fluid to be given

IV. If the horse will not drink voluntarily
are determined by the severity and cause of and there is no obstruction in the small the problem. Laboratory tests to.detem1ine
intestine, hydration may be maintained

GENERAL CONCEPTS REGARDING FLUID NEEDS IN DEHYDRATED

HORSES

Determining

Factor

Formula Used

Amount for a 500-kg Horse

Fluid deficit

% dehydration x body weight (kg) 4o/o-l (JOA, x 500 = 20-50 L

Maintenance

50 mllkg/24 hr

50 x 500 = 25 V24 hr

Fluid losses

Estimate reflux or diarrhea
volwne

Rate of

5QOA, in 1-2 hr; 500Ai throughout

20-35 L in first 1-2 hr; remainder
adn1inistration rest of day
distributed throughout next 23 hr

Adapted, with permission, from Zimmel ON, Management of pain and dehydration in horses with colic. ln Current Thera:py in Equine Medicine, 5, 2003, Robinson, NE, (ed), Elsevier.

COLIC IN HORSES

255
by administering fluids through the tube.

others. This apparent lack of efficacy of

Fluids or medications should not be given
anti-endotoxin antibodies also may indicate
through the nasogastric tube if fluid reflux is
that some of the systemic inflanm1atory
being removed from the stomach, because
responses encountered are triggered by
this indicates either the stomach or the
other bacterial components. Because
small intestine is not emptying properly.

endotoxin itself stimulates the generation of

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a wide array of inflammatory substances

Protection Against Components of
that ultimately produce the pathophysio

Enteric Bacteria: In healthy horses, the
logic effects, neutralizing antibodies should
mucosa! lining of the GI tract restricts
be used as early as possible in the course of
enteric bacteria and their structural
the disease.

components ( eg, endotoxins, lipoproteins,

AB an alternative approach, polyrnyxin B
nucleic acids, flagellin) to the intestinal
has been used to prevent endotoxin from
lumen. These bacterial components exist in
interacting with the horse's inflan101atory
high concentrations in the intestinal lumen,
cells. Polyrnyxin B has well-documented
because they are released when the bacteria nephrotoxicity; however, concentrations die or, in some cases, when bacteria
of polyrnyxin B that bind endotoxin are
multiply rapidly. However, when this
far less than those that cause toxic effects.

mucosa! barrier is disrupted, as occurs with

Polyrnyxin B has been evaluated in several
intestinal ischemia or inflan1rnation, the
experimental studies of endotoxemia
bacterial components can move into the
and is being used in clinical cases at
peritoneal cavity and then be absorbed into

1,000-5,000 U/kg, bid-tid. This forn1 of
the systemic circulation. Based on recent
therapy should be started as early as posresearch studies, equine leukocytes are sible in the clinical course of the disease. In
most sensitive to endotoxins but also
addition, fluid replacement therapy should
respond strongly to other components,
be maintained in hypovolemic horses, and
most notably flagellin. Most studies
serum creatinine concentration should be
perfo1med to date have focused on endotoxclosely monitored. This latter concern is ins, because they are assumed to be the
especially relevant for azotemic neonatal
primary triggers for the systemic inflanm1afoals, because they appear to be more tory responses that occur in many horses
susceptible to the nephrotoxic adverse
with GI disease. These responses can
effects of polymyxin B.

include fever, depression, hypotension,
reduced tissue perfusion, and coagulation

Intestinal Lubricants and Laxatives:

abnormalities. In fact, many equine

A common cause of colic in horses is simple
practitioners refer to these physiologic
obstruction of the large colon by dehyresponses as "endotoxemia." Thus, rnininuzdrated ingesta, sometimes mixed with sand.

ing the inflanm1atory responses to

These impactions generally develop near
endotoxernia is a vital part of colic therapy.

the pelvic flexure or in the right dorsal colon

Prostaglandins are involved in causing
but may involve any portion of the large
many of endotoxin's early ill effects.

colon, descending colon, or cecum. In most

Flunixin megluntine reduces the cellular
instances, lubricants or fecal-softening
production of prostaglandins and can help
agents given through a nasogastric tube
prevent some of their effects. Because
soften the in1pacted ingesta, allowing it to
flunixin can help prevent some of the early
be passed. This form of therapy can be
effects of endotoxemia at dosages less than
aided by the sinmltaneous administration
tl1e recommended dosage (1.1 mg/kg),
of IV fluids. Keeping the horse muzzled is
smaller dosages (0.25 mg/kg) can be
advised to prevent further impaction of feed
administered without masking clinical signs
material while the obstruction is softening.

associated with conditions that require

Mineral oil is the most commonly used
surgery.

medication in the treatment of a large-colon

There is considerable controversy
in1paction. It coats the inside of the intestine
regarding the efficacy of plasma or serum
and aids the norn1al movement of ingesta
that contains antibodies designed to
along the GI tract. It is administered through
neutralize endotoxin. These antibodies
a nasogastric tube, as much as 4 L, once or
are directed against the components of
twice daily, until the impaction is resolved.

endotoxins that are consistent among

Although mineral oil is safe, it is not highly
different gram-negative bacteria. The
effective in treating severe impactions or
results of clinical studies using such
sand in1pactions, because it may sin1ply
antibodies have been conflicting, with
pass by the obstruction without softening it.

evidence of protection being seen in some

Dioctyl soditun sulfosuccinate (DSS) is a
studies and no positive effects identified in
soap-like compound that acts by drawing

256

COLIC IN HORSES
water into the dry ingesta. It is more

Fenbendazole kills migrating strongyles if
effective than mineral oil in softening
given at twice the recommended dosage
impactions; however, it may interfere with
daily for 5 days or at 10 times the recomthe normal fluid absorptive functions of the mended dosage daily for 3 days. As a result
colon and can be toxic. Thus, DSS can be
of common use of these anthelmintics,
given safely only in small quantities two
chronic intermittent colic once thought to

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times 48 hr apait.

be caused by thromboembolism or parasite

A safe and useful compound to treat
larval migration has largely been eliminated
in1pactions, especially those containing
from equine practice.

sand, is psyllium hydrophilic mucilloid.

There is considerable evidence tllat

When mixed with water, it fom1s a
dainage caused by cyatllostomins causes
gelatinous mass that carries ingesta along
colic, diatThea, and loss of condition,
the GI tract. Although usually given through
particularly in young horses. These signs
a nasogastric tube to horses with impacare seen on a seasonal basis and are tions, psylliurn also may be used as a
synchronous with the emergence of large
preventive by mixing the dry powder
nwnbers of encysted larvae into the lumen
into the feed. Horses that live in a sandy
of tile large colon. In temperate areas of tl1e
environment or that persistently develop

Northern hemisphere, tile larvae encyst
impactions may be given psylliwn powder,
during tile winter montl1S and emerge in tile

400 g/500 kg/day, in their feed for 7 days.

late winter and spring, causing ulceration,

This treatment is repeated 2-3 times each
edema, and inflainmation of tl1e mucosa of
year in an effo1t to prevent development
tile large colon. This may result in diarrhea,
of sand impactions.

protein Joss, weight loss, and mild

Strong laxatives that stimulate intestinal
intermittent colic and fever. Horses witl1
contractions are not commonly used to
cyatllostomosis require treatment witll
treat impactions and, in fact, may worsen
larvacidal dosages of anthelmintics such as
the problem. Occasionally, horses with
ivem1ectin, moxidectin, ai1d fenbendazole.

extremely hard inlpactions are treated with

Some horses require analgesics, supportive
magnesillm sulfate, which draws body fluids care, and proper nutritional support.

into tl1e GI tract. Adverse effects inclllde

See also p 316 for a detailed discussion of dehydration and an increased risk of
treatment for Jai·ge and small strongyles.

diai-rhea.

Fluid therapy, whether the fluids are

Surgery: Surgery usually is necessary
administered through a nasogastric tube
if there is a mechanical obstruction to
or IV, is an impmtant and effective part
tile normal flow of ingesta that carmot be
of treating horses with colonic or cecal
corrected medically or if tile obstruction
in1pactions. If an inlpaction does not start to also interferes witll the intestinal blood
break down within 3-5 days, surgery may be supply. The latter conditions result in deatll necessary to evacuate ·the intestine and help
of tile horse unless surgery is performed
restore normal motility.

quickly. Occasionally, surgery is indicated
as an exploratory diagnostic procedure for

Larvicidal Deworming: The normal
horses witll chronic colic tllat have not
migratory routes of the larvae of large
responded to routine medical tllerapy.

bloodworms, particularly Strongylus

Under most circurnstai1ces, horses
vulgaris, have been implicated in many
exhibiting signs of severe abdominal pain
cases of colic. In response to the migratory
nonresponsive to analgesic tllerapy require
and maturation processes of the larvae in
emergency abdominal surgery. Generally,
the cranial mesenteric artery, the wall of the
tile lwnen of tile intestine is completely
artery becomes thickened and forms loose
obstructed, such as occurs with a stranguplaques of inflairunatory tissue. It has been lating obstruction, enterolitl1iasis, or severe
hypothesized that these plaques activate
displacement. Sinlilarly, horses with an
coagulation, resulting in thromboembolism.

abnom1ally distended intestine on rectal

The blood supply to the intestine may be
exanlination and peritoneal fluid witl1 an
reduced, resulting in altered intestinal
increased total protein concentration and
motility, a change in the absorption of
number of erytl1rocytes probably have a
nutrients from the intestine, or death of the
strangulating lesion tllat requires surgical
intestine. Thus, thromboembolism has been
correction. However, these classic findings
presumed to be a cause of recw-rent
tllat characterize horses requiring
episodes of colic and weight loss.

emergency surgery do not al ways exist.

Modem dcworming medications, such as

Some horses with mild or moderate pain
ivermectin and mox.idectin, have activity
may also require surgery, and ajudgment
against migrating S vulgaris larvae.

must be based on a tllorough physical

COLIC IN HORSES

257
examination and other methods of
surgery for inoperative conditions. Swvival
evaluation, including abdominal ultrasonogrates for horses with strangulating raphy. Some of the more commonly used
obstruction and inflanm1atory diseases
indications for surgery in horses with colic
were only 24% and 42%, respectively. In
include w1controllable pain; >4 L of fluid
contrast, horses with an w1defmcd cause
reflux from the stomach; no borborygmi on
for the colic episode had a survival rate of

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auscultation; peritoneal fluid with increased 94%. When the segment of the GI tract was protein, erythrocytes, and toxic neutrophils;
considered, the swvival rates for conditions
and a tightly distended intestine, displaced
affecting the small intestine and stomach
colon, or enterolith or foreign body
were poorer than for those affecting the
identified on rectal exan1ination.

large colon. In addition, conditions that

Perfonning surgery (if indicated) early
interfered with both tl1e passage of ingesta
is critical to success and improves the
and the intestinal blood supply dramatically
prognosis for survival. Therefore, it is more
decreased the chances of smvival. The
in1portant to decide whether the horse
results of more recent studies are far more
should be referred to a clinic where surgery
promising, with survival rates for horses
could be perfom1ed if needed than to
tmdergoing emergency abdominal surgery
determine whether emergency surgery is
often >800A,. Fw.thermore, there have been
definitively required. It is generally prudent
reports docwnenting survival rates of 700A,
to refer the following types of cases: 1) a
for horses requiring resection of stranguhorse that responds initially to an analgesic lated small intestine or correction of
but requires additional analgesic tl1erapy a
large-colon volvulus. In earlier retrospective
few hours later, 2) a horse tlmt continues to
studies, these conditions were associated
exhibit signs of pain despite administration
with survival rates �30%. Although data on
of analgesics, 3) a horse that remains
longtem1 survival (ie, the horse returning
painful but has normal pe1itoneal fluid,
to its intended use) are more difficult to

4) a horse with distended loops of small
obtain, recent findings indicate that most
intestine on rectal exan1ination, or 5) a
horses that die or are euthanized because
horse with large quantities of fluid removed
of serious problems do so within 3 mo
from the stomach but no distended small
after surgery.

intestine palpable on rectal examination.

Values obtained from several variables

When surgery is required, in most
are often combined to predict smvival in
instances, the horse is anesthetized and
horses with colic. Prognostic indicators
positioned in dorsal recwnbency, and the
include pain assessment, intestinal
surgical incision is made on the ventral
distention, mucous membrane color, and
midline. Once the peritoneal cavity is
cardiovascular system function. Smvival
entered, portions of the intestine should
rates are highest for horses with mild
be examined to detennine the definitive
abdominal pain and are lowest for horses
cause of the colic. Correction may involve
with severe pain. Horses with palpable
repositioning a displaced po1tion of
intestinal distention have lower survival
intestine, removing an obstruction, or
rates than horses lacking evidence of
resecting devitalized intestine. When
intestinal distention, and survival rates
devitalized segments of intestine must be
are even lower if no intestinal sounds are
removed or an enterotomy perfom1ed,
audible on auscultation of the abdomen.

postoperative care may include antibiotics,

Red mucous membranes are frequently

IV fluids, polymyxin B, anti.bodies directed
associated with endotoxemia, which
against endotoxin, and NSAIDs to combat
decreases the survival rate. Cardiovascular
endotoxemia. When a displaced segment of
system function reflects the degree of shock
intestine is simply returned to its normal
and, therefore, correlates with the
location, the postoperative care is much
prognosis for survival. For instance, horses
less intense. Each horse must be handled
with low systolic blood pressure or a high
individually, and its treatment needs are
heait rate have a decreased chance of
based on the response to surgery and
survival.

development of complications.

Of the laboratory analyses used to predict
survival, blood lactate concentration and

Prognosis
the anion gap are used most often.

Measurement of blood lactate has been

A large retrospective study in the USA
used as an indicator of tissue perfusion,
docw11ented an overall swvival rate of 600A,
with increasing concentrations of lactic acid
for horses with colic and a survival rate of
corresponding with poor tissue perfusion.

500Ai for those horses undergoing abdominal

In recent studies, changes in blood lactate
surgery, including those euthanized dw·ing
concentration over tin1e have been

258

COLIC IN HORSES
particularly useful to detennine the
sion, and toxemia after the stomach has
prognosis for swvival, with increasing
ruptured. The prognosis for swvival may be
concentrations being associated with a
excellent in most cases of gastric dilatation,
poor prognosis. Furthermore, changes in
but gastric rupture is fatal.

peritoneal fluid lactate concentrations over
time have been used to help identify horses

Gastric Impaction: Impaction of the

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that require emergency abdominal surgery.

stomach is an uncommon cause of colic.

Similarly, the anion gap (the calculated

Although it may be associated with
difference between the measured cations
ingestion of certain feedstuffs ( eg, beet
and the measured anions) reflects the
pulp, pelleted feeds, persimmon seeds,
generation of organic anions, most notably
straw, barley), contributing factors ( eg,
lactic acid, due to reduced tissue perfusion.

diseased teeth, inadequate intake of water,

The concentration of protein in the
and rapid eating) should also be considered.

peritoneal fluid also has been used to

Because the incidence of this condition is
predict swvival, with higher concentrations
low, it is difficult to detennine which factors
associated with a poorer prognosis.

may be most important. The most striking
clinical sign associated with gastric

DISEASES ASSOCIATED WITH
impaction is severe abdominal pain.

COUC BY A! :rOM C lOCATIO

Because of the lack of other characteristic
findings, the diagnosis most often is made

Stomach
at surgery, and the decision for surgery is
based on unrelenting pain. Use of a 3-m

Gastric Dilatation and Gastric
endoscope has made it possible to identify

Rupture: The most common cause of
this problem without surgery.

gastric dilatation in horses is excessive gas

Treatment usually involves repeated
or intestinal obstruction. Gastric dilatation
intragastric administration of saline
may be associated with overeating
carbonated drinks ("soft drinks") if the fermentable feedstuffs such as grains, lush
condition has been identified without
grass, and beet pulp. Presumably, the large
surgery. If the gastric impaction has been
increase in production of volatile fatty acids
identified at surgery, saline or water can be
inhibits gastric emptying. If untreated,
infused into the mass through a needle
gastric dilatation associated with overeating
passed through the wall of the stomach.

can rapidly lead to gastric rupture. If

After the fluid has been injected into the
intestinal obstruction is the cause, the
mass, the stomach then is massaged and the
obstruction most often involves the small
obstruction is broken down. If a nasogastric
intestine. The fluid from the obstructed small tube is in place at the time of surgery, water intestine accumulates in the lumen of the

· may be pumped into the stomach and the
stomach, causing dilatation of the stomach
mass massaged. Gavage is continued after
and retrieval of gastric reflux on passage of
surgery with the hopes of removing some
the nasogastric tube. Gastric dilatation also
of the impacted material, and this can be
may develop in some horses with certain
followed by feeding slurries and pasture
colonic displacements, most notably right
grazing once the in1paction begins to
dorsal displacement of the colon around the
resolve. The prognosis is favorable if the
cecum ( see p 265). It is presumed that the diagnosis has been made without surgery or
displaced colon obstructs duodenal outflow.

if decision to perform exploratory surgery is

Gastric dilatation with fluid and gastric
made early and the impaction can be broken
reflux also are characteristic findings in
down manually at surgery.

horses with proximal enteritis-jejunitis.

Rupture of the stomach is a fatal
complication of gastric dilatation. The

Intestine
stomach generally tears along its greater

Clinical signs of colic may arise due to
curvature. Approximately two-thirds of
obstruction, inflammation, or strangulating
all gastric ruptures occur secondary to
obstruction of the small intestine. The
mechanical obstruction, ileus, and trauma;
prognosis for conditions affecting the small
the remaining cases are due to overload or
intestine is often guarded. Hence, rapid diagto idiopathic causes.

nosis and appropriate treatment are critical.

Clinical signs associated with gastric
dilatation include severe abdominal pain,
lleal Impaction: The most common
tachycardia, and retching. The mucous
condition producing sin1ple obstruction
membranes may be pale. Classically, these
of the lumen of the small intestine is ileal
acute signs are replaced by relief, depres-
impaction. It is most common in the

COLIC IN HORSES

259
southeastern USA, Germany, and the
intestinal distention, peritonitis, or larval

Netherlands. The results of clinical studies
parasite migration. The tissue response to
in the UK indicate that infection with the
ischemia, traumatic tissue handling,
intestinal tapewmm Anoplocephala
foreign material, hemorrhage, or dehydra
perfoliala and ileal impaction are strongly tion results in the formation of fibrinous
associated. In a similar study performed in

(and subsequently fibrous) adhesions.

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the USA, two risk factors for ileal impaction

Clinical signs are seen if the adhesion
were identified: 1) the feeding of Coastal
causes kinking, compression, or stricture

Bermuda hay, and 2) the lack of administraof the intestine.

tion of pyrantel pamoate, an anthelrnintic

Adhesions should be considered if the
with some efficacy against A per.foliata,
horse has had prior abdominal surgery
within the 3 mo preceding development
and a more recent history of recurrent
of the impaction. Further, it has been
abdominal pain. Clinical signs associated
suggested that the impaction develops
with intra-abdominal adhesions range from
secondary to spastic contractions of the
mild, recurrent colic to severe unrelenting
ileal musculature against ingesta.

pain. Most conunonly, intra-abdominal

Clinical signs include the onset of mild to
adhesions cause clinical signs within 60
severe abdominal pain followed by reduced days of the initial surgery if they are going intestinal sounds, gastric reflux, and
to be a significant problem for the horse.

tachycardia. Although early rectal

Surgical treatment involves transection
exan1ination may permit identification of
of the adhesion, resection of the affected
the impaction in the ileum low in the right
intestine, and anastomosis to achieve
caudal abdominal quadrant, subsequent
normal flow of ingesta. Therapeutic agents
distention of the jejunum may make this
purported to reduce the subsequent
identification difficult or impossible. The
formation of additional adhesions then are
most common differential diagnosis is
used. These include the systemic adminisproximal enteritis-jejunitis, and distinguishtration of antinlicrobials, NSAIDs, and instiling the two conditions can often be lation of sterile carboxymethylcellulose into
difficult. Because the horse's condition
tl1e abdomen at the time of closure. The
initially may remain stable and the degree
owner should be informed that adhesions
of abdominal pain may be mild, many
are likely to recur and that the longten11
horses with this condition are not referred
prognosis for horses with extensive
for intensive care or surgery for> 18 hr. The
adhesions is poor.

protein concentration of the peritoneal
fluid may increase if the impaction has

Ascarid Impaction: Young horses,
persisted for this long.

particularly those on farms with inad

Horses with ileal in1paction respond to
equate parasite control programs, may
treatment with fluids and mineral oil if the
develop ascarid impactions of the small
impaction has been identified early (ie,
intestine. These impactions are seen after
before gastric reflux has developed). If
administration of an anthelmintic with high
surgery is indicated, the impacted mass may efficacy againstParascaris equorum. The be mixed with saline or carboxymethylcelanthelmintics most conu11only associated lulose and massaged into the cecum, or an
with this condition are iven11ectin, piperaenterotomy may be performed in the distal zine, and organophosphates. These drugs
jejunum and the ingesta removed through
paralyze the ascarids, resulting in accumuthe incision. Ileus may develop after lation of masses of the wom1s in the smallsurgery. Depending on the degree of intestinal lumen. It has been suggested
damage to the serosal surface of the small
that disruption of the surface of the
intestine at the tin1e of surgery, complicaascarid releases antigenic fluids that tions may develop several weeks after
inhibit intestinal muscular activity,
surgery due to intra-abdominal adhesions

(see
thereby increasing the likelihood of
below).

intestinal obstruction.

Clinical signs range from mild to severe

Adhesions: Intra-abdominal adhesions
abdominal pain, evidence of toxemia, and
generally affect the small intestine and
gastric reflux that may contain ascarids.

usually cause obstruction of the intestinal

Ascarid impaction should be suspected if
lumen, although they may cause stranguthe affected horse is a weanling or yearling, lating obstruction. These adhesions
in poor condition, and has a recent history
develop in response to peritoneal injury
of deworming. Medical treatment with
and, most often, are the result of previous
fluids and intestinal lubricants may be
small-intestinal surgery, chronic small-
successful in some cases. Other horses may

260

COLIC IN HORSES
require surgical inteivention and removal of
be 44%. The horse's feet should receive
the ascarids through multiple enterotomies.

particulai· attention because acute lanlinitis

The prognosis is guarded if surgery has to
has been repmtecl as a common complicabe performed. The owner should be advised tion, with a prevalence of -25%.

that other young horses on the premises
should be treated with anthelmintics that
lntussusception: Most intussusceptions

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have lower efficacy against ascarids, such
that develop in horses are jejuno-jejunal,
as fenbendazole. These initial treatments
ileal-ileal, or ileocecal. The length of
can then be followed with more efficacious
intestine that has become invaginated (the
compounds.

intussusceptun1) into the more clistal
segment of intestine (the intussuscipiens)

Proximal Enteritis-Jejunitis: This
may range from a few centimeters to as
poorly understood disease affects the
much as a meter. Although the precise cause
proximal portion of the small intestine and
of most intussusceptions remains speculahas vaiious names, including proximal tive, alterations in peristalsis due to
enteritis-jejunitis, anterior enteritis, and
enteritis, surgical trawna, pai·asite damage,
duodenitis-jejunitis. TI1e condition has been anU1elmintics, andAnoplocephala recognized in the southeastern and
pe,foliala infection have been suggested.

nmtheastem USA, England, and on the

Horses <3 YT old ai·e affected most

European continent. The cause is unlrnown.

conm1011.ly.

The affected intestine contains lesions

Abdominal pain may be either acute due
varying from hyperemia to necrosis and
to complete obstruction of the intestinal
infiltration of the submucosa with
lwnen or chronic clue to partial occlusion of
inflanm1atory cells. Often, there is edema
the lwnen. If U1e occlusion of the intestinal
and hemorrhage in the vaiious layers of the
lumen is complete, the horse is acutely
intestinal wall.

painful and has gastiic reflux, and distended

Varying degrees of abdominal pain,
loops of small intestine are palpable per
ranging from mild to severe, are characterisrectun1. It may be possible to palpate the tic. When U1e prevalence of the condition
turgid intussusception, especially if ilie
peaked in the 1980s, it was characterized
ileum is involved. Because the strangulated
by vol wninous amounts of gastric reflux,
intussusceptwn is contained wiUlin the
progression from pain to depression, and
intussuscipiens, the WBC count in the
moderate to severe distention of the small
peiitoneal fluid may not reflect U1e degree
intestine on rectal examination. In addition,
of intestinal damage.

the distended duodenwn often was

Treatment requires surgery to reduce the
palpated as it coursed around the base
intussusception, if possible, followed by
of the cecwn. The peritoneal fluid often
resection and anastomosis. Because of ilie
contained an increased concentration of
edema and hemorrhage in the wall of the
protein (>3 g/dL) with a normal nwnber of
affected intestine, it may be difficult to

WBCs, but fuis finding did not consistently
assess the viability of the bowel. Additiondistinguish the condition from otl1er causes ally, ilie dainage to the intussuscepturn may
of small-intestinal disease. Based on
result in the development of adhesions. If
a11ecclotal reports, the prevalence and
the jejunwn is involved, a jejuno-jejunal
clinical seve1ity of the condition have
a11astomosis must be performed. lf the
decreased, at least in regions of the USA
intussusception involves only the ileun1, the
where the condition characteiistically had a
affected intestine must be resectecl and a
more severe course and was accompanied
jejw10-cecal anastomosis pe1fonned. If the
by a high incidence of laminitis.

ileun1 has invaginatecl into U1e cecun1, the

Treatment may be either medical or
temlinal portion of the ileun1 should be
surgical. Medical treatment includes
transected close to the cecum and a
continued gastric decompression until
jejuno-cecal anastomosis pe1fonned. The
the gastiic reflux abates, IV fluids, and
prognosis for survival is good if surgery is
analgesics, as required. Many cliniciai15
pe1fonnecl before the intussusception has
administer penicillin and low doses of
become irreducible. The prognosis is fair
flunixin meglumine; some also administer
to poor in the latter case because of the
neostigmine, lidocaine, or metocloprainide
development of pe1itonitis, ileus, adhesions,
to stimulate small-intestinal motility. Some
a11cl abscess fom1ation.

surgeons, particularly in the UK, believe
exploratory laparotomy and intestinal

Volvulus: A small-intestinal volvulus
decompression result in a more rapid
is seen when ilie intestine rotates on its
recovery. The survival rate associated with
mesenteiic a.xis >180°. As the degree of the
proximal enteiitis-jejunitis is reported to
rotation increases, the vascular supply to

COLIC IN HORSES

261
the intestine is lost. Presumably because of
signs of cai·diovascular deterioration are
its attachment to the cecum, the distal
present, the prognosis for survival is fair
aspect of the volvulus is the ileum in most
to poor.

cases.

Horses with small-intestinal volvulus

Internal Incarceration: The most
have acute pain and an increased heart rate,
conm1on sites for internal incai·cerations

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a prolonged capillaty refill time, and gastric
are mesenteric rents and the epiploic
reflux. Because of the loss of fluid into the
foratnen. Mesenteric rents are defects in
intestine and stomach, these horses rapidly
the small-intestinal mesentery. Problems
become dehydrated and have increased
develop when a segment of small intestine

PCV and plasma protein concentrations.

passes through the mesenteric defect, and

The horse's status may dete1iorate rapidly
the intestine becomes incai·cerated.

because of hypovolemia at1d endotoxemia.

Because the intestine distends with fluid

Rectal exainination generally reveals turgid
and blood, volvulus of the affected segment
distended loops of small intestine, and the
frequently occurs. Mesenteric rents causing
peritoneal fluid contains increased numbers
intestinal incarceration occur in horses of
ofWBCs and protein.

all ages.

Treatment involves surgical correction of

The epiploic foramen is a natural
the volvulus via a ventral midline celiotomy.

opening bounded by the caudate lobe of tl1e
lf the intestine is nonviable, it must be
liver, the portal vein, and the caudal vena
resected and an anastomosis performed.

cava. The distaljejunun1 and ileum ai·e the

The prognosis for survival depends on the
most common portions of the intestine that
duration of illness and atnount of intestine
become incai·cerated through the epiploic
that must be resected. Prognosis is good
foratnen. Although generally the intestine
with early detection and surgery. Horses
passes through the epiploic foran1en from
with a longer period of illness preoperaleft to right, tearing the omentwn in the tively, or those that develop postoperative
process, it also may pass in the opposite
ileus and peritonitis, are at increased risk of
direction to enter the omental bursa. It has
adhesion formation. It has been suggested
been reported that horses > 7 yr old are
that euthanasia is warranted if >500/o of the
affected most frequently by epiploic
length of the small intestine must be
foratnen entrapment. However, tl1e
removed. However, results of an experimencondition also often develops in horses tal study in ponies indicated that removal of

<7yr old.

700/o of the small intestine did not result in

Clinical signs may be vague and sinillai· to
malabsorption provided the ponies were fed those of horses with proxin1al enteritis or several (8) small pelleted meals each day.

pedunculated lipomas. The diagnosis may
have to be made at surgery. Furthermore, in

Pedunculated Lipomas: Colic due to
some cases, because of the position of the
pedunculated lipomas is seen in horses > 10
affected intestine within tl1e omental bw-sa,
yr old. Pedunculated lipomas are suspended the peritoneal fluid available for analysis from the mesentery by a stalk or pedicle,
may be normal.

which wraps around a segment of intestine,

Treatment of horses with either
occluding the lumen of the intestine and
mesenteric rents or epiploic foratnen
interfering with its blood supply. The lipoma entrapments is surgical. The affected frequently forms a knot with the pedicle.

segment of intestine must be exteriorized,

Clinical signs range from depression to
its viability evaluated, and, if necessaiy, a
severe abdominal pain, gastric reflux, and
rapid deterioration in metabolic status.

Distended loops of small intestine ai·e
palpable on rectal exan1ination and can be
identified with abdominal ultrasonography;
the lipoma can be felt per rectum in rare
cases. The peritoneal fluid contains an
increased munber of WBCs and RBCs and
an increased protein content.

Treatment requires transection of the
pedicle and, if necessaiy, resection of the
devitalized intestine. The prognosis
depends on the time between onset of
clinical signs and surgery. If surgery is
performed early, the prognosis is good;

Pedunculated lipoma in a horse. Courtesy of Dr.

however, if surgery is not perfonned until

Sameeh M. Abutarbush.

262

COLIC IN HORSES
resection and anastomosis pe1fom1ed. The
the hernia. Often, the testicle on the affected
prognosis for survival depends on the time
side must be removed, and the affected
between onset and surgery. If surgery is
intestine resected. The prognosis for
performed early in the course of the disease, survival seems to be breed-dependent, the prognosis is good. However, because the with Standardbred horses having a good clinical signs may be vague, the decision to
prognosis and Tennessee Walking Horses

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perform surgery may be delayed, worsening
having a fair to poor prognosis. Presw11ably,
the prognosis.

this reflects the fact that many Tennessee

Walking Horse stallions with inguinal

Inguinal Hernia: Inguinal hernias
hernias show little evidence of pain, which
generally develop in stallions after breeding
delays the decision for surgery.

a mare, trauma, or a hard workout. Hernias
appear to be most common in Tennessee

Walking Horses, American Saddlebreds, and Cecum and Large Intestine Standardbreds. In most cases, the hernia

Impaction: The most common sites of
results in acute colic. The intestine
impaction are the pelvic flexure region
descends through the vaginal ring in
of the left colon, tl1ejunction of the tight
most cases and lies next to the testis and
dorsal colon with the transverse colon, and
epididymis. Physical examination reveals a
the base and body of the cecum. The pelvic
swollen testis that is firm and cool to the
flexure and transverse colon regions are
touch. If the hernia has occurred within
anatomically predisposed to obstruction
hours, the intestine may be palpated in the
because of the dramatic changes in size.

inguinal canal. In this situation, an attempt

The underlying reason for impaction of the
may be made to reduce the hernia by pulling cecwn is unknown, although it has been down on the testis to tighten the boundaries
speculated that cecal muscular activity
of the inguinal canal and then forcing the
is abnormal in affected horses. Other
intestine up toward the vaginal ring. Once
predisposing factors include feed that is too
the incarcerated intestine, which frequently
coarse, diseased or poorly managed teetl1,
includes the ilewn, has become edematous,
and insufficient water intake. In one clinical
it is not possible to reduce the hernia
study, Morgan, Arabian, and Appaloosa
manually. Rectal exan1ination will reveal
breeds were oveffepresented among horses
distended loops of small intestine, with one
with cecal impaction, and it has been
of the loops tracing to the vaginal ting on
proposed that tl1e condition may develop
the affected side. There will be gastric
secondary to infection with the tapeworm
reflux, and the horse's condition will

Anoplocephala peifoliata. In1pactions also
deteriorate rapidly. Peritoneal fluid
may develop secondary to other intestinal
generally reflects the degree of ischemia.

diseases and may be associated with

Surgery involves a ventral midline
prolonged hospitalization. Consequently,
celiotomy and inguinal approach to reduce
the fecal output of horses being treated for
pelvic flexure
junction of right
dorsal colon wtth

I

Most common sites of impaction, cecum and large intestine, in a horse (larger dots indicate more frequent impaction at that site). Illustration by Dr. Gheorghe Constantinescu.

COLIC IN HORSES

263
other abnormalities should be assessed on a
solutions are administered to induce
routine basis. This is especially important in
movement of fluid from the plasma into
horses receiving NSAJDs on a daily basis.

the lwnen of the intestine. This fom1 of

Horses with simple impactions of the
treatment may require administration of
cecum or large colon exhibit mild

>50 L offluid/day to a450-kg horse until
intennittent signs of colic, and there is
the impaction is resolved. Interest has

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minimal evidence of systemic deterioration
increased in using enteral fluid therapy to
unless the impaction has a prolonged
treat horses with impactions, primarily
course. Generally, the heart rate is only
because enteral fluid therapy is significantly
slightly increased. Intestinal sounds are
less expensive than IV fluid therapy. The
usually heard on auscultation of the
clinical results with enteral fluid therapy
abdomen and may be associated with the
have been rewarding, and the results of
onset of pain as the affected portion of the
experimental work in healthy horses have
intestine contracts against the obstruction.

shoW11 that enteral fluid therapy is more

Diagnosis is made on rectal examination.

effective than IV fluid therapy in promoting

Although the most common site of
hydration of colonic contents.

obstruction is considered to be the pelvic

If the large-colon impaction does not
flexure region of the large colon, the
resolve with medical management, surgery
impacted ingesta actually fills much or all of
can be perfom1ed. Generally, the impaction
the left ventral colon. The impacted mass
is approached via a ventral midline
may be felt extending cranially in the
celiotomy, with the affected portion of the
abdomen, and the affected segment of
colon gently exteriorized and positioned on
bowel is identified by palpating the
a sterile colon tray. An enterotomy then is
longitudinal bands on the surface of the
made in the pelvic flexure and the contents
ventral colon. Impaction of the cecw11 is
of the colon removed.

relatively easy to identify, because the mass

Surgery for treatment of cecal impacis situated in the right paralumbar region.

tions requires general anesthesia, a ventral

The cecun1 can be definitively identified by
midline celiotomy, isolation of the cecum
palpating the taut ventral cecal band and
from the celiotomy site, and removal of
the fat and blood vessels overlying the
the contents of the cecum via an entermedial cecal band. Peritoneal fluid analysis otomy. Because impactions have recurred
may be normal, or the total protein
after simple evacuation, some surgeons
concentration may be increased as the
prefer to bypass the cecum with an
course becomes more prolonged.

ileocolostomy.

Cecal impactions tend to cause colic in

The prognosis associated with impachorses >8 yr old. Alternatively, impactions tions involving the large colon is excellent,
may be seen in horses hospitalized for
with a survival rate of >95%. The survival
other reasons and are often associated
rate associated with cecal impactions is
with abrupt rupture of the cecum in these

--80% for those horses that can be treated
cases. Consequently, there is some
medically and 60%-- 700/o for those horses
controversy regarding the best metl10d
requiring surgical intervention.

of treatment. Because medical therapy in

In some geographic areas, the offending
some clinical studies has been unsuccessmaterial may be sand, especially if the ful in 50% of the cases, surgical removal
amount of pasture grass is insufficient and
of the impacting mass followed by an
the horses are fed on the ground. The sand
ileocolostomy has been strongly recomaccwnulates in the right dorsal colon and mended. Other veterinarians report good
transverse colon. Intermittent signs of
results with aggressive medical therapy,
abdominal pain may occur because of the
particularly if abdominal pain associated
weight of the sand in the intestine. More
with the cecal impaction was the primary
severe signs of pain occur when the
reason the horse required veterinary
in1paction occludes the lW11en of the
attention.

transverse colon. Under such circW11-

Medical treatment of horses with cecal
stances, the colon proximal to the
or large-colon in1paction involves the
obstruction distends with gas, resulting in
administration of analgesics as necessary,
extreme pain. It may not be possible to
large volw11es of balanced IV fluids, and
distinguish this condition from an intestinal
intragastric administration of either mineral
displacement or volvulus. Sand also may be
oil or dioctyl sodiwn sulfosuccinate and
identified in the feces by mixing fecal
water. Feed should be restricted until the
material with water in a plastic rectal
impaction is relieved. Many veterinarians
examination sleeve.

consider aggressive fluid therapy to be the

Treatment of sand impaction may be
mainstay of treatment. Balanced electrolyte
either medical or surgical. Medical

264

COLIC IN HORSES
treatment generally involves intragastric
and cecal distention is evident on rectal
administration of psylliurn ( 400 g/500 kg
examination, but the mass rarely is
body wt, daily for 7 days) to purge the sand
palpable because the transverse colon is
from the lwnen. The psylliurn flakes are
cranial to the cranial mesenteric artery.

added to 7.5 L of warm water and rapidly

Analysis of the peritoneal fluid is usually
pumped into the stomach. These treatments
within normal limits unless ischemia of

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are accompanied by analgesics as needed
the colonic wall has developed over the
and IV fluids to promote movement of fluid
enterolith. In areas where the problem
into the intestinal lumen.

is endemic, radiography may be used to

Surgery via a ventral midline celiotomy
identify the enteroliths.

is necessary if the sand completely

Treatment involves surgery via a ventral
obstructs the lumen of the transverse
midline celiotomy to decompress the
colon. The left colon is exteriorized on a
colon and cecum and then to remove the
sterile colon tray, and the sand is removed
stone(s). The left portion of the large
via an enterotomy. The prognosis is usually
colon is exteriorized and positioned on a
good. Problems sometimes develop during
sterile colon tray, the ingesta removed via
surgery if the colon was damaged due to
an enterotomy, and then the enterolith(s)

the extensive weight of the sand or while
removed. If the stone has a flat side or a
the sand is being removed from the
polyhedral shape, this is indicative of
intestine (seep 287).

the presence of one or more additional
enteroliths. Consequently, the rest of

Enterolithiasis: Enteroliths are
the large and small colons must be
concretions composed of magnesium
thoroughly checked for other stones.

ammonium phosphate crystals around a

The prognosis is excellent, with practices
nidus (eg, wire, stone, nail). Enteroliths
in endemic areas reporting survival rates
may be seen singly or in groups and are
of95%.

commonly found in horses in certain
parts of the USA, including California,

Left Dorsal Displacement: Left dorsal
the southwest, Indiana, and Florida.

displacement of the colon is seen when

Enterolithiasis commonly affects Arabian
either the pelvic flexure or the entire left
horses, but the fact that these horses are
colon becomes displaced over the
extremely popular in the aforementioned
renosplenic ligament. Because the
areas confounds the question regarding
renosplenic ligament is not attached to the
breed association. Most horses with
most dorsal aspect of the spleen, a natural
enteroliths are -10 yr old; enterolithiasis
cleft exists between the spleen and left
rarely is seen in horses <4 yr old.

kidney. Although all ages and sexes of

Although not all factors that contribute
horses are affected equally, results of a
to the formation of enteroliths have
clinical study indicate that the displacebeen identified, results of clinical.studies ment is common in young horses.

indicate that large-colon contents from

Because left dorsal displacement results
horses with enteroliths have higher
in simple obstruction of the colon at the
mineral (magnesium, calcium, and
point where it hangs across the ligan1ent,
phosphorus) concentrations and pH th�n
the condition usually is associated with
contents from horses with colic not due
moderate abdominal pain or a prolonged
to enteroliths. A common factor
course of intermittent painful episodes. The
associated with enterolithiasis is the
mucous membranes remain nonnal, and the
consumption of alfalfa hay, which results
heart rate is increased only slightly. The
in a higher pH and increased concentradiagnosis usually is made on rectal tions of calcium, magnesium, and sulfur
exanlination (palpating the pelvic flexure
in the large colon.

over the ligament, palpating the bands of the

Many horses with enterolithiasis have
left ventral colon running dorsocranially to
a history of recurring colic, presumably
the left kidney, and detecting that the spleen
indicating that the enterolith(s) had
is displaced toward the middle of the
caused partial or temporary obstruction
abdomen). The condition also may be
of the colonic lwnen. If the enterolith
identified using ultrasonography. A
becomes lodged at the origin of the
paracentesis may yield blood if the spleen
transverse colon, the colon proximal to the is displaced toward the rniclline.

obstruction distends with gas and the pain

Four fonns of treatment have been used:

is severe. Distention of the abdomen may

1) withholding feed to detern1ine whether
be marked. Heart and respiratory rates are
evacuation of the intestinal contents will
increased, and the mucous membranes
allow the colon to return to its nonnal
may be pale or pink. Generally, colonic
position, 2) rolling the horse to dislodge the

COLIC IN HORSES

265
colon from the ligament, 3) administering

Right Dorsal Colitis: Right dorsal
phenylephrine and/or jogging the horse to
colitis has been recognized with increasing
cause splenic contraction and coITection of
regularity in recent years, particularly
the displacement, or 4) perfom1ing surgery
in, but not limited to, horses receiving
to return the colon to its correct position.

excessive amounts of NSAIDs. Because the

The rolling procedure involves short-term
condition has been identified in horses

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anesthesia (generally xylazine or detomireceiving recommended doses of these dine and ketamine ), elevation of the horse's
drugs, it appears that some horses ar·e
hindlimbs, and rolling the horse 360°.

particularly sensitive to their toxic effects.

Surgery is performed via a ventral midline

The drug most commonly associated with
celiotomy. The advantage of surgery is that
right dorsal colitis is phenylbutazone, but
the viability of the colon can be assessed.

this may reflect the common a11d often

Phenylephrine should not be administered
chronic use of this drug. The most common
to horses >15 yr old because of the
lesions reported in horses with right dorsal
increased risk of fatal hemotThage in aged
colitis are ulceration a11d thickening a11d/or
horses given this drug. If left dorsal
fibrosis of the wall of the right dorsal colon.

displacement of the colon recurs, the

Horses commonly present with
renosplenic space may be sutured closed
abdominal pain, a11orexia, a11d lethargy. In
laparoscopicaUy. Overall, the prognosis is
ma11y cases, the signs are consistent with
good, with most studies rep01ting survival
severe abdominal pain, fever, endotoxemia,
rates >800Ai.

a11d dianhea. Horses with the more chronic
form of the disease present with intermit

Right Dorsal Displacement: The left
tent abdominal pain, weight Joss, lethargy,
colons move laterally around the base of the a11d a11orexia. In most cases, hypoproteinececwn to lie between the cecum and the mia is a common finding on hematology a11d
right body wall. With the most common
may account for ventral edema in some
form of this displacement, the pelvic flexure
horses with the chronic form of the disease.

ends up positioned near the diaphragm. In

The diagnosis is usually based on the
many instances, the displacement may be
history, clinical signs, and hematologic
complicated by twisting of the colon near
findings. In some cases, ultrasonographic
the base of the cecwn. Although there may
evaluation of the colon via the twelfth to
be some interference with venous drainage
fifteenth intercostal spaces may provide
from the affected colon, usually the arterial
evidence of marked thickening of the
supply remains intact.

colonic wall.

Most horses with right dorsal displace

Treatment of affected horses includes
ments exhibit moderate degrees of pain,
discontinuation of NSAIDs, rest, a11d a
and there is slow development of systemic
cha11ge in diet to a complete pelleted feed
deterioration. In some cases, however, the
that contains <!300A, dietary fiber. Some
pain may be severe. Rectal examination
clinicians recommend the feeding of ma11y
may reveal the taenia of the colon running
small meals daily, ma11y recommend the
transversely across the pelvic inlet. It may
inclusion of psylliwn to promote mucosa!

not be possible to palpate the ventral cecal
healing, a11d some administer sucralfate or
band on rectal examination. Some horses
metronidazole. Horses with uncontrollable
with this condition have gastric reflux,
pain may require surgery to resect or bypass
preswnably due to occlusion of the lumen
the affected portion of the right dorsal
of the duodenun1.

colon. The prognosis for horses with right

Some horses with this condition appear
dorsal colitis is guar·ded.

to be stable and may show intennittent
signs consistent with mild abdominal pain.

Volvulus of the Large Colon: Although

Treatment may be conservative, involving
the tenn "torsion" has been used for years attention to fluid needs and administration
to indicate that the colon has twisted on
of mild analgesics. For painful horses,
itself, the involvement of the mesentery
however, surgery must be performed to
between the ventral a11d dorsal colons
locate the pelvic flexure, to exteriorize and
indicates that the condition is a volvulus.

decompress the left po1tion of the colon, if

When viewed from the most common site
possible, and then to relocate the colon to
of the volvulus (the junction between the
its normal position by rotating it around
tight ventral colon a11d the cecwn), the
the cecal base. The twisting of the colon
volvulus most often occw-s in a clockwise
must be identified and coITected. The
direction; the cecwn may or may not be
prognosis for survival is good, provided
involved. If the volvulus is <270°, there may
that the colonic wall is not damaged during
be obstruction of the bowel lwnen without
surgery.

ischemia. If the volvulus is >360°, there is

266

COLIC IN HORSES
strangulating obstruction of the entire left

Impaction and Foreign Body
colon.

Obstruction of the Descending

The onset of colic is sudden, and the

Colon: Abnom1alities involving tl1e
degree of pain may be mild to moderate if
descending (small) colon are infrequent,
the volvulus results only in obstruction of
accounting for <5% of conditions characthe intestinal lumen. When the twist is more terized by colic in one study. The more

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extensive, the pain is severe and the horse
common causes include meconium
may not respond to analgesics. The colon
retention, impaction, and foreign body
is extremely enlarged, and the mesentery
obstruction. Meconi um retention is seen in
between the dorsal and ventral colons is
newborn male foals within the first 24 hr of
edematous on rectal examination. The
life. Affected foals swish their tails from
heart rate is rapid, the horse's condition
side to side, strain to defecate, and roll.

deteriorates rapidly, and there is poor

The diagnosis is made by careful digital
peripheral perfusion. Distention of tl1e
examination. Treatment involves gentle
abdomen usually is marked. Generally,
administration of a wam1, soapy water
results of peritoneal fluid analysis and the
enema. The prognosis is excellent.

degree of colonic involvement are poorly

Impaction of the descending colon is
correlated.

seen in ponies, miniature horses, and adult

Although the cause of colonic volvulus
horses with limited access to drinking
remains unknown, it is presumed to be
water or with other causes of intestinal
associated with a disproportionate
stasis. Most recently, the condition has
amount of gas in the colon. On broodbeen associated with salmonellosis, mare farms, the condition frequently is
although a cause and effect relationship
associated with recent (within 90 days)

has not been proved. Pain may be severe if
or impending parturition, a grass diet, or
the obstruction is complete. In such cases,
highly fermentable feeds. The presence
tympany of the colon occurs secondarily,
of a foal at the mare's side (recent history and ileus results. The diagnosis is made in of parturition) is an additional risk
adult horses by palpating the obstructing
factor.

mass in the ventral portion of tl1e

Treatment of colonic volvulus requires
abdomen on rectal examination. Foreign
surgery to correct the volvulus and
body obstruction of the descending
remove affected bowel, if necessary.

colon must be considered if the horse

Although the technique for removal of90%
is <3 yr old; the offending material may be
of the colon has been perfected in healthy
rubber fencing, nylon fibers from halters
horses, extreme difficulty can be
or lead shanks, hay net, or feed sacks.

encountered if the colon is edematous.

Horses with impactions may be treated

Because the recurrence rate has been
medically with analgesics, IV fluids, and
estimated to be as high as 20% in some
gentle enemas. Often, however, surgery
clinical studies, colopexy pr0cedures have is required to evacuate the colon due to been devised to reduce the recurrence of
severity of pain and gas distention. The
the condition in broodmares. Although
prognosis associated with impaction of
the results of a study involving several
the descending colon is fair, unless it is
university hospitals reported a 27%
complicated by severe colitis after the
survival rate, survival rates >85% are
obstruction has been removed. The
common for practices situated near
prognosis associated with foreign body
broodmare farms.

obstruction is good.

INTESTINAL DISEASES IN RUMINANTS

INTESTINAL DISEASES IN CATTLE the fluid, electrolyte, and acid-base homeostasis. Specific therapy and

Determination of the cause of intestinal
prevention are detailed under the
disease in cattle is based on clinical,
individual disease headings. Intestinal
epidemiologic, and laboratory findings.

diseases of neonates are discussed

Nonspecific therapy includes oral and
separately, although some of the causes
parenteral fluid therapy to restore
also affect older animals.

INTESTINAL DISEASES IN RUMINANTS

267

Bovine Viral Diarrhea and Mucosa!

genotype 1 are represented as la, lb, le,

Disease Complex
etc). CWTently, at least 12 subgenotypes
for BVDV-1 (BVDV-la to BVDV-11) and two

Bovine viral diarrhea (BVD) is most
subgenotypes for BVDV-2 (BVDV-2a and
common in young cattle (6-24 mo old).

BVDV-2b) are recognized.

The clinical presentation can range from

BVDV type 1 and type 2 appear to be
inapparent or subclinical infection to acute

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distributed worldwide; however, the
and severe enteric disease to the highly
prevalence of each type of virus varies
fatal mucosa! disease complex characterconsiderably among regions. The distiibuized by profuse enteritis in association with tion of viral subgenotypes is more restricted,
typical mucosa! lesions. BVD must be
with many viral subgenotypes being found
distinguished from other viral diseases that
only in certain regions of the world and, in
produce diarrhea and mucosa! lesions.

some cases, only certain regions of a country.

These include malignant cata!Thal fever

All BVDV, regardless of genotype or subgeno

(seep 758), which usually is a sporadic
type, are antigenically related. However,
disease in more mature cattle, bluetongue

(seep 738), and rinderpest (seep 771), serologic assays that use serun1 obtained
from convalescent cattle can distinguish
which is cwTently considered to be

BVDV type 1 from type 2. The extent of
eradicated worldwide.

antigenic variation among BVDV of different

Bovine viral diarrhea virus (BVDV), the
genotypes and subgenotypes remains
causal agent of BVD and mucosa! disease
unlmown, but there is concern that the
complex, is classified in the genusPesti
antigenic differences an10ng BVDV may be
virus in the family Flaviviridae. Although
sufficient to affect protection conferred by
cattle are the primary host for BVDV, several vaccination.

reports suggest most even-toed ungulates
are also susceptible. Classically, isolates of

Etiology and Epidemiology: Serologic

BVDV are separated into noncytopathic and
surveys conducted throughout the world
cytopathic biotypes based on their ability or
suggest that BVDV is endemic in the cattle
lack of ability to cause overt cytopathic
population of most cattle-producing
change and cell death in cell cultw·es.

countries. In some countties, BVD is con

Noncytopathic BVDV is the predominant
sidered the single most in1po1tant viral
viral biotype in natw-e, whereas cytopathic
infection of cattle. The prevalence of

BVDV is relatively rare and of little
antiviral antibody in cattle vaiies greatly
epidemiologic relevance. The cytopathic
among countries and geographic regions
biotype arises in cattle that are persistently
because of differing cattle housing
infected with noncytopathic biotype of the
practices, population densities, vaccination
san1e or a genetically similar BVDV strain.

practices, and implementation of different

The switch in biotype is the result of
control or eradication programs. Prevalence
mutations that often involve recombination
of antiviral antibody may be >90% if vaccina-
of noncytopathic viral RNA with itself, with
tion is practiced commonly in a geographic
heterologous viral RNA, or witl1 host cell
region. Although cattle of all ages are

RNA.

susceptible, most cases of overt clinical

Based on comparisons of nucleotide
disease ai·e seen in cattle between 6 mo and
sequence in the viral RNA, there are at

2 yr old.

least two viral genotypes ( distinct genetic

Cattle persistently infected with
groups) of BVDV that can be further
noncytopathic BVDV serve as a natural
divided into subgenotypes or genogroups.

reservoir for virus. Persistent infection

The viral genotypes are tenned BVDV type
develops when noncytopathic BVDV is

1 and BVDV type 2, and both cytopathic
transmitted transplacentally during the
and noncytopathic BVDV are represented
first 4 mo of fetal development. The calf is
in each viral genotype. In recent years,
born infected with virus, remains infected
a new group of atypical pestiviruses, apparfor life, and usually is irnrnunotolerai1t to ently forming a separate species, of which
the resident noncytopathic virus.

cattle are the most likely host species,

Transplacental infection that occw-s
have been recognized. Virus of this third
later in gestation can result in abortion,

Pestivirus genotype are designated as
congenital malformations, or birth of

"HoBi"-like pestiviruses. The subgenohealthy calves that have antibody against types are clusters of viruses within a

BVDV. The prevalence of persistent
viral genotype that are highly similar in
infection varies an1ong countries and
nucleotide sequence of the viral RNA.

between regions within a country. The

(Subgenotypes are designated by lower
estimated mean animal prevalence of
case letters; thus, subgenotypes of BVDV
persistent infection with BVDV is

268

INTESTINAL DISEASES IN RUMINANTS

-1 % ---2% but may approach 4% on dairy
ulcerations of the GI tract, petechial and
farms with endemic BVDV infection. On a
ecchymotic hemorrhages on the serosal
given farm, persistently infected cattle are
surfaces of the viscera, and extensive
often found in cohorts of animals that are
lymphoid depletion are associated with
approximately the same age. Persistently
severe forms of acute BVD. The duration
infected cattle can shed large amounts of
of overt disease may be 3---7 days. High

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BVDV in their secretions and excretions
morbidity with a mortality of �25% is
and readily transmit virus to susceptible
common. Severity of acute BVD is related
herdmates. Clinical disease and reproducto the virulence of the viral strain infecting tive failure often are seen after healthy
the animal and does not depend on viral
cattle come in contact with a persistently
biotype.

infected animal. Although persistently
ln pregnant cattle, BVDV may cross the
infected cattle are important in transmisplacental barrier and infect the fetus. The sion of BVDV, the virus also may be spread
consequences of fetal infection usually
by biting insects, fomites, semen, biologic
are seen several weeks to months after
products, and other animals, including
infection of the dan1 and depend on the
swine, sheep, goats, camelids, and possibly
stage of fetal development and on the strain
wild ruminants.

ofBVDV. lnfection of the dam near the time
of fertilization may result in reduced

Clinical Findings and Lesions: Disconception rates. Infection dming the first ease induced by BVDV varies in severity,

4 mo of fetal development may lead to
duration, and organ systems involved.

embryonic resorption, abortion, growth

Infection of immunocompetent susceptiretardation, or persistent infection.

ble animals with either noncytopathic or

Congenital malformations of the eye and
cytopathic BVDV is termed acute or

CNS result from fetal infections that occur
transient BVD. Inapparent or subclinical
between months 4---6 of development. Fetal
infection without any clinical signs that is
mun1mification, premature birth, stillbirth,
followed by seroconversion is the most
and birth of weak calves also are seen after
common form of infection in the field.

fetal infection.

Acute clinical disease may range from

Persistent infection is an important
mild disease of high morbidity and low
sequela of fetal infection with noncytomortality to severe enteric disease with pathic BVDV. Persistently infected calves
considerable mortality. Biphasic fever
may appear healthy and nom1al in size, or

(-104°F [40°Cl), depression, decreased
they may show stunted growth and be prone
milk production, transient inappetence,
to respiratory or enteric ailments. They
rapid respiration, excessive nasal
often have a short life span, and death
secretion, excessive lacrimation, and

. before 2 yr of age is common. Persistently
diarrhea are typical signs of acute clinical
infected cows always give birth to

BVD. Clinical signs of disease usually are
persistently infected calves, but most calves
seen 6---12 days after infection and last 1---3
sired by a persistently infected bull will not
days. Transient leukopenia may be seen
be infected with virus in utero. Lesions
with onset of signs of disease. Recovery is
attributable to BVDV often are not seen in
rapid and coincides with production of
persistently infected cattle at necropsy.

viral neutralizing antibody. Gross lesions

Antibody against BVD seldom is detected in
seldom are seen in cases of mild disease.

persistently infected cattle in the absence

Lymphoid tissue is a primary target for
of vaccination or superinfection with an
replication ofBVDV, which may lead to
antigenically heterologous BVDV. Persisimmunosuppression and enhanced tently infected cattle exposed to BVDV that
severity of intercurrent infections.

is antigenically different from their resident

Some isolates ofBVDV (BVD type 2) have
noncytopathic virus can produce antiviral
been associated with severe clinical disease
antibody. Therefore, screening for
that manifests as high fever ( -107°F
persistent infection using serologic tests to

[41 °-42°Cl), oral ulcerations, eruptive
identify animals that lack antiviral antibody
lesions of the coronary band and interdigital may not detect some persistently infected cleft, diarrhea, dehydration, leukopenia,
cattle.

and thrombocytopenia. ln thrombocyto

Mucosa! disease is an uncommon but
penic cattle, petechial hemorrhages may be
highly fatal form of BVD occurring in perseen in the cof\iunctiva, sclera, nictitating sistently infected cattle and can have an
membrane of the eyes, and on mucosal
acute or chronic presentation. Mucosal
surfaces of the mouth and vulva. Prolonged
disease is induced when persistently
bleeding from iajection sites also occurs.

infected cattle become superinfected with

Swollen lymph nodes, erosions and
cytopathic BVDV. The origin of the

INTESTINAL DISEASES IN RUMINANTS

269
cytopathic BVDV is usually internal,
apart is necessary to verify recent infection.

resulting from a mutation of the resident

Isolation of BVDV from blood, nasal swab
persistent, noncytopathic BVDV. In those
specimens, or tissues confirms active
cases, the cytopathic virus is antigenically
infection. Identification of persistent
similar to the resident noncytopathic virus.

infection requires detection of virns in

External origins for cytopathic BVDV
clinical specin1ens obtained at least 3 wk
include other cattle and modified-live virns
apart. Colostral antibody can impair the

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vaccines. Cattle that develop mucosal
sensitivity of virns isolation in blood during
disease due to exposure to a cytopathic
the first weeks of life. At necropsy, tissues
virns of external origin often produce
of choice for viral isolation include spleen,
antiviral antibody. Prevalence of persistent
lymph node, and ulcerated segments of
infection usually is low, and many persisthe GI tract.

tently infected cattle do not develop

Alternatives to viral isolation include
mucosal disease, regardless of exposure.

antigen-capture ELISA to detect virus in

Acute mucosal disease is characterized
blood, serum, or tissue biopsies; immunoby fever, leukopenia, dysenteric diarrhea, histochemistry to detect viral protein in
inappetence, dehydration, erosive lesions of frozen or fixed tissues; PCR to detect viral the nares and mouth, and death within a few RNA in clinical specimens; and PCR or in days of onset. At necropsy, erosions and
situ hybridization to detect viral RNA in
ulcerations may be found throughout the GI
fresh or fixed tissues. Differentiation of
tract. The mucosa over Peyer's patches may
viral genotypes and subgenotypes may be
be hemorrhagic and necrotic. Extensive
accomplished by PCR assays alone, or
necrosis of lymphoid tissues, especially
by PCR assays followed by analysis of
gut-associated lymphoid tissue, is seen on
nucleotide sequence, restriction fragmicroscopic exan1ination.

ment analysis, or palindromic nucleotide

Clinical signs of chronic mucosal disease
substitution analysis. Monoclonal
may last several weeks to months and are
antibody binding assays and viral
less severe than those of acute mucosal
neutralization assays also differentiate
disease. Intermittent diarrhea and gradual
viral genotypes.

wasting are common. Coronitis and
eruptive lesions on the skin of the inter

Treatment and Control: Treatment
digital cleft cause lameness in some cattle.

of BVD remains limited primarily to

Lesions found at necropsy are less
suppo1tive therapy. Control is based on
pronounced than, but similar to, those seen
sound management practices that include
in acute mucosal disease. Often, the only
use of biosecurity measures, elimination of
gross lesions seen are focal ulcerations in
persistently infected cattle, and vaccinathe mucosa of the cecum, proxinlal colon, tion. Replacement cattle should be tested
or rectum, and the mucosa over Peyer's
for persistent infection before entry into
patches of the small intestine may appear
the herd. Quarantine or physical separasunken.

tion of replacement cattle from the
resident herd for 2-4 wk should be

Diagnosis: BVD is diagnosed tentatively
considered, and vaccination of replacefrom disease history, clinical signs, and ment cattle for BVD should be done before
gross and rrucroscopic lesions. Diagnostic
commingling with the resident herd.

laboratory support is required when clini

Embryo donors and recipients also should
cal signs and gross lesions are minimal.

be tested for persistent infection. If

Laboratory supp01t also is required in some
vaccination of embryo donors or recipients
outbreaks of mucosal disease or clinically
is warranted, it should be done at least one
severe acute BVD, because eitl1er disease
estrous cycle before embryo transfer is
may appear similar to rinderpest (seep 771) performed. Because BVDV is shed into
or malignant catalThal fever (seep 758).

semen, breeding bulls should be tested for

Laboratory tests for BVDV include
persistent infection before use. Artificial
isolation of virns or viral antigen in clinical
insemination should be done only with
specin1ens and tissues, and assays that detect semen obtained from bulls free of anti-BVDV antibody in serum or milk.

persistent infection.

Because antibody against BVDV can be

Screening cattle herds for persistent
highly prevalent in regions with high
infection can be done by PCR assays using
infection prevalence and/or common use
skin biopsies, blood, or milk; by classical
of BVD vaccines, a single serologic test is
virus isolation metl10ds using serum or
seldom sufficient for diagnosis of recent
buffy coat cells; by antigen-capture ELISA
infection. A >4-fold increase in antibody titer
using serum, buffy coat, milk, or skin
in paired serum san1ples obtained 2:2 wk
biopsies; or by antigen detection using

270

INTESTINAL DISEASES IN RUMINANTS
immunochemical methods on tissue or skin
causative agent, because this organism is
biopsies. Several strategies, based on herd
isolated from the intestines of naturally
size, type of herd being screened, financial
occurring cases at a higher frequency and in
limitations of the herd owner, and testing
higher numbers than from cattle with other
ability of the diagnostic laboratory being
intestinal diseases. Another proposed
used, are available to screen herds for
potential causative agent isAspergillus

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persistent infection. When identified,

Jumigatus, a common fungus in feed and
persistently infected cattle should be
forages. The primary lesion is sin1ilar to that
removed from the herd as soon as possible,
caused by C peifringe,is in young, rapidly
and direct or indirect contact with pregnant
growing animals and consists of an acute,
cattle should be prevented.

localized, necrotizing, hemorrhagic enteritis

Inactivated and modified-live virus
of the small intestine that leads to developvaccines are available. They contain a ment of an intralunlinal blood clot. The clot
variety of strains of BVDV representing
causes a physical obstruction, with
both viral biotypes and viral genotypes 1
proximal accw11ulation of intestinal fluid
and 2. Antigenic diversity among BVDV
and gas and development of hypochloremia,
may affect the efficacy of a given vaccine
hypokalemia, dehydration, and varying
if the vaccine virus or viruses differ
degrees of anemia. The hemorrhagic
significantly from the challenge virus.

enteritis is progressive. Ischemia and

Proper and safe immunization of cattle
necrosis extends through tl1e intestinal wall,
with either inactivated or modified-live
and within 24--48 hr, there is a fib1inous
virus vaccines requires adherence to the
peritonitis, continued electrolyte imbalmanufacturer's instructions. Because ance, profound toxemia, and death.

BVDV is fetotropic and irnmunosuppressive, use of modified-live virus vaccines Epidemiology: Jejuna! hemorrhage
is not recommended in cattle that are
syndrome occurs sporadically, primarily
pregnant or showing signs of disease.

in mature lactating dairy cows in Nortl1

Inactivated viral vaccines may be used in

America and Europe, but it has also been
pregnant cattle. Protection conferred by
recorded in beef cattle. Most cases occur
inactivated vaccines may be of short
in mature dairy cattle in tl1e first 3 mo of
dw·ation, and frequent vaccination may be
lactation, with highest incidence rates during
necessary to prevent disease or reproducthe cold months of the year. Possible risk tive failure. Colostral antibody confers
factors for disease are those associated with
partial to complete protection against
management practices aimed at achieving
disease in most calves for 3-6 mo after
high milk production, such as high fermentbirth. Vaccination of neonatal cattle tnat able carbohydrate content of the diet and
have acquired colostral antibody may not
feeding a total mixed ration. The animal-level
stimulate a protective in1mune response,
disease incidence rate is estimated to be
and revaccination at 5-9 mo of age may be

1 o/c,-2"A,, but outbreaks in a herd can be
necessary. A booster dose of vaccine is
associated with morbidity rates of;,,10%.

often administered before first breeding,

Mortality in general is high, with 8(1>/c,--100% of and additional booster doses of vaccine
affected animals dying within 48 hr.

may be administered in sllbsequent years
before breeding.

Clinical Findings: Cattle affected by
jejuna! hemorrhage syndrome have a
history of sudden anorexia and depression,

Jejuna! Hemorrhage Syndrome
a pronounced reduction in milk produc

(Hemorrhagic bowel syndrome of cattle)

tion, abdominal distention and pain with
kicking at the abdomen, and weakness

Jejuna! hemorrhage syndrome is a sporadic
progressing to recwnbency. Clinical
disease of uncertain etiology that is
findings include depression, dehydration,
observed with increasing frequency in
increased heart and respiratory rates, and
cattle. It is manifest by sudden onset of
pale mucous membranes. The abdomen
abdominal pain, progressing to sternal
may be moderately distended on the right
recumbency, shock, and death.

side, the rwnen is atonic, and fluid sounds
may be elicited by succussion over the right

Etiology and Pathogenesis: The
abdomen. Dark red blood clots may be
etiology of jejuna! hemorrhage syndrome is
fotmd in the feces and rectum. Distended
uncertain but is believed to be multifactoand finn loops of intestine may be palpable rial. Clostridium peifringens type A, a
on deep rectal examination. On laparotnormal inhabitant of the bovine digestive omy, a segment of the small intestine is
tract, has been incrinlinated as an important dark red and distended, with a serosal

INTESTINAL DISEASES IN RUMINANTS

271
surface covered by tags of fibrin. The small

(sometimes accompanied by dysentery),
intestine proximal to the affected segment
a profound drop in milk production,
and the abomasum are distended with gas
variable anorexia and depression, and
and fluid. Ultrasonography may aid in
mild respiratory signs such as couglting.

diagnosis.

The disease has a ltigh morbidity but low

Most affected cattle die witltin 2-4 days
mortality, and spontaneous recovery witltin

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despite intensive fluid and electrolyte
a few days is typical.

therapy. Sudden death without prior
clinical findings may occur. The hemogran1

Etiology: Although the precise etiology of
is variable; serum biochemistry reflects
winter dysentery has not been conclusively
obstruction of the upper small intestine
confirmed, an increasing body of evidence
and sequestration of abomasal secretions
implicates a bovine coronavirus (BCo V),
with resultant hypokalemia and hypochloclosely related to the virus that causes remia.

diarrhea in neonatal calves. Evidence for

Lesions: Necrohemorrhagic jejunitis with

BCoV as the cause of winter dysentery
intraluminal hemorrhage is severe. The
includes the following: 1) clinical signs and
affected segment of intestine is dark red and pathologic findings are consistent with dilated, with tags of fibrin on the serosal
disease induced by BCoV, 2) seroconversion
surface. The lumen contains a firm blood
to BCoV has been demonstrated in affected
clot adherent to the mucosa, and the
cattle, 3) the virus is frequently isolated
affected segment of intestine is necrotic.

from diarrheic feces of cattle that exhibit
clinical signs of winter dysentery, and 4) the

Diagnosis: Diagnosis of jejuna! hemordisease has been reproduced by briefly rhage syndrome can be made either during
exposing BCoV seronegative, lactating
an exploratory laparotomy or at necropsy
cows to a calf experimentally infected with
and is based on the presence of a characterfeces from cows with winter dysentery.

istic focal necrohemorrhagic enteritis of the

Notwithstanding, it has not been possible to
distal small intestine. Differential diagnoses
consistently reproduce winter dysentery
include other causes of physical or
through oral inoculation of adult cattle witll
functional obstruction of the small intestine

BCo V. Concun·ent risk factors, such as
such as intussusception (seep 245), cecal
changes in diet, cold temperatures, closed
dilatation and volvulus, and diffuse
confinement with ltigh anin1al density, poor
peritonitis (seep 670), from right-sided
ventilation, and presence of other microo1°
torsion of the abomasum (seep 238) and
ganisrns, may be required before BCo V
torsion at the root of the mesentery, and
causes clinical disease in adult cattle.

from diseases with melena such as
abomasal ulcer (seep 241).

Transmission, Epidemiology, and

Pathogenesis: BCoV is transmitted via
tile fecal-oral route through ingestion of

Treatment and Control: Fluid and
feed or water contanlinated witll feces from
electrolyte therapy and laparotomy with
clinical cases or clinically healthy carrier
massage of affected bowel loops to break
animals. Viral particles present in respiradown obstructing blood clots and, in tory secretions of affected aninlals may
advanced stages, resection of the affected
furtller enhance transmission. Transmission
segment of the intestine are treatment
of disease is promoted by close confineoptions for jejuna! hemorrhage syndrome.

ment. Winter dysentery is highly contagious

Even with such treatment, the fatality rate is and easily introduced to barns by visitors, very ltigh, and the prognosis is grave. No
carrier animals, and fornites. Winter
preventive strategies have been identified.

dysentery is common in northern climates

A short-term protective effect of a
where animals are housed indoors for

C perfringens type C and D vaccine against extended periods during tile winter months.

hemorrhagic bowel syndrome in some

It is seen frequently in the northern USA,
herds has been reported anecdotally, but

Canada, the UK, Europe, Australia, New
there is currently no corroborating scientific Zealand, Israel, and Japan. Coronaviruses evidence.

survive best at low temperatures and at low
ultraviolet light intensities, which can lead

Winter Dysentery
to a buildup of virus in the environment
during tile colder montlls. Adult lactating

Winter dysentery is an acute, highly
cows tllat have recently calved are most
contagious GI disorder that affects housed
severely affected, but tile disease can affect
adult dairy cattle, primarily during winter.

younger or older aninlals and males.

Clinical features include explosive diarrhea

Mortality rates associated with winter

272

INTESTINAL DISEASES IN RUMINANTS
dysentery are generally low (1%-2%), but

Differential diagnoses for acute diarrhea
morbidity in affected herds is high, with
in adult cattle include bovine viral diarrhea

20%---500Ai of the animals in a herd exhibiting

(BVD), enteric salrnonellosis, and coccidioclinical signs within a few days, and close to sis. These diseases can be excluded by
lOQOA, of animals in the herd exhibiting signs
absence of mucosa! lesions (BVD), negative
within a week. Some degree of immunity to
fecal cultures (Salmonella spp ), and

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winter dysentery appears to develop,
negative fecal flotation ( coccidiosis ), as
because recurrences, if seen in the san1e
well as by the characteristic clinical
herd, are noted at 1- to 5-yr intervals.

presentation of winter dysentery ( rapid

Inflan1111atory mediators that cause
onset of diarrheal disease of short duration
hypersecretion in the small intestine and
in a herd with high morbidity but low
colon are thought to contribute to the
mortality).

volmninous dianhea seen in cattle with
winter dysentery. In addition, destruction of

Treatment and Control: Most cattle
epithelial cells in the colonic crypts results
affected by winter dysentery recover
in transudation of extracellular fluid and
spontaneously. Fresh water, palatable feed,
blood, explaining the hemorrhagic nature
and free-choice salt should be available at
of the diarrhea in some cases.

all tin1es. The use of astringents, protectants, and adsorbents is controversial. IV

Clinical Findings: Winter dysentery is
fluid therapy or blood transfusions may
characterized clinically by an acute onset of
be required in severely affected cattle.

fluid diarrhea and a profolll1d decrease in

There is no vaccine for winter dysentery.

milk production (25o/e>-95% production loss).

Isolation of newly introduced cattle for 2 wk

Feces are liquid and homogenous with little
and isolation of any adult cow with diarrhea
odor, dark green to black, and may contain
is advised to decrease the likelihood of
blood (typically in first-lactation heifers) or
disease introduction into a herd. In an
mucus. A sweet, musty, lll1pleasant odor is
outbreak, access to the premises should be
reported in bams with large nmnbers of
restricted, and all persons in contact with
affected cattle. Nasolacrin1al discharge or
affected cattle should ensure that their
cough may accompany or precede the
footwear and clothing are clean before
diarrhea Other signs include mild colic,
leaving an affected faim.

dehydration, depression, a brief period of
anorexia, and some decrease in body
condition. Occasionally, animals exhibit

Other Intestinal Diseases of Cattle
more severe signs such as passage of feces

Infection with Salmonella spp ( see p 195) with variable amolll1ts of blood, severe
can produce diarrhea in animals of all ages,
dehydration, and weakness. Fatalities are
especially those that ai·e stressed, closely
rare. Diarrhea in individual anin1als has a
stocked, or exposed to a heavily containishort course, and feces return to normal in nated feed or water supply. In older animals,

2-3 days in most animals. Disease in the herd
the disease is manifest by dysentery and
typically subsides in 1-2 wk, but milk
toxemia, and mortality can be significant.

production may take weeks to months to

Rotavirus and coronavirus occasionally
return to nom1al.

cause outbreaks of dianhea in suckling

Lesions: The small intestine may be
calves up to 2-3 mo old. The feces are
dilated and flaccid. Lesions are p1imarily
vollll11inous and may contain mucus.

seen in the large intestine and consist of

Toxemia is not evident and mortality is
cecal and colonic mucosa! h
negligible, but growtl1 is decreased. (See
yperemia,
linear streaks or pinpoint-sized hemor
also D!ARRIIEA IN NEONATAL RUM[NANTS, p 275.) rhages mostly along the colonic mucosa!

Necrotic enteritis of lll1known etiology is
ridges, and blood in the I umen of the large
seen in beef cattle 5-12 wk old, commonly
intestine. Histologic findings may include
affecting several calves within the herd.

widespread degeneration and necrosis of

There is sudden onset of fever, depression,
colonic glandular epithelimn.

and profuse diarrhea. The feces are initially
dai·k green, contain blood, and frequently
stain the perinelll11. Circulai· erosions may

Diagnosis: A diagnosis of winter
be present in the oral mucosa. A proportion
dysentery can be confirmed by demonstratof calves recover after a clinical course of ing coronaviral particles in fecal san1ples via 3-5 days. The clinical course is longer in ELISA or electron microscopy. Seroconverfatal cases; animals have scant mucohemorsion to coronavi.tus in acute and convalesrhagic feces that are passed with tenesmus cent seflll11 samples, taken 8 wk apart, also
and develop a severe non.regenerative
helps confirm the diagnosis.

leukopenia. A secondary fibrinous broncho-

INTESTINAL DISEASES IN RUMINANTS

273
pneumonia may develop. Mortality is high
interaction of a carcinogen (ptaquiloside) in
despite intensive antibiotic treatment. At
bracken fem (Pt.eridium spp, seep 3089) necropsy, there is ulcerative necrosis of the
and papilloma virus.

terminal small intestine and the large

Intestinal obstructions are seen
intestine.

sporadically (seep 245). Cecal dilatation

Coccidiosis ( see p 205) usually is seen in and volvulus are seen predominantly in

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calves >2 mo old but< 1 yr old, especially in adult cattle in the postparturient period.

situations of heavy stocking density and

Intussusception occurring at the distal
overgrazing. It is characterized by dysentery jejunum or proximal ilew11 is the most and tenesmus and may be accompanied by
common cause of complete obstruction in
nervous signs. Intestinal helminthiasis,
both adult cattle and calves. Ileocecocolic,
particularly ostertagiosis (seep 308), is
cecocolic, and colonic intussusceptions are
seen in cattle of the same age group. Type I
seen less frequently in calves and not at all
ostertagiosis is seen in cattle on pasture, but in adult cattle because of the greater Type II ostertagiosis may be seen in housed
strengtl1 of tlle ileocecal ligan1ent and the
animals.

presence of mesenteric fat, which stabilize

Explosive outbreaks of diarrhea in mature this region of the bowel in older cattle.

cattle are associated most commonly with

Intestinal volvulus and volvulus around the
winter dysentery (seep 271) but also with
mesenteric root are seen sporadically at all
salmonellosis when there is heavy
ages. Rarely, intestinal obstruction is caused
contamination of feed or water.

by incarceration and entrapment of the

Chronic diarrhea and wasting often in
small intestine by persistent urachal or
combination with good appetite, occun·ing
wnbilical remnants, by obstruction of the
as a sporadic disease in adult catUe is typical small intestine or descending colon by for paratuberculosis (seep 762). Chronic
phytobezoars and enteroliths, or by
diarrhea and wasting also occurring in
compression from fat necrosis or lipoma.

younger animals may be caused by chronic

Intestinal obstruction can also be caused
salmonellosis and chronic BVD infection.

by congenital disease (seep 168), most

Other possible causes of chronic diarrhea
commonly by atresia coli ( which is seen
include congestive heart failure, uremia, and botll sporadically and in clusters on a farm chronic peritonitis. Persistent diarrhea with
and may be caused by rectal palpation of
unthriftiness, and occasionally wasting in
tlle anlniotic vesicle at 35 and 41 days of
yearling and mature cattle, can be associpregnancy) but also by atresia ani (which ated with a secondary copper deficiency due may be accompanied by urogenital defects to excess molybdenum in the pastures.

and defects of the tail).

Diarrhea may also accompany seleniumresponsive ill-tluift syndromes in growing cattle.

INTESTINAL DISEASES IN SHEEP

Individual cases or outbreaks of diarrhea

AND GOATS
may be associated with dietary indiscretions. Diarrhea may follow cases of simple The causes and circw11stances of diarrhea in
indigestion and is common in grain overload neonatal lambs and kids are sinillar to tllose (seep 222). It also follows ingestion of
in newborn calves. Intensive lambing
toxic amow1ts of chemicals ( eg, arsenic,
practices and shed-lambing increase the
copper, zinc, and molybdenum) or certain
potential for disease and buildup of
poisonous plants and mycotoxicoses;
infectious agents and can be associated with
dipyridyl and organophosphate poisoning
serious outbreaks of diarrhea. The serotypes
can also cause diarrhea.

of enteropathogenic Escherichia coli tllat

Cattle may also harbor organisms such
cause secretory diarrhea in calves also do so
as Escherichia coli 0157:H7, Yersinia
in lan1bs, and the approach to diagnosis,
enterocolilica, and Campylobacterjejuni treatment, and control is sinlilar. Sinlilarly,
in the intestine; although these are rarely
rotavirus, coronavirus, and cryptosporidia
associated with clinical disease in cows,

( see p 209) also cause outbreaks of diarrhea fecal contamination of milk may lead to
in lambs. (See also DIARRHEA IN NEONATAL
outbreaks of gastroenteritis in people who

RUMINANTS, p 275.) Lamb dysentery caused
consume unpasteurized milk or cheese
by Clostridium perfringens type B (see
products. Retail meat products can also be
p 609) is a distinct intestinal disease of lambs
infected if there has been fecal contaminain the first week of life. It is seen principally tion of the carcass at slaughter.

in hill breeds of sheep in the UK and is

Intestinal adenocarcinoma, commonly
characterized by sudden death or diarrhea,
seen in association with bovine enzootic
dysentery, and toxemia. In tlle USA, C
hematuria, is believed to result from the
pe,jringens type C causes a similar

274

INTESTINAL DISEASES IN RUMINANTS
syndrome. Watery mouth or rattle belly (see

Etiology and Pathogenesis: Watery
below), a disease of uncertain etiology
mouth disease has been associated with
associated with fail me of transfer of passive
ingestion of gram-negative bacteria,
immunity, is seen predominantly in the UK.

particularly E coli, that smvive in the

Coccidiosis (seep 206) and GI helminthianeonatal GI tract and translocate from the sis (seep 312), except for haemonchosis,
gut to the bloodstrean1. The strains involved

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are in1portant causes of diarrhea in older
are K99 antigen negative and regarded
nmsing and weaned sheep. Terminal ileitis
normally as nonenteropathogenic and
and villous atrophy, both of unknown
nonenterotoxigenic. The resultant
etiology, are often present in the intestine
bacteremia may be tolerated by the lamb,
of lambs culled because of poor growth.

but > 104 colony-forming units/mL are

GI helminthiasis is the most conunon
associated with release of free endotoxin,
cause of diarrhea in pastmed sheep.

and endotoxic shock develops rapidly.

Coccidiosis develops in association with

Lambs 12-72 hr old with inadequate or
overstocking or intensive indoor housing
delayed access to colostrum are at greatest
and poor sanitation. Salmonellosis ( see
risk Otl1er risk factors that have a negative
p 195) can cause diarrhea in all ages; the
effect on colostrum intake include being
circumstances in y0tmg lan1 bs are similar to
born in larger litters, being born to a dan1
those in calves. It also can cause outbreaks
with poor body condition, and stressors
of diarrhea late in pregnancy and is
such as early castration.

frequently accompanied by abortion.

Salmonellosis is more conunon when sheep
or goats are congregated intensively or

Clinical Findings: Lambs affected with
stressed, particularly by shipping. Yersinia
watery mouth disease are hypothermic,
pseudotuberculosis and Y enterocolitica dull, stop feeding, and, classically, have long
have both been associated with enterocolistrings of saliva drooling from the mouth.

tis and diarrhea in young sheep at pastme

Less obvious cases may have a wet muzzle;
that are debilitated from factors such as
others may show no external signs of
starvation and cold weather. Diarrhea may
excess salivation, but the mouth may be
be present in bluetongue in sheep (see
cold to the touch and contain frothy saliva.

p 738) and is accompanied by typical

Lacrimation may also be seen. The
mucosa! lesions. In goats, diarrhea is often
abomaswn may become distended with gas
prominent in enterotoxemia associated
and liquid, giving the deceptive appearance
with C perfringens type D (seep 610). This of a well-fed Jamb, but if these lan1bs are
is not a feature of the clinical disease in
lifted and shaken gently, a noise associated
sheep but may be present in flockn1ates of
with the alternative nan1e of "rattle belly"

affected sheep. In feedlot sheep, diarrhea
may be heard. Although scoms occasionally
most conunonly is associated with grain
occm, this is not a characteristic featme of
overload, salmonellosis, 0r coccidiosis.

the condition.

Other intestinal diseases of adult sheep

Lesions: Necropsy may reveal a bloated
may manifest with diarrhea. Infection with
and inflamed GI tract, retained meconiun1,

C perfringens type C (strnck, seep 609) pale kidneys and muscle, dehydration, and
manifests with abdominal pain, J;enesmus,
enlarged and reactive mesenteric lymph
and rapid death. Intestinal obstruction due
nodes.

to intestinal accidents occms sporadically
but is usually not seen clinically. Sheep with

Diagnosis: Biochemical and hematologic
paratuberculosis (seep 762) usually show
changes and necropsy findings in lambs
progressive emaciation without diarrhea
affected with watery mouth disease are

Progressive emaciation also is the primary
consistent with endotoxemia and the
sign in adult sheep with intestinal adenocarclinical diagnosis of endotoxic shock cinoma, which can be prevalent in certain

Terminally, lambs develop endotoxemia,
areas, associated with ingestion of bracken
leukopenia, severe hypoglycemia, lactic
fem (seep 3089).

acidemia, and metabolic acidosis.

Differential diagnoses include joint ill or

Watery Mouth Disease in Lambs
navel ill, hypothern1ia, primary starvation,
and infectious enteritis.

(Slavery mouth, Slavers, Rattle belly)

Watery moutl1 disease is a condition of

Treatment: There is no specific
intensively reared lambs occmring dming
treatment for watery mouth disease.

the first days of life. Morbidity in a flock can

Parenteral antin1icrobial and anti-inflan1-
be as high as 30"Ai, and the mortality rate may matory therapy combined with oral exceed 80"Ai.

rehydration are essential; 50-200 mL of an

INTESTINAL DISEASES IN RUMINANTS

275
electrolyte and 5o/e>--l0% glucose solution

12 hr. This discussion emphasizes the
containing a water-soluble antibiotic
disease in calves, but the principles of

(neomycin and/or streptomycin) given
pa.thophysiology and treatment apply to
tid by stomach tube will help maintain
lambs and kids as well.

hydration and provide energy. Systemic
antimicrobial therapy with a gram-negative

Etiology: Several enteropathogens a.re

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spectrum and anti-inflan1matory therapy
associated with diarrhea. in neonates. Their
with NSAIDs or c01ticosteroids to
relative prevalence varies geographically,
counteract the effects of endotoxemia
but the most prevalent infections in most
should also be administered. Purgatives or
areas are Escherichia coli, rotavirus,
enemas may help overcome gut stasis and
corona.virus, and Cryptosporidium
expel the infecting bacteria. Treatment
parvum. Cases of neonatal diarrhea. are
should be continued until signs resolve and
commonly associated with more than one
the lamb is sucking again. Boosting body
of these a.gents, and the cause of most
temperature by external warming may also
outbreaks is multifa.ctorial. Determining
be required. However, such ca.re is timethe particular a.gents associated with an consuming and expensive and carries no
outbreak of diarrhea. can be important,
guarantee of success.

because specific therapy and prophylaxis
are available for some. Also, some a.gents

Prevention: Ewes should be well
have zoonotic risk. Diarrhea. is also present
nourished to ensure a plentiful supply
in septicemic colibacillosis.

of colostrum. Yards, pens, ewes, and

Bacteria: E coli is the most important
equipment should be kept as clean as
bacterial cause of diarrhea in calves during
possible throughout lambing to help control
the first week of life; at least two distinct
the buildup of E coli and keep the incidence types of diarrheal disease are produced by
of disease low. Supplementary feeding of
different strains of this organism. One type
lambs using stored colostrun1 ( ewe, cow, or
is associated with enterotoxigenic E coli,
goat) or commercial colostrum substitute
which has two virulence factors associated
should provide a minin1Um of 50 mUkg
with production of diarrhea. Fimbrial
within 6 hr of birth. Lambs should not be
antigens enable them to attach to and
castrated in the first 24 hr because this
colonize the villi of the small intestine of
depresses colostrum intake.

neonatal calves in the first days of life.

In controlled experiments, a single dose

Strains in calves most commonly possess
of oral antibiotic given within 2 hr of birth

K99 (F5) or F41 fimbrial antigens, or both.

to colostrum-deprived lambs delivered

These antigens are the focus of immunointo a contan1inated indoor environment logic protection. Enterotoxigenic E coli
was as effective as ewe colostrum in
also elaborate a thermostable, nonantipreventing neonatal disease and death in genic enterotoxin (Sta) that influences
all lambs up to 3 days old, despite the
intestinal ion and fluid secretion to
absence of maternal antibodies. Thus,
produce a noninflammatory secretory
antibiotic treatment can provide simple,
diarrhea.. Diarrhea. in calves and lambs also
quick, and inexpensive protection against
has been associated with enteropathogenic
watery mouth disease and is an attractive

E coli that adhere to the intestine to
option for the busy sheep farmer. However, produce so-called attaching and effacing it is important that such treatment be
lesions, with dissolution of the bmsh
targeted to lambs in the high-risk
border and loss of microvillous structure
categories specified above, because
at the site of attachment, a decrease in
indiscriminate dosing may encourage
enzyme activity, and changes in ion
antibiotic resistance.

transport in the intestine. These enteropa.thogens are also called "attaching and effacing E coli." Some produce verotoxin, DIARRHEA IN NEONATAL
which may be associated with a more

RUMINANTS
severe hemorrhagic diarrhea.. The infection
most frequently is in the cecum and colon,

(Scours)

but the distal small intestine can also be

Diarrhea. is common in newborn calves,
affected. The dan1age in severe infections
lambs, and kids. The clinical presentation
can result in edema and mucosa! erosions
can range from mild diarrhea without
and ulceration, leading to hemorrhage into
systemic disease to profuse, acute diarrhea
the intestinal lumen.

associated with rapid dehydration, severe

Salmonella spp, especially S Typhimudisturbance of acid-base and electrolyte rium and S Dublin, but occasionally other balance, and death, sometimes in as few as
serova.rs, cause diarrhea. in calves 2-12 wk

276

INTESTINAL DISEASES IN RUMINANTS

Corona.virus is also conunonly associated
with diarrhea in calves. It replicates in the
epitheliun1 of the upper respiratory tract
and in the enterocytes of the intestine,
where it produces similar lesions to
rota.virus but also infects the epithelial cells

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of the large intestine to produce atrophy of
the colonic ridges.

Other viruses, including Breda virus

(torovirus), a calici-like virus, astrovirus,
and parvovirus, have been demonstrated in
the feces of calves with diarrhea and can
produce diarrhea in calves experimentally.

However, these agents have also been found
in the feces of healthy calves. The importance of these agents in the syndrome of diarrhea in neonates has yet to be determined. The viruses of bovine virus diarrhea and infectious bovine rhinotracheitis are
reported to cause calf diarrhea, but this is
not a conunon manifestation of these

Enterotoxigenic Escherichia coli adhering to the intestine of a 2-day-old calf.

infections.

Courtesy of Dr.

J. J. Hadad and Dr. Carlton Gyles.

Protozoa: Oryplosporidium parzrnm

( see p 209) is a common cause of diarrhea
in calves and lambs. The parasite does not
old. Salmonellae produce enterotoxins but
invade but adheres to the apical surface of
are also invasive and produce inflammatory
enterocytes in the distal small intestine and
change within the intestine. In calves,
the colon. This results in loss of microvilli,
infection commonly progresses to a
decreased mucosa.I enzyme activity with
bacteremia. (See also SALMONELLOSIS, p 195.) villous blunting and fusion Oeading to a

Clostridium pe1fringens types A, B, C,
reduced villous surface absorptive area),
and E produce a variety of necrotizing
and inflanm1atory changes in the submutoxins and cause a rapidly fatal hemorrhagic cosa. Mammalian cryptosporidia lack host enteritis in calves. The disease in calves is
specificity.

rare and usually sporadic. Infection with

Giardia duodenalis is a common
type B or C is a common cause of enteritis.

asymptomatic infection in the intestine of
and dysentery in lambs (seep 609).

young calves and lambs. It has been found

Campylobacte1-jejuni and Ye1·sinia
in the feces of poorly growing calves that
ente1-ocolitica may be present in the feces have a chronic mucoid diarrhea, but there is
of calves and lambs with diarrhea but also
little evidence for a causative association of
may be found in the feces of healthy
this organism with diarrhea in calves or
animals.

lambs.

Viruses: Rota.virus is the most common

Other Causes: Calves fed large amounts
viral cause of diarrhea in calves and lambs.

of milk or inappropriately formulated milk

Groups A and B rota.virus are involved, but
replacers produce a large volume of feces
group A is most prevalent and clinically
with a greater than normal fluid content
important and contains several serotypes of
but do not have a fluid diarrhea with
differing virulence. Rota.virus replicates in
weight loss. Similarly, calves sucking
the mature absorptive and enzyme-produchigh-producing beef cows grazing lush ing enterocytes on the villi of the small
pasture may have loose feces. Milk
intestine, leading to rupture and sloughing
replacers with poor quality, heat-denatured
of the enterocytes with release of virus to
proteins or with excessive amounts of
infect adjacent cells. Rota.virus does not
soybean or fish protein or carbohydrates
infect the inlITlature cells of the crypts. With
of nonrnilk origin have a higher risl5 of
virulent strains of rota.virus, the loss of
producing diarrhea.

enterocytes exceeds the ability of the

There is some evidence that oral
intestinal crypts to replace them; hence,
administration of chloramphenicol,
villous height is reduced, with a consequent
neomycin, or tetracycline to young calves
decrease in intestinal absorptive surface
for 3-5 days can result in villous change with
area and intestinal digestive enzyme
resultant malabsorption and mild diarrhea.

activity.

Prolonged and high-dose antibiotic

INTESTINAL DISEASES IN RUMINANTS

277
treatment of calves can lead to diarrhea
abnormal ainount of fluid is secreted into
associated with bacterial superinfection of
the gut, exceeding the resorptive capacity of
the intestine. Colisepticemia ( see p 7 49) and the mucosa. In malabsorptive diarrhea, the
rnminal drinking ( see p 236) can also be
capacity of the mucosa to absorb fluid and
accompanied by diarrhea
nutrients is impaired to the extent that it
carmot keep up with the normal influx of

Epidemiology and Transmission:

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ingested and secreted fluids. This is usually

Enteropathogens associated with diarrhea
the result of villous atrophy, in which the
are conunonly found in the feces of healthy
loss of mature enterocytes at the tips of the
calves; whether intestinal infection leads to
villi results both in a decrease in villous
diatThea depends on a number of determiheight ( with a consequent decrease in the nants, including differences in virulence
swface ai·ea for absorption) and in loss of
of different strains of a pathogen and the
the brush border digestive enzymes. The
presence of more than one pathogen. The
extent and distribution of villous atrophy
resistance of the calf is of major importance
varies with different pathogens and can
ai1d is lai·gely determined by successful
explain variation in the severity of clinical
passive transfer of colostral inununoglobudisease. Malabsorptive diarrhea may be lins. Colostturn-deprived calves are highly
aggravated by the colonic fermentation of
susceptible to infection with enteropathonutrients that nom1ally would have been gens and develop severe and often fatal
absorbed in the small intestine. Fermentadisease.

tion products, especially lactic acid, appear

The progression of infection, the severity
to draw water into the colon osmotically,
of lesions produced, and the severity of the
which contributes to the severity of
diarrhea can be modulated by immunodiarrhea.

globulins received via colostrum. Immuno

Inflammation contributes to the
globulins act directly on pathogens in the
pathophysiology of diarrhea in most
intestinal lumen during the period of
intestinal infections, and mediators of
colostrum ingestion as well as after,
inflanunation can affect ion flux within
because significant an10unts of circulating
the intestine. Inflammation also leads to
inununoglobulins are re-secreted into the
vascular and lymphatic dainage and to
intestine, especially when the concentrastructural dan1age of the crypt-villus unit.

tion of circulating irnmunoglobulin is high.

Most infectious forms of dian·hea have

The lack of specific antibodies in dains
hypersecretory, inflanunatory, and
that have not been exposed to specific
malabsorptive components, although one
pathogens, and the use of specific vaccines,
usually predominates. These lead to a net
further modulate this influence. Stress
loss of water, sodium, potassium, and
caused by a poor environment, inadequate
bicarbonate; if severe, the calf develops
protection from the weather, or an
hypovolemia, hyponatremia, acidemia,
insufficient or inappropriate diet also
and prerenal azotemia.

increases the risk of disease.

Enterotoxigenic E coli produce the

With all of the enteropathogens, healthy
enterotoxin Sta, which stimulates marked
adult cattle may be carriers and periodically
hypersecretion by activating guanylate
excrete the organism in feces. Excretion
cyclase and by inducing a net secretion of
may increase around parturition and be
sodiwn and chlorine. The membrane-bound
more frequent in prinuparous cows. This
sodiwn-glucose cotransport system remains
can lead to conta.tninated calving areas and
functional but carmot compensate for the
infection of the udder and perineum of the
increased secretory activity. Salmonellae
da.tn. Other sources of infection include the
also elaborate enterotoxins. Inflanunation,
feces of healthy calves and the feces of
leading to necrosis of the enterocyte,
diarrheic calves, which contain large
submucosal inflanunatory infiltration, and
numbers of organisms early in the course of
villous atrophy, is also a major component
infection. A few scouring calves can result
of the pathophysiology of diarrhea
in severe contamination of the calf-rearing
produced by salmonellae, as well as of
ai·ea. Transmission is by fecal-oral contact,
diarrhea produced by enteropathogenic
fecal aerosol, and, in the case of coronavi

E coli and by toxigenic C perfringens.

rns, by respiratory aerosol.

Infections with verotoxin-producing
enteropathogenic E coli result in accumula

Pathogenesis: Diarrhea in neonatal
tion of fluid within the large intestine ai1d
tuminants is usually associated with disease extensive dainage to the large intestinal of the small intestine and can be caused by
mucosa, with edema, hemorrhage, and
hypersecretion or malabsorption. Hypererosion and ulceration of the mucosa, which secretory diarrhea develops when an
results in blood and mucus in the lumen.

278

INTESTINAL DISEASES IN RUMINANTS

Viruses usually produce a malabsorptive

Hemorrhagic enterotoxemia due to
diarrhea by destroying the absorptive cells

C perfringens type B or C is characte1ized
of the mucosa, thus shortening the intestinal by acute onset of depression, weakness, villi. The mechanism by which cryptobloody diarrhea, abdominal pain, and death sporidia produce diarrhea is not completely
within a few homs. It usually develops in
understood, but it appears to have both
vigorous calves just a few days old that have
malabsorptive and inflammatory compolarge appetites and a ready source of milk.

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nents.

Calves affected with C perfringens usually

Inappropriately formulated milk
die before treatment can be instituted.

replacers produce diarrhea by two

Diarrhea due to rotavirus, coronavirus,
mechanisms, both associated with
and other viruses usually is seen in calves
malabsorption. Vegetable (especially

5---15 days old but can affect calves up to
soybean) products are commonly used as
several months of age. Affected calves are
protein sources in the manufacture of milk
only moderately depressed and often
replacers. Depending on the degree of
continue to suck or drink milk. The feces
refinement, these products may contain
are voluminous, soft to liquid, and often
carbohydrates that are indigestible in
contain large amounts of mucus. Diarrhea
young calves. Such carbohydrates are not
conunonly persists for 3 to several days,
absorbed in the small intestine and may
with some cases of coronaviral dian·hea
cont1ibute to diarrhea via colonic fennent a becoming chronic. Cases of viral diarrhea tion. In addition, most calves <3 w k old
that are uncomplicated by other pathogens
appear to have an allergic reaction to soy
commonly respond within a few days to
proteins that results in villous atrophy,
fluid and electrolyte therapy and adequate
leading to diarrhea that is probably
nut1itional support.

malabsorptive.

Cryptosporidiosis (seep 209) is seen in
calves 5---35 days old but most commonly in

Clinical Findings: The major signs are
the second week of life. It is characterized
diaIThea, dehydration, profound weakness,
by persistent diarrhea that does not respond
and death within one to several days of onset.

to therapy. Diarrhea due solely to Crypto

Diarrhea due to enterotoxigenic
sporidium spp is often mild and self-limit

(K99-bearing) E coli is seen in calves
ing, although the severity may be related to

<3---5 days old, rarely later. However, the age
the general strength of the calf and to the
of susceptibility may be extended in the
intensity of challenge with the organism.

presence of other pathogens. Onset is

Combination infections with cryptosudden. Profuse amounts of liquid feces sporidia, rotavirus, and coronavirus are
are passed, and the calves rapidly become
common and result in persistent diarrhea
depressed and recumbent. Calves may Jose
often characterized by emaciation and

> 12"Ai of body weight in fluid, and hypovodeath. Death from hypoglycemia also lemic shock and cteath may occur in 12-24
occurs as a sequela of cryptosporidiosis in
hr. Body temperature may be increased but
calves 3---4 wk of age that have recovered
is commonly normal or subnormal. If fluid
from diarrhea but are still emaciated. Death
and electrolyte therapy is administered
often occurs during a bout of cold weather
early, response is usually good. Disease
and is more likely to occur on fanns where
produced by attaching and effacing E coli is there is a policy of reducing the amount of
seen predominantly in calves from 4 days to
milk fed to calves during periods of

2 mo old and may manifest with diarrhea
diarrhea.

or primarily as dysentery with blood and

Dietary diarrheas are seen in calves <3 wk
mucus in the feces. The clinical course is
old and are characterized by voluminous
short.

feces of pasty to gelatinous consistency.

Diarrhea due to Salmonella spp usually

Initially, the calves are bright and alert and
is not seen in calves <14days old. !t is
have good appetites. Eventually, however,
characterized by feces that are foul smelling
they become weak and emaciated if the
and contain blood, fibrin, and copious
diet is not coITected. Infectious forms
amounts of mucus. Septicemia, with high
of diarrhea are often complicated by
fever and depression progressing to
poor-quality diets or insufficient nutritional
prostration and coma, is the salient
intake.

manifestation of salmonellosis in calves
and, although dian·hea is present, death is

Diagnosis: It is difficult to make a definite usually from septicemic rather than from
etiologic diagnosis for diarrhea based solely
hypovolemic shock. Calves with salmonelon clinical findings. However, the history, losis usually lose weight rapidly and often
age of the animal( s) affected, and clinical
die despite vigorous therapy.

signs may permit a presumptive diagnosis.

INTESTINAL DISEASES IN RUMINANTS

279

Fecal samples can be submitted for
glucose and amino acids and should contain
isolation and characterization of the
sodium, glucose, glycine or alanine,
common enteropathogens. Samples should
potassium, and either bicarbonate or citrate
be taken from several untreated calves in
or acetate as alkalinizing agents. Several
the early stages of diarrhea. Special
commercial preparations are available.

techniques are necessary for the demon

These can be administered by nipple bottle
stration of viruses, cryptosporidia, and
or, if necessary, by stomach tube. The

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K99-bearing E coli. The interpretation of
solutions should be used liberally until
fecal microbiology can be difficult because
the animal is rehydrated.

of mixed infections and because enter

Whether milk should be fed during the
opathogens are conunonly present in the
rehydration period remains controversial.

feces of healthy calves.

Feeding milk may increase fecal volume,

The best diagnostic information is usually but it provides energy to the calf and may obtained by submitting untreated, acutely
promote gut healing. Calves have large
affected animals for necropsy. This allows
energy requirements and little rese1ve.

exanlination of intestinal mucosa for

Electrolyte solutions do not meet calf
evidence of diagnostic lesions and for the
energy requirements, and milk should
presence of enteropathogens such as
not be withheld for >24 hr, if at all.

cryptosporidia. It may be the only way

Calves that are recun1bent, weak, and
that disease such as that associated with
show evidence of water loss of �B"A, of their
attaching and effacing strains of E coli can body weight require IV fluid therapy. These
be diagnosed. The diagnostic value of a
calves are usually acidotic, and the fluid and
necropsy diminishes quickly with time after
base deficits can be con-ected initially by
death; important lesions can disappear
rapidly administering a hypertonic solution
within minutes due to autolysis.

of sodiwn bicarbonate ( either 500 mL of a

Complete laboratory examination can be

4.2% solution, or 250 mL of an 8.4%
expensive, and it has also been argued that
solution), followed by a physiologically
there is little value in expending large
balanced electrolyte solution administered
amounts of money on diagnosis unless there at up to 40 mUkg/hr until the volume deficit are specific control procedures that can be
is corrected. Because diarrheic calves are
implemented based on the infom1ation
frequently hypoglycemic, adding 25-50 g of
gained. In all cases, information on total
dextrose to the electrolyte solution is often
milk or milk replacer consumption should
beneficial in the initial treatment phase.

be obtained. When milk replacer is being

Oral electrolyte solutions should be used
fed, the composition of the diet should be
concun-ently with and after IV fluid therapy
evaluated. Nonspecific immunity should be
to compensate for ongoing fluid and
assessed by detemlining irnmunoglobulin
electrolyte losses.

and vitamin A concentrations in serum.

Although mild diarrhea without systemic
disease is not an indication for antimicrobial therapy, use of parenteral antibiotics Treatment: Many of the factors involved
should be considered whenever calves are
in disease resistance are nonspecific; thus,
systemically ill or recun1bent. Field studies
important preventive measures can be
revealed that at least 30% of diarrheic calves
taken and therapy can be started before an
with systemic disease are bacteremic-a
etiologic diagnosis has been established.

clear indication for parenteral antimicrobial

Treatment includes fluid therapy for water
therapy. Because the large majority of cases
and electrolyte replacement and con-ection
of bacteremia and septicemia in neonatal
of acid-base disturbances, alteration of the
calves are associated with E coli, the
diet, and antimicrobial and anti-inflan1machosen antibiotic should be effective tory therapy.

against gram-negative bacteria.

Fluid and electrolyte therapy is most

In several studies, severely affected
important and should be started as soon as
dia.1Theic calves treated with NSAIDs in
possible regard.less of whether clinical
conjunction with fluid therapy showed
evidence of dehydration has developed
fewer signs of pain, made a faster recovery,

( clinical signs of dehydration are not
and had better weight gains in the reconvaapparent until the calf has lost at least 6% of lescent period. These effects reported for
its body weight in fluid). Calves still able to
several NSAIDs have been attributed to
stand and willing and able to suck can often
their analgesic, anti-inflanunatory,
be treated with oral electrolyte solutions
antipyretic, and antisecretory properties.

alone. Fluids for oral rehydration should

The use of drugs to reduce intestinal
promote the cotransport of sodium with
motility such as hyoscine-N-butylbromide

280

INTESTINAL DISEASES IN RUMINANTS
or atropine is sometimes advocated,
control enterotoxigenic coliba.cillosis. The
because they decrease fecal output.

pregnant dam is vaccinated 6 and 2 wk

Although reducing fecal production may
before pa.rtUiition to stimulate antibodies to
be interpreted as a positive treatment
strains of enterotoxigenic E coli; these
outcome, it can also be seen as sequestraantibodies a.re then passed on to the tion of gut fluid containing bacteria, toxins,
newborn tJu·ough the colostrum (provided

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and undigested nutrients in the intestinal
the calf ingests it). A single booster is given
tract. The literature does not provide any
in subsequent years. Monoclonal K99 E coli
strong supportive evidence for or against
antibody is conunercially available for oral
the use of antimotility drugs.

administration to calves inunedia.tely after

Intestinal gels and adsorbents, such as
bi.tth. It is an effective substitute for the
kaolin and pectin, are in general use, but

K99-specific antibody in the colostrmn of
their only established effect is to increase
vaccinated cows, although calves that
fecal consistency; they do not reduce the
receive this product should also receive
loss of water and ions.

colostrun1 for its nonspecific protection.

Vaccination of pregnant cows with

Prevention and Control: Because of the
rota.virus and corona.vi.tus vaccines
complex nature of diarrhea in neonates, it is
increase the an1ount of specific antibody in

Wlfealistic to expect total prevention-ecocolostrum and milk, but the concentration nomical control is the major objective. The
of antibodies in milk may be insufficient to
incidence of clinical disease and the case
provide local antibody in the intestinal
fatality rate depend on the balance between
lwnen during the period of peak prevalence
the levels of exposure to infectious agents
of infection, which, in calves, is 5-15 days
and the resistance in the calf. Differences in
of age. Controlled trials of commercial
herd size; availability of facilities, land, and
vaccines have shown variable results. The
labor; and general management objectives
addition of small amounts of i.tnmune
make it impossible to recommend specific
colostrum to milk fed during the period of
management procedures applicable to all
susceptibility can provide some protection
situations. However, three broad principles
against disease.

apply in all herds: 1) the degree of exposure
of neonates should be reduced by isolating
diseased animals or by moving calving and

Zoonotic Risk: Several of the a.gents
calf rearing to a separate area, and by practhat produce dia.n-hea. in calves can also ticing good general hygiene; 2) nonspecific
produce diarrheal disease in people.

resistance should be maximized by

Cryptospo1·idium parvum and S Typhiproviding good nutrition to the darn and murium can produce serious disease,
neonate and assming that newborn calves
pruticularly in i.tnmunocompromised
consmne �5% of their body wt of high-qualindividuals. These organisms a.re comity colostrmn, preferably within 2 hr and monly present as subclinica.l infections in
certainly within 6 hr of bi.tth, followed by
the gut of calves and lan1bs; inununocomequivalent a.mounts at 12-hr intervals for promised people should a.void contact with
the next 48 lu·; and 3) the specific resistance
young ruminants and possibly all fru,n
of the newborn should be increased by
animals.

vaccinating the dam or the newborn. A

Cattle, including calves, a.re one of the
significant portion of both naturally
reservoirs for the verotoxic E coli serotype sucking dairy calves and calves handfed

0157:H7 associated with human hemorcolostrun1 do not acqui.t·e adequate amounts rhagic colitis and the hemolytic uremic
of in1munoglobulin because of delayed
syndrome. Infection in people is usually
sucking or feeding, ingestion of an
acquired by conswnption of contan1ina.ted
inadequate volun1e of colostrun1, or
food, but the infective dose is low and the
ingestion of colostrmn of inferior inununopossibility of infection by direct contact globulin concentration. When ti.tne
exists. Other verotoxic E coli associated
constraints on labor preclude an ensured
with human disease cru1 also be isolated
intake of colostrmn by nipple-bottle
from the feces of healthy cattle. HUina.o
feeding, ad.ministration of 4 L of colostrun1
disease from infection with enteric
by esophageal feeder within the first 2 hr of
livestock pathogens has occUl"Ied after
life can be the best colostrmn feeding policy. seemingly trivial contact associated with (See also MANAGEMENT 01' REPRODUCTION:

visits to livestock fairs, petting zoos, and

CAWLE, p 2171.)

fa.rm educational tours. Hand cleansing and

Inununiza.tion of calves against colibacildisinfection should be a component of these losis by vaccination of pregnant dan1s can
visits.

INTESTINAL DISEASES IN HORSES AND FOALS

281

INTESTINAL DISEASES

IN HORSES AND FOALS

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Intestinal disease in horses and foals is

Because of the large volume of the colon
suggested by diarrhea, weight loss,
and cecum of horses, massive fluid losses
hypoproteinemia, and abdominal pain.

can occur in a short time. Thus, dianhea in

(See also COLIC IN HORSES, p 248.)

adult horses can be an explosive event with
morbidity and mortality exceeding that
associated with diarrheal diseases in other
animals and people.

A definitive cause of dianhea can be

SALMONELLOSIS
dete1mined in <500Ai of cases. Yet, treatment
of most horses and foals with diarrhea is

Salrnonellosis (seep 195) is one of the
similar and thus allows supportive
most commonly diagnosed infectious
therapeutic management despite the
causes of diarrhea in adult horses. Clinical
lack of a definitive diagnosis.

manifestations range from no abnormal

Diarrhea in adult horses can be acute or
clinical signs (subclinical canier) to acute,
chronic. Wectious agents that have been
severe diarrhea and even death. The disease
cited as potential causes of acute diarrhea
is seen sporadically but may become an
in adult horses include numerous Salmo
epidemic, depending on the virulence of
nella serovars, Neorickettsia risticii, the organism, level of exposure, and host

Clostridium di.fficile, C pmfringens,
factors. Wection can occw· via contan1ina

Aeromonas spp, coronavirus, and
tion of the environment, feed, or water or by
cyathostorniasis. Other differential
contact with animals actively shedding
diagnoses for acute diarrhea in horses
the bacteria. Stress appears to play an
include ingestion of a toxicant(s), antimiimportant role in the pathogenesis-a crobial-induced colitis, NSAID toxicity, and
history of surgery, transportation, or change
sand enterocolopathy. An acute, fatal
in feed; concurrent disease, paiticularly
diarrheal disease of unknown etiology is

GI disorders (colic); or treatment with
known as colitis-X. Diarrhea that persists
broad-spectrw11 antinlicrobial drugs often

> 1 mo is considered chronic and is often a
precedes the diarrhea.

diagnostic challenge. Clu·onic diarrhea can

Salmonella enterica of the serogroup B
be caused by inflanu11atory or neoplastic
includes S enterica serovar Typhimuriun1
conditions involving the intestine or by
and S enterica Agona, two of the most
disruption of the nom1al physiologic
frequently isolated serovars from horses
process in the bowel. Differential diagwith clinical disease. Knowing the serovar noses include sand enterocolopathy and
and antibiogram can help track or monitor
infiltrative lesions, such as those associated
the type of serovar of salmonellae affecting
with inf1ammatory bowel disease or
any given group or population of horses ( eg,
intestinal lyrnphosarcoma. The body's
tracking nosocomial spread within a
response to certain components of feed may
veterinary hospital). The emergence of
play a role in chronic diarrhea of horses due
multidrug-resistantS entmica isolates is
to bowel inflammation but has not
concerning both in dealing with nosocomial
frequently been established as a cause.

infections a.Ild zoonosis.

Noninflanuuatory conditions of the colon
can also result in diarrhea These include

Clinical Findings: Three forms of
altered fermentation in the large colon,
salrnonellosis have been recognized in adult
which is potentially the result of altered
horses. One is the subclinical carrier, which
intestinal flora or milieu secondary to
may or may not be actively shedding the
antimicrobial treatment, alteration in diet,
organism but has the potential to transmit
or unknown etiologies. Nonintestinal
the bacteria to susceptible animals either by
causes of chronic diarrhea include
direct contact or by contanlination of the
congestive heart failure and chronic liver
environment, water, or feed sources.

disease. The diagnostic approach to these

Multiple fecal cultures may be necessary to
cases is aimed at differentiation of
identify caniers, because the organism is
infiltrative diseases of the intestine from
shed in the feces intemlittently and in small
physiologic causes of diarrhea.

numbers. If stressed, the canier may

282

INTESTINAL DISEASES IN HORSES AND FOALS
develop clinical disease. The national
enrichment techniques along with agars
prevalence of fecal shedding of S enterica
specifically selected to optin1ize recovery of
by nom1al horses in the USA is estin1ated

S enterica is advisable. Because salmonelto be <2%; however, the proportion of lae cannot be consistently cultured from
hospitalized horses shedding is much higher feces, multiple daily samples (generally 3--5) ( -8%). The most common serovars
should be collected from each horse.

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identified among the general population of

Culturing of rectal mucosa! biopsies
horses were S enterica Muenchen and
increases the probability of isolating the

S ente1ica Newport (both serogroup C2).

organism; however, the technique is not

The second form of the disease is
without risk to the horse. Fecal samples
characterized by a mild clinical course, with
that must be mailed should be placed in
signs of depression, fever, anorexia, and soft transport media suitable for enteric but not watery feces. Affected horses may
pathogens at the tin1e of collection and
have an absolute neutropenia. Clinical
shipped on ice. A PCR test is available and,
disease may last 4--5 days and usually is
depending on the prin1ers used, appears to
self-limiting, and S ente1ica can be isolated be more sensitive than routine bacterial
from the feces. Recovered horses may
culture for detection of salmonellae.

continue to excrete the organism in their
feces for days to months; therefore,

Treatment: Treatment of the severe fonn
isolation of the shedding horse and
of salmonellosis is based on IV fluid and
thorough cleaning and subsequent
electrolyte replacement and efforts to
disinfection of the contaminated area
control the host's responses initiated by
are recommended.

tl1e systemic inflammatory response. A

The third form of salmonellosis is
poly ionic isotonic fluid is used for volume
characterized by an acute onset of severe
replacement. Because of active secretion of
depression, anorexia, profound neutropefluid and electrolytes into the lwnen of the nia, and frequently abdominal pain.

intestine, IV fluid volwnes of 40-80 Uday

Diarrhea develops 6-24 hr after the onset
may be necessary. Electrolyte and acid-base
of fever; feces are fluid and foul smelling.

deficiencies are common and are corrected

Affected horses dehydrate rapidly, and
by use of oral and/or IV fluids supplemented
metabolic acidosis and electrolyte losses
with electrolytes. It is difficult to predict
occur as the horse deteriorates. Clinical
the electrolyte status of affected horses.

signs of sepsis and hypovolemic shock can

Deficits should be detem1ined by scrwn
progress rapidly. There may be signs of
biochemical analysis; supplementation
abdominal discomfort, straining, or severe
wiili sodiwn chloride, potassiwn chloride,
colic secondary to ileus, gas distension, and
calciwn gluconate, magnesiwn sulfate, and
colonic inflammation and possible
occasionally sodiwn bicarbonate may be
infarction. Protein-losing enterocolopathy
indicated.

can occur with plasma protein concentra

Antinticrobial treatment in adult horses
tions becoming dangerously low (albumin
with salmonellosis is controversial and does

<2 g/dL) after a few days of diarrhea These
not appear to alter the course of the colitis
horses can become bacteremic because of
or decrease shedding of salmonellae;
bacterial translocation of eoteric organisms, however, it may reduce the likeliliood of and coagulation abnom1alities resulting in
bacterernia. Selection of an antin1icrobial is
disseminated intravascular coagulation can
not easy and should ideally be based on the
occur. If untreated, this fom1 of salmonelsensitivity of the organism isolated.

losis is often fatal.

Resistance patterns vary among Salmonella

Salmonella bacteremia can occur in
isolates and can change over the course of
neonatal foals, especially from farms with
an outbreak. There is potential nephrotoxiendemic salmonellosis (seep 289).

cosis from antinoglycoside antibiotics in
volume-depleted horses; therefore, the
hydration status of the horse should be

Diagnosis: Diagnosis is based on clinical
considered when selecting an antimicrobial.

signs, severe neutropenia, and isolation of

The ideal antibiotic should also be lipid
salmonellae from feces, blood, or tissues.

soluble.

Submission of 10-30 g of feces for culture

The use of GI protectants ( eg, biosponge,
has been more successful in identifying
bismuth subsalicylate, activated charcoal)

salmonellae than has culturing fecal swabs.

may be beneficial. These substances may

It is important to collect and submit feces
bind bacterial toxins. NSAIDs, such as
based on the recommendations of the
flunixin megluntine, help counteract the
laboratory performing the culture. Working
effect of endotoxin, control pain, and
with a diagnostic laboratory that uses
possibly help prevent laminitis. The dosage

INTESTINAL DISEASES IN HORSES AND FOALS

283
ofNSAID used has been quite variable.

colic, fever, and diarrhea in horses of all

Se1ious adverse effects, such as gast1ic and
ages, as well as abmtion in pregnant mares.

colonic ulceration and renal nephrotoxico

The causative agent is Neorickettsia
sis, can result from NSAID treatment, so the

1isticii. The infection of enterocytes of the minimum effective dosage should be used.

small and large intestine results in acute

Equine plasma may be administered to
colitis, which is one of the principal clinical

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correct hypoproteinemia and to supply
signs of PHF. The disease is seen in spring,
coagulation factors and, depending on the
summer, and early fall and is associated
source of the plasma, specific antibodies
with pastures bordering creeks or rivers.

to endotoxin and Salmonella. Colloidal

The epidemiology of PHF has been shown
plasma substitutes such as hetastarch may
to involve a trematode vector. Sporadic
be necessary to maintain oncotic pressure
disease caused by N risticii has been
in horses with substantial protein loss into
reported in dogs and cats; cattle appear to
the GI tract. These colloidal plasma
be resistant to infection. PHF has been
substitutes may be less expensive and
reported in many areas of the USA and
better tolerated than equine plasma in some

Canada using an indirect fluorescent
horses. Often, equine plasma and colloidal
antibody test as evidence of exposure;
plasma substitutes are both used in horses
however, recent studies indicate a high rate
with hypoproteinemia due to colitis.

of false-positive titers with this test, and the

Low-dose polymyxin B (6,000 units/kg,
true geographic range of distribution is
bid) has also been advocated to bind
not !mown. Isolation or detection of the
circulating endotoxin. In controlled trials,
causative agent from clinical cases of PHF
polymyxin B ameliorated some of the
using conventional cell culture or PCR

!mown effects of endotoxemia in horses.

assay has been reported only from

Antimicrobial doses of polymyxin B are

California, Illinois, Indiana, Kentucky,
substantially higher than the dose used to

Maryland, Michigan, New York, New Jersey,
bind endotoxin and may be nephrotoxic.

Ohio, Oregon, Pennsylvania, Texas, and

Low-dose polymyxin B therapy is unlikely

Virginia.

to be nephrotoxic in adequately hydrated
horses receiving IV fluids.

Etiology and Pathogenesis: N risticii
is a gran1-negative obligate intracellular

Prevention: Prevention of salrnonellosis
bacterium with a trophism for monocytes.

is difficult, because the organism is present

Initial morphologic studies of this organism
in the environment as well as in the feces
isolated from cell culture, as well as the
of some healthy animals. In a hospital
serologic responses of N risticii, caused
environment where horses are stressed,
this bacteriwn to be assigned to the genus
may be off feed, and are often receiving

Ehrlichia. However, DNA analyses have
antimicrobial treatment, aggressive
shown N risticii is most closely related to identification and strict isolation of

N helminlhoeca, the agent of salmon
salmonellae-infected horses is indicated.

poisoning in dogs, and Ehrlichia sennetsu,

Biosecurity practices to minimize crossa disease of people in Japan. The organism contamination between hospitalized horses
is not visible in monocytes in blood films
are also advisable. Serotyping, antimicrofrom clinical cases, in contrast to Ana
bial susceptibility profiles and genotyping
plasma phagocytophilum, which is readily
by pulse field electrophoresis, plasmid
identifiable in granulocytes of infected
profile analysis, and phage typing can be
horses.

used to determine whether isolates are

N risticii has been identified in
genetically related and help determine
freshwater snails and isolated from
whether infection is nosocomial.

trematodes released from the snails. N

Owners should be made aware of the
risticii DNA was detected in 13 species of
zoonotic risk of S enterica infection. People immature and adult caddisflies (Trichopworking with infected animals should tera), mayflies (Ephemeroptera),
practice strict hygiene.

damselflies (Odonata, Zygoptera),
dragonflies (Odonata, Anisoptera), and
stoneflies (Plecoptera). Transmission

POTOMAC HORSE FEVER
studies using N risticii-infected

(Equine monocytic ehrlichiosis, Ditch fever,
caddisflies have reproduced the clinical

Shasta River crud, Equine ehrlichial colitis)

disease. One route of exposure is believed
to be inadvertent ingestion of hatched

Potomac horse fever (PHF) is an acute
aquatic insects that carry N risticii in the enterocolitis syndrome producing mild
metacercarial stage of a trematode. The

284

INTESTINAL DISEASES IN HORSES AND FOALS
incubation period is -10-18 days. The
is of limited value as a diagnostic tool,
causative organism is present in the feces
although many infected horses have high
of experimentally infected horses, but the
antibody titers at the time of infection.

biologic significance of this is unknown.

Because of the high prevalence of

Clinically ill horses are not contagious and false-positive titers, interpretation of can be housed with susceptible horses.

the indirect fluorescent antibody test in

Additional studies are needed to deterindividual horses is difficult. Rising paired VetBooks.ir
mine the exact role of the vector and
titers can be helpful. Isolation of the agent
helminth hosts in the complex maintein cell culture, although possible, is nance cycle of N risticii.

time-consuming and not routinely
available in many diagnostic laboratories.

Clinical Findings and Lesions: The

A real-till1e PCR assay that allows
clinical features of PHF are typified
detection of N risticii DNA within 2 hr
initially by mild depression and anorexia,
is a much more feasible test for routine
followed by a fever of 102° -107°F
diagnostic examination. To enhance the

(38.9° -4l.7°C). At this stage, intestinal
chances of detection of N risticii, the sounds may be decreased. Within 24-48 hr,
assay should be performed both on blood
a moderate to severe diarrhea, with feces
and fecal samples, because the presence
ranging in consistency from that usually
of the organism in blood and feces may
seen in cows to watery, develops in -60%
not necessarily coincide.

of affected horses. The onset of diarrhea is
often accompanied by mild abdominal

Treatment: Horses with PHF can be
discomfott. Some horses develop severe
treated successfully with oxytetracycline
signs of sepsis and dehydration. Clinical

( 6.6 mg/kg, IV, bid), if given early in the
signs can be indistinguishable from those
clinical course of the disease. A response
of Salmonella and other infectious causes
to treatment is usually seen within 12 hr.

of enterocolitis. Laminitis can supervene

This is associated with a drop in rectal
as a severe complication of PHF in
temperature, followed by an improvement

20o/o-30% of affected horses. Hematologic
in demeanor, appetite, and borborygmal
findings vary in the early stage of PHF from sounds. If therapy is begun early, clinical leukopenia ( characterized by neutropenia
signs frequently resolve by the third day
and lymphopenia) and thrombocytopenia
of treatment. Generally, anti.microbial
to a nom1al hemogram, despite evidence of therapy is for no more than 5 days. In systemic illness. A common finding in
animals that exhibit signs of enterocolitis,
cases of PHF is a marked leukocytosis,
fluids and NSAIDs should be administered.

which is normally seen within a few days

Laminitis is more common than in other
of onset. PHF may present with all or any
causes of enterocolitis, and if it develops,
combination of these clinical signs.

is usually severe and often refractory to

Several months after clinic!ll disease in
treatment. The overall case fatality rate
pregnant mares, abortion due to fetal
is 5o/o-30%.

infection with N risticii may occur.

Experimentally, pregnant mares infected at

Prevention: Several inactivated,

100-160 days of gestation abort at 190-250
whole-cell vaccines based on the same
days of gestation. The abortion is accompastrain of N risticii are commercially nied by placentitis and retained placenta.

available. Although vaccination has been

Fetal lesions include colitis, periportaJ
reported to protect 78"/o of experin1entally
hepatitis, and lymphoid hyperplasia of
infected ponies, it has been marginally
mesente1ic lymph nodes and spleen.

protective in the field. Vaccine failure has

Necropsy findings in nonpregnant horses
been attributed to antigenic and genomic
with enterocolitis are nonspecific and reveal heterogeneity an1ong the > 14 different diffuse inflammation, mainly in the large
strains of N risticii isolated from naturally intestines.

occuning cases. Furthermore, vaccine
failure may also be due to lack of anti.body

Diagnosis: A provisional diagnosis of
protection at the site of exposure, because

PHF often is based on the presence of typithe natural route of transmission has been cal clinical signs and on the seasonal and
determined to be oral ingestion of the agent.

geographic occurrence of the disease. A

Minimizing insect ingestion in stabled
definitive diagnosis should be based on
horses by turning off barn lights at night,
isolation or identification of N risticii which normally attract the insects, has been
from the blood or feces of infected horses
suggested.

by cell culture or PCR. Serologic testing

No zoonotic risk is known.

INTESTINAL DISEASES IN HORSES AND FOALS

285

CLOSTRIDIA-ASSOCIATED

"colitis-X." Because of the loss of mucosal ENTEROCOLITIS
integrity, bacterial translocation across the

GI tract can occur, resulting in bacteremia

Clostridium difficile and C perfringens due to clostridial or other enteric bacterial
are common causes of enterocolitis in
species. Clinical signs of sepsis or systemic
horses and foals. Antimicrobial administrainflammatory response are often present VetBooks.ir
tion has been associated with C difficile
and consistent with other causes of
diarrhea. Some reports attribute 509'o of
enterocolitis. Clostridiosis cannot be
cases of foal diarrhea to C perfringens.

clinically distinguished from salmonellosis.

C difficile produces toxin A and/or toxin B, Foals affected at <3 days of age with
which cause fluid secretion and lead to

C perfringens-associated enterocolitis
intestinal inflammation. It is common for
often have bloody diarrhea and colic. Fluid
the GI tract of newborn foals to be rapidly
and gas-filled intestine is often identified on
colonized by C difficile, which can be
ultrasound or radiography. In severe cases,
cultured from feces using sensitive
necrotizing enterocolitis occurs with
anaerobic techniques. Nontoxin-producing
thickening and even intramural gas evident
strains are considered commensals.

within the wall of the intestine. Several foals

C difficile can be isolated from various
on a particular farm may be affected, but the
segments of the small and large intestine
disease is typically sporadic.

and rectum of a large proportion of healthy

The role ofCperfringens type A in
horses, and from fecal samples of as many
enterocolitis in neonatal foals is less clear; it
as 8% of healthy horses. Approximately
has been reported that >900A, of foals at 3 days one-third of healthy broodmares and >900A,
of age shed this organism in their feces and
of foals in the general population shed
that C perjr-ingens type A is likely one of the C perfringens in their feces; therefore, it is first bacteria to colonize the intestinal tract
important to determine the presence of a
of newborn foals, in-espective of hygiene
toxin-producing strain.

protocols.

Strains of C perfringens are classified by

C difficile has been associated with enterothe toxins they produce. However, toxins colitis in newborn foals as well as in adult
and toxin-producing strains of C perfrin
horses. It has been identified as a nosoco
gens and C difficile can be detected in mial infection in people, and this may also
healthy as well as in diarrheic horses and
be seen in horses.

foals. The most common type of C perfrin

The mortality rate associated with
gens identified is type A, which can be

C difficile and C perfringens enterocolitis, detected in the feces of as many as 8% of
especially type C, can be high, even with
healthy horses. Type C is rarely identified in
intensive medical treatment.

the feces or environment of healthy
broodmares and their foals but is associated

Diagnosis: Diagnosis is based on
with the highest mortality. Antimicrobial
identification of toxigenic clostridia from
use, food deprivation, and other stressors
fresh fecal samples, reflux, intestinal
have been suggested to predispose horses
contents, or tissue. Blood culture is
to the overgrowth of either or both
indicated in foals and adults with severe

C perfringens and C difficile, leading to GI enterocolitis. Fecal san1ples for culture and
disease. In one report, mares whose foals
detection of toxins or toxin-producing
were being treated with erythromycin
genes should be delivered directly to the
developed fatal enterocolitis associated
laboratory, or shipped overnight, chilled
with C difficile. Clostridial spores can

( not frozen) on ice. San1ples for culture
persist in the environment and can be
must be maintained in an anaerobic
resistant to many disinfectants; therefore,
environment. Isolation of clostridial
nosocomial infection can occur in
organisms requires anaerobic conditions
contaminated environments.

and, depending on the organism, special
growth media. C difficile is inherently
difficult to culture, hence its name.

Clinical Findings: Clinical signs include

Conm1unicating to the laboratory that
sudden death, diarrhea with or without
clostridial enterocolitis is a differential
blood, colic, fever, reduced feed intake, and
diagnosis is critical, because many
lethargy. Disease can range from subclinical
veterinary laboratories do not routinely
to severe enterocolitis to peracute death
culture fecal samples anaerobically unless
before the development of diarrhea. With
specifically requested to do so.

advanced diagnostic techniques, clostridial

Because nonpathogenic serovars are
infections account for a large proportion of
common, a positive culture for C difficile
the previously undiagnosed cases known as
or C perfringens must be confirmed by

286

INTESTINAL DISEASES IN HORSES AND FOALS
identification of toxins or their genes. A
protease that specifically degrades C difficile

PCR test, available at selected laboratories,
toxins A and B. Orally administered DTO
allows differentiation of C perfringens
smectite powder also blinds clostridial toxins
types A, B, C, D, and E based on combinaand may be useful in horses with diarrhea tions of a, [3, e, or, toxins, as well as on Specific antitoxin for C perfringens
identification of the gene coding for the
type C and D has also been used in foals;

[32 toxin. Commercially available tests for
however, it is not approved for this use. The

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clostridial toxins include an ELISA for
benefit of type C and D antitoxin in disease

C difficile toxin A and C perfringens
associated with type A or [32 toxin is
enterotoxin, and a latex agglutination test
unknown, but based on production
for C perfringens enterotoxin. Toxin tests
methods, the a and [32 toxins are unlikely
can be performed in-house, are rapid, and
to be present in high levels in this toxoid.

for C difficile are both sensitive and
specific. Diagnosis of clostridial enterocol

Prevention: No proven effective biologic
itis is often made at necropsy and is based
products are available to immunize horses
primarily on identification of intestinal
or foals against clostridial enterocolitis.

necrosis associated with large gram-posi

When the disease is a problem in multiple
tive rods in intestinal smears. Tissue and
foals on a farm, preventive measures have
fecal specimens must be taken immediately
been implemented, but the efficacy and
after death to avoid degradation of toxins or
safety of these interventions have yet to
an overgrowth of clostridial organisms.

be critically evaluated. These measures
include vaccinating pregnant mares twice

Treatment: Treatment with metronidaat 2- to 4-wk intervals at least 1 mo before zole (15---20 mg/kg, PO, tid-{jid) appears to
foaling with C perfringens type C and D
be beneficial in treating enteric clostridial
toxoid (bacterin products and those with
infections. Pharmacokinetic studies have
oil adjuvants should be avoided); using C
not been performed in foals, but oral and
perfringens type C and D antitoxin
even IV metronidazole appears generally
prophylactically, PO, in newborn foals; and
safe. In some geographic regions, metroniadministering antimicrobials ( eg, dazole-resistant C difficile strains have
metronidazole) prophylactically to foals for
emerged that appear sensitive to vancomythe first 3-5 days of life. The C perfringens cin; however, metronidazole should be used
type C and D toxoid and antitoxin are not
whenever possible.

approved for use in horses; however, these

Supportive care is similar to that for other
products have been used by some owners
causes of equine enterocolitis, often
because of the high mortality rate in foals
requiring large volwnes of IV polyionic
with clostridial enterocolitis on problem
fluids, with supplemental electrolytes
farn1s. Adverse reactions to the C perfrin

(potassiwn, magnesiwn, and calciwn),
gens type C and D toxoid have been
plasma or synthetic colloids for low oncotic
reported in broodmares.

pressure, anti-inflammatories such as

The most important strategy for prevenflunixin meglwnine, and broad-spectrwn tion is good farm hygiene. Clostridial spores
antibiotics if the horse is leukopenic and at
are extremely resilient in the environment

1isk of bacterial trans location across the
and resistant to many disinfectants. Keeping
compromised GI tract. Polymyxin B may
the foaling area and mare as clean as possible
aid in binding systemic endotoxin. Total
during the perinatal period and ensuring
or partial parenteral nutrition to provide
rapid ingestion (by stomach tube if
nutritional support can be useful in foals if
necessary) of colostrwn within 1 hr of birth
milk is withheld or decreased to allow gut
have reduced incidence of disease on some
rest. Foals with colic or profuse diarrhea
contanlinated farms. The mare's hindlegs,
often benefit from milk withdrawal.

tail, and udder can also be washed in soapy

Continuous infusion of IV fluids and
water immediately after foaling to decrease
parenteral nutritional support is optimal but
ingestion of fecal material by newborn foals.

labor intensive and requires separation of

Affected anin1als should be isolated to limit
the foal and mare. However, the course of
cross-infection and contanlination of
diarrhea appears to be dramatically
pastures and stalls.

shortened, thus justifying the more
intensive approach in some severe cases.

COLITIS-X

The yeast Saccharomyces boulardii has
been shown to be protective in clostridial

Colitis-X is not actually a disease but a
diarrhea in other species, and there is some
histmic tern1 used to describe undiagnosed
evidence of beneficial effects in the treatcauses of peracute, fatal enterocolitis in ment of horses with colitis. It produces a
horses characterized by sudden onset of

INTESTINAL DISEASES IN HORSES AND FOALS

·257
profuse, watery diatThea and development
are required to maintain plasma oncotic
of hypovolemic shock. Many affected
pressure if hypoproteinemia occurs
horses have a history of stress. Differential
secondary to protein-losing enteropathy.

diagnoses include peracute salmonellosis,

F1unixin meglurnine may decrease
clostridial enterocolitis, Aeromonas spp
inflarrunation, and polymyxin B can help
colitis, and coronavirus. Salmonella spp
bind endotoxin. Broad-spectrnm antibiotics
and Clostridia clijficile can be difficult to are indicated to treat bacteremia that often

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culture from fluid fecal material, and a
occurs secondary to bacterial translocation
diagnosis of salrnonellosis or clostridial
across the dat11aged GI tract.

enterocolitis can easily be missed. Culture
of GI tissue satnples and mesenteric lymph

CORONAVIRUS
nodes is recommended in addition to
intestinal contents from necropsy cases.

Coronavirus has been identified in the feces

Negative cultures and toxin tests for
of normal foals and those with intestinal
clostridia do not necessarily exclude these
clisease. However, there have been recent
conditions; therefore, thorough disinfection
outbreaks of diatThea and colic in adult
of the premises, hospital facilities, and
horses attributed to coronavirus. Clinical
trailers is recommended in all cases.

signs include anorexia, lethargy, at1d fever.

Clinically, there may be a short febrile

Colic and changes in fecal consistency are
period, but body temperature soon returns
seen in some cases. Occasionally, rapid
to normal or subnom1al. Tachypnea,
progression leads to death ( or euthanasia),
tachycai·dia, and marked depression ai·e
but most cases resolve with suppo1tive care.

present. An explosive diarrhea develops,

Diagnosis is by detection of the orgaitism
followed by extreme dehydration.

in feces by real-time PCR, electron

Sometimes death occurs before diatThea
nticroscopy, and virus isolation. Leukopenia
becomes evident, with severe enterocolitis
due to neutropenia at1d lyrnphopenia are the
observed at necropsy. Hypovolemic and
most common hematologic abnmmalities.

endotoxic shock are manifest by poor
capillary refill tin1e, purplish mucous

PARASITISM
membranes, and cold extremities. Death
may occur within 3 hr of onset of clinical

Both large and small strongyles have
signs. In less acute cases, death occurs
been incriminated as a cause of chronic
within 24-48 hr. At necropsy, edema and
diatThea in horses and foals. The condition
hemorrhage in the wall of the lai·ge colon
associated with small strongyles in horses
and cecum are pronounced, and the
is termed cyathomostomiasis and has
intestinal contents are fluid and often
been reported to result in recurrent colic,
bloo d -stained.

diatThea, atld weight loss. (See GASTROINTESTI

Typically, the PCV is >65% even shortly

NAL PARASITES OF HORSES, p 315.)

after the onset of clinical signs. The

Giardiasis (seep 211) has been reported
leukograt11 ranges from normal to neutropein a limited number of cases as a cause of nia with a degenerative left shift. Metabolic
intennittent diatThea in horses. However,
acidosis and electrolyte disorders ai·e also

Giardia can also be found in the feces of a present.

small nwnber of healthy horses and is rarely

Disease onset is often closely associated
recognized as a cause of diatThea in horses.

with stress, eg, surgery or trat1spo1t. Signs

Cryptosporidia ( see p 209) have been
are similar to those of other diatTheal
identified in the feces of both healthy and
diseases, including peracute sal.rnonellosis,
diatTheic foals. There is evidence that
toxemia caused by Clostridium spp,

Cryplosporidium spp can cause diarrhea

Potomac horse fever, expe1imental
and even death in immunocompetent foals;
endotoxic shock, at1d anaphylaxis. A similar cryptosporidia have been described as a condition may be seen after administration
cause of outbrealcs of foal diatThea on some
of lincomycin to horses. Colitis-Xis the tenn fanns.

reserved for those cases in which no
definitive diagnosis can be made and the

SAND ENTEROCOLOPATHY
horse dies.

Treatment for colitis-X usually is not

Consumption of large atnounts of sand,
effective (by definition) but would be
which then accwnulates in the large
similar to that for sahnonellosis ( see
intestine, can produce diatThea, weight loss,
p 281). Large volumes of IV fluids ai·e
or colic. Sand is ingested when horses or
needed to counter the severe dehydration,
foals are kept on sandy pasture or are fed
and electrolyte replacement is often
hay or grain in a sandy area (paddock, stall,
necessary. Plasma or synthetic colloids
or pasture). Some horses or foals preferen-

288

INTESTINAL DISEASES IN HORSES AND FOALS
tially eat dirt and sand if it is in their environcould provide a histopathologic diagnosis of ment. A diagnosis is based on history of a

:neoplasia or inflainmatory cell infiltrate. A
sandy environment, the presence of sand in
biopsy of the rectal mucosa and duodenal
the feces, "sand sounds" on auscultation of mucosa (via 3-m endoscope) may be
the ventral abdomen, and (if available)

beneficial in diagnosis of inflanimatory
abdominal radiographs that reveal the
bowel disease and should also be cultured
presence of sand in the large colon.

for Salmonella. Full-thickness jejunal,

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Treatment involves use of a hemicellulose
cecal, and colonic biopsies are more reliable
product (psyllium seed hull) administered
for diagnosis of inflan1matory bowel disease
via :nasogastric tube or added to the grain

(seep 291) and can be obtained surgically
daily. Diarrhea generally resolves within 2-3 either by standing flank lapai·otomy or days of initiation of treatment. Generally,
recumbent ventral midline celiotomy.

3-4 wk of treatment is necessary to remove

Surgical exploratory lapai·otomy can
most of the sand and may need to be
provide valuable i:nforn1atio:n but is
repeated if the horse or foal is not removed
expensive and involves substantial 1isks
from the source of sand. Preventive
of poor postoperative healing because
psyllium treatment ( daily for 1 wk each
of hypoprotei:nemia.

month) has been used where sand

Treatment of abdominal :neoplasia or
e:nterocolitis is common. Several psylliwn
inflainmatory bowel disease is often
products are on the market; many horses
unrewarding, but sometimes remission
prefer the pelleted over the powdered form.

of clinical signs can be obtained with

(See ai,so p 262.)

dexainethaso:ne, especially with inflainmatory bowel disease. Improvement of clinical RECURRENT DIARRHEA
signs and laborato1y pai·aineters with
high-dose dexan1ethasone (0.1 mg/kg/day)

Some horses develop semiformed feces
treatment has been reported in three horses
when first introduced to lush pastures,
with clinical signs of GI tract lymphoma of
alfalfa hay, or a temporaiily stressful

T-cell origin. In two horses, the high-dose
situation ( eg, trailer ride, racing, showing,
dexainethasone was followed by a lower
visit to a veterinary hospital). This change
dose (0.01-0.95 mg/kg/day) once clinical
in fecal consistency is not of medical
improvement occmTed. Favorable
significance as long as the horse is healthy
responses persisted for >9 mo. The third
in all other regards, but owners may be
horse had to be maintained on the higher
concerned. It is in1portant that horses with
dose of dexainethaso:ne throughout
diarrhea have a physical exai11inatio:n and
treatment, because signs recUJTed
appropriate laboratory tests to exclude
whenever the dose was lowered. Clinical
infectious causes and to detern1ine whether
signs recurred despite high doses of
treatment is required. Usually, the fecal
dexainethaso:ne, and after 2 mo of treatment
consistency returns to norn1al when the
the horse was euthanized. The mechanism
horse adapts to its new diet or the stressful
of action of the steroid is speculated to be
situation resolves.

control of inflainmation associated with the
condition, as opposed to glucocorticoid

INFILTRATIVE COLONIC DISEASE
induced apoptosis.

Any process that causes a thickening of the
wall of the large colon may interfere with

MISCELLANEOUS CAUSES OF
absorption of fluid and result in chronic

DIARRHEA
diarrhea, weight loss, and sometimes
hypoprotei:nemia. Thickening may be due

Other causes of diaiThea or semiforn1ed
to :neoplasia, inflan1matory cells (such as
to watery feces in horses include grain
lymphocytes, plasma cells, macrophages,
overload, thromboembolic disease of the
or eosinophils), or scai· forniation from
colon, peritonitis, antibiotic treatment,
previous acute colitis.

renal failure, numerous toxicoses ( eg,

Rectal palpation may help detect bowel
blister beetles [cantharidin], salt poisoning,
thickening and mese:nteric lymphadenopaslafrainine, ainitraz, propylene glycol, thy. Abdominal fluid cytology may reveal
phosphorus, seleniwn, nicotine, reserpine,

:neoplastic cells. Ultraso:nography can be
arsenic, mercwy, mo:ne:nsin, organophosused to determine the degree of thickening phates, oleander, Japanese yew, castor
of the bowel wall (if the affected area of
bean, avocado, thorn apple, potatoes, heath,
bowel can be iniaged) and may reveal
algae, acorn or oak, Hypericum, corn
masses in the liver or spleen or on the
cockle, mycotoxicoses, horse tail
peritoneal surfaces; a percutaneous biopsy

[scouring rush]), hyperlipidosis, and

INTESTINAL DISEASES IN HORSES AND FOALS

289
resolving impaction of the large intestine

An acute, fulminant, hemorrhagic
after treatment with oral cathartics such
diarrhea syndrome with high mortality in
as magnesium sulfate.

young foals <10 days old and commonly

<3 days old has been associated with

Clostridium per:fringens type C infection

(seep 285). Enterocolitis has also been
associated with C per:fringeris type A with VetBooks.ir
or without f32 toxin gene. The significance

FOAL HEAT DIARRHEA
of this association is less clear than with

From 4-14 days after bi.Ith, foals often
type C, because type A has been identified in
develop a mild, self-limiting diarrhea.

the feces in >900/o of healthy neonatal foals

During this tin1e, the darn is usually
in a farm-based study. It is possible that the
undergoing her first estrous cycle, hence
nwnber of bacteria and the phase of growth
the name "foal heat dianhea." However,
predispose to disease from type A.

diarrhea can also occur at this ti.Ine in

Infections may be sporadic or seen as
orphan foals; therefore, honnonal activity
outbreaks in multiple foals on a farm.

in the mare is unlikely to be involved in

Severe lethargy and rapid deterioration of
the pathogenesis. Although the cause
cardiovascular status is followed by death
is unknown, it may be associated with
in 24-48 hr in many cases. lntralununal hem-
alterations in the foal's intestinal microbial

01Thage and extensive mucosa! necrosis of
flora or alteration in diet as the foal begins
the small intestine and, in some cases the
to eat small amounts of hay and grain.

colon are fotmd on necropsy.

Coprophagy may also have a role.

Other bacteria that have been associated

The foal remains active and alert and
with diarrhea in foals are Bacter-oides
has a nonnal appetite. Vital signs remain
fragilis, C di.fficile (seep 285), Aer·omonas normal. Feces are semiformed to watery
hydrophila, and Rhodococcus equi.

and not malodorous. Monitoring is

Although R equi prin1arily causes respirain1portant to ensure the foal tory disease (seep 1451), both acute and

's condition
does not deteriorate. Specific treatment is
chronic enteritis can cause diarrhea in
usually not necessary, but application of a
foals 1-4 mo old. The diagnosis is more
protectant to the skill around the perinew11
straightforward if pnewnonia is also
helps prevent scaldmg of the buttocks.

present. When cultured from tracheal wash
fluid, R equi is considered a pathogen;
however, a positive fecal culture is not as

BACTERIAL DIARRHEA IN FOALS
helpful because R equi can be found in the

Bacterial enterocolitis in neonatal foals can
feces of healthy foals. Cla.rithromycin
be a component of neonatal septicemia and
combined with 1ifan1pin is the treatment of
diarrhea can be seen with bacteremia of any choice for R equi infection in foals. Other cause. Organisms commonly involved in
macrolides such as azithromycin or
neonatal bacteremia and subsequent
erythromycin can be used, but erythrodiarrhea in neonatal foals include Salmo
rnycin can predispose to diarrhea and
nella spp, Escherichia coli, and Actinoba
hyperthennia.

cillus spp. Although E coli is the most i.Inportant mediator of systemic sepsis in

Equine Proliferative Enteropathy
newborn foals, it is not as conunon as a
primary cause of diarrhea in foals as it is

(Lawsonia intracellularis infection)

in calves and piglets.

Enteric infection with Lawsonia intracel

Intensive anti.microbial treatment,
lularis causes proliferative enteropathy
correction of fluid loss and electrolyte
resulting in outbreaks of diarrhea, rapid'

abnormalities, and nursing care are needed.

weight loss, colic, lethargy, subcutaneous

Foals should be evaluated to determine
edema, and protein-losing enteropathy in
whether adequate passive transfer of
weanling foals. Lawsonia has a worldwide
colostral antibodies has occuned· if not a
distribution and can affect many other
plasma transfusion is indicated. (See atdo
species, including pigs, rodents, and ratites;

SEPSIS IN FOALS, p 1728.) Markedly hypoproit can survive in the environment for 2 wk teinemic foals will benefit from plasma
and a fecal-oral route of infection is
transfusion and/or administration of a
speculated. L intracellularis enters the
plasma substitute such as heta.starch to
enterocytes, avoidiI1g lysosomal destruci.Inprove oncotic pressure. IV fluid treatment tion. Infected cells continue to divide without correction of the severe hypoproresulting in hyperplastic crypts of im�ature teinemia may induce pulmona.iy or
epithelial cells that have a poorly developed
peripheral edema.

brush border, leading to decreased

290

INTESTINAL DISEASES IN HORSES AND FOALS
enzymatic activity and absorptive function.

Response to treatment is considered

Decreased disaccharide activity results in
confim1ation of the diagnosis. Lack of
maldigestion with subsequent overload
response to therapy after 7-10 days should
of carbohydrates to the large colon and
prompt reassessment of the diagnosis.

osmotic diarrhea. Hypoproteinemia results

Lawsonia is an intracellular pathogen,
from a combination of malabsorption of
so antimicrobials must be lipophilic or

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amino acids and increased small-intestinal
amphoteric to concentrate within the host
permeability and leads to low plasma
cytoplasm. Treatment with oxytetracycline
oncotic pressure and subsequent ventral

(6.6 mg/kg, IV, bid for3-7 clays) followed by
edema. Maldigestion and absorption of
doxycycline (10 mg/kg, bid for 14 days) has
nutrients and protein-losing enteropathy
been successful. Mild cases respond to oral result in weight loss and failure to thrive.

doxycycline alone. Alternatives include

Affected foals range from 3-12 mo old,
erythromycin ( alone or in combination with
but those 4-6 mo old are most commonly
rifai11pin) for 3-4 wk or chloramphenicol.

infected. Stress may be a predisposing

Plasma transfusions ai·e required only in the
factor. Because of their debilitated state,
most severely affected foals. Glucocmtiinfected foals are predisposed to secondary coicls ai·e not reconunended. Response to

GI, skin, and respiratory infections.

therapy is indicated by improvement in

Morbidity and mortality rates are low if
attitude, appetite, and weight gain.

animals are treated appropriately, although

Resolution of hypoproteinemia may take
sudden death has been reported. Marked

4-5 wk and small-intestinal tl1ickening
hypoproteinemia ( <4 mg/clL) with

4-S wk With treatment, -90"!., of foals
hypoalbuminemia ( d.5 g/clL) are the most
usualJy survive.

common laboratory findings. The WBC
count and fibrinogen concentrations tend to

VIRAL DIARRHEA IN FOALS
be nom1al to moderately increased. Anemia,
hyponatremia, hypochloremia, and

Virnses appear to cause diarrhea in foals but
hypocalcemia may be seen. CK concenrarely affect adult horses. Rotavirns is the tration is often milclly increased.

main cause of viral cliai-rhea in foals;

Diagnosis can be confinnecl at necropsy
however, other viruses (eg, coronavirus)

with characteristic intracellular bacteria
have been implicated. Dia.n·hea induced by
observed in silver-stained tissues. L
rotavirns is chai·acterized by depression,
intracellulmis can be confinned using PCR anorexia, and profuse, watery, malodorous analysis and immunohistochemistry on
feces. It is usually seen in foals <2 mo old;
tissues collected at necropsy. Because
younger foals typicalJy have more severe

Lawsonia is an intracellular organism, it
clinical signs. The dia.i-rhea usualJy lasts 4-7
does not grow on standard micro biologic
days, although it can persist for weeks.

culture media, and permissive cell lines are

Rota.vi.ms destroys the enterocytes on the
required for isolation. PCR can be used to
tip of the villi in the small intestine, which
detect£ intracellularis DNA in feces, but
results in malabsorption. Lactase becomes
false-negative results can occur. Serology
deficient, so lactose passing into the large
to detect antibodies to L intracellularis
intestine induces an osmotic diarrhea.

is more sensitive than fecal PCR, but

Diagnosis is made by identification of vi.ms
discrinlination between infected foals and
in the feces by electron microscopy or
exposed foals can be difficult. Indirect
commercial immunoassay kits designed for
fluorescent antibody test and irnmunoperdetection of human rota vims. Requesting oxidase monolayer antibody tests are
that the laboratory test specifically for
currently the best serologic tests available.

rotavirns, collecting feces early in tl1e

An ELISA is also available. Both fecal PCR
course of disease, and sampling several
and serologic testing are recommended.

foals improve the chances of vi.ms

If either test is positive in the presence
detection.

of hypoproteinemia, then treatment is

Treatment is generalJy supportive. Certain
warranted. Foals can remain seropositive
farm management practices a.Ile! disinfection
for 6 mo after clinical signs resolve.

techniques have effectively limited the

Frequently, tra.nsabdominal ultrasonograspread of rotavirns during outbreaks. Sick phy reveals a markeclly thickened smallfoals are highly contagious and should be intestine wall.

isolated in the stalJ in the ba.111 in which the

Differential diagnoses for proliferative
foal originalJy became ill or moved to a
enteropathy include salmonellosis,
designated isolation facility. Personnel
clostridiosis, Neorickettsia 1isticii, R equi,
should wear disposable gloves and cleai1able
parasitic infections, and any cause of
boots and wash their hands with soap before
infiltrative/inflaimnatory bowel disease.

and after hai1clling diai-rheic foals. Foot clips

INTESTINAL DISEASES IN HORSES AND FOALS

291
containing phenolic disinfectants outside

GASTROINTESTINAL NEOPLASIA
the stalls of sick foals should also be used.

Specific stall-cleaning equipment should be

Squamous cell carcinoma of the stomach
designated only for cleaning the stalls of
and the alimentary form of lymphosarcoma
diarrheic foals. Once the stall has been
are the most co nun on forms of neoplasia
vacated, it should be cleaned of particulate
involving the GI tract in horses. Chronic

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material, washed witl1 detergent, and then
weight loss may be the prin1aiy clinical sign.

disinfected witl1 phenolic compounds that

Chronic diarrhea and hypoalburninemia
meet EPA standards. Bleach, chlorhexidine,
may develop when lymphosarcoma has
and quaternary compounds do not appear to
infiltrated the wall of the intestine.

be effective disinfectants for rotavirus. Fecal

Because tl1e incidence of GI neoplasia is
material of sick foals removed from stalls
low, other causes of weight loss should be
should not be spread on pastures used for
investigated first. Diagnosis is usually made
horses and foals, and care should be taken to by exclusion of other causes of weight loss avoid fecal contanunation of alleyways. All
and by histopathologic exatnination of the
stall-cleaning equipment should be
tissue collected by duodenal or rectal
disinfected. Stalls with dirt floors are
mucosa! biopsy during exploratory
difficult to adequately clean and disinfect.

laparotomy or at necropsy. Squan1ous cell

Removal of the top layers of dirt may be
carcinoma of the stomach can be diagnosed
required.

by gastroscopy. An endoscope 2-3 m long is

Arriving horses and foals, including those
necessary to exainine the gastric mucosa of
returning from veterinary hospitals, should
adult horses. In horses with lymphosarbe isolated for �7 days before being coma, enlarged mesenteric lymph nodes or
introduced to the resident population.

thickened bowel may be detected by rectal

A vaccine for pregnant mares to induce
palpation or by ultrasonographic examinacolostral antibodies directed at reducing the tion. Occasionally, neoplastic cells are risk of rotavirus infection in their foals is
identified by cytologic exan1ination of
available.

abdominal fluid. Ultrasonography may
reveal masses in the liver or spleen, as well

MISCELLANEOUS CAUSES OF
as facilitate percutaneous biopsy of the

DIARRHEA IN FOALS
masses. An exploratory laparotomy with
biopsy of intestinal or other masses can

Nutritional diarrhea can result from
provide a definitive diagnosis.

overfeeding ( eg, when a foal is reunited with

Treatment of GI neoplasia in horses is
the mare after a period of separation) and
generally not attempted, and the prognosis
improper nutrition ( eg, orphan foals being
is grave. There have been a few reports of
fed calf milk replacer or sucrose). Lactose
surgical removal of the affected segment of intolerance in foals is rare and can be
bowel. Chemotherapy may be an option for
detem1ined by lactose tolerance challenge
some horses, and corticosteroid therapy
tests or clinical response to supplemental
may prolong survival tin1e in some cases.

lactase. Diarrhea can also develop when
foals consume indigestible substances such

INFLAMMATORY BOWEL DISEASE
as roughage, sand, dirt, and rocks. DiatThea
in foals has been reported to be associated

This collection of diseases includes
with infection by Strongyloides westeri,
granulomatous enteritis (GE), lymphocytic

Parascaris equorum, and C1yptosporid
plasmacytic enterocolitis (LPE), multisys
ium spp. (See also
temic eosinophilic epitheliotropic disease

GASTROINTESTINAL PARASITES

(MEED), and idiopathic focal eosinophilic

01' HORSES, p 315.)

enterocolitis (!FEE). Disease is characterized by infiltration of the small and large intestine with inflammatory cells, including
lymphocytes, plasma cells, macrophages,
and eosinophils. The inflanm1atory condition

The causes for weight loss in horses are
may be limited to only a short segn1ent of the
nun1erous and can involve many body
bowel or be more diffuse. Malabsorption and
systems. This discussion is confined to
a protein-losing enterocolopathy result.

diseases of the GI tract. Protein loss may or

Diarrhea may or may not be a clinical feature.

may not be associated with weight loss. The

Inflammatory bowel disease should be
disorders commonly associated with either
considered in the differential diagnosis of
of these signs are neoplasia, inflammatory
horses with weight loss, recurrent colic, or
bowel disease, and toxicosis from treatment hypoproteinernia, as well as in some horses with NSAIDs.

with generalized skin disease.

292

INTESTINAL DISEASES IN HORSES AND FOALS

Diagnosis is based on clinical signs, low
mural bands, is detected via exploratory
serum protein concentration, possible
laparotomy or necropsy; a diagnosis can be
thickened bowel (identified by ultrasonogmade by subsequent histopathology. Horses raphy or on rectal palpation), malabsorpwith IFEE respond to surgical resection of tion, and intestinal or rectal biopsy.

the diseased segment of intestine. Medical

Malabsorption of carbohydrates occurs
treatment with corticosteroids and feeding

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secondary to severe villous atrophy
small frequent meals has also led to resothroughout the small intestine. Failure to lution of clinical signs after small-intestinal
absorb oral glucose or o-xylose verifies
decompression without resection.

malabsorption from the small intestine.

Histologic diagnosis is subjective and

NSAID TOXICOSIS
should be perfom1ed by a pathologist
experienced in reading equine intestinal

The toxicity ofNSAIDs is related to COX
biopsies. Rectal mucosa! biopsy is useful in
selectively, dosage, and duration (see
the diagnosis of -500A, of cases of GE and
p 2110). It is hypothesized that nonselective

MEED but is rarely helpful in the diagnosis

COX inhibitors have greater risk of toxicity
ofLPE and IFEE. High numbers of
than COX-selective drugs. COX inhibitors
eosinophils and lymphocytes can be
also cause delayed GI healing. The GI tract
identified in the intestinal wall of nom1al
and kidneys are most commonly affected
horses, but overinterpretation should be
by NSAID toxicity. NSAID-induced iJtjury
avoided. The presence of eosinophilic
can occur anywhere in the GI tract, but the
granulomas, vasculitis, and fibrinoid
large colon ( especially the right dorsal
necrosis of intramural vessels is diagnostic
colon) and gastric mucosa appear to be
of MEED. Horses with MEED may have
the most sensitive. The ulcerogenicity of
severe demmtitis, eosinophilic infiltrations
phenylbutazone is greater than that of
in the liver or pancreas, and sometimes
flunixin meglumine, which has greater
marked eosinophilia. Horses with IFEE
ulcerogenicity than ketoprofen. The COX-2
have eosinophilic infiltration restricted to
selective inhibitor firocoxib appears to be
the intestine and have a better prognosis for
safer. Ulcerative lesions in the lai·ge colon
survival. Full-thickness intestinal biopsies
lead to a protein-losing enteropathy, often
can be obtained by using a laparoscopic
with clinical signs of ventral edema,
procedure via a flank incision or by ventral
anorexia, lethargy, weight loss, diarrhea,
midline celiotomy. Because most of the
and colic. Scarring of the right dorsal colon
horses have severe hypoproteinemia at the
can occur leading to large-colon in1pactime of diagnosis, incisional healing can be tions, sometin1es requiring large-colon
problematic.

resection.

The pathophysiology of the various

Phenylbutazone administered at high
syndromes is not well understood. An
doses or for prolonged periods causes a
altered inunune response to a co111111on
protein-losing enterocolopathy in horses.

intestinal factor ( eg, feed, parasites,

However, some horses are inherently
bacte1ia) has been suggested. Histopathosensitive to NSAIDs, and right dorsal colitis logic sin1ilarities exist between GE in
can occur at lower than reconunended
horses, Johne's disease in cattle, and Crohn's dosages. Toxicosis can develop from oral disease in people. Standardbreds seemed to
or parenteral administration of NSAIDs.

be predisposed to GE and MEED, which

Hypoproteinemia (hypoalbuminemia and
suggests possible genetic predisposition.

hypoglobulinemia) is seen due to loss of

Vaiious medical treatments have been
protein into the intestinal lumen, which can
tJied with limited success. Corticosteroids,
occw· without visible ulceration. Renal
dietary alterations, metronidazole, and the
papillary necrosis may also be seen.

anti.metabolite azathiop1ine have been used.

Administration of flwlixin meglumine at

Hypereosinophilic syndrome in people often
high doses or for prolonged periods can
responds to hydroxyurea or vincristine, and
result in a sinillar toxicosis.

sometin1es interferon-a and cyclosporine

Clinical signs ofNSAID toxicity include
are used. Supportive nut1itional care should
difficulty in mastication due to oral and
involve frequent feeding of good-quality,
lingual ulceration, hypersalivation, and
high-energy feeds. The prognosis is grave. If
signs of pain when swallowing due to
only a limited and accessible section of the
esophageal ulceration. Gastric ulceration
bowel is affected, surgical removal may be
can result in recumbency after eating, signs
successful. This is more conunon in IFEE, in
of colic, and anorexia. Horses with colonic
which horses con11110nly present with colic
ulceration can have soft feces, diarrhea, and
rather than weight loss. Focal thickening,
ventJ·aJ edema. Intestinal ulceration ca.11 be
sometimes restricted to circun'lferential
severe enough to allow endotoxin and

INTESTINAL DISEASES IN PIGS

293
bacterial translocation and signs of
transfusion or synthetic colloids can be used
systemic inflammation and septicemia.

to increase plasma oncotic pressure.

Dehydration, fever, and tachycardia can

Longterm dietary management consisting
occur in severe cases. Clinical signs can
of a low-fiber complete pelleted ration fed
occur days to weeks after NSAID therapy.

several times throughout the day, and

More chronic cases present with recurring
elimination of roughage is recommended.

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colic, weight loss, and soft feces.

Corn oil can be given to provide supplemen

A tentative diagnosis can be made based
tal calories and may help heal damaged
on history of NSAID administration, clinical
intestinal mucosa. Psylliurn mucilloid can
signs, and presence of hypoproteinemia.

also promote colonic healing by increasing

Severe cases may have hyponatremia,
the concentration of short-chain fatty acids.

hypochloremia, hypocalcemia, and

Surgery may be required if scarring of the
acidemia in addition to hypovolemia.

bowel has .resulted in partial obstruction of

Ultrasonography may detect thickening
the intestine.

of the colon. Gastric ulceration can be

Prevention of NSAID toxicity involves
confirmed by gastroscopy but requires
limiting the dose and duration ofNSAID
an endoscope 2-3 m long.

treatment, using a COX-2 selective NSAID,

Treatment includes discontinuing use of
or relying on alternative analgesic therapy.

phenylbutazone or any other NSAID. In acute

Monitoring for fecal consistency and sernrn
toxicosis, administration of l gal. of mineral
albumin concentrations are easy methods
oil repeated after 2 hr may be beneficial to
to detect the development of right dorsal
decrease drug absorption. To help prevent
colitis in horses receiving NSAIDs.

gastric ulceration, reducing production of
gastric acid with an H2-receptor blocker ( eg,

SMALL-INTESTINAL FIBROSIS
ranitidine) or a proton pump inhibitor ( eg,
omeprazole) may be beneficial; sucralfate

Extensive fibrosis of the submucosa of the
may be indicated as well. Administration of
small intestine has been associated with
misoprostol ( a synthetic prostaglandin
weight loss and recurrent colic in adult
analogue) may be beneficial but can cause
horses on pasture in n01thern Colorado. All
additional signs of diarrhea and colic. IV fluid
affected horses died or were euthanized
therapy is indicated in cases of hypovolemia,
because of their deteriorating condition.

especially with concurrent azotemia. Plasma

The cause is unknown.

INTESTINAL DISEASES IN PIGS

Pigs of all ages are susceptible to intestinal

CLOSTRIDIUM DIFFICILE
diseases, and diarrhea is the sign conunon

ENTERITIS
to nearly all such disorders. Transmission of
infectious agents that cause enteropathies

C difficile is an important emerging
is by the fecal-oral route. At least 16
pathogen that causes diruThea primarily
different etiologic agents, including
in neonatal swine. The agent was first
bacteria, virnses, and parasites, can cause
recognized as a cause of antibiotic-associprimary intestinal disease. Porcine ated diarrhea in people. It most commonly
ci..rcovi.rus type 2 (PCV 2) vims may be
causes disease in piglets 1-7 days old and in
isolated from the intestines of pigs with
other domestic and laboratory anin1als.

dia.JThea. PCV 2 is the cause of several
multisystemic diseases in pigs, including

Etiology and Pathogenesis: C difficile
postweaning multisystemic wasting
is an anaerobic, gr3111-positive, sporefornling
syndrome ( see p 723). Diarrhea in a herd
rod that is more oxygen-sensitive than
may be due to a single agent, but concurrent

C perjringens. The organism can be
infections are conunon. Because some
demonstrated in the intestine by direct Gr3111
diseases are age-dependent, differential
stain of smears. Survival of C difficile in the diagnosis is best considered by age group
environment and shedding by carrier sows is

(see TABLE 6).

believed to be in1portant in transmission.

294

INTESTINAL DISEASES IN PIGS

IO=ii!i AGE DISTRIBUTION OF DIARRHEAL DISEASES IN PIGS

Age Group

Growing-finishing

Nursing

Weaning
or Breeding

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BACTERIAL DISEASES

Clostridium clijficile entetitis

+++

+

+

C pe1jringens type A enteritis

++

+

C pe1:ftingens type C enteritis

++

Enteric colibacillosis

+++

+++

Intestinal spirochetosis

++

+++

Porcine proliferative enteritis

++

+++

Salmonella enteritis

+

++

+++

Swine dysentery

+

++

+++

PARASITISM

Clyptosporidium sp

+

+

Isospora suis

+++

+

Strnngyloides ransomi

+

+

+

Trichwis suis

++

VIRAL DISEASES

Porcine circovirus diarrhea

+

++

+

Porcine epidemic diarrhea

+++

+ ++

++

Rotaviral enteritis

+++

+++

+

Transmissible gastroenteritis

+++

+++

++

- Rare or does not occur; + Uncon�mon; + + Common; + + + Very conm1on C difficile produces "large clostridial toxins" Diagnosis: Gross lesions are not A and B, which are thought to be involved in
pathognomonic, and diagnosis must be
lesion production. Toxin A is an enterotoxin
confirmed by culture or demonstration of
that causes fluid secretion into the gut
either toxin A or B and histopatholo·gy.

lumen, and toxin B is a cytotoxin.

C difficile can be cultured on selective
media containing cefoxitin, cycloserine,

Clinical Findings: Affected piglets may
taurocholate, and fructose m1der anaerobic
have dyspnea, abdominal distention, and
conditions. The genes of toxins A and B are
scrotal edema. Diarrhea may not be present
identified readily by PCR. The toxins can
in all pigs affected.

also be detected directly in suspensions

Lesions: Ascites, hydrothorax, and
of intestinal contents by commercially
edema of the ascending colon have been
available enzyme inmmnoassays.

reported. Urates are commonly present
in the kidneys. Pasty to watety colonic

Treatment and Control: Based
contents may be seen. Microscopically, the
on minimum inhibitory concentration
colon is primarily affected with multifocal
detenninations, it has been suggested that
exudation of mucus and fibtin plus
e1ythromycin, tetracycline, and tylosin may
submucosal edema.

be useful for treatment of suckling piglets,

INTESTINAL DISEASES IN PIGS

295
and tiamulin and virginiamycin may help to
jejunw11 and ilewn. More chronic cases
reduce levels of the organism in adult swine.

have a thickened small intestine lined by

No controlled studies on the effect of
a pale yellow or gray necrotic membrane
antibiotics on clinical disease have been
tightly adhered to the submucosa.

reported.

Diagnosis: Necropsy is usually sufficient

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CLOSTRIDIUM PERFRINGENS
to establish the diagnosis in the peracute

TYPE A ENTERITIS
hemorrhagic fom1 and in the acute fonn
with jejuna.I emphysema. A rapid prestm1p

Infection of the small intestine by type A
tive diagnosis can be made by demonstratstrains of C peifringens is a milder ing large rod-shaped bacteria in gramcondition and rarer than disease caused by stained mucosa! impression smears.

C pei:fringens type C ( see below). Suckling Histologic demonstration ofvillous necrosis
and sometin1es weaned pigs are affected
with mucosa.I colonization by mm1erous
and exhibit yellow-colored feces with
large gram-positive rods is adequate for
mucous and flecks of blood. Growth rates
confirmation. Subacute and chronic forms
are suppressed but with low to no mortality.

of the disease in piglets 6---14 days old are

The lesions at necropsy are milder and
easily confused at necropsy with Isospora
blood-free as compared with those of
silis ente1itis, but diagnosis is usually

C peiftingens type C enteritis. Diagnosis,
possible by histologic examination of the
treatment, and control are as for C peifrin
jejunw11 and ilewn or by observation of
gens type C enteritis.

clostridia in mucosa.I smears (Gram or

Giemsa stain). Isolates of C peiftingens

CLOSTRIDIUM PERFRINGENS
may be genotyped for the presence of genes

TYPE C ENTERITIS
that code for 13 toxin.

Infection of the small intestine by type C

Treatment and Control: Treatment of
strains of C peif1ingeiis causes a highly pigs with clinical signs is of little benefit
fatal, necrohemorrhagic enteritis. It most
because lesions usually a.re irreversible at
commonly affects piglets 1-5 days old but
the onset of diarrhea. In an acute outbreak,
may be seen in pigs up to 3 wk old (and in
prophylactic administration of type C
other species, seep 609).

antitoxin or antibiotic (or both) parenterally
or PO is protective if given to piglets within

Etiology and Pathogenesis: The

2 hr of birth. The disease tends to recw· on
organism penetrates between the absorpinfected premises. Vaccination of gestating tive cells of the upper jejunum and
sows at 6 and 3 wk before parturition with
elaborates 13 toxin, a potent, heat-labile,
type C bacterin-toxoid confers some passive
trypsin-sensitive exotoxin that causes
lactogenic immunity to subsequent litters, if
necrosis of all structural components of
piglets consun1e colostrwn soon after birth.

the villi. Necrotizing inflammation usually

Once immunized with two doses of bacterinextends to the mucosa.I crypts. The infection toxoicl, sows should receive one dose -3 wk may continue caudally and involve the
before each subsequent farrowing.

ileum, but it rarely affects the colon.

Necrosis of the mucosa is accompanied by
blood loss into the intestinal wall and lumen.

Clinical Findings: Sudden onset of
hemorrhagic diarrhea followed by collapse
and death is characteristic in piglets 1-3 days
old. In less acute cases, brownish liquid
feces develop at 3--5 days. Infrequently, pigs
develop a persistent, pasty, gray diarrhea
and become progressively emaciated. In
peracute cases, the perinea.I region is blood
stained.

Lesions: The small intestines are dark
red, hemorrhagic, and filled witl1 hem01�
rhagic liquid. Less acute cases at 3--5 days

Clostridium perfringens enteritis in a piglet.

may have gas bubbles in the wall of the

Note the large numbers of gram-positive
rods adhering to the necrotic jejunal
jejunun1 and necrosis of tl1e mucosa of the
epithelium. Courtesy of Dr. John Prescott.

296

INTESTINAL DISEASES IN PIGS

EDEMA DISEASE
medication. Prevention includes reducing
predisposing factors, such as dampness

(Escherichia coli enterotoxemia)

and chilling; improving sanitation, such

Edema disease is an acute, highly fatal,
as by replacing solid or slatted concrete
neurologic disorder usually seen 5 days to
flooring with wire-mesh flooring; and

2 wk after weaning and possibly accompavaccinating gestating sows with pilus

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nied by diarrhea (seep 716).

specific vaccines. Pigs lacking receptors
for KSS have been shown to be resistant to

ENTERIC COLIBACILLOSIS
disease caused by enterotoxin-positive

KSS-positive E coli.

Enteric colibacillosis is a common disease
of nursing and weanling pigs caused by

HEMORRHAGIC BOWEL
colonization of the small intestine by

SYNDROME
enterotoxigenic strains of Escherichia coli.

(Mesenteric torsion of the small intestine)

Etiology and Pathogenesis: Certain

Hemorrhagic bowel syndrome affects
strains of E coli possess funbria or pili that rapidly growing swine 4-6 mo old. Pigs die
allow them to adhere to or colonize the
suddenly without evidence of diarrhea,
absorptive epithelial cells of the jejunum
but the small intestine is thin-walled on
and ileum. The common antigenic types of
necropsy and filled with either clotted or
pili associated with pathogenicity are KSS,
unclotted blood. The large intestine usually

K99, 987P, and F41. Pathogenic strains
contains tarry fecal material but no lesions
produce enterotoxins that cause fluid and
suggestive of swine dysentery, salmonelloelectrolytes to be secreted into the intestinal sis, proliferative enteritis, or intestinal lumen, which results in diarrhea, dehydraspirochetosis. The condition can be tion, and acidosis. Infection in neonates is
prevented by the administration of either
commonly caused by KSS and 987P strains,
bacitracin or chlortetracycline in the feed.

whereas postweaning colibacillosis is

When perfonning a necropsy, the mesennearly always due to the KSS strain.

teric root should be palpated before
opening the abdomen. A peracute form of

Clinical Findings: Profuse watery
proliferative enteritis may have similar
diarrhea with rapid dehydration, acidosis,
clinical and gross lesions; however,
and death is common. Rarely, pigs may
histology and culture of the intestine will
collapse and die before diarrhea begins.

discern the presence or absence of

Lesions: Dehydration and distention of
epithelial proliferation and Lawsonia
the small intestine with yellowish, slightly
intracellularis.

mucoid fluid is characteristic. The colon

The cause in most cases is believed due
contains sin1ilar fluid. The fundic portion of
to intestinal volvulus. Predisposing factors
the gastric mucosa is often reddened. Pigs
may include vigorous exercise, handling,
dying suddenly may have patchy cutaneous
fighting, piling, or irregular feeding.

erythema. Histologically, the villi are usually Long-loined pigs may be more likely to of normal length and have many small
develop mesenteric torsion than shorter
bacterial rods adhered tu the absorptive
pigs. Rotation of the entire intestine,
enterocytes.

including the posterior part of the duodenum
and the anterior part of the rectum, around

Diagnosis: Confinnation is based on
the root of the mesentery obstructs venous
histologic observation of villous colonizaoutflow of blood, which causes blood to pool tion; demonstration of KSS, K99, 987P, or
and stagnate in the intestine and soon results

F41 pilus antigens in intestinal scrapings by
in infarction. Rotation may be only partial
inlmunofluorescence or other inlmunologic
and difficult to demonstrate at necropsy,
procedures; and isolation of the organism
which makes diagnosis more challenging.

from the small intestine. Because E coli is a common secondary agent, the possibility of

INTESTINAL SALMONELLOSIS
involvement of other agents such as viruses
or coccidia should be considered.

Enteropathogenic sahnonellae cause
inflanmmtion and necrosis of the small and

Treatment and Control: Therapy
large intestines, resulting in diarrhea that
includes prompt treatment with antibactemay be accompanied by generalized sepsis.

rials and restoration of fluid and electrolyte

All ages are susceptible, but the disease is
balance. Bacterial antibiotic sensitivity
most conu11on in weaned and growingtesting is helpful to identify effective finishing pigs.

INTESTINAL DISEASES IN PIGS

297

Etiology and Pathogenesis:

intestine and liver to differentiate salmonel

Salmonella Choleraesuis kunzendorf (S
losis from proliferative ente1itis and swine

Choleraesuis) is one of the most common
dysentery is a valuable adjunct procedure.

Salmonella species affecting pigs. It
sometimes produces necrotizing enterocol

Treatment and Control: Live avimlent
itis but far more common is a septicemic
vaccines administered either intranasally or

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disease characte1ized by hepatitis,
via the water are very effective for prevenpneumonia, and cerebral vasculitis. S
tion of disease caused by S Choleraesuis.

Typhisuis infection of the intestine results

Avirulent vaccines may also effectively
in necrotizing, nonsuppurative inflammareduce levels of salmonellae in the tissues tion of the mucosa and submucosa of the
of swine at slaughter. Parenteral administraileum, cecum, and colon; frequently, the tion of antibacterials to acutely ill pigs and
mucosa is ulcerative. Usually, there is
medication of the affected group via water
extension to regional lymph nodes and,
or feed may decrease tl1e severity of the
occasionally, generalized septicemia.

outbreak. Neomycin and lli1comycin-spec

Sources of infection for S Choleraesuis and tinomycin are the most often used water

S Typhisuis are primarily asymptomatic medications. Carbadox in the feed is often
carrier pigs but also may include rodents
used as a preventive. Susceptibility testing
and contaminated feed and premises. (See
of the isolated organism is useful to select
also SALMONELLOSIS, p 195.)

an approp1iate antibacterial. Thorough

Numerous other serotypes of salmonellae cleaning and disinfection of contaminated are seen in pigs, some of which have been
facilities and elimination of the source of
associated with human foodbome illness.

the organism decrease tl1e likeli110od of

Common serotypes seen in pigs are
repeated epidemics.

S Typhimurium, S Derby, S Heidelberg, S Worthington, and S Infantis. These serotypes may cause mild to moderate

INTESTINAL SPIROCHETOSIS
diarrhea in swine and may be resistant to
multiple drugs.

Intestinal spirochetosis is a disease of
the large intestine seen in the absence of

Clinical Findings:

Brachyspira hyodysenteriae

Nursing pigs may

( see SWINE
develop diarrhea but usually succumb to

DYSENTERY, p 301). This disease syndrome is
generalized septicemia. Weanling or
being recognized more frequently worldwide.

growing-finishing pigs are febrile and have
liquid feces that may be yellow and contain

Etiology and Pathogenesis: The
shreds of necrotic debris.

primary ca.use of intestinal spirochetosis

Lesions: Pigs infected with S Choleraeis Brachyspira pilosicoli. Other weakly suis have an inflamed, slightly thickened

13-hemolytic Brachyspira assocja.ted with
ileum and colon, usually with necrotic
the condition are B inlermedi a and B
debris on the mucosal surface. Mesenteric
murdochi. B innocens appears not to
lymph nodes are enlarged, edematous, and
ca.use disease at all. B pilosicoli is
sometimes red. Mucosal ulceration may or
emerging as a significant pathogen of
may not be evident. A small an10unt of
people, especially in indigenous populahemorrhage may be seen in acute cases.

tions, homosexuals, and in1munosup

Occasionally, rectal strictures ( see p 300) pressed patients. The organism is transmitmay develop. Other enteropathogenic ted orally and survives extremely well in the
salmonellae, except for S Typhisuis, environment. B pilosicoli has been isolated produce lesions similar to but less severe
from a wide variety of aninlals, including
than those of S Choleraesuis. Lesions of S
waterbirds, rodents, and dogs. It has been

Typhisuis enteritis are distinctive, typically
shown to ca.use diarrheal disease in pigs,
yellow, round (button) ulcers in the colon,
chickens, and people by experimental
cecwn, and less commonly the ileum.

inoculation and in natural occurrence.

The pathogenesis is not well studied, but
apparently the end-on attachment of the

Diagnosis: Culture of feces or intestinal
spirochete to the mucosa! surface interferes
mucosa in a selective medium may yield tl1e
with the absorptive capacity of the colon,
organism. However, salmonellae often are
resulting in di.a.IThea.

isolated (and more reliably) from enlarged
mesenteric lymph nodes by direct streaking
on a selective medium such as brilliant

Clinical Findings: Pigs initially have
green agar or by inoculation of enrichment
sticky feces on the perineum. The feces will
media. Histologic exanlination of affected
appear as wet cement, and a mild diarrhea

298

INTESTINAL DISEASES IN PIGS
may result. Affected pigs may be inappetent
old. Infection causes necrosis and villous
and grow slowly.

atrophy of the ileum and jejunum.

Lesions: The lesions in the large intes

Secondary bacterial infection of the injured
tine are milder than those caused by
intestinal mucosa is common. M01tality

B hyodysente1iae in swine dysentery.

often is 20%-25%, and many pigs are

The volume of the large intestine may be
stunted. Diagnosis can be based on

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increased and distended with thickening of
identification of immature coccidiaJ fonns
the mucosa. In some pigs, a mucohemori11 the intestinal mucosa by direct mucosa]

rhagic colitis develops in association with
smear (Giemsa stain) or by histologic
enlarged mesenteric lymph nodes.

examination of the affected intestine.

Microscopically, spirochetes may be seen

Successful prevention most commortly
attached encl-on to the mucosa! stuface and
depends on thorough cleaning of farrowing
give the appearance of a false bmsh border.

facilities to minimize the number of oocysts.

The mucosa! sUJface has focal erosions with After cleaning, thorough disirlfection with mild catarrhal exudate. Colonic crypts are

500A> bleach has been useful. Coccidiostats
often clilatecl, containing numerous
are sometimes feel to sows 2 wk before
spirochetes.

farrowing or administered PO to pigs from
birth to 3 wk of age.

Diagnosis: Important differential cliag

Adult nodular worms of Oesophagoslo
noses include salmonellosis, proliferative
mum spp in the large intestine cause little enteritis, swine dysentery, and whipworm
harm, but heavy infection by larvae
infection. B pilosicoli and other weakly
encysted in the intestinal wall may lead
f3-hemolytic Brachyspira can be isolated on to emaciation.

selective agar under anaerobic conditions.

Strongyloides ransomi (intestinal

Biochemical tests and preferably PCR
thread worm) larvae can be transmitted via
should be perfo1mecl on Brachyspira
colostrUJn or acquired from contaminated
isolates to confinn species identification.

skin of the dam. Heavily infected piglets
develop severe diarrhea when 10-14 days

Treatment and Control: Treatment and
old, with high mortality. Diagnosis is based
prevention of intestinal spirochetosis is
on direct microscopical observation of
similar to that of swine dysentery. Dmgs
mucosa! scrapings.

such as tianutlin, lincomycin, and carbadox

Trichu1is suis (whipwonns) penetrate
are effective. It is unknown whether the
the mucosa of the cecUJn and colon and
agent can be eraclicated without total
cause multifocal inflammation. Heavy
clepopttlation, as in swine dysentery, but
irlfections cause cliarrhea and emaciation.

because of the reservoir hosts and

The feces are hemorThagic; therefore, heavy
environmental survival it is doubtful.

whipwom1 infections may be confused
clinically with swine dysentery or proliferative enteritis. Diagnosis is based on clirect PARASITISM
observation of whipworms in the large
intestine or on fecal flotation.

See also p 320 and see p 208.

Asca1is siium is the most common

PORCINE EPIDEMIC DIARRHEA
intestinal nematode of pigs. Adults in the
intestine reduce feed efficiency, and heavy

This corona viral cliarrhea affects pigs of all
infections cause emaciation. Larval
ages and clinically resembles transmissible
migration incites inflan1mation in the liver
gastroenteritis (TGE, seep 302) in several
and lungs.

respects.

Cryptospo1idium sp is a coccidium that
attaches to the mucosa] epitheliUJn of the

Etiology and Epidemiology: The
intestine of pigs <!lO clays old. It causes
porcine epidemic cliarrhea (PED) virus is
villous atrophy in the lower small intestine.

not related to any other member of the

MaJabsorption and cliarrhea may result.

Coronaviridae. Pigs are the ortly known

Eimeiia spp are common in pigs, but
host. Antibodies to the virus have not been
overt clisease is seldom seen. Heavy
found in wild pigs or in other anin1aJ
infections may cause significant enterospecies. Infections have been seen in most colitis in young growing pigs.

European countries and in China. In April

Hyostrongylus rubidus is the common

2013, clisease clue to PEDV was cliagnosecl in
stomach worm found in pasture-raised pigs.

the USA for the first time. Large epidemics

It usually causes little harm.

occurred in Europe in 1969; no antiboclies

Isospora suis is a common and important have been found in sera collected before cause of coccidiosis in piglets 6 days to 3 wk

1969. Since then, the virus has become

INTESTINAL DISEASES IN PIGS

299
widespread and endemic in several

TGE. No lesions have been described in the

European count1ies, and acute outbreaks
colon. A consistent finding is acute necrosis
have become rare. On large breeding fanns,
of back muscle.

the virus persists in consecutive litters of
pigs after weaning and after they lose their

Diagnosis: Clirucal differentiation from
immwlity from antibody in the milk. On

TGE is difficult. TGE in its typical epidemic

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these fanns, the virus may be associated
fo1m causes a rapidly spreading diarrhea in
with weailing diarrhea. In Belgiwn, the virus ailimals of all ages, with high mo1tality in is most frequently associated with diai-rhea
neonates. Witl1 PED, the dian·hea spreads at
in feeder pigs, which develops sho1tly after
a slower rate, and although dian·hea is seen
tl1ey ai·e gathered from different breeding
in most of the litters, some litters may
farms and assembled in large fattening
remain healthy even in the absence of
units. The virus was demonstrated in fecal
in1munity. Morbidity is lO()OA, in older pigs,
mate1ial in 8096of these groups. Outbreaks
and tl1ey are severely sick. Acute deaths in
in the USA caused 600Ar 100% mortality in
adults and finishing pigs due to muscle
suckling pigs and mild to severe diaiThea
necrosis and that occw'S during an outbreak
in all pigs of all ages; they were initially
of diarrhea are typical of PED and ai·e not
believed to be outbreaks ofTGE. Spread of
seen with any otl1er infectious diarrhea.

the virus mainly occurs directly through

Laboratory diagnosis in neonates is made
infected pigs and indirectly through
by PCR and/or direct immtmofluorescence
virns-contai11inated fonlites and via
on cryostat sections of small intestine or
trai1sport trucks.

colon. ELISA to detect viral antigens in
feces or intestinal contents is more useful

Pathogenesis: The pathogenesis ai1d
for older pigs. Antibodies can be detected
imnume mechailisms are similar to those
in paired serum sai11ples through ELISAreported forTGE. Oral infection results in blocking.

viral replication in tl1e epitl1elial cells of the
small intestinal villi. Cells on colonic villi

Control: No specific treatment is
also become infected. No other tissue
available. Measures taken during an
tropisms have been shown. Virus is
outbreak are of a general nature. Pigs with
excreted in the feces.

diai-rhea should have free access to water,
and finishing pigs should have feed witl1held

Clinical Findings: DiaiThea is the only
for 1-2 days.

direct virus-induced clirucal sign seen. An

PED virus can be eliminated from herds
acute outbreak on a susceptible breeding
without total depopulation by maxin'h�ing
fann resembles a TGE outbreak and is
immwlity with plaimed infection of the sow
characterized by watery dian·hea in pigs
herd; an "all-in/all-out" management of
of all ages. However, as compared with
farrowing, nw'Sery, and grower rooms; and

TGE, tl1e incubation period is longer (3-4
good sailitation.

days), not all the litters of suckling pigs may

Because PED virus is easily spread during
become sick, and mortality in neonatal pigs
an epidemic by people, anin1als, and
is lower (average 500A,). Also, the disease
fomites, special cai·e should be taken to
within the fann spreads more slowly. In all
prevent spread to tmexposed groups of
outbreaks, signs are most consistently seen
pigs and to neighboring herds. The use of
in feeders, finishers, and adults, which
vacines for prevention has not been well
appeai· to be most susceptible because
docwnented.

outbreaks often start in these age groups.

Older pigs are more lethargic and depressed
with PED than with TGE. Sick pigs appear

PORCINE PROLIFERATIVE
to have colic.

Acute outbreaks in susceptible finishing

ENTERITIS
pigs are characte1ized by watery diarrhea,

(Porcine intestinal adenomatosis,
but a markedly increased nun1ber of acute

Proliferative hemorrhagic enteropathy, Ileitis)

deatl1S may be seen, particularly in pigs
infected towai·d the end of the finislling

Porcine proliferative enteritis is a common
period ai1d in stress-sensitive breeds. Deatl1
diarrheal disease of growing-fmislling and
may even occur during the incubation period. young breeding pigs characterized by hyperplasia and in.fl3.111mation of the ilewn

Lesions: Macroscopic lesions are
and colon. It often is mild and self-limiting
confined to the small intestine, with villous
but sometimes causes persistent clia.JThea,
shortening as the main characteristic. These severe necrotic enteritis, or hemorrhagic lesions closely resemble those seen with
enteritis with high mortality.

300

INTESTINAL DISEASES IN PIGS

Etiology and Pathogenesis: The
has been developed and is useful for
etiology is Lawsonia intracellularis,
confimlation of the presence of L intracel
an intracellular, gran1-negative, small
lularis in lesions. Bacterial culture of
rod-shaped bacterium. The organism has
intestine and lymph nodes to exclude
been cultivated only in cell cultures, and

Salmonella infection, together with
attempts to propagate it in cell-free medium
histologic exanlination and culture of

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have failed. Koch's postulates have been
cecum and colon to exclude swine
fulfilled by inoculation of pure cultures of
dysentery, are essential additional

L intracellularis into conventionally reared procedures. The colon also should be pigs; typical lesions of the disease were
examined for whipworms. L intracellularis
produced, andL intracellularis was
is present in most swine herds, so demonreisolated from the lesions. Inoculation of stration of the organism in feces by PCR or

L intracellularis into gnotobiotic pigs does the presence of antibody in clinically
not cause the disease; therefore, other
nom1al pigs is of little diagnostic value.

factors in the conventionally reared
pig may contribute to development of

Treatment and Control: Vaiious
lesions.

antibacterials administered parenterally to
acutely affected pigs and by feed or water

Clinical Findings: The more common,
to the remainder of the group help reduce
nonhemorrhagic form of the disease often
severity of the enteritis and prevent
affects 40- to 80-lb (18- to 36-kg) pigs and is
development of chronic, irreversible,
characterized by sudden onset of diarrhea.

necrotic enteritis. Porcine proliferative

The feces are watery to pasty, brownish, or
enteritis is one of the first diseases to be
faintly blood stained. After -2 days, pigs
seen in new herds established by surgical
may pass yellow fibrinonecrotic casts that
derivation. A live avirulent vaccine
have fom1ed in the ileum. Most affected pigs
administered via the water is highly
recover spontaneously, but a significant
effective. It should be administered to gilts
nw11ber develop chronic necrotic enteritis
and boars during acclimatization before
with progressive emaciation. The hemorintroduction into a herd.

rhagic form is characterized by cutaneous
pallor, weakness, and passage of hemorrhagic or black, tarry feces. Pregnant gilts RECTAL STRICTURES
may abort.

In growing pigs, rectal strictures are

Lesions: Lesions may be seen anywhere
sequelae of severely traumatized rectal
in the lower half of the small intestine,
prolapses (seep 189) or of infections that
cecum, or colon but are most frequent and
interfere with rectal blood supply. The
obvious in the ileum. The wall of the
fonner cause sporadic cases; the latter may
intestine is thickened, and the mesentery
be epidemic. One cause is Salmonella
may be edematous. The mesenteric lymph

'Iyphimurium infection (seep 296), which
nodes are enlarged. The intestinal mucosa
produces an ulcerative proctitis that heals
appears thickened and rugose, may be
in such a manner that normal function is not
covered with a brownish or yellow
restored. The stricture is reportedly the
fibrinonecrotic membrane, and sometimes
result of fibrosis of the rectal tissue due to
has petechial hemorrhages. Yellow necrotic
persistent ischemia caused by infection in
casts may be found in the ileum or passing
an area of limited blood supply.

through the colon. Diffuse, complete
mucosal necrosis in chronic cases causes
the intestine to be rigid, resembling a garden Clinical Findings: Several bloated pigs in hose. Proliferative mucosal lesions often
varying stages of emaciation are generally
are in the colon but are detected only by
seen in a group of growing pigs. Other
careful inspection at necropsy. In the
clinical signs, including prior outbreaks of
profusely hemorrhagic form, there are red
severe debilitating diarrhea, are common
or black, tarry feces in the colon and clotted
but not always reported. An index finger
blood in the ileum.

rarely can be passed into the rectum
without considerable resi�tance.

Diagnosis: Confimlation is based on

Lesions: At necropsy the colon is grossly
histologic observation of characteristic
distended, and the intestine is filled with gas
proliferation and inflal11ffiation of mucosal
ai1d green feces. The predonlinant lesion is
crypts. L intracellularis ( comma-shaped,
a narrowed rectal canal, due to armular
resembling Campylobacter) can usually be
fibrotic ulcers or rectal strictures found
demonstrated by silver stains. A PCR test

2-5 cm cranial to the anus.

INTESTINAL DISEASES IN PIGS

301

Diagnosis: An epidemic of rectal

Diagnosis: Laboratory procedures are
strictures without prior rectal prolapses is
required. Confirmation is based on histologic
indicative of S Typhimurium infection.

demonstration of villous atrophy in the

Culture of feces and regional lymph nodes
jejunum, electron microscopic demonstrausually yields S Typhimurium. However, it tion of virions in the intestinal contents,
is not possible to determine whether the

PCR, and immunodiagnostic procedures to

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lesion or the infection occuned first.

demonstrate viral antigen in the intestinal
mucosa or feces. Differential diagnoses

Treatment and Control: Early diagnosis
include endemic transmissible gastroente1iand treatment of diarrhea is imperative for tis, porcine epidemic diarrhea, Isospora
control. Good housing, management, and
suis enteritis, and enteric colibacillosis.

sanitation, with "all-in/all-out" movement of pigs is the best method to prevent further

Treatment and Control: There is no
outbreaks. Surgery is not thought to be
specific treatment. Minimizing heat loss
economically feasible.

and providing adequate water to maintain
hydration are helpful. Concurrent infection

ROTAVIRAL ENTERITIS
by enterotoxigenic Escherichia coli is
common; therefore, antibiotic therapy

Rotaviral enteritis is a common disease
may reduce mortality. Providing diaJTheic
of the small intestine of pigs. All ages are
weaned pigs with a warm, dry, draft-free
susceptible, but significant diarrheal
environment and frequent limited feedings
disease usually is seen in nursing or
help prevent starvation, secondary diseases,
post-weaning pigs.

and pe1ma.nent stunting. Vaccine for group A
rotavirus appears beneficial when given to

Etiology and Pathogenesis: The causal
sows before farrowing. Vaccines for groups
rotavirus infects and destroys villous

B, C, and E have not been developed
enterocytes throughout the small intestine,
because of difficulty in virus propagation.

but lesions are most severe in the middle

A serotyping scheme based on virus
third of the intestine. Loss of villous
neutralization indicates a lack of crossepithelium results in partial villous atrophy, protection between isolates within groups.

malabsorption, and osmotic diarrhea. Four
antigenic groups (A, B, C, E) of rotavirus are SWINE DYSENTERY
found in pigs. They are easily spread by
direct contact. Healthy carrier sows may be

(Bloody scours)

fecal shedders during the periparturient
period, thereby exposing their litters to

Swine dysentery is a mucohemorrhagic
infection.

diarrheal disease of pigs that affects the
large intestine.

Clinical Findings: If neonatal pigs do
not receive protective levels of maternal

Etiology and Pathogenesis: The
antibody, they are likely to develop profuse
essential causal agent is Brachyspira
watery diarrhea in 12-48 hr. More com
hyodysenteriae, an anaerobic spirochete
monly, the infection is endemic in a herd,
that produces a hemolysin, although other
and sows have varying levels of antibody in
organisms may contribute to the sevetity of
the colostrum and milk, which provide
lesions. B hyodysenteriae produces strong
varying degrees of passive protection to

13 hemolysis on blood agar under anaerobic
nursing pigs. Diarrhea often begins in pigs
incubation conditions. Other strongly

5 days to 3 wk old or in1mediately after

13-hemolyticBrachyspira have been
weaning. The feces of nursing pigs often are
described that produce lesions of swine
yellow or gray and pasty in the early stages
dysentery when inoculated into pigs,
and progress to gray and pasty after -2 days. namely B suanatina, some strains of B

Diarrhea persists for 2-5 days. Dianheic
intermedia, Brachyspira sp SASK 30446,
pigs become gaunt and rough-haired, but
and B hampsonii. The Brachyspira
mortality usually is low. Weaned pigs have
proliferate in the large intestine and cause
watery feces that contain poorly digested
degeneration and inflanunation of the
feed. Weaners become inappetent and
superficial mucosa, hypersecretion of
noncompetitive, which results in emaciamucus by mucosa! epitheliun1, and tion, stunting, and probably predisposition
multifocal bleeding points on the mucosa!

to pneumonia and other diseases.

surface. The organism does not penetrate
beyond the intestinal mucosa. Decreased

Lesions: The small intestine appears thin
ability of the mucosa to reabsorb endogwalled, and the cecum and colon contain enous secretions from the w1affected small
liquid feces.

intestine results in diarrhea.

302

INTESTINAL DISEASES IN PIGS

Clinical Findings: The first signs are

Etiology and Pathogenesis: The causal
partial anorexia, passage of soft feces, and
coronavirus infects and destroys villous
possibly fever. The course is variable. Some
epithelial cells of the jejunwn and ileum,
pigs die peracutely. More commonly, a
which results in severe villous atrophy,
mucoid diarrhea with flecks of blood and
malabsorption, osmotic diarrhea, and
mucus develops and progresses to a watery
dehydration. The incubation period is -18 hr.

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mucohemorrhagic dia.IThea. After several

The infection spreads rapidly by aerosol or
days, the feces are brown and contain flecks contact exposure. Severe epidemics are offibrin and deb1is. Diarrheic pigs are
more common d wing winter because of
dehydrated, profoundly weak, gaunt, and
survival of the vims in colder temperatures.

emaciated.

Lesions: The diffuse lesions are confined

Clinical Findings: In nonimrnune herds,
to the cecwn, spiral colon, and rectwn. The
vomiting often is the initial sign, followed by
affected mucosa is covered with a layer
profuse watery diarrhea, dehydration, and
of transparent or gray mucus, often with
excessive thirst. Feces of nursing pigs often
suspended flecks of blood in early stages,
contain curds of undigested milk. Mortality
with a mixtme of blood, fibrin, and necrotic
is nearly lOOOA, in piglets <l wk old, whereas
debris in more advanced cases, and a
pigs> 1 mo old seldom die. Gestating sows
yellow, necrotic debris late in the course.

occasionally abort, and lactating sows often
exhibit vomiting, diarrhea, and agalactia.

Diagnosis: Clinical signs and necropsy

Diarrhea in surviving nursing piglets
findings are usually sufficient for a
continues for -5 days, but older pigs may
preswnptive diagnosis. Confinnation
be diarrheic for a shorter period.

is based on demonstration of typical

In large herds with endemic TGE, clinical
histologic lesions in the large intestine and
signs are variable, depending on the level
isolation of strongly 13-hemolytic Brachy
of inununity and magnitude of exposure.

spira by anaerobic culture. ConcwTent
lnununity from antibody in the sow's milk
diseases are not unconunon. Differential
usually is sufficient to protect piglets until
diagnoses include intestinal spirochetosis,
they are 4-5 days old. As the antibody level
proliferative enteritis, salmonellosis, and
in milk decreases, infection and mild
heavy whipwom1 infections.

disease may occur. Depending on the level
of immunity and exposure, diarrhea may be
mild in some litters but severe in others. If

Treatment and Control: Therapeutic use
passive protection is sufficient to protect
of antibacterials is effective if statted early.

pigs throughout the nursing period, diarrhea

Water medication is preferred at first.

often develops during the first few days

Because drug-resistant strains are prevalent,
after weaning.

it is essential to choo�e a drug to which the

Lesions: Piglets dying ofTGE are
organism is sensitive. Bacitracin, carbadox,
severely dehydrated, and the skin is soiled
lincomycin, tylosin, tiarnulin, and virginiarnywith Liquid feces. The stomach usually cin are commonly used. The disease may be
contains milk curd but may be empty. The
eradicated from infected premises without
small intestine is thin walled, and the entire
total depopulation by a persistent and
intestine contains greenish or yellow watery
carefully planned program that includes
fluid and clwnps of undigested milk. Older
treatment of canier pigs with bactericidal
pigs have few remarkable lesions, except
drugs and thorough cleaning and disinfection that the colon contains liquid rather than of vacated facilities. Mice are an important
fonned feces. Villous atrophy can be seen
reservoir of infection for B hyodysenteriae,
by examining the mucosa of the small
and any eradication attempt must include
intestine with a hand lens.

elinlination/reduction of the mouse
population on the farm. In addition,

Diagnosis: Clinical signs in the epidemic

B hyodysenteriae will survive >60 days in fonn ofTGE usually justify a preswnptive
pig waste at refrigerator temperatlffes.

diagnosis. In the mild endemic fonn,
laboratory procedures are required.

TRANSMISSIBLE

Histologic and immunofluorescent

GASTROENTERITIS
examinations of the small intestine to
demonstrate typical lesions and the

Transmissible gastroenteritis (TGE) is a
presence ofTGE viral antigen provide
common viral disease of the small intestine
confirmatory evidence. In some outbreaks,
that causes vomiting and profuse dianhea
hemagglutinating encephalomyelitis (see
in pigs of all ages.

p 728) may cause similar signs.

GASTROINTESTINAL PARASITES OF RUMINANTS

303

Treatment and Control: There is no

TGE virus-infected intestine and feces
specific treatment. Increasing farrowing
in the gestation ration. Because of the
room temperatme to minimize loss of body
obvious hazards associated with this
heat and providing electrolyte solutions to
procedure, it should be undertaken only
combat dehydration are helpful. Adminisif a later epidemic in the farrowing house tration of swine immunoglobulins has been
seems inevitable. The infectious material

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repmted to be beneficial. Weaning older
should be used only in the same herd from
nursing pigs that are consuming creep feed
which it was collected, and the tissues
may reduce mo1tality.

should be as free as possible from other

Protective immunity depends on
pathogens of pigs. TGE virus can be
presence of antibody in the small intestine.

eliminated from herds without total

Passive protection of piglets is provided by
depopulation by maximizing immunity
continual nursing of immune sows. Active,
with planned infection of the sow herd; an
protective immunity develops after

"all-in/all-out" management of farrowing,
infection of the intestinal mucosa with
nursery, and grower rooms; and good
virulent TGE virus. Active infection of
sanitation.

the intestine with virnlent virus provides

Because TGE virus is easily spread during
protective immunity for 6---18 mo due to a
an epidemic by people, animals, and
secretory IgA response. Vaccination of
fomites, special care should be taken to
natmally immune sows boosts inmrnnity
prevent spread to unexposed groups of pigs
sufficiently to protect neonates and is
and to neighboring herds.

particularly useful in endemically infected
herds. Vaccination of swine in herds free of

TGE may not be economically beneficial

OTHER INTESTINAL VIRUSES OF
because vaccines do not induce complete
immunity.

PIGS

Planned infection of pregnant sows at

Other viruses have been isolated from the
least 2-4 wk before farrowing in herds
intestines of pigs but appear not to be
known to be infected with virnlent virus
associated with economically significant
usually provides adequate immunity. This
disease. These include adenovirus and
may be accomplished by mixing ground,
enterovi.rus.

GASTROINTESTINAL PARASITES

OF RUMINANTS

Clinical Findings and Diagnosis: The
are present, the count can be low if egg
clinical signs associated with GI parasitisms production has been suppressed by host are shared by many diseases and condiimmune reaction or recent anthelmintic tions; however, a presumptive diagnosis
treatment. Variations in the egg-producing
based on signs, grazing history, and season
capability of different wom1s ( significantly
is often justified. Wection usually can be
lower for T'tichostrongylus, Ostertagia,
confirmed by demonstrating nematode eggs
andNematodirus than for Haemonchus)

or tapeworm segments on fecal examinamay also distort the trne picture. The ova of tion. However, in clinical evaluation of fecal

Nematodirus, Bunostomum, Strongyloi
examinations, two points should be
des, and Trichuris are distinctive, but remembered: 1) a fecal worm egg count
reliable differentiation of the more conm1on

(nw11ber of worm eggs per gram (EPG) of
species of rnminant strongyle ova is
feces is not always an accmate indication of
difficult. Fecal culture of strongyle eggs can
the number of adult worms present, and 2)

produce distinctive third-stage larvae if
specific identification of certain nematode
differentiation is in1portant premortem.

eggs ( eg, "strongyles") is impractical except The advent of safe and effective
in specialized laboratories. EPG counts can
broad-spectrunl anthelmintics has largely
be negative or deceptively low in the
reduced the need to differentiate the genera
presence of large numbers of inmlature
and species of these parasites. In areas
wonns; even when many adult parasites
where Osterl,agia spp predominate, the

304

GASTROINTESTINAL PARASITES OF RUMINANTS
analysis of sera for increased plasma
clinical significance in lambs, whereas
pepsinogen levels is a useful diagnostic aid.

5,000-10,000 Ostertagia are typically

Generally, increased levels of pepsinogen
required before clinical signs are seen. If the
activity (tyrosine levels >3 IU) are
anin1als have been diarrheic for a few days,
associated with clinical abomasal parasitworms may have been expelled and so the ism. Problems of interpretation may arise in
location, type, and severity of gross lesions

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immune animals under challenge, in which
may also be of considerable diagnostic
there are no clinical signs but the pepsinovalue.

gen levels may be increased because of

Mixed parasite infections should be
a hypersensitivity-type reaction in the
considered when evaluating clinical,
abomasal mucosa. Where H aemonchus spp laboratory, and necropsy findings, because predominate, the traditional estimation of
grazing anin1als rarely have mono-specific

PCV as an indicator of anemia has been
infections in the field.

largely replaced by use of the FAMACHA

The diagnosis of ostertagiosis in cattle
test (see below). In some countries,
during ilie period of larval inhibition (aka
serologic diagnosis (ELISA) of important
arrested development, hypobiosis,
species, such as Ostertagia in cattle, is also cliapause) presents technical problems,
used and based on antibody titers in bulk
particularly for the feedlot industry in the
tank milk samples in dairy herds. Such

USA. Fecal egg counts and plasma
infonnation is used as an indicator of
pepsinogen analysis do not provide useful
pasture challenge at a herd level, as an
information because inhibition occurs
indirect indicator of productivity, and is
within a few days of larval ingestion, before
linked witl1 ilie effectiveness of parasite
either the egg-laying adult stage has been
control strategies.

reached or plasma pepsinogen levels

In many management situations, high
increase. Predisposing factors for inhibition
levels of infection can be expected,
of laivae include age and geographic source
particularly after favorable temperature and of cattle, time of yeai· or season of aiTival, rainfall conditions. "Diagnostic drenching"

previous grazing history and management,
may be recommended when eggs are few
weather conditions prevailing during the
or absent, yet history and signs suggest
last grazing period, and prevalence of
infections, aliliough care should be taken

Ostertagia ostertagi in the source region.

not to treat animals indiscrinlinately to

I.nfo1mation on such factors is not usually
millimize the risk of anthelmintic resistance
available for feedlot cattle. If cattle have
developing.

anived after spring grazing in ilie south of

Routine postmortem exanlinations can
the USA or fall grazing in the north, they
provide valuable parasitologic data about
could have heavy burdens of inllibited
the status of ilie rest of tl1e herd or flock: On
larvae. Lighter calves from areas where
necropsy, Haemonchus, Bunostomum,
prevalence of parasites is high may also

Oesophagostomum, Trichuris, and
have such a problem. It is beconling more

Chabertia adults ( or advanced immature
widely accepted that a significant cause of
worms) can be seen easily. Ostertagia,
clinical disease or feed efficiency problems

Triclwstrongylus, Cooperia, and Nemato
in feedlot cattle is parasitism, possibly
dirus are difficult to see except by their
ostertagiosis. When cattle are brought in
movement in fiuid digesta, and clinically
from a suspect area and at a suspect ti.me of
important infections are easily overlooked.

year, it may be advisable to treat the new

In such cases, the total contents and all
aiTivals promptly with an anthelmintic
washings should be combined to a known
effective against inhibited larvae.

volun1e, and a wom1 count established to
evaluate the severity of the infection. The

Treatment: Effective worm control
number of wom1s found in aliquots of tl1e
cannot always be achieved by drugs alone;
gut contents and scrapings of ilie mucosa
however, anthelrnintics play an important
will enable ilie total worm count to be calcurole. (See also ANTHELMlNTlCS, p 2637.) They lated. However, the smaller nematodes may
may be used to reduce pasture contanlinabe difficult to see against a background of tion, particularly at times when seeding of
digesta, so iliey can be stained (5 min) with
the pasture wiili parasite eggs is .a prerequia strong iodine solution. Once ilie digesta site for development of an infective
and any tissue have been decolorized with
challenge necessai)' to cause clinical

5% sodiun1 thiosulfate, ilie iodine-stained
parasitism. Coordination witl1 other
wmms can be seen easily. The significance
meiliods of control, such as alternate or
of the nun1bers of wom1s present varies
mixed grazing with different host species,
according to worm and host species. For
integrated rotational grazing of different
example, only 100 H aemonchus are of
age groups within a single host species

GASTROINTESTINAL PARASITES OF RUMINANTS

305

(including creep grazing), inclusion of
nematode populations, although they
tannin-1ich forages in pasture, and
require careful adn1inistration if their
alternation of grazing and cropping, are
useful life is to be preserved.

other management techniques that can help

Some narrow-spectrwn anthelmintics,
to provide safe pasture and give economic
such as the salicylanilides, closantel, and
advantage when combined with anthelminrafoxanide, bind strongly to plasma proteins VetBooks.ir
tic treatment.

and have excellent activity against

The "ideal" anthelmintic should be safe,

H aemonchus contort us in sheep and
highly effective against adult and immature
remain in the host for a long time,
stages (including inhibited larvae) of the
conferring prolonged prophylactic activity
important worms, available in convenient
after adn1inistration.

formulations, economical, and compatible

Routes of adn1inistration otl1er than
with other commonly used compounds.

drenching or iitjection ( eg, incorporating

Broad-spectrum anthelmintics currently
into feed, drinking water, and mineral or
available belong to five different chemical
energy blocks) are used to reduce labor
groups: 1) benzirnidazoles (white
costs and may be useful under drylot
drenches), 2) imidazothiazoles (yellow
conditions or when grazing aninlals are
drenches), 3) macrocyclic lactones ( clear
being given supplemental feed. Another
drenches), 4) amino-acetonitrile de1ivaadvantage of these "in-feed" routes is that tives, and 5) spiroindoles. The benzimidacontinual low-level adn1inistration of a drng zoles include thiabendazole, the forerunner
can be achieved and pasture contan1ination
of modem broad-spectrnm anthelmintics,
reduced during periods that are optimal for
which set a new standard in efficacy and is
free-living development of the parasites.

still widely used today.

Disadvantages include erratic consumption

Thiabendazole's ineffectiveness against
of anthelmintic, tissue residues (requiring
inhibited Osterlagia larvae in cattle and
observance of rec01mnended withdrawal
one or two specific worm species led to the
periods), and possible encouragement of
development of other benzimidazoles
drug resistance by continual exposure.

(such as fenbendazole, ox:fendazole, and

Another labor-saving route of adn1inistraalbendazole) and the probenzimidazoles tion is the "pour-on" topical treatment, used (thiophanate, febantel, and netobimin).

for some of the organophosphates ( eg,

These compounds are effective against
tiichlorfon), levanlisole, and avem1ectins. A
most of the major GI parasites of rnrninants number of bolus preparations ( eg, morantel, and have varying levels of activity against
levarnisole, ivennectin, or benzinlidazoles)

inhibited larvae. The imidazothiazoles
release drng in a sustained fashion or in
include levarnisole, morantel, and pyrantel,
pulses at intervals approximately equal to
which also are highly effective, safe,
the prepatent period of the most important
broad-spectrnm anthelmintics but have

GI parasites. The boluses used in cattle have
little activity against inhibited larvae in
been designed to give entire grazing season
cattle. The macrocyclic lactones, which
protection in temperate areas if adminisinclude the averrnectins and milbemycins, tered at turn-out to set-stocked herds.

often administered as pour-on products or

Boluses are also available that provide
by injection, are highly effective against
treatment and subsequent prophylaxis of
adult and larval stages, including inhibited
animals already exposed to contanlinated
larvae of all the common GI nematodes
pasture and harboring parasites. Boluses in
of rnrninants and some of the important
sheep may be used to reduce the peripartuectoparasites. The latter group may persist rient rise in fecal egg output and thus the
in some rnrninant species for several weeks pasture contamination responsible for after a single subcutaneous or topical
disease in their offspring later in the grazing
administration and confer protection
season. Despite their efficacy, some boluses
against reinfection during this period.

used in either cattle or sheep have been

Moxidectin is also persistent after oral
withdrawn from the market because they
administration. Unlike many other
are not commercially viable.

anthelmintics, eprinomectin may also be

Niclosa.mide, morantel, praziquantel, and
used in lactating cows without the need
the newer benzinlidazoles (albendazole,
for a milk withdrawal period. The an1inofenbendazole, and ox:fendazole) are acetonitrile derivatives (monepantel) and
effective against tapewom1S (Moniezia
the spiroindoles ( derquantel) are given
spp) in cattle and sheep. Successful
as oral drenches in sheep, the latter in
treatment of the fringed tapeworm,
combination with abamectin in New

Thysanosorna actinioides, has been

Zealand. Both of these drugs have been
reported using either fenbendazole or
used in the control of multiresistant GI
praziquantel.

306

GASTROINTESTINAL PARASITES OF RUMINANTS

When treating clinically affected animals,
in parasites of cattle has been demonstrated,
the following should be considered: 1)

although much less frequently than in small
provide adequate nutrition; (2) treat all
runlinants; overuse and otherwise indisanimals in the group, as a preventive criminate treatment should be avoided.

measure and to reduce fwther pasture
lf anthelmintic resistance is suspected on
contamination; and 3) either house or move
a fann, a fecal egg count reduction test may

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stock to "clean" pastures to minimize
be conducted onsite that will indicate the
reinfection. The definition of safe pastures
likelihood of resistance. Fifteen to twenty
varies in different climates and depends on
ailimals should be randomly selected and
local knowledge of the seasonal mortality
assigned to eitller control or treatment
of infective laivae. Some authorities have
groups, one for each anthelmintic group
suggested treating only the most severely
selected. Fecal sainples ai·e collected before
affected animals in a flock or herd, ie,
treatment from all groups and then again
targeted selective treatment (TST). Where
either 7 days (after levainisole treatment) or

H aemonchus is a problem in sheep or

14 days (after benzimidazole or macrocyclic
goats, animals most likely to benefit from
lactone treatment) later. Pre- and postsuch treatment can be identified using the treatment fecal worn1 egg counts are tllen

FAMA CHA score card. This links the color
compared and anthelmintic resistance
of the ocular mucous membranes,
suspected if the reduction in output after
measured using a color chart, with the
dosing is <95%.

degree of anemia associated with the

The high cost of developing new
blood-sucking parasite. Animals with the
anthelmintic drugs has encouraged
palest mucous membranes are those likely
researchers to look for alternative
to have the heaviest worm burdens and be
approaches to GI parasite control, such as
chosen for treatment. The severity of
development of a "hidden antigen" vaccine
diarrhea and/or the quantitative fecal egg
againstHaemonchus; the use of tannin-rich
count for parasitic gastroenteritis in sheep
forages (such as clover and lucerne or
or cattle can also be used to detennine the
alfalfa), which have some anthelnlintic
need for individual treatment. The rationale
action; and nematophagous fm1gi.

behind TST is that a very large proportion
of wo1m egg output ( and thus pasture
contamination) is produced by a relatively

General Control Measures
small proportion of the host anin1al

"Control" generally implies the suppression population. Treatment of only these animals
of parasite burdens in the host below that
significantly reduces pasture contamination
level at which economic losses occur. To do
and reduces the overall selection pressure,
tllis effectively requires a comprehensive
exerted by the use of an anthelmintic, for
knowledge of tile epidenliologic and
resistant parasite g�nes. Untreated animals
ecologic factors that govern pasture laival
will continue to pass low numbers of worm
populations and tile role of host irrununity
eggs onto the pasture and so maintain a
in combating infection.

"susceptible" parasite gene pool "in refugia"

The goals of control are as follows:

(ie, unexposed to anthelmintic treatment).

1) prevent heavy exposure in susceptible

In contrast, the established practice of
hosts (recovery from heavy infection is
blanket treatment ai1d movement of stock
always slow), 2) reduce overall levels of
onto a clean pasture may encourage
pasture contamination, 3) minimize tile
emergence of anthelrnintic resistance. A11y
effects of parasite burdens, and 4) encourage
worms can-ying resistance genes surviving
the development of irrununity in tile animals
the treatment will then seed the previously

(less important in fattening anin1als than in
clean pasture with a lai·gely resistant
those to be kept for breeding purposes).

parasite population.

The strategic use of antllelmintics is

Finally, the development of multiple drug
designed to reduce the build up of wonn
resistance in populations of H a.emonchus
burdens and, as a result, pasture contanlina
contorlus, Trichoslrongylus spp, and
tion. The tinling of anthelmintic treatment is

Osterlagia spp in sheep and goats to
based on knowledge of tile seasonal
benzimidazoles, levanlisole, and avermecchanges in infection and the regional tins/milbemycins has been demonstrated.

epidenliology of tl1e various helmintlloses.

Although such resistance is cmTently a

Prompt recognition of circun1stances likely
problem only in certain areas, it should be
to favor development of pai·asitic disease,
considered when other factors have been
eg, weather, grazing behavior, and loss of
excluded, such as improper dosage, rapid
weight and condition, is essential.

reinfection, poor nutrition, or some disease

For exainple, in tile UK, where the pattern
state other than parasitism. Drug resistance
of disease caused by Nemalodirus ballus

GASTROINTESTINAL PARASITES OF RUMINANTS

307
infection in sheep is clearly defined,
anthelmintics in cor\junction with pasture
strategic treatments with two or three doses management to limit reinfection; the latter of an anthelmintic at 2- to 3-wk inteivals,
includes a move to "clean" pastures ( eg,
beginning just before the disease charactergrass conseivation areas or silage or hay istically appears, are recommended. The
aftermath, although anthel.rnintic resistance
timing of these treatments is designed to
concerns should be noted [above]),

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coincide with peak numbers of Nemalodi
alternate grazing with other host species,
rus laivae on pasture in the spring; timing of or integrated rotational grazing in which the latter can be predicted accurately using
susceptible calves are followed by immune
a simple formula that incorporates soil
adults. Alternate grazing with other host
temperatures 1 ft below the surface during
species may be ineffective in areas where

March. Similarly, in the northern USA,
parasite species ( eg, Nematodirus) infect

Canada, and western Europe, pasture levels
both hosts; simple pasture rotation is not
of Osterlagia and other parasites increase
effective, because the bovine fecal mass can
substantially after mid-July, ie, the general
protect laivae from adverse enviroru11ental
pattern of infectivity is minimal in spring
conditions for several months, infecting
but increases rapidly to peak levels in late
rotating calves at a later date.

summer and early fall. Current practices in

In beef herds, anthelmintic treatment at
these areas indicate the effectiveness of
weaning is of value, particularly iitl1e yotmg
two or more carefully timed anthelmintic
cattle are to be retained, eg, as replacement
treatments given during the first grazing
heifer stock or as steers to be fed. Cattle
season after turnout in the spring.

finished on grass should receive treatment

Calculating the inteival between treatments
at weaning and at inteivals tllroughout the
requires knowledge of the parasite's
next 12 mo and, if possible, should be
prepatent period (3 wk in the case of
moved to safe pastmes to maxin1ize

Osterlagia in cattle) and the duration of
liveweight gain.

residual ( or prolonged) activity of the

When cattle carmot be moved readily
anthelmintic being used, ie, the period of
to other pastmes, strategic treatments
protection provided after a single treatment;

(described earlier) may be given to limit
the treatment inteival is calculated as the
contanlination of pastures and rapid
sum of the two. For example, treatment
reinfection. Alternatively, intranmlinal
with a macrocyclic lactone with a 5-wk
boluses may be used in countlies where
period of residual activity at turnout and
approved. In warm temperate regions of tl1e
again 8 wk later should result in highly
world, such as Australia and New Zealand,
effective control of wonn egg output and
the southern USA, and the large cattleminin1al numbers of laivae appearing on raising regions of southern Brazil, Uruguay,
pasture during tl1e fall. No furtl1er treatment
and Argentina, young cattle may be given
is likely to be required, because any laivae
two or more treatments from late SU1111T\er
surviving on pastme from the previous year
and into fall for prevention of large
would have died by the time the prophylactic increases in pasture contan1ination and effect of the second treatment had worn off.

infection during winter and sp1ing. Two or

In other countries, with either a cool or
three strategic treatments, administered
warm temperate climate, similar controls
with a short interval, from the time of
may be used if the seasonal pattern of the
weaning in such regions could be just as
disease is known, but in most regions a
effective as spring treatments in cool
tactical use of anthelmintics is used, eg,
temperate regions. However, survival of
during warm, moist conditions.

infective laivae on pastme from tl1e time of
fall weaning in warm temperate regions is
most often persistent, and longer intervals

Cattle-Special Considerations
between treatlnents ( eg, at weaning, during

Worm problems are seen most frequently in
winter, and in late spring) may be more
young beef cattle from time of weaning and
applicable. In many areas, antllelmintics
several montlls thereafter, and in segregated are simply given at regular intervals after groups of dairy calves during the first
weaning. Inteivals between treatments
season at grass. Immunity to GI nematodes
must necessarily vary according to local
is acquired slowly; two grazing seasons may
parasite epidemiology and tlle duration
be required before a significant level is
of prolonged activity exhibited by the
attained. In endemic areas, cows may
anthelmintic. When Type II ostertagiosis is
continue to harbor low burdens, which may
a problem, treatment with an antl1elmintic
contribute to suboptimal production on
effective against inhibited laivae is
some farms. GI parasitism in young stock
recommended before the expected time
may be controlled by use of broad-spectrum of outbreak.

308

GASTROINTESTINAL PARASITES OF RUMINANTS

Sheep-Special Considerations
large stomac� worm, wire wonn), Osterta

A special strategic treatment is required in
gw, ostertagi (medium or brown stomach
most regions to counter the postparturient
worm), and Trichostrongylus axei (small
relaxation of immunity (resulting in the
stomach worm, seep 319). In some tropical
periparturient rise in worm egg output) seen countries, Mecistocirrus digi/,atus, a large VetBooks.ir
m breeding ewes. The precise timing of such wom1 up_to 40 mm long, is present. H placei treatment varies between regions and for
is pnmanly a parasite in tropical regions,
different species of parasites and will in
whereas O ostertagi and, to a lesser extent, temperate regions, depend on wheth�r ewes T axei are found in more temperate and lambs are turned out onto clean or
climates. Adult male Haemonchus are
contaminated pasture. On clean grazing,
up to 18 mm long, females up to 30 mm.

only the ewes ( with an existing parasite

Ostertagia adults are 6-9 mm long and
burden) act as a source of worm eggs and

Trichostrongylus, -5 mm.

'

therefore, require treatment to prevent

The preparasitic life cycles of the three
pasture contamination and subsequent
groups are generally similar. Larvae hatch
infection of their lambs. Ewes treated
shortly after the eggs are passed in the feces
during the month before lambing should not
and reach the infective stage in -2 wk under
only exhibit a drop in wom1 egg output but
optimal temperatures (-75°F [24°C]).

may also show improved productivity. On

Development to the infective stage is
contaminated pasture, both ewes and lan1bs
delayed during cold weather. In areas with
pass worm eggs in their feces ( ewes from
narrow diurnal temperature variations
their existing wom1 burden and lambs from
those months with a mean maximum '

larvae overwintering on pasture). The aim
temperature of 65°F ( l8°C) and with rainfall
of treating ewes should be to prevent fecal

>2 in. (5 cm) are favorable for development
worm egg output; this can be achieved by
of the free-living stages of H placei, but
treating with an albendazole or ivermectin
where wide fluctuations occur , a mean
anthelmintic bolus (available in some
minimum temperature of 50°F ( 10°C) may
countries), iI\iectable long-acting moxideceffectively limit development. The tin, or medicated feed blocks. In temperate
preparasitic forms of O ostertagi and T axei areas, lambs should be dosed at weaning
develop and survive better in cooler
before a move to clean grazing.

conditions, and their upper limits for sur

A treatment 2 wk before breeding as part
vival are lower than those for H placei. If of a ''.flu�hing" program, is another strategic the ten:iperature is unfavorable or drought
application of anthelmintics. Supportive
conditions eXIst, infective larvae may
management after treatment includes moveremain dormant in the feces for weeks until ment of sheep from contaminated pastures
conditions become favorable again eg after
to cattle pastures, grass conservation areas
heavy rainfall, when large numbers' of
root crops, or pasture not grazed by sheep '

infective larvae emerge onto the surroundfor several months. The latter period varies ing grass.

according to the seasonal pattern of larval

The prepatent period of O ostertagi is
mortality in different countries and may be
normally -3 wk. Ingested larvae enter the
as long as 1 yr in some temperat� countries.

lumen of the abomasal glands and molt by

Sheep are more consistently susceptible
the fourth day; they remain there during the
to the adverse effects of worms than other
prepatent period, growing and undergoing a
livestock, and clinical disease is more
final molt before emerging as young adult
common. lnlmunity to the parasites is
acquired slowly and is generally incomplete.

Frequent treatments may be required,
particularly during the first year of life,
although a good understanding of local
parasite epidemiology will ensure that
such treatments are appropriately timed.

Haemonchus, Ostertagia, and

Trichostrongylus spp

The common stomach worms of cattle are

Abomasal lesions due to Ostertagia. Courtesy

Haemonchus placei (barber's pole worm,
of Or. Sameeh M. Abutarbush.

GASTROINTESTINAL PARASITES OF RUMINANTS

309
worms from the gastric glands onto the
parturition, nutrition, concurrent infection,
abomasal mucosa. During this time, the
and host immune response.

specialized cells (pepsinogen-producing

H placei may also become inhibited over
zymogen cells, acid-producing parietal
winter; they then resume development in
cells) lining parasitized glands are lost and
the spring and infect the pastures with eggs
replaced by hyperplastic, undifferentiated
at a time suitable for their development.

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cuboidal cells, resulting in nodules that may

Both the larval and adult stages are pathobe discrete or confluent. Around the time of genic because of their blood-sucking ability.

worm emergence, the changes seen in

T axei causes gastritis with superficial
parasitized glands also appear in neighborerosion of the mucosa, hyperemia, and ing nonparasitized glands, rapidly extending
diarrhea. Protein loss from the damaged
the effects of the parasite burden. As a
mucosa and anorexia cause hypoproteineresult, in heavy infections, abomasal pH
mia and weight loss. Inhibition does not
may rise from 2 to >6; from a clinical
occur to the same degree.

viewpoint, when pH rises above 4.5,
digestion in the abomasum ceases. A
protein-losing gastropathy results and,

Clinical Findings: Yom1g animals are
together with anorexia and impaired
more often affected, but adults not
protein digestion, leads to hypoproteinemia
previously exposed to infection frequently
and weight loss. Diarrhea is persistent. In
show signs and succumb. Ostertagia and

Type I ostertagiosis, which results from Trichostrongylus infections are characterrecent infection, most worms present are ized by profuse, watery diarrhea that usually
adults, and the response to anthelmintic
is persistent. In haemonchosis and
treatment is good. Type I disease is seen

Mecistocirrus infection, there may be little primarily in calves 7-15 mo old. It is most
or no diarrhea but possibly intermittent
common from time of weaning and ensuing
periods of constipation. Anemia of variable
months in warm temperate regions and in
degree is a characteristic sign of both these
young cattle during summer and early fall in
infections.

cool temperate regions.

Concurrent with the diarrhea of

In Type II ostertagiosis, large numbers O ostertagi and T axei infections, and with of larvae, which had become dormant or
the anemia of heavy Haemonchus infection,
inhibited in development at the early fomth
there is often hypoproteinemia and edema
larval stage, emerge from the glands weeks

(rare in O ostertagi infections), particularly or months later. This is seen primarily in
under the lower jaw (bottle jaw) and
cattle 12-20 mo old. In warm temperate
sometimes along the ventral abdomen.

regions, inhibition-prone larvae are acquired Heavy infections can result in death before in spring, and disease may result when large
clinical signs appear. Other variable signs
numbers of larvae resume development to
include progressive weight loss, wealrness,
the adult stage in late summer or fall. In cold
rough coat, and anorexia.

temperate regions, inhibition-prone larvae

Lesions: WomlS can readily be seen and
are acquired during late autumn and mature
identified in the abomasum, and small
during late winter or early spring.

petechiae may be visible where the wornlS

Larval inhibition in O ostertagi and other
have been feeding. The most characteristic
nematodes is thought to be analogous to
lesions of Ostertagia infection are small,
diapause in insects. It has been interpreted
umbilicated nodules 1-2 mm in dian1eter.

as a survival mechanism in which the

These may be discrete, but in heavy
preparasitic stages on pasture avoid the
infections they tend to coalesce and give rise
adverse conditions of winter in cool regions
to a "cobblestone" or "morocco leather"

and of hot and dry ( or hot and alternately wet appearance. Nodules are most marked in the and dry) conditions of many warm regions.

fundic region but may cover the entire

The factors that cause and later "switch off''

abomasal mucosa and may be accompanied
inhibition are not completely known, but
by a rise in gastric pH to 6---7. As a result,
prolonged experimental cold conditioning of
pepsinogen will no longer be converted to
infective larvae was found to be in1portant in
pepsin and may leak across the damaged
a cool temperate region. In warm regions of
epithelium, leading to high plasma levels.

both northern and southern hemispheres,

TI1ere is also evidence that adult Ostertagia
conditioning of preparasitic stages to
can cause direct hypersecretion of pepsinoinhibition develops principally during spring gen. The increased abomasal pH may also
before the hot and dry conditions of sun1mer. stin1ulate production of gastrin and thus The resumed development or maturation of
hypergastrinemia, which is closely associated
the parasites is likely to be genetically
with the inappetence that may accompany
predetemiined and may be influenced by
infection. Tilis parasite-associated drop in

310

GASTROINTESTINAL PARASITES OF RUMINANTS
intake has been shown to be largely
and rapid weight loss. Diarrhea and
responsible for impaired weight gain. Edema
constipation may alternate. Hypoproteineis often marked and, in severe cases, may mic edema may be present, but bottle jaw is
extend over the abomasum and into the small
rarely as severe as in haemonchosis. Dming
intestine and omentW11.

tl1e patent period, a diagnosis may be made

In T axei infections, the mucosa of the
by demonstrating the characteristic eggs in

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abomasum may show congestion and superthe feces.

ficial erosions, which are sometimes

On necropsy, the mucosa may appear
covered with a fibrinonecrotic exudate.

congested and swollen, with numerous
small hemorrhagic points where the worms

Diagnosis, Treatment, and Control:

were attached. The worms are readily seen

Seep 303 et seq.

in the first few feet of the small intestine,
and the contents are often blood-stained.

Cooperiaspp

As few as 2,000 worms may cause death in

Several species of Cooperia are found in
calves. Local lesions, edema, and scab
the small intestine of cattle; C punclala,
fom1ation may result from penetration

C oncophora, and C peclinata are the most of larvae into the skin of resistant calves.

common. The red, coiled adults are 5-8 mm

For diagnosis, treatment, and control,
long, and the male has a large bmsa. They
see p 303 et seq.

may be difficult to observe grossly. Their life
cycle is essentially the same as that of other

Strongyloides sp
trichostrongylids. These worms apparently

The intestinal thread worm Strongyloides
do not suck blood. Most of them are found
papillosus has an wmsual life cycle. Only
in tl1e first 10---20 ft (3----6 m) of the small
the female worms are found in the intestine.

intestine. The prepatent period is 12-15 days.

They are 3 .5-6 mm long and are embedded

The eggs usually can be differentiated
in the mucosa of the upper small intestine.

from those of the common GI nematodes by

Small, embryonated eggs are passed in the
their practically parallel sides, but a larval
feces, hatch rapidly, and develop directly
cultme of the feces is necessary to
into infective larvae or free-living adults.

definitively diagnose Cooperia infection in The offspring of these free-living adults may
the living animal. ln heavy infections with
develop into another generation of infective

C punclala and C peclinala, there is larvae or free-living adults. The host is
profuse diatThea, anorexia, and emaciation,
infected by penetration of the skin or by
but no anemia; the upper small intestine
ingestion; infective larvae can be transmitshows marked congestion of the mucosa ted in colostrun1 as in other species of the
with small hemorrhages. The mucosa may
genus. The prepatent period is -10 days.

show a fine lace-like superficial necrosis.

Infections are most common in yoWlg

C oncophora produces a milder disease but
calves, particularly dairy stock. Although
can be responsible for weight loss and poor
signs are rare, they may include intermittent
productivity. It is usually necessary to make
diarrhea, loss of appetite and weight, and
scrapings of the mucosa to demonstrate
sometimes blood and mucus in the feces.

Cooperia spp, which must be differentiated

Large numbers of worms in the intestine
from Trichoslrongylus spp, Strongyloides produce catarrhal entetitis with petechiae
papillosus, and in1matme Nemalodirus spp.

and ecchymoses, especially in the

For diagnosis, treatment, and control, see
duodenw11 andjejunum.

p303 et seq.

For diagnosis, treatment, and control, see
p303 et seq.

Bunostomum sp

The adult male Bunoslomum phlebolo

Nematodirus spp
mum is -15 mm long and the female -25 mm. Nemalodirus helvelianus is generally Hookwom1s have well-developed buccal
recognized as the most common bovine
capsules into which the mucosa is drawn;
species, although other species, eg, N
cutting plates at the anterior edge of the
spathiger and N ba.ttus, can also infect buccal capsule are used to abrade the
cattle. The adult males ofN helvetianus are mucosa dming feeding. The prepatent

-12 mm long and the females 18--25 mm. The
period is -2 mo. Infection is by ingestion or
eggs develop slowly; the infective third stage
skin penetration; the latter is more common
is reached within the egg in 2 -4 wk and may
in animals kept in poor conditions.

remain within the egg for several months.

Larval penetration of the lower limbs may

Eggs may accwnulate on pastme and hatch
cause uneasiness and statnping, particularly in lai·ge numbers after rain to produce heavy in stabled cattle. Adult wom1s cause anemia
infections over a short petiod. The eggs are

GASTROINTESTINAL PARASITES OF RUMINANTS

311
highly resistant, and those passed by calves
head is bent dorsally. Because the eggs are
in one season may remain viable and infect
very sinillar to those of Haemonchus
calves the next season. After ingestion of
pla.cei, they are often grouped together on infective larvae, the adult stage is reached in
routine fecal examination. The life cycle is

-3 wk. Wonns are most nwnerous 10--20 ft
direct. The larvae penetrate primarily into

(3--6 m) from the pylorus.

the wall of the lower 10--20 ft (3--6 m) of the

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Signs, which include diarrhea and
small intestine but also into the cecum and
anorexia, usually develop during the third
colon, where they remain for 5--10 days and
week of infection before the worms are
then return to the lumen as fourth-stage
sexually mature; clinical infections may
larvae. The prepatent period in susceptible
be seen in dairy calves from 6 wk onward.

animals is -6 wk. However, in subsequent

Diagnosis is difficult during the prepatent
reinfections, larvae become arrested for
period, but during the patent period it is
some time, and many never return to the
easily made on the basis of the characterlumen (host encystment).

istic eggs. Relatively small numbers of

Young animals suffer from the effects of
eggs are produced. Fecal sampling of both adult worms, whereas in older animals, the healthy and sick calves in an affected
effect of nodules enclosing larval worms is
group will increase the chance of making
more important. Infection causes anorexia;
a diagnosis. Immunity to reinfection
severe, constant, dark, persistent, fetid
develops rapidly. Necropsy may show
dian-hea; weight loss; and death. In older,
only a thickened, edematous mucosa.

resistant animals, the nodules surrounding

For diagnosis, treatment, and control, see
the larvae become caseated and calcified,
p303 et seq.

thus decreasing the motility of the intestine.

Stenosis or intussusception occasionally

Toxocarasp
occurs. Nodules can be palpated per

The ascarid Toxocara vitul01um is a stout,
rectun1, and the wom1S and nodules can
whitish wonn (males 20--25 cm, females
be seen readily at necropsy.

25--30 cm) found in the small intestine of

For diagnosis, treatment, and control, see
calves <6 mo old; older calves are resistant.

p303 et seq.

Larvae hatching from ingested eggs pass to
the tissues and, in pregnant cows, are

Chabertia sp
mobilized late in pregnancy and passed via
the milk to calves. Eggs appear in the feces

Adults of the large-mouth bowel wonn,
of calves from 3 wk of age and are easily

Chabertia ovina, are -12 mm long and bent
recognized by their thick, pitted shells and
ventrally at the anterior end. There is a
dark brown center. In some parts of the
typical direct life cycle. The larvae penetrate
world, the infection is considered serious,
the mucosa of the small intestine shortly
particularly in buffalo calves.

after ingestion and later emerge and pass

For diagnosis, treatment, and control, see
to the colon. The prepatent period is - 7
p303 et seq.

wk. Larvae and adults may cause small
hemorrhages with edema in the colon and
passage of feces coated with mucus. Clinical

Oesophagostomum sp
chabertiosis is seldom, if ever, seen in cattle.

Adults of Oesophagostomum radiatum

For diagnosis, treatment, and control, see

(nodular wom1) are 12-15 mm long, and the
p303 et seq.

Trichuris ovis attached to intestinal wall of a Toxocara canis egg. Courtesy of Dr. Mark Fox.

sheep. Courtesy of Dr. Raffaele Ronca/Ii.

312

GASTROINTESTINAL PARASITES OF RUMINANTS

Trichuris spp
sion of H aemonchus between sheep and

Trichwis spp infections are common in
cattle can occur but not as readily as
young calves and yearlings, but the numbers transmission between homologous species.

of worms are seldom large. The eggs are

Sheep are more susceptible to the cattle
resistant, and infections are likely to persist
species than cattle are to the sheep species.

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on problem premises. Clinical signs are

For descriptions and life cycles, seep 308.

unlikely, but in occasional heavy infections,

Haemonchus is most common in tropical
dark feces, anemia, and anorexia may be
or subtropical areas or in those areas with
seen.

summer rainfall, whereas Ostertagia and

For diagnosis, treatment, and control, see

T a.xei are more common in cooler winter
p303 et seq.

rainfall areas. The latter species predominate in temperate zones.

Tapeworms

Ha.emonchosis in sheep may be classified
as hypera.cute, a.cute, or chronic. In the

The anoplocephalid tapeworms Moniezia
hypera.cute disease, death may occur within
expansa and M benedeni are found in 1 wk of heavy infection without significant
young cattle. The wonns of this group are
signs. The a.cute disease is characterized by
characterized by the absence of a rostellum
severe anemia accompanied by generalized
and hooks, and the segments are wider than edema; anemia is also characteristic of the they are long. The eggs are triangular or
chronic infection, often of low worm
rectangular and are ingested by the
burdens, and is accompanied by progressive
intermediate host, free-living oribatid mites, weight loss. Diarrhea. is not a sign of pure which live in the soil and grass. After 6---16 wk, Haemonchus infection; the lesions are infective cysticercoids are present in the
those associated with anemia. In cases in
mites. Infection occurs after ingestion of
which diarrhea. is present, there may be
infected mites; the prepatent period is -5 wk.

mixed infection with other worm genera.

Moniezia are commonly considered

The a.bomasum is edematous and, in the
nonpa.thogenic in calves, but intestinal
chronic phase, gastric pH increases, which
stasis has been reported.

causes abomasal dysfunction. Mature sheep

For diagnosis, treatment, and control, see
may develop heavy, even fatal, infections,
p 303 et seq.

particularly during lactation.

The lesions, pathogenesis, and signs of

Ostertagia and T a.xei infections are similar to those found in cattle. Even subclinical
infection depresses appetite, in1pa.irs gastric
digestion, and reduces use of metaboliza.ble
energy and protein. Ostertagia is the

Many species of nematodes and cestodes
principal genus involved in the peripa.rturi-
cause parasitic gastritis and enteritis in
sheep and goats. The most in1portant of
these are Haemonchus contortus,

Teladorsagia (Ostertagia.) circumcincta,

Trichostrongylus a.xei, intestinal species of Trichostrongylus, Nematodirus spp,

Bunostomum trigonocephalum, and

Oesophagostomum columbianum.

Cooperia curticei, Strongyloides
papillosus, Trichuris ovis, and Chabertia ovina also may be pathogenic in sheep;
these and related species are discussed
under GI parasites of cattle (seep 308).

Haemonchus, Ostertagia, and

Trichostrongylus spp

The principal stoma.ch worms of sheep and
goats are Haemonchus contortus,

Teladorsagia (Ostertagia) circumcincta,

Ostertagia trifurcata, Trichostrongylus
a.xei ( see GASTROINTESTINAL PARASITES OF CATTLE, p 308), and in some tropical regions,

Haemonchus contortus, heavy infestation,
abomasum of a shee

Mecistocirrus digitatus. Cross-transmis-
p. Courtesy of Dr. Raffaele

Ronca/Ii.

GASTROINTESTINAL PARASITES OF RUMINANTS

313
ent rise in fecal egg counts in sheep, and
winter, with large nw11bers of larvae
heavy infections may cause diarrhea and
appearing during the early grazing period of
depress milk production in ewes. This
the following year. Thus, the lambs of one
output of eggs serves as the main source of
season contaminate the pastures for the
contamination for the lambs. The same type
next season's lambs; fortunately, the life
of inhibited development seen in cattle has
cycle can be broken if the san1e area is not

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been seen with both Ostertagia and
used for lambing each year. Most clinical

Haemonchus in sheep.

infections are seen in lambs 6-12 wk old.

For diagnosis, treatment, and control, see

N battus is seen in the UK and other parts
p 303 et seq.

of Europe and also in North America. Eggs
hatch after a period of chill and then a 1ise in

Intestinal Trichostrongylosis
ambient temperature to a day/night mean of

The life cycle of intestinal Trichostrongylus 10°C (50°F). This occurs in late spring in (Tcolubriformis, Tvitrinus, Trugatus) is
temperate areas. The hatching requirement.<;
direct. The developing larvae burrow
mean that there is generally one generation
superficially in the crypts of the mucosa and of N battus per year, although in the UK, develop to egg-laying adults in 18-21 days.

occasional outbreaks in the autunm have

Anorexia, persistent diarrhea, and weight
been repmted. The parasite can be highly
loss are the main signs. Villous atrophy ( or
pathogenic, because large numbers of
stunting of villi) results in impaired digestion
larvae hatch over a short period at a tin1e
and malabsorption; protein loss occurs
when young lambs are beginning to take in
across the damaged mucosa. There are no
significant quantities of grass. Disease may
diagnostic lesions; a total worm count
be associated with developing larval stages
should be done to evaluate the condition.

and may be seen within 2 wk of challenge,

For diagnosis, treatment, and control, see
ie during the prepatent period (15 days).

p 303 et seq.

Other Nematodirus spp often are fow1d in
low-rainfall regions ( eg, the Karroo in South

Sunostomum and Gaigeria spp

Africa and inland Australia) where other
parasites are rarely seen.

AdultBunostomum trigonocephalum

Nematodirosis is characterized by sudden

(hookwom1) are found in the jejtmtm1. The
onset, "loss of bloom," tmthriftiness, profuse life cycle and clinical findings are essentially diarrhea, and marked dehydration, with the same as for the cattle hookworm ( see
death as early as 2-3 days after an outbreak
p 310), with as few as 100 worms causing
begins. Nematodirosis is commonly
clinical signs. Gaigeria pachyscelis is
confined to lambs or weaner sheep, but in
found in Africa and Asia and resembles
low-rainfall count1y where outbreaks are

Bunostomum in size and fo1m (2-3 cm).

sporadic, older sheep may have heavy

Larvae of G pachyscelis infect the host only infections. The lesions usually consist of
by skin penetration. G pachyscelis is a
dehydration and a nilld catarrhal enteritis,
voracious bloodsucker and probably the
but acute inflanunation of the entire small
most pathogenic hookwonn.

intestine may develop. Counts of� 10,000

For diagnosis, treatment, and control, see
wom1s, together with characteristic signs
p 303 et seq.

and histmy, are indicative of clinical
infections. Affected lambs may pass large

Nematodirus spp
nun1bers of eggs, which can be identified
easily; however, because the onset of

The species of Nematodirus found in the
disease may precede the maturation of the
small intestine of sheep are sinillar in
female worms, this is not a constant finding.

morphology and life cycle to N helvetianus

For diagnosis, treatment, and control, see

(seep 310). Clinical infections are of
p 303 et seq.

considerable importance in the UK, New

Zealand, and Australia, where lamb
mortality may reach 200/o in affected flocks

Oesophagostomum sp
if anin1als are untreated. The parasites are

The nodular worm of sheep, Oesophagosto
also endemic in some parts of the Rocky
mum columbianum, has a similar morphol

Mountain states of the USA, where they
ogy and life cycle to those of the nodular
occasionally cause clinical disease in lan1bs.

worm of cattle ( see p 311 ).

In areas where clinical infections are

Diarrhea usually develops druing the
common, the disease has a characteristic
second week of infection. The feces may
seasonal pattern. Many of the eggs passed
contain excess mucus as well as streaks of
by affected lambs lie dormant through the
blood. As the diarrhea progresses, sheep
remainder of the grazing season and the
become emaciated and weak. These signs

314

GASTROINTESTINAL PARASITES OF RUMINANTS
often subside near the end of the prepatent
skin between the claws, produced by
period, but the continuing presence of
skin-penetrating larvae, resembles the
numerous adult worms may result in a
early stages of footrot and may aid
chronic infection in which signs may not
penetration of the causal agents offootrot.

develop for several months. The sheep

Most infections are transitory and
become weak, lose weight despite a good
inconsequential.

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appetite, and show intennittent diarrhea

For diagnosis, treatment, and control, see
and constipation.

p 303 et seq.

As inununity develops, nodules form
around the larvae; they may become
caseated and calcified. Nodule forn1ation

Trichuris spp
usually is more pronounced in sheep than in

Heavy infections with whipworn1s are not
cattle. Affected sheep walk with a stilted
common but may be seen in very young
gait and often have a humped back. Stenosis lambs or during drought conditions when and intussusception may develop in severe
sheep are fed grain on the ground. The eggs
cases. Diagnosis is difficult during the
are very resistant. Congestion and edema of
prepatent period, at which tin1e it must
the cecal mucosa, accompanied by diarrhea
be based largely on clinical signs.

and unthriftiness, are seen.

For diagnosis, treatment, and control, see

For diagnosis, treatment, and control, see
p303et seq.

p303et seq.

Chabertia sp

Tapeworms

Adult worms cause severe damage to

The pathogenicity of Moniezia, e:rpa,nsa, in the mucosa of the colon, with resulting
sheep has long been debated. Many earlier
congestion, ulceration, and small
observations, which associated this
hemorrhages. Infected sheep are
infection with dia.tThea, emaciation, and
unthrifty; the feces are soft, contain much
weight loss, did not accurately differentiate
mucus, and may be streaked with blood.

between tapeworm infections and infection

Immunity develops quickly, and outbreaks with certain small nematodes ( eg, are seen only under conditions of severe

Trichostrongylus colubriformis ).

stress.

Tapewonns are relatively nonpathogenic,

For diagnosis, treatment, and control, see
but heavy infections can result in mild
p303et seq.

unthriftiness and GI disturbances.

Diagnosis may be made by finding

Strongyloides sp
individual segments (which are much wider

Heavy infections with adult worms cause a
than long) in the feces or lengths of adult
disease resembling trichostrongylosis.

tapeworn1 protruding from the anus or by

Infection is usually by skin penetration but
demonstrating the characteristic eggs on
can also occur via the milk. Damage to the
fecal examination. The life cycle involves an
oribatid mite that lives in the pasture mat.

The prepatent period is 6-7 wk. Infections
are seasonal, in accordance with mite
activity, and unusual in anin1als older tha.i.1

-4-5 mo of age.

Thysa,nosoma, a,ctinioides, the "fringed tapeworm," inhabits the �mall intestine, the
bile ducts, and the pancreatic ducts. It is
commonly found in sheep from the
southern and western parts of the USA and
also South America. Although it has not
been associated with clinical disease, it is
of economic importance because livers are
condenmed when tapeworms are found in
the bile duct.

Thysanosoma aetinioides, adult, in a sheep.

For diagnosis, treatn1ent, and control, see

Courtesy of Dr. Raffaele Roncalli.

p303 et seq.

GASTROINTESTINAL PARASITES OF HORSES

315

GASTROINTESTINAL PARASITES OF HORSES

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GASTEROPHILUS SPP
they pass in the feces. ln the USA, the
presence of gastric infections during the

Horse bots, which are found in the stomach,
winter months is often assw11ed. History of
are the larvae of bot flies, Gasterophilus
the individual horses, knowledge of the local
spp. Three major species are distributed
seasonal cycle of the fly, and observation of
worldwide, and a number of minor species
the yellow to cream-white bot eggs ( 1-2 mm)

are found in parts of Europe, Africa, and
on the horse's hairs all help identify the

Asia. The adult flies are not parasitic and
presence of the parasite in a given herd.

cannot feed; they survive long enough to
mate and lay eggs and die as soon as the
nutrients remaining from the larval stage

Treatment: ln temperate areas, it is
are used, usually in -2 wk. The three
asswned that most animals are infected by
important species can be differentiated in
the end of swnmer. lvem1ectin is effective
any stage of their development. The eggs of
against oral and gastric stages of bots and, G intestinalis (the common bot) are glued
when used as part of a routine parasite
to the hairs of almost any part of the body
control program, provides effective bot
but especially the forelin1bs and shoulders.

control throughout the season. In subtropi

The larvae hatch in -1 wk when stimulated,
cal or tropical areas, some transmission
usually by the animals' licking. The eggs of
may occur throughout the year. Moxidectin

G haemorrhoidalis (the nose or lip bot) are
is effective against gastric stages. Cunent
attached to the hairs of the lips. The larvae
recommendations for control include at
emerge in 2-3 days without stimulation and
least one treatment annually, at the end of
crawl into the mouth. G nasalis (the throat
the bot fly season. In some locations where
bot) deposits eggs on the hairs of the
the bot fly season is long, additional
submaxillary region. They hatch in -1 wk
treatments may be necessary. Although
without stimulation.

there is no satisfactory method to protect

The larvae of all three species apparently
exposed horses from attack by the adult
stay embedded in the tongue or the mucosa
flies, bot control programs, when applied on
of the mouth for -1 mo, after which they
a regional basis to all horses, markedly
pass to the stomach, where they attach
reduce fly numbers and larval infections.

themselves to the cardiac or pyloric
portions and, in the case of G nasalis, to
the mucosa of the first part of the small

HABRONEMA SPP
intestine. After development for -8---10 mo,

The stomach wom1s H abronema muscae,
they pass out in the feces and pupate in the

H microstoma, and Draschia megastoma
soil for 3-5 wk, after which the adult
are widely distributed. The adults are 6---25
emerges. The main pathogenic effect is
mm long. Draschia are found in tun10r-like
caused by larvae, which attach by oral
swellings in the stomach wall along the
hooks to the lining of the stomach. This
margo plicatus. The other species are free
induces erosions and ulcerations at the site
on the mucosa. The eggs or larvae are
of attachment and a hyperplastic reaction
ingested by larvae of house or stable flies,
around it. However, oral stages may cause
which serve as intem1ediate hosts. Horses
sinus tracts in which mucopurulent
are infected by ingesting flies that contain
discharges fonn, especially along the lingual infective laivae or by free larvae that emerge border of the upper, more posterior cheek
from flies as they feed around the lips. (See
teetl1.

also CUTANEOUS HABRONEMIASIS, p 904.)

A catarrhal gastritis may result from

Clinical Findings and Diagnosis: Bots
heavy infections with adult wonns.

cause a mild gastritis, but large nun1bers

Draschia produces the most severe
may be present with no clinical signs. The
lesions-tun10r-like enlargements up to
first instars migrating in the mouth can

10 cm in diameter. These are filled with
cause stomatitis and may produce pain on
necrotic material and a large number of
eating. The adult flies may annoy horses
worms and are covered by intact epithewhen tl1ey lay their eggs. Specific diagnosis limn, except for a small opening tl1rough
of Gasterophilus infection is difficult and which the eggs pass. Rarely, these nodules
can be made by demonstrating larvae as
rupture and cause fatal peritonitis. Larvae of

316

GASTROINTESTINAL PARASITES OF HORSES

H abronema spp and Draschia have been 10-12 wk Large numbers of infective eggs
found in the lungs of foals associated with
can remain viable for years in contanlinated

Rhodococcus equi abscesses (seep 1451).

soil. Adult animals usually harbor very few

Clinical signs usually are absent except
if any worms. The principal sources of
when, rarely, granulomas associated with
infection for young foals are pastures,

Draschia infection lead to mechanical
paddocks, or stalls contanlinated with eggs

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obstruction or rupture.

from foals of the previous year.

Antemortem diagnosis is difficult,

In heavy infections, tl1e migrating larvae
because the eggs are not easily detected
may produce respiratory signs ("sun1mer
using standard fecal flotation methods.

colds"). In heavy intestinal infections, foals

Molecular methods have recently been
show unthriftiness, loss of energy, and
developed for this purpose but would not be occasionally colic. Intestinal obstruction useful for routine use. Wom1s and eggs may
and perforation have been reported.

be found by gastric lavage. Most anthelnlin

Intestinal stages compete for absorption of
tics have not been tested againstHabro
essential anlino acids. Diagnosis is based
nema spp or Draschia sp, although
on demonstration of eggs in the feces. If
ivermectin is effective against their
disease due to prepatent infection is
cutaneous larvae and against adults of
suspected, diagnosis may be confirmed by

H muscae. Moxidectin is also effective
administration of an anthelmintic, after
against adult H muscae.

which large numbers of in1mature worms
may be seen in the feces.

OXYURISSP

On farms where the infection is common,
most foals become infected soon after birth.

Adult pinwom1S, Oxyuris equi, are more

As a result, most of the wom1s are maturing
common in horses <18 mo old and are found when the foals are -4-5 mo old. Treatment primarily in the tem1inal portion of the large
should be started when foals are -8 wk old
intestine. The females are 7.5-15 cm long;
and repeated at 6- to 8-wk inteivals until
males are smaller and fewer in number. The
they are yearlings. All broad-spectrum
gravid females pass toward the rectum to
equine anthel111intics are effective against
lay their eggs, "cementing" them to the
the adult and immature worms in the small
perineum around the anus. Masses of eggs
intestine and, therefore, ascatids are readily
and cement around the anus appear as a
controlled by routine anthelnlintic
white to yellow, crusty mass. The eggs,
administration. However, there have been
which are flattened on one side, become
reports of resistance of P equorum to
embryonated in a few hours and are
ivermectin and moxidectin in North
infective in 4-5 days.

America and Emope. Efficacy on any given

Adult pinwom1S are of little significance
farm should be monitored using a fecal egg
in the intestine but cause perinea! irritation
count reduction test. In cases in which
after egg laying. Rubbing of the tail and anal
veffilinous pneumonia due to Parascaris
regions, with resulting broken hairs and
migration has developed, therapeutic
bare patches around the tail and buttocks, is benefit may be achieved by treatment with characteristic and suggests the presence of
ivermectin or fenbendazole (the latter at
pinwom1s. Fecal exanlination may or may

10 mg/kg/day for 5 consecutive days)

not reveal a pinworm infection. Samples
concmrent with appropriate antinlicrobial
collected around the perinea! region may
therapy. Parascaris infection can be
contain dried female worms or eggs.

effectively prevented by daily ad111inistra

Application of cellophane tape to the skin
tion of pyrantel tartrate once foals are
of the perineum or scraping the area witl1
eating grain regularly.

a tongue depressor may recover ova for
microscopic exanlination, but false-negative LARGE STRONGYLES
tests are common.

Most of tl1e broad-spectrum drugs

The large strongyles of horses ru·e also
recommended for treatment of strongyles
known as blood wom1s, palisade wom1s,

( see below) are effective against pinworms.

sclerostomes, or red worms. The three
major species ru·e Strongylus vulgaris ( µp

PARASCARIS SP
to 25 mm), S edentatus (up to 40 mm), and

S equinus (up to 50 mm). (See also Triodon

AdultPara.scaris equorum are stout,
tophorus spp, below.) Under favorable
whitish worms, up to 30 cm long, with tiu·ee
conditions, the larvae develop to the
prominent lips. The life cycle is sinlilar to
infective stage within 1-2 wk after the eggs
that of Ascaris suum (tl1e roundworm of
are passed. Infection is by ingestion of
pigs, seep 320), with a prepatent period of infective larvae, which exsheath in the intes-

GASTROINTESTINAL PARASITES OF HORSES

317
tine and migrate extensively before developstrongyle infections have been eliminated ing to maturity in the large intestine. The
from closed herds with ivem1ectin
prepatent period is &-11 mo. The larvae of
treatment.

S vulgaris migrate extensively in the cranial Parasite control progran1s are designed to
mesenteric artery and its branches, where
minimize the level of pasture contanlination
they may cause parasitic thrombosis and
and thereby reduce the risks associated

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arteritis. Larvae of the other two species
with migrating larvae. Routine anthelmintic
may be found in various parts of the body,
treatments do this by preventing fecal
including the liver, peri.renal tissues,
excretion of strongyle eggs. (See also
retroperitoneal tissues, and pancreas. These SMALL STRONGYLES, below.) species do not produce lesions in the
mesenteric arteries. Mixed infections of

SMALL STRONGYLES
large and small strongyles are the rule.

More than 40 species of small strongyles

Clinical Findings: Adult large strongyles
in several genera have been found in the
have large buccal capsules and are active
cecum and colon of domestic equids, each
blood feeders; they ingest mucosa! plugs as
with its own site of preference. They have
they move about in the intestine. The
been referred to as trichonemes, cyathoassociated blood loss may lead to anemia.

stomes, and currently cyathostomins. They

Weakness, emaciation, and diarrhea are
belong to the subfantily Cyathostominae of
also common. S vulgaris is important
the family Strongylidae, and -10 species are
because of the dan1age it does to the cranial
particularly prevalent. Most are appreciably
mesenteric artery and its branches. As a
smaller than the "large strongyles," but
result of the interference with the flow of

Triodontophorus spp (sometimes classified
blood to the intestine and th.romboemboas nonmigratory large strongyles) are lism, any of several conditions may follow,
almost as long as Strongylus vulgaris.

including colic; gangrenous enteritis; or

Unlike the large strongyles, small
intestinal stasis, torsion or intussusception,
strongyles do not migrate ext.raintestinally,
and possibly ruptu.re. Cerebrospinal
because early development is confined to
nematodiasis (seep 1312) can cause a
the wall of the intestine. Third-stage larvae
variety of lesions and signs depending on
may progress to the fourth stage without
the part of the CNS affected.

interruption, or they may undergo
hypobiosis and resume development only

Diagnosis and Treatment: Diagnosis
after prolonged periods of dormancy or
of mixed strongyle infection is based on
hypobiosis. When L, emerge from the gut
demonstration of eggs in the feces. Specific
wall, they feed superficially on the mucosa
diagnosis can be made by identifying the
and may ruptu.re capillaries but are less
infective larvae after fecal cultu.re. Serologic pathogenic than the large strongyles. They diagnosis based on a rise in [3-globulins has
molt to the adult stage. An exception is
been recommended but is not specific for

T tenuicollis, which is found in clusters and S '/Yulgaris. Parasitic arterial lesions have can produce severe ulcers in the wall of the
been demonstrated using arteriography in
colon. Generally, however, the resulting
ponies and small horses. Efforts have been
erosions of the mucosa are slight and hard
made to utilize molecular methods and
to visualize. Consequently, it is common to
antibody measu.rements for prepatent
recover thousands of adult wonns from
diagnosis of S vulgaris infections, but these apparently healthy horses that have
techniques are not yet available for standard received limited anthelmintic treatment. In use.

heavier infections, however, disruption may

Colic due to arterial lesions has been
be extensive enough to disttu-b digestive
successfully controlled by anthelmintic
and absorptive function, resulting in loss of
treatments. Ivermectin and rnoxidectin at
condition and even a catarrhal enteritis of
standard dosages are effective against the
the large intestine.

larval stages CL, and L5) of S vulgaris;
fenbendazole and oxfendazole, at dosages

Larval Cyathostominosis: An acute
higher than that for adult parasites, are also
syndrome of sudden weight loss, often with
effective against larval infections. Daily
severe diarrhea, is seen in temperate areas
administration of pyrantel tart.rate
in late winter and spring, particularly in
effectively prevents establishment of
young ponies and horses ( <5 yr old). This
arterial stages of S vulgaris. A number of
is associated with mass emergence of
anthelmintics, including the benzinlidapreviously hypobiotic larvae from the zoles, pyrantel, and ivermectin, are active
intestinal wall as L4. Although of relatively against adult large strongyles. Large
low incidence, larval cyathostominosis is

318

GASTROINTESTINAL PARASITES OF HORSES
nevertheless of concern because response
augmented by corticosteroids and other
to treatment is variable, and prognosis must
appropriate supportive tl1erapy.

be guarded even with intensive therapy. It is
reported more frequently in the UK and

Europe than in the USA

Prevention: Routine or inte1val

Horses with laival cyathostominosis
treatments are traditional and are intended

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generally have a neutrophilia and hypoalbuto nunimize the level of pasture conta.I11inaminemia Hyperglobulinemia, paiticularly tion, thereby reducing the risks associated
involving the !3-globulin fraction described
with accwnulation of mucosal laivae and
as characte1istic in some reports, has been a adult worms. Alternatively, infection may be less consistent finding. Eosinophilia is not a
prevented by daily administration of
consistent finding. Often, strongyle eggs are
pyrantel tartrate. The interval between
not seen on fecal exan1ination. However,
routine treatments depends on the duration
gross obse1vation ofL, or L5 laivae, which
a paiticular drug keeps the feces free of
ai·e often bright red, in the feces is helpful in
eggs and varies from 4-13 wk. The
making a diagnosis. Biopsy of large intestine frequency of treatment is also influenced by via laparotomy also may assist in diagnosis;
the value of the horses and the perceived
rectal biopsy is less reliable. Gross
level of risk, which varies with access to
pathologic findings include typhlitis or
pastw·e, stocking density, and management
colitis with mucosa] hyperemia, hemorpractices. In most cases, these procedures rhage, congestion, ulceration, or necrosis;
are ineffective in the face of widespread
in protracted cases, there may be only
drug resista.I1ce to most compom1ds except
mucosa] tl1ickening. At necropsy, cyathoivem1ectin and moxidectin. Control stomin laivae can be seen as small, gray dots measures should be designed to min.inuze (1-2 mm) in the mucosa, giving it a gritty
the risk of resistai1ce developing in tl1e
sensation on palpation. Transillumination
worm population. This includes presetving
of the mucosa from the serosal surface
the refugia population of the wom1s, ie,
may help in visualizing the laivae.

worms not exposed or affected by tl1e
anthelmintic, and thus reducing the drug

Treatment: Adult cyathostomins are
selection pressure. These populations are
easily removed from the gut lwnen by a
the atTested LJ found in the mucosa and L,1
wide range of anthelmintics, provided that
laivae on the pasture. Fewer treatments
the worm population is susceptible to the
may be effective if given strategically
chosen drug. Benzin1idazole-resista.I1t
according to local epidemiologic and
strains of small strongyles are common in
climatic considerations. Most adult horses
some regions, and pyrantel resista.I1ce has

>3-4 yr old have developed some immunity
been demonstrated in some locations.

to reinfection; thus, only a small portion of

Resista.I1ce to the macrocyclic lactones has
the herd hai·bors the adult wonn populayet to be demonstrated, but concerns exist.

tions and is responsible for conta.I11ination

Drug efficacy and the presence of anthelof the pasture with eggs. Selective treatment mintic resista.I1ce may be deternuned by
of only these infected horses will also
comparing the wom1 egg count at the time
reduce the exposure of the worm populaof treatment and 10-14 days latei::. An tion to ai1thelmintics ai1d selection for
effective drug should reduce the egg count
resista.I1ce. Removal of feces from paddocks
to zero or to very low levels. If resista.I1ce is
and pastw·es aids in control and may also
present, a different anthelmintic class must
reduce the nwnber of anthelmintic
be used, because side resista.I1ce occurs
treatments required.

within chemical groups.

Generally in parasite control progran1s,

Small-strongyle laivae in the intestinal
all horses on a farm should be treated at
mucosa are much more difficult to
some time, and those conmungled on the
effectively remove with anthelmintics.

saine pasture or paddock should be treated

Ivem1ectin has been used with mixed
at the san1e time. Boarded horses or horses
results; lack of efficacy has been reported at
retwning after having been off the prenuses
and above label dosages. Treatment with
for an extended time should be quarantined
large dosages of fenbendazole (10 mg/kg for
ai1d dewormed before being admitted to the

5 consecutive days) or with moxidectin has
herd. In adn1iniste1ing the anthelmintic, all
been reported as effective and can be used
horses should receive the proper dose, as
dming tl1e winter to reduce the risk of laival
deternuned by body weight or an accm·ate
cyathostominosis. Horses already suffering
estimation. Rotating different classes of
from tlus disea5e may not respond to
ai1tl1elnuntics in a fast rotation scheme
treatment if submucosal inflan11nation is too (eg, every few months) or a slow rotation severe. Consequently, treatment must be
scheme (atmually) is widely practiced to

GASTROINTESTINAL PARASITES OF HORSES

319
prevent development of resistant parasite
cephala infections. Colic from disturbances strains, but there is little evidence to
of the ileocecal area is more likely in horses
support the utility of this procedure.

with tapeworm infections than in those not

Whatever program is used, fecal samples
infected. Colic associated with tapewonn
should be examined periodically to monitor
infections often recurs. The site of
the effectiveness of the program and the
attachment of tapeworms frequently

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presence of drug resistance. Treatment can
becomes secondarily infected or abscessed.

be restricted to those horses in a group that

Anoplocephala spp can be effectively
routinely have positive egg counts > 100--200
treated with pyrai1tel salts; normal dosages
eggs per gran1 of feces.

(6.6 mg/kg) of pyrantel painoate are 87%
effective, while double the normal dosage is

STRONGYLOIDES SP

>93"A, effective. Daily administration of
pyrantel tartrate (2.65 mg/kg) removes

Strongyloides westeri is found in the small Anoplocephala spp. Praziquantel
intestine in foals. Adult horses rarely harbor

(0. 75-1 mg/kg) is 89"/er-100% effective in the patent infections, but mares often have
removal of A pm:foliata. Praziquantel ( at
laival stages within their tissues that are

1 mg/kg) appears to effectively remove P
activated by parturition to move into the
rna.millana; pyrantel salts do not. Mixtures manunary tissue and, subsequently, are
of tl1e macrocyclic lactones ivermectin or
transmitted to foals in the milk. However,
mox.idectin with praziquantel are available
the relationship of S westeri infection with and are highly effective against A perfoliata.

diarrhea in foals from 10 days of age has not

On facilities where tapewom1s are
been clearly established. The life cycle of
prevalent, clinical signs of tapeworm
the wom1 in horses is not known to differ
infections can be prevented by pyrantel
significantly from that of Strongyloides in salts administered daily dwing the grazing
pigs (seep 323). Diagnosis can be made
season, or by administration of effective
based on observation of eggs somewhat
oral anthelmintics within an inte1val
more oval and about one-third the length
deworming prograin. Treatment of horses
of strongyle eggs that contain laivae.

according to the latter prograi11 immediately

Ivermectin and oxibendazole effectively
before tum out and at the end of the grazing
remove S westeri. Transmission of laivae to season is likely to be most beneficial.

foals via mare's milk may be prevented by
routine treatment of mares with ivem1ectin
within 24 hr after foaling.

TRICHOSTRONGYLUS SP

TAPEWORMS

The small stomach wonn (hairworm) of
horses, Trichostrongylus atcei, is also

Three species of tapeworms ai·e found in
found in nuninants (seep 308) and,
horses: Anoplocephala magna, A pm:fo
consequently, is generally a clinical problem
liata, and Paranoplocephala mamillana.

only in horses commingled or rotated on

They are 8-25 cm long (the first usually
pasture with ruminants. Adult T axei are being tl1e longest, and the last the shortest).

slender and measure up to 8 nun long.

A magnaandP mamillana usually are in

Details of the life cycle in Equidae have not
the small intestine; A perfoliata is found
been carefully studied, but it is known that
mostly at the ileocecal junction, in the
the laivae penetrate the mucosa. These
cecum, and in the ileum. The life cycle is
worms produce a chronic catarrhal
sinlilai· to that of Moniezia spp in run1inants gastritis, which may result in weight loss.

(seep 312) and involves free-living oribatid

The lesions comprise nodular areas of
mites as intennediate hosts. Diagnosis is by
thickened mucosa surrounded by a zone
demonstration of tl1e chai·acteristic eggs in
of congestion and covered with a variable
the feces, but because the discharge of
amount of mucus. The lesions may be rather
proglottids is sporadic, a single fecal
small and irregularly circmnscribed, or they
exainination may not be diagnostic. ln light
may coalesce and involve most or all of the
infections, no signs of disease are present; in
glandular portion of the stomach, and
heavy infections, GI disturbances may be
erosions and ulcerations may be seen.

seen. Untluiftiness and anemia have been

Definitive diagnosis based on fecal
reported. Ulceration of the mucosa is quite
ex3.111ination is difficult, because the eggs
conunon in the ai·ea of attaclunent of
ai·e sinlilar to strongyle eggs. The feces can

A perjolia.ta and has been suggested as
be cultmed ai1d, in -7 days, the infective
one cause of intussusception. lntestinal
laivae identified. Some of the benzinlidaperforation, peritonitis, and subsequent zoles and ivem1ectin are effective against
colic have been associated witl1Anoplo-

Taxei.

320

GASTROINTESTINAL PARASITES OF PIGS

GASTROINTESTINAL PARASITES OF PIGS

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See also COCCIDIOSIS OF PIGS, p 208.

progran1 as needed but should not be the

In pigs, GI helminths a.re almost always
sole basis of a control program.

present; their main effects are loss of

Various anthelmintics a.re available,
appetite, reduction in daily gain, poor feed
although not all a.re available in every
utilization, and potentiation of other
country. Benzimidazoles, including
pathogens. Only rarely do they cause death.

fenbendazole and flubendazole, a.re

Adequate nutrition helps reduce the adverse available for in-feed administration.

effects of parasitism on feed efficiency and

Flubendazole is available for in-water and
average daily gain.

top dressing use, whereas fenbendazole

Management and control of GI helminths
has an oral fonnulation. Two avermectin
depends entirely on the production system
compounds, iverrnectin and dorarnectin,
in place, with individual programs
a.re available as i.ajectables, whereas only
developed for the circumstances of the
ivem1ectin can be used in-feed. Both
specific farm, including the knowledge of
pyrantel tartrate and leva.misole a.re
which parasites a.re present. Maintaining
available as in-feed formulations, but only
pigs on concrete or entirely on slatted
levantisole can be used in water. Dichlorvos,
floors, as on intensive farms, can successan organophosphate compound, was the fully control those parasites that have
first broad-spectrum deworrner available
intermediate hosts or that require pasture
for pigs and is still in use as an in-feed
conditions for transmission. Stearn cleaning
fom1ulation. Piperazine salts are an older
is highly effective in killing eggs and larvae.

generation of anthelntintic. Despite its

The management approach for outdoor
narrow spectrun1 of activity, it is sti!J widely
situations and nonconcrete floors is aimed
used, available as an in-feed or in-water
at avoiding a buildup of eggs and larvae
formulation.

within the area. Good sanitation is critical

Although anthelrnintic-resistant
because fecal-oral transmission, through
populations of Oesophagostomum sp were
the contamination of food, soil, or bedding,
identified as early as 1987, resistance does
is the primary route by which pigs become
not appear to be a widespread problem.

infected. Direct sunlight or dry conditions

In addition, there is no justification for
shorten the survival of some eggs and larvae
routinely rotating classes of dewormers;
because moisture and warmth a.re needed
rather, choice of product should be made on
for their development and survival, which
the expected efficacy against the parasites
probably accounts for decreased transmispresent (including ectopa.rasites).

sion during hot and cold months. Thermophilic composting of feces and/or bedding

ASCARIS SUUM
before use as fertilizer inactivates Ascaris
suum and Trichuris suis eggs: Both can Adults of the large roundworm, Ascaris
survive for a few hours at 50°C but only a
suum, a.re found in the small intestine and few minutes at 55°C. Most disinfectants
transitorily in the large intestine during
in use on farms, unfortunately, a.re not
expulsion of the worms. Males a.re up to 25
effective against parasite eggs, especially
cm and females up to 40 cm.long, whitish,
those of A suum and T suis. Moving "clean"

and quite thick. Large numbers of eggs a.re
animals to safe pastures will help reduce
produced (as many as 200,000 to 1 million/
parasite buildup, but it must be rememday/female) although shed intermittently; bered that eggs of A suum and T suis a.re they can develop to the infective stage ( eggs
capable of surviving 6-9 and 5--11 yr,
containing L3 Jarva) in 3---4 wk under optimal
respectively, in the environment, and
conditions. In temperate regions, the eggs
reinfection wi!J occur even with 2 -3 yr of
stay dormant in winter ( d5°C) and resume
pasture rest. If it is not possible to rotate
development when temperature rises in the
pastures, pigs may occupy uncleanable
spring. The eggs a.re highly resistant to
ground for many years. In these situations,
chemical agents, but conditions with low
parasites can build up quickly, and control
humidity, heat, or direct sunlight reduce
may be in1possible without the regular use
their survival significantly. Under optimal
of anthelrnintics. Anthelmintic treatments
conditions, eggs may survive for 5--11 yr.

can be incorporated into any broader

When the eggs a.re ingested, the larvae hatch

GASTROINTESTINAL PARASITES OF PIGS

321
in the intestine, penetrate the wall, and
signs, marked unthriftiness and weight loss
enter the portal circulation. After a short
may be seen. Infection generally induces
period in the liver, they are canied by the
development of acquired resistance to
circulation to the lungs, where they pass
reinfection, and prevalence is highest in
through the capillaries into the alveolar
young growing pigs. If the treatment rate is
spaces. Approximately 9-10 days after
very low and the level of herd immunity is

VetBooks.ir
ingestion, the larvae pass up the bronchial
also low, prevalence may be highest in
tree, are swallowed, and return to the small
breedi..ng animals.

intestine by -10-15 days after infection,
where they mature into adult worms.

Diagnosis: During the patent pe1iod,

The first eggs are passed -6-7 wk after
diagnosis can be made by demonstrating the
infection. Lifespan is -6-9 mo. Earthworms
typical eggs (golden brown, thick pitted
and dung beetles can serve as paratenic
outer wall, 50-70 x 40-60 im1) by fecal
hosts.

analysis or by observation of large worms
in feces. Pigs are coprophagic; thus, low

Distribution and Host Range: A suum
egg counts ( <200 eggs/g) may indicate
is found in pigs worldwide. Occasionally,
coprophagy rather than actual infection.

nematodes may establish in sheep; how

A presumptive diagnosis can be made at
ever, ingestion of infective eggs while
necropsy based on demonstration of the
grazing generally results in pneumonia and
typical milk spots; however, other migrating
liver lesions in sheep. Infections can also
parasites ( eg, larvae of Toxocara canis,
be seen in cattle and manifest as an acute,

Stephanurus dentatus) may cause similar
atypical interstitial pneumonia. Whether the lesions. Worms may be demonstrated in U1e human nematode Ascaris lumbricoides
lw1gs (small immatures) and the small
a.nd A suum of pigs are the same is still
intestine (large immatures, adults) at
debated. Current evidence indicates there
necropsy.

is a single interbreedi..ng population of

Ascaiis, and the populations occurring in

Treatment: Supportive tl1erapy, including
pigs or people have only slight phenotypical
treatment for secondary bacterial invaders,
and genotypical adaptive changes.

may be necessary during the respiratory

Regardless, it is clear the pig ascarid is
phase of infection. Many drugs have been
zoonotic, havi.ng been found in people from
used to remove adult ascarids. Piperazine
various areas of the world, particularly
preparations have low toxicity and are
those in close contact with pigs. Visceral
moderately priced. The benzin1idazoles and
larva migrans due to migrating larvae has
probenzimidazoles, dichlorvos, ivermectin,
been described.

levamisole, and pyrantel are effective and
have a broader spectrwn of activity than

Clinical Findings: Adult worms may
piperazine. Hygromycin is active against
significantly reduce the growth rate of
ascarids when administered as a low-le"Oel
you.ng pigs; in rare cases, they may cause
additive to the feed. Less information is
mechanical obstruction of the intestine.

available concerning the control of

Migration of larvae through the liver causes
migratory stages; pyrantel and fenbendazole
hemorrhage, fibrosis, and accumulation of
show activity.

lymphocytes seen as white spots ( called

"milk spots") under the capsule and leadi..ng

MACRACANTHORHYNCHUSSP
to condenmation of the liver at slaughter.

These lesions become visible 7 -10 days

AdultMacracanlhorhynchus hirudina
after infection and will regress within
ceus (thorny-headed worms) are usually

1-4 wk; therefore, their presence indicates
seen in the small intestine. They are 10 cm
recent infection/reinfection. In resistant

(males) to 65 cm (females) long, 3-9 mm
pigs, only a few larvae will reach the liver
thick, and slightly pink with a transversely
and the nwnber of white spots will be low,
wiinkled outer covering; superficially, they
despite continual reinfection. Therefore, the
resemble ascarids. However,milike ascarids,
number of white spots and the liver
tl1e anterior end bears a spiny, retractable
condemnation rate are both poor measures
proboscis or rostellum used for fim1
of herd infection level. In heavy infections,
attachment to the intestinal wall. There is a
the larvae can cause pulmonary edema and
granulomatous inflan1mation at the site of
consolidation, as well as exacerbate swine
attachment resulting in nodule formation,
influenza and endemic pneumonia. Heavily
which will regress -1 mo after the parasite
exposed susceptible pigs show abdominal
is no longer present. The eggs ( dark brown,
breathing, conm10nly referred to as
embryonated, with three embryonic

"thumps." In addition to the respiratory
envelopes, 90-110 x 50-65 µm) passed in the

322

GASTROINTESTINAL PARASITES OF PIGS
feces are ingested by the grubs of various
groups (sows, boars). In patent infections,
beetles that serve as intem1ediate hosts.

typical strongyle eggs (66--80 x 38-4 7 µm)

Pigs become infected by ingesting either
are found in feces, often in large numbers.

grubs or adult beetles, and the infection is

These can be differentiated from those
thus restricted to pigs with pasture access.

of Hyostrongylus by larval culture. At

The prepatent period is 2-3 mo, and
necropsy, tl1e worms and lesions are readily

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longevity is -1 yr. The female can lay
visible. The benzirnidazoles, levamisole,

-260,000 eggs/day for several months.

piperazines, dichlorvos, pyrantel tartrate,

Signs are generally absent; when present,
and ivem1ectin are effective, but anthelnunthey are nonspecific. Antemortem diagnosis tic resistance has been observed for
is difficult, because the ova do not float
benzimidazoles, levamisole, and pyrantel.

reliably in many conventional salt solutions

A diet composed of highly degradable
and thus should be looked for in the
carbohydrates may suppo1t worm control
sediment if using solutions of low specific
by creating utlfavorable conditions, which
gravity. At necropsy, nodules usually can be
decrease worm establislm1ent and
seen through the serosa Because the
fecundity.

proboscis is longer than thejejunal wall is
thick, perforations may occur; however, tile

STOMACH WORMS
inflammatory response generally seals off
any perforation. Clinical signs are not

Five genera of nematodes are found within
generally present; however, when perforathe stomach of pigs. The trichostrongylid tions do occur a fatal peritonitis can result.

Hyostrongylus is relatively common,

Levanusole and ivem1ectin are effective
whereas tile otl1er four spi.rurids (Ascarops,
for treatment. Control depends on avoiding

Gnathostoma, Physocephaius, Simondsia)

use of contan1inated hog lots or pastures or
are less conm1on or geographically linuted.

by regular removal of feces when pigs are

Altl1ough some ( eg, Ascarops strongylina,
kept in sties or small runs.

Physocephalus sexalatus) are more
obvious grossly, only Hyostrongylus

OESOPHAGOSTOMUM SPP
rubidus is considered to be pathologically
significant. H rubidus (the red stomach

Oesophagoslomum spp are prevalent
wom1) is -6 mm long, quite slender, and has
worldwide; 0 dentatum is tl1e most
a direct life cycle, features similar to those
common species, whereas O quadri
of Ostertagia ostertagi of cattle. The
spinulatum appears to be slightly more
prepatent period is -3 wk unless larval
pathogenic. The adults are found in the
inl1ibition occurs; tl1is may be induced by
lumen of the large intestine; they are� 15 mm seasonal changes or repeated illfections, long, slender, and white or gray. The life
explaining why hypobiotic larvae are
cycle is direct. Eggs are passed in the feces;
usually found in older anilnals. As witll
infective L3 are found on pasture within 1 wk H aernonchus contort us of sheep, and can sutvive for -1 yr under optimal
relaxation of inm1Ul1ity associated witll
conditions. Infection results from ingestion
parturition allows inhibited larvae to
ofL3, which penetrate the mucosa of tile
resume development, leading to a periprutularge intestine within a few hours after rient rise in fecal egg counts. A strongylina
ingestion and return to the lun1en in
and P sexalatus, tile tl1ick stomach wom1s, 6--20 days. The prepatent period is -3-6 wk.

are 10-20 mm long, are much stouter tllan H

A periparturient rise in worm egg output has 1ubidus, and have coprophagous beetles as been observed in sows from 2 wk before
intermediate hosts. The prepatent periods
parturition to weaning; however, this
for tl1e spirurids are in tile range of 4-6 wk.

phenomenon is far less constant in pigs than Because of tile free-living larval requiresheep and its epidemiologic in1p01tance is ments (H rubidus) or tile need for an
questionable. Most infections are asympt o intermediate host (all others), illfections are matic, but heavily infected pigs may show
confined to anilnals witll pasture access or
anorexia, emaciation, and GI disturbances.

those kept in straw yards.

The serosa shows small nodules, tl1eir
size reflecting species and previous

Clinical Findings: The patllogenesis
exposure. In severe cases, the intestinal
of hyostrongylosis is sirniJru· to tllat of
wall may be tl1ickened and necrotic. Heavy
ostertagiosis of cattle, includil1g the
infections may reduce tile lactation capacity replacement of parietal cells by rapidly of sows and the body weight of growing
dividing undifferentiated cells, giving rise to
pigs. Infection induces only moderate
nodules on the mucosa! sutface. Gastric pH
inm1Ul1ity; hence, prevalence of nodular
increases as does mucus production,
wo1ms tends to be higher in tl1e older age
resulting in a catarrhal gastritis. Occasion-

GASTROINTESTINAL PARASITES OF PIGS

323
ally, gast1ic ulcerations of the glandular
pa.i·asite of pigs; it is particularly pathogenic
stomach occur but whether this is a direct
in suckling pigs, especially in tropical and
result of the nematode infection is unclear.

subtropical climates. It is of less importance

Light infections are usually asymptomatic.

in adults. Thread worms are unique an1ong

However, when present in large numbers
helrninths, having both parasitic generaor when the host's condition is reduced by tions (females in the small intestine) and

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poor nuttition or other factors, these wonns free-living generations (males a.11d females may cause variable appetite, anemia,
in the SlllTounding environment). Transnusdia.tThea, or weight loss, and may conttibute sion occurs either by skin penetration,
to a thin sow syndrome. H rubidus
emphasizing the in1porta.nce of good
characteristically is found under a heavy
hygiene, or via infective la.tvae in the
catarrhal or mucous exudate. Resun1ed
colostrnrn of lactating sows. Lactogenic
development of inhibited larvae may cause
tra.11sn1ission is lughly efficient in infecting
severe gasttitis and, in addition, contaminewborn piglets. Even without reinfection nate the environment of the young pigs. Egg
of the sow, dormant larvae in the udder may
excretion per female Hyostrongylus wom1
be tt·ansmitted to several consecutive litters
is generally much lower than that of other
of piglets. The adult female worms btuTow
nematode genera.

into the wall of the small intestine, being
found in tU1111els in the epitheliun1 at the

Diagnosis: Clinical signs other than
base of the villi. The prepatent period is
unthriftiness are not obvious. Fecal

4-9 days, depending on the mode of
exan1inations may show the distinctive ova
infection. In light and moderate infections,
of Physocephalus and Ascarops-small
the pigs usually show no signs. In heavy

(35-40 x 17-20 mm), thick-shelled eggs
infections, dian·hea, anemia, and emaciacontaining active larvae. Hyostrongylus tion may be seen, and death may result.

ova resemble those of other strongyle

Infection induces strong i111mttnity; hence,
wonns ( eg, Oesophagostomum ), and fecal
older pigs are usually not clinically affected.

cultures are required to obtain infective

Diagnosis is detem1ined by demonstralarvae for differential diagnosis.

tion of the characteristic small, thin-shelled,

At necropsy, adult worms, especially
embryonated eggs (20-35 x 40-55 µm) in

Physocephalus andAscarops, are readily
the feces. It is impo1tant that feces are
seen. Mucosa! scrapings for microscopic
collected from the rectwn, because fecal
exa.111ination are essential for detection of
droppings often are conta.tninated by
in1mature Hyostrongylus.

free-living nematodes, which may have eggs
indistinguishable from U1e Strongyloides

Treatment and Control: The sa.ine
eggs. F\uthermore, feces must be cooled imprinciples used for control of pa.t-asitic gastromediately to prevent hatcl1ing. At necropsy, enteritis of run1inants apply to the control of
adults may be found in scrapings from the
hyostrongylosis and should not depend
intestinal mucosa, and immature wonns
solely on anthelmintic use. As an exa.inple,
may be recovered from minced tissues
in temperate climates, an a.imual rotation of
using the Baerma.im tecluuques.

pastures with other livestock or crops would

The benzinudazoles and levan1isole arc
reduce pasture contamination. Care must
effective against intestinal infections. If
be taken with rotating livestock if the pigs
administered in the feed for several days
also harbor asca.iid infections. Integration of
before and after parturition, they reduce
a.t1theln1intics depends on their availability
lactogenic transmission to suckling piglets.

and the season, as well as on other farming

Ivennectin is effective against adults a.11d, if
activities. The newer benzimidazoles,
given to the sow 1 -2 wk before fa.tTowing,
probenzinudazoles, and ive1rnectin are highly suppresses larval excretion in the milk.

effective against adult and immature stages

A high level of hygiene is necessary to

(including hypobiotic larvae) of Hyostrongy
dinun.ish larval development as well as
lus. In1plementing measures to control the
multiplication of free-living generations
inte1rnediate hosts of tl1e spirwid nematodes
in the pens.

is usually not required or unproductive.

Treatment for most has not been reported,

TRICHURIS SP
although ivem1ectin has activity against
adultAscarops.

'I'ri.churis suis is found worldwide in pigs.

The adult wonns are 5-6 cm long and

STRONGYLOIDES SP
whip-shaped; the anterior slender portion
embeds within the epithelial cells of the

Strongytoides rnnsomi (pig threadworm)

large intestine, especially the cecwn, with
is a ubiquitous a.t1d common nematode
the thickened posterior third lying free in

324

GASTROINTESTINAL PARASITES OF PIGS
the lumen. Infection is by ingestion of eggs
a short pe1iod of egg-laying (2-5 wk) before
containing an infective first-stage laiva. The
the wonns are expelled by immune-mediated
laiva hatches and penetrates the distal
reactions, and thus little significance can
ileum, cecal, and colonic mucosa The
be given to percentage of egg excreters
nematodes complete all four molts, after
and numbers of eggs per gram of feces.

which the posterior end begins to protrude

Clinical tiichurosis is usually associated

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into the lwnen. The prepatent period is
with the laival stages before eggs are passed

6-8 wk; longevity is 4-5 mo. Light infections, in the feces; in these cases, examining with no clinical signs, are generally the case.

mucosal scrapings taken at necropsy for

Heavy infections may cause inflammatory
smaller stages of the parasite is recomlesions in the cecum and adjacent large mended. Mature parasites are easily found
intestine and may be accompanied by
after ingesta is washed away and can be
diarrhea and untl1riftiness. Clinical infection identified by their size and whip-like form.

is most often seen in young animals;

Dichlorvos, leva.misole, some benzimidaresistance is botl1 acquired and age-related.

zoles, ivermectin, and doramectin are

The double-operculated brown eggs (50-68
effective against the adult worms.

x 21-31 mm) are diagnostic. Eggs are heavy;

Biologically, the eggs are comparable to
thus, good technique with media of proper

Ascaris eggs-they are highly resistant to
specific gravity is essential. Trichurids have
chemicals and may remain infective for

3-4 yr; control relies on thorough cleaning
of the affected area and moving tl1e animals
to clean plots. Trichuris eggs develop
rather slowly (10-12 wk tmder optimal
conditions), and because tl1ey do not
develop at temperatures <l6°C, there is
only one generation per year in temperate
regions.

T suis larvae may hatch in the large
intestine of people, in which the laivae seem
to be able to establish transiently. It is this
feature tl1at has led to intense research
interest in the treatinent of inflammatory
bowel disease, including ulcerative colitis
and Crohn's disease, of people tllfough

Trichuris suis egg. Courtesy of Dr. Bruce Lawhorn.

administration of infective T suis eggs.

FLUKE INFECTIONS IN RUMINANTS

Fasciola hepatica, the most in1portant

Massachusetts, and the Atlantic provinces
trematode of domestic ruminants, is the
of Canada. It is also widespread in some
most common cause of liver fluke disease in
areas in Europe and Asia. Eurytrema spp,
temperate areas of the world. In the USA, it
the pancreatic flukes, parasitize sheep, pigs,
is endemic along the Gulf Coast, the West
and cattle in Brazil and parts of Asia. Several

Coast, the Rocky Mountain region, and
species of paramphistomes or mmen flukes
other areas. It is present in eastern Canada,
are found tllfoughout much of the world.

British Colun1bia, and South America and is
of particular economic in1portance in tl1e

British Isles, western and eastern Europe,

FASCIOLA HEPATICA

Australia, and New Zealand. Fasciola
gigantica is economically important in

(Common liver fluke)

Africa and Asia and is also found in Hawaii.

Fascioloides magna has been reported in

Etiology: Fasciola hepatica (30 x 2-12 nun at least 21 states (USA) and in Europe. ln
and leaf-shaped) is distributed worldwide

North America, Dicrocoelium dendriticum and has a broad host range, including is confined mainly to New York, New Jersey,
people. Economically important infections

FLUKE INFECTIONS IN RUMINANTS

325
and enter the pe1itoneal cavity, where they
migrate to the liver. The time required for
this transit can vary and results in delayed
development rates, which affects the
efficacy of some treatments because many
are effective against flukes only later in their

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development. The young flukes penetrate
the liver capsule and tunnel through the
parenchyma for 6-8 wk, growing and

Adult Fascio/a hepatica (Corazza stain).

destroying tissue. They then enter small bile

Courtesy of Dr. Raffaele Ronca/Ii.

ducts and migrate to the larger ducts and,
occasionally, the gallbladder, where they
mature and begin to produce eggs. The
prepatent period is usually 2-3 mo,
depending on the fluke burden. The minimal
period for the completion of one entire life
cycle is -17 wk. Adult flukes may live in the
bile ducts of sheep for years; most are shed
from cattle within 5-6 mo.

Clinical Findings: Fasciolosis ranges in
severity from a devastating disease in sheep,
alpacas, and llan1as to an asymptomatic
infection in cattle. The course usually is
determined by the munber of metacercariae
ingested. Acute disease occurs 2-6 wk after

Fasciola hepatica egg found on sedimentation. Adding a drop of methylene blue to the the ingestion of large numbers of metacersediment provides contrasting background, cariae (usually >2,000) over a short pe1iod.

making the eggs easier to see. Courtesy of Dr.

In sheep, acute fasciolosis occurs season

Lora Bal/weber.

ally and is manifest by a distended, painful
abdomen; anemia; and sudden death
occurring 2-6 wk after infection. The acute
syndrome can be complicated by concurare seen in cattle, sheep, alpacas, and llamas rent infections with Clostridium novyi, in three fom1s: chronic, which is rarely fatal
resulting in "black disease" ( clostridial in cattle but often fatal in sheep, alpacas,
necrotic hepatitis), although this is now
and llan1as; subacute or acute, which is
less common due to vaccination against
primarily in sheep, alpacas, and llamas, and
clostridial diseases. In subacute disease,
often fatal; and in cor\junction with "black
large numbers (500-1,500) of metacercariae
disease" (INFECTIOUS NECROTIC HEPATITIS, see are ingested over longer periods of tinle;
p 603), which is most common in sheep and
survival is longer(7-10 wk), even in cases
usually fatal.

with significant hepatic damage, but deaths

Eggs are passed in the feces, and
occur due to hemorrhage and anemia.

miracidia develop within as little as

Chronic fasciolosis can be seen in all

9-10 days (at22°-26°C [71.6°-78.8°F]; little
seasons but manifests primarily in late fall
development occurs below l0°C [50°F]).

and winter. It occurs as a result of ingesting

Hatching only occurs in water, and
moderate nun1bers (200-500) of metacermiracidia are short-lived ( -3 hr). Miracidia cariae over longer periods of time; signs
infect lymnaeid snails, in which asexual
include anemia, unthriftiness, submandibudevelopment and multiplication occur lar edema, and reduced milk production,
through the stages of sporocysts, rediae,
but even heavily infected cattle may show
daughter rediae, and cercariae. After 6-7
no clinical signs although their immunity to
wk (or longer if temperatures are low),
other pathogens ( eg, Salmonella spp) may
cercariae emerge from snails, encyst on
be reduced and reactions to the single
aquatic vegetation, and become metacerintradermal test for tuberculosis modified.

cariae. Snails may extend the developmen

Heavy chronic infection is fatal in sheep,
tal period by hibernating during the winter.

alpacas, and llamas.

Metacercariae may remain viable for many

Sheep do not appear to develop
months unless they become desiccated.

resistance to infection, and chronic liver

After ingestion by the host, usually
damage is cumulative over several years.

with herbage, young flukes excyst in the

In cattle, a partial acquired resistance
duoden un1, penetrate the intestinal wall,
develops beginning 5-6 mo after infection.

326

FLUKE INFECTIONS IN RUMINANTS

Lesions: Severity depends on the numto sheep, which must be kept off treated ber of metacercariae ingested, the phase
pasture for 6 wk after application. Other
of development in the liver, and the species
such chemicals are generally too expensive
of host involved. During the first phase,
and have ecologically undesirable effects.

immature, wandering flukes destroy liver

Prevention of livestock access to snailtissue and cause hemorrhage. The second infested pasture is frequently impractical

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phase occurs when the flukes enter the bile
because of the size of the areas involved
ducts, where they ingest blood and dan1age
and the consequent expense of erecting
the mucosa with their cuticular spines. In
adequate fencing.

acute fasciolosis, dan1age is extensive; the

Several drugs are available to treat
liver is enlarged and friable with fibrinous
infected ruminants, including triclabendadeposits on the capsule. Migratory tracts zole, clorsulon (cattle and sheep only),
can be seen, and the surface has an uneven
albendazole, netobirnin, closantel,
appearance. In chronic cases, cirrhosis
rafoxanide, and oxyclozanide. Not all are
develops. The damaged bile ducts become
approved in all countries ( eg, only clorsulon
enlarged, or even cystic, and have
and albendazole are approved in the USA;
thickened, fibrosed walls. In cattle but
none are approved for alpacas and llamas),
not sheep, the duct walls become greatly
and most have long withdrawal periods
thickened and often calcified. Aberrant
before slaughter if used in meat-producing
migrations occur more commonly in cattle,
animals and before milk from treated
and encapsulated flukes may be found in
livestock can be used for human consumpthe lungs. Mixed infections with Fascio
tion. Anthelrnintic resistance by F he'J)atica
loides magna can be seen in cattle.

to various compounds, including albenda

Tissue destruction by wandering flukes
zole, clorsulon, and triclabendazole, has
may create a microenvironment favorable
been demonstrated, furfuer complicating
for activation of clostridial spores.

control programs based only on anthelrnintic usage. The tinling of treatment is also important so that tl1e pharmacokinetics of

Diagnosis: The oval, operculated, golden
brown eggs (130-150 x 65-90 µm) must be
the drug used will result in tl1e optin1al
distinguished from fuose of paramphistomes removal of flukes-each flukicide has (rumen flukes), which are larger and clear.

varying efficacy against different ages of

Eggs of F hepatica carmot be demonfluke. Timing of treatments is deterrnined by strated in feces during acute fasciolosis.

local epiderniologic factors and additional

In subacute or chronic disease in cattle,
treatments by unusually suitable conditions
the nun1ber varies from day to day, and
for parasite multiplication. For example,
repeated fecal sedimentation may be
in the Gulf Coast states of the USA, cattle
required. Diagnosis can be aided by an ELISA should be treated before the fall rainy ( commercially available .in Europe) that
season and again in the late spring. In
enables detection -2-3 wk after infection
norfuwestem USA and in northern Europe,
and well before tl1e patent period. Plasma
cattle should be treated at the end of the
concentrations of -y-glutamyltransferase,
pasture season and, if not housed, again in
which are increased with bile duct damage,
late January or February. In European
are also helpful during the late h1aturation
countries with large susceptible sheep
period when flukes are in the bile ducts. At
populations, computerized prediction
necropsy, the nature of the liver damage is
systems based on rainfall, evapotranspiradiagnostic. Adult flukes are readily seen in tion, nun1ber of wet days per month, and/or
the bile ducts, and immature stages may be
prevalence are used to predict the tinling
squeezed or teased from the cut surface.

and severity of disease. In areas where
heavy infections are expected, sheep may
require treatment in September or October,

Control: Control measures for F hepatica ideally should involve removal of flukes in

January or February, and again in April or
affected animals, reduction of the intem1edi

May to reduce both the chances of acute or
ate host snail population, and prevention of
chronic infections and the output of fluke
livestock access to snail-infested pasture.

eggs for development of future disease.

In practice, only the first of these is used in
most cases. Altl10ugh molluscicides can be

FASCIOLA GIGANTICA
used to reduce lymnaeid snail populations,
those that are available all have disadvan

(Giant liver fluke)

tages that restrict their use. Copper sulfate,

Fasciola gigantica is similar in shape to
if applied before the snail population

Fasciola he'J)atica but is longer (75 mm),
multiplies each year, is effective but toxic
with less clearly defined shoulders, and is

FLUKE INFECTIONS IN RUMINANTS

327

12 mm wide. It is found in warmer climates

(7.5 mg/kg), clorsulon (15 mg/kg), and

(Asia, Africa) in cattle and buffalo, in
closantel (15 mg/kg) have shown efficacy
which it is responsible for chronic
against this fluke in sheep. Currently, no
fasciolosis, and in sheep, in which the
products are approved for use against tins
disease is frequently acute and fatal. The
fluke in the USA. Deer are required for
life cycle is similar to that of F hepatica,
completion of the life cycle; if they can be

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except most parasitic phases are longer,
excluded from the areas grazed by cattle and
the prepatent period is 10-16 wk, and the
sheep, control may be effected. Control of
species of snail intermediate hosts are
the intermediate host (lymnaeid snails) may
different. The pathology of infection,
be possible once it has been identified in a
diagnostic procedures, and control
region and the nature of its habitat exammeasures are similar to those for ined. However, envfronmental concerns are

F hepatica (seep 324).

the same as those for F hepatica.

FASCIOLOIDES MAGNA

DICROCOEUU DENDRmCUM

(Large American liver fluke, Giant liver
fluke)

(Lancet fluke, Lesser liver fluke)

Fascioloides rnagna is up to 100 mm long,

Dicrocoeliurn dend1iticurn is slender

2-4.5 mm thick, 11-26 mm wide, and oval; it

(6--10 mm long x 1.5--2.5 mm wide). It is
is distinguished from Fasciola spp by its
found in many countries and infects a wide
large size and lack of an anterior projecting
range of definitive hosts, including domestic
cone. It is found in domestic and wild
ruminants. Another species, D hospes, is
ruminants; deer are the reservoir host. The
common in West Aflica.

life cycle resembles that of Fasciola spp.

The first intennediate host is a terrestrial

Altl10ugh flukes will mature in cattle, tl1e
snail (Cionella. lubrica., in the USA), from intense encapsulation response fonns a
winch cercariae emerge and are aggregated
closed cyst, so eggs rarely pass out of the
in a mass of sticky mucus (slimeball). The
animal. Pathogeni.city is low, and losses are
slimeballs of cercaiiae are ingested by the
confined p1imarily to liver condemnations.

second intermediate host, which is an

In sheep and goats, encapsulations do not
ant (Fo1micafusca, in the USA), with
occur, and the parasites migrate in the liver
metacercaiiae forming il1 the abdominal
and other organs, causing tremendous
cavity. One or two metacercaiiae in the
damage. A few parasites can cause death
subesophageal gai1glion of the ant cause
due to extensive migrations. Infection with
abnorn1al behavior il1 winch the ants climb

F rnagna appears to be rare in alpacas and
up and remain on tl1e tips of the herbage
llan1as, in which the response milTors that
where they attach themselves, which
seen in cattle. In deer, there is little tissue
increases the probability of ingestion by.

reaction, and the parasites are enclosed in
the definitive host. Once mgested, the
thin, fibrous cysts tl1at communicate with
metacercariae excyst in tl1e small intestine,
bile ducts. Hi.stologically, infected livers
migrate up the main bile duct, and then on
of all species show black, tmtuous tracts
to smaller ducts. They begin laying eggs
fanned by migrations of young flukes.

-10--12 wk after infection. The total life

While the eggs of F rna.gna. resemble
cycle takes -6 mo.

those of Fasciola hepatica, th.is is of limited In cattle, sheep, and goats tl1ere appeai-s
use; eggs usually are not passed by cattle
to be no immunity, and heayy infections
and sheep and probably not by alpacas and
may accumulate ( up to 50,000 flukes in a
llan1as. Recovery of the parasites at
mature sheep) with mmimal pathologic or
necropsy as well as differentiation of
clilucal changes. Cirrhosis can develop,

F hepatica. is necessary for definitive
and the bile ducts may be thickened and
diagnosis. When domestic ruminants and
distended. Economic loss is due primarily
deer share tl1e same grazing, the presence of to condemnation of livers. Clinical signs ai·e disease due to F rna.gna should be kept in
not obvious but may be seen il1 massive
mind. Mixed infections with F hepatica are
infections. Infections in alpacas and llainas
seen in cattle.

are associated with an acute decline in

Oxyclozani.de has been reported to be
condition, recumbency, hypothemua, and
effective againstF rna.gna in white-tailed
anenua. Liver enzyme values tend to be
deer, and triclabendazole has been used in
within nonnal linuts. Severe pathologic
captive and free-ranging red deer. Rafoxachanges occur within the liver and bile ni.de has been used successfully against
ducts, including cmhosis, abscesses, and
natural infections in cattle. Albendazole
granulomas.

328

FLUKE INFECTIONS IN RUMINANTS

The eggs contain a miracidium and are
concentrations of -y-glutarnyl transpeptivery small ( 40 x 25 iun), lopsided, and dase and AST. Losses are reported due to
yellowish brown. Fecal flotation with a
condemned pancreas, but the pathogenesis
solution of high specific gravity (1.30-1.45)

suggests an additional loss of production.

is recommended to detect D dendriticum.

The control of intermediate hosts may

The complex file cycle makes control
not be practical. Treatment with praziquanof intermediate hosts almost impossible, VetBooks.ir
tel (20 mg/kg, for 2 days) or albendazole
because widespread chemical use has

(7.5 mg/kg for sheep, 10 mg/kg for cattle)

damaging ecologic effects on other similar
have reportedly been effective.

organisms. However, keeping ducks,
turkeys, or chickens to eat the snails can
effectively reduce the intermediate host
populations in small areas. Because

PARAMPHISTOMES
infected ants are usually found within

30-50 cm of the base of the nest, covering

(Amphistomes, Rumen flukes, Conical flukes)

nests with tree branches to keep animals

There are numerous species of paramaway from the base can also be useful.

phistomes (Paramphistomum, Calico

Effective anthelrnintic treatments are
phoron, Cotylophoron) in nuninants
available, but most must be administered at
worldwide. The adult parasites are
dosages higher than those recommended
pear-shaped, pink or red, up to 15 mm long,
for F hepalica. Effective anthelrnintic
and attach to the lining of the nm1en.

treatments in both cattle and sheep are

Immature fom1s are found in the duodenun1
albendazole at 15--20 mg/kg in a single dose
and are 1--3 mm long.

or two doses of 7.5 mg/kg on successive

Eggs are passed in the feces, and
days, or netobirnin at 20 mg/kg. Praziquantel
miracidiae hatch in the water and infect

(50 mg/kg) has been shown to decrea5e egg
planorbid or bulinid snails. Development in
shedding by -90% in llamas.

the snail is similar to that in the life cycle of

Fasciola hepatica, with the snail shedding
cercariae that encyst on the herbage. In the

EURYTREMA SPP
ruminant host, the young flukes excyst and

(Pancreatic fluke)

remain in the small intestine for 3--6 wk
before migrating forward through the

Pancreatic flukes have a thick body and
reticulum to the rumen. Eggs are produced
are 8--16 mm long x 6 mm wide. They are

7-14 wk after infection.

parasites of the pancreatic ducts and

Adult flukes do not cause overt disease,
occasionally of the bile ducts of sheep, pigs,
and large munbers may be encountered.

and cattle in Brazil and Asia. Three species,

The immature flukes attach to the duodenal

Eurytrema pancreaticum, E coelomali
and, at tin1es, the ilea! mucosa by means of
cum, and E ovis are recognized. The first a large poste1ior sucker and cause severe
intem1ediate hosts are terrestrial snails
enteritis, possibly necrosis, and hemo,"

(Bradybaena spp ), and the cercariae are
rhage. Affected animals exhibit anorexia,
released onto herbage and ingested by
polydipsia, unthriftiness, and severe
grasshoppers ( ConocephaJ,us spp) or tree
diarrhea. Extensive mortality may occur,
crickets (Oecanthus spp), which are the
especially in young cattle and sheep. Older
second intermediate host. After the anin1al
animals can develop resistance to
ingests a metacercarial-infected grasshopreinfection but may continue to harbor per, the in1mature flttkes excyst in the
munerous adult flukes:

duodemun and migrate to the pancreatic

The large, clear, operculated eggs are
duct, where they mature. The prepatent
readily recognized, but in acute paramperiod of E coelomaticum in cattle is phistomosis there may be no eggs in the

3-4mo.

feces. Exanlination of the fluid feces may

There are no obvious clinical signs, but
reveal immature flukes, many of which
a general weight loss may occur in heavy
are passed in these cases. Diagnosis is
infections. Dicrocoelium-like eggs can be
commonly made at necropsy.

demonstrated in feces. Light infections

Control measures to reduce the host snail
cause proliferative inflammation of the
population are as for control of fasciolosis
pancreatic duct, which may become

( see p 326). Treatments with reported
enlarged and occluded. In heavy infections,
success ( efficacies >90<>A,) are oxyclozanide fibrotic, necrotic, and degenerative lesions

(two doses 3 days apai.t) and the combinadevelop. These result in increased plasma tion of bithional and levai.nisole.

HEPATIC DISEASE IN LARGE ANIMALS

329

HEPATIC DISEASE IN LARGE ANIMALS

Hepatic disease is common in large anin1als.

adenoma), and liver fluke infestation have

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Increases in serum hepatic enzymes and
also been reported in ca.melids.

total bile acid concentration may indicate

The liver can respond to insult in only a
hepatic dysfunction, insult, disease, or
limited nwnber of ways. Fat droplets in ilie
failure. Although liver disease is especially
liver may be an early and often reversible
common in horses and foals, progression to
change. Biliruy hyperplasia is also reversible
liver failure is not.

if the insult is removed early. Necrosis of

Diseases tl1at frequently result in hepatic
hepatocytes indicates more recent drunage.

failure in horses include Theiler disease,

The dead cells are removed by an inflamma

'Iyzzer disease (foals), pyrrolizidine alkaloid tory process and replaced with eiilier new toxicosis, hepatic lipidosis, suppurative
hepatocytes or fibrosis. Unless ilie dysfunccholangitis or cholangiohepatitis, cholelitllition is acute and hepatocellular regeneration asis, and chronic active hepatitis. Obstrucis evident, prognosis for aninlals wiili liver tive disorders (biliary stones, right dorsal
failure is usually unfavorable. Early hepatic
colon displacement, neoplasia, duodenal

:fibrosis may be reversible wiili prompt
ulceration and stricture, hepatic torsion,
recognition and intervention. Chronic
portal vein tlirombosis ), aflatoxicosis,
disease wiili extensive loss of hepatic
leukoencephalomalacia, pancreatic disease, parenchyma and fibrosis, especially wiili kleingrass or alsike clover poisoning, portal
portal bridging, wruTants a poor prognosis.

caval shunts, hepatic abscess, and perinatal
he1pesvirus 1 infections sporadically result

Clinical Findings: Clinical signs of
in hepatic failure. Less frequently, hepatic
hepatic disease may not be evident until
failure is associated wiili endotoxemia,

>60"Ar-80% of ilie liver parenchyrna is
steroid administration, inhalant anesiliesia,
nonfunctional or when hepatic dysfunction
systemic granulomatous disease, drugis secondary to disease in another organ induced amyloidosis, hyperan1monemia in
system. Clinical signs may vruy witl1 ilie

Morgan foals, parasite dan1age, iron toxicity, course of tile disease (acute or chronic), or after neonatal isoeryilirolysis.

primary site of injury (hepatocellular,

In nuninants, hepatobiliary disease is
biliruy ), and specific cause. Onset of signs
associated with hepatic lipidosis, hepatic
of hepatic encephalopatlly and liver failw·e
abscesses, endotoxemia, pyrrolizidine
is often acute regardless of whetller tile
alkaloid and oilier plant toxicoses, certain
hepatic disease process is acute or chronic.

clostridial diseases, liver flukes, mycotoxi

Clinical signs and seve1ity of hepatic
cosis, and mineral toxicosis ( copper, iron,
pathology reflect tl1e degree of compromise
zinc) or deficiency (cobalt). Vitamin E or
of one or more of ilie liver's vital functions,
seleniwn deficiency (hepatosis dietetica),
including blood glucose regulation; fat
aflatoxicosis, ascarid migration, bacterial
metabolism; production of clotting factors,
hepatitis, and ingestion of toxic substances
albwnin, :fibrinogen, nonessential aniino

( eg, coal tar, cyanamide, blue-green algae,
acids, and plasma proteins; bile formation
plants, gossypol) are associated wiili
and excretion; bilirubin and cholesterol
hepatic injury in swine.

metabolism; conversion of runmonia to

Altllough ilie exact incidence of hepatic
urea; polypeptide and steroid hom1one
disease in camelids (llan1as, alpacas) is
metabolism; syniliesis of25-hydroxycholeunknown, it appears to be common in Nortll calciferol; and metabolism and/or

America. Hepatic lipidosis ( secondruy more
detoxification of many drugs and toxins.

often ilian primary) is reportedly the most

Icterus, weight loss, or abnom1al
common liver disease in llan1as and alpacas,
behavior are common in horses witl1 liver
occurring in botl1 crias and adults. Bacte1;al
disease and hepatic failure. CNS signs are

(Salmonella spp, Escherichia coli, Listeria often the initial and predominant sign in spp, Clostridium spp) cholangiohepatitis,
horses with acute hepatic failure, whereas
adenoviral hepatitis and pnewnonia, fungal
weight loss is a prominent sign in most but
hepatitis ( coccidioidomycosis ), toxic
not all horses witll chronic liver disease and
hepatopatlly (copper), haloiliane-induced
failure. Photosensitization and, less
hepatic necrosis, hepatic neoplasia
commonly, bilateral pharyngeal paralysis,

(lymphosarcoma, hemangiosarcoma,
causing inspiratory striclor, diarrhea, or

330

HEPATIC DISEASE IN LARGE ANIMALS
constipation, may be present. Affected
compromised hepatic function results in
cattle usually show inappetence, decreased
phylloerythrin, a photodynarnic metabolite
milk production, and weight loss. Tenesmus
of chlorophyll, entering the ski.ti. Phylloand ascites are seen in cattle but are not erythrin in the skin reacts with ultraviolet
common in affected horses. Weight loss
light and releases energy, causing inflan1mamay be the only sign associated with liver tion and skin damage. Signs of photosensitiabscesses. lcterus, which is most prozation are v3.1.ied but include uneasiness, VetBooks.ir
nounced when the biliary system is
pain, pnuitus, mild to severe dermatitis
diseased, is also common in horses with
with erythema, extensive subcutaneous
acute liver failure. It is more variably
edema, skin ulceration, sloughing of skin
present in horses with chronic liver failw·e
and ophthalmia with lacrimation, photophoor in ruminants. Fasting hyperbilirubinemia bia, and corneal cloudiness. Dern1atitis and
is a more common cause of icterus in horses edema are p3.1.ticul3.1.·ly evident on nonpigand is not associated with hepatic disease.

mented, light-colored or hairless 3.1.·eas of

Occasionally, persistent hyperbilirubinemia
the body and areas exposed to sun.

(p1imarily indirect or unconjugated

Mucocutaneousjw1ctions and patches of
bilirubin) may be seen in healthy horses
white hair are the most conunon sites of

( especially Thoroughbreds) without
photosensitization in cattle. Occasionally,
evidence of hemolysis or hepatic disease. In
the underside of the tongue may be affected.

ruminants, icterus is more commonly due to

Blindness, pyoderma, loss of condition, and
hemolysis and primarily involves increases
occasionally death are possible sequelae.

in indirect bilirubin. Hyperbilirubinemia

Pru1itus may result from photosensitization
caused by obstructive biliary conditions is
or from deposition of bile salts in the skin
rare in goats and sheep.

second3.1.y to alterations in hepatic

Hepatic encephalopathy is associated
excretion.

with behavioral changes in horses,

Diarrhea or constipation may be seen in
nuninants, and swine. The severity of
animals with hepatic disease. Di3.1.Thea is
hepatic encephalopathy often reflects the
more commonly seen in cattle tl1an in
degree of hepatic failure but does not
horses with chronic liver disease or in
differentiate between acute or chronic liver
animals with clu·onic fascioliasis and
failure. Signs of hepatic encephalopathy
hepatotoxic plant poisonings. Ponies and
range from nonspecific depression and
horses witl1 hyperlipemia and hepatic
lethargy to head pressing, circling, aimless
failure may develop di3.I.Thea, l3.111initis, and
walking, dysphagia, ataxia, dysmetria,
ventral edema. Some 3.1.li.mals with liver
persistent yawning, pica, increased
disease have alternating di3.1.Thea 3.11d
friendliness, aggressiveness, stupor,
constipation. Horses with liver failure and
seizures, or coma. Pharyngeal or laryngeal
hepatic encephalopathy frequently develop
collapse with loud, stertorous inspiratory

· colonic impaction due to decreased water
noises and dyspnea occurs in some cases of
intake. Constipation is characteristic of
hepatic failure, especially in ponies. The

Lantana poisoning in goats and other
pathogenesis of hepatic encephalopathy is
mminants.

unknown, but proposed theories include

RecWTent colic, intermittent fever,
anm1onia as a neurotoxin, alterations in
ictems, weight loss, and hepatic encephamonoarnine neurotransmission (serotonin, lopathy may be seen in horses with
tryptophan) or catecholamine neurotranscholeliths that obstruct the conm1on bile mitters, in1balance between aromatic and
duct. Infectious or inflarnmatmy hepatic
short branch chain amino acids resulting in
disease or failure of the liver to prevent
increased inhibitory neurotransmitters
endotoxin from gaining access to t11e

( -y-aminobutyric acid, L-glutarnate ),
systemic circulation may also result in
neuroinllibition due to increased cerebral
intem1ittent fever and colic. Abdominal
levels of endogenous benzodiazepine-like
pain, due to pressure on the liver capsule
substances, increased pern1eability of the
from parenchymal swelling, often is seen in
blood-brain barrier, and impaired CNS
animals with acute diffuse hepatitis or
energy metabolism. Although the signs can
trauma to the capsule itself. Affected
be dramatic, hepatic encephalopathy is
animals stand with an arched back, are
potentially reversible if the w1derlying
reluctant to move, or show signs of colic·. In
hepatic disease can be resolved.

nuninants, pain may be localized to the liver

Photosensitization, which may be seen
by palpation over the anterior ventrolateral
secondary to acute or chronic liver failw·e,
aspect of the abdomen or the last few ribs
must be differentiated from primary
on tl1e right side. Tenesmus followed by
photosensitization (seep 976). Hepatogrectal prolapse is seen in some ruminants enous photosensitization develops when
with liver disease. It may be associated with

HEPATIC DISEASE IN LARGE ANIMALS

331
diarrhea, hepatic encephalopathy, or edema
as depression, weight loss, intermittent
of the bowel from portal hypertension.

fever, and recurrent colic, a.re present

Hypoalburninemia is not as frequently
without an apparent cause. Differentiation
associated with liver disease in horses as
between acute and chronic hepatitis or
previously thought. Due to the Jong half-life
fail me based on the dw·ation of clinical

(-19-20 days in horses, -16 days in cows)

signs before presentation may be misleadand liver reserve for albumin production, ing, because the disease process is often

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hypoalbuminemia is usually a very late
advanced before clinical signs are evident.

event in the disease process. Serum total

Early vague signs of depression and
protein concentrations may be normal or
decreased appetite may be overlooked.

increased because of an increase in

Liver biopsy to detemline the type of

!3-globulins in horses with liver disease.

pathology, degree of hepatic fibrosis

Hypoalbuminemia and hypoproteinemia
present, and the regenerative capabilities
most commonly develop in chronic liver
of the liver parenchyma is necessary to
disease, and they are common findings in
develop a treatment plan and give an

Ila.mas with liver disease. Generalized
accmate prognosis.

ascites or dependent edema may result.

Ascites is related to portal hypertension
caused by venous blockage and increased

Diagnostic Testing: Laboratory tests
hydrostatic pressme and to protein leakage
often detect liver disease or dysfunction
into the peritoneal cavity. The abdominal
before hepatic fail me occms. Routine
fluid present with liver disease usually is a
biochemical tests such as serum enzyme
modified transudate. Hypoalbuminemia can
concentrations are sensitive indicators of
aggravate tl1e ascites, but if it is seen alone,
liver disease, but they do not assess hepatic
it more likely will cause intem1andibular,
function. Dynamic biochemical tests that
brisket, or ventral edema. Ascites is difficult
assess hepatic clearance provide quantitato appreciate in horses and adult cattle tive info1111ation regarding hepatic function.

unless it is extensive. Ascites is a common

Tests of hepatic function a.re useful
finding in calves with liver cirrhosis.

diagnostic and prognostic tools and provide

Anemia may be seen in animals with liver
a guide for the modification of drug-dosing
dysfunction due to parasitic diseases,
regimens.

chronic copper toxicity (in rnrninants ),

Serum Enzyme Concentrations: Serw11
some plant poisonings, or chronic
concentrations of liver-specific enzymes are
inflammatory disease. Anemia in acute
generally higher in acute liver disease than
fasciolosis results from severe hemorrhage
in chronic liver disease. They may be within
into the peritoneal cavity as the larvae
normal lin1its in the later stages of subacute
penetrate the liver capsule. Trauma and
or chronic hepatic disease. The magnitude
feeding activity of adult flukes within the
of increases in hepatic enzymes ( especially
bile ducts cause anemia and hypoproteine

-y-glutamyl transpeptidase) should not be
mia in animals with chronic fasciolosis.

used to dete1111ine prognosis. Hepatic

Chronic inflammatory disease ( eg, hepatic
enzymes are used to determine the presence
abscesses, neoplasia) may cause anemia
of disease but not necessarily the degree of
without accompanying hypoproteinemia.

hepatic dysfunction. Careful interpretation

Clinical signs of severe or terminal
of laboratory values in conjunction with
hepatic fail me include coagulopathies and
clinical findings is essential.

hemorrhage due to decreased production

Sequential measmements of serum
of clotting factors by the liver and possibly

-y-glutamyl transpeptidase or transferase
increased utilization in septic or inflamma

(GGT), sorbitol dehydrogenase (SDH; also
tory processes. A prolonged prothrombin
called iditol dehydrogenase [IDH]), AST,
time is usually seen first because factor VIl
bilirubin, and bile acids are commonly used
has the shortest plasma half-life. Horses
to assess hepatic dysfunction and disease in
may develop a tel111inal hemolytic crisis
large animals. Serum GGT, bilirubin and
ca.used by increased RBC fragility. This has
total bile acid concentrations, and sulfonot been repmted in rnminants.

bromophthalein (BSP®) clearance are not

Fecal color rarely changes in adult
sensitive indicators of liver disease in young
herbivores with liver disease. In young rwnicalves. Although GGT is primarily nants and monogastric aninlals, cholestasis
associated with microsomal membranes in
may result in lighter color feces being
the biliary epitheliun1, it is also present in
passed because of loss of stercobilin, a
the canalicular surfaces of ilie hepatocytes,
metabolite of bilirubin.

pancreas, kidneys, and udder. Because of

Liver disease should always be considminary and milk excreLion of GGT and ilie ered when nonspecific clinical signs, such
rarity of pancreatitis in large anin1als,

332

HEPATIC DISEASE IN LARGE ANIMALS
increased serum GGT concentrations most

Arginase and GLDH are considered specific
commonly indicate bile duct or liver
for acute liver disease, because both have
disease. Some consider GGT to be the single high tissue concentrations in the liver and test of highest sensitivity for liver disease in
short half-lives in the blood. AST is highly
adult large anin1als. Increase of GGT is most
sensitive for liver disease but lacks
pronounced with obstructive biliary
specificity, because high concentrations

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disease. In acute hepatic disease in horses,
come from both liver and skeletal muscle.

GGT may continue to increase for 7-14 days Other AST sources include cardiac muscle, despite clinical improvement and retmn
erythrocytes, intestinal cells, and the
toward normal of other laboratory tests.

kidneys. When CK is sinmltaneously

Reportedly, sernm GGT concentrations
measured to exclude muscle disease and
become increased within a few days of liver
the se1U1n is not hemolyzed, increases in
damage and remain increased until the

AST and LDH-5 are caused by hepatocellutenninal phase. Chronic hepatic fibrosis is lar disease. AST may remain increased
the only liver disease in which an abnormal

10-14 days or longer after an acute,
increase in GGT might not be seen.

transient insult to the liver. AST values are

Neonatal foals have higher GGT concentraoften normal in chronic hepatic disease.

tions due to GGT present in colostrmn and

SDH and AST may be markedly increased
milk. Younger adult horses, especially those
with intral1epatic cholestasis and mildly
in active training, may show a nonspecific
increased with extral1epatic cholestasis.

increase in GGT that is not associated with

Increases in AP and GGT are associated
liver disease or other increases in liver
with i.J.Titation or destmction of biliary
enzymes or se1U1n bile acid concentration.

epitheliun1 and biliary obstruction. AP

GGT is of little value in diagnosing liver
comes from the placenta, bone, macdisease in neonatal calves or lambs, because rophages, intestinal epithelimn, and liver.

it is present in colostrun1 and milk. GGT

AP is increased in very young calves and
activity may also be increased with colonic
foals, probably because of the placental or
displacement or administration of drngs
bone source. In young calves, AP concentra

( eg, corticosteroids, rifampin, benzimidations up to 1,000 IU/L at birth and 500 IU/L at zoles, anthelmintics). Some liver-derived
several weeks of age are considered nonnal.

enzymes are higher in young calves (GGT,

AP concentrations of 152-2,835 IU/L are
alkaline phosphatase [AP], glutamate
reported in foals ( < 12 hr old), and AP
dehydrogenase, lactate dehydrogenase) and activity may remain high compared with foals (AP, GGT, SDH, AST), because they are adult levels for 1-2 mo. In calves ( <6 wk transiently increased or come from sources
old), none of the conunon tests (bilimbin,
other than the liver. Se1U1n levels of hepatic

GGT, GLDH, AP, LOH, AST, or alanine
enzymes also vary in goats with age, breed,
transan1inase) for liver damage or function
and sex. Reference ranges must be
are clinically useful for detection of hepatic
appropriate for the species and age group
disease when used alone. AST and GLDH
being evaluated.

are the most sensitive of the enzymes for

SDH, arginase, omithine carban10yltranshepatic injmy, but AST also increases with ferase (OCT), AST, isoenzyme 5 lactate
muscle damage. AST concentrations in foals
dehydrogenase (LDH-5), glutamate
may be high compared with values of adults
dehydrogenase (GLDH), and AP are also
for many months. This increase is also likely
used to assess hepatic dysfunction and
related to muscle development. Transient
disease. Arginase, SDH, and OCT are
and mild increases in SDH activity may be
liver-specific enzymes in horses, most
noted in some foals <2 mo oki
run1inants, and swine. SDH is most
predictive for active hepatocellular disease,

Serum Total Bile Acid Concentration:

with marked increases in enzyme activity

Se1U1n concentration of bile acids is highly
after hepatocellular dan1age. Mild increases
specific for liver dysfunction but does not
in SDH can also occur with obstrnctive GI
define the type of insult or disease present.

lesions, endotoxemia, anoxia from shock,

Se1U1n bile acid concentrations increase
acute anemia, hyperthermia, and anestl1ewith hepatocellular damage, cholestasis, or sia. Because of their short half-lives, SDH
shunts from the p01tal system to the vena
and LDH-5 are useful in assessing resolution cava. Increases are highest with biliary or progression of liver insult. Both enzymes
obstrnction and portosystemic shunts.

usually retmn to near-normal values 4 days

Se1U1n bile acid concentrations rise early i.J.1
after liver insult, and neither is usually
liver disease and often remai.J.1 high through
increased in chronic liver disease. Rarely, in
the later stages.

severe cases of hepatic failure, SDH may

Total bile acid concentration remains
retmn to normal in spite of a fatal outcome.

increased in horses with chronic liver

HEPATIC DISEASE IN LARGE ANIMALS

333
disease. In horses, there is no diurnal
reference range. In foals, indirect more than
variation, no postprandial rise, and no
direct bilirubin may be increased with
significant hour-to-hour vaiiation in bile
prematurity, neonatal isoerythrolysis,
acid concentrations. Serum total bile acid
septicemia, or a portocaval shunt. Enteritis,
concentration in most healthy horses is
un1bilical infection, intestinal obstruction,

< 10 µmol/L. Concentrations of serum or
and certain drugs ( corticosteroids, heparin,
plasma bile acids >20 µrnol/L have a high
halothane) may also cause hyperbilirubin

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sensitivity ai1d positive predictive value for
emia. Mild, transient physiologic hyperbilidetem1ining liver disease in horses but not rubinemia and icterus may be seen in
in ruminants. Although bile acid concentranewborn foals and calves. Although the tions >30 µrnol/L can be an early predictor
mechanism(s) is not fully known, proposed
of liver failure, caution must be used in
causes include prebirth "loading of
interpretation of mild increases, because
hepatocytes," naturally high RBC destrucbile acid concentrations up to 20 µmol/L
tion at or around birth, inefficiency in
may be seen in horses with anorexia.

bilirubin excretion, or lower hepatocellular

Prolonged, but not short-tem1 ( <14 hr),
ligandin concentrations in neonatal foals
fasting may cause increased serum bile
than in adult horses. In healthy calves <72 hr
acid concentrations in horses.

old, total bilirubin may be as high as 1.5 mg/dL

Interpretation of total bile acid concenand up to 0.8 mg/dL in 1-wk-old calves.

trations is difficult in foals < l wk old.

Direct bilirubin is usually <0.3 mg/dL in

Compai·ed with those in healthy adult
young calves. In healthy foals ( <2 days old),
horses, serum bile acid concentrations in
total bilirubin concentrations may range
healthy foals are considerably greater
from 0.9-4.5 mg/dL, with most being
during the first 6 wk of life. When measuring
uncoajugated bilirubin (0.8----3.8 mg/dL).

serum bile acid concentrations in sick foals,

PrematUJity or illness ( without liver
it is particularly important to have healthy,
disease) may increase uncoajugated
age-matched controls or age-dependent
bilirubin fraction in young foals. Bilirubin
clinical pathology values for reference.

concentrations in healthy foals should be

In dairy cattle, serum bile acid
within adult reference ranges by the time
measurement is of little value in recognizing
tl1ey are 2 wk old. Normal values for total
fatty liver or liver disease or failure because
bilirubin in goats ai·e 0-0.1 mg/dL.

of significant hoUJ"to-hour variations. In

Horses with hepatic disease and failure
recently freshened cows, serUJ11 total bile
most often have significant increases in
acid concentrations are significantly higher
both indirect and direct bilirubin. With liver
tl1an in cows in mid-lactation or in 6--mo-old
dainage in horses or rUJ11inants, most of the
heifers.

retained bilirubin is indirect (uncoaju

Total bile acid concentration may be the
gated), and the direct-to-total ratio usually
best single test for hepatic disease in young
is <0.3 (more than two-thirds is indirect).

calves. In calves, concentrations

Acute liver failure caused by hepatic

>35 µmol/L may indicate liver disease, bile
necrosis results in increases in both indirect
obstruction, or a portosystemic shunt.

and direct bilirubin fractions. In horses with

Reported reference intervals for serum
acute liver failure, the increase in bilirubin
concentration of bile acids are
is primarily because of an increase in the

1.1-22.9 µmol/L for llamas > l yr old and
indirect fraction. Hepatocellular disease

1.8-49.8 µrnol/L for llan1as < l yr old. Bile
should be considered when the indirect
acid concentrations in individual llainas
bilirubin fraction is >25% of the total
may vaiy with feeding or san1pling time of
bilirubin value. Direct-reacting bilirubin
day, remaining within the reference interval. rai·ely exceeds 25%-35% of the total Serum Bile Pigments: Evaluation of
bilirubin in horses. Increases of this
serum bilirubin ( direct and indirect)

magnitude suggest predominant biliaiy
concentration is useful to determine hepatic disease or obstruction. With bile blockage dysfunction in horses and rU1ninai1ts.

or intral1epatic cholestasis, the direct

Increases in bilirubin result from hemolysis,
to-total ratio may be >0.3 in horses or 0.5 in
hepatocellular disease, cholestasis, or
cows. Increases in direct bilirubin may be
physiologic causes. Anorexia in horses
seen in septic foals with intestinal ileus and
causes a physiologic increase in total serum
minimal evidence of hepatocellular
bilirubin to usually <6----8 mg/dL and rarely as dysfunction.

high as 10.5---12 mg/dL, accUJnulating at a

In chronic liver disease, bilirubin
rate of -1 mg/dL for each day of anorexia.

concentrations are often within nom1al

The indirect bilirubin increases 2- to 3-fold,
limits. Adult cattle and calves may have
while the direct bilirubin remains within the
severe liver disease without any increase in

334

HEPATIC DISEASE IN LARGE ANIMALS
serum bilirubin. In cattle, goats, and sheep,
detected because factor VII, a liver-synthecirculating bilirubin concentrations sized vitanlin K--<lependent factor, has the
increase only modestly with severe,
shortest half-life. Serum PT may be rapidly
generalized hepatic disease. The most
prolonged with hepatic failure and is one of
dramatic increases in serum or plasma
the first function tests to return to normal
bilirubin concentrations are due to
with recovery from acute hepatic disease.

hemolytic crises rather than to liver

A normal PT determination, however, does

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dysfunction. In the absence of hemolysis,
not exclude coagulopathy due to vitamin K
total serum bilirubin concentrations
deficiency. Prolonged activated partial

>2 mg/dL indicate in1paired hepatic function
thromboplastin time (APTT) or other
in rwninants.

indications of coagulopathy may be noted

Urobilinogen: Urobilinogen may be
in animals with severe hepatic disease.

detected by dipstick analysis in healthy

Because a nun1ber of factors may influence
horses. Increased concentrations of

PT or APTT values in horses, the ratio of
urobilinogen in urine without hemolysis
clotting time of the horse with suspected
are suggestive of a hepatic dysfunction,
hepatic disease to that of a healthy horse's
portosystemic shunting, or increased
value should be > 1.3 for the test to be
production by intestinal bacteria. Urobilinointerpreted as abnom1al.

gen in the urine indicates the presence of a

Urea, Glucose, Ammonia, and Other
patent bile duct. Absence of urobilinogen

Alterations: Serun1 concentration of urea
may indicate complete biliary blockage,
may be decreased in both acute and chronic
liver disease, or failure to excrete bilirubin
liver failure. Hypoglycemia is conunon in
into the intestine, reduce it by intestinal
foals with hepatic failure. Blood glucose
bacteria, or absorb it from the ilewn. The
concentrations in adult horses with hepatic
correlation between urobilinogen and
dysfunction are frequently normal or
hepatocellular disease in animals is poor.

increased. Hypoglycemia, while less

Urobilinogen is unstable in urine; thus,
common in adult horses and ruminants
analysis must be done within 1-2 hr, or the
with hepatic dysfunction, is more likely in
an1ow1t will be decreased or undetectable.

chronic liver disease. Plasma triglyceride

Serum and Plasma Proteins: Serun1
concentrations are markedly increased in
albwnin and protein concentrations are
ponies, miniature horses, donkeys, and
variable in horses and cattle with hepatic
adult horses with hepatic lipidosis. The
disease. Hypoproteinemia is not conunon
magnitude of increase in serum triglycerin horses with acute liver disease. Serw11
ides may correlate with prognosis in horses.

albwnin is most likely to be reduced in

Alterations in triglycerides, very-lowchronic liver disease due to decreased density lipoproteins, and esterified
functional hepatic parenchyma. In one
cholesterol levels are more common in
study of 84 horses, 13% were hypoalblllllinflllllinants than in horses with hepatic emic. Albwnin concentrations were below
insufficiency. Neonatal foals have higher
minimwn reference values in 18% of horses
blood cholesterol and triglyceride
with chronic liver disease and 6% with acute
concentrations than adult horses.

liver disease. Globulin concentrations were

Plasma ammonia concentrations may be
increased in 64% of the horses. Hyper'

increased with hepatic insufficiency but do
proteinemia due to hyperglobulinemia
not correlate well with severity of hepatic

(polyclonal gammopathy or increase in
encephalopathy except during portocaval

13 -globulins) may develop in horses with
shunts. Increased concentrations of blood
severe acute or chronic liver disease. Total
anunonia and signs of hepatic encephalopaplasma protein concentration is often thy without hepatic failure are reported in
nmmal, but the albunlin to globulin ratio

Morgan weanlings with hyperornitllinemia,
may be decreased.

hyperanunonemia, and nom1ocitrullinuria

Plasma fibrinogen concentration may not
syndrome and in adult horses with primary
be a sensitive test in horses with hepatic
or idiopathic hyperan1monemia. Ingestion
insufficiency. Low fibrinogen concentraof urea or anunonilllll salts is more likely to tions may result from parenchymal
cause increases of blood ammonia and
insufficiency or disseminated intravascular
encephalopathy in cattle than in horses.

coagulopathy. A high fibrinogen concentra

PCV and serum iron concentrations are
tion is associated with an inflammatory
often high in horses with severe liver
response in horses with cholangiohepatitis.

disease. An increased PCV may persist
in the face of fluid therapy and normal

Prothrombin Time: Abnormalities in
hydration status until the W1derlying liver
prothrombin time (PT) are often the first
disease is resolved. Secondary erythrocyto-

HEPATIC DISEASE IN LARGE ANIMALS

335
sis ( with or without increased erythropoihistopathology. Ultrasound can be used to etin concentration) has been noted in some
guide collection of liver biopsy specin1ens
horses with hepatic neoplasia. Increased
and to perfom1 cholecystocentesis and
serum iron concentration is commonly seen
aspiration of abscesses, masses, or bile
in horses with either hepatic and/or
samples (fluke eggs, bile acids, culture).

hemolytic disease.

It is also an accurate, noninvasive way to
monitor the progression or resolution of

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Dye Excretion and Clearance Tests:

Sulfobromophthalein (BSP
disease. In horses, the liver should be

®) or indocyanine green dyes can be used to assess
imaged from both the right and left sides
hepatobiliary transport. The BSP hal f -life is
of the animal.

prolonged when >500A, of hepatic function is

Liver Biopsy: Percutaneous liver biopsy
lost. The nonnal clearance half-life of BSP is is the definitive way to diagnose hepatic

<3.7 min in horses, 2.13 ± 0.19 min in goats,
disease. Histologic evaluation of the liver
and s4 min in sheep. BSP clearance is longer provides valuable information regarding in calves (5--15 min) than in adult cattle
cause and severity of the disease process.

(s5 min). Although dye excretion tests are

Most cases of liver disease are diffuse, so
usually prolonged with hepatic dysfunction,
the sample will be representative of the
they may still be within the nom1al range.

disease. Samples can be obtained blindly,

Hyperbilirubinemia, decreased hepatic
but ultrasonographic guidance decreases
blood flow, and signiiicant cholestasis
the risk of complications (peritonitis due
may falsely prolong BSP clearance, and
to bile leakage or intestinal puncture,
hypoalbuminemia may falsely shorten
hemorrhage, or pneun10thorax). Liver
it. BSP clearance in goats is most often
biopsies can also be obtained during
prolonged with generalized hepatic lipidosis laparoscopy, which offers the additional secondary to pregnancy toxemia. Detem1iadvantage of being able to visualize the nation of BSP clearance time, rather than
surface of the liver and other abdominal
half-life, reportedly is more useful in
organs for evidence of disease.

detection of liver disease. BSP clearance

Samples should be placed in media for
time in healthy fed and 3-day fasted horses
bacterial culture and sensitivity and in
is 10 mUmin/kg and 6 mUminlkg, respecfonnalin for histologic evaluation.

tively. These tests, however, are of limited

Coagulation profiles (prothrombin time,
use in clinical practice because of the lack
partial thromboplastin time, fibrinogen,
of commercially available pharmaceuticalfibrin degradation products, and optional grade BSP. Expense, procedural limitations,
platelet count) may be performed before
and equipment requirements for quantitaliver biopsy to reduce the risk of hemo1�
tion of indocyanine green clearance have
rhage. Liver biopsy may not be advised in
limited its use as a diagnostic test.

an anin1al with clinical or clinicopathologic
evidence of a coagulopathy or a hepatic

Scintigraphy: Biliary patency and
abscess, because hemoffhage or contamihepatocyte function, structure, and blood nation of the peritoneal cavity may result.

flow may be evaluated by hepatobiliary scintigraphy. Radionucleotide liver scans and Radiography: Contrast abdominal
biliary scans can detect alterations in blood
radiography in foals may help diagnose
flow or hepatic masses and biliary
gastroduodenal obstructions and secondary
obstruction (atresia, cholangitis, cholelithicholangiohepatitis. Portosystemic shunts in asis ), respectively. Scintigraphy has been
foals or young calves can be identified with
used in pigs, foals, and Jambs to differentimesenteric portovenography by iltjecting ate biliary obstruction from other causes of
radiopaque contrast solution into a jejunal
hyperbilirubinemia.

mesenteric vein, followed by fluoroscopy or
sequential survey radiographs to monitor

Ultrasonography: Ultrasonography can
the hepatic blood flow.

be used to evaluate liver size, appearance

(shape, texture), and location in horses and

Treatment and Management: Initial
ruminants for diagnosis of hepatomegaly,
treatment of animals with signs of hepatic
hepatolithiasis, biliary dilatation, choledisease or insufficiency is often supportive lithiasis, or focal lesions. Tumors, cysts,
and started before the underlying cause and
abscesses, and granulomas may be seen.

extent of hepatic damage is known. History,

Diffuse diseases are harder to detect than
clinical signs, and laboratory data may give
focal processes, because the former cause
some clue as to the nature of the hepatic
less distortion of normal hepatic architecdisease process, but liver biopsy is usually ture. Diagnosis of diffuse liver disease
required to make a definitive diagnosis and
should be substantiated by biopsy and
to detennine the degree of hepatic iltjury.

336

HEPATIC DISEASE IN LARGE ANIMALS

Specific therapies for hepatic disease
be present. Because rapid correction of the
depend on cause, presence of liver failtu-e,
acidosis may exacerbate nemologic signs,
chronicity, degree of hepatic fibrosis or
acidosis should be corrected gradually by
biliary obstruction, and species affected.

IV administration of fluids with a high

Increases in hepatic enzymes without
concentration of electrolytes. U this fails or
hepatic disease may not requiTe specific
if blood pH is <7.1 (bicarbonate <14 mEq/L),
therapy for the liver but rather for the
bicarbonate may be administered cau

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primary disease.

tiously. Supplemental vitan1ins are optional.

Therapy is most successful when

Adequate fresh water should be available if
intervention is early, hepatic fibrosis is
the animal can swallow nom1ally.

minimal, and evidence of regeneration in

Factors that may contribute to the hepatic
the liver exists. Horses with severe or
encephalopathy should be eliminated.

bridging fibrosis respond poorly because of

Glucose as a 5o/<>-100Aisolution is given to
inadequate potential for liver regeneration.

correct hypoglycemia if present. In addition,

The goals for treatment of large animals
glucose supplementation helps decrease
with hepatic disease or insufficiency are to
blood ammonia concentrations and reduces
control hepatic encephalopathy, to treat the
catabolic gluconeogenesis, protein
tmderlying disease process, to provide
catabolism, and need for hepatic gluconeosupportive care to allow tin1e for liver regengenesis. Unless the animal is hyperglycemi.c, eration, and most in1portantly, to prevent
a continuous IV infusion of glucose (5% at 2
injmy to the animal and those working with
rnUkg/hr or 1 ()OA, at 1 rnUkg/hr) should be
the animal. Anin1als with hepatic encephagiven, even to animals that are not hypoglylopathy often show aggressive and cemic. The infusion rate should be acljusted
unpredictable behavior that can result in
so tlmt euglycemia is maintained. Induction
injury to self or handlers.

of moderate to severe hyperglycemia, rapid
changes in glucose level, and glucosuria

Hepatic Encephalopathy and Hepatic
should be avoided. IV glucose should be used

Failure: Horses with hepatic encephalopain combination with balanced electrolyte tl1y may be aggressive or demonstrate
fluids and not as the sole fluid somce.

repetitive behaviors that make restraint

Therapies directed toward decreasing
difficult. To ensure safety of the anin1al and
either ammonia production in or absorption
handlers, sedation is required. Because
from the bowel include administration of
most sedatives and tranquilizers are
mineral oil, neomycin, lactulose, and
metabolized by the liver, t11eir elimination
metronidazole. Ad.ministration of mineral
half-life may be prolonged in animals with
oil decreases absorption and facilitates
hepatic failure; therefore, dosages should
removal of anm10nia. Passing a nasogastric
be mini.mi.zed initially until it is detem1i11ed
tube in an animal with hepatic encephalopahow the animal responds to lower dosages.

thy must be done cautiously, because nasal

Xylazine or detomi.d_ine given in small doses
bleeding caused by decreased clotting
to effect can be used to control horses
factors may be difficult to control. Oral
exhibiting abnormal behavior. Diazepam
administration of neomycin (10-30 mg/kg,
should be avoided in animals with hepatic
bid-qid for 1-2 days) has been used to
encephalopathy, because it may enhance
decrease an11110nia-producing bacteria in
the effect of -y-aminobutyiic acid on
the intestine. Lactulose (0.2 rnUkg, bid; 0.3
inhibitory neurons and worsen neurologic
ml/kg, PO, qid; or 90-120 ml/450 kg, tid-qid)

signs. Acepromazine should also be
is metabolized to organic acids by bacte1ia
avoided, because it may lower the seizure
in the ilewn and colon . .Reduction in colonic
threshold.

pH reportedly fosters an increased bacterial

Dehydration, acid-base and electrolyte
assinillation of ammonia, decreased
imbalances, and hypoglycemia should be
ammonia production, ammonia trapping in
corrected with approp1iate IV fluids.

the bowel, intestinal microflora changes,

Initially, a balanced polyioni.c solution is
and osmotic catharsis. Rep01tedly, oral
administered for rehydration. Potassiwn
administration of vinegar ( acetic acid) has
supplementation is added (10-40 mEq/L,
the same effect on colonic pH and ammonia
depending on infusion rate) if the animal is
concentration in the gut. Metroni.dazole
hypokalemic or hypophagic. U IV infusion is

(10-15 mg/kg, PO, bid-qid) decreases
not possible in rwninants, rehydration may
ammonia-producing organisms in horses
be attempted by oral administration offlui.ds but should not be used in food animals. U
if rumen motility is normal. Rarely, some
t11e anin1al can swallow, oral drugs can be
horses with hepatic disease have polymixed with com syrup or molasses and cythemia, making evaluation of hydration
given via dose syringe to avoid trauma and
status by PCV difficult. Severe acidosis may
the risk of inducing hemorrhage dming

HEPATIC DISEASE IN LARGE ANIMALS

337 ·
passage of a nasogastric tube. Neomycin,
dysphagia may be a problem. Relatively
lactulose, and metronidazole may all
small amounts should be fed frequently,
potentially induce mild to severe diarrhea
although this recommendation may prove

( salmonellosis) because of disruption of GI
impractical in the longterm for many clients.

flora. Use of the drugs in combination is

The diet should meet energy needs with
more likely to induce diaiThea than any one
readily digestible carbohydrates, provide
of the drugs given alone. Because metroniadequate but not excessive protein, have a VetBooks.ir
dazole is metabolized by the liver, caution
high ratio of branched-chain amino acids to
must be used when administering the drug
aromatic amino acids, and be moderate to
to horses with hepatic failure. Neurologic
high in starch to decrease need for hepatic
signs due to metronidazole toxicosis may
glucose syntl1esis. Fat and salt should not be
mimic hepatoencephalopathy.

added to the diet. Feeds used successfully in

Until the nature of the underlying hepatic
horses include grass or oat hay, com, and
disease is known, treatment with broadsorghum. Small amounts of molasses may spectrurn antin1icrobials is waJTanted if infecbe added to improve palatability and acid tious hepatitis is suspected. A trimethoprirnenergy. Linseed meal and soybean meal sulfa combination is a good empiric choice
have an excellent branched-chain to
because of its activity against gram-negative
aromatic amino acid ratio and may be used
bacteria and its high concentration in bile.

as a protein supplement in small quantities.

Penicillin in combination with an anlinogly

Beet pulp may be substituted for oat or
coside has a broad spectrum of action and
grass hay. Beet pulp may be soaked first
may be of benefit if a Streptococcus sp or an to allow full expansion before being fed.

anaerobic or gram-negative coliform is

Choke may be a problem in some animals
suspected. Enrofloxacin has also been
eating beet pulp.

recommended. First- and second-generation

The feeding of alfalfa hay, alfalfa-containcephalosporins have been used in foals and ing feeds, or otl1er legume hays to horses
in other species. Ceftiofur sodium also has an
with hepatic disease is controversial.

enterohepatic cycle, with -15% of active drug

Although alfalfa hay has a better branchedrecycled through the liver and excreted out chain to aromatic amino acid ratio than
the biliary tree. Ceftiofur has a broader
grass hay, it may have too high a protein
spectrum than most early generation cephalocontent. Feeding grass hay is preferred for sporins and has proved useful to treat
animals with hyperammonemia or signs of
acute or recurrent ascending bacterial
hepatic encephalopathy. A mixed grass/
cholangiohepatitis. Metronidazole may be
alfalfa hay can be fed to horses without
administered when anaerobic infection is
central neurologic signs if weight loss is a
suspected in horses. Specific antimicrobial
problem and the added protein is tolerated.

therapy based on culture and sensitivity of

Grazing grass pastures is allowable as long
a liver biopsy is ideal.

as signs of hepatic encephalopathy are

Pain may be controlled with appropriate
controlled and exposure to sunlightjs
doses of an NSAID ( eg, flunixin meglumine,
avoided.

1.1 mg/kg, IV, bid, or phenylbutazone

Other feeds high in branched-chain

4.4 mg/kg, IV or PO, bid). Vitamin K, (up to
amino acids include sorghwn, bran, or

1 mg/kg, SC; 40-50 mg/450 kg, SC) and
milo. Parenteral or enteral supplement with
plasma transfusions (1-21/100 kg) may be
branched-chain amino acids helps restore
given when coagulopathies develop or
the nom1al ratio of branched-chain to
hypoalbuminemia is present. In some horses aromatic anlino acids. Supplementation with acute hepatic disease and failure,
witl1 vitamins A, D, E, and K might be
antioxidant ( dimethyl sulfoxide, acetylindicated, because these fat-soluble cysteine, vitamin E, S-adenosylmethionine
vitainins are not stored effectively or readily

[SAMe ]), and anti-inflammatory (flunixin
available from a diseased liver. Vitan1in K1
meglumine, phenylbutazone) therapy may
may be indicated in animals with a
be useful. Mannitol has been recommended
coagulopathy. Large amounts of fat should
for treatment of suspected brain edema in
not be fed to meet energy requirements;
fulminant hepatoencephalopathy. Horses
excessive fat may lead to a fatty liver.

with hepatic disease should be protected

Transfaunation (seep 2562) with rumen
from sunlight.

fluid from a healthy cow may help
reestablish nom1al run1inal flora and

Dietary Management: Dietary manenhance the appetite of affected cattle.

agement is essential for management

Animals that will not eat volW1tarily must
of animals with hepatic encephalopathy or
be force fed. A gruel may be given by
acute or chronic hepatopathy. Affected
nasogastric tube in horses and swine or
animals should be fed carefully, because
by orogastric tube or rumen fistula in

338

HEPATIC DISEASE IN LARGE ANIMALS
ruminants. In ruminants, forced feeding
may develop as a potential complication of
of alfalfa meal (15% protein) and dried
administration of ai1y equine plasma or
brewer's grain or beet pulp with potassium
serum product that includes commercial
chloride and nom1al rumen fluid has been
equine plasma. However, other affected
recommended. Alfalfa hay and alfalfa-conhorses have no prior history of exposure taining feeds may be better tolerated by
to such a product. Subclinical IAHD can
cattle than by horses with hepatic disease.

also develop after administration of TAT.

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IV polyionic fluids with 5% dextrose,

Most commonly, only one horse on the
potassiwn chloride, and B vitamins may
premises is affected, although outbreaks
also be needed in animals not consuming
may occur or other horses on the farm
adequate amounts.

may have evidence of liver disease

(increased enzyme levels) without clinical

ACUTE HEPATITIS
signs. Occurrence of the disease in groups
of adult horses during the late summer or

Acute hepatitis can have an infectious, toxic,
early fall (August to November) suggests
or undefined cause. Clinical signs may appear an infectious (viral) or vecto1�spread suddenly, with horses appearing lethargic,
etiology, although supporting evidence is
anorectic, and icteric. Photosensitization,
lacking. The seasonal occurrence could
diatrhea, and clotting abnonnalities also may
reflect the fact that many foaling mares
be seen. Neurologic signs resulting from
receive TAT in the spring of the year along
hepatic encephalopathy and/or hypoglycewith their newborn foals. Lactating mares mia can be most severe in aninlals with acute
that receive TAT at foaling seem to be
fuhninant liver disease. Signs of endotoxemia
more susceptible. A Type III (immune
may be present, depending on the underlying
complex-mediated) hypersensitivity
cause and tile ability of the Kupffer cells to
reaction also has been proposed. Recent
remove endotoxin from the systemic
evidence suggests a viral cause, with a
circulation. Increases in serw11 sorbitol

"Theiler disease-associated virus" of the
dehydrogenase (SDH) and AST activities

Flaviviridae documented in association
indicate acute hepatocellular ir\jury. Serum
with a naturally occurring outbreak of

-y-glutan1yl transpeptidase or transferase

Theilier disease. The offending virus was

(GGT) is increased with cholestasis
identified from diseased horses and was
secondary to hepatocyte swelling. Cholestacharacterized as very similai· to human sis results in hyperbilirubinemia, with the
hepatitis viruses Band C. The newly
direct ( conjugated) fraction ranging from
identified virus was then administered

15%---35% of total in horses. Increased serun1
experimentally to previously naive
total bile acid concentration, decreased
research horses, which developed signs of
glucose and BUN concentrations, and .

Theiler disease, proving that it could be
prolonged coagulation tinles become evident
passed from one horse to another via
as hepatic function progressively worsens.

serum administration and resulting in

Anorexia can lead to hypokalemia_ The CBC
similar disease.

is variable, because it may reflect an
inflanmrntory response with a neutrophilia or Clinical Findings: Onset of clinical signs endotoxemia with a neutropenia, increased
is acute. Acute mortality may be 50"/o---60"Ai, band neutrophils, and toxic"changes.

with overall mortality as high as 88% in
affected horses. Horses with IAHD typically

Idiopathic Acute Hepatic Disease
present with anorexia, hepatic encephalopathy, and icterus. Th� CNS signs are (Theiler disease, Serum hepatitis,
variable, ranging from lethargy to aggres

Postvaccinal hepatitis)

sion or matliacal behavior, central

Idiopathic acute hepatic disease (IAHD) is
blindness, and ataxia. Photosensitivity and
the most common cause of acute hepatitis
discolored urine due to high bilirubin
in horses. It is primarily a disease of adult
concentrations may be seen. Fever is
horses.

present in ---50"A, of cases. Weight loss

(uncommon), ventral edema,jugular pulses,

Etiology and Epidemiology:

ileus, and acute respiratory distress have

Frequently, horses with IAHD show clinibeen seen in some horses with IAHD. These cal signs of hepatic failure 4-10 wk after
findings suggest there may be a subclinical
receiving an equine origin biologic, such as phase before development of overt hepatic tetanus antitoxin (TAT). In some cases, the failure. Intravascular hemolysis with affected horse may not have received TAT
hemoglobinuria may be seen in some
but may have been in contact with another
tern1inal cases. Most cases are sporadic, but
horse that received TAT. Reportedly, IAHD
outbreaks with several horses involved

HEPATIC DISEASE IN LARGE ANIMALS

339
have been reported. Recognition of lAHD

Recovery depends on the degree of
in one horse indicates horses on the same
hepatocellular necrosis. Affected horses
premises should be carefully monitored
that remain stable for 3-5 days and that
for clinical or serum biochemical signs of
continue to eat often recover. Decreases in
hepatic disease.

SDH concentration and prothrombin tin1e

Serum concentrations of GGT, AST, and
along with improvement in appetite are

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SDH are increased. GGT is frequently
the best positive predictive indicators of
further increased during the first few days
recovery. Horses with rapid progression of
of illness, despite clinical improvement and
clinical signs, uncontrollable encephalopaeventual recovery in an affected horse.

thy, hemorrhage, or hemolysis have a poor

Horses with AST values >4,000 IU/L have
prognosis. For affected horses that do
a poor prognosis. AST concentrations
recover, the longterm prognosis is good. In
decrease within 3-5 days in horses that
some horses, progressive weight loss and
improve, and SDH concentrations decrease
death may occur during the months after
even more rapidly. Total serum bilirubin
the initial clinical signs.

concentration is generally higher in horses
with IAHD than in horses with anorexia.

Prevention: Use of TAT is not without

Hyperbilirubinemia is conunon, with the
risk. Routine administration of TAT to partuunconjugated form being > 7Cf'lo of the total.

Iient mares is strongly discouraged. Use of

Serum total bile acid concentrations are

TAT should be restricted to situations necesincreased. Moderate to severe acidosis, sitating tetanus prophylaxis and in which a
hypokalemia, polycythemia, increased
history of active tetanus toxoid immunizaplasma aromatic amino acids, and tion is absent or unknown.

hyperammonemia may also be present.

Lesions: At necropsy, icterus and varying

Acute Hepatic Necrosis in Cattle
degrees of ascites are present. The liver is

Epidemiology and Pathogenesis:

usually small to normal in size but may be

Acute hepatic disease and failure in cattle
enlarged (peracute cases), with a mottled
most commonly results from a toxic insult.

and bile-stained surface. Histologically,

Hepatocellular necrosis with clinical and
there is marked centrilobular-to-midzonal
laboratory evidence of hepatic failure may
hepatocellular necrosis and mild to
develop in cattle after mastitis or metritis
moderate mononuclear infiltrate. Mild to
with clinical signs of endotoxemia.

moderate bile duct proliferation may be

Endotoxin induces hepatocellular necrosis
seen in some animals with more chronic
through both direct and indirect effects on
disease.

the liver. Endotoxin can cause Kupffer cells
to release lysosomal enzymes, prosta

Diagnosis: Diagnosis is based on history,
glandins, and collagenase that damage
abrupt onset of clinical signs, and laborahepatocytes, or it may interact directly with tory alterations suggestive of hepatic insuffithe hepatocytes, causing lysosomal damage, ciency. In some cases, the liver is shrunken
decreased mitochondrial function, and
and difficult to visualize with ultrasononecrosis. Endotoxi n -related hepatocellular graphic examination. A definitive diagnosis
necrosis may be due in part to decreased
can be made only by liver biopsy. Differenhepatic blood flow and liver hypoxia.

tial diagnoses include acute pyrrolizidine
toxicosis, hepatotoxins, acute infectious

Clinical Findings and Lesions: Clinical
hepatitis, acute mycotoxicosis, cerebral
signs include weight loss, anorexia, and
disease, and hemolytic disease.

cessation of milk production. Photosensitization and mild icterus are variable. Serun1

Treatment and Prognosis: There is

SDH, GGT, and AST concentrations are
no specific therapy for IAHD. Supportive
mildly to severely increased. Fatty liver or
therapy (IV crystalloid fluids with glucose
ketosis is not characteristic. The liver may
and potassium added) and treatment of the
be normal in size or mildly enlarged.

hepatic encephalopathy may be successful.

Histologically, there is marked hydropic

Stressful situations, such as moving the
change with varying degrees of hepatic
animal or weaning the mare's foal, may
necrosis.

exacerbate the clinical signs of hepatic
encephalopathy and should be avoided.

Diagnosis: Diagnosis is based on a

Sedation should be used only to control
history of hepatic-related signs developing
behavior that could lead to injury of the
concurrently or after a primary disease
animal or handlers and to allow therapeutic
and endotoxemia. Increases in hepatic
procedures.

and biliary enzymes and absence of ketosis

340

HEPATIC DISEASE IN LARGE ANIMALS
support the diagnosis. Definitive diagnosis
bile stasis, hepatic duct obstruction, and
is based on liver biopsy and by excluding
cholangiohepatitis. Parasite migration
other infectious, toxic, and inflanunatory
ilirough ilie liver may predispose to
causes of hepatic dysfunction. Differential
cholangiohepatitis in some anin1als.

diagnoses include other causes of subacute

Gram-negative organisms, including
or chronic liver disease ( eg, hepatotoxins,

Salmonella spp, Escherichia coli,

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hepatic lipidosis) and conditions causing

Pseudomonas spp, and Actinobacillus
weight loss and hypophagia.

equuli are frequently isolated from ilie liver.

Clostridium spp, Pasteurella spp, and Treatment: Nutiitional and fluid support

Streptococcus spp are less frequently
is often successful in affected cows witl1
recovered.

acute hepatic necrosis after transient
insults. Forced feeding of alfalfa meal (15%

Clinical Findings: Depending on the
protein) and dried brewers' grain or beet
severity of infection and virulence of ilie
pulp witl1 potassium chloride and normal
organism, clinical signs may be acute wiili
nunen fluid is recommended. IV polyionic
severe toxemia, subacute, or chronic. Most
fluids with 5% dextrose, potassium chloride, typically, chola.ngiohepatitis is a subacute and B vitamins may also be needed. Control or chronic disease process, wiili affected of endotoxernia and treatJnent of the primary anin1als showing signs of weight loss, disease condition are essential.

anorexia, inte1mittent or persistent fever, or
colic. Icterus, photosensitivity, and signs of

INFECTIOUS HEPATITIS AND
hyperanunonemic hepatic encephalopailiy

HEPATIC ABSCESSES
are variable. Sorbitol dehydrogenase (SDH),

AST, -y-glutamyl transpeptidase or

Tyzzer Disease
transferase (GGT), coajugated bilirubin,
and total bile acid concentrations are

Tyzzer disease, due to Clostridium
usually increased. Peripheral WBC counts
piliforme (previously Bacillus piliformis ), a,,·e variable, depending on the degree of
causes an acute necrotizing hepatitis,
inflanm1ation and endotoxemia present.

myocarditis, and colitis in foals 8-42 days

Acute, suppmative cholangiohepatitis may
old. (See also p 199.) It has been reported occasionally result in severe septicemia and
in two calves: a 1-wk-old Jersey bull calf
deatl1.

with enteritis and multifocal necrotizing
hepatitis and a second calf with concurrent

Lesions: In acute cases, ilie liver is
cryptosporidiosis and coronaviral enteritis.

swollen, soft, and pale. Suppmative foci

In the latter anin1al, C piliforme was
may be visible beneatl1 ilie capsule or on
identified in hepatocytes and epiilielium
cut surface. Lesions in other systems may
and smooth muscle cells of the ileum and
reflect septicemia and jaundice. Microcecum. Clinical signs included hypophagia, scopically in acute cases, neutrophils are
generalized weakness, dullness, and
present in the portal triads and degenerate
decreased fecal passage.

parenchyma. Purulent exudate is evident
in the ducts. In subacute or chronic

Cholangiohepatitis
cholangiohepatitis, the inflai1unation is
more proliferative and bile duct prolifera

Cholangiohepatitis is a severe inflammation more pronounced. Areas of atrophy, tion of the bile passages and acljacent liver,
regenerative hyperplasia, and periportal
which sporadically causes hepatic fail me
fibrosis may be evident.

in horses and nuninants. It occasionally
occurs secondary to cholelithiasis, duodeni

Diagnosis: Liver biopsy should be
tis, intestinal obstruction, neoplasia, pa,,"

performed to confirm the diagnosis and
asitism, and certain toxins in horses. The
to obtain a liver san1ple for aerobic and
fungal toxin sporidesmin from Pithomyces
anaerobic culture and sensitivity. Differen
chartarum may cause cholangiohepatitis in tial diagnoses include other causes of sheep and cattle.

acute to chronic hepatic disease, weight
loss, colic, or sepsis. If neurologic signs

Etiology: Bacteremia due to an organism
are present, cerebral diseases must be

( eg, Salmonella spp) eliminated in ilie bile, considered. Because cholangiohepatitis is
an ascending infection of the biliary tract
frequently associated with cholelithiasis
after intestinal disturbance, or ileus is
in horses, the presence of one or more
thought to be related to the development
calculi must be excluded; ultrasonography
of cholangiohepatitis. In foals, duodenal
of the liver may prove valuable in this
ulceration and duodenitis may result in
case.

HEPATIC DISEASE IN LARGE ANIMALS

341

Treatment: Treatment based on culture
include Proteus sp, Mannheimia haemo
and sensitivity results from liver tissue
lytica, Staphylococcus epidermidis,
often gives favorable results. Therapy

S aureus, Rhodococcus equi, Erysipelo
consists of longterm (;:,,4-6 wk) antimicro
thrix rhusiopathiae, and the yeast
bial administration, supportive therapy

Candida krusei. In horses, hepatic
with IV fluids, and management of
abscesses often contain Streptococcus spp

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hepatoencephalopathy, if present. Initially,

(S equi equi, S equi zooepidemicus ),
broad-spectrum antimicrobials effective

C pseudotuberculosis, or enterobacteria
against gram-negative, gram-positive, and
after ascending cholangiohepatitis or
anaerobic organisms should be adminisintestinal disease, and anaerobes. In pigs, tered. A combination of penicillin with
hepatic abscesses develop after migration
either a trimethoprim-sulfa or an aminoglyof ascarids into the bile ducts.

coside or enrofloxacin may be used.

The liver is particularly susceptible to

Ampicillin or a cephalosporin can be used
abscess formation, because it receives
instead of penicillin. Ceftiofur sodium has
blood from the hepatic artery, the portal
an enterohepatic cycle and broader
system, and the umbilical vein in the fetus
spectmm and may prove valuable in
and the newborn. Hepatic abscesses are
treatment. Metronidazole can be used
most prevalent in mminants and uncomin horses to treat anaerobic bacteria.

mon in horses. Abscesses are associated

Antimicrobial therapy can be altered
with mmenitis (rumenitis-liver abscess
pending results of culture of tissue
complex), bacteremia, septic portal vein
obtained by liver biopsy. Prognosis is good
thrombosis, and parasite migration or
if fibrosis is not severe, but it is poor if
extension from intestinal disease. They
severe periportal or bridging fibrosis is
can also occur as sequelae of abdominal
present.

surgery. In neonates and young anin1als,
abscesses may develop secondary to

Equine Rhinopneumonitis
ascarid migration, bacterial septicemia, or
ascending infection of the umbilical vein. In

Equine rhinopneumonitis due to equine
horses and cattle, signs may be similar to
herpesvirus 1 is a sporadic cause of
those seen with other abdominal abscesses
interstitial pneumonia, hepatic disease, and
and include intem1ittent colic, intem1ittent
often death in newborn foals. Seep 1452 for fever, and weight loss. Often, liver abscesses
clinical findings, diagnosis, and treatment.

are subclinical in cattle. Hepatic ultrasound
may prove diagnostic. Prognosis is generally

Infectious Necrotic Hepatitis
poor because of lack of response to antimic

(Black disease)

robial therapy or incomplete resolution.

(See also

Infectious necrotic hepatitis, caused by

LIVER ABSCESSES IN CA'l'fLE, p 352.)

Clostridium novyi type B, affects prin1arily sheep but also cattle, horses, and pigs. See

HEPATOTOXINS
p 603 for clinical findings, lesions, and

Hepatotoxins manifest their toxicity by one
control.

or more mechanisms: periacinal ( centrilobular) necrosis, midzonal necrosis, Bacillary Hemoglobinuria
periportal necrosis, cholestasis, biliary

(Red water disease, lcterohemoglobinuria)

hyperplasia, fatty or hydropic change near

Clostridium novyi
necrotic zones, or venous occlusion. Fatal
type D (C haemolyticum)

hepatic insufficiency may result if the initial
is the anaerobic organism that causes
injury is acute and severe. More commonly,
bacillary hemoglobinuria in cattle, other
the hepatic damage from toxins is subacute
mminants, and rarely horses. Seep 601 for
or chronic. In chronic processes, the
clinical findings, diagnosis, and control.

longtern1 result may be cirrhosis. Many
hepatotoxins, especially those in plants,

Hepatic Abscesses
exert toxic effects on multiple organs,

Hepatic abscesses are generally polymicroparticularly the kidneys, lungs, and GI tract.

bial infections; anaerobes are common. The

Definitive diagnosis may be difficult.

p1imary etiologic agent of liver abscesses in

Careful history, inspection of the environcattle is Fusobacterium necrophorum.

ment, laboratory evaluations, liver biopsy, or

In goats, most abscesses are due to
necropsy may be needed to detennine the

Corynebacterium pseudotuberculosis,
offending agent. With acute plant toxicities,

'I'nieperella pyogenes, and Escherichia evidence of hepatotoxic plants may be seen
coli. Organisms less frequently isolated
in the stomach contents or rwnen.

342

HEPATIC DISEASE IN LARGE ANIMALS

Specific antidotes for hepatotoxins are

Hepatic lesions are variable. Most livers
limited. Removal of the animals from the
are friable and are swollen or shrunken. The
source is essential to decrease additional
liver is pale tan or mottled red-brown in
exposure. Administration of an absorbent
color. Hemorrhages may be present in the

( eg, activated charcoal, mineral oil) or
stomach, intestines, and bladder.

laxatives ( eg, mineral oil, magnesiwn

Diagnosis is based on history of iron

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sulfate) or rwnenotomy may decrease
supplementation, clinical signs, and
absorption of toxic elements in acute
necropsy lesions. Serum and liver iron
poisonings. These may not be helpful in
concentrations may be nom1al or increased.

chronic intoxications (ie, pyrrolizidine

Normal iron concentrations in horses are
alkaloid toxicity), in which the toxic agent

66--204 mcg/dL in serwn and 100-300 ppm in
has been ingested over weeks to months
liver tissue. Because serwn iron concentrabefore signs of toxicosis are evident.

tion correlates poorly with total iron stores,

Supportive care includes correction of
serwn ferritin levels are better used as an
electrolyte, metabolic, and glucose
estin1ate of total iron.

disorders via fluid therapy and dietary

Treatment is generally suppo1tive with
management. Hepatic encephalopathy must fluids and nutritional supplementation.

be controlled. Sunlight should be avoided if

Chelation therapy with deferoxan1ine is
photosensitization is present. Antimicrobiw1likely to be successful in either acute iron als may be considered to prevent secondary
toxicosis or chronic hemochromatosis.

pyoderrna. Prognosis is guarded and

Repeated phlebotomy has been attempted
depends on the particular hepatotoxin.

for hemochromatosis. The prognosis is poor.

Chemical and Drug-related Causes

Copper Toxicosis: Acute copper
toxicosis with severe hepatic necrosis and
of Toxic Hepatopathy
death may be seen in cattle 1-4 days after

For COAL-TAil POISONING, seep 3045.

iitjection of copper salt. Copper toxicosis is
seen in sheep and young calves after excess

Iron Toxicosis: Newborn foals ( <3 days
dietary intake of copper and in young goat
old) are especially sensitive to iron overload
kids fed calf milk replacer containing
because of their high serwn iron concentracopper. The prin1ary conditions associated tions, increased ability to absorb iron, and
with copper toxicosis are hemolytic anemia
oversaturation of transferrin at bilth. In
and liver damage. In camelids, ingestion of
adult horses, iitjectable u·on increases body
inappropriate dietary iron concentrations
iron concentration more substantially than
resulted in acute death with few premortem
most oral supplements; liver biopsy will
signs and no evidence of hemolytic crisis.

document increased iron stores, but these

(See also COPPER POISONING, p 3073.)

are rarely if ever associated with clinical
signs of liver disease. Iron toxicosis has been Miscellaneous Chemicals and Drugs reported in calves and young bulls injected

Associated with Hepatotoxicity:

with a ferric ammonium citrate alone or in

Exposure to carbon tetrachloride, chlorincombination with ferrous gluconate.

ated hydrocarbons, hexachlorethane, carbon

Foals given iron at bil'th, especially before disulfide, arsenic, monensin, pentachlororeceiving colostrum, may develop acute toxphenols, phenol, paraquat, halothane icity with clinical signs of hepatic encepha

(goats, llamas), isoflurane, phenobarbital,
lopathy in 2-5 days and a fatal outcome.

tannic acid, copper disodium edetate, and

Serwn bilirubin and blood ammonia
high doses of iverrnectin may cause
concentrations are high, and prothrombin
centrilobular necrosis and hepatic failure.

time is prolonged. Alterations in serwn

Phosphorus causes prin1arily periportal
hepatic enzymes are variable. In adult
changes. Active hepatitis to cirrhosis may
horses, acute toxicosis, although less
be seen after use of isoniazid, nitrofuran,
common, may cause enteric irritation and
halothane, aspirin, or dantrolene in large
cardiovascular collapse with sudden death.

anilnals. Erythromycin, 1ifampin, anabolic

Signs of more chronic hepatic failure,
steroids, phenothiazine tranquilizers, some
including weight loss, icterus, and
diuretics, quinidine sulfate, and diazepam
depression, may be seen with repeated oral
have been associated with cholestasis and
administration of iron. Possible sources of
icterus.

excess iron include inappropriate supplementation, forages high in u·on, iitjectable iron, and leaching of iron into water or feed.

Mycotoxicoses

Calves with iron toxicosis have trembling,

Aflatoxins and furnonisins can cause
vocalizing, bruxism, colic, and convulsions.

hepatic injury and failure in ruminants,

HEPATIC DISEASE IN LARGE ANIMALS

343
swine, and horses. Fusarimn toxicosis is the is eaten and the predominant forage being most corrm1on mycotoxicosis causing liver
fed is the Alsike clover. The toxic principle
failure in horses, whereas aflatoxins only
is an unidentified phototoxin. Photosensisporadically cause hepatic failure in this tivity has been reported in horses, sheep,
species. (See MYCOTOXJCOSES, p 3005.)

cattle, and pigs.

Alsike photosensitivity is also known as

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Blue-green Algae Intoxication

"dew poisoning" because it is seen mostly

Acute hepatotoxicosis may be seen after
when pastures of clover are wet and horses'

ingestion of hepatotoxic cyanobacteria.

skins are moist. It is characterized by
reddened skin after exposure to sun,

(See ALGAL POISONING, p 2956.)

followed by d1y necrosis of the skin or

Hepatotoxic Plants
edema and serous discharge. The muzzle,
tongue, and feet are frequently affected. lf

Pyrrolizidine Alkaloid Toxicity:

the stomatitis is severe, anorexia and weight

Pyrrolizidine alkaloid toxicity most
loss develop.

commonly is a chronic, progressive

Alsike clover poisoning may be fatal, with
hepatopathy, but acute intoxication can
progressive loss of condition and signs of
occur. (See PYRROLIZIDINE ALKALOIDOSIS, p 3150.) hepatic failure and neurologic disturbances.

Colic, diarrhea, and other signs of GI

Kleingrass Toxicosis: IGeingrass
disturbances have been noted. Affected

(Panicum coloratum) can produce
horses may be markedly depressed or
toxicosis in horses and rmninants. IGeinexcited. Prolonged exposure is usually grass toxicosis is a problem in the southrequired before signs of hepatic insuffiwestern USA from late spring to early fall.

ciency are evident. Serum chemistry

Young growing plants are most hazardous
alterations include increased GGT and AST
because of their high sapogenin content,
activities and hyperbilirubinemia, with
believed to be the toxic principle. A similar
direct bilirubin frequently being �25% of the
syndrome is seen in horses in the eastern
total.

USA grazing pasture or fed hay containing

Presun1ptive diagnosis of plant-induced
high concentrations offallPaniC'Um.

hepatopathy is based on history of exposure

Clinical signs include icterus, photosensito plants and multiple animals on a farm tivity, intermittent colic and fever, weight
or in an affected area. Horses in which
loss, and hepatic encephalopathy.

photosensitivity is the primaiy finding may

Photosensitivity may develop around the
recover quickly after being removed to
coronary band and cause lameness. Lesions

Alsike-free pasture. Those with severe
include hepatic and portal fibrosis and
stomatitis or dermatitis require supportive
biliary hyperplasia. Bilirubin, 'Y-glutamyl
care and local treatment of the stomatitis
transpeptidase or transferase (GGT), and
until they heal.

blood animonia concentrations are
increased. Sheep with photosensitivity

Mycotoxic Lupinosis: Mycotmdc
caused by kleingrass ingestion commonly
lupinosis is a worldwide disease of sheep
have a crystalline material in the bile ducts,
and cattle that consun1e lupines containing
canaliculi, and macrophages.

a hepatic mycotoxin produced by the

Presmnptive diagnosis of plant-induced
fungusPhomopsis leptostromiformis. See
hepatopathy is based on history of exposure p 3018 for clinical findings, diagnosis, and to plants and multiple affected animals on a
control.

farm or in an area. Affected animals should
be removed from the kleingrass source, fed

Xanthium (Cocklebur) Toxicosis:

good-quality hay, and protected from

Cockleburs, includingXanthium struma1°
smilight. Local treatment of the photoder
ium, may be found throughout the world.

matitis with antimicrobial or softening

Poisoning is most frequent after ingestion
creams may be needed in severe cases.

of the palatable two-leaf seedling stage or
ground seeds. The burs ai·e highly toxic but

Alsike Clover Toxicosis: Alsike clover
rarely eaten. The mature plant is less toxic

(Trifolium hybridum) causes two
and generally unpalatable. The toxic
syndromes in horses in the USA and
principle is carboxyatractyloside, which

Canada: photosensitivity (trifobiasis) and
directly affects the liver.

Alsike clover poisoning ("big liver disease").

Within hours of toxin ingestion, swine,

Alsike clover grows well on heavy clay soil,
cattle, and horses develop signs of
and an increased incidence of toxicosis is
depression, nausea, weakness, ataxia, and
reported during wet seasons. The disease is
subnormal temperature. Spasms of the
seen mostly when the blossom of the plant
cervical muscles, vomiting, dyspnea, and

344

HEPATIC DISEASE IN LARGE ANIMALS
convulsions may occm. Death may occm
include hyperbilirubinemia with increased
within hours of the onset of signs. Animals
direct ( conjugated) bilirubin, a marked
that survive initial acute poisoning
increase in serum -y-glutamyl transpeptifrequently develop chronic liver disease.

dase or transferase (GGT) activity, and

Affected animals require intensive
increased serw11 total bile acid concentrasupportive care. Mineral oil or activated tion. Sorbitol dehydrogenase (SDH) and
charcoal may be given orally to delay

AST activities are increased but to a lesser

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absorption of the toxic principle. Physodegree. BUN, glucose, and potassiw11
stigmine (5-30 mg, IM) has also been
concentrations may be decreased.

recommended.

Metabolic tests indicate reduced hepatic
function. Activated partial thromboplastin

Miscellaneous Plant Hepatotoxicosis:

time and one-stage prothrombin time may

Hepatotoxins are found in numerous plants,
be prolonged. Leukocytosis, anemia of
including Nolina texana, Agave lechu
chronic disease, hyperproteinemia,
guilla, Phyllanthus abnorrnis, and
hyperglobulinemia, and hyperfibrinogen

Lantana camara. (See RANGE PLANTS OF
emia are often present due to inflamma

TEMPERATE NORTH AMERICA, p 3103.)

tion. Histologic changes include periportal
and intralobular fibrosis, moderate bile

CHOLELITHIASIS,
duct dilatation and proliferation, and
cholestasis. Cultme of the liver may reveal

CHOLEDOCHOLITHIASIS, AND
a bacterial infection.

HEPATOLITHIASIS

Lesions: At necropsy, the liver may be
enlarged or shrunken. The liver is red to

Etiology and Epidemiology:

green-brown and fumer than normal.

Cholelithiasis in horses may cause biliary

Hepatic ducts and the common bile duct
obstruction and concmrent liver disease
are dilated and may contain one or more
or may be an incidental finding at necropsy.

calculi.

It most commonly affects middle-aged

(6-15 yr old) horses with no sex or breed

Diagnosis: Cholelitlliasis should be
predilection. Solitary or multiple calculi may
considered in horses witl1 a histo1y of fever,
be present in the common bile duct
icterus, and recurrent abdominal pain.

( choledocholithiasis ), intrahepatic bile

Other signs of hepatic fail me ( encephalopaducts (hepatolithiasis), or bile duct or thy, photodemrntitis, weight loss) are less
gallbladder in rwninants ( cholelithiasis).

consistently seen with cholelithiasis. A

In large animals, choledocholithiasis is the
marked increase in serum GGT with
most common cause of biliary obstruction,
hyperbilirubinemia ( direct bilirubin >25%)

with horses more frequently affected: The
is supportive. Increases in SDH, AST, and
cause of cholelith formation in horses is not
alkaline phosphatase are often also present,
known. Ascending biliary tract inflammation but when absent despite an increased serum (cholangiohepatitis), intestinal bacterial

GGT make the preswnptive diagnosis of
infection resulting in bile stasis, and a
biliary stasis more justified. Neutrophilic
change in bile composition or cholesterol
leukocytosis with inconsistent increase in
concentration have been proposed.

globulin and fibrinogen concentrations are

Choleliths formed around a foreign body
noted on leukograms. Ultrasonographic
or parasites may occlude the common bile
exan1ination may reveal hepatomegaly
duct. Cholelithiasis and hepatolitl1iasis
with increased echogenicity of the liver,
reportedly are not well recognized as a
thickened distended bile ducts, and
clinical problem in sheep and goats.

hyperechoic regions suggestive of

Incidence in camelids is unknown.

choleliths. Cholelitl1s in horses are most
often visualized in the most cranioventral

Clinical Findings: Clinical signs
portion of the right lobe of the liver,
conunonly seen in horses with choleliths
especially in the sixth to eighth intercostal
or cholangiohepatitis include weight loss,
spaces. Choleliths may be hyperechoic,
abdominal pain, icterus, depression, and
casting an acoustic shadow, or sonolucent.

intermittent fever. Signs of hepatic failure,

Stones may be seen as discrete calculi or
including encephalopathy, photosensitivity, less discrete sludge deposits within the and coagulopathy, occur less frequently.

biliary tract. The thickened distended bile

Clinical signs are often intermittent.

ducts may appear as dilated channels

Complete obstruction of the common bile
adjacent to portal veins. Because of the
duct often is accompanied by persistent
large lung field of horses, choleliths may be
abdominal pain. Laboratory abnormalities
nlissed on ultrasound exan1ination.

HEPATIC DISEASE IN LARGE ANIMALS

345

Treatment: Although biliary obstruction
acute hepatic failure can progress to
in horses is often fatal, choledocholithochronic active hepatitis.

tripsy and choledocholithotomy have been
performed successfully. Prognosis in cases

Clinical Findings: The predominant
requiring choledocholithotomy depends on
clinical signs of chronic active hepatitis are
the severity of concurrent cholangiohepatiweight loss, anorexia, depression, and VetBooks.ir
tis and on the size of the horse. The
lethargy. Icterus, behavioral changes,
procedure is difficult because of limited
diarrhea, photosensitization, and hemorexposure and poor visibility of the common rhage are variably present. Fever may be
hepatic duct. Complications include bile
persistent or intermittent, depending on the
contamination, bile peritonitis, dehiscence,
degree of cholangiohepatitis and fibrosis
bile duct stricture, cholelith refom1ation,
present. Dermatitis of the coronary band
and enterocolitis ( eg, stress-induced,
with regional sloughing of skin may
salmonellosis ). The prognosis is better if the develop. Recent or concurrent abdominal obstruction is corrected by choledochodisease is often reported. Duration of lithotripsy.

clinical signs is variable, extending over

When small calculi or less discrete sludge
days to months. Neurologic signs may seem
deposits are present, resolution by medical
to appear abruptly, even though there is
therapy may be successful. In addition,
histologic evidence of chronic disease.

dissolution of bilirubinate stones, which are

Alkaline phosphatase and -y-glutamyl
common in horses, may be facilitated by
tra.nspeptidase or transferase (GGT) are
concurrent administration of IV dimethyl
moderately increased, as a.re sorbitol
sulloxide ( <20%solution at 0.5-1 mg/kg).

dehydrogenase (SDH) and glutamate

Din1ethyl sulfoxide should be used cautiously dehydrogenase, which indicates ongoing or avoided in horses with coagulopathies or
hepatocyte dan1age. In chronic cases with
signs of hemolysis. Anti-inflammatory agents
marked hepatic fibrosis, enzyme activity
are administered to reduce inflanunation and
may be normal, and BUN and albun1in
provide analgesia. Because cholangitis is
concentrations may be decreased. Serum
often present, longtenn broad-spectrum
total protein is either increased or normal.

antinlicrobial therapy is indicated. Antimi

Globulins are usually increased. Serwn total
crobial choice is best guided by culture and
bile acid concentration is increased, and
sensitivity of the bacte1ia from a liver biopsy,

BSP® clearance prolonged. Cholestasis may
bile duct aspirate, or from the cholelith.

cause hyperbilirubinenlia, with >25%of

Supportive care is provided to manage any
total bilirubin being direct. Witl1 diminishing
degree of accompanying hepatic insuffihepatic function, serum glucose and ciency.

coagulation factors decrease, and one-stage
protl1rombin time and activated partial

CHRONIC ACTIVE HEPATITIS
thromboplastin time become prolonged.

Blood anunonia concentrations may be

Chronic active hepatitis describes any
increased. There may be a neutrophilia or
progressive inflanunatory process within
neutropenia with a left shift if endotoxenlia
the liver. It is a histopathologic diagnosis in
develops. Anorexia can lead to hypokawhich there is evidence of sustained, lemia. Ultrasonography generally reveals
aggressive, chronic liver disease. The
increased echogenicity in the liver,
histologic diagnosis is often cholangiohepaindicative of hepatic fibrosis. The liver may titis, because the inflammatory response is
be smaller than normal, so much so it may
mainly in the periportal areas.

be difficult to identify on ultrasonogra.phy.

Lesions: Grossly, tl1e liver is finn, pale

Etiology: The exact etiology of chronic
brown to green in color, and often small.

active hepatitis is not known. Infectious,

Irregular markings may be seen on the cut
inunune-mediated, or toxic processes are
surface. Histologic lesions are predonlithought to be involved. The early stages are nantly in the periportal areas. Infl=atory
associated with inflammation of the bile
cell infiltration may consist primarily of
ducts and portal areas of the liver.

mononuclear cells, neutrophils with

Extension of bacterial infection through the
bacteria ( often colifom1s), or lymphocytes
bile duct or portal venous drainage may be
and plasma cells. The character of tl1e
responsible for the lesions in animals with
infiltrate may indicate the nature of the
suppurative cholangiohepatitis. When
primary disease process. Biliary hyperplasia
lymphocytes and plasma cells predominate
may be marked if there is cholangiohepatiin the cellular infiltrate, an inlmune-meditis. Variable degrees of necrosis and fibrosis ated process is more likely. Many causes of
are present.

346

HEPATIC DISEASE IN LARGE ANIMALS

Diagnosis: Histologic examination of
with hepatic failure, widespread fibrosis ( or
a liver biopsy is needed for a definitive
severe bridging fibrosis), and disruption of
diagnosis. The tissue should also be
normal hepatic parenchyma.

cultured, although in most cases significant
isolates are not identified.

HYPERLIPEMIA AND HEPATIC

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Treatment: Supportive care should be

LIPIDOSIS
provided, including fluid therapy with
potassium chloride, glucose, and vitamin

Epidemiology and Pathogenesis:

supplementation; dietary management (a

Poor feed quality or decrease in feed intake,
diet low in protein and high in branchedparticularly during a period of high-energy chain amino acids and carbohydrates); and
requirement ( eg, pregnancy, systemic
prevention of exposure to the sun if
disease), may result in hyperlipemia
photodem1atitis is present.

syndrome. Hyperlipemia is seen most

Corticosteroid therapy has been used
commonly in ponies, miniature horses, and
successfully in horses with a lymphocyticdonkeys and less frequently in standard-size plasmacytic infiltrate on liver biopsy.

adult horses. Pathogenesis of hyperlipemia

Reportedly, steroids act to enhance
is complex, with a negative energy balance
appetite, stabilize cell membranes, and
triggering excessive mobilization of fatty
reduce inflammation and connective tissue
acids from adipose tissue, leading to
formation. Different therapeutic regin1ens
increased hepatic triglyceride synthesis and
using prednisolone and dexamethasone
secretion of very-low-density lipoproteins,
have been recommended. One recomconcomitant hypertJiglyceridemia, and fatty mended regimen involves initial administrainfiltration of the liver. The biochemical tion of dexamethasone at 0.04-0.08 mg/kg
etiology of hyperlipemia is overproduction
for4-7 days, followed by a gradual
of triglyceride rather than failure of
reduction in dosage over 2-3 wk depending
triglyceride catabolism.

on response to therapy. Prednisolone

Onset of disease is associated with stress,

(0.5-1 mg/kg/day, PO) may be required for
decreased feed intake, fat mobilization and
an additional 2-4 wk. The risk of inducing
deposition in the liver, and overproduction
lanlinitis or abortion in pregnant animals
of triglycerides, which may be precipitated
with corticosteroids must be discussed
by insulin resistance. ln ponies, hyperwith the owner before initiating therapy.

lipemia is usually a primary disease process

Alternatively, an antifibrotic agent,
associated with obesity, pregnancy,
colchicine (0.03 mg/kg/day, PO), has been
lactation, stress, or transportation.

recommended, but its efficacy in hepatic

Hyperlipemia may develop secondary
failure and safety in pregnant aninlals is
to any systemic disease that results in
unproved. Possible adverse reactions to
anorexia and a negative energy balance.

colchicine in horses include laminitis,

Secondary hyperlipemia is more common
diarrhea, and rarely bone marrow
than primary hyperlipemia in miniature
suppression affecting all cell lines. Malaise,
breeds. Hyperlipemia secondary to a
vomiting, diarrhea, abdominal pain,
systemic disease can be seen in horses
myopathy, alopecia, and bone marrow
of any age and in any condition. Female,
suppression have been reported in people
stressed, and obese donkeys are at highest
and other species. Other drugs recomrisk of developing hyperlipemia regardless mended for arresting or slowing fibrosis
of pregnancy status. Hyperlipemia is most
include pentoxifylline (7.5 mg/kg, PO, bid)

commonly seen in winter and spring.

and SAMe (5 g/day, PO). ln cases compli

Alpacas and llan1as may develop
cated with septic cholangiohepatitis,
hyperlipemia and ketonuria in late stages
broad-spectrun1 antinli.crobials are
of gestation or secondary to disease states.

indicated. Ideally, antimicrobial therapy

Adult camelids and even young crias are
should be based on bacterial culture and
susceptible to hepatic lipidosis during
sensitivity from the biopsy specimen.

disease states.

Fatty liver disease is a complex

Prognosis: Prognosis is variable and is
metabolic disease seen primarily in dairy
best based on liver biopsy and response to
cattle. See p 1018.

therapy. Prognosis is fair to good in aninlals
ln goats, hepatic lipidosis has been
with less severe lesions, especially those
associated with cobalt deficiency. Histowith a lymphocytic-plasmacytic cellular logic lesions are consistent with those
infiltrate that responds well to corticostecharacteristic of white liver disease in roid therapy; however, it is poor in horses
sheep.

HEPATIC DISEASE IN LARGE ANIMALS

347

Clinical Findings: Signs of hyperlipemia
acids, nonesterified fatty acids, and
are nonspecific and variable and may not

13-hydroxybutyrate; high activities of
relate to loss ofliver function. They include

-y-glutamyl transpeptidase or transferase
lethargy, weakness, inappetence, decreased

(GGT) and AST; and hypoproteinemia.

water intake, and diarrhea. Often, there is a
history of prolonged anorexia, rapid weight

Lesions: The liver and kidneys are often
pale, swollen, and friable with a greasy

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loss, and previous obesity. Emaciation,
texture. Microscopically, there is variable
ventral edema, colic, and trembling may be
fat deposition within the hepatocytes and
seen. Serum biochemical values and
epitheliwn of the bile ducts. The hepatic
coagulation testing in miniature horses and
sinusoids may appear compressed and
ponies with hyperlipemia indicate that
anemic with severe fatty infiltration. Gross
impaired hepatic function is common.

and microscopic lesions oftl1e primary

Affected anin1als have grossly opalescent
disease process in ponies and horses may
blood and lipernic plasma. The blood
predominate.

concentrations of all lipids are increased,
especially triglycerides, nonesterified fatty

Diagnosis: Clinical diagnosis of
acids, and very-low-density lipoproteins.

hyperlipemia is often based on the

Donkeys have higher plasma triglyceride
concentrations than do other equids.

signalment, history, clinical signs, and gross

Hypoglycemia is a common finding in
observation of a white to yellow discoloration of the plasma in equids. Plasma or ponies but not in miniature horses with
senl.lll triglyceride >500 mg/dL confirm the
hyperlipemia. Total bile acid concentration
and BSP
diagnosis. Cholesterol may be increased,

® clearance are often nom1al, but
indicating an increase in lipoprotein.

BSP clearance may be prolonged in some

Nonesterified fatty acids, very-low-density
animals. Activated partial thromboplastin
lipoproteins, and 13-hydroxybutyrate
tin1e and one-stage prothrombin time may

(camelids) may also be increased.

be prolonged. AST and sorbitol dehydroge

Laboratory evidence of hepatic dysfunction
nase (SDH) may be normal or increased.

is supportive.

Increased creatinine, isosthenuria, and
metabolic acidosis may develop secondary
to renal disease. BUN and creatinine

Treatment: Correction of the underlying
concentrations are variable. Anorexia can
disease, IV fluids, and nutritional suppo1t
lead to hypokalemia Animals may become
a.re the most essential factors in treatment
neutropenic with increased band neutroofhyperlipemia. Nutritional suppo1t phils. Concurrent pancreatitis has been
reverses the negative energy balance,
reported.

increases serwn glucose concentrations,

Prolonged increase in serum triglyceride
promotes endogenous insulin release, and
concentrations is associated with lipid
inhibits mobilization of pe1ipheral adipose
accwnulation in the liver, kidneys,
tissue. A polyionic electrolyte solution
myocardiwn, and skeletal muscles,
containing supplemental dextrose (50
impairing function of these organs. The liver g/hr/450 kg) and potassiwn (potassiun1
and kidneys become f riable, and death may
chlmide at 20-40 mEq/L) should be given
result from acute hepatic rupture.

IV to hypoglycemic, hypokalemic horses.

Alpacas and llan1as may develop

Glucose adnlinistration may cause
hyperlipernia and ketonuria in late stages of refractory hyperglycemia in animals with gestation, during lactation, or secondary to
insulin resistance. Glucose concentrations,
disease states. Nonspecific clinical signs
renal function, urine output, and semm
include lethargy, anorexia, and recwnbency. electrolyte concentrations should be Hypertriglyceridemia, hypercholesterolmonitored closely. IV fluids and glucose emia, increased SDH activity, metabolic
must be adn1inistered cautiously in
acidosis, azotemia, and ketonuria may be
can1elids with hepatic lipidosis, because
seen. Secondary renal failure may develop.

many are already hypoproteinemic, and

Carnelids appear to be similar to both
glucose regulation in camelids is often
horses (hyperlipidemia) and cattle (ketosis)

challenging. Intermittent bolus administrain their response to severe energy imbaltion ofpolyionic IV fluids rather than ance in late gestation. Hepatic lipidosis is
continuous infusion may more effectively
the most common liver disease found in
maintain hydration without exacerbating
llamas and alpacas. Camelids of various
existing hypoproteinemia.

ages and energy requirements are suscepti

Voluntary enteral nutrition is preferred if
ble, and the pathogenesis is multif actorial.

the affected aninlal will conswne adequate

Common clinical findings include anorexia;
quantities of nutritionally valuable feeds;
weight loss; high concentrations of bile
however, most will not. Frequent feedings

348

HEPATIC DISEASE IN LARGE ANIMALS
of a high-carbohydrate, low-fat diet are

Heparin is used in treatment of hyperpreferred. In animals with inadequate lipemia because it promotes peripheral
oral intake, supplemental tube feeding is
utilization of triglyce1ides a.t1d enha.t1ces
necessary. Commercially available
lipogenesis via stimulation of lipoprotein
high-calorie enteral fo1mulations provide
lipase activity. Heparin may be given IV or
adequate short-term nutritional support.

SC, witl1 recommended dosages of 40--100

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Recipes for home-prepared, liquid

JU/kg, bid. Use of heparin is questionable
tube-feeding diets for horses are also
in affected a.Illl11als with increased hepatic
available. Small frequent feedings are
production ofbiglycerides a.t1d without
required to meet caloric needs without
inlpaired peripheral removal of triglyceroverloading the GI tract. Anin1als should ides. HepariI1 administration may potentiate
be observed after each feeding for signs of
bleeding complications a.t1d is contra.iI1diabdominal discomfort. Body weight, total cated in animals with coagulopathies from
fluid intake, and fecal consistency should
liver dysfunction.

be monitored daily. In a.nin1als that sUIVive,

Nubitional supplementation to prevent
hyperlipemia. usually resolves in 5-10 days,
hyperlipemia. is indicated in minia.tw-e
but enteral feeding should be continued
horses a.t1d donkeys, ponies, horses, a.i1d
until voluntary feed intake is adequate.

ca.inelids with systemic disease associated

Enteral nutritional supplementation and
witl1 hypophagia a.t1d high metabolic
treatment of the primary disease often
dema.i1ds.

reverses hyperlipemia. in miniature horses
and donkeys but less frequently in ponies.

Prognosis: Cliilical biochemical variables

For totally anorectic horses, pa.itial
are not useful prognostic indicators of
parenteral nutrition may be used. The lipid
smvival in ponies with hyperlipemia. In
portion of the solution is omitted. Blood
most instances, sUIVival depends on the
glucose concentration should be monitored
ability to successfully treat the priI11a.iy
at lea.st twice daily to ensw-e that euglycedisease. Prognosis is often poor in ponies, mia. is maintained and that substantial
sta.Ildard-size horses, and ca.inelids.

hyperglycemia. (�180 mg/dL) is a.voided.

In ca.t11elids, pa.itial parenteral nutrition

HEPATIC NEOPLASIA
with enteral supplementation Ca.Il be used
to maintain adequate energy intake a.t1d

Prima.iy hepatic tmnors are uncommon
mininlize fw-ther fat mobilization. Because
in horses a.t1d rmnina.t1ts. They include
of tl1e distinct metabolism of ca.inelids,
hepatocellular carcinoma., chola.t1giocarciparenteral nutrition products must contain noma, a.i1d rarely lymphoma, hepatobla.shigher a.inounts of a.inino acids ( relative to toma (foals, young horses, alpaca cria.s),
nonprotein calories) than traditional

· a.t1d nlixed ha.ina.itoma Chola.t1giocarcifonnula.tions used in other species. Glucose noma. is the most common a.t1d is prin1a.iily
concentrations must be carefully monifound in nliddle-aged or older horses.

tored, because ca.inelids do not a.ssinlila.te

Hepatic carcinomas a.rise from hepatocytes,
exogenous glucose well.

bile ducts, or meta.stasis. Hepa.tocellular

Exogenous insulin administration is
ca.i·ciI1oma.s generally are found in yearlings
recommended for treatment of ia.twgenic
to young adult horses and have also been
hyperglycemia. and hyperlipemia, especially reported in lla.ina.s a.t1d goats. Adenoma.s or when these conditions are resistant to more adenocarcinoma.s of the liver have been conventional therapies. Insulin decreases
reported in cattle. Hepatic fibrosarcoma
mobilization of peripheral adipose tissue by
a.t1d bile duct carciI10ma. with meta.stasis
stimulating lipoprotein lipase activity a.t1d
to the lungs have been reported in goats.

by inhibiting adipocyte hom10ne--sensitive

E1ythrocytosis, large areas of extra.i11edullipase activity. The appropriate dosage of lary hematopoiesis, a.t1d meta.stasis to the
insulin to be used in horses has not been
thoracic cavity have been reported in horses
well established. When insulin is used,
with hepatobla.stoma..

response to therapy, including blood

Lymphosarcoma is the most common
glucose concentrations, must be closely
neopla.sia of the hematopoietic system in
monitored a.t1d the insulin dosage adjusted
horses. As ma.t1y as 37% of horses with
accordingly. Insulin administration may fail
lymphosarcoma have neoplastic involveto lower serum triglyceride or glucose ment of the spleen, a.t1d 41% have neoplastic
concentrations in hyperlipemic a.t1iinals
involvement of the liver. Meta.stasis of
when a.t1 insulin-resistant state is present.

lymphosa.i·coma. of the liver has been
lnsulin treatment in ca.inelids has reportreported in cattle, lla.t11a.s, alpacas, a.t1d goats.

edly been effective in treatment of hepatic

The predominant clinical findings with
lipidosis.

hepatic carcinoma. are lethargy a.i1d weight

HEPATIC DISEASE IN LARGE ANIMALS

349
loss. A progressively enlarging abdomen,

Hepatic Failure in Foals
erythrocytosis, persistent hypoglycemia,
icterus, and hepatic failure may also be seen.

Hepatic failure in neonatal foals may follow

Cholangiocarcinoma causes pronounced
septicemia ( especially Actinobacillus
weight loss before the onset of hepatic
equuli), endotoxemia, perinatal asphyxia,
failure. Liver hepatocellular and biliary

Leptospira Pomona infection, equine

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enzymes may be increased with hepatic
herpesvirus 1, hepatic duct obstruction
carcinoma or cholangiocarcinoma. Serum
secondary to gastroduodenal obstruction,

'Y-glutamyl transpeptidase or transferase
biliary atresia, and iron toxicity. Gastric

(GGT) activity in affected horses is usually
ulcers and duodenitis in foals can cause
very high. Hepatocellular carcinomas are
strictures of the duodenun1 and subsequent
characteristically uniform in appearance
cholangiohepatitis due to bile stasis.

on ultrasonographic examination.

Neonatal isoerythrolysis and hemolysis may

Clinical manifestations of lymphosarcause hypoxic and cholestatic hepatic coma in horses are variable. Early in the
disease. Administration of total parenteral
disease, nonspecific signs such as weight
nutrition may cause cholestasis and
loss, anorexia, and lethargy are seen.

concurrent hepatic disease.

Lymphoma occasionally may diffusely
infiltrate the liver and produce signs of

Biliary Atresia
hepatic failure, jaundice, and severe

Biliary atresia ( extrallepatic) has been
depression. Laboratory findings include
reported in foals and in a neonatal lamb.

hypoglycemia, mild to moderate increases

Affected foals presented for anorexia,
in liver enzymes, hyperbilirubinemia, and
depression, lethargy, poor growth, colic,
abnormally low levels of IgM. Ultrasonopolydipsia, polyuria, pyrexia, and icterus at graphic examination helps to detect splenic
l mo of age. Markedly increased serum
and hepatic neoplasia. In ruminants, signs

'Y-glutamyl transpeptidase or transferase
produced by tumor growth in other organs

(GGT) and bilirubin with mildly increased

(lymph nodes, abomasun1, heart, uterus,
sorbitol dehydrogenase (SDH) suppo1ted a
spinal cord) are often most predominant.

diagnosis of biliary obstruction. Diagnosis

The presence and character of the
of biliary atresia was confirmed at necropsy.

hepatic neoplasia can be con.firmed by liver
biopsy and microscopic exanlination of the

Hemochromatosis
tissue. Atypical lymphocytes or lymphoblasts may be seen in peritoneal fluids and Hemochromatosis is an iron storage disease
peripheral blood of some affected aninlals.

in which hemosiderin is deposited in the

Increased serum cx-fetoprotein concentraparenchymal cells, causing damage and tion may support hepatoblastoma; however,
dysfunction of the liver and other tissues.

this is not conclusive because concentra

The disease is either primary (idiopathic) or
tions may also be increased with hepatocelsecondary. It is reported in people, Mynal1
lular carcinoma.

birds, Salers cattle, and horses.

Etiology: In Salers cattle, the condition

MISCELLANEOUS HEPATIC
appears to be a homozygous recessive

DISORDERS
condition with inappropriate intestinal
absorption of iron, excessive hepatic

Cholangitis
storage, and eventual loss of hepatic
function. In horses, there is no evidence of a

Diseases of the gallbladder are rare in
familial tendency or of excessive iron being
ruminants. Obstruction may be associated
consumed in the diet. Rather, it appears
with liver fluke infestation, foreign bodies,
there is cirrhosis of the liver with secondary
abscesses, neoplasia, suppurative
iron overload. In horses and cattle,
cholecystitis, or abdominal fat necrosis.

increased iron is deposited in the liver.

Rupture of the gallbladder has been
reported in a cow. Cholangitis (inflamma

Clinical Findings and Lesions: In
tion of the biliary system) has been reported horses, primary clinical signs are weight in horses with chronic active liver disease.

loss, lethargy, and intermittent anorexia. In

Mild behavior changes, weight loss, variable cattle, signs include decreased weight gain, colic, icterus, and alterations in hepatic
poor body condition, dull hair coat, and
enzyme activity may be seen in affected
diarrhea. In both species, serum liver
horses. Treatment consists of longterm
enzyme concentrations, including GGT,
antimicrobial and supportive therapy as
alkaline phosphatase, AST, and SDH, are
indicated.

increased. Serum total bile acid concentra-

350

HEPATIC DISEASE IN LARGE ANIMALS
tions are increased in horses, and serum
lobe is inlpaired, resulting in hepatic anoxia,
iron, total iron binding capacity (TIBC), and
deprivation of nutrients, and gradual
percent saturation of the TIBC are usually
atrophy of the right lobe of the liver. No
normal. In some cases, serum iron and
evidence of biliary tract disease has been
ferritin may be increased, but TIBC is not
noted. Colic may be seen. Some horses may
saturated. In cattle, total serum iron, TIBC,
have signs not related to the GI tract.

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and saturation of transferrin are increased.

Iron content of the liver tissue is greatly
increased in horses (no1mal 100-300 ppm)

Hepatic Lobe Torsion
and cattle (normal 84-100 ppm). Hepato

Hepatic lobe torsion can cause colic in
megaly and hemosiderin accumulation in
horses. Liver enzymes and fibrinogen are
the liver, lymph nodes, pancreas, spleen,
increased, but abdominal fluid analysis is
thyroid, kidney, brain, and glandular tissue
vaiiable. Bacteria, including Clostridium
are typically present.

spp, may be fow1d in the necrotic portion
of liver. Exploratory celiotomy may be

Diagnosis: Diagnosis is based on history,
required for diagnosis.

clinical signs, and laboratory findings.

Finding abundant hemosiderin in tl1e

Hepatic Amyloidosis
hepatocytes on histopathologic exanlination of a liver biopsy supports the diagnosis.

Amyloidosis refers to disease characterized

High liver iron concentrations in animals
by the extracellular deposition of amyloid,
with no history of excess iron intake help
a proteinaceous fib1iJ substance, in the
confum tl1e diagnosis. Differential
tissue. Deposition of an1yloid within an
diagnoses include iron toxicosis from
organ distmts normal tissue ai·chitectw·e
exogenous sources and diseases causing
and possibly function. In horses, the liver
chronic weight loss and hepatic dysfunction
and spleen are the most common orgatlS
or disease.

affected by systemic amyloidosis. Reactive
or secondary systemic amyloidosis with

Treatment: Phlebotomies to remove
deposition of amyloid A (AA) fibrils in the
blood and reduce the iron stores have been
liver has been associated with severe
used in treatment of people with hemochroparasitism and chronic infection or matosis. Similar treatment in horses and
inflainrnation in horses. (See also
cattle has been unsuccessful. Deferoxamine AMYLOIDOSES, p 592.) is also used in people to induce a negative
ion balance and reduce the rate at which

Congenital Hepatic Fibrosis
iron accwnulates. The effect in cattle and

In a retrospective study of the records from
horses has not been evaluated.

the University of Berne, Institute of Animal

Pathology, 30 Swiss Freiberger foals with

Right Hepatic Lobe Atrophy in
pathologic lesions compatible with

Horses
congenital hepatic fibrosis were identified.

Affected foals were 1-12 mo old ( average

The tight lobe of the liver is the largest lobe

3. 7 mo). Most showed signs and had
in young horses but frequently atrophies in
clinicopathologic changes reflecting severe
older animals and becomes fibrous. Right
liver damage. Pedigree analysis traced the
hepatic lobe atrophy was previously
disease back to one stallion. Results suggest
considered an incidental postmortem
that congenital hepatic fibrosis in Swiss
finding, but some consider it to be a

Freiberger horses is a recessively inherited
pathologic condition.

autosomal genetic defect. A sinli.lar

Right hepatic lobe atrophy has been
condition has been reported in a calf.

proposed to result from chronic compression of this pmtion of the liver by the right dorsal colon and base of the cecun1. Feeding Primary Hyperammonemia of Adult horses high-concentrate, low-fiber diets

Horses
may contribute to a.tony of the right dorsal

In this syndrome of hyperamrnonemia,
colon with resultant distention; this
blindness and severe neurologic signs are
compresses the right hepatic lobe against
seen in adult horses. The etiology is
the visceral surface of the diaphragm.

unknown, but a prinlaiy intestinal problem

Altl10ugh there is no morphologic evidence
with overgrowth of urease-producing
of direct vascular inlpaim1ent to the right
bacteria within the intestine is suspected.

hepatic lobe, vascular compromise may

The syndrome is neai·ly always associated
result secondary to compression. With
with enteric disease, diarrhea, or colic.

chronicity, the portal circulation to the right

Diarrhea and, in some cases, protein-losing

HEPATIC DISEASE IN LARGE ANIMALS

351
enteropathy may persist for several days. In
controlled by resb.icting protein intake and
most cases, diarrhea or colic precedes the
by careful dietary management. Neomycin
neurologic signs by 24--48 hr. Laboratory
or lactulose are given orally to decrease
abnormalities include increased blood
ammonia production within the bowel.

ammonia concentrations (200-400 µm/1),

Supportive care with polyionic fluids,
severe metabolic acidosis, low plasma
potassiun1, and dextrose may be needed

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bicarbonate (�12 mEq/1) concentration, and to help decrease neurologic signs.

profound hyperglycemia (250-400 mgtdL ).

Serun1 concentrations of liver enzymes,
total bile acids, and bilirubin are nom1al.

Hyperammonemia of Morgan Foals

In most horses, neurologic signs resolve

A syndrome of depression, ill thrift, and
within 2-3 days with supportive treatment
hyperanm10nemia with a variable degree of

(IV fluids, potassium chloride, glucose,
hepatic involvement is seen in Morgan foals.

sodiwn bicarbonate) and administration of

Affected foals have been related, but the
drngs to reduce =onia absorption
cause of the syndrome is undetermined.

(lactulose, neomycin).

Clinical signs are usually first seen around
weaning time. Encephalopathy may
temporarily in1prove with aggressive

Portosystemic Shunts
supportive therapy but recurs after

Portosystemic shunts are seen in foals and
withdrawal of treab.nent. Liver enzymes
calves. Hyperanm10nemia and neurologic
and blood anm1onia concentrations a.re
signs result from liver dysfunction with little increased. Bilirubin concentration is often laboratory or microscopic evidence of liver
nom1al. Pathologic hepatic lesions include
disease.

portal and bridging fibrosis, bile duct
hyperplasia, karyomegaly, and cyto1negaly.

Clinical Findings and Lesions: Clinical

The disease is fatal.

signs are first seen when affected foals are

-2 mo old and sta.It to ingest larger amounts
of grain and forage. N eurologic signs

HYPERBILIRUBINEMIA
include staggering, wandering, blindness,

SYNDROMES
circling, and seizures. Poor growth and
intennittent neurologic signs ( ataxia,

Gilbert Syndrome
wealmess, depression, brnxism, tenesmus)

Gilbert syndrome is a congenital hyperbilirnhave been reported in affected 2- to binemia seen in people (inherited as an

3-mo-old calves. Sernm concentrations of
autosomal dominant trait) and in Southhepatic enzymes are often nonnal. Blood down sheep. It is an unconjugated hyperbiliammonia and total bile acid concentration rubinemia in the presence of normal erythroare increased, and BSP® clearance is cyte life span. A defect in carrier proteins or
prolonged.

conjugating enzyme is suspected. Affected

The liver is often small, with a smooth

Southdown sheep have increased conjuswface, and nonnal in color and texture.

gated and unconjugated plasma bilirnbin

Microscopically, the hepatocytes are small.

concentrations. Hepatic bilirnbin clearance

Portal veins in the triads may be small or
is defective, and affected sheep cannot
absent. Hepatic arteries are often prominent excrete BSP® into the bile. Icterus is and multiple.

variable. Hi.stopathologic lesions are absent
except for pign1ent in the hepatocytes.

Diagnosis: A portosystemic shunt should
be suspected in foals or calves exhibiting
repeated episodes of cerebral signs without

Dubin-Johnson Syndrome
obvious reasons. Signs may be most

Dubin-Johnson syndrome is seen sporadipronounced and associated with feedings.

cally in people and Coniedale sheep. It is a

Catheterizing the mesenteric vein and
failure of conjugated bilirubin to enter the
performing a portogram or nuclear
bile canaliculi. Excretion of bilirubin and
scintigraphy can confirm and locate the
other cor\juga.ted organic anions may be
shunt. In some cases, the shunt may be seen
impaired. Affected sheep may be icteric or
on ultrasonographic examination of the
hyperbilirnbinemic. Sernm conjugated and
liver.

unconjugated bilirnbin concentrations are
increased, and BSP® clearance and bile acid

Treatment: Surgical repair may be
excretion may be delayed in affected
attempted in aninlals in which the site of the Coniedale sheep. HistologicaJJy, the shunt can be identified, but the prognosis is
hepatocytes contain a black, melanin-like
guarded. Clinical signs in some foals may be
pigment.

352

HEPATIC DISEASE IN LARGE ANIMALS

LIVER ABSCESSES IN CATTLE
from the reticulum, direct extension of
infection from omphalophlebitis in neonatal

Liver abscesses are seen in all ages and
calves, and bacteremic diseases.

breeds of cattle wherever cattle are raised.

They are most conunon in feedlot and dairy

Clinical Findings, Lesions, and
cattle fed rations tl1at predispose to

Diagnosis: Cattle with liver abscesses

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rumenitis. Cattle with liver abscesses have
seldom exhibit clinical signs. Detailed
reduced production efficiency. Affected
clinical examination may show periodic
livers are condenmed at slaughter, and
fever, inappetence, and evidence of pain
adhesions to surrounding organs or the
when pressure is applied to the xiphisterdiaphragm may necessitate carcass num and posterior rib cage on the right
trimming. Liver abscesses can also lead
side. Grunting and other signs of pain may
to disease syndromes associated with
occur with movement or when the animal
posterior vena caval thrombosis.

lies down. An episodic drop in milk
production occurs in dairy cattle. Clinical

Etiology and Pathogenesis: Fusobac
signs of omphalophlebitis are commonly
terium necrophorum, a gram-negative,
present when there is liver abscessation
obligate anaerobic bacteriun1, and a
resulting from extension of omphalophlecomponent of normal rumen microflora, is bitis. Acute-phase proteins are increased
the prinlary etiologic agent. Infection in the
early in the course of the disease, and
liver usually originates from a necrobacilserum sialic acid concentrations have lary rumenitis. Two biovars have been
been used for antemortem diagnosis.

inlplicated. Biovar A (F necrophorum

When there are several abscesses or a
necrophorum ), the more virulent, is the
large abscess, leukocytosis with neutropredominant biovar in the rumen microflora philia and increased fibrinogen levels and is isolated, usually in pure culture, from
develop, and serum globulin concentramost cases of liver abscessation. Biovar B
tions may increase. Ultrasonography is an

(F necrophorumfunduliforme) is comaid to diagnosis, but abscesses in the left monly isolated from microabscesses
side of the liver may not be visualized.

in tl1e rumen wall but is less commonly

Feedlot cattle with abscessed livers have
isolated from liver abscesses, in which it is
reduced feed efficiency, and those with
always found in mixed culture with biovar A severely abscessed livers gain 5%-15% less or other bacterial species. Trueperella
per day than cattle without abscesses.

pyogenes, streptococci, staphylococci,

Most liver abscesses a.re occult lesions
and Bacteroides spp are most frequently
that regress to a sterile scar. Untoward
recovered from mixed cultures.

sequelae include peritonitis after abscess

Rumenitis is usually the result of rapid
rupture into the peritoneal cavity, and
intraruminal fem1entation of dietary
sudden death from an anaphylactic or
carbohydrate with subsequent production
toxic reaction when there is rupture of
of lactic acid and increased acidity of the
an abscess into hepatic blood vessels.

ruminal fluid ("grain overload"). Rations

Rupture into hepatic veins can also lead
with high levels of carbohydrate are the
to thrombophlebitis of the posterior vena
principal cause in both da..iry and feedlot
cava with thromboembolic disease,
cattle, but the texture of the feed and
endocarditis, pulmonary thromboernbomethod of feeding can be modifying factors.

lisrn, multiple pulmonary abscesses, and

The incidence of rurnenitis in feedlot cattle
chronic suppurative pneun10nia.

is significantly higher when the cattle are

Aneurysms of the pulmonary artery
transferred directly from a roughage ration
consequent to pulmonary thromboemboto a finishing ration, and when there is poor lism may rupture into airways to result in
feed bunk management. F necropho1um,
hemoptysis, epista.xis, and death. Caudal
alone or with other bacteria, colonizes
vena caval thrombosis may also lead to
through tl1e area of superficial necrosis
portal hypertension with a resulting
produced by tl1e acid rumen contents.

syndrome of hepatornegaly, ascites, and

Leukotoxin may facilitate resistance to
diarrhea.

phagocytosis. Bacterial emboli from the

The rurninal lesions are characterized
lesions invade the hepatic portal venous
by a marked inflanunatory reaction and
system and are transported to the liver,
necrosis. Occasionally, abscesses are found
where they can establish infectious foci
in the deeper layers of the rwnen wall.

of necrobacillosis that eventually develop

Hepatic necrobacillosis lesions of <6 days
into abscesses.

duration are pale yellow and spherical witl1

Other sources of infection in liver
irregular outlines; they are characterized by
abscesses include foreign body penetration
coagulation necrosis of the hepatocytes

MALASSIMILATION SYNDROMES IN LARGE ANIMALS

353
with a surrounding intense zone of
dairy cattle, percutaneous drainage and
hyperemia and inflan1mation. Older
longterm therapy wiili procaine penicillin
abscesses have a core that is progressively

G (22,000 IU/kg) can be attempted, but the
encapsulated by fibrous connective tissue.

prognosis is poor. A vaccine consisting

Abscesses are usually 4-6 cm in diameter.

of the leukotoxoid of F necrophon1,m

Affected livers usually have 3--10 abscesses
combined with a bacte1in of T pyogenes,

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but may have up to 100.

given when cattle enter the feedlot, reduces

Liver condemnation rates as high as 400A,
abscess incidence and severity.

were recorded in a large survey of cattle

The primary control is by managing
slaughtered in the USA. Culture is seldom
ruminal acidosis through the method of
done to confinn the diagnosis. Occasionally,
feeding, diet composition, diligent feed
liver abscesses due to F necrophorum must
bunk management, and use of buffers in
be distinguished from those resulting from
the diet. Fewer ruminal lesions develop
traumatic reticuloperitonitis (seep 230).

when the ratio of concentrate to roughage
is decreased and when the transition
period from a roughage to a finishing ration

Treatment and Control: Tylosin
is lengthened. Increased roughage in the
phosphate fed at 10 g/ton of feed signifiration and multiple daily feedings increase cantly reduces the number of liver
the tin1e of mastication and saliva flow; this
abscesses and increases feed efficiency and
increases buffer to the rumen and provides
weight gain but has little, if any, effect on
a continuous and uniform fennentation
prevalence of ruminal lesions. Virginian1ythat reduces intraruminal acidity, which in cin fed at 16 g/ton of feed or chlortetracyturn lowers the number of ruminal lesions cline fed continually at 70 mg/head/day
and, indirectly, the number of liver
during the finishing period is also used. With abscesses.

MALASSIMILATION SYNDROMES

IN LARGE ANIMALS

Malassinillation is a decreased ability of
understood in large animals. They may be
the GI tract to incorporate nutrients into
due to alterations in gastric fimction or
the body, either due to maldigestion or
activity of rumen mkroflora, abnohnal
malabsorption. Maldigestion is the failure of bacterial proliferation in the small intestine, adequate degradation of clietary constituor a decrease or lack of small-intestinal ents within the GI tract, which is required
brush border enzyme activity ( eg, lactase
to facilitate absorption due to defects in
deficiency). Less likely causes include
pancreatic exocrine function, bile acid
drug-induced alteration in secretion or
content, or brush border enzymes.

excretion of bile salts, or deficiency or

Malabsorption is the failure of passage of
inactivation of pancreatic lipase. Changes
nutrients from the intestinal lumen into
in bile salt concentration may not impair
the bloodstream. Some disease processes
digestion in adult herbivores but may
involve both maldigestion and malabsorpexacerbate diarrhea in milk-fed neonates.

tion, such as is seen in young animals with

Surgical resection or bypass of the djstal
lactase deficiency. Maldjgestion alone is an
small intestine may facilitate bacterial
infrequent cause of malassimilation in large
overgrowtl1 with associated bile salt
animals. In horses, diseases causing
abnormalities.

malabsorption are much more common

Lactose is a disaccharide composed of
than djseases causing maldigestion. In
glucose and galactose. The enzyme lactase,
cattle, small rUl11inants, and camelids,
which catalyzes the degradation of lactose
the forestomach bacteria and protozoa
into its components, is loca}jzed in the
contribute to nutrient degradation, which
small-intestinal brush border of foals and
makes maldigestion a very rare condition.

calves. The degradation is necessary to
facilitate absorption. Primary lactase

Etiology and Pathogenesis: Maldigesdeficiency is inherited as an autosomal tion syndromes are uncommon and poorly
recessive trait in people, but its occurrence

354

MALASSIMILATION SYNDROMES IN LARGE ANIMALS
and mode of inhe1itance in large animals is
small-intestinal resection (short-bowel
poorly documented. Acquired or secondary
syndrome) or from villous atrophy due to
lactase deficiency seems to be more
granulomatous enteritis. Local infiltrative
conunon in large anin1als. It is seen in foals,
or inflammatory disease, edema, or
calves, and crias as a result of intestinal
lymphatic obstruction (granulomatous

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mucosa! changes induced by viral,
enteritis, lymphosarcoma) secondary to
protozoal, and bacterial enteritis. Sloughing
local or systemic causes may interfere
of the small-intestinal epithelial cells, loss of with the ability of the intestinal wall to vi.llous tips, and loss of some or all of the
absorb nutrients. Inefficient absorption
crypt cells result in some degree of lactase
also may develop due to increased
deficiency because ofloss oflactase-secreting mucosa! permeability caused by cellular epithelial cells. Morphologic changes may
da.inage. Metabolic abnormalities may
include partial vi.llous atrophy, crypt
alter the epithelial cells and decrease the
hyperplasia, and infiltration of the lan1ina
available energy for active transport and
propria. Osmotic diarrhea in lactase-deficient maintenance of the carrier proteins or foals and calves occurs due to increased
brush border enzymes. Congenital
undigested/unabsorbed nutrients entering
deficiencies of enzymes normally present
the caudal intestinal parts, subsequently
on the microvilli a.i·e not well recognized
increasing bacterial fermentation,
in large, domestic animals. However,
concentration of osmotically active
neonates and ruminants have low levels
pa.iticles, and retention of water and
of maltase, and ruminants especially
electrolytes in the intestine.

lack sucrase. In most manm1alian

A number of djseases may induce a
species, lactase activity declines
malabsorption syndrome by altering the
with age.

normal absorptive mecha.i1isms of the

In horses, malabsorption is COilUllonly
small intestine. Malabsorption is
caused by the following: 1) inflan1matory or
commonly seen in animals with GI
infiltrative disorders-diffuse lymphosa.i·disease. It may arise from structural or coma of the small intestine (alimentary
functional disorders of the small intestine
lymphoma); enteritis clue to eosinophilic,
or have a multifactorial etiopathogenesis.

lyrnphocytic-plasrnacytic, or basophilic

Malabsorption is often seen concurrently
infiltrate; multisystemic eosinophllic
with enteric protein loss. Either may
epitheliotropic enterocolitis; granulomacause loss of nutrients in the feces and tous enteritis (inflanirnatory bowel disease);
subsequent weight loss. Malabsorption

Lawsonia intracelliilaris ( weanling foals,
is not synonymous with diarrhea in any
yearlings); intestinal ischemia and da.inage
species, although diarrhea may be a
due to migration of Strongyliis vulgaris
common clinical featw-e. Function of the
larvae, small strongyles, or Strongyloides
large intestine may be secondarily altered
westeri (foals) infection; cryptosporidia;
because of changes in the small intestine.

postinfarction inflanunation; a.inyloid

Transient dia.iThea may occur as abnormal
associated gastroenteropathy; multiple
quantities of carbohydrates, protein,
abscessation in tile bowel; tuberculosis;
fatty acids, and bile acids enter the large
histoplasmosis; intestinal Rhodococcus
intestine in the ilea! effluent. These
equi infection; invasive enterocolitis
substances can directly or indirectly

(Salmonella spp ); 2) biochemical or genetic enhance intestinal secretion or decrease
abnormalities----congerutal or acquired
absorption rates. Malabsorption of
lactase deficiency (lactose intolerance),
nutrients may result from insufficient
dietary-induced enteropathy, monosacchaabsorptive surface area, an intrinsic ride transport defect, pancreatic exocrine
defect in the mucosa! or submucosal
insufficiencies; 3) diseases causing
morphology of the intestinal wall, or
inadequate absorptive a.i·ea-villous
obstruction of blood and lymphatic
damage or atrophy clue to viral infection
vessels. Rotavirus infection in younger

( rota virus, coronavirus) or bacterial
animals may cause destruction of
enteritides in foals, cryptosporidiosis,
intestinal villous epitilelial cells, which
intestinal resection; 4) cardiovascular
results in maldigestion due to decreased
disorders-congestive heart fail me,
activity of brush border disaccharidase
intestinal ischemia; 5) lymphatic obstrucenzymes and in malabsorption due tion-lyrnphosarcoma, mesenteric
to decreased absorptive surface area.

lyn1phadenopathy, intestinal lymphangiec

Corona virus and cryptosporidia may have
t.asia, abscessation, thoracic duct obstrucsimilar effects. A decreased absorptive tion; and 6) miscellaneous-drug-induced,
surface area can also result from
heavy metal toxicosis, zinc deficiency.

MALASSIMILATION SYNDROMES IN LARGE ANIMALS

355

In cattle, malabsorption syndromes are
concentrations. Therefore, chronic weight
less frequently documented but likely are
loss or reduced growth rate is a typical
seen most often in calves with diarrhea.

clinical sign.

Diseases that cause malabsorption

Appetite of affected anin1als may be
syndromes in ruminants include diarrhea
normal, increased, or decreased and is,

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caused by viruses, bacteria, or protozoa in
therefore, not very helpful as a diagnostic
calves and young stock. These inflammaparameter. Polyphagia may be seen due to tory changes often result in maldigestion
insufficient nutrient abs01vtion to stimulate
and malabsorption. Another major group
the satiety centers. In small-intestinal
of cattle suffering from malabsorption
malabsorption, decreased feed intake or
syndrome is older cattle with Mycobacte
anorexia is present more commonly,
rium avium subsp paratuberculosis
because the primary disease process causes
infection (Johne's disease). Rare
loss of appetite.

underlying reasons for malabsorption

Feces are frequently normal in consisin rwninants are local or generalized tency and volun1e. Diarrhea may be present
ischemia, protein malnutrition, congestive but is not a consistent feature. In adult heart failure, lymphatic obstruction,
ailirnals, small-intestinal disease must be
parasitism (eg, trichostrongylosis of
ratller extensive before diarrhea develops,
sheep and cattle), or tuberculosis. Oral
because tile colon can compensate and
antibiotics may cause an in1balance in GI
absorb tile increased fluid load. This is
tract flora and interfere with digestion
especially tile case in llamas and alpacas.

and intestinal absorption of nutrients.

In adult horses and rwni.nants, dian·hea

Treatment with high doses of ampicillin,
indicates involvement of tile large intestine.

neomycin, or tetracycline significantly

In young animals in which colonic function is
decreases and delays glucose absorption
not yet fully developed, diarrhea is seen witll
during oral glucose tolerance tests in
small-intestinal and large-intestinal disease.

calves.

Clinical signs of malassimilation may also

New World camelids can be affected by
include exercise intolerance, letllai·gic
most conditions that cause malabsorption
attitude, and vaiiable thirst. Vital signs are
syndrome in rwninants. Virus-caused
usually normal until late in tile disease.

dian·hea ( corona virus) is particularly a

Pyrexia may be seen witll inflaimnatory a11d
problem in young crias. Intestinal protozoa
neoplastic conditions. Abdominal pain may
infection ( eg, Eimeria macusaniensis)

result from bowel inflan1rnation, mesenteric
may result in weight loss and hypoproteinor mural abscesses or adhesions, or partial emia due to malabsorption during either
obstruction. Ascites, dependent edema, and
tile prepatent or patent phase of infection.

weakness may develop later in tile disease

Severe debilitation caused by coccidiosis is
process, especially if enteric protein loss is
typically seen in young aninlals; however,
present. Skin and ocular lesions, vasculitis,
chronic malabsorption caused by chronic
aithritis, hepatitis, and renal disease may
enteritis can also be found in adult llamas
indicate in1munologic reactions, particularly
and alpacas, which typically shed high
with inflaimnatory bowel disease. Skin
nun1bers of tile patllogen.

lesions seen witll malabsorption-related

In swine, malabsorption is poorly
de1n1atosis include a tl1in hair coat, patchy
docw11ented; however, proliferative
alopecia, and focal areas of scaling and crustenteropathy (L intracellularis) can result ing tllat are often syn1rnetrically distributed.

in malabsorption. In piglets, an amylase

Foals and calves with lactose intolerance
deficiency may result in starch malabsorpcommonly show diarrhea, poor growtll rate, tion during tile inlmediate postweaning
and an untllrifty appearance. Some may
period. Diarrhea of other origin ( eg, Escher
experience flatulence, mild abdominal
ich'ia coli) may cause malabsorption
discomfo1t, or bloating after intake of milk.

syndrome in piglets.

In young animals witll acquired lactase
deficiency, clinical signs ( eg, diarrhea,

Clinical Findings: Clinical signs of
dehydration, weight loss) and clinicopathomalassinillation syndrome are variable, logic alterations ( eg, acidosis, hypoglycedepending on tile underlying disease mia and electrolyte abnonnalities) are
condition and the presence or absence of
indistinguishable from those of tile primary
concurrent protein-losing enteropatlly.

enteropathy. The condition of the animal

Malassinlilation syndromes frequently
may improve quickly, and diarrhea may
result in a negative energy balance, and
resolve when milk is witlldrawn.

subsequently in weight loss, muscle

Lesions: The carcass is thin to emaciated,
wasting, and possibly low serum protein
depending on the duration and severity of

356

MALASSIMILATION SYNDROMES IN LARGE ANIMALS
the malassimilation disease. Specific lesions loss, such as renal disease or loss into a depend on the primary underlying disease
third space (peritonewn, pleural space),
process. Ove1t signs of malabsorption do
and by excluding the possibility of
not always correlate with gross and
decreased albwnin production due to
histopathologic changes, emphasizing the
another condition such as liver disease.

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importance of functional disorders.

Standard and contrast radiography of the
bowel may be feasible in foals and small
ponies, calves, and New World camelids.

Diagnosis: Small-intestinal malabsorption Abdominal ultrasonography is a useful cannot be determined by clinical examinadiagnostic tool to determine bowel-wall tion or by routine laboratory data. However,
thickness and intestinal motility, as well
clinical examination may lead to a
as the presence of excess fluid in the
preswnptive diagnosis after more common
abdominal cavity, masses, adhesions, abnorcauses of weight loss have been excluded.

mal positioning of bowel in the abdominal

Detennination of the prin1ary underlying
cavity, and vascular lesions in the cranial
pathologic process is necessary to establish
mesenteric artery.

an appropriate treatment regimen and

When malassimilation is suspected,
prognosis.

a carbohydrate absorption test may be

A complete history should focus on
perfom1ed to assess small-intestinal
duration of condition, precipitating factors,
function. In horses, a gastroscopy to
nutritional history, dewonning and routinP
diagnose lesions in the stomach ( eg,
health care program, previous or concurgranulomas, twnor, ulcers) and duodenum rent diseases, as well as the nwnber, age,
or retention of ingesta should be accomand proximity of other affected animals.

plished before absorption tests are

A thorough physical examination is
performed. For absorption tests, the
perfotmed to correlate physical findings
intestinal disorder must be diffuse and/or
with clinical signs and history. In adult
must affect the delivery to and transit
horses and cattle, rectal palpation is
through the small intestine to be diagnostic.

perfom1ed to determine the presence of

An abnormal or flattened absorption curve
intra-abdominal masses, enlarged lymph
is suggestive of small-intestinal dysfunction.

nodes, adhesions, abnormal positioning or

However, a flattened absorption cwve can
thickening of bowel segments, or abnoralso be caused by other conditions.

malities in the cranial mesenteric artery.

Although absorption tests may indicate the

The kidneys, bladder, and related structures
presence of malassimilation, an etiologic
should also be evaluated.

diagnosis requires a biopsy of intestinal

A CBC and serum biochemical paran1-
mucosa and possibly lymph node. In some
eters ( eg, total protein, albwnin, fibrinogen,
cases, rectal biopsy may reveal focal or
glucose, cholesterol, bilirubin, ketones,
diffuse inflan1111atory infiltration. Bacteriofatty acids, CK, AST, glutamate lactate logic culture of the feces, biopsy samples,
dehydrogenase) help detem1ine general
and fecal examination for leukocytes and
health status of the anin1al; presence of
epithelial cells may confum the presence of
inflammation or an infectious P.rocess;
salmonellae or other invasive organisms. In
involvement of body systems; and
some cases, laparoscopy or exploratory
metabolic, electrolyte, and senun protein
celiotomy is required to obtain the intestinal
status. Urinalysis, abdominocentesis, and
or lymph node biopsies. Surgery may not be
fecal examination for parasite ova, larvae,
advisable in a debilitated animal, because
protozoa, and occult blood should also be
wound healing is poor and dehiscence is a
performed to exclude more common causes potential problem. If undertaken, intestinal of weight loss. Additionally, urinalysis
and lymph node biopsies should be
should be performed to assess whether
obtained for culture, histopathology,
glucose or protein is being excreted via
enzymology, and immunology. Because of
wine, which could be a fwiher cause for
the risk and cost of obtaining appropriate
chronic weight loss.

tissue samples, malassimilation syndrome

Evaluation of plasma protein electrophois often presumptively diagnosed with the resis, fecal pH, bacteriologic culture, and
aid of absorption tests.

immunologic studies may be indicated.

Clinically applicable absorption tests
lntracolonic fermentation of malabsorbed
include o-glucose and o-xylose. These tests
carbohydrates will often reduce the fecal
may help assess small-intestinal fw1ction in
pH in foals and calves. Protein-losing
prenuninant calves, foals, c1ias, and mature
enteropathy can be diagnosed preswnphorses. Indications for an oral o-xylose tively by excluding other causes of protein
absorption test in foals, calves, and possibly

MALASSIMILATION SYNDROMES IN LARGE ANIMALS

357
crias include persistent diarrhea not
retained gastric contents, changes in GI
attributable to infectious agents, poor
transit time and motility, or partial
growth despite normal intake, and.other
obstruction. Further sedation of the animal
signs of maldigestion (repeated episodes of
decreases GI motility and secondarily the
gas colic, bloating, ileus). In monogastnc
absorption. A flat absorption curve may �e
animals, the test solution is administered
also seen in animals with no1mal absorptive

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into the stomach. In ruminants and New
capacity due to a transient decrease in

World camelids, the forestomachs must be
intestinal blood flow or to bacteria in the
bypassed ( esophageal groove, abomasocenlumen ofilie small intestine metabolizing tesis ), because otherwise the sugars are
the test sugar. The test substance rapidly
metabolized by the forestomach flora;
equilibrates with many body fluids ( eg,
however oral carbohydrate tolerance
ascites), which lowers the blood concentrastudies �e not frequently used in rumition of xylose and may result in a flat cwve.

nants. Theo-glucose absorption test has the
advantages of being easy and inexpensive,
o-Xylose Absorption Test: o-xylose is a
and methods to determine blood glucose
pentose also known as wood sugar; only
concentrations are available in most clinical
trace an1ounts are found in feedstuffs of
laboratories. The main disadvantage is that
plant origin. The o-xylose absorption test
results are not only a function of intestinal
measures absorptive capacity of ilie
absorption, but also are strongly influenced
small-intestinal mucosa because functional
by tl1e intensive cellular uptake and
enterocytes actively transport o-xylose
metabolism of glucose after it has been
across ilie mucosa and into tl1e bloodabsorbed. The o-xylose absorption test stream. Subno1mal absorption supports a
more directly measures intestinal absorpdiagnosis of malabsorption. Age and diet tive capacity and is not influenced by
also affect o-xylose absorption in healthy
endogenous factors and intestinal
horses. Foals <3 mo old have a higher peak
enzymatic activity, respectively. Disadvanconcentration of o-xylose after administratages are tlmt o-xylose is m tion tl1an adults. Adult horses maintained on
o_re expensive,
and availability of commercial laboratones
a high-roughage, low-energy diet have a
that perform plasma xylose determinations
higher peak concentration of o-xylose after
is limited. However, o-xylose concentraadministration than tl10se fed a high-energy tions can be measured using classic
diet. Food deprivation can alter o-xylose
photometric techniques, which do not
absorption in horses without overt GI tract
require special equipment and can be
disease, which must be considered when
performed in a clinical laboratory.

interpreting results in horses that are

Glucose or galactose may inhibit the
anorectic regardless of cause.

absorption of o-xylose; therefore, fasting
o-Xylose (0.5-1 glkg in a lO"A,solution) is
is necessary before the test is performed
administered via nasogastric tube to a horse
in horses and preruminant calves. The
iliat has been fasted overnight ( 18---24 hf).

protocols of both tests require prolonged

Heparinized venous blood samples are
fasting, which may be deleterious to sick
collected before o-xylose administration
young foals and calves. The results of both

(time 0) and at 30-min intervals afterward
tests are also affected by gastric emptying
for 4 hr (±6 hr sample). Expected peak
rate (o-xylose has also been used to estimate
values (20-25 mg/dL) should occur between
abomasal emptying rate in cattle), small60 and 120 min after dosing. The normal intestinal transit time, diet, and length of
curve should have a bell shape or inverted V
fasting pe1iod before testing. The shape of
shape with a definable peak plasma xylose
the absorption cwve is influenced by renal
concentration 1-2 hr after administration.

clearance, hypoxia, anemia, systemic and

Peak absolute plasma values should be �15
intestinal bacterial infections, and IgG
mg/dL above baseline values in healthy
concentrations in foals. The age of the
horses. In adult cattle the o-xylose (0.5 g/kg
animals also affects absorption and digestion
in a 5QOA, solution) must be administered by
of glucose, lactose, and o-xylose. Therefore,
abomasocentesis to bypass ilie rumen. Sintiilie control animals must be within a few lar to that in horses, the curve is almost bell
days of age of the affected animal if reference shaped in high-yielding dairy cattle; peak ranges are not available for its age group.

values of 1.1-1.3 mmol/L (16-20 mg/dL)

A delayed peak in the absorption curve
occur -90 min after the solution is
of both the o-glucose and o-xylose test may
administered.

result from delayed gastric emptying
o-Glucose Absorption Test: Glucose
resulting from hypertonicity of the glucose
absorption curves are steeper in pastureor xylose solution, excitement, pain, fed horses than in those fed a higher

358

MALASSIMILATION SYNDROMES IN LARGE ANIMALS
energy ration. Lower peak values are seen
fast (12-18 hr) required. before this test is
in horses on a high-concentrate ration.

performed.. Before performing an oral

The length of the pretest fast influences
lactose intolerance test, grain and hay
the absorption curve. Prolonged fasting
should be withheld for 18 lu·. The calf or
may delay or decrease peak glucose
foal should be prevented from nursing

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concentration, thus giving a false-positive

(muzzled) for �4 hr before administering
result. In two studies, >90% of adult horses o-lactose at 1 g/kg as a 20% solution via with evidence of"total" glucose malabnasogastric tube; the muzzle should be sorption had severe infiltrative lesions of
kept in place for the duration of the test.

the small intestine. The majority of horses

Blood samples are collected into tubes

(18/25) classified with "partial" glucose
containing fluoride oxalate for determinamalabsorption also had obvious pathotion of blood glucose concentrations at 30
logic abnormalities of the small intestine.

min, and immediately before and at 30--min

Perfonnance of the D-glucose absorption
intervals for 3-4 hr after dosing. Blood
test is similar to that of the D-xylose
glucose concentration should be double
absorption test except samples are
that of the resting values within 60-90 min
collected into sodium fluoride tubes. In
of lactose administration. Peak glucose
healthy horses, blood glucose concentraconcentrations should be �35 mg/dL higher tions should peak 90-120 min after
than the baseline in healthy foals.

ad.ministration. This peak should be >85%

Abnormal results suggestive of lactose
above the resting glucose level. Reportedly
intolerance include a delayed, prolonged,
complete malabsorption is defined as a peak or lack of increase in blood glucose

< 15% above resting concentrations; partial
concentration from baseline.

malabsorption is defined as a peak 15%----85%

Lack of an appropriate increase in blood
above resting levels. One of the major
glucose concentration after lactose
disadvantages to the oral glucose absorpadministration may be due to maldigestion tion test is that when using the conventional
or malabsorption. Therefore, if the lactose
protocol sampling is over a 6--hr period. One
tolerance test is abnom1al, a D-glucose or
repo1ted modified protocol requires only

D-xylose absorption test should be
two test samples at O and 120 min after
perfonned to determine whether malabsorpadministration. This modification reporttion or mald.igestion alone is the problem.

edly did not affect the reliability of the test Casein hypersensitivity is distinguished
result.

from lactose intolerance by assessing the
aninlal's response to enzymatically treated

Oral Lactose Tolerance Test: Diagnosis.

and untreated milk. Definitive confim1ation
of acquired. lactase deficiency is usually
of lactase deficiency is through direct
presumptive based on hi�tory, clinical signs,
measurement of mucosa] lactase activity in
and confinnation of presence of associated
the intestinal tissue. However, this is rarely
pathogens. Definitive diagnosis can be
unde1taken in the clinical setting, because a
achieved with an oral lactose tolerance test.

surgical biopsy of the mucosa is required.

Lactose is hydrolyzed within the brush

A hydrogen breath test has also been
border of the small-intestinal en.terocytes
described. for detection of carbohydrate
by lactase to constituent D-glucose and
malabsorption in horses. In a clinical study,
galactose before these monosaccharides
diseased horses showed higher fasting
can be absorbed. Oral lactose tolerance
breath hydrogen levels than.did healthy
testing is directed. specifically at assessing
horses. However, because of the expensive
whether lactase activity is present. Ad.ult
laboratory procedures, the test is not widely
horses (>3 yr old) are lactose intolerant, and used.

the test is unsuitable for adult ruminants
and adult New World camelid.s. The oral

Treatment: The etiology of the primary
lactose tolerance test is of value in
w1derlying disease process must be
evaluating young foals and prenmlinant
detennined before specific therapy for
calves with diarrhea or poor growth.

malassi.milation syndrome can be initiated.

Lactose intolerance has been documented

Specific therapy for most causes of
in foals, calves, and kids.

malassimilation is not available, except for

An oral lactose tolerance test does not
lesions due to parasite dan1age. Anticocdistinguish mald.igestion from malabsorpcidial and larvacidal dewomlings may tion and requires fasting for several hours.

improve the condition; however, a complete

Feeding enzymatically treated milk
healing and return to full absorption

(lactose-free milk) to animals suspected.

capacity is not al ways achievable depending
of being lactose intolerant may be tried
on the damage. Anti-inflammatory agents
before subjecting animals to the lengthy

(eg, NSAIDs, corticosteroids) may also help

MALASSIMILATION SYNDROMES IN LARGE ANIMALS

359
decrease the inflammatory response within
infections in affected came lids may
the affected bowel. Supportive care and
successfully be treated if diagnosed early.

facilitation of nutrient absorption from

Treatment currently involves administramore caudal parts of the intestine must be tion of amproliun1, sulfonamides,
encouraged until the intestinal epitheliwn
ponazuril, or toltrazuril with appropriate

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recovers and new villous cells are produced. supportive care.

Maturation and healing of the intestinal

Horses with malabsorption due to a
absorptive surfaces may take weeks to
disease process or after small-bowel
months in severe cases.

resection must be fed a diet that optimizes

Calves and foals with acquired lactase
digestion of feeds in the large intestine.

deficiency after diarrheal disease (viral,

The diet should provide easily absorbed
bacterial, protozoa!) often respond well to
protein, carbohydrates, fat, and watersupportive care ( correction of acid-base, soluble vitamins and maintain mineral
electrolyte, and glucose abnonnalities)

balance. Increased concentrate-to-forage
and feeding of enzymatically treated milk
ratios decrease digestion of feeds in the
until the small-intestinal mucosa has
large intestine and should be avoided.

regenerated. Foals and calves should

Horses benefit from a fiber-based diet. To
be fed small amounts of high-quality
enhance digestion in the large intestine,
roughage or grain (if they are able to
easily fermentable roughages (eg, alfalfa)

tolerate it) to help meet their energy
should be fed. High-quality fiber, metaboneeds, although enteral feeding should be lized in the cecum and colon to volatile
continued whenever possible. Young foals
fatty acids, may partially compensate for
and calves that do not tolerate feedings of
small-intestinal losses. In young animals,
milk or enzymatically treated milk may
the diet may be supplemented with milk
benefit from short-term ( <24 hr) withprotein if lactase deficiency is not present.

drawal of milk. These animals need

Fat may be added to the diet to enhance
alternative sources of energy and
caloric intake. Calcium, magnesium,
nutrients such as short-term feeding
phosphate, zinc, copper, and iron may

(s24 hr) of glucose-containing electrolyte
need to be supplemented, because they
solutions or, in more severe cases, partial
are absorbed in horses in the small
or total parenteral nutrition. Dietary
intestine only. Water-soluble (especially
change to a soy-based, non-lactoscvitan1in B
containing milk replacer and early

12) and fat-soluble vitamins
should be supplemented parenterally as
weaning are advised for animals with
needed. Excessive supplementation,
nonresponsive lactose intolerance.

which could lead to toxicosis, should

Treatment of inflanunatory bowel
be avoided.

disease in horses has been attempted but is

Horses that will not eat may have to be
often unsuccessful even with aggressive
force-fed via nasogastric tube. The horse
corticosteroid administration. Sulfasalashould be fed small, frequent meals to take zine and isoniazid have been recomadvantage of the limited remaining mended, but their usefulness is unproved.

absorptive ability of the small intestine

Similarly, the usefulness of dimethyl
without overloading it. Preruminant calves
sulfoxide in the treatment of intestinal
that are repeatedly tube-fed may develop
amyloidosis is unknown. Animals with
nuninal acidosis due to deposition of
anaerobic or aerobic bacterial overgrowth
fennentable feed matelial into the rumen
may respond to antimicrobial administra

(nunen drinker) rather than the abomasw11.

tion. Adequate penetration of antimicrobi

Partial or total parenteral nutrition may be
als into inflammatory bowel lesions
necessary for animals that refuse to eat or

(Rhodococcus equi in foals) is doubtful.

that cannot tolerate force-feeding. However,

Successful treatment of Lawsonia
total parenteral nutlition is expensive and
intracellulmis in foals has been achieved
difficult to continue on a long-term basis in
with longterm administration of antimicrohorses or even impossible in nuninants.

bials (erythromycin, azithromycin,
clarithromycin, chloramphenicol, oxytetra

Prognosis: Efforts should be made to
cycline, doxycycline) and aggressive
determine an etiologic diagnosis once
supportive care (fluids, plasma) as dictated malassimilation has been confumed so that by the animal's clinical condition. Any
an accurate prognosis can be given and
treatment attempt of cattle with clinical
appropriate therapy prescribed. Most
signs of Johne's disease have proved to be
conditions causing malassimilation in adult
unsuccessful; slaughter or euthanasia is
large animals warrant a poor prognosis, and
recommended. Eimmia macusa,niensis
treatment is commonly unsuccessful.

360

MALASSIMILATION SYNDROMES IN LARGE ANIMALS

However, parasitic infection of the bowel or
kids with lactase deficiency may respond
its blood supply can respond to anthelminwell to supportive care and dietary tic therapy. Occasionally, a non-neoplastic
management. Prognosis for horses with
infiltration of the bowel may respond to
malabsorption due to inflanunatory bowel
corticosteroids, but the response may be
disease is poor; most reported cases have

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transient in some cases. Calves, foals, and
been fatal.

ABDOMINAL FAT NECROSIS

Hard masses of necrotic fat are occasionally tl1ey compress the abomasum, small identified in the peritoneal cavity of mature
intestine, and spiral colon; obstruct the
cattle, especially the Channel Island breeds,
birth canal; or more rarely compress the

Japanese Black cattle, and beef cattle
ureters. Palpation per rectum is useful
grazing fescue for long periods. The disease
in diagnosis and in detennini.ng prevalence
has also been seen in goats and some
in a cattle herd. Advanced cases in aged
species of deer maintained on pastures
dairy cows may be detected by abdominal
consisting primarily of tall fescue. The
ballottement with the identification of large
masses are commonly mistaken for a
firm masses in the abdomen. Ultrasonodeveloping fetus on palpation per rectum graphic examination of the abdomen
because they feel like "floating corks"

reveals the presence of hyperechoic masses
similar to cotyledons. The masses of
of variable size in the omenturn, with
necrotic fat usually do not cause clinical
localized masses appearing to float in an
signs but in advanced cases can create an
excess of peritoneal fluid. Hyperechoic
extraluminal obstruction that results in
masses adjacent to intestine may be
episodes of moderate abdominal pain,
associated with lun1inal constriction. A
distention of intestine proximal to the fat,
presumptive diagnosis of abdominal fat
and the passage of small amounts of feces.

necrosis can be made using ultrasound

The composition of the deposits in cattle
guided biopsy of the echogenic masses
with fat necrosis is identical to that of fat in
or by direct biopsy during right flank
healthy cows. The abnormal fat deposition
exploratory laparotomy. Less conunonly,
is confined to abdominal fat and is
isolated fat masses may be found freely
consistent with current understanding that
floating in the peritoneal fluid at surgery.

abdominal fat is controlled in a different

The size of tl1e masses usually slowly
manner than fat deposits elsewhere in the
increases, but spontaneous resolution can
body. Fat necrosis has hist01ically been
occur. Removal of cattle from rescue
termed lipomatosis, but this tenn is now
pastures or dilution of fescue intake by
considered inappropriate because the
supplying legwne or other grass pasture
masses are not neoplastic or hyperplastic.

can promote the slow reduction in the size

The etiology is unknown, but one
of masses. Isoprothiolone (50 mg/kg/day,
proposed cause is consun1ption of feeds

PO, for 8 wk) effectively decreases the size
containing high concentrations of
of fat necrosis lesions in Japanese Black

Jong-chain, saturated fatty acids. Fat
cattle.

necrosis is most commonly seen in beef

In affected deer herds, 9QOA, of tl1e females
cattle �2 yr old after prolonged grazing of
may be affected with fat necrosis. Clinical
tall fescue infected with the endophyte
signs include slow development of

Neotyphodium (Acremonium) coenophi
anorexia, depression, and uremia associ
alum (see also ,ESCUE POISO I G, p 3016); fat ated with large masses of necrotic
necrosis is associated with endophyte
abdominal fat constricting the ureters,
infection rates of �65%. Fat necrosis is seen
causing hydrow·eter and hydronephrosis.

throughout the southeastern USA where

A second forn1 of abdominal fat necrosis
tall fescue is the primary pasture plant for
in domestic ani.n1als, less well defined,
grazing.

appears to be related to pancreatitis.

Hard masses of necrotic fat form in the

Although not associated with a clinical
omentum, mesentery, and perirenal fat. The
syndrome, the lesions ( discrete or confluent
masses may cause clinical disease when
masses of necrotic adipose tissue) are

DISEASES OF THE MOUTH IN SMALL ANIMALS

361
usually confined to peripancreatic fat.

most often in sheep but also in pigs,

However, fat necrosis lesions may also
horses, cats, and other species. Little
be found throughout the abdomen.

infom1ation is available about the

A third form, a focal necrosis of
condition in these species, but abdominal
abdominal and retroperitoneal fat
radiography or ultrasonography may help

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(steatitis or yellow-fat disease) is seen
identify focal necrosis in cats.

DISEASES OF THE MOUTH

IN SMALL ANIMALS

For a discussion of developmental diseases
in the oral cavity may affect the gingiva
of the mouth, seep 162. For EOSINOPIIILIC

(gingivitis), nongingival tissues of the

GRANULOMA COMPLEX, seep 971.

pe1iodontiun1 (pe1iodontitis), alveolar

The primary fw1ction of the mouth is to
mucosa (alveolar mucositis), sublingual
introduce food into the digestive tract.

mucosa(sublingual mucositis), lip and

Additional functions include corrunw1icacheek mucosa (labial and buccal mucositis), tion and social interaction, grooming,
lip (cheilitis), oral mucosa (stomatitis),
protection, heat regulation (particularly in
mucosa of the dorsal or ventral tongue
dogs), and grasping objects. The latter is
surface (glossitis), mucosa of the caudal
very important for perfonnance anin1als
oral cavity (caudal mucositis), mucosa

(eg, retrievers, military and police dogs).

fomiing the lateral walls of the pharynx

Similar to other areas of the alimentary

(faucitis), mucosa of the palate (palatitis),
tract, the mouth in the nom1al, healthy state palatine tonsil (tonsillitis), or mucosa of supports a large and diverse population of
the pharynx (pha.iyngitis). The nature
bacteria that lives primarily in biofilrn
and severity of the lesions va.iy greatly
conununities. Unlike other areas of the
depending on the etiology and duration of
body, the mouth also contains nonvital
the disease. Contact mucositis a.Ild contact
surfaces ( enan1el of teeth) that have neither
mucosa! ulceration represent lesions in
local inunune system defenses nor the
susceptible anin1als that are seconda.iy
ability to regenerate through cellular
to mucosa! contact, with a tooth surface
replacement. The oral mucosa! tissues have
bearing the responsible i.nitant, allergen;or
an excellent vascular supply, and the tightly
antigen. They have also been called "contact
adherent gingiva protects the underlying
ulcers" and "kissing ulcers." Stomatitis is alveolar bone from traun1a., them1al injw-y,
infla.irunation of ll1e mucous lining of a.i1y of
and bacterial invasion.

the structw-es in the mouth; in clinical use,

Food prehension requires a complex
the tem1 should be reserved to describe
interaction of the muscles of mastication,
widespread oral inflanunation (beyond
the teeth, the tongue, and the pharyngeal
gingivitis a.Ild periodontitis) that may also
muscles. When any of these become
extend into submucosal tissues ( eg, ma.i·ked
compromised through disease or trauma,
caudal mucositis extending into submucosal
malnutrition and dehydration may result.

tissues may be terrned caudal stomatitis ).

A complete oral examination should be

Periodontal disease, including gingivitis
included in every physical examination,
and periodontitis, is the most common oral
because oral diseases a.re most effectively
problem in small animals. Gingivitis is a
treated when diagnosed early. Unfortugingival inflanunato1y response to the nately, many problems remain hidden in
presence of bacterial plaque on a.Il adjacent
the mouth until they have progressed to
tooth surface. Periodontitis is infla.i1unation
an advanced stage.

of nongingival tissues of the periodontimn

(na.inely periodontal liga.i11ent a.i1d alveolar

ORAL INFLAMMATORY AND
bone); it results from the combination of

ULCERATIVE DISEASE
bacterial pe1iodontopa.thogens and the
host's inunune response that together
lnflanunation of the oral tissues can be
destroy tl1e tootl1-supporting tissues.

either primary or secondary. lnflanunation

(See ai,so PERIODONTAL DISEASE, p 178.)

362

DISEASES OF THE MOUTH IN SMALL ANIMALS

Periapical disease (granuloma, abscess,
of oral mucosa] tissues (particularly the
or cyst) is usually caused by endodontic
gingiva, alveolar mucosa, labial and buccal
disease (spread of infection and inflanunamucosa, sublingual mucosa, and mucosa of tion from within the tooth through the
the caudal oral cavity) and increasing levels
apical foranlina into the periapical tissues).

of discomfort. More significantly, the

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Clinically, a sinus tract may develop that
mucosa of the caudal oral cavity and the
manifests as a circular raised area of
area at and lateral to the palatoglossal folds
inflamed granulation tissue with a central
a.re often severely ulcerated, friable,
drai11ing fistula that opens near the
inflamed, and proliferative. Severe
mucogingivaljunction. The tract can be
ulceroproliferative inflan1mation that
followed to the primary periodontal or
involves this area bilaterally in the back of
pe1iapical lesion, and the etiology resolved.

the mouth is pathognomonic for FS. The

(See also ENDODONTIC DISEASE, p 180.) A
cause is unproved, but it is suspected to
parulis is a true pe1iodontal abscess ( eg, an
result from an inapprop1iate inflammatory
encapsulated mucopmulent lesion within a
response in affected cats to one or more
periodontal pocket).

antigens. A high percentage of affected ca.ts

Other causes of oral inflanunatory

(100% in some studies) are chronic cariiers
conditions include immunopathy ( eg,
of feline calicivirus. FS may be caused by
autoinunune disease, immune deficiency),
the Slllll of multiple sensitivities in an
chemical agents, infectious disease, traun1a,
individual, with antigen on the tooth
metabolic disease, developmental
surfaces, including the root surfaces and
anomalies or conformational anatomy that
periodontal ligament, exceeding a
predisposes to irritation or inflanunation,
threshold.

bums, radiation therapy, or neoplasia.

The most immediate sign is severe pain

Infectious agents that have been associated
when opening the mouth. Cats vocalize and
with oral inflanunation, glossitis, stomatitis,
jlllllp when they yawn or open their mouth
and oral ulcerations include feline
to eat. Halitosis, ptyalism, and dysphagia
herpesvims, feline calicivirus, feline
may be seen. Cats often show an "a.pproachleukemia vims, feline immunodeficiency a.voidance" behavior as they approach their
vims, canine clistemper vims, Barlonella
food in hunger, then hiss and run off in antic
henselae, and certain Le-plospira serovars.

ipation of discomfo1t. lf the condition is

TraLUnatic stomatitis may be seen after oral
severe and of long dmation, weight loss may
exposme to plant material ( embedded plant be evident. The disease is slowly progre s awns) or fiberglass insulation. When sive and may not b e recognized until lesions
chewed, plants of the species Diejfen
have become severe. Mandibular lympha.d
bachia may also cause oral inflammation
enopathy is sometimes present. Pain often
and ulcers. Contact with processionary
prevents adequate exanlina.tion of the oral
caterpillars may also cause severe glossitis.

cavity without sedation or anesthesia.

Thallium is the major heavy metal
responsible for oral lesions; incidence

Diagnosis: Diagnosis is made by visual
of this toxicity is low. Uremia can cause
identification of bilateral inflanunation of
stomatitis and oral ulcers. Recurrent oral
the mucosa of the caudal oral cavity and the
ulcerations are also seen in gray Collies
tissues at or lateral to the pala.toglossal folds
with cyclic hematopoiesis.

dtuing oral examination. In advanced cases,

Signs vary widely with the cause and
the cat will strongly object to opening the
extent of inflammation. Anorexia may be
mouth. Additional tests inciude virus
seen, especially in cats. Halitosis and
isolation (eg, calicivirus and herpesvirus),
drooling are conunon with caudal stomatitis retroviral tests, and evaluation for systemic or glossitis, and saliva r.iay be blood tinged.

disease (eg, renal failme). Although a

The animal may paw at its mouth and resent
defmitive association with Bartonella
any attempt to exanline the oral cavity
infection has not been shown, testing has
because of pain. Regional lymph nodes may
been reconm1ended. In atypical cases
be enlarged.

( LUlilateral involvement, usually proliferative focal lesion), biopsy and histopatho

Feline Stomatitis
logic evaluation is required to exclude oral

(Gingivostomatitis, Caudal stomatitis,
neoplasia or other specific oral disorders.

Lymphocytic-plasmacytic stomatitis)

Most biopsy samples collected from chronic
infla.nunatory or ulcerated lesions reveal a

F'eline stomatitis (FS) is a relatively
predominance of lymphocytes and plasma
uncommon (3% of feline oral problems) but
cells, which indicate the chronic inflanunaserious condition. Affected cats present tory nature of the lesion without elucidating
with progressively worsening inflammation
the primary etiology.

DISEASES OF THE MOUTH IN SMALL ANIMALS

363

Treatment: Partial-mouth extraction
addition, cats that have received repeated

( removal of all premolars and molars) or
corticosteroid treatments have a poorer
full-mouth extraction (removal of all teeth)

prognosis once the teeth are extracted.

and debridement of the associated soft and

Partial- or full-mouth extractions often
hard tissues is the only treatment to provide
result in significant improvement or

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lasting improvement and aid in overall
complete resolution of the inflammation
longtenn control. Partial- or full-mouth
if performed early in the course of the
extractions provide significant improvedisease and before multiple corticosteroid ment in 60%--8()0A, of affected cats when
treatments.

done early in the disease course and when
no root tips or fragments are left behind.

Chronically affected cats treated medically

Canine Stomatitis
for many months have a poorer prognosis

Characteristics of canine stomatitis that
after surgery. Dental radiographs of areas
often manifest as contact mucositis and
with missing teeth are required to check for
contact mucosa! ulceration (also called
retained roots. Any retained root fragments
chronic ulcerative paradental syndrome or
must be removed, because they will prevent

CUPS) include severe gingivitis, multiple
improvement. Postoperatively, medical
sites of gingival recession and dehiscence,
therapy focuses on controlling inflammaand large areas of ulcerated labial and tion, infection, and pain. Oral administrabuccal mucosa acljacent to the surfaces of tion of corticosteroids such as prednisolone
large teetl1. The problem commonly affects
is less effective than SC or IM injection of

Greyhounds, and it has also been seen in
methylprednisolone. An alternative is

Maltese, Miniature Schnauzers, Labrador
transdennal administration of predniso

RetJievers, and other breeds.

lone. In refractory cases, use of interferon
omega may be considered, injected

Diagnosis: Diagnosis of canine stomatitis
intralesionally before the sta.tt of oral
is by clinical observation of the typical oral
administration. Commonly used antibiotics
lesions after excluding other etiologies such
include an1oxicillin-clavulanic acid or
as uremic stomatitis, caustic stomatitis, or
clindan1ycin, but the response to treatment
specific infectious agents. The characterismay be lacking or only transient. Culturing tic lesion is the contact ulcer that develops
the lesions and performing susceptibility
where the lip or cheek mucosa contacts the
tests are rarely indicated, even in chronic or
tooth sruiace, most commonly on the im1er
recurrent infections. Nutritional support is
sruiace of the upper lip acljacent to the
required in chronic cases with severe
upper canine and camassial teeth. These
weight loss and dehydration. Pain control
lesions have also been termed "kissing
with sublingual buprenorphine or a
ulcers" or "kissing lesions," because they transdermal fenta.tiyl patch should also be
are found where the lips "kiss" the teetlt. An considered, along with dietary changes
inunune profile should be done, and a

(nonallergenic, soft palatable foods) and
biopsy considered for histopathology.

administration of topical antiseptics ( eg,
dilute chlorhexidine or zinc ascorbate ).

Treatment: The underlying pathology of

Placement of a feeding tube should be
canine stomatitis is an i.rnmunopatl1y that
considered in debilitated cats that do not
results in an excessive local inflammatory
respond to therapy.

response to the antigens in dental plaque.

Many other treatments for FS have been

Eliminating, or at least minimizing, plaque
reported, including good home oral hygiene, through professional dental cleaning and periodontal therapy, frequent dental
meticulous home oral hygiene (twice daily
cleanings, cyclosporine therapy, laser
tooth brushing) may resolve the problem.

therapy, and bovine lactofenin. Perhaps

However, even slight residual plaque on
with the exception of cyclosp01ine, none of
the tooth sruiaces will perpetuate the
these provide longtem1 resolution. Corticoinflammation and ulcerations. Supplemensteroid adnlinistration alone usually results tal antinlicrobial measures with topical
in significant and inunediate clinical
chlorhexidine gluconate rinses or gels and
improvement from modulation of the
possibly oral antibiotic treatment with
excessive inflanm1atory response, but it is
metronidazole should also be used. In
not recommended except as a last resort.

severe cases, topical anti-inflammatory

Without surgery (ie, partial- or full-mouth
preparations to modulate the inflanmiatory
extractions), repeated use of corticosteresponse may provide comfort. Discomfort roids is frequently required. This treatment
caused by the ulcers complicates efforts
becomes progressively less effective and
to brush the teeth and administer oral
eventually completely ineffective. In
medications. In cases in which discomfort is

364

DISEASES OF THE MOUTH IN SMALL ANIMALS
severe and the owners are unable or
cleaning the folds 1-2 times/day with
unwilling to brush the teeth, extraction of
benzoyl peroxide or a mild skin cleanser,
all teeth associated with ulcers may be
and keeping the area dry. Topical diaper
necessary to remove the contact surfaces
rash cream applied daily may be helpful.

on which plaque accumulates. Although this

Surgical correction ( cheiloplasty) of deep

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may help control the lesions, it is not
lip folds is a more longlasting remedy.

curative, because plaque fom1s on mucosa!

Cheilitis that is u.nrelated to lip folds
srnfaces in the mouth, including the tongue.

usually resolves with minimal cleansing,

In some cases with complete extractions,
appropriate antibiotics if a bacterial
dogs continue to develop lesions due to a
infection is present, and specific treatment
hyperinlmune response to the plaque.

of primary etiologies (eg, autoinlmune skin
disease). Wounds of the lips should be

Lip Fold Dermatitis and Cheilitis
cleaned and sutured if necessary. Treatment

Lip fold de1rnatitis is a chronic, moist
of periodontal disease or stomatitis is
dennatitis seen most conunonly in breeds
necessary to prevent recurrence.

that have pendulous lips and lower lateral

Infectious cheilitis that has spread from
lip folds (eg, spaniels, English Bulldogs,
a lesion elsewhere usually improves with

Saint Bernards) that have prolonged
treatment of the primary lesion, but local
contact with saliva. The lesions may be
treatment also is necessary. With severe
exacerbated when poor oral hygiene results
infection, hair should be clipped from the
in increased salivary bacterial levels. The
lesion and the area gently cleaned and dried.

lower lip folds can become very malod01

Antibiotics are indicated if the infection is

°
ous, inflan1ed, uncomfortable, and swollen.

severe or systemic.

Lip wOLmds, resulting from fights or
chewing on sharp objects, are conunon and

Mycotic Stomatitis
vary widely in severity. Thoms, grass awns,

Mycotic stomatitis caused by overgrowth of
plant burrs, and fishhooks may embed in the the opportunistic yeast Candida albicans lips and cause marked irritation or severe
is an uncommon cause of stomatitis in dogs
wounds. Irritants such as plastic or plant
and cats. It is characterized by stomatitis,
material can produce inflanunation of the
halitosis, ptyalism, anorexia, oral ulceralips. Lip infections may develop secondary tion, and bleeding from the oral tissues. It is
to wounds or foreign bodies or can be
usually thought to be associated with other
associated with inflammation of acljacent
oral diseases, longterm antibiotic therapy,
areas. Direct extension of severe periodonor immunosuppression. Diagnosis is tal disease or stomatitis can produce
confumed by culture of the organism from
cheilitis. Licking areas of bacterial
t11e lesion or by histologic evidence of tissue
dermatitis or infected wounds can spread
invasion.

the infection to the lips and lip folds. Other

Any existing underlying local or systemic
causes of inflanunation of the lips include
diseases affecting tl1e oral cavity should
parasitic infections, autoinlmune skin
be treated. Ketoconazole or a related
diseases, and neoplasia.

benzinl.idazole should be administered until
the lesions resolve, after which antibiotic

Clinical Findings and Diagnosis: Intherapy should be discontinued. An flanm1ation of the lips and lip folds can be
adequate level of nutrition should be
acute or chronic. Animals with cheilitis may
maintained. The prognosis is guarded if
paw, scratch, or rub at their mouth or lip;
predisposing diseases cannot be adequately
have a foul odor on the breath; and
treated or controlled.

occasionally salivate excessively or be
anorectic. With chronic infection of the lip

Acute Necrotizing Ulcerative
margins or folds, the hair in these areas is

Gingivitis
discolored, moist, and matted with a thick,
yellowish or brown, malodorous discharge

(Necrotizing ulcerative gingivostomatitis,
overlying hyperemic and sometimes

Ulceromembranous stomatitis, Necrotizing
ulcerated skin.

ulcerative stomatitis, Vincent stomatitis,

Cheilitis due to extension of infection

Trench mouth)

from the mouth or another area of the body

Acute necrotizing ulcerative gingivitis
usually is detected easily because of the

(ANUG) is a relatively tmconunon disease
primary lesion.

of dogs characterized by severe gingivitis,
ulceration, and necrosis of the oral mucosa.

Treatment: Medical management of lip

F'usobacterium spp and spirochete
fold dermatitis includes clipping the hair,
organisms (Borrelia vincenti), nom1al

DISEASES OF THE MOUTH IN SMALL ANIMALS

365
inhabitants of the mouth, have been
tongue. There may be no inflammation of
suggested as a cause of this disease after
the dorsal surface of the tongue, but the
some predisposing factor increases their
ventral surface is painful, shows acute
numbers or decreases the local resistance
or chronic initation, and frequently is
of the oral mucosa. The role, if any, of these
lacerated by tl1e foreign body. Porcupine

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organisms in causing disease is unknown.

quills, plant material, and other foreign

In people, Bacteroides melaninogeniciis
mate1ials may become embedded so deeply
inlermedius may play a more in1portant
they are not palpable. Insect stings cause
role. Other potential factors are stress,
acute swelling of the tongue.

excess glucocorticoid administration in

In chronic cases of ulcerative glossitis,
susceptible dogs, and poor nutrition.

a thick, brown, foul-smelling discharge

The disease appears first as reddening

( occasionally witl1 bleeding) may be
and swelling of the gingival margins and
present. Frequently, the animal is reluctant
interdental papillae, which are painful,
to allow oral examination.

bleed easily, and may progress to gingival

Fissured, or plicated, tongue (lingua
recession. Extension to other areas of the
dissecta) describes a textural variation of
oral mucosa is common, resulting in
the dorsum of the tongue with deep central
ulcerated, necrotic mucous membranes and or lateral longitudinal grooves. The fissure exposed bone in severe cases, leading to
deepens with age and is therefore thought
osteomyelitis and osteonecrosis. Halitosis is to be acquired from some extrinsic factor.

severe, and the animal may be anorectic

However, it may also represent a developbecause of pain. Ptyalism sometimes mental anomaly. The groove often becomes
occurs, and the saliva may be blood tinged.

deeply filled with hairs tl1at act as a local

Differential diagnoses include severe
irritant, causing inflammation and
periodontal disease, autoin1111une skin
discomfort.

disease, uremia, neoplasia, and other

Any foreign bodies or hairs should be
systemic disease associated with oral
removed, and broken or diseased teeth
lesions.

removed or treated. Bacterial infectious

Diagnosis is made by exclusion of other
glossitis should be treated with an
etiologies.

approp1iate systemic antibiotic. Debride

Treatment of periodontal disease,
ment and dilute chlorhexidine mouthpartial- or full-mouth extractions, debridewashes are beneficial in some cases. Lingual ment of lesions, oral hygiene, antibiotics
curettage is sometimes required if foreign

( amoxicillin-clavulanate, ampicillin,
material is embedded in the tongue. A soft
clindamycin, metronidazole, tetracyclines),
diet and parenteral fluids are administered
and oral antiseptics ( dilute chlorhexidine
as needed. If the animal is debilitated and
solution or gel) are indicated.

unable to eat well for a prolonged p,eriod, a
feeding tube to allow for nutritional support

Glossitis
should be considered. Acute glossitis due
to insect stings may require emergency

Glossitis, an acute or chronic inflammation
treatment.

of the tongue, may be due to infectious

If the glossitis is secondary to another

( calicivirus, herpesvirus, rhinotracheitis
condition, the primary disease should be
virus, leptospirosis ), physical (irritation
treated. Tongue tissues heal rapidly after
from excess calculus and periodontal
irritation and infection have been elimidisease, foreign bodies that penetrate or nated.

become lodged under the tongue, traumatic
wounds), or chemical agents; metabolic

SOFT-TISSUE TRAUMA
disease ( uremia, hypoparathyoidisrn,
diabetes); or other causes such as electric
or thermal burns and insect stings. Foreign

Chewing Lesions
body glossitis is especially a problem in
longhaired dogs that attempt to remove

A proliferative, verrucous lesion along the
plant burrs from their coats.

bite-plane of the cheek or sublingual region

Drooling and a reluctance to eat are
may result from self-trauma when the tissue
common signs, but the cause may go
becomes entrapped between the teeth
undiscovered unless the mouth is carefully
dtuing chewing. Surgical removal of the
examined. Periodontitis may result in
excess tissue prevents further trauma.

reddening, swelling, and occasionally
ulceration of the lateral edges and the tip of

Mouth Burns
the tongue. A thread, string, or other linear

Thermal, chemical, or electric burns
foreign body may get caught under the
involving the mouth are not w1cornmon.

366

DISEASES OF THE MOUTH IN SMALL ANIMALS

The animal should be evaluated and treated
interfere with prehension, mastication, or
for systemic involvement, which may be
swallowing. Occasionally, if the growths are
life-threatening (new-ogenic pulmonary
numerous, the dog may bite them when
edema). The tongue, lips, cheeks, labial and
chewing, causing them to bleed and become
buccal mucosa, and palate are frequently
infected. They may regress spontaneously

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involved with electiic burns. The ir\jwies
within a few weeks to months, and removal
may be mild with only temporary discomis generally not necessary. If necessary, the fort, or they may be destructive with loss
exophytic lesion can be debulked with
of tissue, scar formation, and subsequent
electro- or radiosurge1y or by sharp
deformity or tissue deficits. Chewing on an
resection. Surgical removal of one or more
elect1ic cord is most frequently a problem
of the papillomas may initiate regression.

in kittens, puppies, and pet rabbits. These

The use of commercial or autogenous
animals often have a linear scar across the
vaccines should be considered in very
dorsum of tl1e tongue, outlining tl1e path
severe cases in which the dog caimot
of the electric cord. One or both lip
swallow or breathe nmmally. The selfcommisures may have a scar or woW1d, limiting character of the disease makes
and the acljacent carnassial teeth may be
evaluation of any treatment difficult. Severe
discolored and eventually require endooral papillomatosis may be seen in dontic treatlnent.

iI11mW1ocompromised dogs witl1 lym

The owner may have observed the
phoma.

incident, but more commonly it occurs in

Other wart-like lesions ai·e benign
the owner's absence. The animal hesitates
exophytic proliferations of squan1ous
to eat or diink, drools, and resents handling
epithelium. They are clinically indistinguishof its mouth or face. If tissue destruction is able from virus-induced papillomas but are
marked, ulcerative or gangrenous stomatitis generally slow growing and solitary. They can develop, with secondary bacterial
most commonly remain benign, and surgical
infections. If recent contact with a corrosive removal is curative.

alkaline chemical has occurred, the mouth
should be flushed with mild solutions of

ORAL TUMORS
vinegar or citrus juice; if the chemical was
acidic, a solution of sodium bicarbonate
should be used. Copious flushing of the

Benign Oral Tumors
mouth with water helps remove some of the

Peripheral odontogenic fibromas (previchemical substances. More commonly, the ously called fibromatous epulis or ossifying
animal is seen too long after the exposw-e
epulis) are the most co nun on benign oral
for neutralization to be effective. The hair
twnors. These firm masses involve the
should be clipped and/or �ashed if it is
gingival tissue acljacent to a tooth. They
suspected to be a continued source of a
affect dogs of ai1y age but are most common
chemical that caused the caustic mucosa!

in dogs >6 yr old. Some develop centers of
lesions.

ossification, visible as distinct alveolar bone

Animals that have inflamed oral mucosa
proliferation extending into the soft-tissue
without tissue defects require no specific
mass. They are generally solitary, although
suppmtive treatinent other than a soft or
multiple lesions may be present. The tumors
liquid diet W1til the lesion has healed. If
do not metastasize but may become quite
tissue damage is extensive, treatinent
extensive. They arise from the periodontal
includes lavage with dilute chlorhexidine
ligament of the affected tooth, and complete
solution and conservative tissue debridesurgical removal must include tissues up to ment. The risk of secondaiy infection
and including the periodontal ligainent. This
should be minimized with systemic
usually necessitates conservative resection
ai1tibiotic therapy for several days.

of the neoplastic lesion, exti·action of the
affected tootl1 or teeth, ai1d curettage of the

PAPILLOMAS
extraction sites (ie, removal of remaining
periodontal ligament). Complete excision is

Papillomas are benign growtl1s caused by
curative.

the canine papillomavirus (seep 952). The

The canine acanthomatous ameloblasoral mucosa and commissures of the lip are toma (previously called acanthomatous
most frequently involved, but the growths
epulis) is much more locally aggressive,

(usually multiple but sometimes single)

quickly invading the local tissues including
can involve the palate and oropharynx.

bone. This twnor does not metastasize, but

Papillomas are most conunon in yotmg dogs because of its locally aggressive nature, and appear suddenly, with rapid growth and
surgical excision should include a 1-cm
spread. Signs are seen when the growths
margin of clinically normal tissue (including

DISEASES OF THE MOUTH IN SMALL ANIMALS

367
bony margins) to prevent recun-ence. Radia

Diagnosis: Because of the varied behavior
tion therapy may mininlize disfigurement
of oral and maxillofacial tumors, presurgiwhen treating large twnors. Adequate cal characterization is valuable to plan the
surgical removal is curative.

extent of the required surgery. Biopsy is the
most reliable method to obtain a definitive

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Malignant Oral Tumors
diagnosis; however, a cytologic diagnosis

In dogs, the three most common malignant
from impression smears of a fine-needle
oral twnors are malignant melanoma,
aspirate is possible in many cases.

squamous cell carcinoma, and fibrosar

Therefore, a histologic diagnosis is typically
coma. The incidence of malignant oral
necessary to plan for accurate treatment.

tumors is higher in dogs >8 yr old.

Malignant melanomas are variable in

Squamous cell carcinomas are by far the
appearance, pigmented or nonpigmented,
most common malignant oral neoplasms in
and should be considered in Ll1e diagnosis of
cats; they commonly involve the gingiva
any oral twnor. Squamous cell carcinomas
and tongue and are locally highly invasive.

commonly involve the gingiva or palatine

Fibrosarcomas are the next most common.

tonsils (unilateral), and lymphosarcoma

In cats, these twnors are locally invasive
should be a differential diagnosis for
and, if extensive, carry a poor prognosis.

bilaterally enlarged tonsils. Lymph nodes
and the lw1gs should be evaluated for

Clinical Findings: Signs of malignant oral
regional and distant metastasis.

tumors vary depending on the location and
extent of the neoplasm. Halitosis, reluc

Treatment: Malignant melanomas are
tance to eat, and hypersalivation are
highly invasive and metastasize readily;
corru11on. If the orophary.nx is involved
consequently, tl1e prognosis is guarded to
dysphagia may be present. The tumors'

poor. Surgical resection can extend survival
frequently ulcerate and bleed. The face may
and may be curative, particularly witl1
become swollen as the tumor enlarges and
masses in the rostral areas of the mouth.

invades sun-ou.nding tissue. Regional lymph

However, local recurrence is common.

nodes often become swollen before oral and lmmunotherapy is available as an acljtmct pharyngeal tu.n1ors are seen.

treatment to radical surgery and chemotl1erapy. Nontonsillar squan10us cell carcinomas are locally invasive witl1 a low
rate of metastasis, and the prognosis in
dogs is good with aggressive and complete
surgical resection, radiation therapy, or
both. Tonsillar squamous cell carcinomas
are aggressive and have a poor prognosi£.

Fibrosarcomas have a guarded prognosis
because of tl1eir locally aggressive nature.

RecwTence of twnor growth after resection
is conunon.

In cats, squamous cell carcinoma has a
poor prognosis unless tl1e entire twnor
can be removed, and longterm survival is
usually seen only if diagnosed and treated
early.

SALIVARY DISORDERS

Ptyalism

Ptyalism is drooling of saliva This may be
caused by hypersialosis (hypersecretion of
saliva) or pseudoptyalism (secondary to
confonnational abnonnalities or swallowing disorders in anin1als producing a nonnal quantity of saliva). Both are discussed
togetl1er as ptyali.sm.

Ptyali.sm may result from tl1e following:

1) drugs, toxins, or poisons, eg, organophos

Oral mast cell tumor in a dog. Courtesy of Dr. Ben phates; 2) local irritation or inflanunation

Colmery/11.

associated witl1 stomatitis, glossitis

368

DISEASES OF THE MOUTH IN SMALL ANIMALS

( especially in cats), oral foreign bodies,
mass, frequently in the cervical region. A
neoplasms, i.ajuries, or other mucosa!

ranula may not be seen until it is traumadefects; 3) infectious diseases ( eg, rabies), tized and bleeds. A pharyngeal mucocele
the neivous fonn of distemper, or other
car1 obstruct tl1e airways and result in

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convulsive disorders; 4) motion sickness, fear,
moderate to severe respiratory disti·ess.

neivousness, or excitement; 5) reluctance to

A zygomatic mucocele may result in
swallow or interference with swallowing
exophthalmos or enophthalrnos, depending

(from initation of the esophagus, esophageal
on its size and location.

obstruction by regional pathology, or from

A mucocele is detectable as a soft,
stimulation of GI receptors caused by
fluctuant, painless mass that must be
gastlitis or enteritis); 6) sub lingual lesions
differentiated from abscesses, tumors, and

( eg, linear foreign body, tumor); 7) tonsillitis;
other retention cysts of the neck. Pain or

8) administi-ation of meclicine (particularly
fever may be present if tl1e mucocele
in cats); 9) confonnational defects ( eg,
becomes infected. A salivary mucocele
heavy, pendulous lower lips); 10) metabolic
usually can be diagnosed by palpation and
disorders ( eg, hepatic encephalopathy
aspiration of Light brown or blood-tinged,

[ especially in cats]) or uremia; 11) abscess
viscous saliva. Usually, careful palpation
or other inflanunatmy blockage or condition
with the ani.n1al in dorsal recun1bency can
of the salivary gland.

detenni.ne tl1e affected side; if not,

The possibility of rabies should be
sialography may be helpful.

eliminated before oral examination. The

Surgery is recommended to remove the
underlying cause, local or systemic, should
damaged salivary gland and duct. Periodic
be detenni.ned and treated. Acute moist
drainage if surgery is not an option is usually
dermatitis of the lips and face may develop
only a temporary measure and has the
if the skin is not kept as dry as possible.

potential for iatrogenic infection. Mar·supi

Cleansing with a dilute chlorhexidine
alization is often ineffective. Gland-duct
solution or benzoyl peroxide may be
removal has been recommended for
helpful.

curative treatment of salivary mucoceles.

Salivary Mucocele

Salivary Fistula

A salivary mucocele ( or sialocele) is an

Salivary fistula is an unconunon problem
accun1ulation of saliva in the submucosal or
tl1at can result from trauma to tl1e mandibusubcutaneous tissues after dan1age to the lar, zygomati.c, or sublingual salivary glands.

salivary duct or gland capsule. This is the

Wounds of the paroti.d gland are most likely
most conunon salivary gland disorder of
to develop a fistula Parotid duct i.ajury may
dogs. Although any of the salivar-y glar1ds
be the result of a traumatic wound ( eg, bite
may be affected, the ducts of the subli.ngual
wound), abscess drainage, or prior surgery
arid mandibular glands are involved most
in the area with iatrogenic rupture. The
conunonly. Saliva often collects in the
constant flow of saliva prevents healing,
intennandibu.lar or cranial cervical ar·ea
and a fistula develops.

(cervical mucocele). It can also col.lect fn

History of i.ajury in the gland area,
the sub lingual tissues on the floor of the
location of the fistula, and nature of the
mouth (sublingual mucocele or ranula). A
discharge ar·e characteristic. A salivary
less common site is in the pharyngeal wall
fistula must be differentiated from a

(pharyngeal mucocele) or lower eyelid
draining sinus ( due to a penetrating foreign

(zygomatic mucocele).

body or endodontic disease of a mandibular

The cause may be traumatic or inflan1matooth) in the neck or from sinuses arising tory blockage or rupture of the duct or
from congenital defects. Surgical ligation of
capsule (with damage of par·enchyrna) of
the duct usually results in resolution, but
the sub lingual, mandibular, parotid, or
excision of the associated gland may also
zygomatic salivary gland. Usually, the exact
be necessary.

cause is not detemlined, but a developmental predisposition in dogs has been Salivary Gland Tumors
suggested.

Salivary gland tumors are rare in dogs and

Signs depend on the site of saliva
cats, although cats are affected twice as
accumulation. In the acute phase of saliva
frequently as dogs. Most are seen in dogs
accumulation, the inflanm1atory response
and cats> 10 yr old. There is no clear breed
results in the area being swollen and
or sex predilection, although Pooclles and
painful. Frequently, this stage is not seen by

Spaniel breeds may be predisposed. Most
the owner, and the first noticed sign may be
salivary gland ttunors are malignant, with
a nonpainful, slowly enlarging, fluctuant
carcinomas and adenocarcinomas the most

DISEASES OF THE MOUTH IN SMALL ANIMALS

369
common. Local inftltration and metastasis
apparent pain. The dog may retch and gulp,
to regional lymph nodes and lungs are
which is elicited by mild excitement and
conunon, as is local recurrence after
occurs several times a day. There may be
surgical excision. Radiotherapy, with or
weight loss, reluctance to exercise,

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without surgery, offers the best prognosis.

snorting, lip smacking, nasal discharge,
hypersalivation, inappetence, and

Sialadenitis
depression. Histologically, there are no

Sialadenitis, or inflanunation of the salivary
obvious abnormalities. Excessive saliva
gland, is rarely a clinical problem in dogs
production may be associated with
and cats. However, it is frequently an
increased parasympathetic activity or
incidental finding on histopathology at
changes in sympathetic innervation.

necropsy.

Phenobarbital administration usually

The cause may be trauma from penetratresults in lasting in1provement, providing ing wounds or systemic infection affecting
support for a neurogenic pathogenesis.

the salivary gland or surrounding tissue.

Sialadenitis as a component of systemic

Necrotizing Sialometaplasia
disease has been rep01ted with rabies,
in Dogs
distemper, and the paramyxovirus that

Necrotizing sialornetaplasia has also been
causes mumps in people.

termed salivary gland necrosis or infarction.

Signs include fever, depression, and

There is squamous metaplasia of the
painful, swollen salivary glands. Rupture of
salivary gland ducts and lobules, with
an abscessed gland discharges pus into tl1e
ischemic necrosis of the salivary gland
surrounding tissue or the mouth. Rupture
lobules. It can be seen in dogs (mostly small
ttu·ough the skin may cause a salivary fistula
breeds such as terriers) of all ages, most
to form. Swelling of the parotid gland is
often 3---8 yr old. Affected dogs usually are
most prominent below the ear, swelling of
depressed, nauseous, and anorectic.

the mandibular gland at the angle of the jaw,

Clinical signs include salivary gland
and swelling of the zygomatic gland just
enlargement tl1at may be painful on
caudal to the eye. Zygomatic gland
palpation, weight loss, ptyalism, retching,
involvement may result in retrobulbar swellgagging, regurgitation, and vomiting. Other ing, divergent strabismus of the affected
signs include persistent swallowing, lip
eye, exophthalmos, excess tearing, and
smacking, coughing, tachypnea, dyspnea,
reluctance to open the mouth or eat.

and abdominal respiration. Exan1ination

Abscesses of the zygomatic and parotid
of samples from fine-needle aspirates or
glands are acutely painful; the animal may
biopsies often reveal no abnormalities.

hold its head rigidly and resent any

Diagnosis requires excluding other causes
manipulation involving the head or neck.

of enlargement. Surgical removal of the

Radiographs and laboratory tests are
affected salivary gland produces n1inin1al
usually not helpful, although evaluation of
if any improvement. Pain management,
fluid in an abscess can lead to a diagnosis.

antibiotics (based on culture and sensitivity

Histopathology of salivary gland tissue can
of the fluid/tissue aspirate), NSAIDs,
reveal acute or chronic inflammatory
antiinflarnmatory doses of glucocorticoids,
changes or necrosis.

and control of internal parasites have

Mild sialadenitis requires no treatment,
resulted in favorable responses in some
and recovery is usually rapid and complete.

cases. Phenobarbital administration

A developed abscess should be drained

(1-2 mg/kg, PO, bid, or higher initial doses)

through the overlying skin or, if involving
has resulted in dramatic in1provement in
the zygomatic gland, behind the last upper
several cases, providing more support for a
molar on the affected side. Systemic
neurogenic pathogenesis ..

antibiotics should be administered.

Lack of resolution or recurrence
necessitates cytology of aspirated material,

Xerostomia
biopsy, or surgical removal of the affected

Hypoptyalism is a decreased secretion
gland.

of saliva that can result in a dry mouth

(xerostomia). It can cause significant

Sialadenosis in Dogs
discomfort and difficulty during eating.

It is uncommon in dogs and cats but is very

Sialadenosis is a non-inflanunatory,
common in people who have undergone
non-neoplastic, usually bilateral enlargeradiation therapy for tun10rs of the head ment of the mandibular salivary glands,
and neck that resulted in collateral radiation
associated with regional swelling ( dependir\jury to the salivary glands. As radiation ent on location) and exophthalmos but no
treatment is used more conunonly in

370

DISEASES OF THE MOUTH IN SMALL ANIMALS
veterinary medicine, xerostomia may
salivary gland. Detennination and treatment
become more frequent in anin1als.

of the underlying cause is of prin1ary

Decreased salivary secretion may also result importance. Physiologically balanced from use of certain drugs (eg, atropine),
mouthwashes relieve the discomfort that

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extreme dehydration, pyrexia, or anestheresults from xerostomia. Fluids should be sia It is seen in some dogs with keratoconadministered if the anin1al is dehydrated.

jtmctivitis sicca and can be in1mune-medi

Immunosuppressive therapy is indicated if
ated. Occasionally, it is due to disease of the
inuntme-mediated disease is suspected.

DISEASES OF THE ESOPHAGUS

IN SMALL ANIMALS

CRICOPHARYNGEAL ACHALASIA
neuromuscular disorders are less likely
to respond to surgery but may respond

Cricopharyngeal achalasia is characterized
to treatment of the underlying disease.

by inadequate relaxation of the ciicopharyn

Aspiration pneumonia should be treated
geal muscle, which leads to a relative
aggressively if present.

inability to swallow food or liquids. It is seen
p1imarily as a congenital defect but is
occasionally seen in adult dogs. The cause is DILATATION OF THE ESOPHAGUS
generally unknown, but in adult anin1als it

(Megaesophagus)

may be associated with acquired neuromuscular disorders. Repeated attempts to Megaesophagus may be due to a congenital
swallow are followed by gagging and
defect or may be an adult-onset, acquired
regurgitation. Aspiration pneumonia is
disorder. Congenital defects that may result
a common complication. An accurate
in megaesophagus include vascular ring
diagnosis requires fluoroscopic evaluation
anomalies, esophageal diverticula,
of swallowing after oral administration of
congenital myasthenia gravis, and an
contrast mate1ial alone and mixed with
idiopathic form. (See also CONGENITAL AND
food. Abnormal function (lack of relaxa

INHERITED ANOMALIES OF THE ESOPHAGUS, p 166.) tion) of the cricopharyngeal muscle results

Adult-onset megaesophagus may be
in retention of barium in the posterior
primary (idiopathic) or secondary to
pharynx.

systemic disease. Secondary megaesopha

Treatment consists of cricopharyngeal
gus may be due to myasthenia gravis,
myotomy or cricopharyngeal and thyrophasystemic lupus erythematosus, polymyosiryngeal myectomy, which usually results tis, hypoadrenocorticism, heavy metal
in nonnal swallowing in1mediately after

(lead) toxicity, thalliun1 toxicity, glycogen
surgery. The success rate of surgery
storage disease, neurotoxin-induced
approaches 65%. Dogs with acquired
cholinesterase inhibition, dysautonomia,

CNS disorders including neoplasia, and
possibly hypothyroidism. Esophageal
dilatation may also develop cranial to an
esophageal lesion such as an esophageal
stJ.icture, foreign body, neoplasia, or
exti·aesophageal compression.

The cardinal sign is regurgitation. A
puppy with congenital megaesophagus
characteristically begins to regurgitate at
weaning when it starts to eat solid food.

Affected pups are generally unthrifty and
smaller than their littennates. Pressure
applied to the abdomen may cause
ballooning of the esophagus at the thoracic

Esophagram demonstrating dilatation of the
inlet. Aspiration pneumonia is a complicaesopha_gus (megaesophagus), lateral tion with associated signs of cough, fever,
projection. Courtesy of Dr. Ronald Green.

and sometin1es nasal discharge. Adult

DISEASES OF THE ESOPHAGUS IN SMALL ANIMALS

371
animals that develop megaesophagus also

ESOPHAGEAL STRICTURES
start to regurgitate and ultimately lose
weight. Respiratory signs may predominate,

(Esophageal stenosis)

with little or no apparent regurgitation.

Esophageal st1icture is a pathologic

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Thoracic radiographs reveal air, fluid, or
narrowing of the lw11en that may develop
food in a dilated esophagus. The esophagus
after anesthesia, trauma ( eg, foreign body),
is usually uniformly dilated. A large ventral
ingestion of caustic substances, exposure
deviation may be present cranial to the
to certain drugs (such as doxycycline or
heart. Megaesophagus secondary to a
clindamycin), esophagitis, gastroesophastricture, foreign body, neoplasia, or geal reflux, or tumor invasion. Most
vascular ring anomaly is visualized as a
stiictures develop in the thoracic portion of
dilatation of the esophagus cranial to the
the esophagus. Esophageal tumors a.re rare,
defect only. Strictures, foreign bodies, or
but esophageal sarcomas may be associated
vascular ring anomalies can be excluded
withSpirocerca lupi infection (seep 412), with an esophagram and/or esophagoscopy.

requiring consideration in areas where this

In adult dogs, associated diseases ( eg,
parasite is prevalent. Esophageal compresmyasthenia gravis) should be excluded or, sion by vascular 1ing anomalies or
if found, treated. Surgery is indicated for a
extramural tumors may mimic the signs
vascular ring anomaly. Surgery may not
of st1i ctures.

successfully resolve the clinical signs in

Clinical signs are sinillar to those
longstanding cases with severe esophageal
associated with foreign boclies and include
dilatation cranial to the anomaly. Medical
regurgitation, ptyalism, dysphagia., and pain.

management is indicated for congenital or

An esophagran1 under fluoroscopy is the
acquired idiopathic megaesophagus.

preferred tool for diagnosis, because it

Congenital megaesophagus may resolve as
a!Iows visualization of the number, length,
the animal ages, usually by 6 mo of age. The
location, and severity of strictures.

consistency of the diet that best prevents

Esophagoscopy can also be diagnostic but
regurgitation varies from dog to dog; a soft
does not allow visualization beyond the
gruel works for some, while dry food works
stricture wuess esophageal ba!Ioon dilation
for others. Another possibility is canned
is also performed.

food formed into a meatbalI shape.

Treatment with balloon catheter dilation

Frequent, sma!I meals work best for most
has been the most successful. Bougienage
dogs. Feeding from an elevated position
is another, less available, technique. It
with the forelimbs higher than the
theoretically ca.uses more shear stress on
hindlimbs and holding that position for at
the esophagus but has not been shown to
least 10---15 min after eating a!Iows gravity
have a significantly different compliq1tion
to assist food passage into the stomach.

rate than balloon dilation. Some cases can

Neither surgery nor medications improve
require multiple dilation procedures.

esophageal function. Ultimately, most

Esophageal stents have been used in
animals succumb to aspiration pneun10nia.

strictures that have been refractory to
dilation procedures. However, this method

ESOPHAGEAL DYSMOTILITY
has been limited by a high rate of
complications, including stent migra-

Young dogs may have a disorder of
tion, stent shortening, stent breakage,
esophageal dysmotility without overt
recurrence of stricture, infection,
megaesophagus. Clinical signs can be
megaesophagus, overgrowth of tissue
similar to those of megaesophagus,
into the stent, ptyalism, apparent nausea,
although some dogs without clinical signs
gagging, vomiting, regurgitation, and
have abnormal motility during an esophatracheal-esophageal fistula. Surgical gram. In one study in more than half the
resection of a single stricture is another
cases, the condition improved or resolved
option; however, it is less successful.

with age. Terrier breeds were overrepre

These treatments are likely to induce some
sented. Cats can also have esophageal
degree of esophagi tis, which must be
dysfunction, which can be idiopathic;
treated to decrease the chance of stricture
congenital; or secondary to myasthenia
reformation. The use of corticosteroids,
gravis, mediastinal masses, vascular ring
either systemically or intralesionally, to
anomalies, dysautonomia, and strictures.

help prevent stricture reformation is

Many cats in1prove with medical managecontroversial. No data exist regarding ment such as the use of sucralfate,
the success of this adjunct therapy for

H2-blockers, and metoclopramide.

esophageal strictures in dogs and cats,

372

DISEASES OF THE ESOPHAGUS IN SMALL ANIMALS
but intralesional use has been helpful
esophagus. The administration of corticoin reducing recurrence in people.

steroids to prevent esophageal stricture
fom1ation is controversial. Broad-spectrum

ESOPHAGITIS
antibiotics should be used for concurrent

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aspiration pneumonia and may be useful in

Inflammation of the esophagus is usually
severe esophagitis as an attempt to prevent
caused by foreign bodies, gastroesophageal
bacte1ial invasion and infection.

reflux, and occasionally certain drugs ( eg,
doxycycline). Gastroesophageal reflux is

ESOPHAGEAL FOREIGN BODIES
usually associated with anesthesia, drugs
that decrease lower esophageal sphincter

Esophageal foreign bodies are more
tone (eg, atropine, acepromazine), and
common in dogs than cats. Bones are the
acute or chronic vomiting. Other causes of
most conm1on foreign body, but needles,
esophagitis include ingestion of an irritating fishhooks, wood, rawhide, and dental chew or caustic substance, neoplasia, and
treats may also become lodged in the

Spirocerca lupi infection (seep 412).

esophagus. Objects usually lodge in the

Feeding tubes that traverse the gastroareas of the esophagus with the least esophageal junction may result in gastrodistensibility: the thoracic inlet, over the esophageal reflux. Calicivirus in cats may
heart base, or the caudal esophagus just
also cause esophagitis.

cranial to the diaphragm. Occasionally, an

Regurgitation is the classic sign of
object may lodge in other locations such
esophagitis; others include ptyalism,
as U1e upper esophageal sphincter.

repeated swallowing attempts, pain,

Ptyalisrn, gagging, dysphagia, regurgitadepression, anorexia, dysphagia, and tion, and repeated attempts to swallow are
extension of the head and neck. Mild
signs of an esophageal foreign body. Often,
esophagitis may have no associated
the owner may see the aninlal eat the
clinical signs.

foreign body. The signs depend on the

Endoscopy is the diagnostic tool of
location of the foreign body and on the
choice. It allows visualization of any
degree and duration of obstruction. A
associated problems (eg, foreign body) and
partial obstruction may allow fluids but not
direct assessment of esophageal damage.

food to pass. With a chronic obstruction,

Plain radiographs are of little or no benefit
anorexia, weight loss, and lethargy are
in the diagnosis of esophagitis. An
common.

esophagram under fluoroscopy demon

Perforation of the cervical esophagus
strates any associated esophageal motility
may result in local abscessation or
defects secondary to the esophagi tis and
subcutaneous emphysema; perforation
may demonstrate esophageal wall defects
of the thoracic esophagus may result in
if severe.

pleuritis, mediastinitis, pyothora.x,

Mild esophagitis may require no
pnewnothora.x, bronchoesophageal fistula
treatment. If clinical signs are present, medifomiation, or fatal aortic esophageal fistula cal therapy should be instituted. Esuphagiformation. Esophagitis, mucosal laceration, tis secondary to gastroesophageal reflux
esophageal strictme, and esophageal
is treated by decreasing gastlic acidity,
diverticulwn formation are also potential
increasing lower esophageal sphincter tone, complications. Esophageal stlicture increasing the rate of gastric emptying, and
fonnation is the most conm1on complicaproviding pain control. In most cases, tion associated with an esophageal foreign

Hz-receptor antagonists ( eg, ranitidine,
body. Aspiration pneun1onia may also be
famotidine) are sufficient to decrease
seen secondary to the regmgitation.

gastric acid production; however, in severe

Many esophageal foreign bodies are
cases of esophagitis, a proton pump
radiopaque and can be seen on plain
inhibitor ( eg, omeprazole) is preferred.

radiographs. A contrast esophagram or

Cisapride and metoclopramide increase
esophagoscopy is often required to identify
lower esophageal tone and the rate of
radiolucent foreign bodies. If a perforation
gastlic emptying. Cisapride is more potent
is suspected, an iodinated contrast rnediun1
than metoclopramide. A sucralfate slurry
should be used instead of bariWTI suspenmay also be administered orally for sions. Esophagoscopy pennits evaluation of
esophageal cytoprotection. Soft food, low in both the foreign body and the esophageal fat and fiber, should be fed in small, frequent wall and often allows therapeutic inte1venmeals. Systemic analgesics may be used for tion.

pain relief.

Esophageal foreign bodies, once

If esophagitis is severe, a gastrostomy
diagnosed, should be removed immediately.

tube may be used to completely rest the

Most often, a foreign body can be removed

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

373
per os with a flexible endoscope and
produced, which then contracts, pulling the
forceps. A rigid endoscope can also be used
esophageal wall outward. This diverticulum
if a flexible scope is not available, but care
involves all layers of the esophagus.

must be taken when manipulating the scope

Small diverticula may be subclinical.

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in the esophagus to prevent lacerations or

Large diverticula allow food to become
perforations. If the foreign body is smooth,
trapped in the pouch, leading to postprana Foley catheter can be inserted distal to the dial dyspnea, regurgitation, and anorexia.

foreign body, inflated, then removed orally,

Survey radiographs may show the
bringing the foreign body with it. A large
diverticulun1 if it is full of ingesta or air, but
endotracheal tube can be placed over the
contrast radiographs are best to demonendoscope to remove sharp foreign bodies strate the pouch. Endoscopy will also allow such as fish hooks, which can be drawn up
visualization and can identify ulceration and
into the endotracheal tube and removed
scarring.

without dan1aging the esophagus on the

Small diverticula may be treated with a
way out. If a foreign body cannot be
bland, soft diet fed with the aninlal in an
removed per os, it may be pushed into the
upright position. Large diverticula require
stomach where it can either be digested ( eg,
surgical excision and reconstruction of the
bones), passed, or removed via a gastrotesophageal wall. The prognosis after omy. Surgery is indicated if a perforation
surgery is fair to good.

has occurred or the foreign body cannot be
removed via endoscopy; in one study, the

BRONCHOESOPHAGEAL
recovery rate was 93% after surgery.

However, there is potential for stlicture

FISTULA
fom1ation and complications secondary

Bronchoesophageal fistulas are rarely seen
to the poor wound-healing ability of the
in dogs and cats. They most commonly
esophagus. Esophagitis, if present, should
develop secondary to foreign body
be treated appropriately (see above).

penetration of the esophagus. Fistulas may
develop between the esophagus and any

ESOPHAGEAL DIVERTICULA
part of the respiratory tree. A congenital
form has been described, and Cairn Terriers

Diverticula are pouch-like dilatations of the
may be predisposed. The most common
esophageal wall and may be congenital or
clinical sign is coughing after eating or
acquired. They are rare in dogs and cats.

drinking. Regurgitation may also be seen,

Acquired diverticula are of two types:

and anorexia, fever, and lethargy may be
pulsion or traction. Pulsion diverticula are
related to pneumonia.

caused by increased intra1UI11inal pressure

Survey radiographs may reveal a radioor deep esophageal i.nflanm1ation, which can paque foreign body and pneumonia. Contrast lead to mucosal herniation. Predisposing
esophagrarns will show the communication
conditions include esophagitis, esophageal
between the esophagus and airways. Use of a
stiicture, foreign bodies, vascular ring
small an10unt ofbariun1 is reconm1endedanomalies, megaesophagus, and hiatal iodinated contrast agents are hyperosmolar
hernia. This type of diverticulum involves
and can cause pulmonary edema
the esophageal epithelium and connective

Surgical correction consisting of a ltmg
tissue. Traction diverticula result from
lobectomy and repair of the defect in the
inflammation in the chest cavity in close
esophagus is required. The prognosis after
proximity to the esophagus. Fibrous tissue is surgery is good.

DISEASES OF THE STOMACH AND

INTESTINES IN SMALL ANIMALS

CANINE PARVOVIRUS
acute, irtfectious GI illness in young dogs.

Although its exact origin is unknown, it
is believed to have arisen from feline

Etiology and Pathophysiology:

pa.nleukopenia virus or a related parvovirus

Canine parvovirus (CPV) is a highly conof nondomestic animals. It is a nonenvetagious and relatively common cause of loped, single-stranded DNA virus, resistant

374

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
to many common detergents and disinfectby an increased systemic demand for ants, as well as to changes in temperature
leukocytes. Infection in utero or in pups
and pH. Infectious CPV can persist indoors

<8 wk old or born to unvaccinated dams
at room temperature for at least 2 mo;
without naturally occurring antibodies can

VetBooks.ir
outdoors, if protected from sunlight and
result in myocardial infection, necrosis, and
desiccation, it can persist for many months
myocarditis. Myocarditis, presenting as
and possibly years. In North America,
acute cardiopulmonary failure or delayed,
clinical disease is largely attributed to
progressive cardiac failure, can be seen with

CPV-2b; however, infection with a newer
or without signs of enteritis. However,
and equally virulent strain, CPV-2c, is

CPV-2 myocarditis is infrequent, because
increasingly common, having been
most bitches have CPV antibodies from
identified in at least 15 states. To date, no
irnmUllization or natural exposure.

association has been identified between

CPV strain and severity of clinical disease.

Clinical Findings: Clinical signs of

Young (6 wk to 6 mo), unvaccinated or
parvoviral enteritis generally develop
incompletely vaccinated dogs are most
within 5-7 days of infection but can range
susceptible. Rottweilers, Dobern1an
from 2-14 days. Initial clinical signs may be

Pinschers, American Pit Bull Terriers,
nonspecific (eg, lethargy, anorexia, fever)

English Springer Spaniels, and German
with progression to vomiting and hemor

Shepherds have been described to be at
rhagic small-bowel diarrhea within 24-48
increased risk of disease. Assunling sufficient Irr. Physical examination findings can colostrum ingestion, puppies born to a dam
include depression, fever, dehydration, and
with CPV antibodies are protected from
intestinal loops that are dilated and fluid
infection for the first few weeks of life;
filled. Abdominal pain wanants further
however, susceptibility to infection increases
investigation to exclude the potential
as maternally acquired antibody wanes.

complication of intussusception. Severely

Stress ( eg, from weaning, overcrowding,
affected animals may present collapsed
malnutrition, etc), concwTent intestinal
with prolonged capillary refill time, poor
parasitism, or enteric pathogen infection
pulse quality, tachycardia, and hypother

( eg, Clostridium spp, Campylobacter spp, mia-signs potentially consistent with

Salmonella spp, Giardia spp, coronavirus) sepUc shock. Although CPV-associated
have been associated with more severe
leukoencephalomalacia has been reported,
clinical illness. Among dogs >6 mo old, intact

CNS signs are more commonly attributable
male dogs are more likely than intact female
to hypoglycemia, sepsis, or acid-base and
dogs to develop CPV enteritis.

electrolyte abnormalities. Inapparent or

Virus is shed in the feces of infected dogs
subclinical infection is common.

within 4-5 days of exposure (often-before
clinical signs develop), throughout tl1e

Lesions: Gross necropsy lesions can
pe1iod of illness, and for -10 days after
include a thickened and discolored
clinical recovery. Infection is acquired
intestinal wall; watery, mucoid, or
tlrrough direct oral or nasal contact with •
hemorrhagic intestinal contents; edema
virus-containing feces or indirectly tlrrough
and congestion of abdominal and thoracic
contact with virus-contaminated fomites
lymph nodes; thymic atrophy; and, in the

(eg, environment, personnel, equipment).

case of CPV myocarditis, pale streaks in

Viral replication occurs initially in the
the myocardium. Histologically, inte1?tinal
lymphoid tissue of the oropharynx, with
lesions are characterized by multifocal
systemic illness resulting for subsequent
necrosis of the crypt epithelium, loss of
hematogenous dissemination. CPV
crypt architecture, and villous blunting
preferentially infects and destroys rapidly
and sloughing. Depletion of lymphoid
dividing cells of the small-intestinal crypt
tissue and cortical lymphocytes (Peyer's
epitheliU111, lymphopoietic tissue, and bone
patches, peripheral lymph nodes,
manow. Destruction of the intestinal crypt
mesenteric lymph nodes, thymus, spleen)

epithelium results in epithelial necrosis,
and bone marrow hypoplasia are also seen.

villous atrophy, impaired absorptive

Pulmonary edema, alveolitis, and bacterial
capacity, and disrupted gut banier function,
colonization of the lungs and liver may be
with the potential for bacterial translocation seen in dogs that died of complicating and bacteremia.

acute respiratory distress syndrome,

Lymphopenia and neutropenia develop
systemic inflammatory response synsecondary to destruction of hematopoietic drome, endotoxemia, or septicemia.

progenitor cells in the bone manow and
lymphopoietic tissues (eg, thymus, lymph

Diagnosis: CPV enteritis should be
nodes, etc) and are further exacerbated
suspected in any young, unvaccinated, or

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

375
incompletely vaccinated dog with relevant essential for effective treatment. Dogs must clinical signs, especially those living in or
be monitored for development of hypokanewly acquired from a shelter or breeding lemia and hypoglycemia. If electrolytes and
kennel. During the course of the illness,
serum blood glucose concentration cannot

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most dogs develop a moderate to severe
be routinely monitored, empi1ical
leukopenia characterized by lymphopenia
supplementation of IV fluids with potasand neutropenia. Leukopenia, lymphopesium (potassiwn chloride 20-40 mEq/1) nia, and the absence of a band neutrophil
and dextrose (2.5%--5%) is appropriate.

response within 24 hr of starting treat

If GI protein loss is severe ( albumin
ment has been associated with a poor

<20 g/L, total protein < 40 g/L, evidence of
prognosis. Prerenal azotemia, hypoalbuperipheral edema, ascites, pleural effusion, minemia (GI protein loss), hyponatremia,
etc), colloid therapy should be considered.

hypokalemia, hypochloremia, and

Nonprotein colloids ( eg, pentastarch,
hypoglycemia ( due to inadequate
hetastarch) can be administered in boluses
glycogen stores in young puppies and/or

(5 ml/kg, maximum of20 ml/kg) throughsepsis, potentially a poor prognostic out at least 15 min. The remainder of the
indicator), and increased liver enzyme
maximal dosage of20 ml/kg can be
activities may be noted on the serum
administered as a constant-rate infusion
biochemical profile. Commercial ELISAs
throughout 24 hr, and the volume of
for detection of antigen in feces are widely crystalloids administered decreased by available and have good to excellent

40o/o-6()0A,. Alternatively, transfusion of fresh
sensitivity and specificity, even for the
frozen plasma may partially replace serum
more recently evolved CPV-2c strain. All
albumin while providing serum protease
animals with relevant clinical signs should inhibitors to counter the systemic be immediately tested, so appropriate
inflammatory response. There is no
isolation procedures can be initiated.

evidence to support the use of serwn

Most clinically ill dogs shed large
from dogs recovered from CPV-enteritis
quantities of virus in the feces. However,

( convalescent or hyperimmune serum)

false-negative results can be seen early in
as a means of passive inununization.

the course of the disease (before peak

Antibiotics are indicated because of the
viral shedding), because of the dilutional
risk of bacterial translocation across the
effect of large volume diarrhea, or after
disrupted intestinal epithelium and the
the rapid decline in viral shedding that
likelihood of concurrent neutropenia. A
tends to occur within 10-12 days of
i3-lactan1 antibiotic ( eg, ampicillin or
infection. False- positive results can be
cefazolin [22 mg/kg, IV, tid]) will provide
seen within 4-10 days of vaccination with
appropriate gram-positive and anaerobic
modified-live CPV vaccine. Alternative
coverage. For severe clinical signs and/or
ways to detect CPV antigen in feces
marked neutropenia, additional gran1-
include PCR testing, electron microscopy,
negative coverage ( eg, enrofloxacin
and virus isolation. Serodiagnosis of CPV

(5 mg/kg/day, IM or IV] or gentamicin
infection requires demonstration of a

[6 mg/kg/day, IV]) is indicated. Anlinoglyco4-fold increase in serum IgG titer side antibiotics must not be administered
throughout a 14-day period or detection of
until dehydration has been corrected and

IgM antibodies in the absence of recent
fluid therapy established. Enrofloxacin has

(within 4 wk) vaccination.

been associated with articular cartilage
damage in rapidly growing dogs 2-8 mo old

Treatment and Prognosis: The main
and should be discontinued if joint pain or
goals of treatment for CPV enteritis include
swelling develops. Second- or third-generarestoration of fluid, electrolyte, and tion cephalosporins ( eg, cefoxitin,
metabolic abnormalities and prevention
ceftazidirne, cefovecin, others) can also
of secondary bacterial infection. In the
be considered for their relatively wide
absence of significant vomiting, oral
spectrum of activity against gram-positive
electrolyte solutions can be offered.

and gram-negative bacteria.

Administration SC of an isotonic balanced

Antiemetic therapy is indicated if
electrolyte solution may be sufficient to
vomiting is protracted, perpetuates
correct mild fluid deficits ( < 5%) but is
dehydration and electrolyte abnormalities,
insufficient for dogs with moderate to
or limits oral administration of medications
severe dehydration. Most dogs will benefit
and nutritional support. o:-Adrenergic
from IV fluid therapy with a balanced
antagonists ( eg, prochlorperazine,
electrolyte solution. Correcting dehydra0.1--0.5 mg/kg, SC, tid) can worsen tion, replacing ongoing fluid losses, and
hypotension in hypovolemic animals,
providing maintenance fluid needs are
whereas pro kinetic agents ( eg, metoclopra-

376

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
mide, 0.3 mg/kg, PO or SC, tid, or
protein, and feline interferon-w have not

1-2 mg/kg/day as a constant-rate infusion)

been shown to be beneficial.

may increase the risk of intussusception;

Intussusception, bacterial colonization of
use of either agent should be restricted

IV catheters, thrombosis, urinary tract infec

VetBooks.ir
to dogs that are rehydrated and being
tion, septicemia, endotoxemia, acute
appropriately monitored. In dogs with CPV
respiratory distress syndrome, and sudden
enteritis, maropitant (1 mg/kg/day, IV) and
death are potential complications of CPV
ondansetron (0.5 mg/kg, IV, tid) appear to
enteritis. Most puppies that survive the first
be equally effective at controlling vomiting,

3-4 clays of illness make a full recovery,
although maropitant may be associated
usually witllin 1 wk. With approp1iate
with an improved ability to maintain body
supportive care, 68"Ar-92% of clogs with CPV
weight during illness. Vomiting may persist
enteritis will survive. Dogs that recover
despite antiemetic administration.

develop longterm, possibly lifelong

Antidiarrheals are not recommended,
irnm unity.

because retention of intestinal contents
within a compromised gut increases the risk
of bacterial translocation and systemic

Prevention and Control: To limit
complications. A successful protocol for
environmental contanlination and spread
outpatient treatment of dogs with
to other susceptible animals, dogs with
parvoviral enteritits, consisting of
confinned or suspected CPV enteritis must
maropitant (1 mg/kg/day, SC), cefovecin
be handled with strict isolation procedures

(8 mg/kg, SC, every 14 days), and SC

( eg, isolation housing, gowning and gloving
crystalloid fluids (tid), has been described.

of personnel, frequent and thorough

Previous anecdotal recommendations for
cleaning, footbaths, etc). All surfaces
nuttitional management of CPV enteritis
should be cleaned of gross organic matter
included withholding food and water until
and then disinfected with a solution of
cessation of vomiting. However, evidence
dilute bleach ( 1:30) or a peroxygen,
suggests early enteral nutrition is associated potassiun1 peroxyn10nosulfate, or with earlier clinical improvement, weight
accelerated hydrogen peroxide disinfectant.

gain, and improved gut barrier function. For

The same solutions may be used as
anorectic dogs, placement of a nasoesophafootbaths to disinfect footwear.

geal or nasogastric tube for continual

To prevent and control CPV, vaccination
feeding of a prepared liquid diet ( eg,
with a modified-live vaccine is recom

Clinicare®, or dilute, blended canned diet)

mended at 6-8, 10-12, and 14-16 wk of age,
should be instituted within 12 hr of hospital

· followed by a booster adnlinistered 1 yr
admission. Once vomiting has subsided for
later and then every 3 yr. Because of

12-24 hr, gradual reintroduction of water
potential damage by CPV to myocardial or
and a bland, low-fat, easily digestible
cerebellar cells, inactivated rather than
commercial or homemade ( eg, boiled
modified-live vaccines are indicated in
chicken or low-fat cottage cheese and rice)

pregnant dogs or colostrum-deprived
diet is recommended. Partial or total
puppies vaccinated before 6-8 wk of age.

parenteral nutrition is reserved for dogs

It has been suggested that the presence of
with anorexia >3 days that cannot tolerate
maternally acquired CPV antibodies may
enteral feeding.

interfere with the effectiveness of vaccina

Oseltamivir is an antiviral agent, usually
tion in puppies <8--10 wk old. However,
used to treat influenza virus infections in
current modified-live CPV vaccines are
people. In a single published study of
sufficiently immunogenic to protect puppies
naturally occurring CPV enteritis in dogs,
from infection in the presence of low levels
treattnent with oseltanlivir (2 mg/kg, PO, bid of interfering maternal antibody, and for 5 days) did not decrease duration of
vaccination of 4-wk-old puppies with a high
hospitalization, clinical disease severity, or
antigen titer vaccine results in seroconvermortality. However, treated dogs did not sion and may decrease the window of
experience weight loss or a decrease in
susceptibility to infection. CmTent vaccine

WBC count, as were observed in tmtreated
products protect sinlilarly well against
control dogs. The potential for induction of

CPV-2 as against otl1er strains of the virus.

drug resistance to human or avian influenza

As described above, CPV can remain
viruses has led some to question the
viable in the environment for an extended
appropriateness of oseltamivir administraperiod. In a kennel, shelter, or hospital tion to animals. Other adjunctive treattnents situation, cages and equipment should be such as recombinant human granulocyte
cleaned, disinfected, and dried twice before
colony-stin1ulating factor, recombinant
reuse. The same concepts can be applied to
bactericidal/pern1eability-increasing
a home situation. Removal of contanlinated

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

377
organic material is important in outdoor
only of the bowel but also of the liver,
situations where complete disinfection is
spleen, mesenteric lymph nodes, kidney,
not practical. Disinfectants can be applied
adrenal glands, and heart.

outdoors with spray hoses, but disinfection

Granulomatous colitis (GC) is a rare,

VetBooks.ir
will be less effective than when applied to
breed-specific inflammatory bowel ilisease
clean, indoor surfaces. In a home situation,
of young Boxer dogs. It is seen as a
only fully vaccinated puppies ( at 6, 8, and 12
segmental, thickened, partially obstructed
wk) or fully vaccinated adult dogs should be
segment of bowel (ileum and colon most
introduced into the home of a dog recently
commonly), characterized by the presence
iliagnosed with CPV enteritis. Booster
of macrophages and other inflammatory
vaccination of in-contact healthy dogs that
cells within the lamina propria These
are up-to-date on parvovirus vaccination is
macrophages are not pe1iodic acid-schiff
reasonable but potentially unnecessary given positive. Because of the histologic the extended duration of immunity to CPV.

characteristics, it is important to exclude
inflammation secondary to fungal disease,

COLITIS
intestinal parasites, feline infectious
peritonitis, and foreign material. Treatment

The colon helps maintain fluid and
remains controversial. Although surgery
electrolyte balance and absorb nutrients; it was previously recommended because GC
is also the major site of fecal storage until
was refractory to medical treatment and
expulsion and provides an environment for associated with high mortality rates, recent microorganisms. Disruptions to normal
research using culture-independent
colonic function lead to changes in both
molecular analysis has shown a correlation
absorption and motility; clinically, this
between GC and Escherichia coli invasion
often manifests as large-bowel diarrhea.

witlli.n colonic mucosa] macrophages.

Approximately one-third of dogs with a

Current treatment recommendations for GC
history of chronic diarrhea have colitis.

require antimicrobials effective against E

Chronic colitis is defined as inflammation
coli and that penetrate intracellularly, such of the colon that is present for 2'2 wk.

as enrofloxacin.

Inflammation of the colon reduces the
amount of water and electrolytes absorbed Etiology and Pathophysiology: and changes colonic motility by suppress

Inflammation of the colon may be acute or
ing the normal colonic contractions that
chronic. In most cases, the inciting factors
mix and knead and by stimulating giant
are unknown. Bacterial, parasitic, fungal,
migrating contractions (ie, more powerful
traumatic, uremic, and allergic causes have
contractions that rapidly propel intestinal
been postulated. lnflammation may be the
contents). Colitis has been classified into
result of a defect in mucosal imrnunoregula<
four forms: lymphocytic-plasmacytic,
tion. After initial mucosa] injury, submueosinophilic, neutrophilic, and granulomacosal lymphocytes and macrophages tous. Lymphocytic-plasmacytic is the most
become exposed to luminal antigens and
common form in both dogs and cats. Most
subsequently trigger inflammation.An
dogs are middle-aged, and there is no sex
exaggerated reaction to dietary or bacterial
predilection. There may be an association
factors within the lumen of the bowel,
between colitis and perianal fistula,
genetic predisposition, psychologic
especially in German Shepherds. Cats with
pathology affecting the neurologic or
chronic colitis tend to be middle-aged and
vascular supply to the colon, or sequelae
more commonly purebred. Typically, there
of previous infectious or parasitic ilisease
is an increased number of lymphocytes
have also been implicated.

and plasmocytes in the lamina propria

In acute colitis, there is mucosal

(less frequently in the submucosa and
infiltration with neutrophils and epithelial
muscularis).

disruption and ulceration. Chronic colitis

Eosinophilic colitis is characterized by
is most often characterized by mucosal
an increased number of eosinophils in the
infiltration of plasma cells and lymphocytes,
lamina propria It is less common than
fibrosis, and sometimes ulceration. Goblet
lymphocytic-plasmacytic colitis, the
cells are stimulated to secrete excessive
animals tend to be younger, and it is
quantities of mucus. Absorption of water
more difficult to treat. Infectious agents,
and electrolytes is impaired, and motility is
parasites, and food allergies may be inciting
reduced. Inflammation ilisrupts intracellufactors, but none has been proved. The CBC
lar tight junctions and reduces the
may reveal eosinophilia. Hypereosinophilic
transmucosal electrical potential differsyndrome in cats is a variant of eosinophilic ence, interrupting the ability of the colon
enteritis with eosinophilic involvement not
to absorb soilium. Normal segmentation is

378

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
inhibited; giant migrating muscular
agents ( eg, H capsulatum ). Cases of
contractions proceed down the length of the suspected clostridial colitis (>5 endospores colon and rapidly expel luminal contents.

per field) should be confim1ed by identifying

The inflan1ed bowel is more sensitive to

Clostridium perftingens enterotoxin A

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stretch, and contents entering the colon
and B in feces using a commercially
stimulate strong migrating muscular
available ELISA after a fecal bacte1ial
contractions, an urge to defecate, and
cultw'e is performed.

abdominal discomfort.

A dietary trial is recon1111ended before

Fructooligosaccharides (FOSs) enhance
pursuing more advanced diagnostics. If
colonic microflora and assist in the
clinical signs persist, a CBC, biochemical
prevention and treatment of colonic
profile, and urinalysis should be perfom1ed
disease. These complex carbohydrates are
to exclude other diseases; however, in most
not digested in the small intestine. They are
cases of chronic colitis, the results are
fe1mented by specific colonic bacteria that
nonnal. For cats, feline leukemia virus/feline
use them as an energy source. FOSs
immunodeficiency virus testing is also
promote the growth of beneficial bacteria
recon1111ended as well as a thyrnid level if
and inhibit growth of potentially harmful
age appropriate. Routine abdonlinal
bacteria They are responsible for the
radiographs are also usually no1111al.

production of sho1t-chain fatty acids

Contrast radiographs may occasionally

(SCFAs).

demonstrate intralunlinal na.iTowing, which

SCFAs (acetate, propionate, butyrate) are could indicate an infiltrative disease process.

an important energy source essential for

Ultrasonography allows the visualization of
maintenance of non11al mucosa! health.

colonic mucosa, localized lesions, and the

They help maintain intestinal motility and
size and echogenicity of lymph nodes.

an1eliorate intestinal inflan1111ation.

Colonoscopy is indicated to visually

Alteration of fatty acids leads to mucosa!

inspect the mucosa! surface of the colon
atrophy and injwy.

and to obtain biopsy specin1ens. Prepa.i<1-
tion of the colon is essential to avoid
missing small or subtle lesions because

Clinical Findings: The most common
of residual fecal mate1ial on the mucosa!

clinical sign of chronic colitis is large-
sw-face. Food should be witilheld for
bowel diarrhea, characterized by mucus,

24-48 hr before the procedure, followed
hematochezia, tenesmus, and occasionally
by a combination of enemas and an oral
pain when defecating. There is often an
colonic lavage solution. Several agents can
increased urgency and frequency of
be used to clean the bowel, such as sodiw11
defecation, with decreased fecal volume per picosulfate and bisacodyl. Multiple san1ples bowel movement. Weight loss and vomiting
from tl1e cecUlll and ascending, transverse,
can occur but are uncommon; they are seen
and descending colon should be obtained,
more often when small intestine is involved.

regardless of gross morphologic appear

Clinical signs may wax and wane. Initially,
ance. Because of poor correlation between
the clinical signs may be sporadic, but
gross appearance and histopathologic
progression usually occurs. Physical
results, results should be interpreted in light
exanlination is Ulll·emarkable in most cases.

of tl1e physical exanlination and history.

A thorough rectal exanlination may reveal

A normal mucosa! biopsy or one with
rectal polyps or malignant neoplasms that
evidence of a hyperplastic mucosa, in
can mimic signs of chronic colitis.

coajunction with clinical signs supportive
of large-intestinal diaJThea, is compatible

Diagnosis: The initial approach should
with initable bowel syndrome. Peripheral
include a complete history and physical
eosinophilia is invariably present in cats
examination, including rectal palpation and
with hypereosinophilic syndrome.

evaluation of feces. Fecal smears for

Giardia and fungal elements (Hisloplasma Treatment and Control: If possible, capsulalum, Pylhium insidiosum), fecal
the inciting cause should be identified and
flotation for parasite identification
eliminated. Food should be witllheld for an

('Jhchuris vulpis in dogs, 1'ritrichomonas initial 24-48 hr in animals with acute colitis
foetus in cats), and culture for bacteria
in an effort to "rest" tl1e bowel.

( Campylobacter, Salmonella, Clos t1id

Because shedding of ova by whipworms
ium) are suggested in cases of chronic
is intermittent, therapeutic deworming ( eg,
colitis. Rectal cytology is an important tool
fenbendazole 50 mg/kg/day, for 3 days,
to exclude other causes of large-bowel
repeated in 3 wk and again in 3 mo if there is
diarrhea. It can reveal inflan1111atory cells,
a positive response) should be done even if
neoplastic cells, and certain infectious
results of fecal exa.imnations are negative.

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

379

Supplementing the diet with fiber ( 1-6 tsp
dietaiy management or another drug.

of psylliwn hydrophilic mucilloid or 1-4

Although metronidazole is well tolerated
tbsp of coarse wheat bran/feeding)

in both dogs and cats, adverse effects can
improves diarrhea in many animals. Dietary
occur (mostly neurologic, eg, nystagmus,

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fiber reduces free fecal water, prolongs
ataxia, vestibular signs, seizures), either
lwninal transit time (increasing the opportuwith chronic tl1erapy or at high dosages.

nity to absorb water), absorbs toxins,

However, neurotoxicoses should be
increases fecal bulk and stretches the
reversible within 5-7 days after treatment
colonic smooth muscle, and in1proves
is discontinued.

contractility. However, the addition of fiber

Tylosin, a macrolide antibiotic used
alone rarely results in complete resolution
primarily in food animals, is useful in
of clinical signs of large-intestinal diarrhea
chronic enteropathies, because it interferes
in dogs, and beneficial effects may take as
with bacterial adhesion to the mucosa and
long as 6 wk to become evident. Over time,
has some antibacterial and inmmnomoduthe fiber dose can be reduced or elinlinated lating effects. It targets mainly facultative
in some dogs and a standard dog food
and obligate anaerobic gram-positive
substituted without causing a return of the
bacteria and some gran1-negative bacteria.

diarrhea.

However, E coli and Salmonella are Novel protein diets have effectively
resistant to tylosin. Tylosin is well tolerated
controlled clinical signs of colitis in both
in both dogs ru1d cats with minimal effects.

dogs and cats. The protein source used

Clinical signs resolve more rapidly when
should be one to which the anin1al has not
ru1ti-inflanunatory medication is given,
previously been exposed. In one study,
along witl1 the change in diet. Sulfasalazine,
clinical signs associated with lymphocyticprednisone or prednisolone, and azathioplasmacytic colitis resolved in all dogs prine are used most commonly. Sulfasalawithin -2 wk after feeding a low-residue, zine is often used to treat lymphocyticdigestible, hypoallergenic diet (1 part plasmacytic colitis in dogs (12.5 mg/kg, qid
low-fat cottage cheese and 2 parts boiled
for 14 days, then 12.5 mg/kg, bid for 28
white rice). Thereafter, most dogs were
days). Longterm use is discouraged,
maintained without recurrence of clinical
because it predisposes to keratoconjunctivisigns on conunercially available prescriptis sicca. Sulfasalazine is a prostaglandin tion diets they had not been previously fed.

synthetase inllibitor and has antileukotriene

CwTently, a number of commercially
activity. It consists of mesalamine linked to
available diets contain rice with mutton
sulfapyridine in an azochemical bond; this
or lamb, venison, or rabbit.

linkage prevents absorption in the upper GI

Hydrolyzed diets have also been effective
tract and allows most of tl1e drugs to be
in treatment of colitis. These specialized
transported to the large intestine. Once
diets disrupt the protein structure
it has reached tl1e large intestine, it is metabsufficiently to remove any allergens and olized by cecal and colonic bacteria,
allergenic epitopes and, therefore, prevent
releasing both components. Mesalarnine
inunune recognition.

acts locally to reduce colonic mucosal

If feeding a high-fiber or novel protein
inflanm1ation. Sulfapyridine is believed to
diet is not beneficial, a commercial,
be systemically absorbed and therefore
low-residue diet may be tried, especially
does not have any local therapeutic effect in
one that contains FOSs.

colitis but is blamed for the adverse effects

Cats with lymphocytic-plasmacytic colitis of sulfasalazine. Salicylates are metabolized may respond to dietary management alone
in the liver by hepatic enzymatic processes

( eg, lan1b and rice, horserneat, or a
involving glucuronyl transferase. Because
commercially available diet). In one study,
cats are deficient in this enzymatic pathway,
cats were initially treated with dietary fiber
salicylates have prolonged half-lives in this
or with dietary fiber and pharmacologic
species. Therefore, sulfasalazine is not used
intervention (prednisone, tylosin, or
as the drug of choice in colitis in cats
sulfasalazine). Most cats were eventually
because of the 1isk of salicylate toxicity.

maintained on high-fiber diets or a highly

Glucocorticoids, in combination with
digestible diet.

dietary management and metronidazole, are

Metronidazole is considered one of the
the treatment of choice for chronic colitis in
primary pharmacologic agents in chronic
cats. They may be introduced into the
colitis in cats. Its therapeutic effects include therapeutic plan for dogs when the antiprotozoal and antimicrobial activity and
previously discussed therapies are not
inhibition of some aspects of cell-mediated
successful or if the 5-arninosalicylates result
immunity. It is not usually used as a sole
in adverse effects. !f used in combination
agent but rather in combination with either
with sulfasalazine or metronidazole,

380

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
prednisone may be given at a reduced
complete resolution without relapses
dosage. Prednisone should be started at
appears poor. Most cases of inflammatory

2 mg/kg/day, PO; for 2 wk after clinical signs bowel disease are not curable, and some resolve, the dosage should be reduced by
form of treatment will likely be necessary

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25% every 2-4 wk, which can usually
longterm. For some anin1als, especially cats,
maintain remission.

longterm management of chronic colitis

Cats usually tolerate glucocorticoids very may be possible with diet alone.

well; adverse effects are common in dogs

Most cases of idiopathic lymphocyticand include polyuria, polydipsia, polyphaplasmacytic colitis respond to appropriate gia, GI bleeding, increased susceptibility to
dietary and medical changes. Stricture
infection, iatrogenic hyperadrenocorticism,
formation and extensive fibrosis warrant
and pituitary-adrenocortical suppression.

a more guarded prognosis. Eosinophilic

Budesonide is a nonhalogenated
colitis in dogs responds favorably to
glucocorticoid used in treatment of Crohn's
controlled diets and glucocorticoid therapy.

disease in people. Budesonide undergoes

In cats, the prognosis is more guarded, and
significant first-pass metabolism in the liver; more aggressive treatment with inununotheoretically, this should reduce the adverse suppressive agents is required. Hypereoeffects often seen with traditional sinophilic syndrome is a progressive, fatal
glucocorticoids, because little of the active
disease that has no effective treatment in
drug is systemically available. In one study
anin1als.

of 10 healthy dogs, the pituitary-adrenocor

Histiocytic colitis of Boxers carries a
tical axis was suppressed, but no other
grave prognosis unless treatment is staited
adverse effects were seen.

early in the course of the disease. The

Immunosuppressive drugs are mostly
in1munoproliferative enteropathy of
used in combination with glucocorticoids

Baser\jis also carries a poor prognosis; most
when the response is not satisfactory with
dogs die within 2 yr of diagnosis, although
the latter alone. The most commonly used
some have been reported to live as long as 5
are azathioprine and chlorambucil in dogs
yr. Sinillarly, the prognosis for the diarrheal
and cats. Azathioprine (2 mg/kg/day, and
syndrome reported in Lundehunds is also
then tapered), alone or in combination with
poor.

prednisone, has been used to control
clinical signs associated with lymphocytic

CONSTIPATION AND
plasmacytic colitis. Azathioprine may be
considered in cases that are poorly

OBSTIPATION
responsive to prednisone or to prednisone

Constipation is the infrequent or difficult
with sulfasalazine. The serious adverse
evacuation of feces, which are typically dry
effects of azathioprine in cats (myelosupand hard. Constipation is a common clinical pression and hepatotoxicity) limit its use
problem in small animals. In most instances,
in feline colitis. Instead, chlorambucil
fue problem is easily rectified; however, in

(0.1--0.2 mg/kg or 1 mg/cat, daily initially
more debilitated anin1als, accompanying
until clinical signs are markedly improved,
clinical signs can be severe. As feces remain
which may require 4-8 wk) is used in cats in
in fue colon longer, they become drier,
combination with prednisone if needed.

harder, and more difficult to pass. Obstipa

Cyclosporine has been effective in
tion is intractable constipation charactersteroid-refractory cases of colitis, but it has ized by an inability to evacuate the mass of
not been evaluated in cats. Adverse effects
dry, hard feces; impaction extending from
include GI disturbances, gingival disease,
fue rectum to the ileocolic valve can result.

and alopecia.

Megacolon is a pathologic condition of

Some anin1als also require short-term use
hypomotility and dilation of fue large
of motility modifiers until inflan1mation is
intestine that results in constipation and
controlled. Loperamide (0.1--0.2 mg/kg,
obstipation.

bid-qid) stimulates segmental activity and
slows passage of fecal contents. It also

Etiology and Pathophysiology: Peridecreases colonic secretion, enhances salt staltic waves are responsible for fue aboral
and water absorption, and increases anal
movement of fecal matetial in tl1e colon.

sphincter tone. It is contraindicated in cases

Giant migrating waves fuat occur intennitof infectious colitis ( eg, caused by Salmo
tently furoughout the day move this matter
nella, Campylobacter, or Clostridium).

farther and more rapidly. These waves
constitute the "gastrocolic reflex" and are Prognosis: The short-term prognosis for
common after ingestion of a meal. A
chronic colitis is good for both dogs and
reduction or loss of these waves may
cats. However, longtem1 prognosis for
contribute to constipation. Sinillarly, an

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

381
increase in segmentation wave activity may
the cause, as will a history of ingestion of
predispose to constipation. However, diet
indigestible matelial that may increase fecal
is the most imp01tant local factor affecting
bulk or cause pain that can terminate the
colonic function.

defecation reflex. Other historical factors

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Chronic constipation may be due to
that may be relevant include recent surgery,
intralurninal, extraluminal, or intrinsic
previous pelvic trauma, and possibly

(ie, neuromuscular) factors. Intraluminal
radiation therapy. A complete neurologic
obstruction is most common and is due to
exai1li.nation with special emphasis on
the inability to pass poorly digested, often
caudal spinal cord function should be
furn matter ( eg, hair, bones, litter) mixed
perfonned to identify neurologic causes of
with fecal material. The lack of water intake constipation, eg, spinal cord injury, pelvic or the reluctance to defecate on a regular
nerve trauma, and Manx sacral spinal cord
basis because of environmental ( eg, stress)

defonnity.

or behavioral ( eg, dirty litter box) factors or

Abdonli.nal palpation and rectal
painful anorectal disease predisposes to
exanli.nation, including evaluation of the
formation of hard, dry feces. Intralurninal
prostate and sublun1bar lymph nodes,
tumors may also impede the passage of
should be perfonned to detem1ine the
feces. Extraluminal obstruction may be
presence of perineal hernia, foreign
caused by compression of the colon or
material, pain, or masses. Plain abdominal
rectum from a naiTowed pelvic inlet after
radiographs may help establish the inciting
suboptimal healing of pelvic fractures or
factor(s) of fecal retention and give some
from enlarged sublwnbar lymph nodes or
indication of what the feces contain ( eg,
prostate gland. Colonic stricture due to
bones). A barium enema, ultrasonography,
trauma or neoplasia should also be
or colonoscopy may facilitate demonstraconsidered. Finally, some animals (usually tion of obstructive lesions or predisposing
cats) with chronic constipation or
causes of chronic constipation.

obstipation may have megacolon, likely

A CBC, biochemical profile including a
caused by a lesion of the neuromuscular
serum T level, urinalysis, and detailed
bed of the colon. The etiology of megacolon

4
neurologic exanli.nation should be
often remains undiagnosed. Other diseases
completed in cases of chronic or recurling
that affect neuromuscular control of the
constipation.

colon and rectun1 include hypothyroidism,
dysautonomia, and lesions of the spinal

Treatment and Control: Affected
cord ( eg, Manx sacral spinal cord deforanimals should be adequately hydrated.

mity) or pelvic nerves. Hypokalemia and

Mild constipation can often be treated by
hypercalcemia also adversely affect
dietary adjustment consisting of avoidance
muscular control. Some drugs ( eg, opioids,
of dietary indiscretion, ready access to
diuretics, antihistan1ines, anticholinergic
water and high-fiber diets, and use of
agents, sucralfate, alunli.num hydroxide,
suppository laxatives. Continued or
potassium bromide, and calcium charmellongterm use of laxatives should be blocking agents) promote constipation via
discouraged wuess absolutely necessary
differing mechanisms.

to avoid constipation.

A number of pediatric rectal supposito

Clinical Findings: The classic clinical
lies are available for management of mild
signs of constipation are tenesrnus and the
constipation. They include dioctyl sodium
passage of furn, dry feces. If the passage of
sulfosuccinate (DSS; emollient laxative),
feces is hindered by an enlarged prostate
glycerin (lubricant laxative), and bisacodyl
or sublumbar lymph nodes, the feces may

(stimulant laxative). The use of suppositoappeai· thin or "ribbon-like" in appearance.

lies requires a compliant pet and a willing

Abdominal palpation and rectal exaininaowner. Suppositories car:i be used alone or tion can confirm the presence of large
in coajunction with oral laxative therapy.

volumes of retained fecal matter. Passed

Mild to moderate or recurrent episodes of
feces are often putrid. Some animals are
constipation may require adtninistration of
quite ill and also have lethargy, depression,
enemas or manual extraction of impacted
anorexia, vonli.ting ( especially cats), and
feces, or both. Types of enemas include
abdominal discomfort.

warm tap water (5-10 ml/kg), warm
isotonic saline (5-10 rnllkg) with or without

Diagnosis: A history of dietary indiscrea mild soap to act as an irritant, DSS (5-10
tion and physical evidence of retained feces
mllcat), mineral oil (5-10 mUcat), or
confirms the diagnosis. Detailed informalactulose (5-10 mllcat). Enema solutions tion regarding the duration of constipation
should be administered slowly with a 10--12
and influencing factors may help determine

French rubber catheter or feeding tube.

382

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

Phosphate-containing enemas must be

0.5 ml/kg, PO, bid-tid), magnesium salts ( eg,
avoided in cats.

magnesium citrate, magnesium hydroxide,

If enemas are W1Successful, manual
magnesiwn sulfate), and the polyethylene
extraction of impacted feces may be
glycols. Lactulose is the most effective

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needed. After adequate rehydration, the
agent of this group. The organic acids
anin1al should be anesthetized with an
produced from lactulose fem1entation
enclotracheal tube in place to prevent
stimulate colonic fluid secretion and
aspiration in case the colonic manipulation
propulsive motility. Lactulose osmotically
induces vomiting. Complete removal of all
retains water in the bowel to soften fecal
feces may require 2-3 attempts over as
material. It is also useful in management
many days. Concurrent fluid and electrolyte
of hepatic encephalopathy because it
abnormalities should also be corrected.

decreases lwninal pH, reduces bacterial

Laxatives are classified as bulk-fomling,
production of anm1onia, and favors
lub1ica.nt, emollient, osmotic, or stimulant
formation of anunonium ions that are
types. Most act on fluid transport mechapoorly absorbed. Stimulant laxative nisms and colonic motor stimulation. They
products ( eg, bisacodyl [ cats and small
should be avoided in the presence of
dogs: 5 mg; meditm1-sized dogs: 10 mg; large
dehydration. Bulk-fomling laxatives are
dogs: 15-20 mg]) increase the propulsive
added to the diet. These products are
activity of the bowel. They are contraindidietary fiber supplements of poorly cated in the presence of bowel obstruction.

digestible polysaccharides and celluloses

Colonic prokinetic agents (eg, cisapride)

derived principally from cereal grains,
enhance colonic propulsive motility
wheat bran, and psyllium. They absorb
by activating colonic smooth muscle
water, soften feces, add bulk, stretch the

5-hydroxytryptamine-2A receptors in a
colonic smooth muscle, and inlprove
number of species. Anecdotal experience
contractility. Many constipated cats
suggest that cisapride (0.1-0.5 mg/kg, PO,
respond to dietary supplementation with
bicl-ticl) effectively stimulates colonic
one of these products. Dietary fiber is
propulsive motility in cats with mild to
preferable because it is well tolerated, more
moderate idiopathic constipation. Higher
effective, and more physiologic than other
dosages ( up to 1 mg/kg) may be necessary
laxatives. Commercial fiber-supplemented
in cats with moderate to severe constipadiets are available, or the pet owner may tion. No significant adverse effects have
add psyllium (1-4 tsp/meal), wheat bran
been reported in cats treated with cisapride

(1-2 tbsp/meal), or pumpkin (1-4 tbsp/
at dosages of 0.1-1 mg/kg, PO, bid-tid). Cats
meal) to canned food. Animals should
with longstanding obstipation and
be well hydrated before starting fiber
megacolon are not likely to improve with
supplementation to nlininlize the potential
cisapride therapy.

for impaction of fiber in the constipated

Ranitidine and nizatidine, Hrreceptor
colon.

antagonists, are reported to stimulate

Emollient laxatives are anionic detercolonic motility by inhibiting acetylchogents that increase the miscibility of water linesterase. They stin1ulate motility by
and lipids in digesta, thereby enhancing
increasing the an10W1t of acetylcholine
lipid absorption and impairing water
available to bind smooth muscle muscarinic
absorption. DSS and disoctyl calcium
cholinergic receptors.

sulfosuccinate are emollient laxatives

To prevent recwTence, high-fiber diets
available in oral and enema form. Docusate
are recommended, ready access to water
sodium ( cats: 50-mg capsule/clay; dogs:

should be maintained, and frequent

50-mg capsule, 1-4/day) and docusate
opportunities to defecate allowed.

calciwn (cats: 50-mg capsule, 1-2/day; dogs:

Cases of sinlple intralwninal obstruction

50-mg capsule, 2-3/day) are other exan1ples
due to dietary indiscretion respond well to
of emollient laxatives.

bowel evacuation and prevention of this

Mineral oil and white petroleum are
habit in the future. Chronic constipation

I ubricant laxatives that impede colonic
unresponsive to medical management ( eg,
water absorption and pemlit greater ease of
some cats with megacolon) may respond to
fecal passage. These effects are moderate,
subtotal or total colectomy. Colectomy with
and lubricant laxatives are beneficial only in
colocolonic, ileocolonic, or jejW1ocolonic
mild cases of constipation. Mineral oil use
anastomosis may be performed depending
should be limited to rectal adnlinistration
on the extent of the disease. Mild to
because of the risk of aspiration pneumonia
moderate diarrhea may occasionally persist
with oral administration.

for weeks to months after surge1y, and some

Hyperosmotic laxatives consist of poorly
cats may have recurrent constipation.

absorbed polysaccharides ( eg, lactulose,

Pelvic osteotomy without colectomy has

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

383
been recommended for cats with pelvic
common clinical sign of infection in kittens,
fracture malunion and hypertrophic
upper respiratory tract signs have also been
megacolon of <6 mo duration. In such
reported.

cases, pathologic hypertrophy may be

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reversible with early pelvic osteotomy.

Diagnosis: The viral DNA can be detected

Subtotal colectomy is recommended in cats
in feces by reverse transc1iptase PCR
with pelvic fractures if hypertrophy and

(RT-PCR). Because chronic carriers of
clinical signs have persisted for >6 mo. In

FECV tend to be asymptomatic, FECV can
these cases, hypertrophy is followed by
be assumed to be the cause of the diarrhea
muscular degeneration and pathologic
only after other causes ( eg, infectious,
dilatation, and pelvic osteotomy alone will
dietary, inflanm1atory bowel disease,
not provide relief from obstipation.

neoplasia, etc) have been excluded. The
clinical utility of serologic evaluation for

FELINE ENTERIC CORONAVIRUS
antibodies to FECV is questionable. Positive
coronavirus antibody titers are detected in

Feline enteric coronavirus (FECV) is an
up to 400Ai of pet cats and in up to 900,1, of cats
enveloped, single-stranded RNA virus that is in catteries or multicat households. Positive highly prevalent in domestic cat populations FECV antibody titers are indicative only of worldwide. Infection is often subclinical or
exposure to the virus and are not suggestive
characterized by transient, mild GI illness in
of the etiology of the current disease, do not
kittens. Mutation of FECV to a biotype
co1Telate with the risk of developing FIP,
capable of infection and replication within
and are not diagnostic for FIP. Histologic
macrophages is responsible for developlesions suggestive ofFECV enteritis include ment of feline infectious peritonitis (FIP), a
intestinal villous fusion, atrophy, or
highly fatal, multisystemic disease (see
sloughing. Because these lesions are
p 780).

nonspecific, definitive diagnosis requires
inmmnohistochemical or inummofluores

Etiology and Pathophysiology: Fecal
cent detection of viral antigen in intestinal
shedding ofFECV begins within 1 wk of
epithelial cells.

initial infection and persists at high levels
for2-10 mo, followed by an extended

Treatment, Control, and Prevention:

period ( up to 24 mo) of lower level,

The mild, transient clinical signs are
potentially intermittent, viral shedding.

unlikely to require therapy. Treatment, if

At least 13% of infected cats shed the
required, is symptomatic and supportive
virus indefinitely.

(ie, fluid therapy, oral electrolyte solutions,

Cats become infected through ingestion
a.ntiemetics). There is no specific antiviral
or inhalation of virus-containing feces or
therapy. Death due to the FECV-associated
through contact with contaminated fomites
gastroenteritis is tmcommon.

( eg, litter boxes, mutual grooming, housing,

Control and prevention ofFECV are
personnel). FECV is relatively fragile but
usually a concern only in breeding catteries
can survive in dry environments for up to
and rescue shelters. Ingestion of virus-con7 wk. Close contact between cats ( eg, tan1inated fecal particles should be
catteries and multicat households)

prevented as much as possible. Fecal
facilitates transmission. Vertical transmiscontamination of the environn1ent can be sion from infected queens to kittens does
minimized with sufficient litter box numbers,
occur. Kittens generally do not begin to shed daily litter box cleru1ing, weekly litter box virus before 9-10 wk of age, although viral
disinfection, and clipping/cleaning fur from
shedding as early as 4 wk of age has been
the hind end of long-haired cats. FECV can
repo1ted. Soon after infection, virus may
survive indoors for up to 7 wk under dry
replicate in oropharyngeal tissue, resulting
conditions but is readily inactivated by most
in transient (hours to days) salivary
commercial disinfectru1ts.

shedding. FECV infects and replicates in

Ideally, cats should be housed in small
mature apical epithelial cells of the

(three or four cats), closed groups. The
intestinal villi, causing brush border
room, cages, bedding, and litter boxes
shortening and destruction.

should be disinfected between groups.

Although impractical in a shelter situation,

Clinical Findings: Most FECV infections
cats should be housed in groups according
are clinically inapparent or characterized by
to their antibody (in1munofluorescent
mild, self-limiting gastroenteritis. Occasionantibody test seropositive or seronegative) ally, vomiting and diarrhea can be acute and
and virus shedding (based on fecal PCR)

severe or chronic and unresponsive to
status. Seropositive cats cru1 be retested
treatment. Although diarrhea is the most
eve1y 3-6 mo ru1d moved into seronegative

384

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
groups as their antibody titer decreases. In
confom1ation, a first-degree relative with a
a rescue or shelter situation, cats should be
history of GDV, stress, aggressive or fearful
housed singly. Identification of FECV
behavior, once daily feeding, dry food, rapid
carrier cats requires nine monthly,
conswnption of food, previous splenic

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consecutive positive fecal RT-PCR tests,
disease, and increased gastric ligament
whereas identification of a cat that has
laxity.

eliminated FECV infection requires five

It is unclear whether dilation or volvulus
consecutive negative fecal RT-PCR tests.

occurs first during the development of GDV,

Seropositive cats should be mated only
although it is postulated that volvulus
to other seropositive cats, and seronegative
occurs first. Dilation of the stomach results
cats to other seronegative cats. Kittens born
from accumulation of gas and/or fluid, and
of seropositive matings or to a seropositive
volvulus prevents the normal release of
queen are protected from infection by
these contents. During volvulus, the pylorus
maternally derived immunity until -6 wk
and duodenum first migrate ventrally and
of age. Kittens weaned from seropositive
cranially. Viewed from a caudal to cranial
queens by 6 wk of age are unlikely to
direction, the stomach may rotate from 90°
acquire infection from the queen. Serologic
to 360° in a clockwise fashion about the
testing of kittens should be delayed until
distal esophagus. This rotation displaces the

10-11 wk of age, by which time seroconverpylorus to the left of midline, entrapping the sion is likely.

duodenum between the distal esophagus

New cats should be serologically tested
and the stomach. Depending on the degree
before introduction into a cattery or
of volvulus, the spleen may vary in position
breeding program. Only seronegative and
from the left caudodorsal to the right
virus-free (fecal PCR) cats should be
craniodorsal abdomen. A volvulus of> 180°
introduced into an FECV-free cattery or a
causes occlusion of the distal esophagus.

cattery attempting to elin1inate the virus.

After volvulus of the stomach, gas is

Seropositive cats are less likely to develop
trapped within this compartment and

FIP than seronegative cats when introduced intragastric pressure rises. Gastric outflow to an FECV-endemic environment.

obstruction may be caused by compression

Vaccination with an intranasal, temperaof the duodenum by the distending stomach ture-sensitive FECV mutant is not generally
against the body wall, or it may be due to the
recommended but can be considered in
presence of neoplasia, a gastric foreign
seronegative cats> 16 wk old introduced
body, or pyloric stenosis. Splenic entrapinto an FECV-endemic environment.

ment often accompanies G DV. The

Vaccination will lead to seroconversion and ·progressively distending stomach does not completely protect cats previously
compromises venous retwTL by compresexposed to FECV from developing FIP.

sion of the caudal vena cava. Sequestration
of blood in the dilated splanchnic, renal, and

GASTRIC DILATION AND
posterior muscular capillary beds results in

VOLVULUS
portal hypotension, GI tract ischemia,
hypovolemia, and systemic hypotension.

These factors combine with the Joss of fluid

(Bloat)

in the obstructed stomach and a lack of

Gastric dilation and volvulus (GDV) is an
water intake to produce signs of hypoacute, life-threatening condition that volemic shock. Dogs are at risk-of endoprimarily affects large- and giant-breed toxernia, hypoxemia, metabolic acidosis,
dogs. Immediate medical and surgical
and disseminated intravascular coagulation.

intervention is required to optimize chance
of survival.

Clinical Findings: Dogs may present
with a history of nonproductive retching,

Etiology and Pathophysiology: The
hypersalivation, and restlessness. Acute or
etiology of GDV is unknown, but several
progressive abdominal distention may be
phenotypic and environmental risk factors
noted, or the affected dog may be found
have been identified for developing GDV.

recumbent and depressed with an enlarged

Breeds at risk of GDV include the Great
abdomen.

Dane, German Shepherd, Irish Setter,

Physical examination findings include an

Gordon Setter, Weirnaraner, Saint Bernard,
enlarged or tympanic abdomen. Abdominal

Standard Poodle, and Bassett Hound. No
pain and/or splenomegaly may be apprecisex predisposition exists, and dogs appear ated on abdominal palpation. Progression
to be at increased risk with advancing age.

from gastric dilation to volvulus predis

Other reported predisposing factors include
poses to hypovolemic shock. Signs of
lean body condition, deep/narrow thoracic
shock are common and can include weak

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

385
peripheral pulses, tachycardia, prolonged

Correction of hypovolemia is the first
capillary refill time, pale mucous memtreatment priority and is achieved by rapid branes, and dyspnea. An irregular heait rate
fluid replacement with one or more large
and pulse deficits indicate the presence of
bore (16-to 18-gauge) IV catheters placed in
a cai·diac arrhythmia. Additionally, the
cranial Qugular, cephalic) veins. Shock rate

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expanding stomach may compress the

(90 mllkg/hr) fluid therapy with crystalloids
thoracic cavity and inhibit diaphragmatic
should begin immediately. Fluid therapy
movement, leading to respiratory distress.

witl1 combinations of crystalloids, colloids

(eg, hetastarch at a rate of 10-20 mUkg, IV),

Diagnosis: Suspicion of GDV is usually
or hypertonic saline ( eg, 7% hypertonic
high after considering the history, signalsaline solution with dextran 70 at a rate of rnent, ai1d clinical signs. Radiographs help

5 mUkg over 15 min) can be considered for
distinguish simple gastric dilation from
animals in severe shock, ai1d tl1c rate of

GDV. The prefen-ed radiographic views for
crystalloid fluid infusion reduced by as
identification of GDV are right lateral and
much as 40% if iliese products are used.

dorsoventral recurnbency. Ventrodorsal

These fluid rates ai·e guidelines only, and
positioning must be avoided because of the
fluid resuscitation choices must be tailored
potential for aspiration of gastric contents.

to the individual patient's needs. Flow-by

The right lateral radiograph usually
oxygen should be provided during
reveals a large, distended, gas-filled gastric
stabilization. Electrolyte and acid-base
shadow with the pylorus located dorsal and
disturbances ai·e usually corrected by
slightly cranial to the fundus. The gastric
adequate fluid therapy and gastric
shadow is frequently compartmentalized or
decompression. Because of the potential
divided by a soft-tissue "shelf' between the
risk of endotoxemia ai1d GI trai1slocation of
pylorus and fundus. This shelf, or reverse
bacteria, antibiotics ( eg, ai11picillin 22 mg/kg,

"C" sign, is created by the folding of the tid-qid, and continued for 2-3 days after
pyloric antral wall onto the fundic wall.

surgery) ai·e often given.

Splenic enlargement or malposition may be

Gastric decompression occurs
noted on radiographs. Gas within tl1e gastric concurrently with fluid resuscitation.

wall is suggestive of tissue compromise,

Initial decompression attempts should be
whereas free gas within the abdomen
made with an orogastric tube, which can
indicates gastric rupture.

be performed after sedation with fentanyl

PCV, total solids, electrolytes, blood

(2-5 mcg/kg, IV) or hydro morph one
glucose, and serum lactate levels should

(0.05-0.1 mg/kg, IV), with or without
be evaluated, and blood drawn for a CBC,
diazepain (0.25-0.5 mg/kg, IV). Agents that
serum biochemical profile, and coagulation
cause vasodilation (eg, phenothiazines)

assays. Continuous ECG and blood pressure should be avoided. A stomach tube is monitoring are reconm1ended.

measured from the incisors to the last rib

Prerenal azotemia is a common finding
and marked. The tube must not be placed
in animals with GDV and is secondary to
beyond this marking. The lubricated tube
systemic hypotension. Increased CK levels
is introduced into the mouth (often held
may be present due to striated muscle
open with a roll of tape or bandage
dai11age, and serum potassium levels may
material) while the dog is in a sitting
increase subsequent to cell membrane
position. Some resistance is typically
dainage. Serum ALT and AST levels may
encountered at the esophageal-gastric
increase secondary to hypoxic dainage.

sphincter. Gentle manipulation and

Increased lactate is a common finding and
counterclockwise movement of the tube
is secondary to systemic hypotension and
may be necessary to allow passage of the
inflanm1ation. Hyperlactatemia (>6 mmol/L)

tube into the stomach, but caution must
is associated witl1 an increased likelihood of
be exercised because it is possible to
gastric necrosis and the need for partial
perforate the esophagus with the tube.

gastric resection.

Once the tube enters the stomach, gastric
gas rapidly escapes. Successful passage

Treatment: In1mediate goals in treatment
of a stomach tube does not exclude the
of GDV include restoring circulating volume presence of volvulus. After gas and and gastric decompression. Rapid surgical
stomach contents ai·e released from the
con-ection of the volvulus follows initial
stomach via the tube, the stomach should
patient stabilization. Because duration of
be lavaged with warm water to decrease
clinical signs is one of the risk factors of
the rate of redilation with gas.

GOV-associated death, it is imperative

If an orogastric tube caimot be readily
to recognize and con-ect this condition
passed, percutaneous gastrocentesis may
immediately.

be performed to release excess gastric gas.

386

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

An area (10 cm x 10 cm) over the right
be administered and repeated twice in a
abdominal wall caudal to the last rib and

30-min period if necessary; a continuous
ventral to the transverse vertebral process

IV infusion (30-80 mcglkg/min) may be
is clipped and aseptically prepared.

indicated to control a.iThythmias. Cardiac

Percussion of the area should reveal
arrhythmias associated with GOV are often

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tympany; this helps avoid accidental
difficult to control. If the arrhythmia is
puncture of an overlying spleen. If a
poorly responsive to this therapy, procainatympanic structure is not appreciated, the mide (6--10 mg/kg, IV over 15 min) should be
left paracostal region should be assessed.

given. Life-threatening arrhythmias may

A large-bore needle or over-the-needle
respond to 200/o magnesiwn sulfate
catheter is introduced ttu·ough the skin and

(0.15--0.3 mEq/kg, or 12.5--35 mg/kg, IV
body wall into the stomach at the site of
over 15--60 min).

greatest tympany. Decompression usually

Less common postoperative complicaallows for subsequent passage of an tions can include life-threatening conditions
orogastric tube and lavage of the stomach.

such as sepsis, peritonitis, and disseminated

Surgical correction of GOV rapidly
intravascular coagulation.

follows the initial stabilization. Aseptic

Overall mortality rate associated with
preparation of the abdomen is perfom1ed

GOV is -25o/o-30%. Risk factors associated
before surgery, and a cranioventral midline
with short-tenn death from GOV include
approach is performed. Before correcting
duration of clinical signs >6 hr before
the gastric torsion, the stomach should be
exan1ination, perfom1ing splenectomy and a
decompressed with the help of an assistant
partial gastrectomy, hypotension at any time
placing an orogastric tube or via gastrocenduring hospitalization, peritonitis, sepsis, tesis intraoperatively. The stomach is then
and disseminated intravascular coagulation.

returned to its normal position, and the

Preoperative plasma lactate concentration
stomach and spleen are evaluated for
has been shown to be a good predictor of
ischemia. Any areas of ischemic gastric
gastric necrosis and a negative prognostic
wall are removed, and a splenectomy is
indicator for outcome for dogs with GOV.

perfom1ed if necessary. Extensive gastric

Prophylactic gastropexy is CWTently being
necrosis and necrosis of the gastric cardia
recommended by many veterinary surgeons
are considered poor prognostic indicators.

for breeds at risk or for dogs with relatives

The stomach is emptied of contents, and a
that have been affected by GOV. Prophylactic
gastropexy is perfom1ed to decrease risk of
gastropexy can be performed at fue time
recurrence. Several gastropexy tectuuques
of sterilization surgeries (spay/neuter).

have been described and include a simple

Minimally invasive tectuuques such as
incisional pexy, a circumcostal (belt-loop)

laparoscopic-assisted gastropexy are gaining
pexy, and a tube g:1$trotomy and pexy.

favor. Prophylactic gastropexy has not been

Pre-, intra-, and postoperative monitoring
shown to prevent development of GOV if
should include continuous ECG, intennitpetformed at the tin1e of neuter but has tent blood pressure measurement, and
been shown to help prevent recurrence if
frequent assessment of vital parameters,
perfom1ed at the time of the first GOV

PCV, total solids, electrolytes, blood
correction. However, in one study of five
glucose, and serum lactate.

large dog breeds predisposed to GOV,

Postoperative medical management
mortality was reduced (versus no gastroincludes IV fluid therapy and analgesia.

pexy) ranging from 2.2:fold (Rottweiler) to

Food should be withheld for 48 hr after

29.6-fold (Great Dane). A prospective study
surgery. Antiemetic agents (metocloprareported a median survival time of 54 7 days in mide at 0.2-0.5 mg/kg, SC, or 1-2 mg/kg/day,
dogs that undezwent gastropexy versus 188
constant-rate IV infusion; ma.ropitant at 1
days for dogs that did not. Owners of breeds
mg/kg/day, SC) may be administered in
at high risk of GOV should be educated about
cases of continued vomiting. Postoperative
the risk factors for and signs of GDV, and
cardiac arrhythmias are common, but
advised to seek inunediate veterinary care
treatment is often not indicated. Criteria to
if clinical signs are apparent. Additional
initiate antiarrhythmic therapy include
precautions include avoiding stress, feeding
signs of persistent tachycardia (>140 bpm),
multiple rather than single daily meals,
hypotension (systolic blood pressure <90
avoiding exercise immediately after feeding,
mmHg), hypoperfusion (prolonged capillary and not using elevated food dishes.

refill time, weak pulses), "R on T wave"

pattern ( a phenomenon that predisposes

GASTRITIS
to ventricular fibrillation), or multifocal
ventricular premature contractions. A bolus

Gastritis is a general term used to describe
of 2% lidocaine (2-4 mg/kg, slowly IV) can
a syndrome of acute or chronic vomiting

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

387
secondary to inflammation of the gast1ic

Treatment of acute gastritis is generally
mucosa. Irritation, infection, antigenic
symptomatic and supportive. Small
stimulation, or injury ( eg, chemical, erosion, amounts of oral fluids can be given ulceration) of the gastric mucosa stin1ulates
frequently, with the volun1e increasing as
the release of inflammatory and vasoactive
vomiting subsides. lee ( crushed or cubes)

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mediators with subsequent disruption of
can be provided as the only source of water
gastric epithelial cells, increased gastric
initially. Subcutaneous administration of an
acid secretion, and impaired gastric barrier
isotonic balanced electrolyte solution may
function. Visceral receptors sensitive to
be sufficient to coffect mild fluid deficits
gastric distention, gastric inflammation, and

( <5%). If dehydration is moderate to severe
tonicity of gastiic contents send impulses
or the clinical condition of the animal
via vagal and sympathetic nerves to the
waffants IV fluid therapy, a more extensive
vomiting center of the medulla oblongata,
diagnostic evaluation is indicated. If
thereby stimulating the vomiting reflex.

vomiting is acute, oral intake should be
discontinued for ;;:24 hr. Small amounts of

Acute Gastritis: In acute gastritis,
a bland, low-fat, easily digestible diet ( eg,
vomiting of sudden onset is presumed or
boiled Jean beef, chicken, or cottage cheese
confim1ed to be secondary to inilanunation
and rice, or a commercially available
of the gastric mucosa. Causes include
prescription diet) fed frequently can be
dietary indiscretion or intolerance ( eg,
introduced, with gradual transition to the
ingestion of novel, spoiled, or contaminated
usual diet over 3-5 days.

foods, or of foreign material), drug or toxin

Antiemetic drugs should be used to
ingestion ( eg, antibiotics, NSAIDs,
control vomiting only after an etiologic
corticosteroids, plants, chemicals),
diagnosis has been made or if vomiting is
systemic illness ( eg, pancreatitis, uremic
protracted or severe enough to cause
gastropathy, hypoadrenocorticism),
dehydration or electrolyte imbalances.

endoparasitism ( eg, Physaloplera sp [ dog], Metocloprarnide (0.3 mg/kg, PO or SC, tid,

OUulanus sp [cat]), or bacterial (eg,
or 1-2 mg/kg/day as a constant-rate

H elicobacter-associated disease) or viral
infusion) increases gastric contractions;

( eg, canine parvovirus gastroenteritis, feline
relaxes the pyloric sphincter; and increases
panleukopenia) infection. Vomiting of
gastric, duodenal, and proximaljejw1al
sudden onset is characteristic. The vomitus
peristalsis. It is contraindicated in
may contain bile, food, froth, blood (frank
confinned or suspected GI obstructions.

or digested), or evidence of an ingested

Alternative antiemetics include maropitant
substance ( eg, grass, bones, foreign

(1 mg/kg/day, SC, or 2 mg/kg/day, PO, for
material, etc). Additional clinical signs

5 days) and ondansetron (0.1-1 mg/kg, PO,
depend on the severity and frequency of
once to twice daily). Gastroprotectants
vomiting as well as on the underlying cause.

such as H,-receptor antagonists ( eg,

Diagnosis is usually based on a thorough
famotidine 0.5---1 mg/kg, PO, SC, or IV, bid)

history, clinical findings, and response to
or proton pump inhibitors ( eg, omeprazole
symptomatic treatJnent. A specific diag0.7-2 mg/kg/day, PO, or pantoprazole 1 mg/
nosis should be sought if the animal has had
kg/day, IV) may also be indicated. In dogs,
access to foreign objects or toxins, if
omeprazole may provide better gast1ic acid
clinical signs do not resolve within 2 days
suppression and better prevention of
of symptomatic therapy, if hematemesis
exercise-induced gastritis tl1an famotidine.

or melena are present, if the animal is
systemically unwell, or if abnormalities are

Chronic Gastritis: Chronic gastritis
noted on abdominal palpation. Dogs may
should be considered in animals with
signal the presence of cranial abdominal
intermittent or persistent vomiting that lasts
discomfort by adopting a "praying" posture

> 7 days and that cannot be attributed to

(hindquarters raised and chest and forelegs
dietary indiscretion or intolerance; drug,
held close to floor), which seems to provide
toxin, or foreign body ingestion; systemic
some sense of relief. A CBC, serun1
illness; endoparasitisrn; infection (bacterial
biochemical profile, and urinalysis may be
or viral); or neoplasia. The most corru11on
followed by more specific clinicopathologic
clinical sign is intermittent vomiting of fobd
testing ( eg, basal serum cortisol concentraor bile. Systemic illness, weight loss, and GI tion, adrenocorticotropic hormone [ACTH]

ulceration are infrequent and should raise
stimulation test, evaluation of vomitus for
suspicion of a more se1ious condition or
specific toxins). Diagnostic imaging,
diffuse GI inflammation ( eg, inflan1matory
including plain and/or barium contrast
bowel disease, pythiosis, etc).

abdominal radiographs and abdominal

Histologic evaluation of endoscopic or
ultrasound, may be indicated.

surgical gastric biopsies is required for

388

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
definitive diagnosis and classification of
cil 2 mg [ total dose J every 72 hr; dogs and
chronic gastritis. A CBC, serum biochemical ca.ts: cyclosporine 3---5 mg/kg/day, PO) can profile, urinalysis, total thyroid hormone
be considered.

concentration (cats), basal serum cortisol

Chronic atrophic gastritis is often
concentration possibly with an ACTH-stimchara.cte1ized by marked mononuclear cell VetBooks.ir
ulation test (to exclude canine hypoadrenoinfiltration, thinning of the gastric mucosa, corticism), and fecal evaluation for
and a.trophy of the gastric glands. A unique,
endoparasitism are indicated but are
breed-associated fmm of a.trophic gastritis
frequently unremarkable in animals with
in Norwegian Lundehw1ds has not been
chronic gastritis. Diagnostic imaging (plain
associated with Helicobacter spp infection
and/or barium contrast abdominal
but has been associated with gastric
radiographs, abdominal ultrasound) can
a.denocarcinoma.. The role, if any, of
identify foreign objects, neoplasia, pylo1ic

H elicobacter spp infection in the developstenosis, gastric antral mucosal hypertroment of a.trophic gastritis is unknown.

phy, discrete or multifocal mucosal or mural However, if H elicobacler spp organisms are abnormalities, intra-abdominal lymphadidentified in gastric biopsy specimens, enomegaly, or other intra-abdominal
treatment is indicated (seep 394).

pathology, and is indicated before gastric

Additional treatment options include
biopsy.

dietary management and inmmnosuppres

�phocytic-plasmacytic gastritis
sion as for lymphocytic-plasma.cytic and
and eosinophilic gastritis are characte1'eosinophilic gastlitis (see above); however, ized by diffuse infiltration of the gastric
data with respect to ti·ea.tment efficacy and
mucosa and lamina propria with lymphoprognosis are lacking.

cytes and plasma cells, or eosinophils,

Chronic hypertrophic gastropathy is
respectively. Similar cellular infiltrates may
characterized by diffuse or focal hypertrobe seen in the small intestine. Concomitant phy of the gastric mucosa, muscula.ris, or
lymphoid hyperplasia., mucosal a.trophy, or
both, with variable inflanm1a.tory infiltrates.

mucosal fibrosis is infrequently seen.

The lesion is often most pronounced in the

Dietary allergy or intolerance, occult
pyloric region, with resultant gastric
parasitism, or hyperimmune response to
outflow obstruction. Projectile vomiting
normal antigens have been proposed as
of food within hours of ea.ting may be
possible ca.uses. Eosinophilic gastritis with
described. Older, male, small-breed dogs are
eosinophilia. and/or skin lesions should raise overrepresented (eg, Lha.sa.Apso, Shih Tzu, suspicion for dietary sensitivity or

Maltese, Miniature Poodle). Hypergastrin hypereosinophilic syndrome (ca.ts).

emia. due to exaggerated secretion ( eg,

Animals with mild clinical signs and mild
gastrin-secreting neoplasia., Basertji
histologic lesions may respond to syn1ptogastroenteropa.thy) or inadequate clearance ma.tic care ( see p 387 )', empirical deworm

( eg, hepatic or renal disease, a.chlorhydria.)

ing, and exclusive feeding of a hypoallermay initiate mucosal hypertrophy. Surgical genic or novel protein diet ( eg, balanced
correction via pyloroplasty and/or removal
homemade diet or many conm1ercially
of hypertrophied tissue may be required to
available options). In addition to symptoalleviate clinical signs.

matic care, empirical deworming, and
dietary modification, animals with

GASTROINTESTINAL NEOPLASIA
moderate to severe, histologica.lly
confirmed disease generally require

GI neoplasia. is uncommon in dogs and ca.ts,
inununosuppressive therapy. Prednisone
with gastric tun10rs representing< 1% and

( or prednisolone in ca.ts) is sta.ited at
intestinal twnors d 00/o of overall neoplasia.

2 mg/kg/day, PO (dogs), or2-4 mg/kg/day,
in these species. GI neoplasms tend to be

PO (ca.ts), and tapered to the lowest dosage
malignant. The average age of dogs with GI
that controls clinical signs. Assuming
neoplasia. is 6-9 yr and of ca.ts 10-12 yr.

continued clinical remission, prednisone
therapy is ultimately discontinued and strict

Etiology and Pathophysiology: Speadherence to dietary therapy maintained. If cific etiologic a.gents for GI neoplasia. have
clinical signs persist despite ga.stroprotecnot been identified. The increased 1isk of tant therapy, dieta.iy modification, and

Belgian Shepherds for gastric carcinoma.,
prednisone therapy, treatment with an
and of Siamese cats for intestinal a.denocaradditional inununosuppressive a.gent ( dogs: cinoma. and lymphoma. may reflect genetic
a.za.thioprine 2 mg/kg, PO, every 24--48 hr;
predispositions. Feline leukemia. has been
ca.ts >4 kg: chlorambucil 2 mg [ total dose],
suggested to be an underlying factor in

PO, every 48 hr for 2-4 wk then tapered to
development of feline GI lymphoma., even

2 mg every 72-96 hr; ca.ts <4 kg: chlorambu-
in ca.ts with a negative reti·oviral status.

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

389

H elicobacter infections are associated with may accompany colonic and rectal tumors.

gastric neoplasia in people, but similar

An abdominal mass or organomegaly may
direct links have not been established in
be palpable on physical exan1ination.

dogs or cats.

Abdominal pain and ascites may reflect peri

Adenocarcinomas are the most common
tonitis secondary to a ruptured portion of

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GI neoplasia in dogs and are typically found
neoplastic bowel.

in the duodenum, colon, and rectum.

Gastric adenocarcinomas are common in
dogs and frequently affect the lower 1/3 of

Diagnosis: Routine laboratory studies
the stomach ( eg, lesser cuivature and
and plain radiographs do not show specific
pyloric region). Adenocarcinoma is
changes associated witl1 GI neoplasia.

commonly identified in the feline intestinal

Hypoglycemia is often associated with
tract, especially in the jejwmm and ilewn.

leiomyomaslleiomyosarcomas. Hyper

Adenocarcinomas are very aggressive and
cholesterolemia and increased alkaline
frequently metastasize to regional lymph
phosphatase activity has been seen in some
nodes, liver, and lung. At the time of
nonlymphomatous neoplasia. Microcytic
diagnosis in dogs, as many as 44% of
anemia with or without hypoproteinemia is
intestinal and as many as 95% of gasttic
a common finding with ulcerated masses
adenocarcinomas have metastasized.

and chronic blood loss. Electt·olyte and

Adenomas and carcinomas in situ are
acid-base disturbances may reflect ongoing
uncommonly found in the GI tract of dogs
vomiting and can include hypochloremia,
or cats. These polyp-like masses are usually
hypokalemia, and metabolic alkalosis or
solitary and located in the colon or rectum
acidosis. Para.neoplastic hypercalcemia has
in dogs.

been associated with lymphoma and

Lymphoma is the most common feline GI
intestinal adenocarcinoma.

neoplasia, and it is also common in dogs. GI

Contrast abdominal radiographs may
lymphoma most commonly affects the small reveal mass lesions in the GI tt·act or areas intestine as well as extra-gastrointestinal
of ulceration. Abdominal ultrasonography
organs such as the liver. Two subtypes of
may reveal focal or diffuse thickening of
feline GI lymphoma have been reported:

the GI tract and loss of normal layering.

a low-grade, small-cell lymphocytic

Regional lyn1ph nodes may be enlarged, and
lymphoma and a more aggressive, poorly
splenomegaly and/or hepatomegaly may
differentiated, large-cell, lymphoblastic
accompany some cases of GI lyn1phoma.

lymphoma. Canine GI lymphoma is usually

Ultrasound can facilitate fine-needle
poorly differentiated and aggressive, similar
aspirates or needle biopsy sample collection
to lymphoblastic lymphoma in cats.

for cytologic or histologic analysis.

GI strornal tun1ors (GISTs) are mesenchy

Endoscopy of the upper and lower GI
mal in origin in dogs; they are rarely seen in
tt·act can facilitate identification and
cats. One of the major diagnostic criteria
partial-thickness biopsy of GI neoplasia.

for GISTs include positive c-kit (CDl l 7)

However, endoscopic biopsy collection is
reaction on immunohistochemistry. Before
limited by the small size and superficial
the recognition of GISTs, many of tl1ese
nature of the biopsy, because some GI
tumors were likely classified as leiomyosartumors are submucosal and this technique comas. GISTs typically are found in the
may only collect superficial mucosa A false
cecum and large intestine. In contrast,
diagnosis of gastlitis or enteritis may reflect
leiomyosarcomas are most common in tl1e
inflammation of the mucosa overlying a
stomach and small intestine. The metastatic
neoplastic process. In one study, endoscopic
rate is as high as 30% with leiomyosarcomas
biopsies were adequate to detect feline
and likely lower with GISTs. Uncommon GI
gastlic lymphoma but not adequate to
twnors of dogs and cats include mast cell
differentiate inflanunatory bowel disease
twnors, leiomyomas and leiomyosarcomas,
from lymphoma in the GI tract. Recent
fibrosarcomas, and plasmacytomas.

studies suggest that endoscopic ileal
biopsies aid in the diagnosis of lymphoma

Clinical Findings: Clinical signs of GI
and other GI diseases, compared with
neoplasia depend on the location and extent endoscopic duodenal biopsies. Full-thickof the tumor and its possible metastases or ness smgical biopsies collected via
para.neoplastic syndromes ( eg, hypercalcelaparoscopy or laparotomy may more mia, hypoglycemia). The most common
suitably establish a diagnosis and will allow
clinical signs associated with GI neoplasia
for biopsy of regional lymph nodes and liver
include vomiting (with or without blood),
to evaluate for metastasis. Inununohistoanorexia, weight loss, diarrhea, and chernistry may be required to differentiate
lethargy. Signs of constipation or tenesmus
between types of neoplasia for GI biopsies.

390

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

PCR for antigen receptor rea1Tangement
in perforation, endotoxemia, and hypodetects clonality of a population of volemic shock. Therefore, GI obstruction
lymphocytes and can aid in the ruagnosis of
should be treated as an emergency.

GI lymphoma when perfmmecl on inconclusive biopsy sections, especially in cats.

Etiology and Pathophysiology: GI

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obstruction can be secondary to extralumi

Treatment and Prognosis: Surgical
nal, intramural, or intra!uminal causes. The
excision of the tumor is recommended
most common extraltuninal cause of GI
for nonmetastatic, nonlymphomatous
obstruction is intussusception, in which
neoplasia. Curative resection, with margins
an invaginated segment of the GI tract
of .:4 cm, should be attempted.

becomes enveloped by an antegracle or

The median survival time for GI aclenocarretrograde segment. Intussusception can cinoma in clogs is 10-15 mo if the ttunor was
be secondary to endoparasitic infection,
focal and completely resected but only 3 mo
parvoviral infection, foreign body ingestion,
if metastasis is present at diagnosis.

or neoplasia, but is often idiopathic.

Acljuvant chemotherapy ( eg, carboplatin)

Intestinal intussusception occurs most
may be presc1ibed; optimized chemotherapy
commonly at the ileocecocolic junction.

protocols for treatment of GI adenocarci

Gastroesophageal and pylorogastric
noma have not been rep01ted. GI lymphoma
intussusceptions are uncommon, acute,
is typically treated with chemotherapy.

severe forms of intussusception associated

Phenotypic variations offeline GI lymphoma
with a high mortality rate. German
warrant different treatment strategies.

Shepherds may be prerusposed to

Small-cell (well-differentiated, low-grade) gastroesophageal intussusception.

lymphoma is treated with prednisone (2 mg/ Intestinal entrapment in hernias or kg/clay, PO) and chJorambucil ( either 2 mg
mesenteric rents can result in strangulation

PO every other day or 15 mglm2 daily for 4
of bowel and rapid development of
clays, every 3 wk). The prognosis associated
hypovolemic shock.

with small-cell GI lymphoma is good, with a

Intramural obstruction can be caused by
median survival time of 765 days. Poorly
infiltrative disease such as neoplasia, fungal
differentiated GI lymphoma in dogs and cats infection (eg, pythiosis), and granulomas is poorly responsive to chemotherapy. If

( eg, secondary to feline infectious
treatment is attempted, a multiclrng
pe1itonitis). Pyloric stenosis can cause
chemotherapy protocol ( eg, Wisconsingastric outflow obstruction and has been Maruson) is recommended, but complete
reported as a congenital condition in
remission rates are low, and meruan survival brachycephalic breeds. lntraltuninal times are usually <3 mo. Focal lymphoma
obstruction commonly occurs in dogs and
may be surgically excised, and follow-up
cats secondary to ingestion of a foreign
chemotherapy may be recommended.

body.

GISTs and leiomyosarcomas are slow-grow

Most cases of acute vomiting are not a
ing and slow to metastasize. In a study of
result of GI obstruction and are self-limiting.

dogs with a diagnosis of either leiomyosar

Vomiting may be a result of dietary
coma or GIST, median survival tirtle was 37
inruscretion, parasitic infection, bacterial or
mo after complete resection, although
viral gastroenteritis, anxiety, or motion
another report suggests that GISTs are
sickness. In these cases, treatment usually
associated with a better survival rate than
involves withholding food for !J. short
leiomyosarcomas. Malignant GI neoplasia
period, feeding an easily digested ruet, and
usually has a poor prognosis ( survival <6
offering small amounts of water frequently.

mo), even with surgical and medical

Careful monitoring for persistent vomiting,
tl1erapy. Benign lesions, such as leiomyodepression, abdominal discomfort, and/or mas and colorectal aclenomas, have a good
fever is critical. If vomiting persists,
prognosis with surgical excision.

reevaluation is warranted. Abdominal
palpation should be performed, looking for

GASTROINTESTINAL
signs of a foreign body or abdominal

OBSTRUCTION
discomfort. Careful examination of the oral
cavity in cats, looking for evidence of yam,

GI obstruction often leads to intractable
thread, or needles, is in1portant. Abdominal
vomiting, the consequences of which can be radiographs should be perfonnecl, looking life-threatening and include possible
for radiopaque foreign objects or signs of
aspiration, electrolyte and acid-base
intestinal rustention, indicating possible
disturbances, and dehydration. Depenrung
obstruction.

on the tu1derlying cause of the obstruction,

Obstruction secondary to foreign body
the site can undergo tissue damage resulting ingestion can be partial or complete if the

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

391
foreign body is unable to pass through the
obstruction. Diarrhea, weight loss, lethargy,

GI tract. Linear or small foreign bodies are
and signs of septic shock are less common.

more likely to cause partial obstruction,

Physical exan1ination may be unremarkable
whereas large, round objects often result in
or may reveal signs of abdominal pa.in or
complete obstruction. Foreign bodies are
a palpable intestinal mass. Physical

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usually objects that cannot be digested ( eg,
exan1ination must be thorough and include
plastic, rocks), are slowly digested ( eg,
inspection of the oral cavity, because linear
bones), or are too large to pass through the
foreign bodies in cats may be anchored to

GI tract. Some dogs are indiscriminate
the base of the tongue. If a linear foreign
eaters and will consume such objects,
body is present in the oral cavity, it must be
whereas cats more typically ingest linear
cut inunediately and never pulled in hopes
foreign bodies (eg, string, yarn, dental floss)

of retrieving the foreign body.

while playing with them.

Signs of hypovolemic shock and

GI obstrnction may be due to one or
abdominal pa.in usually accompany cases
more foreign bodies. The decision to treat
of intestinal incarceration.

medically or proceed with surgery can be a
challenge. Some small objects identified

Diagnosis: Laboratory findings associated
radiographically will pass through the GI
with GI foreign bodies include leukocytosis
tract. Passage of these objects can be
with a mild left shift. Marked leukocytosis
monitored with serial radiographs if the
or leukopenia with a degenerative left shift
animal is clinically stable. Failure of these
can be present in cases of GI perforation
objects to pass within 48 hr, serial radioand secondary bacterial pe1itonitis or graphic evidence that the objects are not
sepsis. A wide variety of electrolyte and
moving, or a deterioration of clinical signs
acid-base changes have been described.

necessitate surgical removal. Presence

Proximal GI obstruction has typically been
of uncooked bone matter in the stomach
associated with hypochloremia, hypokashould be monitored but is usually resolved lemia, and metabolic alkalosis, whereas
by normal digestive processes in the
more distal GI obstruction is associated
stomach.

with metabolic acidosis. In a study in dogs,

Regardless of underlying etiology,
hypochloremia and metabolic alkalosis
unresolved GI obstruction leads to
were the two most common changes regarddistention of the more proximal GI tract less of the site of GI obstruction. Hyperlacwith fluid and gas. If entrapment of GI loops tatemia and hemoconcentration (increased
results secondary to hernias or mesenteric

PCV and total solids) are also frequently
rents, strangulation and bowel incarceraidentified.

tion occurs. Venous return is in1pa.ired

Plain ra.diographs may assist in diagnosis
but arterial flow maintained, leading to
of GI obstruction in cases of radiopa.que
congestion, anoxia, and necrosis. Obstrucforeign bodies. Complete obstruction may·
tion or strangulation of bowel can result in
result in radiographic findings such as ileus
devita.lization of the GI tissue and translocaand intestinal loop dilation with fluid and/or tion of bacteria. such as Escherichia coli
gas, whereas linear foreign bodies can
and Clostridium spp from the GI lun1en
create intestinal plication. These findings
to the tissue. If not corrected, edema,
are not specific for GI foreign bodies,
hemorrhage, mucosa! sloughing, and
however, and can be seen witl1 other causes
eventually bowel necrosis occur.

of GI obstruction, including intestinal
stlicture, adl1esions, intussusception, and

Clinical Findings: Intussusception
neoplasia. Conti·ast abdominal radiographs
occurs most conunonly in yotmg dogs.

may be useful in detection of ra.diolucent

Intestinal intussusception typically causes
foreign bodies that create filling defects and
signs of abdominal pain, vomiting, and
in cases of intussusception. Ba.riun1 is
diarrhea with or without blood. More
conunonly used for contrast radiographs,
proxin1al intussusceptions (ie, gastroesophbut if GI perforation is suspected, aqueous ageal, pylorogastric) result in vomiting and
iodine or iohexol should be used instead.

regurgitation.

Abdominal ultrasonography can help

Young cats and y0tmg, large-breed dogs
identify the presence of GI foreign bodies
are more likely to present with signs of
and dilation of intestinal loops with fluid.

foreign body obstruction than older

Transverse sonogra.phic views of intestinal
animals. Clinical signs are variable,
intussusceptions often show a "target-like"

depending on duration, degree, and location
lesion with conccntiic hyperechoic and
of the foreign body but often include
hypoechoic rings. Large amounts of
vomiting and anorexia. Vomiting is less
intestinal gas may obscure the ultrasound
common with distal, small-intestinal
view. Signs of peritonitis and GI perforation

392

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
detectable with radiographs or ultrasound
the foreign body or bodies is recommended
include abdominal effusion or free gas.

to help decrease the risk of postoperative

Abdominal effusion, if present, should be
dehiscence. Linear foreign bodies in cats
cytologically examined to evaluate for
can be particularly challenging, because the

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septic peritonitis. Endoscopic examination
foreign material may be a single piece of
may help identify foreign bodies and mass
thread, yarn, or dental floss that is not
lesions.

palpable, which makes assessment of its
length difficult. Multiple solid, smooth

Treatment: Small, smooth foreign bodies
intestinal foreign bodies can often be
may pass uneventfully through the GI tract.

"milked" through the intestine and removed If this approach is taken, monitoring with
through one incision. Linear foreign bodies
abdominal radiographs to track the
are more likely to cause GI mucosa! damage
movement of the foreign body is recomand devitalization and can affect a large mended. If the foreign body is not moving,
section of the GI tract. Devitalized or
and if obstruction or worsening of clinical
perforated areas of the GI tract must be
signs is apparent, intervention is required.

resected, and the remaining GI tract

In most cases, removal of detected
anastomosed. Intussusceptions are
foreign bodies via endoscopic or surgical
manually reduced or resected, and the
retrieval is recommended because of the
remaining bowel anastomosed if reduction
potential for obstruction or perforation.

is not possible or the bowel loop appears

Detection of colonic foreign bodies is often
compromised. Lapa.roscopic-assisted
incidental, and these usually do not require
exploration and foreign body retrieval is
removal. If a colonic foreign body is causing
gaining popularity among veterinary
clinical signs, endoscopic removal is
surgeons with suitable expertise and
prefen-ed over surgically opening the colon.

equipment.

Fluid, electrolyte, and acid-base distur

After foreign body retrieval, con-ection
bances should be con-ected before
offluid, electrolyte, and acid-base
anesthesia if possible.

disturbances should continue. Peritonitis is

Endoscopic or surgical retrieval of
treated with antibiotics and closed suction
foreign bodies causing GI obstruction is
drains. If the animal is not vomiting, water
associated with a high survival rate. The
may be offered 12 hr after anesthetic
utility of endoscopy is typically limited
recovery. Food may be introduced 12-24 hr
to the retrieval of gastric foreign bodies.

after recovery if there is no vomiting.

Endoscopy cannot assess the GI tract distal
to the pyloric or proximal duodenal region.

Prognosis and Prevention: Outcome

If endoscopy is used to retrieve a proxin1al
for anin1als with GI foreign body obstruc

GI foreign body, the scopE_! should be passed
tion is good if the condition is recognized
into the small intestine as distally as
and treated quickly. Animals with severe
possible for evaluation, with radiographs
clinical signs resulting from systemic
taken before recovery from anesthesia
factors such as concun-ent infection or
to exclude the presence of multiple foreign
debilitation, hypovolemia, and shock are at
bodies.

•
higher risk of delayed healing and incisional

An exploratory laparotomy is indicated
breakdown. Marked preoperative
if a foreign body distal to the pyloric region
hypoalbun1inemia ( <2-2.5 g/dL) is
is present, if there are foreign bodies at
associated with a higher rate. of postoperamultiple locations, if there are signs of septic tive dehiscence. Animals presenting with peritonitis, or if endoscopy is not available.

signs of peritonitis or sepsis have more

Exploratory laparotomy is also indicated
postoperative complications and are at
over endoscopy in cases of suspected
higher risk of enterotomy dehiscence.

intussusception and obstruction secondary

Anin1als with signs of peritonitis, or those
to a mass lesion. The entire GI tract must be
requiring resection of a large amount of
inspected for objects that could cause
intestine leading to short-bowel syndrome,
obstruction. Vitality of the GI tract must also
have a guarded prognosis. Dehiscence of
be assessed, and areas of perforation or
the intestinal surgical site most commonly
ischemia resected. If a linear foreign body is
occurs 3-5 clays after sw·gery at the end of
present in the stomach and extends into the
the lag phase of healing. Until this point,
small intestine, gentle manipulation may
most tensile strength has been provided by
easily free the foreign body from its distal
fom1ation of a fibrin seal that is debrided
attachments, allowing removal through the
by macrophages 3-5 days after surgery.

gastrotomy incision. Otherwise, multiple

Postoperative dehiscence usually requires a
enterotomies may be indicated. The minin1al second surgery and is associated with a high number of enterotomies possible to remove
mortality rate.

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

393

Gastroesophageal and pylorogastric
ulceration can result, exposing the
intussusceptions are associated with a high
submucosa or deeper layers of the GI
mortality rate, and rapid diagnosis and
tissue to the lunlinal contents.

surgical inteivention are essential to

In the normal GI tract, the potential

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maximize chance of survival in these cases.

disruptive properties of the lunlinal

GI obstruction secondary to neoplasia is
contents are balanced by the defense
uncommon, and prognosis depends on the
mechanisms of the GI mucosa! barrier.

type ofneoplasia.

However, many drngs and disease have
the potential to upset the balance between
the harsh luminal contents and the GI

GASTROINTESTINAL ULCERS
protective barrier.

Ulceration and disruption of the GI mucosal

The incidence of GI ulceration in dogs
barrier can be a consequence of several
and cats is unknown. NSAID administradrugs and diseases in small animals. As a tion, neoplasia, and hepatic disease are the
most conunon causes in dogs. NSAIDs can
result, gastroprotectant therapies a.re
widely used in vete1inary patients.

cause direct topical damage to the GI
mucosa, and inhibition of cyclooxygenase

(COX)-1 decreases production of protective

Etiology and Pathophysiology:

prostaglandins. The use of COX-2-specific

The gastric mucosa! barrier is a complex

NSAIDs is thought to decrease GI ulceradefense mechanism that protects the tion, but ulceration and perforation still
normal mucosa from the harsh chemical
occur with use of these medications.

environment of the gastric luminal contents. Corticosteroids potentiate the effects The acids, pepsin, and proteolytic enzymes
ofmucosal damage by decreasing cell
normally present in the gastric lumen have a turnover and mucus production and by pH of 2. The mucous layer provides a weak
stimulating ga.strin (and acid) production.

buffer, maintaining a pH of 4-6 and

Hepatic disease is associated with
neutralizing the acidic luminal contents.

increased ga.stlic acid secretion and

The GI barlier is maintained by a protective
alterations in mucosal blood flow,
layer that includes mucosal cells, tight
potentially leading to ulcer fomrntion.

junctions, and a thick layer of mucus. High

Primary GI neoplasia such as lymphoma,
blood flow to this area supports cellular
adenocarcinoma, leiomyoma, and
metabolism and rapid renewal of injured
leiomyosarcoma can result in ulceration.

cells. Prostaglandins (mainly E and I) help

Additionally, paraneoplastic syndromes
maintain the GI mucosal blood flow and
secondary to ma.st cell tumors and
integlity, increase secretion of.mucus and
ga.strinomas (Zollinger-Ellison syndrome)

bicarbonate, decrease acid secretion, and
have been associated with increased ga.stiic
stimulate epithelial cell turnover. Tight
hydrochloric acid production and ulcerajunctions seal the cellular layers of the tion in dogs.

gastric mucosa, ensrning that the luminal

Other drugs and diseases associated with
contents do not leak into or around these

GI ulceration in dogs include corticosteroid
cells. The small amount of gastric acid that
use in dogs with spinal disease, renal
diffuses into the epithelial cells is quicldy
disease, hypoad.renocorticism, stress,
cleared by the high blood flow to this area.

primary GI disease ( eg, inflan1matory bowel

A defect in the GI mucosa! barrier leads to
disease), extreme exercise (eg, sled dog
a self-perpetuating cycle of mucosal damage.

racing), shock, and sepsis. The role of
lr\jury to this barrier allows hydrochloric

Helicobacter infection in GI ulceration is
acid, bile acids, and proteolytic enzymes to
unknown, because H elicobacter organisms
degrade the epithelial cells, disrupt lipid
have been found in healthy dogs and cats.

membranes, and induce inflammation

GI ulceration is unconunonly reported in
and apoptosis. Back diffusion oflunlinal
cats. Neoplasia ( eg, lymphoma, adenocarcicontents through the tight junctions leads noma) has been associated with GI
to inflammation and hemon-hage of the GI
ulceration in cats, but the cause is often
cells, with further acid secretion mediated by unknown.

inflammatory cells and their products. Mast
cell degranulation occurs, causing histanline

Clinical Findings: Specific clinical signs
release that perpetuates further gastric acid
of GI ulceration include melena, hematemsecretion. The inflanunatory environment esis, and hematochezia. Abdominal pa.in,
also causes decreases in blood flow
anorexia, and signs of underlying disease

( resulting in ischemia ), ability f or cellular
may be present. Cats with GI ulceration
repair, and secretion of mucus and
rarely show specific signs such as melena
cytoprotective prostaglandins. Mucosal
or hematemesis but frequently show signs of

394

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
life-threatening hemon-hage. Animals with

Prophylactic use of H2-blockers and proton
severe ulceration and/or GI perforation may
pwnp inhibitors to prevent GI ulceration is
present with signs of pain, weakness, pallor,
controversial but may be considered in
and shock. Clinical signs of a causative
animals receiving NSAIDs or that have other
factor may be seen. Some dogs and cats with
risk factors.

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GI ulceration do not show any clinical signs.

Cytoprotective agents include antacids
and sucralfate. Antacids are weak bases

Diagnosis: A CBC, serum biochemistry
that help neutralize gastric acid within the
profile, and w·inalysis can help differentiate
stomach lumen. These drugs may also
primary GI disease from non-GI disease and
promote gastric prostaglandin production.

can identify metabolic derangements

Aluminum or magnesium-containing
resulting from GI disease. Additional
antacids are considered the most effective
testing, such as liver function tests or an
agents with the fewest adverse effects,
adrenocorticotropic honnone stimulation
although these drugs can lead to constipatest, may be warranted depending on the tion. Because of their short half-life (2-3 hr),
clinical findings and initial test results.

animals may experience a rebound gastric

Abdominal radiographs generally do not
acidity between doses, and the drugs must
help diagnose GI ulceration, but they can
be given frequently. Sucralfate ( dogs:

help exclude GI obstruction, intussuscep0.5---1 g, PO, bid-tid; cats: 0.25 g, PO, bid-tid) tions, and peritonitis. Abdominal ultrais a polyalun1inW11 sucrose sulfate that sonography may show abnormalities in GI
binds to areas of eroded or ulcerated GI
wall thickness or presence of a mass, but its
mucosa. Because this drug inhibits
primary utility is the identification of non-GI
absorption, it should not be given within
lesions. Endoscopy allows visualization of

1-2 hr of food or other drugs.

the esophagus, stomach, duodenwn, and

The prostaglandin E2 analogue misoproscolon and identification of mucosal lesions tol is used to help prevent NSAID-associand ulcers. Endoscopy also allows for fineated ulcer fonnation but does not assist in needle aspirates of lesions or collection of
mucosa! healing or decrease acid secretion.

biopsy samples, although full-thickness

Prophylactic use of antibiotics can be
smgical biopsies may be required to identify considered in cases of major GI mucosa]

infiltrative disease and tumors. Ulcerated
barrier disruption or shock, or in other
areas should be biopsied only on the
cases when clinicopathologic signs ( eg,
periphery to avoid perforation. Gast1ic fluid
fever, hematochezia, leukopenia, neutrocan be tested for pH to help diagnose philia) suggest that bacterial translocation
hypersecretory states.

is of concern. First-line antibiotic therapy
includes the l3-lactan1s, with additional

Treatment and Control: Primary
gran1-negative coverage if necessary.

treatment of GI ulceration is directed at the
underlying cause. Supportive care may be

Prognosis: The prognosis for GI
required to correct metabolic derangements ulceration in dogs is favorable when tl1e and can include fluid therapy. Medication
tmderlying cause can be treated or removed,
directed at the ulcer itself reduces gastric
ulceration is mild, or tl1e condition is rapidly
acidity, prevents further destruction of GI
diagnosed and treated. Ulceration associmucosa, and promotes ulcer healing. In ated with severe or end-stage conditions ( eg,
general, anti ulcerative therapy should be
hepatic insufficiency) is di{ficult to control.

continued for 6---8 wk.

Mortality rates associated with GI perfora

Gastric acid production is stimulated
tion range as high as 700/o.

by histamine (most potent), gastrin, and

GI ulceration in cats is often related to
acetylcholine. Drugs that decrease acid
neoplasia. Intensive care frequently is
secretion help protect damaged GI mucosa.

needed because of the high prevalence of

H
marked hemorrhage. In one repo1t, median

2- receptor blockers ( eg, cin1etidine,
famotidine) help promote mucosa! healing,
survival of cats with gastric ulceration
and some agents also act as pro kinetics ( eg,
treated with smgery and palliative care
ranitidine). Famotidine (0.5---1 mg/kg, bid,
ranged from 12-15 mo. Cats with GI

PO, SC, or IV) has been shown to be more
ulceration secondary to a non-neoplastic
potent in reducing gastric pH than other Hr
disease have less severe clinical disease and
blockers such as cimetidine or ranitidine.

a good prognosis.

Proton pump inl1ibitors ( eg, omeprazole

0.5---1 mg/kg/day, PO, or pantoprazole

HELICOBACTER INFECTION

0.5---1 mg/kg/day, IV) offer more complete
inhibition of gastric acid secretion and are

H elicobacter spp are commonly fow1d in
therefore useful for more severe ulcers.

the stomachs of both healthy and vomiting

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

395
dogs and cats, but their significance is not
san1ples a large area of the stomach, the
well defined. Although H pylori infections
sensitivity of this test is high.

in people have been linked to gastritis,

Gastric biopsies should be obtained from
peptic ulcers, and a higher rate of gastric
multiple areas in the stomach, because

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neoplasia, similar direct casual relationorganism distribution can be patchy.

ships between H elicobacter infections and

Routine H&E staining is usually sufficient to

GI disease have not been established in
identify organisms, although special silver
dogs and cats.

stains may be required if the organisms have
a glandular location. Mucosa] inflainmation,

Etiology and Pathophysiology:

glandular degeneration, and lymphoid

Helicobacter organisms are spiral or
follicle hyperplasia accompany some
curved, gram-negative, motile, flagellated
infections. Cytology and histopathology is
organisms. H pylO'li is the most commonly
not sufficient to identify specific species.

reported species in human GI infections,

A conunercially available rapid urease test
but non-H pylori organisms (such as H
to detect production of bacterial urease in

.felis, H heilmannii, and H bizzozeronii) gastric biopsies can identify the presence of
are more common in dogs and cats. At least Helicobacterorganisms. However, because 38 differentHelicobacler species have been
cytology and histopathology ai·e highly
identified in animals, and infected animals
sensitive and specific for detection of
can harbor multiple species.

Helicobac/.er infections, w-ease testing may Helicobacter organisms have been
not add further diagnostic information in
identified most conunonly in the gast1ic
some cases.

tissue of dogs and cats, especially in the

Noninvasive tests for Helicobacter
fund us and ca.rdia of the stomach, but
infection available in the research setting
they are also found in the intestinal tract.

include urea breath testing, fecal aJ1tigen

Colonization of gastric mucosa appears to
detection, and serology.

be most prevalent in the surface mucus
layer, as well as within the gastric glands

Treatment: The lack of knowledge
and paiietal cells. There have been sporadic
regarding the pathogenicity of H elicobac/.er
reports of H el'icobacter organisms identified infections in dogs and cats makes treatment in the hepatic tissue of a dog with rnultifocal
decisions difficult. H pylori infections in necrotizing hepatitis, as well as in healthy
people are treated with double or triple
cats and in cats with cholangiohepatitis.

antimicrobial agent therapy plus an acid

Transmission of H elicobacter infections
secretory inhibitor ( eg, clarithromycin,
between groups of dogs or cats is unclear,
ainoxicillin, bismuth, and ranitidine) for
and reservoir hosts have not been defined.

2 wk, and sin1ilar therapeutic approaches

Because of the increased rate of morbidity
have been used in veterinary medicine ..

and mortality associated with H elicobacter

Currently, the role of Helicobacter as a
infections in people, concern ofzoonotic
causative agent of gastritis in dogs ai1d
transmission has been raised (see below).

cats is unclear. Treatment decisions for
dogs and cats should be based on presence

Clinical Findings and Diagnosis:

of Helicobacter, in combination with

Studies report as many as 1 OOOA, of healthy
approp1iate clinical signs and/or gastric
dogs and cats ai·e positive for Helicobacter
lesions. In many veterinai)' studies,
infections; similar infection rates are

Helicobacter infections have been difficult reported in vomiting dogs and cats. In
to eradicate. Reconunended treatment
people, H pylori infection is associated
regimens include ai11oxicillin or tetracywith gastritis, peptic ulcers, and an cline, metronidazole, bismuth subsalicylate,
increased risk of gastric neoplasia. Gastritis, and a proton pump inl1ibitor ( eg, omepravomiting, and diaiThea have been associzole) or H2-receptor blocker ( eg, fan1otiated withHelicobacterinfection, although dine) for 2-3 wk. Other treatment combinaa direct causal relationship has not been tions of omeprazole and azitlu-omycin or
identified. Peptic ulceration is rai·ely
claritlu-omycin have been described.

associated with Helicobacter infections

Although many dogs and cats treated with
in dogs and cats.

the above combinations did not experience

Diagnosis involves upper GI endoscopy
longterm eradication of Helicobacter
or exploratory laparotomy. Swface mucus
infection, when retested, the frequency of
from a large area of the stomach can be
vomiting and gastric lesions did improve
obtained by taking brush san1ples via
with therapy for many patients.

endoscopy. lf organisms are present, they
are readily identified under lOOx oiI-inuner

Zoonotic Risk: Zoonotic transmission of
sion magnification. Because brush cytology Helicobacter infections from dogs and cats

396

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
to people is possible. H canis, H fel'is,
pain are common. Vomiting may precede

H heilmannii, and other species naturally
the onset of bloody diarrhea. Marked,
colonize the stomachs of dogs and cats, and
peracute fluid loss can result in hypothese strains of H elicobacter have been volemic shock before clinically recogniz

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linked to gastritis, ulcers, and lymphoma in
able dehydration. Other historical findings
people. Whereas many strains of Helicobac

( eg, dietary indiscretion, vaccination status,
ter in dogs and cats are genetically distinct etc) are unremarkable. HGE is not
from those implicated in human infections,
considered contagious.

at least one case report documents a
genetically identical strain of H heilmannii

Diagnosis: The diagnosis is typically
infecting pet dogs and a child in the same
based on signalment and acute onset of
house. Although some studies have
clinical signs with hemoconcentration (PCV
suggested a higher risk of H elicobacter

55%) and normal to slightly decreased total
infection in people in contact with dogs and
plasma protein concentration. Selective
cats, other research refutes this. Given the
culture for fecal pathogens ( eg, Clostrid
unknown risk of transmission, proper
ium spp, Salmonella spp, Ye'l·sinia spp, hygiene practices are encouraged, and

Clos tridium spp, Campylobacte'I· spp, identification of infections in dogs and cats
enterotoxigenic Esche'l"ichia coli, etc) and with chronic gastritis and vomiting is likely
evaluation for Closl1idium spp enterotoxin
prudent.

by fecal ELISA can be considered.

Abnormalities on CBC are usually limited

HEMORRHAGIC
to hemoconcentration and neutrophilic

GASTROENTERITIS
leukocytosis. If neutropenia is present,
sepsis and/or parvovirus enteritis may be a

Hemorrhagic gastroenteritis (HGE) is a
concern. Serum biochemical profile may be
syndrome of dogs characte1ized by acute
unremarkable or show mild patlhypoprovomiting and hemorrhagic diarrhea, often teinemia, hypoglycemia (sepsis, decreased
accompanied by hemoconcentration. Young intake with limited hepatic glycogen (median age 5 yr), small and toy breed dogs
stores), and electrolyte abnom1alities

(Yorkshire Terrier, Miniature Pinscher,
consistent with GI loss and decreased

Miniature Schnauzer, Miniature Poodle,
intake (ie, hypokalemia, hyponatremia,

Maltese) are overrepresented. No sex
hypochloremia). There have been anecdotal
predisposition has been identified.

reports of mildly prolonged ( < 10%)

coagulation times ( activated clotting time,

Etiology and Pathophysiology:

prothrombin time, partial thromboplastin

The precise etiology and pathogenesis are
time), potentially attributable to inflan1n1aunclear, but suspicion that HGE is the result tion or interference due to hemoconcentraof infection with or hypersensitivity to tion. If coagulation times are moderately or

Clostridium pe'ljringens seems reasonmarkedly prolonged, coagulopathy or able. Clostridium spp has been identified
disseminated intravascular coagulation
by bacterial culture or immunohistopathol

(DIC) should be investigated. Basal serum
ogy in small-intestinal biopsies from dogs
cortisol concentration should be normal to
with HGE, suggesting an association with
increased ar1d is ar1 appropriate screening
clostridial overgrowth. Acute intestinal
test for hypoadrenocorticism. Radiographic
mucosa! hemorrhagic necrosis and
ar1d ultrasound abnormalities should be
neutrophilic inflammation are the predomilimited to diffuse ileus and fluid-filled loops nant histologic lesions, with the most severe of bowel. Differential diagnoses include lesions occurring in the large intestine.

bacterial, viral ( eg, parvovirus, coronavi-

Histologic mucosa! lesions are not generally rus ), and parasitic (eg, 'I'richuris vulp'is, identified in the stomach, leading some to

Ancylostoma spp, Uncinaria spp)

suggest "acute hemorrhagic diarrhea
gastroenteritis; systemic disturbances with
syndrome" may be a more appropriate
secondary GI involvement ( eg, hypoadrenodescriptor. Leakage of fluid, plasma procorticism, pancreatitis, renal failure, hepatic teins, and RBCs into the intestinal lun1en
disease, etc); coagulopathy (eg, rodenticide
occur secondary to increased intestinal
toxicosis, thrombocytopenia, thrombocypenneability.

topathia, etc); severe GI ulceration;
neoplasia; and GI perforation of ar1y

Clinical Findings: An acute onset of
etiology.

profuse hemorrhagic diarrhea ( often said
to resemble raspberry jam) in a small or

Treatment and Prognosis: Aggressive
toy breed dog is characteristic of HGE.

IV fluid therapy is the mainstay of treatment.

Vomiting, anorexia, lethargy, and abdominal The rate of isotonic fluid administration is

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

397
based on patient perfusion, degree of
pattern (regional enteritis). A neutrophilic
dehydration, and ongoing losses. Dogs
predominance in the inflanunatory infiltrate
markedly hypoproteinemic or in shock may
is rare. A mixed pattern of cellular infiltrate
benefit from synthetic or natural colloid
is described on many occasions. Certain

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( stored or fresh frozen plasma) therapy.

unique IBD syndromes occur more often in

Parenteral antibiotics effective against
some breeds, such as the protein-losing

Clostridium spp ( eg, ampicillin 22 mg/kg,
enteropathy/nephropathy complex in

IV, tid-qid, or metronidazole 7.5 mg/kg, IV,

Soft-coated Wheaten Teniers, immunoprobid) and to decrease the potential for sepsis liferative enteropathy of Basenjis, IBD in
secondary to intestinal bacte1ial transloca

Norwegian Lundehunds, and histiocytic
tion are indicated. Additional antibiotic
ulcerative colitis in Boxers.

coverage for gram-negative bacteria ( eg,
enrofloxacin 5-10 mg/kg/day, IV) is

Etiology and Pathophysiology: The
indicated in animals with sepsis or
etiology of IBD is unknown. Several factors
neutropenia. In a prospective study of dogs
may be involved, such as GI lymphoid tissue
with HGE and no clinical indices of sepsis,

(GALT); permeability defects; genetic,
treatment with amoxicillin-clavulanic acid
ischemic, biochemical, and psychosomatic
did not affect mortality rate, duration of
disorders; infectious and parasitic agents;
hospitalization, or severity of clinical signs.

dietary allergens; and adverse drug

This might suggest not all cases ofHGE are
reactions. IBD may also be immune
due to primary bacterial infection or that
mediated. The intestinal mucosa has a
the bacteria involved may not be susceptibarrier function and controls exposure of ble to amoxicillin-clavulanic acid. Dependantigens to GALT. The latter can stimulate ing on serum potassium concentration,
protective immune responses against pathomaintenance fluids should be supplemented gens, while remaining tolerant of harmless
with potassium chlo1ide at 20--40 mEq/L to
environmental antigens ( eg, commensal
prevent development of hypokalemia.

bacteria, food). Defective irnmunoregula

Hypoglycemic dogs require dextrose
tion of GALT results in exposure and
supplementation (2.5%-5%) of maintenance
adverse reaction to antigens that normally

IV fluids. Additional supportive care,
would not evoke such a response. Although
including antiemetic therapy and dietary
dietary allergy is an unlikely cause of IBD
management, are as described above (see

( except in eosinophilic gastroenteritis),

CANINE PARVOVlRUS, p 373, and ACUTE
it may contribute to increased mucosal

GASTRITIS, p 387). Rehydration with a
permeability and food sensitivity.

balanced oral electrolyte solution ( an initial

Cun·ent evidence supports the likely
volume of 7% dehydration [ to be replaced
involvement of hypersensitivity reactions
over 12 hr J should be offered every 4 hr,
to antigens ( eg, food, bacteria, mucus,.

along with volumes to account for
epithelial cells) in the intestinal lun1en or
maintenance fluid requirements and
mucosa. More than one type of hypersensiongoing losses) may be appropriate for tivity reaction is involved in IBD. For
dogs with mild dehydration and mild
example, type I hypersensitivity is involved
clinical signs.

in eosinophilic gastroenteritis, whereas type

Prognosis is good with appropriate

IV hypersensitivity is likely involved in
treatment. However, serious complications,
granulomatous enteritis. The hypersensitivincluding marked hypoproteinemia, DIC, ity reaction incites the involvement of
sepsis, hypovolemic shock, and death, can
inflanmrntory cells, resulting in mucosal
occur.

inflanunation that impairs the mucosal
banier, in tum facilitating increased

INFLAMMATORY BOWEL DISEASE intestinal permeability to additional antigens. Persistent inflammation may

Idiopathic inflammatory bowel disease
result in fibrosis.

OBD) constitutes a group of GI diseases
characterized by persistent clinical signs

Clinical Findings: There is no apparent
and histologic evidence of inflammatory
age, sex, or breed predisposition associated
cell infiltrate of unknown etiology. The
with IBD; however, it may be more
various forms of IBD are classified by
common in German Shepherds, Yorkshire
anatomic location and the predominant cell

Teniers, Cocker Spaniels, and purebred
type involved. Lyrnphocytic-plasmacytic
cats. The mean age reported for developenteritis is the most common fonn in ment of clinical disease is 6.3 yr in dogs and
dogs and cats, followed by eosinophilic

6.9 yr in cats, but IBD has been documented
inflammation. There are occasional reports
in dogs <2 yr old. Clinical signs are often
of inflammation with a granulomatous
chronic and sometimes cyclic or intem1it-

398

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
tent. Vomiting, diarrhea, changes in
changes may include gas or fluid distention
appetite, and weight loss may be seen. In a
of the stomach and increased total dian1eter
retrospective study of cats with lymphoof small-intestinal loops. Contrast films may cytic-plasmacytic enterocolitis, weight
show diffuse or focal mucosa] irregularities

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loss, intermittent vomiting progressing to
suggestive of infiltrative disease. Loss of
more frequent vomiting on a daily basis,
contrast can be related to ascites.

diarrhea, and anorexia were seen most

Fecal examination is inlpo1tant to
often. Vomiting, melena, and cranial
exclude other causes of mucosa] inflanirnaabdominal pain are often seen with tion, such as nematodes, Giard'ia infection, gastroduodenal ulceration and erosion.

and bacterial infection. Giardia may be

Weight loss, vomiting, diarrhea, ascites, and difficult to detect because of intennittent peripheral edema can be seen in the cases
shedding, and empirical treatment with
of protein-losing enteropathy. Pulmonary
fenbendazole is recommended in all cases.

thromboembolism is a rare complication;

Abdominal ultrasonography can be used
however, it can occur if there is severe
to assess all abdominal organs, examine the
intestinal protein loss (loss of antithrombin
entire intestinal tract, and measw·e wall

Ill). Clinical signs of large-intestinal
thickness ( although the latter measurement
diarrhea, including anorexia and watery
is of no significant value in IBD diagnosis).

diarrhea, are not uncommon.

Small-intestinal hyperechoic mucosal

An association between gastJ.ic dilation
striations are frequently associated with
and volvulus (seep 384) and IBD in dogs
mucosa] inflammation and protein-losing
has also been postulated. In this case,
enteropathy. Ultrasonography also helps
inflan1mation of the bowel may cause
elinlinate the possibility of disease in other
alterations in gastric motility and emptying
organs, localize the disease, and determine
and in GI transit time, thus predisposing to
whether endoscopy would allow biopsy of
dilation and volvulus.

the site.

An association between inflammato1y

Endoscopy allows examination of the
hepatic disease, pancreatitis, and IBD has
esophagus, stomach, duodenum, and
been reported in cats, although an etiology
sometimes the jejunw11, depending on the
for this triad of diseases has not been
size of the animal. Colonoscopy allows
established. However, cats with cholangioexploration of the colon. In some cases, hepatitis should also be evaluated for IBD
gross mucosal lesions may be seen
and pancreatitis. Although unproved, it has
endoscopically, including erythema, friabilbeen suggested that severe IBD in cats may ity, enhanced granularity, erosion, and
progress to lymphosarcoma.

ulceration. In many cases, the endoscopic
appearance is normal. However, biopsy

Diagnosis: There are no specific abn01°
samples should always be taken, because
malities on CBC, biochemical evaluations,
the macroscopic and microscopic
or radiographs.

appearance of the intestinal mucosa are

Hypoproteinemia due to reduced dietruy
poorly correlated. At least six biopsies of
intake and malabsorption or iIJ.creased loss
each segment of the GI tract are recomvia the GI tract may be seen. Hypocalcemia mended. Endoscopy is the easiest way to
and hypocholesterolemia may be attributed
collect biopsy samples, but such samples
to malabsorption. Increases in serun1
are superficial and usually can be collected
amylase as a consequence of bowel
only from the proximal small intestine.

inflammation have been repmted.

One study suggested that ileal biopsies

Hypokalemia secondary to anorexia,
can reveal lesions not apparent in the
potassium loss from vomiting and diarrhea,
duodenum and, therefore, should be
and mild increases in serun1 levels of liver
petionned routinely. More specifically,
enzymes can be expected. Low senun
feline lymphoma was much more likely to
levels of folate and cobalamin because of
be found in the ileum than the duodenum.

malabsorption are also docw11ented.

In some cases, explorato1y celiotomy and

Eosinophilia may be associated with
full-thickness biopsy are necessary to
eosinophilic enteritis; however, this is not a
reveal histopathologic changes at the level
sensitive parameter. Microcytic anemia may of the mucosa ( eg, dilation of the lacteals be present with loss of iron, associated with
in lymphangiectasia). However, wound
chronic loss of blood. Nomesponsive
healing can be compromised if there is
anemia, if present, likely reflects anemia
severe hypoproteinemia or if urgent
of chronic or inflanirnatory disease.

steroid treatment is needed. For this

Erythrocytosis, associated with fluid loss
reason, most clinicians choose to petiom1
from vomiting and diarrhea, and a stress
endoscopic biopsies unless biopsies of
leukogran1 may be seen. Radiographic
other abdominal organs are required.

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

399

Small populations of lymphocytes,

Dogs with large-intestinal diarrhea may
plasma cells, macrophages, eosinophils,
benefit from diets high in insoluble fiber
and neutrophils are normal components
content (seep 379). Supplementation of
of intestinal mucosa! tissue. Increased
dietary fiber alone is rarely effective in
numbers of plasma cells, lymphocytes,
anin1als with severe inflanunatory cell

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eosinophils, and neutrophils in the lamina
infiltrate.

propria are seen in IBD. However, these

Sulfasalazine (and related drugs) are
morphologic features may also be seen with
often used in dogs when IBD is limited to
other causes of GI disease ( eg, Giardia,
the large intestine. In the colon, this drug is

Campylobacler, Salmonella, lyrnphangiecsplit to release 5-aminosalicylic acid, which tasia, lyrnphosarcoma). Although histoexerts its anti-inflan1matory activity in the pathologic assessment of intestinal biopsy
mucosa. The principal adverse effects in
material remains the gold standard for
dogs are keratoconjunctivitis sicca and
diagnosis of many IBDs, it has marked
vasculitis. Because of the risk of salicylate
limitations. Specin1en quality can vary,
toxicity in cats (seep 379), sulfasalazine is pathologic diagnoses are inconsistent, and
not routinely used in feline colitis. Newer
differentiation between nom1al specin1ens
a.minosalicylic drugs without some of
and those showing IBD and even lymphoma
sulfasalazine's adverse effects are
can be difficult. Biopsy must always be
available, eg, olsalazine (dogs: 10-20
considered in relation to clinical signs, and
mg/kg, PO, tid) and mesalan1ine (dogs:

the animal treated accordingly.

10 mg/kg, PO, tid).

The use of antibiotics can be justified in

Treatment and Control: The goals
part by the potential to treat any undiagof therapy are to reduce diarrhea and nosed enteropathogens. Metronidazole
vomiting, promote appetite and weight

(10-20 mg/kg, PO, bid) is the preferred
gain, and decrease intestinal infl=ation.

antibacterial for most fonns ofIBD in small

If a cause can be identified ( eg, dietary,
animals. It may have inu-nunomodulatory
parasitic, bacterial overgrowth, drug
effects. 'Iylosin (10 mg/kg, PO, tid) may also
reaction, etc), it should be eliminated.

have immunomodulatory effects and may

Dietary manipulation by itself may be
have some efficacy in canine IBD. Histioeffective in some cases ( eg, in clu-onic cytic ulcerative colitis of Boxers is
colitis); in other cases, it can enhance the
responsive to enrofloxacin, which supports
efficacy of concurrent medical therapy,
the hypothesis that this pa.iticular fom1 of
allowing for the drug dosage to be reduced

IBD is the consequence of an infection with
or for drug therapy to be discontinued once
a specific organism.

clinical signs are in remission. Corticoste

Corticosteroids may be useful for both
roids, azathioprine, sulfasalazine, tylosin,
small- and large-intestinal disease. Initial.

and metronidazole are among the drugs
dosages are 2 mg/kg/day for prednisone
most often used in management of IBD.

or prednisolone and 0.25 mg/kg/day for

Unless the animal is debilitated, it is
dexamethasone. Adverse effects include
better to institute therapeutic modalities
polyuiia, polydipsia, polyphagia, and GI
sequentially. The frequency and nature of
disturbances ( eg, vomiting, melena,
clinical signs should be monitored, and
diarrhea). Dosages should be tapered every
therapy adjusted as needed. Treatment

7-10 days to the lowest possible dose
should begin with anthelrnintic/antiparasitic required to control clinical signs and, if medication ( eg, fenbendazole at 50 mg/kg/
possible, discontinued altogether. An
day, PO, for 3-5 days). This is followed by
entelic-coated formulation of the glucodietary modification (preferably with an corticoid budesonide has successfully
antigen-limited or hydrolyzed protein diet)

maintained remission in huma.11 IBD. A
for 3--4 wk, then a 3- to 4-wk antibacterial
preliminary study has shown apparent
trial (usually tylosin 10 mg/kg, PO, tid, or
efficacy in dogs and cats, but infom1ation
metronidazole 10 mg/kg, PO, bid), and
on use of this drug is limited. It undergoes
finally trial inmmnosuppressive therapy
substantial first-pass elimination via rapid

(initially prednisolone, 1 mg/kg, PO, bid).

inactivation in the liver; the result is lower

Dietary modification generally involves
systemic bioavailability and reduced effects
feeding a hypoallergenic or elimination diet
on the hypothalamic-pituita.t-y-adrenal axis,
with a source of protein to which the animal
making iatrogenic hyperadrenocorticism
has not been previously exposed ( eg, homeless common than with other glucocortimade diets of lamb and rice or venison and coids. The optimal dosage in dogs is
rice, conu-nercial diets). This diet should be
unknown. Anecdotally, a dosage of
the sole source of food for a minimum of

1 mglm2/day, PO, in dogs, and 1 mg/caUday,

4-6 wk; no treats of any kind should be fed.

PO, in cats, has been recommended.

400

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

In refractory cases, adding an immunonutrients, and it occurs in sequential phases: suppressive drug to corticosteroid therapy
intralurninal digestion, mucosal digestion
may be beneficial. Azathioprine (for dogs)

and absorption, and delivery of nutrients to
and chlorambucil (for cats) can be used. The
the body. Many chronic, small-intestinal
dosage of azathioprine is 2.2 mg/kg/day, PO.

diseases cause malabsorption by interfering

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Adverse effects include myelosuppression,
with one or several of these processes.

pancreatitis, and hepatotox:icity. The dosage

Malabsorptive syndromes have been
of azathioprine can be tapered after several
studied in most detail in dogs, but basic
weeks. Typically, the prednisone is tapered
diagnostic and therapeutic principles are
first (by 25% every 2--3 wk). After prednisone
relevant to other species.

has been tapered to 0.5 mg/kg every other
day without a relapse, then azathioprine is

Physiology: The normal digestive
given every other day. If response to steroids
processes convert polymeric dietary
is poor, even if combined with azathioprine,
nutrients into fom1s (mainly monomers)

cyclosporine can be added at 5--10 mg/kg/
that can cross the luminal surface (brush
day, PO, for at least 8--10 wk. No study has
border) of intestinal absorptive epithelial
been done to compare cyclosporine and
cells (ie, enterocytes). Most digestive
azathioprine. However, one recent study
enzymes are secreted by the pancreas; EPI
suggested that the combination of chloramis thus a major cause of malabsorption.

bucil-prednisolone was more efficient to

Terminal digestion before absorption is
treat chronic enteropathy with concurrent
performed by brush border enzymes, either
protein-losing enteropathy in dogs than the
at the brush border surface of the enteroazathioprine-prednisolone protocol.

cyte in association with transport proteins

Azathioprine is not recommended in cats
for the specific products, or when released
because of sensitivity to adverse effects.

into the intestinal lumen through cleavage

Instead, cats are treated with a combination
by pancreatic peptidases or through loss of
of prednisone and chlorambucil (0.1-0.2
senescent enterocytes.

mg/kg or 1 mg/cat). Clinical signs typically

The main dietary carbohydrates are
improve in 3-5 wk, although 4-8 wk of
starch, glycogen, sucrose, and lactose.

treatment may be needed. A CBC shouJd be

Starch and glycogen are first hydrolyzed by
done every 2 wk to monitor for evidence of
pancreatic amylase to the oligosaccharides
myelosuppression.

maltose, maltotriose, and a-limit dextrins.

Acljunctive treatment may include

These oligosaccharides and ingested
ursodeoxycholic acid in cats ( 10-15 mg/kg/
disaccharides ( sucrose, lactose) ar·e further
day, PO), cobalamine supplementation .

hydrolyzed to monosaccharides by enzymes

(20 mg/kg, SC, every 7 days for 4 wk and then
located on the brush border of the
every 28 days for a further 3 mo) in dogs and
enterocytes. Brush border lactase activity
cats, and other supportive therapy as needed.

declines after weaning, especially in cats,

The response rate to treatment ofIBD is
and animals may become lactose intolerant,
variable. Quality of life tends to be poor, and
especially if the brush border has been
prognosis is guarded. Hypoalbuminemia is a
darnaged by another disease. The final
negative prognostic sign. Prognosis is worse
products of mucosal hydrolysis (glucose,
in cases with severe histologic lesions,
galactose, and fructose) are actively
mucosal fibrosis, eosinophilic enteritis,
transported into the enterocyte by
protein-losing enteropathy, or hypereosinosodium-linked car·rier-111ediated processes, phi.l.ic syndrome. Relapses occur and are most driven by a sodiwn-potassiun1 ATPase.

often precipitated by dietary indiscretion.

Once in the cell, glucose is not used by the
glycolytic pathway but is passed by

MALABSORPTION SYNDROMES
facilitated diffusion via a trar1sport protein
on the basolateral enterocyte membrar1e

Malabsorption is the defective uptake
down a concentration gradient into the
of a dietary constituent resuJting from
extracellular space, ar1d then by diffusion
interference with its digestion or absorpinto the portal venous circulation.

tion, due to either exocrine pancreatic insuf

Protein digestion and absorption follow a
ficiency (EPI) or small-intestinal disease.

similar pattern. Proteolytic enzymes from

Malabsorption typically resuJts in diarrhea,
the stomach and pancreas degrade protein
altered appetite, and weight loss, but a
into a mixture of short-chain oligopeptides,
number of animals ( especially cats) will not dipeptides, and amino acids. Oligopeptides
have overt diarrhea because of the ability of
ar·e further hydrolyzed by brush-border
the colon to conserve water.

peptidases to di peptides and anlino acids

The primary function of the small
that cross the brush-border membrane on
intestine is digestion and absorption of
specific carrier proteins.

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

401

Fat-soluble molecules do not need

Etiology and Pathophysiology:

specific carriers to cross the phospholipid

Malabsorption is a consequence of
bani er of the brush border. However,
interference with mechanisms responsible
intraluminal degradation of large lipids is
for either the degradation or absorption of
essential. Fat in the duodenum stimulates
dietary constituents (see TABLE 7).

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release of cholecystokinin, which, in turn,

Diseases that disrupt the synthesis or
stimulates secretion of pancreatic lipase.

secretion of digestive pancreatic enzymes

After solubilization by bile salt micelles,
cause maldigestion witl1 subsequent
triglycerides are digested by pancreatic
malabsorption, so that the end result is the
lipase to monoglycerides and free fatty
same. An in1portant syndrome is EPI (see
acids. At the enterocyte membrane, the
p 409), which occurs if there is a loss of
monoglycerides and free fatty acids

-85o/<>-900A, of exocrine pancreatic mass. EPI disaggregate from the micelle and are
is characterized by severe maldigestionpassively absorbed into the cell. Released malabsorption of starch, protein, and most
bile acids remain within the lumen and are
notably, fat. In dogs, EPI is most commonly
ultimately reabsorbed by the ileum and
due to acinar atrophy; chronic pancreatitis
undergo enterohepatic recycling. Once
is less common and is seen in older animals,
inside the cell, the monoglycerides and free
and pancreatic hypoplasia is a rare
fatty acids are reesterified to triglycerides
congenital cause. EPI in dogs is often
and incorporated into chylomicrons, which
complicated by secondary antibioticsubsequently enter the central lacteal of the responsive diarrhea, which further disrupts
villus, being delivered to the venous
nutrient digestion and absmption. EPI is
circulation via the thoracic duct. Mediumrelatively uncommon in cats and is most chain triglycerides (C8-C10) may be
frequently due to chronic pancreatitis.

absorbed directly into the pmtal blood,

Intraluminal effects of bacteria can also
providing an alternative route for fat uptake
have important consequences. Bactetial
in case of lymphatic obstrnction, but some
deconjugation of bile salts interferes with
do normally enter the circulation via the
micelle fom1ation, which results in
thoracic duct. Consequently, they are no
malabsorption of lipid. Deconjugated bile
longer recommended in management of
salts and hydroxy fatty acids exacerbate
lymphangiectasia.

diarrhea by stimulating colonic secretion.

•@:i!ii MECHANISMS OF MALABSORPTION

Location

Disease

Mechanism

Lununal

Exocrine pancreatic insufficiency Lack of pancreatic enzymes ( maldigestion)

Antibiotic-responsive diarrhea,

Bacterial activity: bile salt
secondary small-intestinal
deconjugation, fatty acid
bacterial overgrowth
hydroxylation, competition for
cobalanun and nutrients

Mucosal

Inflammatory bowel disease,

Mucosal damage: inflan1rnation,
infectious enteropathies, dietary brush border defects, disturbed sensitivities, neoplastic infiltraenterocyte function, reduction of tion
surface area

Villous atrophy

Reduction in surface area,
immature enterocytes due to
increased cell turnover

Brush border enzyme deficiencies Lactase deficiency, diffuse small-intestinal disease

Postmucosal

Lyrnphangiectasia

Lymphatic obstruction impairs
delivery of chylomicrons

Vasculitis, portal hype1tension

Impaired delivery

402

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

True small-intestinal bacterial overgrowth

This is typified by infection with enter

(SIBO) can be secondary to defective
opathogenic Escherichia coli (which
gastric acid secretion, interference with
specifically cause ultrastructural damage
normal motility or mechanical obstrnction
to micro villi in an attaching-effacing
of the intestine, interference with the
lesion) and by ARD in clogs, which can

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function of the ileocecal valve, and local
cause biochemical damage to the intestinal
immunodeficiency. In other cases, there is
brush border, interfering with enterocyte
no evidence of overgrowth and no defined
function.

cause but a lack of overt mucosal damage.

The main brush border enzyme deficiency

However, a positive response to antibiotic
reported is a relative lactase deficiency,
therapy indicates tl1at the malabsorption is
leading to milk intolerance in adult dogs and
related to bacteria, perhaps in how the
cats. Acquired brush border defects also
innate inunune system (toll-like receptors)

may be seen in tl1e course of generalized
respond to bacterial components. Originally
small-intestinal disease.

called idiopathic SIBO, this syndrome is

Postmucosal obstrnction may be seen
better termed antibiotic-responsive
with lymphatic obstruction ( especially
diarrhea (ARD).

lyrnphangiectasia) and vascular compro

Fat malabsorption may also be seen with
nuse (portal hypertension, vasculitis ).

a deficiency of intraluminal bile salts due to

Intestinal lymphangiectasia causes
cholestatic liver disease, biliary obstrnction,
intestinal protein loss as well as severe
or ileal disease resulting in defective absorµfat malabsorption.

tion of conjugated bile salts.

Usually, in malabsorption a nwnber of

Small-intestinal disease can cause malabnutJ.ients are affected and consequently sorption by reduction of the number or
diarrhea occurs; malabsorption of a single
fw1ction of individual enterocytes. Diffuse
ingredient without any GI signs is rare ( eg,
diseases of the mucosa can result in reduced
selective cobalan1i.n rnalabsorption in Giant
activities of brush border enzymes,

Schnauzers, Australian Shepherds, and
decreased carrier-protein function,

Border Collies). Again, it should be noted
decreased mucosal absorptive swface area,
that the large absorptive capacity of the
and interference with final transport of
colon may prevent overt diarrhea in some
nutJ.ients into the circulation. Weight loss
animals (especially cats) despite significant
may be compounded by reduced nutJ.ient
malabsorption and weight loss.

intake clue to inappetence. In addition, malabsorbecl nutJ.ients exert strong intJ.·aJwninal Clinical Findings: Clinical signs of
osmotic effects that diminish intestinal and
malabsorption are mainly the result of lack
colonic absorption of water and electJ.·olytes,
of nutrient uptake and losses in tl1e feces.

resulting in diarrhea. Tlus may be exacer

The duration, severity, and primary cause
bated if mucosa] clan1age is accompanied by
detem1ine the severity of signs, which
intestinal inflan1mation, which can cause
typically include chronic diarrhea, weight
secretory and pem1eability diarrhea
loss, and altered appetite ( anorexia or

Potential causes of mucosal damage
polyphagia). The absence of diarrhea does
include idiopathic inflammatory-bowel
not exclude the possibility of severe GI
disease (IBD), enteric pathogens ( eg,
disease. Weight loss may be substantial
enteric viruses, pathogenic bacteria,
despite a ravenous appetite, sometimes

Giardia, Histoplasma, Pythium ), dietary
characterized by coprophagia and pica.

sensitivity, ARD, and intestinal neoplasia

Typically, anin1als with malabsorption are

( eg, lymphosarcoma). Histologic changes
systemically well unless there is severe
such as villous atJ.·ophy and infiltration with
inflanunation or neoplasia. Nonspecific
inflan1rnatory cells indicate intestinal
signs may include dehydration, anemia, and
disease but do not identify the tmderlying
ascites or edema in cases of hypoproteincause. For example, lymphocytic-plasmaemia. Tluckenecl bowel loops or enlarged cytic enteritis may be a common response
mesenteric lymph nodes may be palpable,
pattern of the intestinal mucosa to more
especially in cats.

than one provocative agent, particularly
microbial and dietary antigens. Definite

Diagnosis: Chronic diarrhea and weight
associations with parasites, pathogenic
loss are nonspecific signs common to a
bacteria, and dietary sensitivity have been
variety of systemic and metabolic diseases,
demonstrated in dogs, but often the
as well as malabsorption, although,
underlying cause cannot be identified.

typically, systemic diseases cause anorexia.

Mucosa] damage may also occur without

A thorough diagnostic approach in dogs and
obvious changes under light microscopy.

cats with signs suggestive of malabsorption

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

403
is therefore needed to help exclude
is seen more commonly in dogs than cats. In
association with possible underlying
most cases of PLE, serum albun1in and
systemic or metabolic disease. A precise
globulin ai·e both low, but a low albun1in
diagnosis is also important to detennine
alone does not exclude it; inflainmatory
treatment and prognosis.

bowel disease (IBD) and neoplasia are

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The history is particularly important,
rarely associated with hyperglobulinemia as
because it may suggest specific dietary
well as hypoalbun1inemia. Liver enzymes
intolerance, indiscretion, or sensitivity.

(ALT, AST) may be increased as a conse

Weight loss may indicate malabsorption
quence of increased intestinal permeability,
or protein-losing enteropathy (PLE) but
allowing more antigens to reach the liver; in
may also be due to anorexia, vomiting,
such cases, a bile acid stimulation test as
or extraintestinal disease. Small- and
well as ultrasonography should be
large-intestinal diarrhea may be
performed to exclude prin1ary liver disease.

distinguished by a number of features

However, in cats there may be concurrent

(see TABLE 1, p 157). This distinction is IBD and cholangitis. Hypocholesterolemia
more helpful in dogs than in cats, which
may develop with fat malabsorption and is
rarely have exclusively large-intestinal
most notable in lymphangiectasia.

disease. Suspected large-intestinal

Urinalysis is impo1tant to exclude renal
disease in dogs may be further evaluated
causes of hypoalburninemia and/or renal
by colonoscopic biopsy of the large
disease. However, sometimes both may be
intestine. However, if signs of largeseen together ( eg, the familial PLE and intestinal disease are accompanied by
nephropathy of Soft-coated Wheaten
weight loss or large volumes of feces,

Terriers). Hyperthyroidism in cats should be
then there is probably also concurrent
excluded by measuring serwn T, concentrasmall-intestinal disease.

tions. Sero logic tests for feline leukemia and

A thorough physical exainination should
feline inununodeficiency vii.uses should
be performed. Abdominal palpation is
also be performed, not only because both
essential to identify abnormalities, and
may be associated with secondary, chronic
rectal examination is required even when no diarrhea but also because they are large-intestinal disease is suspected, both to
important prognostic factors. Feline
provide a fecal san1ple and possibly to
infectious peritonitis and toxoplasmosis
identify previously unreported melena. ln
have also been described as occasional
older cats, the thyroid should be palpated
causes of chronic diarrhea in cats.

carefully and se1um T, assayed, because

The presence of fat, undigested muscle

1
signs of hyperthyroidism can closely minuc
fibers, or starch in feces may provide
those of malabsorption.

indirect evidence for malabsorption, but

Initial evaluation should include a CBC,
these are unreliable. Feces should be
biochemical profile, urinalysis, fecal
exainined for parasites ( especially
exainination, abdominal ultrasonography
hookwonns and Giardia in dogs and
and, when indicated by clinical signs or

Tritrichomonas and Giardia in cats) and abnormal abdominal palpation, plain
potentially pathogenic bacte1ia (including
radiography. Hematologic correlates in

Salmonella and Campylobacter).

small-intestinal diseases sometimes include

Speciation of Campylobacler isolates by
anemia of chronic blood loss (microcytic,

PCR allows distinction of the pathogenic C
hypochromic) or chronic inflaimnation
jejuni from the more common and probable

( normocytic, nom10chromic ); neutrophilia
coimnensal C upsaliensis. Pathogenic
and/or monocytosis associated with

Escherichia coli are emerging as a
intestinal inflan1mation, infectious
potentially important problem in dogs, but
enteropathies, or neoplasia; eosinophilia
molecular techniques to identify genes
associated with parasitism and eosinophilic
encoding pathogenicity determinants are
enteritis; and lymphopenia that may be
required for diagnosis. Giardia can be
associated with intestinal lymphangiectasia
detected using serial zinc sulfate fecal
in dogs. Lymphocytosis in a dog with
flotations or a commercially available
diarrhea raises the suspicion of hypoad

ELISA; the latter is easier to perform, and its
renocorticism.

sensitivity is better than fecal flotation

Biochemical tests and urinalysis help
perfom1ed by inexperienced personnel.

to exclude systemic diseases that cause

7i'itrichomonas typically causes colitis in chronic diarrhea, most notably hypoadrenocats rather than malabsorption and is best corticism, protein-losing nephropathies,
diagnosed by pouch culture or PCR.

renal failure, and liver disease. Hypopro

Detection of excessive leukocytes on fecal
teinemia frequently is secondary to PLE and cytology may indicate chronic intestinal

404

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
inflammation or the presence of enteric
small-intestinal disease. Folate is absorbed
pathogens. Cytology of rectal scrapings
prirna.iily by the proximal small intestine
may reveal Histoplasma organisms.

Oejunum), whereas cobalan1in is absorbed

Abdominal radiography is more useful
by the distal small intestine (ilewn). As a
when vomiting is present or palpable
result, serum folate concentrations can be

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abnormalities are detected, but ultrasonogdecreased in proximal small-intestinal raphy is an important pa.it of the investigadiseases, serum cobalan1in concentrations tion of most small-intestinal diseases. It
can be decreased in distal diseases, and
can be used to measure intestinal wall
both can be decreased in diffuse enteropathickness, layering, and lwninal diameter thies. Other factors such as the severity,
and to detect other intestinal lesions ( eg,
extent, and duration of a mucosal abnom1almasses, intussusception), mesente1ic ity; dietary intake; and vitamin supplemenlymphadenopathy (in neoplasia and tation also influence these concentrations.

inflanunatory bowel disease), and

In addition, EPI can affect serum folate and
abnormalities in other organs. Mucosal
cobalamin concentrations, and changes in
striations have been associated with
serun1 folate and cobala.inin concentrations
lymphatic dilatation.

are wrreliable for the diagnosis of ARD and

Once obvious dietary, systemic, parasitic,
secondary antibiotic-responsive diarrhea.

and infectious causes of chronic small-intes

The validity of serum folate and cobalamin
tinal diarrhea have been eliminated, the
concentrations as markers of small-intestinext step is differentiation of EPI from nal disease in cats is less clear, but low
intestinal malabsorption; the diagnosis of
serum cobala.inin concentrations may be

EPI is relatively straightforward, whereas
found with both small-intestinal disease and
that of small-intestinal disease is more

EPI. Hypocobalan1inemia is particularly
complex. Nwnerous tests have been used
associated with IBD and alimentary
for dogs and cats with suspected EPI, but
lymphoma and results in metabolic
they are too inaccurate or impractical to be
changes, including methylrnalonic
reconunended. Assay of serum trypsin-like
acidemia, that can lead to anorexia; low
inununoreactivity (TLI) is a highly sensitive
cobalamin concentrations are an indication
and specific test and should be used for
for parenteral supplementation.

diagnosis of EPI. This assay measures

A further indirect approach to detect
trypsinogen, some of which normally leaks
small-intestinal disease is assessment of
from the pancreas into the blood, thereby
intestinal function and penneability by oral
providing an indirect assessment of
administration of test substances that are
functional pancreatic tissue. In EPI,
subsequently measured in blood or urine
functional exocrine tissue is severely
san1ples. Historically, the xylose absorption
depleted and serum TLI c.oncentrations are
test was used to assess intestinal function,
extremely low, clearly distinguishing EPI
but it was insensitive, especially in cats, and
from other causes of malabsorption. This
is no longer used. Measurements of the
test requires a fasted serum sample.

differential absorption of o-xylose/3-o

Species-specific canine and feline TLI
methyl-o-glucose and of intestinal
tests are available.

•
permeability have not been shown to be

The diagnosis of small-intestinal disease
clinically useful. Hydrogen breath testing
is difficult because of limitations of routine
after oral ad.ministration of individual
screening procedures, the need for biopsy,
sugars was considered a sinlple test to
and frequently the absence of diagnostic
detect malabsorption and to assess transit
histologic changes. Bacteriologic culture of
tin1e, but it has also fallen out of favor.

duodenal fluid obtained endoscopically or

Attempts to diagnose ARD by breath
at laparotomy has been used to confinn a
hydrogen or measurement of serum
diagnosis of ARD. However, the exact
unconjugated bile acids were unreliable,
cut-off point at which small-intestinal
because bacterial numbers may not actually
bacterial numbers are considered excessive
be increased in ARD.

is a matter of debate, because numbers> JQ5

IV administration of 51Cr-labeled albumin
total or> 104 obligate anaerobic colony

( or 51CrC13 to label endogenous albumin)

forming units (CFU)/mL may be found in
has been used historically to docun1ent PLE
apparently clinically healthy dogs,
in dogs. Measurement of 3-day fecal
depending on circumstances, including
excretion of this radioactive marker
environment, diet, scavenging, and
provides an estimation of labeled albumin
coprophagia.

and hence protein loss into the intestinal

The assay of serum folate and cobalamin
lumen. However, its use is very limited

(vitamin 812) concentrations can be a
because of the use of radioactive markers.

helpful initial test in assessment of

An alternative approach is the measurement

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS

405
of cx-1 protease inhibitor in the feces. This
descriptive template as a basis for
plasma protein is lost into the intestinal
concordance.

lumen together with albumin, but unlike
albwnin it is an antiprotease and is excreted Treatment: Treatment of malabsorption VetBooks.ir
in the feces essentially intact. Species-speinvolves treatment of the primary cause (if cific assays have been developed. Three
identified), dietary therapy, and managefresh fecal samples passed by spontaneous ment of complications. Management of EPI
evacuation are required; any GI bleeding
in dogs is relatively straightforward (see
invalidates the result.

p 409) and includes feeding a low-fiber

Definitive diagnosis of chronic smalldiet that contains moderate levels of fat intestinal disease typically includes
or highly digestible fat, very digestible
histologic examination of intestinal biopsies carbohydrate, and high-quality protein.

taken by endoscopy or at lapa.rotomy.

Specific treatment involves lifelong

Endoscopy is minimally invasive and allows
supplementation of each meal with
visualization of the mucosa and targeted
pancreatic extract. Powdered extracts
biopsy sampling. However, endoscopic

(1 tsp/10 kg body wt) are preferable to
mucosa! biopsies may not always give an
tablets, capsules, and most enteric-coated
adequate representation of deeper disease
preparations. Fresh or frozen pancreas can
and are limited to the parts of the small
be used as an alternative (100 g/meal for an
intestine (duodenum and sometimes
adult German Shepherd). If the response
proximal jejunum and ileum) that can be
to pancreatic replacement therapy is poor,
visualized via colonoscopy. Endoscopic
secondary antibiotic-responsive diarrhea
biopsy is preferred initially because the risk
may be suspected, and the animal should
of intestinal surgical wound dehiscence
be treated concurrently with oral antibiotcan exceed 10% in debilitated, malnourics for �l mo (see below). Acid suppresished, or hypoproteinemic animals.

sants ( eg, H2-receptor blockers, such as

However, surgery is the preferred option
cimetidine or ranitidine; proton pump
when there is a concern about deeper or
inhibitors, such as omeprazole) may be
extraintestinal disease or a focal lesion. If a
given 20 min before a meal to inhibit acid
laparotomy is performed, multiple elliptical, secretion and to minimize acid degradation longitudinal biopsy san1ples should be
of enzymes in the pancreatic extract, but
collected from the duodenum, jejunum, and
they are expensive and their value is
ilewn; mesenteric lymph nodes should be
questionable. Oral multivitamin supplebiopsied and other organs examined.

mentation should be considered as

Histologic examination of intestinal
supportive therapy, but cobalamin
biopsy specimens can identify morpho

(500-1,000 mcg/wk until normalized)

logic changes in intestinal inflammation
should be given parenterally. Dietary

(including lymphocytic-plasmacytic enterirequirements of cats with EPI can generally tis and eosinophilic enteritis), intestinal
be met by conventional commercial diets,
lymphangiectasia, villous atrophy, and
but pancreatic replacement therapy is still
intestinal neoplasia. The description of
needed, as well as parenteral cobalamin
morphologic abnormalities can provide a
supplementation in cats with low serum
baseline to evaluate response to treatment
cobala.rnin concentrations.

if sequential small-intestinal biopsies are

Effective treatment of small-intestinal
possible. Morphologic abnormalities may
disease depends on the nature of the
also provide prognostic information,
disorder, but therapy may be empirical when
because more severe enteropathies tend to a specific diagnosis cannot be made. In dogs be more difficult to manage. However,
with ARD, a low-fat diet may help by minimizthere may be minimal or no obvious ing secretory diarrhea due to bacterial
abnormalities in certain disorders ( eg,
metabolism of fatty acids and bile salts. Oral

ARD) despite considerable interference
broad-spectrum antibiotic therapy with
with intestinal function. Histologic
oxytetracycline (10-20 mg/kg, tid for 28 days)

descriptions alone provide little informahas been successful. Metronidazole ( 10-20
tion on possible etiology or w1derlying
mg/kg, bid) and tylosin (20 mg/kg, tid) are
mechanisms of damage, which would
effective alternatives; there is rarely a need
clearly assist effective management.

to use other antibiotics, and the nontargeted

Furthermore, inconsistencies in histologic
use of fluoroquinolones should be avoided.

descriptions between pathologists is a

Repeated or longtern1 treatment may be
recognized problem. However, the World
necessary in dogs with idiopathic ARD.

Small Animal Veterinary Association GI

Vitamin supplementation may be helpful,

Standardization Group has published a
particularly for animals with cobalamin

406

DISEASES OF THE STOMACH AND INTESTINES IN SMALL ANIMALS
deficiency. Secondary antibiotic-responsive
be valuable and can minimize the secreto1y
diarrhea. usually resolves with appropriate
diarrhea that is a consequence of bacteria.I
management of the underlying disease, but
metabolism of fatty acids and bile salts.

idiopathic ARD can be difficult to control,

Ora.I prcdnisolone (1 mg/kg, bid for 1 mo,
especially in young Gennan Shepherds,
followed by a reducing dose) is indicated in

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which a.re predisposed to developing the
cases of intestinal disease with a.n obvious
condition.

infla.inma.tory component, such as

Dietary modification is an in1portant
lyrnphocytic-pla.sma.cytic enteritis a.nd
aspect of the management of small-intestinal
eosinophilic enteritis. In more severe cases,
disease in both dogs and ca.ts. Diets generally it may be necessa.iy to add chlora.inbucil contain moderate levels of limited protein

(2-6 mg/m2/da.y, PO, until remission,
sources and highly digestible carbohydrates
followed by drug tapering) in cats or

(to reduce protein antigenicity, reduce
azathioprine (2-2.5 mg/kg/day) in dogs.

osmola.r effects, and improve nutiient

Cats a.i·e often given a.cljunctive metronida.availability) and low to moderate levels of zole ( 10 mg/kg, bid); the beneficial effect of
fat. In addition, they a.re lactose and gluten
meti·onidazole may be a result of a.n inhibition
free; may be fiber-restlicted; and may contain of cell-mediated immune responses as well as increased levels of antioxidants, prebiotics
a.imerobic antibacterial activity. However, the

( eg, fructo-oligosa.ccha.iides ), or omega.-3
value of metronidazole in combination with
fa.tty acids. These additives a.re thought to
prednisolone in the treatment of IBD in dogs
modulate the infla.nunatory response a.i1d
has been questioned.

increase the health of the bacteria.I gut flora

In lymphangiectasia, a severely
and enterocytes. Treatment with an
fat-restricted, ca.!01ie-dense, highly
exclusion diet consisting of a single novel
digestible diet reduces dia.iThea. but tends to
protein source or a hydrolyzed protein
exacerbate weight loss. Supplementation
should be used as tiia.l therapy when dietary
with fat-soluble vitamins is advised, a.nd
sensitivity is suspected. Intestinal infla.inma.additional medium-chain tiiglycerides have tion is sometin1es a manifestation of dietary
been recommended as a.n easily a.bsorba.ble
sensitivity, and an initial exclusion food tiial
fat source that bypasses the lymphatics,
is indicated in mild cases of IBD before other
although this mecha.nism is now doubted.

trea.tinents. Boiled white rice and potato a.re

Prednisone/prednisolone therapy may be
suitable carbohydrate sources, while fish,
beneficial for its anti-infla.inma.tory a.nd
lan1b, or chicken a.re often used as a protein
irrununosuppressive effects, especially if
source, depending on the dietary hist01y.

there is associated lipogra.nulomatous

Cottage cheese, horsemea.t, rabbit, or
lyrnpha.ngitis. The response to trea.tinent is
venison may be acceptable alternatives.

variable; clinical signs may sometimes a.bate

Commercial exclusion diets a.i·e not
for months or even yea.rs, but the longterm
necessa.iy to diagnose food hypersensitivity;
prognosis is grave.

however, they a.re preferred for maintenance

Giardiasis ca.n be tl'ea.ted with metronito reduce potential dietary in1ba.lances.

dazole or fenbendazole, a.nd histoplasmo

Protein hydrolysa.tes may be the most
sis with itraconazole (cats) or ketoconazole
effective diets to detect dietary sensitivity.

( dogs), with or without arnphotericin B.

The response to an exclusion diet is often

In cases of lymphosarcoma, tl'ea.tinent
rapid, but the diet must be fed for at lea.st 3
involves a.n appropriate chemotherapy
and, in a few cases, up to 10 wk before being
regimen, but response is pQor in dogs a.nd
considered a failure. Ora.I prednisolone
in ca.ts with lyrnphobla.stic fom1s. In ca.ts,

(1 mg/kg, bid for� wk, followed by a reductreatinent of small-cell villous lymphoma ing dose) in combination with an exclusion
with oral prednisone a.nd chlora.inbucil is asdiet may be useful in animals in which sociated with prolonged remission.

idiopathic IBD is suspected but dietary
sensitivity has not yet been excluded.

Prognosis: The prognosis in cases of

Trea.tinent of idiopathic inflammatory
ma.labsorption is good if there is a simple
bowel disease should initially attempt to
solution, eg, 85% of cases of EPI respond
elinlinate or control an underlying antigenic
well to enzyme replacement therapy. The
stimulus that may be playing a prima.iy or
prognosis is worse the more severe the
seconda.iy role in the da.inage. Treatinent
small-intestinal pathology. A poorer
should first involve the use of a protein
prognosis has been associated with severe
hydrolysate diet. The diet should comprise
intestinal infla.inrnation, neoplastic disease,
digestible carbohydrate (preferably rice,
severe weight loss, hypoa.lbUOlinemia a.nd
which is most digestible) and high-quality
a.scites (PLE), a.norexia., a.nd hypocoba.laprotein. Restriction of fat content may also minemia.

THE EXOCRINE PANCREAS

407

THE EXOCRINE PANCREAS

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The pancreas has both endocrine and
trauma, such as can be sustained during a
exocrine functions. The exoc1ine pancreas
traffic accident or in cats with high-rise
is made up of pancreatic acinar cells and a
syndrome, can also cause pancreatitis.

duct system that opens into the proximal

Smgery has been considered another risk
duodenum. Pancreatic acinar cells
factor; however, most postsurgical cases of
synthesize and secrete digestive enzymes
pancreatitis are now believed to be due to

( eg, amylase, lipase, and others) or inactive
pancreatic hypoperfusion during anestheproenzyn1es, and zymogens ( eg, trypsinosia. Infectious diseases have been impligen, chymotrypsinogen, proelastase, cated, but the evidence for a cause and
prophospholipase, and others) of digestive
effect relationship is weak in most cases. In
enzymes, which a.re essential for the
dogs, pancreatitis has been reported with
digestion of dietary components such

Babesia canis or Leishmania infection. In as proteins, triglycerides, and complex
cats, Toxoplasma gondii, Amphimerus
carbohydrates. The exocrine pancreas also
pseudofelineus, and feline infectious peritosecretes other essential substances, such as nitis are considered most in1portant.

large an1ounts of bicarbonate, which buffers

Many drugs have been implicated in
gastric acid, intrinsic factor, which is
causing pancreatitis in people, but very few
needed for cobalamin absorption, and
have been confinned in dogs and cats. In
colipase, which is an essential cofactor
general, most drugs should be viewed as
for pancreatic lipase.

potential causes of pancreatitis; cholinesterase inhibitors, calciwn, potassium bromide, PANCREATITIS
phenobarbital, L-asparaginase, estrogen,
salicyla.tes, a.zathioprine, thia.zide dimetics,

Pancreatitis is the most conm1on exoc1ine
and vinca alkaloids are probably the most
pancreatic disease in both dogs and cats.

important.

IL can be acute or chronic, depending on

Many different insults may ultimately
whether the disease has led to permanent
lead to pancreatitis through a common pathchanges of the pancreatic parenchyma, way. Secretion of pancreatic juice decreases
ma.inly atrophy and/or fibrosis. Both acute
during the initial stages of pancreatitis. This
and chronic pancreatitis can be subclinical,
is followed by co-localization of zymogen
mild and associated with vague clinical
granules and lysosomes, leading to
signs, or severe and associated with
activation of trypsinogen to trypsin within
pancreatic necrosis and systemic complicathe co-localized organelles. Trypsin, in tum, tions. Thus a distinction between the two is
activates more trypsinogen and also other
clinically of little significance.

zymogens. Prematurely activated digestive
enzymes lead to local damage of the

Etiology and Pathogenesis: Most
exocrine pancreas with pancreatic edema,
cases of pancreatitis in dogs and cats are
bleeding, inflanm1ation, necrosis, and
idiopathic. However, several 1isk factors
peripancreatic fat necrosis. The ensuing
have been described. Miniature Schnauzers
inflammatory process leads to recrnit:ment
have been identified to be cl.ran1atically
ofWBCs and cytokine production. The
ove1Tepresented in some studies, and it
activated enzymes, and more in1pmtantly,
has been speculated that they may have a
the cytokines circulate in the bloodstream
genetic predisposition similar to that in
and lead to distant complications such as
families of human patients with hereditary
generalized inflammation, disseminated
pancreatitis. Other studies have reported an
intravascular coagulation, disseminated
increased prevalence in Yorkshire Terriers,
lipodystrophy, pancreatic encephalopathy,

Cocker Spaniels, Dachshunds, Poodles, sled hypotension, renal fail me, pulmonary dogs, or other breeds. Dietary indiscretion
fail me, myocarditis, or even multiorgan
is believed to be a conm10n risk factor in
failure.

dogs. Also, hypertriglyceridemia in dogs, if
severe (ie, generally serum concentrations

Clinical Findings: Anorexia(91%),

;,,500 mg/dL), is considered a risk factor for
vomiting (90%), weakness (79%), abdominal
pancreatitis. Hyperadrenocortiscism has
pa.in (58%), dehydration ( 46%), and diarrhea
been cited in some studies as a risk factor

(33%) have been reported as the most
for pancreatitis in dogs. Severe blunt
common clinical signs in dogs with severe

408

THE EXOCRINE PANCREAS
pancreatitis. Clinical signs in cats with
nal ultrasonography is highly operatorsevere pancreatitis are even less specific, dependent, with sensitivities as high as
with anorexia (87%), lethargy (81 %),

35% in cats and 68% in dogs in the most
dehydration (54%), weight loss ( 4 7%),
experienced hands.

hypothermia ( 46%), vomiting ( 46%), icterus

Several diagnostic markers for pancreati

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(37%), fever (190,ii), and abdominal pain
tis have been evaluated in dogs and cats. In

(19%) most commonly repo1ted. Dogs and
general, the clinical usefulness of serum
cats with milder forms of pancreatitis may
lipase and amylase activity is limited in dogs
be subclinical or may have only vague
and even more so in cats. In-clinic tests for
clinical signs, such as anorexia, lethargy, or
the semiquantitative evaluation of serum
clian·hea. The low rate of abdominal pain
pancreatic lipase immunoreactivity are
reported is remarkable given that >900/o of
available. A negative semiquantitative test
hwnan patients with pancreatitis report
suggests that pancreatitis is very w1likely,
abdominal pain, so it is most likely clue to
whereas a positive test suggests pancreatilack of recognition in veterinary patients.

tis. In the latter case, pancreatic lipase
i.nununoreactivity (PLI) concentration

Diagnosis: A history of dietary indiscreshould be measured in a serwn sample and tion combined with vomiting and abdominal evaluated to confirm the diagnosis and to pain may suggest pancreatitis in clogs, but
determine a baseline concentration. This
most cats present with .nonspecific histo1ies
allows use of serum PLI concentration as a
and clinical signs. Findings on CBCs and
monitoring tool for the disease. In both dogs
serwn biochemistry profiles may suggest
and cats, serwn PLI concentration is highly
an inflanunatory disease process but are
specific for exocrine pancreatic function
nonspecific. In clogs, thrombocytopenia and
and is also the most sensitive diagnostic test
neutrophilia with a left shift are common.

for pancreatitis cwTently available (sensitiv

Azotemia and increases in liver enzymes
ity >800/o). However, as for any disease, no
and bilirubin are conunon, nonspecific
test should be used in isolation for diagfindings in both dogs and cats. Thus, while nosis, and all clinical findings should be
basic blood work is not useful for the
used in cortjunction to an·ive at the most
diagnosis of pancreatitis, it is crucial to
appropriate diagnosis.

systematically evaluate the animal and

Pancreatic cytology or histopathology
diagnose systemic complications.

can also be used to definitively diagnose

Abdominal radiographs may show
pancreatitis. Fi.ne-needJe aspiration of the
decreased detail in the proximal abdominal
pancreas is safe and can show acinar cells
cavity and displacement of abdominal
and inflammatory cells, allowing a definitive
organs, but these findings are also
diagnosis of pancreatitis. However, lack
nonspecific and a.diagnosis based on
of inflanunatory cells does not exclude
radiographic findings alone is not reliable.

pancreatitis, because the inflanunatory

However, abdominal radiographs are
infiltrate can be highly localized. Pancreatic
valuable in animals suspected of having
biopsy for histopathologic evaluation may
pancreatitis to exclude other differential
be associated with a higher risk of
diagnoses. Abdominal ultrasonography, if
pancreatitis than fine-needle aspiration ( due
stringent criteria are applied, is highly
to more aggressive pancreatic handling and
specific for pancreatitis, but pancreatic
longer anesthesia). Also, even if the
enlargement and fluid accwnulation around
presence of pancreatitis seems obvious on
the pancreas alone are not sufficient for
macroscopic exan1i..nation of the pancrPas,
diagnosis. A combination of pancreatic
a biopsy specimen should be collected
enlargement, fluid accwnulation around the
because tl1e definitive diagnosis of
pancreas, changes in echogenicity (ie,
pancreatitis requires the identification of an
decreased echogenicity suggesting
inflanunatory infiltrate during 11istopatholpancreatic necrosis, increased echogenicity ogy. Finally, animals with severe pancreatiaround the pancreas suggesting peripancretis are often poor anesthetic risks, and atic fat necrosis, increased echogenicity
exploratory laparotomy or even fine-needJe
suggesting pancreatic fibrosis), and/or a
aspiration may not be justified.

pancreatic mass effect are suggestive of
pancreatitis. Care should be taken not to

Treatment: The mainstay of therapy of
overinterpret findings, because modern
severe pancreatitis is supportive care with
ultrasonographic equipment has a very
fluid therapy, vigorous m011i.toring, and early
high resolution, and pancreatic nodular
intervention to prevent systemic complicahyperplasia may lead to changes in echotions. Fluid therapy should be based on genicity, falsely suggesting the presence of
calculation of degree of dehydration (to be
pancreatitis. Also, the sensitivity of abdomi-
replaced over 4-8 hr if there is no

THE EXOCRINE PANCREAS

409
contraindication), maintenance, and
impact on insulin resistance than glucocorongoing losses ( eg, due to vomiting or ticoids. However, data are limited to date,
diarrhea). In those few cases in which the
and indiscriminate use of glucocorticoids or
cause is known, specific therapy against the
cyclosp01ine in dogs and cats with chronic
inciting cause may be initiated. Antibiotics
pancreatitis should be discouraged.

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are of questionable value and should not be

The prognosis in mild cases is good, but
used routinely. Resting the pancreas is
prognosis in severe cases of pancreatitis is
suggested only if the animal vomits
guarded in both dogs and cats. Systemic
uncontrollably (ie, the animal vomits
complications such as hypothennia,
frequently and violently despite appropriate
acidosis, hypocalcemia, and single- or
antiemetic therapy). In fact, early nutrimultiple-organ failure are considered risk tional support is considered a key compofactors for a poor outcome. It can be nent of successful treatment of human
challenging to identify severe cases early
patients with severe pancreatitis. Also,
during the disease process and prevent
enteral nut1itional support is considered
complications in tl10se animals.

superior to parenteral nutrition. Animals
that vomit should be treated with an
entiemetic, such as maropitant (NKl

EXOCRINE PANCREATIC
antagonist), ondansetron or dolasetron

INSUFFICIENCY

(HT3 antagonists), or in most anin1als a
combination of both. Even animals that do

Exocrine pancreatic insufficiency (EPI) is a
not actively vomit may benefit from such
syndrome caused by insufficient synthesis
antiemetic support, because they may be
and secretion of digestive enzymes by the
nauseated, leading to hyporexia or even
exocrine portion of the pancreas. EPI is less
anorexia. Metoclopran1ide is not considered con1mon than pancreatitis in both dogs and effective as an antiemetic agent and should
cats, but it is the second most common
not be used in these animals. Abdominal
exocrine pancreatic disorder in botl1
pain should be asswned to be present and
species.

treated until contrary evidence is available.

Intermittent meperidine, butorphanol, or

Etiology and Pathogenesis: Pancreatic
buprenorphine may be used in animals with
acinar atrophy is the most common cause of
mild or moderate abdominal pain. Aninlals

EPI in Gem1ai1 Shepherds, Rough Collies,
witl1 severe pain are often treated with a
and Eurasians, whereas chronic pancreaticonstant-rate infusion of an opioid, such as tis is the most con1mon cause in dogs of
morphine, fentanyl, or methadone, or with a
other breeds and cats. Less common causes
combination therapy of fentanyl, ketan1ine,
of EPI in dogs and cats ai·e pancreatic or
and lidocaine. Plasma appears to be helpful
extrapancreatic masses that lead to obstrucin severe cases of canine pancreatitis. It tion of the pancreatic duct. The exocrine
should be given daily until improvement is
pancreas has a remai·kable functional
significant or adverse effects are identified.

reserve, -9QOA, of which must be lost before

Many other treatments have been investiclinical signs of EPI develop. Pancreatic gated in dogs, cats, and people, but
acinar enzymes play an integral role in the
unfortunately none has been shown to be
assimilation of all major macronutrients,
useful.

and a lack of pancreatic digestive enzymes

Aninlals with mild forms of pancreatitis
leads primaiily to maldigestion. However,
should be carefully assessed for the presence animals with EPI also show evidence of of risk factors ( eg, hype1triglyceridemia,
malabsorption, the pathogenetic basis of
hypercalcemia, history of medications that
which is less well understood ( see also
can cause pancreatitis) and concurrent

MALABSORPr!ON SYNDROMES, p 400). The
diseases ( eg, cholangitis, hepatitis,
nut1ients remaining in the intestinal lun1en
inflan1matory bowel disease, diabetes
lead to loose, volunlinous feces ai1d
mellitus ). In dogs, feeding an ultra-low-fat
steatorrhea. The lack of nutrients also
diet is crucial for treatment success. In cats,
causes weight loss and may lead to vitamin
a moderately fat-restricted diet is recomdeficiencies. In anin1als with EPI caused mended. Antiemetic drugs are helpful for
by chronic pai1creatitis, destruction of
animals that may not eat due to nausea.

pancreatic tissue may not be limited to the

If animals do not respond to therapy, a
acinar cells, and concurrent diabetes
trial with prednisone (dogs), prednisolone
mellitus may develop.

( dogs and cats), or cyclosp01ine ( dogs or
cats) may be attempted. Cyclosporine is

Clinical Findings: EPI due to pancreatic
advantageous in animals with concurrent
acinar atrophy is most frequent in young
diabetes mellitus, because it has a smaller
adult Gennan Shepherds but has also been

410

THE EXOCRINE PANCREAS
described in Rough Collies and Eurasians.

I tea.spoon of pancreatic extract. Raw

Dogs and cats with EPI due to other causes
pancreas can be kept frozen for several
are usually middle-aged to older and can be
months without loss of enzymatic activity.

of any breed. Clinical signs most conunonly

Preincubation of the food with pancreatic
reported are polyphagia, weight loss, and
enzymes or supplementation with bile salts

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diarrhea. Vomiting and anorexia are
is not necessary.

observed in some animals and may be a sign

Even though pancreatic enzyme
of concurrent conditions rather than EPI.

supplementation decreases the clinical

The feces are most commonly pale, loose,
signs in almost all animals, nutrient
and voluminous and may be malodorous. In
absorption, especially that of fats, is not
rare cases, watery diruThea may be seen. In
normalized. Feeding low-fat diets to
a small portion of cats with EPI, the high fat
accommodate inlpaired fat digestion has
content of the feces can lead to a greasy
been suggested, but this may further
appearance of the hair coat, especially in
decrease fat assinlilation and lead to
the perianal ru1d ta.ii region.

deficiencies of fat-soluble vitan1ins and/or
essential fatty acids. Some types of dietary

Diagnosis: A serum trypsin-like
fiber interfere with pancreatic enzyme
inrnmnoreactivity (TLI) concentration of
activity, and a diet low in insoluble or

!>2.5 mcg/L in dogs or !>8.0 mcg/L in cats is
nonfermentable fiber should be fed.

diagnostic for EPI. Because digestion of a

Enzyme supplementation alone may not
macronutrient can often be accomplished
lead to complete resolution of clinical signs;
by more than one enzyme, lack of exocrine
cobalan1in deficiency should be considered
pancreatic secretions does not necessarily
as a possible cause. Cobalrunin absorption
lead to clinical signs. For exan1ple, several
depends on adequate synthesis and

Gem1an Shepherds with subclinical EPI
secretion of intrinsic factor. In both dogs
have been reported. These dogs had
and cats, the majority of intrinsic factor is
severely decreased erum TLI concentrasynthesized and secreted by the exocrine tions and a lack of exocrine pancreatic
pancreas, and >80% of dogs and almost all
tissue, but no or only intermittent clinical
cats with EPT are cobalrunin deficient.

signs ofEPI.

Also, cobalrunin deficiency was the only

An assay that measures fecal elastase in
independent risk factor for poor outcome
dogs has been validated. Unfortunately,
in a study of dogs with EPI. Thus, serwn
some healthy dogs or dogs with chronic
cobalrunin and folate concentrations should
small-intestinal disease may have a severely
be routinely evaluated in small animals with
decreased fecal elastase concentration,
suspected EPI. Dogs and cats with
making this test much less reliable than
cobalrunin deficiency, suggested by a
serum TL! concentration.

severely decreased semm cobalan1in
concentration, should be parenterally

Treatment: Most dogs and cats with EPI
supplemented with cobalanlin. Other
can be successfully treated by supplementahypovitaminoses have also been reported in tion with pancreatic enzymes. Powder is
animals with EPI. For exru11ple, vitamin K
more effective than tablets, capsules, and
deficiency leading to a coagulopathy has
especially enteric-coated products. Initially,
been repo1ted in some cats with EPI.

1 teaspoon/10 kg should be given with each

Some anin1als may not respond to
meal for dogs and 1 teaspoon/cat with each
enzyme supplementation a11d cobalan1in
meal for cats. Once the clinical signs have
therapy and likely have concurrent
completely resolved, the dose can be slowly
small-intestinal disease. Aninlals with EPI
decreased until the lowest effective dose
commonly have concurrent small-intestinal
has been reached. However, it should be
dysbiosis and may need antibiotic therapy.

noted that the lowest effective dose can

Inflanrn1atory bowel disease also occurs in
vary between enzyme batches. Oral
some animals with EPI. In those that do not
bleeding has been reported in 3 of25 dogs
respond to therapy, a proton pump inhibitor
with EPI treated with pancreatic enzyme
can also be tried.

supplements; the bleeding stopped in all
three dogs after a dose reduction. Moisten

Prognosis: EPI results from an ineversing the food and pancreatic powder mix ible loss of pancreatic acinar tissue in most
may also decrease the frequency of this
cases, and recovery is rare. However, with
adverse effect.

appropriate management and monitoring,

Fresh pancreas may be a viable alternathese aninlals usually gain weight quickly, tive to the use of powder; 1--3 oz (30-90 g)

pass nonnal feces, and can live a normal life
of raw chopped pru1crea.s can replace
for a nonnal life span.

THE EXOCRINE PANCREAS

411

PANCREATIC NEOPLASMS
cats with pancreatic adenocarcinoma but
may be seen in either species.

Neoplasias of the exocrine pancreas can be

Radiographic findings are also nonspeprimary or secondary and can be classified cific in most cases. Abnormal findings

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as benign or malignant. Most exocrine
include decreased contrast in the cranial
pancreatic neoplasias in dogs and cats are
abdomen suggesting peritoneal effusion,
secondary.

transposition of the spleen caudally, and

Pancreatic adenomas are benign tumors
shadowing in the pyloric region. In some
that are usually singular and can be
cases, abdominal radiographs suggest a
differentiated from pancreatic nodular
cranial abdominal mass. Abdominal
hyperplasia by the presence of a capsule.

ultrasonography generally shows a

Pancreatic adenocarcinoma is the most
soft-tissue mass near the pancreas, but in
common plimary neoplastic condition of
many cases, continuation of the mass with
the exocrine pancreas in dogs and cats but
pancreatic tissue cannot be conclusively
is rare overall in both species.

demonstrated. Also, neoplastic lesions
of neighboring organs may be falsely

Pathogenesis: Benign neoplasms of the
presumed to be of pancreatic origin. Finally,
exocrine pancreas can lead to transposition
animals with severe pancreatitis may show
of organs of the cranial abdominal cavity.

a mass effect in the area of the pancreas on

However, these changes are subclinical in
abdominal ultrasonography that must not
most cases, and the diagnosis is often made
be confused with a pancreatic neoplasia.

as an incidental finding during necropsy.

If peritoneal effusion is present, a san1ple

In rare cases, the neoplastic growth can
should be aspirated and evaluated
obstruct the pancreatic duct and cause
cytologically. However, in most cases
secondary atrophy of the remaining
neoplastic cells do not readily exfoliate into
exocrine pancreas, leading to exocrine
the peritoneal effusion, and no neoplastic
pancreatic insufficiency. Adenocarcinomas
cells are identified on cytology. Fine-needle
may lead to tumor necrosis if the tumor
aspiration or transcutaneous biopsy under
outgrows its blood supply. Tumor necrosis
ultrasonographic guidance can be
causes local inflammation, which can lead
attempted when suspicious masses are
to clinical signs of pancreatitis. Malignant
identified. However, in many cases, the
neoplasms may also spread to neighboring
diagnosis is made at exploratory laparotor distant organs.

omy or necropsy.

Treatment and Prognosis: Pancreatic

Clinical Findings: The presentation of
adenomas are benign and theoretically do
dogs and cats with exocrine pancreatic
not require therapy unless they cause
neoplasia is nonspecific, and many cases
clinical signs due to the effects of an
remain subclinical until late in the disease
intra-abdominal space-occupying lesion.

process. Some animals show clinical signs

However, because the final diagnosis of
suggestive of pancreatitis. Obstructive
pancreatic adenocarcinoma is often made
jaundice may be seen if bile duct obstrucat exploratory laparotomy, a partial tion develops. Clinical signs related to
pancreatectomy should be perfom1ed even
metastatic lesions have also been reported
in cases of suspected pancreatic adenoma.

in some cases of pancreatic adenocarci

The prognosis in these cases is excellent.

noma and may present as lameness, bone

Animals with pancreatic adenocarcinomas
pain, or dyspnea. Finally, paraneoplastic
often present at a late stage of the disease,
alopecia has been reported in cats with
and metastatic disease at the time of
pancreatic adenocarcinoma.

diagnosis is quite common in both dogs and
cats. Common sites for metastasis are the

Diagnosis: Several nonspecific findings,
liver, abdominal and thoracic lymph nodes,
such as neutrophilia, anemia, hypokalemia,
mesentery, intestines, and the lungs, but
bilirubinemia, azotemia, hyperglycemia,
other metastatic sites have also been
and increased hepatic enzyme activities,
reported. In those few cases when gross
have been reported in dogs and cats with
metastatic lesions are not identified at the
pancreatic adenocarcinoma. However,
time of diagnosis, surgical resection of the
results of routine blood tests may be
tumor may be attempted, but clean surgical
unremarkable. Increased serum lipase
margins can almost never be achieved, and
and amylase activities and trypsin-like
owners should be forewarned. Both
inununoreactivity and pancreatic lipase
chemotherapy and radiation therapy have
inununoreactivity concentrations have not
shown little success in human or veterinary
been commonly reported in either dogs or
patients with pancreatic adenocarcinomas.

412

THE EXOCRINE PANCREAS

Thus, the prognosis for dogs and cats with
associated with anesthesia, surgery, and
pancreatic adenocarcinoma is grave.

postoperative care, sw·gery may not be
warranted unless there is clear evidence

PANCREATIC ABSCESSES
of an enlarging mass and/or sepsis in a
medically managed animal.

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By definition, a pancreatic abscess is a
collection of pus, usually in proximity to the

PANCREATIC PSEUDOCYST
pancreas, containing little or no pancreatic
necrosis. Pancreatic abscesses are

A pancreatic pseudocyst is a collection of
considered a complication of pancreatitis,
sterile pancreatic fluid enclosed by a wall
and thus their clinical presentation is
of fibrous or granulation tissue; tl1ese
similar to that of pancreatitis, although most structures are also considered a complicacases are associated with mild chronic tion of pancreatitis. Several cases of
pancreatitis, and clinical signs may be more
pancreatic pseudocysts in dogs and cats
vague. A bacterial infection may or may not
have been described. Clinical signs are
be present, but almost all cases rep01ted in
usually nonspecific and mimic tl10se of
small animals have been sterile. Increased
pancreatitis. On abdominal ultrasonograserum trypsin-like i.nununoreactivity and phy, a cystic structure in close proxin1ity to
pancreatic lipase irnmu.noreactivity
the pancreas can be identified. Aspiration of
concentrations have not been reported in
the pseudocyst is relatively safe and should
dogs or cats with a pancreatic abscess, but
be attempted for diagnostic and therapeutic
anecdotal reports suggest that both serum
purposes. Fluid from a pancreatic
parameters are increased in these animals.

pseudocyst should have few cells and

Surgical drainage and aggressive antimicroshould not contain any evidence of bial therapy are the treatments of choice in
inflammation. Pancreatic pseudocysts can
hwm1.11 patients with an infected pancreatic
be treated medically or surgically. Medical
abscess. Dogs and cats may also respond
management involves ultrasonographicfavorably to surgical drainage. However, in guided percutaneous aspiration and close
one repo1t, only slightly more than 500/o of
monitoring of the size of the pseudocyst.

anin1als swvived the inunediate postsurgi

Surgery may be indicated in animals witl1
cal period. Thus, given tl1e mixed results
persistent clinical signs or when the
and risks, difficultjes, and expenses
pseudocyst fails to regress over time.

GASTROINTESTINAL PARASITES

OF SMALL ANIMALS

SPIROCERCA LUPI

Clinical Findings: Most dogs with S Lupi infection show no cQ.llical signs, but when

(Esophageal worm)

signs are present, they most conunonly
include weight loss, coughing, and dyspnea.

AdultSpirocerca Lupi are bright red worms, When the esophageal lesion is very large 40 mm (male) to 70 nun (female) long,

(usually when it has become neoplastic),
generally located within nodules in the
the dog has difficulty swallowing and may
esophageal, gastric, or aortic walls.

vomit repeatedly after trying to eat. Such

Infections are seen in southern areas of
dogs salivate profusely and eventually
the USA as well as in many tropical and
become emaciated. In addition, dogs may
subtropical regions worldwide (eg, Greece,
develop thickening of tl1e long bones

India, Israel, Japan, South Africa). Dogs are
characteristic of hypertrophic osteopathy.

infected by eating an intermediate host

These clinical signs are suggestive of

(usually dw1g beetle) or a transport host
spirocercosis with associated neoplasia in

(eg, chickens, reptiles, or rodents). The
regions where the parasite is prevalent.

larvae migrate via the wall of the celiac

Occasionally, a dog dies suddenly as the
artery to the thoracic aorta, where they
result of massive hemorrhage into the
usually remain for -3 mo. Eggs are passed
thorax after ruptw·e of the aorta damaged
in feces -� mo after infection.

by tl1e developing worms.

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

413

Lesions: The characteristic lesions are

2 wk apart; 0.5 mg/kg/day, PO, for 42 days;
aneurysm of the thoracic aorta, reactive

0.8 mg/kg, SC, two doses l wk apart;
granulomas of variable size around wonns
additional treatments may be required), and
in the esophagus, and exostoses that bridge
with ivennectin (0.6 mg/kg, SC, two doses
between ventral aspects of thoracic

2 wk apart) combined with prednisolone

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vertebrae. Esophageal sarcoma, often with

(0.5 mg/kg, PO, bid for 2 wk and then
metastases, is sometin1es associated (appartapered), although none of these treatments ently causally) with S lupi infection,
is approved. The specific breed toxicity
particularly in hound breeds. Dogs with
associated with ive1rnectin in Collies and

Spirocerca-related sarcoma often develop
other herding dog breeds also occurs with
hypertrophic osteopatl1y (seep 1205).

dora.mectin. Surgical removal usually is
tmsuccessful because of the large areas

Diagnosis: Diagnosis can be made by
of the esophagus involved.

demonstrating the characteristic small

(11-15 x 30--38 µm), elongated eggs (by

PHYSALOPTERA SPP

NaN03 [specific gravity 1.36] or sugar
flotation) that contain larvae in tl1e feces.

(Stomach worm)

However, eggs are sporadically voided in

Several species of these stomach nemafeces and can be difficult to find. Gastrostodes of dogs and cats are seen throughout copy occasionally reveals a nodule or an
the world. They are usually finnly attached
adult worm. A presw11ptive diagnosis can be to the gastric mucosa. The males are -30 mm made by radiographic examination when it
long, and the females -40 mm. The eggs are
reveals dense masses in the esophagus; a
oval, 42-53 x 29-35 im1, thick-shelled, and
positive-contrast bariwn study may help
la.rvated.

define the lesion. CT is an additional useful

Encysted infective larvae of Physalop
diagnostic tool, with a higher level of
tera spp have been found in several species sensitivity than thoracic radiography for
of insects, including beetles, cockroaches,

S lupi. However, while CT generally
and crickets. Mice and frogs may be
provides more information on the location
paratenic hosts. After the dog or cat ingests
and seve1ity of the infection than radiothe inte,rnediate or paratenic host, graphs, the specificity of the findings for
development of larvae to adults is direct.

S lupi is currently unclear.

Although infections are often subclinical,

Many infections are not diagnosed until
these parasites may cause gastritis that can
necropsy. The granulomas vary greatly in
result in vomiting, anorexia., and dark feces.

size and location in the esophagus but

Bleeding, ulcerated areas remain on the
usually are sufficiently characteristic to be
gastric mucosa when the parasites move to
diagnostic, even if the wom1s are no longer
other locations; in heavy infectioFts, anemia
present. Worms and granulomas may be
and weight loss may develop. Gastroscopy
present in the lungs, trachea, mediastinun1,
is the most efficient means of diagnosis, and
stomach wall, or other abnormal locations.

in1mature wom1s are often found in the

Healed aneurysms of the aorta persist for
vomitus of puppies or kittens. The eggs are
the life of the dog and are diagnostic of
difficult to find in feces, because they do not
previous infection. When sarcomas are
readily float; eggs are best detected by fecal
associated with the infection, the esophasedimentation. ln cats, pyrantel pa.moate geal lesion usually is larger and often

(5 mg/kg, PO, two doses 2-3 wk apart; 20
contains cartilage or bone; metastases
mg/kg, PO, once) and ivem1ectin (0.2 mg/kg,
frequently are present in the lungs, lymph

SC or PO, two doses 2 wk apart) can be used
nodes, heart, liver, or kidneys.

for Physaloptera infections. ln dogs,
fenbendazole (50 mg/kg/day, PO, for 3 days),

Treatment and Control: ln endemic
pyrantel pa.moate (5 mg/kg, PO, two doses
areas, dogs should be prevented from eating

2-3 wk apart; 15 mg/kg, PO, two doses
dung beetles, frogs, mice, lizards, etc, and

2-3 wk apart; 20 mg/kg, PO, once), and
not fed raw chicken scraps. ln Europe,
ivermectin (0.2 mg/kg, SC or PO, two doses
monthly treatment with topical moxidectin/

2 wk apart) can be used. None of these drug
imidacloprid is approved for use in dogs as a regin1ens is approved for treatment of preventive for S lupi infection. Treatment

Physaloptera in either dogs or cats.

of clinical cases is often not practical.

However, efficacy has been demonstrated

OLLULANUS SP
with doran1ectin (0.2 mg/kg, SC, three doses
at 2-wk intervals; 0.4 mg/kg, SC, six doses at

OUulanus lricuspis is a small worm, �l mm

2-wk intervals; 0.5 mg/kg, SC, two doses
long, tl1at infects several animal species,

414

GASTROINTESTINAL PARASITES OF SMALL ANIMALS
typically cats and other felicls, and
of concwTent seconclai-y infections, tllere is
occasionally induces a mild erosive or
little or no fever. Usually in advanced stages,
catanhal gastritis. Vomiting minutes to a
there is shallow, rapid breatlling and fever,
few hours after eating is a common sign.

and the prognosis is grave. Autoinfection

The female wom1s are viviparous, so
may be induced by tile use of corticosteroids

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massive infections can build up endogor oilier factors tllat affect immtmocompeenously. Transmission is via vomitus.

tence. There may be larvae in tissues, and

Diagnosis is by microscopic demonstration
tllese dogs are more likely to die. At
of larvae ( -500 µm) or adult worms in
necropsy, there can be evidence of
vomitus or stomach contents. The use of a
verminous pneun1onia witll large ai·eas of

Bae1marm apparatus enables the separation
consolidation in the lungs as well as mai·ked
of the wom1s from ingesta, after which they
enteritis witll hemonhage, mucosal
are easier to observe. Parasites are rarely
exfoliation, and much secretion of mucus.

seen in feces, because they are usually
digested before being passed. Therapeutic

Diagnosis: First-stage larvae ( -380 µrn
efficacy in cats has been demonstrated with
long) are identified by direct nlicroscopic
fenbenclazole (20-50 mg/kg/clay, PO, for
evaluation of a small quantity of feces.

3 clays) and levanlisole (5 mg/kg, SC, once),

Usually, the Bae1marm technique is used to
although tl1ese are not approved treatments. sepai·ate laivae from fecal material. It is important to use fresh fecal material

STRONGYLOIDES SP
obtained from an infected dog so tile larvae
can be easily differentiated from hookwonn

Strongyloides stercoralis is a small, slender laivae or free-living soil nematodes.

nematode that when fully matme is -2 mm

Occasionally, eggs (50-60 x 30-35 µm) may
long, located at the base of ilie villi in the
be identified by flotation of fresh feces.

anterior half of the small intestine of dogs

Adult female wom1s can be identified by
and cats. The worms are almost transparent
scraping the mucosa of tile small intestine.

and all but impossible to see grossly at

They are only -2 mm long, but tile presence
necropsy. Usually, infections are associated
of eggs in tile uterus easily differentiates
with wann, wet, crowded, unsanitary
them from laivae of other nematodes.

housing. The species found most often in
clogs is identical to that found in people.

Treatment and Control: Poor sanitation

The parasitic worms are all females. The
and mixing of susceptible witll infected
eggs embryonate rapidly, and most laivae
dogs can lead to a rapid buildup of the
hatch before being passed in the feces.

infection in all clogs in a kennel or pen. Dogs

Under appropriate conditions of waimth
witil diarrhea should be promptly isolated
and moistme, development in tl1e environfrom dogs that appear healtlly. Direct ment is rapid; the third larval stage may be
sunlight, increased soil or surface temperareached in little more than a day. Some of tures, and desiccation ai·e deleterious to all
these larvae develop into infective filarifom1 free larval stages. Thorough washing of larvae; others develop into free-living
wooden and impe1vious surfaces witil
wonns iliat mate and produce progeny
steam or concentrated salt or lime
sinlilar to that of the parasitic female. The
solutions, followed by rinsing witil hot
filarifom1 larvae penetrate the skin but also
water, effectively destroys the parasite.

may infect a host via ingestion. Transmain

Because the disease in people can be
mai-y trat1Snlission is possible. Progeny
serious, caution should be exercised when
may be shed in the feces 7-10 days after
handling infected clogs. The disease in
infection. Autoinfection caused by larvae
people (as in dogs) is much more likely to
that developed to the infective stage within
be severe if tl1e person is immunosuptl1e GI tract can result in infections in which pressed.

dogs shed laivae for lengthy periods.

Wections in clogs can be treated with
ive1mectin (0.2 mg/kg, SC or PO, once, with

Clinical Findings: The presence of clinical
a second dose 4 wk later; 0.8 mg/kg, PO,
signs indicates that a heavy infection has
once), fenbendazole (50 mg/kg/day, PO, for
been building up for some weeks. A

5 days, repeated 4 wk later), or tlliabenclabloo d -streaked, mucoid dianhea, usually zole (100-150 mg/kg/clay, PO, for 3 days,
seen in young anin1als during hot hw11id
repeated weekly until laivae are not
weather, is characteristic. Emaciation is
detected in feces-toxicity may be seen
often prominent, and reduced growth rate
with tllis regimen). ln cats, fenbenclazole
may be one of the first signs. Appetite usually

(50 mg/kg/clay, PO, for 3 days) can be used.

is good, and the dog is normally active in the

These are not approved regimens in eitller
earlier stages of the disease. In tile absence
cats or clogs. ln all animals, feces should be

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

415
examined regularly for at least 6 mo after
these patent infections appears to be
treatment to confirm efficacy.

associated with maturation of affested
laivae in the bitch, which migrate to the

ROUNDWORMS
intestine via the lungs. Patency may also
occur as a result of ingestion and matura

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The large roundworms (ascaridoid
tion of larvae that are passed in the feces of
nematodes) of dogs and cats are conunon,
puppies.

especially in puppies and kittens. Of the

After ingestion of infective eggs, larvae of
tlu-ee species Toxocam canis, Toxascaris
ascaridoid nematodes may migrate into the
leonina, and Toxocara cali, the most tissues of many animals and thus provide an
important is Tcanis, not only because its
alternative source of infection, particularly
larvae may migrate in people (as do larvae
for cats and wild carnivores. Such migration
of T cali), but also because infections are also occurs if larvated eggs of To.xocara spp generally common and may impact puppy
are swallowed by people. Most hun1an
health. Also, fatal infections may occasioninfections ai·e asymptomatic, but fever, ally be seen in young pups. T leonina is seen persistent eosinophilia, and hepatomegaly in adolescenVadult dogs and cats. These

(sometimes with pulmonary involvement)

species also infect wild carnivores,
may occur, resulting in a condition known
especially those in zoos or other captive
as visceral larva migrans. Rarely, a laiva
settings.

may settle in the retina and impair vision,

In puppies, the usual mode of infection
resulting in a condition known as ocular
with T canis is transplacental transfer.

larva migrans.

If pups <3 mo old ingest embryonated

The life cycle of T cal'i is similai· to that of infective eggs, the hatched larvae penetrate

T canis, except that no prenatal infection
the intestinal mucosa, reach the lungs via
occurs. Fwthermore, transrnainmary
the liver and bloodstream, are coughed up,
transmission appears to occur only when
swallowed, and mature to egg-producing
queens acquire infection during late
adults in the small intestine. However, when
gestation. Thus, overall, this route of
infective eggs of T canis are swallowed by
infection appears to play a minor role in
older dogs, the larvae hatch, penetrate the
tra11Smission. With T leonina, migration is intestinal mucosa, and migrate to the liver,
restricted to the intestinal wall so that
lungs, muscles, connective tissue, kidneys,
neither prenatal nor transmammary
and many other tissues, where development transmission occurs.

is arrested. In pregnant bitches, these
dom1ant larvae mobilize and migrate into

Clinical Findings and Lesions: The first
the developing fetus; they can be fow1d in
indication of infection in young animals is
the intestine of puppies as early as 1 wk
lack of growth and loss of condition.

after birth. Some larvae migrate to the

Wected animals have a dull coat and often
mammary gland, so pups may also be
are "potbellied." Wom1s may be vomited
infected via the milk. During this perinatal
and are often voided in the feces. In the
period, the inununity of the bitch to ascaricl
early stages, migrating larvae may cause
infection is partially suppressed, and
an eosinophilic pnewnonia, which can be
substantial nwnbers of eggs may be passed
associated with coughing. DiaiThea with
in the feces of the bitch. Development of
mucus may be evident.

In puppies with severe infections,
venninous pnewnonia, ascites, fatty liver,
and mucoid ente1itis are common. Cortical
kidney granulomas containing larvae may
be seen.

Diagnosis: Wection in clogs and cats
is diagnosed by detection of eggs in
feces. Distinguishing the spherical,
pitted-shelled eggs of Toxocara spp

(T canis 80-90 x 75 µm; T cali 65 x 75 µm) from the oval, smooth-shelled eggs of

Toxascaris leonina (75-85 x 60-75 µm) is
important because of the public health

Toxocara can is ova (larger structures) and significance of the former.

Cystoisospora oocysts (smaller structures).

Courtesy of Dr. Andrew Peregrine and Ontario

Treatment and Control: In dogs,

Veterinary College.

compow1ds approved for treatment of

416

GASTROINTESTINAL PARASITES OF SMALL ANIMALS
row1dwom1 infections include fenbendaparticulaJ.·ly children, exposed to potentially zole, milbemycin, moxidectin, piperazine,
contaJ.Uinatecl animals or areas.

and pyrantel (see TABLE 8). In Europe, selan1ectin is approved to treat T canis

Baylisascaris in Dogs

VetBooks.ir
infections with a single dose, whereas in

Canada approved treatment requires two

The raccoon roundworm, Baylisascaris
doses 1 mo apaJ.t. Preventive prograJ.Us for
procyonis, is a common infection of
heaJ.tworm infection using milbemycin,
raccoons in parts of North America and
m1lbemycin/lufenuron, milbemycin/

Europe. Adult parasites reside witllin the
praziquantel, milbemycin/spinosad,
small intestine of raccoons and occasionally
moxidectin/imidacloprid, ivem1ectin/

111 the small mtestine of dogs. It is thought
pyrantel, or ivermectin/pyranteVpraziquanthat dogs become infected via ingestion tel also control intestinal ascarid infections.

of infective eggs or paratenic hosts ( eg,

In addition, selaJ.nectin is approved for this
rodents, rabbits, birds).

indication in some countries but not in the

Ingestion of infective eggs results in

USA (see TABLE 8).

visceral and neural larva migrans in many

Drugs approved for treatment of ascaricl
species, including people. As a result, the
infections in cats include emoclepsicle,
paJ.·asite is a significaJ.1t zoonotic concern.

fenbenclazole, milbemycin, moxiclectin,

Clinical disease has not been reported in
p1perazme, pyrantel, and selan1ectin ( see
clogs with intestinal infections. However,
signs 31.·e likely to be similar to those of

TABLE 9). HeaJ.twonn-preventive progran1S
that use milbemycin, milbemycin/praziquan

T canis infections. In contrast, severe or
tel, moxiclectinfuniclaclop1icl, or seiarnectin
fatal neural laJ.va rnigraJ.1S has occasionally
also control ascaricl infections in cats (see
been repo1tecl in dogs.

Patent intestinal infections appear to

TABLE 9).

Environmentally resistaJ.1t larvatecl eggs
occur uncommonly in clogs. However it is
on the ground and somatic larvae in the
likely that such infecti011S are undercliagbitch are the main reservoirs of infection.

nosed; the eggs of B procyonis are simiJ31.·

Pe1i.natal transmission of infection can be
in appearance to those of T can is, except
greatly reduced by treating bitches with
they are slightly smaller (63---75 x 53-60 µm)

1) daily doses of fenbendazole (25 mg/kg,
and darker in color. Eggs of B procyonis

PO) from day 40 of gestation to day 2 after
may be fotmd in dog feces as a result of
whel
ingestion of raccoon feces; shedding of such

?ing (approved in the UK), 2) ivermectm (0.3 mg/kg, SC) on clays 0, 30, eggs should cease within 1-2 days.

and 60 of gestation, and 10 days after

Adult B procyonis and T canis passed in whelping, 3) ivennectin (0.5 mg/kg) on
feces CaJ.1 be difficult to differentiate· female
days 38, 41, 44, and 47 of gestation or
parasites should be dissected, and the eggs

4) ivennectin (1 mg/kg) on days 20 and 42
exan1inecl for identification.

of gestation; these uses of ivennectin are

Because of the zoonotic potential of
extra-label. Otherwise, to minimize egg

B procyonis eggs, it is in1portant that patent output, pups should be treated as early as
infections in dogs are diagnosed promptly
possible; ideally, treatment should be given
and that appropriate treatment adminis2 wk after birtl1 and repeated at 2-wk tered inunediately. Ivennectin/pyrantel and
intervals to 2 mo of age, and then monthly
milbemycin oxime/lufenuron at approved
to 6 mo of age. Nursing bitches should be
dosages have been shown to exhibit
treated at the saJ.ne times as puppies. In
significant activity against intestinal
cats, perinatal traJ.1S1nission can be greatly
infections in dogs with cure rates of lOOOA,
reduced by treating queens with a single
and 75%, respectively, after treatment with a
close of emoclepsicle/praziquantel spot-on in
single dose. However, these are not
the last week of pregnancy. Kittens should
approved treatment protocols. Dogs should
be treated with an appropriate anthelmintic
be confined and feces/parasites collected
at 3, 5, 7, and 9 wk of age, and then monthly
and disposed of for at least 3 days after
to 6 mo of age. Nursing queens should be
treatment.

treated at the saJ.Ue time as kittens. In other
animals, the appropriate frequency of

HOOKWORMS
preventive treatment for roundwom1s
should be based on a risk assessment of

Ancylostoma caninum is the principal
the animal's environment.

cause of canine hookworm disease in most

Because the eggs adhere to many
tropical and subtropical areas of the world.

surfaces and become mixed in soil and dust

A tubaeforme of cats has a similar but more st1ict hygiene should be observed by peopl;, sparse distiibution. A braziliense of dogs

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

417
and cats is sparsely distributed from Florida
intestine; activation may occur after
to North Carolina in the USA. It is also found removal of adult worms from the intestine.

throughout Central and South America and

Africa. A ceylanicum of dogs, cats, and

Clinical Findings: An acute normocytic,
people is widely distributed throughout
normochromic anemia followed by

VetBooks.ir

Asia, the Middle East, and parts of South
hypochromic, microcytic anemia in young

America. Uncinaria stenocephala is the
puppies is the characteristic, and often fatal,
principal canine hookworm in cooler
clinical manifestation of A caninum
regions; it appears to be the predominant
infection. Surviving puppies develop some
canine hookworm in Canada and the
inimunity and show less severe clinical
northern fringe of the USA, where it is
signs. Nevertheless, debilitated and
primarily a fox parasite. U stenocephala
malnourished animals may continue to be
also is seen in cats. A caninum males are
w1thrifty and suffer from clu·onic anemia.

-12 mm long, females, -15 mm; the other

Mature, well-nourished dogs may harbor a
species are somewhat smaller. The infective
few worms without showing signs; they are
la.ivae of canine hookworms, particularly
of ptimary concern as the direct or indirect
those of A braziliense, may penetrate and
source of infection for pups. Diarrhea with
wander under the skin of people and cause
dark, tarry feces accompa.ilies severe
cutaneous larva migrans.

infections. Anemia, anorexia, emaciation,

The elongate (>65 µm), thin-walled,
and weakness develop in clu·onic disease.

hookworm eggs in the early cleavage stages

(2--8 cells) are first passed in the feces

Lesions: Anemia results directly from the

15--20 days after infection; they complete
bloodsucking and the bleeding ulcerations
embryonation and hatch in 24-72 hr on
that result when A caninum shift feeding
warn1, moist soil. Transmission may result
sites. The an1ount of blood loss due to a
from ingestion of infective la.ivae from the
single worm in 24 hr has been estimated to
environment and additionally, in the case of
be up to 0.1 rnL. There is no intetierence

A caninum, via the colostrun1 or milk of
with erythropoiesis in uncomplicated
infected bitches. Infections with
hookworn1 disease. The liver and other

A
caninum, A braziliense, A tubaeforme, or
organs may appear ischemic, and some fatty

A ceylanicum can also result from la.ival
infiltration of the liver may occur. Hemorinvasion through the skin, but this route is rhagic enteritis with a swollen intestinal
of little significance for U stenocephala.

mucosa that shows red, small ulcers and

Skin penetration in young pups is followed
attached worms is usually seen in acute,
by migration of the la.ivae through the blood fatal cases. A braziliense, A tubaeforme, to the lungs, where they are coughed up and

A ceylanicum, and U stenocephala are not swallowed to mature in the small intestine.

avid blood feeders, and anemia rarely

However, in animals >3 mo old, A caninum
develops. However, hypoproteinemia:is
la.ivae, after migration through the lungs,
characteristic, and serum seepage around
are arrested in the somatic tissues. These
the site of attaclunent in the intestine may
arrested la.ivae a.i·e activated during
reduce blood protein by> lOOAi.

pregnancy, then accw1mlate in the
ln dogs, dermatitis due to la.ival invasion
ma.Illmary gla.i1ds. Arrested development
of the skin may be seen with any of the
may also occw· in the mucosa of the small
hookworn1s but has been seen most
frequently in the interdigital spaces with

U stenocephala; skin infections with

U stenocephala ra.i·ely mature. Pnewnonia
and lung consolidation may result from
overwhelming infections in pups.

•

Diagnosis: The cha.i·acte1istic thinshelled, oval eggs are easily seen on flotation of fresh feces from infected dogs and cats

•

(Ancylostoma spp 52-79 x 28--58 µm;

Uncinaria sp 71-92 x 35--58 �trn). Acute
anemia and death from infections acquired

• via milk may be seen in young pups before

0
eggs are passed in tl1eir feces, ie, as early as

1-2 wk of age.

Hookworm eggs of Ancylostoma (smaller)

and Uncinaria (larger) spp. Courtesy of Dr. Andrew Treatment and Control: Bitches should

Peregrine and Ontario Veterinary College.

be free of hookworms before breeding and

418

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

DRUGS FOR INTESTINAL HELMINTHS OF DOGS APPROVED IN THE

USA AND UK

Drug or Drug

Dosage

Route of

Combination

(mg/kg)

Administration Helminths Active Againsta

VetBooks.ir

APPROVED ONLY IN USA

Fenbendazole

50 , daily for

PO

Toxocara canis, Toxascaris

3 days
leonina, Ancylostoma
caninum, Uncinaria steno-
cephala, Trichuris 'l!Ulpis,

Trichuris pisiformis

Epsiprantel

5.5

PO

D caninum, T pisiformis

Milbernycin oxirne 0.5

PO

T canis, T leonina, A caninum,

T'l!Ulpis

Milbernyci..n oxirne 0.5/30

PO

T canis, T leonina, A caninum,

+ spinosad

Tvulpis

Moxidectin

0.17

SC

A caninum, U stenocephala

Piperazine

48-66b, d

PO

T canis, T leonina

( various salts)

Praziquantel

5---12.5

PO

D caninum, T pisiformis,

Echinococcus granulosusc,

E multilocutarisc

5---11.4

SC,IM

D caninum, T pisiformis,

E granulosus, E multilocitlaris

Pyrantel pa.moate 5 (10 for

PO

T canis, T leonina, A caninum,
dogs s2.3 kg)

U stenocephala

Iverrnectin +

0.006/5

PO

T canis, T leonina,A caninum,
pyrantel parnoate

A braziliense, U stenocephala

Praziquantel +

5/5

PO

T canis, T leonina, A caninum,
pyrantel parnoate ·

A braziliense, U stenocephala,

D caninitm, T pisiformis

Praziquantel +

5/5/25

PO

T canis, T leonina, A caninum,
pyrantel pan1oate

U stenocephala, T'l!Ulpis,

+ febantel

D caninum, T pisiformis,

E granulosus, E multilocularis

Praziquantel +

5/5/0.006

PO

T canis, T leonina,A caninum,
pyTantel parnoate

A braziliense, U stenocephala,

+ ivermectin

D caninum, T pisiformis

APPROVED ONLY IN UK

Fenbendazole

100; 50, daily

PO

T can is, T leonina, Ancylos-
for3 days
toma spp, Uncinaria spp,

Trichuris spp, Taen ia spp

Praziquantel

5

PO

D caninum, T pisiformis,

Taen'ia multiceps, T hydati-
gena, T ovis, E granulosus,

E multilocularis

Selarnectin

6

Topical

Tcanis

Febantel +

15/14.4

PO

T canis, T leonina, A caninum,
pyrantel ernbonate

U stenocephala, T vulpis

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

419

DRUGS FOR INTESTINAL HELMINTHS OF DOGS APPROVED IN THE

USA AND UK (continued)

Drug or Drug

Dosage

Route of

VetBooks.ir

Combination

(mg/kg)

Administration Helminths Active Againsta

Milbemycin ox.ime 0.5/5

PO

T can is, T leonina, A caninum,

+ praziquantel

T vulpis, D caninum, Taenia
spp, Echinococcus spp,

Mesocestoides spp

Praziquantel +

5/14.4/15

PO

T canis, T leonina, A caninum,
pyrantel embonate

U stenocephala, Tvulpisc,

+ febantel

D caninumc, Taenia spp

(T hydatigenac, T pisiformisc),

Echinococcus sppc (E granulosusc, E multilocularisc) Praziquantel +

5/5/20

PO

T canis, T leonina, A caninum,
pyrantel embonate

U stenoceplwla, Tvulpis, D cani

+ oxantel
num, Taenia sppc (Taenia ovisC,
embonate

T pisif<nmisC, T hydatigenaC,

T multicepsc), Echinococcus
sppc (E granuloS1tsC, E multilocularisc), Mesocestoides sppc APPROVED IN BOTH USA AND UK

Milbemycin ox.ime 0.5/10

PO

T canis, T leoninad, A cani

+ lufenuron
num, T vulpis

Moxidectin +

2.5/10

Topical

T canis, T leonina, A caninum,
imidacloprid

U stenocephala, Tvulpis,

Spirocerca litpi•
a Many of these drugs are also approved for use against other types of parasites ( eg, fleas, heartwonn) not listed here.

b Repeat in 10-20 days
c Only some products
c1 Only in the USA

• Only in the UK
kept out of contaminated areas during
followed by a high-protein diet w1til the Hgb
pregnancy. Sanitary quarters should be
level is normal. Heartworm prevention with
provided for whelping and nursing.

products containing milbemycin control

Concrete runways that can be washed at

A caninum, whereas ivermectin/pyrantel,
least twice a week in warm weather are
ivermecti.n/pyrantel/praziquantel, moxidecbest. Sunlit clay or sandy rnnways can be tin, and moxidectin/imidacloprid control
decontaminated with sodium borate

A caninum and U stenocephala. Herut

(1 kg/2 m2).

worm preventives containing pyrantel also

In dogs, fenbendazole, moxidectin, and
have activity againstA braziliense (see
pyrantel are approved for treatment of

TABLE 8) and are approved for this purpose.

A caninum and U stenocephala infections.

Finally, the ir\jectable fonmtlation of

Milbemycin is also approved for treatment
moxidectin for heartworm prevention in
of A caninum infections (see TABLE 8).

dogs also has significant efficacy against

Nitroscanate is also approved for both
infection with A caninum and U steno
hookworms at 50 mg/kg in some countries
cephala for at least 3 mo. For A ceylani

( eg, Canada). When anemia is severe,
cum, the combination product containing
chemotherapy may have to be supported
pyrantel embonate/febantel/praziquantel
by blood transfusion or supplemental iron,
is approved for treatment in Australia.

420

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

DRUGS FOR INTESTINAL HELMINTHS OF CATS APPROVED IN THE

USA AND UK

Drug or Drug

Dosage Route of

VetBooks.ir

Combination

(mg/kg) Administration Helminths Active Againsta APPROVED ONLY IN USA

Epsiprantel

2.75

PO

Dipylidium caninum, Taenia
taeniaeformis

Ivermectin

0.024

PO

Ancylostoma tubaeforme,

A braziliense

Milbemycin oxime

2

PO

Toxocara cati, A tubaeforme

Piperazine (various 48-88b, cl

PO

T catic, Toxascaris leonina
salts)

Praziquantel

4.6-10

PO

D caninum, T taeniaeformis

5-10

SC,IM

D caninum, T taeniaeformis

Praziquantel +

5/20

PO

T cati, A tubaeforme, D caninum,
pyrantel pamoate

T taeniaeformis

APPROVED ONLY IN UK

Fenbendazole

50, daily

PO

T cati, T leonina, Ancylostoma
for3
spp, Uncinaria spp, Ta.enia spp
days;lOO

Praziquantel

5

PO

D caninum, T taeniaeformis,

Echinococcus multilocularis<

8

Topical

D caninum, Taenia spp,

E multilocularis

Milbemycin oxime + 2/5

PO

T cati, A tubaeforme, D caninum,
praziquantel

Ta.enia spp, E multilocularis

Praziquantel +·

5/57.5

PO

T cati, T leonina, D caninum,
pyrantel embonate

T taeniaeformis

APPROVED IN BOTH USA AND UK

Emodepside +

3/12

Topical

T cati, A tubaeforme, D caninum,
praziquantel

T taeniaef01mis, T leoninac1,

E multilocularisd

Moxidectin +

1/10

Topical

T cati, A tubaeforme
imidacloprid

Selamectin

6

Topical

T cati, A tubaefonne
a Many of these dmgs are also approved for use against other types of parasites (eg, fleas, heartwonns) not listed here.

b Repeat in 10-14 days for most products
c Only some products
c1 Only in the USA

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

421

In cats, drugs approved for treatment of A
maintaining cleanliness and eliminating
tubaeforrne include emodepside, fenbendamoist areas, the risk of infection in dogs can zole, ivennectin, milbemycin, moxidectin,
be reduced considerably, although T vulpis
pyrantel, and selamectin (see TABLE 9).

infections can be difficult to control. For

Herutwonn prevention with ivermectin,
anthelmintic treatment of dogs, approved

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milbemycin, milbemycin/praziquantel,
compounds include febantel, fenbendazole,
moxidectin/imidacloprid, or selamectin
rnilbemycin, moxidectin (topical), and
controls A tubaef01me, whereas ivennectin
oxantel ( see TABLE 8). Treatment should be also controls A braziliense ( see TABLE 9).

repeated three times at monthly intervals

When neonatal pups die due to hookbecause of the long prepatent period.

wonn infection, subsequent litters from

Finally, rnilbemycin, rnilbemycin/lufenuron,
the bitch should be treated weekly for A
milbemycin/spinosad, nlilbemycin/
caninum for -12 wk beginning at 2 wk of
praziquantel, and moxidectin/imidacloprid,
age. In addition, fenbendazole (25 mg/kg, PO) when administered for heartworm given daily to pregnant bitches from day 40
prevention, are also approved for control
of pregnancy to day 2 after whelping greatly
of T vulpis infections.

reduces transmammary transmission to

Effective therapy has yet to be described
the pups (approved in the UK). Likewise,
for 'l'richuris infections in cats. If required, treatment of the bitch with ivem1ectin
treatment should be attempted on an

(0.5 mg/kg) on two occasions ( 4-9 days
experimental basis using a compound with
before whelping and 10 days later), or with
approved activity against T vulpis.

moxidectin/inlidacloprid spot-on on day

56 of pregnancy, has the same effect

ACANTHOCEPHALANS

(extra-label use).

Resistance of A caninum to pyrantel has

(Thorny-headed worms)

been reported in parts of Australia.

Oncicola spp

WHIPWORMS

Oncicola canis and other species are rarely found in the small intestine of dogs and cats.

Adult 'i'richwis vulpis are 45-75 nun long

They are white and -8-15 mm long, and
and consist of a long, slender anterior
their thorny heads are embedded in the
portion and a thick posterior third. They
mucosa. The females lay brown, thickcommonly inhabit the cecwn and colon of shelled, embryonated, wide oval eggs
dogs, where they are fumly attached to the

(43-50 x 67-72 µrn). The life cycle is not
wall with their anterior end embedded in
completely known, but it is thought to
the mucosa Thick-shelled eggs with bipolar
include an arthropod intermediate host and
plugs are passed in the feces and become
paratenic hosts such as lizards, birds, or
infective in 1-2 mo in a wam1, moist
am1adillos. Most infections cause no
environment. Although eggs may remain
clinical signs.

viable in a suitable environment for up to 5
yr, tl1ey are susceptible to desiccation. The

Macracanthorhynchus sp
life cycle is direct. After infective eggs are
ingested, the larvae hatch and develop in the Macracanthorhynchus ingens, naturally a wall of the distal ilewn, cecwn, and colon,
pai·asite of raccoons, is occasionally found
and the adults mature in -11 wk. They may
in dogs. The usual obse1vation is of a large
remain for up to 16 mo.

(8-12 cm), white, wrinkled wom1 passed

No signs are seen in light infections, but
in the feces. No clinical signs have been
as the worm burden increases and the
definitively associated with the infection.

inflanunatory (and occasionally hemor

The life cycle requires a nlillipede as an interrhagic) reaction in the cecum and colon mediate host, but other ailirnals may se1ve as
becomes more pronounced, weight loss and pai·atenic hosts. The eggs look similar to diarrhea become evident. Fresh blood may
those of Oncicola canis but ai·e lai·ger ( -50 x be seen in the feces of heavily infected

100 µrn ). Diagnosis of patent infections is
dogs, and anemia occasionally follows.

unlikely, because experimentally induced

Trichwis infections are rarely seen in
infections did not persist after 1-12 days of
cats in North and South America and
patency. No treatment is necessary.

the Caiibbean but may occasionally be
associated with clinical signs similar to

TAPEWORMS
those described for dogs.

(Cestodes)

Treatment and Control: The eggs are

Most urban dogs and cats eat prepared
susceptible to desiccation; therefore, by
foods and have restricted access to natural

422

GASTROINTESTINAL PARASITES OF SMALL ANIMALS
prey. Such animals may acquire Dipylidiwn caninum (the double-pored dog tapeworn1) by ingesting fleas. Cats with
access to infected house (or outdoor) mice
and rats also can acquire Taenia taeniae

VetBooks.ir

Jonnis. In certain pa.its of the world ( eg, India, the Middle East, North Africa,
southeast Asia, southern Europe), dogs and
cats with access to reptiles may acquire

Dipylidium caninum segments. Courtesy of Joyeuxiella pasqualei. Suburban, rural,

Dr.

Andrew Peregrine and Ontario Veterinary College.

and hunting dogs have more access to
vai'ious small mammals, in addition to raw
meat and offal from domestic and wild
w1gulates. A number of cestodes can be
expected in such dogs (see TABLE 10). On sheep rai1ges and wherever wild ungulates
and wild canids are common, clogs may
acquire Echinococcus granulosus (the
hyclatid tapewonn). Sylvatic Echinococcus
mullilocularis (the alveolar hydatid
tapeworm), previously known only from
ai·ctic North America, has been fotmd in
wildlife in miclwestern and western USA
and Canada. The parasite is also endemic in
many parts of central ai1cl eastern Europe,
particularly France, Gern1any, and

Switzerland. Thus far, infections in cats
or dogs are generally rare. However, in

Taenia sp segments. Courtesy of Dr. Andrew addition to multi.pie rep01ts from clogs and

Peregrine and Ontario Veterinary College.

cats in central Europe, the pai·asite has
recently been identified in a few clogs
ith•IH CESTODES OF DOGS AND CATS IN NORTH AMERICA Intermediate Host and

Cestode

Definitive Host

Organslnvadeda

Dipylidium caninum

Dog, cat, coyote, wolf, fox, Fleas and more rarely lice; free other wild canids and
in body cavity
felicls

Taenia taeniaeformis

Cat, dog, lynx, fox, other

Various rats, mice, other
animals
rodents; in large cysts in liver

Taenia pisifonnis

Dog, fox, wolf, coyote,

Rabbits and hares, rarely
other animals
squirrels and other rodents; in
pelvic or peritoneal cavity
attached to viscera

Taenia hydatigena

Dog, wolf, coyote, weasel, Domestic and wild clovenfox hoofed animals, rarely hares
and rodents; in liver and
abdominal cavity

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

423
across Canada. Spirometra mansonoides
methods are required. Direct microscopic
is an uncommon (but not rare) parasite of
examination of fecal samples or fecal
cats and occasionally of dogs along the
flotation may reveal the eggs of Spirametra
eastern and Gulf Coast areas of North
mansonoides, which are sometimes

America.

mistaken for trematode eggs, although they

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Association with infected dogs may result are larger and possess an operculun1 that is in human infection with metacestodes of
often difficult to see.

E g1-anulosus, E multilocularis, 7' multi

Control of tapewonns of dogs and cats
ceps, 7' serialis, or 7' crassiceps in various requires therapy and prevention. Anin1als
tissues (by ingestion of eggs passed in dog
that roan1 freely often become reinfected by
feces), or adultD caninum in the intestine
ingestion of metacestodes in carrion or prey

(by ingestion of infected fleas). The
animals. Dipylidium caninum is different,
presence of metacestodes in livestock may
because it can cycle th.rough fleas that may
limit commercial use of such carcasses or
be associated with confined infected animals.

offal meats. Thus, cestodes of dogs and cats

An accurate diagnosis is necessary for
may be of both economic and public health
effective advice on preventing reinfection.

importance ( see TABLE 11 ).

Effective treatment should remove the

Adult cestodes in the intestine of dogs
attached scolices from the small intestine of
and cats rarely cause se1ious disease, and
infected animals. (See TABLE 10 for specific clinical signs, if present, may depend on the
approved treatments.) For dogs, fenbendadegree of infection, age, condition, and zole and praziquantel are approved for
breed of host. Clinical signs vary from
treatment of Taen-ia spp (ie, more than just unthri.ftiness, malaise, initability, capricious 7' pisiformis, for which epsiprantel is appetite, and shaggy coat to colic and mild
approved); epsiprantel, nitroscanate, and
diarrhea; rarely, intussusception or
praziquantel are approved for D caninum;
blockage of the intestine, emaciation, and
and praziquantel is approved for treatment
seizures are seen.

of Echinococcus spp (see TABLE 8). For Diagnosis is based on finding proglottids
cats, fenbendazole and praziquantel are
or eggs in the feces. The eggs of Taenia spp approved for treatment of Taenia spp (ie,
and Echinococcus spp cannot be differentimore thanjust 7' taeniaejormis, for which ated by microscopic examination; PCR
epsiprantel is approved); epsiprantel and

CESTODES OF DOGS AND CATS IN NORTH AMERICA (continued) Approved

Diagnostic Features of Adult Worm

Comments

Treatme.ntb

Strobila 15-70 cm Jong and up to 3 mm in

Probably most common Dogs and cats:

maxinmm width, 30-150 rostellar hooks of tapeworm of dogs and epsiprantel,
rose-thorn shape in 3 or 4 circles; large
cats; cosmopolitan.

praziquantel
hooks 12-15 µm, smallest 5-6 µm Jong.

Occasionally infects

Segn1ents shaped like cucumber seeds, with people, pa.Iticularly pore near middle of each lateral margin.

infants.

Strobila 15-60 cm long, 5-6 mm in

Common cestode of cats, Cats: epsiprantel,
maximun1 width, 26-52 rostellar hooks in rare in dogs; cosmopolipraziquantel, double row; large hooks 380-420 µm,
tan
fenbendazole
small hooks 250-270 µm long. No neck.

Sacculate lateral branches of uterus
difficult to count.

Strobila 60 cm to 2 m long, 5 mm in

Pa1ticularly common in

Dogs: epsipranmaxi..mun1 width, -34-48 rostellar hooks suburban, farn1, and tel, fenbendain double row; large hooks 225-290 µm,
hunting dogs that eat
zole, praziquansmall hooks 132-177 µm long. Each side rabbits and rabbit
tel
of gravid uterus has 5-10 lateral branches. viscera.

Strobila to 5 m long and 7 mm in
ln farm dogs, more rarely Dogs: praziquanmaximum width; -26--44 rostellar hooks hunting dogs; cosmopoli.- tel, fenbendazole in double row; large hooks 170-220 µm,
tan
small hooks 110-160 µm long. Each side
of gravid uterus 5-10 lateral branches.

424

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

CESTODES OF DOGS AND CATS IN NORTH AMERICA (continued) Intermediate Host and

Cestode

Definitive Host

Organs Invaded8

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Spirometra

Cat, dog, raccoon, bobcat

Copepods, frogs, rodents,
ma.nsonoides
snakes; connective tissue

Diphyllobothrium spp

People, dog, cat, other

Encysted in various organs, or
fish-eating animals
free in body cavity of various
fish

Echinococcus

Dog, wolf, coyote, fox, and Sheep, goats, cattle, pigs, granulosus
several other wild
horses, deer, moose, some
carnivores
rodents, occasionally people
and other animals; co nun only in
liver and lungs, occasionally in
other organs and tissues

Echinococcus

Arctic, red, and gray foxes; Microtine rodents, occasionally multilocul.aris
coyote, cat, dog
in people; in the liver and other
organs

Mesocestoides spp

Many wild canids, felids,

Complete life cycle unknown;
mustelids; other animals,
aithropod intermediate hosts
including dog and cat
suspected; juvenile tetrathy-

1idia in abdominal cavity and
elsewhere of various manunals,
birds, and reptiles; tetrathyridia
in intestine of dogs may enter
abdomen through intestinal
wall.

Taenia multiceps

Dog, coyote, fox, wolf

Sheep, goats, and other
domestic or wild ruminants,
rarely people;. usually in brain or
spinal cord

Taenia serialis

Dog, coyote, fox, wolf

Rabbit, hare, squirrel, rai·ely
people; in subcutaneous
connective tissue or retroperitoneally

Taenia crassiceps

Dog, coyote, fox, wolf

Various rodents, a few records
in people; subcutaneous and in
body cavities

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

425

•H=iif ••• CESTODES OF DOGS AND CATS IN NORTH AMERICA (continued) Approved

Diagnostic Features of Adult Worm

Comments

Treatrnentb

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Strobila 0.5 m long, 8 mm in maximum

Ea.stem and Gulf Coast,

See text for
width. Scolex with 2 grooves and no

North America
extra-label
hooks. Genital pores ventral midline of
treatment
segment.

Strobila to 10 m long, 20 mm in maximum Canada, Ala.ska. and See text for
width but usually smaller. Scolex with 2
various other states of
extra-label
grooves (bothria) and no hooks. Genital the USA, Siberia, and treatment
pores ventral midline of segment.

other areas

Strobila 2-6 mm long with 3-5 segments; Foci an10ng North Ameri Dogs: praziquan28---50 ( usually 30-36) rostellar hooks in can range sheep and
tel
double row; large hooks 27-40 µm, small dogs associating with hooks 21-25 µm long.

them; sylva.tic moosewolf cycle where these
animals are found;
probably cosmopolitan

Strobila 1.2-2. 7 mm long with 2-4

Central and ea.stem

Dogs and ca.ts:

segments; 26-36 rostellar hooks in

Europe, fom1er USSR,
pra.ziquantel
double row; large hooks 23-29 µm, small Ala.ska., and midwestem hooks 19-26 µm long.

USA and Canada; thus
far, significant cycle in
cats and dogs in North

America not recognized.

However, multiple cases
of alveolar echinococcosis have been iliagnosed
in dogs a.cross Canada.

Strobila 10 cm long and 2-5 mm wide.

Rep01ted in dogs and

Dogs: pra.ziquan

Scolex with 4 suckers but no rostellum or ca.ts in midwest and tel
hooks. Genital pore ventral in midline of west; in wild animals worm. Gravid segments with parauterine elsewhere in USA and organ.

Canada

Strobila. 40-100 cm long and up to 5 mm

Rare in domestic

Dogs: praziquanwide. Scolex with 4 suckers and 22-32
carnivores in western
tel, fenbendazole
hooks in double row; large hooks

North America; more

150-170 µm, small hooks 90-130 µm long. common in wild anin1als Vagina with reflexed curve near lateral
excretory canal; 9-26 lateral branches on
gravid uterus.

Strobila. 20-72 cm long and 3-5 mm wide; Primarily in wild canids; Sa.me as for 26-32 hooks in double row; large hooks
considered by some

Tmulticeps

110-175 µm, small hooks 68-120 µm long. authorities as not ilistinct Vagina with reflexed curve near lateral
from T multiceps
excretory canal; 20-25 lateral branches
on gravid uterus.

Strobila. 70-170 mm long and 1-2 mm

Reported from Canada

Same as for
wide. Scolex with 30-36 hooks in double
and northern USA,

Tmulticeps
row; large hooks 158---187 µm, small hooks including Ala.ska 119-141 µm long. Uterus has 16-2lla.teral
branches, sometimes becoming diffuse.

426

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

CESTODES OF DOGS AND CATS IN NORTH AMERICA (continued) Intermediate Host and

Cestode

Definitive Host

Organs Invaded•

Taenia krabbei

Dog, coyote, wolf, bobcat

Moose, deer, reindeer; in

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striated muscle

Taenia ovis

Dog, wild can.ids

Sheep and goat; in skeletal and
cardiac muscle, rarely
elsewhere
praziquantel are approved for treatment of
of embryonation. The first intermediate

D caninum, and praziquantel is approved
hosts are snails found in endemic
for treatment of E mullilocularis (see
locations (eg, Oxytrnma silicula in the

TABLE 9). Outside the USA and UK, praziqu

USA). The cercariae from these snails penantel is approved for use in multiple etrate the skin of yow1g salmonid fishes
countries at 5 mg/kg for treatment of J
and encyst as metacercariae in their
pasqualei in dogs (as praziquantel/pyrantel/ muscles and organs. Dogs and other febantel) and cats (as praziquantel/
animals become infected by eating raw or
pyrantel).

improperly prepared infected fish.

Praziquantel at 7.5 mg/kg, PO, for 2

Because these flukes embed deeply
consecutive days is effective against
between tl1e villi of the intestine, infection

Diphyllobothriiim sp in dogs. Furthermore, with a large number may cause enteritis.

a single dose of 35 mg/kg, PO, eliminates,0

Most infections, however, are complicated
latum from infected cats. Both treatments
through development of the salmon
are extra-label.

poisoning complex caused by rickettsial

Infections with Spii--ometra sp in dogs
organisms, which the fluke transmits (see
and cats can be treated with praziquantel
p 808). Praziquantel (20-30 mg/kg, PO or SC,
at 7.5 mg/kg, PO, for 2 consecutive days.

once) and fenbendazole (50 mg/kg/day, PO,

Spirometra sp infections in cats can also
for 10--14 days) are both effective, but not
be treated with a single dose of praziquanapproved, treatments for dogs.

tel at 30 mg/kg, SC, IM, or PO. Mebendazole

Alaria alata, A can is, and other Alaria at 11 mg/kg, PO, has also been successful.

spp are small (2--6 nun) flukes usually found

All these treatments are extra-label.

in the small intestine of d_ogs, cats, foxes,
mink, and wild carruvores in the western
hentisphere, as well as in Emope, Australia,

FLUKES
and Japan. The anterior part of the body is
flat, and the poste1ior part is conical. The
eggs are oval, light brown, and fairly large

Intestinal Flukes

(98--134 x 62-68 µm). The life cycle includes

Nanophyetus salmincola, the "salmon
freshwater snails ( eg, H elisoma spp) as first poisoning" fluke, is a small ( -0.5 x 0.3
intern1ediate hosts. Cercariae emerge from
mm), oval fluke found in the small
the snails, penetrate tadpoles, and develop
intestine of dogs, cats, and many wild
into mesocercariae. Frogs, snakes, and ntice
fish-eating mammals in the northwestern
then acquire infection by eating tadpoles;

USA, southwestern Canada, and Siberia.

the mesocercariae transfer to tl1ei.r tissues

The eggs, which pass in the feces of
and remain as tltis life-cycle stage. Dogs and
infected hosts, are light brown, 72-97 x
oilier definitive hosts become infected by

35-55 µm, and indistinctly operculated
feeding on these animals. The young flukes
with a small knob at one pole. The life
ntigrate tl1rough various organs of the
cycle includes an extended period (3 mo)

definitive host, including the d.iaphragm and

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

427

CESTODES OF DOGS AND CATS IN NORTH AMERICA (continued) Approved

Diagnostic Features of Adult Worm

Comments

'Ireatmentb

VetBooks.ir

Strobila -20 cm long and up to 9 mm

Reported from Canada

Same as for
wide. Scolex small with 26--36 hooks in
and northern USA,

Tmulticeps
double row; large hooks 146-195 µm,
including Alaska;
small hooks 85-141 µm long. Gravid
considered by some a
uterus has 18-24 straight and narrow
subspecies of T ovis
lateral branches.

Strobila 45-110 cm long and up to 4--8.5

Reported from western

Same as for
mm wide. Scolex with 32-38 hooks in
and central Canada and

Tmulticeps
double row; large hooks 170-191 iun,
the southern USA
small hooks 111-127 µm long. Gravid
uterus has 20-25 lateral branches. Vagina
crosses ovary on poral side of segment.

a In all cases in which the life cycle is known, cats and clogs become infected by eating animals (or parts) that contain the infective metacestode. These intermediate hosts become infected by ingesting tapeworm eggs (except in Mesocestoides, Spimmetra, and Diphylloboth,ium spp, which have an extra stage in the life cycle), which are passed in the feces of the definitive host.

O See TABLE 8 and TABLE 9 for drug dosages.

lungs, before reaching the small intestine.

wall of the intestine, the liver, m1d other

Although the flukes are generally considparts of the body. Lethm·gy, weight loss, ered to be non pathogenic, large numbers
vomiting, and/or dian-hea may develop in
may cause pulmonary hemon-hages during
heavy infections. "Water dermatitis" is
migration or enteritis when they mature in
sometin1es seen when cercmiae penetrate
the small intestine. These flukes may infect
the skin. The eggs do not readily float and,
people. Infections can be treated with
if placed in water, hatch within minutes;
praziquantel using the approved cestocidal
therefore, a sedin1entation method using
dosage ( see TABLE 8 and TABLE 9 for drug 0.85% saline is useful in separating eggs
dosages.). However, such treatment is
from ingesta. In infected dogs, eggs are
extra-label.

passed intermittently, so on a given day eggs

Other species of flukes, usually not
may not be found in feces. Fenbendazole at
pathogenic, have been found occasionally

50 mg/kg/day, PO, for 10 days, is an effective
in the intestine of dogs, cats, and other
treatment. Praziquantel at 25 mg/kg, tid, for
carnivores; these include Heterophyes

2 days is also effective. Both are extra-label
heterophyes in some north African and
uses.

Asian countries; Metagonimus yokogawai
in Asia; C1yptocotyle lingua in the USA,

Canada, Japan, Siberia, and Europe; and

Hepatic Flukes

Apophallus don'icum in No1th America and

Flukes in the bile ducts and gallbladder
eastern Europe. Their life cycles include
cause mild to severe fibrosis. Many species
snails as first intern1ediate hosts and fish
of distome trematodes have been reported
as second intermediate hosts, in which
from the liver of dogs and cats in most parts
metacercmiae become encysted.

of the world. Mild infections may pass

Heterobilharzia americana is fow1d
unnoticed; however, in severe infection,
in the mesenteric veins of dogs and wild
dogs may develop progressive weakness,
aJ.Umals, especially raccoons, in the
ending in complete exhaustion, coma, and
southeastern USA. The eggs pass through
death. The following are some of the most
the tissues of the intestine to the lumen and
commonly encountered trematodes.

then are voided in the feces. From the snail

Opisthorchisfelineus is parasitic in
intermediate host, cercariae escape into
the bile duct, pancreatic duct, and small
water and penetrate the skin of dogs and
intestine of dogs and cats in Italy, eastern
other definitive hosts, migrate to the liver,

Emope, and parts of Asia. 0 viverrini is
mature, and move to the mesenteric vessels.

seen in dogs as well as in domestic and

Granulomas form m·ound the eggs in the
wild cats in southeast Asia. They m·e small

428

GASTROINTESTINAL PARASITES OF SMALL ANIMALS

11-1:11111 CESTODES OF PUBLIC HEALTH IMPORTANCE

Name of

Principal

Host of

Metacestode

Measure-

Interme-

Adult

(Intermediate) ments of
diate

Site of

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Cestodea Worm

Stage

Metacestode Hosts

Metacestode

Taenia

People

Cysticercus

9x5mm

Cattle

Skeletal and
saginala
only

"beef measles"

cardiac muscle

Taenia

People

Cysticercus

6--10 x 5-1 0

Pigs, rarely Skeletal and
solium
only

"pork measles"

mm
dogs
cardiac

(people
muscle,
may be
occasionally
both
nervous
definitive
system
and
interrnedi-
ate hosts)

Diphyllo-

People,

Procercoid

2-25x2.5mm Copepod, Mesenteric
bolhrium dogs, cats, in copepod,
for plerocer-
then fish
tissues, testes,
spp
and other plerocercoid
coid
ovary, muscles
fish-eating in fish
of fish
mammals

Echino-

Dogs,

Hydatid cyst

Diameter

Sheep,

Commonly in
coccus
wolves,

50-lOO mm,
cattle,
liver and lungs,
granulosus foxes, and
sometimes
pigs,
occasionally in
several

�150mm
horses,
other organs
other wild
moose,
and tissues
carnivores
deer;
occasion-
ally people

Echino-

Canids

Alveolar hydatid Variable,

Field m.ice, Usually liver,
coccus
and
cyst
penetrates
voles,
various other
mullilocu- domestic
like neoplastic lemmings, organs and

Laris
cats
tissue
sometimes tissues
domestic
mammals
and people
a Human infections with the mentcestodes of Taenia crassiceps, T multiceps, Mesocestoides spp, and other cestodes not listed here occur rarely. Children occasionally become infected with adult Dipylidiu,n caninurn, which apperu-s to have no medical significru1ce but important aesthetic aspects.

(9 x 2 mm) and elongate. Their life cycle
and severe cases. Treatment of Opislhor
includes certain snails (Bilhynia, sp) and
chis spp infections in dogs may be
cyprinid fishes as intennediate hosts. A
attempted with fenbendazole (200 mg/kg/day,
related species, Clonorchis sinensis, the

PO, for3 days) or praziqua.ntel (20 mg/kg, PO,

Oriental liver fluke of people, also has been
once). Treatment of C sinensis infections in found in the bile ducts and pancreatic ducts
dogs may be attempted with praziquantel
of dogs, cats, and other animals. It is larger

(30 mg/kg/day, PO, for 3 days). All these
tl1an Opislhorchis spp. The operculated
treatments are extra-label.

eggs of these parasites may be identified in

Platynosomum concinnum is a small
the feces of infected animals.

fluke (6 x 2 mm) found in the bile and

Longtenn presence of these flukes in the
pancreatic ducts of Felidae in southeastern
bile duct causes epithelial hyperplasia and

USA, Puerto Rico and other Catibbean
fibrosis of the duct wall. Carcinomas in the

Islands, South America, some of the Pacific
liver or pancreas have been seen in chronic
islands, and parts of Africa. Its life cycle

HEPATIC DISEASE IN SMALL ANIMALS

429
includes the snail Sublima octona and a
clinical signs. Their eggs are small
crustacean (wood louse) as intermediate

(24---30 x 13-16 �l111), and the life cycle
hosts and certain lizards as paratenic hosts.

includes certain freshwater snails and fish

Cats acquire the parasite by feeding on
as intermediate hosts. Treatment of
infected lizards. In mild cases, nonspecific

Metorchis spp infections in dogs may be

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chronic signs oftmthriftiness may be seen.

attempted with praziquantel (20 mg/kg, PO,

Severe infections, however, may cause the
once), although this is an extra-label use.

"lizard poisoning" syndrome, which is

Eurytrema procyonis is a small fluke
characterized by anorexia, lethargy,

(2.1 x 1 mm) commonly seen in the
depression, persistent vomiting, diarrhea,
pancreatic duct of raccoons in the eastern
jaundice, and an enlarged abdomen, leading

USA and occasionally found in the
to death. Treatment with praziquantel
pancreatic duct, bile duct, and gallbladder

(20 mg/kg/day, PO, for 3-5 days, ideally,
of domestic cats. Infection may be
repeated 12 wk later), or nitroscanate
associated with weight loss and intennit

(100 mg/kg, PO, once) has been successful,
tent vomiting. The eggs are medium sized
although these drugs are not approved for

(45-53 x 29-36 pm), and the life cycle
this use. Praziquantel appears to be the
involves a land snail and a second
most effective agent. Bile duct surgery may
intermediate host thought to be an
also be required.

arthropod. Treatment may be attempted

Metorchis albidus and M conjunctus are with fenbendazole (30 mg/kg/day, PO, for 6
two small flukes (5 x 1.5 mm) that have been days) or praziquantel/pyrantel/febantel found in the bile ducts and gallbladder of

(praziquantel and pyrantel each at
dogs, cats, and other carnivores in North

5.8 mg/kg/day and febantel at

America, Europe, and the fom1er USSR.

28.8 mg/kg/day, PO, for 5 days), although

They seldom cause any recognizable
these drugs are not approved for this use.

HEPATIC DISEASE IN SMALL ANIMALS

The liver performs numerous functions,

[GGT]) reflecting cholestasis and iqcreased
including but not limited to lipid, carbohyprotein transcription (enzyme induction).

drate, and protein metabolism; storage,

The liver is predisposed to secondary
metabolism, and activation of vitamins;
injury owing to its sentinel position
storage of minerals, glycogen, and
between the systemic circulation and GI
triglycerides; extra.medullary hematopoietract and because it contains the largest sis; and synthesis of coagulant, anticoagupopulation of fixed macrophages (Kupffer lant, and several acute phase proteins. It
cells) in the body. Macrophage phagocytoalso influences immunologic responses and sis can initiate release of a cascade of
contributes to digestion through synthesis
inflan1111atory cytokines, leading to local
and enterohepatic circulation of bile acids
cellular damage and recruitment of
and detoxification of many endogenous and
inflan1matory infiltrates. The considerable
exogenous compounds, toxins, and
metabolic activity of the liver exaggerates
xenobiotics. Because the liver has a large
its exposure to noxious products,
functional reserve and the ability to
particularly in the centrilobular region,
regenerate, hepatic injury must be
where high cytochrome p450 activity
considerable or chronic and recuffent to
produces noxious products and adducts.

cause overt hepatic dysfunction or failure.

Hepatocytes in this region also are more

Active liver injury is accompanied by
easily injured by hypoxia. The accumulaincreased liver enzyme activity, with tion of hepatic copper and/or iron can
cytosolic transan1inases (ALT, AST)

initiate and augment liver injury through
acutely reflecting altered membrane
oxidative mechanisms.

penneability or viability or the phenom

Clinical signs of liver injury vary
enon of membrane blebbing, and memdepending on the type, mechanism, and brane-affiliated enzyme induction (alkaline
chronicity of the insult. Common clinical
phosphatase [ALP], -y-glutamyl transferase
features may include anorexia, vomiting,

430

HEPATIC DISEASE IN SMALL ANIMALS
diarrhea, weight loss, and fever. With
microvascular shearing ( eg, schistocytes,
severe, diffuse liver injury, animals may
acanthocytes) may be seen. RBC microcytobecome jaundiced and demonstrate sis is conunon in congenital or acquired
polyuria and polydipsia (PU/PD), coagulaportosystemic shunting, although tile tion abnonnalities, and ascites. Ascites
pathologic mechanism remains unclear.

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indicates development of pmtal hyperten

Change in WBC count or distiibution
sion and is typically associated with
are variable. Leukocytosis may reflect
formation of acquired portosystemic shunts
inflan1matory, infectious, necrolytic, or

(APSSs) and concurrent hypoalbwninemia.

diffuse infiltrative hepatic disorders, or

Hepatic encephalopathy (HE) develops in
release of endogenous glucocorticoids
acquired liver disease only when diffuse
or aclministration of glucocorticoids.

fibrosis and APSSs have developed, in acute

Leukopenia can reflect sepsis or toxicosis.

fulminant liver failure, or secondary to

In severe diffuse necroinflarnmat.ory liver
congenital portosystemic shunts ( congeniinjury, damaged sinusoidal microvascula tal malfonnations of the po1tal vein that tme can provoke platelet aggregation,
shunt po1tal blood directly to the systemic
contiibuting to tlrrombocytopenia and
circulation). Fecal color may change with
disseminated intravascular coagulation.

complete occlusion of bile ducts (acholic or
pale-colored feces) or because of increased

COAGULATION TESTS
ente1ic bilirnbi.n elimination (green fecal
color). Hepatomegaly is found witl1 diffuse

Coagulation abnorrnalities can develop as a
infiltrative or storage disorders, acute
result of decreased synthesis or activation
extrallepatic bile duct obstruction
of coagulation factors and anticoagulant

(EHBDO), congenital biliary cystic
proteins produced in the liver (ie, factors V,
malfonnations, or passive congestion,

VU, IX, X, XI, XII, fibrinogen, prothrombin,
whereas microhepatica (small liver) usually
antitlrrombin, protein C, plasminogen,
reflects portal venous hypoperfusion,
a,-macroglobulin, and a1-antitrypsin).

diversion of enteric hepatotrophic factors

Decreased enteric absorption of fat-soluble
nom1ally delivered in the portal circulation,
vitan1ins can lead to vitan1in K -responsive
or the presence of chronic hepatic fibrosis
bleeding in animals with EHBDO or bile
in dogs.

duct inununoirtjury (feline sclerosing
cholangitis), or in cats with HL. Cats witll
liver disease appear predisposed to vitanlin

K-responsive coagulopathies. Conventional
coagulation assessments may not reflect
impending coagulopathies that remain
tmsuspected after physical exanlination,

HEMATOLOGY
analysis of mme or feces, or mucosa!

bleeding tune test. Dogs with congenital or

Depending on the severity and underlying
acquired portosystemic shunting usually
cause of liver disease, a nonregenerative or
develop low protein C activity ( <70"A,
regenerative anemia may develt>p. Severe or activity) that seenlingly reflects the seve1ity acute anemia can impact tile liver as a result
of portosystemic shw1ting. Although
of hypoxia, causing alterations in hepatocoagulation factors may be significantly cyte membranes, leacling to release of
lower in some of these dogs than in
transarninases and induction of ALP.

age-matched control groups·, syn1ptomatic

Altered RBC morphology (poikilocytes,
coagulopathy is rare.

irregularly iITegular RBCs) is common in
cats with cholangiohepatitis and hepatic

ENZYME ACTIVITY
lipidosis (HL). Cats with HL, severe
cholangiohepatitis, and EHBDO also may

Liver disease is often first suspected based
develop Heinz bodies, reflecting oxidative
on increased liver enzyn1e activity. However,
injury that may lead to hemolysis. Severe
abnormally increased liver enzyme activity
hypophosphatemia in HL may develop
is considerably more common than tl1e
secondary to a re-feeding syndrome and
prevalence of liver disease. A wide spectrwn
cause hemolysis severe enough to require a
of nonhepatic disorders may influence liver
blood transfusion; this can be avoided by
enzyn1e activity. It is in1portant to recognize
providing fluid therapy supplemented with
tllat liver enzyn1e measmements are not
potassiun1 phosphate when nutritional
liver fw1ction tests but ratller reflect
support is implemented. In dogs with
hepatocyte membrane integrity, hepatocyte
diffuse necroinflanlillatory liver disease
or biliary epitllelial necrosis, cholestasis, or

( altered sinusoidal perfusion), RBCs with
induction phenomenon.

HEPATIC DISEASE IN SMALL ANIMALS

431

The pattern of liver enzyme abnorn1alities however, both enzymes are present in high in relation to the signalment, history, total
concentrations in liver and several otl1er
bilirubin concentration, serum bile acid
tissues. AST activity is higher in kidney,
values, and comorbid conditions/medicaheart, and skeletal muscle than liver, tions provides the first indication of a
whereas ALT activity is highest in liver.

VetBooks.ir
liver-specific disorder. A full assessment of

Because hepatic ALT activity is 10,000-fold
liver enzyme aberration considers: 1) the
greater than plasma enzyme activity in
predominant pattern of enzyme change
healthy animals, it has high diagnostic utility

(hepatocellular leakage enzymes vs
to detect "liver lesions." The cytosolic
cholestatic enzymes), 2) the magnitude
location of transaminases allows tlleir
of increase of enzyme activity above the
in1mediate release with even minor change
normal reference range ( mild is <3 times
in hepatocellular membrane integrity.

the upper reference range, moderate is 3-9

Unfortunately, indiscriminate leakage limits
times, marked is >10 times), 3) the rate
their diagnostic utility. Nonetheless,
of change (increase or resolution) with
duration and magnitude of transaminase
sequential sampling, and 4) the nature of the activities measured sequentially can predict course of change (fluctuation vs progressive disease activity and severity and roughly increase or decrement). Up to 2.5% of
estimate the number of involved cells.

clinically "normal" animals can have

Hepatic transaminases increase with
borderline abnormal enzyme values.

muscle ir\jury as well as vigorous physical

Recognizing whether enzyme abnormaliactivity in dogs. Persistence of transamities are persistent or cyclic helps categorize nases in plasma contJ.ibutes to tl1eir
likely causes. Investigating liver function
sustained high activities in certain
with paired fasting and postprandial total
disorders. Because transaminase cataboserum bile acids (TSBAs) or urine bile acid/
lism occurs by absorptive endocytosis at tl1e
creatinine measurements (urine collected
hepatocyte sinusoidal border, slow enzyme

4-8 hr after meal ingestion) may expedite
clearance may sustain plasma enzyme
a decision to pursue liver biopsy when
activity in hepatic insufficiency associated
clinical signs remain vague and enzymes are
with liver fibrosis, nodular regeneration,
only mildly increased. Imaging studies help
and development of APSSs.

detect primary underlying disorders that
have secondarily influenced the liver,

Alanine Aminotransferase: The largest
causing increased enzyme activity.

increases in ALT develop with hepatocellu

Ultrasonographic assessment may help
lar necrosis and inflammation. After acute
determine the method of liver biopsy;
severe hepatocyte necrosis, seflll11 ALT
needle biopsies are ill advised in animals
activity increases sharply within 24-48 hr
with microhepatica, ascites, or difficult-toto values often > l 00-fold nonnal, peaking sample focal liver lesions.

during the first 5 days of injury. If the •

Age-appropriate reference ranges for
ir\jurious event resolves, ALT activity
serum liver enzyme activity are essential to
gradually declines to norn1al over 2-3 wk.

interpret laboratory values in puppies and

Altl10ugh this pattern is considered classic,
kittens. Plasma enzyme activities of ALP
some severe hepatotoxins are not
and GGT in neonatal dogs and cats are
associated with increased ALT activity,
remarkably higher than those of adults.

because they inllibit gene ti·anscription

Differences reflect physiologic adaptations
or inte1fere with ALT biosynthesis ( eg,
during the transition from fetal and neonatal aflatoxin B l hepatotoxicity, microcystin life stages, colostrum ingestion, maturation
hepatotoxicity ). A declining ALT also may
of metabolic pathways, growth effects,
represent a paucity of viable hepatocytes in
differences in volun1e of distribution and
end-stage chronic hepatitis or severe acute
body composition, and nutritional intake.

liver disease.

Serum activities of ALP, AST, CK, and LDH

Examples of classic necrotizing
in neonates usually increase greatly dilling
hepatotoxins are carbon tetrachloride,
the first 24 hr of life. In kittens, serum
acetaminophen, and nitrosamine. A single
activities of ALP, CK, and LDH exceed adult
exposure to carbon tetrachloride causes an
values through 8 wk of age. Serum ALP
acute sharp increase in ALT that resolves
increases remarkably in day-old puppies
over the ensuing week. Hepatotoxicity
and kittens after colostrllln ingestion, as
induced by acetaminophen causes a marked
also observed in neonatal calves, lambs,
increase in ALT and AST within 24 hr that
pigs, and foals.

may decline within 72 hr to near normal
values. This toxin is highly dose dependent

Aminotransferases: AST and ALT are
in dogs and cats. Cats are exceedingly
commonly measured to detect liver injury;
susceptible, with hematologic signs

432

HEPATIC DISEASE IN SMALL ANIMALS
dominating after ingestion of as little as 125
sharply increases during the first 3 days to
mg. However, in clogs, a dosage of 200 mg/kg values 10- to 30-fold above normal in dogs may be life-threatening, with susceptibility
and up to 50-fold above nom1al in cats. U
heightened by antecedent exposure to
necrosis resolves, AST activity gradually

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phenobarbital. Hepatocellular necrosis
declines over 2-3 wk. In most cases, AST
induced by nitrosamines increases plasma
pai·allels changes in ALT activity.

ALT activity, but not significantly, until after

Although increased AST activity in the

1 wk of inte1mittent chronic exposure.

absence of abnonnal ALT activity impli

The ALT activity persists for weeks until
cates an extrahepatic enzyme source
necrosis resolves. Low-grade hepatocellular

(notably in muscle injmy), there ai·e clinical
degeneration, observed in some clogs with
exceptions that may relate to severity and
congenital portosystemic shunts, reflects
zonal location of hepatic daniage. In some
delayed enzyme clearance and low-grade
cats with liver disease, AST is a more
hepatocyte dropout; most of these dogs
sensitive marker of liver injury than ALT
have small lipogranulomas reflecting single

( eg, hepatic necrosis, cholangiohepatitis,
hepatocyte dropout/necrosis in the absence
myeloproliferative disease, hepatic
of an inflanm1atory response.

infiltrative lymphoma, and EHBDO).

Acute hepatic necrosis caused by

A sinlilar trend is evident in some dogs.

infectious canine hepatitis increases plasma Because AST is located within the mito

ALT activity by 30-fold, peaking within 4
chondria and free within the cytosol of
days. Thereafter, chronic sustained ALT
hepatocytes, AST in fold increases greater
activity persists as chronic hepatitis
than those of ALT may reflect mitochrondevelops in dogs unable to clear the virus.

drial injury. Dogs treated with glucocorti

Hepatic injury induced by toxins usually
coids may develop mildly increased AST
causes plasma ALT activity to increase,
activity that resolves within several weeks
peak, and return to normal sooner than it
of glucocorticoid withdrawal.

does in infectious viral hepatitis. Chronic
hepatitis, an idiopathic or coppe1�associated Alkaline Phosphatase: Increased persistent or cyclic necroinfla.nunatory liver

ALP activity in dogs is the most conunon
ir\jmy in dogs is associated with vaiying
abnormality on routine biochemical testing;
severities of necrosis and fibrosis. Cyclic
its high sensitivity and low specificity can
disease activity is reflected by plasma
defy cliagnostic interpretation without a
enzyme "flares." At times, plasma ALT
liver biopsy. ALP activity in dogs has the
activity is> JO-fold normal. Enzyme
lowest specificity of routinely used liver
fluctuations contrast with profiles
enzymes as a result of its complexity
associated with single injurious events. In
associated with induction of different
dogs with hepatitis, semm ALT activity
isozymes.

declines as ir\jury resolves, but serum ALP

In dogs at1d cats, tissues containing
activity may increase as a result of
highest ALP activity (in descending order)

regenerative responses (progenitor cell
are intestine, kidney ( cortex), placenta
proliferation, ductal or ovalcell response).

( dogs only), liver, and bone. Distinct serum

Dogs treated with glucocorticoids may

ALP isozyrnes can be extracted from some
develop mildly increased ALT activity that
of these tissues in each species; eg, bone
resolves within several weeks of glucocorti

CB-ALP), liver (L-ALP), and glucocorticoidcoid withdrawal.

induced (G-ALP) isoenzyrnes in canine

Despite high sensitivity of ALT to identify
serum. In dogs, L-ALP and G-ALP are
liver disorders, its lack of specificity to
primarily responsible for high serum
differentiate clinically significant liver

ALP activity, whereas L-ALP is primarily
disease, specific histologic abnormalities,
responsible in cats. Increased ALP activity
or hepatic dysfunction requires that it be
develops in up to 75% of hyperthyroid cats,
interpreted in conjunction with other
depending on the chronicity of the
diagnostic tests.

condition, with B-ALP substantially
contributing.

Aspartate Aminotransferase: AST is

The comparably small magnitudes of ALP
present in substantial concentrations in a
activity in cats with liver disease (2- to 3-fold
wide variety of tissues, especially muscle.

normal) relative to dogs (usually >4- to

Increased AST activity can reflect reversible

5-fold) reflect the lower specific activity of
or i.JTeversible changes in hepatocellular

ALP in feline liver and its shorter half-life.

membrane pe1meability, cell necrosis,

Nevertheless, ALP activity remains
hepatic inflanmiation, and in dogs,
clinically useful in the diagnosis of feline
microsomal enzyme induction. After acute
liver disease when the species-appropriate
diffu e severe hepatic necrosis, serun1 AST
perspective is maintained.

HEPATIC DISEASE IN SMALL ANIMALS

433

The utility of sernrn ALP activity as a
increase within 1 wk, and up to a 9-fold
diagnostic indicator in dogs is complicated
increase within 2-3 wk. Thereafter, activity
by the conunon accumulation of L-ALP and
stabilizes and gradually declines but usually

G-ALP isozyrnes, which can both be induced
not into the nonnal range; the declining

VetBooks.ir
by steroidogenic hormones.

enzyme activity coordinates with develop

Because the B-ALP isozyrne increases
ing biliary cirrhosis c see EXTRAHEPATIC BILE
secondary to osteoblast activity, it is

DUCT OIJSTRUCTION, p 478). Inflammatory
detected in young growing animals and in
disorders involving biliary or canalicular
animals with bone tumors, secondary renal
structures or disorders compromising bile
hyperparathyroidism, and osteomyelitis.

flow increase serun1 ALP activity secondary

However, the minor contribution of B -ALP
to membrane inflammation/disruption and
to total sernrn ALP activity usually does not
local bile acid accumulation. In both dogs
lead to an erroneous diagnosis of cholesand cats, sin'lilar increases in serum ALP
tatic liver disease. Bone remodeling
activity develop in intral1epatic (metabolic,
secondary to neoplasia may not substanbiochemical, sepsis) associated cholestasis tially affect sernrn ALP activity or may cause or obstruction involving the extral1epatic only a trivial increase (2- to 3-fold) in dogs.

biliary structures. Consequently, ALP

In young growing cats, increased B-ALP
activity cannot differentiate between
activity may simulate enzyme activity seen
intra- and extral1epatic cholestatic
in hepatobiliary disease.

disorders.

Although ALT is inunediately released

Many extral1epatic and primary hepatic
from the hepatocellular cytosol in acute
conditions are associated with increased
hepatic necrosis, the small quantities of

L-ALP. In cats, HL (seep 456) is associated membrane-bound ALP are not. It takes
with marked increase in ALP activity and
several days for induction of membranejaundice. The increased ALP seemingly associated enzyme to "gear up" and spill
reflects canalicular dysfunction or
into the systemic circulation. Increased
compression. Although ALP in cats is rarely
sernrn ALP reflects enhanced de novo
affected by anticonvulsants or glucocortihepatic synthesis, canalicular injury, coids, it can increase with diabetes mellitus,
cholestasis, and solubilization of its
hyperthyrnidism, and pancreatitis.

membrane anchor (by bile salts). The

In dogs, prin1ary hepatic inflanunation as
largest increases in serum ALP activity
well as systemic infection or inflanunation

(L-ALP and/or G-ALP 2>100-fold normal)

and exposure to steroidogenic hormones
develop in dogs with diffuse or focal
may induce a glycogen-associated vacuolar
cholestatic disorders, massive hepatocelhepatopathy (VH). When severe, VH has a lular carcinoma, bile duct carcinoma, and
cholestatic effect that seemingly causes
those exposed to steroidogenic hom1ones.

canalicular compression. Although

Although sernrn activity of ALP may be
glycogen-associated VH was initially
normal or only modestly increased in dogs
characterized as a glucocorticoid-initiated
with metastatic neoplasia involving the
lesion, it is now established that nearly 500/o
liver, it may also increase dranmtically in
of dogs with glycogen-associated VH lack
dogs with mammary neoplasia. High sernrn
overt exposure to steroidogenic substances.

ALP activity develops in -55% of dogs with

Chronically ill dogs may produce the G-ALP
malignant and 4 7% with benign mammary
isozyrnes secondary to stress-induced
tumors, with highest ALP activity seen in
glucocmticoid release. Such dogs with
dogs with malignant mixed tumors.

glycogen-associated VH (lacking exogenous

Nevertheless, serum ALP has no value
glucocorticoid exposure) may demonstrate
as a diagnostic or prognostic marker in
normal dexamethasone suppression and
mammary cancer; it remains unclear
adrenocorticotropic hormone (ACTH)

whether disease remission ( surgical,
response tests. However, in some dogs, high
chemotherapy) is followed by a regression

ALP with a glycogen-associated VH signals
in serum ALP activity or whether serum
the presence of atypical adrenal hyperplasia

ALP activity functions as a paraneoplastic
associated with abnonnal sex hormone
marker.

production. There is no consistent

After acute severe hepatic necrosis, ALP
relationship between the magnitude of
activity increases 2- to 5-fold in dogs and
sernrn ALP activity, the presence of high
cats, stabilizes, and then gradually declines

G-ALP activity, or histologic lesions.

over 2-3 wk. Sustained ALP activity usually

Unfortunately, G-ALP is not useful for
correlates witl1 a reparative ductal response
syndrome characterization because it can

(progenitor or oval cell hyperplasia). In
become the predominant ALP isoenzyrne in
cats, EHBDO results in a 2-fold increase
dogs treated with glucocorticoids and in
in ALP within 2 days, as much as a 4-fold
dogs with spontaneous or iatrogenic

434

HEPATIC DISEASE IN SMALL ANIMALS
hyperadrenocorticism, hepatic or nonheor prednisone ( 4.4 mg/kg/day, IM) may patic neoplasia, hepatic inflammation, or
increase GGT activity within l wk to 4-to
numerous diverse chronic illnesses,

7-fold above nonnal and up to 10-fold within
including primary liver disease.

2 wk Dogs treated with phenytoin or

The magnitude of ALP activity induced by primidone develop only a modest increase VetBooks.ir
glucocorticoid administration depends on
in serum GGT activity (up to 2-to 3-fold),
the type of drug and dose given, as well as
unless they develop anticonvulsant
the individual's response. The production of
hepatotox:icosis that is often associated

G-ALP does not in1ply that a dog treated
with marked enzyme activity.

with cortisone has iatrogenic hyperadreno

Cats with advanced necroinfla.mmatory
corticism, a suppressed pituitary-adrenal
liver disease, EHBDO, or inflammatory
axis, or a clinically important glycogenintral1epatic cholestasis can develop a associated VI-I. By comparison, the feline
larger increase in GGT activity relative to
liver is relatively insensitive to glucocorti

ALP Glucocorticoids and other enzyme
coids, with rare development of a glycogeninducers in dogs do not clinically influence associated VI-I or acceleration of hepatocyte
semm GGT in cats. The normal range
lipid vacuole accumulation.

for semm GGT activity in cats is much

In dogs, semm total ALP activity and
narrower and lower than that in dogs;

I.rALP isozyme also may be induced by
therefore, assays must be sensitive enough
administration of certain anticonvulsants
to detect low GGT activity.

(phenobarbital, prirnidone, and phenytoin)

GGT values can be markec!Jy increased
and other drugs; in th.is ci.rcwnstance, the
in dogs and cats with primary hepatic or

ALP activity usually increases 2- to 6-fold
pancreatic neoplasia. However, GGT does
normal. In contrast, semm ALP and l.rALP
not appear to be suitable for SUJveilJance of
did not increase in cats after administration
hepatic metastasis in either species.

of phenobarbital (0.25 grain, bid) for

Like ALP, GGT lacks specificity in

30 days.

clifferentiating between parenchymal
hepatic disease and obstructive biliary
disease. It is not as sensitive in dogs as ALP

Gamma-Glutamyl Transferase:

but does have higher specificity. In cats with

Garnma-gluta.myl transferase (GGT) is a
inflammatory liver disease, it is more
membrane-bound glycoprotein that plays
sensitive but less specific than ALP; these
a critical role in cellular detoxification
two enzymes should be interpreted

(involved with glutathione availability),
sinrnltaneously. The likelihood that HL has
conferring resistance against a number of
developed secondary to necroinflammatory
toxins and drugs. Tissue concentrations
liver disease, EHBDO, or pancreatic disease
of GGT in dogs and cats are highest in the
can be predicted by examining the relative
kidney and pancreas, with lesser amounts
increases in GGT and ALP Necroinflan1111ain the liver, gallbladder, intestines, spleen, tory disorders involving biliary structures,
heart, lungs, skeletal muscle, and erythrothe portal triad, or pa.i1creas are often cytes. However, serwn GGT activity is
associated with a greater fold increase in
largely derived from the liver, altfwugh

GGT tl1an in ALP With the exclusion of
there is considerable species variation in
these underlying disorders, cats with HL
its localization with.in this organ.

usually have a higher fold increase in ALP

Acute, severe, diffuse necrosis is
relative to GGT; tlus has impo1tant
associated with either no change or only
diagnostic utility in disceming the
mild increases (1- to 3-fold normal) in GGT

U11derlying cause of I-IL.

activity that resolve in -10 days. In dogs

Neonatal a.iumals of several species,
with EHBDO, seru.n1 GGT activity increases
including dogs but not cats, develop high

1-to 4-fold above normal within 4 days, and
se1um GGT activity secondary to colostrum

10- to 50-fold within 1-2 wk. Thereafter,
ingestion.

values may plateau or continue to increase
as high as 100-fold. In cats with EHBDO,

OTHER SERUM BIOCHEMICAL
semm GGT activity may increase up to

2-fold within 3 days, 2- to 6-fold within 5

MEASURES
days, 3- to 12-fold within l wk, and 4- to

Albumin: Albumin is produced exclu16-fold within 2 wk. Glucocorticoids and sively by the liver and has a half-life in
certain other microsomal enzyme inducers
healthy dogs estin1ated at -8 days. Because
may stinrnlate GGT production in dogs,
the healthy liver is estin1ated to maintain
sinillar to their influence on ALP. AdnlinisalbU111i.n synthesis at 33"A, maximal capacity, tration of dexa.methasone (3 mg/kg/day)

it has a large reserve capability for albumin

HEPATIC DISEASE IN SMALL ANIMALS

435
synthesis. Albumin functions as an essential

EHBDO. BilirubinLUia can be detected in
transport molecule, maintaining nonnal
healthy dogs because of their ability to
drug-receptor interactions. In liver disease,
conjugate bilirubin in renal tubules (low
decline in albumin concentration comprorenal threshold). However, bilirubinuria in VetBooks.ir
mises its transport functions, increasing
cats is always abnormal and should be
risk of adverse drug reactions (more free or
investigated. Fractionation of total bilirubin
unbound drug). Albumin's large role in
into direct ( cortjugated) and indirect
maintaining colloid osmotic pressure

( uncortjugated) moieties offers little
reflects its lower molecular weight
diagnostic utility. Bilirubin covalently
compared with other plasma proteins and
bound to albLUnin (biliprotein complexes)

its higher intravascular concentration. In
remains in the circulation and is not
inflarnmatory disease or during malnutriexcreted in urine. Chronic retention can tion, albLUnin may increase its transcapillary impart tissue jaLU1dice in t11e absence of escape rate, augmenting distiibution into
bilirubinuria long after a cholestatic
the interstitial space. Th.is phenomenon
disorder has resolved.

hastens onset of hypoalbuminemia in

Common causes of hyperbilirubinemia
anin1als with necroinflanllllatory liver
include increased hemoprotein liberation
disease, long before development of ascites.

( eg, hemolytic anemia, ineffective

Concurrent hypoalbun1inemia and
erythropoiesis, body cavity hemorrhage),
development of hepatic presinusoidal,
bile duct occlusion, ruptured biliary tract,
sinusoidal, or postsinusoidal portal
intrallepatic cholestasis, impaired
hypertension is commonly associated with
hepatobiliary bilirnbin processing, and
ascites in aninlals with chronic severe liver
sepsis. Jaundiced dogs and cats presenting
disease.

with regenerative anemia should be tested

Albunlin also ftmctions as a scavenger of
for hemolytic disorders, including
oxygen radicals and other oxidizing agents.

immune-mediated hemolytic anemia, Heinz

These antioxidant effects may be comprobody hemolysis, zinc toxicity, and erythromised in necroinflammatory liver disease parasites (including hemotropic Myco
and fulminant hepatic failure. Any disease
plasma [cats, dogs] andBabesia [dogs]).

processes promoting an oxidative
environment ( eg, diabetes mellitus, renal

BUN and Creatinine: There are no
disease, hepatic insufficiency, hyperthyroidcharacteristic changes in BUN or creatinine ism) can irreparably damage the albumin
concentrations with liver disorders except
molecule, accelerating its turnover
that low values are associated witl1

(synthesis and catabolism).

pmtosystemic shunting and feeding of a

In many anin1als with liver disease, an
restiicted protein diet ( only BUN, not creatiearly trend toward hypoalbuminernia often nine) formulated to reduce signs of HE. The
reflects systemic inflanllllation ( negative
concentration of BUN reflects nlll11erous
acute phase effect). Only in severe hepatic
variables, including hydration status,
insufficiency ( eg, chronic progressive
nutritional support, enteric bleeding, tissue
hepatitis) is synthetic failure a dtiving cause
catabolism, and the hepatic capacity to
of hypoalbuminemia. Protein-losing
detoxify ammonia. Anorexia, feeding a
nephropathy (glomerular disease) or
low-protein diet, or hepatic insufficiency
protein-losing enteropathy must be
can result in low normal to subnormal
excluded as underlying causes of hypoalbuconcenti·ation of BUN, whereas increased minemia. Glomerular causes are associated
values relative to creatinine ( discordant
with a urine protein:creatinine ratio >3 and

BUN :creatinine ratio) may reflect dehydrahypercholesterolemia, whereas proteintion, enteric bleeding, or consun1ption of a losing enteropathy is associated with panhyhig h -protein diet. Compared with BUN, poproteinemia and hypocholesterolemia.

serum creatinine concentrations are less
affected by dietary protein intake. The low

Bilirubin: Total bilirubin >2.5-3 mg/dL

BUN and low nom1al or low creatinine
results in clinical icterus. Hyperbilirubinconcentration often seen in animals with emia can reflect prehepatic ( eg, hemolysis),
portosystemic shunting reflect increased
hepatic (impaired uptake, intracellular
water tLU11over tl1at increases glomerular
transport, glucuronide cortjugation, or
filtration rate ( up to 2-fold), contiibuting
canalicular elinlination), or posthepatid
to PU/PD. Reduced hepatic synthesis of
extrallepatic causes (EHBDO, biliary tree
creatinine also contributes to low creatinine
rnpture). Total bilirubin concentrations vary concentrations in animals with hepatic markedly with different disease processes.

insufficiency, considering that creatinine

Concentrations are highest in dogs with
depends on hepatic synthesis of creatine
hemolytic disorders and in cats with HL and
in the transmethylation pathway.

436

HEPATIC DISEASE IN SMALL ANIMALS

Glucose: Hypoglycemia is uncommon in
microscopic shunts within the liver
acquired liver disease except end-stage

( congenital microvascular dysplasia) cause
cirrhosis or fulrninant liver failure. The
high TSBA concentrations, particularly in
inability to store hepatic glycogen or
postprandial samples. TSBA concentrations

VetBooks.ir
convert glycogen to glucose is more
are usually lower before a meal than
common in neonates and juvenile small2 hr after a meal. However, --15%--200Ai of breed dogs with congenital portosystemic
dogs and 5% of cats have higher TSBA
shunts. Other causes of hypoglycemia,
concentrations before a meal than after,
including sepsis, insulinoma, iatrogenic
likely reflecting physiologic variables
insulin overdose, rare glycogen storage
influencing the enterohepatic circulation
disorders, or paraneoplastic effects of large
of bile acids (ie, the rate of gallbladder
primary hepatic neoplasia ( canine
contraction, gastric emptying, and intestinal
hepatocellular carcinoma or adenoma) or
transit of bile acids to the ileum where they
other tumors should be considered in an
are actively resorbed). TSBA concentraanimal with suspected liver disease.

tions in dogs >25 µMIL or in cats >20 itMIL
are abnormal either before or after a meal

Cholesterol: All cells in the body except

(fasting ranges should not be applied

RBCs synthesize cholesterol for intracellubecause of the variables influencing the lar use. Cholesterol incorporated in plasma

TSBA enterohepatic circulation). Collecting
lipoproteins is synthesized only in the liver
a single sample for TSBA measurement
and distal small intestine. Bile provides the

( random fasting or a single postprandial
major excretory pathway for cholesterol.

sample) can miss detection of abno1n1al

Hypocholesterolemia may reflect endovalues. Because TSBA concentrations are a crine, metabolic, and nutritional factors as
more sensitive indicator of cholestasis than
well as hepatic insufficiency and portosystotal bilirubin, measuring TSBA concentratemic shunting. Nonhepatic disorders tion is redundant in anin1als with nonhemoassociated with hypocholesterolemia lyticjaundice. Use ofTSBAs as a liver
include hypoadrenocorticism, maldigesfunction test can indicate need for a liver tion/malabsorption, pancreatic exocrine
biopsy. TSBA concentrations should be
insufficiency, severe starvation, cachexia,
routinely measured in all young (6 mo),
sepsis, and hyperthyroidism (cats); hepatic
small, "terrier-like breeds" to detect dogs causes include portosystemic shunting
with microvascular dysplasia (MVD).

( congenital or acquired) and severe hepatic

Finding increased TSBA concentrations in
insufficiency ( eg, end-stage cirrhosis,
apparently healthy, young, terrier-like
fulrninant hepatic failure). Hypercholesterbreeds, including but not restricted to olemia is more common in ill animals and

Yorkshire Terriers, Maltese, Shih Tzus,
requires careful consideration of potential

Miniature Schnauzers, Cairn Terriers,
nonhepatic disorders, including hypothy

Norfolk Terriers, Havanese, Papillons,
roidism, diabetes mellitus, pancreatitis,

Tibetan Spaniels, and Pugs, allows
nephrotic syndrome, hyperadrenocorticism
detection of dogs in which TSBA concentraor treatment with glucocorticoic:16, tion will be misleading if discovered in later
idiopathic dyslipidemias, and rarely a
life during evaluation of illness.

postprandial effect. Hypercholesterolemia
is usually seen in EHBDO and in some

Ammonia: Measurement of blood
animals with diffuse intrahepatic cholestaan1monia can detect hepatic disorders sis, destructive cholangitis, and marked
associated with HE. Ammonia is derived
hepatic regeneration.

predominantly from protein degradation,
with most generated in the intestines from

HEPATIC FUNCTION TESTS
consumed food and enteric bacterial
ureases that catabolize urea into an1111onia
and carbon dioxide. Portal transport of

Total Serum Bile Acids: TSBA
an1monia from the intestines to the liver
concentrations sensitively detect choleresults in a direct 85% detoxification to urea.

static disorders and conditions associated

Ammonia intolerance (in1paired clearance)

with portosystemic shunting. TSBA
occurs in any disorder associated with
concentration should be measured before
portosystemic shunting and in acute
and 2 hr after meal ingestion; fasting is not
fulminant hepatic failure. Ammonia is not
required. Insufficient hepalic mass or
influenced by cholestasis or liver disorders
deviated portal circulation to the systemic
that do not deviate the portosystemic
circulation via extrahepatic portosystemic
circulation or extensively reduce hepatic
shunts ( congenital or acquired) or
parenchyrnal mass.

HEPATIC DISEASE IN SMALL ANIMALS

437

Although ammonia is regarded as a

IMAGING
pivotal cause of HE, animals with overt HE
may have normal blood ammonia concen

Radiography: Routine abdominal

Lrations owing to complicated pathologic
radiographs are useful to detemline liver

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mechanisms driving HE. A single normal
size and may detect irregular liver borders.

ammonia value cannot discount HE in an

Mineralized densities that involve parenanimal with suspected chronic liver disease, chyma or the biliary tree can reflect stasis
and serial ammonia measurements may not
of bile flow, dystrophic mineralization
correlate with an evolving clinical scenario
associated with congenital malformations,
of HE. Thus, ammonia measurements
acquired duct "sacculation," chronic duct
cannot reliably diagnose HE.

inflammation, or choleliths. Choleliths that

Measurement of blood ammonia is
contain enough calcium bilirubinate or
complicated. Spurious hyperammonemia
calciun1 carbonate are radiographically
can reflect slow blood collection, tight
visible. A mass effect in the right cranial
tourniquet technique, conditions promoting
quadrant in suspected EHBDO may
ammonia liberation from muscle (seizures,
represent an engorged gallbladder,
crush injuries), sample contamination
pancreatitis, neoplasia, or focal bile

(human sweat, cigarette smoke, open urine
peritonitis. Radiographic suspicion of
vials), and spontaneous generation in
abdominal effusion (poor abdominal detail)

san1ples not in1rnediately cooled on
may prompt diagnosis of bile peritonitis and
collection or not promptly analyzed.

ascitic effusion. Gas within hepatic

Ammonia is highly volatile, and samples
parenchyma or biliary structures indicates
cannot be mailed for analyses. Blood
an emphysematous process ( eg, cholecystisan1ples should be collected into pre-cooled tis, choledochitis, infected biliary cyst,
tubes and transported on melting ice to the
hepatic abscess, necrotic tumor mass) and
laboratory for analysis within 20 min.

warrants prompt antimicrobial therapy and

Enzymatic-based methodologies are
either surgical intervention or percutanedifficult to standardize. Nonhepatic causes ous, ultrasound-guided aspiration/lavage.

of hyperammonemia also exist, with the

Thoracic radiography can indicate signs of
most common disorders involving bacterial
systemic disease ( eg, metastatic lesions,
infection of the urinary tract with a
pleural fluid). Finding sternal lymphadenopurease-producing organism associated athy is conunon in cats witll the cholangitis/
either with uroabdomen or obstructive
cholangiohepatitis syndrome, in which it
uropathy.

reflects hepatic infla.nunation.

If a random blood ammonia concentra

Altllough cholecystography can be
tion is within nonnal limits but hepatic
accomplished with iodinated contrast given
insufficiency and portosystemic shtmting

PO or IV, contrast radiographic imaging of
suspected, an ammonia tolerance test can
the biliary system is rarely pursued.

be conducted. Ammonium chloride is given

Distribution and concentration of contrast
at 100 mg/kg in a 5% solutfon orally ( can
agents within biliary structures is influenced
induce vomiting) or at 2 mUkg of a 5%
by nun1erous variables, including hyperbilisolution administered rectally (instilled 30
rubinemia and major duct occlusion. At
cm deep) after a cleansing enema, with
best, these agents may disclose cholelitlls,
blood ammonia measured at baseline and
polyps, or sludged bile but are insufficient to
then at 20, 30, 40, or 60 min later. Unfortuconfinn bile peritonitis or to localize the site nately, an ammonia tolerance test may
of leakage. Multisector CT and/or hepatic
induce iatrogenic HE in susceptible
ultrasonography are more useful to discern
animals.

tllese processes.

The presence of ammonium biurate

Contrast studies of the portal vasculature
crystalluria in an animal with high TSBA.s
are tile gold standard for confinnation of a
is pathognomonic for hyperammonemia
congenital portosystemic shunt. Radioand portosystemic shunting. A minimum of graphs should be taken in right and left three urine samples collected at separate
lateral and ventrodorsal positions for best
daily intervals should be inspected to
test sensitivity. Multisector CT imaging
optimize surveillance for crystal discovery.

produces exceptional in1ages and has

In animals on restricted protein intake
replaced radiographic portography for
using diets specifically formulated for
diagnosis of congenital portosystemic
hepatic insufficiency, finding ammonium
shtmts because it allows contrast ir\jection
biurates may be difficult because of the
into a peripheral vessel, can capture
high efficacy of such diets to control
numerous images per second, and allows
hyperammonemia.

wee-dimensional anatomic reconstruction.

438

HEPATIC DISEASE IN SMALL ANIMALS

Ultrasonography: There are many
hemobilia, bacteremia, and vasovagal
diagnostic applications of hepatic
reaction, especially in cats, that may result
ultrasonography: 1) identify distention and
in ventilatory arrest, severe bradycardia,
determine thickness of biliary structures;
and death. If a gallbladder mucocele or

2) verify conunon bile duct obstruction;

EHBDO is suspected, cholecystocentesis is

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3) detect gallbladder mucoceles and
contraindicated. It is better to perfo1m a
cholelithiasis; 4) differentiate between
cholecystectomy for gallbladder mucocele
diffuse and focal hepatic abnormalities;
and surgically decompress EHBDO (relieve

5) identify and detemline dimensions of
or bypass the obstruction).

"mass lesions"; 6) identify pancreatic,
mesenteric, and perihepatic lymphadeno

LIVER CYTOLOGY
megaly; 7) in coajunction with vascular
studies, identify congenital intrahepatic

Ultrasonographic-guided fine-needle
and extrahepatic portosystemic vascular
aspirates are routinely used to confum
anomalies (PSVAs), APSSs, arteriovenous
a diagnosis of HL in cats and to identify
malformations, and hepatic venule
suppurative septic inflammation, neoplasia,
distention reflecting passive congestion;
and glycogen-like VH. However, definitive
and 8) detect small volume abdominal
diagnosis of hepatic disease is otherwise
effusion and small volume of fluid
impossible with liver aspirates because the
sun-ounding the gallbladder. However,
absence of acinar architecture comproalthough abdominal ultrasonography has mises anatomic orientation and correct
become an indispensable diagnostic tool to
interpretation. Cytologic interpretation of
assess the liver and biliary system, its use is
liver aspirates are notoriously discordant
highly operator dependent, and findings
with histologic fmdings on biopsy
must always be reconciled with the history,
specimens. Neither neoplasia nor sepsis can
physical examination findings, and
be definitively excluded using cytology, and
clinicopathologic data. Reconciliation of
inflan1matory disease is too often susdata is best done by the principal clinician pected. Cytology should not be the basis
managing the case, who has the most
to recommend inununomodulatory or
knowledge of the animal's management
antifibrotic medications or longterm
and prognosis.

chelation therapy for copper-associated
hepatopathy. Rather, liver biopsy remains

Computed Tomography: Multisector
the standard for diagnoses of most hepatic

CT imaging, available in specialty referral
disorders.

practices and university teaching hospitals,
can distinguish mass lesions, detect

LIVER BIOPSY
changes in structure of hepatic parenchyma
and the biliary system, identify choleliths,

Hepatic needle true-cut biopsies ( especially
detect abnonnal hepatic perfusion

18-gauge) collected under uJtrasonographic

(involving the portal vein, hepatic artery, or
guidance may yield samples too small and
hepatic vein), and portal thrombi, and can
fragmented for accurate diagnosis because
detail the extent of traumatic hepatobiliary
of a lack of representative acinar units ( at
iajuries.

least 15 portal triads should be sampled).

Furthem1ore, needle biopsies are usually
only collected from the mqre safely sampled

CHOLECYSTOCENTESIS
left-side lobes, which may miss lesions
differentially affecting liver lobes ( eg,

Cholecystocentesis is the aspiration
cholangiohepatitis in cats). Blind-needle
sampling of gallbladder bile; this can be
biopsies done without ultrasonographic
completed using a percutaneous transguidance are hazardous and ill advised in hepatic ultrasound-guided approach,
animals with suspected hepatic hilar or
by laparoscopic assistance, or during
mesenteric lymphadenomegaly; involveexploratory abdominal surgery. Samples of ment of the common bi.le duct, gallbladder,
bile are collected for cytologic investigation
intestines ( eg, inflanllllatory bowel disease,
and culture of aerobic and anaerobic
infiltrative disease), or pancreas; or multiple
bacteria and fungi; collection of bile that
organ abnom1alities. An exploratory
contains particulate debris or sedin1ent has
laparotomy is more appropriate. When
the highest yield to find microorganisms
possible, wedge biopsies or laparoscopic

( cytologically, by culture). Complications of cup forcep biopsies are preferred, because cholecystocentesis may include intrape1;tosamples of adequate size can be easily and neal bile leakage (reduced by using a
safely acquired from multiple liver lobes,
transhepatic approach), hemorrhage,
ensuring accurate disease representation.

HEPATIC DISEASE IN SMALL ANIMALS

439

These methods also permit assessment of
time is more relevant when performed
the gross appearance of the liver. Notably,
inunediately before the procedure. Animals
laparoscopic methods are not recomsuspected to have bleeding tendencies mended when disease of the common bile
should be treated with vitanlin K1
duct or gallbladder is suspected that may

(0.5-1 mg/kg, SC or IM) at 0, 12, and24 hr

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necessitate a decompressive biliary
before tissue sampling. lf buccal mucosa!

procedure, cholecystectomy, or cholestotbleeding tin1e is >5 nlin, a fresh frozen plasma omy. Liver biopsy should always be done
transfusion is indicated, as is administration
even if an obvious biliary abnormality is the
of desmopressin acetate (DDAVP,
predominant disease process, because

0.3-1 mcg/kg diluted in saline), which
underlying histologic liver lesions may
increases plasma vWF 2 -fold over baseline
indicate another primary disease process. It
within 1 hr as well as plasma activity of Factor
is also important to biopsy grossly normal
vm. DDAVP can initiate a hemostatic effect
liver when focal lesions are identified. This
in dogs with type 1 vWF (partial quantitative
practice ensures 1) characterization of
deficiency) but not in dogs with qualitative

"normal" liver histology, 2) determines
defects or complete vWF deficiency. In many
whether an underlying liver disease
people with liver disease, DDAVP has
coexists, 3) investigates histology of liver
improved coagulation ability, although the
distant to the gallbladder in animals
exact mechanisms remain incompletely
undergoing cholecystectomy, and
clarified.

4) provides multiple liver lobe samples
needed to confinn suspected MVD (because
this lesion is variable among liver lobes).

PATHOLOGIC CHANGES IN BILE

Routine biopsy evaluation should include
examination of a cytologic imprint, Gram

(White bile syndrome, lnspissated bile
stain (if suppurative or pyogranulomatous
syndrome, Bilirubin deconjugation)

inflanunation is cytologically detected),

In anin1als with bile stasis, nonabsorbable
routine H&E staining and interpretation,
bile constituents (bile salts, phospholipids,
as well as staining with a reticulin stain
glycoprotei.ns, and cholesterol) are subject

( discloses sinusoidal collapse of the
to concentration or di.I ution when water and
supporting scaffolding of the liver), Masson's
inorganic electrolytes (sodium, chloride,
trichrome (to confirm presence and severity
bicarbonate) are resorbed or added by the
of fibrillar connective tissue deposition),
biliary epithelium. EHBDO can produce a

Prussian blue to identify iron retention in

"white bile" syndrome reflecting the

Kupffer cells (fixed macrophages) and
absence of bilirubin pigments; this usually
hepatocytes (helps confmn lobular
is found in aninlals with an obstructed
involvement in inflanunation, Kupffer cell
gallbladder at the level of the cystic duct or
activation, presence of rare hemochromatoin animals with obstruction of the hepatic sis ), rhodanine stain for copper ( confirms
ducts. Stasis of bile flow also may cause bile
and can be used to quantify copper with
dehydration, promoting a pathologically
digital scanning of the rhodanine-stained
thickened or sludged bile typically dark
section), aerobic and anaerobic bacterial
green to black in color. Formation of a
cultures of liver and bile, and quantification
gallbladder mucocele involves the
of liver metals ( copper, iron, and zinc concenentrapment, retention, dehydration, and trations because these values can help
local overproduction of mucin that lends
evaluate risk of oxidative i.rtjury and need for
a rubbery viscosity to bile. Bile stasis in
zinc supplementation). A tissue sample
obstructed ducts can lead to bilirubin

(formalin fixed) should also be reserved for
deconjugation, which reduces bilirubin
other special case-specific studies such as
solubility and favors cholelith precipitation.

special inununohi.stochemical stains or for

Choleresis (enhanced bile flow) produces

PCR testing for infectious agents.

"watery," dilute bile and is a therapeutic goal Before biopsy, bleeding tendencies should
in disorders associated with bile stasis.

be evaluated by careful review of the history,
physical examination, blood smear (to

NUTRITION
confirm platelets d00,000/µL), routine
coagulation profile (prothrombin time [PT],

Nutritional support has a pivotal influence
activated partial thromboplastin time
in cats with HL and is an important

[APTT]), von Willebrand factor (vWF)

component of at-home treatment in aninlals
activity in high-risk breeds, and a buccal
with slowly progressive hepatobiliary
mucosa] bleeding time. Routine coagulation
disorders. Proper nutritional support
assessments have low reliability to detect
improves quality of life in anin1als with
bleeding risk. The buccal mucosa! bleeding
hepatic insufficiency prone to HE. Diets for

440

HEPATIC DISEASE IN SMALL ANIMALS
animals with hepatobiliary disease should

Energy allowances may require adjustment
be easily digestible, highly palatable,
after the diet is accepted, the animal is
calorically dense, easy for the owner to
stable, and weight and body condition
prepare and feed, and fed frequently as
reassessments confirm a need for higher or
small meals. Objectives are to optimize food lower intake. Estimation of initial energy digestion and assimilation and to achieve
intake is calculated using fom1ulas that

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voluntary food consumption.

predict resting energy requirements in

If animals are anorectic, tube feeding
healthy animals. Formulas for estimation of
should be considered. Nasogastric tubes are initial energy allocations for dogs are 30 x inexpensive, easily placed, and recombody wt (kg) + 70 (for dogs 2-16 kg); 70 x mended as a short-term solution. Esophabody wt(kg}°-75 (for dogs <2 or >16 kg); or gostomy tubes are preferred in cats with HL

99 x body wt (kg)0.67 ( safe initial intake for
for longer dietary support. Use of appetite
a healthy dog).

stimulants remains controversial, because

For cats, 60 x body wt (kg) is often used,
they may delay institution of regimented
unless the cat is markedly overconditioned
nutJ.itional support. In addition, some
or has a subnormal metabolic rate or
commonly used drugs are metabolized in
activity level. Frequent reassessment is
the liver. Diazepam and oxazepam may
necessary with energy allowances tailored
rarely lead to idiopathic fulrninant hepatic
to response.

failure in cats.

Dietary modification for animals with

Dietary Protein Allowance: A diagnosis
liver disease depends on tl1eir clinical
of liver disease should not automatically
status, tl1e definitive diagnosis, and
dictate a need for protein restriction. In fact,
assessment of liver function. Diets should
protein restriction can be detJ.imental in
be balanced and supplemented with
some animals, eg, cats with HL or animals
water-soluble vitamins. In severe choleswith chronic but stable necroinflanllllatory tatic disorders that impede enteric access
liver disease that do not have APSSs or HE.

of bile (eg, EHBDO, advanced sclerosing

Unfortunately, altering nutritional support
cholangitis in cats), fat-soluble vitamins
can be difficult and challenging in anin1als
may become depleted. Vitamin K1 can be
that reject novel diet modifications. Protein
supplemented via parenteral injection of
restriction is appropriate when HE is

0.5-1.5 mg/kg every week (titrated against
suspected, an1lllonimn biurate crystalluria
a thrombotest [PIVKA assay] or PT). If
is observed in an animal with suspected
vitan1in K1 depletion is confinned, vitanlin E hepatic insufficiency, orportosystemic also likely needs supplementation. Because
shunting ( congenital or acquired) is either
vitanlin E is a fat-soluble vitan1in, a unique,
confinned by imaging studies or suggested
water-soluble form may be necessary for
by protein C assessments.

ora.J administration: polyethylene glycol

The protein allowance for an animal with
ac-tocopherol succinate (10 IU/kg/day, PO).

HE should maintain a positive nitrogen

It is important to follow dosing recommenbalance, avoiding tissue catabolism. Because dations, because excessive vitamin K can
maintenance of lean body mass (muscle)

lead to hemolytic anemia (in cats), and
provides a temporary respite from ammonia
excessive vitanlin E can interfere with
toxicity, body condition should be monitored
vitanlin K function.

regularly for comparative estin1ates, with tl1e

Liver function also has considerable
goal being to maintain muscle mass.

influence on glucose homeostasis (glycogen

When protein restriction is deemed
olysis or gluconeogenesis from aniino acids
necessary, initial restriction to 2.5 g protein/
and lactate), detoxification of nitrogen ( urea
kg body wt ( <5 g protein/100 kcal diet) for
cycle), and ketogenesis (from fatty acids).

dogs and 3.5 g protein/kg body wt

In rare circumstances, in animals prone to

( <7 g protein/100 kcal) for cats is advised.

hypoglycemia, low-dose IV glucose may be

Sequential historical, physical, and
transiently needed. Protein modification and
clinicopatl1ologic assessments judge
restriction is used to address insufficient
treatJ.11ent response and guide further
nitrogen detoxification (see below).

tailoring of these recommendations.

Most protein-restricted diets are used in

Energy Allowance: Energy allocation
dogs with chronic, severe liver disease or
should be estimated based on ideal body
that have PSV

A. If a dog responds well to an
weight, with modified diets gradually
initial protein restriction, -0.25--0.5 glkg/day
introduced. Initial intake should be no
can be added, using a tofu or dairy-based
greater tllan 500.Ai of tile calculated daily
protein source. Aninlals should be
energy requirement on day 1, increased to
monitored every 1 -2 wk for signs of HE and

75% on day 2, and then to 100% by day 3-5.

alterations in albunlin, BUN, and appear-

HEPATIC DISEASE IN SMALL ANIMALS

441
a.nee of an1monium biurate crystallrnia
exception is dogs with gallbladder
during dietary protein titration. Three urine
mucoceles, some of wllich have idiopathic
san1ples should be collected: first thing in
hyperlipidemia; in these, feeding a high-fat
the morning, 4--8 hr after feeding, and late
diet can facilitate rapid maturation of the
in the evening to optimize scrutiny for
gallbladder mucocele.

an1monium biurate crystalluria.

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Dietary protein should not be restricted

Micronutrients and Vitamins: Water
in cats with HL, because protein restriction
soluble vitamins should be supplemented
compromises survival. Protein should not

( via IV fluids) in animals with chronic liver
be restricted in most dogs and cats with
disease and cats with HL (see TABLE 12). Cats chronic necroinfian1rnatory liver disorders
are especially susceptible to thiamine (B1),
at the time of diagnosis, because many of
cobalanlin (B12), and vitamin K1 deficiency
these aninlals may have higher protein
when they are chronically inappetent,
requirements than a comparably sized,
treated with antin1icrobials, have severe
healthy, age-matched control for tissue
intestinal or pancreatic disease, or
repair and cell replication. In people with
demonstrate chronic cholestasis. Hypersimilar health status, nitrogen requirements thyroid cats may develop malabsorptive
increase as needed for increased nitrogen
problems and may be more prone to these
utilization (tissue repair and regeneration).

complications when also affected with
cholangiohepatitis or HL. Vitan1in C is not

Modified Protein Quality/Source:

recognized as a commonly depleted

Altering the type and quality of protein
micronutrient in either dogs or cats. Dogs
intake for dogs with HE can help achieve
with copper storage hepatopathy and
good life quality. A high energy:nitrogen
anin1als with large hepatic iron stores
ratio should be maintained, because this
should probably not receive vitan1in C
optimizes use of dietary protein. In dogs,
supplements, because tllis may augment
dairy and vegetable quality protein (soy)

oxidative injury associated with transition
sources work best. Dairy quality protein
metal accU111ulation.

(amoU11t per 8 oz) can be fotmd in the

Supplementation of fat-soluble vitamins
following products: whole milk (8 g in
is important in animals with fat malabsorp157 cal), yogurt (8 g in 139 cal), cottage tion and obstructed bile flow. Vita.nun K
cheese (28-31 g in 200-250 cal), and

1
depletion develops when the enterohepatic
cheddar cheese (57 g in 800-900 cal).

bile acid cycle is inteITupted in anin1als

Alternatively, in dogs, calcirn11 caseinate
demonstrating acholic feces ( eg, EHBDO,
can provide 88 g protein, 2 g fat, and 370
severe destructive [sclerosing ductopenic]

kcal/100 g portion. Using dairy quality and
cholangiohepatitis in cats), HL (cats),
vegetable-derived protein can be estimated
exocrine pancreatic insufficiency, severe
using the Nutritional Analysis Tool 2.0
malabsorptive intestinal disease, after

(hU111an nutrition). In cats, which are pure
feeding a vitamin K -deficient die1i, aninlals
carnivores, a meat-based protein source is
chronically treated with oral antimicrobials,
recon1mended in a balanced diet that
and in anin1als with severe liver disease
contains adequate arginine ( -250 mg/100
causing insufficiency. Vitamin K should be
kcal diet) and tarni.ne for feline metabolism
administered to any jatmdiced animal with

( several commercial presc1iption foods
suspected liver disease as early as possible
meet these requirements).

(0.5--1.5 mg/kg, SC or IM, three times at

12-hr intervals) before invasive procedures

Dietary Fat: There is no need to restrict

(insertion of catheters in large veins,
dietary fat in most aninlals with hepatobilcystocentesis, insertion of feeding tubes, iary disease, because these animals
hepatic aspiration sampling, or liver
typically have no problems with fat
biopsy). In ductopenic feline sclerosing
digestion or assinlilation. Fat ingestion is
cholangitis or chronic EHBDO, animals
in1portant to provide essential fatty acids
require intemlittent vita.Illin K 1 injections
and fat-soluble vitanlins. One exception is

(eg, every 7-21 days), monitored by PIVKA
anin1als with chronic EHBDO or cats with
or PT clotting tests. Overdosing with
sclerosing cholangitis ( destructive cholangivitamin K 1 can lead to symptomatic Heinz tis) with symptomatic "ductopenia" (pale
body hemolytic anenlia in cats.

acholic feces, bleeding tendencies, marked

Vitamin E is an important antioxidant,
jaU11dice). These aninlals have reduced
antiinfian1matory, and antifibrotic used in
entry of bile into the alimentary canal and
necroinflan1matory and cholestatic liver
impaired enterohepatic circulation of bile
disorders. Oral o-u-tocopherol acetate is
acids, linliting emulsification, digestion,
given at 10 IU/kg/day. Higher dosages (100
and assin1ilation of ingested fat. Another

IU/kg/day) are needed in aninlals with

442

HEPATIC DISEASE IN SMALL ANIMALS

FOR MULATION OF A FORTIFIED, WATER-SOLUBLE VITA MIN

SUPPLEMENT" FOR DOGS A N D CATS WITH LIVER DISEASE

Vitamin Supplement

Concentration per mL

Thiamine hydrochloride (vitamin 81)

50mg

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Riboflavin 5' phosphate sodium (vitamin 8

2-2.5mg

2)

Niacinamide (vitamin 83)

50-100 mg
o-Panthenol (vitamin 85)

5-lOmg

Pyridoxine H Cl (vitamin 86)

2-5 mg

Cyanocobalamin (vitanlin 812)

Variable; 0.4-50 mcg (low 812 values
necessitate additional supplementation in deficient cats, SC or IM) 8enzyl alcohol (preservative)

1.5%
a 2 mL/L of N fluid
chronic EH8DO or feline destructive
volun1e and systemic perfusion may prevent
cholangitis ( ductopenic sclerosing cholangior mitigate the severity of organ failure that tis). Alternatively, cx-tocopherol polyethyloften accompanies fulminant hepatic failure ene glycol succinate (water-soluble vitamin

( eg, renal, cardiac, adrenal, pancreatic

E) can be used at 10 IU/kg/day. Dosing of
dysfunction). Lactated Ringer's solution
vitamin E should not exceed recommended
should be avoided in animals with
amounts, because too much vitanlin E can
compronlised lactate metabolism, leading
interfere with vitamin K activity, provoking
to lactic acidosis. Chronic vomiting and
coagulopathies. Too much vitamin E also
diarrhea often accompany fulminant
can impart oxidant injury secondary to
hepatic failure and can lead to dehydration,
accumulation of the tocopheroxy radical.

hypokalernia, hypochloremia, and
metabolic alkalosis. Alkalosis and
hypokalernia can each escalate renal
anrn10nia production, contributing to

FULMINANT HEPATIC FAILURE
hyperan1monemia and HE. Neuroglycopenia can induce neurologic signs that can be Fulrninant hepatic failure is a syndrome
confused with and augment HE. Adnlinistradefined by the abrupt loss of liver function, tion of 0.9"A, NaCl with supplemental
associated with hepatic encephalopathy
vita.nuns and glucose is usually a safe first

(HE) and coagulopathy. Early, appropriate
option uruess portal hypertension and
therapy is critical. In chr@nic or end-stage
ascites complicate the syndrome. Dextrose
liver disease with an acute or chronic insult

(2.5%) and potassium (slidiJlg scale) should
and in acute liver injury with no apparent
be judiciously added to IV fluids, as well as
underlying cause, treatment provides
water-soluble vitanlins (fo1tified 8-soluble
supportive care to allow time for hepatic
vitanlins at 2 ml/L of fluid). Ascites may
regeneration and compensation.

develop in animals with an acute sinusoidal

Specific treatment should be adminiscollapse or acute or chronic fibrosing tered if an underlying cause is detemlined.

hepatic injury.

Decontamination of oral, dermal, and

In cats, a812 injection (250-1,000 mcg
enteric surfaces is mandatory if toxin
total dose, IM or SC) should be considered if
exposure has occurred within 36 hr. If an
severe gut disease, pancreatic disease, or
adverse drug reaction is implicated, the
starvation are suspected; a plasma san1ple
drug in question must be discontinued and
for assessment of812 should be collected
antidotes investigated. Life-threatening
before treatment. Definitive assessment of
infection, cerebral edema, and coagulopamethylmalonic acidemia defines 812
thies are major complications.

adequacy but cannot be completed in a

Attention to fluid, electrolyte, and
timely manner for clinical application in
acid-base balance, glycemic status, and
emergent liver failure. Thianline deficiency
nutritional support optinlizes chance of

(81) can also complicate clinical status,
survival. Restoration of intravascular
producing neurobehavioral signs overlap-

HEPATIC DISEASE IN SMALL ANIMALS

443
ping with HE. Although hyperglycemia must acetate (DDAVP, 0.3 mcg/kg, IV, diluted to be avoided because it can worsen cerebral

1 ()OA, in saline) can sometimes arrest serious
edema, euglycemia must be established
clinical hemorrhage by in1proving primary
before thiamine administration; otherwise,
hemosta.sis. With acute portal hypertension,
thiamine-provoked neuroglycopenia may
diapedesis of blood into the enteric lumen
aggravate neurologic iltjury and clinical
may develop before opening of APSSs;

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signs. Thiamine is especially important in
this can lead to lethal blood loss and/or
cats and can be supplemented PO or slowly
aggravate HE. In this scenario, only a whole
with IV fluids (fortified B-soluble vitamin
blood transfusion or administration of
solution); 25-100 mg/day is reconunended.

packed RBCs and species-specific plasma

Animals with acute liver failure have high
can replace exti·acorporeal losses.

energy expenditure and protein catabolism.

Concurrent propranolol administration may

Nutiitional support should be attempted
reduce portal hype1tension, which may
ente1ically with protein intake initially
lessen the rate of blood loss.

restricted to 2.5 g/kg body wt in dogs and

The goal of therapeutic strategies in

3.5 g/kg body wt in cats, with overt HE. If
fulminant hepatic failure is to prevent the
neurologic signs are inapparent, protein
onset of encephalopathy, limit its severity,
restriction is not advised.

and reduce the risk of cerebral edema.

Broad-spectrum antibiotics should be

Development of cerebral edema is
given empirically if HE, renal failure, or
multi.facto1ial, complex, and incompletely
components of the systemic inflanunatory
tmderstood. Mediators of systemic and local
response syndrome (SIRS) are identified.

inflammation and circulating neurotoxins

As for other suspected bacterial infections

( especially anunonia) contribute to its
involving the liver, a combination of
development. HE also can be precipitated
ticarcillin, meti·onidazole (7.5 mg/kg, bid,
by systemic infection, hypotension, and

PO or IV), and enrofloxacin a.re advised.

systemic vasodilatation. Altered cerebral

In most cases, N -acetylcysteine is
endothelial penneability in response to
administered for the first 2 days to provide
neurotoxins ( eg, ammonia) and inflan1macysteine for glutathione synthesis, to improve tory mediators, inflan1matory responses, microcirculatory perfusion, and to protect
and altered cerebral blood flow are also
against development of SIRS. A loading dose
recognized to trigger or worsen HE.

(140 mg/kg) is initially administered through

The head and neck should be maintained
a 0.25 µM filter and given over 20 min;
in a neutral position, avoiding compression
prolonged infusion can precipitate hyperof jugular blood flow; elevation of the head anunonemia Thereafter, 70 mg/kg is given
and neck can reduce intracra.nial pressure

IV at intervals of� hr for 2 days. Rarely, an
and decrease CSF hydrostatic pressure.

adverse reaction develops, manifesting as

Central venous lines increase risk of serious
urticaria, pruritic rash, vomiting, and most
iatrogenic hemorrhage, which may require
severely as angioneurotic edema
use of compression bandaging. Spontane

When oral medications can be tolerated,
ous hyperventilation sustains a mild
biologically available S-adenosylmethionine respiratory alkalosis that promotes cerebral (SAMe) is reconunended at 20-40 mg/kg/
arterial vasoconstriction, which tends to
day, PO, given on an empty stomach to
reduce intracerebral pressure. Hypoxia
sustain hepatic glutathione adequacy.

must be avoided because of its associated

Initially, vitamin K, (0.5-1.5 mg/kg, IM or
cerebral vasodilatory effect. Marmitol

SC) is given in three doses at 12-hr intervals.

(0.25-0.5 g/kg, given as an IV bolus) can help

Repeated dosing may be necessary in
reduce cerebral edema; boluses can be
animals with overt coagulopathies.

repeated if serum osmolality has not

However, a balanced hemostatic defect with increased. Furosemide (0.5-1 mg/kg, every loss of hepatic procoagulant synthesis

� hr) has been used to increase renal
paralleled by the loss of hepatically derived
elimination of sodium and water. Use of
anticoagulants results in the lack of an overt hypothermia, barbiturate coma, hypertonic coagulopathy. Inhibition of gastric acid
saline, or flumazenil infusions are not
secretion with an H2-receptor antagonist
recommended.

( eg, famotidine, faster onset) or HCl pump
inhibitor ( eg omeprazole, slower onset) is

HEPATIC ENCEPHALOPATHY
advised. Omeperazole inhibits certain p450
cytochromes and may result in polyphar

Hepatic encephalopathy (HE) develops in
macy drug interactions. If overt hemorliver disorders associated with portosysrhagic tendencies are seen, fresh frozen temic shunting, fulminant hepatic failure, or
plasma or cryoprecipitate (for vWF and
cirrhosis (acquired portosystemic shunts,
fibrinogen) may be needed. Desmopressin
reduced functional hepatic mass, intralle-

444

HEPATIC DISEASE IN SMALL ANIMALS
patic shunting of blood around regenerative

Ammonia can influence multiple
nodules). Clinical signs vary but involve
neurotransmitter systems directly
disturbed sensorium ranging from mild

(chemical influence) and indirectly (altered
dullness and an inability to respond to basic
substrate availability for transmitters).

conm1ands to overt abnormalities, including There is substantial evidence that astropropulsive circling, head pressing, aimless cytes play an important role in the

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wandering, wealrness, ataxia, arnaurosis
pathogenesis of HE. Ammonia and other

(unexplained blindness), ptyalism, dementia, endogenous products, inflammatory behavior change (eg, aggression), collapse,
cytokines, and hyponatremia (associated
seizures, and coma. Although the pathowith portal hypertension) induce astrocyte physiologic mechanisms of HE are not
swelling that can lead to brain edema and
completely known, synergistic effects
herniation most common in acute liver
between the failure of the liver to detoxify
failure and acute severe HE.

ammonia and other endogenous substances,

Treatment of acute HE is aimed at
increased cerebral inflanmiatory cytokines,
providing supportive care and rapidly
impaired brain perfusion, development of
reducing neurotoxins produced in the GI
neuronal edema, hypoxia, mitochondrial
tract. Severely encephalopathic animals
dysfunction, neuroglycopenia, and
may be semi comatose or comatose.

oxidative injury are important interdepend

Benzodiazepines and other sedatives
ent mechanisms. Increased production of
should not be administered. Food should
reactive oxygen and nitrogen oxide species
be witl1held until neurologic status
are thought to trigger protein and RNA
improves. Fluids (2.5% dextrose and 0.45%
modifications that deleteriously influence
saline with potassium chloride ai1d vitan1in
brain function. The integrated concept of

B complex added) should be administered

HE explains episodic variability and
to correct dehydration, electrolyte, and
heterogeneous precipitating factors that
acid-base imbalances, but monitoring of
c01Telate with diverse clinical scenarios.

plasma osmolality is essential to avoid

Ammonia plays a key role in HE and is
hypoosmolality. Lactated Ringer's solution
thought to sensitize the brain to numerous
should be avoided, because hepatic failure
other precipitating factors/mediators.

may thwart lactose metabolism and cause

However, blood and cerebral ammonia
lactic acidosis. Cleansing enemas of warm
concentrations are often discordant,
soapy water are followed by retention
disqualifying blood ammonia as a simplistic
enemas of either lactulose or lactitol (3
measure of HE. In healthy animals, most
parts lactulose or lactitol to 7 parts water at
an1monia is removed by hepatocytes,

20 mUkg), lOOA, povidone-iodine solution
converted into amino acids or urea, and

(20 mUkg, rinsed well after 10-15 min
excreted via kidneys in urine. In liver failure
dwell), neomycin (22 mg/kg mixed with
or portosystemic shunting, blood anm1onia
water), or diluted metronidazole (7.5 mg/kg
concentrations increase because of
suspended in water at 10-20 ml/kg) given
inadequate hepatic detoxification. In the
every 8 hr until the animal is neurologically
circulation, ammonia can also be excreted
responsive. Retention enemas should be
by the kidneys (tubular secretion) and used
maintained for 15-20 min by use of a Foley
for glutanline synthesis in skeletal muscle
catheter. Administration ( oral or rectal)

(temporary ammonia detoxification). This
of live Lactobacillus and Biji.dobacillus latter mechanism is why maintenance of
organisms (live yogurt cultures or pro biotic
lean body mass (muscle) is essential in
products) also can assist in displacing
animals with hepatic insufficiency that are
ammonia-producing microbes but remains
susceptible to hyperan1monemia and HE.

a controversial intervention. Metronida

A number of clinical scenaiios ai1d mechazole, neomycin, and povidone-iodine nisms can augment blood an1monia
solutions cai1 directly alter colonic
concentrations and precipitate HE,
bacte1ial flora, decreasing populations of
including dehydration (prerenal/renal
ammonia-producing organisms. However,
azotemia), alkalemia, hypokalemia,
care is warranted in using neomycin with
hypoglycemia, catabolism, infection,
concurrent inflammatory bowel disease

PU/PD, anorexia, constipation, hemolysis,
because increased systemic uptake
blood transfusion, GI hem01Thage, high
can increase potential for renal and
dietary protein, and various drugs ( eg,
otic (cochlear) toxicity. Metronidazole
benzodiazepines, tetracyclines, antihistamust be restricted to s7.5 mg/kg every mines, methionine, barbiturates, organo8 hr (combined oral and rectal dosing); phosphates, phenothiazines, diuretics
higher dosages confer risk of iatrogenic

[ overdosage], metronidazole ( overdosage ),
neurotoxicity (vestibular signs
and ce1tain anesthetics).

initially).

HEPATIC DISEASE IN SMALL ANIMALS

445

Once the animal is stabilized, treatment is
antagonists and sucralfate, control of fever
aimed at preventing recurrence. Proteinand infection, proper hydration, and modified restricted diets should be fed (see
minimal (if any) use of anticonvulsant
p 439). Oral probiotic yogurt and lactulose
medications can help alleviate HE

(0.1-0.5 mI.Jkg, PO, bid-tid, initial dose) can
complications. For additional considerabe used, with initial dose titrated to achieve tions, see p 442.)

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several soft, pudding-like stools per day.

Feeding milk may achieve a similar effect in
some animals. The goal of administration of

PORTAL HYPERTENSION AND
nondigestible carbohydrate is to promote

ASCITES
fermentation in the gut. Concentrated
probiotic organisms can prevent other

Ascites develops secondary to portal
bacteria from growing and replicating
hypertension and low albumin concentrathrough substrate competition and tions. Physiologic responses triggered to
pH-related (acid) growth inhibition or
maintain euvolemia and splanchnic
mechanical cleansing (catharsis) induced
perfusion pressure signal systemic
by fermentation products. These effects
conservation of sodium and water.

diminish uptake of ammonia, inflammatory

Portal hypertension represents circulaand oxidative substrates, lipopolysacchatory dynamics thwarting craniad flow of ride, and other toxic enteric products
blood through the liver. Prehepatic causes
contributing to HE. Unfortunately, the
include stenosis, stricture, or thrombi
efficacy of probiotics remains unestablished involving the extrai1epatic portal vein.

for this purpose.

lntrai1epatic causes include the sequela of

In recalcitrant HE, antibiotic therapy,
chronic hepatitis resulting in collagenizapreferably metronidazole (7.5 mg/kg, PO, tion and capillarization of hepatic sinusoids,
bid) or amoxicillin (13-15 mg/kg, PO, bid)

accumulation of connective tissue
rather than neomycin, is recommended.

encircling pmtal triads or the hepatic venule

Antibiotic therapy works synergistically to

( centrilobular area), architectural
reduce enteric toxins along with indigestremodeling of the liver by fom1ation of ible carbohydrates. Rifaximin (approved for regenerative nodules (cirrhosis), vascular treatment of HE in people in 2010 because of occlusion of hepatic or portal veins ( eg, its few adverse effects and pharmacologic
thrombi, neoplasia, vasculitis), or diffuse
benefits) is a semisynthetic, gut-selective,
dissemination of neoplastic cells within
nonabsorbable oral antibiotic derived from
sinusoids or storage materials (an1yloid
rifamycin and a structural analogue of
within the space of Disse, fat or glycogen
rifampin. It acts locally in the GI tract, with
within hepatocytes). Rarely, arterialization
systemic adverse effects similar to those
of the hepatic parenchyrna by an intra11eof placebo in people. It is active against a patic arteriovenous malformation leads to
variety of aerobic and anaerobic gran1-
arterialization of the intral1epatic circulapositive and gram-negative organisms, as tion and causes portal hypertension and
well as protozoa! infections. In vitro data
ascites. lntrai1epatic causes of portal
indicate that the susceptibility of gramhypertension are categorized as presinupositive organisms to rifaxirnin is greater soidal, sinusoidal, and postsinusoidal.

than that of gran1-negative organisms.

Post-hepatic causes of portal hypertension

Dosing at 5 mg/kg, once to twice daily, has
include obstruction of blood flow from the
been used in a small number of dogs and
liver through the hepatic vein; this can begin
cats with recalcitrant HE with apparent
at the level of the heart ( eg, right heart
positive response. Optimal dosing has not
failure, cor triatriaturn dexter, hemangiosarbeen determined.

coma involving the right atrium), pericar

Clinical signs of HE can be exacerbated
dium ( eg, restrictive pericarditis, pericardia!

by GI bleeding, infection, glucocorticoid use tarnponade ), or vena cava ( eg, thrombi, (enhanced catabolism of tissue protein),
congenital or acquired "kink," heartwormhypoglycemia, neoplasia, fever, azotemia or associated vena ca val syndrome).

dehydration (increased BUN increases

In all cases of hepatic portal hypertenenteric ammonia production), constipation sion, intral1epatic portal hypope1fusion

(increased generation and absorption of

(portal perfusion pressure is -5-8 mmHg)

colonic neurotoxins), metabolic alkalosis
is compensated by an increase in hepatic

(favoring both production of anm1onia by
arterial perlusion that maintains organ
the kidneys and uptake of ammonia across
circulation. This causes hepatofugal
the blood-brain barrier), and use of

(backward) flow of blood into the valveless
diazepan1 and barbiturates (synergetic
portal system and fo1mation of acquired
neuroinhibitors). Use of H2-receptor
portosystemic shunts (APSSs).

446

HEPATIC DISEASE IN SMALL ANIMALS

Compensatory unbalance of sodiwn and
hypotension (response to redistribution of
water homeostasis becomes clinically
removed ascitic fluid) and splanch:nic and
apparent at the onset of pmtal hypertension
renal vasoconstriction. The latter responses
and is typically associated with a subnonnal
increase 1isk of development of the
albumin concentration. Ascitic effusion
hepatorenal syndrome (reversible renal
associated with hepatic disease is usually
vasoconstriction associated with liver

VetBooks.ir
a modified or pure transudate ( serum
failure complicated by ascites). Because
albumin <1.8 gtdL). Consequences of pmtal
there is no access to species-specific
hypertension include development of
albwnin for dogs and cats, polyionic fluids
ascitic effusion, splanch:nic vasodilation,
may be used when therapeutic abdmninorisk of bleeding from APSSs, development centesis to remove large a,,nounts of ascitic
of a portal-enteric vascuolopathy, and
fluid is performed. Large-volume abdominoincreased risk of septic abdominal effusion.

centesis should never be performed without

The standard treatment to reduce
concurrent diuretic administration. In
splanchnic portal hypertension in people is
removiI1g ascitic effusion, the goal is to
nonselective 13-blockade using propranolol,
remove enough volume to ilnprove patient
administered to control or reduce risk of
comfort. Rational use of therapeutic abdomspontaneous bleeding from APSSs. Other inocentesis reduces abdonu:nal pressure,
pha,,macologic interventions remain
in1proves renal perfusion a,,1d ca,,·diac
controversial and have not been shown in
output, and improves response to diuretic
placebo-controlled trials to provide greater
therapy. Once ascitic effusion is mobilized,
benefit. Therapeutic strategies for control of diuretics can often be used intermittently ascites include dieta.J.y sodium restriction,
witl1 concurrent dieta,,y sodiw11 restriction.

administration of diuretics to increase
urina,,y sodium elimination, and therapeutic
abdominocentesis (when necessa,,y). The

PORTOSYSTEMIC VASCULAR
first step is dieta,,y sodium restriction to an

MALFORMATIONS
intake of slOO mg sodium/100 kcal diet (25
mg/kg/day; <0.1 % dry-matter basis in food).

The most common circulatory anomalies of

However, sodium-restriction alone is often
the liver in dogs are microvascular dysplasia
insufficient and too slow in onset for

(MVD) and portosystemic vascular
efficient management. Thus, diuretics are
anomalies (PSVAs, also referred to as
usually also reconunended. Diuretic therapy
portosystemic shunts or portocaval shunts).

should slowly reduce ascites without

Cats also are affected with PSVAs but less
causing dehydration, metabolic alkalosis, or
conunonly than dogs. MVD and PSV As are
hypokalemia. Reducing ascites by slo/o--1.5%
related polygenic disorders affecting
of total body wt/day is reconunended by
small-breed dogs. PSV

As may be extralleinitially using combiI1ed treatment with furopatic (more common in small-breed dogs) semide (1-2 mg/kg, PO, bid) and spironolacor intrallepatic (more common in largetone (loading dosage 2-4 mg/kg x 2--3 doses, breed dogs). MVD has not been characterthen 1-2 mg/kg, PO, bid). Reevaluation eve1y ized in Ja,,·ge-breed dogs or in cats.

7-10 days allows for careful upward titration
of diuretic dosages. Combining a loap

Microvascular Dysplasia
diuretic (furosemide) with spironolactone

MVD is far more common than PSV As in

(aldosterone antagonist) reduces 1isk of
affected kindreds of small "tenier" type
iatrogenic hypokalemia
dogs. A diagnosis of MVD denotes abnom1al
lf ascites is slow to mobilize, measuring
development of the fine (tertiary) branches
the urina,,y fractional excretion of sodium
of the intrallepatic portal veins and is
can help detennine whether dieta,,y
associated with lobular atrophy and a
restriction and diuretic dosiI1g are adequate.

compensatory increase in arte1ial perfusion
lf ascites causes tense abdominal distention

(hepatic arterial buffer response), which
compromising ventilation, appetite, or
manifests as coiling of hepatic a,,te,iole
patient com.fort, therapeutic abdominocenbranches and development of a,,terial twigs.

tesis may be undertaken. In people, 8 g of

The arteriolar response results in increased
human albwnin is administered for every
numbers of tl1ick-walled arterial cross5 L of effusion removed to offset the sections in portal tracts and orphaned
development of postdiuresis circulatory
random arterioles within the hepatic
dysfunction developing --12 hr after effusion parenchyma. Otl1er additional MVD
removal. Postdiuresis circulatory dysfuncmicroanatomic abnormalities va,,iably tion reflects reequilibration of body fluids
include large numbers of binucleate
and worsened hypoalbw11i:nemia (removed
hepatocytes ( especially adjacent to the
by abdonu:nocentesis), leading to systemic
portal tract), merging of hepatic venules

HEPATIC DISEASE IN SMALL ANIMALS

447
with p01tal tracts, abnonnal sinusoidal
features. Needle biopsies restrict the
organization and expansion, thickening of
number of acinai· units sainpled. However,
the tlu·ottiing muscle of the hepatic venule
steps to pursue a definitive diagnosis are
in dogs, and formation of random foci of
not recommended in most dogs with
lipogranulomas. A diagnosis of "po1tal
suspected MVD (no clinical signs, no
hypoplasia" cannot be made on the basis
hematologic or biochemical mai·kers typical

VetBooks.ir
of a liver biopsy, because any reduction in
of PSVA). Instead, it is prudent to consider
hepatic po1tal venous perfusion causes
that a dog at risk of hepatic vascular
identical rnicroanatomic changes. Rather,
malformations has MVD as the underlying
this histologic pattern is better tenned
cause of high TSBAs unless it exhibits

·'po1tal hypoperfusion." Dogs with MVD
clinical (HE) or clinicopathologic features
have high TSBA concentrations but do

(RBC microcytosis, low BUN, creatinine,
not demonstrate clinical illness or otl1er
and cholesterol concenti·ations, low protein
laboratory abnormalities found in dogs witl1

C activity) associated with PSVAs.

PSV As. They do not demonstrate HE, do not
develop ammonium biurate crystalluria,
and typically have a n01mal protein C

Portosystemic Vascular Anomalies
activity. A norn1al lifespan should be

A portosysternic vascular anomaly (PSVA)

expected in dogs witl1 MVD. This diagnosis
is a grossly appai·ent aberrant connection
does not warrant feeding a special diet or
between the extrallepatic pmtal vasculature
liver-specific medications ( eg, lactulose,
a11d the systemic circulation ( connecting a

SAMe, milk tllistle). However, because dogs
branch or tl1e po1tal vein to tl1e vena cava or
with MVD may have trouble metabolizing
azygous vein) that diverts blood to the
drngs tl1at require rapid hepatic delivery
systemic circulation, bypassing the liver.

and extraction, care is necessary when

Reduced portal flow to the liver causes
prescribing certain medications. Because
hepatic lobular ati·ophy. Because tl1e po1tal

MVD is genetically linked with PSV As,
circulation trai1spo1ts microorganisms,

TSBAs should be measured in all young
toxins, n utlients, and otl1er materials from
puppies of predisposed breeds for future
tile intestines to the liver, detow·ed blood is
health care considerations; discove1y of
not cleansed or processed before circulahigh TSBA concentrations during an illness tion to the brain ai1d systemic circulation.

may lead to inappropriate, invasive, and

Consequently, nemotoxic substa!lces that
expensive diagnostic testing. Selection of
ca11 provoke encephalopatllic effects can be
breeding stock in affected kindreds should
circulated directly to the brain, causing HE.

target dogs with normal TSBA concentra

Other noxious products ai1d infectious
tions. However, because the trait is
agents inefficiently removed by the liver in
polygenic, breeding dogs with nonnal
anin1als with PSVAs result in a more severe

TSBAs may result in puppies affected with
clinical challenge to what should be mild

MVD and PSVAs. Once high TSBA
health concerns ( eg, infectious diarrhea,
concentrations are detected in young
infected wounds, dennatitis, tick bites,

( <6 mo) small tenier-type breeds lacking
other).

clinical signs of PSV

A, repeated bi le acid

Congenital PSV As are seen primarily in
measurements are not warranted; TSBA
purebred dogs with extral1epatic PSVAs,
concentrations will remain vaiiably
predomina11tly in small purebred terrierincreased for the ailimal's life. Knowing tl1at type dogs ( eg, Yorkshire Teniers, Maltese,
a dog has high bile acids likely caused by

Shil1 Tzu, Havai1ese, Papillon, Miniatme

MVD will define utility of the TSBA test for

Schnauzers, Pugs, Cairn Teniers, Norfolk
future healtl1 care assessments.

Teniers, Tibeta!l Spaniels, and others).

Definitive diagnosis of MVD is possible

Intral1epatic PSV As predominate in
only by consideration of the liver biopsy and large-breed dogs, including (but not vasculai· imaging studies. Liver biopsy
exclusively) Irish Wolfhounds, Old English
demonstrates lesions identical to tl10se of

Sheepdogs, Labrador Retlievers, a11d

PSV

As. The severity of MVD lesions vaiies

Golden Retrievers. Extrallepatic PSVAs
among liver lobes, necessitating collection
usually aiise from the portal vein, left
of samples from tJu·ee different lobes for
gastiic vein, or splenic vein and connect to
definitive characterization. Liver biopsy by
tile caudal vena cava (most conunon), the
tl1e tru-cut method is strongly discouraged
azygous vein, or rai·ely a11otller systemic
for diagnosis of po1tal hypoperfusion
vessel. An intrallepatic PSVA represents the

(PSVAs, MVD) because tllis diagnosis is
retention of a11 embryo11ic vessel that
based on exanlination of multiple acinar
carries fetal blood from tl1e placenta to tile
units to detect lobular atrophy, portal tiiad
heait, tl1rough tile middle of the liver but
aite1iolaiization, and other chai·acteristic
bypassing the hepatic circulation (ductus

448

HEPATIC DISEASE IN SMALL ANIMALS
venosus). This malformation is only
markedly abnormal. Routine coagulation
occassionally seen in small-breed dogs
assessments ai·e usually within normal
and cats.

limits, but protein C activity is usually <7Cf'lo.

Congenital PSV As in cats are seen

The protein C test is valid for use in dogs.

more frequently in mixed breeds, but the

This test reflects the severity of shunting;
prevalence may be increased in purebred
the lower the value, seemingly the more

VetBooks.ir

Himalayans and Persians. However, the
severe the shunt. In asymptomatic PSVA
higher prevalence of polycystic liver disease dogs with a protein C > 70%, surgical ligation and associated portal hype1tension and
has been very successful. Those with a
acquired portosystemic shunts in these
protein C <700A, may not tolerate complete
breeds complicates diagnosis of PSVAs. In
shunt attenuation.

cats, extrahepatic PSVAs involving the left

Abdominal radiographs reveal microhegastric vein are most common.

patica and "plUlllp" kidneys. AmmoniUlll

Animals with PSV As are often smaller
biurate uroliths are radiolucent and thus
than littermates, fail to thrive, and can
not detected witl1 radiographic imaging.

have other congenital abnormalities ( eg,

U1trasonography can noninvasively identify
cryptorchidism in dogs and cats, heart
a PSVA if done by an experienced operator
murmurs in cats). Clinical signs are highly
using color-flow Doppler in a fasted,
vaiiable, and l(JO/er-20% of affected animals
cooperative patient. However, extrahepatic
may be asymptomatic. The presence of

PSVAs can be missed on ultrasonographic
clinical signs depends on the severity of
imaging and even falsely identified in
pmtosystemic shunting. In symptomatic
animals with MVD. Although discovery of
animals, clinical signs are usually evident by
intrahepatic PSVAs is relatively easy using

6 mo of age in cats ai1d before 1 yr in dogs.

ultrasonography, identification of extrahe

Clinical signs include nausea, ptyalism
patic PSVAs can be challenging because

( especially cats), vomiting, diarrhea, pica,
bowel gas and animal cooperation may limit
intermittent anorexia, PU/PD, an1aurosis
in1aging in critical regions. U1trasono

(unexplained blindness), excessive
graphic exainination can identify radioluvocalization, hallucinations, apparent neck cent uroliths in the renal pelvis or urinai-y
or spinal pain, hematuria, pollakiuria,
bladder. Colorectal portal scintigraphy or
stranguria, uretlrral obstruction associated
splenoportal scintigraphy, available in
with formation of ainmonia biurate uroliths,
specialty clinics or teaching hospitals, can
and additional neurobehavioral signs
clearly determine the presence of portosysreflecting HE. Signs referable to minary temic shunting. However, scintigraphy is
tract calculi may be the only presenting
unable to identify the anatomic location
complaint. Cats with PSVAs have a unique,
of involved shunting vasculature with
homogenous, copper-colored iris that
certainty. Splenoportal scintigraphy
appears to be genetically linked with the
requires percutaneous injection of isotope
disorder; the exception ,is blue-eyed cats.

into tl1e spleen, is considered an invasive

However, because a copper-colored iris is
test, and does not provide better resolution,
typical for Persians and Russian blue cats
specificity, or sensitivity over routine
that do not have a PSVA, it is important to
colorectal scintigraphy to determine the
consider this observation in perspective
presence of portosystemic shunting or
of clinical signs and finding high TSBA
definitively identify the involved vasculaconcentrations.

ture. Contrast radiographic portography,

Laboratory abnormalities may include
the traditional gold standard test to confirm
microcytic RBCs Oow MCV), mild

PSVAs, requires catheterization of a branch
nonregenerative anemia, poikilocytosis
of the pmtaJ vein and injection of radio

(cats), target cells (dogs), mild hypoprodense iodinated contrast to illustrate portal teinemia and hypoalbmninemia, hypoglycevascular anatomy. Noninvasive multisector mia (rare, primarily young toy-breed dogs),

CT has replaced simple contrast radiolow BUN and creatinine, hypocholestergraphic portography, providing better olemia, normal to mildly increased liver
anatomic mapping of po1taJ vasculature.

enzyme activity (ALT, AST, and ALP),

This imaging modality requires short-term
normal bilirubin, dilute urine Olyposthenuanesthesia with contrast injected into a ria or isothenmia), ai1d anu11onia biurate
peripheral vessel and permits 3-dimensional
crystalluria. Fasting and postprai1dial TSBA
anatomic reconstruction of the splanchnic
concentrations are usually markedly
circulation, vascular anomaly, and adjacent
increased; however, measurement of TSBAs viscera. A liver biopsy is always indicated or ainmonia after a prolonged fast may yield
in PSVA patients during surgical shunt
normal values. Postprandial TSBAs and
ligation, or if multiple shunts are noted, to
ainmonia (after NH CI administration) are
determine primary underlying disorders or

4

HEPATIC DISEASE IN SMALL ANIMALS

449
acquired liver diseases that may coexist and
temic shunting. Smvival analyses of >450
require specific intervention.

dogs with PSVAs managed with surgical

Although the treatment of choice for
versus longtem1 medical management
symptomatic PSVAs is surgical attenuation
estimated a median survival time of 11 yT
or ligation, not all dogs can tolerate shunt
for dogs with extra.hepatic PSV As treated
attenuation, and a subset of dogs (asymptosurgically, with no significant difference for VetBooks.ir
matic, minimally symptomatic) swvive with
dogs treated solely by medical management.

good quality of life with medical manage

However, this result is biased, because
ment only. Surgical management of PSVAs
owners of the population of dogs optimally
may include direct shunt ligation at surgery
responding to meclical management were
to the animal's tolerance Uudged by
more inclined to decline surgical intervenmeasurements of portal pressure, vital tion. Median survival time in dogs with
signs, local visceral response) or applicaintra.hepatic PSVAs (n=34) treated tion of an ameroid ring (inner lining
surgically was estimated as 5 yr and was
gradually expands over a few days to slowly
not significantly different from a larger
occlude the shunting vasculature). The
population of dogs treated by medical
most common postsw·gical complication
management alone. In a report of96 dogs
of PSVA attenuation is short-tem1 benign
with intra.hepatic shunts treated by one or
abdominal effusion that typically resolves
more coil emboliza.tion procedures, the
within a few days. The most serious postestimated median survival time was 6 yr.

surgical complication is acute portal hyper

Male clogs with repeated bouts of
tension, characterized by development of
an1rnoniwn biurate urolithiasis requiting
abdominal effusion, bloody diarrhea,
medical or surgical resolution (those
abdominal pain, ileus, endotoxic shock, and
undergoing surgical correction of PSV As
cardiovascular collapse. This complication
in which the shunt could not be fully
requires immediate removal of the shtmt
attenuated as in those on medical manageligature. Other complications include ment) should have a pennanent prescrotal
seizures (rare) and fonna.tion of blood clots
urethrostomy created to allow passage of
within the portal vein. Unf01tuna.tely, in
small calculi. This will a.ve1t subsequent
some dogs, acquired portosystemic shunts
development of an obstructive uropathy.

silently develop at varying intervals after

Overall, prognosis after surgical ligation
surgery for a PSV A. The ligation site also
of a single extra.hepatic PSVA is usually
may be circumvented by formation of a
good. Prognosis is less favorable in dogs
medusa. of vessels around the ligated site or
with multiple acquired shunts secondary to
recana.liza.tion of the PSVA that reestabsevere intra.hepatic portal vein a.tresia. and lishes p01tosystemic shunting several yea.rs
in those with intral1epa.tic shunts. Surgery is
after initial surgery. The greatest risk of
less successful in ca.ts than in dogs, with
insidious postoperative complications is
ca.ts more likely to develop multiple
associated witl1 ameroid constrictors,
acquired p01tosystemic shun ts after PSVA
because the extent of vessel occlusion
ligation. Staging sw·geries to gradually
remains ill defined unless repeat inlaging
attenuate PSV

As in dogs or ca.ts has not
studies are undertaken. In rare cases,
improved outcomes.

an1eroids have eroded through the shtmting

Dogs with relatively asymptomatic PSVAs
vascula.ture, ca.using a.cute collapse,
can often be managed with special diets
hemoa.bdomen, and death that may occw·
indicated for hepatic insufficiency. Lifelong
months after their application. Excellent
dietary suppo1t is required, but good health
outcomes have been observed witl1 careful
and normal lifespan can be achieved.

intra.operative graded ligation of extra.he

However, dogs managed medically ru·e
patic PSV As ( observing p01tal pressure and
always at risk of more severe effects from
visceral response, systemic blood pressure,
health issues involving otl1er organ systems,
and herut rate) as well as with application
infections, or GI signs. The best protein
of a.meroid tings. Surgical intervention for
sources for dogs are soy and daiiy quality
intra.hepatic shunts is more complicated
protein with a protein intake starting at
and less successful. Coil emboliza.tion of

2.5 g/kg/da.y. Red meat, fish, and organ meats
intra.hepatic shunting vessels by intervenmust be a.voided. Additional dairy quality tional radiographic technique is an
protein is usually easily tolerated and can be
alternative procedure but can be associated
used to increase protein, phosphate, and
with adverse effects (portal hypertension,
fermenta.ble carbohydrate intake. Treats
portal or vena. ca.val clot formation) and can
of raw vegetables (eg, broccoli, carrots),
be prohibitively expensive; in addition,
cheese, probiotic yogurt, popcorn, modest
more than a single intervention may be
numbers of dog biscuits, animal crackers,
needed to substantially reduce p01tosys-
and limited supervised activity with rawhide

450

HEPATIC DISEASE IN SMALL ANIMALS
bones can be offered without adverse

Doppler color flow. Although esophageal
consequences. If rawhide chews result in
varicoceles are most common in people,
oral hemorrhage, they should be avoided
this location does not predonlinate in
because swallowed blood can provoke
aiumals. Surgical exploration for shunt
encephalopathic signs. Variation in the
ligation should not be done in ailimals with
need for daily lactulose and metronidazole
suspected PSVAs associated with APSSs,

VetBooks.ir
administration (seep 443) is broad, such
because finding ai1 APSS confirms the
that individualization of treatments is
presence of portal hypertension. Liver
advised. Medically managed dogs remain at
biopsies are needed to determine the
risk of developing HE. Owners should be
underlying cause of portal hype1tension.

educated to recognize early signs of HE

Clinical signs of APSSs include episodic
and complicating health issues, how to

HE, PU/PD, vorniting, diaii:hea (sometimes
administer cleansing and retention enemas,
bloody), and abdorninal effusion. Laboraand how to administer subcutaneous fluids.

tory abnom1alities consistent with a

This training allows early intervention of
primary underlying hepatic disease can be

HE episodes and reduces the nwnber of
seen in addition to markers of shunting
emergency veterinary visits.

(RBC rnicrocytosis, low BUN and creatinine, hypocholesterolernia, anunoniwn biurate c1ystalluria, and subnonnal protein

ACQUIRED PORTOSYSTEMIC

C activity). Hyperbilirubinemia may be

SHUNTS
present, depending on the underlying cause.

Ligation of multiple APSSs is contraindi

Acquired portosystemic shunts (APSSs)

cated, because this is a compensatory
font 1 secondaiy to portal hypertension
response to portal hypertension. Banding
caused by 1) chronic liver disease (fibrosis,
of the vena cava to reduce the extent of
regenerative nodules), 2) congenital severe
shunting is ill advised. Medical treatment
portal vein atresia, 3) acquired dan1age to
to nli.nirnize signs of HE along with sodium
the fine branches of the intral1epatic portal
restriction and combination diuretic
vein (noncirrhotic portal hypertension),
therapy ai·e used to control abdominal

4) hepatic arteriovenous malfonnations,
effusion. Dogs and cats with APSSs can live

5) congenital hepatic fibrosis associated with several yeai·s without clinical signs, some polycystic liver malfonnations ( ductal plate
having a normal lifespan uneventfuJJy when
malfonnations), 6) portal vein thrombosis or
provided with appropriate medical and
stricture, or 7) outflow obstruction through
nut1itional support.

the hepatic vein/venules (thrombosis [Budd

Chiari syndrome], hepatic vein ir\jwy [ veno

OTHER HEPATIC VASCULAR
occlusive syndrome]). The main body of
the portal vein lacks valves and maintains a

DISORDERS
blood pressure of <8 mmHg. Any disorder

Other vascular abnom1alities seen in dogs
diminishing hepatic portal perfusion results
and cats include hepatic arteriovenous
in a hepatic arterial buffer response that

"fistulas," hepatic venous outflow
increases hepatic arterial perfusion.

obstruction, (veno-occlusive disease,

High-pressure retrograde arteljal flow into

Budd-Chiari syndrome), and portal venous
portal vasculature leads to formation of
thromboembolism. These are relatively

APSSs as blood follows the path of least
uncommon compared with PSVAs and MVD
resistance to the vena cava. In animals
ai1d other acquired hepatic disorders.

with extrallepatic portal atresia or portal
thrnmbi, splandmic circulatory hypertension leads to an APSS. In ailimals with Hepatic Arteriovenous
occluded hepatic venular outflow or fibrotic

Malformation
hepatic remodeling, sinusoidal and

A hepatic arteriovenous (AV) malfonnation
postsinusoidal hypertension also results in
is a direct intrallepatic c01mection between
retrograde flow of blood into the valveless
the high-pressure hepatic arterial system
portal system. APSSs represent nests of
and the low-pressure p01tal venous system.

tortuous veins wliting portal vasculature

High-pressure aiterialized blood flows
with the abdominal vena cava.

retrograde into the portal vasculature,

The most common sites of APSSs are
causing intrallepatic and extrallepatic
caudal to the left kidney, in the region of
portal hypertension, ascites, and APSS
the colorectal vasculature, and associated
formation. These may be congenital or, less
with vessels of the spleen. Nests of small
conm10nly, acquired from trawna, biopsy
tortuous vessels can usually be identified
lesions, or neoplasia. Clinical signs of a
during ultrasound examination using
congenital AV malformation initially

HEPATIC DISEASE IN SMALL ANIMALS

451
manifest in young animals and include HE,
defects [ cor tria.tria.tun1 dexter], ca.i·dia.c
abdominal effusion, inappetence, vomiting,
tumors), obstrnction of the caudal vena.

and diarrhea (often bloody). A munnur or
ca.va ( eg, postca.val syndrome associated
bruit associated with tuTbulent blood flow
with hea.itworn1 disease, congenital
may be audible over the affected liver lobe.

"kinking" of the caudal vena. ca.va., vascular Rarely, an intrahepatic AV malformation
or neoplastic thrombosis of the caudal vena.

represents a variant of an intrahepatic
cava., diaphragmatic hernia compressing the

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PSVA.

caudal vena. ca.va), or obstrnction of the

Laboratory abnormalities are identical to
efferent hepatic venous system ( eg, liver
those associated with more conunon PSVAs
lobe torsion, compression by a hepatic

( see p 44 7) and additionally may disclose mass, idiopathic postsinusoidal venous
erythrocyte changes reflecting turbulence
obstruction seconda.i-y to acquired fibrosis
or a shearing effect (ie, schistocytes ).

or hepatic venular destruction, severe

Although ascites is a feature distinguishing
occlusive or obstructive extran1edulla.i-y
an AV malfonnation from a PSVA, dogs with
hema.topoiesis, or hepatic venule obstrucsevere congenital po1tal atresia also may tion by occlusive lipogranulomas (subset
develop abdominal effusion (if they do not
of dogs with extrahepa.tic PSVAs or MVD).

manifest a PSVA). Abdominal ultrasonogra

Clinical features of occlusive disorders
phy can easily identify an intrahepatic AV
include hepa.tomegaly ( unless cause is
malformation (pulsing flow) and the
associated with PSVAs or MVD), ascites,
associated APSS on color-flow Doppler
formation of APSSs, a.i1d signs suggestive of
intenogation. Definitive imaging requires
the underlying prima.i-y disorders. Sin1ple
contrast angiography via the celiac or
passive congestion leads to hepa.tomegaly,
anterior mesenteric artery (former "gold
rnodest increases in liver enzymes, nmmal
standard") or multisector contrast
bile acid concentrations, and a.ii abdominal
angiographic CT ( cun·ent "gold standard").

effusion cha.i·a.cterized as a modified

Multiple AV connections a.re often evident transuda.te. Laboratory abnormalities of within an affected liver lobe. Although surgiveno-occlusive disease (hepatic venule
cal lobectomy or ligation of the nutrient occlusion) or a Budd-Ch.iari syndrome
a.itery is the conventional treatment, many

(tlu·ombosis of the hepatic vein or vena.

affected dogs have other microvascular
cava.) reflect pmtosystemic shunting ( eg,
ma.lforn1ations ca.using intral1epatic
high TSBA concentrations, hypocholeste1"

shunting along with APSSs thwarting
olemia, and usually low protein C activity),
efficacy of lesion ablation. Biopsy of the
mild to moderate increases in hepatic
liver from sites distant to the AV ma.lfonnatransan1inases, and va.i"iable total bi.lirubin tion (other liver lobes) is imperative to
and albtunin concentrations. A modified
detect other intrahepatic vascular
transuda.tive abdominal effusion is
ma.lforn1a.tions. Surgical ma.i1agement has a
common.

clismal prognosis for cure because of the

Thoracic and abdominal radiographs
widespread intrahepa.tic distribution of
help distinguish cardiac from other causal
microscopic vascular malformations and
disorders; these may disclose kinking or
the presence of fimctional APSSs.

in1pingement of the caudal diaplu-agmatic

Intra.vascular a.cryla.inide i.ajection using an
region of the vena cava. Cardiac ultrasonoginterventional radiographic approach is an raphy helps identify ca.uses of passive
alternative salvage procedure. Unfortucongestion ( eg, differentiate between nately, this also c3.!Ulot guarantee clinical
perica.i·dial disease, ca.i·diac tun1ors,
cure because of the complex effect of this
congenital ma.lfom1a.tions, or intrathoracic
ma.lfonnation on hepatic microvascula.ture.

masses compressing the caudal vena cava.).

Limited outcome data for this approach

Abdominal ultrasonogra.phy discloses
describes treatment failures, some
hepatic venular distention in passive
procedural complications ( tmintended
congestion and diminished hepatic venule
emboliza.tion of nontargeted vasculatme ),
size in veno-occlusive or Budd-Chiari
and need for chronic medical rna.i1agement
syndromes associated with hepatic dysfw1cof HE.

tion and APSSs. Treatment a.i1d prognosis
depend on the underlying disease.

Hepatic Vein Outflow Obstruction

HEPATOTOXINS

Hepa.tic venous outflow obstrnction can
result from cardiac or pe1ica.i·dial disorders

Although many drugs have been associated
ca.using passive congestion of the caudal
with hepatic dysfimction, their influence on
vena ca.va. ( eg, right heart failure, perica.i·dial liver pathology varies depending on the disease ca.using ta.inpona.de, congenital
pathornecha.itlsrn of liver i.ajury and the

452

HEPATIC DISEASE IN SMALL ANIMALS
acinar zone of metabolic or circulatmy
concurrent presence of excessive hepatodisturbance.

cellulai· copper seemingly augmented

Primidone, phenytoin, and phenobarbital

NSAID toxicity in Labrador Retrievers. In
can cause acute fulminant liver failure,
dogs, trimethoprim-sulfadiazine also can
chronic cholestatic liver disease, or a
cause idiosyncratic hepatotoxicity that may
diffuse progressive degenerative vacuolar
involve an immune-mediated component. A

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hepatopathy (VH) leading to metabolic
reversible cholestatic hepatopathy or acute/
epidermal necrosis (also known as
subacute massive fatal hepatic necrosis has
necrolytic migratory erythema or hepatobeen observed, sometimes after only a few cutaneous syndrome). Although a diffuse
treatments using a conventional dose.

glycogen-like VH (steroid hepatopathy)

Halothane and methoxyflurane can be
is usually a benign, reversible change
associated with a sensitization reaction
associated with high-dose, longterm
leading to hepatic necrosis in dogs. Xylitol,
glucocorticoid administration, longer-tem1
a commonly used artificial sweetener in
administration of high doses can cause a
human foods, may be an intrinsic hepatodiffuse, severe degenerative VH leading to toxi.n for dogs, with ingestion of small doses
jaunclice (in dogs) and hepatic lipidosis
leading to intractable hypoglycemia and

(in cats). Increases in ALP and, to a lesser
lethal hepatic failure. Toxicity may lead to
extent, ALT are seen as early as 2 days after
death before liver enzyme activity increases.

glucocorticoid administration in dogs.

However, there is some evidence suggesting

Lomustine, a chemotherapeutic agent
a breadth of individual responses to this
used mostly in dogs, causes an idiosyncratic toxin.

unpredictable and progressive hepatitis

Tetracyclines can rai·ely lead to idiosynculminating in cirrhosis. Oxidative ir\jury cratic necrosis in dogs and cats and have
secondary to drng metabolite accumulation
been shown to augment hepatocellular lipid
is a suspected patl1omechanism of liver
accumulation in many species. Itraconazole
ir\jury, because treatment with biologically
and ketoconazole in dogs and cats can
available SAMe before lomustine adminisca.use icliosyncratic hepatotoxicity tration is seemingly protective.

associated with high liver enzyme activity

Danazol, an impeded androgen, can cause and jaundice. Clinical signs resolve with idiosyncratic reversible jaundice in dogs.

drng withdrawal.

Androgenic anabolics can induce hepatic

Acetaminophen preclictably causes
lipidosis in inappetent cats or in cats fed
centrilobular hepatic necrosis in dogs at
a protein-restricted diet. Androgenic
dosages >200 mg/kg. Metl1emoglobinemia
anabolics also increase risk of hepatois also seen. Toxicity in cats is seen acutely cellular carcinoma.

at a much lower dosage (56 mg/kg), with

Thiacetarsarnide, previously used to treat
hematologic signs predominating ( eg,
dirofilatiasis, causes hepatotoxicity owing
methemoglobinemia and Heinz body
to its aisenical content.

hemolysis). (See also p 3029.)

Toxicity is associated with increased ALT

Methimazole hepatotoxicity in cats
activity and, in some dogs, jaundice. High
causing hepatic degeneration and necrosis
liver enzynies were used as an indication to
a.ppeais to be idiosyncratic but also may
suspend therapy; thereafter,llepatic ir\jury
involve inlffiune-mediated mechanisms.

resolved. Mebendazole-associated

Clinical features include inappetence,
idiosyncratic hepatotoxicity caused fatal
jaw1dice, and increased liver enzyme (ALT,
acute hepatic necrosis or chronic hepatitis

AST) activity that resolve after drug
in some dogs. Chronic oxibendazolediscontinuation.

diethylcarbamazine administration in dogs
ln cats, g1iseofulvin-associated hyperbiliwas shown to cause increased ALT and ALP
rubinemia with increased ALT appeais to be
activity, hyperbilirubinemia, periportal
idiosyncratic. Clinical signs and liver ir\jury
hepatitis, and fibrosis. Progressive irtjury
ai·e reversible upon drug discontinuation.

and clinical signs resolved in many but not

Idiopathic diazepan1 toxicity in cats causes
all dogs after drug discontinuation.

fulminant hepatic failure associated with

Many NSAIDs are mitochondrial toxins,
panlobular necrosis; signs of toxicity are
and some are associated with idiosyncratic
evident within several days of initial drng
acute hepatocellular toxicity. In particulai·,
administration. Toxicity has mainly been
carprofen was shown to cause idiosyncratic
seen with medication given PO for behavior
hepatic necrosis in some dogs, particularly
modification or to treat feline lower urinary

Labrador Retrievers. Dogs may recover fully tract disease. Unforttmately, idiosyncratic if toxicity is recognized early and drng
diazepam hepatotoxicity is usually fatal in
administration suspended. Based on
cats. Proactive monitoring of liver enzymes
retrospective liver biopsy inspection, the
can identify adverse reactions early in their

HEPATIC DISEASE IN SMALL ANIMALS

453
course, allowing for prompt drug disconcanine herpesvirus, inadvertent parenteral tinuation. Similar toxicity has also been
iI,jection of an intranasal Bordewlla
seen with oxazepam.

bronchiseptica vaccine in dogs, feline

Other specific hepatotoxins include
infectious peritonitis, and virnlent systemic
aflatoxins, toxins de1ived from amanita
calicivirus infection in cats. Rarely, canine
mushroom (amanitin), blue-green algae
parvovims can lead to hepatic injury as a

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(microcystin), cycad-associated (Sago
result of portal systemic sepsis.

palm) cycasin, and [3-methylamino

Infectious canine hepatitis is caused

L -alanine, a neurotoxic amino acid. There
by canine adenovims 1. 1n addition to acute
are many plants in the Sago palm family,
hepatic necrosis, chronic hepatitis and
which are used as yard oman1entals in
hepatic fibrosis can be sequelae if neutraltemperate climates in North America and izing antibody is inadequate to eliminate the
also are commonly sold as bonsai plants in
infection during the active phase. Seep 798
large retail stores.) Each of these toxins can
for clinical findings, diagnosis, treatment,
cause lethal hepatic necrosis. Other
and control.

chemicals reported to be hepatotoxic

Canine herpesvirus affects neonatal
include heavy metals, certain herbicides,
puppies, causing hepatic necrosis as well as
fungicides, insecticides, and rodenticides.

other systemic changes. It is usually fatal in

(See also TOXICOLOGY, p 2948, et seq.)

puppies.

Important steps to minimize absorption

Accidental parenteral injection of
of ingested toxins or overdose of oral drugs
intranasal B branchiseptica vaccine in
include vigorous decontamination of the
dogs can cause both a local inflammatory
stomach and intestines by gastric lavage,
reaction at the injection site and acute,
induced vomiting, and decreasing ente1ic
nonseptic hepatocellular degeneration and
toxin abSOI])tion. Vomiting can be induced
necrosis that evolves into chronic hepatitis.

within 30 min up to 2 hr after ingestion

There is no known treatment other than
by oral administration of 3"A, hydrogen
symptomatic therapy for chronic inflammaperoxide (2.2 mUkg [ 1 mUlb J to a maxin1um tory liver disease.

of 45 mlldog, repeated once after 10--15 min Feline infectious peritonitis virus is a
if vomiting does not occur) or administracoronavims that causes diffuse pyogranution of apomorphine hydrochloride lomatous inflammation and vasculitis.

(0.03 mg/kg (0.014 mUlb], lV, once; or

Icterus, abdominal effusion, vomiting,
a crushed tablet dissolved in saline
diarrhea, and fever are common clinical

[0.9% NaCl] solution instilled into the
signs. See p 780 for clinical findings,
conjunctival sac and rinsed away with water diagnosis, treatment, and control.

or saline solution after emesis) or syrup of

Virulent systemic calicivirus, a
ipecac given orally ( 1 -2 ml/kg).

recently emerged variant of feline

Activated charcoal without sorbitol
calicivims, can have mortality rates of

(2 g,'kg, PO, repeated every 6-8 hr) may be

33o/er-60% in adult cats. P1imarily identified
administered to reduce absorption of toxins
in shelter or cattery populations, this virus
if the animal is conscious. Activated charcoal causes profound fever, anorexia, marked may also be administered as a high-retention
subcutaneous edema (limbs and face
enema Gastric lavage is important to
especially),jaundice, alopecia, and crusting
prevent absorption in unconscious animals.

and ulceration of the nose, lips, ears, and

High-cleansing colonic enemas should also
feet. Adult cats are most severely affected.

be given, using polyionic warmed fluids in
lndividual hepatocyte necrosis ranging to
dehydrated anin1als. Clinical observation
centrilobular or more extensive necrosis is
suggests that cholestyramine might provide
associated with neutrophilic inflanunatory
benefit for dogs after acute cycad ingestion if foci and intrasinusoidal fibrin deposits.

given after initial enteric decontamination
steps (induced vomiting, gastric lavage). If

Bacterial Diseases
there is no specific treatment for a hepatotoxin, judicious, supportive care should be Leptospirosis: Infections with Lepto
provided.

spira. interrogans serovars Icterohemorrhagiae and Pomona and chronic infections with G1ippotyphosa have been associated

INFECTIOUS DISEASES OF THE
witl1 liver disease in dogs. Other serotypes

LIVER
may also involve the liver. No specific
histologic lesions are pathognomonic.

Viral Diseases

Markedly increased liver enzyme activity

Viral diseases associated with liver dysfuncand hyperbilimbinemia indicate hepatic tion include infectious canine hepatitis,
involvement. However, these parameters

454

HEPATIC DISEASE IN SMALL ANIMALS
may reflect hepatic response to a sepsis
in cats with and without respiratory signs.

syndrome rather than specific organ

Hepatomegaly and increased ALT and AST
invasion in acutely ill dogs. Clinical
activities were notable. Liver samples
and clinicopathologic features of liver
revealed granulomatous inflammation.

involvement may worsen initially with

Treatment with clarithromycin (62.4 mg/cat,
treatment (fever, liver enzymes, hyperbiliru

PO) combined with either clofazimine (25

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binemia), aJa.risch-Herxhein1er reaction.

mg/cat/day, PO, or 50 mg/cat, PO, every

Diagnosis depends on demonstrating a rise
other day) or rifan1picin (5--10 mg/kg, bid,
in convalescent titer or PCR detection of

PO) and a fluoroquinolone or doxycycline
leptospiral DNA in blood or urine.

(5--10 mg/kg, bid, PO) achieved remission in

Identification of organisms in stained liver
affected cats. Relapse should be expected
specimens is difficult. Treatment includes
because of the inununocompromised status
supportive care and specific antimicrobial
of these cats.

therapy. Penicillins are used initially for the

Systemic infections, including gra.nuacute phase, ( eg, an1picillin [22 mg/kg, IV, lomatous hepatitis due to Mycobacterium
qid] or an1oxicillin [22 mg/kg, PO, bid]).

spp has been reported by several investiga

Arninoglycosides ( dose depends on drug
tors in Basset Hounds, Miniature Schnauused; streptomycin was historically used to zers, and additional dogs. Affected dogs are
clear leptospirosis) or doxycycline (5 mg/kg, suspected to have some form of cell

PO, bid for4 wk) are recommended to treat
mediated immunodeficiency (Basset
the carrier phase. Arninoglycosides are

Hounds) or unique exposure to another
currently not reconunended for treatment
infected animal or person. Susceptibility to
of leptospirosis owing to the high risk of
various Mycobacterium spp vary an1ong
causing nephrotoxicity. Special precautions
mammals. M tuberculosis can induce
are reconunended when handling animals
progressive disease in people, nonl1wnan
suspected of having leptospirosis ( and their
primates, dogs, and swine. Clinical signs
urine specimens) because of the zoo no tic
in anin1als infected with M tuberculosis
potential. (See also LEPTOSPIROSIS, p 646.) depend on tl1e route of exposure and degree
of localization of the infection or its

Tyzzer Disease: 'lyzzer disease (see
systemic dissemination. Early infection is
p 199) is a rare but fatal condition caused
subclinical, leading to cachexia, weakness,
by Clostiidium pilijo1me. Infections
anorexia, dyspnea, and a low-grade,
in dogs or cats most conm1only occur
fluctuating fever. Hepatic involvement
in immunocompromised hosts, either
caused increased transaminase activity,
neonatal aninlals or adults affected with
reflecting pyogranulomatous hepatitis.

other conditions. Because C piliforme is a

Many animals infected withMycoba.cte
commensal organism in the intestines of
rium spp are euthanized because of the
laboratory rodents, infection is acquired by
severity of organ involvement at the time
contact with or ingestion of rodent feces
of diagnosis and because of zoonotic
transp01ting bacterial spores. Clinical signs
concerns. Diagnosis of M tuberculosis in an (let11argy, anorexia, abdominal discomfort)

animal should be reported to local health
are acute in onset, and illness rapidly
officials. At least 6-9 mo of treatment using
progresses to death within 24-48 hr. M:arked a multi.drug regin1en is advised; single-agent increase in ALT activity inunediately
treatment is not advised owing to concern
precedes death. Special stains are needed to for emergence of resistant strains.

identify organisms in liver tissue because

Treatment reconunendations include
organisms do not grow in routine bacterial
combined administration of isoniazid,
culture media. Although there is no effective ethambutol, and rifampin, with pyrazinatreatment, a vaccine has been developed for mide sometimes substituted for ethamburesearch colony anin1als.

tol. However, experience in longterm
treatment of dogs is lacking.

Mycobacterium avium Infection:

Diagnosis of Mycobacteri:um can be

Hepatic infection with disseminated M
difficult because many of these organisms
avium has been described in young
are slow growing (requires >l mo), acid-fast

Abyssinian and Somali cats that had an
organisms may not be found in tissue
apparent innate inm1unodeficiency
sections, and PCR from forn1alin-fixed

(unknown cause). The clinical course
tissue may be falsely negative. However,
included vague illness characterized by a

Mycobacteiium sp have also been detected
several month history of weight loss in the
by both histologic staining and by PCR from
face of polyphagia. Marked diffuse
fonnalin-fixed liver specin1ens from dogs
interstitial pulmornu-y infiltrates developed
with pyograulomatous hepatitis.

HEPATIC DISEASE IN SMALL ANIMALS

455

Extrahepatic and lntrahepatic

Mycotic Diseases

Bacterial Infections and Sepsis:

Extrahepatic infection and sepsis can

The most common mycotic infections
cause cholestasis and hyperbilirubinemia.

associated witl1 liver dysftmction are

Increases in semm bilimbin may range from coccidioiclomycosis (seep 637) and moderate to marked, while increases in
histoplasmosis (seep 639). In severely

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liver enzyme activity remain modest. This
affected animals, clinical signs include
type of jaundice has been seen in dogs with
ascites, jaundice, and hepatornegaly, in
leptospirosis and in dogs and cats with
addition to signs associated with otl1er
ill-rlefined sepsis syndromes. Approp1iate
involved organ systems. Anti.fungal
treatment targets the underlying organism
treatment is variable, determined by the
causing infection. Increased liver enzyme
sevelity of infection, organ involvement,
activity in septicemia/sepsis also can reflect
and individual clinical response. Because
bacterial invasion of the liver or hepatocelliver involvement in histoplasmosis is seen lular damage by associated cytokine release
with disseminated disease, aggressive
or hypoxia.

chemotherapy (including combinations of

Animals with acute hepatic failure,
eitl1er itraconazole or ketoconazole and
chronic hepatobiliary disease, and cholesamphotericin B) are recommended.

tatic disorders are predisposed to systemic

Debilitated anin1als have a poor prognosis.

bacterial infection and endotoxemia clue to

Coccidioiclomycosis can be treated
diminished function of hepatic reticuloensuccessfully with several antiI1.mgal dotl1elial cells (hepatic Kupffer cells
medications (itraconazole and tluconazole
comprise the largest fixed macrophage popuare preferred to ketoconazole ). Clu-onic lation in tl1e body) and reduced biliary
treatment (6--12 mo) is required, and
elimination of bacteria cle1ived from the
relapses may occur. Treatment efficacy is
enterohepatic circulation in bile. In acute
determined based on resolution of clinical
fulminant hepatic failure, sepsis or
signs and radiographic lesions and
septicemia may be masked by fever,
reduction in serologic titers. Termination of
hypoglycemia, and leukocytosis that might
treatment should not be based on serologic
also represent clinical manifestations of
titers alone, because tl1ese stabilize and
hepatic injury.

persist in many dogs after clinical recovery.

Animals with chronic disorders causing

Owners must be infonned that discontinustasis of bile flow or with chronic hepatic ing medication may result in relapse.

neoplasia are more likely to develop

Animals recove1ing from CNS infection
intrahepatic infections. Risk factors
should receive lifelong treatment. Similarly,
associated with biliary tract infection
animals with disseminated disease suffering
include advanced age, recent episodes of
infection relapse after treatment discontinucholangitis, acute cholecystitis, choledoation should continue on longtem1 or cholithiasis, and obstructive jaundice.

lifetime treatment with an azole antifimgal.

Treatments tl1at reduce susceptibility to

For chronic treatment, drug doses that
infection and liver injury during fulminant
effectively maintain remission may be lower
hepatic failure and extra.hepatic bile duct
than those needed to induce remission.

occlusion include administration of

N-acetylcysteine, a-tocopherol, glutamine,

Protozoa! Diseases
oral bile acids, and enteric and systemic

Toxoplasmosis: Toxoplasmosis (see
antibiotics. These strategies increase
p 685) can cause acute hepatic failure
microvascular perfusion, reduce ente1ic
associated witl1 hepatic necrosis. Toxo
bacte1ial translocation, augment irmate
plasma gondii is more commonly seen in
immunity, and protect against oxidant
cats positive for feline irnmw1.odeficiency
injury. While awaiting results of culture and
vims and feline leukemia virus. Icterus,
sensitivity (tissue, abdominal effusion, bile),
abdominal effusion, fever, lethargy,
antibiotics against entelic opportunists
vomiting, and dianhea are seen in addition
should be administered empirically,
to clinical signs consistent witl1 CNS, ocular,
avoiding dmgs extensively metabolized in
or pulmonary involvement. Liver disease in
the liver. Combination of a [3-lactarnase-dogs is rare but when seen is either in an resistant penicillin, metronidazole
immunocompromised host or in young dogs

(7.5 mg/kg, PO, bid), and enrofloxacin
and also involves systemic infection. Young

(2.5---5 mg/kg, PO, IM, or IV, bid), may be
dogs may be concurrently infected with
beneficial duling initial treatment when the
canine distemper virus; in these, illness is
underlying infectious cause remains
acute in onset and rapidly fatal. Diagnosis
unclear.

of toxoplasmosis can be difficult; while a

456

HEPATIC DISEASE IN SMALL ANIMALS
positive IgM titer indicates active clinical

However, no correlation has been shown
disease, IgG titers may be found in chronic
between histologic features and breed, sex,
infections and in animals lacking clinical
age, clinical features, or hepatic parasite
disease. Clindamycin (12.5 mg/kg, PO or IM,
load.

bid for 4 wk) is the drug of choice. Because

Treatment is rarely curative, and
clindan1ycin is metabolized in the liver,
prognosis for debilitated animals is poor.

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dosage reduction may be necessary in

Owing to the zoonotic potential of the
severe hepatic insufficiency. Oral clindamyorganism, owners must be informed that cin should be followed by a bolus of water
their pet will never be completely free of
or food to prevent esophageal irritation. In
the disease and that relapses may require
some cases, initial treatment is combined
repeated treatment. This is particularly
with anti-inflan1matory glucocorticoids
important if an owner is immunocompro-
to protect against tissue injmy caused

1nised. In the absence of renal insufficiency,
by inflanm1atory responses initiated by
a high-protein diet is reconunended. The
protozoa] death. Prognosis depends on the
most conunon specific treatment recomdegree of debilitation and stage of disease at mended in the USA is allopurinol initial diagnosis and the associated disorder

(7-20 mg/kg, PO, once to three times daily)

causing inmrnnosuppression. Despite
given for 3-24 mo or indefinitely lifelong;
improvement with treatment, animals
other first-line treatments include meglushould be considered chronicaJJy infected mine antimony (100 mg/kg/day, IV or SC),
and thus must undergo srnveillance for
sodiun1 stibogluconate (30-50 mg/kg/day, IV
recrndescent disease.

or SC), or liposomaJ amphotericin B

(0.25-0.5 mg/kg, IV, every other day until a
total dose of 5-10 mg/kg is achieved).

Leishmaniosis: Canine leishmaniosis (see Numerous other second-line drugs have p 589) is a multisysternic disease caused by
also helped control infections.

protozoan parasites of the genus Leishmania, most conm1only encountered in FELINE HEPATIC LIPIDOSIS
animals that have lived in Mediterranean
countries, Portugal, the Middle East, and

Hepatic lipidosis (HL), the most conunon
some parts of Africa, India, and Central and
acquired and potentiaJJy lethal feline liver

South America. It also is occasionaJly
disease, is a multifactmiaJ syndrome. In
encorn1Lered in dogs in Lhe USA ( especiaJly
most cases, a primary disease process

Foxhounds). A serosurvey of> 12,000 dogs
causing anorexia sets the stage for HL

(Foxhounds, other breeds, wild canids) and
in overconditioned cats. Peripheral fat

185 people in 35 states and 4 Canadian
mobilization exceeding the hepatic
provinces was done to assess geographic
capacity to either redistribute or use fat
distribution prevalence, host range, and
for 13-oxidation (producing energy) leads to
modes of transmission within North
profound hepatocyte cytosolic expansion

America and to assess possible infection in
with triglyceride (fat) stores. In fewer cases,
people. Findings identified Leishmania
inappetence is caused by environmental
spp-infected Foxhounds in 18 states and
stresses ( eg, forced weight loss with

2 Canadian provinces but no evidence of
unacceptable food substitutions, moving
hUlllan infection. North America leishmanito a new household, newly introduced or osis appears widespread in Foxhorn1ds and
loss of pets or fantily members, boarding,
is limited to dog-to-dog transmission.

accidental confinement [ eg, locked in a

However, if the organism becomes adapted
garage, basement, or attic], or an insidefor vector transmission by indigenous only cat being lost outside). The tem1
phlebotomines, the probability of hU111an

"idiopathic HL" is appropriate only when
exposure may greatly increase.

an underlying disease condition or event

Clinical features in dogs with naturaJly
leading to inappetence carmot be identified.

occrnTing leishmaniosis include nonregen

HL has no necroinflanunatory compoerative anemia, increased enzyme (ALP, nent, and the severe cholestasis is caused by

ALT, and AST) activity, hypoaJbunlinemia,
canaJicular compression secondary to
and variable bilirubinernia. Histologic
hepatocyte triglyceride vacuolar distention.

response is characterized by a multifocaJ

The syndrome is associated with a nun1ber
pyogranulomatous hepatitis associated
of metabolic deficits, including low hepatic
with hepatocyte vacuolar degeneration
and RBC glutathione, low plasma tarn"ine,
with phagocytized organisms seen within
low vitamin K, causing coagulopathies in
macrophages. Severity ofliver lesions
some cats, thiamine and/or cobaJanlin
represents sequential stages of hepatic
deficiency and likely other B vitanlin
infection in chronic visceral leishmaniosis.

depletions, and electrolyte aberrations

HEPATIC DISEASE IN SMALL ANIMALS

457

( especially low potassium and low
the entire abdomen for evidence of an
phosphorns).

underlying disease process and include

Clinical signs vary but usually include
evaluation of the biliary tree, gallbladder,
dramatic weight loss (>25%, may include
pancreas, intestinal wall thickness, hepatic
dehydration deficits), lethargy, vomiting,
and mesenteric lymph nodes, kidneys, and
ptyalism, pallor, neck ventroflexion,
urinary bladder, and scrutiny for uroliths in

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hepatomegaly, jaundice, gastroparesis and
the kidneys, ureters, or bladder.

intestinal ileus ( due to electrolyte aberra

Definitive diagnosis is based on the
tions), and retention of omental and
history, physical examination findings,
falciform fat despite diminished peripheral
laboratory features, ultrasonographic
fat stores. Diarrhea is common in HL cats
appearance of the liver, and ultrasoundwith inflammatory bowel disease or enteric guided hepatic aspiration cytology. Liver
lymphoma as primary disease processes.

biopsy is not necessary to diagnose HL;

Classic signs of HE are not seen, and
however, underlying cholangitis/
arnmonium biurate crystalluria is unusual,
cholangiohepatitis or hepatic lymphoma
although bleeding tendencies may develop.

may eventually require biopsy for definitive

Vitamin K, deficiency has been confirmed
diagnosis. Cytology preparations show
in numerous HL cats by observation that
profound vacuolar distention of hepatobleeding tendencies and coagulation test cytes involving >800,1, of hepatocytes
abnormalities resolve with vitamin K,
aspirated. Canalicular cholestasis is
therapy.

conunonly seen. Mistaken aspiration of

Laboratory results reflect the HL
omental fat rather than liver is easily
syndrome as well as the primary underlying
deduced by the absence of hepatocytes.

disease. A nonregenerative anemia,

Treatment ofHL is aimed at correcting
poikilocytosis, increased RBC Heinz bodies,
fluid, electrolyte, and metabolic deficits and
variable WBC count, hyperbilirnbinemia
initiating food intake. Because cats with HL
and bilirnbinmia, mild to marked increases
may have high lactate concentrations and
in ALT and AST, and marked increases in
may not be able to metabolize acetate, 0.9%

ALP are common. In cats with a prin1ary

NaCl is the fluid of choice. Fluids should not
necroinflanllllatory process involving the
be supplemented with dextrose, because
pancreas, liver, bile ducts, or gallbladder,
this will reduce utilization of intraliepatic

GGT activity will be increased, usually
fatty acids for (3-oxidation. Because affected
exceeding the fold increase in ALP. In all
cats are usually overconditioned, fluid
other conditions causing HL, GGT activity
tl1erapy must be based on ideal body weight.

is normal or only modestly increased. The

Overhydration is common when fluid

GGT:ALP relationship is useful in discerning dosage is based on total overconditioned underlying cholangitis/cholangiohepatitis
body weight and can lead to pleural and
and other diseases involving biliary
abdominal effusion and pulmonary edema.

strnctm·es (including pancreatitis). Finding

Fluids should be appropriately supplea high GGT also predicts whether a liver or mented with potassim11 (using the sliding
pancreatic biopsy is indicated. Depending
scale) based on electrolyte status. If initial
on underlying disorders, hypoalbUlllinemia
serum phosphate concentration is low
and hyperglobulinemia may be found.

( <2 mgldL), potassium phosphate should be

Prolonged PT or APTT may develop; the
added at a rate of 0.01-0.03 nunol/kg/hr.

PIVKA clotting time is more sensitive for

Potassimn chloride supplementation must
detection of vitaniin K, sufficiency. In t11e
be judiciously adjusted, considering
earliest stages of the HL syndrome, TSBAs
concurrent potassium phosphate suppleare abnormal before onset of jaundice (this ments to avoid iatrogenic hyperkalemia.

circumstance is rarely encountered).

Potassium phosphate supplements (up to

Peritoneal effusion is rare but when found

0.06 mmol/kglhr) are conllllonJy initiated
represents the prin1ary disease process or
when feeding is started to guard against
iatrogenic fluid overload.

development of severe hypophosphatemia

Ultrasonographic evaluation reveals
associated with the "refeeding syndrome."

homogeneous hyperechoic hepatic

A fortified water-soluble vitamin solution
parenchyma and subjective hepatomegaly.

(2 mIJL of fluids, see TABLE 12, p 442) should Hyperechogenicity is determined by
be added to the IV fluids. Thianiine supplecomparing hepatic parenchyrna to falciform ments (50-100 mg/day) are specifically
fat and the spleen (liver is normally
indicated in HL and provided in water-soluble
hypoechoic vs spleen). Kidneys also may
fluid supplements or by the oral route. Rare
appear hyperechoic because of increased
anaphylactoid reactions and neuromuscular
renal tubular fatty vacuolation. Ultrasonoparalysis have been seen in a few cats treated graphic exan1ination should carefully assess with thiamine by SC or IM injection.

458

HEPATIC DISEASE IN SMALL ANIMALS

A diagnostic blood sample should be

Occasionally, an appetite stin1ulant may
collected for B, determination followed
help initiate feeding early in syndrome

2
by empirical 812 administration
development.

(250-1,000 mcg/cat, SC). Cobalamin

A palatable odiferous food should be
deficiency is seemingly common in HL cats
offered initially. If the cat salivates or
and may predispose individuals to this
objects, all food should be removed because
syndrome. When present, 812 deficiency
of the 1isk of inducing a "food aversion

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confounds intermediary metabolism;
syndrome." If oral feeding is not tolerated,
however, this is confirmed only by
feeding a liquid diet ( eg, CliniCare®) with
assessment of methylmalonic acid, which
supplements via a nasoesophageal tube is
confirms functional 8 insufficiency.

cautiously initiated as a first step. A 5--10 mL

12

Unfortunately, this assessment cannot be
volun1e of tepid water is administered first
promptly completed. Consequently, B,2
to assess the cat's tolerance and response.

supplementation (which has no adverse

If no vomiting or signs of discomfort are
effects) is routinely supplemented with the
noted, the process is repeated with liquefied
less exacting measurement of plasma 812
food. After a few days of nasoesophageal
used to detem1ine propriety of longtem1
feeding, if the cat is judged to be a reasonsupplementation. Treatment witl1 N-acetylable anesthetic risk, an esophagostomy tube cysteine is initiated during the first 2-3 days

CE-tube) is placed with the distal tip 2-4 cm

(140 mg/kg, IV, administered through a
craniad to the esophageal-gastric junction.

0.25-µm filter over 20 min, then 70 mg/kg, IV,

This should be docwnented with a lateral
tid-qid; diluted to a l()OA,solution). N-acetylthoracic radiograph.

cysteine should not be given as a prolonged

A high-protein, calorie-dense, balanced

(>l hr) constant-rate infusion, because it
feline diet is recommended for E-tube
may induce hyperanm10nemia by deviating
feeding. Only rarely should a proteinsubstrates from the urea cycle.

restricted diet be used, because protein

Vitamin K, is given with a small needle
restriction can aggravate hepatic lipid

(0.5--1.5 mg/kg, SC or IM, three doses given at accunmlation. Rather, use of lactulose and 12-hr intervals) before procedures that might
oral amoxicillin or low-dose metronidazole
provoke bleeding ( eg, insertion of a jugular

(7.5 mg/kg, bid) can optimize nitrogen
catheter, esophageal feeding tube, cystocentolerance to allow feeding of a nonnal feline tesis, or hepatic aspiration sampling).

diet (these measures modify enteric flora,

Some cats may develop renal potassium
substrate utilization, and increase colonic
wasting as a result of underlying renal
catharsis or cleansing). A munber of
disease or lipid accwnulation in their renal
metabolic supplements have improved
tubules. The fractional excretion of
recovery of affected cats: taurine (250-500
potassium can be estimated by measming
mg/cat/day), medical grade liquid oral
potassium and creatinine in sin1ultaneously

L-carnitine (250-500 mg/cat/day), vitamin E
collected baseline sernrn and urine san1ples:

(10 IU/kg/day), and potassiun1 gluconate (if
fi·actional potassiun1 excretion= ([urine
hypokalernia is persistent).

potassium/urine creatinine] x [ serun1

Initial feedings are small and given
creatinine/serun1 potassiwn]) x lOOOA,. In a
frequently or by constant-rate infusion. On
hypokalemic cat, a value < 1 % is expected.

the first day, one-third to one-half of the cat's

Values >200A, represent marked renal
energy requirements are fed; the amount fed
potassium wasting and indicate the need for
is then gradually increased over the next
aggressive potassium supplementation. Cats 2-4 days to the ideal intake. If vomiting with prodigious potassium needs should
occurs, electrolytes must be rechecked,
have potassium gluconate added to their
feeding tube position verified, and factors
food as soon as oral intake is established.

relevant to the underlying disease process

This will reduce the concentrations of
considered. Metoclopramide (0.05--0.1 mg/
potassiw11 needed in the IV fluids and associkg, IM, up to tic!, or 0.25--0.5 mg/kg divided ated risk of iatrogenic hyperkalemia
per day as a constant-rate infusion),

Nutritional support is tl1e cornerstone of
ondansetron (0.025 mg/kg, IV, up to bid), or
recovery (seep 439). Feeding is initiated
maropitant (1 mg/kg/day, no more than 5
after the cat is rehydrated and has
days) may be used as antiemetics. Enteric
reasonable electrolyte balance, because
motility may be stimulated by exercise
these are requisite factors enabling nom1al
during owner visits.

enteric motility. Because cats with HL are in

To ave1t development of hypophosmetabolic liver failure, appetite stimulants phatemia induced by re-feeding, which can
are inappropriate; diazepam, oxazepam,
cause weakness, hemolysis, encephalopacyproheptidine, and mirtazepine should not thy, and other adverse effects, sernm
be used and will not recover an affected cat .

phosphorus concentrations should be

HEPATIC DISEASE IN SMALL ANIMALS

459
serially monitored and supplemental
succumb before biliary cirrhosis develops.

potassium phosphate judiciously provided.

Biliary cirrhosis is misidentified in cats with

Routine IV potassium phosphate suppleductal plate malfonnations (a form of mentation is administered when feeding is
polycystic liver disease). Clinical features
initiated to obviate persistent or feedingof biliary cirrhosis include variable inappeinduced hypophosphatemia. If gastritis is tence, cachexia, jaundice, variable liver size,
suspected, an H2-blocker ( eg, famotidine
and ascites. Liver enzymes may be normal.

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or ranitidine) may be used, and carafate

Hypoalbuminemia, hyperglobulinemia,
administered PO (but not via E-tube ). If the
hyperbilirubinemia, and coagulopathies are
cat tolerates oral medications, SAMe at 40
common. The liver may be considered large
mg/kg/day is given between meals once
on abdominal radiographs and appears

N-acetylcysteine treatment is completed.

nodular on ultrasonographic evaluation.

SAMe supplementation must be accompa

Biopsies are needed for definitive diagnosis.

nied by sufficient B12, folate, and other

Coagulation deficits complicate tissue
water-soluble vitaJnins to ensure optimal
sampling and necessitate vitan1in K1
metabolic benefit (metabolism to glusupplementation and fresh frozen plasma tathione and methyl group donation for
transfusions before procedures. Tl'eatment
transmethylation reactions). Use of
is symptomatic, requiring management
ursodeoxycholate in HL may be det1imental
of HE, hypoalbuminemia, EHBDO, and
because TSBAs are extraordinarily high
ascites. Prognosis is generally poor. Biliary
in these cats and because bile acid profiles
cirrhosis is most commonly seen in animals
resemble those associated with EHBDO
with chronic EHBDO caused by obstructive

(increased secondary bile acids). All bile
neoplasia. Although cholecystoenterostomy
acids are toxic to cells in high concentraor choledochoenterostomy can avert tions and, in HL, bile acids are seemingly
progression of EHBDO to biliary cirrhosis,
trapped by canalicular compression.

it introduces recurrent retrograde infection

In the rare circumstance that signs of HE
through biliary structures causing chronic
are encountered, lactulose, amoxici.llin, or
or recurrent septic cholangitis.

low-dose metronidazole (�7.5 mg/kg, PO,
bid) may be useful. In symptomatic pancrea

CANINE CHOLANGIOHEPATITIS
titis, feeding distal to the pancreas is done
using a constant-rate infusion of CliniCare®

Cholangiohepatitis in dogs is rare and
mixed with supplemental pancreatic
usually associated with suppurative
enzymes through ajejunostomy tube.

inflammation and ascending biliary tree

Alternatively, parenteral nutrition can be
infection with a wide variety of bacterial
provided, although this may delay recovery
organisms (both gram-negative and
and provoke hepatic triglyceride retention.

gran1-positive enteric bacteria, Salmonella,

Prognosis for cats with HL is good with

Campylobacterjejuni, coccidiosis). Canine
early diagnosis, full treatment support, and
cholangiohepatitis is most commonly
control of underlying disease. Monitoring
associated with disorders causing stasis
liver enzymes has no value in predicting
of bile flow, biliary mucocele fonnation,
recovery. However, a decline in total
cholelithiasis, and surgical manipulations
bilirubin by 500/llwithin the first 7-10 days
of the biliary tree. Clinical signs include
portends an excellent chance of full
anorexia, vomiting, diarrhea, lethargy,
recovery. Concurrent pancreatitis is a poor

PU/PD, fever, and abdominal pain.

prognostic indicator. Monitoring ALP of

Laboratory abnormalities are consistent
obese cats undergoing weight reduction
with hepatic cholestasis and include
may identify emerging HL that will allow
hyperbili.rubinemia and increased activities
suspension of the weight loss program and
of ALP, GGT, and transaminases. Ultraearly treatment intervention. Recurrence of sonography may or may not reveal

HL is rare in recovered cats.

abnom1alities involving the biliary tree or
gallbladder. In some cases, a coarse hepatic

BILIARY CIRRHOSIS
echogenicity is identified, reflecting portal
tract inflan1matory infiltrates and connec

Biliary cirrhosis refers to periportal bridging tive tissue. In some cases, ultrasonographic fibrosis associated with marked hepatic
findings may indicate need for emergency
architectural remodeling and biliary
surgical intervention ( eg, mature gallbladhyperplasia subsequent to chronic (months) der mucocele, cholelithiasis associated with of EHBDO or years of nonsuppurative

EHBDO). Aspirates or inlpression smears of
cholangiohepatitis. However, it is uncomliver or bile may reveal suppurative septic mon in cats with cholangitis/cholangiohepainflan1mation. Samples collected from liver, titis, because these animals usually
bile, and sections of the biliary tree should

460

HEPATIC DISEASE IN SMALL ANIMALS
be submitted for aerobic and anaerobic
biopsies from Labrador Retrievers and
culture and sensitivity. Antibiotic treatment

Doberman Pinschers from 1980 to 2013
should be based on cultured organisms, and
indicated that dogs of these breeds, with
other treatments should target underlying
and without chronic hepatitis, had
disease processes. Initial treatment with
significantly higher hepatic copper
combination of ticarcillin, metronidazole,
concentrations in the last 10 yr of the study.

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and enrofloxicin is commonly used before

Management of body copper homeostasis
culture and biopsy results are available. For
relies on ntu11erous copper transporters,
best outcome in animals undergoing
chaperones, and binding proteins, as well as
surge1y, antinlicrobials should be started
biliaiy canalicular egress. Copper-associbefore the surgical procedure.

ated hepatopathy is best characterized in

Bedlington Terriers, which have a mutation

CANINE CHRONIC HEPATITIS

( deletion of exon 2) of the CO MMD 1 copper
transpo1ter protein. Careful breeding

Chronic hepatitis that does not focus on
prograins guided by liver biopsy and genetic
biliary structures is more common in dogs
testing (PCR gene mutation test) have
than cats. Several breeds are predisposed
remarkably reduced disease frequency in
including Bedlington Terriers, Labrador

Bedlington Terriers. However, some

Retrievers, Cocker Spaniels, Dobem1an

Bedli..ngton Terriers with biopsy-confirmed

Pinschers, Skye Terriers, Standard Poodles,
copper-associated hepatopathy lack this

West Highland White Terriers, Springer
specific gene mutation.

Spaniels, Chihualmas, and Maltese.

Failure to excrete copper into bile leads

Although there is an identifiable etiology for
to chronic hepatitis and, eventually,
some categories of chronic hepatitis, in
cirrhosis and liver failure. Affected dogs
most cases the cause remains unidentified.

develop high liver copper concentrations by

Increased hepatocellular copper and

1 yr of age (normal: <400 mcg/g dry liver or

Kupffer cell iron stores are common in dogs

400 ppm), which progressively increase
with chronic hepatitis. The degree of metal
during the first 6 yr of life (values may be
accmnulation and its acinar location help

> 12,000 ppm). Liver injmy is reflected by
determine its relevance to tissue injmy.

increased ALT activity and has been shown

Other associated conditions include
in dogs with hepatic copper as low as 600
infectious canine hepatitis, chronic
ppm.

hepatitis secondaiy to infectious processes,

Three disease phases were historically
and chrome exposure to xenobiotics
chai·acterized in Bedlington Terriers. Acute

(including certain drugs, biologic toxins,
hepatic necrosis occurred in dogs <6 yr old
and chemicals). Terminology that reflects
presenting with hepatomegaly, vomiting,
specific etiology or breed predilection, such
lethargy, anorexia,jatu1dice, copper-inas drug-associated chronic hepatitis duced hemolytic anemia, and hemoglobinuinfectious chronic hepatitis, copper-�sociria. Copper-associated hemolytic anemia ated hepatitis, etc, is preferred. The tem1
occurs only with massive hepatic necrosis
idiopathic chronic hepatitis indicates that
which releases lai·ge ainounts of copper into
an etiology has not been determined.

the systemic circulation. Death usually

Histopathologic changes.are generally
occurs within 48-72 hr of onset of cllilical
similar in all cases of chronic hepatitis,
signs. In this group of dogs, untreated
regardless of the underlying cause, and
survivors suffered recurrent bouts of
include a lyrnphocytic-plasmacytic
critical illness induced by stress ( eg,
inflanunation with infiltrates extending into
whelping, attending dog shows, traveling).

hepatic parenchyma, variable single cell or

Another clinical presentation involves
piecemeal necrosis, and in advanced disease
chronic hepatitis associated with clinical
development of bridging fibrosis and nodulal features, including chronic weight loss HE
regeneration. The acinai· zone of involveascites, and jatu1dice. Some dogs devel�p �
ment varies with the tu1derlying cause.

acquired Fanconi syndrome (glucosuria,
an1inoaciduria, metabolic acidosis

Copper-associated Hepatopathy
inappropriately alkaline urine pH): signaling
renal tubular copper toxicity. The last

Copper-associated hepatopathy is a leading
clinical presentation was recognized in
cause of chronic hepatitis in dogs,
yotu1g, cllilically healthy dogs, sin1ply
increasing in prevalence since 1997 when
demonstrating increased ALT activity and
copper supplements in cmmnercial dog
increased hepatic copper concentrations
foods were modified to a more bioavailable

( on liver biopsy). This presentation
fonn. Retrospective evaluation ofliver
progresses to acute hepatic necrosis or

HEPATIC DISEASE IN SMALL ANIMALS

461
chronic hepatitis. Rarely, an affected dog
sources low in copper to raise the dietaiy
remained asymptomatic until another
protein intake to 3.5 g of protein/kg body wt.

disease process caused liver injury

Supplementary protein sources are selected
augmented by excessive hepatic copper
using the USDA food tables (sort based on
stores.

copper concentration), with feeding

Genetic testing is recommended for
a.mounts of selected foods calculated using

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selection of Bedlington Terrier breeding
the Nutritional Analysis Tool 2.0 (hun1an
stock. However, definitive diagnosis of
nutrition). Copper in water should contain
copper-associated hepatopathy requires

<0.1 ppm (0.1 mcg copper/1); if copper
liver biopsy in adult dogs with qualitative
pipes trat1Sport water, flushing the system
copper stains reconciled with quantitative
for 5 min will eliminate any leached copper.

copper measurements.

Ad.ministration of antioxidants is

Many other purebred and mixed-breed
important, because copper induces liver
dogs of all ages also may develop copperdainage through oxidative injwy.

associated hcpatopathy. More commonly

Chelation therapy with o-penicillaini.ne
and perhaps more severely affected are

(15 mg/kg, PO, bid, given 30 min before

Labrador Retrievers; whether the high
feeding, for �4---6 mo) is the gold staildard
breed populaiity influences this observation treatment. Thereafter, clu·onic therapy may remains unclear. Dobennan Pinschers, West be instituted by reducing the o-penicil

Highland White Terriers, and some dogs
lainine dosage by half and administering the
related to Dalmatians also may develop
drug every other day while maintaining
profoundly increased hepatic copper
dietary copper restriction. Alternatively, the
concentrations accompanied by severe liver dog may be treated with zinc acetate ( see injury. A genetic cause has not been
below). Concurrent administration of
identified in any of these breeds. It is
pyridoxine (25 mg/day) is advised during
in1portant to emphasize that copper-associo-penicillainine treatment, because this ated hepatopathy can be the prin1ary cause
drug has antipyridoxi.ne (vitainin B6) effects.

of hepatitis in any dog (purebred or mixed
lf o-penicillami.ne chelation is not tolerated,
breed) and can be definitively diagnosed
trientene hydrochloride can be used
only by liver biopsy. There is no recognized

(5-7 mg/kg, PO, bid, given 30 min before
gender predisposition.

feeding). Caution is warranted with

Histologic features of copper-associated
trientine used at the originally higher
hepatopathy include a focus on the
recommended dose, because this has
centJ.ilobular region (zone 3), finding
induced acute renal failure in dogs with
eosinophilic granules within the cytosolic
severe copper storage hepatopathy.

compartment of hepatocytes and within

An alternative approach to manage
macrophages in areas of single cell necrosis. copper storage hepatopathy is daily Small granulomas develop subsequent to
administration of oral zinc ( acetate,
hepatocyte necrosis and release of copper
gluconate, sulfate) to inhibit copper uptake
granules into the surrounding parenchyma.

from the GI tract (zinc induces enterocyte

Zone 3 lesional-associated parenchymal
metallotheinine, which irreversibly binds
collapse is verified with reticulin staining
copper and prohibits its absorption; copper

( centJ.ilobular collapse) and fibrillar
is subsequently eliminated with effete
collagen deposition with Masson trichrome
enterocytes in feces). Although zinc
staining ( centrilobulai· connective tissue
treatJ.nent theoretically increases dietaiy
deposition). With advanced injury,
options, study of the efficacy of zinc
regenerative nodules and regions of
treatJ.nent in people with Wilson disease
pai·enchymal extinction are seen. The
confirms Wlfeliable control of dietaiy
prominent role of copper in driving tissue
copper uptake. Zinc therapy must not be
injury is verified by finding copper granules
given concurrent with chelation therapy,

( rhodanine staining) in nearly every
because this will thwart efficacy of each
hepatocyte within regenerative nodules.

treatment. Oral zinc is not well tolerated by

Treatment of copper-associated
some dogs, commonly causing vomiting,
hepatopathy requires copper chelation with
nausea, and inappetence. If zinc therapy
concurrent restriction of copper intake
seems more suitable for chronic treatment
from dietary and water sources. Dietaiy
in a specific dog, a loading phase of
copper restriction can be achieved by
elemental zinc at 5-10 mg/kg/day is given in
feeding a prescription diet formulated
two divided doses, 30 min before meals.

for dogs with HE ( delivering 2.2-2.5 g of

Plasma zinc concentrations are monitored
protein/kg body wt). These low-protein
to ensure that circulating zinc is not nearing
formulas can be supplemented with protein
toxic values (>800 ppm). After several

462

HEPATIC DISEASE IN SMALL ANIMALS
months, the dosage can be reduced to

Idiopathic Chronic Hepatitis

2-3 mg/kg/day divided bid, but without
study of radio labelled copper uptake the

Idiopathic chronic hepatitis is defined as
efficacy of treatment in an individual dog
chronic necroinflanunatory self-perpetuatremains unknown.

ing liver disease associated with a

Vitan1in E (10 IU/kg/day, PO) and
nonsuppurative inflan1111atory infiltrate.

biologically available SAMe (20 mg/kg/day,

To qualify as an idiopathic syndrome, an

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PO, on an empty stomach) are recomunderlying cause should have been mended antioxidants that also have
rigorously pursued yet not discovered.

anti-inflan1111atory and potentially anti.fi

Autoin1rnune hepatitis is included in this
brotic effects. Vitamin C is contraindicated
classification. An antinuclear antibody test,
in copper storage hepatopathy, because it
testing for endemic infectious diseases
may foster injurious transition metal

(titer or antigen tests), and investigation of
effects.

d!ug and toxin exposure, along with dietary,

After chelation therapy, it is essential to
environmental, and fan1ily history, must be
continue to limit copper ingestion in food
undertaken. Middle-aged to older adult dogs
and water lifelong. Adherence to a copperare more commonly affected; there a.re no restricted diet and water source may obviate breed or gender predilections.

the need for continual chelation or zinc

Clinical features include variable
therapy.

anorexia or hyporexia, lethargy, weakness,
vomiting, diarrhea, weight loss,jaundice,

PU/PD, and in severe or advanced disease,

Chronic Hepatitis with or without
coagulopathies, ascites, and HE. Earliest

Increased Hepatic Copper in West
laboratory findings are persistent or cyclic

Highland White Terriers: Although
increases in activity of ALT, AST, ALP, and

West Highland White Terriers have been

GGT. With advancing disease, increased
shown to accumulate excessive hepatic

TSBA concentrations a.re followed by
copper, not all dogs with high hepatic
hyperbilirubinemia. Other findings may
copper concentrations develop hepatitis.

include a nonregenerative anemia,

Some dogs with severely increased hepatic
leukocytosis, and hyperglobulinernia. In
copper concentrations die of old age
late-stage disease, portal hypertension
without necroinfla.mma.tory liver lesions.

causes development of APSSs and the

Although West Highland White Terriers with associated laboratory markers ofRBC
chronic hepatitis usually do have high tissue microcytosis, hypocholesterolernia, copper concentrations, they differ from
hypoalbuminemia, prolonged APTT and/or

Bedlington Terriers with copper storage

PT, and an1monium biurate crystalluria. At
hepa.topathy in that: 1) the mode of
this stage, overt signs of HE may manifest.

inheritance has not been determined,

In early disease, liver size is nom1al and

2) maximal copper accumulation occurs
there may be no demonstrable ultrasonoby 6 mo of age and may then decline, graphic lesions. In late-stage disease,

3) overall hepatic copper concentrations
radiographs may demonstrate a small liver
a.re lower than in Bedlington Terriers, and
with nodular lesions detected on ultrasound

4) hemolytic anemia has not been reported.

examination. Ultrasonographic evaluations

Focal hepatitis may be s�en in asymptoalso may disclose ascites and APSSs in dogs matic young adult dogs. Chronic hepatitis is
with advanced liver i.Itjury.

associated with anorexia., nausea, vomiting,

Definitive diagnosis requires liver biopsy
dia.J.Thea.,ja.undice, and later ascites.

to detail acinal distribution of liver i.Itjury,

Increased liver enzymes develop first with
the type of inflanu11atory infiltrates, the
focal disease, followed by increased TSBA
presence of lobular remodeling and fibrosis,
concentrations and then hyperbilirubinemia and accumulation of copper and/or iron.

as the severity of liver injury advances.

Chronic, sustained, unexplained increases

Histopa.thologic changes include multifocal
in liver enzyn1es usually indicate liver
necroinflanunatory hepatitis with typical
biopsy. Biopsy specimens should be
copper-affiliated granulomas and single cell
submitted for both aerobic and anaerobic
necrosis, with advanced disease culminatbacterial cultures and quantification of ing in cirrhosis. Treatments target copper
copper, iron, and zinc. Copper stains must
primarily if an association between
be reconciled with quantitative copper
inflanuna.tion and copper accumulation
measurements to a.void erroneous
is histologically verified. (For treatment
interpretations. Liver biopsies must be large
recommendations, see COPPER-ASSOCIATED
enough to detail at least 15 contiguous

HEPATITIS, p 460, and CANINE CHRONIC HEPATITIS,
portal triads, and biopsies must be ta.ken
p 460.)

from several different liver lobes. Samples

HEPATIC DISEASE IN SMALL ANIMALS

463
collected only from apparent "mass lesions"

chronic hepatobiliary disease include
can lead to erroneous diagnoses. Applicasodium and water retention (which can tion of special stains will disclose the acinar
exacerbate or promote ascites ), catabolic
location of liver injury (reticulin staining);
effects (which can promote HE), GI
presence of collagen deposition of fibrosis
ulceration and enteric bleeding (which can

(Masson's trichrome staining); extent of
precipitate HE), pancreatitis, predisposition
iron accumulation in macrophages, Kupffer
to secondary infections, glucose intoler

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cells, and hepatocytes (Prussian blue
ance, and iatrogenic hyperadrenocorticism
staining); and the extent and location of

(glycogen-like VH).

hepatocellular copper accumulation

Azathioprine is most commonly used at a

( rhodanine staining).

dosage of 1-2 mg/kg/day for 3-5 days, then

Supportive care (nutritional, vitamin
every other day. Beneficial effects may not
supplementation) and use of specific
be seen for up to 8 wk. Because azathiotherapies to slow inflammation and prine can cause bone marrow suppression
fibroplasia and to restore liver antioxidant
and gastroenteric, pancreatic, and rarely
status are recommended. Antibiotics are
liver toxicity, frequent follow-up assessinitially prescribed empirically until results ments are imperative. If azathioprine causes
of the biopsy and tissue cultures become
acute bone marrow suppression (within 1
available, and then adjusted or discontinued mo), treatment is discontinued until based on culture results. Additional
recovery, then restarted with a 25%-50%
treatments include ursodeoxycholic acid as
reduction in dosage. If bone marrow
a hepatoprotectant and anti-inflammatory
toxicity is identified only after chronic
choleretic (15-20 mg/kg, PO, divided bid,
administration (months), azathioprine
given with food), polyunsaturated
should be permanently discontinued.

phosphatidylcholine as an antifibrotic

Pa.ncreatitis and idiopathic hepatotoxicity

(PhosChol® [the specific source used
are rare adverse effects that also mandate
containing 52% of the active antifibrotic
drug discontinuation. Mycophenolate
component dilinoleoylphosphatidylcholine]

mofetil is used in dogs that cannot tolerate

25-50 mg/kg/day, given PO with food),
azathioprine or, alternatively, as an initial
vitamin E as an antifibrotic and antioxidant
immunosuppressant. Recommended dosing

(10 IU/kg/day, given with food), and
is 10-20 mg/kg, PO, bid for 7 -10 days, then
bioavailable SAMe as an antioxidant (20-40
every 24 hr, followed by dosage titration
mg/kg/day, PO, on an empty stomach).

based on patient response. Cyclosporin is

Immunosuppressive drugs are used only
another alternative immunosuppressant
after careful consideration and exclusion
used in combination therapy. Some dogs
of infectious or toxic causes and when an
previously managed well on azathioprine
active disease process (nonsuppurative
have lost remission on conversion to
or pyogranulomatous inflammation) is
cyclosporin. Other dogs started on
characterized on liver biopsy. Prednisolone
cyclosporin as their primary immunoi,upor prednisone is usually started at a dosage pressant have responded well. In the
of 2-4 mg/kg/day, for 7 -10 days and titrated
absence of placebo-controlled clinical trials
downward to a maintenance level of 0.5-1
for treatment of canine immune-mediated
mg/kg, given every 24 hr or on alternate
hepatitis, treatment is individualized to each
days, depending on patient response. In the
dog based on sequential monitoring and,
presence of ascites or APSSs, dexarnethasometimes, follow-up liver biopsy.

sone is used instead of prednisone or

Discontinuation ofirnrnunosuppressive
prednisolone, because it is a synthetic
therapy is not recommended in dogs with
glucocorticoid lacking mineralocorticoid
chronic hepatitis; if drugs are discontinued,
effects. The dose is adjusted considering its
they should be withdrawn gradually, with
longer biologic half-life (72-96 hrs) and
close monitoring ( serum biochemical
higher potency (7-10 fold more than
profiles).

prednisolone or prednisone) such that dexa

Because complete remission is difficult
methasone is used at 0.1-0.2 mg/kg, PO,
to evaluate clinically, a follow-up biopsy
given every 3 days after a daily loading dose
may be required. In most cases, serum
for 3 days. An immunomodulatory agent

ALT activity serves as a surrogate marker
additional to the glucocorticoid is used to
of disease activity. Prognosis is widely
enable titration of the glucocorticoid dosage variable. Some dogs live �5 yr after initial to the lowest effective dose. This reduces
diagnosis. Dogs with ascites require dietary
the dose of each irnrnunosuppressive drug,
sodium restriction and treatment with
reducing their adverse effects and achieving
furosemide and spironolactone (see
a multirnodal immunosuppressive effect.

p 445). Dogs with HE require dietary

Adverse effects of glucocorticoids in
protein modification and may benefit

464

HEPATIC DISEASE IN SMALL ANIMALS
from lactulose and administration of
inflanunatory reaction). Response to
low-dose metronidazole.

treatment is rapid and dramatic if diagnosed

If inunw1e-mediated hepatitis is
early but lifelong management of copperconsidered the definitive diagnosis, careful associated hepatopathy (seep 460) is
consideration should be given before
required. Labrador Retrievers with chronic
administration of routine vaccinations.

nonsuppurative immune-mediated hepatitis

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Nonspecific immune stimulation may
not associated with hepatic copper
adversely stimulate hepatitis and cause
retention are treated lifelong as for
disease flare.

idiopathic chronic hepatitis (see above).

Response to treatment can be dramatic and

Breed-specific Chronic Hepatitis
is especially effective when diagnosis is

Labrador Retrievers: This popular
made early in the disease process.

breed is predisposed to chronic hepatitis
that is commonly associated with patho

Doberman Pinschers: An idiopathic,
logic accumulation of hepatocellular copper chronic, immune-mediated hepatitis (see COPPER-ASSOCIATED HEPATITIS, p 460).

recognized in Doberman Pinschers in the

However, this breed also can develop a
mid 1980s predominantly involved
primary lymphoplasmacytic hepatitis that
middle-aged adult female dogs. Copper
appears to involve in1mune-mediated
retention appears to play a role in some
mechanisms. Clinical features at diagnosis
dogs, which currently contributes to

(in order of highest frequency) include
hepatitis seen in this breed.

jaundice, inappetence, vomiting, lethargy,

In dogs with advanced disease, clinical
and weight loss, with some dogs demonfeatures include cyclic illness involving strating abdominal discomfort, PU/PD, or
anorexia, weight loss, vomiting, diarrhea,
no signs relevant to hepatitis. Common

PU/PD,jaundice, coagulopathies (melena,
laboratory features include a normal PCV,
epistaxis), splenomegaly, microhepatica,
leukocytosis, increased ALT (10-fold),
ascites, and HE. Laboratory features
increased ALP (5-fold), modest or no
may include a nonregenerative anemia,
increases in AST and GGT, hyperbilirubinleukocytosis, thrombocytopenia, increased emia, prolonged APTT, and transient

ALP and ALT activities, hyperbilirubinemia,
glucosuria if severe copper-associated
hypoalbun1inemia, prolonged APTT, and a
hepatopathy is a concurrent problem.

pure or modified transudative abdominal

Ultrasonographic imaging often demoneffusion. Ultrasonography may identify strates hypoechoic and hyperechoic
nodular liver lesions.

parenchymal nodules, subjective microhe

Liver biopsy is necessary for definitive
patica, and less frequently, irregular liver
diagnosis and treatment recommendations.

margins and ascites. A lymphocytic-plasma

Treatment in dogs with inunune-mediated
cytic hepatitis with single cell necrosis and
nonsuppurative hepatitis includes
remodeling may focus on the pmtal tract or
immunomodulation with prednisone
be diffusely disseminated. If pathologic

(1-2 mg/kg/day for several weeks, slowly
copper accun1ulation is a leading cause of
titrated to 0.5 mg/kg/day and if possible, to
the liver injury, inflan1matory responses are
every other day) and antioxidants, with
focused in the centrilobular r11gion. When
or without azathioprine. In dogs with
both disorders coexist, marked lymphoplasdeveloping fibrosis, PhosChol® polyunsatumacytic infiltrates are seen within sinusoids rated phosphatidylcholine is also recomof all acinar zones. Copper-associated mended (25-50 mg/kg, PO, with food).

hepatopathy is not typically associated with

Nutritional support depends on the presence
a marked lymphoplasmacytic infiltrate. In
of HE and the need for copper restriction.

dogs with coexistent lesions, it remains

Prognosis is poor for dogs diagnosed with
unclear whether sensitization to epitopes
advanced nonsuppurative hepatitis. Dogs
on hepatocytes damaged from copper
diagnosed early can achieve remission for
toxicity is the prinlary underlying etiopathoseveral years with prednisone, vitamin E, genesis of the immune-mediated response.

antioxidants, and ursodeoxycholic acid.

Treatment decisions are based on liver

Prognosis for dogs with apparent copperbiopsy findings with routine and special associated hepatopathy can be good if
liver stains and tissue copper quantification.

diagnosed early in the disease process

Copper chelation and restricted copper

(see COPPER-ASSOCIATED HEPATITIS, p 460).

intake (food and water) establishes
complete remission in dogs with overt

Cocker Spaniel Hepatopathy: Chronic
copper overload (>800 mcg/g dry weight

Cocker Spaniel hepatopathy is associated
tissue but lacking a nonsuppurative
with a degenerative vacuolar hepatopathy

HEPATIC DISEASE IN SMALL ANIMALS

465

(glycogen, lipid, and hydropic degenerain1plicated a unique enzyme phenotype tion) associated with low-grade nonsuppuassociated with AAT globules evident in rative inflanunation and sinusoidal
hepatocytes of some but not all Cocker
myofibrocyte activation that leads to

Spaniels. Unfo1tunately, retention of AAT
sinusoidal deposition of fine tendrils of
in damaged or dysfunctional hepatocytes
fib1illar collagen. Disease is typically
may also occur as an epiphenomenon
advanced at initial presentation. Definitive

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of compromised protein transcription
diagnosis by liver biopsy demonstrates
consequent to hepatocellular injury (but
regenerative nodules and marked distortion
usually not retention of globules) as
of the hepatic architecture consistent with
demonstrated in affected dogs. Yet it
micronodular and macronodular cirrhosis.

remains unknown whether AAT plays a role

There is no gender predisposition, and most
in this breed-related syndrome. In people,
dogs are diagnosed as young adults ( 4-4.6
treatment for AAT deficiency is liver
yr, range 2-11 yr). Most dogs lack signs of
transplant.

liver disease antecedent to development of

Treatment is supportive and symptomatic
portal hype1tension, ascites (pure or
using a balanced protocol as described for
modified transudate ), hypoalbun1inemia,
chronic hepatitis. Early glucocorticoid
abrupt onset of HE, and APSSs. Clinical
inununomodulation ( eg, before the diagnosis
signs at presentation may include (in
of liver disease, glucocorticoids prescribed
declining frequency) inappetence, lethargy,
for ear or skin disorders) has seemingly
diarrhea, weight loss, melena, vomiting, and
prolonged survival in affected dogs.

amaurosis. In some dogs, hepatopathy is

However, in dogs with hypoalbuminemia or
discovered during abdominal ultrasonograascites, glucocorticoids are poorly tolerated phy for another health problem. Clinicoand may cause melena, ascites, HE, etc.

pathologic features include modestly

If a glucoco1ticoid trial is undertaken,
increased to nom1al liver enzyme activity,
dexamethasone should be used instead of
hypoalbuminemia, hypocholesterolemia,
prednisone to avoid mineralocorticoid
and increased TSBAs in the absence of
effects. Ursodeoxycholic acid, vitamin E,
hyperbilirubinemia. Nonna! fibrinogen,

SAMe, polyunsaturated phosphatidylchoclotting times, nom1al or increased line (PhosChol®), and individually tailored

C-reactive protein, and subnormal
nutritional support are recommended. A
antithrombin activity argue for a lack of
permanent urethrostomy may be necessary
acute phase marker induction and an
in male dogs that develop ammoniwn
inflan1111atory phenotype. Some dogs have
biurate calculi. Successful treatment of
moderate to abundant copper ( on
severely affected dogs has been possible for
copper-specific staining), which may
several years. Need for copper chelation is
represent copper retention secondary to
based on specific stains and copper
cholestasis (mild copper retention) or a
quantification. Management of HE ( dietary
more primary copper-associated iI\jury
modification, lactulose, low-dose metn;mi

(copper >800ppm). In the latter dogs, foci
dazole, or nonabsorbable orally adminisof hepatocellular damage coordinate with tered antimicrobials), and management
regions of dense copper retention.

of ascites (sodium restriction, diuretics,

Strong sinusoidal staining with alphajudicious therapeutic abdorninocentesis) as smooth muscle actin confinns transformadesc1ibed previously are recommended.

tion of resting stellate cells (Ito cells) that

Dogs receiving glucocorticoids as treatment
nonnally store retinoic acid (vitamin A) into for antecedent health issues before activated myofibrocytes. Although the
hepatopathy diagnosis and dogs treated
lesion has been labeled "lobular dissecting
with glucocorticoids with or without
hepatitis" and Cocker Spaniel "hepatitis,"

azathioprine after diagnosis may have
the minimal inflammation and necrosis
in1proved survival. Additional suppo1tive
and lack of clinicopathologic markers of
treatments reported include ursodeoxyinflan1111ation suggest that "hepatopathy" is cholic acid, antioxidants, and antifibrotics.

better tem1inology. Chronic Cocker Spaniel

Although there was no correction of
hepatopathy studied in Sweden nearly
hypoalbun1inemia in most dogs, survival

20 yr ago investigated whether a genetic
beyond 3 yr of diagnosis was docwnented.

abnormality causing alpha1-antitrypsin

(AAT) deficiency was involved. AAT is

Skye Terriers: Three reports of hepatitis
an important serum protease inhibitor
in Skye Terriers, one characterizing disease
synthesized in the liver and exported to the
in nine related dogs, described no age or
systemic circulation. Study of plasma AAT
gender predilection and clinical signs
protein configuration and immunohistoranging from asymptomatic to end-stage chemistry of AAT in canine liver biopsies
liver failure at time of initial diagnosis.

466

HEPATIC DISEASE IN SMALL ANIMALS

Three separate liver disorders were
staini11g and quantified tissue copper
described: mild inflammation with no

>1,200 ppm). Dogs with zone 3 degeneraevidence of cirrhosis or copper accumulative hepatopathy concurrent with a tion, advanced macronodular cirrhosis with

PSVA usually respond poorly to surgical
cholestasis, and marked copper accumulaor ameroid shw1t attenuation.

tion. Treatment is based on liver biopsy, as

Treatment focuses on management of

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described previously for these disorders.

associated inflanunatory bowel disease

Q1ypoallergenic diets, home-cooked

Maltese Dog Zone 3 (Centrilobular)

nutritionist-formulated or conunercially

Hepatopathy: Maltese dogs have a high
available diets), metronidazole
prevalence of congenital hepatic vascular

(7.5 mg/kg, PO, bid [low dose because of
malfonnations (MVD, PSV As). Dogs with
portal hypoperfusionl), and glucocorticoids

MVD vastly outnumber those with PSVAs.

avoiding use of drugs with mineralocorti

Within kindreds, finding high TSBAs in
coid effects ( eg, clexamethasone, every 3

60o/<r-900/o of dogs confu-ms high Lrail
clays, anti-inflammatory close). Vitamin E
prevalence. Clinicians and breed enthusi

(10 JU/kg/day) and SAMe (20 mg/kg/clay)

asts have been confused by a published
are reconunended for antioxidant and
article proposing that TSBA quantification
antifibrotic benefits. Because a subset of
in Maltese dogs is confounded by interfering severely affected dogs have developed analytes. Liver biopsies from Maltese dogs
thromboemboli involving hepatic venules
with increased TSBA concentrations
and/or portal veins, miniclose aspirin (0.5
strongly refute that supposition, with
mg/kg, PO, once to twice daily) has been

>250 studied cases (600/o lacking PSV As)

prescribed for some clogs tmtil inflammademonstrating lesions of portal hypoperfution abates (assumed based on decline in sion. An inflanunatory and degenerative
liver enzyme activity with maintained
zone 3 ( centrilobular) hepatic lesion
synthetic markers). lnflammation also has
develops in a subset of dogs with the MVD/
been successfully managed with bucleson

PSVA trait; the lesion often coexists with
icle in some dogs. In dogs treated with
marked persistent or cyclic increases of
glucocorticoids, dosage is titrated to
serum ALT activity. Histologic lesions
response (enzymes, clinical features) to
vary in severity and may be progressive,
minin1ize undesirable adverse effects. Some
eventually culminating in ci.nhosis. This
dogs require combined irnmunomodulation
hepatopathy is often associated with conto achieve control of inflammation or current inflammatory bowel disease and
because of unacceptable glucocorticoid
may derive from splanchnic delivery of
effects. In these, azathiop1ine or cycloinflammatory cytokines and inflan1matory sporine are used in combination with or to
cells. Histologic lesions in dogs with
replace glucocorticoids. Ascites is managed
increased serun1 ALT and high TSBA
with sodium restriction and combined
concentrations typically consist of a
furosemide and spironolactone administralymphoplasmacytic infiltrate with or tion. A loading dose of spironolactone
without eosinophils adjacent to and

(2-4 mg/kg, PO, given once) followed by
sheathing hepatic venules (centrilobular,

1-2 mg/kg, PO, bid. Fmosemide is closed at
zone 3). Dogs develop a dege_nerative
l mg/kg, PO, once to twice daily. Diuretic
hepatopathy with lipogranulomas (foan1y
treatment is suspended when ascites is in
macrophage aggregates) located adjacent
remission and reinstituted on recurrence,
to hepatic venules that appear to partially
with continued sodium restriction.

or completely obscure vascular lumen. A
spectrum of histologic severities exists

LOBULAR DISSECTING HEPATITIS
within biopsy sections from an individual
dog. Severe lesions provoke postsinusoidal

Lobular dissecting hepatitis is a unique
intrahepatic po1tal hype1tension and
hepatic reaction pattern rather than a
development of APSSs. Although cilThosis
unique hepatic syndrome. The histologic
has been con.finned in a small subset of
features are typified by liver injmy
dogs, ascites is detected clinically in nearly
associated with intrasilmsoidal nonsuppu75% of those affected. ln dogs with ascites, rative inflanunatory infiltrates leading to
ultrasonography usually discloses hepatic
panlobular sinusoidal fibrosis. Although
parenchymal nodules, a nodular liver
more conunonly described in juvenile to
surface contour consistent with hepatic
young adult dogs and in a small group of
remodeling, and narrowing of hepatic
related Standard Poodles, this disorder
venules on color-flow vascular interrogaseemingly has no breed, gender, or age tion. A small subset of dogs may have
predilection. Weight loss and ascites, with
copper-associated hepatopathy (rhodanine
or without jaundice, are common clinical

HEPATIC DISEASE IN SMALL ANIMALS

467
features. Laboratory abnmmalities include
dogs with hepatic adenomas, hepatocellular
hypoalbuminemia, hypocholesterolemia,
carcinoma, and gallbladder mucoceles.

low BUN, and increased TSBA concentra

Progressive VH merges into ilie classic
tions in nonjaundiced dogs. Liver enzymes
hepatic syndrome associated with ilie
may be normal or mildly or markedly
hepatocutaneous lesion (see below).

increased. APSSs develop due to acquired

Hepatic biopsy is needed for definitive
intrahepatic sinusoidal portal hypertension.

diagnosis, because glycogen-vacuolated

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Hepatic copper concentrations are not
hepatocytes are also seen in necroinflamconsistently increased. The syndrome matory liver disorders. Intrahepatic
conunonly progresses to cirrhosis.

extramedullary hematopoiesis is conunon.

Supportive treatment is reconunended for

It is critical to detern1ine and treat any

HE, ascites, and control of fibroplasia and
underlying disease process. Careful scrutiny
inflammation as described previously.

for adverse drug reactions is also necessary,

Colchicine (0.03 mg/kg, PO, daily to every
wiili a focus on drugs associated with
other day) has been used to control fibrosis

"induction phenomenon." These should
and sinusoidal inflanunation in some dogs.

be discontinued and replaced wiili an

Other dogs have been managed with more
alternative therapy. Clinicians should
conventional immunomodulatory protocols
investigate any use of holistic or herbal
with PhosChol® (polyunsaturated
remedies that may have systemic glucocorphosphatidylcholine with 52% dilinoleoylticoid or adrenocorticotropic ho1mone phosphatidylcholine, 25-50 mg/kg/day),

(ACTH) effects.

used as an antifibrotic with fewer adverse

Nutritional support is impmtant and must
affects. This is a poorly understood and
be individualized. In most cases, a normal
characterized syndrome and in some cases
protein intake is appropriate. VH in dogs
may reflect hepatotoxin exposure.

with hyperlipidemia requires treatment with
a fat-restricted diet ( <2 g fat/100 kcal of

CANINE VACUOLAR
diet). A protein-restricted diet should not be

HEPATOPATHY
fed, unless indicated ( eg, demonstration of

HE or ammoniun1 biurate crystallwia). In

Vacuolar hepatopathy (VI-I) is a commonly
fact, protein restriction may augment
diagnosed canine liver syndrome in which
development of tl1is liver lesion, especially
hepatocytes become markedly distended
if it is associated witi1 hypoarninoacidemia
with cytosolic glycogen with or without
as in the hepatocutaneous syndrome. A
discrete membrane-bound lipid inclusions.

supplemental water-soluble vitan1in is

Glycogen-like VH is associated with typical
recommended for all dogs. Antioxidants
or atypical hyperadrenocorticism or
should be provided, because some
endogenous release of corticosteroids
experimental evidence in1plicates oxidative
in response to chronic stress, illness,
injury in degenerative VH. Ursodeoxycholic
inflammation, or neoplasia. Liver biopsy
acid is reconunended if TSBA concenti;ais often pursued because of unexplained tions are increased.

increases in serun1 ALP activity. Transaminase activity may be only modestly Vacuolar Hepatopathy in Scottish
increased; GGT may or may not be

Terriers: VH associated witi1 a progressive
increased.

increase in ALP activity is common in

Abdominal radiography may reveal

Scottish Terriers. Studies suggest this
hepatomegaly or changes associated with
syndrome is linked with a breed-related
an underlying disease process. Metastatic
abnonnality involving adrenal steroidogendisease or mineralized airways ( chronic esis, leading to overproduction of progeshyperadrenocorticism) may be seen on tins and androgens. Severe progressive VH
tl10racic radiography. Ultrasonography
is first noted in middle-aged dogs and can be
reveals subjective hepatomegaly and
either slowly progressive or progress
hypoechoic hepatic nodules against a
rapidly over a few years to liver failure,
hyperechoic parenchymal background, the
cirrhosis, APSSs, ascites, and hyperbiliruso-called "Swiss cheese pattern" that carmot binemia. Ultrasonographic in1aging be differentiated from infiltrative mass
discloses ilie typical "Swiss cheese" pattern lesions, hepatic fibrosis, nodular hyperplaofVH (described above). High risk of sia, regenerative nodules, or cirrhosis. In
hepatocellular carcinoma is recognized in
some cases, grossly evident hepatic nodules
dogs demonstrating progressive hepatic
carmot be discerned by ultrasound
remodeling. Liver biopsy often discloses
examination. VH usually is the underlying
dysplastic proliferative lesions antecedent
hepatic lesion in dogs with idiopathic
to fom1ation of hepatocellular carcinoma.

nodular hyperplasia and also is common in

Adrenomegaly is conunon and may be

468

HEPATIC DISEASE IN SMALL ANIMALS
bilateral or willateral. Treatment with

HEPATOCUTANEOUS SYNDROME
adrenal-modulating drugs can be hazardous
and appears ineffective. Supportive care as

(Superficial necrolytic dermatitis, Necrolytic
for dogs with declining hepatic function,
migratory erythema, Glucagonoma
monitoring both sequential biochemical
syndrome)

profiles for sudden marked increases in

Hepatocutaneous syndrome is a rare,

ALP or ALT activity that may signal twnor

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chronic, progressive, and usually fatal
formation, and serial ultrasonographic
disorder. Although typically associated with
evaluations for enlarging hepatic mass
diabetes mellitus, the liver lesion is a severe,
lesions are recommended. Early surgical
degenerative, glycogen-like VH that also can
excision of enlarging hepatic mass lesions
accompany pancreatic or neuroendocrine
that likely represent hepatocellular
tumors and severe VH secondary to
carcinomas is recommended to allow
endogenous steroidogenic hormone release
complete excision. A subset of dogs studied
or chronic phenobarbital therapy.

also have copper-associated liver injury that

Bilaterally Synillletric crusting and ulceracannot be inferred on the basis of biochemitive lesions are found on mucocutaneous cal assessments but rather require liver
jtmctions and cutaneous regions susceptibiopsy for definitive diagnosis.

ble to pressure injwy ( eg, footpads, ears,
periorbital regions, and lin1b pressure
points). Skin lesions are characterized by a

METABOLIC DISEASES
marked parakeratotic epidermis. Edema

AFFECTING THE LIVER
tous spaces between cells are filled with
neutrophils, necrotic cells, and debris that

Diabetes mellitus, hyperadrenocorticism,
create an "eosinophilic" layer. Mild
hypothyroidism, and hyperthyroidism can
neutrophilic perivascular inflan1I11ation is
cause changes in the liver.

also seen. Lesions are commonly referred to

HL can develop secondary to diabetes
as "red, white, and blue" on H&E staining mellitus because of increased lipid

( red for parakeratosis, white for edema, and
metabolism and mobilization; notable are
blue for hyperplasia). Skin lesions are seen
hepatomegaly and increased liver enzyme
initially in most affected dogs, but liver
activities. Dogs with diabetes mellitus rarely lesions may precede cutaneous changes.

manifest liver dysfunction unless they

Clinical features include anorexia, weight
develop severe progressive VH associated
loss, lethargy, PU/PD, mild nonregenerative
with the hepatocutaneous syndrome (see
anemia, marked increases in ALP and
below). Most of these dogs have markedly
moderate increases in ALT and AST,
increased ALP with lesser increases in
hyperglycemia, decreased plasma amino
transaminase activity. Diabetic cats also
acid concentrations (by 500/oof normal),
may develop increased ALT and ALP
hypoalbwninemia, and increased TSBA
activities and may become hyperbilirubinconcentrations. High plasma glucagon emic with onset of HL. Diabetic animals
levels are inconsistent. Liver size is variable.

have increased 1isk of pancreatitis that may

On ultrasound, multiple hypoechoic
progressively lead to EHBDO and cholanginodules surrounded by hyperechoic tis. These animals have increased risk of
parenchyma are diffusely scattered
bacterial infections involvingbiliary
throughout the liver, described as a "Swiss
structures (emphysematous cholecystitis,
cheese" pattern. The association between
cholangitis ).

the cutaneous and hepatic lesions is not

Cats with hyperthyroidism usually
understood but is speculated to involve
develop increases in ALP and ALT activities
hypoaminoacidemia or abnormal zinc
and are rarely hyperbilirubinemic. Liver
metabolism. Liver lesions are not necroinfunction is usually normal. The underlying flammatory and are not associated with
cause of altered enzyme activity is not fully
fibrosis or cirrhosis. The prognosis for
understood but postulated to involve toxic
recovery from hepatocutaneous syndrome
effects of excessive thyroxine, malnutrition, in dogs is poor.

cardiac dysfunction, induction phenom

Treatment focuses on correcting amino
enon, and increased bone turnover ( causing
acid deficiencies and providing symptoincrease in the bone isoenzyme of ALP).

matic care for cutaneous lesions and VH. In

Liver enzyn1es return to nom1al with
general, corticosteroids are contraindicated
successful treatment; however, methimafor the skin lesions. A commercial diet high zole also can lead to a drug-associated
in protein or fommlated for dogs with
hepatopathy that resolves only after drug
hepatic insufficiency with an added
discontinuation.

"body-building" amino acid concentrate can

HEPATIC DISEASE IN SMALL ANIMALS

469
be used. Administration of IV amino acids
enzyn1e activity, particularly ALP. Unless the
requires delivery through a catheterized
liver is diffusely remodeled with nodular
jugular vein. Aminosyn l()OA, crystalline
lesions ( secondary to degenerative VH),
amino acid solution (100 mL contains 100 g

TSBA concentrations remain normal.

of amino acids) can be given IV, 500 rnUdog,

Ultrasonographically, nodular hyperplasia
over 8-12 hr. Syn1ptoms from hyperamis associated with hypoechoic hepatic monemia may develop in susceptible dogs
nodules set against a hyperechoic

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(previously demonstrating HE) but should
background (if associated with glycogenresolve within 12 hr after completion of the like VH). Cytology of an aspirate may
infusion. The IV amino acid infusion is
disc1iminate dysplastic, neoplastic, or
repeated 7-10 days later if skin lesions
inflanunatory cells but carmot exclude any
persist; four cycles can be given. If no
of these disorders. Biopsy is necessary to
response is seen, further amino acid
differentiate between nodular hyperplasia,
infusions are futile. Amino acid treatment
dysplastic microscopic nodules, regeneraresults in regression of skin lesions and tive nodules, cirrhosis, and neoplasia.

hepatopathy in some dogs.

Control of concurrent diabetes mellitus
can be challenging, because insulin

HEPATIC NEOPLASIA
resistance suggests involvement of
cotmter-regulatory hormones (glucagon,

Primary hepatic neoplasms are less
glucocorticoids, others). Supportive care
conunon than metastatic neoplasms in the
requires use of appropriate broad-spectrum
liver and are either carcinomas, carcinoids,
antifungals or antibiotics for superficial
sarcomas, or of hemolymphatic origin.

secondary bacterial and fungal invaders,

Metastatic neoplasia of the liver can
zinc methionine supplementation
originate from multiple visceral organs and

(1.5-2 mg/kg/day, PO), water-soluble
can include lyn1phosarcoma. There may be
vitan1ins (doubled daily dose), essential
no c!inicopathologic featmes indicating the
fatty acid supplements, and topical lesion
presence of metastatic neoplasia within the
cleansing. Some dermatologists also
liver.

recommend treatment with rtlacinamide

Primary tumors are most often found in

(250---,'300 mg/dog, PO, bid). Ursodeoxyolder animals ( <9 yr) and can be malignant cholic acid ( 15-20 mg/kg, divided and given
or bertlgn. The most conm1on primary
bid with food) and antioxidants (vitamin E
hepatic neoplasm in dogs is hepatocell ular
and SAMe) are recommended. Identificacarcinoma, whereas the most common tion and treatment of underlying metabolic
primary hepatic neoplasms in cats include
conditions is essential for control. Chronic
biliary adenomas and carcinomas and
phenobarbital therapy has been an
cystadenomas ( not considered a neoplasm)

underlying cause in some dogs. Successful
most common in older cats. Additional
treatment with long-acting somatostatin
tumor types include hemangiosarcomas,

( octreatide; prohibitively expensive) has
carcinoids, and sarcomas in dogs;
been described in a single dog with
lymphomas and myeloproliferative disease
hepatocutaenous syndrome secondary
in cats; and less frequently, leiomyosarcoto metastatic glucagonoma.

mas, GI stromal tumors, and myelolipomas.

NODULAR HYPERPLASIA

Hepatocellular Carcinomas: Hepatocellula.r carcinoma is most conm1on in dogs Nodular hyperplasia (proliferative
but also may occm rarely in cats. Diagnosis
hepatocytes maintaining single-celled
may be initially pursued because of
hepatic cord architecture with nonnal
palpation of an abdominal mass or
reticulin support) occurs as a bertlgn,
recognition of serially increasing ALT, ALP,
age-related microscopic or grossly apparent
or GGT activities. Less commonly, mass
small mass lesion in dogs. It is often
lesions are discovered as the cause of
associated with a VH, lacks a defining
critical abdominal hemorrhage. Radiograremodeled border (as characterizes phy may disclose a large mass lesion or
regenerative nodules), and may be confused emphysematous abscess witrun a necrotic rustologically with adenomatous hyperplatw11or core. Ultrasonography is more sia or hepatic adenoma ( demonstrating
sensitive for detection of mass lesions and
proliferative disorganized hepatocytes
can discriminate single from multiple
fomling thick hepatic cords with din1inlobe involvement. Small hepatocellular ished reticulin support). Although nodular
carcinomas may appear hypoechoic,
hyperplasia does not cause clinical disease,
hy:perechoic, or heteroechoic. However, the
it can be accompartled by increased liver
large size of some masses precludes clear

470

HEPATIC DISEASE IN SMALL ANIMALS
differentiation of tumor impingement on
nase activity) surveillance for ttm1or
or invasion into adjacent viscera and
recurrence.

vasculature. Hepatocellular carcinomas can
occur as a single large mass in one liver lobe

Hepatocellular Adenomas and
with or without smaller masses in other

Adenomatous Hyperplasia or
lobes (massive), as discrete nodules located

Dysplastic Foci: Differentiation of

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in multiple lobes (nodular), or as infiltrative
hepatocellular carcinoma from hepatoceldisease throughout the liver without lular adenoma can be difficult, involving
obvious discrete nodularity (diffuse).

judgement of the degree of dysplasia and

Nodular and diffuse hepatocellular
characterization of the histologic features.

carcinomas, which account for 29"A, and

Like hepatocellular carcinomas, adenomas

10%, respectively, of all hepatocellular
also may be accompanied by microscopic
carcinomas, involve multiple liver lobes and
dysplastic foci in unaffected liver lobes.

are not usually amenable to surgical

Hepatocellular adenomas and dysplastic
removal. Single massive hepatocellular
foci are more conunon in dogs with atypical
carcinomas represent 61 % of all canine
adrenal hyperplasia associated with
hepatocellular carcinomas and are
increased androgen or progesterone
potentially resectable with good outcome.

concentrations. Both lesions are often

1\unors involving the left liver lobes carry
associated with increased liver enzyme
the best prognosis. Hepatocellular
activity (ALP primarily, with more modest
carcinomas are locally invasive and may
change in transaminases). Rather than
spread to local lymph nodes but are slow to
single mass lesions, multiple dysplastic foci
metastasize elsewhere. Multiple histologic
are commonly identified within a single
patterns have been characterized for canine
biopsy sample and among multiple biopsies
hepatocellular carcinoma, including (but
from the same animal. Neoplastic transfornot limited to) solid, clear cell, trabecular, mation of dysplastic foci is suspected.

peliod, pseudoglandular, scirrhous, and

Similar to hepatocellular carcinomas,
anaplastic.

hepatocellular adenomas may outgrow their

Common clinical signs in dogs include
central blood supply, developing a necrotic
weight loss, inappetence, fever, and
core that may serve as a nidus for abscess
lethargy; less common signs include
formation. Mass lesions also may rupture
vomiting, PU/PD, and seizures (hypoglyceand cause critical abdominal hemorrhage.

mia). However, dogs may be asymptomatic

Hepatocellular adenoma is cw·able by wide
until the tumor reaches massive size or
resection, although recurrence is possible in
develops a necrotic core leading to critical
dogs with dysplastic foci. 1\unor margins
abdominal hemorrhage. On abdominal
should be demarcated on submitted
palpation, a mass may be detected, and pain
specimens to enable microscopic assessnotable. Abdominal effusion is uncommon.

ment of the adequacy of mass resection

Laboratory tests may indicate nonregenera

(tumo1�free margin).

tive anemia, RBC microcytosis, thrombocytosis, increased serum activity of ALP and Biliary Adenocarcinomas: Variably

AST, and hypercholesterolemia. High ALT
classified as cholangiocellula.r carcinoma
and AST concentrations may reflect
or adenoca.rcinomas and hepatocellular
invasion of adjacent nonnal tissue or
adenocarcinomas, these tun1ors are the
central tumor necrosis and may indicate a
most common primary malignant hepatic
poor prognosis. Increased ALP may reflect
neoplasm in cats and may derive from
association with increased steroidogenesis
intral1epatic or extral1epatic bile ducts,

(particularly androgens and progestins ).

pancreas, or gallbladder. Pancreatic

Hypoglycemia may develop either due to
adenocarcinomas, invasive into hepatic
large tun1or mass or a paraneoplastic effect.

structures, are also common in cats.

Pulmonary metastases are unconunon.

ln1munohistochemical staining may be

Tun10r margins should be demarcated on
necessary to definitively characterize the
submitted specimens to judge adequacy of
tissue of origin (biliary epithelitm1 vs
mass resection (ttm10r-free margin). Mass
hepatocellular). Biliary cysts can be
excision with wide margins can be curative
mistaken on gross inspection for primary
in both dogs and cats. Liver biopsies from
biliary adenocarcinomas.

regions distal to the tumor are recom

Clinical signs usually include anorexia,
mended in dogs, because antecedent
lethargy, and vomiting, and some cats are
dysplastic foci may portend possible tw11or
jaundiced. Many cats have a history of
recurrence. Finding dysplastic foci should
antecedent liver disease based on historical
increase ultrasonographic and clinicopathobiochemical profiles; histologically, the logic ( a sudden peak in ALP or transami-chronic liver disease is a nonsuppurative

HEPATIC DISEASE IN SMALL ANIMALS

471
cholangiohepatitis. A mass or large liver
abdominal ultrasonography, appear densely
may be palpable. Increased ALT, AST, ALP,
hyperechoic, have a clearly demarcated borand GGT activities and increased cholesder, and are usually small. Aspiration terol and bilirubin concentrations are
cytology can easily characterize the cellular
common. However, some cats with biliary
features. Unless large vessels and biliary
adenocarcinomas have no clinical signs or
structures are compressed, these lesions do
laboratory abnom1alities. Biliary tree
not require surgical removal.

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obstruction is identified in some but not all
cats with neoplasia associated with the

Metastatic Neoplasia: The most
common bile duct and gallbladder.

common tumors metastasizing to the liver

Abdominal radiographs may disclose mass
in dogs include lymphoma, pancreatic
lesions disrupting the hepatic silhouette.

carcinoma, mammary carcinoma,

Ultrasonography usually delineates mass
pheochromocytoma, intestinal carcinoma,
lesions, their dimensions, and lobe location
thyroid carcinoma, fibrosarcoma, osteosarand documents the presence or absence of coma, hemangiosarcoma, mast cell tumors,
biliary tree and/or gallbladder obstruction.

and transitional cell carcinoma. Metastatic

Some cats develop abdominal effusion and
tumors of the liver are less common in cats
carcinomatosis.

but include pancreatic, intestinal, and renal

Surgical resection of neoplastic lesions
cell carcinomas; mast cell tumors; and
associated with biliary structures distal to
lymphoma. Metastatic tumors are often
the porta hepatis and lesions associated
multifocal but may initially exist only within
with the gallbladder is possible. Neoplasia
vascular and lymphatic elements.

involving the common duct may be palliated

Clinical signs can be nonspecific or
with stent placement through the sphincter
specific to the liver and resemble features
of Oddi into the duodenum (poorly
associated with primary hepatobiliary
tolerated by cats) or surgical creation of a
neoplasia, including anorexia, weight loss,
biliary diversion. Some cats survive for
vomiting, PU/PD, and variable hyperbilirumonths with palliative supportive care binemia. Metastatic hepatic neoplasia is

(without surgery) despite total bile duct
more likely to be associated with a
obstruction. However, the longterm
malignant abdominal effusion. Neurologic
prognosis is poor. Metastatic lesions are
signs may indicate metastatic lesions within
often found in the local lymph nodes,
the brain, with associated clinical signs
peritoneum, and lungs.

mistaken for HE. Abnormalities on baseline
hematologic or chemistry profiles may be

Lymphoma: The most common
minimal. Although a nonregenerative
hemolymphatic tumor found in the liver in
anemia may develop, there are no consistboth dogs and cats is lymphoma; this may ent changes in WBC count or distribution.

be primary or metastatic (from primary

Schistocytes may be seen when neoplasia
enteric or multifocal disease). Other
invades hepatic sinusoids, creating a
myeloproliferative diseases and mast cell
shearing effect on RBCs. Eosinophilia
neoplasia also can involve the liver,
can develop with mast cell tumors and
especially in cats. Anin1als with infiltrative
lymphoma, especially in cats. Liver enzymes
hepatic lymphoma may remain asymptomay be normal or variably increased.

matic in regard to clinicopathologic features Hypoglycemia due to large tumor mass except for hyperbilirubinemia and

(enhanced glucose utilization) or a
hepatomegaly. Ultrasonographic imaging
paraneoplastic effect (insulin-like effect) is
may not recognize architectural changes or
sometimes identified. Hyperbilirubinemia
discover nodules or mass lesions. Abdomiand increased AST are more frequent in nal effusion may develop secondary to
canine metastatic disease than in primary
compressive presinusoidal and sinusoidal
hepatic neoplasia. Although radiographic
intrai1epatic portal hypertension. Sampling
findings are variable, ultrasonography can
of the effusion and hepatic aspiration may
discriminate single vs multiple lobe
allow cytologic diagnosis of lymphoma.

involvement from diffuse infiltrative

Circulating blood should first be reviewed
disease. However, aspirates of mass lesions
for presence of neoplastic lymphocytes.

or biopsy is needed for definitive diagnosis.

If one liver lobe is involved, surgical

Myelolipomas: These benign tumors are
removal is recommended. If lymphoma
composed of adipose cells and hematopoior mastocytosis is diagnosed, appropriate etic elements. The cellular composition
chemotherapy may prolong life.

closely resembles cellular elements found

Hepatic hemangiosarcoma is treated
in bone marrow. These tumors are usually
by surgical resection as primary therapy if a
serendipitously discovered during
defined mass lesion is characterized, with

472

HEPATIC DISEASE IN SMALL ANIMALS
follow-up chemotherapy. There is no
growth, abdominal distention due to
specific study of survival expectations of
massive hepatomegaly (glycogen and lipid
dogs with hepatic hemangiosarcoma, with
vacuolation of hepatocytes ), and lethargy
or without surgical debulking or chemoand weakness associated with severe therapy. Surgery is palliative to an·est active
hypoglycemia. Histologic lesions are also
hemorrhage but does not provide longtenn
seen in renal tubular epithelium. Affected
swvival benefit for most dogs with liver
dogs develop lactic acidemia, hypercholes

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involvement. Survival in dogs with grossly
terolemia, hypertriglyceridemia, and
evident metastatic disease have the worst
hyperuricemia. Clinical signs progress to
prognosis, with median sUivival ranging
death or euthanasia by 60 days of age. A
from 68-136 days. A number of combination genetic test is available for type 1 disease chemotherapy protocols have been
in Maltese dogs.

investigated in dogs with hemangiosar

Type III glycogen storage disease,
coma, providing median survival ranging
caused by a deficiency in glycogen
from 145 to 250 days in dogs with incisional
debranching enzymes, has been reported
or excisional biopsies ( all sites of tUinor not
in German Shepherds and Curly Coated
limited to the liver). In a chemotherapy

Retrievers. There is no gender predilecstudy with doxorubin (free or pegylated tion, and an autosomal recessive
liposome-encapsulated drug) compared
transmission has been confirmed.

with a random prospective clinical trial

Clinical signs include abdominal

(n=l 7 for each group), there was no survival distention due to hepatomegaly and mild difference between treatments in dogs with
hypoglycemia. Glycogen stores are
splenic hemangiosarcoma. Pegylated
notable in both liver and skeletal muscle.

liposome-encapsulated doxorubicin was

In Curly Coated Retrievers, the mutation
associated with more adverse effects.

leads to profound hepatocyte glycogen

Another combination protocol for dogs with vacuolation, resulting in progressive advanced-stage noncutaneous hemangiohepatic fibrosis and liver failure. Affected sarcoma ( doxorubicin, dacarbazine, and
dogs also develop a progressive degenvincristine) with nonresectable stage II and erative myopathy. A genetic test is
stage III hemangiosarcoma ( doxorubicin
available for type III disease in Curly
and dacarbazine day 1, vincristine days 8

Coated Retrievers.

and 15, protocol repeated every 21 days for

Diagnosis of these disorders is based on
a maximum of six cycles or until disease
a high index of suspicion considering
progression) was studied. In this study of24
breed affiliation and symptomatic
dogs, a 47.4% response rate (five complete
hypoglycemia. Abdominal radiography
responses, four partial responses) was
reveals hepatomegaly, and ultrasonogr a realized; median time to tUinor progress10n phy reveals hyperechoic hepatic
was 101 days with a median survival of 125
parenchyma consistent with hepatic
days. Significant toxicities included
glycogen or lipid accumulation. Differenhematologic and GI adverse effects.

tial diagnoses include other causes of
juvenile hypoglycemia (including
malnutrition, endoparasitism, transient

MISCELLANEOUS LIVER
fasting hypoglycemia in toy breeds, and

DISEASES

PSVAs) and other causes of muscular
weakness (including endocrinopathies,

Glycogen Storage Disease: Of the four
immune-mediated disorders, infectious
glycogen storage diseases reported in dogs, diseases, hypokalemia, and neuromyopatypes I and III directly affect the liver, thies ). Supportive care consists of fluid
causing massive hepatomegaly in young
support, IV dextrose to achieve euglycepuppies. These disorders are characterized mia, and frequent feedings of a high-carby excessive accumulation of glycogen in bohydrate and protein diet. Diagnosis is
the liver and other organs. Accwnulated
confirmed by tissue enzyme analyses,
glycogen is w1available for conversion to
confirmation of excess glycogen stores in
glucose as a result of defective glycolytic
liver tissue, or genetic testing. Prognosis
enzyme activity.

is poor. Affected dogs and their parents

Type Ia glycogen storage disease,
should be eliminated from breeding
caused by deficiency of glucose-6-
progran1s.

phosphatase-a, has been reported in
toy-breed dogs, particularly Maltese. There Hepatic Amyloidosis: Arnyloidosis is a is no gender predilection, and disease
familial disease of Abyssinian, Sian1ese, and
transmission is autosomal recessive.

Oriental short-hair cats and Chinese

Clinical signs include emaciation, stunted

Shar-Pei dogs. Affected Shar-Pei are more

HEPATIC DISEASE IN SMALL ANIMALS

473
likely to demonstrate episodic fever and

DISEASES OF THE
swollen hocks (Shar-Pei fever) with or
without renal failure, but the liver may also

GALLBLADDER AND
be affected by diffuse amyloid deposition.

EXTRAHEPATIC BILIARY

Affected Abyssinian cats often present with

SYSTEM
clinical signs related to the kidneys or with
complications associated with diffuse

Jaundice is often the primary presenting

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. .

hepatic amyloidosis or amylo1d deposition
sign in animals with disorders involving the
in other organs. 01iental short-hair and
aallbladder or extrailepatic biliary

Siamese cats generally present with

�tructures· abdominal effusion may reflect
amyloid-related hepatic complications.

bile perito:Utis. Finding a higher bilirubin

Other conditions associated with hepatic
concentration in an effusion relative to
amyloidosis include a diversity of chronic
serwn (>10-folcl difference) confams
infections or antigen exposures ( eg,
leakage of bile into the abdominal cavity
coccidioidomycosis in dogs, cyclic
a.i1d constitutes a surgical emergency.

hematopoiesis in Gray Collies, infusion of
porcine insulin in dogs) and hypervitamino

CHOLECYSTITIS
sis A in cats.

Although animals may be asymptomatic

In non-necrotizing cholecystitis,
for long intervals, clinical signs may include inflanm1ation of the gallbladder may involve fever, lymphadenopathy, vomiting,
nonsuppurative or suppurative inflanm1ainappetence, weight loss, PU/PD, Ja tion; may be associated with infectious

_w1d1ce,
and hepatomegaly. Acute presentation for
agents, systemic disease, or neoplas1a; or
severe abdominal hemorrhage subsequent
may reflect blunt abdominal trawna or
to liver lobe rupture usually leads to the
gallbladder obstruction by occlus10n �f the
diagnosis in Oriental short-hair and
cystic duct ( eg, cholelithiasis, neoplas_1a, ?r Sian1ese cats. Ultrasonography can often
choledochitis). Cystic duct occlusion mc1tes
identify a developing hematoma at the site
gallbladder inflanunation secondary to bile
of liver lobe rupture. Aspiration of
stasis· this process is augmented by
abdominal effusion confirms active
mech�ical irritation of a cholelith. The
hemorrhage. Diagnosis can be made by
gallbladder wall thickens, and the_lun1en
aspiration cytology if amyloid fibrils are
distends with a white, viscid, mucm-laden
retrieved. Otherwise, diagnosis is made by
bile (white bile).

identifying an1yloid deposits in a liver

Necrotizing cholecystitis more
biopsy; an1yloid is confirn1ed by tissue
commonly affects miclclle-aged to older

.

staining with Congo red and exammat1on
adult clogs and may develop secondary
under polarized light.

to thromboembolism, blunt abdominal

Because familial an1yloidosis is a
trawna bacterial infection, EHBDO (cystic
progressive systemic disorder, prognosis is
duct obstruction or distal duct obstruction
poor. Cats surviving acute, severe hep
by choleliths, stricture, or neoplasia), or a

�tic
hemorrhage by aggressive adnlin1strat1on of
mature gallbladder mucocele ( causmg tense
blood component therapy subsequently sucgallbladder distention). Extension of an cun1b to renal amyloidosis. (See also
inflanunatory or neoplastic process from
adjacent hepatic tissue also may be an

AMYLOIDOSES, p 592.) Colchicine and din1ethyl

..

sulfoxide have been used to slow progresunderlying cause. Necrotizing cholecystit1s sion of systemic amyloidosis in Shar-Pei
can present with or without gallbladder
dogs and in cats, with limited success.

rupture, or as a chronic syndrome

Anecdotally, hepatic amyloid has regressed
associated with adhesions between the
in Shar Pei treated wit11 colchicine (0.03 mg/
gallbladder, omentwn, and adjacent viscera.

kg/day, daily to every other day). Longterm

Bacteria a.i·e commonly cultured from the
swvival in Shar Pei demonstrating systenuc
gallbladder wall.

. .

.

signs of Sha.i�Pei fever is possible witl1 ea.i·ly

Necrotizing cholecyst1t1s reqwres prompt
institution of colchicine therapy. In
surgical intervention ( cholecystecto�y and
predisposed Shar
potential biliary diversion). Chrucal signs

Pei, a duplication mutation upstream of
usually develop acutely and include abdomit11e hyaluronic acid synthase 2 (HAS2) gene nal pain, fever, and increased liver.enzyme
amplifies production of hyaluronic acid,
activity. However, signs may remam vague
which initiates chronic inflan1mat1on and
and episodic, and hyperbilirubinemia is
a.inyloid fo1mation. Additional genetic
inconsistent.

.

studies have identified complex polygeruc
modifier genes.

Clinical Findings and Diagnosis:_ Signs
of acute cholecystitis include abdommal

474

HEPATIC DISEASE IN SMALL ANIMALS
pain (may only be postprandial), fever,
frozen plasma should be given judiciously
vomiting, ileus, and mild to moderate
based on coagulation tests and a buccal
jaundice. Some animals present in
mucosa! bleeding tinle. Careful exploration
endotoxic shock. The hemogram discloses
of all biliary structures is warranted during
variable leukocytosis, with or without toxic
surgery. Patency of the cystic and common
neutrophils or a left shift. Hyperbilirubinebile ducts must be determined, and viability VetBooks.ir
mia and development of jaundice depend on of the gallbladder ascertained as surgical chronicity, involvement of extrahepatic
assessments are made.

biliary structures, presence or extent of

Cholecystectomy is the treatment of
biliary tree occlusion, bile peritonitis, and
choice in most cases. However, some
endotoxemia. Liver enzyme activity is
animals benefit from a cholecystoentervariable, but ALP and GGT are usually ostomy or choledochoenterostomy to
moderately to markedly increased.

circwnvent a pem1anently occluded distal

Gallbladder rupture leads to pericholecystic common bile duct. Placement of a abscess formation (localized by the
temporary biliary stent may be appropriate
omentwn) or focal or generalized bile
but should be carefully considered because
pe1itonitis. Abdominal radiography may
of the high rate of complications, especially
reveal indistinct detail in the cranial
in cats. Cats with EHBDO secondary to
abdomen consistent with focal peritonitis; a
pancreatitis demonstrate greater morbidity
sentinel intestinal loop may implicate focal
associated with this technique than dogs. In
ileus. Rarely, the gallbladder wall may
one case series of seven cats with EHBDO
become radiodense due to dystrophic
secondary to pancreatitis, after stent
mineralization secondary to chronic
insertion, two cats reobstructed within
inflammation. Choleliths may be found on

1 wk, one cat developed ascending
ultrasonography. Detection of gas within
cholangitis, two cats suffered chronic
the biliary tree or gallbladder heralds an
intermittent vomiting, and two cats died
emphysematous process associated with
during the perioperative period.

sepsis and should prompt antibiotic

San1ples of bile, gallbladder wall,
administration before surgical intervention.

choleliths, and liver tissue should be submit

Consideration of triage for emergency
ted for aerobic and anaerobic culture.

cholecystectomy is appropriate in some

Cytologic evaluations of tissue imprints and
cases. Pericholecystic fluid can be sampled
bile help initial selection of antinlicrobials
using ultrasonographic guidance to confinn

(based on bacterial morphology and Gran1
bile leakage and infection. Comparison of
staining). A combination of metronidazole,
total bilirubin concentration in effusion
ampicillin-clavulanate, and enrofloxacin
versus serwn helps confinn bile leakage.

provides broad protection against

Diagnosis is based on clinical signs,
commonly encountered enteric oppo1tunclinicopathologic features, and ultrasonoists. If only the gallbladder is involved, graphic imaging. Ultrasonographic
sinlple cholecystectomy may be curative.

detection of a thickened gallbladder wall or

If the common bile, cystic, or hepatic ducts
cystic bile duct and tenderness during the
are involved, a more guarded prognosis is
imaging procedure or on deep abdominal
warranted, and longterm antibiotic therapy
palpation may be the only evidence of
recommended.

illness. Because necrotizing cholecystitis is

There are few adverse consequences
often associated with gallbladder mucocele
of cholecystectomy, although episodic
in dogs, early intervention by prophylactic
abdominal pain and diarrhea associated
cholecystectomy may reduce need for
with fat malabsorption have been deemergency surgery.

scribed. Cholecystectomy results in loss
of the absorptive and pressure-regulating

Treatment and Prognosis: Management function of the gallbladder and the fasting of cholecystitis focuses on restoration of
reservoir where bile is concentrated. After
fluid and electrolyte status, treatment with
cholecystectomy, the volwne of bile
broad-spectrw11 antibiotics effective against increases because of reduced sodiwn and enteric opportunists, and prompt surgical
water resorption that nonnally occurs in
intervention. In some cases, colloids and
tile gallbladder, the size of the bile acid
plasma transfusion are necessary (plasma
pool dinlinishes, and tile enterohepatic
preferred to colloids). Because EHBDO is a
circulation of bile becomes continuous. Bile
differential diagnosis, vitan1in K, should be
composition shifts because of the increased
administered (0.5-1.5 mg/kg, IM or SC, three exposure of bile acids to enteric flora with doses at 12-hr intervals) before surgery to
increased formation of secondary bile acids.

avert hemorrhagic complications. If

Aninlals undergoing biliary tree
emergency surgery is necessary, fresh
decompression by biliary enteric anastomo-

HEPATIC DISEASE IN SMALL ANIMALS

475
ses are thereafter susceptible to retrograde
after feeding, confmning lack of movement
septic cholangitis and choledochitis.

of lwninal "sludge." Feeding a dog (100 g of Dogs tolerate this procedure with fewer
food) and recording gallbladder dimensions
clinical signs than cats. Animals should be
at 0, 15, 30, 45, 60, 90, and 120 min, recorded
monitored for fever, inappetence, vomiting,
in cm ([width x height x length] x 0.52)

and signs of cyclic illness. A hemogram
yields the gallbladder volwne in mL. Failure

VetBooks.ir
and liver enzymes should be monitored
to reduce baseline gallbladder volwne by at
quarterly. Chronic or intermittent antimileast 25% suggests dysmotility. Erythromycrobial administration may be needed to cin (0.5-1 mg/kg, PO, one dose) combined
control ascending cholangitis. Fortunately,
with a small meal also may stimulate
illness is usually transient and responsive to
initiation of gallbladder motility; however,
antibiotics. Longterm survival with good
in healthy dogs studied, neither feeding with
quality of life is expected in the absence of
or without erythromycin was consistently
neoplasia. Owners should be instructed to
superior to initiate contraction.

monitor the rectal temperature of animals

Dogs with GBM range in age from 3-14 yr
with cyclic illness to detect episodes of
old with no gender predisposition. Incidence
septic cholangitis to enable institution
is increased in Shetland Sheepdogs,
of at-home antimicrobial therapy.

Miniature Schnauzers, and Cocker Spaniels.

A genetic mutation in the ABCB4 (MDR3)

Emphysematous Cholecystitis/
phospholipase flippase transporter was

Choledochitis
demonstrated in Shetland Sheepdogs and
otl1er dogs with GBM. All affected dogs were

Emphysematous cholecystitis/choledochiheterozygous for tltis mutation.

tis is an uncommon condition associated

Factors predisposing to GBM fom1ation
with gas within the wall or lwnen of the
include middle to older age, endocrinopagallbladder or segments of the biliary tree.

thies (typical and atypical hyperadrenoco1°

In dogs, it has been associated with diabetes ticism, hypothyroidism, diabetes mellitus), mellitus, acute cholecystitis with or without
hyperlipidemia or hypercholesterolemia
cholecystolithiasis, trawnatic ischemia,

(idiopatltic, nephrotic syndrome, feeding of
mature gallbladder mucocele formation,
a high-fat diet, pancreatitis), gallbladder
and neoplasia Gas within the biliary
dysmotility, and cystic hyperplasia of the
structure indicates serious septic inflanunagallbladder mucosa (shown to be inducible tion associated with a gas-forming bacteria
by progestins in dogs). The inciting cause
such as Escherichia coli or Clostridium of mucus hypersecretion or accwnulation
spp. Treatment requires cholecystectomy
is unproved and may be multifactorial.

and antimicrobial therapy based on culture

Nevertheless, mucin imparts important
and sensitivity of bile and involved biliary
viscoelastic properties to bile and likely
tissues. Broad-spectrun1 antibiotic coverage importantly contributes to GBM formation.

should be initiated before surgical

Decreased gallbladder motility leads to
exploration. Use of a 13-lactamase-resistant
lun1inal bile stasis and enhanced absorption
penicillin, with enrofloxacin and metronidaof electrolytes and fluid, promoting biliary zole, is initially indicated until culture and
sludge formation. Dogs with risk factors
sensitivity results are available.

may rapidly mature a developing mucocele
after beginning glucocorticoid therapy or

CANINE GALLBLADDER
a high-fat diet ( eg, some diets for renal

MUCOCELE
disease or hepatic insufficiency). Because
concurrent VH is common, associated

Canine gallbladder mucocele (GBM) is
underlying disorders should be investigated.

characterized by progressive accwnulation
of tenacious, pale yellow to dark green,

Clinical Findings and Diagnosis: Sympmucin-laden bile, which may extend into the tomatic illness averages -5 days, although cystic, hepatic, and conunon bile ducts,
some dogs have vague episodic signs (ie,
resulting in variable degrees of bile duct
inappetence, vomiting, vague abdominal
obstruction. Progressive expansion of a
pain) for months. In decreasing order of

GBM leads to gallbladder ischemia and
frequency, clinical signs include vomiting,
necrosis, bile peritonitis, and sometimes
abdominal discomfort, anorexia or
opportunistic infection. Gallbladder stasis,
hyporexia, jaundice, tachypnea, tachycarperhaps reflecting dysmotility, and dia, PU/PD, fever, diarrhea, and abdominal
distention predispose to cholecystitis. A
distention. Dogs progressing to gallbladder

GBM should be considered when sequential
rupture usually demonstrate abdominal
ultrasonographic examinations fail to
pain,jaundice, tachycardia, tachypnea, and
indicate a reduction in gallbladder volwne
fever. However, occasionally, ruptured

476

HEPATIC DISEASE IN SMALL ANIMALS

GBMs asymptomatic with a free-moving
ultrasonographic evaluations every 6 wk are
congealed mucocele have been imaged in
useful to monitor treatment response or
the peritoneal cavity. Typical clinicopathosyndrome progression. Rarely, an evolving logic indicators include leukocytosis with a

GBM may resolve with medical treatment.

mature neutrophilia and monocytosis and

However, progression in any clinical,
sometimes a left shift, high liver enzyme
clinicopathologic, or imaging parameter

VetBooks.ir
activities (ALP, GGT, ALT, and AST),
indicates poor control and need for surgical
hyperbilirubinemia, and inconsistent
intervention.

hypercholesterolemia. Aerobic bacteria

Cholecystectomy is the best course of
may be cultured from bile or the gallbladder
treatment and is essential for most dogs
wall, with a number of enteric organisms
with clinical signs and clinicopathologic
identified, including Escherichia coli,
findings consistent with biliary tree

Enterobacter spp, Enterococcus spp, inflammation, obstruction, or rupture.

Staphylococcus spp, Micrococcus spp, and Because bile stasis predisposes to

Streptococcus spp. Transhepatic ultrainfection, broad-spectrum antimicrobials sound-guided cholecystocentesis should
should be initiated before surgical
not be pe1fo1rned if a G BM is suspected.

intervention. Examination and staining of

Ultrasonography may detect hepatomegaly
cytologic preparations of bile and imprints
and either a heterogeneous or hyperechoic
of liver and biliary tree biopsies may be
hepatic parenchyma. Hypoechoic "nodules"

invaluable if antibiotic coverage interferes
correspond to a severe VH with formation of with submitted cultures. Evidence of bactereticulin-defined nodules and regenerative ria in cytologic samples or histologic
repair. After gallbladder removal, sequential
confirmation of suppurative cholecystitis
hepatic ultrasonographic evaluations are
or cholangitis indicates a need for chronic
necessary to determine whether parenchypostoperative antimicrobial administramal lesions resolve. A liver biopsy should be tion. The resected gallbladder should be
collected from a liver lobe distant to the
submitted for histopathology (sectioned
gallbladder to evaluate for underlying or
before fixation to allow formalin penetracoexisting disorders; sections collected tion), and a liver biopsy collected distant to
adjacent to the gallbladder contain
the site of surgery. Perioperative mortality
peribiliary glands and numerous ductal
is high for symptomatic dogs with a
elements that may result in erroneous
rnptured gallbladder complicated by
assessments.

sepsis. If bile peritonitis is present, the

Histologically, cystic mucosal hyperplasia peritoneal cavity must be extensively of the gallbladder wall is conunon. All dogs
cleansed with sterile, warm, polyionic
have thick biliary debris; some components
fluids to remove debris, bacteria, and injurimay be profoundly viscous and mucin ous bile salts. Abdominal drains may be
laden, others more liquid, some dark green
necessary. Antibiotics should be administo black, some with white bile, some tered for 4--6 wk after surgery.

contain gritty black matelial, and some

Cholecystotomy for removal of gallbladcontain a finn, organized gelatinous matrix.

der contents without cholecystectomy is

Transmural ischemic necrosis may develop
not advised, because GBMs usually recur.

and lead to necrotizing cholecystitis and

Furthermore, necrosis of the gallbladder
gallbladder mpture. Liver biopsies may
wall may not be grossly evident at surgery,
disclose a VH or mild to moderate portal
leading to postoperative gallbladder
hepatitis or periductal fibrosis; the later
rnpture. After gallbladder resection, chronic
changes reflect associated cholangitis or
choleretic therapy is recommended,
transient biliary tree occlusion. Some dogs
especially for Shetland Sheepdogs in which
lack concurrent hepatic lesions, especially
a genetic risk is surmised for sludged bile.

when cholecystectomy is done preemp

Underlying causes of hyperlipidemia or
tively (before GBM maturation).

endocrine disorders should be identified
and managed appropliately. Clinicopatho

Treatment: Dogs without signs of
logic abnormalities (high ALP usually)

mucocele leakage or biliary tree obstrnction nom1alize after gallbladder removal in most at the time of initial diagnosis may benefit
dogs, except those with associated
from hydrocholeresis induced by adminissuppurative cholangiohepatitis, unresolved tration of ursodeoxycholic acid
endocrinopathies, persistent hyperlipid

(15-25 mg/kg, PO, divided bid and given
emia, or surgical complications of
with food), SAMe (20--40 mg/kg/day, PO,
cholecystectomy. Feeding a proteinafter an overnight fast; food should also restricted, high-fat diet to hyperlipidemic
be withheld for 2 hr after dosing), and
animals may be detrimental and is not
antimicrobial coverage. Biochemical and
recommended.

HEPATIC DISEASE IN SMALL ANIMALS

477

OTHER DISORDERS OF THE
congenital disorders that have been

GALLBLADDER
identified in dogs and cats and reflect
embryo logic malformations involving the

Gallbladder agenesis describes the
ductal plate (po1tal triad). Ductal plate
congenital absence of the gallbladder. In the
malformations (DPMs) reflect embryoabsence of congenital malfom1ations of the genic malfonnations due to dysfunction of

VetBooks.ir
intrahepatic biliary structures, this is an
primary cilia causing defective tubulogeninconsequential abnom1ality.

esis, affecting formation of bile ducts and

Biliary atresia describes the congenital
renal tubules. Either or both organs may be
maldevelopment of intrahepatic biliary
affected. Fibropolycystic syndromes are
structures and is uncommonly encountered.

divided into six categories in people, and

Affected individuals are jaundiced and
this divisional classification also appears
unthrifty at a young age. Prognosis is poor.

relevant to anin1als: 1) diffuse DPMs

A bilobed gallbladder is occasionally
associated with increased deposition of
identified in cats during ultrasonography
extracellular matrix ( congenital hepatic
or at surgery as an inconsequential
fibrosis) causing intrahepatic presinusoidal
abnormality.

portal hypertension, 2) Caroli malforma

Cystic mucosa! hyperplasia of the galltion causing sacculation of large intrahebladder is also known as cystic mucinous patic or interlobular bile duct (may be
hypertrophy, cystic mucinous hyperplasia,
associated with increased deposition of
and mucinous cholecystitis (although it is
extracellular matrix), 3) von Meyenburg
not an inflammatory lesion). The role of
complexes representing microscopic
steroid ho1111ones in lesion induction
isolated DPMs, 4) simple hepatic cysts,
remains w1clea.r but is suspected. There is

5) choledochal cysts representing an
no associated inflammation, and the serosal
appendix-like diverticulum from the
surface of the gallbladder remains intact.

extrahepatic bile duct that can act as an

These hyperplastic lesions are routinely
infection sun1p, and 6) biliary cystadenoidentified in dogs with gallbladder mucocele, mas that likely represent expanding cystic
in which "cystic" structures are filled with malformations involving large biliary ducts
tenacious viscoelastic mucin.

usually located adjacent to the gallbladder

Gallbladder dysmotility is proposed as
and cystic duct. Different malfonnations
an emerging syndrome in dogs and may
can predispose to cholangitis, lead to
precede GBM development. The syndrome
prehepatic portal hypertension, or evolve
may be linked to steroid honnones, based
into space-occupying cystic lesions. A
on early observations of an apparent link
single genetic mutation in cats (autosomal
between mucocele development and
onset dominant polycystic kidney disease)

treatment with progestational compounds.

can lead to biliary ductule malformations

Sex hom1ones (progestins, androgens) have
and hepatic fibrosis, which are commonly
been shown experimentally (in vitro) to
misidentified as advanced biliary cirrhosis
reduce contractility of gallbladder smooth
subsequent to the feline cholangitis/
muscle in experimental anin1al models.

cholangiohepatitis syndrome. Most cats
with this mutation demonstrate polycystic

OTHER DISORDERS OF THE
renal malfo1111ations rather than biliary

BILE DUCTS
malformations, although a small subset of
cats develop diffuse fibropolycystic liver
lesions. Multiple mutations have been

Benign Hepatic or Biliary Cysts: These identified to cause fibropolycystic single cysts are often linlited to one liver
malformations in people, and it is
lobe, usually cause no substantial compressuspected that a similar spectrum of gene sive injmy, and are occasionally discovered
mutations also may underlie similar
serendipitously during ultrasonographic
syndromes in dogs and cats. In some cats,
examinations for other disorders, at
many large hepatic cysts cause profound
surgery, or at necropsy. They do not expand
hepatomegaly, requiring repeated drainage,
to damage adjacent tissues, are not
fenestration, marsupialization, or surgical
associated with increased liver enzyme
resection. Uncommonly, cystic structures
activity, and are considered inconsequenmay become mineralized or complicated by tial. However, they may be problematic if
formation of mineralized choleliths.

they enlarge or interfere with bile flow at

Cats with diffuse DPMs have islands of
the porta hepatis.

normal hepatic parenchyn1a segregated
by bridging portal tracts that represent

Hepatic Fibropolycystic Disorders:

proliferative malformed bile ductules

Hepatic fibropolycystic disorders are
embedded in a complex of extracellular

478

HEPATIC DISEASE IN SMALL ANIMALS
matrix ( dense fibrillar collagen). Extensive
from 1 mm to 8 cm, with masses ranging
connective tissue causes intrahepatic portal
from 5 mm to 12.5 cm. Imaging studies
hypertension, a finn large liver, develop

(ultrasonography or CT) are key to
ment of APSSs, signs of HE, and ascites.

diagnosis.

Affected cats may present with increased

Although surgical excision is the
liver enzyme activity (ALT, AST, ALP) due to
treatment of choice, this may not be

VetBooks.ir
low-grade inflammation or development of
possible if the strncture integrates into the
septic cholangitis or cholelithiasis. Most are
porta hepatis. However, because these
not hyperbilirubinemic or jaundiced. Liver
lesions are often discovered serendipienzymes may be within the normal range, tously, surgical excision is commonly
with diagnostic biopsy initiated by
not indicated. Prognosis after complete
ultrasonographic findings.

cystadenoma excision is good; however,

Biliary dysplastic syndromes rarely ocif surgical intervention is necessary and cur in dogs concurrent with renal cystic
complete excision is not possible, partial
malfom1ations. However, DPMs are as
resection may delay complications from
commonly identified in dogs as in cats.

mechanical invasion of normal tissue.

Affected dogs may develop increased ALP

Repeated aspiration, catheter drainage,
activity and increased TSBA concentramarsupialization, and partial excision have tions. As in cats, extensive connective
been used for palliative management but
tissue deposition in the portal tract can
carry risk of infections. Neoplastic
cause portal-to-portal bridging fibrosi ,
transfom1ation is also possible. Cystadenointrahepatic presinusoidal portal hypertenmas are usually difficult to aspirate owing to sion, APSSs, HE, and ascites.

their complex internal structure.

The only treatment for DPM associated
with bridging portal fibrosis is to palliate HE

EXTRAHEPATIC BILE DUCT
with protein-modified diets and efforts to
alter the enteric microbial flora and pH

OBSTRUCTION

(lactulose, milk, or low-dose metronida

Obstruction of the common bile duct is
zole ). Diuretics and dietary sodiun1
associated with a nun1ber of diverse prin1ary
restriction are used to control ascites.

conditions, including inflammation ( eg,

Sin1ilar syndromes in people are managed
pancreatitis, duodenitis, duodenal foreign
by liver transplantation.

body, etc), cholelithiasis, gallbladder
mucocele, choledochitis/cholecystitis,

Choledochal Cyst: Congenital,
neoplasia, bile duct malformations, parasitic
appendix-like cystic dilation of the
infection, extrinsic compression, fibrosis,
extrahepatic bile duct is recognized
and bile duct stricture. Hepatomegaly
uncommonly in cats. Clinical signs intlude
and distention of intrahepatic bile ducts
fever, abdominal pain, and jaundice,
promptly follow EHBDO. lf obstruction
associated with cyst infection, with the
resolves within a few weeks, resolution of
amotile cyst functioning as an infected
fibrosis and bile duct distention can follow.

sun1p. Surgical exploration is usually

However, obstJ.Uction for >6 wk results in
required for definitive diagnosis. Extirpapersistent peribiliary fibrosis, connective tion of the cystic malformation or its
tissue b1idging between portal tracts,
marsupialization into the common bile duct
remodeling of tile liver consistent witl1
has been a successful treatment. Postoperabiliary cirrhosis, portal hypertension, and tive longtem1 antimicrobial therapy is
formation of APSSs.

guided by bile culture, cytology, and

Complete EHBDO inay result in
repeated ultrasonographic imaging.

development of white bile within the bile
duct or gallbladder, reflecting the absence

Biliary Cystadenoma: These lesions,
of bilirubin pigments in bile; ie, bile cannot
also tenned cystadenomas, bile-duct
enter tl1e distal "stagnant loop" of the ductal adenomas, cholangiocellular adenomas,
system or gallbladder ( cystic duct
cystic cholangiomas, and hepatobiliary
occlusion). Increased ductal mucin
cystadenomas, are benign lesions most
contributes to duct distention and the color
commonly encountered in older cats.

of lwninal contents. ln some cases, tl1e

Well-demarcated, single lesions often have a biliary tree becomes colonized by bacteria, complex internal structure and may invade
which are not cleared because of failed
or compress adjacent hepatic pa.renchyma,
mechanical expulsion of bile and inadcausing compressive atrophy. Cyst contents equate antibiotic penetration into bile.

range from clear, watery fluid to viscous or
solid material; typically there are no bile

Clinical Findings and Diagnosis: Acute
acids or bilirubin. Cyst sizes vary, ranging
complete EHBDO leads to lethargy, cyclic

HEPATIC DISEASE IN SMALL ANIMALS

479
fever, and prompt development of jaundice;
duct palpation is essential to identify
total bilirubin concentration increases
intran1ural mass lesions. A grossly
within 4 hr. Vomiting may be episodic. Some
distended, tortuous common bile duct
animals are intermittently inappetent,
makes the diagnosis apparent. Gentle
whereas others become polyphagic,
gallbladder compression is used to verify
reflecting fat maldigestion due to the lack
obstrnction and tl1e site of restricted bile

VetBooks.ir
of enteric bile acids and consequent fat
flow. The most difficult obstructions to
malabsorption. Hepatomegaly, acholic
confinn and resolve involve hepatic ducts.

feces, and the absence of urine urobilinogen A duodenotomy, cholecystotomy, or (inconsistent) usually develop within the
choledochotomy may be necessary for
first week. Bleeding tendencies may be
passage of a flexible catheter into the
notable within 2---3 wk and are more
common bile duct to ve1ify the site of
common in cats and develop earlier. GI
obstrnction and to allow removal of
ulceration at the pyloric-duodenaljw1ction
inspissated biliary sludge or choleliths.

is common and can lead to considerable

Successful treatment of biliary tract sepsis
blood loss. Even with miniscule enteric
requires mechanical removal of biliary
bleeding, bilirubin pigments gain access to
debris and infectious material and a
the bowel, allowing feces to become brown
decompressive maneuver often involving

(stercobilin fom1ation) and urine to test
a surgical correction. Animals with biliary
positive for urobilinogen, negating the
tree infections tend to become hypotensive
reliability of finding acholic feces and
and a.re susceptible to endotoxic shock
negative wine urobilinogen for EHBDO
during surgery and anesthesia, especially
diagnosis.

cats. Liver biopsy by percutaneous needle

The hemogram may reveal a nonregenor Japa.roscopic methods does not allow erative anemia with chronic obstruction or
safe biliary decompression and may
a strongly regenerative anemia in animals
lacerate distended bile ducts, leading to bile
with substantive enteric bleeding. A
peritonitis; tlms, lapa.rotomy is the optimal
neutrophilic leukocytosis with or without a
manage1ial and assessment approach.

left shift is common. As bile stagnates in the

Controversy exists regarding tl1e need for
biliary tree, serun1 ALT and AST activities
biliary tree decompression in anin1als with
increase. Serun1 ALP and GGT activities

EHBDO secondary to pancreatitis. ln most
increase within 8--12 hr of obstruction and
dogs, obstruction resolves spontaneously
are substantial within a few days. Parenchyover several weeks as the inflan1mation mal necrosis, periductal inflammation, and
resolves. In animals with obstruction
cholestasis sustain serwn transaminase and
persisting beyond 2-3 wk, temporary
cholestatic enzyme activity. In cats, tl1e

(stenting of the bile duct at the sphincter of
magnitude of ALP and GGT a.re Jess

Oddi) or permanent decompression of the
dramatic than in dogs but nevertheless a.re
biliary tree is usually considered. The risk
useful indicators of biliary tree obstruction,
of mortality in dogs with pancreatitis
irtjury, and inflammation. Hypercholesterundergoing extra11epatic biliary surgery olemia develops within 10--14 days of
may be as high as 50%. T:ranshepatic
complete obstruction, reflecting impaired
ultrasound-guided aspiration of the
cholesterol elimination and possibly
gallbladder as a decompressive approach
increased hepatic cholesterol biosynthesis.

has been successfully completed in some

Witl1 chronic obstrnction and development
affected a.nin1als but has high risk of focal
of biliary cirrhosis, serwn cholesterol
or more generalized bile pe1itonitis.

declines, reflecting in1paired cholesterol
synthesis and APSSs. Coagulopathies

CHOLELITHIASIS
associated with vitan1in K deficiency may
develop within 2---3 wk in dogs and earlier

Most choleliths in dogs and cats a.re

(within 1 wk) in cats. Response to vitamin
clinically silent. Diagnosis of this disorder

K, administration is usually dramatic.

has increased subsequent to routine use

EHBDO is confirmed with ultrasonographic
of abdominal ultrasound as a diagnostic
imaging and exploratory lapa.rotomy.

modality. Cholelitl1s are more conunon in
middle-aged to older anin1als, and incidence
may be higher in small-breed dogs. Most

Treatment: Surgical inspection of the
choleliths in dogs and cats contain calcium
liver and biliary strnctures and appropriate
carbonate and calciun1-bilirnbinate
biliary decompression a.re requisites for
pigments and are considered "pigment
optimal therapy. Gross inspection of the
stones." However, many stones do not
gallbladder and common bile duct usually
contain enough mineral for detection on
reveals the site and cause of obstruction;
survey radiographs. Pigment gallstones a.re

480

HEPATIC DISEASE IN SMALL ANIMALS
divided into two categories: "black-pigment"

inm1unomodulatory therapy is appropriate.

stones composed primarily of bilirubin

Vitamin E at 10 U/kg/day can be used for its
polymers, reflecting prolonged hyperbilimantioxidant and anti-inflammatory effects.

binemia, and "brown-pigment" stones

Surgical intervention is necessary if
composed predominantly of calcium
choleliths are associated with cholecystitis,
bilimbinate, which are associated with
are causing cystic duct obstruction, or are

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bacterial infections and biliary stasis. Mucin
occluding the common bile duct. Successful
production, enhanced by local inflammation
treatment of cholecystitis and cystic duct
and prostaglandins, entangles calcium bilimocclusion requires cholecystectomy and binate and bilimbin polymers into cholelith
lavage of the common bile duct. The causal
aggregates. TI1i.s process is augmented by
factors of cholelith formation must be
gallbladder dysmotility and bile stasis.

carefully considered; retaining a diseased
or dysmotile gallbladder imposes risk of

Clinical Findings and Diagnosis: Cholerecurrent lithiasis or necrotizing cholecystilithiasis may be associated with vomiting, tis. In cases in which obstruction of the
anorexia,jaundice, fever, and abdominal
common bile duct is irresolvable, a
pain. However, many animals remain
cholecystoenterostomy is necessary,
asymptomatic or display postprandial
followed by longterm monito1ing for septic
discomfort ( eg, stretching, position of relief, cholangitis. Chronic pulsatile antimicrobial changing postures, wandering, pacing).

administration may be needed to control

Laboratory features of cholelitlli.asis most
retrograde infections of the biliary tree
commonly reflect related chole ystitis or
thereafter. Biopsy of involved biliary
choledochitis, or cholangitis (intral1epatic
structures and liver is essential to determine
choleliths or hepatolithiasis). In anin1als
whether an underlying primary inflan1mawith small duct lithiasis, clinicopathologic to1y, septic, or neoplastic disease is present
features reflect involvement of biliary
and predisposing to cholelith fonnation.

structures (high ALP and GGT activities).

Tissue (liver, bile duct, gallbladder), bile,

Jaundice is only directly related to
and cholelith 11i.dus should be submitted for
cholelithiasis associated witl1 EHBDO or
aerobic and anaerobic bacterial cultures.

sepsis; thus, many animals with cholelitlli.

Cholecystoduodenostomy and cholecysasis are not hyperbilimbinemic. Cholelithitojejunostomy are the most common asis may develop secondary to infection, or
surgical procedures for biliary bypass in
stones may promote infection secondary
small animals. Cystoenteric anastomosis
to amechanical trauma derived from
to the proximal duodenum is most physiocholeliths. Animals with DPMs, especially logic, because it allows bile to enter the

Caroli malfom1ation (sacculation of large
duodenun1 in a position that closely
intrai1epatic bile ducts) are predisposed to
maintains nonnal physiologic responses in
intral1epatic cholelithiasis and infection.

the proximal bowel to allow coordinated

High vigilance for signs of sepsis is
mixing of bile acids and pancreatic enzymes
warranted in any animal with cholelitl1i.asis.

necessary for digestion and assinulation.

The hemogram may be normal or reflect
inflammation or infection. A serwn

BILIARY TREE RUPTURE AND BILE
biochenucal profile Riay be normal or reveal
high cholestatic enzyme activity or evidence PERITONITIS
of obstructive jaundice. Ultrasonography

Rupture of the common bile duct, cystic
can detect stones >2 mm in dian1eter in the
duct, hepatic ducts, or gallbladder is most
gallbladder; however, both skill and luck are often associated with cholelithiasis, needed to recognize stones lodged in
necrotizing choledochitis or cholecystitis,
segments of the common bile duct or in the
blunt abdominal trauma, or neoplasia In
hepatic bile ducts. For animals with small
dogs, necrotizing cholecystitis most often
duct cholelithiasis, biopsy and culture of
occurs as a result of a mature gallbladder
liver tissue is necessary to identify
mucocele that stretches the gallbladder
underlying disease processes and associwall to the extent of causing ischemic ated bacterial infections.

necrosis. Regardless of cause, rupture of
any portion of the biliary tree can lead to bile

Treatment: Medical treatment of
peritonitis. Clinical signs may be minimal
cholelitl1i.asis includes broad-spectrum
early in the disease process, consisting
antibiotics and a choleretic regimen of
only of inappetence and vague abdominal
ursodeoxycholic acid at 15---25 mg/kg, PO,
discomfort. Witl1 chronicity, free bile
divided bid and given with food, and SAMe
initiates an i.nflan1111ato1y reaction ( chemical
at 20---40 mg/kg/day, PO, on an empty
peritonitis), an abdominal effusion
stomach. Liver biopsy dete1mines whetl1er
accumulates, and vivid jaundice develops.

HEPATIC DISEASE IN SMALL ANIMALS

· 481

U1trasonography should guide collection of

CCHS coexists with inflanunatory
abdominal effusion as close to the biliary
processes in the duodenwn, pancreas, and
tree as possible, because this will increase
kidneys ( chronic interstitial nephritis).

detection of free and phagocytized bilirubin

Nwnerous concwTent conditions have been
crystals and bacterial organisms. Abdominal identified in cats with CCHS, whether the adhesions develop with delay in diagnosis
inflan1matory infiltrate is predominantly
and complicate surgical remediation.

neutroph.ilic (suppurative), Jymphocytic or

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Surgical inte1ventions a.re specific to the
lyrnphoplasmacytic (nonsuppurative), or
causal lesions and may involve biliary tree
whether it actively involves bile duct
decompression, cholecystectomy, cholecysdestruction. Disorders associated with totomy, choledochotomy, biliary-enteric
feline CCHS include bacterial infections
anastomosis, or bile duct stent insertion. A

(primary or chronic), septicemia, cholecysliver biopsy should be collected to identify titis, cholelithiasis, EHBDO, trematode
antecedent or coexistent hepatobiliary
infestation, toxoplasmosis, inflammatory
disease. Portions of the ruptured sb:ucture,
bowel disease, primary cholangitis,
bile, and abdominal effusion should be
pancreatitis, neoplasia ( eg, pancreatic or
san1pled and cultured for aerobic and anaerogallbladder or bile duct aclenocarcinoma), bic bacte1ia. Affected tissue and acljacent and bilia.ty cystadenoma, and va.tfous ductal nonacljacent liver tissue should be biopsied.

malfonnations ( eg, choledochal cyst,

The abdominal cavity must be thoroughly
diffuse ductal plate malfonnation [ congenilavaged with sterile wam1 saline to remove tal hepatic fibrosis associated with
bile conta.nlination. Antibiotic coverage
polycystic liver malformation], Caroli
against likely enteric opp01tunists (grammalfonnation).

negative bacteria) and anaerobic flora is

Liver lobe involvement in feline CCHS
reconm1ended, eg, tica.rcillin, piperacillin,
is variable, and the extent a.i1d severity
third-generation cephalosporins, or
of histologic lesions may not be fully
enrofloxacin combined with metronicla.zole.

ascertained on a single liver biopsy or with

Antimicrobial therapy should begin before
small tru-cut biopsies (eg, 18 gauge). Some
surgery and, if sepsis is confirrnecl, continued
biopsy sections may show modest or
for 4-8 wk Antimicrobial selection should be
moderate periductal infla.tnmation and
guided initially by results of cytology and
hepatitis, whereas other liver lobes reveal

Gram staining, and acljusted based on results
complete elimination of bile ducts and lack
of culture and sensitivity. Aninlals with
active inftanm1ation owing to loss of bile
chronic jaundice should receive vita.min K,
duct epitopes that may drive the inflamma

(0.5---1.5 mg,'kg, IM or SC, bid for up to three
tion. Cats with disease in multiple organ
doses) before surgical intervention. Fresh
systems have significantly shorter survival
frozen plasma may be necessary to abate
times if untreated. However, because CCHS
bleeding tendencies during emergency
is slowly progressive, cats can survive
surgery. Antiemetics a.re recommended if the
several yea.rs beyond initial diagnosis
animal is vomiting; Hrreceptor antagonists
without therapeutic interventions.

a.re used if ente1ic bleeding is identified,

Suppurative CCHS causes the most
because these act qu.icl<ly. In a.ninlals with
overt clinical illness. These cats have a
cholelith.iasis and in clogs with gallbladder
shorter duration of illness before presentamucocele, hydrocholeresis (ursodeoxychol.ic tion ( <5 days), with yo=g or middle-aged acid and SAMe) and antioxidants ( vitamin E
adults predominating (ra.i1ge 3 mo to 16 YT).

and SAMe) are recommended postopera

Clinical signs include PYTexia, letha.i·gy,
tively.

dehydration, inappetence, vomiting, and
variable jaundice. Many cats manifest
abdominal pa.in, and some have palpable

FELINE CHOLANGITIS/
hepatomegaly. Clin.icopathologic features

CHOLANGIOHEPATITIS
are simiJa.i· to those of otl1er fom1s of CCHS,

SYNDROME
with moderate to marked increases in
tra.t1Sa.tninases (ALT, AST) and more modest

Feline cholangitis/cholangiohepatitis
increases in ALP and GGT activities.

syndrome (CCHS) is the most common

Surprisingly, some cats lack cholestatic
acquired inflanm1atory liver disease in
enzyme abn01mal.ities. Most cats a.i·e
domestic cats. Both cholangitis and
hyperbilirubinemic, some have concwTent
cholangiohepatitis are more common in
renal a.zotemia, and ma.i1y demonstrate a
cats than dogs. The anatomic difference
left shift and toxic neutrophils on their
between the biliary and pancreatic ducts
leukogran1. Concurrent HL may confuse
in cats compared with dogs has long been
initial assessments. Abdominal ultrasonogconsidered an underlying risk factor. Feline raphy may reveal EHBDO; abnormalities

482

HEPATIC DISEASE IN SMALL ANIMALS
consistent with cholecystitis, choledochitis,
structures, pancreas, or gut, or development
pancreatitis, or inflammatory bowel
of lymphadenopathy. Repeat aspiration
disease; diffuse hepatic parenchymal
cytology or liver biopsy may be necessary.

hyperechogenicity consistent with HL;

Feline lymphocytic portal hepatitis
coarse parenchymal echogenicity; or no
is a diagnosis demonstrating inflan1n1atory
abnormalities. A coarse or heterogeneous
infiltrates without tropism for bile ducts but
hepatic parenchymal pattern sometimes
showing single ceU hepatocyte necrosis.

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recognized may reflect parenchymal

It is presmned that many of these cats are
inflammation and/or periductule or portal
responding to antigens or debris from the
tract fibrosis and inflammation. Thoracic
alimentary canal or reflect inflan1matory
radiography often reveals a large sternal
ceUs delivered in the portal circulation.

lymph node reflecting abdominal inflamma

Otherwise, this diagnosis may represent
tion/sepsis.

mild lesions in cats with CCHS when only

Medical treatment is usually provided
a few portal triads are sampled from a
before surgical intervention (biliary
relatively LUlinvolved liver lobe. Low-yield
decompression surgery for EHBDO,
needle biopsies from cats with nonsuppuracholecystectomy for cholecystitis, cholecystive CCHS may generate this diagnosis. In totomy for cholelithiasis) and liver biopsy.

some cats, however, an inflammatory portal

Disorders causing stasis of bile flow must
tract infiltrate is associated with single cell
be rectified, because they increase risk of
hepatocyte necrosis, qualifying as a true
opportunistic infection involving the biliary
portal hepatitis.

system. Aspiration or biopsy imprint

Nonsuppurative CCHS without
cytology of liver and bile usually reveal
destructive cholangitis is usually a T-cell
bacterial organisms and suppurative
or mixed T -cell with B-ceU mediated
inflammation. Gram-stain characterization
inflammatory syndrome affecting middleof bacteria on cytologic specimens assists in aged or older cats. ConcmTent infection selection of antimicrobial agents and may
with feline leukemia vims or feline
provide the only confu-mation of bacterial
imm tu1odeficiency virus is uncommon, and
infection. Cultures may be negative because
there is no gender or breed predisposition.

of prior antibiotic administration or failure

Duration of illness ranges from 2 wk to
to culture for anaerobic bacte1ia. Comseveral years, with most cats demonstrating monly isolated bacteria include Escheri
signs of illness for several months before
chia coli, Streptococcus, Clostridium,
initial presentation. Clinical signs include

Bacteroides, andActinomyces.

intermittent vomiting and dian-hea and

Treatment involves broad-spectrum
episodic illness characterized by anorexia
antimicrobials effective against anaerobic
or hyporexia, reclusiveness, or self-resolvand gram-negative enteric opportunists, ing jaundice. Hepatomegaly is common. It
ursodeoxycholic acid, SAMe, vitamin E,
is uncommon for nonsuppurative CCHS to
water-soluble vitan1ins, enteral alimentation cause portal hypertension, APSSs, and with a maximum-calorie diet formulated for
abdominal effusion, because cats usually
cats, and judicious administration of fluids
succm11b to the effects of this syndrome
and electrolyte supplements to con-ect and
before diffuse fibrosis evolves. Rather,
maintain hydration and electrolyte status.

cats with these features more likely have

Antioxidants are provided dul'ing critical
fibropolycystic biliary malfom1ations
illness by administration ofN-acetylcysteine (seep 477).

(140 mg/kg initial dose [10%solution in

The hemogran1 is variable, commonly

NaCl], 70 mg/kg thereafter, bid-tid, infused
demonstrating poikilocytosis and Heinz

IV over 20 min through a 0.25-µm filter);
bodies. The leukogram is va.iiable but
when oral administration is possible, SAMe
typically does not display a left shift or toxic
is given by mouth. A combination of
neutrophils. Hyperglobulinemia develops
enrofloxacin, metronidazole, and ampicilwith chronicity; most cats have moderate to linlsulbactam is often initially administered
marked increases in ALT and AST activities
and acljusted based on culture and
with widely variable ALP and GGT activities
sensitivity reports from hepatobiliary or bile depending on cyclic activity of the disease aspirates or tissue san1ples. Antin1icrobial
process. Hyperbilimbinemia is inconsistent
treatment should begin before surgical
and also appears cyclic. Some cats are
intervention (because sepsis compromises
persistently jaundiced secondary to
postoperative survival) and continue for
inflan1n1atory obstruction or destruction

8-12 wk or until liver enzymes nonnalize.

of small and mediun1-sized bile ducts

If liver enzymes remain increased, repeat

(nonsuppurative CCHS with destructive
ultrasonographic assessment is warranted
cholangitis); these often develop symptoto check for abnormalities involving biliary matic coagulopathies responsive to vitamin

HEPATIC DISEASE IN SMALL ANIMALS

483

K administration. Abdominal ultrasonohistologic features that include graphic findings overlap with those of
the following: 1) infiltration of bile ductules
suppurative CCHS; a nonuniforn1 or coarse
with lymphocytes, 2) peripheralization of
parenchymal pattern may be identified.

bile ductules to the margin of portal tracts,

However, cats with marked nonsuppurative

3) evidence of involuting bile ducts,

CCHS may lack ultrasonographic hepatic or

4) lipogranulomas (when ducts have been
biliary abnormalities. Severity of histologic
eliminated), 5) scant lymphoid nodules

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lesions is highly variable within and

(B cells) consistent with an inflammation,
between liver lobes and between cats.

and 6) periductular sclerosing fibrosis

Initial treatment consists of appropriate
without other features suggesting EHBDO.

antin1icrobials (see above), SAMe, vitamin

In some cases, confirmation of bile duct

E, supplementation of B vitamins, enteral
involution and peripheralization to the edge
alin1entation with a maximum-calorie diet
of portal tracts requires immunohistochemformulated for cats, and fluids and istry using a cytokeratin antibody. Marked
electrolyte supplements to correct and
differences between liver lobes in status of
maintain hydration and electrolyte
portal tract inflanlmation may be seen; in
abnonnalities. Broad-spectrum antimicrolobes with elin1ination of biliary ductules, bial coverage ( against anaerobic and
infl=ation can be mild or inapparent.

gran1-negative enteric opportunists) is

Approxin1ately 300,6 of cats with destructive
recommended pending liver biopsy and
cholangitis treated with glucocmticoids
culture results. Longtern1 treatment
develop diabetes mellitus. Involvement
requires in1munomodulation. Ursodeoxyof pancreatic ducts with the T-cell ductal cholic acid is used in cats lacking evidence
targeting inflan1mation may influence this
of destrnctive cholangitis. However,
outcome.

ursodeoxycholic acid is no longer

Symptomatic ductopenic cats require
recommended for cats with destructive
once or twice weekly vitamin K1 iajections
cholangitis based on evidence (experimen

(see JJ 439) and water-soluble vitamin E
tal aninlal models, people with sclerosing

(polyethylene glycol a-tocopherol
cholangitis) that it may provoke small duct
succinate, IOU/kg/day, PO). Overdosing
iajury in destructive cholangiopathies.

vitamin K1 can cause serious hemolytic

First-line inlillunosuppressive therapy is
anemia, and overdosing vitamin E can lead
prednisolone, initially administered at 2-4
to insufficient vitanlin K activity. Affected
mg/kg ideal body weight, PO, daily, with the
cats should be investigated for severe
dose titrated to 5--10 mg/day, administered
inf!anlillatory bowel disease and B12
daily to every other day. Glucocorticoid
adequacy. Hematology and serum
dosing is titrated based on clinical assessbiochemistry features are similar to those ments. Metronidazole (7.5 mg/kg, PO, bid)

of cats with non-duct destructive CCHS.

is also recommended to assist with inlillulnlmunomodulation with prednisolone nomodulation and control of associated
does little to moderate enzyme activity or
inflammatory bowel disease; adding this
hyperbilirubinemia in destructive CCHS
drug may allow reduction of the glucocorwhen used as mono therapy immunosupticoid dose. Continued administration of pression. Instead, methotrexate or

SAMe ( 40-50 mg/kg/day, PO) and vitamin
chlorambucil are used initially with

E (10 U/kg/day) is recommended.

glucocorticoids. Pulsatile methotrexate

As a single agent, SAMe has reduced
is given at a total daily dose of 0.4 mg/cat
nonsuppurative CCHS-associated inflan1madivided into three treatments given on a tion in a few studied cats. Chlorambucil
single day (0.13 mg per dose, PO) once

(2 mg/cat/day, titrated to every other or every every 7-10 days. Alternatively, methotrexthird day) is used in cats that do not respond ate may be given IV or IM with a 500,6 dose
to anti-inflammatory glucocorticoid and
reduction. Folic acid, 0.25 mg/day, PO, is
metronidazole therapy. Treatment usually
concurrently administered to prevent
returns bilirubin concentrations to normal,
methotrexate-associated hepatotoxicity,
but cyclic increases in enzyme activity

GI toxicity, or hematopoietic effects. The
remain although at lower magnitudes.

dosage of methotrexate must be reduced

Cats with nonsuppurative CCHS with
in cats with renal azotemia. Methotrexate
destructive cholangitis (sclerosing
imposes profound immunosuppression at
cholangitis) can eventually develop
the recommended dosage, and careful
widespread small duct destruction causmonitoring for complicating infections is ing permanent hyperbilirubinemia and
essential. Alternatively, treatment with
intermittent acholic feces due to a histochlorambucil, as described above, can be logic progressive "ductopenia." This subset used instead of methotrexate. Concurrent
of CCHS is confirmed by finding defining
treatment with SAMe is recommended,

484

HEPATIC DISEASE IN SMALL ANIMALS
along with low-dose prednisolone and

-15%--85% of cats with access to intermedimetronidazole. Treatment for concurrent ate hosts a.re infected in endent.ic areas.

inflammatory bowel disease with a

After infection, young 11ukes emerge in the
hypoallergenic diet also may be beneficial.

intestines and migrate into the common bile

Cobalamin deficiency must be corrected,
duct, gallbladder, or hepatic ducts, where
with cats ctu-ort.ically supplemented if
they mature within 8-12 wk. Embryonated

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deficiency is proved through laboratory
eggs thereafter pass from bile into the
testing. Low cobalamin concentrations
alimentary canal, where they may be
should raise concern for severe small-bowel
detected in feces a5 early as 12 wk after
malabsorption ( especially small-cell
infection (sedimentation, Baem1ann test).

lymphoma) or severe pancreatic disease.

Clinical signs depend on severity of

In lymphoproliferative disease
infection (parasite burden); however,
masquerading as lymphocytic CCHS,
most infested cats remain asyn1ptomatic.

lesions are characterized by dense portal

Symptomatic cats demonstrate progreslymphocyte infiltrates that penetrate sive illness characterized by progressive
hepatic sinusoids. However, involved
lethargy, fever, hepatomegaly, and
lymphocytes lack convincing morphology
abdominal distention. These cats may
for classification as a neoplastic population;
become jaundiced and emaciated secondthis syndrome may represent a transition ary to anorexia, vomiting, and mucoid
phase between conventional inflammatory
dia.nhea. Chronic fluke infestation can be
disease and overt neoplasia. Treatment with fatal in severely affected cats. First clinical chlorambucil has proved beneficial in some
signs develop between 7 and 16 wk of
cats (2 mg/cat, given every other or every
infection. In some cases, clinical signs
third day), combined with treatments
resolve by 24 wk after infection without
previously described for CCHS. Affected
treatment. A circulating eosinophilia may
cats may smvive for several years with
develop3-14 wk after infection and may
minimal clinical signs. Immunohistochemipersist. In heavily infected cats, ALT and cal staining and other molecular tests

AST activities may increase, while ALP

(investigation of clonality) may help
activity may remain normal or only increase
differentiate this syndrome from lymphoma. mildly. Hyperbili.rubinemia may develop In small-cell lymphoma masquerading
within 7 -16 wk after infection.

as lymphocytic CCHS, dense lymphocytic

Hepatic histologic lesions develop after
pmial infiltrates penetrate hepatic

3 wk and are progressive in persistent
sinusoids. However, this population of cells
infections. Inflammation and distention of
has morphology consistent with a diagnosis
large bile ducts is associated with mixed
of small-cell lymphoma. Treatment with
neutrophilic and eosinophilic inflanlnla.tory
chemotherapy protocols for feline
infiltrates. By 4 mo, severe adenomatous
lymphoma is recommended, along with
biliary hyperplasia and peribiliary
judicious administration of nutritional,
inflammation are well established. By 6 mo,
vitan1in, and antioxidant support. Many of
progressive fibrosis is obvious and evolves
these cats respond to chlorambucil, as
into biliary cirrhosis. Regional lyn1phaddescribed above, for several years. Affected enopathy may be notable. Bile duct
cats may have concwTent intestinal
distention increases with growth of adult
involvement, although some cats with overt
flukes, and when flukes become sexually
hepatic lymphosarcoma have inflanmiatory
mature, bile ducts become fibrotic. During
bowel disease, and some cats with ove1t
this time, serwn transaminase activities
enteric lymphosarcoma have non-neoplasdecline and may normalize. Abdominal tic nonsuppurative CCHS. Evolution of
ultrasonography may reveal apparent
chronic inflammation to a neoplastic
biliary obstruction involving the gallbladder,
process is suspected in each organ system.

common bile duct, and/or intrallepatic
ducts. Gallbladder debris associated with

HEPATOBILIARY FLUKE
flukes may appear as oval hypoechoic

INFECTION
structures having echoic centers. A
thickened gallbladder wall associated with

Infection with liver flukes in endemic
a double-rim sign may reflect cholecystitis.

regions can ca.use acute and chronic

Hypoechoic hepatic parenchyn1a with
cholangitis in ca.ts and less frequently in
prominent hyperechoic portal regions
dogs. The most common fluke infecting cats (ducts) reflects cholangitis and cholangio
isPlatynosomum concinnum in Florida,
hepatitis.

Hawaii, and other tropical areas. Infestation

Canine infection withHeterobilharzia
is acquired by ingesting an infected
americana, a schistisomal fluke, has also
intennediate host, usually a lizard or frog;
been characterized in dogs from Texas,

HEPATIC DISEASE IN SMALL ANIMALS

485

North Carolina, Louisiana, and Florida.

routinely used fecal methods are relatively

Infection is acquired through skin
insensitive for fluke egg detection. In
penetration by cercariae released from
addition, development of bile duct
snails. These forms migrate through the
obstruction and fibrosis may impede
host as schistosomula, reaching the lungs
passage of fluke eggs into bile and feces.

within 5-9 days and liver within 7-45 days.

Suspected fluke infestation is treated with

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Schistosomes grow and mature in liver, with
praziquantel (based on dosing extrapolated
adults migrating to mesenteric veins, where
from experimentally infected anin1als and
they release eggs and also proteolytic
proved to control schistosome infection in
enzymes upon migration to the bowel
dogs). Praziquantel at 20-25 mg,'kg body wt,
lumen. Eggs provoke a granulomatous
tid for 3 days, has been effective in some but
reaction. Healing of the host leads to scar
not all treated anin1als. Eggs may continue
fonnation and organ ir\jury that can result
to be passed in feces for up to 2 mo after
in liver failure and GI malabsorption.

successful treatment in cats, and reinfection

Clinical signs of illness in dogs with
may complicate assessment of treatment
schistosomiasis may manifest as early as a
response. Some infected dogs have been
few days to months after infection. Young
treated with fenbendazole (50 mg,'kg body
adult dogs are more commonly affected.

wt/day, PO, for 10 days) with or without

Common clinical features (in descending
concun·ent praziquantel administration.

order) include lethargy, weight loss,

Prednisolone is used to reduce fluke-associvomiting, diarrhea, inappetence, hypercalated inflanunation (2 mg,'kg/day for 2-4 wk, cemia, PU/PD, and more rarely, melena. The
tapered in 50% decrements every 2 wk).

most conunon hematologic findings are

UrsodeoXYcholic acid is recommended for
lymphopenia and mild to marked thrombobile duct-associated lesions given at 15-20
cytopenia, with eosinophilia being
mg,'kg, PO, divided bid and administered
uncommon. Schistocytes have been seen in
with food to initiate hydrocholeresis.

some dogs, reflecting intravascular shearing

Broad-spectrw11 antibiotic coverage is
ir\jury of RBCs. Common serum biochemireconunended to protect against secondary cal features include modest azotemia (BUN
bacterial infections associated with
and creatinine), hyperglobulinemia, total
migrating or dying flukes. Vitamin E ( l O ill/
and ionized hypercalcemia, and hyperglobukg/day, PO) and SAMe (20-40 mg,'kg/day, linemia. Liver enzyme activity is variable.

PO) are given W1til liver enzymes normalize.

Hypercalcemia is thought to reflect

If necessary, an anti.emetic can be adminisgranulomatous inflanunation. Acquired tered, eg, metocloprarnide (0.2-0.5 mg,'kg,
inununodeficiency (neoplasia, drug

PO or SC, every 6-8 hr) or maropitant (1 mg/
therapy) may increase susceptibility to
kg/day for no more than 5 consecutive days).

infection.

Treatment results ar·e variable, but

Because fluke-infected cats may remain
prognosis is favorable in mild fluke
asymptomatic, diagnosis can be difficult.

infestation. Other rare parasites of the

Eggs may not be detected on fecal examinabiliary tract include Amphimerus tion, because they are only sporadically
pseudofelineus, Metorchis conjunclus, and
passed and demonstrate variable morphol

Eurytrema procyonis. (See also HEPATIC
ogy (inunature and embryonated forms).

FLUKES, p 427.) Similar assessment and

Furthermore, fluke eggs are small, and
treatment strategies are warranted.

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EYE AND EAR

THE EYE

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OPHTHALMOLOGY 488

Physical Examination of the Eye 488

Eyelids 488

Conformational Abnonnalities 488

Inflammation 490

Nasolacrimal and Lacrimal Apparatus 490

Conjunctiva 492

Cornea 493

Anterior Uvea 495

Glaucoma 497

Lens 499

Ocular Fundus 501

Inherited Retinopathies 502

Chorioretinitis 503

Retinal Detachments 503

Optic Nerve 504

Orbit 504

Prolapse of the Eye 504

Ophthalmic Manifestations of Systemic Diseases 505

CHLAMYDIAL CONJUNCTIVITIS 506

EQUINE RECURRENT UVEITIS 508

EYEWORM DISEASE 510

Large Animals 510

Small Animals 512

INFECTIOUS KERATOCONJUNCTIVITIS 512

NEOPLASIA OF THE EYE AND ASSOCIATED STRUCTURES 515

Cattle 515

Horses 516

Dogs 516

Cats 518

OPHTHALMIC EMERGENCIES 1696 (EMG)

THE EAR

DEAFNESS 518

DISEASES OF THE PINNA 520

Arthropod Bite Pinnal Dermatitis 520

Insect Bite Dermatitis 521

Mite Infestations 521

Allergy 522

Aural Contact Dermatitis 522

488

EYE AND EAR

Pinnal Alopecia 522

Ear Margin Seborrhea 523

Sebaceous Adenitis 523

Auricular Hematomas 524

Equine Aural Plaques 524

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Necrotic Ear Syndrome in Swine 524

Miscellaneous Diseases 525

OTITIS EXTERNA 527

OTITIS MEDIA AND INTERNA 531

TUMORS OF THE EAR CANAL 534

Ceruminous Gland Tumors 535

Nasopharyngeal Polyps 535

OPHTHALMOLOGY

PHYSICAL EXAMINATION OF
nasolacrimal system usually do. To avoid

THE EYE
false-positives, samples for corneal and
conjunctiva! cytology that will be analyzed

The initial examination of the eye should
by fluorescent antibody procedures should
assess symmetry, confonnation, and gross
be collected before topical fluorescein
lesions; the eye should be viewed from
staining.

2-3 ft (-1 m) away, in good light, and with

Special examinations such as slit-lamp
minin1al restraint of the head. The anterior
biomicroscopy, ultrasonography, fluoresocular segment and pupillary light reflexes. cein angiography, and electroretinography are exan1ined in detail with a strong light
may require sedation or local, regional, or
and under magnification in a darkened
general anesthesia, depending on the
room. Baseline tests like the Schirmer tear
species.

test, fluorescein staining, and tonometry

(intraocular pressure measurement) may
be followed by ancillary tests such as

EYELIDS
taking corneal and conjunctiva.I cytology
and cultures, everting the eyelids for

The eyelids consist of four parts: 1) the outer
examination, and flushing the nasolacrimal very thin and mobile skin; 2) the strong and system to evaluate the external parts of
encircling orbicularis oculi muscle anchored
the eye, including the anterior segment.

at the medial canthus; 3) the thin and poorly

Diseases of the vitreous and ocular ftmdus
developed fibrous tarsus, which contains
are evaluated by direct and indirect
the sebaceous Meibomian glands and
ophthal.rnoscopy (usually performed after
attaches the lid to the bony orbital rim; and
inducing mydriasis) and vision testing

4) the thin and flexible palpebral conjunc

(menace reflex, obstacle course, dazzle
tiva, which continues to the conjunctival
reflex, etc).

fomix or conjunctival cul-de-sac. Eyelid

Schirmer tear tests and cultures should
disorders may be associated with facial and
be perforn1ed before topical anesthetic is
orbital abnonnalities, specific breeds, and
instilled. Fluorescein staining and eversion
adjunct skin diseases, as well as with many
of the eyelids do not require topical
systemic diseases.

anesthesia, but tonometry, examination
of the bulbar surface of the nictitating

Conformational Abnormalities
membrane, conjunctiva! and corneal

Entropion is an inversion of all or part of
cytology, gonioscopy, and lavage of the
the lid margins that may involve one or both

OPHTHALMOLOGY

489
levator palpebrae
lacrimal gland
superioris m
upper fomb<

\

I
ciliruy body
upper (superior

_r'y
ora serrata
eyelid

�

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"/,

.,
co1tjunctival sac

?

.�

:

""'-
tarsal gland

'•

�_. �

•
eyelashes (cilia)

(r, • f,:, '.�f

_ }l
iris 1.t�

1
anterior chamber� \

":. ••

,,
x
lower (inferior) \

\
eyelid
accesso,y lacrimal

---(' / ' ,
glru1d

;

/
third eyelid
posterior chamber
deep accesso1y
lacrimal gland

The eye and eyelids, median section. Illustration by Dr. Gheorghe Constantinescu.

eyelids and the canthi. It is the most
environmental initants and secondary
frequent inherited eyelid defect in many
bacterial infection can result in clu·onic or
canine and ovine breeds and may also
recurrent conjunctivitis. Topical antibioticfollow cicatrix formation and severe blephacorticosteroid preparations may temporarrospasm due to ocular or periocular pain.

ily control intermittent infections, but

Inversion of the cilia ( or eyelashes) or facial
surgical lid-shortening procedures are often
hairs causes further discomfort, conjunctiindicated. Mild cases can be controlled by val and corneal irritation, and if protracted,
repeated, perioclic lavage with mild
corneal scarring, pigmentation, and
decongestant solutions.

possibly ulceration. Early spastic entropion

Lagophthalmos is an inability to fully
may be reversed if the inciting cause is
close the lids and protect the cornea from
quickly removed or if pain is alleviated by
drying and trauma. It may result from
everting the lid hairs away from the eye with extremely shallow orbits (in brachycephalic mattress sutures in the lid, by subcutaneous
breeds), exophthalmia due to a spaceinjections ( eg, of procaine penicillin) into occupying orbital lesion, or facial nerve
the lid adjacent to the entropion, or by
palpebral nerve blocks. Temporary stay
sutures or surgical staples left in place for

2-3 wk may be used to treat entropion in
vefY young puppies. Established entropion
usually requires surgical correction.

Ectropion is a slack, everted lid margin,
usually with a large palpebral fissure and
elongated eyelids. It is a common bilateral
confonnational abnormality in a munber of
dog breeds, including the Bloodhound, Bull

Mastiff, Great Dane, Newfoundland, St.

Bernard, and several Spaniel breeds.

Contracting scars in the lid or facial nerve
paralysis may produce unilateral ectropion

Bilateral entropion, Shar Pei puppy. Courtesy
in any species. Cortjunctival exposure to
of K. Ge/att.

490

OPHTHALMOLOGY
paralysis. Corneal scarring, pigmentation,

In generalized blepharitis, systemic
and ulceration usually result. Unless the
therapy often is indicated in addition to
cause can be corrected, the therapy is
topical treatment. Supportive therapy of hot
frequent topical lubrication and surgical
packing and frequent cleansing is indicated
shortening or closure of the lateral canthi
in acute cases. Nonophthalmic preparations
either temporarily or permanently.

can be used to treat the eyelids, but caution in

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Excessive nasal skin folds and facial hair
application is indicated to avoid corneal and
may aggravate the damage caused by
coajw1ctival contact and possible irritation.

lagophthalmos.

Abnormalities of the cilia include
extra (distichia) or misdirected eyelashes
on the lid margin. Epiphora, corneal

NASOLACRIMAL AND LACRIMAL
vascularization, and corneal ulceration

APPARATUS
and scarring may result. In many
instances, anomalous cilia are very fine,

The tear production and drainage system
the same color as the surrounding eyelid
is vital for health of the outer eye. Tear
hair, and result in neither clinical signs
glands within the orbit (lacrimal and in
nor damage. However, ectopic cilia
some species Harder gland) as well as
protruding through the dorsal palpebral
the superficial tear gland of the nictitatconjw1ctiva can cause profound pain.

ing membrane (third eyelid) produce the

If the corneal or conjunctiva] damage is
collective preocular or precorneal tear
caused by the extra cilia, excision, cautery, film. This film consists of three layers: or cryothermy of the cilia follicles is
outer lipid (from the Meibomian glands),
indicated. Anomalies of the cilia are
middle aqueous layer (from lacrimal
common and probably inherited in some
and third eyelid glands), and deep layer
dog breeds but are rare in other animal

(mucus) from the goblet cells within the
species. Distichiasis is not treated unless
conjunctiva.

corneal and/or conjunctiva! disease

The tear drainage system consists of
results. Successful removal of distichia
two lacrimal puncta ( except in the rabbit
requires destruction of the follicular base
and pig, which have only one punctum),
of the eyelids while not injuring the eyelid
two canaliculi, the lacrimal sac (within
margin. The most popular method is
the bony lacrimal fossa), and the long
cryotherapy applied at the base of the cilia and often tortuous lacrimal duct (to beneath the palpebral conjunctiva at the
empty tears within the forward nasal
eyelid margin. Depigmentation of the
cavity).

eyelid margin may result after cryotl1erapy

Hypertrophy, inflammation, and prolapse
but usually re-pigments in tl1e subsequent
of the gland of the nictitating membrane
montl1s. Inadequate cryotherapy can result

( cherry eye) is common in young dogs
in distichia recurrence.

and certain breeds ( eg, American Cocker

Spaniel, Beagle, LhasaApso, Pekingese,

English Bulldog). In the acute stage, the red

Inflammation
glandular mass swells and protrudes over

Blepharitis (inflammatio[I of the eyelids)

the leading margin of the nictitans, and
can result from extension of a generalized
there is a mucopurulent discharge.

dermatitis, conjunctivitis, local glandular

Although the swelling may recede for short
infections, or irritants such as plant oils
periods, the gland eventually often remains
or solar exposure. The lids can be the
prolapsed. Because it is.a major tear gland,
original site of involvement for agents that
it should be preserved if possible; the gland
lead to a generalized dermatitis. Dermatoshould be replaced and anchored with phytes (all species), Demodex canis
sutures to the orbital rim, periorbital fascia,

(dogs), D cati or D gatoi (cats), and or nictitans cartilage, or covered with
bacteria such as staphylococci often are
acljacent mucosa ( envelope or pocket
involved. The mucocutaneous junction of
techniques). Partial excision should be
the skin and conjunctiva can be the site of
avoided. Complete excision may predislesions of immune-mediated diseases such pose to keratoconjunctivitis sicca (see as pemphigus. Skin scrapings, cultures,
p 492) in 30%-40% of dogs in later life.

and biopsies may be required for an

Surgical or medical resolution of cherry
accurate diagnosis. Localized glandular
eye still predisposes -20% of tl1ese dogs
infections may be acute or chronic (stye
to future keratoconju.nctivitis sicca.

[glands of Zeis and Moll] and chalazion

Therefore, these dogs should be monitored

[Meibomian glands]).

for several years alter undergoing surgery.

OPHTHALMOLOGY

491
lacrim
l d
r. �
cartilage of the
third eyelid
r

' i

'.

,'_
medial palpebral
comn1issure

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lateral
palpebral

• ,J
commisure
lacrimal puncta�
lacrimal sac

",/

I
nasolacrimal duct----�·/

., .

,,,... ,� , '

_,A' ,;

.. .

'• ,

,

,

I

. "

(

Lacrimal apparatus, dog. Illustration by Dr. Gheorghe Constantinescu.

Dacryocystitis (inflammation of
obstructions. Therapy consists of
the lacrimal sac) usually is caused by
maintaining patency of the duct and
obstruction of the nasolacrimal sac and
instilling topical antibiotic solutions.

proximal nasolacrimal duct by inflamma

Tubing (polyethylene or silicone) or 2-0
tory debris, foreign bodies, or masses
monofilan1ent nylon suture temporarily
pressing on the duct. It results in
catheterized in the duct may be necessary
epiphora, secondary conjunctivitis
to maintain patency during healing. When
refractory to treatment, and occasionally
the nasolacrimal apparatus has been
a draining fistula in the medial lower
irreversibly damaged, a new drainage
eyelid. Irrigation of the nasolacrimal duct
pathway can be constructed surgically
reveals an obstruction of the duct, reflux

(conjunctivorhinostomy or conjunctivoraof mucopurulent discharge from the lostomy) to empty tears into the nasal
lacrimal puncta, or both. Radiographs
cavity, sinus, or mouth.

of the skull after injection of contrast

Im perforate lacrimal puncta are an
material into the duct (dacryocystorhiinfrequent cause of epiphora in young nography) may be necessary to establish
dogs. In foals, atresia of the nasal ( distal)

the site, cause, and prognosis of chronic
end of the nasolacrimal duct is a common

Bilateral inflammation and prolapse of the

Exposure of inflamed, prolapsed nictitating
nictitating membrane (cherry eye), young
membrane using thumb forceps, Boston

Boston Terrier. Courtesy of K. Ge/att.

Terrier. Courtesy of K. Gelatt.

492

OPHTHALMOLOGY
cause of early epiphora and chronic

Subconjunctival hemorrhage may
conjunctivitis. In calves, multiple openings
arise from trauma or blood dyscrasias, von
of the nasolacrimal duct may empty tears

Willebrand factor deficiency, and certain
onto the lower eyelid and medial can thus,
infectious diseases. It does not require
causing chronic dennatitis. Therapy in
therapy, but close inspection is warranted
dogs and foals consists of surgically
to determine whether more important

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opening the blocked orifice and maintainintraocular alterations have occurred. If ing patency by catheterization for several
definite evidence or history of trauma is
weeks during healing.

not present, then systemic examination

Keratoconjunctivitis sicca (KCS)

is indicated to determine the cause of tl1e
is due to an aqueous tear deficiency and
spontaneous hemorrhage.

usually results in persistent, mucopurulent

Chemosis, or conjunctiva! edema,
conjunctivitis and corneal ulceration and
is seen to some degree in all cases of
scarring. KCS occurs in dogs, cats, and
coajunctivitis, but the most dran1atic exan1-
horses. In dogs, it is often associated with
ples are seen with trauma, hypoproteinan autoi.nunune dacryoadenitis of both emia, allergic reactions, and insect bites.

the lacrimal and nictitans glands and is

The latter are treated with topical
the most frequent cause of secondary
corticosteroids and usually resolve rapidly.

conjunctivitis. Distemper, systemic

Specific therapy for the etiologic agent is
sulfonan1ide and NSAID therapy, heredity,
indicated.

and trauma are less frequent causes of KCS

Conjunctivitis is common in all
in dogs. KCS occurs infrequently in cats
domestic species. Primary infectious
and has been associated with chronic feline coajunctivitis caused by different bacteria, herpesvirus l infections. In horses, KCS
viruses, mycoplasma, fungi, and parasites
may follow head trauma.

affect several species. The etiologic agents

Topical therapy consists of artificial tear
vary from infectious to environmental
solutions, ointments, and, if there is no
irritants. The signs are hyperemia,
corneal ulceration, antibiotic-cmticosteroid chemosis, ocular discharge, follicular combinations. Lacrimogenics such as
hyperplasia, and mild ocular discomfort.

topical cyclosporin A (0.2%-2%, bid),

The appearance of tl1e coajunctiva usually
tacrolimus (0.02%, bid), or pimecrolimus
is not sufficiently distinctive to suggest the

( l %) may increase tear production;
etiologic agent, and specific diagnosis
cyclosporine increases tear formation in
depends on history, physical examination,

-80% of dogs with Schirmer tear test values
coajunctival scrapings and culture,

:?: 2 mm wetting/min. Ophthalmic pilocar

Schirn1er tear test, and occasionally biopsy.

pine mixed in food may be useful for

Unilateral coajunctivitis may result from a
neurogenic KCS (dogs 20-30 lb [10-15 kg]

foreign body, dacryocystitis, or keratoconshould be started on 2-4 drops of 2%
junctivitis sicca (see above). In cats, feline pilocarpine, bid). Mucolytic agents ( eg,
herpesvirus l (FHV-1), Mycop/asma, or

HJO/o acetylcysteine) lyse excess mucus

Chla,mydia psitta,ci may produce
and restore the spreading ability of other
coajunctivitis that begins in one eye and
topical agents. In chronic KCS refractory to becomes bilateral after -1 wk. Specific medical therapy, parotid duct ti:ansplantadiagnosis is made most rapidly by tion is indicated. In general, canine KCS
demonstrating the inclusions or tl1e agent
requires longterm (often for life) topical
in coajunctival scrapings. Bilateral
lacrimogenic therapy.

coajunctivitis is common in viral infections
in all species. Herpesviruses produce

CONJUNCTIVA
coajunctivitis in cats, cattle, horses, and
pigs. Purulent discharge indicates a

The conjunctiva consists of the palpebral
bacterial component, but this may be
conjunctiva (lining the posterior eyelids),
opportunistic because of debilitation of
the fomix or conjunctiva! cul-de-sac where
the mucous membrane. Environmental
tl1e palpebral and bulbar coajunctiva
irritants and allergens are common causes
connect, and the bulbar coajunctiva
of coajunctivitis in all species. If a

( covering the anterior globe or episclera)

mucopurulent exudate is present, topical
and nictitating membrane. The coajunctiva
antibiotic therapy is indicated but may not
has important roles in tear dynamics,
be curative if other predisposing factors
immunologic protection, ocular movement, are involved. Mechanical factors such as and corneal healing. Because it is loosely
foreign bodies, environmental irritants,
attached to the episclera, the bulbar
parasites, and eyelid confonnational
coajunctiva is a useful tissue to graft to
defects should be removed or corrected.

weakened, ulcerated corneas.

Selected antibiotics are indicated for

OPHTHALMOLOGY

493
chlamydia] and mycoplasmal infections;
topical antiviral preparations ( eg, 1 % idoxuridine, 3% adenine arabinoside, or 1 %
triiluorothymidine (often instilled tid--qid
and administered for 7-14 days) are
indicated for herpesvirus infections when

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both the cornea and conjunctiva are
involved. Oral supplementation in cats with

250-500 mg of L-lysine daily ( often placed
in the treats) may reduce the severity and
frequency of recurrence of FHV-1
conjunctivitis and keratitis.

Chronic superficial keratitis, early, German

Shepherd. The cornea is progressively

CORNEA
infiltrated with superficial blood vessels,
followed by inflammation (lymphocytes and

The size of the nearly round to oval cornea
plasma cells), and lastly pigmentation.

( vertical/horizontal) varies by animal

Courtesy of K. Gelatt.

species: dog (8.5 x 9.5 mm), cat (8.4 x 8.9
mm), horse (16.6 x 17.9 mm), and cow
by superficial blood vessels. This in1mtme

(15.2 x 16.4 mm). The animal cornea
mediated keratitis is common in Gern1a.n
consists of the superficial epithelium and

Shepherds, Belgian Te,vurens, Border
basement membrane, large and relatively

Collies, Greyhounds, Siberian Huskies, and
acellular stroma, deeper Descemet

Australian Shepherds. Specific therapy
membrane, and deep single layer endotheconsists of topical antibiotics, antiviral or lium. The cornea maintains a strong and
a.ntimycotic agents when appropriate,
durable barrier between the eye and
removal of any mechanical inita.nts, tear
environment, as well as a transparent
replacement when deficient, and corticomedium to pern1it passage of light and steroids or cyclosporin A ( or botl1) when
images into the posterior segment. Corneal
inmume-mediated. The latter may need to
diseases are common in most animal species be continued indefinitely and the frequency and fortunately can be treated successfully
varied depending on the response. Chronic
by medical, surgical, or a combination of
superficial keratitis when immune-mediated
these methods. The accessibility of the
is a. lifelong disease, requiring lifelong
cornea permits several detailed and
topical anti-inflammatory therapy. The
noninvasive diagnostic techniques.

disease appears more aggressive in young

Superficial keratitis is common in all
dogs and in dogs that live outside in higher
species and is characterized by corneal
altitudes. Generally, topical 1% prednisovascularization and opacification, which lone, 0.1% dexa.n1ethasone, or 0.2o/o-l %
may be due to edema, cellular infiltrates,
cyclosporine instilled in both eyes bid-qid is
pign1entation, or fibroplasia. lf ulceration is
sufficient to control the disease and prolong
present, pain-manifest by epiphora and
vision. The intensity of the infla.nllllatory
blepharospasm-is an outstanding sign.

response in both eyes is quite variable and

Unilateral kera.titis frequently is traumatic
may change by age, season, amount of time
in 01igin. Mechanical factors, such as lid
the dog spends outside, and other factors.

confonnational defects and foreign bodies,

To minimize costs and adverse effects, but
should always be eliminated as possible
control the disease, topical therapy is
ca.uses, because improvement will not occur adjusted to the individual animal (topical until they are resolved. Ulcerative keratitis
therapy ranges from one drop in the
may be complicated by secondary invasion
affected eye every other day to as frequent
by bacteria. and, in horses, by saprophytic
as one drop in the affected eyes qid).

fungi. Bilateral superficial kera.titis may be

Interstitial keratitis is a deep
in1mune-media.ted or associated with a la.ck
involvement of the corneal stroma. that
of tears, eyelid conformational defects, or
represents one of the clinical signs
infectious a.gents.

associated witl1 all chronic and many a.cute

Pannus, or Uberreiter disease, is a
cases of anterior uveitis. The corneal
specific, bilateral, progressive, proliferative,
vasculaiization is less branching, finer, and
chronic, superficial keratitis that begins
deeper than in superficial kera.titis; if the
laterally and/or medially at the limbus and
endothelium has been disrupted, corneal
eventually extends from all quadrants to
edema is often marked. Systemic diseases,
cover the cornea. Inflammatory cells
such as infectious ca.nine hepatitis, bovine

(lymphocytes and plasma cells) infiltrate
malignant catarrhal fever, systemic
the cornea from the lirnbus, accompanied
mycoses in many species, and neonatal

494

OPHTHALMOLOGY
septicemias that localize in the eye, can
ulcers to heal within 7-10 days. Early
cause bilateral or unilateral interstitial
reports suggest these keratotomies in cats
keratitis. Therapy is directed at the anterior may predispose to corneal sequestration uveitis, the systemic infection, or both. A
and should be used with great care.

specific, nonulcerative, peripheral, stromal

Nictitating membrane flaps ( or soft contact
keratitis and persistent anterior uveitis
lenses or collagen shields) act as a pressure

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(keratouveitis) occurs in horses; prognosis
bandage and often are therapeutic for
and response to treatment are poor.

shallow ulcers. Medical treatment of deep

Ulcerative keratitis may be divided
ulcers is similar to that of superficial ulcers,
based on onset, depth, and position within
but many deep ulcers also require
the cornea. Ulcerative keratitis (based on
cor\junctival grafts to strengthen and
depth) may be superficial, deep, deep with
maintain the integrity of the cornea.

descemetocele, or perforating. Progression

Corneal sequestration and keratitis
of the corneal ulcer is based on the
appear to be unique to the cat. It occurs in
microbes involved and on the release of
all breeds of cats but may be more frequent
microbe and tissue enzymes that digest the
in the Siamese, Persian, and Himalayan
corneal stroma. Pain, corneal irregularity,
breeds. Initially, a very small dark area
edema, and eventually vascula.rization are
develops within the anterior stroma and
signs of ulceration. A dense, white infiltrate
under intact corneal epitheliun1 (that stains
at the ulcer margin indicates strong
with rose Bengel and occasionally very
leukotaxis and bacterial involvement. To
faintly with topical fluorescein). Eventudetect small ulcers, topical fluorescein may ally, the stromal spot becomes larger and
be required. In dogs and horses, most
either dark brown or black, and is not
ulcers are mechanical in origin; in cattle,
covered by epitheliun1. There is variable
sheep, goats, cats, and reindeer, infectious
pain and a central to paracentral, brown to
agents and mechanical causes are
black opacity composed of necrotic
important; in cats and horses, herpesvirus
stroma, vascularization, and surrounding
infection is a frequent cause. All ulcers
inflammation. Spontaneous extrusion may
have the potential for secondary bacterial
occur, especially with superficial sequescontamination as well as endogenous tra. Treatment consists of superficial
proteinase "melting" of the stroma.

keratectomy of the entire sequestrum,

Therapy for superficial ulcers is usually
that, with deeper lesions, is covered with
medical and consists of topical broadcor\junctival grafts.

spectrum antibiotic(s) administered 3-6

Corneal stromal abscesses in horses
times daily, correction of any mechanical
may be sequelae of healing corneal ulcers
factors, and limited 1 % topical atropine to
or defects and the trapping of bacteria or
maintain iridocycloplegia and reduction of
fungal organisms ( or both) within the
ocular pain. Adverse effects of atropinestroma after reepithelialization. Recently, induced reduced tear production in all
fungi (both Candida and Aspergillus) have species and colic in horses must be
been demonstrated in horses' subepithelial
considered. Antiproteinase therapy for
cornea devoid of iridocyclitis, suggesting
melting stromal ulcers includes topical
another mode of entry. A variable, white to
serum and other drugs, .and for acute
yellow, stromal infiltrate is surrounded by
ulcerations they may be instilled 4-6 times
daily for the first several days. Corneal
healing is monitored by frequent clinical
examinations and gradual reduction in the
size of the fluorescein retention by the
nonepithelialized ulcer.

Syndromes of very slow-healing and
recurrent superficial ulcers occur in dogs,
cats, and horses; in dogs, they may be due
to basement membrane disease causing
faulty attachment of tl1e corneal epithelium,
whereas in cats and horses, and recently in
dogs, herpesvirus should be suspected.

lnitial therapy is ulcer debridement followed
by topical antibiotics and atropine. For
refractory cases in dogs, multiple punctures
or cross-hatching (punctate and grid
keratotomies) of affected corneas with a

Corneal sequestrum, domestic cat.

22-gauge needle stimulates most indolent

Courtesy
of K. Gelatt.

OPHTHALMOLOGY

495
an intense stromal keratitis and vasculari

Female Boston Terriers are affected
zation and a variable but sometimes
more frequently than males (with a mean
intense anterior uveitis. At least seven to
age of -7.5 yr), and this breed's disease has
nine different species of fungi have been
both clinical and histopathology similariisolated in corneal ulcers and stromal ties to those of Fuch corneal endothelial
abscesses in horses, but Aspergillus and dystrophy in people. With the dystrophic

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Pusarium spp are the most frequent
and degenerating endothelium, progressive
isolates. Treatment consists of intensive
but painless bilateral corneal edema
topical and occasional systemic antibiotics
develops starting centrally. With extensive

(and if indicated, antifungals), iridocycloand full-thickness corneal edema, corneal plegics, NSAIDs, and often surgical
epithelial bullae may develop and are quite
removal of the abscess with cor\junctival
painful. Treatment of early cases before
and tectonic corneal grafts.

complete corneal involvement consists

Corneal dystrophies and degenera
of topical hyperosmotics (2%-5% sodium
tions occur frequently in dogs, infrequently chloride or 40% glucose) applied frequently in cats, and rarely in horses. Corneal
and, for advanced cases, thermokeratodystrophies are bilateral and often thought plasty (Salaras procedure) or full-thickness
inherited in dogs. The appearance of these

(penetrating) keratoplasty.

two diseases may be divided into the

Corneal degenerations are often
following categories: 1) part of cornea
unilateral and usually secondary to ocular
affected (epithelium, stroma [anterior,
or systemic diseases. Deposits of triglycermiddle, and deep], and endothelium), ides, cholesterol, and also calcium are

2) area of the involved cornea ( central,
present in corneal degenerations. Corneal
paracentral, and limbal), and 3) possible
degeneration may be associated with other
cause (primary/inherited or secondary).

ocular diseases, such as corneal ulcera

Corneal dystrophies may affect the
tions, phthisis bulbus, lagophthalrnos, and
epithelium and endothelium but appear
prolonged NSAID therapy. If associated
clinically to involve the stroma most
with hyperlipoproteinemias or hyperchofrequently. The corneal degenerations are lesterolemia and high-fat diets, corneal
secondary to other ocular disease or
degenerations can affect both eyes, and
systemic conditions.

these deposits are usually associated with

Corneal dystrophies affecting the
corneal vascula.rization. They also can be
epithelium are associated with recurrent
altered by significant changes in diet. Baby
corneal erosions in dogs. The defective
rabbits or puppies fed whole cow milk may
corneal epithelium fails to normally adhere
develop extensive lipid deposits in the
to its defective basement membrane and
corneal stroma sufficient to impair vision.

results in recurrent superficial erosions

Treatment for most corneal degenerations

(more frequent in the Boxer breed) and
is not usually necessary, unless related to
prolonged healing.

dietary or systemic diseases.

The stromal dystrophies appear as white,
irregular deposits within the different

ANTERIOR UVEA
depths of the stroma and are sometimes
labeled corneal lipidosis. Corneal

The anterior uvea consists of the iris, ciliary
dystrophies are most frequent in dogs,
body, and anterior chamber ( or iridocomeal)

appear inherited in -20 breeds, affect
angle. The iris provides most of the eye color
mostly the corneal stroma, and are usually
as well as an ape1ture (pupil) to regulate the
bilateral. Of the breeds affected, the
an1ount of light that enters the eye and

Siberian Husky corneal stromal dystrophy
posterior segment. Pupil shape varies widely
has been investigated in the greatest detail.

among animal species, including circle,

Most often, the corneal opacities consist
vertical slit, horizontal oval, square, or even
of triglycerides and both intracellular and
multiple pupils. The ciliru-y body processes
extracellular cholesterol. Treatment is not
provide most of the aqueous humor to
usually necessary unless vision is impaired
nourish the anterior segment and remove
or the deposits become irritating. For these
its metabolic wastes, as well as the outflow
lipid deposits to be viewed histologically,
channels ( anterior chamber angle) for
the corneas must be processed as frozen
aqueous humor to reenter the venous
sections and alcohol dehydration
system. The ciliary body musculature also
processing avoided.

regulates lens curvature (accommodation),

The corneal endothelial dystrophies occur which is more lintited in domesticated in dogs and rarely in cats (Manx breed). In
animals than in people. The ciliary body
dogs, it primarily affects older Boston
continues posteriorly as the choroid, and

Terriers, Chihuahuas, and Dachshunds.

diseases of tl1e iris and ciliary body also often

496

OPHTHALMOLOGY
involve the choroid. Diseases of the ante1ior
strate their cystic nature and differentiate
uvea are common in domestic animals.

them from neoplasms. Enlarged and cystic

Persistent pupillary membranes are
dorsal corpora nigra may impair vision
remnants of the normal prenatal vascular
and mimic iridic melanomas in horses.

network that fills the pupillary region.

Surgical excision or aspiration may be

Persistence of pigmented strands across
indicated.

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the pupil from one area of the iris to

Iris coiobomas a.re rare in animals but
another, or to the lens or cornea, is not
occur occasionally in Australian Shepuncommon in dogs and occurs occasionherds. They are usually in the upper iris, ally in other species. In Basenjis, the
mainly in heterochromic irides, and cause
condition is inherited.

an irregularity to the pupil. Viewed closely,

Atrophy of the iris is common in older
the defect involves the iridal anterior
dogs and may involve the pupillary margin
stroma and apparently the sphincter
or the stroma. Atrophy of the pupillary
muscle, but the pigment layer is present.

margin creates a scalloped border and a

Anterior uveitis, or iridocyclitis, when
weakening of the sphincter muscle, which
acute, is manifest by miosis, increased
is manifest as a moderately dilated pupil(s)

protein and cells in the anterior chan1 ber
or by sluggish pupillary light reflexes and

(aqueous flare), low intraocular pressw·e,
increased sensitivity to bright illumination.

bulbar conjw1ctival hyperemia, iridal

Stromal atrophy results in dran1atic holes
swelling, photophobia, and blepharospasm.

in the iris and, often, displacement of the

Secondary glaucoma, cataract, and corneal
pupil. Neither form of atrophy appears to
opacification may be complications.

affect vision. Animals lacking a functional

ConcmTent posterior uveitis or choroiditis
iridal sphincter may show increased
is frequent. Causes of anterior uveitis can be
sensitivity to bright light.

separated into exogenous and endogenous.

Iridic cysts are seen in dogs, cats, and

Penetrating and nonpenetrating trauma
horses. In clogs, they usually are free-floating,
and, rarely, intraocular neoplasms or
pigmented spheres in the aqueous humor
intraocular helrninths are causes of
within the pupil and anterior and posterior
unilateral uveitis. Common causes of
chambers. Although innocuous in most
bilateral uveitis include i.J1m1une-mediatecl
breeds of dogs, anterior uveal cysts (iris
diseases and i.Jlfectious diseases such as
and ciliary body) in Golden Retrievers and
infectious canine hepatitis, feline infectious

Great Danes are associated with exfoliaperitonitis, feline leukemia, feline in1111unotion of pigmented cells, chronic uveitis, deficiency, feline toxoplasmosis, systemic
glaucoma, and cataract formation. In
mycoses in dogs and cats, ca.nine brucellocats, the cysts frequently are not usually sis, leptospi.J·osis in horses, bovine
free-floating but attached at the pupillary
malignant ca.ta.rrhal fever, infectious bovine
margin. In horses, they are present in the
rhinotracheitis, equine viral a.rteritis,
stroma of the iris and more frequently
classical swi.J1e fever, canine ehrlichiosis,
involve blue irides. Because vision is
and neonatal bacterial itlfections Uoint,
infrequently impaired, therapy is rarely
navel, and gut) of calves, lambs, kids, and
necessary, but aspiration or noninvasive
foals. Recurrent uveitis that is at least it1
laser-induced deflation can bs performed.

pa.rt i.J1m1une-media.ted affects horses

Transillumination will usually demon-

(periodic ophtl1almia or recWTent uveitis)

and dogs (panuveitis with dermal clepigmentation or uveode1mal syndrome).

Recurrent and chronic antelior uveitis are
most often associated with complications
and can produce secondary cataract
formation witl1 posterior synechia.e, and
glaucoma.. A thorough history; examination
of the cornea for injuries; physical
exanli.nation; serum serology; and centesis
of the aqueous for culture, serology, and
cytology aid in diagnosis.

Nonspecific therapy consists of topical
mydriatics to maintain pupillary dilation
and movement, topical corticosteroids (if
nonbacte1ial), a darkened environment, and
prostaglandin inhibitors (such as aspirin,

Persistent pupillary membranes, cat. Courtesy
flunixin meglumine, or phenylbutazone).

of K. Gelatt.

lf bacterial in origin, topical, systemic,

OPHTHALMOLOGY

497
and perhaps intraocular antibiotics are
glaucoma, characterized in people by
indicated. Treatment of immune-mediated
normal levels of intraocular pressure and
processes may require systemic or
progressive optic disk damage, has not
subconjunctival as well as topical
been documented in domestic animals. In
cmticosteroids and oral azathioprine.

dogs, the primary (inhe1ited) and secondai-y

Hyphema or hemorrhage in the ante1ior
glaucomas occur in -1. 7% of the canine

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chan1ber has several clinical appearances,
population in North America. The frequency
including the following: 1) small, focal
of bilateral primary breed-predisposed
blood clots suspended within the anterior
glaucomas in purebred dogs is the highest
chamber or adhered to the posterior cornea, of any animal species, except people (0.9%).

iris, or anterior lens capsule; 2) diffuse,

Primary open-angle glaucoma in Beagles
unclotted hemorrhage throughout the
has been associated with the ADAMTSlO
entire anterior chamber, occluding deeper
mutation. In cats, the glaucomas are
eye examination and vision; and 3) multiple
predominately secondary to anterior
layers of recurrent or chronic unclotted
uveitis ai1d neoplasms; however, prirnai-y
hemorrhage (the oldest is a purple or black
open-angle glaucoma occurs in the Siainese
layer in the bottom of the anterior chamber
breed. In horses, the glaucomas appear
and the most recent hemorrhage is the
underdi.agnosed, because applanation
dorsal bright red layer). Causes of hyphema
tonometry is not routinely done; they
include uveitis, trauma, intraocular
appear most frequently in older anin1als,
neoplasia, retinal detachments and retinal

Appaloosas, ai1d witl1 concurrent anterior
tears, systemic hype1tension, coagulation
uveitis. In cattle, the glaucomas have been
factor abnormalities, platelet disorders,
associated with congenital iridocomeal
hyperviscosity, congenital ocular anomaanomalies and anterior uveitis.

lies, anterior segment neovascularization,

Diagnostic procedures essential to
and glaucoma. Resolution of hyphema
manage the glaucomas include tonometry,
requires exit of intact RBCs through the
ophthalmoscopy (direct and indirect), and
aqueous humor outflow channels.

gonioscopy ( visualization of the irido

Acute hyphema generally has a good
comeal angle and anterior ciliary cleft).

prognosis provided the cause is identified

Newer electrophysiologic techniques,
and treated. Recurrent and/or chronic
such as pattern electroretinograms and
hyphema has a poor to guarded prognosis,
visual evoked potentials, estimate damage
because secondary glaucoma or phthisis
to the retinal ganglion cells and their
bulbus is likely. No drugs have been proved
axons and appear to be sensitive
to facilitate resolution of hyphema, but
indicators of glaucoma-related destrucintracameral tissue-plasminogen activator tion of these cells. New, clinical high

(TPA) can dissolve fib1in that is <10-14
resolution imaging techniques, including
days old and release the entrapped RBCs
ultrasound biomicroscopy for anterior
within the anterior chamber. TPA does not
segment changes a.Ild optical coherenGe
prevent future fibrin formation, but topical
tomography for retinal and optic ne1ve
and systemic corticosteroids may.

head changes, permit noninvasive detailed
intraocular examinations. In small

GLAUCOMA
animals, the Schiotz indentation tonometer has been replaced by newer and more The glaucomas are generally related to
accurate applanation tonometers used to
reduced outflow of aqueous humor through
estimate intraocular pressure; in horses
the trabecular mesh work of the anterior
and cattle, only appla.J1ation-type
chamber or iridocomeal angle ( conventional
tonometers can be used.

outflow, -85%), and through the uveoscleral

Intraocular pressure is reasonably
network (through the ciliary body and
consistent in most species (see TABLE 1), subscleral space, -15%). Excessive
and diurnal variations have been
production of aqueous humor in people
documented in dogs, cats, rabbits, and
appears to be rare as a cause of glaucoma
nonhuman primates. Ophthalmoscopy
and has not been reported in ailinlals.

permits detection of the intraocular

Changes in the composition of aqueous
pressure-related damage to the retina a.Ild
hwnor have been reported recently in human optic disk. Gonioscopy is the basis for ai1d animal glaucomas and appear important
classification of all glaucomas; it detects
in the disease genesis and progression.

iridocorneal and sclerociliary cleft

The glaucomas represent a group of
opening outflow changes as the glaucoma
diseases chai·acterized by increased
progresses and helps determine the most
intraocular pressure with resultant retinal
appropriate medical and surgical
and optic disk destruction. Low-tension
treatments. Ultrasound biomicroscopy

498

OPHTHALMOLOGY
itM•ii INTRAOCULAR PRESSURE (IOP) BY APPLANATION TONOMETRY

Species

Tonometer

IOP (mmHg) Mean± soa

Dog

Mac Kay-Marg

15.7 ± 4.2

Tono-PenTM

18.7 ± 5.5

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12.9 ± 2.7

To no-Vet®

10.8 ± 3.1

Cat

Tono-Pen

19.7 ± 5.6

Rabbit

Pnewnatonograph

19.5 ± 1.8

17.9 ± 2.1

Horse

Tono-Pen

29.6± 6.2

23.3± 6.9

Cow

Tono-Pen

26.9 ± 6.7

Llama/alpaca

Tono-Pen

16.6 ± 3.6

Monkey (ketamine)

Tono-Pen

13.6 ± 3.7

Alligator

To no-Pen

23.7 ± 2.1

Ferret

Tono-Pen

22.8 ± 5.5

Rat

Tono-Pen

17.3 ± 5.3

Hawk

Tono-Pen

20.6 ± 3.4

Owl

Tono-Pen

10.8 ± 3.6

" Duplicate figures represent different reports for that species.

(50-100 MHz) permits further examina'.

displacement, and breaks in Descemet
tion of the anterior chamber angle and
membrane (corneal striae) result. Pain
the entire sclerocilia1:y cleft.

usually is manifest by behavioral changes

Clinical signs are traditionally divided
and occasional pe1iorbital pain, ratl1er tllan
into acute and chronic; in reality, most cases
by blepharospasm.

of acute high-pressme glaucoma are

Classification of the glaucomas assists in
superimposed on chronic gl:rucoma rather
tile optimal plan for clinical management
than occurring as singular events. Most dogs and preservation of vision. The choice of with early to moderate chronic glaucoma
medical or smgical treatment, or most
are not taken to the veterinarian because the frequently a combination of both, is based early clinical signs-sluggish to slightly
on the progressive iridocorneal angle
dilated pupils, mild bulbar conjunctiva!

closure that occurs in most of the
venous congestion, and early enlargement
glaucomas. As the glaucoma progresses
of the eye (buphthalmia or megaloglobus )and aqueous humor outflow continues to are so subtle. To detect early glaucoma,
reduce, the need for a combination of
repeated tonometry should be routinely
medical therapies increases. For open-angle
perfom1ed on high-risk breeds of dogs as
glaucoma in dogs, sho1t- and longterm
part of the annual, general physical examin a management is by treatment witll miotics, tion. The clinical signs of acute and often
topical and systemic carbonic anllydrase
markedly increased levels of intraocular
inhibitors, prostaglandins, osmotics, and
pressme are a dilated, fixed, or sluggish

13-blocking adrenergics. These san1e
pupil; bulbar conjunctiva! venous congestreatments are used for initial control of tion; corneal edema; and a finn globe. With
narrow and closed-angle glaucoma, but
prolonged increases of intraocular pressme,
short- and longtem1 management often
secondary enlargement of tl1e globe, lens
requires supplemental smgery, eg, filte1ing

OPHTHALMOLOGY

499
procedures, anterior chamber shunts,
degree of opacification (incipient, immacyclocryotherapy, or laser transscleral ture, mature, hypermature), and shape.

cyclophotocoagulation. Short- and longtern1 Most cataracts can be detected by dilating management of end-stage glaucoma with
the pupil and exanlining the pupiUary region
buphthal..mia and blindness in dogs also
against the retroiUunlination of the tapetal
requires surgery, eg, intrascleral prosthesis,
fund us. Slit-lamp biomicroscopy pernlits
enucleation, cyclocryothermy, or intravitoptimal direct examination of the lens.

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real gentamycin (10-25 mg) combined with

Cataracts (often inherited) are more
l mg dexamethasone. Surgical procedures
common in dogs tlmn in other species ( see
in dogs have traditionally provided only

TABLE 2), and vary by age of onset, rate of
short-term resolution, because the filtering
progression, and original site of cataract
fistulas eventually scar over and fail. More
formation. Other causes include diabetes
recently, ante1ior chamber shunts, with and
mellitus (the second most frequent group of
without valves, offer in1proved results.

cataract surgeries in the dog), mal..nutrition,

Antifibrotic drugs, such as mitomycin C and
radiation, inflammation, and trauma. In cats

5-fluorouracil, may delay or prevent scarring
and horses, most cataracts are secondary to
of the alternative aqueous outflow channels
anterior uveal inflammation. Most rep01ted
and prolong tl1eir function. In cats, medical
inherited cataracts in cats are in young
therapy is usually the mainstay and consists
animals. Population studies on cataracts in
of topical 13-blocking adrenergics ( caution
cattle, rabbits Oaboratory and pet), and
in small cats), topical carbonic anhydrase
guinea pigs suggest spontaneous cataracts
inhibitors, and for those glaucomas
occur not infrequently, but these species
associated with anterior uveitis, topical
infrequently become blind.

and/or systemic corticosteroids. In horses,

In dogs, cataracts that are secondary
single and/or repeated laser transscleral
related to diabetes mellitus are increasingly
cyclophotocoagulation is most effective.

common; tl1ese cataracts represent the
second largest group of cataracts operated

LENS
on in dogs in the USA. The increased blood
glucose causes intralenticular sorbitol to

The optically clear and avascular lens
accw11ulate, which increases the osmotic
consists of (from anterior to posterior) the
forces of tl1e lens, causing the lens to imbibe
anterior lens capsule, anterior cortex,
water and result in fiber swelli.ng, rupture,
nucleus, posterior cortex, and very thin
and death. Typically, these cataracts develop
posterior lens capsule. The lens is formed
rapidly and can occasionally rupture the
early in the development of the eye and
equatorial or posterior lens capsule.

coated with its basement membranes

Cataract surgery appears to yield the same

(anterior and posterior lens capsules),
success rate as for inherited cataracts in
which insulate the lens proteins from the
dogs. Other ocular sequelae of diabetes
later-developing immune system. Hence
mellitus in dogs are occasional small retinal
in later life, if the lens capsule barrier is
hemorrhages, presumed corneal neuropacompromised by trauma or surgery, the thy, and reduced corneal sensitivity. Cats
immune system "attacks" the foreign lens
seem quite resistant to diabetic cataract
material. The sole function of the lens is to
fonnation, perhaps associated with lower
allow unaltered passage of light and images
aldose reductase activity than in dogs.

to the retina. Diseases of the lens involve

Sight may be regained in some young
changes in its transparency.

dogs, cats, and horses when cataracts

Cataracts are an opacity of the lens or its
undergo sufficient spontaneous resorption;
capsule and should be differentiated from
congenital nuclear cataracts in young
the minor lens imperfections in young dogs
aninlals may reduce in size with growth of

(seen on slit-lamp biomicroscopy) and the
the lens to pernlit restoration of vision as
normal increase in nuclear density (nuclear
the animal matures. Animals with immature
sclerosis) that occurs in older animals.

and incomplete cataracts may benefit from

Cataract formation and cataract surgery in
topical ophtl1almic atropine 2-3 times/wk,
people and dogs have many sinillarities, but
which allows vision around a central or
dogs experience more postoperative
nuclear cataract. However, the only
anterior uveitis. Cataract surgery is highly
definitive therapy for cataracts is surgical
effective (95%) in people and is performed
removal of the lens. In dogs and horses,
with advanced nuclear sclerosis and the
cataract extraction, often by phacoemulsi.fifailure of missing two lines on the Snellen cation and with intraocular lens implantaeye acuity test. Cataracts usually are tion, yields best results when perf01med
classified by their age of onset ( congenital,
before cataract maturation is complete and
juvenile, senile), anatomic location, cause,
lens-induced uveitis ( due to leakage of lens

500

OPHTHALMOLOGY

IH=IIII INHERITED CATARACTS IN DOMESTIC ANIMALS

Age of

Breed

Onset

Initial Localization Mode oflnheritance

DOGS

VetBooks.ir

Afghan Hound

6-12mo

Equatorial/posterior

Autosomal recessive
cortex

American Cocker
l-6yr

Posterior/anterior

Autosomal recessive

Spaniel
cortex
polygenetic

Australian Shepherd

2-4yr

Posterior cortex

Autosomal dominant"

Bichon Frise

2-6yr

Posterior/anterior

Autosomal recessive
cortex

Boston Terrier

Congenital Posterior sutures/

Autosomal recessive"

or juvenile
nuclear

Late onset

Equatorial/anterior

Autosomal recessive
cortex

Chesapeake Bay

�l yr

Nuclear/cortex

Incomplete dominant

Retriever

Entelbucher
l-2yr

Posterior cortex

Autosomal recessive

Mountain Dog

German Shepherd

�Swk

Posterior sutures/

Incomplete dominant
cortex

Golden Retriever

�6mo

Posterior subcapsular Incomplete dominant

(triangular)

Labrador Retriever

�6mo

Posterior subcapsular Incomplete dominant

(triangular)

Havanese

2-6yr

Posterior/anterior

Possible autosomal
cortex
recessive

Miniature Schnauzer

Congenital

Nuclear/posterior

Autosomal recessive
cortex

�6mo

Posterior cortex

Autosomal recessive

Norwegian Buhund

�l yr

Nuclear/cortex

Autosomal dominant

Old English Sheepdog Congenital Nuclear/cortex

Autosomal recessive

Rottweiler

�!Omo

Posterior polar/

Unknown
complete

Siberian Husky

�6mo

Posterior subcapsu-

Autosomal recessive

Jar/ posterior sutures

Staffordshire Bull Terrier �6 mo

Posterior sutures/cortex Autosomal recessivea

Standard Poodle

�l yr

Equatorial cortex

Autosomal recessive

Welsh Springer Spaniel Congenital

Nuclear/posterior

Autosomal recessive
cortex

West Highland White

Congenital Posterior sutures

Autosomal recessive

Terrier

( continued)

OPHTHALMOLOGY

501

•4N•ii INHERITED CATARACTS IN DOMESTIC ANIMALS (continued) Age of

Breed

Onset

Initial Localization Mode oflnheritance

HORSES

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Belgian

Congenital

Nuclear/cortex

Autosomal dominant

Morgan

Congenital

Nuclear

Autosomal dominant

CATILE

Holstein-Friesian

Congenital

Nuclear/cortex

Autosomal recessive

Jersey

Congenital

Nuclear

Autosomal recessive

SHEEP

New Zealand Romney Congenital Anterior/posterior

Autosomal domirnmt
cortex
a Associated with mutations in HSF4 gene.

material) is established. Lens-induced
higher levels of postoperative complications
uveitis is intensified by cataract surgery and of glaucoma and retinal detaclunent.

contributes substantially to postoperative
complications. In animals in which cataract

OCULAR FUNDUS
surgery is not performed, continued clinical
monitoring is in1portant. The secondary

The ocular fundus consists of the upper
lens-induced anterior uveitis often requires
tapetal fundus, ventral and surrounding
longterm monito1ing and repeated
nontapetal fundus, retinal vasculature, and
tonometry, with occasional corticosteroid
optic disk ( optic nerve head or optic
and myd.J.iatic therapy. Secondary glaucoma papilla). Histologically, the posterior and phthisis bulbus formation are possible
segment consists, from superficial to deep,
complications.

of the following structures: l) posterior

Lens displacement (subluxation,
sclera; 2) choroid, which contains pigmented
anterior or posterior luxation) occurs in
cells, blood vessels to support the high
all species but is common as a primary
metabolic needs of tl1e outer retina, and tl1e
inherited defect associated with the
tapetum lucidwn to enhance vision in dim

ADAMTSl 7 mutation in several terrier
light (tapetwn cellulosum in carnivores and
breeds. Complete displacement into the
tapetun1 fibroswn in herbivores); 3) retina,
anterior chamber produces acute signs and
which consists of the nine layers of
frequently is accompanied by glaucoma and
neurosenso1y retina and the outer retinal
corneal edema Treatment is surgical removal pigment epitl1eliun1; and 4) the optic disk, by phacoemulsification or intracapsular
where the retinal ganglion axons leave tl1e
lens extraction. Posterior displacement into
eye tJu·ough a weak and fenestrated scleral
the vitreous cavity is asymptomatic or
lamina cribrosa to synapse in the lateral
associated with ocular inflammation or
geniculate body (vision) or middle brain
glaucoma. Subluxated lenses are recognized (pupillary light reflex [Edinger-Westphal by an aphakic crescent and trembling or
nucleus J or dazzle reflex [ mid brain and
instability of tl1e iris (iridodonesis) and lens
rostral colliculi ]). Whereas dogs, cats,

(phacodonesis ). The decision to remove
horses, cattle, sheep, goats, and many oilier
subluxated lenses is based on tl1e severity of species have an upper tapetal fundus, pigs ocular disease tl1at can be attributed to tl1e
and rabbits are typically atapetal.

lens displacement. Lens displacements also

Diseases of tl1e ocular fund us may be
can be produced by trawna, enlargement of
p1irnary or may be manifestations of systemic
the globe witl1 glaucoma, and degenerative
cliseases. Inherited abnonnalities may be
zonular changes witl1 hypermature
congenital or appear later and are in1portant
cataracts. Procedures to remove tl1e lens
in the pathogenesis of retinopathies in dogs
for lens displacement are associated with
and cats. Traun1a, metabolic disturbances,

502

OPHTHALMOLOGY
systemic infections, neoplasms, blood

Labrador Retrievers and Sarnoyeds, retinal
dyscrasias, hypertension, and nutritional
dysplasia may be associated with skeletal
deficiencies are possible underlying causes
dysplasia (shortening) of the forelegs.

for retinopathies in all species.

Progressive retinal atrophy (PRA)

is a group of degenerative reti.nopathies

Inherited Retinopathies
consisting of inherited photoreceptor

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dysplasia and degenerations that have

Collie eye anomaly is a congenital,
a similar clinical appearance. A large
recessively inhe1ited (CEA-CH mutation),
number of mutations and DNA tests have
ocular defect with vaiiable expression in
been reported for these diseases that vary
rough- and smooth-coated Collies. It also is
by breed of dog. The photoreceptor
seen in Shetland Sheepdogs, Border Collies,
dysplasias inherited as autosomal

Australian Shepherds, Lancashire Heelers,
recessive traits in which clinical signs

Long-haired Whippets, Boykin Spaniels, and develop in the first year are seen in Irish Nova Scotia Duck Tolling Retrievers. The

Setters, Collies, Norwegian Elkhounds,
basic lesion is an area of choroidal or

Miniature Schnauzers, and Belgian
chorioretinal hypoplasia that on ophthal

Sheepdogs. The photoreceptor degeneramoscopy appears as a focal, variable-sized, tions inherited as autosomal recessive
pale area lateral to the optic disk. More
traits in which clinical signs develop at
severely affected dogs ( l OO/o-200Ai) can have

3-5 yr are seen in Miniature and Toy
additional colobomatous lesions of the

Poodles, English and American Cocker
optic papilla or peripapillary region and

Spaniels, Labrador Retrievers, Tibetan
occasional retinal detachments (2o/o-5%).

Terriers, Tibetan Spaniels, Papillons,

Intraoculai· hemorrhage may occur. Vision

English Springer Spaniels, Miniature
is not appreciably affected unless retinal

Longhaired Dachshunds, Akitas, and
detachment develops. With recent

Samoyeds. In Siberian Huskies, PRA is
availability of the CEA-CH DNA test,
inherited as an X-linked trait, whereas in
additional breeds of dogs diagnosed

Old English Mastiffs and Bull Mastiffs,
ophthalmoscopically with Collie eye

PRA is inherited as an autosomal
anomaly can be confumed having the same
dominant. Many other breeds of dogs are
mutation as well as potential carrier dogs
also suspected of having inhetited PRA.

within affected breeds before breeding.

In Abyssinian cats, PRA occurs as both

Retinal dysplasia is a congenital, focal,
photoreceptor dysplasia and degenerageographic, or generalized maldevelopment tion. Night blindness is noted early and of the retina that may arise from traun1a,
progresses to total blindness over montlls
genetic defect, or intraute1ine dainage such
to years. Ophthalmoscopic lesions are a
as viral infections. Most forms of retinal
bilateral symmetric increase in reflectivity
dysplasia in dogs are inherited, and many

DNA mutations have been reported.

Maternal viral infections, especially during
early fetal development, can result in
multiple ocular anomalies with retinal
dysplasia in kittens (panleukopenia virus),
lan1bs (bluetongue disease), puppies

(herpesvi.rus), and calves (bovine viral
diarrhea). Breeds of dogs with focal,
geographic, and generalized retinal
dysplasia thought to be inherited as an
autosomal recessive trait include American

Cocker Spaniels, Beagles, Labrador Retrievers, Rottweilers, and Yorkshire Terriers.

Focal areas of retinal maldevelopment may
be asymptomatic or interfere with central
vision. Generalized retinal dysplasia with
retinal detachment, visual i.mpaim1ent, or
blindness is inhetited in English Springer

Spaniels, Bedlington Terriers, Sealyhan1

Terriers, Labrador Retrievers, Dobem1an

Pinschers, and Australian Shepherds. Other
ocular anomalies, including microphthal

Choroidal hypoplasia and peripapillary
mia and congenital cataracts, often
coloboma (arrow), Collie. Both ocular
defects support the diagnosis of Collie eye
accompany the generalized forms. In
anomaly. Courtesy of K. Ge/att.

OPHTHALMOLOGY

503

English Cocker Spaniels suggest vitan1in

E disorders may also be important in the
pathogenesis of this disease complex. A
similar condition in horses, equine motor
neuron disease (seep 1248), has sinlilar
focal yellow-brown areas scattered

VetBooks.ir
throughout the tapetal fund us and has also
been associated with vitamin E deficiency.

Chorioretinitis

Chorioretinitis frequently is a manifestation of systemic infectious disease; it is important as both a convenient diagnostic
clue and a prognosticator of visual function.

Unless the lesions are generalized or involve
the optic nerve, they often are "silent." Scars may be differentiated from active lesions by
the haze and ill-defined borders of the latter.

Progressive retinal atrophy, Miniature Poodle.

Routine ophthalmoscopic examinations of

Changes in tapetal reflectivity, reduced retinal all animals with systemic diseases often vascularity, and early optic nerve atrophy are
permit rapid diagnosis of many specific
consistent with the diagnosis of progressive
diseases. Chorioretinitis may be present
retinal atrophy. Courtesy of K. Gelatt.

with canine distemper, systemic mycoses
in dogs and cats, protothecosis, feline
of the tapetal fund us, decreased pigmentatoxoplasmosis, tuberculosis, bacterial tion of the nontapetal fund us, attenuation
septicemias in young animals, feline
and a decrease in the number of retinal
infectious peritonitis, thromboembolic
vessels, and eventual atrophy of the optic
meningoencephalitis in cattle, bovine
papilla. Electroretinography is often used
malignant catarrhal fever, classical swine
to investigate and diagnose the condition.

fever, and leptospirosis and onchocerciasis

Cortical cataracts are common late in the
in horses. Therapy is directed at the
course of PRA in many breeds and may
systemic disease.

mask the underlying retinopathy. No
effective therapy is available. Blood and

Retinal Detachments
buccal mucosa-based DNA marker and

Retinal detachments occur in most species.

specific gene tests have been developed

In dogs, retinal detachment or separation of
to detect carrier and affected dogs before
the neurosensory retina from the retinal
clinical signs develop in many breeds.

pigment epithelium is associated wlth

The list of breeds affected with inherited
congenital retinal disorders (retinal
retinal degenerations and causative genes
dysplasia and Collie eye anomaly),
continues to increase; for current informachorioretinitis, trauma, intraocular surgery, tion consult the recent literature.

and posterior segment neoplasia. In cats,

Retinal pigment epithelial dystrophy
retinal detachments occur with chorioreti

( central progressive retinal atrophy) is nitis associated with feline infectious seen in Labrador Retrievers, smooth and
peritonitis, feline viral leukemia, and
rough Collies, Border Collies, Shetland
systemic hypertension. In horses, the most

Sheepdogs, and Briards. The condition may frequent causes are trauma, intraocular be inherited in Labrador Retrievers as a
surgery, and recurrent uveitis.

dominant trait with variable penetrance.

Retinal detachments are divided

Early ophthalmoscopic findings ( often
clinically into nonrhegmatogenous (serous,
before clinical signs are apparent) are
exudative, hemorrhagic, secondary to
small foci of irregular pigmentation in the
vitreal syneresis) and rhegmatogenous
tapetal fundus, which eventually coalesce

(with retinal breaks [hole or tear]). Clinical
and fade as reflectivity of the tapetal
signs include mydriasis, anisocoria, vision
fund us increases. The pigmented nontaimpairment, and intraocular hemorrhage.

petal fundus becomes mottled, the retinal

Diagnosis is by ophthalmoscopy and, in
vasculature gradually decreases, and the
eyes with an opaque cornea or lens, ocular
optic disk atrophies. Progressive visual
ultrasonography.

impairment occurs gradually over several

Nonrhegmatogenous serous retinal
years. Cataract formation occurs late in the
detachments are usually treated medically,
disease. There is no treatment. Studies in
with therapy directed at the primary

504

OPHTHALMOLOGY
infections, trauma, reticulosis, toxins, and
other causes. Complete physical and
medical evaluations are usually necessary
to establish the possible diagnoses.

Specific therapies are directed toward the
cause, and systemic corticosteroids are

VetBooks.ir
important to reduce inflammation of and
damage to the optic nerve.

Papilledema is rare in anin1als and often
associated with orbital masses in most
domestic species. Increased intracranial
pressure does not usually result in papilledema in animals, except in calves with avitaminosis A. The optic disk appears raised
above the surface of the adjacent retina, and
venous congestion is present. Vision and the
light pupillary reflexes are not usually
affected unless optic atrophy develops.

Optic atrophy may develop after
glaucoma, trauma, advanced retinal

Early retinal detachment and hemorrhage
developing lateral to the optic disc in a
degeneration, prolonged ocular hypoten

Collie puppy with Collie eye anomaly.

sion, or inflammation. The optic disk

Courtesy of K. Gelatt.

appears depressed and smaller than
normal; it is often pigmented, with marked
reduction in the optic nerve and retinal
vasculature. Both direct pupillary reflex and
disease. Retinal reattachment occurs with
vision are absent. There is no treatment.

resolution of the subretinal exudates and
hemorrhage. Variable retinal degeneration

ORBIT
may follow in the detached areas. Rhegmatogenous retinal detachments with retinal Signs of orbital cellulitis are acute pain
breaks generally require surgical correction. on opening the mouth, eyelid swelling, unilateral prolapse of the nictitating

OPTIC NERVE
membrane, forward displacement of the
globe, and conjunctivitis. Keratitis may

Optic nerve diseases are often difficult to
develop from lagophthalmos. The condition
detect and diagnose. Of the optic nerve
is seen predominantly in large and hunting
diseases, inflammation of the optic nerve
breeds of dogs and is rare in other species.

(optic neuritis) is most frequent.

Foreign bodies ( eg, migrating grass awns)

Optic nerve hypoplasia may be
and zygomatic sialadenitis are additional
inherited in Miniature Poodles; in kittens
causes. Orbital hemorrhage and neoplasia
and calves, it may result from in utero infecmay mimic ini1an1mation, except there is tions with panleukopenia and "bovine viral
usually no pain on opening the mouth. In
diarrhea, respectively. In calves, the cause
acute cases, systemic broad-spectrum
may be maternal avitaminosis A. The
antibiotics are usually curative, but if
condition may be unilateral or bilateral, and swelling behind the last molar is present, it can occur with or without other ocular
drainage of this area is indicated. Wann
anomalies. Bilateral involvement is
compresses and topical lubricants to
manifest as blindness in the neonate; unilatprotect the cornea are also indicated.

eral involvement is often an incidental

Relapses may occur, and radiographs and
finding later in life or becomes manifest if
ultrasonography of the adjacent teeth,
the other eye acquires a blinding disease.

sinuses, and nasal cavity are reconm1ended.

Bilateral optic neuritis produces acute
blindness and dilated and fixed pupils. On

PROLAPSE OF THE EYE
ophthalmoscopy, the optic nerve head or
optic disc is raised, edematous with

Acute prolapse or proptosis of the eye
blurred margins and peripapillary
occurs as a result of trauma. It is common
hemorrhages, venous congestion, and
in dogs and infrequent in cats. Prognosis
often inflan1matory cells in the adjacent
depends on the extent of the traunia, the
retina and vitreous. Causes of optic neuritis breed of dog, depth of the orbit, duration of may vary by species affected and include
the proptosis, resting pupil size, condition
viral, mycotic, protozoan and parasitic
of the exposure keratitis, and other

OPHTHALMOLOGY

505
periocular damage. In cats, proptosis
intraocular hemorrhage, secondary
usually results from severe trauma to the
glaucoma, or retinal detachment.

head; often, other facial bones are fractured.

In cats, systemic diseases frequently

The globe should be replaced as soon as
affect the eye and associated structures.

possible if the animal's physical condition

Eyelid inflammations are often associated
will pemtit induction of general anesthesia
with systemic Demodex cati and D ga,toi, VetBooks.ir

(seep 1696). Treatment consists of

Notoedres ca,ti (scabies), ringworm, and
systemic antibiotics and occasionally
immune-mediated skin diseases. The
corticosteroids, combined with topical
pathogens that commonly cause infecantibiotics and mydriatics. Although the tious diseases of cats, eg, feline herpesviprognosis for retention of vision is guarded, rus 1, Chlamydia, andMycoplasma,,
the globe is usually saved. Return of vision
frequently present as acute and recurrent
occurs in -500/o of dogs but is rare in cats.

cortjunctivitis. Feline herpesvirus 1 is also
associated with ulcerative and stromal
keratitis, proliferative keratocortjunctivi

OPHTHALMIC MANIFESTATIONS
tis, corneal sequestrum, corneal syrn

OF SYST EMIC DISEASES
blepharon, and keratocortjunctivitis sicca.

Feline infectious peritonitis, toxoplasmo

Ophthalmic manifestations of systemic
sis, feline immunodeficiency virus, and
diseases are not uncommon with inherited,
feline leukemia virus often present as
infectious, degenerative, and neoplastic
anterior and posterior uveitis, chronic
disorders in animals. Often, ophthalmic
uveitis, retinal detachment, and secondexaminations can assist in tinlPly identifiary glaucoma. Acute vision loss with cation of the systemic disorder. Diseases
intraocular hemorrhage and retinal
affecting the vascular and nervous systems
detachment in older cats may be secondare likely to show ocular manifestations.

ary to systemic hypertension and is often

Animals with bilateral ocular disease
associated with chronic renal failure or
should be carefully evaluated for systemic
hyperthyroidism. Resolution of intraocudiseases.

lar hemorrhages, repair of the retinal

In dogs, ophthalmic diseases, such as
detachment, and possible restoration of
retinal dysplasia, microphthalmia, and
vision depends on the successful lowering
cataracts, have been associated with
of blood pressure to normal levels, often
dwarfism, albinism, and merling.

using amlodipine, an oral calcium channel

Infectious diseases often involve the uveal blocker.

tract and present as iridocyclitis, choroidi

In horses, systemic infectious diseases,
tis, and panuveitis. They may be caused by such as adenovirus in immunodeficient viruses (distemper, infectious hepatitis),

Arabian foals, equine influenza, strangles
rickettsial diseases ( ehrlichiosis and

(Streptococcus equi), Rhodococcus equi

Rocky Mountain spotted fever), bacteria
infection, leptospirosis, Lyme disease·

(Brucella, ca,nis and Borrelia, burgdo1°

(Borrelia, burgdorferi), and salmonellosis, Jeri), fungi (Blastomyces, Coccidioides, may present as conjunctivitis, anterior

Histopla,sma, Cryptococcus, and
uveitis, or posterior uveitis. Ophthalmic

Aspergillus), protozoa (Toxopla,sma,,
onchocerciasis can be markedly reduced

Neospora,, Leishmania,, and Hepa,tozoon), by frequent administration of ivermectin algae (Prototheca), or parasites (Dirofi
but can present with anterior and
laria, Toxocam, and Diptera, spp ).

posterior uveitis, peripapillary chorioreti

Metabolic diseases associated with eye
nitis, keratitis, keratocortjunctivitis, or
diseases in the dog include diabetes
lateral conjunctiva! vitiligo. Habronemiasis
mellitus (cataract formation), hypocalcepresents with inflammatory cortjunctival mia (cataracts), hyperadrenocorticism
masses of the periocular area ( especially

(corneal disease, cataracts, and lipemia
the medial canthus) associated with the
retinalis), and hypothyroidism (keratoaberrant migration of larvae of Habrone
conjunctivitis sicca, intraocular hemo1�
ma, muscae, H microstoma., and Draschia rhages from increased systemic blood
megastoma. Therapy is usually systemic
pressure, and lipemia retinalis [hyperlipiivermectin.

demia]). Blood and vascular disorders

In cattle, microphthalmia, cataracts,
may present as intraocular hemorrhage,
retinal dysplasia, and retinal detachments
retinal detachment, secondary glaucoma,
are associated with hydrocephalus and in
and pap ill edema. Metastatic neoplasms,
utero infection of calves with bovine viral
such as lymphosarcoma, most often
diarrhea. The same ophthalmic defects
affect the uvea, presenting as persistent
occur in lambs affected in utero with
uveitis, overt intraocular masses,
bluetongue virus. Vitamin A deficiency in

506

OPHTHALMOLOGY
piglets causes microphthaJmia, and in
calves blindness and optic nerve hypoplasia. Vitamin A deficiency in adult or growing cattle results in night blindness,
mydriasis, and eventually total blindness.

OphthaJmoscopic abnormalities include

VetBooks.ir
pap ill edema, retinal degeneration, and
optic nerve atrophy. Vitamin A supplementation may restore vision in animals with night blindness only. Lymphosarcoma in
cattle may present as bilateral progressive
exophthaJmia. Many infectious diseases,
such as rhinotracheitis, malignant
catarrhaJ fever, tlu·omboembolic
meningoencephaJitis, and neonatal
septicemia, may present with conjunctivitis or anterior or posterior uveitis.

Intoxications such as male fem poisoning

(Dryopteiisfllix), bracken fern poisoning

(Pteiidium aquilinum) in sheep,
coumarin poisoning (sweet clover
poisoning) in cattle, and phenothiazine
toxicity in cattle present with clinical
signs of blindness from retinal degenera

Conjunctiva! habronemiasis may be
tion, intraocular hemorrhage, or corneal
concurrent with "summer sores" in horses.

edema. (See also TOXICOLOGY, p 2948.) Courtesy of K. Ge/att.

CHLAMYDIAL CONJUNCTIVITIS

Etiology and Epidemiology: Chlan1y-·

Trachoma and inclusion conjunctivitis
diae are obligate intracellular bacteria that
in people are caused by C trachomatis.

form inclusions witllin the cytoplasm of

Chlamydia-like organisms (Parachla
epitlleliaJ cells. The life cycle of chlamy
mydia acanthamoebae) tlrnt reside and
diae involves an alternation between the
proliferate within free-living an1oeba have
intracellular reticulate body and tile exbeen detected in the eyes of cats, guinea tracellular elementary body, which is tile
pigs, pigs, and sheep witll conjunctivitis.

infectious fonn of tile organism. Several

The patl10genic role of tllese organisms
members of tile fantily Chlamydiaceae
and tlleir amoebic hosts is unclear.

have been associated witll conjunctivitis

Althoug]l tile disease in cats has been
in the host species they infect, including
referred to as feline pnewnonitis, chlan1y

Chlamydia caviae (guinea pigs), C suis
diae rarely cause pnewnonia in cats. The

(pigs), C psittaci (birds), and C pecorwrn infection always involves tile eye, occasion

( cattle and sheep). Altllough chlamydia]

aJJy causing signs of rhinitis, with sneezing
infection has been associated witll keratoand nasal discharge. Altllough antibody conjunctivitis in sheep and goats, a study
titers to C Jelis are common in some cat
that used molecular techniques to detect
populations, tile organism is rarely isolated
chlamydiae in sheep did not find a clear
from clinicaJly heaJtlly cats. Cats witll
association between infection and disease.

chlamydia! conjunctivitis are generally

Chlamydia! conjunctivitis in cats is caused

<l yr old, and cats 2--{) mo old appear to
by Cfelis (fo1merly Chlamydophilafelis).

be at highest risk of infection. Cats witll

C pneumoniae has also been detected in
conjunctivitis tllat are >5 yr old are very
cats witll conjunctivitis using molecular
wllikely to be infected, and cats <8 wk old
metllods. C psittaci has been isolated
may be less at risk because of tile presence
from dogs with keratoconjunctivitis and
of maternal antibody. Transmission occurs
respiratory signs in a dog breeding facility.

as a result of direct, close contact between

CHLAMYDIAL CONJUNCTIVITIS

507
cats, because the organism survives poorly
plasmic chlamydia! inclusions in exfoliative
in the environment. Infected cats also shed
cytologic preparations. Scrapings for
chlamydiae from their rectum and vagina,
cytologic exanlination are prepared by
although whether venereal transmission
lightly but fim1.ly moving a spatula over the
may occur has not been confirmed. There
conjunctiva and smearing the scraped
is weak evidence that chlamydiae may be
material onto a glas.s slide; the preparation is

VetBooks.ir
capable of causing reproductive disease and
air-dried and stained. Chlamydia! inclusions,
larnenes.s in cats, although these as.sociawhich contain reticulate bodies, are round tions have not been definitively documented.

and generally stain purple with Romanow

Chlamydia! infection is one of the most
sky stains. Conjunctiva! cytology from
common causes of conjunctivitis in guinea
guinea pigs generally reveals a neutrophilic
pig populations, in which it is also known
inflan1matory response. Inclusions are
as guinea pig inclusion conjunctivitis (see
generally visible only early in tl1e course of
p 2017). As with cats, young guinea pigs,
infection and sometimes not at all. Melanin
especially those 1-2 mo old, are predisgranules and renmants of some ophthalmic posed. Subclinical disease may also occw·.

preparations may be mistaken for inclu

Rhinitis, lower respiratory tract disease,
sions, leading to false-positives, so oilier
and genital infections, causing salpingitis
diagnostic tests are recommended to
and cystitis in female guinea pigs and
confirm ilie diagnosis.

urethritis in males, may also occur.

Prevention and Treatment: Vaccines

Clinical Findings: In cats, the incubation
are available for chlan1ydiosis in cats but
period after exposure to an infected cat
not for oilier species. Feline chlamydia!

ranges from 3 to 10 days. Signs can include
vaccines do not provide complete
serous to mucopurulent conjunctivitis,
protection from infection but may reduce
nasal discharge, and sneezing. Cats with
disease severity and infection rates. Their
signs of rhinitis in the absence of conj unctiuse may be considered in catteries where vitis are unlikely to be infected with C.felis.

chlamydiosis is endemic.

Early signs include unilateral or bilateral

All Chlamydia isolates are susceptible
conjunctiva! hyperemia, chemosis, and
to tetracyclines. The treatment of choice
serous ocular discharge, with prominent
is doxycycline (10 mg/kg/day) for at least
follicles on the inside of the third eyelid in

4 wk. Systemic ilierapy is superior to
more severe cases. Keratitis is rare, and if
topical ilierapy and is logical given that
present, may be the result of coinfection
organisms are shed from sites otl1er than
with organisms such as feline herpesvirus 1.

the conjunctiva. Treatment for up to 6 wk

The signs are most severe 9-13 days after
has been required to eliminate infection in
onset and then become mild over a 2- to
some cats. All cats in ilie household must be

3-wk period. In some cats, clinical signs
treated. Fluoroquinolones, such as enrofloxacan last for weeks despite treatment, and cin and pradofloxacin, and amoxicillinrecurrence of signs is not uncommon.

clavulanic acid, also have been used to

Untreated cats may harbor the organism
successfully treat feline chlamydiosis,
for months after infection.

although their efficacy may be less than

Guinea pigs may develop mild to severe
that of doxycycline. Aziiliromycin does not
conjunctivitis, with conjunctiva! hyperappear to be effective.

emia, chemosis, and mucopurulent ocular
discharge.

Zoonotic Risk: On rare occasions, C Jelis and C caviae have been isolated from

Diagnosis: Chlamydia! conjw1ctivitis in
people living wiili infected cats and guinea
cats should be differentiated from conpigs. Follicular conjunctivitis was desc1ibed junctivitis caused by feline herpesvirus l
in a single immunocompromised person
and feline calicivirus, and in guinea pigs
who was found to be infected with C Jelis.

from mycoplasmal and other bacterial

There was one report of detection of C
infections ( eg, "pinkeye"). Diagnosis is best caviae in a person with serous ocular
confim1ed using PCR for chlan1ydial DNA
discharge who worked wiili -200 diseased
on conjunctiva! swabs. Cell culture for
guinea pigs. C cavia.e was also detected in Chlamydia is sensitive and specific but not conjunctiva! swabs of tlus person's cat and
widely available or practical for routine
rabbit, ilie latter of which had signs of mild
diagnostic purposes. Special chlamydia!

conjunctivitis. Routine hygiene practices,
transport media is required for transport
such as hand washing before and after
of specimens for cultw-e.

handling sick pets, may reduce the potential

A diagnosis of ocular chlan1ydiosis can
for transmission of iliese organisms from
also be made by demonstration of intracyto-
affected animals to people.

508

EQUINE RECURRENT UVEITIS

EQUINE RECURRENT UVEITIS

(Periodic ophthalmia, Moon blindness, Equine uveitis) VetBooks.ir

Equine recurrent uveitis (ERU) is an
environment. Thus, the underlying cause of
important ophthalmic condition with a
the primary uveitis, genetic composition of
reported prevalence of 2o/o-25%worldwide.

the horse, and environmental factors are all

The classic form of ERU is characterized by
integral to the development of ERU.

episodes of active intraocular inflammation
followed by variable quiescent periods.

Clinical Findings and Lesions: Clinical

However, some horses experience insidious
findings associated with ERU include acute

ERU in which subclinical ocular inflammasigns of active inflammation as well as tion persists without obvious signs of
clu·oruc secondary complications. Changes in
discomfort. With chronicity, the inflammaocular in1muruty allow leukocytes to invade tory bouts cause secondary ocular changes
the uvea and release proinflammatory
such as cataracts, lens luxation, glaucoma,
cytokines such as prostaglandins and
phthisis bulbi, and retinal degeneration. As
leukotrienes. These inflan1matory mediators
a result, ERU is the most common cause of
cause increased vascular permeability within
blindness in horses in the world.

the uvea, breakdown of the blood-oculai·
barrier, iris sphincter muscle spasm,

Etiology and Pathogenesis: ERU is an
decreased aqueous humor production, and
autoinu11w1e syndrome that ensues after an
ciliary body muscle spasm. These changes
initial episode of acute uveitis. Although not
are responsible for the classic signs of acute
every horse with a single bout of uveitis will
uveitis: epiphora, blepharospasm, corneal
develop ERU, horses that have experienced
edema, episcleral congestion, aqueous flare
acute uveitis are at risk of developing ERU
and cell, and fibrin in the ante1ior chatnber.

for several years after the primary episode.

These anterior segment signs often reduce

While nwnerous bacterial, viral, protozoan,
visualization of the posterior segment. Active
parasitic, and noninfectious causes,
posterior segn1ent inflammation Call result in
including ocular trawna, have been linked to
vitreous haze secondary to cellular infiltrate,
the initiation of ERU, the pathophysiology of
fib1inous traction ballds, focal or diffuse

ERU is complex and multifactorial. Of the
retinal detachment, or chorioretirutis.

infectious causes investigated, Leptospim

Chrome sequelae of ERU include corneal
spp, especially L inten-ogans serogroup
scarring, iridal fibrosis, corpora rugra atrophy,

Pomona, have been most studied with regard posterior synechia, cataract, lens dislocation, to their role in the initiation of ERU. The
glaucoma, phthisis bulbi, and chorioretinal
precise mechanisms by which Leptospira
scarring. ERU call be tmilateral or bilateral
spp initiate ERU remain unknown, but it is
and can affect the eyes asyn1metrically.

likely that loss of ocular in1mune tolerance,

Horses with primary ocular disease,
cross-reaction between Leptospira
especially corneal disease, expe1ience
organisms and self-antigen, and intra- and
many clinical signs typical of ERU,
intem1olecular epitope spreading all play
especially epiphora, blepharospasm,
a critical role. There is no gender or age
miosis, and corneal edema. It is critical to
predisposition for ERU. However, Appaloodifferentiate primaiy corneal disease from sas, waimbloods, and draft breeds are

ERU considering the marked differences in
overrepresented among horses diagnosed
treatment. A complete ophthalmic exatllinawith ERU, which suggests a heritable tion at1d fluorescein stain ai·e essential. A
component. Genes of the major histocomthorough ophthalmic examination, includpatibility complex (MHC) have been most ing fundoscopy, is also critical during
widely investigated and likely play a role in
prepurchase or soundness exanlinations.

susceptibility to ERU and/or to leptospirosis

Horses with chronic ERU may exhibit
as an inciting trigger for ERU. The prevasubtle or no ante1ior segment signs but have lence of ERU varies with geographic region,
significat1t retinal degeneration alld thus
with higher rates reported in tropical and
potential for vision compromise.

temperate climates than in arid, dry climates,
an observation that may be pat1ially

Diagnosis: Diagnosis is based on
attributable to differences in persistence
characteristic clinical signs combined with a
of pathogenic Leptospira spp within the
history of recurrent or persistent episodes of

EQUINE RECURRENT UVEITIS

509
uveitis. A thorough ophthalmic examination
other day) doses of oral phenylbutazone or
of the anterior and posterior segment is
aspirin. Although most horses tolerate this
critical to observing signs consistent with
regimen well, these medications can have

ERU and to excluding other primary ocular
adverse GI, hematologic, or renal effects,
diseases. Tonometry should be performed in
and these regimens frequently do not
all cases to exclude glaucoma and document
eliminate recurrence. Systelnic steroids,

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hypotony that is common with ERU.

specifically pred!Iisolone (100-300 mg/day)

Application of fluorescein stain is important
and dexan1etl1asone (5-10 mg/day) have also
to assess corneal epithelial integrity and
been successfully used to treat acute uveitis
exclude reflex uveitis from ulcerative
episodes, but their longtern1 use has been
keratitis. In cases of acute uveitis, a physical
associated with larninitis. Except in cases
examination is performed to exclude
when bacterial infection is present, systelnic
systemic disease. A CBC and serum
antibiotics are not indicated.

biochemistry panel are often warranted as

Topical steroidal medications, including
part of the minimum database. Specific tests
dexamethasone (0.1 % suspension or
may assist in determining the underlying
ointment) and prednisolone acetate (1%
cause of a primary bout of uveitis. Serologic
suspension), are very effective at decreasing
testing for Leptospira spp may confirm expoinflanm1ation. Topical acetate and suspensure to this common risk factor but is not sion preparations of steroids a.re designed to
helpful in determining treatment. Anterior
penetrate tl1e cornea and achieve adequate
chamber or vitreous cavity paracentesis may
uveal concentrations and a.re thus preferred
aid in identifying a causative organism, but
to sodium phosphate fornmla.tions. Topical
this procedure may cause severe intraocular
hydrocortisone should be a.voided, because
damage and is not reconm1ended.

it lacks adequate corneal penetration and
is not sufficiently potent to treat anterior

Treatment, Prevention, and Control:

uveitis. A fluorescein stain is warranted

The primary goals of therapy are to reduce
before initiation of topical steroids, because
inflanm1ation, relieve discomfort, and
tl1ese medications are contraindicated witl1
prevent vision loss. If possible, the specific
corneal ulceration and/or infection. Topical
underlying cause should be diagnosed and
nonsteroidal medications include flurbiproaddressed as part of the initial treatment fen (0.03"Aisolution) and diclofenac (0.1%
regimen. Regardless of whether the
solution); they are less potent than topical
underlying cause is identified, aggressive
steroids but offer a wider safety margin in
treatment with systemic and topical
cases of concurrent corneal disease.

anti-inflanm1atory medications is initiated

Frequency of administration depends on
immediately to rni.ni.rni.ze damage from
inflammation severity; initially, administraintraocular inflammation. Flunixin tion may be 4-6 times daily. With improvemeglumine administered systemically ment in clinical signs, frequency of

( especially IV) is critical to the initial
administration of topical steroidal or
management of acute uveitis in horses. The
nonsteroidal medications can be gradually
typical initial IV dosage is 1.1 mg/kg,
decreased. However, therapy should
administered at the time of diagnosis,
continue for 1 mo after complete resolution
followed by a 5- to 7-day course at a dosage
of active inflanm1ation. Topical atropine ( 1 %
of 0.5-1.1 mg/kg, PO, bid. As inflammation
solution or ointment) ca.uses mydriasis
resolves, the dosage can be reduced to

( which decreases the likelihood of posterior

0.25--0.5 mg/kg once daily or every other clay
synechia fonnation) and cycloplegia. ( which
throughout a 1- to 3-mo treatment pe1iod.

decreases pain associated with ciliary body

Because of the potential for renal toxicity,
muscle spasm) and stabilizes the bloodserum creatini.ne is intermittently monitored a.queous barrier. Atropine is applied topically
if fluni.xin meglunune is used for > 1 mo.

2--3 times daily w1til the pupil is widely

Horses treated with flunixin meglwnine
clilatecl; tl1e frequency can then be adjusted
should also be observed for signs of GI
to maintain myd!iasis. Because atropine
ulceration, and concurrent prophylactic
decreases GI motility, horses treated with
ad!ninistration of omeprazole (2 mg/kg/day,
topical atropine should be monitored for

PO) may be indicated. Iffluni.xin meglunune
signs of ileus. If frequent topical medication
is not tolerated, phenylbutazone (2-4 mg/kg,
is not possible, subconjw1ctival injections of

PO, once to twice daily) or aspirin (10-25
triamcinolone acetanucle (1-2 mg) provide
mg/kg, PO, once to twice daily) can be used
adequate intra.ocular anti-inflanm1atory
alternatively, but neither is as potent or
concentrations for 7 -10 days and are less
effective. Historically, horses with frequent
likely to cause abscess or granuloma
recurrences or chronic, low-grade uveitis
formation than other steroids, including
were managed medically with daily ( or every methylprednisolone acetate (10-40 mg).

510

EQUINE RECURRENT UVEITIS

However, all subconjunctival steroids
aspect of the limbus. The vitreous is then
should be used with caution, because they
replaced with either balanced salt solution
cannot be easily removed once iJ\iected and
or saline. The theorized benefit of this
can have devastating consequences if an
procedure is that organisms, especially
infectious component is present or a corneal Leptospira spp, and/or inflammatory cells ulcer develops.

in the vitreous significantly contribute to

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Two surgical procedures are commonly
the chronic inflanunation ofERU. By
used in longterm management. A suprachoremoving these factors, the frequency and roidal cyclosporine implant is a sustainedseverity of uveitic episodes are minimized.

release medication device that provides ther

Good husbandry practices to manage
apeutic concentrations of cyclosporine A,

ERU ensure proper health maintenance,
an immunosuppressive T-cell inhibitor, for
prevent ocular trauma, and reduce

-3 yr after implantation. During this proenvironmental triggers. Specific managecedure, a cyclosporine A disk ( -5 mm in ment recommendations include routine
diameter) is implanted under a scleral flap
dewornling and vaccinations, proper
created -8 mm posterior to the dorsolatnutrition and dental care, a quality fly mask, eral aspect of the limb us. Horses with
minimizing contact with cattle or wildlife,
implants have markedly fewer uveitic
draining stagnant ponds or restiicting access
episodes than they did before surgery, and
to swampy pastures, effective fly control,
this device results in effective longterm
and frequent bedding changes. Although
control of ERU. Core vitrectomy removes
such measures benefit individual horses, the
virtually all of the vitreous through an
extent to which they impact the clinical
incision posterior to the dorsolateral
course of ERU has not been evaluated.

EYEWORM DISEASE

(Thelaziasis)

LARGE ANIMALS
secretions; the larvae are ingested by the fly
and become infective in 2-4 wk. Infective

Etiology and Epidemiology: Eyethird-stage larvae emerge from the labellae worms (Thelazia spp) are common
of infected flies and are mechanically
parasites of horses and ca.ttle in many
deposited in the host's eye by the fly during
countries, including those of North
feeding. Development of sexually mature

America. Horses are infected primarily by
worn1s takes 1-4 wk in cattle, depending on

T lacrymalis, whereas cattle are mainly
worm species, and 10-11 wk for T lacry
infected by T gulosa, T skrjabini, and
malis in horses. Infections may be found

T rhodesii. The latter is the most common
year-round, but clinical disease outbreaks,
and harmful to cattle in the Old World, but
particularly in cattle, usually are associated
it has not been recently reported in North
with warm season activities of the flies.

America. The prevalence of Thelazia spp

Thelazia sp larvae may overwinter in face
in livestock has declined in at least some
flies. Infection rates generally tend to
areas where macrocyclic lactone endectoincrease witll advancing host age, although cides such as ivennectin and doramectin
some studies report maxin1al levels in hosts
are in common use. Thelazia spp are also

2 -3yr old.

found in pigs, sheep, goats, deer, water
buffalo, dromedaries, hares, dogs and cats

Pathogenesis: The lacrimal gland and its

(seep 512), birds, and people.

ducts are conunon sites for T lacrymalis

The face fly, Musca autumnalis, is the
and T gulosa, with the glands of the
vector of T lacrymalis, T gulosa, and
nictitating membrane and the nasolacrimal

T skrjabini in North America. Feeding
ducts less so. T skrjabini is normally found habits of this fly include a preference for
within the lacrimal ducts of the nictitating
ocular secretions, which are ideal for
membrane. Superficial locations on the
transmission. The life cycle of Thelazia is cornea, in the cortjunctival sac, and under
as follows: female wom1s are ovovivipathe eyelids and nictitating membrane are rous and discharge larvae into the ocular
more typical for T rhodesii, but T lacryma-

EYEWORM DISEASE

511
lis, T skrjabini, and T gulosa may be found yellow, plaque-like "sulfur granules" 1 -2
in these sites, too. Wonns may also be
mm in diameter. Likewise, microfilariae of
found on the periorbital hair or skin dming

Onchocerca sp invade the eye and may
anesthesia or following migration after
result in ophthalmic manifestations.

death of the host. Localized irritation and

Small ( <l mm), raised, white nodules in
inflammation is likely due to the serrated
the pigmented conjunctiva adjacent to

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cuticle of the worms, especially for
the temporal limbus are pathognomonic

T rhodesii. Invasion of the lacrin1al gland of Onchocerca infection. Depigmentation
and excretory ducts may cause inflan1maof the bu I bar conjunctiva in this area is tion and necrotic exudation. Inflan1mation
also common. Other lesions of onchocerof the lacrimal ducts and sac has also been ciasis involve the cornea and include
reported in horses. Mild to severe conjuncedema and punctate or streaking tivitis and blepharitis are common. Also,
opacities of the stroma, superficial
keratitis, including opacity, ulceration,
erosions, and a wedge-shaped sclerosing
perforation, and permanent fibrosis, may
keratitis emanating from the temporal
develop in severe cases, particularly with
limbus. Intraocular structures also may

Trhodesii infection in cattle.

be affected by microfilariae of Onchocerca sp (seep 905). Worms may be Clinical Findings and Diagnosis:

identified morphologically. In addition,

Asymptomatic infections in horses and

PCR and sequencing assays have been
cattle appear to be typical of thelaziasis
developed to confirm the identity of some
in North America. Infection may be
species, but these are not used routinely.

encountered incidentally during surgery
or at necropsy. However, 17ielazia

Treatment and Control: Mechanical
infections in cattle in North America may
removal with forceps after instillation of
not always be innocuous. They may
a local anesthetic is useful for Trhodesii
produce mild conjunctivitis, excessive
in cattle. This also may be feasible for the
lacrimation, localized edema, corneal
more invasive T gulosa or T sk1jabini in clouding, and occasionally, subconjuncticattle or for T lacrymalis in horses.

val cysts. In Europe and Asia, thelaziasis

Irrigation of the eyes with 50-75 mL
is commonly associated with severe
aqueous solution of 0.5% iodine and 0. 75%
clinical manifestations, including
potassium iodide has been recommended
conjunctivitis, photophobia, and keratitis.

for T gulosa and T skrjabini. This also Characteristically, there is chronic
may be effective for T lac1ymalis in
conjunctivitis with lymphoid hyperplasia
horses. Topical application of 0.03%
and a seromucoid exudate.

echothiophate iodide or 0.025% isofluro

A clinically feasible technique for
phate (both organophosphates) has been
reliable detection of adult eyeworrns is
successful for T lacnJmalis in horses.

lacking. Gross inspection of the eyes may

Concurrent use of antibiotic-steroid
reveal the worms and is generally
ointment for the inflammation and
recommended for Trhodesii, commonly
secondary invaders is recommended.

found in the conjunctiva! sac. However,

These topical agents should also be useful

T gulosa and T skrjabini in cattle, and for T gulosa and T skrjabini in cattle.

T lacrymalis in horses, tend to be more

Certain systemic anthelmintics have
invasive and are less apt to be seen. Topical
exhibited activity against eyeworms.

anesthetics allow for tissue manipulation

In cattle, levan1isole at 5 mg/kg, SC,
and are useful for detection and recovery
and ivermectin and doramectin, both at
of worn1s. Microscopic examination of

0.2 mg/kg, SC or IM, have shown activity
lacrimal fluids for embryonated eggs or
against Thelazia spp. Pour-on formulalarvae may be attempted.

tions of ivermectin or doramectin,

Clinical signs may be helpful in
delivered to achieve a dosage of 0.5 mg/kg,
differential diagnosis. Thelaziasis tends
are also effective. Doran1ectin has been
to cause a chronic conjunctivitis. In
approved in the USA for treatment of adult
cattle, infectious keratoconjunctivitis
eyeworms in cattle. For T lacrymalis in

(see below) is an acute, rapidly spreading
horses, single doses of the commonly used
infection of the cornea. In horses,
anthelmintics, including ivermectin,
infective larvae of the stomach worms
administered via stomach tube at 0.2

Draschia and Habronema sp may also mg/kg, have had limited, if any, effect on
produce ophthalmic lesions. These tend
eyeworms. In contrast, the multidose
to occur near the medial can thus of the
regimen of fenbendazole (10 mg/kg/day
eyelid and are raised, ulcerative granulofor 5 days) is efficacious against mas, often containing characteristic

T lacrymalis.

512

EYEWORM DISEASE

Fly control measures, directed especially variegata in Europe and Amiota spp against the face fly, aid in the control of
in Asia.

thelaziasis in cattle and horses. Cattle on

Clinical signs include excessive
dry, open pastures have fewer face flies
lacrimation and epiphora, ocular pruritus,
than those on pastures where shade and
conjunctivitis, keratitis with corneal
water are present.

opacity and ulceration, hyperemia, and

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rarely, blindness. After local anesthetic,
diagnosis and treatment are readily accom

SMALL ANIMALS
plished by observing and removing the
parasites with forceps. Thelazia spp

Thelazia californiensis is found in
infections have been successfully
dogs, cats, and deer in western USA; T
eliminated from dogs with ivermectin
callipaeda is found in dogs, cats, foxes,

SC at 0.2 mg/kg, milbemycin oxime PO
wolves, martens, and rabbits in Europe
at a minimum dosage of 0.5 mg/kg (two
and Asia. T callipaeda appears to be
treatments l wk apart improved efficacy),
spreading in some regions of Europe.

or spot-on treatment with moxidectin 2.5%.

Both species are zoonotic. The worms

Ocular solutions (1% moxidectin or 2%
are whitish, 7-19 mm long, and move in
levamisole) or ointments (1% levamisole
a rapid serpentine motion across the
or 4% morantel) also may be effective.

eye. Up to 100 eyeworms may be seen in

Infection with T callipaeda has been
the conjunctiva! sac, tear ducts, and on
prevented for the full season in dogs with
the conjunctiva under the nictitating
sustained-release moxidectin at 0.17 mg/
membrane and eyelids. Filth flies (Musca
kg, SC, with milbemycin oxime PO at the
spp, Fannia spp) serve as intermediate
dosage recommended for heartworm
hosts and deposit infective larvae on the
prevention, and with ivermectin PO at 0.2
eye while feeding on ocular secretions.

mg/kg. Milbemycin oxime at the minimum

Zoophilic fruit flies have emerged as
oral dosage of 2 mg/kg showed high
potential intermediate hosts of T
therapeutic efficacy in cats infected
callipaeda. These include Phortica
with T callipaeda.

INFECTIOUS KERATOCONJUNCTIVITIS

(Pinkeye, Infectious ophthalmia)

Infectious keraj;oconjunctivitis of cattle,
plasma spp may cause conjunctivitis of
sheep, and goats is characterized by
cattle, either alone or in conjunction with
blepharospasm, conjunctivitis, lac1irnation, M bovis. Infection with IBR virus or other and varying degrees of corneal opacity and
microbes may increase the severity of
ulceration.

infection withM bovis. Another Mornxella Infectious bovine keratoconjunctivitis
species that has been frequently isolated

(IBK) is the most common ocular disease
from eyes of cattle with IBK is Moraxella
of cattle and is seen worldwide. The
bovoculi (not to be confused with Myco
gram-negative rod Moraxella bovis is the
plasma bovoculi). Recent studies do not
only organism demonstrated to cause IBK
support a role for Moraxella bovoculi
in cattle. Seven different serogroups of
as a p1imary pathogen in causing corneal

M bovis are currently recognized. Most
ulceration associated with IBK. It is likely
other ocular infections of cattle are
that Moraxella bovoculi may act as a risk
characterized by conjunctivitis with
factor for IBK by causing conjunctivities
minimal or no keratitis. The primary
similar to other risk factors for infectious
differential diagnosis is infectious bovine
agents such as Mycoplasma spp and IBR
rhinotracheitis (IBR), which causes severe
virus. Moraxella bovoculi has also been
conjunctivitis and edema of the cornea that
reported in cases of infectious keratoconoriginates near the limb us; however, junctivitis in reindeer. Plant awns, face
corneal ulceration is uncommon. Myca-
flies, ultraviolet radiation from bright

INFECTIOUS KERATOCONJUNCTIVITIS

513

Initially, the cornea around the ulcer is cleai·
but within a few hours a faint haze appears
that subsequently increases in opacity.

Les10ns may regress in the eai·Jy stages or
may continue to progress. After 48---72 hr in
severe cases, the entire cornea may become
opaque, blinding tile animal in tl1at eye.

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Blood vessels may invade the cornea from
the limbus and move toward the ulcer at -1
nlITllday. Corneal opacity may result from
edema (hazy white to blue corneas), which

1s a part of tl1e inflammatory process or

Infectious bovine keratoconjunctivitis with
leukocyte infiltration (milky white td yellow corneal ulceration in a calf. Note severe
corneas), which indicates severe infection.

corneal edema (o

Continued active ulceration may cause
pacity), corneal neovascularization, and ep1phora. Courtesy of corneal rupture. Relapse may occur at any

Dr. John A Angelos.

stage of recove1y.

Diagnosis: In all species, presumptive
sunlight, dry and dusty environmental
diagnosis is based on ocular signs and
conditions, and shipping stress are all risk
concurrent systemic disease. It is
factors associated with IBK in cattle. In
important to distinguish iliat the lesions are
cattle, additional risk factors that should be not due to foreign bodies or pai·asites (see considered when making herd managep 510). In IBR, upper respirato1y signs and ment decisions include trace mineral
conjunctivitis predominate, while keratitis
deficiencies such as selenium and copper
accompanied by ulceration is rare. In
deficiency. Flies can also serve as vectors
bovine malignant catarrhal fever, respira
forM bovis.

to1y signs are prominent with primaiy

In sheep
uve1t1s and associated keratitis. Microbial

_and goats, naturally occurring

CO!\Junct1V1t1s or keratoconjunctivitis can
culture may be beneficial in confiTming
be associated with Chlamydia pecorum,
the causative organisms. Chlamydia and

Mycoplasma spp (notably M conjunctivae), Mycoplasma spp require special media· the Moraxella ovis, Colesiota conjunctivae
diagnostic laboratory should be consulted

Listeria monocytogenes, Acholeplasmd
before sample collection. Cytologic
oculi, and Thelazia spp.

evaluation of stained slides prepared from
conjunctival scrapings of sheep and goats

Clinical Findings: The disease usually
may reveal Chlamydia organisms;

IS acute and tends to spread rapidly. In all
however, mtracytoplasmic inclusion
species, young animals are affected most
bodies can be difficult to recognize. PCR
frequently, but animals of any age are
analysis can be used to detect Chlamydia
susceptible. One or both eyes may be
and Mycoplasma spp.

affected. The earliest clinical signs are photophobia, blepha.rospasm, and epiphora; later, the ocular discharge may become mucopu

Prevention and Treatment: Good
rulent. Conjunctivitis, witl1 or without
management practices are of paramount
varying degrees of keratitis, is usually
importance to reduce or prevent spread
present. In sheep and goats, concurrent
of infection in cattle, sheep, and goats.

polyarthritis may be present in association

Separation of infected animals is beneficial
with C pecorum infections. Appetite may be
when possible. Gloves and protective
depressed because of ocular discomfmt or
clothing should be worn and then
visual disturbance tl1at results in inability to
disinfected between animals when
locate food. The usual clinical course vaiies
affected individuals are being handled.

from a few days to several weeks. Most

Temporary isolation and preventive
corneal ulcers in cattle wiili IBK heal wiiliout treatment of animals newly introduced loss of vision; howeve1� corneal rupture and
to the herd may be helpful, because some
permanent blindness can occur in the most
of these animals may be asymptomatic
severe cases.

carriers. Ultraviolet radiation from
sunlight may enhance disease (particularly

Lesions: Lesions vary in severity. In
m cattle); therefore, affected animals
cattle, one or more small ulcers typically
should be provided with shade. Dust bags
develop near the center of the cornea.

or insecticide-impregnated ear tags can be

514

INFECTIOUS KERATOCONJUNCTIVITIS
used to reduce the number of face flies
with penicillin. In the USA, long-acting

(Musca autumnalis), an important vector
oxytetracycline (two injections of 20 mg/
forMbovis.

kg, IM or SC, at a 48- to 72-hr interval) and

M bovis bacterins are available and can
tulathromycin (2.5 mg/kg, SC, given once)

be administered before the beginning of
are currently approved antibiotics to treat
fly season. Cattle should be started on

IBK in cattle. Other effective antibiotics

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M bovis vaccine series 6-8 wk before the
include ceftiofur crystalline free acid (6.6
anticipated first cases of IBK to allow
mg/kg, SC, at the base of the ear) and
time for adequate immune responses to
florfenicol (20 mg/kg, IM, two doses at
develop. The efficacy of current commera 2-day interval). A single injection of cially available M bovis bacterins is
long-acting oxytetracycline (20 mg/kg,
controversial and likely varies because

IM) along with oral oxytetracycline (2 g/
of vaccinal versus outbreak strains of
calf/day for 10 days) fed in alfalfa pellets

M bovis and varying degrees of crosshas also been shown to be effective at protection afforded by vaccination.

reducing severity of IBK during a herd

Vaccination may reduce the severity and
outbreak. Topical applications of
duration of infection in affected animals.

ophthalmic preparations should be

IBR may predispose cattle to infection
applied at least three times a day to be
with M bovis; thus, vaccination of herds
effective, and thus are often not costagainst IBR may reduce outbreaks of effective or practical in herd settings.

M bovis. The use of modified-live IBR

Effective antibiotics for topical ophthalvaccines has been associated with mic use include triple antibiotic,
outbreaks of IBK in cattle; IBR vaccinagentamicin, and a combination oxytetration must be appropriately timed with cycline/polymyxin B ointment. A
cattle shipments so that these events do
third-eyelid flap or partial tarsorrhaphy,
not coincide. Vaccination of cattle with a
which will shade the cornea from
modified-live IBR vaccine could likely
sunlight, together with subconjunctival
exacerbate an outbreak of IBK associated
injection, may reduce morbidity in severewith M bovis and/or Moraxella bovoculi ly affected animals. A temporary eye
because of increased ocular and nasal
patch glued to the hair surrounding the
secretions spreading bacteria between
eye is an inexpensive and easily applied
herdmates as well as corneal epithelial
treatment. The eye patch provides shade,
damage. In recent studies, the efficacy of
prevents exposure to flies, and may help
autogenous Moraxella spp bacterins to
to decrease spread of organisms.

prevent IBK has not been demonstrated

For sheep and goats in which chlamydia!

in randomized controlled field trials.

and mycoplasmal infections are suspected,

Nevertheless, anecdotal evidenee has
respectively, topical tetracycline,
suggested that, for some herds, M bovis
oxytetracycline/polymyxin B, or erythroand/or Moraxella bovoculi autogenous mycin ointments are treatments of choice.

bacterins have provided benefit in

These preparations are all effective against
reducing IBK problems. It is unlikely

ChJ,amydia or Mycoplasma and should be that any Moraxella spp vaccine will ever
applied 3-4 times daily. If topical therapy is
completely control JBK in the face of
not practical, long-acting oxytetracycline
overwhelming challenge from and

(20 mg/kg, IM) or the addition of oxytetraexposure to other risk factors such as cycline to the feed (80 mg/animal/day) may
flies, dust, other infectious agents, and
be beneficial.

trace mineral deficiencies. As such,

Animals with substantial uveitis
planning and implementing a successful
secondary to keratoconjunctivitis that

IBK control program should address
is particularly painful may benefit from
multiple issues that may potentially
topical ophthalmic application of 1%
reduce susceptibility of cattle to IBK
atropine ointment 1-3 times daily. This
beyond just vaccines againstMoraxella
will prevent painful ciliary body spasms
spp.

and reduce the likelihood of posterior

M bovis is susceptible to many
synechia formation that occurs with
antibiotics. Because antibiotic susceptimiosis. Because of mydriasis caused by bility may vary in different geographic
atropine, treated animals should be
locations, bacterial culture and susceptiprovided with shade. Systemic NSAID
bility testing is advised. One common
treatment may be used to provide relief
treatment is bulbar conjunctiva! injection
from secondary uveitis.

NEOPLASIA OF THE EYE AND ASSOCIATED STRUCTURES

. 515

NEOPLASIA OF THE EYE AND

ASSOCIATED STRUCTURES

The different tissues of the eye and
or a hyperkeratotic lesion ( cutaneous

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associated structures can be the site of
horn). While in this benign stage, -30% may
ptimary or metastatic neoplasms. Ophthalspontaneously regress. The tun10r may mic neoplasms vary in histologic type,
become quite large without invading the
frequency, and in1portance in different
globe, but invasion into the eye and orbit
species and are a signillcant group of
and metastasis to parotid and submandibudiseases in veterinary ophthalmology.

lar lymph nodes occur in late stages of the
disease. Diagnosis usually is made by the

CATTLE
typical clinical appearance but can be
confirmed rapidly by cytologic exantina

The most frequent ophthalmic neoplasms in
tion of impression smears. The intraocular
cattle are the squan1ous cell carcinoma comtumor invasion must be differentiated from plex and the orbital infiltration assoseverely damaged and disorganized eyes ciated with lymphosarcoma (seep 743).

after trauma or advanced infectious

The latter, with extensive invasion of the
keratocortjunctivitis (seep 512).

orbital structures, results in progressive

Squamous cell carcinomas may respond
bilateral exophthalmia, reduced ocular
to excision, cryotl1erapy, hyperthermia,
mobility, exposure keratitis, and corneal
radiation therapy, local chemotherapy
ulcerations that can lead to perforation.

using 5-fluorouracil, immunotherapy, or

Ocular squamous cell carcinoma ( cancer
often a combination of these therapies.

eye) is the most common neoplasm of cattle.

Surgical excision is indicated for small

It results in significant economic loss due to
lesions or for debulking the larger lesions
condemnation at slaughter and a shortened
before cryotherapy or hyperthe1mia.

productive life. It occurs more frequently in

Superficial keratectomy can be used to
the Bos taurus than the Bos ind:icus breeds, excise the limbal plaques, papillomas, and
and it is seen most often in Herefords, less
squan10us cell carcinomas. After superfioften in Simmentals and Holstein-Friesians, cial keratectomy and twnor removal,
and rarely in other breeds. The peak age of
cryotherapy, hyperthermia, or a permanent
incidence is 8 yr, actual incidence varies from
bulbar cortjunctival graft have yielded

0.896 to 5.0'Ai an10ng herds. 'I11e cause is
excellent short-term results, but recurmultifactorial, with heritability, sunlight, rence at the same or a different site is -25%.

nutrition, eyelid pigmentation, and perhaps

For advanced lesions confined to the
viral involvement playing roles. The medial
globe, enucleation is reconunended. When
and lateral limbal regions ( corneoscleral
adjacent tissues are affected, removal of the
junction) are affected most frequently, but
globe and all orbital contents ( exenteration)

tile eyelids, cortjunctivae, and nictitating
should be performed. Imrnunotherapy is
membrane may be affected. Bilateral
involvement varies but can be as high as 35%

Eyelid and cortjunctival pigmentation are
highly heritable and can reduce the frequency
oflid squan1ous cell carcinomas, but they have
limited effect on the development of tun1ors of
the cortjunctiva and nictitating membrane.

The cancerous or precancerous lesions are
bilateral or multiple in the same eye in -28% of
cases. Ultraviolet radiation and a high plane of
nutrition are contributing factors. 'I11e viruses
of infectious bovine rhinotracheitis and
papilloma have been isolated from tl1e
neoplasms, but their significance is unknown.

The lesions usually begin as benign,
smooth, white plaques on tl1e cortjunctival
surfaces; they may progress to a papilloma
and then to a squan1ous cell carcinoma or
go directly to the malignant stage. Lid

Squamous cell carcinoma, eyelid, cow.

lesions usually begin as either an ulcerative Courtesy of K. Gelatt.

516

NEOPLASIA OF THE EYE AND ASSOCIATED STRUCTURES
still experimental, and the resulting tumor
is sin'lilar to that in cattle, although
regression may be temporary. Radiation
presentation for treatment is usually earlier,
therapy is not practical in the field but may
and greater emphasis is placed on cosmetic
be an option for valuable animals.

appearance after therapy. Surgical excision

Owners of problem herds should be
for equine squamous cell carcinoma yields
advised of the heritability factor, with

-500/o success when used alone. When

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affected animals and their offspring culled
surgery is combined with cryotherapy,
to decrease the incidence of tumors. Active
hypertherrnia, or local chemotherapy, the
breeding bulls with ocular squamous cell
success rate is markedly increased. As
carcinoma should be culled.

expected, small squamous cell carcinomas
can be excised more widely, and the need

HORSES
for later reconstrnctive blepharoplasties
or corneocoajunctival surgeries is more

In horses, tumors of the skin, eye, and
limited. Often, referral to specialty services
genital system are the most frequent, and
tl1at routinely treat these types of neoplasms

-800/o of eye neoplasms are malignant.

can yield the best possible outcomes. The

Neoplasms of the eyelids and coajunctivae
preventive role of face shields or masks with
are the most frequent ophthalmic tumors
the goal of reduced ultraviolet exposure to
in horses; most are either squamous cell
the external eye is unknown, but their use
carcinoma or sarcoid. Orbital neoplasms
should start at a very young age.

are rare and are usually local extensions

The equine sarcoid (seep 954) generally
of eyelid, coajunctiva, or sinus tumors or
affects young horses ( average 3.8 yr old) and
systemic neoplasms, including lymphosa.rrepresents -400/o of all neoplasms in horses.

coma. lntraocular neoplasms, usually

Because sarcoids are locally destructive and
malignant melanomas, are rare.

have a high recurrence rate after surge1y,

Squamous cell carcinoma occurs most
effective treatment when the periocula.r
frequently in horses 8--10 yr old and may
tissues are involved presents cosmetic and
occur more frequently in those with non- or
functional problems. Sarcoids are grouped
lightly pigmented eyelids. The Appaloosa
into occult, verrncose, nodular, fibroblastic,
and draft breeds are affected most
mixed, and malignant types, and they are
frequently. Ultraviolet radiation may be
divided histologically into neurofibroma,
important, because the incidence in North
neurofibrosarcoma, myxosarcoma, and

America is higher in southern and western
fibromyxosarcoma. They appear initially as
mountainous areas and in areas of increased subcutaneous masses in the eyelids or altitude or mean solar radiation. The eyelids
canthi; they usually enlarge rapidly and may

(-15%), coajunctivae and limbus (-25%),
invade the skin, appearing as red, fleshy
and nictitating membrane ( -300/o) caH be
masses. Treatment is surgery, hypertherrnia,
affected with ulcerative or proliferative
cryotherapy, chemotherapy, radiation, or a
masses. Bilateral involvement is infrequent
combination of these therapies. After

(-15%). Squan10us cell carcinoma of the
attempts to surgically remove the sarcoid,
nictitans is more likely to invade the orbit
recurrence may be rapid and precede wound
than are those from other sites. Treatment
healing. Immunotherapy using BCG (bacille
of ocular squamous cell.carcinoma in horses Calmette-Guerin) as a potentiator of the cellular inunune system is often successful

( -700/o). ll\iections should be repeated at

2- to 4-wk intervals until the mass disappears. Systemic corticosteroids and antiprostaglandins before and after treatment may decrease the likelihood of systemic
anaphylactic reactions. Ganuna radiation
therapy using platinun1-sheathed iridium !92
is highly successful ( -95%) but less
convenient and available and usually
requires a total dose of7,000-9,000 rads.

DOGS

Fleshy mass representing squamous cell

Eyelid neoplasms are the most frequent
carcinoma of the limbus in a white horse. The
group of ophthalmic neoplasms in dogs.

area should be closely examined, because

Adenoma and adenocarcinoma of the
this mass often can be removed by keratecmeibomian gland are the most common lid tomy and covered by a permanent advancing neoplasms ( -600/o) in older dogs; local disfigbulbar conjunctiva! graft. Courtesy of K. Gelatt.

urement and irritation necessitate excision,

NEOPLASIA OF THE EYE AND ASSOCIATED STRUCTURES

517
which is usually successful. Meibomian
is guarded or poor; 25%-400/o of affected

(sebaceous) adenocarcinomas are locally
dogs are euthanized on diagnosis. Surgery,
invasive and histologically malignant but
sometimes combined with chemotherapy,
are not known to metastasize. Lid melanocan often prolong life for �6 mo.

mas, exhibited as spreading pigmented

Corneal and limbal neoplasms are
masses on the eyelid margin or a mass
uncommon in dogs and can be confused

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within the lid, should be widely excised.

with nodular fasciitis and proliferative

Other frequent eyelid neoplasms include
keratocoajunctivitis in Collies. Biopsy is
histiocytoma, mastocytoma, and papilloma
often necessary to establish the diagnosis
and may require biopsy to deternline the
and the specific plan for the best therapy.

best mode of therapy and prognosis. The

Limbal or epibulbar malignant melanomas
vast majority of canine eyelid neoplasms
are focal, usually superficial, pigmented
are treated successfully by only surgical
masses that extend both onto the cornea
excision.

and caudally toward the globe's equator.

Canine conjunctival neoplasms have a

After close intraocular examination (includgreater propensity for maligancy and local ing gonioscopy and B-scan ultrasonograinfiltration than eyelid neoplasms and phy) to detect possible penetration of the
require more extensive surgical excision.

sclera, partial to full-thickness surgical

Because recun-ence may occur, periodic
excision with scleral grafts, cryotherapy, or
reexaminations are recommended.

laser photocoagulation is usually success

Orbital neoplasms in dogs produce
ful. If intraocular extension occw"S,
exophthalmia, coajunctival and eyelid
enucleation is performed.

swelling, strabismus, and exposure

Melanomas are the most common uveal
keratitis. The globe cannot be retropulsed.

neoplasm, are usually pigmented, and most

Usually, there is no pain. Because -900/o of
frequently involve the ilis and ciliary body,
the neoplasms are malignant and -75% arise
with the latter being the site of migin. Chowithin the orbit, the prognosis for longterm roidal melanomas, conunon in people, are
survival is often poor. The most frequently
rare in dogs. Clinical signs of anterior uveal
diagnosed tumors include osteosa.rcomas,
melanomas may iI1clude an obvious mass,
fibrosarcomas, and nasal adenocarcinomas.

persistent ilidocyclitis, hyphema, glaucoma,

The neoplasm type should be detennined
and pain. These melanomas are divided into
histologically, and the extent of the mass
melanocytic melanomas (800/o--900/o) and
detennined by physical exanlination, skull
malignant melanomas (100/o--15%). Metastaradiographs (including special contrast sis is infrequent ( <5%). Ciliary body adenoma
procedures, CT, and MRI), and ultrasonograand adenocarcinoma are the most frequent phy before treatment by surgical excision or
epithelial neoplasms of the anterior uvea.

radiation. Excision of the orbital mass with

Signs may include hyphema, glaucoma, and
the globe and all orbital tissues (including
usually a nonpigmented mass behind the ilis
adjacent bone) may decrease the possibility
and in the pupil. Neoplasms of nemoectoderof recUffence but is more disfiguring, mal origin are rare. Treatment is usually
especially in shorthaired dogs. Prognosis
enucleation. Recent stuclies in ilidal
melanomas, especially in young Labrador

Retrievers, suggest that noninvasive diode
laser photocoagulation may be effective and
can be repeated if necessary, thereby
avoiding enucleation.

Secondary uveal adenocarcinomas are
relatively infrequent and 01iginate from a
nw11ber of distant sites. Other neoplasms,
such as transmissible venereal tun10r and
hemangiosarcoma, may metastasize to the
anterior uvea. Lyrnphosarcoma frequently
involves the anterior uvea and other ocular
structures and may present as bilateral
disease. Systemic therapy with topical and/
or systemic anti-inflammatory treatment for
iI1traocula.r lymphoma may be attempted
using one of several available lymphoma
protocols ( eg, combination of cyclophos

Lid masses in dogs are mostly adenomas or
phamide, preclnisolone, vincristine, and/or
adencarcinomas that arise from the meibomian
doxorubicin), but dogs with botl1 intraocular
glands. Surgical excision is usually effective,
and systemic lymphoma have shmter
with infrequent recurrence. CourtesyofK. Gelatt.

swvival tin1es.

518

NEOPLASIA OF THE EYE AND ASSOCIATED STRUCTURES

CATS

Ocular neoplasms are less frequent in cats
than in dogs and tend to be more malignant. Approximately 2% of feline patients present with neoplasia, and of these, 2% are

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affected with ophthalmic tumors. Eyelid
and conjunctiva! tw11ors are the most
frequent primary ophthalmic neoplasms.

These neoplasms are usually malignant and
more difficult to treat in cats than in dogs.

Squamous cell carcinomas, which are more
conunon in white cats with nonpigmented
eyelid margins, can involve the eyelids,

Diffuse iridal melanoma in a cat, with
conjunctivae, and the nictitating memprogressive pigmentation of the anterior surface of the iris. Courtes
brane; they are pink, roughened, irregular
y of K. Ge/att.

masses or thickened ulcerations. Other less
frequent neoplasms include adenocarcino

Feline lymphosarcoma-leukemia
mas, fibrosarcomas, neurofibrosarcomas,
complex (FeLLC) is the most common
and basal cell carcinomas. Treatment
secondary ocular neoplasm. Cats with
varies with the tumor type, location, and
ocular FeLLC have clinical signs ranging
size and includes surgical excision,
from isolated ocular lesions (affecting one
radiation therapy, and cryotherapy. Prognoor both eyes) to severe systemic illness.

sis for these malignant twnors is poor, with

Corneal abnorn1alities may include
survival of only 1-2 mo.

keratitis, edema, neovascularization,

The most common prin1ary intraocular
corneal infiltrates, and hemorrhages within
neoplasm in cats is diffuse iridal melathe stroma. Ulcerative keratitis may result.

noma, which presents as progressive

Masses can be found in the orbit, globe,
hyperpigmentation of the iris with an
conjunctivae, and eyelids. Pupillary
expanding irregular surface. Pupillary
abnorn1alities, including mydriasis,
abnormalities, secondary glaucoma due
anisocoria, spastic pupil syndrome, "D"

to iridocomeal angle obstruction, and
or reverse "D" pupil shape, and lack of
buphthalmia occur late in the disease.

light-induced pupillary reflexes, may

Enucleation is recommended for masses
develop months before other clinical signs.

that are fast-growing or produce pupillary

Anterior uveitis is the most conunon
abnormalities, iridocorneal angle
clinical finding in FeLLC. Other findings
involvement, and/or glaucoma, because
include ocular hypotension, changes in
metastasis is frequent in advanced cases.

iridal pigmentation and color, keratic

Post-traumatic intraocular sarcoma
precipitates, hyphema, anterior and
occurs in older cats with a history of
posterior synechiae, miosis, and aqueous
chronic uveitis, previous intraocular
flare. Posterior segment changes include
damage, or intraocular injections of
retinal hemorrhages, tortuous dilated
gentamicin. Clinical signs are elther glauvessels, perivascular cuffing, and detachcoma, phthisis bulbi, or chronic uveitis.

ment and degeneration of the retina. Few

Intraocular cartilage and osteoid productherapy studies of cats with ophthalmic tion is common. Early enucleation is
lymphoma exist, but cats with lymphoma
reconunended.

and feline leukemia virus infection have
lower overall survival times.·

DEAFNESS

Deafness-the absence of perception of

Hereditary deafness can be cochleosacsound-and reduced hearing are common cular or neuroepithelial in origin. Cochleoin dogs and cats, and to a lesser extent in saccular deafness is usually seen in dogs
other species. Deafness can be hereditary or with the piebald or merle genes and in cats acquired, and sensorineural or conductive.

with white coat color. It produces deafness

DEAFNESS

519
in one or both ears and is often associated
reversible in mammalian species. Acquired
with blue eyes and white pigmentation.

sensorineural deafness may result from

Pigment-associated deafness also occurs in
intrauterine infection or toxins, otitis
equine, bovine, porcine, and other species.

interna or meningitis, mechanical or noise

This is the most common cause of deafness
trauma, ototoxicity, anesthesia, neoplasms,
in dogs and cats and should be the first
or aging (presbycusis). Loss can be
differential diagnosis considered in an
bilateral or unilateral, and partial or

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animal with any white pign1entation. The
complete. Otitis interna (seep 531) will
condition develops within 1-3 wk after birth
frequently be accompanied by vestibular
secondary to stria vascularis degeneration
signs such as head tilt and circling.

that results from the suppression of

Hunting or military dogs exposed to loud
melanocytes by the pigment gene, leading
percussive sounds such as gunfire
to cochleosaccular neuronal degeneration.

experience cumulative losses that may

Unilaterally deaf anin1als may go undetected
initially go unnoticed. This is often
without brain stern auditory evoked
obse1ved in hunting dogs, in which the
response (BAER) testing but will pass on an
distance at which a trained dog responds
increased deafness risk to offspring if bred;
to commands shrinks by half or more.

inhe1itance does not appear to be simple

A variety of drugs and chemicals are
autosornal. Neuroepithelial deafness is not
ototoxic and vestibulotoxic, especially the
associated with pign1ent patterns, is usually
aminoglycoside antibiotics (gentamicin,
bilateral, and results from primary hair cell
an1ikacin ), antineoplastic drugs ( cisplatin ),
loss over the same time course as cochleosalicylates, diuretics ( ethacrynic acid, saccular deafness; vestibular signs may also
furosemide), and antiseptics (chlorhexbe present ( eg, in Dobem1an Pinschers ).

idine). The toxicity is pem1anent. Aminogly

Congenital deafness ( usually heredicoside toxicity, the most common, functions tary) has been reported in -100 dog breeds
through reactive oxygen species, and
and is especially prevalent in the piebaldhuman studies have shown that coadminiscarrying breeds of Dalmatian, Bull Terrier, tration with aspirin or N-acetylcysteine

Australian Cattle Dog, English Setter,
an1eliorates the toxicity; it is unknown if

English Cocker Spaniel, Boston Terrier, and
postexposure treatment is of value. High

Parson Russell Terrier, and in the different
frequencies are affected first, slowing
merle-carrying breeds. The prevalence of
recognition of the toxicity, which may
deafness in white cats ( dominant white
appear at a delay of weeks after treatment
gene), especially those with blue eyes, is
has been discontinued. Dogs or cats unde1°
high, but blue-eyed cats from Siamese
going general anesthesia for teeth or ear
breeds do not appear to be affected. No
cleaning occasionally awaken bilaterally

DNA testing is currently available to identify deaf, but the mechanisms, which can be carriers of genetic deafness in dogs or cats,
conductive or sensorineural, are unknown.

so BAER testing and selective breeding

Few reports have been seen for procedur.es
are the only available options to reduce
on body regions other than mouth and ear,
prevalence within breeds. A late-onset fonn and no tmilateral deafness from anesthetic of genetic neuroepithelial deafness may
procedures has been reported.

exist in Rhodesian Ridgebacks.

Many geriatric animals develop

Conduction deafness results from
presbycusis. Mid to high frequencies are
obstruction or reduction of sound reaching
affected first, followed by progressive loss
the cochlea, usually from otitis media ( see
at all frequencies. The loss may appear to
p 531), chronic otitis externa (seep 527),
be acute in onset but reflects the animal's
or excess cerurnen, and less commonly
eventual inability to compensate for the
from tympanum rupture or ossicle damage.

progressive loss that had been developing

Resolution of the obstruction or tissue
for some time. There does not appear to be
damage usually restores hearing. Recovery
a gender difference in prevalence. Onset is
after otitis media may require weeks while
typically in the last third of a breed's typical
the body phagocytizes the infection residue,
lifespan and will progress to complete deafaccompanied by progressive recovery of ness if the animal lives long enough.

hearing. Prin1ary secretory otitis media

Unilaterally deaf animals show negligible

(glue ear), especially in Cavalier King
signs, primarily an inability to localize

Charles Spaniels, produces a persistent
sound origins and orienting toward the
conductive deafness that may be treated
good ear, but many compensate and show
by myiingotomy, bulla osteotomy, or
no signs. Bilateral orienting pinnae movetyinpanostomy tubes.

ments persist in urtilaterally deaf anin1als.

Sensorineural deafness results from

Bilaterally deaf anin1als do not respond to
loss of cochlear nerve cells and is not
sound stin1uli but become adept at

520

DEAFNESS
increased attention to other sensations such
used in the clinic. Observations are made
as vision and vibration. Affected animals
for a response to a sound stimulus outside

"key" off the behavior of littermates or other the animal's visual field. Limitations
household pets. Breeders of breeds with
include the inability to identify unilateral
high prevalence often choose to euthanize
deafness, stimulus detection through other
bilaterally deaf (and spay/neuter unilatersenses, blunted responses in stressed VetBooks.ir
ally deaf) animals because of a frequent
animals, and failed responses from expired
outcome of poor quality of life and liabilities
novelty of a repeated stimulus. Failure of a
from owning a deaf dog, such as startle
sleeping animal to waken to an auditory
biting. Bilaterally deaf dogs can be successstimulus that does not activate other fully raised, but more dedication than
senses is a reliable indicator of bilateral
normal is required. Owners of deaf dogs
deafness in the home environn1ent.

should be counseled to protect their pets

Otoscopic examination of the external
against undetected dangers such as motor
ear and tyrnpanun1, radiography of the
vehicles.

tyrnpanic bullae, and neurologic examina

Dogs that lose hearing later in life appear
tion may reveal the cause, especially in
to cope well but on occasion exhibit
conduction deafness, which usually
transient behavior suggestive of auditory
responds to appropriate medical or
sensations similar to subjective tinnitus
surgical treatment. Early intervention in
in people. There is no evidence that deaf
ototoxicity may reduce or reverse loss but
animals otherwise experience pain or
usually is not successful. Once developed,
discomfort from the condition.

sensorineural deafness cannot be reversed,

Identification of deafness is most
and its cause cannot be detemlined. Congeniaccurate with BAER testing at referral tal deafness in breeds with white pigmencenters, but behavioral testing is typically tation is nearly always of genetic origin.

DISEASES OF THE PINNA

A variety of de1matologic conditions affect
canal of horses, cattle, sheep, goats, deer,
the pinna. Rarely, a disease affects the
rabbits, cats, and dogs. Clinical signs include
pinna alone or the pinna is the initial
head shaking, head rubbing, or drooped
site affected. As with all dermatologic
pinnae. Both the animal and tile environconditions, a diagnosis is best made ment should be treated. Treatment involves
with the results of a thorough history, a
mechanical removal of as many ticks as
complete physical and dermatologic
possible with a forceps and spraying or
exan1ination, and with careful selection
dipping the coat witll pyrethrin/pyretllroid
and evaluation of specific diagnostic tests.

products or malatllion. Treatment of

This overview is not all inclusive but
secondary bacterial or yeast otitis extema
discusses diseases that solely or commonly is also important. Precautions to prevent affect the pinna of domestic animals.

rei.nfestations should be instituted.

Gotch ear is a concliti!m described in
cattle, and also in a goat, that results from

ARTHROPOD BITE PINNAL
infestation of the pinna with the Gulf Coast

DERMATITIS
tick, Amblyomma maculatum. Adult ticks
prefer feeding on animal ears, and when

Arttu·opods commonly cause dennatitis of
ticks are present in sufficient numbers the
the pinnae either tlu-ough direct damage
pinna becomes edematous, erythematous,
from the bite of tl1e parasite or as a result of
and crusting at the tick-attaclunent sites.

hypersensitivity. Ticks can cause irritation

Curling of the tip of the ear and excoriaat tile site of attachment and may be found tions may also be seen. Spotted fever group
on tl1e pinna or in the ear canal. The spinous
rickettsiae, such as Rickettsia parkeri,
ear tick (Otobiils megnini), found in tl1e
have been suggested to cause the skin
southwestern USA, south and central
lesions, because ticks removed from the

Americas, southern Africa, and India, is a
pinna of animals with gotch have been, in
soft-shelled tick, the larval and nyrnphal
some cases, positive for Rickellsia spp by
fonns of which parasitize tile external ear

PCR. However, efforts to find the organ-

DISEASES OF THE PINNA

521
isms in skin samples from affected areas
instituted. Mites are much easier to find on
have failed. Removal of ticks and treatment skin scrapings of cats with notoedric of any secondary infection are cw-ative.

acariasis. Treatment options include 2"/o-4%
lin1e sulfur dips ( safe in all species) eve1y 5

INSECT BITE DERMATITIS
days for 4-6 treatments, ainitraz dips at a
strength of250 ppm (in dogs only) applied

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This worldwide problem is caused by
weekly for 4 to 6 treatments, and ivermectin
inflan1mato1y mediators or toxic substances at 200-300 mcg/kg, PO or SC, every 1-2 wk present in the saliva of various hematophafor 3--4 treatments. Treatment response is not gous insects. It typically affects dogs, cats,
consistent when using lime sulfur dips or
and horses. Clinical signs are characterized
amitraz in small anin1als; therefore, these
by small papules and wheals with central
topicals are not good options for a treatment
hemorrhagic crusts that can progress to
trial (ie, mites are not found on skin
multiple small ulcers. Lesions are found on
scrapings). Oral milbemycin oxime has been
the apexes of the pinnae of cats and dogs
reported to be sal·e and effective in the
with erect ears or on the folded surfaces of
treatment of sai·coptic mange in dogs but is
the pirmae of dogs with flopped ears. The
not FDA approved for this purpose. The
causative insect can vaiy with the season
reconrn1ended treatment protocol is
and environment and include, among

2 mg/kg once weekly for 4 to 6 treatments or
others, mosquitoes (Aedes spp, Culex spp ), twice weekly for 3 wk. Selamectin, also extrathe stable fly (Stomo:rys cai,eitrans ), ai1d label, has also shown efficacy; the recomblack flies (Simulium spp ). Mosquitoes can mended protocol is four applications at also cause a hypersensitivity reaction in

2-wk intervals. Moreover, imidacloprid 10%1
cats chai·acterized by inflamrnato1y lesions
moxidectin 2.5% spot-on applied twice at
on the pinnae, face, and feet (see below).

a30-day interval or eve1y 3 wk for three

The rabbit flea (Spilopsyllus cuniculi) is
treatments has been shown to be efficafound mainly in Ew-ope and Australia and cious. There ai·e also anecdotal reports of
can be transmitted to dogs and cats. It
efficacy of these treatment modalities for
adheres tightly to the skin of the host and
treatment of notoedric mange in cats.

typically affects the tip of the pinna, where it Because mites can survive off the host may cause derniatitis. In horses, bites of the
for a variable an1ount of time, all bedding,
stable fly, black flies, and Culicoides spp brushes, tack, and fomites should be treated
can cause a hypersensitivity reaction or
as well. All in-contact a11imals also should
severe dennatitis that results in lesions on
be treated because of the contagious nature
the dorsal and/or ventral trunk and face in
of these acaiioses.

addition to the pinna. Treatment includes fly

Ivermectin is widely used to treat
repellents, controlling the fly population
sai·coptic ma11ge in dogs and has been used
with environmental clean up (manure,
to treat notoedric mange in cats, but it
compost, etc), and insecticides. Topical or
is not approved by the FDA for these
oral short-acting glucocorticoids may be
indications. Therefore, every caution
necessaiy to reduce the inflai11mation and
should be taken, and clients specifically
pruritus in severe cases.

informed of inherent risks with this drug.

Dog breeds susceptible to ivermectin

MITE INFESTATIONS
toxicity include Collies, Shetland Sheepdogs, Australian Shepherds, English Sarcoptes scabiei is a common mange mite

Shepherds, Longhaired Whippets, McNabs,
in pigs and dogs, and Notoedres cati is

Silken Windhounds, and Old English
conunon in cats throughout the world (see

Sheepdogs. Before using ivern1ectin in
also MANGE, p 914). In the USA, sarcoptic a11y of these breeds, a genetic test for the
mange is rare in horses and sheep and is
mutation of the ABCBl (formerly MDRl)

considered a reportable disease. Papular
gene, which encodes for the multi drug
eruptions progress to scaling, crusting, and
tra11sporter P-glycoprotein, should be
excoriations of the ear margins and other
performed. (This test is available at the
parts of the body. Pruritus is severe.

University of Washington.)

Transmission is by direct contact with

N onburrowing psoroptic mites cause
infected animals or contan1inated fomites.

otitis externa in horses and goats. Aninlals

Diagnosis is based on clinical signs, history,
may be asymptomatic or present with
and discovery of mites from multiple skin
pruritus, head shaking, and a drooping ear.

scrapings. Negative scrapings do not

Crusted papules, alopecia, and/or scaling are
exclude the diagnosis, however, because
typically present on the pinnae. Diagnosis is
mites are often difficult to find. If the
confinned by finding the mites on skin
diagnosis is suspected, treatment should be
scraping or in otic exudate, but mites may

522

DISEASES OF THE PINNA
be difficult to find in the ear canal. Ivern1ec

Feline mosquito hypersensitivity is
tin at 200 mcg/kg, PO, every 2 wk for two
an allergic reaction to mosquito bites that
treatments has been shown to be effective.

can cause an ulcerative and crusted
dermatitis of the pinnae, nose, and less
commonly the footpads, eyelids, chin, and

ALLERGY
lips of cats. Lesions progress from wheals
to pa.pules to plaques to crusted ulcers that

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Environmental-induced ( eg, house dust,
coalesce to affect extensive areas. PrW"itus
house dust mites, pollens of trees, grasses
is a consistent sign, and regional lymphadand weeds, molds) or food-induced a.topic enopathy may occur. In severe cases, fever
dermatitis are conunon allergic disorders
or other systemic signs may develop.

of dogs and cats and frequently cause

Histologically, the lesions are characterized
erythema and pruritus of the pinnae and
by severe superficial and deep perivascular
external ear canals. The allergic condition
to interstitial eosinophilic dermatitis, often
predisposes to develop secondary bacte1ial
associated with flame figW"es, foUiculitis,
or yeast otitis externa, which can extend to
and furunculosis. Differential diagnoses
the pinna. In these cases, pa.pules, crusts,
include pemphigus foliaceus, herpesvirus
and lichenification may develop in addition
ulcerative dermatitis, other causes of
to the erythema. Other body sites such as
eosinophilic dermatitis (food allergy, atopy,
the face (ie, periocular region, muzzle, chin), idiopathic), notoedric mange, and a.xilla, groin, and feet are also often affected.

dermatophytosis. Treatment includes

Diagnosis is based on a characteristic
keeping the cat inside and using a pyrethrin
history, clinical signs, and the elimination
repellent (avoid permeth1in-containing
of other pruritic skin diseases. A strict food
products in cats) when exposW"e to
elimination trial is in1portant for animals
mosquitoes is anticipated. Systemic
with year-round clinical signs to determine
glucocorticoids may be necessary in severe
whether food allergens are niggering the
cases. (See also MOSQUITOES, p 888.)

a.topic signs. If food allergy is excluded or is
only part of the allergic condition, intrade1°

AURAL CONTACT DERMATITIS
mal or serologic allergy tests can be
performed to support a presumptive

AW'al contact dern1atitis conm1only affects
diagnosis of environmental-induced a.topic
the concave aspect of the pinna, likely
dermatitis and, more in1portantly, to
because it lacks hair. Topical ear medicainstitute allergen-specific in1.munotherapy.

tions, particularly those containing

It is very in1portant to identify and treat any
anlinoglycosides and/or propylene glycol, are
secondary ear and skin bacterial or yeast
common causes in animals being treated for
infections, because they aggravate the
otitis extema Lesions may develop 1-7 days
allergic dermatitis. Treatment of foodafter starting therapy. Contact dermatitis can induced a.topic dem1atitis consists of solely
also result from ointments applied transde1°
feeding the diet used dW"ing the food trial
mally to the concave aspect of the pinnae.

or avoiding food ingredients known to

Clinical signs include erythema, edema,
trigger the allergic reaction. Treatment
pa.pules that may coalesce and form plaques,
of a.topic dermatitis consists of u�ing
erosions, and/or ulcerations. Pnuitus and
anti-inflanunatory/immunomodulatory
pain are variable. A definitive diagnosis can
drugs, including oral shmt-acting glucocortirarely be made, because mug challenge is not coids such as prednisone or prednisolone
reconm1ended. Discontinuation of all topical
at 1 mg/kg/day and tapering to the lowest
medications is the indicated treatment.

possible dosage administered every other

Changing to a different topical mug is not
day. Cyclospmine at 5 mg/kg/day can also be recommended because most products have used in animals that carmot tolerate or do
identical vehicles, which are the offending
not respond well to glucocorticoid therapy.

cause in most cases.

Omega-3 and/or omega-6 fatty acids can be
used as adjunctive therapy. H1-receptor anti

PINNAL ALOPECIA
histamines typically are not very efficacious
to control the pl'W'itus or inflammation

Symmetrical noninflan1mato1y alopecic
associated with a.topic dermatitis, but their
disorders affecting the pitma, such as
safety profile and relatively low cost make
periodic pinnal alopecia, pattern baldness,
them worthwhile to try. Allergen-specific
and alopecia associated with melanodemia,
immunotherapy based on intra.dermal or
may affect dogs and cats and are typically
serologic test results is cwTently the only
idiopathic.

specific therapy for a.topic dem1atitis and

Periodic pinna.I alopecia in Miniature
should be considered as a treatinent option.

Poodles is characterized by progressive

DISEASES OF THE PINNA

523
bilateral alopecia of the convex surfaces of
dilated follicles filled with keratin debris.

the ear. The hair loss is acute in onset and

Differential diagnoses include sarcoptic
progresses throughout several months, but
mange, pinnal alopecia, proliferative
hair may spontaneously regrow. There are
thrombovascular necrosis, dernrntophytono other clinical signs. A similar condition sis, and frostbite. Dermatophytosis, in
was reported in Siamese cats in which
particular, can cause a scaling pinnal
complete or patchy alopecia of the convex
dermatitis in dogs, cats, and horses, but

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aspect of both pinna develops. Treatment
the ear margin is not typically involved
is unnecessary.

and other areas of the body are generally

Pattern baldness affecting only the
affected as well. Treatment includes
pinna has been reported in Dachshunds,
antiseborrheic shampoos ( eg, sulfur,

Chihuahuas, Italian Greyhounds, and Whipsalicylic acid, benzoyl peroxide), keratolytic pets and is thought to have a hereditary
products, dioctyl sodiw11 sulfosuccinate
predisposition. The age of onset is �l yr of

(DSS), and systemic medications that may
age. Lesions start as thinning of the hair
help n01111alize the abnormal keratinization
coat, and complete pinnal alopecia may
process ( eg, vitan1in A and syntl1etic
occur by 8--9 yr of age. Other commonly
retinoids, essential fatty acids). Topical or
affected areas are the ventral neck and
oral glucocorticoids and pentoxifylli.ne
thorax and the caudal medial thighs. The

(10-15 mg/kg, bid-tid) may be beneficial
hair loss is asymptomatic. Histologically,
when severe inflammation and fissures
the skin is normal, and hair follicles are
develop.

diminished in size but normal in appearance. No effective treatment has been SEBACEOUS ADENITIS
reported, but pentoxifylline (15-20 mg/kg,
bid-tid), melatonin (3 mg for small breeds

Sebaceous adenitis is uncommon in dogs
and 6 mg for large breeds, bid-tid), and topiand rare in cats. The cause is unknown, but cal minoxidil have anecdotally been
the strong predisposition of certain canine
described as helpful. Pattern baldness
breeds suggests that genetics plays a role.

restricted to the pinna has also been

The proposed pathogenesis includes
reported in cats; however, use of minoxidil
cell-mediated immunologic destruction of
in cats should be avoided, because it has
the sebaceous gland; a primary comificabeen associated with death in two cases.

tion disorder of the glandular duct, resulting

Alopecia associated with melanoin obstruction and secondary inflammation derma has been described mostly in
of the gland; an anatomic defect of tl1e

Yorkshire Terriers and occasionally in
sebaceous gland, leading to lipid leakage

Doben11an Pinchers. Alopecia and marked
and a foreign body reaction; or an abnom1al
hyperpigmentation (melanodern1a) are
lipid metabolism, leading to glandular
first noticed between 6 mo and 3 yr of age
destruction. Predisposed breeds include
and affect both pinna and the bridge of the

Standard Poodles, Akitas, Samoyeds,
nose. Other areas such as the tail and feet

Vizslas, Havanese, Springer Spaniels, and
may also be affected. The alopecic and

Lhasa Apsos; however, various otl1er breeds
hyperpigmented skin has a smooth, shiny,
can be affected. Lesions typically affect the
and leathery appearance. The condition
pinnae, forehead, face, tail, and dorsal trunk
tends to worsen as the dog ages, and it
and are characterized by alopecia and
typically does not spontaneously resolve.

adherent scales that cast hair shafts. The

There is no treatment.

severity and characteristics of clinical signs
vary among breeds. Pruritus is variable and

EAR MARGIN SEBORRHEA
mostly associated witl1 secondary bacterial
infection. Histopatl1ologic findings include

This condition is common in Dachshunds,
diffuse absence of sebaceous glands,
although other breeds with pendulous
granulomatous to pyogranulomatous
pinnae may be affected. Lesions usually
i.nflan1mation at tl1e site of previous glands,
affect the apex of the pinnae on both sides
and follicular keratosis. Currently, tl1e most
but can progress to involve the whole ear
efficacious tl1erapy for sebaceous adenitis
margin. The cause is unknown. Lesions
is oral cyclosporine (5 mg/kg/day) in
appear as waxy, gray to yellow scales
association with topical therapy. Oral
adherent to the base of hair shafts. Plugs of
vitamin A (1,000 IU/kg/day) or synthetic
hair can be easily epilated, leaving behind a
retinoids (eg, isotretinoin or acitretin) may
shiny surface to the skin. In severe cases,
be efficacious in some cases. The combinathe ear margins are edematous and fissured.

tion of tetracycline (250 mg, tid, for dogs

Histologic findings include severe hyper

<l O kg; 500 mg, tid, for dogs > 10 kg) or
keratosis and follicular keratosis with
doxycycline (5 mg/kg, bid) and niacinamine

524

DISEASES OF THE PINNA

(250 mg, tid, for dogs <10 kg; 500 mg, tid, for
of horses. Clinically, the lesions are
dogs> 10 kg) is an option for milder cases
characterized by depigmented, hyperkeraor when owners are concerned about costs totic, coalescing papules and plaques
and/or adverse effects associated with
localized to the concave aspect of the pinna.

cyclosporine or retinoids. Topical therapy

Often, both pin.nae are affected. Lesions are
in the fonn of medicated shampoos and
usually asymptomatic, but in some cases

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emollient rinses or sprays should be used
the fly bite itself causes dermatitis and
in cortjunction with systemic therapy.

discomfort. Histologically, the lesions are

Omega-3 and omega-6 fatty acids can also
characterized by mild papillated epidem1al
be used as adjunctive therapy. To help
hyperplasia and marked hyperkeratosis.

soften the adherent scales, a mixture of

Increased size of keratohyalin granules,

7(JJ/o-75% propylene glycol in water can be
koilocytosis, and hypomelanosis may also
sprayed or used as a rinse on the anin1al's
be present in the epidermis. Intranuclear
coat and allowed to act for 2--3 hr before
viral particles have been seen in electron
bathing with a medicated shampoo. Another microscope studies. Various treatments option is to apply baby oil soaks ( undiluted
have been anecdotally tried, with minimal
or diluted with water 1:1) for l-6hr before
to no response. A recent, open-label pilot
bathing with a medicated shan1poo.

study showed that imiquimod cream is
effective in the treatment of aural plaques;

AURICULAR HEMATOMAS
however, the severe inflammation induced
by the drug makes this treatment difficult to

Auricular hematomas are small-to-large.

use, with most horses requiring sedation.

fluid-filled swellings that develop on the

The recommended protocol consists of
concave swface of the pin.nae in dogs, cats,
applying in1iquimod 2 -3 times weekly
and pigs. The pathogenesis for the develop

( nonconsecutive days) every other week.

ment of the lesions is unknown, but head

Frequent applications of fly repellent and
shaking or ear scratching due to pruritus is
stabling the horse during the fly's feeding
almost always involved. In dogs, the
tin1es are important measures to reduce
condition is seen with atopic dermatitis and
discomfort and prevent recurrence. Lesions
food allergy in which the ear canals are the
typically do not regress spontaneously.

primary sites of allergic inflammation,
prwitus, and secondary infection. In pigs,
sarcoptic mange, pediculosis, and meal in the

NECROTIC EAR SYNDROME IN
ears (from overhead feeders) have been

SWINE
in1plicated as a cause of head-shaking that
has led to auricular hematomas. Bites from

(Ear necrosis, Necrotic auricular dermatitis)

other pigs also may be at fault (see below).

Treatment is surgical to allow drainage.

Pigs with necrotic ear syndrome have

After draining and flus
wlilateral or bilateral necrosis of the pinnae,

.hi.ng, several mattress
sutures can be placed to eliminate the
are unthrift;y, and conunonly develop septic

"pocket." The addition of a drain made out of aithritis or die from secondary bacterial
a teat tube, piece of soft urinary catheter,
septicemia. The condition occurs sporadior IV catheter increases the success rate of cally in weaned and growing pigs under all
surge1y. Drainage and glucoc·orticoid
management systems, particularly when
instillation are successful in -509u of cases.

challenged with endemic diseases that may

Drainage is best obtained with a butterfly
influence feed intake.

connection or an IV catheter. Glucocorticoids
are instilled to fill the cavity without causing

Etiology, Transmission, and
skin distention. A short course of a low

Pathogenesis: The causes have not been
anti-inflanunatory dosage of oral glucocortidetenni.ned conclusively. CircW11stantial coids is commonly added to this treatment.

evidence strongly suggests that necrotic ear
syndrome is due to traW11a (fighting) and

EQUINE AURAL PLAQUES
subsequent bacterial invasion of the
dainaged tissue. Another potential factor

Equine aural plaques, also known as
that may contribute to the problem is
papillary acanthoma or ear papillomas, are
inadequate dietary lysine levels in the feed,
caused by papillomavirus. Currently, four
although no scientific data exist to prove
papillomaviruses have been isolated from
this assW11ption.

aural plaques. Black flies (Simulium spp)

Histologic and microbiologic findings
are likely the mechanical vector. The flies
suggest that the aggressive, erosive to
are active at dawn and dusk, when they
ulcerative lesion is due to secondary
attack the head, ears, and ventral abdomen
bacterial infection. In the early phases of

DISEASES OF THE PINNA

525
the disease, large numbers of Staphylococ
sensitivity testing. Trawnatizing events
cus hyicus and low to moderate numbers
should be minimized. Management
of [3-hemolytic streptococci are found in
practices ( ventilation, location and
the surface exudate; later, during the
functioning of waterers, pen design, group
ulcerative and necrotic stage, large
size, mixing) and proper levels of dietary
numbers of the streptococci are found
lysine should be checked and corrected if

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deep in the lesion. It is hypothesized that
deficiencies are detected. Proper immuniza

S hyicus colonizes the trawnatized tissue,
tion against porcine circovirus type 2 is
which prepares the way for the highly
important to reduce the frequency of ear
invasive streptococci that induce the
necrosis on fanns.

changes that lead to ulceration and necrosis. Effo1ts to reproduce the disease by MISCELLANEOUS DISEASES OF
experimental inoculation of the two

THE PINNA
organisms have been unsuccessful.

Spirochetes have also been found in skin

Several inunune-mediated diseases such as
samples from ear lesions using silver stain,
pemphigus foliaceus, pemphigus
and Treponema spp were amplified and
erythematosus, drug eruption, toxic
sequenced from DNA prepared from ear
epidermal necrolysis, and irnmunelesion scrapings and broth cultures.

mediated vasculitis may affect the pinna

However, the primary role of spirochetes in and the ear canal. (See also AUTOIMMUNE SKIN
causing ear necrosis in pigs is unknown at

DISORDERS, p 827.) Other areas of the body
this time. Moreover, porcine circovirus
are typically affected and may include
type 2 infection may contribute to ear
footpads, mucous membranes, mucocutanecrosis, because controlling the infection neousjunctions, nails and nail beds, and the
through systematic vaccination has been
tip of the tail. Inunune-mediated diseases
reported to reduce the frequency of ear
are confinned with biopsy of primruy
necrosis on fanns.

lesions (papules, vesicles, pustules,
erythematous margins of secondary

Clinical Findings, Lesions, and
lesions) and histologic evaluation by a

Diagnosis: The nature and extent of
dermatohistopathologist.

clinical signs depend on the severity of the

Folded ear tips in cats are most often
local lesion and development of secondary
associated with longterm glucocorticoid
bacterial septicemia. Thus, a spectrum of
therapy (eg, daily eye or otic preparations).

signs, including unthriftiness, anorexia,

They may also be caused by solar radiation
fever, septic arthritis, collapse, and death,
damage. Ear folding may not be reversible.

may be seen.

Feline solar dermatitis or actinic

Mild lesions consist of superficial
dennatitis is seen most commonly in white
scratches covered with thin, dry, brown
cats or cats with white pinnae that have
crusts. Mild edema or erythema may be
been chronically exposed to sun. Lesjons
present near the scratches. In more severe
first appear as erythema and scaling on the
cases, thick, brown, moist crusts cover
sparsely haired tips of the ears. Crusting,
deep ulcers. In the most severe cases, there
exudation, and ulceration may develop as
is extensive necrosis. The lesions evolve
the actinic keratosis undergoes transforfrom mild, superficial dermatitis to severe, mation into a squamous cell carcinoma.

deep inflammation with exudation,

During early stages of the disease,
ulceration, thrombosis, and necrosis. In
treatment consists of lin1iting exposure
mild cases, resolution occurs with no loss
to ultraviolet light through confinement
of ear tissue; in severe cases, the margins,
indoors between the hours of 10 AM and
tips, or even the entire pinna may be lost.

4 PM and the use of topical sunscreens.

Diagnosis is made based on the

Squan1ous cell carcinoma of the pinnae is
appearance of the affected ears.

treated with surgical excision followed by
radiation therapy. If surgery and radiation

Management and Control: Tincture of
therapy ru·e not an option, topical
iodine, applied topically bid for 1 wk, has
treatment with irniquirnod crean1 2-3 times
reduced the incidence and severity of the
weekly has shown promising results.

disease. Antibacterial drugs administered in

Feline proliferative and necrotizing
the feed are effective in some herds but not
otitis externa is a rare disease of
in others. Lack of effectiveness could be due unknown cause. It can affect cats from to drug resistance. In cases of antibacterial

2 mo to 12 yr of age, with most cases
ineffectiveness, specimens should be
occurring at 4 yr of age. No breed
collected aseptically from the deep aspect
predilection has been reported, but males
of the ulcerative lesions for culture and
apperu· to be overrepresented. It most

526

DISEASES OF THE PINNA
commonly affects the concave aspect of
defom1ity of the pinnae is to be expected
the pinna and external aural orifice, but
whether or not treatment has been
it can extend into the ear canal. The
instituted.

preauricular, periocular, and perioral

Vasculitis is an uncommon disorder of
regions may also be affected. Lesions are
dogs and cats. Lesions consist of purpura,
characterized by thick hyperkeratotic
erythema, well-demarcated ulcers, crusts,

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crusts covering erythematous plaques that
and sloughing of necrotic tissue. The
may erode or ulcerate. Secondary bacterial
pinnae, tail, and footpads are typically
and yeast infections may aggravate the conaffected. It is usually difficult to detem1ine dition. Most cats appear indifferent to the
the triggering cause, which may be
lesions, but mild pruritus and discomfort
inm1une-mediated, drug-induced, a
may be present when ulceration develops.

concurrent infection, neoplasia, or

Diagnosis is confirmed by the histopathoidiopathic. Differential diagnoses include logic findings, which are characterized by
fight wounds, cold agglutinin diseases,
epidermal hyperplasia associated with
frostbite, and coagulopathies. Treatment
scattered apoptotic-appearing keratinoinvolves identifying and eliminating the cytes that extend to the superficial follicuinciting cause and administering oral, lar epithelium. Parakeratotic hyperkeratoshort-acting glucocorticoids (such as sis is also a feature. Spontaneous
prednisone/prednisolone at 1-2 mg/kg/day,
resolution has been reported to occur in
then tapering to the lowest possible dose
some cases but only after 12-24 mo.

administered every other day), tetracycline

Therapy with topical tacrolimus or oral

(250 mg tid for dogs <10 kg; 500 mg tid for
cyclosporine at 5 mg/kg/day is reported
dogs > 10 kg) or doxycycline (5 mg/kg bid)

to be efficacious.

and niacinamine (250 mg tid for dogs

Proliferative thrombovascular

<10 kg; 500 mg tid for dogs> 10 kg),
necrosis of the pinnae is rare in dogs.

pentoxifylline (15--20 mg/kg, bid-tid), and

There are no known breed, sex, or age
cyclosporine (5 mg/kg/day) or other
predilections, and the cause is unknown.

immunomodulating drugs.

Lesions, which consist of scaly, thickened,

Frostbite may occur in anin1als poorly
hyperpigmented skin surrounding a
adapted to cold climates and is more likely in
necrotic ulcer, begin at the apex of the ear
wet or windy conditions. It typically affects
and spread along the concave surface.

poorly insulated body regions, including the

Eventually, necrosis may deform the
tips of the ears, feet, and tail. The skin may
margin of the pinna. Pentoxifylline (15--20
be pale or erythematous, edematous, and
mg/kg, bid-tid) and/or the combination of
painful. ln severe cases, necrosis and
tetracycline (250 mg tid for dogs <10 kg;
sloughing of the ear tips may follow.

500 mg tid for dogs > 10 kg) or doxycycline .

Treatment consists of rapid, gentle warming

(5 mg/kg bid) and niacinamine (250 mg tid
and supportive care. Amputation of affected
for dogs <10 kg; 500 mg tid for dogs >10 kg) regions may be required but should be have been anecdotally reported to be
delayed until the extent of viable tissue is
efficacious in some cases. Topical
detem1ined, which may take some tin1e.

glucocorticoids are also an option but

Canine juvenile cellulitis is an
must be used carefully becau�e of their
uncommon disorder of puppies and is
atrophogenic effects. If medical therapy
characterized by sterile papules, nodules,
has failed, surgical removal of diseased
and pustules on the face and pinnae, in
tissue should be considered.

addition to submandibular lymphadenopa

Auricular chondritis has been reported thy. It is seen in puppies 3 w.k to 4 mo rarely in cats and dogs. Clinical signs
old and rarely in older animals. Golden
include pain, swelling, erythema, and

Retrievers, Gordon Setters, and Dachsdeformation of the pinnae. Both ears are hunds appear to be at greater risk than
typically affected. Systemic signs may
other breeds. A purulent otitis extema is
accompany some cases, and involvement
common, along with edematous, thickened
of other organs such as the joints, eyes, and pinnae. Systemic signs such as anorexia, heart has been reported. Histologically,
lethargy, and fever may be present in some
lesions consist of lymphoplasmacytic
cases. The diagnosis can be confirmed by
infiltrates, basophilia, and loss or necrosis
biopsy, which shows a pyogranulomatous
of cartilage. Treatment may not be required inflammatory infiltrate with no microorganif the condition is nonpainful and no isms, and by negative bacteriologic culture.

systemic signs are present. Oral glucocorti

Early treatment is recommended to avoid
coids have been reported to be ineffective,
scarring. Prednisone or prednisolone
but dapsone (1 mg/kg/day) has induced

(2 mg/kg, PO, divided bid) should be
remission in some cases. Permanent
tapered slowly throughout 4-6 wk or until

OTITIS EXTERNA

527
the disease is inactive. Antibiotics may
need to be excluded are sterile granuloma
be needed to treat secondary bacterial
and pyogranuloma disease and cutaneous
infection. Cyclosporine at 10 mg/kg/day
reactive histiocytosis; however, other
has been reported to be effective in a case
body sites are commonly affected in these
refractory to glucocorticoid therapy.

diseases. Cases typically respond to oral

Canine sterile nodular granulomaglucoc01ticoids (eg, prednisone/prednisotous dermatitis of the pinna is a rare VetBooks.ir
lone 1-2 mg/kg/day until remission then
condition reported only anecdotally to
tapered) or cyclosporine (5 mg/kg/day);
date. Currently, existence of an age
however, more conservative treatments,
predilection is unknown, and Great Danes
such as topical glucocorticoid (0.01%
and Rottweilers appear to be overrepreflucinolone acetonide plus 60% DMSO) sented. Clinical signs are characterized by
and tetracycline (250 mg tid for dogs
multiple nodules that tend to coalesce and

<10 kg; 500 mg tid for dogs >10 kg) or
are primarily localized to the ear margin.

doxycycline (5 mg/kg bid) combined

Loose to adhered scales typically cover the
with niacinamine (250 mg tid for dogs
nodules. Histopathology shows multiple

<10 kg; 500 mg tid for dogs> 10 kg),
dermal nodules composed primarily of
have been efficacious in some cases.

histiocytes. Leishmaniasis (seep 800) is an Once the disease is in remission, a
important differential diagnosis in endemic
maintenance treatment regimen must
areas. Other sterile nodular diseases that
be instituted.

OTITIS EXTERNA

Otitis extema is inflammation of the
reactions), fungal (eg, aspergillosis),
external ear canal distal to the tympanic
parasites, viral ( eg, canine distemper),
membrane; the ear pinna may or may not
and miscellaneous (auricular chondritis,
be involved. It may be acute or chronic and
eosinophilic diseases,juvenile cellulitis,
unilateral or bilateral. It is one of the most
proliferating necrotitizing otitis of cats).

common reasons for small animals to be

Secondary causes are those that cause
presented to the veterinarian. Clinical signs disease in an abnom1al ear. These causes can include any combination of headshakare relatively easy to eliminate and include ing, odor, pain on manipulation of the ear,
bacteria, fungi, medication reactions,
exudate, and erythema. It can be seen in
overcleaning, and yeast overgrowth.

rabbits (in which it is usually due to the

Factors are elements related to the
mitePsoroptes cuniculi) and is uncommon disease or pet that contribute to or promote in large animals.

the otitis extema by altering the structure,
function, or physiology of the ear canal.

Etiology and Classification System:

Factors are subdivided into predisposing

Causes of otitis extema are now defined
factors, which are present before the
as primary or secondary, with factors that
development of the ear disease, and
contribute to or promote disease. It is also
perpetuating factors, which occur as a
standard of care to determine whether the
result of the inflammation. Predisposing
cause is curable or lifelong management is
factors include conformation of the ear,
required. Primary causes of otitis extema
excessive moisture, obstruction of the ear
are those that create disease in a nonnal ear. canal ( eg, polyp, feline apoc1ine cystadeno

They can cause otitis without any other
matosis ), primary otitis media ( eg, primary
cause or factor and can be subtle; they often
secretory otitis media, otitis media due to
go unrecognized by owners and veterinarneoplasia or respiratory disease), systemic ians until secondary causes develop.

diseases ( eg, catabolic states), and treat

Primary factors alter the ear environment,
ment effects ( eg, alterations of normal
which allows secondary infections to
microflora, trauma from cleaning).

develop. The major primary causes of otitis

Perpetuating factors include changes in
extema are allergy, autoimmune ( eg,
the ear epithelium ( eg, failure of migration),
pemphigus), endoc1ine, epithelialization
ear canal ( eg, edema, stenosis, proliferadisorders, foreign bodies, glandular tion), tyrnpanic membrane ( eg, dilated,
disorders, immune-mediated (eg, drug
ruptured), glandular ( eg, sebaceous

528

OTITIS EXTERNA
hyperplasia), pericattilaginous fibrosis
must have enough light and magnification

( eg, calcification), and middle eat· ( eg, filled
to clearly visualize the external canal to the
with debris, otitis media). This system is
level of the tyrnpanic membrane. Dispos

CU1Tently refen-ed to as the PSPP classificaable otoscopic ear cones are recommended, tion system. A prognosis should be given
because studies have demonstrated
for otitis externa. Curable means that the
contamination of cones. Handheld
component of the problem is readily
otoscopes at·e available with a variety of

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resolved with treatment (for weeks) or via
heads, including magnification options and
surgery. Longterm management indicates
surgical operating heads, that allow for
that the component of the eat· problem may
visualization of the ear canal while
be resolvable, but it can take months of
insetting another instrument. The smgical
treatment. Lifelong treatment indicates that
head is used when biopsies, foreign body
the owner wiU need to play an active role in
removal, or deep flush of the canal is
management for the life of the pet.

anticipated.

A video otoscope provides magnifcation

Clinical Findings and Diagnosis: There of the ear canal and tyrnpanic membrane.

is no recognized sex distribution for otitis

Most have a working charmel through
externa. Yom1g animals may be more
which biopsy instruments, catheters for
commonly affected. There at·e clear breed
flushing debris from the canal, and laser
predispositions for otitis, which directly
tips can be passed. Video otoscopes allow
reflect the breed predispositions for skin
visualization through water and saline to
disease ( eg, allergies in retrievers and
determine the integrity of the tympanic
terriers). The most common historical
membrane and to facilitate sampling and
findings at·e headshaking and amal pm1itus.

culture of tl1e middle eat·.

The first step in physical exanlination is

During an otoscopic examination, the eat·
determination of the severity of pain. This
canal should be inspected for changes in
can be done by gentle palpation or petting
diameter, pathologic changes in the skin,
of the animal. Uthe ear is painful or the
quantity and type of exudate, pat·asites,
degree of discomfort is high, the anin1al
foreign bodies, neoplasms, and changes in
should be sedated before perforn1ing any
the tympanic membrane. The tympanic
further diagnostic testing. The second step
membrane should be examined for
is gentle palpation and manipulation of
evidence of disease or ruptme. However,
the eat· canal and pinna to detern1ine the
in many cases of otitis, the character of the
presence of sweUi..ng, pflllitus, fibrosis, or
eat· canal and tympanic membrane crumot
calcification. The presence or absence of
be visualized at all until the exudate is
these findings will help deternline whether
gently flushed from the canal. Saniples for
advanced diagnostics are needed,
cytologic evaluation and culture should
specifically imaging of the eat· canal. Next,
be obtained before the eat· is flushed.

the outside of tl1e eat· should be examined,

Examination is attempted again after the
noting erythema, edema, crusts, scale,
eat· is dried. In chronic cases, the canal may
ulcers, lichenification, hyperpigmentation,
be too stenotic, either from hyperplasia or
or exudate. The pinnae and periamiculat·
edema, to be exatnined. Systemic glucocorregions should be examined for evidence ticoids given daily for 1 wk may reduce
of selHrauma, erythema, Md primary and
swelling enough to allow exrunination.

secondary skin lesions. Pinna! deformities,

If sedation is not needed, sat11ples for eat·
hyperplastic tissue in the canal, and
diagnostic tests should be collected: skin
headshaking suggest clu-onic otic discomcytology from tl1e external at1d inner fo1t. Uthe otitis is U11ilateral, the Ullaffected
pinnae, cytology of any exudates present,
ear should be examined first to prevent
hair trichogranis and skin scrapings for
iatrogenic contamination of the Ullaffected

Demodex, and eat· swab cytology with
eat· with organisms ( eg, Pseudomonas
mineral oil in yollllg and adult at1in1als
aeruginosa or Proteus mira bilis) that (especially cats, because feline demodicomay be present in the diseased eat·. The sis can present as pruritic otitis). Wood's
llllaffected ear may, in fact, be diseased,
lamp exaniinations need to be done with
meaning that the differential diagnosis list
care, keeping in mind that the key color is
should also include causes of bilateral otitis.

apple-green fluorescense and that sebum

Otoscopic examination is often not
can glow yellow. Dern1atophytosis affects
possible because the ear is painful,
the hair of the pinnae and hairs in the
swollen, or filled with exudate; sedation
concave surface of the ear cat1al.

is usually required. Swelling of the eat·

Cytologic evaluation of exudate or
canal often makes it impossible to see the
cerumen taken from the horizontal eat·
tympanic membrane. A handheld otoscope
canal may provide inrn1ediate diagnostic

OTITIS EXTERNA

529
infonnation. The external ear canals of
refractory ceruminous otitis externa may
most dogs and cats harbor small nwnbers
be associated with localized proliferation
of commensal gram-positive cocci. These
of Demodex sp in the external ear canals of organisms may become pathogenic if the
dogs and cats and may be the only area on
microenvironment is changed and
the body affected.

encourages their overgrowth. Exudate

Microbial cultmes are taken before

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obtained with a cotton-tipped applicator
otoscopy is completed and before any
can be rolled onto a glass slide, stained
cleaning is done. Samples for culture
with a 3-step quick stain or modified
should be taken with a sterile culturette

Wright's stain, and exan1ined under a
from the horizontal canal (the region where
microscope. (A study has shown that
most infections arise) or from the middle
heat fixing is not necessary for ear swab
ear in cases of tympanic rupture. A
cytology.) Smears should be examined
bacterial cultme and antibiotic sensitivity
microscopically under 4X, lOX, and oil
and an antibiotic mean inhibitory
immersion to look for nwnbers and
concentration should be done.

morphology of keratinocytes, bacteria,

Histopathologic changes associated with
yeasts, and WBCs; evidence of phagocytochronic otitis externa are often nonspesis of microorganisms; fungal hyphae; and cific. Histopathologic evidence of a
acantholytic or neoplastic cells.

hypersensitivity response may support a

A stained smear can quickly determine
recommendation for intradermal allergy
whether microbial overgrowth is present.

testing or for a hypoallergenic diet trial. In

Cocca! organisms are usually staphyloaddition, biopsies from animals with chronic, cocci or streptococci. Rod-shaped
obstructive, wulateral otitis externa may
organisms are usually Pseudomonas
reveal whether neoplastic changes are
aeruginosa, Escherichia coli, or Proteus present.

mirabilis; their appearance in large

Radiography of the osseous bullae is
nwnbers indicates that a bacterial culture
indicated when proliferative tissues
with antibiotic sensitivity should be
prevent adequate visualization of the
performed because of their known
tympanic membrane, when otitis media is
resistance to many antimicrobial agents.

suspected as a cause of relapsing bacterial

The presence of many neutrophils
otitis externa, and when neurologic signs
phagocytizing bacteria confirms the
accompany otitis externa. Fluid densities
pathogenic nature of the organisms.

and proliferative or lytic osseous changes

The yeastMalassezia pachydermatis is
provide evidence of middle ear involvefound in low nwnbers in the ear canals of ment. Unfortunately, radiographs are
many healthy dogs and cats. Because
normal in many otitis media cases. CT or
yeasts colonize the swface of the ear canal,

MRI, if available, should be petiormed for
they are most easily found adhered to
cases of severe, chronic otitis.

clumps of exfoliated squamous epithelial
cells. M pachydermatis is identified readily Treatment: Key to treatment is a on microscopic examination and its
discussion with the owner regarding the
nwnbers easily assessed. There is no
suspected or known cause of the otitis
specific nwnber that indicates yeast
externa, whether the otitis is curable, and
overgrowth. The key determining factor is
whether treatment must be longterm for
whether the ears are prw·itic. In addition,
resolution or lifelong management will be
if previous treatment did not include
required. All primary and secondary causes
antifungal therapy and if otitis externa is
and predisposing factors need to be
recurrent, antifungal therapy is warranted.

identified, managed, and treated. Manage

A dark exudate in the canal usually
ment of pain or pruritus must be included in
signals the presence of either Malassezia
the initial treatment protocol. Trarnadol for
spp or a parasite but may also be seen with
the first 5--7 days at 5 mg/kg, PO, tid, may be
a bacterial or mixed infection. In addition
especially beneficial. In addition, otitis
to stained cytology, otic exudate should be
externa is one of the few derrnatologic
examined for eggs, larvae, or adults of the
conditions in which glucocmticoids are
ear mite Otodectes cynotis and for
beneficial in the face of concurrent

Demodex mites in dogs and cats, and
antimicrobial use or sepsis. Glucocorticoids

Psoroptes cuniculi in rabbits and goats.

decrease swelling of the ear canal and may

Smears are made by combining cerwnen
be key to successful treatment. Preclnisone
and otic discharge with a small quantity of
or triamcinolone is used most commonly.

mineral oil on a glass slide. A coverglass

Duration depends on the severity. Ear
should be used, with the smear examined
hygiene is important; in paiticular, the hair
under low-power magnification. Rarely,
from the pre- and periamicular area should

530

OTITIS EXTERNA
be clipped, as well as hair from the surface
be avoided. They cause swelling of the
of the inner pinnae and ends of the ears.

lining of the ear canal and an increase in

This facilitates cleaning and treatment of
glandular secretions, which predispose to
the ears. Plucking of hair from the ear canal
opportunistic infections. Substances that
is conlroversial but may be needed to
are usually not irritating in normal ear
adequately resolve the ear infection. Hair
canals may cause irritation in an ear that is

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plucking is painful and should be done
already inflan1ed. This is particularly true of
under anesthesia.

propylene glycol. Powders, such as those

The first ear cleaning should be clone in
used after plucking hair from the canal, can
the veterinary clinic, and owners should
form irritating concretions within the ear
be instructed not to clean the ears until
canal and should not be used.

recheck in 5-7 days. Owners are often

Systemic therapy should be incorporated
w1able to clean the ears and/or are too
into the treatment regimen in most cases of
aggressive, causing fwther dan1age.

chronic otitis and in any case in which

Owners should initally focus on adminisotitis media is suspected. The most tration of topical and/or systemic drugs
common cause of recw-rent otitis externa
and can begin to clean the ears after the
is undiagnosed otitis media. Failure to use
first recheck and if the otitis is resolving.

systemic antimicrobial therapy is an

It is important to remember that topical
in1portant cause of chronic ear disease in
medications are inactivated by exudates,
dogs. Systemic antibiotics should be used
and excessive cerumen may prevent
when neutrophils or rod-type bacteria are
medications from reaching the epithelium.

found on cytology, in cases of therapeutic

The ears should be gently cleaned with an
failure with topical anti.microbial agents, in
ear cleaner that will remove the debris in
chronic recurring ear infections, and in all
the canal. Thick, d1y, or waxy material
cases of otitis media. (See also SYSTEMJC
requires a ceruminolytic solution such

PliAllMACOTHERAPEUTICS 01' THE INTEGUMENTAllY
as carbamide peroxide or dioctyl sodium

SYSTEM, p 2571.) Yeast infections in dogs
sulfosuccinate (DSS). If rods are seen,
can be treated with oral ketoconazole 5
the ear cleaner should contain squalene,
mg/kg/day, PO, for 15-30 days. Ketoconabecause one possible cause is Pseudomonas, zole should not be used in cats; itraconawhich can produce a biofilm that protects zole 2-3 mg/kg/day for 15-30 days or one
bacteria from antibiotics. The ears should
week on/one week off is recommended.

be thoroughly rinsed with wann water

Duration of treatment will vary
to remove residual ear cleaner. If the
depending on the individual case but
tympanic membrane is ruptured, detershould continue tmtil the infection is gents and DSS are contraindicated; milder
resolved based on reexamination and
cleansers ( eg, saline, saline plus povidone
repeat cytology and culture. Animals with
iodine, Tris EDTA) should be used to flush
bacterial and yeast infections should be
the ear.

physically examined, with cytologies

Effective treatment may require both
evaluated weekly to eve1y other week until
topical and systemic antin1icrobial therapy,
there is no evidence of infection. For most
along with pain medications and glucocoracute cases, this takes 2-4 wk. Chronic ticoids.The duration of treatment may vary
cases may take months to resolve, and in
from 7-10 days to >30 days, depending on
some instances, a therapeutic regimen
the diagnosis. In treatment of acute
must be continued indefinitely.

bacterial otitis externa, antibacterial agents

Methicillin-resistant Staphylococcus
in combination with corticosteroids reduce intermedius and Pseudomonus otitis exudation, pain, swelling, and glandular

(caused by Pseudomonas aeruginosa)

secretions. The least potent corticosteroid
have emerged as frustrating and difficult
that will reduce the inflammation should be perpetuating causes of otitis because of used (seep 2710).

the development of resistance to most

Most commercial topical products
common antibiotics. These infections
contain a combination of antibiotic/
are often chronic in course (>2 mo) and
antifungal and glucocorticoids. The volume associated with marked suppurative of the ear canal in most dogs is 1 mL, and
exudation, severe epithelial ulceration,
adequate treatment requires instillation of
pain, and edema of the canal. Successful
at least this volume twice daily. Products
treatment is multifaceted and should
with an aqueous base or those that have a
include the following steps: 1) identify the
thin film should be used; ointments are to
pri.maiy cause of the otitis and manage it,
be avoided.

2) remove the exudate via irrigation of the

Irritating medications ( eg, home
ear canal, 3) identify and treat concurrent
remedies and vinegar dilutions) should
otitis media, 4) select an appropriate

OTITIS MEDIA AND INTERNA

531
antibiotic from the results of culture and
resistance has been identified through
mean inhibitory concentration on the
culture. However, resistance is developing
organism and use it at an effective dosage
to fluoroquinolones.

for an appropriate duration, and 5) treat
topically and systemically until the

Maintenance Care: Owners should be
infection resolves (weeks to months).

shown how to properly clean the ears. The

The best treatment of chronic otitis is
frequency of cleaning usually decreases

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prevention. In addition to identifying the
over time from daily to once or twice weekly
cause of acute otitis, topical and/or
as a preventive maintenance procedure.

systemic medications should be chosen

The ear canals should be kept dry and well
based on cytology or culture; they should
ventilated. Using topical astringents in dogs
have a narrow spectrum and be specific for
that swim frequently and preventing water
the current condition. Aminoglycosides
from entering the ear canals during bathing
and fluoroquinolone antibiotics should not
should minimize maceration of the ear
be used unless absolutely required for
canal. CJu·onic maceration impairs the
successful treatment but are the most
barrier function of the skin, which
common ingredients in topical otic
predisposes to opp01tunistic infection.

medications. Because many topical

Preventive otic astringents may decrease
products contain a combination of
the frequency of bacterial or fungal
glucocorticoid, antibiotic, and antifungal
infections in moist ear canals. Clipping hair
medications, it is imperative to educate
from the inside of the pinna and around the
the owner on proper use (frequency and
external auditory meatus, and plucking it
duration). Many owners discontinue
from hirsute ear canals, improves ventilatreatment when the ear "looks better" before tion and decreases hunudity in the ears.

the infection is resolved. Polyrnyxin B

However, hair should not routinely be
and fluoroquinolone antibiotics have
removed from the ear canal if it is not
shown the best success in controlling Pseu
causing a problem, because doing so can
domonas infections in cases in which
induce an acute inflan11llatory reaction.

OTITIS MEDIA AND INTERNA

Otitis media, infla.nunation of the nuddle ear tilting or rotating the head towar·d the
structures, is seen in small and large domestic affected side; self-trarm1a can lead to aural •
animals, including dogs, cats, rabbits,
hematoma. The most con1J11on cause of
nmunants, horses, pigs, and camelids. It can
recurrent otitis extema is undiagnosed
be unilateral or bilateral and can affect
otitis media. When otitis extema (see
anin1als of all ages. Although typically
p 527) accompanies otitis media, the
sporadic, outbreaks are possible in herds.

external ear canal may look inflamed and

Otitis media usually results from extension of
contain an abnormal dischar·ge. The pinna
infection from the external ear canal through
or ear canal may be painful and malodorous,
the tympanic membrane or from nugration of
and the hair surrounding the base of the ear
pharyngeal nucroorganisms through the audimay be wet or matted. Because the facial tory tube. Occasionally, infection extends

( cranial nerve VII) and sympathetic nerves
from the inner ear to the nuddle ear, or
course through the middle ear, anin1als with
reaches the nuddle ear by the hematogenous
otitis media may exhlbit signs of facial nerve
route. Primary otitis media has been reported
paralysis ( eg, ear droop, lip droop, ptosis,
in certain breeds of dogs, particularly
collapse of the nostril) and/or Homer

Cavalier King Charles Spaniels. Untreated
syndrome ( eg, nuosis, ptosis, enophtl1alotitis media can lead to otitis interna mos, protrusion of the nictitating

(inflanunation of the inner ear structures) or
membrane) on the same side as the affected
to mpture of an intact tympanic membrane
ear. Exposure keratitis and corneal
with subsequent otorrhea or otitis extema
ulceration may develop. With facial
paralysis, the nasal philtrurn or lip may

Clinical Findings and Diagnosis: Signs
deviate away from the affected side. These
of otitis media include head shaking, rubsigns help to distinguish otitis media from bing or scratching the affected ear·, and
simple otitis externa.

532

OTITIS MEDIA AND INTERNA
apex
endolymphatic

=� r:rckc,tru '"'"

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�
membranous .-=----,; -� ,
utriculus

'

an1pullae

I

/
sacculus
crurn heHcis
pretragic ------4IIF-,...,_::,..,
notch
cochlear duct
inte1tragic notch

Left: Membranous labyrinth, internal ear, dog. Right: External ear, dog. Illustration by

Dr. Gheorghe Constantinescu.

With otitis intema, inflammation impairs
meningoencephalitis, or abscesses, with
function of the vestibulocochlear nerve
signs referable to those conditions. In

( cranial nerve VIII), resulting in hearing loss
horses, severe otitis media/interna can result
and signs of peripheral vestibular disease
in fusion and fi·acture of the tympanohyoid
such as head tilt, circling, leaning or falling
joint; extension of the fractw·e line to the
toward the affected side, general incoordinacalvariw11 can lead to intracranial spread of tion, or spontaneous horizontal nystagmus
infection or cause hematoma and death.

with the fast phase away from the affected

Whereas animals with otitis medial
side. Extension of infection from the inner
intema are usually alert, nonfebrile, and
ear to the brain leads to meningitis,
have a good appetite, those with meningitis
auditory ossicles

)

manubrium
mallei

Deep structures of tympanic bu Ila and tympanic membrane, cat. Illustration by Dr. Gheorghe

Constantinescu.

OTITIS MEDIA AND INTERNA

533
or meningoencephalitis are usually
when started early in the course of the
depressed, febrile, and inappetent. A major
disease. Chronic cases are often refractory
differential diagnosis for otitis media/
to treatment or recur after apparent
intema in mminants is listeriosis. However,
remission. When otitis externa accompain listeriosis, cranial nerves other than VII nies otitis media/interna, the ear should be
and VIII may be affected, causing signs such
examined closely for mites and foreign

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as dysphagia or loss of facial sensation, and
bodies, such as plant awns, and the
affected animals are usually depressed.

discharge cultured for bacteria. Many

In large animals, otitis media and intema
aerobic and anaerobic bacteria have been
are presumptively diagnosed based on
cultured from the ears of animals with
history and clinical signs. A history of
otitis media/interna, and mixed infections
bottle feeding or feeding of contan1inated
are common. Pathogens that warrant
milk to neonates, concurrent or previous
mentioning because of their frequency
respiratory disease, chronic ear infection,
of isolation include Malassezia spp and
or aural foreign body, in conjunction with

Pseudomonas spp in small animals;
typical signs of otitis media/intema, should

Stre'f}tococcus suis in pigs; Streptococcus prompt examination of the ear canal.

spp in horses; Mycoplasma spp in goats;

Otitis media is confinned by visualizing a
and Mannheimia. haemolytica, Pasteur0
bulging, discolored, or ruptured tympanic
ella multocida, Histophilus somni, and
membrane. Although the tympanic

Mycoplasrna bovis in cattle. M bovis is membrane may be visualized using a
particularly problematic in dairy calves fed
simple otoscope in many cases, the
unpasteurized waste milk from cows with
anatomy of the ear canal hinders visualizaintramammary infection. However, other tion in some species, such as horses and
pathogens, such as coliform bacteria,
llan1as; endoscopy, or video otoscopy, is an

Staphylococcus spp, Neisseria spp, alternative approach. Imaging methods
corynebacteria, and Tiue'f}erella pyogenes
assist in diagnosis and assessment of lesion are frequently isolated from the ears of severity. Radiography can detect osseous
affected animals. Isolation of a bacterial
changes in the tympanic bulla and fluid in
pathogen(s) or mites from the ear helps
the tympanic cavity if appropriate
direct initial treatment but does not
positioning and techniques are used.

necessarily imply causation of otitis media/

However, CT and MRI are more sensitive
interna, because the same organisms can
and are the preferred methods when
be isolated from the external ear canals of
feasible. In some cases, diagnosis is made
apparently healthy animals.

only at necropsy, using special techniques

Ear mites, when present, should be treatec
to expose the tympanic region. Diagnosis
with an appropriate systemic antiparasitic
of clinical otitis media/intema in one ear
agent (seep 2576). Topical acaricides can be should always prompt examination of the
instilled into the external ear canal once it
other ear to detennine whether subclinical
is cleaned. Bacterial infection should be
otitis is present.

treated with appropriate systemic antimicro

Otitis media has been reported to be
bial agents (seep 2571), based on culture and present in 16% of dogs with otitis extema
susceptibility test results. If the tympanic
and in >50% of dogs with chronic otitis
membrane is intact, a culture can be
externa. The tympanic membrane has also
obtained via a myringotomy incision with
been reported to be intact in > 70% of cases, a tom cat catheter. It may be possible to and the disease is usually bilateral in dogs.

aspirate fluid. If not, 0.5 mL of sterile water

Primary and secondary causes and factors
can be instilled into tile bulla and tile fluid
of otitis extema can lead to otitis media.

aspirated for culture. No antimicrobial

Diagnosis can be challenging, because
agents are labeled for treatment of otitis
the tympanic membrane can be intact.

media/intema in food-producing aninlals in

Palpation of the tympanic membrane
tile USA, so extra-label drug use guidelines
with a blunt instrument is not an accurate
must be followed and prohibited drugs
method of detem1ining the patency of the
avoided.

tympanic membrane. Advanced imaging

In addition to antin1icrobial and/or
techniques (CT or MRI) are more sensitive
anthelmintic therapy, the external ear canaj
than routine radiographs but are not 1000;6
should be cleaned and flushed if otorrhea
sensitive and specific. In some cases,
or otitis externa is present; physiologic
exploratory (and therapeutic) bulla
saline or dilute antiseptic solutions, such
osteotomy may be necessary.

as iodine,chlorhexidine,or hydrogen
peroxide, are commonly used for flushing.

Treatment and Prognosis: Treatment

Steroids or NSAIDs can help reduce
of otitis media/interna is most successful
inflammation and pain associated with

534

OTITIS MEDIA AND INTER NA
otitis media/interna. Corneal ulceration,
effective lavage. Tyrnpanostomy tubes can be
aw-al hematomas, and concurrent
implanted into the tympanic membrane after
infections should be treated appropriately,
myringotomy to allow continuous drainage
if present, and the animal protected from
in Cavalier King Charles Spaniels with
further self-injury.

primary secretory otitis, but such tubes are
lf the tympanic membrane is intact and
not useful to drain more pw-ulent exudate.

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otitis media/interna does not respond

Early diagnosis and treatment of otitis
sufficiently to systemic antimicrobial and
media/intema can result in complete
anti-inflammatory tl1erapy, myringotomy
resolution of infection and clinical signs.

(perloration of tl1e tympanic membrane) can

However, with severe, chronic, or
be performed to relieve pressw-e and enable
nonresponsive cases, owners should
cultw-e and drainage of fluid from the
be advised that new·ologic deficits and
tympanic cavity. In chronic, nonresponsive
hearing loss may persist even if infection is
or recurrent cases of otitis media/interna, it
resolved. In small anin1als, otitis media may
may be necessary to perlonn bulla
be resolved only by surgery (total ear canal
osteotomy or total ear canal ablation to
abalation), particularly ifmultid..tug-resistant
establish sufficient drainage and enable
bacteria are present.

TUMORS OF THE EAR CANAL

Ear canal twnors may arise from any of the

Chronic infection and inflammation do not
tissues lining or suppo1ting the ear canal,
subside, allowing neoplastic changes to
including the squamous epithelium, the
continue to develop.

ceruminous or sebaceous glands, or the

Incidence of benign and malignant ear
mesenchyrnal tissues. Malignant tumors
tumors is higher in American Cocker
arising from the external ear canal and pinna Spaniels than in other breeds. The density are more common in cats than in dogs.

of glandular tissue in the ear canal of this

True neoplasia in the ear is often
breed may be the reason. Middle-aged to
misdiagnosed during physical examination, older cats are predisposed to benign and because hyperplastic epithelial tissue and
malignant ear canal tumors, whereas
glands can appear as growths along the
young cats (3 mo to 5 yr) are more likely to
canal. Treatment of the infection and
develop nasopha.ryngeal polyps. Clinical
inflammation over time _can change the
signs of an ear canal tumor include
appearance of these growths and, in some
unilateral chronic otic discharge (cerumicases, they will actually disappear. In nous, pw-ulent, mucoid, or hemorrhagic)

contrast, neoplastic growths will not
and necrotic odor, head shaking, and ear
resolve with topical otic therapy.

scratching. Often, aural hematomas result

Although the precise cause of ear canal
from the head shaking associated with ear
tumors is unknown, several theories have
canal tumors. Draining abscesses in the
been postulated. Chronic inflanunation of
parotid region below the affected ear may
the ear canal may lead to hyperplasia,
result. If there is middle or.inner ear
followed by dysplasia and finally neoplasia. involvement, neurologic signs may be Bacterial degradation of the fatty acids and
present, including deafness, vestibular
other products produced in inspissated
signs (eg, head tilt, ataxia, nystagmus),
apocrine secretions from hyperplastic
facial nerve palsy or paralysis (facial
cerwninous glands dw-ing otitis externa
drooping, salivation, and dropping food
episodes may also stimulate carcinogenfrom the lips), Horner syndrome ( eyelid esis in the ear canal. Middle-aged dogs and
droop, pinpoint pupil, and inward rolling
cats are more likely to have benign otic
of the globe), and occasional protrusion of
tumors, whereas dogs and cats > 11 yr old
the third eyelid. In any case of medically
seem to have more malignant tumors. This
refractory tmilateral otitis, a neoplasm
seems to be attributed to chronicity of ear
of the ear canal or middle ear should be
disease rather than simply age. Tumors in
suspected.

the ear canal decrease the lwnen volwne,

Ear canal tumors in dogs are more
which leads to decreased drying of the
likely to be benign than malignant.

canal and impaired drainage of inflan1ma

Malignant otic neoplasms are locally
tory exudates and volatile fatty acids.

invasive, with <10%showing any lymph

TUMORS OF THE EAR CANAL

535
node involvement. Invasion of tumor into
canal surgically. More aggressive surgeries,
the bulla or surrounding tissue indicates
such as total ear canal ablation and bulla
a poorer prognosis. Cats have a higher
osteotomy, are recommended for
incidence of malignant otic tumors. The
malignant tumors of the middle ear. Lateral
most common pinna! neoplasms in dogs
ear canal resection for malignancies results
are sebaceous gland tumors, histiocyin a> 75% recurrence rate. Median survival VetBooks.ir
toma, and mast cell tumors. In cats,
time for animals with malignant ear canal
common pinna! neoplasms include
tumors has been reported to be >58 mo
squamous cell carcinoma, basal cell
in dogs and >11.7 mo in cats. Dogs with
tumors, hemangiosarcoma, and melanoextensive tumor involvement had a less cytic tumors. The most common external
favorable prognosis. Radiation therapy can
ear canal tumors reported in dogs are
be used to treat excised ceruminous gland
ceruminous gland adenomas and
adenocarcinomas in dogs and cats, with a
adenocarcinomas. Other tumors reported

56% 1 -yr survival rate reported. No data are
in the external ear canal of dogs include
available on the efficacy of chemotherapy
inflan1matory polyps, papillomas,
for otic tumors of dogs and cats.

sebaceous gland adenomas, histiocyto

Prognosis of animals with otic neoplasms
mas, plasmacytomas, melanomas,
can best be determined by histopathologic
fibromas, squamous cell carcinomas, and
examination of removed tissues.

hemangiosarcomas. The most common
external ear canal masses reported in cats

NASOPHARYNGEAL POLYPS
are nasopharyngeal polyps, squamous
cell carcinomas, and ceruminous gland

Nasopharyngeal polyps are uncommon,
adenocarcinomas. Lymphoma, fibrosarbenign, smooth, pink, fleshy, pedunculated, coma, and squamous cell carcinomas are
inflammatory growths of connective tissue
occasionally seen in the middle or inner
found in the external ear canals of young
ear of dogs and cats. (See also TUMORS OF'

cats. They arise from the mucosa! lining of

THE SKIN AND SOFT TISSUES, p 942.)

the tympanic bulla, the pharyngeal mucosa,
or the auditory tube. These polyps may be
congenital, or they may result from chronic

CERUMINOUS GLAND TUMORS
bacterial otitis media, commonly found in
cats with upper respiratory diseases. They

(Ceruminous gland adenoma or
are rarely found in dogs. They are not
adenocarcinoma)

neoplastic, and viruses have not been

Ceruminous gland tumors are best
identified in polyp tissue.

visualized in a degreased, clean ear using

Diagnosis involves sedation and deep
a video otoscope. These tumors may be
otoscopic examination of the horizontal
pedunculated or broad based but rise
canal. Purulent discharge from the bulla
above the level of the epithelium. They may may need to be flushed and suctioned be smooth or multilobulated in appearfrom the ear canal to visualize the polyp.

ance. In breeds other than the American

Use of a video otoscope greatly facilitates

Cocker Spaniel, these tumors are often
visualization and treatment of polyps.

primarily in the vertical ear canal. In the

Polyps originating from the eustachian

American Cocker, these tumors can be
tube may be seen by retracting the soft
found in the horizontal ear canal as well.

palate rostrally. Radiography of the bullae

Properly taken, ear canal biopsies can give
may reveal an opacity in the affected
useful information. However, superficial
bulla. CT or MRI may be helpful if a mass
ear canal biopsies are often reported as
is suspected in the tympanic bulla that
polyps with granulation tissue covered by
cannot be seen otoscopically. Definitive
epithelium. Deep en-bloc biopsies of the
diagnosis is made via histopathology.

same tissue are often reported correctly

Surgical removal is curative as long as
as tumors. CT or MRI may be very useful
the entire polyp and stalk are removed.

in assessing the tympanic bulla more

This often involves performing a bulla
completely and in detennining the extent
osteotomy, because the base of the polyp
of tun10r invasion, especially in malignant
is often in the tympanic bulla. Incomplete
tumors.

removal of the base of the polyp by

Surgical removal of benign ear canal
traction avulsion alone leads to rapid
tumors may be accomplished via lateral ear regrowth and return of clinical signs in canal resection for access to the tumor

15o/o-50% of cats. Topical steroids in the
mass. Laser surgery, especially when used
bulla for 30-45 clays seems to retard this
in conjunction with a video otoscope, has
regrowth. Systemic antibiotic therapy
made intraotic removal of these tumors
for the bacterial otitis media is also
relatively easy without having to open the
indicated.

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ENDOCRINE SYSTEM

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INTRODUCTION 538

General Chemical Structure and Function 538

Measurement of Hormones 540

Regulation of Endocrine Systems 540

Pathogenesis of Endocrine Disease 541

Principles of Therapy 542

THE PITUITARY GLAND 542

Hyperadrenocorticism 543

Nonfunctional Pituitary Tumors 54 7

Hirsutism Associated with Adenomas of the Pars Intermedia 54 7

Adult-onset Panhypopituitarism 548

Juvenile-onset Panhypopituitarism 549

Diabetes Insipidus 550

Feline Acromegaly 551

THE THYROID GLAND 552

Hypothyroidism 553

Non-neoplastic Enlargement of the Thyroid Gland (Goiter) 558

Hyperthyroidism 559

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM

METABOLISM 561

Calcium Physiology and Calcium-regulating Hormones 561

Hypercalcemia in Dogs and Cats 562

Hypercalcemia of Malignancy 563

Primary Hyperparathyroidism 564

HypercalcemiaAssociated with Hypoadrenocorticism 565

Renal Failure 565

Idiopathic Hypercalcemia of Cats 565

Other Causes of Hypercalcemia 566

Diagnostic Tests 567

Treatment 568

Hypercalcemia in Horses 570

Hypocalcemia in Dogs and Cats 570

Hypoparathyroidism 570

Other Causes of Hypocalcemia 5 71

Treatment 572

Hypocalcemic Disorders of Horses 572

THE ADRENAL GLANDS 573

Adrenal Cortex 573

Hyperadrenocorticism 573

Hypoadrenocorticism 574

Adrenal Medulla 575

538

ENDOCRINE SYSTEM

NEUROENDOCRINE TISSUE TUMORS 576

Adrenal Medulla 576

Thyroid C-cell Tumors 577

Chemoreceptor Organs 578

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THE PANCREAS 579

Diabetes Mellitus 579

Functional Islet Cell Tumors 582

Gastrin-secreting Islet Cell Tumors 583

ENDOCRINE SYSTEM INTRODUCTION

The endocrine system encompasses a group
sized initially as larger products (prepro-
of tissues that release hormones into circor pre-fom1s) that undergo processing to ulation for travel to distant targets. An
authentic hormone inside tl1e cell before
endocrine tissue is typically a ductless gland
secretion. Embedded in the gene coding for

( eg, pituitary, thyroid) that releases its
protein structure are amino acid sequences
hormones into capillaries permeating the

(signal peptides) that conununicate to the
tissue. These glands are richly supplied with
cell that these molecules are destined for
blood. However, nontypical endocrine tissues tl1e regulated secretory pathway. Other also contribute important hom1ones to
post-translational modifications may occur
circulation, eg, secretion of atrial natriuretic
during processing, including folding,
peptide from the heart, erythropoietin from
glycosylation, disulfide bond formation, and
the kidney, insulin-like growth factor from
subunit assembly. The folded and processed
the liver, and leptin from fat. New hormones
hormone is then stored in secretory
continue to be discovered. Some act only on
granules or vesicles in preparation for
a single tissue, whereas others have effects
release by the exocytotic process. Release
on virtually all cells of the body. The effects
of hormone is triggered by unique signals;
of hormones on tl1eir targets are variedeg, secretion of PTH is stimulated by a from enhancement of nutrient uptake to
decline in the concentration of ionic or free
altering cell division and differentiation,
calcium present in the extracellular fluid
among many others.

bathing the parathyroid chief cells. In most
cases, cells producing protein/polypeptide

GENERAL CHEMICAL STRUCTURE hormones store significant amounts of AND FUNCTION
these substances intracellularly; therefore,
they can respond quickly when increased

There are three main chemical categories of
amounts are needed in circulation. Generhom1ones: protein/pol ally, protein/pol
ypeptides, steroids,
ypeptide hormones have
and those made from modified an1ino acids.

relatively short half-lives in blood (minutes)

and do not travel in blood-bound carrier

Protein/Polypeptide Hormones:

proteins ( exceptions exist, eg, insulin-like

Examples of protein/pol
growth factor 1 is highly protein bound).

ypeptide hom1ones
include adrenocorticotropin (ACTH) from

Protein/polypeptide hormones act on their
the pituitary, insulin from the pancreas,
target cells by binding to receptors located
and parathyroid hormone (PTH). These
on the cell surface. These receptors are
honnones range in size from three an1ino
proteins and glycoproteins embedded in the
acids (thyrotropin-releasing hom1one) to
cell membrane that traverse the membrane
considerably larger proteins with subunit
at least once so that tl1e receptor is exposed
structure ( eg, luteinizing hormone). They
to both tl1e extracellular and intracellular
are produced in their endocrine tissue of
environments. There are several classes or
origin by transcription/translation of the
types of cell surface hom1one receptors tl1at
gene coding for the hormone and syn the-
translate tl1e hormonal message to tl1e cell

ENDOCRINE SYSTEM INTRODUCTION

539
interior by different means. Some are the
enzymes ( eg, isomerases, dehydrogenases)

G-protein (guanosine) coupled type, with
rapidly convert the molecule to the approseven transmembrane spanning domains.

priate steroid hormone. The identity of the

After hormone binding, these receptors
final steroidal product is thus dictated by the
activate a G-protein that is also located in the
set of enzymes expressed in that tissue.

membrane. One or more of the G-protein

Steroid hom10nes are hydrophobic and

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subunits affects other downstream
pass through cell membranes easily. In the
molecules (known as effectors) such as
blood, they are bound to a great extent to
enzymes ( eg, adenylate cyclase or phosphocairier proteins. Albumin binds many lipase C) or ion channels. Activation may
steroids fairly loosely; in addition, specific
result in production of a second messenger,
binding globulins exist for many steroid
such as cyclic AMP, that can then bind to
hormones. Most of the steroid hormone in
protein kinase A, causing its activation and
circulation is botmd to catTier proteins, and
subsequent phosphorylation of other
a small fraction circulates free or unbound.

proteins. Thus, signal transduction is a

This latter fraction is thought to be available
cascading and often an1plifying series of
for target cell entry, ie, the biologically
events triggered when a hormone binds to its
active portion. A rapid equilibrium exists
receptor. The ultin1ate effects in target cells
between protein-bound and unbound
are multiple and include such things as
steroid in extracellulai· fluid. Possible roles
triggering secretion, increasing uptake of
for steroid hormone-binding proteins
a molecule, or activating mitosis. Other
include aiding in tissue delivery of steroids
receptors, such as the one for insulin, not
by providing an even distribution to all cells
only bind h01mone but also act as enzymes,
within a target tissue, buffe1ing against large
with the ability to phosphorylate tyrosine
fluctuations in free honnone, and prolongresidues. The phosphorylated tyrosines in ing the half-life of steroids in blood. Relative
turn serve as docking sites for downstream
to protein/polypeptide hon11ones, steroids
signaing proteins.

usually have longer half-lives, often in the

Cell surface receptors are dynamic;
range of many minutes to hours.

their numbers and/or activity change with

Steroid hormones act on target cells via
physiologic conditions. In some cases,
receptors located in the cell interior. These
such as exposure to excessive amounts of
receptors are generally found in the nucleus,
hom1one, receptor down-regulation can
although some appeai· to reside, when
occur. Down-regulation and a decline in
unoccupied, in the cytoplasm. There are
target tissue responsiveness may be due
several classes of steroid receptors-those
to internalization of receptors after ligand
for glucocorticoids, rnineralocorticoids,
binding or to desensitization whereby
progestins, etc. Steroid receptors comp1ise
the receptor is chemically modified and
a family of related proteins that also show
becomes less active. Conversely, a lack of
homology to receptors for the thyroid
hormonal exposure can lead to an increase
hormones and vitan1in D. The receptor has
in receptor numbers on target cells
regions or domains that CatTY out specific

( up-regulation). Diseases have been linked
tasks: one for recognition and binding of the
to mutations in hormone receptors, which
steroid, another for binding to a specific
can result in inactivation or constitutive or
region on chromosomal DNA, and a third for
nonhom1onal activation of the pathway.

helping regulate the transcriptional complex.

In some instances, a single an1ino acid

Steroid hormones enter targets by diffusing
substitution is responsible.

through the cell membrane and then binding
to the receptor, causing a confom1ational

Steroid Hormones: Steroid honnones
change in the new complex. This, in turn,
are derivatives of cholesterol and include
leads to release of associated proteins ( eg,
products of the adrenal cortex, ovaries,
heat-shock proteins) and movement to the
and testes as well as the related molecule,
nucleus (if necessary), followed by binding
vitamin D. Unlike protein/polypeptide
of the complex to regions of DNA located
hormones, steroid hormones are not stored
near specific steroid-regulated genes. The
in large amounts. When needed, they are
result is a change in the rate of transc1iption
rapidly synthesized from cholesterol by a
of specific genes, either increasing or
se1ies of enzymatic reactions. Most of the
decreasing their expression. Thus, steroid
cholesterol needed for rapid steroid
hon11ones prin1aiily function by affecting the
hormone synthesis is stored intracellularly
production rates of specific messenger RNA
in the tissue of origin. In response to
and proteins in targets. Steroid action is
approp1iate signals, the precursor is moved
relatively slow in onset (hours) but may
to organelles ( mitochondria and smooth
be long lasting because of the duration of
endoplasmic reticulum), where a series of
production and half-lives of the messenger

540

ENDOCRINE SYSTEM INTRODUCTION

RNA and proteins induced in target cells.

nanomolar (10-9) range. In recent years,

It is increasingly clear that some steroids
nonradioactive tags, "sandwich-type"

also act via nongenomic mechanisms. For
assays, and ELISA methods have been
exan1ple, many of the anti-inflammatory
developed for hormone measurement.

effects of glucocorticoids are thought to be

Accurate measurement in veterinary
due to the glucocorticoid-receptor complex
species presents some challenges, because

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binding to, and inhibiting the action of, pronormal concentrations of a given honnone inflan1111ato1y transcription factors inside
can vary significantly between species. For
cells.

example, normal total T4 concentrations

Steroids in the blood are elin1inated by
in dogs and cats are -4 tin1es lower than
metabolism in the liver. Reduced forms are
those in people. Concern about crossproduced and subsequently coajugated reactivity is important; protein/polypeptide
to glucuronic acid and sulfate. These
hmmones vary in amino acid composition
metabolites a.re freely soluble in blood and
and in other structural ways ( eg, patterns
are eliminated from the body by renal
of glycosylation) across species. As a
excretion and tllrough the GI tract. Small
consequence, antibodies made against a
amounts of free steroid h01mone are also
pa1ticular hormone may not recognize that
directly excreted by the kidneys.

material from another species. Finally,
while steroid hormones are structurally

Modified Amino Acid Hormones:

identical across species ( cortisol in dogs

This class of hom1ones is made by chemiis identical to that in people), substances cal modification of amino acids, mainly
present in the serwn of a given species can
tyrosine. They include thyroid hormones
sometimes interfere in an assay, leading
and the catecholamines epinephrine and
to inaccurate results. Overall, it is
norepinephrine. Thyroxine (T4) and
important that a laboratory providing
triiodothyronine (T3) are stored in the
measurement of a particular hormone in a
thyroid as a part of thyroglobulin;
species demonstrate that the assay is valid
secretion of these hormones involves
in that species and that the laboratory has
thyroidal cell uptake and breakdown of
established normal ranges.

this large molecule liberating T and T

4

3•

Thyroid hormones act on targets much

REGULATION OF ENDOCRINE
like steroids; they are relatively water
insoluble, transported by carrier proteins

SYSTEMS
in blood, and act on targets via intracellu

Secretion of honnones is regulated by a
lar receptors. Catecholamines are
system of sensing elements possessing the
manufactured by hydroxylation, decarmeans to detect need for both increased and boxylation, and methylation of tyrosine
decreased secretion. The particular sensing
and are secreted into the blood from the
network, feedback elements, and network
adrenal medulla: They have exceedingly
of control responses are wlique for each
short half-lives ( <5 min), are not protein
hormone. Hormonal pathways maintain
bow1d, and act on targets via cell surface
homeostasis, and adjustments in secretion
receptors ( o.- and 13-adrenergic receptors).

usually result in changes that will help maintain the status quo. In addition, secretion MEASUREMENT OF HORMONES
and activity of a particular hormone may be
adjusted upward or downward in response

Because hormones circulate in low quanto challenges such as chronic stress, disease, tities in blood, accurate measurement of
or change in nutritional status. TI1e concept
these substances requires sensitive assays,
of negative feedback and its relationship to
usually in the fom1 of a competitive
control of hom1onal patl1ways is in1portant
inmmnoassay. The original method (still
in understanding pathway regulation and
widely used) is radioinununoassay
evaluation of endocrine function tests. For
employing an antibody directed against the example, insulin is released in response to hormone and a radio-labeled form of the
an increase in glucose concentration bathhormone. The labeled hormone competes ing the 13-cells in the pancreatic islets of
with unlabeled hormone for antibody

Langerhans. One of insulin's actions is to
binding sites. A standard curve containing
lower glucose concentrations in extracellular
known amounts of ho,mone is used for
fluid by enhancing its uptake in target tissues.

comparison to calculate the concentration

TI1is decline in glucose leads to reductions in
of hom10ne in patient samples. The use of
insulin secretion. In patients suspected of
radioactive tags permits detection of low
having an insulin-secreting twnor, the finding
concentrations of hormone, which
of a low blood glucose concentration
typically circulate in the pico- (l0-12) or

(hypoglycemia) together with an increased

ENDOCRINE SYSTEM INTRODUCTION

5·41
insulin concentration demonstrates
sufficient amounts to cause clinical signs; eg,
inappropriate feedback, characteristic of
certain tumors ( apoc1ine gland tumors of the
such a tumor. In another exan1ple, patients
anal sac in dogs, lymphoma) can manufacshowing increased blood calciwn concentrature PTH-related protein that can mimic PTH
tions should have low levels of PTH in
action, resulting in hypercalcemia
circulation. Measurement of high PTH levels

Syndromes associated with deficient
in such patients indicates a malfwlction at
or absent honnone secretion also have

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the level of the parathyroid, most often
multiple causes. Endocrine tissue
associated with parathyroid adenoma
destruction secondary to cell-mediated

Secretory patterns of hormones vary
autoin1mune attack is often believed to
tremendously. The thyroid honnones tend
be the cause. Examples of endocrine
to have less variability than the steroid
hypofunction resulting from prin1ary tissue
hormones and show only moderate daily or
loss include canine hypothyroidism, type
weekly variation. In contrast, blood levels

1 diabetes mellitus, primary hypoparathyof the adrenal steroid cortisol show much roidism, and primary hypoadrenocorticism.

more fluctuation, with occasional bursts

In early stages of tissue loss, compensatory
of secretion followed by periods of low
mechanisms involving feedback pathways
activity (low blood levels) occurring
stimulate activity (hom10ne production)

throughout the day.

from the remaining tissue. For example, in
prin1ary hypoadrenocorticism (Addison

PATHOGENESIS OF ENDOCRINE
disease), secretion of pituitary ACTH

DISEASE
increases as the adrenal co1tex disappears.

The increased trophic support results in full

Endocrine diseases can arise from many
activation of the remaining tissue and often
causes. Hormones can be over- or underproprovides sufficient hormone secretion to duced, receptors can malfwlction, and
delay signs of deficiency until tissue loss
normal pathways for hormone removal may
simply eliminates the hom10nal source.

be disrupted. Clinical signs consistent with

Disorders resulting in clinical signs of
malfwlction in an endocrine tissue may
endocrine hypoactivity may also occur
develop because of a problem originating in
due to disruption in tissues distant from
the source of the hormone itself or may be
the hormone source. Secondary hypothydue to disruption in another location that is roidism results from pituitary thyroidsecondarily affecting hormone secretion or stimulating hormone insufficiency that
action.

reduces the stimulus needed at the thyroid

In veterinary medicine, the most common
for T4 and T 3 production and secretion.

types of endocrine disease are hormonal

Patients receiving glucocorticoid therapy
overproduction associated with either a
may experience atrophy of the cortisoltumor or hyperplastic tissue manufacturing producing zones in the adrenal cortex.

excessive amounts of hormone, and

The exogenous steroid initiates Regative
hormonal deficiency due to destruction
feedback on the pituitary gland, suppressof the endocrine tissue source. Common ing ACTH secretion and leading to adrenal
diseases associated with hormonal
cortical atrophy. Another potential cause
overproduction are hype1thyroidism in cats
of endocrine hypofunction relates to tissue
and hyperadrenocorticism (Cushing disease) loss secondary to compressive and/or in dogs. Often, the abnom1al endocrine
destructive growth of nonfunctional
tissue not only overproduces hom1one but
twnors.

also fails to respond nom1ally to feedback

Endocrine disease and related malasignals, contributing to inappropriate release dies also result from alterations in tissue
of hmmone. Hom10nal overproduction from
responsiveness to hormones. An impo1tant
an endocrine tissue can also result from
example is type 2 or non-insulin-dependent
stimulation arising from a secondary source;
diabetes mellitus, in which relative
eg, renal disease can result in parathyroid
insensitivity to insulin is observed, often
hyperplasia and oversecretion of PTH.

associated with obesity. Nephrogenic

Hyperphosphatemia occurs as a consediabetes insipidus is due to renal insensitivquence of some types of renal disease. This ity to the actions of vasopressin (antidiuleads to decreased fmmation of the active retic hormone). The renal insensitivity to
form of vitamin D, 1,25-dihydroxycholecalvasopressin in this syndrome may relate to ciferol ( calcitiiol). In tum, low calcitriol
congenital abnom1alities in the vasopressin
concentrations contribute to low calciwn
receptor but more often is secondary to
levels in exti·acellular fluid, which act as a
other diseases ( eg, pyometra, hyperadrenostimulus for PTH secretion. Nonendocrine corticism) or abnormalities in ion concentissues can produce and secrete hormones in ti·ations ( eg, hypokalemia, hypercalcemia).

542

ENDOCRINE SYSTEM INTRODUCTION

PRINCIPLES OF THERAPY
response and other suitable measures
such as therapeutic blood monitoring (eg,

Endocrine diseases involving hyperactivity
post-pill measurement ofT concentramay be treated surgically (tumor removal), 4
tions, measurement of sodium and
by radiotherapy ( eg, 1311 for hyperthyroidpotassium in serum in patients with ism), or medically ( eg, methimazole as an
primary hypoadrenocorticism). Replace

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antithyroid drug). Syndromes of ho1mone
ment therapy is often required for a time
deficiency are often successfully managed
after surgical removal of an endocrine
by sin1ply replacing the missing hormone(s), twnor. However, remaining normal tissue such as insulin treatment in diabetes
that was atrophied as a consequence of
mellitus or thyrnid hormone replacement
the disease often recovers activity in a
therapy in hypothyroidism. Replacement
fairly short period of tinle, obviating need
therapy for deficiencies related to protein/
for lifelong replacement therapy. Animals
polypeptide honnones can present a
show significant variation in drug
challenge. Often, the species-specific
bioavailability; thus, a proper dosing
version of the hom1one is not available, the
schedule should be tailored to each
drug may need to be injected several times
patient.

per day, or the possibility of antibody

Glucocorticoids a.re commonly used
fo1mation and anaphylaxis must be
therapeutic drugs, particularly because of
considered. Steroid and thyroid ho1111ones
their anti-inflamma.tmy and anti-allergic
can usually be administered orally. Some
activity. Proper use requires an understandprotein/polypeptide hormones or analogues ing of their adverse effects, including the
are effective when given by routes other
potential appearance of signs of hyperthan ir\jection ( eg, the anti diuretic hormone adrenocorticism resulting from longterm
analogue desmopressin acetate is effective
therapy or from use of potent derivatives.

when administered by a variety of routes).

Such adverse effects can be minimized by

Hormonal replacement therapy should
use of orally administered glucocorticoids
be monitored by assessment of clinical
given on alternate days.

THE PITUITARY GLAND

The pituita.J.y gland Q1ypophysis) is
enter an actively synthesizing phase in
composed of the adenohypophysis ( ante1ior response to increased demand for a lobe) and the neurohypophysis (posterior
particular hormone. Secretory cells in the
lobe).

adenohypophysis a.re often subdivided into
chromophils (acidophils, basophils) and

Adenohypophysis: The adenohypophychromophobes based on interaction of the sis, which surrounds the pa.rs nervosa of the
secretory granules with pH-dependent
neurohypophyseal system to varying
histochemical stains.

degrees in different species, consists of the

Acidophils a.re further subdivided
pa.rs distalis, the pars tuberalis, and the pa.rs
into somatotrophs that secrete growth
intennedia. The pa.rs distalis is the largest
hormone (GH, somatotropin) and
pa.rt and contains multiple populations
lactotrophs that secrete prolactin.

of endocrine cells. The pars tuberalis

Basophils include gonadotrophs that
functions primarily as a scaffold for the
secrete both luteinizing hormone (LH) and
capillary network of the hypophyseal portal
follicle-stimulating hom10ne (FSH), and
system. The pars intermedia forms the
thyrotrophs that secrete thyrotropic
junction between the pa.rs distalis and pa.rs
hormone (thyroid-stimulating hormone
nervosa. It contains two populations of cells

[TSH]). Clu·omophobes include the
in dogs, one of which synthesizes adrenoendocrine cells involved in the synthesis corticotropic hormone (ACTH).

of ACTH and melanocyte-stin1ulating

A specific population of endocrine cells in
hormone (MSH), nonsecretory follicular
the pa.rs distalis (and in the pars intermedia
cells, and undifferentiated stem cells.

for ACTH in dogs) synthesizes and secretes

Endocrine cells in the adenohypophysis
each of the pituitary trophic ho1111ones.

are under the control of corresponding

Pituitary cells have a secretory cycle and
hypothalamic-releasing ho11110nes. These

THE PITUITARY GLAND

543
releasing ho1mones are conveyed by the
several hundred times lai·ger than the
hypophyseal portal system to specific
antidiuretic dosage, ADH has a pronounced
cells in the adenohypophysis, where they
pressor effect, which may also lead to
stinmlate the rapid release of prefonned
coronary constriction. The contractile
trophic horn1ones.

mechanism of the capillaries, as well as GI

Separate hypothalamic-releasing
ai1d uterine muscle, is stimulated, and a

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horn1ones regulate the rate of secretion of
prolonged increase in blood pressure
each trophic hormone from the adenohypofollows.

physis. For most pituitary trophic horn1ones,

Oxytocin has specific effects on the
negative feedback control is accomplished
smooth muscle of the uterus and the
by a feedback loop involving the blood
myoepithelial cells of the mat1Unaty gland.

concentration of the hormone produced by

It has no established physiologic function
the target endocrine gland ( eg, thyroid
in tl1e male, although an effect on spem1
gland, adrenal cortex, ovary, and testis).

trai1sport has been suggested.

Honnones such as prolactin, GH, and MSH
have more complex feedback mechanisms.

HYPERADRENOCORTICISM

For example, prolactin affects primatily the
mat1l.lllary gland, and GH has its principal

(Cushing disease)

effect on the liver-both nonendocrine
tissues. The negative feedback in such cases

Hyperadrenocorticism may be divided
includes metabolites and other messengers
into two broad categmies. One category,

( eg, insulin-like growth factor I produced
pituitary-dependent hyperadrenocorticism,
by the liver). In the case of GH, there is an
arises from adenomatous en!ai·gement of tl1e
inhibitory (somatostati.n) as well as
pituitary gland, resulting in excessive ACTH
stimulatory (GR-releasing hormone)

production. The other category, adrenalhypothalamic regulator.

dependent disease, is associated with
functional adenomas or adenocai·cinomas of

Neurohypophysis: The neurohypophythe adrenal gland. Ectopic ACTH secretion sis (pars nervosa, postelior lobe) has three
has not been repo1ted in dogs; however, in
anatomic subdivisions. Secretion granules
people, ectopic ACTH secretion is associthat contain the neurohypophyseal ated with ce1tain lung tu.n1ors. Iatrogenic
hormones, ie, antidiuretic hormone (ADH,
hyperadrenocorticism results from clu·onic
vasopressin) and oxytocin, are synthesized
excessive exogenous steroid administration.

in the hypothalatnus but are released into
the bloodstream in the pars nervosa. The

Clinical Findings: Hyperadrenocorticism
infundibular stalk joins the pat'S nervosa
is seen in middle-aged to older dogs (7-12 yr
to the overlying hypothalanms.

old); -85% have pituitary-dependent hyper

ADH, an octapeptide synthesized in the
adrenocmticism (PDI-I), and -15%have
hypothalamus, is packaged into membraneadrenal tu.n101"S. Breeds in which PDH is lirnited granules with a con-esponding
conunonly seen include Miniature Poodles,
binding protein (neurophysin) and

Dachshunds, Boxers, Boston Terriers, ai1d
transported to the pars nervosa, where it is

Beagles. Large-breed dogs often have adrenal
released into the circulation. ADH binds to
tu.nlors, and there is a distinct predilection in
specific receptors in the distal part of the
females (3: 1 ). In cats, hyperadrenoco1ticism
nephron and collecting duct of the kidney;
is found in middle-aged to older cats, with a
it increases the renal tubular reabsorption
slight predilection in females (60"Ai).

of water from the glornerular filtrate.

The output of ADH is directly related to the
degree of hydration of the body. Hydration
of the body inhibits release of ADH, whereas
dehydration or injection of hypertonic
electrolyte solutions favors release of ADH,
which in turn causes increased water
resorption from the glomerular filtrate,
resulting in dilution and decreased
osmolarity of body fluids. Bat'biturates, ether,
chloroform, morphine, acetylcholine,
nicotine, and pain increase ADH release,
which leads to less urine fonnation. Ethanol
inhibits ADH release, which leads to diuresis.

Hyperadrenocorticism in a 7-yr-old intact,

The pressor effect of ADH is less promfemale Miniature Poodle. Cocrtesyof inent than the at1tidiuretic effect. At a dosage Dr. Stephen White.

544

THE PITUITARY GLAND

The most common clinical signs in dogs
diabetes mellitus and insulin resistance. The
and cats are polydipsia, polyuria, polyphahemogra.m is characterized by evidence of gia, heat intolerance, lethargy, abdominal
regeneration ( eryth.rocytosis, nucleated
enlargement or "potbelly," panting, obesity, RBCs) and a classic stress leukogra.m
muscle weakness, and recunent urinary

( eosinopenia, lymphopenia, and mature
tract infections. The panting and increased
leukocytosis). Basophilia is occasionally

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respiratory rate may be a result of the
seen. Many dogs with hyperadrenocortienlarged liver pushing against the diaphragm cism show evidence of winary tract and limiting the depth of respiration.

infection without pyuria (positive culture),

Dem1atologic manifestations of hyperadrenbacteriwfa, and protei.nuria resulting from ocorticism in dogs can include alopecia
glomerulosclerosis. In cats, polydipsia and

( especially truncal), thin skin, phlebectasias,
polyuria are a result of concurrent diabetes
comedones, bruising, cutaneous hyperpigmellitus, and urine specific gravity is usually mentation, calcinosis cutis, pyodenna,
high. In dogs, cortisol-induced interference
dermal atrophy ( especially around scars),
with ADH binding results in hyposthenuria,
secondary demodicosis, and seborrhea. In
and central diabetes insipidus may occur as
cats, the most striking dennatologic sign is
a result of pituitary tumor enlargement.

increased skin fragility; many cats present
with self-inflicted cutaneous wounds.

Diagnosis: There is no single test or

Secondary infections ( especially respiracombination of tests that is 100% accurate tory) are also common in cats.

for diagnosing hyperadrenocorticism. The

Uncommon clinical manifestations
sensitivity and specificity of individual tests
include hypertension, pulmonary th.romor combinations of tests are increased when boembolism, bronchial calcification,
they are applied to a patient population likely
congestive heart failure, and new·ologic
to have hyperadrenocorticism. The diagnosis
signs, such as polyneuropathy or myopathy,
should be based on appropriate clinical signs
behavior changes, blindness, or pseudomyofollowed by suppmting minimun1 database tonia. Hypercortisolemia may be evident as
abnormalities ( eg, high cholesterol, SAP),
weakening of collagen manifesting as
and confirmed via an approptiate screening
cranial cruciate rupture (small dog) or a
test for hyperadrenocorticisrn. If screening
nonhealing corneal ulceration. Reproductest results are inconclusive, or if laboratory tive signs of hyperadrenocotticism can
abnonnalities associated with hyperadrenoinclude perianal adenoma in a female or corticism ( eg, increased SAP) are noted in a
castrated male, clitoral hypertrophy in
dog without clinical signs, the dog should be
females, testicular atrophy in intact males,
retested 3--6 mo later rather than treated
or prostatomegaly in castrated male dogs.

without a definitive diagnosis. In particular,

In dogs, serum chemistry abnom1alities

. the diagnosis of sex steroid-induced
associated with hypercortisolemia include

Cushing disease may be especially difficult.

increased seflllll alkaline phosphatase

The urine cortisol to creatini.ne ratio

(SAP), increased ALT, hypercholester

(UCCR) is a highly sensitive test to
olemia, hyperglycemia, and decreased BUN. differentiate healthy dogs from those with Hypercholesterolemia is due to steroid
hyperadrenocorticism, but it is not highly
stimulation of lipolysis. SAP is inqeased
specific because dogs with moderate to
primarily from induction of a specific
severe nonadrenal illness also exhibit
hepatic isoenzyn1e; some also comes from
increased ratios. UCCR should be deterhepatic glycogen deposition and vacuolizamined based on free-catch urine collected at tion impinging on the biliary system. SAP is
home by the owner. The stress of transportseldom increased in cats ( <2096), because ing the dog to the veterinary hospital, the
they lack the specific hepatic isoenzyn1e for
stress of cystocentesis, or both, can be
it. Increased seflllll ALT and AST are caused
enough to cause a falsely increased UCCR.

by hepatocellular necrosis, glycogen

An increased UCCR should be confirmed
accumulation, and swollen hepatocytes.

with an ACTH stimulation test, an IV

Decreased seflllll phosphorus may be a
low-dose dexarnethasone suppression
result of increased urinary excretion due

(LDDS) test, or an oral LDDS test.

to polyuria. Abnormalities noted on the

The LDDS test is the screening test of
biochemical profile may also include
choice for canine hyperadrenocorticism
hyperglycemia due to increased gluconeowhen properly used. Only 5o/<r-8% of dogs genesis and decreased peripheral tissue
with PDH exhibit suppressed cortisol
utilization through insulin antagonists.

concentrations at 8 hr (ie, are false

Approxin1ately 100/o of Cushingoid dogs are
negatives). In addition, 300/o of dogs with
diabetic; however, in cats with hyperadren

PDH exhibit suppression at 3 or 4 hr
ocorticism, almost 800/o present with ovett
followed by "escape" of suppression at 8 hr;

THE PITUITARY GLAND

545
this pattern is diagnostic for PDH, making
the pituitary can be suppressed by
further testing UIUlecessary. The major dissupra.physiologic concentrations of steroid.

advantage of the LDDS test is the lack of

Dogs with autonomous cortisol-producing
specificity in dogs with nonadrenal illness:

adrenal tumors have maxin1ally suppressed

>500A, of dogs with nonadrenal illness have a

ACTH production via the nonnal feedback
positive LDDS test. In such cases, the dog
mechanism; therefore, administration of

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should be allowed to recover from the
dexamethasone, no matter how high the
nonadrenal illness before testing for
dose, caimot suppress serum cortisol
hyperadrenocorticism with an LDDS test.

concentrations. In dogs with PDH, however,

Another option, particularly in cats, is to
the high dose of dexan1ethasone is able to
perfom1 an oral LDDS test using the UCCR
suppress ACTH and, hence, cortisol
as the discrin1inator. In this test, morning
secretion. One inlporta.Ilt caveat is that dogs
urine is collected for a baseline on days 1 and
with pituitary macroadenomas (15%-500A,of

2. On the second day after urine collection,
dogs with PDH) do not suppress on the
three doses of dexan1ethasone at 0.1 mg/kg

HODS test.

(cats) or0.01 mg/kg (dogs) is administered

Measurement of endogenous plasma
every 6 hr and a urine sample is collected for

ACTH concentrations is the most reliable

UCCR measurement the next morning. The
way to discrinlinate between PDH and adrefirst two samples can be combined into a nal tumors. Dogs with adrenal tumors have
single "pre" or baseline sample. lf the UCCR
low to w1detectable ACTH concentrations;
does not decrease into the normal range
in contrast, dogs with PDH have normal to
after oral dexamethasone, the diagnosis of
increased ACTH concentrations. Recently,
hyperadrenocorticism can be confim1ed.

researchers have found that the addition of

The ACTH stinlulation test is used to
the protease inhibitor, aprotinin, to whole
diagnose various adrenopathic disorders,
blood in EDTA tubes inhibits the degradaincluding endogenous or iatrogenic tion of ACTH. San1ples may be collected,
hyperadrenocorticism and spontaneous
spun in a nonrefrigerated centrifuge, and
hyperadrenocorticism. As a screening test
kept for as long as 4 days at <4°C.

for the diagnosis of naturally occurring

Diagnostic imaging of the pituitary and
hyperadrenoco1ticism, it has a diagnostic
the adrenal glands can be accomplished via
sensitivity of -80%--85% and a higher
abdominal radiography, ultrasonography,
specificity than the LDDS test. In one study, CT, or MRI. Abdominal radiographs should only 15% of dogs with nonadrenal disease
be perfonned in all dogs that do not
had an exaggerated response to ACTH
suppress on an HODS; -300/o--500A, of dogs
stinlulation. Adrenal tumors may be
with adrenal tunlors have a mineralized
particularly difficult to diagnose using an
mass in the area of the adrenal glands.

ACTH stinlulation test; however, an ACTH

Abdominal ultrasonography is a more
stimulation test is the test of choice for
sensitive way to identify adrenal twnors. In
iatrogenic hyperadrenocorticism.

addition, liver metastasis or invasion into

Dogs with adrenal sex steroid excess may the vena cava may be demonstrated in dogs have negative ACTH stimulation and LDDS
with adrenal cai·cinomas. CT or MRI of the
tests, because serum cortisol concentrabrain or abdominal cavity in dogs that do tions are normal. This may be due to excess
not suppress on the HODS may demonstrate
cortisol precursors. Increases in progeste1�
unilateral adrenal enlargement (500Ai),
one, 17-0H-progesterone, androstenedione,
pituitary macroadenoma (25%), or pituitary
testosterone, and estrogens may require
microadenoma (25%).

dynamic adrenal testing using the ACTH
stinlulation test and measurement of sex

Treatment and Prognosis: Three
steroids in addition to cortisol.

treatment options are available for

After the diagnosis of hyperadrenocortihyperadrenocorticism in dogs. Medical, cism has been confinned, differentiation of
surgical, and radiation therapy have all been
pituitary- versus adrenal-dependent disease
used with varying degrees of success.

may be necessary. Although most dogs with

Dogs with PDH may be treated using the
hyperadrenocorticism have PDH, in atypical
adrenolytic agent mitotane (o,p' -DOD),
cases ( eg, anorectic dogs with hyperadrenobeginning with an induction dosage of corticism ), a differentiation test is appropri25-50 mg/kg/day for 7-10 days. Dogs ate. In particular, differentiation of PDH
should be monitored for signs of

( often macroadenomas) from adrenal
hypoadrenocorticism, such as anorexia,
tumors is often necessaiy in large breeds.

vomiting, and diarrhea; if such signs

The high-dose dexamethasone suppresoccur, mitotane therapy should be sion (HD DS) test works on the principle
discontinued and glucocorticoids
that autonomous ACTH hypersecretion by
administered. Water consumption or

546

THE PITUITARY GLAND
appetite may be measured to provide an
as well. Selegiline is an irreversible
endpoint for therapy; water consumption
monoamine oxidase (type B) inhibitor that
should decrease to <60 mllkg/day (dogs).

increases dopamine levels. Dopamine

After 7--10 days of therapy with mitotane
inhibits ACTH release from the pituitary
or a reduction in water or food consumpgland. However, only --200,1, of cases with tion, an ACTH response test should be

PDH can be expected to respond; no
performed to determine whether cortisol
significant changes in serum cortisol or

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suppression is adequate. Cortisol levels
creatinine, ACTH stimulation, or LDDS
measured both before and after the ACTH
have been noted with selegiline therapy.

response test should be in the normal

Treatment of iatrogenic hyperadrenocorrange. To maintain suppression of cortisol ticism should include a change to an oral,
secretion, mitotane is administered at a
short-acting steroid such as prednisone or
dosage of 50 mg/kg/wk. Dogs on longterm
prednisolone. Gradually, the steroid dose
treatment with mitotane should have an
is decreased from -1 mg/kg to 0.5 mg/kg
examination and ACTH response test
throughout several weeks and then tapered
every 3-4 mo. Gradually increasing
to an alternate-day schedule until the
dosages of the drug are often required to
adrenal glands can respond to ACTH
maintain adequate clinical remission.

stimulation. Monthly ACTH stin1Ulation

Adverse effects of mitotane at the
tests may be performed to detern1ine when
recommended dosage include GI irritation
steroid treatment can be discontinued.

(vomiting and anorexia), CNS disturbances

Surgical removal of unilateral adrenal

(ataxia, weakness, seizures), mild
adenomas or adenocarcinomas may be
hypoglycemia, and a moderate increase in
indicated in some cases; however, surgical

SAP. Signs such as depression or ataxia can
and anesthetic complications (eg, hypotenbe alleviated by dividing the daily dose into sion) may develop secondary to hypoadtwo equal parts administered at 8- to 12-hr renocorticism, which occurs immediintervals. Persistence of CNS signs after ately after surgical removal of the tumor.

mitotane is discontinued suggests an

Median survival for dogs with carcinomas
expanding pituitary macroadenoma.

treated with surgical excision was 778

Reports have demonstrated the efficacy of
days. The metastatic rate was 5% at time of
the adrenal enzyme inhibitor trilostane in the
surgery and 14% longterm. With unilateral
treatment of PDH in dogs. Studies in dogs
adrenalectomies, mortality within 1 mo
with hyperadrenocorticism have shown that
after surgery was 14%--60%; overall rate
trilostane is an effective steroid inhibitor
for cure for adrenal tumors was -500,1,.

with minimal adverse effects. Trilostane

Medical treatment of adrenal tumors is
must be administered daily and often twice
difficult, because they tend to be resistant
daily to achieve a decrease in glucocorticoid
to.the effects of mitotane. Adrenal tun1ors
secretion from the adrenal glands. Mineraloare relatively resistant to mitotane; dogs co1ticoid insufficiency, which is.reversible,
require as much as four times the dose of
can also be seen in anin1als receiving
mitotane to respond, and clinical response
trilostane; a few cases of adrenal necrosis
tends to be less favorable. Finally, if the
with permanent adrenal insufficiency have
dog is showing neurologic signs ( eg,
been seen after trilostane administration.

anorexia, stupor, or seizures) and a large

Trilostane may prove to be a reasonable
pituitary tumor (macroadenoma) is
alternative to rnitotane therapy for PDH in
identified, radiation therapy of the
dogs. Dogs with sex steroid imbalance also
pituitary gland is indicated. Newer types
may benefit from tJilostane therapy, because
of radiation therapy ( cyberknife, gamma
the enzyme inhibitor affects precursors of
knife) may prove to be superior to
cortisol synthesis in addition to inhibiting
previously available modalities and can
cortisol synthesis itself.

treat pituitary tumors in <3 days with

Radiation therapy of pituitary tumors is
minimal adverse effects. Results of
associated with a high rate of response;
radiation therapy in dogs show that this is
however, most dogs and cats require
an effective method of treatment with low
ancillary trilostane or mitotane therapy for morbidity; however, it may take several several months after radiation treatment
months for the signs of PDH to subside.

because of residual ACTH secretion. In

These dogs do well longterm, however,
dogs with PDH undergoing hypophysecbecause the primary disease process tomy, 80"A, achieved remission, with an 11 % (pituitary tumor) has been addressed.

recurrence; thyroid and glucocorticoid

Prognosis of dogs with PDH has been
support may be needed after surgery, and
estimated to be -2 yr with or without
animals may lose the ability to secrete
me1.lical therapy. Radiation treatment
vasopressin, leading to diabetes insipidus
of pituitary tumors causing PDH or

THE PITUITARY GLAND

547
hypophysectomies is associated with a
severely compress the overlying hyporelatively good longtenn prognosis (2-5 yr). thalamus, which is the primary center for Prognosis of dogs with unilateral
homeostatic regulation of body temperaadrenalectomy was 18 mo.

ture, appetite, and cyclic shedding of hair. ln
addition, pars intermedia adenomas secrete

NONFUNCTIONAL PITUITARY
increased amounts of alpha melanocyte

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TUMORS
stin1Ulating hmmone (MSH), a factor in the
growth of a long hair coat in winter.

Nonfunctional pituitary tumors are
uncommon in most species. Chromophobe

Clinical Findings and Lesions: Signs
adenomas appear to be endocrinologically
of PPID include polyuria and polydipsia
inactive, but they may cause compression

(PU/PD), poor muscle tone, weakness,
atrophy of adjacent portions of the pituitary
somnolence, abnom1al distribution of
gland and extend into the overlying brain.

adipose tissue, swelling of the periorbital

Clinical disturbances occur because of
fossa, lantinitis, increased susceptibility to
either a lack of secretion of pituitary trophic
infections, intermittent hyperpyrexia, and
hormones and diminished target organ
generalized hyperhidrosis. Hirsutism often
function ( eg, adrenal cortex) or dysfunction
becomes evident because of failure of the
of the CNS. Affected animals often are
cyclic seasonal shedding of hair. Before
depressed, incoordinated, and weak and
generalized hirsutism is observed, horses
may collapse with exercise. (See also
may have longer hair on the legs, ventral

ADULT-ONSET PANHYPOPITUrrAlllSM, below.)

abdomen, and throat latch. Eventually, the

Endocrinologically inactive pituitary
hair over most of the trunk and extremities
adenomas often attain considerable size
becomes long (up to 4-5 in. [10-12 cm]),
before they cause obvious signs ( or death).

abnormally thick, wavy, and often matted.

The proliferating tun1or cells incorporate

Pars intermedia adenomas are the most
the remaining structures of the adenohypoconunon pituitary twnors in horses. They physis and infundibular stalk. The entire
are yellow to white, multinodular, and
hypothalamus may become compressed
compress the pars nervosa. Horses with
and replaced by the tun10r.

PPID may have hyperglycemia (insulinresistant) and glycosuria. It is not known HIRSUTISM ASSOCIATED WITH
why some horses with PPID become insulin

ADENOMAS OF THE PARS
resistant and others do not. However,
cortisol and other hormones that may be

INTERMEDIA
present in increased concentrations in
horses with PPID are insulin antagonists.

(Hypertrichosis)

Plasma immunoreactive adrenocortico

Hirsutism is the long, nonshedding hair coat
tropin and alpha-MSH levels may range
that develops in older horses (typically ;o,18
from modestly to extremely increased.

yr old) and is associated with pituitary pars

Blood cortisol concentrations generally
inte1media dysfunction (PPID) caused by an remain in the normal range but lack normal adenoma of the cells of the pars intermedia
diurnal rhythm and escape suppression by
of the pituitary gland. Such adenomas often
administration of dexamethasone much
more quickly than in healthy anin1als.

Diagnosis: Hyperglycemia and insulin
insensitivity are suggestive of pituitary
adenoma in horses, but because they occur
in horses with equine metabolic syndrome

( see p 1006) or other insulin dysregulation syndromes, they are not diagnostic of PPID.

Other nonspecific findings include an
absolute or relative neutrophilia, eosinopenia, and lyrnphopenia; lipemia; hypercholesterolemia; and a mild, nom1ochromic, normocytic anemia. Liver enzymes may be
increased. Electrolytes are usually nom1al.

Urinalysis is nom1al except for occasional
glycosuria and a low to nonnal specific

Hirsutism in a
gravity.

pony, associated with advanced
pituitary pars mtermedia dysfunction. Courtesy

Definitive diagnosis is based on
of Dr. Janice Kritchevsky.

evocative testing or measurement of

548

THE PITUITARY GLAND
resting endogenous ACTH concentrations.

function. Thus, most require diligent

Dexamethasone ( 40 mcg/kg, Thl) often will
attention to good husbandry. Pergolide, a
not suppress cortisol levels to at least 300Ai
clopaminergic a.gonist, is currently the only
of baseline or to < 1 mcg/dL, as it does in
a.gent demonstrated to decrease endoghealthy horses 6--15 hr after administration.

enous ACTH concentrations in horses with

In addition, cortisol concentrations return

PPID. Statting dosages a.re 0.006--0.01

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to within 800Ai or greater of baseline values
mg/kg/day, PO. This typically results in a

24 hr after dexamethasone administration
dose of 0.5-1 mg/day. If this amount does
in horses with PPID. Healthy horses have
not result in improvement in clinical signs
suppressed cortisol levels 24 hr after
and enclocrinologic testing, it may be
dexamethasone administration. Horses with
increased gradually. Reported adverse

PPID react with an exaggerated response to
effects of pergolide therapy include depresdomperidone administration. Increase in sion and anorexia.. Often, these signs are
plasma endogenous ACTH to �lOOOAi of
transitory and resolve over time. If they do
baseline levels 2-4 hr after administration
not, the dose may be decreased temporarily
of domperidone at 5 mg/kg, PO, is consistent or split and given twice daily. Altl10ugh its with PPID. Horses with PPID have an
use has not been docmnented to result in
increase in plasma endogenous ACTH
improvement in clinical signs when given
concentration 10 min after administration of
alone, cyproheptadine at a dosage of 0.6--1.2

1 mg thyroid-releasing honnone (TRH), and
mg/kg/day, PO, may exert synergistic effects
the TRH stimulation test is believed to be the when combined witl1 pergolide, and the most sensitive means to detect a pituitary
combination may result in outcomes better
tumor. Horses expe1ience a seasonal rise in
than those achieved with pergolide alone.

endogenous ACTH in the autumn (August

Trilostane, a competitive 3-[3 hydroxysteroid
through November in the northern
dehydrogenase inhibitor, has not been inveshemisphere). Healthy horses a.re less likely tigated adequately in the horse, although its
to have a decreased cortisol concentration
use has improved clinical results.

in response to dexa.methasone administration and may demonstrate an exaggerated ADULT-ONSET
response to domperidone or TRH in the

PANHYPOPITUITARISM
autumn as well. For this reason, unless there
are season-specific nonnal values available

Endocrinologically inactive, nonfunctional
for the testing being performed, it is
pituitary tmnors develop most conunonly in
recommended to perform diagnostic testing
adult to aged animals; there is no apparent
for PPID from January through July.

breed predisposition. The most common

Differential diagnoses include syndromes
cause is a chromophobe adenoma a.rising in
resulting in chronic debilitation, eg, poor
the pa.rs distalis. Other infrequent ca.uses
management and nutrition, parasitism, and
include extensive inflanuna.tory destruction
chronic systemic diseases. The PU/PD must
of pituitaty tissue, ischemic necrosis of the
be differentiated from that due to chronic
pituitary due to infarction from invasion of
renal disease or diabetes insipidus. The
tmnor cells, parasitic or septic emboli,
hyperglycemia, glycosuria, and PU/PD must
diffuse necrosis associated with toxemia,
be differentiated from that ca.used by
invasion by neoplasms a.rising in adjacent
primary diabetes mellitus. High insulin
strnctm·es ( eg, meninges, sphenoicl bone,
concentrations or an increased glucose to
nasal cavity, etc), and widespread hem01°
insulin ratio must be differentiated from
rhage and subsequent scarring after
primary hyperinsuli.nemia. ( equine
tra.mna.tic iqjmy. Dogs and cats with
metabolic syndrome). Pheochromocytomas nonfunctional a.denomas develop clinical (seep 576) may ca.use hyperhidrosis,
disturbances related to a la.ck of secretion
hyperglycemia., and tachypnea, although
of pituitary trophic hormones and
they usually a.re nonfunctional and found
diminished target organ function or
only incidentally at necropsy. Differential
to dysfunction of the CNS.

diagnosis for hi.rsutism includes being of the

Bashkir Curly breed or having a congenital

Clinical Findings: Affected animals
curly coat a.bnonna.lity. There is no other
often a.re depressed and i.ncoordinated
recognized condition in which adult horses
and collapse with exercise. Occasionally,
acquire a long, curly hair coat. For this
they exhibit a change in attitude, become
reason, hirsutism can be considered a
unresponsive to people, and develop a
positive diagnostic test for PPID.

tendency to hide at the slightest provocation. In chronic cases, there may be Treatment: Horses with PPID a.re
evidence of blindness, with dilated and
relatively fragile, with poor immune
fixed pupils clue to compression and

THE PITUITARY GLAND

549
disruption of optic nerves by dorsal exten

Skin atrophy and loss of muscle mass
sion of the pituitary tumor. Affected dogs
may be related to a lack of protein anabolic
often show a progressive weight loss with
effects of growth hom10ne in an adult dog
muscle atrophy due to loss of the protein
or cat. Interference with the secretion of
anabolic effect of growth hormone.

pituitary trophic honnones often results in

Compression of the cells that secrete
gonadal atrophy resulting in either

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gonadotropic hormones or the corredecreased libido or anestrus.

sponding releasing hormone from the
hypothalamus results in atrophy of the

JUVENILE-ONSET
gonads. Disturbances of water balance

PANHYPOPITUITARISM
result from interference with the
synthesis of antidiuretic hormone (ADH)

(Pituitary dwarfism)

or its release into capillaries of the pars
nervosa. The posterior lobe, infundibular

Pituitary dwarfism occurs most frequently
stalk, and hypothalamus are compressed
in German Shepherds but has been
or disrupted by neoplastic cells.

reported in other breeds such as the Spitz,

Animals with panhypopituitarism appear

Miniature Pinscher, and Karelian Bear Dog.

dehydrated despite increased water

It is inherited as a sin1ple autosomal
consumption. Dogs and cats with large
recessive trait.

nonfunctional pituitary tumors usually

Pituitary dwarfism is usually associated
excrete large volun1es of dilute urine with a
with a failure of the oropharyngeal ectolow specific gravity (!>l.007) and may break denn of the cranial pharyngeal duct
housetraining. Clinical signs are not highly

(Rathke's pouch) to differentiate into
specific and can be confused with those of
trophic-hom10ne-secreting cells of the pars
other CNS disorders ( eg, brain tumors or
distalis. Consequently, the adenohypophyencephalitis) or chronic renal disease.

sis is not completely developed. The

Hypopituitarism caused by pituitary
second most common cause is craniophartumors should be included in the differenyngioma, a benign twnor derived from the tial diagnosis of diseases characterized
oropharyngeal ectoderm ofRathke's
by incoordination, depression, polyuria,
pouch. Compared with otl1er types of
blindness, and sudden behavioral changes
pituitary neoplasms, these tumors tend to
in adult or aged animals. Because the
develop in younger dogs. Craniopharyngioblindness is central in origin, ophthalmomas cause subnonnal secretion of growth scopic exan1ination usually does not reveal
hormone, which results in dwarfism.

significant lesions. There is no effect on
body stature associated with compression

Clinical Findings: Dwarf pups are
of the pars distalis and probable interferindistinguishable from normal littem1ates ence of growth hormone secretion,
up to 2 mo old. Subsequently, the slower
because these tumors usually arise in dogs
growth rate compared with littennates,
that have already completed their growth.

retention of puppy coat, and lack of prin1ary

Parakeets with chromophobe adenomas
guard hairs gradually become evident.

often develop exophthalrnos due to

Gem1an Shepherds with pituitary dwarfism
extension of neoplastic cells along the
appear coyote- or fox-like, owing to their
optic nerve.

small size and soft, woolly coat. Bilaterally
syn1metric alopecia develops gradually and

Lesions: Endocrinologically inactive
often becomes complete except for the
pituitary adenomas usually reach considerhead and tufts of hair on the legs. Pennaable size before they cause obvious signs or nent dentition is delayed or completely
death. The proliferating tun10r cells incorabsent. Closure of the epiphyses is delayed porate the remaining structures of the
as long as 4 yr depending on the severity of
adenohypophysis and infundibular stalk
the hormonal insufficiency and is caused by

The entire hypothalamus may be comdeficiencies of botl1 thyroid-stimulating pressed and replaced by tumor.

honnone and growth hormone. The testes

Thyroid glands in dogs and cats with
and penis are small, calcification of the os
large pituitary adenomas often are smaller
penis is delayed or incomplete, and the
than normal, although to a much lesser
penile sheath is flaccid. The ovarian cortex
degree than the adrenal cortex. The adrenal
is hypoplastic, and estrus is irregular or
glands are small and consist primarily of
absent. Lifespan is shortened because of the
medullary tissue surrounded by a narrow
resulting secondary endocrine dysfunction,
zone of cortex. Seminiferous tubules are
such as hypothyroidism and hypoadrenosmall and show little evidence of active corticism. Puppies with panhypopituitarism
spennatogenesis.

often have a shrill bark

550

THE PITUITARY GLAND

Lesions: Pituitary cysts fill with mucus

Etiology: The hypophyseal fom1 develops
and eventually occupy the entire pituitary
as a result of compression a11d destruction of
area, resulting in severe compression of the
the pms nervosa, inftmdibular stalk, or supra.pars nervosa and infunclibular stalk.

optic nucleus in the hypothalainus. The

Craniopharyngiomas are large, solid, cystic
lesions responsible for the disruption of
areas that extend into the overlying

ADH synthesis or secretion in hypophyseal
hypothalamus. They may also grow along
diabetes insipid us include large pituitary

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the ventral aspect of the brain, where
neoplasms ( endoc1inologically active or inacincorporation of several cranial ne1ves tive), a dorsally expa11cling cyst or inflai1m1aresults in specific nerve function deficits.

to1y granuloma, and trawnatic injwy to the
skull witl1 hemon-hage a11d glial proliferation

Diagnosis: Levels of thyroxine, triiodoin the neurohypophyseal system.

thyronine, and c01tisol are reduced or in the
low-normal range. In those animals with an
equivocal change in basal hormone level,

Clinical Findings: Affected animals
excrete large voltm1es of hypo tonic urine
the responses to challenge by exogenous
and &ink equally lai·ge ai11ounts of water.

thyrotropin or adrenocorticotropin are

Urine osmolality is decreased below normal
subno1111al, owing to the hypoplasia or
plasma osmolality ( -300 mOsm/kg) in both
atrophy of the thyrnid gland and adrenal
cortex. Other useful diagnostic aids include
hypophyseal and nephrogenic forms, even if
the animal is dep1ived of water. The increase
comparison of height with that of litterof mine osmolality above that of plasma mates, evidence of delayed epiphyseal
closure or dysgenesis on skeletal radioin response to exogenous ADH in the graphs, and skin biopsy. Cutaneous lesions
hypophyseal fo1m, but not in the nephroinclude hyperkeratosis, follicular keratosis, genic form, is useful in the clinical differentiation of the two forms of the disease.

hyperpigmentation, adnexal atrophy, loss
of elastin fibers, and a loose network of

Lesions: The poste1ior lobe, infundibular
collagen fibers in the dennis. Hair shafts
stalk, and hypothalainus are compressed
are absent, and hair follicles are primarily
or disrnpted by neoplastic cells. This
in the telogen stage of the growth cycle.

inten-upts the nonmyelinated axons U1at

The activity of somatomedin C (insulintranspo1tADH from its site of production like growth factor 1) is low in dwaif dogs.

(hypothalanrns) to its site of release (pars

Intermediate somatomedin C activity is
ne1vosa).

present in phenotypically normal ancestors
suspected to be heterozygous carriers.

Diagnosis: This is based on chronic poly

Assays for somatomedin C provide an
uria that does not respond to dehyru·ation
indirect measurement of circulating growth
and is not due to primary renal disease. To
ho1mone activity in dogs with suspected
evaluate the ability to concentrate urine, a
pituitary dwarfism. Basal levels of
water deprivation test should be done if the
circulating canine growth ho11110ne are
animal is not dehydrated ai1d does not have
reported to be detectable but low (n01mal
renal disease. The bladder is emptied, and
range: 1.75 ± 0.17 mg/mL) in pituitary
water and food are withheld (usually 3--8 hr)

dwaifs and do not increase after a
to provide a maxi.mwn stinrn.lus for ADH
provocative test for secretion via clonidine
secretion. The animal should be monitored
injection (30 mcg/kg, IV) as they do in
carefully to prevent a loss of >5% body wt
healthy dogs. Insulin hypersensitivity has
and severe dehydration. Urine and plasma
been demonstrated in pituitary dwarf dogs,
osmolality should be detennined; however,
probably due to a chai1ge in insulin receptor
because these tests are not readily available
nw11bers or affinity of binding in response
to most practitioners, urine specific gravity
to the low level of growth honnone.

is frequently used instead. At the end of the
test, wine specific gravity is> 1.025 in those

DIABETES INSIPIDUS
animals with only a paitial ADH deficiency
or with antagonism to ADH action caused

Central diabetes insipid us is caused by
by hypercortisolism. There is little change
reduced secretion of antidiw·etic hormone
in specific gravity in tl1ose anin1a.ls with a

(ADI-I). When target cells in the kidney lack
complete lack of ADH activity, whether due
the biochemical machinery necessaiy to
to a prima1y loss of ADH or to tmresponsiverespond to the secretion of n01mal or ness of the kidneys.

increased circulating levels of ADH,

An ADH response test should follow to
nephrogenic diabetes insipid us results.

differentiate ai11ong conditions that may

It occurs infrequently in dogs, cats, ai1d
result in large volwnes of urine that is
laboratory rats, and rarely in other ai1imals.

chronically low in specific gravity but

THE PITUITARY GLAND

551 ·
othe1wise normal. These include nephrochronic nephritis with a wine specific gravity genic diabetes insipidus (an inability of the
that is usually low and shows evidence of
kidneys to respond to ADH), psychogenic
renal failure (protein, casts, etc).

diabetes insipidus (a polydipsia in response
to some psychological disturbance but a

Treatment: Polyuria may be controlled
normal response to ADH), and hypercortiusing desmopressin acetate, a synthetic solism (which results in a paitial deficiency
at1alogue of ADH. The initial dose is 2 drops

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of ADH activity due to the antagonistic
applied to the nasal mucosae or conjunctieffect of cortisol on ADH activity in the vae; this is gradually increased until the
kidneys). This test also cai1 be used to
minimal effective dose is detem1ined.

evaluate aninlals in which a water

Maximal effect usually occurs in 2-6 hr and
deprivation test could not be perfonned.

lasts for 10-12 hr. Water should not be

Urine specific gravity is detem1ined at the
restricted. Treatment should be continued
start of the test, desmopressin acetate is
once or twice daily for the life of the aninlal.

administered (2-4 drops in the conjunctiva!

sac), the bladder is emptied at 2 hr, and

FELINE ACROMEGALY
urine specific gravity is measured at set
intervals ( 4, 8, 12, 18, and 24 hr) after ADH

Acromegaly, or hypersomatotropism,
administration. Specific gravity peaks at
results from chronic, excessive secretion

> 1.026 in anin1als with a primary ADH
of growth hom10ne in the adult at1in1al.

deficiency, is significantly increased above

Acromegaly in cats is caused by a growth
the level induced with water deprivation in
hormone-secreting tumor of the at1terior
those with a partial deficiency in ADH
pituitary. In cats, tl1ese tumors grow slowly
activity, and shows little change in those
and may be present for a long time before
with nephrogenic diabetes insipidus.

clinical signs appeai·.

If osmolality is measured, the ratio of
urine to plasma osmolality after water

Clinical Findings: Feline acromegaly
deprivation is >3 in healthy aninlals, 1.8-3
occurs in older (8-14 yr) cats and appears to
in those with moderate ADH deficiency,
be more common in males. Clinical signs of
and <1.8 in those with severe deficiency.

uncontrolled diabetes mellitus are often the

The ratio of urine osmolality after ADH
first sign of acromegaly in cats; therefore,
administration as compared with water
polydipsia, polywia, ai1cl polyphagia are the
deprivation is >2 in animals with primary
most common presenting signs. Net weight

ADH deficiency, between 1.1 and 2 in those
gain of lean body mass in cats with
with inhibitors to ADH action, and < 1.1 in
uncontrolled diabetes mellitus is a key sign
those unresponsive to ADH.

of acromegaly. Organomegaly, including

As an alternative to the water deprivation
renomegaly, hepatornegaly, and enlargetest, or in cases in which this test does not ment of endocrine organs, is also seen.

establish a definitive diagnosis, a closely

Some, but not all, cats show the classic
monitored therapeutic trial with desmoenlai·gement of extremities, body size, jaw, pressin ( see below) can be performed.

tongue, and forehead that is characteristic

Again, all other causes of polyuria and
of acromegaly in people. Some of the most
polydipsia should initially be excluded,
striking ma.J.1ifestations are seen in the
limiting the differential diagnosis to central
musculoskeletal system and include ai1
diabetes insipidus, nephrogenic diabetes
increase in muscle mass and growth of the
insipid us, and psychogenic polydipsia. For
acral segments of tl1e body, including the
cats, tl1e owner should measure the aninlal's paws, chin, at1d skull. Stridor may be 24-hr water intake 2-3 days before the theradetected as a result of increased soft-tissue peutic trial with desmopressin, allowing
enlargement of tl1e epiglottis at1d surroundfree-choice water intake. The intranasal ing tissues. Cai·diovasculai· abnom1alities
prepai·ation of desmopressin is adn1inissuch as cai·diomegaly (radiographic and tered in the coajw1ctival sac ( 1-4 drops,
echocardiographic), systolic murmurs, and
bid) for 3 -5 days. A drainatic reduction
congestive heart failure develop late in the
in water intake (>50"A,) during tl1e first
disease cow-se. Azotemia also develops late
treatment clay strongly suggests an ADH
in the course of the disease in -500Ai of
deficiency and a diagnosis of central
acromegalic cats. Neurologic signs of
diabetes insipidus or partial nephrogenic
acromegaly in people, such as peripheral
diabetes insipidus.

neuropathies (pai·esthesias, caipal tunnel

Diabetes insipidus also needs to be dissyndrome, sensory at1d motor defects) and tinguished from other diseases witl1 polyuria
parasellar manifestations (headache at1d

The most common are diabetes mellitus with
visual field defects), are not generally
glycosuria and high urine specific gravity, and detected in acromegalic cats.

552

THE PITUITARY GLAND

Impaired glucose tolerance and insulin
hormone or insulin-like growth factor 1
resistance resulting in diabetes mellitus are

(IGF-1) concentrations in suspected cases.

seen in all cats with acromegaly. Measure

Unfortunately, feline growth hormone
ment of endogenous insulin reveals
assays are no longer available. Serum IGF-1
dramatically increased serum insulin
concentrations are often dramatically
concentrations. Despite severe insulin
increased in acromegalic cats (as in affected

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resistance and hyperglycemia, ketosis is
people). Currently, the most definitive
rare. Hypercholesterolemia and mild
diagnostic test is CT of the pituitary region.

increases in liver enzymes are attributed

Results of CT, coupled with the exclusion of
to the diabetic state. Hyperphosphatemia
other disorders that cause insulin resistance
without azotemia is also a common

(llyperthyroidism, hyperadrenocorticism)

clinicopathologic finding. Urinalysis is unreand clinical signs and laboratory abnonnalimarkable except for persistent proteinuria.

ties, support a diagnosis of acromegaly.

In a recent study, acromegaly was the
most common (25%) underlying cause of

Treatment and Prognosis: Medical
non-insulin-dependent diabetes mellitus in
therapy in people includes the use of
cats, and it should be suspected in any cat
dopamine agonists, such as bromocriptine,
that does not respond to standard therapy
and somatostatin analogues ( octreotide ).

for type 2 diabetes mellitus (high-protein,

Treatment with octreotide has been
low-carbohydrate diet and glargine insulin) unsuccessful in acromegalic cats. The lack within 4 mo of initiating therapy.

of efficacy of the long-acting somatostatin

Lesions: Gross necropsy findings in acroanalogues may result from species-specific megalic cats may include a large expansile
tissue binding. Radiation therapy probably
pituitary mass, hypertrophic cardiomyopaoffers the greatest chance for success with thy with marked left ventricular and septa!

low rates of morbidity and mortality. The
hypertrophy (early) or dilated cardiomyopadisadvantages include the slow rate of thy (late), hepatomegaly, renomegaly,
tumor shrinkage (>3 yr) and the occurrence
degenerative joint disease, lumbar vertebral
of hypopituita.J.ism, cranial and optic nerve
spondylosis, moderate enlargement of the
damage, and radiation injury to the
parathyroid glands, adrenocortical
hypothalamus.

hyperplasia, and diffuse enlargement of the

The short-te1111 prognosis in cats with
pancreas with multifocal nodular hyperplauntreated acromegaly is fair to good. Insulin sia. Histopathologic exan1ination of the
resistance is generally controlled satisfactoendocrine glands reveals acidophil rily by using large doses of insulin divided
adenoma of the pituitary; adenomatous
into several daily doses. Mild cardiac
hyperplasia of the thyroid gland; and
disease can be managed with diuretics and
nodular hyperplasia of the adrenal cortices,
vasodilators. The longterm prognosis is
parathyroid glands,
relatively poor, however, and most cats die

�d pancreas.

of congestive heart failure, chronic renal
failure, or signs of an expanding pituitary

Diagnosis: A definitive diagnosis requires
mass. The longterm prognosis may improve
measurement of increased plasma growth
with early diagnosis and treatment.

THE THYROID GLAND

All vertebrates have a thyroid gland.

carotid artery near the origin of the

In mammals, it is usually bilobed and
vertebral artery.

located just caudal to the larynx,

Ectopic or accessory thyroid tissue
adjacent to the lateral surface of the
is relatively common in most species,
trachea. The two lobes may be connected especially dogs and cats. It may be located by a fibrous isthmus (eg, ruminants,
anywhere from the larynx to the diaphragm
horses), or a connecting isthmus may be
and may be responsible for maintaining
indistinct (eg, dogs, cats). The gland is
nom1al thyrnicl function after surgical
extremely vascular. In birds, it is found
thyroidectomy. In addition, ectopic thyroid
within the thoracic cavity; both lobes are
tissue occasionally is the site of hyperplalocated near the syrinx, adjacent to the sia or neoplasia.

THE THYROID GLAND

553

Physiology: Thyroid hormones are the
thyroid horn1ones also stimulate mitochononly iodinated organic compounds in the drial oxygen consumption. These changes
body. Thyroxine (T4) is the main secretory
a.re linked directly to the calorigenic effect
product of the nonnal thyroid gland.

of thyroid honnones. More chronic effects

However, the gland also secretes 3,5,3' -
invariably a.re related to the cellular actions
triiodothyronine (T3), reverse T3, and other
that require interaction with nuclear T3

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deiodinated metabolites. T3 is -3-5 tin1es
receptors, foUowed by an increase in
more potent than T., whereas reverse T3 is
protein synthesis crucial to physiologic
thyromimetically inactive.

processes such as growth, differentiation,

Although all T4 is secreted by the thyroid,
proliferation, and maturation.

a considerable amount of T 3 is derived from

Thyroid honnones, in physiologic quan

T, 1; therefore, T4 has been called a proh01°
tities, a.re anabolic. In coajunction with
mone. Its activation to the more potent T3 is
growth hormone and insulin, protein
a step regulated individually by peripheral
synthesis is stimulated and nitrogen
tissues.

excretion is reduced. However, in excess

Thyroid ho1mone secretion is regulated

01ype1thyroidism), they can be catabolic,
primarily via negative-feedback control
witil increased gluconeogenesis, protein
through the coordinated response of
breakdown, and nitrogen wasting.

the hypothalamic-pituitary-thyroid axis:

thyrotropin-releasing honnone (TRH) binds

HYPOTHYROIDISM
to the thyrotroph ceU in the pituitary and
stimulates secretion of thyrotropin

In hypothyroidism, impaired production

(thyroid-stimulating honnone, TSH), which
and secretion of tile tl1yroid hormones
binds to the follicular ceU membrane and
result in a decreased metabolic rate. This
stinrnlates thyroid honnone synthesis and
disorder is most common in dogs but also
secretion.

develops rarely in otiler species, including

Thyroid h01mones a.re water-insoluble
cats, horses, and otiler large, domestic
lipophilic compounds that a.re bound to
animals.

plasma proteins (thyrnxine-binding protein,
thyroxine-binding prealbun1in [ transthyre

Etiology: AJU1ough dysfunction anywhere
tin ], and albunlin). The major function of
in tile hypotilalamic-pituitary-thyroid a.xis
the thyroid honnone-binding proteins is
may result in tilyroid honnone deficiency,
probably to provide a hormone reservoir in

>95% of clinical cases of hypotilyroidism in
the plasma and to "buffer" hormone delivery dogs appear to result from destruction of into tissue. In healthy �uthyroid animals,
tile tilyrnid gland itself (primary hypotlw0.1%of total semm T
roidism ). The two most common causes of

4 is free (not bound
to thyroid honnone-binding proteins),
adult-onset primary hypotilyroidism in dogs
whereas -1 % of circulating T
include lymphocytic tilyroiditis and idippatllic

3 is free.

Evidence suggests that the fractions of
atrophy of tile tl1yroid gland. Lymphocytic
circulating free T and free T dete1mine the
tilyroiditis, probably immune-mediated, is

4

3
an1ount of honnone available for uptake by
characterized histologically by a diffuse
tissues.

infiltration of the gland by lyn1phocytes,
plasma cells, and macrophages and results

Action of Thyroid Hormones: Thyroid
in progressive destruction of follicles and
honnones act on many different cellular
secondary fibrosis. Idiopatllic atrophy of tl1e
processes; however, no single reaction or
thyrnid gland is characterized histologically
metabolic event can be equated with their
by loss of thyroid pa.renchyma and
action. Although both T4 and T3 have
replacement by adipose tissue. (See also
intrinsic metabolic activity, T3 is 3-5 times

AUTOIMMUNE THYROIDITIS, p 831.)

more potent in binding to the nuclear

In dogs, the most common cause of
receptors and sinlila.rly more potent in
secondary hypotilyroidism is destruction
stimulating oxygen conswnption.

of pituitary thyrotrophs by an expanding,

Effects of thyroid hormones generally a.re
space-occupying tumor. Because of tile
divided into two categories: tl10se that maninonselective natme of tile resulting fest within minutes to homs after honnone
compressive atrophy and replacement
receptor binding and do not require protein
of pituitary tissue by such large tumors,
synthesis, and those that manifest later
deficiencies of otiler ( one or more) pituitary

(usually >6 hr) and require synthesis of new
hormones also usually occm.

proteins. About half the increase in oxygen

Other rare fonns of hypothyroidism
consun1ption produced by thyrnid
in dogs include neoplastic destruction
h01mones is related to activation of the
of tilyrnid tissue and congenital ( or
plasma membrane-bound Na+/K+ ATPase;
juvenile-onset) hypotily:roidism. Congenital

554

THE THYROID GLAND
primary hypothyroidism may result from

Clinical Findings: Although onset is
one of various forms of thyroid dysgenesis
variable, hypothyroidism is most common

(eg, athyreosis, thyroid hypoplasia) or
in dogs 4--10 yr old. It usually affects midfrom dyshormonogenesis (usually an to large-size breeds and is rare in toy and
inherited inability to organify iodide).

miniature breeds. Breeds repmted

Congenital secondary hypothyroidism
to be predisposed include the Golden

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(associated with clinical signs of

Ret1iever, Doberman Pinscher, Irish Setter,
disproportionate dwarfism, lethargy, gait

Miniature Schnauzer, Dachshund, Cocker
abnormalities, and constipation) has been

Spaniel, and Airedale Terrier. There does
reported in Giant Schnauzers, Toy Fox
not appear to be a sex predilection, but

Terriers, and Scottish Deerhounds.

spayed females appear to have a higher

Congenital secondary hypothyroidism
risk of developing hypothyroidism than
also has been reported in Gennan
intact females.

Shepherds with pituitary dwarfism

A deficiency of thyroid ho1mone affects
associated with a cystic Rathke's pouch.

the fw1ction of all organ systems; as a

However, the degree ofTSH deficiency in
result, clinical signs are diffuse, variable,
these dogs is variable, and clinical signs
often nonspecific, and rarely pathognoare usually caused primarily by deficiency monic. Although the disorder should be
of growth hormone (rather than thyroid
highly suspect, overdiagnosis should be
hormone).

avoided, because many diseases, especially

In cats, iatrogenic hypothyroidism is the
those of the skin, can easily be misdiagmost common form. Hypothyroidism nosed as hypothyroidism.

develops in these cats after treatment for

Many of the clinical signs associated with
hyperthyroidism with radioiodine, surgical
canine hypothyroidism are directly related
thyroidectomy, or use of an antithyroid
to slowing of cellular metabolism, which
drug. Although naturally occurring
results in development of mental dullness,
hypothyroidism is an extremely rare
lethargy, exercise intolerance, and weight
disorder in adult cats, congenital or
gain without a corresponding increase in
juvenile-onset hypothyroidism does also
appetite. Mild to marked obesity develops
occur. Recognized causes of congenital
in some dogs. Difficulty maintaining body
hypothyroidism in cats include intrathyroitemperature may lead to frank hypotherdal defects in thyroid hormone biosynthesis mia; the classic hypothyroid dog is a

(dyshonnonogenesis), an inability of the
heat-seeker. Alterations in the skin and coat
thyroid gland to respond to TSH, and
are common. Dryness, excessive shedding,
thyroid dysgenesis. All reported cats with
and retarded regrowth of hair are usually
hypothyroidism have had the primary
the earliest dennatologic changes.

(thyroidal) disorder. Secondary (pituitary)

Nonpruritic hair thinning or alopecia
or tertiary (hypothalamic) hypothyroidism

( usually bilaterally syn1rnetric) that may
has not been well described in either
involve the ventral and lateral trunk, the
juvenile or adult cats but has been reported
caudal surfaces of the thighs, dorsum of the
after severe head trauma.

tail, ventral neck, and the dorsurn of the

In foals, congenital hypothyroidism
nose is seen in about two-thirds of clogs
may develop when pregnant mares graze
with hypothyroidism. Alopecia, sometimes
plants that contain goitrogens, or are fed
associated with hyperpigmentation, often
diets either deficient in or containing
starts over points of wear. Occasionally,
excessive amounts of iodine. Most
secondary pyodenna (which may produce
commonly, congenital hypothyroidism
pruritus) is seen.

develops in association with a specific

In moderate to severe cases, thickening
syndrome of neonatal foals characterized
of the skin occurs secondary to accwnulaby thyroid gland hyperplasia together tion of glycosanlinoglycans ( mostly
with multiple congenital musculoskeletal
hyaluronic acid) in the dennis. In such
anomalies. This syndrome, reported most
cases, myxedema is most common on tl1e
commonly in western Canada, has been
forehead and face, resulting in a puffy
referred to as either thyroid hyperplasia
appearance and thickened skin folds above
and musculoskeletal deformities
the eyes. This puffiness, together with slight
syndrome or as congenital hypothyroiddrooping of the upper eyelid, gives some ism and dysmaturity syndrome and may
clogs a "tragic" facial expression. These
be related to feeding a high nitrate diet
changes also have been described in the
to pregnant mares. In adult horses,

GI tract, heart, and skeletal muscles.

hypothyroidism appears to be very rare

In intact dogs, hypothyroidism may cause
but, as in other species, is commonly
vaiious reproductive disturbances: in
misdiagnosed.

females, failure to cycle (a11estms) or

THE THYROID GLAND

555
sporadic cycling, infertility, abortion, or
iatrogenic hypothyroidism, but it is not a
poor litter survival; and in males, Jack of
consistent sign. Bilaterally syn1metric alopelibido, testicular atrophy, hypospennia, cia, except for pim1al involvement, does not
or infertility.

appear to develop, but focal areas of

A variety of neurologic disorders,
alopecia over the craniolateral carpi, caudal
including megaesophagus, laryngeal
hocks, and dorsal and lateral tailbase have

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paralysis, facial nerve paralysis, and
occasionally been seen. However, in many
vestibular disease, have been related to
cats with mild iatrogenic hypothyroidism,
hypothyroidism. However, all such
very mild or no obvious clinical signs are
peripheral and central nervous disease is
seen. In young cats with congenital or
uncommon, at least compared with the
juvenile-onset hypothyroidism, the clinical
metabolic and dermatologic changes
signs are more obvious and include
commonly seen in hypothyroid dogs. In
disproportionate dwarfism, severe lethargy,
addition, such neurologic signs do not
mental dullness, constipation, inappetence,
always resolve after thyroid ho1mone
and bradycardia.

replacement therapy.

Myxedema coma, a rare syndrome, is the

Diagnosis of Hypothyroidism:

extreme expression of severe hypothyroid

Hypothyroidism is probably one of the
ism. The course can develop rapidly;
most overdiagnosed diseases in dogs.

lethargy progresses to stupor and then

Many diseases and conditions can mimic
coma. The conunon signs of hypothyroidhypothyroidism, and some of the clinical ism (eg, hair loss) are usually present, but
signs, even in dogs with normal thyroid
other signs, such as hypoventilation,
function, can improve after administration
hypotension, bradyca.rdia, and profound
of exogenous thyroid honnone. In addition,
hypothe1mia, are usually seen as well.

a variety of nonthyroidal factors (eg,

During the fetal period and in the first few
nonthyroidal illness and prior administramonths of postnatal life, thyroid hormones tion of certain drugs) can lead to low serum
are crucial for growth and development
thyroid hom1one measurements in
of the skeleton and CNS. Therefore, in
euthyroid dogs, cats, and other species.

addition to the well-recognized signs of

Definitive diagnosis of canine hypothyroidadult-onset hypothyroidism, disproporism requires careful attention to clinical tionate dwarfism and impaired mental
signs and results of routine laboratory
development (cretinism) are prominent
testing. Tests that may confirn1 the diagnosis
signs of congenital and juvenile-onset
include measurement of the serum
hypothyroidism. In primary congenital
concentrations of total T
hypothyroidism, enlargement of the thyroid

4, free T4, and TSH;
provocative thyroid function tests (eg, TSH
gland (goiter) also may be detected, dependstimulation test); thyroid gland imaging; and ing on the cause of the hypothyroidism.

response to thyroid hormone supplementa

Radiographic signs of epiphyseal dysgention. Choice and interpretation of diagnostic esis (underdeveloped epiphyses throughout
tests is based heavily on the index of
the Jong bones), shortened vertebral bodies,
suspicion for hypothyroidism.

and delayed epiphyseal closure are

There are well-recognized clinicopathocommon.

logic abnormalities associated with

In dogs with congenital hypopituitarism
hypothyroidism, the severity of which

(pituitary dwarfism, see p 549), there may
usually correlates with the severity and
be variable degrees of thyroidal, adrenoc01�
chronicity of the hypothyroid state.

tical, and gonadal deficiency, but clinical

These changes are nonspecific and may be
signs are primarily related to growth
associated with many other diseases in
honnone deficiency. Signs include
dogs. Their presence, however, adds
proportionate dwarfism ( rather than the
supportive evidence for a diagnosis of
disproportionate fom1 of dwarfism
hypothyroidism in a dog with relevant
characteristic of congenital hypothyroidclinical signs. The classic hematologic ism), loss of primary guard hairs with
finding associated with hypothyroidism,
retention of the puppy coat, hyperpigmentafound in 400h-500/o of cases, is a normocytic, tion of the skin, and bilaterally symmetric
n01mochromic, nonregenerative anemia.

alopecia of the trunk.

The classic serum biochemical abnormality

In adult cats, clinical signs associated
is hypercholesterolemia, which occurs in
with advanced or severe hypothyroidism

-800/o of dogs with hypothyroidism. The
include lethargy, dullness, nonpruritic
value of serun1 cholesterol dete1mination as
seborrhea sicca, hypothem1ia, decreased
a screening test for hypothyroidism cannot
appetite, and occasionally bradycardia.

be overemphasized, because cholesterol con

Obesity may develop, especially in cats with centrations are a sensitive and inexpensive

556

THE THYROID GLAND
biochemical marker for this disease in dogs.

tions have secondary hypotllyroidism,

Other clinicopathologic abnorn1alities may
pituitary TSH deficiency is extremely rare,
include high serum concentrations of triand most dogs with normal TSH concentraglyce1ides, alkaline phosphatase, and CK.

tions (ie, a false-negative result) have

Total T, concentration is the most
primary hypothyroidism. In contrast, falsely
commonly performed static thyroid
high serum TSH concentrations (ie, a

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hormone measurement and is a good initial
false-positive result) are occasionally found
screening test for hypothyroidism, with a
in euthyroid dogs witll nontllyroidal illness.

diagnostic sensitivity of -900/o. A dog or

Thus, serum TSH detemlina.tions should
cat with a T concentration well within
never be evaluated alone but always in

4
reference range limits may be assumed to
coajunction with tlle dog's history, routine
have normal thyroid function. However, a
laboratory a.bnonnalities, and total or free
subnormal basal T concentration alone is

T concentrations.

4
not diagnostic; it may indicate an animal

4 The TSH stimulation test evaluates U1e
that is norn1al, hypothyroid, or suffering
response of tlle tllyrnid gland to exogenously
from a nonthyrnidal illness with a secondadministered TSH and is a test of tllyroid ary decrease in the basal T, concentration
reserve. It is an accurate test of thyroid

(sick euthyroid syndrome; see below).

function in dogs but its use is linlited by the

Because only the unbound fraction of
expense and limited availability ofTSH. The
sernm T is biologically active, measureprotocol requires collection of a serum 4
ment of free T has been hypothesized to be
sample for measurement of a basal T

4
more useful to differentiate euthyroid <logs

4,
followed by administration of bovine TSH
from hypothyroid dogs than total T concengiven IV at a dosage ofO. l U/kg ( maximum 4
trations. However, most single-stage solid
dose 5 units). A second sample for
phase (analogue) commercial assays for
measurement ofT is collected 6 hJ' later.

free T, do not appear to be superior

4
to

Human recombinant TSH is available,
measurement of total T, in dogs, probably
although expensive, and may be frozen for
because of differences in serum binding
at least 8 wk with no loss of potency. The
proteins. A free T, assay that uses an
recommended dose is 75 mcg, IV, with
equilibrium dialysis step ( direct dialysis)

collection of 0- and 6-hl' samples. Results
has better accuracy than the analogue
a.re similar to those obtained using the
meU1ods. Compared with the total T, assay,
bovine product. Results may reveal a
the free T, assay by dialysis has greater
normal response, a blunted response (sick
diagnostic sensitivity and specificity.

euthyroid syndrome), or no response

Because T3 is the most potent thyroid

(hypothyroidism).

hormone at the cellular level, it would seem

Botll ultrasonography and scintigra.phy
logical to measure its concentration for'

of the thyroid gland have been evaluated as
diagnostic purposes. However, serum T3
diagnostic tests for hypotllyroidism in dogs.

concentrations may be low, nonnal, or

Witll an experienced radiologist, use of

(occasionally) high in dogs with documented tllyroid sonography (ie, decreased hypothyroidism. The diagnostic value of a
echogenicity and decreased thyroid
serum T3 detennination is particularly weak volume) can be an effective ancillary during early thyroid failure because the
diagnostic tool to differentiate between

"failing" thyroid tends to increase the
canine hypotllyroidism and euthyroid sick
relative synthesis and secretion of T 3 versus
syndrome. The best imaging technique may

T,
be tlle use of technetium 99m (99mTc)

1• In hypothyroid dogs in which values for
serum T3 are high, anti-T3 antibodies, which
uptake and imaging of the Ulyroid gland.

produce spurious results in most T3 ra.dioim-

With quantitative measurement of thyroidal

1mmoassa.ys, should be suspected.

99mTc uptake, there is little to no overlap

Detennina.tion of serum TSH concentrabetween dogs wiili primary hypoiliyroidism tions by use of a valid species-specific TSH
and dogs wiili nonthyroidal illness.

assay can be a useful a.cljunctive test for

In some cases, Uie most practical
hypothyroidism in dogs, cats, and horses.

approach to confirming the diagnosis of

Aninlals with primary hypothyroidism (by
hypothyroidism is a therapeutic trial using
fay the most common type) would be
appropriate guidelines. Every attempt
expected to have low serum T and/or free
should be made lo exclude nonthyroidal

4

T concentrations with high endogenous
illness before starting a therapeutic trial.

4

TSH concentrations. Unfortunately, serum

There is no evidence that thyroid hormone

TSH concentrations remain within the
supplementation is beneficial in dogs with
reference range in 20%-40% of dogs with
sick euthyroid syndrome, and it may be
confirmed hypothyroidism. Although a few
detrimental. Thyroxine supplementation
dogs with nonnal serum TSH concentra.-
should be started at a dosage of 20 mcg/kg

THE THYROID GLAND

557

(administered without food, on an empty
hypothyrnidism is suspected in a dog with
stomach), once to twice daily. Objective
circulating thyroid hom10ne autoantibodcriteria should be used to assess the ies, serwn free T4 concentratfon should be
response to treatment. If response to
cletem1ined to help confirm the diagnosis.

treatment is positive, the clinician should
be prepared to withdraw therapy to

Nonthyroidal Factors That Affect

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confirm that clinical signs return. This will

Interpretation of Thyroid Function
ensure that dogs with thyroid-responsive

Tests: Certain breeds have nonnal thyrnid
diseases (ie, those in which the clinical
honnone ranges that differ from most other
signs improve because of the nonspecific
breeds. Few have been evaluated, but
effects of thyroid hormone or unrelated

Greyhounds have serum total T, and free T
to therapy) do not remain on thyroid

4
concentrations that are considerably lower
supplementation for life. If therapy is
than those of most other breeds. Scottish
unsuccessful, therapeutic monitoring

Deerhounds also have total T, concentrashould be pel'formed to identify the cause tions that are well below ilie mean
of treatment failure. Because an incorrect
concentration of dogs in general, and other
diagnosis is the most common cause of
sight hounds may have similar findings.

treatment failure, the clinician should be

Alaskan sled dogs have serum total T4, T3,
prepared to withdraw therapy and pursue
and free T4 concentrations that are below
other diagnoses.

the reference range of most pet dogs,

In cats, hypothyroidism can also be
particularly during periods of intense
diagnosed on the basis of finding low to
training or racing.

low-n01mal serum concentrations of total

Illness not involving ilie thyroid gland can

T
alter thyrnid function tests and has been

4, free T4, and T3, with high serum TSH
concentrations. A feline-specific TSH assay
labeled "nonthyroidal illness" or "euthyroid is not available, but tl1e canine TSH assay can sick syndrome." Any illness can alter be used as a test for feline hypothyroidism.

thyroid function tests, causing a fairly
consistent decrease in total T

Diagnosis of Thyroiditis:

1 and T3

Circulating
concentrations in proportion to the severity
antithyroglobulin antibodies can be
of illness. Serum TSH concentration is
detected in as many as half of dogs with
increased in SoA.--1096 of dogs with nonthyrnihypothyroidism and are believed to reflect a dal illness. Serum free T, measured by
state of autoimmune thyroiditis. Measureequi.librimn dialysis is less likely to be ment of these antibodies in breeding studs
affected but can be increased or decreased.

and bitches has been proposed as a method

However, in dogs wiili substantial
to identify dogs with autoin1mune thyroid
nonthyrnidal illness, the free T, is likely to
disease. Serum thyrnglobulin autoantibocly

1
be decreased. Testing of thyroid function
detem1inations may be a useful adjunctive
should be postponed until the nonthyroidal
diagnostic aid for hypothyroidism.

illness is resolved. If this is not possible,

However, the test can never be used alone
measurement of T
are
to confirm a diagnosis of hypothyroidism,

4, TSH, and free T4
indicated.

because a positive antithyroglobulin

Glucocorticoids, phenobarbital,
antibody titer may occur in euthyrnid dogs
sulfonamides, clomipran1ine, and aspirin
with early stages of lymphocytic thyroiclitis.

are known to commonly alter thyroid

Identification of these autoantibodies
function tests. Glucocorticoids suppress
supports the diagnosis if the clog has clinical
total T and sometimes free T, concentrasigns and other laboratory data consistent 4
tions. Phenobarbital causes decreased total
with the disorder.

T and mildly increased TSH. Sulfonamides

Although extremely rare in dogs,

4
can induce overt primaiy hypothyroidism
circulating thyrnid hormone autoantiboclies
with clinical signs and thyroid function tests

(anti-T3 or anti-T4 antibodies) are occasionthat support the diagnosis. All changes are ally detected and also are believed to reflect
reversible when the medication is
a state of autoimmune thyroiditis. These
discontinued. Dozens of drugs affect
antibodies, which can be formed against
thyroid function and thyroid function tests
either T3 or T,1 ( or both), produce a spurious
in people, so many others likely affect
increase in ilie apparent T 3 or T4 concentraai1imals as well.

tions, into the hyperthyroid range in most
dogs. Of all the thyroid hormones, only

Treatment: Thyroxine (T4) is the iliyroid
measurement of free T4 (by dialysis) is not
hom10ne replacement compound of choice
affected by autoantibodies directed at T or
in dogs and cats. With few exceplion8,

4

T3, because the serum autoantibodies are
replacement therapy is necessaiy for the
removed in the dialysis step. Therefore, if
remainder of the anin1al's life; careful initial

558

THE THYROID GLAND
diagnosis and tailoring of treatment is
many goitrogenic areas throughout the
essential. The reported replacement
world before the widespread supplementadosages for T
tion of iodized salt to anin1al diets. Although

4 in dogs and cats range from a
total dosage of 0.01--0.02 mg/lb (0.02--0.04
outbreaks of iodine-deficient goiter are now
mg/kg), daily, given once or divided bid
sporadic and fewer animals are affected,
without food ( on an empty stomach).

iodine deficiency is stiU responsible for

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The most important indicator of the
most non-neoplastic goiters seen in large
success of therapy is clinical improvement. domestic animals.

Reversal of changes in coat and body

Iodine atoms are a part of the thyroid
weight should be assessed only after 1-2
hormones thyroxine and triiodothyronine;
mo of therapy. When clinical improvement
thus, insufficient iodine reduces the
is marginal or signs of thyrotoxicosis are
ability of the thyroid to make these
seen, the clinical observations can be
hormones. With reduced circulating
supported by therapeutic monitoring of
thyroid hormone levels, the pituitary
serum thyroid hormone concentrations
secretes more thyroid-stimulating

("post-pill testing"). With once-daily
hormone (TSH), which acts as a stimulus
administration ofT4, the peak serum
for hyperplasia of the thyroid gland and
concentration ofT, generally should be
subsequent development of a goiter. The
slightly high to high-normal 4-6 hr after
hyperplastic gland may, and usually does,
dosing and should be low-normal to
compensate for the reduced availability
normal 24 hr after dosing. Animals on bid
of iodine; therefore, goiter is in no way
administration probably can be checked at
synonymous with hypothyroidism. Fetal
any time, but peak concentrations can be
thyroid glands are more susceptible to
expected at the middle of the dosing
the effects of high or low iodine intake;
interval (4-6 hr) and the nadir just before
animals born to females on iodine-deficient
the next dose. After the dosage is
diets are more likely to develop severe
stabilized, serum T4 (with or without T3)

thyroid enlargement and have clinical
concentrations should be checked
signs of hypothyroidism.

1-2 times per year.

Goiter caused by iodine deficiency is

If clinical signs of hypothyroidism remain
most common in newborn pigs, lambs, and
despite the use of reasonable doses of
calves in iodine-deficient areas. The thyroid
thyroid horn10ne, the foUowing must be
lobes of the young animal usually are at
considered: 1) the dosage or frequency of
least twice norn1al size, soft, and dark red.

administration is improper; 2) the owner is

In severe cases, there is an accompanying
not complying with instructions or is not
lack of hair ( especially in pigs) or wool
successfully administering the medication;

Oambs ). The neck is usually grossly

3) the aninrnl is not absorbing the medicaenlarged, and the skin and other tissue may tion well, or is metabolizing and/or excreting be thickened, flabby, and edematous. In it too rapidly; 4) the medication is outdated;
mildly affected animals, treatment with
or 5) the diagnosis is incorrect.

iodized salt ( containing >0.007% iodine)

may resolve the goiter and associated

NON-NEOPLASTIC
clinical signs, but many die before or soon

ENLARGEMENT OF THE
after birth. Prophylaxis is more effective

THYROID GLAND
than treatment. Using stabilized iodized
salt or ensuring that the ration is balanced

(Goiter)

for iodine content is recommended in all
areas known or suspected to be iodine

An enlarged thyroid gland is, by definition,
deficient.

a goiter. Non-neoplastic and noninflammatory enlargements of the thyroid gland Iodine Toxicity: Goiter and h
develop in all domestic mammals as well as
ypothyroidism occur in foals of dams fed excess iodine birds. The major causes of goiter include
during gestation. Mares supplemented with
iodine deficiency, ingestion of goitrogenic
iodine at �35 mg/day may produce affected
substances, dietary iodine excess, and
foals. Foals receive the excess iodine both
inherited enzyme defects in the biosynthein utero and via the milk, because mares on sis of thyroid horn1ones. Many animals
high-iodine diets secrete higher than normal
with goiter appear to remain euthyroid,
amounts of iodine in their milk. Clinical
but clinical signs of hypotl1yroidism may
signs vary and may include goiter,
develop in some, especially in newborns.

weakness, and musculoskeletal abnormalities. Mares are invariably asymptomatic.

Iodine Deficiency: Thyroid hyperplasia

Foals may improve or recover once the
due to iodine deficiency was conm10n in
excess iodine is removed.

THE THYROID GLAND

559

Goitrogenic Substances: Certain
sparse coat, myxedematous swelling of
plants may produce goiter when ingested
subcutaneous tissues, and weakness. Many
in sufficient an1ounts, especially in the
affected animals die shortly after bilth or
absence of adequate iodine intake.

are very sensitive to adverse environmental

Soybeans are most notable, but cabbage,
conditions.

rape, kale, and turnips all contain less

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potent goitrogens. Cooking or heating ( and

HYPERTHYROIDISM
the usual processing of soybean meal)

destroys the goitrogenic substance in these

Excessive secretion of the thyroid
plants. All of the goitrogenic substances act
hormones, T4 and T3, results in signs that by interfering with production of thyroid
reflect an increased metabolic rate and
hormone. As with iodine deficiency, the
produces clinical hyperthyroidism. It is
pituitary responds to the reduced circulatmost common in middle-aged to old cats ing thyroid honnone levels by increasing its
but also develops rarely in dogs.

secretion ofTSH, which results in thyroid

Functional thyroid adenoma ( adenomagland enlargement. In adult animals the tous hyperplasia) is the most conunon
disease is usually not significant, but severe
cause of feline hyperthyroidism; in --7CJ'lo
thyroid enlargement and hypothyroidism
of cases, both thyroid lobes are enlarged.

may develop in newborns.

Thyroid carcinoma, the prin1ary cause of
hype1thyroidism in dogs, is rare in cats

Congenital Hypothyroidism and

(1%-2%of hyperthyroidism cases).

Dysmaturity Syndrome of Foals:

Congenital hypothyroidism and dysmatmity

Clinical Findings and Diagnosis: The
syndrome of neonatal foals was first
most common signs include weight loss,
recognized in the early 1980s and is
increased appetite, hyperexcitability,
characterized by hyperplasia of the thyroid
polydipsia, polyuiia, and palpable enlargegland, goiter, and multiple congenital ment of the thyroid gland. GI signs are also
musculoskeletal anomalies. It is most
common and may include vomitiI1g,
conunon in western Canada but has been
diatThea, and increased fecal volwne.

seen in the Pacific Northwest and sporadi

Cardiovascular signs include tachycru·dia,
cally in other areas of the USA. There is no
systolic murnmrs, dyspnea., cru·diomegaly,
sex or breed predilection. Foals with this
and congestive heatt failure. Ra.rely,
syndrome are born after a prolonged gesthype1thyroid ca.ts exhibit a.pathetic signs ( eg, ation (340-400 days) but appear dysmature
at1orexia, lethargy, and depression); weight
with pliable ears, muscle weakness, and
loss remains a conunon sign in these cats.

incomplete skeletal development. Conunon

High basal serwn total thyroid hormone
musculoskeletal defects include flexural
concentration is the hallmark of hyperthydefomtities of the forelimbs, ruptured tendroidism and confirms the diagnosis.

ons of the common digital extensor muscles, Although serun1 total T, concentrations are mandibular prognathia, and inunature

1
high in most cats with hyperthyroidism,
carpal and tarsal bones. Multiple cases may

-5o/e>--Hl0A, of ca.ts have norn1al T values.

appear on a farm, with no recurrence in

4

Most ca.ts with normal serum T values have
subsequent years. The underlying etiology is

4
either mild or early hyperthyroidism or
unknown but may be the result of diets that
hyperthyroidism with concurrent nonthycontain high levels of nitrate ( eg, greenfeed) roidal illness, which has caused suppression combined with low iodine intake or
of a high total T concentration to within
ingestion of an unidentified goitrogen. Most

4
reference range limits. In these ca.ts, a high
affected foals either die or are euthanized
free T, concentration along with consistent
within the first week of life.

1
history and physical exan1ina.tion findings is
diagnostic of hype1thyroidism.

Familial Dyshormonogenetic

Goiter: Fanillial dyshonnonogenetic

Treatment: Cats with hyperthyroidism
goiter has been repmted in sheep, cattle,
can be treated by ra.dioiodine therapy,
goats, and pigs and appears to be inherited
thyroidectomy, chronic administration of
as an autosomal recessive trait. Essentially,
at1 antithyroid drug, or lifelong nutlitional
it is a genetic enzyn1e defect in the
therapy (iodin e -deficient diet). Radioactive
biosynthesis of thyroid hormones. As with
iodine provides a silnple, effective, and safe
iodine deficiency, reduced thyroid hormone
treatment and is considered the trea.tlnent
production leads to secretion of increased
of choice. The ra.dioiodine is concentrated
levels ofTSH and subsequent goiter. Clinical within the thyroid tun1or, where it signs may include subnormal growth rate,
selectively in·a.diates and destroys
absence of normal wool development or a
hyperfunctioning thyroid tissue.

560

THE THYROID GLAND

Surgical thyroidectomy is also an
the tachycardia, tachypnea, hypertension,

�ffective treatment for hyperthyroidism
and hyperexcitability associated with
m cats. With unilateral thyroid tumors,
hype1thyroidism.

r1emithyroidectomy corrects the hyperthy

Oral cholecystographic agents ( eg,
roid state, and thyroxine supplementation
ipodate, iopanoic acid, or diatrizoate
usually is not necessary. For bilateral
meglumine) acutely inhibit conversion

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thyroid tumors, complete thyroidectomy is
of peripheral T4 to T3. In one study of
indicated, but parathyroid function must be
hyperthyroid cats, administration of
preserved to avoid postoperative hypocalcalcium ipodate nom1alized serum total cemia. Thyroxine supplementation should

T3 concentrations and produced clinical
be started 1-2 days after complete
improvement in >600/o of cats treated.

thyroidectomy. If iatrogenic hypoparathylpodate (308 mg iodine/500 mg calcium roidism develops, treatment with vitamin D
ipodate) is no longer marketed in the USA,
and calcium is also indicated.

but iopanoic acid (333 mg iodine/500 mg

Treatment with methimazole, an
iopanoic acid) and diatrizoate meglumine
antithyroid drug, controls hyperthyroidism

(370 mg iodine/mL) have been used
by blocking thyroid hormone synthesis.

anecdotally in hyperthyroid cats at

Carbimazole is a similar antithyroid drng
comparable dosages. None of these drugs
available in many European countries,
provides complete resolution of clinical

Australia, and Japan; it exerts its effects
signs or biochemical features associated
through immediate conversion to methimawith hype1thyroidism. In addition, waning zole after administration. Propylthiouracil,
of the thyroid-lowering effect is common
another antithyroid drug, is not recomafter 3 mo of therapy with any of these mended for use in cats because of the high
drugs.

incidence of serious adverse effects

A fouth treatment option for cats witl1

( especially hemolytic anemia and thrombohyperthyroidism is the use of a prescription cytopenia ). The recommended initial daily
diet with severely restricted iodine levels
dose of methimazole is 2.5-5 mg in two

(Hill's® y/d Feline Thyroid Health TM). The
divided doses. The dosage is acljusted to
basis for using this diet is that iodine is an
maintain circulating thyroid hormone
essential component of both T4 and T3;
concentrations within the mid-normal range witl10ut sufficient iodine, tl1e thyroid cannot and is given daily. Adverse effects, the more
produce excess thyroid honnones. This is
serious of which are ag.ranulocytosis and
an iocline-deficient diet, containing iodine
thrombocytopenia, develop in <5% of
levels below the minimun1 daily requiretreated cats. If this occurs, methimazole ment for adult cats. A major indication for
should be discontinued and supportive
use of this diet for management of feline
therapy instituted; these adverse reactions
hypeithyroidism is in cats that are not
should resolve within 2 wk. To maintain
candidates for definitive treatment of the
normal levels of thyroid hormone ·and to
underlying thyroid tumor( s) with surgery or
monitor for adverse reactions during the
radioiodine, which remain the treatments of
first 3 mo of treatment (when the most
choice. In addition, nutritional management
serious adverse effects associated with
could be considered in cats whose owners
methi.mazole therapy develop), CBCs and
are not able to give oral medication or i.n
serum thyroid hormone determinations
cats that develop adverse effects from
should be repeated at 2- to 4-wk intervals,
methimazole or carbin1azole.

with the drug dosage acljusted as necessary.

Most hyperthyroid cats exclusively fed

Subsequently, serum T concentrations
this iodine-restricted diet become euthyroid

4
should be measured at 3- to 6-mo intervals
in 8-12 wk. This therapy appears to be more
to monitor dosage requirements and
effective in cats with only moderate
response to treatment.

increases ofT than in cats with severe

The use of medical therapy other than

4
hyperthyroidism. Despite some advantages,
methin1azole may be required if adverse
nutritional management has disadvantages:

effects develop. For the most part, these

1) feeding this diet can only control (by
alternative medical therapies are for
withholding "fuel" for the thyroid tumor)

short-tem1 use and are only recommended
but not cure hypertl1yroidism; 2) cats fed
before use of a more permanent treatment
this diet must not eat any other cat diet,
option.

table food, or treats, because even tiny

Propranolol and atenolol are the most
amounts of iodine can render the diet
frequently used [3-adrenoceptor blocking
ineffective in controlling hyperthyroidism;
agents in hyperthyroid cats. These drugs do
and 3) relapse will occur if the diet is
not lower the circulating T concentration
stopped, so the cat must eat only this diet

4
but are used to symptomatically control
for the rest of its life.

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

561

In dogs, a thyroid tumor causing
and use of radioactive iodine therapy, alone
hyperthyroidism should always be
or in combination, may be indicated
presumed to be a carcinoma until proved
depending on the individual. The hyperthyotherwise. This is in contrast to the case roid state can be medically controlled by
in hyperthyroid cats, in which thyroid
daily administration of an antithyroid drug
carcinoma is present in <5%.

such as methimazole or carbimazole (5-15

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Treatment of thyroid neoplasia and
mg/dog, bid), but such treatment will not
hyperthyroidism in dogs is dictated by the
prevent tumor growth or metastasis.

size of the primary tumor, extent of local

Because canine hyperthyroidism is almost
tissm: invasion, presence of detectable
always associated with thyroid carcinoma,
metastasis, and available treatment options.

the longterm prognosis in these dogs is poor

Surgery, chemotherapy, cobalt irradiation,
to grave.

THE PARATHYROID GLANDS AND

DISORDERS OF CALCIUM METABOLISM

The physiology and disorders of calcium

The calcium ion is an essential structural
and phosphate metabolism, Lhe function of
component of the skeleton and plays a key
vitamin D ( which acts more like a honnone
role in muscle contraction, blood coagulathan a vitamin), and the formation of bone tion, enzyme activity, neural excitability,
are all tied together in a common system
secondary messengers, hmmone release,
along with two other regulatory hms
and membrane permeability. Precise control
manes-parathyroid hormone (PTH) and
of calcium ion in extracellular fluids is vital to
calcitonin. Therefore, PTH, calcitonin, and
health. Three major ho1mones (PTH, vitamin
vitamin D are discussed in this chapter

D, and calcitonin) interact to maintain a
together with the associated disorders of
constant concentration of calcium, despite
calcium homeostasis.

va.iiations in intake and excretion. Other

Because aberrant calcium and phosphohormones, such as adrenal corticosteroids, rus metabolism is reflected in the skeletal
estrogens, thyroxine, somatotropin, and
system, specific syndromes are presented
glucagon, may also contiibute to the
in that section. (See also DYSTROPHIES
maintenance of calciun1 homeostasis.

ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND

VITAMIN D, p 1050.)

Parathyroid Hormone: PTH is
synthesized and stored in the chief cells

CALCIUM PHYSIOLOGY
of the parathyroid glands. Synthesis is

AND CALCIUM-REGULATING
regulated by a feedback mechanism

HORMONES
involving the level of blood calcium (and,
to a lesser degree, that of magnesium).

The concentration of calciun1 in the blood

In addition, biological an1ines, peptides,
of mammals is -10 mg/dL, with some
steroids, and several classes of drugs can
variation due to species ( eg, as much as 13
influence PTH secretion.

mg/dL is normal in horses and rabbits), age,

The p1irnary function of PTH is to control
dietary intake, and analytic method.

calcium concentration in the extracellula.i·

Calcium in plasma or serum exists in three
fluid, which it does by affecting the rate of
forms or fractions: 1) Protein-bound
tra.t1Sfer of calcium into and out of bone,
calcium accounts for approximately
resorption in the kidneys, and absorption
one-third of the total serum calcium
from the GI tract. The effect on the kidneys
concentration. Protein-bound calcium canis the most rapid, causing reabsorption of not diffuse through membranes and thus is
calcium and excretion of phosphorus. The
not usable by tissues. 2) Ionized or free
major initial effect on bone is to mobilize
calcium is the physiologically active fonn
calcium from the bone to the extracellular
that accounts for 500/<>-tiO"Ai of total calciun1
fluid; later, bone formation may be enhanced.

concentration. 3) Complexed or chelated

PTH does not directly affect calcium
calcium is bound to phosphate, bicarbonate, absorption from the gut. Its effect is mediated sulfate, citrate, and lactate and accounts for
indirectly by regulation of synthesis of the

-lO"A, of the total calciun1 concentration.

active metabolite of vitamin D.

562

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

Vitamin D: The second major hormone
hormone to protect against development
involved in the regulation of calcium
of hypercalcemia.

metabolism and skeletal remodeling is

Calcitonin exerts its effects by interactvitamin D, which includes cholecalciferol ing with target cells, primarily in bone and

(vitamin 03) of animal origin, as well as
kidney. The actions of PTH and calcitonin
ergocalciferol (vitan1in 02) of plant origin.

are antagonistic on bone resorption but

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Vitamin D has long been considered an
synergistic on decreasing the renal tubular
essential dietary ingredient, but in several
reabsorption of phosphorus. The
species, including sheep, cattle, horses,
hypocalcemic effects of calcitonin are
pigs, and people, vitamin D can be formed
primarily the result of decreased entry of
in the skin from a cholesterol metabolite
calcium from the skeleton into plasma,

(7-dehydrocholesterol) after exposure to
resulting from a temporary inhibition of
ultraviolet light. In contrast, dogs and cats

PTH-stimulated bone resorption. The
are not able to synthesize vitamin 03
hypophosphatemia develops from a direct
adequately in the skin and mainly depend
action of calcitonin, which increases the
on dietary intake.

rate of movement of phosphorus out of

Vitan1in D must be metabolically
plasma into soft tissue and bone and
activated before it can function physiinhibits the bone resorption stimulated by ologically. The biologic actions of vitamin

PTH and other factors. Although many

D depend on hydroxylation in the liver and
effects have been attributed to calcitonin
kidneys to form the biologically active
at pharmacologic doses, their physiologic

1,25-dihydroxyvitamin D (calcitriol). This
relevance is suspect. Physiologically,
conversion in the kidneys is the ratecalcitonin has at best a minor role in limiting step in vitamin D metabolism,
regulating blood concentrations of
and it is partly responsible for the delay
calcium. Neither chronically high (eg, as
between vitamin D administration and
in animals with medullary thyroid cancer)

expression of its biologic effects. PTH and
nor chronically low ( eg, as in animals after
conditions that stimulate its secretion, as
surgical removal of the thyroid gland)

well as hypophosphatemia, increase the
circulating calcitonin concentrations
formation of the active vitamin D metaboresult in any changes in the serum calcium lite. High circulating phosphorns concenconcentration.

trations have the opposite effect. Under
certain conditions, prolactin, estradiol,
placental lactogen, and possibly somato

HYPERCALCEMIA IN DOGS AND
tropin have a similar enhancing effect.

CATS

Increased secretion of these hormones,
either alone or in combination, appears to

Hypercalcemia can be toxic to all body
be important in the efficient adaptation to
tissues, but major deleterious effects occur
the major calcium demands of pregnancy,
in the kidneys, nervous system, and
lactation, and growth.

cardiovascular system. The development
of clinical signs from hypercalcemia

Calcitonin: Calcitonin is a 32-amino acid
depends on the magnitude of the calcium
polypeptide hormone secreted by the
increase, how quickly it develops, and its
parafollicular cells CC-cells) of the thyroid
duration. Serum total calciw11 concentragland in mammals and by ultimobranchial tions of �15 mg/dL may not be associated
tissue in avian and other nonmammalian
with systemic signs, but serum concentraspecies. The concentration of calcium ion tions of> 18 mg/dL are often associated
in extracellular fluids is the principal
with severe, life-threatening signs.

stimulus for the secretion of calcitonin

Polydipsia and polyuria are the most
by C-cells. In hypercalcemia, the rate of
common signs of hypercalcemia and result
secretion of calcitonin is increased greatly
from an impaired ability to concentrate
by rapid discharge of stored honnone from
urine and a direct stimulation of the thirst

C-cells into interfollicular capillaries.

center. Anorexia, vomiting, and constipa

Hyperplasia of C-cells occurs in response
tion can also develop as a result of
to longterm hypercalcemia. When blood
decreased excitability of GI smooth
calcium is lowered, the stimulus for
muscle. Decreased neuromuscular
calcitonin secretion is diminished. The
excitability may lead to signs of generalized
storage of large amounts of prefom1ed
weakness, depression, muscle twitching,
hormone in C-cells and rapid release in
and seizures.

response to a moderate rise in circulating

There are many potential causes of
calcium probably reflect the physiologic
hypercalcemia ( see TABLE l ). In hypercalcerole of calcitonin as an "emergency"

mic dogs, neoplasia (lymphosarcoma) is

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

563

•4i=i•i• CAUSES OF HYPERCALCEMIA IN DOGS AND CATS

Acromegaly

Apocrine gland adenocarcinoma

Carcinoma (squamous cell, mammary, bronchogenic, prostate, thyroid, nasal cavity) VetBooks.ir

Chronic and acute renal failure

Factitious: lipemia, postprandial, young dog ( <6 mo old) Granulomatous disease

Hematologic malignancies (bone marrow osteolysis)

Humoral hypercalcernia

Hypercalcemia of malignancy

Hyperthyroidism

Hypervitaminosis D: iatrogenic, plants (eg, day-bloomingjessamine), rodenticides, antipsoriatic cream

Hypoadrenocorticism (Addison disease)

Iatrogenic disorders: excess calcium or oral phosphate binders Idiopathic hypercalcemia of cats

Laboratory error

Lymphoma (lyrnphosarcoma)

Metastatic or primary bone neoplasia

Multiple myeloma

Myeloproliferative disease (rare)

Primary hyperparathyroidism

Skeletal lesions: osteomyelitis, hypertrophic osteodystrophy the most common cause, followed by
are lymphoma and squamous cell carcihypoadrenocorticism, primary hyperparanoma Prin1ary hyperparathyroidism occurs thyroidism, and chronic renal failure. Other
in cats but not as frequently as in dogs.

causes of hypercalcemia in dogs, in an

Rarely, hypercalcemia is seen in cats with
approximate incidence order as seen in
hyperthyroidism.

practice, include vitamin D toxicosis,
apocrine gland carcinoma of the anal sac,
multiple myeloma, carcinomas (lung,

Hypercalcemia of Malignancy
manunary, nasal, pancreas, thymus, thyroid,

Malignancy is the most common cause of
vaginal, and testicular), and finally, certain
persistent hypercalcemia in dogs and is a
granulomatous diseases (blastomycosis,
common cause in cats. In hypercalcemia
histoplasmosis, schistosomiasis ). Approxiof malignancy, the hypercalcemia mately 70% of hypercalcernic dogs are also
primarily results from increased osteoazoternic. However, azoternia is uncommon clastic bone resorption, but increased
in dogs with hyperparathyroidism.

renal tubular resorption and increased

In cats, idiopathic hypercalcemia appears intestinal absorption may also play a role.

to be the most frequent cause of a high total

Factors that may be produced by tun1ors
calciwn concentration, followed by renal
and result in hum oral hypercalcemia of
failure and malignancy. Ionized hypercalcemalignancy include PTH, PTH-related mia in conjunction with chronic renal
protein (PTHrP), transforming growth
failure is more conunon in cats than dogs.

factor, 1,25-dihydroxyvitamin D, prosta

The most common tumor types associated
glandin E2, osteoclast-activating factor,
with hypercalcernia of malignancy in cats
and other cytokines (interleukin-1,

564

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM
interleukin-2, and -y-interferon). Although
cally different from tl1ose without hypercalmany tumors have been associated with cemia, survival times are considerably less
hypercalcemia in people, malignancyindicating that hypercalcemic lymphomas'

associated hypercalcemia in dogs has
have a poorer prognosis. (See also CANINE
been most commonly linked to lymphoma, MALIGNANT LYMPHOMA, p 40, and FELINE LEUKEMIA VetBooks.ir
adenocarcinoma of the apocrine glands

VIRUS AND RELATED DISEASES, p 790.)

of the anal sac, and multiple myeloma.

Other tumors (thymoma, squan1ous cell

Adenocarcinoma of the Apocrine
carcinoma, nasal carcinoma, hemangio

Glands of the Anal Sac: This tumor
sarcoma, and undifferentiated adenocarusually occurs in older dogs of either sex cinoma) have also been associated with
with hypercalcemia developing in -90% df
hypercalcemia in dogs. In cats, humoral
cases. Humoral mechanisms are most
hypercalcemia of malignancy occurs less
likely responsible for the hypercalcemia,
frequently tl1an in dogs but has been
because a PTH-like protein has been
reported with squan1ous cell carcinoma
identified from tumor tissue in dogs.

multiple myeloma, and l

This tumor is usually malignant and has
ymphoprolifera�
tive diseases.

metastasized to regional lymph nodes by
the time of diagnosis. Surgical resection

Lymphoma (Lymphosarcoma): The
is associated with reduction of serum
most common tumor associated with
calcium. Failure to remove all of the
hypercalcemia in dogs, lymphoma is
tumor or recurrence of the tumor usually
also one of the tumors associated with
results in recurrence of hypercalcemia.

hypercalcemia in cats. The pathogenesis

De�pite surgical excision, radiation, and
of the hypercalcernia may involve two
vanous chemotherapy protocols, the
general mechanisms. One is local
tumor usually recurs within a few
elaboration of an osteolytic factor that
months, and prognosis is poor.

induces resorption of bone and mobilization of calcium when the bone marrow Multiple Myeloma: This malignancy
is infiltrated by tumor cells. The other,
in dogs and cats has been associated
probably more important, is humoral
with hypercalcemia in 10%--15% of cases.

hypercalcemia in which neoplastic cells

The pathogenesis of the hypercalcemia
produce a humoral factor that acts at a
is most likely multifactorial. Myeloma
distance from the tumor. As evidence for
cells are known to produce osteoclastsecretion of a humoral substance by activating factor in people, which may
tumor cells, increased bone resorption,
partially account for the hypercalcemia.

phosphaturia, and urinary excretion of

The presence of extensive bony lysis
cyclic adenosine monophosphate (cAMP) may also contribute to the increased have been documented in dogs with
serum calcium. Although serum protein
lymphoma. Serum concentrations of both concentration is usually increased in PTH and 1,25-dihydroxyvitamin D are
multiple myeloma, increased protein
generally low in these dogs, but PTHrP
binding of calcium rarely accounts for
has been detected in dogs wiJ;h lymphoma the hypercalcemia. Treatment of multiple ( see
myeloma with chemotherapy has been

TABLE 2).

Of dogs with lymphoma, 10%-40% have
associated with longterm survival, but
concurrent hypercalcemia, and a large
the presence of associated hypercalcenumber of tl1ese cases also have tl1e mia, light chain proteinuria, and
mediastinal form of lymphoma. Although
extensive bony lesions is associated
detectable l
with a shorter survival time.

ymphadenopatl1y is usually
present, hypercalcernia may be the first
abnormality noted. A tl1orough physical

Primary Hyperparathyroidism
examination, together with thoracic and

Primary hyperparathyroidism results from
abdominal radiographs, abdominal
excessive secretion of PTH by one or more
ultrasonography, multiple lymph node
abno1mal (usually neoplastic) parathyroid
aspirates or biopsies, and multiple bone
glands. It is relatively rare in dogs and cats.

marrow aspirates may be necessary to

Persistent hypercalcemia is characteristic.

make the diagnosis. Treatment with

Solitary adenoma of the external or internal
glucocorticoids (eg, prednisone) lowers
parathyroid gland is the most common
serum calcium concentrations; however,
cause of primary hyperparathyroidism,
steroids are lympholytic and make
whereas parathyroid carcinoma has been
identification of lymphoma difficult.

infrequently reported. Hyperplasia of one

Alt11ough remission rates in dogs with
or all four paratl1yroid glands has been
lymphoma and hypercalcemia are not statisti-
described but is very rare.

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

565

Clinical Findings: Polydipsia, polyuria,
treatment exists for primary hyperparathyanorexia, lethargy, and depression are the roidism, although treatment for hypercalcemost common signs, but many animals mia can be done if surgery is declined.

with milder degrees of hypercalcemia may
be asymptomatic. Constipation, weak

Hypercalcemia Associated with
ness, shivering, twitching, vomiting, stiff

VetBooks.ir

Hypoadrenocorticism
gait, and facial swelling are less often
reported.

Mild hypercalcemia (�15 mgtd.L) has been
repo1ted in as many as 300/o of dogs with
hypoadrenocmticism (Addison disease).

Diagnosis: Hypercalcemia, normal to

Multiple factors may result in the hypercallow serum phosphorus, and low urine cemia, including increased calciun1 citrate
specific gravity are the most consistent

(complexed calcium), hemoconcentration
findings. Azotemia commonly develops

(relative increase), increased renal
as a consequence of moderate to severe
resorption of calcium, and increased affinity
hypercalcemia. In hypercalcemic animals
of serum proteins for calcium. Although
that still have relatively normal renal
total serun1 calcium concentrations may be
function (normal serum creatinine and
increased, the ionized fraction usually
urea nitrogen concentrations), determiis nom1al. The hypercalcemia resolves nation of serum PTH is helpful in
quickly with successful treatment for
diagnosis. The finding of high-normal
hypoadrenocorticism.

to high serum PTH concentrations in
hypercalcemic animals with normal renal
function is consistent with primary

Renal Failure
hyperparathyroidism, whereas the finding In cats, chronic renal failure (usually of low PTH concentrations is consistent
associated with chronic interstitial
with hypercalcemia of malignancy.

nephritis) appears to be the most common

Ultrasonography of the parathyroid
cause of hypercalcemia. The pathogenesis
glands is a useful diagnostic technique
of the hypercalcemia is not known, but the
but requires an ultrasound unit with a
ionized calcium concentrations remain
high frequency transducer in the 7.5- to
nom1al. In dogs, renal failure caused by

10-MHz range to achieve the necessary
familial renal disease is more often
resolution. Normal parathyroid glands are associated with hypercalcemia than are not always visualized on ultrasonographic
other forms of chronic renal failure.

examination, but enlarged parathyroid

Hypercalcemia may also be present in
glands appear as rounded hypoechoic or
acute renal failure during the polyuric
anechoic structures associated with the
phase, but this is rare.

thyroid gland. Finding a solitary parathyroid gland in a hypercalcemic animal Idiopathic Hypercalcemia of Cats.

supports a diagnosis of primary hyperparathyroidism, whereas finding multiple A syndrome in young to middle-aged
enlarged parathyroid glands is compatible
cats, first described in the early 1990s,
with secondary hyperparathyroidism.

involves hypercalcemia that occurs

Ultrasound cannot distinguish a parathywithout obvious explanation. It has roid adenoma from an adenocarcinoma.

been suggested that the feeding of

Exploratory surgery of the cervical region
acidifying, magnesium-restricted diets
is a diagnostic alternative if no other
predisposes cats to idiopathic hypercalcause of hypercalcemia can be detercemia. Another plausible hypothesis is mined.

that excessive dietary vitamin D content
in some cat foods may contribute to
this condition. Total serum calcium is

Treatment: The most cost-effective and
increased for months to years, often
expedient approach to management is
without obvious clinical signs in the
surgical exploration of the neck and
early stages. Ionized calcium is
removal of the abnormal parathyroid tissue.

increased, sometimes out of proportion

Percutaneous ultrasound-guided chemical
to the increase in total serum calcium.

( ethanol) or heat ablation of the parathyroid Longhaired cats may be over-represented; has been used and may be a feasible
most are not azotemic at initial diagnosis
alternative to surgery in some cases.

but may later develop azotemia. PTH

Attempts to lower the serun1 calcium
levels are either low or remain within the
concentration with IV fluids (saline) an<l
reference range, PTHrP is not detectable,
furosemide before surgery or ablation may
and 25-hydroxyvitamin D and calcitriol
be beneficial (seep 568). No medical
levels are within normal limits.

566

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

Intensive treatment for idiopathic
bisphosphonates in cats are currently
hypercalcemia is rarely indicated,
unknown, but alendronate appears to
because hypercalcemia has developed
be relatively safe for use in cats.

gradually and is relatively longstanding,
and dramatic clinical signs are usually

Osteolytic Lesions
absent. Most cats can be treated as

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outpatients with dietary change either

Hypercalcemia resulting from tumor
alone or in combination with drug
invasion or metastasis to bone develops
therapy.

very rarely in anin1als. P1imary bone tumors

Diet modification is recommended as

( eg, osteosarcoma) and neoplastic cells
a firs
within the bone marrow ( eg, multiple

_t-line treatment. If an acidifying diet

IS bemg fed, 1t should be discontinued.

myeloma) may occasionally produce

A number of different diets have been
hypercalcemia. The mechanisms whereby
recommended, including high-fiber diets,
bony neoplasia may produce hypercalcemia
kidney diets, or diets developed to
include mechanical destruction by the
prevent calcium oxalate urolithiasis.

infiltrating cells ( as occurs with metastatic

Others recommend feeding canned diets
twnors and osteosarcoma) and local
with a composition similar to what cats
production of osteoclast-activating factor
would eat in the wild (ie, 40%-60% of

(as occurs with multiple myeloma).

calories as protein, 30%-50% fat, and< 15%

Bacterial and mycotic osteomyelitis can
carbohydrates). No matter what t
also occasionally produce hypercalcemia.

ype of
diet is chosen, it is best to feed a wet-only

The hypercalcemia may result from direct
diet to promote urinary dilution and
bone lysis or may be mediated by bonelessen the chance of calcium oxalate resorbing factors ( eg, prostaglandins,
stone formation. Administration of
osteoclast-activating factor).

prednisone results in longterm decreases
in ionized and total calcium concentra

Other Causes of Hypercalcemia
tions in some cats.

If normocalcemia has not been

Hypervitaminosis D: Vitanlin D toxicity
restored after a dietary feeding trial of
refers to the effects of excessive intake of

6-8 wk, treatment with glucocorticostebioactive metabolites of vitamin D. Toxicity roids or bisphosphonates should be
caused by ergocalciferol (vitanlin DJ or
considered. Prednisone is given orally at
cholecalciferol (vitanlin 03) can occur from

5 mg/caUday for 1 mo before reevaluaexcessive dietary supplementation ( most tion. If the serum ionized calcium
common in young growing dogs) for
concentration is normal, this dose is
treatment of primary hypopa.rathyroidism.

continued for several months. Ifthe

Both of these f01ms of vitamin D have a slow
ionized calcium value is still increased
onset of action and prolonged duration
the dosage is gradually increased to 10'...20
making correct dosing difficult. Treatm�nt is
mg/caUday as needed to restore normocdirected at discontinuing the supplement or alcemia. Alternatively, treatment with the
decreasing the dose of vitanlin D. Toxicity
bisphosphonate alendronate can be
caused by calcitriol (1,25-dihydroxyvitanlin
instituted, starting at 10 mg orally once

D), the most active fom1 of vitanlin D, most
weekly; the dosage can be increased to
commonly occurs after treatment of

20-30 mg per week, as needed. It is
primary hypoparathyroidism. Calcitriol is
extremely important to administer
also the active ingredient in some rodentialendronate after a 12-hour fast, because cides, but these p(oducts are no longer
food significantly reduces drug absorpwidely available in the USA.

t10n; the fast should also be continued for

In dogs, a newly emerging cause of
at least 2 hr after alendronate administravitanlin D toxicity is ingestion of the tion. Erosive esophagitis is a known
calcitJiol analogue, calcipotriene (also
adverse effect of oral bisphosphonates
called tacalcitol), which is a topical
in human patients. Although the risk of
preparation used to treat psoriasis in
development of esophagi tis in cats is
people. Calcipotliene toxicity in dogs can
unknown, the owner can give 5-6 mL of
result in severe metastatic calcification in
the GI tract, kidney, and otl1er tissues; the

:,vater to the cat with a dosing syringe

1mmed1ately after administration of the
condition is commonly fatal.

alendronate; a small amount of butter
applied to the cat's lips may increase

Housepla
licking and salivation and promote the

�ts: Certain house plants ( eg,

Cestrum diurnum [the day-blooming
transit of the pill to the stomach. The
jes�arnine], Solanum malacoxylon,
longterm safety and efficacy of oral

Trisetumfiavescens) may contain a

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

567
substance similar to vitamin D that may
should be treated by surgical removal,
cause hypercalcemia when ingested.

chemotherapy, or radiation therapy.

Problems may arise when hypercalcemia is

Granulomatous Disease: Hypercalcecomplicated by renal failure, or when mia associated with granulomatous disease primary hyperparathyroidisrn or occult arises from an alteration of endogenous
malignancy is suspected. In these cases, the

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vitamin D metabolism. Macrophages
cause of hypercalcemia may not be obvious,
activated in response to granulomatous
and additional steps must be taken to
inflarrunation can develop the capability to
differentiate primary hyperparathyroidism
convert vitan1in D precursors to the active
from occult tumors causing hypercalcemia.

fonn of vitamin D (ie, calcitriol) in an
unregulated manner. A similar alteration

Ionized Calcium: Because the ionized
of vitamin D metabolism in people may
calcium fraction is the biologically active
explain hypercalcemia in non-Hodgkin
form and the component that regulates
lymphoma, Hodgkin lymphoma, and
production of PTH, measurement of the
lymphomatoid granulomatosis.

ionized calcium concentration is the first

In companion animals, hypercalcemia
step in evaluation of calciun1 abnormalities.

related to granulomatous disease has been
reported in disseminated histoplasmosis,

If ionized calcium is nom1al, even if total
calcium is increased, no further diagnostics
blastomycosis, coccidiomycosis, tubercuare warranted.

losis, and schistosomiasis. Animals with

If ionized calcium is
increased, then PTH and PTHrP detem1inahypercalcemia related to granulomatous tions should be considered if there are no
disease are expected to have high serum
obvious causes of the hypercalcemia.

concentrations of ionized calcium and low

In many cases of hyper- or hypocalcemia,
values for PTH. Serum calcium concentrathe total calcium and ionized calciwn tions return to nom1al with treatment (ie,
concentrations are highly correlated (see
antifungal drugs and surgical removal).

TABLE 2). However, in some instances the
concentration of total calcium does not
reflect the status of ionized calcium. In dogs

Diagnostic Tests for Hypercalcemia
with renal failure, total calciun1 is high, but

The first step in investigating hypercalcemia ionized calcium is nonnal or surprisingly is to exclude the possibility of spurious test
low. In this situation, the total calcium
results. Ideally, a fasting sample should be
increase seems to reflect increased amounts
resubmitted, because sample conditions
of calciun1 complexed to anions, an effect

(Iipemia or hemolysis) can artifactually
that would not be identified in albun1inincrease total serum calcium values adjusted calciun1 concentrations.

reported by colorimetric analyzers.

Ionized calcium is measured in serum or

If the hypercalcemia is repeatable,
heparinized plasma by an instrument using a
ionized calcium should be measured,
calcium-specific electrode. Serwn ionized
because it is a better reflection of the
calciun1 may be falsely high when collected
biologically active form of calcium. Total
in serum separator tubes. There is simultaor adjusted total calcium are not reliable neous measurement of pH, which affects the
measurements of calcium status.

binding of calcium to protein in an inverse

In some animals with persistent ionized
manner. An increase in pH is accompanied
hypercalcemia, identification of the cause
by a decrease in ionized calcium. Serum
will be obvious after analysis of history
samples collected and handled in anaerobic

(vitall1in D exposure, drugs, ingestion of
conditions provide the best results with
houseplants) and physical examination
ionized calcium assays. Samples collected in
findings (masses, organomegaly, cancer, or

EDTA tubes are unsuitable, because EDTA
granulomatous disease). In other animals,
binds available ionized calciw11.

the cause will not be obvious, and
hematology, serum biochemistry, body

Parathyroid Hormone: Assay of PTH
cavity imaging, cytology, and histopatholis the next step in evaluation of calcium ogy may be required. In many animals, use
abnom1alities, once hypercalcemia has
of specialized assays, including measurebeen confirmed by measurement of the ment of PTH, PTHrP, and/or vitan1in D is
ionized calcium concentration. Evaluation
necessary to confinn a diagnosis.

of PTH can reveal whether the parathyroid

If lymphadenopathy is present, a lymph
glands are responding appropriately to the
node aspirate or biopsy should be performed change in calcium concentration or whether to check for lymphosarcoma. If a twnor of
inapprop1iate production of PTH is the
the anal sac is found, surgical removal
cause of the disorder. If calcium metabolism
should be attempted. Any other neoplasm
is normal, small increases of ionized

568

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM
calcium inhibit secretion offYI'H and small

See TABLE 2 for a summary of the
decreases of ionized calcium prompt
anticipated fYI'H, ionized calcium, and
release offYI'H.

fYI'HrP values in the various disorders

Serum or plasma fYI'H detenninations are
causing hypercalcemia. Generally, the
very useful in evaluation of hypercalcemic
fYI'H level is no1mal to high with primary,

VetBooks.ir
dogs and cats. Animals with primary
secondary, or tertiary hyperparathyroidism.

hyperparathyroidism should have

The fYI'H level is low with other causes of
mid-normal to high concentrations offYI'H,
hypercalcemia ( eg, hypervitanlinosis D,
whereas those with most other fom1s of
malignancy associated, renal failure,
hypercalcemia have low fYI'H concentrahypoadrenocorticism).

tions (see TABLE 2).

Parathyroid Hormone-related

Treatment of Hypercalcemia

Protein (PTHrP): Hypercalcemia

A mild degree of hypercalcernia may not
associated with nonparathyroid neoplasia
be immediately dangerous; there is time
is often caused by production of a humoral
to establish a definitive diagnosis before
factor, fYI'HrP, that has parathyroid
starting treatment. In animals with severe
hormone-like bioactivity. Since its
clinical signs associated with hypercalcediscovery in the 1980s, fYI'HrP has been mia, diagnostic and therapeutic efforts
found to be associated with a variety of
may proceed concurrently. No single
tumors that cause hypercalcemia of
treatment protocol is consistently
malignancy in people.

effective for all causes of hypercalce-

Assay of fYI'HrP can be used to confirm
m ia; each animal must be approached
hypercalcemia of malignancy ( see TABLE 2).

individually, and the cause of the

There is a relatively high prevalence of
hypercalcemia must be determined. The
positive results in dogs with apocrine gland
definitive treatment of hypercalcemia is
adenocarcinoma of the anal sac, lymphoma,
treating or removing the underlying cause.

or other miscellaneous tumors. However,

Unfortunately, the cause may not be
humoral hypercalcemia of malignancy
apparent, and supportive measures must
always remains a differential diagnosis in
be taken to decrease the serum calcium
a hypercalcemic dog with a low fYI'H and
concentration. The goal of all supportive
a normal or negative fYI'HrP In cats, high
treatment is to enhance urinary excretion
fYI'HrP is also consistent with humoral
of calcium and to prevent calcium
hypercalcemia of malignancy, especially
resorption from bone.

in cats with carcinoma.

Fluid Therapy: Volun1e expansion

Vitamin D Metabolites (Calcidiol and
with 0.9% saline, -100-125 mllkg/day,

Calcitriol): Because metabolites of

IV, decreases hemoconcentration and
vitamin D are chemically identical in all
increases renal calciwn loss by in1proving
species, radioimmunoassays developed for
glomerular filtration rate and sodiwn
use in people are satisfactory for measureexcretion, which results in less calciwn ment in animals. Calcidiol (25-hydroxyvitareabsorption.

min D) concentration is a good.indicator of
vitamin D ingestion and can be used to

Diuretics: Loop diuretics such as
diagnose hypervitaminosis D.

furosemide (2-4 mg/kg, bid-tid) increase

Vitamin D metabolites resulting from
calcium excretion by the kiQneys; however,
the ingestion of cholecalciferol present in
higher dosages may be needed. If dehydrarodenticides can be measured with the tion is present, fluid therapy should be
calcidiol assay. Toxicity from ingestion of
instituted first because volume contraction
cholecalciferol or ergocalciferol would be
and further hemoconcentration may worsen
detected by an increase of calcidiol that
the hypercalcemia. Thiazide diuretics are
may persist for weeks after exposure.

contraindicated in hypercalcernia, because

Assay of calcidiol also may be used to
these agents decrease calcium excretion by
confirm toxicity from ingestion of
the kidneys and worsen the hypercalcemia.

rodenticides that contain vitan1in D3 as
the active ingredient.

Glucocorticoids: Glucocorticoids

Calcipotriene, the vitamin D analogue
such as prednisone (1-2 mg/kg, bid) or
found in anti psoriasis creams, is not
dexameiliasone (0.1-0.2 mg, bid) provide
measured with the assay for calcidiol but
a second tier of treatment for hypercalcewould be detected in the assay for calcitriol.

mic cases that do not respond adequately

Unfortunately, the calcitriol assay is not
to IV fluids and furosemide. They reduce
widely available for clinical use.

bone resorption of calcium, reduce

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

569

CHARACTERISTIC LABORATORY ABNORMALITIES ASSOCIATED WITH

COMMON CAUSES OF HYPERCALCEMIA

1,25-

Total

Ionized Intact Dihydroxy- Phos-

Diagnosis

Calcium Calcium PTH
vitaminD
phorus PTHrP

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Primary

High

High

Normal Normal

Normal Negative
hyperthyroidism
to high
to low

Malignant

High

High

Low

Low to

Normal Positive
hypercalcemia
to low-
normal
to low

(some-
normal
times)

Hypoadrenocor- Low,

Normal

Nmmal Normal

Normal Negative
ticism (Addison normal,
to high
disease)

or high

Chronic renal

Low,

Normal

Normal Low to

High

Negative
failure
normal,
to low
to high
normal
or high

Hypervitamino-

High

High

Low

Low to

Normal Negative
sis D ( calcitriol
to low-
normal
to high
or calcitriol
nmmal
analogue)

Hypervitamino-

High

High

Low

High

Normal Negative
sis D (D2 or D3
to low-
to high
toxicity)

nonnal

Granulomatous High

High

Low

Low to

Normal Negative
disease
to low-
nom1al
to high
nonnal

Idiopathic

High

High

Nonna! Normal

Normal Negative
hypercalcemia
of cats
intestinal calcium absorption, increase
of osteoclasts. Pamidronate is the most
renal calcium excretion, and are cytotoxic
commonly used parenteral drug; the
to malignant lymphocytes, leading to
recommended dosage in dogs is 1-2 mg/kg,
substantial reduction in serum calcium

IV, mixed in 0.9% saline given throughout
concentration in animals with hypercalce2 hr. In cats, alendronate is the most mia secondary to lymphoma, myeloma,
common oral preparation used to control
hypervitaminosis D, granulomatous
idiopathic hypercalcemia. Adequate
disease, and hypoadrencorticism.

hydration is essential when treating with

However, use of glucocorticoids may
bisphosphonates, because these drugs may
make definitive diagnosis of the underlycause nephrotoxicity, especially at higher ing cause of the hypercalcemia difficult.

doses. The drug can be repeated in 3-4 wk

This is especially true with lymphosarcoma, if needed.

because steroids are lymphocytolytic and

Mithramycin, an inl1ibitor of RNA synthemay alter lymph node architecture and sis in osteoclasts, is an effective treatment
patterns of lymphocyte infiltration in bone
for hypercalcemia; the dosage is 25 mcg/kg,
marrow.

IV, given throughout 4-6 hr. A single dose is
usually successful in normalizing the serum

Miscellaneous Agents: The third tier
calcium concentration; effects last from a
of treatment is to add a bisphosphonate,
few days to several weeks. Adverse effects
mithramycin, or calcitonin for more
may include thrombocytopenia, nephrolongterm control of hypercalcemia.

toxicity, and hepatotoxicity but are unlikely

Bisphosphonates assist in lowering serum
after a single dose. However, this drug must
calcium by reducing the number and action
be used with extreme caution.

570

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

Calcitonin inhibits bone resorption by
are reported in horses witl1 tl1e disorder.

inhibiting the activity and formation of

Additional tests to exclude oilier conditions
bone osteoclasts. The dose of calcitonin is
associated witl1 hypercalcemia may include

4-8 U/kg, SC, bid-tid. Calcitonin is the
measurement of PTHrP and vitantin D
most rapidly acting hypocalcemia agent,
metabolite concentrations.

causing serum calcium to decrease within

As in other species, the definitive

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a few hours after administration. Its effect
treatment of equine hypercalcemia is
is rather transient, however, and the
treating or removing the underlying
maximal reduction in calcium is not as
cause. Unfortunately, the cause may not
great as that seen with bisphosphonates
be readily apparent, and supportive measor mithran1ycin.

ures (eg, fluid therapy, diuretics, and/or

Calcimimetics, a new class of drugs, are
glucocorticoids) must sometimes be used
calcium-sensing receptor agonists. The
to enhance urinary excretion of calcium
mostly conm10nly used drug of this class
and to decrease the serum calcium
is cinacalcet. By interacting witl1 the
concentration.

calcium-sensing receptors in the parathyroid glands, these drugs reduce the secretion of PTH and can effectively

HYPOCALCEMIA IN DOGS AND
suppress circulating PTH in all fom1s of
hyperparatl1yroidism. They have become a

CATS
major therapy for secondary hyperparatl1y

Hypocalcemia causes tl1e major clinical
roidism associated with renal failure as well
manifestations of hypoparatl1yroidism by
as for treatment of primary hyperparathyincreasing tl1e excitability of botl1 the roidism.

central and peripheral nervous systems.

Peripheral neuromuscular signs classically
include muscle tremors, twitches, and

HYPERCALCEMIA IN HORSES
tetany. Generalized convulsions, resembling
tl1ose of an idiopathic seizure disorder, are

Like dogs and cats, horses can develop
the predominant CNS manifestation of
hypercalcemia due to several disorders,
hypoparatl1yroidism.

including chronic renal failure, vitan1in D
toxicosis, and prin1ary hyperparatl1yroidism. The most common cause of Hypoparathyroidism
hypercalcemia in horses is chronic renal

Hypoparatl1yroidism is a metabolic disfailure. The equine kidney is important order characterized by hypocalcemia and
in tl1e excretion of calcium; tl1erefore,
hyperphosphatemia and either transient
impaired renal calcium excretion associor permanent PTH insufficiency. The ated witl1 normal intestinal calcium
spontaneous disorder is uncommon in dogs
absorption may explain tl1e hypercalcemia
and rarely reported in cats. Iatrogenic irtjury
found in these horses.

or removal of tl1e paratl1yroid glands during

Humoral hypercalcemia of malignancy
tl1yroidectomy for treatment of hyperthyhas been reported to be associated with roidism is the most common cause in cats.

gastric squamous cell carcinoma,

Postoperative hypoparatl1yroidism
adrenocortical carcinoma, squamous cell
secondary to pa.ratl1yroidectomy for
carcinoma of the vulva, lymphosarcoma,
paratl1yroid tumor may occur because of
and ameloblastoma. These horses have
atrophy of tl1e remaining glands in eitl1er
hypercalcemia, hypophosphatemia,
dogs or cats.

increased serum concentrations of

PTHrP, and decreased serum concentra

Diagnosis: Diagnosis is based on
tions of PTH.

history, clinical signs, laboratory

Intoxication witl1 ergocalciferol or
evidence of hypocalcemia and hype r cholecalciferol has been reported in phosphatemia, and exclusion of other
horses. Ingestion of plants containing
causes of hypocalcemia ( eg, hypopro1,25-dihydroxyvitamin D-like compounds teinemia, malabsorption, pancreatitis,

(Solanum malacoxylon, S sodomaeum,
renal failure). If idiopathic hypopa.rathy

Cest?um diurnum, Trisetumfiavescens)

roidism is suspected, it should be
causes typical clinical signs of vitantin D
confirmed by histologic examination of
intoxication, including hypercalcemia.

the parathyroid glands and documenta

Primary hyperparatl1yroidism is a rare
tion of parathyroid atrophy or destrucdisorder in ponies and horses. As in dogs tion. Because the parathyroid glands are
and cats, hypercalcemia, hypophosphanot grossly evident in animals with temia, and high serum PTH concentrations
hypoparathyroidism, a unilateral

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM

571
thyroidectomy should be performed to
should be directed at lowering the serum
ensure that adequate parathyroid tissue
phosphate concentrations by dietary
is available for examination. Determinarestriction of phosphorus and intestinal tion of serum PTH concentrations might
phosphate binders. (See ai,so RENAL
be helpful in the diagnosis of idiopathic

DYSFUNCTION IN SMALL A IMALS, p 1512.)

hypoparathyroidism and may thereby

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eliminate the need for cervical explora

Hypoproteinemia: Animals with
tory surgery and histologic verification.

hypoaJbuminemia may be hypocaJcemic
because of a decrease in the protein-bound

Treatment: Treatment is directed at
fraction of caJciun1, but the ionized caJciwn
restoring the serum caJciwn concentration
fraction may remain nonnaJ. Clinical signs
to the low end of the normal range. This
of hypocaJcemia do not usually develop. The
should include use of caJciwn supplements
magnitude of hypocaJcemia is usually mild.

and vitamin D for either iatrogenic or
idiopathic forms of hypoparathyroidism.

Pancreatitis: When hypocaJcemia occurs

If hypocaJcemic tetany or seizures are
in animals with pancreatitis (seep 407), it is present, calcium should be administered IV
usually mild and subclinicaJ. The exact
immediately. For maintenance of normocaJmechanism is unknown, but a commonly cemia, oral calcium should be administered
accepted theory is that calcium is
together with a vitamin D preparation.

precipitated in the form of insoluble soaps

The major complication associated
through saponification of peripancreatic
with treatment of hypoparathyroidism
fatty acids fom1ed subsequent to release of
is hypercalcemia, which develops as
the pancreatic enzyme lipase. More recent
a consequence of overtreatment with
work suggests that hypocaJcemia may
calcium and vitamin D. If this occurs,
result from a shift of calcium into soft
calcium and vitamin D therapy should
tissues, especially muscle.

be temporarily discontinued; saline and
furosemide should be administered if

Puerperal Tetany: Puerperal tetany
hypercalcemia is severe (seep 568).

( eclampsia, seep 992) is an acute, life

With idiopathic hypoparathyroidism,
threatening disease caused by an extreme
longterm management with vitamin D
fall in circulating caJciwn concentrations in

(with or without calcium supplementathe lactating bitch or queen. Severe tion) is necessary. In contrast, with
hypocaJcemia associated with eclampsia
iatrogenic hypoparathyroidism, spontadevelops during the nursing petiod (several neous recovery of parathyroid function
days to several weeks postpartun1). The
or accommodation of calcium-regulating
pathophysiology remains poorly undermechanisms to the absence of PTH may stood but appears to result from an
occur weeks to months after surgery.

imbalance between the rate of inflow ( eg,
bone resorption, GI absorption) and outflow

( eg, rnan1mary gland) from the extracellular

Other Causes of Hypocalcemia
caJciwn pool. Treatment consists of slow IV

Renal Disease: Chronic renal failure
administration of caJcimn ( see below) and
is probably the most frequently encounweaning of the litter, if possible.

tered cause of hypocalcernia. Azotemia
and hyperphosphatemia result from

Phosphate Enema Toxicity: Hypertonic
decreased glomerular filtration rates.

sodiwn phosphate ( eg, Fleet®) enemas may

Mechanisms of hypocaJcemia include
result in severe biochemical abnom1aJities,
decreased renal tubular calcium
especially when administered to dehydrated
resorption, hyperphosphatemia,
cats with colonic atony and mucosa]

decreased formation of 1,25-dihydroxyvidisruption. Hypematremia and hyperphostamin D, hypoalbuminemia, and chelation phatemia result from the colonic absorption
of calcium with oxalate. Parathyroid
of sodiwn and phosphate from the enema
gland hyperplasia occurs to maintain
solution, as well as transfer of intravascular
serum calcium in normal ranges. High
water to the colonic lwnen (because of the

PTH concentrations result in increased
hypertonic enema). Hyperphosphatemia
bone resorption. The hypocalcemia
leads to precipitation of serum caJciwn with
associated with renal failure, however, is
resultant hypocaJcemia. Clinical signs of
rarely clinically significant (ie, muscle
phosphate enema toxicosis, which result
tremors, twitches, tetany, or convulsions
from these electrolyte and fluid alterations,
do not develop). In addition, most animals include shock and neuromuscular with chronic renal failure have normal
initability. Treatment consists of IV volwne
serum calcium concentrations. Treatment
expansion with an electrolyte-poor solu-

572

THE PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM
tion (eg, 5%dextrose in water), as well as
preparations of vitamin D available,
treatment of hypocalcemia (see below).

including vitamin 02 (ergocalciferol),
dihydrotachysterol, and 1,25-dihydroxy

Chelating Agents: EDTA ( ethylenedivitamin D (calcitriol). The dosage and aminetetraacetic acid), citrated blood, and
duration of response of these drugs
oxalic acid ( a metabolite of the ethylene
depends on the form used. For vitamin

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glycol in antifreeze) all complex calciwn

02, the initial required dosages are
and can cause hypocalcemia Animals with
generally 4,000-6,000 JU/kg/day, whereas
ethylene glycol intoxication (seep 3046)

the final dosages required to maintain
also have severe metabolic acidosis,
normocalcemia range from 1,000-2,000
azotemia, and hyperphosphatemia from the

IU/kg, once daily to once weekly. For
oliguric renal failure, which results from
dihydrotachysterol, initial loading
calciwn oxalate crystal precipitation in the
dosages of 0.02-0.03 mg/kg/day are
renal tubules.

usually administered, with maintenance
dosages of 0.01-0.02 mg/kg given every

Treatment of Hypocalcemia

24-48 hr. For 1,25-dihydroxyvitamin D, a
daily dosage of 0.025-0.06 mcg/kg (25-60

The definitive treatment for hypocalcemia
ng/kg/day) is generally required. Because
is to eliminate the underlying cause.

the available capsule sizes (250 and

Supportive measures, including the

500 ng) are not well formulated for the
following, to restore normocalcemia can
small body size of most dogs and cats,
be administered pending the diagnosis.

and these capsules cannot be readily
divided, it may be desirable to contact a

Parenteral Calcium: Hypocalcemic
pharmacist who can reformulate these
tetany or convulsions are indications for the
products to a size that is appropriate for
immediate TV administration of lOOA, calciun1
the individual pet. With all vitamin D
gluconate (1-1.5 mUkg), which should be
preparations and dosage regimens, the
slowly infused throughout a 10-min period.

development of iatrogenic hypercalcemia

Close monitoring is mandatory; if bradycaris a common complication of treatment.

dia or shortening of the QT interval occurs,
the TV infusion should be slowed or
temporarily discontinued.

HYPOCALCEMIC DISORDERS OF

Once the life-threatening signs of

HORSES
hypocalcemia have been controlled,
calciwn can be added to the rv fluids and

Primary hypoparathyroidism is a rare but
administered as a slow continuous infusion well documented disorder in horses.

( eg, 10% calciwn gluconate, 2.5 mUkg

Affected horses have clinical signs
every 6-8 hr). The rate of calciwn
consistent with hypocalcemia (ataxia,
administration should be adjusted as
seizures, hyperexcitability, synchronous
necessary to maintain a normal serum
diaphragmatic flutter, tachycardia,
calcium concentration, and the infusion
tachypnea, muscle fasciculation, and
should be continued for as long as
ileus). As in other species, the diagnosis
necessary to prevent r�cwTence of
is based on the finding of low serum
hypocalcemia. Although this continuous
concentrations of calcium and PTH with
calciwn infusion will maintain normocalcehigh levels of phosphorus. As described mia, its effects are short-lived; hypocalceabove, treatment with intravenous and mia will recur within hours of stopping the
subsequently oral calcium combined with
infusion unless other treatment is given.

large doses of vitamin D should result in
the remission of clinical signs associated

Oral Calcium: Oral calciwn supplementawith hypoparathyroidism.

tion may be beneficial in some conditions

Sepsis is one of the most common causes

(eg, hypoparathyroidism, puerperal tetany).

of hypocalcemia in horses admitted to

The daily requirements are 1-4 g for dogs
veterinary hospitals. Total and ionized
and 0.5-1 g for cats. The daily dose of
hypocalcemia are common in horses with
calciwn should be based on the amount of
severe GI disease and sepsis. Hypocalcemia
elemental calciwn in the product, rather
with inappropriately low serum PTH
than on the weight of the calciwn salt.

concentrations also has been reported in
foals. The underlying cause of hypocalce

Vitamin 0: In some conditions,
mia in foals remains to be determined.

vitamin D supplementation is necessary

However, these foals may possibly have
to increase calcium absorption from the
some fom1 of hypoparathyroidism
intestines. There are three main
associated with sepsis.

THE ADRENAL GLANDS

573

THE ADRENAL GLANDS

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The adrenal glands of mammals are located
the spread of infection. Glucocorticoids
near the cranial pole of the kidneys. They
may impair the immunologic response at
consist of two distinct parts, the outer
any stage, from the initial interaction and
cortex and inner medulla, that differ in
processing of antigens by cells of the
morphology, function, and origin.

reticuloendothelial system, through the
induction and proliferation of inununo

ADRENAL CORTEX
competent lymphocytes and subsequent
antibody production. Inhibition of a number

The adrenal cortex is subdivided into
of lymphocyte functions forms pazt of the
three layers, or zones, although the
basis for inununosuppression.

demarcation between zones often is

Glucocorticoids may have a profound
indistinct. The zona glomerulosa, the outer
negative effect on wound healing. High
zone, is responsible for the secretion of
therapeutic doses of adrenal corticosteroids
mineralocorticoid hormones. The zona
or the syndrome of hyperadrenoc01ticism
fasciculata, the middle zone, comprises
may cause wound dehiscence after surgery.

-700,1, of the cortex and is composed of cells

The inhibition offibroblast proliferation and
that contain abundant cytoplasmic lipid and
collagen synthesis leads to a decrease in
the glucocorticoid hormones. The zona
scar tissue fom1ation.

reticularis, the inner zone, is responsible

Progesterone, estrogens, and androgens
for the secretion of sex steroids.

are adrenal sex hormones. Excess secretion

Mineralocorticoids, of which the most
may be associated with a neoplasm of the
potent naturally occurring one is aldosterzona reticularis. The maztifestation of one, are adrenal steroids that have their
virilism, precocious sexual development, or
principal effects on ion transport by
feminization depends on which steroid is
epithelial cells, resulting in a loss of
secreted in excess, sex of the individual, and
potassium and retention of sodium. Sweat
age of onset. In addition, a syndrome termed
glands and the electrolyte "pumps" in
atypical hyperadrenocorticism has been
epithelial cells of the renal tubule respond
reported in association with excessive
similarly. In the distal convoluted tubule of
production of adrenal sex steroids. The
the mammalian nephron, a cation-exchange symptoms mirror those of Cushing mechanism resorbs sodium from the
syndrome (seep 543), despite normal or
glomerular filtrate and secretes potassium
low levels of cortisol concentrations after
into the lumen. These reactions are
provocative testing. Dogs with thls synaccelerated by mineralocorticoids and drome have increased concentrations of
proceed more slowly in their absence. A
one of several adrenal steroids, which lead
lack of secretion of mineralocorticoids
to the clinical signs. Treatment options are

(Addison disease) may result in a lethal
sinillar to those used in the management of
retention of potassium and loss of sodium.

Cushing syndrome.

Cortisol and lesser amounts of corticosterone are the most important glucocorticoid hormones secreted by the adrenal HYPERADRENOCORTICISM
gland in many species. In general, the
actions of glucocorticoids on carbohydrate,

(Cushing syndrome)

protein, and lipid metabolism result in

Hyperadrenocorticism may be the most
sparing of glucose and a tendency to result
frequent endocrinopathy in adult to aged
in hyperglycemia and increased glucose
dogs but is infrequent in other domestic
production. In addition, they decrease
animals. The clinical signs and biochemilipogenesis and increase lipolysis in adipose cal abnormalities result primarily from tissue, which results in release of glycerol
chronic excess production of cortisol.

and free fatty acids.

Increased cortisol levels in dogs may result

Glucocorticoids also suppress inflammafrom one of several mechanisms. The most tory and immunologic responses, thereby
common is an adenoma or hyperplasia
attenuating associated tissue destruction
of the adrenocorticotropic hormone
and fibroplasia. However, high levels of

(ACTH)-containing cells of the pituitary
glucocorticoids reduce resistance to
gland (pars distalis or pars intermedia),
bacteria, viruses, and fungi, which favors
which results in bilateral adrenal cortical

574

THE ADRENAL GLANDS
hypertrophy and hyperplasia. This form
excretion by the kidneys is reduced and
of the disease is referred to as pituitaryresults in a progressive increase in serum dependent hyperadrenocorticism
potassium levels. Hyponatremia and

(Cushing disease) and is seen in -90% of
hypochloremia result from renal tubular
cases. Functional adrenal twnors, a far
loss. Severe hyperkalemia may result in
less frequent cause of hyperadrenocortibradycai·dia and an irregular heart rate with VetBooks.ir
cism in dogs, may secrete cortisol or sex
changes in the ECG. Some dogs develop a
steroids, resulting in a variety of clinical
pronounced bradycardia (heatt rate s50
signs. Many of the clinical signs and
bpm) that predisposes to weakness or circubiochemical abnormalities seen with latory collapse after mininlal exertion.

naturally occurring hyperadrenocorti

Although the development of clinical
cism can be induced by longterm, daily
signs is often unnoticed, acute circulatory
administration of large doses of corticocollapse and evidence of renal failure steroids. Dogs develop a spectrum of
frequently occur. A progressive decrease in
clinical signs and laboratory abnormalities
blood volume contributes to hypotension,
as a result of the combined gluconeoweakness, and microcardia. Increased genic, lipolytic, protein catabolic, and
excretion of water by the kidneys, because
anti-inflammatory effects of the glucocorof decreased reabsorption of sodium and ticoid hormones on many organ systems.

chloride, results in progressive dehydration

The disease is insidious and slowly
and hemoconcentration. Emesis, diar-
progressive. (For discussion of the clinical
rhea, and anorexia are conm1on and
signs, laboratory abnormalities, diagnosis,
contribute to the animal's deterioration.

and treatment of hyperadrenocorticism,

Weight loss is frequently severe. Sinular
seep 543.)

clinical signs are seen in cats with
hypoadrenocorticism.

HYPOADRENOCORTICISM

Decreased production of glucocorticoids
results in several characteristic functional

(Addison disease)

disturbances. Decreased gluconeogenesis

A deficiency in adrenocortical hormones is
and increased sensitivity to insulin
seen most commonly in young to middlecontribute to the development of moderate aged dogs and occasionally in horses. The
hypoglycemia. In some dogs, hyperpigmendisease may be familial in Standard Poodles, tation of the skin is seen because of the lack

West Highland White Terriers, Great Danes,
of negative feedback on the pituitary gland

Bearded Collies, Portuguese Water Dogs,
and increased ACTH release. Atypical
and a vatiety of other breeds. The cause of

Addison disease has been reported in dogs
primary adrenocortical failure usually is
and is associated with hypocortisolemia
unknown, although most cases probably
witl1 normal electrolytes. Clinical signs are
result from an autoinunlll}e process. Other
similar to those seen in dogs with both
causes include destruction of the adrenal
glucocorticoid and mineralocorticoid
gland by granulomatous disease, metastatic
insufficiency.

tumor, hemorrhage, infarction, adrenolytic

Lesions: The most conm1on abnom1ality
agents ( mitotane ), or adrenal enzyme
in dogs is bilateral idiopathic adrenocortical
inhibitors (trilostane).

•
atrophy, in which all layers of the cortex are
markedly reduced in thickness. The adrenal

Clinical Findings: Many of the funccortex is reduced to one-tenth or less of its tional disturbances of chronic adrenal
normal thickness and consists primarily of
insufficiency are not highly speciiic;
the adrenal capsule. The adrenal medulla is
they include recurrent episodes of gastrorelatively more prominent and, with the enteritis, a slowly progressive loss of
capsule, makes up the bulk of the remaining
body condition, and failure to respond
adrenal glands.

appropriately to stress. Although

All three zones of the adrenal cortex are
hypoadrenocorticism is seen in dogs
involved, including the zona glomerulosa,
of any breed, sex, or age, idiopathic
which is not under ACTH control; however,
adrenocortical insufficiency is most
no obvious pituitary lesions have been seen
common in young female adult dogs.

in dogs with idiopathic adrenal c01tical

This may be related to its suspected
atrophy.

immune-mediated pathogenesis.

A destructive pituitary lesion that

A reduction in secretion of aldosterone,
decreases ACTH secretion is characterized
the principal mineralocorticoid, results
by severe atrophy of the inner two cortical
in marked alterations of serum levels of
zones of U1e adrenal gland; the zona
potassium, sodiun1, and chloride. Potassium
glomerulosa remains intact.

THE ADRENAL GLANDS

575

Diagnosis: A preswnptive diagnosis
function, and glucose should be monitored
is based on the history and supportive
regularly to assess response to tllerapy.

( although not specific) laboratory abno1�

In cases of severe, nonresponsive
malities, including hyponatremia, hyperhyperkalemia, l()OA, glucose in 0.9% saline kalemia, a sodiwn:potassiurn ratio of <25:1,
can be given for 30-60 min to increase
azotemia, mild acidosis, and a norrnocytic,
potassiwn movement into tlle cells. Regular

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normochromic anemia. Severe GI blood loss insulin (0.25---1 U/kg) administered IM will has also been reported. Occasionally, mild
enhance glucose and potassiwn uptake, but
hypoglycemia is present. The hyperkalemia

1()% glucose (20 mL per unit of insulin)

results in ECG changes: an elevation
should be administered IV concmTently to

( spiking) of the T wave, a flattening
avoid hypoglycemia.

or absence of the P wave, a prolonged

For longterm maintenance therapy, the

PR interval, and a widening of the QRS
mineralocorticoid desoxycorticosterone
complex. Ventlicular fibrillation or asystole
pivalat.e (DOCP) is administered at 2.2 mg/kg,
may occur with potassium levels > 11 mEq/1. IM or SC, every 25---28 days. Electrolytes Differential diagnoses include primary GI
should be measured at 3 and 4 wk after
disease (especially whipworm infection),
the first few injections to detemtine the
renal failure, acute pancreatitis, and toxin
duration of action. Alternatively, fludrocortiingestion. For definitive diagnosis, evaluation sone acetate is administered PO at 10-30
of adrenal function is required. After
mcg/kg/day. Serum electrolytes should be
obtaining a baseline blood sample, ACTH
monitored weekly until tlle proper dose is

(gel or synthetic) is administered. Gel
detemlined. Some dogs ( especially dogs on
preparations are administered IM, and a

DOCP) also require daily oral glucocorticoid
second blood sample is obtained 2 hr later.

therapy to adequately control clinical signs.

Synthetic preparations are administered IM Replacement doses ofprednisone (0.2--0.4
or IV with a second blood san1ple 1 hr later.

mg/kg/day) are required in -50% of dogs.

Baseline (resting) cortisol concentrations

Additional glucocorticoid supplementation

>2.5 mcg/dL effectively exclude the diagnosis may be required (2-5 times maintenance) ofhypoadrenocorticism, whereas values <2.5 during tinles of illness or stress. Dogs with mcg/dL require the use of ACTH stimulation
atypical Addison disease require only
testing to confirm the diagnosis. Affected
replacement doses ofprednisone, altllough
dogs have low baseline cortisol levels, and
it is recommended that electrolytes be
there is little response to ACTH administramonitored every 3 mo for tlle first year after tion in classic and atypical cases. This test
diagnosis. Dogs with chronic hypoadrenoco1�
can be completed in most animals bef ore
ticism should be reexantined every 3-6 mo.

replacement honnone therapy is started.

Treatlnent of horses with hypoadrenocorticism is sinillar-aggressive replacement of Treatment: An adrenal crisis is an acute
fluids, steroids, and glucose if needed in an
medical emergency. An IV catheter should
adrenal crisis. Supportive tllerapy and resf
be inserted, and an infusion of 0.9"A, saline
are indicated in cases of chronic Addison
begun. lf the dog is hypoglycemic, the saline
disease.

should include 2.5%-5% dextrose. The hypovolemia is corrected rapidly by adrniniste1�

ADRENAL MEDULLA
ing 0.9"A, saline (60-70 ml/kg over the first

1-2 hr). Urine output should be assessed to

The adrenal medulla, although apparently
detennine whether the dog is becoming
not essential to life, plays an in1portant role
anuric. Fluids should be continued, at a rate
in response to stress or hypoglycemia.. It
appropriate to match ongoing losses, until
secretes epinephrine and norepinephrine,
the clinical signs and laboratory abnormaliwhich increase cardiac output, blood ties have resolved.

pressure, and blood glucose, and decrease

Prednisolone sodiun1 succinate (22-30

GI activity.

mg/kg) or dexamethasone sodiun1 phosphate

Pheochromocytomas (see below) may

(0.2-1 mg/kg) may be used in tlle initial
develop in domestic animals, most often in
management of shock. Dexan1ethasone will
cattle and dogs. These secrete epinephrine,
not interfere with cortisol measurements
norepinephrine, or both. Clinical signs a.re
clwing tlle ACTH stimulation test. Preclnisooften absent, and tumors may be incidental lone or prednisone should be given at 1 mg/
findings during evaluation for other
kg, bid, for the first few days oftllerapy and
conditions or at necropsy.

tl1en at 0.25-0.5 mg/kg/day. Mineralocorti

Other adrenal tun10rs, such as neuroblascoid replacement tl1erapy (see below) is also tomas and ganglioneuromas, may a.iise in
begun to help with electrolyte imbalances
the chromaffin cells of tlle sympathetic
and hypovolemia. Electrolytes, renal
ne1vous system.

576

NEUROENDOCRINE TISSUE TUMORS

NEUROENDOCRINE TISSUE TUMORS

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Neuroendocrine cells are characterized by

For discussions of insulinoma and
their ability to produce and secrete a
gastrinoma, see p 582 and p 583.

neuromodulator, transmitter, or hormone.

In addition, these cells contain dense core

Carcinoids: Carcinoids are a heterolosecretory granules, the storage site for the gous group of NETs that occur in various
secreted product(s). New·oendocrine cells
regions of the GI tract. In dogs and cats,
am capable of releasing this product in a
carcinoids have been reported to occur
regulated manner by classic exocytosis.

in the stomach. The most common sign

N euroendocrine cells differ from classic
reported in affected anin1als is chronic
neurons in that they lack axons and
vomiting. In people (but not yet docusynapses. Certain molecules, particularly mented in companion animals), carcinoids
those of the granin family ( eg, chromograserve as a source of serotonin or histamine.

nin) are synthesized and stored in neuroen

Excessive release of these transmitters can
docrine cells and serve as immunohistologic cause a syndrome of flushing, hypotension, markers.

wheezing, and diarrhea.

Previously, neuroendoc1ine cells were
classified as antine precursor uptake and
decarboxylation (APUD) cells and were

Glucagonoma: Glucagonomas have been
believed to be solely derived from
found in a small number of dogs. Interestneuroectoderm. However, more recent ingly, affected animals show cutaneous
evidence supports a more diverse embryolesions characterized by a superficial logic origin.

necrolytic dermatitis affecting mucocutane

Tumors that arise from this cell type
ous junctions, footpads, elbows, or the
comprise a fanl.i.ly of neuroendocrine twnors, abdomen.

or NETs. Because of the diffuse distribution
of cells, particularly within the GI tract, NETs TUMORS OF THE ADRENAL
are found in a wide variety oflocations.

MEDULLA

Overall, NETs are rare twnors in people and
animals. Some NETs oversecrete their

Pheochromocytomas: Pheochronormal product, and the excessive levels mocytomas occur in domestic species,
result in the observed signs. Other NETs are
including dogs and cats. Incidental masses
nonfunctional, and clinical signs instead
in the area of the adrenal glands are being
result from physical forces associated with
discovered with greater frequency
expansion and/or metastasis.

because of the increased use of abdominal

Examples of NETs include carcinoids,
ultrasound and other imaging techniques.

gastroenterohepatic tumors (gastrinoma,

Pheochromocytoma, although rare,
insulinoma, glucagonoma), pheochromocyshould be a differential diagnosis toma of the adrenal gland, medullary
whenever such a mass is identified.

carcinoma of the thyroid gland, some

Pheochromocytomas arise from the
pituitary tumors, small-cell lung cancer,
adrenal medullary chromaffin cells that
multiple endoc1ine neoplasia (MEN types 1
normally synthesize and secrete the
and 2), and twnors of the chemoreceptor
catecholamines epinephrine and
organs. Interestingly, devil facial tumor
norepinephrine. These tumors have been
disease, a devastating transmissible cancer
identified more often in dogs than in cats,
affecting Tasmanian devils ( see p 2044 ),
usually affect only one gland, and tend to
appears to be an NET. NETs are identified
occur in older animals. They are often
and classified by their microscopic appearlocally invasive (may result in thrombus ance, the immunohistologic identi-formation in the adjacent vena cava) and
fication of classic new·oendocrine cell
metastasize in -25% of cases. Diagnosis
markers (such as chromogranin A), and
of pheochromocytoma is challenging.

staining for their characteristic transmitter

Clinical signs are nonspecific and may
or hormonal product.

appear sporadically, possibly related
to periodic or intermittent release of
lnsulinoma and Gastrinoma: Insucatecholantines. In addition, signs may linoma (functional islet cell twnor) is the
vary depending on which catecholan1ine
most common NET in domestic species.

predominates. Signs reported in most dogs

NEUROENDOCRINE TISSUE TUMORS

577
include weight loss, anorexia, depression,
guishing these tun1ors from other thyroid
weakness, and occasional collapse. Dyspcarcinomas is challenging with light nea and tachycardia may be seen, and
microscopy alone, and confinnation
hypertension is common; indirect blood
requires immunohistologic staining. These
pressure measurement can help establish
tumors are usually well encapsulated and
the diagnosis. Imaging, such as ultrado not show the tendency for metastasis VetBooks.ir
sonography or CT scans, is very useful in
other thyroid carcinomas exhibit. Overseconfirmation of a suspected adrenal mass.

cretion of calcitonin has not been clearly

Although surgical removal is the treatment documented in affected animals. Perhaps of choice, animals with pheochromocyrelated to excessive release of prostaglantoma present an anesthetic risk secondary dins or serotonin, diarrhea is a common
to the cardiovascular effects of the
clinical sign in dogs with C-cell tumors of
catecholamines. Surgery is additionally
the thyroid.

complicated by the tendency toward local
invasion of these tumors and their
proximity to large vessels.

Adenomas: C-cell adenomas appear in
one or both thyroid lobes as discrete, single

Adrenal Medullary Hyperplasia:

or multiple, gray to tan nodules. Adenomas

Diffuse or nodular adrenal medullary
are smaller ( ---1---3 cm in diameter) than
hyperplasia appears to precede the
carcinomas and are separated from the
development of pheochromocytomas in
thyroid parenchyma by a thin, fibrous
bulls with C-cell tumors of the thyroid
connective tissue capsule. The acljacent
gland. This diffuse proliferation of
thyroid is compressed but not invaded by
chromaffin cells is nonencapsulated but
the tumor. In horses, C-cell adenomas may
compresses the surrounding adrenal cortex.

result in a palpable enlargement in the

In bulls with prominent diffuse medullary
anterior cervical region. Larger C-cell
hyperplasia, there are often a few small foci
adenomas incorporate most of the thyroid
of intense nodular proliferation of
lobe, but a rim of dark brown-red thyroid
medullary cells.

often is present on one side.

THYROID C-CELL TUMORS

Carcinomas: Thyroid C-cell carcinomas
cause extensive multinodular enlargements

Tumors derived from C-cells (parafollicuof one or both thyroid lobes and may lar, ultimobranchial cells) of the thyroid
incorporate the entire thyroid gland. lf
gland are most common in adult to aged
present, metastases in anterior cervical
bulls and horses and in certain strains of
lymph nodes usually are large and have
laboratory rats. A high percentage of aged
areas of necrosis and hemorrhage.

bulls has been reported to develop C-cell

Pulmonary metastases are infrequent and·
tumors (<!300Ai) or hyperplasia of C-cells and appear as discrete tan nodules throughout ultimobranchial derivatives (<!l5%---200Ai).

all lobes of the lung.

These have not been seen in cows fed

The chronic stimulation of C-cells by
similar diets. The incidence in bulls
longterm dietary intake of excess calcium
increases with advancing age and is often
may be related to the high incidence of
associated with development of increased
these tumors in bulls; adult bulls frequently
vertebral density. Multiple endocrine
were fed diets with 3.5---6 tin1es the amount
tumors, especially bilateral pheochromocyof calcium normally reconunended for tomas and occasionally pituitary adenomaintenance, and incidence of the tumors mas, are detected coincidentally in bulls
declined significantly when calcium intake
with C-cell tumors. A high frequency
was reduced.

of thyroid C-cell tumors and pheochromo

Syndromes associated with abnormalities
cytomas has been reported in a family of
in the secretion of calcitonin are recognized

Guernsey bulls, which suggests an
much less frequently than disorders
autosomal dominant pattern of inheriinvolving parathyroid hormone (PTH).

tance. A diffuse or nodular hyperplasia of

Hypersecretion of calcitonin has been
secretory cells in the adrenal medulla often
repo1ted in people, bulls, and laboratory
precedes the development of pheochromorats with medullary ( ulti.rnobranchial) cytoma.

thyroid neoplasms derived from C-cells.

In dogs, C-cell tumors of the thyroid

Osteosclerotic changes have been reported
occur as a small percentage of all thyroid
in bulls with Utis syndrome, but the
tun1ors (estimates range from O.lo/o-12%),
relationship of longterm excess calcitonin
but the incidence may be higher. Distin-
secretion to the pathogenesis of the skeletal

578

NEUROENDOCRINE TISSUE TUMORS
lesions and their occurrence in other
are infrequent in dogs with amtic body
species is w1clear.

carcinomas. Nonetheless, the local and

In dogs, the histologic grading of thyroid
physiologic effects are important,
carcinoma has been important in prognoincluding those of adenomas.

sis, although histologic type has not. Of

Aortic body tumors in animals are not
greater importance is the volume of tumor
functional (ie, they do not secrete excess

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and its relation to the potential for
hom1one into the circulation) but, as
metastasis; also, the more deeply fixed the
space-occupying lesions, may result in
tumor is to underlying structures, the less
various functional disturbances. These
likely surgical resection will be complete.

include manifestations of cardiac

Surgery is the primary therapy, but some
decompensation due to pressure on the
form of adjuvant therapy is reasonable
at1ia or vena cava ( or both) associated with
because of the potential for metastatic
larger aortic body adenomas and carcinospread and residual nonresectable tissue.

mas. Aortic body tumors tend to be more

A combination of radiotherapy and
benign than carotid body twnors. They
chemotherapy would be ideal in theory, and
grow slowly by expansion and exert
there is increasing interest in such combined
pressure on the vena cava and atria. Aortic
therapy. For the rather rare functional
body carcinomas may invade locally into
thyroid carcinoma in dogs, treatment with
the atria, pericardium, and adjacent large,

131 I would be a reasonable choice.

thin-walled vessels.

Carotid body tumors arise near the

CHEMORECEPTOR ORGANS
bifurcation of the common carotid artery,
usually as a unilateral, slow-growing

Chemoreceptor organs are sensitive
mass. Adenomas are usually 1-4 cm in
barometers of changes in the carbon
diameter. The bifurcation of the carotid
dioxide and oxygen content and pH of the
artery is incorporated in the mass, and
blood and aid in the regulation of respiratumor cells are firmly adherent to the tion and circulation. Although chemoretunica adventitia. Complete excision or ceptor tissue appears to be widely
biopsy often is difficult because of the
distributed in the body, tumors (chemodechigh degree of vascularity and intimate tomas) develop principally in the aortic
relationship with major arterial trunks

(more frequent in animals) and carotid
in the neck.

(more frequent in people) bodies. These

Malignant carotid body tumors are
tumors are found primarily in dogs and
larger and more coarsely multinodular
rarely in cats and cattle. Brachycephalic
than adenomas. Although carcinomas
breeds of dogs, such as the Boxer and
appear to be encapsulated, tumor cells

Boston Terrier, are predisposed to tumors
invade the capsule and penetrate into the
of the aortic and carotid bodies.

walls of adjacent vessels and lymphatics.

Aortic body tumors appear most

The external jugular vein and several
frequently as single masses or as multiple
cranial nerves may be incorporated by the
nodules within the pericardia! sac near
neoplasm. Metastases of carotid body
the base of the heart. They vary conside r tumors occur in -30% of cases and have ably i n size (0.5-12.5 cm), with earcinobeen found in the lung, bronchial and mas generally larger than adenomas.

mediastinal lymph nodes, liver, pancreas,

Solitary, small adenomas either are
and kidneys. Multicentric neoplastic
attached to the adventitia of the pulmotransformation of chemoreceptor tissue nary artery and ascending aorta or are
occw-s frequently in brachycephalic
embedded in the adipose connective
breeds of dogs.

tissue between these major vascular

The histologic characteristics of
trunks. Larger adenomas may indent the
chemodectomas are essentially sinillar
atria or displace the trachea, are
whether derived from the carotid or ao1tic
multilobular, and partially surround the
body.

major arterial trunks at the base of the

Although the etiology of carotid and
heart.

aortic body tumors is unknown, it has been
ln dogs, malignant aortic body tumors
suggested that a genetic predisposition
occw- less frequently than adenomas.

aggravated by chronic hypoxia may

Carcinomas may infiltrate the wall of
account for the higher risk in certain
the puln1onary artery to form papillary
brachycephalic breeds. Carotid bodies of
projections into the lumen or invade
several mammalian species, including
through the wall into the lumen of the atria.

dogs, have tmdergone hyperplasia when

Altl10ugh tumor cells often invade blood
subjected to chronic hypoxia by living in
vessels, metastases to the lungs and liver
a high-altitude environment.

THE PANCREAS

579

THE PANCREAS

The endocrine function of the pancreas is
conditions. Pancreatic � cells are able to

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perfonned by small groups of cells, the
respond to a specific physiologic stimulus
islets of Langerhans, that are completely
with release of stored hormone in a
surrounded by acinar (exocrine) cells that
modulated fashion, rather than releasing
produce digestive enzymes. The endocrine
all of the stored hormone at once.

and exocrine portions of the pancreas are

Insulin affects, either directly or
closely related during development, and
indirectly, the function of every organ in the
evidence suggests that islet, acinar, and
body. Tissues that are especially responsive
ductal cells arise from a common multipoto insulin include skeletal and cardiac tential precursor cell.

muscle, adipose tissue, fibroblasts, liver,

Pancreatic islets contain et, �. and o

WBCs, mammary glands, caiiilage, bone,
cells, each of which synthesize a unique
skin, ao1ta, pituitary gland, and peripheral
polypeptide hom10ne. � cells account for
nerves. The main function of insulin is to

600/o---700/o of the islet-cell population and
stimulate anabolic reactions involving
secrete insulin, et cells secrete glucagon,
carbohydrates, fats, proteins, and nucleic
and o cells secrete somatostatin.

acids. Liver, adipose cells, and muscle are

The pancreatic islets function as discrete
three principal target sites for insulin.

microendocrine organs. They are distrib

Insulin catalyzes tl1e fonnation of macrouted throughout the pancreas with a molecules used in cell structure and energy
characteristic pattern of cellular interrelastores, and it regulates many cell functions.

tionships to assure an appropriate balance

In general, insulin increases the transfer of
of hormones. Afferent vessels and nerves
glucose and certain other monosaccharides,
enter the islet in the peripheral tricellular
some amino acids and fatty acids, and
region. The close anatomic relationship
potassium and magnesium ions across the
of et, �. and o cells in this heterogeneous
plasma membrane of target cells. It also
co1iical region allow it to function as a local
decreases the rate of lipolysis, proteolysis,
glucose sensor, pennitting a coordinated
ketogenesis, and gluconeogenesis.

output of insulin and glucagon in response

Glucagon is secreted in response to a
to fluctuations in blood glucose. Specialized
reduction in blood glucose. It promotes
tight junctions between membranes of
mobilization of stores of energy-yielding
adjacent endocrine cells tend to partition
nutrients by increasing glycogenolysis,
the intercellular space and may pennit
gluconeogenesi.s, and lipolysi.s. At physiosomatostatin to exert a direct local logic concentrations, glucagon increases

(paracrine) inhibitory effect on glucagon
both hepatic glycogenolysis and gluconeoand insulin release.

genesis, thereby increasing blood glucose.

Insulin is formed initially as a single

Insulin and glucagon act in concert to
polypeptide chain of81-S6 amino acid
maintain the concentration of glucose in
residues. This prohonnone (proi.nsulin)

extracellular fluids within relatively narrow
contains the A and B chains of the insulin
limits. A glucose sensor in tl1e pancreatic
molecule, plus a connecting peptide.

islets controls the relative ainounts of

Proinsulin is converted enzymatically to
insulin and glucagon secreted. Glucagon
insulin before storage in membrane-limited
controls glucose release from the liver into
secretory granules.

the extracellular space, and insulin controls

The major physiologic stimulus for the
glucose transport from the extracellular
release of insulin from � cells is an increase
space into insulin-sensitive tissues such as
in the concentration of glucose in the
fat, muscle, and liver.

extracellular fluid. Specific glucoreceptors
that bind with glucose exist on the plasma
membrane of� cells. An appropriate level of DIABETES MELLITUS
extracellular calcium is required for insulin
secretion. Other sugars (fructose, mannose,

Diabetes mellitus is a chronic disorder of
ribose), amino acids Oeucine, arginine),
carbohydrate metabolism due to relative or
hormones (glucagon, secretin), drugs
absolute insulin deficiency. Most cases of

(sulfonylurea, theophylline), short-chain
spontaneous diabetes occur in middle-aged
fatty acids, and ketone bodies may also
dogs and middle-aged to older cats. In dogs,
stimulate insulin secretion under certain
females are affected twice as often as males,

580

THE PANCREAS
and incidence appears to be increased in

Infection with certain viruses in people
certain small breeds such as Miniature
may cause selective islet damage or

Poodles, Dachshunds, Schnauzers, Cairn
pancreatitis and has been suggested to be

Teniers, and Beagles, but any breed can be
responsible for certain cases of rapidly
affected. In one study, obese male cats were
developing diabetes mellitus. This has yet
more commonly affected than females; no
to be documented in dogs or cats. The

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breed predilection is seen in cats.

selective degeneration and necrosis of

13 cells is accompanied by infiltration of the

Etiology and Pathogenesis: The
islets by lymphocytes and macrophages.

pathogenic mechanisms responsible for

Stress, obesity, and administration of
decreased insulin production and secretion corticosteroids or progestogens may are multiple, but usually they are related to
increase the severity of clinical signs.

destruction of islet cells, secondary to

Complete expression of the complex
either immune destruction or severe
metabolic disturbances in diabetes mellitus
pancreatitis (dogs) or amyloidosis (cats).

appears to be the result of a bihormonal

Chronic relapsing pancreatitis with
abnormality. Although a relative or absolute
progressive loss of both exocrine and endodeficiency of insulin action in response to a crine cells and their replacement by fibrous rising extracellular glucose concentration connective tissue results in diabetes
has long been recognized as the major
mellitus. The pancreas becomes firm and
hormonal abnormality, the importance of an
multinodular and often contains scattered
absolute or relative increase of glucagon
areas of hemorrhage and necrosis. Later in
secretion has been appreciated more
the course of disease, a thin, fibrous band
recently. Hyperglucagonemia in diabetes
of tissue near the duodenum and stomach
may be the result of increased secretion of
may be all that remains of the pancreas.

pancreatic glucagon, enteroglucagon, or

In other cases, the numbers of 13 cells are
botl1. Increased glucagon appears to
decreased, and the cells become vacucontribute to development of severe olated; in chronic cases, the islets are
hyperglycemia by mobilizing hepatic stores
difficult to find. Insulin resistance and
of glucose and to development of ketoacidosecondary diabetes mellitus are also seen sis by increasing the oxidation of fatty acids
in many dogs with spontaneous hyperin the liver.

adrenocorticism and after chronic
administration of glucocorticoids or

Clinical Findings: The onset of diabetes
progestins. Pregnancy and diestrus also
is often insidious, and the clinical course
can predispose to diabetes mellitus. In
chronic. Common signs in dogs include
dogs, but not cats, progesterone leads to
polydipsia, polyuria, polyphagia with weight
release of growth hormone from manunary loss, bilateral cataracts, and weakness. The tissue, resulting in hyperglycemia and
disturbances in water metabolism develop
insulin resistance. Obesity also predisposes prin1arily because of an osmotic diuresis.

to insulin resistance in both dogs and cats.

The renal threshold for glucose is -180

Cats with diabetes mellitus usually have
mg/dL in dogs and -280 mg/dL in cats.

specific degenerative lesions localized

Diabetic anin1als have decreased
selectively in the islets of Langerhans,
resistance to bacterial and fungal
whereas the remainder of the pancreas
infections and often develop chronic or
appears to be normal. The selective
recurrent infections such as cystitis,
deposition of amyloid in islets, with
prostatitis, bronchopneumonia, and derdegenerative changes in 13 cells, is the most matitis. This increased susceptibility to
common pancreatic lesion in many cats
infection may be related in part to impaired
with diabetes. The an1yloid appears to arise
chemotactic, phagocytic, and antimicrobial
from islet-associated polypeptide (IAPP),
activity associated with decreased
which is secreted together with insulin from neutrophil function. Radiographic the 13 cells. Cats are unable to process IAPP
evidence of emphysematous cystitis (rare)

normally, which leads to excessive
due to infections with glucose-fermenting
accumulation and conversion into an1yloid.

organisms (such as Proteus sp, Aerobacter As cats age, a greater percentage of their
aerogenes, and Escherichia coli), which islets contain an1yloid. Cats with diabetes
results in gas formation in the wall and
have a greater percentage of their islets
lumen of the bladder, is suggestive of diabeaffected with larger amow1ts of amyloid tes mellitus. Emphysema also may develop
than age-matched cats without diabetes.

in the wall of the gallbladder in diabetic

The amyloid or IAPP ( or both) lead to
dogs.

physical disruption of the 13 cell and insulin

Hepatomegaly due to lipid accumulation
resistance, resulting in diabetes.

is common in diabetic dogs and cats. The

THE PANCREAS

581
fatty liver results from increased fat mobi

In dogs with poor glycemic control on
lization from adipose tissue. Individual liver

NPH or lente insulin, use of the basal
cells are greatly enlarged by the accumulainsulin cletemir should be considered.

tion of multiple droplets of neutral lipid. In

Because of its potency, the starting dosage
cats, hepatic lipidosis may occur in conof detemir is 0.1 U/kg, bid, with reassessjunction with diabetes mellitus.

ment of clinical signs and glycemic control

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Cataracts develop frequently in dogs
in 1 wk.

(not cats) with poorly controlled diabetes

It is usually preferable to have blood
mellitus. The lenticular opacities appear
glucose testing perfonned at home to avoid
initially along the suture lines of lens fibers
changes in the pet's routine and the stress of
and are stellate ("asteroid") in shape.

in-hospital testing. Studies in both dogs and

Cataract formation in dogs is related to the
cats have shown that at-home monitoring
unique sorbitol pathway by which glucose
improves glycemic control and increases
is metabolized in the lens, which leads to
the likelihood of obtaining remission in
edema of the lens and disruption of nom1al
diabetic cats. In cats, high-protein diets
light transmission. Although the same
along with insulin therapy are initiated,
sorbitol pathway seems to be present in
with reevaluation in 5-7 days. In newly
cats, the development of cataracts is rare.

diagnosed cats, insulin glargine is the

Other extrapancreatic lesions associated
insulin of choice. Glargine is a long-acting
with diabetes mellitus in people, such as
basal insulin. Used in cor\junction with
nephropathy, retinopathy, and micro- and
high-protein, low-carbohydrate diets, it is
macrovascula.r angiopathy, are rare in dogs
associated with remission of diabetes and
and cats.

discontinuation of insulin therapy in

80%-90"Ai of cases within the first 3-4 mo of

Diagnosis: A diagnosis of diabetes
treatment. NPH, lente, or PZI insulins may
mellitus is based on persistent fasting
also be used in cats, with Stal.ting dosages
hyperglycemia and glycosuria. The normal
ranging from 1 to 3 units, bid. However,
fasting value for blood glucose in dogs and
these insulins a.re not associated with high
cats is 75-120 mg/dL. In cats, stress-induced
rates of diabetic remission.

hyperglycemia is a frequent problem, and

The use of oral hypoglycemic agents
multiple blood and urine samples may be

(glipizide) has been evaluated in diabetic
required to confinn the diagnosis. Measurecats. Glipizide is a sulfonylurea that ment of serum fructosan1ine can assist
stimulates the release of insulin from
in differentiating between stress-induced
functional 13 cells. Glipizide should not be
hyperglycemia and diabetes mellitus. In
used in thin or ketonuric cats when absolute
cases of stress-induced hyperglycemia, the
insulin deficiency is likely and exogenous
fructosan1ine oncentrations are normal. In
insulin administration is required. Glipizide
all cases, a search should be made for drugs
is administered at an initial dose of2.5 mg,
or diseases that predispose to diabetes.

bid, PO, in cor\junction with dietary
management. Clinical response is seen at

Treatment: Longterm success depends on 3-4 wk. Short-tenn success is seen in 50"Ai of the understanding and cooperation of the
treated cats, with longterm success rates
owner. Treatment involves a combination of

(> 1 yr) of --15%. Alternatively, glirnepiride
weight reduction, diet, insulin, and possibly
and glyburide ( other sulfonylureas) may be
oral hypoglycemics. Intact females should
administered to cats at 2 mg/day (glirnebe neutered. In cats, recent evidence has pi.ride) or 0.625 mg/day (glyburide).

supported the use of high-protein, low

Acarbose, an oral a-glucosidase inhibitor,
carbohydrate diets. In dogs, diets that are
has also been used in cats at a dose of
high in fiber and complex carbohydrates are

12.5-25 mg, bid-tid, in cor\junction with diet
preferred. Diet and weight reduction alone
and/or insulin to control hyperglycemia.

will not control the disease, so initial

Ketoacidosis is a serious complication of
therapy with insulin is required. Most dogs
diabetes mellitus and should be regarded as
require two doses of insulin a day. In
a medical emergency. Therapy includes
general, NPH or lente is the initial insulin of
correcting dehydration by administration
choice at a close of 0.5 U/kg, bid. With twice
of IV fluids, such as 0.9% NaCl or lactated
daily injections, two meals of equal calories

Ringer's solution; reducing hyperglycemia
are given at the time of insulin administraand ketosis by administration of crystalline tion. Diets high in simple sugars (semin1oist
zinc (regular) insulin; maintaining serum
foods) should be avoided. Clinical signs and
electrolyte levels, especially potassium,
serial blood glucose determinations are
through supplemental administration of
used to monitor therapy after initial
appropriate electrolyte solutions; and
stabilization at home for 5-7 days.

identifying and treating underlying and

582

THE PANCREAS
complicating diseases, such as acute
restlessness. Periodic seizures may occur,
pancreatitis or infections.

and episodes of collapse resembling

Numerous insulin regimens have been
syncope have also been reported.

used in treatment of ketoacidotic diabetes

Clinical signs are characteristically
mellitus. In the intermittent insulin
episodic and occur initially at widely
regimen, regular insulin at 0.2 U/kg, IM,
spaced intervals but become more

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is the initial dosage, followed by hourly
frequent and prolonged as the disease
administration ofO.l U/kg. Once the serum
progresses. Hypoglycemic attacks may
glucose is <250 mg/dL, the insulin is adminbe precipitated by physical exercise istered SC at 0.25-0.5 U/kg, every 4-6 hr,

(increased use of glucose) or fasting
with careful monitoring of the serum

( decreased availability of glucose), as well
glucose at 1- to 2-hr intervals. During
as by ingestion of food (stimulation of insuaggressive treatment with insulin, blood lin release). Adntinistration of glucose
glucose levels may fall rapidly, and the
rapidly alleviates the signs.

addition of 2.5%---5% dextrose to the IV

The predominance of clinical signs
fluids may be required.

relating to the CNS demonstrates the

When insulin therapy has been instiprimary dependence of the brain on the tuted, the blood glucose should be
metabolism of glucose for energy. When the
checked frequently until an adequate
brain is not supplied with glucose, cerebral
maintenance dose has been detemtined.

oxidation decreases and manifestations of

Once the animal is on maintenance therapy anoxia appear. Because clinical signs are and its condition is stable, it should be
compatible with p1imary disease of the
reassessed every 4-6 mo.

CNS, functional islet cell tumors may be
misdiagnosed as idiopathic epilepsy, brain

FUNCTIONAL ISLET CELL
tumors, or other organic neurologic disease.

TUMORS

Repeated episodes of prolonged and severe
hypoglycemia may result in irreversible

The most frequent pancreatic islet tumor
neuronal degeneration iliroughout the
is an islet cell carcinoma derived from
brain. Pem1anent neurologic disability
insulin-secreting 13 cells. These neoplasms
probably accounts for the terminal coma,
frequently are hormonally active and
unresponsiveness to glucose, and eventual
secrete excessive an1ounts of insulin,
death of some dogs.

which causes hypoglycemia. Endocrine

Lesions: lnsulinomas usually appear as
pancreatic tissue appears to be derived
single, yellow to dark red, spherical, small
from multipotential ductal epithelial cells,

(l-3 cm) nodules visible from the serosal
which differentiate into one of the se.veral
surface. They occur as single or occasionally
cell types present within the islets. Gastrin,
multiple nodules in the same or different
somatostatin, PaI\Creatic polypeptide, and
lobes of the pancreas. They are of similar
vasoactive intestinal peptide may also be
consistency to or slightly firmer than the
produced in excess in islet cell tumors.

surrounding pancreatic parenchyrna. A thin

[3-cell neoplasms of the pancreatic islets
layer of fibrous connective tissue separates

(insulinomas) are seen most frequently in
the neoplasm from the adjacent parendogs 5-12 yr old. They are conunon in chynia. Insulinomas frequently metastasize
ferrets and have also been less frequently
to regional lymph nodes or the liver ( or both)

reported in cats and in older cattle.

before diagnosis. True benign adenomas of
islet cells are rare.

Clinical Findings: The clinical signs seen
with insulinomas result from excessive

Diagnosis: A blood glucose detemtination
insulin secretion, which leads to an
should be done on all older dogs with a
increased rate of transfer of glucose from
history of periodic weakness, collapse, or
the extracellular fluid to body tissues and
seizures. Fasting hypoglycentia (s60 mg/dL)

thus to severe hypoglycentia. The clinical
in a middle-aged to older dog is strong
signs are a reflection of the hypoglycentia
support for an insulinoma. Serun1 insulin
and are not specific for hyperinsulinism
concentrations taken at the time of
associated with [3-cell neoplasms. Initial
hypoglycemia are normal to increased in
signs include poste1ior weakness, fatigue
animals with an insulinoma. Differential
after exercise, generalized muscular
diagnoses for hypoglycemia include
twitching and weakness, ataxia, mental
hypoadrenocorticism, hepatic failure,
confusion, and changes of temperament.

large extrapancreatic neoplasms, sepsis,

Dogs are easily agitated, and there are
polycythemia, insulin overdosage, and
intermittent periods of excitability and
laboratory error.

THE PANCREAS

583 .

Treatment: Although insulinomas are
secreting 13-cell neoplasms. The few docuusually solitary in dogs, the entire pancreas mented cases have had anorexia, hematemshould be examined carefully for multiple esis, intermittent diarrhea ( usually with
tLUnors. Complete excision of the ttunor
dark blood present), progressive weight
ameliorates the hypoglycemia and
loss, and dehydration. The prominent
associated neurologic signs, unless there
functional distLU·bances appear to result

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have been irreversible changes in the CNS.

from multiple ulcerations of the GI mucosa

If there are nonvisible metastases,
that develop from gastrin hypersecretion.

hypoglycemia may persist after surgery.

Even though the potential for malignancy

Lesions: Animals studied with the
of insulinomas is high, many dogs live > 1 yr

Zollinge1�Ellison-like syndrome have had
with acceptable quality of life if all visible
single or multiple tumors of varying size in
tumors are debulked at surgery. Dogs with
the pancreas. The tumors were firm on
inoperable tumors may be managed fairly
palpation because of an increase of fibrous
well with multiple feedings per day and
connective tissue in the stroma, and all had
glucocorticoid administration (0.5-1
evidence of metastasis before diagnosis.

mg/kg/clay). Diazoxide (20-80 mg/kg/day,
divided into three equal doses) may also

Diagnosis: Serum gastrin levels have
alleviate clinical signs in some dogs,
been evaluated in a limited number of clogs
although problems with availability have
with gastrinomas. Gastrin levels in a dog
limited its use. The chemotherapeutic
with a Zollinger-Ellison-like syndrome
agent streptozotocin has been investigated
varied from 155 to 2, 780 pg/mL, whereas
for the treatment of islet cell tumors in
the mean serum gastrin in clinically normal
dogs and may be considered after surgical

( control) dogs was 70.9 pg/mL. Recurrent
resection.

gastric or duodenal ulcers in dogs with no
identified cause warrants exploratory

GASTRIN-SECRETING ISLET CELL
surgery and careful inspection of the

TUMORS
pancreas.

Gastrinomas of the pancreas have been

Treatment: Excision of the gastrinreported in people, dogs, and a cat. Hype1�
secreting mass in the pancreas can be
secretion of gastrin in people results in the
attempted. However, all such tumors

Zollinger-Ellison syndrome, consisting of
that have been studied in dogs have had
hypersecretion of gastric acid and
evidence of local invasion into adjacent
recurrent peptic ulceration in the GI tract.

parenchyma and had metastasized to

The tumors, derived from ectopic amine
regional lymph nodes and liver. The clogs
precursor uptake decarboxylase (APUD)

had either single or multiple ulcerations in
cells in the pancreas, produce an excess of
the gastric or duodenal mucosa associated
the hormone gastrin, which normally is
with free blood in the lumen. Medical
secreted by cells of the antral and duodenal management with H2-receptor antagonists mucosa.

(famotidine or ranitidine) or the protonplllllp inhibitor omeprazole may temporar

Clinical Findings: These tumors are rare;
ily alleviate clinical signs in animals with
they occur less frequently than the insulin-
inoperable disease.

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GENERALIZED

CONDITIONS

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MORE THAN ONE SPECIES

ACTINOBACILLOSIS 589

ACTINOMYCOSIS 590

AMYLOIDOSES 592

ANTHRAX 593

BESNOITIOSIS 597

CHLAMYDIOSIS 598

CLOSTRIDIAL DISEASES 601

Bacillary Hemoglobinuria 601

BigHead 602

Blackleg 602

Infectious Necrotic Hepatitis 603

Malignant Edema 604

Botulism 605

Clostridium difficile and Clostridium perfringens Infections 607

Enterotoxemias 609

Clostridium perfringens Type A 609

Clostridium perfringens Types B and C 609

Type D Enterotoxemia 610

Tetanus 611

Clostridial Vaccines 613

CONGENITAL AND INHERITED ANOMALIES 613

Akabane Virus Infection 620

Border Disease 622

COXIELLOSIS 623

ERYSIPELOTHRIX RHUSIOPATHIAE INFECTION 625

Swine Erysipelas 626

Nonsuppurative Polyarthritis in Lambs 628

Postdipping Lameness in Sheep 629

FOOT-AND-MOUTH DISEASE 629

FUNGAL INFECTIONS 632

Aspergillosis 633

Blastomycosis 634

Candidiasis 636

586

GENERALIZED CONDITIONS

Coccidioidomycosis 637

Cryptococcosis 637

Epizootic Lymphangitis 639

Histoplasmosis 639

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Hyalohyphomycosis 640

Mycetomas 640

Oomycosis 641

Penicilliosis 643

Phaeohyphomycosis 643

Rhinosporidiosis 644

Sporotrichosis 644

Zygomycosis 645

LEPTOSPIROSIS 646

Dogs 650

Horses 652

Ruminants 653

Swine 654

LIGHTNING STROKE AND ELECTROCUTION 655

LISTERIOSIS 656

LYME BORRELIOSIS 659

MELIOIDOSIS 661

NEOSPOROSIS 663

NOCARDIOSIS 666

PERITONITIS 670

PLAGUE 677

RHODOCOCCOSIS 679

SWEATING SICKNESS 684

TOXOPLASMOSIS 685

TUBERCULOSIS AND OTHER MYCOBACTERIAL INFECTIONS 687

Cattle 689

Sheep and Goats 689

Deer and Elk 689

Horses 690

Elephants 690

Pigs 690

Dogs 690

Cats 690

Rabbits 690

GENERALIZED CONDITIONS

587

Guinea Pigs 691

Nonhuman Primates 691

Free-ranging and Captive Hoofed Animals 691

Marine Mammals 691

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Mycobacterial Infections Other than Tuberculosis 692

TULAREMIA 692

VESICULAR STOMATITIS 694

HORSES

AFRICAN HORSE SICKNESS 696

EQUINE GRANULOCYTIC EHRLICHIOSIS 697

EQUINE INFECTIOUS ANEMIA 699

EQUINE VIRAL ARTERITIS 701

GLANDERS 706

HENDRA VIRUS INFECTION 707

SEPSIS IN FOALS 2089 (MGN)

PIGS

AFRICAN SWINE FEVER 711

CLASSICAL SWINE FEVER 713

EDEMA DISEASE 716

ENCEPHALOMYOCARDITIS VIRUS INFECTION 718

GLASSER'S DISEASE 720

NIPAH VIRUS INFECTION 721

PORCINE CIRCOVIRUS DISEASES 723

PORCINE HEMAGGLUTINATING ENCEPHALOMYELITIS 728

PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME 729

STREPTOCOCCAL INFECTIONS 731

Streptococcus suis Infection 731

Streptococcus dysgalactiae equisimilis Infection 734

Streptococcus porcinus Infection 734

Other Streptococcal and Enterococcal Infections 735

SWINE VESICULAR DISEASE 735

TRICHINELLOSIS 736

VESICULAR EXANTHEMA OF SWINE 738

588

GENERALIZED CONDITIONS

RUMINANTS

BLUETONGUE 738

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BOVINE EPHEMERAL FEVER 741

BOVINE LEUKOSIS 743

BOVINE PETECHIAL FEVER 745

CAPRINE ARTHRITIS AND ENCEPHALITIS 747

COLISEPTICEMIA 749

CRIMEAN-CONGO HEMORRHAGIC FEVER 751

HEARTWATER 751

HISTOPHILOSIS 754

HEMORRHAGIC SEPTICEMIA 756

MALIGNANT CATARRHAL FEVER 758

NAIROBI SHEEP DISEASE 760

PARATUBERCULOSIS 762

PASTEURELLOSIS OF SHEEP AND GOATS 765

PESTE DES PETITS RUMINANTS 766

RIFT VALLEY FEVER 768

RINDERPEST 771

TICKBORNE FEVER 772

TICK PYEMIA 774

WESSELSBRON DISEASE 775

SMALL ANIMALS

CANINE DISTEMPER 777

CANINE HERPESVIRAL INFECTION 779

CANINE LYMPHOMA 40 (crn)

FELINE INFECTIOUS ANEMIA 28 (cm)

FELINE INFECTIOUS PERITONITIS 780

FELINE LEUKEMIA VIRUS AND RELATED DISEASES 790

FELINE PANLEUKOPENIA 796

INFECTIOUS CANINE HEPATITIS 798

ACTINOBACILLOSIS

589

LEISHMANIOSIS 800

RICKETTSIAL DISEASES 803

Ehrlichiosis and Related Infections 803

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Rocky Mountain Spotted Fever 806

Murine Typhus 807

Salmon Poisoning Disease and Elokomin Fluke Fever 808

ACTINOBACILLOSIS

Actinobacillosis refers to a group of

The natural host of A equuli is tl1e horse, diseases caused by gram-negative
and infections are seen in botll foals and
coccobacilli in the genusActinobacillus.

adult horses. Disease in foals may manifest as

Although there are >22 different bacterial
diarrhea, followed by meningitis, pneumonia,
species in this genus, only four (A pleuro
purnlent nephritis, or septic polyarthritis
pneumoniae, A suis, A equuli, and A

( sleepy foal disease or joint-ill). Infection
lignieresii) are frequently associated with may be acquired tlrrough a contaminated
disease in animals.

umbilicus or by inhalation or ingestion. The

A pleuropneumoniae causes contagious
incidence of foal infection is reduced witll
pleuropneumonia in pigs (seep 1469).

greater attention to sanitation in tile foaling

Disease ranges from acute, severe fibrinous
environment, and maternal antibodies in
pleuropneumonia to subacute or chronic
colostrum are often protective. Abortions,
infection with pleuritis and pulmonary
septicemia, nepluitis, peritonitis, and
abscessation. Immune complexes fanned
endocarditis may result from A equuli
as a result of host response may damage
infection in adult horses. A syndrome of
endotl1elial cells, resulting in vasculitis and
acute peritonitis in adult horses associated
tlrrombosis, with edema, necrosis, infarcwitllA equuli has been described in Australia tion, and hemorrhage. Infection is usually
as well as sporadically in oilier parts of tile
restricted to pigs <5 mo old. A pleuropneu
world. A equuli isolates have also been
rnoniae may be nonnal mucosa! flora in pigs, recovered from fetuses of mares affected cattle, and sheep. Diagnosis is by culture of
with mare reproductive loss syndrome;
tile organism from nasal swabs or lung tissue
however, it is not clear whether tile bacteria
at necropsy. Molecular techniques such as
is directly associated with tile pregnancy

PCR have also been developed to detect tile
loss. In botll foals and adult horses, several
presence of A pleuropneumoniae in tissue
other bacteria can cause the san1e clinical
san1ples. Treatment involves use of antidisease syndromes as A equitli. Therefore, biotics, including penicillin, tetracycline,
definitive diagnosis of A equuli relies on
spectinomycin, cephalosp01ins, or
isolating the bacteria by culture. Infected
fluoroquinolones. Control focuses on good
horses may be treated witll chloramphenicol,
management combined witll tile use of
gentamicin, or tllird-generation cephalosporvaccines or eradication of the infection ins, depending on tile nature of tile Infection
from tile herd by depopulation.

and tile ability to achieve therapeutic

A suis is part of the nom1al flora of the
concentrations at tile site of infection.

oral cavity of pigs. It causes septicemia in

13-Lactam antibiotics and potentiated sulfonayom1g pigs and arthritis, pneumonia, and nlides have been recommended; however,
pericarditis in older pigs. It may also cause
resistance to botll of these types of
septicemia, artluitis, pneumonia, and
antibiotics is occasionally reported.

purulent nephritis in neonatal and post

A arthritidis, previously classified as
natal foals. Disease follows a break in tl1e

Bisgaard taxon 9, has been isolated from
integrity of tile oral mucosa or may be
horses witll arthritis and septicemia.

associated with in1munosuppression.

A lignieresii causes tun1orous abscesses

The organism is typically susceptible to
of tl1e tongue, usually referred to as wooden
sulfonamides and cephalosporins.

tongue. It is seen prin1arily in cattle but also

590

ACTINOBACILLOSIS
chemistry findings are generally nom1al.

Gross pathology generally reveals a firm,
pale tongue containing multifocal nodules.

These nodules are often filled with thick

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yellow-white pus. Histologically, the
primary lesion is a granulomatous abscess.

This fom1 of actinobacillosis is found
worldwide but is sporadic and thus difficult
to prevent. Herd outbreaks are possible and
are generally associated with consw11ption
of coarse, abrasive feeds that encourage
formation of lesions in the mouth. Soditun

Actinobacillosis in a cow. Note the characteriodide is the treatment of choice in istic large granulomas in the substance of the
actinobacillosis in ruminants. IV sodium
tongue. Courtesy of Dr. John Prescott.

iodide (70 mg/kg of a 10%---200/o solution) is
given once and then repeated once or twice
at 7- to 1 0 -day intervals. lf clinical signs of
in sheep, horses, pigs, and dogs. It is a rare
iodine toxicity develop (including dandruff,
cause of disease in chickens. The organism
diarrhea, anorexia, coughing, and excessive
may also cause pyogra.nulomatous lesions
lacrimation), iodine administration should
in soft tissues associated with the head,
be discontinued. Clinical improvement is
neck, limbs, and occasionally the lungs,
often seen within 48 hr of therapy, and
pleura, udder, and subcutaneous tissue. A
treatment is usually successful when only
lignieresii is part of the normal mucosal
the tongue is involved. Systemic antibacteflora of the upper GI tract and causes rial agents, such as ceftiofur, penicillin,
disease when it gains access to adjacent soft ampicillin, florfenicol, and tetracyclines may tissue via penetrating wounds. It causes
be effective and are primarily recommended
localized infections and can spread via the
in severe cases of actinobacillosis or in cases
lymphatics to other tissues. The primary
refractory to sodium iodide therapy. Surgical
lesion associated with A lignieresii
debulking of lesions, especially if they
infection in cattle is a very hard, diffusely
intetfere with breathing, may be useful. This
swollen, painful tongue. This leads to
is pa.iticularly true when la.i·ge granulomaexcessive salivation, the inability to tous masses that do not respond to medical
prehend food nom1ally, and sometimes a
therapy are present. Prevention of
visibly enlarged tongue that protrudes from
actinobacillosis in ruminants primarily relies
the mouth. On palpation, the tongue will
on avoidance of coarse, stemrny feedstuffs
feel very hard. Diagnosis requires culture
and pastures full of hard, penetrating plant
and biopsy of the lesion. Pus from an
awns (ie, foxtails or thistles).

abscess crushed between two glass slides

A ureae has caused upper respiratory
may show club-like spicules of calcium
tract infections in people and abortions in
phosphate, giving the appearance of sulfur
pigs. In addition, A actinoides has
granules <l mm diameter. No re1iable
occasionally been associated with
serologic tests are available for actinobacilsuppurative pneumonia in calves and losis, and the hematologic and clinical
seminal vesiculitis in bulls.

ACTINOMYCOSIS

Members of the genusActinomyces are

A bovis is the etiologic agent of lun1py jaw gran1-positive, anaerobic, non-acid-fast
in cattle. It has also been isolated from
rods, many of which are filamentous or
nodular abscesses in the lungs of cattle and
branching. Branches are< 1 µrn in diameter,
infrequently from infections in sheep, pigs,
as opposed to fungal fila.inents, which are
dogs, and other manirnals, including chronic

> 1 µm in diameter. Although they a.i·e
fistulous withers and chronic poll evil in
nom1aJ flora of the oral and nasopharyngeal
horses. Lumpy jaw is a localized, chronic,
membranes, several species are associated
progressive, granulomatous abscess that
with diseases in animals.

most frequently involves the mandible, the

ACTINOMYCOSIS

591
maxillae, or other bony tissues in the head.

A israelii is primarily associated with

Disease is seen when A bovis is introduced chronic granulo.matous infections in
to underlying soft tissue via penetrating
people but has also been isolated rarely
wounds of the oral mucosa from wire or
from pyogranulomatous lesions in pigs
coarse hay or sticks. Involvement of adjacent and cattle. Treatment involves surgical VetBooks.ir
bone frequently results in facial distortion,
debridement and administration of
loose teeth (making chewing difficult), and
penicillin.

dyspnea from swelling into the nasal cavity.

A naeslundii has been isolated from

Any pait of the head can be affected;
suppurative infections in several anin1al
however, the alveoli around the roots of the
species, the most common being aborted
cheek teeth are frequently involved. The
porcine fetuses.

primary lesion appears as a slow-growing,

A suis causes pyogranulomatous porcine firm mass that is attached to or pait of the
mastitis, chai·acterized by small abscesses
mandible. Ulceration fonns in some cases,
containing thick, yellow pus surrow1ded by
with or without fistulous tracts, and drainage
a wide zone of dense connective tissue.

of purulent exudate may occur. Preswnptive

Yellow "sulfur granules" may be scattered
diagnosis is often based on clinical signs. The throughout the pus, as in A bovis in cattle.

diagnosis can be confumed by culture of the

Chronic, deep-seated abscesses may
orgailism from the lesion; however, this
fistulate. Sows may also develop ventral
requires anaerobic conditions and is
subcutaneous granulomatous lesions, and
frequently negative. A Grain stain of purulent occasional pyogranulomatous infections matetial will reveal gran1-positive, clubdevelop in lungs, spleen, kidneys, and other shaped rods and filainents ( sulfur granules).

organs. Diagnosis is based on clinical signs

Radiology of the head is also useful; the
and on isolation and identification of the
prin1ary radiographic lesion consists of
etiologic agent. Treatment is rarely
multiple, centrally radiolucent areas of
successful, primarily due to the inability
osteomyelitis swTounded by periosteal new
of an antibacterial agent to penetrate the
bone and fibrous tissue. As a last resort, a
infected tissue. Infected tissue may be
biopsy sainple can be taken with a trephine
surgically removed to salvage sows for
and submitted for histopathology.

slaughter.

The goal of treatment is to kill the bacteria

A hordeovulneris is a rare cause of cailine and stop the spread of the lesion. However,
actinomycosis, which can present with
the hard mass will usually not regress
either localized abscesses or systemic
significantly. Sodiwn iodide is the treatment
infections such as pyogra11ulomatous
of choice in rwninant actinomycosis.

plemitis, peritonitis, visceral abscesses, or

Sodiwn iodide (70 mg/kg of a 10%-20%
septic aithritis. A common predisposing
solution, IV) is given once and repeated
factor is the presence of tissue-nligrating
several tinles at 7- to 10-day intervals. If signs foxtail grass (Hordeum spp) paiticles, and of iodine toxicity develop (eg, dandruff,
the primary route of infection appears to be
diarrhea, anorexia, coughing, and excessive
via inhalation of the bacteria. Histo1y a11d
lacri.mation ), iodine administration should
clinical signs may contribute to the
be discontinued or treatments given at
diagnosis, but demonstration of the
longer intervals. Sodiwn iodide has been
causative agent by Grain stain a11d bacterioshown to be safe for use in pregnant cows logic culture is necessary for confirmation.

and presents little risk of causing abortion.

Treatment includes surgical debridement

ConcwTent administration of antimicrobiand/or longterm treatment with penicillin, als, including penicillin, florfenicol, or
cephalosporins, or sulfonanlides. Pyothorax
oxytetracycline, is recommended. Surgery
is frequently seen in canine actinomycosis
to debride large .mai1dibular lesions has also
ai1d requires repeated drainage of the chest
been described in conjunction with iodine
in addition to antimicrobial therapy.

and antin1icrobial therapy. Because A bovis

A viscosus causes cutaneous actinomyis pait of the normal oral flora in rwninants, cosis in dogs, which appears as localized
control focuses on avoiding coarse, stem.my
subcutaneous abscesses. These usually
feeds or feeds with plant awns that nlight
occur secondary to perforating injuries
dan1age the mucosal epitheliwn. When
caused by bite wounds or foreign bodies.

.multiple cases are seen in a herd, it is not

The most common sites for abscesses are
from the contagious nature of the pathogen
the head, neck, thorax, and abdomen.

but the widespread exposure to a risk factor

A viscosus ca11 also cause pneun10nia,

( eg, coarse feed).

pyothorax, and rarely pyogranulomatous

A actinoides is occasionally found as a
meningoencephalitis. Diagnosis may be
secondary invader in enzootic pnewnonia
based on history and clinical signs,
of calves and seminal vasculitis in bulls.

including the presence of soft, grayish

592

ACTINOMYCOSIS
white granules in the pus or exudate.

sulfonamides, or cephalosporins may be

Cytology ( of pus or pleural fluid) is useful
successful if begun early in the clinical
and will reveal gram-positive, filamentous
course. A successful outcome is more
organisms. Definitive diagnosis is based on
likely with cutaneous infections, which
isolation and identification of A viscosus.

should also be treated with the same

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Treatment of pyothorax with penicillin,
antimicrobials.

AMYLOIDOSES

The amyloidoses are diseases that result from deposited in mesenchymal tissues, eITors in protein folding. When new proteins
especially nervous tissues and joints.

are made, their peptide chains nonnally fold

It is rare in domestic animals.

into the corTect shape. Sometimes, howeve1�

At least 20 other proteins have been
the peptide chains fold incotTectly and fonn
shown to misfold, fonn 13-sheets, and
highly stable 13-sheets that are insoluble and
become deposited in the tissues as amyloid.

resistant to proteolytic digestion. When this

There are also hereditary anwloidoses, such
insoluble protein is deposited in tissues, it is
as those described in Abyssinian cats and
called amyloid. Amyloid proteins may be

Chinese Shar-Pei dogs, in which mutations
deposited in a localized fashion or widely
result in protein misfolding. Some amyloid
distributed throughout the body. 111ey cause
is formed in all aged animals ( senile
damage by displacing nom1al cells. If critical
systemic an1yloidosis ); eg, in aged dogs,
organs such as the kidneys, liver, or heart are
amyloid is commonly deposited in the
extensively disrupted, the disease may be
media of meningeal and cortical aiteries.

fatal. Amyloidosis can affect all domestic

Tunlor-like amyloid nodules and subcutailemanunals, and minor, asymptomatic ous amyloid have been repo1ted in horses.

deposition of amyloid proteins is conunon

Some forms of amyloid may be transmitin aged animals.

ted between animals. The most important

The most common fom1 of a.myloid is
of these are the transmissible spongiform
generated by rnisfolding of the major
encephalopathies, such as bovine spongiacute-phase protein, serum amyloid A (SAA). form encephalopathy (seep 1284) and Levels of SAA in the blood climb significantly
scrapie (seep 1288). These are caused by
in anin1als with severe inflanunation. If SAA
the production of misfolded prion proteins.

fails to fold cotTectly, it forms a very stable

Indeed, even AA ainyloid is somewhat
protein called AA an1yloid. Amyloidosis thus
transmissible, because experimental
develops as a result of chrop.ic inflanunatory
adn1inistration of small amounts of amyloid
diseases, chronic bacterial infections, and
protein to an animal can accelerate its
malignant tun1ors. It is a conunon cause of
development. Cheetahs are especially prone
death in horses aggressively inununized for
to arnyloidosis and shed an infectious fonn
antiserum production. AA amyloid is usually
of arnyloid protein in tl1eir feces.

deposited in parenchymal organs, such as

Because of its diffuse distribution and
the spleen, where it may not cause clinical
insidious onset, an1yloidosis is difficult to
signs. If tl1e kidneys are involved, the
diagnose clinically. However, an1yloidosis
presence of an1yloid in glomeruli may lead to
should be suspected if progressive renal
severe proteinuria, eventually resulting in
or hepatic failure develops in animals
renal failure and death. There is no practical
subsequent to chronic infections or
treatment for this fonn of amyloidosis,
inflanunation. There is no specific therapy
altl10ugh removal of the source of inflanunathat can prevent the development of tion may slow amyloid deposition and hence
amyloidosis or promote the resorption of
progression of the disease.

fibrils. Animals with persistent inil.anuna

Misfolding of inununoglobulin light
tion should be treated to reduce the severity
chains generates a second form of amyloid,
of their inflammatory response and hence

AL amyloid. This cormnonly results from
the availability of SAA. Amyloidosis is
the overproduction of monoclonal light
readily recognized at necropsy and in
chains in animals with plasma cell tun10rs
histologic sections by its affinity for dyes

(myelomas). AL amyloid tends to be
such as Congo red.

ANTHRAX

593

ANTHRAX

(Splenic fever, Siberian ulcer, Charbon, Milzbrand)

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Anthrax is a zoonotic disease caused by the
are usually associated with drought,
sporefo1ming bacterium Bacillus anthra
flooding, or soil disturbance, and many
cis. Anti1Tax is most common in wild and years may pass between outbreaks. During
domestic herbivores ( eg, cattle, sheep,
interepidemic periods, sporadic cases may
goats, camels, antelopes) but can also be
help maintain soil contan1ination. But it is
seen in people exposed to tissue from
now absent from some countiies in western
infected animals, to contantinated animal

Europe, north Africa, and east of the
products, or directly to B anlhracis spores Mississippi in the USA.

under certain conditions. Depending on

Human cases may follow contact with
the route of infection, host factors, and
contaminated carcasses or animal products.

potentially strain-specific factors, anthrax

The risk of hun1an disease in these settings
can have several different clinical presentais comparatively small in developed tions. In herbivores, anthrax commonly
countiies, partly because people are
presents as an acute septicemia with a
relatively resistant to infection. However,
high fatality rate, often accompanied by
in developing countries, each affected cow
hemorrhagic lymphadenitis. In dogs,
can result in up to 10 human cases because
people, horses, and pigs, it is usually less
of home slaughter and sanitation issues.

acute although still potentially fatal.

In cases of natural transmission, people

B anthracis spores can remain viable in exhibit primarily cutaneous disease (>95%
soil for many years. During this time, they
of all cases). GI antl1Tax (including
are a potential source of infection for
pharyngeal antlirax) may be seen among
grazing livestock but generally do not
human populations after consumption of
represent a direct risk of infection for
contantinated raw or undercooked meat.

people. Grazing animals may become

Under ce1tain artificial conditions ( eg,
infected when they ingest sufficient
laboratories, animal hair processing
quantities of these spores from the soil. In
facilities, exposw·e to weaponized spore
addition to direct transmission, biting flies
products), people may develop a highly fatal
may mechanically transmit B anthracis
forn1 of disease known as inhalational
spores from one animal to another. The
anthrax or woolsorter's disease. Inhalalatter follows when there have been rains tional antiu·ax is an acute hemorrhagic
encouraging a high fly hatch and reporting
lymphadenitis of the mediastinal lynrph
has been delayed on the index ranch, such
nodes, often accompanied by hemorrhagic
that there are 4-6 moribund or dead cattle
pleural effusions, severe septicemia,
for the flies to feed on. Feed contaminated
meningitis, and a high mo1tality rate. Of late,
with bone or other meal from infected
injection antilfax has emerged in coajuncanimals can serve as a source of infection tion with contan1inated heroin.

for livestock, as can hay muddy with

The precise incidence of anthrax among
contaminated soil. Raw or poorly cooked
animals in the USA is unknown. Throughout
contantinated meat is a source of infection
the past hundred years, animal infections
for zoo carnivores and omnivores; anthrax
have been seen in nearly all states, with
resulting from contantinated meat
highest frequency from the Midwest and
consumption has been reported in pigs,

West. Presently, antilfax is enzootic in west
dogs, cats, mink, wild carnivores, and

Texas and nortl1west Minnesota; sporadic in
people.

south Texas, Montana, eastern North and

South Dakota; and only occasionally seen

Epidemiology: Underdiagnosis and
elsewhere. The annual incidence of human
unreliable reporting make it difficult to
antlirax in tl1e USA has declined from -130
estimate the true incidence of anthrax
cases annually in the beginning of the last
worldwide. However, anthrax has been
century to no reported cases in 2004-2005.

reported from nearly every continent and is

In addition to causing naturally occurring
most common in agricultural regions with
anthrax, B anlhracis has been manufactured neutral or alkaline, calcareous soils. In
as a biologic warfare agent. B anthracis was these regions, anthrax periodically emerges
used successfully as a weapon of terrorism
as epizootics among susceptible domestiin 2001, killing 5 people and causing disease cated and wild animals. These epizootics
in 22. Probably because of the metl1od of

594

ANTHRAX
delivery (via mail), no !mown animal disease
ln acute anthrax of cattle and sheep, there
resulted from this attack. Weaponized spores is an abrupt fever and a period of exciterepresent a threat to both human and animal ment followed by depression, stupor,
populations. The World Health Organization
respiratory or cardiac distress, staggering,
has estimated that 50 kg of B anlhracis
convulsions, and death. Often, the course

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released upwind of a population center of
of disease is so rapid that illness is not

500,000 could result in 95,000 deaths and
observed and anin1als are found dead. Body

125,000 hospitalizations. The effect on
temperature may reach 107°F (41.5°C),
animal populations has not been estin1ated,
rumination ceases, milk production is
but because livestock are more susceptible
materially reduced, and pregnant anin1als
to B anlhracis infection than primates,
may abo1t. There may be bloody discharges
the outcome of an aerosol attack with
from the natural body openings. Some

B anlhracis spores against livestock would
infections ru·e characterized by localized,
result in higher and earlier mortality and
subcutaneous, edematous swelling that can
morbidity rates than among a human
be quite extensive. Areas most frequently
population. Subsequent to the 1979
involved are the ventral neck, thorax, and

Severdlovsk incident, human cases were
shoulders.

seen up to 4 km from the source, but dead

The disease in horses may be acute. Signs
sheep were noted 64 km downwind, and in
may include fever, chills, severe colic,
villages between.

anorexia, depression, wealmess, bloody
diarrhea, and swellings of the neck,

Pathogenesis: After wound inoculation,
sternwn, lower abdomen, and external
ingestion, or inhalation, spores infect
genitalia. Death usually occurs within
macrophages, gem1inate, and proliferate. ln

2-3 days of onset.

cutaneous and GI infection, proliferation

Although relatively resistant, pigs may
can occur at the site of infection and in the
develop an acute septicemia after ingestion
lymph nodes draining the site of infection.

of B anlhracis, chru·acterized by sudden

Lethal toxin and edema toxin are produced
death, oropharyngitis, or more usually a
by B anlhracis and respectively cause local mild chronic fom1. Oropharyngeal anthrax
necrosis and extensive edema, which are
is characterized by rapidly progressive
frequent characteristics of the disease. As
swelling of the throat, which may cause
the bacteria multiply in the lymph nodes,
death by suffocation. ln the chronic form,
toxemia progresses and bacteremia may
pigs show systemic signs of illness and
ensue. With the increase in toxin producgradually recover with treatment. Some tion, the potential for dissemi..'lated tissue
later show evidence of anthrax infection in
destruction and organ failure increases.

the cervical lymph nodes and tonsils when

After vegetative bacilli are discharged from
slaughtered ( as apparently healthy animals).

an animal after death (by carcass bloating,
lntestinal involvement is seldom recognized
scavengers, or postmortem exan1ination),
and has nonspecific clinical characte1istics
the oxygen content of air induces sporulaof anorexia, vomiting, diarrhea (sometimes tion. Spores are relatively resistant to
bloody), or constipation.

extremes of temperature, chemical
ln dogs, cats, and wild carnivores, tl1e
disinfection, and dessication. Necropsy is
disease resembles that seen in pigs. ln wild
discouraged because of the potential for
herbivorous animals, the expected course
blood spillage and vegetative cells to be
of illness and lesions varies by species but
exposed to air, resulting in large nwnbers
resembles, for the most prut, anthrax in
of spores being produced. Because of the
cattle.

rapid pH change after death and decomposi

Lesions: Rigor mortis is frequently absent
tion, vegetative cells in an unopened carcass or incomplete. Dark blood may ooze from quickly die without sporulating.

tile mouth, nostrils, and anus with marked
bloating and rapid body decomposition.

Clinical Findings: Typically, the

If the carcass is inadve1tently opened,
incubation period is 3-7 days (range
septicemic lesions are seen. The blood is

1-14 days). The clinical course ranges from
dark and thickened and fails to clot readily.

peracute to chronic. The peracute form

Hemorrhages of various sizes ru·e common

( common in cattle and sheep) is characteron the serosal surfaces of the abdomen and ized by sudden onset and a rapidly fatal
thorax as well as on the epicardium and
course. Staggering, dyspnea, trembling,
endocardium. Edematous, red-tinged
collapse, a few convulsive movements, and
effusions commonly are present under the
death may occur in cattle, sheep, or goats
serosa of various organs, between skeletal
with only a brief evidence of illness.

muscle groups, and in the subcutis.

ANTHRAX

595

Hemorrhages frequently occur along the

Specific diagnostic tests include bacte1ial

GI tract mucosa, and ulcers, particularly
culture, PCR tests, and fluorescent antibody
over Peyer's patches, may be present. An
stains to demonstrate the a.gent in blood
enlarged, dark red or black, soft, semifluid
films or tissues. Western blot and ELISA
spleen is common. The liver, kidneys, and
tests for antibody detection are available in

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lymph nodes usually are congested and
some reference labora.t01ies. Lacking other
enlarged. Meningitis may be found if the
tests, fixed blood smears stained with
skull is opened.

Loeffler's or MacFa.dean stains can be used

In pigs with chronic anthrax, the lesions
and the capsule visualized; however, this
usually are restricted to the tonsils, cervical
can result in -200/o false positives.

lymph nodes, and surrounding tissues. The

In livestock, anthrax must be differentilymphatic tissues of the area are enlarged ated from other conditions that ca.use
and are a mottled salmon to brick-red color
sudden death. In cattle and sheep,
on cut sruiace. Diphtheritic membranes or
clostridial infections, bloat, and lightning
ulcers may be present over the surface of
strike ( or any ca.use of sudden death) may
the tonsils. The area around involved
be confused with anthrax. Also, acute
lymphatic tissues generally is gelatinous
leptospirosis, bacillary hemoglobinuria,
and edematous. A chronic intestinal form
anaplasmosis, and acute poisonings by
involving the mesenteric lymph nodes is
bracken fem, sweet clover, and lead must
also recognized.

be considered in cattle. In horses, acute
infectious anemia, purpura, colic, lead

Diagnosis: A diagnosis based on clinical
poisoning, lightning strike, and sw1stroke
signs alone is difficult. Confinnatory
may resemble anthrax. In pigs, acute
laboratory examination should be
classical swine fever, African swine fever,
attempted if anthrax is suspected. Because
and pharyngeal malignant edema are
the vegetative cell is not robust and will not
diagnostic considerations. In dogs, acute
survive 3 days in transit, the optimal san1ple
systemic infections and pharyngeal
is a cotton swab dipped in the blood and
swellings due to other causes must be
allowed to dry. This results in sporulation
considered.

and the death of other bacteria and
contaminants. For carcasses dead >3 days,

Treatment, Control, and Prevention:

either the nasal turbinates should be

Anthrax is controlled through vaccination
swabbed or turbinate samples removed.

programs, rapid detection and reporting,

Pigs with localized disease are rarely
quarantine, treatment of asymptomatic
ba.cteremic, so a small piece of affected
anin1als (postexposure prophylaxis), and
lymphatic tissue that has been collected
burning or burial of suspect and confinned
aseptically should be submitted. Before
cases. In livestock, anthrax can be
submission, the receiving reference
controlled largely by annual vaccination of
laboratory should be contacted regarding
all grazing a.nin1als in the endemic area and
appropriate specimen la.belling, handling,
by in1plementation of control measures
and shipping procedures.

druing epizootics. The nonencapsulated

Sterne-strain vaccine is used almost
universally for livestock in1munization.

Vaccination should be done at least 2--4 wk
before the season when outbreaks may
be expected. Because this is a live vaccine,
antibiotics should not be administered
within 1 wk of vaccination. Before
vaccination of dairy cattle during an
outbreak, all of the procedures required
by local laws should be reviewed and
followed. Human anthrax vaccines
currently licensed and used in the USA and

Europe are based on filtrates of artificially
cultivated B anthracis.

Early treatment and vigorous implementation of a preventive program are essential Bacillus anthracis, methylene blue stain of to reduce losses among livestock. Livestock
tissue smear, high power. Note the intense
at risk should be in1rnediately treated with a
red stain of the large capsule of this
long-acting antibiotic to stop all potential
organism. Courtesy of the Department of
incubating infections. This is followed by

Pathobiology, University of Guelph.

vaccination -7-10 days after antibiotic

596

ANTHRAX
treatment. Any animals becoming sick after
slaughter, and meat of uncertain origin
initial treatment and/or vaccination should
should be avoided. Routine vaccination
be retreated immediately and revaccinated
against anthrax is indicated for individuals
a month later. Simultaneous use of
engaged in work involving large quantities
antibiotics and vaccine is inappropriate,
or concentrations of B anlhracis cultures VetBooks.ir
because available commercial vaccines
or activities with a high potential for aerosol
for animals in the USA are live vaccines.

production. Laboratory workers using

Animals should be moved to another
standard Biosafety Level 2 practices in
pasture away from where the bodies had
the routine processing of clinical sainples
lain and any possible soil contamination.

are not at increased risk of exposure to

Suspected contan1inated feed should be

B anlhracis spores. The risk for workers immediately removed. Domestic livestock
who come into contact with imported
respond well to penicillin if treated in the
animal hides, furs, bone meal, wool, anin1al
early stages of the disease. Oxytetracycline
hair, or bristles has been reduced by
given daily in divided doses also is effective.

improvements in industry standards and

Other antibacterials, including amoxicillin,
import restrictions. Routine preexposure
chloramphenicol, ciprofloxacin, doxycyvaccination is reconm1ended for people in cline, erythromycin, gentamicin, streptomytllis group only when these standards and cin, and sulfonanlides also can be used, but
restrictions ai·e insufficient to prevent
their effectiveness in comparison with
exposure to ai1tlu·ax spores. Routine
penicillin and the tetracyclines has not
vaccination of veterinarians in the USA
been evaluated under field conditions.

is not recommended because of the

In addition to therapy and inm1Unization,
low incidence of animal cases. However,
specific control procedures are necessary to vaccination may be indicated for veterinarcontain the disease and prevent its spread.

ians and other high-risk individuals handling

These include the following: 1) notification
potentially infected ailimals in areas where
of the appropriate regulatory officials;
there is a high incidence of anthrax cases.

2) rigid enforcement of quarantine ( after

The CDC has reconunended that those at
vaccination, 2 wk before movement off the
risk of repeated exposure to B anlhracis
fann, 6 wk if going to slaughter); 3) prompt
spores in response to a biotetTorism attack
disposal of dead animals, manure, bedding,
should be vaccinated. Those groups include
or other contaminated material by
some emergency first responders, federal
cremation (preferable) or deep burial;
responders, and laboratory workers.

4) isolation of sick animals and removal of

Vaccination in anticipation of a tetTorist
well ailirnals from the contanlinated areas;
attack is not recommended for other

5) cleaning and disinfection of stables,
populations.

pens, milking banis, and equipment used

For people, postexposure prophylaxis
on livestock; 6) use of ihsect repellents;
against B anthracis is reconunended after 7) control of scavengers that feed on
an aerosol exposure to B anlhracis spores.

animals dead from the disease; and 8) obser

Prophylaxis may consist of antibiotic
vation of general sailitary procedures by
tl1erapy alone or the combination of
people who handle diseased animals, both
antibiotic therapy and vaccination, if
for their own safety and to prevent spread
vaccine is available (most hwnan vaccines
of disease. Contaminated soils are very
are not live). Although there is no approved
difficult to completely decontaminate, but
regin1en, the CDC has suggested that
formaldehyde will be successful if the level
antibiotics may be discontinued after three
is not excessive. The process generally
doses of vaccine have been administered
requires removal of soil.

according to the staI1dard schedule

Human infection is controlled through

(0, 2, and 4 wk). Because of availability and
reducing infection in livestock, veterinary
ease of dosing, doxycycline or ciprofloxacin
supervision of animal production and
may be chosen initially for antibiotic chemoslaughter to reduce human contact with prophylaxis until the susceptibility of the
potentially infected livestock or animal
infecting orgailism is determined. Penicillin
products, and in some settings either pre- or
and doxycycline are approved by the FDA
postexposure prophylaxis. In countries
for treatment of anthrax in people and have
where anthrax is common and vaccination
traditionally been considered the drugs of
coverage in livestock is low, people should
choice. Both ciprofloxacin and ofloxacin
avoid contact with livestock and animal
have demonstrated in vitro activity against
products that were not inspected before

B anthracis. Although naturally occurring and after slaughter. In general, consun1ption B anthracis resistance to penicillin is of meat from animals that have exhlbited
infrequent, it is reported; resistaI1ce to other
sudden death, meat obtained via emergency
antibiotics has been noted. Antibiotics are

BESNOITIOSIS

597
effective against the germinated form of

12 mo. If subsequent exposures occur,

B anlhracis but are not effective against the additional vaccinations may be required.

spore form of the organism. Spores may

There are no definitive recommendasurvive in the mediastinal lymph nodes in tions for postexposure prophylaxis after
the lungs for months without gernlination
cutaneous or GI exposures of people to

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in nonhuman prin1ates.

B anthracis. Based on the slow progression

There are cun-ently no approved
of disease, low fatality rate, and ease of
vaccination regimens for postexposure
antibiotic treatment of cutaneous anthrax,
prophylaxis after B anthracis exposures.

and the general low risk of cutaneous

Although postexposure chemoprophylaxis
disease after natural exposure, postexpousing antibiotics alone has been effective sure prophylaxis is not reconunended after
in animal models, the definitive length of
direct cutaneous exposure to contan1inated
treatment remains unclear. Antibiotic
animals or animal products. However,
chemoprophylaxis may be switched to
immediate washing of the exposed areas is
penicillin VK or amoxicillin in children or
advised. Those exposed should be advised
pregnant women once antibiotic susceptiof the signs of cutaneous anthrax (ie, an bilities are known and the organism is found inflamed but painless area with or without to be susceptible to penicillin. The safety
circumferential small vesicles, enlargement
and efficacy of anthrax vaccine in children
of the regional lymph nodes) and should
or pregnant women has not been studied;
seek medical assistance if illness develops.

therefore, a recommendation for use of

Because of the high fatality rate and rapid
vaccine in these groups cannot be made.

progression of GI anthrax, se1ious

Although the shortened vaccine regimen
consideration should be given to initiating
has been effective when used in a postexpopostexposure antibiotic prophylaxis for sure regimen that includes antibiotics, the
those who consun1e contan1inated
duration of protection from vaccination is
undercooked or raw meat. There is no
not known. The existing evidence suggests
current indication for vaccination after
that vaccine protection is adequate for
either cutaneous exposure or ingestion.

BESNOITIOSIS

Besnoitiosis ( originally nan1ed globidiosis)

in donkeys in Africa, southern France,
is a cyst-forming, usually nonfatal disease

Mexico, and in a number of locations in the
caused by a number of different species of

USA. B bennetti is also found in horses,
the apicomplexan protozoaBesnoitia.

especially, but not only, those living in the

Lesions are conunonly seen in the dennis
tropics. B jellisoni and B wallacei have and in mucous and serous membranes, as
been described from rodents; B tarandi
well as in other tissues. These Besnoitia
from reindeer or caribou; B darlingi from
species tend to be confined to specific
lizards, opossums, and snakes; and
animal hosts that include large and small

B sauriana from lizards. Viscerotropic
mammals, as well as reptiles.

strains of B besnoiti have been isolated
from African antelopes; and serologic

Etiology and Transmission: The most
evidence of infection was detected in red
significant condition in domestic animals is
and roe deer. Wildlife in Australia and blue
that of cattle, in which B besnoiti causes
duiker, impala, and blue wildebeest in Africa
economic loss through reduced milk
have been affected; to date it has not been
production, infertility and sterility, skin
reported in cattle in North America. A recent
lesions, and increased mortality; similar
addition to these species and their hosts is
effects are likely with B caprae in goats in B oryctofelisi in Argentinian rabbits.

Africa, southern Europe, and New Zealand.

It is thought that these parasites may

Recent studies indicate that infection is
have both definitive and intermediate hosts,
being detected more commonly in cattle in
and although the cat is often named as the

Europe (ie, Spain, Portugal, Italy, Germany,
likely candidate for the role of definitive

Switzerland, Hungary, and Greece).

host, this has not yet been clearly defined

B bennelli has been reported to be present
for mostBesnoitia sp. Various animals,

598

BESNOITIOSIS
usually rodents or small mammals, such
periostitis, endostitis, lymphadenitis,
as woodrats and opossums, have been
pnewnonia, periorchitis, orchitis, epididysuggested as intem1ediate hosts.

mitis, arteritis, and perineuritis. Severely

These Toxoplasma/Neospora-like orgaffected animals become emaciated.

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anisms multiply in endothelial, mac

Although mortality is low, convalescence is
rophage, and other cells and produce
slow in severe cases. Severely affected bulls
characteristic large, thick-walled cysts filled can become permanently sterile. Affected with bradyzoites. These, along with the
animals remain carriers for life. The disease in
oocyte stage in cats and the tachyzoite stage goats is sinlilar to that in cattle. In horses, the in other animals, are the infectious forms.

clinical signs are similar but tend to be less

The true route(s) of transmission remains severe or invasive. Infected donkeys, which unclear despite many experimental and
are most commonly young ( <2 yr old), also
epidemiologic attempts. Experimental
present with sinlilar signs and symptoms,
cyclic transmission with intestinal sexual
which are often more severe than those seen
stages in a definitive host-the cat-has
in horses.

been reported for B besnoiti, B wallacei,

The appearance of cysts in the scleral
and B darlingi, and experimental
coajunctiva and nasal mucosa are useful
transmission using genetically modified
diagnostic indicators. Parasitologic
mice and tissue culture has been achieved
diagnosis is made by finding the crescentwith B oryctofelisi. Transmission of shaped bradyzoites in biopsies or skin/

B besnoili from cattle to cats has not been conjunctiva! scrapings.

substantiated by subsequent studies. The
suggestion that biting insects may trans-

Prevention and Treatment: B besnoiti
mit B besnoiti mechanically remains a
infections are economically important to
possibility but has not been substantiated;
cattle owners in endemic areas because of

Besnoitia spp can be transmitted artificially mortality (although usually dOOAi), sterility to suitable hosts by needle inoculation of

(which may be temporary or pem1anent),
tissues that contain cysts. Water or feed
loss of condition, lower market value, and
contaminated by infected cat feces are
damage to the hide.

other possible routes of transmission.

Although the route of transmission
remains tmclear, cattle are usually isolated

Clinical Findings: Infected cattle often
and protected from biting insects and ticks
show no clinical signs other than a few cysts
to reduce transmission, and then treated
in the scleral coajunctiva or a localized, scaly,
symptomatically. In some countries, cattle
papular dennal change. Illness begins with
are in1111Wlized with a live, tissue culturefever followed by wann, painful swellings adapted vaccine. Chemotherapy remains
ventrally (anasarca). Swollen lymph nodes,
very linlited and only minimally effective.

diarrhea, anorexia, photophobia, rhinitis, and

Both antin1ony and sulfanilan1ide complex
orchitis also are seen. Anasarca gives way to
prevented cyst development by B besnoiti
sclerodermatitis. The skin becomes hard,
in rabbits, and oxytetracycline may have
thick, and wrinkled and develOP!i cracks that
some therapeutic value if given early in the
allow secondary bacterial infection and
disease course. Clindamycin has been used
myiasis to develop; movement is painful.

to treat cats, but this has no positive effect

There is loss of hair and epidennis. In
on the stages present in other animals.

addition to the skin lesions, there may be

Ponazuril has been found to be generally
focal, disseminated myositis, keratitis,
ineffective in infected donkeys.

CHLAMYDIOSIS

Bacteria of the order Chlan1ydiales are
organism can infect any eukaryotic host
ubiquitous, obligate intracellular gramcell, resulting in various infections.

negative bacteria. Within the host cell, they

Chlamydia! taxonomy with two genera,
replicate via a unique developmental cycle

Chlamydia and Chlamydophila, was
competing with the host for intracellular
proposed in 1999 but is no longer valid. A
nutrient pools. Virtually any chlamydia!

single genus, Chlamydia, is now used, as

CHLAMYDIOSIS

599
well as nine species (abortus, caviae,felis,

Transmission and Zoonotic Risk:

muridarum, pecorum, pneumoniae,

Recent studies indicate that host specificity
psillaci, suis, and trachomalis ). Genome of different species is not as cleat· as
comparison revealed a high level of
previously thought. Most members of the
sequence conservation and synteny across
genus Chlamydia have shown to be

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taxa with the major exception of the human
transmissible an10ng species, including
pathogen C trachomatis. Two additional
people. Zoonotic transmission from animals
new species have been discovered recently,
to people is well known for C psittaC'i,
ie, C avium and C gallina.cea.

C abortus, and C felis. Conversely, chlamydia! species of people have been

Etiology and Epidemiology: 'Iradidetected in numerous animal species.

tional classification of chlanwdiae was

'Iransmission of avian C psittaci strains
based on host and/or disease association,
to people may result in atypical pneumonia
without a high degree of consistency.

or even life-threatening acute illness (ie,

Different efficiencies in infectivity and
psittacosis in people). Trat1Smission
replication determine consistent, but not
between companion parrots and dogs or
absolute, associations between chlamydia!

cats, respectively, has also been associated
strain, host, and disease manifestation. The
with clinical cases. Fmthennore, C psittaci

Chlamydia species known so far were
has been found in numerous other
traditionally attributed to their main hosts.

manu-nalian species ( eg, cattle, swine,

C abortus (formerly C psittaC'i serotype 1) horses, small run1inants, rodents, wildlife).

is an agent causing primaiily abortion in

An association between C psittaci
small ruminants, mainly sheep ( ovine
genotypes with host species has recently
enzootic abo1tion, now ovine chlamydiosis;
been detected, but tl1e pathogenetic
seep 1338) and goats (seep 1340). C caviae relevance as well as the zoonotic potential
was found in guinea pigs and was related to
of non-avian C psillaci strains have yet to ocular and urogenital infections. C felis is be defined.

associated with acute or chronic cor\junctivi

C abortus may cause abortion and fetal
tis (seep 506), rhinitis, and bronchopneumodeath in pregnant women after transmission nia in both stray and domestic cats.

from goats or sheep. It has also been found

C muridarum was isolated from a mouse
in other animals (cattle, swim', wild suic1aP,
colony with pneun1onia Infections with
horses, and birds). Zoonotic risks resulting

C pecorum are ubiquitous in cattle herds
from these hosts and the role of this
with multiple organ manifestations (see also
patl10gen in these hosts are unknown.

ABORTION IN LARGE ANIMALS, p 1332). C pneumo

Natural transmission of C felis mostly
niae is a respiratory pathogen in people and occurs through close contact with other
is involved in community-acquired respirainfected cats, their aerosol, and fomites, b9t tory tract infections as well as exacerbations
the pathogen has also been found in dogs.

of clu-onic obstructive airway diseases.

With respect to people, there is clear

C psittaci is the causative agent of avian
evidence that C felis acquired from cats
chlamydiosis (seep 2808), fonnerly called
may occasionally cause keratocor\juncpsittacosis or omithosis in psittacine birds or tivitis. Reports are rare, attributing this
poultry/fowl, respectively. In swine, C suis
pathogen to serious systemic disease or

(former porcine serovar of C trachomatis)

atypical pneumonia.

is the most prevalent chlatnydial agent that

The known hwnan pathogen C pneumo
might be involved in multiple infection sites
niae was detected in cats with cor\junctiviof the body. C trachomatis causes a variety tis and also infects koalas, horses, and frogs.

of diseases in people, such as trachoma,

C trachomatis, the other human pathogen,
mogenital infection, and lyrnphogranuloma
was found in pigs and birds so far.

venereum. With respect to the two new

The risk of zoonotic transmission of other
species, C avium has a!Teady been identified chlamydia! species found in numerous as a pathogen in pigeons and in psittacines,
animal species beside their main hosts,
whereas the role of C gallinacea in poultry including the two new species C avium and
has yet to be defined.

C gallinacea, has yet to be defined.

With the availability of molecular
diagnostic tools, the presence of chlamydiae

Clinical Findings: Chlamydia! infections
has been frequently noticed in clinically
do not present a typical clinical pictlffe. In
inconspicuous anin1als (pets and farm
general, they affect multiple organs and can
anin1als). Epidemiologic data indicate that
generate a variety of clinical manifestations,
chlamydia! infections are disseminated
ranging from acute to chronic inflanu-nation
worldwide, but the epidemiologic imporand from a severe to a mild or even tance of these findings is still unknown.

subclinical course. Because aerosol

600

CHLAMYDIOSIS
transmission of the pathogen is one of the

C abortus in equine recurrent airway
main infection routes, the respiratory
obstruction as trigger factors of inflai11-
system is often involved.

mation or indicators of severe disease.

In birds, avian chlamydiosis is accompa

Based on serologic data, most chlan1ydiaJ
nied by coajunctivitis, serositis, fib1inoperiinfections ill farm aninlaJs do not necessaiily VetBooks.ir
carditis, hepato- or splenomegaJy, anemia,
result ill clinical illness. However, they may
and leukocytosis or monocytosis. Dogs
lead to chronic -persistent or recurrent
infected by C psittaci (most likely transmitchlai11ydiaJ infections on a subclinicaJ level.

ted from birds) present a clinical picture of

Because of the potential role of chlamydiae as
bronchopnetm1onia that may include fever
bystanders, copathogens, or etiologic agents
and dry cough, but also keratocor\junctivitis,
of latent persisting illfections, clinically

GI signs (vomiting, diarrhea), and even
illapparent chlamydial illfections are
neurologic signs. In cats, infections with
probably economically more ill1po1tant than

C felis clinically result in rhinitis, coajunctirare outbreaks of severe chlamydia] disease.

vitis, and/or bronchopneun1onia, but
seropositive cats are often asymptomatic.

Lesions: Acute pulmonary lesions

Lambs delivered by ewes with C ahortus
include bronchiolitis, severe focal
infection may develop acute chlamydia]

pnew11onia, and dystelectases. Disseminapnetm1onia. They become feb1ile, lethargic, tion of chlan1ydiaJ bodies in lung tissue is
and dyspneic and develop a serous and later
usually accompanied by an influx of
mucopuru.lent nasal discharge.

macrophages, granulocytes, and activated

In cattle and pigs, chlamydia] infections

T cells. Pulmonary edema may occur.

must be regarded as widespread but often

Disturbances in gas exchange and acid-base
w1derdiagnosed. Chlamydiae detected so
status (hypoxemia and/or respiratory
far in cattle herds include ma.in.ly C
acidosis) or even acute respiratory distress
pecorum, but also C abortus, C psillaci, are attributed to multiple disorders in
and C suis. In pig herds, C suis dominates, pulmonary functions.

but C psillaci, C abortus, C perorum, and

Bronchoil1terstitiaJ pneumonia and
even C trachomatis have been found in
alveoli tis may be accompanied by
parallel. Mixed infections a.re common in
progression to type II pnew11ocyte
herds and even in individual aninlaJs.

hyperplasia and interstitial thickening due

Clinical pictures of bovine and porcine
to illgress of mixed inflanunatory cells.

chla.mydioses are highly variable, although

Lyrnphocytic aggregates are frequently seen
most infections remain clinically inapparai·ound airways and pulmonary vessels.

ent. Cun-ent knowledge suggests these

In chronic ( often subclinicaJ) chlamydia]

infections manifest clinically when they
infections, macroscopic exa.Illination of the
coincide with additional 1isk factors. In
respiratory tract reveals only mild lesions
acute infection, clinical symptoms include
or a few foci of a.telectasis, predominantly
fever and depression. Respiratory disorders
affecting the apical lobes. Histologic lesions
may affect upper airways as well as the
may include neutrophi.l inflanunation, folliculower respiratory tract and result in lai· bronchiolitis, and active lymphoid tissues
pneumonia with the typical signs (nasal

(tonsils, tracheobronchiaJ and pulrnonaiy
secretions, dry hacking cough, and
lymph nodes, etc). Both activated bronchusdyspnea). In reproducing cows and sows, a.ssociated lymphoid tissue of bronchioles
ch.lamydiaJ infections might be associated

(bronchiolar cuffing) and hyperplastic
with abo1tion, disorders in fertility, and
bronchial and bronchiolar epithelium
mastitis. Other disease manifestations of
contribute to chronic small airway obstrucacute chlamydiosis include enteritis and tion and persistent airflow limitation.

diarrhea., polyaithritis (seep 1065),
kera.tocoajunctivitis, encephaJomyelitis

Diagnosis: Neitl1er clillicaJ signs nor

(seep 1308), pericai·ditis, or hepatitis. In lesions allow a definitive diagnosis of
chlamydia-positive herds, newborns are
chlan1ydiosis. Detection of Chlamydia
free of chlamydiae but stait to acquire
species is not part of routine veterinary
chlai11ydiaJ infections within 2 wk of bilth.

bacteriologic diagnosis, and infections

Thus, young anil11aJs develop more clinical
caused by these intracellular pathogens
signs than older ones.

have long been underestil11ated because

Equine chlai11ydiosis has been desc1ibed
of the requi.i·ement for special laboratory
as variable. Bronchopneun1onia may be
facilities. Isolation of the pathogen st1ictly
accompanied by abortions in mares,
depends on cell culture techniques.

polyarthritis in foals, hepatitis, and fatal

Confirmation of chlamydia] infection
cases of encephaJomyelitis. Recent data
requires collection of an appropriate clinical
indicate a role of C psittaci and/or
sample from the aninlaJ, followed by direct

CLOSTRIDIAL DISEASES

601
detection of the organism using a suitable
elicits ste1ilizing immunity and virtually 100%
diagnostic test. In vivo, swabs (nasal,
protection from disease does not apply to
ocular, rectal, vaginal), tracheal washing,
chlamydiae. However, therapeutic vaccinaor bronchoalveolar lavage fluid are useful.

tion may neve1theless provide substantial

Chlamydia! inclusion bodies may be
health and economic benefits. To prevent

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detected in affected tissues. Appropriate
abortion in small ruminants, C abortus live tests include direct impression smears and
vaccines are available. There is, however, an
cytologic staining, cell culture isolation of
ongoing and controversial discussion
the agent, immunofluorescence tests, and
whether the vaccine strain might even be
nucleic acid amplification-based tests
involved in enzootic abortion. Vaccines

(PCR and microarray techniques).

against C Jelis are available for pet cats, but Because most chlamydia! infections do not little has been repo1ted about their efficacy.

elicit sufficiently high changes in antibody

Several antimicrobials ( eg, tetracyclines,
levels, serologic detection is generally more
quinolones, macrolides, lincosamides,
suitable for prevalence surveys than for
rifamycins) can inte1fere with chlamydia!

the retrospective diagnosis of chlamydia!

replication. Tretracyclines or fluoroquinoinfection. Species-specific serologic tests lones ( eg, enrofloxacin) are generally the
are still lacking. Most commercially available
dlugs of choice. Treatment must start as

ELlSA methods may detect infections
early as possible and continue for at least
caused by tl1e family Chlamydiaceae but do

7clays.

not differentiate between chlanwdial species.

No antibiotic treatment for chlan1ydiae is

Sensitivity and specificity of tl1ese serologic
bactericidal. It is suspected iliat antibiotics
tests are much lower than direct detection
frequently induce persistent chlamydia!

of the antigen by PCR.

infections by reducing antichlamydial
immunity clue to suppression of antigen

Prevention and Treatment: The classic
production while not completely eliminatconcept of prophylactic inmmnization that ing chlamydiae.

CLOSTRIDIAL DISEASES

Clostridia are relatively large, anaerobic,
constant weat to successful livestock
sporeforming, rod-shaped, gram-positive
production in many parts ofilie world.

organisms. They are found either as living

Clostridial diseases can be divided into
cells (vegetative fonns) or as dom1ant
two categories: 1) those in which the
spores. Their natural habitats are soils
organisms actively invade or when locally
and intestinal tracts of anin1als, including
dom1ant spores are activated and repropeople. Dormant spores of several duce in the tissues of the host, with the
clostridial species have been found in
production of toxins that enhance the
healthy muscular tissue of horses and
spread of infection (the gas-gangrene group,
cows. The endospores are oval, sometimes
the clostridial cellulitides group); and
spherical, and are located centrally,

2) those characterized by toxemia resulting
subtem1inally, or tenninally. The vegetative
from the absorption of toxins produced by
fom1s of clostridia in tissue fluids of
organisms within ilie digestive system (the
infected animals occur singly, in pairs, or
enterotoxemias), in devitalized tissue
rarely in chains. Differentiation of the

(tetanus), or in food or canion outside the
various pathogenic and related species is
body (botulism). Clostridial diseases are not
based on cultural characte1istics, spore
spread from anin1al to anin1al.

shape and position, biochemical reactions,
and ilie antigenic specificity of toxins or
surface antigens. The genomes of many

BACILLARY HEMOGLOBINURIA
clostridia have been sequenced and are
available online. Pathogenic strains or their

(Red water disease)

toxins may be acquired by susceptible

Bacillary hemoglobinuria is an acute,
animals by eitl1er wound contamination or
infectious, toxemic disease caused by
ingestion. Diseases thus produced are a

Clostridium haemolyticum. It affects

602

CLOSTRIDIAL DISEASES
primarily cattle but has also been found in
tentative diagnosis. The most striking sign is
sheep and rarely in dogs. It occurs in the
the typical port-wine-colored urine, which
western part of the USA, along the Gulf of
foains freely when voided or on agitation.

Mexico, in South America, Great Britain, the The presence of the typical liver infarct is Middle East, India, Japan, and other parts of
sufficient for a prestm1pti.ve diagnosis. The

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the world.

normal size and consistency of the spleen
serve to exclude anthrax and anaplasmosis.

Etiology: C hae1nolyticu1n is a soilborne Bracken fern poisoning and leptospirosis
organism naturally fotmd in the GI tract of
also should be considered. Diagnosis can be
some cattle. It can survive for long periods
c011.fim1ed by isolating C haemolyticum from in contaminated soil or in bones from
the liver infarct, but the organism is difficult
carcasses of infected animals. After
to culture. Rapid and accurate diagnosis can
ingestion, latent spores ultimately become
be made by demonstrating the organism in
lodged in the liver. The incubation petiod is
the liver tissue by a fluorescent anti.body or
extremely vaiiable, and onset depends on
in1munohistochemical test or by demonstratthe presence of a locus of anaerobiosis in ing the toxin in the fluid in the peritoneal
the liver. Such a nidus for germination is
cavity or in a saline extract of the infai·ct.

most often caused by liver fluke (Fasciola

PCR has also been used to diagnose clinical
hepatica) infection, rarely by high nitrate bacillary hemoglobinuria in a cow in Japan.

content of the diet, accidental liver
puncture, liver biopsy, or any other cause

Control: Early treatment with penicillin
of localized necrosis. When conditions for
or tetracyclines at high doses is essential.

anaerobiosis ai·e favorable, the spores

Whole blood transfusions ai1d fluid therapy
germinate, and the resulting vegetative
also are helpful early in the disease.

cells multiply and produce 13 toxin (phos

C haemolyticum bacterin prepared from
pholipase C). This causes intravascular
whole cultures confers immunity for -6 mo.

hemolysis, resulting in hemolytic anemia

In areas where the disease is seasonal, one
and hemoglobinuria.

preseasonal close is usually adequate; where
the disease occurs throughout the year,

Clinical Findings: Cattle may be found
semiat111ual vaccination is necessary. Cattle
dead without premonitory signs. Usually,
in contact with aninlals from areas where
there is a sudden onset of severe depression, this disease is endemic should be vaccifever, abdominal pain, dyspnea, dysentery, nated, because the latter may be carriers.

and hemoglobinuria. Anemia and jaundice
are present in varying degrees. Edema of the

BIG HEAD
brisket may occur. Hgb and RBC levels are
quite low. The duration of clinical signs

(Swollen head)

varies from -12 hr in pregnant cows to

-3---4 days in other cattle. Mortality in

Big head is an acute, infectious disease,
untreated animals is -95%. Some cattle
caused by Clostridium novyi, C sordellii,
suffer from subclinical attacj<s of the disease or rarely C chauvoei, characterized by a and thereafter act as intrnune carriers.

nongaseous, nonhemorrhagic, edematous
swelling of the head, face, and neck of young

Lesions: Dehydration, anemia, and
rams. Tilis infection is initiated in yow1g rains
sometimes subcutai1eous edema ai·e seen.

by fighting or continual butting of one

There is bloody fluid in the abdominal and
another. It has also been associated with
thoracic cavities. The lungs are not grossly
tl1e practice of dipping immediately after
affected, and the trachea contains bloody
shearing. The bruised and battered
froth with hemorrhages in the mucosa TI1e
subcutaneous tissues provide conditions
small intestine and occasionally U1e Jai·ge
suitable for growth of patl10genic clostridia,
intestine are hemorrhagic; their contents
and the breaks in the skin offer an opportuoften contain free or clotted blood. An nity for their entrance. Treatment is with
ischemic infarct in the liver is characteristic;
broad-spectrwn antibiotics or penicillin.

it is slightly elevated, lighter in color than the
surrounding tissue, and outlined by a bluish
red zone of congestion. The kidneys ai·e dark,

BLACKLEG
friable, and usually studded with petechiae.

Blackleg is an acute, febrile, highly fatal

The bladder contains purplish red urine.

disease of cattle and sheep caused by

After death, rigor morti.s sets in quickly.

Clostridium chauvoei and characterized
by emphysematous swelling, commonly

Diagnosis: The general clinical picture
affecting heavy muscles ( clostridial
and postmortem findings usually permit a
myositis). lt is found worldwide.

CLOSTRIDIAL DISEASES

603

Etiology: C chauvoei is found naturally edema. The lesions may be seen in any
in the intestinal tract of animals. Spores
muscle, even in the tongue or diaphragm. In
remain viable in the soil for years and are
sheep, because the lesions of the spontanepurported to be a source of infection.

ously occurring type are often small and

Outbreaks of blackleg have occurred in
deep, they may be overlooked. Occasionally,

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cattle on farms in which recent excavailie tissue changes caused by C septicum, tions have occurred or after flooding. The

C novyi, C sordellii, and C pmjringens may organisms probably are ingested, pass
resemble those of blackleg. At times, both
through the wall of the GI tract, and after

C septicum and C chauvoei may be isolated gaining access to the bloodstream, are
from blackleg lesions, particularly when the
deposited in muscle and other tissues
carcass is examined <!24 hr after death,

( spleen, liver, and alimentary tract) and
which allows time for postmortem invasion
may remain donnant indefinitely.

of the tissues by C sordellii. Field diagnoses In cattle, blackleg infection is endogare confirmed by laboratory demonstration enous. Lesions develop without any history
of C chauvoei in affected muscle ( standard of wounds, although bruising or excessive
methods: culture and biochemical identificaexercise may precipitate disease in some tion). The samples of muscle should be
cases. Commonly, the animals that contract
taken as soon after death as possible. The
blackleg are of the beef breeds, in excellent
fluorescent antibody test for C chauvoei is health, and gaining weight. Outbreaks occur rapid and reliable. A PCR is available and in which a few new cases are found each
reported to be very good for clinical san1ples
day, sometimes for several days. Most cases
but not for environmental san1ples.

are seen in cattle from 6---24 mo old, but
thrifty calves as young as 6 wk and cattle as

Control: A multivalent vaccine containing
old as 10-12 yr may be affected. The disease

C chauvoei, C septicum and, where needed,
usually occurs in sununer and fall and is

C novyi antigens is safe and reliable for
uncommon during the winter. Interestingly,
cattle and sheep. Calves 3-6 mo of age
in sheep, the disease is almost always the
should be vaccinated twice, 4 wk apart,
result of a wound infection and often
followed by annual boosters before the
follows some fonn of injury such as
anticipated danger period ( usually spring
shearing cuts, docking, crntching, or
or early summer). In an outbreak, all
castration. The case fatality rate approaches susceptible cattle should be vaccinated and 1000/o. In New Zealand, blackleg is seen more treated prophylactically with penicillin frequently in sheep.

(10,000 JU/kg, IM) to prevent new cases for
as long as 14 days. Cattle should be moved

Clinical Findings and Lesions: Usually,
from affected pastures. Vaccine failure has
onset is sudden, and a few cattle may be
been observed locally and attributed t9 a
found dead without premonitory signs.

deficient spectrun1 of antigens in the

Acute, severe lameness and marked
vaccine. In such instances, a bacterin
depression are common. Initially, there is
vaccine is produced with local, previously
a fever but, by the time clinical signs are
identified clostridial strains of C chauvoei.

obvious, body temperature may be nom1al

Naive ewes should be vaccinated twice
or subnormal. Characteristic edematous

1 mo before lambing and then with yearly
and crepitant swellings develop in the hip,
boosters. In outbreaks in flocks of ewes,
shoulder, chest, back, neck, or elsewhere. At
prophylactic penicillin and antisernrn
first, tl1e swelling is small, hot, and painful. As treatments are recommended. Young sheep the disease rapidly progresses, the swelling
should be vaccinated before going to
enlarges, there is crepitation on palpation,
pasture. Immunity in young sheep is
and the skin becomes cold and insensitive
relatively short. Clostridial vaccines are
with decreased blood supply to affected
reported to create a weaker inunune
areas. General signs include prostration and
response in sheep and goats than in cattle.

tremors. Death occurs within 12--48 hr. In

Carcasses should be destroyed by burning
some cattle, the lesions are restricted to the
or buried deeply in a fenced-off area to limit
myocardiwn and the diaphragm.

heavy spore contamination ofilie soil.

Diagnosis: A rapidly fatal, febrile disease
in well-nourished young cattle, particularly

INFECTIOUS NECROTIC HEPATITIS
of the beef breeds, wiili crepitant swellings
of ilie heavy muscles suggests blackleg. The

(Clostridium novyi infection, Black disease) affected muscles are dark red to black and

Infectious necrotic hepatitis is an acute
dry and spongy, have a sweetish odor, and
toxemia of sheep that is sometimes seen in
are infiltrated with small bubbles but little
cattle and is rare in pigs and horses.

604

CLOSTRIDIAL DISEASES

Etiology and Pathogenesis: The
flukes, or by otherwise reducing the
etiologic agent, Clostridium novyi type B,
fluke infection of sheep. However, these
is soilbome and present in the intestines
procedures a.re not always practical, and
and livers of herbivores; it may be present
active in1munization with C novyi aluminw11-VetBooks.ir
on skin surfaces and dormant in muscles
precipitated toxoid seems more effective
and is a potential source of wow1d
and can be also perfonned during outbreaks.

infections. Fecal contanlination of pasture

Longterm in1munity is produced by one
by carrier anin1als is the most important
vaccination. After this, only new introducsource of infection. The organism multitions to the flock (lambs and sheep brought plies in areas of liver necrosis caused by
in from other areas) need to be vaccinated.

migration of liver flukes and produces a

This is best clone in early sununer. Pasture
powerful necrotizing toxin (Of.toxin). The
contanlination can be rnininuzed by proper
disease is distributed worldwide, wherever
disposal of carcasses (bwTiing).

sheep and liver flukes are both found, and is
increasing in cattle where liver flukes are

MALIGNANT EDEMA
accidentally introduced.

C novyi has been suspected but not yet

Malignant edema is an acute, generally fatal
confim1ed as a cause of sudden death in
toxemia affecting all species and ages of
cattle and pigs fed high-level grain diets, and
anin1als and is usually caused by Clostrid
in which preexisting lesions of the liver
ium Se'J)ticum. Other clostridial species
were not detectable. The lethal and
have been isolated, indicating mixed
necrotizing toxins damage hepatic
infections. Additional clostridia in1plicated
parenchyma, thereby pem1itting the
in wound infections include C chauvoei,
bacteria to multiply and produce a lethal

C pe1fringens, C novyi, and C sordellii.

amount of toxin.

The disease occurs worldwide.

Clinical Findings: Usually, death is

Etiology and Pathogenesis: C se'J)ti
sudden with no well-defined signs. Affected
cum is found in soil and intestinal contents
animals often are 2-4 yr old, tend to lag
of anin1als throughout the world. Infection
behind the flock, asswne sternal recwnordinaiily occurs through contamination of bency, and die within a few hours. Most
wounds containing devitalized tissue, soil,
cases occur in the sun1111er and early fall
or some other tissue debilitant or through
when liver fluke infection is at its peak. The
activation of dormant spores. Wounds
disease is most prevalent in well-nowished
caused by accident, castration, docking,
adult sheep and seems to be limited to
insanitaiy vaccination, and parturition may
anin1als infected with liver flukes. Diffe1°
become infected. Potent clostridial toxins
entiation from acute fascioliasis may be
cause local and systemic signs, often
difficult, but peracute deaths of anin1als that
resulting in death. Local exotoxins cause
show typical lesions on necropsy should
excessive inflai11mation, resulting in severe
arouse suspicion of infectious necrotic
edema, necrosis, and gangrene. Risk factors
hepatitis.

include IM injections in horses; sheaiing,
docking, and lan1bing in sheep; and

Lesions: The most characte1istic gross
traun1atic parturition and castration in
lesions are grayish yellow, necrotic foci in
cattle. Horses and probably cows have
the liver along migratory tracks of the yow1g dmmant spores present_ in muscle tissues.

flukes. Histologically, the liver lesions
include central eosinophilic inflanm1ation

Clinical Findings: General signs, such as

(fluke induced) surrounded by coagulation
anorexia, intoxication, and high fever, as
necrosis with an outer rin1 of neutrophils.

well as local lesions, develop within 6-48 hr

The lesion is positive for gram-positive rods.

after predisposing ir\jwy or activation of

Other common findings are an enlarged
dom1ant spores. The local lesions are soft
pe1ica.rdial sac filled with straw-colored
swellings that pit on pressure and extend
fluid and excess fluid in the peritoneal and
rapidly because of the fom1ation of large
thoracic cavities. Usually, there is extensive
quantities of exudate that infiltrate the
rupture of the capillaries in the subcutanesubcutaneous and intranmscular connecous tissue, which causes the adjacent skin tive tissue of the affected areas. The muscle
to twn black (hence the common name,
in such areas is dark brown to black.

black disease).

Accwnulations of gas in subcutaneous
tissue and along muscle fascias may or may

Control: The incidence may be lowered
not be present. These muscle infections are
by reducing the nwnbers of Lymnaea spp
extremely painful, and systemic toxemia
snails, the intermediate hosts for the liver
may evolve. Extensive local sloughing of

CLOSTRIDIAL DISEASES

605

C chauvoei in a blackleg/malignant edema
vaccine and is available in multivalent
vaccines. In endemic areas, animals should
be vaccinated before they are castrated,
dehomed, or docked. Calves should be

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vaccinated at -2 mo of age. Two doses 2-3 wk
apart generally give protection. In high-risk
areas, annual vaccination is indicated, as is
revaccination after severe trauma

Treatment with high doses of parenteral
penicillin, tetracyclines, or broad-spectrum
antibiotics is indicated early in the disease.

Clostridial myonecrosis due to C perfringens

Although injection of penicillin directly into
type A in a horse. Courtesy of Dr. Henry Stampf/i.

the periphery of the lesion may minimize
spread of the lesion, the affected tissues
usually slough. Supportive therapy with

NSAIDs (flunixin meglunline for cattle and
horses) is recommended. Local treatment
skin and tissues is often seen in progressed
includes surgical incision of skin and fascia
states of malignant edema. Severe edema of
to allow drainage. Animals with systemic
the head of rams develops after infection of
toxic signs will need supportive treatments
wounds inflicted by fighting. Malignant
such as IV perfusion.

edema associated with lacerations of the
vulva at parturition is characterized by
marked edema of the vulva, severe toxemia,

BOTULISM
and death in 24--48 hr.

(Lamziekte)

Diagnosis: Sinularity to blackleg (see

Botulism is a rapidly fatal motor paralysis
p 602) is marked, and differentiation made
caused by ingestion of the toxin produced
on necropsy is unreliable; laboratory
by Clostridium botulinum types A-G.

confirmation is the only certain proce

The spore-fomling anaerobic organism
dure. Horses and pigs are susceptible to
proliferates in decomposing animal tissue
malignant edema but not to blackleg. An
and sometimes in plant material.

important differential diagnosis in these
species is anthrax (seep 593).

Etiology: Botulism is in most cases an

C septicum also causes braxy in sheep, intoxication, not an infection, and results
a highly fatal infection characterized by
from ingestion of toxin in food. There are
toxemia and inflammation of the abomasal
seven types of C botulinmn, differen'tiated wall. This disease seems to be confined
on the antigenic specificity of the toxins: A,
mostly to European sheep fed on "frosted"

B, C1, D, E, F, and G. Types A, B, and E are
pasture.

most important in people; C, in most animal

Diagnosis can be confirmed rapidly on
species, notably wild ducks, pheasants,
the basis of fluorescent-antibody staining of
chickens, mink, cattle, and horses; and D in

C septicum from a tissue smear. However,
cattle. In horses, the most common type in

C septicum is an extremely active post

North America and Europe is type B (>85%
mortem invader from the intestine, and its
of USA cases), and in the western USA type
presence in a specimen taken from an

A has been reported in only two outbreaks,
animal that has been dead for �24 hr is not
both in people, known to have been caused
significant. PCR can be used for direct
by type F. Type G, isolated from soil in
identification and differentiation of

Argentina, is not known to have been
clostridia associated with malignant edema.

involved in any outbreak of botulism. The

The presence of type ill echinocytes or
usual source of the toxin is decaying
spheroechinocytes in blood smears may
carcasses or vegetable materials such as
help diagnose immune-mediated hemolytic
decaying grass, hay, grain, or spoiled silage.

anemia associated with clostridial

Toxins of all types have the same pharmacoinfections in horses. Fine-needle aspirates logic action. Like tetanus toxin, botulinun1
and Gram stain may confu111 the presence
toxin is a zinc-binding metalloprotease that
of gran1-positive rods before confirmation
cleaves specific proteins in synaptic
by anaerobic culture.

vesicles. Motor neuron surface receptors
vary for the different botulinum toxins,

Control: Bacterins are used for inlmunizaexplaining some of the species differences tion. C septicum usually is combined with
in susceptibility to the different toxins.

606

CLOSTRIDIAL DISEASES

The exact incidence of botulism in
syndrome. Gastric ulcers, foci of necrosis
animals is not !mown, but it is relatively low
in the liver, abscesses in the navel and lungs,
in cattle and horses, probably more frequent wounds of the skin and muscle, and in chickens, and high in wild waterfowl.

necrotic lesions of the GI tract are

Probably 10,000-50,000 birds are lost in
predisposing sites for development of

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most years, with losses reaching 1 million
toxicoinfectious botulism. This disease of
or more during the great outbreaks in the
foals and adult horses appears to resemble
western USA. Most affected birds are ducks, "wound botulism" in people. Type B toxin is although loons, mergansers, geese, and
often implicated in botulism in horses and
gulls also are susceptible. (See also BOTULISM
foals in the eastern USA. Toxicoinfection is

IN POULTRY, p 2889.) Dogs, cats, and pigs are
also suggested as a cause of equine grass
comparatively resistant to all types of
siclrness ( equine dysautonomia, seep 1257).

botulinum toxin when challenged orally;

Botulism in mink usually is caused by
however, there are recent individual case
type C strains that have produced toxin in
reports mentioning botulism in dogs.

chopped raw meat or fish. Type A and E

Most botulism in cattle occurs in South
strains are occasionally involved. Botulism

Africa and South America, where a
has not been reported in cats but occurs
combination of extensive agriculture,
sporadically in dogs. Type C toxin is usually
phosphorus deficiency in soil, and
responsible, but there have been reports in

C botulinurn type D in animals creates
which type D was incriminated.

conditions ideal for the disease. The
phosphorus-deficient cattle chew any bones

Clinical Findings and Lesions: The
with accompanying bits of flesh they find on
signs of botulism are caused by flaccid
the range; if these can1e from an animal
muscle paralysis and include progressive
carrying type D strains of C botulinurn,
motor paralysis, disturbed vision, difficulty
intoxication is likely to result. Any animal
in chewing and swallowing, and generalized
eating such material also ingests spores,
progressive paresis. Death is usually due to
which germinate in the intestine and, after
respiratory or cardiac paralysis. The toxin
death of the host, invade the musculature,
prevents release of acetylcholine at motor
which in tum becomes toxic for other
endplates (neuromuscular jtmction).

cattle. Type C strains also cause botulism

Passage of impulses down the motor
in catUe in a sin1ilar fashion. This type of
nerves and contractility of muscles are
botulism in cattle is rare in the USA,
not hindered. No characteristic gross and
although a few cases have been reported
histologic lesions develop, and pathologic
from Texas under the name ofloin disease,
changes may be ascribed to the general
and a few cases have occurred in Montana.

paralytic action of toxin, particularly in the

Hay or silage contaminated with toxinmuscles of the respiratory system, rather containing carcasses of birds or mammals
than to the specific effect of toxin on any
and poultry litter fed to cattle have also
particular organ.

been sources of type C or type D toxin for

Epidemics have occurred in dairy herds
cattle ("forage botulism"). Big bale silage in which up to 65% of adult cows developed
and haylage seem to be a particwar risk and
clinical botulism and died 6-72 hr after the
result in botulism problems if fermentation
onset of recun1bency. Major clinical findings
fails to produce a low and stable pH ( <4.5).

included drooling, decreased tongue tone,

Botulism in sheep has been encow1tered in
dysphagia, inability to urinate, and sternal

Australia, associated not with phosphorus
recwnbency that progressed·to lateral
deficiency as in cattle, but with protein and
recumbency just before deat11. Skin
carbohydrate deficiency, which results in
sensation is usually nonnal, and withdrawal
sheep eating carcasses of rabbits and other
reflexes of the limbs are weak. Initially,
small anin1als found on the range. Botulism
clinical signs resemble second-stage
in horses often results from forage
partwient paresis (seep 988), but the cows
contan1inated with type C or D toxin. In six
do not respond to parenteral calciwn
out of eight outbreaks of equine botulism
therapy.

associated with type A, the source of

Reported clinical signs in horses are very
infection was confirmed to be hay or silage.

sin1ilar, with progressive muscle paresis,

Toxi coinfec tious botulism is the name
recwnbency, dysphagia, and decreased
given the disease in which C botulinurn
muscle tone (tail, tongue,jaw), respiratory
grows in tissues of a living animal and
distress, and death.

produces toxins there. The toxins are

In the shaker foal syndrome, foals are
liberated from the lesions and cause typical
usually <4 wk old. They may be found dead
botulism. This has been suggested as a
without premonitory signs; most often, they
means of producing the shaker foal
exhibit signs of progressive syn11netric motor

CLOSTRIDIAL DISEASES

607
paralysis. Stilted gait, muscular tremors, and

CLOSTRIDIUM DIFFICILE AND
the inability to stand for >4-5 min are salient

C PERFRINGENS INFECTIONS
features. Other clinical signs include
dysphagia, constipation, mydliasis, and

Clostridium difficile is a large, gram-posifrequent mination. As the disease progresses, tive, anaerobic, spore-forming motile rod VetBooks.ir
dyspnea with extension of the head and
and is the major cause of antibiotic-associneck, tachycardia, and respiratory arrest ated colitis in people. C difficile-associ
occur. Death ensues most often 24-72 hr
ated diarrhea and disease develops
after the onset of clinical signs due to
spontaneously in a variety of other species
respiratory failure. The most consistent
including horses, pigs, calves, dogs, cats,
necropsy findings are pulmonary edema and
han1sters, guinea pigs, rats, and rabbits.

congestion and excessive pericardia! fluid,

C difficile produces protein toxins A, B, ancV
which contains free-floating strands of fibrin.

or the binary toxin CDT in the intestine.

Toxin A is an enterotoxin that causes

Diagnosis: Although sporadic cases of
hypersecretion of fluid into the intestinal
botulism often are suspected because of the
lun1en and also causes tissue dan1age.

characteristic motor paralysis, it is difficult

Toxin B is a potent cytotoxin that induces
to establish the diagnosis by demonstrating
inflanunation and necrosis. The mechanism
the toxin in anin1al tissues or sera or in the
of action of CDT is not known. Disruption
suspect feed. Commonly, the diagnosis is
of colonic micro flora together with the
made by eliminating other causes of motor
presence of toxigenic C dijj'icile strains
paralysis (flaccid paralysis). Filtrates of the
that overgrow in the intestines are the
stomach and intestinal contents should be
prerequisites for disease. Diagnostic tests
tested for toxicity in mice, but a negative
for C difficile toxins include cell cytoxicity answer is unreliable. Primary supportive
assays and ELISA on fecal san1ples,
evidence is provided by feeding suspect
anaerobic culture, and PCR to discrin1inate
material to susceptible animals. In peracute
between toxigenic and nontoxigenic
cases, the toxin may be detectable in the
strains. C p@:fringens is widely distributed blood by mouse inoculation tests but
in the soil and the GI tract of anin1als and is
usually is not detectable in the average
charactetized by its ability to produce
field case in fann animals. Use of ELISA
potent exotoxins, some of which are
methodology for detection of the toxin
responsible for specific enterotoxemias.

makes it feasible to test large munbers

Five types (A, B, C, D, and E) have been
of san1ples, increasing the chances of
identified and produce one or more of four
diagnosis confirmation. In toxicoinfectious
major toxins (alpha, beta, epsilon, and
botulism, the organism may be cultured
iota). C p@fringens type A is most conunon
from tissues of affected anin1als.

and the most variable strain in toxigenic
properties. Alpha toxin production is

Treatment and Control: Any dietary
associated with gas gangrene, traumatic
deficiencies in range animals should be
infections, avian and canine necrotic
corrected and carcasses disposed of, if
enteritis, colitis in horses, and diarrhea in
possible. Decaying grass or spoiled silage
pigs. C pmfringens types B and C cause
should be removed from the diet. Inmmnizasevere enteritides, dysentery, toxemia, and tion of cattle with types C and D toxoid has
high mortality in young lambs, calves, pigs,
proved successful in South Africa and
and foals (beta toxin). 'Iype C causes

Australia. Toxoid is also effective in
enterotoxemia in adult cattle, sheep, and
immunizing mink and has been used in
goats. The diseases are listed below, categopheasants.

rized as to cause and host.

Botulinmn antitoxin has been used for
treatment with varying degrees of success,
depending on the type of toxin involved

Clostridia-associated Enterocolitides
and the species of host. Treatment of ducks
in Horses
and mink with type C antitoxin is often

Clostridium dilf'icile and C pmfringens successful; however, such treatment is
have been implicated in this acute, sporadic
rarely used in cattle. Early administration of
disease of horses characterized by diarrhea
antitoxin (type B) specific or polyvalent to
and colic. Because of uncertainty about
foals before recmnbency (30,000 ill, IV) is
the etiology, the condition has also been
reported to be successful. Supportive care
referred to as idiopathic colitis, but there is
in valuable animals is essential; prognosis
now good evidence that these organisnu; are
is poor in recmnbent animals. In endemic
responsible for enterocolitis in horses in
areas (eg, Kentucky), vaccination with type
approximately 20%-30% of cases of acute

B toxoid appears to be effective.

diarrhea. (See also p 285.)

608

CLOSTRIDIAL DISEASES

Etiology: C difficile may be found in low the intestinal mucosa. Horses with anterior
concentrations in the feces of as many as
enteritis will mostly have hemorrhagic
lO"Aiof healthy horses. C difficile and duodenitis.

C perfringens organisms may be present in
soil or the environment and be ingested by

Diagnosis: Clinical features of the disease

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horses. The factors that t1igger disease are
ai·e sinlilar to those of acute salmonellosis
not well known, but it is presumed that

(seep 195), Potomac horse fever (see
some alteration in the nom1al flora permits
p 283), or monocytic ehrlichiosis. The
excessive multiplication of the bacteria,
identification of C pe'l:fringens as the cause which produce toxins capable of causing
of diarrhea in horses depends on demonstraintestinal damage and systemic effects.

tion of the presence of enterotoxin or the

Predisposing factors that have been
gene for CPE in the feces or intestinal fluid
suggested include change in diet and
and the absence of other likely etiologic
antibiotic therapy. Other host factors that
agents. Most C pe'lfringe'lis fow1d in the
may determine whether disease develops
intestine of horses lack the gene for CPE
include age, inununity, and presence or
expression. Large numbers of C perfringens
absence of intestinal receptors for the
in anaerobic fecal culture of horses with
clostridial toxins. Recent antibiotic therapy
diaJThea is not diagnostically significant.

is a common feature of the history of horses

The diagnosis of C difficile diarrhea is
with C dl(ju;ile-induced diarrhea Certain
suggested by a history of recent treatment
antibiotics, notably macrolides and especially with antibiotics and is supported by erythromycin ethylsuccinate, 13-lactam antibidemonstration of the presence of C difficile
otics, and trimethoprim/sulfonarnide, are
toxin A and/or B in a freshly passed or frozen
more likely than others to be associated with
fecal sample submitted to a laboratory using

C difficile colitis. Mares with foals that are a human ELISA validated in horses, with
being treated with erythromycin ethylsuccigood sensitivity and specificity. The toxin nate appear to be at high risk Elimination of
gene may be identified by PCR ribotyping.

roughage from the diet before surgery is also
reported to predispose to C cll(ju;ile colitis.

Control: Steps may be taken to reduce the

Acute diarrhea has been reproduced in
opportunity for C difficile infections in
healthy neonatal foals using C difficile spores horses. Proper isolation procedures and
and vegetative cell fomis. Acute anterior
infectious disease control should be applied
enteritis ( duodenitis-jejunitis, seep 285) has to high-risk horses receiving antibiotics.

also been associated with C difficile in a

The environmental load of C difficile spores case-control study.

may be reduced by surface disinfection with

C pe'ljhngens type A is believed to cause
spo1icidal disinfectants, and the spread
diarrhea by elaboration of an enterotoxin
may be reduced by hand washing and by

(CPE), which is released during sporulation
isolation of infectious horses and foals.

and stimulates intestinal epithelial cells to

There are no control measures available
secrete excess fluid into the lumen. A novel
for prevention of C perf1inge'lis-induced
necrotizing toxin, called 132, produced by
diarrhea. Oral metronidazole ( 15 mg/kg, tid)

some strains of C pe'ljhngenS, has recently is recommended for treatment of either of
been strongly associated with colitis in
these clostridial infections. Metronidazole
horses.

might be teratogenic, so its use should be
avoided if possible in pregnant mares.

Clinical Findings: Foals and adult horses
may be affected. Typically, there are signs of

Clostridium difficile in Swine
abdominal pain and diarrhea witl1 or without
blood. There may be abdominal distention,

Clostridium difficile has emerged as an
especially in cases of
inlportant cause of diarrhea in neonatal

C difficile-induced
diaiThea. Dehydration, toxemia, and shock
swine. In some studies, it has been identified
may develop, and the mortality rate is
as tl1e second most frequent cause of
variable. One or several animals on a faim
diarrhea in 1- to 7-day-old pigs. Mesocolonic
may be affected. Horses with anterior
edema is a characteristic feature of the
enteritis have associated severe recurrent
disease seen in almost all affected pigs, but
nasogastric reflux, fever, and malaise.

this lesion is not pathognomonic. Diagnosis
of the disease depends on detection of

Lesions: The characteristic lesion is a
toxins as desc1ibed for the disease in
necrotizing enterocolitis-typhlitis. There is
horses. Porcine, equine, bovine, and canine
severe loss of colonic and cecal mucosa!

C difficile isolates may show an antinlicroepithelial cells, hemorrhagic colitis and bial susceptibility profile overlapping tl1at of
typhlitis, and thrombosis in capillaries of
isolates from hwnan patients, raising tl1e

CLOSTRIDIAL DISEASES

609
possibility for interspecies transmission of
strains of other types. C perftingens

C difficile. Donmnt C dijficile spores have enterotoxin (CPE) is the principal toxin
been fow,d in meat of pigs and beef cattle.

involved in Cpeijringens foodbome illness

Some of the ribotypes isolated were similar
and is associated with nonfood borne
or identical to human pathogenic strains.

diarrheal disease in different animals.

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C perfiingens also produces a necrotizing

Clostridium difficile in Dogs
toxin associated with necrotic enteritis in

Cwstridium difficile has not been
poult1y (seep 2802) and dogs, colitis in
established as a p1imary pathogen in dogs.

horses, and diarrhea in pigs. C peifringens

However, human toxigenic C difficile strains type A is in1plicated in a rarely occurring
have been frequently isolated from rectal
hemorrhagic cliarThea in clogs and has been
swabs of dogs visiting hwnan patients in
associated with nosocomial and acquired
hospitals. Hw,1an ELISA for C difficile toxins acute and chronic diarrhea in clogs. The does not perfo1m well in dogs with diarrhea
acute form is characterized by a necrotic
and has poor sensitivity and specificity.

enteritis in which there is massive

Approximately lOOAi of asymptomatic dogs
destruction of the villi and coagulation
shed toxigenic C difficile in feces.

necrosis of the small intestine. Many lar·ge,
grar11-positive rods ar·e visible in fecal
smear·s, and large nwnbers of C perjringens

Clostridium difficile in Calves
type A are recovered on anaerobic culture

Clostridium difficile has been identified
of feces of dogs with acute diarrhea. Fecal
as a potential cause of diarrhea in yow,g
tests ar·e not useful in cletem1ining the cause
calves. The disease could not be reproduced of diarThea, however, because of a high in colostrwn-deprived neonatal calves with
nw,1ber of false-positive results. A
spores or vegetative cells. C difficile has commercial ELISA for CPE in dogs is quite
been fow,d in high prevalence in veal calves
specific. PCR for CPE gene expression in
early in the veal production process.

clogs is being evaluated. Type A strains from
pigs with diarrhea have produced entero

C/ostridium perfringens in Adult
toxin in vitro, and anti-enterotoxin

Cattle
antibodies in sows indicate that enterotoxin
is produced in vivo. Enterotoxin has also
ln the past few years, hemorrhagic bowel,
been demonstrated in the feces of pigs with
bloody gut, or jejw,al hemorrhage
diarrhea but not in feces of healthy aninlals.

syndrome has emerged sporadically in

C peij1ingens isolated from pigs with
individual, high-producing dairy cows in
diarrhea are typically nonenterotoxigenic
early lactation. Although no specific
but produce the cytotoxic 132 toxin, which
etiology has been established, it is assw,1ed
possibly plays a role in disease. Experimentl1at Clostridium perjringens type A is tal disease has been produced in pigs
involved, because large nw,1bers of this
challenged orally with C peijhngens type A.

clostridia may be recovered in most
cases. The clinical course is peracute,
with anorexia, colic, drop in milk yield,

Enterotoxemia Caused by C/ostridium
hemorrhage into the intestine, and sudden
perfringens Types B and C
death despite aggressive supportive and

Wection with C peifringens types B and C
surgical treatment. Gross postmortem
causes severe enteritis, dysentery, toxemia,
findings include severe hemorrhage and
and high mortality in yow,g lambs, calves,
necrosis in tl1e intestines. Prevention
pigs, and foals (see TABLE 1). Types Band C
consists of optinlizing nutritional manageboth produce tl1e highly necrotizing and ment and avoiding sudden feed changes.

lethal beta toxin responsible for severe

Autogenous vaccines in affected dairy herds intestinal damage. This toxin is sensitive to have been tried with anecdotal success.

proteolytic enzymes, and disease is
associated with inhibition of proteolysis in

ENTEROTOXEMIAS
the intestine. Sow colostrW11, which contains
a trypsin inhibitor, has been suggested as a

(C/ostridium perfringens infections)

factor increasing the susceptibility of yow,g

Enterotoxemia Caused by
piglets. Type C also causes enterotoxemia in
adult cattle, sheep, and goats.

C/ostridium perfringens Type A

Type A strains of C perfringens are

Clinical Findings: Lamb dysentery is an
commonly fow,d as part of the normal
acute disease of lan1bs <3 wk old. Many may
intestinal microflora of animals and lack
die before clinical signs are seen, but some
some of the powerful toxins produced by
newborn lan1bs stop nursing, become

610

CLOSTRIDIAL DISEASES

ENTEROTOXEMIA CAUSED BY CLOSTRIDIUM PERFRINGENS

TYPES BAND C

Disease

C perfringens Type

Host

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Lamb dysentery

TypeB

Lambs s3 wk old

Calf enterotoxemia

TypesBandC

Well-fed calves sl mo old

Pig enterotoxemia

TypeC

Piglets in first few days of life

Foal enterotoxemia

TypeB

Foals in first week of life

Struck

TypeC

Adult sheep

Goat enterotoxemia

TypeC

Adult goats
listless, and remain recumbent. A fetid,
animals of any age. It is most common in
blood-tinged diarrhea is common, and
lambs eitller <2 wk old or weaned in
death usually occurs within a few days. In
feedlots and on a high-carbohydrate diet
calves, there is acute diarrhea, dysentery,
or, less often, on lush green pastures. The
abdominal pain, convulsions, and opisthotodisease has been suspected in well-noui0
nos. Death may occur in a few hours, but
ished beef calves nursing high-producing
less severe cases suivive for a few days, and
cows grazing lush pasture and in sudden
recovery is possible. Pigs become acutely
death syndrome in feedlot cattle; however,
ill within a few days of birth and there is
supportive laboratory evidence in the latter
diarrhea, dysentery, reddening of the anus,
is lacking.

and a high fatality rate; most affected piglets
die within 12 hr. In foals, there is acute

Etiology: The causative agent is
dysentery, toxemia, and rapid death. Struck

C pe1J1ingens type D. Predisposing factors in adult sheep is cha.racte1ized by death
are essential, the most common being the
without premonitory signs.

ingestion of excessive amounts of feed or

Lesions: Hemorrhagic enteritis with
milk in the very young and of grain in
ulceration of the mucosa is the major lesion
feedlot lambs. In young lan1bs, the disease
in all species. Grossly, tl1e affected portion of usually is restricted to ewes with single the intestine is deep blue-purple and appears lambs, because ewes with twins seldom at first glance to be an inf!Lfction associated
give enough milk to allow enterotoxemia to
with mesenteric torsion. Smears of intestinal develop. In the feedlot, the disease usually is contents can be examined for large numbers
seen in lambs switched rapidly to high-grain
of gram-positive, rod-shaped bacteria, and
diets. As starch intake increases, it provides
filtrates can be made for detection of toxin
a suitable mediuin for overgrowth of C
and subsequent identification by neutralizapmjhngmis, producing epsilon toxin. The tion witll specific antisera.

toxin causes vascular damage, particularly
in capillaries of tlle brain. Many adult sheep

Treatment and Control: Treatment is
carry strains of C pmfringens type D as part usually ineffective because of the severity of
of their normal intestinal rnit:roflora, which
tlle disease but, if attempted, includes specific is the source of organisms that infect the hyperimmune sera and oral antibiotics. The
newborn. Most such carriers have
disease is best controlled by vaccination of
nonvaccinal antitoxin serum titers.

tlle pregnant dam during tlle last third of
pregnancy, initially witll two vaccinations

Clinical Findings: Usually, sudden deaths

1 mo apart and annually tllereafter. When
in tlle best-conditioned lambs are the first
outbreaks occur in newborn animals from
indication of enterotoxernia. In some cases,
unvaccinated dams, antiserun1 should be
excitement, incoordination, and convuladministered in1111ediately after birth.

sions occur before death. Opisthotonos,
circling, and pushing the head against fixed

Type D Enterotoxemia
objects are conunon neurologic signs;
frequently, hyperglycemia or glycosuifa is

(Pulpy kidney disease, Overeating disease)

present. Diarrhea may or may not develop.

This classic enterotoxemia of sheep is seen

Occasionally, adult sheep are affected too,
less frequently in goats and rarely in cattle.

showing weakness, incoordination,

It has a worldwide distribution and affects
convulsions, and death within 24 hr. In

CLOSTRIDIAL DISEASES

611
goats, the course of disease ranges from
lambs, ewe in1.111unization probably is the
peracute to chronic, with signs that vary
most satisfactory method of control.

from watery diarrhea with or without blood

Breeding ewes should be given two
to sudden death. Affected calves not found
injections of type D toxoid in their first year,
dead show mania, convulsions, blindness,
a booster injection 4--6 wk before lan1bing,

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and death within a few hours. Subacutely
and each year thereafter.

affected calves are stuporous for a few days

Enterotoxemia in feedlot lambs can
and may recover. In goats, diarrhea and
be controlled by reducing the amount of
nervous signs are seen, and death may
concentrate in the diet. However, this may
occur over several weeks. Type D enteronot be economical, and i.Inrntmization of all toxemia occasionally is seen in young
lan1bs with toxoid on entering the feedlot
horses that have overeaten.

likely will reduce losses to an acceptable

Lesions: Necropsy may reveal only a
level. 1\vo injections, 2 wk apart, will
few hyperemic areas on the intestine
protect lambs through the feedrng period.

and a fluid-filled pericardia! sac. This is

When alunlllwn-precipitated toxoids or
particularly the case in young lan1bs. In
bacteriI1s are used, the injection should be
older animals, hemorrhagic areas on the
given at such a site that the local cold
myocardiwn may be found as well as
abscesses, which conunonly develop, can
petechiae and ecchymoses of the abdomibe removed easily during nom1al dressing nal muscles and serosa of the intestine.

and will not blemish the carcass.

Bilateral pulmonary edema and congestion
frequently occur but usually not in young

TETANUS
lambs. The rumen and abomasum contain
an abundance of feed, and w1digested feed

(Lockjaw)

often is found in the ilewn. Edema and
malacia can be detected microscopically in

Tetanus toxemia is caused by a specific
the basal ganglia and cerebellwn of lambs.

neurotoxin produced by Clostiidium

Rapid postmortem autolysis of the kidneys
tetani in necrotic tissue. Almost all
has led to tl1e popular name of pulpy kidney mammals are susceptible, although dogs disease; however, pulpy kidneys a.re by
and cats are relatively more resistant than
no means always found in affected young
any other domestic or laboratory manunal.

lambs and are seldom found in affected

Birds are quite resistant; the lethal dose for
goats or cattle. Hemorrhagic or necrotic
pigeons and chickens is 10,000-300,000
enterocolitis may be seen in goats.

times greater ( on a body wt basis) than that
for horses. Horses and lambs seem to be the
most sensitive of all species, with the

Diagnosis: A preswnptive diagnosis
possible exception of people. Although
of enterotoxemia is based on sudden,
tetanus is worldwide in distribution, there
convulsive deaths in lan1bs on carbohyare some areas, such as the northern Rocky drate-rich feed. Smears of intestinal

Mountain section of the USA, where the
contents reveal many short, thick,
organism is rarely found in the soil and
gram-positive rods. Confinnation .requires
where tetanus is almost unknown. In
demonstration of epsilon toxin in the
general, the occurrence of C tetani in the
small-intestinal fluid. Fluid, not ingesta,
soil, especially in cultivated soil, and the
should be collected in a sterile vial within a
incidence of tetanus in people, horses, and
few hours after death and sent under
lambs is higher in the warmer parts of the
refrigeration to a laboratory for toxin
various continents.

identification. Chloroform, added at 1 drop
for each 10 mL of intestinal fluid, will

Etiology and Pathogenesis: C tetani,
stabilize any toxin present. Although
an anaerobe with temlllal, spherical spores,
inlmunologic tests have been developed
is found in soil, especially cultivated soil,
to replace the traditional mouse assay for
and intestinal tracts. In most cases, it is
detection of toxin, they are less sensitive.

introduced into the tissues through wounds,

A PCR for detection of epsilon toxin gene
particularly deep puncture wounds, that
is available for identification of the isolates
provide a suitable anaerobic environment.

as either type B or D.

In lambs, however, and sometinles in other
species, tetanus often follows docking or

Control: The method of control depends
castration. Sometin1es, the point of entry
on the age of the lambs, the frequency with
cannot be fow1d because the wound itself
which the disease appears on a particular
may be minor or healed.

property, and tl1e method of husbandry. If

The spores of C tetani are unable to grow
the disease is seen consistently in young
in nom1al tissue or even in wounds if the

612

CLOSTRIDIAL DISEASES
tissue remains at the normal oxidationspasms disturb circulation and respiration, reduction potential of the circulating blood.

which results in increased heart rate, rapid

Suitable conditions for multiplication occur
breathing, and congestion of mucous
when a small amount of soil or a foreign
membranes. Sheep, goats, and pigs often fall

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object causes tissue necrosis. The bacteria
to the ground and exhibit opisthotonos when
remain localized in the necrotic tissue at the
startled. Consciousness is not affected. In
original site of infection and multiply. As
dogs and cats, localized tetanus often
bacterial cells undergo autolysis, the potent
presents as stiffness and rigidity in a limb
neurotoxin is released. The neurotoxin is a
with a wound. The stiffness progresses to
zinc-binding protease that cleaves synaptoinvolve the opposing limb and may advance brevin, a vesicle-associated membrane
anteriorly. The appearance in generalized
protein. Usually, toxin is absorbed by the
tetanus is sinillar to that described for horses
motor nerves in the area and travels
except that the partially open mouth with the
retrograde up the nerve tract to the spinal
lips drawn back (as seen in people) is usually
cord, where it causes ascending tetanus.

evident. Young, large-breed dogs seem to be

The toxin causes spasmodic, tonic
most commonly affected.

contractions of the voluntary muscles by

Usually, the temperature remains slightly
interfering with the release of inhibitory
above normal, but it may rise to 108° -110°F
neurotransmitters from presynaptic nerve

( 42° -43°C) toward the end of a fatal attack
endings. If more toxin is released at the site

In nilld attacks, the pulse and temperature
of the infection than the surrounding nerves
remain nearly normal. Mortality averages
can take up, the excess is carried off by the

-80% ( -50"A, in dogs in one study). In
lymph to the bloodstrean1 and thus to the
animals that recover, there is a convalescent

CNS, where it causes descending tetanus.

period of2-6 wk; protective immunity

Even minor stimulation of the affected
usually does not develop after recovery.

animal may trigger the characteristic tetanic
muscular spasms. The spasms may be

Diagnosis: The clinical signs and history
severe enough to cause bone fractures.

of recent trauma are usually adequate for

Spasms affecting the larynx, diaphragm,
a clinical diagnosis of tetanus. It may be posand intercostal muscles lead to respiratory sible to confirm the diagnosis by demonfailure. Involvement of the autonomic strating the presence of tetanus toxin in
nervous system results in cardiac arrhythserun1 from the affected animal. In cases in mias, tachycardia, and hypertension.

which the wound is apparent, demonstration of the bacterium in gram-stained Clinical Findings: The incubation period
smears and by anaerobic culture may be
varies from one to several weeks but usually attempted.

averages 10-14 days. Localized stiffness,
often involving the masseter muscles and

Treatment and Control: When
muscles of the neck, the hindlin1bs, and the
administered in the early stages of the
region of the infected wound, is seen first;
disease, curariform agents, tranquilizers, or
general stiffness becomes pronounced -1
barbiturate sedatives, in conjunction witl1
day later, and tonic spasms and hyperesthe300,000 IU of tetanus antitoxin IV, bid, have sia become evident. Because of their high
been effective in the treatment of horses.

resistance to tetanus toxin, dogs and cats

Good results have been obtained in horses
often have a long incubation period and
by injecting 50,000 IU of tetanus antitoxin
frequently develop localized tetanus;
directly into the subarachnoid space
however, generalized tetanus does develop
tlrrough tl1e cistema magna. Such therapy
in these species.

should be supported by draining and

The reflexes increase in intensity, and the
cleaning the wounds and administering
animal is easily excited into more violent,
penicillin or broad-spectrun1 antibiotics.

general spasms by sudden movement or

Good nursing is invaluable during the acute
noise. Spasms of head muscles cause
period of spasms. The horse should be
difficulty in prehension and mastication of
placed in a quiet, darkened box stall with
food, hence the common name, lockjaw. In
feeding and watering devices high enough
horses, the ears are erect, the tail stiff and
to allow use without lowering the head.

extended, the anterior nares dilated, and the

Slings may be useful for horses having
third eyelid prolapsed. Walking, turning, and
difficulty standing or rising.

backing are difficult. Spasms of the neck and

The same approach as described for
back muscles cause extension of the head
horses is used in treatment of dogs and cats,
and neck, while stiffness of the leg muscles
except that caution must be exercised in the
causes the animal to assume a "sawhorse"

IV administration of antitoxin, because the
stance. Sweating is common. General
equine antitoxin may induce anaphylaxis. In

CONGENITAL AND INHERITED ANOMALIES

613
one study, antitoxin was given to dogs with

CLOSTRIDIAL VACCINES
tetanus only after an intradermal test to
detect hypersensitivity reactions. In

Vaccination is frequently practiced for
addition, all dogs received IV penicillin and
protection of animals against clostridial
some also received metronidazole orally.

diseases. A wide variety of vaccines is

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A combination of chlorpromazine and
available, singly or in combinations that
phenobarbital or diazepan1 may be used
consist of bacterins, toxoids, or .mixtures of
to reduce hyperesthetic reactions and
bacterias and toxoids. Single vaccination
convulsions.

with most clostridial vaccines does not

Active in1munization can be accomprovide adequate levels of protection plished with tetanus toxoid. If a dangerous
and must be followed by a booster dose
wound occurs after in1munization, another
witllin 3-6 wk. Vaccination of young
injection of toxoid to increase the circulatanin1als does not yield adequate protective ing antibody should be given. If the anin1al
immunity until they are at least 1-2 mo
has not been immunized previously, it
old. Therefore, most vaccination strategies
should be treated with 1,500-3,000 IU or
target the pregnant dam so that maxinlal
more of tetanus antitoxin, which usually
immunity is transferred to the neonate in
provides passive protection for as long as
colostrun1. Most commercial vaccines are

2 wk. Toxoid should be given simultaneinactivated and usually contain 2-, 4-, 7-, or ously with the antitoxin and repeated in

8-way combinations of clostridial organ30 days. Even though it is not scientifically isms/toxoids. These should be optimally
based, yearly booster injections of toxoid in
timed for provision of maxinlal protection
animals are advised; in people the toxoid is
at tlle most likely age of susceptibility.

given every 10 yr. The toxoid vaccination

Tetanus toxoid is con1.111only used as a
interval is currently debated among vaccine
single vaccine in horses but is often used in
recommendations for sport horses. Mares
combination in sheep, goats, and cattle. In
should be vaccinated during the last 6 wk of
sheep and goats, a common combination is
pregnancy and foals vaccinated at 5-8 wk of
tetanus toxoid plus Clostridiiim pe,frin
age. In high-risk areas, foals may be given
ge,is types C and D. In cattle, a combination tetanus antitoxin in1.111ediately after birth
frequently used in feedlots is a 4-way
and every 2-3 wk until they are 3 mo old, at
vaccine that consists of killed cultures of
which time they can be given toxoid. The

C chauvoei, C septicum, C novyi, and
decision to vaccinate lan1bs or calves

C sordeUii to protect against blackleg
depends on the prevalence of the disease in
and malignant edema. A more complex
the area. All anin1als that have recovered
clostridial vaccine that contains C perfrin
from tetanus should be regularly vacci
ge,is types C and D in addition to the
nated. Anin1als surviving tetanus do not
components of the 4-way vaccine may be
build a good in1munity and should be
used to protect cattle against enterotox,
vaccinated with tetanus toxoid.

emias as well. The addition of C hae,nolyti

All surgical procedures should be
cum extends the protection to include
conducted with the best possible aseptic
infectious necrotic hepatitis. The clostridial
techniques. After surgery, animals should be
vaccines often cause tissue reactions and
turned out on clean ground, preferably grass
swelling and should therefore be adminispastures. Only oxidizing disinfectants such as tered to cattle in the neck and by the SC
iodine or chlorine dependably kill tlle spores.

ratller tllan the IM route.

CONGENITAL AND INHERITED ANOMALIES

Embryonic and fetal development are the
developmental disruption results in a
result of a complex series of well orchesdeviation from normal tllat is present or trated events. When properly accomplished, apparent at birth, the defect is said to be the outcome is a healtlly neonate. Errors in
congenital. Other developmental defects
the sequential steps of development may be
may not become apparent until later in life,
followed by embryonic loss, fetal death,
and although tlle disruptive event occurred
fetal mmnmification, abortion, stillbirtl1,
before birth, the defect is not strictly
birth of nonviable neonates, or birth of
classified as congenital. Although the event
viable offspring with defects. When a
or agent resulting in disrupted development

614

CONGENITAL AND INHERITED ANOMALIES
remains w1defined for many recognizable
diagnostic tools and genomic testing, allow
congenital conditions, technologic
a more detailed W1derstanding of maiw
advances in the field of teratology have
observed congenital anomalies. It is likely
identified an increasing nW11ber of specific
that as these technologies improve, the
genetic, environmental, and infectious
etiology of other conditions will be cla.tified.

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agents as etiologic determinants of certain

Chromosomal abno1malities occurring
cases of defective fetal development.

during gametogenesis or fe1tilization may

Teratogens are agents or factors that
result in embryo lethal anomalies or
cause development of physical defects
occasionally in abnonnal but viable
in the embryo or fetus. The tinting of
offspring. Errors in oogenesis ca.t1 be
teratogenic exposw·e influences the
associated with increased maternal age in
eventual outcome. Although zygotes, the
several species and may result in failure of
cells resulting from the union of gametes,
fertilization, reduced emb1yo vi.ability, or
are relatively resistant to the effects of
in deficiencies expressed during fetal
most teratogens, they may be affected by
development. Chromosomal errors such as
chromosomal alterations or aberrations
trisomy, in which there are three instances
that occm during the process of gametogenof a pa.tticulai· chromosome instead of esis or fertilization, as well as by genetic
the normal two, have been rep01ted in
mutations that may be passed from one or
veterina.ty medicine, and increasing
both parents. As the zygote develops into
availability of kaiyotyping and ancillaiy
the embryo and organogenesis progresses,
chromosomal analysis have increased
susceptibility to environmental teratogens
recognition of these defects. Aging of
and teratogenic infectious agents increases.

gan1etes after suboptin1al timing of

As the conceptus ages fwther, the fetus
insemination represents another somce of
becomes increasingly resistant to environchromosomal abnorn1ality leading to errors mental teratogens. Late-differentiating
in embryonic and fetal development. All cells
structures such as the palate, cerebellwn,
of the defective embryo may be aneuploid
and urogenital system remain at risk well

(the presence of an abnorn1al number of
into the fetal period.

chromosomes in a cell) or various degrees

Sin1ilar, and perhaps indistinguishable,
of mosaicism (the presence of two or more
defects may be induced by more than one
populations of cells with different genotypes
agent. Exposure to toxic or infectious
in one individual who has developed from a
agents at critical phases of embryonic or
single fertilized egg) may exist.

fetal development may induce congenital

Chromosomal and epigenetic abnorn1alianomalies that closely resemble heritable ties may occm during assisted reproductive
conditions. With increased awareness of
techniques that involve oocyte collection,
the in1p01tance of inherited anomalies by
culture, and fertilization. Bovine pregnanbreeders and breed associations, practitioncies resulting from somatic cell nucleai·
ers and diagnosticians must be thorough
transfer or, to a lesser extent, from in vitro
in investigating cases, to avoid failing to
fe1tilization, are at increased risk of
recognize conditions that may be heritable
development of abnormal offspring
and to avert in1properly in1plicating •
syndrome due to failmes in physiologic
breeding lines as a cause.

mechanisms necessaiy for proper fetal and

Structural and fw1ctional congenital
placental development. These errors in
defects have been described in all domestic
development and placentation can result in
species. Although congenital defects a.re
fetal death, abortion, abnorn1ally iai·ge or
often classified or described by the body
small birth weights, or bitth of defective
system or pa.it prin1arily involved, such
neonates, and ai·e often associated with
classification systems are complicated by
dystocia.

frequent simultaneous involvement of
multiple body systems. Even so, descriptive

Inherited Defects
classifications provide a basis for comparison and allow for estimation of the time Inherited defects resulting from mutant
of the disruptive event relative to fetal
genes present in breeding lines or families
development, and sometimes etiology
have been seen in all breeds. They may be

(see
expressed in typical patterns of inheritance

TABLE 2).

such as the conunon sitnple autosomal
recessive pattern typified by the recently

Etiology
described a.rthrogryposis multiplex

Identification of molecular signals that
anomaly of Angus cattle. Dominant defect
gttide sequential development of orga.t1s and
traits are inhetited as well and are
organ systems, coupled with moleculai·
sometin1es selected for.

CONGENITAL AND INHERITED ANOMALIES

615

SOME COMMON CONGENITAL DEFECTS OF DOMESTICATED

ANIMALS

Amelia

Absence of a limb or limbs

Arthrogryposis

Persistent flexure or contracture of a joint or joints VetBooks.ir

Atresia

Absence or closure of a normal body opening or passage Brachygnathia

Abnormally short lower jaw

Campylognathia

Cmved jaw

Cheiloschisis

Abnorn1al division of the lip (harelip)

Cryptorchidism

Failure of the testis to descend into the scrotum

Hemirnelia

Absence of all or part of the distal half of a limb

Hernia

Abnormal protrusion of an organ or portion of an organ through a defect or natural opening

Hydranencephaly Virtual absence of cerebral hemispheres and replacement by CSF

Hydrocephalus

Abnormal fluid in the cranial vault accompanied by enlargement of the head

Kyphosis

Abnormally increased convexity of the thoracic spine Microophthalmia Abnormally small eye

Palatoschisis

Fissure of the palate ( cleft palate)

Perosomus

Developmental anomaly characterized by a greatly deformed body or trunk

Polydactyly

Supernumerary digits

Porencephaly

The presence of cavities in the brain developed during fetal life Prognathia

Marked projection of the lower jaw

Schistosomia

Developmental anomaly characterized by fissure of the abdominal wall

Scoliosis

Lateral deviation of the spinal axis

Syndactyly

Fusion of the digits

Thoracoschisis

Fissure of tile thoracic wall, which may result in herniation of lung tissue

Some polygenetic defects require
frequency in tile population. Sin1ilarly, while
inclusion of more tilan one interacting gene.

tile Overo color pattern is attractive to some

Rat tail syndrome, a congenital fon11 of
horse breeders, animals homozygous for
hypotrichosis in cattle, is controlled by
this color pattern a.r·e often affected with a
genes at two interacting loci.

lethal congenital a.r1omaly due to failure of

Because animals heterozygous for
intestinal tract innervation secondary to
undesirable or lethal recessive traits often
ileocolonic agangliosis. It is recommended
cannot be detected by visual examination,
to include only one Overo pa.r·ent in a
and sometimes exhibit a phenotype tilat
ma.ting. The dominant inheritance of
is thought to be desirable, inadvertent
polledness in dairy goats is associated with
selection may help spread genetic defects
coinheritance of a recessive allele tlla.t
in a particular breed. For exa.rnple, cattle
results in masculiniza.tion of homozygous
heterozygous for tibial hemin1elia. reportfemales (tlle so-ca.lied polled intersex goat).

edly have rear limb confon11ation and hair

Restrictive breeding progra.rns tilat ensure
coat characteristics preferred by some
at least one member of the breeding pair
breeders, and phenotypic selection of
has horns a.r·e recommended to a.void this
certain sires may have increased the allele
defect.

616

CONGENITAL AND INHERITED ANOMALIES

Heritable defects in metabolic function
developed after description of the condition
may result in embryonic or fetal death, birth
provided breed associations and breeders
of nonviable neonates, or birth of comproopportunities to minimize the effects or mised offspring that stuvive. Such defects
eliminate the conditions.

may be lethal in utero or early in the

By the time detrimental genetic

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postnatal period, or animals may survive in
conditions are recognized in a population or
a compromised form. Careful observation
breed, the abnmmal allele is often widely
and diagnostic evaluation are required to
distributed. Early recognition and detection
properly identify these conditions and link
are desirable to minimize this possibility. All
them to pedigree information.

congenital anomalies should be investi

Deficiency of monophosphate synthase
gated, and when a condition apperu-s to

(DUMPS) is a lethal autosomal recessive
have an underlying genetic component,
trait formerly widely dispersed in Holstein
appropriate techniques to assess pedigree
cattle. When breeding of two DUMPS
infonnation and identify the mutated
carriers results in a homozygous embryo,
homozygous phenotype should be explored.

apparently nonnal fertilization and

A structured system of reporting and
embryonic development is followed by
recording, beginning with accurate clinical
death of the fetus in early gestation.

and pathologic descriptions, is necessruy to

Screening of sires destined for use in
centralize data and focus attention on
artificial insemination has successfully
physical and physiologic abnonnalities that
reduced the incidence of DUMPS.

may be genetic in 01igin. Pedigree analysis

CitrulJinemia in cattle results in
and test mating of closely related animals
disruption of the urea cycle due to
coupled with recently developed DNAarginosuccinate synthetase deficiency and based testing have the potential to identify
is lethal in the homozygous state. Affected
specific genetic aben-ations, in some cases
calves appear healtl1y at birth but develop
relatively rapidly after recognition of the
increased blood an1monia concentrations
defect. Most breed associations have
and die within a few days.

procedures to repmt congenital anomalies

Defects found on the X chromosome,
and work with pathologists, geneticists, and
such as the one responsible for canine
molecular biologists to identify emerging

X-linked muscular dystrophy in Golden
genetic defects.

Retrievers, Labrador Retrievers, and other

Once known genetic recessive conditions
breeds, are expressed in males carrying
ru·e identified, several options exist to
only a single copy of a defective allele. Both
minimize their occurrence. For complex
pa.rents are unaffected, with the dam
vertebral malformation, testing of alJ
carrying a single copy of the defective

Holstein sires entering artificial inseminagene on an X chromosome.

tion progrruns was chosen. BulJs were

For a partial list of inherited disorders
identified as being either cruTiers or free of
with a known molecular basis, see TABLE 3.

the defect. The resulting decline in use of

Use of elite genetic lines in domestic
semen from carrier bulJs led to a decrease
species increa5ed with the rapid and
in the occwTence of the condition and the
widespread adoption of reproductive
aJJelic frequency within the breed. Other
technologies, pruticularly rutificial
genetic recessive conditions in the srune
insemination, embryo transfer, and in vitro
breed, including bovine leukocyte adhesion
fe1tilization. Dissemination of undetected
deficiency and DUMPS were handled
genetic recessives to a large portion of the
similarly, and the recently Identified
population domesticaJJy and intemationaJJy
brachyspina syndrome will likely be
has been an inadve1tent and unintended
managed in the san1e marmer. The extensive
consequence. As the percentage of animals
use of artificial insemination in dairy cattle
canying undesirable recessive traits grows,
allows this strategy to have a rapid impact.

an increased opportunity for breeding

In breeds or species with less use of
geneticaJJy related individuals is followed
rutificial insemination, a more aggressive
by the expression of the undesirable
approach may be required. After recognition
phenotype. Complex vertebral malformaof artJu·ogiyposis multiplex, tl1e American tion in Holstein-Friesian dairy cattle was

Angus Association mandated testing and
spread intemationa!Jy primarily due to the
identification of alJ sires in active artificial
influence of a single Holstein sire from the
insemination progrruns. They also required

USA and his offspring. Similarly, arthrogenetic testing to dete1mine canier status of gryposis multiplex in Angus cattle received
aJJ anin1als with suspect pedigrees submitted
international attention due to the influence
for registration. No certificate of registration
of a popular bulJ, his offspring, ru1d
will be issued to cruTier anin1als born after a
descendants. In both cases, genetic testing
specified date. Similar requirements for

CONGENITAL AND INHERITED ANOMALIES

617

IM=liii CONGENITAL DISORDERS WITH A KNOWN MOLECULAR BASIS

Species

Disorder

Cat

Gangliosidosis (GMl, GM2)

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Mucopolysaccharidosis (I, VI, VII)

Muscular dystrophy (Duchenne, Becker)

a-Mannosidosis

Dog

C3 deficiency
a-Fucosidosis

Glycogen storage disease (I, VII)

Hemophilia B

Krabbe disease

Leukocyte adhesion deficiency

Mucopolysaccharidosis (I, VII)

Muscular dystrophy (Becker, Duchenne [X-linked])

Myotonia

Narcolepsy

Nephritis, X-linked

Pyruvate kinase deficiency of RBCs

Rod-cone dysplasia

Severe combined immunodeficiency

Tremor, X -linked
von Willebrand disease III

Cattle

Arthrogryposis multiplex (Angus, Angus-influenced breeds) Brachyspina syndrome (Holstein)

Chediak-Higashi syndrome

Complex vertebral malforn1ation (Holstein)

Citrullinemia

Deficiency of uridine monophosphate synthetase (Holstein) Ehlers-Danlos syndrome (II, V)

Glycogen storage disease

Goiter, familial (Holstein)

Leukocyte adhesion deficiency
ac-Mannosidosis

13-Mannosidosis

Maple syrup urine disease

Muscular hypertrophy (Shorthorn, Maine-Anjou)

Pulmonary hypoplasia with anasarca (Shorthorn)

Progressive degenerative myeloencephalopathy (Brown Swiss) Protoporphy1ia

Spinal muscular atrophy (Brown Swiss)

Syndactyly (I-Iolstein, Angus)

Tibial hemimelia (Shorthorn, Maine-Anjou)

Sheep

Ceroid lipofuscinosis

Chondrodysplasia

Glycogen storage disease IV

Goat

Goiter, familial

13-Marmosidosis

Mucopolysaccharidosis III

Reduced casein concentration

Polled intersex syndrome

Horse

Hyperkalemic periodic paralysis (Quarter horse, Paint, others) Megacolon

Severe combined immunodeficiency (Arabians)

Pig

Hypercholesterolernia

Malignant hypertherrnia

618

CONGENITAL AND INHERITED ANOMALIES
animals with pedigrees tracing to carriers of

In cattle, ingestion of several species of
neurogenic hydrocephalus have been put in
lupines (Lupinus laxiflorus, L caudatus,
place by this breed association. Extensive

L sericeus, or L nootkatensis) has resulted testing and identification of carrier
in "crooked calf disease," characterized by individuals is used by the American Quarter
jomt contractures, torticollis, scoliosis or

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Horse As ociation to minimize the incidence
kyphosis, cleft palate, or combmations of
of hyperkalemic pe1ioclic paralysis.

these defects. The quinolizidine alkaloid

As new genetic recessive abno1malities
anagyrine is identified as the teratogen, and
are identified and characterized, genetic tests the critical window for exposure is 40--70 days to detennine canier status can be developed.

gestational age. Ingestion of Lfonnosus

Breed associations and breeders will adopt
causes sinillar skeletal defects and cleft
testing and identification strategies similar to
palate in cattle and goats; the teratogen is the
those mentioned above. However, implemenalkaloid pipeiidiI1e. With either toxiI1, defects tation of testing strategies will be more
are thought to be related to an alkaloidal
complicated for nonlethal defects and for
toxin-induced mhibition of fetal movement
conditions in which heterozygotes have a
dming clitical gestational peliods. Peliodic
phenotype perceived as desirable.

losses due to lupine-induced crooked calf
disease occur iI1 the western USA after
mgestion by cattle on rangeland.

Environmental Teratogens

Conium maculatwn (poison hemlock)

Environmental teratogens include plant
causes contracture defects and occasionally
toxins, viruses, drngs, trace elements,
cleft palate in cattle, goats, sheep, and pigs.

nutlitional deficiencies, and physical agents

Both the plant and seed contain the
such as irradiation, hype1thennia, uterine
teratogenic alkaloidal toxin coniine.

positioning, and perhaps pressure dming

Ingestion ofNicotia.na tabacum
rectal examination for pregnancy. Although

( cultivated tobacco) produces skeletal
the defects produced in the neonate may
defects m pigs sinillar to those induced in catresemble or mimic heritable defects, they do tle and pigs by Lupinus spp and C macula
not follow a familial pattern. Specific causes
tum. Congenital an1elia and hemilnelia in
may be difficult to identify but often follow
piglets that occun-ed when pregnant sows
seasonal patterns associated with growth
were allowed access to tobacco stalks are
characteristics of toxic plants or availability
seldom seen today due to changes in swine
of suitable vectors of arthropodborne
management. Nicotiana glauca (tree
virnses. Although congenital anomalies
tobacco) also induces conti·acture defects
may follow maternal disease due to plant
and cleft palate in cattle, sheep, and goats.

intoxication or viral infection, teratogenic

Otl1er plants suspected of causing similar
effects sometimes occur in the absence of
defects in calves include Senecio spp,
observed clinical signs in the dam.

Cycadales, Blighia, Papaveraceae,

Biologically active products produced by

Colchicum, Vinca spp, and lndigofera
many plants are known to be teratogens.

spicata and related plants. Sudan grass

(See also POISONOUS PLANTS, p_3103.) Ingestion (Sorghum vulgare) has been inc1iminated
may result in abortion, birth of nonviable
as a cause of congenital joint contracture
neonates, or production of neonates that are in horses, and S sudanense may cause abnonnal at bilth. Production losses can be
arthrogryposis in calves.

significant if large mun be rs of anilnals gaiI1

Pregnant mares consuming fescue
access to affected plants at c1itical times m
pasture or fescue hay infected with the
embryonic or fetal development. Veratrum
fw1gal endophyteNeotyphodiitm coenocalifornicum (skunk cabbage) has been phialum are at risk of abortion, prolonged
ilnplicated as a cause of fetal gigantism,
gestation, hypogalactia, and delivery of
prolonged gestation, and craniofacial
weak or dysmarure foals (seep 3016).

defonnities iI1 sheep grazing rangelands

Ergovaline and other ergot alkaloids
containing the plant. Cyclopanune, a
produced by the endophyte are tl1e cause
steroidal alkaloidal compound produced
of fescue toxicosis. Endophyte-free fescue
by the plant, is the teratogenic agent. Expe1iand fescue infected by nontoxic strains of mental dosing with this toxin iI1 ewes on
endophyte reportedly can be grazed safely
day 13-15 of pregnancy can cause a variety
by pregnant mares.

of congenital anomalies. Ingestion on day

Congenital hypothyroidism in foals has

14 specifically induces synophthalmia or
been lmked to mcreases of dietary nitrate
cyclopean defect. Ewes exposed later i11
concentrations in pregnant mares m
gestation may deliver healthy lan1bs,
western Canada and to dieta.Iy exposure of
illusti·ating the critical interaction of time
late gestation mares to N coenophialum
of exposure and gestational age.

infected fescue.

CONGENITAL AND INHERITED ANOMALIES

619

Pesticides, herbicides, phannaceutical
gestational day 120. These animals serve as
agents, and other chemicals have been
a major rese1voir of infection.

incriminated as teratogenic agents.

Pestivi.J.us infections in other species also

Cun:enUy, drngs and chemicals undergoing
result in congenital defects. Infection of

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approval processes in the USA, Canada, and
pregnant ewes with border disease virus
many otl1er countries must be tested for

(seep 622) may manifest as embryonic and
teratogenic potential before commercial
fetal death or congenital defects involving
licensing. Products may be labeled with
the integumenta.ry, nervous, skeletal,
instructions to specifically avoid use in
endocrine, and immune systems. Defects
anin1als that are pregnant or may be
include tremors, ataxia, abnonnal hair coat,
pregnant. Other products may be labeled
low birth weight, facial and ocular
as safe for pregnant anin1als once the fetus
abnom1alities, depressed immune response,
exceeds a specified gestational age. When
and birtl1 of small, weak lan1bs with poor
using some herbicides, it may be necessary to growth and viability. Infection of pregnant withhold animals from pasture for specified
ewes with BVDV from cattle has produced
periods after application. Extra-label use of
identical congenital anomalies in sheep.

pharmaceutical agents in pregnant animals

Classical swine fever (seep 713), a
and inadvertent exposure to pesticides and
pestivi.J.us infection of swine, was once
other chemicals carries inherent risks,
known as hog cholera. The vims has been
including adverse effects on the developing
eradicated in the USA but remains a major
fetus. Practitioners and producers should be
cause of swine disease in some areas.

aware of the potential for pregnancy loss or

Prenatal infection can result in congenital
development of congenital anomalies after
defects similar to those seen in cattle
ad.ministration of therapeutic agents or
infected with BVDV.

exposure to pesticides and chemicals and

Cache Valley vi.J.us inJection of pregnant
should exercise appropriate caution when
ewes may result in anomalies in their lambs,
using such products.

including ruthrogryposis, torticollis, scoliosis,
lordosis, hydranencephaly, microcephaly,
porencephaly, and cerebellar and muscular

Infectious Agents
hypoplasia This bunyavi.J.us is spread by

Prenatal viral infections may be teratogenic
mosquitoes and is found in tl1e USA, Canada,
in cattle, sheep, goats, pigs, dogs, and cats
and Mexico. Other run1inant species may be
but have rarely been inc1iminated in
affected, and other btmyavi.J.uses have been
congenital defects in horses. The stage of
reported to cause similru· congenital defects.

fetal or embryonic development at the time

Bluetongue virus, an orbivims endemic
of exposure determines the type and extent
in many areas of North America, South
of the anomalies observed. Viral infection in

America, Africa, and parts of Asia, has
late gestation may result in fetal infection
recently expanded its range in Europe. In
and seroconversion without observed
utero exposure may induce hydranencephclinical signs, while exposure during earlier aly, porencephaly, and arthrogryposis in
stages may induce pregnancy loss or induce
sheep, and it can result in abortion,
congenital defects.

stillbirths, arthrogryposis, campylognatlua,

Production of neonates with congenital
prognathia, hydranencephaly, and "dununy
anomalies after in utero infection may
calf' syndrome in cattle. Other orbiviruses
follow observable clinical disease in tl1e
such as Chuzan virus and perhaps epizootic
dam; however, anomalies are also seen
hemorrhagic disease may cause abortion,
without history of disease during pregnancy.

congenital defects, and neonatal losses

On occasion, use of modified-live virus
sinillar to bluetongue vi.J.us.

vaccines in pregnant animals has produced

Akabane virus (see below), an orbivirus
congenital defects; such use is discouraged.

present in many tropical and subtropical

Pestivirns infections are teratogenic in
areas, is spread by Culicoides spp (biting
many species. Bovine viral diarrhea vims
nudges). Infection of naive anin1als can be

(BVDV) is an10ng tl1e most economically
followed by transpla.cental infection of the
significant infectious agents affecting cattle
fetus and may produce defonnities sinillru·
worldwide, and prenatal infection can cause to those seen with viruses such as a variety of congenital defects in survivors,
bluetongue and Cache Valley vi.J.us.

including cerebellar hypoplasia, brachyg

Congenital cerebellar hypoplasia in kittens
nathia, alopecia, ocular defects, internal
has long been recognized as a result of
hydrocephalus, and impaired in1munocominfection of pregnant queens with feline petence. Irnmunotolerant, persistently
panleukopenia vi.J.us. Infection of pregnant
infected animals may result from fetal
ferrets with feline panleukopenia vi.J.us also
infection with noncytopathic BVDV before
cru1 result in congenital cerebellar hypoplasia.

620

CONGENITAL AND INHERITED ANOMALIES

Nutritional Factors
development of the GI and urogenital

Deficiency of one or more nutrients during
systems accompany this condition. The
pregnancy may result in congenital defects
body, lin1bs, and organs cra.tlial to the

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in the newborn. Microminerals and vitanlins developmental defect in the spinal cord are implicated in a vatiety of developmental
appear normal. The condition is fatal,
defects. Severe deficiencies may interrupt
resulting in stillbirth or requiting euthanasia
pregnancy or result in weak or nonviable
on hwnane grounds. Dystocia is a frequent
young.

complication. Although there a.i·e sugges

Iodine deficiency may cause congenital
tions of inheritance, no definitive cause is
goiter or cretinism in all species. Copper
recognized. Aberrations in the homeobox
deficiency is a cause of enzootic ataxia in
gene fanlily, responsible for cranial to
lan1bs. Manganese deficiency can result in
caudal patterning, may be involved.

congenital limb defomtities in calves. Vitanlin

Schistosomus reflexus, a fatal congenital

D deficiency may cause neonatal rickets, and
disorder seen in ruminants, is characterized
vita.tllin A deficiency may cause eye defects or by severe retroflexion of the spinal colw1m, harelip. Experimentally, teratogenic effects
resulting in positioning of the hindlimbs
have been induced by deficiencies of choline,
adjacent to the skull, ankylosis of appenriboflavin, pantothenic acid, cobala.tnin, and dicular joints, and failure of closure of
folic acid, and by hypervita.tilinosis A
the abdonlinal wall with consequential
presence of abdonlinal viscera outside the
body. Other anomalies, including thora

Physical Agents
coschisis, may accompat1y the condition.

Congenital joint contracture after birth of

The presence of an affected fetus results in
relatively large calves or foals, or associated
dystocia, frequently requiring surgical
with cases of twin pregnancy in these
intervention or fetotomy. Some reports
normally monotocous species, is a result of
utilizing pedigree analysis suggest a genetic
restricted motion due to uterine crowding.

etiology, but no specific defect or mode of

Many cases are mild and potentially
inhetita.tlce has been found. Interestingly,
self-correcting after birth.

cases involving one affected calf and a

Torticollis, scoliosis, and limb abnormalihealthy co-twin have been reported.

ties in foals have been associated with

Fetal anasarca is a fatal anomaly seen in
intrauterine fetal positioning after
several breeds of dogs. The cause remains
transverse or caudal presentation. Pervious
w1krlown and may vary from breed to
urachus in foals is reportedly associated
breed. This condition frequently results in
with umbilical cord twisting.

·dystocia due to the disproportionately large

In cattle, aggressive tra.i1srectal palpation
fetus at term. Single or multiple pups within
of the anmionic vesicle before day 42 of
a litter may be affected.

gestation ( eg, during pregnancy diagnosis)

may disrupt vascular supply to the intestinal

AKABANE VIRUS INFECTION
tract and induce atresia coli. Most cases of
this malformation are seen in Holstein cattle, Akabane is an insect-tra.t1Smitted virus that and a genetic predisposition may exist. At
causes congenital abnonnalities of the CNS
least one report suggests an autosomal
in rwni.nants. Disease due to Akabane virus
recessive inherita.tlce pattern for atresia coli.

has been recognized in Australia, Israel,

Japan, and Korea; antibodies to·it have been

Gestational Accidents of Unknown
found in a nwnber of countries in southeast

Etiology

Asia, the Middle East, and Africa. The
disease affects fetuses of cattle, sheep, and

In many cases of congenital anomalies, the
goats. Asymptomatic infection has been
etiology or predisposing factors remain
demonstrated serologically in horses,
w1known. Some specific anomalies of
buffalo, deer, and pigs (but not in people)

unknown etiology occur frequently enough
in endemic areas.

to be readily recognized by veterinarians in
the field.

Etiology, Epidemiology, and Trans

Perosomus elwnbis is a congenital
mission: The causal agent, Akabane virus,
anomaly that occurs prirna.tily in cattle but
is an orthobunyavirus and member of the
also in small rwllinants and swine. Affected

Sin1bu serogroup of the fa.tni.ly Bunyaviricalves have agenesis of segments of the dae. It is spread by biting midges ( Culi
lurnbosacral spinal cord and vertebral
coides spp) in Australia, Japan, and Kenya
colwnn, with secondary hypoplasia,

Akabane virus is common in many
arthrogryposis, and ankylosis of the pelvic
tropical and subtropical areas between
limbs. Other anomalies associated with

-35°N and 35°S. In these endemic areas,

CONGENITAL AND INHERITED ANOMALIES

621
herbivores are bitten by the vectors,

( arthrogryposis ), and sometimes also
become infected at an early age, and
torticollis, kyphosis, and scoliosis with
develop a long-lasting immunity by the time
associated neurogenic muscle atrophy due
of breeding; thus, congenital abnormalities
to loss of spinal motor neurons. These

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are seldom seen. However, under favorable
abnormalities usually cause dystocia and
environmental conditions such as an
can result in severe obstetric complications,
extended humid summer, the vector (and
sometimes resulting in infe1tility and even
hence the vims) may spread beyond its
death of cows. The first calves born with
usual range into new areas, and outbreaks
arthrogryposis are less severely affected
of congenital infection may be expected.

than those born during the next 4-6 wk

These outbreaks usually occur at the

Initially, only one or two joints may be
northern or southern limits of the vector
affected on a single limb, but later cases can
distribution or in areas of higher altitude.

have severe fixation of multiple joints on

Similarly, pregnant ruminants from virusseveral or all limbs. Calves infected at and vector-free areas moved to vims80-120 days of gestation are usually born infected areas are at risk
alive and, if able to stand, walk poorly and

The incidence of Akabane virus----induced
are depressed and blind. These calves have
disease is influenced by the time of gestation
varying degrees of cavitation of cerebral
at which infection occurs and by the strain
hemispheres, ranging from porencephaly
of virus. Infections in cattle dwing the last
to severe hydranencephaly. The latter is

3 mo of pregnancy result in a relatively low
common, especially among those infected in
incidence of disease (5%-1 QOA, of calves are
the earlier stages of pregnancy. Some calves
affected). The peak incidence is seen after
may be affected with both arthrogryposis
infection in the third and fourth months,
and hydranencephaly. Calves with severe
when up to 4()0A, of calves may be born with
hydranencephaly may be aborted in
defects. Some strains of Akabane vims
midgestation. A useful differential diagnostic
produce a very low incidence of abnormalifeature is the virtual absence of either gross ties ( <20%) even at the most susceptible
or histologic lesions in tl1e cerebellum,
stages of gestation, whereas the most severe
distinguishing Akabane vims infection from
can cause disease in up to 800A, of infected
other teratogenic viruses such as bovine
animals.

viral diarrhea virus (BVDV, see p 267).

In sheep and goats, disease is seen but the

Infrequently, strains of Akabane vims are
distinct sequential manifestation of different
encountered that cause disease when calves
abnormalities seen in cattle does not occur
are infected in the first few weeks of life. A
because of the shorter period of gestation
range of neurologic signs and pathology
and the shorter pe1iod of susceptibility.

consistent with an acute viral encephalitis

Most abnormalities develop after infection
may be seen. In Japan, strains of Akabane
between days 28-56 of gestation. Few, if
vims that cause disease in adult cattle have
any, abnormalities are seen after infection
also been described.

at other times. However, it is not known

In small nuni.nants, the lesions of
whether infection in large or small
arthrogryposis and hydranencephaly are
nuni.nants very early in gestation results in
often seen concurrently and are common in
lethal infection, with abortion of the fetus.

the same animals. In lambs and kids, a range
of other defects may occur, including

Clinical Findings and Lesions: The
pulmonary hypoplasia and hypoplasia of the
clinical signs and pathology of Akabane
spinal cord. Most Akabane-i.nfected lambs
vims infection depend on the species of
or kids are stillborn or die soon after bi.Ith.

animal and time of infection. In a herd of

Abmtions are also seen.

cattle with an extended or year-round

Akabane virus-induced congenital
calving period, the full range of abnormaliabnormalities ( especially arthrogryposis ties may be seen. The most severe defects
and hydranencephaly) have been suspected
are seen after susceptible cows have been
in horses, but laboratory confinnation has
infected between -80-150 days of gestation;
been inconclusive.

however, calves can be affected at most
times after the first 2 mo of gestation. Calves

Diagnosis: A presumptive diagnosis can
infected late in pregnancy may be born alive
be made on the gross CNS lesions, but the
but unable to stand and may have a flaccid
disease must be differentiated from other
paralysis of the limbs, or may be incoordiinfectious and genetic conditions. Infection nated and on necropsy show a disseminated
can be conflrmed by testing sera or body
encephalomyelitis. Those infected earlier
fluids ( eg, pericardia! or pleural fluid) from

(120-180 days of gestation) have rigid
unsuckled, affected offspring and their danlS
fixation of limbs, usually in flexion
for antibodies against Akabane vims. While

622

CONGENITAL AND INHERITED ANOMALIES
the detection of antibody in maternal serum
related to the vi.Iuses of classical swine
does not confum Akabane as an etiologic
fever (seep 713) and bovine vu·al diarrhea/
agent, its absence is definitive for exclusion.

mucosal disease (seep 267). Surviving

Other vectorborne viruses ( and also
lainbs are persistently vu·emic, and the vu·us
non-vectorborne viruses such as BVDV) can

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is present in thei.I· excretions and secretions,
cause congenital defects identical to those
including semen. Cattle, goats, and pigs are
of Akabane virus. Aino virus, a relative of
also susceptible to infection with border

Akabane, is found in Australia, Japan, and
disease vims. Persistently infected
several other countries where Akabane
individuals have been demonstrated in all of
virus is found and has been an infrequent
the aforementioned species from natural
cause of disease in cattle. In late 2011,
in-utero infection. Tra.t1Smission of border

Schmallenberg, a newly recognized
disease virus to cattle can occur l'rom
orthobunyavirus, spread throughout most of commingled grazing with persistent or western Europe and extended to the UK and
acutely infected sheep. Acute infections in
also north to Scandinavian countries. This
imnumocompetent a.t1i.I11als ai·e usually

Sin1bu virus caused disease indistinguishtransient and subclinical and result in able from Akabane infection in sheep,
i.Inmunity to challenge with homologous
although the incidence of congenital defects
but not heterologous strains of virus.

was generally low compared with that

Vi.Ius acquired in early pregnancy by
caused by Akabane virus. Disease was
previously unexposed ai1inlals crosses the
occasionally seen in cattle but at a very low
placenta and invades the fetus. Placentitis
prevalence. In Japan, Chuzan vi.Ius, a
occurs 10-30 days after infection and may
reovi.I1.1s, is transmitted by Culicoides
cause fetal death with expulsion, resmption,
oxyslorna and causes congenital infection in or mummification. Abortion may occur at any calves sinillar to Akabane virus. ln the USA, stage of pregnancy and may pass unnoticed

Cache Valley vi.I"Us, another vectorborne
because there is little maternal malaise.

bunyavirus unrelated to Akabane virus, has
ln sustained pregnancies, tl1e virus
been associated with congenital defects in
becomes widely distributed in fetal tissues,
sheep and perhaps cattle in some states.

but patl10logic changes are most obvious iI1
tl1e skin, skeleton, and CNS. Affected lan1bs

Treatment and Control: There is no
may be born 2-3 days early, and many die
specific treatment for animals affected by
before or at weaning. ln swvivors, the

Akabane vims infection. Measures should
cli.Ilical signs gradually regress, but such
be directed at the prevention of infection of
anin1als remam persistently infected and
susceptible animals with Akabane virus
excrete virus for the remamder of their lives,
during pregnancy. Introduction of stock
exposing tl1eir progeny and floclanates.

from nonendemic to endemic areas should

Death from a syndrome si.Inilar to bovine
be done well before first breeding. Effective
mucosal disease may occur iI1 these clinically
vaccines are available in Japan.

"recovered" hairy-shaker sheep at any time.

ln naive flocks exposed to bovine viral
diarrhea virus (BVDV), up to 500Ai or more

BORDER DISEASE
of lan1bs born may be affected witl1 border

(Hair
disease. Thereafter, the prevalence decliI1es,
y shaker disease)

although tl1e disease may become endemic

Border disease (Britain) or hairy shaker
when "recovered" lambs ace retained for
disease (Australia and New Zealand) is a
breeding. The virus is most commonly
congenital disorder of lambs characterized
introduced into susceptible flocks by tl1e
by low bi.Ith weight and viability, poor conforaddition of persistently infected sheep or mation, tremor, and an excessively hairy
pregnant ewes carrying an infected fetus.

bi.Ith coat in norn1ally smooth-coated breeds.

However, sheep can also acquire infection

Goat kids may also be affected, and a si.Inilar
from transiently or persistently infected
condition occasionally occurs in calves.

cattle. F or practical purposes, it should be

The disease has been recognized in most
assumed that sheep and cattle are equally
sheep-reaiing areas of the world, includi.I1g
susceptible to all strai.I1s of border disease
the western USA. There are currently seven
virus and BVDV, even though at least four
recognized genotypes (BDV-1 to BDV-7) for
phylogenetic groups of pestiviruses have
the border disease virus.

been identified in domestic runlinants.

Etiology, Pathogenesis, and Epidemi

Clinical Findings: Affected flocks
ology: Border disease is caused by
probably are recognized first at lan1bing time
infection of the fetus in early pregnancy
by an increase in the number of barren ewes
with a pestivi.I1.1s (F1aviviridae) closely
and iI1 tl1e bi.Ith of undersized lan1bs with

COXIELLOSIS

623
excessively hairy and sometimes excessively
chemistry, or PCR. When testing blood in
pigmented fleece. Skeletal abnorn1alities that newborn lambs, precolostral blood is ideal may be seen in newborn lambs include a
because colostral antibody can mask virus
decreased crown-rump length, shortened
for up to 2 mo. Virus can be isolated from

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tibia and radius, and a sho1tened longitudinal
serum or buffy coat cells in cell cultures, but
axis of the cranium. Some lambs exhibit
a viral antigen detection ELISA using
involuntary muscular tremors, particularly
heparinized or EDTA blood is available.

of the trunk and hindlegs. The tremors are

Reverse transc1iptase-PCR can also be used
reduced at rest and exacerbated by
to detect viral RNA in clinical specinlens
purposeful movement. In others, skeletal
and to type runlinant pestiviruses.

defects such as dropped pasterns and

Other causes of ovine abortion ( eg,
mandibular brachygnathia may predominate. bluetongue, Chlamydia, listeriosis, Affected lambs have a poor survival rate. In

Salmonella, Campylobacter, Rickettsia
survivors, nervous signs gradually disappear
spp, Toxoplasma gondii, and Akabane
within 3-4 mo. Even in the absence of typical
virus) should be considered in the
haily-shaker lambs, outbreaks of low fe1tility
differential diagnosis. In live-born lambs,
in ewes and poor viability and ill-thtift in
border disease must be differentiated from
lambs may be associated with border disease swayback (enzootic ataxia), bacterial virus infection.

meningoencephalitis, focal symmetric
encephalomalacia, and "daft lan1b" disease.

Lesions: In severe cases, abnorn1al
development of the cerebrum may be seen
at necropsy, resulting in hydrocephalus,

Control: There is no effective treatment
hydranencephaly, porencephaly, or
for persistently infected lan1bs. Bulk tank
microcephaly. Cerebellar hypoplasia or
milk samples can be tested for antibodies to
cerebellar dysplasia may also occur.

BVDV to screen for the presence of virus

Otherwise, the characteristic lesions are
witllin dairy sheep flocks. Serology should
microscopic and involve the white matter of
be pe1iormed on the dan1s of affected
the CNS. There is a deficiency of myelin and
lan1bs. Most should have high levels of
an increase in interfascicular glial cells, in
antibody and be immune to further
which myelin-like lipid droplets may
challenge with tl1e same strain of virus in
accumulate. These changes are most obvious subsequent pregnancies. Those that do not in the newborn and gradually resolve.

have antibody titers should be screened for
vims to identify any that are persistently

Diagnosis: Clinical findings usually allow
infected. Recovered lan1bs should not be
a diagnosis, although abnormal hairiness of
retailled for breeding but can be mixed with
the birth coat may not be apparent in
replacement stock well before breedin_g
rough-coated breeds of sheep. The
season to maxinlize opportunities for the
diagnosis can be confirmed by histologic
latter to become infected and develop
demonstration of the pathognomonic
immunity before subsequent matings. There
lesions in the CNS and with immunocytois no effective vaccine. BVDV vaccines for chemical stailling of the virus. In typical
cattle cannot be recommended for use in
hairy-shaker lambs, the virus or viral
sheep, because border disease vimses most
antigen may be demonstrated readily in
commonly isolated from sheep are
blood and tissues by virus isolation,
antigenically distinct from BVDV most
fluorescent antibody tests, inlmunohisto-
common in cattle.

COXIELLOSIS

Coxiellosis is a zoonotic bacterial infecassociated with Coxiella burnetii is widely tion associated primarily with parturient
known as Q fever. Coxiella is considered

1Ull1inants, although domestic animals
a potential agent of bioterrorism because
such as cats and a variety of wild aninlals
of its low infectious dose, stability in the
have been identified as sources of human
environment, and capability for aerosol
infection. The zoonotic infection in people
dispersion.

624

COXIELLOSIS

Etiology, Epidemiology, and Transmis

Clinical Findings and Diagnosis: Infec
sion: Coxiellosis is caused by the
tion in ruminants is usually subclinical but
gram-negative coccobacillus C burnetii.

can cause anorexia and late abortion. When

Although classically considered a rickettsial
infection is subclinical, animals shed much

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agent, recent phylogenetic analyses suggest
lower bacterial loads of the orgaitism than
that C burnetii is more closely related to
when abmtion occurs. Reports have

LegioneUa and F'ranciseUa than to the genus implicated C burnetii as a cause of Rickettsia. It resides and reproduces in the infertility and sporadic abortion with a
acidified phagolysosomes of host mononecrotizing placentitis in 1uminants. New cytes and macrophages. Two forms exist:

evidence has shown an association of
the large cell variant is a vegetative form

C burnetii with subclinical mastitis an10ng found in infected cells, and the small cell
dairy cows, although additional work
variant is the extracellular infectious form
regarding causality is required before
shed in milk, urine, and feces and found in
this can be considered clinically valid.

high concentration (109 IDoofg) in placental

Experimental infection in cats causes
tissue and anmiotic fluid. The small cell
transient fever, dullness, and anorexia
variant is resistant to heat, drying, and many
lasting several days.

common disinfectants and remains viable

In domestic nmtinants, gross lesions are
for weeks to years in the environment. Once
nonspecific, and differential diagnosis
a domestic ruminant is infected, C burnetii
should include infectious and noninfectious
can localize in mammary glands, supran1ai11-
agents that cause abortion. ln1munofluoresmary lymph nodes, placenta, and uterus, cence test on paired sera taken �2 wk apart
from which it may be shed in subsequent
can be used to detect recent infection;
parturitions and lactations.

however, shedding of C burnetii may occur

The epidemiology of C burnetii is
in the absence of a measurable semm
complex because there are two major
antibody titer in up to 200/o of infected
patterns of transmission. In one, the
aitimals. Culture, immunohistochentical,
orgaitism circulates between wild aitimals
and PCR tests may be used to identify
and their ectoparasites, mainly ticks; the

C burnetii in tissues. Studies conducted in other occurs in domestic ruminants,
veterinary diagnostic laboratories suggest
independent of the wild animal cycle.

that C burnetii is often found concmrently

Ixodid and argasid ticks can act as
with other orgaitisms isolated in cases of
reservoirs of the orgaitisrn. Distribution is
infectious abmtions, so mixed infections
worldwide ( except New Zealand), and the
may be irnpo1tant. Seasonal variability in
host range includes various wild and domesshedding of the orgaiusm hinders interpretic mammals, arthropods, and birds. The tation of a single PCR test. Shedding is
disease is enzootic in most areas where
highest in the periparturient pe1iod and
cattle, sheep, and goats are kept. In the
may drop below detectable levels for a

USA, seroprevalence studies have shown
significant period during the year despite
significant variability in prevalence of
persistent infection.

antibodies to C burnetii based on
difference in test population, test used, and

Treatment and Control: Q fever in
time of year. Evaluation of bulk tank ntilk
people is a notifiable disease in tl1e USA,
san1pling of USA cattle dairies has
primarily because of its status as a possible
demonstrated prevalence of the organism at
bioterrorism agent; reporting requirements
the farm level of 77% to >900/o. In a comprefor animals vary by state. Vaccines for hensive seroprevalence study conducted in
people and anin1als have been developed

Canada, 48.6% of sheep operations and
but are not commercially available in the

63.2% of goat operations had at least one

USA. Vaccination has prevented infection
positive aitimal. Not surprisingly, seroprevawhen administered to uninfected calves and lence in veterinarians and small runtinant
has in1proved fertility and reduced shedding
farmers is also high.

in previously infected animals.

The greatest risk of transmission occurs

There is little evidence-based data to
at parturition by inhalation, ingestion, or
suggest that antibiotic treatment in aitimals
direct contact with birth fluids or placenta.

provides significant benefit. Human clinical

The organism is also shed in milk, urine, and disease is typically treated with tetracyfeces. High-temperature pasteurization clines, but significant benefit from
effectively kills the orgarusm. Ticks may
tetracycline treatment has not been
transmit the disease among domestic
demonstrated in controlled studies in
ruminants but are not thought to play an
abortion outbreaks of sheep in Europe.

epidentiologically important role in

Despite the lack of evidence, some
transmission of disease to people.

practitioners still advocate the use of

ERYS/PELOTHRIX RHUS/OPATHIAE INFECTION

625
parenteral tetracyclines during abortion
associated with human abortions, and
storms. In known infected herds, the
pregnant women should take precautions
periparturient period represents a
to prevent exposure.

significant risk period for transmission

The majority of outbreaks in people have

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because of the large amount of environmenbeen associated witl1 wind dispersion of tal contamination associated with abortion.

desiccated reproductive products,

Standard abortion control measures,
contanlinated with C bwnetii, from sites
including prompt removal of aborted
where sheep, goats, or cattle are kept.

materials ( using zoonotic precautions),

Farmers and veterinarians are at risk while
segregation of animals by pregnancy status,
assisting birthing. Slaughterhouse workers
and diagnostic evaluation of abortions, are
are at risk from contact with infected
all warranted.

carcasses, hair, and wool. Transmission may
also occur by consumption of unpasteur

Zoonotic Risk: Q fever occurs more
ized milk. Handling of infected tissue poses
frequently in persons who have occupaa threat to laboratory personnel. Q fever has tional contact with high-risk species. The
been seen in personnel and hun1an patients
clinical presentation in people is highly
in medical institutions where latently
variable clinically, ranging from a self-limitinfected sheep were used for research.

ing, influenza-like illness to pneumonia,

Medical facilities using ruminants in
hepatitis, and endoca.rditis. C burnetii is research should attempt to purchase
highly infectious, and a single organism can
animals from flocks free of coxiellosis
reportedly cause infection via the aerosol
or use male animals when possible. In
route in people. Individuals who have
addition, workers should use adequate
artificial heart valves are at particular risk,
personal protective equipment to protect
as well as anyone who is significantly
against small droplet and aerosol exposure
immunocompromised. C burnetii has been
du.ring high-tisk medical procedures.

ERYSIPELOTHRIX RHUSIOPATHIAE INFECTION

(Erysipelas, Nonsuppurative polyarthritis, Postdipping lameness) Erysipelolhtix rhusiopathiae is a
frozen or chilled pork, cured and smoked
significant bactetial pathogen of swine,
ham, and feed byproducts such as dried
turkeys, and sheep. It is distributed
blood.

worldwide and has also been isolated from

E rhusiopathiae is a nornnotile,
cattle, horses, dogs, cats, mice, rats, fresh
gram-positive, facultative anaerobic bacillus.

and saltwater fish, domestic poultry, and

It is catalase negative, coagulase positive,
a variety of wild birds and mammals. Erysipoxidase negative, resistant to high salt eloid, a condition characterized by localized concentrations, and produces H2S on triple skin infections and cellulitis, may develop in
sugar iron media. Colonies of E rhusi
people who work with infected animals,
opathiae are either smooth or rough, with
infected carcasses, or infected animal
rough colonies being slightly larger, with
byproducts.

iITegular edges. On agar media, colonies are

The bacterium can survive in the soil for
clear, circular, and very small (0.1-1.5 mm in
up to 5 wk; however, soil is not an effective
dian1eter) after 24 hr of incubation, but they
growtl1 medium, and the organism is unable
increase in size after 48 hr.

to smvive for extended petiods of time in

The organism is very hardy and can
the environn1ent. Soil and surface water
swvive and grow in a wide range of pH and
contamination represent routes of
environmental temperatures. E rhusi
exposure. Asymptomatic earners are the
opathiae has demonstrated the ability to
usual source of infectious organisms, but
resist the action of several classes of
the bacteria may also be introduced to
disinfectants used in anin1al production
animal production w1its by sw-face water
units, including alcohols, aldehydes,
runoff, wild manm1als, wild birds, pets, and
oxidizing agents, and phenols. Classes of
biting insects. E rhusiopathiae has food
disinfectants and/or compounds considered
safety implications, because it can survive
to effectively inactivate E rhusiopathiae
for several months in animal tissues such as
include hypochlorites (bleach) and caustic

626

ERYSIPELOTHRIX RHUSIOPATHIAE INFECTION
soda (lye; NaOH). The organism is sensitive
tend to develop protective active in1munity
to the [3-lactam (penicillin, ampicillin),
as a result of exposure to the organism,
cephalosporin ( ceftiofur ), and tetracycline
which does not necessarily lead to clinical
classes of antibiotics and is resistant to
disease. E rhusiopathiae is excreted by

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sulfonamides.

infected pigs in feces and oronasal
secretions, effectively contaminating the
environment. When ingested, the organism

SWINE ERYSIPELAS
caz1 survive passage through the hostile

Infectious disease caused by E1ysipelo
environment of the stomach and intestines
thrix rhusiopathiae in pigs is known as
a11d may remain viable in the feces for
erysipelas and is one of the oldest recogseveral months. Recovered pigs and nized diseases that affect growing and adult
chronically infected pigs may become
swine. Up to 509'o of pigs in intensive swine
caniers of E rhusiopathiae. Healthy swine
production areas are considered to be
also may be asymptomatic caniers. Infection
colonized with E rhusiopathiae. The
is by ingestion of contaminated feed, water,
organism commonly resides in the tonsillar
or feces and tJu·ough skin abrasions.

tissue. These typical healthy cartiers can
shed the organism in their feces or oronasal

Clinical Findings: The acute az1d chronic
secretions and are an important source of
forms of swine e1ysipelas may occur in
infection for other pigs.

sequence or separately. Pigs that succumb

Disease outbreaks may be acute or
to the acute septicemic fom1 may die
chronic, and clinically inapparent infections suddenly without previous clinical signs.

also occur. Acute outbreaks are character

This form occurs most frequently in
ized by sudden and unexpected deaths,
growing and finishing pigs. Acutely infected
febrile episodes, painful joints, and skin
pigs are depressed, febrile (104°-l08°F
lesions that vary from generalized cyanosis

[ 40° -42°C]), and reluctant to stand and
to the often-desc1ibecl dian10nd skin
move. Affected pigs squeal excessively

(rhomboid wticazia) lesions. Chronic
when handled, require assistance to stand,
erysipelas tends to follow acute outbreaks
and prefer to lie down soon after being
and is characterized by enlaz·gedjoints and
forced to stand. Affected pigs may also walk
lan1eness. A second fon11 of chronic
stiffly on their toes and shift weight from
erysipelas is vegetative valvular endocaz·dilimb to limb when standing. Anorexia and tis. Pigs with valvulaz· lesions may exhibit
thirst are common, and feb1ile pigs will
few clinical signs; however, when exerted
often seek wet, cool areas to lie clown. Skin
physically they may show signs of
discoloration may vazy from widespread
respiratory distress, lethargy, and cyaz1osis,
erythema and purplish discoloration of tl1e
and possibly suddenly succumb to the
eaz-s, snout, and abdomen, to diaznondinfection.

shaped skin lesions almost anywhere on the
body, but particularly on the lateral and
dorsal regions. The lesions may occur as

Etiology: Growth of E rhusio)Jathiae on discrete, pink or purple areas of varying size
nonentiched media produces pinpoint,
tl1at become raised and firm to the touch
nonhernolytic colonies after incubation for
within 2-3 days of illness. They may

24 lu·. After 48 hr of incubation, a zone of
disappear over the cow-se of a week or
incomplete hemolysis becomes evident
progress to a more chronic type of lesion,
az·ound colonies. The genus of Erysipelo
conunonly referred to as diaz11oncl skin
thrix is subdivided into two major species: disease. If tmtreated, necrosis and

E rhusiopathiae and E tonsillarum. In separation of large areas of skin can occur,
addition, there are other strains that
and the tips of the ears and tail may become
constitute one or more additional species
necrotic and slough.

known asE species 1, E species 2, E species Clinical disease is usually sporadic

3, and E inopinata. At least 28 different
and affects individuals or small groups,
serotypes of E1ysipelolhrix spp are
but sometin1es larger outbreaks occur.

recognized, and pigs az·e considered to be

Mo1tality is vatiable (0-100%), and death
susceptible to at least 15. Field cases of
may occur up to 6 days after the first signs
swine erysipelas are predominately caused
of illness. Acutely affected pregnant sows
by E rhusiopathiae serotypes la, lb, or 2.

may abort, probably due to the fever, and

On farms where the organism il; endemic,
lactating sows may show agalactia.

pigs are exposed naturally to E rhusi

Untreated pigs may develop the chronic
opalhiae when they are young. Matemalform of the disease, usually characterized detived az1tibodies provide passive inununity by chronic arthritis, vegetative valvular and suppress clinical disease. Older pigs
endocaz·ditis, or both. Such lesions may also

ERYS/PELOTHRIX RHUSIOPATH/AE INFECTION

627
be seen in pigs with no previous signs of
likely to be seen in at least some cases
septicemia Valvular endocarditis is most
and would suppott a clinical diagnosis.

common in mature or young adult pigs and

Rhomboid urticaria. or diamond skin
is frequently manifest by death, usually from lesions are almost diagnostic when VetBooks.ir
embolism or cardiac insufficiency. Chronic
present; however, similar lesions can also
arthritis, the most common form of chronic
be seen with classical swine fever virus
infection, produces mild to severe
infection (seep 713), Actinobacillus suis lan1eness. Affected joints may be difficult to
septicemia., or the porcine dermatitis and
detect initially but eventually become hot
nephropa.thy syndrome. Isolation of E
and painful to the touch and later visibly
rhusiopathiae from blood of affected pigs,
enlarged. Dark purple, necrotic skin lesions
especially after enrichment, is possible in
that commonly slough may be seen.

acute cases and helps establish a diagnosis.

Mortality in chronic cases is low, but growtll

In addition, molecula.i· metllods capable of
rate is retarded.

detecting E rhusiopathiae DNA in affected

Lesions: At necropsy, acutely infected
tissues or blood (ie, PCR assays) can also
pigs may exhibit skin lesions, enlarged and
be used. Recently, immunohistochemical
congested lymph nodes, edematous and
methods to demonstrate the organisms in
congested lungs, splenomegaly, and
formalin-fixed paraffin-embedded tissues
hepatomegaly. Petechial hemorrhages
have become available and are useful in
may be seen on the kidneys and heart.

cases when pigs have been treated with

In chronic erysipelas, valvular endocardiantimicrobials before sa.inple submission.

tis is seen as proliferative, granular growths

A rapid, positive response to penicillin
on the heart valves, and embolisms and
therapy in affected pigs supports a
infarctions may develop. Artllritis may
diagnosis of a.cute erysipelas because of
involve joints of one or more legs, and
tile sensitivity of tile organism to penicillin.

the intervertebral a.iticula.tions may be

Clu-onic erysipelas ca.11 be difficult to
involved. Affected joints may be enlarged,
definitively diagnose. Arthtitis and
with proliferative, villous synovitis and
la.ineness, coupled witll tile presence of
increased viscosity of synovial fluid,
vegetative valvular endocarditis postmorinflan1ma.tory exuda.tes, and tllickening of tem, may support a presmnptive diagnosis
tl1e joint capsule. Proliferation and erosion
of chronic erysipelas. However, these
of articular cartilage may result in fibrosis
lesions can be ca.used by oilier infectious
and ankylosis of tllejoint.

a.gents. A positive culture of valvula.i·
vegetations or demonstration of E

Diagnosis: Diagnosis of erysipelas is
rhusiopathiae DNA in tile lesions by PCR is based on clinical signs, gross lesions,
definitive for diagnosing chronic erysipelas.

response to antimicrobial therapy, and

Serologic tests carmot reliably diagnose
demonstration of tile bacterium or DNA
erysipelas but can be useful to detemline
in tissues from affected a.ilimals. Acute
previous exposure or success of vaccinaerysipelas can be difficult to diagnose in tion protocols, because a.11tibody titers
individual pigs showing only fever, poor
should increase after vaccination. For tllis
appetite, and listlessness. However, in
purpose, ELISAs and complement fixation
outbreaks involving several animals, the
tests are available in selected laboratories.

presence of skin lesions and la.ineness is

Differential diagnoses to consider include
conditions tlla.t can precipitate gross lesions
suggestive of a.cute septicemia.. Septicemic
salmonellosis due to Salmonella Cholera.esuis infection, classical swine fever due to pestivirus infection, and septicemia. and
endoca.i·ditis due to Streptococcus suis
infection should be considered, based on
similarity of lesions. Glasser's disease ( see
p 720) due to Haemophilus parnsuis
infection and Mycoplasma hyosynoviae
infection can precipitate sinillar changes in
synovial tissues and joints of affected pigs.

Treatment: E rhusiopathiae is sensitive to Acute, severe skin form of swine erysi
penicillin. Ideally, affected pigs should be
pelas
with extensive small, raised, pink/red lesions
treated at 12-hr intervals for a mininllUll of
and some developing dark scabs. Courtesy of

3 days, although longer durations of therapy

Dr. Ranald D. A. Cameron.

may be necessary to resolve severe

628

ERYSIPELOTHRIX RHUSIOPATHIAE INFECTION
infections. On an economic basis, penicillin

(6-16 wk old) characterized by high
is the best choice for antibiotic therapy, but
morbidity and moderate to severe lameness
an1picillin and ceftiofur also yield satisfacwith enlargement of affected joints.

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tmy results in acute cases. When iltjecting
large numbers of affected pigs is in1practical, Etiology: The infectious agent of tetracyclines delivered in the feed or water
nonsuppurative polyarthritis, ErzJsipelo
may be useful. Fever associated with acute
thri.x rhusiopathiae, is thought to infect
infections can be managed by administration the aninlal through wounds created as a of NSAIDs such as flunixin meglumine or by
result of tail docking and castration
delivery of aspirin in the water. Erysipelas
procedures. However, outbreaks may
antiserum is described as an effective
also occur after "bloodless" procedures,
adjunct to antibiotic therapy in treating
particularly during extended periods of wet
acute outbreaks but is not commonly
weather, which increases the level of stress
available. Treatment of chronic infections is
and appears to enhance the survivability of
usually ineffective and not cost effective.

the organism in the environment. E rhusiopathiae localizes in joints via hematog

Prevention: Vaccination against E rhusi
enous dissemination and infects the
opathiae is very effective in controlling
synovial membrane. Progression of the
disease outbreaks on swine farms and
synovial infection results in synovitis and
should be encouraged. Cessation of
damage to articular cartilage and underlying
vaccination on some farms has been linked
subchondral bone.

to disease outbreaks. Ir\jectable bacterins
and attenuated, live vaccines delivered via

Clinical Findings and Lesions: Sudden
the water are available and provide extended onset of moderate to severe lameness in a duration of inlmunity. Optimal tinling of
high number of growing lambs is suggesvaccination may vary from farm to farm.

tive of nonsuppurative polyarthritis.

When E rhusiopathiae is endemic in the

Lameness typically occurs in two or more
production environment, vaccination should
limbs, and the joints most often affected
precede anticipated outbreaks. Susceptible
are the carpus and hock. Affected lambs
pigs may be vaccinated before weaning, at
are reluctant to move and spend extended
weaning, or several weeks after weaning.

periods of time in sternal recumbency.

Male and female swine selected for addition

Growth is often severely depressed.

to the breeding herd should be vaccinated

Progression of the condition results in
with a booster 3--5 wk later. Thereafter,
proliferation of the synovial membrane,
breeding stock should be vaccinated twice
thickening of the joint capsule without
yearly. Vaccines should not be administered
significant joint effusion, and eventual
to aninlals undergoing antibiotic therapy,
erosion of articular cartilage.

because antibiotics can interfere with the
subsequent inunune response to the vaccine.

Vaccination failures may occqr in some

Diagnosis: Sudden onset of lameness
in a large number of growing-age lambs is
herds due to management stresses that
suggestive of polyarthritis due to E rhusi
compromise the inlmune system of
opathiae. Because joint effusions are
vaccinated pigs. Antigenic differences
minimal, attempts to obtain a sample from
between serotypes in vaccines and serotypes affected joints for culture and other circulating on farms can also result in
incomplete inlmunity and disease outbreaks, diagnostics may be unsuccessful.

but this is a rare event because there is good
cross-protection among the major E rhusi

Prevention and Treatment: Vaccina
opathiae strains infecting pigs.

tion should be considered on premises

In addition to vaccination, attention to
where the disease is a recurring problem.

sanitation and hygiene and elimination of

Adopting strict antiseptic techniques and
pigs with clinical signs suggestive of
maintaining hygienic conditions for tail
erysipelas infection represent other viable
docking and castration are recommended
methods that may help control the disease
but may not prevent the condition. The
on swine farms.

so-called "bloodless" methods of performing both procedures may reduce the chances of wound contanlination, but

NONSUPPURATIVE
outbreaks are still possible. Administration

POLYARTHRITIS IN LAMBS
of penicillin for 5 days is recommended for
effective treatment of the nonsuppurative

Nonsuppurative polyarthritis is an
polyarthritis. Administration ofNSAIDs
infectious condition of older, growing lambs helps improve lan1eness.

FOOT-AND-MOUTH DISEASE

629

POSTDIPPING LAMENESS IN
acute postdipping lan1eness. Outbreaks may

SHEEP
also occur when sheep must walk through
wet and muddy areas that are heavily

Postdipping lameness affects lambs and
contaminated with tl1e organism.

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adult sheep. It is characterized by severe
lan1eness that results from infection caused

Clinical Findings: Two to 4 days after
by the penetration of Erysipelothrix
dipping, a variable number (up to 90%, but
rhusiopalhiae through skin abrasions in
usually -25%) of sheep in tl1e flock may be
the hoof. Postdipping lan1eness, which
lame in one or more limbs. Affected limbs
normally occurs in outbreaks, has been
appear nonnal except for the hoof and
described in most sheep-raising countiies.

pastern regions, where the coronary band

Because of the reduced usage of sheep dips
may be swollen, hot, and painful. Most
in recent years, this manifestation is seen
sheep recover spontaneously in 2-4 wk with
less frequently now.

nothing more se1ious than a slight loss of
body weight. In some outbreaks, however,

Etiology: With time and repeated use,
administi·ation of penicillin for 5 days may
dipping solutions, which have little or no
be necessary to salvage affected sheep.

bacteriostatic activity, become heavily

Septicemia and polyarthtitis are not
contaminated with various species of
common with this condition.

bacteria. E rhusiopalhiae is a common
contaminant, and its presence in the dipping Prevention and Treatment: Discarding vat, sometimes in enormous numbers, leads
heavily contaminated dips is the best way to
to infection of skin wounds during dipping.

prevent infection with E rhusiopathiae and

Small skin abrasions in the region of the
the lan1eness associated with tllis condition.

hoof and fetlock joint are a common portal

Using an appropriate bacteriostat in dip
of entry. Lesions extending from these
solutions may reduce the incidence of the
wounds to tl1e laminae of the hoof cause
condition.

FOOT-AND-MOUTH DISEASE

Foot-and-mouth disease (FMD) is a llighly

Western Europe. In endenlic countries,
communicable viral disease caused by an

FMD places economic constraints on the

Aphthovirus of the family Picornaviridae.

international livestock trade and can be

There are 7 serotypes: A, 0, C, Asia 1, and
easily reintroduced into disease-free areas

SAT (Southern African Tenitories) 1, 2, and
unless strict precautions are in place.

3. Fmther diversity is found in strains within

Outbreaks can severely disrupt livestock
each serotype. It primarily affects clovenproduction and require significant resources hooved animals of the order Artiodactyla.

to control, as in the 2001 UK outbreak.

Livestock hosts include cattle, pigs, sheep,
goats, and experimental infections in

Epidemiology and Transmission: FMD
alpacas and llamas. FMD virus has also been
is endenlic in many countries of the Middle
reported in > 70 species of wild artiodactyls,

East, Afiica, Asia, and in parts of Soutl1
inclucling bison, giraffes, Indian elephants,

Ame1ica. Where FMD still occurs, serotypes
and several species of deer and antelope.

are not mlifonnly distributed. Six of the 7

The disease is characterized by fever and
serotypes have occu!l'ed in Africa (0, A, C,
vesicles in the mouth and on the muzzle,

SAT-1, SAT-2, SAT-3), 4 in Asia (0, A, C,
teats, and feet and is spread through direct

Asia-1), and 3 in South America (0, A, C).

contact or aerosolized virus via respiratory

North and Central Ame1ica, Australia, New
secretions, milk, semen, and ingestion of

Zealand, Greenland, Iceland, and Western
feed from infected aninlals (meat, offal,

Europe are free of FMD. In 2001, FMD was
milk). In a susceptible population, morbidity
inti·oduced into the UK, where it spread to
reaches 100% with rare fatalities except in
lreland, the Netherlands, and France. The
young animals. FMD was once distributed
highly virulent pan-Asiatic serotype O
worldwide but has been eradicated in some
causing the outbreak was the san1e found
regions, including North America and
throughout Asia.

630

FOOT-AND-MOUTH DISEASE

The virus is transmitted via direct or
quaternary an1rnonium compounds,
indirect contact with infected secretions
hypochlorite, and phenols are less effective
and excretions (including semen and milk),
disinfectants, especially in the presence of
mechanical vectors (people, horses, dogs,
organic matter.

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cats, birds, vehicles), and air currents over

FMD is shed into milk in dairy cows
land or water. The vims can enter the body
before clinical signs develop, so there is
via inhalation, ingestion, or through skin
opportunity for virus to spread fann to fam1
wounds and mucous membranes. Breeding
and from cow to calf via raw milk FMD may
is a possible route of transmission for the
survive pasteurization depending on the

SAT viruses in African buffalo populations.

method (ltigh temperature sh01t time, ultra

An example scenario for introduction into a
high temperature, laboratory pasteurizapreviously FMD-free area is for a susceptition); the lipid component of milk protects ble population, such as pigs, given imported
virus during heating. FMD virus survives up
food derived from an infected animal (meat,
to 20 wk on hay or straw bedding, in dry
offal, milk). Virus then spreads from pigs,
fecal matter for up to 14 days in sun1rner, in
which can expire up to 3,000 times more
a fecal slw·ry for up to 6 mo in winter, in
virus than cattle, to more susceptible cattle
wine for 39 days, and in soil for 3 ( swnmer)

hosts via aerosol. Vims was reported to
to 28 (winter) days.

travel over water >250 km ( 155 miles) from

The incubation period of FMD is variable

Brittany, France, to the Isle of Wight, UK,
and depends on the host, environment, route
in 1981, but it usually travels no more than
of exposure, and virus strain. After infection

10 km ( -6 miles) over land. FMD has high
with FMD vims, the average incubation
agroterrorism potential because of its
period for sheep and goats is 3-8 days, �2
infectivity, high transmissibility through
days for pigs, and 2-14 days in cattle. The
wind and inanimate objects, and potential
incubation period can be as short as 18 hr
for large economic losses.

for host-adapted strains in pigs, especially

People can act as mechanical vectors of

W1der intense direct contact.

FMD by carrying virus on clothing or skin.

FMD is not considered a public health

Clinical Findings: Clinical signs in cattle
problem, but there are reports of people
include pyrexia of -104 ° F, followed by
who work in FMD vaccine laboratories who
vesicular development on tl1e tongue, hard
have developed antibodies to the virus.

palate, dental pad, lips, gums, muzzle,

There are few reports of people with
coronary band, interdigital cleft, and teats in
laboratory-confirmed cases of clinical
lactating cows. Acutely affected individuals
illness between 1921 and 1969. The disease
may salivate profusely, stamp their feet, and
in people is usually short-lived and mild,
prefer to lie down. Ruptured oral vesicles
with symptoms including"vesicular lesions
can coalesce and fonn erosions but heal
and influenza-like illness.

rapidly, roughly 11 days after vesicle
formation. Feet vesicles take longer to heal

Pathogenesis: The primary site of
and are susceptible to bacterial infection
infection and replication of FMEl is in the
leading to chronic lameness. Secondary
mucosa of the pharynx. The virus may also
bacterial mastitis is common due to infected
enter through skin lesions or the GI tract.

teat vesicles and resistance to milking. After

Once distributed throughout the lymphatic
vesicular disease develops, cattle quickly
system, the virus replicates in the epithelose condition and milk yield, which can lium of the mouth, muzzle, teats, feet, and
persist chronically.

areas of damaged skin ( eg, knees and hocks

Infected pigs show mild lameness and
of pigs). Vesicles then develop at the organs
blanching around the coronary band and
and rupture within 48 hr. More than 500A, of
may develop a fever of up to 107°F. Affected
ruminants that recover from illness and
pigs become lethargic, huddle among other
those that are vaccinated and have been
pigs, and have little interest in feed. Vesicles
exposed to virus can carry virus particles in
develop on the coronary band, heel of the
the pharyngeal region-up to 3.5 yr in cattle, foot including accessory digits, snout, 9 mo in sheep, and >5 yr in African buffalo.

mandible, and tongue. Additional vesicles

FMD virus is environmentally resistant
may form on the hocks and knees of pigs
and inactivates outside the pH range 6-9
housed on rough surfaces. Depending on
and desiccation and at temperatures >56°C
the severity of vesicles, the horn of the foot

(132.8°F). It is resistant to lipid solvents
may completely slough off and cause
such as ether and chloroform, but sodium
chronic lan1eness in recovered pigs. Young
hydroxide (lye), sodiun1 carbonate (soda
pigs <14 wk old may die without clinical
ash), citric acid, and acetic acid (vinegar)

signs of illness because of viral dan1age to
are effective disinfectants. Iodophores,
the developing myocardium.

FOOT-AND-MOUTH DISEASE

631

Lameness is usually the first clinical sign
method for countries with endemic FMD for
of FMD infection in sheep and goats. This is
viral antigen detection and serotyping (OIE
followed by fever and vesicular develop

TerTestrial Manual 2012). ConcrnTent virus
ment on the interdigital cleft, heel bulbs,
isolation may be performed, preferably in

VetBooks.ir
coronary band, and mouth. Vesicles may
primary bovine thyroid cell culture.

also form on the teats of lactating animals

Detecting nucleic acids via RT combined
and rarely on the vulva and prepuce.

with real-time PCR is more sensitive and

Secondary infections result in reduced milk
rapid than conventional methods and may
yield, chronic lameness, and predisposition
be more useful when samples contain low
to other viral infections, including sheep/
concentrations of virus. ELISA is preferred
goat pox (seep 869) and peste des petits
over complement fllCation tests because of
ruminants (seep 766). Similarly to young
its increased sensitivity and specificity, but
pigs, infection in inm1ature sheep and goats
complement fixation may be performed if
results in death without clinical signs due to

ELISA reagents are not available. Commerheart failure.

cially available lateral flow devices have not

Experimentally infected camelids are
yet been validated by the OIE.

commonly reported to have mild clinical

Serologic tests for FMD are used to
illness, if at all, but can have severe
certify animals for import/export (ie, trade),
infections resulting in salivation and mouth
confirm suspected cases ofFMD, test
lesions and sloughing of the footpad and
efficacy of vaccination, and provide
skin of the tarsal and carpal joints. Water
evidence for absence of infection. Testing
buffalo can have mouth and foot lesions,
cut-offs may be set at different levels for
which heal faster and are less severe than
herd-based surveillance versus certifying
those in cattle. FMD infections in wildlife
freedom of infection for trade purposes.

resemble clinical illness in their domestic

The choice of serologic test depends on the
counterparts, but more severe lesions such
vaccination status of the animals. Serologic
as sloughing of antlers or toe horn are
tests for antibodies to the viral structural
repmted.

( capsid) proteins cannot be used in
vaccinated animals, because FMD vac

Diagnosis: In cattle and pigs, the clinical
cines induce antibodies to these proteins.

signs of FMD are indistinguishable from

Detection of antibodies to nonstructural
those of vesicular stomatitis (seep 694),
proteins, which are expressed only during
and in pigs from those of swine vesicular
virus replication, can be used to determine
disease (seep 735) and vesicular exanpast or present infection with any of the 7
thema (seep 738). Therefore, laboratory
serotypes, whether or not tl1e animal has
confirmation is essential for diagnosis of
been vaccinated. However, they are less

FMD and should be performed in specialsensitive and may result in false-negatives in ized laboratories that meet OIE requirecases with limited virus replication such as ments for Containment Group 4 pathogens.

vaccinated animals that become infected,

Countries lacking access to a national or
because the vaccine suppresses viral
regional laboratory meeting these
replication (OIE Ten-es trial Manual 2012).

guidelines should send specimens to an OIE

FMD reference laboratory. The tissue of

Treatment, Control, and Prevention:

choice for san1pling is vesicular epitheliun1

The OIE classifies countries and regions as
or fluid. At least 1 g of epithelium should be

FMD-free without vaccination, FMD-free
placed in a transport medium of phosphatewith vaccination, suspended FMD-free buffered saline (PBS) or equal parts glycerol status with or without vaccination, and and phosphate buffer with pH 7.2-7.6.

unrecognized (World Organization for

Samples should be kept refrigerated or

Animal Health, 2013). The CU1Tent global
transported on ice. lf vesicles are not
status ofFMD distribution shows geopresent, oropharyngeal fluid can be graphic areas of viral "hotspots" where FMD
collected via probang cup or pharyngeal
prevalence indices are highest over long
swabbing for virus isolation or reverse
periods of time. They are commonly located
transcription PCR (RT-PCR). Serun1 (blood)

in poor countries where veterinary services
samples may also be tested by these means
and resources are inadequate to control or

(OIE Terrestrial Manual 2012). Repeated
eradicate FMD. Combined use of trade and
sampling may be necessary to identify a
movement restrictions of animals and
carrier, because virus presence may be low
animal products has not completely
and fluctuate.

prevented introductions of FMD into

Laboratory diagnosis is usually per

FMD-free areas. These viral incursions into
forn1ed via antigen capture-ELISA or
coU11tries or regions where FMD is not
serotyping ELISA. This is the preferred
enzootic are usually controlled by slaughter

632

FOOT-AND-MOUTH DISEASE
of all infected and susceptible animals,
mass slaughter is not possible, strict
strict restriction of animal and vehicle
quarantining and movement restriction
movement arow1d infected premises,
should be enforced. However, quarantine
proper carcass disposal, and environmental
may not be long enough to prevent carrier

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disinfection, without the use of vaccines.

aninlal movement after an outbreak. When

Inactivated virus vaccines are limited in
mass euthanasia is perfom1ed, infected
their use, because they protect for only
carcasses must be disposed of via incinera4-6 mo against the specific serotype( s) tion, burial, or rendering on or close to the
contained in the vaccine and protect
infected premises. Scavengers and rodents
aninlals from clinical illness but not viral
should be prevented or killed to prevent
persistence in the pharyngeal region;
mechanical dissemination of virus.

therefore, they can induce a carrier state.

Buildings should be cleaned with a mild

Additionally, it is difficult to distinguish
acid or alkali disinfectant and fumigation,
infected animals from vaccinated aninlals
and people that have come into contact with
unless purified killed vaccines are used.

virus may be asked to decontaminate their

Therefore, vaccination is used more in
clothing and avoid contact with susceptible
enzootic countries to protect producing
animals for a period of tin1e.

aninlals, particularly high-yielding dai1y

In some regions, FMD persistence in
cattle, from clinical illness because
wildlife populations, such as the wild
slaughter of all at-risk individuals may be

African buffalo, can make FMD eradication
economically unfeasible and can cause
unrealistic. Control measures, such as
food shortages.

fencing of wildlife reserves to prevent

Rapid disease reporting is essential to
contact with domestic livestock, have
control an FMD outbreak in nonendemic
helped linlit the spread of virus in certain
countries. Veterinarians who encounter
areas. A twice-yearly vaccination buffer
any vesicular disease in the USA should
zone in livestock proximal to endemic
immediately inform their state or federal
wildlife reserves may additionally help
veterinary authorities. After an outbreak,
decrease outbreak occurrence.

tracing is done through epidemiologic

There is no specific treatment for FMD,
inquiries to help identify the source of
but supportive care may be allowed in
disease introduction. In countries where
countries where FMD is endemic.

FUNGAL INFECTIONS

(Mycoses)

Systemic mycoses are infections with fwlgal
losis and candidiasis, which may be focal
organisms that exist in the envirorunent,
or systemic.

enter the host from a single portal of ently,

Clinical findings and gross lesions are
and disseminate within the host usually to
often suggestive of systemic mycoses, but
multiple organ systems. The soil reservoir is
definitive diagnosis requires microscopic
the primary source of most infections, which identification, culture of the organism, or can be acquired by inhalation, ingestion, or

PCR. Identification of the fW1gus and the
trawnatic introduction of fwlgal elements.

tissue reaction via microscopic exanlination

(See also DERMATOPHIJJ)SIS, p 858.)

of exudates and biopsy material is adequate

Pathogenic fwlgi establish infection in
for diagnosis of histoplasmosis, cryptococapparently normal hosts, and such diseases cosis, blastomycosis, coccidioidomycosis,
as histoplasmosis, coccidioidomycosis,
and rhinosporidiosis. Other diseases, such
blastomycosis, and cryptococcosis are
as candidiasis, aspergillosis, zygomycosis,
regarded as primary systemic mycoses.

phaeohyphomycosis, hyalohyphomycosis,

Opportunistic fwlgi usually require a host
and oomycosis (pyth.iosis and lagenidiosis ),
that is debilitated or immunosuppressed to
usually require more than microscopic
establish infection. Prolonged ad.ministraevaluation for a definitive diagnosis. Some tion of antimicrobials or immunosuppresof these fungi are also common contantisive agents appears to increase the nants of cultures; thus, tissue invasion and
likelihood of infection by the opportunistic
reaction must be demonstrated for the
fwlgi that cause diseases such as aspergil-
culture isolation to be considered signifl-

FUNGAL INFECTIONS

633
cant. Serology may be useful for diagnosis
the disease grossly resembles tuberculosis

( and prognosis) of some mycotic diseases

(seep 687).

such as coccidioidomycosis, pythiosis, and

In the absence of pneumonia, infected
lagenidiosis. Antigen titers have proved
cows generally have no signs except for

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useful for cryptococcosis, histoplasmosis,
abortion; a dead fetus is aborted at 6-9 mo
and blastomycosis.

gestation, and the fetal membranes are

For treatment, see discussions of specific
retained. Lesions are found in the uterus,
systemic mycoses (below) and see SYSTEMIC
fetal membranes, and often the fetal skin.

Pl·IARMACOTl·IERAPEUTICS OF' THE INTEGUMENTARY

In the uterus, the intercaruncular areas are

SYSTEM, p 2571.

grossly thickened, leathery, dark red to tan,
and contain elevated or eroded foci covered

ASPERGILLOSIS
by a yellow-gray adherent pseudomembrane. Maternal caruncles are dark red to Aspergillosis is caused by several Aspergil
brown, and the adherent fetal cotyledons
lus spp, especially Afumigatus and A are markedly thickened. Cutaneous lesions
terreus. A niger, A nidulans, A viridinu
in abmted fetuses consist of soft, red to
lans, Ajlavus, andAfelis are being
gray, elevated, discrete foci that resemble
recognized more commonly with increasing

1ingworm.

use of molecular techniques for identifica

In horses, epistaxis and dysphagia are
tion. Aspergillus infection is found
comn1on complications of gutturomycosis
worldwide and in almost all domestic

(seep 1463). The infecte<I guttural pouch is animals and birds as well as in many wild
characterized by a necrotizing inflan1mation
species. It is primarily a respiratory infection
and is thickened, hemorrhagic, and covered
that may become generalized; however,
by a friable pseudomembrane. Mycotic
tissue predilection varies among species.

rhinitis characterized by dyspnea and

The most conunon forms are pulmonary
nasal discharge has also been described.

infections in poultry and other birds; mycotic Aspergillosis can be a rapidly fatal disease abortion in cattle; guttural pouch mycosis in
associated with diffuse pulmomuy invasion.

horses; infections of the nasal and paranasal

In these cases, acute enteritis is often a
tissues, interve1tebral sites, and kidneys of
predisposing factor. The colitis is thought
dogs; and sinonasal, sino-orbital, and
to result in a profound neutropenia that
pulmonary infection in domestic cats.

decreases the inununocompetence of the
host, followed by the invasion of Aspergil

Clinical Findings and Lesions: In
lus from disrupted intestinal mucosa.

birds, aspergillosis (seep 2901) is primarily Locomotor and visual disturbances,
bronchopulmonary, with dyspnea, gasping,
includi.n.g blindness, may occur when the
and polypnea accompanied by somnolence,
infection spreads to the brain and optic
anorexia, and emaciation. Mycotic tracheitis nerve.

has also been described. Torticollis and

In dogs, aspergillosis is typically localized
disturbances of equilibrium are seen when
to the nasal cavity or paranasal sinuses and
infection disseminates to the brain. Yellow
is usually caused by infection with A
nodules of varying size and consistency or

Jumigatus. Nasal aspergillosis is seen
plaque lesions are found in the respiratory
mainly in dolichocephalic breeds; it begins
passages, lungs, air sacs, or membranes of
in the poste1ior region of the ventral
body cavities. Fur-like growth of fungus may maxilloturbinate with signs of lethargy, be found on the thickened walls of air sacs.

Other species with bronchopulmonary
aspergillosis may have nodular lesions in the
lungs or an acute pneumonia accompanied
by serosanguineous fluid in the pleural
cavity and a fibrinous pleuritis.

In ruminants, aspergillosis may be
asymptomatic, appear in a bronchopulmonary form, cause mastitis, or cause placentitis and abortion. Mycotic pneumonia may be rapidly fatal. Signs include pyrexia; rapid, shallow, stertorous
respiration; nasal discharge; and a moist
cough. The lungs are firm, heavy, and
mottled and do not collapse. In subacute
to chronic mycotic pneumonia, the lungs

Aspergillus fumigatus from canine nasal
contain multiple discrete granulomas, and
infection. Courtesy of Ontario Veterinary College.

634

FUNGAL INFECTIONS
nasal pain, ulceration of the nares, sneezing, lesions. Systemic disease is usually unilateral or bilateral sanguinopurulent
diagnosed by culture of the organism, often
nasal discharge, frontal sinus osteomyelitis,
from urine. A blood and urine galactomanand epistaxis. Gross lesions vary considernan antigen assay for diagnosis of systemic VetBooks.ir
ably with site of infection, but the mucosa
aspergillosis in dogs has been described to
of the nasal and paranasal sinuses may be
have moderate sensitivity and specificity.

covered by a layer of necrotic material and
white to gray-white fungal growth. The

Treatment: In clogs, topical treatment is
mucosa and the underlying bone may be
considered the treatment of choice for nasal
necrotic with loss of bone definition on
and paranasal aspergillosis. Several surgical
radiographs or CT.

techniques and drug regin1ens have been

Disseminated disease in dogs is seen
used with varying success. Clotrimazole
most often in middle-age, female German
formulated in a polyethylene glycol base is

Shepherds and usually involves A le1Teus,
generally considered the first-line treat

A deflectus, and A niger. The clinical signs ment. It can be adnunistered through
of disseminated aspergillosis may include
indwelling tubes trephinecl into tl1e frontal
lethargy, lameness, anorexia, weight loss,
sinuses or via the nares as a single infusion.

muscle wasting, pyrexia, hematuria, urinary If infusion is via the nares, Foley catheters incontinence, generalized lymphadenopaare used to instill 0.5 g in each side of the thy, and neurologic deficits. Lesions are
nasal cavity. The infused solution is left in
frequently found in the abdominal and
place for 1 hr, during which the dog's
thoracic lymph nodes, kidneys, spleen, and
position is changed periodically to
vertebrae. Discospondylitis is conunon.

maximize penetration. There is an -8QOA,

In cats, sinonasal and sino-orbital disease success rate using local infusions in tlus is seen most often. Aspergillosis is rare in
marmer. Enilconazole, 10 mg/kg, instilled
cats compared with dogs. Sinonasal disease
bid for 7 -14 days, via tubes implanted
can present similarly to the disease in dogs,
surgically into the frontal sinuses, has also
but sino-orbital disease can be very
been used with a similar success rate. Drugs
aggressive, often causing severe facial
given systemically have included ketoconaswelling. In some cases, a mass in the zole, itraconazole, fluconazole, voriconapterygopalatine fossa or ulceration of the zole, and posaconazole. Fluconazole
hard palate may be seen. The CNS may be

(2.5--10 mg/kg, divided bid) and itraconazole
invaded, causing neurologic signs.

(5-10 mg/kg/day) are cost-effective options.

Ketoconazole (5--10 mg/kg, bid for 6--8 wk),

Diagnosis: Radiographs in dogs with
although cost-effective, is not as effective
nasal aspergillosis may show generalized
clinically. Vmiconazole (3--6 mg/kg/day) is
radiolucence of the nasal cavity secondary
probably the most effective of the azole
to turbinate tissue destruction. Frontal
antifungals for treating aspergillosis, but the
sinus osteomyelitis is seen in as many as
cost is much higher than that of the other

80% of dogs. Cross-sectional imaging via CT
choices.

is more sensitive than plain radiographs in

In horses, surgical exposure and
demonstrating consistent changes.

curettage have been used to treat gutturo

Visualization of fungal plaques by rhinosmycosis. Topical natarnycin and oral copy together with serologic and either
potassium iodide have been reported
mycologic or radiographic evidence of
effective in cases of Aspe1!]illus infection.

disease is often how a diagnosis is made.

Itraconazole (3 mg/kg, bid for 84-120 days)

A diagnosis based on culture results alone
has been reported effective in Aspergillus
is not appropriate, because aspergilli are
rhinitis in horses.

ubiquitous and can be isolated from Lhe

Bovine mastitis has been treated
nasal cavities of healthy dogs. Positive
successfully with combined intra-arterial
culture results should be supported by
and intraman1mary irtjection with miconademonstration of narrow, hyaline, septate, zole.

branching hyphae within lesions or by
serologic tests. The agar-gel double-diffu

BLASTOMYCOSIS
sion test for serum antibody is generally
considered unreliable. Dogs with systemic

Blastomycosis, caused by the dimorphic
disease usually have neutrophilia, often
fungusBlastomyces dermatitidis, is
with a left shift, and a nonregenerative
characterized by pyogranulomatous lesions
anemia. Azoternia, hyperglobulinemia,
in various tissues. It is most common in
hypoalbununemia, and hypercalcemia are
people, dogs, and cats but has also been
common. Ultrasound usually reveals
described in such widely divergent species
abdominal lymphadenopathy and renal
as horses, ferrets, deer, wolves, African

FUNGAL INFECTIONS

635
lions, bottlenosed dolphins, and sea lions. It
uveitis, glaucoma, and retinal detachment.

appears not to be a disease of cattle, sheep,

Lameness associated witl1 fungal osteomyor pigs. Blastomycosis is generally limited elitis or severe paronychia occurs in
to No1th Ame1ica, and most cases have
approximately one quarter of affected dogs.

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occurred in the Mississippi, Missouri,

CNS signs are uncommon, occurring in <5%

Tennessee, and Ohio River basins and along
of dogs, but they may be more common in
the Great Lakes and the St. Lawrence
cats. The pattern of systemic involvement is

Seaway. There is an endemic area in the
sinlilar in cats, but cats are affected far less

Pacific northwest. Even within these river
conm10nly than dogs. Hematuria and
basins, the organism is found in geographidysmia may be seen with urogenital cally restricted areas. Beaver dan1s and
blastomycosis.

other habitats where soil is moist, acidic,
and rich in decaying vegetation may serve

Lesions: Gross lesions consist of few
as the ecologic niche for the organism, but it to numerous, variable-sized, irregular, is often difficult to find in the environment.

firm, gray to yellow areas of pulmonary

The organism has also been recovered from
consolidation and nodules in the lungs and
pigeon and bat feces. Rain, dew, or fog may
thoracic lymph nodes. Dissenlination may
play a c1itical role in liberating the infective
result in nodular lesions in various organs
conidia, which then are aerosolized and
but especially the skin, eyes, and bone.

inhaled. When respiratory defenses are

Cutaneous lesions are single or multiple
overwhelmed or inm1unosuppressed,
papules, or chronic, draining, nodular
disseminated disease occurs via hematogpyogranulomas.

enous spread from the lungs. Cutaneous
lesions may result from a primary entry

Diagnosis: Blastomycosis should be
through the skin or, more commonly, by
considered in dogs with draining cutaneous
dissemination from a pulmonary focus.

nodules and signs of respiratory disease. In

Needle-stick iltjuries to veterinary
cats, respiratory tract involvement is seen
personnel after aspiration of cutaneous
most frequently, followed by involvement of
lesions from infected animals have resulted
the CNS, regional lymph nodes, skin, eyes,
in primary cutaneous infection. Ocular
and GI and urinary tracts. Radiographic
lesions tend to develop first in the posterior
findings in the lungs include noncalcified
segment, resulting in granulomatous
nodules or consolidation, with enlargement
chorioretinitis and retinal detachment.

of the bronchial and mediastinal lymph

Ante1ior segment involvement often
nodes. The predominant patterns on
follows, resulting in anterior uveitis and
thoracic radiographs are those of diffuse
panophthalrnitis.

nodular interstitial and peribronchial
densities. Commonly, the bronchial lymph

Clinical Findings: The signs vary with
nodes are greatly enlarged and appear in
organ involvement and are not specific.

radiographs as dense masses. Diagnosis can

Weight loss may be accompanied by
be made from biopsy of tissue or aspirated
coughing, anorexia, lymphadenopathy,
specimens taken from cutaneous lesions or
dyspnea, ocular disease, lan1eness, skin
other involved organs by tl1e presence of
lesions, and fever. Dry, harsh hmg sounds
thick-walled yeast that often have daughter
from lung lesions are common in dogs with
cells budding from a broad base. These
blastornycosis. Signs of pulmonary
round to ovoid, pale pink (H&E) blastoinvolvement are seen in as many as 85% of spores measure 8-25 µm and have a
affected dogs. Severe pulmonary involverefractile, double-contoured wall. They may ment results in hypoxemia, which indicates
be empty or contain basopllilic nuclear
a poor prognosis. Lymph node involvement
matelial and have single, broad-based buds.

is seen in approximately half of affected

An antibody response, detected by agar gel
dogs, which is about tl1e same proportion of
immunodiffusion, usually occurs, but tllis
dogs tl1at have cutaneous involvement. Skin
response is neither sensitive nor specific
lesions may include proliferative granulowhen attempting to make a definitive mas and subcutaneous abscesses that
diagnosis. An enzyme inmlunoassay for
ulcerate and drain a serosanguineous
antibodies to rBAD-1 repeat has shown
discharge. The skin lesions are often very
improved sensitivity. A recently developed
small and multifocal in dogs, but large
antigen enzyme immunoassay has been
abscesses are occasionally seen, especially
used in both serun1 and urine to detect
in cats. The planun1 nasale, face, and nail
cell-wall galactomannan that is inmlunologibeds are most often involved. Signs of cally indistinguishable in histoplasmosis
ocular blastomycosis are seen in 30%--500A,
and blastomycosis. Although the titer is not
of affected dogs and include blindness,
useful in differentiating between tl1e two

636

FUNGAL INFECTIONS
infections, it helps diagnose the presence
considered a cause of arthritis in horses
of one of these two systemic my coses.

and mastitis and abortion in cattle.

Fungemia and Candida peritonitis have

Treatment: Itraconazole (5 mg/kg/day) is
been noted in dogs with perforating

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the treatment of choice for dogs and cats
intestinal lesions after surgery, and
with blastomycosis. A minimum of 2 mo of
mucosa! and cutaneous candidiasis has
treatment is necessary, and the drug should
been noted in immunosuppressed dogs
be continued until active disease is not
and in dogs with diabetes mellitus.

apparent. Clinical cure can be expected in

-700/o of dogs, with recurrence months or

Clinical Findings and Lesions: Signs
years after treatment noted in -20% of
are variable and nonspecific and may be
treated dogs. Most dogs will respond to
associated more with the primary or
retreatment with itraconazole. Other azoles
predisposing conditions than with the
such as fluconazole and ketoconazole are
candidiasis itself. Calves with forestomach
not as effective as itraconazole, but a study
candidiasis have watery diarrhea, anorexia,
evaluating cost-effectiveness of fluconazole
and dehydration, with gradual progression
showed it to be a less expensive alternative,
to prostration and death. Affected chicks
despite longer treatment times. In
are listless and have reduced feed intake
fulminating cases of blastomycosis,
and growth rate. Porcine candidiasis affects
especially those with evidence of hypoxthe oral, esophageal, and gastric mucosa, emia, combination therapy with an1phowitl1 dian-hea and emaciation the most tericin B and itraconazole is recommended.

consistent signs.

Short courses of anti-inflammatory dosages

Gross lesions of the skin and mucosae are
of glucocorticoids have been advocated
generally single or multiple, raised, circular,
during the first few days of treatment by
white masses covered with scabs. The
some, but steroid use is controversial and
organism can penetrate keratinized
may actually worsen the prognosis. The
epithelium and cause marked keratinous
prognosis is best for dogs with only mild
thickening of the mucosae of the tongue,
lung disease, is more guarded for dogs with
esophagus, and run1en. In birds, the crop
moderate to severe lung disease, and is
and esophageal lesions are white, circular
poorest for dogs with CNS involvement.

ulcers with raised surface scabs that
produce thickening of the mucosa; an easily

CANDIDIASIS
removed pseudomembrane is common.

Candidiasis is a localized mucocutaneous

Diagnosis: Fungal organisms are
disease caused by species of the yeast-like
numerous in proliferating epithelial tissue,
fungus Candida, most commonly C
and diagnosis can be made by examination
albicans. It is distributed worldwide in a
of scrapings or biopsy specimens from
variety of aninlals. C albicans is a normal mucocutaneous lesions. C albicans are
inhabitant of the nasopharynx, GI tract,
ovoid, budding yeast cells (2-4 µm in
and external genitalia of many species of
diameter) with thin walls, or they occur in
aninlals and is opportunistic in causing
chains that produce pseudohyphae when
disease. Factors associated with candidal
the blastospores remain attached after
infections are disruption of mucosa!

budding division. Filamentous, regular, true
integrity; indwelling, intravenous, or urinary hyphae also may be visible. The fungal cells catheters; administration of antibiotics; and
generally are limited to epithelial tissue and
inununosuppressive drugs or diseases. The
rarely extend deeper.

organism most frequently infects birds ( see
p 2791), in which it involves U1e oral

Treatment: Nystatin ointment or topical
mucosa, esophagus, and crop. Superficial
application of amphotericin B or !%iodine
infections limited to the mucous memsolution may be useful in the treatment of branes of the intestinal tract have been
oral or cutaneous candi.diasis. Amphotericin
described in pigs and foals. Systemic

B, 500 g in 1 L of 5% dextrose, was adminiscandidiasis has also been described in tered IV, every 48 hr for 24 days and then
cattle, calves, sheep, and foals secondary
every 72 hr for 15 days, to successfully
to prolonged antibiotic or corticosteroid
resolve arthritis induced by C fumata in a
therapy. In cats, candidiasis is rare but has
horse. Fluconazole (5 mg/kg/day, PO, for
been associated with oral and upper

4-6 wk) was also used to successfully treat
respiratory disease, pyothorax, ocular
disseminated candidiasis in foals. Itraconalesions, intestinal disease, and urocystitis.

zole and an1photericin B lipid complex are

Infections are rare in dogs and horses.

considered the treatments of choice in dogs,

However, Candida spp have been
but few cases have been treated.

FUNGAL INFECTIONS

637

COCCIDIOIDOMYCOSIS
of some foci may contain purulent exudate
and fungal organisms. Some lesions may

(Valley Fever)

have mineralized foci.

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Coccidioidomycosis (Valley Fever) is a
dustbome, noncontagious infection caused

Diagnosis: In endemic areas, coccidioidoby the dimorphic fungus Coccidioides mycosis should be considered in dogs with
immitis. Infections are limited to arid and chronic bronchopulmonary disease and
semiarid regions of the southwestern USA
when pulmonary nodules and enlarged
and to similar areas of Mexico and Central
lymph nodes are found on thoracic
and South America. Although many species
radiographs. The lesions are pyogranuloof animals, including people, are susceptimas that contain C immitis free in the ble, only dogs are affected significantly.

exudate and in epithelioid and multinucle

Placental infection leading to abortion
ate giant cells. The organisms vary in size
and osteomyelitis have been described
and appear as relatively large (20-80 µm,
in horses. Ruminants and pigs may have
up to 200 µm) spherules with a doublesubclinical infections with lesions restricted contoured wall. The mature spherules to foci in the lungs and to thoracic lymph

(sporangia) contain endospores (sporangionodes. Inhalation of fungal spores is the spores) 2-5 µm in diameter. Diagnosis is
only established mode of infection, and
established by demonstrating the spherules
spores may be carried on dust particles.

in tissues. Serum can also be tested by agar

Epidemics may occur when rainy periods
gel immunodiffusion (AGID) assays for
are followed by drought, resulting in dust
detection of precipitin and complementstorms. Most bovine infections are fixing antibodies. Currently, most commercontracted in dusty feedlots.

cial laboratories run AGID assays for IgG
and IgM antibodies; results of these assays
are specific but relatively insensitive. An

Clinical Findings and Lesions: The
enzyme in1munoassay for Coccidioides
disease varies from inapparent ( cattle,
galactomarman antigen useful in htunan
sheep, pigs, dogs, cats) to progressive,
infections has proved insensitive in dogs.

disseminated, and fatal ( dogs, nonhuman

A presumptive diagnosis can be made
primates, cats, and people). Coccidioidowhen serology is positive in an anin1al with mycosis is primarily a respiratory disease
consistent clinical signs. Attempts to culture
that ranges from self-limiting to chronic.

tl1e fungus should be restricted to those

Dissemination occurs in -200A, of canine
laboratories equipped to handle such
infections, with many tissues, especially
dangerously infective cultures.

eyes, joints, and bone, affected. Clinical
signs can vary greatly, depending on organ

Treatment: Disease is often sel.f:limiting,
involvement and severity of infection. Dogs
but if chronic respiratory signs or multisyswith disseminated disease may have temic disease are present, longterm
chronic cough, anorexia, cachexia,
antifungal therapy is needed; with
lameness, enlargedjoints, fever, and
disseminated infection, treatment of at least
intermittent diarrhea. Dissemination to the

6-12 mo is typical. Fluconazole (2.5-10 mg/
skin with draining ulceration may occur, but kg/day) is the most commonly used drug to primary infection through the skin is rare.

treat disseminated or chronic respiratory

Cats infected with C immitis most often
infections. Ketoconazole (10-30 mg/kg/day)

present with dermatologi.c signs ( draining
and itraconazole (10 mg/kg/day) are also
skin lesions, subcutaneous granulomatous
commonly used to treat dogs with coccidioimasses, abscesses), fever, inappetence, and domycosis but are more expensive and have
weight loss. Less common clinical signs in
a higher incidence of adverse effects.

cats include respiratory ( dypsnea),

Amphotericin B may be the most effective
musculoskeletal (lameness), neurologi.c,
antifungal drug, but it is highly neplu·otoxic.

and ophthalmologic abnormalities.

It may be indicated in anin1als that either do

Approximately 500A, of infected cats appear
not improve or are unable to tolerate tl1e
to have disseminated disease.

azole antifungals.

Gross lesions may be limited to the lungs,
mediastinurn, and thoracic lymph nodes, or

CRYPTOCOCCOSIS
may be disseminated to various organs.

Lesions are discrete, variable-sized nodules

Cryptococcosis is a systemic ftmgal disease
with a firm, gray-white cut surface, and
that may affect the respiratory tract ( esperesemble those of tuberculosis (seep 687).

cially the nasal cavity), CNS, eyes, and

The nodules are pyogranulomas composed
skin (particularly of the face and neck of
of epithelioid and giant cells, and the center
cats). The causal fungi, Cryptococcus

638

FUNGAL INFECTIONS
neo.formans and C gattii, exist in the nodes, spleen, liver, thyroid, adrenals,
environment and in tissues in a yeast form.

pancreas, bone, GI tract, muscle, myocar

Infection occurs worldwide. The fungi are
dium, prostate, heart valves, and tonsils.

found in soil and fowl manure, especially

Lesions associated with cryptococcosis

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in pigeon droppings. Transmission is by
vary from a gelatinous mass, consisting
inhalation of spores or contan1ination of
of nun1erous organisms with minimal
wounds. In avian droppings, it may occur
inflanunation, to granuloma formation. The
in a noncapsulated form as small as 1 µrn,
lesion is usually composed of aggregates of
which can be inhaled into the deeper
encapsulated organisms within a connecportions of the lungs. Cryptococcosis is tive tissue reticulw11. The cellular response
most common in cats but also is seen in
is primarily macrophages and giant cells
dogs, cattle, horses, sheep, goats, birds, and
with a few plasma cells and lymphocytes.

wild animals. In people, many cases are

Epithelioid giant cells and areas of caseous
associated with a defective cell-mediated
necrosis are less conunon than with the
immune response.

other systemic mycoses.

Clinical Findings and Lesions: Bovine

Diagnosis: The most rapid method of
cryptococcosis has been associated only
diagnosis is cytologic evaluation of nasal
with cases of mastitis, and many cows in a
exudate, skin exudate, CSF, or samples
herd may be infected. Affected cows have
obtained by paracentesis of the aqueous
anorexia, decreased milk flow, swelling and
or vitreous chambers of the eye or by
firmness of affected quarters, and enlarged
impression smears of nasal or cutaneous
supramammary lymph nodes. The milk
masses. Gram stain is most useful; the
becomes viscid, mucoid, and gray-white, or
organism retains the crystal violet, whereas
it may be watery with flakes. The disease in
the capsule stains lightly red with safranin.

horses almost invariably is a respiratory

India ink is also used to visualize the
ailment with obstructive growths in the
organism, which appears unstained and
nasal cavities.

silhouetted against a black background.

In cats, upper respiratory signs secondary It is not as definitive as Gram stain unless to nasal cavity infection are most common
budding is seen, because lymphocytes, fat
and include sneezing; mucopurulent,
droplets, and aggregated India ink particles
serous, or hemorrhagic unilateral or
may be confused with the organism. Wright
bilateral chronic nasal discharge; polypstain has been used most often in diagnoslike mass( es) in the nostril; and/or a firm, ing canine and feline cases, but this stain
subcutaneous swelling over the bridge·
can cause the organism to shrink and the
of the nose. Cutaneous lesions are also
capsule to become distorted. New
common and are characterized by papules
methylene blue and periodic acid-Schiff
and nodules that are fluctuant to firm.

(PAS) stains are better than Wright stain for

Larger lesions tend to ulcerate, leaving a
this reason. Because cytologic evaluation is
raw surface with a serous exudate.

rapid, in1pression smears or potassium

N eurologic signs associated with cryptocochydroxide preparations should always be cosis of the CNS may include depression,
made of suspected cryptococcal lesions.

changes in temperament, seizures, circling,

If no organisms are seen, a biopsy of the
paresis, and blindness. Ocular abnormalilesion can be taken; part of the sample can ties may also develop, including dilated
be used for culture and the rest processed
unresponsive pupils and blindness due to
for routine histology. The organism can be
exudative retinal detachment, granulomastained with H&E, but the capsule does not tous chorioretinitis, panophthalmitis, and
stain. The organism is more easily visualized
optic neuritis.

with PAS and Gomori methenanline silver

In contrast to cats, dogs often have
stains, but the capsule does not stain with
dissen1inated disease with CNS or ocular
these, either. The best stain for Cryptococ
involvement. Clinical signs are often related
cus is Mayer mucicarmine because of its
to meningoencephalitis, optic neuritis, and
ability to stain the capsule. Immunofluoresgranulomatous chorioretinitis. Lesions in cent staining can also be used. The large
the nasal cavity of many dogs have been
capsule and thin cell wall of Cryptococcus
reported, but they are usually not the
differentiate it from Blastomyces.

primary finding or reason for presentation.

Cryptococcus, by its budding and lack of

Approximately 500A> of dogs have lesions in
endospores, can be distinguished from
the respiratory tract, usually the lungs, and

Coccidioides immitis.

most have granulomas present in multiple

Detection of cryptococcal capsular
systems. Structures often involved in order
antigen in serum, urine, or CSF is a useful,
of decreasing frequency are kidneys, lymph
rapid method of diagnosis in those

FUNGAL INFECTIONS

639
suspected cases in which the organism is
macrophages and appear in H&E sections
not identified. A latex agglutination test is
as globose or oval bodies (3-4 µm) with a
commercially available in kit form. The
central basophilic body surrounded by an
antigen titer can also be used to help
unstained zone. The organism closely

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detennine response to therapy.

resembles H capsulatum. Serologic testing

The organism can be cultured from
is available with serum agglutination titers
exudate, CSF, urine, joint fluid, and tissue
of 1:80 or higher reported to be positive.

samples if a large enough sample volwne is

Positive titers may be reflective of past
available. Sabouraud agar with antibiotics is exposure, with specificity for current used if bacterial contamination is likely.

infection being low.

Treatment: Fluconazole (2.5-10 mg/kg/

Treatment: No completely satisfactory
day) or itraconazole (10 mg/kg/day) are
treatment is known. Surgical excision of
considered the treatments of choice.

lesions combined with antifw1gal drugs

Arnphotericin B can be given SC (0.5-0.8

(an1photelicin B) could be used.

mg/kg diluted in 0.45% saline containing

2.5% dextrose; 400 mL for cats, 500 mL for

HISTOPLASMOSIS
dogs <20 kg, 1,000 mL for dogs >20 kg), 2-3
times per wk. Amphote1icin B lipid complex Histoplasmosis is a chronic, noncontagious, ( 1-2 mg/kg for cats or 2-3 mg/kg for dogs)

disseminated, gra.nulomatous disease of
can also be given 3 times/wk for 12-15
people and other animals caused by the
treatments. Flucytosine can be used alone;
dimorphic ftmgusHistoplasma capsula
however, drug resistance may develop, so
tum. The organism is conunonly found in
combination therapy with amphotericin is
soil that contains bird and bat manure. It
recommended.

produces mycelial growth in the soil and in
culture at room temperature and grows in a

EPIZOOTIC LYMPHANGITIS
yeast fo1m in tissues and in cultures at 37°C.

Histoplasmosis is found worldwide.

Epizootic lymphangitis is a chronic

Endemic areas in the USA include the
gra.nulomatous disease of the skin, lymph

Mississippi and Ohio River valleys. Infection
vessels, and lymph nodes of the limbs and
has been described in many animal species,
neck of Equidae caused by the dimorphic
but disease is unconunon to rare in all but
fungus Histoplasmafarciminosum. The
dogs and cats. Infection is commonly via
disease is seen in Asian and Mediterranean
aerosol contamination of the respiratory
areas but is unknown in the USA. The
tract, and the lungs and thoracic lymph
fungus fo1ms mycelia in nature and yeast
nodes are the sites of plimary infection,
forms in tissues and has a saprophytic
although the GI tract may be a prin'lary site
phase in soil. Infection probably is acquired
of infection, especially in dogs. The
by wound infection or transmission by
organisms enter the bloodstream from a
bloodsucking insects.

primary focus and become dissenlinated
throughout the body; they may localize in

Clinical Findings and Lesions: The
bone marrow or the eyes, where they
disease is characterized by freely movable
produce cholioretinitis or endophthalmitis.

cutaneous nodules, which 01iginate from
infected superficial lymph vessels and

Clinical Findings: The signs vary and are
nodes and tend to ulcerate and undergo
nonspecific, reflecting the va.iious orga.t1S
alternating periods of discharge and
involved. Chronic GI signs, especially large
closure. Affected lymph nodes are enlarged
intestinal diarrhea, a.i·e usually most obvious
and hard. The skin covering the nodules
in dogs, but cats tend to have respiratory and
may become thick, indurated, and fused to
nonspecific clinical signs. Many dogs have
the underlying tissues. Lesions also may be
a protracted course of weight loss to
present in the lungs, conjunctiva, cornea,
emaciation, chronic cough, persistent
nasal mucosa, and other organs. The
dian·hea, fever, anemia, hepatomegaly,
nodules are pyogranulomas with a thick,
splenomegaly, lymphadenopathy, a.i1d
fibrous capsule and contain thick, creamy
nasopharyngeal and GI ulceration. Obstrucexudate and the causative organisms.

tive respiratory difficulty due to tracheobrondtial lymphadenopathy also has been seen in Diagnosis: The clinical features are highly dogs. Dissemination may involve the skin, in suggestive. Diagnosis can be confirn1ed by
which weeping, ulcerated, nodular lesions
microscopic exanlination of exudates and
develop. Polyarthropathy, cholioretinitis,
biopsy specimens. The yeast fonns of the
and retinal detachment have also been
organisms distend the cytoplasm of
reported in a dog wiU1 dissenlinated

640

FUNGAL INFECTIONS
histoplasmosis. Acute histoplasmosis may

Aspergillus or Penicillium or the class be fatal after 2-5 wk. In cats, disseminated

Zygomycetes) that in tissue fo1m hyphal
infection is common. Clinical signs may be
elements with hyaline or clear walls.

nonspecific but often include respiratory

Examples of genera causing hyalohyphomy

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difficulty, fever, depression, anorexia and
cosis in people and other anin1als include
weight loss. Lymphadenopathy, hepatomeg

Acremonium, Fusariiim, Geotrichum
aly, ocular disease ( coajunctivitis, granu

Paecilomyces, Pseudallescheria, Sage:io
lomatous chorioretinitis, retinal detachment,
mella, Phialosimplex, Geosmithia,
optic neuritis), lameness, and cutaneous

Geomyces, and Scedosporiiim. Hyalonodules or ulcers may also be seen.

hyphomycosis is far less common than

Lesions: Gross lesions include enlargephaeohyphomycosis.

ment of the liver, spleen, and mesenteric
lymph nodes; ascites; yellow-white,

Clinical Findings: Lesions range from
vaiiable-sized nodules in the lungs; and
local cutaneous, subcutaneous corneal
enlargement of bronchial lymph nodes. The
or nasal mucosa! disease to dis;eminate'd
enlai·ged liver may have multiple, scattered,
disease involving the lungs and multiple
uTegular-shaped, pale yellow foci of
other organ systems. Disseminated and
granulomatous inflainmation. Pale foci may
corneal forn1s have been reported most
be present in the myocai·diun1, and the small conunonly. Anin1als presenting with intestine may have thickened, gray walls
cutaneous lesions should be evaluated for
and ulceration of the mucosa.

systemic disease. Animals being treated
with immunosuppressive drugs for immune

Diagnosis: Histoplasmosis should be
mediated disease may develop cutaneous
considered when the clinical signs include
hyalohyphomycosis and not have lesions at
weight loss, chronic diarrhea, respiratory
other sites, whereas inununocompetent
distress, enlarged bronchial lymph nodes,
aninlals that develop hyalohyphomycosis
and pulmonary nodules. Nistoplasma
most often do have disseminated disease
organisms are usually nun1erous in affected
or at least disease that is not confmed to
tissues, and a definitive diagnosis can often
the skin.

be made by fine-needle aspiration and
exfoliative cytology. Cytology of bone

Diagnosis: The several causative fwlgi
marrow may be diagnostic in cats. Tissue
carmot be identified by their histologic
biopsy may be required if cytology is not
features in tissues; culture isolation and/or
diagnostic. Histoplasma organisms are

.

PCR are required.

difficult to detect with routine H&E stain but
stain well with PAS, Gomori methenaniine

Treatment: Surgical removal with or withsilver, and G1idley fungal stains. Yeast forms out azole anti.fungal therapy is the treatment
in macrophages and giant cells ai·e round to
of choice for local disease. Disseminated
ovoid (1-4 µrn) structures with a thin cell wall disease typically carries a grave prognosis.

and a thin, clear zone between the cell wall

Treatment with newer azole antifw1gals
and cellular cytoplasm. H capsui,atum can
and/or ainphotericin B lipid complex may
also be cultured from tissue specin1ens,
be attempted and is most likely to be
fine-needle aspirates, and body fluids. Antigen effective if in1munosuppressive drugs testing usmg a quantitative antigen ELISA can can be tapered.

be performed on urine, seruni, and CSF.

Cross-reactivity occurs with blastomycosis.

MYCETOMAS

!reatment: ltraconazole (10 mg/kg/day)

Mycetomas are granulomatous nodules of

IS the treatment of choice for disseminated
the subcutaneous tissues that contain tissue
histoplasmosis in dogs and cats, although
grains or granules. Within the grains are
fluconazole is probably also effective.

dense colonies of the organism. When such

Ketoconazole, 10-15 mg/kg, bid for 4--6 mo,
lesions ai·e caused by fungi, they are known
may be effective in early or mild cases of
as eun1ycotic mycetomas. The causal agents
histoplasmosis in dogs. For severe cases,
of ewnycotic mycetomas include a variety
concwTent treatment with ainphotericin B or
of saprophytic geophi.lic fungi. Ewnycotic
ainphotericin B lipid complex is suggested.

mycetomas caused by pigmented fungi such
as Curvularia spp and Madurella spp are called black- or dai·k-grain mycetomas.

HYALOHYPHOMYCOSIS

White-grained mycetomas are caused by
unpigmented fwlgi such as Acremonium

Hyalohyphomycosis is infection caused by
spp and Scedosporium apiospermum (the
nonpigmented fungi ( other than the genera
asexual state of Pseudallescheria boydii).

FUNGAL INFECTIONS

641

Clinical Findings and Lesions: Most
tme fungi but are aquatic pathogens in the
eumycotic mycetomas are confined to the
kingdom Stramenopila. They are more
subcutaneous tissue, but white-grain
closely related to algae than fungi but cause
mycetomas may be extensions of abdomidisease that closely resembles zygomycosis VetBooks.ir
nal cavity disease. Peritonitis or abdominal

(seep 645). Organisms of significance in
masses are typically seen in white-grain
veterinary medicine include va.Jious species
mycetomas. Black-grain mycetomas are
of Saprolegnia and Achy la ( eg, S diclina ), usually characterized by relatively poorly
which are the common agents of cutaneous
circwnscribed cutaneous nodules on the
disease in fishes; Pythium insidiosum, the
extremities or face. The lesions may
cause of a cutaneous and subcutaneous
ulcerate or form fistulas. When the feet or
mycosis in horses (bursatti, swan1p cancer,
lin1bs are involved, the infection may extend leeches), a cutaneous, subcuta.J1eous, 3.11d to the W1derlying bone.

GI disease in dogs, and a cuta.J1eous and

The fungal mycelia proliferate in the
para.J1asal disease of cats; and Lagenidium
lesions and organize into aggregates known
spp, the cause of cutaneous and systemic
as granules or grains. In these granules, the
lesions and la.J·ge-vessel aneurysms in dogs.

myceliW11 is compact and frequently bizarre

Pythiosis is a common disease of domestic
and distorted in fom1. Chlamydospores are
animals in some tropical and subtropical
frequent, especially at the periphery, and the areas of the world. In dogs, pythiosis is most mycelium may or may not be embedded in
often encountered in southeast Asia,
an amorphous, cement-like substance.

eastern coastal Australia, South America,

Histologically, the granules are frequently
and in the USA, especially along tl1e Gulf
surroW1ded by eosinophilic deposits.

coast. In the USA, the disease most often is

Granules may be of various colors and sizes, seen in fall and winter months.

depending on the species of fungus
involved.

Clinical Findings and Lesions: In
horses, lesions are large, roughly circular,

Diagnosis: A presumptive diagnosis
granulomatous, ulcerated, fistulated
can be made if there are grains within the
nodules, or subcutaneous swellings with
exudate of draining tracts. For cytology, the
yellow-gray necrotic masses or cores. The
grains should be examined for the presence
lesions are most conunon on tl1e legs
of fungal elements. If no tissue grains are

( especially the lower limbs), abdomen,
foW1d in the exudate, a biopsy of the lesion
chest, and genitalia. Distribution of lesions
should be taken for histopathologic
is attributable to the aquatic nature of the
exaTI1ination. Cultures should be performed
to confirm cytologic findings and to identify
the causative agent. Either tissue grains or
biopsy specimens should be cultmed.

Treatment: The prognosis for abdominal
mycetomas is guarded, because tissue
involvement is usually extensive. Cutaneous
mycetomas, while not life-threatening, are
often difficult to resolve. Radical surgical
excision, including limb amputation, may
be effective for some cases of cutaneous
mycetomas. Effectiveness of antifungal
chemotherapy has been reported in only
a few cases. In one report, fluconazole,

50 mg/day for 6 wk, was used to successfully
treat a dog with intra-abdominal maduromycosis. In another report, longtenn treatment with itraconazole, 5-10 mg/kg/day, failed to
resolve a disseminated Acremonium
infection in a dog.

OOMYCOSIS

(Pythiosis, Lagenidiosis)

Oomycosis is caused by pathogens in the

Prominent granulation tissue and inflammation due to Pythium insidiosum in a horse.

class Oomycetes. These organisms are not

Courtesy of Dr. Corrie Brown.

642

FUNGAL INFECTIONS
organism. The lesions are pruritic, disextremities, tail head, venti·al neck, or charge a mucosanguineous exudate, and
perineum are affected most commonly.

often are self-trawnatized. The granulomas

Pythiosis in cats is rare and typified by
contain fi.1111, yellowish, coralliform masses
eit11er cutaneous or nasopharyngeal

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of necrotic tissue lrnown as "kunkers,"

lesions.

which may be removed intact. Kunkers are

Lagenidiosis is an oomycotic infection
foci of coagulative necrosis in vessels that
of dogs characterized by progressive,
have become sequestered from the
multifocal cutaneous and subcutaneous
surrounding tissue; they contain broad,
lesions, most often affecting tl1e extremibranching aseptate hyphae and are 1-10 µm ties, marmnary region, perinewn, or trw1k.

in diameter. Bone involvement may be a

Regional lymphadenopathy is common. At
featw-e of chronic pythiosis. Enteric
least two species of Lagenidium have been
pythiosis in horses is characterized by
shown to affect dogs. One of the Lagen
fibrosing and stenotic GI lesions containing
idium spp causes more aggressive
intralesional foci of caseous material and
cutaneous infection wi.tl1 systenuc
fungal hyphae.

involvement, whereas a less aggressive

Specin1ens removed at sw-gery or

Lagenidium spp tends to cause more
necropsy consist of fibrous tissue with
slowly progressive cutaneous disease.

irregularly spaced, fiml, focal areas of

Cutaneous lesions are characterized as firm
necrosis that vary in size and color.

dermal or subcutaneous nodules, or as

Microscopically, alterations vary from foci
ulcerated, thickened, edematous areas of
of acute exudative infianunation with
deep celluJitis with regions of necrosis and
numerous eosinophils to a granulomatous
nun1erous draining tracts. In contrast to the
reaction with sequestered areas of necrosis
clinical course of cutaneous pythiosis, in
and a fran1ework of hyphae that ar·e
dogs with aggressive Lagenidium spp,
thick-walled, branching, and slightly
involvement at distant sites is often seen.

in-egular in width.

Thoracic and abdominal lymph nodes,

GI and cutaneous forms of pythiosis
lungs, and especially great vessels may be
are seen and are characterized by severe
affected. Aninlals witl1 great vessel or
granulomatous and eosinophilic inflanunasublun1bar lymph node involvement tion. Pinsidiosum infection is seen most
typically have cutar1eous or subcutaneous
often in the GI tract of young adult dogs,
lesions on the hindlimbs and often develop
especially Labrador Retiievers. The
hindlirnb edema. Great vessel anewysms
stomach, proxinlal small intestine, and
may acutely rupture, resulting in hemoileocolicjunction are affected most abdomen and sudden death.

commonly, but any part of tl1e intestine,
esophagus, and colon can be diseased. Clini

Diagnosis: In horses, lesions of pythiosis
cal signs include vomiting, weight loss, and
are similar· to those of zygomycosis ( see
anorexia. The weight loss can be severe,
p 645) and may be confused with cutaneous
but affected dogs usually do not appear
habronenliasis (seep 904), excessive
systemically ill until late in the disease. The
granulation tissue, and certain equine
lesions are typically characterized by severe neoplasms. In pythiosis, tl1e necrotic cores transmural thickening of the gastJic or
are distinct from the surrow1ding tissue,
intestinal wall, wi.th mesenteric lymphadand a seropw'lllent discharge from the sinus enopathy in which the lymph nodes are
tracts is prominent. The lesions contain
embedded in a large, fim1 granulomatous
in-egular, branching ( at 1ight angles), rarely
mass involving the surrounding mesentery.

septate hyphae, 4-8 µm in diameter.

Bowel ischemia, infarction, or acute

In dogs, diagnosis can be made by
hemoabdomen may develop due to
isolation of P insidiosum from infected
extension of disease into mesenteric
tissues. Culture identification or PCR has
vessels. Enteric pyogranulomas typically
been used. Inm1unoblot serology for
consist of necrotic foci infiltrated and
detection of anti-? insidiosum antibodies
surrounded by neutrophils, eosinophils,
is available and appears to be both sensitive
epithelioid macrophages, plasma cells, and
and specific. Immunoblot serology for
multinucleated giant cells. Etiologic agents
detection of anti-Lagenidium antibodies in
may not be apparent on sections stained
caiune serum can provide a preswnptive
wi.th H&E. Sections stained wi.th Gomori
diagnosis of lagenidiosis but must be
methenamine silver show branching, rarely
interpreted in conjunction with results of
septate hyphae.

serologic testing for Pin idiosum infection Cutaneous pytluosis is typified by
because of the potential for cross-reactivity
nonhealing wounds, invasive masses, and
in serwn from dogs wi.th pythiosis. The
ulcerated nodules with draining tracts. The
histologic features of lagenidiosis are

FUNGAL INFECTIONS

643
similar to those of pythiosis and zygomyco

Clinical Findings and Lesions: Dogs
sis. However, Lagenidium hyphae are
witll nasal penicilliosis have chronic
usually much larger and visible on H&Esneezing and an acute to clu·onic nasal stained tissues. Definitive diagnosis of
discharge tllat varies from intermittent

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lagenidiosis and pythiosis is best made by
hemorrhagic to intermittent or continuous
culture and PCR identification.

mucoid or mucopurulent. Radiographic
findings include areas of turbinate

Treatment: The prognosis for pythiosis
destruction with increased radiolucency.

or lagenidiosis is poor if surgical excision

Grossly, tlle nasal mucosa has foci of
cannot be done. Complete surgical excision
necrosis and ulceration; microscopically,
is the treatment of choice, but the disease is
fungal hyphae may fom1 a thick mat over
often too extensive at the time of diagnosis
an intact mucosa acljacent to these foci.

to allow complete resection. In animals with Systemic disease often affects long bones, lesions limited to a single distal extremity,
resulting in lameness.

amputation is reconunended. Medical
therapy for pythiosis should include

Diagnosis: Diagnosis is based on ftmgal
itraconazole (10 mg/kg/day) and terbinafine
culture, character of tl1e lesions, presence

(5-10 mg/kg/day). Steroids may decrease
of fungal hyphae, and a positive agar-gel
inflammation and improve clinical signs in
double-diffusion test. Cultural isolation of
the short term. Treatment with ampho
aPenicillium sp must be accompanied
tericin B lipid complex can also be
by demonstration of tissue invasion by
attempted. Approximately 2()0A, of dogs with
the ftmgus for confirmation. In tissues, P
pythiosis respond to longtem1 antifungal
marne.[fei closely resemble the yeast phase therapy. Lagenidiosis appears to be poorly
of Hisloplasma capsulaliim.

responsive to medical therapy. In horses,
the prognosis is guarded, and timely

Treatment: Very little has been repo1ted
recognition and treatment are essential
concerning treatment of penicilliosis.

for successful management. Factors tl1at

Surgical turbinectomy with curettage has
influence prognosis include size and site
been combined witll flushing of U1c nasal
of lesion and duration of infection. Small
cavity with 1 % tincture of iodine or
lesions of short duration tllat have not
povidone-iodine ( 10: 1) and oral thiabendainvaded critical strnctures usually respond zole. Fluconazole, 2.5-5 mg/kg/day for 2 mo,
best to treatment. Surgical excision,
has been used to successfully treat some
immunotherapy, or a combination of both
dogs with nasal penicilliosis.

may be effective. lnununotllerapy consists
of a series of intradermal or SC irtjections of

PHAEOHYPHOMYCOSIS
killed, sonicated, whole-cell hyphal antigens
or precipitated soluble antigens of the

Phaeohyphomycosis refers to chronic
causative fungus. Subcutaneous abscesses
cutaneous, subcutaneous, mucosa!,
at the sites of irtjection, osteitis, or
cerebral, or systemic infection caused by
deep-seated laminitis may be a complicaone of several genera and species of tion of such therapy. Surgical removal plus
pigmented fungi of the family Dematiaceae.

systemic or local administration of

Several ftmgal genera have been rep01ted to
amphotericin B may be a satisfactory
affect people and other animals, including
treatment if the disease is localized.

Allernaria, Bipolaris, Cladophialophora

(Xylohypha, Cladosporiiim), Curvu.laria,

PENICILLIOSIS

Exophiala, Fonsecaea, Moniliella,

Phialophora, Ramichloridium, and

Wections with Penicillium spp are rare in

Scolecobasidium. Fungi in this category are domestic animals. In dogs, infections of tlle
saprophytic, widely distributed organisms
nasal cavity, lungs, lymph nodes, and bones
found in soil, water, and decaying vegetable
have been reported. Nasal disease is most
matter. Infection may result from fungal
conunon and behaves similar to nasal
implantation into tissue at the site of an
aspergillosis. In cats, the fungus has been
irtjury.

isolated from tlle nasal cavity, orbital
cellulitis and sinusitis, and lungs. It has also

Clinical Findings and Lesions: Phaeobeen reported to cause systemic disease in hyphomycosis has been described in cows,
captive toucanets (P griseofulvum) and
cats, horses, and dogs. The most conunon
bamboo rats (P marnejfei) in southeast
clinical presentations include ulcerated

Asia. Penicillium spp are widely distribcutaneous nodules of the digits, pinnae, uted in nature and are found in soils, grains,
nasal plan um, and nasal/paranasal tissues in
and various foods and feeds.

cats. The nodules may ulcerate and have

644

FUNGAL INFECTIONS
draining fistulous tracts. These pyogranupassages. The cutaneous lesions may be lomas contain pigmented, septate hyphae
single or multiple, sessile or pedunculated.

with irregular enlargements and thin

The nasal polyps and cutaneous lesions
walled, budding, yeast-like forms.

have a granulomatous, fibromyxoicl

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Granulomatous meningoencephalitis
inflammatory component and contain
caused by pigmented fungi has been
the fungal organism.

reported in dogs and cats. Dogs treated
with multiple immunosuppressive agents,

Diagnosis: Rhinosporidiosis may be
especially cyclosporine, appear to be
confused with other granulomatous lesions
predisposed to developing multifocal
of the nasal mucosa and skin, including
cutaneous lesions. Systemic clissemination
aspergillosis, entomophthoromycosis,
is most likely in animals treated with

"nasal granuloma," and cryptococcosis.

irnmunosuppressive drugs.

Microscopic demonstration of spherules

(sporangia) ofR seeberi in biopsy

Diagnosis: Phaeohyphomycosis can be
specimens confinns the diagnosis. The
diagnosed by microscopic examination of
spherules may be numerous, vary in size
exudate and biopsy specin1ens, which

(up to 300 µm), have thick walls that stain
reveals pigmented, dark-walled, irregularly
periodic acid-Schiff positive, and contain
septate filan1entous hyphae (2-6 µm in
endospores 4-19 µm in diameter. Developdiameter) or yeast-like cells. Infected ing stages of varying size without spores are
tissues may be grossly pigmented, giving
distributed throughout the lesion.

an appearance of melanoma. The several
causative fungi cannot be identified by their

Treatment: Surgical excision of the
histologic features in tissues; cultural
lesions is considered standard, but
isolation and/or PCR are required. The
recurrence is corrunon. Amphotericin B
differential diagnosis should include
and itraconazole have been described for
neoplasia, other granulomas, and epidermedical treatment but are generally not moid cysts.

as effective as surgery.

Treatment: Phaeohyphomycosis is

SPOROTRICHOSIS
generally poorly responsive to treatment.

Wide excision of cutaneous or subcutane

Sporotrichosis is a sporadic, chronic,
ous lesions is recommended, followed by
granulomatous disease of people and

6-12 mo of treatment with itraconazole (10
various domestic and laboratory animals
mg/kg/day). Nonresectable disease should
caused by Sporoth1ix schenckii. The
be treated with itraconazole. Voriconazole
organism is dimorphic and forms mycelia
or posaconazole m(ly be more effective, but
on vegetation and in Sabouraud dextrose
voriconazole is not recommended in cats. In agar at 25° -30°C (77° -86°F) but is yeast-like dogs being treated with in1munosuppressive in tissue and media at 37°C (98.6°F). It is therapy, the prognosis may be better if the
ubiquitous in soil, vegetation, and timber; is
immunosuppressive drugs ( especially
distributed worldwide; and in the USA is
cyclosporine) can be discontinued.

most commonly found in coastal regions
and river valleys. lnfection usually results

RHINOSPORIDIOSIS
from direct inoculation of the organism into
skin wounds via contact with plants or soil

Rhinosporidiosis is a chronic, nonfatal,
or penetrating foreign bodies. Disseminated
pyogranulomatous infection, primarily of
disease caused by inl1alation of spores is
the nasal mucosa and occasionally of the
rare.

skin of horses, cattle, dogs, cats, and aquatic

Sporotrichosis has been reported in clogs,
birds, caused by the fungus Rhinosporid
cats, horses, cows, camels, dolphins, goats,
ium seeberi. Uncommon in North America,
mules, birds, pigs, rats, armadillos, and
it is seen most often in India, Africa, and
people. Zoonotic infections can occur. The

South America. The organism has not been
cat may be the species with the greatest
cultured, and its natural habitat is unknown.

zoonotic potential, and transmission from

Traun1a may predispose to infection, which
cats to people has been reported without
is not considered transmissible.

evidence of trauma.1n contrast, transmission from other infected species appears to Clinical Findings and Lesions: Infecrequire inoculation of previously traumation of the nasal mucosa is characte1ized by tized skin. The large number of organisms
polypoid growths that may be soft, pink,
shed from the wound and in the feces of
friable, lobulated with roughened surfaces,
infected cats is believed to be responsible
and large enough to occlude the nasal
for the increased zoonotic potential of feline

FUNwAL INFECTIONS

645
sporotrichosis. Epidemics of sporotrichosis successfully. Alte:rnatively, a supersaturated have been reported in Brazil. Data from
solution of potas&iwn iodide, administered
these studies support the in1portance of

PO, has been used with some success;
cats in the zoonotic transmission of the
therapy is continved 30 days beyond
organism. Caretakers of infected cats were
apparent clinical ,eure. During treatment,

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four times more likely to become infected
the anin1al shoulcf be monitored for signs
than others living in the same household.

of iodide toxicity: anorexia, vomiting,
depression, muscle twitching, hypothennia,

Clinical Findings and Lesions: Sporotricardiomyopathy, ,eai·ciiovascular collapse, chosis may be grouped into three forms:

and death. Cats aee especially sensitive to
lymphocutaneous, cutaneous, and
iodides and the development of iodism.

disseminated. The lymphocutaneous fom1
is the most common. Small, firm dennal to

Zoonotic Risk: Sporotrichosis is an
subcutaneous nodules, 1-3 cm in diameter,
important zoonos is, with animal-to-hmnan
develop at the site of inoculation. As
tra.J1S1nission well docwnented. St1ict
infection ascends along the lymphatic
hygiene must be abserved when handling
vessels, cording and new nodules develop.

anin1als ( especiallY cats) with suspected or

Lesions ulcerate and discharge a serohemdiagnosed sporottichosis. People in contact orrhagic exudate. In cats, lesions are most
with infected anirtials should be informed of
often seen on the head, especially on the
the contagious nature of the disease when
bridge of the nose and pin.nae. Although
therapeutic optio(1S are discussed.

systemic illness is not seen initially, chronic
illness may result in fever, listlessness, and
depression. Respiratory signs may be

ZYGOMYCosrs
apparent. The cutaneous fonn tends to
remain localized to the site of inoculation,

(Basidiobolomyco9is, Conidiobolomycosis,
although lesions may be multicentric.

Entomophthoromycosis)

Disseminated sporotrichosis is rare but

Zygomycosis is used to describe infection
potentially fatal and may develop with
with fungi in the ciass Zygomycetes ai1d two
neglect of cutaneous and lymphocutaneous
genera in tl1e ordef Entomophthorales,
forms or if the anin1al is inappropriately

Basidiobolus ai1d Conidiobolus. Trne treated with corticosteroids. Infection
zygomycete infectJons are rare, but
develops via hematogenous or tissue spread conidiobolomyco�is ai1d basidiobolomycofrom the initial site of inoculation to the sis are more comrr1on ai1d cause pyograi1ubone, lungs, liver, spleen, testes, GI tract, lomatous lesions grossly and histologically
or CNS.

similar to those caused by pythiosis ai1d
lagenidiosis. This iS prirnaiily aJ1 infection of

Diagnosis: Diagnosis can be made by
the nasopharyngeol mucosa ai1d subcutaneculture (samples obtained from unopened ous tissue of horses ai1d rai·ely other
lesions) or microscopic exan1ination of the
anin1als (llamas, s]'leep) by C coronatus,
exudate or biopsy specimens. In tissues and

C incongruus, C t(),mprauges, or B rana-exudate, the organism is present as few to

1um. These ubiquitous fungi are present in
numerous, cigar-shaped, single cells within
soil and decaying vegetation ai1d, in the case
macrophages. The fungal cells are
of basidioboli, the GI tracts of amphibiai1s,
pleomorphic and small (2-10 x 1-3 µm);
reptiles, ai1d macropods. C coronatus
buds may be present and give the appearaffects almost exclusively the mucosa of the ance of a ping-pong paddle. A fluorescent
nose ai1d mouth. Basidiobolus infects the
antibody technique has been used to
lateral aspects ofwe head, neck, ai1d body.

identify the yeast-like cells in tissues.

C coronatus is also an important insect In species other than cats, Sporothrix
pathogen.

organisms are often sparse in exudate and
infected tissue, so that diagnosis usually

Clinical Findings: Ulcerative pyograi1urequires culture. In cultures, a true lomas of the rnuc01ts membra.J1e of the
myceliwn is produced, with fine, branching,
nasopharyngeal tis:,ue, mouth, or nodular
septate hyphae bearing peai0shaped conidia growths of tl1e nasal mucosa ai1d the lips on slender conidiophores.

may be seen with conidiobolomycosis,
resulting in mechartical obstruction of the

Treatment: Itraconazole (10 mg/kg/day)

nasal cavity, dyspnea, ai1d nasal discharge.

is considered the treatment of choice for

Local disseminatiofl mto the retropharynsporotrichosis. Treatment should be congeal, retrobulbar, of other tissues of the face tinued 3-4 wk beyond apparent clinical
may be noted. Lesions in basidiobolomycocure. Terbinafine has also been used sis are usually single, circular, ulcerative,

646

FUNGAL INFECTIONS
pruritic nodules of the skin of the upper
sis (seep 904) and oomycosis (see
body. Fistulous tracts discharge a serosanp 641) but can be differentiated by microguineous fluid from the lesions, which scopic examination of tissues. In H&E
frequently are traumatized. Extension to
sections, the fungus appears as holes and

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regional lymph nodes results in swelling
elongated channels, and many hyphae
of the nodes and development of yellow
have a wide eosinophilic cuff; in sections
necrotic foci. Lesions may contain a creamy,
stained for fungi, the organism consists
yellow central core of necrotic tissue.

of large, branching, sometimes septate,

Disseminated basidiobolomycosis is rare but 2.5-25 µm hyphae. Cultural examination has been described in dogs and a mandrill.

is required to identify the causative

Lesions: In excised tissues or necropsy
fungus.

specimens, a thickened fibrotic dermis has
scattered, red or crean1y white areas. The

Treatment: Longtem1 itraconazole adminlesions, which contain hyphal fonns, a heavy istration is recommended for treatment of infiltrate of eosinophils, and sequestered
nasopharyngeal infection. Altl10ugh lesions
areas of necrosis, have histologic features
often regress, recurrence is common after
of infectious granulornas.

treatment is discontinued. Cutaneous
zygomycete infections should be treated

Diagnosis: Clinically, zygomycosis may
with wide surgical resection followed by
be confused with cutaneous habronemia-
longtem1 itraconazole.

LEPTOSPI ROSIS

Leptospi..rosis is a zoonotic disease with a
identified in 9 species of Leptospira, with worldwide distribution caused by infection

6 species being regarded as intermediate in
witl1 any of several pathogenic serovars of
pathogenicity, and 6 being nonpathogenic.

Leplospira. The disease affects virtually all Some of the conunon leptospiral pathogens
m=als and has a broad range of clinical
of domestic animals now have different
effects, from mild, subclinical infection to
species nan1es. For example, L interrogans
multiple-organ failure and death.

serovar Grippotyphosa is now L kirschneri
serovar Grippotyphosa. The two types of

Etiology: Leplospira are aerobic,
serovar Hardjo have been formally split into
gram-negative spirochetes that are
two species: serovar Hardjo type hardjofastidious, slow growing, and have bovis (found in the USA and much of the
characteristic corkscrew-like motility. The
world) is now L borgpetersenii serovar
taxonomy of Leplospira is complex and can Hardjo and the less conunon serovar Hardjo be confusing. Traditionally, Leplospira
type hardjo-prajitno (found primarily in tl1e
were divided into two groups; the patho

UK) is now L interroga'YJ,S serovar Hardjo.

genic Leptospira were all classified as

The revised nomenclature is now reflected
members of L interrogans, and the
in the scientific literature but not on labels
saprophytic Leptospira were classified as
for vaccines and phannaceutical products.

L bijlexa. Within each of these species,

Fortunately for clinicians, the serovar and
leptospiral serovars were recognized, with
serogroup names remain in common use

>250 different serovars of pathogenic
and are useful when discussing the

Leplospira identified (based on surface
epidemiology, serology, clinical features,
antigens) throughout the world. The
treatment, and prevention of leptospirosis.

serovars are often grouped into antigenically related serogroups. With the increased Host Susceptibility, Epidemiology,
use of genomic infom1ation for the
and Transmission: Essentially all
classification of bacteria, the genus
mammals are susceptible to infection with

Leptospira was reorganized. There are
pathogenic Leptospira, although some
currently 21 recognized genomospecies of
species are more resistant to disease.

leptospires, including both pathogenic,

Among conunon companion animals and
intem1ediate, and nonpathogenic organlivestock, leptospirosis is most frequently isms. Pathogenic leptospires are now
recognized in cattle, swine, dogs, and

LEPTOSPIROSIS

647
horses. Cats have historically been
clinical signs, and a short renal phase of
considered to be resistant to disease but
infection. Diagnosis of incidental host
have been shown to seroconvert on
infections is less problematic because of a
exposure to leptospires. Recent evidence
marked antibody response to infection and
suggests that the role of leptospires in the

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the presence of large numbers of organisms
pathogenesis of feline renal disease should
in tissues of infected animals. Examples of
be reexamined. Leptospirosis in wildlife is
this type of infection are serovar Grippotycommon, although the disease is most often phosa infection in dogs or serovar Icteronoticed only when the wildlife serve as a haemorrhagiae infection in cattle and
source of infection for domestic animals or
swine.

people.

Characterization of a host/serovar inter

Leptospi.rosis is found throughout the
action as a maintenance or incidental host
world. The infection (and disease) is more
infection is not absolute. For exan1ple,
prevalent in warn1, moist climates and
swine and cattle infected with serovar
is endemic in much of the tropics. In

Pomona behave as a host intermediate
temperate climates, the disease is more
between the two forms, with the organism
seasonal, with the highest incidence after
persisting in the kidneys but the host
pe1iods of rainfall.

showing a marked antibody response to

Although >250 serovars of pathogenic
infection.

Leplospira are recognized, a subset of

Transmission an1ong maintenance hosts
leptospiral serovars are prevalent within
is often direct and involves contact with
a particular region or ecosystem and are
infected urine, placental fluids, or milk. In
associated with one or more maintenance
addition, the infection can be transmitted
hosts, which serve as reservoirs of infection
venereally or transplacentally with some

(see TABLE 4). Maintenance hosts are often host/serovar combinations. Infection of
wildlife species and, sometimes, domestic
incidental hosts is more commonly indirect,
animals and livestock. Each serovar
by contact with areas contaminated with
behaves differently within its maintenance
urine of asymptomatic maintenance
host species than it does in other, incidental
hosts that shed leptospires in their urine.

host species. In maintenance hosts,

Environmental conditions are critical in
leptospirosis is generally characterized by a
determining the frequency of indirect
high prevalence of infection, relatively mild
transmission. Survival of leptospires is
acute clinical signs, and persistent infection
favored by moisture and moderately warm
in the kidneys and sometimes the genital
temperatures; survival is brief in dry soil
tract.

or at temperatures <l 0°C or >34 °C. The

Diagnosis of maintenance host infecorganisms are killed by freezing, dehydrations is difficult because of relatively low tion, or direct sunlight.

antibody responses and the presence of few
organisms in the tissues of infected animals.

Pathogenesis: Despite the many serovars

Examples of this type of infection are
of Leplospira and host species, t11e key
serovar Bratislava infection in swine and
steps in pathogenesis of the disease are
serovar Hardjo infection in cattle. In
sin1ilar in all host/serovar combinations.

incidental hosts, leptospirosis is character

Leptospires invade tl1e body after penetratized by a low prevalence of infection, severe ing exposed mucous membranes or

COMMON MAINTENANCE HOSTS OF THE PATHOGENIC

LEPTOSPIRES ASSOCIATED WITH DISEASE IN DOMESTIC ANIMALS

IN THE USA AND CANADA

Leptospiral Serovar

Maintenance Hosts

Canicola

Dogs

Pomona

Pigs, cattle, opossums, skunks

Grippotyphosa

Raccoons, muskrats, skunks, voles

Hardjo

Cattle

Icterohaemorrhagiae

Rats

Bratislava

Pigs, mice (?), horses(?)

648

LEPTOSPIROSIS
damaged skin. After a variable incubation

Diagnosis: Diagnosis of leptoEl>Pirosis
period ( 4-20 days), leptospires circulate in
depends on a good clinical and v1accination
the blood and replicate in many tissues
history and laboratory testing. I))iagnostic
including the liver, kidneys, lungs, genital
tests for leptospirosis include th1ose

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tract, and CNS for 7 -

10 days. During the
designed to detect antibodies a�ainst the
period of bacteremia and tissue colonizaorganism and those designed to detect the tion, the clinical signs of acute leptospirosis,
organism in tissues or body fluid1s. Serologic
which vaiy by serovar and host, occur.

testing is recommended in each case,

Agglutinating antibodies can be detected in
combined with one or more tect:miques to
sernm soon after leptospi.remia occurs and
identify the organism in tissue mr body
coincide with clearance of the leptospires
fluids.

from blood and most organs. As the

Sero logic assays are the most- commonly
organisms are cleared, the clinical signs
used technique to diagnose leptc0spirosis in
of acute leptospirosis begin to resolve,
anin1als. The microscopic aggluttination test
although damaged organs may take some

(MAT) is most frequently used. n involves
time to return to normal function. In some
mixing appropriate dilutions of 53ernm with
cases, severely damaged organs may not
live leptospires of serovars prev,alent witl1in
recover, leading to chronic disease or death.

the region. The presence of antill:>odies is

At this point, the disease in incidental and
indicated by the agglutination oJf the
maintenance hosts diverges. Leptospires
leptospires, with the reported titter being the
remain in the tubules of the kidneys of
highest dilution of serun1 tllat re,sults in 500;6
incidental hosts for a short period of time
agglutination. The MAT is a corruplex test to
and are shed in the urine for a few days to
perfonn and interpret, and it rec,.uires the
several weeks. In maintenance hosts,
maintenance of live leptospiral cultures. An
however, leptospires often remain in

ELISA test to diagnose canine l�ptospirosis
the renal tubules, genital tract, and less
is offered by a commercial labocatory in tile
commonly, the eyes, despite the presence of

USA. This test detects antibodie·s to LipL32,
high levels of sernm antibody. Leptospires
a membrane protein found on pl!lthogenic
are shed in the urine and genital secretions
leptospires. The currently avaib,.ble assay
of persistently infected anin1als for months
provides a qualitative negative o.r positive
to years after initial infection, and these
result and will also detect antibodies
anin1als become an important reservoir of
induced by vaccination. A comp,arison of
infection, with the potential to transmit
this test to the MAT has not beer'I reported,
infection to other reservoir hosts or to
and it is likely that the numerical titers
incidental hosts at risk of developing
provided by the MAT will provide more
clinical disease.

diagnostically useful information than a
qualitative ELISA.

Clinical Findings: The clinical signs of

Interpretation of serologic results from
leptospirosis depend on the host species,
the MAT is complicated by a nu(llber of
the pathogenicity of the strain and serovar
factors, including cross-reactiviJ!;y of
of Leptospira, and the age an_d physiologic antibodies, antibody titers induced by
state of the animal. Subclinical infections
vaccination, and lack of consensus about
are common, particularly in the maintethe level of antibody titer that in.dicates nance host. In incidental hosts, leptospiroinfection. Antibodies produced :in an animal sis is an acute, systemic, often febrile illness
in response to infection with a given serovar
characterized by renal and/or hepatic
of Le'J)tospira often cross-react with other damage. In addition, there may be effects
serovars. In some cases, these patterns of
on other body systems resulting in clinical
cross-reactivity are predictable based on
problems such as uveitis, pancreatitis,
the antigenic relatedness of the various
bleeding, hemolytic anemia, muscle pain,
serovars of Le'J)tospira, but tl1e 9attems of or respiratory disease.

cross-reactive antibodies vary between host

In botl1 incidental and maintenance hosts
species. Paradoxical reactions may occur
that are pregnant at tile time of infection,
with the MAT early in the course of an acute localization and persistence of the organism infection, with a marked agglutinating in the uterns may result in fetal infection,
antibody response to a serovar other than
with subsequent abortion, stillbirth, birth
the infecting serovar. In additior1, there is
of weak neonates, or birth of healthy but
evidence of lack of consistency between
infected offsp1ing. In general, incidental
diagnostic laboratories. For the�e reasons,
hosts abort acutely, whereas in maintethe infecting serovar in an indivJdual animal nance hosts, abortions or other reproduccarmot be reliably identified as the serovar tive sequelae may be delayed by several
to which the animal develops the highest
weeks or months.

titer. The real value of the MAT is in

LEPTOSPIROSIS

649
providing a numerical titer to allow
begun. Culture of leptospires requires
comparison of acute and convalescent
specialized culture medium, the organisms
values.

are fastidious and slow-growing, and

Widespread vaccination of dogs and
diagnostic laboratories rarely culture
livestock with leptospiral vaccines also
specimens for the presence of leptospires.

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complicates interpretation of leptospiral

Thus, culture is of little value to clinicians.

serology. In general, vaccinated animals
develop relatively low agglutinating

Prevention: Avoidance of exposure to
antibody titers (1: 100 to 1:400) in response
free-ranging wildlife and domestic animals
to vaccination, and these titers persist for
that may be maintenance hosts for

1-4 mo after vaccination. However, some

Leptospira is difficult because rodents,
animals develop high titers after vaccination
raccoons, opossun1s, and skunks are
which persist for �6 mo.

frequently found in rural and urban

Consensus is lacking as to what
environments. The cornerstone of
constitutes a diagnostic titer for leptospiral
leptospirosis prevention is vaccination with
infection. A low antibody titer does not
polyvalent inactivated vaccines. Inmmnity
necessarily exclude a diagnosis of
to leptospirosis is believed to be serovar
leptospirosis, because titers are often low
specific and, therefore, vaccines are
in acute disease and in maintenance host
formulated for various species to include
infections. In cases of acute leptospirosis, a
the relevant serovars. There are cruTently

4-fold rise in antibody titer is often observed
no leptospiral vaccines for horses. Leptoin paired serum samples collected 7-10 days spiral vaccines are generally designed and
apart. Diagnosis of leptospirosis based on a
evaluated for the ability to prevent clinical
single serum sample should be made with
signs of disease, although some vaccines
caution and with full consideration of the
have also been shown to significantly
clinical picture and vaccination history of
reduce renal colonization and urine
the animal. In general, with a compatible
shedding.

clinical history and vaccination >3 mo ago, a
titer of 1:800 to 1:1,600 is good presumptive

Zoonotic Risk: People are susceptible
evidence of leptospiral infection. The use
to infection with most of the pathogenic
of paired acute and convalescent titers is
serovars of Leptospira but are incidental
strongly recommended whenever possible.

hosts and, therefore, not important

Antibody titers can persist for several
reservoirs of infection. Occupational
months after infection and recovery,
exposure is a rick factor, and veterinarians,
although there is usually a gradual decline
veterinary staff, livestock producers, and
with time.

dairy workers are at increased risk. In

Immunofluorescence can be used to
addition, recreational exposure to waters
identify leptospires in tissues, blood, or
contaminated with urine of domestic
urine sediment. The test is rapid and has
animals or wildlife presents a risk. Animal
reasonable sensitivity, but interpretation
owners have contracted leptospirosis via
requires a skilled laboratory technician.

contact with infected companion animals

Immunohistochemistry is useful to identify
and livestock.

leptospires in formalin-fixed tissue but,

The principal route of infection is contact
because there may be small numbers of
with infectious body fluids (blood in acute
organisms present in some tissues, the
cases or urine) via mucous membranes. In
sensitivity of this technique is variable. A
people, the disease varies from subclinical
number of PCR procedures are available,
to severe and can be fatal when renal or
and each laboratory may select a slightly
hepatic failure occurs. The most common
different procedure. Unfortunately, few
signs are fever, headaches, rash, ocular
publications have confirmed the validity of
pain, myalgia, and malaise. Transplacental
all the commercially available PCRs, which
infection, abortion, and infection of infants
likely vary considerably in their perforvia breast feeding have been described, mance. PCR techniques allow detection of
making exposure of pregnant women of
pathogenic leptospires in blood, urine, or
particular concern. Laboratory techniques
tissue samples but do not determine the
are necessary for a definitive diagnosis.

infecting serovar. Culture of blood, urine,

Because diagnosis of leptospirosis in
or tissue specimens is the only method to
animals is difficult based on clinical signs,
definitively identify the infecting serovar.

veterinarians may wish to implement an

Blood may be cultured early in the clinical
infection control program in which animal
course; urine is more likely to be positive
body fluids are handled only with gloved

7-10 days after clinical signs appear. Culture
hands and hand washing is routine. It is also
is rarely positive after antibiotic therapy has
essential for staff to take precautions when

650

LEPTOSPIROSIS
handling or nursing animals suspected or
sex of dog is susceptible to leptospirosis,
confirmed to have leptospirosis. Appropriand the diagnosis should not be excluded on ate precautions include wearing gowns,
the basis of signalment or lifestyle. Canine
shoe covers, and gloves to avoid contamileptospirosis is not restricted to large-breed nating exposed skin or spreading organdogs, male dogs, or dogs with a predomi

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isms. Face shields should be worn when
nantly outdoor lifestyle.

handling wet bedding or cleaning cages,

Acute kidney injury has been the most
stalls, or rnns to avoid contact of aerocommon presentation for canine leptospirosolized organisms with mucous memsis in recent years. Affected dogs may branes.

present with lethargy, anorexia, vomiting,
abdominal pain, and history of polyuria,

LEPTOSPIROSIS IN DOGS
oliguria, or anuria. Dogs that survive acute
renal failure may return to baseline or

Dogs are the maintenance host for
progress to chronic kidney disease.

Leptospira interrogans serovar Canicola,

Leptospirosis should also be considered in
and before widespread vaccination
any dog with previously diagnosed chronic
programs, serovars Canicola and Icterokidney disease that develops "acute-onhaemorrhagiae were the most common chronic" kidney injury. Renal tubular
serovars in dogs in the USA. The prevalence
dan1age in leptospirosis may manifest as
of canine serovars has shifted significantly
cylindrmia, proteinuria, or glycosuria.

in the last 20 years; currently the most

In people, acute kidney injury due to
prevalent serovars are believed to be
leptospirosis is often nonoligmic and can

Grippotyphosa, Pomona, and Bratislava;
be associated with hyponatremia and
however, this belief is largely based on
hypokalemia. These electrolyte changes
serologic results that are now known to
have also been noted in canine leptospi..robe inaccurate in predicting the infecting sis, along with the expected changes of
serovar in dogs with leptospirosis. The
azotemia, hyperphosphatemia, and acidosis
serovars that cause disease in dogs are
of renal failure. Hyperkalemia is also
likely to vary with geographic region and
possible. Polyuria and polydipsia (PU/PD)

the presence of reservoir hosts. Unfortuin the absence of azotemia is a less conu11on nately, current understanding of the
manifestation of the renal effects of
serovars that cause natural disease in dogs
leptospirosis. PU/PD may be due to a
is limited by tl1e fact that isolation of
decrease in glomernlar filtration rate that is
leptospires is rarely perfonned; thus,
sufficient to cause loss of renal concentratstudies to date have relied on serologic data. ing ability without azotemia. However, As noted above, it is now accepted that the

PU/PD can also be due to nephrogenic
results of the MAT do not reliably predict
diabetes insipidus.

the infecting serovar in dogs ( or people)

Acute liver disease may accompany acute
with leptospirosis; thus, the trne infecting
renal failure in dogs with leptospirosis, or it
serovar is unknown in most cases. Howmay occur alone. Affected dogs may be ever, it is likely that the serovars that cause
icteric, and serurn biochemistry analysis
disease in dogs are those circulating in local
reveals increased bilirubin and alkaline
wildlife. Experimental infections and
phosphatase. ALT is typically less markedly
isolation of organisms from a small number
increased than alkaline phosphatase. In
of sick dogs have shown that serovars
people and dogs, the jaundice of acute

Icterohaemorrhagiae, Canicola, Auturnnaleptospirosis appears to be associated lis, Pomona, Bratislava, Sejroe, and Ballun1
with minimal histopathologic changes in
are capable of causing disease in dogs.

the liver, suggesting that it is due to the

Knowledge of the infecting serovar in dogs

"cholestasis of sepsis" ratller than to
is essential for epidemiologic studies and
hepatocellular damage.

vaccine development; it is less important for

Muscle pain, stiffness, weakness,
clinicians managing individual cases. It is
trembling, or reluctance to move can be
currently not Imown whether specific
seen in dogs with leptospirosis. These may
serovars are associated with specific
be the result of vasculitis, myositis, or
clinical signs in dogs, and there is no
nephritis. Myalgia is commonly reported in
published evidence to guide therapy based
hun1an leptospirosis and is associated with
on serovar identification. It is, however,
the septicemic phase of the disease.

extremely impmtant for veterinarians to

Less common manifestations of canine
maintain a high inclex of suspicion for
leptospirosis include bleeding disorders
leptospirosis, because this is a zoonotic
characterized by petechial hemorrhages,
disease and has a wide range of clinical
epistaxis, melena, and hematemesis. These
presentations in dogs. Any age, breed, or
findings are most likely due to vasculitis.

LEPTOSPIROSIS

651

Affected dogs may also be thrombocytofriable with an accentuated lobular pattern penic; however, platelet counts are rarely
and may have a. yellowish brown discoloralow enough to be responsible for spontanetion. The kidneys may have white foci on ous bleeding. The causes and mechanisms
the subcapsula.i· surface. Microscopic
of bleeding disorders in leptospirosis are
findings in the liver may include mild

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poorly understood, but they have been
random hepatocytic necrosis, nonsuppura.suggested to be associated with endothelial tive hepatitis, and intral1epatic bile stasis,
cell damage. Pulmonary hemorrhage is now
while swollen tubula.i· epithelial cells,
one of the most common clinical signs in
tubular necrosis, and a mixed infla.n1111ato1y
outbreaks of hun1a.n leptospirosis. This is a
reaction may be seen in the kidneys.

less common finding in canine leptospirosis;

Idea.lly, a combination of serology and
however, cough or dyspnea, or radiographic organism detection should be used for abnom1alities have been noted in a number
diagnosis of ca.nine leptospirosis. Serology
of affected dogs. Uveitis is an uncommon
is the most frequently used diagnostic test
manifestation of leptospirosis in dogs. It
for dogs. Acute and convalescent titers may
appears to be infrequently associated with
be necessary to confim1 a diagnosis; hence,
experimental ca.nine leptospi.rosis, but rare
tl1e use of the MAT is preferred over the
case reports exist. Additional clinical signs

ELISA. PCR-based tests a.i·e widely
reported in dogs with leptospirosis include
available, and collection of both blood and
vomiting, diarrhea, weight loss, fever,
urine sa.inples before adnlinistration of
hypothermia, oculonasal discharge,
antibiotics should be considered for
lymphadenopa.thy, effusions, and edema.

maximal sensitivity. The results of a.II

CBC changes may include neutrophilia,
diagnostic tests should be interpreted in
lymphopenia., monocytosis, and mild
light of tl1e animal's vaccination history,
anemia. These changes are nonspecific;
clinical signs, and cli.nicopathologic
however, mild to moderate thrombocytopefindings.

nia is seen in >500A, of cases and, if detected

Renal failure and liver disease a.i·e
in combination with azotemia or evidence
treated witl1 fluid tl1erapy and other
of cholestasis, should prompt diagnostic
supportive measures to maintain normal
testing for leptospirosis. Coagulation
fluid, electrolyte, and acid-base balance.

abnonnalities may include increased fibtin

Supportive measures may include a.ntiemetdegradation products and prolonged ics, GI protecta.nts, phosphate binders,
prothrombin tinle (PT) or activated partial
and hepatic suppo1t medications. Renal
thromboplastin time (APTT). Urinalysis
replacement therapy with intennittent
may reveal hyposthenuria., isosthenuria, or
hemodialysis or continuous renal replacehypersthenuria, depending on the degree ment therapy should be considered for dogs
of renal involvement. Other changes may
that are a.nuric or oliguric despite appropriinclude proteinmia, glucosuria, cylind.ruria, ate suppmtive tl1erapy. Antibiotic therapy
hema.turia, and pyuria Leptospirosis could
is indicated whenever leptospirosis is
also potentially be associated with renal
suspected and should be instituted before
tubular acidosis.

confinnatory test results are available. There

Reticulonodular pulmonary opacities
a.re no experimental studies in dogs to guide
have been desc1ibed in the thoracic
selection of antibiotic protocols for this
radiographs of dogs with leptospirosis and
species. Cun·ent recommendations are to
attributed to pulmona.iy hemorrhage. These
treat with doxycycline (5 mg/kg/day, IV or
changes may be diffuse or predominantly

PO) for 2 wk For dogs that ca.1U1ot tolerate
involve the ca.udodorsal lung fields.

doxycycline, initial tl1erapy with a penicillin

Abdominal radiogra.phs may be unremarkis appropriate, but this should be followed able or may show renomegaly or hepatoby a 2-wk course of doxycycline to eliminate megaly. Changes noted on ultrasonography
the renal ca.iTier phase of infection. Dogs
include renomegaly, pyelectasia, increased
recently exposed to leptospirosis may be
cortical echogenicity, perinephric effusion,
treated prophylactica.lly with oral doxycyand a hyperechoic medullary band.

cline for 14 days.

However, these changes are not specific for

Con1111ercial ba.cterins for dogs a.i·e
leptospirosis, and absence of these findings
available for serovars Ca.nicola, Icterodoes not exclude the diagnosis.

haem01Thagia.e, Gtippotyphosa, and

Gross necropsy findings can include

Pomona. Vaccinated dogs may potentia.lly
jaundice, effusions, and petechial or
be susceptible to infection with other
ecchymotic hemorrhages on any orga.11,
serovars, although this has not been tested
pleural, or peritoneal surface. The kidneys
in an experinlental setting. In general,
and liver may be enlarged, and lungs may be
currently available vaccines provide good
wet, heavy, and discolored. The liver is often protection from clinical disease and also

652

LEPTOSPIROSIS
appear to reduce renal colonization and
between years. The reason for the yearly
urine shedding. Concerns exist regarding
variation in incidence of abortions is not
hypersensitivity reactions after leptospiral
clear. Serovar Pomona type kennewicki is
vaccination in dogs, but these appear to be
responsible for most of the leptospiral

Ulljustified based on more recent studies
abortions in North America, but serovars

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and perhaps associated with the use of

G1ippotyphosa and Hardjo have also been
more highly purified vaccines. Canine
reported. Skunks, raccoons, and red foxes
challenge studies have demonstrated
are known to harbor Pomona type
duration of inununity of at least 1 yr; thus,
kennewicki. Most abortions occur after
prior recommendations for vaccinating

9 mo of gestation, and rarely a live foal may
every 6 mo are no longer justified.

be born ill from leptospirosis. Macroscopic

Because leptospirosis is a zoonotic
lesions are edema, areas of necrosis in the
disease, all veterinary personnel should
chorion, and placentitis that does not
take appropriate precautions when
involve the cervical star. Microscopic
handling known or suspected infected
lesions include necrosis and calcification of
animals. Such dogs do not need to be placed
the placenta. Placental disease may result in
in isolation but should be nursed with
the mare developing hydroallantois.

barrier precautions, paying particular

Macroscopically, the fetal liver may have
attention to avoiding exposure of skin or
yellow discoloration. Liver disease in the
mucous membranes to urine or blood.

fetus is a multifocal necrosis and giant cell

Infected dogs should be allowed to urinate
hepatopathy. Tubulonephrosis and
in designated areas that can subsequently
interstitial nephritis may be detected in the
be cleaned and disinfected. The organisms
kidneys of the aborted fetus. Inflainmation
are killed by all commonly used disinfectof the umbilical cord (funisitis) may be ants. Owners of dogs recently diagnosed
recognized by diffuse yellowish discolorawith leptospirosis should be advised of the tion. Aborting mares typically have very
zoonotic nature of the disease and contact
high leptospiral antibody titers at the time of
their physicians with any health concerns.

abortion and, although quite variable, the

Owners should wear gloves when cleaning
time of urine shedding of leptospires after
up urine and should wash their hands after
an abortion is often 2-3 mo.

handling the dog, at least until the course of

Occasionally, Leptospira interrogans
antibiotic therapy is completed.

serovar Pomona causes fever and acute
renal failure in horses. The kidneys become

LEPTOSPIROSIS IN HORSES
swollen as a result of tubulointerstitial
nephritis, and urinalysis may reveal

In the USA and Canada, Leptospira
hematuria and pyuria without visible
interrogans serovar Pomona type
bacteria. On rare occasions, multiple
kennewicki and serovar·Grippotyphosa are
weanling or yearling horses may be affected
the most common causes of equine leptospiwith fever and acute renal failure after infecrosis. The prevalence of leptospirosis in tion.

horses is unknown, but serologic evidence

The most in1portant clinical disease
indicates a higher incidence than is
associated with L interrogans serovai·
apparent clinically. Antibodies to serovar

Pomona infection in adult horses in North

Bratislava are reported frequently in horses

America and L kirschneri serovar
in the USA and in Europe; horses are

Grippotyphosa in Europe is equine
thought to be a maintenance host for this
recurrent uveitis (ERU). ERU is believed to
organism, and clinical disease has not been
be an inunune-mediated disease sometimes
confirmed with Bratislava infections. Acute
involving antibody against certain

Pomona infections also commonly cause

Leptospira antigens, specifically the LruC
cross-reacting antibodies for Bratislava and
outer membrane protein, which cross

Icterohaemorrhagiae on the MAT, which
reacts with tissues of the lens, cornea, and
may explain some of the commonly
possibly retina. Live Leptospira organisms
observed high titers to Bratislava. Clinical
can be found in the aqueous or vitreous fluid
leptospirosis in horses is most commonly
of horses with ERU. High concentration of
associated with abortions, acute renal
antibody againstL interrogans serovar
failure, rarely pulmonary or systemic illness

Pomona in the aqueous humor, compared
in foals, and most importantly recurrent
with serum titers, also suggests persistent
uveitis.

local antigenic stimulation. Survival of the

Leptospira, interrogans serovar Pomona
organism in the face of high ocular antibody
abortions may account for -13% of bacterial
indicates an absence of cells or molecules
abortions in mares in endemic regions,

(eg, complement) involved in bacterial
although incidence vaiies considerably
clearance, suggesting an ocular immune

LEPTOSPIROSIS

653
privilege similar to that of the CNS.

testing of aqueous fluid may be the only way

Recurrent episodes of the disease may be
to confinnLeptospira-associated uveitis. In related to a Thl 7 response of autoreactivity

ERU, the organism is most commonly found
following mimicry and inter- or intramoin the vitreous rather than aqueous fluid, lecular epitope spreading, or both.

which limits the practical application of

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Genetic factors are likely involved in the
ocular fluid PCR testing.

disease process, helping to explain why

In acute disease, systemic antibiotics
only some horses infected with Leptospira
such as enrofloxacin, penicillin, tetracydevelop uveitis. Appaloosas are thought to clines, or aminoglycosides are useful, but
be genetically predisposed, and specific
this has not been proved to be the case with

MHC markers on ECAl, ELA class 1, and an
recurrent uveitis. There are no leptospiral

ELA class II microsatellite are strongly
vaccines approved for horses, although
associated with the disease. The prevalence
many vete1inarians have used vaccines
of ERU is unknown, but reports suggest that approved for cattle on horse farms that have

:2c 1 % of horses will develop the disease
endemic Leptospira abortions or uveitis.

during their lifetime. It is probable that
some cases of ERU are not associated with

Leptospira infection, and this may vary by

LEPTOSPIROSIS IN RUMINANTS
geographic region. In some regions, more

Leptospiral serovars of major importance
than 500/o of ERU cases are associated with
in cattle are Hardjo and Pomona in North
persistent ocular infections with Lepto

America, with serovars Grippotyphosa,
spira. Leptospira-associated uveitis may

Bratislava, Icterohaemorrhagiae, and
cause corneal, anterior chamber, and

Canicola occasionally implicated. The most
posterior chamber disease. Therefore,
commonly documented cause of leptospiroclinical findings may vary from corneal sis among cattle in the USA and throughout
edema, clinically quiet retinal lesions
much of the world is serovar Hardjo, for
observed on funduscopic examination, and
which cattle are the maintenance host. Risk
most dramatically recurrent and progresfactors for Hardjo infection in cattle have sive painful uveitis. The chronic disease
been reported to include open herds, access
of the globe may cause cataracts, retinal
to contaminated water sources, co-grazing
degeneration, or even glaucoma.

with sheep, and use of natural breeding.

Diagnosis of Leptospira abortion is best

Serovar hardjo has the ability to colonize
accomplished by fluorescent antibody
and persist in the genital tract of infected
testing (FAT) or inununohistochemical
cows and bulls.

evaluation of the placenta, umbilical cord,

Many leptospiral infections in cattle are
fetal liver, or fetal kidney. The sensitivity
subclinical, particularly in nonpregnant and
and specificity of the FAT in these tissues
nonlactating anin1als. Acute or subacute

(but not urine) are nearly 1000/o. Examinaleptospirosis is most commonly associated tion of silver-stained kidney samples in
with incidental host infections and occurs
horses with renal disease does not yield
during the leptospiremic phase of infection.

high accuracy, because there may be

Clinical signs associated with chronic
false-negative and false-positive findings,
infections are usually associated with
likely a result of nonpathogenic serovars.

reproductive loss through abortion and

PCR testing is preferred for evaluation of
stillbirth. Persistent colonization by serovar
fluids, such as urine, ocular fluids, and

Hardjo of the uterus and oviducts may be
blood. Marked increases in serun1 antibody
associated with infertility characterized by
titers often accompany Leptospira
increased services per conception and
abortions or acute renal failure, but serw11
prolonged calving intervals.

titers may be low in horses with recurrent

Uncommonly, severe acute disease
uveitis because of the chronic and localized
occurs in young stock infected with
nature of infection. Acute L interrogans
incidental serovars, particularly serovar
serovar Pomona infections often cause

Pomona and less commonly Icterohemormarked increases in antibody titers to rhagiae. Clinical signs include high fever,
several serovars ( especially Icterohemorhemolytic anemia, hemoglobinuria, rhagiae and Bratislava, but the noninfecting
jaundice, pulmonary congestion, occasionserovar titers usually decline much more ally meningitis, and death. In lactating cows,
quickly over several weeks than the titers to
incidental infections may be associated with
the actual infecting serovar. Collection of a
agalactia with small quantities of bloodvoided urine sample after furosemide tinged milk. A less severe form of this "milk
administration may in1prove sensitivity of
drop syndrome" may occur in Hardjo

PCR, darkfield staining, or culture testing. A
infected lactating cows in the absence of
combination of serology, culture, and PCR
other clinical evidence of infection. In

654

LEPTOSPIROSIS
lactating cows, incidental infections have
giae, and Hardjo. These vaccines provide
been reported to cause blood-tinged milk.

good protection against disease caused by

The chronic phase of disease is assoc i each of these serovars, with the possible ated with fetal infection in pregnant cows
exception of serovar Hardjo. Experimental
presenting as abortion, stillbirth, or birth
and field evidence indicates that some

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of premature and weak infected calves.

traditional five-way leptospirosis vaccines

Infected but healthy calves also may be
do not provide good protection from
born. Abortion or stillbirth is commonly the
serova.r Ha.rdjo irlfection. New vaccines
only manifestation of infection but may
have been introduced to address this issue.

sometimes be related to an episode of

If a primary goal of a vaccination program
illness up to 6 wk (Pomona) or 12 wk
is protection of cattle against Hardjo, care

(Hardjo) earlier. Abortions associated with
should be taken in selection of a vaccine
incidental host infection tend to occur late
product. In general, annual vaccination of
term and in groups or so-called "abortion
all cattle in a closed herd or low incidence
storms." ln contrast, abortions occurring
area, or twice-yearly vaccination in an open
after infection with serovar Hardjo tend to
herd or high incidence area, is the most
be more sporadic and can occur mid- to late
effective approach to control.

pregnancy and several months after initial

Relative to cattle and pigs, sheep and
infection.

goats have been considered resistant to

Diagnosis of incidental host infections
leptospfral infection, with low seroprevain cattle is relatively straightforward. ln lences and only a small number of
general, infected animals develop high titers serogroups being irnplicated in clinical to the infecting serovar; an antibody titer
disease. Sheep can serve as a maintenance

> 1 :800 at the time of abortion is considered
host for serovar Hardjo and therefore
evidence of leptospfrosis. Leptospfres can
spread Wection to cattle. lncidental
be demonstrated in placenta and the fetus in infections may cause sporadic outbreaks of some cases by inmmnofluorescence, PCR,
acute disease characterized by hematuria,
and inununohistochemistry. Diagnosis of
hemoglobinuria,jaundice, and death
serovar Hardjo infection is more difficult

(usually in lan1bs), and occasional
and requfres a combination of approaches.

abmtions.

Serology alone often fails to identify
animals infected with serovar Hardjo,
because seronegative shedders are conunon

LEPTOSPIROSIS IN SWINE
in infected cattle herds. The recommended
diagnostic testing strategy includes the

Leptospira interrogans (serovars Pomona,
primary use of a test (inununofluorescence

Icterohaemorrhagiae, Canicola, Hardjo, and
or PCR) to detect the organism in the urir1e

Bratislava), L borgpetersenii (serovars
from a sample of cattle·in the herd followed

Sejroe and Tarassovi), and L kirschneri
by serologic testing to provide insight into

(serovar Grippotyphosa) are all reported to
the likely infecting serovar of Leptospira.

infect pigs. Serovars Pomona and Bratislava

Cattle with acute leptospu·osis can be
are uniquely adapted to swine; others are
treated with the label dosage of tetracycline, maintained in other species but sometin1es oxytetracycline, penicillin, ceftiofur,
infect swine. Swine are maintenance hosts
tilmicosin, or tulathromycin. Leptospires
for serovar Bratislava, and Wected pigs
also are highly susceptible to erythromycin, rarely develop signs typical of acute tiamulin, and tylosin, although these
leptospfrosis-rather, reproductive failure
antibiotics cannot be relied on to remove
as evidenced by infertility and sporadic
the renal carrier state. lf\iectable, longabortion is the most common clinical sign, acting oxytetracycline (20 mg/kg) and
and venereal transmission may occur.

sustained-release ceftiofur have been

Serovar Pomona, in contrast, is of
shown to effectively eliminate shedding
intermediate pathogenicity for swine, with
in cattle infected with serovar Hardjo.

acute clinical signs seen in young pigs and

Vaccination can be combined with
abortions ( often in groups) occurring in
antibiotic treatment in the face of an
pregnant swine. Although Pomona
outbreak of leptospirosis, but vaccination
infections are associated with acute,
alone will not reduce urinary shedding. All
sometimes severe clinical signs suggestive
appropriate withdrawal times should be
of an incidental host infection, pigs often
observed.

remain Wected and shed serovar Pomona

Bovine leptospfrosis vaccines available in for weeks to a few months after infection.

the USA and Canada are pentavalent and

This feature of Pomona infection can be
contain leptospfral serovars Pomona,
associated with high rates of pig-to-pig

Grippotyphosa, Canicola, Icterohaemorrha-
transmission among swine reared in

LIGHTNING STROKE AND ELECTROCUTION

655
confinement. Incidental infections may
leptospirosis, as described in calves, has
occur from strains belonging to the
been described in piglets but is rare.

G1ippotyphosa, lcterohaemorrhagiae,

Treatment and control are similar to those
and Canicola serogroups.

described for cattle, using a combination

Abortions occurring 2-4 wk before term
of medication either to prevent infection

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are the most common manifestation of
or to decrease shedding, vaccination,
leptospirosis in pigs. Piglets produced at
rodent and small mammal control, and
term may be dead or weak and may die
feed and water free of Leptospim
soon after bilth. The p1incipal differential
organisms. Immunization through use of
diagnosis is porcine reproductive and
bacterins is widely practiced in breeding
respiratory syndrome (seep 729),
herds and will reduce the prevalence of
although brucellosis, parvovirus, and
infection and abo1tions. The bacterin

SMEDI (stillbirth, mummification,
must be serovar specific for protection.

embryonic death, and infertility) share

Bacterins should not be expected to
some features with leptospirosis. Acute
eliminate infection in carriers.

LIGHTNING STROKE AND ELECTROCUTION

Injury or death of an animal due to
stanchion or a metal creep or guard rail can
high-voltage electrical currents may be the
result in widespread distribution of an
result of lightning, fallen transmission
electric current throughout the stable (see
wires, faulty electrical circuits, or chewing
also STRAY VOLTAGE IN ANIMAL HOUSING, p 2113) on an electrical cord. Electrocution due to
tl1at may result in signs of water deprivation
lightning stroke is seasonal and tends to be
or feed refusal.

geographically restricted. Investigation of

Death from electric shock usually results
possible electrocution should always
from cardiac or respiratory arrest. Passage
proceed with caution, because the
of current through the heait usually
electrification resulting from broken
produces ventricular fibrillation, and
transmission wires, for example, may still
involvement of the CNS may affect the
be present. Once the site is clearly safe, the
respiratory or other vital centers.

investigation should include the location
of the dead animals, examination of all

Clinical Findings: Vaiying degrees of
affected animals, and necropsy of those
electric shock may occur. In most il1stances
that died.

of electrocution by lightning stroke, death is

Ce1tain types of trees, especially
instantaneous and the animal falls without a
hardwoods such as oaks and those that are
struggle. Occasionally, the anin1al becomes
tall and have spreading root systems just
unconscious but may recover in a few
beneath the ground surface, tend to be
minutes to several hours; residual ne1vous
struck by lightning more often than others.

signs ( eg, depression, paraplegia, cutaneous

Electrification of such roots charges a wide
hyperesthesia, blindness) may persist for
surface area, particularly when the ground
days or weeks or be permanent. Singe
is already damp; passage of charged roots
marks on or damage to tl1e cai·cass, damage
beneath a shallow pool of water causes it to
to the immediate envfronment, or both,
become electrified. A tile drain may spread
occur in -90"Ai of cases of lightning stroke
an electric charge throughout its course.

but are less likely to be fom1d if the ai1imal

Fallen or sagging transmission wires also
is electrocuted by standing on electrified
may electrify a pool of water, fence, or
earth. Singe marks tend to be linear and are
building, and an anilnal may also dfrectly
more commonly found on the medial sides
contact such wires. Differences exist in
of the legs, although rai·ely much of the
conductivity of soil; loan1, sand, clay,
body may be affected. Beneatl1 the singe
marble, and chalk are good conductors (in
marks, capillary congestion is conunon; the
decreasing order), whereas rocky soil is not. arboreal pattern chai·acteristic of lightning Accidental electrocution of farm animals
stroke can be visualized best from the
in a barn or adjacent confinement pen
dermal side of the skin by subcutaneous
usually occurs as a result of faulty wiring.

extravasations of blood. Singe marks are

Electrification of a water or milk line
rai·ely found on recovered animals. Smaller

656

LIGHTNING STROKE AND ELECTROCUTION
animals such as pigs that contact electrified
superficial lymph nodes of the head, neck,
water bowls or creeps may be killed
and thoracic limbs, and to a lesser extent
instantly or be thrown some distance by the
in the hindquarters. Probably the best
strength of the shock. Electrocuted pigs are
indication of instantaneous death is the
often recumbent and may have sustained
presence of hay or other feed in the animal's

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spinal, pelvic, or limb fractures, resulting
mouth; supportive evidence includes the
from severe muscular contractions.

presence of nonnal ingesta ( especially in the
run1en), lack of frothy ingesta (frothy bloat),

Diagnosis: The diagnosis is almost always
and presence of normal feces in the lower
made on circumstantial evidence, ie,
tract and occasionally on the ground behind
location of the carcass(es) and absence of
the animal. Few conditions affecting
any disease processes when examined by
livestock cause such peracute death
necropsy. The presence of dead animals
clustered in a small area
under a tree, hanging through or near a wire

Farm animals often are insured against
fence, or clustered around a light pole is
lightning stroke, and the insurance claims
strong evidence of electrocution by lightning agent or the veterinarian requested to sign stroke even in the absence of physical
an insurance form should closely observe
evidence like recent burning of tree bark
the situation that initiated the claim. The
or splitting of poles or boards in a fence.

investigator should ascertain that the

Rigor mortis develops and passes quickly.

animal actually died in the high-risk location

Postmortem distention of the rumen occurs
rather than having been moved after death.

rapidly and must be differentiated from

This could be done to merely clean up or
antemortem rurninal tympany (seep 227); in
to deliberately confuse the investigation.

both conditions, the blood tends to clot

Similarly, examination of recent weather
slowly or not at all. The rnucosae of the upper
information confirming thw1derstonns is an
respiratory tract, including the turbinates and in1portant part of the process to substantisinuses, are congested and hemorrhagic; ate an insurance clain1. A well-documented
linear tracheal hemorrhages are common,
description of where the animal(s) died and
and large blood clots are occasionally found
the results of a necropsy examination are
in the trachea, but the lungs are not
usually acceptable to support an insurance
compressed as in bloat. All other viscera are
claim of lightning stroke.

congested, and petechiae and ecchymoses
may be found in many organs. Due to

Treatment: Those animals that survive
postmortem rurninal distention, the poorly
may require supportive and symptomatic
clotted blood is passively moved to the
therapy. Euthanasia is warranted for those
periphery of the body, resulting in postmoranimals recumbent with fractures or severe tem extravasation of blood in muscles and
muscle injuries.

LISTERIOSIS

(Listerellosis, Circling disease)

Listeriosis is a sporadic bacterial infection

4°-44°C (39°-111 °F). Its ability to grow
tl1at affects a wide range of animals,
at 4°C is an important diagnostic aid (the
including people and birds. It is seen

"cold enrichment" method) for isolation
worldwide, more frequently in temperate
of the organism from brain tissue but not
and colder clin1ates. There is a high
from placental or fetal tissues. Primary
incidence of intestinal carriers. Encephalitis isolation is enhanced under microaeroor meni:ngoencephalitis in adult ruminants philic conditions. It is a ubiquitous
is the most frequently recognized fom1.

saprophyte that lives in a plant-soil
environment and has been isolated from

Etiology and Epidemiology: Listeria

-42 species of domestic and wild mammals
rnonocylogenes is a small, motile, gramand 22 species of birds, as well as fish, positive, nonsporeforming, extremely
crustaceans, insects, sewage, water,
resistant, diphtheroid coccobacillus that
silage and other feedstuffs, milk, cheese,
grows under a wide temperature range
meconium, feces, and soil.

LISTERIOSIS

657

The natural reservoirs ofL monocy

The uterus of all domestic animals,
togenes appear to be soil and mammalian
especially ruminants, is susceptible to

GI tracts, both of which contan1inate
infection with L monocylogenes at all
vegetation. Grazing animals ingest the
stages of pregnancy, which can result in
organism and fmther contaminate
placentitis, fetal infection and death,

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vegetation and soil. Animal-to-animal
abortion, stillbirths, neonatal deaths,
transmission occurs via the fecal-oral
rnet1itis, and possibly viable carriers. The
route.

metritis has little or no effect on subsequent

Listeriosis is primarily a winter-spring
reproduction; however, Listeria may be
disease of feedlot or housed ruminants. The
shed for;:,! mo via the vagina and milk.

less acidic pH of spoiled silage enhances

Infections acquired via ingestion tend to
multiplication of L monocytogenes.

localize in the intestinal wall and result in

Outbreaks typically occur 2'10 days after
prolonged fecal excretion. It has been
feeding poor-quality silage. Removal or
postulated that contan1inated silage results
change of silage in the ration often stops the
in latent infections, often approaching lOO"A,
spread of listeriosis; feeding the same silage
of the exposed herd or flock, but clinical
months later may result in new cases.

listeriosis in only a few animals.

Pathogenesis: Listeria organisms that Clinical Findings: Encephalitis is the
are ingested or inhaled tend to cause
most readily recognized fonn of listeriosis
septicemia, abo1tion, and latent infection.

in ruminants. It affects all ages and both

Those that gain entry to tissues have a
sexes, sometimes as an epidemic in feedlot
predilection to localize in the intestinal wall,
cattle or sheep. The course in sheep and
medulla oblongata, and placenta or to cause
goats is rapid, and death may occur 24-48 hr
encephalitis via minute wounds in buccal
after onset of signs; however, the recovery
mucosa.

rate can be up to 3()0A, with prompt,

The various manifestations of infection
aggressive therapy. In cattle, the course is
occur in all susceptible species and are
less acute, and the recovery rate approaches
associated with characteristic clinical

50%. Lesions are localized in the brain stern,
syndromes: abortion and perinatal mortality and the signs indicate dysfunction of nerve in all species, encephalitis or rneningoennuclei, including those of the third to cephalitis in adult ruminants, septicemia in
seventh cranial ne1ves.

neonatal rmninants and monogastric

Initially, affected animals are anorectic,
animals, and septicemia with myocardial
depressed, and disoriented. They may
or hepatic necrosis ( or both) in poultry ( see
propel themselves into comers, lean against
p 2839).

stationary objects, or circle towar·d U1e

Listeric encephalitis affects sheep, cattle,
affected side. Facial paralysis with a
goats, and occasionally pigs. It is essentially
drooping ear·, deviated muzzle, flaccid lip;
a localized infection of the brain stern that
arid lowered eyelid often develops on the
develops when L monocytogenes ascends
affected side, as well as lack of a menace
the trigeminal nerve. Clinical signs vary
according to the function of damaged
neurons but often ar·e mlilateral and include
depression (ascending reticular activating
system), ipsilateral weakness (long tracts),
trigeminal and facial nerve paralysis, and
less commonly, circling (vestibulocochlear
nucleus). Neurologic signs indicating
bilateral cranial nerve deficits are occasionally seen in lambs <4 mo old.

Septicemic or visceral listeriosis is most
common in rnonogastric animals, including
pigs, dogs, cats, domestic and wild rabbits,
and many other small mammals. These
animals may play a role in transmission of

L monocytogenes. This fonn is also found
in young ruminants before the rumen is
functional. Although rare, septicemia has
been reported in older domestic ruminants
and deer. The septicemic fom1 affects
organs other than the brain, the principal

Right-sided facial and trigeminal nerve paralysis with profuse salivation caused by listeriosis lesion being focal hepatic necrosis.

in a goat. Courtesy of Dr. Philip Scott.

658

LISTERIOSIS
response and profuse, almost continuous,

Specimens of choice ru·e brain from ruli.mals
salivation; food material often becomes
with CNS involvement and aborted placenta
impacted in the cheek due to paralysis
and fetus. If p1imruy isolation attempts fail,
of the masticatory muscles. Terminally
grow1d brain tissue should be held at 4 °C
affected anin1als fall and, unable to rise,

(39°F) for several weeks and recultured

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lie on the same side; involuntary running
weekly. Occasionally, L monocytogenes
movements are common.

has been isolated from spinal fluid, nasal

Listeric encephalitis may recur on the
discharge, urine, feces, ru1d milk of clinically
san1e premises in successive years. The
ill rwninants. Serology is not used routinely
nwnber of animals clinically involved in an
for diagnosis, because mruiy healthy
outbreak usually is <2% but in exceptional
animals have lli.gh L'isteria titers. lllllmmocircwnstances may reach 100/o-30% in a fluorescence is effective for rapidly
flock of sheep.

identifying L monocytogenes in smears Listeric abortion usually occurs in the last
from anin1als dead or aborted from
trimester without premonitory signs. Fetuses listeriosis and from milk, meat, and other usually die in utero, but stillbirths and
sow·ces.

neonatal deaths occur. The abortion rate

Listeriosis can be differentiated from
varies and may reach 200A, in sheep flocks.

pregnancy toxemia in ewes (seep 1021) or

Fatal septicemia of the dan1 secondruy to
ketosis in cattle (seep 1024) by careful
metiitis is rru·e. Encephalitis ru1d abo1tion
clinical examination, CSF changes, and
usually do not occur simultaneously in the

3-0H butyrnte concentrations well below
same herd or flock. However, the clinical

3 mmoVL. Fwthe1more, facial and ear
pattern in sheep in the UK has been changing;
paralysis are absent in pregnancy toxemia
abortions, encephalitis, and diarrhea ru·e
or ketosis. ln cattle, the unilateral signs of
increasing, and outbreaks of abortions and
trigeminal and facial paralysis ( often subtle)

encephalitis occur together in the san1e flock. help differentiate listeriosis from bovine Listeriosis is relatively uncommon in pigs, spongiform encephalopathy (seep 1284), with septicemia occurring in those < l mo
thromboembolic me1li.ngoencephalitis (see
old ru1d encephalitis in older pigs; it has a
p 754), polioencephalomalacia (seep 1281),
rapid, fatal course of 3-4 days.

sporadic bovine encephalomyelitis (see

Lesions: ln listeric encephalitis, there
p 1308), and lead poisoning (seep 3078).

are few gross lesions except for some

Rabies (seep 1302) must always be
congestion of meninges. Microscopic
considered in the differential diagnosis of
lesions are confined primarily to the pons,
listeriosis. Aili.n1als with brain abscesses
medulla oblongata, and anterior spinal cord .. and coenurosis (seep 1311) present with ln septicemic listeriosis, small necrotic
circling, contralateral blindness, and
foci may be found in any organ, especially
proprioceptive deficits, but show no cranial
the liver. In calves that die when <3 wk old,
ne1ve deficits. Vestibulru· disease is conunon
in addition to focal hepatic necrosis, there is in growing rw1linants; these animals frequently mru·ked hemorrhagic gastroentypically show ipsilateral spontaneous teritis.

nystagmus or strabismus, and remain bright
ln aborted fetuses, there is slight to
and alert without ttigeminal nerve
marked autolysis, clear to blood-tinged fluid
dysfunction.

in the serous cavities, and nun1erous small
necrotic foci in the liver, especially in the

Treatment and Control: Recovery
right half. Necrotic foci may be found in
depends on early, aggressive Mtibiotic
other viscera such as lung and spleen.

treattnent. If signs of encephalitis ru·e

Shallow erosions, 1-3 mm, may be present
severe, death usually occurs despite
in abomasal mucosa. Autolytic changes may treatment. L monocytogenes is susceptible mask these lesions. Gran1-stained smerus
to penicillin (the dmg of choice), ceftiofur,
of abomasal contents reveal numerous
erythromycin, and trimetl1oprim/sulfonagram-positive, pleomorphic coccobacilli.

mide. High doses are required because
of the difficulty in achieving minin1w11
bactericidal concentrations in the brain.

Diagnosis: Sru11ples of lurnbosacral CSF

Penicillin G should be given at 44,000 U/kg
can be collected under local anesthesia. ln
body wt, IM, daily for 1-2 wk; the fust
cases of listeriosis, the CSF has an increased iajection should be accompanied by the protein concentration (0.6-2 g/L [normal
srune dose given IV. Suppo1tive therapy,

0.3 g/L]) and a mild pleocytosis composed
including fluids and electrolytes, is required
of lru·ge mononuclear cells.

for animals having difficulty eating and

Listeriosis is confinned only by isolation
drinking. High-dose dexan1ethasone
and identification of L monocytogenes.

( 1 mg/kg, IV) at first examination is

LYME BORRELIOSIS

659
considered beneficial by some but is concaution. Aborted fetuses and necropsy of troversial and will cause abo1tion during the septicemic animals present the greatest last two trimesters in cattle and after day
hazard. In cases with encephalitis,

135 in sheep.

L monocytogenes is usually confined to the

Results with vaccines have been
brain and presents little risk of transmission

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equivocal, which together with the sporadic
unless the brain is removed. People have
nature of the disease, lead to questions
developed fatal meningitis, septicemia, and
about the cost-benefit of vaccination. In
papular exanthema on the arms after
an outbreak, affected animals should be
handling aborted material. Pregnant
segregated. lf silage is being fed, use of the
animals (including women) should be
particular silage should be discontinued
protected from infection because of danger
on a trial basis. Spoiled silage should be
to the fetus, with possible abortion,
avoided. Com ensiled before being too
stillbi.Jth, and infection of neonates.

mature and grass silage containing additives Although hwnan listeriosis is rare (upper are likely to have a more acid pH, which
esti.Jnate of 12 cases per million population
discourages multiplication of L monocy
per yr), mortality can reach 500/o. Most cases
logenes.

involve older patients, pregnant women, or
imrnunocompromised people.

Zoonotic Risk: Whether animals serve as

L monocytogenes can be isolated from
a reservoir of infection for people may be
milk of mastitic, aborting, and apparently
questioned, because Lis leria organisms
healthy cows. Excretion in milk is usually
have been isolated from feces of a
intennittent but may persist for many
significant number of apparently healthy
months. Infected milk is a hazard, because
people as well as other animals. However,
the organism may survive certain forms of
despite this and the apparently low
pasteurization. Listeria also have been
invasiveness of L monocytogenes, all
isolated from milk of sheep, goats, and
suspected material should be handled with
women.

LYME BORRELIOSIS

(Lyme disease)

Lyme borreliosis is a bacterial, tick-transexperimental conditions. Tick vectors of mitted disease of animals ( dogs, horses,

B burgdorferi sensu Jato are hard-shelled
probably cats) and people. Many additional

Ixodes ticks. In the USA, these are primarily mammalian and avian species become

I scapularis in the northeast and Midwest
infected but do not develop overt clinical
and I paciji.cus on the Pacific coast. I signs. Areas of greatest incidence in the

1icinus and I persulcatus are the primary USA are regions in the northeast (particuvectors in Europe and Asia. B miyamoloi larly the New England states), the upper
is another member of the genus Borrelia.

Midwest, and the Pacific coast. Lyme

Although this spirochete is transmitted by
borreliosis also occurs in moderate climatic
ixodid ticks and may cause infections in
regions of Europe and Asia.

mammals characterized by clinical signs
such as fever, headache, fatigue, and muscle

Etiology and Transmission: On the
aches, the bacterium is a relapsing,
basis of DNA analysis, 19 different
fever-causing organism.

genospecies fall within the Borrelia
lxodid ticks hatch from eggs as unin
burgdorferi sensu Jato complex. Within this fected larvae. Both larvae and nymphs may complex, the most important spirochete
acquire spirochetes from Borrelia-carrying
species are B burgdorferi sensu stricto
hosts. Small mammals, especially rodents,

(North America, Europe), B afzelii
play a major role as reservoir hosts. Birds

(Europe, Asia), B bavariensis, and B
and lizards may also harbor certain Bon-elia
garinii (Europe, Asia), all of which are
species and serve as reservoir hosts.

pathogenic for people. Only B burgd01feri

Infection rates of the vectors vary according
sensu stricto has been shown so far to be
to region and season and can be as high as
pathogenic for domestic animals under

500/o in adult ticks. After tick attachment,

660

LYME BORRELIOSIS

>24 hr elapse before the firstB burgdo1:feri
reacting samples are rechecked with
sensu Jato organisms are transmitted into
specific confinnatory tests. Western blot
the host's skin. Stable infection of the host
or LIA testing helps to differentiate tlle
occurs at >53 hr into the blood meal.

in1mune response elicited by infection

Therefore, early removal of attached ticks
from that induced by vaccination.

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reduces the potential for spirochete

Alternatively, blood or senun samples
transmission. B burgdorferi sensu Jato
can be tested with peptide-based assays
organisms are not transmitted by insects,

(C6 peptide), which is specific for infectionbody fluids (urine, saliva, semen), or bite induced antibodies. However, demonstration
wow1ds. Experimental studies have shown
of specific antibodies indicates exposure to
that dams infected before gestation may
bacte1ial antigen only and does not equate to
transmit spirochetes to their pups in utero.

clinical disease. Approximately 5%-100,6 of
dogs in central Europe carry Borrelia-specific

Clinical Findings: Nwnerous clinical
antibodies witl1 no clinical signs. Additionally,
syndromes have been attributed to Lyme
false-negative results can occur with the
borreliosis in domestic animals, including

C6 peptide assays shortly after infection.

limb and joint disease and renal, neurologic,

Long incubation periods, persistence of
and cardiac abnormalities. In dogs,
antibodies for months to years, and the
intermittent, recurrent lameness; fever;
disassociation of the antibody response from
anorexia; lethargy; and lymphadenopathy
the clinical stage of disease make diagnosis
with or without swollen, painful joints are
by blood testing alone impossible.

the most common clinical signs. The second

Lymphocyte stimulation tests are
most common syndrome associated with
available that measure the cellular inunune

Lyme borreliosis is renal failure, which is
response to Borrelia. In culture, Borrelia generally fatal. It is characterized by uremia,
antigens are processed by antigen-presenthyperphosphatemia, and severe proteining cells with which specific lyn1phocytes losing nephropathy, often accompanied by
interact. Released cytokines (eg, interleuperipheral edema. Bernese Mountain Dogs kin-! beta) in the culture supernatant are
and Labrador Retrievers in particular often
correlates for preceding B01Telia infections show high Borrelia-specific antibody levels; of the host. Scant inforn1ation is available in
inlmune complexes in kidney tissues lead to
terms of the test's sensitivity and specificity.

severe inflammation. In hwnan medicine,

Isolation of B burgdo1feri sensu Jato
single case reports have described abnormalby culture or detection of specific DNA ities with bradycardia with the cardiac fom,
by PCR from joints, skin tissue samples, or
of Lyme borreliosis, whereas facial paralysis
other sources may also help in diagnosis.

and seizure disorders are thought to be

However, direct detection of the organism
expressions of the neurologic form.

is difficult, time conswning ( up to 6 wk for
culture), and in most cases produces

Diagnosis: Diagnosis is based on history,
negative results. Only a positive result is
clinical signs, elinlination of other diagnomeaningful. Blood samples are generally ses, laboratory data, epidemiologic
negative, because the organism resides in
considerations, and response to antibiotic
tissue and not in the circulation.

therapy. Autoimmune panels, CBC, blood

Clinical signs of Lyme borreliosis are
chemistry, radiographs, and other laboratory nonspecific. In addition to other orthopedic data are generally nonnal, except for results
disorders ( eg, trawna, osteochondritis
pertaining directly to the affected system
dissecans, inlmune-mediated diseases),

( eg, soft-tissue swelling in limbs, neutrophil
other infections should be considered.

accun1ulation in synovial fluids of affected

Anaplasma phagocytophilum can also
joints, uremia in renal disease).

induce intermittent, recurrent lan1eness.

Serologic testing for antibodies specific

A phagocytophilum is transmitted by the
for B burgdorferi sensu Jato is an adjunct
same tick genus, and epidemiologic studies
to clinical diagnosis. Antibodies can be
have revealed that up to 30% of all dogs in
detected with ELISA (including rapid test
central Europe carry antibodies specific
systems), Western blots, line inmmnoassays
for tllis agent. Mixed infections should be

(LIA), and with fluorescent bead-based
considered when clinical signs are apparent.

multiplex assays. Because of their low
specificity, indirect in1munofluorescent

Treatment: Antibiotic therapy is indicated
antibody assays are no longer recomin all cases with clinical signs attributed to mended. The standard procedure for

Lyme borreliosis. Antinticrobials in tlle
antibody detection is a two-tiered approach
tetracycline ( eg, doxycycline 10 mg/kg, PO,
in which san1ples are screened with a
bid) and penicillin ( eg, an10xicillin 20 mg/kg,
sensitive ELISA, and only positively

PO, tid) groups are effective, and rapid

MELIOIDOSIS

661
response is seen in limb and joint disease in
strong antibody response predominately
most cases, although incomplete or transient to OspA (lysate vaccines) or only against resolution of signs occurs in a significant

OspA (recombinant vaccines). During the
number of affected animals. Doxycycline is
tick's blood meal, antibodies against OspA
preferred over penicillins, because mixed
bind to Borrelia organisms residing in the

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infections with other tickbome pathogens
tick. Bound antibodies prevent spirochete
are often found in animals with clinical signs. migration within the tick and consequently Clinical and research data indicate that

Borrelia transmission from ticks to hosts.

low-level infection in animals, including

Later, during the blood meal, B burgdor
people, may persist despite antibiotic
feri sensu lato organisms in the engorging
therapy. In dogs, standard antibiotic doses
tick stop producing OspA and begin
and treatment for 4 wk have been demonexpressing new proteins, OspC and others, strated to be effective. If clinical signs recur,
before transmission. Development of
the antibiotics mentioned above can be used
vaccines that contain multiple B burgdor
again, because persistent infection is not the
feri antigens that may contribute to
result of acquired antibiotic resistance.

enhanced protection is being pursued.

Prolonged antibiotic therapy (>4 wk) may

In endemic areas, dogs should be
be beneficial for animals with continuing
vaccinated before natural exposure to ticks
disease signs.

to attain the highest degree of protection.

Symptomatic therapy directed toward the

Dogs that have been exposed to ticks
affected organ system and clinicopathologic
should be tested serologically for estababnom1alities is also in1portant, especially in lished infection before vaccination.

renal disease. In limb and joint disease, the

Postinfection vaccination has little to no
use ofNSAIDs concurrent with antibiotic
therapeutic effect on established infections.

therapy may lead to confusion over the

1\vo doses of vaccine should be adminissource of clinical in1provement and make tered SC to dogs <!9-12 wk old at 3-wk
diagnosis based on therapeutic response
intervals, or according to label directions.

difficult.

Because antibody levels often drop quickly
after the initial two in1munizations,

Control and Prevention: Tick
additional booster vaccinations should be
avoidance plays an important role in disease administered twice within the next year, control. Although highly effective repellents preferably at 6-mo intervals (suggested and acaricides in collars, sprays, and
schedule: spring, fall, spring) with armual
spot-ons are available for use on dogs, lack
vaccinations thereafter.

of owner compliance in application may
often be a barrier to effective, longtem1 tick
avoidance.

Zoonotic Risk: Lyme borreliosis is an

Killed, whole-cell bacterins to prevent
in1portant zoonotic disease. Aninlals and ·

Lyme borreliosis in dogs have been in use
people are infected during the blood meal of
since the early 1990s. Vaccines that contain hard-shelled ticks (Ixodes spp ). Companion only recombinant outer surface protein A
and fam1 animals are not the source of

(rOspA) have since been licensed for use
infection in people. Pets may bring
in dogs. Vaccines are available in Europe
unattached infected ticks into the housethat contain antigens from different hold and subsequently the vectors may be
species of the B burgdorferi sensu lato
passed on to other animals or people during
complex. All current vaccines induce a
close contact.

MELIOIDOSIS

(Pseudoglanders, Whitmore disease)

Melioidosis is a bacterial infection of

Etiology and Epidemiology: The
animals and people. It is often associated
etiologic agent is Burkholderia pseu
with suppurative or caseous lesions,
domallei, an oval, motile, gran1-negative,
comprising a mixed purulent and granufacultative anaerobic bacillus with bipolar lomatous response that can occupy any
staining. The organism is ubiquitous
body organ.

throughout southeast Asia, northern

662

MELIOIDOSIS

Australia, and the South Pacific. Its
other hospital or surgical equipment have
distribution is predominantly tropical and
been reported.

subtropical with "hyperendemicity" in the
top end of the No1them Territory of

Pathogenesis: The virulence of

Australia and northeast Thailand. The true

B pseudomallei appears to vary among

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boundaries of its endemicity are ambiguisolates, but these virulence factors are not ous because of movement of the organism
well understood. Molecular-typed clonal
and its ability to travel to and exist in
outbreaks have produced a range of
temperate regions (eg, southwest
different clinical presentations, which

Australia, France), where it may cause
indicate that host factors and infecting dose
sporadic disease and outbreaks.

may be just as important in detennining the

B pseudomallei has been introduced to
severity of disease. The incubation period
new environments with the export of
ranges from a few days to months or even
animals, and shipments of contaminated
years. B pseudomallei is a facultative
soil and water could potentially produce
intracellular pathogen that can remain
the same results. Reports of possible
donnant for many years before emerging
autochthonous melioidosis have also
as an active infection.

come from India, Pacific islands, Central
and South America, the Caribbean, Africa,

Clinical Findings: Signs can vary widely
and the Middle East.

within a species, depending on the site of

B pseudomallei is a widespread
infection, and range from acute to chronic.

saprophyte and has been isolated from

Fever, anorexia, or swollen glands may be
various soil types and surface water of
noted. Subclinical infection is common.

varying depths. Melioidosis outbreaks have

Infection may be associated with single or
coincided with heavy rainfall and flooding
multiple suppurative or caseous nodules/
associated with high humidity or temperaabscesses, which can be located in any ture. Major excavations and disturbances
organ tissue with vaiiable effects. Disease
in plumbing resulting in contamination of
most likely due to percutaneous inoculation
water supplies have also resulted in
often develops at distant sites without
outbreaks.

evidence of active infection at the inocula

Melioidosis is most commonly seen
tion site. The organs most conunonly
in sheep, goats, and pigs; other affected
affected include the lungs, spleen, liver,
species include cattle, buffalo, horses,
and associated lymph nodes.

mules, deer, camels, alpacas, dogs, c;,ts,

Goats often develop mastitis, and aortic
dolphins, wallabies, koala, primates, birds,
aneurysms have been reported. The
tropical fish, reptiles, and people. Laborarespiratory system is involved preferentially tory animals affected by melioidosis include
in sheep; signs ca.ti include fever, severe
hamsters, guinea pigs, rabbits, mice, and
coughing, respiratory distress, and
rats. Host susceptibility and disease
mucopurulent nasal and ocular dischai·ge.

manifestations vary between species. The

CNS disease, with signs that include
introduction of naive livestock to endemic
circling, incoordination, blindness,
regions may predispose them to disease, as
nystagmus, and spasms, has been seen in
seen with sheep, goats, pigs, and camelids.

cattle, horses, sheep, and goats. Pigs often

Other species ( eg, dogs and cats) may
have asymptomatic lesions on the spleen
succumb to infection due to inrnmnocomthat are incidental findings at slaughter.

promising conditions.

Lameness due to septic.arthritis and
osteomyelitis can occur. Fatalities often

Transmission: Wection is thought to
occur in association with acute fulminating
be opportunistic and prin1arily a result of
infections or when vital organs ai·e affected.

transmission from the environment ( eg,

Various forms of melioidosis have been
contanlinated soil and surface waters)

reported in horses; signs may include
rather than from animal to animal. The
weakness, edema and lymphangitis of the
most conunon routes of infection are via
lin1bs, mild colic, diarrhea, coughing, or
percutaneous inoculation, contanlination of
nasal discharge. Skin infections may
wounds, ingestion of soil or contanlinated
resemble fungal eczema initially, progresscarcasses, or inhalation. Transplacental ing to become papular. In dogs, disease may
infection resulting in abortion has been
be acute, subacute, or chronic. In acute
reported in goats. Transmission during
cases, septicemia with fever, severe
breeding and other means of host-to-host
diarrhea, and fulminant pneumonia are
transmission may occur. Laboratorycommon. Subacute cases may present as a acquired infection and iatrogenic infection
skin lesion with lymphangitis and lymphadvia contan1inated antiseptics, ir\jections, or enitis; untreated cases may progress to

NEOSPOROSIS

663
septicemia. Chronic disease can occur in

Treatment may be expensive, prolonged,
any organ with clinical signs that include
and possibly unsuccessful, with the risk of
anorexia, myalgia, edema of the limbs, and
recrudescence once treatment is disconskin abscesses.

tinued. The possibility of underlying

Lesions: Multiple abscesses that contain
immunosuppressive conditions should be

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thick, caseous greenish yellow to off-white
investigated in less susceptible species.

material a.re noted at necropsy. The organs

With severe disease, treatment regimens
most conunonly involved a.re the lungs,
can follow guidelines for hw11an melioidospleen, lymph nodes, liver, and subcutanesis with initial intensive therapy using the ous tissues. Exudative bronchopnernnonia,
newer 13-lactams (ceftazidime and the
consolidation, and abscesses may be found
ca.rbepenems), possibly in combination
in the lungs of anin1als with respirat01y
with cotrimoxazole for up to 2 mo. This
disease. Nodules and ulcers may be found
should be followed by subsequent
on the nasal mucosa and septunl and on
eradication therapy for a minin1wn of
the tmbinates; these may coalesce into

3 mo with high-dose cotrimoxazole or
in-egular plaques. Meningoencephalitis,
conventional combination therapy using
severe enteritis, supptu"ative polya.rthritis,
chloramphenicol, cotrimoxazole, and
and other syndromes also have been
doxycycline or amoxicillin/clavulanate.

reported.

Preventive measures a.re more practical
and economical in intensive farming
environments and involve raising tl1e

Diagnosis: T11e clinical signs of melioidosis animals off the soil, especially avoiding a.re not diagnostic because of the protean
exposing animals to muddy or water-inunnature of the disease. For a definitive dated regions and providing clean drinking
diagnosis, isolation and identification of the
water via chlorination and filtration.

organism a.re required. The organism can be Minimization of environmental contamiisolated from lesions and discharges. It is nation by diseased animals is also an
possible to culture the organism on routine
important control measure. There is no
diagnostic media; however, Ashdown's
effective vaccine.

media is prefen-ed because of a consistently
distinctive colony morphology and odor.

Zoonotic Risk: Melioidosis has zoonotic

Gram-stained smears of exudate or pus
potential. Infected a.ilinlals ca.i1 shed the
can sometimes identify bipolar "safety
organism in wound exudates and,
pin"-shaped, gran1-negative rods. Serologic
depending on tile site of infection, from
tests such as complement fixation and
other solll"ces, including nasal secretions,
indirect hemagglutination are effective
milk, feces, and urine. Mastitis in goats is a
herd surveillance tools. More recently, DNA
common manifestation, and B pse1.idomal
probes and PCR tests have been developed.

lei has been isolated from milk, resulting in the requirement for pasteurization of

Treatment and Prevention: Treatment commercial goats' milk in the tropics.

with the appropriate antibiotics should be

Infected aninlal ca.i·casses a.re condemned
based on culttu"e and sensitivity results.

at the abattoir.

NEOSPOROSIS

Neospora caninum is a microscopic
water buffalo, and ca.inelids, although they
protozoan parasite with worldwide
may be less susceptible than cattle.

distribution. Many domestic (eg, dogs,

A second Neospora species, N hughesi,
cattle, sheep, goats, water buffalo, horses,
is a cause of myelitis in horses and
chickens) and wild and captive animals
shares clinical features with equine

(eg, deer, rhinoceros, rodents, rabbits,
protozoa! myelitis, which in North and
coyotes, wolves, foxes) can be infected.

South America is usually caused by

Neosporosis is one of the most common

Sarcocystis neurona (seep 1309). The
causes of bovine abortion, especially in
life cycle of N hughesi is unknown.

intensively farmed cows. Neosporosis

Discussion in this chapter deals only
abortion also occurs in sheep, goats,
with N caninum infection.

664

NEOSPOROSIS

Epidemiology: Neosporosis in cattle
placentas) and deer and are presun1ed to
herds manifests in both endemic and
become infected by consuming raw meat
epidemic abortion patterns, but it is also
diets, barnyard chickens, and a variety of
possible for a herd to have a high infection
wild animals.

prevalence without a noticeable abo1tion

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problem. Both endemic and epidemic

Clinical Findings: Most neosporosis
transmission patterns in cattle are
abortions occur in mid to late gestation.

positively associated with the presence

Congenitally infected calves may be
and number of dogs in and around farms.

born weak or with neurologic deficits.

Endemic abortion is mainly associated

However, most congenital infections
with recrudescence of latent organisms
are subclinical.

during pregnancy followed by tra.nsplacen

In dogs, subclinical infection is the rule,
tal transmission to the fetus, although
although there are a greater variety of
occasional transmission from dogs or
exceptions. Litters or individual puppies
other canids may compound the problem.

may develop progressive hindlimb paresis

Epidemic abo1tion is a possible conseassociated with polyradiculoneuritis, quence of sudden large-scale transmission
myositis, and muscle atrophy. Adult
to pregnant cattle, presumably by ingestion dogs may have encephalomyelitis, focal of a mixed ration or water that has been
cutaneous nodules or ulcers, pneumonia,
contan1inated with infected canine feces.

peritonitis, hepatitis, or myocarditis with

The use of mixed rations in dairy herds
use of immunosuppressive drugs.

probably accounts for the greater
prevalence of neosporosis in dairy cattle

Diagnosis of Bovine Abortion:

than in extensively grazed beef cattle.

Because neosporosis is only one of many
causes of abortion, diagnostic efforts

Transmission: Dogs are definitive hosts
should focus on an array of possible
of N can in um and are capable of shedding causes. Aborted fetuses should be
oocysts in feces after eating tissues of
submitted to a veterinary diagnostic
infected animals. Gray wolves, coyotes,
laboratory, together with placenta and
and dingoes are also definitive hosts, and
a serwn san1ple from the aborting dam.

many other wild canids are suspected.

Examination of multiple fetuses increases

Neospora oocysts have an impervious
the odds of accurate diagnosis. If it is
shell that enables survival in soil and water impractical to submit an entire fetus, for prolonged periods after canine feces
as many of the following specimens as
have decomposed. Intermediate hosts
possible should be submitted to exclude
such as cattle become infected by
other causes of abortion: aseptically
ingesting oocysts. Cattle do not produce
collected and chilled lung, liver, spleen,
oocysts and thus do ilot transmit infections and abomasal fluid; an eyeball for nitrate horizontally to other cattle, but latent
testing; formalin-fixed spec:imens of brain
infection may endure permanently in their

(even if soft), lung, thymus, liver, kidney,
tissues and is transmitted to canids by
spleen, adrenal gland, skeletal muscle ( eg,
carnivorism.

tongue and diaphragm), and placental

In cattle, N caninum can be transmitted cotyledon; serum from the aborting dam;
transplacentally from an infected cow to
and thoracoabdominal fluid from the fetus
the developing fetus, an event that may
for serology.

occur in multiple pregnancies of the same

A diagnosis of neospoi"osis abortion
cow. Because most congenital infections
can be made with great confidence from the
are subclinical, congenitally infected heifer following constellation of findings: 1) lack of calves may be retained and added to the
other etiologic agents; 2) nonsuppurative
breeding herd and, in turn, may pass
inflan1mation in multiple fetal organs,
infections transplacentally to their own
especially including the brain, heart, and
offspring. This endogenous transplacental
skeletal muscle; 3) irnmunohistochemical or
transmission may enable transgenerational PCR detection of Neospora in fetal tissues; maintenance of the parasite even if the
and 4) Neospora seropositivity of the dam or herd does not have frequent transmission
fetus. However, such unequivocal findings
from dogs. Exogenous transplacental
are not always present. A lesion that is nearly
transmission may occur when a previously
specific for neosporosis abortion in cattle is
uninfected cow ingests Neospora oocysts
multifocal cerebral necrosis surrounded
during pregnancy and the fetus becomes
by nonsuppurative leukocytic reaction.

infected.

Confidence in the diagnosis increases with

Dogs have been shown to become
the strength of the Neospora antibody level infected by eating infected cattle (including
in the aborting dam, with high seropositive

NEOSPOROSIS

665
reactions at the time of abortion having

Treatment: There is no approved treatgreater predictive value than low seroposiment for neosporosis in cattle. Clinical tive reactions. Neosporosis is generally
neosporosis in dogs is treated with prolonged
excluded in seronegative darns.

administration of clindamycin or potentiated

Toxoplasmosis is a more common cause
sulfa drugs. The prognosis is negatively

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of abo1tion in sheep and goats and has
associated with the severity of presenting
lesions similar to those of neosporosis, but
clinical signs and with delayed treatment.

toxoplasmosis abortion in cattle is rare or

The prognosis is poor in puppies if disease
nonexistent.

has progressed to hi.ndlimb paresis with

Serologic testing of multiple cows or
atrophied, rigid limbs.

heifers can be used as an alternative or
complementary method to determine

Control: Currently, there are no available
whether neosporosis is a major reproduc

Neospora vaccines for cattle or dogs.

tive problem in a herd. This strategy can

It is common for dairy and beef herds
be helpful when investigating herds with
to have at least a small percentage of
endemic abortion problems. Serum samples Neospora-infected cattle. Although should be collected from aborting dan1s and
reducing the risk of Neospora transmisfrom an equal number of matched sion is a useful goal, complete eradication
herdmates with normal gestation (generally
from a herd is usually impractical.

<!lO per group). Sera should be tested and

Contan1ination of feedstuffs used in
classified for Neospora antibodies. If most mixed rations by canine feces should be
cows in the aborting group are seropositive
avoided. Large dairies can consider
and few are seropositive in the normal
erecting dog-proof fences around the area
group, then .neosporosis should be
in which feedstuffs are stored outdoors,
suspected as a cause of abortion in the
and automatic gates can be installed to
herd; this may be confirmed by statistical
facilitate the daily traffic of heavy
comparison. If most aborting cattle are
machinery. Smaller dairy farms may be
seronegative, then neosporosis is unlikely
able to protect feedstuffs within tradito be a major problem.

tional buildings such as barns, grain bins,
and silos.

Diagnosis of Canine Neosporosis:

In addition to protecting feedstuffs,

Clinically affected dogs often have
herds with endemic neosporosis

Neospora antibody levels much higher
abortions may consider not retaining
than levels seen in subclinically infected
heifer calves born to seropositive cows,
individuals. Biopsy of clinically affected
thereby reducing the number of congenitissues demonstrates nonsuppurative intally infected replacement heifers that flammation and may reveal the presence
enter the breeding herd. If this technique
of protozoa! organisms, but irnrnunohistois used, seropositive dairy cows could be chemistry or PCR may be required to debred using beef semen. For seropositive tect the organisms or to differentiate them
cows with valuable genetics, the use of
from other protozoa.

embryo transfer to Neospora-seronegative

Dogs with symptomatic neosporosis
surrogates, a technique that blocks
usually do not shed oocysts in feces. The
endogenous transmission, can be
finding of Neospora in routine fecal floats is considered.

serendipitous, because dogs typically shed

Dead stock, offal from home slaughter,
oocysts for only a period of days or weeks
and placentas should be discarded in a
after ingesting tissue of an infected animal.

mariner that prevents ingestion by dogs

The tiny oocysts are round to slightly oval
to reduce the risk that dogs will become
and 10-11 microns in diameter; in compariinfected and shed Neospora oocysts on the son, Giardia cysts are oblong and
farm. Dogs seropositive for Neospora have
approximately 9 x 13 microns, and coccidia
reduced likelihood for future shedding
are 2-4 times the diameter of Neospora. A
of oocysts than do seronegative dogs;
smooth outer contour helps to differentiate
therefore, serologic testing of farm dogs

Neospora oocysts from pitted pollen grains
is seldom useful.

of similar size. The oocysts are nearly
identical to those of Hammondia

Zoonotic Risk: Despite its similarity to
heydorni, a closely related parasite that has Toxoplasma, Neospora infection has not
not been associated with systemic disease
been clearly associated with any hwnan
in dogs or with abortion in ruminants. PCR
disease. Laboratory workers should guard
may be necessary to distinguish between
against inoculation, which caused fetal
oocysts of N caninum and H heydomi.

lesions in parenterally inoculated primates.

666

NOCARDIOSIS

NOCARDIOSIS

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Nocardiosis is an opportunistic, noncontamolecular speciation. Thus, because of gious, pyogranulomatous to suppurative
the taxonomic transition of Nocardia
disease of domestic animals, wildlife, and
speciation, for purposes of this chapter, the
people.

remaining text will use the former Nocardia

Mastitis, pnew11onia, abscesses, and
spp (in reference to the old classification) or
cutaneous/subcutaneous lesions are the
molecular species detection of Nocardia (in
major clinical manifestations of nocardiosis
reference to the new taxonomy).

in livestock and companion animals.

To date, >90 valid species of Nocardia

Nocardia species are aerobic actinomyare recognized. Of these, >30 have been cetes that belong to the order Actinomydescribed as causes of opportunistic human cetales, which comprises a complex group
infections, and at least 30 as responsible for
of pathogens, including the generaRhodo
animal diseases. Recent use of molecular
coccus, Mycobacterium, and Corynebacte
techniques has led to large taxonomic
rium, which are related to severe infectious changes in the Nocardia classification, and diseases and usually refractory to convennew species continue to be described.

tional therapy.

Epidemiology: Nocardia spp are

Etiology: Nocardia is a pleomorphic, ubiquitous organisms, a component of
gram-positive, facultative intracellular
normal soil microflora; they are commonly
bacteriWll, nonmotile and non-spore-formfoWld in soil, organic material, freshwater ing. In Gram smears, it appears as rods,
and saltwater, dust, compost vegetation,
cocci, or coccobacilli forms with characand other environmental sources.

teristic Jong or branching filaments and a

Nocardiosis is considered an uncommon
tendency to fragment into rods and cocci.

disease in animals and people. However,

When cultured, some species of Nocardia
reports of animal nocardiosis have
produce aerial filaments. Components of
increased worldwide.

the cell wall, particularly mycolic acids,

Infections in livestock and companion
render Nocardia spp partially acid-fast.

animals caused by Nocardia spp are

Pathogenic Nocardia spp are st1ictly
acquired by inhalation, traW11atic percutaaerobic, growing over a wide temperature neous introduction of the microorganism,
range (l0°-50°C [50°-122°Fl).

ingestion, or by the intramanllllary route.

In past decades, Nocardia species

The occurrence of disease and infective
identification has been traditionally based

Nocardia spp may vary geographically,
on phenotypic methods, including
influenced by animal ma.11agement
hydrolysis of different substrates ( casein,
strategies as well as environmental factors,
xanthine, hypoxanthine, and tyrosine),
such as dry, dusty, or windy conditions.

carbohydrate assin1ilation (glucose,

Nocardia spp is considered an agent of
glycerol, galactose, glucosamine, inositol,
mastitis of environmental origin in cattle
adonitol, and trehalose ), and antin1icrobial
and small rW11inants. Nocardial mastitis
susceptibility profile. Based on this former
usually affects herds witll a history of
classification, the most important pathoinadequate milking management and/or genic species for animals and people were
poor hygiene conditions before and after
represented by tile Nocardia asteroides
milking. Man1mary infections are predomicomplex (N asteroides, N nova, N
nantly caused by soil contanlination of teat
farcinica), N brasiliensis, N pseudobrasil
dips, udders, and milking equipment during
iensis, N otitidiscaviarum, and N transva
washing procedures and by intran1arnrnary
lensis. However, diagnosis based
infusion therapy. Dairy herds affected by
exclusively on phenotypic assays leads
nocardial mastitis also have a history of
to misidentification or is insufficient to
inadequate concentrations of antiseptics in
distinguish some species of Nocardia. More teat dips. Outbreaks of nocardial mastitis recently, studies in domestic animals and
have been reported associated witll dry-cow
people have revealed that speciation of
tllerapy ( eg, neomycin) or improper

Nocardia requires confirmation by
intramammary therapy.

molecular methods. However, most of tile

In companion animals, disease transliterature about nocardiosis in animals and mission is related to the inoculation of
people was published before this new
organisms tllrough pW1cture woW1ds

NOCARDIOSIS

667
or foreign bodies, or secondary to bites,
of domestic ruminants. More recently,
wounds, or scratches after cat fights. Canine based on 16S rRNA sequencing, N nova and infections have rarely been related to

N farcinica were the most frequent species
inhalation of the bactelium. The occurrence
detected in 80 different cases of bovine
of nocardiosis in dogs and cats is intimately
mastitis in Brazil and, unexpectedly,

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associated with underlying immunosup

N puris, N veterana, N cyriacigeorgica,
pressive disorders, particularly dogs

N arthril'idis, and N africana were infected by distemper virus and cats
identified as well.

affected by leukemia or in1n1 unodeficiency

Nocardial mastitis is generally charactervirus. Canine nocardiosis occurs at any age ized by a history of chronic evolution and is
group and in both sexes, although it appears
usually refractory to antimicrobial therapy.

to affect mainly males, particularly between

Classically, clinical cases of mammary
l -2yr old.

nocardiosis were predominantly seen in one

Nocardiosis in horses is recognized as
or two animals in the herd, duling lactation
an opportunistic infection and is usually
or the dry peliod. Clinical examination of
related to inlffiune disorders. In most
the udder shows enlargement, edema,
reported cases of equine clinical nocardiofibrosis, either diffuse or multifocal nodules, sis, there were underlying in1n1unosuppresand occasionally draining tracts. Strip cup sive problems, particularly pituitary pars
testing reveals serous to purulent milk
intermedia dysfunction (seep 54 7) or severe secretion, showing white to yellow particles combined immw10deficiency in Arabian

("sulfur granules"). Infected cows have high foals (seep 818).

somatic cell counts. Less frequently, the
organism may disseminate from the

Pathogenesis: Pathogenicity of
man1n1ary gland to other organs, causing

Nocardia in domestic anin1als is attributed regional lymphadenitis and pyogranulomato the virulence of the st.rain, the structure tous lesions.

of the bacterial cell wall, host susceptibility,

Bovine Farcy: This particular manifestaroute of transmission, coinfection with tion of bovine nocardiosis is usually limited
inlffiunosuppressive diseases, and
to the tropics. Bovine farcy is caused by
development of pyogranulomatous lesions.

former N farcinica. Occasionally,

However, the outcome of Nocardia

Mycobacteriumfa1-cinogenes and
infections is intimately linked to the ability

M senegalense are also identified in similar of the st.rain to resist the initial neut.rophil
lesions. Bovine farcy is an uncommon cause
and activated macrophage attack and the
of chronic lymphangitis, lymphadenitis, and
cell-mediated inlffiune response.

cutaneous nodules. Initially, the lesions

Immune response against nocardial
consist of cutaneous nodules, particularly
infections is plimalily cell-mediated. These
in the leg and neck regions. These nodules
intracellular organisms are able to inhibit
may slowly enlarge and coalesce to lesions
phagosome-lysosome fusion in neut.rophils
of up to 10 cm in dian1eter, which rarely
and macrophages because of the presence
ulcerate. The lymphatic vessels appear
of mycolic acids in their bacterial cell wall.

cord-like.

Nocardia is also resistant to acids,
oxidative enzymes ( ca.ta.lase and superoxide

Horses: Noca.rdiosis is an uncommon
dismutase ), and other enzymatic mechadisease in horses. Most nocardial infections nisms of phagocytic cells. In addition, some
in horses were described involving former
toxins have been identified inNocardia spp

N asteroides and occasionally N brasilien
that appear to contribute to the vi..tulence of
sis. More recently, based on molecular
pathogenic st.rains.

assays, N nova was desclibed causing

Nocardia does not induce an effective
recurrent airway obstruction in a horse.

hwnoral in1mune response mediated by the

Severe pnewnonia, pleuritis, disseminated
action ofB lymphocytes.

(systemic) abscesses in organs, cutaneous
lesions, mycetomas, and rarely, abortion

Clinical Findings: Mastitis, cutaneous/
represent the main clinical signs of equine
subcutaneous lesions, abscesses in organs,
noca.rdiosis.

and pnewnonia are the most con1n1on

Systemic nocardiosis occw-s by
clinical signs of noca.rdiosis in livestock
hematogenous dissemination of bacteria
and companion animals.

causing abscesses in various organs.

Pulmonary nocardiosis is charactelized by

Mastitis in Ruminants: Former
increased respiratory rate, cough, labored

N asteroides, N nova, N otitidiscavimum,
breathing, and nasal secretion. Cutaneous
and N farcinica are the most con1n1on
and subcutaneous lesions are generally
species desclibed in man1n1ary nocardiosis
secondary to t.rawnatic introduction of

668

NOCARDIOSIS

Nocardia into the skin, leading to pyoder

Jar and mesenteric lymphadenitis was
matitis, cellulitis, and cutaneous nodules
reported in pigs. Nocardiosis in wildlife and
located anywhere in the body. The lesions
fishes generally causes organ abscesses and
may ulcerate and have an odorless, gray to
pneun1onia.

white discharge. Mycetomas are another

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type of cutaneous infection and consist of
chronic and progressive skin lesions caused

Diagnosis: Routine diagnosis is based on
after transcutaneous inoculation of
epidemiologic findings, clinical signs, and

Nocardia spp. Painless nodules, purulent to microbiologic exanlination. Samples of necrotic, commonly form, usually limited to
abscesses, skin, tracheobronchial lavage
the site of injury, and occasionally show
fluid, milk, aspirates, organs, or other
purulent discharge through the sinus tract.

tissues should be cultured on sheep blood

Abortion rarely occurs in mares. Two
and/or Sabouraud agar and incubated
cases were reported in Arabian and
aerobically for 2-7 days at 37°C and 25°C

Thoroughbred mares at -6 mo of gestation,

[98.6°F and 77°FJ, respectively. However,
both with histocy of failure to maintain
growth of some Nocardia spp in culture
gestation to term. Fetal necropsies showed
media is slow, and incubation should be
lesions in lung and liver. N asteroides was extended for at least 2 wk. Colonies are
cultured from the uterus of the Arabian
circular, convex, smooth or rough, finnly
mare.

adherent to agar surface, odorless, with
various carotenoid-like pigments ( cream,

Companion Animals: In dogs and cats,
former N asteroides, N brasiliensis,
white, orange, pink, or red), and present

N otitidiscaviarum,
aerial hyphae and typical powdecy and dry
and N nova are the
surface, like fungal organisms. Because
most frequent species identified. Recently,

Nocardia
based on molecular methods, N africana,
spp are ubiquitous in the

N elegans,
environment, microbiologic isolation of a
and N tenerifensis were
small number of organisms from clinical
reported in cats, and N abscessus in a dog.

specimens must be evaluated together with

Superficial skin, ly:mphocutaneous, and
clinical signs and other diagnostic methods.

thoracic infections, as well as disseminated

Microscopically, gram-positive, typically
forms, are the major clinical pictures of
nocardiosis in dogs and cats. Cutaneous/
filamentous organisms are seen, with a
subcutaneous abscesses with fistulous
tendency to fragmentation. Modified

Ziehl-N eelsen stain shows partially acid-fast
tracts, ulcers, mycetomas, and regional
organisms. Fine-needle aspiration has been
lyrnphadenitis are frequent clinical
used in the diagnosis of skin nocardiosis in
manifestations of the disease, associated
companion animals. Gram, Giemsa, and
with local skin or lyrnphocutaneous lesions
panoptic stains show filamentous organin cats and resembling human nocardiosis.

isms in aspirated specimens. The leukogram

Skin lesions are seen mainly in the
reveals mainly leukocytosis with neutroextremities, flank, nose, and neck areas.

philia and monocytosis, whereas the

Canine and feline pulmonary nocardiosis
are characterized by mucopurnlent
ecythrogram shows moderate anemia.

Radiographic images of dogs with
oculonasal discharge, anorexia, hype1therpulmonary nocardiosis show diffuse mia, weight loss, cough, dyspnea, and
inflammation, nodules, abscesses, and lobar
hemoptysis. Other systemic or disseminated
forms of the disease in companion animals
consolidation. Differential diagnoses in
domestic animals include infections with
are represented by the presence of

Actinomyces
abscesses or lesions in two or more sites,
or Streptomyces spp because
of the similarities in microbiologic
including liver, kidneys, spleen, eyes, bones,
appearance and clinical signs. Face and jaw
joints, and abdominal lymph nodes, as well
as development of pe1itonitis, pleuritis,
enlargement in cattle and horses caused by
oral nocardiosis should be differentiated
and pyothorax. GI infection can lead to
fromActinomyces bovis (actinomycosis,
gingivitis, halitosis, and ulceration of the
seep 590), Actinobacillus lignieresii
oral cavity. Rarely, the organism affects the

(actinobacillosis, seep 589), and Staphylo
urinary tract and heart. Nocardial infection
coccus aureus
in the CNS is associated with seizures,

(botcyomycosis).

Postmortem examination of internal
alertness, and deficits in proprioception.

organs and tissues reveals abscesses and/or

Miscellaneous: Bovine or equine oral
numerous small to large nodules, discrete to
infection secondary to ingestion of fibrous
coalescing, of white to gray color. Histologic
foods can lead to development of pyogranufindings of nocardiosis are characterized by lomatous lesions in the jaw. Abortion may
pyogranulomatous to suppurative lesions
also occur in sows and cows. Submandibu-
with areas of necrosis. The lesions or

NOCARDIOSIS

669
nodules show a suppurative, necrotic

Long-term therapy ( 1-6 mo in domestic
center containing filamentous organisms
anin1als and 6-12 mo in people) is required
surrounded by macrophages, lymphocytes,
because of clinical relapses after short-tern1
and plasma cells. Occasionally, epithelioid
protocols. In companion animals, surgical
and multinucleated giant cells are found.

procedures ( debridement, drainage,

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Histolopathology sometin1es reveals small,
extirpation of foreign bodies, and washing
soft granules in discharges of lesions,
of lesions with antiseptic solutions) are
formed by microcolonies of the organism.

indicated in cutaneous/subcutaneous

Lymph nodes are enlarged.

lesions and osteomyelitis. However,

Different serologic (immunodifusion,
antin'licrobial therapy is successful in only
complement fixation, and ELISA) and

30%--500,i, of cases of mastitis in cattle and
cutaneous hypersensitivity tests have been
goats, as well as in pulmonary or extrapulproposed to diagnose nocardiosis in monary ( disseminated or systemic)

animals. However, host animals commonly
infections in companion animals and
develop a nonspecific antibody response
horses. The mortality of animal nocardiosis
against Nocardia, limiting the use of
is attributed mainly to underlying condiserologic tests in routine diagnosis.

tions, delayed diagnosis, and in1proper

Currently, phenotypic diagnoses of
therapy.

Nocardia spp have been confinned using
molecular metl10ds, including PCR,
restriction endonuclease analysis of

Control and Prevention: There are no
amplified 65--kDa heat shock protein gene
specific or effective measures to control

(hsp65), 16S rRNA gene sequence, essential
animal and human nocardiosis, probably
secretory protein A ( secAl ), gyrase B
because of the wide distlibution of the

(gyrB), and DNA-DNA hybridization. These
microorganism in the environment.

molecular techniques offer a timesaving and

In companion animals, immunosuppresreliable means of speciation and have led to sive pathogens or debilitating conditions
a number of taxonomic changes and the
should be investigated as predisposing
identification of new species of Nocardia.

factors to development of nocardiosis.

Control and prevention of nocardial
mastitis is based on measures recom

Treatment: Animal and human nocardiomended for environmental agents. Thus, sis is usually refractory to conventional
the best measures to control and/or
therapy because of the intracellular location prevent nocardial mastitis remain the early of the bacterium, development of pyogranumicrobiologic diagnosis of mastitis, proper lomatous lesions, and antimicrobial
hygiene conditions, cleaning the environresistance patterns.

ment during milking, correct antiseptic

The antimicrobial susceptibility profile
concentrations in post- and mainly iu
varies dramatically between Nocardia
pre-dipping solutions, high-q_uality water to
spp and geographic areas. The National
wash the animals and milking equipment,

Conunittee for Clinical Laboratory
removal of organic material from the

Standards approved an in vitro standardized milking area, and appropriate intramamsusceptibility test for Nocardia by broth mary therapy procedures. Because of poor
microdilution. The modified disc diffusion
success rates in treatment of manimary
method has been used as well.

infections, segregation of infected anin1als,

Trirnethoprim-sulfonamides, arninoglychemical drying of affected quarters, or cosides (an1ikacin, gentamicin), linezolid,
culling of animals are also recommended
amoxicillin-clavulanate, imipenem, and
in control of nocardial mastitis in dairy
some cephalosporins ( cefotaxime, ceftriaherds.

xone) are considered drugs of choice for
nocardiosis therapy in animals and people.

Public Health Considerations: Human

Ampicillin, clarithromycin, doxycycline,
nocardiosis is an opportunistic disease. In
erythromycin, and minocycline are descsome countries, the clinical impact of nocar

Iibed as treatment alternatives for animals.

diosis is fragn1entary, indicating that

Combined therapy using an'likacin with
diagnosis of disease may be neglected or
sulfonamides, and amikacin with imipenem
underestimated. Curiously, reports of
or cephalosporins ( cefotaxime, ceftriaxhuman nocardiosis have recently increased one) also have been proposed. lntramamall over the world. Although the disease mary infusions of trin1ethoplim-sulfontypically occurs in immunocompromised amides, cephalosporins or arninoglycosides
patients, nocardiosis has been described in

(gentamicin) have been used for 5-7 days to i.nununocompetent people as well. Former treat clinical mastitis in cattle and goats.

N asteroides complex is the main species

670

NOCARDIOSIS
described in human nocardiosis. Currently,
people. Cases of cutaneous/subcutaneous
based on molecular methodologies and
nocardiosis have been reported in some
rearranged taxonomy, N cyriacigeorgica,
patients, secondary to bites or scratches

N brasiliensis, N asteroides, N nova,
of clinically ill dogs and cats. However,

N farcinica, N transvalensis, N pseudobra
human nocardiosis is apparently not

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siliensis, and N otitidiscaviarum have most directly transmitted person-to-person or frequently been detected in human patients.

by nosocomial infections. Interestingly,

Pneumonia, cutaneous-subcutaneous
studies have shown great similarity
lesions, mycetoma, and neurologic
between Nocardia spp involved in human
manifestations are the most common
and animal infections. Experimental
clinical signs. However, clinical cases of
studies regarding temperature resistance
human nocardiosis are intimately associusing former N asteroides and N
ated with inununosuppressive or debilitat
brasiliensis isolated from bovine milk
ing disorders, such as AIDS, organ transand submitted to time/temperature plants, cirrhosis, diabetes, alcoholism,
conditions used in usual pasteurization
rheumatic and malignancy diseases
procedures indicated a potential risk of

(lymphosarcoma, lymphoma), or prolonged

Nocardia transmission by milk.

use of corticosteroids.

Precautions should be taken an10ng

The environment is the natural
human patients who have immune
reservoir of Nocardia spp for human and
dysfunctions or debilitating diseases, with
animal infections. Most cases of transmisspecial reference to contact with soil or sion to people probably occur by
organic material from environments
inhalation of the organism in dry and
contaminated by domestic animals,
warm climate regions (aerosolization).

contamination of traumatic cutaneous

Trauma with skin inoculation is another
lesions, or close contact with animals
form of transmission of the bacterium to
suspected of having nocardiosis.

PERITONITIS

Peritonitis is an inflammation of the se_rous

Peritonitis occurs secondary to another
membranes of the peritoneal cavity. It may
disease as the result of exposure of the
be a primary diseas_e or secondary to other
peritoneal cavity to nonspecific infectious
pathologic conditions. Different infectious
or noninfectious agents. It is often acute and
and noninfectious agents may cause
frequently results in a progressive, systemic
peritonitis, which may result in a variety of
disease. Secondary septic peritonitis is
clinical manifestations, disease progression, commonly associated with perforation of and outcome. Peritonitis fnay be acute or
and leakage from GI organs ( eg, traumatic
chronic, septic or nonseptic, local or
reticuloperitonitis in cattle), with subsediffuse, or adhesive or exudative. The quent processes allowing transmural
term "tertiary peritonitis," used in human migration of bacteria ( eg, neoplasia,
medicine for particular cases of chronic
intestinal ischemia), or with perforation/
peritonitis with a small number of bacteria
rupture of or leakage from other infected
or fungi, is not used in veterinary medicine.

viscera ( eg, abscesses in liver, spleen,
omentun1, cystitis, endometritis, pyometra).

Etiology: Primary peritonitis is less

Furthermore, migration of parasites
common than secondary peritonitis
through the abdominal cavity may also
and may be infectious or idiopathic. In
result in leakage of chyme with subsequent
infectious primary peritonitis, infectious
septic peritonitis. Perforating wotmds of the
agents spread via the bloodstream into the
abdominal wall ( eg, dog bites) or dehisperitoneal cavity of animals that are often cence of abdominal wound closure may
inununocompromised. Such infectious
result in laceration of viscera and inoculaagents include feline corona.virus (FCoV), tion of foreign material and microorganisms
which causes feline infectious peritonitis
into the peritoneal cavity.

(FIP); Nocardia spp; Mycobacterium spp; Microorganisms associated with septic

Haemophilus parasuis; and other
peritonitis usually reflect the source of
infectious agents. Progression of primary
contan1ination. A mixed bacterial population
peritonitis tends to be chronic.

is seen in GI tract perforation, whereas

PERITONITIS

671
perforation of nongastrointestinal viscera
always aseptic. The originally aseptic

( eg, urinary or gall bladder, uterus, prostate)

peritoneal inflanm1ations may later become
or hematogeous infection of the peritoneal
septic. In addition, intraperitoneal adminiscavity may be more typically associated with tration of drugs or fluids may result in
aerobic organisms, includingEsclwichia
temporary inflanm1at01y reactions of the

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coli, Streptococcus equi zooepidemicus,
peritoneum. Because New World can1elids

Staphylococcus, Proteus, Rhodococcus,
show severe inflanmiatory reactions to

Klebsiella, Salmonella, Enterobacter,
infections withDicrocoelium de,itriticum,

Pseudomonas, or Corynebacte,ium.

peritonitis may develop subsequent to the

Secondary aseptic peritonitis occurs after
severe hepatitis. In large anin1als, peritonitis
contamination of the abdominal cavity with
is most commonly seen in cattle, less often in
chemical irritants ( eg, bile, urine, drugs) or
horses, and rarely diagnosed in pigs, sheep,
intestinal ischemia Common conditions are
and goats. It is a serious and often fatal
urolithiasis and rnpture of the Uii.nary or gall
condition in cats (FIP). For conunon causes
bladder; however, these conditions are not
of peritonitis in vaiious species, see TABLE 5.

l#H•il COMMON CAUSES OF PERITONITIS

Species

Cause

Cattle

Traumatic reticulope1itonitis; rnmenitis; abomasal ulcer (perforation); abomasal volvulus; cecal torsion; dystocia (uterine torsion, cesarean section); metritis or pyometra; abdominal surgery; intestinal, rectal, or uterine rnpture; liver or abdominal abscess rnpture; omphalitis ( calves); fat necrosis/pancreatitis; neoplasia (eg, mesothelioma, ileal adenocarcinoma); iatrogenic (eg, rectal perforation, liver biopsy, intraperitoneal i.Itjection, rw11enocentesis); green algae infection (rare); Setaria infection (rai·e) Horses

Parasitic (larval) migration; intestinal injUIY and ischemia ( colic); abdominal abscess rupture (Rhodococcus, Streptococcus); abdominal surgery (colic surgery, castration); gastric, intestinal, or uterine rupture; gastroduodenoenteritis, colitis; omphalitis, persistent urachus, or bladder rupture (foals); gastric ulcer (perforation); fat necrosis/pancreatitis; neoplasia ( eg, cholangiocellular carcinoma); penetrating trallllla to abdominal wall; iatrogenic ( rectal perforation, intraperitoneal injection) Small ruminants

Primary peritonitis (Mycoplasma spp ); parasitic (larval) migration ( eg, liver fluke, lungwom1, Seta1ia sp ); traumatic reticuloperitonitis (less common than in cattle); abdominal abscess rupture; neoplasia ( eg, mesothelioma, cholangiocellular carcinoma); iatrogenic ( eg, liver biopsy, intraperitoneal injection) New World canlelids Sequela of parasitic migration/acute hepatitis ( dicrocoeliosis of special importance); pe1forating third-compartment or duodenal ulcers; sequela of urolithiasis/ruptured urinary bladder; traumatic reticuloperitonitis (rare)

Pigs

Glasser's disease (Haemophilus parasuis); intestinal (ileal) perforation; dystocia; sequela of septicemic infections (Salmonella Choleraesuis, Streptococcus siiis ); polyserositis (Mycoplasma hyorhinis) Dogs and cats

Feline infectious peritonitis (FCoV); ingested intestinal foreign bodies; gastric, intestinal, rectal, bladder, or uterine rupture; abdominal or intestinal surgery; gastric and duodenal ulcers/
perforation; abdominal neoplasia ( eg, mesothelioma); hepatitis, gallbladder diseases/rupture; pancreatitis/fat necrosis; gastric dilatation volvulus (dog); penetrating trauma to abdominal wall; Candida albicans (rare); Neospora caninum (rare)

672

PERITONITIS

Pathogenesis: Inflammation of the

Clinical Findings: Clinical signs vaiy
peritonewn is the result of a vaiiety of
depending on the type and etiology of
possible pathogenetic pathways that
peritonitis. Affected animals may develop
are species-dependent ( eg, peritoneal
toxemia and septicemia, shock, hemorinflammatory response in cattle is rhage, abdominal pain, paralytic ileus, fluid

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characterized by extensive fibrin fonnation,
accwnulation, and adhesions in varying
horses tend to develop exudative peritonidegrees. However, there are reports of tis) and mainly influenced by etiology ( eg,
apparently clinically healthy animals having
primaiy or secondaiy, septic or nonseptic ).

chronic bacterial peritonitis.

Because of the release of inflammato1y

Shock, hypotension, acid-base disturmediators after contact with mechanical, bances, and circulatory collapse after acute
chemical, or infectious agents, serosal
septic peritonitis associated with rupture of
capillaiy permeability is increased and
intestines or utems often lead to sudden
results in leakage of plasma proteins,
death. These animals normally show only
solutes, and water into the peritoneal cavity.

limited clinical signs of peritonitis. In less

Exudation of protein-rich fluid may result in
severe cases, abdominal pain and fever are
hypoproteinemia and facilitates bacte1ial
common. Hypothem1ia can also be seen as
proliferation. The combined effect of large
a result of dehydration, hypovolemia, and
fluid losses into the peritoneal cavity and
sepsis. Abdominal pain may be permanent
vasodilatory effects of absorbed toxins may
and severe, characterized by guarding the
produce profound hypotension and
abdomen, stiff gait, or recwnbency. In all
hypovolemia. The inflan1IT1ation may
species, pain responses are most evident
decrease the animal's antioxidative capacity in the early stages. Abdominal distention, and result in oxidative stress.

which may be inapparent, usually is due

Rupture or perforation of the forestomto accwnulation of peritoneal exudates, ach, stomach, or intestine with spillage of
paralytic ileus, or peritoneal adhesions.

large vohunes of gastric or intestinal

Fecal output is often decreased, although
contents and rupture or perforation of the
frequency of defecation may be increased in
contaminated uterus leads to an acute
tl1e early stages of peritonitis. Animals with
septic peritonitis. Toxins produced by
secondaiy pe1itonitis may also show clinical
bacteria and tissue breakdown are readily
signs associated with the primaiy disease.

absorbed through the peritoneum and have

Rectal palpation is a useful diagnostic
severe systemic effects leading to hypotechnique to evaluate the peritoneum and tension, shock, systemic inflammatory
accessible abdominal organs in large
response syndrome (SIRS), and dissemianimals; however, local peritonitic nated intravascular coagulation (DIC).

processes in the cranial abdomen ( eg,

Endotoxins and acid-base and electrolyte
trawnatic reticuloperitonitis in cattle)

disturbances directly affect cardiac
do not result in clinical signs that can be
function, leading to reduced cardiac output
diagnosed by rectal exan1ination. Abdomiand circulatory failure. Paralytic ileus is nal radiography may be used in small
considered to be a frequent result of acute
animals. In horses and cattle, radiography
peritonitis, causing functional.obstruction
can be also used as a diagnostic tool, but
and an increased mortality rate. Large
high-power x-ray macl1ines are required;
volwnes of inflan1rnatory exudates may be
therefore, this technique is limited to
secreted into the peritoneal cavity during
stationaiy units in vete1inaiy clinics.

peritonitis and may lead to impaired

Generally, ultrasonography is the most
respiration by impinging on the diaphragm.

valuable diagnostic tool to exan1ine the

Spillage of small an10unts of gastric or
abdominal cavity and assess the extent,
intestinal content ( eg, after transcutaneous
localization, and character of peritonitis.

run1enocentesis, bar suture techniques for

Additionally, ultrasonography allows a
left displaced abomaswn surgery) nom1ally
guided abdominocentesis, which can be
result in local peritonitis.

used (in both large and small anin1als) to

Chronic peritonitis is often characterized
obtain fluid for cytologic and biochemical
by extensive secretion of fibrinogen and
exainination and bacte1iologic culture.

subsequent formation of fib1inous/fibrous

Diagnostic peritoneal lavage can be used
adhesions. Such adhesions help localize
if peritoneal fluid caJU1ot be obtained by
the inflainmatory process ( eg, trawnatic
abclominocentesis. Diagnostic laparoscopy
reticuloperitonitis in cattle, type 3 abomasal
or laparotomy can be considered to verify
ulcers in cattle) but may cause mechanical
the diagnosis. Diagnostic laparotomy is
or functional obstruction of the GI tract.

frequently used in cattle because it is

Chronic peritonitis in horses often results
inexpensive, can be performed in standing
in recurrent colic episodes.

position, and is associated with few or

PERITONITIS

673
minor complications; it also makes
palpation may be painful, and abdominal
additional diagnostic procedures unnecesmasses may be detected. Icterus may be sary and can often be combined with
present in generalized biliary peritonitis in
therapeutic measures.

small animals. Abdominal radiographs may

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Cattle: Clinical signs of peritonitis in
reveal GI obstruction, bowel dilatation, free
cattle are often nonspecific and characterabdominal air, ascites, or radiodense foreign ized by reduced feed intake, drop in milk
matelial. Loss of serosal details in radioproduction, and decreased rumination graphs indicates abdominal fluid.

activity. In chronic cases, rurninal con

Diagnosis: Laboratory analyses are
tractions may be present but reduced in
helpful to confirm the clinical diagnosis and
intensity. Abdominal percussion may reveal
determine the severity of peritonitis, and
rurninal tympany or pneumoperitoneum.

should include a CBC and several biochemi

Moderate fever is typical during the first
cal paran1eters in blood and peritoneal fluid.

24-36 hr in cattle with acute, local

Acute, diffuse pe1itonitis with toxemia
peritonitis. High fever suggests acute,
is usually accompanied by leukopenia,
diffuse peritonitis. Cattle with peritonitis
neutropenia, and a marked increase in
often have a shuffling, cautious gait with a
immature neutrophils ( degenerative left
rigid arched back, and grunt when walking
shift). In less severe acute peritonitis,
or passing urine or feces. Deep palpation of
leukocytosis may occur as a result of
the abdominal wall and pain provocation
increased neutrophil production. Acute,
tests result in pain response. Chronic
localized peritonitis may reveal a nonnal
peritonitis is associated with develop-

WBC count with a regenerative left shift. The
ment of fibrous adhesions. Depending on
total WBC count in chronic peritonitis may
localization, rectal palpation may reveal
be normal, with an occasional increase in
adhesions between intestinal loops and
lymphocytes and monocytes. Anemia may
peritoneum. Cattle may suffer from chronic
occur due to hemorrhage into the peritoneal
indigestion (Hoflund syndrome, abomasal
cavity but is also commonly associated with
impaction) or toxemia, with periods of
chronic inflan1matory processes. A nw11ber
acute, severe illness caused by partial
of abnonnalities of serum biochemical
intestinal obstruction. The majolity of cattle
parameters ( eg, total protein, albumin,
develop a localized pelitonitis by extensive
fibrinogen, bilirubin, LDH, alkaline phosfibrin formation; however, in a few cases the phatase, CK) may accompany peritonitis.

abdominal cavity contains large volumes of

Hypoalbunlinemia, hyperglobulinemia, and
turbid, infected peritoneal fluid.

hyperbilirubinemia are frequently present.

Small Ruminants, New World Camelids,

Generally, the changes in hematologic and
and Pigs: Generally, the clinical signs in
biochemical parameters indicate inflan1masmall ruminants, New World camelids, and tory processes and tissue damage, but they
pigs are similar to those in other animals.

are not pathognomonic for peritonitis.

However, peritonitis is rarely diagnosed .

The peritoneal fluid is a plasma dialysate
clinically in pigs, sheep, or goats, although 1t
witl1 specific physical and chemical
is not an uncommon finding on routine meat
properties that depend on membrane
inspection after slaughter of pigs. It is more
permeability, concentrations and electrical
common in llamas and alpacas.

charges of ions, and osmotic pressure. The
fluid contains cells deriving from the

Horses: Clinical signs include colic,
distended intestines on rectal examination,
mesothelium and the blood or Jyn1phatic
gastric reflux, and occasionally diarrhea.

vessels. Under physiologic conditions,

Rectal palpation may reveal tacky, dry
peritoneal fluid is a tJ.·ansudate, whereas
mucosa and in some cases fibrinous or
pelitonitis results in a fluid that is typically
fibrous adhesions between intestinal loops
characterized as an exudate. Analysis of
and other abdominal organs. Intestinal
peritoneal fluid is a useful diagnostic
peristaltic sounds are reduced. Tachycardia, method in gastroenterology, because tl1e fluid generally reflects abdominal condiweak pulses, poor pelipheral perfusion, and fever are common. Weight loss and
tions. The volume of peritoneal fluid is
intermittent abdominal pain (colic) may be
frequently increased in peritonitis. In cases
seen in horses with chronic peritonitis.

of septic peritonitis, samples of peritoneal
fluid should be exanlined microbiologically

Dogs and Cats: In small animals,
to characterize infectious pathogens.

anorexia and depression are nonspecific

The parameters of the classic transudatesigns of peritonitis, often accompanied by exudate categorization system are shown in
vomiting and decreased defecation. The

TABLE 6. A peritoneal fluid showing properabdomen may be distended. Abdominal ties of both a transudate and an exudate is

674

PERITONITIS
conunonly called a modified transudate. Use
fluid and serum is lower than 1:2. The SAAG
of a scoring system allows further classificais calculated by subtracting the peritoneal tion as mild, moderate, or severe peritonitis.

fluid albumin concentration from the serum

In practice, however, analysis of peritoneal
concentration. The cutoff value of 11 g/L for
fluid may be inconsistent, leading to
people seems suitable for monogastric

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inconclusive results. Therefore, the diagai1in1als. However, the reference values for nostic value of this traditional concept is
protein ratio and SAAG ai·e not applicable to
limited. To improve the sensitivity of the
dairy cattle, mainly because of their higher
distinction between an exudate and
serwn protein and albumin concentrations
transudate of pleural and peritoneal effusions than those of monogastric anin1als and in human medicine, Light's criteria (fluid to
people. In addition, in cattle, the protein
serum protein ratio >0.5, fluid to serum LDH
ratio a.11d SAAG did not show higher
ratio >0.6, or fluid LOH activity >200 U/L),
diagnostic values than the total protein
cutoff values for ratios between peritoneal
concentration in peritoneal fluid alone.

fluid and plasma or serum of vaiious

In healthy anin1als, glucose concentration
paraineters (eg, lactate, glucose, enzymes),
is the saine in both serum and peritoneal
a.11d the serum-ascites albumin gradient
fluid. Bacterial infection of the peritoneal

(SAAG) have been established. These
cavity results in a major decrease of
concepts have been applied to some animal
peritoneal glucose concentration. A
species (ie, horses, cattle, small anin1als ).

peritoneal fluid:serum ratio of glucose

Under physiologic conditions, the ratio
concentrations <0.5 is highly sensitive and
between lymphocytes and neutrophils is
specific for septic peritonitis. Because in
close to 1: 1. Acute peritonitis usually results
anin1als with septic peritonitis the glucose
in an increased number of leukocytes, and
concentration in peritoneal fluid frequently
the percentage of neutrophils ca.11 be
falls below the detection limit, it is often not

60%--900A,. However, in cases of peracute
even necessal}' to measure the glucose
septic inflanm1ation, the number of
concentration in serum.

leukocytes may decrease due to necrosis

Intestinal ischernia results in an increase
and cell dainage. Histologically, a high rate
of L-lactate concentration in plasma and
of degenerative leukocytes ( cytolysis,
peritoneal fluid. Although an association
kai,1orrhexis, or kal}'olysis) can be found.

exists between L-lactate concentration in

In chronic peritoneal inflanunation, the
pe1itoneal fluid and plasma, L-lactate in
proportion of neutrophils decreases and the
peritoneal fluid is considered to be more
proportion of monocytes increases. The
closely coJTelated to the severity of intespresence of intra- or extracellular bacteria tinal ischemia. Physiologically, L-lactate
confirms septic peritonitis. Grain-staining
concentration in peritoneal fluid is lower
enables differentiation between gran1-posithan that in plasma (in healthy horses, the tive and grain-negative bacteria and
ratio is --1:2). This ratio is reversed in colicky
facilitates early antibiotic treatment.

horses with intestinal ischemia, cows with

The physiologic total protein concentraabomasal volvulus, and dogs with gastiic tion in peritoneal fluid is 20--25 g/L. The
dilatation volvulus. Similar to that in horses,
nom1al protein ratio between peritoneal
an increased L-lactate concentration in

CHARACTERISTICS OF TRANSUDATES AND EXUDATES IN CATTLE, HORSES, DOGS, AND CATS

Parameter

Species

Transudate

Exudate

Total protein (g/dL)

All

<2.5

>3

Specific gravity

All

<1.020

>1.025

Cell count (109/L)

Cattle

0.5--5

>8

Horses

0.5--5

>8

Dogs, cats

<3

>5

Color

All

Colorless to yellow

Variable

Turbidity

All

Clear to moderate

Moderate to opaque

Bacteria

All

Absent

May be present

PERITONITIS

675
peritoneal fluid has been found in cattle with
cows with displaced abomasun1. However,
abomasal volvulus and dogs with gastric
the origin of the ALP was not exclusively
dilatation volvulus. In addition, lactate is
the dainaged stomach or intestine. Other
also a bacterial metabolite (predominately
sources of the increased ALP activity in
o-lactate ); therefore, increased lactate
these cases include hepatocytes and

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concentration in peritoneal fluid may also
granulocytes. Normally, serum ALP activity
indicate septic peritonitis. The accuracy
does not show major changes during
of peritoneal lactate concentration in
intestinal ischemia.

differentiating septic and nonseptic

Increased concentrations of protein and
peritonitis varies between species ( eg,
globulin in serum and peritoneal fluid are

90%--950/oin dogs but 65%--700,1, in cats).

often seen in cats with FIP However,

Inflammation can be monitored using
neither paraineter is accurate enough for
acute phase proteins such as C-reactive
diagnosis, especially if measured in serum.

protein or haptoglobin (in cattle) as

Calculation of the albwnin:globulin ratio
markers. Acute phase protein concentramay in1prove the diagnostic value. The tions are increased in peripheral blood and
traditional Rivalta's test simply differentiin peritoneal fluid in animals with peritoniates transudates from exudates. Although it tis; however, these paran1eters are general
produces false-positive results in cats with
indicators for inflammation and not specific
septic bacterial peritonitis, it still seems
for peritonitis.

useful for FIP diagnosis. The widely used

Fibrinogen concentration in peritoneal
paraineter o.-1-acid glycoprotein indicates
fluid may be increased in animals with
infla.nunation but is not specific for FIP
peritonitis. However, fibrinogen concentra

Serun1 anti-feline coronavirus (FCoV)

tion has lin1ited diagnostic value, because
antibody titers must be interpreted
there is only a weak association between
critically, because many healthy cats are
peritoneal and blood fibrinogen concentraanti-FCoV-antibody positive. The diagnostic tion. An increased concentration of the
value of anti-FCoV antibody titers in
fibrin degradation product o-dimer indicates peritoneal fluid is still under discussion. A intestinal ischemia and inflammation with
number of advanced diagnostic methods
high sensitivity and specificity. Nonna!

( eg, in1rnunofluorescent staining of FCoV
values for hwnan plasma are <0.3 mg/L.

antigen in peritoneal macrophages, ELISA

Reference values for small animals and
to detect ai1tigen-antibody complexes in
horses seem to be similar to those in people.

serum, reverse transcriptase-PCR) have

The peritoneal fluid D-dimer concentration
been introduced as diagnostic measures to
in healthy cows is <0.6 mg/L; increased
improve accuracy of FIP diagnosis.

values indicate peritonitis with high

Generally, the laboratory tests performed
sensitivity and specificity.

on peritoneal fluid are superior to those that
lnflan1mation, intestinal ischemia, and
use serwn. Further immunohistochemistry
reperfusion affect the activities of several
for intracellular FCo V antigen in macroenzymes (alkaline phosphatase [ALP], AST, phages derived from ocular or dennal

CK, LDH) in peritoneal fluid and peripheral
lesions ofFIP cats may aid the diagnosis.

blood. CK activity is primarily increased in

(See ai,so FELINE INFECTIOUS PERITONITIS, p 780.) serum and peritoneal fluid in cases of
intestinal ischemia. The origin of CK is
thought to be the muscular layer of the

Prognosis: Although the mesothelium of
strangulated, ischemic intestines. However,
the peritoneum is able to regenerate rapidly,
other tissues ( eg, striated muscle after colic
peritonitis must be considered a severe,
episodes in horses) may be sources of
life-threatening disease with a guarded
higher CK activities; therefore, the
prognosis. Prognosis strongly depends on
sensitivity and specificity of CK are low.

the character and severity of the disease

LDH activity is a measure of inflai11maand, therefore, must be determined tory response and has been used to
individually. General survival rates of
differentiate exudate from transudate

500/o--700A, have been reported, with much

(peritoneal fluid:serum LDH ratio >0.6; LDH
lower rates for return of productivity in
activity of peritoneal fluid >200 U/L). The
fann animals. In horses, the prognosis for
reference values for monogastric animals,
further use in equestrian sport is guarded.

but not those for cattle, are similar to those

Furthermore, horses that survive peritonitis
for people. For cattle, a cut-off value of960
frequently suffer from recurrent colic

U/L has been identified.

episodes. Despite new developments in

An increase of ALP during intestinal
therapy, the prognosis for cats with FIP
ischemia and reperfusion has been found in
remains poor. It is still a lethal disease
peritoneal fluid of horses with colic and
with no effective long-term treatment.

676

PERITONITIS

Treatment: Adequate therapy depends on
removing septic and proinflanunatory
the diagnosis and the results of physical
material from the abdominal cavity. Whereas
examination and laboratory analyses. In
the removal of septic peritoneal fluid is
severe cases of septic peritonitis, the initial
generally accepted as beneficial, the efficacy
treatment must be directed toward saving the of repeated peritoneal lavage is under VetBooks.ir
life of the animal and stabilizing cardiovascudebate. Whereas some reports describe lar and other organ fonctions. In severe cases, positive effects, others clainl that intensive euthanasia is a consideration. Therapy
lavage may disturb healing of the epithelium
should include treatment of hypovolernid
a.t1d result in fwther spread of the inflanm1atoxemic shock, aggressive anti-inflammatory tion. The composition of tl1e lavage solution
therapy, and treatment of the metabolic and
is also under debate; there are no or very
rheologic disturbances ( eg, electrolyte and
few advantages to adding antibiotics or
acid-base disorders, disseminated intravasa.i1tiseptics. The decision to manage cular coagulation). Replacement fluids,
pe1itoneal ch'llinage is based on the severity
electrolytes, plasma, or whole blood may be
of the case, expetience level, intensive care
necessary to maintain cardiac output and
possibility, a.t1d equipment. Maintena.t1ce
improve circulation. It is of major in1portance of ch·ain patency ca.t1 be difficult, e pecially to prevent circulatory failure from complicain cattle, caused by the extensive fibrin tions of disseminated intravascular
fonnation in the abdominal cavity. In
coagulation. Antioxidative treatment using
a.tlinlals treated by pe1itoneal drainage or
vitanlins C and E or short-acting glucocortilavage, serum protein a.t1d electrolyte levels coicls might be useful. Additional prokinetic
should be monitored pe1iodically, because
chugs might be necessary to increase and
both are lost with drainage of exudate.

coordinate the motility of the GI tract.

Nuttitional support should be a.t1tici

Appropriate antin1icrobial therapy should
pated, because ma.t1y aninlals with
be started once septic peritonitis is
peritonitis will not eat. Enteral nuttition
suspected or confinned. Peritoneal fluid
helps to maintain the healtl1 of the intestinal
samples should be obtained for cuiture and
mucosa; however, vomiting (dogs and cats)

sensitivity testing. Parenteral broad-spectrum or a.t1orexia may force the consideration of antimicrobial therapy must be applied
alternatives. In rumina.t1ts a.t1d New World
initially. Arninoglycoside or fluoroquinolone
camelids, tra.t1Sfaunation using rumen fluid
antibiotics are effective against gram-negative obtained from other a.t1in1als or conm1erorganisms, and penicillins or cephalosporcially available products has proved ins are effective against gram-positive
beneficial. In certain aninlals, total or pa.itial
bacteria. The antimicrobial drug may be
parenteral nuttition may be necessary to
changed later according to the results of
provide a portion of the nuttitional
cytology and cultme and sensitivity testing.

requirements while enteral nuttition is

Antimicrobial and anti-inflammatory
being initiated. Administration of a.t1tioxitreatment should continue through the dants and vitamins should be considered.

healing period.

Vomiting is sometimes a sequela of

If possible, therapy should be initiated to
peritonitis in small aninlals; antiemetic
eliminate the cause of]1eritonitis. In animals treatment is indicated in such cases.

with suspected leakage of abdominal

Feline coronaviral infection may cause a
organs, surgery should be pe1fo1med
p1irnary feline infectious peritonitis (FIP).

inlrnediately to explore the abdomen and

Therapy is palliative ( eg, interferon therapy,
repair the defects, followed by peritoneal
glucocorticoids, sup·portive therapy) and
lavage with an isothem1ic, isotonic,
directed towa.i·d slowing down the inflambalanced electrolyte solution before the mation. However, no effective long-term
abdominal cavity is closed. Aithough
therapy is available. Commercial vaccines
frequently performed, there is no proven
for prophylaxis are available in some
clinical benefit in adding antin1icrobial
countties; however, there are conflicting
drugs to the lavage solution. Solutions
reports on their efficacy a.t1d safety. The
containing antiseptics ( eg, povidone-iodine) vaccine is not effective when administered also have no proven clinical benefit and may to aninlals already exposed to FCo V; even function as chemical irritants and
however, it may offer some protection when
exacerbate the inflammation. Hepa.tin
achninistered to seronegative aninlals.

treatment may be considered in cases of

In chronic adhesive peritonitis, laparos

DIC and may prevent extensive fib1in
copy or laparotomy may be considered to
formation within the peritoneal cavity.

cut adhesions that prevent intestinal

The application of abdominal drains and
motility or to remove/drain intestinal
subsequent lavage is possible in small and
abscesses. However, the success of such
large aninlals to treat severe peritonitis,
interventions might be limited.

PLAGUE

677

PLAGUE

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Plague, caused by Yersinia pestis, is an
membrane contact with secretions or
acute and sometimes fatal bacterial
tissues of an infected rodent or rabbit or
zoonosis transmitted primarily by the fleas
by the bite of an infected flea People are
of rats and other rodents. Enzootic foci of
usually exposed by an infected flea bite but
sylvatic plague exist in the western USA and are sometimes exposed due to contact with throughout the world, including Eurasia,
infected aninlals or via respiratory droplet

Africa, and North and South America. In
transmission from pneumonic cases. Risk
addition to rodents, other mammalian
factors for cats acquiring plague include
species that have been natw·ally infected
hunting and eating rodents and rabbits,
with Y pestis include lagomorphs, felids,
visiting an enzootic plague area, finding
canids, mustelids, and some ungulates.

dead rodents around the yard or areas that

Domestic cats and dogs have been known
the aninlal frequents, and exposure to
to develop plague from oral mucous
infected fleas. Plague epizootics cause
membrane exposure to infected rodent
nearly 100% mortality in affected wild
tissues, typically when they are allowed to
rodent and rabbit populations. Once their
roam and hunt in enzootic areas. Birds and
host has died, Y pestis-infected rodent and other nonrnammalian vertebrates appear to
rabbit fleas will seek other hosts, including
be resistant to plague. On average, 10
cats and dogs, and potentially be transhuman plague cases are reported each year ported into homes. Rodent and rabbit flea
in the USA; most are from New Mexico,
species are different from dog and cat fleas

California, Colorado, and Arizona. Most

( Ctenocephalides spp ), although most
human cases result from the bite of an
veterinarians and pet owners will not be
infected flea, although direct contact with
able to visually distinguish flea species. Dog
infected wild rabbits, rodents, and occasionand cat fleas are rare in most plague-enzootic ally other wildlife and exposure to infected
areas of the western USA; therefore, fleas
domestic cats are also risk factors.

on pets in these areas may be more likely to
be fleas from wildlife, including rodents or

Etiology: Y pestis is a gram-negative, rabbits.

nonmotile, coccobacillus belonging to the

Enterobacteriaceae family. It exhibits a
bipolar staining, "safety pin" appearance

Pathogenesis: F1eas become infected
when stained with Wright, Giemsa, or
with Y pestis when feeding on a bacteremic

Wayson stains. Y pestis grows slowly even
mammal. It has been thought that most flea
at optimal temperatures (28°C [82.4°F]) and
transmission of plague occurs when the
can require <!48 hr to produce colonies.

bacteria multiply and block the flea's

Several types of media can be used to grow
digestive tract, preventing it from digesting

Y pestis, including blood agar, nutrient
subsequent blood meals; the flea then
broth, and unenriched agar. Colonies are
regurgitates the plague bacteria and
small (1-2 mm), gray, nonmucoid, and have
inoculates the host on which it is attempta characteristic "ha11m1ered copper" appearing to feed. Recent experiments have ance. Different virulence factors are
shown that some species of unblocked
expressed by the organism at different
fleas are better transmitters of plague.

temperatures and environments, allowing

These fleas became infectious within a day
the organism to survive in flea vectors and
of feeding and remained infectious for <!4
then be transmitted to and multiply in
days, also inoculating the host on which
mammalian hosts. The organism does not
they are feeding with plague bacteria that
survive for long at high temperatures or in
have been multiplying within the flea's
dry environments.

upper GI tract. In mammalian hosts, plague
presents clinically in one of three forms:

Epidemiology and Transmission:

bubonic, septicemic, or pneun1onic. After

Y pestis is maintained in the environment
inoculation into the skin by a flea bite or
in a natural cycle between susceptible
into mucous membranes by contact with
rodent species and their associated fleas.

infectious secretions or tissues, the

Commonly affected rodent species include
bacteria travel via lymphatic vessels to
ground squirrels (Spermophilus spp) and
regional lymph nodes. These infected
wood rats (Neotoma spp ). Cats and dogs
lymph nodes are called buboes, the
are usually exposed to Ypestis by mucous
typical lesion of bubonic plague.

678

PLAGUE

Secondary septicemic plague can develop

Dogs infected with plague are less likely
when the organism spreads from the affected
to develop clinical illness than cats,
lymph nodes via the bloodstream but can also
although cases have been seen in enzootic
occur without prior lymphadenopathy
areas. Symptomatic plague infection has

(primary septicemic plague) and affect
been docun1ented in three naturally infected

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numerous organs, including the spleen, liver,
dogs; clinical signs included fever, lethargy,
healt, and lungs. Pneumonic plague can
submandibular lymphadenopathy, a
develop from inadequately treated septicemic purnlent interrnandibulal· lesion, oral cavity plague (secondaly pnew11onic plague) or
lesions, and cough.

from infectious respiratory droplets (pri.maly

Cattle, horses, sheep, and pigs are not
pnew11onic plague), typically from a coughing known to develop symptomatic illness pnetunonic plague patient ( aninlal or hwnan). from plague, whereas clinical illness has been documented in goats, camels, mule

Clinical Findings and Lesions: The
deer, pronghorn antelope, nonhuman
clinical presentation of plague in cats is most
primates, alld a llalna. Infected mountain
commonly bubonic plague. The incubation
lions and bobcats have shown clinical
period ranges from 1-4 days. Cats with
signs and mortality similal· to those of
bubonic plague typically present with fever,
domestic cats.

anorexia, lethal·gy, and an enlal·ged lymph
node that may be abscessed and draining.

Diagnosis: Plague must be differentiated

Oral alld lingual ulcers, skin abscesses,
from other bacterial infections, including
ocular dischal·ge, diarrhea, vomiting, and
tularemia (seep 692), abscesses due to
cellulitis have also been docw11ented. A
wounds ( cat fight bites), and staphylococretrospective review of 119 naturally infected cal and streptococcal infections. During
cats found that 53"A, of cats had bubonic
acute illness, preferred filltemortem
plague; of those, 75% had submandibulal·

Salllples for culture include whole blood,
lymphadenopathy, with bilateral enlargement lymph node aspirates, swabs from draining in-'/. of cases. Affected lymph nodes show
lesions, alld oropharyngeal swabs from
necrosuppurative inflalrunation, edema, and
cats with oral lesions or pneun1onia.

hemorrhages and contain numerous Y peslis

Diagnostic sal11ples should be taken before
organisms. In experimentally infected cats,
filltibiotics are ad.ministered. Y peslis
fever was as high as 106°F ( 41 °C), peaking -3
cultures Call take 48 hr for visible growth to
days after exposure; mortality was as high as
develop. An air-dried glass slide smear of a

6(Y>A, in untreated cats. Ten of 16 (62.5%) cats
bubo aspirate can be used for a fluorescent
exposed orally developed enlarged lymph
filltibody test that detects the Fl filltigen on
nodes in the medial retropharyngeal,

Y peslis cells. This test Call be performed in submandibulal·, sublingual, and tonsillar
a matter of hours in fill experienced
regions, palpable 4--0 days after exposure.

laborato1y and is both sensitive alld

Y peslis was isolated from the throats of 15 of specific.

these cats. In 6 subcutaneously exposed cats

Postmo1tem specimens should include

(mimicking a flea bite), none had palpably
samples of liver, spleen, and lung (for
enlal·ged lymph nodes in the head or neck
pnewnonic cases) alld affected lymph
region, but four had subcutaneous abscesses
nodes. In areas where tularemia is also
at the inoculation site.

present, Salllples should be collected under

Cats with primaly septicemic plague have
a biosafety hood, or the entire animal
no obvious lymphadenopathy but present
submitted to a veterinary diagnostic
with fever, lethargy, and anorexia. Septic
laboratory where aerosol precautions Call
signs may also include diarrhea, vomiting,
be implemented. Serologic antibody tests
tachycal·dia, weak pulse, prolonged
can be confinnatory but require acute alld
capillaly refill time, disseminated intravasconvalescent Salnples taken 2-3 wk apart, cular coagulopathy, and respiratory distress. demonstrating a 4-fold rise in filltibody titer.

Prin1ary pneun1onic plague has not been

Single acute sera are often negative if taken
docun1ented in cats. Cats with secondaly
early in the cow-se of illness or Call be
pneun1onic plague may present with all the
problematic in fill enzootic al·ea where
signs of septicemic plague along with a
aninlals may retain filltibody titers from
cough and other abnom1al lung sounds.

previous exposw·es.

Characteristic necropsy findings Call include
livers that are pale with light-colored

Treatment: Because of the rapid
necrotic nodules, enlarged spleens with
progression of this disease, treatment for
necrotic nodules, and lungs with diffuse
suspected plague (filld infection control
interstitial pnewnonia, focal congestion,
practices) should be started before a
hemorrhages, and necrotic foci.

definitive diagnosis is obtained. Streptomy-

RHODOCOCCOSIS

679
cin has been considered the drug of choice
interventions are critical when an animal
in human cases but is difficult to obtain and
is suspected to have plague. Animals
rarely used today. Gentan1icin is currently
with signs suggestive of plague should be
used to treat most human plague cases and
placed in isolation, with infection control
should be considered a suitable alternative
measures inlplemented for the protection

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choice in veterinary medicine for seriously
of staff and other animal patients without
ill aninmls, although it is not approved for
waiting for a definitive diagnosis. The use
this purpose. Aninlals with renal failure
of gloves, surgical masks, eye protection
require adjusted dosages.

(if splashes or sprays are anticipated),

Doxycycline is appropriate for treatment
patient isolation (animal or human),
of less complicated cases and to complete
and standard hygiene and disinfection
treatment of seriously ill anin1als after clinical procedures for protection from potentially in1provement. Tetracycline and chloran1-contan1inated respiratory droplets, body
phenicol are also options. Penicillins are not
fluids, and secretions from the patient
effective in treating plague. In treatment

(animal or human) are essential. Of the 23
studies with experimentally infected mice,
human patients who developed cat-associthe fluoroquinolones perfom1ed as well as ated plague in the USA between 1977 and
streptomycin. F1uoroquinolones have not

1998, 6 were veterinary staff; the rest were
been studied in any veterinary clinical trials,
cat owners or others handling a sick cat.

but there is growing evidence from their use

After pneumonia has been excluded, or
in enzootic areas that they are effective in the
once there is evidence of clinical inlprovetreatment of plague in dogs and cats. The ment after 72 hr of appropriate therapy,
recommended duration of treatment is 10-21
isolation procedures may be relaxed, but
days, with clinical improvement (including
standard disinfection and hygiene
defervescence) expected within a few days
procedures should continue.

of treatment initiation.

Local or state public health officials

The duration of infectivity in treated cats is should be notified promptly when plague not definitively known, but cats are thought
is suspected to help conduct appropriate
to be noninfectious after 72 hr of appropriate
diagnostic tests, initiate an environmental
antibiotic therapy with indications of clinical
investigation, and assess the need for
in1provement. During this infectious period,
fever watch or prophylactic antibiotics in
cats should remain hospitalized, especially if
potentially exposed people. To decrease the
there are signs of pneumonia. Human cases
risk of pets and people being exposed to
have occurred in cat owners trying to give
plague, pet owners in enzootic areas should
oral medications at home, exposing them to
keep their pets from roaming and hU11ting,
contact with the oral cavity and associated
linlit their contact with rodent or rabbit
infectious secretions.

carcasses, and use appropriate flea control.

Epidemiologic data, fact sheets, public

Prevention and Zoonotic Risk: Along
education brochures, and other information
with treatment and diagnostic consideraon plague is available on the Web sites of the tions, protection of people and other

CDC and the New Mexico Depaiiment of
animals and initiation of public health

Health.

RHODOCOCCOSIS

Rhodococcosis is a pyogranulomatous

Co1ynebacterium, and Nocardia. R equi
disease of domestic animals, wildlife, ai1d
is a facultative intracellular opp01tunistic
people. It is caused by Rhodococcus equi
pathogen. In Grai11 smears, the bacteria

(fonnerly Corynebacterium equi), the
appear as gram -positive rods, cocci, or
pathogenicity of which has been mainly
rod-shaped (pleomorphic) organisms.

attributed to the presence of virulence

The virulence of R equi is intinlately
associated antigens and plasmids.

associated with its ability to survive and
multiply inside macrophages, mainly the

Etiology: Rhodocucc:us spp belong to presence of a large plasmid that contains
the aerobic actinomycetes in the order
genes encoding a number of proteins associ

Actinomycetales, which is taxonomically
ated with virulence (Vap ). Seven genes have related to the generaMycobacterium,
been classically associated with R equi

680

RHODOCOCCOSIS
virulence, the most important being the
orgai1S and developing pyogenic reactions

VapA plasmid because of its probable
in the liver, spleen, kidneys, bones, brain,
regulatory action over other genes. This
and lymph nodes.

gene regulation of R equi is a complex

The basis of pathogenicity is attributed to

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mechanism, influenced by vaiious factors,
the ability of the organism to survive and
including iron and magnesium availability,
multiply inside macrophages, subsequently
as well as environmental conditions such as
destroying these phagocytic cells. Other
temperature and pH.

factors that contribute to the pathogenesis
include the iron acquisition mechanism and

Epidemiology: R equi has been isolated the presence of phospholipase C and
from a wide vaiiety of species, including
cholesterol oxidase (so called "equi
horses, cattle, swine, sheep, goats, dogs,
factors"). In nonequine species, in1munocats, camelids, birds, and wild animals.

suppressive conditions of the host may

R equi is distributed worldwide. It is enable a virulent or less virulent strains to
widespread in surface soil, particularly in
persist inside phagocytes.

feces of foals and other herbivores, and in

Passive humoral immunity generated by
their environment. R equi may survive up ingestion of mare colostrum contributes to
to 12 mo in soil and can multiply in a wide
the control of R equi infection in foals.

temperature range (15°-40°C) and neutral

However, Immoral response by itself does
pH (6.5-7.3).

not confer complete protection. Consistent

Inhalation of soil dust particles is
evidence supports the essential role of
considered the main route of infection for
cellular in1mune response in control of
domestic animals. Contan1inated water and

R eqiii infections.

food is a less frequent route of infection,
except for swine. Infected sputum may be

Clinical Findings: Suppurative bronchoswallowed by foals with pneumonia, pneurnonia and ulcerative colitis in foals,
causing ulcerative colitis and mesenteric
lymphadenitis in cattle and swine, and
lyrnphadenitis. Foals showing clinical and
cutaneous or organ abscesses are the major
subclinical disease may spread R equi via clinical manifestations of rhodococcosis in
aerosol.

domestic animals. R equi infections are Risk factors associated with a higher
frequently found only in foals and swine,
prevalence of disease in horses include
whereas they ai·e rare or uncommon in
large numbers of foals and mares, transient
small ruminants, companion animals, birds,
equine population, high foal density, foals
and wildlife.

born to mares that shed high numbers of the

In horses, R equi is a commensal
microorganism in the feces, and inadequate
intestinal organism; it can actively multiply
transfer of maternal ai1tibo(j.ies. Poor animal in the intestines of foals up to -3 mo old and management, housing, seasonal effect on
can also be isolated from the feces of adult
foals' birth, and environmental conditions
horses. Suppurative bronchopneumonia is

(eg, dry, dusty, windy) have also been
tl1e primary clinical sign in foals. Foals are
reported as predisposing conditions.

affected between 2 wk and 6 mo of age,

VapA plasmid is usually found ii1 foal and
although foals 1-3 mo old are most
bovine rhodococcosis cases, indicating a
commonly affected, possibly because of the
major risk of infection to companion
decline in maternal antibodies at -6 wk of
animals by contact with livestock or their
age. On endemic farms, it is estimated that
environment.

5o/o-4QOA, of foals may develop clinical signs,
and up to 5()0A, of cases may be fatal. Foals

Pathogenesis: The outcome of exposure

>6 mo old appear to be refractory to
to R equi is strongly influenced by the
development of clinical signs. (See also
virulence, infective dose, and age and

Rf/0/JOCOCCUS EQUI PNEUMONIA IN FOALS, p 1451.) immune response of the host. Virtually all

Initially, foals show nonspecific signs,
foals are exposed to R equi shortly after
including fever, lack of appetite, and
birth, although most do not develop clinical
reluctance to move and suckle. Most foals
signs. Adult horses are commonly resistant
with lung infections show respiratory
to the clinical disease, because they have
distress, with tachycardia, tachypnea, and
developed effective immune responses
a strong inspiratory effo1t manifested by
againstR equi.

abdominal movement and nostril flaring. On

R equi may invade the animal via the
auscultation, inspiratory and expiratory
respiratory or digestive tracts or the skin.

wheezes and crackles are possibly audible,

It then spreads through hemolyrnphatic
predominantly in the cranioventral region.

vessels, reaching different tissues and

Decreased ailway sounds suggest

RHODOCOCCOSIS

681
consolidation, extensive abscess fom1ation,
lymph nodes caused by R eqiti observed in
or occasional pleural effusion. Mucous
slaughterhouses resemble those caused by
membranes may be pale or cyanotic. Weight

Mycobacterium spp, a major cause of swine
loss, cough, and serous to mucopurulent
lymphadenitis (seep 690).

nasal secretion are not consistent signs.

Rhodococcosis is rare in dogs and cats,

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Typically, the disease is insidious in foals
although it is more conunonly reported in
because of the ability of horses to compencats than in dogs. The most common routes sate for respiratory lesions, making early
of infection in dogs and cats are traumatic
diagnosis difficult.

percutaileous introduction of microorgan

Abdominal R equi infections in foals are
isms, p1imary contamination of wounds, or
clinically manifest by diarrhea, ulcerative
secondary to scratches in cat fights. Most
colitis, mesenteric lymphadenitis,
cats present with cutaileous lesions on one
abdominal abscesses, typhlitis, and
extremity, along with localized swelling,
peritonitis. Foals rarely develop intestinal
ulcers, and fistulas with purulent drainage.

signs without pulmonary signs, but

The lesions are conunonly painful, and
intestinal lesions are found in --30%--5096 of
usually no systemic signs are seen. Regional
foals with pulmonary rhodococcosis. Colic,
lymph nodes may be enlarged. Respiratory
diarrhea, and weight loss are the major
and visceral involvement represents the
clinical signs of the intestinal fmm.

systemic or disseminated form of disease.

Immune-mediated polysynovitis affects

Pyothorax is usually caused by dissemina

--20%--30% of foals, caused by immune
tion of the organism from mediastinal
complex deposition in joints. Any joint may
lymph nodes. These animals present witl1
be involved, although the tibiotarsal and
fever, ai1orexia, dyspnea, and weight loss.

stifle joints are most commonly affected.

In visceral infections, there is abdominal

Synovial fluid aspiration reveals nonseptic
distention with palpable fluid, splenomemononuclear pleocytosis, without isolation galy, hepatomegaly, and mesenteric
of R equi. Septic aithritis of foals is another lymphadenomegaly. Underlying conditions,
joint lesion caused by R equi. Different from including irnmunosuppressive viral immune-mediated polysynovitis, the septic
infections, should be investigated in cats
lesion is usually combined with lan1eness
with rhodococcosis.

signs.

In rwninants, lymphadenitis (mesen

A variety of other R equi infections are
teric, submaxillary, and bronchial),
sporadically seen in horses, including
pneumonia, pyometra, ulcerative lyn1phancellulitis, ulceration, subcutaileous gitis, and occasionally mastitis have been
abscesses, lymphangitis, lymphadenitis,
reported in cattle and buffalo. Pneumonia is
renal abscesses, pleuritis, hepatitis, and
the most common clinical picture in goats.

hepatoencephalopathy. Ocular signs, such

Sporadic abortion and organ abscesses
as hypopyon and immune-mediated uveitis,
have been reported in sheep and goats.

may be seen. Osteomyelitis causing ataxia,
decubitus, and limb paralysis is uncommon.

Diagnosis: Periodic clinical exainina

Rai·ely, R equi is associated with abortion, tions, WBC counts, serum fibrinogen levels,
placentitis, and infertility in mares, and it
serologic tests, and diagnostic imaging have
has been occasionally isolated from equine
been proposed as measures for early
semen.

diagnosis, mainly because of the insidious

Clinical manifestations in adult horses
and precocious characteristic of foal
are uncommon. The disease probably
rhodococcosis. Weekly physical exaininaaffects immunocompromised horses, or tion, including thoracic auscultation, is an
animals co infected with in1munosuppreseffective clinical practice for early sive agents, infected by plasmid strains
diagnosis. Monthly or more frequent
expressing VapA. The predominant clinical
monitoring of increased WBC counts
signs in adult horses ai·e sinillar to those in

(> 13,000 cells/µL), serum fibrinogen
foals, with suppurative bronchopneumonia,
concentration (>400 mg/clL), and thoracic
pleuritis, enteritis, lymphadenitis, and
ultrasonography are also valuable
osteomyelitis.

procedures for early diagnosis. Efficacy

In swine, R equi infections ai·e basically
of periodic inununodiffusion testing in
restricted to the lyn1phatic tract. Usually,
predicting individual cases in affected foals
pyogranulomatous cervical lymphadenitis
is controversial.

is seen, although mesenteric, bronchial, and

Supportive clinical and epidemiologic
otl1er lymph nodes may be involved. R equi
findings are in1po1tant in presumptive
has also been isolated from apparently
diagnosis, but diagnosis by isolation,
normal lymph nodes. Occasionally,
microbiologic culture, and phenotypic
pneumonia may be seen. Gross lesions in
characterization of R equi is considered the

682

RHODOCOCCOSIS

"gold standard." Tracheobronchial lavage,
and continuous exposure to R equi in the
skin, synovial and pe1itoneal fluid, organs,
environment. In addition, these tests have
and abscesses are the main clinical
failed to differentiate between healthy and
specimens used. On staining, the presence
sick foals and, therefore, are inappropriate
of gram-positive pleomorphic organisms
for diagnosis of individual cases.

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supports a presumptive diagnosis, although

Detection of R equi-speci.fic DNA by
this preliminary identification of the

PCR is also available for rapid and reliable
organism should be carefully evaluated,
diagnosis. However, because R equi can be
because few bacteria may be present m
fotmd in the trachea of foals without
some clinical samples. Tracheobronchial
pulmonary signs, PCR may be positive in
lavage is the main clinical specimen for
healthy anin1als. Thus, epidemiologic
isolation of R equi in foals. However, the
aspects, clinical signs, hematologic tests,
organism may occasionally be isolated
imaging findings, microbiologic culture,
from the trachea of foals without signs of
and/or molecular assays must all be
pneumonia. Nasal swabs of foals are not
considered in making a diagnosis.

indicated as evidence of rhodococcos1s
because of contamination with local

Lesions: Suppurative abscesses with
microflora. Likewise, the presence of
necrotic areas and regional lymphadenitis

R equi in the nasal region is not predictive are the major gross lesions seen at necropsy.

of pulmonary infection.

Typically, pulmonary lesions reveal multiple

R equi is naturally isolated from feces
fim1 nodules, atelectasis, congestion, and
of most livestock species, especially foals.

cavitary lesions. Multiple miliary lesions

Despite the fact that foals often swallow
may be seen as well. Multifocal enteritis,
sputum containing R equi, <200,1, of foals typhlitis, mesenteric lymphadenitis, and

.

confinned with pulmonary rhodococcos1s

Peyer's patches reaction are seen in cases
show positive fecal isolation of bacterium.

of intestinal involvement. Abdontinal

R equi can be isolated from feces, soil, or dissentination is characterized by peritoniother contantinated samples. Potentially tis and organ abscesses. Septic arthritis,
contaminated material, including feces, soil,
hypopyon, and vertebral osteomyelitis ar�
and sand of parks and yards, should be
signs indicative of hematogenous disselTllsubmitted to selective culture media nation. Abortion, placentitis, and fetal

Neutrophilic leukocytosis, hyperfibrinoinfection are w1common.

"enemia and hyperglobulinemia are the

Histologically, tl1e tissue and organ lesions

�1ost co�sistent hematologic findings in
are characterized as pyogranulomatous
foals with rhodococcosis. Thrombocytosi.s
lesions containing foci of necrosis. The
and monocytosis are variable findings.

lesions reveal numerous gram-positive

Serum amyloid A (SM), an acute-phase
pleomorphic organisms phagocytized by
protein, has been proposed as an inflammamacrophages, multinucleate giant cells, and tory marker of rhodococcosis because of
fewer neutrophils. Moderate infiltrate of
increased SAA levels in foals with R equi
plasma cells and lymphocytes are also fotmd.

infections. Abdominal and thoracic

The primary pathogens that should be
effusions are usually exudates and reveal
differentiated from R eqiii as causal agents increased protein levels and nucleated cell
of foal respiratory diseases are Salmonella
counts.

spp, Streptococcus equi, influenza virus,

Thoracic, abdominal, and joint radiograherpesvirus, and migrating stages of phy have also been used in diagnosis. Initial

Parascaris equorum. Differential diagnosis
pneun10nia is characterized by a mild to
of R equi causing intestinal manifestations moderate, diffuse bronchointerstitial
should be perfonned with Clostridium
pattern, revealing small nodules and
spp, Salmonella spp, Escherichia coli,
possibly cavitary masses, which can

Strongyloides westeri, rotavirus, and
be multiple and large in severe cases.

coronavims. Septic artllritis caused by R

Occasionally, mediastinal lymphadeno
equi should be differentiated, especially
megaly is seen. Thoracic ultrasonography
from Salmonella spp and Stre-ptococcus
is valuable to evaluate mainly peripheral
equi. Swine lymphadenitis caused by
lung lesions.

Mycobacterium spp should be differenti

Serologic assays ( eg, agar-gel in1rnunoated from R eqili because of similar diffusion, ELISA, synergistic hemolysis
appearance of lyn1ph nodes at the

_
inhibition) have been proposed for use m
slaughterhouse.

diagnosis, particularly of horses. However,
titer results have varied greatly, probably

Treatment: Treatment involves appropribecause of differences in antigen preparaate antimicrobial therapy, surgical drainage, tion, interference of maternal antibodies,
debridement, and supportive care.

RHODOCOCCOSIS

683

R equi is typically refractory to conven

Surgical drainage of abscesses and
tional antimicrobial therapy. Successful
debridement are indicated in some
therapy varies dramatically between animal
cutaneous lesions. Hydration and adequate
species, probably because of the intracellunutrition are reconu11ended as supportive lar location of the pathogen, development of care. NSAIDs may be used to control fever VetBooks.ir
pyogranulomatous lesions, and antimicroand in animals with arthritis.

bial resistance patterns of the isolates.

Despite appropriate antimicrobial

Antimicrobial susceptibility profile of
therapy and supportive care, domestic
animal and human strains usually shows in
animals with respiratory distress, tachycarvitro sensitivity to rifampin, erythromycin, dia, severe thoracic in1aging abnormalities,
arninoglycosides (lincomycin, gentamicin),
and osteomyelitis have a poor prognosis.

and imipenem. However, lipid-soluble drugs
are the antimicrobials of choice because of

Control and Prevention: Control
the need for adequate tissue and cellular
procedures are recommended to maximize
penetration, particularly into macrophages.

the resistance of foals to infection and to

Since 1980, the standard effective
reduce infection pressure in their environchemotherapy protocol for foals is based on ment. Adequate transfer of colostral administration of rifan1pin (5 mg/kg, PO,
inu11unoglobulins to foals is essential.

bid, or 10 mg/kg/day, PO) and erythromycin

Different measures have been proposed to

(25mgfkg, PO, tid, or37.5mgfkg, PO, bid).

prevent and control animal rhodococcosis,

These drugs have a synergic effect, and their particularly in foals, including decrease in combined use decreases resistance rates.

environmental exposure to R equi, passive

Throughout the past decade, the macrolides immunization (hyperimmune plasma), clarithromycin (7.5 mg/kg, PO, bid) and
active inu11unization (vaccination), and
azithromycin (10 mg/kg/day, PO) have been
early diagnosis of disease.

investigated as treatment alternatives

The exposure of domestic animals,
because of their bioava.ilability, stability,
particularly foals, to R equi in the environand higher concentration in the cells than ment is theoretically tlle ma.in risk factor for
erythromycin. The combination of rifampin
transmission. A high number of mares and
and clarithromycin has shown better
foals on fam1s, and high density, leading to
efficacy than rifampin-erythromycin or
higher levels of R equi in manure, appear
azithromycin-rifan1pin.

to be predominant risk factors for equine

The duration of treatment is variable,
rhodococcosis. Thus, decreasing the
although 4-8 wk is frequently recomnumber of mares and foals and reducing mended. Therapy may be extended in
foal density have been recommended on
complicated cases in foals. However, after
farms with endemic rhodococcosis.

a longer course of therapy, some foals may

Removal of excess manure from livedevelop antibiotic -associated colitis. Recent stock paddocks, stalls, and pastures could resistance of R equi isolates to rifampin and theoretically decrease growth of R equi, erythromycin have been described,
and consequently, tlle risk of infection.

especially with use of these drugs as

However, high concentrations of pathomonotherapy.

genic R equi are usually found in tlle feces Azithromycin has been used as an alternaof foals, because they commonly swallow tive to erythromycin in foals with adverse
sputum containing virulent strains and
signs after the use of erythromycin,
excrete the pathogen in their feces. Wected
including respiratory distress and diarrhea.

foals should be isolated and their manure

However, there is a paucity of infom1ation
removed inlmediately to help control the
regarding prolonged use (;,,4 wk) and
disease.

adverse effects of this drug.

Direct involvement of dust as the major

In companion animals, combined therapy 1isk factor for livestock rhodococcosis is using rifan1pin (10 mg/kg/day, PO) and
controversial. Nevertheless, irrigation of
clarithromycin (7.5-12.5 mg/kg, PO, bid) for
paddocks and stalls, as well as growing

2 -5 wk may be recommended. Combined
grass in foal environments tl1at a.re
treatment using lincomyci.n (20 mg/kg, PO,
excessively dusty, may decrease aerosolbid, for 7 -10 days) and gentamicin (5-8 mg/
ization.

kg/day, SC, IM, or IV, for 5 days) has been

The use of hyperinu11une plasma as an
effective in some cats, although longterm
alternative prophylactic measure for equine
therapy or a second course of antimicrobipassive inm1w1ization aga.i.nstR equi is als may be necessary. Erythromycin (15 mg/
based on the protective action of plasma
kg, PO, bid, for 14 days) may be combined
components (inlmunoglobulin, interferon,
with rifampin or other drugs in treatment of
complement factors, cytokines, and
dogs and cats.

fibronectin). Hyperirnmune plasma

684

RHODOCOCCOSIS
decreases the severity of clinical signs in
and field conditions using VapA vaccines
foals, although it does not seem to have a
have shown enhanced clearance of R equi.

curative effect or to shorten the course of

Administration of oral live VapA vaccines
disease. Protocols for administration are
has induced high concentrations of

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variable, but hyperimmune plasma is most

VapA-specific antibodies, despite being
effective when used before exposure to R
considered impractical for vaccination
equi. Most commonly, 1 L of hyperimmune
of a large nun1ber of animals. Efforts are
plasma ( or 20 mlJkg of foal), IV, is used for
ongoing to develop vaccines using modem
foals 1---60 days old. The initial dose for foals
concepts, such as transposons, and
is variable, given at 1-10 days of age, and
recombinant and DNA vaccines containing
followed by a second dose at 30--50 days of

VapA antigen, which induces humoral and
age. However, because foals are challenged
especially cellular immune response.

early (in the first days of life), the first dose is probably the most effective for protection.

Zoonotic Risk: Traditionally, contact with

Different vaccines have been developed
soil or manure, or inhalation of aerosols
to induce active immunity in foals. Most
contaminated by livestock, represents the
foals challenged with virulent R equi strains major routes of transmission of R equi to develop a protective and prolonged in1mune people. Alternatively, human infection may response. However, insufficient neonatal
occur by transcutaneous trauma, ingestion,
response or relative immunologic immatuor wound contamination. Recent evidence rity, interference with maternal antibodies,
supports that consumption of pork
and the intracellular location of R equi limit products or undercooked pork may be
the active immunization of foals in field
a probable route of infection to people
conditions.

because of contamination of the meat

Killed vaccines have shown ineffective or
with lymph node content or feces.

controversial results in inducing a cellular

R equi has emerged as a pulmonary
immune response againstR equi.

pathogen among immunocompromised

Infection withR equi strains without
people. Therefore, it is recommended that

VapA and VapB genes does not induce immunocompromised people avoid contact
protection of foals, indicating that virulent
with livestock and their environment, as
strains are essential for composition of
well as consumption of undercooked pork
effective vaccines. Studies in experimental
products.

SWEATING SICKNESS

Sweating sickness is an·acute, febrile,
sweating sickness-positive strain. The
tickbome toxicosis characterized mainly by
potential to produce toxin is retained by
a profuse, moist eczema and hyperemia of
ticks for as long as 20 generations, and
the skin and visible mucous membranes.

possibly longer. Attempted experimental

It is essentially a disease of young calves,
transmissions between affected and healthy
although adult cattle are also susceptible.

anin1als by contact or inoculations of blood

Sheep, pigs, goats, and a dog have been
have been tmsuccessful.

infected experimentally. It occurs in

Graded periods of infestation of a
eastern, central, and southern Africa and
susceptible host by "infected" ticks have
probably in Sri Lanka and southern India
different effects on the host. A very short
period has no effect; the animal remains

Etiology: The cause of sweating sickness
susceptible. A period just long enough to
is an epitheliotropic toxin produced by
produce a reaction may confer in1munity,
females of certain strains of Hyalomma
but if the exposure is >5 days, severe clinical
truncatum. The toxin develops in the tick,
signs and death may result. Recovery
not in the vertebrate host. Four tick salivary
confers a durable immunity, which may
gland proteins with molecular mass ranging
last <!4 yr. Other closely related forms of
from 27-33 kDA have been proposed to be

H t1uncatum toxicoses have been described.

associated with sweating sickness immunodominance, whereas a 32 kDA band salivary Clinical Findings: After an incubation
gland protein was found to be unique to a
period of 4-11 days, signs appear

TOXOPLASMOSIS

685
suddenly and include hyperthermia,
of the spleen, and congestion of the liver,
anorexia, listlessness, watering of the
kidneys, and meninges are found, in
eyes and nose, hyperemia of the visible
addition to the skin lesions. Experimentally
mucous membranes, salivation, necrosis
infected adult cattle showed typical lesions
of the oral mucosa, and hyperesthesia.

of moist eczema, and mucous membrane

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Later, the eyelids stick together. The skin
changes were accompanied by a marked
feels hot, and a moist dermatitis soon
decrease in circulating leukocytes with
develops, starting from the base of the
severe neutropenia.

ears, the axillae, groin, and perineum and
extending over the entire body. The hair

Diagnosis: For diagnosis, it is essential
becomes matted, and beads of moisture
to determine the presence of the vector.

may be seen on it. The skin becomes

'Typically, there is a generalized hyperemia
extremely sensitive and emits a sour odor. with subsequent desquamation of the Later, the hair and epidermis can be
superficial layers of the mucous membranes
readily pulled off, exposing red, raw
of the upper respiratory, GI, and external
wounds. The tips of the ears and the tail
genital tracts, and profuse moist dermatitis
may slough. Eventually, the skin becomes
followed by superficial desquan1ation of the
hard and cracked and predisposed to
skin.

secondary infection or screwworm
infestation. Affected animals are sensitive

Prevention and Treatment: Control
to handling, show pain when moving, and
of tick infestation is the only effective
seek shade.

preventive measure. Adult ticks show a

Often, the course is rapid, and death may
predilection to attach in the tail switch.

occur within a few days. In less acute cases,

Removal of ticks, symptomatic treatment,
the course is more protracted and recovery
and good nursing care are indicated.

may occur. Mortality in affected calves is

Non-nephrotoxic antibiotics and anti30%-700,1, under natural conditions.

inflan1matory agents are useful to combat

Morbidity in endemic areas is -lO"Ai. The
secondary infection. Immune serun1 can be
severity of infection is influenced by the
an effective specific treatment, although
nwnber of ticks as well as by the length of
associated with problems of donor availabiltime they remain on the host.

ity, possible serun1 contamination, and IV
administration of a relatively large volume.

Lesions: Emaciation, dehydration,

A refined precipitated irnmunoglobulin
diphtheroid stomatitis, pharyngitis,
suspension proved ineffective as a specific
laryngitis, esophagi tis, vaginitis or posthitis,
treatment, probably because of low conedema and hyperemia of the lungs, atrophy centrations of effective in1munoglobulins.

TOXOPLASMOSIS

Toxoplasrna gondii is a protozoan parasite
transplacental transfer of tachyzoites from
that infects people and other warm-blooded
mother to fetus. T gondii initiates
animals, including birds and marine
enteroepithelial replication in unexposed
man1mals (seep 1865). It has been found
cats after ingestion of uncooked meat
worldwide from Alaska to Australia.

containing tissue cysts. Bradyzoites are
released from tissue cysts by digestion in

Etiology and Pathogenesis: Felids are
the stomach and small intestine, invade
the only definitive hosts of T gondii; both intestinal epitheliwn, and undergo sexual
wild and domestic cats therefore serve as
replication, culminating in the release of
the main reservoir of infection. There are
oocysts (10 µrn dian1eter) in the feces.

three infectious stages of T gondii:

Oocysts are first seen in the feces at 3 days
tachyzoites (rapidly multiplying fom1),
after infection and may be released for as
bradyzoites (tissue cyst form), and
long as 20 days. Oocysts sporulate (become
sporozoites (in oocysts).

infectious) outside the cat within 1-5 days,

T gondii is transmitted by consun1ption
depending on aeration and temperature,
of infectious oocysts in cat feces, consun1pand remain viable in the environment for tion of tissue cysts in infected meat, and by
several months. Cats generally develop

686

TOXOPLASMOSIS
immwlity to T gondii after the initial

Diagnosis: Diagnosis is made by biologic,
infection and therefore shed oocysts only
serologic, or histologic methods, or by
once in their lifetime.

some combination of these. Clinical signs

After being consumed in uncooked meat
of toxoplasmosis are nonspecific and are

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containing tissue cysts (carnivores) or in
not sufficiently characte1istic for a definite
feed or drink contaminated with cat feces
diagnosis. Antemortem diagnosis may be
containing oocysts (all warm-blooded
accomplished by indirect hemagglutination
animals), T gondii initiates extra.intestinal assay, indirect fluorescent antibody assay,
replication. Bradyzoites and sporozoites,
latex agglutination test, or ELISA. IgM
respectively, are released and infect
antibodies appear sooner after infection
intestinal epithelium. After several rounds
than IgG antibodies but generally do not
of epithelial replication, tachyzoites emerge
persist past 3 mo after infection. Increased
and disseminate via the bloodstream and

IgM titers(> 1:256) are consistent with
lymph. Tachyzoites infect tissues throughrecent infection. In contrast, IgG antibodies out the body and replicate intra.cellularly
appear by the fowth week after infection
until the cells burst, causing tissue necrosis.

and may remain increased for years during

Tachyzoites measure 4 --6 x 2-4 µrn in
subclinical infection. To be useful, IgG
diameter. Young and irnrnunocompronlised
titers must be measured in pa.ired sera from
animals may succwnb to generalized
the acute and convalescent stages (3-4 wk
toxoplasmosis at this stage. Older animals
apart) and must show at least a4-fold
mount a powerful, cell-mediated immune
increase in titer. Additionally, CSF and
response to the tachyzoites (mediated by
aqueous hun10r may be analyzed for the
cytokines) and control infection, driving the
presence of tachyzoites or anti-T gondii
tachyzoites into the tissue cyst or bradyantibodies. Postmortem, tachyzoites zoite stage. Tissue cysts are usually seen
may be seen in tissue impression smears.

in neurons but also seen in other tissues.

Additionally, microscopic examination of

Individual cysts are microscopic, up to 70
tissue sections may reveal tl1e presence
µrn in diameter, and may enclose hundreds
of tachyzoites or bradyzoites. T gondii is
of bradyzoites in a thin, resilient cyst wall.

morphologically similar to otl1er protozoan

Tissue cysts in the host remain viable for
parasites and must be differentiated from
many years, and possibly for the life of the

Sarcocystis species and Neospora
host.

caninum.

Clinical Findings: The tachyzoite is the

Treatment: For anin1als other tl1an
stage responsible for tissue dan1age;
people, treatment is seldom warranted.

therefore, clinical signs depend on the

Sulfadiazine (15-25 mg/kg) and pyri.methnumber of tachyzoites released, the ability of an1ine (0.44 mg/kg) act synergistically and the host inunune system to linlit tachyzoite
are widely used for treatment of toxoplasspread, and the organs damaged by the mosis. Although these drugs are beneficial if
tachyzoites. Because adult irnrnunocompegiven in the acute stage of the disease when tent animals control tachyzpite spread
there is active multiplication of the parasite,
efficiently, toxoplasmosis is usually a
they will not usually eradicate infection.

subclinical illness. However, in young

These drugs are believed to have little effect
animals, particularly puppies, kittens, and
on the bradyzoite stage. Certain other
piglets, tachyzoites spread systemically and
drugs, including diarninodiphenylsulfone,
cause interstitial pneumonia, myocarditis,
atovaquone, and spiramycin are also used
hepatic necrosis, meningoencephalomyelito treat toxoplasmosis in difficult cases.

tis, chorioretin.itis, lyrnphadenopathy, and

Clindamycin is the treatment of choice for
myositis. The corresponding clinical signs
dogs and cats, at 10-40 mg/kg and 25-50
include fever, diarrhea, cough, dyspnea,
mg/kg, respectively, for 14 -2 1 days.

icterus, seizures, and death. T gondii is also an important cause of abortion and stillbirth

Prevention and Zoonotic Risk:

in sheep and goats and sometimes in pigs.

T gondii is an important zoonotic agent. In After infection of a pregnant ewe, tachysome areas of the world, as much as 600Ai of zoites spread via tl1e bloodstream to
tl1e human population has serum IgG titers
placental cotyledons, causing necrosis.

to T gondii and are likely to be persistently Tachyzoites may also spread to the fetus,
infected. Toxoplasmosis is a major concern
causing necrosis in multiple organs. Finally,
for people with immune system dysfuncin1munocompromised adult animals ( eg, tion. In these individuals, toxoplasmosis
cats infected with feline in1munodeficiency
usually presents as meningoencephalitis
virus) are extremely susceptible to develand results from the emergence of T gondii oping acute generalized toxoplasmosis.

from tissue cysts located in tile brain as

TUBERCULOSIS ANO OTHER MYCOBACTERIAL INFECTIONS

687
inununity wanes rather than from primary
to 67°C (152.6°F) or by cooling to -13°C

T gondii infection. Toxoplasmosis is also

(8.6°F). Toxoplasma in tissue cysts are also a concern for pregnant women because
killed by exposure to 0.5 kilorads of gamma
tachyzoites can migrate Lransplacentally
irradiation. Meat of any animal should be
and cause birth defects in human fetuses.

cooked to 67°C (152.6°F) before consump

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Infection with T gondii, may occur after
tion, and tasting meat while cooking or
ingestion of undercooked meat or
while seasoning should be avoided.

accidental ingestion of oocysts from cat

Pregnant women should avoid contact with
feces. To prevent infection, the hands of
cat litter, soil, and raw meat. Pet cats should
people handling meat should be washed
be fed only dry, canned, or cooked food.

thoroughly with soap and water after

The cat litter box should be emptied daily,
contact, as should all cutting boards, sink
preferably not by a pregnant woman. Gloves
tops, knives, and other materials. The stages should be worn while gardening. Vegetables of T gondii in meat are killed by contact
should be washed thoroughly before eating,
with soap and water. T gondii organisms
because they may have been contaminated
in meat can also be killed by exposure to
with cat feces.

extreme cold or heat. Tissue cysts in meat

There is currently no vaccine to prevent
are killed by heating the meat tiU'oughout
toxoplasmosis in people.

TUBERCULOSIS AND OTHER

MYCOBACTERIAL INFECTIONS

Tuberculosis (TB) is considered a

�2 mo, and M avium may survive in soil
reemerging, infectious granulomatous
for �4 yr.

disease in animals and people caused by

All types may produce infection in host
acid-fast bacilli of the genusMycobacte
species other than their own. M tuberculorium. Although commonly defined as a sis is most specific; it rarely produces
chronic, debilitating disease, TB occasionprogressive disease in animals other than ally assumes an acute, rapidly progressive
people and nonhun1an primates, infrecourse. The disease affects practically all quently in dogs and pigs, and has very rarely
species of vertebrates. The widespread
been isolated from skin lesions in exotic
occurrence of multidrug-resistant (MDR)

birds. M bovis can cause progressive
strains and extensively drug-resistant
disease in most warm-blooded vertebrates,

(XDR) strains of M tuberculosis is of
including people. M caprae, an organism
concern to clinicians and public health and
closely related to M bovis, has been isolated regulatory officials involved in the control
from people, goats, cattle, and several otl1er
of disease. Bovine TB is still a significant
species in Europe. M avium a.vium is the
zoonosis in nonindustrialized countries of
species of most importance in birds, but it
the world. Signs and lesions are generally
has a wide host range and is also patl10genic
sinillar in the various species.

for pigs, cattle, sheep, deer, mink, dogs,
cats, certain exotic hoofed animals, and

Etiology: The main types of M tuberculo
some cold-blooded animals. M avium
sis complex (mammalian tubercle bacilli)

hominissuis is the cause of tuberculosis in recognized are M tuberculosis, M canettii,
people, swine, and other animals. M gena

M bovis, M capra.e, M pinnipedii, M
vense and other pathogenic mycobacteria
micro ti, M mungi, and M africanum. The are infrequently isolated from exotic and

M avium complex includes M avium
free-living wild and domestic birds ( see
avium (avian tubercle bacilli), M avium
p 692). M intracellulare causes disease in
hominissuis (isolated from people, swine,
cold-blooded animals and has been isolated
and other manunals ), and M intracellulare.

from many other species.

The types differ in cultural characteristics
and pathogenicity. Several serovars of M

Pathogenesis: Inhalation of infected
avium avium are recognized; however,
droplets expelled from the lungs is tile usual
only serovars 1, 2, and 3 are patl10genic for
route of TB infection, although ingestion,
birds. M bovis may sruvive on pasture for
particularly via contaminated milk or water,

688

TUBERCULOSIS AND OTHER MYCOBACTERIAL INFECTIONS
also occurs. Intrauterine and coital methods

Diagnosis: The single most inlporta.nt
of infection are recognized less commonly.

diagnostic test for TB is the i.ntradem1al

Inhaled bacilli are phagocytosed by alveolar tuberculin test. Old tuberculin prepared macrophages that may either clear the
from the cultme filtrate of M tuberculosis

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infection or allow tl1e mycobacteria to
is used to detect disease in nonhuman
proliferate. In tl1e latter instance, a prin1ary
prin1ates exposed to M tuberculosis or
focus may form, mediated by cytokines

M bovis. In other animals, purified protein associated with a hypersensitivity reaction
derivatives (PPDs) prepared from tl1e
that consists of dead and degenerate
culture filtrate of M bovis or M avium can macrophages surrounded by epithelioid
be used. Diagnosis based on clinical signs
cells, granulocytes, lymphocytes, and later,
alone is very difficult, even in advanced
multinucleated giant cells. The purulent to
cases. Radiography is useful in nonhmnan
caseous, necrotic center may calcify, and
primates and small animals. Microscopic
the lesion may become surrounded by
exanlination of sputum and other disgranulation tissue and a fibrous capsule to charges is sometimes used. Necropsy
fom1 the classic "tubercle." The primary
findings of the classic "tuberculous"

focus plus similar lesions formed in the
granulomas are often very suggestive of the
regional lymph node is known as the
disease. Confirmation of diagnosis is by

"primary complex." In alin1entary forms of isolation and identification of the organism,
disease, tl1e primary focus may be found in
with culture usually taking 4-8 wk, or
the pharynx or mesenteric lymph nodes or,
by PCR, which requires only a few days.

Jess commonly, in the tonsils or intestines.

Molecular techniques, such as restriction

The cellular composition of and presence of
fragment length polymorphism (RFLP) or
acid-fast bacilli in tuberculous lesions differ
variable number tandem repeat (VNTR)

between and witllin host species.

provide definitive information useful in

The primary complex seldom heals in
animals and may progress slowly or rapidly.

conducting epidenliologic investigations.

Dissemination through vascular and

The delayed-type hypersensitivity
lymphatic channels may be generalized and
response of the host, responsible for much
rapidly fatal, as in acute miliary TB. Nodular
of the pathology of TB, is fundan1ental to
lesions may form in many organs, including
the tuberculin skin test widely used for
tl1e pleura, peritoneum, liver, kidney, spleen, diagnosis in large aninlals. The single skeleton, mammary glands, reproductive
intradermal (SID) test involves inoculation
tract, and CNS. A prolonged, chronic course
of PPD prepared by precipitation of protein
may also ensue, with lesions usually having
from the culture filtrate of M bovis. PPD
a more localized pattern of distribution.

preparations in1prove specificity. In a
reactor, the antigen stimulates a local
infiltrate of inflanm1atory cells and causes

Clinical Findings: The clinical signs of TB skin swelling tJ1at can be detected by reflect the extent and location of lesions.

palpation and measured by calipers. The

Generalized signs include progressive
reaction is read at 48---72 lu· for maximmn
emaciation, lethargy, weakness, anorexia,
sensitivity and at 96 hr for maximlUll
and a low-grade, fluctuating fever. The
specificity. Test sites used vary in sensitivity
bronchopneun10nia of the respiratory fonn
and between countries/areas and include
of the disease causes a chronic, intemlittJ1e neck region, caudal fold at the tail base, tent, moist cough with later signs of
and vulval lip. One disadvantage of the
dyspnea and tachypnea. The destructive

M bovis SID test is that cross-reactions may lesions of the granulomatous bronchopneuoccur in anin1als infected with M kansasii, monia may be detected on auscultation and

M avium, M tuberculosis, M avium
percussion. Superficial lymph node
paratuberculosis, or other mycobacteria
enlargement may be a useful diagnostic sign that share some antigenic determinants when present. Affected deeper lymph nodes
withM bovis.

cannot always be palpated, but they may

In areas with a high incidence of avian
cause obstruction of the airways, pharynx,

TB or other mycobacterial infections such
and gut, leading to dyspnea and runlinal
as paratuberculosis, the comparative
tympany.

tuberculin skin test can be used, with

In pigs, lesions caused by M avium homi
biologically balanced M bovis and M avium nissuis or M avium avium are most often PPD tuberculins inoculated sinlultaneously
seen in lymph nodes associated with the
but at separate sites in the neck The agent

GI tract, although generalized disease
causing sensitization provokes the greater
involving the liver, lung, and spleen does
skin reaction. Other diagnostic tests used
occur.

for TB include the thermal test, which may

TUBERCULOSIS AND OTHER MYCOBACTERIAL INFECTIONS

689
detect a pyrexic peak (104°F [>40°C]) at
slaughter has been used widely in tile UK,

6----8 hr after SC inoculation with tuberculin.

USA, Canada, Germany, New Zealand, and

The Stormont test uses an intradermal

Australia. In some European countries,
inoculation of PPD followed by a second
where test and slaughter would have been

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inoculum at the same site 7 days later. The
impractical, varying forms of test and
test is read for swelling 24 hr later.

segregation have been used, witll test and

False-negative results may occur in
slaughter used only in the final stages of
animals with poor immune response such
eradication.

as those in the early stages of infection,

The BCG (bacille Calmette-Guerin)

nonresponsive cases in advanced disease, or
vaccine, sometin1es used to control TB
old animals. Cattle that have recently calved
in people, has proved to provide little
may also have false-negative results. Current
protection against virulent M bovis in most research is focused on the identification
animal species, and inoculation often
of antigens such as secretory proteins and
provokes a severe local granulomatous reacgenetically engineered proteins of M bovis for tion. Moreover, ECG-vaccinated animals use in improved in vitro diagnostic tests.

usually respond on the tuberculin skin test.

Serologic tests such as ELISA appear to be of
limited diagnostic use, consistent with the

CATTLE
lesser role of antibody compared with the
cellular immune response in TB. In vitro

Most of tile general discussion above
cellular assays have been developed (ie,
applies to bovine TB. The introduction of
interferon--y assay) using WBCs stimulated
milk pasteurization was a major step in the
with M bovis antigen and may be used as a
fight against Mycobacterium bovis TB and
supplemental test to the widely used SID test;
continues to be an important control
however, they have not come into widespread procedure in many nonindustrialized use in many nonindustrialized countries
countries.

because of cost and the necessity to conduct
cellular assays in the laboratory witllin 24 hr

SHEEP AND GOATS
after collection of blood specin1ens.

Lesions caused by Mycobacterium bovis in
the lungs and lymph nodes of sheep and

Control: The main reservoir of M bovis
goats are similar to tllose seen in cattle, and
infection is cattle. However, other animals
the organism may sometimes disseminate
have been found to be reservoirs in some
to oilier organs. Sheep and goats are quite
countries, including badgers and red deer
resistant to M tuberculosis infection. The

(England, Ireland); red deer, possums, and
intradermal skin test is commonly used for
ferrets (New Zealand); mule deer, whitediagnosis. The comparative tuberculin skin tailed deer, elk, and American bison (North
test conducted in tile cervical region using

America); African buffalo (South Africa);
biologically balanced pwified protein
and water buffalo (Australia). The
dclivative tuberculins of M bovis and
prevalence of disease in such reservoirs

M avium can be used to differentiate
influences the incidence of disease in other
sensitization to oilier mycobacteria. The
species. Carnivores and scavengers can
responses should be observed at 48 and
acquire M bovis by consumption of infected

72 hr for induration and swelling.

carcasses. These species include lion,
coyote, wolf, hyena, cheetall, black bear,

DEER AND ELK
bobcat, and leopard. Warthogs, ferrets,
raccoon, European wild boar, opossums,

Tuberculosis due to Mycobacterium bovis
and feral pigs have also been found to be
is an important problem in most species of
infected withM bovis.

farmed and wild cervids, including axis

The three principal approaches to the
deer, fallow deer, roe deer, mule deer, sika
control of TB are test and slaughter, test and deer, as well as red deer/elk/wapati. Deer segregation, and chemotllerapy. The test
appear to be unusually susceptible to M
and slaughter policy is the only one assured
bovis infections. M avium infections may of eradicating TB and relies on tile slaughter
produce sinlilar lesions. M tuberculosis
of reactors to the tuberculin test. In an
infection is tmcomn1on. Tuberculous
affected herd, testing every 2 mo is
lesions may be confined to isolated lymph
recommended to rid tile herd of individuals
nodes of tile head, or they may be found
tllat can disseminate infection. Routine
extensively in lymph nodes and organs
hygienic measures aimed at cleaning and
after a rapid, fulminating disease course.

disinfecting contaminated food, water

Abscessation in deer should always raise
troughs, etc, are also useful. Test and
suspicions of tuberculosis. A presumptive

690

TUBERCULOSIS AND OTHER MYCOBACTERIAL INFECTIONS
diagnosis may be made using the tuberculin
tl1e ear or in skin of the vulva is often useful
skin test and/or by in vitro cellular assays
for diagnosis. Test responses should be

(blood lymphocyte immune-stimulation test obse1ved at 48 hr after iJ\iection of tuberculin.

or 'I interferon assay), or a combination of

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these tests. Infection should be confirmed

DOGS
by an organism-based test.

Dogs may be infected with Mycobacterium

HORSES
tuberculosis, M bovis, and occasionally with M avium complex or Mfortuitum,

Horses are relatively resistant to tuberculocommonly from a hwnan or bovine source.

sis caused by Mycobacterium tuberculosis; Tuberculous lesions are usually found in the however, they are susceptible to M bovis.

lungs, liver, kidney, pleura, and peritoneum;

When tuberculosis does develop, tubercuthey have a gray appearance, usually with a lous, noncalcified lesions are often found in
noncalcified, necrotic center. Lesions a.re
the liver, mesenteric lymph nodes, lungs,
often exuda.tive and can produce a large
and other sites. Tuberculin test results are
quantity of straw-colored fluid in the thorax.

rather erratic.

False-negative tuberculin tests a.re often seen
in dogs. Ra.diogra.ph.s and a thorough lustory

ELEPHANTS
are useful in diagnosis. Treatment is not
often recommended. Affected dogs in close

Tuberculosis due to Mycobaclerium
contact with people should be euthanized
tuberculosis has been reported in captive
because of public health concerns.

elephants. Lesions most often involve the
lw1g and associated lymph nodes. Nonspe

CATS
cific responses are obse1ved on tuberculin
skin tests and on some in vitro in1munologic

Ca.ts are quite resistant to infection with
tests; therefore, diagnosis should be made

Mycobaclerium tuberculosis but are
on an organis m -based test of trunk washes.

susceptible to M bovis, M avium complex, or Multidrng regin1ens, including isoniazid

M micmti. M lepraemurium has been
and rifan1pin, have been developed that
isolated from granuloma.tous lesions in the
eliminate shedding of M tuberculosis in
skin. Some unclassified acid-fast bacilli have
discharges and mininuze development of
also been isolated. Contaminated nulk
mug-resistant strains. It is important to
ca.using GI tract lesions, typically in the
emphasize that d!ug sensitivity tests should
mesente1ic lymph nodes, is tl1e most
be conducted to determine the susceptibility common circumstance, and historically this of the organism. Also, blood concentrations
was responsible for a very high percentage of
should be monitored periodically to confinn
tuberculous ca.ts in Europe. Rapid, hema.togthey are high enough to kill the bacte1ia.

enous dissemination to other organs,
including tl1e lungs and regional lymph

PIGS
nodes, can occur. Infected skin or deeper
wounds sometimes give rise to tuberculous

Pigs are susceptible to M tuberculosis,
sinuses. Lesions have a central area of

M bovis, and M avium complex. M avium necrosis, usually witl10ut calcification. The
avium and M avium hominissuis are most tuberculin skin test is considered unreliable
frequently isolated; serologic identification of in cats. Diagnosis may be assisted by isolates is useful in epiderniologic investigaradiography and ELISA Identification of tl1e tions. Granulomatous lesions are most often
organism is necessary to confirm a diagnosis.

fow1d in the cervical, submandibular, and

Efficacious treatment protocols are not
mesenteric lymph nodes, but in advanced
available. Therefore, it is recommended tl1a.t
disease lesions may also be found in the liver
ca.ts infected with M bovis be eutha.nized
and spleen. Typically, enlarged nodes contain because of public health concerns.

small, white or yellow, caseous foci, usually
without any evidence of mineralization. Pigs

RABBITS
witl1 disease due toM tuberculosis may
have similar regionalized lesions. Pigs are

Naturally occurring, or so-called spontaneparticularly susceptible toM bovis, which ous tuberculosis in rabbits is an unconunon
is usually acquired from shared grazing or
fu1ding; most cases are ca.used by Mycobac
ingestion of contaminated dairy products.

terium bovis or M avium. Rabbits

This can ca.use a rapidly progressive,
apparently become infected when exposed
disseminated disease with caseation and
to other tuberculous a.nin1als or by ingesting
liquefaction of lesions. The single intra.dermilk from tuberculous cattle. M avium has mal test conducted on the dorsal surface of
been reported in rabbits that are housed in

TUBERCULOSIS AND Orn ER MYCOBACTERIAL INFECTIONS

691
close contact with domestic or exotic
isolates. Efficacy is lin1ited, and there are
birds infected with M avium. Rabbits are
overriding argu.n1ents against therapy, based
relatively resistant to M tuberculosis; such on the removal of infected animals, zoonotic
infections are seldom reported. Rabbits
risks, and the danger of developing drng

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infected with M avium complex may
resistance. Exacerbations may occm·.

develop miliary lesions involving the Jung
and liver. Tuberculin skin tests may be

FREE-RANGING AND CAPTIVE
conducted on the skin of the abdomen. Test
sites should be observed for induration and

HOOFED ANIMALS
swelling at 24 and 48 hr after injection of

The major wildlife reservoirs of Mycobacte

M bovis purified protein delivative.

rium bovis infection in addition to cervids are Afiican buffalo, wood bi.son, North

GUINEA PIGS

American bi.son, white-tailed and mule deer,
lechwe, and elk. Also, brushtail possums and

Guinea pigs are quite susceptible to infection

European badgers are considered reservoirs
with either Mycobactmium tuberculosis or
of M bovis infection. Other species in which M bovi,S. Lesions are most often seen in the M bovis infection has been rep01ted but not parenchyma of the Jung and adjacent lymph
in1plicated as rese1voirs and are considered
nodes. Also, guinea pigs are susceptible to
spillover hosts include fennic fox, coyote,
certain serovars of M avium complex with

Arabian oryx, muntjac, in1pala, sitatunga,
lesions seen in lymph nodes associated with
sp1ingbok, moles, voles, hares, eland, yak,
the GI tract. Tuberculin skin tests can be
bactrian can1el, wildebeest, European wild
conducted by injection of purified protein
goat, large spotted genet, tapir, moose, otters,
delivative of M bovis and of M avium ( 1: 100
feral water buffalo, hedgehogs, European
dilution containing 5,000 tuberculin units) at wild boar, greater kudu, tiger, white and
separate sites in the skin of the abdomen.

black rhinoceros, and giraffe. M tuberculosis

'TI1e preferred iajection site is 2 cm posterior
has been isolated from oryx, black rhinocto the xyphoid cartilage and 2 cm lateral on eros, Asian elephant, addax, and Rocky
each side of the Jinea alba. The iajection sites

Mountain goats. Tuberculous lesions vary in
should be observed at 24 and 48 hr for induraconsistency from purulent to caseous and tion and swelling. The presence of erythema
often involve the lungs and regional lymph
at the injection site is of little or no signifinodes, with liver, spleen, and serosal surfaces cance.

as other potential sites. Tuberculin skin tests
are conducted in the cervical region using

NONHUMAN PRIMATES

M bovis purified protein derivative (PPD)

containing 5,000 tuberculin units prepared

In monkeys and large apes, Mycobactmium
for veterinary use. Nonspecific responses
tuberculosis, M bovis, andM avium
may occur in some species with no hi.story of
complex can cause severe disease of the
tuberculosis. Therefore, it may be necessary
lungs and other organs. Epidemics in plimate to use biologically balanced PPDs prepared colonies may be caused by contact with
from M avium and M bovis iajected at infected human caregivers. Transmission is
separate injection sites. Skin tests are
usually by aerosol with respiratory infection,
observed for swelling and induration at
but the oral route is also possible. Bacilli may

48and 72hr.

also be shed in mine. Old tuberculin is used
in skin tests in preference to purified protein
derivative (PPD), because it provides greater

MARINE MAMMALS
sensitivity in detecting animals infected with

Mycobacterium pinnipedii ( a seal-adapted

M tiiberculosis or M bovis. Biologically variant of M bovis) causes tuberculous
balanced PPDs prepared from M bovis or
lesions in fur seals and sea lions. The

M avium can be injected intradem1ally at
organism has been isolated from four species
separate sites on the abdomen to conduct a
of fur seals and two species of sea lions in
comparative test. Skin tests are observed at
several countries as well as from some

24, 48, and 72 hr for induration and swelling.

other animals. In seals, the organism causes

Tuberculins prepared for use in people are
lesions in the peripheral lymph nodes,
not of sufficient potency to elicit a response
spleen, peritoneun1, and lungs. The presence
in no.nhU111an plimates. Treatment of cases of of acid-fast organisms in the granulomatous tuberculosis in nonhU111an plimates has been
lesions va.iies. Aerosols are considered the
attempted using drugs that have had success
main route of transmission. Because of the
in people, eg, isoniazid, ethan1butol, and
zoonotic risk, precautions should be taken

1ifarnpin. Drug sensitivity tests should be
when handling these animals. (See also
conducted to deteffi1ine sensitivity of

MYCOBACTERIOSIS IN MARINE MAMMAI.S, p 1863.)

692

TUBERCULOSIS AND OTHER MYCOBACTERIAL INFECTIONS

MYCOBACTERIAL INFECTIONS
pigs, cattle, and certain nonhuman primates.

OTHER THAN TUBERCULOSIS

M xerwpi, a slowly growing scotochromogen, has been isolated from pigs, seafowl, Mycobacteria found in soil and water have
and amphibians. These organisms should

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been isolated from tissues of animals.

be differentiated from M gordonae and

Mycobacleliumfoituitum, a rapidly growing M .fla,vescens and from other slowly growing organism highly resistant to penicillin G,
scotochromogenic mycobacteria that are
streptomycin, ampicillin, sulfamethoxazole,
common contaminants of water.

and chloramphenicol, has been associated

Numerous nonpathogenic, nonphotowith mastitis in cows, pulmonary infections chromogenic mycobacteria that closely
in dogs, lymph node lesions in pigs and
resemble potential pathogens can be
certain exotic animals, and cutaneous lesions isolated from water and soil; M nonchromo
in cats and dogs. Drug susceptibility tests
genicum, M gastri, M triviale, and
indicate the organism is inhibited by

M terrae, which closely resemble strains of capreomycin and by ethionamide. M chew
the M avium complex, may be differenti
nae, another rapidly growingMycobaclelium ated by in vitro laboratory examinations, similar to Mfortuitum in biochemical
including molecular techniques.

reactions, has been isolated from contami

Although opportunistic mycobacteria
nated wounds and ir\jection abscesses.

usually do not produce progressive disease,

These organisms must be distinguished
they may be important in inducing transient
fromM phlei, M srnegmatis, andM vaccae,
tuberculin skin sensitivity in animals. The
which are rarely if ever pathogenic.

application of comparative skin tests, using

Fish and other cold-blooded animals
biologically balanced purified protein
may be infected with M marinum, certain
derivative tuberculins prepared from culture
serovars of M avium complex, or M intra
filtrates of M bovis and M avium, provides cellula,re, which have been recognized as
useful information on tl1e possible cause of
human pathogens. A photochromogenic
tuberculin skin sensitivity. Tuberculins
organism, M kansasii, has been isolated prepared for veterinary use, containing
from pigs, cattle, and nonhuman primates.

-5,000 tuberculin units per test dose, should

These organisms can be differentiated by
be used for skin tests in free-ranging,
biochemical and seroagglutination tests.

captive, wild, and exotic aninlals.

M avium paratuberculosis, the cause of

M lepraemurium, a nonphotochromo

Johne's disease, has been isolated from
genic, slow-growing, acid-fast bacillus,
domestic and wild ruminants (see al.so
causes a disease in cats and rats similar in

PARATUBERCULOSIS, p 762). It is a slowly
some respects to leprosy in people. It can
progressive diarrheal disease resulting in
be grown on media containing cytochrome
weight loss and emaciation. Lesions are

C and a-ketoglutarate. M leprae, the cause
most often seen in the ileocecal valve and
of leprosy in people, has been found in
associated lymph nodes. Diagnosis should
spontaneously occuning disease in
be based on an organism-based test. No
armadillos. This organism has not been
treatment is available.

grown on artificial culture medium;

M scrofulaceum, a scotochromogen, has
however, M leprae DNA can be identified
been isolated from lymph node lesions in
by molecular techniques.

TULAREMIA

Tularemia is a bacterial septicemia that
ing, gram-negative coccobacillus antiaffects >250 species of wild and domestic genically related to Biucella spp. It is a
mammals, birds, reptiles, fish, and people.

facultative intracellular parasite that is

It is listed as a category A bioterrorism
killed by heat and proper disinfection but
agent because of the potential for fatality,
survives for weeks or months in a moist
airborne dissemination, and societal
environment. It can be cultured readily on
disruption if released.

blood supplemented with cysteine but must
be differentiated from other gram-negative

Etiology: The causative bacterium,
bacteria on blood agar. The taxonomic

Prancisella tularensis, is a nonspore-form-
status of Francisella has been revised and

TULAREMIA

693
debated, but recent consensus establishes
infected tick, but people who prepare or
the subspecies F tularensis tularensis,
eat improperly cooked wild gan1e are also
associated with type A tularemia; F
at increased risk. Dogs, cats, and other
tularensis holarctica, which causes type B
carnivores may acquire infection from

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tularemia; and a third type, C, associated
ingestion of an infected carcass. Case
with F novicida, which has low virulence
reports have implicated cats as a source
and is less common than the other two.

of infection in people.

Type A has been found predominantly in

North Ame1ica and is more virulent; in

Clinical Findings: The incubation period
people, the mortality rate may be as high as
is 1-10 days. The most severely and

3()0A, if untreated. Type Bis less virulent and
conm10nly affected livestock species are
occurs in both the Old and New Worlds.

sheep; Type A tularemia is particularly
pathogenic for lagomorphs, and cats and

Epidemiology and Transmission:

nonhuman primates have been reported to

Among domestic animals, sheep are the
be infected. The clinical presentation
most common host, but clinical infection has depends on host species, subspecies of the also been reported in cats, dogs, pigs, and
bacteria, and route of infection. Sheep and
horses. Cats are at increased risk because
cats may be subclinically infected or
of predatory behavior and appear to have
develop bacteremia, fever, and respiratory
an increased susceptibility, whereas cattle
infection. Cats may also develop ulceroglanappear to be resistant. Little is known of the dular or oropharyngeal disease, presumably
true incidence and spectrum of clinical
through exposure to infected prey items.

disease in domesticated animals. Important

Clinical signs include increased pulse and
wild animal hosts for F tularensis tularen
respiratory rates, coughing, diarrhea, and
sis include cottontail and jackrabbits,
pollakiuria with lymphadenopathy and
whereas the most common vectors are the
hepatosplenomegaly. Prostration and death
ticks Dernwcentor andersoni (the wood
may occur in a few hours or days. Sporadic
tick), Amblyomma americanum (the lone
cases are best recognized by signs of
star tick), D variabilis (the American dog
septicemia. Outbreaks in untreated lambs
tick), and Chrysops discalis (the deer fly).

may have up to 15% mortality.

Animal hosts of F tularensis holarctica are lagomorphs, beaver, muskrat, voles, and

Lesions: The most consistent lesions are
sheep. Ticks, flies, fleas, and exposure
rniliary, white to off-white foci of necrosis in
to contaminated water sources are all
the liver and sometimes in the spleen, lung,
associated with transmission of this
and lymph nodes. Organisms can be readily
subspecies, which has also been found to
isolated from necropsy specinlens by use of
persist naturally in a water-associated
special media. The infective dose required to
amoeba
transmit this pathogen is extremely low; thus,

Natural foci of infection exist in North
risk of infection dming necropsy or to

America and Eurasia. Although found in
laboratory personnel is significant, and
every state except Hawaii, tularemia is most
special procedures and facilities are essential.

often reported in the southcentral and
western USA ( eg, California, Missouri,

Diagnosis: Tularemia must be differenti

Oklahoma, South Dakota, and Montana).

ated from other septicemic diseases

Tularemia can be transmitted by aerosol,

( especially plague and pseudotuberculosis)

direct contact, ingestion, or arthropods.

or acute pneumonia. When large nun1bers of

Inhalation of aerosolized organisms (in the
sheep show typical signs during periods of
laboratory or as an airborne agent in an act
heavy tick infestation, tularemia or tick
of bioterrorism) can produce a pneumonic
paralysis (seep 1314) should be suspected.

form. Direct contact with, or ingestion of,

Tularemia should be considered in cats with
infected carcasses of wild anin1als ( eg,
signs of acute lymphadenopathy, malaise,
cottontail rabbit) can produce the
oral ulcers, and history of recent ingestion
ulceroglandular, oculoglandular, oropharynof wild prey.

geal (local lesion with regional lymphadeni

Diagnosis of acute infection is confirmed
tis ), or typhoidal form. Immersion in or
by culture and identification of the
ingestion of contaminated water can result
bacteriun1, direct or indirect fluorescent
in infection in aquatic anin1als. Ticks can
antibody test, or a 4-fold increase in
maintain infection transstadially and
antibody titer between acute and convalestransovarially, making them efficient cent serum specimens. A single titer of �1:80
reservoirs and vectors.

by the tube agglutination test is presumptive

The most common source of infection
evidence of prior infection. When tularemia
for people and herbivores is the bite of an
is suspected, laboratmy personnel should

694

TULAREMIA
be alerted as a precaution to reduce the risk
tetracycline and chloramphenicol are
of laboratory-acqulred infection. In some
bacteriostatic, they should be continued
jurisdictions, tularemia in animals is
for 14 days to minimize the risk of relapse.

reportable to public health authorities.

Early treatment is important to minimize

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1isk of fatality. Because of the substantial

Treatment and Control: Streptomycin,
sylvatic ( wildlife and tick) component of the
gentamicin, and tetracyclines are effective

Francisella life cycle, control is limited to at recommended dose levels. Gentamicin
reducing arthropod infestation and to rapid
should be continued for 10 days. Because
diagnosis and treatment.

VESICULAR STOMATITIS

Vesicular stomatitis is a viral disease caused
and 2012. The largest outbreak in the past
by two distinct serotypes of vesicular
decade occurred in 2005 and affected nine
stomatitis virus-New Jersey and Indiana.

states. Vesicular stomatitis viruses are

Vesiculation, ulceration, and erosion of the
endemic in South America, Central America,
oral and nasal mucosa and epithelial sruface and parts of Mexico but have not been seen of the tongue, coronary bands, and teats are
naturally outside the Western hemisphere.

typically seen in clinical cases, along with

The virus can be transmitted through direct
crusting lesions of the muzzle, ventral
contact with infected animals with clinical
abdomen, and sheath. Clinical disease has
disease (those with lesions) or by bloodbeen seen in cattle, horses, and pigs and feeding insects. In the southwestern USA,
very rarely in sheep, goats, and llan1as.

black flies (Sirnulidae) are the most likely

Serologic evidence of exposure has been
biologic insect vector. In endemic areas,
found in many species, including cervids,
sand flies (Lutzomyia) are proven biologic
nonhuman primates, rodents, birds, dogs,
vectors. Other insects may act as mechanical
antelope, and bats.

vectors. Exposure to insects that carry the
virus is often associated with nearby moving

Etiology: The viruses are members of the
water sources such as creeks or rivers or
family Rhabdoviridae and genus Vesiculovi' irrigation of pastures. Experimental studies rus. Vesicular stomatitis viruses are the
have shown that feeding of infected insects
prototypes of the Vesicutovirus genus.

on mucosa! srufaces and nonhaired areas of

They are bullet shaped and generally 180 nm the body were more often associated with long and 75 nm wide. The genomic structure development of lesions at those sites than if is a single strand of negative-sense RNA
insects fed on haired areas of the body. The
composed of five genes (N, P, M, G, and L,
prevalence of clinical cases in a herd is
representing the nucleocapsid protein,
generally low (10%-209fi), but seroprevalence
phosphoprotein, matrix protein, glycowithin the herd may approach lOOOAi. Viremia protein, and the large protein, which is a
has not been detected in livestock species
component of the viral RNA polymerase).

that exhibit clinical signs of vesicular

Although there are many members of the
stomatitis, although experimental studies

Vesiculovirus genus, the New Jersey and
have shown transmission of virus, presum

Indiana serotypes are of particular interest
ably via lymphatics, between co-feeding
in the Western hemisphere. These two
black flies on cattle. Virus is routinely
viruses are sinlilar in size and morphology
isolated from active lesions in affected
but generate distinct neutralizing antibodies animals, and these lesions serve as a source in infected animals. They have both been
of virus spread by direct contact and contamisolated in recent outbreaks in the USA.

ination of shared feed and water stations.

Many vertebrate species have serologic

Epidemiology and Transmission:

evidence of exposure and may serve as reser

Vesicular stomatitis is seen sporadically in
voirs of infection. No definitive reservoir or
the USA. Outbreaks historically occurred in
amplifying host of vesicular stomatitis
all regions of the country but since the 1980s
viruses in the USA has been identified.

have been limited to western states and
occur seasonally, usually May through

Clinical Findings: The incubation period

October. Outbreaks occurred in the USA in
is 2-8 days and is typically followed by a

1995,1997,1998,2004,2005,2006,2009,2010, fever. By the time animals develop other

VESICULAR STOMATITIS

695
signs and are exanlined, however, they are

Treatment, Control, and Prevention:

rarely febrile. Ptyalism is often the first sign

No specific treatment is available or
of disease. Vesicles in the oral cavity are
warranted. Cachexia can be avoided by
rarely seen in naturally occurring cases
providing softened feeds. Cleansing lesions
because of rupture soon after formation;

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with mild antiseptics may help avoid
therefore, ulcers are the most common
secondary bacterial infections. Management
lesion seen during initial exan1ination.

factors suggested to reduce risk of exposure

Ulcers and erosions of the oral mucosa,
to the virus include limiting time on pasture
sloughing of the epithelium of the tongue,
dming insect season, providing shelters or
and lesions at the mucocutaneousjunctions
barns during insect feeding times, and
of the lips are commonly seen in both cattle
implementing other procedures that reduce
and horses. Ulcers and erosions on the teats
aninlal contact with insects, such as
are not uncommon in cattle and may result
application of insecticides. This should
in secondary cases of mastitis in dairy cows.

include application to the inner surface

Coronitis with erosions at the coronary band of the pinna, where black flies feed. If are seen in some cattle, horses, and pigs,
livestock need to be kept on pasture during
with subsequent development of lameness.

outbreaks of vesicular stomatitis, then

Crusting lesions of the muzzle, ventral
keeping them pastured away from moving
abdomen, sheath, and udder of horses are
smface water (such as streams, irrigation
typical during outbreaks in the western USA. canals, or rivers) may reduce the risk of Loss of appetite due to oral lesions, and
exposure to Vesiculovirus. Affected aninlals lan1eness due to foot lesions, are nom1ally
should be isolated, and movement of other
of short duration, because the disease
anin1als from the affected premises
is generally self-limiting and resolves
restricted. Vesicular stomatitis is a
completely within 10-14days. Virus-neutralreportable disease in most areas, including izing antibodies to either serotype persist
the USA, so state and federal aninlal health
and have been documented in individual
officials must be notified when it is
horses that had previous clinical disease for
suspected. Commercially produced

>8 yr after an outbreak, but reinfection can
vaccines are not available in the USA, but
occur after a second exposure.

vaccines for livestock are available in some

Latin American countries.

Diagnosis: In most areas, including the

Veterinarians act as a part of the surveil

USA, vesicular stomatitis is a reportable
lance network as they examine animals
disease. Samples for diagnostic purposes are
involved in shows, exhibitions, races, and
generally taken by a foreign anin1al disease
interstate or international movement in order
diagnostician or other regulatory veterinarto write a health certificate (ie, ce1tificate of ians and are tested by officially designated
veterinary inspection). When practitioners
government laboratories. Diagnosis is based
observe suspect cases of vesicular stomatitis,
on the presence of typical signs and either
they should report to both their state and
antibody detection through serologic tests,
federal animal health officials. Reporting will
viral detection through isolation, or detecprompt a regulatory investigation. Mucosa!

tion of viral genetic material by molecular
swab and serum samples from suspected
techniques. San1ples for viral isolation may
animals are submitted for testing to
include vesicular fluid, epithelial tags from
veterinary diagnostic laboratmies. During
lesions, or swabs of lesions. Vesicular
outbreak years, data regarding laboratorystomatitis viruses are easily propagated in confinned cases of vesicular stomatitis, along
cell culture. Three commonly used serologic
with the number of premises with cases, are
tests are competitive ELISA, virus neutralizaposted on the Web site of the Animal and tion, and complement fixation. PCR tests

Plant Health Inspection Se1vice of the USDA.

may also be used to identify the virus. Of
primary concern in diagnosis is differentia

Zoonotic Risk: The vesicular stomatitis
tion of vesicular stomatitis from clinically
vi.ruses are zoonotic and may cause
indistinguishable but much more devastating self-limiting influenza-like disease (headviral diseases, including foot-and-mouth ache, fever, myalgia, and weakness) lasting
disease in ruminants and swine (seep 629),

3--5 days in people working in close contact
swine vesicular disease (seep 735), and
with the virus ( eg, laboratory exposure,
vesicular exanthema of swine (seep 738).

direct contact with lesions in infected

Horses are not susceptible to foot-andaninlals ). Rarely, people can develop vesicles mouth disease. Both noninfectious and
on the buccal and pharyngeal mucosa, lips,
infectious causes of oral lesions must be
and nose. More severe signs, including
considered.

encephalitis, are rare.

696

AFRICAN HORSE SICKNESS

AFRICAN HORSE SICKNESS

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African horse sickness (AHS) is an insectdisappears when cold weather stops or borne, viral disease of equids that is endemic
significantly reduces vector activity. The
to sub-Saharan Africa It can be acute,
virus also has been isolated from the dog tick
subacute, or subclinical and is characterized

Rhipice'f)halus sanguineus sanguineus,
by clinical signs and lesions associated with
and the can1el tick Hyalomma dromedarii
respiratory and circulatory irnpainnent.

dilling the winter in southern Egypt, where
the disease is endemic. AHSV has apparently

Etiology and Epidemiology: AHS is
been transmitted between dogs by infected
caused by African horse sickness virus
mosquitoes. Furthermore, dogs, and possibly

(AHSV), which is 55--70 nm in diameter
large African carnivores such as lions and
and of the genus Orbivirus in the family
leopards, can be infected by ingestion of

Reoviridae. There are nine immunologically
meat from AHSV-infected equids. However,
distinct serotypes of AHSV. The virus is
it is generally considered that dogs and other
inactivated at a pH of <6 (but is stable at
large carnivores, ticks, and mosquitoes play
higher pH), or by formal.in, !3 -propiolactone,
little part in the epidemiology of AHS.

acetylethyleneimine derivatives, or radiation.

In endemic regions of Africa, the

Clinical Findings and Lesions: Mortalappearance of AHS may be preceded by ity depends on the vintlence of tl1e particseasons of heavy rain that alternate with ular AHSV strain and susceptibility of the
hot and dry climatic conditions, which favor
host. In naive populations of horses, which
transmission by the insect (biting midge)

are the most susceptible equids, mortality
vector. Outbreaks in central and east Afiica
may reach 900/o in epidemics. The acute
have occasionally extended to Egypt,
respiratory forn1 is characterized by an
the Middle East, and southern Arabia In
incubation period of 3-5 days, interlobular

1959-1961, a major epidemic, caused by
edema, and hydropericardium. Death

AHSV serotype 9, extended from Africa
occurs in -1 wk. A fever of 40°--40.5°C
through the Near East and Arabia as far as

(104°-105°F) for 1-2 days is followed by

Pakistan and India, causing the deaths of an
dyspnea, spasmodic coughing, and dilated
estin1ated 300,000 equids. A further epidemic
nostrils. The animal stands with its legs
of the same serotype in 1965--1966 centered
apart and head extended. The conjunctivae
on northwest Africa (Morocco, Algeria,
are congested, and tl1e supraorbital fossae
and Tunisia) but also extended briefly into
may be edematous. Recovery is rare, and
southern Spain. This outbreak in Spain was
the animal dies of anoxia, congestive heart
eliminated by a vigorous vaccination and
failure, or both. At necropsy, pulmonary
slaughter campaign. In July 1987, AHS
edema is especially visible in the intralobucaused by AHSV serotype 4 was 1'eported lar spaces. The lungs are distended and
in central Spain, due to the importation of
heavy, and frotl1y fluid may be foU11d in the
infected zebra from Namibia The outbreak
trachea, bronchi, and bronchioles. There
lasted until the cold weather started in
may be pleural effusion. Thoracic lymph

October 1987; however, the virus survived
nodes may be edematous, arid the gastric
the winter and caused disease in southern
fundus may be congested. Petechiae are

Spain, Portugal, and Morocco in subsequent
found in tl1e pericardiun1, and there is an
years before its elimination in 1991. AHS
increase in pericardial fluid; however,
outbreaks continue to occur in endemic
cardiac lesions usually are not outstanding.

regions of southern and eastern Africa, and

The abdominal viscera may be congested. A
in 2007, AHS serotype 2 was reported in West
frothy exudate may ooze from the nostrils.

Africa (Nigeria and Senegal), and serotype

The pulmonary forn1 is the predominant

7 in Senegal. Outbreaks of AHS caused by
form in dogs, which are usually infected by
any one of several serotypes have recently
ingesting virus-contaminated meat.

been reported in Ethiopia.

The cardiac forn1 of AHS is subacute with
an incubation period of 1-2 wk. A fever

Transmission: Culicoides spp are the of <l wk is followed by edema of tl1e
principal vectors of all nine serotypes of
supraorbital fossae. Swelling may extend

AHSV, with C imicola usually considered to
to the eyelids, facial tissues, neck, thorax,
be the most important. Consequently, AHS
brisket, and shoulders. Deatl1 usually
is seen druing warm, rainy seasons, which
occurs witl1.in 1 wk and may be preceded by
favor propagation of the vectors, and
colic. The mortality rate is -500/o. Petechiae

EQUINE GRANULOCYTIC EHRLICHIOSIS

697
and ecchymoses on the epicardium a.nd

Prevention and Control: There is no
endocardiurn are prominent. The lungs are
specific treatment for animals with AHS
usually flaccid or slightly edematous. There
apart from rest and good husbandry. Compare yellow, gelatinous infiltrations of the licating and secondary infections should

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subcutaneous and intramuscular tissues,
be treated appropriately during recovery.

especially along the jugular veins and

AHSV is typically noncontagious and
ligan1entum nuchae. Other lesions in.Clude
spread exclusively via the bites of infected
hydropericardiurn, myocarditis, hem or

Culicoides spp or by the direct inoculation rhagic gastritis, and petechiae on the ventral of infectious material (via blood-feeding surface of the tongue and peritoneurr1-insect.s, needles, etc). Various methods

A mixed pulmonary and cardiac fo:l'I11 is
of control may be attempted, such as
most commonly seen in outbreaks, with a
introducing animal movement restrictions
mortality rate in horses of -80%.

to prevent infected animals initiating new

Subclinical AHSV infection occurs in
foci of infection, and husbandry modificapartially immune equids, such as thrnte tion to deny or reduce vector access to
previously vaccinated against t11e dis�ase,
susceptible or infected animals ( eg,
or in equids naturally infected with
stabling in vector-proof housing). It is rarely
live-attenuated vaccine strains of AH/3V.

possible to completely eliminate popula

Subclinical infections are also characteristions of vector Culicoides, especially in tic in zebras and certain other equids.

extensive pasture systems.

Live-attenuated virus vaccines are

Diagnosis: In endemic areas, clinici:tl signs available for iim11UI1ization of equids against
and lesions may lead to a presurnptiv(

AHS. These are typically based on cell
diagnosis. However, laboratory confu'lllaculture-attenuated viruses and generally tion is essential for definitive diagnosi $ and provide good, but not absolute, protection.

determination of the serotype; the latfer is

Annual revaccination is recommended in
imp01ta.nt for control measures. Anticoaguregions where these vaccines are used.

lated blood should be obtained at the peak

However, there are increasing concerns
of fever and transported ( at 4 °C) to th�
regarding use of live-attenuated AHSV
laboratory. Spleen samples collected (.tom
vaccines because of their potential
freshly dead anin1als should be kept on ice.

reversion to virulence, capacity for

Presence of virus is best detected by
transmission by vector Culicoides midges,
group-specific reverse-transcriptase
and reassortrnent of their gene segment.s
polymerase chain reaction (RT-PCR).

with other vaccine and field strains of

AHSV also can be isolated by intracertbral
virus, leading to the creation of novel virus
inoculation of suckling mice or in marnmaprogeny. Inactivated and subunit vaccines lian or insect cell cultures. Although nOt
avoid these potential drawbacks and,
widely available, indirect sandwich EJ.JSA
assUI11i.ng they are commercially available,
is also useful for rapid identification of
would likely be used after incursion of

AHSV antigen in tissues from anin1als that

AHSV into previously unaffected regions.

have died from acute infection.

Transport of equids from countries where

Serotyping of AHSV previously relii!d on

AHSV occurs to virus-free areas is subject to
virus neutralization test.s using type-specific
strict regin1ens of testing and quarantine,
antisera, which take �5 days. The recfht
although the precise requirements may vary
development of type-specific RT-PCR can
from country to country. The presence of
now confirm the serotype of an AHSV
antibodies alone should not preclude such
within 24 hr.

movement.s as long as AHSV is not present.

EQUINE GRANULOCYTIC EHRLICHIOSIS

Equine granulocytic ehrlichiosis is an

Etiology, Epidemiology, and
infectious, noncontagious, seasonal disease, Transmission: The causal rickettsial originally seen in the USA in northern
agent was initially termed Ehrlichia equi,

California but now recognized in manf
but based on DNA sequence relationships,
states where the tick vector occurs; it ts also
the organism is now referred to as
seen in Europe, Africa, and South Amt-rica.

Anaplasma phagocytophilum. It is not

(See also POTOMAC HORSE FEVER, p 283.) similar or clinically related to anaplasmo-

698

EQUINE GRANULOCYTIC EHRLICHIOSIS
sis in cattle. The organism has a wide host
fever, which is highest during the first
range; naturally occurring infections have

1-3 days of infection at 103° -104 °F
been seen in horses, burros, dogs, llamas,

(39.5°-40°C), persists at 102°-104°F
and rodents. A rickettsia infection in

(39°-40°C) for 6--12 days. Signs become

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people, the human granulocytic anaplasmore severe over several days. Rarely, mosis (HGA) agent, caused by a similar
myocardial vasculitis may cause transient
strain as the equine infection, has been
ventricular arrhythmias. Other clinical
identified in cases of human illness in the
presentations for acute infection have
upper midwestern and northeastern states
included recumbency and severe
in the USA and many other countries
myopathy. Any concurrent infection (eg,
worldwide.

a leg wound or respiratory infection) can

A phagocylophilum frequently infects
be exacerbated. Cytoplasmic inclusion
horses wherever the tick vector (lxodes
bodies are few during the first 48 hr and
sp) is present. States in which clinical
increase to 30%-40% of circulating
infection has been confirmed include
neutrophils at days 3-5 of infection. The

Connecticut, Illinois, Arkansas, Washingdisease is seasonal in California, occurring ton, Pennsylvania, Colorado, Minnesota,
in the late fall, winter, and spring.

New York, Massachusetts, and Florida.

It has also been confirmed in British

Lesions: Gross petechiation, ecchy

Columbia, Sweden, Great Britain, and
moses, and edema develop in the subcutis

South America.

and fascia. Vasculitis is regional, with the
subcutis and fascia of the legs predomi

A phagocylophilum resembles the
etiologic agents of tickborne fever (see
nantly affected.

p 772), bovine petechial fever (seep 745),
and the HGA agent based on morphology,

Diagnosis: Demonstration of the charcell tropism, and 168 rRNA gene sequence acteristic cytoplasmic inclusion bodies in a
data. It is present in cytoplasmic vacuoles
standard blood smear is diagnostic.

of neutrophils and occasionally eosino

However, inclusion bodies are difficult to
phils during the acute phase. Blood smears
see in the first day or two of fever. PCR
stained with Giemsa or Wright-Leishman
can detect A phagocylophilum DNA in
stains reveal one or more loose aggregates
unclotted blood or buffy coat smears. An

(morulae or inclusion bodies, 1.5-5 µm
indirect fluorescent antibody test can detect
in diameter) of blue-gray to dark blue
rising antibody titers to A phagocylophi
coccoid, coccobacillary, or pleomorphic
lum. Differential diagnoses include viral
organisms within the cytoplasm of
encephalitis, primary liver disease, equine
neutrophils.

infectious anemia, purpura hemorrhagica,

The infection can be transmitted
and viral arteritis.

experimentally to susceptible horses by
whole blood from infected horses or from

Treatment and Control: Oxytetrapeople with HGA. The incubation period is cycline is extremely effective against A

1-3 wk. I pacijicus (the western black
phagocylophilum, and systemic treatment
legged tick) and I scapularis can transmit
with tetracycline, 7 mg/kg/day, IV, for

A phagocylophilum to horses.

8 days, has eliminated the infection.

The zoonotic risk of infection to people

Penicillin, chloran1phenicol, and streptovia horses has not been observed to occur.

mycin have no inhibitory effect. Horses

Although horses and people appear to be
treated early in infection for shorter
infected with strains of the same agent, it
durations may relapse within the following
is believed that human exposure occtus
few weeks. Horses with severe ataxia and
through tick bites, and not by direct
edema may benefit from short-term
transmission from horses to people.

corticosteroid treatment ( dexan1ethasone,

20 mg/day, for 2-3 days). The risk of
laminitis appears to be very low; no

Clinical Findings: Severity of signs
la.mini tis has occurred in clinical cases or
varies with age of the horse and duration
experimental infections. Recovered horses
of the illness. Signs may be mild. Horses
are solidly immune for �2 yr and are not

<l yr old may have a fever only; horses
believed to be carriers. Persistence of

1-3 yr old develop fever, depression, mild
infection has been suggested with some
limb edema, and ataxia. Adults exhibit

European strains, but further verincation is
the characteristic signs of fever, partial
required. Tick control measures are mandaanorexia, depression, reluctance to move, tory for control of disease. There is no
limb edema, petechiation, and icterus. The vaccine.

EQUINE INFECTIOUS ANEMIA

699

EQUINE INFECTIOUS ANEMIA

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Equine infectious anemia (EIA) is a
of tl1e clinical signs associated with tl1e
noncontagious, infectious disease of horses
acute fom1 of EIA result from infection of
and other Equidae. It is caused by an RNA
macrophages and tl1e release of pro-inflamvirus classified in tl1e Lentivirus genus, matory mediators or cytokines, specifically
family Retroviridae. EIA can present as an
ttm1or necrosis factor ex, IL-1, IL-6, and
acute, subacute, or chronic infection. On
transfonning growth factor 13. This response
occasion, tl1e virus can be a cause of
togetl1er witl1 suppression of platelet
significant morbidity and mortality. The
production are believed to be tl1e factors
most frequently encountered fom1 of the
responsible for tl1e tl1rombocytopenia that
disease is tl1e inapparent, chronically
is a characteristic feature of EIA. In
infected carrier.

addition, immune responses play a major
role in the patl1ogenesis of EIA. Platelets

Transmission and Pathogenesis:

from infected horses have significant

Under natural conditions, the most
amounts of bound IgG or IgM, which leads
important mode of transmission of EIA is
to their immune-mediated destruction,
by tl1e transfer of virus-infective blood by
contributing to botl1 splenomegaly and
blood-feeding insects between horses in
hepatomegaly.

close proximity. Virus is found free in tl1e
plasma or cell associated, principally in
monocytes and macrophages of infected

Clinical Findings: The clinical findings
animals. Altl1ough infection is considered
and course of EIA are variable, depending
primarily blood borne, all tissues and body
on the virulence of tl1e virus strain, viral
fluids are potentially infectious, especially
dose, and susceptibility of the horse. After
during episodes of clinical disease when
an incubation period of 15-45 days or longer
viral burdens are high. Transmission of EIA
in naturally acquired cases of infection, clasby biting flies is purely mechanical; tl1e virus sic cases of the disease progress through does not replicate in tl1e vector. The chance
three clinical phases. An initial or acute
of transmission of EIA is directly proporepisode lasting 1-3 days is characterized by tional to tl1e volun1e of blood retained on tl1e fever, depression, and tl1rombocytopenia.

moutl1parts of tl1e insect after feeding. In

Because these signs can be mild and
tl1at respect, horse flies, deer flies, and to a
transitory, tl1ey are often overlooked.

lesser extent, stable flies are likely tl1e most

Typically, this initial phase is followed by a
efficient vectors. It is also because they
prolonged period associated with recurring
are capable of triggering host defensive
episodes of fever, thrombocytopenia,
behavior tl1at interrupts feeding and results
anemia, petechiation on mucous memin tl1eir seeking a new susceptible host to branes, dependent edema, muscle
complete tl1eir blood meal.

weakness, and loss of condition. The

Additionally, EIA can be readily
interval between episodes can range from
transmitted iatrogenically through use of
days to weeks or months. In most cases, the
blood-contaminated syringes, needles, or
episodes of clinical disease subside witl1in a
surgical equipment, or by transfusion
year, and infected horses become inapparof infective blood or blood products.

ent carriers and reservoirs of EIA virus.

Infrequently, transplacental transmission

Many of tl1ese horses remain clinically
can occur in infected mares tl1at experience
nom1al.

one or more clinical episodes during

Altl1ough tl1e foregoing represents tl1e
pregnancy. There is evidence, altl1ough
most commonly described clinical course of
circun1stantial, from a significant outbreak
the disease, some outbreaks of EIA can be
ofEIA in an equine hospital in Ireland, of
associated with peracute infection in which
probable spread of tl1e virus by direct or
tl1e primary viral infection is uncontrolled;
indirect transfer between horses in stalls
tllis can result in a very high fever, severely
sharing tl1e same barn.

reduced platelet counts, and acute

A very close relationship exists between
depression, leading to deatl1. In view of tl1e
presence and severity of clinical signs of
wide variation in response seen in natural

EIA and tl1e amount of virus present in
cases of infection, it is not possible to
infected anin1als. Viral burdens are highest
confim1 a diagnosis of EIA based solely
during febrile episodes of tl1e disease. Many
on clinical grounds.

700

EQUINE INFECTIOUS ANEMIA

Lesions: Gross lesions frequently seen in
other equids. The only recognized exception
acute cases of EIA include enlargement of
to this rule is the progeny of seropositive the spleen, liver, and abdominal lymph
mares, which may possess maternal
nodes; dependent edema; and mucosa!

antibodies to the virus after ingesting

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hemon-hages. Chronic cases of infection are colostmm. In most cases, passive antibody characterized by emaciation, pale mucous
against EIA virus wanes and is no longer
membranes, petechial hemon-hages,
detectable in the Coggins test by 6-8 mo of
enlargement of the spleen and abdominal
age; detectable antibody may persist up to
lymph nodes, and dependent edema.

12 mo, however, if ELISA testing is used.

Histopathologically, there is a nonsuppura

The Iisk associated with maintaining
tive hepatitis and, in some cases, a
infected breeding stock varies. Field studies
glomerulonephritis, periventricular
have indicated excellent success in raising
leukoencephalitis, meningitis, or encephalitest-negative foals from inapparent carriers tis. Proliferation of reticuloenthelial cells is
of EIA vims. The 1isks of infection in utero
evident in many organs, especially in the
increase dramatically if clinical signs of EIA
liver, where there is also accumulation of
are seen in the mare before parturition.

hemosiderin in Kiipffer cells. Perivascular

Unfortunately, it is not possible to
accumulation of lymphocytes can be found
accurately detemune the risk posed by any
in various organs.

equid infected by EIA virus. Inapparent
carrier horses maintain low-level viremias
that may increase under stressful circum

Diagnosis: A provisional clinical diagnosis
ofEIA must be confirmed by demonstration
stances. As compared with seronegative
of antibodies to the virus in blood. Although
healthy horses, inapparent carriers have
the internationally accepted serologic test is
increased serum globulin concentrations
the agar gel immunodiffusion or Coggins test, and lymphocyte subset changes that are there is increasing acceptance of a variety of
consistent with inunune activation or

ELISA tests, either competitive or synthetic
chronic inflammation. Because EIA virus
antigen-based, because they can provide
persists in infected equids for life, most
rapid results. Because ELISA tests can give a
regulatory agencies assun1e all equids
higher rate of false positives, all ELISA
seropositive for EIA virus pose the same
positive results must be confin-ned by the
high Iisk.

Coggins test. When used in combination,

In the USA, seropositive horses must be

ELISA and agar gel inununodiffusion tests
placed under quarantine witlun 24 hr after
provide the highest level of sensitivity
the positive test results are known. The
combined with specificity. The Western blot
quarantine area must provide separation of
is a supplemental test that can be resorted
at least 200 yd from all other equids. After a
to in cases of conflicting results with other
confin-natory test is performed, seroposidiagnostic tests. A problem witl1 available tive horses must be permanently identified
serologic tests is that they can give negative
using the National Uniform Tag code
results when testing sera collected within the
nun1ber assigned by the USDA to the state
first 10-14 days of infection. Whereas the vast in which the reactor was tested, followed majolity of horses infected with EIA virus
by the letter "A." This identification may will have seroconverted by 45 days, there
take the form of a hot brand, chemical
have been exceptional cases in which the
brand, freezemark, or lip tattoo, and it must

.

interval has been �90 days. Virus detection
be applied by a USDA representative.

assays such as the reverse transcliption PCR

Reactor horses must be removed from the
assay are not routinely used to diagnose EIA.

herd by euthanasia, slaughter, or quarantine

Notwithstanding their sensitivity, they may
at the premises of oligin. They may move
not detect virus in carrier horses with very
interstate only under official permit to a
low viral loads. Although the animal
federally inspected slaughter facility or a
inoculation test is highly sensitive for
federally approved diagnostic or research
detection ofEIA virus, for logistical and
facility, or to return to the premises of
economic reasons, it is no longer in vogue
origin. After a reactor is detected in a herd,
as a means of diagnosis of EIA.

testing for EIA must be performed on all
horses on the premises and repeated until
all remaining equids on the premises test

Treatment and Control: No specific
negative. These horses must be retested at
treatment or safe and effective vaccine is

30- to 60-day intervals until no new cases
available. Because equids infected with EIA
are found. Quarantine on the premises is
virus present the only known source of
released when tests on the entire herd have
infection, antibody-positive animals should
been negative for at least 60 days after the
be kept at a safe distance ( -200 m) from
reactor equids have been removed.

EQUINE VIRALARTERITIS

701

All equids shipped across state lines

12 mo as part of a routine health program.

in the USA must be tested for EIA with

More frequent testing may be indicated in
a negative result within 12 mo before
areas that perennially have a high incidence
transport. All equids sold, traded, or
of EIA. Owners of equids entering shows or
donated within a state must have tested
competitive events should present proof to

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negative for EIA no more than 12 mo before event officials of a negative EIA test. All new change in ownership and, preferably, no
equids introduced to a herd should have a
more than 60-90 days. All equids entering
negative EIA test before entry or be isolated
horse auctions or sales markets are
while tests are pending. Vector control
required to have a negative test before sale, practices, including application of or the horse must be held in quarantine
insecticides and repellents and environmenwithin the state unW the test results are tal insect control, should be in1plemented.

known.

Good hygiene and disinfection principles

It is recommended that horse owners
should be maintained to prevent iatrogenic
implement an EIA control plan for their
infection of horses with contaminated
premises. All horses should be tested every needles, syringes, or equipment.

EQUINE VIRAL ARTERITIS

(Epizootic cellulitis-pinkeye, Equine typhoid, Rotlaufseuche) Equine viral arteritis (EVA) is an acute,
geographically different isolates. Pathocontagious, viral disease of equids caused genicity also valies 3lllong viral strains, with
by equine arteritis virus (EAV). Typical
some capable of causing moderate to severe
cases are characterized by fever, depressigns of disease whereas others only induce sion, anorexia, leukopenia, dependent
a fever.

edema ( especially of the lower hind

After respiratory exposure, EAV invades
extremities, scrotum, and prepuce in the
the upper and lower respiratory tract and
stallion), cortjunctivitis, supra- or pelimultiplies in nasopharyngeal epitilelium orbital edema, nasal discharge, respiratory
and tonsillar tissue and in bronchial and
distress, skin rash, temporary subfertility
alveolar macrophages. Infected cells of the
in affected stallions, abortion, and
monocytic lineage and CD3+ T lymphocytes
infrequently, illness and deatl1 in young
transport the virus to the regional lymph
foals. A vaiiable percentage of postpubertal
nodes, where it undergoes a furtiler cycle of
colts and stallions become carriers and
replication before being released into tile
semen shedders after infection with EAV.

bloodstre3lll. The cell-associated viremia
that follows ensures dissemination of EAV

Etiology and Pathogenesis: EAV is a
throughout tile body. By day 6-8, the virus
small, enveloped single-stranded positivelocalizes in the vascular endothelium and sense RNA virus and the prototype virus of
medial myocytes of the smaller blood
tl1e genusArterivirus, fainily Arteliviridae,
vessels, especially the artelioles, and causes
order Nidovirales. It has 10 open reading
a panvasculitis. It can also be found in the
fran1es (ORFs), of which ORFs 2a, 2b, 3,
epithelium of certain tissues, particularly

4, 5, 5a, 6, and 7 encode the viral structural
tile adrenals, seminiferous tubules, tilyproteins. EAV is one of tile tJu·ee most roid, and liver. Vascular lesions include
important equine viral respiratory patiloendothelial swelling and degeneration, gens. The virus is not especially resistant
neutrophilic infiltration, and necrosis of tile
outside the body, and survival �37°C can be
tunica media of affected vessels. These
short-lived. In contrast, EAV can maintain
lesions give rise to edema and hemorrhage,
infectivity in tissues or bodily fluids for
which ai·e believed to result from activation
extended periods at storage temperatures
of tile proinfl3lllmatory cytokines IL-1 beta,
equal to or below freezing. It can remain

IL-6, IL-8, and possibly TNF-a. Maximal
viable in frozen semen for many years.

vascular irtjury occurs by about day 10,

Altilough only one major serotype ofEAV
after which lesions begin to resolve.

has so far been identified, the prototype

Based on expelimental infection of

Bucyrus strain, genomic and antigenic
pregnant mares with the expelimentally
vaiiation exists an1ong temporally and
derived highly vi.mlent Bucyrus strain of

702

EQUINE VIRAL ARTERITIS

EAV, abortion is believed to result from a
phase of infection. It is primarily responsimyometritis that gives rise to irnpainnent of ble for transmission of EAV among naive
the placental circulation and death of the
equids kept in close contact ( eg, at
fetus. However, this is unlikely to represent
racetracks, shows, sales, veterinary

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the pathogenesis of abortion in naturally
hospitals, and under conditions of
acquired cases of EAV infection, which has
intensive management on breeding farms).

yet to be determined.

EAV can also be transmitted venereally by

Except in certain infected stallions that
the acutely infected mare and by the
become carriers of the virus, EAV is no
acutely or chronically infected stallion.

longer detectable in tissues and body fluids

Mares can be readily infected by the
beyond day 28 after primary infection.

venereal route after breeding to a carrier

However, stallions that remain persistently
stallion either by live cover or artificial
infected harbor the virus principally in
insemination with fresh-cooled or
certain accessory sex glands, especially the
c1yopreserved semen. There is evidence
ampulla of the vas deferens, where it can
that EAV can be spread through embryo
remain for many years. Some carrier
transfer. Infection can also be spread
stallions may shed EAV from their
through indirect contact with virus-conreproductive tracts for an extended period.

taminated fomites (eg, breeding shed
equipment, shanks, or twitches) or on the

Epidemiology and Transmission:

hands or apparel of animal handlers.

While the natural and experimental host

The carrier state has been confinned in
range of EAV is restricted p1incipally
sexually mature intact males, specifically
to equids, there are very limited data to
postpubertal colts and stallions, but not in
suggest the virus may also infect alpacas
mares, geldings, sexually in1mature colts, or
and llamas. There is no evidence that EAV is
fillies. Establishment and persistence of
transmissible to people. Based on serologic

EAV in the reproductive tract of stallions is
srnveys and reported outbreaks of equine
testosterone-dependent. The carrier stallion
viral arteritis, EAV is present in equine popuis the natural reservoir of EAV and is lations in many countries worldwide, with
responsible for its dissentination and
the notable exceptions of Japan and
persistence in equine populations.

Iceland. The prevalence of infection varies

Frequency of the carrier state can vary
widely both between countries and among
from <lOOA, to >700A,. There is evidence that
breeds in the same country. It is frequently
stallions witl1 CD3+ T lymphocytes that are
highest in Standardbreds and Warm bloods.

susceptible to EAV infection are at higher

Despite the widespread global distribution
risk of beconting carders than stallions with
of EAV, laborato1y-confinned outbreaks of
the CD3+ T lymphocyte-resistant pheno

EVA are relatively unconunon. However,
type. Persistently infected stallions shed
this situation appears to be changing in

EAV constantly in the spem1-lich fraction of
more recent years, with an increase in the
the semen but not in any other secretions or
nrnnber of verified occurrences of the
excretions. Duration of tl1e carrier state can
disease being reported. A major factor
range from weeks to many years. Persistent
contributing to this change is the continued

EAV infection clears spontaneously in a
growth in tl1e volun1e of international trade
variable percentage of stallions, with no
in horses and equine semen.

evidence of subsequent reversion to a

The epidemiology of EVA involves virus-,
shedding state. Existence of the carrier
host-, and environment-related factors,
state does not appear to impair the fertility
including variability in pathogenicity among
of infected stallions nor otherwise adversely
naturally occurring strains of the virus,
affect their clinical condition. Carrier
modes of transmission, occurrence of the
stallions also serve as tl1e p1incipal means
carrier state in stallions, and tl1e nature of
by which genetic diversification of EAV can
acquired inunrntity to infection. Outbreaks
occur, with potential emergence of novel
of EVA are most often linked to the
viral variants.

movement of infected animals or the

Compared with other equine respiratory
shipment of virus-contantinated semen.

viruses, EAV stimulates a stronger,

Frequently, viral transmission occurs with
longer-lasting inunrntity that is protective
ntinimal if any detectable clinical signs in
against development of clinical disease,
acutely infected equids.

including abortion and establishment of the

Transntission of EAV can occur by
carrier state in stallions. High levels of
respiratory, venereal, and congenital
neutralizing antibodies that frequently
routes or by indirect means. Spread by the
persist for at least 2-3 yr can be stimulated
respiratory route is the principal mode of
by natural exposure to tl1e virus and by
dissemination of the virus during the acute
vaccination.

EQUINE VIRALARTERITIS

703

Clinical Findings: Exposure to EAV may
pregnant at tin1e of exposure; this occurs
result in clinical or asymptomatic infection,
primarily by the respiratory route through
depending on the relative pathogenicity
direct proximity with an acutely infected
of the virus strain involved, viral dose, age
animal. Abortion occurs 1-4 wk later. Mares

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and physical condition of the animal, and
exposed very late in gestation may not abort
various environmental factors. Most cases
but give birth to a foal congenitally infected
of primary infection are asymptomatic.

with the virus. Mares that abo1t from EAV

Onset of the acute phase of EAV infection,
infection have not been proved to be less
whether associated with clinical signs or
fertile.

not, is preceded by an incubation period

Stallions with EVA may w1dergo a period
of 3-14 days, which varies mainly with the
of short-term subfertility. This has been
route of exposure. The interval is usually
observed in individuals that develop a high

6-8 days after venereal transmission of the
and prolonged fever and extensive scrotal
virus. Clinical signs can differ in range and
edema. Affected stallions may exhibit
seve1ity between disease outbreaks and
reduced libido associated with decreases
between affected individuals in the same
in total and progressively motile spenn,
outbreak. Any combination of the followcurvilinear velocity, percentage of live ing may be seen: fever lasting 2-9 days,
spennatozoa, and percentage of morpholeukopenia, depression, anorexia, limb logically normal spem1atozoa The changes
edema (especially of the lower hindlimbs),
in semen quality are believed to result from
and edema of the scrotum and prepuce.

increased intratesticular temperature

Less frequently encountered signs include
and not from the direct effectofEAV on
conjunctivitis, lacrimation and photophospermatogenesis and testicular fw1ction.

bia, periorbital or supraorbital edema,

There is strong evidence that fever and
rhinitis and nasal discharge, edema of the
scrotal edema exert independent effects on
ventral body wall (including the mammary
semen quality. Semen changes can last for
glands of mares), an urticarial-type skin

14-16 wk before returning to nonnal. No
reaction ( often localized to the sides of the
longterm adverse effects on fertility have
face, neck, or over the pectoral region,
been seen in fully recovered stallions.

although it can be generalized), stiffness

The frequency and severity of clinical
of gait, dyspnca, petechiation of mucous
illness associated with EAV infection
membranes, diarrhea, icterus, and ataxia.

tend to be greater in very yoW1g, old, or

Strains of EAV can cause abortion
debilitated individuals and Wlder adverse
throughout much of pregnancy (3 mo to
climatic conditions. Regardless of severity
more than 10 mo). Abortion may occur late
of clinical signs, affected horses invariably
in the acute phase or early in the convalesmake complete recoveries, even in cent phase of the infection, with or without
the absence of symptomatic treatment.

prior clinical signs of EV

A. In natural

Mortality in older horses is very rarely
outbreaks, abortion rates can vary from
encoW1tered in natural outbreaks. However,

<10% to as high as 600/o. There is no evidence
it can occur in neonatal and in yoW1g foals
confinning that mares bred with EAV-infecup to a few months of age that succumb tive semen will abort later in gestation.

from a fulminating pneumonia or pneu

Mares that abort from the virus are already
moenteritis.

Lesions: The gross and microscopic
lesions in fatal cases of EVA reflect the
extensive and considerable vascular damage
caused by the virus; these desctiptions are
primarily based on e:Kperimental infection
with the highly pathogenic Bucyrus strain
of EA

V. The most significant gross findings
include edema, congestion, and hemorrhages, especially in the subcutis of the limbs and abdomen; excess peritoneal,
pleural, and pericardia! fluid; and edema
and hemorrhage of the intra-abdominal and
thoracic lymph nodes and of the small and
large intestine, especially the cecwn and
colon. Pulmonary edema, emphysema and
interstitial pnewnonia, enteritis, and infarcts

Equine viral arteritis, scrotal edema. Courtesy
in the spleen have been repo1ted in natw-ally
of Dr. Peter J. Timoney.

acquired fatal cases of the disease in foals.

704

EQUINE VIRAL ARTERITIS

Aborted fetuses are often partly
fetuses not infrequently are somewhat
autolyzed. Gross lesions are usually absent;
autolyzed at time of expulsion and very
if present, they are limited to an excess of
often are devoid of any gross and even
fluid in body cavities and a variable degree
microscopic lesions. In contrast, herpes

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of interlobular pulmonary edema. The
virus-infected fetuses are invariably fresh
vascular damage and immune-mediated
and usually display characteristic gross
lesions seen in older animals are seldom
and microscopic lesions.

found in infected fetuses.

Laboratory confirmation of a provisional

The characteristic microscopic lesion
clinical diagnosis of EVA should be pursued
seen in cases of EAV infection is a vasculitis,
without delay in suspected outbreaks. This
involving primarily smaller arterioles and
can be based on virus isolation, detection
venules. Histologically, changes can range
of viral nucleic acid, visualization of viral
from vascular and perivascular edema, with
antigen by immunohistochemical exantinaoccasional lymphocytic infiltration and tion, or demonstration of a recent hurnoral
endothelial cell hypertrophy in mild cases,
antibody response by testing paired (acute
to fibrinoid necrosis of the tunica media,
and convalescent) sera collected 3-4 wk
extensive lymphocytic infiltration, necrosis
apart.

and loss of endothelium, and thrombus

The most appropriate samples for virus
formation in severe cases. Microscopic
isolation and/or detection of viral nucleic
lesions are frequently not seen in cases of
acid by reverse transcriptase-PCR (RT-PCR)

abortion. If present, vasculitis has been seen are nasopharyngeal swabs or washings and in the placenta and the brain, liver, spleen,
unclotted ( citrated or EDTA) blood
and lungs of tl1e fetus.

samples. To optimize the chances of

Fatal cases of EAV infection in young
isolation or detection, samples should be
foals are characterized by interlobular
collected as early as possible after the
edema, congestion and mononuclear cell
onset of clinical signs or suspicion of EAV
infiltration in the lungs, and lymphoid
infection. After collection, swabs should
depletion and hemorrhage in lymphoreticube transferred directly into viral transport lar tissues. Focal hemorrhages and necrosis
mediun1 and shipped refrigerated or frozen
of the intestinal mucosa have been
in an insulated container via an overnight
described when there is an associated
delivery service to a laboratory capable of
enteritis.

testing for tltis infection. Unclotted blood
san1ples should be transported refrigerated
but not frozen.

Diagnosis: The symptomatology of EVA

In suspect cases of EAV-related abortion,
can mimic that of a range of other respiravirus detection should be attempted from tory and nonrespiratory equine diseases.

placental tissues and fluids and from fetal

Accordingly, laboratory exanunation of
lung, liver, lymphoreticular tissues
appropriate specimens is essential to

( especially thymus), and peritoneal or
confirm diagnosis. Equine influenza, equine
pleural fluid. Chorioallantoic membrane
herpesvirus I and 4-related di.seases,
and fetal lung are fue tissues of choice for
infection with equine rhinitis A and B
recovery of virus. When EAV is suspected
viruses or equine adenoviruses, and purpura in deaths of young foals or older horses, a hemorrhagica are among the more common
wide range of tissue specimens, especially
equine illnesses that clinically resemble
the lymphatic glands in the thoracic and

EVA. The latter must also be differentiated
abdominal cavities and related organs,
from equine infectious anemia, toxicosis
should be collected and submitted for
caused by hoary alyssurn (Berteroa
laboratory exrunination, including
incana), and allergy-induced urticaria.

histologic and immunohistochemical

Several foreign diseases that should be
testing.

considered in a differential diagnosis of EVA

Detection of the carrier state in a stallion
include Getall virus infection, dourine, and
is based initially on detennination of the

African horse sickness (seep 696).

individual's serologic status for EA

V. In the

Abortion caused by EAV must be
absence of a certified history of vaccination,
differentiated from fuat due to equine
stallions with a serum neutralizing antibody
herpesvirus 1 or 4. A helpful but not always
titer �1:4 should be considered potential
reliable distinguishing featme is that mares
carriers of the virus until proven otherwise,
that abort because of EAV may display prior
based on an absence of detectable EAV in
clinical signs of EVA, whereas mares that
their semen. Confirmation of the canier
abort because of equine herpesvirus seldom
state is based on demonstration of virus in
exhibit any premonitory clinical evidence of a semen sample containing fue spe1m-rich infection. Fwtherrnore, EAV-infected
fraction of the ejaculate either by isolation

EQUINE VIRAL ARTERITIS

705
of virus in cell culture or its detection
protects against development of EVA,
by RT-PCR. Under controlled laboratory
including abortion, and establishment of
conditions, sensitivity of virus isolation and
the carrier state in stallions. Although
real-time RT-PCR are essentially equivalent
the vaccine is safe and in1munogenic for
for detection of EAV in stallion semen;
stallions and non pregnant mares, the

VetBooks.ir
however, the RT-PCR assay has the
manufacturers do not recommend its use
advantage of providing a more rapid result.

in pregnant mares, especially in tl1e final

The carrier state can also be determined by

2 mo of gestation or in foals <6 wk of age,
test breeding a stallion to two seronegative
wliess tmder circun1stances of high lisk of
mares and checking the mares for
exposure to natural infection. Experimental
seroconversion 28 days after breeding.

and field studies have shown tl1at tl1ere are

Of the serologic assays evaluated for
no adverse consequences to vaccinating
detection of antibodies to EAV, the
pregnant mares up to 3 mo before foaling
complement-enhanced virns neutralization
and duling the in1mediate postpartum
test continues to be tl1e most reliable for the
peliod. However, there is a low lisk of
diagnosis of acute EAV infection and for
abortion in mares vaccinated dwing tl1e
seroprevalence studies. A number of ELISA
last 2-3 mo of pregnancy. Mi11in1izing or
tests have been developed, only a few of
elin1inating direct or indirect contact of
which offer comparable but not equivalent
unprotected horses witl1 infected animals
sensitivity and specificity. None of the
or witl1 virus-infective semen is critical to
available serologic tests can differentiate
tl1e success of any prevention program.

antibody titers resulting from natural

The plirnary focus of current control
infection from those due to vaccination.

programs is to rest1ict the spread ofEAV in
breeding populations and to reduce tl1e risk

Treatment, Prevention, and Control:

of outbreaks of virns-related abortion, deatl1

There is no specific antiviral treatment
in young foals, and establishment of tl1e
currently available for EVA. Aside from
carrier state in stallions and postpubertal
young foals, vittually all naturally affected
colts. Although EAV has occasionally been
horses make complete clinical recoveries.

responsible for extensive outbreaks of

Symptomatic treatment ( eg, antipyretic,
disease at racetracks, shows, sales, and
anti-inflammatory, and diuretk drngs) is
vete1inary hospitals, tl1ese have been so
indicated only in severe cases, especially in
sporadic tl1at no specific control programs
stallions. Prompt symptomatic treatment of
have been developed to prevent such
stallions with a high or prolonged fever and
occurrences.

significant scrotal and preputial edema can

Effective control programs are predireduce the likelihood of short-term cated on observance of sound managesubfe1tility. Good nursing care, adequate ment practices similar to tl1ose recom,
rest, and a gradual return to normal activity
mended for other respiratory infections.

are indicated. There is no effective

These include isolation of new arrivals on a
treatment for EVA-related cases of
premises for 3-4 wk before allowing them
pneun1onia or pneun10enteritis in foals.

to co-n1ingle with tl1e resident equine

Because congenitally infected foals are
population, maintenance of pregnant
very productive sources of EAV and their
mares in small isolated groups, identificachances of survival are essentially nil, tion of carrier stallions, armual immw1izaearly euthanasia should be considered to tion of noncarrier breeding stallion
minin1ize the lisk of further spread of the
populations, and vaccination of colts at
virus to any susceptible contacts, especially

6--12 mo of age to minimize their risk of
pregnant mares and young foals. Although
becoming carriers later in life. Carrier
there is some evidence that temporary
stallions should be managed separately and
down-regulation of circulating testosterone
bred only to naturally seropositive mares
by GnRH inm1urrization or through the use
or mares vaccinated against EV A. Because
of a GnRH antagonist promotes clearance
fresh-cooled or frozen semen can be an
of EAV from the reproductive tract of
important source of EAV, it should be
carrier stallions, neither strategy has yet
tested by a laboratory with appropriate
been adequately validated.

diagnostic expertise to confirm its negative

EVA is a manageable and preventable

EAV status, especially if imported. When
disease that can be controlled by obserbreeding a mare artificially with virnsvance of sound management practices infective semen, the san1e precautions
together with a targeted vaccination
apply as if breeding by live cover to a
program. Only one commercial vaccine, a
carrier stallion.

modified-live virus product, is currently
ln tl1e event of a suspected outbreak of
available in North Amelica. The vaccine

EVA, relevant anin1al healtl1 autl1olities

706

EQUINE VIRAL ARTERITIS
should be promptly notified, with affected
equipment that might have come in contact
and in-contact horses isolated, and
with infected animals should be thoroughly
restrictions immediately in1posed on
sanitized. Vaccination of the at-risk equine
movement of horses onto and off the
population on a premises should be
affected premises. Appropriate specimens
se1iously considered as a means of

VetBooks.ir
should be collected as soon as possible after restricting further transmission of EAV and onset of clinical signs and submitted for
of expediting control and resolution of an
laboratory confumation of a diagnosis of
outbreak. Movement restrictions should not

EVA. Breeding activity should be suspended be lifted w1til at least 3 wk after the last on breeding farms to minimize risk of
clinical or suspected case of EVA or
further spread of the infection. Stalls and
laboratory-confumed case of EAV infection.

GLANDERS

(Farcy)

Glanders is a contagious, acute or chronic,
subsequently, a tllick, mucopurulent nasal
usually fatal disease of Equidae caused by
discharge and respiratory signs. Deatil

Burkholderia mallei and characterized by
occws within a few days. The chronic
serial development of ulcerating nodules
disease is common in horses and is seen
that are most commonly found in tl1e upper
as a debilitating condition with nodular or
respiratory tract, ltmgs, and skin. Felidae
ulcerative lesions of tile skin and internal
and other species are susceptible, and
nares. Infected animals may live for years
infections are usually fatal. The organism is
and continue to disseminate t11e organism.

infectious for people, with a 95% fatality rate In some, the infection may be latent and in untreated septicemia cases, and is considpersist for long periods.

ered a potential bioterrorism agent.

Nasal, pulmonary, and cutaneous forms

Glanders is one of tile oldest diseases
of glanders are recognized, and an animal
known and once was prevalent worldwide.

may be affected by more tilan one fonn at a

It has now been eradicated or effectively
time. In the nasal form, nodules develop in
controlled in many countries, including tile
the mucosa of tile nasal septunl and lower

USA. In recent years, tile disease has been
paiis of tile turbinates. The nodules
reported in the Middle East, Pakistan, India,
degenerate into deep ulcers witll raised

Mongolia, China, Brazil, and Africa.

irregular borders. Characteristic starshaped cicatrices remain after tile ulcers Etiology: Burkholderia mallei, a clonal heal. In the early stage, tile submaxillary
gran1-negative facultative intracellular
lymph nodes are enlarged and edematous
obligate pathogen, is present in nasal
and later become adherent to the skin or
exudates and discharges from ulcerated
deeper tissues.

skin of infected animals. Glanders is

In the pulmonary form, small, tuberclecommonly contracted by ingesting food or like nodules, which have caseous or
water contanlinated with nasal discharges
calcified centers surrounded by inflainmaof carrier animals, by contact with harness tory zones, are found in the lungs. If the
components, and by ingestion of meat from
disease process is extensive, consolidation
affected horses. The organism is susceptible of the lung tissue and pneumonia may be to heat, light, and disinfectants; survival in a
present. The nodules tend to break down
contanlinated area is limited to 1-2 mo.

and may discharge tlleir contents into the

Humid, wet conditions favor survival. A
bronchioles, resulting in extension of tile
polysaccharide capsule is an important
infection to the upper respiratory tract.

virulence factor and enllances survival in

In the cutaneous form ("farcy"), nodules the environment.

appear along the course of the lymph
vessels, particulai·Jy of tile extremities.

Clinical Findings: After an incubation

These nodules degenerate and fom1 ulcers
period of 3 days to 2 wk, acutely affected
that discharge a highly infectious, sticky
animals usually have septicemia, high fever
pus. The liver and spleen also may show

(as high as 106°F [41 °Cl), weight loss, and
typical nodular lesions. Histologically, there

HENDRA VIRUS INFECTION

707
may be vasculitis, thrombosis, and
complement fixation and may become
infiltration of degenerating inflammatory
positive as early as 3 days after infection.

cells.

PCR based on 168 and 238 rRNA gene
sequences may be used for specific

Diagnosis: The typical nodules, ulcers,
identification.

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scar fonnation, and debilitated condition
may provide sufficient evidence for a

Prevention and Treatment: There is no
clinical diagnosis. However, because these
vaccine. Protective immunity involves T cell
signs usually do not develop until the
responses elicited by live attenuated
disease is well advanced, specific diagnostic bacteria. Prevention and control depend on tests should be used as early as possible.

early detection and elimination of affected

Culture of B maUei from lesions confirms
anin1als, as well as complete quarantine and
the diagnosis. A test for delayed hyperrigorous disinfection of the area involved.

sensitivity is pe1forn1ed by intrapalpebral

Treatment is given only in endemic areas
inoculation of mallein, a secreted glycoprobut does not reliably produce a bacteriotein of B mallei found in culture supernalogic cw-e. Doxycycline, ceftrazidirne, tant. Wected hypersensitive horses develop gentamicin, streptomycin, and combinaa purulent conjunctivitis within 24 hr and tions of sulfazine or sulfamonomethoxine
swelling of the eyelid. Complement fixation
with trimethoprim were effective in the
is also used to screen for infection.

prevention and treatment of experimental

Competitive ELISA is more sensitive than
glanders.

HENDRA VIRUS INFECTION

Hendra virus was first described in 1994
ruses. Hendra virus is genetically and
after an outbreak of acute respiratory
antigenically closely related to Nipall virus
disease in a Thoroughbred training stable in

(seep 721), with which it shares >900A, Australia in which horses and one person
aniino acid homology. Both viruses have
were fatally infected. Sporadic cases
been classified in a new genus, Henipavi-
continue to occur in eastern Australia,

1us, in the subfanilly Paramyxovi1inae.

typically presenting as an acute febrile

It is increasingly evident that Hendra
illness and rapidly progressing with varivirus strain variation is minimal and that able system involvement, notably acute
clinical presentation and pathology more
respiratory and/or severe neurologic
likely vary with the route of infection.

disease. Fruit bats ( suborder Megachirop

Histo1ically, interstitial pneun1onia of
tera) are the natw-al reservoir of the virus.

variable severity was the principal finding in

Hendra virus is classified as a biosafety
natw-ally infected horses and in experimen

Level 4 agent ( defined as posing a high risk
tally infected horses exposed by the
of life-threatening disease in people), and
respiratory or parenteral routes. Hendra
the use of safe work practices and personal
virus has a specific tropism for vascular
protective equipment is essential to manage
tissues, regardless of route of challenge. In
the risk of human exposure. The earlier
early infection, the vascular lesions may
names of equine morbillivirus and acute
include edema and hemorrhage of vessel
equine respiratory syndrome are no longer
walls, fibrinoid degeneration with pyknotic
appropriate.

nuclei in endothelial and tunica media cells,
and numerous giant cells ( syncytia) in the

Etiology and Pathogenesis: Hendra
endotheliun1 and sometin1es the tunica
virus is a large, pleornorphic enveloped
media of affected vessels (both venules and

RNA virus. Although initially considered to
arterioles). The virus becomes more widely
be more closely related to members of the
distributed in various tissues throughout the
genus Morbillivirus than to other genera
body as infection progresses, presumably as
in the family Paramyxoviridae, subsequent
a result of a leukocyte-associated viremia.

studies showed limited sequence homology

Virus has been demonstrated in the vascular
with respiroviruses, morbilliviruses, and
endothelium of subarachnoid and cerebral
rubuloviruses and negligible immunologic
vessels and in the vasculature of the renal
cross-reactivity with other paramyxovi-
glomerulus and pelvis, lamina propria of the

708

HENDRA VIRUS INFECTION
stomach, spleen, various lymph nodes, and
lungs) sometimes observed temli.nally in
myocardium. When respiratory disease is
naturally affected horses could plausibly
present, there is progressive destruction of
provide a source of virus for aerosol
alveolar walls, with the appearance of alveotransmission. Hendra virus has been fow1d VetBooks.ir
lar and intravascular macrophages. In
in the wine, blood, and nasal and oral
addition to its vascular tropism, Hendra
secretions of naturally infected horses and
virus can also be neurotropic, causing
cats. Based on available field and laboratory
neuronal necrosis and focal gliosis. A
data, infection of people or anin1als appears
feature of one outbreak at an equine
to require direct contact with virus-infective
veterinary clinic in Australia in 2008 was
secretions (lung exudates), excretions
severe neurologic disease and an absence

(urine), body fluids, or tissues. Although
of respiratory disease. Thus, Hendra virus

Hendra virus appears to have linlited
should no longer be regarded as causing
infectivity, the case fatality rate in individupredominantly respiratory disease in als that become infected is high: 75% in
horses.

horses, 57% in people.

Available epidenliologic, serologic, and

Epidemiology and Transmission: Natvirologic evidence implicates fruit bats as urally occurring disease caused by Hendra
the natural reservoir ofHendra virus.

virus has been reported only in horses and

Serologic surveys have revealed a high
people. Experimentally, disease has been
prevalence of neutralizing antibodies in
produced in cats, han1sters, ferrets,
wild-caught fruit bats (Pteropus spp) in
monkeys, pigs, and guinea pigs, but not in

Australia and Papua New Guinea. The
mice, rats, rabbits, chickens, or dogs. The
geographic distribution of the virus in fruit
clinical response and pathologic findings in
bats appears to be limited to Australia and
cats are very sinlilar to those seen in horses.

Papua New Guinea, although a transition of

Hendra virus infection and disease in horses Hendra-like to Nipa11-like viruses may occur has only been reported in Australia, and
beyond Australia. lnfection in fruit bats
events are sporadic and infrequent, with 14

( either natural or experimental) causes no
events recorded between 1994 and 2010.

evident disease. There is field and experi

Most of these were single horse events.

mental evidence of vertical transnlission,

Thus, Hendra virus appears to have limited
with isolates recovered from the uterine
infectivity, and under field conditions,
fluid and fetal tissues of a grey-headed flying
tra.nsnlission between infected and
fox (P poliocephalus) and a black flying fox noninfected horses occurs infrequently.

(P alecto ). The infrequent occurrence and

However, the frequency of Hendra virus

. sporadic nature of equine cases suggest that
infection in horses has increased since 2011, exposure of horses to Hendra virus is, at with 18 incidents in 2011, 8 in 2012, 8 in
least in part, a chance event. The modes of

2013, and 3 in 2014 (up to October), with
transnlission between bats, and from bats to
extended geographic locations (between
horses, are uncertain, as are factors that
far north Queensland to north New South
may facilitate spillover. Hendra virus has

Wales, Australia). In July 2011, a d_og on
been identified in the birtlli.ng fluids,
a property with horses infected with Henplacental material, aborted pups, and urine dra virus (in Queensland) was identified
of naturally infected fruit bats and in the
as seropositive without any clinical signs.

urine of experimentally infected fruit bats.

In July 2013, a dog on a property (in New

The related Nipal1 virus has been detected

South Wales) with Hendra virus infection
in bat urine and on fruit partially eaten by
in a horse was confirmed to be infected
bats. Horses are hypothesized to be infected
with the same virus. Further research is
through contact with food or water
underway to investigate whether these incontanli.nated with material from infected creased incidents in horses were because
fruit bats, but tl1e definitive mechanism
remains to be detemli.ned.

of greater public awareness in reporting
the disease or whether environmental or

Clinical Findings: Because of its affinity
ecologic factors triggered tllis increased
for endothelial cells, Hendra virus can cause
number of cases and extended geographic
a range of clinical signs in horses. The
occurrence.

predominant clinical presentation may

Experin1entally, attempted transnlission
depend on wllich organ system sustains the
from virus-infected horses to in-contact
most severe or compronlising endothelial
horses or cats has been unsuccessful.

damage.

Nonetheless, the possibility of respiratory

Hendra virus infection should be
transmission can.not be excluded. The
considered when tl1ere is acute-onset fever
frothy nasal discharge ( originating from the
and rapid progression to death, possibly

HENDRA VIRUS INFECTION

709
associated with either severe respiratory or
spleen, heart, stomach, kidneys, and brain).

neurologic signs; however, the absence of

Widespread fibrinoid degeneration of small
these should not preclude consideration of
blood vessels is seen in many organs,

Hendra virus. Infection is not always fatal,
including the lungs, heatt, kidneys, spleen,
with 25% of !mown cases having recovered
lymph nodes, meninges, GI tract, skeletal

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from clinical disease.

muscle, and bladder. Antigen specific for

Clinical signs that should prompt a veteri Hendra virus can be demonstrated by immunarian to consider Hendra virus infection nohistochemical staining in the vascular
include acute onset of illness, fever, and
lesions and along alveolar walls. lntracytorapid deterioration. Respiratory signs can plasmic viral inclusion bodies can be seen in
include pulmonary edema and congestion,
infected endothelial cells by electron (but
respiratory distress (increased respiratory
not light) microscopy. When respiratory
rate), and terminal nasal discharge, which
disease is predominant, the principal gross
may be clear initially and progress to stable
lesions are severe edema and congestion
white or blood-stained froth. Neurologic
of the lungs and marked dilatation of the
signs can include "wobbly gait" progressing subpleural lymphatics. The airways are
to ataxia, altered consciousness (apparent
filled with thick froth, which is often
loss of vision in one or both eyes, aimless
blood-tinged. Additional lesions seen in
walking in a dazed state), head tilt, circling,
some affected horses include increased
muscle twitching (myoclonic spasms have
pleural and pericardia] fluids, congestion
been seen in acutely ill and recovered
of lyn1ph nodes, hemorrhages in various
horses), urinary incontinence, recumbency
organs, and slightjaundice.

with inability to rise, terminal wealrness,

Microscopically, the primary lesions are
ataxia, and collapse. Other clinical signs
those of an acute interstitial pneumonia.

may include depression, highly increased

Severe vascular damage, with serofibrinous
heart rate, facial edema, muscle trembling,
alveolar edema, hemorrhage, thrombosis of
anorexia, congestion of oral mucous
capillaries, necrosis of alveolar walls, and
membranes, colic-like symptoms (generally alveolar macrophages are evident in the quiet abdominal sounds on auscultation of
lungs.

the abdomen in pretenninal cases), and

If new·ologic disease is predominant,
stranguria in both males and females.

lesions of nonsuppurative meningitis or

Proximity to fruit bat roosts or feeding sites meningoencephalitis, including perivascushould increase the index of suspicion.

lar cuffing, neuronal degeneration, and focal

Where horses are paddocked, Hendra
gliosis, have been seen.

virus infection is more likely to manifest as
a single sick or dead horse than as multiple
cases. Most paddock infections have

Diagnosis: Hendra virus infection should
involved a single fatally infected horse with be considered when there is acute onset no transmission to in-contact companion
fever and rapid progression to death, but a
horses. However, on several occasions,
nonfatal outcome should not preclude
one or more companion horses have
consideration of Hendra virus. Confirmabecome infected after close contact with tion of the diagnosis is based on laboratory
the index case before or at the time of
exanlination of approp1iate specimens to
death. Where horses are stabled, it appears detect virus, viral antigen, viral nucleic acid, that Hendra virus has the potential to
or specific antibodies. The approach to
spread either through close direct contact
specimen collection should reflect the
with infectious body fluids, or through
serious zoonotic potential ofHendra virus
indirect transmission via contaminated
and should incorporate appropriate
fomites, including inadvertent humanmeasures to avoid hun1an exposure.

assisted transfer. Hendra virus infections

Minimum recommended samples include
in horse stables to date have resulted in
a blood sample (whole and/or EDTA) and
multiple horses becoming infected, which
nasal, oral , and/or rectal swabs. These can
appear to have arisen from a horse infected be taken from both live and dead horses.

in a paddock or outside yard being brought Necropsy specimens, both fresh and fixed in into the stable.

lOOA, formalin, of lung, kidney, spleen, liver,
lymph nodes, and brain will increase the

Lesions: The presence oflarge endothelikelihood of reaching a conclusive lial syncytial cells on histopathology is
diagnosis but also potentially increase the characteristic of Hendra virus infection.

risk of human exposure. The number and

Although most prominent in pulmonary
type of specin1ens collected should follow a
capillaries and arterioles, these cells are
careful risk analysis by the veterinarian to
also seen in other organs (lymph nodes,
prevent human exposure and consider

710

HENDRAVIRUS INFECTION
many factors, including personal protective

Prevention focuses on minimizing
equipment available, training, and prior
contact with fruit bat body fluids/contamiexperience. If there are personal safety nants and includes simple, practical
concerns, only a minimal set of samples
measures such as placing feed and water

(blood, swabs) should be collected.

containers under cover and minimizing the

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Submitting a combination of EDTA blood,
nwnber of bat food trees/shrubs (fruiting
serum, nasal, oral, and rectal swabs should
and/or flowering) in horse paddocks or
be sufficient to detect Hendra virus
excluding horses from the vicinity of such
infection in a horse highly suspected to be
trees/shrubs. Control is based on euthanasia
infected. Recommended procedures for
and deep burial of cases; monitoring,
safe handling of suspect Hendra cases are
isolating, and restricting movement of
available at the Biosecurity Queensland
in-contact animals; and disinfection of

Web site (www.daff.qld.gov.au).

potentially contaminated surfaces.

The virus can be isolated in a range of cell
lines; Vero cells are the cell line of choice.

Zoonotic Risk: Human infection with

Viral cytopathic effect, which typically

Hendra virus has a 57% case fatality rate.

develops after 3 days, is characterized by

All hwnan infections have occurred from
syncytia formation in infected cells. Virus
handling infected horses (both live horses
isolation and other diagnostic tests
and dead horses at necropsy), so great care
involving live virus should only be
should be taken to ensure the personal
attempted under biosecurity Level 4
safety of all people in contact with suspect
conditions. Sero logic confirmation of
or confirmed equine cases. Neither
infection is based on testing acute and
bat-to-hun1an nor hun1an-to-human
convalescent sera collected 2-4 wk apart in
transmission has been recorded.

a virus neutralization test. Presence of the

Protocols to minimize risk of human
characteristic vascular lesions on histopaexposure should be in1plemented on thology is highly suggestive of the infection;
suspicion of Hendra virus infection in a
specificity of the lesions can be confinned
horse, not on confirmation. An outline
by immw10chemical labeling with Hendra
of the approach developed by Biosecurity
virus reference antiserum.

Queensland includes the following steps to

African horse siclmess can clinically
minimize risk. First, a plan should be made
mimic Hendra virus infection and should
in advance that outlines how Hendra virus
be considered in the differential diagnosis.

risks will be managed by the practice and

Other causes of sudden death that must be
individual veterinarians in that practice.

excluded include anthrax, botulism, certain

This includes 1) taking precautions based
bacterial infections ( eg, pasteurellosis,
on suspicion ofHendra virus and not
equine influenza, peracute equine herpeswaiting for confirmation of infection; virus 1 infection), snake bite, and plant or

2) isolating sick or dead horse( s) from
chemical poisoning.

people and all other animals, including pets;

3) limiting hwnan contact with in-contact

Treatment, Prevention, and Control:

horses to only essential people; 4) promoting

There is no specific antivira1 treatment for
personal hygiene ( especially hand washing,

Hendra virus infection. A vaccine,
showering) for in-contact staff; 5) identifycontaining a noninfectious protein ing hazards and taking steps to minimize the
component (G protein) of the virus, has
risks associated with tlwse ( eg, if deconbeen developed; it was introduced in taminating an area, avoid generating

November 2012 and is available through
splashes and aerosols by not using a
accredited veterinarians in Australia.

high-pressure hose); 6) infonning people

Healthy horses can be vaccinated from 4 mo who may be potentially exposed such as of age with two doses at a 21-day interval,
owners, handlers, and others (including
followed by boosters every 6 mo. Studies
other veterinarians and veterinary
are being conducted to determine whether
assistants) of the risk and the appropriate
the period of booster vaccination can be
procedures to be followed; and 7) referring
extended to 1 yr.

to relevant animal health and public health

Confinned cases should be euthanized on
authorities.

hwnane grounds and to limit risk of hwnan

Second, adequate personal protective
exposure. In Australia, euthanasia of
equipment should be used: 1) all exposed
recovered seropositive horses is also
skin, mucous membranes and eyes
recommended, because the currently
should be protected from direct contact;
available evidence cannot exclude the

2) inhalation of airborne particulates should
possibility of recrudescence in these
be prevented; 3) regular hand washing and
animals.

washing of exposed skin with soap should

AFRICAN SWINE FEVER

711
be promoted; and 4) cuts and abrasions
saliva, and urine) and tissues from sick or
should be covered by wateHesistant
dead horses should be treated as potentially
occlusive dressings that are changed as
infectious and appropriate precautions
necessary.

taken to prevent any direct contact with,

In particular, blood and other body fluids
splash back of, or accidental inoculation

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( especially respiratory and nasal secretions,
with these body fluids.

AFRICAN SWINE FEVER

African swine fever (ASF) is a highly

The disease is limited to all breeds and
contagious hemoIThagic disease of pigs that
types of domestic pigs and European wild
produces a wide range of clinical signs and
boar. All age groups are equally susceptible.

lesions that closely resemble those of

In Africa, the virus produces inapparent
classical swine fever (seep 713). It is an
infection in two species of wild swineeconomically important disease that is waithog (Phacochoerus aethiopicus) and
enzootic in many African countries and the
bushpig (Potmnochoerus porcus )-and in

MediteITanean island, Sardinia. In June
the soft tick Oniithodoros moubata. When

2007, ASF was confirmed for the first time
the disease was endemic in southern Spain
in Georgia in the Caucasus region. Since its
and Portugal, a different species of soft tick,
introduction into Georgia, Af1ican swine

O erraticus, becaine infected with the virus.

fever virus (ASFV) has spread rapidly into

Several other 01nithodoros spp that are not vast areas of western and southern Russia,
usually associated with pigs or wild swine
where it is CUJTently (2013) circulating
have been infected experimentally. ASF
out of control in domestic and wild pig
has been reported in a large number of
populations. The virus has spread to the
countries in Africa south of the Sahara,
edges of Europe, with outbreaks reported
either as an enzootic disease or as sporadic
in both the Ukraine and Belarns in 2013,
epidemics in domestic pigs. The first spread
putting at risk the very large pig populations
of the disease outside Africa was into
present in Eastern Europe.

Europe (Portugal) in 1957 as a result of
waste from airline flights being fed to pigs

Etiology and Epidemiology: ASFV is
neai· Lisbon airpmt. Although this incursion
a large, enveloped, double-stranded DNA
of disease was almost certainly eradicated,
virns that replicates primarily in cells of
a further outbreak occuJTed in 1960 in
the mononuclear phagocytic system. It is

Lisbon, and ASF then remained endemic in
cuJTently classified as the only member of
the Iberian peninsula until the mid-1990s.

a family called African swine fever-like

Outbreaks of ASF were repmted in a
viruses (Asfarviridae ). The prolonged
nw11ber of other European countries during
period during which ASF has been an
the 20th century, including Malta (1978),
enzootic disease in Africa is likely to have

Italy (1967, 1980), France (1964, 1967, 1977),
led to the selection of viruses of varying

Belgiun1 (1985), and the Netherlands (1986).

virulence. Distinct genotypes of ASFV have

The disease was eradicated from each of
been differentiated by sequence analysis
these countries but has remained endemic
of the genomes of viruses obtained from
in Sardinia since its introduction in 1978.

different geographic areas over a long time.

Owing the 1970s, ASFV spread to the

The virus is highly resistant to a wide pH

Caribbean and South America. An outbreak
range and to a freeze/thaw cycle and can
in south Brazil in 1978-1979 was eradicated
remain infectious for many months at room
by stai11ping out, and Brazil regained its
temperature or when stored at 4 °C. Virus in

ASF-free status in December 1984.

body fluids and serum is inactivated in 30

The spread of ASF out of Africa has been
min at 60°C, but virus in unprocessed pig
a relatively rai·e event, but in June 2007 ASF
meat, in which it can remain viable for
was confirmed in pigs in the former Soviet
several weeks, can be inactivated only by
republic of Georgia in the Caucasus region.

heating to 70°C for 30 min. Although ASFV

Genetic analysis revealed the genotype of
can be adapted to grow in cells from
tl1e Georgia isolate to be closely related to
different species, it does not replicate
isolates in circulation in Mozainbique,
readily in any species other than swine.

Madagascar, and Zainbia. It is therefore

712

AFRICAN SWINE FEVER
likely that pigs were fed ASFV-contamitract and is also present in secretions and nated pig meat transported by ship from
excretions containing blood.

the southeastern part of Africa. By July

Pigs that survive infection with the less

2007, the outbreak had spread to 56 of61
virulent isolates may be persistently

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districts in Georgia; soon after, outbreaks
infected and have circulating antibody,
of ASF were reported in neighboring
although tl1ey do not excrete virus or
regions, including the autonomous republic transmit virus to their offspring in utero.

of Abkhazia, Armenia, and Nagorno-Kara

Their role in the epidemiology of the disease
bakh. Later in the year, infection of wild
is not fully understood; however, they are
boar was confirmed in the Russian republic
resistant to disease when challenged with
of Chechnya. In 2008, the spread of ASF
related highly virulent isolates, indicating
continued into North Ossetia; it then
some level of cross-protective inununity
jumped over 1,000 km into Orenburg,
between strains.

illustrating its potential for rapid spread
over long distances. By October 2008, a

Clinical Findings and Lesions: Pertotal of21 outbreaks of ASF had been acute, acute, subacute, and chronic forms
officially reported in five Russian adminisof ASF occur, and mortality rates vary from trative divisions. From 2009-2013, the virus O to lOOOAi, depending on the virulence of has continued to spread within the Russian
the virus with which pigs are infected.

Federation, and there are currently (Oct

Acute disease is characterized by a short

2013) two main expanding hotbeds of
incubation petiod of 3-7 days, followed by
infection in Russia, one in the southern part high fever ( up to 42°C) and death in 5 -10
of the center of the Rostov region (Oblast)

days. The least variable clinical signs are
and the other in the Tver region (Oblast)

loss of appetite, depression, and recumand the adjoining areas. In 2013, outbreaks bency; other signs include hyperemia of
of ASF were reported in both the Ukraine
the skin of the ears, abdomen, and legs;
and Belarus, putting at risk large pig
respiratory distress; vomiting; bleeding
populations in eastern Europe.

from the nose or rectum; and sometimes
diarrhea Abortion is sometimes the first

Transmission and Pathogenesis: ASFV
event seen in an outbreak. The severity
is maintained in Africa by a natural cycle
and distribution of the lesions also vary
of transmission between warthogs and the
according to virulence of the virus.

soft tick vector O moubata, which inhabits

Hemorrhages occur predominantly in
warthog burrows and from which it is
lymph nodes, kidneys ( almost invariably
wilikely ever to be eliminated. The sprea(l
as petechiae), and heart; hemorrhages in
of virus from the wildlife reservoirs to
other organs are variable in incidence and
domestic pigs can be py the bite of an
distribution. Some isolates produce an
infected soft tick or by ingestion of warthog
enlarged and friable spleen; straw-colored
tissues. Virulent viruses produce acute
or blood-stained fluid in pleural, pericardia!,
disease, and all body fluids and tissues
and peritoneal cavities; or edema and
contain large amounts of infectious virus
congestion of the lungs. Some viruses of low
from the onset of clinical disease until
virulence have been isolated in Europe and
death. Pigs infected with less virulent
produce nonspecific clinical signs and
isolates can transmit virus to susceptible
lesions. Chronic disease is characterized by
pigs as long as 1 mo after infection; blood is
emaciation, swollen joints, and respiratory
infectious for as long as 6 wk, and transmisproblems. This form of tli.e disease is rarely sion can occur if blood is shed. Pigs usually
seen in outbreaks.

become infected via the oronasal route by
direct contact with infected pigs or by

Diagnosis: ASF cannot be differentiated
ingestion of waste food containing
from classical swine fever (hog cholera) by
unprocessed pig meat or pig meat products.

either clinical or postmortem exanlination.

The primary route of infection is the upper

San1ples of blood, serum, spleen, tonsil, and
respiratory tract, and virus replicates in the
gastrohepatic lymph nodes from suspected
tonsil and lymph nodes draining the head
cases should be submitted to the laboratory
and neck, with generalized infection rapidly
for confirmation. Virus can be isolated by
following via the bloodstrean1. High
inoculation of primary cultures of pig
concentrations of vims are then present in
monocytes, in which it produces hemadall tissues. The factors that produce the sorption of pig red cells to tl1e surface of
hemorrhagic lesions are not fully defined,
infected cells. Classical swine fever virus
but severe disruption to the blood clotting
does not replicate in these cells. There are
mechanism plays a major role. Virus is
nonhemadsorbing viral isolates, some of
excreted mainly from the upper respiratory
which produce virulent disease. These

CLASSICAL SWINE FEVER

713
isolates produce only a cytopathic effect

Control: There is no treatment for ASF,
in pig leukocytes. Confinnation of ASF in
and all attempts to develop a vaccine have
these cases has to be performed by either
so far been unsuccessful. Prevention

PCR or an antigen-detection ELISA. Viral
depends on ensuring that neither infected
antigen can be detected in infected tissue
live pigs nor pig meat products are

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smears or sections by staining with labeled
introduced into areas free of ASF. All
antibodies (several enzyme-labeled tests are successful eradication programs have available, eg, immunofluorescence), and
involved the rapid diagnosis, slaughter,
viral DNA by PCR or hybridization of
and disposal of all animals on infected
nucleic acid probes to tissue sections. The
premises. Sanitary measures must also be
most appropriate tests to detect antibody
applied and include control of movement
in serum or tissue fluids are the ELISA
and treatment of waste food. Subseand indirect immunofluorescence.

quently, a serologic survey of all pig farms

Other differential diagnoses include
within a specific control zone must be
hemorrhagic bacterial infections and
conducted to ensure that all infected pigs
certain types of poisons.

have been identified.

CLASSICAL SWINE FEVER

(Hog cholera, Swine fever)

Classical swine fever is a contagious, often

Etiology and Epidemiology: CSF is
fatal, disease of pigs clinically characterized
caused by a small, enveloped RNA virus
by high body temperature, lethargy,
in the genusPestivirus of the family
yellowish diarrhea, vomiting, and a purple

Flaviviridae. Classical swine fever virus
skin discoloration of the ears, lower

(CSFV) is antigenically related to the otl1er
abdomen, and legs. It was first described in
pestiviruses, mainly to bovine viral dian·hea
the early 19th century in the USA. Later, a
virus (BVDV, seep 1436) of cattle and to
condition in Europe termed "swine fever"

border disease virus (BDV, seep 622) of
was recognized to be the same disease. Both sheep. These viruses are highly prevalent in names continue to be used, although in
bovine and ovine populations and can infect
most of the world the disease is now called
pigs. Although infections of pigs with
classical swine fever (CSF) to distinguish it
ruminant pestiviruses in most cases do not
from African swine fever (seep 711), which
lead to clinical disease and are rapidly
is a clinically indistinguishable disease but
cleared, infections with both BVDV and
caused by an unrelated DNA virus. Because

BVD induce an antibody response in swine.

of the severe economic impact of CSF,

Therefore, antibody disc1imination tests
outbreaks are notifiable to the OIE. CSF has
must be applied to differentiate CSF
the potential to cause devastating epideminfections from infections caused by ics, particularly in countries free of the
runlinant pestiviruses. Transmission of
disease. In these countries, vaccination is
rwninant pestiviruses to pigs usually
allowed only under emergency circwnrequires direct contact with cattle, sheep, or stances. In case of a new outbreak, strict
goats. CSFV naturally infects members of
measures are enforced to control spread,
the Suidae fan1ily, ie, domestic and wild
eg, culling of infected and disease suspect
pigs.

herds and strict movement restrictions. This

In the laboratory, CSFV is cultured in cells
can have severe consequences for the swine
of porcine origin, notably in the PK-15 cell
industry, especially in densely populated
line (porcine kidney), but does not generally
livestock areas. Awareness and vigilance
cause a visible cytopathic effect. The virus
are essential, so that outbreaks are detected
has only one serotype, although some minor
early and control measures instituted
antigenic va.iiability between strains is seen.

rapidly to prevent further spread of CSF.

Strains can be typed for epidenliologic

The "high risk period," ie, the tin1e between mapping purposes by sequencing tl1e entire
introduction of the virus and detection of
viral genome or specific regions of the viral
the outbreak, must be kept as short as
genome (ie, 5'UTR, E2, and NS5B regions)

possible.

combined with phylogenetic analysis.

714

CLASSICAL SWINE FEVER

CSFV is moderately fragile and does not

CSFV within herds for long periods has
persist in the envirorunent or spread long
been observed. Infections of sows during
distances by the airborne route. However,
pregnancy with low to moderately vi.J.ulent
it can survive for prolonged periods in a
strains of CSFV may lead to in utero
moist, protein-rich envirorunent such as
infections of fetuses. These infections lead

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pork tissues or body fluids, particularly if
to litters born persistently infected with
kept cold or frozen. Virus survival times

CSFV that ai·e carriers of the vii.us and
up to several years have been observed in
source for new infections. Persistently
frozen pork meat. CSFV may also survive
infected carrier pigs usually do not show
months in chilled or cured cuts.

clinical signs but constantly shed CSFV into

CSF has a worldwide distribution. It is
the envirorunent. Therefore, it is particuconsidered endemic in certain countlies larly important to consider CSFV infections
of Central and South America, in the
while investigating herds presenting with

Catibbean basin, and in many pork-producunexplained reproductive failures that ing countries in Asia. Australia, New
include clinical manifestations in piglets

Zealand, Canada, and the USA are free of
such as congenital tremor or congenital
the disease, as well as most countries of
abnorn1alities.

western and central Europe, although
sporadic outbreaks occur in Europe. CSF is

Clinical Findings and Lesions: CSF is
considered endemic in several countries in
characterized by fever, hemorrhages, ataxia,
eastern Europe. The main source of CSFV
and purple discoloration of the skin;
infection is the pig, either via infected live
however, the clinical presentation varies,
animals or via uncooked pork products.

depending on host characteristics and the

In areas where CSF is endemic, the major
particular virus strain causing the infection.

concern relates to the spread of disease

CSF occurs in several forms, including
through movement of infected animals,
highly lethal, acute, chronic, or subclinical.

which may lead to widespread outbreaks,

Acute forms of CSF, associated with highly
particularly in areas where there is largevirulent CSFV strains, ai·e chai·acterized scale transport of pigs ainong farms or to
by an incubation period that is typically
slaughter houses. In Europe, CSFV is

3-7 days, with death occurring within 10
considered endemic in wild boar populadays after infection. Fever >41 °C ( 105.8°F) tions, and infected wild boars are a source
is usually seen and persists until terminal
for CSF outbreaks ainong domestic pigs.

stages of the disease when body tempera

However, the most probable source of CSFV ture drops and becomes subnorn1al.

infection for wild boars is contatninated

Constipation followed by diarrhea and
garbage or even "spillover" from infected

· vomiting is corrunon.

domestic pigs. The outcome of such

The principal lesion produced by CSFV
infections mainly depends on the size
infection is a generalized vasculitis,
and density of the wild boar populations
clinically manifested as hemorrhages and
affected. Outbreaks in small populations
cyanosis of the skin, notably at the ears,
of wild boat-s living within natural confmes,
lower abdomen, and extremities. There may
such as valleys, tend to be self-limiting,
also be a generalized erythema of the skin.

and the disease fades away over ti.me. In

Vasculitis in the CNS leads to incoordinacontrast, infections leading to outbreaks tion (ie, staggering gait) or even convulin large areas densely populated with wild sions. Histologically, nonsuppurative
boars often become endemic.

encephalitis with a characteristic vascular

Another major risk for CSF outbreaks is
cuffing is corru11on. At necropsy, the
the accidental introduction of CSFV into
principal findings are widespread petechial
herds through illegally imported pork meat
and ecchyrnotic hemorrhages, especially in
or pork products that often find their way
lymph nodes ( eg, mai1dibular and retrointo the porcine food chain via swill feeding.

pharyngeal), tonsils, larynx, kidneys,

However, CSFV is readily inactivated by
spleen, urinary bladder, and ileun1.

heat (ie, cooking), which emphasizes the

Infarction may be seen, particularly in the
importance of enforcing regulations for
periphery of the spleen. Subacute and
heat treatment of swill feed. In addition,
chronic forn1s of the disease are also
many countries have completely banned
characterized by high fever, staggering gait,
swill feeding practices.

cough, diarrhea, purple discoloration of the

Mechanical transmission by vehicles and
skin, and death. In the subacute form, death
equipment, as well as by personnel (notably
generally happens within 20-30 days after
veterinarians) travelling between pig fatms,
infection; in the chronic form, death may
are also significant means of spread of CSF
occur much later. Subacute and chronic
within infected areas. The persistence of
forn1s of the disease are associated with

CLASSICAL SWINE FEVER

715

CSFV strains of moderate to low virulence,
of CSFV antibodies are pursued. Nasal
respectively. Low virulence strains can
swabs and/or tonsil scrapings are combe difficult to detect; the only clinical monly collected clinical sainples used to
expression may be poor reproductive
detect the virus (ie, viral RNA).

performance of sows and the birth of piglets

Significant ainounts of CSFV are shed
with neurologic defects ( eg, congenital
from infected animals into the environment

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tremor). In chronic fonns of CSF after an
via the oronasal route, paiticularly early
initial acute febrile phase, infected animals
during infection. Detection of CSFV antigen
may show an apparent recovery but then
can be performed using direct immunofluorelapse, with anorexia, depression, fever, rescence on frozen tissue sections,
and progressive loss of condition (ie,
particularly in tonsil sainples using specific
marked weight loss). Macroscopically, in
antibodies. Antigen detection can also be
addition to the lesions described above,
done using ELISA; however, this assay has

"button" ulcers may develop in the intestine, low sensitivity and is only useful for particularly near the ileocecaljunction.

screening for the presence of CSFV at the

Histologically, atrophy of the thymus and
herd level. More commonly, viral nucleic
depletion of lymphoid follicles in lymph
acid detection is done using reverse
nodes are seen.

transctiptase (RT)-PCR. The assay is highly
specific and can differentiate CSFV from

Diagnosis: CSF is first detected by

BVDV and BDV. Standardized methods such
veterinarians in the field. Because clinical
as RT-PCR can be scaled up to screen lai·ge
signs manifested by CSFV-infected pigs
nwnbers of sainples, giving rapid results
are also seen with other diseases of swine,
while retaining high sensitivity. This is
laboratory confinnation is always required.

particulai·ly useful to screen herds during

Clinically, the differential diagnosis varies
an outbreak of CSF.

according to the course of the disease,

For virus isolation, cell cultures are
and primaiily includes Africai1 swine
inoculated with tissue suspensions or WBCs,
fever. Hemorrhagic lesions must also be
fixed after 2 -3 days, and the virus is detected
distinguished from those seen in porcine
using specific antibodies directed against
dennatitis and nephropathy syndrome

CSFV ( eg, fluorescent or enzymatic
and postweaning multisystemic wasting
methods). Final results may not be available
syndrome. Hemolytic disease of the
for 4-7 days. This method is labor intensive
newborn, porcine reproductive and
and time conswning. Virus characterization
respiratory syndrome, Aujeszky disease,
using virus-specific monoclonal antibodies
parvovirus, thrombocytopenic purpura,
or RT-PCR is performed to differentiate
anticoagulant poisoning ( eg, warfarin),

CSFV from the other pestiviruses. Positive
and salt poisoning should also be considresults of antigen detection or virus isolation ered as possible differential diagnoses.

are not confirmed until vims identification is

Septicemic diseases, including salmonellocompleted. Virus neutralization tests and sis, erysipelas, pasteurellosis, actinobacil

ELISA tests are available to detect antibodlosis, Haemophilus s·u·i::; infections, and ies against CSFV. Because the virus is
eperythrozoonosis may resemble CSF.

noncytopathogenic in culture, the neutrali

Congenital infections with ruminant
zation test requires an additional immunopestiviruses can resemble CSF reproductive staining step to reveal the presence of failures caused by low virulence strains of
neutralizing antibodies. ELISA tests are

CSFV. Poor reproductive perfom1ance in
suitable for large-scale serology when large
sows can also be associated with pseudoranwnber of sainples are processed, ie, for bies, parvovirus, and other noninfectious
surveillance purposes. Cross-reactions
causes.

between pestivirus antibodies are seen in

Virologic tests are essential to confirm
diagnostic tests. The presence of antibodies
the diagnosis of CSF. Advice on sainple
against ruminant pestiviruses in pigs may
submission should be sought from the
hainper the serologic diagnosis of CSF.

laboratory. Suitable tissues to detect the

BVDV or BDV-specific antibodies are
presence of the virus are tonsils, lymph
sporadically detected in pig populations.

nodes (mandibular, retropharyngeal,

Risk factors related with run1inant pestivirus
gastrohepatic, and mesenteric), spleen,
antibodies in pigs are associated with the
kidney, and ileun1. Whole blood collected
presence of cattle on the saine fann and high
with EDTA as anticoagulant can be used for
density of sheep and/or goats in the area.

virus isolation or virus detection, particu

Some commercial ELISAs can distinguish
lai-ty during the viremic phase of the

CSF from BVDV or BDV antibodies, although
infection. Clotted blood sainples (serum)

confirmatory testing is advised usually via
are taken when serologic tests for detection
neutralizing peroxidase-linked assays.

716

CLASSICAL SWINE FEVER

New generations of CSFV marker

Countries free of CSF usually implement
vaccines have been developed to make
preventive measures to avoid outbreaks
emergency vaccination compatible with
of CSF by controlling movement of live
control of CSF. The application of a
animals and pork products at borders.

marker vaccine is possible if tests such as

Countries free of CSF forbid the use of

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ELISA can distinguish between antibodies
prophylactic vaccination. In countries
produced in response to a natural
where CSF is endemic, prophylactic
infection and those produced by vaccinavaccination is regularly practiced and is tion. This is the DIV A principle ( differenmandatory in some cases. Prophylactic tiation of infected from vaccinated
vaccination has been used worldwide as a
animals) that is based on detection of
tool to control and eradicate CSF. In these

CSFV-specific antibodies that develop in
countries, herds affected by an outbreak are
the host only with CSFV infection but not
quarantined and if possible eliminated.

on vaccination with a marker vaccine.

Emergency ring vaccination around the

These assays have been developed as
outbreak is done to prevent further spread
necessary companion tests for CSF
of CSFV. CSF live attenuated vaccines are
marker vaccines.

safe and highly efficient, being able to
induce protection shortly after vaccination

Control: CSF is a notifiable disease.

(within 3 days after vaccination). Several

Control is usually strictly regulated by local
live attenuated vaccines, such as the
laws that establish strict sanitary measures.

Chinese lapinized vaccine CC-strain), the

No treatment is available. Outbreaks in

Japanese GPE-strain, and the French
countries free of CSF are controlled rapidly

Thiverval strain, have been developed and
via culling of infected animals and
used in different countries. More recently,
preemptive slaughter of susceptible animals
subunit CSFV vaccines containing only the
within determined distances from the focus.

major viral surface glycoprotein of the virus

Restriction of movement within a wellhave been licensed. Although these vaccines defined radius from the outbreak is applied
have DIVA capabilities, they lack the
to contain spread of the infection.

efficiency of live attenuated vaccines. Oral

Eventually, emergency vaccination can be
vaccination of wild boars has been used
authorized to control the further spread of
successfully within tl1e European Union

CSFV. Countries will regain their CSF-free
using a live attenuated vaccine delivered
status ( no antibodies or virus detected)

via baits. Oral vaccination has been a key
after establishing that CSFV is no longer
strategy to control CSF, particularly where
present in the national pig herd.

parenteral vaccine delivery is not feasible.

EDEMA DISEASE

(Escherichia coli enterotoxemia)

Edema disease is a peracute toxemia
associated primarily with enterotoxigenic
caused by specific pathotypes of Escheri

E coli. A new variant of Fl8 has been
chia coli that affect primarily healthy,
identified on strains of E coli that carry the rapidly growing nursery pigs. Other names

Stx2e gene, but the role of these strains in
for edema disease include "gut edema" or
edema disease is not known. The Shiga

"bowel edema" because of the prominent
toxin-producing£ coli implicated in edema
edema of the submucosa of the stomach
disease most commonly belong to four
and mesocolon.

specific serotypes: 0138:KSl:NM,

0139:Kl2:Hl, 0141:K85ab:H4, and

Etiology and Pathogenesis: Edema

0141:K85ac:H4. However, other serotypes
disease is caused by hemolytic E coli that
of E coli may be implicated, and strains of produce Fl8 pili and Shiga toxin 2e (Stx2e,
serogroup O 14 7 have been dominant in
also known as verotoxin 2e or VT2e). The
parts of the USA. These 0147 strains

Fl8 pill have two major antigenic variants,
typically carry the Hl 7 flagella, but some

Fl8ab and Fl Sac; F l 8ab is characteristic
have Hl4 or H4. Some of these 0147 strains
of edema disease strains, and Fl8ac is
are not typeable with O 14 7 specific

EDEMA DISEASE

717
antiserum but can be identified by their
associated with weaning, including the

O antigen genes.

stresses of mixing pigs, changes in diet,

Pigs become infected initially by a
and the loss of milk antibodies from the
contaminated environment or the sow.

intestine, appear to be important elements

Spread of infection among perunates is
in enhancing the susceptibility of weaned

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facilitated by the large numbers of edema
pigs to the disease.

disease-producing E coli that are shed by
colonized pigs. Some strains of E coli that Clinical Findings: Clinical signs range
cause edema disease also carry genes for
from peracute death with no signs of illness
enterotoxins and can cause diarrhea as well
to CNS involvement with ataxia, paralysis,
as edema disease. Ingestion of edema
and recumbency. Edema disease usually
disease strains of E coli is followed by
occurs 1-2 wk after weaning and typically
colonization of the intestine in pigs in which
involves the healthiest animals in a group.

intestinal epithelial cells carry receptors for

The disease is seen occasionally in nursthe FIS pill. Expression of the receptors ing pigs or in adult pigs. The average
is age-related, so younger pigs are less
morbidity is 300/o-400Ai, and the mortal-
susceptible to colonization than older pigs.

ity among affected pigs is often as high

Some pigs carry a specific mutation in a
gene required for expression of the
as 900A,. Pe1iocular edema, swelling of the
receptors and are thereby resistant to
forehead and subrnandibular regions, dysinfection.

pnea, and anorexia are common.

Resistance/susceptibility is detem1ined

Lesions: Edema disease is primarily a
by a single locus with a dominant susceptidisease of the vasculature, and gross lesions bility allele and a recessive resistant allele;
consist of subcutaneous edema and edema
it is possible to select resistant pigs, which
in the subrnucosa of the stomach, particucan be identified by a simple PCR test that larly in the glandular cardiac region. The
identifies presence or absence of the
edema fluid is usually gelatinous and may
specific mutation. Some concern about
extend into the rnesocolon. The edema may
selection for resistance to FIS+ E coli
be accompanied by hernon-hage. Fibrin
has been expressed, because a very high
strands may be found in the peritoneal
association between presence of the marker cavity, and serous fluid may be found in for resistance to FIS+ E coli and presence
both the pleural and peritoneal cavities.

of the marker for stress susceptibility was

Microscopically, a degenerative angiopathy
shown in Swiss Landrace pigs. However,
affecting arteries and aiterioles and
this association does not exist in Belgian
necrosis of the smooth muscle cells in the
pigs.

tunica media are present. Lesions of focal

Stx2e produced in the intestine of
encephalomalacia in the brain stern are
colonized pigs is responsible for the major
characteristic and thought to result from
clinical signs and pathology seen. This
vascular damage, leading to edema and
cytotoxin inhibits protein synthesis, leading
ischemia.

to cell death. The toxin is absorbed from the
intestine and targets vascular endothelium

Diagnosis: A clinical history of peracute
in specific sites believed to have high
death in healthy, well-conditioned, recently
concentrations of the toxin receptors
weaned pigs, along with observation of
globotriaosyl ceran1ide and globotetraosyl
periocular edema and extensive edema of
ceramide. A study showed that edema
the stomach and mesocolon, are helpful
disease strains of E coli may colonize the
in diagnosis. There may be a charactermesenteric lymph nodes and produce Stx2e istic squeal due to edema of the larynx.

there. This may be an additional site from
which the toxin is absorbed into the

Diarrhea may precede the signs of edema
bloodstream. The Stx2e toxin binds readily
disease if the E coli responsible also posto pig RBCs, which may transport the toxin sesses genes for enterotoxins. Characterto various sites in the body. Sites highly istically, the stomach is full of dry feed.

susceptible to the toxin include the

Diagnosis is easily made in an outbreak in
submucosa of the stomach, the colonic
which the full range of clinical signs and
mesentery, the subcutaneous tissues of the
pathologic features are likely to occur. It
forehead and eyelids, the larynx, and the
is more difficult when only a few animals
brain. Damage to vascular endothelium
are affected or when the disease occurs
results in edema, hemon-hage, intravascular
in an atypical age group. Isolation and
coagulation, and microthrombosis.

chai·acterization of the E coli are required High-protein diets increase the susceptifor a definitive diagnosis. Culture of the bility of pigs to the disease. Factors
small intestine and colon typically yields

718

EDEMA DISEASE
a heavy growth of hemolytic E coli, but in
difficult. Several experimental approaches
some cases the organism may no longer
have been shown to be effective, but none
be present in the intestine at the time of
are economical to date. These methods
death. Demonstration that the hemolytic
include feeding a high-fiber and low-protein

E coli isolated is an edema disease strain
diet, reducing the an10unt of feed given to

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may be done by PCR amplification of the
weaned pigs, vaccinating by a systemic
genes for the Fl8 pili and Stx2e. Recently,
route with Stx2e toxoid, oral vaccination
quantitative PCR for several pig bacte1ial
with an Fl8+ nontoxigenic E coli, passive
enteropathogens, including edema disease
systemic inm1m1ization with antitoxin, and
strains of E coli, was shown to be a rapid
passive oral immlll1ization with anti-Fl8
and sensitive method for detection and
antibodies. Mucosa] inunlll1ization with
quantification of these bacteria in pig feces.

purified Fl8 firnbriae has proved to be

Serotyping of the isolate is useful to track
ineffective, possibly because the pmtion of
tl1e persistence of a pruticular type of the
the Fl8 firnbria that binds to the intestine is
organism on a farm. The Fl8 pili are not
a small fraction of the total firnbrial
readily expressed on organisms that are
strncture. Incomplete protection was
cultured, but tl1e genes that encode them
reported after vaccination of pigs witl1
are easily detected by PCR.

the receptor portion of the Fl8 firnbriae
conjugated with F4 firnbriae. Two in1portant

Treatment and Control: Because the
developments are the rapid and inexpensive
onset of disease is often sudden and the
methods for plllification of Stx2e toxin
com-se rapid, treatment is often ineffective.

or toxoid and the demonstration that

Oral medication with antibiotics via the
inm1lll1ization of pregnant sows with Stx2e
drinking water may be used to protect
toxoid resulted in protection of their
clinically unaffected pigs in a herd in which
weaned offspring against a challenge with
cases of the disease have been detected.

a lethal dose of Stx2e toxin. The flagella of

Antibiotic sensitivity should be determined

Fl8ab edema disease E coli has been shown
on the isolate from an affected pig;
to be involved in adherence to pig intestinal
medication should be changed if the initial
epithelial cells in vitro and could be a new
choice was ineffective. Control is also
target for vaccines against edema disease.

ENCEPHALOMYOCARDITIS

VIRUS INFECTION

Encephalomyocarditis (EMC) is a.

mummification, and apparent reproducsignificant viral infection of swine and tive failure. Type A strains cause porcine
zoologic manunals. It is caused by members
reproductive problems, whereas type B
of the genus Cardiovirus in the family
strains cause heart failure. With the

Picomaviridae and recognized in many
recognition of porcine reproductive and
parts of the world. Although EMC virus
respiratory syndrome (PRRS) in 1987,

(EMCV) isolates from various regions and
however, the overall significance ofEMCV-1
countries have differed in pathogenicity and as a cause of reproductive disease in swine virulence, until recently all EMC viruses
has been questioned. The high mutation rate
were considered to exist as a single
of the PRRS arterivirns complicates the
serotype (EMCV-1). A cru·diovin.1s isolated
maintenance of reliable diagnostic PCR
from a wood mouse in Germany in 2012 was
assays for that virus, while a concurrent
distinguished from EMCV-1 by serologic

EMCV infection may be easily detected by
and molecular means and has been
virus isolation. Most outbreaks of EMCV
designated EMCV-2. Although EMCV-1
infection have been associated with captive
infects a wide variety of hosts, the host
aninlals in swine production lll1its, primate
range and pathogenicity of EMCV-2 remains
research centers, and zoos. Sudden death
to be deteffilined.

is often the first indication of infection. A

Swine may die acutely at any age due to
variety of exotic manunals have been fatally
associated myocardial failure or may be
afflicted with EMC in zoologic parks in tile
affected with neru0term abortions, fetal

USA, Australia, and other pruts of the world

ENCEPHALOMYOCARDITIS VIRUS INFECTION

719
and have included African elephants,
from conceptuses in cases of reproducrhinoceroses, hippopotamuses, sloths, tive failure due to near-term abortions
llamas, various antelope species, and many

(107-111 days of gestation), stillbirths, and
types of nonhuman primates ( chimpanzees,
mummifications. Reproductive problems
orangutans, baboons, monkeys, lemurs,
have been reported to involve sows of all

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etc). An episode of lion deaths at a zoo in the parities, often persisting in affected herds USA was associated with the feeding of the
for 2 -3 mo, but the possibly more significarcass of an African elephant that had died cant contribution of PRRS should be
of EMC, and a spontaneous outbreak of fatal investigated.

EMC was reported in free-ranging African
elephants at Kruger National Park in South

Africa in 1995. Reports of outbreaks of

Diagnosis: Because the pale necrotic

EM CV-associated disease are solicited and
heart muscle lesions that may be seen in
recorded at the Pirbright Institute in the UK.

fatal EMC infections are also seen in septic
infarction or vitamin E/selenium deficiency,

Epidemiology: Cardioviruses are small,
a definitive diagnosis requires virus
nonenveloped viruses that are almost
recovery and identification. Heart, liver,
always associated with rodents, and the
kidney, and spleen collected from acutely
disease in other mammalian species has
dead animals or abortuses are the specioften been attributed to spillover from mens of choice for virus isolation. Because
populations of wild mice and rats. These,

EMC viruses are very stable, they may be
and presumably other rodent species, shed
recovered from frozen tissues.

the viruses in feces and urine, which may

Sero logic diagnosis via virus neutralizacontaminate food and water supplies of tion, hemagglutination-inhibition, or ELISA
large mammals. Ingestion of rodents dead
is possible if acute and convalescent sera
or dying of EMC may be another means of
are collected, but the frequency of
infection. Pigs shed virus in nasal secresubclinical EMC infections makes single tions and feces during the first 3 days of
serum detenninations of little value in
experimental infection. During this short
aborting sows. Detection of antibody
period, the virus may be transmitted to
against EMC viruses in stillborn or large
other pigs by contact. Cardioviruses are
mununified fetuses is significant for fetal
resistant to adverse environmental
infection, however, because maternal
influences and may remain infective
immunoglobulins are not passed across the
for weeks to months under favorable
placenta in swine.

conditions.

Treatment, Control, and Prevention:

Clinical Findings and Lesions: The

There is no specific treatment for EMC, but
disease is named for its predilection for
mortality may be minimized by avoiding
the CNS and cardiovascular systems of
stress or excitement in animals at risk. EMC
experimental mice, and both encephaloviruses appear to cycle in rodents and are tropic and cardiotropic strains have been
most likely to affect swine and zoo animals
defined. In swine and zoologic species,
when rodent populations are high. Rodent
however, acute and subacute deaths are
control is thus critical to minimize exposure
almost always attributed to the destructive
of susceptible species. Prompt and proper
effects of the virus on the myocardium, with
disposal of animals that have died of the
resultant cardiac insufficiency, puhnonary
disease is also recommended. EMC viruses
edema, and frothy transudation into the
are inactivated by the judicious use of many
respiratory tract. Affected animals often
disinfectants labeled for livestock use.

appear to have asphyxiated in their own

Killed vaccines for the prevention of
respiratory fluids. Other clinical signs may
myocarditis in weaned swine have been
include fever, anorexia, listlessness,
patented but are no longer commercially
trembling, staggering, dyspnea, and
available in the USA except as autogenous
paralysis. Mortality approaching 100% has
products. The current impetus for vaccine
been described in suckling swine but
development has come largely from zoos
becomes successively lower in older age
and amusement parks where EMC has been
groups. Strains of EMC viruses that target
problematic. Success with a genetically
the pancreas and are diabetogenic in
engineered attenuated virus vaccine has
experimental mice have been recognized,
been reported in primates, pigs, and various·
but the significance of this finding for other
zoologic hoofstock species. Commercial
mammals has not been established.

EMCV vaccine production has been lin1ited

EMC viruses are known to cross the
by the apparent lack of need in most
placenta in swine and have been recovered
domestic livestock situations.

720

ENCEPHALOMYOCARDITIS VIRUS INFECTION

Zoonotic Risk: EMC viruses have rarely

EMCV infections are common in many parts
been recognized as the cause of human
of the world; most are asymptomatic or not
illness, and the severe myocarditis and acute
recognized. Human disease has been
fatal infections seen in many other species
characterized by fever, chills, nausea,
have not been reported in people. Nevertheheadache, nuchal rigidity, delirium, delusions, VetBooks.ir
less, serologic surveys have revealed human
vomiting, photophobia, and pleocytosis.

GlASSER'S DISEASE

(Porcine polyserositis, Infectious polyarthritis)

Pigs can be colonized by different microorsystemic invasion by H parasuis are still ganisms before weaning, but some of those
unknown. Moreover, the correlation
early colonizing agents are potentially
between serovar and virulence is not clear,
pathogenic. This is the case with Haemo
and strains belonging to the same serovar
philus parasuis, a commensal organism
may vaiy in virulence. Serotyping also has
of the upper respiratory tract of swine that
been used as the basis to establish
causes severe systemic disease charactervaccination criteria, but the cross-protecized by fibrinous polyserositis, arthritis, and tion between different serovars is variable
meningitis. Disease has a sudden onset,
and difficult to predict. Therefore, current
short comse, and high morbidity and
metl10ds of H parasuis identification and mortality. Young aninrnls ( 4---8 wk old) are
characterization are primarily genotyping
primaiily affected, although sporadic

(fingerprinting or sequencing methods).

disease can be seen in adults ( eg, introduc

The identification of virulence genes has
tion of a naive adult to a healthy herd).

received increased attention because of the

Survivors can develop severe fibrosis in the
possibility of differentiating strains with
abdominal and thoracic cavities, which can
pathogenic potential as well as of developresult in reduced growth rate and carcass ing vaccines.

condemnation at slaughter. Glasser's
disease is seen worldwide, and its incidence
appears to have increased since the intro

Clinical Findings: Clinical signs are seen
duction of porcine reproductive and respiramainly in pigs 4---8 wk old, although the age tory syndrome (seep 729).

of affected animals may vaiy, depending on
the level of acquired maternal immunity.

Etiology: The causal agent, H parasuis,

Peracute disease has a short course and
is a small, gram-negative pleomorphic
may result in sudden death without the
bacterium of the family Pastemellaceae that presence of characteristic gross lesions; requires V factor (NAD) supplementation
petechiae may be seen in some organs in
but not X factor (hem.in) for growth. In the
these cases, indicating septicemia.

laborato1y, H parasuis grows on enriched

The typical clinical signs of acute
chocolate agar; it can also be cultured in

Glasser's disease include high fe'ver
blood agar with a staphylococcal nmse

( 41.5°C [ 106. 7°F]), severe coughing,
streak. However, H parasuis is fastidious,
abdominal breathing, swollen joints, and
and its isolation in pme cultme from

CNS signs such as lateral decubitus,
diseased animals is usually difficult and
paddling, and trembling. These signs may be
frequently complicated because of
seen jointly or independently. Chronically
antibiotic treatments. Fifteen serovars of
affected animals may have a reduced

H parasuis have been reported, but a high
growth rate as a result of severe fibrosis
percentage of the evaluated isolates cannot
in the thoracic and peritoneal cavities.

be typed. Wide differences in serovar

Dyspnea and coughing not usually
virulence have been described. Serovars
associated with Glasser's disease have been

1, 2, 4, 5, 12, 13, 14, and some isolates that
described, together with H parasuis
cannot be typed are usually isolated from
isolation from the lungs of pigs with
systemic disease cases, while serovars
cata!Thal purulent bronchopneumonia

3, 6, 7, 9, and other nontyped isolates
and even fibrinohemorrhagic pneumonia.

are frequently isolated from the upper

However, H parasuis is not considered
respiratory tract. The factors involved in
a significant cause of coughing.

NIPAH VIRUS INFECTION

721

Disease prevalence is modulated by
collected from clinically affected animals
concomitant environmental stressors as
that were euthanized increase the chances
well as by viral infections affecting the
of isolation. Recently, a multiplex PCR
immune system, mainly porcine reproductechnique able to differentiate between virutive and respiratory syndrome and porcine lent and nonvirulent isolates has been

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circovirus type 2 systemic disease.

developed. This technique might be used

Lesions: Peracute disease may cause
to prevent introduction of pigs carrying
petechiae in some tissues, with no gross
potentially virulent strains onto farms that
lesions observed. Histologically, these pigs
are free of clinical Glasser's disease.

show septicemia-like microscopic lesions

Differential diagnoses of Glasser's
such as DIC and microhemorrhages.

disease include infections by Streptococcus

Increased fluid in the thoracic and
suis, Mycoplasma hyorhinis, septicemic
abdominal cavities, without the presence of

Escherichia coli, Actinobacillus suis,
fibrin, can also be seen in peracute cases.

Erysipelothrix rhusiopathiae, and

Acute systemic infection is characterized

Salmonella Choleraesuis.

by development of fibrinous polyserositis,
arthritis, and meningitis. The fibrinous

Treatment and Control: H parasuis
exudate can be seen on the pleura,
is one of the few gram-negative organisms
pericardium, peritoneum, synovia, and
that can be successfully treated with
meninges and is usually accompanied by
synthetic penicillin. Other antimicrobials
an increased amount of fluid. Fibrinous
used include ceftiofur, ampicillin, enropleuritis may be accompanied by craniofloxacin, erythromycin, tiamulin, tilmicosin, ventral consolidation ( catarrhal-purulent
florfenicol, and potentiated sulfonamides.

bronchopneun10nia). Lack of characteristic

Individual treatments must be given
gross lesions is also common in swine
parenterally to see a significant effect, and
showing CNS signs. Chronically affected
all pigs in the affected group (notjust those
pigs usually have severe fibrosis of the
showing clinical signs) should be treated.

pericardium and pleura, which may or may

Preventive treatments can be given via
not be present in the peritoneal cavity.

water or feed medication. Either conunercial or autogenous vaccines can be used to Diagnosis: Diagnosis is based on
control H parasiiis infection, although their observation of characteristic clinical signs
efficacy has been variable. The broad range
and lesions, in association with detection of
of potentially pathogenic serovars and geno

H parasuis in affected swine by isolation or types has impaired the development of a by molecular methods such as PCR.

universal vaccine for H parasuis.

Most current diagnostic methods do not

Homologous protection between isolates
differentiate virulent from nonvirulent
from the same serovar group is relatively
isolates, so it is important to sample only
satisfactory, whereas heterologous
from systemic sites such as pleura,
protection is restricted to a few serovars.

pericardium, peritoneum,joints, and brain.

So far, several "universal" (independent

Isolation of H parasuis from the upper
of serovar) vaccine prototypes have been
respiratory tract has no relevance in the
experimentally developed but are not yet
diagnosis of systemic infection. Samples
commercially available.

NIPAH VIRUS INFECTION

(Porcine respiratory and neurologic syndrome, Barking pig syndrome) Nipah virus disease is a relatively newly
disease was eradicated from the national
discovered disease of swine and people
commercial swine population by control
associated with infection with a novel
efforts. Fruit bats of the genus Pteropus
paramyxovirus named Nipah virus. This
appear to be reservoirs of the virus.

disease emerged in Malaysia in 1998 and

1999. It was linked to severe encephalitis

Etiology and Epidemiology:

among people occupationally exposed to

The etiologic agent, Nipah virus (genus
infected pigs in Malaysia and Singapore. The Henipavirus, family Paramyxoviridae),

722

NIPAH VIRUS INFECTION
is an enveloped, negative-sense, singleby bats, are other documented means of stranded RNA virus. The virus is closely
infection in Bangladesh. Person-to-person
related to Hendra virus (seep 707), the
transmission, although not evident in
only other member of the genus. The

Malaysia, has also occurred in south Asia
human outbreak in Malaysia and Singapore

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followed contact with infected swine and

Clinical Findings: Because of the danger
resulted in encephalitis with -400,6 case
of hun1an infection from infected pigs and
mortality. The virus is assumed to have been
the emergency setting, clinical observations
introduced into the swine population from
were not detailed in the field during the
one of the two species of Pteropus found
original epidemic. Most pigs developed a
with antibodies during investigation of the
febrile respiratory disease with a severe
outbreak. Pteropus spp range from the
cough that led to the local nan1es for the

Western Pacific through southeast Asia, and disease--"ba.rking pig syndrome" and south Asia down through coastal African

"one-mile cough." Encephalitis was also
islands, including Madagascar. Several
noted, particularly in the sows and boars
species of Pteropus have been found with
in affected facilities. The proportion of
antibodies, suggesting that the virus or
animals with each fom1 of the disease is
closely related viruses occur in other areas
uncertain, although the respiratory form
within the range of this genus of bats. In
predominated. Overall mortality within

Malaysia, genetic analysis of vims from
affected facilities was also not well
human and swine clinical materials strongly
docwnented but probably was not >5%
supported a single introduction of the virus
among all age groups.

with spread through the commercial swine
population. There was evidence of infection

Diagnosis: Laboratory diagnosis can be
among several other species of domestic
made by isolation of the virus, identification
animals, including dogs, cats, and horses.

of the RNA by use of reverse transcriptase

Hun1an encephalitis caused by Nipal1

PCR, detection of antigens in tissues by
viruses in south Asia has been a regular
in1111unohistochemical staining with specific
occurrence since 2001 in Bangladesh and
antibodies, or serologic tests such as
more recently in adjacent areas of India.

indirect ELISA and virus neutralization

In these areas, epidemiology has not
tests. The virus is considered biosafety level
supported the role of intem1ediary domestic 4 in the USA and Australia, and stringent species but rather more direct transmission
laboratory containment at limited
from the flying fox reservoir of the virus.

laboratories is a special consideration.

More recently, f.mit bats belonging to tl1e
family Pteropidae, but not the genus

Treatment: Treatment of affected swine

Pteropus, were found to harbor related
was not attempted during the Malaysian
virnses in Africa.

emergency. Human patients required
intensive care with ventilation support

Transmission and Pathogenesis:

to manage the encephalitis; no specific

Wection in pigs is asswned to have been
treatment is available. Ribavirin was
a transfer from the reservoir baE species to
administered to some patients, but
pigs. Once the virus was introduced into an
subsequent studies in laboratory animals
intensive swine husbandry setting, infection
suggest that it is ineffective.

of animals within premises was rapid, and
serologic tests suggested that nearly all pigs

Control and Prevention:· Control of
on an affected premise were infected.

the epidemic/epizootic in Malaysia was

Transmission between premises was
dependent on the initiation of strict
thought to be by poor biosecurity procequarantine procedures and the slaughter of dures and movement of infected anin1als.

all swine from affected facilities. Adherence

Experin1ental infection of swine with Nipal1
to appropriate biosecurity and quarantine
virus in a high biosecurity facility in Geelong procedures within facilities, as with other supported that transmission between swine
contagious diseases, is of paramount
in close contact occurred readily. In south
importance in preventing spread of the

Asia, infection of people appears to occur
infection. An active swveillance and
by indirect means from the reservoir fmit
slaughter program successfully eliminated
bats; contamination of sap collected in pots
the virus from the national commercial
on palm trees is a recurring means of
swine population, which has remained free
infection in regular cases occurring in
of infection. Presence of the virus in

Bangladesh. Other similar circumstances,
reservoir species of bats in a wide
such as contact with trees contaminated by
geographic range emphasizes the imporbats or consumption of fruit partially eaten tance of good disease surveillance and

PORCINE CIRCOVIRUS DISEASES

723
biosecurity practices to promote early
of nearly all human Nipal1 virus infections in
detection and confine the disease to initial

Malaysia..

premises should reintroduction occur.

Continued sporadic clusters in horses and
subsequent human cases with Hendra vims

Zoonotic Risk: Transmission of the virus
in Australia, with serious disease in some of

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from infected pigs to people was largely in
these clusters, emphasize the irnp01ta.nce
an occupational setting, and a study of risk
of use of appropriate personal protective
factors associated with human infection
equipment in vetelina.ry clinical examinasuggests that close contact with live tions or postmortem procedures when
infected swine was the means of infection

Hendra. or Nipal1 virus infection is suspected.

PORCINE CIRCOVIRUS DISEASES

(Postweaning multisystemic wasting syndrome, Porcine dermatitis and nephropathy syndrome)

A novel, noncytopa.thogenic, picoma.virus

PCVD is the PCV2-subclinical infection
like contaminant in the porcine kidney cell

(PCV2-SI), which is linked with growth
line PK-15 (ATCC-CCL33) was described in
retardation without overt clinical signs.

1974. This a.gent was later shown to be

Porcine dermatitis and nephropa.thy
a small, nonenveloped virus containing a
syndrome (PDNS) is also included as a
single-stranded, circular DNA genome; it

PCVD, although there is still no proof
was named porcine circovirus (PCV). PCV
of PCV2 as the antigen linked with this
antibodies in swine were found to be
immunocomplex disease. PCV2 has also
widespread, and experimental infections
been associated with porcine respiratory
with this virus in pigs did not result in
disease complex, although its in1pa.ct is
clinical disease, suggesting that PCV was
probably linked to the occurrence of
nonpa.thogenic.

PCV2-SD. PCV2-SD and PCV2-SI a.re the

A new disease was described in Western

PCVDs considered to severely in1pa.ct swine

Canada during the early and mid 1990s. The
production worldwide, but the introduction
etiology was unlmown, and the condition
of efficacious vaccines to the market has
was named postweaning multisystemic
largely a.meliorated their effects.

wasting syndrome (PMWS). Affected pigs,
ma.inly nul'Sery pigs, showed primarily poor

Etiology and Pathogenesis: Circovigrowth rate, ill thrift, and/or wasting, and ruses are small (17-22 nm in dian1eter),
they were histopathologically characterized
nonenveloped viruses that contain a single
by systemic inflan1.111a.tory lesions. In the
strand of circular DNA. There are two types
late 1990s, an apparently novel PCV-like
of porcine circovims, although only PCV2 is
virus was isolated from PMWS-a.ffected
considered pathogenic. Phylogenetic
pigs. The new virus was antigenically and
studies have shown that at least three
genetically distinct from the PCV contamigenotypes of PCV2 exist(PCV2 a, b, and c).

nant of PK-15 cell cultures. Subsequently,

Recent studies suggested a genotype shift

PCV isolates from diseased pigs were

(from a to b; PCV2c has been retrospecdesignated as porcine circovirus type 2
tively detected in Denmark during the
viruses (PCV2) and the original PCV from

1980s) coincidental with major outbreaks

PK-15 cell cultures as porcine circovirus
of PCV2-SD in North America, Japan, and
type 1.

some European countries. It is not clear

PCV2 has been further associated with a
whether differences in virulence exist
nun1ber of disease syndromes in pigs, so the
among or within PCV2 genotypes.

term porcine circovirus disease (PCVD)

Serologic surveys show that PCV2 is
was proposed as a collective name.

widespread in swine, independent of the

Recently, the terms PCV2-systernic disease

PCV2-SD status of the farm. Results from

(PCV2-SD) and PCV2-reproductive disease
retrospective serologic studies indicate that

(PCV2-RD) have been proposed to replace

PCV2 has been infecting pigs for >50 yea.rs

PMWS and PCV2-associa.ted reproductive
so far, and phylogenetic studies indicate
failure, respectively. Moreover, it is
that PCV2 has probably circulated in pigs
cun-ently thought that the most in1portant
duling the past 100 yea.rs.

724

PORCINE CIRCOVIRUS DISEASES

Initially, PCV2-SD was identified in high
particles. However, epithelial and endothehealth herds that were free of most common lial cells seem to be the main target for PCV2
swine pathogens. However, under field
replication, as well as a small proportion of
conditions, swine that show signs of
macrophages and lymphocytes.

PCV2-SD usually are infected with multiple

Much less is known regarding the

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agents, including porcine parvovirus,
pathogenesis of other PCVDs. PCV2 is able
porcine reproductive and respiratory
to replicate in fetuses as well as in zona
syndrome virus, Mycoplasma hyopneumo
pellucida-free embryos. Moreover, an
niae, Actinobacillus pleuropneumoniae,
experiment with embryos exposed to PCV2

Pasteurella multocida, Haemophilus
and then transferred to receptor sows
parasuis, Staphylococcus spp, and
suggested that infection can lead to

Streptococcus spp.

embryonic death. Therefore, it is believed

Accounts of multiple attempts to
that one of the potential outcomes of PCV2
experimentally reproduce PCV2-SD have
infection in sows could be return to estrus.

been published. Some early trials ( using

Transplacental transmission of PCV2 has
tissue homogenates from pigs affected with
been demonstrated. However, experiments

PCV2-SD or a PCV2 isolate) reproduced
using pregnant sows inoculated intranasally

PCV2-SD-like histologic lesions but not the
have yielded variable results. When
wasting condition. However, occasional
successful, those studies have shown that
studies subsequently reproduced clinical

PCV2 may cause fetal death, similar to that
disease and lesions consistent with
of porcine parvovirosis, with live pigs

PCV2-SD using only PCV2, preswnably, as
together with dead piglets and mUTilffiies
inoculwn. Consequently, it was suggested
of different sizes.

that PCV2 infection, linked to other

PONS is considered a type III hypersensicofactors, was necessary for the consistent tivity reaction in which the antigen present
development of full clinical disease. It
in the immune complexes is unknown. It
appears that a nwnber of factors, such as
has been speculated that PCV2 could be
age and source of pigs, envirorunental
the antigen, but there is no definitive proof
conditions, genetics, the nature of the PCV2
that PCV2 causes PD NS lesions. Indirect
inoculwn used, and the in1munologic status
evidence exists, such as significantly higher
of the pig at PCV2 infection, play a
serum antibody titers to PCV2 in affected
significant role in the consistent experimenpigs compared with healthy or PCV2-SDtal reproducibility of the disease. In fact, the affected pigs.

more consistent and repeatable PCV2-SD
disease models have been obtained using

Epidemiology and Transmission:

infectious and noninfectious cofactors as

PCV2 is considered a ubiquitous virus
triggers. Also, the coinfection of PCV2a and
in countries with and without PCVDs,
b genotypes has been linked to reproducincluding PCV2-SD. PCV2 infection and tion of clinical disease under experimental

PCV2-SD have also been described in
conditions. The mechanisms by which other wild boars. The disease has been reported viruses or inlmunostimulation may trigger
worldwide.

tl1e development of wasting in PCV2-.

Transmission may be by direct contact
infected pigs is still unknown. High loads of
with infected pigs. PCV2 has been detected

PCV2 in blood, lymphoid, and oilier tissues
in almost all potential excretion routes such
and in potential excretion routes are
as nasal, ocular, and bronchial secretions;
associated with the expression of disease.

saliva; urine; and feces. The virus can be

When multisystemic disease and wasting
found in semen, but the practical imporis apparent, danmge to the inlmune system tance of this is probably negligible. Artificial
is the main feature suggesting that affected
insemination (Al) of sows with PCV2-
pigs have an acquired immunodeficiency.

infected semen from experimentally

Lymphocyte depletion of lymphoid tissues,
inoculated boars did not result in sow
changes in peripheral blood mononuclear
infection or fetal infection. However, when
cell subpopulations, and altered cytokine
such Al was perfonned with PCV2-spiked
expression patterns have all been demonsemen, reproductive problems were strated in pigs naturally and experimentally
developed. Therefore, it seems that
affected with PCV2-SD.

reproductive disease linked to Al is

The identification of cells that support
possible, but only when semen has a high

PCV2 replication has been a matter of
virus load, which is wilikely under natural
controversy. The large amount of PCV2
conditions. Although not demonstrated, it is
virus antigen found in the macrophages and
asswned that contact with contaminated
dendritic cells of diseased pigs appears to
fomites, exposure to contanlinated feeds
be the result of accwnulation of viral
or biologic products, multiple use of

PORCINE CIRCOVIRUS DISEASES

725
hypodermic needles, or biting insects may
by PCV2-SD, a variable proportion of pigs
play a role in transmission.

developed ilie systemic disease, while most

PCV2 may persist in swine for several
had only subclinical infection. PCV2-SI had
months under either experimental or field
been unnoticed for many years until the
conditions. Convalescent swine may carry
advent of vaccines drew attention to this

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virus for extended periods and be important condition. Vaccinated pigs have an increased in disease transmission. PCV2 is fairly

ADWG compared with nonvaccinated,
resistant to commonly used disinfectants
apparently healthy counterparts. Such
and to irradiation, probably allowing it to
difference has been demonstrated to vary
accumulate in the environment and be
between 10-40 g/d, depending on the farm.

infective for new groups of susceptible pigs

PCV2-RD characterized by late-term
if rigorous sanitary measures are not
abortions and stillbirths in the absence or
followed. The decline of colostral antibody
presence of other well-lrnown reproductive
titer in pigs is associated with onset of
pailiogens seems to be the hallmark of

PCV2-SD in late nursery or finishing pigs.

clinical PCV2 infection in sows. Most of

Transplacental infection with PCV2 has
these descriptions come from North America
been documented, but it is not lrnown
and usually occur in start-up herds. Return to
whether pigs infected in utero are able to
estrus due to embryonic death as a potential
subsequently develop clinical PCV2-SD.

outcome of intrauterine PCV2 infection has

Some reports have suggested that
been suggested based on experimental data.

anin1als other than swine may be infected

However, there are no field data unequivowith PCV2 or PCV-like viruses. However, cally supporting this effect.

results of serologic studies for antibody

PDNS may affect nursery and growing
against PCV in cattle and other livestock
pigs and, sporadically, adult anin1als. The
have been contradictory, and experimental
prevalence of the syndrome in affected
induction of disease using PCVl or PCV2 in
herds is relatively low ( <1%), although
species of livestock other than swine has
higher prevalences (>200/o) have been
not been successful. Mice may be able to
described occasionally. Pigs with severe
replicate and harbor the virus.

acute disease die wiiliin a few days after the
onset of clinical signs, due to acute renal

Clinical Findings:

failure with a significant increase in serum

PCV2-SD is characterlevels of creatinine and urea. Surviving pigs ized by overt weight loss. Disease often
tend to recover and gain weight 7-10 days
occurs in the fattening units in pigs 8-18 wk
after the begi.Jming of the syndrome.

old, although the disease can be also seen in

Affected pigs have anorexia, depression,
older or y0tmger pigs. Morbidity is typically
prostration, stiff gait and/or reluctance to 5%-200/o among cohorts in the late nursery or
move, and normal temperatures or mild
finishing stages. Mortality in swine with signs
fever. The most obvious sign in the acute
of PCV2-SD can occasionally be >500/o. In
phase is the presence of irregular, red-toaddition to death loss, PCV2-SD in finishing purple macules and pa.pules on the skin of
pigs may cause a substantial increase in
the hindlirnbs and perinea! area, although
time to reach market weight, resulting in
distribution may be generalized in severely
economic Joss. Growth retardation, wasting,
affected ani.Jnals. With ti.Jne, the lesions
and dyspnea are the clinical signs seen most
become covered by dark crusts and fade
frequently in outbreaks. Pallor, anemia,
gradually (usually in 2-3 wk), someti.Jnes
jaundice, diarrhea, and palpable inguinal
leaving scars.

lymphadenopathy also are seen in some
affected pigs. A low-grade fever (104° -106°F

Lesions: PCV2-SD is diagnosed by

[ 40° -41 °C]) iliat lasts several days may be
characteristic histopathologic findings in
seen as well. Overcrowding, poor air quality,
affected pigs. Grossly, lymph nodes may
insufficient air exchange, and commingled
be substantially enlarged and pale on cut
age groups seem to exacerbate ilie course of
swface, the thymus atrophied, and the
the disease. Usually, only a few pigs in a group tonsils thinner than normal. Splenic infarcts show wasting. The onset of disease may be
also may be present in a low proportion of
acute, leading to deaili wiiliin a few days in
pigs affected with PCV2-SD. Histopathosome pigs. Other pigs show a more chronic Jogic lymphoid lesions are characteristic,
disease and fail to gain weight or thrive.

showing lymphocytic depletion and

PCV2-SI is believed to occur in pigs that
granulomatous inflammation, someti.Jnes
become infected witl1 the virus and suffer
with the presence of multinucleate giant
from growth retardation ( significantly lower
cells and an1phophilic botryoid intracytoaverage daily weight gain [ADWG]) but not plasmic inclusion bodies of different sizes
overt clinical signs. In fact, in a farm affected caused by accumulation of PCV2 particles.

726

PORCINE CIRCOVIRUS DISEASES

Lesions in the lung are common in

Histologically, a moderate to severe
affected pigs; their severity is influenced
nonpurulent interstitial nephritis with
by duration of disease and presence of
dilation of renal tubules is also seen. Usually,
concurrent infections. Gross lung lesions
both skin and renal lesions are present, but
may include failure to collapse, firmness,
in some cases, skin or renal lesions may

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diffuse pulmonary edema, mottling, and
occur alone. Lymph nodes may be enlarged
consolidation. Microscopically, a variable
and red due to blood drainage from affected
degree of lymphohistiocytic interstitial
zones with hemorrhages (mainly skin).

pneumonia to granulomatous bronchointer

Histopathologically, PCV2-SD-like lesions
stitial pneumonia with bronchiolitis and
such as lymphocyte depletion and histiobronchiolar fibrosis can be seen.

cytic and/or multinucleate giant cell

Grossly, the liver may appear icteric and/
infiltration ( although less severe) are usually
or atrophic in a low proportion of affected
found in lymphoid tissues of affected pigs,
pigs. lnterlobular connective tissue may be
although to a milder degree.

prominent. Microscopic lesions range from
single cell necrosis ( apoptosis) with mild

Diagnosis: The PCV2-SD case definition
lymphocytic infiltration of portal zones to
includes three main diagnostic criteria:

extensive lymphohistiocytic periportal

1) clinical signs of wasting or ill thrift,
hepatitis with diffuse necrosis of hepato2) presence of gross and microscopic cytes. The kidneys may be enlarged and

( moderate and severe) lesions characterisshow scattered to diffuse white foci on the tic of the disease, and 3) presence of viral
cortical surface. Microscopic lesions
antigen or DNA (moderate to high amount)

include interstitial lymphohistiocytic
in the microscopic lymphoid lesions.

infiltration. Other lesions seen in affected

Visualization of viral DNA or antigen in
pigs include gastric ulceration (probably
lesions is usually done using in situ
due in part to a prolonged fattening period
hybridization or irnmunohistochemistry,
in chronically affected pigs) and occasional
respectively, and moderate to high amounts
multifocal lymphohistiocytic myocarditis.

of virus are linked to the disease. A herd
ln severely affected pigs, lymphohistiocytic
case definition has been proposed, which
infiltrates can be seen in virtually all tissues.

includes two main criteria: 1) significant

PCV2-SI pigs do not show gross lesions
increase of mortality and number of runt
attributable to PCV2 infection. These
pigs or pigs failing to gain weight or thrive in
animals may show microscopic lymphoid
comparison to previous values for the farn1,
lesions similar to those seen in pigs with
and 2) fulfillment of the three individual

PCV2-SD, although only to a mild degree.

criteria listed above in at least one of five
ln PCV2-RD, stillborn and nonviable

· examined pigs. Differential diagnoses
neonatal piglets show chronic passive
include conditions causing increased
congestion of the liver and cardiac
mortality and growth retardation, such as
hypertrophy with multifocal areas of

PRRS, chronic respiratory disease, Gliisser's
myocardial discoloration. The key
disease, salmonellosis, porcine intestinal
histopathologic feature is fibrosing and/or
adenomatosis, and many others.

necrotizing myocarditis in fetuses .•

Because PCV2 is ubiquitous and the virus

PONS is easy to detect from a clinical
replicates in individual pigs for weeks to
point of view because of the red-to-dark
months, isolation of virus, detection of PCV2
macules and papules, which correspond

DNA in serum or tissues, or detection of
microscopically to necrosis and hemorrhage PCV2 antibodies in serum is not'sufficient secondary to necrotizing vasculitis of dermal to establish a diagnosis of PCV2-SD.

and hypodermal capillaries and arterioles.

Antibodies against PCV2 may be detected

N ecrotizing vasculitis is a systemic feature,
by ELISA, indirect fluorescent antibody, or
but it is more prominent in the skin, renal
inununoperoxidase staining of infected cell
pelvis, mesentery, and spleen (splenic
cultures. Viral isolation can be done on
infarcts may also be present as a result of
several porcine cell lines (mainly porcine
necrotizing vasculitis of splenic arteries or
kidney cells) using serum, bronchiolar
arterioles). Apart from skin lesions, pigs that
lavage fluid, or tissue homogenates. Viral
die acutely with PONS have firm, bilaterally

DNA can be detected using PCR in most
enlarged kidneys, with a fine granular
tissues or in serum from affected pigs.

cortical surface and edema of the renal

Several tissue san1ples from multiple pigs
pelvis. The renal cmtex displays multiple,
may be required for detection of virus in
small, reddish pinpoint lesions, similar to
cases of chronic disease. Virus quantificapetechial hemorrhages, which microscopition in serum by real time quantitative PCR
cally correspond to enlarged and inflan1ed

( qRT-PCR) has been suggested as a potential
glomeruli (fibrinonecrotizing glomerulitis).

diagnostic method in live pigs. Values of

PORCINE CIRCOVIRUS DISEASES

727

> 107 PCV2 genome copies/mL of sennn
effective control measures before the
usually have been linked with PCV2-SD
advent of PCV2 vaccines were focused
occurrence. However, PCV2 infection is
on control or eradication of these triggers.

extremely common in clinically healthy pigs, The most widely used control measures and interpretation of positive qRT-PCR
were the use of antibiotics to prevent

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results is not always straightforward.

concurrent bacterial infections, improve

The diagnostic approach of PCV2-SI is of
ment of biosecurity and sanitary measures
less interest for clinicians, because lack of
such as isolation of affected pigs and
overt clinical signs plus demonstration of
disinfection of pens after their use,
infection by PCR would be enough to
decreasing stressors (eg, high stocking
establish such a diagnosis. Values of> 105
density, inadequate ventilation, inador 106 PCV2 genome copies/mL of sernm equate temperature control), and control
usually have been linked with the subcliniof concomitant viral infections, especially cal infection.

PRRS. Other prevention and control

The diagnosis of PCV2-RD should include
measures used on young pigs before
the following criteria: 1) late-term abortions
the anticipated time of onset include
and stillbirths, sometimes with hypertrophy
injection of vitamins, IP injection of
of the fetal heart, 2) extensive fib rosing and/
serum harvested from finishing pigs, and
or necrotizing myocarditis, and 3) high
vaccination against common pathogens.

concentrations of PCV2 in the myocardial

Currently, control of PCV2-SD as well as
lesions and other fetal tissues. Differential

PCV2-SI is based on use of PCV2 vaccines.

diagnoses for PCV2-RD include PRRS,

There are four major commercial vaccines
porcine parvovirus, pseudorabies (Aujeszky worldwide (plus a higher number with disease), leptospirosis, and other diseases
regional availability, mainly in southeast
that cause late abortions, stillbirths, and

Asia). The first conunercial vaccine was
weak piglets. So far, there are no formal
based on an inactivated PCV2 isolate and
criteria to diagnose a putative return to
was licensed for use in sows and gilts. The
estrns associated with PCV2 infection.

same vaccine was later licensed for use in

However, the occurrence of such signs
piglets. Subsequently, three more vaccines
together with evidence of viral circulation
have been developed, all for use in piglets
during the clinical episode should be

-2--3 wk old or older. Two of these are
demonstrated.

subunit vaccines (PCV2 capsid protein

The case definition for PONS is relatively
produced in a baculovirus system), and the
simple and includes two main criteria: 1)

third is an inactivated virus constructed by
presence of hemorrhagic and necrotizing
replacing the capsid gene of the nonpathoskin lesions, mainly located on the hindgenic PCVl with that of PCV2. In addition to lirnbs and perinea! area, and/or swollen and
significantly reducing mortality and runting
pale kidneys with generalized cortical
percentages, these vaccines seem to
petechiae, and 2) presence of systemic
improve ADWG, batch unifornlity, slaughter
necrotizing vasculitis as well as necrotizing
weight unifonnity, and feed conversion rate.

and fibrinous glomernlonephritis. From a

All commercial PCV2 vaccines are based
diagnostic point of view, detection of PCV2
on PCV2a isolates, but cross-protection has
is not included in the diagnostic criteria.

been demonstrated against PCV2b. All PCV2

Differential diagnosis of PONS depends
vaccines are able to generate both cellular
on the most significant pathologic outcome.

and hwnoral inunune responses, which are

Cutaneous manifestations may be confused
believed to be the key features to control
with classical and African swine fever,
the subsequent PCV2 infection that occurs
swine erysipelas, septicemic salmonellosis,
under field conditions.

infection withActinobacillus suis, porcine

No treatment has proved successful for
stress syndrome, transit erythema

PONS. Only those epizootic cases with

(urine-soaked floors, chemical burns, etc),
moderate to high morbidity and mortality
and other bacterial septicemias. Differential rates may be important in terms of diagnoses for kidney lesions include
economic losses. Treatment using a wide
classical and African swine fever, swine
range of antin1icrobial agents has been
erysipelas, and septicemic salmonellosis.

unsuccessful. Because the antigen

Sernm biochemical analyses may help
responsible for triggering PONS is not
differentiate PONS from other diseases;
known, no preventive recommendations are
urea and creatinine concentrations are
indicated. hnportantly, the use of PCV2
markedly increased.

vaccines worldwide has significantly
reduced occurrence of this condition,

Treatment and Control: Because
emphasizing tl1e putative implication of

PCV2-SD is a multifactorial disease,

PCV2 in its pathogenesis.

728

PORCINE HEMAGGLUTINATING ENCEPHALOMYELITIS

PORCINE HEMAGGLUTINATING

ENCEPHALOMYELITIS

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(Vomiting and wasting disease, Coronaviral encephalomyelitis) Porcine hemagglutinating encephalo

(VWD) and the encephalitic fom1s, are
myelitis, a viral disease of young pigs, is
confined almost exclusively to pigs <4 wk
characterized by vomiting, constipation,
old. The "VWD form" has an incubation
and anorexia and results either in rapid
period of 4-7 days. Repeated retching and
death or chronic emaciation (vomiting and
vomiting are seen. Pigs start suckling but
wasting). Also, motor disorders due to acute soon stop, withdraw from the sow, and encephalomyelitis (hemagglutinating
vomit the milk they have ingested. They dip
encephalomyelitis) are often seen during
their mouths into water bowls but drink
field outbreaks.

little, possibly indicative of pharyngeal
paralysis. The persistent vomiting results

Etiology, Epidemiology, and Patho
in a rapid decline of condition. Neonatal
genesis: The causal coronavirus, porcine
pigs become dehydrated, cyanotic, and
hemagglutinating encephalomyelitis virus
comatose and die. Older pigs continue to

(PHEV), is of a single antigenic type, and it
vomit, although less frequently than in the
grows in several types of porcine cell
early stage of the disease. They lose appetite
cultures, in which it causes syncytia. It
and become emaciated. A large distention
agglutinates RBCs of several animal
of the cranial abdomen can develop. This
species. Pigs are the only natural host. The

"wasting" state may persist for 1-6 wk until virus is spread via aerosol. It has no public
the pigs die of starvation. Mortality
health significance.

approaches 100% within the litter, and

Based on virus detection and/or serology,
survivors remain pem1anently stu.nted.

PHEV Infection has been reported from

The "encephalomyelitic fom1" also starts
several countries in Europe and from North
with vomiting, usually 4-7 days after birth.

and South America (Argentina), Australia,

Vomiting continues intemlittently for
and Asia (China, Taiwan, South Korea);

1 -2 days, but it is rarely severe and does
thus, it appears to be widespread. The virus
not result in dehydration. After 1-3 days,
is endemic in most breeding herds, and a . generalized muscle tremors and hyperherd immunity exists. The infection usually esthesia are seen. The pigs tend to walk
remains subclinical. Immune sows transfer
backward, often ending in a dog-sitting
maternal antibodies to their piglets, which
position. They soon become weak, are
are protected until they have developed an
unable to rise, and paddle their limbs.

age resistance; thus, clinical outbreaks are

Blindness, opisthotonos, and nystagmus
rare. However, if the virus enters a
also occur. After a few days, they become
susceptible herd with neonatal"piglets,
dyspneic, comatose, and die. More recently,
morbidity and mortality may be high.

some outbreaks have been reported from

The virus first replicates in the nasal

Taiwan and South Korea in which pigs
mucosa, tonsils, lungs, and to a very limited

30-50 days old showed motor disorders.

extent, in the small intestine. From these

Morbidity and mortality of the encephalosites of entry, the virus invades defined myelitic form are high ( as much as 100%) in
nuclei of the medulla oblongata via the
neonatal pigs but both decrease with
peripheral nervous system and subseincreasing age. Both clinical forms of PHEV
quently spreads to the entire brain stem, and infection may be seen during an outbreak possibly to tl1e cerebrun1 and cerebellum.

on the same farm.

Vomiting is tl10ught to be caused by viral

From onset to disappearance, an
replication in the vagal sensory ganglion.

outbreak on a farm lasts 2-3 wk. Disap

Wasting is due to vomiting and delayed
pearance of disease coincides with the
emptying of the stomach, which is the result
development of immunity in sows in late
of virus-induced lesions in the intramural
pregnancy, which subsequently protects
plexus. Infection of cerebral and cerebellar
piglets via maternal antibodies.

neurons may cause motor disorders.

Lesions: Cachexia and abdominal
distention are seen in chronically affected

Clinical Findings: Both clinical synpigs. Their stomachs are dilated and filled dromes, the vomiting and wasting disease
with gas. Microscopically, perivascular

PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME

729
cuffing, gliosis, and neuronal degeneration
appear. Therefore, the acute serum must
are fow1d in the medulla in 700h---10()0/c, of pigs be collected immediately after disease with nervous signs and in 200/o-600/c, of pigs
starts.

with VWD. Neuritis of peJipheral senso1y

Differential diagnoses include pseudoraganglia, particularly the trigeminal ganglia, bies (seep 1300) and teschovirns encepha

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is seen regularly. Degeneration of the
lomyelitis (seep 1307). Respiratory signs in ganglia of the stomach wall and perivascuolder pigs and abortions in sows are part of lar cuffing are found in 15o/o-85% of pigs with
a pseudorabies outbreak. ln teschovirus

VWD. The lesions are most pronounced in
encephalomyelitis, older pigs are usually
the pyloric gland area.

involved.

Diagnosis: A laboratory diagnosis can be

Control: There is no treatment. Once signs
made routinely by virus isolation from the
are evident, the disease runs its coLu-se.

brain stem and, to be successful, the pigs

Spontaneous recove1ies are rare. Piglets
are preferably euthanized within 2 days
born from noni.nmnme sows dwing the
after signs appear. It is difficult to isolate the
outbreak can be protected by being
virus from pigs that have been affected for
injected, at birtl1, either with hyperimrnune

>2-3 days. Other diagnostic techniques,
semm or, if this is not available, witl1 pooled
based on antigen or nucleic acid (RT-PCR)

serwn collected from older sows at a
detection, have been developed and applied
slaughterhouse. However, the time lapse
recently.

between diagnosis and cessation of the

A significant rise in antibody titer can be
disease is usually too sho1t for this
demonstrated in paired serum samples.

procedure to be effective. Maintaining the

Because of the rather long incubation
virus on tl1e farm (thus retaining naturally
period, pigs may start to build up a low
induced i.rnnnmity in the sows) avoids
antibody titer 2-3 days after the first signs
outbreaks in piglets.

PORCINE REPRODUCTIVE AND

RESPIRATORY SYNDROME

Porcine reproductive and respiratory
earlier animals to those that have not been
syndrome (PRRS) was first reported in the
previously exposed.

USA in 1987. Since then, outbreaks of PRRS

The primary vector for transmission
and successful isolation of the virus have
of the virus is the infected pig. Contact
been confirmed throughout Notth America
transmission has been demonstrated
and Europe.

experimentally, and spread of virus from
infected seedstock oJiginating from a single

Etiology and Epidemiology: The
source has been desc!ibed. lntroduction
etiologic agent is a virus in the group
of infected seedstock can lead to the

ArteJiviJidae. The virus is enveloped and
introduction and coexistence of genetically
ranges in size from 45 to 80 mm. lnactivadiverse isolates of PRRS virus on the san1e tion is possible after treatment with ether
farm. Controlled studies have indicated that
or chloroform; however, the virus is very
infected swine may be longtern1 carriers,
stable under freezing conditions, retaining
with adults able to shed PRRS virus for up
its infectivity for 4 mo at -70°C (-94°F). As
to 86 clays after infection, and weaned pigs
the temperature Jises, infectivity is reduced
able to harbor virus for 157 days. Experi

(15-20 min at 56°C [132.8°F]).

mentally infected boars can shed virus in

After infection of a naive herd, exposure
the semen up to 93 days after infection.

of all members of the breeding population

Aerosol transmission of the virus has
is inconsistent, leading to development of
been confirmed as an indirect route of
naive, exposed, and persistently infected
transmission and may depend on isolate
subpopulations of sows. This situation is
pathogeni.city. Highly virulent isolates that
exacerbated over time through the addition
produce high titers of virus in blood and
of improperly acclimated replacement gilts
tissues have been shown to be spread via
and leads to shedding of the virus from
aerosols at a significantly higher frequency

730

PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME
than less pathogenic isolates. Environmeninterstitial pneun1onia in cesarean-derived/
tal factors, such as wind direction and
colostnl.111-deprived (CD/CD) piglets after
velocity, significantly impact spread via
intranasal inoculation.

this route as well. PRRS virus can also be

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transmitted by fomites, such as contaminated needles, boots, coveralls, transport Diagnosis: The most commonly used
vehicles, and shipping containers. Farm
serologic assay is the ELISA It measures
persorn1el are not a risk, unless hands are

IgG antibodies to PRRS virus. It cannot
contan1inated with blood from viremic pigs.

measure the level of ilrn11wlity in an a.nil11al

Finally, transmission via certain species of
or predict whether the a.nilnal is a carrier.

insects (mosquitoes [Aedes vexans] and

Titers are detected within 7 -10 days after
house flies [Musca domestica]) has been
mfection and can persist for up to 144 days.

reported.

Tests for PRRS virus include PCR, virus
isolation, and in1111unohistochemistry.

Clinical Findings: PRRS appears to have

Nucleic acid sequencing of the open reading
two distinct clinical phases: reproductive
frame 5 region of the virus is an excellent
failure and postwea.ning respiratory
tool for epidemiologic investigations in the
diseases. The reproductive phase of the
field to confirm similarity between isolates
disease includes increases in the number
recovered from different sites. Recently,
of stillborn piglets, mummified fetuses,
oral fluid san1pling has been widely applied
premature fan-owings, and weak-born pigs.

as a means to sample a population of pigs.

Stillbilths and mummies may increase up

This method is cost effective and convenito 25%-35%, and abo1tions can be > l ()OA,.

ent and can be used for botl1 virus and

Anorexia and agalactia are evident in
antibody detection at the pen level.

lactating sows and result in i11crea.sed

(30"/o--500;6) preweaning mortality. Suckling
piglets develop a characteristic thumping

Treatment and Control: Cun-ently, there
respiratory pattern, and hlstopathologic
a.re no effective treatment programs for
exan1mation of lung tissue reveals a severe,
acute PRRS. Attempts to reduce fever using
necrotizmg, interstitial pnew11onia. PRRS is

NSAIDs (aspirin) or appetite stimulants
capable of crossing the placenta m the third

(B vitanlins) appear to have minimal benefit.

and possibly second tri111ester of gestation.

The use of antibiotics or autogenous

Piglets may also be born viremic and
bacterins to reduce the effects of opportuntransmit the virus for 112 days after istic bacterial pathogens has also been
mfection. Perfo1mance after weaning is also reported; however, results have been mixed.

affected. Infection with PRRS virus results

Prevention of mfection appears to be the
in destruction of mature alveolar macprilnary means of control. Understanclmg rophages, which has led to the hypothesis
the PRRS status of replacement gilts and
that mfection results in inlmune suppresboars, as well as proper isolation and sion; however, controlled studies indicate
acclimatization of mcommg stock, are
that the virus may actually enhance specific
critical measures to prevent viral introducparameters of tl1e ilnmw1e response.

tion. Pigs should be retested on arrival at the

Outbreaks of the reproductive form of
isolation facility and 45----60 days later, before

PRRS have been reported to last 1-4 mo,
entry to the herd. Elilnination of existmg
dependmg on the facilities and initial healtl1
mfection by multisite production and
status of the pigs. In contrast, the postweansegregated early weanmg has also been ing pneumonic phase can become chronic,
described. Although these strategies have
reducing daily gain by 85% and increasmg
had some success, the longterm risks of
mortality to lOo/o--25%. Nun1erous other
reinfection appear high. Prevention of viral
pathogens are commonly isolated along
spread by nursery depopulation has been
with PRRS virus from affected nursery or
described. This is successful when virus
finishing pigs. Other bacteria such as
transmission is not occuning m the sow

Streptococcus suis, Escherichia coli,
herd ( usually 12-18 mo after initial

Salmonella Choleraesuis, Haemophilus
outbreak), but the nurse1ies and growing/
parasuis, and Mycoplasma hyopneumo
finishing pigs are still mfected. All nursery
niae have been reported, as well as viruses pigs are removed from the farm to be
such as porcme respiratory coronavirus and
finished elsewhere. The nurseries are then
swine influenza virus. Finally, differences in
aggressively washed and disinfected and
the clinical response to PRRS virus may also left empty for 7-14 clays, after which they be due to strain variation. Studies have
can be used normally. The technique has
demonstrated the ability of different
successfully elimmated PRRS virus from
isolates to induce varymg degrees of
several herds, and pigs have remained

STREPTOCOCCAL INFECTIONS IN PIGS

731
seronegative (for >l yr) to market age;

LUlidentifiable routes. This has resulted in an
production in the nurseries has improved,
increased level of biosecurity on farms.

both in growth rate and mortality.

Strict quarantine and testing progran1s, the

Commercial modified-live vaccines have
purchase of PRRS virus-naive breeding

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been licensed and have been effective in
stock and semen, sanitation of transport
controlling outbreaks, reducing shedding,
vehicles, and strict protocols of fomite and
and preventing economic losses.

personnel movement between farms are

Elimination of PRRS virus has been
critical components of an effective
demonstrated to be possible on an
program. Recent advances in monitoring
individual farm basis. Metl10ds such as
the status of artificial insemination centers
whole herd depopulation-repopulation, test
include PCR analysis of blood samples
and removal, and herd closure have been
collected from ilie auricular vein (blood
docwnented as effective methods to
swab). In addition, the application of air
eliminate PRRS virus from endemically
filtration to artificial insemination centers
infected herds. Unfortunately, a nun1ber
and breeding herds has been shown to
of eradication efforts have failed because
significantly reduce the risk of airborne
of introduction of new isolates thrnugh
entry of the virus.

STREPTOCOCCAL INFECTIONS IN PIGS

Of the bacterial group of gran1-positive
considered a normal inhabitant of the upper
cocci comprising the genera Streptococcus,
respiratory tract ( especially nonvirulent

Enterococcus, and Peptostreptococcus,
strains) and can be easily f0tmd in tonsils,
streptococci constitute the most significant
which are considered a natural niche. It can
pathogens of swine. Streptococci are also
also be isolated from the reproductive and
as ociated wiili infectious conditions of

GI tracts of clinically healthy pigs.

people, cattle, sheep, goats, and horses.

Relative to pigs, S suis (an et-hemolytic

Etiology and Pathogenesis: S suis

Streptococcus) is by far U1e most imp01tant possesses antigens somehow related to
agent of infectious diseases in this group,

Lancefield group D streptococcus , but it is
affecting mainly nursing and recently
taxonomically far from other members of
weaned pigs. Septicemia, meningitis,
this group. It is considered a facultatively
polyserositis, polyarthritis, and bronchoanaerobic, gram-positive, nonn1otile coccus, pneumonia are associated with S suis
oriented in chains of varying lcngilis. S suis
infections. Streptococcus dysgalactiae
produces et-hemolysis (incomplete
equisimilis is considered the most
hemolysis) on blood agar and is catalase
important 13-hemolytic Streptococcus
negative. It has a worldwide distribution, and
involved in lesions in pigs, and it has been
originally 35 serotypes based on capsular
judged to be of etiologic significance in
antigens had been described (serotypes 1 to
autopsy reports. S porcinus, ·another

34 and serotype 1/2). However, there is still

13-hemolyticStreptococcus, has been
some controversy, because serotypes 20, 22,
associated particularly in the USA with a

26, 32, 33, and 34 have been suggested as not
contagious clinical entity in growing pigs
being part of ilie S suis species. Nonetheless, known as streptococcal lymphadenitis,jowl
ilie nun1ber of serotypes considered as
abscesses, or cervical abscesses. Enterohighly virulent is relatively small and cocci reside in the intestinal tract and may
depends mainly on geographic location.

cause disease in multiple species. In pigs,

Most studies on virulence factors of S suis
tl1e E faecium species group, mainly
have been performed witl1 serotype 2 only.

E durans and E hirae, are especially associ

'Iype 2 virulent and nonvirulent strains exist,
ated with enteritis and diarrhea.

but characte1ization of virulence factors is
still incomplete. Capsular polysaccharide is

STREPTOCOCCUS SUIS INFECTION so far U1e most in1portant critical virulencP
factor. However, well encapsulated

S suis is a significant pathogen of swine and nonvirulent serotype 2 strains do exist.

one of the most important causes of bacterial Some proteins, such as the muran1idasemortality in piglets after weaning. It is released protein, the extracellular factor,

732

STREPTOCOCCAL INFECTIONS IN PIGS
and the hemolysin (suilysin), constitute
maternal antibodies are no longer present.

virulence-related proteins for serotype 2

Clirtical infections are seen mainly in
strains isolated in Europe and Asia but not
weaned pigs (2-5 wk after weaning),
for North American strains. So far, there is
growing pigs, and less frequently, suckling

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no single true predictor of pathogerticity.

piglets and adult aninrnls. Transmission

In fact, serotype 2 strains from different
between herds occurs by the movement
continents are phenotypically and genotypiand mixing of healtl1y caii:ier pigs. The cally very different. Most strains from Asia
introduction of a highly vintlent strain into
and Europe belong mainly to the sequence
a naive herd may result in subsequent onset
type or STl, as characte1ized by multilocus
of disease in weaned and/or growing pigs.

sequence typing, and are highly vimlent.

However, some herds with animals

Sero type 2 strains from North America
hai·boring vimlent strains but not showing
belong to ST25 and ST28, presenting lower
illness may suddenly develop serious
vintlence capacities, which may explain the
clinical disease in the presence of other
importance of other serotypes in this
predisposing factors such as overcrowding,
continent, such as serotypes 3 and 1/2.

poor ventilation, excessive temperature

The mechanisms that enable S suis to fluctuations, mixing of pigs with an age
disseminate throughout the anin1al are not
spread of >2 wk, and coinfections with other
weJI understood. The bacterium is able to
pathogens. Disease outbreaks due to S suis spread systemically from the nasopharynx,
infection have been frequently repmted with
occasionally resttlting in septicemia and
coinfections of porcine reproductive and
death. The palatine and pharyngeal tonsils
respiratory syndrome virus (seep 729).

are both potential portals of entry for S

S suis might also be transmitted via fomites suis, leading to subsequent hematogenous
and flies, although probabilities are low.

or lymphogenous dissemination. Survival of

Although S suis has been isolated from the organism once in the bloodstream may
different mainmal species and birds, the
be facilitated by the capsular polysacchaimportance of such reservoirs is unknown.

ride as weJI as ceJI wall components, which
ef'ficiently hamper phagocytosis. lf S suis Clinical Findings: Even when the carrier
does not cause acute fatal septicemia,
rate in pigs is near lOOOA,, tl1e incidence of the bacteria are able to reach the CNS via
disease vaiies from period to period and is
mechanisms that are only partially
usually <5%. However, in the absence of
elucidated, such as invasion of brain
treatment, mortality rates can reach 2QOA,.

microvascular endothelial ceJls or through

The earliest sign is usually fever, which may
the choroid plexus epithelial ceJls. In both
occur irtitially without oilier obvious signs. It septicemic and CNS cases, excessive host
is accompartied by a pronounced septicemia
inflan1mation seems to play an important
that may persist for several days if untreated.

role in the pathogenesis of infection.

Dming this period, there is usually a
fluctuating fever and variable degrees of

Epidemiology and Transmission:

inappetence, depression, and shifting

S suis is present in all parts of the world laineness. In peracute cases, pigs may be
in swine intensive areas. Serotypes 1 -9
found dead with no premortitory signs.

(including serotype 1/2 that shares antigens

Meningitis is the most striking feature and
with serotypes 1 and 2) represent > 7096 of S
the one on which a presll.l11ptive diagnosis
suis isolates recovered from diseased pigs, is usually based. Pigs in the early stages of
mainly in North America where most
meningitis may hold their ears back and
studies have been done. Serotype 2 is, in
squint their eyes. Other eai·ly nervous signs
general, the most prevalent worldwide, but
include depression, incoordination, and
its importance is lower in North America
adoption of tmusual stances ( eg, dog-sitand higher in Asia and some countries in ting), which soon progress to inability to

Europe, such as France. Serotype 9 is the
stand, paddling, opisthotonos, convulsions,
most frequently isolated type in other
and nystagmus. Swollen joints and lan1eness

European countries, such as Spain,
are indicative of polyarthritis, which is

Germany, and the Netherlands.

common in Nmth America. Endocarditis is

Most clirtically healthy pigs are carriers of
also a frequent finding in older piglets, with
multiple serotypes of S suis, although a few affected pigs dying suddenly or showing
are colonized by vintlent strains. Piglets
signs of dyspnea, cyanosis, and wasting.

become colonized with S suis from vaginal

Signs of respiratory disease may be seen in
secretions during parturition and while nurssome outbreaks, although the role of S suis ing. Asymptomatic carriers serve as a source as a pri.maiy agent of pnell.l11ortia, in the of infection for their pen mates after they are absence of other pathogens, remains mixed and commingled in the nursery, when
contr·oversial.

STREPTOCOCCAL INFECTIONS IN PIGS

733

Lesions: Lesions are mainly seen in

Mycoplasma hyorhinis; meningitis caused
weaned and growing pigs and are associated
by H parasuis; endocarditis caused by
with lymphadenopathy, meningitis, arthritis,

E1ysipelothrix rhusiopalhiae; septicemia
and endocarditis. Polyserositis similar to
caused by H parasuis, Actinobacillus suis, VetBooks.ir
that seen in Gla.sser's disease is sometimes

Escherichia coli, E1ysipelothrix rhusio
seen. Lesions may include fibrinopurulent
pathi ae, or Salmonella Choleraesuis; and exudates in the brain, swollen joints,
polyarthritis caused by otl1er streptococci,
fibrinous serositis, and cardiac valvular
staphylococci, E coli, or A suis.

vegetations. Splenomegaly and petechial
hemorrhages indicating septicemia are

Treatment, Control, and Prevention:

common. Significant microscopic lesions

Prompt recognition of the early clinical
are usually limited to the brain, heart, and
signs of streptococcal meningitis, followed
joints. The predominant lesions are
by i..nunediate parenteral treatment of
neutrophilic meningitis and chorioiditis,
affected pigs witl1 an appropriate antibiotic,
with hyperemic meningeal blood vessels,
is currently the best method to maximize
and fibrinopurnlent or suppurative
survival. The early stages of meningitis may
epicarditis. Evidence of encephalitis, edema,
be difficult to detect, so weaned pigs should
and congestion of the brain may be present.

be observed 2--3 times daily on farms where

The choroid plexus may have disruption of

S suis infections are a problem. Resistance the plexus brush border, and fibrin and
of isolates to penicillin has been repmted
inflammatory cell exudates may be present
and varies among countries, but extended
in the ventricles. Microscopic lesions do not
spectrum 13-lactarns such as ampicillin and
seem to be associated with a given serotype.

arnoxicillin appear to retain some good
effectiveness. Treatment can also be

Diagnosis: Presumptive diagnosis is
administrated via the drinking water or in
generally based on history, clinical signs, age
an1oxicillin-medicated feed. However,
of animals, and gross lesions. Isolation and
because of the method of spread of the
serotyping of the infectious agent and
disease, treatment needs to be started
evaluation of microscopic lesions in affected
quickly. Whichever method of medication is
tissues confirm the diagnosis. After isolation,
used, treatment should be continued for at
biochemical identification of S suis isolates least 5 days. Administration of an antirecovered from diseased animals is possible inflammatory preparation is sometimes
with a minimum of biochemical tests.

recommended to reduce inflammation of

Serotyping is important to confirm and
affected tissues and improve the overall
implement preventive measures, and several
condition of pigs with S suis meningitis.

multiplex PCR tests to easily serotype S suis

Treatment of sows with antibiotics before
strains have been repmted (and can be used farrowing may reduce pathogen transmis-.

by any laboratory). Validated and specific
sion to piglets, although results are
serologic tests to detect antibodies are not
controversial.

available for S suis. Genetic characteriza

Vaccines available in the field are
tion, including multilocus sequence typing, is bacterins (inactivated whole cells), and they done in some laboratmies and is particularly
have proved to be relatively ineffective in
useful for epidemiologic studies. For
preventing outbreaks. If somehow useful,

European and Asian strains of serotype
the protection would be serotype-specific.

2, detection of the murarnidase-released

Because affected animals are in general
protein, the extracellular factor, and the

6-10 wk old, interference wiili maternal
hemolysin (suilysin) by PCR as an indication
antibodies should be considered. In
of virnlence can also be done.

addition, the adjuvant used seems to play an

Detection ofvirnlent strains of S suis
important role; a bacterin with a water-in-oil
from tonsils or nasal cavities can.not be
emulsion as an adjuvant provided better
done, because universal virulence factors
results than the same bacterin with an
are unknown. These sites are highly
alwninum hydroxide-based adjuvant.

contaminated, and traditional bacterial

Sow vaccination also had poor results.

isolation has a low sensitivity. Strains

One main problem is thats suis is one of
isolated from tonsils must be confumed by
several bacterial pathogens iliat have been

PCR as being S suis, because biochemical
able to defeat eradication efforts in nursing
tests are not able to correctly differentiate
or early weaned pigs, because anin1als are
this bacterial species from other streptoalready colonized inunediately after or even cocci normally present in the upper respiradwi.ng farrowing.

tory tract of swine.

Streptococci are susceptible to the action

Differential diagnoses include polyseroof aldehyde, biguanide, hypochlorite, iodine, sitis caused by Haemophilus parasuis or
and quaternary anunoniwn disinfectants.

734

STREPTOCOCCAL INFECTIONS IN PIGS

Zoonotic Risk: Human infections with S
be seen 15-30 days after onset and may
suis can result in septicemia, meningitis,
become more severe. Fibrosis and mulpermanent hearing loss, endocarditis, and tiple focal abscessation of periruticular
arthritis. In Western countries, mortality has
tissues and hypem·ophy of synovial villi

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been reported to approach 7%, and most
also occur. Endocarditis occurs but is difcases are related to employment in the ficult to diagnose antemo1tem. Lesions
swine industry (ie, pig farmers, abattoir
consist of yellow or white vegetations of
workers, persons transpo1ting pork, meat
different sizes, often covering the entire
inspectors, butchers, and vete1inarians ). In

Asia, the general population is at risk, and
smface of the affected valve.

mortality rates can be >20%. S suis is
considered one of the most common causes

Diagnosis: Diagnosis of streptococcal
of adult meningitis in Thailand, Vietnan1,
septicemia, artluitis, or endocarditis is best
and Hong Kong. Serotype 2 and, to a lesser
accomplished by necropsy and bacteriologic
extent, serotype 14 are mainly involved
exanunation of affected pigs. Only small
in htunan cases. Transmission to people
nun1bers of organisms or no orgfillisms may
occurs via contamination of skin wow1ds or
be isolated from affected joints, especially
mucous membranes by blood or secretions
when inflanll1lation is advanced.

from infected pigs or by consuming raw
meat or blood (as is the case in Asia). The

Treatment and Prevention: fl-hemolytic
disease is considered to be m1derdiagnosed
streptococci ru·e sensitive to l3-lactan1
and m1den-eported in several countlies.

antibiotics. Long-acting antibacte1ial agents
may be beneficial, and ti·eatment should be
given before inflammation is well advanced.

STREPTOCOCCUS DYSGALACTIAE There are no recent repo1ts about vaccina

EQUISIMILIS INFECTION
tion against these sti·eptococci. Autogenous
bacterins ru·e sometimes used, and there

Alpha-and nonhemolytic streptococci of
were repo1ts of a reduced incidence of

Lancefield group C are defined as S dysgal,ac
arthritis when sows were vaccinated before
liae dysgawctiae, whereas fl-hemolytic
farrowing. However, no recent data have
streptococci belonging to groups C, G, or L
confinned such information.

are named S dysga1actiae equisimilis.

Adequate intake of colostrmn may ensme

In swine, fl-hemolytic S dysgalactiae
that piglets receive protective antibodies.

equisimilis usually belong to Lancefield

Traumatic injwies to the feet and legs should
group C. Although members of the normal
be minirnized by reducing the abrasiveness
flora, they are considered the most
of the floor swface in the fruTowing ru·ea
in1portant l3-hen10lytic streptococci

S dysgalactiae is not recognized as a
involved in lesions in pigs, and these agents
zoonotic pathogen.

were judged to be of etiologic significance
in autopsy reports. These streptococci are
common in nasal and throat secretions,

STREPTOCOCCUS PORCINUS
tonsils, and vaginal and preputial secre

INFECTION
tions. Vaginal secretions and milk from
postpruturient sows are the most likely

(Streptococcal lymphadenitis, Jowl abscess,
sources of infection for the piglets.

Cervical abscess)

Streptococci enter the bloodstrean1 via

S porcinus Lance field group E has been
skin wounds, the navel, and tonsils. A
associated in the USA with a contagious
bacteremia or septicemia occurs, and
clinical entity in growing pigs known as
the orgfillisms then settle in one or more
streptococcal lymphadenitis,jowl
tissues, giving rise to ruthritis, endocarditis,
abscesses, or cervical abscesses. Losses due
or meningitis.

to this disease in the USA were important
in the 1960s, but its incidence has since

Clinical Findings and Lesions: Infecdeclined, and the disease is not recognized tion is usually first seen in pigs 1-3 wk old.

as an inlportant economic entity in other

Joint swelling and lan1eness ru·e the most
countries, where the bacterium represents
obvious and persistent clinical signs.

only a few percent of the microorganisms

Increased temperatures, lassitude,
isolated from abscesses in swine. Interestroughened hair coat, and inappetence may ingly, it was recently reported that almost
also be noted. Early lesions consist of

20% of tonsils from a slaughterhouse were
periarticular edema; swollen, hyperemic
positive for S porcinus. Although pathology synovial membranes; and tmbid synovial
is not frequently seen, the pathogen is still
fluid. Necrosis of articular crutilage may
prevalent in swine.

SWINE VESICULAR DISEASE

735

Transmission is possible by contact or

S poi·cinus Lancefield groups P, U, and V
ingestion of food or water contaminated by
have been isolated from lungs, genital organs,
purulent material from abscesses or feces
and brains of pigs. However, no histologic
containing the organism. Organisms infect
lesions could be associated with their

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the pig through the mucosa of the pharynpresence. S porcinus groups P and V have geal or tonsillar surfaces and are carried to
also been associated with abortions in pigs.

the lymph nodes, primarily of the head and

Many strains of S porcinus have been
neck region, where abscesses are formed.

recovered from the human female

Abscesses may be seen at slaughter, and
genitourinary tract. However, it has been
enlargement of lymph nodes in the throat
reported later that these strains belong to a
region may be evident. S poi-cinits is also different and new species, Streptococcus
occasionally found in the vaginal mucus of
pseudoporcinus sp nov (novel species).

sows and the semen and prepuce of boars.

It is generally considered to be a secondary

OTHER STREPTOCOCCAL AND
invader.

Scattered miliary abscesses develop in

ENTEROCOCCAL INFECTIONS
the mandibular, parotid, or retropharyngeal

Bacterial streptococcal strains were isolated
lymph nodes within 7 days after infection.

from the lungs and kidney of two pigs with

By 21 days, abscesses measuring 5---8 cm in
lesions associated with pneumonia and
dian1eter are common; they destroy the
septicemia, respectively. The two isolates
internal structure of affected nodes and may were recovered from different animals, extend into adjacent tissues. Developing
on different farms located in difference
abscesses may reach the skin, rupture, and
provinces of Spain, and in different years.

drain in 7 -10 wk The drained lesions heal

The isolates were classified as a new
by granulation, leaving a dense, fibrous,
species, Streptococcus plurextontm sp nov
subcutaneous tract that resolves after

(novel species). Other isolates associated
several weeks. Deep-seated abscesses may
with pnew11onia were also defined as a new
remain undetected until slaughter and tend
species, Streptococcus porci sp nov. So far, not to drain into the pharynx.

there are no data about the habitat and/or

S porcinits is sensitive to penicillins, and virulence properties of these two species.

antibiotic therapy will usually resolve acute

Enterococci are known as part of the intesinfections if detected. However, anti.biotic tinal flora, but some strains can extensively
treatment is not usually successful in
colonize the mucosa! surface of the small
treating swine with established abscesses
intestine. Some enterococcal species that
or in eliminating carriers. Resistance to
show typical adhesion to the apical surface
tetracycline has been repo1ted, but pulsing
of the enterocytes of the small intestine of
tetracyclines in the feed at the therapeutic
young anin1als have been described as
level of 400 g/ton is commonly used in an
associated with diarrhea in different species,
attempt to control this condition. Vaccinaincluding piglets 2-20 days old. Taxonomic tion (autogenous) is possible but has not
studies have shown that most of these
been widely used, because cervical
enterococci are members oftheEJaecium
abscesses are not a widespread problem.

species group, mainly E durans and E hirae.

SWINE VESICULAR DISEASE

Swine vesicular disease (SYD) is typically a

Pigs are considered the only natural host
transient disease of pigs in which vesicular
of the virus, although it can infect sheep
lesions appear on the feet and snout and in
in close contact with infected pigs and
the mouth. SYD is usually mild in nature and
infection of one laboratory worker was
may infect pigs subclinically. However, the
reported. SYD has been reported only in
disease is of major economic importance,

Europe and Asia, having been first identified
because it must be differentiated from
in Italy in 1966 and subsequently in Hong
foot-and-mouth disease, eradication is

Kong, Japan, Taiwan, and 16 other councostly, and embargoes on export of pigs and tries in Europe. Although SYD virus was
pork products are often imposed on nations
eradicated from Japan in the mid-1970s and
not free of SYD.

most European countries by the mid-1980s,

736

SWINE VESICULAR DISEASE
it has remained endemic in Italy and caused

Diagnosis: Diagnosis is confirmed by
sporadic outbreaks of disease in other
laboratory tests on epithelial samples, feces,

European countries during the 1990s and
or serum. Virus detection is by antigenin Portugal in 2003, 2004, and 2007.

detection ELISA, virus isolation, or

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reverse-transcriptase PCR. Serology

Etiology: The causal agent is an enteroviis by antibody-detection ELISA or virus rus of the family Picornaviridae. It belongs
neutralization test, but low specificity may
to the species Human enterovirus B and is
be a concern, particularly in older animals.

thought to have evolved from the human

In clinical cases, the preferred specimens
pathogen coxsackievirus B5, with which
are lesion material collected in phosphateit shares a close antigenic and genetic buffered saline. Subclinical infection may
relationship. There is only one serotype
be detected by testing of pen-floor feces
of SVD vims, although isolates may be
using reverse-transcriptase PCR or virus
differentiated by antigenic or genetic typing
isolation.

and may differ in virulence. SVD virus is
transmitted by direct or indirect contact or

Control: Countries free of the disease
by feeding infected pork or pork products.

can remain so by controlling the in1port

Infection is via the oral route or through skin
of pigs and pork products or by ensuring
abrasions and can give rise to viremia, fecal
that pork products are treated (heat or
viral shedding, and generalized vesicles that
otherwise) to kill the virus. Feeding of
rupture to release large amounts of virus.

garbage to pigs may be banned or regulated
to ensure thorough cooking. Any suspected

Clinical Findings and Lesions: The
outbreak should be reported to the approprimary signs are fresh or healing vesicular priate authorities. lfSVD does occur,
lesions on the feet, especially the coronary
control is by zoosanitary measures,
band, and less often other areas such as the
including restrictions on pig movement.

mouth, lips, teats, or snout. The lesions may

There are no commercially available
be mild or inapparent, especially when pigs
vaccines. Extensive serosurveillance is
are kept on soft bedding. The lesions are
necessary to detect subclinically infected
similar to those of foot-and-mouth disease
herds, and seroreactor herds must be

(seep 629), vesicular exanthema of swine
followed up by clinical inspection and

(seep 738), and vesicular stomatitis (see fecal virus testing. The virus is extremely
p 694); however, affected pigs usually do
resistant in the environment and is stable
not lose condition, and the lesions heal
over a wide pH range (2.5-12); thus,
rapidly. Nervous signs have been desc1ibed
disinfection of premises, trucks, and
but are rarely seen in the field. The OIE
equipment must be thorough. The most
recommends that any outbreaks of
effective disinfectants are strong alkalis,
vesicular disease in pigs should be assumed
although hypochlorites or acid-containing
to be foot-and-mouth disease until proved
iodophors can be used when organic
otherwise by laboratory testing.

material is not present.

TRICH IN ELLOSIS

(Trichinosis)

Trichinellosis is a parasitic disease of public

50 years due in part to the move to modern
health in1portance caused by the nematode
production facilities (confinement) that

'I'richinella spiralis. Human infections are reduces or elinlinates exposure to rodents
established by consumption of insuffiand other wildlife.

ciently cooked infected meat, usually pork
or bear, although other species have been

Etiology and Epidemiology: The
implicated. Natural infections are found in
genus 'I'richinella is currently considered wild carnivores; trichinellosis has also been
a complex of nine species and three
found in horses, rats, beavers, opossums,
additional genotypes (T6, TS, and T9) of
walruses, whales, and meat-eating birds.

undeternlined taxonomic status. Other than

Most mammals are susceptible. The number for the existence of two clad es defined by of human cases has declined in the past
the presence or absence of a collagen

TRICHINELLOSIS

737
capsule (cyst) surrounding the parasite in
after infection and is completed by 4-8 wk,
the muscle, there are few distinct morphoat which time the latvae are infective. The logic differences. Ta.xon identification is
cell degenerates as the larva grows, and
based on characteristics such as reproducthen calcification occms ( at different rates tive isolation, infectivity to certain hosts,
in various hosts). Larvae may remain viable

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resistance to freezing, geographic cruising
in the cysts for yeai·s, and their development
range, PCR and DNA sequencing, and
continues only if ingested by another
isoenzyme analysis. T spiralis (Tl) is the
suitable host. The diaphragm, tongue,
most common and widely distributed of the
masseter, and intercostal muscles are
encapsulated species affecting people and
among those most heavily involved in pigs.

domestic animals in temperate regions; it

If larvae pass through the intestine and
has high infectivity for pigs and rodents,
are eliminated in the feces before matmaexhibits low resistance to freezing, and is tion, they ai·e infective to other animals.

broadly infective for most sylvatic hosts.

The other cyst-forming species include

Clinical Findings and Diagnosis: Most

T nativa (T2), found in arctic carnivores;
infections in domestic and wild animals go

T b1itovi (T3), found throughout the entire
undiagnosed. ln people, heavy infections

Emopean continent, northwest Africa, and
may produce serious illness with tlu·ee
southwest Asia; T murrelli (T5), restricted
clinical phases (intestinal, muscle invasion,
to North Ame1ica; Tnelsoni (T7), found
and convalescent) and occasionally death.

only in eastern Africa; and the most recently

Although antemortem diagnosis in
named Tpatagoniensis (Tl2), found in
animals other than people is rai·e, tJ.ichinel

Argentina. There are three other encapsulosis may be suspected if there is a history lated genotypes: Trichinella T6, which is
of eating rodents, wildlife carcasses, or raw,
very sin1ilar to Tnativa and is fow1d in
infected meat. Microscopic exatnination
carnivores of North Ame1ica; TS, which
of a muscle biopsy sample ( usually tongue)

shows similarities to T britovi and is
may confinn but not necessarily exclude
present in carnivores of Africa; and T9,
trichinellosis. ELISA is a reliable test to
which has been identified only in sylvatic
detect anti-Trichinella antibodies.

hosts from Japan but is genetically more

Seroconversion may not occur for weeks
similar to T murnlli of the USA. There are
after infection, although as little as 0.01
three additional species-T pseudospiralis
larvae per gram of meat can be detected.

(T4), Tpapuae (TlO), and T zimbabwensis

(Tll), which constitute the nonencapsu

Control: TreatJ.nent is generally in1practilated clade (lack a cyst in the muscle).

cal in animals. The objective is Lo prevent

Tpseudospiralis has a cosmopolitan
ingestion by any animal, including people,
distribution and is the only species capable
of viable Trichinella cysts in muscle
of infecting mammals and birds. T papuae

(trichinae). ln pigs, this may be accomwas first identified in pigs from Papua New plished with good management that

Guinea, but its presence is suspected to
includes controlling rodents, cooking
extend into Australasia and southeast Asia.

gai·bage (fed to the pigs) for 30 min at 212°F

T zimbabwensis is present in sub-Sallaran

(100°C), and preventing cannibalism (ie, ta.ii

Africa Both T papuae and T zimbabwensis biting) and access to wildlife cai·casses.

are capable of infecting crocodiles.

Inspection of meat for viable trichinae at

Infection generally occurs by ingestion of
tl1e time of slaughter (by trichinoscopic or
larvae encysted in muscle. The cyst wall is
digestion methods) is effective to prevent
digested in the stomach, and the liberated
hwnan infection in many cotmtries. ln
larvae penetrate into the duodenal and

North America, the asswnption is that pork
jejunal mucosa. Within -4 days, the larvae
may be infected; therefore, those products
develop into sexually mature adults. After
that appear as "ready to eat" must be
mating, the females (3-4 nun) penetrate
processed by adequate heating, freezing, or
deeper into the mucosa and discharge living
curing to kill trichinae before mai·keting.

larvae (up to 1,500) throughout 4-16 wk

Other pork should be cooked to assme that

After reproduction, the adult wonns die
all tissue is heated to an internal temperaand usually are digested. The young laivae tme of 145°F (63°C) for roasts or 160°F

(0.1 mm) migrate into the lymphatics,

(71 °C) for ground meats. Freezing pork
are carried via the portal system to the
at an appropriate temperatme for an
petipheral circulation, and reach striated
appropriate time is also effective (5°F
muscle, where they penetrate individual

[-l5°C] for 20 days, -9.4°F l-23°C] for 10
muscle cells. They grow rapidly (to 1 mm)

days, or -22°F [-30°C] for 6 days). Freezing
and begin to coil within the cell, usually 1
cannot be relied on to kill trichinae in meat
per cell. Capsule formation begins -15 days
other than pork

738

VESICULAR EXANTHEMA OF SWINE

VESICULAR EXANTHEMA OF SWINE

(San Miguel sea lion virus disease)

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Vesicular exanthema of swine (YES) is an
seal meat, and perch-like fish in California.

acute, highly infectious disease character'

SMSV can produce lesions indistinguishable
ized by fever and fom1ation of vesicles on
from those uf VES in pigs, and the diverse
the snout, oral mucosa, soles of the feet,
pool of marine caliciviruses on the west
coronary band, and between the toes.

coast of the USA are a reservoir of potential

VES has been reported only in the USA,
swine pathogens. 1\vo marine caliciviruses,
and not since 1959, but it remains of historic
serotype SMSV-5 and an unknown virus,
in1p01tance because of its clin.ical similarity
have been isolated from vesicular lesions
to foot-and-mouth disease. Since 1972, San
or throat washings of two people with

Miguel sea lion virus (SMSV), a virus
vesicular lesions, but the viruses ar·e consiindistinguishable from VES virus (VESV), dered of minimal significance to public
and related calicivimses have been isolated
health.

from marine mammals on the west coast of

In pigs, the clinical disease is indistinthe USA.

guishable from foot-and-mouth disease

VESV, SMSV, and related vimses are

(seep 629), vesicular stomatitis (see
members of the genus Vesivirus in the
p 694), and swine vesicular disease
fan1ily Caliciviridae. Many inmmnologically

(seep 735).

distinct serotypes have been demonstrated

Presun1ptive diagnosis in pigs is based on

(13 types ofVESV from pigs and at least 16
fever and the presence of typical vesicles,
types of SMSV from marine sources). In
which break within 24-48 hr to fom1
addition, a number of serotypes have been
erosions. Diagnosis can be confirmed
isolated from other host species and named
by ELISA, reverse-transcriptase PCR,
accordingly: bovine, prinlate, cetacean,
complement-fixation tests, arid electron
walrus, skunk, mink, rabbit, and reptile
microscopy on epithelial tissue, or after
cal.iciviruses. In some cases, serotypes
passage in swine tissue cultures. Serum
initially isolated in terrestrial animals ( eg,
neutralization tests and electron microsreptile calicivirus) have subsequently been copy are also used.

found in marine mammals. All of these

Suspected cases of vesicular exanthema
viruses ( except for SMSV-8, SMSV-12, and
should be reported inlmediately to the
mink cal.icivirus) fom1 a single virus species, appropriate authorities. Feeding of food vesicular exanthema of swine virus.

scraps (garbage, swill) to pigs is illegal in

SMSV has also been isolated from
many countries and can be done only under
vesicular lesions on marine mammals,
license and after cooking in the USA.

BLUETONGUE

Bluetongue is ar1 infectious arthropod-borne cattle are subclinical. Bluetungue (the viral disease prin1arily of domestic and wild
disease caused by BTV) is usually considmrninants. Infection with bluetongue virus ered to be a disease of in1proved breeds of

(BTV) is common in a broad band across the
sheep, particularly the fine-wool and mutton
world, which until recently stretched from
breeds, although it has also been recorded

-35°S to 40°-50°N. Since the 1990s, BTV has
in cattle and some wild ruminant species,
extended considerably north of the 40"' and
including white-tailed deer (OdocoileilS
even the 50'h parallel in some parts of tl1e
virginianus ), pronghorn antelope
world ( eg, Europe). The geographic

(Antilocapra americana ), and desert
restriction is in part related tu the climatic
bighorn sheep (Ovis canadensis) in Nmth
and envit·onmental conditions necessary to

America, and European bison (Bison
support the Culicoides vectors. Most
bonasus) and captive yak (Bos grunniens infections with BTV in wild mminants and
grunniens) in Europe.

BLUETONGUE

739

Etiology and Transmission: Bluetongue

Embryo transfer is regarded as safe,
virus is the type-species of the genus
provided that donors are not viremi.c and an

Orbivirus in the family Reoviridae. There
appropriate washing procedure for emb1yos
are at least 24 serotypes worldwide,
is used. Transplacental transmission of field
although not all serotypes exist in any one
strains of BTV from dan1 to fetus, leading to

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geographic area; eg, 13 serotypes (1, 2, 3, 5,
the birth ofviremic calves, is reported in

6, 10, 11, 13, 14, 17, 19, 22, and 24) have been
cattle, but the epidemiologic significai1ce
reported in the USA and 8 serotypes (1, 2, 4,
of this mechanism is unclear. Accidental

6, 8, 9, 11, and 16) in Europe. Distribution
infection has been reported in dogs in the
of BTV throughout the world parallels the

USA after administration of a modified-live
spatial and temporal distribution of vector
canine virus vaccine that was contaminated
species of Culicoides biting midges, which
with BTV. Serologic evidence of infection
are the only significant natural transmitters
with BTV has been fow1d in wild and captive
of the virus, as well as the temperatures
carnivores in Africa and Europe, perhaps as
at which BTV will replicate in and be
a result of ingesting virus-infected viscera.

transmitted by these vectors. Of more than

The epidemiologic in1portai1ce of this oral

1,400 Culicoides species worldwide, fewer
infection mechanism is at present
than 30 have been identified as actual or
uncertain. Serologic evidence of BTV
potential vectors of BTV to date. Continued
exposure has been demonstrated in
cycling of the virus an1ong competent
domestic dogs fed commercial diets.

Cul'icoides vectors and susceptible
ruminants is critical to viral ecology. In the

Clinical Findings: The course of the

USA, the principal vectors are C sonorensis
disease in sheep can vary from peracute to
and C insignis, which limit the distribution chronic, with a mortality rate of2%-900Ai.

of BTV to southern and western regions. In

Peracute cases die within 7--9 days of
northern and eastern Australia the principal
infection, mostly as a result of severe
vector is C brevitarsis, whereas in Africa, pulmonary edema leading to dyspnea,
southern Europe, and the Middle East it is
frothing from the nostrils, and death by

C imicola,. In northern Europe, the major
asphyxiation. In chronic cases, sheep may
vectors are species within the C obsoletus
die 3--5 wk after infection, mainly as a result
dewulji complex. In each geographic region, of bacterial complications, especially secondary vector species may attain local
pasteurellosis, and exhaustion. Mild cases
in1portance.

usually recover rapidly and completely. The

Vectors become infected with BTV by
major production losses include deaths,
in1bibing blood from infected vertebrates;
unthriftiness during prolonged convalestransovarial transmission has not been cence, wool breaks, and reproductive
reported. High affinity of the vin1s to blood
losses.

cells, especially the sequestering of viral

In sheep, BTV causes vascular endothelial
particles in invaginations ofRBC memdamage, resulting in changes to capillary branes, contributes to prolonged viremia in
permeability and subsequent intravascular
the presence of neutralizing antibody. The
coagulation. This results in edema, congesextended viremia in cattle ( occasionally up tion, hemorrhage, inflammation, and
to 11 wk), and the host preference of some
necrosis. The clinical signs in sheep are
vector species of Culicoides for cattle,
typical. After an incubation period of 4--6
provide a mechanism for yeai0round
days, a fever of 105°-107.5°F ( 40.5° -42°C)

transmission in domestic ruminants in
develops. The aninlals are listless and
locations where the vector-free (winter)

reluctant to move. Clinical signs in young
period is relatively short. Mechanical
lai11bs are more apparent, and the mortality
transmission by other bloodsucking
rate can be high ( up to 30%). Approximately
insects is of minor significance.

2 days after onset of fever, additional

Vector-borne transmission through
clinical signs may be seen, such as edema

Culicoides spp is the primary way BTV
of lips, nose, face, submandibulai· area,
spreads. Virus concentrations in secretions
eyelids, and sometimes ears; congestion of
and excretions are minimal, making direct,
mouth, nose, nasal cavities, coajunctiva,
indirect, or aerosol transmission unlikely.

and coronary bands; and laineness and

However, in-contact transmission of BTV
depression. A serous nasal discharge is
serotype 26 has been demonstrated in goats. common, later becoming mucopurulent.

The significance of this fonn of transmis

The congestion of nose and nasal cavities
sion in the ecology of this serotype is not
produces a "sore muzzle" effect, the tenn
known. Semen from viremic bulls can serve
used to describe the disease in sheep in
as a source of infection for cows through
tl1e USA. Sheep eat less because of oral
natural service or artificial insemination.

soreness and will hold food in tl1eir moutlls

740

BLUETONGUE
to soften before chewing. They may champ
hemorrhages, hydrothora.x, hydroperica.rto produce a frothy oral discharge at the diun1, perica.rditis, and pneumonia.

corners of the lips. On close examination,

In many areas of the world, BTV infection
small hemo1Thages can be seen on the
in sheep, and especially in other rwnina.nts,

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mucous membranes of the nose and mouth.

is subclinical. Laboratory confinnation is

Ulceration develops where the teeth come
based on vims isolation in embryonatecl
in contact with lips and tongue, especially in chicken eggs or manm1alian and insect cell areas of most friction. Some affected sheep
cultures, or on identification of viral RNA
have severe swelling of the tongue, which
by PCR. The identity of isolates may be
may become cyanotic ('blue tongue") and
confirmed by the group-specific antigeneven protrude from the mouth. Animals capture ELISA, group-specific PCR,
walk with difficulty as a result of inflanunainununofluorescence, immunoperoxidase, tion of the hoof coronets. A purple-red color serotype-specific virus neutralization tests, is easily seen as a band at the junction of the
serotype-specific PCR, or hybridization with
skin and the hoof. Later in the course of
complementary gene sequences of group- or
disease, lan1eness or torticollis is due to
serotype-specific genes. For vims isolation,
skeletal muscle dan1age. ln most affected
blood (10-20 mL) is collected as early as
anin1als, abno1mal wool growth resulting
possible from febrile animals into an
from dennatitis may be seen.

anticoagulant such as heparin, sodium

Clinical signs in cattle are rare but may
citrate, or EDTA and transported at 4 °C
be similar to those seen in sheep. They a.re

(39.2°F) to the laboratory. For longterm
usually limited to fever, increased respirastorage when refrigeration is not possible, tory rate, lacrimation, salivation, stiffness,
blood is collected in oxalate-phenolglycerin
oral vesicles and ulcers, hyperesthesia,

(OPG). Blood to be frozen should be
and a vesicular and ulcerative denna.titis.

collected in buffered lactose peptone and

Susceptible cattle and sheep infected during stored at or below -70°C ( -94°F). Blood pregnancy may abort or deliver malforn1ecl
collected at later times during the vi.remic
calves or lambs. The malfonnations include
period should not be frozen, because lysing
hydranencephaly or porencephaly, which
of the RBCs on thawing releases the
results in ataxia and blindness at birth.

cell-associated vims, which may then be

White-tailed deer and pronghorn antelope
neutralized by early humoral anl ibody. The
develop severe hemorrhagic disease leading vims does not remain stable for long at to sudden death. Pregnant dogs abmt or

-20°C ( -4 °F). ln fatal cases, specimens of
give birth to stillborn pups and then die in
spleen, lymph nodes, or red bone marrow

3--7 clays.

are collected and transported to the
laboratory at 4 °C (39.2°F) as soon as

Diagnosis and Lesions: The typical
possible after death.

clinical signs of bluetongue enable a

A serologic response in 1UI11inants can be
presumptive diagnosis, especially in areas
detected 7-14 days after infection and is
where the disease is endemic. Suspicion is
generally lifelong after a field infection.

confirmed by the presence of pete�hiae,

Current reconunended serologic techniques
ecchymoses, or hemorrhages in the wall of
for detection of BTV antibody include agar
the base of the pulmonary artery and focal
gel inununodiffusion and competitive
necrosis of the papillary muscle of the left

ELISA. The latter is the test of choice and
ventricle. These highly characteristic
does not detect cross-reacting antibody to
lesions a.re usually obvious in severe
other orbivirnses, especially anti-EHDV
clinical infections but may be barely visible ( epizootic hemorrhagic disease virus) in mild or convalescent cases. These
antibody. Various fonns of the serum
lesions are often described as pathognoneutralization test, including plaque monic for bluetongue, but they have also
reduction, plaque inhibition, and rnicrotiter
been seen occasionally in other ovine
neutralization, can be used to detect
diseases such as hea.rtwater, pulpy kidney
type-specific antibody.

disease, and Rift Valley fever. Hemorrhages
and necrosis a.re usually found where

Prevention and Control: There is
mechanical abrasion damages fragile
no specific treatment for anin1a.ls with
capillaries, such as on the buccal surface
bluetongue apart from rest, provision of soft
of the cheek opposite the molar teeth and
food, and good husbandry. Complicating
the mucosa of the esophageal groove and
and secondary infections should be treated
omasal folds. Other autopsy findings
appropriately during the recovery period.

include subcutaneous and intermu cular

Prophylactic inununization of sheep
edema and hemorrhages, skeletal
remains the most effective and practical
myonecrosis, myocardial and intestinal
control measw·e against bluetongue in

BOVINE EPHEMERAL FEVER

741
endemic regions. Attenuated and inacti

During an outbreak, when one or a limited
vated vaccines against BTV are commernumber of serotypes may be involved, cially available in some countries. Three
vaccination strategy depends on the
polyvalent vaccines, each comprising five
serotype(s) causing infection. Use of

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different BTV serotypes attenuated by
vaccine strains other than the one(s)

serial passage in embryonated hens' eggs
causing infection affords little or no
followed by growth and plaque selection in
protection and is not recommended.

cell culture, are widely used in southern

The potential risk from vaccine virus

Africa and elsewhere, should epizootics of
reassortment with wild-type viral strains,
bluetongue occur. A monovalent (BTV type
virus spread by the vectors to other

10) modified-live virus vaccine propagated
susceptible ruminants, and reversion to
in cell culture is available for use in sheep
virulence of vaccine virus strains or even
in the USA. Use of vaccines with different
the production of new BTV strains of
serotypes does not provide consistent
uncertain virulence should also be
cross-protection. Live-attenuated vaccines
considered. The use of inactivated
should not be used during Culicoides
vaccines in BTV incursions into northern
vector seasons, because these insects

Europe has played a major part in
may transmit the vaccine virus( es) from
controlling virus spread in those regions
vaccinated to nonvaccinated animals, eg,
where significant cover (>80%) has been
other ruminant species. This may result in
achieved.

reassortment of genetic material and give

Control of vectors by using insecticides

1ise to new viral strains. Abortion or
or protection from vectors may lower the
malfomiation, particularly of the CNS, of
number of Culicoides bites and subsefetuses may follow vaccination of ewes and quently the risk of exposure to BTV
cows with attenuated live vaccines during
infection. However, these measures alone
the first half and the first trin1ester of
are unlikely to effectively halt a bluetongue
pregnancy, respectively. Passive inununity
epidemic and should be regarded as
in lambs usually lasts 2-4 mo.

mitigation measw·es to be used alongside a

The control of bluetongue is different in
comprehensive and vigorous vaccination
areas where the disease is not endemic.

program.

BOVINE EPHEMERAL FEVER

(Three-day sickness)

Bovine ephemeral fever is an insecthas been demonstrated using panels of transmitted, noncontagious, viral disease
monoclonal antibodies and by epitope
of cattle and water buffalo that is seen in
mapping. Several closely related

Africa, the Middle East, Australia, and
ephemeroviruses (including Berrimall

Asia. Inapparent infections can develop
virus, Kimberley virus, Malakai virus,
in Cape buffalo, hartebeest, waterbuck,

Adelaide River virus, Obodhiang virus,
wildebeest, deer, and possibly goats. Low

Puchong virus, kotonkan virus, and
levels of antibody have been recorded in

Koolpinyah virus) have been identified.

several other antelope species and giraffe, However, of these, only kotonkan virus but the specificity has not been con

(isolated in Nigeria) has been associated
firmed.

with clinical ephemeral fever in cattle.

BEFV can be transmitted from infected to

Etiology and Epidemiology: Bovine
susceptible cattle by IV inoculation; as little
ephemeral fever virus (BEFV) is classified
as 0.005 mL of blood collected during the
as a member of the genus Ephemerovirus
febrile stage is infective. Although the virus
in the family Rhabdoviridae (singlehas been recovered from several Culicoides stranded, negative sense RNA). The virus
species and from Anopheline and Culicine
is ether-sensitive and readily inactivated
mosquito species collected in the field, the
at pH levels below 5 and above 10.

identity of the major vectors has not been

Although no evidence of immunogenic
proved. Transmission by contact or fomites
diversity is reported, antigenic variation
does not occur. The virus does not appear to

742

BOVINE EPHEMERAL FEVER
persist in recovered cattle, which often have All clinical cases have a neutrophilia with a lifelong inununity.

the presence of many immature fonns,

The prevalence, geographic range, and
although this is not pathognomonic.

severity of the disease vary from year to

Serofibrinous inflammation in ti1e tendon

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year, and epidemics occur periodically.

sheaths, fascia, and joints, together with

During epidemics, onset is rapid; many
pulmonary lesions, may substai.1tiate a
animals are affected within days or 2---3 wk. preswnptive diagnosis.

Bovine ephemeral fever is most prevalent

Laboratory confirmation is by serology,
in the wet season in the tropics and in
rarely by virus isolation. Whole blood
summer to early autumn in the subtropics
should be collected from sick and apparor temperate regions (when conditions ently healthy cattle in affected herds and
favor multiplication of biting insects); it
must be sufficient to provide two aiJ0dried
disappears abruptly in winter. Virus spread blood smears, 5 mL of whole blood in appears to be limited by latitude rather
anticoagulant (not EDTA), and ---10 mL of
than topography or availability of
serwn. A differential WBC count on blood
susceptible hosts. Morbidity may be as
smears can eiti1er suppmt or refute a
high as 80%; overall mortality is usually
preswnptive field diagnosis.

1 % ---2%, although it can be higher in

Virus is best isolated by inoculation of
lactating cows, bulls in good condition,
mosquito (Aedes albopictus) cell cultures
and fat steers (10%---30%). However,
with defibrinated blood, followed by
reported overall mo1tality rates have
transfer to baby han1ster kidney (BHK-21 or
exceeded 10% in outbreaks in several

BHK-BSR) or monkey kidney (Vero) cell
countries in recent years.

cultures after 15 days. Suckling mice may
also be used for primary isolation by

Clinical Findings: Signs, which occur
intracerebral inoculation. Isolated viruses
suddenly and vary in severity, can include
ai.·e identified by PCR, neutralization tests
biphasic to polyphasic fever ( 40° -42°C
using specific BEFV antisera, and ELISA

[ 104°-107.6°F]), shivering, inappetence,
using specific monoclonal antibodies. The
lacrimation, serous nasal discharge,
neutralization test and the blocking ELISA
drooling, increased heai.t rate, tachypnea
are recommended for antibody detection
or dyspnea, atony of forestomachs,
ai.1d give similar results. A 4-fold 1ise in
depression, stiffness and lameness, and a
antibody titer between paired sera collected
sudden decrease in milk yi.eld. Clinical

2---3 wk apart confun1s infection.

signs are generally milder in water buffalo.

Affected cattle may become recumbent

Treatment and Control: Complete
and paralyzed for 8 hr to > 1 wk. After
rest is the most effective treatment, and
recovery, milk production often fails to
recovering animals should not be stressed
return to normal levels until tl1e next
or worked because relapse is likely.

lactation. Abortion, with total loss of the

Anti-inflanm1atory drugs given early and in
season's lactation, occurs in ---5% of cows
repeated doses for 2---3 days ai.·e effective.

pregnant for 8---9 mo. The virus does not

Oral dosing should be avoided unless ti1e
appear to cross the placenta or affect ti1e
swallowing reflex is functional. Signs of
fertility of the cow. Bulls, heavy cattle, and
hypocalcemia are treated as for milk fever
high-lactating dairy cows are the most

(seep 988). Antibiotic treatment to control severely affected, but spontaneous
secondary infection and rehydration witi1
recovery usually occurs within a few days.

isotonic fluids may be warranted.

More insidious losses may result from

Attenuated vims vaccines appeai.· to
decreased muscle mass and lowered
be effective but should be used only in
fertility in bulls.

endemic areas. Inactivated virus vaccines
have not produced longtem1 protection

Lesions: Bovine ephemeral fever is an
against experimental challenge with
inflai.1unatory disease. The most common
virulent virus and cannot guarantee lasting
lesions include polyserositis affecting
immunity, but they may boost the
pleural, pericardia!, and peritoneal surfaces; immunity produced by live virus vaccine.

serofibrinous polysynovitis, polyai.thritis,

Alti1ough a subunit vaccine that protects
polytendinitis, and cellulitis; and focal
against field and laboratory challenge has
necrosis of skeletal muscles. Generalized
been described, it is not commercially
edema of lymph nodes and lungs, as well as
available. The efficacy of vector control
atelectasis, also may be present.

remains uncertain, because the insect
vectors have not been fully identified.

Diagnosis: Diagnosis is based almost

There is no evidence that people can be
entirely on clinical signs in an epidemic.

infected.

BOVINE LEUKOSIS

743

BOVINE LEUKOSIS

(Bovine lymphosarcoma, Leukemia, Malignant lymphoma) VetBooks.ir

Lyrnphosarcoma in cattle may be sporadic
eradication programs in place that have
or result from infection with bovine
led to negligible rates of BLV infection.

leukemia virns (BLY); the latter is often

Although voluntary control progrruns ru·e
referred to as an enzootic bovine leukosis.

in place in the USA, prevalence is high

Sporadic lymphosa.rcoma in cattle is
compru·ed with much of the rest of the
unrelated to infection with BLV. Despite the
world. The most recent surveys in the USA
lack of association, animals with sporadic
estimate tl1at 44% of dairy and lOOAi of beef
lymphosarcoma may possibly be infected
cattle are infected with the virns. Prevawith the vims. Sporadic lymphosarcoma lence tends to increase on dairies with
manifests in three main fo1111s: juvenile,
increasing herd size, while the converse is
thyrnic, and cutaneous. Juvenile lyrnphosru�
true in beef cattle. In general, the prevalence
coma occurs most often in anin1als <6 mo
of viral infection increases with age.

old, thyrnic lyrnphosarcoma affects cattle

Cattle are infected witl1 BLV tlu-ough the

6-24 mo old, and cutaneous lymphosart:rru1sfer of blood and blood products that coma is most common in cattle 1-3 yr old.

contain infected lymphocytes. Once
infected, cattle develop a lifelong ru1tibody

Etiology, Transmission, and Epidemi
response, primarily to tl1e gp51 envelope
ology: Enzootic bovine leukosis is caused
protein ru1d the p24 capsid protein.

by BLV, an exogenous C-type oncogenic

B lymphocytes harbor tl1e integrated
retrovirus of the BLV-humru1 T-lyrnphotropic provims but rarely express viral proteins virns group. BLV has a stable genome, does
on tl1eir cell sU1face. The exact site of viral
not cause chronic viremia, ru1d has no
replication ru1d expression that drives the
preferred site of proviral integration.

inunune response remains elusive.

Despite the lack of preferred proviral

Under experimental conditions, most
integration sites, the tumors generated by
routes of viral exposure can successfully
the virus in a single individual are typically
transmit infection. However, mru1y of these
monoclonal and have a single integration
settings are unlikely to be encountered
site. The vims escapes the immune
naturally. Mru1y bodily fluids, including urine,
response by low levels of viral replication.

feces, saliva, respiratory secretions, semen,

It appears that replication is blocked at
uterine fluids, ru1d embryos, have been examthe transcriptional level, but the mechru1ism ined for tl1eir ability to transmit BLV arid ru·e is not completely understood.

considered to be noninfectious. Only on rare

The prevalence of BLV infection varies
occasion has virus been found in these fluids.

from country to country. Many European

Colostrun1 from BLY-positive cows contains
countries, Australia, ru1d New Zealru1d have
virus ru1d has been found to be infectious
experimentally. However, colostrnrn also
contains lru·ge ru11ounts of ru1tibody, ru1d it
is believed that the protective effects of
colostral ru1tibody outweigh the infectious
potential when colostrum is administered in
a nom1al fashion.

Most BLV trru1smission is horizontal.

Close contact between BLV-negative ru1d

BLV-positive cattle is thought to be a risk
factor. Mru1y common fa.i111 practices have
been in1plicated in viral transmission,
including tattooing, dehorning, rectal
palpation, if\iections, ru1d blood collection.

Vectors such as tabru1ids ru1d other large
biting flies also may transmit the virus.

Vertical tra.i1smission may occur tr3l1splacentally from ru1 infected dam to the fetus, intrapa.iturn by contact with infected blood,

Cutaneous lymphosarcoma.

or postpartum from the dam to the ca.If

Courtesy of Dr. Peter
through ingestion of infected colostrum.

Constable.

744

BOVINE LEUKOSIS

Any material that is blood contaminated or

Dyspnea, bloat, jugular distention,
lymphocyte rich has the potential to infect
tachycardia, anterior edema, and fever
anin1als with BLV.

have been documented. The affected cell
population is an immature, poorly

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Pathogenesis: There are three main
differentiated lyn1phocyte. Cutaneous
outcomes in cattle infected with BLV. Most
lymphosarcoma presents as cutaneous
animals remain persistently infected with no
plaques, 1-5 cm in diameter, on tl1e neck,
outward signs of infection. Approximately
back, nunp, and thighs. Regional lymph

299'o of BLY-infected cattle develop persistent nodes may also be enlarged. This fonn of lymphocytosis, while <5% of BLY-infected
lyrnphosarcorna may undergo spontaneous
cattle develop lymphosarcoma.

remission; however, relapses may occur.

Persistent lymphocytosis is sometimes
referred to as a preneoplastic syndrome,

Lesions: Animals with BLY-associated
but tl1ere is no convincing evidence tl1at
lyn1phosarcoma commonly show lesions
affected cattle have an increased risk of
in tl1e central or pe1ipheral lymph nodes,
developing lyn1phosarcoma. The lympholeading to Jyn1phadenopathy. Lesions of tl1e cytes present in persistent lymphocytosis
abomasw11 may lead to signs of cranial
are not neoplastic, altl1ough tl1ey may have
abdominal pain, melena, or abomasal
mild reactive changes consistent with
outflow obstruction. Pelvic limb paresis
normal blood smears in cattle. Persistent
progressing to paralysis can occur in
lymphocytosis is considered a benign
animals with extradural spinal lesions.

condition associated witl1 BLV infection.

Retrobulbar lesions cause protrusion of tl1e

For this reason, it is often overlooked.

globe, resulting in exposure keratitis and

However, tl1ese cows may serve as a
eventually proptosis. Lesions of the right
rese1voir of infection. The increased
atriun1 may be mild and Wldetectable
lymphocyte count is attributed to a 45-fold
clinically, or may cause arrhythmias,
increase of infected CD5• and a 99-fold
mun11w-s, or heait failure. Uterine lesions
increase in infected CD5- B cells. It has
may lead to reproductive failure or abortion.

been suggested that cows witl1 persistent

Lesions of the internal organs typically
lymphocytosis may be at greater risk of
involve the spleen, liver, or kidneys ai1d
passing BLV infection on to their calves in
ureters. Lesions of the spleen are often
utero and may show decreased milk producinitially asymptomatic but may result in tion and alteration of milk components.

rupture of the spleen and exsanguination

Lymphosarcoma is rarely seen in
into tl1e peritoneal cavity. Lyn1phosarcoma
animals <2 yr old and is most corru11on in.

of the liver is often asymptomatic but may
tl1e 4- to 8-yr-old age group. Less tl1an 5% of
lead to jaundice and liver failure. Disease of

BLY-infected cattle develop lymphosartl1e kidney and ureter can lead to abdominal coma. Lymphosarcoma, including botl1
pain and the subsequent development of
sporadic and enzootic forms, is one of the
hydroureter or hydroneplu-osis and clinical
main causes of condemnation of adult dairy
signs associated witl1 renal failure.

cows at slaughter.

Lyn1phosarcoma may appear as
yellow-tan, discrete nodular masses or a
diffuse tissue infiltrate. The latter pattern

Clinical Findings: Clinical signs associresults in an enlarged, pale organ and can ated witl1 development of lymphosarcoma
be easily misinterpreted as a degenerative
are highly variable, because tl1e affected
change ratl1er than neoplasia. Histologically,
organ( s) will dictate tl1e predominant
tl1e twnor masses are composed of densely
clinical signs.

packed, monomorphic lymphocytic cells.

Juvenile lymphosarcoma is often
characterized by a sudden onset of diffuse

Diagnosis: Lymphosarcoma is often
lymphoid hyperplasia witl1 or witl1out
included on tl1e differential diagnosis list for
visceral organ involvement. Weight Joss,
many diseases because of tl1e wide range of
fever, tachycardia, dyspnea, bloat, and
clinical findings. Viral infection is diagnosed
posterior paresis have all been described
by serology or virology, persistent Jymphowith tlus form of lymphosarcoma. Procytosis is identified by hematology, and found Jymphocytosis (>50,000/µL) often
neoplastic tun1ors are identified by histologic
accompanies this fatal form of bovine
exanunation of biopsies. Positive serology or
lyrnphosarcoma. Thynuc lyn1phosa.rcoma
virology for BLV confinns viral infection but
may involve the cervical or intrathoracic
not tl1e presence of lymphosarcoma
tl1yn1us, or botl1. Clinical signs associated

Serology is tl1e most common and reliable
witl1 this form of Jymphosa.rcoma depend
way to diagnose infection witl1 BLV. Agar gel
heavily on tl1e location and size of tl1e
inu-nunodiffusion is still recognized by most
tun1or. A cervical swelling may be evident.

countlies as tl1e official import/export test,

BOVINE PETECHIAL FEVER

745
but ELISA is the most common test for
resources, including money, time, and
routine diagnostic use. Serology is mrreliable
available workforce.

in calves that have ingested colostrum from

BLV-positive cows because of the passive
acquisition of maternal antibodies that

Prevention: Eliminating the movement

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typically wane by 4--6 mo of age. PCR is a
of blood from infected anin1als to naive
sensitive and specific assay for diagnosis of
animals is the cornerstone of prevention

BLV infection in peripheral blood lymphoprotocols. In calves, feeding colostrun1 from cytes. This test can identify proviral DNA of
seronegative cows is often advocated.

BLV in the lymphocytes of infected animals

However, most epidemiologic evidence
and differentiate positive from negative
suggests that the protective effect of
calves in the presence of maternal antibodies. colostral antibody outweighs the risk of The diagnosis of lymphosarcoma must
infections, particularly in high prevalence
be made by cytology or histopathology.

herds. The replacement of whole milk

Cytologic diagnosis is sometimes difficult
feeding with high-quality milk replacer may
because of the frequency of blood
also be considered. Bloody milk should
contamination of the aspirates.

never be fed to calves.

Cautery or other bloodless methods of

Treatment and Control: There is
dehoming should be used. Equipment used
no treatment for viral infection or for
for castration, tattooing, ear tagging, or
lymphosarcoma in cattle, although
implanting should be adequately cleaned
parenteral corticosteroids can transiently
and disinfected between animals.

decrease the severity of clinical signs.

Transmission can be decreased in adult

Eradication programs have been develcattle by changing rectal sleeves in between cows. Artificial insemination or embryo
oped but success has been variable, pritransfer (using negative recipients) may marily because of the expense and high
limit transmission. In beef herds, the use of
prevalence of infection among cattle in
a negative bull may linut transmission, but
the USA relative to tl1e economic cost
natural service is an uncommon method
of disease. The most commonly recomof viral transmission wtless breeding is mended eradication protocol is as fol-traumatic.

lows: 1) identify infected animals using a

Additional recommendations include
serologic test, 2) cull seropositive animals
disinfection of equipment that has come in
inunediately, 3) retest the herd in 30-60
contact with blood or body tissue. Single
days, 4) use PCR to test young calves and as
use, disposable needles should always be
a complementary test to clarify test results
used for blood collection and IM injections.

in herds with a low prevalence of infection,

It is preferable to use single-use disposable
and 5) repeat testing and cull until the entire
needles for vaccination, but the risk of
herd tests negative. Testing is then repeated
transmitting BLV virus via SC vaccination
every 6 mo. The herd is declared free when
is low. Handling facilities that become
there have been no positive tests for 2 yr.

contan1inated with blood should be

Additions to the herd should have two
cleaned between animals. Fly control helps
negative tests 30 and 60 days before arrival.

nunimize the potential for tabanid-associ

When test and cull programs are econoated transmission. Blood transfusions and mically untenable, test and segregation
vaccines containing blood, such as those
programs have been reconm1ended but
used for babesiosis and anaplasmosis, are
are rarely implemented. These programs
particularly potent ways to spread the
necessitate rwrning two completely
disease, and donors must be carefully
separate operations and require additional
screened.

BOVINE PETECHIAL FEVER

(Ondiri disease)

Bovine petechial fever is a rickettsiosis

Kenya and Tanzania at altitudes >5,000 ft
of cattle characterized by high fever,

(1,500 m), although it is considered likely to
hemorrhages, and edema. Its occwTence
occur in neighboring countries with similar
has been confirmed in the highlands of
topography. The importance of bovine

746

BOVINE PETECHIAL FEVER
petechial fever lies in its threat to dairy
as the animal begins to recover. Marked
development in the highlands of eastern
cortjunctival edema and hemorrhage

Africa, but no outbreak has been reported

("poached egg eye") are characteristic in
for more than a decade.

some severe cases. The cortjunctival sacs
are swollen and everted around a tense and

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protmding eyeball, and there may be blood

Etiology and Epidemiology: The
in the aqueous humor. Pregnant cows may
disease is caused by Ehrlichia ondiri,
abort, most likely from the high fever. Other
an intracellular rickettsia that resides in
clinical signs are absent. The case mortality
cytoplasmic vacuoles of circulating
rate in untreated cases can be as high as 500/o
leukocytes. The organism can multiply after
in imported animals or in animals newly
experimental infection in cattle, sheep, goats,
introduced to the area. Latent infections
bushbuck, duiker, impala, Thomson's
develop after recovery in some animals,
gazelles, and wildebeest, and hence, probably especially in indigenous stock and in in most domestic and wild rwninants. E
ondiri
bushbuck. After recovery from the disease,
is believed to be endemic in wild
affected cattle are immune against
ruminants, particularly bushbuck, and it
experimental challenge for -2 yr.

sporadically overspills into domestic cattle
grazing forest edges or scmbs.

Lesions: Typically, eosinopenia and

The disease is restricted to scmb or forest lymphopenia are marked, followed by edge areas that have heavy shade, a thick
an equally pronounced neutropenia.

litter layer that provides high relative

Anemia is characteristically a sequela,
humidity, and a residual population of
and organisms can be demonstrated in
bushbuck and duiker, the two wild

Giemsa-stained smears of blood or spleen.

ruminants believed to be the main

At necropsy, widespread serosal and
an1plifying and reservoir hosts. It is seen
mucosa! hemorrhages and edema are
sporadically throughout the year in
accompanied by lymphoid hyperplasia.

imported breeds of cattle. It is not known

Organs frequently affected include the
how the disease is transmitted. As in other
heart, GI tract from the forestomach to
rickettsial infections, an arthropod vector
the colon, liver, gallbladder, kidneys, and
is suspected, but extensive attempts to
urinary bladder. The edema is characterincriminate ticks, biting insects, and mites ized by gelatinous fluid in the intennuscuhave failed.

lar connective tissue, lymph nodes, and
abomasum. No characteristic histologic
abnormalities have been described, but

Pathogenesis: The route of infection is
there is vascular proliferation with
not known, butE ondiri can be seen in
prominent endothelial swelling and
circulating granulocytes (neutrophils and
mild mononuclear infiltration.

eosinophils) and monocytes while cattle are
ill, and in the spleen at necropsy. Electron
microscopic studies have shown that E

Diagnosis: In areas where the disease is
ondiri can also infect endothelial �nd
endemic, a histo1y of movement to forest

Kupffer cells, and it may be free in capillary
edge areas, coupled with clinical signs and
lumens in the heart. It is believed that£
postmortem lesions, allows for a presun1p
ondiri initially multiplies in the spleen, with tive diagnosis. Definitive diagnosis requires subsequent spread to other areas. Damage
demonstration of the causal organism in
to the vascular endothelium would explain

Giemsa-stained smears of blood or spleen
the hemorrhages and edema, as in many
or by electron microscopy. E ondiri stains
other rickettsial infections.

blue with Giemsa and can be seen as small
bodies (0.4 µm), larger bodies (1-2 µm),
groups of small and large bodies, and

Clinical Findings: The disease is
groups or morulae of small bodies. They are
characterized by a high, fluctuating fever,
seen in cytoplasmic vacuoles and are most
apathy, lowered milk yield, and widespread
commonly seen in neutrophils. Tissue
petechiation of mucous membranes. After
suspensions (spleen) can also be inoculated
an incubation period of 4-14 days, animals
into susceptible cattle or sheep. Blood
develop a high fever; 2-3 days later, most
smears from the recipient animal should be
animals appear dull, and petechiae may be
made daily for as long as 10 days, by which
seen on mucous membranes, particularly
time E ondiri should be detectable in
the lower surface of the tongue and the
neutrophils. The disease is difficult to
vaginal mucosa These hemorrhages
differentiate from other hemorrhagic
enlarge over several days and then regress
diseases of cattle such as Rift Valley fever,

CAPRI NE ARTHRITIS AND ENCEPHALITIS

747
acute trypanosomosis (hemorrhagic
successfully to treat early experimental

Tr1.Jpanosoma vivax), acute theileriasis,
cases but a.i·e ineffective in advanced cases.

heartwater, hemorrhagic septicemia, and

The former is said to be more effective. In
bracken fem poisoning.

endemic areas, the disease can be prevented
by avoiding areas associated with previous

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Treatment and Control: Dithiosemica.i�
cases. However, this may not always be
bazone and tetracyclines have been used
practical.

CAPRINE ARTHRITIS AND ENCEPHALITIS

Caprine artluitis and encephalitis (CAE)

frequent introductions of new aninlals into
virus infection is manifested clin.icaJJy as
a herd). Prevalence of infection increases
polysynovitis-arthritis in adult goats and
with age but is not influenced by sex. Most
less commonly as progressive paresis
goats are infected at an early age, remain

(leukoencephalomyelitis) in kids. Subclinivirus positive for life, and develop disease cal or clinical interstitial pneumonia, induramonths to years later.

tive mastitis ("hard udder"), and chronic

The chief mode of spread of CAE is
wasting have also been attributed to
through ingestion of vi.ms-infected goat
infection with this vi.ms. Most CAE vi.ms
colostrum or milk by kids. The feeding
infections, however, are subclinical.

of pooled colostrunl or milk to kids is a

Infection with the CAE virus decreases the
particularly risky practice, because a few
lifetime productivity of dairy goats and is a
infected does will spread the virus to a large
barrier to exportation of goats from North
number of kids. Hmizontal transmission

America.

also contributes to disease spread with.in

CAE vi.ms infection is widespread among
herds and may occur through direct
dairy goats in most industrialized countries
contact, exposure to fomites at feed bw1ks
but rare an10ng indigenous goat breeds of
and waterers, ingestion of contaminated
developing countries unless they have been
milk in milking parlors, or serial use of
in contact with imported goats. In countries
needles or equipment conta.illinated with
such as Canada, Norway, Switzerland,
blood. Unlikely methods of transmission, as

France, and the USA, seroprevalence of
indicated by experimental studies, include

CAE virus is >65%.

in utero transmission to the fetus, infection
of the kid dwing parturition, and infection

Etiolo�y, Epidemiology, and Patho
through breeding or embryo tra.J1Sfer.

genesis: The CAE virus is an enveloped,

The pathogenesis of CAE is not fully
single-stranded RNA lentivi.ms in the fan1ily
w1derstood. Vi.ms-infected macrophages

Retrovi.ridae. There are several, geneticaJJy
in colostrw11 and milk are absorbed intact
distinct isolates of the vi.ms that differ in
through the gut mucosa Wection is
vi.mlence.

subsequently spread throughout the body

The CAE virus of goats is closely related
via infected mononuclear cells. Periodic
to the ovine lentivi.mses causing ov.ine
viral replication and macrophage maturaprogressive pneun1onia and maedi-visna in tion induces the characteristic lyrnphopro

North America and Europe, respectively.

liferative lesions in target tissues such as the

Cross-species transmission is possible
lungs, synoviun1, choroid plexus, and udder.

through feeding of infected milk and

Persistence of the CAE vi.ms in the host
colostrun1. Therefore, the ov.ine and cap1ine
is facilitated by its ability to become
lentivimses are now commonly referred to
sequestered as provirns in host cells.

as small rwninant lentivimses.

Infection induces a strong hwnoral and

CAE vi.ms infection is widespread in
cell-mediated inunune response, but neither
dairy goat breeds but unconunon in
is protective.

meat- and fiber-producing goats. Th.is has
been attributed to genetics, management

Clinical Findings: Clinical signs are seen
praclices such as feeding colostrunl and
in -200Ai of CAE vi.ms-infected goats during
milk from a single dam to multiple kids,
their lifetime. The most common manifesta and industrialized farming practices ( eg, tion of infection is polysynovitis-arthlitis,

748

CAPRI NE ARTHRITIS AND ENCEPHALITIS
which is primarily seen in adult goats but
multiple, small, white foci, and do not
can occur in kids as young as 6 mo old.

collapse. The bronchial lymph nodes are

Signs of polysynovitis-arthritis include joint
invariably enlarged. Histologic findings
capsule distention and varying degrees of
include chronic interstitial pneumonia with

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lameness. The carpal joints are most
mononuclear cell inflltration in alveolar
frequently involved. The onset of arthritis
septae and in perivascular and peribronmay be sudden or insidious, but the clinical chial regions. In does witl1 udder induration,
course is always progressive. Affected goats mononuclear infiltration of periductular lose condition and usually have poor hair
stroma obliterates normal man1mary tissue.

coats. Encephalomyelitis is generally seen
in kids 2--4 mo old but has been described

Diagnosis: A presumptive diagnosis
in older kids and adult goats. Affected kids
can be based on clinical signs and history.

initially exhibit weakness, ataxia, and

Infectious arthritis caused by Mycoplasma
hindlimb placing deficits. Hypertonia and
spp and traumatic aithritis are differential
hyperreflexia are also common. Over time,
diagnoses for arthritis induced by CAE
signs progress to paraparesis or tetraparesis virus. Differential diagnoses for the and paralysis. Depression, head tilt, circling, progressive pai·esis ai.1d pai·alysis exhibited opisthotonos, torticollis, and paddling have
by young kids should include enzootic
also been described. The interstitial pneuataxia, spinal cord abscess, cerebrospinal monia component of CAE virus infection
nematodiasis, spinal cord trauma, and
rarely produces clinical signs in kids.

congenital anomalies of the spinal cord

However, in adult goats with serologic
and vertebral colwnn. If the neurologic
evidence of CAE virus infection, chronic
exainination indicates brain involvement,
interstitial pneumonia that leads to
polioencephalomalacia, listeriosis, and
progressive dyspnea has been documented.

rabies should be considered as possible

The "hard udder" syndrome attributed to
causes. The pulrnonai-y form of caseous

CAE virns infection is characterized by a
lyrnphadenitis may have a similai· clinical
firm, swollen mammary gland and agalactia
presentation to the pulmonary form of CAE
at the time of parturition. Milk quality is
in adult goats.

usually unaffected. Although the mam

Botl1 an agar gel inunw10diffusion test
mary gland may soften and produce close
and ELISA for CAE virus are considered
to normal amounts of milk, production
sufficiently reliable for use in control
remains low in many goats with indurative
programs. The agar gel inunw10diffusion
mastitis.

test is reported to be more specific but less
sensitive than the ELISA. A positive test

Lesions: Pathologic lesions of CAE
result in an adult goat in1plies infection but
virus infection are generally described as
does not confirm that the clinical signs are
lyrnphoproliferative wi.th degenerative
caused by CAE virus. Kids infected at birth
mononuclear cell infiltration. Lesions in
develop a measurable antibody response
joints are characterized by thickening of the 4-10 wk after infection. However, positive joint capsule and marked proliferation of
test results in kids <90 days old usually
synovial villi. In chronic cases, soft-tissue
reflect colostral antibody transfer. Negative
calcification involving joint capsules,
test results do not reliably exclude CAE
tendon sheaths, and bursae is not uncomvirus infection, because the time for mon. Severe cartilage destruction, rupture
postinfection seroconve�ion is variable
of ligan1ents and tendons, and periarticular
and occasional goats have a very low titer
osteophyte formation have also been
that may not be detectable. Low antibody
described in advanced cases. Microscopic
titers are conm10n in late pregnancy.

features of articular lesions include synovial Because of the limitations of serologic cell hyperplasia, subsynovial mononuclear
testing, definitive diagnosis of clinical CAE
cell infiltration, villous hypertrophy,
requires demonstration of characteristic
synovial edema, and synovial necrosis.

lesions in biopsy specimens or at necropsy.

Gross lesions associated with the neuro

Virus isolation or PCR to demonstrate
logic form of CAE include asynm1etric,
presence of viral antigen in tissues may be
brownish pink, swollen areas, most
used to further substantiate the diagnosis.

corrunonly in the cervical and lumbosacral
spinal cord segments. Histopathologically,

Treatment and Control: There are no
these lesions are characterized by multispecific treatments for any of the clinical focal, mononuclear cell inflanm1atory
syndromes associated with CAE virus
infiltrates and varying degrees of demyeliinfection. However, supportive treatments nation. On gross exanlination, lw1gs of
may benefit individual goats. The condition
affected goats are firm and gray-pink with
of goats with the polysynovitis-arthritis may

COLISEPTICEMIA

749
be improved with regular foot trimming, use
control ofCAE: 1) permanent isolation
of additional bedding, and administration of
of kids beginning at birth; 2) feeding of

NSAIDs such as phenylbutazone or aspirin.

heat-treated colostrum ( 45°C [ 113°F] for

Goats with encephalomyelitis can be

60 min) and pasteurized milk; 3) frequent
maintained for weeks with good nursing
serologic testing of the herd (semiannuaJ!y),

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care. Antimicrobial therapy is indicated to
with identification and segregation of
treat secondary bacterial infections that
seronegative and seropositive goats; and
may complicate the interstitial pneumonia

4) eventual culling of seropositive goats. If
or indurative mastitis components of CAE
the control progran1 includes segregation of
virus infection. Providing high-quality,
herds into seropositive and seronegative
readily digestible feed to goats positive
groups, groups should be separated by
for CAE virus may delay the onset of the
a minimum of 6 ft (1.8 m), and shared
wasting syndrome.

equipment should be disinfected using

In commercial herds, one or more of the
phenolic or quaternaiy ammoniwn
following have been recommended for
compounds.

COLISEPTICEM IA

(Septicemic colibacillosis, Septicemic disease)

Septicemia caused by Escherichia coli is a
oropharyngeal mucosa but can also occur
common disease of neonatal calves, and to
across the intestine or via the wnbilicus
a lesser extent lan1bs. It may present with
and un1bilical veins. Septicemic strains of
signs of acute septicemia or as a chronic

E coli produce endotoxin, which results in
bacteremia with localization.

shock and rapid death. There is a period of
subclinical bacteremia that, with virulent

Etiology and Epidemiology: The
strains, is followed by rapid development
disease is caused by specific invasive
of septicemia and death from endotoxemic
serotypes of E coli that possess virulence
shock. A more prolonged course, with
factors enabling them to cross mucosal
localization of infection, polyaithritis,
surfaces, overcome the bactericidal plasma
meningitis, and less commonly uveitis and
factors, ai1d produce bacteremia and
nephritis, is seen with less virulent strains.

septicemia. The main deteffilinant of the

Chronic disease also develops in calves
disease is deficiency of circulating inm1unothat have acquired mai·ginal levels of globulins as the result of a failure in passive
circulating inununoglobulin. The organism
trat1Sfer of colostral inmmnoglobulin.

is excreted in nasal and oral secretions,

Colisepticemia is seen dming the first
urine, and feces; excretion begins dwing
weeks of life, with the highest incidence
the preclinical bacteremic stage. Initial
in aninlals 2-5 days old. Bacteremia and
infection can be acquired from a contatnisepticemia in calves and lambs are most nated environment. In groups of calves,
commonly associated with E coli and to a
trat1Smission is by direct nose-to-nose
lesser extent Salmonella spp. Approxicontact, urinary and respiratory aerosols, mately 30% of diat-rheic calves with severe
or as the result of navel sucking or fecalsystemic clinical signs were found to be oral contact.

bacterernic or septicemic, with E coli the
most commonly isolated pathogen from

Clinical Findings and Diagnosis:

blood cultures.

In the peracute and acute clisease, the
clinical course is sho1t (3-8 hr), and signs

Transmission and Pathogenesis:

are related to development of septic shock.

It is assumed that the primary source of the

Fever is not prominent, and the rectal
infection is the feces of infected aninlals,
temperature may even be subnonnal.

including the healthy darns and neonates,

Listlessness and an early loss of interest in
and diarrheic newborn aninlals, which act
sucking are followed by depression, poor
as multipliers of the organisms. Invasion
response to external stimuli, collapse,
occurs prirnaiily through the nasal and
recumbency, cold extremities, and coma.

750

COUSEPTICEMIA

Tachycardia, a weak pulse, and prolonged
volumes of balanced electrolyte solutions
capillary refill time are seen. The feces are
over several hours is essential to correct
loose and mucoid, but severe diarrhea is
hypovolemia and assure adequate
not seen in uncomplicated cases. Tremor,
peripheral tissue perfusion; fluids should
hyperesthesia, opisthotonos, and convulinclude glucose to correct hypoglycemia.

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sions are seen occasionally, but stupor

The beneficial effect of NSAIDs has been
and coma are more common. Mortality
attributed to their anti-inflammatory,
approaches lO()DA,. With a more prolonged
antipyretic, and analgesic properties.

clinical course, the infection may localize.

Glucocorticoids have also been proposed

PolyaiiJrritis, ophthalrnitis, omphalophlebito treat septicemia, although their benefits tis, and meningitis may occur within the first for treatment of sepsis are less well week of the initial bacteremic phase.

established.

No single laboratory parameter is
considered reliable for early diagnosis

Control and Prevention: Calves
of septicemia. A moderate but significant
that acquire adequate concentrations
leukocytosis and neutrophilia are seen
of immunoglobulin from colostrum are
early, but leukopenia is more common in
resistant to colisepticemia. Therefore,
severe and advanced cases. A left shift
prevention depends primarily on
of neutrophils and signs of toxicity of
management practices that ensure an
neutrophils as well as hypoglycemia are
adequate and early intake of colostrum.

common findings. Because failure of

The adequacy of the farm's practice of
transfer of passive inmmnity is the single
feeding colostrum should be monitored,
most important predisposing factor,
and corrective strategies applied as
subnom1al serum IgG and total protein
required. In North American Holstein
concentrations are common. Subnonnal
dairy herds, natural sucking does not
platelet counts ai·e the result of a consumpguarantee adequate concentrations of tive coagulopathy. In cases of arthritis, the
circulating immunoglobulins, and calves
joint fluid has an increased inflammatory
should be fed 2-4 L of first-milking
cell cotmt and protein concentration. With
colostrum containing a minimal total
meningitis, the CSF shows pleocytosis
mass of 100 g of IgG, using a nipple bottle
and an increased protein concentration;
or an esophageal feeder, within 2 hr of
organisms may be evident on microscopic
birth; this is followed by a second feeding
exanunation. Less conm1only, other
at 12 hr. A cow-side immunoassay test
bacteria, including other Enterobactecan assist in selection of colostrum with riaceae, Streptococcus spp, and Pasteur

�dequate immunoglobulin concentration.

ella spp, produce septicemic disease in

Although the circulating concentration
young calves. These organisn1s are more
of immunoglobulin required to protect
common in sporadic cases than as causes
against colisepticemia is low, high conof outbreaks. They produce similar clinical centrations are desirable to decrease
disease but can be differentiated by culture.

susceptibility to other neonatal infectious

As with colisepticemia, the primary
diseases.

detenninant of these infections is a failure

When natural colostrum is not available
of passive transfer of colostral inm1 unofor a newborn calf, commercial colostrum globulins.

substitutes containing 25 g oflgG will

The diagnosis is based on history and
provide sufficient inm1w10globulin for
clinical findings, demonstration of a severe
protection against colisepticemia if fed
deficiency of circulating IgG, and ultimately,
early in the absorptive period. Plasma
demonstration of the organism in blood or
containing at least 4 g and preferably 8 g of
tissues.

IgG, administered parenterally, will provide
some protection for older calves that have

Treatment: Treatment requires
not been fed colostrunl and are unable to
aggressive antimicrobial, fluid, and
absorb immunoglobulins from the intestine.

anti-inflainmatory therapy. Although blood

Small-volume hyperimmune serum is of
cultures are reconm1ended to retrospecbenefit only when it contains antibody tively confirm the diagnosis, antin1icrobial
specific to the particular serotype associtherapy must be initiated in1mediately in ated with an outbreak. The risk of early
any animal suspected of being septic.

infection should be minimized by hygiene

Because there is no time for sensitivity
in the calving area and disinfection of the
testing, the initial choice should be a
navel at birth. To minimize transmission,
bactericidal drug that has a high probabilcalves reared indoors should be in separate ity of efficacy against gram-negative
pens (without contact) or reared in calf
orgai.1isms. Administration IV of large
hutches.

HEARTWATER

751

CRIMEAN-CONGO HEMORRHAGIC FEVER

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Crimean-Congo hemorrhagic fever (CCHF)

Clinical Findings and Diagnosis: In
is a severe hemorrhagic viral disease of
experimental inoculations, sheep and cattle
people acquired from infected ticks, tissues
become infected but develop only transient
of infected wild or domestic animals, and
and mild increases of body temperature
from human patients with the disease.

with little evidence of clinical disease.

Viremia levels and duration are relatively

Etiology and Epidemiology: The
low and short, and antibodies are detectable
etiologic agent, CCHF virus (genus Nairovi
shortly after cessation of viremia. Reverse
rus, family Bunyaviridae), is an enveloped
transcriptase-PCR assays can detect the
negative-sense, trisegmented, single-stranded
virus, but primer design should match the

RNA vi.ms. The virus has been reported in a
vi.ruses found in the region in which human
wide area from South Africa through
patients, or other materials, have originated.

southern Europe, Eurasia, and into parts

Some tests (principally IgG ELISA) can
of western China The virus is principally
detect antibodies for the remainder of the
associated with ticks of the genus Hya
life of the animal, while other tests, such as
lomrrw, although it has also been isolated complement fixation and indirect fluoresfrom other genera of ixodid ticks. The global cent antibody, can detect antibodies for
distribution of the virus roughly approxisho1ter pe1iods after infection. Antibody mates that of Hyalomma spp ticks. Recent
prevalence in adult livestock species in
analyses of the genome of the virus suggest
endemic regions can be >50%.

that there is significant genetic diversity
somewhat correlated with geographic origin

Treatment: The antiviral dmg ribavirin has
of the virus. However, anomalies to this
been used in treatment of human disease in
pattern suggest that dispersal of host ticks

South Africa, although placebo-controlled
by migratory wildlife such as birds or the
trials have not been completed. Lack of
movement of livestock (by people) may act to
significant clinical disease in livestock
perturb the "normal" geographic distribution warrants no treatment considerations.

of CCHF virus subpopulations.

Control and Prevention: Control

Transmission and Pathogenesis: The
strategies for human infection include the
virus replicates in the host tick as it passes
avoidance of tick bites through the use of
from larval through adult stages (transstarepellents and appropriate protection dial transmission), and it can also be
when slaughtering or grooming animals.

transmitted from one generation to the

Movement of naive animals into endemic
next (transovarial transmission). Thus, the
areas provides opportunity for vertebrate
tick not only is a vector but also can be a an1pli.fication of the virus and increasing
reservoir of the virus via vertical transmisoccupational risk to butchers and hide sion. Small rodents, lagomorphs, and birds
preparers; tick control when naive animals
have all been incriminated as sources of
and endemic stock are mixed is paramount.

infection of immature stages of the tick,

Medical personnel should use appropriate
while mostHyalomma spp ticks are
barrier nursing techniques and universal
multihost and use larger vertebrates as the

(standard) precautions when handling
host for the adult stage of their life cycle.

suspect patients.

HEARTWATER

(Cowdriosis)

Heartwater is an infectious, noncontagious,
and the islands of the Comores, Zanzibar,
tickbome rickettsial disease of mminants.

Madagascar, Sao Tome, Reunion, and

The disease is seen only in areas infested by

Mauritius. Heartwater was introduced to
ticks of the genusAmblyomma. These
the Caribbean, and it and its vector (A
include regions of Africa south of the Sallara variegatum) are endemic on the islands of

752

HEARTWATER

Guadeloupe and Antigua. A variega tum,
challenged. There is no, or only partial,
but not the rickettsia, has since spread to
cross-protection between different stocks
several other islands despite attempts at

(strains) of E 1-uminantium. Most of these
eradication. Possible spread to the mainstocks ai·e infective for, but cannot be VetBooks.ir
land threatens the livestock industJy of
serially passaged in, mice; however, a few
regions from northern South America to
are pathogenic to mice infected by the IV

Centi·al America and the southern USA.

route.

In heartwater endemic areas in southern

Af1ica, it is estimated that mortalities due to

Pathogenesis: The pathogenesis
the disease are more than double those due
of heaitwater has not been elucidated;
to bacillaiy hemoglobinuria (red water, see
however, the tick probably infects the host
p 601) and anaplasmosis (seep 18)

via organisms in the saliva or regurgitated
combined. Cattle, sheep, goats, and some
gut content while feeding. Replication of
antelope species are susceptible to
the E ruminantium organisms in the tick
heartwater. In endemic areas, some animals
probably occurs in the intestinal epithelium
and to1toises may become subclinically
and is significai1tly ainplified. Once in the
infected and act as reservoirs. Indigenous
host, the organisms may replicate first

African cattle breeds (Bos ·indic'Us),
within the regional lymph nodes with
especially those with years of natural
subsequent dissemination via tl1e bloodselection, appear more resistant to clinical streai11 to invade endothelial cells of blood
heartwater than B taurus breeds.

vessels elsewhere in tl1e body. In domestic
ruminants, there does seem to be a

Etiology and Transmission: The
predilection for endothelial cells of the
causative organism is an obligate intrabrain. Organisms cai1 often be fow1d in cellular parasite, previously known as
colonies ( commonly but mistakenly

Cowdria ruminantium. Molecular
referred to as morulas) within tl1e cytoevidence led to reclassification of several plasm of endotl1elial cells. Colonies can vaiy
organisms in the order Rickettsiales, and it
in size, as can tl1e organisms that reside in
is now classified as Ehrlichia ruminan
them. Generally, small-sized organisms are
tium. Under natural conditions, E rumi
found in lai·ger colonies and vice versa. The
nantium is transmitted by Amblyomnia
smaller organisms are usually referred to
ticks. These three-host ticks become
as elementary bodies and represent the
infected during either the larval or nymphal
infective stage, tl1e larger orgaJ1isms as
stages and transmit the infection during one
reticulated bodies and the proliferative
of the subsequent stages (transstadial

.stage, and those in between as intermediate
transmission). The progeny of an infected
bodies.

female tick are most probably not infective

During the febrile stage, and for a short

(ie, there is no epidemiologically significant
while thereafter, the blood of infected
transovarial transmission). This and the
animals is infective to susceptible ai1in1als
fact that ticks are indiscriminate feeders
if subinoculated. Signs and lesions are
probably play a role in the low infeftion
associated witl1 functional iI\iwy to the
rate in tick populations.

vascular endothelium, resulting in increased

E 1-uminantium can be propagated
vascular pe1meability without recognizable
experimentally by se1ial passage, either by
histopathologic or even ultrastructural
inoculating infective blood into, or by
pathology. The concomitant fluid effusion
feeding infected nymphal or adult stages of
into tissues and body cavities precipitates
a vector tick on, susceptible animals. The
a fall in arterial pressure ai1d general
organism can also be propagated in tissue
circulatory failure. The lesions in peracute
culture, most reliably in endothelial cells,
and acute cases are hydrothorax, hydroperibut also in primaiy neutrophil cultures and cardiun1, edema and congestion of the lungs
macrophage cell lines. At room temperaand brain, splenomegaly, petechiae and ture, infective material loses its infectivity
ecchymoses on mucosal and serosal
within a few hours, but the organism,
swfaces, and occasionally hemorrhage into
together with suitable c1yoprotectants, may
the GI tract, particularly the abomaswn. The
be viably preseived in liquid nitrogen for
typically straw-colored effusions ai·e high in
years.

large-molecular-weight proteins, including

Immunity to heartwater appears to be
fibrinogen; hence, this fluid readily clots on
chiefly, if not exclusively, cell mediated,
exposure to air. The an1ount of effusion
because spleen cells from an immune donor
seen, particularly in body cavities, is not
inoculated into susceptible recipients
necessaiily proportionate to the concentraprotects, whereas serum from an immune tion of pai·asitic colonies detected in
donor fails to protect recipients when
endothelial cells.

HEARTWATER

753

Clinical Findings: The clinical signs are

Using immunoperoxidase staining
dramatic in the peracute and acute forms.

methods, a definitive diagnosis can be made

In peracute cases, animals may drop dead
on any formalin-fixed tissue samples, even
within a few hours of developing a fever,
from autolyzed carcasses. The contrasting

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sometimes without any apparent clinical
color makes the search for and identificasigns; others display an exaggerated tion of the rickettsial colonies much quicker,
respiratory distress and/or paroxysmal
although the substructure of the colonies
convulsions. In the acute form, animals
should be identified before the diagnosis
often show anorexia and depression along
is confffmed. Because of the natme of the
with congested and friable mucous
test, false-positive reactions may arise with
membranes. Respiratory distress slowly
some closely related organisms. On brain
develops along with nervous signs such
squash smears, Chlamydia pecorum can as a hyperaesthesia, a high-stepping stiff
be confused with E ruminantium, but
gait, exaggerated blinking, and chewing
histopathology or the immunoperoxidase
movements. Terminally, prostration
technique allow differentiation. Serodiagwith bouts of opisthotonus; "pedaling,"

nosis of animals previously exposed to

"thrashing," or stiffening of the limbs; and the disease, ie, recovered from subclinical
convulsions are seen. Diarrhea is seen
or clinical infection, still poses problems.

occasionally. In subacute cases, the signs

Several tests are in use, including several
are less marked and CNS involvement is
indirect fluorescent antibody and ELISA
inconsistent.

tests. All serologic tests, including an ELISA
that uses recombinant antigen, are plagued

Diagnosis: In clinical cases, heartwater
by cross-reactions with sera from anin1als
must be differentiated from a wide range
infected with one of several Ehrlichia or of infectious and noninfectious diseases,

Anaplasma organisms (false positive) and especially plant poisonings, that manifest
the fact that immw1e cattle on repeated
with CNS signs. In acute clinical cases in
exposme may become seronegative (false
endemic areas, clinical signs alone may
negative). DNA probes, available at research
suggest the etiology, but demonstration of institutions, can be used together with PCR
colonies of organisms in the cytoplasm of
technology. A combination of a pCS20 probe
capillary endothelial cells is necessary for and probes to 168 ribosomal RNA of several a definitive diagnosis. Traditionally, this is of the stocks are used routinely to exaniine done with "squash" smears of cerebral or
samples from aninlals when pemlits for
cerebellar gray matter stained with
movement of aninlals from endemic to

Romanowsky-type stains. Low concentranonendemic areas are required. Real-time tion Giemsa stain developed for 30 min

PCR has also come into use.

gives the best color differentiation and
batch-to-batch consistency. Organisms in
autolyzed material lose their stainability,

Treatment, Control, and Prevention:

and diagnosis then becomes difficult.

Oxytetracycline at 10 mg/kg/day, IM, or

For the "brain squash smear," a piece
doxycycline at 2 mg/kg/day will usually
of gray matter ( -3 x 3 mm) is macerated
effect a cme if administered early in the
between two microscope slides; the
course of heartwater infection. A higher
softened material is then spread like a
dosage of oxytetracycline (20 mg/kg) is
blood smear with the material pushed
usually required if treatment begins late
rather than pulled along. A slight lifting
dming the feb1ile reaction or when clinical
of the spreader slide about every 5 -10 mm
signs are evident. In such cases, the first
creates several thick ridges across the
treatment should preferably be given slowly
slide, from which capillaries are arranged

IV. A minimum of three daily doses should
straight and parallel in the thin sections
be given regardless of temperature; if fever
of the smear for easier examination. The
persists, oxytetracycline treatment should
endothelial cells of all the capillaries on a
continue for a fomth and fifth day. If the
smear should be carefully scrutinized for
fever still does not abate, a potentiated
presence of the dark purple colonies made
sulfona.nlide at 15 mg/kg/day, IM, has been
up of clusters of individual organisms
successful. The withdrawal tin1es for milk

(granules) of E ruminantium. The size and meat after treatment with doxycycline,
of the granules can vary between animals,
short- or long-acting oxytetracycline, and
or smears from the same animal, or even
sulfona.nlides must be observed based on
between colonies on the same smear,
local regulations.

but is usually uniform within a particular

Corticosteroids have been used
colony.

as supportive therapy (pred.nisolone

754

HEARTWATER

1 mg/kg, IM), although there is debate as to

16 [for the more resistantB indicus
the effectiveness and rationale for their use.

breeds], sheep and Angora goats on day

Diazepam may be required to control

11, and Boer and crossbreed goats on
convulsions.

clay 12). Yow1g calves ( <4 wk old), lambs,

Affected animals must be kept quiet in a
and kids ( < 1 wk old) have an innate

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cool area with soft bedding and be totally
age-related resistance to heartwater,
undisturbed; any stimulation can preempt
so if challenged by natural or induced
a convulsive episode and subsequent
infections within this time period, most
death.

recover spontaneously and develop a

Vaccination can help with the control
reasonable immunity.

of heartwater; however, it is neither easily

Control of tick infestation is a useful
administered nor monitored and gives varipreventive measure in some instances but able to no cross-protection to the vaiious
may be difficult and expensive to maintain

E ruminantium stocks. The "infection
in others. Excessive reduction of tick
ai1cl treatment method" for immunization
numbers, however, interferes with the
is in use in southern Africa, where infected
maintenance of adequate in1.rnunity
sheep blood containing fully virulent
through regulai· field challenge in endemic
organisms of the Ball 3 stock is used for
areas and may periodically result in heavy
infection, followed by monitoring of rectal
losses.

temperatw-e and antibiotic therapy after a

Chemoprophylaxis involves a series
fever develops. In certain circumstances,
of oxytetracycline ir\jections to protect
the "controlled" infection is followed by
susceptible anin1als from contracting
preventive "block treatment" without
heaitwater when introduced into endemic
temperature recording ( cattle on day
areas while also allowing them to develop

14 [susceptible B taui-us breeds] or day
a natural inununity.

H ISTOPH I LOSIS

Histophilosis, or Histophilus somni

H somni is considered a conunensal of
associated disease, is a common disease
bovine mucous membranes. Pathogenic
in North An1erical") cattle. It also has been
and nonpat110genic strains of H somni are
reported to occur sporadically in beef
found in the sheath and prepuce of males,
and dairy cattle worldwide. H somni
the vagina of females, and in the nasal
predominantly causes an acute, often
passages of both sexes. Nasal and
fatal, septicemic disease that cai1 involve
w-ogenital secretions ai·e believed to be
the respiratory, cardiovascular, musculosow·ces of the organism. The orgaitlsm may skeletal, or nervous systems, either
colonize the respiratm-y tract, presumably
singly or together in confined cattle. The
after inhalation, and gain access to the
reproductive system is often affected
bloodstreain vi.a that route. Colonization of
without clinical signs or other systemic
the male and female reproductive tracts
involvement; however, herd infertility
may involve venereal spread.

has been reported to occur more
frequently.

Epidemiology: Recently weaned calves
are at ltlgher risk of infection and death from

Etiology and Transmission: H somni
histophilosis than are previously weaned
is a gram-negative, nonmoWe, nonsporeolder calves, yearlings, or matw-e animals.

forming, nonencapsulated, pleomorphic

The risk of infection with H somni is highest coccobacillus that requires an enriched
early in tl1e feeding period, with "high-risk"

medium ai1d a microaerophilic atmosphere
calves in confinement establishing peak
for cultw-e. I -Iemolysis on blood agar
titers to H somni at -21-23 days after
occurs within 48 hr due to an exotoxin
anival. Although calves are generally
produced by most disease-causing isolates.

exposed to H somni earlier in the feeding

Pathogenic and nonpathogenic strains
period, the average time on feed for calves
have been differentiated. The virulence
that die of histophilosis has been reported to
of the orgaiusm may vai-y by region and
be 30-60 days. Sudden death due to peracute
age group.

septicemia usually occurs within 21 days

HISTOPHILOSIS

755
after anival, although it may occur
involved and may include rapid respirathroughout the feeding period. Reproductive tion, stiffness, muscle weakness, ataxia, disease manifestations, including granular
lan1eness, and severe behavioral changes.

vulvovaginitis, abortion, and mastitis, can

Animals affected with pleuritic histophilosis

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affect individual beef and dairy cattle or
are usually found dead without any
more of the herd.

treatment history; if alive, they may exhibit
extreme dyspnea Animals with myocarditis
display very poor exercise tolerance and

Pathogenesis: Septicemia is likely
required for most fom1s of histophilosis.

may collapse and die when movement to a
handling facility is attempted. Animals with

Strains of H somni that cause disease adhere the encephalitic fom1 and early depression to the endothelium of vessels, resulting in
rapidly proceed to recun1bency, with
contraction, exposure of collagen, platelet
occasional signs of hyperesthesia before
adhesion, and thrombus fom1ation. The
death. Anin1als fotmd dead and confim1ed
primary disease mechanism likely involves a
with H
ttu·ombus, rather than a thromboembolism
somni infection often have a history
of treatment for undifferentiated fever or
as once thought. Some bacterial strains may
depression in the previous
adhere to the endothelium in vessels of

14 days.

the pleura, myocardium, pericardiw11,

Closer individual examination usually
synovium, or a variety of other tissues ( eg,
reveals a febrile animal. Polypnea and/or
brain, larynx). Interruption of the blood
dyspnea may be evident overtly and are
supply in those areas results in the fonnation easily co11fimled by auscultation.

of an infarction with destruction of tissue

Hypoxemia associated with a malfunctionand the formation of a necrotic sequesing pulmonary or cardiovascular system trwn. The development of clinical signs is
can be easily confused with other clinical
associated with the extent of organ system
signs such as depression or even blindinvolvement. The susceptibility of individual ness. A sterile blood sample obtained from anin1als and variations in the preference
an untreated animal at this time tests
of strains of the organism for vessels in
positive for
different tissues may be important in the

H somni in a high percentage
of cases.

development of the different fom1S of the
disease, but these have not been extensively

Lesions: Feedlot cattle that die of
studied.

possible histophilosis should be exan1ined

The apparent preference of H somni for at necropsy. These animals may exhibit an
different organ systems has defined the
array of postm01tem findings, including
changing character of histophilosis. Initially,
fibrinous pleuritis without bronchopnetm10-
the disease presented primarily as an
nia, a focal myocardial lesion ( often in the
encephalitic syndrome that changed to one
papillary muscle of the left ventricle),
in which plewitic and myocardial foffilS
fibrinous pericarditis, bronchopneumonia,
predominated. Anecdotal observations
polyartluitis, and a fibrinous laryngitis. Less
suggest that the organism may be changing
conm10n gross postmortem lesions include
again ( eg, from a focal to a more generalized
polyserositis, fibrinous gonitis, and a
myocarditis ). Recent microbiologic
fibrinopurulent meningitis. Probably the
exanlinations of the organism have identified most common lesion seen in the feedyard a variety of mechanisn1S that contribute to its is that of "left heart failure" associated diverse virulence and ability to withstand
with a marked necrotic sequestnun in
treatment.

the myocardial wall.

Reproductive disease has not been

In animals that survive long enough
associated with systemic infection; the
to allow the pathology to progress, the
inflammation appears to be more local, even fibrinous portion of the lesions becomes though the pathogenesis in these situations
fibrotic, and the infarctions or sequestrae
is not well understood.

in the heart or larynx liquefy and wall off
to become an abscess. Lesions of the

Clinical Findings: Sudden death is
reproductive tract may include suppurative
usually the first indication of H somni
vaginitis, cervicitis, and endometritis.

infection in a group of confined anin1als and
is often mistaken by the stock attendants as

Diagnosis: A definitive diagnosis is based
evidence of a digestive tract upset such as
on sampling and examination of affected
bloat. A profound depression has been
tissues collected during a necropsy or
described as the most noticeable clinical
clinical exan1ination. A diagnosis at
sign of encephalitic histophilosis. Other
necropsy of "left heart failure" with a
findings are deteffilined by the system( s)

concomitant myocardial lesion or a

756

HISTOPHILOSIS
carcass in which the thoracic space is
with a sustained-action antinlicrobial or an
filled with fluid and fibrin with little
oral antimicrobial supplement in tile feed
pneumonia is considered definitive for hison arrival at tl1e feedlot or in the face of tophilosis. Historically, isolation of the
occurring cases to reduce histophilosis

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organism from CSF, brain, blood, urine,
mortality is scant. This contrasts with the
joint fluid, or other sterile, internal organs
evidence that H somni is susceptible in
or fluids has been used to confirm the
vitro to a wide range of antinlicrobials,
diagnosis. Because H somni is a commenincluding florfenicol, tilmicosin, tulathrosal of the mucous membranes of cattle, the mycin, tetracyclines, trimetlloprimbacterium should be isolated in predomisulfadoxine, fluoroquinolones, and nant or pure culture from the respiratory
ceftiofur. Historically, the precise
or urogenital tract to be considered a
mechanism by which tile organism is able
significant etiologic agent. This may be
to avoid systemic antimicrobial blood
difficult, because antimicrobial treatment
levels has not been well understood.

often interferes with recovery of the

Recently, it has been postulated that as
organism. The characteristic histologic

H somni proliferates, it forms biofilms lesion is suppurative with heavy infiltrathat allow it to adhere to the endothelium tions of neutrophils in all tissues where
and to withstand an otherwise adequate
localization of the bacteria occurs.

level of an antimicrobial.

Currently, the diagnosis is usually

Bacterins containing different strains
confirmed with molecular techniques
of the organism have been used to
such as inununohistochemical staining
immunize cattle againstH somni. A
of H&E-stained tissues or a fresh lesion
favorable humoral response generated by
swab subjected to a specific PCR test.

a single immunization with a commercial
vaccine has been shown to be improved

Treatment and Prevention: A major
when boosted with a second immunizahindrance to successful treatment of tion. Calves initially immunized before
individual histophilosis cases is the

"turn out" (estimated age to be 2 mo) difficulty in identifying affected anin1als
will respond to a second immunization
early in the course of disease because of its
anamnestically on their arrival at
often rapidly fatal nature. Antimicrobial
the feedlot after weaning. Although
treatment is most effective in tl1e early
protection with current bacterins and
stages of disease. Florfenicol (20 mg/kg, IM,
immunogens against histophilosis
repeated in 48 hr, or 40 mg/kg, SC, once)

morbidity and mortality has been
may be tile antimicrobial of choice if
reported, the ability of immunization to
histophilosis is tile tentative diagnosis
consistently spare cattle from the disease
in an individual aninlal.

is compromised when immunization and

Evidence supporting tile use of
challenge occur at the same time (ie,
prophylactic or metaphylactic treatment
arrival at the feedlot).

HEMORRHAGIC SEPTICEMIA

Hemorrhagic septicemia (HS) is an acute,
outbreaks occurring in southern Europe.

llighly fatal fom1 of pasteurellosis that

The only confirmed outbreaks of HS in the
affects mainly water buffalo, cattle, and

Americas occurred in bison in Yellowstone
bison. It is considered the most econonli

National Park, most recently from
cally important bacterial disease of water

1965-.1967. Natural disease occurs
buffalo and cattle in tropical areas of Asia,
infrequently in pigs, sheep, and goats and
particularly in soutlleast Asia, where water
has been reported in can1els, elephants,
buffalo populations are high. Disease is
horses, donkeys, yaks, and various species
most devastating to smallliolder fanners
of deer and other wild runlinants.

where husbandry and preventive practices
are poor and free-range management is

Etiology: Classical HS as defined by the
common. HS is also an important disease in

OIE is caused by Pasteurella multocida

Africa and the Middle East, witl1 sporadic
serotypes B:2 and E:2 (Carter and Heddle-

HEMORRHAGIC SEPTICEMIA

757
ston classification system). Serotype B:2
disease these signs may easily be overhas been identified in most areas where the looked. Acute disease can persist up to 3
disease is endemic, whereas serotype E:2
days, and less often 5 days, and is characterhas been found only in Africa. Septicemic ized by fever of 104°-l06°F (40°-41.l °C),

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pasteurellosis that is clinically similar to HS
apathy or restlessness and reluctance to
can be caused by a wide variety of other P
move, hypersalivation, lacrirnation, nasal
multocida serotypes and has been reported
discharge that begins as serous and
worldwide.

progresses to mucopurulent, subcutaneous
swelling in the pharyngeal region that
extends to the ventral neck and brisket

Transmission, Epidemiology, and

(and sometimes the forelegs), progressive

Pathogenesis: The tonsils of up to 5%
respiratory difficulty, cyanosis, terminal
of healthy water buffalo and cattle are
recumbency, and possibly abdominal pain
colonized by small numbers of P multocida
with diarrhea.

serotype B:2 or E:2, which can be
shed during periods of stress. Common

Lesions: The characteristic lesion of
stressors associated with outbreaks

HS is swelling of the subcutis and muscle
include high temperature and humidity,
of the submandibular region, neck, and
concurrent infection (blood parasites or
brisket by clear to blood-tinged edema
foot and mouth disease), poor nutrition, or
fluid. Serous to serofibrinous fluid may
work stress. Although outbreaks can occur
also be present in the thorax, pericardium,
at any time, disease is most prevalent
and abdominal cavity. There is typically
during the rainy season. Increased
widespread congestion with petechiae and
outbreaks associated with high rainfall are
ecchymoses in tissues and on serosal
most likely due to the multiple stressors
surfaces. Hemorrhages are often most
present during this time and the moist
prominent in the pharyngeal and cervical
conditions, which prolong the survival
lymph nodes. Pulmonary congestion
time of the organism in the environment.

and edema, sometimes with interstitial

Infection occurs by contact with infected
pneumonia, and gastroenteritis may occur
oral or nasal secretions from either healthy
in some cases.

carrier animals or animals with clinical
disease, or by ingestion of contan1inated
feed or water. Infection begins in the tonsil

Diagnosis: Clinical diagnosis of HS in
and adjacent nasopharyngeal tissues.

endemic areas is based on history, lapses in

Subsequently, bacterernia leads to
vaccination, environmental conditions, and
dissemination and rapid growth of bacteria
the characteristic clinical signs and lesions
in various locations, tissue iajury, a host
of disease. Although typical outbreaks of HS
cytokine response, and release of
are not difficult to recognize in endemic·

Jipopolysaccharides that results in a
regions, acute salrnonellosis, anthrax, and
rapidly progressing endotoxemia. Clinical
noninfectious toxicities should also be
signs can appear 1-3 days after infection,
considered. Sporadic cases are more
and death can occur within 8-24 hr after
difficult to diagnose clinically and could be
the first signs develop. ln endemic areas,
confused with blackleg, lightning strike, or

HS affects older calves and young adults,
snakebite. A definitive diagnosis of HS is
and morbidity and mortality are variable.

based on isolation of P multocida serotype
ln non endemic areas, epizootics can occur

B:2 or E:2 ( or other less common serotypes
with high morbidity and mortality that can
recognized by the OIE as causing HS) from
reach 100%. Water buffalo tend to be more
the blood and tissues of an animal with
susceptible and have more severe clinical
typical signs. Various other P multocida
disease than cattle. Recovery can stimulate serotypes can cause HS-like disease in acquired immunity to homologous and
cattle and water buffalo, which must be
often heterologous strains of P multocida,
differentiated from classical HS. The
and some of these animals become healthy
passive mouse protection test using specific
carriers that can provide a source of

B:2 and E:2 immune rabbit sera has been
infection for future outbreaks.

used in Asia ;rnd Africa to identify these
serotypes. More precise tests, such as
indirect hemagglutination, coagglutination,

Clinical Findings: Many cases of HS are
cotrnter irnmunoelectrophoresis, and
peracute and result in death within 8-24 hr.

in1munodiffusion tests have also been

These anin1als often have fever, hypersalivaused in some laborato1ies. More recently, tion, nasal discharge, and difficult respiramolecular techniques, including pulsed field tion, but because of the sho1t duration of
gel electrophoresis, southern blots, and

758

HEMORRHAGIC SEPTICEMIA

PCR-based protocols, have been used to
annually. Although it provides the best
differentiate between capsular and somatic
inunuruty, it is unpopular in the field
serotypes. The PCR techniques are most
because of its viscosity and difficulty
feasible for use in endem_ic areas and can be
of admirustration. Oil-based vaccines
used with vaiious samples, including blood,
combined with tween 80 or saponin have

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tissues, or bacteria from broth or plate
also been used in attempts to increase
cultures.

the ease of administration or inm1une
protection. The commonly used alun1-

Treatment and Prevention: Antimicroprecipitated and aluminum hydroxide bials are effective against HS if adminisgel vaccines have shorter durations of tered very early in the ilisease. However,
immunity, and twice yearly booster
because HS progresses rapidly, therapy is
vaccinations are recommended. It is
often unsuccessful. During outbreaks, any
important that the vaccines are made from
ammal with a fever should be treated with
the strains of P mullocida, circulating in the IV antim_icrobials as soon as possible to
regions of intended use to obtain maximal
qwckly obtain systemic bactericidal
effectiveness. Attenuated or modified-live
antimicrobial concentrations. Various
vaccines have been used with some
sulfonarrndes, tetracyclines, perucillin,
success. A live avirulent vaccine prepai·ed
gentainicin, kai1amycin, ceftiofur, enrofrom aPmultocida serotype B:3(4) of floxacin, tilm_icosin, and chlorainpherucol
fallow deer origin seems effective and is
have been used effectively to treat HS.

recommended for use by the Food and

However, plasmid-and chromosomal

Agricultural Organization of the Uruted
meiliated multidrug resistance seems to

Nations (FAO) in southeast Asia. Various
be increasing for some strains of P multo
modified-live and suburut vaccines made
cida, and resistance to tetracyclines and
from either purified or recombinant
perucillin has been reported for serotype
bacterial components have also been

B:2.

investigated experimentally.

Killed vaccines are most commonly
used for prevention and include bacterins,

Zoonotic Risk: The P multocida
alum-precipitated and aluminum hydroxide
serotypes that cause HS have not been
gel vaccines, and oil-acljuvant vaccines.

recovered from hw11an infections. However,
ln animals >3 yr old, an irutial two doses,
because many serotypes of P multocida

1-3 mo apart, is recommended, followed
have the potential to infect people,
by booster vaccinations once or twice
appropriate precautions should be taken
yeai·ly. The oil-acljuvant vaccine provides
when dealing with suspected cases of HS
protection for 9-12 mo and is given
or HS-like ilisease.

MALIGNANT CATARRHAL FEVER

(Malignant head catarrh, Snotsiekte, Catarrhal fever, Gangrenous coryza) Malignant catan-hal fever (M CF) is an
normally is seen sporailically and affects
infectious systemic ilisease that presents
single ammals. MCF is typically fatal;
as a variable complex of lesions affecting
however, there are outbreaks in which
mainly ruminants and rarely swine. It is
several ammals are affected, with evidence
principally a disease of domestic cattle,
of recovery and mild or inapparent
water buffalo, Bali cattle (banteng),
infections in some cases. It also occasion

Ame1ican bison, and deer. In adilition
ally presents as chrome alopecia and weight
to these farmed animals, MCF has been
loss. Its ilistribution is essentially worlddescribed in a variety of captive ruminants wide, mirroring that of the principal
in mixed zoologic collections. In some
carriers, domestic sheep and wildebeest.

species, such as bison and some deer, MCF

MCF has long been a major problem in
is acute and highly lethal, capable of
farmed deer operations, and in recent years
affecting large nun1bers of ammals. With
has emerged as a severe threat to the
occasional exceptions, the disease in cattle
conm1ercial bison industry.

MALIGNANT CATARRHAL FEVER

759

Etiology: MCF results from infection
infection than cattle. As agricultural
by one of several members of a group of
systems involving bison and deer producclosely related ruminant ganunaherpesvition have developed, MCF has become ruses of the Rhadinovints genus. Although
more troublesome. It is a leading cause of
the MCF group of ruminant rhadinoviruses
infectious disease losses on New Zealand

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currently comprises approximately 10
deer fanns. In bison exposed to large
lrnown members, only a few are lrnown to
numbers of adolescent sheep, losses can be
be pathogenic under natural conditions.

devastating. Approximately 800 head died

The principal caniers and their viruses are
in one outbreak in the USA in 2003. The
sheep (ovine herpesvirus-2), wildebeest
incubation period is variable and ranges

(alcelaphine herpesvirus-1), and goats
from 14 to >200 days from initial exposure.

( caprine herpesvirus-2). Another strain

Among animals that survive, infection
or unidentified origin has caused MCF in
is lifelong. Some susceptible species,
white-tailed deer. Virtually all clinical cases
including cattle and bison, may be latently
are caused by the sheep or wildebeest
infected. Recrudescence of latent infections
viruses.

is possible and must be considered for cases

The viruses are maintained within the
wiili no known history of contact witl1
sheep and wildebeest populations in sinlilar
carriers.

but not identical patterns. Lambs are infected

MCF is transmitted only between cartiers
usually at 3--6 mo of age by aerosol transmisand clinically susceptible animals. Affected sion from other individuals within the flock
animals do not transmit MCF to their
and begin to actively shed virus at -6-9 mo
cohorts.

of age. Shedding decreases at -10 mo, with
adults shedding at a much lower rate than

Clinical Findings: Acute MCF cases
adolescents. Wildebeest calves, in contrast,
caused by ovine herpesvirus-2 and
are infected in the perinatal period by
alcelaphine herpesvirus-1 are similar
horizontal and occasional intrauterine
clinically and pathologically. Disease course
transmission, and actively shed virus until
may range from peracute to chronic. Cases

4---6 mo of age. Transmission is by transfer of
in deer and bison are often peracute with
virus-laden nasal secretions by direct contact
sudden death. Deer that survive for a few
or poorly defined airborne routes. Transmisdays and bison usually develop hemorsion from sheep to cattle has been demonrhagic diarrhea, bloody urine, and corneal strated at distances of at least 70 m in cattle
opacity before expiring. High fever
and at distances of up to 5.1 km in bison. In

(106°-107°F [41 °-41.5°C]) and depression

Africa, most wildebeest-associated MCF is
are conm1on. Other possible signs include
seen around the time of wildebeest calving;
catarrhal inflanm1ation; erosions and
however, sheep-associated MCF (SA-MCF)

mucopurulent exudation affecting the
does not follow the san1e pattern. Ewes
upper respiratory, ocular, and oral mucosa; do not shed virus in placental tissues or
swollen lymph nodes; lameness; and CNS
secretions and do not experience more
signs (depression, trembling, hyporesponfrequent shedding episodes around lan1bing siveness, stupor, aggressiveness, convultime. The only rational and established sions). Historically, MCF has been
factors contributing to seasonality of SA-MCF desctibed as having several "foffi1S"-mild, are climatic influences on virus survival and
peracute, head and eye, intestinal, etc.

the age-related shedding patterns in Jambs.

There is little basis for this division and it

The epidemiology of the caprine MCF virus
is of little utility. Variation in organ system
appears sinlilar to that of sheep.

involvement sometimes can be seen in the

The severity of SA-MCF outbreaks
san1e outbreak and is at least partially
depends on factors such as the total numrelated to survival time after disease onset.

bers, population density, and species of

On average, the tin1e to death in European
susceptible hosts involved; the closeness
cattle breeds is somewhat longer ilian in
of contact; and the amount of shed virus
deer, bison, water buffalo, and Bali cattle.

available for transmission. Cases usually are In cattle, swollen lymph nodes and severe seen sporadically in European breeds of
eye lesions (panophthalrnitis, hypopyon,
cattle (Bos taurus ), because they are a
corneal opacity) are more frequent, and
relatively resistant species. By contrast, Bali hemorrhagic enteritis and cystitis less cattle, bison, and some but not all cervid
frequent, tl1an in deer and bison. Peripheral
species (eg, white-tailed deer, Pere David's

( centripetal) corneal opacity is an important
deer) are highly susceptible. Infectious
clinical sign suggestive of MCF in cattle.

dose of virus is a prin1ary deteffi1inant of

Skin lesions ( erythema, exudation,
infection and clinical disease, with bison
cracking, crust formation) are common
being > 1,000 times more susceptible to
in animals that do not succumb quickly.

760

MALIGNANT CATARRHAL FEVER

Hematologic changes are variable, and
infectious bovine rhinotracheitis, and
an inflan1matory leukogram may not be

East Coast fever (theileriosis). When
present, even in febrile aninmls with severe

CNS involvement is prominent, MCF
lesions. As many as 25% of cattle experience
can resemble rabies and the tickbome

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chronic disease, and sometin1es the disease
encephalitides. A history of contact witl1 a
waxes and wanes. Mortality rates in
carrier species (sheep, goats, or wildebeest)

clinically affected anin1als generally
can be helpful, although recrudescent cases
approach 95%. However, in limited
can be seen without such a history. Reliable
circumstances, survival in cattle can be
and specific laboratory assays for antibody
higher, although survivors can rarely return
and for viral DNA are available. The test of
to normal production.

choice for clinical diagnosis is PCR to detect

In a few outbreaks, the goat MCF virus
viral DNA. Preferred tissues for testing are

( capri.ne herpesvirus-2) induced disease in
anticoagulated blood, kidney, intestinal
white-tailed and Sika deer. These cases
wall, lymph node, and brain.

were subacute to chronic, with weight loss,

Serology is used to survey healthy
dem1al inflai1U11ation, and alopecia as the
ai1imals and is indicative only of infectionprimary signs. Whether this strain of virus latent infection a.I11ong susceptible aninlals
causes disease in species otl1er than deer is
may render serology alone inconclusive
not known.

evidence of cunent disease. Several

Lesions: The disease is systemic, and
seroassays ai·e available, including viral
lesions may be found in ai1y organ, although
neutralization, in1munoperoxidase,
severity and frequency varies greatly. The
immunofluorescence, and ELISA. The
p1incipal lesions are inflan1111ation ai1d
polyclonal assays are ha.I11pered by
necrosis of respiratory, alimentai-y, or
cross-reactivity. The monoclonal-based
urinary mucosa! epitl1elium; subepithelial
competitive ELISA is cun-ently the most
lymphoid infiltration; generalized lymphoid
specific and detects ai1tibody against all of
proliferation and necrosis; and widespread
tl1e known MCF group viruses. Only PCR
vasculitis. Mucosa! ulcerations and
can disc1iminate between the different
hemorrhage are common. Hemorrhages
viruses.

may be present in many pai·enchymatous
organs, paiticularly lymph nodes. A classic

Treatment and Control: The prognosis
but not pathognomonic histologic lesion is
is grave. No treatment has been found to
fibrinoid necrosis of small muscular
provide any consistent benefit. Stress
aiteries, but vessels of all types may be
reduction of subclinical or mildly affected
inflained, including those in the brain. Promanimals is indicated. No vaccine is currently inent white nodules representing intranmral available. Sheep can be produced tl1at are and perivascular proliferation may be
free of virus by early weaning and isolation.

apparent, particularly in the kidneys.

The only other effective control strategy is
sepai·ation of can-iers from susceptible

Diagnosis: Diagnosis of MCF i� based on
species. When large numbers of potent
clinical signs, gross and histologic lesions,
shedders ai·e present, such as in la.I11b
and laboratory confirmation. Primary
feedlots, distances > l kn1 may be necessary
differential diagnoses include bovine viral
to protect highly susceptible species such as
diarrhea/mucosa! disease, rinderpest,
bison.

NAIROBI SHEEP DISEASE

Nairobi sheep disease (NSD) is a tickbome
and Republic of Congo. Human infections
viral disease of sheep and goats chai·acterare rare; however, accidental infections ized by fever and hemorrhagic gastroenterihave been reported an10.ng laboratory tis, abortion, and high mortality. The disease workers, resulting in fever, joint aches, was first identified near Nairobi, Kenya,
and general malaise. The African field rat
in 1910, and NSD virus was shown to be

(A rvicathus abysinicus nubilans) is a
the causative agent in 1917. The disease
potential reservoir host. NSD is a reportable
is endemic in Kenya, Uganda, Tanzania,
disease in tl1e USA and is one of the OIE

Somalia, Ethiopia, Botswana, Mozan1bique,
listed diseases.

NAIROBI SHEEP DISEASE

761

Etiology and Transmission: NSD virus
hindquarters soiled with feces ( or a mixture
is classified in the genusNairovirus, family of blood and feces) and dehydration,

Bunyaviridae, and is possibly the most
especially in anin1als with prolonged
pathogenic virus known for sheep and
scouring. Also common are conjunctivitis

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goats. It is identical to or closely related
and dried crusts around the nostrils as a
to Ganjam virus, a tickbome infection of
result of nasal dischai·ge. Necropsy findings
sheep, goats, and people in India. Genetic
include enlarged and edematous lymph
and serologic data demonstrate that
nodes; mild splenomegaly; and hemor

Ganjarn virus is an Asian vaiiant of NSD
rhages in the GI (particularly the abomavirus. Both Ganja.in and NSD viruses are sun1), respiratory, and female genital tracts,
phylogenetically more closely related to
as well as in the gallbladder, spleen, and

Hazara virus than Dugbe virus. In addition,
heait. Petechial and ecchyrnotic hemorthe NSD virus is serologically related to rhages in the mucosa of the cecum and

Dugbe virus, another tickbome infection in
colon frequently appear as longitudinal
cattle, and to Crimean-Congo hemorrhagic
striations and are sometimes the only lesion
fever virus (seep 751). lt is transmitted
evident. Subserosal hemorrhages may be
transovaiially and transstadially by the
seen in the cecum, colon, gallbladder, and
brown ear tick, Rhipicephalus appendicu
kidneys. Conjunctivitis with d1ied crusts
latus, in which it cai1 survive up to 800 days.

around the nostrils is often noted. Common

The unfed adult ticks can transmit NSD
histopathologic lesions are hyperplasia of
virus for >2 yr after infection. Other
lymphoid tissues, myocai·dial degeneration,

Rhipicephalus spp and A mblyomma
nephrosis, and coagulative necrosis of the
variegatum ticks also may transmit the
gallbladder.

disease. The virus is shed in wine and feces,
but the disease is not spread by contact.

Clinical Findings: In natural outbreaks,

Diagnosis: The occurrence of a disease
disease usually occurs 5-6 days after
in sheep or goats with high mortality
susceptible animals move to areas infested
accompanied by a tick infestation is
with R appendiculatus. Clinical signs
suggestive, especially if it follows movebegin with a steep rise in body temperature ments into endemic areas or cha11ges in tick

(41 °-42°C [105.8°-107.6°F) that persists for populations that have been induced by 1-7 days. Leukopenia and viremia usually
heavy and prolonged rainfall. Confin11ation
coincide with the febrile phase. Diarrhea
of suggestive signs and lesions requires
usually appears 1-3 days after the onset of
detection of virus or viral antigen and
fever and worsens as infection progresses.

antibodies. The preferred specimens are

Illness is manifest by depression; anorexia;
plasma from febrile anin1als, mesenteric
mucopurulent, blood-stained, nasal
lymph nodes, spleen, a11d serum. Personal
discharge; occasional conjunctivitis;
protective equipment should be used when
and fetid dysentery that causes painful
conducting a necropsy and handling the
straining. Pregnant animals frequently
agent in the laboratory. Mouse inoculation
abort. In peracute and acute cases, the time a11d cell cultures can be used for primary between the appearance of disease and
isolation of virus. Sheep are the most
death is usually 2-7 days but may be as
sensitive a!lirnals for isolation, whereas a
long as 11 days in less acute cases.

baby hainster kidney cell line and lainb or

Experimental infection has shown that
han1ster kidney cell cultures are the most
indigenous Persian fat-tailed and European sensitive cells. Agai· gel inununodiffusion, breeds of sheep are equally susceptible;
complement fixation, and ELISA can be
however, mortality rate in the field is as
valuable for detection of antigen in the
high as 70%-90% for indigenous breeds of
infected tissues or tissue culture. New
sheep and 30% for exotic and cross-breeds.

probes have been developed targeting the

The clinical signs in goats are similar to

S and L segments of Dugbe virus a11d can
those in sheep but less severe, although
potentially be used as a rapid diagnostic

80%mortality has been reported. The
tool for NSD. Antibodies in infected or
presence of colostral immunity not only
recovered ailimals can be detected by
protects lambs and kids from early
inlrnunodiffusion, complement fixation,
exposure to infection but also allows
indirect fluorescent antibody tests,
development of active immunity, enabling
hemagglutination, and ELISA.

survival in tick-infested areas.

Differential diagnoses include peste des
petits run1inants (seep 766), Rift Valley

Lesions: The most striking features on
fever (seep 768), heartwater (seep 751),
external exai11ination of the carcass are the
and salmonellosis (seep 195).

762

NAIROBI SHEEP DISEASE

Treatment and Control: No specific
the range of the tick vector extends. Two
antiviral agent is available for treatment.

types of experin1ental vaccines have been

Unaffected animals in the flock may be
developed-a modified-live virus vaccine
treated with acaricides ( eg, pyrethroids in a
attenuated in mouse brain and an inacti

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grease, cypermethrin "pour-on" products,
vated oil adjuvant vaccine. A single dose of
various dip preparations). Longtem1 tick
the modified-live vaccine produces rapid
control is not cost-effective in endemic areas.

immunity; however, revaccination is

In endemic areas, clinical signs are not
necessary to maintain full protection.

seen unless susceptible animals are

Two doses of the inactivated vaccine are
introduced. Such animals should be
required to elicit good protection. Neither of
vaccinated, as should those exposed when
these vaccines is produced commercially.

PARATUBERCULOSIS

(Johne's disease)

Paratuberculosis is a chronic, contagious
expansion or replacement purchases; the
granulomatous enteritis characterized in
infection is introduced via subclinically
cattle by persistent diarrhea, progressive
infected carriers.

weight loss, debilitation, and eventually

Wection is acquired early in life-often
death. It is considered a listed disease by
soon after birth-but clinical signs rarely
the OIE, meaning it is a priority disease for
develop in cattle <2 yr old, because
international trade. The etiologic agent,
progression to clinical disease occurs

Mycobacterium para tuberculosis, also
slowly. Resistance to infection increases
known as Mycobacterium avium subsp
with age, and cattle exposed as adults are
para.tuberculosis, is believed capable of
much less likely to become infected.

infecting and causing disease in all other

Infection is acquired by ingestion of the
mminants (eg, sheep, goats, llamas, deer)

organism when nursing on contaminated
and in captive and free-ranging wildlife.

teats; consumption of milk, solid feed, or

The infection has also been recognized in
water contan1inated by the organism;
omnivores and carnivores such as wild
or licking and grooming behavior in a
rabbits, foxes, weasels, pigs, and nonhucontan1inated environment. In the later, man plimates. Distlibution is worldwide.

bacteremic stages of infection, intrauterine

National control programs include those
infections can be seen. After ingestion and
established in Australia, Norway, Iceland,
uptake in the Peyer's patches of the lower

Japan, The Netherlands, Denmark, Ontario,
small intestine, this intracellular pathogen

Canada, and the USA. The highest
infects macrophages in the GI tract and
published prevalence is in dairy cattle, with
associated lymph nodes. It is possible that

20%-8()0,6 of herds infected in many of the
some animals may elin1inate infection
major dairy-producing countries. Limited
through a cell-mediated in1mune response
information is available about the
that encourages microbiocidal activity in
prevalence in other species. The disease
macrophages, but the frequency with which
is of economic in1portance for the goat
this occurs is unknown. In most cases, the
industry in Spain and the sheep industry
organisms multiply and eventually provoke
in Australia.

a chronic granulomatous enteritis that
interferes with nutrient uptake and

Etiology and Pathogenesis:

processing, leading to the cachexia typical

M paratuberculosis is excreted in large
of advanced infections. This may take
numbers in feces of infected anin1als and in
months to years to develop and is usually
lower numbers in their colostrun1 and milk.

paralleled by a decline in cell-mediated

It is resistant to environmental factors and
immunity, a rise in serun1 antibody, and
can survive on pasture for > 1 yr; survival in
bacteremia with dissen1ination of the
water is longer than in soil. The infection is
infection beyond the GI tract. Fecal
usually acquired through the fecal-oral
shedding begins before clinical signs are
route; the dose needed to infect an animal is
apparent, and animals in this "silent" stage not known. Introduction of the disease into
of infection are in1portant sources of
a non.infected herd is usually through herd
transmission.

PARATUBERCULOSIS

763

Clinical Findings: Paratuberculosis in

Diagnosis: There are many commercattle is characterized by weight loss and cially available tests for paratuberculosis,
diarrhea in the late phases of infection, but
each with their own advantages, disadvaninfected animals can appear healthy for tages, and appropriate application. The

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months to years. In cattle, diarrhea may be
assays focus on detecting the organism in
constant or inte1mittent; in sheep, goats,
feces or tissue (culture, PCR), on finding
and other ruminants, diarrhea may not be
evidence of cellular immune response to
seen. It typically does not contain blood,
infection (skin testing, interferon--y), or on
mucus, or epithelial debris and is passed
detecting antibody to M para.tuberculosis
without tenesmus. Throughout weeks or
antigens (ELISA). Use of different tests
months, the diarrhea becomes more severe,
in combination can increase diagnostic
further weight loss occurs, coat color may
sensitivity. Given the biology of the
fade, and ventral and intermandibular
infection and the need to manage it on a
edema may develop due to a protein-losing
herd basis, diagnostic information should
enteropathy. This leads to low concentrabe gathered for a group of animals rather tions of total protein and albumin in plasma,
than for an individual case. An animal
although gamma globulin levels are normal.

showing signs of disease is more likely

In dairy cattle and goats, milk yield may
to provide diagnostic evidence of the
drop or fail to reach expected levels.

infection (shedding, antibody production)

Animals are alert, and temperature and
than an animal at the preclinical stage of
appetite are usually normal, although thirst
infection. Necropsy with culture and
may be increased. The disease is progreshistopathology on multiple tissues is the sive and ultimately terminates in emaciation gold standard for definitive diagnosis.

and death. In infected herds, the mortality

Ziehl-Neelsen stains of tissue samples for
rate may be low for a number of years, but
acid-fast bacteria usually reveal abundant
as many as 50% of animals may be infected
mycobacteria in lesions; however, in some
subclinically with associated production
cases, a careful search still may not reveal
losses. The disease in sheep and goats is
their presence. Acid-fast staining of an
similar, but diarrhea is not a conunon
impression smear made from the ileum of
feature, and advanced cases may shed wool
a cow with typical pathology is a quick,
easily. In cervids ( deer and elk), the course
low-cost (albeit insensitive) method to
of the disease may be more rapid.

arrive at a preliminary diagnosis. Biopsy
of full-thickness sections of ileum and

Lesions: A diverse array of pathology
regional lymph nodes for culture and
may be seen in infected animals, ranging
histopathology may provide a definitive
from a complete lack of gross lesions to a
diagnosis; however, this approach is
thickened and corrugated intestine with
usually restricted to particularly valuable
enlarged and edematous neighboring lymph
animals. M paratuberculosis has been
nodes. Often, there is no correlation
isolated from a wide variety of tissue
between clinical signs and the severity of
sites, but the mcscnteric and ileocecal
lesions. Carcasses may be emaciated, with
lymph nodes, ileum, and liver are most
loss of pe1icardial and perirenal fat in more
frequently recommended for diagnostic
advanced, cachectic cases. Intestinal
sampling.

lesions can be mild, but typically the distal

Serologic tests are rapid, low-cost
small-intestinal wall is diffusely thickened
methods for antemortem confirmation of
with a nonulcerated mucosa tiu·own into
a clinical diagnosis; sensitivity is >85% in
prominent transverse folds. Lesions may
clinically affected anin1als. They are also
extend proximally and distally to the
useful to detect infection in clinically
jejw1um and colon. Serosal lymphangitis
normal cattle in the later stages of infection
and enlargement of mesenteric and other
that are shedding large numbers of M
regional lymph nodes are usually apparent.

paratuberculosis; sensitivity is -45%. Of the Histologically, there is a diffuse granulomaserologic tests, those based on ELISA tous ente1itis characte1ized by the
technology offer the highest sensitivity and
progressive accumulation of epithelioid
specificity and are best used to determine
macrophages and giant cells in the mucosa
the infection prevalence in a herd.

and submucosa of the gut. Sparse to myriad

Quantitative use of ELISA to identify
acid-fast organisms may be seen within the
animals for selective culling or isolation in
macrophages. Often, there is no correlation
herds may be a cost-effective strategy for
between clinical signs and the severity of
disease control; higher
lesions. Sheep, goats, and deer sometimes

ELISA values are associated with higher
develop foci of caseation with calcification
probabilities of infection and higher rates of
in the intestinal wall and lymph nodes.

fecal shedding. Fecal culture is more

764

PARATUBERCULOSIS
sensitive and more specific than serology,

A routine testing progran1 for adults
but the organism grows very slowly (2--4
can help focus efforts in controlling the
mo) and the assay is more costly than
disease. Low-cost tests (eg, ELISA) have
serology. Pooling of fecal samples ( eg, five
the greatest cost benefit for commercial

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san1ples per pool) or culture of manure
dairy herds that are confirmed infected by
from farm sites where cattle commingle
culture or PCR. Animals testing positive,

( environmental sampling) can establish a
particularly heavy shedders or that have
herd's infection status at a lower cost,
strong-positive ELISA results, should be
despite some reduction in test sensitivity.

sent to slaughter as soon as economically

Proficiency at isolation of this pathogen
feasible. Retesting at least annually
varies significantly among laboratolies. Use
should be continued until herd tests
of a laboratory that has passed a proficiency
indicate a low ( <5%) infection prevalence.

test is recommended. Most strains infecting

Because intrauterine infection can occur,
sheep will not grow on solid media but may
more aggressive control programs include
be isolated using liquid culture media
culling of calves from dams that have or
systems. Genetic probes for an element
develop signs of the disease. Herd
specific for M paratuberculosis DNA, such
replacements should be obtained from
as 18900, can be used in conjunction with
herds believed to be free of the disease,
culture
and the replacements themselves should
or directly on fecal samples. Commercial
be tested before introduction to the

PCR kits are as sensitive and specific as
new herd. More general procedures to
fecal culture and much more rapid. Cost of
minimize fecal contamination on the
culture and PCR is comparable.

farm can also help, eg, elevating food

Tests of cell-mediated in1munity, such as
and water troughs, providing piped water
the intradennal Johnin test, lymphocyte
in preference to ponds, and harrowing
transformation test, and interferon-'(, are
frequently to disperse feces on pasture.

used more on a research basis and may be

Herd owners should be advised that
negative in advanced clinical cases. The
paratuberculosis control takes at least 5 yr.

genome of M paratuberculosis has been

The formulation of M paratuberculosis
desclibed and may provide the basis for
vaccines varies by manufacturer. In many
new diagnostic approaches.

countries, their use is subject to approval by

Tests that have fallen out of favor
regulatory agencies and may be restricted to
because of reports of low sensitivity and/or heavily infected herds. Vaccination of calves specificity are microscopic examination

<l mo old can reduce disease incidence but
ofZiehl-Neelsen-stained fecal san1ples
does not prevent shedding or new cases of
and the IV Johnin test. The complement
infection in the herd. Vaccination thus does
fixation (CF) test also reportedly is less
not eliminate the need for good manageaccurate than other serologic tests. The ment and sanitation. In the goat industry

CF test is still required by many countries
in Spain and Australia, vaccination has
for importation of animals, although many
increased productive herd life. Cattle
of the reagents used in the CF test are
inoculated with an inactivated whole-cell,
made to different specifications in
mineral-oil vaccine develop granulomas,
different countries, resulting in a lack
one to several inches in diameter, at the site
of standardization.

of inoculation (brisket) and may react
positively on subsequent tuberculin tests.

Control: No satisfactory treatment is

Accidental self-inoculation can result in
known. Control requires good sanitation
severe acute reactions wiili sloughing and
and management practices aimed at
chronic synovitis and tendinitis.

limiting the exposure of young animals
to the organism. Calves, kids, or lan1bs

Zoonotic Risk: There are conflicting
should be birthed in areas free of manure,
data on ilie involvement of the causative
removed from the dam immediately after
organism in Crohn disease, a chronic
birth in the case of dairy cattle, bottle-fed
granulomatous enteritis of unknown cause
colostrum that has been pasteurized or
in people. However, M paratuberculosis is
obtained from dams that test negative,
consistently detected by PCR in people with
and then reared segregated as much as

Crohn disease. This fact, coupled wiili its
possible from adults and their manure
broad host range, including nonhun1an
until > 1 yr old. Use of milk replacer is
p1imates, indicates that paratuberculosis
recommended instead of waste milk
should be considered a zoonotic risk until
unless the milk has been pasteurized.

the situation is claiified.

PASTEURELLOSIS OF SHEEP AND GOATS

765

PASTEURELLOSIS OF SHEEP AND GOATS

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Past,eureUa and Mannheimia organisms inclement weather, poor ventilation,
are (3 -hemolytic, gram-negative, aerobic,
handling, and transpottation, leaves sheep
nonmotile, nonsporeforrning coccobacilli in
and goats susceptible to respiratory viral
the family Pasteurellaceae. This family tends
infections. Parainfluenza 3, adenovirus type
to inhabit the mucosal surfaces of the GI,

6, respiratory syncytial virns, possibly
respiratory, and genital tract of mammals.

bovine adenovirus type 2, ovine adenovirus

Many are known as opportunistic secondary
types 1 and 5, and reovirus type 1 cause
invaders. Some species show preferences for
primary respiratory infections that are
specific surfaces and hosts. Updating of
rarely life threatening but predispose to
phylogenetic data has resulted in renaming
secondary M haemolytica infections.

based on gene sequence analysis. As a result,

Respiratory infections with Mycoplasma

P haemolytica biotypes A and T were
ovipneumoniae and Bordetella paraper
reclassified asM haemolytica (biotype A)

tussis have also been reported to be
and P trehalosi (biotype T). More recently,
associated with secondary M haemolytica

P trehaiosi has been reclassified as
infections. The combination of stressors

Bibersteinia trehalosi. Each isolate of M
and primary infections are thought to break
haemolytica andB trehalosi is designated
down the m ucosal barrier integrity of
witl1 a biotype and serotype. M haemolytica
the lower respiratory tract, allowing M

A2 is the most common strain isolated from
haemolytica to colonize, proliferate,
sheep and goat respiratory pasteurellosis,
and induce significant tissue damage.

although A6, Al3, and Ant have been reported

The vi.rnlence of M haemolytica and
in sheep and Ant in goats. M haemolytica A2

B trehalosi is mediated by the action of
is routinely reported from cases of mastitis in
several factors, including endotoxin,
sheep. B trelw.losi T3, T4, TIO, and Tl5 have leukotoxin, and capsular polysaccharide,
been most often associated with the systemic
that afford the bacteria advantages over
or septicemic form of pasteurellosis affecting
host immunity. The leukotoxin is particulambs. These serotypes have been regrouped larly in1portant in the pathogenesis, because
to B trehalosi biotype 2, and a new biotype 4
it is specifically toxic to ruminant leukohas been added. B trehalosi is often isolated cytes, resulting in fibrin deposition in lungs
from the lungs of sheep, goats, and cattle,
and on pleural surfaces. The lipopolysacbut pathogenicity is variable and may be charide endotoxin contributes to adverse
incidental. P multocida has also been
reactions in the lungs and also leads to
reported as a cause of pneumonic pastesystemic circulatoty failure and shock.

urellosis in sheep and goats and has been

The capsular polysaccharide prevents the
isolated in herd outbreaks of septic artl1ritis. phagocytosis of the bacteria and assists M haemolytica is the most commonly
in attachment to the alveolar epithelial
isolated bacteria in clinical cases, followed
surlace. Survival of the acute phase of
closely by B trehalosi, with P multocida pneumonic pasteurellosis depends on the
seen less frequently.

extent of lung involvement and damage in
the lower respiratory tract. Sheep and goats

Etiology and Pathogenesis: M haemo
that recover may have chronic respiratory
lytica and B trehalosi are distributed problems, including reduced lung capacity
worldwide, and diseases caused by them
and weight gain efficiency if <C20"A, of the are common in sheep and goats of all ages,
lung was damaged. In one review, there was
although the prevalence of serotypes may
no association between virulence and the
vary by region and flock. M haemolytica,
presence of hemolysis on blood agar culture

B lrehalosi, and P muUocida are common plates.

commensal organisms of the tonsils and
nasopharynx of healthy sheep and goats.

Clinical Findings and Lesions: B treha

The presence of multiple Pasteurella spp
losi mainly causes septicemia and systemic
may serve to keep the bacterial populations
pasteurellosis in sheep <2 mo old. The
in check, because there appears to be some
systemic fom1 of pasteurellosis caused
interference with growth when multiple
by B trehalosi is characterized by fever,
species are present. For these organisms to
listlessness, poor appetite, and sudden
cause infection, a combination of stressors,
death in young sheep. The organism is
including heat, overcrowding, exposure to
t110ught to move from the tonsils to the

766

PASTEURELLOSIS OF SHEEP AND GOATS
lungs and pass into the blood. This results in of fluoroquinolones is prohibited in the USA septicemia and localization of the infection

Treatment is frequently unrewarding unless
in one or more tissues such as the joints,
begun very early in the disease process
udder, meninges, or lungs. P multocida has
because of rapid progression of lung dan1age

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been reported to be isolated from polyand endotoxin release. Parenteral fluids and arthritis in young Jambs. M haemolytica
anti-inflan1matory agents are in1porta.nt
has been reported from cases of mastitis,
acljtmcts to antibiotic t11erapy. Altl10ugh
especially in sheep. All of these bacteria can
septicemic pasteurellosis has favorable
cause a severe fibrinonecrotic pneun10.nia in antimicrobial susceptibility, response to sheep and goats. The disease is charactertherapy is often disappointing. Administering ized by acute onset of illness, very high
prophylactic antibiotics to at-risk lambs may
fevers, dyspnea, anorexia, and often death.

be beneficial.

Diagnosis: The differentiation of

Prevention: Pasteurellosis prevention
pasteurellosis from other causes of
would be desirable given the economic costs
respiratory disease is based on the high
of treatinent, losses, and reduction of weight
mmtality and rapid progression to death.

gains in survivors. Commercial vaccines are

Diagnosis of pneumonic and septicemic
available for cattle but unfortw1ately are
forms of pasteurellosis is based on .necropsy
specific for M haemolytica Al, and tl1ere examination, gross and histopathologic
is little or no cross-protection against
findings, and isolation of organisms from a

M haemolyticaA2 expe1irnentally.

range of tissues. Lesions include subcutane

Commercial vaccines for M lwemolytica
ous hemoIThage; epithelial necrosis of the

A2 are available in the UK and have been
tongue, pharynx, esophagus, or occasionally
reported to be beneficial in reducing death
the abomasum and intestine; enlargement
losses and decreased weight gains from
of tonsils and retrophary.ngeal lymph
both septicemic and pneumo.nic fonns of
nodes; and peracute, multifocal, embolic,
pasteurellosis. An intranasal recombinant
necrotizing lesions in the Jung and liver.

vaccine has protected lambs challenged

There is better coITelation with PCR analysis withPmultocida,, but tllis vaccine is not of lung tissue than with microbial culture in
commercially available. There are no
identifying the presence of M haemolytica, commercial vaccines in the USA, but

B trehalosi, andPmulticoda.

producers can get autogenous bacteri.ns for
their flocks; however, evidence that these

Treatment: Early identification of
are efficacious is anecdotal. Prevention of
respiratory disease and introduction of
respiratory viruses by using a vaccination
effective antibiotic therapy is necessary.

prog:ran1 would be expected to decrease

Death losses are high in severely affected
respiratory pasteurellosis by preventing
animals. Antimicrobial susceptibility patterns
the initial insult that allows colonization.

of M haemolytica, B trehalosi, and Pmulti

Inclusion of prophylactic antibiotics, mainly
coda have shown resistance to penicillins
tetracycline, in the feed during tl1e rnontllS

( all three organisms), sulfadirnetJ\oxine (P
of the year with the highest incidence is a
multocida ), and tetracyclines (B trehalosi).

common management practice. Avoidance

Ampicill.i.n, ceftiofur, danofloxacin, enrofloxaor reduction of known stressors such as cin, florfe.nicol, tiirnethoprirn-sulfan1ethoxaheat, overcrowding, exposure to inclement zole, and tulathromycin would be expected to weather, poor ventilation, handling, and have good efficacy, although extra-label use
transportation should also be considered.

PESTE DES PETITS RUMINANTS

Peste des petits ruminants (PPR) is an

Africa. Goats and sheep appear to be
acute or subacute viral disease of goats
equally susceptible to the virus, but goats
and sheep characterized by fever, necrotic
exhibit more severe clinical disease. The
stomatitis, gastroenteritis, pneumonia,
virus also affects several wild small
and sometimes death. It was first reported
run1inant species. Cattle, buffalo, and pigs
in Cote d'Ivoire (the Ivory Coast) in 1942
are only subclinically infected. People are
and subsequently in other parts of West
not at risk.

Pf:STE DES PETITS RUMINANTS

767

Etiology and Epidemiology: The
and pigs can become naturally or expericausal virus, a member of the Morbillivirus mentally infected with PPR virus, but these
genus in the family Paramyxoviridae,
species are dead-end hosts, because they do
preferentially replicates in lymphoid tissues
not exhibit any clinical disease and do not
and epithelial tissue of the GI and respiratransmit the virus to other in-contact VetBooks.ir
tory tracts, where it produces characteristic
anin1als of any species.

lesions.

PPR has been reported in virtually all
parts of the African continent, except for

Clinical Findings: The acute form of PPR
the southern tip; the Middle East; and the
is accompanied by a sudden rise in body
entire Indian subcontinent. In the last 15 yr,
temperature to 40° -4 l.3°C ( 104 ° -l06°F).

PPR has rapidly expanded within Africa and Affected anin1als appear ill and restless and to large parts of Central Asia, SouU1 Asia,
have a dull coat, dry muzzle, congested
and East Asia (including China).

mucous membranes, and depressed

Because PPR virus and the now-eradiappetite. Early, the nasal discharge is cated rinderpest virus (seep 771) are crossserous; later, it becomes mucopurulent protective, it is possible that the recent
and gives a putrid odor to the breath. The
rapid expansion of the PPR virus within
incubation period is usually 4-5 days. Small
endemic zones and into new regions may
areas of necrosis may be observed on the
be because of disappearance of the crossmucous membrane on the floor of the nasal protection previously afforded by natural
cavity. The conjunctivae are frequently
rindcrpest infection of small ruminants and/ congested, and the medial can thus may or the hitherto use of rinderpest vaccine to
exhibit a small degree of crusting. Some
prevent small ruminant infection with PPR
affected anin1als develop a profuse
virus in certain endemic areas. Based on
catarrhal conjunctivitis with matting of the
this theory, PPR virus has the potential to
eyelids. Necrotic stomatitis affects the
cause severe epidemics, or even pandemics,
lower lip and gum and the gmTiline of the
in more small ruminant populations in an
incisor teeth; in more severe cases, it may
increasingly expanding area of the
involve the dental pad, palate, cheeks and
developing world.

their papillae, and the tongue. Diarrhea may

At a local level, such epidemics may elimibe profuse and accompanied by dehydranate the entire goat or sheep population of tion and emaciation; hypothermia and deatl1
an affected village. Between epidemics,
follow, usually after 5-10 days. Broncho

PPR can assume an endemic profile.

pneumonia, characterized by coughing,

Mortality and morbidity rates vary within
may develop at late stages of tl1e disease.

an infected country, presumably due to

Pregnant anin1als may abort. Morbidity and
two factors: the varying inmrnne status of
mo1tality rates are higher in young anin1als
the affected populations and varying levels
than in adults.

of viral virulence.

Lesions: Emaciation, conjunctivitis, and
stomatitis are seen; necrotic lesions are

Transmission: Transmission is by close
observed inside the lower lip and on
contact, and confinement seems to favor
the adjacent gum, the cheeks near the
outbreaks. Secretions and excretions of
commissures, and on the ventral surface of
sick animals are the sources of infection.

the tongue. In severe cases, the lesions may

Transmission can occur during the incuextend to the hard palate and pharynx. The bation period. It is generally accepted that erosions are shallow, with a red, raw base there is no carrier state. The common
and later become pinkish white; they
husbandry system whereby goats roam
are bounded by healthy epitheliun1 that
freely in urban areas contributes to spread provides a sharply demarcated margin. The and maintenance of the virus. There are
rumen, reticulun1, and omasum are rarely
also numerous instances of livestock
involved. The abomasum exhibits regularly
dealers being associated with the spread
outlined erosions that have red, raw floors
of infection, especially during religious
and ooze blood.

festivals when the high demand for

Severe lesions are less common in
animals increases the trade in infected
the small intestines than in the mouth,
stock.

abomasum, or large intestines. Streaks of

Several species of gazelle, oryx, and
hemorrhages, and less frequently erosions,
white-tailed deer are fully susceptible; these
may be present in the first portion of the
and other wild small ruminants may play a
duodenum and tem1inal ileum. Peyer's
role in the epidemiology of the disease, but
patches are severely affected; entire
few epidemiologic data are available for
patches of lymphoid tissue may be

PPR in wild small ruminants. Cattle, buffalo, sloughed. The large intestine is usually

768

PESTE DES PETITS RUMINANTS
more severely affected, with lesions
detection, and serum (from unclotted
developing around the ileocecal valve and at blood) for antibody detection, The virus the cecocolic junction and rectum. The
neutralization test may also be used to
latter exhibits streaks of congestion along
confinn an infection if paired serum

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the folds of the mucosa, resulting in the
samples from a surviving animal yield rising
characteristic "zebra-striped" appearance.

titers of <!4-fold. PPR must be differentiated

Petechiae may appear in the turbinates,
from other GI infections ( eg, GI parasites),
larynx, and trachea. Patches of bronchorespiratory infections ( eg, contagious pneumonia may be present.

cap1ine pleuropneumonia), and such other
diseases as contagious ecthyma, heartwa

Diagnosis: A presumptive diagnosis is
ter, coccidiosis, and mineral poisoning.

based on clinical, pathologic, and epidemiologic findings and may be confinned by viral Control: Local and federal authorities
isolation and identification. Historically,
should be notified when PPR is suspected.

simple techniques such as agar-gel

PPR is also an OIE-reportable disease
immunodiffusion have been used in
worldwide. Eradication is recommended
developing countries for confirmation and
when the disease appears in previously
reporting purposes. However, PPR virus

PPR-free countries. There is no specific
cross-reacts with rinderpest virus in tl1ese
treatment, but treatment for bacte1ial and
tests. Virus isolation is a definitive test but is parasitic complications decreases mortality labor intensive, cumbersome, and takes a
in affected flocks or herds. An attenuated
long time to complete. Currently, antigen

PPR vaccine prepared in Vero cell culture
capture ELISA and reverse transcriptionis available and affords protection from PCR are the preferred laboratory tests for
natural disease for > l yr. Encouraged by
confinnation of tl1e virus. For antibody
the successful global eradication of
detection (such as might be needed for
rinderpest, international organizations
epidemiologic surveillance, confirmation of
such as OIE, Food and Agriculture
vaccine efficacy, or confinnation of absence Organization of tl1e United Nations (FAO), of the disease in a population), competitive
and International Atomic Energy Agency

ELISA and virus neutralization are the

(IAEA) are making plans (2015) for global

OIE-recommended tests. The specimens
eradication of PPR. The available homolorequired are lymph nodes, tonsils, spleen, gous PPR vaccine would play an important
and whole lung for antigen or nucleic acid
role in that effort.

RIFT. VALLEY FEVER

Rift Valley fever (RVF) is a peracute or
three-segmented, single-stranded,
acute, mosquito-borne, zoonotic disease
negative-sense RNA genome with a total
of domestic and wild ruminants in Africa,
lengili of-11.9 kb. Each of tl1e segments,

Madagascar, and tl1e Arabian Peninsula.

L (large: 6.4 kb), M (medium: 3.9 kb), and

Large outbreaks of clinical disease are

S (small: 1.7 kb), is contained in a separate
usually associated witl1 heavy rainfall and
nucleocapsid witl1in tl1e vilion. Remarkably
localized flooding. During epidemics, the
little genetic diversity has been found
occurrence of abo1tions in livestock and
between RVF virus isolates from many
deaths among young animals, particularly
countries, and no significant antigenic
lambs, togeilier with an influenza-like
differences have been demonstrated, but
disease in people, is characteristic.

differences in pailiogenicity are seen. The

However, infections are frequently
disease is endemic in many tropical and
subclinical or mild.

subtropical regions of Afiica, Madagascar,
and tl1e Arabian Peninsula. Thought to have

Etiology and Epidemiology: RVF virus
been miginally confined to Lhe Rill Valley
belongs to tl1e genus Phlebovirus and is a
region of eastern and southern Africa, ilie
typical Bunyavirus. An enveloped spherical
virus has recently expanded its range, wiili
particle of80-100 nm in dian1eter, it has a
major outbreaks having occurred in Egypt

RIFT VALLEY FEVER

769
since 1977, West Africa since 1987,

Jambs is high (90%-100%), and animals

Madagascar since 1990, and the Arabian
usually die within 2-3 days. Adult sheep

Peninsula in 2000. Particularly large
are less susceptible, with lOo/o-30%
epidemics with large numbers of human
mortality; the incubation period is
cases occurred in Egypt in 1977-1978 and in

24-72 hr, and animals show a generalized

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Kenya in 2006-2007. It is considered a threat
febrile response, lethargy, hematemesis,
to regions further afield, where competent
hematochezia, and nasal discharge,
mosquito vectors are present. Sporadic,
although infection may also be inapparent.

large epidemics have occurred at 5-10 yr

Calves are less susceptible than lan1bs, but
intervals in d1ier areas of eastern Africa,
mortality may still be as high as 70%;
and Jess frequently in southern Africa.

clinical signs are similar to those in sheep,

Outbreaks are usually associated with
but icterus is more common. Disease in
periods of abnormally heavy rainfall or, in
adult cattle is often inapparcnt, but they
some cases, with localized flooding due to
may show anorexia, Jacrimation,
dam building or flood irrigation. Dwing
salivation, nasal discharge, dysgalactia,
interepidemic periods, the virus may remain and a bloody or fetid diarrhea, with a dormant in eggs of floodwater-breeding
mortality of 5o/o-10%. Sometimes, abortion
aedine mosquitoes in the dry soil of small,
may be the only sign of infection; the
ephemeral wetlands (dambos or pans). In
aborted fetus is usually autolyzed. In
some areas, this transovarial transmission
pregnant ewes, abortion rates vary from
is believed to be the most important inter5% to almost 1000,.{, in different outbreaks epidemic survival strategy of the vims;
and on different farms; abortion rates in
however, inapparent cycling of the vims
cattle are usually <10%. Vaccination of
between vectors and wild or domestic
ewes with live Smithburn strain vaccine
mammalian hosts has been shown to occur
may result in early embryonic death,
in many areas. RVF virus may also spread by congenital CNS anomalies and arthromovement of viremic animals and possibly gryposis, or abortion or stillbirth. Clinical
by wind-borne mosquitoes. When emergence signs and abmtions have also been of infected mosquitoes, or introduction of
reported in goats, and occasionally in
vims to an area, coincides with abnormally
camels, water buffalo, and some wild
wet conditions and the presence of a
ungulate species. In people, RVF is usually
highly susceptible host population, a large
inapparent or associated with a selfepidemic may ensue when the vims is limiting febrile illness characterized by
amplified in ruminants and spread locally by abrupt onset of malaise, myalgia, and many species of mosquitoes or mechaniarthralgia. A minority ( lo/o-2%) may cally by otl1er insects. The incidence of RVF
develop severe disease with ocular lesions,
peaks during the late rainy season. In areas
encephalitis, or severe hepatic lesions with
witl1 cold winters, both the disease and
hemorrhages; in such cases, the fatality
vectors may disappear after the first frost.

rate may be lOo/o-20%.

In warmer climates where insect vectors
are present continuously, seasonality is

Lesions: The hepatic lesions are sin'li.lar
not seen.

in all species and vary mainly with the age

People are readily infected through blood
of the affected individual. The most severe
aerosols from infected animals during
lesions, seen in aborted fetuses and
slaughter, or by exposure to infected animal
newborn Jambs, are moderately to greatly
tissues, abo1ted fetuses, mosquito bites,
enlarged, soft, friable livers with irregular
and laboratory procedures. Therefore,
congested patches. Numerous grayish white
veterinarians, farm laborers, and abattoir
necrotic foci are invariably present but may
workers are particularly at risk. People can
not be clearly visible. Hemorrhage and
also act as an1plifying hosts and introduce
edema of the wall of the gallbladder and
the disease (via mosquitoes) to animals in
mucosa of the abomasum are common.

wunfected areas.

Intestinal contents are dark chocolatebrown. In all animals, the spleen and peripheral lymph nodes are enlarged and

Clinical Findings: Clinical signs of
edematous and may show petechiae.

RVF tend to be nonspecific, rendering it

Histopathologically, the liver lesions are
difficult to recognize individual cases. The
severe and extensive, with hepatic necrosis
incubation period is 12-36 hr in lambs, and
being the most striking microscopic lesion
a biphasic fever of up to 108°F ( 42°C) may
of RVF in all domestic animals and people.

develop. Affected animals are listless and
reluctant to move or feed and may show

Diagnosis: RVF should be suspected
signs of abdominal pain. Mmtality in young when abnormally heavy rains and flooding

770

RIFT VALLEY FEVER
are followed by widespread occurrence of
virus can readily be produced in large
abortions and mortality among newborn
quantities, is inexpensive, and induces a
animals characterized by necrotic
durable immunity 6-7 days after inoculahepatitis, concurrent with influenza-like tion. It should normally not be used for
disease in people handling animals or their
protection of pregnant animals, because

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products.

it may cause abortion, congenital defects,

The necropsy of infected animals poses
and hydrops amnii in the ewe; however,
considerable risk to the operator and
its use may be contemplated during an
should be performed only by trained
outbreak when possible adverse effects
personnel, using appropriate personal
may be outweighed by the dangers of
protective equipment. The virus can
natural infection. Although not proved, it
readily be isolated from tissues of aborted
is theoretically possible for the attenuated
fetuses and the blood of infected animals.

virus to revert to virulence. A small-plaque

The viral titer in these tissues is often high
variant and a mutagen-induced strain have
enough to use organ suspensions as
been investigated as potential vaccine
antigen for a rapid diagnosis in neutralizacandidates but have not been accepted as tion, complement fixation, ELISA, agar gel
replacements for the Smithburn strain.

diffusion tests, or staining of organ

More recently, a naturally attenuated
impression smears; however, these tests
avirulent isolate of Rift Valley fever, clone
should be supplemented by isolation in

13, has been used in a commercially
suckling mice or hamsters injected
available vaccine. It is not advisable to use
intracerebrally or in cell cultures such as
live attenuated vaccines in nonendemic
baby han1ster kidney (BHK21), monkey
countries. Possible future recombinant
kidney (Vero), chicken embryo-related

DNA vaccines and viral strains with

(CER) and mosquito cells, or primary
deletions of the major virulence genes
kidney and testis cell cultures of lambs.

should offer a better alternative. Control

Detection of viral nucleic acid by PCR is
of vectors, movement of stock to highpossible, and reverse transcriptase-PCR
lying areas, and confinement of stock in
tests have been described. Virus can be
insect-proof stables are usually impractidemonstrated in organ sections using cal, instituted too late, and of little value.

immunohistochemical stains.

Much work has gone into attempts to

All conventional serologic tests can be
predict RVF outbreaks using meteorologic
used to detect antibody against RVF virus
and remote-sensing data to identify highand are helpful in epidemiologic studies. In risk areas and time periods; this has been
some areas, however, serologic surveys may somewhat successful in predicting be complicated by cross-reactivity between
outbreaks in eastern Africa but less so in

RVF virus and other phleboviruses; virus
southern Africa. However, outbreaks
neutralization tests are the most specific in
cannot yet reliably be predicted and
this situation. An IgM ELISA can demonare usually of sudden onset. Therefore, strate recent infection using a single serum
routinely immunizing lambs at 6 mo of age,
sample.

which should afford lifelong protection, is

Wesselsbron disease (seep 775) and
advisable. The offspring of susceptible e
other insect-borne viral diseases tend to
wes can be immunized at any age. Pregnant
occur under the same climactic conditions.

ewes and cattle can be vaccinated with a

RVF mortality associated with hepatic
formalin-inactivated vaccine, which elicits
lesions should be distinguished from
a better immunity in cattle and· is safe in
hepatotoxic plant and algal intoxications;
pregnancy. Revaccination after 3 mo is
bacterial septicemias such as pasteurellosis, advisable to induce an inlmunity that will salmonellosis, and anthrax; and other viral
last> 1 yr and to confer colostral inlmunity
infections such as Nairobi sheep disease
to the offspring.

and peste des petits ruminants. When
abortion is the only finding, other important

Zoonotic Risk: Because RVF virus can
diseases such as brucellosis, leptospirosis,
cause a severe and potentially fatal disease
chlamydiosis, campylobacteriosis, Coxiella
in people, those involved in the livestock
burnetii infection, and salmonellosis
industry should be made aware of the
should be elim.i.nated.

potential dangers of exposure to RVFinfected aninlals and tissues. Appropriate Control and Prevention: Immunizaprotective measures should be taken when tion remains the only effective way to
investigating cases of abortion, handling
protect livestock from RVF. The mouse
potentially infected animals, and collecting
neuro-adapted Smith burn strain of RVF
diagnostic samples.

RINDERPEST

771

RINDERPEST

(Cattle plague)

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Historically, ri.nderpest virus was a scourge
rus, closely related to the viruses causing that wrought economic havoc throughout
peste des petits ruminants, canine

Africa, Asia, and Europe. The need to combat distemper (seep 777), and measles. Strains rinderpest provided the impetus for the
of varying virulence for cattle occwTed and
establislunent of the first modem veterinary
could be differentiated genetically.

school in Lyon (France) in 1762. After several However, a single serotype of the virus decades of success in eradicating rinderpest
existed, and a vaccine prepared from any
from Europe, the disease recuffed unexpectstrain could protect against all strains.

edly in Belgium in 1920, and renewed efforts

Rinderpest virus is shed in nasal and
to eradicate it resulted in the creation of the
ocular secretions and can be transmitted

World Organization for Animal Health (OIE)

during the incubation period (1-2 days
in 1924. Shortly after the creation of the Food
before onset of fever). Transmission
and Agriculture Organization (FAO) of the
required direct or close indirect contact

United Nations in 1946, the OIE and FAO
between susceptible aninlals and sick
signed a cooperation agreement in 1952.

animals shedding the virus. The role of

Since then, the two organizations (FAQ and
fomites in transmission was negligible,

OIE) have been major participants in several
because the virus is fragile, being inactiglobal can1paigns to combat rinderpest, vated witltln 12 hr of exposure to atmoswhich cuhninated in global eradication of pheric heat and light. There was no carrier
the disease in 2011. In fact, the last reported
state, and recovered animals acquired

1inderpest outbreak occurred in Kenya in
lifelong immunity. In endemic areas, young

2001, but a 10-yr active surveillance period
cattle became infected after maternal
was necessary before global eradication
in1munity disappeared and before vaccinal
could be declared. Rinderpest is only tl1e
immunity began, with possible auxiliary
second viral disease, after smallpox, to have
cycles in wild ungulates.

been successfully eradicated worldwide.

The successful eradication of ri.nderpest
shows that smallpox eradication in 1980 was Clinical Findings: After an incubation not an unrepeatable feat and should provide
period of 3--15 days, fever, anorexia,
a certain degree of confidence to the internadepression, and oculonasal discharges tional community that concerted, sciencedeveloped, followed by necrotic lesions on based efforts can result in future successes.

the gums, buccal mucosa, and tongue. The

Rinderpest virus is biologically similar to
hard and soft palates were often affected.

the virus of peste des petits mmi.nants ( see

The oculonasal discharge became mucop 766), which has been targeted by the OIE
purulent, and the muzzle appeared dry and
and FAQ as the next aninlal disease for
cracked. DiaiThea, the final clinical sign,
global eradication.

could be watery and bloody. Convalescence

Rinderpest was a disease of clovenwas prolonged and could be complicated by hoofed aninlals characterized by fever,
concurrent infections due to inununosupnecrotic stomatitis, gastroenteritis, pression. Morbidity was often lQ()OA, and
lymphoid necrosis, and high mortality. In
mortality was up to 9()0A, in epidemic areas,
epidemic form, it was the most lethal plague
but in endemic ai·eas morbidity was low and

!mown in cattle. All wild and domesticated
clinical signs were often nilld.

species of the order Artiodactyla were

Lesions: Gross pathologic lesions
variably susceptible to ri.nderpest, although
occtUTed throughout the GI and upper
dissemination of the virus largely depended
respirato1y tracts, either as areas of
on continual transmission among domestinecrosis and erosion, or congestion and cated cattle, domesticated buffalo, and yaks.

hemorrhage, the latter creating classic

The virus also infected goats and sheep,

"zebra-striping" in the rectwn. Lymph nodes leading to wider-diagnosis of the clinically
could be enlarged and edematous, with
similar peste des petits runlinants in regions
white necrotic foci in the Peyer's patches.

where the two diseases coexisted.

Histologic lesions included lymphoid and
epithelial necrosis with viral-induced

Etiology, Epidemiology, and Trans
syncytia, and intracytoplasntlc and
mission: Rinderpest virus is aMorbillivi-intranuclear inclusions were often seen.

772

RINDERPEST

Diagnosis: Clinical and pathologic
period between occurrence of the last
findings were sufficient for diagnosis in
outbreak and the official declaration of
endemic areas and after initial laboratory
eradication, active rinderpest smveillance
confirmation of an outbreak. In areas
in recent endemic areas included the

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where rinderpest was uncommon or
testing of all susceptible cloven-hoofed
absent, laboratmy tests had to be used to
animals presenting with erosive stomatitis.

differentiate it from bovine viral diarrhea
in particular, as well as East Coast fever,

Control: Active immunity was Lifelong,
foot-and-mouth disease, infectious bovine
whereas maternal immunity lasted 6-11 mo.

rhinotracheitis, and malignant catarrhal

Control in endemic areas was by in1munizafever. Viral isolation and detection of tion of all cattle and domestic buffalo> 1 YT
specific viral antigens in affected tissues
old with an attenuated cell culture vaccine.

using an immunocliffusion test was the
ln these areas, outbreaks were controlled
standard, but simpler, more rapid and more
by quarantine and "ring vaccination" and
discriminating tests, such as immune
sometimes by slaughtering. ln epidemics,
capture ELISA and reverse transcriptionthe disease was best eliminated by imposing PCR (RT-PCR), were favored toward the
quarantine and by slaughte1ing affected
end of the eradication can1paign. The
and exposed animals. Control of anin1al

RT-PCR technique allowed phylogenetic
movements was paramount to control
characterization of the virus and helped
rinderpest; many outbreaks were clue to the
trace the migin of strains in new outbreaks.

introduction of infected cattle to hitherto

A simple lateral flow penside test for field
uninfected herds. The lessons learned from
use also proved useful in the final stages
this huge success will be instrun1ental in the
of the eradication campaign. In the 10-yr
fight against peste des petits rnminants.

TICKBORNE FEVER

(Pasture fever)

Tickborne fever is a febrile disease of
stages of development, as in chlamydiae,
domestic and free-living rnminants in the
but rather are rickettsial colonies within
temperate regions ofE.urope. It is prevalent
cytoplasmic vacuoles.

in sheep and cattle in the UK, Ireland,

The disease is transmitted by the hard

Norway, Finland, The Netherlands, Austria,
tick I 1icinus. Adult ticks infected as larvae and Spain. Disease is transmitted by the
or nymphs can transmit the disease as can
hard tick Ixodes ricinus. A similar disease nymphs infected as laivae, but infections do
transmitted by other ticks has been
not appear to pass from the adult female to
described in India and South Africa. The
the laiva via the egg. The rickettsiae can
main hosts are sheep and cattle, but goats
survive in infected ticks for long periods
and deer are also susceptible.

and, because I ricinus can swvive wued
for > 1 yr awaiting a new host, ticks infected

Etiology: The causative agent is now
in their previous instar can still be infective
classified as a member of the order
after long periods of hibernation. The ready

Rickettsiales, family Anaplasmataceae,
transmission of infection by injecting
asAnaplasma phagocytophilum, which
infected blood suggests that the organism
includes the granulocytic agents formerly
could be transmitted mechanically by biting
known as Ehrlichia phagocytophila,
insects. In addition, if the organisms

Ehrlichia equi, and the agent of human
reported to cause a similar disease in
granulocytic ehrlichiosis.

rnrninants in India and South Af1ica are

The organism infects eosinophils,
indeed A phagocytophilum, it is most likely neutrophils, and monocytes, in that order.

that ticks other than I ricinus a.i·e involved.

Cytoplasmic inclusions are visible as
grayish blue bodies in Giemsa-stained blood Clinical Findings: After infestation witl1
smears and may contain one or more
infected ticks, the incubation period may be
rickettsial particles of variable size and

5--14 days, but after il,iection with infected
shape. The varied morphologic types in the
blood, the incubation period is 2-6 days. In
cytoplasmic inclusions do not represent
sheep, the main clinical sign is a sudden

TICKBORNE FEVER

773
fever (105° -108°F [ 40.5° -42.0°C]) for 4-10
infected throughout the pe1iod of bacteredays. Other signs are either absent or mild, mia. The nwnber of circulating thrombobut the animals generally appear dull and cytes is also rep01ted to be depressed
may lose weight. Respiratory and pulse
during the febrile period, and tile occasional
rates are usually increased, and a cough
hemorrhagic syndromes associated with

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often develops.

tickbome fever are probably related to the

In cattle, the disease is known as pasture
reduction in circulating th.rombocytes.

fever in many parts of Europe, including

Finland, Norway, Austria, Spain, and

Diagnosis: In sheep, tile onset of high

Switzerland. The disease occurs as an
fever in tick-infested areas during the spring
annual minor epidemic when dairy heifers
and summer in association with hematoand cows are turned out to pasture in the logic changes and the presence of incluspring and early summer. Within days, the sions within granulocytes or the detection
cows are dull and depressed, with a marked
of specific DNA by PCR is diagnostic. PCR
loss of appetite and milk yield. Affected
and other molecular methods are particucows usually suffer from respiratory larly useful during the late stages of primary
distress and coughing. Clinical signs are
bacteremia and during persistent infection
more obvious and last longer in newly
when it is difficult to detect inclusion bodies
purchased animals than in home-bred
in blood smeai"S. Clinical disease usually is
animals. Often, veterinary advice is sought
seen only in young lambs born in tickafter a sudden drop in milk yield.

infested areas or in older animals newly

Abortions affect susceptible ewes and
introduced to such areas. Demonstration of
cows newly introduced onto tick-infested
typical inclusion bodies in blood smeai"S or
pastures during the last stages of gestation,
specific DNA by PCR should indicate the
with abortions occurring 2-8 days after the
association of tickbome fever and cases of
onset of fever. Except for aborting ewes,
tick pyemias and abortions, particularly
death due to tickbome fever is rare. The
when abortions occur after pregnant
semen quality of infected rams and bulls
animals are moved from tick-free to
may be greatly reduced. Variations in
tick-infested pastures. Wection could be
severity of the clinical effects may be
established retrospectively by demonstratrelated to differences between strains of ing a rise in aJ1tibody titers by indirect

A phagocytophilum or in host susceptibility.

imrnunofluorescence or ELISA.

Perhaps the most significant effect of

In affected dairy cattle, tile main signs ai·e
infection is its serious impairment of
abortions a!ld a sudden drop in milk yield.

hwnoral and cellular defense mechanisms,

The other common clinical sign in infected
which results in increased susceptibility to
cattle is respiratory illness after a herd is
secondary infections such as tick pyemia,
introduced to tick-infested pastures.

pnewnonic pasteurellosis, louping ill, and

Tickbome fever must also be considered
listeriosis.

when abortions a!ld stillbirtlls, particularly
in heifers, occur soon after tlleir introduc

Lesions: Tickbome fever is charactertion to tick-infested pastures. Therefore, in ized by transient but distinct hematologic
areas where the disease is enzootic, blood
changes. A modest neutrophilia develops
smeaJ"S must be exainined for the presence

2-4 days after natural or experimental
of organisms in all cases of abortion in
infection and is followed by a severe
sheep a!ld cattle and when milk yield drops
leukopenia due to lymphocytopenia and
suddenly soon after the animals have
neutropenia. The lymphocytopenia lasts
returned to pasture.

4-6 days, whereas the neutropenia develops
progressively and becomes more marked

Treatment and Control: The short

-10 days after infection. Studies witl1
acting oxytetracyclines ai·e regarded as the
monoclonal antibodies that recognize
most effective treatment, because otl1er
surface markers for lymphocyte subsets
aJ1tibiotics such as penicillin, streptomycin,
have shown that both T and B lymphocytes
a!ld ampicillin do not prevent relapses.

are reduced. The number of circulating

SulfaJ11etha.zine has also proved useful. If
eosinophils is also depressed for as long as
dairy cattle are treated with oxytetracy2 wk. After the febrile period has subsided, clines within a few days of infection, the
the number of monocytes may increase. At
pyrexia is reduced quickly aJ1d milk yield
the peak of reaction, >90% of circulating
restored.

neutroph.ils and eosinoph.ils may be

There are three important aspects of
infected. The monocytes are predominantly
control: vector control, chemotherapy, a!ld
infected during the later stages of bactereimmunity. Effective control Call be achieved mia, whereas the granulocytes are usually
by eliminating or markedly reducing

774

TICKBORNE FEVER
contact with the tick vector either by
as 3 wk and helps reduce secondary
grazing sheep and cattle on tick-free
infections such as tick pyemia, pasteurelpastures in lowland areas or by use of losis, and colibacillosis. It may also improve
acaricides. In sheep practice, this comgrowth rate.

monly involves keeping ewes and lan1bs in a

Several aspects of inln1unity remain

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fenced, relatively tick-free pasture until the
controversial, but it is generally accepted
lan1bs are -6 wk old. Lambs also benefit
that sheep and cattle are immune to
from improved nutrition of the ewes.

challenge after recovery from one or

Dipping lambs within 1-2 wk of birth is not
two bouts of clinical disease caused by
commonly practiced because of difficulties
tickbome fever. The immunity may last for
of gathering the lambs on widely dispersed
several months but wanes rapidly if the
hill farms, the risks of mismothering, and
animals are removed from tick-infested
the relatively short duration of protection
areas. Secondary infections are usually
provided by acaricides, possibly because of
milder as residual immunity persists. There
the short fleece and rapid growth rate of
is a variable degree of cross-protection
lambs. However, dipping twice with a 2- to
among strains of A phagocytophilum. No

3-wk interval or use of pour-on preparations
effective vaccines are available to protect
or smears applied before lambs are moved
ruminants from clinical tickbome fever.

from lambing fields to hill pastures

However, if susceptible aninlals are being
reportedly controls ticks effectively.

brought into tick-infested pastures, it may

Pregnant aninlals should not be moved
be sensible to deliberately infect them
from tick-free to tick-infested pastures.

before introduction and treat them with

In enzootic areas, treatment with
oxytetracyclines before or immediately
long-acting tetracyclines may be used as a
after the onset of fever. This allows
prophylactic measure. When susceptible
multiplication of the organism and therefore
aninlals, particularly pregnant ewes and
stimulation of immune responses without
cows and newborn lambs, are to be moved
uncontrolled clinical disease; a minimum
from tick-free to tick-infested areas, it may
duration of bacteremia may be required for
be necessary to combine dipping with
protective immunity to develop. Because
prophylactic use of long-acting tetracynot all strains of A phagocytophilum are clines. Such treatment of lambs in the first
cross-protective, strains specific to the area

2 -3 wk of life can be protective for as long
must be used.

TICK PYEMIA

Tick pyemia affects lambs 2-12 wk old
superficial wounds, or through the infected
and is characterized by debility, crippling
umbilicus. However, there is clinical and
lan1eness, and paralysis. Pyernic abscesses
experimental evidence that I ricinus does
are common in joints but may be found in
not simply act as a vector directly injecting
virtually any organ. The disease causes
staphylococci into the bloodstream. The
significant economic loss through debilitamain role of I ricinus is as a vector of the tion and death. The disease is enzootic in
rickettsial agentAnaplasma phagocytophi
many regions of the UK and Ireland where
lum, which causes tickbome fever ( see
the tick Ixodes ricinus is common, and it is p 772), which in tum creates factors
likely to be present in other parts of Europe
favorable to development of pyemia Lambs
where the same tick is found.

affected with tickbome fever have severe
leukopenia, and their peripheral blood

Etiology: Staphylococcus aureus is
neutrophils are less capable of phagocyregarded as the main cause of the pyemic tizing and killing S aureus. Experimental
abscesses, because it has been isolated
studies have shown that lambs with
consistently from superficial and deeptickbome fever were more susceptible seated lesions and it is rare to find other
to experin1ental infections with S aureus
bacteria. The bacteria are believed to gain
during the period of neutropenia and that as
entry into the bloodstrean1 either by direct
many as 300/o of lambs with tickbome fever
inoculation during tick feeding, from local
may develop staphylococcal infections.

WESSELSBRON DISEASE

775

The epidemiology of the disease is closely
septicemic diseases. Tick pyemia may also
related to the biology of I ricinus. The resemble other suppurative infections of
disease is limited to areas populated by
the newborn, including navel ill and joint

I ricinus and to seasons of the year
ill due to infections by other bacteria such
climatically favoring high tick population
as streptococci and Trueperella pyogenes.

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and activity.

Clinical Findings: Abscesses form in

Treatment and Control: Treatment of
various parts of the body, mainly in the joints, clinical cases of tick pyemia with penicillin tendon sheaths, and muscles, resulting in
or tetracycline can be effective, provided
lameness-hence the common use of the
the lesions are not too advanced.

tem1 "crippled Jambs." In some outbreaks,

Control of tick infestation is the most

>30% of lambs may be affected; they are
effective prevention. This can be achieved
usually dull and lame and often suffer from
either by restricting lambs and ewes to
loss of body condition. Internal abscesses
low-ground, tick-free pastures for the first
withoutjoint lesions may result in no clinical
few weeks of life or by dipping ewes before
signs other than the loss of condition, but

Jambing and administering aca.iicides as
when lesions are present in the CNS, there
dips or smears on lambs. In young lambs,
may be ataxia, paraplegia, or other nervous
pour-on preparations of cypermethrin or
signs. ·me crippling disease lasts for days or
smears applied before Jan1bs are moved
weeks, but the disease may also appear as an
from lambing fields to hill pastures
acute septicemia. On occasion, there may
reportedly control ticks effectively.

be sudden deaths resulting from multiple

Ad.ministration of long-acting oxytetracyinternal abscesses without other visible cline at the time of risk Ca.J.l help prevent both
signs. As many as 5096 of affected lambs
tickbome fever and tick pyem.ia during the
may die, and the survivors recover slowly.

first weeks of life. A single irtjection at

Lesions: Apart from the joints and other
double the standard dose given at 3 wk of
superficial structures, abscesses are
age can significantly reduce mortality and
commonly found in the liver, lungs, and
morbidity in young hill lambs on tickkidneys. They may also be present in the

.infested pastme and inlprove weight gains
meninges of the spinal cord and in the
and condition in the remainder. Prophylactic
pericardiun1 and myocardium. The
treatment with a long-acting antibiotic may
diaphragm, thymus, and adrenal glands are
prevent development of tickbome fever
less conunonly affected. Ticks are often
for as long as 3 wk, without pyrexia and
found attached to an inflamed area.

inununosuppression, so that the incidence
of tick pyemia and other infections such as

Diagnosis: History and clinical signs are
pasteurellosis and colibacillosis are reduced ..

valuable indicators. The restriction of the

Although treatment with oxytetracycline
disease to tick-infested areas, its occurrence
may inhibit tl1e development of in1munity,
during seasons of tick activity, and demonif the Jan1bs eventually develop tickbome stration of A phagocytophilum or specific
fever, they are several weeks older and

DNA by PCR in the blood of affected lambs
apparently less susceptible to tick pyemia.

or other sheep in the flock are diagnostic

Deliberate expos me of Jambs by irtjections,
features. Isolation of S aureus from lesions followed by treatment with oxytetracycline,
and the absence of other bacteria will help to
could provide some i.J11munity before the
confirm tick pyemia The Joss of condition

Jambs enter tick-infested areas; however,
and ill-thrift without lameness may be
strains specific to the area must be used
difficult to recognize as tick pyemia, and the
because some strains of A phagocytophilum
acute condition can be confused with other
have no cross-inlrnunity.

WESSELSBRON DISEASE

Wesselsbron disease is an acute, arthropodinfrequent although likely under-reported.

borne flavivi.Jus infection of mainly sheep,

Newborn Jambs and goat kids are most
cattle, and goats in sub-Sallaran Africa.

susceptible, and mortality may occur.

Infection is common, but clinical clisease is

Infection in adult sheep, cattle, and goats

776

WESSELSBRON DISEASE
is usually subclinical, but disease may
of Rift Valley fever, and severe fetal
be severe in sheep with preexisting liver
teratology of the CNS is seen after
pathology. Occasional abortion in ewes,
experimental infection. Use of the
together with congenital malformation of
attenuated vaccine in pregnant ewes may

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the CNS with arthrogryposis of the ovine
result in early embryonic death, severe

( and also the bovine) fetus and hydrops
teratology of the CNS, arthrogryposis,
arnnii in ewes, is seen. Incidental spillover
hydrops arnnii, abortion, or fetal mummifioccurs to people, causing a nonfatal, cation. In people, mild to severe, nonfatal
influenza-like disease.

influenz a -like symptoms are seen.

Lesions: In newborn and young

Etiology and Epidemiology: Wesselsbron disease is caused by a flavivirus, animals, a moderate to severe icterus and
which is an enveloped, positive-sense
hepatomegaly are seen with Wesselsbron

RNA virus. It has not been well characterdisease; the liver is yellowish to orange ized but has properties typical of a
brown. Petechiae and ecchymoses are
hemagglutinating flavivirus. It has been
commonly found in the mucosa of the
isolated from vertebrates and arthropods
abomasum, the contents of which are
from many sub-Saharan African countries,
chocolate-brown in color. Histopathology
and serologic surveys provide evidence
reveals mild to extensive necrosis of the
of its occurrence in other countries.

parenchyma as well as individual or small,

Evidence of infection has been reported in scattered groups of necrotic hepatocytes.

cattle, sheep, goats, camels, pigs, donkeys, Lesions in adult animals are usually much horses, ostriches, and wild ruminants.

milder.

Based on the distribution of aedine
mosquitoes associated with Wesselsbron

Diagnosis: The clinical signs and
disease, the incidence of infection is likely
epidemiology, together with a relatively
greater than is generally realized. The high high mortality in lambs, are an indication prevalence of antibodies in warmer and
of Wesselsbron disease. It should,
moister coastal areas of southern and
however, be distinguished from Rift Valley
eastern Africa suggests that domestic
fever, and the two diseases may occur
herbivores may play a significant role in
together. The virus can be isolated from
maintenance of the virus, and activity
almost all organs of lambs that have died
appears to occur year round. In drier
during the clinical stage of the disease.

areas, however, seroprevalence is

Intracerebral inoculation of newborn mice
generally lower, with irregular disease
is the best method of isolation. The virus
outbreaks occurring, usually in conjunccan be distinguished from that of Rift tion with Rift Valley fever. (seep 768)

Valley fever by intraperitoneal inoculation
when abnormally heavy rains lead to
of weaned mice; Wesselsbron disease
an abundance of floodwater-breeding
virus will not kill such mice, whereas Rift
mosquitoes. People may become infected

Valley fever virus will. Confirmation of the
by mosquitoes or by handling organs from
viral identity can be accomplished by
infected animals.

•
virus neutralization.

Serodiagnosis has been based on

Clinical Findings: After an incubation
hemagglutination-inhibition, complement
period of 1-3 days in newborn lan1bs,
fixation, and virus neutralization. Flavivirus
nonspecific signs of illness, including
cross-reactivity is marked in li.emagglutinafever, anorexia, listlessness, weakness, tion-inhibition tests but less so in compleand increased respiration, become ment fixation, a test that is specific in cattle
evident. Death may occur within 72 hr. In
sera. Nevertheless, homologous Wesselscalves and adult sheep, goats, and cattle, bron titers greatly exceed heterologous
nonfatal febrile or inapparent infection
flavivirus titers.

occurs. Occasional abortion, congenital

CNS malformations with arthrogryposis,

Control: Production of an attenuated
and hydrops amnii are seen in ewes.

vaccine was discontinued shortly before

Wesselsbron disease and Rift Valley fever

2000. Incidence of disease is low in sheep,
share many clinical and pathologic
but injudicious use of the vaccine in
features. However, Wesselsbron disease
pregnant ewes resulted in severe economic
is usually milder, producing much lower
losses in the past due to abortion and fetal
mortality, fewer abortions, and less
malformations. Attempts to control
destructive liver lesions. The virus
mosquito vectors are of little value as
appears to be more neurotropic than that
a preventive measure.

CANINE DISTEMPER

777

CANINE DISTEMPER

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Canine distemper is a highly contagious,
may be accompanied by serous nasal
systemic, viral disease of dogs seen
discharge, mucopurulent ocular discharge,
worldwide. Clinically, it is characterized
letl1argy, and anorexia. GI and respiratory
by a diphasic fever, leukopenia, GI and
signs, typically complicated by secondary
respiratory catarrh, and frequently
bacterial infections, may follow; rarely,
pneumonic and neurologic complications.

pustular dern1atitis may be seen. Encepha

Its epidemiology is complicated by the large
lomyelitis may occur in association with
number of species susceptible to infection.

these signs, follow tl1e systemic disease, or

The disease is seen in Canidae ( dog, fox,
occur in the absence of systemic manifestawolf, raccoon dog), Mustelidae (ferret, tions. Dogs surviving the acute phase may
mink, skunk, wolverine, marten, badger,
have hyperkeratosis of the footpads and
otter), most Procyonidae (raccoon,
epitl1elium of tl1e nasal planun1, as well as
coatirnundi), some Viveridae (binturong,
enamel hypoplasia in incompletely erupted
palm civet), Ailuridae (red panda), Ursidae
teetl1.

(bear), Elephantidae (Asian elephant),

Overall, a longer comse of illness is
primates (Japanese monkey), and large
associated with tl1e presence of neurologic

Felidae. Domestic dogs (including feral
signs; however, tl1ere is no way to anticipate
populations) are considered to be the
whether an infected dog will develop
reservoir species in most, if not all,
neurologic manifestations. CNS signs
locations. Antigenic drift and strain
include circling, head tilt, nystagn1us,
diversity is increasingly docun1ented in
paresis to paralysis, and focal to generalized
association witl1 outbreaks in wild species,
seizures. Localized involuntary twitching of
domestic dogs, and exotic animals held in
a muscle or group of muscles (myoclonus,
zoos and parks.

chorea, flexor spasm, hyperki.nesia) and
convulsions characterized by salivation and,

Etiology and Pathogenesis: Canine
often, chewing movements of the jaw
distemper is caused by a paran1yxovirns

("chewing-gun1 fits") are considered classic closely related to the vimses of measles
neurologic signs. Emerging viral strains may
and rinderpest. The fragile, enveloped,
be associated witl1 greater neurotropism;
single-strand RNA vims is sensitive to lipid
increased morbidity and mortality from
solvents, such as etl1er, and most disinfecneurologic complications has been tants, including phenols and quaternary
observed.

an1monium compounds. It is relatively

A dog may exhibit any or all of these
unstable outside tl1e host. The main route of
multisystemic signs during the course
infection is via aerosol droplet secretions
of tl1e disease. Infection may be mild and
from infected animals. Some infected dogs
inapparent or lead to severe disease with
may shed virus for several montl1s.

most of the described signs. The course of

Virus initially replicates in the lymphatic
the systemic disease may be as short as 10
tissue of the respiratory tract. A cell-associdays, but the onset of neurologic signs may ated vi.remia results in infection of all
be delayed for several weeks or months as a
lymphatic tissues, which is followed by
result of chronic progressive demyelination
infection of respiratory, GI, and urogenital
within the CNS.

epitl1eliun1, as well as the CNS and optic

Clinicopathologic findings are nonspenerves. Disease follows vims replication in cific and include lymphopenia, with the
tl1ese tissues. The degree of viremia and
possible finding of viral inclusion bodies
extent of viral spread to various tissues is
in circulating leukocytes very early in the
moderated by tl1e level of specific hum oral
course of tl1e disease. Thoracic radiographs
immunity in tl1e host during tl1e viremic
may reveal an interstitial pattern typical of
period.

viral pneumonia

Chronic distemper encephalitis ( old dog

Clinical Findings: A transient fever
encephalitis, [ODE]), a condition often
usually occurs 3-6 days after infection,
marked by ataxia, compulsive movements
and there may be a leukopenia ( especially
such as head pressing or continual pacing,
lymphopenia) at this time; tl1ese signs may
and incoordinated hypern1etria, may be
go unnoticed or be accompanied by
seen in fully vaccinated adult dogs without
anorexia. The fever subsides for several
a history suggestive of systemic canine
days before a second fever occurs, which
distemper infection. Although canine

778

CANINE DISTEMPER
distemper antigen has been detected in the
strains has also been desc1ibed; this assay
brains of some dogs with ODE by fluoreswould be of particular value in epidemiocent antibody staining or genetic methods, logic investigations or in outbreaks in
dogs with ODE are not infectious, and
non-canine species. Antibody titers or
replication-competent virus has not been

ELISA can be pe1formed on CSF and

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isolated. The disease is caused by an
compared with peripheral blood; a
inflammatory reaction associated with
relatively higher level in the CSF is typical of
persistent canine distemper virus infection
natural infection versus vaccination. Viral
in the CNS, but mechanisms that trigger this
antigen inununofluorescent assay (IFA) or
syndrome are unknown.

fluorescent in situ hybridization for viral

Lesions: Thyrnic atrophy is a consistent

DNA can be perfom1ed on biopsies from
postmortem finding in infected young
the footpads or from the haired skin of
puppies. Hyperkeratosis of the nose and
the dorsal neck
footpads is often found in dogs with

At necropsy, diagnosis is usually
neurologic manifestations. Depending on
confinned by histologic lesions, IFA, or
the degree of secondaiy bacterial infection,
both. These sainples are often negative
bronchopneumonia, ente1itis, ai1d skin
when the dog is showing only neurologic
pustules also may be present. In cases
manifestations or when circulating ai1tibody
of acute to peracute death, exclusively
is present (or both), requiring that the
respiratory abnormalities may be found.

diagnosis be made by CSF evaluation or

Histologically, canine distemper virus

RT-PCR as described above.

produces necrosis of lyn1phatic tissues,
interstitial pneumonia, and cytoplasmic and

Treatment: Treatments are syn1ptomatic
intranuclear inclusion bodies in respiratory,
ai1d supportive, aimed at lin1iting secondaiy
winaiy, and GI epithelium. Lesions found
bacterial invasion, supporting fluid balin the brains of dogs with neurologic ance, and controlling neurologic manicomplications include neuronal degenerafestations. Broa d -spectrum antibiotics, tion, gliosis, noninflainmatory demyelinabalanced electrolyte solutions, pai·enteral tion, pe1ivascular cuffing, nonsuppurative
nutrition, antipyretics, analgesics, and anleptomeningitis, and intranuclear inclusion ticonvulsai1ts are used, and good nursing
bodies predominately within glial cells.

cai·e is essential. No single treatment is
specific or wlifonnly successful. Experi

Diagnosis: Distemper should be
mental in vitro work with antiviral agents
considered in the diagnosis of ai1y feb1ile
shows promise, but these agents have not
condition in dogs with multisystemic
yet been widely used.

manifestations. Characte1istic signs

Unfortunately, treatment for acute
sometimes do not appeai· until late in the
neurologic manifestations of distemper is
disease, and the clinical picture may be
frequently unsuccessful. If the neurologic
modified by concurrent parasitism and
signs are progressive or severe, the owner
nwnerous viral or bacterial infections.

should be appropriately advised. With

Distemper is sometimes confused with
prompt, aggressive care, dogs may recover
other systemic infections such as leptocompletely from multisystemic manifestaspirosis (seep 650), infectious canine hepations, but in other cases, neurologic signs titis (seep 798), or Rocky Mountain
may persist after GI and respiratory signs
spotted fever (seep 806). Intoxicants such
have resolved. Some dogs with chronic
as lead or organophosphates can cause
progressive or vaccine-induced forms
sinmlta.neous GI and neurologic signs. A
of neurologic disease may respond to
febrile catarrhal illness with neurologic
immunosuppressive tl1erapy with antisequelaejustifies a clinical diagnosis of inflanunatory or greater dosages of
distemper.

glucocorticoids.

In dogs with multisystemic signs, the
following can be exainined by immuno

Prevention: With the potential increasing
fluorescent assay or reverse transcriptase
virulence of emerging strains and the wide

(RT) PCR: smears of conjw1ctival, tracheal,
host range of canine distemper virus,
vaginal, or other epithelium; the buffy coat
widespread vaccination of domestic dogs is
of the blood; urine sediment; or bone
essential. Successful immUllization of pups
matTow aspirates. Commercially available
with canine distemper modified-live virus
quantitative R T -PCR can usually distinguish

(MLV) vaccines depends on the lack of internatural infection from vaccinal virus. A ference by maternal antibody. To overcome
combined two-step RT-PCR to distinguish
this batTier, pups are vaccinated with MLV
vaccinal strains from emerging wild-type
vaccine when 6 wk old and at 3- to 4-wk

CANINE HERPESVIRAL INFECTION

779
intervals until 16 wk old. Alternatively,

Assocation of Zoo Veterinarians recommeasles virus vaccine induces inmrnnity mends its extra-label use in many at-risk
to canine distemper virus in the presence
species held in zoos and parks. Historically,
of relatively greater levels of maternal
annual revaccination has been standard
distemper antibody. MLV measles vaccine is
because of the breaks in protection that can

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administered IM to pups 6---7 wk old and is
occur in stressed, diseased, or immunosupfollowed with at least two more doses of pressed dogs, and because vaccines have

MLV distemper vaccine when 12-16 wk old.

been labeled for annual use. Substantial

Many varieties of attenuated distemper
evidence supports the finding that
vaccine are available and should be used
inm1unity induced by MLV distemper
according to manufacturers' directions.

vaccines lasts �3 yr. However, in most

MLV vaccines should not be used in
cases, this remains an extra-label use of the
late-pregnant or early-lactation bitches.

vaccine; thus, decisions to revaccinate less

MLV vaccines can produce postvaccinal
often than annually should be considered
illness in some imrnunosuppressed dogs.

in light of local prevalence of the disease

A recombinant canarypox vector vaccine
and other potential risk factors, as well as
expressing distemper vims proteins is
industry and professional organization
licensed for use in ferrets; the American
recommendations.

CANINE HERPESVIRAL INFECTION

Canine herpesvirus is best known as a severe
occurs in fetal or neonatal puppies from in
viral infection of puppies worldwide, which
utero infection, or infection in the fil'St 3 wk
often has a lO()OA, mortality rate in affected
of life. After tllis tin1e, natural resistar1ce to
litters. Increasingly sensitive molecular
infection improves as puppies mature and
diagnostics have enabled its recognition in
maintain a higher body temperature.

adult dogs with upper respirntory infection,

Infection of susceptible aninlals results in
ocular disease, vesicular vaginitis or
replication of CHV in the surface cells of the
posthitis, and in dogs with no clinical signs.

nasal mucosa, pharynx, and tonsils. In the

As is typical of herpesvirnses, recovery from
case of newborn susceptible pups or other
clinical disease is associated with lifelong
dogs with compromised in1rnune response,
latent infection. Only canids ( dogs, wolves,
viremia and invasion of diverse visceral
coyotes) are known to be susceptible. The
organs occur. Primary systemic infection
seroprevalence in dog populations worldwide is associated with a high degree of viral ranges from 200A, to 98% depending on the
shedding; shedding by latently infected
region. Because latently infected animals may aninlals after clinical or subclinical recmdestransiently convert to seronegative status, any ence is of lesser severity and duration.

seroprevalence study likely underestimates
the tme rate of exposure and carriage.

Clinical Findings: Deaths due to CHV
infection usually occur in puppies 1-3 wk old,

Etiology and Pathogenesis: The
occasionally in puppies up to 1 mo old, and
disease is caused by an enveloped DNA
rarely in pups as old as 6 mo. Typically, onset
canine herpesvirus (CHV) that is sensitive
is sudden, and death occul'S after an illness
to lipid solvents (such as ether and
of !>24 hr. If clinical signs ar·e obse1ved, they chlorofonn) and most disinfectants. CHV is
may include lethar·gy, decreased suckling,
relatively unstable outside the host, so close
diarrhea, nasal dischar·ge, conjunctivitis,
contact is required for transmission.

corneal edema, erythematous rash, rarely

Transmission usually occurs by contact
oral or genital vesicles, and the notable
between susceptible individuals and the
absence of fever. Thoracic radiographs show
infected oral, nasal, or vaginal secretions of
a diffuse unstrnctured interstitial pattern that
shedding dogs. Many dogs shedding vims
is typical of viral pnemnonia, but, in contrast
exhibit no clinical signs. Inm1unologically
to other viral diseases of puppies, leukocytonaive pregnar1t bitches are at risk of acute sis may be present.

infection, which may be traI1Sn1itted to

Older dogs exposed to or experimentally
fetuses or neonatal pups; previously infected inoculated with CHV may develop a mild bitches are unlikely to traI1Sn1it infection.

rhinitis, which may be part of the "kennel

TI1e most significar1t systenlic disease
cough" syndrome (infectious tracheobron-

780

CANINE HERPESVIRAL INFECTION
chitis, seep 1490) or a vesicular vaginitis spleen by cell culture techniques and
or posthitis. There are also reports of
subsequent identification by PCR and
conjunctivitis and dendritic corneal ulcers
sequencing, transmission electron
in the absence of other upper respiratory
microscopy, immunoftuorescence, or
signs. Acutely infected pregnant bitches

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fluorescence in situ hybridization. The
may abort a litter, or deliver a partially
tissues should be submitted to the
stillborn litter; however, they seldom exhibit laboratory refrigerated but not frozen.

other clinical signs, and future breedings are
likely to be successful.

Treatment: Therapy is typically

Lesions: The characte1istic gross lesions
unrewarding in systemically affected
at necropsy consist of disseminated focal
puppies, and the prognosis for puppies that
necrosis and hemorrhages. The most
do survive is guarded because damage to
pronounced lesions are seen in the lungs,
lymphoid organs, brain, kidneys, and liver
cortical portion of the kidneys, adrenal
may be iITeparable. Before onset of clinical
glands, liver, and GI tract. All lymph nodes
signs in littermates or other nearby puppies,
are enlarged and hyperemic, and the spleen
reaiing in incubators at an increased
is swollen. Lesions may also be found in the
temperature (95°F [35°CJ, 50%relative
eyes and CNS. The basic histologic lesion is
hwnidity), and/or passive iinmunization
necrosis with hemo1Thage in the adjacent
with intraperitoneal senm1 may reduce
parenchyma. The inflammatory reaction in
losses within an exposed litter. Lin1ited
many organs may be limited, but marked
studies with antiviral agents such as
neutrophilic and mononuclear infiltration
vidarabine are inconclusive, but iinmediate
is seen in ocular lesions. Single, small,
recognition and treatment would be needed
basophilic, intranuclear inclusion bodies
to have any possibility of success.

are most common in areas of necrosis in the

Adult dogs with ocular, respiratory, or
lung, liver, and kidneys; occasionally, they
genital disease often experience mild and
are seen as faintly acidophilic bodies
self-liI11iting signs. Ophthalmic antiviral
located within the nuclear space.

cidofovir (0.5% bid) has been used successfully in one reported case of primary ocular Diagnosis: 1n systemically affected
iI1fection in an adult dog ai1d may be useful
puppies, CHV infection may be confused
for persistent or painful ocular lesions.

with infectious canine hepatitis (seep 798), but it is not accompanied by the thickened,

Prevention: No vaccine is available in the
edematous gallbladder often associated with

USA Infected bitches develop antibodies,
the latter. The focal areas of necrosis and
and litters subsequent to the first infected
hemorrhage, especially those that are seen in
litter receive maternal antibodies in the
the kidneys, distinguish it from hepatitis and
colostrw11. Puppies that receive maternal
neosporosis (seep 663). CHV causes serious
antibodies may be infected with the virus,
disease only in very young puppies. The rapid but disease does not result. Isolation of pregdeath and characteristic lesions distinguish it nant bitches from other dogs during the last from canine distemper (seep 777). •

3 wk of gestation and first 3 wk postpartw11,

Hemagglutination, ELISA, and immw10-
with excellent hygiene by hW11an handlers,
fluorescence antibody tests are available,
is the most effective way to minimize risk to
and PCR is highly sensitive and specific
puppies. Because of the high seroprevalence
when used on fresh tissue and fluid samples. among adult dogs and because virus may be 1n cases of neonatal mortality, the diagnosis
shed by asymptomatic individuals, complete
typically is made postmo1tem with virus
avoidance of exposure is not a reasonable
isolation from fresh lung, liver, kidney, and
management strategy for most dogs.

FELINE INFECTIOUS PERITONITIS

Feline infectious peritonitis (FIP) is an

Coronavirus-specific antibodies ai·e
iinmune-mediated disease triggered by
present in as many as 90% of cats in
infection with a feline coronavirus (FCoV).

catteries and in as many as 500A, of those in

FCoV belongs to the family Coronaviridae,
single-cat households. However, <5% of
a group of enveloped, positive-stranded

FCoV-infected cats develop FIP in multicat

RNA viruses frequently found in cats.

households.

FELINE INFECTIOUS PERITONITIS

781

Geographic Distribution: FCoV
outbreaks. No consistent mutation has yet
infection and FIP occur worldwide with
been identified, although studies have
similar prevalence and are found in domessuggested sequence differences in the spike tic and wild cats. FCoV strains can be
proLein, membrane protein, or NSP3c

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classified into serotypes I and II, depending
correlate with disease manifestation.

on their antigenetic relationship to canine

Recent studies have found feline coronavicoronavirus (CCV), and these subtypes vary ruses to have intact NSP3c genes, whereas
in propo1tion among different countries.

most isolates from diseased tissues of FIP

Among FCoV strains isolated in the field in
cases had disrupted NSP3c genes. Findings
the USA and Europe, 70%--95% are serotype
suggested that 3c-inactivated viruses only

I. In contrast, in Japan serotype II predomirarely replicate in the intestine, which nates. Most cats with FIP are infected with
possibly explains the rare incidence of FIP

FCoV serotype I. However, both serotypes
outbreaks. In additional work, it was
can cause FIP and both can cause clinically
concluded that mutation of the S l/S2 locus
inapparent FCo V infections.

and modulation of a furin recognition site

FCoV belongs to the same taxonomic
nom1ally present in the S gene of ente1ic
cluster of coronaviruses as transmissible
coronaviruses is a critical contributing
gastroenteritis virus, porcine respiratory
factor for development of FIP.

coronavirus, CCV, and some hw11an

The second hypothesis for the developcoronaviruses. In many species, corona viment of FIP is the existence of distinct ruses have a relatively restricted organ
circulating virulent and avirulent strains in a
tropism, mainly infecting the respiratory
population, and exposure to the pathogenic
and/or GI tracts. In cats and mice, however,
strain, the viral load, and the cat's inunune
coronavirus infections can, in certain
response detern1ine whetl1er FIP will
circumstances, involve multiple organs.

develop. It is likely both viral genetics and

In addition to cats, other fetid species are
host immunity play a role. In both hypothsusceptible, and FCo Vis also an in1portant eses, the key pathogenic event in the
pathogen in non domestic felids. There was
development of FIP is tl1e massive
evidence of FCo V infection in 195 of 342
replication of FCo V in macrophages. If
nondomestic felids in southern Africa,
the cat does not eliminate macrophages
which included both wild and captive
infected with replication-competent virus
anin1als. There is also a high incidence of
early in infection, the presence of tl1e virus

FIP in nondomestic felids in captivity in the
within circulating macrophages initiates an

USA and Europe. Cheetai1s in captivity
ultin1ately fatal arthus-type in1mune-mediseem to be highly prone to developing FIP; ated reaction, which defines FIP.

loss of genetic diversity and a genetic

Factors that increase FCo V replication in
deficiency in their cellular in1munity is
the intestines (and increase the probability
thought to predispose them to the disease.

of the mutation) include young age, breed

Although FIP can only occur in felids, a
predisposition, in1mune status, stress,
clinically similar condition in ferrets is
corticosteroid treatment, and surgery, as
associated with ferret systemic coronavirus. well as dosage and virulence of the virus and reinfection rate in multicat households.

Etiology and Pathogenesis: FIP is a

Crowded environments, such as catteries
sporadic disease thought to be caused by
or shelters, also may increase stress and
viral variants that develop within each
exposure to FCoV. Whenever FCoV
specific cat. The pathogenesis of FIP is
infection exists, so does the potential
tmclear, but there are two main hypotheses.

for development of FIP

The "internal mutation theory" states that After a cat becomes infected with
cats are infected with the primarily

FCo V via fecal-oral transmission ( or less
avirulent FCo V that replicates in enteroconunonly, inhalation), the main site of viral cytes; in some cats, a mutation occurs in
replication is the intestinal epithelium.

a ce1tain region of the FCo V genome that

Replication of FCo Vin the cytoplasm can
creates a new phenotype with the ability
destroy intestinal epithelial cells, leading
to replicate within macrophages. The
to diarrhea in some cats. In many cats,
presence of highly virulent strains of FCo V
infection persists for weeks to months in
capable of consistently inducing FIP
the absence of clinical signs. These cats
suppmt this theory, albeit under experished FCoV either intennittently or mental conditions. Several researchers
continually and act as a source of infection
speculate that some circulating feline
for other cats. Previously, it was believed
enteric coronaviruses are closer to mal<ing
that avirulent FCo V remained confined to
critical mutations necessary for developthe digestive tract, did not cross the gut ment of FIP, possibly explaining FIP
mucosa, and did not spread beyond the

782

FELINE INFECTIOUS PERITONITIS
intestinal epithelium and regional lymph
develop FIP; the number is even lower
nodes. However, PCR can detect FCoV in
in a single cat environment. The risk of
the circulating macrophages of healthy
developing FIP is higher for young and
cats from households with endemic
inununocompromised cats because the

FCo V, indicating that a virulent FCo V may
replication ofFCoV in these animals is less

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also cause viremia.

controlled and, thus, the critical mutation is

FIP is an immune complex disease
more likely to occur. More than half of the
involving viral antigen, antiviral antibodies,
cats with FIP a.re < 12 mo old. Sexually intact
and complement. Within weeks after
cats, males, and purebred cats have a higher
macrophage invasion and replication,
incidence of FIP. Epidemiologic data
virions a.re found in the cecwn, colon,
suggest that the cat's genetic background
intestinal lymph nodes, spleen, and liver
contiibutes to the manifestation of FIP.

after distribution by macrophages in the

Investigators have desciibed va.Iiation in
whole body, including the CNS. There a.re
breed resistance and susceptibility to FIP.

two possible explanations for the events

Susceptibility to FIP is a polygenic inhe1ited
that follow viral dissemination from the
trait in Persians and Bim1ans. Breeds with
intestines. The first proposed mechanism is
higher prevalence of FIP include Abyssinthat FCoV-infected macrophages leave the ian, Bengal, Birn1an, Himalayan, Ragdoll,
bloodstream and carry virus into the tissues. and Rex.

The virus attracts antibodies, complement

FCoV is shed mainly in the feces. Infecis fixed, and more macrophages and tion is generally via the oronasal route. After
neutrophils arc attracted to the lesion; as a
natw·al infection, cats begin to shed virus in
consequence, typical pyogranulomatous
feces within 1 wk. In very early infection, it
changes develop. The alternative explanamay be found in saliva, respiratory tion is that FIP occurs as a result of
secretions, and urine. When naive cats in
circulating immune complexes lodging in
multi.cat households first encounter FCoV, it
blood vessel walls, fixing complement, and
is likely that all will become infected ( and
leading to development of the pyogranudevelop antibodies); most will shed virus lomatous changes. It is assumed that these
intetmittently for a period of weeks or
antigen-antibody complexes are recognized months. Some cats become chronic FCoV
by macrophages but a.re not, as they should
shedders, providing a continual source for
be, presented to killer cells, and thus a.re not reinfection of other cats. Cats that a.re destroyed.

antibody-negative a.re very unlikely to shed,

In addition to virus, chemota.ctic
whereas approxin1ately one-third of all
substances, including complement and

FCoV antibody-positive cats shed virus.

inflammatory mediators, a.re released from

Cats with high antibody titers a.re more
infected macrophages. Complement
likely to shed FCoV. They also a.re more
fixation leads to the release of vasoactive
likely to shed consistently and higher
amines, which cause endothelial cell
a.mounts of the virus. Most ca.ts with FIP
retraction and thus increased vascular
also shed non-mutated FCoV; however, the
penneability. Retraction of capillary endovirus load in feces seems to decrease after a thelial cells allows exudation of plasma
cat has developed FIP.

proteins and, hence, development of

The major sources of FCo V for naive cats
characteristic protein-rich exudates.

a.re litter boxes shared with shedding cats.

Inflanunatory mediators activate proteo

Also, continuous reinfection through the
lytic enzymes that cause tissue damage.

contaminated litter box of a cat already
infected seems to play an important role in

Epidemiology and Transmission:

the endemic survival of the virus. Ra.rely,

FCoV and FIP a.re a major problem in
virus can be transmitted through saliva, by
multicat households. The virus is endemic
mutual grooming, sharing t11e same food
in environments in which many cats a.re
bowl, and through close contact. Sneezed
kept together in a confined space ( eg,
droplet transmission is also rare but
catte1ies, shelters, pet stores). FCoV is
possible. It is uncertain whether FCoV
found less commonly in free-roaming
transmission occurs to a significant degree
community cats, because they do not
at cat shows. Transmission by lice or fleas
typically use the same locations to bury
is considered unlikely. Transplacental
their feces; shared litter boxes a.re a major
transmission can occur but is very
source of transmission in multi.cat
uncommon under natural circumstances.

households.

Most kittens that a.re removed from contact

Although the prevalence ofFCoV
with virus-shedding adult cats at 5---6 wk of
infection is very high in multicat houseage do not become infected. Most comholds, <5% of cats in these situations monly, kittens a.re infected at the age of

FELINE INFECTIOUS PERITONITIS

783

6----8 wk at a time when their maternal
for the diagnostic approach, because there
antibodies wane, mostly through contact
is nearly always effusion to a greater or
with feces from their mothers or other
lesser degree in combination with more

FCoV-excreting cats.

or less granulomatous changes present in

FCo V is a relatively fragile virus that is
cats with FIP. In addition, the fmms can

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destroyed by most household disinfectants
transfonn into each other. Cats with FIP
and detergents. However, it may survive in
may be alert or depressed. Some eat with a
cold or d1y conditions ( eg, in carpet) for as
normal or even increased appetite; others
long as 7 wk outside the cat. Indirect fomite
are anorectic. Fever, weight loss, and/or
transmission is possible, and the virus can
icterus may be noted.

be transmitted for a sho1t time via clothes,

In cats with ascites, an abdominal swelling
toys, and grooming tools.

is commonly noticed. Fluctuation and a fluid
wave may be present; in less severe cases,

Clinical Findings:

fluid can be palpated between tl1e intestinal

Feline Coronavirus Infection: FCoV
loops. Abdominal masses can sometimes be
infection can cause a transient and clinically palpated, reflecting omental and visceral mild diarrhea and/or vomiting due to
adhesions or enlarged mesenteric lymph
replication ofFCoVin enterocytes. Kittens
nodes. Thoracic effusions may cause
infected with FCo V may have a history of
dyspnea, tachypnea, open -mouth breathing,
stunted growth or upper respiratory tract
or cyanotic mucous membranes. Auscultasigns. Occasionally, the virus may cause tion reveals muffled heart sounds. In cats
severe diarrhea witl1 weight loss, which may with pericardia! effusions, heart sow1ds are be unresponsive to treatment and continue
muffled and typical changes can be seen on
for months. However, most FCoV-infected

ECG and echocardiography. Effusions can
cats do not show clinical signs.

be visualized by diagnostic in1aging ( eg,
radiographs, ultrasound) and verified by a

Feline Infectious Peritonitis: Clinical
fluid centesis.

signs of FIP vacy depending on organ

In cats wifuout obvious effusion, in which
involvement. Many organs, including the
mainly granulomatous changes are present,
liver, kidneys, pancreas, CNS, and eyes,
signs are often vague and include fever,
can be involved. The clinical signs and
weight loss, lethargy, and decreased
pathologic findings are a consequence of the appetite. If the lungs are involved, cats can vasculitis and, less commonly, organ failure
be dyspneic, and thoracic radiographs may
resultant from damage to the blood vessels
reveal patchy densities in the lungs.

that supply them. In all cats with nonspe

Abdominal palpation may reveal enlarged
cific clinical signs, such as chronic weight
mesenteric lymph nodes and irregular
loss or fever of unknown origin resistant to
kidneys or nodular irregularities in other
antibiotic treatment or recurrent in nature,
viscera Presenting clinical signs sometimes

FIP should be on the list of differential
can be unusual. In some cats, abdominal
diagnoses.

tumors are suspected, but FIP is finally

The length of time between infection and
diagnosed at surgery or necropsy.

development of clinical signs is unknown

Cats with F1P frequently have ocular
and depends on the inlrnune response of the lesions. The most common ocular lesions individual cat. Disease generally becomes
are retinal changes, and a retinal examinaapparent from a few weeks to 2 yr after the tion should be pe1formed in all cats with
mutation has occurred. Cats are at greatest
suspected FIP. FIP can cause cuffing of tl1e
risk of developing FIP in the first 6-18 mo
retinal vasculature, which appears as fuzzy
after infection with FCoV; the risk decreases grayish lines on either side of the blood to -4% at 36 mo after infection.

vessels. Occasionally, granulomatous

Previously, three different forms of FIP
changes are seen on the retina. Retinal
were distinguished: 1) an effusive,
hemorrhage or detachment may also occur.

exudative, "wet form"; 2) a noneffusive,

These changes, however, are not pathognononexudative, granulomatous, parenchymamonic; similar changes can be seen in other tous "d1y fom1"; and 3) a mixed form. The
systemic infectious diseases, including
first form was characterized by a fibrinous
toxoplasmosis, systemic fungal infections,
peritonitis, pleuritis, and/or pericarditis
and feline inununodeficiency virus or feline
wifu effusion in the abdomen, thorax, and/
leukemia virus infection. Uveitis is another
or pericardium, respectively. The second
common manifestation. Mild uveitis can
form was characterized by granulomatous
manifest by color change of the iris. Uveitis
changes in different organs that may include may also manifest as aqueous flare, with fue eyes and CNS. Differentiation between
cloudiness of the anterior chan1ber, which
tl1ese fo1ms is not useful and is of value only
can be detected in a darkened room using

784

FELINE INFECTIOUS PERITONITIS
focal iJlumination. Large numbers of

Difficulties arise from the lack of noninvainflammatory cells in the anterior chan1ber sive confinnatory tests in cats without
settle on the back of the cornea and cause
obvious effusion. Obtaining and analyzing
keratic precipitates, which may be hidden
effusion is minimally invasive and much
by the nictitating membrane. Hemorrhage
more sensitive than diagnostic tests in
into the anterior chamber can occur. If
blood. In cats with no effusion, several

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aqueous humor is sampled, it may reveal
paran1eters including history, clinical signs,
increased protein and pleocytosis.

laboratory changes, and level of antibody

Neurologic signs are common in cats with titers should be considered to dete1mine FIP. These are variable and reflect the area
whether to use invasive confmnative
of CNS involvement. The lesions are usually
diagnostic methods.

multifocal. The most common clinical
sign is ataxia followed by nystagmus and

Hematology and Serum Biochemistry:

seizures. In addition, incoordination,

WBC counts can be decreased or increased.

intention tremors, hyperesthesia, behavioral

Lyn1phopenia is commonly present, mainly
changes, and cranial ne1ve involvement
caused by apoptosis of uninfected T cells,
can be seen. If cranial ne1ves are involved,
prin1arily CDS• T cells, as a result of high
neurologic signs such as visual deficits and

TNF-a concentrations produced by
loss of menace reflex may be present. When
vims-infected macrophages. However,

FIP lesions are located on a peripheral nerve lyn1phopenia in combination with or the spinal column, lan1eness, progressive
neutrophilia can occur in many severe
ataxia, or paresis may be seen. Finding
diseases in cats. A mild to moderate
hydrocephalus on a CT scan is suggestive
nomegenerative anemia is another
of neurologic FIP. In a study of 24 cats with
nonspecific finding that may be seen

FIP with neurologic involvement, 75% were
in almost any chronic disease i.n cats.

fow1d to have hydrocephalus on postm01�

The most common laboratory abnommlity
tern examination.

in cats witl1 FIP is an increase in total serum

Solitary mural intestinal lesions have
protein concentration caused by increased
been described in cats with a histologic
globulins, mainly-y-globulins, which occurs
diagnosis of FIP. Diarrhea, vomiting, or
in > 7(1'/o of cats with FIP. Total protein in cats obstruction can occur, and a suspected
with FIP can reach very high concentrations
neoplastic mass can be found in the colon
of�l2 gtc!L. The albwnin to globulin ratio,
or ileocecocolicjunction, with associated
however, has a significantly higher diagnostic
lymphadenopathy, and a markedly
value to distinguish FIP from other diseases
thickened and finn segment of bowel with
than total serum protein or-y-globulin
multifocal pyogranulomas extending
concentrations, because serwn albUl11in also
through the intestinal wall on histology.

may decrease. Albun1in loss in cats with FIP

Skin fragility syndrome was described in
may be caused by glomerulonephritis
a cat with FIP, -and other skin lesions ( eg,
secondary to inm1une complex deposition,
nodular skin lesions, papular skin lesions,
by loss of protein due to exudative enteropapododermatitis) may be present as well.

thy in cases of granulomatous changes in the

Reproductive disorders, neonatal deaths,
intestines, or by extravasation of protein-rich
and fading kittens ar{! not usually associated fluid during vasculitis. An optimal cut-off withFIP.

value of0.8 was detem1ined for the albun1in
to globulin ratio ( specificity 82%, sensitivity

Lesions: Histology of lesions is usually

8C/'/o). If the serum albrn11in to globulin ratio is pathognomonic and is traditionally

<0.8, the probability that the cat has FIP is
considered the gold standard for diagnosis
high (92% positive predictive value [PPV]); if
ofFIP. H&E-stained samples typically
the albwnin to globulin ratio is >0.8, the cat
contain localized perivascular mixed
likely does not have FIP (61 % negative
inflanm1ation with macrophages, neutropredictive value [NPV]). Reference labphils, lymphocytes, and plasma cells. FCoV
orato1ies have variation in techniques for
can be identified by inm1unohistochemistry
measurement of serwn proteins. Senun
in the macrophages within the lesions.

protein electrophoresis may be perfo1med

Pyogranulomas may be large and consoliin cats witl1 suspected FIP to distinguish a dated, sometin1es with focal tissue necrosis,
polyclonal from a monoclonal hypergan1maor numerous and small. Lymphoid tissues in globulinemia to differentiate FIP ( and other
cats with FIP often show lymphoid
chronic infection) from ttunors such as
depletion caused by apoptosis.

multiple myelomas or other plasma cell
ttm10rs. However, hyperglobulinernia is

Diagnosis: Reliable and rapid diagnosis
generally nonspecific and reflects active
of FIP is in1porta.nt but can be challenging.

inflanmmtion.

FELINE INFECTIOUS PERITONITIS

785

Other laboratory parameters, including
yellow effusions of sticky consistency are
liver enzymes, bilimbin, urea ( or BUN),
considered typical, the presence of this
and creatinine, can be variably increased
type of fluid in body cavities alone is not
depending on the degree and localization
diagnostic. Cases with pure chylous effusion
of organ damage but are not helpful in
have been reported. Usually, the protein
establishing an etiologic diagnosis.

content is very high (>3.5 g/dL), consistent

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Hyperbilimbinemia and ictems are often
with an exudate, whereas the cellular
seen in cats with FIP. High bilimbin (in the
content is low ( <5,000 nucleated cells/mL),
absence of hemolysis) and increased liver
resembling a modified transudate or even
enzyme activity should raise the suspicion
pure transudate. Major differential diagnoses
of FIP
for these effusions include inflanunatory

High serwn levels (>3 mg/mL) of a-1-acid
liver disease, lymphoma, heart failure, and
glycoprotein (AGP), a semm acute phase
bacte1ial peritonitis or pleuritis. LDH activity
protein that is increased in cats with FIP,
typically is high (>300 IU/L). Cytology is
can supp01t diagnosis, but levels also are
vatiable but often consists predominantly of
increased in other inflanunatory conditions;
macrophages and nondegenerate neutrothus, these changes are not specific.

phils (in much lower numbers than seen with

Additionally, AGP may also be high in
bacterial infection). These effusions can
asymptomatic cats infected with FCoV,
usually be differentiated from bacterial
especially in households where FCo V is
infection or lymphoma by the presence of
endemic. However, the most prominent
malignant cells, degenerate neutrophils,
increases in serwn AGP concentration have
or intracellular bacteria on cytology and
been recorded in cats with FIP Levels of
bacterial growth on culture, respectively.

AGP in semm and effusions increased 2- to

The albumin to globulin ratio of the effusion

5-fold in cats with FIP, more than in diseases
can be measured: a ratio of <0.5 is strongly
such as neoplasia and cardiomyopathy. In
correlated with FIP, with a PPV between 66%
a study with a small number of cases,
and 95%, depending on the prevalence of FIP
measurement of semm AGP concentrations
in the cat's envirorn11ent. An albwnin to
was demonstrated to be most helpful,
globulin ratio >0.81 has a lOOOAi NPV,
because it was the only diagnostic test in
essentially excluding FIP
complete concordance with inununohisto

Rivalta's test is a sinlple, inexpensive
chemistry. Two factors must be considered
method that does not require special
when evaluating AGP concentration to
laboratory equipment and can be perfom1ed
support a clinical diagnosis of FIP: the
easily in private practice. It is very useful in
magnitude of the increase in concentration
cats to differentiate between effusions
and the pretest probability of FIP ( compatcaused by FIP and effusions caused by otl1er ible history and clinical findings). Semm
diseases. The high protein content and high
an1yloid A (SAA), another acute phase
concentrations of fibrin and infla.nunatory
protein, increases 10-fold in the semm of
mediators lead to a positive reaction. To
cats with FIP compared with asymptomatic
perform the test, a transparent reagent tube
cats exposed to feline enteric coronavimses.

( 10 mL) is filled with -8 mL distilled water, to

SAA may be a useful biomarker in the future. which 1 drop of acetic acid (highly concen

Diagnostic Imaging: A recent study
trated vinegar, 98%) is added and mixed
highlighted specific concurrent ultrasonothoroughly. On the surface of this solution, 1
graphic findings that should increase the
drop of the effusion fluid is carefully layered.

index of suspicion for FIP, including

If the drop disappears and the solution
abdominal lymphadenopathy, peritoneal
remains clear, the Rivalta's test is defined as
or retroperitoneal effusion, renomegaly,

.negative. If the drop retains its shape, stays
irregular renal contour, hypoechoic
attached to the surface, or slowly floats
subcapsular echogenicity, and diffuse
down to the bottom of the tube (drop- or
changes within the intestines. In most cats
jelly-fish-like), the test is defined as positive.

in the study population, the liver and spleen

Rivalta's test has a high PPV (86%) and a very
were normal in echogenicity. A nom1al
high NPV (96%) for FIP Positive results can
abdominal ultrasound does not exclude
sometin1es be seen in cats with bacterial
the possibility of FIP infection.

peritonitis or lymphoma. Those effusions,
however, are usually easy to differentiate

Effusion Fluid: Tests on effusion have
through macroscopic exanlination, cytology,
a much higher diagnostic value than tests
and bacterial culture.

performed on blood. Fluid can be obtained
through ultrasound-guided fine-needle

Cerebrospinal Fluid: Analysis of
aspiration or by using the "flying cat
cerebrospinal fluid (CSF) from cats with
technique" in case of ascites. Although clear
neurologic signs due to FIP lesions may

786

FELINE INFECTIOUS PERITONITIS
reveal increased protein (50-350 mg/dL with

Feline Coronavirus Reverse Transcripa normal value of <25 mg/dL) and pleocytotase PCR: FCoV reverse transcriptase PCR
sis (100-10,000 nucleated cells/mL)

in blood is used with increasing frequency as
containing mainly neutrophils, lymphocytes, a diagnostic tool for FlP. However, so far, no and macrophages ( a relatively nonspecific

PCR has been developed that can definifinding). Many cats with neurologic signs tively diagnose FlP. PCR can be false-nega

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caused by FIP have nonnal CSF. In one
tive ( eg, because the assay requires reverse
study, typical CSF findings in cats with FIP
transcription of viral RNA to DNA before
were a protein concentration >200 mg/dL
amplification of DNA, and degradation of
and a WBC count of> 100 cells/itL, which

RNA can occLrr clue to contan1ination with
consisted predominantly of neutrophils.

ubiquitous RNAases) or false-positive ( eg,

Measurement of Antibodies: There is
the assay does not distinguish between
no FIP-specific antibody test; all that can
vimlent and avirulent FCoV strains and will
be measured is antibodies against FCoV.

not discrin1inate FCo V from coronavimses

Antibody titers measured j.n serum are
of other species). Furthermore, viremia
extensively used as a diagnostic tool.

appears to occur not only in cats with FIP

However, most FCoV antibody-positive cats
but also in healthy carriers. FCoV RNA has
never develop FlP. Thus, antibody titers
been detected in the blood of cats with FIP
must be interpreted extremely cautiously
but also in healtl1y cats that did not develop
and should never be used as tl1e sole test to

FlP for as long as 70 mo. Therefore, tl1e
diagnose FlP. Antibody testing still has a
results of PCR tests in general must be
certain role h1 the diagnosis and, more
interpreted carefully, and PCR catmot be
importantly, in the management of multicat
used as a tool to definitively diagnose FlP.

households, when done by appropriate

PCR has been used to detect rcov in
methodologies and when results are
fecal samples, and it is sensitive and useful
properly inte1preted. However, antibody
to clocw11ent that a cat is shedding FCo Vin
testing can only be useful if the laboratory
feces. The strengtl1 of the PCR signal in
is reliable and consistent. Low or mediwn
feces correlates with the amount of virus
titers have no diagnostic value. If interpreted present in the intestines. These results can carefully, however, ve1y high titers can be of
be useful to detect cats that chronically
certain diagnostic value. A very high titer in
shed high virus loads and that pose a high
a cat with compatible clinical signs (1: 1,600)

risk in multicat households.

has a 94% PPV for FlP; a negative titer has a
lmmunostaining of Feline Coronavirus

90% NPV for FIP Cats with high antibody

Antigen: Direct staining ofFCoVs within
titers are more likely to shed FCo V and to
macrophages by inununofluorescence in
shed more consistently higher amotµ1ts
cytocentrifuged effusions or inu11 unohistoof the vi.ms. Thus, the titer is directly chemistry in tissue is considered the most
correlated with virus replication rate and tl1e specific test to confirm FlP. Inm1unostai11ing an1ount of vims fn the intestines. S creening
crumot differentiate between tl1e "hru·mless"

a cattery for the presence of FCo V or

FCoV and FIP-causing FCoV, butfmding
screening a cat before introduction into an
irLfected macrophages in characteristic

FCoV-free cattery are additional indications.

pyogranulomatous lesions or in inflruruna

Measuring antibodies in fluids ( eg,
tory effusions is highly associated with FlP.

effusion, CSF) other than blood has been

In a recent study in which a large nwnber of
investigated. D etection of anticoronavirus
cats with coniinnecl FIP and controls with
antibodies in effusion fluid has a PPV ofOO'Ai
other confirmed dis!'!ases were investigated,
and aNPVof29"Aifor diagnosis ofFIP.

positive imrnunofluorescence staining of

Presence of antibodies in effusion is
intracellular FCoV anti.gen in macrophages
correlated with tl1e presence of antibodies in
of tl1e effusion was 100%predictive ofFIP.

blood; thus, antibody titers in effusions are

Unfortunately, the NPV of the test is not
not very helpful. One study investigating the
very high (57%), which can be explained by
diagnostic value of antibody detection in CSF
low nwnbers of macrophages on effusion
reported a very good correlation to the
smears resulting in negative staining.

presence of FIP when compared with

Inm1unohistochemistry can be used to
histopathology; however, two studies
detect the expression ofFCoV antigen in
investigating a large nun1ber of cats presented tissue and is also 100% predictive of FIP if to veterinary teaching hospitals revealed no
positive. However, invasive methods (eg,
significant difference in antibody titers in CSF
laparotomy or laparoscopy) are usually
from cats with neurologic signs due to FIP
necessary to obtain appropriate tissue
compared witl1 cats with other nemologic
san1ples. Eitl1er histology itself is confirmadiseases confinned by histopathology.

tive, or immunohistochemistry staining of

FELINE INFECTIOUS PERITONITIS

78.7

FCoV antigen in tissue macrophages can be

Immune modulators ( eg, Propionibacle
used to diagnose FIP.

rium acnes, acemannan, tylosin, promodulin, interferon-a) have been used to treat Treatment, Control, and Prevention:

cats with FIP. However, controlled trials are

Because of the high prevalence of FCo V
lacking, and anecdotal reports often lack
antibodies in healthy cats, widespread
definitive diagnosis. It has been suggested
antibody testing of healthy cats is not an

VetBooks.ir
that these agents may benefit infected
appropriate screening test for FIP in pet
ani.nlals by restoring compromised inunune
cats. Nor should cats in shelters be screened function. However, a nonspecific stimulafor antibodies before adoption. No tion of the inunune system would seem to
treatment of healthy antibody-positive
be contraindicated in FIP, because clinical
cats has been shown to prevent developsigns develop and progress as a result of an ment of FTP.

immune-mediated response.

Treatment of cats with FIP remains

A nun1ber of studies have investigated
frustrating and is lin1ited to the cases that
effectiveness of various antiviral treatments
respond favorably within the first few days.

in cats with FIP, including interferons and

The prognosis for a cat with FIP is very
libavirin. To date, none have proved to be
poor. In a prospective study including 43
very successful. See TABLE 7.

cats with confirmed FIP, the median survival

Interferons have been used frequently in
after the definitive diagnosis was 9 days.

cats with FIP. Human interferon-a has a

Some cats, however, may live for several
direct antiviral effect, and in vitro antiviral
months. Factors that indicate a poor
efficacy against an FIP-causing FCoV strain
prognosis and a short survival time are low
has been demonstrated. In a controlled

Karnofsky score (index for quality of life),
study, cats with confirmed FIP treated with
low platelet count, low lymphocyte count,
interferon-a at 106 IU/kg in combination
high bilirubin concentration, and a large
with Propionibacterium acnes survived for
amount of effusion. Seizures are an

-3 wk. Feline interferon-w is available in
unfavorable prognostic sign; they are
some European cow1tries and Japan.

significantly more frequent in cats with

FCoV replication is i.nllibited by feline
marked extension of the inflan1matory
interferon-win vitro, but there was no
lesions to the fore brain. Cats that show no
statistically significant difference in the
improvement within 3 days after treatment
mean survival time of cats enrolled in a
initiation are unlikely to show any benefit
randomized placebo-controlled doublefrom therapy, and euthanasia should be blind treatment trial. Cats survived for
considered. Longer survival or remission

3-200 days, regardless of whether they
from clinical signs is rare.

received the drug or placebo.

Supportive treatment is aimed at suppressing the immune overreaction, usually Management of Exposed Cats:

using corticosteroids. However, there are

When a cat in a household develo{ls FIP,
no controlled studies that indicate whether
all in-contact cats will have already been
corticosteroids have any beneficial effect.

exposed to the same FCoV. Under natural

Cats treated with corticosteroids have shown circwnstances, it appears that the FIP-causanecdotal improvement for as long as ing virus strain is not excreted in such cases,
several months. Inununosuppressive drugs
and FIP is not transmitted from cat to cat.

such as pred.nisolone (2-4 mg/kg/day, PO)

However, under experimental conditions it
are commonly used. More potent cytotoxic
has been possible to transmit FIP-causing
drugs such as cyclophosphamide ( 4 mg/kg/
virus from a cat with FIP to in-contact cats.

day) have also been suggested. Cats with

Still, it appears to be relatively safe for a cat
large effusions benefit from removal of the
with FIP to remain in the same household
fluid; ir\jection of dexan1ethasone into the
with cats that have already been in contact
abdominal or thoracic cavity may follow
to the FCo V strain. However, it is not

(1 mg/kg/day until no effusion is present).

recommended to allow contact between

Cats with FIP should receive supportive
a cat with FIP and any new "naive" cat.

therapy, including fluids and nutritional

Kittens, which are more susceptible to FIP
support, and their quality of life should be
than adults, should not be introduced to
monitored. Anecdotal reports suggest that
households with a recent history of FIP.

ozagrel hydrochloride, a thromboxane

If a cat has been euthanized or has died
sy.nthetase inhibitor that inhibits platelet
due to FIP, the owner should wait 2 mo
aggregation, and pentoxifylli.ne, a drug that
before obtaining another cat. FCoV can
decreases vasculitis and inhibits several
remain infectious for at least 7 wk in the
cytokines (such as interleukins and TNF-a),
environment, particularly where litter boxes
may be beneficial in some cats.

are in use. Other cats currently in the

788

FELINE INFECTIOUS PERITONITIS
household are most likely infected with
and other rnulticat homes, there is virtually
and shedding FCoV. Cats are conunonly
nothing to prevent FIP
presented to the veterinarian for evaluation

Various tactics have been used to
after contact with a cat with FIP or a
eliminate FCo V from an endemic cattery.

suspected or known virus excretor. The

Reducing the number of cats ( especially of
owner may want to know the prognosis for
kittens <12 mo old) and keeping suspected

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the exposed cat or whether it is shedding

FCoV-contarninated surfaces clean can

FCo V. Such cats will likely be antibody
minimize population loads of the virus.

positive, because 95%-lOOOAi of cats exposed

Antibody or fecal PCR testing and removal
to FCoV become infected and develop
of positive cats should be performed to stop
antibodies -2-3 wk after exposure. A few
exposure and reinfection of recovered cats.

cats may be resistant to FCo V infection.

Approximately 1 13 of antibody-positive cats Some cats in FCoV-endemic multicat
excrete virus; thus, every antibody-positive
households continuously remain antibody
cat should be considered infectious. After
negative. The mechanism of action for this

3-6 mo, antibody titers can be retested.

resistance is unknown.

Alternatively, PCR testing of ( several) fecal

Although exposed cats will most likely
samples can be performed to detect chronic
have antibodies, this is not necessarily

FCo V carriers; these cats should be
associated with a poor prognosis. Most
removed. In large, multicat environments,
cats infected with FCoV will not develop

400/o-600Ai of cats shed virus in their feces at FIP, and many cats in single- or two-cat
any given time. Approximately 200Ai will shed
households will eventually clear the
virus persistently. If a cat remains persisinfection and become antibody negative in tently PCR-positive for >6 wk, it should be
a few months to years (usually -61110). If
placed in a single-cat environment or with
titers are monitored, cats should be retested
other chronic shedders.

( using the same laboratory) every 6--12 mo

Kittens of FCo V-shedding queens are
until the antibody test is negative. Some cats often protected from infection by materwill remain antibody positive for years. The nally derived antibodies until they are 5-6
value of serial antibody or PCR testing is
wk old. An early weaning protocol for
mostly limited to protocols aimed at
prevention of FCo V infection in kittens has
creating FCoV-free closed catteries.

been proposed and consists of isolation of
queens 2 wk before parturition, strict

Management of Multicat Households:

quarantine of queen and kittens, and early

In most multicat households with unusually
weaning at 5 wk of age. Early removal of
high cat numbers, FCo V is endemic and FIP
kittens from the queen and prevention of
is almost inevitable. Households of <5 cats
infection from other cats may succeed in
may spontaneously and naturally become
keeping kittens free of infection. Kittens

FCo V-free, but in households of> 10 cats per should be taken to a new home (with no group, this is almost impossible because

FCo V -infected cats) at 5 wk of age. Although
the virus passes from one cat to another,
straightforward in concept, the protocol
maintaining the infection. In these
requires quarantine rooms and procedures

FCoV-endemic environments, such as
to ensure that new virus does not enter.

breeding catteries, shelt,ers, foster homes,

Special care must be taken during this

DRUGS THAT HAVE BEEN SUGGESTED FOR USE IN FELINE

INFECTIOUS PERITONITIS CASES

ABCD Recommendation

Druga

Comment

(EBM LeveJb)

ANTIVIRALS

Ribavirin

Active in vitro but toxic in cats

Not reconunended (2)

Vidarabin

Active in vitro but toxic in cats

Likely ineffective ( 4)

Human interferon-a, Although effective in vitro

Ineffective (2)

SC, high dose
against FCoV, SC treatment did
not work in an experimental trial

FELINE INFECTIOUS PERITONITIS

789

DRUGS THAT HAVE BEEN SUGGESTED FOR USE IN FELINE

INFECTIOUS PERITONITIS CASES (continued)

ABCD Recommendation

Druga

Comment

(EBM Levelb)

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Human interferon-ex, No trials. Only acts as immu

Contraindicated (4)

PO,low dose
nostimulant if given orally;
inunune stinrnlation should be
avoided in cats with FIP

Feline interferon-w

Single placebo-controlled study No benefit was observed (level of naturally occurring cases and 1 study); may require further one uncontrolled study
studies in view of anecdotal
clinical evidence ( 4)

Polyprenyl

Upregulation biosynthesis of

May have some beneficial
immunostinrnlant
mRNA ofTHl cytokines,
effect in noneffusive FIP (3);

(investigational
uncontrolled study treating three controlled studies required drug)

noneffusive cases, long survival

IMMUNOSUPPRESSANTS

Prednisolone/

No controlled studies; some

Currently supportive treatment
dexarnethasone
cats improved during treatment of choice (3); if effusion is (immunosuppresand survived for several
present, dexamethasone
sive doses)

months; does not cure FIP
intrathoracic or intraperitoneal
may be helpful

Pentoxyfylline

Aimed at treating vasculitis

Ineffective in one case study ( 4)

Ozagrel

Thromboxane synthesis inhibitor Controlled studies needed (3) hydrochloride
aimed at treating inflammatory
response; only used in two cases
with beneficial effect

Cyclosporin A

Irnrnunosuppressive; no

Not recommended; more directpublished studies
ed against cellular inlfnunity
than humoral (lack of data) ( 4)

Cyclophospharnide Irnrnunosuppressive; no

Might be considered in combinapublished studies
tion with glucocorticoids ( 4)

Chlorambucil

Immunosuppressive; no

Might be considered in combinapublished studies
tion with glucocorticoids ( 4)

Azathioprine

Toxic in cats; irnmunosuppres

Not recommended ( 4)

sive; no published studies

Acetylsalicylic acid To treat inflammatory response May have some beneficial (aspirin), platelet
as well as vasculitis; no
effect, but adverse effects
inhibitory dosage
published studies
possible if used in combination
with high-dose glucocorticoids
a Many of the treatments listed represent extra-label use for treatment of FIP.

b Evidence-based medicine (EBM) level 1 = confirmed by randomized controlled clinical trials in target species; EBM level 2 = confhmed by randomized controlled experimental studies in target species; EBM level 3 = suppmted by case series, other experimental studies, nonrandomized clinical trials; EBM level 4 = based on expe1t opinion, case reports, studies in other species. Modified, with permission, from Feline infectious pe1itonitis. Guidelines of The Ew-opean Advisory Board on Cat Diseases (ABCD), © 2012 Advisory Board on Cat Diseases.

790

FELINE INFECTIOUS PERITONITIS
period to socialize the kittens. The success
understand that FCoV is an unavoidable
of early weaning and isolation depends on
consequence of endemic FCo Vin multicat
effective quarantine and low numbers of
environments. Good husbandry practices
cats ( <5) in the household.

and facilities that can be cleaned easily may

Another possible approach is to
minin1ize virus spread.

maxin1ize heritable resistance to FIP in

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breeding catteries. Genetic predisposition

Vaccination: A vaccine developed with a
plays a role in the disease but is not
temperature-sensitive mutant of the FCoV
completely understood. Full-sibling
strain DF2-FIPV, which is reported to
littennates of kittens with FIP have a higher
replicate in the cool lining of the upper
likelihood of developing FIP than other cats
respiratory tract but not at higher internal
in the same environment. A cat that has two
body temperature, is available in the USA,
or more litters in which kittens develop FIP

Canada, and Europe. This vaccine is
should not be bred again. Particular
administered intra.nasally and produces
attention should be paid to pedigrees of
local inununity (IgA antibodies) at the site
toms in which FIP is overrepresented.

where FCoV first enters the body (the

Because line breeding often uses valuable
oropharynx), as well as cell-mediated
tomcats extensively, eliminating such
immunity. Vaccination in an FCoV-endemic
anin1als may have an effect on in1proving
envirorm1ent or in a household with known
overall resistance.

cases of FIP is not effective, probably

In shelters, prevention of FIP is virtually
because most cats are already seropositive
in1possible unless cats are strictly separated
for FCo V. The vaccine is labeled for use
and handled only through sterile handling
begiru1ing at 16 wk of age, which may be
devices (comparable to isolation w1its).

too late to protect kittens against FCo Vin

Isolation is often not effective because
endemic populations. Most cats develop

FCoV is easily transported on clothes,
systemic antibodies after vaccination, thus
shoes, dust, and cats. There appears to be
making the establishment and control of an
significant correlation between the number

FCoV-free household difficult. The American
of handling events outside the cages and

Association of Feline Practitioners lists the
stress and the percentage of antibody -posi

FIP vaccine as "not reconm1ended."

tive cats. Studies have shown dran1atic
increases in fecal shedding of FCo V in
infected cats after entering an animal

Zoonotic Risk: Although corona.viruses
shelter. Half of the cats that were originally
shared with anin1als, such as severe acute

FCoV-negative were shedding FCoV within
respiratory syndrome (SARS) and Middle

1 wk of entering the shelter environment.

East respiratory syndrome (MERS), are

Shelters should have written information
responsible for severe respiratory disease
sheets or contracts infom1ing adopters
outbreaks in people, there is no indication
about FCo V and FlP Personnel should
that FCo Vis infectious to people.

FELINE LEUKEMIA VIRUS AND

RELATED DISEASES

(Feline lymphoma and leukemia, Lymphosarco�a)

Feline leukemia virus (FeLV) remains one of tion, diagnosis, and management of FeLV for the most important infectious diseases of
veterinary practitioners in private practice,
cats globally. It manifests primarily through
animal shelters, and catteries ( see TABLE 8).

profound anemia, malignancies, and
immunosuppression and infects domestic

Etiology and Epidemiology: FeLV is a
cats and other species of Felidae. In the
retrovirus in the family Oncovirinae. Other
laboratory, cells from a much wider range
oncoviruses include feline sarcoma virus,
of species can be infected by some strains
mouse leukemia viruses, and two human
of the virns.

T-lymphotropic viruses. Although oncogen

The Feline Retrovirus Management
esis is one of their more dramatic effects,

Guidelines published by the American
oncoviruses cause many other conditions,

Association of Feline Practitioners is a key
including degenerative, proliferative, and
resource for expert consensus on preven-
inununologic disorders.

FELINE LEUKEMIA VIRUS AND RELATED DISEASES

791
itM•i:I SUMMARY OF CLINICAL MANAGEMENT OF FELINE RETROVIRUS

Test cats that

Sick regardless of age and previous test status
are:

Entering a new household

30 days since last high potential for exposure

At risk with unknown infection status

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Receiving routine veterinary care and have outdoor access or live in a home with FeLV-positive cats

Candidates for blood donation

Vaccinate cats

Kittens, as part of the initial vaccination series
that are:

Often outdoors

In transient group situations such as foster homes or temporary colony housing

Living with known FeLV-positive cats

Note: All cats should be tested for FeLV before vaccination.

Diagnostic

Antigen tests do not detect previous vaccination.

considerations

Positive results on immunofluorescent assay or PCR confirm positive infection status, but a negative result creates a discordant situation that clouds confirmation of true infection status.

Current test modalities cannot exclude the potential of a regressive infection with subsequent negative tests after any initial positive result.

Management of Infected cats may have a good quality of life.

infected cats

Although many cats succumb within 3 yr of diagnosis, others remain clinically healthy for multiple years.

Preventive veterinary care, including frequent physical examination, laboratory monitoring, core vaccination, spay/neuter surgery, dental prophylaxis, and parasite control, is essential.

Avoid transmission to other cats by preventing access to outdoors and other uninfected cats in household.

Many antiviral and inununotherapeutic treatments are described in early trials or anecdotal use, but none has both wide availability and demonstrated clinical efficacy in controlled field studies.

Adapted from the Feline Retrovirus Management Guidelines, American Association of Feline Practitioners, 2008.

There are four FeLV subgroups of clinical
attributed to testing and vaccination efforts.

in1portance. Almost all naturally infected

In the USA, 3.1 % of cats in a large, nationcats are originally infected by FeLV-A, the wide data set tested positive for FeLV in
original, archetypical fom1 of the virus.

2010, with increased risk an10ng outdoor

Additional mutated forms of the original
cats, unneutered males, and cats with other

FeLV-A subtype as well as FeLV-B, FeLV-C,
disease conditions (particularly respiratory
or FeLV-T may develop in infected cats.

disease, oral disease, and abscessation).

FeLV-B increases the frequency of

Prevalence was highest in the mid western
neoplastic diseases; FeLV-C is strongly
and western regions of the USA and lowest
associated with development of erythroid
in the northeast. Seroprevalence surveys of
hypoplasia and consequent severe anemia;
varying statistical power have found rates
and FeLV-T has the propensity to infect and
of positive test results to range from 3.6%
destroy T lymphocytes, leading to lymphoid
in Germany and Canada to 4.6% in Egypt
depletion and immunodeficiency. Viruses of
and 24.5% in Thailand.

all four subgroups are detected (but cannot

Persistently infected, healtlly cats serve
be distinguished) by commonly used FeLV
as reservoirs ofFeLV for botll vertical and
diagnostic test kits.

horizontal viral transmission. Oronasal

The prevalence of FeLV infection
contact with infectious saliva or urine
documented in cross-sectional surveys
represents the most likely mode of
in North An1erica has been declining
horizontal transmission; vertical transmisthroughout the past three decades and is sion in utero or through nursing is also

792

FELINE LEUKEMIA VIRUS AND RELATED DISEASES
conunon. Tears and feces may contain
followed by complete clearance of viral
vims but are not considered to be clinically
infection. However, improved sensitivity of
significant in disease transmission or

PCR testing has revealed that antigen-negadiagnostic detection. Although direct tive cats may still harbor FeLV provirus in
contact, mutual grooming, and shared
tissues; this is termed regressive infection.

litter trays and food dishes are the prin1ary

It is believed that cats with regressive

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methods of horizontal transmission,
infections generally are aviremic, do not
infection through bite wow1ds is possible.

shed infectious virus, and do not develop

In a national (USA) study, FeLV infection

FeLV-associated diseases; however, they are
was diagnosed in 9% of cats w1dergoing
considered carriers with the potential for
treatment for bite wounds, approximately
reactivation and future shedding. It is likely
three ti.mes the rate for cats in general.

that FeLV can be transmitted by blood

Because FeLV is a fragile, enveloped virus,
transfusion from cats with regressive
horizontal transmission between adults
infection, so feline blood donors should
usually requires prolonged, intimate contact. have PCR testing performed as a screening In addition, the dose required for oronasal
test before donating. The incidence of
transmission of the vims is relatively high.

regressive infections and the causes and

FeLV is considered to be an age-dependfrequency of reactivation of viral shedding ent disease; yow1g kittens are at higher risk

,unong these cats are incompletely underof progressive infection and more rapid stood. Focal infections, rare in natural
disease progression, whereas adults display
infections, involve viral replication in
some degree of age resistance. However,
specific tissues, such as the eyes or bladder,
transmission can occur at any age, and
releasing low levels of viral antigen and,
factors affecting clinical comse of disease
therefore, variable results on diagnostic
are complex and incompletely understood.

testing.

Disorders Caused b

Pathogenesis: After oronasal inoculay FeLV: FeLVrelated disorders are numerous and include tion, the vims first replicates in oropharynanemia, neoplasia, irnmw1osuppression, geal lymphoid tissue. From there, virus is
inunune-mediated diseases, reproductive
carried in blood mononuclear cells to
problems, enteritis, neurologic dysfunction,
spleen, lymph nodes, epithelial cells of
and stomatitis.

the intestine and bladder, salivary glands,

The anemia caused by FeLV is typically
and bone marrow. Virus also appears in
nonregenerative and nom1ochromic. Less
secretions and excretions of these tissues
conunonly, macrocytosis or regenerative
and in peripheral blood leukocytes and
hemolytic anemia is seen in only 1 ()OA, of
platelets. Viremia is usually evident 2-4.wk

FeLV-induced anemia. cases. The cause of
after infection. The acute stage ofFeLV
nonregenerative anemia is usually bone
infection occurring 2-6 wk after infection is
marrow suppression due to viral infection
rarely detected but typically characterized
of the hematopoietic stem cells and the
by mild fever, malaise, lymphadenopathy,
supporting stromal cells. Platelet dysfuncand blood cytopenias. Cats w1able to mow1t tion, tlirombocytopenia, and neutropenia
an adequate immune response become
are all possible sequelae as well.

persistently viremic and develop a

Lymphoma is the most frequently diagprogressive infection, often leading to fatal nosed malignancy of cats. Tuniors such as
disease. Oncogenesis occurs when FeLV
lymphoma and lymphoid leukemia develop
vims inserts into tl1e host cellular genome,
in as many as 300A, of cats with progressive
either in proximity to an oncogene resulting FeLV infections. Regressive infections are in activation or directly into the oncogene
also implicated in the occurrence of these
itself to form a recombinant subgroup virus
ttunors in the absence of viremia, but cats
such as FeLV-B tl1at can induce new neowith progressive infections may face an plastic activity in any cell the recombinant
increased risk of lymphoma development as
vims enters.

high as 60-fold. Most American ca.ts with

The most recent classification system
mediastinal, multicentric, or spinal forms
for FeLV labels infections as progressive,
of lymphoma are FeLV-positive. However,
abortive, regressive, and focal. Progressive
these forms of lymphoma are becoming
infections are defined by uninhibited viral
less common as the prevalence of FeLV
replication with subsequent persistent
decreases. Diffuse GI lymphoma is now
viremia and probable eventual manifestamore likely to be found in FeLV-negative tion of clinical disease. Previously, most
cats of middle or older agf' and can be
adult cats were thought to have abortive
difficult to differentiate from inflan1matory
infections in which transient viremia was
bowel disease. Fibrosarcomas and

FELINE LEUKEMIA VIRUS AND RELATED DISEASES

793
quasi-neoplastic disorders such as multiple
and early mortality collectively termed
cartilaginous exostoses ( osteochondroma

"fading kitten syndrome." It is likely that tosis) can be FeLV-associated. Other types
transmission from infected queens to their
of tumors share a suspected but not yet
kittens is the single greatest source of FeLV
clearly defined link with the FeLV virus.

infections.

Leukemia is characterized by the

Coinfection with FeLV and feline panle

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neoplastic proliferation of hematopoietic
ukopenia virus (FPV) has been inlplicated
cells originating in the bone marrow,
in feline panleukopenia-like syndrome
including neutrophils, basophils, eosino

(FPLS), which is also termed FeLV-associphils, monocytes, lymphocytes, megakaryoated enteritis. FPLS resembles feline panleucytes, and erythrocytes. Feline leukemias kopenia both clinically and histopathologiare strongly associated with FeLV infection cally and is characterized clinically by
and typically involve neoplastic cells
progressive anorexia, depression,
circulating in the blood. Lymphoid
vomiting, hemon-hagic diarrhea, weight
leukemias are further classified as acute and loss, gingivitis, oral ulceration, severe chronic. Acute lymphocytic leukemia is

:neutropenia, and septicemia FPV antigen is
characterized by lymphoblasts circulating
inconsistently present on diagnostic testing
in the blood, whereas chronic lymphocytic
in tl1ese cases, and the pathogenesis and
leukemias have an increased number of
exact role of each virus in the development
circulating lymphocytes with mature
of this syndrome are incompletely
morphology.

understood.

The immunosuppression caused by FeLV

Although neurologic disorders associcreates increased susceptibility to bacterial, ated with FeLV are most often caused by
fungal, protozoal, and viral infections.

compression of the brain and spinal cord

Numbers of neutrophils and lymphocytes in
by lymphoma tumor tissue, a mechanism
the peripheral blood of affected cats may be
for :neuropathology is also suspected to
reduced, and those cells that are present
result in peripheral neuropathies, urinary
may be dysfunctional. Many FeLV-positive
incontinence, and ocular pathology,
cats have low blood concentrations of
including anisocoria, mydriasis, Homer
complement; this contributes to FeLV-assosyndrome, and central blindness even in ciated immunodeficiency and oncogenicity,
the absence of visible compressive lesions
because complement is vital for some fom1s on diagnostic imaging. If antineoplastic of antibody-mediated tumor cell lysis.

therapy is planned, it is inlportant to

Immune complexes formed in the
distinguish neoplasia from neuropathy.

presence of moderate antigen excess can

Stomatitis is more classically associated
cause systemic vasculitis, glomerulonephriwith FIV infection, but FeLV infection can tis, polyarthritis, and a variety of other
also predispose cats to chronic ulcerative
inunune disorders. In FeLV-infected cats,
proliferative gingivostomatitis. Clinical
inlmune complexes form under conditions
sequelae include pain, anorexia, and tooth
in which FeLV antigens are abundant and
loss. An immune-mediated mechanism is
anti-FeLV IgG antibodies are sparse, a
likely, particularly in combination with
situation ideal for the development of
coinfectio:ns such as feline calicivirus.

immune-mediated disease.

Reproductive problems are commonly

Diagnosis: Testing for FeLV infection is
associated with FeLV infection. Fetal
recommended when cats are first acquired,
death, resorption, and placental involution
before vaccination against FeLV, if there has
may occur in the middle trimester of
been potential exposure or bite wound from
pregnancy, presumably as a result of
a cat of w1known or positive retro viral
in utero infection of fetuses by virus
status; annually if they live in a household
transported across the placenta in
witl1 FeLV-positive cats; before blood
maternal leukocytes. Abortion typically
donation; and regularly if they have outdoor
occurs in late gestation accompanied by
access. For cats entering a new home or
risk of bacterial endometritis, especially in
known to be at high risk of exposure, testing
neutropenic queens. Transmission during
should be repeated 30 days after the first test
birth and nursing constitutes the greatest
in case of recent infection that has not yet
risk of producing live, viremic kittens.

resulted in detectable circulating antigen.

There is some evidence that regressively

Documentation of a previous :negative test
infected queens may pass virus on to their
does not negate the need for repeat testing
kittens either in utero or in milk. Neonatal
in the above situations. Prior vaccination
kittens are at risk of rapidly progressive
does not interfere with diagnostic testing
infection with clinical manifestations of
unless perfom1ed in1mediately before blood
hypothermia, dehydration, failure to nurse,
collection for antigen testing.

794

FELINE LEUKEMIA VIRUS AND RELATED DISEASES

Three types of tests are now readily

PCR testing on whole blood, bone
available for clinical use: immunochromama.J.Tow, and other tissues is increasingly tography (such as ELISA), inununofluoresavailable through diagnostic laboratories, cent assay (IFA), and PCR. Virus isolation
although validated sensitivity and specificis considered the gold standard diagnostic ity studies are often lacking. Real-time PCR
test but is not generally available to private
offers great potential to provide extremely

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practitioners. ELISA or other point-of
sensitive detection of FeLV rapidly after
care antigen test kits can be used in the
infection and can be useful to detect
veterinary clinic to detect the presence of
regressive infections and resolve conflicting
soluble FeLV p27 antigen in whole blood
test results if a positive result is obtained.

or serum using a lateral flow test kit or a

Diagnosis of FeLV-induced neoplasia is
multi-well plate. Saliva and tears are not
similar to that of other tumors. Cytologic
considered to be reliable samples for testing examination of fine-needle aspirates of purposes. Several different test kits are
masses, lymph nodes, body cavity fluids ( eg,
available; most have sensitivities and
pleural effusion), and affected organs may
specificities of -98%.

reveal malignant lymphocytes. Bone

IFA tests for the presence of FeLV p27
ma.J.Tow examination may reveal leukemic
and other structural core antigens in the
involvement, even when the peripheral
cytoplasm of cells. In clinical practice,
blood appears normal. Biopsy with
peripheral blood smears are usually used
histopathologic exar11ination of abnormal
for IFA, but cytologic preparations of bone
tissues is often necessary for diagnostic
marrow or other tissues can also be used.

confimrntion. Cellular phenotyping via flow

IFA requires submission to a diagnostic
cytometry, immunocytochemistry, or other
laboratory and cannot detect infection
techniques can provide additional
until bone marrow involvement occurs.

diagnostic information.

False-negative test results may occur
because of leukopenia or lack of bone

Treatment and Prognosis: Unfortuma.J.Tow involvement, whereas technical nately, no curative treatment cwrently
error is most often the cause of false-posiexists to eradicate retroviral infection.

tive results. Like ELISA, IFA carmot detect

In vitro studies have yielded cautiously
regressive infection because of the lack
promising results suggesting virus-supof sufficient viral antigen production.

pressing activity of FDA-approved drugs

Historically, cats with nonregenerative
used to treat HIV and other myelodysplastic
ar1emia or other cytopenias and negative
syndromes against FeLV virus ( eg,

FeLV antigen tests on blood samples were
raltegravir, tenofovir, gemcitabine,
subjected to bone marrow testing in sear·ch
decitabine ). Further research is needed
of occult FeLV infections. Several recent·
to demonstrate efficacy and safety in vivo
studies have indicated this is unnecessary,
and in field trials, as well as to address
because cats with Fel:.V-associated bone
affordability of these drugs for most cat
ma.J.Tow suppression invariably have
owners. Feline interferon omega and hW11an
positive results on blood tests.

interferon alpha have been associated with

Discordant results between tests, often a
improved survival, but concerns swroundpositive initial ELISA followed by negative ing availability, cost, and absence of strong
results on either repeat ELISA or IFA, may
evidence in controlled field studies have
reflect the inconsistent antigen circulation
limited their widespread integration into
during various stages of FeLV infection,
standard treatment protocols for FeLV.

technical error, or possibly regressive

Anecdotal reports of various antiviral
infection status. These cats are generally
and inu11unotherapeutic agents to reverse
considered presw11ptively infected and
viremia, inlprove clinical signs, and prolong
potential sources of infection until further
survival are abundant. Controlled studies
clarification is possible. Standard recomusing naturally infected cats have either not mendations to resolve discordant testing
been performed or have not confirmed
dictate repeating both tests in 30-60 days
anecdotal observations. Treatment efficacy
using sernm instead of whole blood. It is not
must be demonstrated in controlled clinical
uncommon for cats, especially kittens, to
trials, because spontaneous reversion to
test negative on a subsequent test. This
seronegative status or prolonged survival
could indicate a false-positive on the first
is not uncommon, even in the absence of
test, a false-negative on the second test, or
medical treatment.

development of a regressive or abortive

Some FeLV-positive cats can live without
infection status. Once a single positive test
major disease complications for years with
result has been obtained, it can be difficult
routine prophylactic care, good husbar1dry,
to ever know the true status of the cat, even
minin1al stress, and avoidance of secondary
if subsequent tests are negative.

infections. Infected cats should be kept

FELINE LEUKEMIA VIRUS AND RELATED DISEASES

795
strictly indoors to reduce the risk of
attain a complete remission live an average
exposure to infectious agents and to
of9 mo, whereas survival an10ng FeLVprevent transmission of the virus to other positive cats averages 6 mo. Cats not treated
cats. Routine vaccinations should be
or those not responding to treatment
administered based on individual risk
survive an average of2-o wk.

assessment and in compliance with local

Many protocols for treatment of feline

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laws. Use of inactivated vaccines could be
lymphoma have been published; most use
considered because of concerns regarding
similar drugs with differing schedules of
use of live vaccines reverting to virulence in
administration. One widely used protocol
immunocompromised animals, although
consists of an intensive induction phase
this does not appear to be common. FeLV

(vi.ncristine weekly for4 wk, cyclophosvaccinations should not be administered, phamide every 3 wk on the same day as
because there is no evidence to suggest a
vi.ncristine, and prednisolone daily),
benefit after infection. Physical examinafollowed by a less intensive maintenance tions focusing on external parasites, skin
phase (vi.ncristine and cyclophosphan1ide
infections, dental disease, lymph node size,
given every 3 wk on the san1e day, and
and body weight should be performed
prednisolone continued daily). Treatment is
semiannually, along with a routine program
continued for 1 yr or until relapse. With this
for parasite control and annual fecal, CBC,
protocol, 79% of cats attained remission,
chemistry panel, and urinalysis testing. All
and average survival was 150 days.

infected cats should be neutered. Owners

Changing the maintenance protocol to
should be advised to watch for signs of
doxorubicin every 3 wk provided an average

FeLV-related disease, particularly secondremission of281 days. When relapse occurs, ary infections. Although FeLV-positive cats
the dn1g reginlen can be changed and a
often respond well to treatment, therapy for
second remission achieved; however,
such infections or other illnesses should be
second remissions seldom last as long as
early and aggressive because of irnrnunothe fiJst.

compromise.

Another popular chemotherapy protocol

Because FeLV is historically associated
involves an initial treatment with L-asparawith rapid and grave disease, the modem ginase and vi.ncristine. Treatment is
prognosis varies considerably depending on continued with daily prednisolone and husbandry, veterinary care, and individual
alternating doses of cyclophosphamide,
in1mune system variation. Large-scale
vincristine, and doxorubicin for a total of
studies have demonstrated an average
three cycles. When relapse occurs, the
survival of2.4 yr after diagnosis among
protocol is started again. Using this
positive cats ( versus 6 yr after testing for
protocol, the median survival has been
negative control cats), with 50% mortality
reported to be 210 days. Other protocols
in 2 yr and 80% mortality by 3 yr after
incorporating alkylating agents such as
diagnosis. Progression of disease is much
mustargen and procarbazine have
more rapid in kittens, whereas some adult
demonstrated efficacy as well, sometimes
cats remain healthy for many years and may
even after other combination therapies
succumb to conditions unrelated to their
have not achieved remission.

retroviral status.

Most lymphomas have an intermediate or
high histopathologic grade and are clinically

Lymphoma Treatment: Feline lymaggressive, except for a subset identified phoma can be treated with cytotoxic dn1gs.

as small-cell lymphoma or lymphocytic

These drugs may cause significant toxicities
lymphoma. Small-cell lymphomas are
if not dosed and administered properly.

characterized by a diffuse infiltration of

Most cytotoxic drugs are also carcinogens
malignant lymphocytes throughout affected
and must be handled properly. Before
organs, typically intestines, and can often be
administering these drugs, veterinarians
successfully treated with less aggressive
should familiarize themselves with proper
chemotherapy. Administration of prednisodosing and administration procedures, lone and chlorambucil orally daily for 4
appropriate monitoring of the patient,
consecutive days every 3 wk has been used.

toxicities and complications, and safe

Using these drugs in clinical trials to treat
handling to prevent exposure of veterinary
small-cell lymphoma involving the GI tract
personnel and owners to the agents and
produced a median swvival of963 days. If
their metabolites.

other sites were involved, with or without

Approximately 50% of cats with

GI disease, the median survival was 636
lymphoma that are treated obtain a
days.

complete remission, defined as no clinical

In addition to small-cell lymphoma, large
evidence of disease. FeLV-negative cats that
granular lymphocyte lymphoma also affects

796

FELINE LEUKEMIA VIRUS AND RELATED DISEASES
the intestinal tract. This is an extremely

Management Guidelines include the
aggressive disease, with a response to
reconunendation that all kittens should
chemotherapy of -3QOA, and a median
receive the two-dose FeLV vaccination as a
survival of 57 days. An intestinal mass is
component of the routine initial vaccination
usually present and may cause intestinal
series and should also receive a booster
obstruction.

vaccination l yr later. This is prudent,

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Acute lymphocytic leukemia is treated
because rehoming and lifestyle changes
with the same protocol as lymphoma, but
such as outdoor access frequently occur as
only -25% of cats obtain remission for an
cats mature. Annual revaccination after
average of 7 mo. Chronic lymphocytic
maturity would depend on tl1e cat's risk of
leukemia typically carries a much better

FeLV exposure.

prognosis than the acute fonn and is best

The adult cat's risk of exposure to
treated with chloran1bucil and prednisolone

FeLV-positive cats should be assessed, and
given every other day on alternating days.

vaccines used only for those cats at risk.

Leukemias other than lymphocytic are

FeLV vaccines have been associated with
rarely treated because of severity of illness
development of sarcomas at the vaccination
at diagnosis and poor response to therapy.

site, although the risk of tumor development
is very low. Uninfected cats in a household

Prevention and Control: FeLV virus
with infected cats should be vaccinated;
is unstable in the environment and is
however, vaccination is not universally
susceptible to all common detergents and
protective, and other means of reducing
disinfectants. In a hospital or boarding
transmission to uninfected cats, such as
setting, infected cats may be kept in the
physical separation, should also be used.

general population as long as they are

While testing of cats in an anin1al shelter
housed in separate cages. Medical and
environment is considered optional for
surgical equipment contaminated with body
individual housing, FeLV status should be
fluids, even when dried, can be fomites for
detennined before placement in group
infection. Thorough cleaning and sterilizahousing and is recommended at tl1e time tion of equipment, strict attention to
of adoption or foster home placement.

washing contaminated hands, and avoid

Because tests are not 10(.)0A, accurate, shelter
ing reuse and sharing of single use and
cats placed in group housing should be
consumable supplies between patients are
vaccinated against FeLV, especially in
critical practices to prevent iatrogenic
longtenn conditions such as sanctuaiies.

transmission.

Because of the equivalent prevalence of

FeLV vaccines are non-core and are

FeLV among feral and free-roaming pet cats
intended to protect cats against FeLV
and the role of neutering in decreasing the
infection or to reduce the likelihood of
spread of infection, expending resources on
persistent viremia. Types of vaccines

FeLV testing is not considered a mandatory
include killed whole vims, subunit, and
component of conununity trap-neutergeneticalJy engineered. Vaccines may vary retum progran1s.

in protective effect, and manufacturers'

clain1s and independent comparative

Zoonotic Risk: Some strains of FeLV can
studies should be carefully noted. Vaccines
be expe1irnentally grown in human tissue
are indicated only for uninfected cats,
cultures, leading to concerns of potential for
because there is no benefit in vaccinating
transmission to people. Studies addressing
an FeLV-positive cat.

tl1is concern have shown no evidence that

The American Association of Feline
any zoonotic risk exists, and there are no

Practitioners (AAFP) Feline Retrovirns
known cases of zoonotic transmission.

FELINE PANLEUKOPENIA

(Feline infectious enteritis, Feline parvoviral enteritis) Feline panleukopenia is a highly contagious, temperature in the environment, if often fatal, viral disease of cats that is seen
protected in organic material. Feline
worldwide. Kittens are affected most
panleukopenia is now diagnosed infreseverely. The causative parvovirus is very quently by veterinaiians, presumably as a
resistai1t; it can persist for 1 yr at room
consequence of widespread vaccine use.

FELINE PANLEUKOPENIA

797

However, infection rates remain high in
most queens passively transfer sufficient
some unvaccinated cat populations, and the
antibodies to their kittens to protect them
disease occasionally is seen in vaccinated,
during the period of susceptibility.

pedigreed kittens that have been exposed to
a high virus challenge.

Clinical Findings: Most infections are
subclinical, as evidenced by the high

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Etiology, Transmission, and Patho
seroprevalence of anti-FPV antibodies
genesis: Feline panleukopenia virus
among unvaccinated, healthy cats. Those

(FPV) is closely related to mink entelitis
cats that become ill are usually < l yr old.

virus and the type 2 canine parvoviruses

Peracute cases may die suddenly with little

(CPV) that cause canine parvoviral
or no warning (fading kittens). Acute cases
enteritis. FPV can cause disease in all felids
show fever (104°-107°F [40°-41.7°Cl),
and in some members of related fan1ilies
depression, ·and anorexia after an incuba

( eg, raccoon, mink), but it does not harm
tion period of 2-7 days. Vomiting usually
canids. Conversely, some cw-rently
develops 1-2 days after the onset of fever; it
circulating CPV strains (CPV-2a, -2b, and
is typically bilious and W1felated to eating.

-2c) have been shown to cause a panleuko

Diarrhea may begin a little later but is not
penia-like illness in domestic cats and
always present. Extreme dehydration
larger felids. In some parts of Asia, CPV
develops rapidly. Affected cats may sit for
strains are reported to Iival FPV as the
hours at their water bowl, although they
major cause of feline panleukopenia,
may not drink much. Terminal cases are
although FPV still dominates worldwide.

hypothem1ic and may develop septic shock

Vaccines that contain FPV only provide
and disseminated intravascular coagulation.

some protection to cats against disease

Physical exan1ination typically reveals
caused by CPV, but it has been suggested by
profound depression, dehydration, and
some autholities that inclusion of CPV-2c in
sometimes abdominal pain. Abdominal
feline vaccines would broaden and improve
palpation-which can induce in1mediate
the degree of protection provided.

vomiting-may reveal thickened intestinal

Virus particles are abundant in all
loops and enlarged mesenteric lymph
secretions and excretions during the acute
nodes. In cases of cerebellru· hypoplasia,
phase of illness and can be shed in the feces
ataxia and tremors with nom1al mentation
of survivors for as long as 6 wk after
are seen. Retinal lesions, if present, appear
recovery. Being highly resistant to
as discrete gray foci.

inactivation, parvoviruses can be trans

The duration of tllis self-linuting illness
ported long distances via fomites ( eg, shoes, is seldom >5--7 days. Mortality is highest clothing). However, FPV can be destroyed
in young kittens <5 mo old.

by exposure to a 1:32 dilution of household
bleach (6% aqueous sodium hypochlolite),

Lesions: There are typically few gross

4% formaldehyde, and 1 % glutaraldehyde for lesions, altllough dehydration is usually 10 min at room temperature. Peroxygen
marked. Bowel loops are usually dilated and
disinfectants are also highly effective.

may have thickened, hyperemic walls.

Cats are infected oronasally by exposure

There may be petechiae or ecchymoses on
to infected anin1als, their feces, secretions,
tile intestinal serosal surfaces. Perinatally
or contan1inated fomites. Most free-roaming infected kittens may have a noticeably small cats are thought to be exposed to the virus
cerebellum. Histologically, the intestinal
during their first year of life. Those that
crypts are usually dilated and contain debris
develop subclinical infection or survive
consisting of sloughed necrotic epitllelial
acute illness mount a robust, long-lasting,
cells. Blunting and fusion of villi may be
protective in1mune response.

present. Eosinophilic intranuclear inclusion

FPV infects and destroys actively dividbodies are seen only occasionally in ing cells in bone marrow, lymphoid tissues,
fmmalin-fixed specimens; use ofBouin's or
intestinal epithelium, and-in very young

Zenker's fixative will increase the likelihood
anin1als-cerebellum and retina. In
of seeing these.

pregnant queens, the virus may spread transplacentally to cause embryonic resorption, Diagnosis: A presun1ptive diagnosis is
fetal mummification, abortion, or stillbirth.

usually based on compatible clinical signs

Alternatively, infection of kittens in the
in an inadequately vaccinated cat and tile
pelinatal period may destroy the germinal
presence of leukopenia ( nadir 50-3,000
epithelium of the cerebellwn, leading to

WBC/µL). Neutropenia is a more consistent
cerebellar hypoplasia, incoordination, and
finding tllan lymphopenia. Total WBC
tremor. FPV-induced cerebellar ataxia has
counts <2,000 cells/µL are associated with
become a relatively rare diagnosis, because
a poorer prognosis. During recovery from

798

FELINE PANLEUKOPENIA
infection, there is typically a rebound
preferable for the occasional cat that is
neutrophilia with a marked left shift.

severely anemic. Parenteral, broad-spectrun1

Diagnosis can sometimes be con.fumed
antibiotic therapy is indicated; however,
using an in-office immunoch.romatographic
nephrotoxic drugs ( eg, gentanucin,
test kit intended for detection of fecal CPV
anukacin) should be avoided until dehyantigen. However, fecal antigen is detectdration has been corrected. Antiemetic VetBooks.ir
able only for a short time after infection.

therapy ( eg, metoclopranlide, ondansetron,

False-negative results are common.

ma.ropitant) may provide some relief and

Differential diagnoses include other
allow earlier enteral feeding of soft, easily
causes of profound depression, leukopenia,
digested food. Parenteral nutrition is
and GI signs. Salmonellosis (seep 195) and
indicated for severely affected cases.

infections with feline leukemia virus (FeLV,

Recombinant feline interferon omega
seep 790) and feline immunodeficiency

(rFeIFN; 1 MU/kg/day SC for 3 days) should
virus (seep 821) should be considered.

be considered for use in the treatment of

Concurrent infection with FeLV and FPV
feline panleukopenia. Although rFeIFN is not
can cause a panleukopenia-like syndrome
approved by the FDA for this purpose, it is
in adult cats.

approved and effective in the treatment of
canine parvoviral enteritis.

Treatment and Prevention: Successful

Excellent inactivated and modified-live
treatment of acute cases requires vigorous
virus vaccines that provide solid, longfluid therapy and suppmtive nursing care in lasting immunity are available for preventhe isolation unit. Electrolyte disturbances tion of feline panleukopenia. Live vaccines

( eg, hypokalemia), hypoglycemia, hypoproshould not be given to cats that are teinemia, anemia, and opportunistic
pregnant, in1rnunosuppressed, or sick,
secondary infections often develop in
or to kittens <4 wk old. Most authorities
severely affected cats. Anticipation of these
recon1rnend that kittens receive two or
possibilities, close monitoring, and prompt
three modified-live vaccine doses SC,
inte1vention are likely to improve outcome.

3--4 wk apart. The first vaccination is usually

IV fluid replacement and maintenance with
given at 6-9 wk of age. The last dose of the
a balanced isotonic crystalloid solution ( eg,
initial vaccination series should not be
lactated Ringer's solution with calculated
administered before the kitten is 16 wk
potassium supplementation) is the
old, to ensure that interfering maternal
foundation of therapy. B vitamins should
antibodies do not inactivate the modifiedbe added to the infusion, together with 5%
live virus. Exposure to virus should be
glucose if hypoglycemia is suspected or
avoided until 1 wk after the initial vaccinaproved. In addition to crystalloid infusion, tion series has been completed. Cats should
transfusion of fresh-frozen plasma helps
be revaccinated 1 yr later, and triennially or
support plasma oncotic pressure and
less frequently thereafter, although some
provides clotting factors to severely ill,
manufacturers continue to recommend
hypoproteinemic kittens. Whole blood is
annual revaccination.

INFECTIOUS CANINE HEPATITIS

Infectious canine hepatitis (ICH) is a
of the disease in wild and feral hosts,
worldwide, contagious disease of dogs
reinforce the need for continued
with signs that vary from a slight fever and
vaccination.

congestion of the mucous membranes to
severe depression, marked leukopenia, and

Etiology and Pathogenesis: ICH is
coagulation disorders. It also is seen in
caused by a nonenveloped DNA vims,
foxes, wolves, coyotes, bears, lynx, and
canine adenovirus 1 (CAV-1), which is
some pinnipeds; other carnivores may
antigenically related only to CAV-2 ( one of
become infected without developing
the causes of infectious canine tracheoclinical illness. In recent years, t11e disease bronchitis, seep 1491). CAV-1 is resistant to has become uncon1rnon in areas where
lipid solvents (such as ether), as well as to
routine immunization is done, but periodic
acid and fonnalin. It survives outside the
outbreaks, which may reflect maintenance
host for weeks or months, but a 1 o/o-3"/o

INFECTIOUS CANINE HEPATITIS

. 799
solution of sodium hypochlorite (household

Clinicopathologic findings reflect the
bleach) is an effective disinfectant.

coagulopathy (prolonged prothrombin time,

Ingestion of urine, feces, or saliva of
thrornbocytopenia, and increased fibrin
infected dogs is the main route of infection.

degradation products). Severely affected

Recovered dogs shed virus in their urine
dogs show acute hepatocellular injury
for �6 mo. Initial infection occurs in the

(increased ALT and AST). Proteinuria is
tonsillar crypts and Peyer patches, followed
common. Leukopenia typically persists

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by viremia and disseminated infection.

throughout the febrile period. The degree

Vascular endothelial cells are the primary
of leukopenia varies and seems to be
target, with hepatic and renal parenchyrna,
correlated with the severity of illness.

spleen, and lungs becoming infected as

On recovery, dogs eat well but regain
well. Chronic kidney lesions and corneal
weight slowly. Hepatic transaminase
clouding ("blue eye") result from immuneactivities peak arotmd day 14 of infection complex reactions after recovery from
and then decline slowly. In -25% of
acute or subclinical disease.

recovered dogs, bilateral corneal opacity
develops 7-10 days after acute signs

Clinical Findings: Signs vary from a slight disappear and usually resolves spontanefever to death. The mortality rate ranges ously. In mild cases, transient corneal
from 10%-30% and is typically highest in
opacity may be the only sign of disease.

very young dogs. Concurrent parvoviral or

It has long been thought that chronic
distemper infection worsens the prognosis.

hepatitis may develop in dogs that have low

The incubation period is 4-9 days. The first
levels of passive antibody when exposed,
sign is a fever of>104°F (40°C), which lasts
although a recent PCR-based study did not

1-6 days and is usually biphasic. If the fever
confirm this theory.

is of short duration, leukopenia may be the
only other sign, but if it persists for >1 day,

Lesions: Endothelial dan1age results in
acute illness develops.

"paint-brush" hemorrhages on the gastric

Signs are apathy, anorexia, thirst,
serosa, lymph nodes, thymus, pancreas,
conjunctivitis, serous discharge from the
and subcutaneous tissues. Hepatic cell
eyes and nose, and occasionally abdominal
necrosis produces a variegated color
pain and vomiting. Intense hyperemia or
change in the liver, which may be normal
petechiae of the oral mucosa, as well as
in size or swollen. Histologically, there is
enlarged tonsils, may be seen. Tachycardia
centrilobular necrosis, with neutrophilic
out of proportion to the fever may occur.

and monocytic infiltration, and hepatocel

There may be subcutaneous edema of the
lular intranuclear inclusions. The gallbladhead, neck, and trunk. Despite hepatic der wall is typically edematous and
involvement, there is a notable absence
thickened; edema of the thymus may be
of icterus in most acute clinical cases.

found. Grayish white foci may be seen in

Clotting time is directly correlated with
the kidney cortex.

the severity of illness and is the result of
disseminated intravascular coagulation

Diagnosis: Usually, the abrupt onset of
induced by vascular endothelial comproillness and bleeding suggest !CH, although mise, coupled with failure of the liver to
clinical evidence is not always sufficient to
rapidly replace consumed clotting factors.

differentiate !CH from distemper (see

It may be difficult to control hemorrhage,
p 777). Definitive antemortem diagnosis
which is manifest by bleeding around
is not required before institution of
deciduous teeth and by spontaneous
supportive care but can be pursued with
hematomas. CNS involvement is w1usual
commercially available ELISA, serologic,
and is typically the result of vascular
and PCR testing. PCR or restriction
injury. Severely infected dogs may develop
fragment length polymorphism is required
convulsions from forebrain damage. Paresis
to definitively distinguish CAV-1 from
may result from brain stern hemorrhages,

CAV-2, if clinically necessary. Postm01tem
and ataxia and central blindness have also
gross changes in the liver and gallbladder
been described. Foxes more consistently
are more conclusive, and diagnosis is
have CNS signs and intermittent convulsions confirmed by virus isolation, inm1unofluoduring the course of illness, and paralysis rescence, characteristic intranuclear
may involve one or more limbs or the entire
inclusion bodies in the liver, or PCR or
body. Respiratory signs usually are not seen
fluorescence in situ hybridization studies
in dogs with !CH; however, CAV-1 has been
of infected tissue.

recovered from dogs with signs of infectious
tracheobronchitis despite high serologic

Treatment: Treatment is symptomatic
titers against parenteral disease.

and supportive. The goals of therapy are to

800

INFECTIOUS CANINE HEPATITIS
limit secondary bacterial invasion, support
often combined with other vaccines.

fluid balance, and control hemorrhagic

Vaccination against !CH is recommended at
tendencies. Broad-spectrum antibiotics
the time of canine distemper vaccinations.

and intravenously administered balanced

Maternal antibody from immune bitches
electrolyte solutions with 5% dextrose
interferes with active immunization in
supplementation are indicated. Plasma or
puppies until they are 9-12 wk old.

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whole blood transfusions may be necessary

Attenuated CAV-1 vaccines have produced
in severely ill dogs.

transient unilateral or bilateral opacities of

Although the transient corneal opacity
the cornea, and the virus may be shed in

(which may be seen during the course of
urine. For these reasons, CAV-2 attenuated

!CH or associated with vaccination with
live vims strains, which provide crossattenuated CAV-1 vaccines) usually requires protection against CAV-1, are preferentially
no treatment, atropine ophthalmic ointment
used because they have very little tendency
may alleviate the painful ciliary spasm
to produce corneal opacities or uveitis, and
sometimes associated with it. Dogs with
the vims is not shed in urine. Historically,
corneal clouding should be protected
a.rmual reva.ccina.tion against ICH was
against bright light. Systemic corticosterstandard, and vaccines are labeled for oids are contraindicated for treatment of
annual use. Increasing evidence suggests
corneal opacity associated with !CH.

that immunity induced by MLV CAV-1
irtjectable vaccines lasts �3 yr, although this

Prevention: Modiiied-live vims (MLV)

remains an extra-label use of commercially
irtjectable vaccines are available and are
available vaccines.

LEISHMANIOSIS

(Visceral leishmaniasis)

Leishmaniosis is a disease caused by

USA. It is also of concern in nonendemic
protozoan parasites of the genus Leishma
countries where imported disease
nia and transmitted through the bites of
constitutes a veterinary and public health
female phlebotomine sand flies. More than
problem.

23 species of Leishmania have been
described, most of which are zoonotic.

Transmission: Leishmania is a diphasic The most importantLeishmania parasite
parasite that completes its life cycle in two
to affect domestic animals is L infantum,
hosts: a sand fly that harbors the flagellated
also known as L chagasi in {4tin America.

extracellular promastigote form and a

Dogs are the main reservoir host for human
manunal in which the intracellular
visceral leishmaniosis caused by L
an1astigote parasite forn1 develops.

infantum, and the disease is potentially

Transmission is a complex process that
fatal in dogs and people. Because the
requires special adaptation between the
internal organs and skin of the dog are
sand fly host and the particular Leishmania
affected, the canine disease is termed
species transmitted. There are numerous
viscerocutaneous or canine leishma.niosis.

species of sand flies, only a minmity of

Cats, horses, and otherrnan1mals can be
which are competent vectors of Leishma
infected by L infantum or other Leishmania. Dogs with or without clinical signs are nia species. The disease in ca.ts is rarer than infectious to sand flies and may transmit in dogs and may manifest in cutaneous or
leishmaniosis. Congenital vertical
visceral organs. L braziliensis, the cause
transmission of canine Jeishmaniosis from
of tegumentary canine leishmaniosis, is
an infected darn to its offspring has been
widespread in regions of South America and reported but appears to be uncommon.

may geographically overlap withL chagasi.

Transmission by transfusion of blood

Canine leishmaniosis is a major zoonosis
products from infected dogs has been
endemic in> 70 countries. It is prevalent in
shown to cause infection in recipients.

southern Europe, Africa, Asia, South and

Direct dog-to-dog transmission by contact

Central America, and sporadically in the
has been suggested as a mode of disease

LEISHMANIOSIS

801
transmission in an effort to explain the
considerable bleeding. A mild form of
spread of infection among kenneled
papular dermatitis has been reported in

Foxhounds in the USA in the absence of
dogs with no other signs of disease. Ocular
proven sand fly vectors. At present, the
or periocular lesions include keratoconvalidity of direct transmission is unknown.

junctivitis and uveitis.

Clinical laborato1y findings include mild

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Clinical Findings: Dogs are infected by
to moderate nomegenerative or more rarely

L irifantum promastigotes deposited into the regenerative anemia in 600/o-73% of the dogs; skin via the bites of infected sandilies. The
thromobocytopenia is less common. The
promastigotes invade host macrophages
most consistent serun1 biochemistry findings
and replicate as intracellular amastigotes.

in dogs with clinical canine leishmaniosis are

The inunw1e responses mounted at the time
serwn hyperproteinemia with hyperglobuof infection and thereafter appear to be the linemia and hypoalbwninemia, frequently
most important factor in detem1ining
expressed by a decreased albunlin:globulin
whether a persistent infection will develop
ratio. Marked hyperglobulinemia with no
and progress from subclinical to clinical
apparent cause in dogs from Leishmania
disease. The incubation period may last
endemic regions should suggest possible
months to years, during which the parasite
canine leishmaniosis. Grossly increased
disseminates from the skin throughout the
activities of liver enzymes or azotemia are
host's body (prin1arily to the hemolymphatic found in only a minority of infected dogs.

system organs). Age, breed, host genetics,

Some degree of renal pathology is present
nutrition, concurrent diseases, and other
in most dogs with canine leishmaniosis.

factors may also influence the progression

Subsequent renal failure due to inununefrom infection to clinical disease.

complex glomerulonephritis may eventually

Canine leishmaniosis is a multisystemic
develop and is believed to be the main
disease with a highly variable spectrum of
natmal cause of death. The presence of
inunune responses and clinical manifestaproteinwia should be evaluated and kidney tions. In endemic areas, the prevalence of
disease staged with measurement of the
dogs carrying infection is much higher than
urine protein:creatini.ne ratio.

those demonstrating clinical disease.

Clinical disease is associated with a marked

Lesions: The typical histopathologic
antibody response that does not confer
finding in canine leishmaniosis is granuprotection. In fact, immune-mediated lomatous inflammation associated witl1 a
mechanisms are responsible for much of
variable nwnber of Leishmania arnastithe pathology in canine leishmaniosis.

gotes with macrophages. Protective

The typical history reported by owners
inununity aga.instLeishmania parasites is
of dogs with clinical disease due to L
mediated through CD4•T11 cells and tl1e
irifantum includes the appearance of skin
activation of a complex cascade of cytokine
lesions, ocular abnormalities, or epistaxis.

mediators. Circulating inunune complexes

These are frequently accompanied by
and antinuclear antibodies can be detected
weight loss, exercise intolerance, and
in anin1als with canine leishmaniosis, and
lethargy. The main physical examination
deposition ofin1mune complexes in the
findings are dermal lesions in 80%-900/o of
kidneys, blood vessels, and joints occurs as
the dogs, lymphadenomegaly in 62%-90%,
infection progresses. Glomerulonephritis
ocular disease in 16%--81%, splenomegaly in
associated with the renal inunune comlQO/c,-53%, and abnormal nail growth plexes is a hallmark of th.is disease. Renal

(onychogryphosis) in 200/o-31%. Other
pathology, including glornerulonephritis and
clinical findings may include polyuria and
interstitial nephritis, is evident by histopapolydipsia due to kidney disease, vomiting, thology, even if not manifested clinically in
colitis, melena, and lameness due to joint,
most dogs infected with L infantum.

muscle, or bone lesions. The sole presenting
signs of disease could be epistaxis, ocular

Diagnosis: Diagnostic tests include a
abnormalities, or manifestations of kidney

CBC, biochemical profile, urinalysis, and
disease without dermal abnormalities. The
one or more specific tests to confirm
dem1al lesions associated with canine
infection. Quantitative serology is useful,
leishmaniosis include exfoliative dermatitis, especially when compatible clinical signs which can be generalized or localized over
are present. High antibody titers are found
the face, ears, and limbs. Ulcerative,
in 800/o-l 000/o of dogs with clinical disease
nodular, or mucocutaneous dermatitis are
and could be conclusive of a diagnosis.

also seen. Cutaneous ulcers over the ears

Vruious quantitative serologic methods to
or other locations may be associated with
detect anti-Leishmania antibodies have

802

LEISHMANIOSIS
been developed, including indirect

75---100 mg/kg, SC, for4-8 wk combined
inm1Unofluorescence assays, ELISA, and
with allopurinol (10 mg/kg, PO, bid, for
direct agglutination assays. Purified

6-12 mo or longer as needed). Allopurinol
recombinant antigens such as rK39 are also
may also be used as a single therapeutic
used to detect leishrnaniosis in dogs and
agent at the same dose. Miltefosine (not
people. Serologic cross-reactivity with
approved for use in dogs in the USA) at
trypanosomes may be found in regions

2 mg/kg/day, PO, for 4 wk can also be

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where Trypanosoma infection is prevalent,
combined with allopurinol (10 mg/kg, PO,
particularly with T c1Uzi in Latin America.

bid) as an alternative to N-methylglucanline

Detection of parasite-specific DNA by
antimoniate. Treatment frequently achieves

PCR allows sensitive and specific diagnosis
only temporary clinical i.Jnprovement in
of infection. Several different assays with
dogs and often does not eli.Ininate the
various target sequences using genomic
parasites. Treated dogs can remain carriers
or kinetoplast DNA (kDNA) have been
of infection and may relapse. They may
developed for canine leishrnaniosis. PCR
remain infectious to sand flies. Stopping
can be performed on DNA extracted from
treatment with allopurinol is reconlffiended
tissues, blood, or even from histopathologic
only when clinical signs disappear,
specimens. Assays based on kDNA are
hematologic and serum biochemistry abnorthe most sensitive for direct detection in malities return to normal, and the animal
infected tissues. Bone marrow, lymph node,
becomes seronegative by a quantitative
conjunctiva! swabs, or spleen samples are
laboratory serologic test.

superior to blood with most of the CLUTent

Specific repellent topical insecticides

PCR techniques.

effectively reduce sand fly bites and disease

Leishmania an1astigotes can be
transmission. A deltan1ethrin-i.Jnpregnated
demonstrated by cytology from lymph
collar and a spot-on formulation of
nodes, spleen, skin impressions, bone
permethrin and irnidacloprid have been
marrow, or joint fluids stained with Giemsa
shown to confer protection against sand
stain or a quick commercial stain. Detection
fly bites. The application of protective
of amastigotes by cytology is sometimes
insecticides is recommended for dogs in
m1rewarding because of a low nun1ber of

Leishmania-endemic areas, dogs traveling
detectable parasites, even in dogs with
to sites of iilfection, and infected dogs (to
full-blown clinical disease. Leishmania
reduce potential transmission). Purifiedparasites may also be viewed in histopathofraction commercial vaccines against logic formalin-fixed, paraffin-embedded
canine leishrnaniosis are marketed in
biopsy sections of the skin or other infected

Europe and Brazil, and other vaccines
organs. Identification of parasites within
are under development.

tissue macrophages may be difficult;
inlffiunolabeling with iI1lffiunohistochemical staining can v.erify the presence of Zoonotic Risk: Hwnan visceral leishmani

Leishmania in the tissue.

osis caused by L infantum is a serious

Detection of infection in dogs with no
public health problem in areas where canine
clinical disease for purposes such as
leishmaniosis is endemic and dogs are the
in1portation to nonendemic countries or use main reservoir of infection. It is mostly a as blood donors may require PCR, which is
disease of yow1g children. Malnutrition has
the most sensitive diagnostic technique.

been recognized as a risk factor and may

Cross-sectional studies of dog populations
explain why this disease is more prevalent
in highly endemic areas have shown that
an1ong children in poor countries than
infection rates can reach 65o/er800/o.

among those in affluent ones, despite high

Typically, only approximately 100/o-13%
prevalence rates in the canine populations.

marlifest clinical signs of disease, 26% are

Hwnan disease is also prevalent in
seropositive and include sick and subcliniinm1w1osuppressed individuals; HIV
cally infected dogs, and an additional
patients are the predominant risk group for

400/o-600/o are carriers positive only by tissue
hun1an leishmaniosis in southern Europe.

PCR.

HIV and leislunaniosis coinfection has been
reported from >33 countries worldwide and
does not respond well to therapy. Efforts to

Treatment: The main protocol used for
control canine leislunaniosis and the hwnan
treatment of canine leishmaniosis includes
disease in endemic areas focus on disrupting

N-methylglucamine antirnoniate (not
the transmission of infection and preventing
approved for use in dogs in the USA) at
canine infection at the population level.

RICKETISIAL DISEASES

803

RICKETTSIAL DISEASES

EHRLICHIOSIS AND RELATED
sanguineus, which is found worldwide·

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INFECTIONS
accordingly, canine monocytic ehrlichi�sis
also has a worldwide enzootic distribution.

In the past, a number of obligate intracellu

Acute E can is cases may resemble
lar organisms that infect eukaryotic cells
infection with Rickettsia rickettsii (the
were classified in the genusEhrlichia on
agent of Rocky Mountain spotted fever
morphologic and ecologic grounds. With
which can also b� transmitted by the b;own
newer genetic analyses, these agents have
dog tick). Rhipicephalus ticks become
been reclassified into the genera of
infected with E can is after feeding on

Ehrlichia, Anaplasma, and Neorickellsia, infected dogs, and ticks transmit infection
all of which are in the family Anaplasmatato other dogs during blood meals taken in ceae. However, usage of the tern1 "ehrlichiosuccessive life stages. Blood transfusions sis" to broadly describe these infections
or other means by which infected WBCs
may still persist.

can be transferred, may also transmit the
pathogen. E chaffeensis and E ewingii

Etiology: Canine ehrlichiosis is primarily
have sylvan cycles in the environment that
caused by Ehrlichia canis, which
involve tick species and wildlife reservoir
predominantly involves monocytes;
hosts. In the USA, E chaffeensis and E
although it is not considered a primary
ewingii are transmitted by Amblyomma
zoonosis, human infection with this agent
americanum, the lone star tick, and
has been occasionally reported. Another
white-tailed deer are thought to play an
common ehrlichial pathogen of dogs is E
important role as reservoir hosts. Dogs are
chaffeensis, which causes a monocytic
also considered a possible reservoir for
form of illness and is the primary species

E ewingii. A case of humanE ewingii
causing human ehrlichiosis infection in the
contracted via blood infusion has been

USA. Human cases are reported throughout
reported, and organ transplantation of
the mid to southeastern and central USA.

E chaffeensis infection has been suspected.

Several published reports of monocytic

The ecologic cycle for the EML agent has
ehrlichiosis in cats suggest that feline
not yet been elucidated but is suspected
infection may occur, albeit uncommonly.

to involve Ixodes scapularis, the black

E ewingii, which primarily infects the
legged tick.

granulocytes of susceptible hosts, has

A phagocytophilum is transmitted by
been isolated from dogs and people in the

Ixodes species of ticks; in the northeastern southern, western, and midwestern USA. In

USA, infection is transmitted by l'Scapula

2009, an organism either identical or related
ris, whereas infection in western states is to E muris was identified as a cause of
primarily associated with I pacijicus, the
human illness in the upper Midwest; the

Western black-legged tick. In nature, the
role of this E muris-like (EML) agent as
enzootic cycle is most likely associated with
a possible pathogen of dogs or cats is
small rodents. People and domestic animals
currently unknown.

are incidental hosts of these pathogens.

A phagocytophilum, formerly known

Human-to-hun1an transmission via
as both E equi and the agent of hun1an
transfusion of packed RBCs has been
granulocytic ehrlichiosis, has been reported
reported; the risk of canine-associated
as a cause of illness in dogs. It is known to
infections after blood transfusion is
cause human illness in the USA, prin1arily
unknown.

m northeastern, upper midwestern, and

A platys is transmitted by R sanguineus western states. Infection with this agent is
and is enzootic in many parts of the USA
most appropriately referred to as anaplasand worldwide. Coinfection withE canis mosis, and the pathogen is found predomimay occur, because the same tick vector nantly in granulocytes.

is responsible for transmission of both

A platys, which infects platelets, is the
pathogens.

cause of infectious cyclic thrombocytopenia of dogs.

Clinical Findings: In dogs, E canis
causes the most potentially severe clinical

Epidemiology: E canis is transmitted presentation of the Ehrlichia spp. Signs
by the brown dog tick, Rhipicephalus
arise from involvement of the hemic and

804

RICKETISIAL DISEASES
lymphoreticular systems and commonly
lum appear clinically similar to acute E
progress from acute to chronic, depending
canis infection, but the clinical course is on the strain of organism and immune
usually more self-lim.iting. Shlfting leg
status of the host. In acute cases, there is
lan1eness and fever of unknown origin may
reticuloendothelial hyperplasia, fever,
be present. Thrombocytopenia and mild
general.ized lymphadenopathy, splenomegleukopenia or leukocytosis may occur VetBooks.ir
aly, and thrombocytopenia. Variable signs
during the acute course of infection, whlch
of anorexia, depression, loss of stan1ina,
is clinically more discrete. Chronic can.ine
stiffness and reluctance to walk, edema
d.isease, as seen with E canis infection, is of the limbs or scrotwn, and coughing or
not typically seen with other infections.

dyspnea may be seen. Most acute cases are

Dogs infected with A platys generally
seen in the warmer months, coincident with
show minimal to no signs of infection
the greatest activity of the tick vector.

despite the presence of the organism in

Clu·onic cases may present at any time
platelets. The primary finding is cyclic
of year.

thrombocytopenia, recurring at 10-day

During the acute phase of E canis
intervals. Generally, the cyclic nature
infection in dogs, the hemograrn is usually
diminishes, and the thrombocytopenia
nom1al but may reflect a mild nom10cytic,
becomes mild and slowly resolves.

nmmochromic anemia; leukopenia; or mild
leukocytosis. Thrombocytopenia is

Lesions: During the acute or self-limiting
conunon, but petechlae may not be evident,
phase of E canis infections, lesions
and platelet decreases may be mild in some
generally are nonspecific, but splenomegaly
animals. Vasculitis and inunune-med.iated
is common. Histologically, tl1ere is
mechanisms induce a thrombocytopenia
lymphoreticular hyperplasia and ly:mphoand hemorrhagic tendencies. Lymph node cytic and plasmacytic perivascular cuffing.

aspiration reveals hyperplasia. Death is rare

In chronic cases, these lesions may be
during this phase; spontaneous recovery
accompanied by widespread hemorrhage
may occur, the dog may remain asymptoand increased mononuclear cell infiltration matic, or chronic d.isease may ensue.

in perivascular regions of many organs.

Chronic ehrlichiosis caused by E canis
may develop in any breed, but certain

Diagnosis: Because tlu·ombocytopenia is
breeds, eg, German Shepherds, may be
a relatively consistent finding with these
pred.isposed. Seasonality is not a specific
infections, a platelet count is an important
hallmark of clu·onic infection, because
screening test. Clinical d.iagnosis may be
appearance of chronic signs may be variably confirmed by demonstrating the organisms delayed after acute infection. In chronic
within WBCs or platelets, seen in intracytocases, the bone marrow becomes hypoplasplasmic inclusion bod.ies called morulae.

tic, and lymphocytes and plasmacytes

Th.is method of diagnosis lacks sensitivity,
infiltrate various organs. Clinical findings
because low nwnbers of organisms make
vary based on the predominant organs
demonstration difficult. More commonly,
affected and may include marked splenoa diagnosis is made by a combination of megaly, glomerulonephritis, renal failure,
clinical signs, positive serwn indirect
interstitial pnewnonitis, anterior uveitis,
fluorescent antibody (IFA) titer, and
and meningitis with associated cerebellar
response to treatment. In-house tests for
ataxia, depression, paresis, and hyperesthe

E can is, A phagocytophilum, A platys, and
sia Severe weight loss is a prominent

E ewingii based on enzyme in1munoassay
finding.

methods are also available, The antibody

The hemogran1 is usually markedly
response may be delayed for several weeks;
abnormal in chronic cases. Severe
thus, serologic testing may not be a reliable
thrombocytopenia may cause epistaxis,
diagnostic tool early in the course of tl1e
hematuria, melena, and petechlae and
disease. Furthermore, antibodies can
ecchymoses of the skin. Variably severe
persist for months or years after infection,
pancytopenia (mature leukopenia,
making in-house tests for tl1e organisms
nonregenerative anemia, thrombocytopeproblematic for confirmation of acute nia, or any combination thereof) may be
infection, particularly in highly enzootic
seen. Aspiration cytology reveals reactive
areas where many dogs may have antibodlymph nodes and, usually, marked ies to these agents because of previous
plasmacytosis. Frequently, polyclonal, or
infections. Testing of paired sera and
occasionally monoclonal, hypergarnmademonstration of increased antibody titers globul.inemia develops.

is recommended to confirm infection when

Other ehrlichial infections caused by E
possible, although treatment of suspected
chaffeensis, E ewingii, or A phagocytophi-cases should never be delayed or withheld

RICKETISIAL DISEASES

805
on the basis of test results, either positive or
therapy, body temperature is expected to
negative. Serologic cross-reactivity is strong return to normal within 24-48 hr after between E canis, E clwffeensis, and E
treatment. In chronic cases associated
ewingii; some cross-reactivity to A
withE canis infection, the hematologic
plwgocytophilum is also seen. In people,
abnonnalities may persist for 3-6 mo,
the EML agent shows cross-reactivity to E
although clinical response to treatment

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chaffeensis. In some areas, -500/o of dogs
often occurs much sooner. Supp01tive
infected with E canis also have a titer to A therapy may be necessary to combat
platys, which likely reflects coinfection;
wasting and specific organ dysfunction;
cross-reactivity between these agents is not
platelet or whole-blood transfusions may
seen.

be required if hemorrhage is extensive.

PCR has been used to detect and identify

Concurrent broad-spectrwn antibiotics
specific Ehrlichia and Anaplasma species may be needed if the dog has severe
in infected people and animals. Samples
leukopenia. The E canis antibody titer
appropriate for PCR include blood, tissue
should be measured again within 6 mo of
aspirates, or biopsy specimens of reticuillness to confirm a low or seronegative loendothelial organs, such as lymph nodes,
status indicative of successful therapy.

spleen, liver, or bone marrow. PCR can also

Serwn titers that persist at lower but
be used to detect the effectiveness of
positive levels should be rechecked in
treatment in clearing infection. PCR is not
another 6 mo to ensure that they are not
routinely available through commercial
increasing.

veterinary laboratories, although some
veterinary schools and research institutions
offer it. PCR is available through several

Prevention: Prevention is enhanced by
commercial human laboratories.

controlling ticks on dogs, through use of

During the acute stage, differential
reliable methods. In particular, medications
diagnoses include other causes of fever and
and products with proven efficacy againstR
lymphadenomegaly ( eg, Rocky Mountain
sanguineus are imp01tant to use. Because
spotted fever, brucellosis, blastomycosis,

R sanguineus infestations can be
endocarditis), inunune-mediated diseases
problematic in kennels and around homes,

(eg, systemic lupus erythematosus), and
and longtem1 tick control is needed for
lymphosarcoma. During the chronic stage
management, use of effective long-acting
of E canis infection, differential diagnoses collars on all susceptible dogs might be
include estrogen toxicity, myelophthisis,
considered; collars containing propoxur,
immune-mediated pancytopenia, and other
amitraz, or flumethrin have proven activity
multisystemic diseases associated with
against R sanguineus. Prevention of
specific organ dysfunction ( eg, glomerulotransfusion-associated transmission can be nephritis ).

reduced by using seronegative screened
blood donors. although new donors with a
negative screen carmot be presumed free of

Treatment: The drug of choice for
infection for several weeks because they
infection with Ehrlichia and Anaplasma
may be incubating infection. Prophylactic
spp is doxycycline because of its superior
administration of tetracycline at a lower
intracellular penetration and bacteriostatic
dosage (6.6 mg/kg/day, PO) is effective in
properties against rickettsiae. Doxycycline
preventing E canis infection in kennels
is recommended for dogs of all ages. If
where disease is endemic. Treatment must
infection is suspected, dogs should be
be extended for many months through at
treated empirically; treatment should not
least one tick season if the endemic cycle is
be withheld or delayed pending laboratory
to be successfully elinlinated, and tick
results. Early seronegative tests should not
control should be in1plemented as well.

be considered a reason to stop therapy,
because antibodies may take :?:l wk to

Zoonotic Risk: E chaffeensis, E ewingii, develop in acute cases. The recommended
and A plwgocytophilum are considered
dosage of doxycycline in dogs is 5-10 mg/
zoonoses. Despite the occurrence of
kg/day, PO or IV, for 10-21 days. Tetracydisease in both animals and people, the cline (22 mg/kg, PO, ti.ct) can also be used
involvement of a required intermediate tick
for ;:,2 wk in acute cases and 1-2 mo in
vector for transmission means dogs and
chronic cases. Two doses of i.rnidocarb
other infected animals do not pose a direct
dipropionate (5-7 mg/kg, IM), 2 wk apart,
transmission risk in normal circumstances.

are variably effective against both ehrlichio

Infection in dogs may indicate a heightened
sis and some strains of babesiosis. In acute
risk of human infections related to tick
cases receiving appropriate antibiotic
exposure in a given area.

806

RICKETISIAL DISEASES

ROCKY MOUNTAIN SPOTTED
documented in a single hun1an case and

FEVER
should be considered when selecting canine
blood donors. Direct transmission from

(Rickettsia rickettsii infection)

dogs to people has not been reported,
although hun1an infection may occur after

Etiology: Rocky Mountain spotted fever
contact of abraded skin or cof\iunctiva with

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(RMSF) is a disease of people and dogs
tick hemolymph or excreta duiing removal
caused by Rickettsia rickettsii. R rickettsii
of engorged ticks from pets.

and closely related members of the spotted
fever group of rickettsiae are considered

Clinical Findings: Dogs are highly
endemic throughout much of North, South,
susceptible to clinical infection witl1
and Central America. These pathogens are

R rickettsii; in contrast, it is rarely
transmitted primarily through the bites of
diagnosed in cats. Early signs in dogs may
infected ticks. The ability of genetically
include fever (up to 105°F [40.5°C]),
similar rickettsial organisms, such as R
anorexia, lymphadenopathy, polyarthritis,
parkeri, to cause clinically similar disease coughing or dyspnea, abdominal pain, vomitin dogs is unknown. Because of their ing and diarrhea, and edema of the face or
susceptibility to R rickeltsii and relatively extremities. Petechial hemorrhages of the
higher rates of tick exposure, dogs may
conjunctiva and oral mucosa may be seen in
serve as excellent sentinels of risk for R
severe cases. Focal retinal hemorrhage may
iickettsii infection in people. Clusters of be seen during the early course of disease.

disease are frequently reported in defined

Neurologic manifestations such as altered
geographic areas, and temporally associmental states, vestibular dysfunction, and ated infections may be seen in both dogs
paraspinal hypcresthesia may occur.

and their owners.

Thrombocytopenia is common.

Leukopenia develops during the early
stages of infection and, in untreated cases,

Epidemiology: In the USA, Dermacentor
variabilis (the American dog tick) and
is followed by progressive leukocytosis.

D andersoni

Sernrn biochemical abnom1alities may

(the Rocky Mountain wood
tick) are considered the primary vectors
include hypoproteinemia, hypoalbuminemia, azotemia, hyponatremia, hypocalcefor R rickettsii. In South America, several Amblyomma
mia, and increased liver enzyme activities.

spp of ticks have been
implicated in transmission. The organism

Case fatality rates of -lo/o--100,.6 are expected.

has also been isolated from Rhipicephalus

Lesions: Vascular endothelial damage
sanguineus ticks (the brown dog tick),
is due to direct cytopathic effects of the
which appear to be the primruy vector in
rickettsiae. Severity of the necrotizing
some focal ru·eas of Arizona, particularly
vasculitis can be directly correlated to the
on American Indian tribal lands, and may
infective dose. Vascular endothelial drunage
also play an as-yet unappreciated role in
and thrombocytopenia contribute to
outbreaks elsewhere in the USA. R san
development of petechiae and ecchymoses.

guineus ticks are also associated with

Necrosis of the extremities (acryl gangrene)

transmission of R rickettsii in Central
or disseminated intra vascular coagulation

America and with large city-based"

can develop in severely affected dogs.

outbreaks in Mexico. The pathogen is
acquired by larval and nymph stages of ticks Diagnosis: Currently, there are no while feeding on infected vertebrate hosts
in-house diagnostic tests available for
and is also passed from female ticks to
diagnosis of acute RMSF in dogs. Indirect
progeny through transovarial transmission.

fluorescent antibody titer (IFA) is preferred

An estimated < 1 % of Dermacentor spp ticks for serologic testing. However, because of
cruzy R iickettsii, even in areas considered the high incidence of cross-reacting
highly endemic. In highly enzootic regions
antibodies to a vaiiety of nonpathogenic
of Arizona where R iickettsii is transmitted spotted fever group rickettsiae, as well as
by the brown dog tick, as many as 5% of
longtenn persistence of antibodies after
ticks may be infected.

acute RMSF infection, demonstration of a

Seroprevalence in dogs from endemic

4-fold 1ise in titer should be documented in
areas ranges from 4.3o/o--77%, but these
conjunction with a compatible clinical
values do not accurately reflect infection
syndrome. Differential diagnoses include
rates because of the detection of crossother causes of fever of unknown origin.

reacting antibodies to other genetically

The therapeutic response is usually
similar rickettsiae. RMSF transmission
dramatic, as it is in other canine rickettthrough blood transfusion has been sial diseases. Animals with neurologic

RICKETISIAL DISEASES

807
dysfunction may have residual deficits.

studies of dogs in emerging areas may help

Immunity appears to be lifelong after
predict human risk of infection. Particunatural infection; therefore, recurrent larly in areas where transmission occw-s
episodes should not be attributed to RMSF.

viaR sanguineus, close cooperation
between veterinary, medical, and public

Treatment: Antibiotic treatment should
health officials is in1portant to achieve
be administered based on clinical suspicion
control.

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without waiting for results of serologic
tests, because delayed administration of
antibiotics may result in higher rates of

MURINE TYPHUS
severe or fatal outcome. Doxycycline is the
treatment of choice, regardless of age of the

(Rickettsia typhi infection, R felis infection) dog, and should be administered at a dosage Rickeltsia lyphi, the causative agent of of5-10 mg/kg/day, PO or IV, for 10-21 days.

murine typhus, and Rfelis are zoonotic

Tetracycline at 22 mg/kg, PO, tid for 2 wk is
pathogens maintained primarily in rodent
also effective. Chlorarnphenicol has been
reservoirs (rats, mice) that may also be
used to treat RMSF in the past, but its use
associated with enzootic cycles involving
is associated with higher rates of fatal
opossun1s and domestic cats. Infection is
outcome in hun1an patients, and it is not
transmitted to people and other animals
recommended. Other broad-spectrum
through contact with infected fleas.

antibiotics are ineffective againstR
rickettsii infection, and there is some

Epidemiology: Infection in people
evidence in hun1an cases that use of
is primarily thought to occur through
fluoroquinolones may actually worsen
exposure of abraded skin with infectious
infection. Early seronegative tests should
flea feces; aerosolization of infectious
not be considered a reason to stop therapy,
materials may occur in limited settings.

because antibodies may take �1 wk to

Dogs and cats are presumably exposed in a
develop in acute cases. Suppo1tive care for
similar fashion. Although known to occur
dehydration and hemorrhagic diathesis may worldwide, currently fewer than several be necessary. Because of alterations in
hundred human cases of murine typhus are
vascular integrity, conservative rates of fluid reported in the USA each year. Enzootic administration are advised. Precautions
infection is the most commonly reported
should be taken for the safe removal and
from southern Texas, California, and
control of ticks. In settings in which

Hawaii, although the disease is believed

R rickettsi i transmission from R san
to be underreported.

quineus is suspected, medications and
products with proven efficacy against this

Clinical Findings: Clinical illness
tick species are important to use. Because
associated with canine and feline infec

R sanguineus infestations can be
tion with R lyphi and Rfelis is not well problematic in kennels and around homes,
docwnented, but evidence of exposure
and longterm tick control is needed for
based on presence of antirickettsial
outbreak control, use of effective longantibodies has been noted, particularly acting tick collars on all susceptible dogs
in association with outbreaks of hun1an
might be considered; collars containing
disease. Although a role as a possible
propoxur, arnitraz, or flumethrin have
rese1voi.r for infection has been suggested,
proven activity againstR sanguineus.

particularly for cats, the importance of
domestic animals in maintenance of

Zoonotic Risk: R rickettsii is considered enzootic cycles has not been well elucia zoonotic pathogen. The potential for dated. Nonetheless, dogs and cats may, at
household clustering and large urban
a minimwn, serve as a source of fleas that
outbreaks, particularly in areas with
may pose a transmission risk to people.

transmission by brown dog ticks, makes

Regular flea control is recommended to

RMSF a disease of significant public health
reduce risk of flea-associated transmission
concern. Although clinical disease occurs
to people.

in both animals and people, the involvement of a required intermediate tick vector Diagnosis: An indirect fluorescent
for transmission means dogs and other
antibody (IFA) titer assessed in paired sera
infected animals do not pose a direct
is preferred for serologic testing and is most
transmission risk in normal circumstances.

commonly used in coajunction with

Wection in dogs indicates a heightened
environmental assessments around a
risk of human infections related to tick
human outbreak. There is some degree of
exposure in a given area, and serologic
antibody cross-reactivity with antibodies

808

RICKETISIAL DISEASES
from other rickettsial infections, including
become infected by ingesting trout, salmon,

R rickettsii, so assessments should ideally or Pacific giant salan1anders that contain
be made with paired sera. PCR of whole
the encysted metacerca.ria stage of the
blood may also be used, but its utility in
rickettsia-infected fluke. In the dog's
assessing canine and feline infection is
intestine, the metacercarial flukes excyst,
unknown because the animals may not
embed in the duodenal mucosa, become

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exhibit clinical signs during periods of
gravid adults, and transmit the rickettsiae
rickettsemia, making it difficult to deterto monocytes-macrophages. The fluke mine the optimal time for assessment.

infection itself produces little or no clinical
disease. A recent repmt of SPD in two

Treatment: In the absence of clinical
captive Malayan sun bears underscores the
signs, specific treatment is not recomneed to consider this etiology in non-native mended. If clinical illness associated with
exotic species with compatible exposure

R typhi or Rfelis infection is suspected in and clinical histories.

a dog or cat, doxycycline may be administered at a dosage of 5-10 mg/kg/day, PO
or IV, for 10-21 days. Animals should be

Epidemiology: The life cycle of Neo
provided with routine preventive treat
rickettsia helminthoeca is maintained by
ments to control fleas. Control progran1s
the release of infected fluke ova in the feces
involving animal removal from an area of
of the ma.nunalian host. Infected miracidia.

enzootic activity should be accompanied by
develop from these ova and infect the snails
pesticide treatment of the environment to

Juga plicifera and Juga silicula to form prevent fleas feeding on people after the
infected redia.e. Redia.e develop into
removal of prefeITed blood-meal hosts.

infected cerca.iia.e that a.re released from the
snail, penetrate the salmon or trout, a.i1d

Zoonotic Risk: R typhi is considered a develop into encysted metacercaria.e
zoonotic pathogen. Serologic evidence of
infected withNe01ickettsia. The cycle is
exposure or past infection in dogs or cats
completed when man1111als eat the fish, and
indicates a heightened 1isk of human
infected metacercaria.e become infected
infections in a given area, and flea control
gravid adults and pass Neorickettsia to
for pets is an essential component of
fluke eggs. Although Ne01ickettsia infection of dogs is not required for the life cycle of
disease control.

Neorickettsia, mammalian infection is
required to maintain U1e trematode life

SALMON POISONING DISEASE
cycle. Transmission by cage-to-cage contact,

AND ELOKOMIN FLUKE FEVER
rectal thermometers, or aerosols is rare.

There a.re no age, sex, or breed predilec

(Neorickettsia spp infection)

tions; however, the disease prevalence is

Salmon poisoning disease (SPD) is an acute, higher when the availability of trema.todeinfectious disease of can.ids, in which the infected fish is greater. Infected fish are
infective agent is transmitted through the
found in the Pacific Ocean from San
various stages of a fluke in a snail-fish-dog

Francisco to the coast of Alaska, but SPD is
life cycle. The name of the dise.ase is
more prevalent from northern California. to
misleading, because no toxin is involved.

Puget Sound. It is also seen inland along the

Elokomin fluke fever (EFF) is an acute
rivers of fish migration. SPD also has been
infectious disease of can.ids, feITets, bears,
reported in southern California and Brazil.

and raccoons that resembles SPD but has a

The snail is the primary factor for geowider host range. In people, Neorickettsia graphic limitation, but dogs fed under
sennetsu causes a disease known as
cooked or raw fish from the superma.i·ket

Sennetsu ehrlichiosis, and in horses
may have developed SPD.

N risticii causes a disease known as

Potomac horse fever; these have not been

Clinical Findings: In SPD, signs appear
reported as a cause of illness in dogs except
suddenly, usually 5-7 days after ea.ting
for one report of N ri.sticii in Illinois.

infected fish, but may be delayed as long
as 33 days, and persist for 7-10 days before
culminating in death in up to 90% of

Etiology: SPD is caused by N helmin
untreated anin1als. Body temperature pea.ks
thoeca and is sometimes complicated by a
at 104°-107.6°F (40°-42°C) 1 -2 days later,
second agent, N elokominica, which causes then gradually declines for 4-8 days and EFF. The vector for these Ne01ickettsia
returns to nonnal. Frequently, a.i1imals
agents is a small fluke, Nanophyetus
a.re hypothermic before death. Fever is
salmincola. Dogs and other anin1als
accompanied by depression and complete

RICKETISIAL DISEASES

809
anorexia in virtually all cases. Persistent
yellowish brown, rough-surfaced, and
vomiting usually occurs by day 4 or 5.

-87-97 x 35-55 µm, with an indistinct

Vomiting occurs in most cases, and
operculum and a small, blunt point on the
diarrhea, which develops by day 5-7,
opposite encl. During the first day or two,
often contains blood and may be severe.

few ova may be passed. Inti·acellular

Dehydration and extreme weight loss occur. organisms have been demonstrated by VetBooks.ir

When severe, the GI signs are clinically

Romanowsky staining on lymph node
indistinguishable from those of canine
aspirates in -70% of cases. PCR testing to
parvoviral infection. Generalized lyrnphaddetect DNA-specific N helminlhoeca ( or enopathy develops in -60% of cases. Nasal

Neorickettsia genus) is recommended for
or conjunctiva! exudate may be present and
accurate diagnosis. Serologic testing using
mimic signs of distemper. Neutrophilia is
the N helminthoeca organism has been
conunon, but a marked, absolute leukopedeveloped. Other causes of fever of nia with a degenerative left shift may occur.

unknown 01igin, generalized lyrnphadenop

Th.rombocytopenia is repo1ted in 94% of the
athy, vomiting, and diruThea are differential
cases. Serum chernistiy values are nom1al.

diagnoses. When diruThea and exuclative

Clinically, EFF is a milder infection than
coajunctivitis occur, distemper should be

SPD. Severe GI signs are less conunonly
considered.

seen in EFF infections, and lyrnphadenopathy may be a more pronounced finding.

Case fatality rates with EFF are lower, at

Prevention and Treatment: Currently,

-HJO/o of untreated cases.

the only means of prevention is to restrict
t11e ingestion of uncooked salmon, ti·out,

Lesions: Infection appears to chiefly
steellieacl, and sin1ilar freshwater fish. In
affect the lymphoid tissues and intestines.

animals that recover, a profound hw11oral

There is enlargement of the GI lymph
inunune response persists, but there is no
follicles, lymph nodes, tonsils, thymus, and
cross-resistance between N helminlhoeca
to some extent, the spleen, with microand N elokominica. Sulfonru11ides are not scopic necrosis, hemorrhage, and hyperplaeffective and may exacerbate the clinical sia Remarkable abdominal or mesenteric
disease. Recommended treatinent is
lyrnphadenomegaly may be seen. A variable
pru·enteral oxytetracycline (7 mg/kg, JV, tid
but often severe nonhemorrhagic enteritis
for 5 days) or doxycycline (10 mg/kg, bid for
is seen throughout the intestine with SPD

7 clays). Oral tetracycline or doxycycline is
but is less commonly seen with EFF.

contraindicated because of in1pinging GI

Microscopic foci of necrosis also appear
signs. Animals usually succwnb because
aprut from the follicles. Nonsuppurntive
of dehydration, electi·olyte and acid-base
meningitis or meningoencephalitis has been
imbalances, and anemia. Therefore, general
identified in some dogs.

supportive therapy to maintain hydration
and acid-base balru1ce, while meeting

Diagnosis: Fluke ova are found on fecal
nutlitional requirements and conti·olling
exan1ination in -92% of cases, which
diarrhea, is often essential. Judicious use of
supp01ts the diagnosis. The ova are oval,
whole blood tr3l1Sfusions may be helpful.

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IMMUNE SYSTEM

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THE BIOLOGY OF THE IMMUNE SYSTEM 811

Physical Barriers 812

Innate Immunity 812

Complement 813

Cells oflnnate Immunity 813

Adaptive Immunity 814

Antibody Responses (Humoral Immunity) 815

Cell-mediated Immunity 816

Immunologic Memory 817

Cytokines 817

Regulatory Cells 817

IMMUNOLOGIC DISEASES 817

Immunodeficiency Diseases 818

Primary Immunodeficiencies 818

Defects in Innate Immunity 818

Deficiencies in Adaptive Immunity 819

Diagnosis 821

Secondary Immunodeficiencies 821

Virus-induced Immunodeficiencies 821

Excessive Immune Function 822

Excessive Innate Responses 822

Excessive Adaptive Responses 823

Type I Reactions (Atopic Disease, Anaphylactic Reactions) 823

Type 11 Reactions (Antibody-mediated Cytotoxic Reactions) 826.

Type Ill Reactions (Immune Complex Disease) 828

Type IV Reactions (Cell-mediated Immune Reactions) 830

Tumors of the Immune System 831

Gammopathies 832

THE BIOLOGY OF THE IMMUNE SYSTEM

Animals are under constant threat of
nisms that can be thought of as a series
invasion by a diverse range of microorof barriers. These mechanisms include ganisms that seek to enter the body and
physical barriers to invasion such as a
exploit its resources for shelter and food.

tough, thick skin or the ability to cough

To ensure survival and prevent such
and sneeze. The second line of defense is
exploitation, the body combats the most
a "hard wired" system of innate immunity
dangerous of these invaders with an
that depends on a rapid, stereotyped
equally complex set of defensive mecha-
response to stop and kill both bacterial

812

THE BIOLOGY OF THE IMMUNE SYSTEM
and viral invaders. This is typified by the
centers largely on the presence of the huge
process of acute inflammation and by the
and in1mensely complex nom1al conimensal
classic sickness responses such as a fever.

nlicrobiota. Potential invaders may be

The third line of defense is the highly
unable to colonize the intestine in the
complex, adaptable, and incredibly
presence of a well-adapted population
effective adaptive immune system.

of conm1ensal nlicrobes. If all else fails,

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Innate immune responses are highly
invaders may be rapidly removed from
effective against opportwlistic organisms
the GI tract by vonliting and diarrhea
or those of low virulence, but by their very

The intestinal nlicrobiota plays a critical
nature cannot do more than delay highly
role in maintaining animal health. First, it is a
pathogenic nlicrobial invaders. Longterm
source of nutrients, especially in herbivores,
resistance and swvival depends on adaptive in which it provides a means of exploiting a immmlity. The adaptive immune system is
cellulose-rich diet and a source of essential
effective against a wide variety of pathovitanlins. This nlicrobiota also plays a gens. Its effectiveness improves each time
critical role in the defense of the body. The
it is activated in response to nlicrobial
large, well-adapted nlicrobial population
invasion. Because the body accumulates
excludes many potential pathogens through
in1mune memory cells as it ages, adaptive
competition. More importantly, the constant
immunity provides an almost insunnountstimulus provided by the presence of the able barrier to most potential invaders. In
nlicrobiota effectively stimulates the correct
its absence, the animal dies.

development of the adaptive immune system

The adaptive immune system faces
and regulates the level of inflanm1ation
complex challenges. Many different
mediated by innate immune systems.

nlicroorganisms, including bacteria, viruses,
protozoa, and helnlinths, may attempt

INNATE IMMUNITY
invasion. The optimal inimune responses to
this diversity of invaders must also be very

Microbes that succeed in penetrating the
diverse. For example, invaders such as
physical barriers of the body are rapidly
bacteria that live outside body cells are best
detected, and the innate defenses are
attacked by an antibody-mediated (or
activated. Although multiple innate
humoral) immune response, whereas
mechanisms exist, acute inflammation is
virnses living within cells are best destroyed the central feature of innate immunity.

by the killing of infected cells through

The first step in the inflammatory process
cell-mediated mechanisms.

is the early detection of either invading
organisms or damaged tissues. Most

PHYSICAL BARRIERS
invaders are recognized by patternrecognition receptors that bind and The physical barriers on the surface of the
recognize conserved molecules expressed
body play a significant role in slowing or
on nlicrobial surfaces. There are many
blocking microbial invasion. Very few
different pattern-recognition receptors,
nlicroorganisrns can penetrate intact skin;
but the most in1portant are the toll-like
instead, invaders usually enter through
receptors (TLRs). TLRs are a family of at
wounds or by being irtjected, such as by
least 10 different receptors found on the
mosquito bites. Skin wounds heal rapidly to
surface or in the cytoplasm of cells such
reestablish the protective barrier. A complex as macrophages, intestinal epithelial cells, population of nom1al skin bacteria tends to
and mast cells. The TLRs on cell surfaces
exclude new invaders, while antinlicrobial
bind to molecules commonly expressed by
molecules in sweat can kill many would-be
extracellular bacteria such as lipopolysacinvaders. In the airways, the structure of the charides or lipoproteins. The cytoplasnlic
upper respiratory tract serves as an effective TLRs, in contrast, bind to the nucleic acids filter of small particles. The airways
of intracellular viruses. Once they bind
themselves are lined with a layer of adhesive their ligands, the TLRs trigger the mucus that can entrap nlicrobes. The mucus
production of proteins such as intercontains multiple antinlicrobial proteins leukin 1 (IL-1) or interferon a (IFN-a).

such as defensi.ns, lysozyme, and sur

IL-1 and the otl1er cytokines produced
factants. "Dirty" mucus is constantly being in response to TLR stimulation then trigger
replaced by clean mate1ial as ciliary action
acute inflammation. They initiate the
carries it to the pharynx where it is
adherence of circulating leukocytes to
swallowed. Coughing and sneezing remove
blood vessel walls close to sites of invasion.

larger irritants from tl1e airways and nasal

These leukocytes, especially neutrophils,
passages and are essential defensive
then leave the blood vessels and nligrate
reactions. The defense of the intestine
to invasion sites, attracted by nlicrobial

THE BIOLOGY OF THE IMMUNE SYSTEM

813
products, small proteins called chemo

Complement
kines and molecules from damaged
cells. 'once they anive at the invasion site,

Although acute inflanunation is central to
the neutrophils bind invading bacteria,
the processes of innate inm1unity, the body
ingest them through the process of
possesses other innate defenses. Tissues .

phagocytosis, and kill the ingested
contain antinlicrobial peptides that can bmd

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organisms. This killing is largely mediated
and kill invading bacteria. These include
by a metabolic pathway called the
detergent-like molecules such as the
respiratory burst that generates p
defensins or cathelicidins that can lyse

_otent
oxidants such as hydrogen peroXIde and
bacterial cell walls, enzymes such as
hypochloride ions. Neutrophils, however,
lysozyrne that kill many gram-positive
have minimal energy reserves and can
bacteria, and iron-binding proteins such
undertake only few phagocytic events
as hepcidin or haptoglobin that prevent
before they are depleted.

bacterial growth by dep1iving them of

Even if the initial inflammatory response
essential iron supplies. Perhaps the most
is successful in killing all invaders, the body
in1portant of these innate defenses is the
must still remove cell debris, eliminate any
complement system, winch consists of a
swviving microbes and dying neutrophils,
complex group of -30 proteins that act
and repair the damage. This is the task
collectively to kill invading microbes. The
of macrophages. Tissue macrophages
prin1ary function of the complement system
originate as blood monocytes
is to bind two proteins called C3 and C4

: They, like
neutrophils, are attracted to sites of
ilTeversibly to nlicrobial surfaces. Once
microbial invasion and tissue dan1age by
bound these complement components may
chemokines and damaged tissues, where
either kill microbes by rupturing them using
they finish off any swviving invaders.

another protein called C9 or sin1ply coat

.

They also ingest and destroy any remamthem so that they are rapidly and effectively ing neutrophils, thus ensuring that 1:he
phagocytized by leukocytes.

.

neutrophil oxidants are removed without

The complement system can be acti-
toxic spills occurring in the tissues. Finally,
vated in tlu-ee ways. One way, called the
another population of these macrophages
alternative pathway, is niggered by the
begins the process of tissue repair.

presence of bacterial surfaces that consist

.

Macrophages that complete the destrnctive
largely of carbohydrates and can bi.t1d the
process are optinlized for microbial destrnccomplement protei.11 C3. Once bound, the tion and are called Ml cells. Macrophages

C3 acts as an enzyme to activate and bind
optimized for tissue repair and removal of
more C3. These CS-coated bacteria are
damaged tissues are called M2 cells.

rapidly and effectively phagocytized and

Many of the molecules produced as a
destroyed. Alternatively, srniace-bound C3
result of inflammation and tissue damage,
can activate additional complement
such as IL-1 and tumor necrosis factor,
components that eventually cause a p,otein
can reach the bloodstream where they
called C9 to insert itself withm bacterial cell
circulate. They enter the brain and trigger
walls where it causes bacterial rupture. A
sickness behavior; for example, they alter
seco�d complement-activating pathway is
the thermoregulatory centers to cause a
triggered when bacterial surface carbohy-.

fever, act on appetite-controlling centers to drates bind to a mannose-bmding protem m suppress appetite, and act on sleep centers
serum. This binding activates an enzyme
to produce sleepiness and depression.

pathway that leads to activation of C3 or C9.

They also mobilize energy reserves from

The third, or classic, pathway of coml?leadipose tissue and muscle. This sickness ment activation is triggered when antibodbehavior is believed to enhance the defense ies bind to microbial swiaces. It is thus of the body by redirecting energy toward
triggered by adaptive immune responses. As
fighting off invaders.

with the mannose pathway, this eventually

Circulating cytokines from inflammatory leads to activation of C3 and C9. Because of sites also act on liver cells, causing the cells its potential ability to cause severe tissue to secrete a mixture of "acute-phase
damage, the complement system is carefully
proteins," so-called because thei
regulated through multiple complex

_r blood
levels climb steeply when acute mflammaregulatory pathways.

tion develops. Different species have different acute-phase proteins, including serum Cells of Innate Immunity
amyloid A, C-reactive protein, and many

The key to an effective innate immune
different iron-binding proteins. Acuteresponse is prompt recognition of invasion phase proteins also serve to promote
and a rapid cellular response. Several cell
innate immunity.

types function as sentinel cells; three of the

814

THE BIOLOGY OF THE IMMUNE SYSTEM
most important are macrophages, dendlitic

ADAPTIVE IMMUNITY
cells, and mast cells. These cell types express
pattern recognition receptors such as TLRs

Innate in1munity, although critical to the
and can sense the presence of microbial
defense of the body, is insufficient to
invaders. They also express multiple other
guara11tee protection. It lacks the
receptors that can detect microbes and
flexibility to respond optin1ally to a
tissue dan1age. When these receptors are
diversity of microorga11isms a11d by its

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engaged, they signal through a molecule
very nature may cause significa11t tissue
called NF-KB to tum on the production of
dainage. A third layer of defense is
cytokines such as IL-1, IFN-a, and TNF-a.

required that can act automatically in

They also release vasoactive and pain
response to microbial invasion, generate
molecules such as histamine, leukotrienes,
resista11ce proportional to the threat, a11d
prostaglandin, and specialized peptides that
improve with experience. These are the
initiate the vascular events in inflan1rnation.

key features of the adaptive immune

The purpose of inflan1mation is to ensw·e
system. Adaptive immune responses are
that leukocytes are delivered as promptly as
of two major types: a11tibody (hwnoral)

possible to sites of microbial invasion. This
immunity directed against extracellular
involves attracting these cells from tl1e
invaders, and cell-mediated immwuty
bloodstrean1 where they circulate and
directed against intracellulai· invaders.

inducing them to migrate through tl1e

Adaptive immune responses are
tissues to the invasion sites where they
complex a11d must be very carefully
engulf and kill invaders. There are three
regulated. The immune defenses of the
major leukocyte populations that can kill
body constitute a potent system of protecinvaders. Granulocytes are especially tion that must be carefully controlled to
effective at killing invading bacteria. They
minimize dainage to normal tissues. As a
engulf the invaders, activate a metabolic
result, a major pmtion of the immune system
pathway called the respiratory burst, and
is devoted to the production of regulatory
generate letl1al oxidizing molecules such as
cells that function to ensure that adaptive
hydrogen peroxide and hypochloride ions
immune responses occur only under
that kill most ingested bacteria. Eosinophils
appropriate circun1sta11ces. If these
are specialized killers of invading parasites.

regulatory pathways fail, disease or death

They contain enzymes that are optimized to
may result.

kill migrating helminth larvae. The third

The adaptive immune system functions
major killing cell population are Ml
through a series of steps that must occur
macrophages. These cells migrate into areas sequentially for eitl1er a11 antibody-mediated of microbial invasion more slowly than
or cell-mediated il11rnune response to occur.

granulocytes. However, they are capable of

The first step involves the capture and
sustained and effective phagocytosis. They
processing of foreign antigens. Once
contain the highly lethal antj.microbial
processed, these antigens are transported to
factor nitric oxide and thus can kill
cell surfaces, where they can be recognized
organisms resistant to neutrophil killing.

by lymphocytes carrying receptors for

When inflanrn1ation leads to activation of
specific antigens. Each a11tigen receptor is
macrophages, they secrete a cytokine called highly specific, a11d each lymphocyte IL-23. This, in tum, acts on a popuiation of
expresses only a single fom1 of a11tigen

T cells (called Th17 cells), causing them to
receptor. Thus, millions of cells have tl1e
secrete IL-17. IL-17 recruits granulocytes to
potential to recognize millions of a11tigens.

sites of inflai11rnation, infection, and tissue

To ensure that only foreign a11tigens trigger
dainage.

adaptive irnmwuty, cells with (eceptors that

While mai1y leukocytes are optimized to
bind and respond to nom1al body a11tigens
kill invading bacteria, viruses also present a
are selectively killed early in their developpotent threat. Natural killer (NK) cells are a ment. The surviving cells are located within
population of innate cells optimized to kill
lymphoid orga11s at sites where they ca11
virus-infected cells. NK cells, a form of
most effectively encounter antigens on
lymphocyte, ca11 kill virus-infected or other
microbial invaders, triggering tl1em to

"abnormal" cells tl1at fail to express major respond by motmting in1rnune responses.

histocompatibility complex (MHC) class I

There are tJu·ee major populations of
molecules. MHC class I molecules bind to
lymphocytes: B cells that are responsible

NK cell receptors and switch off their killing for antibody responses, effector T cells abilities. In tl1e absence of this signal, the
that are responsible for cell-mediated

NK cells bind to target cells, ir\ject them
in1mune responses, a11d regulatory T cells
with apoptosis-inducing proteins, and kill
tl1at control these responses and minimize
them.

inappropriate responses.

THE BIOLOGY OF THE IMMUNE SYSTEM

815

Antibody Responses {Humoral

Antibodies: Antibodies are composed of

Immunity)

proteins called in1111unoglobulins. Mammals
use five different classes of antibodies:

Antibodies are protein molecules that seive
in1111unoglobulin G (lgG), IgM, lgA, IgE, and
as B-cell antigen receptors that can be

IgD. The class of immunoglobulin secreted
synthesized in large quantities and secreted
by B cells and plasma cells depends on their

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by the cell into the bloodstrean1 where they
location. Cells located in lymphoid organs
circulate. These proteins are produced by
within the body secrete IgM and IgG,

B cells and from B cell-derived plasma cells.

whereas cells located on body surfaces

Antibodies bind to foreign molecules and
secrete IgM, lgA, and IgE.

mark them for destruction by phagocytic

IgG is the most abundant immunoglobucells or complement-mediated lysis. Plasma lin found in the bloodstrean:i and plays the
cells are differentiated B cells optimized to
major role in eliminating organisms that
synthesize and secrete enom1ous quantities
succeed in penetrating deep into the body.

of antibodies. Antibodies are critical to host

IgM seives as a "back-up" for IgG and is
defense against extracellular invaders such
usually confined to the bloodstream. IgM is
as most bacteria, some blood parasites, and
produced early in the antibody response,
viruses traveling between cells.

when its high effectiveness compensates

B cells originate in the bone marrow and
for its low quantity.

reside in lyn1phoid tissues such as lymph

IgA is produced by B cells and plasma
nodes, bone marrow, Peyer's patches, and
cells located on mucosa! surfaces. As a
the spleen. Each B cell is covered by several
result, IgA is produced and secreted in large
thousand identical antigen receptors and
amounts into the upper respiratory tract,
can bind and respond to only a single
the GI tract, tears, sweat, etc. In these
antigenic molecule. When a microbe enters
locations, it complements the physical
the body, it will inevitably encounter B cells
barriers of the body and prevents microbial
that can bind to some of its surface antigens. invasion. IgE seives as a "back-up" for IgA As a result of antigen binding, and under
and is also mainly produced on body
suitable circun1stances, these B cells divide
surfaces. IgE is optinuzed to control
repeatedly and differentiate into two
invasion by parasites such as helminths or
subpopulations. One subpopulation is
arthropods. However, it also mediates a
composed of antibody-producing plasma
rapid acute inflammation in allergic states
cells, which are capable of enormously
and hence may mediate life-threatening
increased protein synthesis and are the
anaphylaxis. The function of lgD is unclear,
major sources of antibodies. The other
but it is believed to be of minimal signifisubpopulation is composed ofB cells that cance.

develop into memory B cells and persist in
lymphoid tissues for months or years. When

T Cell Help: Most antibody responses are
an animal encounters an antigen for a
regulated by the need to receive prior
second time, these memory B cells respond
approval from T cells. The T cells in tum
rapidly, producing large numbers of plasma
are activated only when they bind antigen
cells (and more memory cells). As a result,
fragments presented by specialized antigenthe anin1al mounts a vastly improved presenting cells called dendritic cells.

antibody response and the invader is rapidly

Dendritic cells are macrophage-like cells
elin1inated. Subsequent exposure to a
that capture and process foreign antigens.

microbe leads in turn to the accumulation

Their name derives from their many long,
of more memory cells, resulting in better
thin, filamentous processes or dendrites
protection and virtually guaranteeing that
that extend through tissues to form an
the organism will never be able to cause
effective antigen-trapping web. For
disease in that anin1al. This response is the
example, a subpopulation of dendritic cells
basis of all vaccination programs.

(Langerhans cells) is found in the dennis,

Although simple in concept, B cell
where its web of dendrites traps microorresponses and antibody production are ganisms seeking to enter the body through
made more complex by the need to ensure
damaged skin. Dendritic cells capture and
their careful regulation. Thus, a B cell is not
phagocytize invading microorganisms.

usually able to respond to a b0tmd foreign

Fragments of these foreign antigens persist
antigen unless it also receives "permission"

within the dendritic cells, where they
in the form of a second signal from cells
become attached to receptor molecules
called helper T cells. These T cells in tum

(major histocompatibility complex [MHCJ
can only be activated if they are presented
molecules). Once fonned, these antigenwith antigen under carefully controlled receptor complexes move to the cell surface
circwnstances.

where they can be recognized by T cells.

816

THE BIOLOGY OF THE IMMUNE SYSTEM

The receptors in dendritic cells that bind
whereas the other (DC2 cells) triggers
and present antigen fragments are specialantibody formation. These dendritic cell ized proteins encoded by genes clustered
populations send different messages to T
together in the MHC ( originally identified
cells, because they use different cytokines
as the antigens that cause graft rejection,
for signaling; DCl cells secrete IL-12,
hence their unusual nan1e ). There are many
whereas DC2 cells secrete IL-1. In tum,

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thousands of different MHC molecules
these different cytokines stimulate two
expressed within an animal population but
different T cell populations: Th l, which
relatively few (3-6) different molecules
promotes cell-mediated in1munity, and Th2,
expressed in any individual anin1al. Because
which promotes B cell responses and
they play a critical role in binding antigen
antibody production. Thl cells secrete
fragments and activating T cells, MHC
a mixture of cytokines typified by
molecules effectively detennine whether an
interferon-')! (IFN-')I). Th2 cells secrete
individual can respond to a foreign antigen.

a mixture of cytokines typified by IL-4.

An individual anirnal possesses MHC

B cells will usually respond optimally to a
molecules that can bind many, perhaps most,
foreign antigen only if they are stimulated
foreign antigens, but not all of them. If an
by the presence ofIL-4 from Th2 cells.

animal lacks MHC molecules that can bind
an antigen, it will be unable to respond to
that specific antigen. The set of antigens to

Cell-mediated Immunity
which an individual can respond (and against As described above, cell-mediated inunune which it is protected) are determined by its
responses are required to combat intracel

MHC haplotype. All domestic animal species
lular invaders such as viruses and some
possess their own unique MHC. The
intracellular bacteria. The immune system
receptors coded for these genes are named
blocks virus infections by killing tl1e cells
after the specific species; thus, Bo LA is the
that they infect. The cells responsible are
name of these molecules in cattle, ELA in
called effector, or cytotoxic, T cells. Like
horses, SLA in swine, etc.

T cells, effector T cells w1dergo develop

As with B cells, T cells possess specific
ment and selection witllin the thymus, so
antigen receptors on their surface that are
any T cells capable of killing nom1al healthy
generated randomly when the cells are first
cells are elinlinated. The surviving T cells
produced. As T cells mature within the
are released into the body, where they
thymus, cells with receptors that can bind
circulate continuously tllrough the tissues
normal body components are killed.

seeking out abnonnal cells.

Surviving T cells can respond only to

All nucleated cells produce many different
foreign antigens. The antigen receptors on
proteins when ftmctioning nom1ally.

T cells, like those on B cells, are identical

Virus-infected cells, however, are forced by
on any single cell. Unlike those on B cells,
tl1e virus to produce viral proteins. The body
however, the receptors can recognize
therefore requires that all nucleated cells
antigen only when it is bound to an MHC
send a sample of their newly synthesized
molecule. Thus, when a dend1itic cell
proteins to the cell surface. This involves the
presents MHC-associated antigen to T cells,
cell diverting a small sample of each newly
only those T cells witb appropriate
formed protein and fragmenting it in a
receptors will bind to the dendritic cells.

complex enzyme system called a protea

Once in contact, the cells exchange signals
some. The resulting protein fragments are
that confirm that the T cell is responding to
then attached to MHC molecules and carried
a correctly processed antigen. After T cells
to the cell surface, where they are available
receive all the necessary signals, they
for inspection by effector T cells. If the cell's
secrete a mixture of cytokines that pennit
receptors do not engage a protein fragment,
their attached B cells to respond to antigens
nothing happens. If, however, their antigen
and allow antibody production to proceed.

receptors bind to a foreign antigen fragment

Antibodies are produced in response
in an MI-IC-protein complex, tl1e T cell will
to, and directed against, extracellular
be signaled to kill the offending cell. Like
bacteria. Cell-mediated responses, in

B cells, effectorT cells function only if they
contrast, are directed against viruses and
receive permission from a helper T cell,
intracellular bacteria. The detennination
specifically a Thl cell. The cytokines from
as to the appropriate form of the immune

Thl cells, especially IFN-')I, must be present
response is made at an early stage in the
if an effector T cell is to kill its target.

immune response. Thus, there are two

Effector T cells bind tightly to target cells
populations of dendritic cells that can trap
expressing foreign antigens and then signal
and process antigens. One population (DCl them to destroy themselves through cells) triggers cell-mediated in1munity,
apoptosis. The T cells ir\ject their targets

IMMUNOLOGIC DISEASES

817
with enzymes called granzymes that trigger
come into physical contact and exchange
this process. As a result, effector T cells
signals through receptors within the contact
eliminate virus-infected cells but not
area or immunologic synapse. Exan1ples
normal, healthy cells. Most effector T cells
include the contact between T cells and
die within a few days once they are no
dendritic cells or between effector T cells and
longer needed, but a few survive to become
their targets. ln1mune cells can also signal

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long-lived memory cells that respond rapidly nearby cells by secreting small signaling should the animal encounter the virus again.

proteins called cytokines. Several hundred

Effector T cells are especially effective at
different cytokines have been identified.

killing target cells that produce foreign

Signaling cells secrete a mixture of cytokines
antigens. However, some intracellular
that then bind to receptors on nearby cells.

organisms, especially intracellular bacteria,

The target cell receives multiple signals that
are best destroyed by other cell-mediated
it must integrate to respond appropriately.

mechanisms. In these cases, TFN--y from Thl

Cytokines, acting through their specific
cells activates M 1 macrophages. As a result,
receptors, can turn the synthesis of specific
bacteria that can survive within normal
proteins on or off. They can cause the target
macrophages are rapidly destroyed by
cell to divide or differentiate, and they may
activated macrophages.

nigger apoptosis. With hundreds of different
cytokines acting in complex mixtmes it is

Immunologic Memory
sometin1es difficult to predict exactly how
a specific target cell will respond. Major

The effectiveness of adaptive immunity is
fan1ilies of cytokines include the interleukins
largely a result of its ability to recognize
that mediate signaling between leukocytes,
antigens encountered previously and to
interferons that mediate interactions
mount an enhanced and accelerated
between cells and have significant antiviral
response against them. The more an animal
activity, growth factors that regulate growtl1
encounters an antigen, the greater will be its and differentiation of many different cell immune response. 1mmw1ologic memory
types, and tun10r necrosis factors that
depends on the presence of persistent
modulate inflan1matory responses.

populations of memory cells that accwnulate as an anin1al ages. These memory cells Regulatory Cells
may be very long-lived or, more likely, turn
over very slowly. As a result, animals may

The adaptive immune system is carefully
make small an1ounts of antibodies to
regulated by several different cell populavaccine antigens for many years after tions. The most important are T ..,8 cells,
vaccination. Cell-mediated memory may
which secrete a mixtme of cytokines that
also be due to the development of very
inhibit conventional immw1e responses.

long-lived populations of memory T cells.

They serve to turn off an in1mune response

The effectiveness of vaccines in inducing
once it has completed its task ans the
long-lasting immunity depends in large part
invading microorganism is eliminated. T res
on their ability to induce memory cell
cells also play a central role in preventing
populations.

the development of autoimmunity. Anotl1er
important population of regulatory T cells

Cytokines
are called Thl 7 cells. These cells, so called
because they secrete IL-17, regulate the

The cells of the adaptive in1mune system
innate immw1e system and the development
communicate in several ways. They can
of inflan1mation.

IMMUNOLOGIC DISEASES

The primary role of the immune system is
immunity (seep 812) and adaptive
the detection and destruction of invading
in1munity (seep 814). Protection within
microorganisms. Because of the great
the first few days of microbial invasion
diversity of microbial invaders, the immune is the responsibility of the "hard-wired"

system has evolved an equally complex
innate immune system. Longterm
mixture of protective mechanisms. These
protection is the responsibility of the
may be simply classified as innate
adaptive immune system.

818

IMMUNOLOGIC DISEASES

In general, disease associated with the

PRIMARY IMMUNODEFICIENCIES
immune system takes two forms: insufficient in1mune function causing inlmunodefi

Defects in Innate Immunity
ciencies, manifested as increased susceptibility to infections, and diseases resulting Phagocytosis is a central feature of innate
from excessive in1mune function, resulting
inununity. Phagocytic cells are found

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in hypersensitivities and autoin1munity.

underlying the mucous membranes and

Under certain circumstances, normally
skin and in tile bloodstream, spleen, lymph
protective inlmune responses can cause
nodes, meninges, synovial membrane,
significant tissue damage. In general,
bone marrow, and around blood vessels
excessive innate immune responses do this
tlu·oughout tile body. Phagocytes are
by triggering inappropriate inflan1mation
either in the tissue (histiocytes, synovial
leading to collateral damage to nearby
macrophages, Kupffer cells, etc) or in tile
tissues, or by producing vastly excessive
blood (neutrophils and monocytes).

amounts of inflammatory cytokines.

Phagocytes have receptors for inlmuno

Excessive adaptive immune responses, in
globulins and complement on their surfaces
contrast, can cause damage by multiple
that assist in tile engulfment ( opsonization)

mechanisms. One simple classification
of foreign material coated with specific
divides diseases due to excessive adaptive
antibody (opsonins) or complement, or
immune responses into four distinct types.

both. Phagocytosis involves chemotaxis of

Each involves the activities of different cell
tile phagocyte toward foreign, noxious, or
populations or complement. Type I is
damaged tissues; adherence of microorganmediated by mast cells and eosinophils, isms to the plasma membrane of the

Type II by complement and some macphagocyte; incorporation of tile organisms rophages, Type III by neutrophils, and
into a phagosome; and activation of the

Type IV is T cell-mediated.

respiratory burst and lysosomal enzymes in

Inflan1mation and limited tissue
the phagosome, leading to microbial death
destruction are features of the normal innate and destruction.

and adaptive inlmune responses. Clinical
disease occurs when this inflan1mation is

Deficiencies in Phagocytosis:

excessive or in an inappropriate location.

Deficiencies in phagocytic activity can This may be due to external environmental
be due to acquired or congenital defects in
factors, such as the composition of the
any of these steps, or simply to a deficiency
intestinal microflora, together with genetic
of phagocytic cells tllemselves. They often
and hormonal influences.

manifest as an increased susceptibility to
bacterial infections of tile skin, respiratory
system, and GI tract. These infections

IMMUNODEFICIENCY
respond poorly to antibiotics. Secondary

DISEASES
phagocytic deficiencies include disorders
that lead to profound and chronic depres

In1munodeficiency diseases manifest
sions of WBCs. Feline leukemia virus
clinically as a predisposition to infections.

infection, feline panleukopenia virus

They are usually recog11ized when an animal infection, feline in1munodeficiency virus makes multiple visits to a veterinarian for
infection, tropical canine pancytopenia,
infections that would normally be relatively
idiopathic granulocytopenias, drug-induced
easy to control. Two major groups of
granulocytopenias (antineoplastic drugs,
inununodeficiency disease occur. One
estrogens, anticonvulsants, sulfonamides,
group is inherited as a result of mutations
etc), and myeloproliferative disorders are
or other genetic disease. These p1imary
some of the conditions in which secondary
or congenital in1munodeficiency diseases
infections can develop as life-tllreatening
usually develop in very young animals ( <6
complications.

mo old). The second group of inm1unodefi

A cyclic decrease of all cellular elements,
ciency diseases are secondary to some
most notably neutrophils, occurs in the
other stimulus such as a viral infection
peripheral blood and lowers tile resistance
or tumor. These secondary or adaptive
to infection of certain lines of gray Collies
diseases tend to occur in adult anin1als. One
and Collie crosses.

otller general rule in diagnosing inununode

Congenital abnonnalities tllat lead to
ficiencies is tllat defects in tile innate and
impaired phagocytosis are well documented
antibody-mediated inlmune systems tend to
in people. Deficiencies of opsonins,
result in uncontrollable bacterial infections,
complement factors, chemotactic abilities,
whereas defects in tile cell-mediated
and myeloperoxidase have been recognized
immune system tend to result in overin people but not in oilier animals. Chediakwhelming viral and fungal infections.

Higashi syndrome results from a defect in

IMMUNOLOGIC DISEASES

819
phagosomal function and has been recorded

Deficiencies in Adaptive Immunity
in cats, mink, cattle, and orcas. Chronic
granulomatous disease has been recognized

Humoral Immunodeficiencies: These
as an X-linked defect in some Irish Setters
deficiencies may be acquired or congenital.

(canine granulocytopathy syndrome). Some

Acquired deficiencies are seen in neonates
lines of Weimaraners develop bacterial
that do not receive adequate maternal

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septicemias ( usually manifested by bone and antibodies (failure of passive transfer) or joint infections) as puppies. The underlying
in older animals due to conditions that
causes of these defects are unknown; some
decrease active inununoglobulin synthesis.

of the affected dogs have lower than normal

Failure of passive transfer occurs in species
levels oflgM and IgG, and their WBCs have a
that use colostrum as the major source of
bactericidal defect.

maternal antibodies. It is commonly
associated with recurrent infections in

Leukocyte Adhesion Deficiency:

calves, lambs, and foals. Failure of passive

Leukocyte adhesion deficiency is an
transfer can occur when the young animal
autosomal recessive primary immunodefifails to nurse properly dUiing the first ciency. It has been described in people, Irish several days of life or when the dam's Setters, and Holstein cows. The deficiency
colostrum contains low levels of specific
results from the absence of an integrin, an
antibodies. Defects in the absorption of
essential surface glycoprotein expressed on
in1rnunoglobulin from ingested milk may also
leukocytes. Clinically, it is characterized by
occur. lmmunoglobulin levels <400 mg/dL
recurrent severe bacterial infections,
in a postnursing serum san1ple indicate
impaired pus formation, and delayed wound a failure of passive transfer in foals.

healing. Infected animals usually have

Premature weaning of calves is a problem in
severe pyrexia, anorexia, and weight loss.

dairy herds and is a leading cause of failure

Response to antibiotic therapy is usually
of passive transfer in dairy calves. Newborn
poor. Extreme, persistent leukocytosis may
animals that do not receive sufficient
occur (>100,000 WBCs/mL) and consists
maternal antibodies often succun1b to fatal
predominantly of mature neutrophils.

bacterial or viral infections of the GI and

The integrin deficiency prevents blood
respiratory tracts.

leukocytes from leaving blood vessels

Hypogamrnaglobulinemia of clinical
and entering the tissues, so they cannot
significance can be associated with any
contribute to the defense of tissues against
disorder that interferes with antibody
infections.

synthesis. Tun1ors, such as plasma cell
myelomas or lymphosarcomas that secrete

Complement Deficiencies: A congenilarge amounts of monoclonal antibody, can tal deficiency of C3 has been described in
be associated with profound antibody

Brittany Spaniels. These dogs developed
deficiencies. This is because the tumor cells
recurrent bacterial infections, especially
outcompete normal inununoglobulinskin diseases and pneumonias. Although producing cells, or because regulatory
complement is necessary for opsonization
pathways inhibit inununoglobulin
and neutrophil chemotaxis, bacterial
production. Anin1als with tUinors that
infections do not always develop in people
produce monoclonal antibodies may have
or laboratory animals with complement
severe secondary infections. Some viral
deficiencies, because the existence of
infections, eg, canine distemper and canine
multiple pathways provides a way to
parvovirus, may damage the in1rnune
activate the system even if one pathway is
system so severely that antibody production
blocked. Diagnosis is based on a blood test
is virtually stopped.

showing reduced C3 levels.

Congenital hypogarnrnaglobulinemia

A congenital deficiency in the Cl inhibitor has been recognized either alone or in has been recognized in people and occurs
combination with defects in cell-mediated
rarely in dogs. This can lead to uncontrolled
immlll1ity ( combined inununodeficiency,
complement activation and inflammation.

seep 816). Deficiencies in IgG subclasses

Affected animals have recurrent bouts of
have been seen in some breeds of cattle;
facial edema.

IgM deficiency has been described in

There is no specific treatment for
horses; and IgA deficiencies have been
complement deficiencies. Vaccination and
described in Beagles, German Shepherds,
antibiotics are used to prevent and treat
and Chinese Shar-Pei. Cattle with IgG
infection. As with all inherited diseases,
subclass deficiency are usually asymptosubsequent breeding programs must be matic. Older foals witl1 IgM deficiencies
carefully assessed to prevent the reappeardevelop respiratory infections. Dogs with ance of the disease in future generations.

IgA deficiency, like their human counter-

820

IMMUNOLOGIC DISEASES
parts, are prone to chronic skin infections,
production of functional antigen receptors.

chronic respiratory infections, and possibly

Sporadic cases of CID have also been seen
allergies. IgA deficiency of Beagles appears
in Toy Poodle, Rottweiler, and mixed-breed
to be due to a defect in the secretion oflgA,
puppies. Affected dogs are frequently
because IgA-positive cells are present in
asymptomatic during the first several

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normal numbers. Some German Shepherds
months of life but become progressively
have lower IgA levels than other breeds and
more susceptible to microbial infections as
a higher incidence of intestinal infections.

maternal antibody wanes. Puppies with CID

IgA deficiency in Shar-Pei is highly variable;
are clinically nonnal until 6--12 wk of age.

some have negligible serum and secretory

The most common cause of death from CID
levels, and some have normal serum levels
is canine distemper as a consequence of
and low or negligible secretory levels. Like
routine irnmunization with modified-live

German Shepherds, affected Shar-Pei
virus distemper vaccine. Arabian foals with
have more problems than expected with

CID frequently succumb to adenovirus
allergies. Dogs with these immunodefipneumonia or other infections when -2 mo ciency syndromes may have a higher than
old. The foals are persistently lymphopenic.

usual incidence of autoimmune diseases

Precolostral serum samples have no
and autoantibodies, such as autoimmune
detectable lgM antibody. Immunoglobulin
hemolytic anemia, thrombocytopenia, and
levels are normal initially but then
systemic lupus erythematosus. Longterm
progressively decrease compared with
treatment with broad-spectrum antibiotics
levels in normal foals. At necropsy, the
is required and is often unsatisfactory.

thymus is difficult to identify and is architec

Transient hypogammaglobulinemia
turally abnormal. Lymphocyte numbers are
has been recognized most frequently in
depleted in the lymph nodes, Peyer's
foals and puppies. It may be more common
patches, and spleen. A PCR test can confim1
in Spitz-type puppies than in other breeds.

CID in foals and the presence of the gene in

It results from a delayed onset of immunoheterozygote animals. As a result of such globulin production in the newborn and is
testing, the prevalence of equine CID has
associated with defects in both TH function
declined significantly.

and the B cell response to foreign antigens.

Puppies with this condition develop

Selective Immunodeficiencies: A large
recun·ent respiratory infections at 1-6 mo
number of immunodeficiency diseases have
of age but recover by 8 mo. Affected foals
yet to be fully analyzed, so their precise
frequently develop clinical signs of
mechanisms remain unknown. For
hypoganunaglobulinemia ( usually
example, Rottweiler puppies have a breed
respiratory infections) at -6 mo of age when predilection for severe and often fatal their maternal antibody reaches a very low
canine parvovirus infections (seep 373).

level. After aJ!Other 3-5 mo they begin to

Their resistance to other infections is
produce immunoglobulin. Appropriate
essentially normal, and the basis of this
antibiotic treatment and supportive therapy
selective immunodeficiency is unknown.

is often sufficient.

Persian cats have a predilection toward
severe, and sometimes protracted,

Deficiencies in C II-mediated
dermatophyte infections (seep 874). In

Immunity: Deficiencies in cell-mediated
some Persian cats, the fungal infections
immune responses are associated with
invade the dennis and cause granulomatous
thymic aplasia, an absent or very small
disease (mycetomas).

thymus. This has been seen in some inbred

Mink with the Aleutian coat color
lines of dogs, cats, and cattle; these anin1als
mutation are susceptible to chronic
were deficient in cell-mediated immune
parvovirus infection and so develop
functions, as well as having pituitary

Aleutian disease (seep 1872). Other strains dysfunction.

of mink are susceptible to infection with
this virus but do not develop clinical

Combined Immunodeficiency
disease. This is due to inherited Chediak

Diseases: If both humoral and cell

Higashi syndrome.

mediated in1mune responses are deficient,

Focal and systemic aspergillosis (see
they are classified as combined immunodep 633), and mycoses due to related fungi, ficiencies (CID). These result from inherited affect certain types of dogs. Long-nosed defects in the earliest lymphocyte
breeds, in particular German Shepherds and
progenitors. An autosomal recessive CID

Shepherd-crosses, are prone to develop
has been identified in Arabian foals and
focal aspergillosis in the nasal passages.

Basset Hounds. It results from a defect in

Systemic aspergillosis is seen almost

DNA repair enzyn1es and prevents the
exclusively in German Shepherds. It is

IMMUNOLOGIC DISEASES

821
characterized by fungal pyelonephritis,
bacterial antigens), decreased cellular
osteomyelitis, and discospondylitis. The
inlrnunity, and reduced complement levels.

organism can be isolated readily from blood
lnllllune responses to FeLV infection also
and urine.

appear to suppress immunity to the feline
infectious peritonitis (FIP) coronavirus and

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Diagnosis of Primary
may lead to reactivation of quiescent FIP.

(See also p 790.)

Immunodeficiencies

Recunent persistent infections in young

Simian Type D Retrovirus: This
anin1als suggest some fom1 of immm1odefiviral infection of macaques has a similar ciency. A complete differential leukocyte
pathogenesis to that of FeLV infection of
count will reveal whether all leukocyte
cats but can ·induce even more severe
types are present in appropriate numbers.

in1munodeficiency. Type D retrovirus

Immunoglobulin deficiencies can only
infection of macaques can cause severe
be detected by means of a quantitative
disease in adolescent animals. Affected
inlmtmoassay such as radial in1munodiffumacaques may either die within several sion, although turbidity tests such as those
months with fever, lymphadenopathy,
used for the diagnosis of failure of passive
and opportunistic infections of the CNS,
transfer are relatively easy to perfom1 and
respiratory tract, and intestines; become
may provide useful diagnostic information.

lifelong asymptomatic carriers; or

Primary inlmunodeficiencies as genetic
sometimes recover fully.

diseases are generally not treatable and, if
diagnosed, steps should be taken to ensure

Simian Immunodeficiency Virus (SIV):

that parent animals that carry defective

This lentivirus is closely related to human
traits are no longer used for breeding.

immunodeficiency virus. Many strains of

SIV exist in nature. The common hosts are

SECONDARY

African primates such as African green

IMMUNODEFICIENCIES
monkeys, sooty mangabeys, mandrills,
baboons, and other guenons. Transmis

In adult animals, inlmtmodeficiencies often
sion between infected and noninfected
occur as a consequence of virus infections,
monkeys is probably a result of bites or in
malnutrition, stress, or toxins. These are
utero exposure. SIV is not present in native
called secondary immm1odeficiencies.

populations of Asian primates. It rarely

Virus-induced secondary immunodeficiencauses disease in the host African species.

cies are the most important of these.

If infected animals are under heavy stress,
as in captivity, some may develop

AIDS-like disease. SIV, especially of sooty

Virus-induced Immunodeficiencies
mangabey origin, causes sev�re disease in

One way in which viruses survive in infected macaques (rhesus, stump-tail, pig-tail, animals is by inlrnunosuppression. For
bonnet, etc). The immunosuppression
example, canine distemper virus infects
associated with SIV can last for weeks or
and kills lymphocytes, causing a profound
years. Encephalitis (usually asymptomatic
combined immunodeficiency in affected
except for wasting) and lymphomas are
puppies. This infection is associated with
frequent consequences of SIV infection in
a progressive decline in inlmunoglobulin
macaques.

levels and increased susceptibility to
organisms normally controlled by cellular

Feline Immunodeficiency Virus (FIV):

immunity such asPneumocystis and

FIV has been identified in domestic and wild

Toxoplasma. Parvoviral infection in both
felids. The infection is endemic in cats
dogs and cats also causes a profound
throughout the world. Virus is shed in the
depression in the resistance to fungal
saliva, and biting is the principal mode of
infections such as aspergillosis, mucortransmission. As a result, free-roaming, mycosis, or candidiasis in the inlrnediate
male, and aged cats are at greatest risk of
postrecovery period.

infection. FIV infection is uncommon in
closed purebred catteries. After infection,

Feline Leukemia Virus (FeLV): FeLV is
there is a transient fever, lymphadenopathy,
associated with an increased susceptibility
and neutropenia. Most cats then recover
to secondary and opportunistic infections.

and appear to be clinically normal for many

Acquired in1munodeficiency in FeLV
months or years before progressive
infection is multifactorial. Infected cats can
inlmunodeficiency develops. Cats with
have deficiencies of neutrophils, decreased
acquired immunodeficiency induced by FIV
synthesis of antibodies ( especially to
then develop chronic secondary and

822

IMMUNOLOGIC DISEASES
opportunistic infections of the respiratory,
a high proportion of neutrophils in the

GI (including mouth), and urinary tracts,
synovial flu.id cell population. The excessive
as well as the skin. FIV-infected cats have
inflan1mation is believed to be due to the
a higher than expected incidence of
deposition of immune complexes in the syno

FeLV-negative lymphomas, usually of
via with subsequent complement activation.

the B-cell type, and myeloproliferative

An erosive arthritis has also been

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disorders (neoplasia and dysplasias).

recognized in cats. It tends to occur in older
male cats and frequently is associated with

Bovine Immunodeficiency-like Virus:

feline syncytia-fomung virus infection. The

Th.is lentiv.irus has been isolated from cattle
development of disease in cats is much
with persistent lymphocytosis, hemolymmore insidious than in dogs.

phadenopathy, and BLV-negative lympho

Canine rheumatoid arthritis responds
sarcomas. The overall prevalence in North
poorly to systenuc glucoco1ticoids alone.

American cattle appears to be -1 %, although Immunosuppressive agents with antiin some herds it may be as much as 15%. The inflammatory activity such as cyclophosvirus does not appear to be pathogenic.

pharn.ide and azatl1ioprine are used with
glucocorticoids to treat these disorders;

NSAIDs (eg, aspirin, carprofen, etodolac,

EXCESSIVE IMMUNE
melox.ican1) may bring relief.

FUNCTION

Plasmacytic-Lymphocytic Synovitis:

There are many different ways by which

Possibly a variant of rheun1atoid arthritis,
excessive immune function can cause
tl1is synovitis occurs in medium-sized and
disease or death. These include excessive
large breeds of dogs. Although multiple
innate responses, excessive adaptive
joints often are involved, the disease has
responses, and tumors of the immune
a predisposition for the stifle. The most
system.

common clinical sign is hindl.in1b lameness
and anterior drawer motion of the stifles.

EXCESSIVE INNATE RESPONSES

Lyn1phocytes, plasma cells, and neutrophils predominate in t11e synovial fluid, While acute inflammation is a defensive
although in some cases the flu.id is
process and central to innate immunity, it
essentially normal. Gross inspection of the
may occur without appropriate provocation joint shows proliferation of the synovial and in locations where it causes discomfort,
membrane and stretching or rupture of the
tissue dan1age, or systemic disease. This
cruciate ligan1ents. Treatment is as for
results in significant morbidity and resulting canine rheumatoid arthritis, above.

disability.

Idiopathic Polyarthritis: Arthritis of

Canine Rheumatoid Arthritis: This
unknown etiology is most conunon in large
disease results from excessive, uncontrolled
dogs, particularly German Shepherds,
inflan1mation around joints. It manifests

Dobennan Pinschers, retrievers, spaniels,
initially as a shifting lameness with
and pointers. In toy breeds, it is most
soft-tissue swelling around involved joints. frequent in Toy Poodles, Yorkshire Teniers, Within weeks or months, the disease
and Chihualmas, or mixes of these breeds.

localizes in individual joints, and characteris

There is no evidence of a prin1ary chronic
tic radiographic changes develop. The
infectious disease process or of systemic
earliest radiographic changes consist of
lupus erythematosus. Arthritis is often the
soft-tissue swelling and a loss of trabecular sole manifestation.

bone density in the area of the joint. Lucent

Diagnosis is based on the history of cyclic
cyst-like areas frequently are seen in the
antibiotic-unresponsive fever, malaise, and
subchondral bone. The most prominent
anorexia, with stiffness or lameness. Bony
lesion is a progressive erosion of cartilage
changes are not seen on radiographs until
and subchondral bone in the area of synovial
the disease is well established. Even then,
attachments, resulting in loss of articular
radiographic changes are mild and can
cartilage and collapse of the joint space.

minuc degenerative joint disease. Synovial

Angular deformities often occur, and
flu.id contains leukocytes but is sterile.

luxation of the joint is a frequent sequela.

TI1e disease may be controlled with daily

Defomuties are most frequent in the carpal,
high-<lose glucocorticoids followed by
tarsal, and phalangealjoints and less
low-<lose, altemate-<lay therapy. Treatment
frequent in the elbow and stifle. Synovial
usually can be discontinued after 3--5 mo.

flu.id exan1ination shows a sterile, inflamma

Dogs with poor response to such therapy
tory synovitis, with increased cell count and

(>500Ai) may be treated with more potent

IMMUNOLOGIC DISEASES

823
inmrnnosuppressive drugs such as azathiomay generate vastly excessive cytokine prine or cyclophosphamide in addition to
production, most notably IL-1, TNF-ot, IL-8,
glucoco1ticoids. Gold salts help augment
and IL-6. This massive cytokine release has
glucoco1ticoid tl1erapy in some animals.

been called "a cytokine storm." High doses of cytokines are toxic and induce severe

Immune-mediated Meningitis: This
acidosis, fever, lactate release in tissues,

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disease occurs in adolescent or young adult an uncontrollable drop in blood pressure, Beagles, Boxers, German Shorthaired
increased plasma catecholamines, and

Pointers, and Akitas but is very rare in
eventually renal, hepatic, and lung iitjury
other pure and mixed breeds. The clinical
and death. The procoagulant-anticoagulant
signs consist of cyclic episodes of fever,
balance is upset so that endothelial
severe neck pain and rigidity, reluctance to
procoagulant activity is enhanced, while
move, and depression. Each attack lasts
many anticoagulant pathways are inhibited,

5-10 days, with intervening periods of
leading to disseminated intravascular
complete or partial normality lasting
coagulation and capillary thrombosis.

approximately a week. During attacks,

All these effects are initiated by excessive
protein and neutrophils in the CSF are
triggering of toll-like receptors leading to a
increased. The lesion is an arte1itis,
massive and uncontrolled release of
primarily of the meningeal vessels, but
cytokines. The cytokines damage vascular
occasionally of other organs as well. The
endothelial cells, activating them so that
disease is often self-limiting over several
procoagulant activity is enhanced, which
months; attacks become milder and less
leads to blood clotting. The nitric oxide
frequent. Glucocorticoid therapy reduces
causes vasodilation and a drop in blood
the severity of attacks. In some anin1als,
pressure. The widespread damage to
the disease becomes chronic and only
vascular endotheliwn eventually causes
partially amenable to therapy.

organ fail me. Multiple organ dysfunction

A more severe form of this meningitis has
syndrome is the end stage of severe septic
been reported in young Bernese Mountain
shock. It is characte1ized by hypotension,

Dogs. The disease in this breed is somewhat
insufficient tissue perfusion, uncontrollable
cyclical, but the resolution in intervening
bleeding, and organ failure caused by
periods is less than in other species. CSF
hypoxia, tissue acidosis, tissue necrosis,
abnormalities resemble those seen in other
and severe local metabolic disturbances.

breeds. The condition requires longtenn,

The severe bleeding is due to disseminated
high-dose glucocorticoid therapy.

intravascular coagulation. The sensitivity

A syndrome of meningitis, often
of manm1als to septic shock varies greatly.

associated with polyarthritis, is seen in

Species with pulmonary intravascular
young Akitas. The dogs show severe
macrophages ( cat, horse, sheep, and pig)

episodes of fever, depression, cervical pain
tend to be more susceptible ilian dogs.

and rigidity, and generalized stiffness.

Affected dogs grow slowly and often appear

EXCESSIVE ADAPTIVE
unthrifty. The condition responds poorly to

RESPONSES
glucocorticoid and combination irnrnunosuppressive therapy, and most affected dogs Excessive activity of the adaptive in1rnune
are euthanized as young adults. In older
system can lead to inflammation and tissue

Akitas, a milder and more drug-responsive
damage, autoinm1uni.ty, or amyloidosis.

form of the disease is seen, which may be

For many years it has been customary to
associated with pemphigus foliaceus, uveitis,
classify excessive adaptive immune system
and plasmacytic-lymphocytic tlwroiditis.

function into four types on the basis of the
mechanisms involved.

Systemic Inflammatory Response

Syndrome

Type I Reactions

In severe infections or after massive tissue

(Atopic disease, Anaphylactic reactions)

damage, large amounts of cytokines and

Type I, or immediate hypersensitivity,
reactive oxygen and radicals enter the bloodencompasses these IgE-mediated reacstream and cause a fonn of shock known as tions to other, nonparasitic antigens. This
systemic inflan1matory response syndrome.

inflai1m1ation may be minor or local, or

Septic shock is the name given to the
severe and generalized. In its most extreme
systemic inflammatory response syndrome
form, it causes a potentially lethal shock
specifically caused by severe infections and
syndrome called anaphylaxis. Anaphylaxis
associated with traun1a, ischemia, and
is an acute systemic manifestation of the
tissue iitjury. Animals with severe infections
interaction of an antigen (allergen) binding

824

IMMUNOLOGIC DISEASES
to IgE antibodies attached to mast cells
associated with constriction of hepatic
and basophils. This binding of antigens to
veins, which results in portal hypertension
cell-bound lgE antibodies tdggers the
and visceral pooling ofbloocl. GI signs
release of biologically active inflammatory
rather than respiratory signs are more apt
mediators, including histamine, leukotrienes, to be seen in dogs. Supportive therapy, in VetBooks.ir
eosinophilic chemotactic factors, platelet
addition to treating respiratory distress,
activating factor, kinins, serotonin,
consists of the administration of epinephproteases, and cytokines. These molecules rine (both locally and systemically as
directly affect both the vascular system,
needed). IV fluids for the treatment of
causing vasodilation and increased
shock, antihistamines ( systemically for
vascular permeability, and smooth
severe acute anaphylaxis or orally as a
muscles, causing contraction. Additionally,
means to control chronic signs of allergy or
they attract pro-inflammatory eosinophils
milder allergic signs), and corticosteroids if
to the triggering site.

needed. Ancillary support of blood pressure

The severity of anaphylaxis depends on
and respiration may be necessary.

the type of antigen, the amount of IgE

Urticaria! reactions (hives or
produced, and the amount of antigen and
angioedematous plaques) of the skin and
route of exposure. If the animal has been
subcutaneous tissue and acute edema of
previously sensitized by exposure to an
the lips, conjunctiva, and skin of the face
allergen (antigen) and produces IgE

(facial-conjunctiva! angioedema) are less
antibodies; then injection of the sensitizing
severe forms of'Iype I hypersensitivity.

antigens directly into the bloodstream can

Hives are the least severe reaction and
result in anaphylactic shock and related
may not be associated with other clinical
reactions ( eg, hives, urticaria, facial-conabnormalities. Facial-conjunctival edema junctiva! edema). If the sensitizing allergen
is more severe and can be associated
enters through the mucous membranes or
with mild to moderately severe systemic
the skin, allergic reactions tend to be more
anaphylaxis. These reactions usually
localized. Agents that can trigger anaphyfollow administration of vaccines or drugs, lactic and allergic reactions are numerous
ingestion of certain foods, or insect bites.

and include the venom of stinging and

Urticarial reactions and facial-conjunctival
biting insects, vaccines, drugs, foods, and
edema occur in most species and usually
blood products.

resolve spontaneously within 24 hr. Not all
urticarial reactions are mediated by Type I

Systemic AnaphylaJtis (Generalized
hypersensitivity. (See also URTICARB., p 857.) Anaphylactic Reactions): Anaphylac

Milk allergy occurs occasionally in cows
tic shock occurs in sensitized anin1als
and less frequently in mares. This occurs
after exposure to antigens in sensitizing
when a cow makes IgE autoantibodies to
vaccines or drugs, ingestion of foods, or
its own milk components, notably casein.

insect bites. Clinical signs occur within

�en intramamrnary pressure rises, these
seconds to minutes after exposure to the
milk proteins gain access to the circulation
allergen. In most domestic animals, the
and induce a 'Iype I hypersensitivity. The
lungs are the primary target organs, and
reaction can be localized or systemic.

the portal-mesenteric vasculature is a

Recovery occurs once the aninlal is milked.

secondary target; this is reversed in dogs.

Mast cell degranulation in the pulmonary

Localized Anaphylactic Reactions:

vasculature causes constriction of

Allergic rhinitis, manifest by serous nasal
bronchial airways or pulmonary veins
discharge and sneezing, is less common in_
and pooling of blood and edema in the
domestic animals than in people. Often, it IS
pulmonary vascular bed, which results
seasonal, correlating with pollen exposure.

in severe respiratory distress. Mast cell

Nonseasonal rhinitis may be associated
degranulation in the portosystemic
with exposure to ubiquitous allergens, such
vasculature causes venous dilatation and
as molds, danders, bedding, and feeds.

pooling of blood in the intestines and liver.

Recurrent airway obstruction in horses (see

Clinical signs can be localized or
p 1455) is probably a reaction to chronic
generalized and include restlessness and
d
exposure to molds present in moldy hay an
excitement, pruritus around the head or
poorly ventilated stables. Summer snuffles
site of exposure, facial edema, salivation,
is a seasonal allergic rhinitis occurring
lacrimation, vomiting, abdominal pain,
commonly in Guernsey or Jersey cattle
diarrhea, dyspnea, cyanosis, shock,
placed on certain types of flowering
incoordination, collapse, convulsions, and
pastures in late summer and early autumJl·
death. In dogs, the major organ affected by

Allergic rhinitis can be diagnosed tentatively
anaphylactic shock is the liver, and signs are by the following: 1) identification of

IMMUNOLOGIC DISEASES

825
eosinophils in the nasal exudate,

Hat.ion of the lungs, aerophagia, cyanosis,

2) demonstration of a favorable response to and frantic attempts to obtain air.

antihistamines, 3) disappl',u-ance of signs

Intestinal allergies (food allergies)

when the off end_ing allergen is removed, or
are principally seen in dogs and cats,

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4) occ3:'ionally, its se::_�sonal nature. �kin
particularly kittens. (See also p 855 and
testing is not ru_1 acc�nate means to diagnose p 2379.) Allergic gastritis is manifest by nasal allergies m ruumals.

vomiting, which occurs 1 to > 12 times

Chronic allergic bronchitis has been
weekly, within 1-2 hr of eating. The
characte1ized in dogs. A dry, harsh, hacking
vomitus may be tinged with bile. In cats,
coue1h that is easily precipitated by exertion
vomiting may be the sole sign; dogs may
or by pressure on the trachea is a characteralso have intermittent loose feces. Cats istic clinical sign. The disease may be
and dogs with allergic gastritis are usually
seasonal or occur year-round. Usually, it is
healthy except for vomiting, although
not associated with other signs of illness.

there can be loss of weight and coat

Toe bronchial exudate is lich in eosinophils
condition in severe cases. Allergic
and free of bacteria Chest radio graphs are
entelitis is associated with a mild
normal, and there may or may not bea
inflammation of the small intestine but
low-grade peripheral eosinophilia. The
with little or no eosinophilia. Feces
condition is treated with bronchodilators
usually are normal in volume and
and expectorants ( aminophylline and
frequency but vary from semif ormed to
potassium iodide or guaifenesin). Glucowatery. They may be extremely odorous, corticoids will alleviate clinical signs,
especially in cats. Affected animals may
especially when their use can be limited to
be excessively thin despite good appetite.

certain seasons or to low-dose, alternate

Skin lesions and poor coat are commonly
daytherapy. Avoidance of the offending
associated with food allergies in cats but ·
allergen( s) usually is not possible.

less commonly in dogs. The allergy often

Allergic bronchiolitis is most common
develops after episodes of viral, bacterial,
in cats. It is manifest by a low-grade cough,
or protozoal entelitis (a phenomenon
wheezing, some dyspnea, and increased
known as allergic breakthrough).

peribronchiolar density on radio graphs, and Eosinophilic enteritis, the most severe it may be mistaken for other conditions
form of allergic intestinal disease,

( allergic asthma or lungworm disease).

manifests by moderate to severe inflam

Early in the course of the disease, clinical
mation of the intestines and a pronounced
signs can be modified by antihistamine
eosinophilia. Diarrhea, weight loss, and
therapy, but if the disease increases in severpoor coat condition are usually evident.

ity, moderate to high dosages of corticoster�

The prevalence of allergic colitis is greater
oids may be necessary. The offending
in cats than in dogs, although in general it
allergen usually is not Identified.

is not common. In dogs, it is often

Eosinophilic bronchopnewnopathy
associated with frequent defecation and
occurs most frequently in dogs but has been
soft, mucus-laden and sometimes bloody
recognized in all species. It is associated with feces; in cats, it most frequently manifests diffuse inflammatory infiltrates in the lungs
by more normal feces coated or spotted
and a pronounced peripheral eosinophilia; ·
with fresh blood. (For diagnosis and
frequently, the serum globulins are increased. treatment of food allergies, seep 855.) Unlike in allergic bronchitis, affected animals

Atopic dermatitis (seep 853) is a
are often dyspneic or tire easily with exercomplex pruritic; chronic skin disorder that cise. Diffuse bronchial exudate contains
occurs in many species but has been studied
numerous eosinophils. The specific
mostly in dogs. Some animals with a.topic
offending allergen is rarely identified.

dermatitis may have a genetic predisposition

Glucocorticoids are the treatmentof choice.

that leads to excessive production of

A similar syndrome is also associated with
reaginic (lgE) antibodies. It has been
resident or migratory parasitic infections of
estimated that -100/4 of all dogs suffer from
the lungs in young animals.

atopy, with a breed predisposition in teniers,

. Allergic asthma occurs most frequently

Dalmatians, and retrievers. Atopic dermatitis
m cats, in which the signs are similar to
of dogs often is triggered by inhaled

�ose in people. It occurs more frequently
allergens, eg, house dust mites, pollens,

� summer and after going outdoors;
molds, and danders. Atopic dogs often chew

Individual attacks can be transient and
at their feet and axillae. Excessive sweating
mild, or protracted and severe (status asthis especially noticeable in hairless areas. The rnaticus ). Mild attacks may manifest as
severity of the skin lesions are greatly

Wheezing and coughing; in severe attacks,
increased by licking, scratching, flea
there may be expiratory dyspnea, hyperin-
infestation, and secondary bactelial or yeast

826

IMMUNOLOGIC DISEASES
infection. Atopic skin lesions in cats are
throml>ocyl,openia is found in GO% of cases.

either miliary (small scabs) and widespread,

IMHA can be associated with systemic lupus
or larger and more localized. Localized
eiythematosus or with Iymphoreticular
lesions are often pnuit.ic.

malignancies. Drugs or infections may trigger

In cats, food allergens probably are a
episodes of hemolytic anemia or thrombocy

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more common cause of skin lesions than
topenia in many sp�cies. More often than not,
are inhaled allergens. Sweet itch ( see
the initiating cause IS unknown.

p 887) is a seasonal allergic dermatitis of

IMHA occurs in several clinical forms:

horses associated with certain insect bites,
peracute, acute or subacute, chronic, cold
especially night-feeding Culicoides.

agglutinin disease, and red cell aplasia. Most

Intensely pruritic lesions appear along the
cases are treatable, but relapses are
dorswn from the ears to tail head and
common. (See also p 10.)

perianal area Similar allergic skin reactions

Pera.cute IMHA is seen mainly in
to insect bites can be seen around the ears
middle-aged, larger breeds of dogs. Affected
and face of cats and dogs. (For diagnosis
dogs are acutely depressed and have a rapid
and treatment, seep 853.)

decrease in PCV within 24-48 hr with
bilirubinemia, variable icterus, and

Type II Reactions
sometimes hemoglobinuria Initially, the
anemia is nonresponsive, but it may respond

(Antibody-mediated cytotoxic reactions)

within 3-5 days. Thrombocytopenia may

Type II reactions occur when an antibody
also be present. Anti.globulin tests are often
binds to an antigen present on the surface
negative, and spherocytes may or may not
of cells. This bound antibody can then
be present, but tube or slide agglutination of
activate the classical complement pathway,

RBCs is marked. The autoagglutination is
resulting in cell lysis, phagocytosis, or
not dispersed by saline dilution, hence the
antibody-mediated cytotoxicity. Many
term hemolytic anemia with in-saline
different antigens may trigger this cell
agglutinins. The serum usually contains
destruction, but an infection in a genetically
autoantibodies that cause agglutination
predisposed animal appears to be a major
of most donor RBCs. The prognosis of
triggering pathway. Cross-reactive
peracute IMHA is poor even with prompt
antibodies can develop during infections.

and vigorous therapy. The most effective

These cross-reactive antibodies directed
therapy involves immediate use of high
toward an infectious agent may bind to
dosages of glucocorti.coids plus cyclophosnormal tissue antigens and trigger antibodyphamide, together with a compatible blood mediated cytotoxicity. For example, in
transfusion. If incompatible blood must
streptococcal infection in horses, a
be used, the animal should first be heparincross-reaction between Streptococcus equi ized and maintained on heparin for 10 days.

antigen and vascular basement membranes

Even without transfusion, heparinization
can occur, leading to purpura hemorrhagica.

may be beneficial for the first 2 wk or more.

Pathogens such as Babesia or Mycoplasma Bovine hemoglobin blood substitute and
haemofelis, which parasitize cells, trigger an human immunoglobulins can be used as
immune response that destroys those cells
supportive therapy until immunosuppressive
as part of the protective mechanism. The
treatment reduces the destruction ofRBCs.

most common manifestations of'lype II

Acute IMHA is the most common fonn
hypersensitivity involve blood cells. These
of the disease, with a breed predilection
include hemolytic anemia if RBCs are
in Cocker Spaniels. Initial signs are pallor,
involved, leukopenia involving WBCs, or
fatigue, and less commonly, icterus.

thrombocytopenia involving platelets. Under Hepatosplenomegaly is a prominent sign.

some circun1Stances, a cytotoxic attack on

The WBC count may be increased due to
vascular epithelial cells will cause a
bone marrow hyperplasia. Autoaggluvasculitis with local vascular leakage.

tination ofRBCs is uncommon, and the
anti.globulin test is generally positive. The�e

Immune-mediated Hemolytic Anemia
animals usually respond well to glucocort1•

(IMHA) and Thrombocytopenia:

coid therapy. If a favorable response is not

The production of autoantibodies against
seen within 7-10 days, cytotoxic drugs
erythrocyte or platelet antigens leads to

( cyclophosphamide or azathioprine) should
anemia and thrombocytopenia, the most
be added to the regimen.

common 'lype II reactions. Antibody and

Chronic IMHA differs from the acute
complement attach to RBCs either directly or form in that the PCV falls to a constant level indirectly via an absorbed antigen and then
and remains there for weeks or months.

mediate RBC destruction, resulting in a

The bone marrow is either normal or
severe, life-threatening anemia Concurrent
hyperresponsive, and the anti.globulin test

IMMUNOLOG IC DISEASES

827
is often negative. Chronic IMI IA is relatively

Animals wit h immune-mediated
more con�n�on in cats_than in d_ogs. Usually,
thromhocyt.openia that show only petechial
the anenua 1s responsive early m the course
and ecchymotic hemorrhages, with no
of disease but responds minimally or not at
significant blood loss and megakaryocytes
all by the time it bcconws severe. Initial
in the marrow, may be treated initially with

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�eatmcnt is with glucoc01ticoids; ifthere is
glucocorticoids. The clinical signs should
no response within 2 wk, cytotoxic dmgs
abate and the platelet count begin to rise
maY be added to the regimen.

after 5-7 days. If the platelet count has

Cold agglutinin disease is an IMHA
not increased significantly by 7-10 days,
of dogs and horses. Its cause is usually
cyclophosphamide, azathioprine, or
unknown but may be secondary to infection,
vincristine can be added to the glucocortiother autoimmune diseases, or neoplasia coid regimen. In animals with megakaryo

The IgM autoantibodies can be agglutinating
cytes in the marrow and severe blood loss, a
ornonagglutinating. Complete agglutination
more rapid response to therapy is desirable.

does not occw- at body temperature but only

Such animals are treated with a single
when the blood is chilled; thus, it is more
injection of vincristine combined with daily
frequent in colder climates and seasons.

glucocorticoids; a favorable response

Initial signs may be of a hemolytic disease·
usually occw-s after 3-5 days. If the blood
in the agglutinating type, vascular blockage
loss is life-threatening, platelet-rich whole
may lead to necrosis of the nose, tips of the
blood should be administered. If the platelet
ears and tail, digits, scrotum, and prepuce.

count has risen by day 7, remission is

Diagnosis is based on a reversible autoagglumaintained on glucocorticoids alone. If there tination that occurs only at 4 °C. The direct
is no response after 7 days, a second dose of
antiglobulin reaction is usually negative for
vincristine is given. If the platelet count is

IgG, frequently positive for C3, and usually
still low after 2 wk, vincristine is discontinpositive for IgM if the reaction is performed ued and either cyclophosphamide or
in the cold. Mortality is high. In the absence
azathioprine is added. Animals with
of an obvious initiating cause such as
thrombocytopenia and no megakaryocytes
infection or neoplasia, the disease is best
respond much more slowly to glucocorticontrolled with high doses of glucocorticoids coids, or to glucocorticoids and vincristine.

in combination with cyclophosphamide.

Preferred treatment for these animals is with

Red cell aplasia ( see p 13) is most prednisolone and cyclophosphamide, and a
common in dogs. It occurs in two forms, one response should not be expected earlier than in post.weanling to adolescent puppies and

1-2 wk after beginning therapy. Therapy may
the other in adults. Unlike in IMHA, the bone
be discontinued in most animals with
marrow shows a selective depression of
immune-mediated thrombocytopenia 1-3
erythroid elements; granulocytes and
mo after the platelet count retw-ns to
platelets are unaffected. Therefore, the
normal. Some animals have a persistent
peripheral anemia is unresponsive. The
thrombocytopenia despite drug therapy, or
immune attack is directed against erythroid
they can be maintained in remission only
stem cells, and the antiglobulin test is usually with chronic high-dose treatment. The negative. Treatment is usually as for chronic
alternatives are to allow the animal to live

IMHA, but recovery may be very slow.

with the thrombocytopenia if signs are

Immune-mediated thrombocytopenia minimal or to use longterm combination is common in dogs. It occw-s more often in drug therapy with glucocorticoids and either females than males. The most frequent
vincristine, azathioprine, or cyclophosphaclinical signs are hemorrhages of the skin mide. Splenectomy is seldom curative by
and mucous membranes. Melena, epistaxis, itself but may allow use of lower and safer and hematuria may be accompanying
dosages of immunosuppressive drugs.

features and can cause profound anemia.

Hemolytic anemia and thrombocytopenia

Autoimmune Skin Disorders: In these
som�times occw-together. Immunediseases, affected animals make autoanti

�ed1ated thrombocytopenia usually is
bodies against the intracellular cement
diagnosed on the basis of low peripheral
proteins in the epidermis. This promotes

Platelet counts despite a pronounced megalocal proteolysis, leading to separation of karyocytosis in the marrow. Occasionally,
the epidermal cells ( acantholysis) and
megakaryocytes may be selectively absent development of vesicles within the skin.

from the marrow. Tests for antiplatelet

Although not strictly a Type II disease, it
antibodies are difficult to conduct, so
is best considered here.

diagnosis is usually made on clinical

Pemphigus foliaceus is the most

Presentation and response to therapy.

common of these diseases, occurring

(See also p 46.)

more often in dogs than in cats and horses.

828

IMMUNOLOGIC DISEASES

It is characterized by the development of

Myasthenia Grav!s: My�the�ia gravis
erosions, ulcerations, and thick encrustais an autoimmune disease m which tions of the skin and mucocutaneous
autoantibodies directed against the
junctions. The absence of lesions in the
acetylcholine receptors on muscle cells
mouth, and the widespread thick, crusty
cause receptor degradation or blockage

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nature of the skin lesions, tend to
and so block neuromuscular transmission.

differentiate pemphigus foliaceus from

The disease is characterized by extreme
the much rarer pemphigus vulgaris.

generalized muscle weakness, which is

Autoantibodies in the skin react with
accentuated by mild exercise. Megaesoph.

intracellular cement (desmoglein),
agus due to paralysis of
resulting in its degradation and separation

_esophageal
muscles is a frequent pnmary or accompa.

of the cornified and uncornified cell
nying complaint in _dogs. Thyrno
layers. Immunosuppression is required to

_mas ar_e
often associated with myastherua gravis m
treat the disease. High doses of glucocortipeople but are uncommon in domestic coids are used initially, but low-dose,
species. Administration of a s�ort-acting
alternate-day therapy is used once the
anticholinesterase ( edrophoruum
disease is under control. More potent
chloride) produces a dramatic increase
immunosuppressive drugs such as
in muscle strength. Treatment is with a
cyclophosphamide or azathioprine may
long-acting anticholinesterase. Chronic
be used with glucocorticoids in cases
immunosuppressive drug therapy for this
unresponsive to steroids. Animals that
disease is logical. Autoantibodies to the
respond poorly to initial therapy, or
acetylcholine receptors can be detected
require high dosages of drugs to control
in the serum of affected animals by an
lesions, have a poor longterm prognosis.

indirect immunohistopathologic assay

Pemphigus vulgaris is a much less
using normal muscle as a substrate.

common autoimmune skin disease than
pemphigus foliaceus. It is characterized by

Type Ill Reactions
vesicle formation along the mucocutaneous junctions of the mouth, anus, prepuce, (Immune complex disease)

and vulva, and in the oral cavity. Other

Antigen-antibody complexes (immune
areas of the skin are only mildly involved.

complexes) deposited in tissues may cause

Because the epidermis of animals is
acute inflammation. By activating the
relatively thin ( compared with human
classical complement pathway, the
skin), these blisters rupture rapidly and
complexes produce potent chemoattractform erosions; consequently, characteristic ants that attract large numbers of neutrobullae are seldom seen. The vesicles phils. These cells, especially if they release
develop as a result of suprabasilar
their enzymes and oxidants, cause acute
acantholysis. Secondary bacterial infection inflammation and tissue damage. The most·
often complicates the lesions, and if
frequently affected sites include the joints,
untreated, the disease is often fatal. It is
skin; kidneys, lungs, and brain.

treated with high doses of glucocorticoids

The prerequisite for the development of·
alone or in combination with other drugs ·
such as cyclophosphamide, azathioprine,
immune complex disease is the persistent
presence of soluble antigen and antibody.

or gold salts. Pemphigus vulgaris is
difficult to maintain in remission, and the

These form insoluble immune complexes
that become trapped on the basement
longterm prognosis of affected animals is
membrane of small blood vessels. The
fair to poor.

deposited immune complexes then activate

Bullo us pemphigoid is a rare canine skin
the classical complement
disease recognized most often in Collies and
pathway.

Complement fragments attract neutrop!ill-5

Doberman Pinschers. Lesions are often
and are also directly vasoactive, triggenng
widespread but tend to be concentrated in
a vasculitis. Antigens persist
the groin. The involved skin resembles a
for a number
ofreasons, including chronic infections
sever� scald. Bullae also develop; they are
and certain neoplastic
subep1dermal and may be full of eosinophils.

conditions,
particularly

Autoantibodies to the basal lamina can be
lyrnphoreticular neoplasms,_th

Chronic antigen
detected in immunohistopathologic sections.

exposure also occurs WI
inhaled antigens

The treatment of choice is prednisolone and
and, in such cases,
immune complexes
azathioprine used in combination; remission
form in the alveolar
walls.

is frequent, but continual drug therapy at

Lastly, some animals respond to
self-ant
relatively high dosages may be required to
igens, which then act as a source of
chronic antigen
keep the disease under control. The longterm

�xposure. In many cases,
the origin of the antigen
prognosis is poor.

within these
immune complexes cannot be determined,

IMMUNOLOGIC DISEASES

829

The location of the immune complexes is
antigenic dusts. The most potent antigens of
largely detemtlned by the route by which
this type arc those contained in the spores
antigen enters the body. Inhaled antigens
ofthermophilic actinomycetes from moldy
give rise to a pneumc_mitis, antigens that
hay. Inhalation of these spores causes
enter through the skin cause local skin
farmer's lung disease in people and a similar

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lesions, and antigens that access the
condition in cattle (seep 1441). Hypersensibloodstream fonn immune complexes that tivity pneumonitis is characterized by the
are deposited in renal glomeruli or joints.

onset ofrespiratory distress 4-6 hr after
clinical signs are therefore variable but may exposure to moldy hay. The most effective include fever, cutaneous signs (such as
treatment is removal of the source of the
erythema multiforme ), and polyarthritis
antigen; otherwise, corticosteroid therapy

(shifting-leg l�en�ss or painful, swollen
may help.

joints). Other �1� �elude ataxia, behavior
change, protemuna, 1sosthenuria,

Systemic Lupus Erythematosus (SLE):

polydipsia, polyuria, or nonspecific signs

This complex autoimmune disease occurs
such as vomiting, diarrhea, or abdominal
in dogs, is rare in cats, and has been
pain. Diagnosis is based on the elimination
reported in large animals. It has two
of more common causes of clinical signs.

consistent immunologic features: immune

Supporting evidence to confirm the

·
complex disease and a tendency to produce
diagnosis includes establishing a temporal
multiple autoantibodies. Clinically, it
relationship if a drug or infectious agent is
reflects a combination of Type II and III
suspected as the cause, identifying chronic
mechanisms. Antibodies to nucleic acids
infections or malignancies, and perlorming
are the diagnostic hallmark of SLE, but in
histopathology and immunohistochemistry
many individuals, antibodies to RBCs,
on biopsies to identify immune-mediated·
platelets, lymphocytes, clotting factors,
vasculitides or nephritis. ·
immunoglobulin (rheumatoid factors),

Therapy should include supportive ·
and thyroglobulin are also present. The
treatment, removal of the causative agent,
presence of autoantibodies to nucleic acids,
or treatment of the underlying disorder ( eg,
antinuclear antibodies (ANA), can be
appropriate antibiotic therapy for bacterial
diagnostic of the disease. Either the
infections, surgical drainage of abscesses or immune complex or the autoantibody infected tissue, therapy for heartworm
component of the disease tends to
disease, the withdrawal of drugs).

predominate in a given animal. Immune

Immwwsuppressive therapy may be need�d complex deposition around small blood to prevent the continued deposition of
vessels may lead to synovitis, dermal
i

· ·
mmune complexes.

reactions, oral erosions and ulcers,
myositis; neuritis, meningitis, arteritis,

Menibranoproliferative Glomerulone
rnyelopathy, glomerulonephritis, or
phritis: This lesion is caused by immune
pleuritis. Glomerulonephritis is one of the
complexes that form within the bloodmajor life-threatening complications of SLE
stream and are filtered out in the glomeruli
in cats but not in dogs. Psychosis, a major

(see p 1517). In effect, the insoluble sign of SLE in people, is also seen in animals
complexes collect on the glomerular
with SLE. Autoimmune hemolytic anemia
basement membrane. Depending on
or thrombocytopenia, or both, are the most
their size, they may be deposited on the
common presentations of SLE in animals.

subendothelial or subepithelial surface of

SLE is characterized by the presence of
the membrane. Secondary glomerulonephri ANA, and tests for these or the associated tis occurs as a sequela of chronic infectious, lupus cells may help in diagnosis. However, neoplastic, or immunologic disorders.

some healthy animals may have ANA, and

Animals with idiopathic glomerulonephritis
not all animals with SLE have detectable

(�50% of cases) usually have signs of renal

ANA in their blood. Diagnosis of SLE must
disease, whereas secondary glomerulo'netherefore be based on the entire clinical Pluitis is often a relatively minor part of a
syndrome-notjust on the presence or
more serious disease.

absence of ANA.

SLE usually can be treated with

�Ypersensitivity Pneumo�itis: �e�
glucocorticoids. Initially, they are used

�aled antigens meet circulating antibodies in high daily doses, and when remission in the walls of the alveoli, immune
occurs alternate-day, low-dose therapy is
complexes form in the alveolar walls and
used. Drug treatment should be continued
trigger acute inflammation. Hypersensitivity for 2-3 mo after all clinical signs have Pneumonitis is most common in large
resolved. Cyclophosphamide or azathioanimals exposed over a long time to prine, or both, are used in combination

830

IMMUNOLOGIC DISEASES
with glucocorticoids in animals with SL�
that is diftlcult to control with glucocorllcoids alone.

Vasculitis: Vasculitis mediated by

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immune complexes occurs in animals,
especially dogs and horses. Lesions are
most prevalent in the dermis of the distal
limbs and mucous membranes of the
mouth, paiticularly the palate and tongue

(dogs) and lips 010rses ). Involvement of.

the nose, ears, eyelids, cornea, and anus 1s
less common. Early lesions develop as
reddened areas that rapidly form shallow
erosions. A scab quickly forms over dermal

Purpura hemorrhagica, ocular lesions, in a
erosions. Limb edema is common in horses
horse. Courtesy of Dr. Thomas Lane.

and a less frequent but equally striking sign
in dogs. Vasculitis is a feature of SLE in
severe equine recurrent uveitis (see
some animals but most often is idiopathic.

p 508) is associated with immunologic

Drug-induced vasculitis has been well
reactions to Leptospira or Onchocerca spp.

recognized in dogs. The vasculitis is

This periodic ophthalmia results from
detected on histopathologic and irnmuno-
autoimmune attack Antibodies against
histopathologic examination of superficial
some serovars of Leptospira can crossand deep biopsies taken from the margins react with retinal antigens and so trigger
of lesions.

severe ophthalmia. Uveitis caused by

Vasculitis is treated by withdrawal of

Toxoplasma and feline infectious peritoni-.

off ending drugs and, if necessary, by
tis virus infections of cats may also have an
immunosuppressive drug therapy.

immunologic basis.

Glucocorticoids used alone or in combination with other agents such as azathioprine Type IV Reactions
or cyclophosphamide are usually used to
treat non-drug-induced cases.

(Cell-mediated immune reactions)

Cell-mediated immune reactions occur

Periarteritis Nodo'sa (Polyarteritis
when antigen triggers TH 1 responses.

Nodosa, Necrotizing Polyarteritis):

Multiple cytokines as well as activated

This rare disease of domestic animals is
macrophages and cytotoxic T cells are
caused by deposition of immune complexes
produced. The infiltration of mononuclear
and inflammation in walls of small and medicells and the elaboration of a variety of um-sized arteries. Among farm animals, it is
inflammatory molecules from these cells in
most common in pigs, usually associated
tissues result in the pathologic processes
with erysipelas and streptococcal inf ecof cell-mediated immune reactions. The tions, and is attributed to a 'fype III reaction
antigens usually responsible for the
to these bacteria or to their vaccines. It has
development of Type IV reactions include
been reported in cats, although it may be
intercellular bacteria or parasites, some
mistaken for the non effusive form of feline
viruses, chemicals, and (in certain
infectious peritonitis.

situations) cellular antigens. The lesions
commonly occur in the skin (allergic

Other Type Ill Reactions: Purpura
contact dermatitis) when the antigen c?II_les
hemorrhagica of horses is a severe
into contact with the skin. The diagnosis 15
nonthrombocytopenic purpura (see p 4 7)

based on eliminating other causes of
that often follows a Streptococcus equi
disease and on histology. The goals of
respiratory infection; it is mediated by
treatment are to idE:ntify and elinunate
immune complexes of antibody and
the source of antigen responsible for the
streptococcal antigen deposited in vascular
reaction and to provide anti-inflammatory
basement membranes.

or immunosuppressive therapy as required.

Anterior uveitis ("blue-eye," see p 495) is an immune complex-mediated reaction

Granulomatous Reactions: T cellthat frequently occurs in the recovery stage mediated granulomatous reactions may 1
of infectious canine hepatitis (seep 798).

also occur around persistent infectious

It results from the reaction of serum
foci. These reactions to microorganisms
antibodies with uveal endothelial cells
such as mycobacteria, Coccidioides spp,
infected with canine adenovirus 1. Similarly, Blastomyces.spp, and Histoplasma spp,

IMMU NOLOG IC DISEASES

831
dpossibly feline infectious peritonitis
plasmacytic-lymphocytic inliltrate. When

��-us, nuiy be a result of_chronic c.cn- _
sufficient glandular tissue is destroyed,

1

1
ediatrd immune reactrnns and oca 1zed
in
the dogs develop Addison syndrome

... ci·ophage activation. Although
lllo

-

(adrenoco1tical insufficiency, see p 574).

d ,

.

f" . l

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en-mediate mmunuty e 1cct1ve y

The condition is sometimes associated

�ontrols these types of infections in most
with autoimmune thyroiditis (see above).

animals, for poorly understood reasons,
these same mechanisms are only partially

Keratitis Sicca: Keratitis sicca is a "dry effective in others. The�e granulomatous
eye" syndrome that occurs in dogs. It can
reactions are charactenzed by the
occur in either a primary form or secondary
development of a fibrous stroma and an
to chronic use of sulfonamides. It results
infiltration of macrophages, giant cells, and from immune-mediated destruction of the lymphocytes around the persistent antigen. lacrirnal glands and is similar to Sjogren syndrome of people. Affected dogs may .

Lymphocytic Choriomeningitis:

respond favorably to cyclosporine.

Lymphocytic choriomeningitis, a viral
eye drops.

infection of mice (see p 2025), results from the destruction of virus-infected cells by

TUMORS OF THE IMMUNE

T cells, leading to CNS damage and a ·

SYSTEM
choriomeningitis.

The cells of the immune system may

Old-dog Encephalitis: Old-dog
become neoplastic. This may result in the
encephalitis (seep 777) may also result from production of tumor cells that are :nonfunccell-mediated immune mechanisms directed tional and hence lead to immunodeficienagainst cells persistently infected with cies. Alternatively, they may be functional,
canine distemper virus. The initiating
and some cancerous B cells may produce
canine distemper virus infection is usually
large'quantities of immunoglobulins.

clinically inapparent and may precede the

· Tumor cells escape from the immune
development of encephalitis by many years. attack by relying on both immunosuppression and tumor cell modification. The Allergic Contact Hypersensitivity:

demonstration that even bulky, invasive

Allergic contact hypersensitivity results
tumors can undergo complete remission
from chemicals reacting with and
under appropriate stimulation ( eg; IL-2) has
modifying normal dermal proteins. The
shown that it is indeed possibleto treat
modified pioteins trigger a cell-mediated,
some cancers successfully by immune
immune response, which causes inflamma manipulation.

tion and damages the skin ( eg, poison oak

Lymphomas are common tumors in dogs
and poison ivy reactions in people). This
and cats.-The normal adaptive response
reaction has been described in dogs, ·
requires a burst of rapid proliferation of
cattle, and horses and usually occurs as
lymphocytes. On occasion,-however, this
a result of contact with sensitizing
proliferation may be uncontrolled, and
c�emicals incorporated in plastic food.

lymphoid neoplasms result. Because
dishes, plastic collars, and drugs placed
lymphocytes are present in all organs;
on the skin.

lymphoid tumor development can occur in
any organ. Lymphomas can be multicentric,

Autoimmune Thyroiditis: . Autohnmune mediastinal, GI, renal, nervous, or leukemic.

thyroiditis in dogs is characterized by

Less commonly, 'they occur in the eyes, skin,
destruction of the thyroid gland by an
a
or nose. To determine the stage of the
utoimmune process that has both humoral disease, CBC, serum chemistry profiles, (Type II) and cell-mediated (Type IV)

abdominal ultrasound, abdominal
tomponents. It is particularly prevalent in
radiographs, and bone marrow analyses are
ob�rman Pinschers, Beagles, Golden

Re
useful. lmmunofluorescent staining and
trievers, and Akitas. Hypothyroidism (see immunophenotyping can be pe1formed in

:53) may be the sole manifestation of the
dogs and cats to characterize lymphomas.

ease or may be a clinical or sub clinical

They may be either T cell or B cell in origin.

c?mponent of a broader autoimmune

Most cases of canine lymphosarcoma,
disorder such as systemic lupus erythematos

Mare k's disease, calf leukosis, and feline

Us or panendocrinopathy.

leukemia are ofT-cell origin, as are
thymomas. Many T-cell lymphomas are

Adrutoimmune Adrenalitis: Autoimmune
a
associated with a simultaneous inununoenalitis has been reported in dogs. The a
suppression manifest by a predisposition
drenal glands are slowly destroyed by a
to recurrent infections.

832

IM MUNOLOGIC DISEASES

Adult bmi.nc and ovinc lcnkosis,
proteins of any immnnoglobulin clac,s or
alirncntarv feline leukemia, and avian
imnnmoglobulin subunits (light chains or
leukosis �re usually of B-ccll oiigin. Under
heavy chains). Mycloma proteins in dogs
some circumstances, neoplastic B cells may
are commonly IgG or IgA and less comdcYelop into plasma cells. Plasma-cell monly IgM. Myelomas of the IgA type are

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tumors arc known as myelornas. Because
particularly common in Doberman
neoplastic plasma cells can secrete

Pinschers. Myeloma proteins in cats and
irnmunoglobulins, they give Iise to
horses usually are IgG and, uncommonly,
gamrnopathies (see below).

IgM, IgG3 (horses), or igA.

Clinical signs depend on the location

GAMMOPATHIES
and severity of the primary neoplasm and
on the amount and type of immunoglobulin

Garnmopathies are conditions in which
secreted. Plasma-cell myelomas frequently
serum immunoglobulin levels are greatly
develop in marrow cavities of flat bones of
increased. They can be classified either as
the skull, ribs, and pelvis, and in the
polyclonal (increases in all major immunovertebrae and cause severe bone erosion.

globulin classes) or monoclonal (increases

Pathologic fractures of diseased bone can
in a single homogeneous immunoglobulin).

lead to spinal pain and lameness.

Polyclonal gammopathies result from

Disease can result from the presence of
chronic stimulation of the immune system.

the monoclonal protein itself. For example,

They can therefore be caused by chronic
some forms of amyloidosis (see p 592) are
pyodermas; chronic viral, bacterial, or
due to deposition of immunoglobulin light
fungal infections; granulomatous bacterial
chains in tissues (SAA amyloid). Hypervisdiseases; abscesses; chronic parasitic cosity syndrome occurs in 20% of dogs with
infections; chronic rickettsial diseases, such IgM or IgA monoclonal proteins if the as tropical canine pancytopenia; chronic
protein levels in blood are high. In this. ,
immunologic diseases, such as systemic
syndrome, plasma viscosity can be many
lupus erythematosus, rheumatoid arthritis,
times normal, resulting in profound
and myositis; or by some neoplasia. In many vascular disturbances, thrombosis, and cases, there is no obvious predisposing
bleeding. Depression, blindness, and
cause. In some animals, the gammopathy
neurologic manifestations can be due to
may initially be monoclonal because of the
hemorrhage in the nervous system and
predominance of a.single immunoglobulin
retina. Some IgM monoclonal proteins are
class (usually IgG). This has been seen in
cryoglobulins and aggregate in vitro and in
cats with non effusive feline infectious
vivo when the plasma is cooled. Animals
peritonitis and in dogs with chronic tropical
with cryoglobulinemia often develop
canine pancytopenia.

gangrenous sloughs of the ear tips, eyelids,

Monoclonal gammopathies are
digits, and tip of the tail, especially during
characterized by the production of large
cold weather. Animals with monoclonal
amounts of a single immunoglobulin
gamrnopathies may have depressed levels
protein. Monoclonal gammopathies are
of normal immunoglobulins and are
either benign (ie, associated with no
therefore immunodeficient.

underlying disease), or more commonly,

Imrnunoglobulin-secreting tumors
associated with immunoglobulin-secreting
usually are treated with appropriate
tumors.

chemotherapy. Plasmapheresis may be

'Tumors that secrete monoclonal
required to lower serum viscosity in aniantibodies originate from plasma cells mals with clinical signs ofhyperviscosity

(myelomas ). Myelomas can secrete intact
syndrome.

I NTEG U M ENTARY

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SYSTEM

INTRODUCTION 837

Dermatitis 838

Dermatologic Problems 839

Diagnosis of Skin Diseases 839

History 839

Physical Examination 840

Laboratory Procedures 840

Common Dermatologic Problems 841

Alopecia 841

Pruritus 843

Principles of Topical Therapy 844

CONGENITAL AND INHERITED ANOMALIES 845

Congenital Anomalies of the Skin 846

Hereditary Alopecia and Hypotrichosis 846

Hyperplastic and Seborrheic Syndromes 84 7

Pigmentary Abnormalities 848

Defects of Structural Integrity 849

Cutaneous Manifestations of Multisystemic and Metabolic Defects 850 ·

Congenital and Hereditary Neoplasms and Hamartomas 852

·

ALLERGIC- SKIN.DISEASES

. . · _·

.

ATOPIC DERMATITIS 853

Canine Atopic Dermatitis 853

Feline Atopic Dermatitis 855

FLEA ALLERGY DERMATITIS 882

FOOD ALLERGY 855

URTICARIA 857

, BACTERIAL SKIN DISEASES ·

DERMATOPHILOSIS 858

EXUDATIVE EPIDERMITIS 860

INTERDIGITAL FURUNCULOSIS 862

PYODERMA 863

VIRAL SKIN DISEASES

,

· , ·

,

CONTAGIOUS ECTHYMA 866

Pox DISEASES 867

CoWpox 868

Pseudocowpox 868

834

INTEG UMENTARY SYSTEM

Lumpy Skin Disease 868

Sheeppox and Goatpox 869

Swinepox 870

Cowpox Virus Infections in Cats and Other Species 870

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ULCERATIVE DERMATOSIS OF SHEEP 872

FUNGAL SKIN DISEASES

DERMATOPHYTOSIS 872

Cattle 874

Dogs and Cats 87 4

Horses 875

Pigs, Sheep, and Goats 875

PARASITIC SKIN DISEASES

CATTLE GRUBS 876

Hypoderma spp 876

Dermatobia hominis 878

Lechiguana 879

CUTEREBRA INFESTATION IN SMALL ANIMALS 879

FLEAS AND FLEA ALLERGY DERMATITIS 880

FLIES 885

Dipterans with Biting Mouth parts 885

Black Flies . 886

Sand Flies 887

Biting Midges 887

Mosquitoes 888

Horse Flies and Deer Flies 889

Stable Flies 890

Hom Flies 891

Buffalo Flies 892

Tsetse Flies 892

Sheep Keds 893

Spider Flies/New Forest Flies 893

Hippoboscid or Louse Flies 894

Dipterans with Nonbiting Mouthparts 894

Face Flies 894

Head Flies 895

Filth-breeding Flies 895

Eye Gnats 896

Dipterans that Produce Myiasis 897

Facultative Myiasis-producing Flies 897

Obligatory Myiasis-producing Flies 899

Cochliomyia hominivorax 899

Chrysomya bezziana 900

Wolves (Warbles) of Small Animals 901

INTEGUMENTARY SYSTEM

835

Gray Flesh Flies 901

African 1\unlm Flies 002

Pseudomyiasis 903

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HELMINTHS OF THE Sl<IN 904

Cutaneous Habronemiasis 904

Dracwzculus Infections 904

Elaeophorosis 904

Onchocerciasis 905

Para.filaria Infection 906

Pelodera Dermatitis 907

Stephanofilariasis 907

LICE 908

Cattle 910

Sheep and Goats 911

Horses and Donkeys 912

Pigs 913

Dogs and Cats 913

MANGE 914

Cattle 914

Sheep and Goats 917

Horses 918

Pigs 919

Dogs and Cats 920

TICKS 925

Important Ixodid Ticks 928

Amblyomma spp 928

Anomalohimalaya spp 930

Bothriocroton spp 930

Cosmiomma sp 930

Dermacentor spp 930

Haemaphysalis spp 931

Hyalomma spp 932

Ixodes spp 934

Margaropus spp 935

Nosomma sp 935

Rhipicentor spp 935 ·

Rhipicephalus spp 935

Important Argasid Ticks 938

Argas spp 938

Carias spp 938

Ornithodoros spp 939

Otobius spp 939

Tick Removal 940

Tick Control 940

836

INTEGUMENTARY SYSTEM

NEOPLASTIC SKIN DISEASES

TUMORS OF THE SKIN AND SOFT TISSUES 942

Epidermal and Hair Follicle Tumors 943

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Benign, Nonvirus-associated Papillomatous Lesions 943

Basal Cell Tumors and Basal Cell Carcinomas 944

Intracutaneous Comifying Epitheliomas 944

Squamous Cell Carcinomas 945

Keratinized Cutaneous Cysts 94 7

Tumors of the Hair Follicle 948

Cutaneous Apocrine Gland Tumors 949

Apocrine Gland Tumors of Anal Sac Origin 950

Eccrine Gland Tumors 950

Sebaceous Gland Tumors 950

Hepatoid Gland Tumors 951

Primary Cutaneous Neuroendocrine Tumors 952

Papillomas 952

Equine Sarcoids 954

Connective Tissue Tumors 955

Benign Fibroblastic Tumors 955

Soft-tissue Sarcomas 955

Fibrohistiocytic Tumors 957

Peripheral Nerve Sheath Tumors 958

Adipose Tissue Tumors 958

Vascular Tumors 959

Cutaneous Smooth Muscle Tumors 961

Undifferentiated and Anaplastic Sarcomas 961

Lymphocytic, Histiocytic, and Related Cutaneous Tumors 961

Lymphoid Tumors of the Skin 961

Cutaneous Mast Cell Tumors 963

Tumors with Histiocytic Differentiation 966

Transmissible Venereal Tumors 967

Tumors of Melanocytic Origin 967

Metastatic Tumors 969

MISCELLANEOUS SKIN DISEASES

ACANTHOSIS NIGRICANS 970

EOSINOPHILIC GRANULOMA COMPLEX 971

Cats 971

Dogs 972

Horses 972

HYGROMA 973

MISCELLANEOUS SYSTEMIC DERMATOSES 973

NASAL DERMATOSES OF DOGS 975

PARAKERATOSIS 975

INTEGUMENTARY SYSTEM

837
pHOTOSENSITIZATION 976
congenital Photosensitization in Sheep 978
p1TYRIASIS ROSEA IN PIGS 979

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SADDLE SORES 979

SEBORRHEA 980

. INTEGU M ENTARY SYSTEM INTRODUCTION .

The skin is the largest organ of the body
the lipid content of the skin are critical to
and, depending on the species and age,
this function. The vitamin D precursor,
may represent 12%-24% of an animal's

7-dehydrocholesterol, is formed in the
body weight. The skin has many functions,
epidermis. The epidermis is thickest in large
insluding serving as an enclosing barrier
animals. The stratum corneum is continuand providing environmental protection, ously shed or desquamated.

regulating temperature, producing

Melanocytes are located in the basal cell
pigment and vitamin D, and sensory
layer, outer root sheath, and ducts of
perception. Anatomically, the skin
sebaceous and sweat glands. They are
consists of the following structures:

responsible for the production of skin and
epidermis, basement membrane zone, ·
hair pigment (melanin). Production of
dermis, appendageal system, and
pigment is under hormonal and genetic
subcutaneous muscles and fat.

control.

Langerhans cells are mononuclear

Epidermis: The epidermis is composed
dendritic cells that are intimately involved
of multiple layers of cells ·consisting of
in regulating the immune system of the skin.

keratinocytes, melanocytes, Langerhans

They are damaged by excessive UV light
cells, and Merkel cells.

· ·
exposure and glucocorticoids. Antigenic

Keratinocytes function to produce a
and allergenic material is processed by
protective barrier. They are produced from
these cells and transported to local and

�olumnar basal cells attached to a basement
nodal T cells to induce hypersensitivity
membrane. The rate of cell mitosis and
reactions. Epidermal proteins may also
subsequent keratinization are controlled by
cortjugate with exogenous haptens,
a variety of factors, including nutrition,
rendering them antigenic.

hormones, tissue factors; immune cells in

Merkel cells are specialized sensory cells
the skin, and genetics. The dermis may also
associated with skin sensory organs, eg,
exert significant control over the growth of
whiskers and tylotrich pads.

the epidermis. It has been hypothesized that

Photoperiod and reproduction cycles may

Basement Membrane Zone: This
affect the epidermis in animals. Glucocortiarea serves as a site for attachment of basal

�oids decrease mitotic activity; disease and
epidermal cells and as a protective barrier
inflammation also alter normal epidermal
between the epidermis and dermis. A
gr?wth and keratinization. As keratinocytes variety of skin diseases, including several migrate upward,they undergo a complex
autoimmune conditions, can cause damage

Process of programmed cell death or
to this zone. Vesicles are an example of a
keratinization. The goal of this process is to
damaged basement membrane zone.

Produce a compact layer of dead cells called
the stratum corneum which functions as an Dermis: The dermis is amesenchymal impermeable barrier to the loss of fluids,
structure that supports, nourishes, and to
ele�trolytes, minerals, nutrients, and water, some degree, regulates the epidermis and

:Vhile preventing the penetration of
appendages. The dermis consists of ground

�ectious or noxious agents into the skin.

substance, dermal collagen fibers, and cells
e structural arrangement of keratin and

(fibroblasts, melanocytes, mast cells, and

838

INT[C,Ul\\[N TI\IN SYS l 1. 1\,I IN l l\l 11 )ll( · 1 1< lN
occ:1...-.;ionall\' C(lsi1101 ihils, Ill 'Ill n 11 ihils, Thi• hnir 1·1 1:11. :tlso ll<'lps 1·orH·1•al or
lYrnphncytt's, histincylt's, am! pl:1sma cl'lls).

t':lllH>t1llag1• l hl' ani111:1l.

Blond n'�...;ds n.'sponsihk fur tht'rt11on•g11la

Si•ha1·1•011s gl:1nds an• si111pll' or l>ranchert tinn, lll'lYl' pkxl!Sl'S ass1 )('iat t•d \\'ith
alv<'ol:tr, hol<HTilH' glmHls 1 11:11. sr•1:rdr•
cut:mt'ous St'nsation. and both I\\Wlinall'd
sl'ht1111 int o f ill' hair follil'l<·s and onto lhe

:md 1mn\Yl'linatt'd n<'lYl'S an' pn•st'nl in the
q>id<'t'!llal smface. TIH•y are prcscnl in large VetBooks.ir
tknnis. �lot or 1w1Ycs an' p1immilv adn'ncrgic
nnmlwrs nPar U1P m11coc11Umco11sjunetion

:me! im1en ·at
intcnligital spaces, dorsal neck are
l' blood , '<'sst'ls and am.'cl or pili
a, rump '

muscll's. Excl'pt in hm�cs, apoctinc glands do
chin, ancl tail area; in some species, they ar�
not appe:u- to be inne1Yated. Sensory nl'rves
pmt of the scent-marking system. For
are dishibutl'd in thc dcm1is, hair follicles,
exmnple, in cats, sebaceous glands are
and specialized tactile stn1ctures. The skin
present on the face, dorsum, �nd �.ail in high
responds to the sensations of touch, pain,
concentration; cats mark temtones by
itch, heat, and cold.

mbbin<1 their face on objects and depositing
a layer �f sebum laced with feline facial

Appendageal System: These strnctures pheromones. Se bum is a complex lipid grow out of ( and are continuous with) the
material containing cholesterol, cholesterol
epidemlis and consist of hair follicles,
esters, triglycerides, di.ester waxes, and
sebaceous and sweat glands, and specialfatty acids. Se bum is important to keep the ized strnctures ( eg, claw, hoof). The hair
skin soft and pliable and to maintain proper
follicles of horses and cattle are simple, ie,
hydration; it gives the hair coat sheen and
the follicles have one hair emerging from
has antimicrobial properties.

each pore. The hair follicles of dogs, cats,

Sweat glands ( epitrichial [ formerly
sheep, and goats are compound, ie, the
apocrine] and atrichial [ formerly eccrine])

follicles have a central hair surrounded
are part of the therrnoregulatory system.

by 3-15 smaller hairs all exiting from a

The evaporation of sweat from the skin is
common pore. Animals with compound hair the primary body cooling mechanism for follicles are born with simple hair follicles
horses and primates and, to a lesser degree,
that develop into compound hair follicles.

pigs, sheep, and goats. There is some

The growth of hair is controlled by a
clinical evidence to suggest that limited
nlllllber of factors, including nutrition,
sweating occurs in dogs and cats, and that it
hom10nes, and photoperiod. The growing
may have a minor role in cooling the body.

stage of the hair is referred to as anagen,

Dogs and cats therrnoregulate primarily by
and the resting stage (mature hair) is
panting, drooling, and spreading saliva on
referred to as telogen. The transitional stage their coats (cats). Cats also sweat through between anagen and telogen is catagen.

their paws, especially when excited; this is

Animals normally shed their hair coat in
most commonly seen as wet paw prints on
response to changes in temperature and
surfaces, eg, examination tables.

photoperiod; most anin1als undergo a shed
in the early spring and early fall. The size,

Subcutaneous Muscles and Fat:

shape, and length of hair is controlled by

The "twitch muscle" (panniculus carnosus)

genetic factors but may be influenced by
is the major subcutaneous muscle. The
disease, exogenous drugs, nutritional
subcutaneous fat (panniculus adiposus)

deficiencies, and environment. Hormones
seives many functions, including insulation;
have a significant effect on hair growth.

reservoir for fluids, electrolytes, and energy;

Thyroxine initiates hair growth, and
and shock absorber.

glucocorticoids inllibit hair growth. The
primary functions of the hair coat are to
provide a mechanical barrier, to protect the

DERMATITIS
host from actinic damage, and to provide

Inflamma
thermoregulation. In most species, trapping
tion of the skin can be produced
by numerous
dead air space between second
agents, including external
ary hairs
irritants,
conserves heat. This requires that the hairs
bums, allergens, trauma, and
infection
be dry and waterproof; the cold-weather

(bacterial, viral, parasitic, or
fungal).

coat of many animals is often longer and

It can be associated with conctu�
rent internal
finer to facilitate heat conservation. The
or systemic disease; hercdi:

tary
hair coat can also help cool the skin. The
fact.ors also may be involved. Allergies
fom1 an import
warm-weather coat of animals, particularly
ant group of etiologic factors,
especially
large animals, consists of shorter thicker
in small animals.

.

The
hairs and fewer secondary hairs. This
skin's response to insult is genenanatomic change allows air to move easily cally called dermatitis and manifests as anY
through the coat, which facilitates cooling.

combination of pruritus, scaling, eryt�1crtta,
thickening or lichenification of the skin,

INTEGUMENTARY SYSTEM INTRODUCTION

839
llYPerpigmentation, oily seborrh�a, od?r,
d hair loss. The usual progression of a

.u;in disease involves an underlyin? trigger

( disease syndrome) that causes pnmary

Definitive diagnosis of the causes of various
lesions such � papules, pustules! �d
skin diseases requires a detailed history,
vesicles. Pnmtus 1s a �ommo� �hmcal sign physical examination, and appropriate VetBooks.ir
in 111any diseases, and 1�1_co��1t1ons that
diagnostic tests. Many skin diseases look
are not inherently prunt1c, 1t 1s often
alike, arid a definitive diagnosis is made
present because of secondary infections or over time by including or excluding possible 35 a result of production of inflammatory
causes, evaluating responses to therapy, ·
mediators. As the iriflammatory changes
ancVor process of elimination.

progress, crosting and scaling develop. If
the process involves the deeper dermis;
exudation, pain, and sloughing of the skin

History
may'occm,-. Secondary bacterial and yeast

A careful dermatologic history is critical to
infections' corrimonly develop as a'result of interpret the physical examination :findings skin inflammation. As dermatitis oe·comes
and choose appropriate diagnostic tests.

chronic, acute signs of inflammation ( eg,

A complete general history should be
erytnema) subside and primary lesions
obtained, including information about prior
become obscured by signs of chronic '�
illnesses, vaccinations, husbandry (housing,
infl_ammatfon (thickening of the skin,·-·; ( f
feeding practices, etc), changes in attitude
hyperpigrrientation, scaling, seborrhea).

and food consumption, elimination

Often, theskin·becomes drier; ifpruntus ·
practices, exposure to other animals, and
is not a comporierit of. the u,nderlyjng I • _. I .

travel within the past 6-12 mo. This should ·
trigger, it will often develop at this stage.'

be followed by a detailed dermatologic

Resolution of dermatitis requires . . . :- :, '

history. Use of a preprinted history form can
identification of the underlying cause arid:: be very useful for chronic or complicated treatment of secondary infections or other
cases: Agood history is important, because
complications.

·
many skin diseases that look similar are
differentiated based on interpreting clinical

DERMATOLOGiC 'PROBLEMS
signs and historical patterns.

The following information should be

Dermatitis is a nonspecific terin us#ally . !

obtained: 1) the primary complaint; 2) length
used until the demiatologic history,· clinical
of time the problem has been present; 3) age
signs, and physical examiriatioh can more
at which the skin disease started ( distinct
precisely define the problem: Derm:atolbgic age:predilections are seen in many diseases, problems are a major category of clinical ' : eg; de:modicosis' and dermatophytosis findings that can be caused by a number of
in pediatric animals and signs of atopic
skin qiseases; many skin diseases look alike dermatitis in animals 1 '--3 yr old); 4) breed and are differentiated by working through

(breed predilections include a predisposition
diagnostic flow charts and a process ·of
of Cocker Spaniels to primary disorders
elimination. The most common dermatoof keratinization, and of terriers to atopic l�gic problems include pruritus, alopecia,
dermatitis); 5) presence and severity · .

Cnistirtg and scaling, otitis; nohhealing
of pruritus (including licking, rubbing,
wounds, nodules and tumors, and
scratching, or chewing behavio�wne:rs
ulcerative disorders. In some species, such often do not realize licking may be a sign as cats, there may be well-recognized
of pruritus ); 6) how the disease started and
subcategories of dermatologic problems:·
its progression (diseases that begin with

C eg, he�d and neck pruritus, symmetric,: · :

pruritus may lead to self-trauma and

�opec1a, eosinophilic exudation/dermati-,:

subsequent development ofsecondaryskin
tis, etc). Defining the major dermatologic • . lesions [alopecia, seborrhea] or infections P�oblem will help ·create a specific · ··

[bacterial or yeast pyoderma]); 7) type and
differential

;
diagnosis list and aid selection '

o
progression of lesions noted by the owner;
f �ppropriate diagnostic tests. The

8) evidence of seasonality ( suggesting fleas,
aruma1•s dermatologic problem may or may

�
allergic skin disease, or weather-related
ot be the owner's chief complaint. It is,
diseases); 9) area on the body the problem
llnP0rtant to be sensitive to owners'

was first noticed (ie, regional patterns seen in

Perceptions of problems or complaints,·•
e
atopic dermatitis [ typically the face and feet],
specially if odor or aesthetics are involved, cheyletiellosis [primarily dorsal], scabies

�d _to _address them ( eg, bathing to

[primarily ventral]; and endocrine hair loss

�ze odor while the key problem is

[usually involves the trunk and spares the
eing evaluated). -

. ·

· -
head and legs]); 10) any previous treatments

840

INTEGUMENTARY SYSTEM I NTRODUCTION
and the responses to such (ic, antibiotic-

Some ksions may be either primary or
responsive skin diseases suggpst a bactcnal
secondary, depending on the <:ause of the
cause; pnnitus that respond
disease. Tlwse include alopecia, scale,

� t� sma)l
doses of glucoc011icoicts, antilust.anm
crusts, follic11lar casts (ph

�cs,

_1gging of hair
or essential fatty acids snggests al
follicles with visible keralm), comedones

_lergic

VetBooks.ir
dennatitis ); 11) frequency of batlung and

(blackheads), and pigmentary changes.

.

when the last bath was given (recen� b:1tlung
may obscure or change important c_luucal

Laboratory Procedures for Skin
lesions excessive bathing and wetting of

Diseases
the skht can predispose to skin �ease);

S!dn Scrapings: Skin scrap

12) presence of fleas, ticks,

�gs :rre part

_or �tes;

13) otl1er contact animals (ie, e
of the basic database for all skin dis
videnc
eases.

_e of

There are two types of skin sc
contagion which suggests fleas, scabies,

�apings, .

cheyl;tiellosis, or dermatophytosis ); 14) the
superficial and deep. Supe�c1al scrapm�
environment of the animal (housing changes
do not cause capillary bleeding and pro':de
can influence the development of certain
information from the surface of the epiderskin diseases, eg, contact dermatitis, conmis. Deep skin scraping� collect.material tagious diseases); and 15) signs or reports ?f
from within the hair follicle; cap1�lary ·,
systemic illness ( endocrine [ eg, hypothyrmdbleeding indicates that the sampling was .

ism and hyperadrenocorticism] disorders
deep enough. Skin scrapings are used
and metabolic diseases [ eg, diabetes mellitus, primarily to determi1:1e the p�esence or renal disease liver disease] should be noted,
absence of mites. Skin scrapmgs are best
because the �kin can be the first place signs
perf orrned using a skin-�cr�ping spatula,
of systemic illness are noted).

which is a thin metal weighing spatula
commonly found in pharmacy or chemical
supply catalogs. These spatulas are reusable

Physical Examination
and do not cause injury.

A complete physical examination should
always be performed. Many skin diseases

Combing of the Hair Coat: This
are manifestations of systemic diseases,
technique, commonly ref erred to as "flea
eg, hypothyroidism, hyperadrenoco1:1icism, combing," is useful to collect large amounts hepatocutaneous syndrome, systeffilc
of skin debris and trap cutaneous parasites.

lupus erythematosus. (See also MISCELLANE

Combings are particularly useful to find
ous SYSTEMIC DERMATOSES, p 973.) A good
fleas, ticks, lice, and some mites. A clean
dermatologic examination requires very
scrub brush or curry comb can be used to
close inspection of the entire hair coat and
collect material into a flat container ( eg, pie
skin under strong lighting; flashlights may
plate) in large animals.

be necessary to exarnine the skin of large
animals. It is important to examine the

E}tamination of Hairs: Microscopic
ventrum of the animal, where many primary examination of hair shafts can be used to lesions and cutaneous parasites are found.

look for evidence of self-trauma, dennato

Clinical lesions are described in a variety
phyte infections (requires clearing agents
of ways. Gross lesions can be described as
and special staining), dysplastic hairs, and
focal, multif ocal, or diffuse in distribution,
sometimes, genetic diseases of the hair coat.

followed by a description of the affected
region ( eg, mucocutaneous, truncal). On

Cytology: Cutaneous and auricul�
closer inspection, lesions may be further
cytology
described as primary or secondary. Primary
is helpful to identify bactenal,
lesions include macules or patches (nonfungal, and, possibly, neoplastic skin elevated areas of discoloration); pa.pules
diseases. At least 4-6 impression smears
or plaques ( elevated lesions, the latter
should be made; several slides should be
coalescing); pustules, vesicles, or bullae
saved for examination at a reference

(fluid-filled lesions); wheals (flat-topped,
laboratory if necessary. When performing
steep-walled, solid elevations of the skin
impression smears of the skin, the glass ·te
arising from histamine release); or nodules
slide should be placed directly over the si
or tumors (large solid elevations of the skin).

to be sampled. An index finger or th�b d

Secondary lesions include epidermal
should be placed directly over the slide an
collarettes (late stage of a pustule), scars,
very firm pressure exerted. AltemativelYthe
excoriation (areas of self-trauma), erosions
clear acetate tape can be used to sample
or ulcers (loss of the epidermis), fissures,
skin. Adequate sampling will produce a e
lichenification (increased thickening and

"thumb print" from the surface. At least on hyperpigrnentation of the skin), and calluses. slide should be heat fixed with a match or lighter before staining. In most cases, a

INTEGUMENTARY SYSTEM INTRODUCTION

841

Romanowsky-type stai� is adequate. In
urinalysis may be helpful to identify the
nrritic animals, matenal should be scraped cause. In dogs with recurrent infections,

�-oin beneath nail beds .md smeared onto
these tests may identify an underlying

1355 slides for �1ea� fixing, s�ining, and
subclinical disease.

g ytolomc exanunat:1on. Specimens should

VetBooks.ir

�e ex�ined und_er 4x_, !Ox, and oil
lntradermal Slcin Testing: This test is not
jnUnersion magnification.

necessarily required to make a diagnosis of
atopic dermatitis. A positive intradermal

Fungal Cultures: Dermatophyte
skin test reaction indicates past exposure
infections are best identified with a fungal
to a particular allergen. Inhalant allergies
culture on either dermatophyte test medium are best diagnosed based on a compatible or on plain Sabouraud agar. Plates that are
history, physical examination findings, and
easily inoculated are pref erred; glass,
judicious use of intradermal skin testing or
screw-topped jars are difficult to inoculate
in vitro testing for allergies: Intradermal
and obtain samples from and are best

, 1 , skin testing is recommended for animals in
avoided. Cats are best sampled using a new
which immtinotherapy is indicated because
toothbrush aggressively combed over the
ofthe severity or duration of allergic signs.

affected lesions. Dogs can be sampled with

Potential drug interactions that can interfere
either a toothbrush or via a hair plucking
with testing should be considered before
technique. In large animals, hairs should be
intradermal skin testing is performed.

gently wiped with alcohol before collecting
to minimize contaminant growth. Interme-

In Vitro Diagnostic Tests: In vitro •
diate and deep fungal organisms are·best
diagnostic tests (ELISA or RAST tests) are
cultured at a reference laboratory using a,
an·alternative to intradermal skin testing.

skin biopsy specimen (6-8 mm in size ):r

Although in vitro tests are considered less
reliable because of the large number of,

Bacterial Cultures: • Intact pustules can be false-positive reactions, most complications cultured by rupturing the pustule with a.. i' . in interpretation are the result of poor ·
sterile needle· and swabbing the lesion with
patient selection. Like intradermal skin·
asterile culture swab. Lesions should :n:otbe tests/in vitro tests reflect exposure and : scrubbed before sampling. Deep pyodermas. must be 'interpreted in light of the animal's• .

are best cultured from a skin.biopsy. ··;
clinical signs and ·history.

(6,;-8 mm). The reference laboratory should
be informed as to what pathogens are
suspected, because this may affect how the

-·��

;:_ .. -..:d ;l\ ) .. �
exudate is cultured. Systemic and topical •.,

�H.,
agents should be withheld for at least 72 hr,,

. , , ...

.,

'

1-..::

before sampling. .

; 1 ; '., • , : The two most common dermatologic problems are alopecia and pruritus.

Biopsy: Skin biopsies are indicated in �y ·
case that appears severe, unusual; or does·, . , ALOPECIA not respond to appropriate therapy. Lesions
should not be scrubbed before biopsy;

(Ha_ir loss)

1 '.

because surface pathology is important in;

Alopecia is the partial or complete lack of
the diagnosis of many skin diseases. Beveral
hairs in areas where they are normally
samples from a variety of lesions should be
present If an animal is presented for the
submitted for examination. Primary lesions
problem of hair loss and pruritus is present,
should be sampled whenever possible;. . · · the problem ofpruritus should be investi

?therwise, the report is often not very helpful gated first ( see p 843).

� making a diagnosis or narrowing a list of·
diffe�ential diagnoses. Biopsy specimens .· Etiology: There are many causes of rTe _examination by a pathologist familiar. alopecia; any disease that can affect hair Wi skin diseases of animals. Direct immun
follicles can cause hair loss. There are two
ofluorescence is not necessary to diagnose broad etiologic categories of alopecia:

;��imm�e skin diseases; routine histo-

1) congenital or hereditary and 2) acquired.

ology IS the test of choice.

Acquired alopecia is further divided into

Rou
two categories: inflammatory and nonin-
tine Blood and Urine Tests: In
flammatory.

:�s� dermatologic cases, these tests do

Congenital or hereditary alopecia ( see
r.r° elp to make a definitive diagnosis.

s
p 846) has been described in cows, horses,
th ystemic signs of illness are present,
dogs, cats, and pigs. Hairless breeds of mice,
en a CBC, serum chemistry panel, and
rats, cats, and dogs have been bred and

842

INTEGUMENTARY SYSTEM I NTRODUCTION
developed for personal and rcscar('h
collars. Harely, excessive grooming may be
interests. Congenital alopccia may or may
the cnusP of hair loss in some animals,
not be hereditary; it is caused by a lad< of
particularly cats.

development of hair follicles ,mcl is apparent

Feline endocrine alopccia is no longer
at, or sho1tly after, birth. Animals with
recognized as a bona fide syndrome; the
tardivc alopecias are born with normal
cun-cnt name is feline acquired symmetric

VetBooks.ir
coats, c.md focal or generalized hair loss
alopccia. To date, there is no documented
occurs when the animal sheds its juvenile
evidence of an endocrine disease in these
coat or when it becomes a young adult.

cats, and the symmetric alopecia seen is a

Exan1ples of this include pattern baldness of clinical sign of an underlying disease, most Dachshunds, color dilution alopecia ( most
commonly a pruritic disease. The most
commonly seen in Doberman Pinschers ),
common cause off eline symmetric alopecia
and certain types of follicular dysplasias.

is flea allergy dermatitis. In cats that do not

Acquired alopecia encompasses all other
have an obvious flea infestation, a CBC With
causes of hair loss. In this type of alopecia,
differential is recommended; many cats that
the animal is born with a normal hair coat,
have flea allergy dermatitis have an eosinohas or had normal hair follicles at one time, philia. This finding may help convince
and is or was capable of producing strucowners to pursue flea control as a first turally normal hairs. Acquired alopecia
diagnostic step.

may be noninflammatory, as is seen in
endocrine alopecia or some types of

Clinical Findings and Lesions: The
immune-mediated alopecia, or inflammaclinical signs of hair loss may be obvious or tory. Inflammatory acquired alopecia is the
subtle, depending on the disease. Congenimost common cause of alopecia. Acquired tal or hereditary hair loss is commonly
alopecia develops because a disease
symmetric and not accompanied by many
destroys the hair follicle or shaft, inteiferes
inflammatory changes; in some cases, the
with the growth of hair or wool, or causes
areas of hair loss are localized to one region
the animal discomfort ( eg, pain, pruritus ),

( eg, ear flaps) or to well-demarcated areas.

leading to self-trauma and loss of hair.

The clinical signs of acquired hair loss are

Diseases that can directly cause destrucvaried and often influenced by the underlying tion or damage to the hair shaft or follicle
cause( s ); the pattern of hair loss may be
include bacterial skin diseases, dermatophy�
focal, multifocal, symmetric, or generalized.

tosis, demodicosis, severe inflammatory

Inflammatory changes such as hyperpigmendiseases of the dermis ( eg, juvenile cellulitis, t.ation, lichenification, erythema, scaling,
deep pyoderma), traumatic episodes
excessive shedding, and pruritus are

( eg, bums, radiation), and rarely, poisonings
common. Some causes of acquired alopecia
caused by mercury, thalliun1, and iodine.

may predispose the animal to development of

These diseases tend to be inflammatory.

secondary skin diseases, such as a bacterial

Diseases that can directly inhibit or slow.

pyoderma or sebon-hea Pruritus is variable,
hair follicle growth include nutritional
depending on the primary cause. In
deficiencies (particularly protein deficienendocrine alopecias, the hair loss usually cies), hypothyroidism, hyperadrenocortidevelops in a symmetric pattern, often in cism, and excessive estrogen production or
wear areas first; pruritus is uncommon unless
administration (hyperestrogenism, Sertoli
there is a secondary infection. Contrary to
cell tumors, estrogen injections for
previous thought, hair loss is not generally an
mismating). Temporary alopecia in horses,
early clinical sign of an endocrine alopecia.

sheep, and dogs can occur during preg

Many owners seek veterinary assistance
nancy, lactation, or several weeks after a
because of perceived excessive shedding.

severe illness or fever. Marked hair loss

Shedding may be abnormal (excessive) if it

( effluvium) is common in cats after
results in obvious loss of the hair coat and
respiratory infection. These types of
areas of alopecia. A common cause of
alopecia tend to be noninflammatory unless
abnormal shedding is bacterial pyodenna.

a secondary skin infection develops.

If, however, the shedding is not accompa

Pruritus or pain is a common cause of
nied by development of patchy or symmetacquired inflammatory alopecia in animals.

ric hair loss, it is likely that it is just a stage

Diseases that commonly cause pruritus or
in the natural replacement of the hair coat.

pain include infectious skin diseases ( eg
bacterial �yoderma and dermatophytosi� ),

Diagnosis: An accurate diagnosis of the
ectoparas1tes, allergic skin diseases ( eg,
cause of alopecia requires a careful history
atopic dermatitis, food allergy, contact,
and physical examination. Key points in
insect hypersensitivity), and less commonly, the history include recognition of breed neoplastic skin diseases. Friction may cause predispositions for congenital or hereditarY
local hair loss, eg, poorly fitted halters or
alopecias; the duration and progression of

INTEGUMENTARY SYSTEM INTRODUCTION

843
ions; anci thryn'.st'n�•p or absl'IH'l' or prnri

Ies
lilH'rn t.lwt. c<H1<h1ct: sP11sat. ions al. 10-20 ml cvicirncr of contn�10n, 01· nondt'rmat otttS:

Sl'(' rnrry IIH' Wc'll-lncalized pricking itch

.'problrtns, t'�, polvmia and pnlydipsia.

10f �
sc·nsation. In c<mtrw-il., UH' S<'nsalion of

1�:-siral pxamination, the distrihut.ion or burning itch is t ransmit.t.ed via nonrnyeli-Oi .1 11._ slumld lH' nott'd ( focal, nmlt.il'oc:tl, l
nat <'d fih('rs that con cl net semmtions at 2 m/

.r51011�

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1�1,·c ('°l'lll'rnlizt'd). and tlw hairs

,,,nr
sec. Both or these fibers enter the dorsal root
l .

, c,

::,;, � t1itll'd to <kt l'nninl' wlH'tlwr th<'y are of the spinal cord, ascend through the dorsal

��'.�(1 shrd from till' hair follicle or broken

�'h,��

.

.

S'

f
colunm, and cross into the lateral spinothaoff-the lattl'!' s��<.'stmg pnmtus. 1g1�s o lamic tract. From there they go to the
srcondmY skm mf cct.10ns or ectoparas1tes
thalamus and on to the sensory cortex.

1 ould be noted, and a careful nondennato

The mediators ofpruritus are controver

: �ic examination should be pe1fonned.

0
sial and may vary depending on the species.

1Itltial diagnostic tests include skin

These putative mediators include histacrapings for ectoparasites (particularly mines (released from mast cell degranula1emode.·r�lites); cm:nbh�g ofthe_hair coat tion), proteolytic enzymes (proteases), and
for fleas, nutes, and bee; nnpress10n smears
leukotrienes. Proteases are released by
of the skin for evidence of bacterial or yeast fungi, bacteria, and mast cell degranulation, infections; fungal cultures for identification
and during antigen-antibody reactions.

of dem1atophytosis; and exanlination of

Leukotrienes, prostaglandins, and thromplucked hairs, !ooking at both the shaft and boxane �' which are broken down from
the ends for eVIdence of dermatophytosis or arachidornc acid, are pro-inflammatory.

that the hairs were chewed off. In many

Essential fatty acids, particularly glinocases of bacterial pyoderma, impression s
lernc acid, have been used to counter the
mears of the skin do not show neutrophils
inflammation mediated by leukotrienes and
and/or cocci, but they may show large
thromboxane A2• The sensation of pruritus
numbers of shed keratinocytes. N eutrophils may be affected by a variety of factors, and cocci are seen if pustules or recently
including boredom, competing sensations,
ruptured pustules are sampled.

and anxiety. Stress may potentiate pruritus

If these tests do not identify or suggest an
via the release of opioid peptides.

underlying cause, a skin biopsy may be
indicated to evaluate hair follicle structures,
numbers, and anagen/telogen ratios and to

Etiology: · Pruritus is a clinical sign and
look for evidence of bacterial, fungal, or
not a diagnosis or specific disease. In
parasitic skin infections. In addition, skin
general, the most common causes of
biopsies are often needed to confirm
pruritus are parasites, infections, allergic
congenital or tardive causes of hair loss and
skin diseases, and miscellaneous causes
to identify inflammatory or neoplastic

( eg, cutaneous neoplasia). Many diseases
causes of hair loss. Skin biopsies from
that are nonpruritic (eg, endocrinopathies)

nonnal and abnormal sites should be·.

become 'pruritic when the animal develops
submitted for evaluation. CBC, serum
secondary bacterial or yeast infections.

chemistry panels, and urinalyses are
generally.only helpful when an endocrinopa Diagnosis: A thorough dermatologic thy is suspected. Specific endocrine function history and physical exanlination should tests can be performed based on findings of
be performed. Parasitic causes of pruritus,
routine laboratory work or clinical signs.

including Dmnodex; fleas and ticks, conta

Treatme
gious mites, and lice, should be excluded,
nt: Successful therapy depends on
the
because they are most common. Skin
underlying cause and specific diagnosis.

scrapings can exclude ( or include) various
mite infestations, including Dmnodex.

PRURITUS

However, some mite infestations ( eg,

Otching)

Sarcoptes, Cheyletiella, Psoroptes, Clwrioptes) might be missed on skin scrapings.

�tus is defined as an unpleasant sensation If a mite infestation is suspected, a response Within the skin that provokes the desire to
to therapy trial should be undertaken. The
scratch.

most commonly used drug in these cases

Patho
is ivermectin. Fleas can be excluded or
physiology: Pruritus may be well
or Po
included based on a history offlea control,
orly localized. It may manifest as
response to flea control, or finding evidence

�harp or diffuse, burning sensation.

tho
offlea infestation via a flea combing. Flea
ar ugh the skin is richly innervated, there

'lb
control practices can also exclude louse
no known specialized pruritus receptors.

e
infestations.

sensation of itch is transmitted via a

8Peci

The next most important group of pruritic
a!ized set of afferent fibers. Myelinated diseases to exclude is infectious causes of

844

INTEGUMENTARY SYSTEM INTRODUCTION
skin disease. These include bacterial

Animals with idiopathic pruritus or those in
infections (primarily staphylococcal
which treatment of the underlying disease
infections, Malassezia overgrowth, and does not eliminate the pruritus ( eg, atopic
dermatophytosis ). A fungal culture should
animals) require medical management of
be perfom1ed in any cat presented for
pruritus. Currently, evidence-based revi

.

ews

VetBooks.ir
pnuitus. It is also highly recommen�ed m
of antipruritic do not support the use of
dogs that are newly acquired, any arumal
antihistamines to control pruritus.

with a possible history of e:x1>osure and/�r

Essential Fatty Acids: Essential fatty
compatible clinical signs, or when there 1s
acids are rarely effective as sole antipruri
a history of people with skin dis
tic

_ease . .

agents and are not suitable for acute flares

Concurrent bacterial and yeast inf ect1ons
of pruritus. If they are beneficial, it is a
are increasingly recognized as a common
longterm therapy.

cause of pruritus in dogs, cats, and large
animals. Bacterial pyoderma is underdiag

Glucocorticoids: Glucocorticoids are the
nosed in cats, and a response to therapy
most effective drugs in the management of
trial may be needed to exclude or include it.

pruritus. However, they cannot be used

Infectious causes of pruritus commonly
safely for longterm management because of
induce clinical signs of hair loss, scaling,
adverse effects ( eg, �uppression of adrenal
scales piercing hairs, odor, and/or greasy
function risk of development of diabetes
seborrhea. Marked pedal pruritus and facial mellitus,' risk of secondary urinary tract . ·
rubbing are common in animals with
infections). In addition, owners can rarely
concurrent yeast and bacterial infections.

tolerate the common adverse effects

Before pursuing allergies as a cause of pruri (polydipsia, polyuri� polyph��a, and

.,
tus or performing skin biopsies or other
panting) for long penods. Anti-inflammatory
more expensive and/or invasive diagnostic
dosages range from 0.5-1 mg/kg/day, PO, for
testing, a concurrent bacterial and yeast

5-10 days and then eveiy other day. Topical
infection should be excluded. A 21-30 day
spray formulations of triamcinolone acetate
concurrent course of an antibiotic effective
are highly effective and good alternatives to .·
against Staphylococcus spp ( eg, cephalexin oral steroids.

30 mg/kg, PO, bid) and a systemic antifungal

Other Systemic AntipruriticAgents:

( eg, ketoconazole, itraconazole, or

Cyclosporine modified is a highly effective · ·
fluconazole 5-10 mg/kg/day, PO) should be
nonsteroidal drug for control of pruritus. Toeprescribed. If the pruritus resolve�, then only formulation that can be used is modified
existing pruritus was due to a microbial
cyclosporine. The dosage is 5 mg/kg for
infection.

dogs and 7 mg/kg for cats. Maximal benefit···

It is possible that the,initial trigger has
can take as lohg as 30 days to observe. Once··
long passed or is seasonal. However, if the
efficacy is established, dose tapering to
animal's pruritus is unchanged or only
every other day can be attempted. Common
somewhat better, the most likely underlyingadverse effects include vomiting and cause is allergic ( assuming parasitic causes
diarrhea ( common) and gingival hyperplahave been excluded). The most common sia Oess common). Another drug for control
causes of allergic pruritus are insect bite
ofpruritus in dogs is oclacitinib, a Janus
hypersensitivity ( eg, flea allergy, mosquito
kinase inhibitor that provides rapid relief
bite allergy, fly bite), food allergy, and atopic from pruritus and inflammation in dogs with dermatitis. F1.ea allergy dermatitis and
short- and longterm allergic skin disease. , ,
insect bite hypersensitivity are excluded
based on response to insect control.

Animals that do not have insect bite
hypersensitivity but are seasonally pruritic
most likely have atopic dermatitis. Animals
with year-round allergic pruritus have atopic See also SYSTEMIC PHARMACOTHERAPEUTICS OF
dermatitis and/or food allergy. Food allergy
is excluded or included based on response

THE INTEGUMENTARY SYSTEM, p 2571.

_ Topical therapy is an important part of
to a diet trial and provocative challenge.

.

veterinary dermatology. It is often beneficl�

Atopic dermatitis is a clinical diagnosis; in
in improving the cosmetic appearance
vitro allergy testing and intradermal skin
or odor of the animal, pending the final
testing show only antigen exposure
diagnosis. It can be beneficial as an acijunct
patterns. These tests are used to determine
to systemic therapy. Finally, it may be the
the contents of an immunotherapy vaccine.

preferred method of treatment for some
diseases, eg, flea infestations.

Treatment: Successful therapy depends

The following are some basic guidelines to
on identification of the underlying cause.

consider when prescribing topical therapy:

CONGENITAL AND INHERITED ANOMALIES OF THE INTEG UMENTARY SYSTEM

845

1) As much of the hair coat as possible should Antiparasitic shampoos are "flea be removed when treating skin diseases.

shampoos." In most cases, the amount of
aood grooming practices facilitate topical
insecticide in these products is not adequate
therapy and can significantly help shorten the to kill all the fleas in a severe infestation.

course of disease. 2) TI1e cooperation of the

However, these products are excellent
wner ( and animal) should be evaluated
routine cleansing products. Medicated

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Wore any topical therapy is prescribed.

shampoos include antimicrobial and

S) Animals tend to groom off topical products antiseborrheic products. The most widely and may vomit after ingestion. The risk of
used antibacterial shampoos contain
toxicity is a constant wony for owners. Local chlorhexidine or benzoyl peroxide.

ointtnents, gels, and sprays are best used

Antiseborrheic shampoos contain some
sparingly, under occlusion, and for specific
combination of tar, sulfur, and salicylic
diseases. Such medications often sting when
acid-ingredients that are keratoplastic and
applied to the skin, especially many of those
keratolytic. Tar is recommended for. oily
instilled into the ears. Many agents also may
seborrhea, and sulfur and salicylic acid are
mat the hair. 4) Tepid water is the temperarecommended for scaly seborrhea. Most ture of choice for bathing animals. 5) The old
animals benefit from products that contain
adage, "If it's wet, dry it and if it's dry, wet it,"

all three agents; however, tar products are
has some truth to it; however, this advice
contraindicated in cats.

should not be carried to extremes. Exudative ·

When a medicated shampoo is used, the
lesions, eg, areas of pyotraumatic dermatitis,
animal should be washed in a cleansing
heal faster if they are kept clean and covered
shampoo before the medicated shampoo
with an antibiotic ointment or gel (previous
and rinsed well. Medicated shampoos
recommendations suggested aggressive
often are not good cleansing agents, do
astringent use). Dry, lichenified skin is often
not lather well, or do not work well in the
pruritic, and the judicious use of emollients
presence of organic debris. The medicated
may be beneficial. 6) The animal should be
shampoo should be applied evenly to the
monitored closely for possible development
hair coat after being prediluted in water.

of irritant or allergic contact dermatitis from

Prediluting the shampoo will facilitate it
topical agents. Many topical agents have very being rinsed from the coat and minimize similar bases or ingredients, and changing
the potential for irritant or allergic contact
from one to another may only exacerbate the dermatitis. Depending on the shampoo, problem. 7)0wners should be given careful
the concentration of shampoo to water
and thorough instructions on how to
will vary between 1:3 and 1:4. If possible,
administer the therapy.

the medicated shampoo should be allowed
to have a contact time of 10 min with the

Shampoo Therapy: , ·shampoos are the
skin and then rinsed thoroughly from the
most corrtrnonly used topical treatments.

coat. Shampoo residue is a common cause

There are three broad classes of shampoos:

of irritant reactions. Finally, the medicated
cleansing, antiparasitic, and medicated.

shampoo should be used often, usually 2-3

Cleansing shampoos remove dirt and
times/wk during the early stages of
excess oils from the coat. These products
therapy.

include over-the-counter dog grooming

The use of medicated antimicrobial
shampoos, fl.ea shampoos, and many mild
shampoo therapy is mcreasing because of
human products. These products lather
concerns over development of methicillin

Well and must be rinsed from the coat.

resistant staphylococcal infections.

CONG E.N ITAL AN D ; IN H ERITED ANOMALI ES

OF TH E I NTEG U M ENTARY SYSTEM

Congenital dermatoses of the skin may be
f
tions are referred to as tardive developmenenetic or arise during embryo genesis tal defects. Both congenital and tardive
eca�e of
developmental dermatoses are fairly
rn
nongenetic factors. Genetic

Utations that cause skin anomalies may be common in domestic animals of all species, resent at birth or become apparent weeks
with the greatest number of well-defined

0 rnonths later. These late-onset manifest.a- defects described in cattle and dogs.

846

CONGENITAL AND INHERITED ANOMALIES OF TH E INTEGUMENTARY SYSTEM

CONGENITAL ANOMALIES OF
comcdonicus, linear organoid nevi, and

THE SKIN
follicular hamartomas are known to occur

In horses, cannon keratosis and linear

Epitheliogenesis imJJerfccta ( aplasia
epidermal nevi have been described.

cutis) is a congenital discontinuity of

Doubtless, similar defects occur in all
squamous epithelium. It is seen in cattle
species. Mixed, or organoid, nevi consist

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(autosomal recessive trait), horses, swine,
of circumscribed collections of densely
sheep, cats, and dogs, although it is rare in
packed adnexal structures (pilosebaceous
the latter three species. In cattle, affected
nevus and pilosebaceosudoriferous nevus)

breeds include Holstein-Friesian, Hereford,

Collagenous nevi are nodules composed

Ayrshire, Jersey, Shorthorn, Angus, Dutch
of focal collagen hyperplasia that displ ac e Black Pied, Swedish Red Pied, and German
the normal structures of the skin. Most

Yellow Pied. It is common in swine, in
lesions are alopecic, with pigmented, pitted
which large lesions are obvious at birth as
surfaces. When not extensive, nevi can be
glistening red, well-demarcated discontiexcised; otherwise there is no known nuities in the skin or mucous membranes.

effective treatment.

Infection and ulceration are early conse

Dermoid sinuses or cysts are seen in quences. One or more hooves or claws

Thoroughbred horses and Rhodesian
may be deformed or absent; in some

Ridgebacks (in which they are inherited)

affected animals, there are other associated and occasionally other breeds of dogs.

congenital anomalies. The condition is

These are cystic structures lined with skin
fatal when extensive, but small defects can
in which exf oliated skin, hair, and glandular
be surgically corrected. Ultrastructural
debris accumulate. They are caused by
evaluation of this condition in American
failure of complete separation of the neural

Saddlebred foals has demonstrated a
tube from the epidermis during embryogenrelationship withjunctional epidermolysis esis; cysts are found on the dorsal midline
bullosa ( see p 850).

·
and are rarely associated with spinal cord .

Focal cutaneous hypoplasia and
neural deficits. They can be removed by , ·
subcutaneous hypoplasia are congenital,
surgical excision.

circumscribed hypo plastic defects of

Follicular cysts develop by abnonnal ..

multiple or deeper skin layers in swine.

hair follicle morphogenesis and by retention

The lesions manifest as skin depressions in
of follicular or glandular products. They may
which all skin layers or the subcutaneous
be congenital when caused by the failure of
fat layers fail to develop· normally.

the follicular orifice to develop normally.

A nevus is a circumscribed developmen

Congenital cysts are most commonly
tal defect of the skin, whereas a hamaridentified in Merino and Suffolk sheep.

torna is a hyperplastic mass formed as a

Periauricular ( dentigerous) cysts are seen in
result of a developmental defect in any
horses and, although present at birth, may
organ. Both nevi and hamartomas have
not be recognized until adulthood. Wattle ·
been described as congenital skin defects,
cysts are seen in Nubian goats; these arise
but the problem may not become obvious
from the bronchial cleft. Porcine wattles are
until later in life. fu dogs, sebaceous nevi,
seen fairly frequently in all breeds of swine.

pigmented epidermal nevi, inflammatory

These are teat-like growths on the lower jaw.

linear verrucous epidermal nevi, nevi

HEREDITARY ALOPECIA AND

HYPOTRICHOSIS

Alopecia is the absence of hair; hypotrichosis, which is much more common, is the presence ofless hair than normal. Although
these defects can be generalized, they
commonly develop in patterns that spare
the extremities or correlate with hair color.

These ectodermal defects can be congenital
or tardive and can be associated with
abnormal or absent adnexa, with defects in
other ectodermal structures ( such as teeth,
claws, and eyes), or with skeletal and other
developmental defects. There are various

Collagenous nevus in a dog. Courtesy of Dr.

modes of inheritance in those instances in

Robert Dunstan.

which familial occurrence has been studied,

CONGENITAL AND INHERITED ANOMALIES OF THE INTEGUMENTARY SYSTEM

847

X-linked ectodennal dysplasia has been
hypotrichosis, is seen in black and white
ported in Germ�m Shepherds. Hairless
piebald dogs. The hypotrichosis develops

��eds of dogs ( eg, l\kxic�m Hairless,
shortly after birth and affects only the

Chinese Crested, Ame1ican Hairless Tenfor) black-colored areas. This syndrome is best and cats (Sphinx) have been bred_for these
known in the Papillon and Bearded Collie.

ctodennal defects. Many sporadic cases
e

Recent genetic analysis in Large Munster

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f ectodennal defects are described in
landers has indicated an autosomal

�ogs most often in males. Affected dogs,
recessive inheritance in this breed. A
inclt;ding most of the hairless �ree�s, often
similar follicular dysplasia is reported in
have patchy or pattern hypotnchos1s as
nonpiebald breeds. Other types of follicular
well as associated dental anomalies. All
dysplasias of uncertain cause include
animals with abnormal follicular developseasonal flank alopecia of Boxers and ment are prone to_ comedone formation,

Airedale Terriers and various woolly
hair follicle infect10ns, and hair foreign-
syndromes and post-clipping alopecia in
body granulomas.

Spitz-type breeds. Familial h

At least 13 types of hypotrichosis have
ypotrichosis of

Irish Water Spaniels develops at 2-4 yr of
been described in cattle, affecting' Angus,
age, and a dominant mode of inheritance

AyrShire, Brangus, Holstein-Friesian,
has been suggested. The condition formerly

Hereford, polled Hereford, Guernsey,
known as growth hormone-responsive

Gelbvieh, Jersey, as well as Normandyalopecia in Pomeranians and other breeds Maine, Anjou-Charolais, and Simmeiltal
is now called alopecia X, reflecting the
crosses. Most have autosomal recessive or
complexity of factors, hereditary and othersex-linked modes of inheritance. Associated wise, influencing these syndromes.

defects include failure of horn development,

In cats, follicular dysplasia is seen in the
hypophyseal hypoplasia, macroglossia,

Devon Rex. In horses, both color dilution
dental anomalies, abnormal coat coloration, alopecia and black hair follicle dysplasias and death Q.ethal hypotrichosis ). Viable
are·occasionally reported, especially in
hypotrichosis, hypotrichosis with anodon.:

Appaloosas. Congenital progressive
tia, semihairlessness, streaked hairlessness, hypotrichosis has been reported in a blue black hair follicle dysplasia (Holstein), and
roan Percheron. Reported hair shaft
cross-related hypotrichosis (rattail) are·
structural abnormalities of dogs and cats
specific types described in cattle.

include pill torti (American Wrrehaired Cat),

In sheep, hypotrichosis is rarely-reported, trichorrhexis nodosa, and spiculosis (Kerry with the best known syndrome affecting the Blue Terrier).

Polled Dorset. 'This involves the hair of the
face most severely, but the wool is-also of

HYPERPLASTIC AND SEBORRHEIC
poor quality. In goats, hypotrichosis is

SYNDROMES ,
associated with congenital goiter. In swine;
two forms of hypotrichosis are known

Many anomalies affect keratinization; some

(Mexican Hairless, German), one of which
are associated with hereditary hypotriis associated with goiter and death in the choses (see p 846); whereas others are
homozygote.

·

·
associated with systemic metabolic

In dogs, there are several tardive follicle derangements. Those for which none of·
dysplasias, including color dilution
these associations has yet been made are a
alopecia This is found in some dogs
diverse group of syndromes that may affect
bearing the coat color genotype dd, which
localized parts of the· epithelium or that may
renders black genotypes blue and liver
be generalized. Among the latter are the
genotypes beige or fawn. This syndrome is
poorly characte�ed congenital or familial
best known in Doberman Pinschers but is
seborrheic syndromes, the best known of
also commonly seen in color dilute
which is idiopathic seborrhea of Spaniels

Dachshunds, Italian Greyhounds,

· ··
and idiopathic facial dermatitis of Persian

Greyhounds, Whippets, Yorkshire Terriers, cats. Hereditary congenital follicular

?11d tricolor hounds and has been reported
parakeratosis is a syndrome of female Rottma Gennan Shepherd. Recently, "silver ·
weilers and Siberian Huskies. It is a severe

Labrador Retrievers" with color dilution
keratinization defect associated with
alopecia have been reported. Affected dogs various noncutaneous abnormalities.

are bom with normal hair coats but before

Cutaneous ichthyoses are charac

� Yr of �ge b�gin to develop fo�culitis and
terized by abnormal and hypertrophic

Yll0trichosIS that is progressive and
epithelial proliferation, with accumulation

Confined to the blue-or fawn-colored areas. of extensive scale and hyperkeratosis on the

�la�k hair follicle dysplasia, a similar but
skin surface. Cases have been described
artier developing and more complete
mostly in cattle and dogs, but chicken and

848

CONGENITAL AND I NHERITED ANOMALIES OF THE I NTEGUMENTARY SYSTEM
several mouse models arc also known, and
disease is nol uniformly fatal, but affected
there is om' re1rnrt in a llama. In cattle, the
survivors are stunted. There is no effective
severity varies; some forms arc lethal
trcalmenl.

shmily after bitth. Affected breeds include

Familial footpad hyperkeratosis is

Red Poll, Flicsim1, Holstein, Brown Swiss,
reported in Irish Teniers and Dogues de

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Pinzgauer, and Chianina.

Bordeaux. All pads of all feet are involved

Cm1ine ichthyosif onn dennatoses are
from a young a�e, although the disease is not
also heterogeneous and occur sporadically
usually congerutal. When hyperkeratosis
in a number of breeds, including Doberis severe, horns, fissures, and secondary man Pinschers, Rottweilers, Irish Setters,
infection cause pain and lameness. No other

Collies, English Springer Spaniels, Cavalier
skin lesions are present. Treatment is

King Charles Spaniels, Golden Retrievers,
symptomatic, with soaking, keratolytic and

Labrador Retrievers, and terriers (including
emollient treatments, with treatment of

Parson Russell Terriers). There is some
bacterial pyoderma. No reports of the use
evidence of a familial inheritance pattern
of synthetic retinoids are available. Major
in Parson Russell Terriers and Golden
differential diagnoses for footpad hyperkera

Retrievers. In dogs, the body is covered with tosis include hepatocutaneous syndrome, a large adherent scales that may flake off in
disorder of keratinization, and pemphigus.

large sheets. The planum nasale and digital

Granulomatous sebaceous adenitis
pads may be markedly thickened in some
is an idiopathic disease that destroys the
forms; the latter usually is associated with
sebaceous glands and, in some breeds of
apparent discomfort. Clinical management
dogs, is associated with a severe seborrheic
is difficult, but signs may be ameliorated
and alopecic dermatosis. It is hereditary
with keratinolytic shampoos or solutions
in Standard Poodles and suspected to be

( eg, selenium disulfides, lactic acid, benzoyl familial in Akitas. It first manifests itself in peroxide) and with hurnectants ( eg, lactic
young adults, but inapparent carriers are
acid, urea, propylene glycol, and essential
known in Poodles. Marked hyperkeratosis
fatty acid preparations). Experimental use
precedes development of hair coat
of synthetic retinoids has been helpful.

abnormalities, which begin as loss of

Control of secondary pyoderma is
normal hair kinkiness and progress to
frequently required.

patchy alopecia Akitas tend to have more

Psoriasiform-lichenoid dermatosis
seborrhea oleosa and less alopecia than
affects young English Springer Spaniels and

Poodles. Response to treatment is
is presumed to be genetic. The erythematous, inconsistent and incomplete. Mildly symmetric lesions, which consist of papules
affected dogs are treated with antiseborand plaques on the pinnae and inguinal rheic shampoos and treatment of pyodenna
region, are covered with scales and become
as needed. Severely affected dogs have
increasingly hyperkeratotic if left untreated.

benefited from propylene glycol or hot oil

In some affected dogs, the lesions may
treatments. Some dogs respond to oral
even t ually spread, and the skin is severely supplementation with omega-3 fatty acids,
greasy. Spontaneous remissions and a
and some respond to synthetic retinoids.

waxing and waning course are recorded.

Spontaneous remission has been recorded.

Some dogs respond to antibiotic treatment or Recently, modified cyclosporin to synthetic
e A (5 mg/kg/
retinoids, but most are refractory day, PO) has been very effective in the.

to therapy. Cyclosporine therapy has been
treatment of many dogs.

used with mixed results in some dogs.

Pityriasis rosea of pigs is a familial
disease in which the mode of inheritance is
not known. (See p 979 for clinical findings

PIGMENTARY ABNORMALITIES·
diagnosis, and treatment.) Derma to sis

Many
vege
associations between skin and coat

_tans of Landrace pigs is a hereditary,
possibly
color and
congenital,
developmental anomalies have
disorder with an
autosomal
been
recessive
recorded in domestic animals. Some
mode of inheritance.

It must
of
be
the
differentiated
associations with hypotrichosis are
in the early stages
from pityriasis
discussed
rosea.

under hereditary alopecia

This is a more serious
disease

(see p
and

846).

affects the hooves as well as

.·

Albinis
the skin. Lesions begin
m
as
appears to be rare in domestic
macules and
papules and are
animals. True
scaly as
albinis
in pityriasis
m is always associated
rosea.

with pink or pale

They later become
irises
covered
and
with
with visual
browndefects and increased
black crusts and are
risk
associated
of solar
with coroni radiation-induced neoplasms of the s�-
tis and hoof deformity. Piglets fail to thrive

It has been noted in Icelandic
and
sheep and 111
eventually develop pneumonia; the

Guernsey, Austrian Murboden, Shorthorn,

CONGENITAL AND INHERITED ANOMALIES OF THE INTEGUMENTARY SYSTEM

849
wn Swiss, and Charolais cattle. Albinism in some breeds of dogs (Belgian Tervuren, aro t be differentiated from extreme white

Rottweilcr). Affected animals develop
rnUS tting or piebaldism mHl dominant white. somewhat symmetric macular depigmentasp 5 ° 1e animals with extreme piebaldism or
on

·
tion of the skin that occasionally also affects
l

· t ct

I ·
donlinant wlute mve associa e neuro og1c
the hair coat and claws or hooves. The onset

VetBooks.ir
malies or deafness, or suffer death in
is usually in young adulthood. Most lesions ,

�iro. Lethal white foal_ syndrome is one
are on the face, especially the muzzle or
ti at results from breedmg two Overo
planum nasale or around the eyes. Depigp�ts- In dogs and cats, dominant white mentation may wax and wane. Complete
r extreme piebaldism can be associated

0
remission may occur but is rare. There is no
u
accompanying systemic or cutaneous patholvitll nilateral or bilateral deafness and :

'ometnnes with blue irides or iris hetero-
ogy. No treatment is available; treatments

�
used
hromia. White cats with bilateral-blue eyes
in people with vitiligo are unlikely to
have a 75% chance of deafness. In dogs,
provide significant cosmetic results in
deafness may also be associated with merle
animals,
hair coats and is found in Dalmatians, . ·

Lentigo in orange and orange-faced

Sealyham Terriers, harlequin Great Danes,
male cats is marked by the development of

Collies, and white Bull Terriers: Cyclic
asymptomatic, pigmented macules. Lesions
neutropenia may be found in gray or pale
are first seen on the lips and eyelids at
merle Collies. In Rhodesian Ridgebacks, . .

< 1 yr of age. Other sites include the planwn
pale coat color is associated with cerebellar nasale and gingivae.'Lentigines are not .

degeneration. In Chediak-Higashi syndrome· precancerous and have no medical

(see p 50) of cats and cattle (Herefords,·
consequence.

Japanese Black, Brangus ), coat color: · ·

Acquired aurotrichia of Miniature
dilution (blue smoke in cats) is associated· -. Schnauzers is afainilial syndrome in which with neutrophil and platelet abnormalities
hair along the dorsal midline changes to
and shortened life span: This is inherited as
golden from the normal black or gray of
an autosomal recessive trait. Male tricolor
this breed. The onset is usually in young
cats ( calico and tortoiseshell) are sterile ·
adulthood. The change may be associated
because the gene for orange is X-linked and . with thinning in the hair coat but no other recessive, and males have the abnormal·
cutaneous or systemic signs.·ln most dogs,

XXY gen()type. '

. ,
coat color reverts to normal within 1-2 yr.

Pigmentary abnormalities may be
acquired, and some of these may be ·

DEFECTS OF STRUCTURAL
hereditary or familial, as in vitiligo. As a

INTEGRITY
familial disease; vitiligo is best recognized in

Arabian horses ( Arabian fading syndrome,

This category includes genetic defects in
pinky syndrome); it may also be familial in
structural elements responsible for the
cattle (Holstein-Friesian), Siamese cats, and
integrity of the epidermis and dermalepidermaljunction, as well as some dermal structural anomalies.

Cutaneous asthenia ( dermatosparaxis,

Ehlers-Danlos syndrome) is a: group of •
syndromes characterized by defects in
collagen production. This results in a variety
of clinical signs including loose, hyperextensible, fragile skin; joint laxity; and other connective tissue dysfunctions. These
collagen defects have beeh described in
cattle (Belgian Blue and White, Charolais,

Hereford, 'Holstein-Freisian, Simmental),
a goat, sheep (Norwegian Dala, Border

Leicester-Southdown, Finnish-Merino cross,

Romney, White Dorper); pigs (Large

White-Essex cross), horses (Quarter horse,

Arabian cross), rabbits (New Zealand white),
cats (Himalayan and domestic shorthair),
mink, and dogs ( a litter of Garafiano

Shepherds, sporadically in several breeds).

The mode of inheritance has been demon

Vitili . ·

.

strated for Himalayan cats (recessive) and
ofo go in an adult Golden Retriever. Courtesy
r. 5tephen White.

·
domestic shorthair cats (dominant).

850

CO'.\JGENtTAL AND INHERITED ANOMALIES OF THE INTEGUMENTARY SYSTEM

Clinical fpatures incluclP f ragilP skin from the first weeks of life. The most, sever the time of birth. wounds that heal ";th thin lesions are on tiH' feet, with sloughin: scars. delayed wound healing, pendulous
hooves, claws, or f�1otpads, and oral m�� 0
skin. and hematoma and hygroma
membrane and facial and perigenital ski Us
fommtion. ln lan1bs, rupture of the GI tract

(erosions). Except for epidennolysis n

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and arterial ane�'SillS are features. and the bullos� simple�, these �li�eases arc, fatuJ
disease is fatal in lambs and cal,·es. In

Carunc berugn familial chronic
horses. the onset is later and tl1e lesions are
pemphigus is a mechanobullous disorct er
well circumscribed. consisting of hyperexthat is caused by a defect in cell-to-cell tensible and somewhat fragile skin. In dogs
adhesion in the epidermis. This disorder h
and cats. the disease is not fatal, and older
been described in a family of English Sett as
animals dc,·elop hanging folds of skin and

It develops within a few weeks of birth an�rs.

exhibit e:x1ensi,·e scarring; some have joint
causes crusting alopecic lesions on the
la.tin· or ocular anomalies.

pressure points of the skin that slowly

Diagnosis is based on clinical signs and
enlarge as the puppies grow. The disease
histoparhologic studies of the collagen
is benign, and no treatment is reported.

structure, which require age and breed

Familial acantholysis, reported in New
matched controls. For diagnosis in cats and

Zealand Angus calves, is a similar syndrome
dogs, a skin extensibility index has been

This fatal syndrome is reported to be an
de\"eloped. There are anecdotal reports of
autosomal reces.sive trait.Affected calves
imprm-ement of affected dogs with vitamin
develop erosions, with collarettes and crusts

C supplementation. The major differential
in areas subjected to trauma Some show
diagnosis in adult cats is feline hyperadreno partial separation of the hooves. Diagnosis corticisrn with acquired skin fragility.

in both puppies and calves is established

The epidermolysis bnllosa syndromes
by skin biopsy of newly forming lesions.

are a group of congenital and hereditary

Cutaneous mncinosis is thought to be
diseases that result from defects in the
a familial problem in some lines of Chinese
dermal-epidermal attachment structures.

Shar-Pei. Normal Shar-Pei have more

These are knm\"n as mechanobullous
cutaneous mucin than other dogs, but in
diseases. because minor cutaneous trauma
some young dogs, cutaneous mucin
results hi dermal-epidermal separation with formation in the dermis is so excessive that formation of flaccid bullae that soon
the skin exhibits pronoW1ced folding and
rupture, leaving glistening, flat erosions.

mucinous vesiculation. Diagnosis is by skin

Syndromes are classified according to the
prick of the vesicles and observatiori of
ultrastructural location of the epidermalthe strings of mucus that have the same dermal defect: simplex, in the epidermal
appearance as normal joint fluid or,
basal cell layer;jW1ctional, within the
alternativelY, by skin biopsy. The syndrome
basement membrane; and dystrophic,
is partially responsive to corticosteroids,
below the basement membrane in the
but they are contraindicated because of the
subepidermal anchoring fibrils.

young age of the affected dogs. As these

In large animals, lesions are most
dogs mature, the severity of the syndrome
conunon on the gingivae, palate, lips, _
may abate, but it can be exaggerated by the
tongue, and feet. Some forms of epi<;lermolydevelopment of allergic skin disease, which sic; bullosa are scarring, and most are fatal.

is conunon in the breed. The major

In large animals, epidermolysis bullosa
differential diagnosis is hypothyroidism.

syndromes are known in calves (Sirnmental,

Brangus ), domestic buffalo, lambs (Suffolk,

South Dorset Down, Scottish Blackface,

CUTANEOUS MANIFESTATIONS

Weisses Alpenschaf, Welsh MoW1tain ), and

OF MULTISYSTEMIC AND

Belgian foals. All three forms of epidermoly

_

M_E_TA
sic; bullosa have been characterized in dogs

_

BO

_

LI_C_D_E_F_E_C_

TS

____

..--
and cats. Epidermolysis bullosa simplex has Baldy calf syndrome of female HolsteinS, been described in Collies and Shetland
as the name implies, is associated wi� ·

Sheepdogs. JW1ctional epidermolysis
hypotrichosis. This autosomal recessive
bullosa ha5 been reported in a Toy Poodle
trait is lethal to male fetuses. Affected

German Shorthaired Pointers, mixed-bre�d
calves appear normal at birth but ! 0s�
dog.5, and Siamese cats and tentatively

· c11:-2
condition and patches of hair be�o
id�ntified in �eaucerons. Dystrophic
ed
mo later. The skin then becomes thicken
ep1dermolysis bullosahas been reported in
and wrinkled, and the tips of the ears rnaY
a domestic shorthair cat and a Persian and
e
curl. Calves salivate profusely and bee:�
in Golden Retrievers and Akitas. Lesions
emaciated, and affected female calves
may be present at birth or develop within
boliC
by 6-8 mo of age. The W1derlying meta

CONGENITAL AND INHERITED ANOMALIES OF THE INTEGUMENTARY SYSTEM

851
defect is not lmmrn. A similar appParing
onset. in adulthood has been recorded.

rndrotnr, known a.s congenital anemia,

Progression oflcsions is variable, and

S) rskeratosis, and progressive alopecia, individual pups within a litter may be affected

�desc1ibe<l in polled llerC'ford calves of

15
mildly to severely. Skin lesions appear in

.

ct

II .

either sex. Anenua an sma �1ze are noted
areas of increased trauma and are seen on

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at bilth and become progressively more
the face, ear tips, tail tips, and lateral surfaces
severe. Alopecia, abnom1al curly hair, and
of the extremities. Skin lesions, which
hyperkeratosis begin around the muzzle and consist of erosion, crusting, and alopecia, are ear margins and become more extensive as
exacerbated by heat and sun exposure. The
the calves mature. Later, the skin becomes
muscles affected most severely are on the
markedly wrinkled, and neurologic
head and extremities. Diagnosis is estababnommlities develop. Calves have diarrhea lished by evaluation oflittermates and family and die before 6 mo of age.

history, skin biopsy, electromyography, and

Familial vasculopathy has been
muscle biopsy, which must be performed
described in German Shepherds and Parson early in the course of the disease. There are Russell Teniers. In these dogs, the skin
reports of disease amelioration with dosages
lesions develop shortly after the first set
of corticosteroids, vitamin E, and.orriega-3
of puppy vaccinations and seem to be
fatty acids, but severely affected dogs rarely
exacerbated after subsequent vaccinations.· respond satisfactorily to treatment.

The main cutaneous signs a.re footpad swell Pentoxifylline (10 mg/kg, PO, bid) has been ing and depigmentation that may progress
helpful in many dogs.

to ulceration; all footpads are typically

Hereditary lupoid dermatosis of
affected. Crusting and ulceration of the ear

German Shorthaired Pointers is first noted
and tail tips and depigmentatioil of the ·
when the dog is ~6 mo old. It begins with
plan um nasale are also features. As the dogs scaling and crusting onthe head and mature, the disease may resolve, but pad
dorsum and quickly progresses to
lesions may be so severe that euthanasia
generalized scaling with erythema The
iswarra:nted. No lmown treatment is
dermatopathy appears to be either painful
unifortnly·effective, although some dogs
or pruritic. Affected dogs become pyrexic
appear to respond to high dosages of
and develop lymphadenopathy. Some
corticosteroids. A severe form of neutro-
develop a poorly characterized enteropathy;
philic vasculitis recently described in_ ·
most lose condition. As the name implies,
young Chinese Shar-Pei may be familial.

skin biopsy specimens reveal features of a

Familial dermatomyositis is an ' ·
lupus-like dermatitis. The disease is
idiopathic inflammatory disease of the skin
progressive and ultimately fatal. No
and inuscles of young Collies and Shetland
successful treatment has been reported.

Sheepdogs. The mode of inheritance is· · · ' 1; ·

Hereditary zinc deficiency syndromes
reported to be autosomal dominant in
are best known in cattle and have also been

Collies, but there is some evidence of a role ' ·' described in dogs. In cattle, these syndromes for an unidentified infectious agent in•the ·
include hereditary parakeratosis, lethal trait
pathogenesis. A vasculopathy is associated

A46, edema disease, and hereditary thymic
with the early inflammatory stages of the
hypoplasia Affected breeds include
disease in the skm and muscle; in both · ·

Friesian, Shorthorn, Angus, and Black Pied.

tissues, the eventual sequela is atrophy. The

These syndromes all become apparent
onset is typically at <6 mo of age, although
within days to weeks of birth and are
characterized by symmetric, mostly acral,
hyperkeratosis; crusting and unthriftiness;
susceptibility to infection; and early death.

Affected calves exhibit cortjunctivitis,
ptyalism, rhinitis, and diarrhea and often
succumb to pneumonia In most breeds of
cattle, the trait appears to be autosomal
recessive and associated with intestinal
malabsorption of dietary zinc, which is more
or less responsive to dietary zinc supplementation. In some breeds, the defect in absorption is absolute, and parenteral
administration of zinc is needed to achieve
remission. Because such treatment is rarely
feasible in production animals, these are

Familial derm
lethal traits. Diagnosis is established by
a;omyositis in a Collie. Courtesy
of Dr.

excluding dermatophilosis (see p 858) and

Robert Dunstan.

852

CONGENITAL AND INHERITED ANOMALIES OF THE INTEGUMENTARY SYSTEM
by skin biopsy ( showing mostly parnkerntoeryt.hropoietic porphyria (see p DSG) is sis ), by measming serum zinc levds, mul hy
common and more severe. It is report tn_ore
necropsy findings that includ<' hypoplm,ia or
several breeds (including Shorthorn Cdin
thymus and lymph nocll'S.

Holstcin-Friesian,_ and l�ereford) as �n

In dogs, there arc two familial zinc
autosomal recess��e �rmt: In addition t

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deficiency syndromes. In ·white Bull Teniers,
o
severe photoscns1tivity, signs include
lethal acroderrnatitis is characterized
red-brown disc�loration ?f teeth, bones
by retarded growth; progressive, acral,
urine; regenerative anemia; and stuntect' flnd
hyperkeratotic de1n1atitis; and pustular
growth. Teeth and urine from affected
dem1atitis around mucocutaneous junctions. animals �uo�esce ?range under a Wood's These signs are apparent by IO wk of age
lamp. Skin bmpsy IS also useful in diagn osis.

and are later accompanied by diarrhea,

Leukocyte adl1esion deficiency in
pneun10nia, and death before 2 yr of age.

Holstein cattle is an inherited disease

In older dogs, footpad hyperkeratosis and

( autosomal recessive) with many manife
paronychia contribute significantly to
tat.ions. It is fatal before adulthood. Skin smorbidity. The severity of the cutaneous lesions are frequently seen in affected
disease can be ameliorated somewhat
calves and include de
by control of secondary bacterial and

_rmatitis and vasculitis

This disease can be diagnosed by molecu}�

Malassezia infections and, with aggressive
methods with PCR analysis of fresh or fixed
medical treatment, the lives of affected
tissue providing identification of affected
dogs can be prolonged. These dogs do not
carrier, and normal cattle.

,
respond to oral zinc therapy. A familial
zinc-responsive dermatopathy that is

CONGENITAL AND HEREDITARY
manifest mostly by cutaneous lesions and

NEOPLASMS AND HAMART0MAS
is responsive to supplemental oral zinc is
seen in Alaskan Malamutes, Huskies, and

Congenital neoplasms are common in large

German Short.haired Pointers. Signs develop animals. Mastocytosis, melanocytosis, at weaning or later in life and consist of
cutaneous lymphosarcoma, and vascular
crusting and hyperkeratosis of the extremi
hamartomas are found in calves. Melanoties and mucocutaneous junctions. Often, cytomas may also arise shortly after birth in
bitches will develop signs associated with
calves and may be hereditary. These are
estrus or whelping and lactation. Secondary
thought to be benign.

Malassezia infections are common.

Melanomas are seen in Duroc..Jersey and

Diagnosis is established by skin biopsy and

Sinclair miniature pigs as familial traits.

response to oral zinc supplementation.

These may undergo spontaneous remission

'fyrosinemia has been described in a
or may behave as malignant tumors. Piglets

German Shepherd puppy. It was compared
have also been described with vascular
to a type of tyrosinemia in people and thus
hamartomas and with congenital fibropap·
thought to be hereditary. Clinical manif esta
illomatosis, which is likely infectious.

tions included erosions and ulcerations of

Congenital tumors are rare in dogs and
the footpads and nose and bullous lesions
cats. One dog with a giant congenit.al
and depigmentation of the skin, loss of claws, pigmented nevus had a malignant melaand eye lesions. It must be differentiated noma develop within the lesion. In cats,
from the familial vasculopathy of German
familial benign mastocytosis is described

Shepherds described above. In the puppy,
in young Siamese cats.

serum tyrosine levels were 20-30 times

A syndrome of multiple collagenous
above normal levels, and urine specimens
nevi is seen in some families of German
contained similar high concentrations.

Shepherds and

Porphyria
is called nodular der
is an inherited defect in the
matofibrosis.

metabolism

Aff
of
ected dogs are ad
hemoglobin and its

1�ose

Dozens
byproducts. In
of skin lesions may occur, an
cattle, accumulation of
on t
aberrant
he
porphyrins
feet of
in
ten ulcerate or cause foot
the skin increases
e iS
de
sensitivity
formiti
to ultraviolet
es and lameness. This syndro�
light. (Porphyria has
ara
been described in

_cutaneous
cats and
marker f
swine but does

�r renal cystaden�scrnoma and
not result
uterine
in photosensit
le1omyom
ivity.

a. Pr?gr

) In cattle,
sive dermal collagenosis is a similar
there are two types of inherited porphyries.

disease of post.pubertal male :minia

Bovine protoporphyria has been

��
reported in pigs. It is thought to be hereditaIY
crossbred Limousin cattle and is inherited
an ues on
characterized by symmetric, firill platl
as an autosomal recessive trait. Signs
of
the trunk that consist of thick bundl�S 8,ll
include photodermatitis and photophobia
d
collagen replacing the nom1al deJ.1lllS al

Affected calves may die, but mature animals panniculus. A connection with intern, may be less severely affected. Bovine
malignancy has not been reported.

ATOP IC DERMATITIS

853

Urticaria pigmcntosn is caused by
and crusted papular eruption on the head,
t cell hypcq)lasia and has been
neck, and legs. Diagnosis is made by skin

�1�rtbed in cats. Affected cats have
biopsy. There is evidence of a familial
n�:uifocal, pattially coalescing macular
history.

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ATOPIC DERMATITIS

Atopic dermatitis (AD) is a genetically

Terrier, Shih Tzu, and West Highland White
predisposed inflammatory and pruritic

Terrier. The age of onset is generally
allergic skin disease with characteristic
between 6 mo and 3 yr. Clinical signs usually
clinical features. It is most commonly
occur on a seasonal basis but may be seen
associated with IgE antibodies to environyear-round with time. Pruritus is the mental allergens. The atopic phenotype ( see characteristic sign of AD. The feet, face, clinical signs, below) can be seen in animals ears, flexural surfaces of the front legs, with IgE-mediated skin disease, food allergy, axillae, and abdomen are the most or a condition called "atopic-like dermatitis" frequently affected areas. Primary lesions (AID). ALD is defined as a pruritic skin
consist of erythematous macules, patches,
disease in dogs with characteristic features
and small papules. Lesions that develop · ;
of AD but negative tests for IgE antibodies.

secondary to self-trauma include alopecia,

Feline atopic dermatitis has many
erythema, scaling, salivary staining,
similarities to canine atopic dermatitis.

hemorrhagic crusts, excoriations, lichenification, hyperpigmentation, superficial Etiology and Pathogenesis: The
staphylococcal pyoderma, Malassezia and
etiology and pathogenesis of AD is combacterial overgrowth, and allergic otitis plex and involves a genetic predisposition, · externa Chronic or recurrent otitis is the impairment of the normal barrier function
only complaint in a small number of animals.

of the skin, and immunologic aberrations. ·,

Animals with AD are thought to be ·

Diagnosis: The diagnosis is challenging
genetically predisposed to become
and is based on signalment, clinical signs,
sensitized to allergens in the environment: : · and disease history and not on laboratory Allergens are proteins that, when inhaled
tests. Prospective studies have revealed the
or absorbed through the skin, respiratory·
following clinical features compatible with
tract, or GI tract, evoke allergen-specific · , .. a diagnosis of AD: onset of clinical signs lgE production. These allergen-specific IgE before 3 yr of age, dogs that live mostly molecules affix themselves to tissue mast
indoors, glucocorticoid-responsive pruritus,
cells or basophils. When these primed cells pruritus without skin lesions, affected front come in contact with the specific allergen · · feet, affected ear pinnae, nonaffected ear again, mast cell degranulation results in the margins, and nonaffected dorsolumbosacral release of proteolytic enzymes, histamine,
areas. These clinical signs can overlap with
ta�Ykinins, and other vasoactive amines,
other diseases, so parasites, pruritic
eading to inflammation ( erythema, edema, microbial overgrowth, food allergy, and flea and P�tus ). The skin is the primary target
o
allergy need to be excluded. Allergy testing
rgan m dogs and cats, but rhinitis and

(intradermal or serologic) is a diagnostic aid
as�hma can also occur in ~ 15% of affected
that measures increased levels of tissueantrnals.

bound or circulating IgE; alone, it is not
diagnostic but rather reflects exposure. The

�INE ATOPIC DERMATITIS
primary reason to pursue intradermal or

Clinical F
serologic allergy testing is to identify the

· d.

·
le . . m ings: There IS no sex predi-
off ending allergens in an individual animal
cti�n m Canine AD. There are breed
and to formulate specific immunotherapy.

b�edilections, but the prevalence within a

Test results are significant only if the
an�ed l�gely depends on the genetic pool
off ending allergens identified are compatre
d gion. Breeds predisposed to
ible with the history or seasonality of

ShVelop:ment of AD include Chinese
pruritus. Animals with classic clinical signs

Re ar:Pei, Wrrehaired Fox Terrier, Golden
but negative allergy tests are given the

Lab triever, Dalmatian, Boxer, Boston Terrier,
diagnosis of ALD.

r

Immunotherapy
act
would be
orRetriever, LhasaApso, Scottish
difficult if not impossible in these animals.

854

ATOPIC DERl'v1J\TITIS

Treatment: AD and ALO cannot lw c·11n'<l.

con1t'orta\Jly wit h t l_1is drng alo11P. Tanoli

Client l'dncation is import:mt, lwcansP this

!llllS oint 11w11I. prnvtdl's a hl'll<'lil. in anir 11, •11 k is a lifdong; dist':ISP t hat rcqnin's lifl'long
with mon• loC'aliz('d h�sions. I IOWPV(•

·
r <1
m�ma�t'HH�nt and n'�1lar prngn'ss chl'cks.

t I t l

. ' rue,�
in tl11s cat.l'gory enc <� IP rnor<' expen8ivt

:\lanag
than other sympt.omat.w treatm

L'Hll'Ht options depend on tlll' sevnity
ent<;.

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of th(' clinical signs and wlwtht'r th('

Another oplion is ocladtinib (a.Janus
prnritus is seasonal or year rorn�d.

kinase inhibitor), which has been shoWn t

AYoidimce of allergens: Tlns may be
be safe and effective in control of Prurituso
the best choice, but it is difficult, if not.

lmmunotherapy: Immunotherapy or
impossible, to do unless a specific allergen

ASIT is arguably the best treatment option
can be identified.

for AD, because it is the only therapy that

Relief from pruritus: By definition, this
potentially leads to remission of signs
is a prnlitic skin disease; itching may be

,vithout addition of other medications. It
relieved via antipruritic drugs alone or in
remains the treatment of choice of most
combination with allergen-specific
dermatologists and allergists. ASIT attempts
irnnmnotherapy (ASIT [see below]).

to increase an animal's tolerance to

Bathing and coat hygiene: Bathing
environmental allergens (subjectively
dogs with AD may decrease pruritus. In dogs measured when an individual is exposed to with a history of flares due to microbial
an identified allergen without developing
overgrowth, routine use of antimicrobial
clinical signs). Although the mode of action
shampoos can be of benefit. Except for the
is not completely understood, the primary
use of lipid-containing shampoos, there is no theory states that IgG increases during the evidence of benefit from shampoos or condi first few months of hyposensitization and tioners that contain oatmeal, pramoxine,
exerts a blocking effect on circulating
antihistamines, or corticosteroids.

allergens by binding them and preventing

Recognition and control of flare
mast cell degranulation. Another theory
factors: A relapse of clinical signs in a dog states that immunotherapy causes a shift
that is otherwise well controlled should
away from TH2 toward TH1 by enhancing
prompt an investigation into what caused

-y-interf eron expression. After an iJtjection,
the exacerbation of pruritus. Recognized
however, allergen-specific IgE levels may
flare factors include, but are not limited to,
also increase when immunotherapy is
fleas, food and environmental allergens,
initiated due to a response to the additional
secondary microbial overgrowth, and poor
allergen load from the immunotherapy
coat hygiene. These need to be investigated
injections. This may result in increased
before using systemic antipruritic drugs.

pruritus in some animals. Reducing the

Antipruritic drugs for acute flares: In
amount of allergen given often alleviates
many dogs, the flare may present as allergic
this reaction, and with time, allergenotitis, and topical use of otic corticosteroids specific IgE levels decrease. However, may be adequate. There is good evidence for decreased IgE levels and clinical improvea short course of a topical triamcinolone or ment are not always directly correlated.

hydrocortisone aceponate spray for local

ASIT can be administered via iJtjections
pruritus. If the pruritus is too severe or
or allergy drops, which are equally effective.

extensive to be controlled with topical

Imrnunotherapy is best considered for
formulations, then oral steroids may be
animals with problematic clinical signs that
needed. Options include prednisone, predni occur for several months dwing the year.

solone, or methylprednisone administered

For injections, the animal must also be

PO at 0.5 mg/kg, once to twice daily, until
cooperative enough to receive allergy
clinical signs are in remission. Tacrolimus,
injections. For allergy drops, the owner
cyclosporine, or essential fatty acids are
th
must be able
u
to handle the a
nlikely to be beneficial for acute flares.

nimal's mou
and be able and willing to aclminist�r �e

Antipruritic drugs for chronic AD:

drops

Systemic reviews of clinical trials have not
twice a day every day. The cntena
for succes
shown conclusively that omega-3 and
sful hyposensitization inclutle
appropriate
omega-6 essential fatty acids alone are
interpretation of test results,
careful
likely to reduce pruritus. Use may help
selection of allergens, adequate I of
control of
improve coat quality. Cyclosporine can
secondary infections, contr?

other allergies
provide relief similar to that seen with

(food or flea), systematic
administration
glucocorticoids. A reported 50% reduction
of immunotheraPf . ns
injections, and periodic comnrn�catl
in pruritus in 70% of dogs with AD given

'flie
between the owner and veterin
cyclosporine A parallels the response seen
anan- th
longterm conunitrnent needed from bo
with glucocorticoids but with fewer adverse the owner and the veterinarian for effects. Some animals can be maintained
successful immunotherapy cannot be

FOOD ALLERGY

855
vcrcmphasizcd. _The owner must be wi�ling a hypersensitivity reaction to inhaled or 0 � }

o low instructions accurately, be patient,
contacted environmental allergens. The age
t d0communicatc effectively with the

�

. .

of onset is variable but generally is <5 yr.

teiinadan. The vctennanan must

The signs may be seasonal or nonseasonal.

ve o!!Ilize and treat other primary or second Purebred cats may have a higher risk than rec c;uses ofpruritus and manage flare
domestic shorthaired cats. As in dogs,

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f;arYtors (eg, otitis, pyodenna, Malassezia
ac
pruritic cats may have several clinical
h

. . . ) tl
dennatitis, insect ypersens1t1vity as 1ey
presentations ( eg, miliary dermatitis,
occur and guide the owner through these
symmetric alopecia, eosinophilic granuhallenges until improvement is seen.

loma complex, head and neck pruritus) that

�nptomatic therapy is required in almost
are consistent ·with a diagnosis of AD but
every case during the induction period and
that must be differentiated from other
at various times of the year ( see above).

diseases with similar clinical signs.

Allergen selection is determined by ·

Differential diagnoses include flea allergy, ·
correlating the positive allergens on the test various mite infestations ( eg, Cheyletiella, results with the prominent allergens during

Demodex, Notoedres, Sarcoptes, Oto-
the tinle of year when the animal is symptodectes ), mosquito bite hypersensitivity, food matic. If the test shows positive results for
allergy, autoimmune disease ( eg, pemphigus
pollens that have no clinical relevance ( egi
foliaceus), dennatophytosis, and cutaneous
high pollen'count during a period when the
neoplasia. A thorough review of the cat's
animal is not pruritic, positive reaction to an history and complete dennatologic and allergen not in the geographic area), then
physical examination, along with the
either the allergic reaction is mild ( sub- ·
standard flea combing, skin scrapings, and
threshold) or it is a false-positive reaction.

fungal cultures, are mandatory first steps.

Either way; the allergen is not included in

The diagnosis of AD is made when the other
the allergen mixture.

differential diagnoses have been eliminated.

Allergen protocols vary but usually have

Response to glucocorticoids is excellent
induction and maintenance periods. During · initially but decreases over time.

the induction period, the dosage of allergen

Intradennal allergy testing and hyposengradually increases until an arbitrary sitization procedures in cats are similar to
maintenance dosage is reached'. Once the ·
those used in dogs, but the intradermal test
maximal dosage is given, tl1is rri.ainteriance
results are more difficult to read because
level is continued. The interval between
the reactions are less dramatic and dissipate
maintenance dosages may vary from 3-4 ..

more rapidly in cats. The same avoidance
days to 3 wk. Adjustments in the interval are recommendations made for dogs apply to based on the animal's response. Owners are
cats. Symptomatic therapy includes conadvised not to expect inuch response for 6
trol of secondary infections and use of
mo and are asked to commit to at least l yr·
antipruritic' drugs. The approved formula-
of therapy before deciding the usefulness of tion of cyclosporine for use in cats is liquid; immunotherapy. The best assessment of
the dosage is 7 mg/kg, and it can be
response is to compare the degree of disease administered PO or in food. After 30 days, or discomfort between similar seasons.

the dosage can be tapered to every other
day in ~ 70% of cats and to twice a week in

!_!LINE ATOPIC DERMATITIS

~50% of cats. Response to iminunotllerapy
is similar to fuat in dogs ( see above); owners

Feline AD is similar to canine AD. It is a
are advised to commit to 1 yr of therapy

Pruritic disease in which affected cats have
before deciding its usefulness.

(Adverse.food reactio"ns)

!t�rse food reactions comprise allergic
terms are frequently interchanged, because
o
no; ns _termed food allergy as well as
the precise immunologic processes of most
int Fergic reactions termed food ·

0
adverse food reactions are usually not
erance. On a practical level, these
known. Immunologic reactions types I, III,

856

FOOD ALLERGY
and IV are thought to be tlw most likely
protein source is hydrolyzed to small
causes, but this is cm\il'clmal for most
moll'CUlar weights that an• not allerge
reported cases in small animals. F'oO(l

It is PsUmal.ed that hydrolyzat.ion ofthnic, allergil'S an' very rare in hcrbivon's. Jn this

11rotdn may still trigger an allergic res e
chapter, tht' more commonly used term .

in -101¼, of ;min mis allergk to the unhict�nse
food allergy will be used for all adverse iood lyzcd form.

o-

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reactions.

Thc trial diet should be fecl for up to

Food allergy is - 10% as common as atopic 3 mo. The key point in any food elimin t'

dennatitis in dogs and perhaps as common
diet trial is that only the designated foict'0n as atopic dennatitis in cats. The history is
ingredients can be fed. Thus, no treats
that of a nonseasonal pnuitus, with little
flavored toys, medications, or toothp�t
variation in the intensity ofpnuitus from
are allowed. If marked or complete .e
one season to another in most cases. Most
resolution �n the pn�t_us �nd clinical signg
repo1is do not suggest a breed predilection;
occurs dunng the ehmmat10n diet trial
however, one report indicated an increased
food allergy can be suspected. To confurn
relative risk in Labrador Retrievers, West
that a food allergy exists and that the

Highland White Terriers, and Cocker
clinical improvement was not just

Spaniels. Food hypersensitivities have been coincidental, the animal must be chalreported in Soft-coated Wheaten Terriers lenged with the previously fed food
in association with protein-losing enteropaingredients and a relapse of clinical signs thy and nephropathy. The age of onset is
must occur. The return of clinical signs
variable, from 2 mo to 14 yr old. One report
after challenge is usually between 1 hr and
indicated that most food allergies begin at

14 days. Once a food allergy is confinned,

< 12 mo of age. In adult-onset food allergy,
the elimination diet should be reinstituted
most dogs have been fed the off ending
until clinical signs resolve, which usually
allergen for >2 yr.

takes <14 days. At this point, previously fed

The distribution ofpruritus and lesions
individual ingredients should be added to
varies markedly between animals. Ear
the elimination diet for up to 14 days. If
canal disease that manifests as pruritus
pruritus recurs, the individual ingredient is
and secondary infection with bacteria
considered positive for having a causative

(usually Staphylococcus pseudintermerole in the food allergy. If pruritus does not
dius, Pseudomonas spp) or yeast
recur, the individual ingredient is not

(Malassezia pachydermatis) is common considered important in causing the
and may be the only presenting complaint. clinical signs.

Other patterns seen include blepharitis,

The number of off ending food allergens
generalized pruritus, generalized
varies from one to five ingredients. The most
seborrhea (scaling), a papular eruption,
frequently identified causative allergens in
or a distribution pattern that may mimic
canine food allergy include beef, chicken,
that of atopic dermatitis (feet, face, and
eggs, com, wheat, soy, and milk. Once the
ventrum) or flea allergy dermatitis ( dorsal off ending allergens are identified, control lumbosacrum and hindlegs ). The most
of the food allergy is by strict avoidance,
common areas of involvement include the Concurrent diseases (such as atopic derears, feet, inguinal region, axillary area, matitis or flea allergy) may complicate the
proximal anterior forelegs, periorbital
identification of underlying food allergies.

region, and muzzle. The degree ofpruritus Infrequently, a dog will react to new food is usually moderate to severe. Response
allergens over time.

to glucocorticoids varies from poor to

Clinical presentations of food allergy in
excellent.

cats include miliary dermatitis, feline

There is no reliable diagnostic test other
synunetric alopecia, eosinophilic gran��
than a strict food elimination diet. Sero logic loma complex (primarily the eosinop�i testing and intradermal testing for food

!S
plaque), and severe head and neck prun
allergens have proved unreliable. The ideal

No breed
food elimination diet should be balanced

, sex, or age predilection is s_e:•

Age of onset
and nutritionally complete and not contain
varies from 3 mo to 11 YI·
one study, however,
any ingredients that have been previously

46% of affected ca�
became symptomatic at �2 yr of age, an
fed. Many diets contain novel protein or

Siamese cats represented 3�% o[the �� 5

�
carbohydrate sources ( eg, venison and
e,·

Resp
rice). However, if a previously fed ingredionse to glucocortic01ds IS vana uent but about two-thir
ent is present in the elimination diet, and the
ds of cats show exce e to
response initially. In many cats, �espons ated animal is allergic to that ingredient, the diet
glucocorticoids becomes poor with repe ail trial will be a failure. Another option is the
treatments. As with food allergy in dogs,
use of hydrolyzed protein diets, in which the elimination diet should be fed for up to

URTICARIA

857

3 n1o. The elimination diet should not con

Time unt.il relapse ol' pruritus after
tain any previously fed ingredients. Food
challenge with the offending food varies
liJlUilation diets can be difficult in cats,
from 16 min to 10 days. The most fre

�ecause many cats are reluctant to change
quently identified food allergens in cals
diets. Cats should n_ot ?e s_tarv�d or forced include fish, beef, milk, and chicken.

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into eating a new ehmmat1on diet because

Avoidance of the offending allergens will
of the serious nature of hepatic lipidosis
control the clinical signs associated with
that may be induced by prolonged anorexia. the food allergy.

·U RTICARIA

(Hives, Nettle rash)

Urticaria is characterized by multiple
limbs, or perineum. In horses, dermatophyplaque-like eruptions that are formed by tosis (ringworm) and pemphigus foliaceus
localized edema in the dermis and that often may present as urticaria early in the disease.

develop and disappear suddenly. It occurs

In horses, vasculitis may also present with
in all domestic animals but most often in
urticaria
horses� Allergic urticaria may be exogenous
or endogenous. Exogenous hives rri�y be

Clin!cal Findings: The wheals or plaques
produced by toxic irritating products of
appear within a few minutes or hours
the stinging nettle, the stings or bites of
of exposure to the causative agent. In
insects; topicai'rriedications, or exposure
severe cases, the cutaneous eruptions are

. to chemicals (eg, carbolic acid, turpentine,
preceded by fever, anorexia, or dullness.

carbon disulfide, or crude oil). Nonirnrnuno

Horses often become excited and restless.

logic factprs stich as pressure, sunlight,

The skin lesions are elevated, round, flatheat, exe·rcise, psychologic stres_s, ap.d topped, and 0.5--8 in. (1-20 cm) in diameter;
genetic abnormalities inay precipitate or
they may be slightly depressed in the center.

intensify urticaria. Pruritus is not always

They can develop on any part of the body
present, particularly in horses. . , . .

but are seen mainly on the back, flanks,

Sensitive animals, particularly shprt�
neck, eyelids, and legs. In advanced cases,
hair�d dogs and purebred horses/also
they may be found on the mucous memrarely may exhibit dermographism, a branes of the mouth, nose, cmtjunctiva,
phenomenon wherein pressure applied to . .

rectum, and vagina In general, the lesions
the skin produces linear urticaria! lesions:

disappear as rapidly as they arise, usually

The clinical significance is oolmown.

within a few hours.

Endogenous urticaria may develop after

In sheep, lesions usually are seen only
exposure to topical, inhaled,. or ingested
on the udder and hairless parts of the

�ergens or administration of medications;
abdomen. In pigs, eruptions have been seen
it has been seen mostly in horses and dogs.

around the eyes, between the hindlegs, and

In horses, it has been noted in the course of on the snout, abdomen, and back

�I conditipns, particularly severe constipa

In general, the prognosis is favorable.

tion or inflammation of the intestinal

Fatalities are rare and are probably due to
mucosa A unique form of urticaria in cattle anaphylaxis or associated angioedema has been described chiefly in the Channel
involving the respiratory passages.

Island breeds (Jersey, Guernsey), which

Chronic urticaria is a diagnostic
b�come sensitized to the casein in their own challenge. All allergens in an environment

�k ("milk allergy"); it occurs in cases of should be considered potential causes, and

�k retention or unusual engorgement of

. i
elimination of exposure instituted, if

�dder with milk Urticaria has been seen possible. Persistent urticaria! lesions,

: itches during estrus. In young horses,
particularly those that progress to

�gs,. and pigs, urticaria may be associated
thickened crusts, should be biopsied.

With mtestinal parasites. Angioneurotic
ed�ma is a life-threatening variant of

Treatment: Acute urticaria usually

�!Caria in which there is diffuse subcuta-
disappears spontaneously. The rapideous edema, often localized to the head, acting glucocorticoids, eg, hydrocortisone

858

URTICARIA
sodium succ-inate or prcdnisolom· sodium
disappc•ar hut rPturn rapidly if the aller
succinate or hcmisuccinate are reported to
is 1101 C'li1'.1inat:ed. { lsually, local treatrntn be useful. Dl'x�mwthasmw (0. 1 mg/kg) has
oft he ksrons ts not necessary. In chro ,nt
nic
bet.>n useful in dogs, cats, and horst> s.

urticaria in horses, the antihistamine

Antihistamirws arc of questionable value
hydroxyzine at 0.4-0.8 mg/kg, bid, orth
and may induce urticaria if given IV.

tricydic antidepressant doxepin (Whic�

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Epinephrine may be given in life-threatenhas antihistaminic properties) at 0.6 Tngfk ing situations. The lesions promptly
bid, may be useful.

g,

DERMATOPH ILOSIS

(Dermatophilus infection, Cutaneous streptothricosis, Lumpy wool, Strawberry footrot)

This infection of the epidermis, seen
between animals, through contaminated
worldwide but more prevalent in the
environments, or possibly via biting insects.

tropics, is also erroneously called mycotic

It has been isolated only from the integudermatitis. The lesions are characterized by ment of various animals and is restricted to exudative dermatitis with scab fom1ation.

the living layers of the epidemlis. Asympto

Dermatophilus congolensis has a wide
matic chronically infected animals are
host range. Among domestic animals, cattle, considered the primary reservoir.

sheep, goats, and horses are affected most

Factors such as prolonged wetting by rain,
frequently, and pigs, dogs, and cats rarely. It
high humidity, high temperature, and various
is commonly called cutaneous streptothriectoparasites that reduce or permeate the cosis in cattle, goats, and horses; in sheep, it natural barriers of the integument influence is termed lumpy wool when the wooled
the development, prevalence, seasonal
areas of the body are affected. Infection in
incidence, and transmission of dennatcamel herds has been related to drought and ophilosis. Ticks and lice are major predispoverty. Recent isolates from chelonids may posing factors in cattle and sheep, respecrepresent a new species of Dermatophilus.

tively.

It is also a common disease in farmed

The organism can exist in a quiescent
crocodiles. The few human cases reported
form within the epidermis until infection is
usually have been associated with handling
exacerbated by climatic conditions. Epidem·
diseased animals.

ics usually occur during the rainy season.

Moisture facilitates release ofzoospores

Etiology, Transmission, and Epidemifrom preexisting lesions and their subseology: D congolensis is a gram-positive, quent penetration of the epidermis and
non-acid-fast, facultative anaerobic
establishment ofnew foci of infection. High
actinomycete. It is the only currently
humidity also contributes indirectly to �e
accepted species in the genus, but a variety
spread of lesions by allowing increases tn
of strains can be present within a group
the number of biting insects, particularly
of aninlals during an outbreak. It has
flies and ticks, that act as mechanical
two characteristic morphologic forms:

vectors. Shearing
filamentous hyphae and motile zoospores.

, dipping, or introducmg
an infected animal into a herd or flock can

'.fhe hyphae are characterized by branchspread infe mg filaments (1-5 µrn in diameter) that
ction.

.

Derm
ultimately fragment by both transverse
atophilosis is contagious onlY J.Il kiJ1
that any
and longitudinal septation into packets
reduction in systemic or l�cal 5 tio!l
of coccoid cells. The coccoid cells mature
resistance favors establishment of infec
and subsequent
into flagellated ovoid zoospores (0.6-1 µrn
disease.

in diameter).

. n t11e

Pa

The natural habitat of
thogenesis: To establish infec�o !

D congolensis is
te
infe
unlmown. Attempts to isolate it from soil
ctive zoospores must reach a �kill 51e
where
have been unsuccessful, although it is
the normal protective barriers � ut
redu
probably a saprophyte in the soil. It is
ced or deficient. The respirat�rJ : de
of low conc
believed to be spread by direct contact
entrations of carbon dio:lO res
from the skin attracts the motile zoo5P 0

DERMATOPHILOSIS

859
iscrptihk :m'Hs 011 tlw skin surface.

tos
ohiwrwcl i11 I.Im'<' sl.agPs: I ) hairs malted

�pOI'('Sgenninatl' to produn' hyph:w,
togPt.her as pai11l.-hrnslt lc�sions, 2) crusl.

Z�?ch pl'IH'tntt<' into ti!(' living <'pidl'nnis or scah formal.ion as the inil.ial lesions

" � snbsl'<lm'ntlv spr<'ad in all directions coalesce, and :l) accumulations of'

:�n; th<' initial f'. )<'\lS. l lyphal penct�·ation cutaneous keratinized material forming

1

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sesm1 acull' mflammatory reachon.

call
wart-like lesions that arc 0.5-2 cm in
t I
t ' r .•

N tnntl r<'sistance o t 1c acu c nhect.Ion
diameter. Typical lesions consist ofraiscd,

. �uc to phngocytosis of the infective
matted tufts of hair. Most lesions associated

15 ospores, but once infect.ion is established,
zo

.

.

with prolonged wetting of the skin are

I
there is little Or ,no lllllllllllltr, n l�lOSt acute
distributed over the head, dorsal surfaces

• uections, the filamentous mvas1on of the
ofthe neck and body, and upper lateral

�pidem1is ceases in 2-3 wk, and the lesions
surfaces of the neck and chest. Cattle that
heal spontaneously. In chronic infections,
stand for long periods in deep water and
the affected hair follicles and scabs are sites mud develop lesions in areas such as skin from which intermittent invasions of
folds of the flexor surfaces of the joints.

non.infected hair follicles and epidermis

Dairy cows may present with papular
occur. The invaded epithelium comifies and crusted lesions on the udder. Lesions separates in the form of a scab. In wet scabs, initiated by biting flies (mechanical vectors) moisture enhances the proliferation and
are found primarily on the back, whereas
release of zoospores from hyphae.-The high
lesions induced by ticks are primarily on the
carbon ilioxide concentration produced
head, ears, axillae, groin, and scrotum.

by the dense population of zoospores

Chronic lumpy wool infections are
accelerates their escape to the skin surface,
characterized by pyramid-shaped masses
thus completing the unique life cycle.

of scab material bound to wool fibers. The
crusts are primarily on the dorsal areas of

Clinical Findings: Dermatophilosis is
the body and prevent the shearing of sheep;
seen in animals at all ages but is most
spiny plants often predispose to lesions on
prevalent in the young, in animals chronithe lips, legs, and feet. Strawberry footrot is cally exposed to moisture, and in irnrnunoa proliferative dermatitis affecting the skin suppressed hosts. Lesions on a host can
from the coronet to the carpus or hock
vary from acute to chronic. Age, sex, and

Lesions on horses with long winter hair
breed do not seem to affect host susceptibilcoats are similar to those of cattle, ity. Pruritus is variable. Most affected
developing with matted hair and paint

'animals recover'spontaneously within 3 wk
brush lesions leading to crust or scab
of.the initial infection (provided chronic
formation with yellow-green pus present
maceration of the skin does not occur). In
under larger scabs. With short SUillffier hair,
general, the onset of dzy weather speeds
matting and scab formation is uncommon;
healing.

loss of hair with a fine paint-brush effect can

Uncomplicated skin lesions heal
without scar formation. These infections
be extensive. Persistent wetting of pasterns
in wet yards, stables, or at pasture leads to
usually have little effect on general health.

Animals with severe generalized infections
lower limb infection; white legs and the
often lose
white-skinned areas of the lips and nose are
condition, and movement and
prehension are difficult if the feet, lips, and
more severely affected. Generalized disease
muzzle
is also associated with prolonged wet
are severely affected; these animals
are often
weather. Outbreaks occur on farms with
sent to slaughter as incurable.

Deaths occ
previously affected horses.

asionally occur, particularly in

Histopathologic examination reveals
calves and lambs because of generalized
disease with
the characteristic branching hyphae with
or ½ithout secondary bacterial

!nf ection
multidimensional septations, coccoidal
and secondary fly or screwworm
infestatio
cells and zoospores in the epidermis. The
n. The primary economic
consequen
org�isms are usually abundant in
ces are damaged hides in cattle,

�ctive

Wool loss
lesions but can be sparse or absent m
in sheep, and lameness and loss
of perfonn
chronic lesions.

ance in horses when severely

�ected around the pastern area. Cattle

'Yith lesio

Diagnosis:

ns

Presumptive diagnosis
covering >500/4 of the body are
likely to beco
depends largely on the appearance of
me seriously ill.

lesions in clinically diseased animals and

· lesions: Distribution of the gross lesions demonstration of D congolensis in stained on catt�e, sheep, and horses usually correl
smears or histologic sections from scabs. A
ates With the predisposing factors that
definitive diagnosis is made by demonstratrect�ce or permeate the natural barriers of ing the organism in cytologic preparations,
the integument. In cattle, the lesions can be isolation via culture, and/or via skin biopsy.

860

DERMATOPHILOSIS

An indin'cl Huon'Sl't'nt antibody l<'chniq1w
spira111yci11, penicillin <i, arnpicillin
and a singll' dilution ELlSA ll'st have hC'<'ll chlora111phc11icol, streptomycin, � O . .

Xi
devl'lo1wd for lat-gt' sC'rologic and epidemiotdracyclirws, and novobiocin. 'I\vo do Cllhn, logk smY<.'ys. The most practical diagnostic of long-acting oxytctracycline (20 mJes test is c:vtolo•
l day apart have shown to be cura

1 ic examination of fresh crusts
tive . g)

VetBooks.ir
and/or i·mpre�-,ion smears of the underside
of cattle and 100% ofsheep, <:omparectln�5%

Wit h
of freshly avulsed lesions. Fresh crusts are
cure rates of 71 % in cattle and 80% in h
minced on a glass microscope slide with a
for a single dose. In food-producing �p
stelile scalpel blade in several drops of
topical ap�licati�ns of lime sulfur are a ais,
sterile saline. The slide is allowed to air dry
cost-effective adjuvant to antibacterial
and is then stained "rith a fast Giemsa or
therapy. Insecticides applied extemaU

Romanowski stain. The organisms are seen
frequently used to control biting insec� are
under oil immersion as 2-6 parallel rows of

In horses, the lesions s�ould be gently
gram-positive cocci that look like railroad
soaked and removed. Topical antibacte • a1
tracks. Differential diagnoses include
shampoo therapy is effective as adjuvan�
dem1atomycoses in most species, warts
therapy. Chlorhexidine is recommended
and lumpy skin disease ( see p 868) in cattle,

Topical treatment with povidone-iocline �
contagious ecthyma (see p 866) and ulcerasuperior to parenteral oxytetracycline al o ne tive dermatosis (see p 872) in sheep, and

(100% and 66% effective, respectively).

demrntophytosis (see p 872) and immune

Isolating clinically affected animals
mediated scaling diseases of horses ( eg,
culling affected animals, and controlllilg
pemphigus foliaceus ).

ectoparasites are methods used to break
the infective cycle. Preventing chronic

Treatment and Control: It was
maceration of the skin and keeping the
previously thought that because acutely
animals dry are important. Zinc levels
infected animals usually heal rapidly and
should be checked in the feed of cattle
spontaneously, treatment was indicated
because outbreaks have been associat�d
only for cosmetic reasons in food-producing "1th zinc deficiencies.

animals. However, in certain parts of the
world, the disease is associated "1th

Zoonotic Risk: Dermatophilosis can be
significant morbidity and mortality, loss of
transmitted to people. Direct contact with
body condition, decreased milk production
an infected animal can lead to infections
and increased somatic cell counts in milk.

on the hands and arms. Affected animals

Treatment is recommended in horses
should be handled with gloves, and thorough
because the lesions interfere "1th use and
hand washing with an antibacterial soap is
are painful. Organisms are susceptible to a
recommended after contact with an infected

"1de range of antimicrobials: erythromycin, animal.

EXUDATIVE EPIDERMITIS

(Greasy pig disease)

Exudat�"'.e epidermitis is a generalized
d�rmatit�s that occurs
ex
in 5-
ist. Abra
to 60-day-old
sions on the face, feet, and
pi�s and is characterized by sudden

�egs o: lacerations on the body preced e d onset
with morbidity of 10%-90%
mfect1
and

0n. Such injuries
mort
are usually cause
rt
of 5%�90%: The acute form
by
usually
fighting or by abrasive surfaces such 85
af�:cts

�ucklmg piglets, whereas
new
a chronic
concrete. Other predisposing factors
form
is more commonly seen
that
in weaned
may affect the severity and prog:ess
pigs

It has b�en reported

.

from
of the
most s"1ne-
disease include immunity, hygien_ e ,
producmg areas of the world
nutrition, and the presence of mange rnites

�esions �re caused by
or

Sta
anyt
phylococcus
hing that damages the skin. Mature
hyi?us, which can produce an exfoliative

�ows that have acquired a high level ? f
to� but se�ms unable to penetrate

1mm
intact

�nity from previous exposure � I
skin. Both virulent and
prov
avirulent
ide
strains
protection to piglets via th�If iJ1
colostrum. The incidence is often hig her

EXUDATIVE EPIDERMITIS

861
the alTected area a black color. Vesicles and
ulcers may also develop on the nasal disk
and tongue. The feet are nearly always
involved, with erosions at the coronary
band and heel; the hoof may be shed in rare

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cases. In the acute disease, death occurs
within 3-5 days. In older animals, the
chronic form of the disease is seen as thick,
crusty lesions over the entire body or as
discrete circumscribed lesions that do not
coalesce. Mortality is low except in very
young suckling piglets. However, recovery
is slow and growth is retarded and often
associated with diarrhea, emaciation, and.

Chronic exudative epidermitis over the entire
dehydration.

body in a 5-wk-old weaner pig. Courtesy of Dr.

Necropsy of severely affected pigs

Ranald D. A. Cameron.

reveals marked dehydration, congestion
of the lungs, and inflammation of the
peripheral lymph nodes. Distention of the
kidneys and ureters with mucus, cellular
gilt litters and in newly established SPF
casts, and debris is common in peracute
herds in which most breeders are gilts.

and acute forms of the disease. Diff eren

Pigs develop resistance with age, but
tial diagnoses include sarcoptic mange.·

S hyicus may be recovered from the skin

(see p 919),-nutritional deficiencies
of older pigs, the vagina of sows, and the ·
including zinc (parakeratosis, seep 975),
preputial diverticulum qfboars'. These
ringworm (see p 872), and pityriasis rosea
inapparent carriers serve as a source of

(see p 979).

contamination for naive herds. Suckling
pigs are usually infected by their dams; in'

some cases during birth from sows with

Treatment: The causative organism is
vaginal infections, or from contamination
inhibited by many antibiotics, including
in the farrowing unit. Suckling piglets are
amoxicillin, ampicillin, erythromycin,
the most commonly and severely affected, lincomy_cin, p�nicillin, tylosin, trimetho- , but cross-infection occurs after .mixing at
prim-sulfonamide, the aminoglycosides,
weaning with a morbidity of as much as .

and cephalosporins. Successful treatment

80%. However, mortality is usually low in
requires that the antimicrobial be given in
this age group. The incidence appears to
high dosages early in the disease and for
have increased because of pig production 7-10 days. Success is greatest when units with high stocking densities and_
antimicrobial therapy is combined with
possibly earlier weaning. There are recent daily applications of antiseptics to tlle reports of exudative epidermitis associ�.

entire body surface._Treatment is less
a�ed with ST398 methicillin-resistarit S
effective in very young pigs and ineff ec-
aureus (MRSA) infections, but a causal
tive in advanced cases. In severe

. ,
role has not been clearly demonstrated.

outbreaks, in-contact pigs should also be
given antibiotics for several days. Sows
due to farrow, and their housing, should

Clini�al Findings and Lesions: The · ' be thoroughly disinfected to prevent

:t s1� are listlessness and reddening of outbreaks. Hygiene in the weaner e skin m one or more piglets in the litter.

accommodation and strategic in-water or

Affected pigs rapidly become depressed
in-feed medication for 3:-5 days will help

'.1Jld refuse to eat. Body temperature may
control outbreaks after weaning. Other

�crease early in the disease but thereafter
procedures that may decrease the severity

18 near normal. The skin thickens and
of an outbreak include clipping the needle
reddish brown spots (macules) appear
teeth of newborn pigs, providing soft

!�und the eyes, nose, lips, and ears from
bedding; segregating infected animals,

. ch serum and sebum exude. The lesions and avoiding mixing of animals to mcrease in size and develop a vesicular or
decrease the possibility of skin lesions

PUStuiar appearance.

due to fighting. Autogenous bacterins have

The
gr body is rapidly covered :with a moist,
been used with some success to reduce
e
b asy exudate of sebum and serum that
the incidence of disease in chronically
ecomes crusty. Accumulation of dirt gives infected herds.

862

I NTERDIGITAL FURUNCULOSIS

INTERDIG ITAL FU RU NCU LOSIS

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Interdigital ftmmcles, often incorrectly

Lesions caused by a foreign body eg
referred to as interdigital cysts, are painful
awn, are usually solitary and are �ft�;fass
nodular lesions located in the interdigital
on a front foot; rec�ence is not conun��d
webs of dogs. Histologically, these lesions
these cases. If bactena cause the interdi . III
represent areas of nodular pyogranulomafurunculosis, there may be several noctuf taI es
tous inflammation-they are almost never
with new lesions developing as others
cystic. Canine interdigital palmar and
resolve. A common cause of recurrence .

plantar comedones and follicular cysts is a
the granulomatous reaction to the prese lS
recognized syndrome that may be a subtype of free keratin in the tissues.

nee
of interdigital furuncles or a separate

Dogs with interdigital comedones and
disease.

follicular cysts typically present with
lameness and draining tracts. Skin lesions

Etiology: The most common cause is a
are not often seen unless the hair coat is
deep bacterial infection. Many dog breeds
clipped. Areas of alopecia and thickened

( eg, Chinese Shar-Pei, Labrador Retriever,
firm, callus-like skin with multiple

English Bulldog) are predisposed to
comedones are typical.

bacterial interdigital furunculosis because
of the short bristly hairs located on the

Diagnosis: For furunculosis, the
webbing between the toes, prominent
interdigital webbing, or both. The short
diagnosis is often based on clinical signs
shafts of hairs are easily forced backward
alone. The major differential diagnoses are
into the hair follicles during locomotion
traumatic lesions, foreign bodies, follicular

(traumatic implantation). Hair, ie, keratin,
comedon� cysts, and neoplasia, although
is very inflammatory in the skin, and
the latter IS rare. The most useful diagnostic
secondary bacterial infections are comtests include skin scrapings for Demodex mon. Less commonly, foreign material is
mites, impression smears or fine-needle
traumatically embedded in the skin.

aspirates to confirm the p�esence of an

Demodicosis (see p 920) may be a primary
inflammatory infiltrate. Unusual or
cause ofinterdigital furunculosis. Canine
recurrent lesions should be excised for
atopic dermatitis (see p 853) is 'also a
his�opathologic examination. Solitary
common cause ofrecurrent interdigital
lesions may require surgical exploration to
furunculosis.

find and remove foreign bodies such as

The cause of canine interdigital palmar
grass awns.

�d plantar comedones and follicular cysts

J:?efinitive diagnosis of palmar and plantar

IS unknown but most likely involves trauma
follicular cysts requires a skin biopsy.

resulting in epidermal arid follicular inf-

H�)\�ever, these cysts are suspected when
undibular hyperkeratosis acanthosis
clinical examination reveals draining tracts
plugging or narrowing of the follicul�
associated with callus-like lesions or obvious
opening, and retention of the follicular
comedone formation. Moderate to extensive
contents.

compact hyperkeratosis and acanthosis of
the epidermal and follicular infundibulwn is

Cli�ical Findings and Lesions: Earl
found. Follicular cysts consisting of keratin
lesions of interdigital furunculosis may Y
are conunon. Often, lesions are complicated
appear as focal or generalized areas of
by secondary infection and concurrent
erythema and papules in the webbing of the
bacterial furunculosis.

�eet t�at, if left untreated, rapidly develop
mto smgle or multiple nodules. The latter

Treatment: Bacterial interdigital
usually ar� 1-2 cm in diameter, reddish
furuncles respond bestto a combination_of
purple, shiny, and flucttiant; they may
topical and
ruptuz:e when palpated and e
systemic therapy. Treatment 15
xude a bloody
best based on culture and susceptibility,
matenal. Interdigital furuncles are most
bec<l:use these are
commonly found on the dorsal aspect of
deep infections and _rnaY
req�e longter
the paw but may also be found ventrally.

m therapy, particularlf if
multifocal. Pending culture, applicatlO� 0:

Furuncles �e usually painful, and the dog
waim water compresses and topical tnP1.

may be obviously lame on the affected foot
antibiotic

( or feet) and lick and bite at the lesions.

ointment or mupirocin antibio?c
ointment are recommended. Foot soakS Jll

PYODERMA

863
hlorhexidine s?lution arc also helpful.

Lesions in confined dogs are likely to recur

�ecause the les1�ms arc pyog1:a�ul_omaunless the dog is removed from wire or tons, it may be difficult. for antib1ot.ics to
concrete smfaces. In some chronic cases,
enetrate th�n�; t�1erefore, >8 wk of

.

surgical excision or surgical correction of

;
the webbing via fusion podoplasty may be
ys teinic antib1ot1c therapy may be reqmred

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for lesions to completely resolve. These
needed. Alternatively, pulse antibiotic
lesions are often_ com�licated by concurrent therapy (full dosage therapy 2-3 times/wk) ftfalassezia spp infections. Oral ketoconaor chronic low dosage antibiotic therapy zole or itraconazole (5-10 mg/kg) for 30

( eg, 500 mg/day/dog, PO) may help
days may be indicated. The presence
maintain clinical remission and provide
of Malassezia can be documented by
pain relief in dogs with chronic lesions.

cytologic exam_ination of nail bed d�bris

This therapy is recommended only when
and/or impression smears of the skin.

the inciting cause cannot be identified

Chronic, recurrent interdigital furuncu

( eg, idiopathic pyoderma ), treated ( eg,
iosis is most often caused by inappropriate
anatomic predisposition), orresolved
antibiotic therapy (too short a course,

( eg, chronic infection caused by foreign
wrong dosage, wrong drug), concurrent
body material or keratin).·
corticosteroid administration, demodico

Treatment ofinterdigital palmar and
sis, an anatomic predisposition;· or a foreign plantar comedones and follicular cysts body reaction to keratin. Lesions that recur can be successfully accomplished by despite therapy can also be a sign of an
laser therapy. Postoperative care is time
underlying disease, eg; atopy, hypothyroidintensive, with hydrotherapy and bandage ism; or concurrent M alassezia infection.

changes once or twice daily.

Pyod�rm�literally means "pus in the,·skin"

losis are ref erred to as deep. Etiologic
and can be caused by infectious, inflamma-:- .

classification refers to the pathogenic
tory, and/or n�oplastic etiologies; any .

organism involved in the infection ( eg,
condition that results in the accumulation
staphylococci, streptococci, etc). Wections
of neutrophilic exudate can be termed 3:, , .. . are superficial and secondary to a variety of pyoderma Most commonly, however, :.

other conditions.

pyoderma refers to bacterial infections of
the skin. Pyodermas are common in dog�_

Etiology: Bacterial pyod�rma is usually
and less common in cats.

triggered by an overgrowth/overcoloniza-

. , Bacterial pyode_rmas are eithe! simple

. tion of normal resident or transient flora . .

�ections or complex infections.Simple

The primary pathggen of dogs is. Staphyloinfections are those occurring in young coccus pseudintermedius.

�als that are triggered-by one-time or . , •

�unple events, eg, flea inf e�tation. Complex
infections are recurrent and are associated

With underlying diseases, such as 3:llergies

�flea allergy, atopic dermatitis, food allergy), m!ernal diseases (particularly endocrinop3:�
thies such as hypothyroidism or hypera_drenocorticism ), seborrheic conditions (I?cluding follicular or sebaceous gland
dise?5es ), parasitic_ diseases ( eg, Demodex_
ca?tis), or anatomic predispositions (�g,
kin

� folds). Either simple or complex
recti�ns can be superficial or deep. ,
a_ctenaI pyodermas limited to the

' .

epidennis and hair follicles are ref erred to
as superficial whereas those that involve

Superficial pyoderma in a dog. CourtesyofDr.

t.he dernus, d�ep dermis, or cause furuncu-

Stephen White.

864

PYODERMA

Nonnal rc>si<lcnt bacteria in canine skin
prcsenl, hut follicular pustules and
also include coagula..c;c-negative st,1phyloerythcrna arc often absent in shorthair cocci, streptococci, Micrococcus sp, and
breeds, making diagnosis difficult. Col�d

Acinctobncter. Transient lmcte1ia in canine and Shetl�ncl Sheepdogs of�en have dirt3
skin includeBncillus sp, Corynebacteriurn
areas of w1despr�ad alopecia with l11ilct Use
sp, Esclwrich.:ia coli, Protens 1nirabilis,
e1ythema and epidermal collarette

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andPseudomonas sp. These organisms may formation at the leading edge of the play a role as secondary pathogens, but
expanding area, often mimicking an
often S pseudintermedius is required for

�ndocrinopathy. Pustules and crusts are
a pathologic process to ensue. Nonnal
mfrequently found.

resident bacte1ia in feline skin include

The hallmarks of deep pyoderrna ind

Acinetobacter sp, Micrococcus sp,
are ·
pam,
t·
crus mg, d
o or, d
an
o
exudatio gs
n of
coagulase-negative staphylococci, and
blood and pus. Erythe�a, swelling,

O'.-hemolytic stTeptococci. Transient
ulcerations, hem?�hagic crus1:5 and bullae
bacteria in feline skin include Alcaligenes
hair loss, and dranung tracts with serohern�
sp, Bacillus sp, Escherichia coli, Proteus orrhagic or purulent exudate may also be
mirabilis, Pseudomonas sp, coagulaseseen. The bridge of the muzzle, chin, positive and coagulase-negative staphyloelbows, hocks, interdigital are�, and lateral cocci, and O'.-heinolytic streptococci.

stifles are more prone to deep infections

The most important factor in superficial
but any area may be involved. Acral lick '

pyodermas that allows a bacteria to
granulomas an d areas o f pyotraumatic
colonize the skin surface is bacterial
dermatitis are also clinical manifestations of
adherence, or "stickiness," to the keratinodeep pyoderma. Interdigital furunculosis cytes. Wann, moist areas on the skin, such

(see p 862) is another manifestation of
as lip folds, facial folds, neck folds, axillary
deep pyoderma. Plant awns, naked keratin
areas, dorsal or plantar interdigital areas,
from hair shafts or ruptured hair follicles,
vulvar folds, and tail folds, often have higher and other foreign bodies play a significant bacterial counts than other areas of skin
role in the inflammatory process associated
and are at an increased risk of infection.

with deep pyodermas.

Pressure points, such as elbows and hocks,

Superficial pyoderma in cats is usually
are prone to infections, possibly because of
due to Staphylococcus spp. It is often
follicular irritation and rupture due to
overlooked and underdiagnosed. The
chronic repeated pressure. Any skin disease most common clinical finding is scaling, that changes the normally dry, desert-like
particularly over the lumbosacral area;
environment to a more humid environment
scales pierced by hairs are a common
can predispose the host to overcolonization
finding. Intact pustules are almost never
of the skin with resident and transient
found. Feline pyoderma is most common in
bacteria
allergic skin diseases, parasitic diseases,
and feline chin acne.

Clinical Findings and Lesions: The

Miliary dermatitis can be a clinical
most common clinical sign of bacterial
manifestation of superficial pyodenna. Cats
pyodenna in both dogs and cats is excessive with deep pyodermas often present with scaling; scales are often pierced by hairs.

alopecia, ulcerations, hemorrhagic crusts,

Pruritus is variable. In dogs, superficial
and draining tracts. Eosinophilic plaques
pyoderma commonly appears as multif ocal
are a common clinical presentation of deep
areas of alopecia, follicular papules or
pyoderma secondary to an allergic dis�ase.

pustules, epidermal collarettes, and serous

Recurrent
crusts.

nonl1ealing deep pyodenna J1l

The trunk, head, and proximal
cats can
extremities
be
are
associated with systemic
most often affected.

diseas

Shorthaired
e, such
breeds
as feline immunodefici�ncY
often present with
virus
multiple
or
superficial
feline leukemia virus, or atypical
papules that look
similar to
mycobacteria
urticaria because the inflammation in and around the follicles causes the hairs

Diag
to stand
nosis:

more erect.

The diagnosis of s�p_erficial

These hairs are
often easily epilated,

P;Yoderma
an
is usually
important
based on clinical u}

feature
es,
that helps
s
to distinguish
igns-hair
superficial
loss, scaling, erythema, pap
pyodenna from
pustule
true urticaria
s, and epidermal collarette?.

in which
hairs do not epilate.

Differential

In bacterial
diagnoses for sup�rficial
pyoderma
gzO),
affected hairs
pyoder
epilate and
ma
progress
include demodicosis ( see P
to form'

iS
focal

Ma
areas
lassezi
of alopecia
a

0. 5-2
dermatitis, dermatoph
cm in

�05
diameter.

and

(see p

At the margins of the

872),
hair loss,
other causes of fo11iculit15,
mild
epidermal
uncom
collarette
mon
formation
crusting diseases such as
may be
pemphigus foliaceus. Diagnosis of

PYODERMA

865
pyodenna shoul� also _include steps to
pyoclcrmas typically require 8-12 wk or

'denti(Y any prf'dtsposmg causes.

1
longer to resolve completely.

Identification of the dennatologic lesions

Amoxicillin, penicillin, and tetracycline
described above allo�vs a tentative
arc inappropriate choices to treat superfidiagnosis of superfic1� pyodenna. Direct cial or deep pyo<lermas, because they are
impression smears of n�tact pustules, areas
ineffective in 90Wi of these cases. Fluoro

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tmderlying crusts or ep1den11al collarettes,
quinolones should be used only if based
or 1noist e1ytl1�rnatous areas may reveal
on culture and susceptibility.

cocci, rods, or mflarnrnatory cell infiltrates.

Topical antibiotics may be helpful in focal

Impression smears of areas of hair loss and
superficial pyoderma A 2% mupirocin
scaling may only reveal large numbers of
ointment penetrates skin well and is helpful
exfoliative keratinocytes. One of the most
in deep pyoderma, is not systemically
important reasons to do impressions is to
absorbed, has no known contact sensitiza-
detennine whether a concurrent M alasse

. tion, and is not used as a systemic antibiotic zia infection or overcolonization is present· that would increase the likelihood of there is a symbiotic relationship between
cross-resistance. It is not very effective

Staphylococcus andMalassezia, and both
against gram-negative bacteria. This
are found in ~50% of cases. The infection
ointment should not be used in cats with
will not resolve without concurrent
any known or suspected history of renal
systemic antimicrobial therapy. Multiple
disease, because the preparation contains
deep skin scrapings are needed to exclude
propylene glycol. Neomycin is more likely
parasitic infections, particularly Demodex to cause a contact allergy than other
canis. Dermatophyte cultures should be
topicals and has variable efficacy against
done to exclude dermatophytosis. Bacterial gram-negative bacteria Bacitracin and culture and susceptiblity testing is highly
polymyxin B are more effective against
recommended because of the increased '

gram-negative bacteria than other topical
prevalence of methicillin-resistant ·
antibiotics but are inactivated in purulent

Staphylococci.

extidates.

Accurate test results are most likely

Attention to grooming is often overobtained from intact pustules or induced looked in the treatment of both superficial
rupture of deep lesions: Caution should be
and deep pyoderma The hair coat should be
exercised in.interpreting culture results
clipped in: animals with deep pyoderma, and
from samples stibinitted from crusted
a professional grooming is recommended in
lesions, papules, epidermal collarettes,and·
medium-to longhaired dogs with generalfistulous tracts, because contamination of ized superficial pyoderma Clipping will
the sample is more likely than mth samples
remove excessive hair that can trap debris
obtained from a closed lesion. Pending
and bacteria and will facilitate grooming.

culture and susceptibility, topical anti

Longhaired cats usually benefit most from
microbial therapy is recommended, using
having the hair coat clipped.

chlorhexidine-based baths or solutions. ·.

Dogs with superficial pyoderma should

The most common underiying triggers
be bathed 2-3 times/wk during the first 2 wk
of superficial pyoderina include fleas, flea
of therapy and then 1-2 times until the
allergy dermatitis, a.topic dermatitis, food
infection has resolved. Dogs with deep
allergy, hypothyroidism, hyperadrenocortipyoderma may require daily hydrotherapy.

c�m, and poor grooming. Appropriate

Medicated shampoos should be prediluted
diagnostic testing and treatment of

1:2 to 1:4 before application to facilitate
underlying triggers is mandatory. The most
lathering, dispersal, and rinsing. Appropricommon causes of recurrent bacterial ate antibacterial shampoos include benzoyl

PYoderma mclude failure to identify an
peroxide, chlorhexidine, chlorhexidineunderlying trigger, antibiotic undertreatketoconazole, ethyl lactate, and triclosan.

ment ( dosage too low or duration of therapy Shampooing will remove bacteria, crusts, to? short), concurrent use of glucocortiand scales, as well as reduce the pruritus, co1ds, wrong antibiotic, or wrong dose.

odor, and oiliness associated with the
pyoderma Clinical improvement in

Treatment: The primary treatment of
superficial pyodermas may not be evident
sup,e1:ficial pyoderma is with appropriate
for at least 14-21 days, and recovery may

:tib�o?cs for <!21, and preferably 30, days.

not be as rapid as expected.

clinical lesions ( except for complete

Of increasing concern is the development

�egrowth of alopecic areas and resolution of of methicillin-resistant staphylococci, and yPerpigmented areas) should be resolved
narrow-spectrum antibiotics should be
f�r at least 7 days before antibiotics are
used in treatment of pyoderma to minimize
discontinued. Chronic, recurrent, or deep
development of resistance. Recurrent

866

PYODERMA
bacterial pyodenna, deep pyodcnna,
helpful. Avoid�ncc of fluo�·oquinolones
and/or animals with a history of extensive
second- and third-generat1on cephalos anct
t0
antibiotic use are best treated based on
rins as empirical therapy is important •
culture and sensitivity. Concurrent
minimize the development ofmultistr�
aggressive topical antimicrobial therapy is
resistant staphylococci.

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CONTAG IOUS ECTHYMA

(Orf, Contagious pustular dermatitis, Sore mouth) Contagious ecthyma is an infectious
ousjunction of the lips and around empting
dermatitis of sheep and goats that affects
incisor teeth and _may exte�d to the mucosa
primarily the lips of young animals. The
of the buccal cavity. Occasionally, lesions
disease is usually more severe in goats than
are found on the feet and around the
in sheep. People are occasionally affected
coronet, where secondary bacterial
through direct contact.

infection withDermatophilus congolensis
commonly causes "strawberry footrot."

Etiology and Epidemiology: The

Ewes nursing infected lambs may develop
causal parapoxvirus is related to pseudolesions on the teats extending onto the cowpox (see p 868) and bovine papillar udder skin. The lesions develop as papules
stornatitis (seep 215). Infection occurs by and progress through vesicular and pustular
contact. The virus is highly resistant to
stages before encrusting. Coalescence of
desiccation in the environment, having been numerous discrete lesions often leads to the recovered from dried crusts after .12 yr. In
formation of large scabs, and the prolif era•
the laboratory, it is also resistant to glycerol
tion of dermal tissue produces a verrucose
and to ether.

mass under them. When the lesion extends

Contagious ecthyma is found' worldwide
to the oral mucosa, secondary necrobaciland is common in young lambs reared losis (see p 1429) frequently develops.

artificially and in older lambs during late

During the course of the disease (1-4 wk),
summer, fall, and winter on pasture, and
the scabs drop off and the tissues heal
during winter in f eedlots.

without scarring. During active stages of

Clinical Findings and Diagnosis:

infection, more severely affected lambs do

The
not eat normally and lose condition.

primary lesion develops at the rnucocutane-

Extensive lesions on the feet cause
lameness. Mastitis, sometimes gangrenous,
may occur in ewes with lesions on the teats.

The lesion is characteristic. The disease
must be differentiated from ulcerative

�ermatosis (see p 872), which produces tissue destruction and craterif orrn ulcers.

Ecthyma usually affects younger animals
than does ulcerative dermatosis, althou�
this criterion can only be used presumpave}y.

Foot-and-mouth disease (seep 629) and bluetongue (see p 738) infection sho�� �
considered if morbidity is high and clirUC

•

.

dfever.

signs mclude salivation, lameness, an . of

Staphyloccocal folliculitis affects the s�ct
the muzzle and surrounding the eyes .. Dir
demonstration of virus in scab matenal bY d
electron microscopy has now been repl�i:

by PCR as the diagnostic method of ch01

Proliferative contagious ecthyma (orf) lesion
f ?r
exte

�cthyma Historically, positive �ere!l·

.nd� from the mucocutaneous junction of
tia
the lips in a sheep.

tion

Courtesy of Dr. Philip Scott.

�ould be obtained by inoc�awi,g eeP·
susceptible and ecthyma-inum.uuzed sh

POX DISEASES

867

Treatment and Control: Both parenfair immunity in all parts of the USA ( with teral and topical antibioti�s 1�rny h�lp
an occasional exception more usually seen

01nbat secondary bacterial mfection
in goats). Vaccine breaks appear to be due
cf the skin lesions. In endemic areas,

0
to the virulence of the infecting strain rather
propriate repellents and lai:vicides
than to differences in antigenicity of the vac

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:itould be applied to the lesions to prevent
cine. Sheep immunized against contagious

111yiasis. The virus �s transmissible to
ecthyrna remain susceptible to ulcerative
people, and the lesions, usually confined to
dermatosis.

the hands and face, are more proliferative

Live vaccines should be used cautiously
and occasionally very distressing.

to avoid contaminating uninfected

Veterinarians and sheep handlers should
premises, and vaccinated animals should be
exercise reasonable protective precautions segregated from unprotected stock until the and wear disposable gloves. Diagnosis in
scabs have fallen off. A small amount of the
people is established by transmitting the
live vaccine is brushed over light scarificaviruS to sheep; a complement-fixation test tions of the skin, usually on the inside of the
may be of value.

thigh or behind the elbow or caudal fold.

Sheep that have recovered from natural

Lambs should be vaccinated when ~ 1 mo
infection are highly resistant to reinfection.

old. For best results, a second vaccination

Despite a multiplicity of imrnunogenic virus

~ 2-3 mo later is suggested. N onimmunized
strains, the presently used commercial·
lambs should be vaccinated ~ 1-2 mo before
single-strain live vaccines have produced
entering infected feedlots.

Pox diseases are acute viral diseases that
smallpox, cowpox, monkeypox, etc, are
affect many animals, including people and
closely related to vaccinia virus and are
birds. Some poxviruses also cause zoonoses. classified within the genus Orthopox. The

'fypically, lesions of the skin and mucosae . ·
avian poxviruses, the myxoma viruses, and
are widespread and progress from macules
some of the other poxviruses ( eg, swineto papules, vesicles, and pustules before pox) are species-specific. The viruses of
encrusting and healing. Most lesions contain orf, pseudocowpox, and bovine papular multiple intracytoplasmic inclusions, which
stomatitis are parapoxviruses. It has been
represent sites of virus replication in
recognized that several orthopoxvirus
infected cells. In some poxvirus infections,
infections of domestic animals and people;
vesiculation is not clinically evident, but
notably cowpox and monkeypox, are
microvesicles can be seen on histologic
acquired from rodent reservoir hosts:

ex�ation and, in some, proliferative

Many of these rodent hosts have not been
lesions are characteristic.

.

. ·
unequivocally identified. Thus, although

Infection is acquired either by inhalation
the use of adjectives such as "cowpox" and or through the skin ( eg, sheeppox ). In

"monkeypox" to describe these viruses

�� m:stances (eg, fowlpox, swinepox),
may be epidemiologically inaccurate and
misnomers, their retained use reflects both
b' � VIrus IS transmitted mechanically by

Iting arthropods. Infection may be
historical association and, until a better
foUowed by generalized lesions ( eg,
nomenclature evolves, pragmatism (see
sheeppox) or remain localized ( eg, pseudop 870).

c?wpox). Strains of poxvirus with reduced

Poxvirus infections can be confirmed in

VIrulence are used to immunize against
the laboratory using several diagnostic
some infections, the classic example being
techniques. The orthopoxviruses can

�e. global _eradication of smallpox in people usually be isolated in cell culture and by inoculation of embryonated eggs. Examinav Y �uruzation with strains of live acclllla virus.

tion of clinical samples by negative-staining
t Po�es can be classified according
electron microscopy is frequently used to
o the
visualize virus particles. PCR is widely used
p
ir physicochemical and biologic
roperties. Immunologically, the viruses of to further characterize virus isolates.

868

POX DISEASES

COWPOX
a parapoxvi_rns ar�d is widespread world.

wiclP. Tlw virus ol pseudocowpox is

In this mild, l'ntptin' disl':ISt' or dairy cows,
rel
t O t hos1•_or ('OJ1L_agio11s ('Cti1_y�1a (see
ksions are Sl'l'l\ on till' uddl'r and teats.

JJ situ
and hovmc pap1l_lar sl,011_1,_1!,1tts (see p 2l

Although oncl' common, cowpox is now

G) )

These parapox�1�us<:s <hller rnorphol
t'xtn'lH,l'lY ran' and reported only in western
o 'i-·
cally from vaccmia v1n1s and other g

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Europe csee also p 870).

poxviruses. They have a lh�ited host ran g

The ,in.is of co"l)OX is closely related
and cannot be propagated m fertile eggs e

.mtigenically to vaccinia and smallpox
and they will grow in some cell culture
virnses. Indeed, the first two c,m be
s '

although relatively poorly.

differentiated only by sophisticated

Lesions begin as small, red papules on
laborat01y techniques. Before vaccination of
the teats or udde_r. These may be _followed
the general population against smallpox was
rapidly by scabbmg, or small vesicles or
discontinued, some outbreaks of cowpox
pustules may develop before scabs fo
in cows in North America and Europe were
rm.

Scabs may b� abun?ant but c� be removed
due to infection with vaccinia from recently
without causmg pam. Granulat10n occurs
vaccinated persons. Vaccinia-related viruses
beneath the scabs, resulting in a raised
continue to cause occasional outbreaks
lesion that heals from the center and leaves
of teat infections in dairy cattle in South
a characteristic h<?rseshrn� or circular ring

America and buffalo in the Indian subcontiof small scabs. This stage IS reached in nent These viruses often spread to people

-7-12 days. Some lesions persist for several
in contact with cattle. The epidemiology of
months, giving the affected teats a rough
these viruses is unknown, but it has been
feel and appearance, and more scabs may
suggested that they are vaccine viruses that
form. The infection spreads slowly
spread to animals during the smallpox
throughout milking herds, and a variable
vaccination campaigns.

percentage of cows shows lesions at any

The disease spreads by contact during
time. Cattle may become reinfected in
milking. After an incubation period of 3-7
subsequent lactations.

days, during which cows may be mildly

The scabbed lesions may be confused
febrile, papules appear on the teats and udder. with mild traumatic injuries to the teats and Vesicles may not be evident or may rnpture
udder. Scabs examined with an electron
readily, leaving raw, ulcerated areas that form
microscope frequently show characteristic
scabs. Lesions heal within 1 mo. Most cows in virus particles.

a milking herd may become affected. Milkers

Control of infection within a herd is
may develop fever and have lesions on the
difficult and depends essentially on hygienic
hands, arms, or face. Occasionally, cowpox in measures, such as teat dipping, to destroy people can cause generalized disease, and
the virus and prevent transmission. Little
fatalities have been recorded.

immunity appears to develop.

Cowpox or vaccinia infection may be

People may become infected with
confused with bovine herpes mammillitis
painless but itchy purplish red nodules that

(seep 1385); because the lesions of these
are generally present on the fingers or
two conditions are superficially similar,
laboratory confirmation is required. The
hands. These lesions cause little disturbance and
viruses of cowpox and vaccinia can be
disappear after several weeks.

easily visualized by electron microscopy.

Although they cannot be distinguished from

LUMPY SKIN DISEASE

-----------------
each other, their morphology by electron

Lumpy skin
microscopy is distinct from that of pseudodisease is an infectious, tl
eruptive
cowpox virus and bovine herpes mammil

, occasionally fatal disease_ of c� e
chara
litis virus. Both vaccinia and cowpox
cterized by nodules on the skin an ·a.J
vir
other p
uses grow readily in cell cultures.

arts of the body. Secondary ��cten
infecti

Measures to prevent spread of cowpox
on often aggravates the co�ditiond ill
within a herd must be based on segregation

Traditionally, lumpy skin disease_1s foun
and hygiene. Cowpox and vaccinia viruses
southern and eastern Africa, but ID the
are important causes of zoonoses.

1970s it extended northwest throu� t}l.e
continent into sub-Saharan west Africa.

Since 2000, it has spread to sever�

PSEUDOCOWPOX

2013 wl.lS
countries of the Middle East and ll1
confirmed in Turkey.

(Milker's nodes, Paravaccinia)

Etiology and Epidemiology: The

Pseudocowpox, a common, mild infection
oi,
causal vir
of the udder and teats of cows, is caused by
us is related to that of sheePP

The prototype strain is known as the

POX DISEASES

869

Neethling �OA'Vi�1s. Lumpy skh� disease
and the disease is called bovine herpes
appears ep1denucal�y o� spor�d1cally. .

mammillitis (see p 1385).

Frequently, new foci of mfcct1on appear m

Pseudo-lumpy skin disease is a milder
areas far removed from the initial outbreak. disease than true lumpy skin disease, but Its incidence _is highest in �ct �umme�
differentiation depends essentially on

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weather, but 1t may occur m wmter. It 1s
isolation and identification of the virus.

most prevalent along water courses and on

Histologic and ultrastructural examination

}ow ground. Beca�se_ quarantine restricof nodules may be helpful. Poxlike tions designed to liimt the spread of
intracytoplasmic inclusion bodies or
infection have failed, biting insects have
eosinophilic intranuclear herpesvirus
been suspected as vectors; however,
inclusions may be seen in the nodules.

outbreaks have occurred under conditions

Dermatophilus congolensis also causes
in which insects practically could be
skin nodules in cattle (see p 858).

excluded. Experimentally, three species of
hard ticks found in Africa have been shown

Prevention and Treatment: · Quarantine
to biologically transmit the virus. Because
restrictions are of limited use. Vaccination
the disease can be experimentally
with attenuated virus offers the most
transmitted by infected saliva, contact
promising method of control. The viruses
infection is considered as another route of
of goatpox and sheeppox passed in tissue
infection. African buffalo are suspected as
culture also have been used.

maintenance hosts in Kenya. •

Administration of antibiotics to control
secondary infection and good nursing care

Clinical Findings: A subcutaneous
are recommended.

ir\jection of infected material produces a
painful swelling and then fever, lacrima

SHEEPPOX AND GOATPOX
tion, nasal discharge, and hypersalivation,
followed by the characteristic eruptions on

Sheeppox and goatpox are serious, often
the skin and other parts of the body in :-500/4 fatal, diseases·characterized by widespread of susceptible cattle. The incubation period
skin eruption; Both diseases are confined to
is 4-14 days.

. ,
parts of southeastern Europe, Africa, and

. The nodules are· well circumscribed, ·· · .

Asia The poxviruses of sheep and goats
rourid, slightly raised, finn; and painful and

( capripoxviruses) are closely related, bothinvolve. the entire cutis and the mucosa of·
antigenically and physicochernically. They
the GI; respiratory, and genital tracts. ·
are also related to the virus of lumpy skin

Nodules.·may develop on the muzzle and
disease ( see above). Reports on the natural within the nasal and buccal mucous
susceptibility of sheep to the virus of
membranes; Theskinnodules contain a ; ·
goatpox and vice versa are conflicting; at
finn; creamy-gray or yellow mass of tissue.

least some strains seem capable of infecting

Regional lymph nodes are ·swollen, and · , .

both species.

edema develops in the.udder, brisket, and

The incubation period of sheeppox is 4--8
legs. -Secondary infection sometimes occurs days and that of goatpox 5-:-14 days. The and causes extensive suppuration and · ·
clinical picture is similar in the two diseases
sloughing; as a result, the animal may.

but is generally less severe in goats. Fever
become extremely emaciated, and

· ·
and a variable degree of systemic distur

�uthanasia may be warranted. In time, the
bance develop. Eyelids become swollen, and
no_dliles either regress, or necrosis of the .

mucopuntlent discharge crusts the nostrils.

skin results in hard,· raised areas ("sit-fasts") c

Widespread skin lesions develop and are
l�arly separated from the surrounding
most readily seen on the muzzle, ears, and
skin. These areas slough to leave ulcers,
areas free of wool or long hair. Palpation can

Which heal and scar.,. . , .

· · · detect lesions not readily seen. Lesions start Morbidity is 5%--500/4; mortality is usually
l
as erythematous areas on the skin and

�w. The greatest loss is due to reduced milk

Yie
progress rapidly to raised, circular plaques
ld, loss of condition and rejection or ·, ·
re
with congested borders caused by local
duced value of the hide.

inflammation, edema, and epithelial
hyperplasia Although microvesicles are

D�agnosis: The disease may be confused

Wit
present histologically, vesicles and pustules
h Pseudo-lumpy skin disease, which is are not evident clinically. VIrUS is abundant

=ed by a herpesvirus (bovine herpes- , ·
in skin lesions at this stage. As lesions start
c . . 2). These diseases can be similar
to regress, necrosis of the dermis occurs and
w�cally, although in some parts of the . ,
o
dark, hard scabs form, which are sharply
c r d the herpesvirus lesions seem · ·

0
separated from the surrounding skin.

nfined to the teats and udder of cows,

Regeneration of the epithelium beneath the

870

POX DISEASES
scabs takes seYcral \\'l'C'ks. Whl'll scabs arc
lous<) (/ /cw11wlopinus sit.is). The diseas
n.'moYed, a star-shaped scar, free or hair or
also 111ay be t.ra1��m1iU.ed, P�>ssibly bet.w
wool. remains
e:

. In scVl'rc cases, lesions can
farms, by other msccls aclmg as mech
develop in the lungs. In some sheep and in
a.nt
carriers.

Ca\
ct'11ain breeds, the disease may be mild or

Recovered pigs are immune. There is
the infection inapparcnt.

specific treatment. Eradication of lice isno

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It has been sug<Tcsted that tnmsmission
important.

may be airborne� �1ay occur by direct
contact ,vith lesions, or mechanically by

COWPOX VIRUS INFECTIONS I
biting insects.

N

CATS AND OTHER SPECIES

The disease in either species must be
differentiated from the milder infection,

Many orthopoxvirus infections of domesti
contacious ecthyma ( orf, see p 866), which animals and people result from "spill ove/
mainl; causes cmsty, proliferative lesions
from rodent reservoir hosts. Although
arotmd tl1e mouth.

traditionally described as infecting cattle

Infection results in solid and enduring
infections of cattle with cowpox virus ar�
immunity. Live, attenuated virus vaccines
now very rare. Domestic cats in Europe are
induce longer immunity than inactivated
now the most commonly recognized species
virus vaccines. Live, attenuated, lumpy skin
clinically affected by cowpox virus.

disease virus also can be used as a vaccine

Cowpox infections are apparently restricted
against sheeppox and goatpox.

to Europe. The virus has not been isolated
in the Americas, but there is a single report

SWINEPOX
of raccoonpox virus ( a related orthopo:xvirus) causing a paw lesion in a cat in Canada Swinepox is an acute, often mild, infectious
disease characterized by skin eruptions that Etiology and Epidemiology: All affects only pigs. It is present in the USA,
orthopox isolates from domestic cats in
particularly in the Midwest, and has been

Europe are currently considered to be
reported from all continents, although the
cowpox virus, although molecular characincidence is generally low.

terization indicates significant heterogeneity

Historically, vaccinia virus was involved
in isolates that may be indicative of different
in some outbreaks; currently, swinepox
rodent hosts. Infection due to cowpox virus
virus appears to be the only cause. The
has also been recorded in other domestic
disease described here is that caused by the
species ( dogs, horses, and llamas } and in a
latter. Swinepox virus is distinct from other
wide range of captive species in various
poxviruses and does not protect against

European zoos. Cowpox virus is also
infection with vaccinia virus. It will grow on infectious to people, and cat-to-human pig cell cultures but not embryonating eggs.

transmission has been recorded. Owners

It is relatively heat stable and survives for
should be advised accordingly.

-10 days at 37°C (98.6°F).

It is assumed that because of a domestic

The disease is most frequently seen in
case of raccoonpox infection in a cat in
young pigs, 3-6 wk old, but all ages may

Canada with a localized infection of a paw,
be affected. After an incubation period of
cats may become infected when hunting.

-1 wk, small red areas may be seen most

Most affected cats come from rural
frequently on the face, ears, inside the legs,
environments and are known to hunt
and abdomen. These develop into papules
rodents; the initial lesion is often described
and, within a few days, pustules or small
as having originated as a small bite-like
vesicles may be seen. The centers of the
wound.

pustules

Infection in cats
become
has a marked
dry and scabbed and are
surrounded
seasonal incidence, with most cases
by a raised, inflamed zone so
that the lesions
occurring between September and
appear urnbilicated. Later,
dark scabs

November

(1-2 cm

. Cat-to-cat transmission can �J
in diameter) form
giving affected piglets
occur but usually results in only subclinIC
a spotted appe�ance. These eventually
infection.

·
drop or are rubbed

.

off without leaving a

The significa
scar.

nce of the disease an? its

Successive crops
oflesions can occur
relat
so
ively
that
recent recognition in cats 15 an
all are not
ti.Jl
at the same stage.

enigm

The
a. It may have always been pr�se
early stage of the , ,

�
disease may be
the feline
accompanied
population but not recogruze ·
by mild fever
i.nc1
inappetence, and dullness.

Alternatively, the disease may be incre.

Few pigs die of

:et

'

uncomplicated
in
swinepox.

importance as a result of a change ei
in the

Virus is abundant
epidemiology of the disease, in the
in the lesions and can
reservoir
be transferred from
host, or in the nature of the
pig to pig by the biting
dominant biotype of the virus itself.

POX DISEASES

871
pathogenesis: The most comrnon_routc
epidermis covers the skin beneath the
f entry appears to be through the skm, but

0
scabs, early scar tissue is present, and there

-onnstl inf cction is also possible. After
is a moderate, mainly mononuclear cell
f�cal replicat.io1� and dcv�lopment of a
infiltrate.

riinary skin lesion, the VIrus spreads to

In rarer cases, in which the disease has
iocal Iyinph �10de�, and a leukocyte_-
generalized, lesions may also be present in

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associated VIrenua develops. The VIrenuc
the liver, lungs, trachea, bronchi, oral
phase may be associated with pyrexia and
mucosa, and small intestine.

depression and, du�ng th�s perio_d, virus can
be isolated from vanous tissues, mcluding

Diagnosis: If multiple, well-circumscribed
the skin, turbinates (and sometimes lungs),
skin lesions are present, and especially if
and lymphoid organs. Widespread

.

there is a history of hunting or exposure to a
secondary skin lesions appear a few days
rural environment, a presumptive diagnosis
after the onset of viremia, and new lesions
may be based on clinical signs. Cowpox
continue to appear for 2-3 days, at which
virus infection also should be suspected
time the viremia subsides:

when skin lesions do not respond to
antibiotics. Differential diagnoses include

Clinical Findings: Most affected cats '

miliary dermatitis, feline herpesvirus or
have a history of a single primary skin
calicivirus infection, eosinophilic granulesion, �sually on the head, neck, or a loma, bite wounds, ringworm, and other
forelimb. The primary _lesion can vary from
chronic bacterial or fungal conditions.,
a sm'all, scabbed wound to a large abscess.

Presumptive arid rapid diagnosis can be

Appro�ately 7-1 o·days after the primary
made in most cases from unfixed scab,
lesion appears, widespread secondary
exudate, or biopsy material examined for
lesions begin to appear. Throughout 2-4
characteristic brick-shaped orthopox
days, these develop into �screte, circular, .. virions by electron microscopy. A more ulcerated papules -:--0.�l. cm in diameter.

accurate and sensitive method of diagnosis

The ulcers soon become covered l:>y scabs,
is by PCR, or isolation of virus in cell culture
and he.aling is usually complete, by -6 wk.

or on the chick chorioallantois. Fixed

Many cats show no signs other· than skin
biopsy material for histologic examination
lesions, but -20% may develop 'mild coryza
and serum for antibody determination also
or conjunctivitis. Sorrie. cats may also. be
can be sent to the laboratory.

pyi:e:idc, depi-ess�d, and' inappetenf ch.iring
the viiemic phase just before and during

Treatment and Control: In both
the early development of secondary ..

domestic cats and cheetahs, it is important
lesions. Concurrent.bacterial infection,
that cowpox be diagnosed promptly, . .

Pa.rticularly of the prilnary lesions, may .

because steroid treatment, which is often
give·rise to systemic.signs. However, most
used in-therapy of other skin conditions, is
domestic cats recover uneventfully. More
contraindicated. Although the disease is
se".ere puhnonary diseas·e is oocommon in
often severe in cheetahs, in domestic cats
dom�stic cats but frequently occurs in
supportive treatment (broad-spectrum
cheetahs and is often fatal in both 'species.

antibiotics, fluid therapy) is generally

More severe disease in domestic cats is
successful, and mortality is low.

o�en associated with nnrnunqsuppression,

Because it seems that infection in domestic
either after treatment with corticosteroids cats is mainly sporadic and acquired from or associated with infection with feline
chance contact with an infected wildlife
leukemia or immunodeficiency viruses.

reservoir, it is difficult to control the exposure
of outdoor cats to this virus. In wildlife parks,

Lesions: Because most cats survive
s
where big cats are at risk from contact with

� biopsies generally are the only tis�ue
small wild rodents, and especially where the

:�able for histologic examination. Early . · disease has already occurred, vaccination i51�ns consist of areas of epidermal hyper-may be helpful. Vaccinia virus appears to be

� asia_and hypertrophy with vesiculation of-

�=� e
oflow pathogenicity in domestic cats, and

Pnckle cell layer. Many of the epidermal · cheetahs appear to be refractive. Currently,

?Orde�g such vesicles contain charac-

1.af
management of outbreaks among large cats
tic eos�ophilic cytoplasmic inclusions. depends on prompt diagnosis and segregae tion of affected animals to reduce the
pi�r, th�re IS ulceration and necrosis of the
enms
possibility of cat-to-cat spread. Rodent

Phili
and replacement by an eosino- .

Ah c coaguium of necrotic cells and fibrin ..

control s_hould be evaluated and premises
is eavy, mixed inflammatory cell exudate
disinfected. At ambient temperatures,

1 �resent in the dermis surrounding the
esi
poxviluses are relatively resistant and may
on. As healing ensues, a thin layer of
remain infective in dried crusts for months.

872

ULCERATIVE DERMATOSIS OF SHEEP

U LCERATIVE DERMATOS IS O F S H EEP

{Lip and leg ulceration, Venereal balanoposthitis and vulvitis) VetBooks.ir

Ulcerative dennatosis is an infectious
lesion. Differentiation between this
disease of sheep caused by a vims similar
lesion and that of contagious ecth a
yrn (s
to the ecthy:ma virns. It manifests in two
p 866), which is essentially proliferative:

somewhat distinct fom1s, one characterized
character, is fundamental. In most cases
by fonnation of ulcers around the mouth and on removal of the scabs, the lesions of nose or on the legs (lip and leg ulceration),
ulcerative dermatosis are craterifonn or
and the other as a venereally transmitted
ulcerative, whereas lesions of contagioUs
ulceration of the prepuce and penis or vulva
ecthyma are proliferative. The question
of the similarity of the agents of these

Clinical Findings: The lesion, regardless
two conditions is not clearly defined, but
of location, is an ulcer with a raw crater that inoculation of sheep previously immunized bleeds easily, varies in depth and extent, and against contagious ecthyma helps in making contains an odorless, creamy pus; it is
a diagnosis. It is also difficult, and in some
covered from the beginning with a scab.

instances impossible, to differentiate

Face lesions occur on the upper lip,
between ulcerative posthitis and vulvitis
between the border of the lip and the nasal

( see p 1372) and ulcerative dermatosis
orifice, on the chin, and on the nose. In
without resorting to sheep inoculation.

severe cases, the ulcers may perforate the
lip. Foot lesions are seen anywhere between Prevention and Treatment: Infected the coronet and the carpus or tarsus.

sheep should be isolated, and those with

Venereal lesions partially or completely
genital lesions should not be bred. Recovecy
surround the preputial orifice and may
takes 2-8 wk and is not greatly influenced
become so extensive as to cause phinlosis.

by treatment. Therapy is usually not

Rarely, the ulcers may extend to the glans
attempted unless the animals are to be bred
penis so that the ram becomes unfit for
soon, lip lesions interfere ,vith eating, foot
natural breeding. In ewes, edema, ulceralesions make the animals so lame that they tion, and scabbing of the vulva have less
are losing condition, or secondary bacterial
serious consequences.

infections become severe.

There are no noticeable early systemic

Treatment consists of removing the scabs
reactions. Morbidity rates of 15%-20% are
and all necrotic tissue from the ulcers and
usual, although up to 60% of a flock may
applying any one of the following preparabe infected. Often, the disease remains tions: silver nitrate (styptic pencil), stro
unrecognized until the lesions are so
ng
tincture of iodine, 300/o copper sulfate
advanced that signs of lameness or
s�lution, 4% formaldehyde, 5% cresol (sheep disturbed urination become apparent.

dip), or sulfa-urea powder. Foot and lower
leg lesions can be treated with copper

Diagnosis: Diagnosis depends entirely on
sulfate or formaldehyde solutions in
recognition of the characteristic ulcerative
footbath troughs .. .

DERMATOPHYTOSIS

(�ingworm)

Dermatophytosis is an infection of
anim
keratinized tissue (skin, hair, and claws) by
als are susceptible. In developed
countri
one of the three genera of fungi collectively_
es, the greatest economic and
c
human health consequences come front

�ed dermatophytes-Epidermophyton,

Microsporum, and Trichophyton. (See also dermatophytosis of domestic cats and ii
cattle. A few dermatophyte species are 50 d

FUNGAL INFECTIONS, p 632.) These pathogenic
inhabit
fungi are found worldwide, and all domestic
ants (geophilic ); eg, M gypse:1'rn an

T terrestre, and cause disease in arurnals

DERMATOPHYTOSIS

873
tMt :U\' l'�yosed whik digging or rooth,g.

I )pr111nl.ophytm1iH IH di:1gnosl'd hy fungal

Othl'r:-pl'Cll'� :ll'-' \'�lst-adaph'l� t(� !Woph:

c11lt 11re, ex:unl11ntio11 wit.h n Wood'H lamp,

(·uttht\lpopluhl'). q�. ,ll audou1 1111 and 7
and din•cl. mkroHcopic 1�xnminat.ion of hair

,;,bl'll m, �md inft'ct oth_l'r animals rarelv.

or skin seal<'. F1111gal eulturc is Uw most

'fh(' 1110..--t impm1ant n�1m1nl pat.lu lgens
acc11rat <' mctms of diagnosiH. Dcrmat.ophytc
worldwidl' :u'l.)1'! ca111.-:, M .cmpse11111, 1'

test medium (DTM) may ue used in a

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,,11.-nta.c1l'oJ)hJ1tcs, Tcq,11imrn1, T vmTucoclinical setting. Selected lesions should sum, :md...lf ,w,!um. lhese_sl;)ecies are
have the hair clipped to a length of -0.a em.

zoonotk, especial�r M can1B mfections of

The m·ea should be gently patted with an
doint'Stic cats mtd T ve,·mcoswn of cattle
alcohol-moistened sponge and then patted

:uid kunbs. Th� zoophilic species are
dry to reduce contamination with saprommsmitt�d pmnanly by contact with phytic fungi. Hair stubble and skin scale are
infected individuals and contaminated
collected for placement on the growth agar.

fomites such as furniture, grooming tools,

The container is then loosely capped to
or tack E>...1>osure to a dennatophyte does
prevent drying. Incubation at room
not ahvays result in infection. TI1e liketemperature is sufficient except when lihood of infection depends on several
culturing for T verrucosum from food and
factors, including the fungal species, host
fiber animals, in which case incubation at
age, immunocompetence, condition of

37°C is necessary. T equinum requires
exposed skin surfaces, host grooming
nicotinic acid if subcultured from primary
behavior, and nutritional status. Infection
growth, and some T verrucosum isolates
elicits specific immunity, both humoral
require thiamine or thiamine and inositol.

and cellular, that confers incomplete and

Dermatophyte growth is usually apparent
short-lived resistance to subsequent
within 3-7 days but may require up to 3 wk
infection or disease. New information
on any type ofDTM. Dermatophytes
concerning dermatophytic virulence factors,
growing on DTM cause the medium to
notably secreted proteases involved in the
change to red at the time of first visible
invasion of keratin, aspects of host immune
colony formation, Dermatophyte fungi have
response against dermatophytes, and new . ,.- , white to buff-colored, fluffy to granular molecular tools available for studying derma mycelia. Saprophytic contaminant colonies tophytes should hasten development of safe.

are white or pigmented and almost never
and effective vaccines against dermatophyproduce an initial color change on DTM.

tosis in species without vaccination options. Definitive diagnosis and species identifica

Under most circumstances, dermatotion require removal of hyphae and phytes grow only in keratinized tissue, and
macroconidia from the surface of the
advancing infection stops when reaching
colony with acetate tape and microscopic
living cells or inflamed tissue. Infection
examination with lactophenol cotton blue
begins in a growing hair or in the stratum
stain. Dysgonic strains do exist, but lack of.

corneum, where threadlike hyphae develop growth of suspected ringworm is most from the infective arthrospores or fungal
likely due to lack of expertise in culture
hyphal elements. Hyphae can penetrate the
technique and fungal identification or to
hair shaft and weaken it, which, together
disease processes other than ringworm that

With follicular inflammation, leads to a
cause clinical signs.

common clinical sign of patchy hair loss.

. The Wood's lamp is useful as a screening

As the infection matures, clusters of arthrotool for M can is infections in cats and dogs.

�res develop on the outer surface of

Infected hairs fluoresce yellow-green;
infected hair shafts. Broken hairs infected
however, only s50% of M can is infections

With spores are important sources for
fluoresce, and other fungal species in
spread of the disease. Under experimental
animals do not. Therefore, negative Wood's
conditions, the housefly, Musca domestica, lamp examinations are not meaningful.

can 1:ransmitM canis mechanically with its False-positive examinations may occur and 0 ::t body surface for as long as 5 days. The are especially likely in oily, seborrheic skin

� . cal relevance is yet to be determined.

conditions. Fluorescing hairs should always
be cultured to confirm the diagnosis.

d inflammation and host immunity

�el.op, further spread of infection is

Direct microscopic examination of hairs
bited, although this process may take
or skin scrapings may cnlumce clinical
several weeks. Thus, for most healthy
suspicion by demonstrating characteristic
adult hosts, dermatophyte infections arc
hyphae or arthrospores in the specimen.

Self.limiting. In young or debilitated animals The technique is more useful in diagnosing and, to some extent in Yorkshire Terriers
dermatophytosis in large animals than in

:d l�nghaired bre�ds of domesti� cats,
small animals. Hairs (preferably white ones)

ection may be persistent and widespread. and scrapings from the periphery of lesions

874

DERMATOPHYTOSIS
m-e examined for fungal elements in a wel
decrease the number of new inf ectect
pn .. 'paration of 20% potassium hydroxide
h

The duration or immunity is long las ercts.

that has been gently wanned or incubated in
t'

The vaccine prevenls development
a lmmirlity chamber overnight.

0 fg,
clinical lesions, transmission to othe r

An ELISA for the serodiagnosis of c,mine
animals, and contamination of the

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<lennatophytosis has been researched but is environment. A vaccination prograrn not commercially available. The sensitivity
combined with a cleaning and disinf e t'

and specificity is· high and similar to that
protocol can help eliminate sig
c 1
ns o

0n
f
of ftmgal cultme with DTM, but positive
ringworm and eradicate it from the herd
results can be seen after elimination of the

Vaccination has greatly reduced the
denuatophyte infection. Cross-reactivity
incidence of zoonotic disease in farrners
between the vruious derrnatophytes would
their �oll:5eholds, :"eterinarians,_ and pe not
o
allow for species identification, which is

�le
working m abatf:mr� and �enes. No liv
important for identification of the source of
e
attenuated vaccme 1s available in North
infection.

America.

CATTLE

DOGS AND CATS

Trichophyton verrucosum is the usual

In dogs, -70% of cases are caused by
cause of ringworm in cattle, but T menta

Microsporum canis, 200/o by M gypseum
grophytes, T equinum, Microsporum
and 100/o by Triclwphyton mentagrophyt�sgypseum, M nanum, M canis, and others in cats, 98% are caused by M canis. The
have been isolated. Dermatophytosis is

Wood's lamp is useful in establishing a tentamost commonly recognized in calves, in tive diagnosis of dermatophytosis in dogs
which nonprmitic periocular lesions are
and cats but cannot be used to exclude this
most characteristic, although generalized
type of infection. Definitive diagnosis is
skin disease may develop. Cows and heifers
established by DTM culture (see p 872).

are reported to develop lesions on the chest

Detection of infection in asymptomatic
and limbs most often, and bulls in the
carrier animals is facilitated by brushing
dewlap and intermaxillary skin. Lesions are
the coat with a new toothbrush and then
characteristically discrete, scaling patches
inoculating a culture plate with the
of hair loss with gray-white crust formation,
collected hair and scale by pressing the
but some become thickly crusted with
bristles to the surface of the medium.

suppmation. Ringworm as a herd health

The clinical appearance of ringworm in
problem is more common in the winter and
cats is quite variable. Kittens are affected
is more commonly recognized in temperate
most commonly. Typical lesions consist of
climates and in English rather than Zebu
focal alopecia, scaling, and crusting; most
breeds of cattle.

are located around the ears and face or

Many topical treatments have been
on the extremities. Cats with clinically
reported to be successful in cattle, but
inapparent infections can serve as a source
because spontaneous recovery is common,
of infection to other cats or people.

claims of efficacy are difficult to substanti

Occasionally, dermatophytosis in cats
ate. Valuable individual animals should still
causes feline miliary dermatitis and is
be treated, because this may well limit both
pruritic. Cats with generalized derrnatop h yprogression of existing lesions and spread tosis occasionally develop cutaneous
to others in the herd. Thick crusts should
yt
ulcerated nodules lmown as derrnatop h e be removed gently with a brush, and the
granulomas or ps�udomycetomas. D e von
material burned or disinfected with

Rex cats can have a maculopapular
hypochlorite solution. Treatment options
hyperpigmented, crusted disease l?�t
depend on allowed usage of some agents
histopathologically is an eosinophilid
in animals destined for slaughter. Agents
mastocytic dermatitis.

reported to be of use include washes or

· c

Lesions in dogs are classic�Y alop e �
sprays of 4% lime sulfur, 0.5% sodium
aY
scaly patches with broken hairs. Dogs
hypochlorite (1: 10 household bleach),
also develop regional or gene�alized

0.5% chlorhexidine, 1 % povidone-iodine, •
uies and
folliculitis and furunculosis with pap
natamycin, and enilconazole. Individual
topustules. A focal nodular form of d e i:111 a lesions can be treated with miconazole or
phytosis in dogs is the kerion reactIO_I1·
clotrimazole lotions.

Generalized ringworm in adult dog� 1

A live attenuated fungal vaccine is in use

� bY
uncommon and is usually accomp arue
in some countries other than the USA. The
otJS or

�uno?eficiency, especial�Y_ end�;
vaccine has been used in control and
ren·
iatrogeruc hyperadrenocorticISID-
eradication programs to successfully

1 ions
tial diagnoses for classic ringwonn e s

DERMATOPHYfOSIS

875

. dogs include demodic?sis, bact�1:ial
tcrhinanne (30-40 mg/kg/day), and
fomculitis, and se�lO_rrhe1c dcrmaht1s. .

fluconazole (5-10 mg/kg/day). Fluconazole

Dennatophyto�1s,1�1 dogs and shm�hrured may he the least effective of these drugs.

cats 111ay be self-lnmtmg, but rcsolut1�n can

Terbinafme was found to be at levels higher
be hastened by trcat�ncnt. Another pnmary
thru1 the minimum inhibitory concentration

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bjective of therapy 1s to decrease

0
on the hair of treated animals for 5.3 wk
wiroiunental contamination ru1d prevent
ei
after 2 wk of daily therapy. This may
read ofinf ection to other ru1imals ru1d
indicate its potential for use as a pulse
ieople. Although no controlled studies exist therapy drug after 2 wk of daily administrathat prove clip�ing o� the h�� coat sh�rtens tion. None of these drugs is approved for
the duration of infection, clinical studies ..

use in domestic lli1imals in the USA. In
support this recommendation, at least for
addition, ketoconazole is often a cause of
cats with long hair ru1d/or generalized : . ·
ru1orexia in cats ru1d is not used as often in
dennatophytosis, even if it initially worsens
this species. Systemic and topical treator spreads the lesions. Environmental ments for dermatophytosis should be
decontamination with bleach (1:10 dilution) continued until a negative brush culture is orenilconazole solution (0.2%) is effective.

obtained. A brush culture is usually

Whole-body topical therapy may hasten a submitted after a minimum of 1 mo of clinical cure (if not a mycologic cure) ru1d
therapy or when clinical lesions are minimal
decrease environmental contamination.

to resolved. In chronic disease and/or

Based on in vitro ru1d in vivo studies,
challenging environments, the endpoint of
whole-body lin1e sulfur dips (1:16);0.2%
treatment may more appropriately be two
enilconazole rinses, 2% miconazole, ru1d a
or three consecutive negative fungal
combined 2% miconazole/chlorhexidine
cultures obtained at weekly or biweekly
shampoo were found to be ru1tifungal.

intervals. Efficacy ofluf enuron either to

These may be appropriate for adjunctive
treat orpreventM can.is infection has not
therapy.' Enikonazole rinse is not currently
been confirmed in controlled studies.

available in the USA iri a formulation
approved for dogs ru1d cats. Topical use • .· ·
of enilconazole may have been the cause · •

HORSES
of hypersalivation, idiopathic muscle
wealmess, ru1d slightly increased serum ALT' Tric�phyton equinum a:nd Tmentagro
concentration in one study. Local lesions
phyt,es are the primary causes of ringworm
can be treated effectively with topical
in horses, althoughMicrosporum gypseum,
miconazole or clotrimazole.

M can is, ru1d T verrucosiim have also been For chronic or-severe cases and for
isolated. Clinical signs consist of one or more.

ringworm in longhaired breeds of cats and · patches of alopecia ru1d erythema, scaling, Yorkshire Terriers, systemic treatment is
ru1d crusting, whi_ch are present to varying ,
indicated:Itraconazole, fluc6nazole,· '

degrees. Early lesions may resemble
terbiriafine, ketoconazole, ru1d griseofulvin
papular tµiicariabut progress with crusting
have all been used successfully. The · ·
and hair loss within a few days. Diagnosis is
microsized formulation of griseofulvin cru1
co�ed py culture. I)ifferential diagnoses
b�
include dermatop:tmosis, pemphigus

�ed in dogs (25-100 mg/kg, daily or in
di".1ded doses) and in cats (25-50 mg/kg,
foliaceus, and bacterial folliculitis. Transmisdaily in divided doses) ru1d is best absorbed sion is by direct contact or by grooming·
when given with a fatty meal. The ultramiimplements ru1d tack. Most lesions are seeri crosized formulations should be used at
in the saddle ru1d girth areas ("girthitch'J
lower d�sages (10....'..15 mg/kg/day); There is

Treatment is generally topical because
no vetennary-labeled griseofulvin currently systemic therapy is expensive ru1d of approved for use in dogs ru1d cats in the
unproven efficacy. Whole-body rinses

USA Cats may develop bone marrow
as described earlier for cattle may be recom

:P.l)ression, especially neutropenia, at
mended, ru1d individual lesions treated with

. gher doses as idiosyncratic reactions. This clotrimazole or miconazole preparations.

� more common inf eline imrtl.unodefi

Grooming implements ru1d tack should be
ciency virus-positive cats. In both dogs and disinfected, ru1d affected horses should be ca!S, GI upset is a fairly common sequela of isolated.

griseofulvin administration.

·

. tr Other effective treatments include

PIGS, SHEEP, AND GOATS

� acohazole (5-10 mg/kg/day, or pulse
e
an: PY 5-10 mg/kg/day for 28 days then on

Dermatophytosis in pigs is usually caused
te

We rnate-week regimen [ 1 week on, 1
e
by Microspo1�m nanum. Lesions are rings
k Off]), ketoconazole (5-10 mg/kg/day), of inflammation or brown discoloration

876

DERMATOPHYTOSIS
that. spn'ad centrifugally up to a diameter
when lambs are sheared for show, or m
of G cm. Lesions are f
a
a irly asymptomatic in
develop later ��s a consequen�e of con Y.

adults, and ringworm in swine is generally
nation from clippers _at sheanng. lnfec�
of little economic consequence. Zoonotic
lambs should not be 1
infections in f

�sued _ce_rtificates /
a rm workers are not
transport to show until �h� m.f ection is or
common.

cleared. Because there 1s little evidenc

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t

Ringwonn is a common, troublesome
h
lambs with a functional rumen absorb e at
problem in show lambs but is othe1wise
griseofulvin to effective levels, treatrne t.

uncommon in production flocks of sheep
best acc�mplished_with sodi� h yP oc�:

and goats. The infecting species include
rite solutions or enilconazole nnses (wh

M canis, M gypse-um, and Trichophyton
available). In healthy lambs, as in othe ere
r
verrucoswn. Lesions in lambs are most
species, th�se infections are �elf-limitin
often noticed on the head, but widespread
g
but resolut10n may not be evident in tim�
lesions under the wool may be apparent
fo
show purposes.

r

CATTLE G RUBS

Hypodermosis of cattle in the northern
eggs hatch in 3-7 days, and first-stage larvae
hemisphere is caused by bot fly larvae
travel to the base of the hair shaft and

( cattle grubs or ox warbles) of Hypoderma
penetrate the skin. Normally, the first-stage
spp ( order Diptera, family Oestridae). In
larvae travel through the fascial planes

Central and South America, larvae (tropical
between muscles, along connective tissue,
warbles) of Dermatobia hominis (order·
or along nerve pathways. They secrete

Diptera, family Cuterebridae) are important proteolytic enzymes that facilitate their pests of cattle.

movement. Dilling fall and winter, larvae
migrate toward two different regions,

HYPODERMA SPP
depending on the species. H lineatum
larvae migrate to the submucosal connec1\vo species of Hypoderma, H bovis tive tissue of the esophageal wall, where

( common cattle grub) and H lineatum
they accumulate for 2-4 mo. H bovis larvae

(northern cattle grub), are economically
migrate to the region of the spinal canal,
important and primary pests of cattle. They
where they are fonnd in the epidural fat
are found between 25° and 60° latitude in between the dura mater and the periosteum
the northern hemisphere in >50 countries of for a simil.ar period.

North America; Europe, Africa, and Asia. In

Beginning in early winter, the larvae

North America, H lineatum is found in
arrive in the subdermal tissue of the back of

Canada, the USA, and northern Mexico,
the host, where they make breathing holes
whereas H bovis is generally found north of

( central puncturn) through the skin. Cysts
the 35 th parallel. Occurrence in cattle and or warbles form aronnd the larvae, which

American bison was historically common.

undergo two molts (second and third stage).

However, widespread use of macrocyclic

The warble stage lasts 4-8 wk FinallY,
lactones have decreased the prevalences of
third-stage larvae emerge through the

H lineatum andH bovis in cattle in North
breathing holes, drop to the ground, �d

America. H tarandi parasitizes native

-3
pupate. Flies emerge from the P

Cervidae and reindeer in arctic and

��ae in l ctul t
mo, depending on weather conditions,
subarctic regions. Larvae of Hypoderma
do not feed, live <1 wk. Th li
e fe
flies, which
spp also have been reported in horses,
cycle is complete
sheep, goats, and people.

in 1 yr.

are

For the two species, seasonal events
similar

Life Cycle: AdultHypod
except that those for H linea::;
erma, lmown
vi,s,
occur
also as heel flies or gad flies, are ~ 15 mm

~6-8 wk earlier than those of

These events
long, hairy, and bee-like in appearance. In
vary from year to ye3.: but_ c
correlate with
late spring or early summer, they attach
local and regional clima\r
conditions
their eggs on the hair of cattle, particularly

. Larvae first appear in backs
cattle about
on the legs and lower body regions. The
mid September in southef!l

USA but not nntil late January or later U1

CATTLE GRUBS

877

:rt11em USA. Grubs first emerge from the
usually results in healing of the lesions

�o ck dming the hc,t half of November in
without complications. Carcasses and hides
r:xas and dming the first I_1alf of March in of cattle infested with cattle grnbs show

Montana. Wlwn both species ,�re present,
marked evidence of the infestation and are
tliird-stage huvae may appear m the back
reduced in value.

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for -5--6 mo; when only one species is

An infested animal may have 1 to �300
present, the lmva� m�� appear for -3-4 mo.

warbles but generally <100; infested herds

The activity of ovipos1ting (by female flies)

often have individual animals with no
is at its height from January to March in
larvae. Young animals are most heavily
southem USA and from May to July in
infested.

northem USA.

If migratingHypoderma die in esophageal tissue (H lineatum) or near the spinal Clinical Findings and Pathogenesis:

cord (H bovis ), they can cause severe,

During periods of sunshine on warm days,
sometimes fatal, reactions. These reactions
cattle may run with their tails high in the air appear to be related to the numbers of when chased by fem ale heel flies, particularvae but are rare in any case.

larly H bovis. This behavior in cattle is

Death of first-stage larvae ofH lineatum
referred to as "gadding" and is a strategy in the submucosal connective tissue of
to avoid female flies and their attempt to
the esophagus causes inflammation of the
deposit eggs. Not all stampeding or gadding
esophageal wall, dysphagia, drooling, and
of this kind is the result of heel fly attacks,
bloat. Again, recovery is usually rapid and
because this activity has been seen in the
complete ( 48-72 hr after treatment), but in
absence of heel flies. Gadding in cattle
severe cases, the bloat may be fatal. Rupture
may result in loss of production, altered
of the esophagus may be caused by
reproduction, self-ir\iury, or death.

attempted passage of a stomach tube in an

In otherwise healthy cattle, H bovis
affected animal.

larvae and their secretions in the epidural

Death of first-stage larvae of H bovis in
fat of the spinal canal are associated with
the spinal canal of cattle after systemic
dissolved connective tissue, fat necrosis,
insecticide treatment has resulted in
and inflammation. Sometimes, the inflastiffness, ataxia, muscular weakness, and mmation extends to the periosteum
paralysis of hindlimbs. Recovery is usually
and bone, producing a localized area of
rapid and complete, but occasionally,
periostitis and osteomyelitis. Occasionally,
paralysis may be permanent.

the epineuriurn and perineuriurn may•

Concurrent with the decrease in the
become involved. In rare severe cases,
prevalences of H lineatum and H bovis in paralysis or other nervous disorders may
cattle, widespread use of macro cyclic
occur. Similarly, H lineatum in the
lactones has also led to a decline in the
submucosa of the esophagus may cause
clinical relevances of these parasites in
sufficient inflammation and edema in the

North America. However, serologic surveys
surrounding tissues to hinder swallowing
have demonstrated that cattle are still
or eructation. It is unusual, however, for
exposed to Hypoderma spp. Should
clinical signs of parasitism to be evident
treatment programs stop or move away
during the migratory phase.

from products that have efficacy against

· · Penetration of the skin by newly hatched

Hypoderma spp, clinical signs due to
lruvae may produce a hypodermal rash,
infestation will likely reappear.

most often in older, previously infested
cattle. The points of penetration are painful Diagnosis: Third-stage larvae of and inflamed and usually exude a yellowish Hypoderma spp are found in warbles, the serum:. Warbles may be found in the back
furuncle-like nodules or cysts along the
from tailhead to shoulders, and fromtopline back of cattle. On recovery from a warble, to about one-third the distance down the
third-stage larvae can be easily differentisi�es. Usually, the warbles are firm and r
ated. H bovis is longer (27-28 mm) and has
aised considerably above the normal
co
no spines on the tenth segment and a funnelntour of the skin. In each warble, there is a
shaped spiracular plate. H lineatum is

�reathing hole, ranging in size from a small slightly shorter (25 mm) and has spines on slit to a round hole (3-4 mm in diameter) for

�
the tenth segment and typically a flat
ore mature larvae. Generally, secondary
spiracular plate. In cases of bloat or
lllfection is depressed; however, warbles
paralysis, the presence of disintegrating
may occasionally develop in large,

8
grubs and the associated hemorrhage and

�PPurating abscesses. The emergence

0
tissue damage distinguishes animals that
the third-stage larvae their forced
e
are parasitized from those that are not.

xpulsion, or their death within the cysts

ELISA-based tests have been developed to

878

CATTLE GRUBS
of the heel fly season. They should not b
treated later than 8-12 wk before the e
anticipated first appearance of grubs in th
backs, because adverse reactions may e
occur when migrating larvae are killed

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Where systemic insecticides cannot·
be used, Hypoderma spp larvae can be
controlled by applying tetrachlorvinphos
dust to the warbles in the back. The dUst
should be applied to the animal's back anct
worked into the grub holes. Because new
grubs continue to appear in the back,

Hypoderma spp, third-stage larva. Courtesy of
treatment must be repeated every 30-45

Dr. Raffaele Ronca/Ii.

days during the warble season.

On small groups of tractable animals
mechanical extraction by instrument 0�.

detect anti-Hypoderma antibodies in sera
hand expulsion (ie, squeezing) of the
and milk. These ELISA tests are often used
individual larva is effective. Larvae can also
to measure risk of exposure and do not
be removed by carefully iajecting 1 mL of 3%.

correlate well with observation of clinical
hydrogen peroxide with a blunt cannula
hypodermosis in cattle.

through the central puncturn. However, care
must be used to not rupture or pierce the

Treatment and Control: Systemic
larvae during removal. Rarely, when these
insecticides in various formulations are .

procedures are performed carelessly, larvae
available for treatment. Pour-on products
are crushed or pierced, inducing an
containing macrocyclic lactones ( doramecanaphylaxis-type reaction. This anaphlyaxis tin, eprinomectin, ivermectin, or mo:xidecis believed to result from the overwhelming tin) are poured evenly along the midline of
and sudden release of Hypoderma spp
the back Some products must not be
antigens. Experimental studies have also
applied when the skin or hair coat are wet
demonstrated that this anaphylaxis-type
or when rain is expected to wet cattle within reaction is due to the release of toxins from 6 hr. The application site should be free of

Hypoderma larvae.

skin lesions, mud, or manure. Cattle

Research to develop vaccines against
stressed by castration, overheating,

Hypoderma spp infestations was convaccination, or shipping should not be ducted as early as the 1950s. Even though
treated.

some natural and recombinant antigens

In the USA, registrations of most, if not
were demonstrated to have efficacy against
all, systemic organophosphate insecticides

Hypoderma spp infestations, the high
for cattle grub control have been cancelled,, efficacy and ease of use of macrocyclic and the practices of dipping or spraying
lactones have precluded modem vaccine
cattle for cattle grub control have been
development.

replaced by pour-on and/or iajectable
treatments.

Doramectin and ivermectin are systemi

DERMATOBIA HOMINIS
cally active against Hypoderma larvae

The
when injected
tropical

SC. Ivermectin
warble fly or torsalo, on e o�the
is also
available as
most
an oral
importan
paste.

t parasites of cattle in Latin

The injectable
and pour-on systemic

America, is
treatments
distributed between southern
are
approved for control of

Mexico and northern Argentina. LarV�

Hypoderma and
other myiasis-causing
stages
flies in
are found in many hosts, including
many
countries.

cattle, sheep, goats, pigs, buffalo, dog s , Eprinomectin and
cats,
moxidectin
rabbits, and people. Cattle and �o� s
pour-on
formulations are approved
are
for
infected
treatment
most commonly. D hom!nis
of .

both beef and dairy cattle.

is

Otherwise,
thought to initiate the lesion that gi ves
use of rise

�gs fo
to lechiguana, a disease of cattl e C see

� cattle grub control is prohibited in
darry amrnals of breeding
below
age.

).

· ·

Because
res�dues may be present in cattle for varying
penods after treatment,

Life
withdrawal

Cycle: The adultfly is 12-15 nun 10Ilg times
for all treatments must be observed.

and has a short life span ( 1-9 days). The 5

In areas where
adult fly

Hypoderma spp are
fastens its eggs to different typ e ,
prevalent, cattle, especially
of insects
calves, should

( 49 have been described �s .

be treated as soon as possible
vectors
after
at
the
of D hominis in Latin Aro e ?ca
end
th
most are mosquitoes or muscoid fli e s)

CUTEREBRA INFESTATION IN SMALL ANIMALS

879
transp01t them to warm-blooded
al\jaccnt areas ( chest, neck, shoulders, and
the� where they hatch as the insects feed. ribs). Most cattle aff ecled have only h05

�ne
f�ae penetrate the skin of the animal swelling, but two swellings are occas10nally T��-n a few minutes of hatching and
seen. The regional lymph nodes are

W1 ;;n in the subcutaneous tissue for 4-18

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rem,...

·

·
enlarged and without treatment may
d tl l
k During tius per10 , 1e arvae grow
become enormous.

'\i1 m warbles with breatl1ing holes. When
wi

Mannheimia gra,nulomatis has been
ttire the larvae leave the host and drop

1na ,
recovered from lesions and is considered
d

Af
the m-ound, burrow, an pupate. ter
f
causal. The lesion that gives rise to
e pupal period, which lasts 4-11 wk, the
lechiguana is initiated by D hominis larvae.

�es emerge as adults. The complete life

M granuwmatis is consistently recovered
cycle takes 11-17 wk
from lesions of the clinical disease, and it is
thought to be mainly responsible for the

Clinical Findings and Pathogenesis:

characteristic tissue changes. The involve

I,arval penetration of the skin is accompament of a myofibroblast-like cell population nied by pain and local inflammation, and
that expresses mRNA for type I collagen is
pus gradually forms. Infested hides are
suggested to be associated with the increase
condemned at slaughter, and production of
of collagen deposition. It has also been
milk and meat is reduced. In 1982, it was esti demonstrated that macrophages activated by mated that cattle infested with D hominis

M granulomatis induce fibroblast prolif era-
resulted in a yearly reduction in weight of
tion. The habitat or source of M granuloma-

40.6 g/larva. In 2014, combining losses due
tis is not known. It has not been recovered
to reduced weight gain and hide damage,
from cattle without lechiguana.

infestation by D hominis in cattle raised in

Risto logically, lesions consist of focal

Brazil was estimated to cost producers $383
proliferation of fibrous tissue infiltrated by
million USD annually. Efforts to characterize plasma cells, eosinophils, lymphocytes, and and produce antigeni<; proteins that confer
sometimes neutrophils. The primary lesion
immunity againstD hom_inis have resulted .. is an eosinophilic lymphangitis, which in identification of a candidate vaccine, with results in eosinophilic abscesses, with 900/4 efficacy in immunized ,cattle;
occasional rosettes containing bacteria in

Treatment and Control: Different
their centers. The subcutaneous, tumorous
contact and systemic insecticides iri various mass produced may attain a size as large as .

formulations are available for treatment.

40 x 50 cm in 2 mo. Without treatment,

Generally, iJ hominis infestations in cattle
death occurs after 3""' 11 mo, probably due are susceptible to systemic organophosto inanition resulting from the enormous phates and macrocyclic lactone endecto-swellings.

cides, which may be approved and available

When well established, the disease is
locally.

clinically obvious. Diagnosis is confumed
by recovery of M granulomatis and

Lechiguana
observation of the characteristic histopathologic lesions.

Lechiguana is a sporadic; chronic disease of

Treatment with chloramphenicol (3 g/day
cattle that, thus far, has been reported only
for 5 days) or danofloxacin mesylate (1.25
from southern and southeastern Brazil, in
mg/kg/day for 3 days) results in rapid
areas where infection by Dermatobia
reduction of swellings, with almost
hominis is common. It is characterjzed by
lar
complete regression in 30 days. Conducting
ge, hard, subcutaneous swellings that
de
susceptibility tests is advisable before using
velop rapidly, mainly in the scapular and
other antimicrobials.

CUTEREBRA INFESTATION IN SM.ALL ANIMALS

� opportunistic, parasitic infestation of
o
are less host-specific and are usually
r gs, cats, and ferrets is caused by the

0den
associated with dog and cat infestations.

t or rabbit bot fly Cuterebra spp

Rarely, cats and dogs may be infested with

�rderDiptera, family Cuterebridae). Flies

Hypoderma spp or Dermatobia hominis.

th! .US�ally host-and site-specific relative to Ferrets housed outside may be infested by lI' life cycle. However, rabbit Cuterebra

Hypoderma or Cuterebra spp.

880

CUTEREBRA I N FESTATION IN SMALL ANIMALS

Etiology: Adult Cuterebm flies arc
abnonnal bc_>dY temperatures ( either
large �md bee-like and do not feed or bite.

hrpcr� hen�ua _or l�ypothennia). One

Females deposit eggs around the openings
h1stoncal f mdmg m cats with neural k:y
of animal nests, burrows, along rnn ways of
signs caused by Oulerebra inf estati ogi?

the nonnal hosts, or on stones or vegetation
an acute episode of violent sneezingons Is

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in these areas. A female fly may deposit 5-15 to months before c!inical presentati �eeks eggs per site and >2,000 eggs in her lifetime.

Common neurologic findings inclu o
de

Animals become infested as they pass
blindness, abnormal mentation, ands·
through contaminated areas; the eggs hatch
of unilateral prosencephalic disease. lgtls
in response to heat from a nearby host. In

Idiopathic vestibular signs in cats may b
the target host, the larvae enter the body
due to a?�rrm:t migr�t�on of the Parasite
through the mouth or nares during

Definitive diagnosis 1s made b
e
y findin
grooming or, less commonly, through open
and ident�g-a larva. In cats, CT scansg
wounds. After penetration, the larvae
may help identify larvae. Second insta.r
migrate to various species-specific
larvae are 5-10 mm long and are gray to
subcutaneous locations on the body, where
cream in color. Third instar larvae are dark
they develop and communicate with the air
thick, heavily spined and are the stage mo�
through a breathing pore. After ~30 days,
commonly seen by veterinarians.

the larvae exit the skin, fall to the soil, and
pupate. The duration of pupation varies

Treatment: Suspect lesions should be
depending on the environmental factors and explored by carefully enlarging and probing winter diapause.

the breathing pore or fistula with mosquito
forceps. It is not unusual for the parasite to

Clinical Findings and Diagnosis:

retreat into the opened pore, making it

Cuterebra lesions are most common in the
difficult to grasp. Covering the breathin
summer and fall when the larvae enlarge
g
pore with white petroleum jelly for 10-15
and produce a fistulous swelling ~ 1 cm
minutes before grasping the parasite can
in diameter. Dogs, cats, and ferrets are
make it easier to remove. The lesion should
abnormal hosts for this parasite; aberrant
not be squeezed, because this may rupture
migrations can involve the head, brain,
the larva and lead to a chronic foreign body
nasal passages, pharynx, and eyelids. In the
reaction and secondary infection. There are
skin, typical lesions are seen around the
anecdotal reports of larval rupture causing
head, neck, and trunk. The hair is often
anaphylaxis. If possible, the larva should be
matted, and a subcutaneous swelling is
removed in one piece; recurrent abscesses
present beneath the lesions. Cats often
at the site of previous Cut ere bra infestation groom the area aggressively. Pain at the
suggest residual infection or remaining
site is variable and usually associated with
pieces of larva The area should be
secondary infections. Purulent material
thoroughly flushed with sterile saline,
may exude from the lesion; the most
debrided (if necessary), and allowed to
common differential diagnosis is an
heal by granulation. Healing may be
abscess or foreign body.

slow. Ivermectin has been described

Free-roaming cats are more likely to
as a treatment for cats with CNS cuteredevelop lesions than indoor cats. Clinical briasis. Diphenhydramine ( 4 mg/kg, �
signs are often associated with the CNS and
is administered 1-2 hr before ivennectm
typically occur between July and Septem

( 400 mcg/kg, SC) and dexamethasone
be!. Cats may have depression, lethargy, or

(0.1 mg/kg, IV). Ivermectin is not approved
selZllfes; upper respiratory infections; or
for use in cats.

FLEAS AND FLEA ALLERGY DERMATITIS

There are >2,200 species of fleas recognized

Echidnophaga gallinacea (the poultrY t
worldwide. In North America, only a few
sticktight flea). However, by far_them�!. cat
species commonly infest dogs and cats:

fi l
prevalent flea on dogs and cats IS_ C Js

Ctenocephalidesfelis (the cat flea),
and
fleas cause severe irritation in a.rum

Ctenocephalides canis (the dog flea), Pulex rgy
people and are responsible for flea allt
simulans (aflea ofsmall mamrnals), and
r of
dermatitis. They also serve as the vec 0

FLEAS AND FLEA ALLERGY DERMATITIS

881

}ms-like �ickcU.si,�e m1d Ba rt o II clla sp
receive I.he proper stimulus to emerge, it
typd arc the mtennNhat.<' host. for filatid and all '

.

C 11
can remain quiescent in I.he cocoon for
stode paras1lt'S. at. cas haVt' been found several weeks unut a suitable host arrives.

�: infest >50 diff crent mmnmalian and avian

Emergence can be delayed up to 3G0 days

1iosts throughout t11e world. h� N ort.h
if preemcrged adults arc protected from

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Anleiica, the most commonly mfcsted hosts desiccation. Newly emerging fleas move to are domestic and wild ca.nids, domestic and
the top of the carpet pile or vegetation,
vild felids, raccoons, opossums, fetTets, and where they are more likely to encounter a

�omestic rabbits.

passing host. Under ideal conditions of
temperature (27° C [80.6° F]) and relative Transmissio�, Epidemiology, and
humidity (90%), a newly emerged cat flea
pathogenesis: Cat fl�as deposit their
can survive ~ 12 days before requiring a
eggs in the pelage of their host. The eggs are blood meal; at 500/4 relative humidity, this pearly white, oval with rounded ends, and
interval drops to -3 days. It is these newly

0.6 nun long. They readily fall from the
emerged unfed fleas that inf est animals
pelage and drop onto bedding, carpet, or
and bite people. There is generally minimal
soil, where hatching occurs in ~ 1-:--6 days.

inter-host movement of cat fleas. However,

Newly hatc�ed flea larvae are 1-5 mm long,
it has been documented that before Cf elis
slender, white, segmented, and sparsely
reaches reproductive status, there can be
covered with short hairs. Larvae are
some limited movement on and off hosts.

free-living, feeding on organic debris found

Cat fleas that have found a preferred host
in their environment and on adult flea feces

( eg, dog, cat, opossum, etc) and have
which are essential for successful

'. initiated reproduction generally do not
development. F1ea larvae.avoid direct light
leave their host unless forced off by
and actively move deep in carpet fibers or
grooming or insecticides.

under organic debris (grass, branches,

Depending on temperature and humidity,
leaves, or soil).·
the entire life cycle of the cat flea can be

La.Ivae are susceptible to desiccation,
completed in as little as 12-14 days or can
with prolonged exposures to relative
be prolonged for up to 350 days. However,
humidity <50% being lethal. The areas
under typical household conditions with
within a home with the necessary humidity
normal pet and human activity, cat fleas
are limited, and suitable outdoor sites are
complete their life cycle in 3-8 wk.

even rarer. F1ea development occurs

Adults begin feeding almost immediately
outdoors only where the ground is shaded
once they find a host. Female cat fleas can
and moist (1 %-200/4 soil moisture content)

consume 13.6 µL of blood daily, which is
and where the flea-infested animal spends

15 times their body weight. After rapid
a significant amount of time so that adult
transit through the flea, the excreted blood
flea feces will be deposited inta. the larval
dries within minutes into reddish black
environment. In the indoor environment,
fecal pellets or long tubular coils (flea dirt).

flea larvae probably survive only in the

F1eas mate after feeding, and egg producprotected microenvironment deep within tion begins within 24-48 hr off emales

C3.IJ)et fibers, in cracks between hardwood
taking their first blood meal. Female cat
floors in humid climates, and on unfinished
fleas can produce up to 40-50 eggs/day
concrete floors in damp basements. The
during peak egg production, averaging
larval stage usually lasts 5-11 days but may

27 eggs/day through 50 days. Individual
be prolonged for 2-3 wk, depending on
females may continue to produce eggs
availability of food and climatic conditions. for> 100 days.

After completing its development, the

Cat fleas are susceptible to cold. No stage
mature laiva produces a silk-like cocoon in of the life cycle ( egg, larva, pupa, or adult) which it pupates. The cocoon is ovoid, ~0.5 can survive exposure to <3° C (37.4 ° F) for cm long, whitish, and loosely spun. F1ea
several days. Therefore, cat fleas survive
cocoons can be found in soil, under
winters in north temperate climates as
vegetation, in carpets, under furniture, and adults on untreated dogs and cats or on on animal bedding. Once the pupa has fully small wild mammals ( eg, raccoons or developed (1-2 wk), the adult flea can
opossums) in the urban environment. As
e1!1erge from the cocoon when properly
these animals pass through yards in the
s��ated by physical pressure, carbon
spring or set up nesting sites in crawl spaces
dioXJ.de, substrate movement, or heat.

or attics, the eggs laid by surviving female

The preemerged adult ( which is a fully
fleas drop off and subsequently develop to
fonnect adult flea) residing in the cocoon is
adults. Cat fleas may also survive the winter
the stage that.can extend the longevity of
as preemerged adults in microenvironments
the flea. If the preemerged adult does not
protected from the cold.

882

FLEAS AND FLEA ALLERGY DERMATITIS

Fll'�lS can cause iron-deficiency anemia in dev<'lop naturally in dogs continually lwmily infl•sted hosts, particularly in young
exposed t.o flea bites. Although the
m1imals. Fleas in the genus Cte11or.ephnf-idcs pathophysiol�g� of FAD in c�ts is poorly have been repmted to produce anemia in
understood, s1m1lar mechanisms may exi
poultry, dogs, cats, goats, calves, and sheep.

st,

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Cat fleas are also involved in disease

Clinical Findings: Clinical signs
transmission. Mmine typhus, caused by
associated with FAD are variable and

Rickettsfo typhi and Rickettsiafelis, is a depend on frequency of flea exposure
mild to severe feblile disease of people
duration of disease, presence of seco�ct
charactelized by headaches, chills, and skin
or other concurrent skin disease, degre ary
rashes, with infrequent involvement of the
of hypersensitivity, and effects of prevji
kidneys and CNS. The disease is seen in
or current treatment. Nonallergic animafs
people and many small mammals along the
may have few clinical signs other than s
southeastern, southwestern, and Gulf
occasional scratching due to annoyance
coasts. In the USA, the plincipal transmisof flea bites. Those that are allergic Will sion cycle involves opossums and cat fleas.

typically have a dermatitis characterized

Cat fleas also serve as the intermediate host
by pruritus.

of the nonpathogenic subcutaneous filarid

In dogs, the pruritus associated with FAD
nematode of dogs, Dipetalonema
can be intense and may rnanif est over the
reconditum. Dipylidium caninum, the
entire body. Classic clinical signs are
common intestinal cestode of dogs and cats papulocrustous lesions distributed on the (and rarely children), develops as a
lower back, tailhead, and posterior and
cysticercoid in C felis, C can is, and .

inner thighs. Dogs may be particularly

Trichodectes can is. F1ea larvae ingest the sensitive in the flanks, caudal and medial
eggs of the tapeworm, which develop into
thighs, ventral abdomen, lower back, neck,
cysticercoids in the body of the flea. When
and ears. Affected dogs are likely to be
grooming themselves, dogs and cats may
restless and uncomfortable, spending much
ingest infected fleas, and the cysticercoids
time scratching, licking, rubbing, chewing,
are released.

and even nibbling at the skin. Hair may be
stained brown from the licking and is often

FLEA ALLERGY DERMATITIS
broken off. Common secondary lesions
include areas of alopecia, erythema,

F1ea allergy dermatitis (FAD) or flea bite
hyperpigmented skin, scaling, papules, and
hypersensitivity is the most common
broken papules covered with reddish brown
dermatologic disease of domestic dogs in
crusts. The rump and tailhead areas are
the USA. Cats also develop FAD, which is
typically the first, most evident, areas
one of the major causes offeline miliary
affected. As FAD progresses and becomes
dermatitis. FAD is most prevalent in the
chronic, the areas become alopecic,
summer, although in wann climates flea
licheni:fied, and hyperpigmented, and the
infestations may persist throughout the
dog develops secondary bacterial and yeast
year. In north temperate regions, the close
infections.

association of pets and their fleas with

In extremely hypersensitive dogs,
human dwellings creates conditions that
extensive areas of alopecia, erythema, and
permit a year-round problem. Temperature
self-trauma are evident. Traumatic moist
extremes and low humidity tend to inhibit
dermatitis (hot spots) can also occur. As
flea development.

the disease becomes chronic, generalized_

When feeding, fleas inject saliva that
alopecia, severe seborrhea, hyperkeratosIS,
contains a variety of histamine-like
and hyperpigmentation may develop.

compounds, enzymes, polypeptides, and

In cats, clinical signs vary from miniJnal
amino acids that span a wide range of sizes
to

(
severe, depending on the degree_of

40-60 �} and induce Type I, Type IV, and
sensitivity. The primary dermatitis IS a :S
basophil �ypers_ensitivity. F1ea-naive dogs
pa.pule,
e�os�d mtemuttently
which
to
often
flea
becomes crusted.

bites develop
miliary
either immediate (15 min) or delayed (24-48
dermatitis is typically found ?n �e
back, neck,
hr) reactions, or both, and detectable levels
and face. The miliary les!ons f
not actual
of
flea bites but a manifestation°

�0th �irculating IgE and IgG antiflea
a systemi
antib?dies. Dogs exposed continuously to
c allergic reaction that leads to
gene
flea bites have low levels of these circulating
ralized pruritus and an eczematous b
rash
antibodies and either do not develop skin

. Pruritus may be severe, evidence? }

repeat
reactions or develop them later and to a
ed licking, scratching, and che�o·

Cats
considerably reduced degree. This could
with FAD can have alopecia, facial
dermatitis, exf oliative dermatitis, and
indicate that immunologic tolerance may

"racing stlipe" or dorsal dermatitis.

FLIES

893

SHEEP KEDS
after shcming, and best results arc obtained
if an insecticide that has a residual activity

�cp kcd, Melophagus ovinus, is
of �3-4 wk is used. By this means, the keds

111e 5 f tllC most widely <listributc<l an<l that emerge from the pupae are also killed.

? nc 0 rau1 t external parasites of sheep.

Modem treatments to control lice also

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� 1 P<:,, :,.e also ke<ls tliat parasitize deer in 1•1e1 .... ,u
control keds.

NortllAmeiica (L1,'f�ptena depressa and

Dipping is an effective method of

M [ipoptenaferrisi ).

1 e
treatment. Completely submerging the

� eds are wingless dipter�s. _The adult is sheep in vats ensures the destruction of all

� 7 n1m Jong, brown o� reddis� m color, an�
keds present but, in most instances, does
covered with short, bnstly hrurs. The head 1s not kill the pupated larvae; a long-acting short and broad, and the legs are strong and
insecticide is required to kill newly
aimed with stout claws.

emerging keds. Large flocks of range

The female gives birth to a single, fully ·
sheep should be treated in a permanently
developed larva, which is cemented to the
constructed dipping vat. Smaller flocks
wool and pupates within 12 hr. A young ked
and farm flocks may be successfully
emerges after ~22 days. Females live
treated in portable, galvanized-iron

100-120 days and produce ~ 10 larvae during dipping vats or in smaller tanks, tubs, this time; males live ~80 days. The entire life or canvas dipping bags.

cycle is spent on the host. Keds that fall off·

Spraying may be as effective as dipping
the host usually survive < 1 wk and present
and is more convenient in some areas.

little danger of infestation to a flock Ked

Pressures of 100-200 lb/sq in. (7-14 kg/cm 2 ) nwnbers increase during the winter and
for short wool and 300-350 lb/sq in. (21-28
early spring when they spread rapidly
kg/cm 2 ) for long wool are commonly used.

through a flock, particularly when sheep are

Shower dipping is also sometimes used;
assembled in close quarters for feeding or
the sheep are held in a special pen and
shelter.

showered from above and below until the
fleece is saturated. The run-off is returned

Pathology: To feed, sheep keds pierce.the for recirculation, and the concentration of skin with their mouthparts and suck blood.

insecticide used is the same as for dipping.

They usually feed on the neck, breast,

The concentration of the insecticide can
shoulder, flanks, and rump but not on the
drop rapidly and become ineffective if the
back where dust and other debris collect in
instructions for replenishment are not
the wool. Ked bites cause pruritus over
followed explicitly.

much of the host's body; sheep often bite,

Jetting involves the forceful application
scratch, and rub themselves, thus damaging of the insecticide by means of a hand-held, the wool. The fleece becomes thin, ragged,
multiple-jet comb drawn through the short
and dirty. The excrement of the keds causes fleece. Although a little slower and less a permanent brown discoloration, which is
effective than dips or sprays, jetting may be
likely to reduce the value of the wool. Keds
advantageous for smaller flocks because it
also cause a defect in hides called a cockle, · . is economical and does not require a which affects the grade and value of the
permanent installation.

sheep skin. Infested sheep, particularly

Spot-on or pour-on formulations of the
lanibs and pregnant ewes, may lose vitality
newer pyrethroids are easy to apply and
and become unthrifty. Heayy infestations
c
very effective.

an considerably reduce the condition of
the hos

Powder dusting fits well into managet and even cause anemia. Keds also ment practices at shearing time. It is rapid,
transmit Trypanosoma melophagium, a
nonp
economical, and avoids wetting the animals.

athogenic protozoan parasite of sheep. Various types of equipment for dusting are available commercially.

�iagnosis: Close �pection of the

Ulllaged, dirty wool and underlying skin
reveals infestation by

SPIDER FLIES/NEW FOREST FLIES
the unique appearance of these wingless, hairy flies. · · ·

The spider or new forest fly, Hippobosca
equina, is widely distributed throughout

:;eatment and Control: Shearing
mo

Europe, Asia, and Africa. These winged
sh �es many pupae and adults. Thus,
ea
keds parasitize horses and rarely cattle
tr nng before lambing and subsequent
eatrnen
throughout the UK. Its bite is characterized
t of the ewes with insecticides to
control th
as a nuisance and disturbance to large
e remaining keds can greatly
domestic animals. It has a predilection for

�:du�e 1:he possibility of lambs becoming
feeding sites in the perineal region and
aVily infested. Sheep are usually treated
between the hind legs.

884

FLEAS AND FLEA ALLERGY DERMATITIS

Administration of topical or systemic
dl•monst.rat.cd aclivit.y against. adult fie
rl'sidual inst'ctichks and administ.rat.ion

:me! 1�rovidcs prolo�1gccl residual ovici:I:_
of topical, il\i<'ct.ablc, or oral IGHs have

1
activ1l.y, Ums rcducmg the potential for
become the prl'fencd methods to eliminate
genetic select.ion. Not only have topical!

flea infestations. ScV<'ral of these inscctiapplied IGHs been shown t.o be ovicidaJ Yb VetBooks.ir
cidt..'S and IG Rs have very effectively
orally administered or injectable (cats ' Ut
controlled fleas on pets living in infested
lufcnuron also provides ovicidal activ-i�nly)

premises. Field studies have shown that

Although not an IGR, selamectin also Y.

af oxolaner, fipronil with or without the
demonstrates ovicidal activity in cats
addition of (S)-methoprcnc, i.midacloprid,

Many pet owners mistakenly think that
indoxacarb, fluralaner, lufenuron (with an
flea products either kill all newly acquired
adulticide), selan1ectin, and spinosad can
fleas within seconds to minutes or
effectively control flea infestations, without
completely repel the�. But repellency ma
the need for premise treatment. Flea inf esta sometimes be noneXIStent, and residual Y
tions can be eliminated via regular monthly
products do not kill most fleas within
use of topical and systemic approaches,
minutes. Often fleas may live for &-24 hr
because most fleas are killed before and/or
and consume blood before being killed.

directly inhibited from reproducing.

Therefore, close scrutiny of treated pets

However, even if the systemic or topical
in an infested environment occasionally
insecticide used is 100% effective, control of results in a few flea sightings on pets for up an existing infestation will typically take 2-3 to 8 wk and occasionally longer until the mo because of the existing flea life stages in
infestation is eliminated.

the environment.

An additional complication for pet

If residual flea products are applied at the owners is infestation of the yard by wildlife appropriate dose and treatment intervals,
feral cats and dogs, or other infested pets.

residual activity between applications may

Often owners will treat their pets, but do not
be adequate to kill many newly acquired
realize the environment their pet frequents
fleas before egg production is initiated.

may be constantly infested with fleas by

However, flea survival and reproduction
wildlife or feral animals ( especially cats).

may occur before the next application for a

Even when pets go outdoors for only brief
variety of reasons: 1) residual activity < 100% periods, they are susceptible to becoming within the labeled time frame, 2) rate offlea infested. Additionally, people can act as kill slows during the third or fourth week,
carriers, bringing fleas into the household

3) delayed or infrequent product reapplicaand infesting unprotected pets.

tion, 4) simple Wlder-dosing, and 5) mechan

In cases of severe, massive flea infestaical removal of water-soluble insecticides tions or severe pet or human flea allergy,
during bathing or swimming. These probtreatment of the premises may be necessary.

lems may result in delays in control or

Pet owners should begin by conducting a
outright treatment failures.

mechanical control program. Helpful

Some of the currently available residual
procedures include washing pet blankets,
flea products may not be 1000/4 effective
throw rugs, and pet carriers; in addition,
against all cat flea strains between labeled
pet sleeping and resting areas should be
reapplication periods because of genetic
vacuumed thoroughly to help remove flea
variability of different flea populations.

eggs and larvae. Seat cushions and pillows

Many of the factors that allow flea
on sofas and chairs should be removed and
infestations to persist could possibly lead to vacuu genetic
med, and special attention given to
selection of resistant flea populacrevices
tions. Surviving
in sofas and
fleas
chairs and to areas
may be capable of
beneath sofas or beds where flea eggs and

�roducing viable eggs. Continued reproduction must feces
be halted
may drop fr
to
om the pet and ac
prevent persistent
cumub
flea infestations
late.

and selection

Intermittent-light flea traps can al_s
for

� e
resistant
fleas. Reproduction
bene
can
ficial. The overall goal of mechanic
be prevented by
a�trat
intervention is to reduce preexisting
ill

_ion of topical or systemic IGRs,
which provide prolonged
biomass of
residual
immature and adult life stages
ovicidal
activity, interrupting
the prem
future
ises. In addition, treatment of the
flea developtill
ment even after
premi
residual
ses with
activity
adulticides and IGRs maY s
of an

1
insecticide is
be
diminished.

necessary in some infestations; Contr_

Application
dl
of
methoprene
mar
or
be
pyriproxyfen
achieved by using insecticide�
to the hair coat

�oil
res
of dogs and cats rapidly kills developing
idual activity ( or by repeated app�c\
flea
on
of
eggs in addition
short
to residual

-acting insecticides) in comb Ula
ovicidal activity.

with an

The combination of

IGR to prevent development of
fipronil/(S)-methoprene flea eggs
or other
and larvae. Methoprene and
adulticidaJ/ovicidal products has
pyriproxyf en are the currently available

FLIES

885

JGRs for premise application. Insecticides
feasible in some situations or may not
d JGRs can be applied by broadcast
r
occur rapidly enough to control clinical
atment Q1and pmnp sprayers or
r
signs of FAD. Supportive medical therapy

� ssUl ized aerosols) or with total release must be instituted to control pruritus and

�erosols or "foggers." During application, secondary skin disease in hypersensitive

VetBooks.ir
the smface of all rugs and carpets must
animals. Systemic glucocorticoids are
be treated adequately. Efforts should be
often needed to control inflammation and

&rected to areas where flea eggs and larvae
associated pruritus. Short-acting predaccunmlate, such as carpets, cracks, grooves nisone or prednisolone can be adminisin hardwood floors, behind baseboards, tered initially at a dosage of 0.5-1 mg/kg/day,
under the edge of rugs, beneath furniture
tapering the dosage arid using alternate

(beds, tables, and sofas), and within closets.

day therapy until the lowest dose possible

In severe infestations, a second treatment
that still controls the pruritus is given.

may be necessary 7-10 days later because

As soon as flea control is accomplished,
of continued emergence of adult fleas from
the glucocorticoid can be discontinued.

cocoons hidden deep within carpets.

Anti-inflammatory therapy should never

Elimination of fleas in the yard can be an
be used as a substitute for flea control.

important aspect of flea control. Outdoor

Secondary bacterial skin infection can be
treatments ( eg, imidacloprid, cyfluthrin,
associated with FAD. Systemic antibiotics
fenvalerate) should concentrate on primary are commonly used to control the pyoderma areas of flea development, including
and thus reduce the associated inflammaprotected rnicrohabitats such as dog tion and pruritus. Selection of an approprihouses, within garages, under porches, and· ate antibiotic should be based on bacterial in animal lounging areas beneath shrubs or
cultures and results of antibiotic sensitivity
other shaded areas. Spraying flea control
tests.

products over the large expanse of a

Hyposensitization consists of adminisshade-free lawn generally is not beneficial in tering allergens to a hypersensitive animal controlefforts and is poor environmental
on a regular basis in an attempt to ob tarn a
practice.

state of clinical nonreactivity to flea bites.

Despite the efforts of pet owners, the

The: effectiveness of currently available
total elimination of fleas may not be .

whole flea extracts is controversial.

Ftl ES

.· i · ., ·.

Flies belong to the order Diptera, a l�ge,
vertebrate hosts and produce a condition
comp l ex order of insects. Most members
known as myiasis.

of this order have two wings ( one pair) as, ·
a�ults. However, there are a few wingless
dipterans. Dipterans vary greatly in size,
food source preference, and in the
d e yelopmental stage that parasitizes the

�al or produces pathology. As adults,

Blood-feeding dipte'rans can be classified

Pterans may intermittently feed on
ve
based on which sexes feed on vertebrate
rtebrate blood or on: saliva;'tears, or
m
blood and on food preference. In certain
ucus. These dipterans are referred to
species of dipterans, only the females feed

'.18 Periodic parasites and may serve as
on vertebrate blood, which is required for
mtermediate hosts for helminth parasites
egg laying; these species include black flies,

�r for protozoan parasites. They may also
te
sand flies, biting midges, mosquitoes, horse
mately
flies, and deer flies. In other species of
d
feed both on feces and on food
an m
ba �y P?ssibly serve as vectors for
blood-feeding dipterans, both male and
c

. .

et �a, Vll'Uses, spirochetes, chlamydiae,
female flies feed on vertebrate blood; these
l
de� �ae (maggots), dipterans may
species include stable flies, horn flies,
s el op
kin

� the subcutaneous tissues of the
buffalo flies, tsetse flies, sheep keels, and

, respiratory passages, or GI tract of
hippoboscid or l ouse flies.

886

FLIES

BLACK FLIES

Pathology: . B1·<·:u1sc or t.h_Pir !.iny, serrate 11111ut hp;1rls, l<'nWIP black flH•s mflict
l\h,mlw1� ofthe family Sinmlid:ll' arl'

Pain. d
hit<'s. Till' '.'ars,_1wck, h_1!ad, _and ahdorne/UI eommonly called black llies (although their

('att ic an� Jav�ml.1) fl'Pchng si_t.Ps. _In adcli of coloration may \'ary from black to gray to
f.io
to Jocal

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yt.'llow to olive) or buffalo gnats (becau�l:

_rea�:t.1ons (rednc-ss, 1tchmg, Whr.ai:

at the lntc site, there may be general
s)

their thorn.'\: is humpl'd over the head, gtvmg conditions that va� in intensity with the the appe,mmce of a buffalo's hu�np ): Black
sensitivity of the ammal and the number
flies me the tiniest of the blood-tce<lmg
of
bites. Attacks by large numbers of black
dipterans, 1-6 nun long. They hav� broad,
flies can cause severe damage and high
unspotted wings with thick, pronunent .

mortality in livestock. People may be
veins along tl1c ante1ior margins. Black fhes
sintllarly attacked.

have compow1d eyes; eyes off emales are

Death from bla�k �Y at.tac� apparently
distinctly separated, whereas those of the
results from a toxm m the saliva, which
males are contiguous above the antennae.

increases capillary permeability and

The palps have five segments. Fem�e b�ack permits the fluid from the circulatory flies have scissm'-like mouthparts with tiny,
system to ooze into t�e body �avity and
sharp, serrated edges. The female flies
tissue spaces. The amrnal rapidly succumbs
require a blood meal to lay eggs. Males are
to a mass attack but can recover quickly if
never bloodf eeders but instead feed on
protected from further attacks. Reduced
nectar from flowers.

milk, meat, and egg production may result

Although there are > 1,000 species of
from less extensive attacks. Certain specie
black flies, only a few are considered
s
of black flies sometimes cause losses in
important as pests. Black flies feed on all
poultry, either by direct attack or through
classes of livestock, wildlife, birds, and
transmission of Leucocytozoon spp. In
people.

Africa, Simulium damnosum and S neavei

Black flies are distributed throughout the
are important as vectors of Onchocerca
world in areas where conditions permit
spp. S neavei is an important vector of
development of the immature forms. Larvae O volvulus. In Central America, S ochra
nearly always are found in swiftly flowing,
ceum, S metallicum, S callidum, and
well-aerated water; shallow mountain

S exiguum are important vectors of
torrents are favored breeding places. Some

Onchocerca spp. S ochraceum and
species breed in larger rivers; others live in

S metallicum
temporary or sernipennanent streams.

also are vicious biters.

Black flies are particularly abundant in the

Diagnosis: Black flies are most often
north temperate and subarctic zones, but
collected in the field and not found on the
many species are found in the subtropics
and tropics where factors other than
animals. Adult flies can be identified by
seasonal temperatures affect their
their small size, humped back, prominent
developmental and abundance patterns.

venation in the anterior region of the wings,
and tiny, serrat

Larval black flies are cylindrical and
ed mouthparts. Identification
attach themselves by a large posterior
of black flies to genus and species is
sucker. On the anterior end are the
probably best left to an entomologist.

mouth parts and a pair of brush-like organs.

Treatment and Control: If public funds

The larvae are carnivorous. Just below the
and trained supervisory personnel are .

mouthparts is an arm-like appendage called
available, large-scale control of black fli�s JS
the proleg. Larvae attach to rocks or other
possible by treating breeding streams with
solid objects in the stream, sometimes
an approved
clinging to aquatic or emergent vegetation.

larvicide. However, black fly
control is

The mature larva spins a triangular cocoon
difficult because of the large
number
on the floor of the stream. The oblong pupa
of flowing water breeding sites.

Streams
has one dorsal and one ventral respiratory
can be treated using the natural
product
tube, the branches of which float out of the

, Bacillus thuringiensis var ali3Il
israelen
cocoon.

sis, a product with no manun
toxicity.

Black flies produce one to six generations

. 1ves
per year, depending on the species and

Treatment of streams and 1ivers wvo
climatic conditions. Adult female feeding
techniques similar to those used by
activity may last from 2-3 wk to 3 mo. Adult
mosquito abatement programs. � � ru1;eir
black flies may fly 8--1 1 miles ( 12.,.. 18 km)

pesticides should not be used owing to
from swiftly flowing streams; migrating
potential negative effects on the e�vrron�er
windbome swarms have been known to
ment. Pesticide treatments involVU1:g ��o
travel �250 km
surfaces

.

or large land areas are subJec
governmental regulation and must be

FLIES

887
perfonncd with_ due regard for possible
rcticulocndothelial cells of capillaries, the
deleterious environmental eff ect.s and
spleen, and other organs but may be seen in
residues in foo� products.

monocytes, polymolJ)honuclear leukocytes

Adult black flies ;u-e small enough to pass
and macrophages of people, dogs, cats,
through window screens or may come
horses, and sheep (see p 800).

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indoors on or within a pet's hair coat. More
often, tl1e adult fe_male flies prefer to feed

Diagnosis: Like black flies, sand flies can outdoors and d�mg the daylight hours.

most often be collected in the field and are

Because black �es feed predominantly
not found on animals. They can be identified
during the daylight hours, it is wise to limit
by their small size and hairy wings and
exposure of pets to swiftly flowing streams.

bodies. Identification of genus and species
pet owners concerned about black fly bites
is probably best left to an entomologist.

may use over-t�e�counter insect repellents.

Aerosols contarrung pyrethrins may provide Treatment and Control: Insecticide only temporary relief.

spraying of larval habitat is usually not

Because area-wide control of black
possible because of the difficulty of
flies is difficult and expensive, livestock
accessing breeding sites. Removal of dense
producers frequently resort to the daily
vegetation discourages breeding. Spraying
use ofrepellents to protect their animals.

of residual insecticides on surfaces in the

Extension entomology personnel should be home is the main way to control sand flies; contacted for the latest approved recomhowever, this is ineffective for species that mendations and withdrawal times.

bite away from the home. In general, populations of sand flies have been reduced SAND FLIES
as a result of intense mosquito control
programs. Deltamethrin-impregnated

The phlebotomine sand flies, Phlebotomus
collars may be recommended to dog owners
spp (Old World sand flies) and Lutzomyia
to protect their pets from sand fly bites.

spp (New World sand flies), are members
of thefamily Psychodidae. These flies are
confined primarily to the tropical and

BITING MIDGES
subtropical regions of the world. Members
of these genera are tiny, moth-like flies,

The biting midges, "no-see-urns," or punkies

~ 1.5-4 mm long. The legs are as long as the
belong to the family Ceratopogondiae. The
antennae, comprising 16 segments that
most common biting midges are Culicoides
often have a beaded, hairy appearance;
spp. They are associated with aquatic or·

They are commonly known as sand flies,
semi.aquatic habitats, eg, mud or moist soil
moth flies, or owl midges. The key
around streams, ponds, and marshes. Biting
morphologic feature for identification is
midges are tiny gnats (1-3 mm long) and,
that the body of the sand fly is covered
like black flies, inflict painful bites and suck with fine hairs; The females have piercing
the· blood of their hosts, both people and
mouthparts and feed on blood of a variety
livestock.

of warm-blooded animals, including people.

�any species feed on reptiles. Male sand

Pathology: Culicoides spp are vicious
flies suck moisture from any available
biters and can cause intense irritation and.

s_ource and are even said to suck perspiraannoyance. In large numbers, they can tion from people. Sand flies tend to be active cause livestock to be nervous and interrupt

?nlY at night and are weak fliers; their flying their feeding patterns. These gnats tend to

� d�terred by air currents, even slight ones.

feed on the dorsal or ventral areas of the
unng the day, sand flies seek protection in host; feeding site preference depends on the cr��ces and caves, among vegetation, and
species of biting gnat. They fly only in the

Within ?ark buildings. They often seek
warm months of the year and are most
protection within rodent and armadillo
active before and during dusk. They feed
burrows; these mammals can serve as
often on the mane, tail, and belly of horses.

�servoir hosts for Leishmania spp. Sand

Horses often become allergic to the bites,
es bree
scratching and rubbing these areas, causing
th
d in dark, humid environments
at have a supply of organic matter that
alopecia, excoriations, and thickening of the
terves as food for the larvae. They do not
skin. This condition has several names,
reed in aquatic environments.

including culicoid hypersensitivity in .

Canada, Queensland itch in Australia,

:�tholo�y: These tiny flies serve as an

Kasen in Japan, sweat itch, and sweet itch.

Because it is often seen during the warmer

P/trmediate host for Leishmania spp, a

0 ozoan parasite that infects the
months of the year, it is also referred to as

888

FLIES
summer dermatitis. These fli<'s also serve
have_h<�<:n dc>s�:rihPd worldwide, with _1
as the intenncdiate host. for 011rhor.erca

5
spccH'S found m the temperate regions fO

C<'l'Vicalis; the microfilariac of this

· NI

.

o

Nmth Anwnca. osqmtoes are found in
nematode arc found in the skin of horses.

such diver�e areac, as salt marshes of the

Onchocerciasis (see p 905) is a nonseacoastal plams to snow J?Ools above 14,0oo f VetBooks.ir
sonal dennatosis that is similar to sweet itch ( 4,300 m) to the gold mrnes of India 3,6QQ ft but usually is less pnuitic and affects the

(1,100 m) below sea level. The volume of t
head, neck, and belly. These flies also
water in which mosquitoes will breed van es
transmit the bluetongue vims (see p 738)

from that within an empty can or tree hole
in sheep and cattle.

to large shallow pools of accumulated
standing water from either rain or sno�

Diagnosis: Like black flies and sand �es,
melt.

biting midges are most often collected m

Mosquitoes lay their eggs either on the
the field and not found on the animals. In
surface of standing water ( eg, Aedes and
contrast to the clear, heavily veined wings of Psorophora spp) or on a substrate ( such black flies, the wings of Culicoides spp are as damp soil) where the eggs hatch after
mottled. Identification is probably best left
inundation from rainfall, irrigation, snow
to an entomologist.

melt, etc. Larval mosquitoes are known as
wrigglers, whereas pupal mosquitoes are

Treatment and Control: Lruvae may
known as tumblers. These stages are always
be attacked in their breeding grounds.

aquatic and are found in a wide variety of

Extension entomology personnel should be habitats. Large numbers of mosquitoes can contacted for the latest approved recombe produced from eggs laid in relatively mendations.

small bodies of water. Some species have

Bio Kill Stable SprayTM, a modified
several generations per year. The flight
perrnethrin, is approved for the spraying of
habits of adult mosquitoes vary with the
stables and horseboxes to aid in the control
species; some Aedes sp migrate many miles
of biting midges. A backpack or handheld
for their aquatic, larval habitat. In strong
bulk pesticide spray pack, turbo-blower, or
winds, mosquitoes may be carried great
fogger should be used. A fine spray should
distances. Some species overwinter as eggs,
be produced under pressure, in the amount
while others overwinter as adults.

of 500-750 mL per stable ( stable size: 3 m x

3.5 m to 4 m x 4 m). All surfaces in the stable Pathology: Only female mosquitoes should be sprayed. A reappHcation 7-10
actively take a blood meal so that they can
days later is needed. Thereafter, application lay eggs. Males feed on nectar, plantjuices, every 3-4 wk should provide ample product and other liquids. Mosquitoes annoy buildup on the walls.

livestock, cause blood loss, and transmit

Because Culicoides spp are poor flyers,
disease. Also, the toxins injected at the ti.me
an electric fan may be used in the stable to
of biting may cause systemic effects. The
create air movement around the horses. Fly
feeding oflarge numbers of swarming
repellent ear tags attached to the horse's
mosquitoes can cause significant anemia in
mane and tail (not approved in the USA);
domestic animals. Although they are Imown
pyrethrurn synergized with piperonyl
for spreading malaria, yellow fever, dengue,
butoxide, applied weekly; butoxypolyproand elephantiasis in people, mosquitoe� 3:e pylene glycol 800, applied daily; stable
probably best known
blankets; and fine screens on stable doors
in veterinary medicine
as
and windows have been used with mixed
the intermediate host for the canine
heartwo
success. Topical insecticides such as
nn, Dirojilaria immitis, and as the
vectors
pyret�
of the equine viral encephalitides,

_( eg, cypermethrin or cyfluthrin),
especially m pour-on formulations, may also including West Nile virus.

A
be used to control these adult pests in large
nopheles quadrimaculatus is the . rn
interm
animals.

ediate host for malaria (Plasmodiu
spp) in people and other primates. Aedes
aegypti is the yellow fever mosquito,

MOSQUITOES
transmitting this virus among people. f

Pso

Mo
ro

�q�toes are members of the family
phora columbiae is a sever� peSt �

Culic1dae. Important genera include Aedes
both livestock and people in the nee fie\.

Anopheles, Culex, Culiseta, andPsoro-
of Louisiana and Arkansas. Culex tarsa is
is an
phora. Although they are tiny, fragile
important vector of Western equine
ence
dipterans, mosquitoes are perhaps some of
phalitis and is found in the western, iS
centr
the most voracious of the blood-feeding
al, and southern USA. Aedes veX��e
an impor
arthropods. Approximately 300 species
tant nuisance species found J..I1

Midwest. Aedes albopictus is a recently

FLIES

889

. troduced Asian species that also spreads

Valuable animals should be housed in closed
u�now fever, dengu�, and equine encephali or screened buildings and the mosquitoes

� certain Mm1.-wnrn spp are severe pests
inside killed with a fog or aerosol formula

�liivestock in Florida. In Central and South
tion of an approved insecticide. Temporary

Aineiica, the adult female bot fly Dermatorelief may be afforded by a spray or "wipe VetBooks.ir
bia hominis fastens her eggs to a species of on" of materials commercially available.

psorophora mosquito, which then transmits

Walking pets or allowing pets free range,
them to tl1e mammalian host during feeding. outdoor access in the early morning or early evening hours when adult mosquitoes are

Diagnosis: Adult mosquitoes are most
most abundant should be avoided to reduce
often collected in the field and are not found exposure to mosquito bites. Imidacloprid on animals, Adults are 3-6 mm long and
has been used as a topical prevention and
slender, with small, spherical heads and
treatment of ticks, fleas, and mosquitoes on
long legs. The wing veins, body, head, and
dogs and puppies ?.7 wk old, weighing >2 lb
legs are covered with tiny, leaf-shaped

(0.91 kg). It has been shown to repel adult
scales. The long, filamentous antennae have female mosquitoes for as long as 4 wk.

14-15 segments and are plumose in the

Unfortunately, it cannot be used on cats.

males of most species. They also have

Mosquitoes are not attracted to light; thus,
proboscides designed for lacerating tiny
electrocution devices are not helpful in
blood vessels and sucking up pooled blood.

mosquito control and may actually be

Identification of the plethora of mosquito
detrimental, because they may destroy
species ( adult, larval, and pupal stages) is
beneficial insects that prey on mosquitoes.

probably best left to an entomologist.

A combination of two compounds,
imidacloprid and permethrin, works to

Treatment and Control: Area control of repel and kill the many species of bloodmosquitoes usually involves the cooperafeeding mosquitoes that often feed on dogs.

tion of many individuals and can be

Monthly application of this product repels
accomplished successfully by experienced
and kills mosquitoes, preventing their
personnel with proper equipment. Areas
blood-feeding activity and ostensibly
that can serve as breeding sites for mosquito helping to prevent transmission of larvae should be eliminated or reduced. In··
organisms such asDirojilaria immitis
addition; area programs generally include
from dog to dog. This product may not be
extensive use oflarvicides; however,
used on cats.

mosquito larvicides can disrupt the normal
ecologic balance within an ecosystem.

HORSE FLIES AND DEER FLIES

Recently, the use of various species of fish
as biologic controls has been successful. In

Tab anus spp (horse flies) and Chrysops
massive emergence of adult mosquitoes,
spp (deer flies) are large (up to 3.5 cm

Particularly when disease transmission is a
long); heavy bodied, robust dipterans with
concern, application of an insecticide active powerful wings and very large eyes. They against the adult may be necessary.

are swift fliers. These flies are the largest in Caution is advised with area treatment
the dipteran group, in which only the
programs, because many nontarget
females feed on vertebrate blood. Horse
organisms ( eg, fish, shrimp, bees) may be
flies are larger than deer flies; many horse
exposed to insecticides. A local extension
flies are highly colored. Deer flies are
entomologist should be consulted regarding medium sized; they have a dark band appropriate materials for use on animals or passing from the anterior to the posterior Within premises. Large-scale programs
margin of the wings and a yellow to brown
usually are coordinated by mosquito
abdomen with black patches and longitudiabatement district or other government nal bands.

agencies.

Adult horse flies and deer flies lay eggs in

It is difficult for individual producers to

Pr
the vicinity of open water. Larval stages are

?tect their animals; residual sprays on the found in aquatic to semiaquatic environ

�als d? not prevent feeding females
ments, often buried deep in mud at the

0m landing, and currently available
bottom oflakes and ponds. The developing

�epellen
larval stages have sharp mandibles and are
on _ts do not confer adequate protec�
d
fr unng massive emergence. Protection
predatory on smaller vetebrates and inverteom adult mosquitoes may be provided by f
brates; they will even lightly nip at the toes

0und and, in some cases, aerial applicaof people wading in shallow water. This is on of an insecticide at the time of
an unusual dipteran fly in that both larval

�ergence. Depending on local conditions,
stages and adult flies are capable of

Protection may be of short duration.

inflicting pain as they bite.

890

FLIES

Pathology: Adults arc seen in stmtmN,
brownish gray, the oul.er of four thor
particularly in sunlight. Adult. females of
stripes is hrokcn, and the abdom(•n h�ic
both species foed in the vicinity of open
checkered appearance. It ha<; a bayon , a
water and have reciprocating, scissor-like like, needle-sharp proboscis that �heetn mouthpart.s, which they use to lacerate
rcst, protrudes forward from the 'heacl at

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tissues and lap up the oozing blood. They

The wings, when at rest, are widely sp·
consume 0. 1-0.3 mL of blood at a single
at the tips. These flies are found throuriad
feeding. Bites are painful and irritati�g.

out the world. In the USA, they are foug

These flies feed primarily on large amin the mid western and southeastern nd mals such as cattle and horses, which
states.

beco�e restless when the flies are

The larval and pupal forms develop in
present. Site preferences include the
decaying organic matter, including grass
underside of the abdomen around the
clippings and seaweed along beaches. In the
navel, the legs, or the neck and withers.

mid western USA, larvae can be found in Wet

Horse flies and deer flies feed a number of areas around the edges of hay stacks and times in multiple feeding sites before they silage pits. Where cattle are fed hay, become replete. When disturbed by the
breeding can occur at the edge of the
animal's swatting tail or by the panniculus feeding area where hay has become mixed reflex, the flies leave the host, yet blood
with urine and feces. The life cycle in the
continues to ooze from the open wound.

field can be completed in 2-3 wk, and adults

These flies may act as mechanical
may live �3--4 wk.

transmitters of anthrax, anaplasmosis,
tularemia, and the virus of equine

Pathology: Both male and female stable
infectious anemia.

flies are avid blood feeders, feeding on any
warm-blooded animal. Stable flies stay on

Diag nosis: These flies can be identified by the host for short periods of time, during their large size, powerful wings, compound
which they obtain blood meals. This is an
eyes, and lacerating scissor-like mouthoutdoor fly; however, in the late fall and parts. Species identification of intact adult
during rainy weather, it may enter barns.

and larval horse and deer flies is probably

Horses are the preferred hosts. The fly
best left to an entomologist.

usually lands on the host with its head and
proboscis pointed upward and inflicts

Treatment and Control: Horse flies
painful bites that puncture the skin and
and deer flies are the most difficult to
bleed freely. It is a sedentary fly, not moving
control of all of the bloodsucking flies.

on the host. Stable flies usually attack the

Many of the adulticide compounds used for
legs and ventral abdomen and may also bite
other biting flies can kill both horse and
the ears. They can be a problem in cattle
deer flies. However, because these flies
feedlots in the Midwestern USA. The
are intermittent feeders that alight on the
damage inflicted to cattle is caused by the
host for only a short time, they may not be
painful bite and blood loss, and the irritation
exposed to these compounds long enough
results in a reduced efficiency in converting
to be affected. Thus, larger doses of the
feed to meat or milk. In pets, stable flies
compounds may be required.

pref er to feed on the tips of the ears of dogs

Horse fly traps have been effective when
with pointed ears, especially Gennan
used around cattle confined to manageable

Shepherds.

areas. For livestock, pyrethroid pourons

Stable flies are mechanical vectors of
function as limited repellents. Self-applicaanthrax, surra, and equine infectious tion techniques are usually not effective for
anemia. They
horse and deer flies.

are the intermediate host for

Habronema muscae, a nematode found in

Manipulation of these flies' aquatic
the stomach of horses.

habitat has been attempted by removing
unnecessary woody plants from residential

D.

Stable flies are il ·ctentified

1agnosis:

eas Y 1
areas or draining wet areas. Application of
fthe
by their size
insecticides in the water may have

( about the same as that 0
house fly),
detrimental environmental effects.

coloration, and bayonet-like the
proboscis that protrudes forward from
head.

STABLE FLIES

Treatm

The stable fly, Stomoxys calcitrans, is
ent and Control: The main
considerat
often called the biting house fly. It is about
ion in stable fly control is }f
sanitatio
the same in size and general appearance
n, which can effect up to gQ9o feed
control. Area
as Musca domestica, the house fly. It is
s along fence rows, under or
bunks, or wherever manure and straW

FLIES

891
decaying matter can accumulate should
least clisturbed by tail switching. On hot,
be kept clean, h�cau�e the�e substrates
smmy days, horn flies accumulate on the

-ovide the medmm m wluch the larval fhes ventral abdomen.

��velop. If good sanitation procedures are

Newly emerged flies seeking their host
practiced, che1�1ical_ contr?� is less likely to may travel 7-10 miles (11-15 km) but

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be needed. Vanous msect1c1des can be
usually find a host in much shorter
sprayed where flies may be resting in barns
distances. Migration seldom occurs over
or on fence rows.

any great distance. In the southern USA, fly

Stable flies feed on the lower portions
populations on individual animals may be
of cattle, around the legs and belly,
in the thousands, especially on bulls not
including the udder. They usually feed
receiving chemical treatment; in the north,
only once or twice daily for short periods, they may not exceed 100, although the thus rnininlizing exposure to compounds
damage inflicted is similar.

applied to these areas. Often, insecticides
applied to these _body regions are rubbed

Pathology: Horn flies feed frequently
off by contact with dense vegetation and

(as many as 20 times/day), sucking blood
mud or rinsed off when dairy cattle are
and other fluids; fem ale flies are more
rinsed before milking. Direct animal
aggressive than males. Feeding causes
application of sprays and dusts may be
pain, annoyance, and blood loss in cattle.

used in some instances to protect large

Irritated animals also lose weight because
animals. Insecticides tised for direct
of their less efficient use of feed. Heavy
animal application usually have short
infestations cause lesions along the ventral
residual activity. This type of application
midline of the animal. Horn flies cause
is quite labor intensive.

great economic losses annually in the USA;

•A combination of two compounds,

14% reductions in weight gains on range
imidacloprid and permethrin, works to
cattle. and losses of 12-14 lb (5--6 kg/head)

repelS calcitrans. Monthly application
in weaned calves are common. In dairy
repels these flies and prevents their blood
cattle, milk production may be reduced
feeding on dogs, but the product does not

10%-20%. These flies also serve as the
kill this type of biting fly.

intermediate host for Stephanofil,aria
stilesi (see p 907), a :filarial parasite that

HORN FLIES
produces plaquelike lesions on the ventral
abdomen of cattle.

The.common name of Haematobia
irritans comes from the fact that these

Diagnosis:· Horn flies can be easily
flies often cluster in the hundreds around
identified by their dark color, size ( ~3-6 mm
the base of the horns of cattle .. This major
long, approximately half the size of a stable
pest of cattle is found in most cattlefly), and bayonet-like proboscis that producing areas of the world.· Populations
protrudes forward from the head.

are common in Europe, North Africa, Asia

Minor, and the Americas. Throughout .

Treatment and Control: Horn flies

North America, horn flies are found almost are relatively easy to control with exclusively on cattle, but they will feed on
whole-animal chemical sprays and with
h?rses, sheep, goats, and wildlife. Horn
self-treating devices ( eg, dust bags or back
flies are found-in much larger numbers and rubbers) in a forced-use manner. Dust for longer periods of time in the southern
bags are most effective when cattle are
and southwestern USA.

required to pass under them daily to reach

Adult horn flies spend their entire life on
water or mineral supplements. Dust bags
th:ir host, and fem ales leave only to
f
leave a deposit of insecticides along the

VJ.posit eggs on fresh cow feces, where
dorsum, the areas where horn flies spend
arva1 and pupal development occurs. In the
so
most of their time. Back rubbers allow
uthern USA, the life cycle can be as short cattle to treat themselves as they scratch.

as 1 wk, but in cooler climates and in the . The insecticide should be diluted with a

�ring or fall, development can take 2-3 wk· good grade of mineral oil according to some wanner areas ( south Florida and
label instructions. Feed additives pass

�thernmost Texas), horn flies reproduce
through the animal to kill larval stages

OUghout the year.

that develop in fresh cow feces. All
h When the air temperature is <70° F (21 °C), animals must consume a minimum dose h 0lll flies cluster around the base of the
tllls
of a feed additive regularly. Insect growth
of cattle. In warmer climates, the flies regulators also prevent development

�h n cluster in large numbers on the
of larvae in cow feces. When used

0ulders, back, and sides; these areas are according to label directions,

892

FLIES
insecticid0-impregnated cattle ear tags
remove -801¼1 of the buffalo flies each r

(cg, pyret.hroids) release small amo1mts
the cat.Uc pa!-;s through. When cattle 1rne
of insectiddes that are distribute cl over
through the trap every day or every tass
e
the ;.mimal during grooming or nibbing.

day, sufficient fly control is usually conct

Animals should be tagged at or near the
achieved.

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beghming of fly season, the tags removed_at
or near the end of fly season, and alternative TSETSE FLIES
methods with nonpyrethroid insecticides
used near the end of fly season. Pour-on

The tsetse flies, Glossina spp, ar;----.

insecticide fornmlations are also effective
important blood-feeding flies found in
against horn flies. These compounds are

Africa (latitude 5°N to 20°S). Tsetse flie
applied to cattle in measured doses based
are narrow bodied, yellow to dark bro�
on body weight. Most of these pour-ons
and 6-13.5 mm long. When resting, their '

function as contact insecticides.

wings are held over the back in a scissorlike configuration. The thorax has a dull BUFFALO FLIES
greenish color with inconspicuous spots
or stripes. The abdomen is light to dark

Buffalo flies, Haematobia irritans
brown.

exigua, are similar to horn flies in size and Both sexes are avid blood feeders. One
appearance and in feeding and breeding
copulation renders a female fly fertile for
habits. The buffalo fly is a primary pest of
her lifetime, during which she can produce
cattle and water buffalo but occasionally
as many as 12 larvae. She produces one
feeds on horses, sheep, or wildlife. It is
larva at a time, retaining it within her uterus·
distributed throughout northern Australia after -10 days, the larva is deposited on and New Guinea and is found in parts of
loose, sandy soil, where it digs in and begins
southern, southeastern; and eastern Asia
pupation within 60-90 min. This pupation
as well as Oceania; it is not found in New
period averages -35 days, after which the

Zealand. Its life cycle is similar to that of
adult emerges. Adult flies feed avidly on
the horn fly; the adult leaves the host long
vertebrate blood approximately every 3
enough to oviposit on fresh manure,
days.

where development occurs. The life cycle
may take as few as 7-10 days, depending

Pathology: Tsetse flies serve as the
on weather conditions.

intermediate hosts for several species of
trypanosomes that cause fatal diseases of

Pathology: Buffalo flies irritate and
both domestic animals ( nagana) and people
annoy animals, usually biting about the

(African sleeping siclmess ). Trypanosomes
shoulders and withers. Bite wounds may
invade the blood, lymph, CSF, and various
provide a site for screwworm ( Chrysomya
organs of the body, such as the liver and
bezziana) infection. During hot weather,
spleen. Nagana, a related complex in cattle
the flies move to shaded parts of the body.

caused by Trypanosoma brucei, has

Affected animals suffer blood loss and are
occurred throughout enormous areas
irritated by the flies; feed efficiency and
estimated to be as great as one quarter of
production may be affected adversely.

the African continent. The disease is fatal to
horses, mules, camels, and dogs. Cattle,

Diagnosis: Buffalo flies can be identified by sheep, and goats usually survive, except their dark color, size ( approximately half that when parasitized by certain strainS. ManY
of a stable fly), and bayonet-like proboscis
wild ungulates native to Africa show no
that protrudes forward from the head.

evidence of harm. (See also TRYPANosoMJASIS, p 35.)

Treatment and Control: Insecticides
should be avoided in the treatment of

Diagnosis:

d
buffalo fly populations. Many of the chemi

Tsetse flies can be identifi! ng
by their
cals used to treat these flies result in meat
honeybee-like appearance, thet ;e
prob
res�dues. Buffalo flies have developed
oscis with its onion-shaped_bulb � the
base,
resistance to the synthetic pyrethroids
and the unique wing venation Wl d
and to some of the organophosphates.

characteristic cleaver- or hatchet-shape

Buffalo fly traps have been developed in
cell in the center of the wing.

Australia. The trap consists of a rounded
fl

Treatm
i scail
clear plastic tent through which the cattl�
ent and Control: Tsetse . !

be
walk The flies are brnshed off the cattle
controlled by catching and trapplllo

(tsetse
within the tent and are then trapped inside
traps), bush clearing, fly �cree:

repelle
where they die of desiccation. These traps
nts, insecticides, and sterile Ill
release techniques.

FLIES

893

SHEEP KEDS
after shcming, and best results arc obtained

;..---

,,. , .,

.

.

if an insecticide that has a residual activity
hecp kcd, 1l1e .op rn.57us mnnus, 1s

'fl1e 5
of 2:!3-4 wk is used. By this means, the kcds
f tl\C most widely distributed and
that emerge from the pupae are also killed.

? ne 0 ruu1 t external parasites of sheep.

Modem treatments to control lice also

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� l P�e :,.e also keds t11at parasitize deer in 1.1e1 ,u
control keds.

NortliAmeiica (fa?�ptena depressa and

Dipping is an effective method of

�eolipoptenaf en·isi ).

1
treatment. Completely submerging the

Keds are wingless dipter3:11s. _The adult is sheep in vats ensures the destruction of all

� 7 nm1 Jong, brown o� reddis� m color, an�
keds present but, in most instances, does
covered with short, bnstly hrurs. The head 1s not kill the pupated larvae; a long-acting hort and broad, and the legs are strong and
insecticide is required to kill newly

!nned with stout claws.

emerging keds. Large flocks of range

The female gives birth to a single, fully
sheep should be treated in a permanently
developed larva, which is cemented to the
constructed dipping vat. Smaller flocks
wool and pupates within 12 hr. A young ked
and farm flocks may be successfully
emerges after ~22 days. Females live
treated in portable, galvanized-iron

100-120 days and produce ~ 10 larvae during
this ti
dipping vats or in smaller tanks, tubs,
me; males live ~80 days. The entire life or canvas dipping bags.

cycle is spent on the host. Keds that fall off

Spraying may be as effective as dipping
the host usually survive < 1 wk and present
and is more convenient in some areas.

little danger of infestation to a flock Ked

Pressures of 100-200 lb/sq in. (7-14 kg/cm 2 ) numbers increase during the winter and
for short wool and 300-350 lb/sq in. (21-28
early spring when they spread rapidly
kg/cm 2 ) for long wool are commonly used.

through a flock, particularly when sheep are

Shower dipping is also sometimes used;
assembled in close quarters for feeding or
the sheep are held in a special pen and
shelter.

showered from above and below until the
fleece is saturated. The run-off is returned

Pathology: To feed, sheep keds pierce,the for recirculation, and the concentration of skin with their mouthparts and suck blood.

insecticide used is the same as for dipping.

They usually feed ·on the neck, breast,

The concentration of the insecticide can
shoulder, flanks, and rump but not on the
drop rapidly and become ineffective if the
back_where dust and other debris collect in
instructions for replenishment are not
the wool. Ked bites cause pruritus over
followed explicitly.

much of the host's body; sheep often bite,

Jetting involves the forceful application
scratch, and rub themselves, thus damaging of the insecticide by means of a hand-held, the wool. The fleece becomes thin, ragged,
multiple-jet comb drawn through the short
and dirty. The excrement of the keds causes fleece. Although a little slower and less a pennanent brown discoloration, which is
effective than dips or sprays, jetting may be
likely to reduce the value of the wool. Keds
advantageous for smaller flocks because it
also cause a defect in hides called a cockle, ·. is economical and does not require a which affects the grade and value of the
permanent installation.

sheep skin. Infested sheep, particularly
l

Spot-on or pour-on
ambs
formulations of the
and pregnant ewes, may lose vitality
and b
newer pyrethroids are easy to apply and
ecome unthrifty. Heayy infestations
can c
very effective.

onsiderably reduce the condition of
the hos

Powder dusting fits well into managet and even cause anemia. Keds also ment practices at shearing time. It is rapid, transmit Trypanosoma melophagium, a
nonpat
economical, and avoids wetting the animals.

hogenic protozoan parasite of sheep. Various types of equipment for dusting are available commercially.

�iagnosis: Close �pection of the
amaged, dirty wool and underlying skin
reveals infestation by the

SPIDER FLIES/NEW FOREST FLIES
unique appearance of these wingless, hairy flies. · · ·

The spider or new forest fly, Hippobosca

I
equina, is widely distributed throughout

;eatment and Control: Shearing
mo

Europe, Asia, and Africa. These winged
sh �es many pupae and adults. Thus,
e
keds parasitize horses and rarely cattle
tr aring before lambing and subsequent
eatrne
throughout the UK. Its bite is characterized
nt of the ewes with insecticides to
control th
as a nuisance and disturbance to large
e remaining keds can greatly
domestic animals. It has a predilecti

�
on for

:du�e 1:he possibility of lambs becoming
feeding sites in the perineal region and
aVi}y infested. Sheep are usually treated
between the hind legs.

894

FLIES

The winged adult is ~ 10 mm long with a
and mucus. Face flies are usually not
flattened, sluiveled body. The life cycle is
considered blood feecle:s because their
similar to that of Melophagus ovinus, in
mouthparts are a sponging type and n t o
that the female produces one larva at a time, piercing or bayonet-like, as are those f i
and at the time of maturity the larva falls

Stomoxys calcitrans. However, they 1

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away from the female fly and pupates in the
blood-feeding flies, disturb them durin ° 10w soil.

feeding process, and then lap up the bl gthe

'li"eatment is rarely indicated, but many of and body fluids that accumulate on theooct the repellents used for other blood-feeding
host's skin. Face flies are found on
periodic parasites may be used.

that are outdoors and usually do no�
animals into barns.

ow

HIPPOBOSCID OR LOUSE FLIES

Face flies are found on range cattle
throughout southern Canada and most

The hippoboscid or louse flies, Pseudoof the USA. The mouthparts consist of lynchia and Lynchia spp, are winged
sponging Iabellae, and there are four
versions of the keds. They infest many song
longitudinal stripes on the abdomen.

birds, rapt.ors, and pigeons. The pigeon fly,

Although similar in appearance to the

P canariensis, is an important parasite of
common house fly, face flies can be
domestic pigeons throughout the tropical
differentiated by the closeness and angles
and subtropical regions of the world. It is
of the interior margins of the eyes and by
found throughout the southern USA and
the distinctive coloration of the face and
northward along the Atlantic coast to New
abdomen. Speciation requires the skills

England. These dark brown flies have long
of a trained entomologist.

wings (6.5-7.5 mm) and are able to fly

Cattle are the principal host of the face
swiftly from the host.

fly in the USA, but face flies will also feed
on horses and probably sheep and goats.

Pathology: Hippoboscid flies move about

The face fly is a pest of range cattle; it is not quickly on their avian hosts and bite and
seen in f eedlot situations and thus is not a
suck blood from parts that are not well
parasite of confined cattle. The eggs are laid
feathered. They may serve as intermediate
in fresh cattle feces in rangeland situations
hosts for many avian blood protozoans of
and hatch in ~ 1 day. The yellowish larvae
the genus Har:nnoproteus. Pigeon flies
develop in 2-4 days and, when mature, leave
readily attack people who handle adult
the manure to pupate in the surrounding
birds; the bite is said to be as painful as a bee soil. The complete life cycle from egg to sting, and its effects may persist for 2:5 days.

adult requires 12-20 days, depending on
climatic conditions. The diapausing adult

Diagnosis: Close inspection of the riiffled overwinters within buildings and other
feathers and underlying skin reveals
protective places.

infestation by the unique appearance of
these winged, swiftly flying flies.

Pathology: Faceflies annoythehostand .

ultimately interfere with the host's produc- .

Treatment and Control: Anyflies on the

.

tivity. Females feed on facial secretions, such
birds can be killed by spraying the birds
as tear fluid, nasal mucus, and saliva, to
with permethrin. Thorough cleaning of the
obtain
premises
protein for egg development. Toe
and destruction of the debris are
irritation
essential
around the host's eyes stimulates
for control. Spraying the loft with
the

P:rme
flow of tears, which attracts even more
tm:m, whe� coupled with cleaning,
will
flies. •

··
alleviate the inf esta.tion.

Face flies also feed on other fluid sources,
such as blood from wounds and milk on all
calves' faces. Because face flies have � m
rough spines (prestomal teeth) on thelf

�p�m�g mouthparts, they can caustlle eye
rrnta.tion and mechanical damage. t? f

FA
tissue

CE FLIES
of the host. The feeding actiVItJ 0
face flies enhances transmission of

Face flies, Musca

Morax
autumnalis,
ella
are
bovis (see p 512). Face flies
so ·
named because
tt

!hey
can
gather
also serv
around
e as intermediate hosts fo�
the eyes·
ari
and muzzles of livestock,

Thelazi
particularly
a spp ( see p 51 O) and for Para.ft
cattle.

They may also
bovicola
be found on the

(see
withers
p 906).

neck, brisket, and sides. Their mouthp�
are adapted

Diag
for sponging up saliva,
nosis:

tears,

• Adult face flies are mofP;
logically similar to house flies. These

FLIES

895
ecics can be diff crentiated only by minor

Flies, attracted by the blood, settle on these

�fercnces in ere position.and color_ofthe
self-inflicted lesions and extend the margins
abdornen. Speciat1on r?qmres the sla�ls
by their feeding activity. Sheep of all ages
of a trained enton�olog1st. In �eneral, 1f a
are involved, but breeds with horns and
edium-sized fly 1s seen feedmg around the
without wool on the head are most severely

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:�es and nosttils of a cow or horse, it is ·
affected.

most probably a face fly.

Head flies also atrack people, deer,
horses, cattle, and rabbits. Although no

Treat�ent and Control: , Control of face
corresponding broken head lesions develop
flies is d�cul!- Muc� �ff01t has be�n made
in cattle, the occurrence of summer mastitis
using vanous msect1c1des and application

( due to Trneperella pyogenes) and the
techniques, such as dust bags, mist sprays,
seasonal activity of head flies are closely
and wipe-on formulations. Also, insecti-
associated, especially in Denmark. Head
cides and insect growth regulators are used
flies may also be involved in the spread of
as feed additives. However, results are
myxomatosis in rabbits (seep 1950).

usuallyless than satisfactory. The introduction of insecticide-impregnated ear rags has Treatment and Control: The develop- ·
provided somewhat better control, but
ment, emergence, and congregation of
generally, seasonal face fly reduction of only• head flies, which occur away from farm 70o/o-80% has been achieved; even with two··; areas, preclude the traditional methods of tags ( one in each ear) per animal.·
insecticide spraying of generalized breeding
sites and resting habitats.· Control at the

HEAD FLIES
point of conract between the feeding adult
insects and the mammalian hosts is also

(Plantation flies)

limited in value. With sheep, the retention of
organophosphate compounds or pyrethrin

Head flies or planration flies; Hydrotaea
derivatives on the susceptible head areas
irritans, are nonbiting flies found in largeis of short duration, which necessitates numbers in riortherrl European countries, . ·
impractical reapplications in free-ranging
especially Denmarkand Great Brirain,
animals. Use of insecticide-impregnated ear
where they are pests of cattle; sheep, and
rags in cattle decreases the incidence of ·
other livestock. This fly resembles the · . :. · · '· summer mastitis, presumably by reducing house fly and'is·-~� 7 mrn fong. The thorax·
transmission by head flies.·

·
is black with gray patches, the abdomen is

Removal of livestock from infested
olive green; and the wing bases are orange
locations during the fly season is the orily
yellow.·L .. ,
completely effective way to prevent

•·Head flies are a nuisance to domestic
damage. Once brokenheads have occurred;
animals and people because they are
the housing of sheep is the only successful
attr_acted to the mouth, nose; ears,·eyes, and , method to stop further fly damage.

wounds to feed on secretions: Unlike other·

Hydrotaea spp;'H°irritans produces orie -,

FILTH-BREEDING FLIES ' :

generation per year, with three larval instar
stages.' Eggs deposited in latesummer hatch The following adult dipterans are often out laivae within a few days: The sapropharef erred to as filth-breeding flies: Musca gous s�ge is brief, before development to
domestica (the house fly); Calliphora,
re stage that is predatory on other insect

Phaenicia, Lucilia; and Phormia spp (the aivae:Overwintering occurs as late�srage
blow flies or bottle flies); Sarcophaga spp

�aivae. Adults are most active from early · · · .· (the flesh flies); Fannia spp (the little house

. une until late September and are common
flies); Muscina spp (the false srable flies); Ill. the vicinity of thickets or woodlands in
andHermetia illucens (the black soldier

;�tey shelter between perio� of
flies). Large populations of these adult flies
are often found around facilities associated
with animal feces. Larval stages may be

:a�hology: In Great Brirain, sheep are
associated with skin wounds conraminated
attainly affected. Large swarms of flies,
with bacteria or with a matted hair coat
racte
co
d by the movement of animals;
conraminated with feces (see p 897). The
e ngregate to feed on secretions from the
life cycle of M domestica will be used as a ai�� and nose and on the cellular debris
represenrative example of the life cycles of •
the assorted filth-breeding flies.

Pe � grown horn base. To alleviate the
th ��tent irriration, sheep scratch and rub . ·

The house fly is commonly found around

" e
b u- e
livestock and poultry operations, where it
k ads, resulting in raw wounds or . . · ·
ro en heads," especially on the poll: ·.

readily breeds in accumulating manure

896

FLIES
sources. It is a nwdimn--sizl'd (as l:u-gl' as
to mini111iz(' (ly hrc�'ding. If solid rnanur

9 mm), grayish fly with four dark t.honwic

11ta11agl'llll'llL pracl.1<'<'8 ar<' applied, e stripes ,md sponging, nonbit.ing mout.hparls l'ff<!':'s �ho11�d �)l• �11rn1�� to �Pd�l(:(\ n1anure d('si�wd for sucking semiliquicl rood ( ther{'

11101st.uw. lf ,I lrq11ul lll,lllllW pr(, l8 1tsec1

�u·e 1;0 1rnmdibh.'s or maxillae). 'l'he lahium is rn:1111rrc should not be_! allo�ecl to accu�

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e�1):.mdl'd into two labellae that can transfer late ahovc the watcrlme, <!ti.her floatir u.

fluids and semitluids.

or sticking to the sides, because this i�g

After oviposition, the cn'ainy-whitl',
ideal site for fly reproduction.

.

Insectici�
banana-shaped egg ( -1 nun long) hatches m should be consiclcre<l as supplementar es 6-12 lu-in optimal conditions. The eggs are
to sanitation and
y

_manageme�t measures
not resistant to drying, and few appear to
aimed at preventmg fly breedmg. Residua)

smvive temperatw:e; >40°C or <15°C.

sprays providing 2-4 wk control with on

Larvae may develop in a few days to 3 wk,
treatment may be applied to fly-restin e
depending on the temperature and
g
surf aces. Space sprays, mists, or fogs With
availability of food. When temperature for
quick knockdown but no residual action
larval development is optimal ( -36°C), the
can be used for immediate reduction of
larvae develop to pupae in -6 hr. Pupae
high numbers of adult flies. Other measur
persist 4-5 days in wann weather. After the
es
for control of adult flies include use of
adults emerge, the flies search for food and
insecticide resin strips or various fly baits.

copulate after a few days. The life cycle is

These measures also can be applied directly
usually completed in -3 wk, although it can
to fly-breeding sources; however, this
be completed in as little as 10-14 days under should be considered only for fly-breeding favorable conditions. In temperate climates, spots that cannot be eliminated by nonnal it is thought that house flies overwinter as
sanitation practices.

pupae.

EYE GNATS

Pathology: Even though these flies do not
feed on blood, annoyance caused by their

The eye gnats or the eye flies (Hippelates
movement on and off animals can lead to
spp) are very small (l.5--2.5 mm long) flies
reduced performance. In addition, they
that frequently congregate around the eyes
have been implicated in the transmission of as well as mucous and sebaceous secrenumerous pathogens (helminth, protozoan, tions, pus, and blood.

bacterial, and viral) of people and other

In the desert and foothill regions of
animals. Large populations of these adult
southern California, adult Hippelates flies
flies often are found around poorly managed are present throughout the year; they are livestock or poultry facilities and become a
annoying from April through November.

public annoyance. These are synanthropic

During the peak months, they are noticeable
flies, ie, they are often associated with
in the early morning and late afternoon.

human dwellings. The flies are "vomit drop"

They gather in deep shade, such as among
feeders and fly from feces to food, spreading densely planted shrubs or in the shade of a bacteria on their feet and within their
dwelling. The eggs are ~0.5 mm long, fluted,
disgorged stomach contents.

and distinctly curved. They are deposited on
or below the surface of the soil. The larvae

Diagnosis: All adult filth-breeding flies
hatch and feed on decaying organic matter,
have similar sponging, nonbiting mouthincluding excrement. The larval stage lasts parts, designed for sucking semiliquid food.

7-11 days. During the winter months, the

The identification of adult flies is probably
larval and pupal stages may persist for manY
best left to a specialist. House flies are
weeks. Pupation occurs close to the s�;ce
medium-sized, grayish flies with four dark
of the soil
thoracic stripes. A preliminary identification
and lasts -6 days. The entire we
cycle lasts ~ 21 days. The adults are
of blow flies or bottle flies may be made on

. d
generally
the basis of the metallic coloring o{the
strong flyers, flying both with an
against the
a
wind.

?ults .. Flesh flies are medium-sized, grayish
flies with a checkerboard abdominal
ctedto

Pathology:

pattern.

Some species are attra pie,
the genital organs of mammals; for ex�

H pallipes

Treatment and Control: A thorough
clusters around a dog's peWS·

These gnats
sanitation program is necessary to control
quietly approach the� sonie
mamm
fly populations in and around livestock and
alian hosts. They usually alight
distance
poultry facilities. All manure accumulations
from their feeding site 3:11d then and
cr�wl over the skin, or fly internuttentlh
should be removed at least twice a week or
ost,
alight, thus
handled properly, if stored on the premises,
avoiding annoyance to the

They are persistent and, if brushed awaY,

FLIES

897
quicklY return to continue �1�gor�ing

Phaenicia,, I.,udl-in, and Plwrrn:ia spp (the
tlteinselves. They are nonb1tu�g flies;
blow flies or bot.tie llies); and Sarcophaga

110wever, the_labcllae have spmes ti1at
spp (the flesh flies). Their adult st.ages are
scarify host tissm: and all?w cntranc_e of
synanthropic flies, ie, they are often
athogcnic orgamsrns. lhppelates fhes
associated with human dwellings and

VetBooks.ir

�ften hover �ound the body �rificcs of
readily fly from feces to food. Larval stages
calves, yearlmgs, pregnant he1f e1?, and
are usually associated with skin wounds of
lactating cows. They feed on lacnmal fhnd,
any domestic animal that have become
fattY body secreti?ns, milk droplets, �d on
contaminated with bacteria or with a
secretions at the tips of the teats of animals.

matted hair coat contaminated with feces.

Hippelates flies also serve as vectors for

In the larval stages, the characteristics of

TruepereUa pyogenes ( summer mastitis)

the distinctive posterior spiracular plates
andMoraxella bovis (pinkeye, see p 512).

and the cephalopharyngeal skeleton are
unique for each species and are used for

Di�gnosis: These small flies have
identification.

sponging type mouth parts. Although eye

The life cycle of M domestica is a
gnats have much smaller mouthparts, they
representative example of that of the
closely resemble house flies in form and
filth-breeding flies (see p 895). Several
structure and have short aristate antennae.

species of blow flies cause myiasis in sheep.

Primary flies in the USA and Canada are

Treatment and Control: Repellents, ·

Phormia regina and Protophormia
such as those recommended for mosqui
terraenovae (the black blow flies) and
toes, provide temporary relief from eye

Lucilia sericata (the green bottle fly).

gnats. Applications of insecticides on a

L illustris, Cochliomyia macellaria
community-wide basis ( as would take place (secondary screwworm), and some others with mosquito abatement) may provide
are usually secondary invaders. L cuprina
temporary control of adults, but more adults is the most important primary fly in invade the treated area after the insecticide

Australia and South Africa; L sericata in
has dissipated.

·

Great Britain; and L cuprina, L sericata,
and Calliphora stygia in New Zealand.

'·�·-:··: ·�i.®WUC:@�lS�m�,�(:.�'.-?:. Pathology: In normal conditions, adult flies of these genera lay their eggs in feces or
in decaying animal carcasses. In facultative
myiasis, the adult flies are attracted to a

Larval dipterans may develop in the
moist wound, skin lesion, or soiled hair
subcutaneous tissues of the skin or organs
coat. A common site is the breech, where
of many domestic animals, producing a
flies may be attracted to wool soaked with
condition known as myi.asis. There are two
urine or feces. As adult female flies feed in
types of myiases based on degree of host
these sites, they lay eggs, which hatch
dependence. In facultative myiasis, the fly
within 24 hr if conditions are moist. Larvae
larvae are usually free-living; however, in

(maggots) move independently about the
certain circumstances, these larvae can adapt wound surface, ingesting dead cells, themselves to a parasitic dependence on a
exudate, secretions, and debris, but not live
host In obligatory myiasis, the fly larvae
tissue. This condition is known as strike
are completely parasitic, ie, they depend on
or fly strike. The larvae irritate, injure, and
the host to complete the life cycle. Without
kill successive layers of skin and produce
the host, obligatory parasites will die.

exudates. Maggots can tunnel through the
thinned epidermis into the subcutis. This
process produces tissue cavities in the skin

FACULTATIVE MYIASIS
that measure up to several centimeters in

�ODUCING FLIES
diameter. Once established, strikes can

F
spread rapidly and attract more blow flies,
acuitative m,nasis-producing flies of

Vet
secondary as well as primary. Mild strikes
e '

.,.

ch nn� importance covered in other
can cause rapid loss of condition, and bad
a
h pters mclude Gasterophilus spp in
o
strikes can be fatal, Unless the process is
rs

( es (seep 315), Oestrus ovis in sheep
halted by appropriate therapy, the infested

:JP 1473), and Cuterebra spp in dogs
animal may die from shock, intoxication,
c
di ats (see p 879). The following larval
histolysis, or infection. A peculiar, distinct,
r Pterans are often referred to as facultapungent odor penneates the infested tissue

�e myi_asis-producing flies: Musca
and the affected animal. Advanced lesions
rnestica (the house flies); Calliphora,
may contain thousands of maggots.

898

FLIES

The body of the sheep also may lH' struck. !r?atn�cnt �nd Control: Blow fl This is usually associated with soaking rains mlest.atlon of I.he breech can be effe�
that eaUSl' the development. of fleece rot,
controlled for -G-8 wk hy tagging . lively O
often eharact{'liZl'ct by discoloration due to
cmtching (ie, wool is shom bet wee� th

Psc11domo11as spp or dcnnatophilosis.

legs and around the tail). ComplN� ·h e

Other sites arc the horns of nuns, wool
controls outbreaks involving other 8 earing VetBooks.ir
around the prepuce, sides where feet with
the body. Wool removed from arouiJrl'l Of
footrnt come in contact with fleece, and
head and the prepuce can prevent st -the_
wounds.

these areas. Urine staining of the cru� ; 1n

As adults, these flies can be pestiferous

Merino ewes can be virtually eliminat Of
ect
in veterinruy clinics, f ain1S, or poultry
by removal of breech wrinkles (Mule
operations. The flies ai·e vomit drop feeders
operation), and fecal contamination�
and fly from feces to food, spreading bacteria greatly reduced by docking tails at the�e on their feet and from their disgorged
joint. Scouring should be controlled. Oct d
stomach contents.

and associat�d ��isture a1:tract flies anctors

These fly laivae have also been associated stimulate oVIpos1t1on, particularly durin with toxic effects in chickens. Botulism
hot, humid weather.

g

(seep 2889), also known as limberneck in

Chemoprophylaxis consists of wetting t
chickens, has been associated with ingestion complete saturation of susceptible areas 0
of large numbers of laivae of Lucilia caesar, with suitable insecticidal and larvicidal Plwenicia sericata, and other species of
preparations, such as the organophosphat
flies. Cwstridium botulinum multiplies in
e
insecticides or cyromazine, a specific
carrion, where it may be picked up by fly
larvicide in dips and sprays. Jetting is the
laivae breeding in that medium and then
most efficient procedure-insecticide is
passed on to chickens that eat the maggots.

forced into the fleece, usually locally to the

Dead animals should be quickly and
breech and along the back and head, under
safely disposed of, preferably by
high pressure. Protection can last 6-8 wk
incineration.

but where the primary fly is resistant ( eg,'

L cuprina in Australia), it may last only2-3
wk. Weekly application of agents such as

Diagnosis: Strikes should be diagnosed
ronnel (2.5%) under pressure to wounds
early; behavior of sheep is a good indicator
until healed can be highly beneficial,
of myiasis. Affected animals become
particularly for screwworm infestation.

depressed, stand with their heads down, do

Before suitable agents are applied, all wool
not feed, and attempt to bite the infested
should be removed from the struck area and
areas. Screwworm may be suspected if the
laivae are associated with wounds.

around it.

The species of myiasis-producing flies

Burning or deep burying of the carcass
can be definitively identified by closely
may be a valuable general hygienic measure
examining the larvae. The extreme caudal but may have little effect on primary strikes.

ends of several third-stage larvae infesting The main source of primary flies is the struck the wound should be sliced using a
sheep. A genetic manipulation approach has
scalpel blade held perpendicularly to
been
the
used to control a strain of blow fly in
larval body. When the sliced caudal ends

Australia; male flies are partially sterile but
ar:e placed cut surface down on a glass
transmit a gene that causes blindness in
shde, _covered with a coverglass, and
female offspring.

exammed under a compound microscope

Treatment and control measures for
a dichotomous key can be used to identif; myiasis in dogs and cats are limited. If the genus or genera of flies within the
these larvae are detected in small animals,

�o�nd. The unique spiracular plates are
immediate therapy is necessary. The hair
distmct for a particular genus, much
coat
like
should be clipped to determine the f
a human fingerprint. Several specimens
extent of the lesion and to remove manY O d should be examined because more than
the larvae present in the hair. Removing IT13o ·
on� genus may be present within the
gots_from existing deep tissue pockets::.

les�on. The first larvae to hatch in the

?e difficult, and sedating or even anestb
les10n often
siofl
create a favorable medium
mg the animal may be necess�- The 1�.

attractive to flies of other genera. Also
should be examined on successive day ' t

.

.J:fferen
the possibility of obligatory myiasis

�dult flies lay eggs in the wound at uw e
caused by Cochliomyia hominivorax
times, and hatching of larvae may not b

(see below) or Chrysomya bezziana (see synchronous.

. a15
p 900) should be considered depending

Depressed, febrile, and prostrat� 3!lciu
on geographic locale.

should be treated accordin° to thelf c dies
signs. Ideally, culture and s�nsitivitY stu

FLIES

899
hould be pc1fonned on samples or

5
that can be used as an advantage in biologic
pings of the wounds. If secondary
control. Adult, flies usually mate when
i�crial or fungal infect.ions are present,

3-4 clays old, and gravid females arc ready
a� ni stration of broad-spectmm
to oviposit when -G days old. In warm
antibiotics is advisable.

weather, the life cycle may be completed in

VetBooks.ir

Witll respect to prevention, owners

21 days. Only female flies feed and oviposit
hould be educated about the effectiveness
on wounds; males and younger, virgin

�f treating all skin wounds. Animals with
females gather to mate in vegetation,
kin wounds should be confined to fly-free
especially flowering vegetation.

�eas. The hair coat should be kept clean of
urine or feces and should not be permitted

Pathology: Newly infested wounds
to become matted. Contaminated wounds
contain screwworm larvae of a single age;
and matted hair coats soaked in urine or
older, larger wounds may contain larvae
feces rapidly attract adult myiasis-producing of various ages and of different species flies. The control of adult flies in the field
of flies. The malodorous, reddish brown
and the destruction of their breeding places
fluid produced in the wound usually drains
are excellent preventive measures. All areas and may stain the hair or wool around or should be free of opened garbage cans and
below the wound. As annoyance increases,
decaying carcasses or carrion.

the infested animal seeks protection by
retreating to the densest available shade.

OBLIGATORY MYIASIS

Even a small and relatively inconspicuous

PRODUCING FLIES
wound infested with screwworm larvae
attracts not only more screwworm flies

Many dipteran flies produce larvae that
but also facultative myiasis-producing
must lead a parasitic existence and result in
flies. Necrotic tissues attract even more
obligatory myiasis. Only one fly in North
flies. The wound can become greatly

America, Cochliomyia hominivorax, is a
enlarged due to multiple infestation and,
primary invader of fresh, uncontaminated
unless treated, usually results in death of
skin wounds of domestic animals. Another
the animal.

species of screwworm, Chrysomya
bezziana, is found in Africa and southern

Diagnosis: The parasitic larvae are

Asia, including Papua New Guinea.

tapered and have mouth hooks at the
narrow end and breathing spiracles at the

Cochliomyia h_ominivorax
wide end. Body segments are ringed with
spines. Fully grown larvae can be as long as

(Primary screwworm, New World
r5 cm.-Larva
screwworm)

; are often identified by their
wood screw shape and appearance and

Cochliomyia hominivorax is distributed
can be distinguished from the larvae of
throughout the neoarctic and neotropical
the facultative myiasis-producing flies by
regions of the western hemisphere. As
the darkly pigmented tracheal tubes on
a result of massive state, federal, and
the dorsal aspect of the posterior end of
international eradication programs, extant
third-stage larvae. These tubes can be easily
populations of C hominivorax are no
visualized through the larval cuticle.

longer found in the USA or Mexico; isolated

Adult screwworm flies are similar in

�eports are often traced to importation of
appearance to other blow flies. The adult
infested animals from locations where the
stage is never recovered in a veterinary case
screwworm is still prevalent. Extant
scenario. They are bluish to bluish green,

Populations are found in Central and South have a reddish orange head and eyes, and America and in certain Caribbean Islands.

are slightly larger than a house fly. If

Adult female flies lay batches of 200--400
eg
collected, they are difficult to distinguish
gs in rows that overlap like shingles in a
from other blow flies or bottle flies.

��s on the edge of a fresh wound. After

Identification of adult screwworms is
w 21 hr, larvae hatch, crawl into the
probably best left to an entomologist.

1;und, and burrow into the flesh. The
ae

Aft feed on wound fluids and live tissue.

Treatment and Control: Screwworm
w er 5-7 days, grown larvae exit from the
infestation must be reported to both state
s 1und, fall to the ground, and burrow in the and federal autilorities. C hominivorax has

� to pupate. The pupal period varies from been eradicated from the USA but occasion7 tur!Y�o 2 �o, depen�g on �he temperaally enters tile country surreptitiously on tur · eezmg or sustained soil temperae
imported animals. In tile USA, if a wound is
br s
e <46° F (8° C) kill the pupae. Adults thought to be infested with screwworm
ed Only once during their lifetime, a fact larvae, the USDA can be contacted.

900

FLIES

Screwworms in wounds can be killed

Adult screwwonns are usually not seen
by direct application of a wound dressing,
in the field. The adult fly has a dark metallic
called a smear. Such smears, which contain
green body with abdominal segments with
lindane or ronnel, may be difficult to find
nanow ba11ds along the posterior margins.

in the USA because of the eradication

The legs are black or partially brown. The

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program. Smears are best applied with a
face is ora11ge/yellow. The first lruval stage

1-in. (2.5-cm) paint brush and should reach
probably goes wmoticed because of its
all of the many pockets formed by the
small size, as long as 3 mm at the time of its
burrowing larvae in deep wounds. A thin
molt to the second stage. The second stage
layer should also be applied to the skin
is quite similar to the third but is 4-9 mm
sunounding the wound to protect it from
long. The third-stage larvae are large, as
reinfestation. Wounds may also be treated
long as 18 mm. The body is composed of
with aerosol, dust, or foam formulations of

12 segments that have broad encircling
coun1aphos, lindane, or ronnel. To protect
bands of spinules. All three stages are
animals from infestation and also to kill
maggot-like in their appearru1ce a11d have
larvae in small wow1ds that are difficult to
posterior spiracles that are unique to the
detect, anin1als can be sprayed thoroughly
species. The posterior end of the larva has
with ronnel or sprayed with or dipped in
its spiracular plate located in a deep cleft at
coun1aphos.

the end of the eighth abdominal segment.

The spiracular plates a.re Jru·ge and well

Sterile Male Release Eradication
separated. The peritreme and the three

Program: In 1958, the USDA initiated a
breathing slits are wide.

progran1 in the southeastern states to

C bezziana produce a particularly vile
eliminate screwworms by the sterile male
myiasis. Female flies are attracted to open
release technique. When reared rutificially
wounds of people a11d domestic and wild
and exposed to irradiation shortly before
animals, laying their eggs in masses of
they emerge from the pupae, male flies are

150-500 at the edge of wounds or near body
able to mate but sterile. The female mates
orifices. Larvae develop to the third stage
only once and, when mated with a sterile

-2 days after hatching. They burrow deep
male, lays eggs that do not hatch. Thereinto the wound such that only their fore, release of sufficient nun1bers of sterile posterior ends ru·e visible. The entire larval males in an area throughout a period of
stage lasts 5-6 days. The pupal stage lasts
time leads to eradication. By 1959,

7-9 days in tropical conditions a11d longer
screwworms had been eliminated from
in cooler environments. The adult flies

Florida.

emerge later to mate, locate a new host,

This program was expanded to cover
and continue the cycle. Female flies mate
the rest of the area involved in the USA and
only once during their lifetime-a fact
then, via ajoint Mexico-USA agreement,
paramount in prevention a11d control.

to include most of Mexico. This, along with

Under favorable conditions, there may be
the use of screwworm attractant and an

�8 generations per year.

insecticide system that attracted and killed
adults, led to eradication of screwwmms

Pathology: The larvae of C bezziana a.re from Mexico. There is interest in expanding
obligatory wound pru-asites, never developthis area throughout Central America and ing in carcasses or decomposing orga11ic
the Caribbea11. However, until this has been
material. Although female flies are attracted
achieved, constant vigilance by all who deal
to open wounds, occasionally eggs are
with anin1als in the southern USA a11d
deposited on the unbroken, soft skin of

Mexico is necessary to detect a11 infestation
various parts of the body, especially if
quickly and to eradicate it before the flies
contanlinated by blood or mucous dischru·ge.

reproduce a11d spread.

When the lruvae hatch, they bunow into
the flesh of the host, using their hooked

Chrysomya bezziana
mouthparts to scrape away at the tissues
a11d lacerate the fine blood vessels. Larvae

(Old World screwworm, Oriental fly,
are voracious blood feeders. Outing the

Bezzi's blow fly)

bloodsucking phase, only the caudal ends of

Chrysomya bezziana is fow1d in Africa, the the maggots with their blackish peritremes Indian subcontinent, and southeast Asia
remain visible at the surface of the lesion,
from Taiwan in the north to Papua New
enabling the larvae to breathe. As ma11y

Guinea in the south. This fly is not
as 300 maggots have been seen in some
indigenous to Australia. Owing to its
wounds. In W1treated woW1ds, the destrncgeography, the most likely potential port of tive activity of the larvae may lead to the
entry for C bezziana to the USA is Hawaii.

death of the anin1al within a very short time.

FLIES

901

Secondary infestation with the facultative

Gray Flesh Flies
myiasis-producing flies (seep 897) may
complicate treatment and control.

The gray flesh fly, Wahifahrlia vigil, is
responsible for cutaneous myiasis in North

America, particularly in southern Canada

Diagnosis: The identification of the
and the northern part of the USA. The adult
rarely observed adult flies and their
flies have been recorded from the New

VetBooks.ir
associated larval stages is best left to an

England states to Alaska, but most reports
entomologist. A definitive diagnosis can be
made only after obse1vation, extraction,
are from eastern sections of Ca11ada and the
neighboring northeastern parts of the USA.

and identification of typical larvae. Diagno

All reports of infestation ai·e in the skin of
sis may often be made by residence in or
healthy animals, particularly the unbroken
history of travel to an area endemic for
skin of the young.

C bezziana. If a wound is thought to be

All three larval stages are maggot-like
infested with larvae of C bezzia,na, samples in their appearance and have posterior should be collected and sent to appropriate spiracles unique to the species. The first eradication officials.

larval stage is 1.5 mm at hatching and grows
to 3.5 mm at the time of its molt to the

Treatment and Control: Treatment of
second stage. The third stage is 7-18.5 mm
screwworn1 infestation involves killing the
long. Its posterior end is narrow, and it is
larvae in the lesions, promoting healing, and
covered with many irregular rows of small
preventing secondary reinfestation with
spines that have dai·k points and are
larvae of the facultative myiasis-producing
directed posteriorly. This larva is better
flies. The extent of the lesions is detemlined
adapted to maintain an attachment to living
by clipping the hair coat and removing as
tissues. The oral hooks are strongly
many larvae as possible. The larvae that are
developed. The posterior end of the larva
removed should be killed to prevent them
has its spiracular plate located in a deep pit
from pupating and developing into adults.

formed by the mai·gins of the segment. The

Larvae located deep within tissues must be
postelior spiracles have wide slits and a
extracted.

strong peritreme.

Ivermectin at dosages of 50, 100, and 300

The gray flesh fly is larviparous-it
mcglkg administered to infested cattle
deposits laivae instead of eggs on healthy,
resulted in lOOOA, larval mortality for at least
uninjured skin of suitable hosts, particu6, 12, and 14 days, respectively. Depending larly young animals. Larvae penetrate
on their age, larvae swvived in established
the unbroken skin and forn1 a boil-like
strikes after treatment at 200 mcglkg.

(fmuncular) swelling. Development to

Mortality was lO()OA, in larvae up to 2 days old the infective third-larval stage is usually but less in older laivae. However, many of
completed in 9 -14 days. The pai·asites then
the larvae that survived ivermectin therapy
drop to the ground and pupate for --;11-18
failed to develop to the adult stage. After
days, varying with the season of the year
treatment with 200 rncg/kg, residual
a11d the temperature. When cold weather
protection lasted 16--20 days, 2-3 times that
approaches, the pupation period is greatly
of most insecticide smears.

prolonged. Under laboratory conditions, it

All wounds on domestic animals should
has been observed to last 7 mo. Parasites
be properly dressed, and all elective surgical swvive the winter in pupal forn1. Adults procedures avoided during the fly season.

emerge a11d mate after -3-4 days. Female

The fact that the female flies mate only
flies begin larviposition -1 wk late1�
once during their lifetin1e is an important
depositing 6--16 laivae at a tin1e. Female
fact to consider in the control of C bezzi
flies live for 35-40 days; males seldom
ana. Pupal flies exposed to irradiation lead swvive >3 wk.

to sterile adults that can be released to mate
with wild male and female flies. As a result,
no viable offspring are produced in the wild.

Pathology: Female W vigil deposit active larvae near or directly on the host. Although
larvae usually penetrate unbroken skin, in

Wolves (Warbles) of Small Animals
small aJlimals, penetration may go deeper

Laivae of the genus Cuterebra are often
tha11 the dermal tissue, even into the
referred to as wolves, warbles, rabbit bots,
coelornic cavity.

or rodent bots. These fly larvae infest the

The first indication that a11 ailimal is
skin of rabbits, squirrels, mice, rats, chipinfected is exudation of seruni a11d matting munks, and occasionally dogs and cats.

oftl1c hair coat over the site of penetration.

(For clinical findings, diagnosis, a11d
ln light-skinned animals, a small inflarnrnatreatment, seep 879.) to1y area, with a tiny hole visible in the

902

FLIES
center or to one side, is noticeable. These
opening may be helpful before removing
lesions may be palpated as they develop. On
lai-vae with forceps. Lidocaine hydrochlothe third or fourth day, the larvae are 1.5-2
ride can also be injected into the furu:ncular
cm long and produce abscess-like lesions
lesion to facilitate extraction. Great care
resembling those of Hypodmma spp in
should be taken during the extraction
cattle. These lesions vary in size, shape,
process to avoid rupturing larvae in situ,

VetBooks.ir
position, and the number of larvae they
although anaphylaxis has not been
contain. The hair coat often becomes parted reported. Antibiotics should be prescribed.

over the swnmit of the lesions and reveals

W vigil often infects young mink. A
an opening 2-3 mm in diameter. The
teaspoon of ronnel can be placed in the
posterior aspect of the larva is visible in
bedding of mink nest boxes as a control
these openings, through which it breathes.

measure; however, ronnel should not be

Openings are generally circular and
used in the bedding of kits <3 days old.

well-defined; however, if several larvae are

Protection can be provided by using wire
present in a single lesion, the shape of the
gauze to keep flies out of cages.

opening is quite variable. Small animals
infected with <!5 larvae for several days

African Tumbu Flies
become emaciated, and the skin becomes
dry and loses its luster.

(Mango fly, Skin maggot fly, Ver du Cayor,

The penetration of the skin by the larvae,

Worms of Cayor)

their development in the subcutaneous

The African tun1bu fly, Cordylobia
tissues, and secondary bacterial infection
anlhropophaga, is responsible for another
produce intense irritation and inflan1maboil-like (furu:nculru") myiasis in both people tion. Attempts by the animal to remove the
and animals in Africa, pruticularly in the
larvae or relieve the irritation tend to
sub-Sal1aran regions.

aggravate the condition. Young ru1in1als may

The adult flies are non parasitic and as a
die from exhaustion. It has also been
result are not seen by owners or veterinarsuggested that the lru-vae may produce toxic ians. They are stout, compact flies, 6-12 mm
secretions. W vigil has been isolated from
long. They are light brown, with diffuse
the skin of young children, particularly
blue-gray patches on the thorax and dark
infants.

gray on the posterior part of the abdomen.

The face and legs are yellow. The second

Diagnosis: Adult gray flesh flies are
and third-stage larvae are the stages usually
nonparasitic and as a result will probably
seen in the animal's skin.

not be seen by owners or veterinarians.

Second-stage larvae are slightly

They are large grayish flies ( -13 mm long),
club-shaped and exhibit large, black
about twice the size of a house fly. The
cuticular spines directed posteriorly and
dorsal surface of the thorax is marked with
distributed irregularly over segments 3-8.

three longitudinal bands, and the dorsal

Segments 9-11 are almost bare when comsurface of the abdomen has three wellpared with the preceding segments. The defined rows of oval black spots that are
segments have a few rows of small, pale
confluent with one another.

spines posteriorly. Segment 12 is densely

The identification of adult flies and their
covered with these spines. Segment 13 is
associated larval stages should be left to an
indistinctly demai·cated, lacking spines
entomologist. The presence of a dennal
but possessing two pair of short proswelling with a central opening may lead cesses. Each tracheal tube opens through
to a tentative diagnosis of myiasis due to
two slightly bent slits: The second-stage

W vigil. A definitive diagnosis can be made larvae are 2.5--4 mm long. The size of
only after extraction and identification of a
advanced second-stage larvae varies
typical larva. Extensive descriptions and
greatly, as does the size of third-stage
dichotomous keys for the three larval stages larvae. Fully mature larvae are 1.3-1.5 cm are available. A tentative diagnosis may
long. The body is cylindrical with 12
often be made by a history of either
identifiable segments. Curved spines
residence in or travel to a geographic area
that are directed posteriorly are densely
endemic for W vigil.

arranged at least up to segment 7; the
last 5 segments may be either partially

Treatment and Control: Larvae must be
or densely covered with spines.

extracted from the skin. Applying heayy oil,

After fertilization, female flies produce
liquid paraffin, or petrolatun1 jelly to the

100-500 banana-shaped eggs, usually
opening of the lesions will occlude
depositing them in dry, shady, sandy soil
the airway of the lru-vae. Applying a small
that has often been contaminated by urine
an10unt of chloroform or ether to the
or feces. Eggs are never deposited on the

FLIES

903.

skin of the host. Eggs hatch after 1-3 days,

Treatment and Control: Larvae can
and the larvae are initially 0.5-1 mm long.

be removed by coating the breathing pore

Larvae can swvive as long as 15 days while
with a tllick, viscous compound, such as
waiting for a host and can penetrate the host heavy oil, liquid paraffin, sticking plaster, or in as little as 25 sec. After penetration,
petrolatum jelly. Clogging the pore causes
larvae reside in a cavity in the demlis and
the larva to become hypoxic and leave the
hypoclermis. This cavity communicates to

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cavity in search of oxygen. Light pressure
the external environment by means of a
at the edge of the lesion also aids in larval
central breathing pore, which corresponds
removal.

to the caudal end of the larva with its

Lidocaine hydrochloride can be injected
spiracles. A single larva is found in each
into the furuncular lesion to facilitate larval
cavity, within which the larva develops to
extraction with thumb forceps. Surgical
the second and third stages. Larvae require
excision is usually unnecessary and

7-15 days to mature and then emerge
unwarranted while tl1e larvae are alive but
through the breathing pore and drop to the
is used to remove dead or decaying larvae.

ground, where they pupate. Adult flies

Great care should be taken during the
emerge 10-20 days later, and the cycle
extraction process to avoid rupturing larvae
begins again.

in situ, although anaphylaxis has not been

Rats and dogs are the usual definitive
reported. Antibiotics should be prescribed.

host; however, people, mice, monkeys,

Adult flies should be killed if seen indoors.

mongooses, squi.lTels, leopards, boars,

Larvae should be removed from animals
antelopes, cats, goats, pigs, rabbits, guinea
entering the house and destroyed. All rats
pigs, and chickens can be infested.

should be killed and burned. Prevention of
an infestation depends on cleanliness and

Pathology: Clinically, the infestation is
regular disinfection of the anin1al's sleeping
characterized by a small erythematous
quarters. In the case of valuable animals (eg,
papule that appears 2 -3 clays after larval

Angora rabbits), flies may be kept out of
penetration. Within days, the papule
rabbit pens using wire gauze.

enlarges until it becomes a nodule that

Because the adult female flies lay eggs in
resembles a boil (furuncle ); hence, the
sandy soil contaminated by feces or urine,
description furunculoid myiasis. At the
the parasite can be controlled in the pet's
center of the nodule is a pore tlu·ough
environment by prompt removal of the pet's
which serous fluid oozes. This fluid can
feces and by covering U1ination sites on the
be hemorrhagic or purulent and contains
premises witl1 a layer of dirt.

larval feces.

Dogs with thin, soft skin seem to be more
suitable hosts for larval development than

PSEUDOMYIASIS
dogs with tllick skin. Preferential sites of
infestation are the feet, genitals, tail, and

In pseudomyiasis, dipteran larvae have
axillae. ln endemic areas, mild infestations
been accidentally ingested and are found
in dogs do not produce clinical distress.

within an animal's GI tract, where they

Massive infestation may induce marked
arc not able to continue their developswelling and edema, especially if larvae ment. Dogs or cats infested with larvae of
are in close proximity to each other. Larvae
the facultative myiasis-producing flies in
can penetrate deep into tissues and cause
wounds or in the hair coat often ingest
considerable damage and even death.

larvae while licking or grooming. These
larvae pass through the GI tract and

Diagnosis: The presence of a dermal
appear in the feces undigested. Dipteran
swelling with a central opening may lead
larvae may also be passed in the feces
to a tentative diagnosis of myiasis due to
when a roaming dog or cat ingests carrion

C anthropophaga. A definitive diagnosis can that contains maggots; these maggots be made only after extraction and identificapass to the external environment tion of typical larvae. The identification of
undigested.

adult flies and their associated larval stages

Pseudomyiasis can also occur if feces
should be left to an entomologist.

submitted for parasitologic exanunation are

A tentative diagnosis may often be made
not fresh. Adult facultative-myiasis flies may
by a history of either residence in or travel
have laid their eggs in these feces, and larval
to a geographic area endemic for C anlhro
development may have begun.

pophaga. However, the parasite has also

Eristalis tenax, the rat-tailed maggot,
been diagnosed in travelers and their
may be seen in the gutter behind cows in
accompanying pets from geographic areas
dairy barns. These maggots are associated
where the parasite is not found.

with liquid feces and with feces that have

904

FLIES
not been removed from the environment.

on their posterior end. Many farmers

The larvae are known as rat-tailed maggots
erroneously assume that the cows
because their breathing pores are found at
defecated these maggots. The adults are
the tip of a long, siphon-like breathing tube
nonparasitic, free-living flies.

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HELMINTHS OF THE SKIN

CUTANEOUS HABRONEMIASIS
their anterior end is protruded on contact
with water. Females produce characte1istic

(Summer sores, Jack sores, Bursatti)

long, thin-tailed larvae. Water fleas ( Cyclops

Cutaneous habronemiasis is a skin disease
sp) are the intermediate host in which
of Equidae caused in part by the larvae of
infective larvae develop. Dogs become
the spirurid stomach worn1s (seep 315).

infected through ingestion of contaminated

When the larvae emerge from flies feeding
water or a paratenic host (frogs).

on preexisting wounds or on moisture of the

Subcutaneous, serpentine, inflammatory
genitalia or eyes, they migrate into and
tracts and nonh.ealing, crater-like, edemairritate the tissue, which causes a granutous skin ulcers are seen. Infections are rare lomatous reaction. The lesion becomes
but are occasionally fow1cl in animals that
chronic, and healing is protracted.

have been around small lakes and bodies

Diagnosis is based on finding nonh.ealing,
of shallow, stagnant water. Treatment is
reddish brown, greasy skin granulomas that
by careful, slow extraction of the parasite.

contain yellow, calcified material the size of

Administration of miridazole or benzimiclarice grains. Larvae, recognized by spiny zole compounds may be useful.

knobs on their tails, can sometinles be

D medinensis, the guinea worm of
demonstrated in scrapings of the lesions.

parts of Africa, Asia, and the Middle East,

Many different treatments have been tried,
although primarily a parasite of people,
most with poor results. Symptomatic
is also found in clogs and other animals.

treatment, including use of insect repellents, may be of benefit, and organophos

ELAEOPHOROSIS
phates applied topically to the abraded
surface may kill the larvae. Surgical removal (Filarial dermatosis, "Clear-eyed" blindness, or caute1ization of the-excessive granula

Sorehead)

tion tissue may be necessary. Treatment

Elaeophora schneideri is a parasite of
with ivennectin (200 mcg/kg) has been
mule deer and black-tailed deer found in the
effective, and although there may be
mountains of western and southwestern USA
temporary exacerbation of tbe lesions
and in Nebraska; it also has been found in

(presumably in reaction to the dying larvae), white-tailed deer in southern and southeastspontaneous healing may be expected.

ern regions in the USA Adult parasites are

Moxidectin at 400 mcg/kg also appears to be 60-120 mm long and usually are found in active against H abronema spp in the
the conunon carotid or internal maxillary
stomach. Control of the fly hosts and
arteries. The microfilariae, which are -275
regular collection and stacking of manure,
µm long and 15-17 µm thick, normally are
together with anthelmintic therapy, may
found in skin capillaries on the forehead
reduce the incidence.

and face. Development in the intermediate
hosts, horse flies of the genera Tabanus and

DRACUNCULUS INFECTIONS

Hybomitra, requires -2 wk. Infective larvae invade the host as tl1e horse fly feeds, migrate

Dracunculus 'insignis is found mainly in the to the leptomeningeal arteries, and develop
subcutaneous connective tissues of the legs
to inunature adults in -3 wk These young
of raccoons, mink, and other animals,
adults migrate against the blood flow and
including dogs and cats, in North America
establish in the common carotid arteries,
and possibly other parts of the world. The
where they continue to grow. The parasites
females (<!300 mm long) are much longer
reach sexual maturity -6 mo later and begin
than the males ( -20 mm). They produce
producing microfilariae. The life span of
ulcers in the skin of their host, through which adults is 3-4 yr.

HELMINTHS OF THE SKIN

905

Clinical Findings: Clinical disease
occurs in 18--20 days. No treatment is
has not been reported in mule deer and
available for the cerebral form of the
black-tailed deer; therefore, they are
disease.

considered to be the normal definitive
hosts. When horse flies transmit the

ONCHOCERCIASIS
infective larvae to elk, moose, domestic

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sheep and goats, sika deer, and possibly

The taxonomic status of the three species
white-tailed deer, the larvae develop in the of Onchocerca currently recognized in the leptomeningeal arteries and cause

USA, and other previously recognized
ischemic necrosis of brain tissue,
species, is under debate. 0 cervicalis is
resulting in blindness, brain damage, and
found in the ligamentum nuchae and
sudden death. Blindness in these animals
possibly other sites in Equidae. In cattle,
is characterized by absence of opacities in

O gutturosa locates in the ligamentum
the refractive media of the eye ("clearnuchae, and O lienalis in the gastrosplenic eyed" blindness).

ligament. Adults are associated with

Domestic sheep and goats, especially
connective tissues; they are very thin and
lambs, kids, and yearlings, may die suddenly 3--60 cm long. Microfilariae are found in the 3-5 wk after infection. Death is usually
dennis and on rare occasions circulating in
preceded by incoordination and circling and
peripheral blood. The microfilariae lack a
often by convulsions and opisthotonos.

sheath and are 200-250 µm long with a

Numerous thrombi occur in the cerebral
short, sharply pointed tail. Culicoides spp and leptomeningeal arteries. One or more

( see p 887) are the intermediate hosts for young adultE schneideri accompany each

O cervical is, and Simulium spp for thrombus. If sheep or goats survive the early

O gutturosa and O lienalis.

infection, a raw bloody dermatitis on the
poll, forehead, or face ("sorehead")

Clinical Findings: 0 cervicalis has been develops 6--10 mo later. Lesions occasionassociated with fistulous withers, poll evil, ally develop on the legs, abdomen, and feet.

dermatitis, and uveitis in horses. However,

These lesions are an allergic dermatitis in
because O ceruicalis in large nUI11bers is
response to the microfilariae lodged in
cmnmon in horses without these diseases,
capillaries. Lesions persist, with periods of
there is some debate about its role in the
intermittent and incomplete healing for
pathogenesis of these conditions.

-3 yr, followed by spontaneous recovery.

Adults in the ligan1entUin nuchae induce

Hyperplasia and hyperkeratosis develop in
inflanunatory reactions ranging from acute
the epidermis of the parasitized area.

edematous necrosis to chronic granulomatous changes, resulting in marked fibrosis Diagnosis: Differential diagnoses include
and mineralization. Mineralized nodules are
coenurosis (Taenia, seep 1311), cerebromore common in older horses. Although cortical necrosis (seep 1281), and
lesions are found in these areas, presumably
enterotoxemia (seep 609). Elaeophorosis
associated with dead parasites, it is
should not be considered unless sheep have
generally agreed that fistulous withers and
been in endemic areas dUiing the SUinmer.

poll evil are not caused by O ceruicalis

Diagnosis in lambs, kids, or elk yearlings
infections.

or calves usually is made at necropsy;

Microfilariae concentrate in the skin of
numerous thrombi and parasites are found
the ventral midline. Large numbers can be
in the common carotid, internal maxillary,
foUlld in horses without dermatitis as well as
cerebral, and leptomeningeal arteries.

in horses with dermatitis of the face, neck,

Presun1ptive diagnosis in mature sheep is
chest, withers, forelegs, and abdomen.

based on history and location and type of

These lesions may be pflllitic and often
lesion. The skin lesion must be differentiinclude areas of scale, crusts, ulceration, aloated from that of ulcerative dermatosis pecia, and depigmentation. The dermatitis

(seep 872). Confirmation is by recovery
may be associated with an immunologic
of microfilariae from the lesion or by postreaction to dead and dying microfilariae.

mortem recovery of the adult parasites. A

Although the pathogenesis of these lesions
skin biopsy of the lesion is macerated in
is unclear, treatment with microfilaricidal
isotonic saline solution and allowed to
drugs may result in dramatic inlprovement.

stand �6 hr at room temperature. The skin is

Allergic reactions to the bites of small flies
strained off and the fluid examined for the
may produce sinlilar lesions or exacerbate
typical microfilariae.

microfilaria-associated dem1atitis. Thus,
diagnosis of Onchocerca-associated der

Treatment: Piperazine salts (220 mg/kg,
matitis may be based on responsiveness to

PO) are effective. Complete recovery
microfilaricidal treatment.

906

HELMINTHS OF THE SKIN

Microfilaiiae also accumulate in the eyes

Clinical Findings: The only external signs
of horses, but not all agree that a clear
of infection in cattle m·e focal cutaneous
association has been made between
hemorrhages ("bleeding spots") that may
microfilariae and equine uveitis (seep 508)

ooze for some hours before clotting and
or other ocular lesions in horses.

drying in the matted hair of the coat.

Bleeding spots ai·e induced by the female

Diagnosis: The most effective method of
worm, which causes the formation of a

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diagnosis is by ski.Ji biopsy, preferably a
small nodule, perforates the skill, and
full-thickness biopsy �6 mm. The tissue is
oviposits in the blood dripping from the
minced and macerated in isotonic saline for central wound. The tiny eggs contain the several hours. Microfilai·iae ai·e concenfirst larval stage ( rnicrofilariae) of the trated and stained with new methylene blue parasite. In both the northern and southern after removal of skill pieces. The microhemispheres, bleeding spots are markedly filariae can be differentiated microscopiseasonal, being most conu11on in spring and cally from Setaria spp, found in the blood
em·ly summer. Most bleeding spots occur
of cattle, and Equidae by the presence of a
along the dorswn of the m1i.Jnal, pmticuJm·ly
sheath around Setaria.

in the forequarters.

The inve1tebrate hosts are face flies of the

Treatment: No treatment is effective
genus Musca (subgenus Eiimusca), which against the adults. Ivennectin (200 mcg/kg)

ingest the eggs when feeding at the bleeding
and moxidectin ( 400 mcg/kg) are efficaspots. M aulumnalis has been identified as cious (>99"Ai) against microfilmiae and
a host in Sweden, M lusoria and M xan
produce marked clinical improvement in
lhomelas in South Afi"ica, and M vit1·ipen
horses with onchocercal dermatitis. A small
nis in Asia. Development to infective
portion of horses infected with O cervicalis
third-stage larvae in the fly takes 10-12
react to the treatment with a marked,
days. Transmission to cattle probably
edematous ventral midline swelling 1-3
occurs when the flies feed on wounds,
days after treatment. Ocular lesions have

ParajUa1ia bleeding spots, or oculm·
also been reported. These reactions usually
secretions.

resolve spontaneously, but symptomatic

Because of seasonal bleeding and the
treatment may be necessmy
cutaneous nodules, severe infections of

P bovicola have been rep01ted to i.Jnpair
the productivity of worki.J1g bullocks in

PARAFILARIA INFECTION

India; however, the major in1po1ta.J.lce of

ParajUaria in beef-producing countries

Parafilaria bovicola
is dainage to the subcutaneous tissues.

Carcasses of i.Jlfected ani.Jnals display

This filarial pai·asite of cattle causes
irregular, edematous, greenish yellow
subcutaneous l�sions that resemble
lesions that resemble brnising. These are
brnising. It also has been reported from
usually superficial but occasionally
water buffalo (Biibalus biibalis ). The worm underlying muscles are extensively
is whitish; adult females are 50-65 mm long,
involved. Lesions are most severe during
and males 30-35 nun. It is found in Asia
the spri.J1g and summer.

(Philippines, Japan, Russia, Pakistan,

Trimmed carcasses are often seriously

India), Europe (Bulgaria, Romania, Frm1ce,
disfigured and consequently downgraded.

Sweden), and Africa (Morocco, Tunisia,

In severe cases, the carcass may be

Rwanda, Burundi, South Africa, Namibia,
condemned. Lesions are more common and

Botswana, Zin1babwe). A specimen was
severe in bulls than in steers, which in tum
recovered in Canada from a bull imported
are less severely affected than female
from France, but P bovicola does not
ani.Jnals.

appear to have established itself on the

American continents and has not been

Diagnosis: The seasonal bleeding spots
reported from Australia.

are sometimes confused witl1 those caused

ParajUaria infection has been identified
by thorns, wi.J"e, ticks, or biting insects. For as a source of considerable economic loss
differentiation, either fresh or dried blood
to the beef industries of South Africa and
should be mixed with water in a test tube

Sweden, despite their climatic differences.

and centrifuged. The characteristic eggs m·e

It is fow1d primarily in range cattle in the
found on microscopic examination of the
savaJ.llla areas of southern Afiica, whereas
sedi.Jnent.

in Sweden it has emerged as a problem in

Carcass lesions can be differentiated
cattle following spring turnout to pasture
from bruising by the presence of nun1erous
after winter housing.

eosinophils in Giemsa-stained impression

HELMINTHS OF THE SKIN

907
smears made from the lesions. In addi

PELODERA DERMATITIS
tion affected tissue has a characteristic,
disagreeable, metallic smell.

(Rhabditic dermatitis)

Usually, only small numbers of wom1s are This rare, nonseasonal, acute dem1atosis present in affected carcasses and are often
results from invasion of the skin by laivae
difficult to find because of their color and
of the free-living saprophytic nematode
the accompanying inflammatory reaction.

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Pelodera strongyloides. The laivae are

Affected tissues can be incubated in wam1
ubiquitous in decaying organic matter and
saline to facilitate the recovery of parasites.

on or near the surface of moist soil but are

An ELISA for the detection of antibodies
only occasionally pai·asitic. Exposure to
againstP bovicola is available.

the laivae occuts through direct contact
with infested material such as damp, ftlthy

Treatment and Prevention: Ivermectin
bedding. The laivae may not be able to

(200 mcg/kg) or nitroxynil (20 mg/kg) given
invade healthy skin; preexisting dermatoses

SC reduces the number and surface area of
or environmental conditions favoring

Parafilaria lesions. Animals should be
maceration of the skin, eg, constant
treated at least 70-90 days before slaughter
exposure to mud or damp bedding, may
to provide sufficient time for lesions to
facilitate invasion. Pelodera dermatitis has resolve. The treatment-to-slaughter interval
been reported in dogs, cows, horses, sheep,
should not be > 120 days, because unafguinea pigs, and people.

fected laival fonns of the parasite may

Typically, lesions are confined to body
induce fresh lesions as they mature.

areas in contact with the infested material,

In trials in Sweden, use of pyrethroidsuch as tl1e extremities, ventral abdomen impregnated ear tags gave good control of
and thorax, and perinewn. Affected skin is
flies and reduced parafilarial lesions at
erythematous and partially to completely
slaughter by 75%. Ear tagging all cattle in an
alopecic, with papules, pustules, crusts,
area resulted in total control of the parasite.

erosions, or ulcerations. Pruritus is usually

The use of residually active, synthetic
intense but can be moderate or even absent.

pyrethroid dips has also effectively reduced

Differential diagnoses include demodicosis,
transmission.

canine scabies, dem1atophytosis, pyo

It may be possible to screen imported
derma, and other rare cutaneous laival
animals with an ELISA to prevent spread of
infestations such as hookworm dermatitis,
the disease to unaffected countries or, in
dirofi.lariasis, dipetalonemiasis, and strongycoajunction with residual insecticides and loidiasis.

effective anthelmintics, to eradicate new

Diagnosis is confinned easily by finding
foci of infection.

live, motile P strongyloides laivae in skin scrapings of affected areas. The laivae ai·e

Parafilaria multipapillosa
cylindrical and -600 x 38 irm. Histologic
exainination of skin biopsy speGin1ens

P miiltipapillosa is found in the subcutanereveals laivae in the hair follicles and ous tissues of horses in various parts of the
superficial de1111is and usually an inflammaworld; it is especially common in the tory dermal infiltrate. The laivae are readily

Russian steppes and eastern Europe. It 1s
cultivated on blood agar plates at 77°F
similar in size, appeai·ance, life cycle, and

(25°C).

development to P bovicola. Bloodsucking

Effective treatment consists primarily

Haematobia spp are thought to be the
of removing and destroying moist, infested
inve1tebrate hosts.

bedding mate!ial and moving the animal to a
ln spring and summer, the parasite causes clean, dry environment. Usually, spontaneskin nodules, particularly on the head and ous recovery ensues. It may be desirable
upper forequarters. These bleed transiently
to dip or spray the affected aJ1imals with
but often profusely ("summer bleeding")

an insecticidal preparation at least twice
ai1d then resolve; other hemorrhaging
at weekly intervals. Short-term use of
nodules develop as the parasite moves to a
corticosteroids may be indicated if pru!itus
different site. Occasionally, the nodules
is severe.

suppurate. The nodules and bleeding are
unsightly and interfere with harnesses of
working horses but generally are of little

STEPHANOFILARIASIS
consequence. The clinical signs are
pathognomonic.

(Filarial dermatitis of cattle)

No satisfactory treatment has been

Stephanofilaria stilesi is a small, filai·ial reported, but fly control may reduce the
parasite that causes a circumscribed
incidence.

dermatitis along the ventral midline of

908

HELMINTHSOFTHESKIN
cattle. It has been reported throughout the
pa.rakeratosis develop in the epidennis of

USA but is more common in the west and
the parasitized area
southwest. Adult worms are 3-6 mm long

Deep skin scrapings a.re ma.cerated in
and usually are found in the dermis, just
isotonic saline solution and examined
beneath the epidem1al layer. Microfilariae
microscopically for adults or microfilariae.

are 50 µm long and a.re enclosed in a

The microfilaria.e must be differentiated

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spherical, semirigid vitelline membrane.

from microfilaria.e of Onc/wcerca lienalis,

The intermediate host for S stilesi is the

O gutturosa, and Setaria spp, which a.re female horn fly, Haematobia irritans
much larger (200-250 µm), and Pelodera

( see p 892). Hom flies feeding on the lesion strongyloides (see above), a small
ingest microfilaria.e that develop to thirdfree-living nematode occasionally sta.ge infective larvae in 2-3 wk. The infective responsible for a moist, superficial larvae are introduced into the skin as the
dermatitis. The rhabditiform esophagus
horn fly feeds.

of P strongyloides is not found in filarial The dem1atitis develops along the ventral
nematodes.

midline, usually between the brisket and

No approved treatment is available for
navel. With repeated exposure, the lesion

S stilesi, but topically applied organophosspreads and often involves the skin posphates (trichlorfon 6o/o-100Ai, daily or on terior to the navel. Active lesions a.re
alternate days for 7 days) have proved
covered with blood or serous exudate,
effective against other species of Step
while cluonic lesions are smooth, d1y,
hanofil,aria. Ivennectin is reported to be
and devoid of hair. Hyperkeratosis and
effective against microfilaria.e of S zaheeri.

LICE

(Pediculosis)

Numerous species of lice pa.rasitize
long, although the species infesting animals
domestic animals. Lice are largely host
may range from 1-8 mm long. The claws of
specific, living on one species or several
the legs a.re adapted for clinging to and
closely related species. Lice are obligate
moving among hairs or feathers; the size
ectoparasites and depend on the host to
and shape of the claws tend to be specialcomplete their life cycle. Recent taxonomic ized for the average width of a hair shaft of
changes have complicated the orders and
the host species. This characteristic plays
suborders of lice. In general, lice are divided an important role in host specificity. The into two categories: bloodsucking ( or
mouthpa.rts also aid in attachment to the
sucking) lice ( order Anoplura) and chewing
host. Chewing lice have ventral chewing

(or biting) lice (formerly the order
mandibles; they feed on epidermal debris,

Mallopha.ga., now composed of three
primarily skin scales, sebaceous secretions,
suborders). Bloodsucking lice are parasites
and feathers, if applicable. The heads of
of manunals, whereas chewing lice infest
chewing lice have a blunted appearance,
both mammals and birds. Lice Jive within
with the head being wider than the thorax.

the microenvironment provided by the skin

As the name implies, bloodsucking lice have
and its hair or feathers, and are transmitted
piercing mouthpa.rts that allow them to feed
primarily by contact between hosts. All life
on the blood of their host. In contrast to the
stages occur on the host, although lice may
heads of chewing lice, those of bloodsucksurvive off the host for a period of time. In ing lice have a pointed appearance, and the
temperate regions, lice a.re most abundant
heads a.re narrower than the thorax. When
during the colder months and often are
not in use, their mouth part stylets are
difficult to find in the summer. Infestations
retracted within the head. The distinction
are most often seen on stressed anin1als,
between chewing lice and bloodsucking lice
and husbandry and individual health are
is important when choosing an effective
in1portant in treatment and management of
therapy for treatment of pediculosis.

these parasites. (See also p 2875.)

On mammalian hosts, louse eggs,
sometimes called "nits," are glued to hairs Etiology and Pathogenesis: Lice are
near the skin surface and are pale,
wingless, flattened insects, usually 2-4 mm
translucent, and suboval. The three

LICE

909 ·
nymphal stages, of increasing size, are
embedded in the skin. Diagnosis may be
smaller than adults but otherwise resemble
aided by use of a magnification device. An
adults in habits and appearance. Approxiotoscope, without the otoscopy cone, may mately 3-4 wk are required to complete one
be useful for this purpose.

generation, but this varies by species. Adult

Pediculosis of livestock is most prevalent
lice are visible to the naked eye, but
during the winter; severity is greatly reduced
magnification is often required to identify
with the approach of summer. Infestations

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the species.

of both chewing and sucking lice may

Pediculosis can result in dermatologic
become severe. In dairy herds, the young
disease, production loss, and occassionally
stock, dry cows, and bulls may escape early
anemia due to blood loss. Additionally, lice
diagnosis and suffer more severely. Young
may be vectors of more arthropod-borne
calves may die, and pregnant cows may
infections than previously believed. Lice
abort.

have been shown to transmit viruses,

Transmission usually occurs by host
bacte1ia, fungi, and protozoa. Most of the
contact. Lice dropped or pulled from the
research has focused on agents transmitted
host die in a few days, but disengaged ova
by human lice species that are known to
may continue to hatch over 2-3 wk in warm
transmit a variety of pathogens to their
weather. Therefore, premises recently
hosts, including the causative agents of
vacated by infested stock should be
epidemic typhus (Rickettsia prowazekii),
disinfected before being used for clean
louse-borne relapsing fever (Borrelia
stock
recurrentis ), and trench fever (Bartonella reC'Un·entis ), among others. Until recently, Treatment: Successful louse control is a
relatively few diseases were known to be
multifactorial process. Factors to address
vectored by domestic animal lice. A number
include treatment of the affected animal( s ),
of agents are now known or suspected to be
treatment of contact animals, environmenvectored by lice.

tal control, and properly addressing the
stressors that either permitted initial

Clinical Findings and Diagnosis:

infestation or exacerbated infestation.

Pediculosis is manifested by pruritus and

Effective treatment results in prompt
dermal irritation, with resultant scratching,
in1provement of clinical signs. Specific
rubbing, and biting of infested areas. A
pediculosis treatments are discussed below.

generally unthrifty appearance, rough coat,

It is the practitioner's duty to recommend
and lowered production in farm animals is
a saJe and effective treatment regimen. In
common. In severe infestations, there may
the USA, ectoparasiticides are regulated by
be loss of hair and local scarification.

the Environmental Protection Agency

Extreme infestation with bloodsucking lice

(EPA) or the FDA Center for Veterinary
can cause anemia. In sheep and goats,

Medicine. As a general rule, if a product
rubbing and scratching often results in
is applied topically to an animal to treat
broken fibers, which gives the fleece a
ectoparasites, and the compound is not

"pulled" appearance. In dogs, the coat
absorbed systemically, it likely falls under
becomes rough and dry and, if lice are
the jurisdiction of the EPA. If a product is
numerous, the hair may be matted. Sucking
administered parenterally, or if it is applied
lice cause small wounds that may become
topically for systemic absorption, it likely
infected. The constant crawling and
falls under the jurisdiction of the FDA. This
piercing or biting of the skin may cause
distinction is important for practitioners to
restless behavior in hosts.

recognize, because there is no legal

Diagnosis is based on the presence of lice. extra-label use of products regulated by the The hair should be parted, and the skin and

EPA. Label directions must be followed
proximal po1tion of the coat examined
regarding species treated, product
under good lighting conditions. The hair of
concentration, product dosage, individuals
large animals should be parted on the face,
allowed to administer application, and
neck, ears, topline, dewlap, escutcheon, tail
re-treatment interval. Because products
base, and tail switch. The head, legs, feet,
regulated by the FDA are approved animal
and scrotum should not be overlooked,
drugs, extra-label use may be allowed under
particularly in sheep. On small animals, the
the Animal Medicinal Drug Use and
ova are more readily seen. Occasionally,

Clarification Act (AMDUCA) (seep 2748
when the coat is matted, the lice can be seen and seep 2637). The Food Animal Residue when the mass is broken apart. Biting lice

Avoidance Databank (FARAD) can
are active and can be seen moving tJu·ough
be consulted for extra-label drug use
the hair. Sucking lice usually move more
recommendations and calculated meat
slowly and are often found with mouthparts
and milk withdrawal times.

910

LICE

Treatment of individual animals may be
at1d H quad·1ipertuses ). Except for
aided by debulking the infested coat if

H quadripertuses, these lice have a cosweather and coat type pennit. Clipping an mopolitan distribution, ie, they are found
infested animal's long, heavily soiled, or
throughout most of the world. H quadriper
matted coat can immediately reduce the
tuses, the cattle tail louse, is a tropical parasite burden on an affected animal,
louse that has extended its distribution
allow topical products to be distributed
into subtropical areas. In the USA, H

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evenly, and allow for treatment of second
quad1ipertuses has been reported in
aiy infections if present. Many compounds

California, Florida, and in other Gulf Coast
effectively kill adult and nymphal life stages, states. The cattle tail louse is known to but few have been tested for ovicidal
parasitize both Europeat1 and Zebu breeds
capabilities. Therefore, many sources
of cattle.

recommend re-treatment at intervals of

Cattle, especially young anin1als, may

7-10 days until the infestation has been
be infested with multiple species of lice
controlled. Contact animals should also be
simultaneously. S cap'illal'us and H eitry
treated to prevent spread of infestation
sternus infestations ai-e more often recogwithin a herd, flock, or household. Animal nized on mature anin1als, whereas L vituli
equipment or bedding should be washed
is more commonly seen on calves and on
frequently with hot, soapy water until
daily stock. For all age classes of cattle,
infestation is controlled. Finally, addressing
stressors such as high stocking density,
animal overcrowding, poor feed quality, and
poor feed quality, gestational status,
underlying health issues are the fmal steps
and tmderlying health issues are often
to manage pediculosis and prevent
contributing factors to susceptibility and
recmTence. New animals should be
degree of infestation. For site predilection
quarantined at1d inspected for infestation
on the host, see TABLE I.

before herd or flock integration.

Pathogenesis and Disease Transmis

CATI LE
sion: Pediculosis in cattle can decrease
weight gain at1d milk production, result

In temperate climates, domestic cattle may
in weight loss, and cause hide and hair
be infested with one species of chewing
dan1age. Some sources have reported up
louse (Damalinia bovis, fom1erly Bovicola to goA, reduced gain in cattle moderately to
bovis) at1d four species of bloodsucking
heavily infested with lice.

lice (Linognathus vituli, Solenopotes

L vituli can serve as a mechanical vector
capillatus,Haernatopinus eitryslernus,
for Anaplasma marginale, the causative
itM•il SITE PREDILECTION OF CATILE LICE

Site Predilection

CHEWING LICE

Damalinia bovis

Most conm1only found on dorsum

( cattle biting louse,

Infestation may extend cranially to head at1d caudally to red louse)

tailliead

BLOODSUCKING LICE

Linognalhus vituli

Most commonly found over withers, lateral shoulders, and (long-nosed cattle louse) dewlap

May have generalized distribution over animal

In early infestations, may be found in clusters

In heavy infestations, may be found over most of body Haernatopinus

Often found on front half of host from ears to dewlap e'ltrysternus

Westations tend to be heavier in anterior portions of the ( short-nosed cattle louse) body, including the ears, during warm weather Solenopotes capillatus

Found in distinct clusters, mainly on head and face

(little blue cattle louse)

Heavy infestations may extend to dewlap or surround eyes Haeniatopinus

Adults often confined to the tail, eggs commonly noted on quadripertuses
tail switch

( cattle tail louse)

LICE

911.

agent of bovine anaplasmosis (seep 18).

pour-on method has become a popular

Outside the USA, H eurystemus populaway to apply insecticides. Self-treatment tions have been found to contain multiple
devices also can be used, such as back

Rickettsia spp, but the role lice play in
rubbers, oilers, dust bags, and ear tags.

transmitting rickettsial agents is not well

Cattle dips have fallen out of favor in the
understood.

USA because of the labor-intensive nature
of the process and amount of chemical

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Treatment: A vaiiety of compounds
needed to keep vats charged with active
effectively control lice in cattle, including
compound. The compound chosen must be
synergized pyrethrins; the synthetic pyreappropriate for the animal's age, reproducthroids cyfluthrin, permethrin, zetacypertive status, and production system. The methrin, and cyhalothrin (including
treatment of meat and dairy animals must
ganuna-and lambda-cyhalothrin) (beef cattle be restricted to uses specified on the only); the organophosphates phosmet,
product label, and all label precautions
chlorpyrifos (beef and nonlactating dairy
should be carefully observed. Appropriate
cattle only), tetrachlorvinphos, coumaphos,
meat and milk withdrawal times must be
and diazinon (beef and nonlactating dairy
observed. In most countries, regulatory
cattle only); and the macrocyclic lactones
agencies specify tissue residue limits
ivermectin, eprinomectin, and dorainectin.

of insecticides and carefully regulate

Pour-on formulations are effective against
insecticide use on livestock. All regulabiting and bloodsucking lice, whereas tions are subject to change, and pertinent
injectable fonnulations are primarily
current local Jaws and requirements
effective against bloodsucking lice.

should be determined before treatment.

Multiple pour-on formulations of 5%

Husbandry issues ( overcrowding, poor
permetluin/5% piperonyl butoxide, 5%
feed quality, etc) and underlying health
cliflubenzuron/5% permethrin, and gainrnaconditions in animals should be addressed.

cyhalothrin are labeled for season-long

Treatment will be most effective if stock
control ( -3-4 mo) oflice on beef and dairy
trailers, chutes, and other areas cattle have
cattle. Although both anlitraz and spinosad
contacted are cleaned ai1d treated with an
are effective against lice, the last cattle
appropriate premise spray.

products containing amitraz were removed
from the USA market in 2014. Spinosad
formulations for use on cattle were officially

SHEEP AND GOATS
discontinued in the USA in 2010.

Certain Brahman and Brahman-cross

Sheep may become infested with one
cattle have organophosphate hypersensitivspecies of chewing louse, Damalinia ovis ity, which should be considered when

(formerly Bovicola ovis ), and three species selecting a treatment compound.

of bloodsucking lice: Linognathus pedalis, L

Because of ease of application and
ovillus, and L africanus ( see TABLE 2). Outside reduced stress to the treated animal, the
the USA, D ovis is also referred to as'the sheep ltti=i•fi SITE PREDILECTION OF SHEEP LICE

Site Predilection

CHEWING LICE

Damalinia ovis

Most corrunonly found on the dorsum

(sheep biting louse)

Infestation may extend cranially to head and caudally to tailliead

BLOODSUCKING LICE

Linognathus pedalis

Confined to hairy parts of the foot, except in very heavy ( sheep foot louse)

infestations

Linognathus ovillus

Usually found on hairy parts of the sheep's skin

(sheep face and body

As populations increase, lice spread to other parts of body louse)

Linognathus africanus

Often found on flanks of sheep

(African blue louse)

Fom1s clusters

Slippage of wool is common

912

LICE
body louse. Despite its name, L af7icanus is HORSES AND DONKEYS
found outside Africa, including in the USA,

Centra!Amelica, and India. L africanus has

Horses and donkeys may be infested by two
also been reported from a valiety of hosts,
species of lice, Haematopinus asini, the
including goats and several species of deer.

horse bloodsucking louse, and Damalinia

Goats can be pa.rasitized by three types
equi, the horse biting louse. D equi is also of chewing lice, namely Da.malinia ca.prae
called Wemeckiella equi and was formerly

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(formerly Bovicola caprae), D limbala
known asBovicola equi, 'I'richodectes equi,

(fo1merly B limbata), and D crassipes
and T parumpilosus. Both species a.re

(formerly Holokarlikos crassipes); and
distlibuted worldwide. D equi is a small
two types of bloodsucking lice, namely
louse, 1-2 mm long, and H asini is 3-3.5

Linognalhus slenopsis and L africanus. L
mm long. There have been repmts of
slenopsis is fow1d on both short-haired and poultry chewing lice (seep 2876) infesting

Angora breeds of goats. L slenopsis has
horses when poultry and horses a.re housed
occasionally been reported from sheep in
in the same facilities. This problem is
valious parts of the world. It is found mostly exacerbated when the poultiy ai·e removed on the long-haired parts of the hindlegs and
without concurrent aiumal or premise
back. Severe infestations are ra.re. D caprae, ti·eam1ents, leaving horses as the only host the goat biting louse, is most frequently
available.

fow1d on short-haired goats. Both D cras

Stressors such as high stocking density,
sipes and D limbala (the Angora goat biting poor feed quality, gestational status, and louse) are se1ious pests of Angora breeds.

underlying health issues ai·e often
contlibuting factors to susceptibility and

Pathogenesis and Disease Transmis
degree of infestation. Longer body hair,
sion: Affected animals often rub vigo1°
whether a winter coat or featheling, appears
ously on fencing and pens, dan1aging the
to allow for higher densities of lice to be
coat and causing excoliations. Pediculosis
sustained, because they have greater
is one cause of "wool slip" in sheep.

surface ai·ea to infest. Infestations are most

Sheep and goat lice are not known to
common in winter and ea.rly sp1ing. For site
vector any disease agents within the USA
predilection on host by species of louse, see

TABLE 3.

Treatment: Pyrethlins and pyrethroids are
labeled for control of lice in sheep and goats.

Pathogenesis and Disease Transmis

Shea.ting may be necessaiy to achieve
sion: D equi and H asini a.re not known to effective louse control on sheep and goats.

vector any disease agents in the USA

Re-treatment is often necessai-y. Husbandly
issues and individual health issues within the Treatment: A valiety of compounds flock or herd should be addressed. Shea.ting
effectively control lice on horses, including
must be done carefully, because clippers
synergized pyrethrins, synthetic pyrethroids,
may carry lice from animal to animal.

and the organophosphate cow11aphos.

'Ireatment of meat a.11d daily animals

Diazinon is no longer labeled for use on
must be restlicted to uses specified on the
horses in the USA
product label, and all label precautions

Pyrethrin and pyrethroid sprays are the
should be ca.refully observM. Appropriate
most popular method for lice control on
meat and milk withdt·awal tin1es must be
horses in the USA. Pyrethrin or pyreobserved.

throid formulations also are available
itM•M SITE PREDILECTION OF EQUINE LICE

Site Predilection

CHEWING LICE

Damalinia equi (also called

Found most commonly on the liner hairs of the body

Werneckiella equi)

Found on lateral aspects of the neck, flanks, and base of the tail

BLOODSUCKING LICE

Haemalopinus asini

Found most commonly at roots of the forelock and
mane, around base of tl1e tail, and on hairs just above the hoof ( especially in breeds with feathering)

LICE

913
in wipe-on, pour-on, and powder appli

Treatment: A variety of compounds
cations. Coumaphos is available as a
effectively control lice on swine, including
powder or spray. Caution is warranted in
synergized pyrettuins; pyrethroids; the
mares with foals at their side, because the organophosphates phosmet, coumaphos, foals may be exposed to larger amounts
and tetrachlorvinphos; and the macrocyclic
of the compound than intended, espelactones ivermectin and doramectin.

cially with powdered formulations. When

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Amitraz is no longer available for use on
using sprays, certain formulations require
swine in the USA. Although eprinomectin is
soaking the hair to the skin, including
used in cattle, this compound should not be
mane and tail, whereas others may
used in unapproved animal species, because
require only a light, misting application.

severe adverse reactions, including

Label instructions should be read
fatalities, may result.

carefully, and the manufacturer consulted

For severe infestations in swine, dust
if necessary.

formulations can be used to treat bedding.

Depending on the severity of infestation,

Husbandry and underlying health issues
the coat may be clipped. Long hair such as
should be addressed.

feathers on certain breeds, winter coats,
or resultant from endocrine disorder ( eg,

DOGS AND CATS
pituitary pars intermedia dysfunction, see
p 54 7) may make treatment more difficult.

Dogs can be infested with one species of

Husbandry issues ( overcrowding, poor
bloodsucking lice, Linognathus setosus,
feed quality, etc) and underlying health
and two species of chewing lice, Tricho
conditions should be addressed. Treatment
dectes canis andHeterodoxus spiniger.

will be most effective if trailers, stalls, wash

H spinigeris considered rare in North
racks, and other areas where horses have

America. It is distributed worldwide but
contacted are cleaned and treated with an
appears to be more corrunon in wanner
appropriate premise spray.

environments; infestations are heavier on
animals in poor physical condition. H spiniger exhibits atypical behavior for a chewing PIGS
louse-it is a blood-feeder. Dogs neglected

Domestic pigs are infested with only one
or in poor health may become heavily
species of louse, Haematopinus suis, the
infested with L setosus, which tends to
hog louse. This very large (5-6 mm) sucking prefer longhaired breeds. T canis prefers louse is common on domestic swine worldthe head, neck, and tail of the host, and it wide. Swine pediculosis is more common
may be found around wounds and body
in smaller or backyard populations than in
openings. Infestations may be heavy on very
large, commercial operations. Nymphal lice
young and very old animals. lnfested dogs
are normally found on the inside of the ears
rub, bite, and scratch the affected area and

( often in the ear canal), on the skin behind
have a rough, matted coat.

the ears, in the folds of the neck, and on

Cats can be infested with one species
the medial aspects of the legs. In severe
of chewing lice, Felicola subrostratus,
infestations, H suis may be found
although there are rare reports of
elsewhere on the body.

H spiniger on feral cats in other regions

H suis can cause severe anemia, espof the world. The louse may be seen more ecially in piglets, because of the amount of
frequently on older, longhaired cats that
blood imbibed by this large louse species.

are unable to groom themselves.

Extreme pruritus and subsequent self

Practitioners should be able to
trauma (alopecia, erythema, excoriations,
distinguish Phthirus pubis, the human
and crusting) can be seen as hogs alleviate
crab louse, from the lice of dogs and
the irritation associated with the lice
cats. This species may be presented for
feeding.

identification by owners who claim to
have found them on an animal. P pubis
does not typically infest dogs or cats;

Pathogenesis and Disease Transmis
there have been only two reports of dogs
sion: H suis is a vector of swine pox virus, infested with P pubis, both of which
and it has also been implicated as a vector
occurred from sharing bedding with a
of Eperythrozoon suis and E parvum, the person who was severely infested.

causative agents of swine eperythrozoono

With widespread use of monthly flea and
sis and of African swine fever virus in
tick preventives, pediculosis in dogs and
regions where these agents are endemic.

cats has become rare in the USA. Infestation

Except for swine pox virus, transmission of
is usually seen on debilitated, feral, stray, or
these agents by H suis is considered rare.

shelter animals.

914

LICE

Pathogenesis and Disease Transmis

( eg, flumetluin/imidacloprid collar).

sion: T canis can serve as an intennecti-Selrunectin, in1idacloprid, and fipronil have
ate host to the double-pored tapeworm,
all been used successfully to treat lice on Dipylidium caninum. This parasite of dogs
dogs and cats.

and cats can occasionally infect people. H

Although carbrunates are effective
spiniger has been found to contain the filruial against lice, carbaryl-containing collars VetBooks.ir
nematode Acanthocheilonema reconditum
were removed from the USA market in 2010,

(formerly Dipetalonema reconditum ), but
and propoxur-containing collars will no
its competence as a vector has not been
longer be available for sale in the USA after
demonstrated.

April 1, 2016. Extra-label use of ep1inomectin or doran1ectin may result in fatalities.

Treatment: A variety of compounds

Currently, spot-on products are the most
effectively control lice on dogs and cats,
popuiru· way to treat lice in dogs and cats.

including many of the topical, monthly flea

However, other fonnulations, such as
and tick control products. Pyrethrins and
collars, shrunpoos, sprays, or dusts, are
pyrethroids are very effective pediculicides.

available for insect control on pets.

However, caution must be exercised when

If the animal is heavily matted or longusing these products on cats, because this haired, treatment may be facilitated by
species is highly sensitive to pyrethrins and
clipping the coat. Bedding should be washed
pyrethroids, lacking the ability to metabofrequently in hot, soapy water or treated lize high doses. Limited pyretluin or
with an approved bedding or premise spray
pyrethrin products are labeled for use on
until the infestation is controlled. Certain
cats; the products either contain very low
fipronil products are labeled for this use.

concentrations of the active compound or

Nutritional deficiencies or concurrent health
are available in a slow-release formulation
conditions should be addressed.

MANGE

(Cutaneous acariasis, Mite infestation)

Mange is a contagious disease characterized

Successful mange treatment is a
by crusty or scaly skin, pruritus, and
multifactorial process, including treatment
alopecia. Mange is a general tenn for
of the affected animal(s), treatment of
cutaneous acariasis and is the result of
contact animals, and environmental
infestation with one of several genera of
control. Isolation of affected animals for
parasitic mites, including Chorioptes,

2 wk is often recommended to prevent or

Demodex, Psorobia (forn1erly Psorergates ), limit spread of contagious mites. Care Psoroptes, Sarcoptes, and others. The term
should be taken to prevent contact of naive

"scabies" most appropriately refers to
animals with potentially infested fomites
infestation with Sarcoptes sp mites (ie,

(eg, animal bedding, feed and water
sarcoptic mange); however, this term is
buckets, tack ru1d other equipment).

commonly misused to refer to any type

Specific treatments are discussed for
of mange.

each species below.

Historically, mange in large rulimals was a
reportable disease because of the severity

CATTLE
of clinical signs and contagiousness.

However, widespread use of macrocyclic

Sarcoptic Mange (Scabies): Sarcoptes
lactones beginning in the 1990s has
scabiei var bovis is a highly contagious provided effective treatment and decreased
disease spread by clirect contact between
the prevalence. As a result, mange is no
infested and naive anin1als or by contan1ilonger a federally reportable clisease in the nated fomites. Lesions caused by tllis

USA. However, some types of mange in
bwTowing mite start on the head, neck, and
large animals remain reportable to certain
shoulders and can spread to other parts of
state agencies, although this may change
the body. The whole body may be involved
as the lists are revised.

in 6 wk. Pruritus is intense, and papules

MANGE

915
develop into crusts; the skin thickens and
from Texas, New Mexico, Oklal10ma,
forms large folds. Diagnosis is made by deep Kansas, Colorado, and Nebraska. Clinical skin scrapings, skin biopsy, or response to
signs of P ovis infestation are rare in dairy therapy. S scabiei var bovis can be cattle. These mites pierce host tissue at1d
transmitted to people and result in a
feed on seru.n1 and oilier fluid secretions
transient, self-li.n1iting dennatitis.

from the bite wound. Exudates coagulate

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The following compounds are approved
to form thick, scabby crusts. Alopecia is
for use against sarcoptic mange mites in
conunon wiili exudative dennatitis.

cattle at the labeled injectable and pour-on

Westations are intensely pruritic, with
dosages: doramectin, eprinomectin, and
papules, crusts, excoriation, and lichenificaivern1ectin. Hot lime sulfur dips or sprays tion on the shoulders and rump initially,
may be used, following the label instrucspreading to cover almost ilie entire body.

tions for species-specific dilution, with

Secondary bacterial infections are common
treatment repeated at 12-day intervals as
in severe cases. Death in untreated calves,
needed, usually for a maximum of three
weight loss, decreased milk production, and
treatments. Phosmet is also labeled for use
increased susceptibility to oilier diseases
against sarcoptic mange mites in cattle; two
can occur.

treatments may be required. Label

Treatment can be done by spray dipping
instructions for dilution (multiple dilutions
or vat dipping; topical application of nonsysare listed) should be followed as appropritemic acaricides; and oral, topical, or ate. Certain spray fonnulations of pern1ethinjectable forn1ulations of systemic drugs.

rin are labeled for use against sarcoptic

Spray dipping is time consuming but useful
mange mites, but it is generally not confor small herds, whereas vat dipping has sidered tl1e compound of choice. If
fallen out of favor in the USA because of
pennetlui.n is used, the animals should be
expense and the difficulty in managing
wet thoroughly with the product and
proper concentrations of therapeutic
re-treated in 10--14 days.

compow1ds and proper cleanup. Toxaphene

Practitioners and producers should take
spray (0.5%--0.6%) was used historically;
care to note whether the compound, dose,
however, all uses of toxaphene were baimed
and forn1ulation are appropriate for the age
in the USA in 2001 and prohibited internaof the aninlal and the production system in tionally tJu·ough ilie Stockl10lm Convention
use. Eprinomectin and moxidectin pour-on
on Persistent Organic Pollutants, effective
formulations, as well as hot lime sulfur, are

2004.

approved for use on dairy animals in the

In the USA, the following treatments are

USA.

labeled for use against P ovi s in cattle at the labeled dosages: injectable dorarnectin,

Psoroptic Mange: Psoroptic mange in
injectable ivermectin, and moxidectin
cattle is caused by infestation with

(pour-on and injectable forn1ulations). Hot

Psoroptes ovis. Current taxonomic and
lime sulfur dips or sprays may be used,
systematic classification of Psoroples spp
following the species-specific dilution
indicates thatP ovis and P cuniculi ( ear labeled on the package, with treatment
canker in rabbits, ear mange in sheep and
repeated at 12-day intervals as needed,
goats) are strains or variants of the same
usually for a maximum of three treatments.

species, with P ovis being found primatily

Of iliese, only pour-on moxidectin and hot
on ilie backs and flanks of infested aninlals
lime sulfur are approved for use on dairy
and P cuniculi in the ears. P ovis is not aninlals. Certain spray fonnulations of
zoonotic.

permethrin are labeled for use against

P ovis is a nonbuITowing mite that lives
mange mites in cattle, but it is generally not
on the skin surface. All stages of the mite
considered the compound of choice. If
are found on the host, and transmission is
pern1etlui.n is used, the aninlals should be
through direct contact of infested and
tl1oroughly wet with the product and
susceptible hosts. Trat1Smission is also
re-treated in 10--14 days. Outside the USA,
possible through contact with contaminated other treatments are available and labeled environments or fomites, because P ovis
for the control of mange, including
can survive off the host for ;o.2 wk under ilie
flumethrin pour-on (2 mg/kg, repeated 10
right conditions.

days later), 0.3% cownaphos, O.lo/ophoxi.m,

P ovis is a common parasite of cattle with 0.075% diazinon, and 0.025--0.05% arnitraz.

a dist1ibution limited to continental Europe

There are currently no arnitraz products
and parts of the USA. It can be found in
labeled for use on cattle in the USA.

range and feedlot beef cattle from the

Diazinon is available for use on cattle only
central and western states, with the lai·gest
in an ear tag formulation in the USA; it is not
numbers of outbreaks histo1ically reported
labeled for treatment or prevention of

916

MANGE
mange. Products labeled for treatment and
should be repeated at 12-day intervals if
control of sarcoptic mange in cattle are
needed. Of these, the pour-on formulations
considered effective against? ovis.

of eprinomectin and moxidectin as well as
hot lime sulfur are approved for use on dairy

Chorioptic Mange (Le� Mange, Foot
animals in the USA.

and Tail Mange, Symbiotic Mange,

Barn Itch): Chorioptic mange in cattle is

Demodectic Mange (Follicular

VetBooks.ir
caused by infestation with Clwrioptes bovis Mange, Bovine Demodicosis): or C texanus. Species of Chorioptes are not Three species of Demodex are known to
host specific, and C bovis can be found on
infest cattle: D bovis, D ghanensis, and
domestic ruminants and horses through

D tauri. D bovis is the most conunon and
out the world. Chorioptic mange caused
infests hair follicles of cattle worldwide.

by infestation with C bovis is the most

D ghanensis infests meibomian glands of
common type of mange in cattle in the
cattle from Ghana, and D tauri has been

USA. C lexanus has been reported on cattle
recovered from hair follicles and sebaceous
from Brazil, China, Germany, Israel, Japan,
glands of cattle from Czechoslovakia

Malaysia, South Korea, and USA. C bovis

Species of Demodex are host specific and
and C texanus are not zoonotic.

not zoonotic.

C bovis live on the skin surface and do

Demodex spp are unique among parasitic
not burrow. Life cycle stages include egg,
mites, because they are elongated with
larval, two nymphal, two female, and one
sh01t, stwnpy legs. Their distinct morpholmale stage. Eggs are deposited on the skin, ogy is a preswned adaptation to living in
and secretions from female mites help
hair follicles and sebaceous glands of their
secure eggs to the surface of their hosts.

hosts. All life cycle stages are found on the

Eggs require 5-6 days to hatch, whereas
host and include egg, laivae, two nymphs,
each larval and nymphal stage requires 3---5
and adults. These mites feed on sebwn,
days for development. The entire life cycle
protoplasm, and epidermal debris.

may be completed in 21-26 days and

Transmission of D bovis occurs through
depends on temperature and hwnidity.

close contact of infested and naive hosts,

Transmission is by direct contact of infested with the transfer of mites from infested and naive hosts. C bovis can live off their dams to neonates being the primary route.

host for up to 3 wk and can be transmitted

Lesions consist of follicular papules and
to cattle through contact with contaminated nodules, especially over the withers, neck, fomites and housing.

back, and flanks. Invasion by D bovis results C bovis likely feeds on sloughed skin cells in chronic inflainmation, with formation of and other surface debris. While feeding,
ulcers, abscesses, and fistulae due to

C bovis irritates the host skin, causing
follicular rupture or secondary staphylococabrasions that become contanlinated with cal infection. Pruritus is absent. Infestation
secretions and feces from the mites. Most
of D bovis may result in considerable cattle are subclinically infested with
damage to hides. Cattle of any age are

C bovis. However, C bovis may cause an susceptible to demodectic mange, although
allergic, exudative, mildly pruritic, flaky
disease is more evident in the young. Most
dermatitis. Lesions include nodules,
cases are seen in dairy cattle in late winter
papules, crusts, and ulcets that typically
or early sp1ing. Infestation with D bovis is begin at the pastern and spread up the legs
usually subclinical, and infestation may
to the udder, scrotum, tail, and perinewn.

Self-trawna and alopecia may be evident.

Lesions and clinical signs appear in late
winter and spontaneously regress during
swnmer months. Chorioptic mange is less
pathogenic than sarcoptic or psoroptic
mange in cattle. Diagnosis is by observation
of mites in skin scrapings.

In the USA, the following treatments are
approved for use against C bovis at the
labeled dosages: pour-on doramectin,
eprinomectin (both pour-on and irtjectable
formulations), and pow"--On moxidectin. Hot
lime sulfur dips or sprays are labeled for use
against cho1ioptic 1nites and may be used
following the label directions for species

Demodex bovis, skin lesions. Courtesy of Dr.

specific di! ution. Lime sulfur treatment

Raffaele Ronca/Ii.

MANGE

917
extend for many months. Diagnosis is by
be repeated every 12 days if needed. Certain
observation of mites in deep skin scrapings.

fonnulations of permethrin sprays are

Recovery is usually spontaneous; conselabeled for mange in sheep and goats. As quently, treatment is rarely perfom1ed. If
witll cattle, permetluin is generally not
tl1erapy is instituted, tile macrocyclic
considered the compound of choice, but if
lactones listed for treatment of Sarcaptes
used, tile animals should be tl1oroughly wet

VetBooks.ir
scabiei var bavis or Chariaptes avis should with tile product and re-treated in 10-14
be considered.

days. Topical treatments are more likely to
be effective if sheep are freshly shorn. Oral

Psorergatic Mange (Itch Mite): Psara
ivermectin sheep drench is not labeled for
bia bas (formerly Psarergates bas) is a small treatment or control·of mange. Altllough
mite tllat lives in tile superficial layers of
single doses of oral ivern1ectin have been
cattle skiI1. In most instances, P bas is
shown to reduce tile nun1ber of Psaraptes
nonpathogenic, and few cattle exhibit clinical avis mites witllin 24 hr, a single oral dose is signs of infestation. On rare occasions, mild
not considered curative. For these reasons,
pruritus, alopecia, and increased licking and
extra-label drug use of macrocyclic lactones
rubbing have been attributed to infestation
in sheep and goats is common. However,
witll P bas. This mite has been reported from practitioners should consider compounds
cattle in tile USA, Canada, tile UK, and Soutll
labeled for a large range of species, tile

Africa. P bas is not zoonotic. The disease
production system of tile animals treated,
does not cause significant economic losses;
and any warnings against use in species
tllerefore, animals are usually not treated.

not listed on the label. Outside the USA,

The macrocyclic lactone products labeled for ir\jectable ivermectin is approved to treat use for sarcoptic, chorioptic, and psoroptic

P avis in sheep at the labeled dosage of 200
mange likely control tllis infestation
mcg/kg, two doses given 7 days apart.

effectively.

Sarcoptic Mange: Sarcaptes scabiei

SHEEP AND GOATS
var avis infests sheep, and S scabiei var caprae infests goats, throughout tile world.

It is the practitioner's duty to recommend a

However, S scabiei var avis is rare in the safe and effective treatment regin1en, but

USA. This mite infests nonwooly skin,
tllis proves difficult when treating mange in usually on tile head and face. Typical of sheep and goats. In tile USA, ectoparasitiscabies, lesions manifest witll formation cides are regulated by the Environmental
of crusts and intense pruritus. Affected

Protection Agency (EPA) or the FDA
aninlals have decreased reproduction,

Center for Veterinary Medicine. As a
meat gain, and milk yield. In goats, S scabiei
general rule, if a product is applied
var caprae is responsible for a generalized topically to an aninlal to treat ectoparaskin condition characterized by marked sites, it likely falls under the jurisdiction of
hyperkeratosis. Lesions start usually on tile
the EPA. If a topical product is used to treat
head and neck and can extend to tile inner
both external and internal parasites, it
thighs, hocks, brisket, ventral abdomen,
likely falls under jU1isdiction of tile FDA.

and axillary region. Botll S scabiei var avis This distinction is inlportant for practitionand S scabiei var caprae are zoonotic.

ers to recognize, because there is no legal

Consistent witll otller aninlal vruiants of
extra-label use of products regulated by the Sarcaptes, zoonoses are initiated from EPA. Label directions must be followed
direct contact with infested aJlin1als but
regarding species treated, product
are self-linliting infestations.

concentration, product dosage, individuals
allowed to administer application, and

Chorioptic Mange: Chariaples bavis
re-treatment interval. Because products
infests sheep and goats worldwide.

regulated by the FDA are approved animal

Prevalence of C bavis is more common in
drugs, extra-label drug use may be allowed
rruns tllan ewes or lrunbs. Infestation of
under the Aninlal Medicinal and Drug Use

C bavis on goats is fairly common, witll
and Clarification Act (AMDUCA). (See also
most of a herd infested. Distribution of
p 2748 and seep 2637.) The Food Animal
lesions is tile srune as tllat in cattle, with

Residue Avoidance Databank (FARAD)

papules ru1d crusts seen on the feet ru1d legs.

can be consulted for extra-label drug use

Most sheep ru·e subclinically infested witll
recommendations and calculated meat

C bavis. However, C bavis can cause and milk withdrawal tinles.

exudative dermatitis on the lower legs and

Hot lime sulfur spray or dip is labeled for
scrota of ran1s ( scrotal mange). Semen
use against sarcoptic, psoroptic, and
quality may be affected, presU1nably due to
chorioptic mites in sheep. Treatment should increased temperature of infested scrota.

918

MANGE

Psoroptic Mange (Sheep Scab, Ear
affected. However, intense generalized

Mange): Psoroptes ovis is a highly
prnritus and scaliness, with matting and loss
contagious and severe infestation of sheep.

of wool can result from infestation with

This mite has been eradicated from sheep

P ovis. All breeds of domestic sheep are
in Canada, New Zealand, and the USA.

susceptible. Because of their small size, the

However, sheep scab persists in many
mites are difficult to find in skin scrapings.

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countries, including some in Europe.

This disease can cause significant economic

Intense prnritus leads to large, scaly,
losses through weight loss and wool
crnsted lesions that develop in more
damage. Treatments effective against
densely haired or woolly parts of the body.

sarcoptic, chorioptic, and psoroptic mange

Lesions begin on the back and side but may
in sheep are expected to be efficacious for
become generalized and cover a large
psorergatic mange.

portion of the body. Anin1als bite, lick, and
scratch in response to the prnritus, which

HORSES
results in wool loss and secondary bacterial
infection. If affected sheep are not treated,

The last large anin1al mange reportable to
infested animals may become emaciated
the OIE was horse mange, but this was
and anemic and possibly die.

removed in 2006. Mange in horses was

Psoroptic mange ( ear mange) in goats and removed from the list of federally reportsheep is caused by P cuniculi, which is able diseases in the USA prior to this date,
likely a variant of P ovis. P cuniculi typically although it remains reportable to some state infests the ears of goats but can spread to
veterinary agencies.

the head, neck, and body. Infestation of

P cuniculi in goats can be common, with

Sarcoptic Mange: Sarcoptes scabiei var 80%---900/o of a herd infested. Disease can
equi is rare but is the most severe type of range from subclinical to scaling, crnsting,
mange in horses. The first sign of infestation
inilanunation, alopecia, ear scratching, head
is intense pruritus due to hypersensitivity
shaking, and nibbing of ears and head to
to mite products. Early lesions appear on
alleviate irritation. Although the course is
the head, neck, and shoulders. Regions
chronic, the prognosis is good with
protected by long hair and lower parts of
appropriate treatment.

the extremities are usually not involved.

Lesions start as small papules and vesicles

Demodectic Mange (Ovine Demodico
that later develop into crnsts. Alopecia
sis, Caprine Demodicosis): Demodex
and crnsting spread, and the skin becomes
ovis infests sheep, and D caprae infests lichenified, fanning folds. If infestations are
goats. Demodectic mange in sheep is not
not treated, lesions may extend over the
common, whereas D caprae are relatively
whole body, leading to emaciation, general
common in goats. Lesions are similar to
weakness, and anorexia. Negative skin
those in cattle. In goats, nonprnritic papules
scrapings do not exclude the disease; biopsy
and nodules develop, especially over the
may establish a diagnosis.

face, neck, shoulders, and sides or udder.

Hot lime sulfur spray or dip is labeled

Demodectic mange in goats occurs most
for use against sarcoptic, psoroptic, and
commonly in kids, pregna.ot does, and dairy
chorioptic mites in horses. Treatment
goats. The nodules contain a thick, waxy,
should be repeated every 12 days if needed,
grayish material that can be easily expressed; following the species-specific dilution on mites can be found in this exudate. The
the label. Although certain spray fom1uladisease can become chronic. Historically, in tions of permethrin are labeled for use
some cases, localized lesions in goats have
against mange in horses, it is generally not
been managed by incision, expression, and
considered the compound of choice. If
infusion with Lugol's iodine or rotenone in
permethrin is used, the anin1als should be
alcohol (1:3). This practice should not be
thoroughly wet with the product and
continued or condoned. Rotenone, a
re-treated in 10---14 days. Although not
plant-derived ketone once a popular
labeled for treatment of mange in horses,
pesticide and ectoparasiticide approved for
two doses of oral ivermectin at 200 mcg/kg
use in organic fanning, is now available only
given 14 days apart (field studies), or a
as a piscicide in the USA and Canada.

single treatment of oral moxidectin at

400 mcg/kg, have effectively treated

Psorergatic Mange (Itch Mite,
psoroptic, chorioptic, and sarcoptic

Australian Itch): Psorobia ovis (formerly mange in horses.

Psorergates ovis) is a common skin mite of
sheep in Africa, Australia, New Zealand, and

Psoroptic Mange: Psoroptes ovis

South An1erica. Most infested sheep are not

(formerly P equi) and P cuniculi (likely a

MANGE

919
variant of P ovis) both infest horses. P ovis or D caballi. Demodex mites infest hair
is rare in horses. However, infestations can
follicles and sebaceous glands. D equi lives produce lesions on thickly haired regions of
on the body, and D caballi on the eyelids
the body, such as under the forelock and
and muzzle. Demodectic mange is rare in
mane, at the base of the tail, under the chin,
horses but can manifest as patchy alopecia
between the hindlegs, on the udder, and in
and scaling or as nodules. Lesions appear

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the axillae. P cunicul'i can sometimes cause on the face, neck, shoulders, and forelimbs.

otitis extema in horses and may cause head

It has been reported in association with
shaking. Pruritus is characteristic. Lesions
pituitary pars intermedia dysfunction
start as papules and alopecia and develop

(seep 54 7) and chronic corticosteroid
into thick, hemorrhagic crusts. Psoroptic
treatment. Pruritus is absent; therefore,
mites a.re more easily recovered from skin
secondary infections due to excoriation are
scrapings than are sarcoptic mites. Topical
rare. Therapy is rarely done, although there
and oral treatments recommended for other
is limited evidence that the macrocyclic
types of mange are effective. Hot lin1e sulfur
lactones may be effective. Lesions have also
is labeled for use aga.instPsoroptes in
been reported to resolve without treatment.

horses ( see above). Although not labeled
for treatment of mange in horses, oral

Trombiculidiasis (Chiggers, Harvest
ivermectin at 200 mcg/kg given for two

Mite): Trombiculid mites can parasitize
doses 14 days apart (field studies), or a
the skin of horses, especially during the
single treatment with oral moxidectin at
late summer and fall. The adult mites live

400 mcg/kg, has effectively treated
on inve1tebrates and plants; the larvae
psoroptic, chorioptic, and sarcoptic
normally feed on small rodents, but they
mange in horses.

can oppo1tunistically feed on people and
domestic animals, including horses. Lesions

Chorioptic Mange (Leg Mange):

consist of severely pruritic papules and

Chorioptic mange is caused by infestation
wheals on the face, lips, and feet. At the
with Chorioptes bovis (fom1erly C equi)

time of diagnosis, a topical pyrethrin or
and is the most common fonn of mange
pyrethroid labeled for horses can be used
in horses. Draft horses are commonly
to kill any remaining larvae still feeding.

infested, although all breeds are suscepti

Symptomatic treatment with a g]ucocortible. Lesions caused by C bovis start as a coid for pruritus can be added to minin1ize
pruritic dermatitis affecting the distal limbs
further self-trauma and associated
around the foot and fetlock. Papules are
secondary infections. Any secondary
seen first, followed by alopecia, crusting,
infections should be treated. Repellents
and thickening of the skin. A moist dem1-
may help prevent infestation.

atitis of the fetlock develops in chronic
cases. Wested horses may stamp their feet

Straw Itch Mite (Forage Mite): These
or rub one foot against the opposite leg or
mites usually feed on organic material in
object. Chorioptic mange is a differential
straw and grain and can opportunistically
diagnosis for "greasy heel" in draft horses.

infest the skin of horses. Papules and

The signs subside in summer but recur with
wheals appear on the face and neck if
the return of cold weather. The disease
horses are fed from a hay rack, and on the
course is usually chronic without treatment,
muzzle and legs if fed from the ground.

but the prognosis is favorable when treated.

Pruritus is va.iiable. Treatment for

Topical and oral treatments recommended
trombiculidiasis may be used for straw itch
for other types of mange are effective.

mite infestations.

Hot lime sulfur is labeled for use against

Chorioptes in horses (see above).

PIGS

Treatment is aided by clipping long hair
from infested areas. Although not labeled

Mange in pigs is principally due to
for treatment of mange in horses, oral
infestation withSarcoptes scabiei var suis.

ivermectin at 200 mcg/kg given for two

Rarely, infestation with Demodex phyl
doses 14 days apart (field studies), or a
loides has been reported to cause clinical
single treatment with oral moxidectin at 400
disease in pigs.

mcg/kg, has effectively treated psoroptic,
chorioptic, and sarcoptic mange in horses.

Sarcoptic Mange: Sarcoptic mange,
caused by infestation with Sarcoptes
scabiei var suis, is of primary importance in Demodectic Mange (Equine Demodi
pigs worldwide. S scabiei var suis in a herd cosis): Demodectic mange in horses is
typically becomes established after
caused by infestation with Demodex equi
introduction of infested breeding stock.

920

MANGE

Transmission of S scabiei var suis can mange in swine. In swine, lime sulfur dips
occur rapidly through direct contact of
ar·e repeated at intervals of 3-7 days to treat
infested and naive pigs. However, transmismange, unlike in other species in which sion to naive pigs is also possible through
they are repeated every 12 days. Label
contact with fomites contaminated with
instructions must be followed closely,

S scabiei var s·u·is. Survival of the mite eggs because there are three possible lime sulfm

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away from the host is limited. However,
dilutions for use on swine. Unlike phosmet,
exposure for as little as 24 hr to contamilime sulfur spray can be applied to suckling nated pens that were recently vacated by
pigs. Certain spray formulations of
infested pigs resulted in transmission of the
pem1ethrin am labeled for use against
mite. Laboratory experiments indicated that mites on swine, but it is generally not S scabiei var suis did not survive >96 hr at considered the compound of choice. If
temperatures <25°C or >24 lu· at 20° -30°C.

pennethrin is used, animals should be wet

Survival was <l lu· at temperatures >30°C.

thoroughly with the product and re-treated

Unless pigs originated from SPF colonies or
in 14 days. Phosmet spray is approved for
after mange eradication programs, all pig
sarcoptic mange in swine at the speciesherds must be considered potentially specific dilution instructions on the label.

infested even if aca.ricides a.re used

A single treatment is usually effective, but
routinely.

a second treatment can be applied 14 days

Lesions due to infestation with S scabiei
later if necessary. Phosmet should not be
var siiis usually start on the head, especially applied directly to suckling pigs. Couthe ears, then spread over the body, tail, and ma.phos sprays are available for use on
legs. Itching can be intense and associated
swine in the USA, but they are labeled only
with a hypersensitivity reaction to the mites. for control of lice.

As the hypersensitivity subsides, typically
after several months, the thickened, rough,

Demodectic Mange (Swine Demodi
dry skin is covered with grayish crusts.

cosis): Demodectic mange caused by

Infestations are negatively coITela.ted with
infestation with Demodex phylloides is
daily weight gains and feed conversion in
possible in pigs. Clinical signs of D phyl
pigs.

loides infestation include reddening of the Experimental studies of S scabiei var
skin, pustules, and alopecia. Although rare
suis in pigs have demonstrated that
in domestic pigs, D phylloides infestation
infestation alters the microbial community
car1 be common in wild boars without overt
on the skin. Comparing the microbiome of
signs of clinical disease. In wild boars, the
bacteria. on pigs witl10ut S scabiei var suis highest prevalence and greatest numbers
versus that of infested pigs showed that
of D phylloides were found in sebaceous
noninfested pigs had low relative abunglands in eyelids and cheeks. D phylloides dances of Staphylococcus, whereas the
can also be found a.round the eyes, mouth,
relative abundance of Staphylococcus
snout, ventral neck, ventrun1, and thighs.

increased significantly on pigs with

There is no reliable treatment.

S scabiei var suis during the comse of infestations. Specifically, tl1e staphylococci

DOGS AND CATS
population shifted from S lwminis to that
of the more pathogenic S chromogenes as

Sarcoptic Mange (Canine Scabies):

scabies progressed.

Sarcoples scabiei var canis infestation Diagnosis is best performed by combinis a highly contagious disease of dogs ing different approaches: dermatitis score
found worldwide. 111e mites are fairly host
recorded at slaughter, scratching index,
specific, but anin1als (including people) that
observation of clinical signs of mange, ear
come in contact with infested dogs can also
or skin scrapings for microscopic examinabe affected. Adult mites are 0.2-0.6 mm long tion, and ELISA for detection of specific
and roughly circular· in shape; their surface
antibodies. The usefulness of ea.ch criterion
is covered with small triangular spines, and
may vary according to the group age. This
they have four pairs of sh01t legs. Females
global approach is particularly useful during are almost twice as large as males. The an eradication campaign.

entire life cycle (17-21 days) is spent on the

Injectable dora.rnectin and ivennectin are
dog. Females burrow tunnels in the stratmn
labeled for use a.gainstS scabiei var suis comeun1 to lay eggs. Sa.rcoptic mange is
and are considered highly effective
readily transmitted between dogs by direct
treatments. In some instances, a second
contact; transmission by indirect contact
dose of macrocyclic lactone 14 days later
may also occur. Clinical signs may develop
may be necessary for complete resolution.

anytime from 10 days to 8 wk after contact

Hot lime sulfur is labeled for use against
with an infected animal. Asymptomatic

MANGE

921
carriers may exist. Intense pruritus is
milbemycin oxirne and ivennecti.n, which
characteristic and probably due to
are not registered for treatment of sarcoptic
hypersensitivity to mite products. Primary
mange in dogs, have been reported to be
lesions consist of papulocrustous eruptions
effective depending on the dosage and
with thick, yellow crusts, excoriation,
route of administration. The recommended
erythema, and alopecia. Secondary
dosage for milbemycin oxi.me is 2 mg/kg,
bacterial and yeast infections may develop.

PO, weekly for 3-4 wk; potential toxicity

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'Typically, lesions start on the ventral
should be considered in dogs with averabdomen, chest, ears, elbows, and hocks mectin sensitivity. Ivennectin (200 mcg/kg,
and, if w1treated, become generalized. Dogs

PO or SC, 2-4 treatments 2 wk apart) is very
with chronic, generalized disease develop
effective and usually.curative. Ivermectin at
seborrhea, severe thickening of the skin
this dosage is contraindicated in avermecwith fold fonnation and crust buildup, tin-sensitive breeds. Additionally, the
peripheral lymphadenopathy, and
microfilaremic (Diroji.laria immilis)

emaciation; dogs so affected may even die.

status of the dog should be evaluated before

"Scabies incognito" has been described in
treatment with a macrocyclic lactone. For
well-groomed dogs; these dogs, infested
topical treatment, hair can be clipped, the
with sarcoptic mites, are prwitic, but
crusts and dirt removed by soaking with an
demonstrating the mites on skin scrapings
antiseborrheic shan1poo, and an acaricidal
is difficult because the crusts and scales
clip applied. Lime sulfur is highly effective
have been removed by regular bathing.

and safe for use in young aninlals; several

Atypical, including localized, clinical forms
dips 7 days apart are reconunended.

that are probably linked to extensive use

Amitraz is an effective scabicide, although
of insecticides or acaricides are being
it is not approved for this use. It should be
increasingly seen.

applied as a 0.025% solution at 1- or 2-wk

Diagnosis is based on the history of
intervals for 2-6 wk. In addition, the owner
severe pruritus of sudden onset, possible
must observe certain precautions to avoid
exposure, and involvement of other
self-contanlination. Fipronil spray was
aninlals, including people. Making a
repo1ted to be effective but should be
definitive diagnosis is sometimes difficult
considered an aid in control rather than a
because of negative skin scrapings.

p1irnary therapy. Treatment can be topical

Concentration and flotation of several
or systemic, and should include all dogs in
scrapings may increase chances of finding
contact.

the mites, eggs, or feces. Several extensive
superficial scrapings should be done of the

Notoedric Mange (Feline Scabies):

ears, elbows, and hocks; nonexcoriated

This rare, highly contagious disease of cats
areas should be chosen. A centrifugation
and kittens is caused by Notoedres cali,
fecal flotation using sugar solutions may
which can opportunistically infest other
reveal mites or eggs. A specific and sensitive aninlals, including people. The mite and its commercially available ELISA to detect
life cycle are similar to the sarcoptic mite.

specific antibodies has been developed and

Pruritus is severe. Crusts and alopecia are
may be useful. Because mites can be
seen, particularly on the ears, head, and
difficult to detect, if Sarcoples is on the neck, and can become generalized. Mites
differential diagnosis list but no mites are
can be found quite easily in skin scrapings.

found, a therapeutic trial is warranted.

Treatment consists of both topical and

Systemic treatments of scabies are based
systemic therapies. Nonapproved but
on administration of macrocyclic lactones,
effective and safe treatments include
some of which are FDA approved for this
selarnectin (6 mg/kg, spot-on) and
purpose. Among them, selan1ectin is given
moxidectin (1 mg/kg, spot-on, in the
as a spot-on fom1ulation at 6 mg/kg. This
imidacloprid-moxi.dectin formulation).

drug appears to be safe, even in ivem1ectin

Ivermectin (200 mcg/kg, SC) has also been
sensitive breeds. Another is the imidacloused. Another effective topical therapy is prid-moxidectin formulation, which may be
lime sulfur dips at 7-day intervals.

used on dogs as young as 7 wk of age. In
some countries, moxidectin is also

Otodectic Mange: Otodectes cynotis
registered for treatment of scabies. It is
mites are a common cause of otitis extema,
available as a spot-on fo1mulation in
especially in cats but also in dogs. Mites that
combination with imidacloprid and should
belong to the fanilly Psoroptidae are usually
be given in two doses of 2.5 mg/kg, 4 wk
found in both the vertical and horizontal ear
apart; additionally, oral uptake should be
canals but are occasionally seen on the
prevented in breeds at risk of avennectin
body. Clinical signs include head shaking,
sensitivity. Other endectocides, such as
continual ear scratching, and ear droop.

922

MANGE

Pruritus is vaiiable but may be severe. Dark

Both topical and systemic acaricides are
brown cerurnen accumulation in the ear
effective against cheyletieUosis, although no
and suppurative otitis extema with possible
dmgs ai·e currently licensed for this
perforation of the tympanic membrane
indication. In addition to treatment of the
may be seen in severe cases. Affected and
affected aitimals, it is necessary to treat aJJ
in-contact animals should receive approin-contact anin1als. Topical dmgs include VetBooks.ir
p1iate parasiticide treatment in the ears.

lime sulfur, fipronil spot-on and spray,

Systemic therapies have been approved
permethrin, and amitraz (the latter two
and include topically applied selamectin
dmgs are contraindicated in cats).

and moxidectin. Direct applications to the

Extra-label systemic dmgs include
external ear canal of cats using approved
sela.rnectin spot-on, mllbemycin oxirne
ivermectin and milbemycin fo1mulations

(PO), and ivern1ectin (SC). Care must be
ai·e also effective. As a general rule, ear
taken to avoid or minimize the risks of
cleansing with an appropriate ceruminolytic adverse reactions as described above (see agent is indicated with any therapy.

p 920). The treatment period depends on
the selected drng but must be long enough

Cheyletiellosis (Walking Dandruff):

to eradicate the mites from botl1 tl1e anin1als

Cheyletiella blakei infests cats, C yasguri and their environment, which can be
infests dogs, and C parasitovorax infests
difficult in anin1al commLU1ities ( eg,
rabbits, although cross-infestations are
breeding colonies, kennels). In practice,
possible. This disease is very contagious,
treatment lasts 6-8 wk and should continue
especially in animal communities. Hwnan
for a few weeks beyond din ical cure until
infestation is frequent. Mite infestations ai·e
parasitologic cure is achieved.

rare in flea-endemic areas, probably
because of the reguJai· use of insecticides.

Canine Demodicosis: Canine demodico

These mites have four pairs of legs and
sis occurs when large nLU11bers of Demodex
prominent hook-like mouthparts. They live
canis mites inhabit hair folJicles and
on the surface of the epidermis, and their
sebaceous glands. In small nwnbers, tl1ese
entire life cycle (3 wk) is spent on the host.

ntites are part of the normal flora of canine

Female mites can, however, survive for as
skin and usually cause no clinical disease.

long as 10 days off the host. Clinical disease

The ntites are transmitted from dan1 to
is characterized by scaling, a dorsal distribupuppies during nursing within the first 72 hr tion, and pruritus, which varies from none
after birth. The mites spend their entire life
to severe. Cats can develop dorsal cmsting
cycle on the host, and the disease is not
or generalized miliary dermatitis. Asymptoconsidered to be contagious. The pathomatic carriers may exist. The mites and eggs genesis of demodicosis is complex and may not be easy to find, especially in
not completely LU1derstood; evidence of
animals that are bathed often. Acetate tape
hereditary predisposition for generalized
preparations, superficial skin scrapings, and
disease is strong. In1mLU1osuppression,
flea combing can be used to make the
natural or iatrogenic, can precipitate the
diagnosis.

disease in some cases. Secondary bacterial
deep folliculitis, f=culosis, or ceUulitis
may occur, leading to a guarded prognosis.

Three forms of demodicosis are seen
in dogs: localized demodectic mange,
juvenile-onset generalized demodicosis,
and adult-onset generalized demodicosis.

Localized demodicosis is seen in dogs
usually < 1 yr old, and most of these cases
resolve spontaneously. Lesions often consist
of one to five well-demarcated small areas of
alopecia, erythema, and scaling. Lesions are
usually confined to areas aroLU1d the lips,
periorbital area, and forelimbs but may be
foLU1d in other locations. Pmritus is usually
absent or mlld. A small percentage of these
cases, especially the diffuse localized fonns,
progress to a more severe generalized fom1.

Juvenile-onset generalized demodicosis
is the result of an inherited in1mLU1ologic
defect with functional abnormality asso

Chey/etie/la sp. Courtesy of Dr. Michael W Dryden.

ciated with the cell-mediated inm1LU1e

MANGE

923
system. It is a severe disease of young
crosses. However, idiosyncratic toxicity may
dogs with generalized lesions ( erythema,
be seen in any breed. Testing for m utation in
papules, alopecia, oily seb01Thea, edema,
the MDRl al.lele (ABCBl) may be required
hyperpigmentation, and crusts) that are
before initiating therapy. Local and systemic
usually aggravated by secondary bacterial
corticosteroids are contraindicated in
infections (pyodemodicosis ). Accompanyany animal diagnosed with demodicosis.

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ing pododermatitis is common. Dogs can

Secondary bacterial infections must be
have systemic illness with generalized
treated aggressively with an approp1iate
lymphadenopathy, lethargy, and fever
antibiotic. Antiparasitic therapy must be
when deep pyoderma, furunculosis, or cellucontinued not only .until clinical signs abate litis is seen. Diagnosis is not difficult; deep
but also until at least two consecutive
skin scrapings or hair plucking typically
negative skin scrapings are obtained at 1-mo
reveal mites, eggs, and larval fonns in high
intervals. Although some dogs respond
numbers. The third form is adult-onset
rapidly, others may need several months of
generalized demodicosis and clinically
treatment. Recurrence within the first year
appears sinillar to juvenile-onset generalof treatment is not uncommon. As the sole ized demodicosis but is seen in adult dogs.

prophylactic measure, dogs developing

It is typically associated with or triggered
juvenile-onset generalized demodicosis
by some neoplastic process or debilitating
should not be used for breeding.

disease that may be producing inu11unosuppression, such as malignant lymphosar

Feline Demodicosis: Feline demodicosis
coma, malignant melanoma, hyperadis an uncommon to rare skin disease caused renocorticism, hypothyroidism, diabetes
by at least two species of demodectic mites.

mellitus, etc. However, in many cases an

Demodex cati is thought to be a normal
underlying in1rnunosuppressive condition
inhabitant of feline skin. It is a follicular
may not be found.

mite, sintilar to but narrower than the

Localized demodicosis can generally be
canine mite, that can cause either localized
left untreated. The prognosis for this form is or generalized demodicosis. One other usually good, and spontaneous recovery is
species of Demodex ( named D gatoi) is frequent. In contrast, treatment is required
shorter, with a broad abdomen, and is found
in cases of generalized demodicosis, for
only in the stratum comeum. lt causes a
which prognosis is guarded. Hair clipping
contagious, transmissible, superficial
and body cleansing, especially with benzoyl
demodicosis that is frequently pruritic and
peroxide shampoo used for its follicular
can be generalized. In follicular localized
flushing activity, may be required. Wholedemodicosis, there are one or several areas body amitraz dips (0.025%) applied every 2
of focal alopecia most conunonly on the
wk remains the only approved treatment in
head and neck. In generalized disease,
the USA for generalized dernodicosis.

alopecia, crusting, and potential secondary

Higher concentrations (0.05%) and shorter
pyoderma of the whole body are seen. The
treatment intervals (1 wk) may be more
generalized form is often associated with
efficient.

an underlying inununosuppressive or

A number of other protocols are
metabolic disease such as feline leukemia
commonly used for refractory generalized
vims infection, feline inununodeficiency
demodicosis. Among macrocyclic lactones,
virus infection, diabetes mellitus, or
milbemycin oxime (0.5-1 mg/kg/day, PO),
neoplasia. In some cases, cemminous otitis
moxidectin, and ivermectin have all
extema is the only clinical sign.

demonstrated varying degrees of effective

Diagnosis is made by superficial (D gatoi)

ness. Moxidectin is available as a spot-on
and deep (D cati) skin scrapings, although
formulation in combination with a flea
mite munbers are often small, especially
product (imidacloprid) and should be given
with D gatoi. Medical evaluation is
at 2.5 mg/kg at 1-4 wk intervals. More
indicated in cats with generalized disease.

frequent applications are associated with

Dennatophyte cultures are essential,
higher degrees of success. Other reportedly
because dermatophytosis and demodicosis
successful but unapproved systemic treatcan be concomitant conditions. Prognosis ments include mox:idectin ( 400 mcg/kg/day,
of generalized demodicosis is unpredictable

PO) and ivermectin (300-600 mcg/kg/day,
because of its potential relationship with

PO). For the latter, different therapeutic
systemic disease. Some cases spontaneprotocols have been proposed with a ously resolve. Weekly lime sulfur dips (2%)

gradually increased dosage and thorough
are safe and usually effective; an1itraz
monitoring of treated anin1als to detect any

(0.0125o/o--0.025%) has been used but is not
potentially toxic effect. lvermectin is
approved for use in cats and can cause
contraindicated in Collies and Collie
anorexia, depression, and diarrhea. The use

924

MANGE
of antiparasitic macrocyclic lactones has
epidennis of the parasitic larval stage of
been repo1ted but their efficacy is unclear.

Straelensia cynotis. This mite belongs to
a fainily close to the family Trombiculidae.

Trombiculosis: Trombiculosis is a

To date, the life cycle is largely unknown,
common, seasonal, noncontagious acariasis
and the disease has been reported only in
caused by the parasitic larval stage of

France, Portugal, Spain, and Italy. Transmis

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free-living mites of the fan1ily Trombiculidae
sion occurs mainly in rnral and small-sized

(chiggers). It can affect domestic carnivores,
hunting dogs, probably through contact
other domestic or wild man1mals, birds,
with containinated soil, litter, and other
reptiles, and people. Two common species
terrestrial habitat of foxes. No contagion
found in cats and dogs, Neotrombicula
has been reported to congeners and people.

autumnalis and Eut1vmbicula alfreddugesi, S cynotis has distinct differences from are reported in Europe and in America,
other trombidioid mites, especially in
respectively. Adults (harvest mites) and
clinical presentation, histopathologic
nymphs look like small spiders and live on
features, and response to treatment.

rotting detritus. In temperate areas from

Straelensiosis is sudden in onset and
sUTI1rner to fall, dogs and cats can acquire the
may be accompanied by systemic signs
laivae as parasites when lying on the ground
such as anorexia and prostration. Lesions
or walking in suitable habitat. In wai1.ner
are painful, variably pnuitic, and either
regions, infestation occurs throughout the
generalized or multifocal, most often
year. The laivae (0.25 mm long) attach to the
affecting the dorsal regions of the head and
host, feed for a few days, and leave when
trunk. The characteristic erythematous
engorged. At that time, they are easily
papules and nodules resemble small craters.

identified as ovoid, 0. 7 mm long, orange to

Scaling, pustules, and crusts can be seen.

red, inlrnobile dots, usually found clustering

Differential diagnoses include bacterial
on the head, ears, feet, or ventrum. Pathofolliculitis, sarcoptic mange, and gunshot.

genicity is through traumatic and proteolytic

Microscopic examination of sainples
activities. Hypersensitivity reactions are
obtained from deep skin scrapings may help
suspected in some animals, because pruritus
identify the Jaivae (0. 7 nun long, 0.45 mm
may vary from none to severe. Lesions
wide), each in a thick-walled cyst. The
include erythema, papules, excoriations, hair
larvae, which resembleNeotrombicula, are
loss, and crusts. When present, intense
more easily visualized by histopathology.

prmitus can persist for hours to several days

The prognosis is favorable; a self-cure
even after the laivae have left the animal.

generally occurs after several months if

Diagnosis is based on history and clinical
reinfestation is prevented. However,
signs. The infestation is a seasonal threat to
management of clinical signs is difficult.

free-ranging dogs and cats. Differential

Arnitraz may be somewhat effective.

diagnoses include other p1uritic dermatoses.

Diagnosis is confirmed by careful exainina

Lynxacariasis: Feline lynxacaiiasis is a
tion of the affected areas. Microscopic
quite common but to date geographically
exainination of sainples obtained from skin
restricted (Australia, Brazil, Hawaii, Florida,
scrapings may help to identify the larvae,

North Carolina, Texas) parasitic dem1atitis
which have an oval-shaped body densely
caused by the fur mite Lynxacarus
covered with setae, six long1egs, and curved
radovskyi, which belongs to the fainily
pedipalps terminating in claws.

Listrophoridae. The life cycle remains

Management is difficult. The most useful
poorly described, and this species has not
approach, if feasible, consists of keeping
been repo1ted from hosts other than cats.

pets away from areas known to harbor lai·ge

Infestation typically occurs by direct
nun1bers of mites to prevent reinfestation
contact, but fomites may be important for
during periods of 1isk. The application of
transmission. Clinical signs include a
pyrethroids (dogs only) with repellent-like
salt-and-pepper appearance of the hair
activity to prevent infestation has yielded
coat, variable pruritus, and alopecia.

variable results. Fipronil and permeth1in

Diagnosis is based on visualization of mites

(dogs only) can be used, both for preven

(0.5 mm long) using a magnifying glass or
tion and treatment of infested aninlals.

on isolation of any parasitic stage in skin

Symptomatic treatment may be required
scrapings or acetate tape preparations.

in cases of severe pruritus.

Treatment with acaricidal sprays, weekly
lime sulfur dips, and ivennectin (300 mcg/kg,

Straelensiosis: Canine straelensiosis

SC) are effective. The only case of contagion
is a rare, noncontagious, sporadic, but
to people that has been reported involved
potentially emerging pai·asitic dermatitis
a transient rash in an owner with a heavily
caused by the temporary encystment in the
infested cat.

TICKS

925

TICKS

Ticks are obligate ectoparasites of most

There are four developmental stages: egg,

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types of terrestrial vertebrates virtually
larva, nymph, and adult. All larvae have
wherever these animals are found. Ticks are three pairs of legs; all nymphs and adults large mites and thus are arachnids,
have four. Adults have a distinctive genital
members of the subclass Acari. They are
and anal area on the ventral body surface.

more closely related to spiders than to

The foreleg tarsi of all ticks bear a unique
insects. The -850 described species are
sensory appai·atus-Haller's organ-to
exclusively bloodsucking in all feeding
sense carbon dioxide, chemical stimuli
stages. Ticks transmit a greater variety of

(odor), temperature, humidity, etc.

infectious organisms than any other group

Pheromones stin1ulate group assembly,
of arthropods and, worldwide, are second
species recognition, mating, and host
only to mosquitoes in te1ms of their public
selection.

health and veterinary importance. Some of

Certain tick species that parasitize
these agents are only slightly pathogenic to
livestock can survive several months, and
livestock but may cause disease in people;
occasionally a few years, without food if
others cause diseases in livestock that are
environmental conditions pemtit. Tick host
of tremendous economic in1portance. In
preferences are usually limited to a
addition, ticks can harm their hosts directly
particular genus, fanlily, or order of
by inducing toxicosis ( eg, sweating sickness vertebrates; however, certain ticks are

[seep 684], tick paralysis [seep 1314]

exceptionally adaptable to a variety of
caused by salivary fluids containing toxins),
hosts, so each species must be evaluated
skin wounds susceptible to secondaiy
sepai·ately. The larvae and nymphs of most
bacterial infections and screwworm
ixodids that pai·asitize livestock feed on
infestations, and anemia and death.

small wildlife such as birds, rodents, small

International movement of animals infected
carnivores, or even lizards.

with the tick-transmitted blood parasites

In the Argasidae, the leathery dorsal

Theileria, Babesia, and Anaplasma spp surface lacks a hard plate (scutum). Male
and Ehrlichia (Cowdria) ruminantium is
and female argasids appear to be much
widely restricted.

alike, except for tile larger size of the female

Movement of tick-infested livestock over
and differences in external genitalia. The
great distances is an in1portant factor in the
argasid capitulum (mouthparts) arises from
extensive distribution and prevalence of
the anterior of the body in laivae but from
many tick species and tickborne disease
the ventral body surface in nymphs and
agents. A number of introduced tick species
adults.

thrive in the vast grazing and browsing

In the Ixodidae, the male dorsal surface
environments established during recent
is covered by a scutwn. The scutum of the
centuries of hun1an and livestock populaixodid female, nymph, and laiva covers only tion explosions. Conversely, introduction of
the anterior half of the dorsal surface. The
livestock into areas with exotic tick species
ixodid capitulun1 arises from the ante1ior
and tickborne agents to which they have no
end of the body in each developmental
in1munity or innate resistance often results
stage.

in significant losses.

Two of the three fanlilies of ticks
parasitize livestock: the Argasidae

Argasid Parasitism

(argasids, "soft ticks") and the Ixodidae

The world's argasid tick fauna comprises

(ixodids, "hard ticks"). Although they share 185 species in four genera, nainely Argas,
certain basic properties, argasids and

Carias, Ornithodoros, and Otobius, in the ixodids differ in many structural, behavfainily Argasidae. The Argasidae are highly ioral, physiologic, ecologic, feeding, and
specialized for sheltering in protected
reproductive patterns. Tropical and
niches or crevices in wood or rocks, or in
subtropical species may undergo one, two,
host nests or roosts in burrows and caves.

or rai·ely three complete life cycles annually.

Some argasid species ai·e known to survive

In temperate zones, there is often one
for several years between feedings. Most
annual cycle; in northern regions and at
of these leathe1y parasites inhabit tropical
higher elevations in temperate regions, at
or warm, temperate environments with
least 2-4 yr are required by most species.

long dry seasons. Hosts are those that

926

TICKS
either rest in large numbers near the

The majority of nearly 37 species
argasid microhabitat or return from time
belonging to the genus Ornitlwdaros
to time to rest or breed there. Soft ticks
inhabit animal burrows and lairs in hot, arid
can be a serious pest in poultry and pig
climates and feed on most any potential
operations in tropical and subtropical
hosts that enter their habitat. Larvae in this
countries. Blood loss and subsequent
nidicolous genus do not feed, which may be
anemia can be significant and substantially related to the fact that these ticks dwell in VetBooks.ir
affect weight gains and egg-laying
btuTows that may house hosts irregularly.

performance. Massive infestations can

A few species have adapted to living in
cause numerous fatalities.

crevices of walls and under fences where

An argasid population typically
livestock are confined and also are pests of
parasitizes only a single kind of vertebrate people. Certain species are vectors of and inhabits its shelter area. Argasids use
relapsing fever spirochetes (Barrelia spp)

multiple hosts, ie, the larvae feed on one
and African swine fever virus; some species
host and drop to the substrate to molt; the
cause toxicosis, and one species (0 caria
several nymphal instars each feed
ceus) transmits a spirochete causing
separately, drop, and molt; adults feed
epizootic bovine abortion in the western
several times (but do not molt). Argasid

USA. Ntunerous Ornithadaras-transmitted
nymphs and adults feed rapidly (usually
salivary toxins or arboviruses cause

30-60 min). Larvae of some argasids also
irritation or febrile illnesses in people.

feed rapidly; others require several days

The unique argasid genus Otabius (see
to engorge fully. Adult argasids mate off
p 939) has ttu·ee species, which do not feed
the host several times; afterward, females
in the adult stage. 0 megnini ( spinose ear
deposit a few hundred eggs in several
tick) is exceedingly specialized biologically
batches and feed between ovipositions.

and structurally. It infests the ear canals of

Most of the 57 describedArgas spp
pronghorn antelope, mountain sheep, and
parasitize birds that breed in colonies in

Virginia and mule deer in low rainfall
trees or against rock ledges; others parasitize biotopes of the western USA, Mexico, and cave-dwelling bats. Few feed on reptiles or
western Canada. Cattle, horses, goats,
wild manUTials, and none on livestock.

sheep, dogs, various zoo animals, and

Several species have become important
people are sinlilarly infested. This
pests of domestic fowl and pigeons; among
well-concealed parasite has been transthese are the vectors of Barrelia anserina ported with livestock to western South

(avian spirochetosis) and the rickettsia

America, Galapagos, Cuba, Hawaii, India,

Anaplasma (Aegyptianella) pullarum

Madagascar, and southeastern Africa.

(aegyptianellosis). Argas spp also cause

Notably, adults have nonfunctional
tick paralysis and transmitPasteurella
mouthparts and remain nonfeeding on the
multacida (agent of fowl cholera), and
ground but may survive for almost 2 yr.

many are vectors of a variety of a.rboviruses,

Females can deposit as many as 1,500 eggs
some of which infect people.

in a 2-wk period. Laivae and two nymphal

Genus Carias includes 88 species,
instars feed for 2-4 mo, mostly in winter and
most of which are parasites of mammals,
spring. There can be two or more generaespecially bats and rodents. Depending on tions per year. People and other animals
the species, they inhabit de'hs or roosts of
may have severe irritation from ear canal
bats located in caves or tree holes or rodent
infestations, and heavily infested livestock
burrows. Several species parasitize colonial
lose condition during winter. Tick paralysis
nesting birds and dwell in the substrate or
of hosts and secondary infections by laival
under stones and debris in ground-level bird
screwworms are reported. 0 megnini is
colonies. Many of these ticks parasitize only
infected by the agents of coxiellosis/Q fever,
a single host species or a group of closely
tularemia, Colorado tick fever, and Rocky
related hosts. However, some Carias ticks

Mountain spotted fever. Another species, 0
will feed on people and domestic animals if
lagaphilus, feeds on the heads of jackrabthe p!irnary host is not available. C kelleyi, a bits (hares) and rabbits in western USA.

tick associated with bats and bat habitats,
has been reported to can-y a novel spotted
fever group Rickettsia and a relapsing fever lxodid Parasitism
spirochete closely related to Barrelia

The Ixodidae number >600 species, occupy
turicatae. The seabird tick C capensis has many more habitats and niches than do
been shown to transmit West Nile virus to
ai·gasids, ai1d parasitize a greater nun1ber of
ducklings. The American C puert01icensis
vertebrates in a wider vai'iety of environand C talaje are potential vectors of Afiican ments. Most ixodid species have a
swine fever virus.

three-host life cycle, others have a two-host

TICKS

927
cycle, and a few have a one-host cycle. Each
the development of each stage and, in the
ixodid postembryonic developmental stage
case of females, oviposition.

(larva, nymph, adult) feeds only once but
for a period of several days. Males and

Three-host lxodids: Most ixodids have
females of most species that parasitize
a three-host cycle. The recently hatched
livestock mate while on the host, although
lruvae quest for a suitable host, usuaJly from
some mate off the host on the ground or in
vegetation, feed for several days, drop, and

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burrows. Males take less food than females
molt to nymphs, which repeat these
but remain longer on the host and can mate
activities and molt to adults. Of the
with several females. During inactive
tlu·ee-host species that parasitize livestock
seasons, few or no females are found
or dogs, a few have immatures and adults
feeding, even though males may remain
tl1at parasitize the san1e kind of host; these
attached to the hosts. Such males may
often develop tremendous population densicontribute to transmission of pathogens to ties. The success of ixodid species that
new susceptible animals by serial interhost
require smaJle1°size hosts for inunatures
transfer. Larval and nymphal population
depends on the availability of those hosts in
activity generally peaks during the "off
the livestock browsing and grazing grounds.

seasons" of adults, although in some species The natural hazards inherent in the there is overlap in the seasonal dynamics of
three-host cycle have been compensated for
immatures and adults.

by the benefits afforded adaptable tick

The ixodid males, except those in the
species by a.i1in1al husbandry practices.

genus Ixodes, become sexually mature only

Only certain ixodids specific for herbivores
after beginning to feed, after which they
have adapted to coexistence with livestock,
mate with a feeding female. Only after
and therein lies the answer to nun1erous
mating does the female become replete and
livestock tick problems in Africa, where
proceed to develop eggs. She then detaches,
hosts for adults and in1matures ru·e
drops from the host, and over a period of
abundant.

several days deposits a single batch of many
eggs on or near the ground, usuaJly in

Two-host lxodids: Some ixoclids,
crevices or w1der stones, leaf litter, or
especiaJly those tl1at parasitize wandering
debris. Depending on species and quantity
ma.i11mals ( and also birds in certain cases)

of female nourishment, the egg batch
in inclement envirorunents of the Old World,
usually numbers 1,000-4,000 but may be
have developed a two-host cycle in which

> 12,000. The female dies after ovipositing.

lruvae and nymphs feed on one host, and

Notably, ixodids ( except one- and two-host
adults on another. As in three-host species,
species, which use vertebrate host anin1als
both hosts may be different or may be the
as habitat for much of their life cycle) spend
sa.ine species. Two-host parasites of

>90"A, of their lifetin1e off the host, a fact of livestock thrive in both inclement and
utmost significance in planning control
clement envirorunents and are difficult to
measures. The several-day feeding process
control. This is especially true of two-host
progresses slowly; the baJloon shape
species that feed in the ears and anal areas
characte1istic of engorged lruvae, nymphs,
of livestock.

and females develops only during the final
half day of feeding and is followed by

One-host lxodids: Among the most
detaching. The dropping tin1e at certain
economically important ticks ru·e several
hours of the day or night is governed by a
one-host species. These parasites evolved
circadian rhythm closely associated with
together with herbivores that wandered in
the activity cycle of the principal host.

extensive ranges in the tropics (Rhipiceph

It is also important, especially in
alus [Boophilus] spp, Dermacentor nitens, understanding the epidemiology of
etc) or in temperate zones (D albipictus,
tickbome pathogens, to know whether

Hyalomma scupense). Larvae, nymphs,
in1matures of an ixodid species feed on the
and adults feed on a single animal until the
same host species as do the adults, or on
mated, replete females drop to the ground
smaJler vertebrates. Where acceptable
to oviposit.

smaller-sized hosts are scarce, immatures of
some ixodid species can feed on the san1e

Feeding Sites: Each species has one or
livestock hosts as adults; immatures of
more favored feeding sites on the host,
other species seldom or never do so.

although in dense infestations, other areas

The proximity of acceptable hosts, air
of the host may be used. Some feed chiefly
temperature gradients, and atmospheric
on the head, neck, shoulders, and escutchhw11idity during resting and questing eon; others in the ears; others around the
periods are among the factors that regulate
anus and under tl1e tail; and some in the

928

TICKS
nasal passages. Other common feeding sites
parasitize a variety of livestock, pets, and
are the axillae, udder, male genitalia, and
wildlife as well as people. Activity in the
tail brush. Immatures and adults often have

USA continues from early spring to late
different preferred feeding sites. Attachfall. Feeding sites on domestic and wild ment of the large, irritatingAmblyomma
mainmals are usually skin areas with sparse
spp is regulated by a male-produced
hair; wounds at these sites predispose
aggregation-attachment pheromone, which
livestock to attack by the screwworn1 fly

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ensures that the ticks attach at sites least

Cochliomyia hominivorax.

vulnerable to grooming.

A ammicanum is a vector of Prancisella
tularmisis, the etiologic agent of tularemia; IMPORTANT IXODID TICKS

Ehrlichia chaffeensis, which causes monocytic ehrlichiosis in people; E ewingii, The important ixodid ticks include
which causes granulocytic ehrlichiosis in

Amblyomma spp, Anomalohimalaya spp, dogs and people; and a recently described

Both1iocroton spp, Cosmiomma sp,

Panola Mountain Ehrlichia closely related

Dermacentor spp, Haemaphysalis spp, to the agent of heaitwater, which is patho

Hyalomma spp, Ixodes spp, Margaropits genic to at least goats and people. This tick
spp, Nosomma sp, Rhipicentor spp, and also transmitsRickettsia amblyommii,

Rhipicephalus spp.

Borrelia lonesta1i, and the Heartland
virus pathogenic to people. A Coxiella sp

AMBLYOMMA SPP
symbiontic bacteria, closely related to
the agent of Q fever, can be present in tl1e

More than half of the -140 knownAmbly
majority of ticks in a population but is
omma species are endemic to the New
unknown to cause infections in people

World. Amblyomma ticks are large,
or otl1er animals. A ammicanum may
three-host parasites. They have eyes and
cause tick paralysis in people and dogs. In
long, robust mouthparts. They are more or
addition, Lone star virus (Bunyaviridae) has
less brightly ornamented and generally
been isolated from a single A ame1icanum
confined to the tropics and subtropics.

nymphal tick that had been removed from

Adults and immatures of37 species in this
a woodchuck (Ma1mota monax) in
genus parasitize reptiles, which together

Kentucky.

with ground-feeding birds, are often hosts

A cajennense, tl1e Cayenne tick, ranges
of inunature Amblyomma ticks that have
from South America into southern Texas.

adapted, in the adult stage, to parasitizing

This species is found most conunonly in dry
manunals. Their long mouthparts make
tropical habitats and lower elevations of

Amblyomma ticks especially difficult to
subtropical highlands. As with A ameiica
remove manually and frequently cause
num, each active stage is indiscriminate in serious wounds that may become secondai�
host choice: livestock and a large variety of
ily infected by bacteria or screwworms and
avian and man1malian wildlife serve as
other myiasis flies.

hosts. People are severely irritated by

Several Af1icanAmblyomma that infest
clusters of A cajennense larvae ("seed livestock are vectors of Ehrlichia
ticks") in wooded and high-grass areas.

(Cowdria) ruminantium, the rickettsial

Most adults attach on the lower body
agent that causes herutwater (seep 751),
surface, especially between the legs; some
whereas New WorldAmblyomma spp cariy
feed elsewhere on the body. Activity
agents of monocytic and granulocytic
continues throughout the year. A cajenn
ehrlichioses as well as several Rickettsia
ense is a vector o(R rickettsii in Central spp, includingR rickettsii, the agent of
and South America from Panaina to

Rocky Mountain spotted fever.

Argentina and has been expe1imentally

A ammicanum, the lone-stat· tick, is
shown to transmit Ehrlichia ruminan
abundant in the southern USA from Texas
tium. Wad Medani virus (an Orbivirus,
and Missouri to the Atlantic Coast and

Reoviridae), an African virus transported to
ranges northward into Maine. Southward,

Caribbean islands by A variegatum
its distribution extends into no1thern
infested cattle from Senegal, has been

Mexico. Because of the changing climate,
isolated from A cajennmise inJainaica.

the geographic range of this species

A maculatum, the Gulf Coast tick, is an
continues to expand.

important pest of livestock, particularly

The scutum is distinctive because of pale
cattle, from South America to southern
ornainentation in males and a conspicuous,

USA. Optimal habitats are warm areas with
silvery spot ("star") near the posterior
high rainfall, near seacoasts. Immatures
margin in females. Larvae, nymphs, and
usually parasitize birds and small
adults are indiscriminate in host choice and
mainmals; adults parasitize deer, cattle,

TICKS · 929
horses, sheep, pigs, and dogs. Adult feeding for "provisionally free" certiiication by 200�
activity is chiefly in late summer and early
altl1ough St. Kitts was reinfested in 2004.

fall but may begin later after a dry summer.

Host preferences are sinillar to those of

Most adults infest the ears, where the

A hebraeum but also include can1els. The
feeding wounds are initial sites of screwbites of the tropical bont tick are severe.

worn1 infestations. Clustered feeding

They may result in septic wounds and
adults also cause much irritation to the
abscesses, inflanm1ation of tlle teats of

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upper parts of the neck of cattle and to the
cows, and considerable damage to hides
hun1ps of Brahman cattle. A maculatum is
and skins. Adults feed chiefly during rainy
the primary vector of R parkeri,, and in
seasons, inm1atures during dry seasons.

some tick populations as many as 500;6 of

Most adults attach to tlle underside of the
individual ticks may be infected with this
host body, on the genitalia, and under tlle
pathogen.

tail.

A imitator parasitizes livestock from

A variegatum injuries to hosts and

Central America to southern Texas; it has
transmission of E ruminantium are simila
been shown to transmitR rickettsii in
to those of A hebraeum but also include the Mexico. Occasional pests of livestock
spread of acute bovine dern1atophilosis ( se(
in tropical America are A neumanni
p 858). This tick is not considered to be an

(Argentina), A ovale and A parvum
effective vector of N ai.robi sheep disease

(Argentina to Mexico),A tigrinum (much
virus but is a secondary vector of Crimeanof South America), and A lapirellum Congo hemorrhagic fever virus. Dugbe virui

(Colombia to Mexico).

has been isolated from A variegatum in

A testudinarium inhabits Asian tropical
six countries north of the equator; the
wooded environments from Sri Lanka and

Thogoto and Bhartja viruses are also

India to Malaysia and Vietnam, Indonesia,
associated with this tick in vaiious areas

Borneo, Philippines, Taiwan, and southern
north of tlle equator. Notably, yellow fever

Japan. Adults are particularly abundant
virus has been isolated from A variegatum
on wild and domestic pigs and also infest
collected from cattle in the Central African
deer, cattle, other livestock, and people.

Republic and has been demonstrated to be
lnlrnatures parasitize birds and small
transovarially transmitted to the progeny of
man1mals as well as people. In India and Sri
infected females. Jos virus infects A varie

Lanka, adultA integrum and A mudlairi
gatum from Ethiopia to Senegal and has
also parasitize livestock, wild ungulates,
been tra.I1Sported in this tick to Jainaica.

and people.

A lepidum, the East African bont tick,

A hebraeum, the southern Africa bont
inhabits xeric savanna environments
tick, inhabits warm, moderately hwnid
from northern Tanzania to central Sudan.

savannas of South Africa, Namibia,

A gemma, the gem-like bont tick, occurs in

Botswana, Zimbabwe, Malawi, Mozamsimilar environments of Tanzania, Somalia, bique, and Angola In1matures feed on

Kenya, and Ethiopia. A small variety of tlle
various small mai11mals, ground-feeding
buffalo bont tick, A cohaerens,'is abundant birds, and reptiles. Adults infest livestock,
on cattle in Ethiopian highlands, but from
antelope, and other wildlife. Adults,

Zaire to Tanzania tlle larger variety of A co
attached chiefly to body areas with
haerens parasitizes chiefly Cape buffalo.

relatively little hair, cause se1ious wounds

Other African Amblyomma ticks of Cape
that become secondarily infected by
buffalo and various other large man1mals,
bacteria and the screwworm Ch1ysomya
including livestock, are A pomposum of
bezziana. Like other AfricanAmblyomma
hwnid highland forests in Angola, Zaire,
ticks (bont ticks) that pai·asitize livestock,

Uganda, southern Sudan, Kenya, and

A hebraemn is an in1portant vector of Ehrli

Zimbabwe, and A astrion of West Africa
chia ruminantium and the principal
and Zaire.

vector of Rickettsia africae, the agent of

In Central and South America, nwnerous

African tick bite fever, in southern Africa.

Amblyomma spp parasitize livestock and

A va.riegatum, the tropical African bont
dogs, often in lai·ge nwnbers. Among tllose,
tick, is an easily visible, brightly colored

Amblyomma and A ovale adults feed
parasite found throughout sub-Sallai·an
primai·ily on cainivores and A parvum on
savaimas southward to the range of
carnivores ai1d armadillos. A awicularium

A hebraemn, and also in southern Arabia
has been found on wild hosts of tlle families
and several islands in the Indian and

Mynnecophagidae and occasionally

Atlantic Oceans and tlle Caribbean. An

Didelphidae, Caviidae, Chinchillidae,
eradication program is in progress in the

Hyclrochaeridae, Muridae, Canidae,

Caribbean; St. Kitts, St. Lucia, Montserrat,

Mustelidae, and Procyonidae; it tra.I1Srnits

Anguilla, Barbados, and Dominica qua.lilied

R rickettsii in Brazil. A pseudoconcolor has

930

TICKS
been found occasionally on wild hosts of

D albipictus, and D dissimitis, the the family Didelphidae. A naponense is

De1macentor life cycle is of the typical
common on peccaries, and A oblongogut
three-host pattern.

tatiim has been found on a variety of hosts D nite11S, the one-host tropical horse tick, in several South and Central Ame1ican
is of considerable veterinary importance. It
countries. The South American tapir
originally parasitized deer (Mazama) in the (Tapirus lerrestris) seems to be the
forests of northern South America. With the

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primary host for the adult stage of
introduction of Equidae and other livestock

A la.tepunctatum, A scalpturatum, and
into its habitat, it adapted to these anin1als.

A incisum. A dissimile is a common

Spending its entire parasitic life deep in the
parasite of reptiles and true toads of the
hosts' ears, this parasite was easily spread
genus Bufo, from Argentina northward to
by human activities to other areas of the
southern Mexico, the Caribbean islands,

Americas, including Florida and Texas. In
and southern Florida.

addition to ear cavities, each active stage
may infest nasal passages and the mane,

ANOMALOHIMALAYA SPP
ventral abdomen, and perianal area.

D nitens transmits Babesia. ca.batli

The three Anomalohimalaya spp are found
transovarially to successive generations
in mountains of Central Asia-Panlir, Tian
and is important in the horse-racing

Shan, Tibet, and Himalayas. All stages of
industry. It also is an experimental vector
these three-host ticks parasitize rodents,
of Anaptasma marginale to cattle.

shrews, and less frequently hares.

Another American one-host species,

D albipictus, the winter or moose tick,

BOTHRIOCROTON SPP
ranges from Canada and nmthern USA
into western USA and Mexico. A brownish

Genus Bothriocroton (formerly
form, sometimes called D nigrolineatus,

Aponomma) includes seven species of ticks
is distributed from New Mexico to southern
indigenous to Australia and Papua New
and eastern USA and may merit subspe

Guinea (B oudemansi). Bothriocroton spp
cies, if not full-species, rank. The larvalresemble Amblyomma spp except they nymphal-adult feeding period on a single
have no eyes. In this group, B aruginans
host (moose, deer, elk, or domestic cattle or
is a parasite of wombats; B concolor and
horses) extends from fall to spring. Heavily

B oudemansi are ectoparasites of echidnas
infested hosts may die. D albipictus causes in Australia and Papua New Guinea,
the often fatal "phantom moose disease" of respectively. The other four species in this

Canada, is a secondary vector of Colorado
genus parasitize reptiles almost exclusively.

tick fever virus, and is an experimental

B hydrosauri, the blue-tongued lizard tick, vector of B cabatli; it is a natural vector is the reservoir of Rickettsia honei on
of A marginale in OkJal10ma.

Flinders Island, Australia.

In Mexico and central America,

D dissimilis parasitizes a variety of equine

COSMIOMMA SP
and ruminant hosts and may be a one-host
tick on horses.

Genus Cosmiomma contains a single

The Rocky Mountain wood tick,
species, C hippopotamensis,.which is

D andersoni, is found from Nebraska
found in southwestern and eastern Africa. It
westward to the western mountains
feeds primarily on white and black rhinocer

(Cascades and Sierra N evadas ), in northern
oses and less frequently on antelopes.

New Mexico and Alizona, and in western

Canada.

DERMACENTOR SPP

The American dog tick, D variabilis,
is found west of the Cascades and Sierra

Of the 36Dermacentorspp , 19 inhabit

Nevadas, in Mexico, from Montana to Texas
temperate zones. Of the tropical species,
and east to the Atlantic, and in eastern

D (Anocenter) nitens is of major veterinary Canada. Both species may cause tick
in1portance, although others may transmit
paralysis in livestock, wildlife, and people.

zoonotic infections, and adults may be

They are the primary vectors of Rickettsia
common on wildlife such as pigs, deer, and
rickettsii, the agent of Rocky Mountain
antelope. Inunatmes infest chiefly rodents
spotted fever (seep 806). D ande1·soni is and lagomorphs. De1macentor spp in cold
also the chief vector of Colorado tick fever
areas and D nitens in tropical America have virus and transmits Powassan virus, A
specialized life cycles and seasonal
marginale, A ovis, and the agents of
dynan1ics of activity, each of which must be
tularemia and coxiellosis/Q fever. D
considered separately. Except for D nitens,
variabilis is an experin1ental vector of A

TICKS

931
marginme, B caballi, and B equi. In addition,

HAEMAPHYSALIS SPP
sawgrass virus, Ehrlichia cha.ffeensis, and E
ewingii have been detected in questing D

Few of the 166 species of Haemaphysalis
variabilis adults. Adults of both species
parasitize livestock, but those that do are
parasitize livestock and wildlife, including
economically in1portant in Eurasia, Africa,
deer, bison, and elk, but those of D variabilis

Australia, and New Zealand. Some
prefer skunk, raccoon, puma, etc, and
haemaphysaline parasites of wild deer,

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domestic dogs. Immatures feed on rodents
antelope, and cattle have adapted to
and other small wild manunals. A related,
domestic cattle and, to a lesser extent, to
biologically similar species, D occidentalis, is sheep and goats. Others, originally specific restricted to the Pacific lowlands and
for various wild sheep.and goats, have
foothills from Oregon to Baja California and
adapted chiefly to the domestic breeds of
is a natural vector of A marginale.

these aninlals. A few African species that

In western USA and Mexico, D paru
evolved together with carnivores now
mapterus, D hunteri, and D halli parasitize parasitize domestic dogs. In1111atures of various hares and rabbits, mountain sheep,
species that parasitize livestock generally
and peccaries, respectively. These ticks
feed on small vertebrates, but there are a
seldom make contact with livestock.

few notable exceptions. All Haemaphysalis

D hunteri is an experimental vector of
spp have a three-host life cycle. They are

A mmginale and A ovis. In Costa Rica small (unfed adults <4.5 mm long), brownish
and Panama, D latus infests tapirs.

or reddish, and eyeless. Most have very short

In Eurasian steppes, forests, and
mouthparts. Different species cause tick
mountains, D marginatus, D reticulatus,
paralysis and are vectors of the agents that
and D silvarum, collectively, are vectors
cause coxiellosis/Q fever, tularemia, and
of Rickettsia slovaca and R ramtltii (the brucellosis, and of Theileria orientalis, T
causative agents of tickborne lymphadenopa
ovis, Babesia major, B motasi, B canis,
thy ), R sibiiica (the agent of Siberian tick Anaplasma mesaeterum, etc.

typhus), Babesia bovis, B caballi, B equi,

H punctata, the red sheep tick, is widely

B can is, Theileria ovis, and A ovis, together distributed where sheep, goats, and cattle
with the agents of tularemia and coxiellosis/Q feed in certain open forests and shrubby fever, and Russian spring-summer encephapastures from southwestern Asia (Iran and litis. D marginatus is found in forests,
former USSR) to much of Europe, including
marshes, semideserts, and alpine zones from
southern Scandinavia and Britain. It usually

France to southwestern Siberia, Kazakhstan,
does not appear in large nw11bers.

Xirtjiang Uygur Autonomous Region of China,
ln1111atures infest birds, hedgehogs, rodents,

I.ran, and northern Afghanistan. D reticulatus
and reptiles. H punctata can cause tick
ranges from Ireland and Britain to northwestparalysis. In addition to transmitting ern Siberia and Xirtjiang, China, in meadows,

A naplasma, Brucella, Theileria, Babesia
floodplains, and deciduous and deciduousspp , and tularemia, different H punctata conifer forests. D silvarum ranges from
populations are infected by Russian
central Siberia and northeastern China to
spring-summer encephalitis virus, Tribec

Japan in marshes, meadows, shrubby and
virus, Bhanja virus, and Crin1ean-Congo
secondary forests, and farmlands in taiga
hemorrhagic fever virus. H concinna
forest areas. Some males in populations of
is found in Central Europe, East and
each of these three species remain attached

Southeast Asia, China, and Japan. It is found to the host during winter. Adults and
in humid scrubby forests as well as in
immatures may overwinter on the ground.

meadows and peat-lands but avoids dense

Greatest adult activity is from early spring to
forests. H concinna can transmit tularemia, summer with a lower peak in fall. Larvae and
several Rickettsia spp, including mildly
nymphs are active from spring through fall.

pathogenic R heilongjiangensis, and

The life cycle may be completed in 1 yr or
several encephalitis viruses.

extended by one or more swnmer or winter

H sulcata adults parasitize livestock
diapauses to 2-4 yr.

(chiefly sheep and goats) from northwest

About 12 other Dermacentor spp inhabit
ern India and southern former USSR to
certain lowland, mountain steppe, and

Arabia, Sinai, and southern Europe.

semidesert areas of temperate Asia. Their

H parva adults parasitize these hosts from
adults are commonly taken from camels,
southwestern former USSR and the Near
cattle, horses, sheep, and goats. In tropical

East to the Mediterranean area (but not

Asia, the several species of the Dermacen

Egypt). Immature H sulcata are especially
tor subgenus Indocentor are parasites of common on lizards, but the range of hosts
wild pigs; they also infest larger wildlife but
of larvae and nymphs of both species is
seldom if ever feed on livestock.

similar to that of H punctata.

932

TICKS

H longicornis is a parasite of deer and

HYALOMMA SPP
livestock in Japan and northeast Asia; there
is a bisexual form (race) in southern areas

Hyalomma ticks are often the most
and a parthenogenetic race in northern areas. abundant tick parasites of livestock, The latter has been introduced into Australia, including camels, in warm, arid, and New Zealand, and the Pacific islands, where
semiarid, generally harsh lowland and
it preserves this unusual reproductive ability.

middle altitude biotopes, and those with

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Immatures usually parasitize small manm1als
long dry seasons, from central and
and birds but may also feed on livestock;
southwest Asia to southern Europe and
heavy population densities may become
southern Africa. Of the -30 known
serious pests of deer and livestock. This tick

Hyalomma spp, at least half are imporis the chief vector of Theileria orienlalis and tant vectors of infectious agents to also transrnitsBabesia ovala, B gibsoni, and livestock and people. The three-host life
the agents of coxiellosis/Q fever, Powassan
cycle predominates in this genus, but
encephalitis, and Russian spring-summer
some species have either a one- or
encephalitis. Larval feeding causes acute
two-host cycle. Some three-host species
dern1atitis in people.

can develop in one- or two-host cycles, a

H inermis is found in lowlands from
facultative ability unique to tl1is ixodid
nmthern Iran and southwestern forn1er
genus. Hyalomma spp are mostly

USSR to central and southeastern Europe to moderately large to large ticks with Italy, where it prefers deciduous and mixed
long mouthparts.

forests as well as grasslands. It can cause

In the subgenus Hyalomma.sta,
tick paralysis. Other Eurasian haemaphysaimmatures of the single species, H aegyp
lines of livestock are H pospelovashtromae
l'ium, parasitize tmtoises and small wildlife (mountains of southern fonner USSR and
and livestock from Pakistan to both sides of

Mongolia), H kopetdaghicus (Caspian Sea
tl1e Mediterranean basin. Adults are specific
area, mountains of former USSR, and Iran),
for tortoises.

and H tibetensis, H xinjiangensis, and

The subgenus Hyalommina is found on

H moschisuga (China).

the Indian subcontinent and in Somalia.

Of the several Haemaphysalis spp para

Each of the six species has a three-host
sitizing livestock in southeast Asia, tlu·ee
cycle. Immatures parasitize small mammals,
are especially noteworthy: H bispi1wsa
especially rodents. Adult host preferences
ranges to Pakistan, Bangladesh, Nepal,
among livestock reflect the wild gazelle,

Bhutan, Sri Lanka, and Malaysia, and
bovine, caprine, or ovine group with which
transmits Babesia spp to cattle, sheep, and each species evolved. 1\vo species infest
dogs; H spinigera is the chief vector of
chiefly cattle and the domestic buffalo:

Kyasanur Forest disease virus in people in

H brevipunclata (India and Pakistan) and

Kamataka state, India; and H anomala

H kumari (India, Pakistan, Afghanistan,
ranges from the Nepal lowlands to Sri Lanka
northwestern Iran, and Tadzhikistan).

and the mountains of northwestern Thailand. Three usually parasitize sheep and goats: In temperate Asia, 18 other haemaphysa

H hussaini (India, Pakistan, Burma), H rhi
lines parasitize livestock: 9 high in the
picephaloides (Dead Sea and Red Sea

Himalayas and outlying mountains, and 9 in
areas), and H arabica (Yemen and Saudi
northeastern Russia, Korea; and Japan. Yak

Arabia). H punt (Somalia and Ethiopia)

and yak-cattle hybrids are an1ong the
feeds on antelope, camels, cattle, sheep,
livestock hosts of Himalayan haemaphysaand goats.

lines. Several Hin1alayan species appear to

The subgenus Hyalomma contains ticks
prefer sheep and goats.

of veterinary and public health importance

H leachi, the yellow or African dog tick,
that affect cattle, sheep, goats, horses,
is found in tropical and southern Africa. It
camels, dromedaries, dogs, cats, and
can transmit canine and feline babesiosis,
people. Chief among these is the two-host

Mediterranean spotted fever, coxiellosis/Q

H anatolicum anatolicum, which ranks
fever, and Boutonneuse fever. Ot11er haemahigh an1ong the world's most damaging ticks physalines that infest livestock in highland
and has been widely distributed by can1els,
forests or lowland, humid, secondary or
cattle, and horses in steppe and semidesett
riparian forests in sub-Saharan Africa are
environn1ents from central Asia to

H parmala (Ethiopia and Kenya, Central

Bangladesh, the Middle and Near East,
and West Africa, toAngola),H aciculifer

Arabia, southeastern Europe, and Africa

(Ethiopia to Cameroon and Zin1babwe,
north of the equator. Inm1atures and adults
introduced into South Africa), H 1ugosa
generally infest the san1e kinds of hosts.

(southern Sudan and Uganda to Ghana and

Nymphs and unfed adults spend the dry and

Senegal), and H silacea (Zululand and
winter season in crevices in stone walls,
eastern South Africa).

stables, and weedy or fallow fields. When

TICKS

933.

immatures infest smaller mammals, birds,
inm1atures; ha.res also may be infested.

or reptiles, the life cycle type is three-host.

Adults pa.rasitize livestock, particularly

In addition to significantly weakening
camels. The subspecies from east to
affected anin1als, causing weight loss,
west, H asiaticum kozlovi, H asiaticum
reduced fertility, and decreased milk
asiaticum, and H asiaticum caucasicum,
production, H anatolicum anatolicum
a.re of veterinary and medical importance.

transmits Theileria annu/,ata, Babesia

Three additional tJu·ee-hostHyalomma

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equi, B caballi, Anaplasma marginale,
spp that pa.rasitize camels and other

Trypanosoma theileri, and at least five
livestock a.re H dromedarii (India to Africa a.rboviruses; it is a significant vector of
north of the equator), H schulzei ( eastern

Crinlean-Congo hemorrhagic fever virus

Iran to Arabia and northern Egypt), and
to people.

Hfranchinii (SY1ia to Tunisia). In1ma

Immatures of the subspecies H anatoli
tures pa.rasitize rodents and other small
cum excavatum ( a three-host parasite)

manunals, birds, and reptiles; those of
infest chiefly burrowing rodents in

H dromedarii also infest livestock.

somewhat different biotopes in the same

H dromedarii is of veterinary and medical
environments asH anatolicum anatoli
importance; the other two species have
cum. Adults of both species may infest the
been little investigated.

same aninlal. Distribution of H anatolicum

H detritum, an important vector of
excavatum is somewhat more limited than

Theileria annulata, is a tJu·ee-host species; that of H anatolicum anatolicum, but its
both adults and immatures pa.rasitize
winter season population densities a.re often livestock. Its biotopes ar·e humid areas in greater. A closely related species, H lusi
steppes, deserts, and semideserts from
tanicum, replacesH anatolicum anatoli
southern China, Mongolia, and Nepal
cum from central Italy to Po1tugal,
lowlands to southern Europe and northern

Morocco, and the Canary Islands; it is

Africa. H impellatum ranges from Iran and
associated with equine and bovine

Arabia to northern Tanzania and Chad.

babesiosis. In addition to livestock, deer

Adults pa.rasitize livestock; inlmatures feed
and rabbits serve as hosts.

on rodents and other small manunals, birds,

The H marginatum complex consists
and reptiles.

of four species, each apparently invariably

H scupense, a one-host parasite of cattle
two-host. Adults pa.rasitize livestock and
and horses in southwestern fonner USSR
wild herbivores. lnlmatures primarily
and southeastern Europe, is unusual (like
pa.rasitize birds. Rodents a.re rarely, if ever,

Canadian strains of Dermacentor albipic
pa.rasitized. Ha.res and hedgehogs a.re
tus) in that it overwinters on ti1e host, which secondary hosts. This group includes
often suffers greatly from the Jong feeding

H marginatum marginatum (Caspian
period of nurnerous larvae Oate fall),
area of Iran and former USSR to Portugal
nymphs (winter), and adults (spring).

and northwestern Africa), H marginatum

H scupense is a vector of T annulata and 1ujipes ( soutl1 of the Salla.ra to South Africa, B equi.

also Nile Valley and southern Arabia), H mar

In addition to the several species already
ginatum turanicum (Pakistan, Iran,
mentioned, the African savarmas harbor five
southern former USSR, Arabia, parts of
other Hyalomma spp of livestock and
northeastern Africa-introduced witi1
wildlife: H (Euhyalomma) glabrum
sheep from Iran to Karoo ), and H marginatruncatum ( southeastern Egypt to southern tum isaaci (Sri Lanka to soutl1ern Nepal,

Africa), H albiparmatum (souti1ern Kenya,

Pakistan, northern Afghanistan). Ticks
northern Tanzania), H erythraeum ( eastern
belonging to the H marginatum complex

Somalia and Ethiopia, Yemen), H impres
a.re major vectors of the Crinlean-Congo
sum (western Sudan, West Afiica), and
hemorrhagic fever virus. They also transmit

H nitidum (Central African Republic, West

Rickettsia aeschlimannii and several

Africa). The preferred hosts of its adults a.re

Babesia, Anaplasma, Theileria, and
large herbivores such as zebras, gemsbok,

Trypanosoma spp that infect wildlife,
and eland. In1matures of these three-host
livestock, and people. H truncatum can
species generally infest small mammals,
cause paralysis in livestock, pets, and
less often ground-frequenting birds and
people.

reptiles. H truncatum glabrum, which

The H asiaticum complex includes three
causes bovine sweating sickness and
species with three-host life cycles and
lameness and also human and ovine tick
inhabits deserts, semideserts, and steppes
paralysis, is a vector of Crimean-Congo
from southwestern China, Mongolia, and the hemorrhagic fever virus, Coxiella burnetii southern fonner USSR into the Middle East

(Q fever), andRickettsia conorii (African
as far as Iraq. Rodents a.re the chief hosts of
tick typhus, Boutonneuse fever).

934

TICKS

/XODESSPP
northern islands of Japan. The life cycle
can be completed in 3-4 yr but can last
lxodes spp, the largest genus of the family up to 7 yr in regions with a short summer

Ixodidae, contains 249 species and is highly
season. It is one of the main vectors of
specialized both stmcturally and biologi

Russian spring-summer encephalitis virus
cally. So far as is known, all Ixodes spp have and Borrelia biirgd01fe1-i. In addition, it a three-host life cycle. Almost all inhabit
transmits Babesia spp, Eh?'lichia muris, VetBooks.ir
temperate or tropical forest zones or
and the agents of human and ovine
wooded or shmbby grasslands; fewer are
anaplasmoses and tularemia.

adapted to humid areas in semideserts or to

Other Asian representatives of the
arctic or sub-Antarctic nesting colonies of

I 1·icinus group are I sinmsis of China; marine birds. Hosts are a wide vaiiety of

I kashmfricus of mountainous northern
birds and mammals and a few reptiles. Most

India, Pakistan, and Kyrgyzstan; I pavlov
species parasitize burrowing hosts or those
skyi of the southern Siberian mountains of
that return regularly to caves, dens, or

Russia; and I kazakstani of mountain taiga
terrestrial or arboreal nesting colonies. The
and deciduous forest in Kazakhstan,
few Ixodes spp that parasitize wande1ing

Kyrgyzstan, and Turkn1enistan.

artiodactyls or perissodactyls are excep

In the Americas, representatives of the
tionally adaptable; they also parasitize

I ricinus group include I scapiila1is,
livestock and ai·e important pests or vectors
l pacificus, I affinus, I jellisoni,
of agents that infect livestock and people.

I minor, and I muris. I scapiilaris is The I 1icinus group of Eurasia,
distributed throughout the eastern and
northwestern Africa, and North and South
northcentral USA and southern Canada.

An1erica is especially important. I 1icinus,

It is a vector of Borrelia burgd01feri, the the so-called sheep tick and prototype of
agent of Lyme disease, and A phagocy
this group, inhabits relatively humid, cool,
tophilmn, which causes granulocytic
shrubby and wooded pastures, gardens,
anaplasmosis in people, horses, and dogs.

windbreaks, floodplains, and forest through

It also transmits Babesia. micro ti, the
much of Europe to the Caspian Sea and
agent of human babesiosis in coastal
northern Iran, and also northwestern Africa. areas from Rhode Island to Virginia, and Its life cycle is 2-4 YT, depending on
an E muris-like agent causing granuloenvironmental temperature. (In drier, cytic ehrlichiosis in people and rodents
waimer, eastern Mediterranean biotopes,
in the mid western USA. The chief hosts

I 1icinus is replaced by I gibbosus, which of adult I scapularis are deer; livestock
completes its life cycle in 1 yr.) I ricinus
seldom graze in the wooded zones
laivae feed on small reptiles, birds, and
inhabited by this tick. Adults of I pa
man1mals. Nymphs feed on small and
cificus parasitize livestock from Baja
medium-sized vertebrates, and adults feed

California to British Columbia and in
chiefly on herbivores and livestock. All
inland pockets of Idaho, Nevada, and
stages, especially nymphs and adults,

Oregon. I pacificus and I neotoma.e
parasitize people. Male I ricinus take little transmit the agents of Lyme disease,
or no food and can mate either on or off the
tularemia, and a rickettsia of the Rocky
host. Unfed adults often mate while on

Mountain spotted fever group; I pacificus
vegetation. Adult activity peaks in spring; in
also transmits A phagocytophilum. The
some populations, there is a lower peak of
tick bites cause slowly healing ulcers.

adult activity in the fall. Chief ainong the

A related species, I affinis, ranges from
numerous arboviral diseases tra11Smitted by

South Carolina and Florida to Argentina.

I 1icinus a.i·e louping ill, tickborne

It is recorded chiefly from' wildlife and has
encephalitis, and Crimean-Congo hemornot been shown to be a vector.

rhagic fever. Other agents transmitted to

In Africa, only four Ixodes spp have
livestock are Coxiella burnetii, Anaplasma adapted to livestock. Chief among these is marginale, Babesia divergmis, and
the South African paralysis tick, I 1ubicun

A phagocytophilum, various strains of
dus, of humid hill and mountain karoo
which cause bovine, ovine, and human
vegetation in South Africa. Its salivaiy
granulocytic airnplasmoses.

toxins cause a flaccid tetraplegia in

I pm·sulcatus, the taiga tick, is closely
livestock, people, dogs, and jackals.

related to I 1icinus and has similar host

Immatures parasitize the rock hai·e, other
preferences. It ranges from the central and
hares, and elephant shrews. Other parasites
eastern mountains ofEmope through the
of livestock in African highlands are
lowland forests from the Baltic Sea and

I drakenbm·gensis (Natal), I lewisi

Karelia eastward through the Siberian taiga

(Kenya), and I cavipalpus (southern Sudan
to the Seas of Japan and Okhotsk and the
to Zimbabwe and Angola).

TICKS

935

. I holocyclus, the Australian paralysis tick, NOSOMMASP

1s considered the most medically important
of the Australian tick fauna. Although most

Adults of the single species in this genus,
cases of tick bite are uneventful, some can

N monstrosum, particularly parasitize wild
result in life-threatening illnesses, including
and domestic buffalo, and also people,
paralysis, ti.ck typhus, and severe allergic
livestock, and wildlife, through much of
reactions. The species is found throughout

India, Nepalese lowlands, Bangladesh,

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the year in a variety of habitats, particularly

Thailand, and Laos. Inunatures parasitize
wet sclerophyll forests and temperate
chiefly murid rodents.

rainforest areas, across the hun1id coastal
regions of eastern Australia. Adults are

RHIPICENTOR SPP
more abundant in the spring and early
sun1mer, larvae in mid to late sunllller, and

The genus Rhipicenlor is composed of two
nymphs during winter. Natural hosts include species, namely R bicornis and R nultalli, bandicoots, kangaroos, possun1s, birds, and
and both are fom1d only in Africa south of
sometimes even reptiles, but it regularly
the Sal1ara. R bicornis feeds on goats,
attaches to domestic animals, including
cattle, horses, dogs, and carnivores in southdogs, cats, cattle, and horses, and occasionern and central Africa. R nultalli has a ally people. The tick injects a neurotoxin
widespread distribution in South Africa.

that causes progressive motor paralysis,

Immature stages feed on elephant shrews.

respiratory depression, and death in aninlals The preferred hosts of the adults are that have no immunity to the toxin. Most
domestic dogs, leopards, and South African
cases of tick paralysis seen by veterinarians
hedgehogs. The life cycle of these ticks
are in dogs and cats, but other species can
probably takes a year to complete in the
be affected. The condition has been
field.

recorded in sheep, cattle, goats, llamas, and

Muscovy ducks. Fatal cases have occurred

RHIPICEPHALUS SPP
in people. In the larger species, the younger
and smaller animals are likely to be affected. Approxinlately 60 of the 81 rhipicephalid I 1ubicundus, the karoo paralysis tick,
species are found in sub-Sallaran Africa.

may cause paralysis in sheep and goats in

The other rhipicephalid species have
southern Africa. The immature stages of
tl1eir origins in Eurasia and northern Aliica,

I rubicundus can be found on scrub hares
with R sanguineus and R (Boophilus)

and elephant shrews. The life cycle of the
microplus being spread by hLU11an activities tick is -2 yr. The ticks can often be found
into Asia, Australia, and the Americas.

along the lower line of the neck, chest, and

Adults of most species parasitize wild and
belly. The active period for adult ticks
domestic artiodactyls, perissodactyls, or
begins usually late in sununer and reaches
carnivores. Inunatures feed mostly on
peak levels in autunul and early winter
smaller man1mals; however, of those that

(April/May) and declines thereafter. The
parasitize rodents or hyraxes, and of tl1ose
paralysis commonly occurs from February
that parasitize artiodactyls, a few feed on
and reaches a peak in April and May.

the same host as the adults. The rhipicephalid life cycle is typically three-host,

MARGAROPUS SPP
but in the Mediterranean climatic zone

(long, warm sLU11mer with low rainfall)

Ticks of the genusMargaropus resemble

R bursa has a two-host cycle. In sub

Rhipicephalus (Boophilus) ticks but do

Sallaran Africa with long dry seasons,
not have festoons or ornamentations. They

R evertsi and R glabroscillalum also have are characterized by greatly enlarged
two-host cycles. In contrast, each of the
posterior legs and a prolonged median
five species in subgenus Boophilus has a
plate. The three highly specialized
one-host life cycle that may be completed
beady-legged, one-host Margaropus spp are in 3---4 wk (see below).

restricted to limited areas of Africa. M reidi

A nLU11ber of Rhipicephalus spp have
and M wileyi are recorded from giraffes in
long been difficult to identify or have been
the Sudan and in Kenya and Tanzania,
incorrectly identified. Current concepts of
respectively. M wileyi is also known to
tick phylogeny, taxonomy, and nomenclaparasitize zebras and gnu. M winthemi, a ture are based on molecular analyses.

winter-feeding parasite of zebras, horses,
and less often otl1er livestock and antelope,

Subgenus Boophilus spp

1s confined to mountains of South Africa

Each of the five Rhipicephalus (Boophi
and may contribute to loss of condition
lus) spp has a one-host life cycle that may during winter.

be completed in 3---4 wk and results in a

936

TICKS
heavy tick burden. Under these conditions,

Philippines) westward to India, Sti Lanka,
acaricide resistance becomes a major

Nepal, Pakistan, and western Afghanistan.

problem in control efforts. Zebu cattle,

R pilans infests livestock and wildlife in
which have served for centuries as hosts of

Indonesia and Borneo. Immatures of both

R (BJ microplus in the Indian region, have
species feed chiefly on rodents, also on
developed resistance to feeding by large
shrews, hares, and smaller carnivores.

numbers of ticks and are used (purebred or

From central Europe to Kazakhstan,

VetBooks.ir
crossbred) in integrated control programs.

R rossicus, R schulzei, and R pumilio are R (BJ microplus, considered the world's
of medical and veterinary importance. In
most important tick parasite of livestock,
southwestern Europe, R pusillus infests
has been introduced from the bovid- and
dogs as well as European rabbits, foxes,
cervid-inhabited forests of the Indian region
and wild pigs. R turanicus, as presently
to many areas of tropical and subtropical
recognized, ranges from China, southern

Asia, n01iheastern Australia, Madagascar,
fon11er USSR, India into southern Europe,
the coastal lowlands of southeastern Africa
and Africa as far south as South Africa.

to the equator, and much of South and

A member of the taxonomically difficult

Central America, Mexico, and the Carib

R sanguineus group, "R turanicus" and its bean. R (BJ microplus and R (BJ annula
vatious populations, which may represent
tus were eradicated from the USA after a
separate species, requires ftuiher studies of
long, costly control program. Constant
its abilities as a vector.

surveillance is maintained to prevent their

An easily recognized two-host species,
reintroduction. R (BJ annulatus of

R bursa, rat1ges from the western Meditersouthern former USSR, the Middle East, and ranean area of Europe to Iran and Kazakhthe MediteITanean area, was introduced stan. Adults and inunatures parasitize
witl1 livestock of the early Spanish
livestock, hares, deer, wild sheep and goats,
colonialists into northeastern Mexico but
people, and infrequently dogs. It causes
has not spread into Central America. In
ovine paralysis and transmits Crimeat1-

Africa, south of the Sallara and north of the

Congo hemorrhagic fever virus and other
equator, cattle movements probably
viruses to people, and numerous microbial
account for tl1e many R (BJ annulatus
diseases of livestock such as vatious
populations.

species of Babesia, Anaplasma, and

R (BJ decoloratus, which ranges from

Theileria ( notably Theileria parva, the soutl1ern Africa to the Sallara, is being
agent of East Coast Fever, often fatal for catreplaced in the southeastern part of this tle), Ehrlichia (CowdriaJ ruminantium
area by R (BJ microplus. In more humid

(the agent of heattwater), and Trypano

West African zones, R (BJ annulatus mixes
soma vi,vax ( an agent of sleeping sickness).

with or is totally replaced by R (BJ geigyi.

The best known Aftican rhipicephalid,

Scattered R (BJ geigyi populations are

R sanguineus, the kennel tick or brown dog
found as far east as southern and central
tick, has spread worldwide with domestic

Sudan. The only boophilid restricted to
dogs. It is now established in buildings as fat·
sheep and goats ( and occasionally horses)

north as Canada at1d Scandinavia at1d as far
is R (BJ kohlsi of Syiia, Iraq, Israel, Jordan, soutl1 as Australia In Africa, the Near East,
western Saudi Arabia, and Yemen. R (BJ
and parts of southern Europe, adults
microplus is an expe1im�ntal vector of
parasitize wild and domestic carnivores,

Babesia equi and has been collected from
sheep, goats, camels, other livestock, and
the nasal passages of equids in Panama.

various wild mat11mals, especially hares and

This tick and R (BJ annulatus are major
hedgehogs. Immatures in nature in this area
vectors of Babesia bigemina, B bovis, and
feed on small matm11als. However, in urban

Anaplasma marginale. R (BJ decoloratus
situations everywhere, dogs are virtually the
is an efficient vector of B bigemina and
only hosts of inunatures at1d adults. People

A marginale but does not tra.nsmitB bovis are attacked infrequently, more often in
orB equi.

situations when children play and sleep in
close contact with heavily infested dogs.

Strains of adultR sangiiineus that feed on

Subgenus Rhipicephalus spp
cattle are recorded in parts of Mexico and in

Tropical Asia is the home of five Rhipiceph

Tahiti. This tick is active throughout tl1e year
alus (RhipicephalusJ spp; adults of
in the tropics and subtropics but only from
two species parasitize domestic animals.

spring to fall in temperate zones. Newly

R haemaphysaloides infests all types of
active adults and nyinphs are frequently
livestock, and wild antelope, deer,
seen climbing walls from floor-level cracks.

carnivores, and hares in continental

R sanguineus is a vector of Babesia canis, southeast Asia ( and Taiwan and the

Ehrlichia canis, Rickettsia. conorii,

TICKS

937

R ma.ssiliae, R rickettsii, and R rhipi

The two-host African rhipicephalids are
cephali, Crimean-Congo hemorrhagic fever

R evertsi subspecies and R glabroscu
virus, and Thogoto virus. In southcentral
tatum. R evertsi evertsi, a large, beady

USA, R sanguineus is associated with
eyed, red-legged tick, a parasite of the
scattered foci of Leishmania mexicana.

East African zebra, parasitizes all types of

Certain American populations have become
herbivorous wildlife and livestock (but

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resistant to insecticides. The hymenopteran
seldom pigs). Immatures and adults infest

( chalcid) parasite of ticks, Hunterellus
the same hosts; immatures are also
lwoke'li, frequently infests nymphal
recorded from hares. It ranges from South

R sang1iineus in East Afiica.

Africa through eastern Africa east of the

R appendiculatus, the brown ear tick,

Nile to southern Sudan and is established
is a major pest in cool, shaded, woody and
in the mountains of Yemen. Scattered foci,
shrnbby savannas from southern Sudan and
introduced by domestic animals, are
eastern Zaire to Kenya and South Africa.

found west of the Nile. Immatures feed in

Adults and immatures feed in the ears of
the ear canal; adults feed mostly around
cattle, other livestock, and antelope, but
the anus and under the tail but also in the
also on other areas when the infestation
axillae and groin and on the sternum.

is massive. lnunatures may infest small

Large numbers on a single host are
antelope and carnivores, and occasionally
common on Equidae and are difficult to
rodents. Engorged females lay as many as
control because of their concentrations in

5,000 eggs. The life cycle lasts 3-9 mo.

difficult-to-reach feeding sites. Adult

Seasonal activity is closely associated with
females lay as many as 7,000 eggs. The life
temperature and rain periods. As many as
cycle takes 36 mo to complete, depending
three generations a year can follow in
on weather conditions. R evertsi evertsi
regions with two rainy seasons. R appen
transmits Babesia equi, Theile1'ia parva
diculatus is the major vector of the

(secondary vector), Bon·elia. theileri,

Theileria parva group of diseases (East

Rickettsia cono1'ii, and Kerai, Wad

Coast fever, Corridor disease, Zimbabwe

Medani, and Thogoto viruses. The
malignant theileriosis) and Nairobi sheep
banded-legged (Hyalomma.-like) western
disease virus, and is also a vector of T tau
subspecies, R eve1'tsi mimeticus, found
rotragi, Ehrlichia bovis, R conorii, and
from western Botswana to Namibia,

Thogoto virus. Heavy infestations on

Angola, and Zaire, is like the nominate
susceptible Bos taurus cattle cause a
subspecies in host preferences, feeding
sometimes fatal toxemia, loss of resistance
sites, and life cycle.

to various infections, and severe damage to

The tiny R glabroscutatum has become
the host's ears.

a common pest of sheep, goats, and other

The closely related R zambeziensis, with
livestock in the arid, small-shrub savanna of
similar host preferences, is found in drier
southeastern Cape Province, South Africa
lowland savannas in Tanzania, Zin1babwe,

Kudu and other small antelope are also

Zambia, Botswana, and Transvaal; it also is
infested. The few records of immatures are
a vector of East Coast fever. Other species
from rodents.

closely related to R appendiculatus include The R pravus group, currently under

R nitens in the Cape Province of South
taxonomic study, consists of four or

Africa and R duttoni in Angola and Zaire.

more species of which the adults feed

The ivory-ornamented R pulchellus, a
on livestock and herbivorous wildlife
parasite of zebras, also infests livestock and

(including hares); immatures feed on
gan1e aninlals in savanna habitats east of the elephant shrews (insectivores), hares, Rift Valley from southern Ethiopia to
and other small mammals. R pravus, a

Somalia and northeastern Tanzania Adults
brown, convex-eyed tick, is found in
and in1rnatures generally infest the same
shrubby and wooded savannas in east
host; however, in1rnatures also feed on

Africa. It is infected by Kadam virus. The
hares, and larvae ("seed ticks") are
closely related R occulatus, a parasite of
notmiously annoying pests of people.

hares, and another related, unnamed

R p1ilchell1is feeds in the ears and on the parasite of livestock are found in
lower abdomen, chiefly dtuing wet seasons.

southern Africa.

This tick is a vector of Babesia equi ( among The difficult-to-classify R punctatus
zebra), Theile1ia spp, Trypanosoma
group of parasites of livestock and wild
theile1'i, Rickettsia con01'ii, several
artiodactyls consists of R punctatus

Bunyaviridae (Crimean-Congo hemorrhagic (Angola, Mozambique, Tanzania), R kochi fever virus; Nairobi sheep disease; and

( neavi) (Botswana to Kenya and Zaire), and

Kajiado, Kismayo, and Dugbe viruses), and
an as yet unnan1ed species from Zimbabwe

Barur virus.

and South Africa.

938

TICKS

The R capensis group is also under
and big gan1e animals; R supe1·tritus also is study. Originally parasites of the Cape
found on carnivores.

buffalo, these species now parasitize
livestock and wildlife in Namibia and

South Africa (R capensis and R gertrndae ), East Africa (R compositus and The important argasid ticks include Argas

R longiis ), and West Africa to southspp, Carios spp, Ornithodoros spp, and VetBooks.ir
western Sudan (R pseudolongus ).

Otobius spp.

Above 5,900 ft (l,800 m) altitude in

East African forest and shrub zones,

ARGASSPP

R hurti and Rjeanelli infest livestock and Cape buffalo and other large game

Most of the 57 known Argas spp are specific animals. R hurti also inhabits mountains
for birds or bats; a few parasitize wild
in Zaire. Both species feed chiefly in the
terrestiial mammals or Galapagos giant
hosts' ears; Rjeanelli also feeds in the
tortoises. A pe1·s-ici1s (the fowl or poulti-y tailbrush.

tick) is an imp01tant poultry pest worldwide

R simus, the prototype of the R simus in warm climates. A miniatus (the South group and long considered to be a

American chicken tick) and A radiatus (the
well-established species, is divided into

N01th American bird tick) can present a
several species. R simus sensu stricto is problem for traditional or outdoor poultry
found through central and southern
operations from Caribbean to Central

Africa, roughly south of latitude 8°S,

America.and from Caribbean to 01th
where it is a competent experimental

America, respectively. The species of
vector of Anaplasma marginale and A
importance in tra.nsmittingAegyptianella
centrale. In eastern and northern Africa,
pullorum and Borrelia anse1ina to poultry R simus is replaced by a less punctate
are A persicus ( many tropical and
species, R praetextatus, which ranges
subtropical areas of the world), A m-boreus from central Tanzania to Egypt. Adults of

(much of Africa, including Egypt), A af1i
both species parasitize livestock, dogs,
columbae (tropical Africa), A walke1·ae
wild carnivores, large and medium-sized

(southern Africa), and A miniatus (South
game animals, and people. Occurrence
and Central America). Other species that
and densities on livestock are inexplicainfest poultry appear to transmit both bly erratic. Immature stages feed on the

A pullorum and B anse1ina. (See also
common burrowing rodents in savannas.

p 2876.) Tick paralysis is caused by feeding

Both species cause tick paralysis of

A pe1··sicus, A m·boreus, A walke1-ae,
people and transmit Rickettsia conorii

A miniatus, A rad'iatus, and A sanchezi and Coxiella burnet'ii. In Kenya, R prae

(USA). These and otherA1:gas spp can
textatus is a vector of Thogoto virus and
cause great irritation when feeding on
may be a secondary vector of Nairobi
people.

sheep disease virus. West of the Nile,
these species are replaced by R senega

CARIOSSPP
lensis and R muhsamae.

Much literature regarding R tricuspis

Most of the 88 Carios spp are species

(Tanzania to South Afrtca) and R lunulatus
specific parasites of bats and rodents.

(West Af1ica to Etruopia and Tanzania) has

Several species infest birds nesting in rocks
been incorrect. The chief feeding site of
and caves. These ticks norrna.lJy live
both on livestock and wildlife is the
alongside their hosts in caves, hollow trees,
tail brush, but other parts of the host may
and rock crevices, and therefore rarely
also be feeding sites.

come in contact with domestic animals.

R sanguineus and R turanicus of the However, in locations where bats occupy

R sanguineus group are described above.

roof cavities, their parasites may present a

Related species are R camicasi and R be1°
problem for people and their pets. Ticks
geoni of n01theastem Africa, R guilhoni C kelleyi in North America and C vespe1·til
and R moucheti of West Africa, and two
ionis in Europe, which in nature feed almost widely distributed "fom1s" of R sulcatus, exclusively on rock- and ti·ee-roosting bats,
which are under study.

have been found in massive numbers in

Two quite distinctive species often
homes with associated bat colonies and
confused with R appendiculatus are R su
have been reported to attach to people. Nest
pe1·tritus (Natal to southern Sudan) and
parasites of colonial birds such as C amblus,

R muhlensi (Kenya and southern Sudan

C capensis, and C denmm·ki may pose a to Central Africa). Adults of both species
distinct threat to breeding colonies and are
parasitize cattle, Cape buffalo, antelope,
known to cause the death of chicks.

TICKS

·939

ORNITHODOROS SPP

O tholozani (0 papillipes, also O crossi) infests burrows, caves, stables, stone and

Most of the 37 Ornithodoros spp inhabit
clay fences, and human habitations in
protected niches in burrows, caves, dens,
semi.desert, steppe, and long dry-season
cliffsides, and bird colonies. Among the few
environments from China, southern f01mer
that parasitize livestock, 0 sa.vignyi and

USSR, northwestern India, and Afghanistan

O co1iaceus are exceptional, because they
to Greece, northeastern Libya, and eastern

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have eyes and because they restjust below

Mediterranean islands. Nun1erous rodents,
or above ground level under the shade of
hedgehogs, porcupines, and domestic
trees and rocks where livestock and game
anin1als support O lholozani populations.

animals rest and sleep. 0 savignyi, the sand People develop severe, sometimes fatal, ta.mpan, lives in semiarid areas from

Persian relapsing fever when bitten by

Namibia to India and Sri Lanka and is often

O lholozani infected with Borrelia persica.

tremendously abundant. It can cause fatal

O lahorensis, originally a parasite of wild tick paralysis in calves. People and tethered
sheep resting in the lee of cliffsicles, is an
livestock suffer severe in.itation, allergy,
inlpo1tant pest of stabled livestock in
and toxicosis from sand tampan bites, and
lowlands and mountains of Tibet, Kaslunir,
paralysis and death of animals are recorded.

and southern forn1er USSR to Saudi

O co1iaceus, the "pajaroello" of h.illside Arabia and Turkey, Greece, Bulgaria, and
scrub oak habitats from northern California

Yugoslavia. The two-host life cycle and long
and Nevada to Chiapias, Mexico, occupies
wintertime attaclunent of O laho1·ensis is
deer beds under trees and near large rocks.

biologically remarkable. It is deleterious

It is well known for irritating deer and
to livestock held for much of the winter
cattle, and in people, its bite causes a severe
in heavily infested stables; it may cause
skin reaction. Epizootic bovine abortion,
paralysis, anemia, and toxicosis, and it
caused by an unnamed bacterum (in the
transmits the agents of piroplasmosis,
order Myxococcales), is transmitted by
bmcellosis, coxiellosis/Q fever, tular·emia,

O co1iaceus. 0 gurneyi shelters in treeand possibly Bo1nlia persica, the agent of shaded soil in arid zones of Australia where

Persian relapsing fever.

kangaroos and people rest; livestock are

O turicala parasitizes rodents that live in rare or absent in these habitats.

burrows, crevices, or caves; owls; snakes;

Among the numerous Ornilhodoros spp
tortoises; and also domestic pigs and other
that inhabit burrows, several species are
livestock in southern USA and Mexico.

either naturally infected with African

Contrary to most Ornithodoros feeding
swine fever (ASF) virus in Africa or have
patterns, inunature O tu1icata engorge in
the laboratory-confirmed ability to harbor

<30 min, but adults may attach for as long as
and transmit the agent in Europe and the

2 days. 0 tiiricata has been associated with Americas. The natural reservoir and vector diseases of pigs, and serious toxic reactions of ASF virus is O porcinus, which is
and secondary infections can r�sult when
abundant in burrows of tropical African
people are bitten.

pigs and also of antbears and porcupines.

O.furucosus parasitizes people and

It has secondarily adapted to human dwelllivestock in houses and stables in northings and domestic animal shelters, where western South America. Other South
it lives in the cracks of walls and floors.

American pests of livestock and people,

Domestic pig populations in the vicinity
probably originally parasites of the peccary,
of infected wild pigs can be decimated by
are O braz'iliensis and O rostratus.

ASF. Wild and domestic pigs are not
involved in the epidemiology of Boirelia
dutloni,

OTOBIUSSPP
the agent of human African
relapsing fever, which is transmitted by

Otobius megnini, which is exceedingly

O moubata. ASF virus has been transspecialized biologically and structurally, ported in infected meat to Spain where
infests the ear canals of pronghorn

O marocanus, an inhabitant of rodent
antelope, mountain sheep, and Virginia and
burrows and pig sties, is an efficient
mule deer in low rainfall biotopes of
vector. 0 marocanus is also a reservoir
western USA and in Mexico and western
and vector of Borrelia hispanica, the

Canada. Cattle, horses, goats, sheep, dogs,
agent of Spanish-northwest African human and people are sinillarly infested. This relapsing fever. ASF has likewise been
well-concealed parasite has been transintroduced in Brazil, Haiti, the Dominican p01ted with livestock to western South

Republic, and Cuba. The American O tur

America, Galapagos, Cuba, Hawaii, India,
icala, 0 dugesi, and O coriaceus arc Madagascar·, and southeastern Afiica.

potential vectors of ASF virus.

Notably, adults have nonfunctional

940

TICKS
mouthparts and remain nonfeeding on the
will not cause the tick to "back out" and in ground but may survive for almost 2 yr.

fact, may cause more disease-carrying tick

Females can deposit as many as 1,500 eggs
saliva to be deposited in tile wound.

in a 2-wk period. Larvae and two nymphal
instars feed for 2--4 mo, mostly in winter and
spring. There can be two or more genera

VetBooks.ir
tions per year. In contrast with most other

The main reasons for tick control are to
ticks, the bites of O megnini are painful for protect hosts from irritation and production
the hosts. People and other animals may
losses, formation of lesions tllat can become
suffer severe irritation from ear canal
secondarily infested, danrnge to hides and
infestations, and heavily infested livestock
udders, toxicosis, paralysis, and of greatest
lose condition during winter. Tick paralysis
importance, infection witll a wide variety of
of hosts and secondary infections by larval
disease agents. Control also prevents the
screwworms are reported. 0 megnini is
spread of tick species and the diseases they
infected by the agents of coxiellosis/Q fever,
transmit to unaffected areas, regions, or
tularemia, Colorado tick fever, and Rocky
continents.

Mountain spotted fever, although its ability
to transmit these pathogens to the hosts

Cultural and Biologic Control: These
is uncertain. The second Otobius sp, 0
measures can be directed against both the
lagophilus, feeds on the heads of jackrabfree-living and parasitic stages of ticks. The bits (hares) and rabbits in western USA.

free-living stages of most tick species, botll
ixodid and argasid, have specific requirements in terms of microclimate and are CK REMOVAl!

restricted to particular microhabitats witllin
tile ecosystems inhabited by tlleir hosts.

Ticks found attached to people or domestic

Destrnction of these microhabitats reduces
animals should be removed immediately.

the abundance of ticks. Alteration of the

The longer a tick remains attached to the
environment by removal of certain types of
skin, the more pathogen- and/or toxinvegetation has been used in tile control of containing saliva is being injected into the

Amblyomma americanurn in recreational
host. Therefore, prompt removal is
areas in southeastern USA and in tile
imperative. Several tick removal devices
control of Ixodes rubicundus in South
are on the market, but ticks are most

Africa. Control of argasid ticks such as
effectively removed by a plain set of

Argas persicus and A walkerae in poultry fine-tipped tweezers.

can be achieved by eliminating cracks in

The CDC recommends the following
walls and perches, which provide shelter to
method of tick removal: 1) Use tweezers to
the free-living stages.

grasp the tick as close to tl1e skin surface as

The abundance of tick species can also be
possible. 2) Pull upward with steady, even
reduced by removal of alternative hosts or
pressure. 3) Do not twist the tick, because
hosts of a particular stage of the life cycle.

this will cause the mouthparts to break off

This approach has occasionally been
and remain in tile skin. If tllis happens and
advocated for control of tlrree-host ixodid
the moutllparts cannot ea§ily be removed
ticks such as Rhipice-phalus appendicula
with clean tweezers, leave it alone and let
tus, Amblyomrna hebraeum, and Ixodes
the skin heal. Chances of a local infection
nibicundus in Africa, and Hyalomma spp being caused by remaining tick moutllparts
in southeastern Europe and Asia.

are insignificant compared witll tile risk of

Rotation of pastures or pasture spelling
pathogen transmission by an attached cick.

has been used in control of tile one-host

4) Avoid crnshing tile tick. Do not squash
ixodid tick Rhipice-phalus (Boophilus)

tile tick with your fingers; tile contents of
microplus in Australia. The method could
tile tick can transmit disease tllrough skin
also be applied to oilier one-host ticks, in
abrasions. 5) After removing tile tick,
which tile duration of the spelling period is
tlloroughly clean the bite area and your
determined by tile relatively short life span
hands witll nibbing alcohol, an iodine scrnb,
of tile free-living laivae. However, it has
or soap and water.

minimal application to multihost ixodid

Avoid folklore remedies such as
ticks or argasid ticks because of the long

"painting" tile tick witll nail polish or
survival periods of tile unfed nymphs and
petroleum jelly or using a hot match to make adults.

the tick detach from the skin. The goal is to

Predators, including birds, rodents,
remove tl1e tick as quickly as possible, not
shrews, ants, and spiders, play a role in
to wait for it to detach. Using irritants such
some areas in reducing tile numbers of
as petroleum jelly, a hot match, or alcohol
free-living ticks. In the New World, fire ants

TICKS

941

(Pheidole megacephala) are noteworthy

Acaricides are most commonly applied
tick predators. Engorged ticks may also
to livestock by use of dips or sprays, with
become parasitized by the larvae of some
dips being considered the more effective.

wasps (Hymenoptera), but these have not

In recent years, several other means of
significantly reduced tick populations.

acaricide application have been developed,

Zebu (Bos indicus) and Sanga(aB la-u
including slow release of systemics from
rns, B indicus crossbreed) cattle, the
implants and boluses, slow release of

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indigenous breeds of Asia and Afiica,
conventional acaricides from inlpregnated
usually become very resistant to ixodid
ear tags, pom0ons (which are applied on the
ticks after initial exposure. In contrast,
back and spread rapidly over the entire

European (B lam-us) breeds usually remain
body surface), and spot-ons (which are
fairly susceptible. The tick resistance of
similar but have less ability to spread).

Zebu breeds and their crosses is being

Acaricides are usually applied as dusts or
increasingly exploited as a means of control
washes on cats, and as dusts on dogs and
of the parasitic stages. The introduction
fowl.

of Zebu cattle to Australia has revolution

For many years, pyreth:roids and
ized the control of R microplus on that
organophosphates fom1ulatecl as dusts,
continent. Use of resistant cattle as a
dips, or collars were used on clogs and cats
means of tick control is also becoming
to control ticks. With the advent of the
important in Africa and the Americas. In
phenylpyrazoles, long-lasting spray and

Africa, infestations of ixodicl ticks on
convenient spot-on formulations were
livestock and wild ungulates may also be
introduced. Pyretllfoids are available as
reduced by oxpeckers (Buphagus spp ),
highly concentrated spot-on products that
which are birds that feed on attached ticks.

are labeled only for dogs because of their
toxicity in cats. Use of these concentrated

Chemical Control: See also ECTOPARASITIpyrethroids is not advised on dogs if a cat is cwEs, p 27 48.

even in the same household.

Control of ticks with acaricides may be
directed against the free-living stages in the

Vaccines: An advance of potentially great
environment or against the parasitic stages
importance has been the production, using
on hosts. Control of ixodicl ticks by
biotechnology, of a promising vaccine
acaricicle treatment of vegetation has been
againstR microplus. The inlmunizing agent
clone in specific sites ( eg, along trails) in
is a concealed tick antigen, not nom1ally
recreational areas in the USA and elseencountered by the host. The in1IDune where, to reduce the risk of tick attachment
mechanism it stimulates is different from
to people. This method has not been
that stinlulated by exposure to ticks (ie, tick
recommended for wider use because of
feeding). The antigen was derived from a
environmental pollution and the cost of
crude extract of partially engorged adult
treatment of large areas. Dog kennels,
female ticks. It stin1ulates the pro.duction of
barns, and hun1an dwellings may also
an antibody that damages tick gut cells and
require periodic treatment with acaricides
kills the ticks or drastically reduces their
to control the free-living stages of ixoclicl
reproductive potential.

ticks such as the kennel tick, Rhipicepha

Prospects of developing similar vaccines
lus sanguineus.

against other ixodid tick vectors of cattle

The free-living stages of argasid ticks,
diseases of major veterinary importance are
which infest specific foci such as fowl nms,
not clear. Rhipicephalus ticks are good
pigeon lofts, pig sties, and human dwellings,
candidates for such vaccines in that they
are more frequently and more effectively
are one-host ticks and show a marked
treated with acaricides.

preference for bovine hosts, which act as

Treatment of hosts with acaricides to
the principal reservoir of perhaps the most
kill attached larvae, nymphs, and adults of
inlportant group of disease agents (Babesia
ixodid ticks and larvae of argasid ticks has
spp) these ticks transmit. By contrast, most
been the most widely used control method.

other tick vector species of agents that

In the first half of the century, the main
cause inlportant cattle diseases ( eg,
acaricide was arsenic trioxide. Subsequently,
anaplasmosis, heartwater, theileriosis) are
organochlo1ines, organophosphates,
three-host ticks, which infest not only cattle
carbamates, amidines, pyretl1roids, and
but also wild ungulate species, for which
avermectins have been used in different
vaccination is not feasible. Moreover, many
parts of the world. The introduction of new
wild tmgulate hosts of the vector ticks serve
compounds, such as the phenylpyrazoles,
as reservoirs of these disease agents. For
has been necessary because of the developthese reasons, vaccines against nonboophiment of resistance in tick populations.

lid vector ticks may be unable eitller to

942

TICKS
eradicate the ticks or to eliminate important
cost-containment strategies requires better
sources of the disease agents they transmit.

knowledge of the dynamic associations
among the disease agents, their vertebrate

Control Strategies: Initially, the main
hosts, the tick vectors, and the environment.

uses of acaricides were for tick eradication,

Strict quarantine measures to prevent
prevention of spread of ticks and tickbome
reintroductions are enforced in countries
diseases (quarantine), and eradication
from which ticks and tickborne diseases

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and control of tickbome diseases. The
have been eradicated. Climate-matching
eradication programs were successful in
models, geographic infmmation systems,
some ecologically marginal subtropical
and expe1t systems ( models based on
areas, such as southern USA and central
expert knowledge and aitificial intelligence)

Argentina where Rhipicephalus spp and
are being used to identify unaffected areas
babesiosis were eradicated, and southern
in which tick pests could become estab

Africa where East Coast fever ( caused by
lished if introduced.

Theileria parva. parva) was eradicated.

Control of these diseases will require use

The programs were less successful in the
of the principles of endemic stability ai1d
ecologically more favorable tropical areas
development of improved recombinant
of northeastern Australia, Central America.,
vaccines. A current, promising strategy is
the Caiibbean Islands, and East Africa.

the identification of receptor sites on the

In the areas where eradication was not
midgut of vector ticks and the development
achieved, costs of maintaining intensive tick of antibodies tlrnt bind with these sites, control programs often have become
thereby blocking tick-ingested tickborne
prohibitive. For this reason, integrated
pathogens from infecting the tick. Cattle
biologic and chemical control strategies are
irtjected with receptor-site antigens may
being adopted. The effectiveness of these
produce antibodies that feeding ticks ingest.

TUMORS OF THE SKIN AND SOFT TISSUES

Cutaneous tumors are the most frequently
hamartoma (nevus) is a localized
diagnosed neoplastic disorders in domestic
developmental defect associated with
animals, in pa.it because they Call be
enlargement of one or more elements of the
identified easily a.nd in pa.it because the
skin. A sebaceous han1aitoma., for exa111ple,
constant exposure of the skin to the
refers to a localized region of tl1e skin where
external environment predisposes this
sebaceous glands are extremely prominent
organ to neoplastic tra.I1Sformation.

and sometimes rnalfon11ed. Although by

Chemical carcinogens, ionizing radiation,
strict definition hai11aitomas are present at
and viruses all have been implicated, but
birth, they may occasionally take a long time
hormonal and genetic factors may also play
to reach a clinically apparent size and may
a role in development of cutaneous
not be diagnosed until ai1 animal is mature.

neoplasms.

To confuse matters f.urther, some lesions

The skin is a complex structure composed with clinical and histologic features of of various epithelial ( epidennis, a.dnexa),
congenital han1aitomas may develop in
mesenchymal (fibrous connective tissues,
adult aninlals. Such "acquired" han1aitomas blood vessels, adipose tissue), and neural
ai·e difficult to separate from benign
and neuroectodermal tissues (pe1ipheral
epithelial ai1d mesenchymal neoplasms.

nerve, Merkel cells, melanocytes), all with

In hw11ai1 medical literature and some
the potential to develop distinctive tw11ors.

veterinary texts, the tern1 "nevus" is used Because cutaneous tumors ai·e so diverse,
synonyn10usly witl1 hamaitoma.. A benign
their classification is difficult and often
neoplasm is localized, noninfiltrative, and
controversial. There is also controversy
because it is surrounded by a capsule, easily
regarding the criteria used to define whether excisable. A neoplasm of intermediate a lesion that arises in tl1e skin or soft tissues
malignancy is locally infiltrative and
is neoplastic and, if so, whether it is benign
difficult to excise but does not metastasize.

or malignant. To avoid confusion, the follow

A malignant neoplasm is infiltrative
ing ten11s are used in this discussion: A
witl1 metastatic potential.

TUMORS OF THE SKIN AND SOFT TISSUES

943

Although cutaneous neoplasms
neoplasms not surgicalJy resectable, or
characteristically are nodular or papular,
when surgical intervention would cause
they also can occur as localized or
unacceptable physical irnpainnent.

generalized alopecic plaques, erythematous

Chemotherapy can be used either systemiand pigmented patches and plaques, calJy (and if appropriate, intralesionalJy) as
wheals, or nonhealing ulcers. The variability a primary method for treatment of in clinical presentation can make distinmalignant neoplasms or as an adjw1ct to VetBooks.ir
guishing a neoplasm from an inflanunatory
surgery or radiation therapy. In the skin,
disease difficult; furthermore, distinguishradiation is most commonly used to treat ing a benign tumor from a malignant tumor
round cell tumors ( eg, lyrnphosarcomas,
is even more subjective because sarcomas
mast cell twnors, transmissible venereal
or carcinomas early in their development
tumors, etc) or solid tumors that cannot be
may palpate as discrete, encapsulated
excised completely. Although generalJy
masses. To establish a definitive diagnosis,
palliative, long remissions may sometimes
histopathology is generalJy required.

be obtained with radiation therapy. Other

Cytologic evaluation is very useful and
fom1s of therapy include hyperthennia.,
should be used to exclude mast cell tumor
laser therapy, photodynamic therapy,
before surgery so that wide adequate
antiangiogenic tl1erapy, metronomic
margins are planned as appropriate. For
therapy, gene therapy, irnmunotherapy, and
some neoplasms (eg, round cell tumors),
multimodal therapy using a combination or
cytology can rival or even surpass the value
sequencing of various therapies.

of histologic examination.

Therapy depends largely on the type of
tumor, its location and size, and signalment

EPIDERMAL AND HAIR FOLLICLE
of the animal. For benign neoplasms

TUMORS
associated with neither ulceration nor
clinical dysfunction, no therapy may be the

Cerurninous gland tumors are discussed in
most prudent option, especialJy in aged

TUMORS OF' THE EAR CANAL ( see p 535).

companion anin1als.

Fine-needle aspiration cytology should
be perfom1ed initially on alJ tumors to

Benign, Nonvirus-associated
detennine the type of tw11or and treatment

Papillomatous Lesions
planning. For more aggressive neoplastic

For a discussion of papillomas (viral warts),
diseases or for benign tumors that inhibit
the most common, viral-induced neoplasms
nom1al function or are cosmeticalJy
of the skin, seep 952. Benign, proliferative unpleasant, there are several therapeutic
lesions not associated with papilloma virus
options. For most, surgical intervention
infection can have a gross morphology
with complete excision provides the best
similar to that of papillomas.

chance of a cure with the least cost and

Epidermal hamartomas (nevi) are rare
often with the fewest adverse events.

proliferations identified only in dogs, most

Histologic assessment of margin status
often in the young. The disease may be
is useful to predict local recurrence of
heritable in Cocker Spaniels. Grossly,
cutaneous malignant tun1ors in dogs and
epidennal nevi appear as pigmented,
cats treated by means of excision alone.

hyperkeratotic, vaguely papillated papules

However, method accuracy varies among
and plaques that a.re occasionalJy arranged
tumor types and grades. Recurrence times
in a linear pattern. Some forms are
suggest postsurgical follow-up should
associated with pustules and acantl1olytic
continue for �2 yr. Careful postsurgical mancells. They are benign, but their appearance agement is recommended for anin1als with
is unpleasant, and the extensive hyperkeraboth in.filtrated and close tumor margins.

tosis is prone to secondary bactelial

Lumpectomy is adequate for benign
infection. Localized lesions can be excised;
lesions, but if a malignancy is suspected, the dogs with multiple lesions or lesions too lesion should be removed with wide (3 cm)

large to be surgicalJy removed may be
surgical margins. For tumors that cannot
responsive to isotretinoin or etretinate.

be completely excised, partial removal or

Hyperkeratosis may be transiently
debulking may prolong the life of the animal
controlled by use of topical keratolytic
and increase the effectiveness of radiation
shampoos and emollients.

or chemotherapy. Cryosurgery is also

Congenital papillomas of foals are rare
an option, although it is more effective
and probably a developmental defect rather
for benign, superficial lesions than for
tl1an a result of papilloma virus infection.

malignant cutaneous neoplasms. Radiation

They are found anywhere on the body but
therapy is of most value for infiltrative
most conunonly on the head. Thoroughbreds

944

TUMORS OF THE SKIN AND SOFT TISSUES
may be predisposed. Present at birth, the
predisposed breeds such as Wirehaired
lesions are often several centimeters in diam

Pointing Griffons, Kerry Blue Terriers, and
eter, hairless, pedunculated, and exophytic,

Wheaten Terriers. These tumors are found
with a papillated surface reminiscent of a
most commonly on the head ( especially the
cauliflower. They are benign, and excision is
ears), the neck, and forelimbs. Older
curative.

domestic longhair, Himalayan, and Persian

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Canine warty dyskeratomas are rare,
cats are the breeds most at risk. Feline basal
benign neoplasms of uncertain derivation
cell tumors may develop almost anywhere
but with histologic features of follicular or
on the body. In both dogs and cats, these
apocrine neoplasms (or both). They appear
tumors generally appear as firm, solitary,
grossly as verrucous papules or nodules
encapsulated, and often hairless or
with a keratotic, umbilicated center.

ulcerated nodules that may be pedtmcu

Excision is curative.

lated; they vary in size from <l cm to> 10 cm
in diameter. In cats more often than dogs,

Basal Cell Tumors and Basal Cell
these tumors are often densely pigmented,

Carcinomas
and on cut section, they can be difficult to
distinguish from dermal melanocytomas.

(Basal cell epitheliomas, Basaliomas,

Cystic variants are also more common in

Trichoblastomas, Basosquamous cell
cats. Although basal cell tumors are benign,
carcinomas)

they are expansive neoplasms and may be

Basal cell tumors represent a heterogeassociated with extensive ulceration and neous group of cutaneous epithelial
secondary inflammation. Complete excision
neoplasms recognized most commonly in
is curative.

cats, less commonly in dogs, occasionally

Basal cell carcinomas are more
in horses and sheep, and seldom in other
frequently recognized in aged cats than in
domestic animals. These neoplasms are
dogs. Persian-type breeds are predisposed.

composed of a proliferation of small

They often appear as ulcerated plaques on
basophilic cells that exhibit morphology
the head, extremities, or neck. Unlike
reminiscent of the progenitor cells of the
benign basal cell tumors, these carcinomas
epidermis and adnexa. As these tumors
generally have continuity with the
have been examined more closely, evidence
epidem1is, are locally invasive, and may be
of differentiation (follicular, sebaceous, etc)

multicentric. Altl10ugh evidence of vascular
has been discovered, giving justification for
invasion may be identified on histologic
reclassification. For exan1ple, in dogs, what
sections, local or systemic metastasis rarely
in the past was called a basal cell tumor is
occurs. Consequently, surgical excision is
best characterized as a trichoblastoma, a
the treatment of choice.

tumor of hair bulb (the site of the follicle

In dogs, most basal cell carcinomas have
that produces the hair shaft) origin.

llistologic evidence of cornification, a

Some reclassification schemes have
feature they have in common with
suggested that the use of the term basal cell
squamous cell carcinomas. Therefore, they
tumor be restricted to a benign neoplasm in
are generally called basosquamous cell
cats (the derivation of which has yet to be
carcinomas. These tumors are generally
defined). Because this revisep terminology is recognized in older dogs. Saint Bernards, being adopted slowly, traditional terminol

Scottish Terriers, and Norwegian Elkogy will be used herein. That is, a benign hounds are most at risk. Unlike canine basal
proliferation of basal cells will be called a
cell tumors, basosquamous cell carcinomas
basal cell tumor; a malignant proliferation
do not tend to develop on.the head and can
will be called a basal cell carcinoma. In
be found almost anywhere on the body
domestic animals, most basal cell tumors
where they have continuity with the
are benign and originate in the mid to deep
epidernlis and appear as exoendophytic
dermis, indicating probable adnexal
nodules or plaques. These twnors are
derivation. These features distinguish basal
locally invasive but seldom metastasize.

cell tumors in domestic animals from those

Surgical excision is the treatment of choice.

in people, the latter being locally invasive

(ie, they are true carcinomas) and originat
lntracutaneous Cornifying
ing in the epidemlis. ln addition, solar injury

Epitheliomas
is a common cause of neoplasms derived
from basal cells in people, but its role in

(Keratoacanthoma, lnfundibular keratinizing
inducing basal cell tumors of other animals
acanthoma)

is unknown.

Intracutaneous cornifying epitheliomas are

Canine basal cell tumors generally
benign neoplasms of dogs and possibly cats.

develop in middle-aged to older dogs of

As in human keratoacanthomas, these

TUMORS OF THE SKIN AND SOFT TISSUES

945
lesions most likely arise from the hair
especially in the face and ear tips of white
follicle and not from the interfollicular
cats and in the ventral nonpigmented skin of
epidermis. They can develop anywhere on
dogs, prolonged exposure to sUlllight on
the body, with the back, tail, and extremities sparsely haired, minimally pigmented areas the most common sites affecting middleof the body is a major predisposing factor.

aged dogs. Norwegian Elkhounds, Belgian

The grooming habits of cats also expose

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Sheepdogs, Lhasa Apsos, and Bearded
them to particulate carcinogens from

Collies are most likely to develop these
cigarette smoke and flea collars. In addition,
tun10rs, with Nmwegian Elkhounds and
a tmique form of feline squamous cell

Lhasa Apsos at risk of developing generalcarcinoma associated with papilloma virus ized lesions. The most characteristic
infection has been described (see below).

presentation is a papule or nodule with a

In dogs, squamous cell carcinomas are
central comified pore that may protrude
the most frequently diagnosed carcinomas
above the epidermal sUiface, giving the
arising in the skin. Two forms are recogappearance of a horn; however, many of nized: cutaneous and subungual. Cutane
these tumors never have continuity with
ous squamous cell carcinomas are
the epidermis and may appear solely as
tUinors of older dogs, with Bloodhounds,
comified cysts. These tumors are benign

Basset Hounds, and Standard Poodles at
and treatment is optional, provided a
greatest risk. Lesions conunonly arise on the
definitive diagnosis has been established
head, distal extremities, ventral abdomen,
and there is no self-trauma, ulceration, or
and perineum. Most cutaneous squan1ous
secondary infection. Tumor wall rupture
cell carcinomas appear as finn, raised,
releases keratin into sunounding tissues,
frequently ulcerated plaques and nodules;
evoking a pyogranulomatous and granusometin1es they can be extremely exophytic lomatous inflammatory response. Excision
and have a wait-like sUiface. The etiology of
is curative; however, dogs are prone to
most of these tumors is undefined; however,
develop additional tun10rs over time. For
some are induced by prolonged solar ir\jury.

animals with a generalized fom1 of the

These usually develop on ventral abdomidisease, oral retinoids ( eg, isotretinoin or nal, preputial, scrotal, and inguinal skin in
etretinate) may be of therapeutic benefit.

white-skinned, shorthaired breeds such as

Dalmatiat1S, Bull Terriers, Pit Bulls, and

Squamous Cell Carcinomas

Beagles. Lesions develop in a ventral

(Epidermoid carcinomas, Prickle cell
location because the poorly haired skin has
minimal shielding from ultraviolet radiation,
carcinomas)

many animals sun themselves lying on their

Thought to arise from either the epiderbacks, and perhaps because solar radiation mis or the epithelium of the superficial
reflects from the ground. Before a carci

(infundibular) regions of the outer root
noma develops, anin1als acquire focal zones
sheath of the hair follicle, squamous cell
of lichenification, hyperkeratosis, anct
carcinomas have been recognized in all
erythema known as solar keratosis (solar
domestic anin1als. Although most arise
dermatosis, actinic keratosis, senile
without prior cause, in many species,
kcratosis).

Subungual squamous cell carcinomas
are most conunonly found in older Giant
and Standard Schnauzers, Gordon Setters,

Briai·ds, Ken-y Blue Terriers, Standard

Poodles, and Scottish Terriers. Generally, all
are darkhaired breeds, and a dark coat color
has been associated with development of
subungual squamous cell carcinomas that
arise from the nailbed epithelium and
invade tl1e medullary and cortical bone of

P3. They may arise on multiple digits, often
appeai· on different extremities, and may
metastasize via lymphatics to regional
lymph nodes and lungs in as many as 13% of
cases. Females have a slight predilection,
ai1d both fore- and hindlimbs are equally
predisposed to tumor development.

Solar-induced squamous cell carcinoma in the

In cats, cutaneous squamous cell
white skin of a Dalmation dog. Courtesy of Dr.

carcinomas most conunonly develop in

Alice Villalobos.

cor\junction witll chronic solar ir\jury.

946

TUMORS OF THE SKIN AND SOFT TISSUES

Consequently, they usually develop on the

In goats, squamous cell carcinomas
pinnae, frontal ridges, eyelids, nose, or lips
develop most frequently in females, in
of cats that have white skin in these regions.

which twnors develop on the perineal and

There is no breed or sex predilection. As in
vulvar regions and on tile skin of tl1e teats
dogs, solar keratosis or carcinoma in situ
and udders. Both males and females can

( early superficial stage) often precedes
develop sun-induced tun1ors on the ears.

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development of a malignant tw11or.

Although Angoras are most at risk, Saanan

Recently, coat-associated particulate
goats occasionally develop squamous cell
carcinogens from exposure to cigarette
carcinomas on the udder in association with
smoke and flea collars have been identified
papillomas. The role papilloma vi.ruses play
as lisk factors for cats with oral squamous
in tumor progression is considered
cell carcinoma Lesions not caused by sun
contiibutory.

exposure may develop on the digits and are

Squamous cell carcinomas are extremely
presun1ed to be metastatic from primary
uncommon in swine.

squamous cell carcinomas of the lung, but

Most squan1ous cell carcinomas are
primary subungual fonns are uncommon in
solitary lesions; however, multiple tumors
cats.

may develop in conjunction with solar

Cutaneous squamous cell carcinomas are
injury in tl1e "field cancerization" model.

the most common malignant neoplasm in

They appear as endophytic or exoendohorses. They generally develop in adult or phytic lesions, the former as raised,
aged horses with white or part-white coats;
irregular de1mal masses with an ulcerated
breeds at risk include Appaloosa, Belgian,
surface, and the latter as raised, irregular

American Paint, and Pinto. Although they
dermal masses covered by a papillated
can arise anywhere on U1e body, tl1ese
epidermis. Cats initially exhibit small
twnors most commonly arise in nonpigcrusting facial sores tllat do not heal. The mented, poorly haired areas near mucous
lesions often persist for months before
membranes. Thus, the pe1iorbital regions,
defects appear on tl1e ear tips, nares, and
lips, nose, anus, and external genitalia
eyelids. Subungual squamous cell carcino

( especially tl1e penile sheath) are sites most
mas of dogs are first identified by lan1eness
likely to be affected.

or nail malformation, an infection that

In cattle, these tumors are most common
mimics chronic osteomyelitis, or loss of the
in breeds with white hair and poorly
claw of the affected digit. In cattle with
pigmented skin ( especially Holsteins and
involvement of the horn, the first sign is

Ayn;hires) and, as in horses, develop around distorted growth.

the mucous membranes, usually at the

Squamous cell carcinomas are charactermucocutaneousjunctions, particularly the istically invasive into adjacent soft and bony
periocular and vulvar regions. In India,
tissues. Infrequently, in cattle, they regress
squamous cell carcinomas of the horn core
spontaneously. In small animals, longterm
are common in aged bullocks. The most
sUIVival and the likelihood of metastasis are
common cause is actinic injury. Solar
correlated with histologic differentiation.

keratoses often precede development of an

Well-differentiated tumors are slowly
invasive tumor; genetic factors, in1munodeprogressive or remain localized; undifferenficiency, and vi.ruses may also way a role.

tiated tumors are more likely to metastasize

In sheep, squamous cell carcinomas are
or recur witllin 20 wk of excision. In
of economic significance in some parts of
general, failure of tream1ent is due to late
the world. In a study in Australia, they were
diagnosis and lack of control of local
responsible for more than one-third of all
disease rather tllan metastasis.

condenmations before slaughter. The

For dogs and cats, surgical excision, such

Merino breed is most at risk, and females
as amputation of tile involved digit or
more so than males. The most conm1on
pinnae or nosectomy, is the treatment of
sites are the poorly haired skin of the ears,
choice, and margins of at least 2 cm are
lips, muzzle, and the vulvar lips after they
recommended. One review of 117 digit
have been externalized by a Mules
masses in dogs found tllat 25% of tile lesions
operation to prevent fly strike. Tumors at
were squamous cell carcinomas and 66%
these sites develop in conjunction with
were subungual lesions. These dogs had a
solar injury, which is heightened when

95% 1-yr sUIVival after an1putation; however,
animals ingest photosensitizing plants.

if tile lesion originated in otller parts of tile

Tumors of the ears also develop more
digit, 1 -yr sUIVival was 600A,. Excision may be
frequently after a procedure such as ear
combined with radiation or chemotllerapy.

tagging. Squamous cell carcinomas can

Feline squamous cell carcinomas are more
develop from follicular cysts on sites not
radiosensitive than tllei..r canine counterconm1only exposed to sunlight.

parts. Still, tile 1-yr sUIVival rate is <lOOA,

TUMORS OF THE SKIN AND SOFT TISSUES

947
for invasive neoplasms. Cryosurgery and
associated witl1 the presence of a papilloma
hype1therntia can be very helpful for local
virus. The tem1 in situ refers to a malignant
therapy especially in early ( carcinoma in
proliferation of epidem1al and follicular
situ) lesions, but controlled studies have not outer sheath cells that are not invasive into been done to detemline their effectiveness.

the W1derlying dennis. UnfortW1ately,

Intralesional implant chemotherapy with
lesions may progress over time into a,_1

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5-fluorouracil (dogs only), cisplatin (dogs
invasive carcinoma. Metastasis is extremely
only), or carboplatin along with retinoids

W1conrn1on. These lesions usually develop
and photodynan1ic therapy has been used
in systemically ill or immW1osuppressed
with variable success. Intratumoral
cats ru1d are believed to be virally induced.

injection of nasal planwn squamous cell

They have not been an1enable to therapy;
carcinomas in cats using carboplatin in a
however, cryotherapy of local lesions and
water-sesame seed oil emulsion resulted in
topical imiquin1od as described above may
a 7fJJ/o general response with 1 -yr progresincrease tin1e to progression.

sion-free survival rate of -5fJJ/o. 111 dogs with
multiple ventral actinic keratoses, topical
dinitrochlorbenzene or 5-fluorouracil (5%)

Keratinized Cutaneous Cysts
may be of benefit. Cats should not be given

Most keratinized cuta.J.1eous cysts are
any fonn of 5-fluorouracil therapy. More
malformations of the hair follicle. They a,_·e
recently, the use of topical inrn1W1omodulatcommon in dogs; occasionally identified in ing antineoplastics such as imiquimod
cats, horses, goats, and sheep; and rare in
crean1 applied topically on lesions twice
cattle and pigs. Excision is the treatment of
daily for 2 wk creates a local application site
choice. Vigorous squeezing of these lesions
inflanunatory reaction and often resolves
is contraindicated, because it often incites a
lesions. Imiquin1od stimulates Toll-like
severe foreign body infla,_mnatory response
receptor 7 and dendritic cells, modifying
due to the release of keratin into surroW1dimmune responses to destroy the targeted ing tissues.

carcinoma cells. The response may be

Infundibular follicular cysts
enhanced by tl1e application of 6 joules of

(epidem1oid cysts, epidennal inclusion
cold laser tl1erapy to the lesions every 2 wk
cysts, erroneously called sebaceous cysts)

Wltil regression. Limiting exposure to
a,_·e the most common. They are a cystic
ultraviolet radiation may help prevent
dilatation of the upper portion of the outer
solar-induced squamous cell carcinomas in
sheath of the hair follicle (the infundibudogs and cats. This may be accomplished by lum) lined by a layer of stratified cornifying
using UV window screens, sW1screen, and
epithelial cells indistinguishable from the
keeping companion animals indoors during
epidennis. These cysts vary in size from
hours of peak swilight between 10 AM and

2 mm to >5 cm (lesions <5 nun in diameter

2 PM. Tattoos, magic markers, and sW1Screen are often called milia). The only domestic are used with vruiable success.

animals identified at risk are Merino sheep,

In horses, radiotherapy using swiace or
in which these cysts are often multiple and
interstitial brachytherapy is the treatment of may progress to squan1ous cell carcinomas.

choice for squrunous cell cru·cinomas. Other

As with all folliculru· cysts, these are usually
options include 90Sr or l9"2J:r implants, wide
solitary, papular to nodular lesions that are
surgical excision ( especially for neoplasms
freely movable. They a,_·e generally prui;ially
of the third eyelid, penis, and prepuce), and
compressible on palpation and occasioncryosurgery. Immunotherapy, with either an ally have a small opening through the
autogenous vaccine made from the tumor
epidermis from which the cystic contents
tissue suspended in FreWld's adjuvant, or
can be extruded. On cut surface, they are
nonspecific immW1omodulation using
filled with a gray, brown, or yellowish,

Corynebactmium parvum, has had some
granular, "cheesy" mate1ial that is lwnenal success in treating ocular or horn core
keratin.

squrunous cell cru·cinomas in cattle.

Isthmus catagen cysts (trichilenrn1al

Feline multicentric squamous cell
cysts, pilar cysts, cystic intracutaneous
carcinoma in situ (feline Bowen disease)

comifying epithelioma) are follicular cysts
is a disease of aged (> 10 yr old) cats and
that have the keratinization pattern of the
may be associated with in1mW1osuppreslower portion of the outer root sheath. They sion. There is no defined breed or sex
have been definitively identified only in dogs
predilection. Clinically, lesions appear as
and (rru·ely) in cats.

multiple discrete, erythematous, black or

Matrix cysts are follicular cysts in which
brown hyperkeratotic plaques and papules.

the wall resembles the epitheliw11 of the

Lesions are nonpruritic, and ulceration is
hair bulb (the matrix portion of the hair

W1c01mnon. Their development is
follicle) and the inner root sheath. They

948

TUMORS OF THE SKIN AND SOFT TISSUES
occur predominantly in dogs and cats. Many commonly found on the head. Poodles may progress to pilomatricomas (seep 948).

be predisposed. These tumors are derived

Hybrid cysts (panfollicular cysts) are from the lower portion of the outer root follicular cysts that have a combination of
sheath and often have areas of transition
the characteristics of epidermal inclusion,
into basal cell tumors. They have little in
trichilemmal, and matrix cysts and that are
common with a tumor of the same name in

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found predominantly in dogs and cats.

people that represents an old wart. They

Many progress to trichoepitheliomas
appear as firm, ovoid masses, 1-7 cm in

(see below).

diameter, that are encapsulated but expand

Dermoid cysts are congenital malformaover time. Excision is curative.

tions found most commonly on the dorsal

Trichofolliculomas are extremely rare
midline of the head or along the vertebral
follicular tumors of dogs composed of the
column. They are most commonly identified
inferior and isthmic regions of multiple
in Boxers, Kerry Blue Terriers, and
abortive follicles that extrude their lumenal

Rhodesian Ridgeback dogs; Thoroughbred
contents into a dilated abnom1al cystic
horses; and possibly Suffolk sheep. Typically
infundibulum. Too few have been recogmultiple, they differ from other follicular nized to detemiine age, breed, or sex
cysts in that on cut surface they contain fully
predilection. Considered by some to be
formed hair shafts. They are arguably the
more a hamartoma than a true neoplasm,
only true epidem1al inclusion cysts, because
these tumors are benign, and complete
they most likely represent an embryonal
surgical excision is curative.

invagination of the epidemiis with associ

Trichoepitheliomas are cystic hair
ated adnexa. These adnexa are responsible
follicle neoplasms of dogs and, less
for the hair shafts within the cyst Jun1ens.

commonly, cats, in which all elements of

Keratomas are cystic lesions in the hoof
the hair follicle (infundibulum, isthmus,
wall of the toe or, Jess frequently, the quarter and inferior portions) and the patterns of or heel in simple or cloven-hoofed anin1als.

comification they produce are represented.

They often develop secondary to a

The epithelium and comification of the
traumatic injury. Although often asymptoinfundibular and isthmic portions predomatic, they commonly induce lameness and minate. Benign and malignant fom1S are
deformity of the hoof wall or sole and may
recognized. In dogs, these lesions can
be associated with distal phalangeal lysis.

be seen at any age but are fotmd most

Keratomas are seldom >5 cm in diameter
commonly during late middle age. Many
and contain white to brown laminated
breeds are predisposed, including Basset
keratin, often with a necrotic center

Hounds, Bull Mastiffs, Irish Setters, Standard
associated with secondary inflan1mation.

Poodles, English Springer Spaniels, and

When Jan1eness is present, surgical excision

Golden Retrievers. There is no defined sex
and curettage of the underlying bone, if
predilection. Tumors can develop anywhere
affected, is the treatment of choice.

on the body but are most common on the

Dilated pores ofWmer are rare,
trunk in dogs and on the head, tail, and
hair-follicle neoplasms recognized only in
extremities in cats. Benign foffi1S appear as
aged cats. Males may be predisposed. These
palpably encapsulated cystic nodules ( 1-5
lesions most often develop on-the head.

cm in diameter) in the dermis and subcuta

Clinically, they appear as solitary, domeneous fat. Expansion of cysts or self-trauma shaped lesions with the appearance of a
may induce ulceration associated with
giant comedo. Compact keratin may
extrusion of lumenal keratin that appears
protrude through (above) the surface,
as a condensed, yellow, granular, "cheesy"

giving them the appearance of a cutaneous
material. Excision is curative; however,
horn. These lesions are benign, and
aninlals that develop one such tun1or are
complete excision is curative.

prone to develop additional lesions at other
sites. This is especially true for Basset

Tumors of the Hair Follicle

Hounds and English Springer Spaniels.

Malignant trichoepitheliomas are

The hair follicle is a complex structure
much less common than benign trichoepicomposed of eight different epithelial theliomas and are differentiated by their
layers. Hair-follicle tun1ors display a similar
local invasiveness; continuity with the
complexity, and much work needs to be
epidemtis; and association with extensive
done to characterize them further. They are
inflan1mation, necrosis, and fibrosis.

most common in dogs, less frequent in cats,

Metastasis is uncommon. Wide surgical exciand rare in other domestic animals.

sion is the treatment of choice and is often

Tricholemmomas are rare, benign,
curative in those tumors that are invasive
hair-follicle neoplasms of dogs, most
but have minin1al metastatic potential.

TUMORS OF THE SKIN AND SOFT TISSUES

949

Pilomatricomas (hair matrix tumors,
straight duct that flows into the folliculai·
calcifying epitheliomas of Malherbe) are
infundibulun1. In domestic animals, all hair cystic hair-follicle neoplasms recognized
follicles have apocrine glands. Apocrine
almost exclusively in dogs. Unlike trichoglands in dogs and cats are also present in epitheliomas, in which all elements of the
association with the anal sac, and modified
follicle are represented, in pilomatricomas
apocrine glands, known as cerunlinous

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only the cells of the matrix region of the
glands, are present in the external auditory
inferior part of the hair follicle and the
meatus. In most mainmals, apocrine glands
cornification patterns they produce (hair
produce an odiferous, oily compound that is
shaft and inner root sheath) are present.

a sexual attractant, a territorial marker, ai1d

Benign and malignant fonns are recognized.

a warning signal. In horses and cattle, these

Benign tumors are most common on the
glands play a role in thennoregulation by
trunk of middle-aged dogs. Ken-y Blue and
producing sweat.

Wheaten Terriers, Bouviers des Flandres,

Apocrine gland tumors and malfonna

Bichons Frises, and Standard Poodles are
tions are most common in dogs and cats.

most at risk. Grossly, these tumors are

Three diseases of apocrine glands of haired
indistinguishable from trichoepitheliomas,
skin have been characterized.

but their cystic contents are often gritty

Cystic apocrine gland dilations
because of mineralization. Excision is the

(apocrine gland cysts, cystic apocrine gland
treatment of choice. As in trichoepitheliohyperplasia, apocrine cystomatosis) are mas, when one such lesion develops,
best characterized as hainartomas. Two
additional lesions often develop over time.

forms exist: a cystic form in which one or

Malignant pilomatricomas (malignant
more cysts develop in the mid to upper
hair matrix tumor, matrical carcinoma) are
dermis with a poor association with hair
rare and have been identified most often in
follicles, and a more diffuse form characterdogs. They are a tumor of old dogs and ized by cystically dilated apocrine glands
grossly characterized as solitary or
associated with multiple hair follicles in
multinodular, vaiiably cystic tumors that
nontraun1atized skin. Both ai·e found in
are often firmly attached to subjacent soft
middle-age or older dogs and, less
tissues. Because they ai·e invasive, they are
commonly, cats. The head and neck are the
difficult to excise, and recurrence is
most conunon sites where these lesions
common after attempts at surgical excision.

develop. In both species, lesions appear as

They often metastasize to draining lymph
fluctuant detmal cysts or as translucent
nodes and internal organs, especially the
bullae. Complete excision is curative;
lungs. Aggressive surgery is recommended.

however, this may be difficult to accomplish

It is unknown whether they respond to
in the more diffuse forn1.

radiation or chemotherapy.

Apocrine gland adenomas are
diagnosed almost exclusively in clogs, cats,

Cutaneous Apocrine Gland Tumors
and rarely horses. Two types are recognized

Sweat glands are of two types: apocrine and
based on whether their histologic appeareccrine. Apocrine glands ai·e tubular glands ance primarily resembles the secretory or
with a coiled secretory portion and a long,
cluctular portion of tl1e apocrine gland.

Apocrine adenomas resemble the
secretory region of the apocrine glands.

They ai·e fow1cl in older dogs and cats. Great

Pyrenees, Chow Chows, and Alaskan

Malainutes are the most commonly affected
breeds. The head, neck, and extremities are
the most frequent sites of development. In
cats, apoc1ine aclenomas are more likely to
be seen in males, and no breed appears at
greater risk than any other. The vast
majority of apocrine aclenomas occur on the
head, especially the pinnae. In horses, no
age, sex, or breed association is known. The
pinnae and vulva are the most likely regions
to develop these tumors. In all species, these
tumors appear as firm to fluctuant cysts,
seldom >4 cm in diaineter. They contain
varying an1ounts of clear to brownish fluid.

Ceruminous gland carcinoma, right ear of a

In cats, the luminal fluid may be darkly
cat. Courtesy of Or. Alice Villalobos.

pigmented, and apocrine cysts can be

950

TUMORS OF THE SKIN AND SOFT TISSUES
confused clinically with melanocytomas,
tissue with increased BUN and creatinine
especially when present on the inner aspect
values. These tumors are often highly infiltraof the ears. Apocrine d uctular adenomas tive into the pelvic canal and conunonly
are less conunon. They are found in older

(90%) metastasize to the sublmnba.r lymph
dogs and cats and are putatively derived
nodes or to distant internal organs ( 400Ai).

from or show differentiation toward

Wide surgical excision, including involved

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apocrine ducts. In dogs, these tumors are
lymph nodes, is the treatment of choice.

most commonly recognized in Peekapoos,

Even if the tumor cannot be totally resected,

Old English Sheepdogs, and English
debulking can be of value in dogs with

Springer Spaniels. They are often smaller,
pseudohyperpa.rathyroiclism, because the
fumer, and less cystic than apocrine
hypercalcemia is related to the production
adenomas. Because they often consist of a
of paratl1om1one-like hormone from the
large population of basal cells and because
total twnor volume. Adjunct chemotl1erapy
evidence of ductula.r differentiation can be
along with tyrosine kinase inhibitors,
extremely subtle, these tumors are often
metronomic chemotherapy, and radiation
diagnosed histologically as basal cell tun10rs therapy may also be of benefit to increase (seep 944). Apocrine adenomas and
time to progression, but few clogs are
apocrine ductular aclenomas are benign, and reported to live > l YT after the tun1or has complete surgical excision is curative.

been recognized.

Apocrine gland adenocarcinomas of
haired skin are rare in all domestic animals

Eccrine Gland Tumors
but most frequently identified in older dogs
and cats. In clogs, Treeing Walker Coon

Eccrine glands are the coiled, tubular, sweat
houncls, Norwegian Elkhouncls, German
glands present on the footpads of carni

Shepherds, and mixed-breed dogs are most
vores, the frog of ungulates, the carpus of
at risk; in cats, Siamese may be predisposed. pigs, and the nasolabial region of run1inants.

In botl1 species, this tumor most commonly

Ttunors derived from these glands are
arises in axillary and inguinal regions-sites
extremely rare and have been identified
that allow it to be easily confused clinically
only on the footpads of dogs and cats. Most
and histologically with manunary gland
are malignant and invasive. These tumors
ductular adenocarcinomas. Apocrine gland
are reported to have a high potential to
adenocarcinomas generally are larger than
metastasize to draining lymph nodes.

adenomas and have a variable clinical
appearance ranging from fibrotic dermal

Sebaceous Gland Tumors
nodules to ulcerated plaques. They are

Tumors and tumor-like conditions of
locally invasive and frequently metastasize
sebaceous glands are conunon in clogs,
to draining lymph nodes. Less conunonly,
infrequent in cats, and rare in other
skin and lung metastasis may occur.

domestic animals. Based on morphologic

Complete surgical €Xcision is the treatment
more tllan on behavioral features, four
of choice. Little is known about response to
categories of benign sebaceous gland
adjunct chemotherapy.

proliferations have been described. In
people, in which a roughly sintilar clas

Apocrine Gland Tumors of Anal Sac
sification scheme is traditionally used, it has
been proposed that all benign sebaceous

Origin
gland tumors be called sebaceomas.

Apocrine gland tumors of anal sac origin

Sebaceous gland hamartomas are
have been definitively identified only in
solitary lesions reported only in dogs. These
clogs, although anecdotal reports suggest
lesions are distinguished from sebaceous
they may also be seen in cats. Older English
gland hyperplasias and adenomas because

Cocker and Springer Spaniels, Dachshm1ds,
they are linear or circumscribed, several

Alaskan Malanmtes, Gem1an Shepherds,
centimeters in length or diameter, and
and mixed-breed dogs are most at risk.

usually identified shortly after birtll.

Unlike hepatoid gland tumors (seep 951),

Sebaceous gland hyperplasias (senile
these apocrine gland tun1ors have no sex
sebaceous hyperplasias) represent a
predilection. They most commonly appear
senile change in dogs and cats. In dogs,
as deep, firm, nodular masses near tl1e anal

Manchester, Wheaten, and Welsh Terriers
sac. As these lesions grow, they may
are at greatest risk. In cats, there is no breed
compress the rectum and induce constipapredilection, but females develop these tion. Some of tl1ese tun1ors are associated
lesions more frequently than males. In both
with paraneoplastic hypercalcemia, which
species, the skin of the head and abdomen
causes anorexia, weight loss, polyuria and
are affected most conunonly. Sebaceous
polydipsia, and mineralization of renal
hyperplasias conunonly appear as papillated

TUMORS OF THE SKIN AND SOFT TISSUES

951
masses seldom > 1 cm in diameter, often
chemotherapy for any of these lesions has
with a shiny, keratotic surlace.

been defined. Oral retinoids may prevent

Sebaceous gland adenomas are seen
recurrence of sebaceous hyperplasia, but
in all domestic animals but are so
their use remains poorly defined, and
common in older dogs and cats they can
consultation with a vete1inary oncologist or
be considered primarily a small animal
dem1atologist is strongly recommended.

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neoplasm. Coonhounds, English Cocker

Spaniels, Cocker Spaniels, Huskies,

Hepatoid Gland Tumors

Samoyeds, and Alaskan Malamutes are
the canine breeds most likely to develop

(Perianal gland tumors, Circumanal gland
these tumors; Persians are the feline
tumors)

breed most predisposed. In dogs, these

These common neoplasms arise from
tumors frequently are clinically indistinmodified sebaceous glands that are most guishable from sebaceous hyperplasias,
abundant in the cutaneous tissues around
but they tend to be larger (typically >l
the anus but may also be present along the
cm). They are often multiple and may
ventral midline from the perineun1 to the
develop anywhere on the body but are
base of the skull, the dorsal and ventral
commonly found on the head. Sebaceous
tail, and in the skin of the lumbar and sacral
adenomas may be covered with a
regions. Because androgens stin1ulate
serocellular crust and exhibit pleocellular
the development of hepatoid glands, the
inflammation and superficial pyoderma.

incidence of proliferative lesions of hepatoid

Sebaceous gland epitheliomas are a
glands in intact, male dogs is three times that
variant of sebaceous adenoma distinin females.

guished by lobules composed primarily of

Benign hepatoid gland tumors are divided
basal progenitor cells rather than mature
into hepatoid gland hyperplasias and
sebocytes. Because they often have
adenomas; however, as with benign
irregular lobules that extend into the deep
sebaceous gland tumors, there is a
dermis, they can occasionally be confused continuun1 from hyperplasia to adenoma.

with sebaceous carcinomas. These tumors Here, they will be considered as a single are found in older dogs and rarely in cats.

entity. Hepatoid gland adenomas are most

They appear as ulcerated nodules that
common in aged dogs. Siberian Huskies,
may be several centimeters in diameter.

Samoyeds, Pekingese, and Cocker Spaniels

A papillated epidermal surface and
are most commonly affected. Tumors may
pigmentation are variable findings.

develop at any site where hepatoid glands

Sebaceous gland adenocarcinomas
are present, but 9096 are found in the perianal
are rare in domestic animals. They ru·e
region. Grossly, they appear as one or (more
recognized almost exclusively in dogs and
commonly) multiple intraderrnal nodules
cats, generally in middle-aged or older

0.5--10 cm in diruneter. Larger lesions
animals. Cavalier King Charles Spaniels;
commonly ulcerate, and hemorrhagic,

Cocker Spaniels; and Scottish, Cairn, and
proteinacious material can often be

West Highland White Terriers are most at
extruded with local pressure. Large tumors
risk Male dogs and female cats may be
cru1 compress the anal canal and make
predisposed. These lesions are often
defecation difficult. Up to 95% of male dogs
ulcerated and may be indistinguishable
respond completely to castration; in those
from sebaceous epitheliomas or other
that do not, the pituitary-adrenal axis should
cutaneous carcinomas. They are locally
be evaluated and, ifno abnormality is
infiltrative and may metastasize to regional
detected, the dog should be reevaluated for
lymph nodes late in the disease.

the presence of a low-grade hepatoid gland

Once a diagnosis is established, treatment adenocarcinoma. Excision may be used is optional for benign sebaceous gland
concun·ently to remove extremely large
tumors unless they are secondarily inflamed or ulcerated tumors that have become and infected. For malignant adenocarcinosecondarily infected. Surgery is the mas, excision is the treatment of choice, but
treatment of choice for females with
complete removal can be difficult because
hepatoid gland adenomas but may need to
of the infiltrative nature of this tumor;
be repeated, because recurrence is common.

adjunct radiotherapy may be required. Even

Radiation therapy is also an option and has a
benign sebaceous gland growths recur if

2-yr cure rate of 69% for benign tun1ors.

remnants are left at the surgical site. In

Cryosurgery is another therapeutic
addition, animals that develop one
alternative, but because of the complication
sebaceous gland hyperplasia or adenoma
of fecal incontinence, should be used only
often develop new lesions at other sites
when tumors are not amenable to surgical
over time. No established protocol of
intervention. Diethylstilbestrol has been

952

TUMORS OF THE SKIN AND SOFT TISSUES
used in the past as an alternative to
papilloma viruses: people have >20; cattle,
castration, but because of severe adverse

6; dogs, 3; and rabbits, 2. Different
effects, including aplastic anemia and cystic
papilloma viruses often have considerable
prostatic hyperplasia, it should be used with
species, site, and histologic specificity. The
extreme caution, if at all. Antiandrogens may virus is transmitted by direct contact, have a role as an alternative to castration.

fomites, and possibly by insects. Papillomas

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Hepatoid gland adenocarcinomas are
have been reported in all domestic animals,
uncommon canine neoplasms that generally
birds, and fish. Multiple papillomas
appear as nodular lesions affecting the

(papillomatosis) of skin or mucosa!

perianal region. These tun1ors are found in
smfaces generally are seen in younger
male dogs 10 times more commonly than in
anin1als and are usually caused by viruses.

females. Siberian Huskies, Alaskan

Papillomatosis is most common in cattle,

Malamutes, and Bulldogs are most likely to
horses, and dogs. Single papillomas are
develop this tun1or. Histologic evaluation is
more frequent in older animals, but they
the best means of diagnosis; however, there
may not always be caused by viral infection.

is debate about how to distinguish low-grade

When lesions are multiple, they may
malignant tun1ors from hepatoid adenomas,
be sufficiently characteristic to confinn
because well-differentiated fom1s can be
the diagnosis; however, there are many
confused with adenomas, and anaplastic
simulants of warts, and a definitive
fonns can be confused with apocrine gland
diagnosis requires identification of the
adenocarcinomas of anal sac origin. These
virus or its cytopathic effects on individual
tun1ors have metastatic potential and often
cells-a change known as koilocytic atypia
spread to regional lymph nodes. Treatment
or koilocytosis.

consists of wide surgical excision including

In cattle, warts commonly are found
involved lymph nodes and, possibly,
on the head, neck, and shoulders, and
subsequent radiation. These tun1ors are
occasionally on the back and abdomen. The
generally not responsive to castration or to
extent and duration ofilie lesions depend
estrogen therapy; however, some studies
on ilie type of virus, area affected, and
show that the use of masitinib and other
degree of susceptibility. Warts appear -2 mo
tyrosine kinase inhibitors may overcome
after exposure and may last �l yr. Papillochemoresistance, inhibit the proliferation of matosis becomes a herd problem when a
tun1or cells, and prevent the emergence of
large group of young, susceptible cattle
metastasis. These findings may increase the
becomes infected. Immwuty usually
benefit of combining targeted agents with
develops 3--4 wk after initial infection,
various fom15 of chemotherapy such as oral
but papillomatosis occasionally recurs,
piroxicam and capecitabine or with
probably due to loss of immwuty.

metronomic chemotherapy to prevent or

Aliliough most warts appear as epidermal
treat local recwTence and metastatic
proliferations iliat have a keratotic surface
disease. The overall prognosis is guarded.

resembling a cauliflower (verruca vulgaris),
some bovine papilloma viruses (bovine

Primary Cutaneous Neuroendocrine
papilloma types 1 and 2) involve dermal

Tumors
fibroblasts and keratinocytes and appear as
a papulonodule with a warty surface. Such

(Merkel cell tumors, Atypical histiocytomas,
fibropapillomas may involve ilie venereal

Trabecular carcinomas, Extramedullary
regions, where they can cause pain,
plasmacytomas)

disfigurement, infection of the penis of

In veterinary medicine, the diagnosis of
young bulls, and dystocia when ilie vaginal
tun1ors derived from Merkel cells (tactile,
mucosa of heifers is affected.

neurosecretory cells of epithelial derivation

A form of persistent cutaneous papillopresent in the basal cell layer of the matosis with smaller nwnbers of papillomas
epidennis) has fallen in disfavor, and most
may be seen in herds of older cattle. A
pathologists consider this tumor to be an
bovine papilloma virus has been demonextramedullary plasmacytoma. Merkel cell strated in bladder tumors associated wiili
tumors most likely develop in animals but
bracken fem ingestion (seep 3089) and in
are not recognized as such.

upper GI tract papillomas of cattle in

Scotland. It is believed that ilie papilloma

Papillomas
virus acts as a co-carcinogen. When bovine
papilloma virus type 1 or 2 is injected into

(Warts)

the skin of horses, a dermal tmnor similar to

Papilloma viruses are small, doubleequine sarcoid develops.

stranded DNA viruses of the Papovaviridae

In horses, small, scattered papillomas
family. Some manm1als have several distinct develop on ilie nose, lips, eyelids, distal legs,

TUMORS OF THE SKIN AND SOFT TISSUES

953
penis, vulva, mammary glands, and inner
pigs, they are very rare and when present
surfaces of the pirmae, often secondary to
a.re identified as solitary or multiple lesions
mild abrasions. They can be a herd problem,
on the face or genitalia. (For discussion of
especially when young horses are kept
papillomatosis in rabbits, seep 1950.)

together, but regress in a few months, as a

A cutaneous fibroma occurs in whitefoal's immune system matures. When they tailed, black-tailed, and mule deer, and in

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develop in older horses, they often persist
antelope, moose, and caribou. It is ca.used
for> 1 yr. So-called aural plaques are also
by a papilloma vims that resembles a bovine
thought to be a flat form of papilloma
papilloma virus and is found only in the

(vem1ca planum). Equine papillomas are
epitl1eliun1 that cove� the tumors.

disfiguring but benign. They should be

Infectious papillomatosis is a self-limiting
distinguished from verrucous equine
disease, although the duration of warts
sarcoid (seep 954).

varies considerably. A variety of treatments
ln dogs, three clinical presentations of
have been advocated without agreement on
canine papilloma virus infection have been
efficacy. Surgical removal is recommended
described. The first is canine mucous
if the warts a.re sufficiently objectionable.

membrane papillomatosis, which

However, because surgery in the early
primarily affects young dogs. It is charactergrowing stage of warts may lead to recized by the presence of multiple warts on urrence and stimulation of growth, the
oral mucous membranes from lips to
warts should be removed when near their

(occasionally) the esophagus and on the
maximum size or when regressing. Affected
conjunctiva! mucous membranes and
animals may be isolated from susceptible
acljacent haired skin. When the oral cavity
ones, but with the long incubation period,
is severely affected, there is interference
many are likely to have been exposed
with mastication and swallowing. A viral
before the problem is recognized.

etiology has been clearly established for

Vaccines are of some value as a preventhese lesions. Azithromycin therapy has tive but are of little value in treating cattle
been shown to speed up regression in dogs.

that already have lesions. Because wart

The second presentation is cutaneous
viruses are mostly species-specific, there
papillomas, which are indistinguishable
is no merit in using a vaccine de1ived from
from the warts that develop on or around
one species in another. An intralesional
mucous membranes. However, they are
lymphocyte T-cell inlmunomodulator,
more frequently solitary and develop on
which stimulates T cells and endogenous
older dogs. Cocker Spaniels and Kerry Blue
interleukin 2 levels, may benefit individual

Terriers may be predisposed. A definitive
animals that develop multiple or persistent
viral etiology has not been established, and
warts. ln addition to azithromycin, topical
lesions may be confused with cutaneous
imiquirnod cream may also help the immune
tags. A syndrome characterized by papisystem to resolve these warts in dogs.

llomatosis of one or more footpads has

When the disease is a herd problem, it
also been described. Clinically, lesions
can be controlled by vaccination with a
appear as multiple, raised keratin horns. A
suspension of ground wart tissue in which
viral etiology has been suggested but not
the virus has been killed with formalin.

proved. The third presentation is cutane

Autogenous vaccines may be more effective
ous inverted papillomas, which have
than those commercially available. It may
more in common clinically with intracutabe necessary to begin vaccination in calves neous comifying epitheliomas. ln this
as early as 4-6 wk of age with a dose of
disease of young, mature dogs, lesions most

-0.4 mL intradermally given at two sites.

commonly develop on the ventral abdomen,

The vaccination is repeated in 4-6 wk and
where they appear as raised papulonodules
at 1 yr of age. Immunity develops in a few
with a keratotic center. Infrequently, viral
weeks but is unrelated to whatever
papillomas in dogs may progress to invasive
mechanism is involved in spontaneous
squamous cell carcinomas.

regression. If the animal was exposed to
ln cats, papilloma virus infection appears
the virus before vaccination, immunity
most commonly as a multi centric squamous
may develop too late to prevent warts. A
cell carcinoma (seep 945). The typical
vaccination program must be in effect for
warty lesions associated with papilloma

-3---6 mo before its preventive value will be
virus infection in most species are not
evident. Vaccination should be continued
present. Papillomas may affect the skin of
for �l yr after the last wart disappears,
goats, and infection on the teats has been
because the premises may still be contamireported to induce malignant transfonnanated. Stalls, stanchions, and other inert tion. ln sheep, papillomas a.re rare and most
materials can be disinfected by fumigating
commonly appear as fibropapillomas. In
with formaldehyde.

954

TUMORS OF THE SKIN AND SOFT TISSUES

EQUINE SARCOIDS
particular breeds and bloodlines appear to
be more susceptible to the disease.

Equine sarcoids are the most commonly

The mode of transmission has not
diagnosed tumor of equids, representing
been confirmed. BPV-1 has recently been

200A, of all equine neoplasms and 36% of all
detected in several conunon fly species ( eg,
skin tumors in horses. Studies suggest there
house fly and stable fly), and because there

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is no significant gender or age predisposiis an apparent predilection for sarcoid tion.

development at wound sites, it has been

Equine sarcoids are rarely life threatenproposed that flies may act as vectors as ing but can compromise function and be a
they move between wound sites on different
major economic concern. Sa.rcoids may
horses. Alternatively, BPV infection may
also cause significant welfare dilemmas,
be transmitted via stable management
particularly in developing countries where
practices, such as the sharing of contan1iequids, principally donkeys, are widely used nated tack, or be passed into existing as work anin1als ( eg, brick-carrying donkeys wounds from contaminated pasture.

in India).

There is a wide range of therapies for

Sarcoids can occur as single or multiple
sarcoids, and many tumors recur. Pedunculesions in different forms, ranging from lated sarcoids with a discernible neck are
small, wart-like lesions to large, ulcerated,
ideally suited to ligation with mbber bands
fibrous growths. Six distinct clinical entities
or elasticized suture material, usually in
are recognized: 1) Occult-flat, gray,
combination with a topical preparation
hairless, and persistent; often circular or
once the twnor is detached. Other
roughly circular. 2) Vemicose-gray,
conunonly used treatments include
scabby, or warty in appearance and may
cryotl1erapy, surgical or laser excision,
contain small, solid nodules; possible surand local inunune modulation (Bacillus face ulceration; well-defined or cover large,

Cal.rnette-Guerin [BCG] therapy). Surgical
ill-defined areas. 3) Nodular-multiple,
excision with margins of at least 0.5-1 cm
discrete, solid nodules of variable size; may
is reconunended. Preplaced sutures or
ulcerate and bleed. 4) Fibroblastic-fleshy
releasing incisions are often needed for
masses, either with a thin pedicle or a wide,
primary closure. Local radiotherapy
flat base that commonly bleed easily; may

(interstitial brachytherapy), using
have a wet, hemorrhagic surface. 5) Mixedpennanently in1planted radon-222 or variable mixtures of two or more types.

gold-198 seeds or removable needles of

6) Malevolent-an extremely rare,
radiun1-226, cobalt-60 or, more often,
aggressive tumor that spreads extensively
iridium-192 (192Ir) implants, is a highly
th.rough the skin; cords of tumor tissue
effective treatment for tun10rs less
intersperse with nodules and ulcerating
amenable to traditional therapy ( eg, those
fibroblastic lesions.

on the limbs or around the eye). However,

Lesions can develop anywhere on the

1921.r implants and other radioisotopes are
body but are most common in the para.geniexpensive and not widely available but may tal region, the ventral thorax and abdomen,
be the best option for recurrent aggressive
and the head. They frequently are seen at
lesions. Sarcoids have a 15%--82% recw�
sites of previous injury and scarpng. Equine
rence rate if treated by surgical excision
sarcoids can resemble other skin tun10rs
alone. Excised sarcoids often regrow more
such as benign fibropapillomas and also
aggressively within 6 mo, which may be due
other cutaneous conditions such as
to activation of latent BPV in apparently
exuberant granulation tissue (proud flesh).

normal tissue surrouncling the lesion. Larger

An individual lesion on a horse can be
tun1ors may require a combination of
difficult to diagnose, but multiple tumors
th.era.pies ( eg, surgical debulking or C0

( often of more than one type) with

2
laser vaporization followed by topical or
characteristic features on an individual
intracavitary chemotherapy or local
horse make the clinical diagnosis reasonelectrochemotherapy).

ably straightforward. A definitive diagnosis

Several pron1ising treatments now
can be made by biopsy; however, acquiring
available or in the final stages of clinical
the sample carries the risk of triggering a
trials include the use of intra-tun10ral
considerable and uncontrollable expansion
bioabsorbable cisplatin beads/emulsion (9%
of the lesion.

recurrence rate), the application of topical

Bovine papillomavirus (BPV), primarily
in1iquirnod every other day for 32 wk or until
types 1 and 2, is now considered the main
resolution (600Ai), autologous in1plantation,
etiologic agent of equine sarcoids. There
and topical acyclovir crean1s for treatment
may also be a genetic predisposition
of flat, occult sarcoids (68% response rate)

associated with equine leukocyte antigens;
or applied to the wound bed of larger

TUMORS OF THE SKIN AND SOFT TISSUES

955
tumors removed by surgical excision.

develops -3--5 yr after t11e skin lesions are

Acyclovir is relatively inexpensive and has a
recognized. No known therapy can prevent
wide safety margin, but its method of action
development of tl1e renal and ute1ine
is w1known. Other products used to treat
neoplasms.

sarcoids are topical ointments that contain

Acrochordons ( cutaneous tags, soft
heavy metals, thiouracils, and 5-fluorourafibromas, fibrovascular papillomas) ai·e VetBooks.ir
cil; an escharotic salve containing bloodroot distinctive, benign, cutaneous lesions of powder extract and zinc chloride; and an IV
older dogs. These lesions ai·e common, may
immw10stimulant of nonviable Propioni
be single or multiple, and can develop in any
ba.cterium acnes and BCG. The developbreed, although large breeds may be at ment of preventive and/or therapeutic
increased risk Most commonly, they appear
vaccines may fom1 a significant pa.it of
as pedW1culated exophytic growths, often
disease control strategies in the future, but
covered by a verrucous epidem1al surface.

trials so far have shown limited success.

Treatment is optional, but a biopsy is

A novel therapeutic approach using small
recommended to confinn the diagnosis.

interfering RNA molecules to target viral

Acrochordons are an1enable to excision,
gene expression is being investigated. This
electrosurgery, and cryosurgery, but dogs
technique has been shown to selectively
that develop one are prone to develop
destroy BPV-1-infected equine skin cells in
others over time.

vitro.

Fibromas are discrete, generally cellular proliferations of dermal fibroblasts.

Histologically, they resemble collagenous

CONNECTIVE TISSUE TUMORS
nevi or cutaneous tags. Fibromas occur in

Benign Fibroblastic Tumors
all domestic species but are primarily a
tw11or of aged dogs. Dobem1an Pinschers,

Collagenous nevi are benign, focal,

Boxers (predisposed to developing multiple
developmental defects associated with
ttm10rs), and Golden Retrievers are most at
increased deposition of dennal collagen.

risk. The head and extremities are tl1e most

They are common in dogs, W1common in
likely sites. Clinically, the lesions appeai· as
cats, and rare in large animals. They
discrete, generally raised, often hairless
generally are fow1d in middle-aged or older
nodules originating in the dermis or
anin1als, most frequently on the proxin1al
subcutaneous fat. They palpate as either
and distal extremities, head, neck, and areas
firm and rubbery (fibroma durum) or soft
prone to trauma. They are sessile to raised,
and fluctuant (fibroma molle ). These
dennal nodules, often with a papillated
lesions are benign, but complete excision is
surface. 1\vo fom1s are seen: one develops
recommended if they change appearance or
in the interfollicular dermis or subcutat1egrow large.

ous fat that is not accompanied by adnexal
involvement, and one incorporates adnexa
and induces enlai·ged, often malformed

Soft-tissue Sarcomas
follicles, sebaceous glands, and apocrine

Th.is group of malignancies includes equine
gla.11ds. This latter form has been called
sarcoids, fibromatoses, fibrosarcomas,
focal adnexal dysplasia. Excision of
malignant fibrous h.istiocytomas, neurofiboth fom1s is generally curative although, brosai·comas, leiomyosarcomas, rhabdoinfrequently, expansive fom1s have been myosarcomas, and vaiiants of liposai·coidentified that may grow too large to be mas, angiosarcomas, synovial cell
surgically removed.

sarcomas, mesotheliomas, and meningi

Generalized nodular dermatofibrosis
omas. As a group, sarcomas ai·e widely

( dermatofibromas ), recognized rai·eJy
recognized, yet poorly characterized
in German Shepherds (believed to be a.11
neoplasms. The confusion stems in part
inhe1ited, autosomal dominant trait) and
from tl1e fact tl1at spindle-cell sai·comas
even less commonly in other canine breeds,
demonstrate much greater morphologic
is a syndrome in which multiple collagenous heterogeneity than carcinomas; often, nevi are associated with renal cystadenofeatures of one sarcoma are intermixed carcinomas and, in females, multiple uterine with features of another. Consequently, it is leiomyomas. Skin lesions, first recognized
widely accepted that the cell of origin
when animals are 3--5 yr old, are characte1°
of all soft-tissue sarcomas is a primitive
ized by the development of multiple
mesenchyn1al cell tl1at can differentiate in
collagenous nevi varying from barely
many different directions. Th.is makes it
palpable to large and nodular, generally on
difficult to define histopatl10logic c1iteria
the lin1bs, feet, head, and trunk They may
necessaiy for making an unequivocal
be symmetrically distributed. Renal disease
diagnosis of specific spindle-cell sarcomas.

956

TUMORS OF THE SKIN AND SOFT TISSUES

In addition, comparing neoplastic
in1pression of complete encapsulation;
mesenchymaJ cells with the nom1aJ cell they these tumors should not be "shelled out,"

most closely resemble does not imply origin
because neoplastic cells are usually present
from those cells.

in the pericapsular connective tissues. Many

A second cause for the confusion stems
sarcomas are shaped like an octopus, with
from the difficulty in deteffilining whether
tentacles that extend deeply into the tumor

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these are benign or malignant or what their
bed. Except for equine sarcoids, cryosurbiologic behavior will be in certain locations gery is usually not used for these tumors or breeds. Most spindle-cell sarcomas of
because some types, most notably
domestic aninlals are locally infiltrative,
fibrosarcomas, are resistant to freezing.

difficult to excise, and yet seldom metasta

Spindle-cell sarcomas generally do not
size. Because, by definition, only malignant
respond well to conventional doses of
tumors have metastatic potential, these
radiation; however, higher doses have been
tumors should be considered benign;
reported to control -50% of them for 1 yr.

however, again by definition, benign

Surgical debulking followed by intraoperaneoplasms are not infiltrative, and those tive placement of carboplatinum-containing
tumors should be considered malignant and
biodegradable beads, intracavitary
treated aggressively from the start. In
chemotherapy with follow-up intratumor
human pathology, infiltrative but nonmetasbed chemotherapy, and/or follow-up tasizing mesenchymaJ spindle-cell tumors
radiation therapy are options to enhance
have been defined as sarcomas of intermedilocal control.

ate malignancy, a concept used below.

Chemotherapeutic protocols for

Clinically, four general principles relate
sarcomas that include targeted therapy
to spindle-cell sarcomas and soft-tissue
agents such as tyrosine kinase (T-K)

sarcomas: The more superficial the
inl1ibitors have become more accepted as a
location, the more likely the tumor is to be
means of treatment. Most older protocols
benign ( deep tumors tend to be malignant).

involve the use of adriamycin often in

The larger the tumor, the more likely it is
combination with other agents, including
to be malignant. A rapidly growing tumor
cyclophosphanlide, vincristine, dacaris more likely to be malignant than one bazine, and methotrexate. Some clinicians
that develops slowly. Benign tumors are
prefer to use a combination of carboplatin,
relatively avascular, whereas most mali

T -K inhibitors, and metronomic chemothe1"

gnancies are hypervascular. The type
apy, whereas others rotate carboplatin with
of sarcoma, its size, location, stage and
adriamycin. Although chemotherapy may
histologic grade (low, intermediate, high
cause temporary adverse events, it can

[ or I, II, ill]), which depends on the degree
improve the length and overall quality of
of differentiation, the number of mitotic
life; it is seldom curative.

figures per 10 high-power fields, and percent

Fibromatosis ( aggressive fibromatosis,
that is necrotic, will help guide treatment
extra-abdominal desmoids, desmoid
planning.

tumors, low-grade fibrosarcomas, nodular

Surgical excision is the treatment of
fasciitis) is a sclerosing and infiltrative
choice. Wide excision or an1putation should
proliferation of well-differentiated
be performed when anatomically.feasible
fibroblasts derived from aponeuroses and
because spindle-cell sarcomas often
tendon sheaths. They are generally seen on
infiltrate along fascia] planes, making it
the heads of dogs, especially Doberman
difficult to determine from gross exanlina

Pinschers and Golden Retrievers, where
tion the peripheral margins of the tumor.

they are commonly diagnosed as nodular

The best, if not only, opportunity to
fasciitis. In veterinary medicine, the term
completely remove a spindle-cell sarcoma
nodular fasciitis is applied to two different
is during the first surgical attempt. A
diseases: one that behaves as a fibromapresurgical biopsy should be performed tosis and one that commonly affects the
and, if possible, tumor imaging with CT
periocular tissues (known as canine fibrous
or MRI or ultrasound to provide a clear
histiocytoma [seep 957]). Fibromatoses
surgical plan that includes the intention
are infrequently diagnosed in cats and
of complete removal, with biopsy samples
horses. Grossly, fibromatoses are generally
submitted for margin determinations. Those indistinguishable from infiltrative fibrosarsarcomas that recur have a greater potential comas; however, they can be differentiated
for metastasis, and the time to recurrence
on histologic exanlination. Focal lymphoid
often shortens with each subsequent
nodules are scattered throughout the
attempt at excision. In addition, many
tissues. The fibromatoses are locally
soft-tissue tumors have a pseudocapsule,
infiltrative, with essentially no metastatic
which on gross examination gives the
potential. If feasible, wide, complete

TUMORS OF THE SKIN AND SOFT TISSUES

957
excision with local control techniques as
over the lumbar areas. Although commonly
described above is the treatment of choice
classified as fibrosarcomas, vaccinationat diagnosis. Recurrence is common, and site sarcomas are extremely heterogeneous
radiation therapy may be of value for local
and may be appropriately called malignant
control.

fibrous histiocytomas (giant cell tumors),

Fibrosarcomas are aggressive
liposarcomas, osteosarcomas, or chondro

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mesenchymal tumors in which fibroblasts
sarcomas.

are the predominant cell type. They are the

Wide and deep surgical excision is the
most common soft-tissue tumors in cats and treatment of choice for fibrosarcomas, but are also common in dogs but rare in other
because the necessary margin extent is
domestic anin1als. In dogs, these tumors are
commonly underestimated, recurrence
most conunon on the trunk and extremities.

is conunon (> 700Aiwithin 1 yr of the initial

Gordon Setters, Irish Wolthounds, Brittany
surgery). The rate of recurrence is >90%for

Spaniels, Golden Ret1ievers, and Doberman
vaccine-associated sarcomas. Even when

Pinschers may be predisposed. Fibrosarcosurgical excision is clinically and histologimas vary markedly in their appearance and cally complete, recurrence is still the rule.

size. Neoplasms arising in the dermis may

Therefore, multimodal therapy combining
appear nodular. Those arising in the
presurgical imaging, aggressive surgery,
subcutaneous fat or subjacent soft tissues
intracavitary chemotherapy with carbomay require palpation to identify. They platin, followed by radiation therapy and IV
appear as firm, fleshy lesions involving the
carboplatin every 21 days for 4---0 treatments
dermis and subcutaneous fat and often
with tyrosine kinase (T-K) inhibitors as
invade musculature along fascial planes.

adjunctive therapy may yield the best

When tumors are multiple, they are usually
results. Chemotherapy with carboplatin,
found within the san1e anatomic region.

doxorubicin and cyclophosphamide, or

Fibrosarcomas with abundant interstitial
dacarbazine, along with T-K inhibitors, has
proteoglycans ( connective tissue mucins)

been recommended for nonresectable
are called myxosarcomas or myxofibrotumors. Initial results using a biologic sarcomas. Myxosarcomas remain poorly
response modifier (used intratun1orally
defined in veterinary medicine, and many of
before excision and followed by radiation
them could be characterized as variants of
therapy) appear promising. Further work
liposarcomas or malignant fibrous
suggests that its effectiveness as an adjunct
histiocytomas. Fibrosarcomas in dogs are
to surgery and radiation may increase
invasive tun10rs; -1 OOAi metastasize. Factors
tun10r-free intervals up to 200Ai compared
that affect whether a fibrosarcoma can be
with historical controls.

completely excised include the skill of the
surgeon; rate of growth ( as defined by the
mitotic index and quantity of necrosis);

Fibrohistiocytic Tumors
degree of cellular atypia; and the tumor's

These pleomorphic, mesenchymal tumors·
infiltrative nature, size, and location (which
composed of fibroblasts and histiocytic
may require imaging to define properly).

cells ( often present as multinucleated giant

Three forms of fibrosarcoma are
cells) remain poorly defined in veterinary
recognized in cats: a multicentric form in
medicine. A lesion called canine fibrous
the young (generally <4 yr old) caused by
histiocytoma (nodular granulomatous
the feline sarcoma virus (FSV); a solitary
episclerokeratitis, nodular fasciitis,
form in the young or old, in which FSV has
proliferative keratoconjunctivitis,
not been implicated; and a fibrosarcoma
cortjunctival granuloma, Collie granuloma)

that develops in the soft tissues where cats
is recognized at the episcleral junction and
are commonly vaccinated (seep 2169). An
cornea primarily in young to middle-aged
association with rabies and feline leukemia

(2-4 yr old) Collies, but the histologic
virus vaccinations is better defined than
features are more suggestive of a granuwith vaccinations for other viral or lomatous inflan1.111atory response than a
bacterial diseases. Aluminum hydroxide
neoplasm. As might be expected for a nonin

(commonly used in adjuvants) has been
fectious inflammatory process, these are
identified in vaccine-induced fibrosarcogenerally responsive to sublesional mas, and a prolonged proliferation of
injections of 10-40 mg of methylpred.nisofibroblasts in response to the adjuvant lone.

may predispose these cells to undergo

Malignant fibrous histiocytomas
neoplastic transformation. These tumors

( extraskeletal giant cell tumors, giant cell
appear as nodules or plaques between the
tun1ors of soft parts, dem1atofibrosarcoshoulder blades, in the soft tissues of the mas) are most frequently found in the skin
proximal hindlimbs, or less commonly,
and soft tissues of cats, occasionally found

958

TUMORS OF THE SKIN AND SOFT TISSUES
in horses and mules, and rarely in the skin of indolent nature, treatment is optional; also, other domestic species, including dogs. In
additional tun1ors often develop spontanecats, malignant fibrous histiocytomas are ously at other sites over ti.me. In dogs, cats,
most common on the distal extremities or
and horses, most are locally infiltrative but
ventral cervical regions of the aged but
do not metastasize. Complete excision is
may also be diagnosed at vaccination sites.

the treatment of choice. When mai·gins are

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In horses and mules, these have been
nanow or insufficient, followup radiation
described as giant cell tumors of soft parts.

therapy, postoperative intralesional tumor

Seen in young adult to middle-aged Equidae, bed chemotherapy ( using the patient's they are firm, nodular to diffuse swellings
serum mixed with the chemotherapy agent),
that are white on cut surface, with variable
electrochemotherapy, or systemic
hemorrhage. Malignant fibrous histiochemotherapy with carboplatin or cytomas are sarcomas of intermediate
metronomic chemotherapy may increase
malignancy. They are locally invasive and
the tun1or-free interval.

tend to recur after attempts at complete
excision but seldom metastasize. Radical
excision is reconunended.

Adipose Tissue Tumors

Lipomas are benign tun1ors of adipose

Peripheral Nerve Sheath Tumors
tissue, perhaps more accurately characte1�
ized as hainartomas. They are conunon in

Amputation neuromas (traun1atic
dogs, occasionally identified in cats and
neuromas) are non-neoplastic, disorganized horses, and rare in other domestic species.

proliferations of pe1ipheral nerve paren

In dogs, they generally develop in older,
chyma and stroma that form in response to
obese females, mosL conunonly on U1e Lrunk
amputation or traun1atic irtjury. They are
and proxin1al limbs. The breeds most at
most conunonly identified after tail docking
risk are Doberman Pinschers, Labrador
in dogs or neurectomy in the distal

Retrievers, Miniature Schnauzers, and
extremities of horses. The most common
mixed-breed dogs. Older, neutered male
clinical presentation is a yotmg dog that

Siainese cats ai·e predisposed, and tun10rs
continuously traumatizes its docked tail. In
are most commonly found on the ventral
horses, such a lesion appears as a firm,
abdomen. Obesity does not appear to be a
often painful swelling at a neurectomy
factor in the development of lipomas in cats.

surgery site. Excision is curative.

Affected horses are generally <2 yr old.

Neurofibromas and neurofibrosar

Lipomas typically appear as soft, occasion
comas (perineuromas, neurilenunomas,
ally pedunculated, discrete nodulai· masses,
nerve sheath tunlors, hemangiopericytoand most are freely movable. In dogs and mas, neurothekomas, schwannomas) are
cats, >5% ai·e multiple. In general, these
spindle-cell twnors that arise from the
tunlors float when placed in fom1alin.

connective tissue components of the

A rare variant of this twnor, diffuse
pe1ipheral nerve. They are believed to aiise
lipomatosis, has been identified in
from Schwarm cells, but they could also

Dachshunds. Virtually the entire skin is
arise from mesenchyrnal cells, which
affected, resulting in prominent folds on the
produce the nonmyelinat�d connective
neck and truncal skin. Many lipomas merge
tissues that surround the myelinated ne1ve
imperceptibly with the adjacent nonfiber. In dogs, forms of this twnor cai1 be neoplastic adipose tissue, making it difficult
virtually indistinguishable from hemangioto detennine when the entire lesion is pericytomas and may be the san1e tunlor.

excised. Lipomas with-an abundant

In dogs and cats, peripheral nerve sheath
connective tissue stroma (fibrolipomas ),
tun1ors of the skin ai·e found in older
cartilaginous stroma ( chondrolipomas ), or a
a.Ilin1als. In cattle, they have a suspected
prominent vascular component ( angiolipogenetic basis, may be multiple, can develop mas) are also recognized. Despite their
in both the young and old, and are generally
benign nature, lipomas should not be ignored
an incidental finding at slaughter; they arise
because they tend to enlarge over tin1e, and
from the deep nerves of the thoracic wall
their gross presentation may be indistinand viscera, and cutaneous involvement is guishable from that of infiltrative Ji po mas
rare. Regai·dJess of the species, these
or liposarcomas (see below). Excision is
tun1ors appear as white, finn, nodules.

curative. In dogs, dietaiy restiiction to 7ff'/o

Attachment to a peripheral nerve may
of nonnal intake for several weeks before
occasionally be noted. Both benign and
surgery may allow for better definition of the
intermediate-grade malignant variants
surgical mai·gins of the tumor.

ai·e recognized. Benign tun10rs are most

Infiltrative lipomas (intra- and interconunon in cattle in which, because of their muscular lipomas) are rare in dogs and

TUMORS OF THE SKIN AND SOFT TISSUES

959
even less common in cats and horses. In
predisposed to developing disseminated
dogs, they are most conunon in middle-aged hemangiomas (angiomatosis) in the skin females, usually on the thorax and limbs.

and internal organs. In pigs, these lesions

The breeds (dogs) most at risk are the same
generally develop in the scrotal or pe1ineal
as those for lipomas. These tumors are
skin of Yorkshire, Berkshire, and less
poorly confined, soft, nodular to diffuse
commonly Chester White boars. In the first
swellings that typically involve the
two breeds, the disease is believed to be

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subcutaneous fat and nnderlying muscle
genetically transmitted. Hemangiomas are
and connective tissue stroma. Infiltrative
single to multiple, circwnscribecl, often
lipomas, which dissect along fascia! planes
compressible, red to black nodules. The
and between skeletal muscle bnndles, are
lining epidermis may be unaffected or
considered sarcomas ofintennediate
ulcerated or papillatecl. Small, superficial
malignancy. They rarely metastasize.

hemangiomas tl1at often appear as a "blood

Aggressive excision is recommended, and
blister" are known as angiokeratomas.

amputation may be necessary.

When erythrocytes are sparse or absent

Liposarcomas are rare neoplasms in all
within vascular lumens, the tem1 lyrnphandomestic animals. Most are recognized gioma is applied. Hemangiomas are benign,
in older male dogs in which they usually
but their tendency to ulcerate and grow
develop on the trunk and extremities;
quite large, along witl1 the in1portance

Shetland Sheepdogs and Beagles may be
of confinning the diagnosis to make a
predisposed. In cats, feline leukemia virus
prognosis, indicate removal. Excision is the
infection has been infrequently associated
treatment of choice; however, in large
with their development; whetl1er this is a
animals in which the lesions may be large
coincidence or such infections play a
and involve the distal extremities, this may
causative role remains unclear. Liposarcobe difficult. In these cases, cryosurgery or mas are nodular and soft to finn. They may
radiation therapy may be necessary. Except
exude a mucinous fluid when sectioned.

in dairy cattle with angiomatosis, develop

Many have palpable, partially encapsulated
ment of additional tumors at new sites after
areas, but these zones should not be
complete excision is nnconunon.

construed as evidence of a benign tumor.

Hemangiopericytomas ( canine

Liposa.rcomas are malignant neoplasms that spindle-cell sarcoma, canine malignant have a low metastatic potential but are
fibrous histiocytoma, canine neurofibrosarfrequently pseudoencapsulated. Wide coma, canine perineuroma) are corrunon in
excision is reconunended. Recurrence is
dogs and rare in cats (if they occur at all).

conunon, so followup radiation therapy is

This twnor was initially named because it
indicated in cases with insufficient margins.

was thought to be derived from fibroblastic
cells that suffouncl small vessels; however,

Vascular Tumors
the appropriateness of the nan1e remains a
topic of debate. These tun1ors develop most

Hemangiomas of the skin and soft tisconunonly on the distal extremities and sues are benign proliferations that closely
thorax of older clogs. Females appear to
resemble blood vessels. Whether these
be predisposed, and Sibelian Huskies,
are neoplasms, hamartomas, or vascular
mixed-breed clogs, Irish Setters, and
malfom1ations remains w1defined, and no

Gennan Shepherds are most at risk.

clear criteria exist that allow for their

Hemangiope1icytomas typically present as
separation. They are most commonly
firm, multilobulated, solitary lesions with
identified in dogs, occasionally in cats and
irregular borders, most commonly in the
horses, and rarely in cattle and pigs; they are subcutaneous fat but sometimes in the an exceptional finding in other domestic
demlis. They are of intem1ediate maliganin1als. In dogs, they are tumors of adult nancy and have limited metastatic potential.

clogs and most corrunonly develop on the

Complete excision with adequate margins is
tflll1k and extremities. Many canine breeds
the treatment of choice but, because of the

(including Gordon Setters; Boxers; and
infiltrative nature of these tumors, excisions

Airedale, Scottish, and Kerry Blue Terriers)

are incomplete or margins are nan·ow in
are considered to be at risk. Cats most
most surgeries; therefore, -300/o recur. If the
frequently develop hemangiomas when they fixst excision of any sarcoma does not have are adults. Lesions are most corru11on on the
adequate margins, ie, clean, wide surgical
head, extremities, and abdomen. In horses,
margins ("complete" may include na.D"ow they are most common on tl1e distal
margins not considered adequate for local
extremities of young ( <l yr old) animals.

tumor control), followup surgery to remove

In cattle, they may be seen as congenital
the tumor bed and increase the margins is
lesions or in older animals. Dairy cattle are
indicated. At surgery, intracavitary

960

TUMORS OF THE SKIN AND SOFT TISSUES
chemotherapy with carboplatin or
the skin or underlying soft tissues. Less

5-fluorouracil mixed with the patient's
frequently, they appear as a poorly defined
serum, and/or intraoperative radiation
bruise. All grow rapidly, often are associated
therapy with followup intratumor bed
with large zones of necrosis and thrombochemotherapy, and/or followup radiation sis, and typically are red to black on cut
therapy may increase the tumor-free
section. Tumors often diagnosed as

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interval.

lymphangiosarcomas may have much less

Angiosarcomas, arguably the most
lun1enal blood, and the vascular spaces are
aggressive of all soft-tissue tumors, are comtypically filled with serum. Characteristiposed of cells that have many functional cally, angiosarcomas create their own
and morphologic features of nom1al
vascular space by dissecting through soft
endothelium. Although these tumors are
tissues. Distant metastasis, especially to
often divided into hemangiosarcomas ( of
the lungs and liver, is common. In other
purported blood vessel origin) and
domestic animals, these tun1ors do not
lymphangiosarcomas ( of lymphatic vessel
appear to behave as aggressively, and
origin), such a distinction is arbitrary. The
postexcisional recurrence rather than
tenn angioendothelioma is also used.

metastasis is more common.

These tumors generally arise spontane

For all species, because of the aggressiveously. In the nonpigmented skin of dogs ness of these nodules, wide excision with
with short, often white coats, chronic solar
intraoperative placement of carboplatin
iajury may induce transfom1ation in the
beads or intracavitary carboplatin mixed
superficial vascular plexus, which initially
with the patient's serum may be the
appears as a hemangioma and then protreatment of choice. Solar-induced canine gresses to a malignant vascular twnor. The
cutaneous hemangiosarcomas generally do
light-skinned breeds prone to actinically
not have an aggressive biologic behavior,
induced dermal angiosarcomas are
although numerous lesions may continue to

Whippets, Italian Greyhounds, White
appear over a period of several years.

Boxers, and Pit Bulls. Pathologists often

Superficial lesions are easily destroyed with
diagnose these lesions as cutaneous
topical cryotherapy, which may control the
hemangiosarcomas. Because histogenesis
disease for years; however, if lesions
of dermal hemangiosarcoma is often related
become large (>l cm) or cystic, they are
to that of chronic solar irritation, predisbest controlled with excision. If multiple posed breeds should be protected from sun
cystic lesions appear, the aninlal may
exposure. Dermal hemangiosarcomas have
benefit from a combination of local control
a moderately high potential for malignancy;
and antiangiogenic therapy. Avoidance of
therefore, wide surgical excision is the
further sun irradiation injury may reduce
treatment of choice for tumors >0.5 cm.

the development of new lesions; however,

Cryosurgery or laser surgery can effectively
previously exposed skin may continue
control multifocal, small, early lesions.

to develop lesions as a result of "field

When metastasis occurs, it is by the
cancerization." Adjuvant chemotherapy
hematogenous route to the lungs and
consisting ofvincristine, doxorubicin, and
spleen. Up to one-third of splenic hemangiocyclophosphamide (the VAC protocol) has sarcomas arise in the skin or p,eripheral
been reported to shrink angiosarcomas;
tissue and end up in the spleen because of
splenic filtering of cells in the bloodstream.

Angiosarcomas of the skin and soft
tissues are seen in all domestic animals but
are most common in dogs, generally in adult
or aged aninlals. In dogs, they most
frequently develop on the trunk, hip, thigh,
and distal extremities. In addition to the
breeds prone to actinically induced
angiosarcomas, Irish Wolfhounds, Vizslas,

Golden Retrievers, and German Shepherds
are also at risk. In cats, this tumor is seen
most commonly in older, neutered males,
on the extremities and trw1k. Cats with skin,
subcutaneous, or visceral involvement
develop distant metastasis. Angiosarcomas
can vary markedly in appearance. Most

Solar-induced cutaneous hemangiosarcoma,
older Bulldog. Lesions appear as multiple,
commonly, they appear as one or more
red, flat or blood-filled cysts in sun-exposed
erythematous nodules present anywhere in
non pigmented skin. Courtesy of Dr. Alice Villalobos.

TUMORS OF THE SKIN AND SOFT TISSUES

961
carboplatin is also helpful. However, the
combination of the intraoperative and
effects of chemotherapy for systemic
followup oncologic therapy techniques
control or radiation therapy for local
described above, because the first surgery
control and longterm survival remain to be
with immediate followup is most important
defined. Electrochemotherapy delivering
in determining outcome. The prognosis is
bleomycin and platinum-containing drugs
generally poorer for anaplastic sarcomas

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into tumors has shown cytotoxic efficacy
than for undifferentiated sarcomas.

leading to endothelial cell death in 1 to 3
treatment sessions under heavy sedation.

LYMPHOCYTIC, HISTIOCYTIC,

These agents may also be administered
intraoperatively. The role of NSAIDs such

AND RELATED CUTANEOUS
as piroxicam, meloxicam, etc, is still not

TUMORS
completely understood and may vary from
drug to drug. Antiangiogenic or angiostatic

Lymphoid Tumors of the Skin
compounds such as canine recombinant

Canine extramedullary pla.sma.cytoma.s
canstatin that attack the blood supply of

(atypical histiocytomas, cutaneous neuroentun10rs may control and prevent metastadocrine tumors [seep 952], reticulw11 cell ses; however, results of clinical trials remain sarcomas, cutaneous nodular an1yloidosis) elusive.

a.re relatively common cutaneous tumors.

Although tl1eir derivation was long debated,

Cutaneous Smooth Muscle Tumors
neoplastic cells characteristically express
cytoplasmic inlmunoglobulin and may

Because they either a.re not recognized
produce primary amyloid, leaving little
or do not develop vvith any regularity in
doubt as to their lymphoplasma.cytic origin.

domestic animals, cutaneous smooth

These tumors of dogs and, rarely, ca.ts a.re
muscle tumors (leiomyomas or leiomyomost frequently identified on the head sarcomas) are diagnosed rarely. Those

(including ea.rs, lips, and oral cavity) and
reported generally have been malignant and
extrentities of mature to aged animals.

found in dogs and cats. Usually, they are

Cocker Spalllels, Airedales, Scottish
firm cutaneous masses. Leiomyomas are

Teniers, and Standard Poodles are most at
small and tend to be limited to the demtis,
risk. The tun1ors are generally small ( <5 cm)

whereas leiomyosa1·comas are larger
a11d sometimes pedtmculated. Most of tl1ese
and most arise from ( or extend into)

the subcutaneous fat. The behavior of
tumors are locally confmed, and complete
but conservative surgical excision is the
malignant smooth muscle tumors remains
treatment of choice. Infrequently, extra.cpoorly defined. Complete excision is the utaneous plasmacytomas may be locally
treatment of choice for both leiomyomas
invasive or multiple ( or both), especially
and leiomyosarcomas. They have been
when they occur in tl1e oral cavity.

responsive to vincristine chemotherapy

Recurrence has also been correlated
given IV weekly for 6 wk then tapered; they
witl1 the presence of amyloid (seep 592).

may also respond to oral masitinib therapy

Treatment for tl1ese tumors targets local
and other tyrosine-kinase inhibitors.

control using localized techniques described
above. For recurrent, invasive twnors, more

UNDIFFERENTIATED AND
aggressive attempts at excision may be

ANAPLASTIC SARCOMAS
required. When tumors a.re multiple or when
surgical excision is not feasible, radiation

These malignant mesenchymal tumors
therapy appears to be the best secondary
are difficult to characterize microscopitTea.tment. For tumors resistant to radiation cally. Undifferentiated sa1·comas la.ck
and for those filllmals unable to receive
distinctive features ( eg, architectural
radiation therapy, systemic treatment
patterns, cytoplasmic and nuclear features,
with chemotherapeutic a.gents, including
cell products). Anaplastic sarcomas have
melphalan, chloran1bucil, cyclophosphamost of the following features: variations mide, and glucocorticoids, have been
in size and shape of nuclei, nuclear hyperrecommended and have yielded longterm chromasia., striking irregularity of chromasurvival.

tin pattern, abnormal ntitotic figures,

Cutaneous lymphosarcoma may
and large numbers of ntitotic figures. As
occur as a disease in which the skin is tl1e
such, ana.plastic sarcomas are generally
initial and prin1ary site of involvement, or
undifferentiated, but undifferentiated
it may be secondary to systentic, internal
sarcomas do not have to be anaplastic. In
disease. (See also CANINE MALIGNANT LYMPHOMA, both cases, excision should be deep and
p 40; BOVINE LEUKOSIS, p 7 43; and FELINE
wide, with 3-cm margins along with a

LEUKEMIA VIRUS AND RELATED DISEASES, p 790.)

962

TUMORS OF THE SKIN AND SOFT TISSUES

Cutaneous lymphosarcoma is rn1common
tine (an alkylating nitrosourea), retinoids
but has been identified in all domestic
with and without glucocorticoids, and
species. In general, two distinct forms are
high-dose li.noleic acid supplementation
recognized-an epitheliotropic fom1 (in

( safflower oil at 3 mUkg, 3 consecutive
which there is infiltration by malignant
days/wk) may occasionally achieve partial
lymphocytes into the epidermis and adnexa) or complete remission. Studies show that and a nodular, nonepitheliotropic fom1.

a lymphocyte T-cell inunrn1omodulator,

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Both usually express smface and cytoplaswhich signals the differentiation of late mic antigens characteristic of T cells; this,
stage CD4 lymphocytes and causes
along with the frequent identification of at
apoptosis of malignant T cells, is a
least small foci of epitheliotropism in many
reasonable adjrn1ctive therapeutic agent
cases of "nonepitheliotropic" forms in dogs to use and may improve the clinical course
and cats, suggest they may be different
in some cases.

variants of the san1e till1lor.

ECL is rare in cats and tends to develop

Epitheliotropic cutaneous lymphoin older anin1als. Lesions often follow a sarcoma (ECL, mycosis fill1goides) is the
defined progression, appearing initially
most frequently recognized fonn of
as a crusty plaque that is variably pruritic.

cutaneous lymphosarcoma in dogs and

Biopsies of early lesions are often diagnosed
arguably cats. It is a disease of middle-aged
as lymphocytic mural folliculitis. In many
and older dogs, and Poodles and Cocker
cases in which this diagnosis is applied, the

Spaniels may be predisposed. Classically,
lesions evolve into rn1equivocal cutaneous
the lesions progress from patch to plaque to
lyrnphosarcoma. In contrast to ECL in dogs,
tumor; however, one or any combination of
epitheliotropism is often extremely subtle
these three primary lesions may be present.

in cats. Little is known about therapy or

For example, a fonn of ECL known as
whether therapy used in dogs would be

Pagetoid reticulosis has minin1al to no
effective if used in cats; however, since the
dennal involvement, and cutaneous lesions
availability of a lymphocyte T -cell inmmalways appear as erythematous patches.

nomodulator for use in cats witll feline

Another common feature of the disease in
leukemia virus, it can be offered as a viable
dogs is the presence of areas of alopecia due option.

to follicular atrophy caused by infiltration of

Nonepitheliotropic cutaneous
neoplastic cells into the outer sheath and
lymphosarcoma (NECL) is the most
lU1Tien of hair follicles. Although most cases
recognized form of cutaneous lymphosarare associated with diffuse cutaneous coma in all domestic animals but dogs and
involvement, forms limited primarily to
cats. In dogs, NECL is most common in
mucous membranes or the footpads have
middle-aged or older animals. Lesions are
been identified. Because of the variable
nodules or plaques that most conunonly
clinical appearance of this till11or, diagnosis
develop on tile trunk They generally are
based on clinical features can be very
multiple, although solitary lesions may be
difficult, and early stages can be confused
noted, especially in cats. In many cases,
with allergic, autoinlmrn1e, endoc1i.ne,

NECL is grossly indistinguishable from the
infectious, or seborrheic diseases. Most
tU1Tior stage of ECL. A definitive diagnosis
cases are limited to the cutis rn1til late in the
is in1porta.nt because NECL in dogs is
course of the disease. ECL.with concurrent
generally more aggressive than ECL, and
leukemia is known as Sezary syndrome.

systemic involvement occurs commonly

In dogs, ECL is a slow to moderately
and early in the course of the disease.

progressive disease for which a nmnber of

Various modes of tllerapy, including
therapies have been attempted. To date, all
excision, chemotherapy, and less frequently
appear more effective in improving the
radiotherapy, have been used as monotherclinical features of the disease than in apy and in combination. Excision is the
prolonging an affected dog's life. Methchlochoice when the disease is limited to a rethamine (nitrogen mustard) has been
solitary tmnor, and complete cures have
used in the past as a topical therapy, but
occasionally been obtained. Excision
because large areas of a dog's body may
or cryosurgery in more diffuse fonns
be affected (including the mucous
infrequently elicit longterm remissions.

membranes) and because of its sensitizing

Chemotherapy or chemoilnmrn1ologic
potential in people, it is infrequently used.

protocols used for otller forms of canine

The disease is often transiently responsive
lymphosarcoma should be considered as
to steroids. Chemotherapeutic agents, such
palliative. The average remission tilne
as combinations of adria.mycin, chloran1buis-Smo.

cil, cyclophospharnide, doxorubicin, and

In cats, NECL is a rare disease of
vincristine, are variably effective. Lomus-
middle-aged or older animals. The role of

TUMORS OF THE SKIN AND SOFT TISSUES

963
feline leukemia virus remains undefined.

occurrence of unknown etiology. Cutane

The lesions are plaques or nodules that
ous lymphosarcoma of young cattle is
may be solitary or multiple, alopecic or
presumed not to be associated with bovine
haired, and ulcerated or lined by an intact
leukemia virus infection (seep 743) and
epidermis. Feline NECL is aggressive; even
presently has an unknown etiology. The
when complete excision of a solitary nodule lesions are typically nodular, involve the is attempted, recurrence is conunon. No
dermis or subcutaneous fat, and are often

VetBooks.ir
definitive therapy is known; however,
ulcerated. There is no known therapy.

using a combination of lomustine, steroids,
linolenic acid ( oil of evening primrose), and

Cutaneous Mast Cell Tumors
injections of a lymphocyte T-cell inununomodulator may be of some value.

(Mastocytomas, Mast cell sarcomas)

In horses, NECL (nodular lymphosar

These tumors are the most frequently
coma, subcutaneous lymphosarcoma,
recognized malignant or potentially
lymphohistiocytic lymphosarcoma) may be
malignant neoplasms of dogs. In addition,
recognized at any age but is most conunon
visceral and leukemic fom1s can occur.

in young and middle-aged animals. Fitm,

A viral etiology has been speculated but
nonulcerated nodules are most common in
remains controversial. Tun10rs may be seen
the subcutaneous fat of the ventral body
in dogs of any age ( average 8-10 yr). They
surface. Microscopically, two types of
may develop anywhere on the body surface
nodular lymphosarcoma are recognized in
as well as in internal organs, but the limbs
horses. The most common consists of a

( especially the posterior upper U-ligh ),
mixture of histiocytes and small, wellventral abdomen, and thorax are the most differentiated lymphocytes, occasionally
conunon sites; -lOOA, are multicentric.

with plasmacytoid features; the second

However, studies suggest that multiple
consists of a monomorphic population of
tumors do not cany a worse prognosis when
large atypical lymphocytes, with only
tl1ey are all adequately excised if grade 1 or
occasional histiocytic cells. Differentiation
low grade. Initial size at the time of surgery
between these two fonns is important
is highly predictive of outcome; tun10rs >3
because most cases of cutaneous lymphocm correlate with decreased survival time.

sarcoma in horses with a monomorphic

Tun10rs that are incompletely excised, grow
pattern of cells have internal involvement,
rapidly, or arise from mucocutaneous
and the disease progresses rapidly. In
junctions, muzzle, ventrun1, prepuce, or
contrast, the lymphohistiocytic form seldom subungual areas or in animals with clinical is associated with internal involvement, and
signs at diagnosis are associated with more
affected horses may live for years. As the
aggressive biologic behavior.

lymphohistiocytic forn1 progresses, the

Many breeds appear to be predisposed,
nodules tend to become more frequent on
especially Boxers and Pugs (in which
the ventral cervical regions. In many cases,
tumors are often multiple), Rhodesian
euthanasia may be wan·anted when

Ridgebacks, and Boston Terriers. Tlie
pharyngeal involvement induces dyspnea.

tumors vary markedly in size, and clinical

Because of the expense of cytotoxic drugs,
appearance alone cannot establish a
therapy is generally limited to glucocortidiagnosis. Most commonly, they appear as coids administered orally or intralesionally;
raised, nodular masses that may be soft to
remission, if induced, is usually short term.

solid on palpation. Although they often

In cattle, cutaneous lymphosarcoma is a
seem encapsulated, mast cell tumors in
disease of young anin1als (generally <4 yr
dogs are seldom discrete. Rather, they
old). It is one of the sporadic bovine
consist of a highly cellular center surleukosis syndromes that is not transmissirounded peripherally by a halo of smaller ble. The tern1 sporadic bovine leukosis is
numbers of mast cells that palpate as
usually reserved for calf,cutaneous,and
nonnal skin. Dogs can also develop clinical thymic types of lymphoma, which are
signs associated wiili the release of
defined by the young age of occurrence and
vasoactive products from the malignant
the distribution of tun1ors. The cause or
mast cells. Most common is gastroduodenal
causes are not known. Only lymphomas
ulceration that may be present in up to 25%
caused by bovine leukemia virus infection
of cases. Cytologic evaluation of Wrightshould be termed leukosis or enzootic stained, fine-need.le aspirates or impression
bovine leukosis. There may also be
smears can be used to establish the
lymphosarcomatous conditions that do
diagnosis of mast cell tumors in dogs. All
not fall into either the sporadic or enzootic
skin twnors should be examined by finebovine leukosis categories, ie, adult needle aspiration cytology before excision
multicentric lymphoma with sporadic
to exclude mast cell tumor. lfilie surgeon is

964

TUMORS OF THE SKIN AND SOFT TISSUES
aware that the tumor is of mast cell origin,
three multinucleated cells/10 hpf, three
a surgical plan for wide and deep excision
bizarre nuclei/IO hpf, and karyomegaly in
will yield the best results. All mast cell

J()OA, of the cells. These high-grade features
tumors should be submitted for biopsy to
confer a prognosis of a 4-mo survival time
detemline margins and grade, because
vs >2 yr for low-grade mast cell tumors.

cytology is not a substitute for histopathol

Because of the difficulty of subcategorizing
ogy-only the latter has been well
canine mast cell tumors, all should be

VetBooks.ir
correlated with prognosis. However, certain
treated as at least potential malignancies.

cytologic features can be used to identify

The Mast Cell Tun10r Panel to detemline
high-grade tumors. Two systems of
prognosis and treatment guidance can
histopathologic grading have been defined,
be requested for grade II tumors at the
the Bostock system of 1973 and the Patnaik

Diagnostic Center for Population and
et al system of 1984. To avoid confusion, it is Animal Health at Michigan State University.

essential to know which system is being

Treatment depends on the clinical stage
used. The conunonly used Patnaik grading
of the disease and the predicted aggressive
system has the following designations:

biologic behavior. For Stage I tumors ( a
grade 1 = low grade, grade II = intermediate
solitary tumor confined to the dennis
grade, grade III= high grade. Up to 80% of
without nodal involvement), the preferred
canine mast cell tumors are classified as
treatment is complete excision with a wide
grade II and are further divided into
margin; at least 3 cm of healthy tissue
subgroups of low grade II (mitotic index 5:5)

surrounding all palpable borders should
and high grade II (mitotic index >5) along
be removed in an attempt to excise both
with characteristics that may predict
the nodule and its surrouncling halo of
clinical behavior in this large category.

neoplastic cells. Intraoperative cytology

Although there is believed to be a benign

(examination of impression smears at the
variant of canine mast cell tumor, there is no excised tissue margins) can guide the clinical or microscopic means of identifying
surgeon, who should continue to remove
it. In addition, small mast cell tumors may
tissue until the margins are adequate and
remain quiescent for long pe1iods before
free of mast cells. If histologic evaluation
becoming aggressive. A subcutaneous
suggests that tl1e tumor extends beyond the
variant of canine mast cell tumor, which
surgical margins, reexcision or tun1or bed
does not have a primary infiltrative dermal
excision should be attempted. Because
involvement, occU1Ted in -lOOA,ofbiopsied
mast cells are sensitive to radiation, intratissues in one study. This variant appeared operative radiation therapy is an option
most frequently in the hindlimb, with 66%
along with followup external beam
having incomplete excision, most comradiation therapy, which may be curative monly at the deep margin. These tumors
if the remaining tumor is small or microhave intermediate histologic grade, a lower scopic. Combination or multimodal
rate of recurrence.( only 9"Ai), and extended
treatments using radiation therapy (if
mean survival times, with only a 6% rate of
affordable), with intralesional chemothermetastases.

apy and or local hyperthemlia or electro

Up to 65% of incompletely excised mast
chemotherapy along with systemic
cell tumors do not recur. This suggests that
chemotherapy including tyrosine-kinase
their biologic behavior is not always
inhibitors, may be more effective than
aggressive and that aggressive treatn1ent
radiation alone to control biologically and
may not always be warranted. Specialized
locally aggressive mast cell tumors.

stains can be used to distinguish tumor

There is no agreed upon mode of therapy
grades more adequately. Proliferation
for Stage II-IV mast cell tumors; however,
marker expression can help detemline the
the advent of multikinase inllibitors
likelihood that an incompletely removed
represents a new option, which when used
mast cell tumor will recU1· or metastasize.

in combination with cytotoxic chemother

The combination of Ki-67 >23/grid;
apy, requires dose reduction to avoid
proliferating cell nuclear antigen, Agnor
adverse events. Standard care options for
count >54; mutations in exon 8 and exon 11

Stage II tumors ( a solitary tumor with
of c-Kit gene; and increased PCNA levels are regional lymph node involvement) include prognostic for local recurrence and a poor
excision of the mass and the affected
prognosis. Correlation of test results with
regional node (if feasible), prednisolone,
survival times can be useful but is not
and radiotherapy, used either singly or in
always a reliable predictor of the outcome.

combination. Tl.iamcinolone or dexametha

There is agreement on cytologic features for sone sodium phosphate, nlixed with the high-grade mast cell tumors: seven or more
patient's serun1 and irtjected evenly into
mitotic figures/IO high-power fields (hpf),
the tissues of tl1e tun10r bed at the time of

TUMORS OF THE SKIN AND SOFT TISSUES

965.

surgery or postoperatively as a followup
respond regardless of their c-Kit status.

series, may also help reduce recurrence.

A study of 202 client-owned dogs with or

Intraoperative radiation therapy and/or
without prior treatment, having measurable
followup external beam therapy is still
cutaneous grade II or III mast cell tumors
considered the highest standard of care but
without nodal or visceral metastasis, found
is often declined because of cost. Injections
that masitinib (12.5 mg/kg/day, PO) was a
into the tumor bed after incomplete
relatively safe and beneficial treatment

VetBooks.ir
excision using hypotonic, deionized, or
option. Another clinical trial fow1d that
distilled water has been debated. Treatment
toceranib (3.25 mg/kg, PO, every 48 hr), a
of Stage m ( multiple dermal tumors with or
receptor tyrosine kinase inhibitor, results in
without lymph node involvement) or Stage
inhibition of Kit phosphorylation in canine

IV (any twnor with distant metastasis or
mast cell twnors and was of clinical benefit
recurrence with metastasis) tumors is
with continued use. Note that the toceranib
generally considered palliative. One
dosage stated on the package insert may
recommended therapy is prednisolone
lead to unacceptable toxicity. Veterinary

(2 mg/kg, PO, for 5 days, followed by a
oncologists are the most informed sources
maintenance dose of 0.5 mg/kg/day) or
for clinical application using these novel
intralesional injections of triamcinolone
tyrosine kinase inhibitor drugs against mast

(l mg/cm diameter of tumor, every 2 wk).

cell twnors, which may also benefit other

Treatment with H1- and Hz-receptor
malignancies.

antagonists for the peripheral and gastric

In cats, cutaneous mast cell tumors are
effects of histamine, respectively, may be
the second most common skin tun1or;
indicated for animals with systemic disease
however, the disease is seen only occasionor clinical signs referable to histamine ally in practice. In addition to cutaneous
release. Chemotherapy with vinca alkaloids
tumors, primary splenic, systenuc,

(vincristine, vinblastine), L-asparaginase,
leukenuc, and GI fom1s have been
and cyclophosphanude has also been used
recognized. Two distinct variants of the
with some effectiveness. Prednisone and
cutaneous form occur-a mast cell type
vinblastine used as adjuvant chemotherapy
analogous to, but not identical with,
to incomplete surgical resection conferred
cutaneous mast cell tumors in dogs, and
an apparent improvement over historical
a histiocytic type unique to cats. Feline
survival data using surgery alone, yielding a
cutaneous mast cell tumors may be either

57% 1- and 2-yr disease-free state and a 45%
solitary or multiple. Piin1ary splenic,
survival at 1 and 2 yr for dogs with grade m
systenuc, recurrent, and multiple tun10rs
tumors. In 19 dogs on a high dose of

(five or more) are associated with a guarded
lomustine given every 21 days, 42% of mast
prognosis.

cell tumors showed measurable responses,

The mast cell type is most common. It is
ranging from stable to partial with one
found primarily in cats >4 yr old and may
complete response. Neutropenia appears 7
develop anywhere on the body butmost
days after treatment, with neutrophil counts commonly on the head and neck. The of 1,500 cells/µL. Vinc1istine doses must be
tumors are single, alopecic nodules,
lowered if used in combination with multigenerally 2-3 cm in diameter, that occasionkinase inhibitors. Lomustine at metrononuc ally extend into the subcutaneous fat.

doses given daily along with multikinase

Lymphoid nodules are common; eosinophils
inhibitors may be helpful and may avoid the
are rare. Unlike mast cell tumors in dogs,
adverse events associated with high-dose
those in cats are generally benign; atypia
lomustine.

and clinical behavior are poorly correlated.

Novel small molecule multikinase

Surgical excision is the treatment of choice;
inhibitors such as masitinib mesylate and

3096 of tun10rs recur after surgery and some
toceranib phosphate are available to treat
metastasize. Cryotherapy may be a good
mast cell tumors and have been shown to be option to treat multiple recurrent small very helpful in management of difficult
lesions to avoid anesthesia. Recurrent
cases. They inhibit the c-Kit tyrosine kinase
tumors may respond to chemotherapy,
receptor, an activated or mutated protoradiation therapy, and novel small molecule oncogene associated with the development
targeted therapy (see above).

of mast cell tumors. Tissue sampling to

The histiocytic type of cutaneous mast
detemune the biologic aggressiveness
cell tun10r in cats is recognized primarily in
of mast cell tmnors and to look for the

Siamese cats <4 yr old. Lesions may develop
presence of the mutated tyrosine kinase
anywhere on the body and appear as
c-Kit receptor has been recommended
multiple ( rniliary ), small (generally 0.5-1 cm
before starting treatment, although
in diameter), firm, subcutaneous papuloevidence shows that many mast cell tumors nodules. Usually, the older the cat, the fewer

966

TUMORS OF THE SKIN AND SOFT TISSUES
the lesions. This variant may be difficult
systemic illvolvement; purely cutaneous
to distinguish morphologically from a
fom1s have been recognized occasionally.

granulomatous inflanunatory response.

Because some of these tumors are reported
to resolve spontaneously, treatment may

Tumors with Histiocytic
not be necessary.

Differentiation

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In horses, mast cell tumors are unconunon

Tumors with histiocytic differentiation
and generally benign, although metastasis
comprise a group of poorly defined ski11
has been reported and should be considered.

diseases all characterized by a proliferation

There has been debate as to whether mast
of histiocytes (tissue macrophages) in the
cell tumors are actually a neoplastic process
absence of any !mown stimulus.

or an unusual inflanunatory response;

Cutaneous histiocytomas are common
however, they are currently considered a
in dogs and rare in goats and cattle; it is
neoplastic process caused by a gain of
debatable whether they are found ill cats.

function mutation of the Kit proto-oncogene.

Strong immunohistochemical evidence

Lesions may develop anywhere on the body
suggests that in dogs they are derived
but are most common on the head and legs.

from Langerhans (i11traepidennal antigen

'Iypically, tl1ere is a single, solitary mass in
processing) cells. These tun10rs are
the dermis or subcutaneous fat that rarely
typically seen in dogs <3.5 yr old but can
expands to involve the underlying musculabe seen at any age. English Bulldogs, ture. Erythema and wheal formation (Darrier Scottish Terriers, Greyhounds, Boxers, and sign) is not a clinical feature of equine

Boston Terriers are most at risk. The head
mastocytoma. Most affected horses are male, (illcluding the pnmae) and limbs are the with an average age of 7 yr ( range 1-18 yr).

most conunon sites of involvement. These

The tumor begins as a nodule composed of a
classic "button twnors" appear as solitary, generally monomorphic proliferation of mast smooth, pillk, raised nodules that are cells. As the lesion evolves, the mast cells are
generally covered by alopecic skin, or they
limited to aggregates in a fibrous stroma that
may be ulcerated. They are freely movable.

surrounds large foci of liquefactive necrosis

Although a conunon neoplasm, histiocytocontaining numerous eosinophils. In the late mas are not always easy to diagnose
stages, the necrotic foci undergo dystrophic
histologically and can be confused with
mineralization, and mast cells may be very
granulomatous inflanunation, mast cell
difficult to identify. Once mineralization
tumors, plasmacytomas, and cutaneous
occillS, the lesion is gritty on sectioning.

lymphosarcomas. Canine histiocytomas

The classification system used to grade mast
should be considered benign, and most
cell tumors in dogs is unreliable in horses
resolve spontaneously within 2-3 mo
because of the variable histologic appearwithout treatment. Surgical excision is ance of tumors i11 this species. Alopecia and
optional once the diagnosis is established
ulceration are variable features.

(which can often be made via cytology).

A variant of cutaneous mast cell tumor is

In goats and cattle, histiocytomas are
seen in newborn foals, in which tl1e lesions
extremely rare and behave the san1e as
may become generalized but regress over
those in dogs. Histiocytomas have also been
tune, suggesting an equine equivalent of
reported in young cats; however, they most
urticaria pigmentosa in people·.

likely represent the histiocytic form of mast

Conventional therapy for equine
cell tumor ill cats.

metastatic mast cell cancer is suboptnnal.

Cutaneous histiocytosis is associated

Excision is the treatment of choice;
with development of numerous plaques and
however, lesions have been reported to
nodules involving the dermis or subcutanemetastasize occasionally. Affordable ous fat. It is rare ill dogs and can develop at
protein tyrosine kinase inhibitors or "small
any age but is most common in yow1g
molecule" drugs such as masitinib mesylate
adults. Chinese Shar Pei, Collies, Border
and toceranib phosphate that selectively

Collies, Shetland Sheepdogs, Briards,
target mutated fo1ms of tl1e c-Kit tyrosille

Bernese Mountaill Dogs, Golden Retrievers,
kinase receptors may become available in
and Gem1an Shepherds may be predisthe future.

posed. Shai"Pei have excessive ski11 folding

In pigs and cattle, mast cell tumors are
and severe cutaneous mucinosis due to an
rare. In pigs, most appear as discrete,
accumulation of dermal hyaluronan, a
solitary, cutaneous nodules. Most are
protein associated with angiogenesis and
benign but disseminated, and leukemic
tumor cell motility. The nodules and plaques
variants do occur. In cattle, most are
tend to wax and wane, and tl1e extremities
malignant and characterized by multiple
and trunk are nwolved most commonly.

cutaneous nodules often accompanied by

Lesions also occur on the face and nasal

TUMORS OF THE SKIN AND SOFT TISSUES

967
plan um, and swelling of the nares may
spleen, and bone marrow. The disease may
cause difficulty breathing. Lesions are
be episodic in its clinical presentation, but it
nonprmitic, and larger lesions may ulcerate.

is progressive and eventually fatal.

Cutaneous histiocytosis seldom involves

Malignant histiocytosis is seen in male
internal organs, but its diffuse nature and

Bernese Mountain Dogs ( mean age at onset
the unsightly appearance often force the

7 yr) and, less frequently, in other canine
owner to consider eutl1anasia. Various
breeds. The lungs, lymph nodes, and liver

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fonns of therapy have been tried, including
are the most common organs affected, and
systemic glucocorticoids and a combination the disease tends to spare the skin. Grossly, of glucocorticoids and chemotherapy and
the lesions appear as large, solitary, finn
more recently in combination with
masses that may cause pleural effusion or
masitinib and other tyrosine kinase
efface large portions of affected internal
inhibitors. Leflunomide without steroids
organs. The disorder is rapidly progressive
has been used as well as azathioprine and
and does not wax and wane as does
cyclosporine. Response is variable; the
systemic histiocytosis. Few dogs survive
lesions in some dogs respond rapidly and

>6mo.

pern1anently, whereas in others, lesions are

Vatious chemotherapeutic regimens
either transiently improved or unchanged.

mentioned above have been used to treat

The histiocytoses of Bernese
both fonns; hopefully, masitinib and other

Mountain Dogs are systemic, familial
tyrosine kinase inl1ibitors used in combinadisorders of unknown etiology with two tion with vincristine or other combinations
manifestations: a more indolent and
of antineoplastic drugs will be of benefit.

generally cutaneous form known as

Bovine thyrnosin fraction 5 may help induce
systemic histiocytosis and a more
remissions, especially in the systemic fonn.

aggressive fonn in which skin lesions are

However, both fonns of the disease are
rare, known as malignant histiocytosis.

ultin1ately fatal.

Malignant histiocytosis has been infrequently identified in other canine breeds. In systemic histiocytosis, males (mean age at

Transmissible Venereal Tumors
onset 4 yr) are affected more often than

See also CANINE TRANSMISSIBLE VENEREAL TUMOR, females. There are multiple cutaneous
p 1408. These can also develop initially on
nodules, papules, and plaques involving the
haired skin due to inoculation via cutaneous
skin ( especially of the scrotum), nasal
injuries.

mucosa, and eyelids. The lesions are poorly
circumscribed and variably alopecic and
may be ulcerated; they develop in waves

TUMORS OF MELANOCYTIC
and slowly regress, only to recur several

ORIGIN
months later. The clinical disease tends to
become more severe with each new wave of

These tumors are most common in dogs,
eruptions. Although the skin is the primary
gray horses, and miniature pigs; uncorrm10n
target organ, lesions may also develop in
in goats and cattle; and rare in cats and
other organs, including lymph nodes,
sheep. The temlinology used to describe
melanocytic lesions in veterinary medicine
is different from that used in human
dennatology. In animals, the tern1s
melanocytoma and malignant melanoma
are used to describe benign and malignant
melanocytic proliferations, respectively. In
people, a benign melanocytic proliferation

( whether congenital or acquired) is called a
nevus, and the tenn melanoma by definition
refers to a malignancy (ie, in people, there
are no benign melanomas). In addition,
although solar injury is a common cause
of melanocytic tumors in people, actinic
damage is seldom associated with
development of analogous tumors in
domestic animals.

Malignant histiocytosis and pleural effusion

Dogs: Mela1.1ocytomas of the skin are
in thorax of a dog. Courtesy of Dr. Alice Villalobos.

diagnosed much more frequently than

968

TUMORS OF THE SKIN AND SOFT TISSUES
malignant melanomas. They most comcomplete excision with adequate margins monly develop on the head and forelimbs
and an acceptable postsurgical cosmetic
in middle-aged or older dogs. There may
appearance and survival. Lesions at rostral
be a predilection for males. Miniature and
locations on the maxilla or mandible

Standard Schnauzers, Doberman Pinschers,
allowed the best survival times of 10.9 mo

Golden Retrievers, hish Setters, and Vizslas
in one study. Melanomas are generally
are the breeds in which these tumors are
considered insensitive to radiation

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most commonly recognized. They can
therapy, and there is no established
appear as macules or patches; as papules
chemotherapeutic protocol shown to
or plaques; or as elevated, occasionally
be highly effective. Survival times range
pedunculated masses. Most have a
from 1 -36 mo, indicating that individual
pigmented surface. Although generally
variations in host defense mechanisms
solitary, lesions may be multiple, especially
and aggressiveness of the tumor may play
in the breeds at risk. These tumors are
a role in establishing a prognosis. The
benign, and complete excision is curative.

nuclear protein Ki67 has been established

Malignant melanomas most commonly
as a highly sensitive and specific immunodevelop in dogs somewhat older than histochemical marker for predicting the
those that develop melanocytomas.

outcome of oral malignant melanoma,

Miniature and Standard Schnauzers and
with indices >19.5 corresponding to lower

Scottish Terriers are most at risk. The
survival times. A mitotic index of >4/10
mucocutaneousjunctions of the lips, in
high-power field and a nuclear atypia
the oral cavity (seep 366), and in the
score of >30% also indicate poor survival
nail beds are the most common sites of
times. In one study of 117 dogs with digit
development. Malignant melanomas of
masses, 24 had melanoma and a median
haired skin are rare, and most arise on the
survival time of 12 mo, with 42% alive at
ventral abdomen and the scrotum. Males

1 yr and 13% alive at 2 yr.

are affected more commonly than females.

A series of novel xenogeneic gene

Most malignant melanomas appear as
therapy vaccinations using plasmid DNA
raised, generally ulcerated nodules that
encoding human tyrosinase can induce an
are variably pigmented depending on
immune response in dogs, resulting in
the melanin content; some malignant
antibody and cytotoxic T-cell responses
melanomas are amelanotic. When present
that may shrink their melanomas. A canine
on the mucocutaneous regions of the lip,
melanoma vaccine was shown to have
the tumors may be pedunculated with a
potential therapeutic value for dogs as an
papillated surface; when present in the nail adjuvant therapy for completely removed bed, they appear as swellings of the digit,
oral melanoma and for some advanced
often with Joss of the nail and destruction
malignant melanoma cases in clinical trials
of underlying bone, mimicking osteomyeliin the New York area. It was conditionally tis. Whenever a toe is festering in an older
licensed in the USA in 2007; however, no
dog, radiographs and a deep punch biopsy
benefit was found in a study that followed
that includes bone are indicated for

23 vaccinated dogs and 17 nonvaccinated
diagnosis. Canine malignant melanomas
dogs in Michigan. A clinical trial using
are locally aggressive and have a high
masitinib in combination with the canine
potential for metastasis; however, there
melanoma vaccine in dogs with melanomas
is considerable variability in reported
expressing mutated c-Kit and another
survival times. Reported median survival
study that adds doxorubicin for nonmutimes for dogs with oral malignant tated c-Kit are being �valuated for efficacy.

melanomas treated with definitive surgery

Chondroitin sulfate proteoglycan-4 is an
alone are 511 days for WHO stage I disease, immunohistochemical biomarker and a 324 days for stage II, and 336 days for stage potential immunotherapeutic target for III disease. A comprehensive study found
canine malignant melanoma, as in people.

that up to 32% of oral melanocytic tumors
in dogs exhibited less aggressive biologic
behavior, which emphasizes the need to

Cats: Cutaneous melanocytic neoplasms
accurately classify them in clinical trials.

are uncommon and most often identified on

Treatment generally consists of
the head ( especially the pinnae), neck, and
complete excision; however, the infildistal extremities in middle-aged or older trative nature of the tumor may make
cats. An association with the oral cavity and
achieving adequate margins difficult.

subungual regions is less well defined than

When present on the digits, amputation is
in dogs, and a higher percentage are
indicated; when present on the mandible,
malignant. Excision is the treatment
a hemimandibulectomy may allow for
of choice.

TUMORS OF THE SKIN AND SOFT TISSUES

969

Horses: Most melanocytic neoplasms are
pigs and Duroc and Duroc crosses.

in gray horses, in which the coat turns gray

Selective breeding in these strains has

( or white) with age. They are especially
increased the prevalence of tumors. These
common in Lipizzaners, Arabians, and
tumors develop both pre- and postnataJly,

Percherons, and 800/o of gray or white horses anywhere on the body. Generally multiple, of these breeds may be affected. They are
they can appear as pigmented macules or
generaJly recognized in older horses but
patches with smooth borders; as raised,

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usuaJly begin their development when
often ulcerated pigmented lesions; or as
animals are 3-4 yr old. The perineum and
deeper, slightly raised, blue masses. Deeply
the base of the tail are the most common
invasive melanomas are often associated
sites of development, but these tumors
with metastatic disease. The lymph nodes
may develop in any location, including the
and lungs are the most common sites of
parotid area. The tumors are often multiple
metastasis. Not all of these twnors become
and may appear as coalescent, frequently
invasive, and many undergo spontaneous
pedunculated nodules that often extend
regression associated with an intense
in a linear arrangement up the tail base.

lymphocytic infiltrate. Melanocytic lesions

They increase in size and number over tin1e.

in pigs are not treated; because of the

Although most are benign, invasive variants, heritable nature of the disease, prevention some with metastatic potential, can
by selective breeding is reconunended if
develop. Most are black on cross-section.

lesions are frequently recognized in a herd.

Many gray horses have evidence of lymph
node involvement; however, there is debate

Cattle: Melanocytic neoplasms in cattle
as to whether this represents metastasis or
develop infrequently anywhere on the body.

whether the intranodal melanocytes and

They can be found at any age but are most
melanophages represent a stin1ulation of
commonly recognized in young animals;
extracutaneous melanocytes that are
congenital forms have been recognized.

normally present in the lymph node.

Angus cattle appear to be predisposed. Most

Treatment consists of surgical or cryosurgicommonly, the tun10rs are large nodular cal removal; however, affected horses are
masses, densely pigmented on cut surface,
predisposed to develop additional tumors
and benign. Excision is curative for most;
over time. Little is known about the use of
however, rare malignant variants have been
radiation or chemotherapy for the
recognized with distant metastasis.

treatment of equine melanocytoma or
malignant melanoma. Cimetidine was

Sheep: Melanocytic neoplasms in sheep
reported to be of value in controlling
are most common in middle-aged or older
recurrence, but followup studies did not
animals but have been recognized in
find benefit. Electrochemotherapy or
neonates. They are most common in
intralesional chemotherapy with cisplatin

Suffolks and Angoras, in which they appear
or carboplatin after surgical debulking may
as multiple, densely pigmented dermal or
be of benefit in the treatment oflarge or
subcutaneous masses. They should be
inoperable masses. Recurrent tumors do
considered malignant; metastasis is
not develop resistance to cisplatin, and they
common.

can be treated a second time, sometimes
with good results.

Goats: Melanocytic tumors in goats are

Melanocytic neoplasms ofnongray
rare. They are most common in middle-aged
horses are rare tumors usually found on the
or older animals and possibly in Angoras.

trunk and extremities of young ( often <2 yr

There may be a site predilection for the
old) horses. They may represent expansion
coronary band and udder. Lesions are seen
of a congenital lesion. Masses characteristias solitary or multiple masses with variable caJly appear as solitary nodules. Most are
pigmentation on cut surface. Most tend to
benign; however, congenital malignant
grow rapidly, and metastasis is common.

melanomas may infrequently develop. Such
tumors are invasive, with little metastatic

METASTATIC TUMORS
potential. Surgical excision or cryosurgery
is the treatment of choice. If the tun10rs are

The spread of a prin1ary neoplasm to the
benign and surgically extirpated, the
skin is unusual in domestic animals. It is
prognosis is excellent. For invasive tumors,
occasionaJly identified in dogs; less
the prognosis is guarded.

commonly in cats; and rarely in horses,
cows, sheep, goats, and pigs. Although

Pigs: Melanocytic neoplasms of pigs are
all malignant neoplasms are capable
seen as congenital lesions and sporadicaJly
of secondary cutaneous involvement,
in adults of the Sinclair (Hormel) miniature
metastatic potential is greatest in man1mary

970

TUMORS OF THE SKIN AND SOFT TISSUES
gland adenocarcinomas, squamous cell
features of a metastatic site. This is because
carcinomas, transitional cell carcinomas,
only a small population of cells in the
transmissible venereal tumors, pulmonary
primary tumor have the potential for
adenocarcinornas, and angiosarcomas.

metastasis, and these cells may have

Although appearance is variable, the lesions
different microscopic features. In cats,
most commonly are multiple, ulcerated
pulmonary adenocarcinomas appear to
papulonodules. Early cutaneous metastasis
preferentially metastasize to the distal

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is characterized by aggregates of neoplastic
extremities, and when carcinomas are
cells within superficial and deep dem1al
diagnosed on multiple feet, radiographic
vessels. As these lesions evolve, they
examination for a primary lung tumor
extend into the dermis and are associated
should be performed. Cutaneous metastawith effacement of adnexa. Generally, it sis is usually a feature of aggressive tumors
is difficult to distinguish the prinlary
and is associated with a guarded to poor
neoplasm based on the morphologic
prognosis.

ACANTHOSIS NIGRICANS

Acanthosis nigricans is a clinical reaction in
not necessarily present in both the axillary
dogs characterized by axillary and inguinal
and inguinal region, nor are they necessarily
hyperpign1entation, lichenification, and
symmetric. In primaiy acanthosis nig1icans,
alopecia.

secondary inflammatory lesions (ie,
lichenification) most commonly develop

Etiology and Clinical Findings: Acanas a result of confom1ational friction.

thosis nigricans is a disorder of hyperpig

Postinflan1matory hyperpigmentation is
mentation. There is no sex predilection.

triggered by inflai11mation and/or friction.

Primary acanthosis nigricans is a genoder

Lesions can develop into severe areas of
matosis that can occur in many breeds but
hyperpign1entation, with marked lichenifiparticularly Dachshunds. Clinical signs are cation, hair loss, and seborrhea. Often,
usually present by 1 yr of age in th.is breed.

these areas are odiferous and may be

Secondary acanthosis nigricans or
painful. The edges of these lesions are often
postinflamrnatory hyperpigmentation can
e1ythematous; this is a sign of secondary
occur in any breed of dog and at any age; it
bacterial and/or yeast pyoderma. With time,
is most common in breeds predisposed to
lesions may spread to the ventral neck,
conditions that result in inflammation of the
groin, abdomen, perinewn, hocks,
axillary or inguinal region due to conformaperiocular ai·ea, and pinnae. Prnritus is tional abnormalities, obesity, endocrinopavariable and is usually the result of thies ( eg, hypothyroidism; hyperadrenocor secondary microbial overgrowth (staphyloticisrn, sex hormone abnormalities), axillary coccal or Malassezia dermatitis) or and inguinal prnritus associated with atopic
prnritus from the underlying disease.

dem1atitis, food allergy, contact dermatitis,
primary disorders of keratinization, and

Diagnosis: The physical findings
skin infections ( eg, staphylococcal
compatible with a clinical diagnosis of
pyodem1a, Malassezia dennatitis).

prinlary acanthosis nigricans are not

Clinical signs start with increased
difficult to recognize. Postinflanlffiatory
pign1entation in the axillary and/or inguinal
hyperpigrnentation is a clinical sign of an
region. In primary acanthosis nigricans,
underlying disease and should be aggresthe hyperpigmentation is initially diffuse sively evaluated through a careful history
and noninflammatory. It tends to develop
and physical exainination to identify the
unifo1mly in the affected areas. In
underlying trigger. Skin scrapings should be
secondary acanthosis nigricans, the
perfonned to exclude demodicosis, and
distribution is patchy and often starts with
impression smears should be performed to
a lacey appearance. It may not develop in
confinn suspected bacterial and Malasse
all areas at the same time. Inflan1mation is
zia infections. Postinilainmat01y inflanm1amild but becomes more severe with time.

tion associated with endocrinopathies is not

Lesions of postsecondary inflanimation are
prnritic, and testing for thyroid and adrenal

EOSINOPHILIC GRANULOMA COMPLEX

971 ·
disease may be useful in older dogs;
alternate days; melatonin, 2 mg/day/dog,
endocrine skin diseases are not pruritic

SC, for 3-5 days, then weekly or monthly
unless accompartied by secondary skin
as needed. The concurrent treatment
infections. Intradermal skin testing and/or
of secondary bacterial or Malassezia
a food trial may be necessary. Skin biopsies
infections is helpful and is required before
are usually not necessary to confirm prin1ary systemic glucocorticoids are administered; disease and are usually not helpful in identiantimicrobial therapy is compatible VetBooks.ir
fication of underlying disease associated
with the other therapies. Antiseborrheic
with secondary disease, with the possible
sha.I11poos are often beneficial for removing
exception of primary seborrhea. In some
excess oil and odor but must be used
cases, skin biopsy can identify secondary
frequently (ie, 2-3 times/wk).

bacterial infections not previously

In postinflai11matory hyperpigmentarecognized. The presence of such infection, most of the lesions will resolve after tions is common; secondary infections are
identification and correction of the
underdiagnosed in this condition. In most
underlying cause. Some residual lacey
cases, it is useful to treat the secondary
hyperpigmentation may remain. Treatment
bacterial and/or Malassezia infections
of secondary bacterial and yeast ove1°
before proceeding with other diagnostic
growth is critical. If the dog has not been
tests.

previously treated for a staphylococcal
bacterial infection of the skin, therapy with

Treatment: Primaiy acanthosis nigricans
narrow-spectrw11 drugs based on culture
in Dachshunds is not curable. In some
and susceptibility and/or use of topical
dogs, lesions do not progress beyond a
chlorhexidine spray or baths is recomcosmetic problem. If infla.I11mation is mended. Culture is recommended to
present, early cases may respond to
minimize development of methicillinai1timicrobial sha.I11poo therapy and local resistant staphylococci. Yeast infections
topical glucocorticoids, eg, tria.I11cinolone
may be successfully treated with concuracetate spray or betamethasone valerate rent oral itraconazole or ketoconazole
ointment. As lesions progress, more

(5-10 mg/kg). Affected dogs benefit greatly
aggressive systemic therapy may be useful.

from appropriate antin1icrobial therapy and

The following systemic therapies have been
antisebo.rrheic sha.I11poos (2-3 times/wk). If
used, alone or in combination, with varying
the lesions are caused by friction, emoldegrees of success: vitan1in E, 200 IU, PO, lients may be beneficial.

bid, for 2---3 mo; systemic glucocorticoids,

Clinical signs resolve slowly, possibly

1 mg/kg/day, PO, for 7-10 days, then on
over months.

EOSINOPHILIC GRANULOMA COMPLEX

The cause of this group of diseases that

Eosinophilic Ulcer: This wellaffects cats, dogs, and horses is primarily an circW11scribed, erythematous, ulcerative
underlying hypersensitivity reaction. This is
lesion, often neither painful nor pruritic, is
particularly true in cats and horses. Insect,
usually found on the upper lip. Some ai·e assoenvironmental, and dietary hypersensitiviciated with a hypersensitivity to flea bites.

ties have been documented in cats, while

Although reported to occur, progression to
insect hypersensitivity has been seen in
squa.I11ous cell carcinoma is extremely rare.

some equine cases and in a smaller nw11ber

Histology shows an ulcerative dermatitis,
of cartine cases. Genetic predisposition and
with a cellular infiltrate of eosinophils,
bacterial infections have also been noted as
neutrophils, plasma cells, and mononuclear
causes in cats. In all species, idiopathic
cells predominating. Mild to moderate
cases exist.

fibroplasia is common. Peripheral eosinophilia is not as common as in the eosinophilic CATS
plaque or the linear granuloma. Occasional
cases due to pyodem1a or den11atophytes

In cats, three disease entities have been
have been reported; thus, a fungal culture of
grouped in the complex.

the surrounding hairs is recommended.

972

EOSINOPHILIC GRANULOMA COMPLEX

Eosinophilic Plaque: This well

Progestational dmgs, such as megestrol
circwnscribed, erythematous, raised lesion
acetate or medroxyprogesterone acetate,
is most commonly found in the medial thigh
have also been effective; however, they are
and abdominal regions; it is extremely
not recommended because of their
pmritic. Regional lymphadenopathy can be
potential adverse effects.

seen. Histology shows a diffuse eosinophilic
dermatitis with marked epidermal inter- and

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intracellular edema and vesicles containing

DOGS
eosinophils. Mast cells may also be present
in the dermis. Peripheral eosinophilia is

In dogs, the lesions reported as eosinophilic
conunon.

granulomas histologically resemble the
eosinophilic granuloma of cats, with marked

Eosinophilic Granuloma: These
collagen degeneration sun-ounded by a
typically raised, well-circwnscribed,
granulomatous and eosinophilic infiltrate.

yellowish to pink lesions may be found

These lesions may be seen as ulcerated or
anywhere on the body but are most
vegetative masses in tl1e oral cavity or, less
conunon on the caudal thighs and in the oral commonly, as plaques, nodules, or papules cavity. When these lesions develop on the
on the lips and other areas of the body. Any
head, face, bridge of the nose, pinnae, or
breed may be affected, but Siberian Huskies
pads of the feet, mosquito bites may be the
and Cavalier King Charles Spaniels may be
inciting cause. The caudal thigh lesions are
at greater risk.

usually distinctly linear. Histologically, a

Most lesions respond to c01ticosteroids,
granulomatous inflammatory response
and therapy is usually oral prednisone or
surrounds collagen fibers. Tissue and
prednisolone (0.5-2 mg/kg/day initially,
peripheral eosinophilia are marked when
tapenng the dosage throughout 20-30 days).

the lesions are in the mouth but vary when

Lesions recur in some dogs, in which case
lesions are on the skin.

low-dose, every-other -day corticosteroid
therapy is indicated.

Treatment: Hypersensitivity disorders

Canine eosinophilic furunculosis is a

(allergy to fleas, food, or inhalants) should
closely related disease. It has been reported
be investigated by instituting strict flea
in many breeds but typically is seen in
c_ontrol, testing for environmental allergens
long-nosed large breeds or curious small

(mtradennal or in vitro), and conducting
breeds ( eg, terriers) with potential access to
dietary elimination trials. Hyposensitizawasps, bees, ants, spiders, etc. It is thus felt tion, continued insect control, and dietary
to be due to arthropod bites or stings.

management should be used when

Consistent with this, the disease may be
appropriate. Antibiotic therapy (amoxicilvery rapid in onset, leading to nasal/muzzle lin-clavulanate, cephalosporins, or
swelling, exudation, and pain. Large,
fluoroquinolones) should be t1ied empiriswollen erythematous lesions on the muzzle cally, especially in refractory cases. If no
are the most common lesions, but in some
underlying cause can be detennined and the dogs similar lesions may be seen on the condition is refractory, corticosteroids, such head, periocularly and around the pinna.

as methylprednisolone acetate ( 4 mg/kg, IM, lnlpression smears often show eosinophils.

once every 2 wk for 2 -3 iI\jections ), oral

Although diagnosis is usually done on a
prednisolone (2-4 mg/kg/day), or oral
clinical basis, histologic confirmation will
triamcinolone (0.8 mg/kg/day), can be tried.

show lesions similar to that of the canine

Oral corticosteroids should be tapered to
eosinophilic granuloma but with more
alternate days ( or to every tl1ird day in the
eosinophilic infiltration into the epidermis
case of triamcinolone) and dosages reduced and follicular wall, a fumnculosis, and when used for long-te1m management.

fewer areas of eosinophilic debris-coated

Long-acting iI\jectable methylprednisolone
collagen. Treatment is as described for
acetate should not be used more often than
feline eosinophilic granulorna.

every 12 wk because of the potential to
induce hyperadrenocorticism and/or

HORSES
diabetes mellitus. Cyclosporine (7 mg/kg/day)

has been used successfully in the eosino

In horses, the disease also has been termed
philic granuloma and plaque, less so in the
equine eosinophilic granuloma with
lip ulcer. This may require laboratory
collagen degeneration, nodular necrobiosis
monitoring ( at least twice yearly) for
of collagen, and collagenolytic granuloma.

metabolic (eg, renal) changes, although

The lesions are nodular, nonulcerative, and
internal organ dysfunction is relatively rare.

nonpruritic. They often a.re found in the

MISCELLANEOUS SYSTEMIC DERMATOSES

973
saddle, central truncal, and lateral cervical
roid ir\jections. Mineralized lesions often
areas and may have a gray-white central
require excision. Triamcinolone acetonide
core. Older lesions may become mineral

(3-5 mg/lesion) or methylprednisolone
ized. Both insect bites and trauma have
acetate (5-10 mg/lesion) is effective. No
been suggested as causes, although the
more than a total of 20 mg trian1cinolone
occasional onset during winter in cold
acetonide should be administered
climates and in noncontact saddle or tack
sublesionally at any one time because of the

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areas suggests multifactorial causes.

potential to induce lanlinitis. Horses with

Histology reveals multifocal areas of
multiple lesions may be treated with oral
collagen fibers surrounded by granulomaprednisone or prednisolone at 1.1 mg/kg/day, tous inflammation containing eosinophils.

for 2 -3 wk. ln horses with recurrent lesions,

Thus, histologically, this lesion is similar to
intradennal allergy testing, particularly
eosinophilic granuloma of cats and dogs.

with insect antigens, is recommended.

Solitary lesions may be treated with

Hyposensitization and insect control
surgical excision or sublesional corticoste-
can be palliative in some cases.

HYGROMA

A hygroma is a false bursa that develops
over pressure points is in1perative to
over bony prominences and pressure points,
prevent further trauma. Surgical drainage,
especially in large breeds of dogs. Repeated
flushing, and placement of Penrose drains
traun1a from lying on hard surfaces
are indicated for chronic hygromas. Small
produces an inflammatory response,
lesions can be treated with laser therapy.

which results in a dense-walled, fluid-filled

Areas with severe ulceration may require
cavity. A soft, fluctuant, fluid-filled, painless
extensive drainage, extirpation, or skin
swelling develops over pressure points,
grafting procedures. Use of intrahygromal
especially the olecranon. If longstanding,
corticosteroids is not recommended. Severe
severe inflan11.11ation may develop, and
lesions can develop into decubital ulcers.

ulceration, infection, abscesses, granulo

Hygromas can become complicated with
mas, and fistulas may occur. The bursa
comedones and furunculosis. Furthermore,
contains a clear, yellow to red fluid.

some dogs develop follicular cysts or

If diagnosed early and if still small,
calcinosis cutis circumscripta at these sites.

hygromas can be managed medically via

A skin biopsy of atypical lesions or lesions
aseptic needle aspiration, followed by
that do not respond to conservative medical
con-ective housing. Soft bedding or padding
therapy is recommended.

MISCELLANEOUS SYSTEMIC DERMATOSES

A number of systemic diseases produce
mentioned briefly below and are also
various lesions in the skin. Usually, the
described in the chapters on the specific
lesions are noninflammatory, and alopecia is disorders.

common. ln some instances, the cutaneous

Dermatosis may be associated with
changes are characteristic of the particular
nutritional deficiency, especially of proteins,
disease. Often, however, the de1matosis is
fats, minerals, some vitamins, and trace
not obviously associated with the underelements. However, this is uncommon in lying condition and must be carefully
dogs and cats fed modem, balanced diets.

differentiated from primary skin disorders.

Siberian Huskies, and occasionally other

Some of these secondary dennatoses are
breeds, may develop a disease similar to

974

MISCELLANEOUS SYSTEMIC DERMATOSES
parakeratosis in pigs and require addiseen. Intact female dogs with hom1onal tional zinc in their diet ( elemental zinc at
in1balances are usually pruritic and have

2-3 mg/kg/day). Zinc-responsive dermaa papular eruption, manmmry tissue toses also have been reported in cattle,
enlargement, and frequent estrous cycles.

sheep, goats, and llamas and may be

The skin lesions of both disorders may begin
associated with either a higher individual
in the ingu.inal or flank region and progress

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requirement or a dietary deficiency. The
cranially. De1matosis due to neutering is not
latter may be precipitated by oversupplecommon in dogs and cats; when it does mentation of calcium. A zinc-responsive
occm, it is generally nonpruritic, witl1 mild
dermatosis has also been reported in a
alopecia in the perineal or ingu.inal areas.

dingo and a red wolf.

Dermatoses have been seen in hypotl1y

Dermatitis is sometimes seen in associaroidism (seep 553). The skin lesions are tion with disorders of internal organs,
characterized by diminished hair growth
such as tl1e liver, kidneys, or pancreas.

and bilaterally symmetric alopecia. The skin

Hepatic parenchyrnal dysfunction has
is dry, scaly, thickened, and sometimes cool
been associated witl1 superficial necrolytic
to tl1e touch. Pyoderma and seborrhea may
dermatitis (hepatocutaneous syndrome,
occur. The margins of the pinna may
diabetic dem1atosis) in old dogs and rarely
develop excess scale. In rare cases,
in cats. This has been associated witl1
cutaneous myxedema develops.

hypoaminoacidemia. The cutaneous lesions

Faulty production of hypophyseal
include erythema, crusting, oozing, and
hormones may rarely cause dermatoses.

alopecia of the face, genitals, and distal

Hypopituitarism is characterized by
extrem.ities, as well as hyperkeratosis and
alopecia, especially in the axillary regions
ulceration of the footpads. The skin disease
and on the lateral thorax and abdomen.

may precede the onset of signs of tl1e

Hyperadrenocorticism also is manifest by
internal disease. H.istopathologic findings
skin changes such as hyperpigmentation,
are diagnostic and include superficial
alopecia, seborrhea, calcinosis cutis, and
perivascular to lichenoid dem1atitis, with
secondary pyoderrna. In cats, the skin
marked diffuse parakeratotic hyperkeratosis becomes extremely friable. In diabetes and striking inter- and intracellular edema
mellitus, pruritus and secondary infection
lim.ited to the upper half of the epidermis.

sometimes occur, especially in cats with

Hyperglucagonem.ia has also been
generalized Malassezia sp infection.

docw11ented in dogs with th.is syndrome;

The can.ine nasal m.ite (Pneumonys
however, dogs tend to have hepatic
soides caninum, seep 1480) is a parasite
parenchyrnal dysfunction more conu11only
fow1d in the nasal cavity and sinuses of the
tl1an glucagonomas. In dogs, therapy relies
dog. P caninum infection in dogs causes
on IV or oral ammo acid treatment or
nonspecific clinical signs of the upper
smgical removal of the glucagonoma. Skin
respiratory tract, such as sneezing, reverse
fragility syndrome ( excessive skin fiiability)

sneezing, rhinitis, in1paired scenting ability,
in cats has been seen in association with
and pawing at the muzzle.

pancreatic or hepatic neoplasia, hepatic

Rarely, underlying neurologic disorders,
lipidosis, or adrenal dysfunction. Pancreatic
especially in dogs, may manifest as
neoplasia has also been associated with
cutaneous lesions. These include sensory
crusting of the footpads ancl alopecia in cats.

neuropathies in English Pointers and

A generalized nodular dermatofibrosis

Longhaired Dachshunds, cauda equina
syndrome in Geiman Shepherds, and
syndrome, pseudorabies, neoplasia of
occasionally other breeds, associated with
peripheral ne1ves, and �yringomyelia and/or
renal cystadenomas, cystadenocarcinomas,

Chiari-like malfo1111ation of Cavalier King
or renal epithelial cysts, has been reported.

Charles Spaniels. Clinical signs generally

H.istopathologic exan1.ination of the skin
include pruritus and/or scratching
nodules reveals dense collagen fibrosis.

( sometimes "air scratching" in some cases Poisoning by thallitm1 sulfate (rat
of syiingomelia/Chiaii-like malfmmation)

poisons, seep 3165), ergot (seep 3012), but also manifest as pain in the cauda
mercury (seep 3080), and iodides may
equina syndrome and self-mutilation in
cause various skin changes. Hyperkeratosis
the sensory neuropath.ies.

in cattle can be caused by chlorinated

Treatment of all the above conditions
naphtl1alene toxicity.

depends on a specific etiologic diagnosis.

In dogs, dermatosis can develop as a result Once th.is is established a11d ma11aged, the of endocrine dysfunction (see THE ENDOCRINE
skin lesions usually need only syi11ptomatic

SYSTEM, p 538 et seq). ln males with Sertoli
cai·e ( eg, control of scratching) until they
cell tw11ors, bilateral alopecia and occasional resolve with resolution of the prin1ary pruritus with a papular eruption may be
disease.

PARAKERATOSIS

975

NASAL DERMATOSES OF DOGS

(Collie nose, Nasal solar dermatitis)

Nasal dermatoses of dogs may be caused

AUTOIMMUNE SKIN DISORDERS, p 827.) A sudden

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by many diseases. Lesions may affect the
onset of nasal swelling, erythema, and
haired bridge of the muzzle, the planum
exudation is often eosinophilic furunculonasale, or both. In pyoderma, dermatophysis; this is thought to be caused by an tosis, and demodicosis, the haired portions
arthropod sting or bite. The protozoal
of the muzzle are affected. In systemic lupus disease leishma.niasis may cause depigerythematosus or pemphigus, the whole mentation of the nasal planun1.

muzzle is often crusted (with occasional

Treatment depends on the cause. Diagexudation of serum) or ulcerated. In nostic tests should include skin scrapings,
systemic and discoid lupus, and occasionbacterial and fungal cultures, and biopsies ally in pemphigus and cutaneous lymfor both histopathology and immunologic phoma, the plan um nasale is depigmented,
testing, although such testing is not used as
erythematous, and eventually may ulcerate.

often as in the past because of the increase in

The normal "cobblestone" appearance of
veterinary dem1atopathologists who may be
the nasal plan um is effaced.

able to make the diagnosis based on histo

Nasal dennatosis due to solar radiation
pathology alone. If systemic lupus erythemaprobably is not as conunon as previously tosus is considered, blood for an antinuclear
thought and may often be a misdiagnosis for antibody test should be obtained.

the lupus variants. In true nasal solar

If the diagnosis is nasal solar dermatitis,
dennatitis, the nonpigmented areas of the
a topical c01ticosteroid lotion (betamethaplan um nasale are affected first, and sone vale rate, 0.1 %) may help relieve
occasionally the bridge of the nose may
inflanunation. Exposure to sunlight must be
become inflamed and sometimes ulcerated.

severely ctutailed. Topical sunscreens may

The lesions are worse in the sununer,
be effective but need to be applied at least
although lupus and pemphigus may also
twice daily. Treatment for eosinophilic
show this seasonal variation.

furunculosis is systemic corticosteroids,

Any of the diseases listed above may
prednisone or prednisolone at 1 mg/kg, bid,
affect the periocular areas. (See also
for 1 wk, after which the dosage should be

SYSTE�nc LUPUS ERYTIIEMATOSUS, p 829, and
gradually decreased over the course of 1 mo.

PARAKERATOSIS

Parakeratosis is a nutritional deficiency
weaned pigs has further reduced the
disease of6- to 16-wk-old pigs characterlikelihood of the disease.

ized by lesions of the superficial layers of

Signs are limited to the skin, although
the epidermis. It is a metabolic disturbance
mild lethargy, anorexia, and growth
resulting from a deficiency of zinc (see also
depression may be seen in severe cases;
p 2337) or inadequate absorption of zinc
there is little if any pruritus. The
due to an excess of calcium, phytates,
outstanding lesions are symmetrically
or other chelating agents in the diet.

distributed areas of excessive and

Predisposing factors include rapid growth,
abnormal keratinization of the epidermis
deficiency of essential fatty acids, or
with the formation of horny scale and
malabsorption due to GI diseases.

fissures. Brown spots or papules are first

Parakeratosis is unlikely in commercial
seen on the ventrolateral areas of the
swine unless errors have been made in diet
abdomen and inner thigh, pastern,
formulation, but it may be seen in backyard fetlock, hock, and tail regions. These pigs. The widespread use of high zinc levels lesions coalesce to involve larger areas in feed to prevent enteric disease in
until the entire body may be covered. The

976

PARAKERATOSIS
scale is horny, dry, and usually easily

Highly satisfactory results can be
removed. Occasionally, secondary
obtained by adjusting the intake of calcium
infection of the cracks and fissures causes or zinc, or both. Nursery pig diets should them to fill with dark, sticky exudate and
contain 0.8%--0.85% calcium ( with standarddebris, which may resemble exudative ized total tract digestible phosphorus of
epidermitis (seep 860); however, this

0.4%-0.45%) and 100 mg/kg of zinc, assuming
usually occurs in younger piglets. Chronic daily feed intake of 280-500 g. Grower diets VetBooks.ir
sarcoptic mange and deficiencies of B
should contain 0.6%--0.65% calcium and
vitamins or iodine must also be consid60 ppm zinc, whereas finisher diets should ered in the differential diagnosis. Clinical
contain 0.45o/<r-0.5% calciw11 and 50 ppm
signs, skin biopsy, and low serum levels of zinc. Sow and boar diets should contain 0.9%
zinc and alkaline phosphatase help
calcium and 150 ppm zinc. Correction of the
confirm the diagnosis.

deficiency results in rapid recovery.

PHOTOSENSITIZATION

Photosensitization occms when skin
react with a photodynan1ic a.gent. These

( especially areas exposed to light and
high-energy molecules initiate reactions
lacking significant protective hair, wool, or
with substrate molecules of the skin,
pigmentation) becomes more susceptible to ca.using the release of free radicals that in ultraviolet light because of the presence of
twn result in increased pennea.bility of
photodynanuc agents. Photosensitization
outer cell and lysosomal membranes.

differs from sunbmn and photodennatitis,

Damage to outer cell membranes allows for
because both of these conditions result in
leakage of cellular potassiun1 and cytoplaspathologic skin changes without the nuc extrusion. Lysosomal membrane
presence of a photodynamic agent.

damage releases lytic enzyn1es into the cell.

In photosensitization, W1Stable, lugh

This can lead to skin ulceration, necrosis,
energy molecules a.re formed when photons
and edema. The time interval between
exposme to the photodynarnic agent and the
onset of clinical signs depends on the type of
agent, its dose, and the exposme to sW1light.

Photosensitization is typically classified
according to the source of the photodynamic agent. These categories include primary (type I) photosensitivity, aberrant
endogenous pigment synthesis (type II)

photosensitivity, and hepatogenous

( secondary, type III) photosensitivity. A
foW'th category termed idiopathic (type IV)

photosensitivity has been described.

A wide range of chenucals, including
some that are fungal and bacterial in origin,
may a.ct as photosensitizing agents.

However, most compounds that are
in1portant causes of photosensitivity in
veterinary medicine are plant-derived.

Photosensitiza.tion occurs worldwide and
can affect any species but is most corrunonly
seen in cattle, sheep, goats, and horses.

Primary Photosensitization: Primary
photosensitiza.tion occurs when the

Photosensitization, causing cracking and
photodynamic agent is either ingested,
peeling of the skin, in an adult horse. Courtesy
irtjected, or absorbed through the skin. The
of Dr. Stephen White.

a.gent enters the systenuc circulation in its

PHOTOSENSITIZATION

977 .

native fom1, where it results in skin cell

Thus, when it reaches the skin, it can absorb
membrane damage after the anin1al is
and release light energy, initiating a photoexposed to ultraviolet light. Examples of toxic reaction.

primary photosensitizing agents include

Phylloerythrin has been incriminated
hypericin (from Hypericum pe1foratum
as the phototoxic agent in the following

[St. John's wort]) and fagopyrin (from
conditions: common bile duct occlusion;

Fagopyrum esculentum [buckwheat]).

facial eczema (seep 3015); lupinosis (see VetBooks.ir

Plants in the families Umbelliferae and
p 3018); congenital photosensitivity of

Rutaceae contain photoactive furocou

Southdown and Corriedale sheep (see
maiins (psoralens ), which cause photosenp 978); and poisoning by numerous sitization in livestock and poultry. Ammi
plants, including Ttibulis te1-restris
majus (bishop's weed) and Cymopte1-us

(puncture vine), Lippia rehmanni,
watsonii (spring parsley) have produced

Lantana camara, several Panicum spp photosensitization in cattle and sheep,

(kleingrass, broomcorn millet, witch
respectively. Ingestion of A majus and
grass), Cynodon dactylon, Myoporum

A visnaga seeds has produced severe
laetum (ngaio), andNarthecium
photosensitization in poultry. Species of
ossifragum (bog asphodel).

Trifolium, Medicago (clovers and alfalfa),

Photosensitization also has been reported

Erodium, Polygonum, and Brassica have in anin1als that have liver damage associbeen inc1irninated as prin1ary photosensitizated with various poisonings: pyn-olizidine ing agents. Many other plants have been
alkaloid ( eg, Senecio spp, Cynoglossum suspected, but the toxins responsible have
spp, Heliotropiiim spp, Echium spp [see not been identified ( eg, Cynodon dactylon
p 978]), cyanobactelia (Microcystis spp,

[Bermudagrass]). Additionally, coal tar

Oscillatoria spp ), Nolina spp (bunch derivatives such as polycyclic ai·omatic
grass), Agave lechuguilla (lechuguilla),
hydrocarbons, tetracyclines, and some

Holocalyx glaziovii, Kochia scoparia,
sulfonamides have been reported to cause

Tetradymia spp (horse brush or rabbit
primary photosensitization. Phenothiazine
brush), Bmchiaria brizanlha, Brassica
anthelmintics have been reported to cause
napus, Tlifolium pratense and T hyb1i
primary photosensitivity in cattle, sheep,
dum (red and alsike clover), Medicago
goats, and swine.

saliva, Ranunculus spp, phosphorus, and
carbon tetrachloride. Phylloerythrin is

Aberrant Pigment Metabolism: Type
likely the phototoxic agent in many of these

II photosensitivity due to aberrant pigment
poisonings.

metabolism is known to occur in both cattle
and cats. In this syndrome, the photosensi

Type IV Photosensitivity: Photosensitivtizing porphyrin agents are endogenous ity in which the pathogenesis is unknown or
pigments that arise from inhelited or
the photodynainic agent is not identified is
acquired defective functions of enzyn1es
classified as type IV. One such example
involved in heme synthesis. Bovine
involved a case of primary photosehsitivity
congenital erythropoietic porphyria (see
in cattle presumed to be caused by Thlaspi
p 986) and bovine erythropoietic protopor
arvense (field pennycress), even though
phyria (seep 852) are the most commonly
field pennycress has not been reported to
reported diseases in this category.

cause photosensitization. Outbreaks of
photosensitization have been reported in

Secondary (Hepatogenous) Photo
cattle exposed to water-damaged alfalfa hay,
sensitization: Secondary or type Ill
moldy straw, and foxtail-orchardgrass hay.

photosensitization is by far the most

These cases were suspected to be hepatogfrequent type of photosensitivity observed enous in origin. Ranunculus bulbosus
in livestock. The photosensitizing agent,

(buttercup) has also been presun1ed to be a
phylloerythrin (a porphyrin), accumulates
cause of hepatogenous photosensitization.

in plasma because of impaired hepatobiliary Other plants associated with photosensitizaexcretion. Phylloerythrin is derived from tion include winter wheat ( cattle), Medicago
the breakdown of chlorophyll by microorspp (alfalfa), Brassica spp (mustards), and ganisms present in the GI tract. Phyllo

Kochia scoparia (fireweed). Many of these
erythrin, but not chlorophyll, is normally
plants are believed to be type I photosensiabsorbed into the circulation and is tizers. Forages such as oats, wheat, and red
effectively excreted by the liver into the
clover have been suspected in cases of
bile. Failurn to excrete phylloerythrin due
photosensitization and may be associated
to hepatic dysfunction or bile duct lesions
with specific environmental conditions such
increases the amount in the circulation.

as heavy rainfall.

978

PHOTOSENSITIZATION

Clinical Findings and Lesions: Dem1ato

Treatment: The prognosis for animals
logic signs associated with photosensitivity
with hepatogenous photosensitization and
are similar regardless of the cause.

porphyria is poor; however, the prognosis

Photosensitive animals are photophobic
for animals with primary photosensitization
immediately when exposed to sunlight and
is generally good. Treatment involves
appear agitated and uncomfortable. They
mostly palliative measures. While photosen

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may scratch or rub lightly pigmented,
sitivity continues, animals should be shaded
exposed areas of skin ( eg, ears, eyelids,
fully or, preferably, housed and allowed to
muzzle). Lesions initially appear in
graze only during darkness. The severe
white-haired, nonpigmented, or hairless
stress of photosensitization and extensive
areas such as the nose and udder. However,
skin necrosis can be highly debilitating and
severe phylloerythrinemia and bright
increase mortality. Corticosteroids, given
sunlight can induce typical skin lesions, even parenterally in the early stages, may be in black-coated animals. Erythema develops
helpful. Secondary skin infections and
rapidly and is soon followed by edema. If
suppurations should be treated with basic
exposure to light stops at this stage, the
wound management techniques, and fly
lesions soon resolve. When exposure is
strike prevented. The skin lesions heal
prolonged, lesions may progress to include
remarkably well, even after extensive
vesicle and bulla fonnation, serum
necrosis.

exudation, ulceration, scab fom1ation, and
skin necrosis. The final stage involves skin
sloughing. In cattle, and especially in deer,

CONGENITAL
exposure of the tongue while licking may

PHOTOSENSITIZATION IN SHEEP
result in glossitis, characterized by
ulceration and deep necrosis. Irrespective

Southdown and Corriedale sheep may
of coat color, cattle may develop epiphora,
inherit a hepatobiliary incompetence that
corneal edema, and blindness.

results in photosensitization.

Depending on the initial cause of the

In mutant Southdown sheep, the inherited
accumulation of the photosensitizing agent,
defect involves hepatic uptake ofunconjuother clinical signs may be seen. For gated bilirubin and organic anions. Plasma
example, if the photosensitivity is hepatoglevels of unconjugated bilirubin are enous, icterus may be present. In bovine
consistently increased and, because bilirubin
congenital erythropoietic porphyria,
is partially excreted, icterus is not a clinical
discoloration of dentin, bone (and other
feature. Phylloerythrin is less effectively
tissues), and urine often accompanies the
excreted, and affected lambs become
skin lesions. Photodermatitis is the sole
photosensitized when they first begin grazing
manifestation seen in bovine erythropoietic
green plant material. Unless chlorophyll
protoporphyria.

is excluded from the diet, or exposure to
sunlight is prevented, lesions and stress of

Diagnosis: Diagnosis of photosensitizaphotosensitization result in death within tion is based on clinical signs, evidence or
weeks. Mutant sheep so protected develop
history of exposure to photosensitizing
progressive renal lesions in which radial,
agents or hepatotoxins, and characteristic
fibrous bands fom1 in the medulla, along
lesions. Photophobia in combination with
with increasing nun1bers of cystic tubules.

erythema and edema of hairless, nonpig

The changes ultimately result in renal
mented areas of skin is strongly suggestive
insufficiency and death. The liver is small,
of the disease. The period from exposure
with pericanalicular deposits of lipofuscin.

to photodynan1ic or hepatotoxic agents to

This semilethal trait appears to be inherited
the onset of clinical signs can vary from
as a simple recessive trait. Elinlination of
several hours up to 10 days. Clinical signs;
carriers is the only feasible control.

increased serum biochemical measure

In mutant Corriedale sheep, the
ments, including sorbitol dehydrogenase,
hepatocellular incompetence involves
ganuna glutamyltransferase, alkaline
excretion of conjugated bilirubin and other
phosphatase, and direct bilirubin; and gross
conjugated metabolites. There is no obvious
or histologic signs of liver disease help
icterus, but phylloerythri.n excretion is
support a diagnosis of hepatogenous photosufficiently impaired to produce photosensisensitization. A preswnptive diagnosis of tization. Hepatic pigmentation is obvious
porphyria is based on signalment (sex,
grossly. Brown-black, melanin-like pigment
breed, age) combined with clinical signs,
is confined to centrilobular parenchyn1al
and a definitive diagnosis can be made by
cells. This condition is transmitted as an
measuring porphyrin levels in blood, feces,
autosomal recessive trait. Control is by
and urine.

detection and removal of carriers.

SADDLE SORES

979

PITYRIASIS ROSEA IN PIGS

(Porcine juvenile pustular psoriasiform dermatitis)

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Pityriasis rosea is a sporadic disease of
unlrnown etiology of pigs, usually 8---14 wk
old, but occasionally as young as 2 wk and
very rarely in pigs as old as 10 mo. One or
more pigs in a litter may be affected. The
disease is mild, but transient anorexia and
diarrhea have been reported. The initial
skin lesions are cha.racte1ized by small
erythematous papules, which rapidly
expand to fom1 a ring ( collarette) with
distinct raised and reddened borders.

The lesions enlarge at their periphery, and
adjacent lesions may coalesce. The center
of the lesion is flat and covered with a

Pityriasis rosea lesions, hindlimb, pig. Note
bran-like scale overlaying normal skin.

the small, ring-like early stage lesions and the
older, expanding larger rings healing centrally

The lesions are found predominantly on
as they expand. Courtesy of Dr. Ranald D. A. Cameron.

the ventral abdomen and inner thighs but
occasionally may be seen over the back,
neck, and legs. Characteristically, there is
no pruritus, and recovery is spontaneous in
not resemble pityriasis rosea in people

6---8 wk Treatment is generally considered
clinically or pathologically.

unnecessary. Diagnosis can usually be

Lesions appear to be more extensive in
made from the characteristic lesions, but
pigs reared in high stocking densities with
laboratory tests, culture, and biopsy may be
high an1bient temperatures and high
used to differentiate it from dem1atomycohumidity. Under these conditions, secondsis, exudative epidermitis, dermatosis ary bacterial infection ( eg, Staphylococcus
vegetans, and swinepox.

hyicus) is common. Treatment is of little

The disease is considered to be partially
value and does not affect the course of the
hereditary, pigs of the Landrace breed being
disease; however, treatment aimed at
most commonly affected, but the mode of
controlling secondary infections may be
inheritance is uncertain. The disease does
warranted.

SADDLE SORES

(Collar galls)

The area of riding horses that is under

Affected areas show hai.r loss and are
saddle, or the shoulder area of those driven
swollen, warm, and painful. The serous or
in harness, is frequently the site of injuries
purulent exudate dries and fonns crusts.

to the skin and deeper soft and bony tissues.

Advanced lesions are termed "galls." When

Clinical signs vary according to the depth of
the skin and underlying tissues are more
injury and the complications caused by
severely dan1aged, abscesses may develop.

secondary infection. Emaciated horses are

These are characterized as warm, fluctuatat increased risk Sores affecting only the ing, painful swellings from which purulent
skin are characterized by inflammatory
and serosanguineous fluid can be aspirated.

changes that range from e1ythematous to

Severe damage to the skin and subcutis
papular, vesicular, pustular, and finally
or deeper tissues results in dry or moist
necrotic. Frequently, the condition starts as
necrosis. Chronic saddle sores are
an acute inflammation of the hai.r follicles
characterized by a deep folliculitis/
and progresses to a purulent folliculitis.

furunculosis (boils) with fibrosis or a

980

SADDLE SORES
localized indurative and proliferative
antibiotics. Hematomas should be aspirated
dermatitis. Lesions are usually caused by
or incised. Necrotic tissue should be
poorly fitting tack.

removed surgically. In severe folliculitis and

Identification and elimination of the
furunculosis, antibiotics, ideally chosen on
offending portion of tack is more important
the basis of culture and sensitivity, are
than any other treatment. Excoriations and
always indicated. Scars and/or leukotrichia

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inflammation of the skin of the saddle and

( white hairs) are cmmnon sequelae of
harness regions are treated as any other
healed areas. Recurrence of hematomas,
dermatosis. Absolute rest of the affected
seromas, and/or sloughing skin upon initial
parts is necessary. During the early or acute
saddlings of a young Quarter horse or Paint
stages, astringent packs (Burow solution)

horse should elicit suspicion of the genetic
are indicated. Chronic lesions and those
disease hereditary equine dennal asthenia.

superficially infected may be treated by

A simple DNA test, performed on the hair
warm applications and topical or systemic
bulbs of the tail, will confirm this diagnosis.

SEBORRHEA

Primary idiopathic seborrhea is a skin
underlying causes are endocrinopathies and
disease seen in dogs and rarely in cats. It is
allergies. The goal is to identify and treat
characterized by a defect in keratinization
any underlying cause of the seboIThea.

or comification that results in increased

Palliative therapies that do not comproscale formation, occasionally excessive mise the diagnostic evaluation should be
greasiness of the skin and hair coat, and
instituted concurrently to provide as much
often secondary inflanunation and
inunediate relief as possible.

infection. Secondary seborrhea, in which a

Underlying diseases may present with
primary underlying disease causes sinillar
seboIThea as the primary clinical problem.

clinical signs, is more common than primary The signalment (age, breed, sex) and hisseborrhea. Seborrhea in horses is usually tory may provide clues in diagnosing the
secondary to either pemphigus foliaceus or
underlying cause. Environmental allergies
equine sarcoidosis ( chronic granulomatous

( atopic dermatitis) are more likely to be the
disease).

underlying cause if age at onset is <5 yr,
whereas an endocrinopathy or neoplasia

Etiology, Clinical Findings, and

( especially cutaneous lymphoma) is more

Diagnosis� Primary seborrhea is an
likely if the seboIThea begins in middle-aged
inherited skin disorder characterized by
or older animals.

faulty keratinization or comification of the

The degree of pruritus should also be
epidermis, hair follicle epithelium, or claws.

noted. If pruritus is minimal, endocrinopa

It is seen more frequently in American
thies, other internal diseases, or certain

Cocker Spaniels, English Springer Spaniels,
diseases limited to the skin ( eg, demodi

Basset Hounds, West Highland White
cosis or sebaceous adenitis) should be

Terriers, Dachshunds, Labrador and Golden
excluded. If pruritus is significant, allergies

Retrievers, and Geiman Shepherds. There is
and pruritic ectoparasitic diseases ( eg,
usually a familial history of seborrhea,
scabies, fleas) should be considered. The
suggesting genetic factors. The disease
presence of pruritus does not exclude
begins at a young age ( usually < 18---24 mo)

nonpruritic disease as the underlying
and typically progresses throughout
cause, because the presence of a pyodenna,
the animal's life. A diagnosis of generalized

Ma.la.ssezia. infection, or inflanunation
primary idiopathic seborrhea should be
from the excess scale can cause significant
reserved for cases in which all possible
pru1itus. However, a lack of pruritus helps
underlying causes have been excluded.

to exclude allergies, scabies, and other

Most seborrheic animals have secondaiy
pruritic diseases as the underlying cause.

seborrhea, in which a primary underlying

Other important considerations include
disease predisposes to excessive scaling,
the presence of polyuria, polydipsia,
crusting, or oiliness, often accompanied by
or polyphagia; heat-seeking behavior;
superficial pyoderma, Ma.la.ssezia (yeast)

abnormal estrous cycles; occurrence of pyoinfection, and alopecia. The most conunon demrn; the influence of seasonality; diet;

SEBORRHEA

981
response to previous medications
minirnwn database. Exrunples of diagnostic

(including corticosteroids, antibiotics,
clues include increased serun1 alkaline
antifungals, antihistanunes, or topical
phosphatase ( which may suggest hypertreatments); zoonosis or contagion; and the adrenocorticism or previous steroid
environment. The duration and severity of
therapy), cholesterol (which may suggest
disease as well as level of owner frustration
hypothyroidism), blood glucose (which

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are important factors in determining the
suggests diabetes mellitus), and BUN or
aggressiveness of the diagnostic plan.

creatinine ( which may suggest renal

A thorough physical exanunation,
disease).

including internal organ systems and a
comprehensive dermatologic examination,

Treatment: Palliative therapy is needed
is the first step in identifying the underlying
to keep the animal comfortable while the
cause. The dermatologic exan1ination
underlying cause is identified and secondshould docwnent the type and distribution ary skin diseases are corrected. For
of the lesions; the presence of alopecia; and
treatment of pyoderma, an antibiotic with
the degree of odor, scale, oiliness, and
known sensitivity against Staphylococcus
texture of the skin and hair coat. The
pseudinle7medius should be appropriate.

presence of follicular papules, pustules,

Exrunples of such antibiotics are amoxicilcrusts, and epidem1al collarettes usually lin-clavulanate 13. 75 mg/kg bid, cephalexin
indicates the existence of a superficial

20-30 mg/kg bid-tid, cefpodoxin1e 5-10
pyodenna. Hyperpigmentation indicates a
mg/kg/day, lincomycin 20 mg/kg bid, ciprochronic skin irritation (such as pruritus, floxacin 30 mg/kg/day, enrofloxacin 5-10
infection, or inflan1111ation ), and lichenificamg/kg/day, marbofloxacin 3-6 mg/kg/day, tion indicates chronic pruritus. Yeast
azithromycin 10 mg/kg/day, 4 days/wk,

(Malassezia spp) infection should always
doxycycline 5 mg/kg bid, trimethoprin1-sulfa
be considered when evaluating a seborrheic

30 mg/kg bid, clindamycin 11 mg/kg bid, and
animal.

chloramphenicol 50 mg/kg tid in dogs and

Secondary infection plays a significant

12.5-20 mg/kg bid in cats. Because most
role in most cases of seborrhea. The sebwn
staphylococcal infections in seborrhea
and keratinization abnom1alities that are
cases are superficial pyodermas, they
col11ll1on in seborrhea frequently provide
should be treated for a minimwn of 4 wk.

ideal conditions for bacterial and yeast

With the increase in methicillin-resistant
infections. The self-traun1a that occurs in

S pseudintermedius, S aureus, and
prwitic animals increases tl1e likelihood of

S schleiferi, it is now strongly recoma secondary infection. Often, coagulasemended to perform a bacterial culture of positive Staphylococcus spp or Malassezia any animal with pyoderma that does not
spp are present. The infections add to the
begin to respond to an antibiotic after 3-4
pruritus and are usually responsible for a
wk. Epidermal collarettes may be cultured
significant amount of the inflan1rnation,
using a dry sterile culturette rolled across
papules, crusts, alopecia, and scales.

the collarettes. Although metnicillin-resistant

One of the first diagnostic steps is to

S pseudinte7medius infections are more
obtain superficial cytology of the affected
difficult to treat, they are not more virulent
areas to identify the quantity and type of
or visually striking than those due to
bacteria or yeast present. If nwnerous cocci
methicillin-susceptible S pseudinte1me
and neutrophils are present, pyoderma is
dius. Previous (ie, within the past year)

likely. In addition to systemic therapy,
hospitalization, surgery, or previous
topical shampoos will aid in tl1e treatment
antibiotic treatment are all possible risk
of secondary infections. In a seborrheic dog
factors for development of methicillinwith pruritus, the infection may cause all or resistant S pseudinte1medius infections.

most of the pruritus. Instead of considering

Malassezia may be treated systemically
allergies as the underlying disease in tl1ese
with an azole such as ketoconazole or
dogs, nonprw·itic diseases ( eg, endofluconazole (5 mg/kg/day, for4 wk). In crinopathies) may be uncovered by
addition to addressing any secondary
addressing the infections.

infections, antipruritic therapy and

After the infections have been addressed,
shrunpoo therapy are usually needed to help
other diagnostic tests that should be
control the seborrhea and speed tl1e return
considered include multiple deep skin
of tl1e skin to a normal state. Shan1poo
scrapings, dermatophyte culture, in1prestherapy can decrease the nun1ber of sion smears, trichograms, and flea combing.

bacteria and yeast on the skin surface, the

If these ru·e negative or nom1al, a skin
amount of scale and sebwn present, and the
biopsy, CBC, serum biochemical profile, and level of pruritus; it also helps normalize the complete urinalysis will complete the
epidermal turnover rate.

982

SEBORRHEA

In the past, seborrhea has been classified

Animals with mild scaling and no oiliness
as seborrhea sicca ( dry seborrhea),
need mild shampoos that are gentle,
seborrhea oleosa ( oily seborrhea), or
cleansing, hypoallergenic, or moisturizing.

seborrheic dermatitis (inflanunatory

These shampoos are indicated for animals
seborrhea). Most seborrheic animals have
that have mild seborrheic changes, are
varying degrees of all three of these
initated by medicated shan1poos, or bathed

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classifications of seborrhea.

too often. These products often contain

Most products contained in shampoos
emollient oils, lanolin, lactic acid, urea,
can be classified based on their effects as
glycerin, or fatty acids. Emollient sprays or
keratolytic, keratoplastic, emollient,

1inses are often used in conjunction with
antipruritic, or antimicrobial. Keratolytic
these shan1poos.

products include sulfi.u-, salicylic acid, tar,

Aninials with moderate to marked scaling
selenium sulfide, propylene glycol, fatty
and mild to marked oiliness should be
acids, and benzoyl peroxide. They remove
bathed with shan1poos that contain sulfur
stratw11 cornew11 cells by causing cellular
and salicylic acid. Both agents are
damage that results in ballooning and
keratolytic, keratoplastic, antibacterial, and
sloughing of the surface keratinocytes. This
antipruritic. In addition, sulfi.U' is antiparareduces the scale and makes the skin feel sitic and antifungal. Some of these
softer. Shampoos containing keratolytic
shampoos also contain ingredients that are
products frequently exacerbate scaling
antibacterial, antifungal, and moisturizing,
during the first 14 days of treatment because which can help control secondary the sloughed scales get caught in the hair
pyoderma, Malassezia spp, and excessive
coat. The scales will be removed by
scaling. Shampoos that contain ethyl lactate
continued bathing, but owners should be
lower the cutaneous pH (which has a
warned that the scaling often worsens
bacteriostatic or bactericidal action by
initially. Keratoplastic products help
inhibiting bacterial lipases), nom1alize
nonnalize keratinization and reduce scale
keratinization, solubilize fats, and decrease
fonnation by slowing down epidennal basal
sebaceous secretions. These actions also
cell mitosis. Tar, sulfur, salicylic acid, and
result in potent antibacterial activity.

selenium suliide are exan1ples of kerato

In the past, dogs with moderate to severe
plastic agents. Emollients ( eg, lactic acid,
scaling and moderate oiliness were often
soclium lactate, lanolin, and nw11erous oils,
treated with tar-containing shampoos.

such as corn, coconut, peanut, and

However, because tar shampoos usually
cottonseed) are indicated for any scaling
have an unpleasant odor and can be
dermatosis, because they reduce transepiinitating, along with poor owner complidermal water loss. They are most effective ance, they usually are no longer recomafter the skin has been rehydrated and are mended.

excellent adjunct products after shampoo

In anin1als with severe oiliness and
ing. Antibacterial agents include benzoyl
minimal scaling, profound odor, erythema,
peroxide, chlorhexidine, ethyl lactate,
inflammation, and a secondary generalized
tris-EDTA, and triclosan. Antifungal
pyode1ma or Malassezia dermatitis are
ingredients include chlorhexidine, sulfi.U',
often present. Shampoos that contain
ketoconazole, and miconazole. Boric and
benzoyl peroxide provide strong degreasing
acetic acids are also used as"topical
actions along with potent antibacterial and
antimicrobials.

follicular flushing activities. Because

It is important to know how individual
benzoyl peroxide shan1poos are such strong
shampoo ingredients act, as well as any
degreasing agents, they can be irritating and
additive or synergistic effects they have,
drying. Other antibacterial shampoos a.re
because most shampoos are a combination
better suited in animals that have superficial
of products. The selection of approp1iate
pyodenna without significant oiliness.

antiseborrheic shampoo therapy is based on These shampoos usually contain 2%-4%
hair coat and skin scaling and oiliness, of
chlorhexidine ( often in assoication with
which there are four general presentations:

tris-EDTA) or ethyl lactate. The follicular

1) mild scaling and no oiliness, 2) moderate
flushing action of benzoyl peroxide makes it
to marked scaling and mild oiliness (the
helpful for animals witl1 numerous
most common), 3) moderate to marked
comedones or with demodicosis. Benzoyl
scaling and moderate oiliness, 4) mild
peroxide gels (5%) are good choices when
scaling and marked oiliness. These
antibacterial, degreasing, or follicular
categories are intended to guide the type of
flushing actions are desired for focal areas,
shampoo therapy necessary; however, all
such as in localized dernodicosis, canine
factors for each individual animal should
acne, or Schnauzer cornedone syndrome.

be considered.

However, these gels also may be irritating.

METABOLIC DISORDERS

INTRODUCTION 984

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Metabolic Storage Disorders and Inborn Errors of Metabolism 984

Production-related Metabolic Disorders 985

CONGENITAL ERYTHROPOIETIC PORPHYRIA 986

CUTANEOUS MANIFESTATIONS OF MULTISYSTEMIC

AND METABOLIC DEFECTS 850 (rTG)

DISORDERS OF CALCIUM METABOLISM 987

Hypercalcemia in Dogs and Cats 562 (END)

Hypercalcemia in Horses 570 (END)

Hypocalcemia in Dogs and Cats 570 (END)

Hypocalcemic Disorders in Horses 572 (END)

Hypocalcemic Tetany in Horses 987

Parturient Paresis in Cows 988

Parturient Paresis in Sheep and Goats 991

Puerperal Hypocalcemia in Small Animals 992

Hypocalcemia as an Electrolyte Disturbance in Small Animals 995

DISORDERS OF MAGNESIUM METABOLISM 995

Hypermagnesemia 996

Hypomagnesemic Tetany in Cattle and Sheep 996

Magnesium as an Equine Dietary Supplement 998

Subclinical Hypomagnesemia in Critically Ill Animals 998

DISORDERS OF PHOSPHORUS METABOLISM 999

Hypophosphatemia 1000

Hyperphosphatemia 1002

Postparturient Hemoglobinuria 1002

DISORDERS OF POTASSIUM METABOLISM 1003

Hypokalemia in Adult Cattle 1004

Hyperkalemia 1005

EQUINE METABOLIC SYNDROME 1006

FATIGUE AND EXERCISE 1008

Fatigue during High-intensity Exercise 1009

Fatigue during Prolonged Exercise 1011

Prevention of Fatigue 1012

FEVER OF UNKNOWN ORIGIN 1015

HEPATIC LIPIDOSIS 1018

Fatty Liver Disease of Cattle 1018

Feline Hepatic Lipidosis 456 (ma)

984

METABOLIC DISORDERS

Hyperlipemia and Hepatic Lipidosis in Large Animals 346 (DIG) Pregnancy Toxemia in Cows 1020

Pregnancy Toxemia in Ewes and Does 1021

KETOSIS IN CATTLE 1024

Subclinical Ketosis 1027

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MALIGNANT HYPERTHERMIA 1027

METABOLIC OSTEODYSTROPHIES 1054 (Mus)

TRANSPORT TETANY IN RUMINANTS 1030

METABOLIC DISORDERS INTRODUCTION

Metabolic diseases may be inherited or

Australian Silky TeITiers and Dalmatians.

acquired, the latter being more common and

Ceroid lipofuscinosis is seen in English
significant. Metabolic diseases are clinically

Setters, Cocker Spaniels, Dachshunds,
important because they affect energy produc

Chihuahuas, Salukis, Border Collies, and
tion or damage tissues c1itical for survival.

domestic cats. Mannosidosis is seen in

Persian and domestic cats. Glycogenosis is
seen in Silky Terriers and in domestic

METABOLIC STORAGE
shorthaired and Norwegian forest cats.

DISORDERS AND INBORN

Globoid cell leukodystrophy (Krabbe

ERRORS OF METABOLISM
disease) is seen in Cairn Terriers, West

Highland White Terriers, Beagles, Bluetick

Storage diseases and inborn eITors of

Hounds, Poodles, and domestic shmtmetabolism are classified as either genetic hai.red cats. Mucopolysaccharidosis type I
or acquired. These diseases are characteris seen in Siamese, Korat, and domestic ized by the accumulation or storage of
shorthaired cats; type IV is seen in Siamese
specific lysosomal enzyme.substrates or
cats. In dogs, mucopolysaccharidosis is
byproducts within cells because of partial
seen in Miniature Pinschers, Plott Hounds,
or complete deficiency of those enzymes.

and mixed-breed dogs and is associated

Although lysosomal storage diseases are
with lameness. Diseases associated with
often widespread throughout the body, the
decreased RBC survival and anemia
majority of clinical signs are due fo the
include pyruvate kinase deficiency in
effects on the CNS.

Basenjis, Beagles, and West Highland

Genetic storage diseases are nan1ed

White and Cairn Terriers; phosphofructokiaccording to the specific metabolic nase deficiency in English Springer and
byproduct that accumulates in the

American Cocker Spaniels; and porphyria
lysosomes. Animals are typically normal at
in Siamese and domestic shorthaired cats.

birth, then manifest clinical signs within

In large animals, a-mannosidosis occurs in
the first weeks to months of life. These

Angus, Murray Grey, Simrnental, Galloway,
diseases are progressive and usually fatal,
and Holstein cattle. 13-Mannosidosis is seen
because specific treatments do not exist. In in Saler cattle and Nubian and Nubian-cross small animals, the gangliosidoses (GM, and goats. Generalized glycogenosis (GMi) is GM;) are seen in Siamese, Korat, and
seen in Holstein cattle and Suffolk sheep.

domestic cats, and in Beagle crosses,

Generalized glycogenosis (GM2) is seen in

German Sho1thaired Pointers, and

Shorthorn and Brahman cattle, and in pigs.

Japanese Spaniels. Sphingomyelinosis is

Globoid cell leukodystrophy is seen in polled
seen in German Shepherds and Poodles

Dorset sheep. Other identified diseases that
and in Siamese and domestic shorthaired
are manifest by neurologic signs and appear
cats. Glucocerebrosidosis is seen in
to be inherited include neuronal lipodystro-

METABOLIC DISORDERS INTRODUCTION

985
phy in Angus and Beefmaster cattle, shaker
production. They are therefore correctly
calf syndrome of homed Hereford cattle,
considered production diseases. However,
maple syrup urine disease of Hereford and
they are also metabolic diseases because
polled Shorthorn cattle, and hereditary
management of the animal is directed at
neuraxial edema of polled and homed
production, which at its peak is beyond

Hereford and Hereford-Friesian cross cattle.

the capacity of that animal's metabolic

There have been no reports of lysosomal
reserves to sustain a particular nutrient at

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storage diseases in horses; however,
physiologic concentrations. For example,
inhe1ited diseases manifest by neurologic
parturient paresis of cows ( see p 988)

signs include inherited myoclonus of
occurs when the mass of calcium in the

Peruvian Paso foals and congenital
mammary secretion is greater than the
encephalomyelopathy in Quarter horses.

cow's diet or its skeletal reserves can

Other inherited diseases that involve
supply. Comparable situations occur with
basic errors of metabolism in various
magnesium and glucose metabolism, and
tissues include goiter of sheep and goats,
with phosphorus in relation to postparturiinherited parakeratosis ( edema disease) ent hemoglobinuria (seep 1002).

of cattle, osteogenesis imperfecta of

Most production-induced metabolic
sheep and cattle, and possibly cardiomydiseases result from a negative balance opathy of cattle, the hypotrichoses, baldy
of a particular nutrient. In some cases,
calves, photosensitization of sheep (see
dietary intake of the nut1ient is rapidly
p 978), dermatosis vegetans and porcine
reduced because of an ongoing, high
stress syndrome (seep 1027) of pigs,
metabolic requirement for that nutrient.

dermatosparaxia and Ehlers-Danlos

Examples include pregnancy toxemia in
syndrome of cattle, hemochromatosis of
ewes (seep 1021), protei n -energy malnut1icattle (seep 349), and Marfan syndrome in tion in beef cattle (seep 2248), fat cow
cattle. Many other inherited defects,
syndrome in dairy cattle (seep 1018), and
especially those based on abnormal
hyperlipemia in ponies (seep 346).

growth of collagen, cartilage, and bone,

Furthennore, some diseases may be precipialso are likely to have basic errors of tated when producers, prirnazily because of
metabolism of structural tissues. Many
economic concerns, are compelled to not
disorders of metabolism have been
supplement the diet of animals that already
described involving dysfunctions of
have a substandard nutritional plane.

the immune system.

Exertional rhabdomyolysis of horses (see

Acquired storage diseases are caused by
p 1178) is az10ther production-induced metaingestion of plants that contain inhibitors bolic disease. In this case, the production
of specific lysosomal catabolic enzymes.

activity ( draft or racing) is maintained by

Chronic ingestion of locoweed plants
and matched to a level of caloric intake.

(Astragalus or Oxytropis spp) results in Management decisions not to work or race
an acquired neurologic storage disease.

these horses without a concomitant

Several toxic components, including locoine, decrease in caloric intake may result in swainsonine n-oxide, and indolizidine
accwnulation of muscle glycogen to
alkaloids, interfere with cx-mannosidase
dangerous levels. Disease results when
activity. Horses are most susceptible to
work is resumed and the production of
intoxication; however, cattle, sheep, and
lactate exceeds its metabolism.

goats can also be affected. (See also p 3103.) The difference between productionrelated metabolic diseases and nutritional PRODUCTION-RELATED
deficiencies is often subtle. Typically,

METABOLIC DISORDERS
nutritional deficiencies are longterm,
steady-state conditions that can be

Although the development of the following
corrected through dietary supplementation.

diseases is largely related to production or

Metabolic diseases are generally acute
management factors, the pathogenesis of
states that dramatically respond to the
each disease is primarily related to
systemic administration of the deficient
alterations in metabolism. In most cases,
nutrient or metabolite, although affected
the basis of disease is not a congenital or
anin1als may require subsequent dietary
inherited error in metabolism, but rather
supplementation to avoid recurrence.

an increased demand for a specific nutrient An in1portant aspect of dealing with that has become deficient under certain
production-induced metabolic diseases
conditions. Diseases such as hypocalceis accurate and rapid diagnosis. Ideally, mia, hypomagnesemia, and hypoglycemia
diagnostic tests can be used to predict the
are augmented by management practices
occurrence of disease before its clinical
directed toward in1proving and increasing
onset.

986

CONGENITAL ERYTHROPOIETIC PORPHYRIA

CONGENITAL ERYTHROPOIETIC PORPHYRIA

(Porphyrinuria, Pink tooth, Osteohemochromatosis)

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Congenital erythropoietic porphyria (CEP)

Heterozygous animals seem to be normal,
is a rare hereditary disease of cattle, pigs,
but homozygous recessive animals are
cats, and people that results from a
affected at birth with reddish brown
significant yet variable decrease in
discoloration of the teeth, bones, and urine
uroporphyrinogen III synthase (UROthat persists for life. The excess copropo1°
synthase) activity. URO-synthetase is the
phyrin I and uroporphyi·in I in the w·ine
fowih enzyme in the heme biosynthesis
colors it an amber or reddish brown. Bones,
pathway, and it nomially converts
wine, and teeth ( especiaJly the deciduous
hydroxymethylbilane to uroporphyrinogen
teeth) fluoresce pink when irradiated with

III. With decreased URO-synthase activity,
near-ultraviolet light. Prolonged exposure to
hydroxymethylbilane accwnulates
sunlight causes typical lesions of photosenp1irnarily in e1ythrons and is nonenzymatisitization with hyperemia, vesicle fonnation, cally converted to uroporphyrinogen I.

and superficial necrosis of unpigmented

Further decarboxylation of uroporphyrinoportions of the skin. Severity of the skin gen I leads to the fonnation of various
lesions depends on the intensity of the solar
porphyrinogen I isomers, with coproporradiation and the extent of cutaneous phyrinogen I occurring as the ftnal product.

pigmentation found in specific families of

Coproporphyrinogen I cannot be further
ani.mals. A normochromic, hemolytic
metabolized to heme and is thus nonphysianemia with macrocytes and microcytes ologic. Porphyrinogen I isomers are
and marked basophilic stippling develops.

pathogenic when they accwnulate in large

Splenornegaly eventually develops. The
amounts and are oxidized to their corretexture of bones is not altered except in sponding porphyrins. Accun1ulation of
cases in which bones have increased
porphyrinogen isomers in bone man-ow
fragility because of a diminished cortex.

erythroid precursors results in cell damage

Affected animals are generally of mediwn
and hemolysis. Porphyrin I isomers are also
to good condition wlless solar injury has
released into circulation and deposited in
occurred. Some animals become progresskin, bone, and other tissues. Cutaneous sively unthri.fty wlless protected from
photosensitivity occurs, because porphyswilight. A similar disease, bovine rins deposited in skin are photocatalytic and
protoporphyria (seep 852), causes
cytotoxic. Preswnably, exposure of skin to
photosensitivity only in Li.mousin cattle
swilight ( and other sources of long-wave
and people. A recent molecular study of
ultraviolet light) leads to phototoxic

CEP in cattle supports the hypothesis that
excitation of isomers, formation of oxygen

CEP is caused by a mutation affecting the
radicals, and subsequent tissue and vessel

URO-synthetase gene; however, additional
damage. Urinary porphyiin excretion is
functional studies are needed to identify
greatly increased (100-1,000 ti.mes normal)

the exact causative mutation.

and prirnatily consists of uroporphyrin I and

In people, a series of porphyrias caused
coproporphyrin I with lesser an1ounts of
by defective functions of enzymes in
other isomers. Although isomer I porphyrins porphyrin-heme biosyntliesis have been predominate, isomer ill porphyrins ai·e also
described and grouped according to their
increased.

presenting signs. These vary broadly and

CEP was first reported in Soutl1 African
may include severe cutaneous lesions on

Shorthorn cattle; however, most cases have
exposed areas of the body, acute photosensince been reported in the Holstein breed. It sitivity reactions, serious liver daniage, and
is inherited as a sin1ple autosomal recessive
acute attacks of neurologic dysfunction.

and is usually confined to herds in which

In animals, the recognized diseases ai·e
inbreeding or close line-breeding is
commonly classified as CEP, congenital
practiced. It has been recognized in the
erythropoietic protoporphyria, or por

USA, Canada, Denmark, Jamaica, England,
phyria. It is likely that aJl of the syndromes

South Africa, Australia, and Argentina. This
described in people also occur in animals
broad geographic distribution suggests that
and that a broader classification could be
the disease likely is found worldwide and
used.

probably affects all meat-producing

Porphyria in swine is rare and incomanimals, especially cattle, swine, and sheep.

pletely described. Affected pigs have

DISORDERS OF CALCIUM METABOLISM

987
discoloration of teeth and excessive
inherited as an autosomal dominant trait
uroporphyrin in urine. In contrast to CEP in

(as in some pig models), whereas in
cattle and people, affected swine are not
people and cattle, the disease is inherited
anemic and do not present with signs of
as an autosomal recessive trait. It is now
photosensitization. The specific genetic
understood that cats with the CEP-like
defect is unknown; therefore, its relevance
phenotype and autosomal dominant

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to CEP in other animals is also unknown.

inheritance actually have feline acute

Nonetheless, the disorder is inherited as
intermittent porphyria and not CEP.

an autosomal dominant trait.

Diagnosis should be based on the

Recently, the first feline model of
excretion of abnom1al uroporphyrins, the
human CEP due to deficient URO-synthase brown discoloration ofthe teeth (which activity was identified by characteristic
fluoresce when irradiated with nearclinical phenotype and confirmed by ultraviolet light), the appearance of
biochemical and molecular genetic
discolored urine, and hemolytic anemia.

studies. In this case, sequencing of the

The recessive genetic character is
cat's URO-synthetase gene revealed two
widely distributed in cattle, but the clinical
homozygous, missense mutations in
condition is comparatively rare. Clinically
exons 3 and 6. This synergistic interaction
normal heterozygotes have lower levels
of two rare amino acid substitutions in the of uroporphyrinogen III cosynthetase URO-synthase polypeptide resulted in the
than do normal animals, but laboratory
feline model of human CEP. Previously,
identification of the carrier state is
cats presenting with brownish discolored
impractical because of the low incidence
teeth that fluoresced pink under UV light
of the disease and is not widely used.

and increased URO and coproporphyrino

Morbidity can be controlled by keeping
gen concentrations were believed to have
affected animals indoors and out of direct

CEP. The disease was also observed to be
sunlight.

DISORDERS OF CALCIUM METABOLISM

HYPOCALCEMIC TETANY
prolonged physical activity ( eg, endurance

IN HORSES
rides) results from sweat loss of calciuo1,
increased calcium binding during hypochlo

(Transport tetany, Lactation tetany,
remic alkalosis, and stress-induced high

Eclampsia)

corticosteroid levels. Corticosteroids inhibit

H
vitanlin D activity, which leads to decreased
ypocalcemic tetany in horses is an uncommon condition associated with acute intestinal absorption and skeletal mobilizadepletion of serun1 ionized calcium and tion of calcium. Stress and lack of calcium
sometimes with alterations in serun1
intake have been associated with transport
concentrations of magnesium and
tetany. Occasionally, hypocalcemic tetany
phosphate. It occurs after prolonged
may be precipitated by hypocalcemia after
physical exertion or transpmt (transport
blister beetle ingestion (seep 3157).

tetany) and in lactating mares (lactation
tetany). Signs are variable and relate to

Clinical Findings: The severity of clinical
neuromuscular hyperirTitability.

signs corresponds with the serun1 concentration of ionized calcium. Increased Etiology: Mechanisms of hypocalcemia
excitability may be the only sign in mild
include decreased absorption from the
cases. Severely affected horses may show
intestines; increased loss of calciwn from
synchronous diaphragmatic flutter (see
the kidneys, sweat, or milk; or inhibition
p 1183), anxious appearance, and signs of
of osteolysis due to alterations in parathytetany, including increased muscle tone, roid hormone, calcitonin, or vitanlin D. In
stiffness of gait, muscle tremors, prolapse of
lactating mares, high milk production and
the third eyelid, inability to chew, trismus,
grazing of lush pastures appear to be
salivation, recun1bency, convulsions, and
predisposing factors. Hypocalcemia after
cardiac arrhythmias. In lactating mares,

988

DISORDERS OF CALCIUM METABOLISM

U" not treated, the disease may take a
rus throughout gestation. In times of
progressive and sometimes fatal course
increased calciun1 demand such as
over 24--48 hr.

lactation, fasting should be avoided and

Differential diagnoses include tetanus,
high-quality forage such as alfalfa or
endotoxemia, colic, exertional rhabdomycalciW11-containi:ng mineral mixes should olysis or other muscle disorder, seizure
be provided. Stress and fasting during

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disorder, laminitis, and botulism.

transport should be minimized. In
endw·ance horses, water and electrolyte

Diagnosis: A tentative diagnosis is based
deficits associated with prolonged exercise
on clinical signs, history, and response to
and sweating may be prevented by
treatment. Definitive diagnosis requires
provision of a sufficient water supply and
demonstration of low serw11 levels of
electrolyte supplementation.

ionized calcium. Most laboratories measure
only total (protein-bound and free) serum
calci w11, which is an acceptable diagnostic

PARTURIENT PARESIS IN COWS
test in most cases. However, discrepancies
may arise in alkalotic and hypoalbw11inemic (Milk fever, Hypocalcemia) horses. Alkalosis increases albumin binding

Parturient paresis is an acute to peracute,
of calcium, which results in a decreased
afeb1ile, flaccid paralysis of mature dairy
concentration of ionized calcium. Thus,
cows that occurs most commonly at or soon
alkalotic horses may have non11al total
after pa.Iturition. It is ma.Jlliest by changes
serw11 calciW11 while exhibiting signs of
in mentation, generalized paresis, and
hypocalcemia. Likewise, hypoalbuminemic
circulatory collapse.

or acidotic horses may have decreased total
serw11 calciw11 without developing signs of

Etiology: Dairy cows will secrete 20-30 g
hypocalcemia. Total serum calcium can be
of calciw11 in the production of colostrwn
adjusted for albumin concentration by the
and milk in the early stages of lactation.

following formula:

This secretion of calciw11 causes serun1
calciw11 levels to decline from a normal of
adjusted Ca2+ = measured Ca2+ - serw11

8.5-10 mg/dL to <7.5 mg/dL. The sudden
albumin concentration+ 3.5
decrease in serw11 calciwn levels causes
hyperexcitability of the nervous system and

Treatment: IV administration of calcium
reduced strength of muscle contractions,
solutions, such as 200/o calcium boroglucoresulting in both tetany and paresis.

nate or solutions recommended for

Parturient paresis may be seen in cows
treatment of peripa.Iturient paresis in cattle,
of a.Jly age but is most common in highusually results in full recovery. These producing dairy cows entering their third
solutions should be administered slowly
or later lactations. Incidence is higher in

( over 20 min) at 250-500 mU500 kg, diluted

Charmel Island breeds.

at least 1:4 in saline or dextrose, and the
cardiovascular response should be closely

Clinical Findings and Diagnosis: Pa.Jtumonitored. An increased intensity of heart rient paresis usually occurs within 72 hr of
sounds is expected. If arrhytlupias or
parturition. It can contribute to dystocia,
bradycardia develop, the IV treatment
uterine prolapse, retained fetal membranes,
should be discontinued immediately. Once
metritis, abomasal displacement, and
the heart rate has returned to normal, the
mastitis.

infusion may be resWlled at a slower rate. If

Parturient paresis has three discernible
the horse does not improve within 1-2 hr of
stages. During stage 1, animals are
the initial infusion, a second dose may be
a.Jllbulatory but show signs of hypersensitivgiven, although laboratory verification of ity and excitability. Cows may be mildly
hypocalcemia is indicated. Some horses
ataxic, have fine tremors over the flanks and
require repeated treatments over several
triceps, and display ea.I· twitching and head
days to recover from hypocalcemic tetany.

bobbing. Cows may appear restless,

Mildly affected horses may recover without
shuffling tlleir rear feet and bellowing. If
specific treatment. If the tetany is associcalciW11 tllerapy is not instituted, cows will ated with physical exertion, incorporating
likely progress to the second, more severe
magnesiw11 into the solution may be
stage.

advisable.

Cows in stage 2 are unable to stand but
can maintain sternal recun1bency. Cows are

Prevention: A balanced feed ration
obtunded, anorectic, a.Jld have a dry muzzle,
should be provided to supply adequate
subnorn1al body temperature, and cold
aJ11ounts and ratios of calciWll and phospho-
extremities. Auscultation reveals tachycardia

DISORDERS OF CALCIUM METABOLISM

989
and decreased intensity of heart soW1ds.

administration of calciwn. Magnesiwn is

Peripheral pulses are weak. Smooth muscle
also necessary for appropriate parathyroid
paralysis leads to GI stasis, which can
hormone (PTH) secretion and activity in
manifest as bloat, failure to defecate, and
response to hypocalcemia. Most products
loss of anal sphincter tone. An inability to
available to veterinarians contain phosphite
urinate may manifest as a distended bladder salts as tl1e source of phosphorus. However, on rectal exanunation. Cows often tuck
phosphorus found in blood and tissues of

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their heads into their flanks, or if the head is
cattle is primarily in the fmm of tl1e
extended, an S -shaped cUIVe to the neck
phosphate anion. Because no patl1way
may be noted.

exists for the conversion of phosphite to the

In stage 3, cows lose consciousness
usable phosphate form, it is unlikely these
progressively to the point of coma. They are
solutions are of any benefit in addressing

Wlable to maintain sternal recW11bency,
hypophosphatemia.

have complete muscle flaccidity, a.re

Calciwn is cardiotoxic; therefore,
unresponsive to stimuli, and can suffer
calciW11-containing solutions should be
severe bloat. As cardiac output worsens,
administered slowly (10--20 min) while
heart rate can approach 120 bpm, and
cardiac auscultation is performed. If severe
peripheral pulses may be undetectable.

dysrhythmias or bradycardia develop,

If untreated, cows in stage 3 may survive
administration should be stopped W1til the
only a few hours.

heart rhythm has returned to normal.

Differential diagnoses include toxic

Endotoxic animals a.re especially prone to
mastitis, toxic metritis, other systemic toxic
dysrhythmias caused by IV calciwn therapy.

conditions, traun1atic ir\jwy ( eg, stifle injW)',

Adnunistration of oral calcium avoids the
coxofemoral luxation, fractured pelvis,
risks of ca.rdiotoxic adverse effects and may
spinal compression), calving paralysis
be useful in mild cases of parturient paresis;
syndrome ( damage to the 16 lwnbar roots
however, it is not reconunended as the sole
of sciatic and obturator nerves), or compartapproach for clinical milk fever cases.

ment syndrome. Some of these diseases, in

Products containing calciW11 chloride are
addition to aspiration pneun1onia, may also
effective but can be caustic to oral and
occur concurrently witl1 parturient paresis
pharyngeal tissues, especially if used
or as complications. (See also p 1188.)

repeatedly. Calcimn propionate in
propylene glycol gel or powdered calciw11

Treatment: Treatment is directed toward
propionate (0.5 kg dissolved in 8-16 L water
restoring normal serun1 calciwn levels as
administered as a drench) is effective, less
soon as possible to avoid muscle and nerve
injurious to tissues, avoids the potential for
damage and recun1bency. Reconunended
metabolic acidosis caused by calciun1
treatment is IV ir\jection of a calciwn
chloride, and supplies the gluconeogenic
gluconate salt, although SC and IP routes
precmsor propionate. Oral administration
are also used. A general rule for dosing is
of 50 g of soluble calcium results in -4 g qf

1 g calcium/45 kg (100 lb) body wt. Most
calcium being absorbed into the circulation.

solutions are available in single-dose,

Regardless of the source of oral calcium,

500-mL bottles that contain 8-11 g of
it is important to note that cows with
calciwn. In large, heavily lactating cows,
hypocalcemia often have poor swallowing
a second bottle given SC may be helpful,
and gag reflexes. Care must be exercised
because it is thought to provide a prolonged
during administration of calciun1-containing
release of calciwn into the circulation. SC
solutions to avoid aspiration pnewnonia.

calcium alone may not be adequately

Gels containing calcium chloride should not
absorbed because of poor peripheral
be adnunistered to cows unable to swallow.

perfusion and should not be the sole route

Hypocalcemic cows typically respond to
of therapy. No matter what route is used,

IV calciwn therapy inunediately. Tremors
strict asepsis should be used to lessen the
are seen as neuromuscular fw1ction returns.

chance of infection at the ir\jection site.

Improved cardiac output results in stronger

Solutions containing formaldehyde or >25 g
heart sounds and decreased heart rate.

dextrose/500 mL are irlitating if given SC.

Return of smooth muscle fwlction results in

Many solutions contain phosphoms and
eructation, defecation, and urination once
magnesiun1 in addition to calcium. Altl10ugh
the cow rises. Approximately 75% of cows
administration of phosphoms and
stand within 2 hr of treatment. Animals not
magnesiwn is not usually necessary in
responding by 4--8 hr should be reevaluated
uncomplicated parturient paresis,
and retreated if necessary. Of cows that
detlimental effects of their use have not
respond initially, 25%---30% relapse witlun
been reported. Magnesium may protect

24-48 hr and require additional therapy.

against myocardial irritation caused by the

Incomplete milking has been advised to

990

DISORDERS OF CALCIUM METABOLISM
reduce the incidence of relapse. Histori

An important strategy to decrease blood
cally, udder inflation has been used to
pH in pe1ipartwient cattle is to reduce tl1e
reduce the secretion of milk and loss of
potassiwn content of the diet. It is essential
calcium; however, the 1isk of introducing
to include com silage as a major portion of
bacteria into the manm1ary gland is high.

the d1y cow's diet, because it tends to have
the lowest content potassiwn of available

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Prevention: Historically, prevention of
forages. Alfalfa is another forage source that
parturient paresis has been approached by
may prove beneficial in maintaining proper
feeding low-calcium diets during the dry
blood pH. ln the past, including alfalfa in a
period. The negative calcium balance
dry cow ration was not considered ideal
results in a minor decline in blood calciw11
because of the high calcium content.

concentrations. This stimulates PTH

However, it has since been detennined that
secretion, which in tum stimulates bone
calcium has little effect on the alkalinity of
resorption and renal production of 1,25
cow's blood. Withholding potassium
diliydroxyvitamin D. Increased 1,25
fertilizers on fields used to grow dry cow
diliydroxyvitanlin D increases bone calciwn forages is another way to decrease potassium release and increases the efficiency of
levels in hay fed to dry cows. Alternatively,
intestinal calcium absorption. Although
readiiy absorbable anions can be added to
mobilization of calcium is enhanced, it is
tl1e diet to increase the total negative charges
now known that feeding low-calcium diets
in the blood, allowing more H+ to exist,
is not as effective as initially believed.

decreasing the pH of the blood. Anionic salts

Furthermore, on most dairy farms today, it
to consider include calciw11 chloride,
is difficult to fonnulate diets low enough in
magnesium chloride, magnesiw11 sulfate,
calciw11 ( <20 g absorbed calcium/cow/day),
calcium sulfate, anunoniw11 sulfate, and
although the use of dietary straw and
anm1onium chloride. Research evaluating
calcium-binding agents such as zeolite or
the acidifying activity of different anionic
vegetable oil may make this approach more
salts has resulted in the following equation
useful.

that describes the ion balance in rations:

Alternative methods to prevent hypocalcemia include delayed or incomplete DCAD =(Na+ + K+)-(CJ- + s-2)

milking after calving, which maintains
pressure within the udder and decreases

The target value for close-up dry cow
milk production; however, this practice may
rations is-15to +15 mEq/100 g d1y matter.

aggravate latent mammary infections and

Sodium and potassium should be provided
increase incidence of mastitis. Prophylactic
as close to the required levels as possible
treatment of susceptible cows at calving

(0.1 % dietary dry matter sodium, and 1 %
may help reduce parturient paresis. Cows
dietary dry matter potassiwn). Chloride
are administered either SC calcium on the
should be added to the ration to offset the
day of calving or oral calcium gels at calving
effects of low levels of potassium on blood
and 12 hr later.

alkalinity. ln general, providing -0.5% less

Most recently, the prevention of
dietary chloride than the concentration of
parturient paresis has been revolutionized
potassiw11 being fed will result in appropriby use of the dietary cation-anion difference ate acidification. Urine pH provides an

(DCAD), a method that decreases the blood
inexpensive and relatively accurate
pH of cows during the late prepartw11 and
estimate of blood pH in dairy cattle. Mean
early postpartwn period. This method is
urine pH ranges from -6-6 .5 are optimal to
more effective and more practical than
manage DCAD and prevent milk fever. Urine
lowering prepartum calcium in the diet. The
should be measured >24 hr after addition of

DCAD approach is based on the finding that
an anionic diet in pre-fresh cows.

most dairy cows are in a state of metabolic

An important drawback to feeding
alkalosis due to the high potassium content
anionic salts is poor palatability, which can
of their diets. This state of metabolic
be overcome by using a mixture of anionic
alkalosis with increased blood pH
salts within a moist, palatable ration such as
predisposes cows to hypocalcemia by
com silage, brewer's grain, distiller's grain,
alte1ing the confonnation of the PTH
or molasses. Although sulfate salts are more
receptor, resulting in tissues less sensitive
palatable than chloride salts, they are less
to PTH. Lack of PTH responsiveness
effective in acidifying the blood. Dietary
prevents effective use of bone calcium,
sulfur should be >0.22"A, dry matter to
prevents activation of osteoclastic bone
support rumen microbial amino acid
resorption, reduces renal reabsorption of
synthesis but <0.4% dry matter to avoid
calcium from the glomerulus, and inhibits
neurologic signs associated with sulfur
renal conversion to its active form.

toxicity. If dry matter intake drops> 1 kg/day

DISORDERS OF CALCIUM METABOLISM

991
in a group of pre-fresh dry cows fed an
of increased calcium requirements, usually
acidifying diet, the dose of anions should be
dw'ing late gestation. This results in a low
decreased to the point that dry matter
serum calciwn concentration, paiticularly
intake is restored.

in anin1als pregnant with multiple fetuses.

Administration of vitamin D3 and its

Some cases are complicated by concurrent
metabolites effectively prevents parturient
pregnancy toxemia. Ewes that are both

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paresis. Large doses of vitamin D (20-30
hypocalcemic and hyperketonemic may not
million U/day), given in the feed for 5---7 days be able to produce endogenous glucose as before parturition, reduces the incidence.

readily as ewes that are only hyperketone

However, if administration is stopped >4
mic, leading to the risk of more severe
days before calving, the cow is more suscepdisease developing when both conditions tible. Dosing for periods longer than those
are present. Partuiient paresis can occur at
recommended should be avoided because
any time from 6 wk before to 10 wk after
of potential toxicity. A single injection (IV or
parturition; however, the greatest demand

SC) of 10 million IU of crystalline vitamin D
for calcium because of mineralization of the
given 8 days before calving is an effective
fetal skeleton occurs 1-3 wk prepartum,
preventive. The dose is repeated if the cow
particulai·Iy when multiple fetuses are
does not calve on the due date. Newer
present in utero. Whenever an abrnpt
compounds used (where available and
decrease in calciwn intake occurs, the body
approved) in lieu of vitamin D and less
requires 24-72 hr to activate the metabolic
likely to cause hypervitaminosis include
machinery necessai-y to mobilize stored

25-hydroxycholecalciferol, 1,25-dihydroxycalciun1. Mobilization of stored calcium can cholecalciferol, and la-hydroxycholecalcifbe inadequate to meet the animal's needs erol. After calving, a diet high in calciwn is
in older ewes and does, in animals with
required. Administe1ing large doses of
chronic calcium deficiency, and when diets
calciwn in gel fonn (PO) is commonly
ai·e calcium deficient. Exainples of forages
practiced. Doses of 150 g of calciun1 gel are
with low calciw11 levels include cereal hays
given 1 day before, the day of, and 1 day
or pasture, poor-quality grassy hays ai1d
after calving.

pasttll'e, and com silage. Most grains also

Use of synthetic bovine PTH may prove to contain little calcium but additionally have be superior to administration of vitamin D
high levels of phosphorns, causing an
metabolites. Vitamin D metabolites enhance inverse calcium:phosphorns ratio, GI calciwn absorption, whereas PTH
increasing dietary risk. Vitamin D deficienenhances GI calcium absorption and cy, which occurs in housed run1inants
stimulates bone resorption. PTH is
during winter months, also depresses
administered either IV 60 hr before
calciun1 absorption from the GI tract.

parturition, or IM 6 days before parturition.

Drawbacks to the use of PTH include

Clinical Findings and Diagnosis: Charincreased labor requirements for adminisacteristically, parturient paresis occurs in tration, as well as the availability of such
outbreaks, with most cases occun'ing in the
compow1ds.

last few weeks of gestation, although it is
not uncommon for individual animals to

PARTURIENT PARESIS IN SHEEP
be affected. Usually, <5% of aitimals ai·e
affected, but severe outbreaks may involve

AND GOATS
up to 300/o of the flock. The onset is sudden

(Milk fever, Hypocalcemia)

and often follows-within 24 hr-an abrnpt
change of feed, a sudden change in weather,

Parturient paresis in pregnant and lactating
or short periods of fasting imposed by
ewes and does is a.disturbance of metabocircwnstances such as shearing or lism characterized by acute-onset hypocaltransportation ( see also p 1030). In early cemia and rapid development of
hypocalcemia in sheep, the most commonly
hyperexcitability and ataxia, progressing to
noted signs are stiff gait, ataxia, salivation,
depression, recumbency, coma, and death.

constipation, and depressed rnmen motility,

Unlike parturient paresis in dairy cattle,
progressing to hyposensitivity, bloat, recumwhich primarily occurs within a few days bency, loss of anal reflex and, if untreated,
of calving, the condition in ewes and does
death. Tachycardia may be present; heart
usually occurs before and less commonly
sounds are quieter than normal. Often when
after parturition. This condition may be
recwnbent, ewes are in a sternal frog-lying
underdiagnosed in some situations.

position, with the hindlegs extended behind.

Goats have a similar presentation, although

Etiology: Paitw·ienl paresis is caused by a muscle tremors are more commonly seen decrease in calcium intake under conditions thai1 in sheep.

992

DISORDERS OF CALCIUM METABOLISM

A working diagnosis is based on the
as well as vitamin D levels, may help to
history and clinical signs. In outbreaks
prevent further cases in pregnant animals.

occurring before parturition, pregnancy

Sudden dietary changes or other stressors
toxemia (seep 1021) is the main differential should be avoided during late gestation, and diagnosis. These diseases also occur
risk factors for pregnancy toxemia
concurrently. A tentative diagnosis of acute
investigated.

hypocalcemia is supported by a dramatic

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and usually lasting response to slow IV

PUERPERAL HYPOCALCEMIA IN
administration of calcium. Diagnosis can
be confirmed by testing serum calcium

SMALL ANIMALS
levels before treatment. Urine ketone or

(Postpartum hypocalcemia, Periparturient
serum [l-hydroxybutyrate levels should
hypocalcemia, Puerperal tetany, Eclampsia)

always be evaluated at the same time.

Hypocalcemia is often classified as total

Puerperal hypocalcem.ia is an acute,
semm calcium levels <2 mmol/L or, if
life-threatening condition usually seen
expressed as ionized calcium, <1.1 mmol/L. at peak lactation, 2-3 wk after whelping.

Normal values are reported as 2.8-3.2

Small-breed bitches with large litters are
mrnol/L for sheep and 2.2-3.05 nrn101/L for
most often affected. Hypocalcemia may also
goats. (To convert from mrnol/L to mg/dL,
occw· during parturition and may precipidivide the value by 0.25.) Animals with low tate dystocia.

serum albumin, such as occurs with

Johne's disease and clinical GI parasitism,

Etiology and Pathogenesis: Hypocalmay have low total serum calcium and cemia most likely results from loss of
normal ionized calcium.

calcium into the milk and from inadequate
dietary calciwn intake. This imbalance

Treatment and Prevention: Treatment
in calcium metabolism occurs because
should be initiated immediately, usually
calcium mobilization from bone into the
administered as calciwn borogluconate IV
serwn pool is insufficient to maintain

(50-150 mL of a 23% solution). Calciumthe efflux of calcium leaving through the containing products that also contain
manunary glands. Heavy lactational
phosphoms and magnesium, as well as
demands from large puppies or a large litter
dextrose, likely have additional therapeutic
are often noted. The incidence is increased
value. Oral or SC administration of a
in small breeds of dogs, although puerperal
calcium solution helps to prevent relapse.

hypocalcemia can occur in any breed,

During treatment, the heart should be
with any size litter, and at any time during
monitored, and therapy slowed or stopped
lactation. Rarely, it occurs during late
if arrhytlm1ias occur. For ease of IV
gestation in bitches. Although uncommon
administration, it may be preferred to
in queens, it may occur during early
increase the volwne of the product by
lactation. In dogs, supplementation
adding 50-150 mL of a 23% calcium
with oral calcium during pregnancy may
borogluconate or gluconate solution to 1 L
predispose to eclarnpsia during peak
of a 5% dextrose solution and administering
lactation, because excessive calcim11
this volume over 10 min. Dietary modificaintake during pregnancy causes downregutions to increase the cal.cium:phosphoms lation of the calcium regulatory system and
ratio (>1.5:1) and ensure total calciwn in the subsequent clinical hypocalcemia when diet meets NRC requirements (see TABLE 1), calciun1 demand is high.

CALCIUM REQUIREMENTS OF A MEAT EWE AND DAIRY DOE

DURING GESTATION AND LACTATION

Calcium Requirements (g/day)

70-kg adult
with twins

Early gestation Late gestation Early lactation Mid lactation Ewe (meat)

6.5

8.8

7.9

6.5

Doe (parlour

6.6

6.6

20.7

21.4
milked)

Adapted, with pennission, from Nutrient Requirements of Small Ruminants, Animal Nutrition Seties, 2007. National Academy of Sciences, National Academy Press, Washington DC.

DISORDERS OF CALCIUM METABOLISM

993

Inadequate production of parathyroid

Clinical Findings: Panting and restlesshormone (PTH) during the hypocalcemic ness are early clinical signs. Mild tremors,
crisis is not responsible for eclampsia in
twitching, muscle spasms, and gait changes
dogs. In dairy cows with a similar condition

( stiffness and ataxia) result from increased

(seep 988), production of PTH is adequate,
neuromuscular excitability. Behavioral
but the pool of osteoclasts for PTH to
changes such as aggression, whining,
stimulate is not. The small osteoclast pool
salivation, pacing, hypersensitivity to

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results from feeding a high level of dietary
stimuli, and disorientation are frequent.

calcium during the nonlactating period,

Severe tremors, tetany, generalized seizure
which suppresses parathyroid gland
activity, and finally coma and deatl1 may be
secretion of PTH and stimulates parafollicuseen. Hyperthermia may occur in severe lar C-cell secretion of calcitonin. Hypocalcecases. Prolonged seizure activity may cause mia at partwition interferes with the release cerebral edema. Tachycardia, hypertl1em1ia, of acetylcholine at the neuromuscular
polyuria, polydipsia, and vomiting are
junction, which is nonnally mediated by
sometimes seen. Historically, the bitch has
extracellular calciwn entering presynaptic
been otherwise healthy and the neonates
nerve terminals through voltage-gated
have been thriving.

calcium channels and triggering the fusion

Although hypocalcemia usually occurs
of acetylcholine-filled synaptic vesicles with postpartwn, clinical signs can appear the presynaptic nerve terminus. The paresis
prepartum or at parturition. Mild hypocalceseen in cattle, rather than the tetany seen in mia (serum calcium concentration >7 mg/dL
dogs, is probably the result of a combination but below the normal reference range) may of factors. Cows often have concurrent mild
contribute to ineffective myometrial
hypermagnesemia. Magnesium is a
contractions and slow the progression of
calcium-channel antagonist and plays a key
labor without causing any other clinical
role in modulating any activity governed by
signs.

intracellular calcium fluxes. Cows also have

Heavy panting may produce a respiratory
increased volatile fatty acids ( which are
alkalosis. Ionized calciwn is the physiologiinhibitory at neuromuscular synapses), and cally available fraction; it is affected by
cows have a higher threshold potential at
protein concentration, acid-base status
new·omuscularjw1ctions than do dogs.

(aJkalosis favors protein binding of serum

In dogs with hypocalcemia, unlike cows,
calciwn and will decrease blood levels of
excitation-secretion coupling is maintained
the biologically important ionized calcium,
at the neuromuscular junction. The low
thus exacerbating hypocalcemia), and other
concentration of calcium in the extracelluelectrolyte imbalances. Thus, the severity of lar fluid has an excitatory effect on nerve
clinical signs may not correlate with total
and muscle cells, because it lowers the
calcium concentration.

threshold potential (voltage level at which
sodiun1 channels become activated) so it is

Diagnosis: Diagnosis is often made from
closer to the resting membrane potential.

the signalment, history, clinical signs, and

With hypocalcemia, sodiun1 channels
response to treatinent. A pretreatinent total
become activated ( opened) by very little
serum calciun1 concentration <7 mg/dL
increase in membrane potential from their

( <6 mg/dL in cats) confirms the diagnosis.

normal, negative level. Therefore, the nerve

(IV therapy with calcium is often started,
fiber becomes highly excitable, sometimes
however, before serum calcium concenti·adischarging repetitively without provocation is detennined.) A serum chemistry tion rather than remaining in the resting
profile is useful to exclude concurrent
state. The probable way that calcium ions
hypoglycemia and other electi·olyte
affect the sodium channels are that calciw11
imbalances. Prolongation of the QT interval
ions bind to the exterior surfaces of sodium
and ventiicular premature contractions may
channels. The positive charge of these
be seen on the ECG.

calciun1 ions alters the electlical state of the

Differential diagnoses include other
sodiun1 channel protein, thus altering the
causes of seizures such as hypoglycemia,
voltage level required to open the sodium
toxicoses, and primary neurologic disorders
channel. Because of the loss of stabilizing
such as idiopathic epilepsy or meningoenmembrane-bound calciwn ions, nerve cephalitis. Other causes of irritability and
membranes become more permeable to
hypertl1ermia such as metritis and mastitis
sodium ions and require a stimulus of lesser
should also be excluded. If the parathyroid
magnitude to depolarize. Tetany occurs as a
glands are functioning nom1ally, serum PTH
result of spontaneous repetitive firing
will be increased in the face of hypocalceof motor nerve fibers. Hypoglycemia can mia. Low or undetectable serum PTH in a
occur concurrently.

hypocalcemic animal is strongly suggestive

994

DISORDERS OF CALCIUM METABOLISM
of primary hypoparathyroidism (seep 1057).

The bitch may remain nonresponsive

A commercially available hwnan intact-PTH after correction of hypocalcemia if cerebral assay has been validated in both cats and
edema has developed. Cerebral edema,
dogs; PTH-calcimn curves are also similar
hyperthermia, and hypoglycemia should
in cats and dogs.

be treated if present. Fever usually
resolves rapidly with control of tetany, and

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Treatment and Prevention: Slow IV
specific treatment for fever may result in
administration of lOOA, calcimn gluconate is
hypothennia.

given to effect (0.5---1.5 mUkg over 10-30

It is best not to let the puppies or kittens
min; 5---20 mL is the usual dose). This usually nurse for 12-24 hr. During this period, they results in rapid clinical in1provement within
should be fed a milk substitute or other

15 min. Muscle relaxation should be
appropriate diet; if mature enough, they
inunediate.

should be weaned. If tetany recurs in the

During administration of calcimn, heart
san1e lactation, the Jitter should be removed
rate should be carefully monitored by
from the bitch and either hand raised
auscultation or by ECG for bradycardia or

( <4 wk old) or weaned (>4 wk old).

arrhythmias. Signs of toxicity from too rapid

After the acute crisis, elemental calcimn
administration of calcimn include
at 25---50 mg/kg/day in three or four divided
bradycardia, shortening of the QT interval,
doses is given PO for the remainder of the
and premature ventricular complexes. If an
lactation. Again, the dose of calcimn is
arrhythmia develops, calcimn administrabased on the amount of elemental calciun1
tion should be discontinued until the heart
in the product (ie, calcimn carbonate tablets
rate and rhythm are normal; then adminiscontain 295 mg elemental calciwn/1 g tration is resmned at half the original
tablet). ln dogs, the dosage is usually
infusion rate.

1-4 g/day, in divided doses. In cats, the

It is important to calculate the dosage
dosage of calcimn is -0.5---1 g/day, in divided
of calcium based on elemental (available)

doses. Longte1m maintenance therapy with
calcium, because different products vary
oral vitamin D and oral calcimn supplemenin the amount of calcimn available. The tation usually requires a minim w11 of
dosage of elemental calcium for hypocal24-96 hr before an effect is achieved.

cemia is 5---15 mg/kg/hr. Calcium gluco

Hypocalcemic animals should, therefore,
nate, 10%, contains 9.3 mg of elemental
receive parenteral calcimn support during
calcium/mL. Calcium chloride, 27%,
the initial posttetany period. Calcimn
contains 27.2 mg of elemental calcimn/mL.

carbonate is a good choice because of its

Thus, for 10% calcium gluconate the
high percentage of elemental calcimn,
dosage is 0.5-1.5 ml/kg/hr, IV, and for
general availability in drugstores in the form

27% calcium chloride the dosage is
of antacids, low cost, and lack of gastric

0.22-0.66 ml/kg/hr, IV. Calcium gluconate,
initation. The dosage of calcimn can be
as a 10% solution, is recommended
gradually tapered to avoid wmecessary
because, unlike calcium chloride, calcium
therapy; there is usually sufficient calcimn
gluconate extravasation is not caustic.

in commercial pet food to meet the needs

Once the animal is stable, the dose of
of dogs and cats. However, to avoid acute
calcium gluconate needed for initial
problems of hypocalcemic tetany, oral
control of tetany may be difuted in an
calcimn supplementation should continue
equal volmne of normal (0.9%) saline and
throughout lactation.

given SC, tid, to control clinical signs.

Vitamin D supplementation is used to

(Calcium chloride cannot be given SC.)

increase calcium absorption from the

Alternatively, 5-15 mg of elemental
intestines. The concentration of serum
calcium/kg/hr can be continued IV. This
calcimn should be monitored weekly.

protocol effectively supports serum

The dosage of l,25-dihydroxyvitan1in D
calcium concentrations while waiting for

(calcitriol) is 0.03-0.06 mcg/kg/day.

oral vitamin D and calcium therapy to

Calcitriol has a rapid onset of action
have effect. Ideally, serum calcium

(1-4 days) and short half-life ( <l day).

concentration should be maintained

Iatrogenic hypercalcemia is a common

>8 mg/dL. Serum calcium concentrations
complication of this therapy. If hypercal

<8 mg/dL indicate the need to increase the
cemia results from overdosage, it can be
dosage of parenteral calciwn, whereas
rapidly corrected by discontinuing
concentrations >9 mg/dL suggest that it be
calcitriol. The toxic effects resolve in 1-14
reduced. The aim of longterm therapy is to
days. This is a much briefer period than
maintain the serum calciw11 concentration
that seen with dThydrotachysterol (1-3 wk)

at mildly low to low-normal concentraor ergocalciferol (vitamin D2; 1-18 wk) tions (8-9.5 mg/dL).

therapy.

DISORDERS OF MAGNESIUM METABOLISM

995

Corticosteroids lower serum calcium and, dogs and cats. The incidence of hypocaltherefore, are contraindicated. They may cemia is 16% in critically ill dogs and 24%
interfere with intestinal calcium transport
ln dogs with sepsis. Hypocalcemia is best
and increase urinary loss of calcium.

detected by measuring ionized calcium

Owners should be warned that puerperal

( <2.5 mEq/L), which is the biologically
hypocalcemia is likely to recur with future
active form, rather than total or corrected
pregnancies. Preventive steps to consider in
calcium. Hypocalcemia, hypovitaminosis

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the bitch include feeding a high-quality,

D, and metabolic acidosis occur in dogs
nutritionally balanced, and appropriate diet
with induced endotoxemia. LPS may
during pregnancy and lactation, providing
mediate a decrease in vitamin D-binding
food and water ad lib during lactation, and
protein, with subsequent Joss of vitamin D
supplemental feeding of the puppies with
in the urine. Also, dogs with blunt and
milk replacer early in lactation and with
penetrating traumatic injuries, particusolid food after 3-4 wk of age. Oral calcium larly abdominal trauma, are significantly
supplementation during gestation is not
more likely to have ionized hypocalcemia
indicated and may cause rather than

(16%incidence). These dogs spend longer
prevent postpartum hypocalcemia. Calcium
time in the hospital and ICU, require more
administration during peak milk production
intensive therapies, and are less likely to
may be helpful in bitches with a history of
survive (57% survival rate) than dogs with
puerperal hypocalcemia.

normocalcemia (89% survival rate).

Hypocalcemia from critical illness or

HYPOCALCEMIA AS AN
traumatic injury can cause clinical signs

ELECTROLYTE DISTURBANCE IN
similar to those of puerperal hypocalce

SMALL ANIMALS
mia (hyperexcitability, including tremors,
twitching, spasms, or seizures, or more

Hypocalcemia is also an important
subtle signs related to cardiovascular
electrolyte disturbance in critically ill
collapse).

DISORDERS OF MAGNESIUM METABOLISM

Magnesium (Mg) homeostasis is not under
movement of calciun1 into smooth muscle
direct hormonal control but is mainly
cells, giving it a pivotal role in cardiac
determined by absorption from the GI tract;
contractile strength and peripheral vascular
excretion by the kidneys; and the varying
tone. Low ionized Mg concentrations
requirements of the body for pregnancy,
accelerate the transmission of nerve
lactation, and growth. Magnesiun1 is the
impulses. Clinical manifestations of severe
second most common intracellular cation
hypomagnesemia include muscle weakness,
after potassium, with 500/er-60% of total body
muscle fasciculations, ventricular

Mg distributed in bone, 40%-50% in soft
arrhythmias, seizures, ataxia, and coma
tissues, and <1% in the extracellular fluid.

Sin1ilar to calciwn, sernm total magne

Therefore, plasma Mg does not provide
sium (tMg) can be divided into three fotms.

an indication of intracellular or bone Mg

The physiologically active (free) fraction is
stores. Intracellular Mg is required for
ionized magnesium (i.Mg2+), whereas the
activation of enzymes involving phosphate
protein-bound and chelated fractions are
compounds such as ATPases, kinases, and
unavailable for biochemical processes.

phosphatases; and for synthesis of RNA,

Serwn iMg2+ cannot be accurately

DNA, and protein. Magnesium is a cofactor
calculated from serun1 tMg and albumin
for >300 enzymatic reactions involving ATP,
concentrations; therefore, serum iMg2+
including glycolysis and oxidative
concentration must be determined by direct
phosphorylation. It is also in1portant in
measurement. Because iMg2+ concentrathe function of the Na+/K+-ATPase pun1p, tions represent the functional pool of sernm
membrane stabilization, netve conduction,

Mg, detetmination of i.Mg2+ may provide a
ion transportation, and calciw11 channel
better physiologic assessment of Mg status
activity. Magnesiun1 also regulates the
than does tMg. A commercially available

996

DISORDERS OF MAGNESIUM METABOLISM
ion-selective electrode for Mg allows
administered as a cathartic for treatment of
routine measurement of iMg2+ concentralarge-intestinal inlpactions. This is followed tions.

by recumbency, tachycardia (120 bpm), and

Magnesiwn is cleared by glomerular
tachypnea (60 breaths/min). Signs subside
filtration and, in the absence of renal
after treatment with slow IV infusion of
disease, renal homeostatic mechanisms will
calciun1 gluconate (23%solution). Hyperattempt to maintain Mg balance. When the magnesemia has been repo1ted in cats with

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diet contains excessive Mg, renal tubular
renal failure that were receiving IV fluid
resorption decreases, maintaining serum
therapy. As plasma Mg concentrations
concentrations of Mg within narrow
exceed 2.5 mmol/L, tl1ere may be ECG
physiologic limits. Renal excretion of Mg
changes with prolongation of the PR
may be used to evaluate Mg balance.

inteival; at 5 mmol/L, deep tendon reflexes

IV administration of large doses of Mg is
disappear, followed by hypotension ai1d
safely used to concurrently diagnose and
respiratory depression. Cardiac a.JTest may
treat hypomagnesernia. The IV Mg retention
occw·with blood Mg levels >6.0-7.5
test, which involves the determination of
mmol/L.

urinary Mg retention, has become the gold
standard to detennine Mg status in human
medicine and has been validated in horses,

HYPOMAGNESEMIC TETANY IN
dogs, and cattle. Anin1als deficient in Mg

CATILE AND SHEEP
will retain a large proportion of the
administered Mg, whereas animals with

(Grass tetany, Grass staggers)

sufficient Mg will excrete most of it.

Hypomagnesernic tetany is a complex

Fractional clearance relates the amount
metabolic disturbance characte1ized by
of substance excreted to the amount filtered hypomagnesemia (plasma tMg <1.5 mg/dL
by the glomerulus without the need for

[ <0.65 mmol/L]) and a reduced concentravolwnetric urine collection. Fractional tion of tMg in tl1e CSF ( <1.0 mg/dL [0.4
clearance can be calculated by using
mmol/L]), which lead to hyperexcitability,
concurrently collected spot san1ples of
muscular spasms, convulsions, respiratory
urine and serum and by measuring the condistress, collapse, ai1d deatl1. Adult lactating centrations of creatinine and the electroanimals are most susceptible because of the lyte of interest. This allows assessment of
loss of Mg in milk. Hypomagnesemic tetany
urinary electrolyte excretion without the
occurs mainly when ailirnals are grazed on
need for timed urine collections and takes
lush grass pastures or green cereal crops
into account variability in urine concentrabut can occur in lactating beef cows fed tion due to hydration status.

silage indoors. It is rare in nonlactating

Run1inants are more prone to hypocattle but has occwTed when undernourmagnesemia than monogastric animals.

ished cattle were introduced to green

The variation in Mg metabolism among
cereal crops.

species is mainly because of anatomic and
physiologic differences in digestive tracts.

Etiology: The disorder occurs after a

Ruminants absorb Mg less efficiently than
decrease in plasma Mg concentration when
noruuminants (35%vs 700Aiof intake). The
absorption of dietaiy Mg is unable to meet
rumen is the main site of absorption, and
the requirements for maintenance (3 mg/kg
there are active transport mechanisms.

body wt) and lactation (120 mg/kg milk).

Absorption from the large intestine occurs

This can arise after a reduction in food
with high Mg intakes. In noruuminants, the
intake during inclement weather, transport,
small intestine is the main site of absorpor when cows graze shmt-grass dominant tion. Species differences in Mg metabolism
pastw·es containing <0.2% Mg on a
are attributable to variation in both
dry-matter basis. Low herbage availability
absorption efficiency of Mg from the gut and ( <1,000 kg dry matter/hectare) results in reabsorption of Mg by the kidney tubules.

liveweight losses during lactation, and
plasma Mg decreases because insufficient

Mg is obtained from body tissues mobilized

HYPERMAGNESEMIA
during loss of liveweight to support
lactation.

Hypermagnesemia (plasma Mg concen

Mg absorption from tl1e rwnen may be
tration >2 mg/dL [1.1 nrn101/Ll) is a rare
reduced when potassitm1 and nitrogen
condition reported only in monogastric
intakes are high and soditun and phosphoai1in1als. Horses show signs of sweating and rus intakes are low. Soils naturally high in
muscle weakness within 4 lu- of receiving
potassiwn ai1d those fertilized with potash
excessive oral doses of magnesiun1 sulfate
and nitrogen are high-risk areas for

DISORDERS OF MAGNESIUM METABOLISM

997
hypomagnesemic tetany. The more comundetectable in cows with hypomagneseplex mineral interactions are likely to be mic tetany. Mg concentrations <1.8 mg/dL
involved in herds in which hypomagnese-

(0. 75 mmol/L) in the vitreous hun1our of the

1nic tetany occurs in first- and secondeye removed from anin1als within 24 hr after calving cows as well as in older cows.

death are indicative of hypomagnesemic

Cows often do not develop signs of
tetany.

hypomagnesemic tetany until blood

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calcium concentrations are <0.8 mg/dL

Treatment: Animals showing clinical

(0.35 mmol/1), which commonly occurs
signs require treatment immediately with
in cattle grazing green cereal crops. The
combined solutions of calciun1 and Mg,
hypocalcemia arises from either a reduction preferably given slowly IV while monitoring in calcium intake or absorption, or both.

the heart (seep 988). The response to

Lush grass pastures and green cereal crops
treatment is slower in anin1als with
may predispose cattle to metabolic
hypomagnesemic tetany than in anin1als
alkalosis (urine pH >8.5) with a reduced
wiU1 hypocalcemia alone, because of the
available pool of ionized calcium and
time it takes to restore Mg in the CSF The
magnesiun1, thereby increasing the risk of
aninlal should not be stimulated during
hypocalcemia and hypomagnesemia. Urine
treatment, because this could trigger fatal

Mg concentrations are a useful guide to Mg
convulsions. Additional Mg sulfate (200 mL
status and are undetectable in cows with
of a 500A, solution/cow) can be given SC.

hypomagnesemia.

After treatment, cows should be left to
respond without stin1Ulation and then

Clinical Findings: In the most acute fom1,
moved off the tetany-prone pasture, if
affected cows, which may appear to be
possible. Animals must be provided with
grazing normally, suddenly throw up their
hay treated with 2 oz (60 g) of Mg oxide
heads, bellow, gallop in a blind frenzy, fall,
daily; if this is not done, the condition can
and exhibit severe paddling convulsions.

recur within 36 lu- after initial therapy.

These convulsive episodes may be repeated
at short intervals, and death usually occurs

Prevention: Mg must be given daily to
within a few hours. In many instances,
aninlals at risk, because the body has no
aninlals at pasture are found dead without
readily available stores. Daily oral
observed illness, but an indication that the
supplements of Mg oxide (2 oz [ 60 g] to
animal had convulsions before death may
cattle and l/3 oz [ 10 g] to sheep) should be
be seen from marks on the ground. In less
given in the danger period. Most Mg salts
severe cases, the cow is obviously ill at ease, are unpalatable and must be combined with walks stiffly, is hypersensitive to touch and
other palatable ingredients such as
sound, urinates frequently, and may
molasses, concentrates, or hay. Feeding hay
progress to the acute convulsive stage after
alone may be all that is required to prevent
a period as long as 2-3 days. This period
hypomagnesemic tetany in herds in which
may be shortened if the cow is transpo1ted
only old cows (>6 yr) are affected.

or driven to a fresh pasture. When animals

If slow-release intraruminal Mg devices are
have hypocalcemia and hypomagnesemia,
administered, the aninlals also should be
the signs shown depend on which
provided with hay. Fertilizers containing Mg
predominates. With hypomagnesemia,
effectively increase herbage Mg only on
tachycardia and loud heart sounds are
certain soil types. Herbage may be dusted
characteristic signs.

with powdered Mg oxide (500 g/cow) or

Clinical signs of hypomagnesemic tetany
sprayed with a 2% solution of Mg sulfate
in sheep occur when hypomagnesemia
at intervals of 1-2 wk. If rainfall exceeds

(plasma tMg <0.5 mg/dL (0.2 mmol/L])

40-50 nrm within 2-3 days of dusting, the
occurs concomitantly with hypocalcemia
herbage will require another dusting.

(plasma tCa <8 mg/dL [2.0 mmol/L]). The

Out-wintered stock should be protected
disease in lactating ewes occurs under
from wind and cold and provided with
essentially the san1e conditions and has
supplementary food. Sheep and cattle
the same clinical signs as in cattle.

should have access to hay, particularly
when grazing either green cereal crops or

Diagnosis: Diagnosis is usually conpastures fertilized with potassium or firmed by response to treatment, followed
nitrogen ( or both).

by confirmation of hypomagnesemia in
samples taken before treatment. Tetany usually occurs when plasma tMg is < 1.2 mg/dL

Hypomagnesemic Tetany in Calves

(0.5 m.11101/L) in cattle and <0.5 mg/dL

Magnesium absorption efficiency in calves

(0.2 nunol/1) in sheep. Urine Mg is usually
fed milk falls from 87% at 2-3 wk to 32% at

998

DISORDERS OF MAGNESIUM METABOLISM

7---8 wk of age. Hypomagnesemic tetany

The maintenance Mg requirement for
occurs in 2- to 4-mo-old calves being fed
horses has been estimated at 13 mg/kg body
milk only, or in younger calves with chronic
wt!clay and can be provided by a diet
scours while being fed milk replacer.

containing 0.16% Mg (1,600 ppm of feed) or

Clinical signs are similar to those of
by adding Mg oxide at 31 mg/kg/day, MgC03
hypomagnesemic tetany in adult cattle
at 64 mg/kg/day, or MgS04 at 93 mg/kg/day.

(see above) and include hyperexcitability,

This may be important when formulating

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muscular spasms, convulsions, and death.

oral replacement fluids for inappetent

Hypomagnesemic tetany in calves must
horses. For a 500-kg horse, this would
be differentiated from acute lead poisoning
equate to Mg oxide at -16 g/day, MgC03

(seep 3078) , tetanus (seep 611), strychnine at 32 g/d, orMgSO, at 47 g/day. Growing,
poisoning (seep 3170), polioencephalomalactating, and exercising aninlals may lacia (seep 1281), and enterotoxemia
require double these amounts. Horses that
caused by the toxin of Clost1idiiim pe1frin
are obtaining adequate feed by grazing, with
gens (seep 609). Analysis of bone aids
hay or grain, are unlikely to be Mg deficient.

diagnosis-nom1al bone has a Ca:Mg ratio

Horses are able to absorb 3()0A,-6()0A, of the
of 70:l; in hypomagnesemic calves, the ratio Mg provided in their feed, which is higher may be <!90: 1.

than the absorption rate in ruminants.

Affected calves require prompt treatment

If a pasture is considered Mg deficient
with a 10%solution of Mg sulfate (100 mL,

(winter pastures with little herbage that

SC) followed by Mg oxide at 10 g/day, PO.

have been fe1tilized with potash and /or

Provision of good-quality legwne hay and a
nitrogen), then renal excretion of Mg may
sta.Iter ration from 2 wk of age prevents the
be used to evaluate Mg balance. With low
disorder.

dietary Mg intake, urinary Mg excretion falls
to negligible levels. Renal Mg excretion is
measured in urine collected tlu·oughout

MAGNESIUM AS AN EQUINE

24 hr (mg/kg/day). The fractional clearance

DIETARY SUPPLEMENT
of Mg can be detennined by expressing the
renal Mg clearance relative to tl1e creatinine

Diel:a!y Mg deficiency in horses is very
clearance and requires only a single sample
rare, unless extreme conditions combine
each of urine and serun1. Fractional
to result in decreased consw11ption and
clearance of Mg in healtl1y horses fed grass
increased demand, eg, long-distance
hay ranges from 15% to 35%, ai1d values <6%
transportation of unfed lactating mares
indicate inadequate dietary Mg intake. A Mg
or prolonged administration of enteral
retention test to assess total body status has
or parenteral fluid or nutrition solutions
been evaluated in horses receiving
deficient in Mg. Despite this, Mg supple

Mg-deficient diets, but tl1is test offered no
ments have been advocated by laymen as a benefit over pe1fo11ning fractional calming agent or as an acijunctive therapy
clearances and requires 48 hr of volwnetric
for equine metabolic syndrome, and even
urine collection.

to prevent laminitis. There is no evidence
that these uses are beneficial or effective,
and such practices should be discouraged.

SUBCLINICAL

One randomized placebo controlled study

HYPOMAGNESEMIA IN
showed no difference in either insulin

CRITICALLY ILL ANIMALS
sensitivity or morphometric variables in
horses supplemented with Mg (8.8 g/cl)

Subclinical hypomagnesemia is conunon in
and chromiun1. Although sedation can be
critically ill horses and small aninlals and
seen in horses administered >500 g of
can increase the severity of the systemic

MgS0 as a cathartic via stomach tube,
inflanunatory response syndrome; worsen

4
low level Mg supplemenL5 are unlikely to
the systemic response to endotoxin; and
influence behavior, and larger amounts
lead to ileus, cardiac arrhythmias,
would be unpalatable in the feed or even
refractory hypoka.lemia., and hypocalcemia.

dangerous if administered as repeated

Low serum Mg concentrations have been
dosages via nasogastric tube (seep 996).

reported to occur in 65% of critically ill

Recommended doses of 3-10 g are
people, 39%--46% of clogs and cats in the
unlikely to have a clinical benefit.

intensive care tmit (ICU), 49% of hospital

However, low-level supplementation is
ized horses, 54% of equine surgical colic
considered relatively safe even if not
patients, and 78% of horses with enterocolefficacious, because excess Mg will be itis. In hun1an and canine ICU populations,
readily excreted by the kidneys in animals
hypomagnesemic patients had higher rates
with normal renal ftmction.

of concurrent hypokalemia and hypona-

DISORDERS OF PHOSPHORUS METABOLISM

999
tremia and a longer length of hospitalizathe precise regulation of serum Mg tion. In another study, 54% of equine surgical concentration by the kidney, Mg does not colic patients had low iMg levels, and these
have a complex homeostatic endocrine
horses had a significantly greater prevaregulating mechanism. Tllis is in contrast lence of postoperative ileus.

to calciwn, which is tightly regulated by

Although diets for horses and small
parathyroid honnone (PTH), calcitonin,

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animals are rarely deficient in Mg,
and calcitriol. However, PTH, vitamin D,
subclinical acute hypomagnesemia is very
calcitonin, arginine vasopressin, glucagons,
common in critically ill animals. Serum Mg
and calciw11 concentrations do influence Mg
concentration may be low as a result of
absorption and excretion to some degree.

altered Mg homeostasis, cellular or

Mild hypocalcemia and hypomagnesemia
tllird-space redistribution, GI loss of Mg,
stimulate PTH release, but severe Mg
or diuresis secondary to aggressive fluid
depletion and acute hypennagnesemia
therapy with IV fluids unsupplemented
decrease PTH release. Consequently,
with Mg.

parallel detennination of calciw11 and

Hypocalcenlia is also frequently seen in

PTH concentrations is in1po1tant in the
tl1e equine ICU. Although the mechanism of
investigation of Mg homeostasis.

action is unknown, serum Mg may influence

If longtem1 fluid therapy is required to
serwn calciwn concentrations; hwnan
support an inappetent animal in the I CU, Mg
hypocalcemic patients witl1 concurrent
should be supplemented. A constant rate
hypomagnesemia are often refractory to
infusion of Mg sulfate at 50-150 mg/kg/day,
calciwn therapy unless the low serun1 Mg

IV (0.1-0.3 ml/kg/day of the 50"A, solution),
levels are identified and corrected. Despite
provides daily requirements.

DISORDERS OF PHOSPHORUS METABOLISM

Phosphorus (P) is a macromineral witl1 a
extracellular space (ECS), which includes
pletl1ora of important biologic functions. In
blood serun1 or plasma. In the ECS,
addition to being essential for tl1e structural
phosphorus is present either as Pi, fanning
stability of bones and teetl1, cell membranes
the metabolically relevant fraction, or as

(phospholipids ), and nucleic acid molphospholipids. The extracellular Pi fraction ecules, phosphorus plays an in1po1tant role
is largely ( -85%) ionized ( either H2PQ,,- or
in metabolic activity such as carbohydrate

HP0,.2-), while - HJ<>,6 is protein botmd and
and energy metabolism tl1at inherently

5% is complexed with other minerals such
depends on the capacity to phosphorylate
as calciwn or magnesiwn.

intermediate metabolites and to store

The concentration of Pi in the ECS and
energy released during oxidation in
thus in serum is dictated by tl1e equilibriwn
high-energy phosphate bonds such as ATP
between Pi uptake from the digestive tract;
or phosphocreatine. Phosphorus is an

Pi excretion in urine ( monogastric species),
integral component of2,3-DPG, a comsaliva (ruminants), and milk; the uptake or pound tl1at regulates oxygen release from
release of Pi from bone; and compartmental
hemoglobin and tl1erefore is critical for

Pi shifts between the ECS and ICS.

oxygen delivery to tissues. Inorganic

Accordingly, hypophosphatemia that is
phosphoms (phosphate, P0
defined as subnormal se1wn or plasma Pi

4, or Pi) is
also an important buffer in the body.

concentration can be caused by decreased

In the body, phosphorus is present as a
oral phosphoms uptake, increased
stable inorganic phosphate (Pi), an organic
phosphorns loss, increased cellular
phosphate ester, or a phospholipid. By far
phosphorus uptake, or a combination of
tl1e largest fraction of the body phosphorus
these factors. Because only increased

( -85% of total body phosphorus) is
phosphorns loss and decreased phosphorus
incorporated into bone in an insoluble
uptake are associated with phosphorus
inorganic phosphate fonn ( dihydroxyapadepletion of the body but compartmental tite). The remainder is largely located in the
shifts of phosphorus between tl1e !CS and
intracellular space (ICS, -14%), while <1%

ECS can strongly affect the extracellular Pi
of the total body phosphorus is found in the
concentration, the serwn Pi concentration

1000

DISORDERS OF PHOSPHORUS METABOLISM
is an unreliable parameter to assess the
phosphorus depletion. These signs appear
phosphorus status of an animal. Despite
to be the result of decreased energy and prothe difficult interpretation of the serum Pi tein intake in animals that are anorectic due
concentration, it is still the most commonly
to phosphorus depletion. ln later stages,
used measurement of phosphorus status in
animals may develop pica, osteomalacia,
veterinary medicine.

abnormal gait, and lameness, and eventually
become recun1bent.

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Acute hypophosphatemia has been

HYPOPHOSPHATEMIA
associated with anorexia, muscle weakness,
muscle and bone pain, rhabdomyolysis,

Etiology and Pathogenesis: Chronic
increased fragility of RBCs, and ensuing
phosphorus deficiency is commonly caused
intravascular hemolysis. Other potential
by inadequate feed intake or inadequate
effects of hypophoshatemia are neurologic
phosphorus content in the ration over an
signs preswnably related to the altered
extended time. This can be seen in grazing
energy metabolism, impaired cardiac and
animals in arid regions with low phosphorus respiratory function ( decreased contractilcontent in soil. Phosphorus depletion can ity of striated and heart muscle), and
also result from chronic renal tubular
dysfunction of WBCs and platelets that are
disease due to impaired renal reabsorption
believed to be caused by ATP depletion.

of phosphorus (eg, Fanconi syndrome) or
ln cattle, hypophosphatemia occurring at
primary hyperparathyroidism causing
the onset of lactation is widely believed to
increased renal phosphorus excretion.

be associated with periparturient recwn

Hypophosphatemia is a common finding
bency and the downer cow syndrome (see
in horses with chronic renal failure.

p 1188). However, this association is based

Acute phosphorus losses associated with
on empirical observation and is not
hypophosphatemia are a well-recognized
supported by unequivocal evidence.

problem in high-yielding dairy cows at the

Postparturient hemoglobinuria is another
onset of lactation. The sudden onset of
but rare condition seen in high-yielding
phosphorus losses through the marnmary
dairy cows in the first days of lactation. It
gland at the onset of lactation and the
is characterized by acute intra.vascular
decreased feed intake around parturition
hemolysis and hemoglobinwia., frequently
are believed to be the major contributors to
with fatal outcome.

periparturient hypophosphatemia of dairy

It is currently not well understood
cows. Nonetheless, periparturient
whether the above-mentioned clinical signs
hypophosphatemia has also been docuand conditions are ca.used by low levels of mented in mastectomized cows, indicating
phosphorus in the blood or by overall
that other mechanisms, such as compartdepletion of phosphorus in the body.

mental shifts, impaired intestinal absorp

Necropsy findings in cases of chronic
tion, or increased ·losses tlu·ough the
phosphorus depletion are those specific to
digestive or urinary tracts, must contribute
rickets or osteomalacia.. Carcasses appear
to this phenomenon.

emaciated with a dull hair coat. Fractures

Hypophosphatemia without phosphorus
of ribs, vertebrae, or the pelvis, as well as
depletion may occur after oral or parenteral
widened growth plates and costochondral
carbohydrate administration and after
junctions, angular defonnities, and
parenteral insulin administration as a result
shortened long bones are common.

of increased cellular phosphorus uptake in
combination with glucose. Alkalemia and

Diagnosis: Phosphorus depletion is not
respiratory alkalosis enhance cellular
readily diagnosed in living animals. Because
phosphorus uptake and therefore also have
chronically phosphorus-depleted animals
a hypophosphatemic effect.

can maintain the serum Pi concentration
within nonnal limits by mobilizing Pi from
bone, and because the serum Pi concentra

Clinical Findings and Lesions: Signs
tion can be decreased even in the absence of
of chronic phosphorus depletion are most
phosphorus depletion, the Pi concentration
commonly seen in cattle fed a phosphorusin serum is an wrreliable proxy to diagnose deficient diet over several months. Young
chronic phosphorus depletion. Although
animals grow slowly, develop rickets, and
acute phosphorus depletion can reflect
tend to have a rough hair coat, whereas
accurately in the serum Pi concentration,
adult animals in early stages may become
the considerable diurnal variation, effects of
lethargic, anorectic, and lose weight.

physical activity, and feed intake complicate

Decreased milk production and fertility
the interpretation of results from a single
have en-oneously been att1ibuted to
blood sample. Dextrose administered

DISORDERS OF PHOSPHORUS METABOLISM

1001
parenterally shortly before blood sampling
solutions. In cattle, rapid administration
can decrease the serum Pi concentration by
of sodium phosphate salt solutions is

>30%; 4-6 hr should elapse between the end
commonly practiced. Mono- or di basic
of dextrose infusion and blood san1pling to
phosphate salts (either Na HP0 or
allow the serum Pi concentration to return

2

4

NaH,P0,
to baseline. Other factors that can affect the

1) infused IV rapidly increase the
serum Pi concentration. Tribasic
serum Pi concentration include physical
phosphate (N3,iP0

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exercise shortly before blood sampling or

4) is a caustic detergent
that cannot be used under any circumthe site of blood collection. Vigorous stances for PO or IV phosphorus supplephysical activity can result in markedly mentation. An issue with the IV infusion of
decreased serum or plasma Pi concentraphosphorus salt solutions is that unbound tions for > 1 hr.

Pi in plasma reaching the kidney is filtered

Determination of the bone density or
by the renal glomeruli and must then be
bone phosphorus content in a rib biopsy has reabsorbed in the renal tubules. Because been proposed as a reliable parameter to
tubular reabsorption is a saturable
diagnose chronic phosphorus depletion in
process, infusing Pi at a rate that increases
cattle. Nonetheless, the bone phosphorus
plasma Pi concentration above the renal
content is slow to respond to changes in
threshold disproportionally increases
dietary phosphorus supply, which means
renal Pi excretion and therefore only
the nutritional history has a strong impact
transiently increases the plasma Pi
on the mineral content of fresh bone. The
concentration. This explains the shortphosphorus content in fresh bone is lived effect ( <2 hr) of sodium phosphate
therefore a good indicator of body
solutions when administered as an IV
phosphorus reserves but not of current
bolus as recommended for cattle. Rapid
dietary phosphorus supply. Furthermore,
administration of sodium phosphate salts
obtaining bone biopsies is impractical under causes transient but severe hyperphosfield conditions, and detennination of bone phatemia and therefore bears the risk of
phosphorus content is generally restricted
causing hypocalcemia due to precipitation
to postmortem examination or research
of calcium phosphate salts. This risk of
activities. Alternatively, the extent of bone
calcium phosphate precipitation also
resorption activity can be determined by
precludes the parenteral administration
measuring the urinary hydroxyproline
of phosphate salts in combination with
concentration, an amino acid liberated
parenteral calcium or magnesium
from collagen as bone is demineralized.

infusions. Infusing phosphorus salts

Radiographic examination of bone will
slowly over several hours results in a more
reveal reduced radiopacity of the bones in
sustained effect and reduces the risk of
chronically phosphorus-depleted animals.

hypocalcemia. Currently, no sodium

Feed samples can be submitted to
phosphate salt-containing solutions are
detemline the phosphorus content in the
approved by the FDA for IV admipistration
ration, allowing an estimate of phosphorus
in cattle; therefore, any effective IV
intake if the daily feed intake is known. ln
phosphate administration is off-label.

grazing aninlals, the phosphorus concentraln cattle, solutions containing not tion in either soil or in a fecal sample can be
phosphate but phosphite (P03), hypophosdetem1ined and used as an indirect and phite, or organic phosphorus compounds
crude parameter to assess adequacy of the
such as butaphosphan or toldimphos are
dietary phosphorus content.

often used to supplement phosphorus IV,
frequently in combination with calcium,

Treatment and Prevention: Chronic
magnesiun1, and other minerals. However,
phosphorus depletion and hypophosthese phosphorus compounds are not phatemia is most effectively treated by
suitable to correct hypophosphatemia,
providing sufficient amounts of feed with
because mammals are unable to convert
adequate phosphorus content; however,
phosphite or the above-mentioned organic
the most appropriate treatment approach
compounds into phosphate (PO,) and so do
for acute phosphorus depletion and
not contribute to the biologically active
hypophosphatemia is controversial. IV
plasma Pi pool. Even when organic
administration of phosphorus-containing
phosphorus compounds are usable
solutions is often recommended as the
metabolically, phannaceutical products
most appropriate approach. In small
containing organic phosphorus compounds
animals, this is achieved by slow IV
adnlinistered at label dose do not provide
infusion of sodium phosphate salt
nearly enough phosphorus to correct severe
solutions, or in case of concomitant
phosphorus depletion, which would be the
hypokalemia of potassium phosphate
primary indication for IV treatment.

1002

DISORDERS OF PHOSPHORUS METABOLISM

Mild to moderate phosphorus depletion

HYPERPHOSPHATEMIA
can be treated effectively by oral Pi
supplementation either by adding dairy

Physiologically increased serum and plasma
products to the diet (monogastric species)

Pi concentrations are seen in young and
or by providing solutions of sodium
growing anin1als due to enhanced intestinal
phosphate salts for oral consumption. Oral phosphorus uptake and decreased renal Pi administration rapidly increases plasma phosphorus excretion, presun1ably to VetBooks.ir

Pi concentration and is safe and effective,
facilitate bone mineralization. Pathologibut it may not be appropriate in vomiting cally increased extracellular phosphorus
and possibly in diarrheic animals. In
concentrations can be the result of
cattle, oral sodium phosphate salts
hemoconcentration, decreased renal
increase the plasma Pi concentration
excretion, decreased intracellular uptake,
within 3-4 hr and exert a sustained effect
or cellular release of phosphorus after cell
lasting> 12 hr. Other phosphate salts that
lysis. Decreased urinary phosphorus
have been proposed for rapid correction
excretion in association with chronic renal
of hypophosphatemia in cattle include
failure is the most common cause of
monopotassium phosphate and monocalhyperphosphatemia in many monogastric cium phosphate. Dicalcium phosphate is
species except horses. In ruminants,
commonly used for longterm supplemenhyperphosphatemia is commonly seen in tation of phosphorus-deficient diets but
dehydrated anin1als and is most likely due
because of its poor solubility characteristo hemoconcentration and a concomitant tics is unsuitable for rapid correction of
reduction in saliva production. Massive
hypophosphatemia.

tissue irtjury with rhabdomyolysis results in

Phosphorus depletion in healthy
damaged cell membrane integrity, which
grazing animals is prevented by assuring
leads to release of phosphorus together
sufficient feed intake with adequate
with other predominantly intracellular
phosphorus content. In animals grazing on compounds such as potassium into the phosphorus-deficient soils, depletion may
extracellular space. Hypoparathyroidism
be prevented by fertilizing the soils with
may result in hyperphosphatemia due to
phosphorus or by supplementing feeds or
increased renal phosphorus reabsorption
the water supply with phosphate salts. In
in the absence of PTH. Incidental cases of
the dairy industry, overfeeding phosphosevere acute hyperphosphatemia were rus is more common because of the widely reported after repeated treatment with held but incorrect assumption that
enemas containing hypertonic sodimn phosfeeding phosphorus in excess of the daily phate solutions in people and small
requirements improves fertility and milk
ruminants.

production. Research consistently

Hemolysis occuning dtu-ing or after
confirms that phosphorus concentration
blood sample collection results in release of
of 0.42% in dry matter _is adequate for
intracellular phosphorus from RBCs and
high-yielding dairy cows.

therefore gives erroneously high serun1 Pi

Currently, no effective approach to
concentrations. Therefore, hemolytic blood
prevent hypophosphatemia and phosphosamples should not be used to determine rus depletion at tl1e onset of lactation is
the serun1 or plasma Pi concentration.

known. Feeding higher amounts of dietary

Hyperphosphatemia as it occurs during
phosphorus during tlle last weeks of
hemoconcentration or decreased glomerugestation is contraindicated, because it lar filtration is unlikely to be of any clinical
decreases the intestinal absorption rate
relevance. In more severe cases, concomiof phosphorus and increases the risk of tant hypocalcemia may result from
periparturient hypocalcemia. The dietary
precipitation of excessive phosphorus with

Ca:P ratio that appears to be essential in
calciun1 and cause muscle fasciculations
horses and other species to prevent
and tetanic muscle contractions. In
secondary hypo- or hyperparathyroidism is sustained cases, precipitation of calciumnot imp01tant in ruminants. Cattle tolerate phosphate salts results in extraskeletal

Ca:P ratios between 1:1 and 8:1, provided
tissue mineralization with a potentially fatal
the ration meets minimal requirements for
outcome.

both minerals. This peculiarity in
ruminants can be explained by the high

POSTPA RTURIENT
salivary phosphorus concentration (5- to

10-fold the concentration in serum) and

HEMOGLOBINURIA
the large amounts of saliva produced that

Postparturient hemoglobinuria is a sporadic
alter the Ca:P ratio of the rumen content
condition seen worldwide that most
considerably.

commonly affects individual high-yielding

DISORDERS OF POTASSIUM METABOLISM

1003
dairy cows at the onset of lactation. It is
lactation. Hemoglobinuria may best be
characterized by development of peracute
diagnosed by noting failure of the urine
intravascular hemolysis and anemia with
to clear with centrifugation ( excluding
potentially fatal outcome. Beef and
hematlllia) and presence of concurrent
non.lactating cattle are rarely affected. The
severe anemia. Intravascular hemolysis
exact cause is tmlrnown, but phosphorus
caused by Babesia (seep 21) or Theileria depletion or hypophosphatemia has been

(seep 33) may be excluded by blood smear

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incrinlinated as a major predisposing factor.

analysis, and staridard laboratory methods

Severe intracellular phosphorus depletion of can be used to exclude leptospirosis (see RBCs is lrnown to increase osmotic fragility
p 646) or bacillary hemoglobinuria (see
of the RBCs, possibly predisposing to
p 601). Diagnostic testing and feed or
intravascular hemolysis. Although marked
pasture analysis can be perfom1ed to
hypophosphatemia is commonly diagnosed
identify toxic plants and deficiency of
in affected animals, most cases of severe
phosphorus, copper, and other antioxidants.

hypophosphatemia are not associated with

Transfusion of large quantities of whole
intravascular hemolysis, suggesting that
blood is the best treatment for severely
hypophosphatemia is not the sole causative
affected cows. Crystalloid fluids may be
factor responsible for postpartUiient
beneficial if blood is not available and may
hemoglobinlllia. A sinular condition
protect the kidneys against toxic and anoxic
reported in New Zealand was associated
damage, but monitoring the PCV and the
with copper deficiency, potentially making
total protein concentration is required to

RBCs more susceptible to oxidative stress.

prevent third spacing due to tile decreased

Other potential causes are hemolytic or
intravascular oncotic pressure. Par·enteral
oxidative plant toxins ( often from Brassica.

treatment witil monosodium dihydrogen
spp, sugar beets, or green forage).

phosphate (60 g in 300 mL of sterile water)

Clinical cases are rare, but when they

IV followed by oral treatment witil 200--300
occur the case fatality rate is high
g of sodium phosphate salts every 12 hr is

(10%--3Q<>A,). With clinical disease, rapid
suitable to rapidly correct hypophosintravascular hemolysis leads to severe phatemia. Copper glycinate (120 mg
anemia, tachycardia, wealrness, hemogloavailable copper) has been recommended binlllia witl1 dark brown or red urine, and
in cases in which copper deficiency is
pallor over several days. Milk production
suspected as the underlying cause. The
drops rapidly. Affected cows also may have
efficacy of these treatments to prevent
fever, diarrhea, and t.achypnea. Cows that
further hemolysis is not documented. No
survive the hemolytic c1isis may take
sodium phosphate or copper glycinate
several months to recover completely.

solution approved for parenteral adminis

Convalescent cows and cows with
tration by the FDA is currently available
subclinical disease develop icterus and
for use in ruminants. The use of these
evidence of increased erythropoiesis.

compounds in dairy cows is therefore

Diagnosis is usually made by recognition
extra-label. Correction of mineral deficienof clinical signs, particularly dark urine and cies and elimination of plant toxins from
anemia during the characteristic stage of
the diet may help prevent recurrence.

DISORDERS OF POTASSIUM METABOLISM

PotassiUin homeostasis is mainly deterpotassium excretion is aldosterone, which mined by the balance between absorption of is released from the zona glomerulosa of the potassium from tile GI tract and subsequent
adrenal gland in response to hyperkalemia
excretion by tile kidneys (all animals) and
and otiler factors. One of aldosterone's
saliva (in adult ruminants). Transport of
prinlary actions is to enhance the secretion
potassium is passive in the small intestine
of potassium ions in the distal renal tubules
and active in tile colon under tile influence
and collecting ducts. At least 95% of whole
of aldosterone. The most important
body potassiun1 is intracellular, witil
hoimone affecting renal and salivary
skeletal muscle containing 60%-75% of the

1004

DISORDERS OF POTASSIUM METABOLISM
intracellular potassium. Marked changes in

HYPOKALEMIA IN ADULT CATTLE
serum or plasma potassium concentrations
alter the resting membrane potential of

Hypokalemia occurs commonly in
cells, because the potassium gradient
inappetant adult cattle, particularly in
generated by Na+fK+-ATPase is the main
lactating dairy cows because of the
cause for the negative electtic potential
additional loss of potassium in the milk.

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across cell membranes. Therefore,
hypokalemia or hyperkalemia alters the

Etiology: Hypokalemia is common in
resting membrane potential, resulting in
adult cattle with prolonged inappetence
clinically significant changes in cellular

(>2 days), or in those receiving more than
and organ function. Hypokalemia usually
one iI\jection of corticosteroids that have
indicates whole body depletion of
mineralocorticoid activity, eg, isoflupredone
potassiwn, whereas in hyperkalemia, whole
acetate. This is because mineralocorticoid
body potassium status cannot be inferred
activity enhances renal and GI losses of
because many animals with hyperkalemia
potassium. Hypokalemia is extremely rare
have concurrent acidemia and whole body
in adult rwninants witl1 adequate dry matter
potassium depletion.

intake.

Hypokalemia can occur in any animal
receiving large volumes of IV fluid or having

Clinical Findings and Diagnosis: Ania marked and sustained reduction in feed mals with hypokalemia have generalized
intake. The clinical signs in most animals
muscle weakness, depression, and muscle
with mild to moderate hypokalemia are mild fasciculations. Severely affected anin1als and nonspecific. Severe hypokalemia is
are unable to stand or lift their head from
associated with ventroflexion of the head
the ground.

or recumbency due to generalized muscle

Serw11 biochemical analysis is required to
weakness and cardiac arrhythmias,
confirm a suspected diagnosis of hypokaincluding both atrial and ventricular lemia. A serwn potassium concentration
premature complexes that may lead to more <2.5 mEq/L reflects severe hypokalemia; complex cardiac arrhythmias. Prolonged
most anin1als will be weak, and some will be
and profound hypokalemia can result in a
recumbent. A serum potassium concentramyopathy that is difficult to treat. Cats can tion of 2.5-3.5 mEq/L reflects moderate
be affected by a hypokalemic polymyopathy hypokalemia, and some cattle will be (seep 1201), and Burmese cats have an
recumbent or appear weak with depressed
autosomal recessive disorder that leads

GI motility. In addition to measurement of
to hypokalemic myopathy (seep 1232).

serwn potassium concentration, measure

Hyperkalemia usually results from
ment of serw11 concentrations of sodium,
inadequate urinary excretion of ingested
chloride, calcium, and phosphorus, and
potassium and is common in monogastric
serum activities of CK and AST can be very
animals with urinary tract obstruction
helpful in guiding treattnent. Aciduria may
and bladder rupture. Hyperkalemia in
be present in response to a marked
horses and ruminants can also result
decrease in urine potassium concentration.

from exertional rhabdomyolysis, because
skeletal muscle contains a large percent

Treatment: Oral potassiwn administraage of whole body potassium. Hypertion is the treatment of choice for hypoka.kalemia also occurs in heavily muscled lemia. Inappetant lactating dairy cattle

Quaiter horses and related breeds as a
should be treated with 60-120 g of feed
genetic disorder (hyperkalemic periodic
grade KC! twice at a 12-hr inte;rval, with the
paralysis, seep 1047). Hyperkalemia is

KC! placed in gelatin boluses or adminisfrequently present in dogs with hypoadtered by ororuminal intubation. Adult cattle renocorticism (seep 574). Severe
with severe hypokalernia ( <2.5 mEq/1)

hyperkalemia is associated with generalshould initially be treated with 120 g of KC!

ized muscle weakness, depression, and

PO, followed by a second 120-g dose of KC!

cardiac conduction disturbances that

12 hr later, for a total 24-hr treatment of 240
may lead to lethal cardiac arrhythmias.

g KC!. Higher oral doses are not recom

Pseudohyperkalemia. in serum can occur
mended, because they can lead to diarrhea,
in animals with thrombocytosis as a result
excessive salivation, muscular tremors of
of the excessive release of intra.cellular
the legs, and excitability.

potassium stores from platelets during

Potassiwn is rarely administered IV; the
clotting. Pseudohyperkalemia in serum

IV route is used only for initial treatment
and plasma occurs when extensive
of recumbent rwninants with severe hypohemolysis is present due to the high kalemia and rumen a.tony, because it is
potassium concentration in RBCs.

much more dangerous and expensive than

DISORDERS OF POTASSIUM METABOLISM

1005
oral treatment. The most aggressive IV treatamplitude or loss of the P wave, widened ment protocol is an isotonic solution of KC!

QRS complexes, and symmetric T waves

(1.15%), which should be adrn.inistered at

(narrowing of T wave duration and

<3.2 ml/kg/hr, equivalent to a maximal

"tenting" of the T wave). The ECG effects
delivery rate ofK+ at 0.5 mEq/kg/hr. Higher
of hyperkalemia are exacerbated by the
rates of potassium administration run
presence of hyponatremia, aciclemia, at1cl
the risk of inducing hemodynamically
hypocalcemia. The ratio of serum sodium

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important anhythmias, including premature to potassium concentration is importa11t ventricular complexes that can lead to
in development of cardiac arrhythmias;
ventiicular fibrillation and death.

hyperkalemia in the presence of hyponatremia (sodium:potassium ratio <25:1) is Prevention: Oral administration of
commonly associated with the occurrence
potassium is a mandatory component of
of cardiac arrhythmias at1d ECG abnorfluid and electrolyte adrninisti·ation to malities.

inappetant cattle. Ensuring adequate
dry-matter intake is the best method to

Treatment: Hyperkalemia should
prevent hypokalemia in adult cattle.

initially be treated by IV administration
of 0.9% NaCl to increase the rate of urine

HYPERKALEMIA
production in dehydrated animals with
a patent urinaiy system, at1d in selected

Etiology: Hyperkalemia is common
cases by IV administration of sodium
in neonatal ruminants with diarrhea.,
bicai·bonate, glucose, insulin, a11d
dehydration, a.cidemia, and strong ion
sometimes calcium. Urine should be

(metabolic) acidosis. Hyperka.lemia.often
removed from the abdomen of a11imals
accompanies acidemia., because low blood
with obstructive urolithiasis a11d ruptured
pH results in intracellular acidosis a11d
bladder, a11d urethral patency established.

leakage of potassium from the intracellular

Sodium bicarbonate is administered to
compaitment to the extra.cellular space.

correct systemic at1d intracellulai· acidosis.

Hyperkalemia is common in neonatal foals

The rationale for IV glucose at1d insulin
with uroabdomen secondary to ruptured
administration is that insulin-mediated
bladder associated with parturition, a11d in
glucose entl)' into cells is accompa11ied
male cats with uroa.bdomen secondary
by movement of potassium from the
to obstructive urolithiasis and bladder
extra.cellular space to the intra.cellular
rupture. Hyperkalemia. is rare in steers,
compaitment. The rationale for calcium
wethers, and bucks with obstructive
administration is that calcium counteracts
urolithiasis a11d bladder or uretlu·al rupture,
many of the deleterious effects of
because excess potassium is secreted in
hyperkalemia on a.rrhythmogenesis, a11d
adult ruminant saliva and affected a11in1als
the IV administration of calcium may
have a decrease in potassiw11 intake due to
therefore improve cardiac output.

illness. Hyperkalemia can be present in

However, hypertonic saline (2,400
horses and ruminants with exertional
mOsm/1) is just as effective as hypertonic
rhabdomyolysis clue to da1nage to skeletal
sodium bicarbonate in decreasing
muscle cells.

hyperkalemia and hyperkalemia-associated
bra.dyarrhythmias, probably because of

Clinical Findings and Diagnosis: Severe
hypernatremia-mediatecl intra.cellular
hyperkalemia. is usually associated with
movement of potassium, extra.cellular
depression, weakness, lethargy, cardiac
volume expa11sion, and increased rate of
arrhythmias, and ECG a.bnom1alities,
urine production. The focus of treatment
pa1ucularly when the serw11 potassiW11
in hyperkalemia should therefore be
concentration is > 7 m.Eq/L. Severe ca.rdioidentification a11d correction of aciclemia, toxic effects are evident when the serw11
plasma volume expa11sion to assist in renal
potassiW11 concenti·a.tion is 8-11 m.Eq/L.

excretion of potassium, and increasing the

Serum biochemical analysis is required
serum sodium concentration. Glucose and
to confirm a suspected diagnosis of hyperinsulin do not appear to be routinely ka.lemia. In addition to measurement
needed to correct hyperkalemia.

of serum potassium concentration,
measurement of serum concentrations of

Prevention: Hyperkalemia ca11 be
sodium, calcium, phosphorus, urea, and
prevented by early diagnosis and treatment
crea.tinine; the serum activities of CK a11d
of its most conm10n causes. Hyperkalemic

AST; and blood gas analysis can be helpful
periodic paralysis can be prevented in
in guiding treatment. ECG may reveal
horses by feeding a low-potassium diet or
bradyarrhythmias, suppression in P wave
the oral administi·ation of acetazol3111icle.

1006

EQUINE METABOLIC SYNDROME

EQUINE METABOLIC SYNDROME

(Insulin dysregulation syndrome, Equine syndrome X,

Peripheral Cushing disease)

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Equine metabolic syndrome (EMS)

necrosis factor and other inflan1matory
describes a characteristic collection of
mediators. Increased fat stores in the liver
clinical signs and clinicopathologic changes
may also predispose to insulin resistance
in equids. It is found in both horses and
due to down-regulation of insulin receptors.

ponies and has also been recognized in

Experimentally, high blood insulin levels
donkeys. Affected animals typically are
lead to lanlinitis in horses and ponies.

obese, with increased condition score

Insulin has vasoregulatory actions. Insulin
overall and increased adiposity in the neck
resistance can decrease nitric oxide
and tailhead regions. Laminitis, both chronic production and promote vasoconstriction.

and acute, is common. Hyperinsulinemia

Altered glucose and insulin levels may also
with norrnal blood glucose concentrations
lead to altered epidermal cell function and

(insulin resistance) is the primary clinical
glucose uptake by epidermal laniinar cells.

pathologic finding. Other associated signs

These effects predispose horses with EMS
include infertility, altered ovarian activity,
to develop laminitis.

and increased appetite. Other laboratory

Horses with EMS respond to high
findings include hypertriglyceridemia,
carbohydrate meals with an exaggerated
increased serum concentrations of leptin,
increase in insulin, a higher than expected
and arterial hypertension. Previously, this
blood glucose level, and a very slow return
cluster of clinical signs in horses was
of blood glucose concentrations to baseline
referred to as hypothyroidism, peripheral
values. This indicates a resistance to the

Cushing disease, prelaminitic syndrome, or
peripheral effects of insulin (EMS) and/or

Syndrome X. EMS replaces these earlier
an inability to metabolize oral carbohydrate
tenns. EMS may be the end result of an
nom1ally (insulin dysregulation).

inability to properly metabolize dietary

EMS may be a predisposing factor for
carbohydrate, and many horses exhibit
pituitary pars intem1edia dysfunction
exaggerated glucose and insulin responses

(PPID; also called equine Cushing disease).

to an oral hexose load before developing

Both endoc1ine disorders can occur
true insulin resistance. Any abnormality in
concurrently in middle-aged and older
carbohydrate metabolism in horses has
horses. Horses with EMS should therefore
been termed insulin dysregulation.

be monitored to detect the onset of PPID.

EMS first develops in horses 5-16 yr old.

(See ai,so p 547.)

Breeds most commonly affected include
ponies, Saddlebred, Tennessee Walking,

Clinical Findings: There is no clinical

Paso Fino, Morgan, Mustang, and Quarter
picture that is pathognomonic for insulin
horses. Thoroughbreds and Standardbreds
resistance. Horses may exhibit all the phenoinfrequently develop EMS. There is no typic characteristics of EMS with normal
recognized sex predilection.

responses to evocative testing. In most
instances, the animals in question are obese

Etiology and Pathogenesis: The
because of excess calorie intake rather than
underlying reason why some horses develop any underlying metabolic alteration.

EMS and others do not is not known. There

Affected horses typically are obese witl1 a
appears to be a genetic disposition, both
body condition score >6 out of9. Even if the
within and between breeds. Affected horses
overall condition score is not extremely high,
may possess a "thrifty" gene that enabled
there is increased fat deposition in the neck,
their ancestors to survive in harsh
leading to a "cresty" appearance. Fat
environments. This increased efficiency of
deposition over the ribs and over the top line
energy metabolism becan1e maladaptive in
to the tail head is also common. Geldings may
modem environments with plentiful,
have increased fat deposition in the prepuce,
nutrient-dense feedstuffs.

whereas mares may have increased fat

The common denominators behind many
deposition around the manimary gland. Larniof the signs associated with EMS appear to nitis is a common finding. Horses brought in
be increased adiposity, insulin resistance,
for evaluation with no previous history of
and hyperinsulemia. When obesity
lanlinitis often show evidence of prior
develops, adipose tissues elaborate leptin
episodes such as abnom1al hoof growth rings
and other adipokines as well as tumor
and radiographic evidence of third phalanx

EQUINE METABOLIC SYNDROME

1007
rotation or pedal osteitis. Laminitis may

To document insulin resistance, the horse's
occur secondary to ingestion of feeds high in
ability to handle glucose should be evaluated.

soluble carbohydrates, either in the fom1 of

Because a subset of horses are nom1al in all
lush pasture or high-carbohydrate hays and
respects except for their ability to handle an
supplements. This can result in bouts of
oral carbohydrate load, an oral sugar test
larninitis developing in the spring, when new

(OST) or oral glucose test (OGT) should be

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pasture growth appears, and in the fall, when
perfom1ed. The OST is easy to perform in
night temperatures are below freezing.

North America, where com syrup is readily

Horses with EMS may not lose weight
available, whereas the OGT can be perwithout extreme feed restriction; owners fonned in other parts of the world. The OST
conunonly report that affected horses
is perfo1med by fasting the horse for 6-8 hr
remain obese even when fed minimal
and then giving an oral dose of com syn.1p at
amounts. Obesity may be exacerbated by

0.15 mllkg. Blood should be collected at 60
larninitis, which may limit exercise. Horses
or 90 min after administration of the com
appear to have increased appetites and often
syrup for insulin detemlination. An insulin
will eat continually as long as feed is
concentration >60 mU/L is abnormal. The
available. Infertility and abnonnal reproduc

OGT is performed by giving a fasted horse
tive cycles occur in mares affected with EMS. 0.5 kg of chaff-based feed to which dextrose Lesions: Increased general adiposity
powder at 1 g/kg has been added. An insulin
and laminitis are often documented. The
concentration >87 mU/L in a blood sample
pituitary gland is normal in younger horses
collected 2 hr later is abnonnal. To detemline
with EMS, but lesions consistent with PPID
whether insulin can stimulate normal glucose
may be found in older horses with EMS that
uptake by peripheral tissues, an insulin
are concurrently affected by EMS and PPID. tolerance test can be petformed. This is accomplished by collecting a baseline blood

Diagnosis: Diagnostic testing for EMS
sample for glucose concentration, giving
should concentrate on documenting insulin
regular human recombinant insulin at
resistance while excluding PPID. The

0.1 IU/kg, IV, and then collecting a second
presence of obesity and the cresty neck
blood sample for glucose concentration 30
phenotype is not sufficient to make a
nlin later. A second blood glucose concentradiagnosis. A careful dietary history and tion that does not decrease to 50% or less of
physical exanlination are essential.

the baseline value indicates insulin

Establishing baseline body condition score
resistance. Other diagnostic testing that has
and neck circumference will enable
been described includes the IV glucose
assessment of the horse's response to
tolerance test or a combined glucose-insulin
treatment. Even if there is no history of
response test. The oral glucose tolerance test
laminitis, careful exanlination of the feet,
can be altered by delayed gastric emptying or
including lateral in1ages of P3, are indicated. poor GI absorption and is less desirable.

Because many conditions, including diet,

Because of the large number of blood
pain, and stress, can affect blood glucose
samples required and the fact that change
and insulin levels, diagnostic testing should
from baseline--not absolute glucose
be performed in a controlled manner in a
values-is of interest, a hand-held glucomlow-stress environment. If the horse has eter to detemline blood glucose concentralarninitis, diagnostic testing should be tion may be used when perfomling these
delayed unW the feet have stabilized and
tests.

are relatively pain free.

Tests for PPID such as measuring

Blood glucose concentrations are in the
endogenous ACTH concentration, the
normal range or only slightly increased with
dexamethasone suppression test, domperi

EMS. If persistent hyperglycemia is
done response test,or thyroid releasing
documented, concurrent PPID should be
ho1mone response test are normal in horses
strongly suspected. Because many factors
with EMS. Positive results indicate that the
influence blood glucose and insulin levels, a
horse is concurrently affected by EMS and
one-time blood insulin measurement should PPID, which can occur in older horses.

be used only as a screening test for insulin

Detection of PPID is important, because it is
resistance. Insulin should be determined
thought that PPID exacerbates insulin resisafter the horse has been fasted for 6-8 hr.

tance in horses previously affected by EMS.

This can be done by leaving only one flake
of hay with the horse after 10 PM the night

Treatment and Prevention: Treatment
before and then collecting the blood sample
for EMS involves dietary management and,
the next monling. If those conditions are met, if diet and exercise is not sufficient to treat a blood insulin concentration >20 µU/rnL is
the condition, medical therapy. Correction
suggestive of insulin resistance.

of the diet may be all that is needed to

1008

EQUINE METABOLIC SYNDROME
return the horse to normal body weight.

laminitis, walking as pain allows may be of

Dietary carbohydrate restJ.iction is essensome benefit.

tial to decrease glycemic and insulinemic

Weight reduction should be docwnented
response; total calorie intake is restricted to by scale weight or weight tapes. In addition, reduce body weight. Pasture access should
neck thickness and diameter can be
be eliminated or severely restricted. Use of
monitored over time. If increased exercise

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a grazing muzzle may aid in decreasing
and dietary modification is not sufficient to
pasture ingestion.

decrease body weight, medical therapy may

The nonstructural carbohydrate (NSC)

be of benefit.

content of forage should be determined by

The thyroid hormone thyroxine, in
feed analysis. This can be calculated by
the form of levothyroxine sodiwn, will
adding starch and water-soluble carbohyaccelerate weight loss and thereby in1prove drate percentages. Ideally, NSC should
insulin sensitivity when combined with
comprise <lOOA, of the hay dry matter, and it
dietaty interventions in horses. Horses
should never exceed 16%. Soaking hay in
weighing >350 kg can be given 48 mg/day,
water for 60 min has been recommended to

PO; smaller horses and ponies should receive
lower water-soluble carbohydrate concentra24 mg/day, PO. TreatJ.nent pe1iods of3-6 mo tions, but the actual amow1t reduced is
are often needed to achieve desirable weight
exti·emely variable; hence, this is not a
loss. At that time, the horse should be
reliable method to produce a low-NSC
weaned off the medication over 3-4 wk.

forage. Supplements should be given to

If feed intake is not limited concwTently,
add needed vitamins and minerals but not
treatJ.nent with levothyroxine is unlikely
additional calories. Complete feeds that are
to resolve clinical signs.

fom1ulated to be low in digestible energy and

Metfonnin is poorly absorbed in cquids
carbohydrate specifically designed for horses but may decrease postprandial glucose and with insulin resistance may be used in place
insulin levels .. It may lead to in1provement
of forage and supplements. Numerous
in hyperinsulinemic horses at a dosage of
dietary supplements have been suggested to

30 mg/kg, PO, tid or bid. It should be given
increase insulin sensitivity, including

30 min before a meal if possible. However,
cinnamon, chromitun, and magnesiwn. None
the longte1m efficacy and safety of
has been shown to in1prove insulin sensitivity metfonnin has not been established in in horses in experimental situations.

horses. If it is used, blood glucose should

Horses should initially be fed 1.5% of their be carefully monitored. Use of metformin ideal body weight in forage per day. This
should be discontinued if hypoglycemia
amount can be lowered to 1.25% and then
is docwnented.

to 1 % of ideal body weight after 30 days, if

Prevention of EMS should focus on
necessary. Sudden feed restriction should
maintaining normal weight in horses,
be avoided, because it may lead to hyperparticularly in high-risk breeds. Because lipemia and further exacerbate insulin
these horses may be more efficient users of
resistance. Increasing the amount and level
ingested calories than others, it is imperative
of exercise will increase the rate of weight
to feed appropriately to maintain an ideal
loss. The amount of exercise necessary to
condition score and not to use arbitrary
provide maximal benefits has not peen
feeding guidelines. Particular care should be
established, but five sessions per week that
exercised when turning horses on pasture
include at least 30 min of trotting and
during tin1es of high-soluble carbohydrate
ltmging is a realistic goal. In horses with content, eg, spring and autumn.

FATIGUE AND EXERCISE

Muscular fatigue during exercise is the
ture, hydration status, electrolyte conceninability to continue to perfonn at tl1e same trations, external motivation, and the
level of intensity, resulting from the inability
animal's desire to work. As effort increases,
of t11e muscles to produce force. Fatigue
glycogen depletion, intracellular acidosis,
may occur drning botl1 aerobic and
and accwnulation of metabolic by-products
ai1aerobic exercise, and at submaximaJ
will contJ.ibute to the onset of fatigue.

effort depending on the ambient tempera-

Fatigue during exercise can also be the

FATIGUE AND EXERCISE

1009
result of pathologic conditions, including
serotonin, altered amino acid metabolism,
diseases that affect oxygen uptake, energy
and changes in extracellular ions. Central
metabolism, or neuromuscular function.

fatigue is associated with decreased

This chapter will focus on muscular fatigue
motivation, lethargy, tiredness, and loss of
in nonnal, healthy animals.

muscle coordination. However, the cause

Fatigue is considered a normal conseof central fatigue is multifactorial, and the VetBooks.ir
quence of exercise of prolonged duration or
response to tl1ese stimuli is highly variable.

high intensity, and is regarded as an intrinsic For example, some horses can continue safety mechanism. Without the onset of
endurance exercise at speed despite severe
fatigue, or if fatigue is delayed for a time,
hyperthennia, dehydration, and plasma
structural damage to the myocytes and
electrolyte disturbances.

supportive tissues may occur. Most
knowledge of fatigue has been described in
horses using high-speed treadmill exercise,

FATIGUE DURING HIGH
to allow for investigation of the respiratory,
cardiovascular, and metabolic responses

INTENSITY EXERCISE
during exertion. Tests involved include

For all intensities of exercise, there is a
spirometry, arterial blood gases, hematodegree of anaerobic metabolism, but for logic analysis, kinematics, electromyograbrief, high-intensity exercise, anaerobic phy, and muscle biopsies. Fatigue in these
metabolism predominates. Catabolism
studies has been defined as the inability or
of creatine phosphate and glycogen is
unwillingness of the horse to maintain the
the anaerobic source of energy during
same velocity as the treadmill at a
high-intensity exercise. This type of
detennined speed despite minimal
exercise at an individual animal's highest
encouragement. Horses run to the point of
attainable speed cannot be maintained for
fatigue on a treadmill exhibit characteristic

>30-40 seconds. Thereafter, fatigue occurs
changes in gait, including decreased stride
and the animal slows down.

frequency and a longer stride length.

Fatigue has been classified into two
types: peripheral and central. Peripheral

Energetics of Exercise and Fatigue:

fatigue is described as fatigue secondary to

The contribution of aerobic or anaerobic
altered muscle function. The primary cause
energy pathways during exercise depends
is failure of ATP to resynthesize with
on the duration and energy demands of the
accun1ulation of ADP and inorganic
event. In short, intense exercise lasting
phosphate ions. Studies of muscle

20-30 seconds ( eg, Quarter horse races
metabolism after exercise to identify

[400 ml, some Greyhound races), 600A,of
peripheral fatigue have relied mainly on
energy demands is supplied by anaerobic
muscle biopsies and direct measurement of
sources. For intense exercise at maximal
muscle glycogen, creatine phosphate, ATP,
speeds for a longer duration ( eg, Standard-.

ADP, inosine monophosphate, inorganic
bred or Thoroughbred races [1,600-2,100 m]

phosphate, glycolytic intem1ediary
lasting 1-3 min), it has been estimated that
products, pH, and other metabolites. Other
the energy supply is 20%-300A, anaerobic. In
studies have investigated the expression of
contrast, events lasting many hours ( eg,
mRNA in muscle tissue to monitor
endurance races for horses, camels, and
adaptations in gene expression of proteins
dogs) have >900A, of energy demands met
that regulate oxygen-dependent metaboby aerobic sources.

lism, glucose metabolism, and fatty acid

Dming brief, high-intensity exercise,
utilization. Indirect serum biomarkers
fatigue is secondary to engagement of
associated with fatigue may include lactate,
muscle fibers that heavily rely on anaerobic
an1monia, hypoxanthine and xanthine,
metabolism. The higher the intensity, the
ammonia, markers of oxidative damage
greater the anaerobic demand. Fatigue is

(thiobarbituric acid reactive substances,
the result of an increase in hydrogen ions,
glutathione, and glutathione peroxidase),
lactate, inorganic phosphate, anllllonia, and
inJlan1matory mediators, and lymphocytes.

ADP, and a decrease in ATP, phosphocre

Central fatigue is defined as an alteration
atine, and pH in active muscle cells.

in the signals arising from the CNS, directly

Clinically, fatigue is initially identified by a
decreasing perfonnance by modifying the
decrease in exercise intensity or a drop in
frequency of the action potential in the
the maximal speed.

motor neurons. Central fatigue may occur

As anaerobic metabolism increases,
secondary to pain, dyspnea, perceptions
lactate production is directly correlated to
of exertion, hypoglycemia, hyperthermia,
the percentage of type IIB muscle fibers
ammonia accumulation, increases in
present and corresponds to the accmnulation

1010

FATIGUE AND EXERCISE
of protons in the muscle tissue. Intracellular

Similar to ATP depletion, muscle
acidosis caused by lactate accumulation has
glycogen concentration decreases up to 300;(,
a negative feedback effect on the glycolytic
after a single exercise bout and by as much
enzymes required for energy production and
as 500;(, with repeated bouts of intense
mitochondrial respiration, resulting in a
exercise. Again, depletion varies between
decline in ATP concentrations. Lack of ATP
muscle fiber types, with greater depletion

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prevents calcium recycling through the
seen in type IIB muscle fibers. Glycogen
sarcoplasmic reticulum, resulting in
depletion may play a role in fatigue, in that
accumulation of calcium in the sarcoplasm
horses that perform repeated bouts of
and slowing of the relaxation phase of
exercise before an anaerobic exercise
muscle contraction. Acidosis also interferes
session may be at increased risk of fatigue
with excitation-contraction coupling by
because of the slow rate of glycogen
interfering with calcium binding to troponin
repletion in this species.

C, reducing the ability of the muscles to

During high-intensity exercise, the
contract. Unfortunately, there is no
normal equilibrium between release of
correlation between muscle lactate
potassium from recruited muscle and
concentration and placement in a race, or
uptake by inactive muscle fibers is lost,
plasma lactate concentrations and perforresulting in a continual increase of mance indexes.

extracellular potassium until the onset of

A decrease in muscle ATP after maximal
fatigue. Changes in the ratio of intracellular
exercise has been noted in conjunction with
to extracellular potassium across the
high muscle lactate concentrations. For highsarcolemrna alter the resting membrane intensity exercise, eg, a Thoroughbred race
potential and decrease sarcolemma
lasting 2 min, intramuscular stores of ATP
excitability and the ability to generate an
can decrease from 14% to 500h. Depletion of
action potential. Reduced excitability

ATP varies by muscle fiber type. In type I
contributes to reduced calcium release by
fibers, depletion is negligible, whereas in
the sarcoplasmic reticulum (a process that
type IIB fibers, ATP loss is significant. Low
requires ATP) and a consequent reduction
levels of ATP impair optimal functioning for
in the force of muscle contraction. This
muscle contraction, reuptake of calcium by
loss of force may relate to the idea of an
the sarcoplasmic reticulum, and the sodiwn
inherent safety mechanism, in that plasma
potassium exchange. Fatigue is associated
potassium rapidly declines after cessation
with depletion of phosphocreatine stores
of exercise by reuptake into the now
and accumulation of ADP and inorganic
inactive muscle.

phosphate. A correlation between stride

Intracellular acidosis as a result of lactate
length and muscle ADP accumulation has
accumulation has been blan1ed for the
been seen at the time of fatigue.

decrease in efficiency or force of muscle
contractions. However, in vitro research has

Muscular Fatigue:. Increased ADP
demonstrated a protective effect of lactic
concentration results in accumulation of
acidosis or hydrogen ions in maintaining

AMP, inosine monophosphate, allantoin,
sarcolemma function and muscle force
anunonia, and uric acid in horses. In
production in the face of potassium shifts
treadmill studies, the decre�e in muscle
within the cell and plasma associated with

ATP during intense exercise is correlated
intense exercise.

with an increase in plasma uric acid
concentration 30 min after exercise.

Thermoregulation and Fatigue:

Running time during treadmill tests is

Fatigue during high-intef.lsity exercise is
co1Telated with uric acid concentrations
also influenced by environmental condiafter exercise. Significant but low correlations. Intense exercise in hot conditions is tions have also been found between racing
associated with earlier onset of fatigue,
performance of Standardbred pacers and
due to increased blood flow to the skin for
uric acid concentrations after a race.

thermoregulation at the expense of cardiac

Ammonia accumulation in plasma is
output and oxygen delivery to the exerciscorrelated to decreased ATP and increased ing muscle. Attenuation of normal increases
muscle lactate. It has been postulated that
in muscle blood flow during exercise in
anunonia accumulation in the plasma may
hot environments has been suggested as a
contribute to fatigue. However, infusion
contributor to the onset of fatigue. There is
with anunonium acetate during treadmill
also a central effect of high temperatures,
exercise until fatigue did not significantly
resulting from increased blood temperature
affect time to fatigue, suggesting plasma
at the hypothalamus. Early onset of fatigue
ammonia levels do not have a role in fatigue
in hot conditions is thought to be a produring intense exercise.

tective response to avoid heat stroke.

FATIGUE AND EXERCISE

1011 .

FATIGUE DURING PROLONGED
damage to the kidneys, GI mucosa, and

EXERCISE
lamina of the hoof.

Sweating is associated with the loss of

Fatigue as a result of prolonged exercise
electrolytes, mainly sodium, potassiwn and
depends on the duration and intensity of the
chloride, as well as calcium and magnesium.

activity, liver glycogen stores, the an1bient

Alterations in muscle electrolytes can

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temperature, and mechanisms of central
contribute directly to signs of fatigue. The
fatigue. Prolonged exercise mainly depends
most common acid-base alteration resulting
on aerobic metabolism. Fatigue during
from electrolyte imbalances is metabolic
prolonged exercise has been associated
alkalosis. Aerobic energy metabolism of
with depletion of glycogen stores in muscle
endurance events produces minimal
and liver, and with hypoglycemia. Intramusamounts of lactic acid; therefore, alkalosis cular glycogen provides 5QOA, of the energy
caused by alterations in strong ions
during the first 30 min of submaxinlal

(hypochloremia and hypokalemia)

exercise but drops to <200Ai after 1 hr. Blood
predominates. Depletion of magnesium and
glucose makes a smaller contribution,
calcium may contribute further to
providing only lOOAi of total energy utilized.

neuromuscular dysfunction, causing ileus,

Although circulating fatty acids may provide cardiac arrhythmias, and synchronous an energy source during prolonged
diaphragmatic flutter. Unlike endurance
exercise, fatigue will set in before these
riding, anaerobic metabolism predominates
fat stores are completely exhausted.

in 3-day eventing and combined driving,

In prolonged exercise, the heat generated
resulting in metabolic acidosis during tl1e
during aerobic ATP resynthesis imposes a
event. After recovery, which can range from
high thermoregulatory demand on the

30 min to 2 hr after the event, lactate is
aninlal. Only 25% of the total energy
oxidized and the acidosis resolves.

produced by the muscles is converted to

Metabolic alkalosis will then predominate.

mechanical energy, leaving 75%-SQOA, of

Horses affected by exhausted horse
that energy that must be removed as heat.

syndrome demonstrate a range of symp

Physiologic responses to heat production
toms, from changes in attitude and gait
include sweating and/or panting to remove
inconsistencies to colic, laminitis, clinical
excess heat from the body. Complications
signs of myopathies (hard muscle bellies,
from these compensatory mechanisms
pain on palpation), depression, ataxia, and
include dehydration, acid base and
eventually recumbency. Persistent
electrolyte disturbances (which are
tachycardia and tachypnea are noted
implicated as causes of fatigue), exhaustion, despite rest, and rectal temperature may be and even death (which can occur after

<!42°C (107.6° F). Perfusion abnormalities
prolonged exercise).

and signs of dehydration may be seen.

Sweating may be inappropriate or absent.

Exhausted Horse Syndrome: Horses

Treatment involves cooling tl1e hor.se and
occasionally develop severe clinical signs of
providing fluid therapy to restore circulating
fatigue at endurance events, despite current
volw11es. Hyperthermic horses should be
preventive practices, including evaluation
moved to shade and treated with cool or
of recovery at rest stops. Horses that
cold water sponge baths, cold hosing, or
compete in sports that include 3-day
misting fans. Water should be scraped off
eventing, endurance rides, or combined
the haircoat and reapplied repeatedly, to
driving are at risk of presenting with
prevent an insulating layer of water from
life-threatening exhaustion. In hot
forming. Application of ice water should be
conditions, horses may lose body fluids at
avoided, as well as alcohol baths or direct
a rate of 10-15 Ilhr through sweat during
ice application, to prevent tissue dan1age.

prolonged exercise. Urgent treatment of

Cool-water enemas, or peritoneal and
fluid and electrolyte deficits and hyperthergastric lavage, may help to reduce body mia (rectal temperatures >40.5°C [104.9°F])

temperature in severe cases.

may be required. Exhausted horses may

Isotonic balanced electrolyte solutions

Jose up to 10% of their body weight in water,
may be provided for dehydration by
with some having body fluid deficits of up to
nasogastric intubation if the horse has

40 L, depending on their size. Water lost as
nom1al borborygmi. Horses may be given
sweat is mainly lost from the extracellular
up to 8 L initially, with subsequent adminisfluid and circulating plasma. Decreased tration of 4--8 L every 1-2 hr, as needed.

blood volume reduces perfusion to vital

Commercial electrolyte mixtures for horses
organs and hampers thermoregulation. In
are suitable, but hypertonic, hypotonic, and
severe cases, cardiovascular compromise
alkaline solutions should not be used. In
may result in multiorgan failure, including
severe cases, IV fluid therapy is preferred.

1012

FATIGUE AND EXERCISE

A shock dose of a balanced electrolyte

In experimental studies, a nillder fom1 of
solution should be provided initially
overtraining has been reproduced, without

(20---40 mIJkg bolus) with addition of
any evidence of red cell hypervolemia,

100 mL 23% calcium gluconate per 5 L, and
inappetance, or adrenal gland exhaustion.

5% dextrose. Additional fluids and additives

However, this syndrome was associated with
should be based on reevaluation of serum
a decrease in the plasma cortisol response to

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chemistries and hydration status.

intense exercise, suggesting that overtrain

Additional treatments may include
ing is associated with dysfunction of the

NSAIDs for muscle pain and colic,
hypothalainic-pituitary-adrenal axis. Recent
administered simultaneously with fluid
research has shown that overtrained horses
therapy to prevent renal injury, and
have altered growth hormone activities, with
phenothiazines for anxiety caused by
an increase in the normal pulsatile growth
myopathies. Anticonvulsant medications
hormone activity overnight, in addition to
may be required, and dexamethasone may
altered glucose metabolism. Biomarkers of
help reduce cerebral edema. DMSO may be
skeletal muscle metabolism are cun-ently
useful to further reduce inflammation, and
being investigated as a means to identify
low-molecular-weight heparin can be
overtraining syndrome but require invasive
administered to treat coagulopathies.

muscle biopsies for measurement.

Environmental temperature and htunidity

Overtraining syndrome should be
have a major impact on the severity of
suspected in horses with evidence of
disturbance of the horse's fluid balance
sustained decreased performance in
during prolonged exercise. It is important to
association with one or more physiologic or
ensure adequate hydration before an event,
behavioral signs. While no single physiologic
especially after long trailer rides to the
mai·ker is able to identify tl1e syndrome,
competition, and to provide access to fluids
clinical signs in horses may include
during and after exercise to reduce the
decreased body weight, increased heart rate
likelihood of dehydration. Administration
during exercise, decreased plasma cortisol
of supplementary fluids, electrolytes, and
response to exercise, and increased plasma
glucose before and during competition, when concentrations of muscle enzymes or gamma allowed by doping regulations, may reduce
glutamyl transferase. Behavioral signs are a
the incidence of exhausted horse syndrome.

consistent and eai·ly marker of overtraining
syndrome, and development of a behavioral

Overtraining Syndrome: Highly intense
score to assist in early detection of over
exercise training over many weeks can
training syndrome in horses is warranted.

result in a fonn of chronic fatigue refen-ed
to as overtraining syndrome. Racehorse

PREVENTION OF FATIGUE
trainers have long used the terms "overtraining," "staleness," or "sourness" to Physical Training: Physical training is the
describe a syndrome of poor pe1f01mance,
most effective way to reduce fatigue and
failure to recover from exercise, and
increase capacity for exercise. Physiologic
prolonged fatigue that does not resolve for
responses to training that contribute to
weeks or months. By definition, signs of
increased exercise capacity include
overtraining syndrome should persist after
increases in the maximal rate of oxygen

>2 wk of rest or reduced physical activity.

transport, cardiac stroke volume, muscle

A less severe form of overtraining syndrome
capillaiy density, circulating blood volume,
is termed "oven-eaching," which is also a
and total hemoglobin content. Hypertrophy
syndrome of poor performance and fatigue,
of muscle cells occurs, coupled with
but athletic recovery in oven-eaching
increases in concentrations of mitochontypically occurs from a few days to 2 wk dria, glycogen, and enzymes concerned with
after a reduced workload.

cellular energy production.

Overtraining syndrome was first reported

Sport-specific training can result in
in Swedish Standardbred trotters based on
specific adaptions. For exan1ple, sprint
observations of horses with signs of fatigue
training can result in decreased proportions
and poor performance combined with
of slow-twitch muscle fibers, whereas
weight loss, inappetence, and signs of
endurance training can result in increased
stress, including tachycardia, nervousness,
oxidative capacity of fast-twitch muscle
muscle tremors, sweating, and diarrhea.

fibers. Sprint training also modulates the

The severity of clinical signs of overtraining
ionic changes associated with intense
was associated with the degree of red cell
exercise, including decreased potassium
hypervolemia, and horses exhibited adrenal
efflux from working muscles, resulting in a
exhaustion that may be sinillar to parasymsmaller increase in plasma potassium and pathetic overtraining reported in people.

delayed onset of fatigue. Training also

FATIGUE ANO EXERCISE

1013
modulates the exercise-induced decline in
which fatigue occurs. Although a metabolic
both calcium reuptake by the sarcoplasmic
aJkaJosis could be induced, administration
reticulum and caJcium-ATPase activity
of sodiU111 bicarbonate before intense
associated with fatigue.

treadmill exercise did not have any

Adaptations to training in skeletal muscle
significant effect on metabolic response to
depend on the training intensity. Horses
exercise. In Greyhotmds, a dose of sodiU111

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trained at intensities >800/o of their maximal
bicarbonate at 0.4 g/kg did not have a
oxygen uptake (V02maJ had an increase in
significant effect on race time in races
their percentage of fast-twitch muscle fibers

>400 m long. However, there may be an
and an 8% increase in the buffering capacity
ergogenic effect when sodilll11 bicarbonate
of exercised muscle. These responses did
is administered at high dosages. Sodium
not occur in horses trained at 400/o ofV02ma.,·
bicarbonate at a dosage rate of 1 g/kg (by

Heart rate meters can be used to guide
nasogastric tube) increased the time to
the intensity of training to improve the adapfatigue in horses nmning on a treadmill, and tive response to training. Heart rates that
it was concluded that treatment at this dose
result in 80% ofV02 are -900/o of maximal
affected perfonnance.

max
heart rate, which typically ranges from 210

Energy supply and hydration are
to 240 bpm in horses. Heart rate meters can
frequently manipulated in hU111an athletes
be used to measure an individual horse's
to lirnit fatigue during endtrrance exercise.

heart rates dming slow and fast exercise

Dehydration before exercise results in higher
and to calculate the exercise velocities that
core temperatures dttring exercise in horses.

result in heart rates of90"/oof maximal heart

It would be inappropriate for an anin1aJ to
rate. Blood lactate after exercise can also be begin an endurance exercise with suboptiused to measure tl1e appropriate training mal hydration. Horses are more susceptible
intensity. At an exercise intensity of 800/o
to hypertl1em1ia during prolonged exercise

V02
plasma lactate concentrations
than people because of tl1eir high body mass
max,
during treadmill exercise are in the range
to swface area ratio, which inhibits heat loss.

of 4-10 mmol/L.

Equine them1oregulation also results in
extreme changes to total body fluid status,

Warm-up: Wann-up before exercise
and there is increasing interest in the way
significantly increases the time to fatigue
of linuting these excessive responses to
dming intense exercise. Warm-up increases
exercise by preexercise fluid administration.

muscle temperature before exercise,

Hyperhydration by administration of
increases the rate at which oxygen uptake
electrolytes or saline solutions orally before
increases, and reduces lactate accU111ulaexercise will result in expansion of the tion by enhancing aerobic metabolism. The
blood volLU11e during the event. Studies
effect is similar whether tl1e warm-up is
suggest that hyperhydration before
low intensity (5-10 min at 500/o V02max),
prolonged exercise helps conserve plasma
moderate intensity (1 min at 700/o V02max),
volm11e during exercise but does not lower
high intensity (1 min at 115% V02max), or a
body temperature or improve arterial
combination of low- and high-intensity. The
hypoxemia. Maintenance of euhydration
practical in1portance of this finding is that a
with water or a carbohydrate-electrolyte
warm-up before competition involving
solution during exercise improves perfusion
intense exercise is likely to increase the
parameters and sweating rates and reduces
time to fatigue during Quarter horse,
heat storage. Horses should be acclimated

Thoroughbred, and Standardbred races.

to hot environments before competition.

Horses should not be given large meals

Manipulation of Acid-Base Balance,

( equal to half the ration) 1-2 hr before

Diet, and Hydration: It has been
intense exercise, because plasma volume is
suggested that fatigue during intense
decreased for at least 1 hr after a large meal.

exercise may be delayed by manipulation of

Large meals may also shift fluid to the
acid-base status before exercise to increase

GI tract, reducing cardiovascular and
the plasma-buffering capacity. Although
tl1ermoregulatory function dming exercise.

some trainers have administered sodiU111

Feeding smaller rations every 4 hr does not
bicarbonate before races, this practice is
result in changes in plasma volLU11e. A
now banned by many racing administrasho1t-tenn reduction in fiber intake before tions. The treatment does alter blood pH
high-intensity racing (fed as -1% of body wt
and lactate concentrations during exercise;
in hay for 3 days before high-intensity
however, the effect of aJkaJinizing solutions
exercise) is a strategy to reduce GI water
on equine perfonnance is equivocal. Studies
volume and, hence, body weight. For
using bicarbonate at a dosage of 0.6 g/kg
endurance exercise, feeding before
have not shown an effect on the time at
exercise, especially high-fiber feeds, is likely

1014

FATIGUE AND EXERCISE
to be beneficial, because the increased
needed for high-intensity exercise. Adding
water in the GI tract can be an important
fat to the diet also affects the metabolic and
reservoir for water and electrolytes to
thermoregulatory response to exercise.

replace sweat losses. Feeding high-fiber

Feeding vegetable oil at a rate of 100/o-12% of
feeds also increases voluntary water intake.

the total diet on a dry-matter basis has been

Glucose supplementation may be
suggested, but horses must be acclimated to

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important in lintiting fatigue in endurance

!ugh-fat diets. In horses not acclimated, fat
exercise in horses. Endurance time during
supplementation can slow the rate of muscle
treadmill running was prolonged by the
glycogen repletion.

IV infusion of a glucose solution during

Creatine has been used in horses as an
exercise. Plasma glucose was higher than
ergogenic aid, but there is no evidence of its
controls, and plasma lactate and body
efficacy. Horses receiving 25 g of creatine
temperature were lower at the point
monohydrate bid for 6.5 days did not have
of fatigue. These results suggest that
significantly different run times until fatigue
supplemental glucose during exercise
on a treadmill than control horses.

prolongs performance time in horses. This

Supplementation with creatine also had no
increase may be due to increased glucose
significant effect on muscle or blood
availability, reduced reliance on anaerobic
creatine concentrations at rest or after
energy production, lower core temperature,
exercise until fatigue.

and better maintenance of plasma volun1e.

An association between plasma vita.min E

In endurance horses, hydrolyzable starches
concentration and performance has been
and sugars fed within 3 hr of a race may
described in sled dogs. Dogs with a higher
increase glucose utilization in the short
prerace vita.min E concentration were more
tem1 but inhibit lipid oxidation, which could
likely to finish the race and were less likely
be detrin1ental for energy production.

to be withdrawn during tl1e race for poor

Glycogen concentration in skeletal
health, fatigue, or other reasons. Vita.min E
muscle before perfom1a.nce is relevant to
concentrations for the dog team overall
fatigue during both short-tennlintense and
were not associated with speed during the
prolonged endurance exercise. Depletion of
race. Additional studies are needed to
muscle glycogen before exercise causes a
investigate whether tl1e reduced signs of
decrease in anaerobic power generation and
fatigue are directly linked to higher vita.min
capacity for high-intensity work. Intense or

E concentrations in the bloodstream.

prolonged exercise depletes the muscle
glycogen stores, and it may take 48 hr for

Recovery: Recovery of horses after
glycogen to be replenished in the horse.

endurance exercise is influenced by tl1e

Although modest increases in glycogen
rehydration strategy used. After prolonged
stores may be obtained using high-starch
treadmill exercise and furosemide-induced
diets in the horse, no benefit on performance dehydration, horses offered a saline has been shown. On the contrary, highsolution (0.9% NaCl) as the initial rehydracarbohydrate diets have increased heart tion fluid maintained a plasma sodium
rates and blood lactate concentrations
concentration higher than that of control
during intense exercise. Use of glucose or
horses. The recovery of body weight was
other carbohydrate solutions before racing
more rapid than in horses offered plain
to promote perfonnance in Standardbred
water. A similar study noted ambient
and Thoroughbred racehorses has no
temperature fluids were more palatable
scientific basis.

(20°C [68°F]) and increased voluntary

Fat supplementation is now a widespread
intake. Water intake can also be increased
practice in diets for athletic horses and can
by providing a saline solution (0.9% NaCl)

increase perfom1ance during endurance
both during and after endurance exercise.

exercise. Increased free fatty acid concentra

Sodiun1 chloride solutions may increase
tions in the bloodstream before prolonged
plasma chloride and accentuate a
exercise results in an increased use of fat as
metabolic acidosis; as a result, isotonic
an energy source and in higher blood glucose
polyionic electrolyte solutions fom1ulated
and muscle glycogen concentrations during
specifically for horses should be selected.

exercise. The shift to increased use of fat as a When providing electrolyte solutions, fuel results in lower respiratory demands for
horses may need to be trained to drink
exercise, because less carbon dioxide must
these fluids, and plain water should always
be expired when more fat is used for energy.

be available. However, use of electrolyte

Fat adaptation appears to facilitate the
solutions should be encouraged, especially
metabolic regulation of glycolysis by sparing
in horses required to compete on consecuglucose and glycogen at low-intensity work tive days, such as in endurance rides and
and by promoting glycolysis when power is

3-day events.

FEVER OF UNKNOWN ORIGIN

1015

FEVER OF UNKNOWN ORIGIN

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In both veterinary and human patients,
temperatures in the range of 103°- l06°F
fever may indicate infectious, inflamma

(39.5°-41.l °C).

tory, immune-mediated, or neoplastic

An increase in the hypothalamic set-point
disease. In most cases, the history and
may be initiated by exogenous pyrogens,
physical examination reveal the cause of
which include drugs, toxins, and viral or
the fever, or the fever resolves spontanebacterial products ( eg, endotoxin ). These ously or in response to antibiotic therapy.

pyrogenic stimuli lead to the release of

However, in a small percentage of patients,
cytokines, termed endogenous pyrogens,
the cause of fever is not readily apparent,
from inflammatory cells. Ultimately, locally
and the problem becomes persistent or
synthesized prostaglandin E2 in the
recurrent. These patients are said to have
hypothalamus is responsible for increasing
fever of unknown origin (FUO).

the set-point, resulting in fever.

In human medicine, classic FUO is
defined as fever >101 °F (38.3°C) on

Etiology and Pathogenesis: FUO may
several occasions over a period >2-3 wk
be defined as fever that does not resolve
with no diagnosis established after 3
spontaneously in the period expected
outpatient visits or 3 days in the hospital.

for self-limited infection and for which a

There is no recognized definition of this
cause cannot be found despite considerable
syndrome in veterinary medicine, making
diagnostic effort. This excludes patients
it difficult to determine its true prevathat respond to antibiotic therapy (and do lence. FUO is probably less prevalent now
not relapse) and patients in which the cause
than in the past because of improved
of fever is determined from initial history,
diagnostic technology ( eg, imaging,
physical examination, or laboratory tests,
molecular diagnostic tests).

or in which fever resolves spontaneously.

Infectious, immune-mediated, and
neoplastic disease are the most common

Body Temperature Regulation: Body
causes of FUO in dogs. In a study of 101
temperature is regulated by the hypothaladogs with fever, 22% had immune-mediated mus. This area of the brain acts as a
diseases, 22% primary bone marrow
thermostat to maintain temperature as
abnormalities, 16% infectious diseases,
close as possible to a normal set-point. The

11.5% miscellaneous conditions, 9.5%
hypothalamus receives input from internal
neoplasia, and 19% genuine FUO. In cats,
and external thermoreceptors, and it
the cause is more likely to be infectious,
activates physiologic and behavioral
but there are fewer published data on
activities that influence heat production,
feline cases than on canine cases. In a case
heat loss, and heat gain.

series of horses with FUO, 43% had

Hyperthermia refers to any increase
infectious disease, 22% neoplasia, 6.5%
in body temperature above the normal
immune-mediated disease, 19% miscellarange. Fever is a particular form of neous causes, and in 9.5% the cause was
hyperthermia in which the heat loss and
not determined. In farm animals, the most
heat gain mechanisms are adjusted to
likely causes of FUO are infectious or
maintain body temperature at a higher
inflammatory diseases such as pneumonia,
hypothalamic set-point; thus, fever is
peritonitis, abscesses, endocarditis,
essentially a regulated hyperthermia. In
metritis, mastitis, polyarthritis, and
nonfebrile cases of hyperthermia ( eg, heat
pyelonephritis.

stroke, exercise-induced hyperthermia,
malignant hyperthermia, seizure), body

Diagnosis: The key to diagnosis of FUO
temperature is increased by abnormal and is to develop and follow a systematic plan unregulated heat loss, heat gain, or heat
that allows for the detection of both
production, and the hypothalamic
common and uncommon causes of fever.

set-point is not altered. Depending on

The plan should always include repetition
their severity, these conditions can
of relevant tests, because findings can
potentially result in body temperatures
change over time. Owners should be

;,cl06°F (41.1 °C). In comparison, most
informed that diagnosis of FUO may
patients with true fever have body
require considerable time and patience

1016

FEVER OF UNKNOWN ORIGIN
and may demand more advanced or
carefully about specific clinical signs,
expensive diagnostic tests. Nevertheless,
because these may help localize the source
simple and inexpensive tests may also
of the fever. The physical exan1ination
reveal diagnostic clues that eventually
should be detailed; always include fundic,
point to the cause of the fever. In one
neurologic, and rectal exan1inations; and
retrospective study of fever in dogs,
repeated frequently.

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radiography, cytology, and bacterial or
fungal cultures of tissues or fluids were

CBC and Serum Chemistry Profile: The
found to be the most useful diagnostic

CBC and chemistry changes in animals with
tests.

FUO are often nonspecific but may suggest

A staged or tiered approach to diagnosis further diagnostic tests. For example, bile can assist in choosing appropriate tests.

acids assay may be indicated in an animal

The first stage should include history,
with changes suggestive of hepatic
physical examination, ophthalmic and
dysfunction. The CBC should always be
neurologic examinations, CBC, fibrinogen, accompanied by blood smear evaluation to serum chemistry profile, urinalysis and
detect parasites or morphologic changes.

urine culture, feline leukemia virus and

Urine Culture: This test is always
feline immunodeficiency virus tests (cats), indicated to evaluate FUO in small animals, and usually thoracic and abdominal
regardless of the appearance of tl1e urine
radio graphs in small animals. Any
sediment.

medications that could induce fever

Radiography and Advanced Imaging:

should be discontinued. In the second
stage, some first-stage tests may be

Thoracic and abdominal radiographs are
repeated (particularly the physical
useful screening tools for the early
localization of fever. Skeletal radiographs
examination), and additional specialized
tests are performed. These may be
and contrast radiographs may subsequently
be considered, depending on initial findings.

dictated by abnormal findings in the first

For exan1ple, myelography may be used to
stage of testing or may be determined by
investigate back pain. The use of techniques
consideration of the most common known
such as CT or MRI is determined by the
causes of FUO. Tests included in this stage results of initial diagnostic testing or by include blood cultures, arthrocentesis,
abdominal ultrasonography, lymph node
consideration of the body system of
aspiration, aspiration of other organs or
interest, eg, MRI is particularly useful to
evaluate the CNS. Advanced imaging with
masses, analysis of body fluids (eg, fluid
nuclear scintigraphy or positron emission
from body cavities, milk samples,
tomography is used in human patients with
reproductive tract secretions), rectal
cytology, fecal culture, echocardiography

FUO but is not yet widely reported in
veterinary medicine.

(in the presence of a murmur), long-bone
and joint radio graphs, contrast radio

Ultrasonography and Echocardiogra
graphs, serology, and molecular diagnos
phy: Abdominal ultrasonography may
tic tests. In the third stage, earlier tests
reveal a source of fever in the abdomen,
may be repeated again, as well as
such as neoplasia, peritonitis, pancreatitis,
additional specialized proceck!res. These
or abscesses. The thoracic cavity, limbs, and
procedures are most likely to be chosen
retrobulbar areas may also be exan1ined by
on the basis of previous findings but may
ultrasound. Echocardiography is indicated
also be considered when all previous
at the early stages of evaluation of the FUO
testing has been unrewarding. Examples
patient with a murmur. This may aid in the
include echocardiography (in the absence
detection of endocarditis, although this
of a murmur), dental radiographs, bone
diagnosis should also be based on
marrow aspiration, bronchoscopy and
signalrnent, characteristics of the heart
bronchoalveolar lavage, CSF analysis, CT,
murmur, and blood culture results.

MRI, laparoscopy, thoracoscopy, biopsies,

Bone Marrow Evaluation: Bone
exploratory surgery, or trial therapy.

marrow cytology and histology should be

History and Physical Examination:

evaluated in any animal with unexplained

Epidemiologic characteristics such as

CBC abnormalities. Bone marrow disease
vaccination, parasite control, exposure to
is a common cause of FUO in small
vectors, and travel history should always
animals; therefore, bone marrow
be reviewed. The response to previous
aspiration and biopsy, if possible, should
medications should be determined, as well
also be included in the second stage of
as the presence of illness in other animals
diagnostic testing in these patients. When
or people. Owners should be questioned
obtaining bone marrow aspirates from

FEVER OF UNKNOWN ORIGIN

1017
cats, a sample should be saved for possible
diagnose systemic lupus erytl1ematosus
molecular diagnostic testing for feline
or rheun1atoid arthritis, respectively.

leukemia virns.

Microbiology, Cytology, and

Arthrocentesis: Because immune

Histology: Fine-needle aspirates are safe
mediated polyartlu·itis is a common cause
ai1d simple to obtain from effusions,
of FUO in dogs, aithrocentesis of multiple
masses, nodules, orgai1s, tissues, ai1d body

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joints is included in the second stage of
fluids. Fluids should be exainined cytologidiagnostic testing in this species, even if the cally ai1d also submitted for microbiologic
joints are nom1al on palpation. Some dogs
or molecular diagnostic testing. Tissue
with steroid-responsive meningitis-arteritis
biopsies are generally obtained in the
also have concurrent inunune-mediated
second or third stages of diagnostic
polyarthritis; therefore, arthrocentesis
testing, after clinical signs or initial
should be performed in dogs with spinal
diagnostic tests have localized the fever.

pain. Infectious polyarthritis is more

When biopsies are obtained, sufficient
commonly recognized in large ai1imals,
samples should be submitted for histopain which arthrocentesis is ai1 importai1t thology, appropriate culture (aerobic ai1d
diagnostic test.

ai1aerobic, fungal, mycoplasmal, mycobac

CSF Analysis: CSF sainpling is recomterial, etc), moleculai· diagnostics, ai1d mended for dogs with FUO if less invasive
special stains. If exploratory surgery is
tests do not reveal the cause of the fever.

perfom1ed, biopsies should be obtained

Fluid should be submitted for cytology,
from several sites.

protein measurement, ai1d culture.

Treatment: In some FUO cases a specific

Blood Culture: Blood cultures are
diagnosis is not reached, or diagnostic
recommended in all animals with unextesting is discontinued, leading to plained fever. The techniques used should
consideration of therapy in the absence of
allow the collection of adequately large
a diagnosis. Options include ai1tibiotics,
volun1es of blood under aseptic conditions.

ai1tifungal agents, ai1d anti-inflammatory

If the size of the ai1imal allows collecting
or immunosuppressive therapy ( usually
more thai.1 one set of sainples for blood
with corticosteroids). Trial therapy may
culture, using appropriately sized aerobic
resolve the clinical signs or confirm a
ai1d ai1aerobic bottles increases the
presumptive diagnosis, but it is also
sensitivity ai1d specificity of the test.

associated with significai1t risk. Before

Special enrichment culture methods
pursuing a therapeutic trial, the owner
may be considered for certain organisms,
should be informed of the potential risks
eg, Barlonella spp.

ai1d should be committed to careful

Infectious Disease Testing: Tests
monitoring of the ai1imal for aJ.1 appropriavailable for the diagnosis of infectious ate length of time. The therapeutic trial
diseases include assays for detection of
should be based on a tentative diagnosis
ai1tibodies or ai1tigen in blood, body fluids,
ai1d should define the parai11eters to be
or tissues. Molecular diagnostic tests detect
followed ai1d the criteria used to deternucleic acid, with PCR being the most mine treatment success or failure. If aJ.1
common in this category. Selection of these
ai1imal is likely to be referred for in-depth
tests should be based on the signalrnent,
investigation of FUO, trial therapy should
clinical signs, ai1d epidemiologic characternot be started because it may affect the istics of the animal. Interpretation of test
results of further testing.

results requires aJ.1 understanding of disease

In true fever, the increase in body
prevalence, vaccination history, ai1d
temperature is regulated; therefore, cooling
sensitivity ai1d specificity of the test. When
methods such as water baths work against
requesting PCR-based assays, it is in1porta.J.1t the body's own regulatory mecha.J.1isms.

to use laboratories that have quality

It is also likely that fever itself has some
mai1agement prograins that address test
beneficial effects, particulai·ly in infectious
perfo1mai1ce ai1d consistency, ai1d control
diseases. However, fever cai.1 lead to
for sainple contan1ination.

ai1orexia, lethargy, ai1d dehydration. Thus,
a.J.1imals with FUO may benefit from IV

Other Serologic Tests: The value of
fluid therapy or ai1tipyretic medications.

immune pai1els or autoai1tibody screens in

Exainples include NSAIDs such as aspirin,
small ai1imal patients with FUO is unclear.

carprofen, ketoprofen, ai1d meloxican1 in

Neither ai1tinuclear ai1tibody nor rheun1asmall a.J.1imals, and flunixin meglumine or toid factor titers alone should be used to
phenylbutazone in large animals.

1018

HEPATIC LIPIDOSIS

HEPATIC LIPIDOSIS

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FATTY LIVER DISEASE OF CATTLE
with the amount of available body fat
reserves moderates the degree of

Fatty liver results from a state of negative
triglyceride accumulation. Excessive
energy balance and is one of the important
intracellular triglyceride accumulation
metabolic diseases of postparturient dairy
in liver cells results in disturbed liver
cows. Although often considered a
function and cell damage. Fatty liver can
postpartum disorder, it usually develops
develop within 24 hr of an animal going off
before and during parturition. Periparturifeed. Although lipid accumulation in the ent depression of feed intake, and endocrine liver is a reversible process, the slow rate changes associated with parturition and
of triglyceride export as lipoprotein causes
lactogenesis contribute to development of
the disorder to persist for an extended
fatty liver. Cows that are overconditioned at
period. Depletion of the liver lipid content
calving are at highest risk. Fatty liver can
usually begins when the cow reaches
develop whenever there is a decrease in
positive energy balance and may take
feed intake and may occur secondary to the
several weeks to fully subside.

onset of another disorder. Fatty liver at

Fatty liver is not a consequence of
calving is commonly associated with ketosis positive energy balance or overfeeding.

(seep 1024).

Energy consumption above requirements
for maintenance and productive purposes

Etiology: Mobilization of body fat
will not directly result in deposition of
reserves that is triggered by hom1onal cues
triglyceride in hepatic tissue. Triglyceride
in states of negative energy balance results
deposition will occur only if the animal
in the release of nonesterified fatty acids
becomes overconditioned and consequently

(NEFAs) from adipose tissue. The liver
reduces feed intake.

retains -15%-200/o of the NEFAs circulating
in blood and thus accumulates increased

Clinical Findings: There are no pathognoamounts du1ing periods when blood NEFA monic clinical signs of fatty liver disease in
concentrations are increased. The most
cattle. The condition is often associated
dramatic increase occurs at calving, when
with feed intake depression, decreased milk
plasma concentrations are often >1,000
production, and ketosis. Increased blood
µEq/1. Concentrations can reach that level

NEFA concentration has been associated
if the animal goes off feed. NEFAs taken up
with impaired immune function and a
by the liver can either be oxidized or
proinflammatory effect, presumably
esterified. The primary esterification
reflecting in increased incidence of clinical
product is triglyceride, which can either be
mastitis, metritis, and other periparturient
exported as part of a very low density
infectious diseases. However, cause and
lipoprotein (VLDL) or be stored iu liver
effect has not been established. Metabolic
cells. In ruminants, export occurs at a very
consequences of triglyceride accun1ulation
slow rate relative to many other species
in the liver include reduced gluconeogenbecause of impaired VLDL synthesis.

esis, ureagenesis, hormone clearance, and

Therefore, under conditions of increased
hormone responsiveness. Consequently,
hepatic NEFA uptake and esterification,
hypoglycemia, hyperammonemia, and
triglycerides accumulate. Oxidation of
altered endocrine profiles may accompany

NEFAs leads either to the production of
fatty liver.

ATP in the tricarboxylic acid cycle or to the

Fatty liver is likely to develop concurformation of ketones through peroxisomal rently with another disease, typically
or !3-oxidation. Ketone formation is favored
disorders that are seen at or shortly after
when blood glucose concentrations are low.

calving. These include metritis, mastitis,

Conditions that lead to low blood glucose
abomasal displacement, or hypocalcemia.

and insulin concentrations also contribute

Field observations suggest that response to
to fatty liver, because insulin suppresses fat
treatment of concurrent disorders is poor if
mobilization from adipose tissue.

cows have extensive triglyceride infiltration

The greatest increase in liver triglycerof the liver. Cows slow to increase in milk ide typically occurs at calving. The extent
production and feed intake after calving are
of feed intake depression before and after
likely to have fatty liver. However, fatty liver
calving or during disease in combination
is probably the result rather than the cause

HEPATIC LIPIDOSIS

1019
of poor feed intake. Fatty liver is often

13-hydroxybutyra.te concentration in blood
associated with obese cows and downer
has become a popular way to identify
cows (seep 1188) but is unlikely to be a
herds that may be at risk of developing
direct cause of the downer cow syndrome.

fatty liver. Measurement of plasma NEFA

Overconditioned cows exhibit more
concentration is more expensive and
pronounced feed intake depression before
requires submission of blood samples to

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and after calving than nonobese cows and,
a diagnostic laboratory. In addition to
therefore, are susceptible to fatty liver.

extreme variations in plasma NEFA

Although obesity predisposes to fatty liver
concentrations among animals, there is
disease, it is not restricted to obese cows.

extreme variation in a single individual,

Similarly, obese cows do not necessarily
because concentrations increase
have fatty liver.

dramatically immediately before and after
calving. Therefore, a large number of

Diagnosis: Diagnostic tools for fatty liver
animals must be san1pled at a consistent
are of limited value. Fa.tty liver is usually
time relative to calving. Ca.re must be taken
diagnosed after the animal has been off feed
not to excite animals before sampling
or has died because of another disease.

blood, because NEFAs increase rapidly

A positive diagnosis does not mean that
in response to stress; samples should be
clinical signs of illness are the result of fatty
drawn at standru·dized times using
liver, and misinterpretation of a positive
standardized procedures. The plasma
diagnosis is common.

NEFA concentrations at which triglyceride

Liver biopsy is a minimally invasive
accun1Ula.tes in the liver have not been
procedure that is the only direct and most
established but are probably -600 µEq/L
reliable method to determine severity of
and higher. These concentrations are
fatty liver in dairy cattle. Measurement of
common within 24-48 hr of parturition.

total lipid or triglyceride content by

However, prolonged exposure of the liver
gravin1etric or chemical methods after
to concentrations >600 µEq/L will likely
extraction from tissue by organic solvents
lead to fatty liver. Primiparous cows are
is necessary for quantitative assessment;
less susceptible to fa.tty liver during perihowever, these assays are not routinely ods of increased plasma NEFAs. Thereconducted in commercial laboratories.

fore, mature animals should be sampled

Estimation of triglyceride content by
when using plasma NEFAs as a predictor
flotation characteristics of the tissue in
of fatty liver. To screen a herd for the
copper sulfate solutions of varying specific
prevalence and severity of hepatic
gravity is rapid, easy, and available for use
lipidosis, detem1ination of plasma NEFAs
under field conditions.

not eru·lier than 1 wk antepartum is

Blood and urine metabolites or blood
recommended. Even though plasma NEFA
enzyme activity have been proposed as
concentration is a direct para.meter for the
indirect diagnostic para.meters. Blood
lipid mobilization and thus the liver lipid
glucose concentrations are low and blood
accumulation, after parturition the plasma

NEFA and 13-hydroxybutyra.te concentra13-hydroxybutyra.te concentration has been tions are high when conditions are
found to more accurately reflect the
conducive to the development of fatty liver.

severity of hepatic lipidosis.

Blood cholesterol concentration is usually

Microscopic evaluation can be used to
low when fatty liver occurs, which may
estimate the volwne of the tissue occupied
reflect an impaired ability of the liver to
by fat. Estimates obtained by this method
secrete lipoproteins. AST, ornithine
agree fairly well with chemical detenninadecarboxylase, and sorbitol dehydrogenase tion of triglyceride when expressed as a
are hepatic enzyn1es that may be positively
percentage of tissue dry weight. Mild,
associated with liver triglyceride and liver
moderate, and severe fatty liver are often
damage. The total bilirubin concentration
defined as <20%, 20o/o-40"Ai, and >40% fat in blood is often positively associated with

(percentage of cell volume), respectively,
the NEFA concentration in blood. Blood
but these values have little meaning relative
metabolites or enzyn1es are unreliable
to impact on physiologic function or clinical
indices of the degree of fatty liver, because
signs of the animal. However, clinical signs
nom1al concentrations vary widely an1ong
potentially associated with fatty liver
animals. The same problem exists when
disease are rarely seen in animals with <10%
attempting to detem1ine liver function by
fat in wet liver tissue. Use of ultrasonogrameasuring sulfobromophthalein clearance phy as an alternative noninvasive procedure
from blood.

is being developed to detemline the severity

With the availability of handheld devices
of fatty liver but is not yet routinely
allowing cowside testing, measuring
available.

1020

HEPATIC LIPIDOSIS

Prevention and Treatment: Reducing
catecholamine-mediated increases in fat
severity and duration of negative energy
mobilization.

balance is crucial to prevent fatty liver. This

Other than longterm IV infusion of
can be achieved by avoiding overcondiglucagon, there is no proven treatment for tioning cattle, rapid diet changes, unpalatfatty liver. Repeated IV bolus administration able feeds, periparturient diseases, and
of 500 mL of 5001o dextrose solution is

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environmental stress. Cows within a herd
commonly used in dairy practice and can be
should enter the dry period with an average
combined with administration of propylene
body condition score (BCS) of3-3.5 (scale:

glycol 250 mL, PO, bid. Dextrose adminis1 = thin, 5 = obese). Thin cows (BCS !>2.5) tration at a continuous infusion rate of up to
can be fed additional energy during the dry

40 g/hr, IV, suitable to increase the plasma
period to replenish condition without fear
glucose concentration to 100--150 mg/dL
of causing fatty liver. Overconditioned
without surpassing the renal threshold for
cattle (BCS 2:4) should not be feed restrictglucose, can be used in a clinical setting.

ed, because this will promote fat

Although this treatment effectively
mobilization from adipose tissue and
suppresses lipolysis and ketogenesis,
increase blood NEFAs and liver triglyceride.

treatment-induced hyperglycemia is likely

The critical time for prevention of fatty
to negatively affect feed intake. It is
liver is -1 wk before through 1 wk after
therefore advisable to reduce the infusion
parturition, when cows are most susceptirate after 2-3 days and to determine ble. Cows that are candidates for preventive
whether the animal is able to maintain
measures are those that are overcondinonnoglycemia as the parenteral glucose tioned or starting to go off feed. Propylene
supply decreases.

glycol, 300-600 mllday, given as an oral

Use of glucocorticoids in cows with fatty
drench during the final week prepartum has
liver is controversial because of their
effectively reduced plasma NEFAs and the
potential lipolytic effect. Recent literature
severity of fatty liver at calving. Propylene
suggests that short-term treatment with
glycol can be fed, but feeding may not be as
dexamethasone does not induce lipolysis
effective if the full dose is not consumed in a in dairy cows. The gluconeogenic effect of short period of time. Glycerin may be a less
glucocorticoids that is well docun1ented
expensive alternative to propylene glycol.

in several monogastric species has thus far

Glucose or glucose precursors are
not been confirmed in cattle. The welleffective, because they may cause an insulin established hyperglycemic effect of
response. Insulin is antilipolytic, ie, it
glucocorticoids in cattle has primarily been
decreases lipid mobilization from adipose
attributed to an in1paired glucose uptake
tissue. Slow-release insulin compounds are
by the mammary gland in treated cows. In
available but are not approved for use in
addition, glucocorticoids are thought to
food-producing animals. A single 100 IU
have a positive effect on feed intake. In

IM dose of a 24-hr slow-release insulin
theory, effective treatments would be those
immediately after calving may be prophythat enhance lipoprotein triglyceride export lactic. Higher doses may cause severe
from the liver. However, compounds that
hypoglycemia and should not be used
are known lipotropic agents in nonrun1iwithout concurrent glucose administration.

nants have not been proved to be effective

Glucagon stimulates glycogenolysis,
in ruminants. IV administration of choline,
gluconeogenesis, and insulin production.

inositol, methionine, and vitamin B,2 are

In contrast to that in nonruminants, the
often suggested as treatments, but scientific
lipolytic effect of glucagon in ruminants is
data are insufficient to support their use.

negligible. Glucagon (10 mg/day, IV, for 14

Oral administration of these compounds is
days) is effective at reducing liver triglycernot effective, because they are degraded in ide. A more practical protocol for use of
the rumen. In essence, treatment is the
glucagon to prevent fatty liver has not been
same as prevention; attempts should be
established. Niacin is an antilipolytic agent
made to avoid negative energy balance and
that may have potential for prevention of
to mininlize fatty acid mobilization from
fatty liver, but unequivocal evidence
adipose tissue. Once positive energy
supporting niacin supplementation of
balance is attained, liver triglyceride can be
animals at risk is not available.

reduced significantly in 7 -10 days.

Minimizing stress is important for
prevention of fatty liver. Sudden changes

PREGNANCY TOXEMIA IN COWS
in environment should be avoided. For
example, changes in ration, housing,

Pregnancy toxemia in cows is similar to the
temperature, herdmates, etc, may cause
condition in small ruminants and is the
a reduction in feed intake and trigger
result of fetal carbohydrate or energy

HEPATIC LIPIDOSIS

1021
demand exceeding maternal supply during
variable increases in serum activities of
the last trimester of pregnancy. It is
muscle or liver enzymes, as well as
precipitated by large or multiple fetuses,
clinicopathologic evidence of infection,
feed low in energy or protein or high in
metabolic acidosis, internal organ dysfuncpoorly digestible fiber, and health condition or failure, and circulatory collapse.

tions that increase energy demand or

Hepatic lipidosis in cortjunction with large

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decrease ability to take in nourislunent ( eg,
or multiple fetuses is a common necropsy
lameness and oral diseases). Cold, snowy
finding; evidence of muscle pressure
weather may contribute by increasing the
necrosis and toxemia may also be found.

animal's energy requirement and by

Successful treatment requires early
covering available forage. Inflammation is
identification of the disease. There are few
also increasingly being associated with
differential diagnoses, and pregnancy
disorders of energy metabolism; inflammatoxemia must be considered a factor in any tory mediators tend to promote mobilizadisease that affects cattle in late gestation.

tion of lipid stores and antagonize the

Cattle that have lost weight but are still eating
actions of insulin. The fetoplacental unit
may be managed by feeding concentrate or
uses carbohydrate for energy and removes
propylene glycol (0.5-1 g/kg/day for up to
these compounds from the blood in an

5 days). Anorectic cattle must be treated
insulin-independent fashion. When this
aggressively, because the decrease in
demand exceeds maternal supply, adipose
energy intake causes the disease to progress
tissue is mobilized to supply energy as
rapidly. Propylene glycol can be force-fed, or
acetate or ketone bodies, sparing carbohydextrose given IV (0.5 g/kg at least once a drate consumption by other maternal
day). Cattle with dehydration, organ dysfunctissues. However, only a small amount of tion, or metabolic acidosis should be treated
new carbohydrate is generated from fat
with large volumes (20----60 Ilday, PO or IV) of
metabolism (from glycerol). This condition
electrolyte fluids; if IV fluid administration is
is more severe than ketosis (seep 1024)

practical, continuous dextrose infusion (5%)

because fetal demand increases during
is recommended. Protarnine zinc insulin
pregnancy, while milk demand can decline

(200 U, SC, every 48 hr) may be given after
in response to negative energy balance.

dextrose administration to suppress

Although the mechanism is unknown,
ketogenesis. However, insulin is not
clinical disease develops in some cows with
approved for use in cattle in the USA. Recun1-
negative energy or carbohydrate balance.

bent cattle may benefit from good nursing

Proposed mediators of clinical disease
care (seep 1188) but rarely respond to
include glucose deficiency with intermittent
treatment. To decrease the energy drain of
hypoglycemia, ketone body accumulation
any cow with pregnancy toxemia, induction
with metabolic acidosis or appetite
of parturition or removal of the fetus by
suppression, and death of the fetus with
cesarean section should be considered.

secondary infection and toxemia. Individual

On the herd level, the disease can be
cows of any breed can be affected, but herd
prevented by adequate attention to nutrition
problems are most common in beef cattle,
and health care of cattle in late gestation.

which frequently are managed so that late

For tl1c individual cow, recognition of the
pregnancy coincides with the poorest
precarious state of energy and carbohydrate
availability of feed. Both thin and fat cows
balance during late gestation dictates
can be affected, but the first noted abnorn1alcareful monitoring of energy intake, ity often is loss of body condition over
attitude, and fat mobilization, especially

1-2 wk. Decreased appetite, rumination,
during times of illness or other stress.

fecal production, and nose-licking are
general signs of illness. With time, affected
cows become markedly depressed, weak,

PREGNANCY TOXEMIA IN EWES
ataxic, and recumbent. Opisthotonos,

AND DOES
seizures, or coma may be seen terminally.

Ketonuria is present from the early stage of

(Twin lamb disease, Pregnancy ketosis)

disease and is the most specific finding; even

Pregnancy toxemia affects ewes and does
mild ketonuria should not be found in
during late gestation and is characterized by
healthy pregnant cows until a few days
partial anorexia and depression, often with
before calving. Inexpensive ketone meters
neurologic signs, progressing to recumare now available and augment the older bency and death. It is seen more often
techniques of nitroprusside tablets or strips.

in anin1als carrying multiple fetuses.

Hypoglycemia is also common, but excited

Generally, clinically affected animals have
or seizuring cows may have hyperglycemia
other risk factors, at either the individual or

With more advanced disease, there may be
flock/herd level.

1022

HEPATIC LIPIDOSIS

Epidemiology and Pathogenesis:

responsive to insulin production when

The primary predisposing cause of pregnancy nutritional intake is inadequate. Ewes toxemia is inadequate nutrition during late
fitting these criteria may quickly shift from
gestation, usually because of insufficient
subclinical ketosis to clinical pregnancy
energy density of the ration and decreased
toxemia if feed intake is acutely curtailed by
rumen capacity as a result of fetal growth.

such events as adverse weather, transport,

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In the last 4 wk of gestation, metabolizable
handling for shearing or preventive
energy requirements rise dramatically. For
medication, or other concomitant disease
example, the energy requirement of a 70-kg

(footrot, pneumonia, etc). These variants
ewe carrying a single lamb is 2.8 Meal/day in
of pregnancy toxemia have been tem1ed
early gestation compared with 3.45 Meal/day primary pregnancy toxemia (thin ewes and in late gestation, or an increase of 23%. This
inadequate nutrition), estate ketosis (fat
change is more dramatic in ewes bearing
ewes), and secondary pregnancy toxemia
twins, with an energy requirement of 3.22

( ewes suffering from other disease). Dairy

Meal/day in early and 4.37 Meal/day in late
does often experience ketosis after kidding
gestation (36% increase), and in ewes

(serum 13-hydroxybutyrate [BHBJ >1.7
bearing triplets, with an energy requirement
mmol/1), which may or may not be
of 3.49 Meal/day in early and 4.95 Meal/day
connected with pregnancy ketosis before
in late gestation ( 42% increase). Dairy goats
kidding. Ketosis after kidding appears to be
have similar changes in needs.

more common in herds using a complete

In late gestation, the liver increases
pelleted ration.

gluconeogenesis to facilitate glucose
availability to the fetuses. Each fetus
requires 30-40 g of glucose/day in late

Clinical Findings: Early clinical signs can
gestation, which represents a significant
be detected by an observant producer. Most
percentage of the ewe's glucose produccases develop 1-3 wk before parturition.

tion and which is preferentially directed

Onset earlier than day 140 of gestation is
to supporting the fetuses rather than the
associated with more severe disease and
ewe. Mobilization of fat stores is increased increased risk of mortality. Decreased in late gestation as a way to assure
aggressiveness at feeding, particularly with
adequate energy for the increased
grain consumption, indicates a problem.

demands of the developing fetus( es) and

Animals will spend more tin1e lying and
impending lactation. However, in a
have more frequent bouts of lying than their
negative energy balance, this increased
healthy herdmates. As the disease advances,
mobilization may overwhelm the liver's
ewes or does may also show signs of
capacity and result in hepatic lipidosis,
listlessness, aimless walking, muscle
with subsequent impairment of function.

twitching or fine muscle tremors, opisthoto

Additionally, twin-bearing ewes appear to
nos, and grinding of the teeth. This progresshave more difficulty producing glucose es (generally over 2-4 days) to blindness,
and clearing ketone bodies, thus increasataxia, and finally sternal recumbency, ing their susceptibility to pregnancy
coma, and death. Cerebral hypoglycemia
toxemia.

coupled with ketosis, ketoacidosis, and

Females with a poor body condition
reduced hepatic and renal function lead to
score (BCS ,,;2) or that are overconditioned
the clinical signs and fetal death. Blood

(BCS �4) and carrying more than one fetus
glucose levels may return to normal or even
are most at risk of developing pregnancy
become high terminally, possibly indicating
toxemia, although the condition can occur
death of the fetus( es). Septicemia develops
even in ideally conditioned ewes on an
in the ewe or doe after fetal death.

adequate ration. Susceptible, thin ewes or

Lesions: Postmortem changes demondoes develop ketosis because a chronically strate varying degrees of fatty liver, enlarged
inadequate ration is offered or because
adrenal glands, and often include multiple
other diseases limit intake ( eg, lameness,
fetuses in a state of decomposition
dental disease) and, with increasingly
indicating premortem death. Very thin
insufficient energy to meet increasing fetal
animals may appear starved ( eg, serous
demands, the ewe or doe mobilizes more
atrophy of the kidney and heart fat).

body fat, with resultant ketone body

However, these signs alone are not
production and hepatic lipidosis. Overconpathognomonic for death due to pregnancy ditioned anin1als may have depressed
toxemia. Postmortem samples of aqueous
appetites, and adipose mobilization quickly
humor or CSF can be analyzed for BHB.

overwhelms the liver's capacity, resulting

Levels >2.5 and 0.5 nunol/1, respectively, are
again in hepatic lipidosis. In addition, there
consistent with a diagnosis of pregnancy
may be a population of aninrnls less
toxemia.

HEPATIC LIPIDOSIS

1023

Diagnosis: Laboratory findings in
glandinF
individual animals may include hypoglyce2a (dinoprost [10 mg, IM] or cloprostenol [75 mcg/45 kg body wt]).

mia (often <2 mmol/L), increased urine

Contributing factors ( eg, nutrition, housing,
ketone levels ( evaluated by commercial
illness, other stressors) should be con-ected
qualitative test strips), increased serum
for the group, and feeding management

BHB levels (nom1al <0.8 mmol/L, subcliniassessed ( eg, adequate feeder space, feeding VetBooks.ir
cal ketosis �0.8 mmol/L, and clinical disease
frequency, protection from adverse weather).

>3 mmol/L), and occasionally hypocalce

Treatment of advanced cases of
mia. Hypoglycemia is not a consistent
pregnancy toxemia is frequently unrewardfmding, with up to 400,6 of cases having ing. If a ewe or doe is .µready comatose,
normal glucose levels and up to 200,6 having
htunane euthanasia is wan-anted, and
hyperglycemia. If the diagnosis needs
treatment should focus on the rest of the
further confurnation, CSF glucose levels
flock. However, if the female is valuable and
may be more accurate than blood; they
the owner wishes to pursue treatment
remain low even when serum glucose
despite the poor prognosis, then aggressive
rebounds in advanced cases after fetal
therapy should be directed against the
death. BHB is a more reliable indicator of
ketoacidosis and hypoglycemia. Before
disease severity than are blood glucose
starting this therapy, it should be deterlevels. Nonesterified fatty acids can also mined whether the fetuses are alive ( eg,
be increased above 0.4 mmol!L, indicating
real-time or Doppler ultrasonography). If
likely hepatic lipidosis, resulting in in1paired
the fetuses are alive and within 3 days of a
hepatic function.

calculated due date (gestation length 14 7

Although hypocalcemia is often found in
days), then an emergency cesarean section
cases of pregnancy toxemia, it should also
may be considered if economically viable.

be considered when formulating hypoth

If the fetuses are dead or too premature to
eses regarding recumbent late gestational
stuvive a cesarean section, it is less stressful
sheep and goats (seep 991). This is sinularly to the ewe or doe to induce early parttu·ition
true with hypomagnesemia, which is a
with dexamethasone (as above). Prophylaccommon finding in cases of pregnancy tic antibiotics ( usually procaine penicillin G
toxemia but should also be considered as
at 20,000 IU/kg/day) are appropriate if the
a differential diagnosis for periparturient
fetuses are thought to be dead.

CNS disease. Other CNS diseases to be

Hypoglycemia can be treated by a single
considered include polioencephalomalacia,
injection of 50% dextrose, 60-100 mL, IV,
pulpy kidney disease ( enterotoxemia),
followed by balanced electrolyte solution
rabies, scrapie, maedi visna/ovine
with 5% dextrose. IV drips and lower
progressive pneumonia, lead poisoning,
dextrose levels in solution might cause less
chronic copper toxicity, and listeriosis.

of a diuretic effect; however, this is often

These can be differentiated based on
impractical in a field setting. Repeated
clinical and laboratory findings or during
boluses of IV glucose should be avoided,
necropsy.

because they may result in a refractory
insulin response. Insulin can be adminis

Treatment: Ewes or does in the early
tered (20-40 IU protamine zinc insulin,
stages (ie, are ambulatory, have a decreased

IM, every other day). Calcium (50-100 mL
appetite for grain, and are showing few
of a commercial calcium gluconate or
nervous signs) can often be treated successborogluconate solution, SC) can be given fully with oral propylene glycol (60 mL, bid,
safely without serum biochemistry data.

for 3 days, or 100 mllday). Adding oral

If serum biochemistry demonstrates
calciun1 (12.5 g calcium lactate), oral
hypocalcemia, -50 mL of a commercial
potassium (7.5 g KC!), and insulin (0.4
calcium solution can be given by slow IV

IU/kg/day, SC) has increased survival rates.

injection while monitoring the heart. Oral

Oral commercial calf electrolyte solutions
potassium chloride (KC!) can be given as
containing glucose may also be given by
well, because serum potassium levels are
stomach tube at a dose of3--4 L, qid, or
often depressed. Use of flunixin megludrenched as a concentrated solution. It may mine at 2.5 mg/kg improved survival rate
also be prudent to induce parturition/
of ewes and their lan1bs, although the
abortion if the ewe or doe is also thin or fat
mechanism is unknown. Although
and cannot manage fetal demands that late in aggressive therapy and intensive nursing pregnancy. This can be done by adn1inistercare may be successful, it is not unusual ing dexan1ethasone (20 mg, IV or IM).

to see case fatality rates > 40%. Given the

Parturition is expected within 24--72 hr, with
cost, it is prudent to share the guarded
most anin1als giving birth within 36 hr. Does
prognosis with owners before undertaking
may also benefit by the addition of prosta-
treatment.

1024

HEPATIC LIPIDOSIS

A sample of late-gestation ewes or does
it convenient to feed pregnant ewe-lainbs or
can be tested for serum BHB levels to
doelings with twin-bearing females and thin,
determine the extent of the risk in tl1e rest
single-bearing females because of the added
of the flock. Generally, 10-20 anin1als in late
energy young animals need for growili. With
gestation should be san1pled (3%-200A, of the
prolific breeds, triplet-bearing ewes and
pregnant flock). The risk of the flock can
thin, twin-bearing ewes can be fed together.

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be determined based on the mean value of

Overconditioned females (ie, BCS ;:,4) are
these results: nom1al (low risk) 0-0. 7 mmol/L, not as common but may be seen in small moderate underfeeding (moderate risk)

hobby flocks. Fat females are much less

0.8---1.6 mmol/L, and severe underfeeding
responsive to therapy, and owners should

(high risk) 1. 7---3.0 mmol/L. Other diseases
be advised on how to avoid fue problem
should be treated (eg, footrot). Females
tl1rough proper feeding management.

off feed should be separated from the

However, late pregnancy is not fue tin1e to
group and hand fed, keeping in mind they
reduce BCS in overconditioned females.

should be able to see the group to feel

BHB serun1 levels can be used as a flock
comfortable.

screening test to detect flocks at risk of
pregnancy toxemia. In flocks wifu values

Prevention: Ewes or does should not enter
ranging from >0.8---3 rnrnol/L, feeding
the last 6 wk of gestation with a BCS <2.5; this management should be corrected quickly can be prevented by good feeding manageto avoid clinical disease.

ment, eg, adequate feeder space for pregnant

Reseai·ch has supported fue use of
anin1als, sorting (based on BCS, fetal
ionophores, particularly monensin, in
numbers, and anin1al size), forage analysis
transition dairy cows to prevent subclinical

(for energy, digestible fiber, and protein
ketosis and oilier early postpartum diseases.

levels), and ration fonnulation. During the

Ionophores in1prove feed efficiency by
last 6 wk of gestation, grain is required as a
changing microf1ora populations in the
source of carbohydrates in the ration to
run1en, resulting in increased feed efficiency
maintain the health of multiple-bearing
ai1d production of propionic acid, followed
females. Amount vaiies depending on forage
by in1proved gluconeogenesis. There is some
quality, adult body weight and condition
evidence fuat monensin may be beneficial
score, and number of fetuses, but protein
for late-gestation ewes ( although not for
must also be balanced for rumen microbes to
dairy goats); it in1proved feed efficiency
make optimal use of available cai·bohydrates.

by lowering feed intake. Treated ewes also

Producers should ideally assess BCS at
showed lower serun1 BHB levels in late gestabreeding and midgestation, usually at the tion, with no adverse effects on lamb birth
time of pregnancy scanning, so that thin
weights. It may help prevent ketosis in
animals can be fed as a separate group. It
postpartum dairy goats. Lasalocid has been
takes -6 wk to raise BCS by 1 point, so early
sintilarly studied. Again, feed intake was
inte1vention is in1portant to avoid latesuppressed, but lan1b survival was better in gestation problems. If real-time ultrasound
tl1e treatment group. More work needs to
scanning allows for fetal number determinabe done with both drugs to assess their tion, then anin1als should also be managed
use in preventing pregnancy toxemia in
based on fetal numbers. Producers may find
prolific ewes.

KETOSIS IN CATTLE

(Acetonemia, Ketonemia)

Ketosis is a common disease of adult cattle.

nation and abnormal gait, bellowing, and

It typically occurs in dairy cows in early
aggression, are occasionally seen. The
lactation and is most consistently charactercondition is worldwide in distribution but is ized by partial anorexia and depression.

most common where dairy cows are bred

Rarely, it occurs in cattle in late gestation,
and managed for high production.

at which time it resembles pregnancy toxemia of ewes (seep 1021). In addition to Etiology and Pathogenesis: The
inappetence, signs of nervous dysfunction,
pathogenesis of bovine ketosis is incomincluding pica, abnormal licking, incoordi-pletely understood, but it requires the

KETOSIS IN CADLE

1025
combination of intense adipose mobilizawith excessive adipose stores (body tion and a high glucose demand. Both of
condition score �3. 75 out of 5) at calving
these conditions are present in early
are at a greater risk of ketosis than those
lactation, at which time negative energy
with lower body condition scores. Lactating
balance leads to adipose mobilization, and
cows with subclinical ketosis (seep 1027)

milk synthesis creates a high glucose
are also at a greater risk of developing
demand. Adipose mobilization is accompaclinical ketosis and displaced abomasum VetBooks.ir
nied by high blood serum concentrations of
than cows with lower serum BHB concennonesterified fatty acids (NEFAs). During trations.

periods of intense gluconeogenesis, a large
portion of serum NEFAs is directed to

Clinical Findings: In cows maintained in
ketone body synthesis in the liver. Thus, the
confinement stalls, reduced feed intake is
clinicopathologic characterization of
usually the first sign of ketosis. If rations are
ketosis includes high serum concentrations
offered in components, cows with ketosis
of NEFAs and ketone bodies and low
often refuse grain before forage. In
concentrations of glucose. In contrast to
group-fed herds, reduced milk production,
many other species, cattle with hyperlethargy, and an "empty" appearing ketonemia do not have conCU1Tent acidemia. abdomen are usually tl1e signs of ketosis The serum ketone bodies are acetone,
noticed first. On physical exan1ination,
acetoacetate, and (3-hydroxybutyrate
cows are afebrile and may be slightly

(BHB).

dehydrated. Rumen motility is variable,

There is speculation that the pathogenbeing hyperactive in some cases and esis of ketosis cases occlllTing in the
hypoactive in others. In many cases, there
immediate postpartum period is slightly
are no other physical abnom1alities. CNS
different than that of cases occuning closer
distmbances are noted in a minority of
to the time of peak milk production. Ketosis
cases. These include abnom1al licking and
in the immediate postpartum period is
chewing, witl1 cows sometimes chewing
sometin1es described as type II ketosis.

incessantly on pipes and other objects in

Such cases of ketosis in very early lactation
their surroundings. Incoordination and gait
are usually associated with fatty liver ( see
abnormalities occasionally are seen, as are
p 1018). Both fatty liver and ketosis are
aggression and bellowing. These signs
probably pa.it of a spectrum of conditions
occm in a cleai· minority of cases, but
associated with intense fat mobilization in
because the disease is so common, finding
cattle. Ketosis cases occlllTing closer to
anin1als with these signs is not unusual.

peak milk production, which usually occurs
at 4-6 wk postpaiturn, may be more closely

Diagnosis: The clinical diagnosis of
associated with underfed cattle experiencketosis is based on presence of risk factors ing a metabolic shortage of gl uconeogenic

(early lactation), clinical signs, and ketone
precursors than with excessive fat
bodies in urine or milk When a diagnosis of
mobilization. Ketosis at this time is
ketosis is made, a thorough physical
sometimes described as type I ketosis.

exan1ination should be perfom1ed, because

The exact pathogenesis of the clinical
ketosis frequently occurs concurrently with
signs is not known. They do not appear to
other peripaiturn diseases. Especially
be associated directly with serum concencommon concurrent diseases include trations of either glucose or ketone bodies.

displaced abomasum, retained fetal

There is speculation they may be due to
membranes, and metritis. Rabies and otl1er
metabolites of the ketone bodies.

CNS diseases are important differential
diagnoses in cases exhibiting neurologic

Epidemiology: All dairy cows in early
signs.

lactation (first 6 wk) are at risk of ketosis.

Cow-side tests for the presence of ketone

The overall prevalence in cattle in the first
bodies in urine or milk are critical for

60 days of lactation is estimated at 7%-14%,
diagnosis. Most commercially available test
but prevalence in individual herds varies
kits are based on the presence of acetoacsubstantially and may exceed 14%. The peak etate or acetone in milk or urine. Dipstick prevalence of ketosis occms in the first 2 wk tests are convenient, but those designed to of lactation. Lactational incidence rates
detect acetoacetate or acetone in urine are
vary dran1atically between herds and may
not suitable for milk testing. All of these
approach 1 OOOAi. Ketosis is seen in all pa.ii ties tests are read by observation for a paiticular ( although it appears to be less common in
color change. Care should be taken to allow
primipai·ous animals) and does not appear
the appropriate time for color development
to have a genetic predisposition, other tl1an
as specified by the test manufactmer.

being associated with dairy breeds. Cows

Handheld instruments designed to monitor

1026

KETOSIS IN CATILE
ketone bodies in the blood of human
suppresses both adipose mobilization and
diabetic patients are available. These
ketogenesis but should be given in
instrwnents quantitatively measure the
combination with glucose or a glucocorticoncentration of BHB in blood, wine, or coid to prevent hypoglycemia. Use of insulin
milk and may be used for the clinical
in this manner is an extra-label, unapproved
diagnosis of ketosis.

use. Other therapies that may be of benefit

In a given animal, urine ketone body
in refractory ketosis cases are continuous

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concentrations are always higher than milk

IV glucose infusion and tube feeding. (See
ketone body concentrations. Trace to milclly also p 1018.) positive results for the presence of ketone
bodies in mine do not signify clinical

Prevention and Control: Prevention of
ketosis. Without clinical signs, such as
ketosis is via nutritional management. Body
partial anorexia, these results indicate
condition should be managed in late
subclinical ketosis. Milk tests for acetone
lactation, when cows frequently become too
and acetoacetate are more specific than
fat. Modifying diets of late lactation cows to
wine tests. Positive milk tests for acetoacincrease the energy upply from digestible etate and/or acetone usually indicate
fiber and reduce the energy supply from
clinical ketosis. BHB concentrations in milk
starch may aid in partitioning dietary energy
may be measured by a dipstick method that
toward milk and away from body fattening.

is available in some countries, or by the

The d1y period is generally too late to
electronic device mentioned above. The
reduce body condition score. Reducing

BHB concentration in milk is always higher
body condition in tl1e dry period, particuthan the acetoacetate or acetone concentralarly in the late dry pe1iod, may even be tion, making the tests based on BHB more
counterproductive, resulting in excessive
sensitive than those based on acetoacetate
adipose mobilization prepaitwn. A critical
or acetone.

area in ketosis prevention is maintaining
and promoting feed intake. Cows tend to

Treatment: Treatment of ketosis is
reduce feed conswnption in the last 3 wk of
aimed at reestablishing normoglycemia
gestation. Nutritional management should
and reducing serum ketone body concenbe ain1ed at minimizing this reduction.

trations. Bolus IV administration of 500 mL

Controversy exists regarding the optimal
of 500Ai dextrose solution is a common
dietary characteristics during this period.

therapy. This solution is very hyperosmotic

It is likely that optimal energy and fiber
and, if administered perivascularly, results
concentrations in rations for cows in the
in severe tissue swelling and irritation, so
last 3 wk of gestation vary from farm to
care should be taken to ensure that it is
fai,n. Feed intake should be monitored and
given IV. Bolus glucose therapy generally
rations adjusted to meet but not greatly
results in rapid recovery, especially in
exceed energy requirements throughout the
cases occurring near peak lactation (type I
entire dry period. For Holstein cows of
ketosis). However, the effect frequently is
typical adult body size, the average daily
transient, and relapses are common.

energy requirement throughout the dry

Administration of glucocorticoids,
period is between 12 and 15 Meal expressed
including dexan1ethasone pr isoflupredone
as net energy for lactation (NE,). After
acetate at 5-20 mg/dose, IM, may result in
calving, diets should promote rapid and
a more sustained response, relative to
sustained increases in feed ai1d energy
glucose alone. Glucose and glucocorticoid
consumption. Early lactation rations should
therapy may be repeated daily as necesbe relatively high in nonfiber carbohydrate sary. Propylene glycol administered orally
concentration but contain enough fiber to

(250-400 g/dose [8-14 oz]) once per day
maintain run1en health and feed intake.

acts as a glucose precursor and is effective

Neutral-detergent fiber concentrations
as ketosis therapy. Indeed, propylene
should usually be in the range of 28%-30%,
glycol appears to be the most well
with nonfiber carbohydrate concentrations
documented of the various therapies for
in the range of 38%-41%. Dietary paiticle
ketosis. Overdosing propylene glycol leads
size will influence tl1e optimal proportions
to CNS depression.

of carbohydrate fractions. Some feed

Ketosis cases occurring within the first
additives, including niacin, calciwn

1-2 wk after calving (type II ketosis)

propionate, sodium propionate, propylene
frequently are more refractory to therapy
glycol, and rumen-protected choline, may
than cases occurring nearer to peak
help prevent and manage ketosis. To be
lactation (type I). In these cases, a
effective, these supplements should be fed
long-acting insulin preparation given IM at
in the last 2-3 wk of gestation, as well as

150-200 IU/day may be beneficial. Insulin
during the period of ketosis susceptibility.

MALIGNANT HYPERTHERMIA

1027

In some countries, monensin sodium is

In addition to laboratory detem1ination
approved for use in preventing subclinical
by spectrophotometry, handheld devices
ketosis and its associated diseases. Where
manufactured to monitor blood ketone
approved, it is recommended at the rate of
body concentrations in human diabetic

200-300 mg/head/day.

patients have been evaluated for use in
monitoring subclinical ketosis in cows.

SUBCLINICAL KETOSIS

These instruments use whole blood rather

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than sernm for BHB detennination, making

Subclinical ketosis is defined as high serum
them particularly practical for on-farm use.

ketone body concentrations without

The whole blood BHB concentration is very
observed clinical signs. Subclinically
close to the serw11 concentration, so the
affected cows are at increased risk of
interpretation of results obtained from
clinical ketosis and displaced abomasum
either the handheld device or laboratory
and are also less fertile than those with
analysis is similar.

nom1al sernm ketone body concentrations.

Diagnosis of subclinical ketosis requires

Furthermore, they appear to have reduced
definition of a concentration above which
milk production. Detennination of serum
cows are considered to be subclinically
f3-hydroxybutyrate (BHB) concentrations
ketotic. Concentrations between 1,000 µM
is considered the best way to detect and

(10.4 mgtdL) and 1,400 µM (14.6 mgtdL) are
monitor subclinical ketosis, because the
used. Recommended strategies for herdcow-side tests mentioned above are level testing are to test at least 12 animals in
insufficiently sensitive and specific in
the first 60 days of lactation. If> 1()% are
detecting subclinical increases in sernm
subclinically ketotic, it should be considered

BHB concentrations. Sernm concentrations
evidence of a herd-level problem and prompt
may be detem1ined spectrophotometrically
a review of nutritional management. Some
by traditional clinical laboratory means. The farms use the handheld BHB meters to test BHB concentrations in blood or sernm
all cows in early lactation. Cows diagnosed
samples are reasonably stable; thus,
with subclinical ketosis are treated with
rigorous san1ple handling precautions are
propylene glycol. Such an approach is labor
not necessary to transport the specin1ens
intensive but has been demonstrated to
to the laboratory. The test is sensitive to
reduce further disease occtuTence in subclinhemolysis, however, so hemolysis should ically ketotic animals and to improve milk
be avoided during sample collection, and
production in treated animals. Such an
serum should be separated from the clot
approach should not replace sound
before shipment to the laboratory.

nutritional management procedures.

MALIGNANT HYPERTHERMIA

(Porcine stress syndrome)

Malignant hyperthemua (MH) is a rare,
contraction occurs, leading rapidly to a
life-threatening, inherited disorder that
potentially fatal hypennetabolic state
can lead to metabolic disease of skeletal
known as an MH episode. More than 300
muscles in susceptible animals after

RYRl variants have been identified, and 31
exposure to Lriggering agents such as
of those mutations have been confirmed to
halogenated inhalation anesthetics,
cause MH according to the molecular
depolarizing neuromuscular blocking drugs, genetic guidelines of the European stress, and/or exercise. A mutation in the

Malignant Hyperthemua Group. Different
ryanodine receptors (RYRl locus) on the
mutation loci within the RYRl receptors
sarcoplasmic reticulum iliat surrounds
have been shown to be responsible for MH
myofibrils of skeletal muscles alters the
syndrome in different species.

function of calcium release channels, which
results in massive release of calcium into

Etiology and Clinical Findings: MH is
the cytoplasm of the myofibrils. As a resull,
considered to be a clinical syndrome rather
generalized, extensive skeletal muscle
than a single disease, because research

1028

MALIGNANT HYPERTHERMIA
indicates that multiple environmental
ln pigs, MH is also referred to as porcine
and genetic factors cause a complex of
stress syndrome. Breed susceptibility
pathophysiologic events. Contrary to
varies, with Pietra.in, Portland China, and
general belief, a full-fledged MH episode,

Landrace pigs very susceptible to MH, and
with a sudden and rapidly progressive

Large White, Yorkshire, and Hampshire pigs
course of symptoms, does not occur
much less so. In the past, halothane was the

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frequently. ln most cases, MH is a subtle
most frequently reported trigger of MH in
disorder. Pigs and people seem to be most
pigs. Isoflurane has been reported to trigger
susceptible, but MH has also been reported

MH in pigs of susceptible breeds, but only
in dogs, cats, and horses. In people and
one instance of isoflurane-induced MH has
dogs, both parents must carry the mutant
been reported in a potbellied pig. Sevofluchromosome for the autosomal recessive rane-induced MH also has been reported in
gene to result in clinical expression in
purebred Poland China pigs. Episodes of
offsp1ing. ln pigs, the mutant autosomal

MH induced by desflurane have been
gene is dominant, so that a single copy of
reported in Large White, Pietra.in, and
the mutant chromosome, carried by either

Pietran-mixed pigs. There have been no
parent, can result in clinical expression in
reports of isoflurane- or sevofluranethe offspring, ie, 500/() of offspring are induced MH in cattle.

susceptible to MH.

In dogs, MH syndrome has been

Interestingly, most MB-susceptible
reported in Pointers, Greyhounds,
animals, including people, do not suffer

Labrador Retrievers, Saint Bernards,
from signs of muscle disease in everyday

Springer Spaniels, Bichon Frises, Golden
life. In people, the incidence of MH

Retrievers, and Border Collies. There are
episodes during anesthesia is between
distinct differences in the clinical signs of

1:5,000 and 1:50,000 per 100,000 anesthet

MH seen in dogs and those in pigs and
ic events. The MH episode may develop at
people. The first obvious indication of an
first exposure to an anesthetic triggering
imminent MH episode in dogs is the rapid
agent, but in some cases, as many as three
and dramatic increase in C02 production,
exposures must occur before a fullas evidenced by a sudden increase in fledged MH crisis develops. In domestic

ETC02 concentration. Body temperature
animals, it is unclear whether multiple
may increase during the episode, but this
exposures to the triggering agent are
occurs much later than the increased
required before developing a full-fledged

ETC02. In a study in which a colony of
episode. This is because the clinical signs

Doberman-German Shepherd-Collie dogs
ofMH can be so subtle that the episode
were challenged with halothane/succinylgoes unrecognized.

choline, the dogs that developed MH

MH can occur at any time during
syndrome all had a mutation on the
anesthesia or in the early postoperative
calcium-release channels in the RYRl
period. The clinical signs of MH are often
receptors. However, this mutation was
a sudden and dramatic rise in body
identified on a different loci (Tl640) than
temperature and end-tidal C02 (ETC02),
that responsible for MH syndrome in pigs
followed by muscle fasciculation, muscle

(R614C) and in people (CFAOl). Another
rigidity, tachypnea, tachycardia,
mutation, RYRl V54 7 A, has also been
arrhythmias, myogloblnuria, metabolic
shown to be involved in MH syndrome in
acidosis, renal failure, and often death.

dogs. The incidence rate of MH syndrome

The prognosis is usually poor once
associated with anesthesia in dogs is
clinical signs are recognized. Triggering
reported to be 2.1 % in Canada, 0.43% in
agents ofMH include stress (eg, excitethe USA, and 0.23% in England, with a ment, transportation, and preanesthetic
mortality rate of 0.11%in both Canada and
handling), exercise, halogenated
the USA.

inhalation anesthetics (eg, halothane,

MH syndrome in horses is difficult to
isoflurane, sevoflurane, and desflurane),
recognize, because it can easily be confused
and depolarizing neuromuscular blocking
with other myopathies commonly assodrugs (eg, succinylcholine). Of the ciated with anesthesia in horses. Unlike
halogenated inhalation anesthetics,
in pigs, dogs, and people, signs of MH
halothane is claimed to be the most
syndrome in horses tend to be slow to
potent triggering agent, and it is no longer
develop and are often observed only after �3
used in western countries. The use of
hr of anesthesia. ln addition to the clinical
succinylcholine, another potent triggersigns of anesthetic-related MH seen in other ing agent, has been gradually restricted
species, intraoperative cardiac arrhythmia
by international anesthesia societies.

( eg, premature ventricular contraction),

MALIGNANT HYPERTHERMIA

1029
postanesthetic myositis, and increased
detomidine, dexmedetomidine, romifiserum potassium and CK have also been dine ), dissociative anesthetics ( eg,
seen in MR-affected horses. Clinical signs
ketamine, tiletarnine-zolazeparn),
similar to those of MI-I syndrome such as
propofol, etomidate, opioids (eg,
hypercarbia, increased body temperature,
morphine, hydromorphone, fentanyl,
and hyperkalemia, are also seen in horses
butorphanol, buprenorphine), N20,
with hyperkalemic periodic paralysis ( see
nondepolarizing neuromuscular blocking

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p 1047), a genetic mutation of sodiwn
drugs (eg, atracurium, vecuronium,
channels. Thus, a definitive diagnosis
rocuronium), and local anesthetics (eg,
should be confirmed by in vitro contracture
lidocaine, mepivacaine, bupivacaine).

test (IVCT) or DNA analysis. Prognosis of

MH-susceptible animals should be kept
horses suffering an MH episode during or
calm and stress minimized by administerafter anesthesia is usually poor because ing effective preanesthetic medication
of the lack of response to syn1ptomatic
before induction and maintenance of
treatments and difficulty in management of
anesthesia. Azaperone at 0.5-2 mg/kg, IM,
complications such as myositis, fractures,
provided 100% protection against MH in
and/or seizures.

susceptible Pietrain pigs.

Treatment ofMH is most effective when

Diagnosis: Currently, the gold standard
signs ofMH (eg, muscle rigidity, sudden
for diagnosis of MI-I is IVCT, which is based rise in body temperature and ETC02) are on muscle fiber contracture in response
recognized early and treated aggressively.

to triggering agents such as halothane

Treatment is largely syn1ptomatic and
or caffeine. However, IVCT requires a
includes immediate discontinuation of
surgical procedure (ie, muscle biopsy), is
inhalation anesthetic and use of ice packs
expensive and available only at specialized and alcohol baths. Controlled ventilation testing centers, and may produce
using a machine flushed free of anesthetic
equivocal as well as false-positive and
agent should also be instituted as soon as
false-negative results. DNA analysis is an
possible to remove excessive C02 and
alternative to the IVCT; it requires only
maintain normal blood pH and acid-base
a small blood sample to be sent to an
status. Dantrolene (a specific ryanodine
accredited diagnostic laboratory to screen
receptor antagonist) has proved effective
for RYR l mutation. An animal is diagnosed for treatment (1-3 mg/kg, IV) and as MI-I susceptible if 1 of the 31 known
prophylaxis (5 mg/kg, PO, up to 10 mg/kg)

causative mutations is detected. However,
of MI-I. Animals with cardiac arrhythmias,
the diagnostic classification of many RYRl
such as tachycardia or severe premature
mutations remains difficult because their
ventricular contractions, can be treated
pathophysiologic impact with regard to
with lidocaine (1-2 mg/kg, IV), if needed.

initiating an MI-I episode is not yet clear.

Calcium chloride and calciwn gluconate

Therefore, an IVCT is required to exclude
are not recommended. Hyperkajemia

MI-I susceptibility in case of an unclassified should be treated with controlled RYRl mutation or if RYRl mutation is
ventilation, and 50% dextrose (0.5 ml/kg,
absent. Other minimally invasive

IV) and/or insulin (0.25-0.5 U/kg, IV) can
diagnostic tests for identification of MI-I
be administered to promote movement of
susceptibility are in development
extracellular potassium into cells. Sodium
bicarbonate (1-2 mEqlkg, IV) can be

Treatment and Prevention: Because
administered to maintain normal blood
of few effective drugs available to treat
pH in the presence of metabolic acidosis.

MI-I, stress before anesthesia should be

Balanced electrolyte solutions, 5%
minimized, and using anesthetics that are
dextrose in water, and normal saline are
known triggering agents should be avoided acceptable for supportive fluid therapy; to prevent an MI-I episode in susceptible

Ringer's lactate with added calcium
animals. Total IV anesthesia and/or
should not be used. Dantrolene should be
regional/local anesthetic techniques can
administered to affected animals. Testing
be safely used as alternative procedures to
for disseminated intravascular coagulaallow surgery on MH-susceptible animals.

tion, which often results when body

Drugs that can be safely administered to
temperature exceeds 41 °C (131.4°F), is

MI-I-susceptible animals include phenoprudent, as well as observation of the thiazine derivatives (eg, acepromazine),
urine for myoglobinuric renal failure due
butyrophenone derivatives (eg, droperito severe muscle damage. Affected dol, azaperone), benzodiazepine derivaanimals should be closely monitored for tives ( eg, diazeparn, rnidazolan1, zolazsigns of MI-I for 48-72 hr, because 25% may eparn), cxz-agonists (eg, xylazine,
ell.'Perience recrudescence.

1030

TRANSPORT TETANY IN RUMINANTS

TRANSPORT TETANY IN RUMINANTS

(Railroad disease, Railroad sickness, Staggers)

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Transport tetany occurs after the stress of
hypomagnesemic, but others show no
prolonged transport, typically in cows and
measurable biochemical abnonnalities. No
ewes in late pregnancy, although it is also
specific lesions are found at necropsy other
seen in lan1bs transported to feedlots and in
than lesions associated with prolonged
cattle and sheep transported to slaughter.

recumbency, most commonly ischemic

Crowded, hot, poorly ventilated transport
muscle necrosis. In lambs, early signs
vehicles (railroad cars or trailers) with
include restlessness, staggering, and parminimal or no access to feed or water tial h.indlimb paralysis followed by lateral
appear to predispose anin1als to the
recwnbency. Death can occur rapidly or
condition; however, prolonged travel by
after 2-3 days of recw11bency. In lambs, mild
foot is also a risk factor. The disease is
hypocalcemia may be noted. Recovery rates
characterized by recumbency, GI stasis,
are fair even with treatment. The relationand coma, and is generally fatal.

ship of clinical signs with transport or

Although cows in late gestation are most
forced, prolonged exercise is diagnostic.

commonly affected, the disease is also seen

Some animals respond to treatment with
in cows tl1at have recently calved, as well as
combinations of parenteral calcium,
in bulls, steers, and dry cows. Risk factors
magnesiwn, and glucose. IV i[\jections of
include heavy feeding before shipment,
calciwn borogluconate (25%solution at
deprivation of feed and water for >24 hr

400-800 mUcow or 100 mUewe) or
during transit, and unrestricted access to
calciwn borogluconate with magnesium
water and exercise inm1ediately after
sulfate (5% solution, san1e volumes) can be
arrival. Exposure to hot environmental
administered slowly. A dose of 50 mUday
conditions is also associated with an
can be given SC to affected lambs in
increased incidence. Although the specific
feedlots. Repeated injections may be
cause of tetany is unknown, the condition
warranted, but failure to respond is
may be a form of acute hypocalcemia
common (500/o) and most likely due to
precipitated by late pregnancy and early
concurrent muscle necrosis. Additional
lactation, or by fasting before or during
treatment considerations include IV admintransit. Physical stress is undoubtedly istration of large volumes of polyionic
related. Hypomagnesemia may be a
fluids such as lactated Ringer's solution.

precipitating factor in cattle and a

Anin1als should be offered good quality
contributing factor in sheep.

feeds (eg, alfalfa hay), fresh water, and soft

Clinical signs in cattle may occur while in
bedding with good footing underneath.

LransiL or as long as 48 hr after artival. Early

Sedation may be necessary if animals are
clinical signs include restlessness and
hyperexcitable or convulsing.

excitement, trismus, and grinding of teeth.

If prolonged transport times of cows or

A staggering gait may be seen, and later, if
ewes in advanced pregnancy is unavoidable,
recwnbent, cattle often demonstrate
animals should be fed a restricted diet
paddling of the h.indlegs. Rwnen hypomotilseveral days before shipment, then provided ity and GI stasis are seen, and anin1als
adequate feed, water, and rest pe1iods
become completely anorectic. Tachycardia
during transport. Administration of
and rapid, labored respiration may develop.

ataractic agents (unless transport is to

Abortion may be a complication. Cattle that
slaughter) such as promazine hydrochloride
do not recover gradually become more
before loading is recommended, especially
obtunded to the point of coma and die
for nervous animals. Upon unloading at the
within 3-4 days. Moderate hypocalcemia
destination, anin1als should be allowed
and hypophosphatemia may be seen in
limited access to water for tl1e first 24 hr and
cattle. Some sheep are hypocalcemic and
minimal exercise for 2-3 days.

MUSCULOSKELETAL

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SYSTEM

INTRODUCTION 1039

CONGENITAL AND INHERITED ANOMALIES 1042

Multiple Species 1042

Contracted Flexor Tendons 1042

Dyschondroplasia 1042

Dystrophy-like Myopathies 1043

Glycogen Storage Disease 1043

Malignant Hyperthermia 1027 (MET)

Muscular Steatosis 1043

Myopathy Associated with Congenital Articular Rigidity 1044

Osteochondrosis 1044

Osteogenesis Imperfecta 1044

Osteopetrosis 1044

Syndactyly and Polydactyly 1045

Cattle 1045

Arthrogryposis 1045

Brown Atrophy 1045

Double Muscling 1045

Limber Leg 1045

Perosomus Elumbis 1045

Spine Defects 1046

Horses 1046

Angular Limb Deformities 1046

Digit Malformation 1046

Dwarfism 1046

Glycogen Branching Enzyme Deficiency 1046

Hernias 104 7

Hyperkalemic Periodic Paralysis 1047

Spine Defects 104 7

Tying-up Syndrome 1048

Sheep 1048

Spider Lamb Syndrome 1048

Pigs 1049

Splayleg 1049

Small Animals 1049

Apodia 1049

1032

MUSCULOSKELETAL SYSTEM

Ectrodactyly Syndrome 1050

Polydactyly 1050

Syndactyly 1050

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DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS,

AND VITAMIN D 1050

Nutritional Osteodystrophies 1051

Rickets 1051

Osteomalacia 1052

Enzootic Calcinosis 1052

Vitamin D3 Toxicity 1054

Metabolic Osteodystrophies 1054

Fibrous Osteodystrophy 1054

Primary Hyperparathyroidism 1054

Renal Secondary Hyperparathyroidism 1056

Hypoparathyroidism 1057

SARCOCYSTOSIS 1058

LARGE ANIMALS

ARTHROPATHIES 1060

Arthritis 1060

Traumatic Arthritis 1060

Osteochondritis Dissecans 1061

Subchondral Cystic Lesions 1062

Septic Arthritis 1062

Osteoarthritis 1063

Bursitis 1064

Capped Elbow and Hock 1064

Fistulous Withers and Poll Evil 1064

Chlamydia! Polyarthritis-Serositis 1065

Tenosynovitis 1066

LAMENESS IN CATTLE 1066

Diagnostic Procedures 1066

Physical Examination of a Lame Cow 1067

Locomotion Scoring 1068

Computerized Recording of Digital Lesions 1068

Distal Digital Anesthesia for Diagnostic and Surgical Procedures 1068

Radiography 1069

Arthrocentesis andArthroscopy 1070

Risk Factors Involved in Herd Lameness 1070

Preventive Procedures 1073

Footbaths 1073

Functional Claw Trimming 107 4

Prevalent Lameness Disorders in Intensively Managed Herds 107 4

Digital Dermatitis 1075

MUSCULOSKELETAL SYSTEM

1033

Pododermatitis Circumscripta 1076

White Line Disease 1077

Toe Necrosis Syndrome 1078

Sole Hemorrhage 1079

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Thin Sole 1079

Heel Erosion 1079

Other Disorders of the Interdigital Space 1080

Interdigital Dermatitis 1080

Interdigital Phlegmon 1081

Interdigital Hyperplasia 1082

Disorders of the Hom Capsule and Corium 1082

Laminitis 1082

Double Sole 1084

Foreign Body in Sole 1084

Vertical Fissures 1085

Horizontal Fissures 1085

Corkscrew Claw 1086

Slipper Foot 1086

Disorders of the Bones and Joints 1086

Ankylosing Spondylosis 1086

Degenerative Arthropathy 1086

Coxofemoral Luxation 1087

Patellar Luxation 1087

Fetlock Dislocation 1087

Hip Dysplasia 1087

Fractures 1088

Septic Arthritis of the Distal Interphalangeal Joint 1088

Serous Tarsitis 1088

Neurologic Disorders Associated with Lameness or Gait Abnormalities . 1088

Suprascapular Paralysis 1088

Radial Paralysis 1089

Ischiatic Paralysis 1089

Obturator Paralysis 1089

Femoral Paralysis 1089

Peroneal Paralysis 1090

Tibial Paralysis 1090

Spastic Syndrome 1090

Spastic Paresis 1091

Soft-tissue Disorders Causing Lameness 1091

CarpalHygroma 1091

Rupture of the Gastrocnemius Muscle 1091

Rupture of the Peroneus Tertius Muscle 1091

Tarsal Cellulitis 1092

LAMENESS IN GOATS 1092

Caprine Arthritis and Encephalitis 1093

Contracted Tendons in Kids 1093

1034

MUSCULOSKELETAL SYSTEM

Copper Deficiency 1093

Epiphysitis 1093

Footrot and Foot Scald 1094

Joint-ill 1094

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Laminitis 1095

Mycoplasmosis 1095

Trauma 1095

White Muscle Disease 1095

LAMENESS IN HORSES 1096

The Lameness Examination 1097

Imaging Techniques 1098

Arthroscopy 1101

Regional Anesthesia 1101

Disorders of the Foot 1107

Osseous Cyst-like Lesions in the Distal Phalanx 1107

Bruised Sole and Corns 1107

Canker 1108

Fracture ofNavicular Bone 1108

Fracture of Distal Phalanx 1108

Keratoma 1109

Laminitis 1109

Navicular Disease 1112

Pedal Osteitis 1114

Puncture Wounds 1114

Pyramidal Disease 1115

Quittor 1115

Quarter Crack 1116

Scratches 1116

White Line Disease 1116

Sheared Heels 111 7

Sidebone 1117

Thrush 1117

Disorders of the Pastern and Fetlock 1118

Fractures of the First and Second Phalanx 1118

Fractures of the Proximal Sesamoid Bones 1119

Osteoarthritis of the Proximal Interphalangeal Joint 1119

Palmar/Plantar Metacarpal/Metatarsal Nonadaptive Bone Remodeling 1120

Sesamoiditis 1120

Chronic Proliferative Synovitis 1120

Digital Sheath Tenosynovitis 1121

Disorders of the Metacarpus 1121

Tendinitis 1121

Suspensory Desmitis 1122

Inferior Check Desmitis 1123

Bucked Shins 1123

Exostoses of the Second and Fourth Metacarpal Bones 1123

MUSCULOSKELETAL SYSTEM

1035

Fractures of the Small Metacarpal (Splint) Bones 1124

Fracture of the Third Metacarpal (Cannon) Bone 1124

Disorders of the Carpus 1125

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Fracture of the Carpal Bones 1125

Subchondral Bone Disease of the Third Carpal Bone 1126

Tearing of the Medial Palmar Intercarpal Ligament 1126

Osteoarthritis of the Carpus 1126

Distal Radial Exostosis and Osteochondroma of the Distal Radius 1126

Carpal Hygroma 1127

Rupture of the Common Digital Extensor Tendon 1127

Disorders of the Shoulder 1127

Developmental Diseases 1127

Fractures 1128

Bicipital Bursitis 1129

Infection 1129

Suprascapular Neuropathy 1129

Osteoarthritis of the Shoulder 1130

Disorders of the Elbow 1130

Developmental Orthopedic Disease 1130

Fractures 1131

Osteoarthritis of the Elbow 1131

Collateral Ligament Injury 1131

Disorders of the Metatarsus 1131

Bucked Shins/Dorsal Cortical Fractures of the Third Metatarsal Bone 1131

Exostoses of the Metatarsal Bones 1132

Diaphyseal Fracture of the Third Metatarsal Bone 1132

Incomplete Longitudinal Fractures of the Plantar Aspect of the Third Metatarsal Bone 1132

Focal Bone Reaction and Avulsion Fractures of the Third Metatarsal Bone 1132

Fractures of the Second and Fourth Metatarsal Bones 1132

Enostosis-like Lesions of the Third Metatarsal Bone 1133

Disorders of the Tarsus 1133

Failure of Ossification of the Distal Tarsal Bones 1133

Osteoarthritis of the Distal Tarsal Joints 1133

Osteoarthritis of the Talocalcaneal Joint 1135

Osteoarthritis of the Tarsocrural Joint 1135

Synovitis/Capsulitis of the Tarsocrural Joint 1135

Osteochondrosis of the Tarsocrural Joint 1135

Osteitis of the Calcaneus 1136

Fractures of the Distal Tarsal Bones 1136

Fracture of the Talus 1136

Fracture of the Fibular Tarsal Bone (Calcaneus) 1136

Fracture of the Lateral Malleolus of the Tibia 1136

Tarsal Joint Luxation 1136

Desmitis of the Collateral Ligaments of the Tarsus 1137

Rupture of the Fibularis (Peroneus) Tertius 1137

1036

MUSCULOSKELETAL SYSTEM

Stringhalt 1137

Curb 1138

Disorders of the Tarsal Sheath 1138

False Thoroughpin 1138

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Luxation of the Superficial Digital F1exor Tendon from the Tuber Calcanei 1139

Gastrocnemius Tendinitis 1139

Calcaneal Bursitis 1139

Capped Hock 1140

Disorders of the Stifle 1140

Osteochondrosis 1140

Subchondral Cystic Lesions 1140

Meniscus and Meniscal Ligament Iajuries 1141

Cranial and Caudal Cruciate Ligament Iajuries 1141

Collateral Ligament Iajuries 1141

Intermittent Upward Fixation of the Patella and Delayed Patella Release 1142

Fragmentation of the Patella 1142

Patellar Luxation 1142

Patellar Ligament Iajuries 1143

Gonitis and Osteoarthritis 1143

Chondromalacia of the Femoral Condyles 1143

Fractures 1143

Disorders of the Hip 1144

Luxation of the Coxofemoral Joint 1145

Pelvic Fracture 1145

Osteoarthritis and other Coxofemoral Joint Diseases 1145

Disorders of the Back and Pelvis 1146

Spinal Processes and Associated Ligaments 1146

Articular Process-Synovial Intervertebral Articulation Complexes 114 7

Vertebral Bodies and Discs 1147

Muscle Strain and. Soreness 1147

Lumbosacral Junction Abnormalities 114 7

Sacroiliac Joint Abnormalities 114 7

Developmental Orthopedic Disease 1148

Osteochondrosis 1148

Physitis 1149

Flexural Deformities 1150

LAMENESS IN PIGS 1151

Pigs in Farrowing Houses 1156

Pigs in Nurseries 1158

Pigs in Grower/Finisher Areas 1160

Breeding Gilts, Sows, and Boars 1162

LAMENESS IN SHEEP 1166

Interdigital Dermatitis 1167

Contagious Footrot 1167

MUSCULOSKELETAL SYSTEM

1037

Benign Footrot 1167

Virulent Footrot 1167

Foot Abscess 11 70

Impacted or Infected Oil Gland 1170

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Interdigital Fibroma 1170

Septic Laminitis 1171

MYOPATHIES IN RUMINANTS AND PIGS 1171

Infectious Myopathies 11 71

Clostridial Myonecrosis 1171

Sarcocystosis 11 72

Nutritional Myopathies 1172

Nutritional Myodegeneration 1172

Hypokalemic Myopathy 1173

Nutritional Myopathy of Pigs 117 4

Toxic Myopathies 1175

Plant Toxins 1175

Ionophores 1175

Traumatic Myopathies 1175

Muscle Crush Syndrome of Cattle 1175

Genetic Myopathies 1175

Caprine Myotonia 11 75

Congenital Muscular Dystonia in Belgian Blue Cattle 1175

Phosphorylase Deficiency in Charolais Cattle 1175

Porcine Malignant Hyperthermia 1176

Porcine RN(-) Glycogen Storage Disease 1176

Pseudomyotonia 1176

MYOPATHIES IN HORSES 1176

Exertional Myopathies 11 78

Infectious Myopathies 1180

Immune-mediated Myopathies 1182

Muscle Cramping 1182

Myotonic Disorders 1184

Nutritional Myopathies 1185

Plants Causing Myopathies 1186

Toxic Myopathies 1186

Traumatic and Anesthetic Myopathies 1186

Hereditary and Congenital Myopathies 1187

BOVINE SECONDARY RECUMBENCY 1188

SMALL ANIMALS

LAMENESS 1192

The Lameness Examination 1193

Pain Management 1193

1038

MUSCULOSKELETAL SYSTEM

ARTHROPATHIES AND RELATED DISORDERS 1194

Aseptic Necrosis of the Femoral Head 1194

Patellar Luxation 1194

Osteochondrosis 1195

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Elbow Dysplasia 1196

Hip Dysplasia 1196

Degenerative Arthritis 1197

Septic Arthritis 1197

Immune-mediated Arthritis 1198

Neoplastic Arthritis 1198

Polyarthritis 1198

Joint Trauma 1198

Cranial Cruciate Ligament Rupture 1198

Joint Fractures 1199

Palmar Carpal Breakdown 1199

Hip Luxation 1199

MYOPATHIES 1200

Yellow Fat Disease 1200

Labrador Retriever Myopathy 1200

Great Dane Myopathy 1200

Fibrotic Myopathy 1200

Myositis Ossificans 1201

Polymyositis 1201

Masticatory Myositis 1201

Feline Hypokalemic Polymyopathy 1201

Malignant Hyperthermia 1201

Exertional Myopathy 1202

Muscular Trauma 1202

Muscle Tumors 1203

OSTEOPATHIES 1203

Developmental Osteopathies 1203

Angular Deformity of the Forelimb 1203

Craniomandibular Osteopathy 1203

Hypertrophic Osteodystrophy 1204

Multiple Cartilaginous Exostoses 1204

Panosteitis 1204

Retained Ulnar Cartilage Cores 1204

Scottish Fold Osteodystrophy 1204

Osteomyelitis 1204

Hypertrophic Osteopathy 1205

Nutritional Osteopathies 1205

Bone Tumors 1205

Bone Trauma 1205

MUSCULOSKELETAL SYSTEM INTRODUCTION

1039

MUSCULOSKELETAL SYSTEM

INTRODUCTION

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The musculoskeletal system consists of
peripheral axon, the neuromuscular
bones, cartilage, muscles, ligaments, and
junction, and the muscle fibers innervated
tendons. Primary functions of the musculoby the neuron. Each cif these components skeletal system include support of the body,
must be functionally intact for the muscle to
provision of motion, and protection of vital
contract properly. The ventral motor neuron
organs. The skeletal system serves as the
is the final common pathway conducting
main storage system for calcium and
nemal impulses from the CNS to the
phosphorus and contains critical compomuscle.

nents of the hematopoietic system. Many

The transmission of a ne1ve impulse
other body systems, including the nervous,
at the neuromuscular junction involves
vascular, and integumentary systems, are
massive release of acetylcholine from small
inteITelated, and disorders of one of these
synaptic vessels, where it is stored. The
systems may also affect the musculoskeletal acetylcholine fills the synaptic cleft between system and complicate diagnosis.

the nerve temlinal and the muscle fiber

Diseases of the musculoskeletal system
membrane, where most of it is destroyed by
most often involve motion deficits,
cholinesterase witllin a fraction of a second.

functional disorders, and lameness. The

This short period of activity is sufficient to
degree of impairment depends on the
excite the muscle fiber membrane, which
specific problem and its severity. Skeletal
results in a significant increase in memand articular disorders are by far the most brane permeability to sodiun1 ions and
common and have the greatest economic
allows rapid influx of sodiwn into the
impact. In horses and dogs, musculoskeletal muscle fiber. The sodium ion increases the injuries are a major source of debilitating
end plate potential, which elicits electrical
pain, economic loss, and loss of athleticism.

cwTents that spread to the interior of the

Degenerative joint disease is much more
fibers, where they cause a release of
common and has a greater economic
calcium ions from the sarcoplasmic
importance than acute traumatic injuries or
reticulun1. The calcium ions initiate, in turn,
respiratory diseases in performance horses.

the chemical events of the contractile

Several studies estimate that problems
process. When this occurs in all the muscle
involving the fetlock and carpal joints
fibers innervated by each motor neuron
account for 25o/er-28% of horses lost from

(possibly tl10usands), muscle contraction
training. In addition, tendon injury is a
results.

common debilitating injury in performance

Normal muscle, comprising many motor
horses. The healing response is prolonged,
units, is dynainic, and its function and
and the resultant repair tissue is usually of
structme can be influenced by many
inferior mechanical strength. Consequently,
diseases. Complete paralysis, paresis, or
the prognosis for return to previous levels
ataxia may be caused by primary muscular
of performance is poor. In dogs, cranial
dysfunctions of infectious, toxic, or
cruciate ligament injury with resulting
congenital origin. However, in most
osteoarthritis is the most common
instances the primary disorder can be
musculoskeletal injury resulting in
attributed to the nervous system ( eg,
lameness. Although perhaps less common,
tetanus, rhinopneumonitis, cailine
primaiy muscular diseases, neurologic
distemper, protozoa] myelitis), with the
deficits, toxins, endocrine aberrations,
musculai· system merely representing the
metabolic disorders, infectious diseases,
effector organ. Disorders tl1at affect the
blood and vascular disorders, nutritional
neuromuscular junction ( eg, myasthenia
imbalances or deficits, and occasionally
gravis, hypocalcemia, hypennagnesemia)

congenital defects are diagnosed as well.

can result in muscle fatigue, weakness, and
paralysis. The neuromuscular junction can

DISORDERS OF MUSCLE
also be affected by muscle-relaxing drugs

( eg, curare, succi.nylcholine, M99), ce1tain

The structural and functional unit of
antibiotics, and toxins ( eg, botulism,
skeletal muscle is the motor unit. It consists
tetanus, venoms).

of a ventral motor neuron with its cell body

Disorders prin1ari.ly of the muscle
in the central horn of the spinal cord and its
membrane and, to some extent, of the

1040

MUSCULOSKELETAL SYSTEM INTRODUCTION
actual muscle fibers are called myopathies.

disorders are caused by excessive protein

Muscle membrane disorders may be
intake of growing animals. Either deficiency
hereditary ( eg, myotonia congenita in goats) or excess intake of certain vitan1ins, particuor acquired ( eg, vitamin E and selenium larly vitamins A and D, may influence
deficiencies, hypothyroidism, and
growth and development of bone. Aseptic

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hypokalemia). Myopathies involving the
physitis or special osteochondrotic
actual muscle fiber components include
conditions of the physes may be caused
muscular dystrophy, polymyositis,
by zinc toxicity or copper deficiency.

eosinophilic myositis, white muscle disease,

Trawnatic causes of bone disorders
and exertional rhabdomyolysis. Various
represent the vast majority of cases and
laboratmy tests, eg, histopathologic
include fractures, fissures, periosteal
examination, determination of serum
reactions as a result of trawna, sequestrum
enzyme levels, electromyographic studies,
formation, and insertion desmopathies or
thermography, and determinations of
tendinopathies, respectively. Lack of weight
conduction velocity, are very useful in
bearing, lameness, reduced motion,
confirmation of a specific diagnosis.

instability, pain, heat, or swelling usually
accompany these disorders.

DISORDERS OF TENDONS

DISORDERS OF JOINTS

Tendons act as bridging and attachment
structures for the muscles; some bridge

Articulations are divided into synarthrodial
long gaps between the muscle bellies and
joints and diarthrodial joints. Synarthrodial
target bone and, therefore, are prone to
joints are osseous components united by
injury themselves, especially because they
fibrous tissue or cartilage. Synarthrodial
are often loaded to the extreme and are only joints are practically immovable and are minimally capable of elastic elongation. A
rarely associated with joint disease other
prin1e example is the superficial flexor
than fractures. Diarthrodial joints are
tendon of horses, which is frequently
mobile; the opposing bone ends are covered
iajured by partial tearing that leads to
by articular hyaline cartilage and are
tendinitis. Another acquired injury of
separated by a joint cavity filled with
tendons involves traumatic disruptions.

synovial fluid. Articular cartilage serves

Because of tl1e relatively poor blood supply
to distribute weight-bearing forces and to
of both tendons and ligaments, healing is
minimize friction between adjacent skeletal
always prolonged with inelastic scar tissue,
components during movement. Normal
and the injured tendon never returns to its
synovial fluid and articular cartilage express
original strength. Therefore, management
a glycoprotein to provide boundary
of tendon and ligament injuries requires
lubrication to the articular cartilage and
patience with conservative longterm
synovial membrane during weight bearing.

rehabilitation. Reinjwy is common.

The synovial fluid also nourishes the
articular cartilage.

DISORDERS OF BONE

Diarthrodialjoints are most frequently
involved in pathologic changes. These

Bone diseases are generally congenital
changes can involve the joint capsule,
or hereditary, nutritional, or traumatic.

synovial membrane, hyaline articular

Congenital disorders include in utero
cartilage, and subchondral bone. Damage to
malfom1ations and atavisms, such as
intra-articular ligaments and the menisci in
polydactyly or persistent ulnae or fibulae
the stifle joint can affect the stability of the
in foals; examples of genetic defects are
joint and propagate damage to the joint.

atlanto-occipital malformations in Arabian

Joint disorders may be caused by trauma,
horses or certain cases of spinal ataxia (see
chronic inflammation, developmental
p 1228), canine hip dysplasia, and abnormal
factors, or infections. Severe trawna
bone fonnation such as that caused by
frequently results in luxation, subluxation,
paratl1yroid hypoplasia.

fracture, or instability of ajoint. Direct

Bone defects due to nutrition are caused
penetration of the joint capsule may also
primarily by imbalances or deficiencies in
lead to septic arthritis, which is characterminerals, particularly the trace minerals ized by an increase in synovial WBCs
such as copper, zinc, and magnesium.

resulting in an increased concentration of

Calcium and phosphorus concentrations
proteolytic enzymes within the synovial
must also be present in the correct ratio.

fluid. The severe inflan1.111atory response

Osteomalacia represents the classic
within the joint can quickly lead to
example of imbalanced or deficient calcitun
breakdown of the articular· hyaline
and phosphorus intake. Other nutritional
cartilage. Bacterial and fungal infections

MUSCULOSKELETAL SYSTEM INTRODUCTION

1041
involving synovial structures are typically

Several medications have specific
recognized based on their extreme heat,
chondroprotective actions to treat articular
swelling, pain localized to the joint, and
cartilage damage. Structure-modifying
lameness that is often severe. All cases of
osteoarthritis drugs ( eg, glycosaminoglysynovial sepsis require immediate and cans, pentosan polysulfate, hyaluronic

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aggressive treatment to preserve the joint.

acids) slow down the progression of

Developmental defects include osteoosteoartluitis by mitigating the rate of chondritis dissecans, equine ataxia, angular
cartilage degradation and enhancing matrix
limb deformities, and lumbar disc syndrome
synthesis. Intra-articulai· hyaluronic acid
in certain breeds of dogs. Extension of
administration reduces synovial inflanun a physitis into the adjacent joint and damage tory effects and may also reestablish
due to continuous abnonnal weight bearing
boundary lubrication within the joint cavity.

in animals with angular limb deformities are

The autogenous substance interleukin
other inciting causes of joint disease.

receptor antagonist protein (IRAP) has

Chronic inflammation of joints and
been used effectively to control joint
surrounding structures is most common in
inflanunation in some horses.

articulations associated with locomotion.

Joint homeostasis involves the simultaneous synthesis and degradation of extracel

DIAGNOSIS AND TREATMENT OF
lular matrix components of the cartilage.

MUSCULOSKELETAL DISORDERS

The responses of the synovial membrane
and articular cartilage are critical to

In all cases of musculoskeletal pain and
accommodate the mechanical and chemical
lameness, diagnostic procedures to
demands placed on the joint. In pathologic
determine the nature, extent, and exact
conditions, the biosynthetic activity of the
location of the ir\jury must be performed.

cells does not compensate for the loss of

Evaluation of the source of pain ai1d
matrix components through mechanical
lameness always starts with a thorough
and enzymatic degradation. This results in a
history, inspection, and physical exanlinanet loss of caitilage and compromised joint tion to look for sources of heat, swelling,
function.

and pain on manual palpation. Hoof testers

Osteoarthritis is a degenerative,
should be applied to determine whether
progressive disease of diarthrodialjoints.

pain is present within the hoof capsule.

It has a multifactorial etiology; aging,

Next, the gait and locomotion of the aninlal
trauma, mechanical forces, conformation,
are evaluated. In a weight-bearing lameness,
hormonal, and genetic factors contribute
the lan1e leg always bears less weight and
to varying degrees. It is a major cause of
often has a shorter duration of beaiing
musculoskeletal pain, morbidity, and
weight. In swinging leg lameness, the lame
decreased performance in all species.

leg abducts or adducts to avoid flexion of

Although pathologic changes occur in
a painful joint. These findings can be
multiple joint tissues, loss of articular
measured objectively using a force plate or
cartilage is the hallmark of the disease.

a gait analysis system. In horses, flexion

Cartilage damage is recognized clinically
tests of joints followed inunediately by
when sufficient joint damage occurs to
lan1eness evaluation at a trot may help
cause synovitis or lameness. As damage
localize pain. After determining which limb
accumulates, cartilage fibrillation or
is lan1e, diagnostic analgesia (intra-articular
complete eburnation can occur at areas of
or perineural) can be used to localize the
high stress. Histologically there is loss of
painful gait to a specific anatomic structure
proteoglycan staining, decreased cell
or a region of the affected limb. After
viability, and advancement of the tidemark
localization, diagnostic imaging techniques
of calcified cartilage. The loss of proteoglycan be performed to evaluate the soft-tissue cans is accompanied by an increase in
structures and bones. These diagnostic
cartilage matrix water content and a
procedures include radiography, ultrareduction in stiffness. The biomechanically sonography, MRI, CT, nuclear imaging,
compromised cartilage is more susceptible
and thermography. When joint sepsis is
to further damage.

suspected, synovial fluid analysis of

Corticosteroids and NSAIDs have been
affected joints is necessary for diagnosis.

widely used for symptomatic treatment of

After these procedures, a diagnosis can be
osteoarthritis. The benefit of these drugs is
made, treatment instituted, and a prognosis
rninin1ized in extensive cartilage loss in
given based on the diagnosis, extent of
which chondrocyte replacement is an issue,
disease, and expected response to therapy.

and their inappropriate use may exacerbate

Therapeutic options for diseases of the
the progression of degenerative chai1ge.

musculoskeletal system include rest,

1042

MUSCULOSKELETAL SYSTEM INTRODUCTION
restricted or modified activity, immobilizaduring the past few years with the use of tion of diseased or injured structures in
regenerative medicine, in which growth
splints and casts, NSAIDs, co1ticoste-
factors and mesenchymal cell therapy
roid administration, physical therapy,
have been used to augment healing. A

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acupuncture, extracorporeal shock wave
return to a useful life for many animals is
therapy, and surgical repair. Therapeutic
possible when diagnosis and subsequent
options for management of musculoskeltreatment is done early in the disease etal disorders have greatly expanded
process.

CONGENITAL AND INHERITED ANOMALIES

OF THE MUSCULOSKELETAL SYSTEM

Congenital and inherited anomalies can
to stretch the ligan1ents, tendons, and
result in the birth of diseased or defonned
muscles, helps treat these intermediate
neonates. Congenital disorders can be due
cases. Severe cases require tenotomy of one
to viral infections of the fetus or to ingestion or both flexor tendons. A bandage cast may of toxic plants by the dam at certain stages
sometimes be indicated. Extreme cases may
of gestation. The musculoskeletal system
not respond to any treatment.

can also be affected by certain congenital
neurologic disorders.

Dyschondroplasia

Dyschondroplasia of genetic origin is seen

MULTIPLE SPECIES
in most breeds of cattle. The forms range

Contracted Flexor Tendons
from the so-called Dexter "bulldog" lethal, Contracted flexor tendons a.re probably
the most prevalent abnormality of the
musculoskeletal system of newborn foals
and calves. An autosomal recessive gene
causes this condition. In utero positioning
may also affect the degree of disability.

At birth, the pastern and fetlocks of the
forelegs and sometimes the carpal joints are
flexed to varying degrees due to shortening
of the deep and superficial digital flexors
and associated muscles. A cleft pala'te may
accompany this condition in some breeds.

Slightly affected animals bear weight on the
soles of the feet and walk on their toes.

More severely affected animals walk on the
dorsal surface of the pastern and fetlock
joint. If not treated, the dorsal surfaces
of these joints become damaged, and
suppurative arthritis develops. Rupture of
the common digital extensor can occur as a
sequela. This condition should be differentiated from a.rthrogryposis.

Mildly affected animals recover without
treatment. In moderate cases, oxytetracycline may be administered to relax the flexor muscles, and a splint can be applied
to force the animal to bear weight on its
toes. The pressure from the splint must not
compromise the circulation, or the foot may
undergo ischemic necrosis. Frequent

Ruptured common digital flexor tendon as
a sequela of contracted flexor tendons in a
manual extension of the joints, attempting
foal. Courtesy of Dr. Reid Hanson.

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM

1043
in which the calf is invariably stillborn, to

Europe. Affected dogs, generally males,
mildly affected animals.

develop progressive muscular weakness,

The brachycephalic dwarfs common
dysphagia, stiffness of gait, and muscular
in Hereford cattle in the 1950s largely have
atrophy. Microscopically, the distinctive

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been eliminated through genetic selection.

change is lack of dystrophia, a protein

Short faces, bulging foreheads, prognaconcentrated in the sarcolenuna and thism, cleft palate, large abdomens, and
essential for normal membrane function.

short legs are characteristic. They are

Some dogs die with accompanying
approximately half normal size. The
cardiomyopathy. A similar X-linked
dolichocephalic dwarf, most commonly
dystrophy witll a lack of dystrophia is
seen in Angus cattle, is of the san1e general
described in cats. A second type of
body conformation as the brachycephalic
dystrophy involves Labrador Retrievers in
dwarf, except that it has a long head and

North America, Europe, and Australia.

does not have eitller a bulging forehead or

Clinical signs, which include stiffness,
prognatllism. The short-faced calves are
exercise intolerance, and muscular atrophy,
frequently referred to as "snorter" dwarfs develop by 6 mo of age. Autosomal
because of their labored and audible
recessive inheritance is implicated.

breatlling. Botll types are of low viability

A further dystrophy was described in
and susceptible to bloat. Their carcasses
dysphagic Bouviers in Europe.

are undesirable, and they are rarely kept
except for research purposes.

Glycogen Storage Disease

Dyschondroplasia of tile appendicular
and axial skeletons also is seen in dogs. The

(Glycogenosis)

fo1mer is reported in Poodles and Scottish

Glycogen storage disease (GSD) is tile result

Terriers, the latter in Alaskan Malamutes,
of defects in tl1e processing of glycogen

Basset Hounds, Dachshunds, Poodles, and
syntllesis or breakdown witllin muscles, liver,

Scottish Terriers. In some breeds (Bassets,
and oilier cell types. GSD can be genetic or

Dachshunds, Pekingese), the appendicular
acquired. Genetic GSD is caused by any
dyschondroplastic characteristics are
inborn error of metabolism (genetically
an important feature of breed type. In
defective enzyn1es) involved in tllese

Malamutes, the condition is accompanied
processes. In livestock, acquired GSD is
by anemia.

caused by intoxication witll tile alkaloid
castanospe1mine. Progressive muscular

Dystrophy-like Myopathies
weakness and inability to rise properly may

Numerous examples of progressive
be seen in animals witll GSDs. Five of tile 11
myopathies have been described in animals;
types of GSDs characterized in people have
many are heritable, and many resemble
been identified in animals (types I, II, ill, VII,
various types of muscular dystrophy in
and VIII). Affected species include cattle,
people. Affected muscles have a variety
sheep, dogs, cats, horses, Japanese quail, rats,
of degenerative and atrophic changes.

and mice. Type II g]ycogenosis in Shmthorn

In Meuse-Rhine-Y ssel cattle of Holland, a
and Bralm1an cattle has been well docuprogressive fatal myopathy of tile diaphragm mented and is inherited as an autosomal and intercostal muscles has been described.

recessive disorder. Affected cattle develop

Another dystrophy in cattle is weaver
muscular weakness and die at 9 -16 mo of
syndrome in Brown Swiss. Hyperplasia,
age, often witll accompanying cardiomegaly
commonly called double muscling ( see
and congestive heart failure. Morphologic
p 1045), is a congenital myopathy found in
and biochemical study reveals extensive
some European breeds of cattle. Progressive intralysosomal and cytoplasmic glycogen myopatllies have been repmted in Merino
deposits. Corriedale sheep and Lapland dogs
sheep in Australia ( an inherited autosomal
also develop type II glycogenosis.

recessive), in Pietrain pigs (Pietrain creeper

Myophosphorylase deficiency (type V
syndrome), and in dogs, cats, chickens,
glycogenosis) is an autosomal recessive
turkeys, and mink Inherited muscular
disorder in Charolais cattle. Affected cattle
dystrophy of mice and hamsters has been
show exercise intolerance and may have
studied extensively; tile hamsters have
increased serum activities of skeletal
severe myocardial lesions and serve as a
muscle-origin enzymes.

model for studies of cardiomyopatlly.

Several types of muscular dystrophy are

Muscular Steatosis
seen in dogs. An X-linked Duchenne-like

Muscular steatosis is a condition in which
muscular dystrophy is reported in Golden
muscle fibers have been replaced by fatty

Retrievers in tile USA and in Irish Terriers in
deposits and is seen occasionally in cattle,

1044

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM
sheep, and pigs at slaughter. Sometimes

Osteochondrosis
the occurrence of muscular steatosis is
indicated before slaughter by an abno1mal

Osteochondrosis is a disturbance in
gait, but usually the condition is not found
endochondral ossification that is someuntil a carcass is butchered. The condition times classified as dyschondroplasia. The

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may be difficult to establish, and it is often
immature articular cartilage may separate
only the restriction of muscular steatosis to
from the underlying epiphyseal bone, which
a single muscle group in an otherwise poorly
sometimes dissects completely free and
marbled carcass that makes it conspicuous.

floats loose in the synovial cavity, resulting

In pigs, there is evidence that the onset of
in accompanying synovitis or the retention
muscular steatosis is accompanied by lipid
of pyramidal cores of physeal cartilage
accumulation in muscle fibers. No clinical
projecting into the metaphysis. Often, these
disease results, and the cause is unknown.

two lesions are seen simultaneously in the

The gross lesions are symmetric, pale areas
san1e bone. The disease develops during
in affected muscles, especially of the back,
maximal growth when the biomechanical
neck, and upper limbs. Microscopically,
stresses are greatest in the immature skeleton
many muscle fibers are replaced by fat cells.

(4--Smo in dogs, 80-120 lb [36--54 kg] in pigs).

It is most common in large and giant breeds
of dogs (seep 1195) and in rapidly growing

Myopathy Associated with
pigs (seep 1161), horses (seep 1148), turkeys, Congenital Articular Rigidity
and chickens (seep 2932).

(Arthrogryposis)

This syndrome, one of the more common

Osteogenesis lmperfecta
congenital defects of calves, is characte1ized Osteogenesis i.rnperfecta is a generalized, by rigid fixation of the limbs in abnom1al
inherited bone defect in cattle, dogs, and
postures; it often produces dystocia. The
cats, characterized by extreme fragility of
muscle weakness and imbalance of muscle
bones and joint laxity attributable to any of a
power around the joints elicits a physiologic
large number of possible mutations of type I
compensatory collagenic response, which
collagen. The mechanical properties of the
replaces atrophied muscle fibers with

"soft" part of the collagen/mineral composite connective tissue and thickens the joint
in the bone appear to be altered. The long
capsule sufficiently to result in prenatal
bones are slender and have thin cortices.

fixation of limb segments at the joint.

Calluses and recent fractures may be

Affected animals may have other anomalies,
present. The sclera of the eyes may be bluish.

including hydrocephalus, palatoschisis, and

The inheritance is most likely polygenic.

spinal dysraphism. The condition may be
lethal, but some mildly affected animals
recover completely. The muscle lesions may

Osteopetrosis
be primaiy in some types of the disease, but

Osteopetrosis is a metabolic bone disease
the neural lesions generally are primaiy,
characterized by a systemic increase in
and the muscular alterations represent
skeletal mass. It is a rare disease that
denervation atrophy. Congenital articular
appears to be inherited as a simple
rigidity is seen in cattle, sheep, horses, and
autosomal recessive trait in Angus,
pigs. Numerous etiologic factors have been

Sinm1ental, Dutch Holstein-Freisian and
recognized. In cattle, these include viral

Hereford cattle. It is also seen in dogs and

(Akabane virus [seep 620], bluetongue virus
foals. It is characterized by premature

[seep 738]) and plant (Lupinus sp, seep 3018) stillbirth 10 days to 1 mo before tenn, teratogens, and a heritable recessive trait in
brachygnathia inferior, impacted molar

Charolais (see ARTHROCRYPOSIS, p 1045). In
teeth, and easily fractured long bones. Bone
sheep, plant Oocoweed) and viral (Akabane,
marrow cavities are absent and replaced by

Wesselsbron [seep 775] teratogens, Rift
primaiy spongiosa. The fetal-like abnormal

Valley fever [seep 768]), parbendazole
intran1edullaiy bone consists of chondroexposure, and inherited autosomal recessive osseous tissue. Foran1ina of the skull and primaiy myopathies of Merino and Welsh
long bones are hypoplastic or aplastic. The

Mountain lan1bs may cause congenital
cranium is thickened and compresses the
articular rigidity. In pigs, the condition may
brain. Extensive mineralization is present
be inherited as an autosomal recessive, or
in vessel walls and neurons of the brain.

result from deficiency of vitamin A or

Diagnosis is confirmed by a longitudinal
manganese or from exposure of pregnant
bisection of long bones revealing the
sows to plant toxins ( eg, tobacco, thomapdiaphyses filled with a plug of bone instead ple, hemlock, and black cherry).

of marrow.

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM

1045

Syndactyly and Polydactyly
brown lipofuscin pigment granules

Syndactyly, or mule foot, is the partial or
accumulate under the sarcolenuna or
complete fusion of the digits of one or
centrally in the muscle fibers. The
more feet. Reported in numerous cattle
inheritance pattern of one affected and

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breeds, it is most prevalent in Holsteins
three norn1al offspring suggests that this
and is inherited as a simple autosomal
condition may result from inheritance of
recessive condition. The forefeet are
a sin1ple recessive gene.

affected most often, but one or all four feet
may be affected. Animals affected with

Double Muscling
syndactyly walk slowly, usually have a

Double muscling is an overdevelopment
high-stepping gait, and may be more prone
of the musculature of the shoulder, back,
to hyperthermia.

rump, and hindquarters, separated by deep

Polydactyly is a genetic defect of cattle,
creases, particularly between the semitensheep, pigs, and occasionally horses. In its dinosus and biceps femoris, and between
most common form, the second digit is
the longissimus dorsi muscles of either side.

developed but the medial dewclaw is

Necks of double-muscled cattle are shorter
missing. The toes may be fused to give rise
and thicker, and their heads appear smaller.

to polysyndactyly. Rarely one or all four

Associated disorders include hypoplastic
limbs have the condition. Polydactyly in
reproductive tracts, delayed reproductive
cattle appears to be polygenic, with a
age of maturity, and lengthened gestation
dominant gene at one locus and a homoand increased birth weights combined with zygous recessive at another.

dystocia. The condition is seen in various
beef breeds, including Charolais, Santa

CATILE

Gertrudis, South Devon, Angus, Belgian

Blue, Belgian White, and Piedmontese.

Arthrog ryposis

Double muscling is caused by a pair of

Arthrogryposis is ankylosis of the limbs,
incompletely recessive genes that result
usually combined with a cleft palate and
in the inhibition of myostatin activity in
other growth deformities. It is seen in all
various degrees of the condition. Succinic
breeds of cattle, paiticularly Charolais. At
dehydrogenase activity is significantly
birth, affected calves exhibit joints fixed in
decreased in affected calves.

abnormal positions and frequently have
scoliosis and kyphosis. They are usually

Limber Leg
unable to stand or nurse. Muscle changes,
notably atrophy, have also been seen. In

Limber leg is a hereditary condition of Jersey
the spinal cord, necrosis of neurons and
cattle, apparently controlled by a simple
lesions of the white matter may be seen.

lethal autosomal recessive gene. Some

Arthrogryposis has more than one etiology
affected calves are born dead. Living calves
and pathologic entity. The arthrogryposis
appear nonnal at birth but are unable to
syndrome in Charolais is caused by an
stand because of incompletely formed
autosomal recessive gene with complete
muscles, ligaments, tendons, andjoints. The
penetrance in the homozygous state.

shoulder and hip joints can be rotated in any

Teratogens identified as causing arthrodirection without apparent discomfort.

gryposis include plants such as lupines

Diagnosis is based on signs, necropsy

(anagyrine as the toxic agent) that are
findings, and identification of carrier animals.

ingested by pregnant cows between day

40 and 70 of gestation. Prenatal viral

Perosomus Elumbis
infections with the Akabane (seep 620) or

Perosomus elurnbis is an occasionally found
bluetongue (seep 738) virus cru.1 also cause congenital anomaly of unknown etiology
arthrogryposis.

that is characterized by partial or complete
agenesis of the lumbar, sacral, and

Brown Atrophy
coccygeal area and accompanied by
posterior birnelic artlu·ogryposis character

(Xanthosis, Lipofuscinosis)

ized by ankylosis of joints with associated

In dairy cattle with brown atrophy, the
malformations of the musculature. Affected
skeletal muscles and myocardium are
calves caimot use their hindlegs and must be
yellow-brown to bronze. The masseter
euthanized. The defect is suspected to be
muscles and the diaphragm ai·e affected
inherited. A reduced nwnber of vertebrae
most frequently. No clinical disease results.

has been repo1ted rarely but also has been

Certain breeds ( eg, Ayrshire) are more
claimed to be a genetic defect. The condition
predisposed than others. Microscopically,
has also been repo1ted in sheep and pigs.

1046

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM

Spine Defects
transection and periosteal elevation of the

There are several defects of the spinal
distal radius on the concave side of the
column that include short spine lethal,
defect or tl1rough transphyseal bridging
atlanto-occipital fusion, kyphosis ( dorsal
of the physis on the convex side. These

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arching of the back), lordosis (ventral),
surgeries must be performed before the
scoliosis (lateral), and torticollis (twisted).

physeal growtl1 plates close (as early as

These defects may occur alone, in combina2-4 mo of age for fetlocks), and success tion with, or associated with defects of other depends on continued growth and body systems, particularly of the CNS.

development of the bones. Sequential
examinations and radiographs are
necessary to follow spontaneous improve

HORSES
ment or to establish a need for surgery.

Angular Limb Deformities

Without treatment, the prognosis for
severe carpal valgus is poor. The confom1a

In these congenital or acquired skeletal
tional anomaly leads to early degenerative
defects, the distal portion of a limb deviates
joint disease. Likewise, deformity of the
laterally or medially early in neonatal life. In
cuboidal carpal bones contributes to a poor
utero malposition, hypothyroidism, trauma,
prognosis. However, with early detection,
poor conformation, excessive joint laxity,
careful evaluation, and proper surgical
and defective endochondral ossification of
treatment, most foals respond favorably.

the carpal or tarsal and Jong bones have
been implicated. One to four limbs may be
affected, depending on the severity of the

Digit Malformation
condition.

Digital malfonnations include supernumer

The carpus is affected most frequently,
ary digits (polydactyly), hypoplasiaof
but the tarsus and fetlocks are occasionally
phalanges, such as the navicular bone, and
involved. The deviation is obvious but varies bipartite and tripartite navicular bone in in severity. A lateral deviation ( valgus) of up
which there is incomplete ossification of
to 6° of the distal portion of a limb may
the navicular bone.

be regarded as normal. Most foals are
asymptomatic, but lameness and soft-tissue

Dwarfism
swelling can accompany severe deviations.

Dwarfism is tl1e lack of appropriate growth,

Outward rotation of the fetlocks invariably
resulting in a smaller horse. A dwarf horse
accompanies carpal valgus. Foals with
can be proportionate or disproportionate.

defective ossification of the carpal cuboidal

Proportionate dwaifs are a result of a
bones or excessive joint laxity are
deficiency in growth hormone, whereas
frequently lame as th.e legs become
disproportionate dwarfs are a result of
progressively deviated. Affected limbs must
abnormal tl1yroid hom10ne levels. The latter
be palpated carefully to detect ligament
results in a foal with musculoskeletal
laxity and specific areas that may be painful. immaturity, characterized by delayed Diagnosis should include a precise
cuboidal bone development, a large head,
determination of the site arid cause for the
silky hair coat, floppy ears, and mandibular
deviation. The distal radial metaphysis,
brachygnathia. Determination and
physis, epiphysis, or cuboidal bones may
interpretation of either growth hormone
be the site of deviation. Radiography helps
assays or thyroid ho1mone function is not
detect physeal flaring, epiphyseal wedging,
entirely developed or understood in horses,
and deformation of carpal bones. Mildly
hence the importance of clinical diagnosis.

affected foals frequently improve spontane

Efforts toward characterizing thyroid
ously.

function ai1d growili hormone levels should

Treatment depends on the severity of the
be undertaken to prevent overdiagnosis of
condition and tissues affected. Excessive
this condition. A nitrate toxicity theory has
joint laxity, with or without cuboidal carpal
been confinned in certain foals born with
bone involvement, requires tube casts or

"congenital hypotl1yroid syndrome."

splints. The fetlock and phalangeal region
should not be included in the casts, which
should protect the weak joint from trauma

Glycogen Branching Enzyme
but allow restricted exercise to maintain

Deficiency
tendon and ligan1ent tone. Such limb

Glycogen branching enzyn1e (GBE)

support may be required for as long as 6 wk.

deficiency may be a common cause of

Physeal and epiphyseal growth disturneonatal mortality in Quarter horses and bances are also amenable to surgical
related breeds that is obscured by the variety
correction through hemicircumferential
of clinical signs that resemble other equine

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM

1047
neonatal diseases. Affected foals lack the

Hyperkalemic Periodic Paralysis
enzyme necessary to store glycogen in its
branched form and therefore cannot store

Hyperkalemic periodic paralysis (HYPP)

sugar molecules. The disease is fatal; heart
is marked by sudden attacks of paralysis
muscle, brain, and skeletal muscles are
which, in severe cases, may lead to collapse

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unable to function. Clinical signs ofGBE
and sudden death. It is an inherited misdeficiency may include transient flexural sense mutation in the gene encoding the
limb deformities, stillbirth, seizures,
alpha chain of the adult skeletal muscle
respiratory or cardiac failure, and persistent
sodiun1 channel, resulting in increased
recumbency. Leukopenia, high serwn CK,
sodium pern1eability across the skeletal

AST, and -y-glutamyl transferase are present
muscle cell membrane. Quarter horse, Paint
in most affected foals. Gross postmortem
horse, and Appaloosa progeny tracing back
lesions are inconclusive. Muscle, heart, or
to the Quarter horse sire "Impressive" can liver samples contain abnom1al periodic
be affected with this disease and must be
acid-Schiff-positive globular or crystalline
eliminated from any reproductive program.

intracellular inclusions in amounts

Most affected horses are heterozygotes. A
proportional to the foal's age at death.

sequela of HYPP in horses that undergo

Accumulation of an unbranched polysacchageneral anesthesia is malignant hyperthe1°
ride in tissues is suggested by a shift in the
mia syndrome (seep 1027).

iodine absorption spectra of polysaccharide
isolated from the liver and muscle of affected Spine Defects foals. Skeletal muscle total polysaccharide

Skeletal malfonnations include scoliosis
concentrations are reduced, but liver and

(lateral deviation of the back), synostosis
cardiac muscle glycogen concentrations are

(fusion of vertebrae), lordosis ( ventral
normal. Several glycolytic enzyme activities
dorsal deviation of the back), kyphosis
are normal, whereas GBE activity is virtually

(dorsal deviation of the back), torticollis
absent in cardiac and skeletal muscle, as well (twisted neck), and wry nose (twisted nose).

as in liver and peripheral blood cells. GBE

Although all of these conditions are
activities in peripheral blood cells of dams of
uncommon in foals, congenital scoliosis is
affected foals and several of their half-sibencountered most frequently. On clinical lings or full siblings are -500Ai of controls.

exanlination, it is often difficult to assess

GBE protein in liver is markedly reduced to
the severity. A better appreciation of the
absent in affected foals. Pedigree analysis
condition can be obtained by radiographic
supports an autosomal recessive mode of
exanlination. In mild cases, improvement is
inheritance.

spontaneous and may be complete. Even in
the more severe cases, there is rarely any

Hernias
obvious abnormality in gait or maneuverability. However, these foals frequently are Hernias are defects in the muscle wall that
not raised because they appear unlikely to
pennit intestines/organs to move into an
be able to withstand being ridden or worked.

abnormal location. An umbilical hernia is

Anotller occasional congenital deformity is
the incomplete closure of the abdominal
tllat of synostosis (fusion of vertebrae), which
wall at the umbilicus. Larger umbilical
may be associated with secondaiy scoliosis.

hernias should be surgically repaired to

Radiography is necessary for confim1ation.

prevent incarceration of bowel. A congeni

Congenital lordosis (swayback) is
tal diaphragmatic hernia is an opening in the associated with hypoplasia of the interverthoracic diaphragm, permitting the tebral articular processes. In adult horses,
displacement of abdominal organs into the
degrees of acquired lordosis and kyphosis
thorax. These hernias usually go undetected (roachback) are occasionally seen, which until the horse is presented for GI signs
contribute to back weakness. Diagnosis is

(colic) rather than respiratory issues.

based on the clinical appearance and can be

Inguinal hernias are commonly seen in
con.finned by radiography, which reveals an
certain breeds, particularly Standardbred
undue curvature of the vertebral column,
and draft horses. They are most common in
usually in the cranial thoracic region
male foals, and a large scrotal sac is seen.

(T5--10) in lordosis and in tlle cranial lumbar

Affected horses rarely present with signs of
region (Ll-3) in kyphosis.

colic. The hernia should be reduced on a

Other, less common skeletal malformadaily basis, and most cases will resolve in tions include incomplete closures of the bony

4-6 mo. In cases presented with signs of
spinal canal ( cervical meningomyelocele,
colic or when there is edema in the inguinal/
spina bifida) and hydrocephalus ( abnormal
ventral area (ruptured hernia), surgical
accumulation offluid in the cranial vault with
repair is advised.

resultant enlargement of the head).

1048

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM

Tying-up Syndrome
grain and sweet feed completely and

(Equine rhabdomyolysis syndrome, Exertional
feeding fats such as rice bran or vegetable
rhabdomyolysis, Myoglobinuria)

oils stabilizes blood sugar and provides fat
for energy metabolism. It is essential tl1at

See also p 1178. Tying-up syndrome in
horses witl1 PSSM be turned out as much

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Thoroughbreds is an inherited abnormality
as possible and exercised often, even if
in the way calcium is regulated by
only for 10 min/day. Horses witl1 mild to
membrane systems in the skeletal muscle.

moderate clinical signs might be able to

The narrow genetic origin of Thoroughreturn to full athletic pe1formance with breds and the common lineage of the
cai·eful dietat)' and management changes,
pedigrees of horses with tying-up would
which include regular daily exercise
support the possibility of an inherited trait.

without extended periods of inactivity.

The disease might lie dorn1ant unless

Breeding horses witl1 PSSM has at least
specific factors trigger the calcium
a 500A, chance of passing the trait on to
regulatory system to malfunction. Initiating
offspring.

events include stress, excitement, lameness,
high-grain diets, and exercise at submaximal speeds.

SHEEP

A different form of tying-up is polysaccharide storage myopathy (PSSM). It is characterized by the accumulation of

Spider Lamb Syndrome
glycogen polysaccharides in skeletal

Hereditat)' chondrodysplasia, or spider
muscle. The recent identification of a
lamb syndrome, is an inherited, semilethal,
genetic mutation for PSSM revealed that
musculoskeletal disease affecting lambs
there are actually no less than two forms of
primarily of Suffolk or Hampshire breeds.

this disease. A form of PSSM called type l

Because the syndrome is a recessive

PSSM is caused by a mutation in the
genetic disorder, a lan1b is afflicted only if
glycogen synthase gene. Type l PSSM
both parents pass on the mutation. Thus, it
occurs in many Quarter horses and related
is critical. to identify carriers, which are
breeds, draft breeds, some Wam1blood
structw-al.ly normal anin1als with only one
breeds, and several other breeds. It has not
copy of the mutation. The location of the
been identified in Thoroughbreds to date.

locus causing spider lamb syndrome is

This mutation causes the muscle to
along the distal end of ovine chromosome
continually make glycogen. Consequently,

6. This mutation causes an inactivation of
when beginning exercise, horses have
normal fibroblast growth factor receptor 3,
trouble switching over to bum glycogen for
which produces skeletal. overgrowth in
energy ratl1er than storing glycogen in their
animals homozygous for the gene. La.tubs
muscles. Affected horses.develop stiffness,
have pronounced medial deviation of the
muscle cramping, and soreness with light
carpus and hock and are unable to stand
exercise probably due to a deficit of energy
without distress. Pathologic changes in
generation in tl1eir muscles. Some horses
the skull reveal a rounding of the dorsal
witl1 this disorder also have an increased
silhouette, producing a "Roman nose"

sensitivity to insulin, further increasing
appeara.11ce and a narrowed elongation of
storage of glycogen in the muscle. PSSM
the occipital. condyles. The thoracic and
type l horses are often calm, sedate horses
lwnbar vertebrae are moderately kyphotic,
that tie-up after a lay-up, especially when
which causes a dorsal rounding of the
fed grain. They tend to be found in
backline. The stemebrae are dorsally
disciplines such as halter and pleasw-e
deviated, leading to a flattening of the
horse perforn1ance and do not usually
sternum. The forelimbs have a medial
perfonn well at speed.

deviation of the carpal joints with a bowed

Type 2 PSSM has a slightly different
radius and ulna and irregular tl1ickening of
microscopic appearance, and the genetic
the growth plate cartilage. The hindlimbs
cause is yet unknown. It occurs in Quaiter
have medially deviated hocks and bowed
horse-related breeds, Warmbloods, and
tibiae, which also have thickened, irregular
likely other light horse breeds, possibly
growth plates. Muscle atrophy is also
including Thoroughbreds. Whereas type l
predominant. The regulation of liver

PSSM can be diagnosed by a DNA-based
insulin-like growth factor (IGF) and
blood or hair root test, type 2 PSSM requires IGF-binding proteins may be involved exainination of a muscle biopsy. Treatment
in the physical manifestations of this
of both forms of PSSM involves supplying
disorder. It is suggested that the condition
horses with an alternative sow-ce of energy
is inherited in a simple autosomal recessive
such as fat ratl1er than sugai·. Eliminating
pattern.

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM

1049

PIGS
stress-sensitivity of the heavily muscled
pa.rent(s) may be a contributing factor.

However, any cause of stretching of the

Splayleg
adductor muscles increases the incidence.

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(Spraddleleg, Myofibrillar hypoplasia)

Stretching can result from slippery or

In splayleg, a condition of neonatal pigs,
sloping floors, struggling while legs are
caught in cracks in the floor, or as tl1e result
the hindlegs are spread apart or extended
of damage to nerve pathways from
forward because of weakness of the
intrauterine viral infections .. Mycotoxins
adductor muscles relative to the abductors.

have been suggested to play a role in some

The condition is seen at or soon after birth
cases. The general nutrition of the sow
and can present in a number of forms. In the

"stars" form, both sets of limbs are splayed ( choline, methionine, and vitan1in E levels)

may influence the incidence, but benefits
out sideways, such that the pig cannot stand
from feeding supplements to sows is
and can move about only by crawling or
questionable.

shuffling. The most common fom1 of the

The clinical signs are distinctive. In utero
condition is hindleg splays; the back legs
infections with hemaggluti.nati.ng encephalisplay out sideways and forward, causing the tis virus, enteroviruses, other viluses, and
pig great difficulty in standing on its hind
postpartwn bacterial meningeal infection
end. Many will "dog sit" and shuffle around and trauma should be considered. The
on their backsides. This can lead to
affected muscles are generally hypoplastic,
considerable skin trauma and secondary
infection. Front leg splays also occur. The
and the small muscle fibers contain few
myofibrils, as would be found in muscles
hindlin1bs work nom1ally, but the front legs
of normal fetuses nearing parturition.

splay out sideways such that the pig moves

Frequently affected muscles include the
around with its chin on the ground. Such
pigs have great difficulty nursing, and
semitendinosus, longissimus dorsi, and
triceps.

mortality levels are high. The incidence of

Dry, nonslippery floors should be
splayleg is greater in the Landrace than in
provided, with no cracks in which the legs
other breeds.

can become trapped, especially for the first

Histologically, there is a continuous

2 days. Pigs should be protected from ir\jury
gradation in myofibrillar content between
by the sow, and adequate suckling should be
normal and severely affected muscles.

ensured. In affected piglets, the hindlegs

Myofibrils in affected fibers are scanty and
should be secured together above the hocks
small in cross section. No other morphowith a loose "figure 8" of adhesive tape for logic or histochemical abnom1alities have

2-4 days. Appropriately treated pigs usually
been detected. The cause of the condition
recover within a week, although few
remains obscure. Newborn piglets of hybrid
recover if the front legs are also affected.

stock tested for defects of neuromuscular

Glucocorticoids should not be administered
transmission by stimulation electromyography reveal that congenital myofibrilla.r late in gestation. Highly susceptible blood
lines should be eliminated.

hypoplasia is not prin1arily a myasthenialike syndrome, but that either excitationcontraction coupling or the contractile SMALL ANIMALS
mechanism itself is primarily affected.

Selection for increased litter size
indirectly increases the genetic potential for

Apodia
sows to create a uterine environment more

Few reports of apodia have appeared in the
likely to produce litters with splayleg pigs
literature. It is likely that this condition
and should be treated as a trait of the sow,
occurs more frequently tllan is docun1ented,
rather than of the individual pig. Affected
but affected animals probably eitl1er die, are
pigs a.re susceptible to overlaying,
euthanized by breeders without being
starvation, and chilling because of poor
brought to a veterinarian, or are just not
mobility. Mortality may reach 500A,. Genetic
reported. Congenital absence of tile forearm
influence has been demonstrated. There
or hand is a relatively common abnormality
are significant differences in the incidence
in people. Most defects are transverse
among litters of different sires and breeds.

(an1elia) and unilateral. Lower limb

It is seen more frequently in males than
deformities are less common and also
females and in pigs of lower birth weight.

usually unilateral. No fanlilial tendencies

The syndrome also may be produced if
have been seen, and intrauterine an1putaglucocorticoids are administered during tion by anmiotic bands is thought to be a
pregnancy, and it appears possible that
common cause of amelia. Longitudinal limb

1050

CONGENITAL AND INHERITED ANOMALIES OF THE MUSCULOSKELETAL SYSTEM
deficiency, or hemimelia, probably results
fusion. No breed or sex predilection has
from defective development of the
been noted. Studies of this defect in cats
embryonic limb bud.

indicate that it is inherited as an autosomal

Few cases of hemimelia in dogs and
dominant with variable expressivity.

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cats have been reported. Radial agenesis
appears to be the most common of these

Polydactyly
defects. Affected animals have medially
directed angular defom1ities of the affected

In dogs and cats, preaxial polydactyly is by
limbs. There may be complete or partial
far the more common fom1 (an additional
agenesis of either one or both radii with a
digit or digits on the medial side of the paw).

compensatory increase in the diameter of

In cats, it is inherited as an autosomal
the ulna. Tibial agenesis is less common.

dominant trait with variable expressivity. A

The fibulae are markedly enlarged in
similar inheritance pattern appears to apply
affected animals.

to the occurrence of multiple dewclaws in
dogs, as is seen in Great Pyrenees. Lateral
polydactylism occurs less frequently. There

Ectrodactyly Syndrome
is no apparent clinical significance to these

Maldevelopment of the central rays of the
conditions, other than an increased
lin1bs may produce longitudinal splitting of
propensity for trawnatic injury of the partial
the extremities. Split hand or foot may be
supemwnerary digits.

sporadic, but autosomal dominant and
recessive forms of this condition, some

Syndactyty
tin1es tenned the "lobster claw" defect, have Syndactyly involves bony and/or soft tissue
been described. The defect also occurs as
union of two or more digits, with varying
part of several syndromes. Splitting is most
degrees of involvement. Few cases of
common between the first and second metasyndactyly in dogs and cats have been carpals, although all variations have been
reported. Because few clinical problems
seen. Other abnormalities associated with
are associated with the malfonnation,
this defect include digit contractures, digit
tl1is syndrome is probably more common
aplasia, and metacarpal hypoplasia and
than reported.

DYSTROPHIES ASSOCIAT ED WITH

CALCIUM, PHOSPHORUS, AND VITAMIN D

The principal causes of osteodystrophies
acts primarily on the GI tract to increase
are deficiencies or imbalances of dietary
absorption but also affects the bone,
calciwn, phosphorus, and vitan1in D, as well
thereby increasing availability of elemental
as dysregulation of parathyroid hormone
calciwn. Through a negative feedback loop,

(PTH) activity. Their interrelationships are
it also contributes to the regulation of PTH
complex and not easily defined.

secretion.

The primary source of calciwn and

PTH secretion occurs in response to a
phosphorns is the diet. These elements are
low circulating calcium ion concentration
absorbed in amounts depending on the
and depends on the availability of magnesource of the minerals, intestinal pH, siwn. The target organs of PTH are the
and dietary levels of vitamin D, calciwn,
kidneys, bones, and intestines. In the
phosphorus, iron, and fat. If vitamin D or its
kidneys, PTH promotes renal tubular
activity is decreased, calciwn and phosphoabsorption of calciwn while enhancing the rus absorption are reduced. Vitamin D is
renal excretion of phosphorus, as well as
obtained either furough the diet or by
the activity of lcx-hyclroxylase, the enzyn1e
production when the skin is exposed to
responsible for activation of vitan1in D3 in
swilight (ultraviolet radiation). Before
the kidney. In the intestine, PTH promotes
vitan1in D can be used, it must be processed
absorption of calciwn. PTH also facilitates
into its metabolically active fom1 in two
mobilization of calcim11 and phosphorus
consecutive hydroxylation steps by the liver
from bone by allowing utilization of calciwn
and kidney. Vitamin D3 ( cholecalciferol)

from the osteoid matrix. In ruminants, PTH

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D

1051
increases the salivary excretion of
develop locomotor disturbances within
phosphorus in exchange for bicarbonate.

4 wk, even though the high content of

Specific bony lesions are associated with
digestible protein (>500/o on a weight basis)

abnonnalities in absolute or relative
and fat promotes rapid growth, the animals
amounts of vitamin D, calcium, phosphorus,
appear well nourished, and their coat

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and PTH. Often, in addition to the deficiency
maintains a good luster. The predominant
or excess in one element, this also causes a
clinical signs are reluctance to move,
secondary pathology due to feedback
posterior lameness, and ataxia. The kittens
mechanisms, altered ratios, or concomitant
often stand with characteristic deviation of
metabolic deficiencies. Specific disease
the paws. The skeletal disease becomes
syndromes can be classified as nutritional,
progressively more severe after 5 -14 wk.

metabolic, or genetic in nature. Classic

The kittens become quiet and reluctant to
exan1ples of nutritional osteodystrophics
play; they assume a sitting position or
are rickets, osteomalacia, enzootic
sternal recumbency with the hindlin1bs
calcinosis, or hypervitaminosis D. Fibrous
abducted. Nonnal activities may result in
osteodystrophy and hyperparathyroidism
the sudden onset of severe lameness due
are common metabolic osteodystrophies.

to incomplete or folding fractures of one

Genetic osteodystrophies can be caused by
or more bones. Lameness is the initial
defects in phosphate transporters or genetic
functional disturbance in growing dogs and
abnonnalities in the hormonal regulation of
may vary from a slight limp to inability to
phosphorus homeostasis. Examples of
walk. The bones are painful on palpation,
genetic defects associated with osteodystroand folding fractures of long bones and phies include X-linked hypophosphatemia
vertebrae are common.

and hereditary hypophosphatemic rickets.

Swine kept in confined housing are
susceptible to rickets because of their rapid
growth rate combined with lack of exposure
to sunlight. Fwthennore, diets for market
swine are fom1ulated to maximize growth
of lean muscle mass with little consideration of requirements for bone fom1ation.

RICKETS

Diets with excessive amounts of calcium

(three times normal concentrations) have

Rickets is a disease of the bony growth
caused rickets-like signs in growing Great
plate and thus only affects young, growing

Danes. Several other bone pathologies such
animals. The most common causes are
as retained cartilaginous cores, osteochondietary insufficiencies of phosphorus or drosis, and stunted growth were seen in
vitamin D. Calcium deficiencies can also
these dogs as well.

cause rickets, and while this rarely occurs
naturally, poorly balanced diets deficient in
calciwn have been said to cause the disease.

Diagnosis: Typical microscopic lesions

As in most diets causing osteodystrophies,
associated with rickets are in1paired
the abnom1al calcium:phosphorus ratio is
endochondral ossification, which are most
most likely the cause.

prominent in fast-growing bones. Growth
plates are widened and irregular, and joints

Clinical Findings and Lesions: The
appear enlarged. Trabecula of the spongiosa
characteristic lesions of rickets are failure of are thinner, predisposing to infarctions and both vascular invasion and mineralization in
hemorrhage. Radiographic examination of
the area of provisional calcification of the
large bones and joints is the most reliable
physis. This pathology is most obvious in the in vivo diagnostic tool for rickets. The metaphyses of the long bones. There may be
radiopacity of rachitic bones is charactera wide variety of clinical signs, including istically less than that of nom1al bone.

bone pain, stiff gait, swelling in the area of

Growth plates appear widened and
the metaphyses, difficulty in rising, bowed
irregular.

limbs, and pathologic fractures. On radio

Plasma alkaline phosphatase activity is
graphic examination, the width of the
conunonly increased. Concentrations of
physes is increased, the nonmineralized
senun phosphorus and vitamin D may be
physeal area is distorted, and the bone may
altered depending on the primary cause of
show decreased radiopacity. In advanced
rickets. In cases associated with phosphocases, angular limb deformity can be seen rus or vitanlin D deficiencies, concentradue to asynchronous bone growth.

tions of these compounds in serum are

Animals fed all-meat diets are conunonly
subnom1al. Hypocalcemia is seen in
affected. Kittens fed beef heart exclusively
advanced stages.

1052

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D

Treatment: Correction of the diet is
the most conunon clinical findings. Pica
the primary treatment for rickets. The
may predispose affected animals to esophaprognosis is good in the absence of geal obstruction, reticuloperitonitis,
pathologic fractures or irreversible damage
botulism, or other intoxications.

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to the physes. lf the animals are housed,
exposure to sunlight ( ultraviolet radiation)

Diagnosis: To establish a firm diagnosis of
will also increase production of vitamin 0
osteomalacia, the diet should be evaluated

3
precursors.

for calcium, phosphorus, and vitanlin D con

Many homemade diets for dogs are
tent. There is radiographic evidence of
deficient in minerals and have altered
generalized skeletal demineralization, loss
calcium:phosphorus ratios. Therefore,
of lamina dura dentes, subperiosteal
a high-quality commercial food, or one
cortical bone resorption, bowing deformidesigned by a credentialed veterinary ties, and multiple folding fractures of long
nutritionist, is reconu:nended.

bones due to intense localized osteoclast
proliferation. Levels of hydroxyproline, an

OSTEOMALACIA
anlino acid released into blood during bone
mineralization, can be detemlined to assess

(Adult rickets)

the extent of ongoing bone mobilization. If
dietary calcium and phosphorus content

Osteomalacia has a pathogenesis similar to
cannot readily be determined ( eg, in grazing
that of rickets but is seen in mature bones
animals), soil or fecal samples can be
and associated with disruption of nonnal
analyzed as crude proxies for dietary
bone remodeling. Because bones mature
at different rates, both rickets and osteointake of these minerals.

Laboratory values used to assess renal
malacia can be seen in the same animal.

function should be within normal limits in

Osteomalacia is characterized by an
animals with nutritional osteodystrophy.

accumulation of excessive unmineralized
osteoid on trabecular surfaces.

Treatment: Animals with osteomalacia

Clinical Findings: Animals with osteoshould be confined for several weeks after malacia are unthrifty and may exhibit
initiation of the supplemental diet.

pica. Nonspecific shifting lamenesses are

Response to therapy is rapid; within 1 wk
common. Fractures can be seen, especially
the animals become more active, and their
attitude improves. Jumping or climbing
in the ribs, pelvis, and long bones. Spinal
defonnation such as lordosis or kyphosis
must be prevented, because the skeleton is
still susceptible to fractures. Restrictions
may be seen.

can be lessened after 3 wk, but confinement

In horses, nutritional osteodystrophy is
known as bran disease, miller's disease,
with limited movement is indicated until the
skeleton returns to nonnal (response to
and "big head." The diet of pampered treatment should be monitored radiographihorses is often too high in grains and low in forage; such a diet is high in phosphorus
cally ). Complete recovery can be achieved
within months in anin1als with no or only
and low in calciun1. Many 6f the obscure
lamenesses of horses have been attributed
minor limb and joint deformities.

to nutritional osteodystrophy. The
pathologic changes are similar to those in

ENZOOTIC CALCINOSIS
other species, with the provisos that the
bones of the head are particularly affected

(Enteque seco, Enteque ossificans,
in severe cases and that gross or micro

Espichamento, Espichacao, Manchester
scopic fractures of subchondral bone ( with
wasting disease, Naalehu disease,
consequent degeneration of articular

Weidekrankheit)

cartilage and tearing of ligan1ents from

Enzootic calcinosis is a disease complex
periosteal attachments) are dominant
of run1inants and horses caused by plant
clinical signs. Unilateral facial deformity
poisoning or mineral imbalances and
due to secondary (nutritional) hypoparathycharacterized by extensive calcification of roidism has been reported in a 1-yr-old filly.

soft tissues. The prevalence of the disease in

Nutritional osteodystrophy can occur in
cattle varies widely (100/o-500/o) in areas of
cattle grazing on arid, infertile soils deficient Argentina, Brazil, Papua-New Guinea, in phosphorus if they are not given adequate Jamaica, Hawaii, and Bavaria. It is said to mineral supplementation. Affected animals
cause up to 600/o mortality and affect 17% of
are unthrifty and have a rough hair coat.

the sheep in southern Brazil and Mattewara

Weight loss, shifting lin1b lameness, limb

(India), respectively. Incidence elsewhere
defom1ities, and spontaneous fractures are

(Australia, Israel, South Africa, and

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D

1053
southern USA) is less well documented, and
affected, and some anin1als even walk
in many areas enzootic calcinosis is rare or
or graze on their knees. The distal joints
nonexistent.

become abnormally straight. When affected

Etiology and Pathogenesis: Known
animals are forced to walk, their gait is

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causes of enzootic calcinosis fall into two
awkward, stiff, and slow, and their steps are
categories: plant poisonings and mineral
short. After walking only short distances,
imbalances in the soil, the first probably
breathing becomes shallow and diaphragbeing the more in1portant. Cestrum matic, the nostrils are flared, and the head
diurnum (wildjasmine, day-blooming
and neck are extended. Tachycardia is a
jessamine, king-of-the-day), 'I'risetum
common finding, and heart murmurs may be
jl.avescens (golden oats or yellow oat grass), audible on auscultation. Jugular venous Nierembergia veitchii, Solanum esuriate,
pulse is prominent in some cases.

S torvum, and S malacoxylon contain As the disease progresses, U1e animal

1,25-dihydroxycholecalciferol ( calcitriol)

loses weight and becomes weak, listless,
glycoside or a substance that mimics its
reluctant to stand, or even recumbent. The
calcinogenic action. Studies indicate that
coat becomes shaggy, dull, and faded,

S malaco:x:ylon has the required enzyme
particularly in cattle. There is wasting of
systems for synthesis of calcitriol from
muscles, a prominent skeleton, tucked up
vitanlin D
abdomen, kyphosis, and raised tailhead.

3.

The imbalance of minerals in certain

Appetite is usually unimpaired but
soils, as well as at higher altitude ( up to
sometimes becomes depraved. Calcification

1,500 m above sea level), have been thought
of vessels is sometimes palpable on rectal
to be the main etiologic factors; higher
examination.

altitude is considered to favor the growth of

Osteodystrophy is seen in calcinosis due
plants like golden oats at the expense of
to T jl.avescens and C d'iurnum toxicities other plants less suited for this location.

in Bavarian cattle and Florida horses,

Osteodystrophy of bulls after prolonged
respectively. Severely affected horses stand
intake of excessive calcium is a sinlilar
with forelimbs somewhat abducted and
condition; calcification of the cardiovasculuxated caudally at the shoulder joints. The lar system associated with aging and such
flexor tendons, particularly the suspensory
cachectic diseases as tuberculosis is not
ligaments, are painful. Fetlock joints are
identical. Excessive vitamin D
overextended to varying degrees.

3 and normal
or excessive calcium intake induces aortic

Lesions: Degeneration and calcification
calcification and atherosclerosis in
of soft tissues are seen, with emaciation
runlinants.

and varying an1ounts of excess fluid in the

Normally, the conversion of25-hydroxythoracic and abdominal cavities and cholecalciferol ( calcifediol) to calcitriol
pericardia! sac. The cardiovascular'system
in the kidneys is controlled by a feedback
is the fu-st to be involved, followed by lung,
mechanism. The calcitriol-like factor in the
kidney, and tendons. The heart and aorta
leaves of plants bypasses this mechanism,
show the most pronounced abnormalities.

and more calcium is absorbed than can be

The left side of the heart is more affected
accommodated physiologically. Hypercalthan the right. Calcification of the bicuspid cemia promotes calcitonin production,
valves results in valve insufficiency and
calcinosis, and osteoporosis.

systolic heart murmurs. White, elevated

Changes in plasma calcium, phosphorus,
plaques of irregular size and shape are seen
and magnesiwn are different in different
on the luminal surface; in advanced cases,
species. Horses develop hyperphosphathese are seen throughout the length of the temia; plasma calcium remains nom1al
aorta and its main branches. Mineral
but rises with excess doses of calcitriol. In
deposits are found on the pleura, on the
cattle and small ruminants, high serun1
surface and edges of the diaphragmatic
inorganic phosphorus with increased or
and apical lobes of lungs, in the renal
normal serum calcium concentrations have
artery and pelvis of the kidney, and on the
been reported in animals with enzootic
ligaments and tendons (particularly of the
calcinosis.

forelimbs). Capsular thickening and
irregular erosions of articular surface of

Clinical Findings: Enzootic calcinosis is
cartilage and joints are seen, especially
progressive and chronic, extending for
of the carpus and hock.

weeks or months. The earliest signs are

The basic histologic evidence is necrosis
stiffness and shifting limb lameness, most
and calcification of connective tissue,
pronounced when the aninlal rises after
followed by cellular proliferation in the
prolonged rest. Forelimbs are particularly
affected area.

1054

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D

Diagnosis: Diagnosis of enzootic
breathing, and lan1eness, followed by
calcinosis is usually based on the history,
weakness, recumbency, and even death can
combined with clinical signs such as
be seen in anin1als with vitanlin D3 toxicosis.

emaciation, lameness, and listlessness, as

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well as cardiac and respiratory abnonnali

Lesions: Lesions are consistent with
ties, but may be difficult at early stages.

soft-tissue calcification described under

Abnonnal serw11 calcium, phosphorus, and
enzootic calcinosis (seep 1053).

magnesium concentrations and increased
activity of alkaline phosphatase in

Diagnosis: Diagnosis of vitan1in D3
combination with the presence of plants
toxicity is usually based on a history of
with calcinogenic action in the feed or on
repeated vitamin D3 injections in combinapastw·e are further clues.

tion with the clinical signs mentioned

Imaging techniques such as radiography
above.

and ultrasonography can be used to
visualize soft-tissue calcification.

Treatment and Control: No practical
treatment for vitamin D3 toxicity is currently
available. Education of producers

Treatment and Control: No practical
treatment reversing soft-tissue calcification
concerning the risks and toxic dose of
is currently available. Removal of the causal
parenteraJJy administered vitamin D3 will
factor(s) is essential, but when the disease
help avoid accidental overdoses.

is associated with the mineral content of the
soil, control may be difficult. Change of
pasture, forage, and environment may effect
clinical improvement. Careful pasture
management to limit the density of
calcinogenic plants can effectively reduce
the disease prevalence. Feeding oat grass

FIBROUS OSTEODYSTROPHY
hay cut after blooming rather than having
anin1als graze on oat grass pasture may

(Rubber jaw syndrome)

reduce the problem, because calcinogenicity of the plant decreases with maturity and Primary Hyperparathyroidism
with drying. Experinlentally, daily

In prinlary hyperparathyroidism (seep 564), administration of 15 g of aluminum
there is excess production of parathyroid
hydroxide, PO, prevented the development
honnone (PTH) by an autonomous
of calcinosis in sheep fed T jlavescens.

functional lesion in the parathyroid gland.

The nom1al control mechanisms for PI'H

VITAMIN D
secretion by the concentration of blood

3 TOXICITY
calcium are lost, and the parathyroid

IatrogenicaJJy induced calcinosis, in tl1e
produces excess PTH despite increased
form of vitamin D3 toxicity, is a condition
levels of blood calciwn. This disease is
occasionaJJy reported in cattle that is very
encountered infrequently in older dogs, and
sinlilar to enzootic calcinosis. Parenteral
it does not appear to be a sequela of renal
administration of vitamin 03 10-14 days
secondary hyperparathyroidism (seep 1056).

before the predicted calving date is

PTH acts on cells of the renal tubules
considered an effective strategy to prevent
initially to promote the excretion of
periparturient hypocalcemia (milk fever) in
phosphorus and retention of calcium. A
dairy cows. Because of the narrow margin
prolonged increased secretion of PTH
between therapeutic and toxic doses,
results in accelerated osteocytic and
vitamin D3 toxicity can occur either after a
osteoclastic bone resorption. Mineral is
single overdose or after repeated tl1erapeuremoved from tl1e skeleton and replaced by tic doses injected at short intervals.

inunature fibrous connective tissue. Fibrous

Commonly, toxicity is due to the repeated
osteodystrophy is generalized throughout
injection of therapeutic doses in cows that
the skeleton but is accentuated in local
did not calve within 2 wk of the initial
areas such as the cancellous bone of the
treatment and thus are considered at
skull. The increased PTH levels also inhibit
increased risk of developing periparturient
the renal tubular resorption of phosphorus.

hypocalcemia.

The lesion in the parathyroid gland in
dogs is usuaJJy an adenoma, occasionaJJy a

Clinical Findings: Animals with vitanlin 03 carcinoma, composed of active chief cells.

intoxication become anorectic, lose weight,

Usually, adenomas are single, light
and develop acetonemia within 2-3 wk after
brown-red, and located in the cervical
the overdose. Tachycardia, shallow
region near the thyroid gland.

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D

1055

Clinical Findings: In primary hyperparasensitive radioimmunoassays or immunothyroidism, lameness follows severe radiometric assays.

osteoclastic bone resorption, and fractures

The intact PTH assay or dual-site assays
oflong bones occur after minor physical
can be perfom1ed using either serum

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trauma. Compression fractures of

(preferred) or plasma that has been
weakened vettebral bodies may exert
separated and frozen ( -70°C [-94°FJ in
pressure on the spinal cord and nerves,
either glass or plastic tubes) as soon as
resulting in motor and sensory dysfunction.

possible after collection. Using this method,

Facial hyperostosis with partial
circulating levels of PTB in most animals
obliteration of the nasal cavity (by poorly
are near 20 pglmL ( dogs, 20 ± 5 pglmL; cats, mineralized woven bone and highly

17 ± 2 pglmL), with levels in nonhuman
vascular fibrous connective tissue) and loss
primates being slightly lower (normal
or loosening of teeth has been seen in dogs.

values also vary an10ng laboratories). PTH

This may result in an inability to close the
assays that use antibody generated against
mouth properly and development of
the carboxy terminal end of the human
gingival ulcers. The maxillae and ran1i of the
molecule usually give Jess consistent results
mandibles often are coarsely thickened by
in animals other than people.

the excess woven bone. Bones of the skull

Differential diagnoses include other
are markeclly thinned by the increased
causes ofhypercalcemia, such as vitamin D
resorption and have a characteristic
intoxication ( overdosage ), enzootic

"moth-eaten" appearance radiographically.

calcinosis (seep 1052), malignant neo

In advanced cases, the mandible can be
plasms witl1 osseous metastasis, and
twisted gently due to loss of osteoid and
hum oral hypercalcemia of malignancy (see
severe fibrous osteodystrophy-hence the
p 563). The hypercalcemia ofhypervitaname "rubber jaw" syndrome.

minosis D may be as high as that in prinmry
hyperparathyroidism but is accompanied

Lesions: Histologic demonstration of
a 1irn of normal tissue and a partial to
by varying degrees ofhyperphosphatemia
complete fibrous capsule in an enlarged
and normal serum alkaline phosphatase
parathyroid suggests an adenoma rather
activity. Skeletal disease usually is absent,
than focal hyperplasia. Chief-cell carcinobecause the increased concentrations of mas tend to be larger than adenomas and
blood calcium and phosphorus are de1ived
fixed to the underlying tissues ct ue to local
principally from augmented intestinal
infiltration of neoplastic cells.

absorption rather than from bone
resorption.

Malignant neoplasms with osseous

Diagnosis: Although other laboratory
metastases may cause moderate hypercalfindings may be variable when diagnosing cemia and hypercalciuria, but the alkaline
primary hyperparathyroidism, hypercalcephosphatase activity and serum phosphorus mia is consistent and results from accelerlevel usually are normal or only slightly ated release of calcium from bone. The blood increased. These changes are believed to be calcium in healthy dogs is -10 ± 1 mgld.L,
due to the release of calciun1 and phosphodepending on age and diet ( and assay rus into tl1e blood from areas of bone
method). Senun calcium values consistently
destruction at rates greater than can be

> 12 mgld.L indicate hypercalcernia. Dogs
cleared by the kidneys and intestine. Bone
with primary hyperparathyroidism usually
involvement is more sharply demarcated
have a serwn calcium of �12-20 mgld.L. The
and localized to the area of metastasis.

blood phosphorus is low or in the low-nonnal Osteolysis associated with tun10r metastarange (s4mgld.L). The urinary excretion ses results not only from a physical
of phosphorus, and often of calcium, is
disruption of bone by proliferating
increased and may result in nephrocalcinoneoplastic cells but also from local sis and urolithiasis. Accelerated bone
production of humoral substances that
matrix metabolism is reflected by
stimulate bone resorption, such as
increased urinary excretion of hydroxyproprostaglandins and interleukin-I.

line. Serwn alkaline phosphatase activity

Primary parathyroid hyperplasia has been
may be increased in animals with overt
described in Gem1an Shepherd pups. The
bone disease. Demonstration of increased
condition was associated with hypercalcelevels of PTH by a species-specific assay in mia, hypophosphaternia, increased
an adult to aged dog with hypercalcemia,
immunoreactive PTH, and increased
hypophosphatemia, and evidence of
fractional clearance of inorganic phosphogeneralized bone disease provides rus in the urine. Clinical signs include
conclusive evidence ofpri.mary hyperstunted growth, wealcness, polyuria, parathyroidism. PTH can be measured by
polydipsia, and a diffuse reduction in bone

1056

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D
density. IV infusion of calcium fails to
surgery, or recurs after initial in1provement,
suppress the autonomous secretion of PTH
a second adenoma or metastases from a
by the diffuse hyperplasia of chief cells in all carcinoma should be suspected.

parathyroids. Lesions include nodular

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hyperplasia of thyroid C cells and widespread mineralization of the lungs, kidneys, Renal Secondary
and gastric mucosa. The disease is inhe1ited

Hyperparathyroidism
as an autosomal recessive.

Renal secondary hyperparathyroidism

Hypercalcemia also may be associated
is a complication of chronic renal failure
with multifocal osteolytic lesions associcharacterized by increased endogenous ated with septic emboli, complete
levels of parathyroid ho1mone (PTH). lt is
immobilization, osteosarcoma, hypoadrenomore common than primary hyperparacorticism (Addison-like disease), hypocalcitl1yroidisrn. In contrast to primary hypertoninism due to a destructive thyroid lesion, parathyroidism, renal secondary
chronic renal disease, hemoconcentration,
hyperparathyroidism tends not to be
or hyperproteinemia. Hypercalcemia is
autonomous. It is seen frequently in dogs,
detected occasionally in dehydrated
occasionally in cats, and rarely in other
animals but usually is mild. It is attributed
species.

to fluid volun1e contraction that results in

With progressive renal disease, serum
hyperproteinemia and increased concentrahyperphosphatemia develops as the tions of ionized and nonionized calcium; it
glomerula.r filtration rate decreases.

resolves rapidly after fluid therapy.

Hyperphosphatemia leads to lower serum
concentration of ionized calcimn. Renal

Treatment: The objective in treating
synthesis of calcitriol is also reduced.

primary hyperparathyroidism is to eliminate Calcitriol nonnally acts on the intestine and the source of excessive PTH production. An
kidneys to maintain normal calcium levels.

attempt should be made to identify all four

Decreased ionized calcimn and calcitriol
parathyroid glands before excising any
concentrations cause an increase in serllln
tissue. Single or multiple adenomas should

PTH concentrations. As glomerular
be removed in toto. If all identifiable
filtration rate decreases with advancing
parathyroids in the cervical region appear
renal disease, PTH concentrations
to be of nonnal or smaller size, and the
progressively increase, leading to the
diagnosis is reasonably certain, surgical
clinical manifestations of renal secondary
exploration of the thorax near the base of
hyperparathyroidism.

the heart may be necessary to localize the
parathyroid neoplasm.

Clinical Findings: The predominant

Removal of the functional parathyroid
signs of renal insufficiency ( eg, vomiting,
lesion results in a rapid decrease in
dehydration, polydipsia, polyuria, and
circulating PTH levels, because the half-life
depression) are usually present. Skeletal
of PTH in plasma is < 15 min. Because
lesions range from minor changes with early
plasma calciun1 levels in <!f!imals with overt

( or mild) renal disease to severe fibrous
bone disease may decrease rapidly and be
osteodystrophy of advanced renal failure.

subnormal within 12-24 hr after surgery,

The volmne of affected bones usually is
they should be monitored frequently.

normal (isostatic), particularly in older dogs

Postoperative hypocalcemia ( ::;6 mg/dL) can
because of the slow onset of renal failure
result from the following: 1) depressed
and lower metabolic activity of bones.

secretory activity of chief cells due to

Hyperostotic bone lesions, such as facial
suppression by the chronic hypercalcemia
swelling, may be seen in younger dogs in
or injury to the remaining parathyroid tissue which deposition of unmineralized osteoid during surgery, 2) abruptly decreased bone
by hyperplastic osteoblasts and production
resorption due to decreased PTH levels, and of fibrous connective tissue exceed the rate 3) accelerated mineralization of osteoid
of bone resorption.

matrix fom1ed by the hyperplastic

Skeletal involvement is generalized but
osteoblasts, which was previously
not unifom1. Lesions become apparent
prevented by the increased PTH levels
earlier and reach a more advanced stage in

(known as "hungry-bone syndrome").

certain areas, such as cancellous bones of

Infusions of calcium gluconate to maintain
the skull. Resorption of alveolar bone
the serum calcium between 7.5 and 9 mg/dL,
occurs early and results in loose teeth,
plus feeding high-calcium diets and
which may be dislodged easily and interfere
supplemental vitanlin D therapy, corrects
with mastication. As a result of accelerated
this serious postoperative complication.

resorption of cancellous bone of the maxilla

If hypercalcemia persists for � 1 wk after
and mandible, bones become softened and

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D

1057
pliable ("rubber jaw" syndrome), and the

Prognosis: If untreated, secondary
jaws fail to close properly. This often results
hyperparathyroidism results in irreversible
in drooling and protrusion of the tongue.

hypertrophy of the pa.rathyrnid glands, a

Severely demineralized mandibles are
condition also known as tertiary hyperpara

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predisposed to fractures and displacement
thyroidism. In this stage, hyperparathyof teeth from alveoli. Long bones are less roidism becomes un.responsive to treatment
dramatically affected. Lameness, stiff gait,
and requires surgical extirpation of the
and fractures after minor trauma may result
hypertrophic parathyroid glands.

from increased bone resorption.

Lesions: All parathyroid glands are
enlarged, initially due to hypertrophy of

HYPOPARATHYROIDISM
chief cells and subsequently by compensatory hyperplasia. Although the parathyroids In hypoparathyrnidism (seep 570), either
are not autonomous, the concentration of
subnormal an1ounts of parathyroid
hom1one (PTH) are secreted, or the

PTH in the peripheral blood often exceeds
that of primary hyperparathyroidism.

hom1one secreted is unable to interact

Changes such as osteoclastosis, marrow
nom1ally with target cells. It has been
fibrosis, and a higher concentration of
recognized p1irnarily in dogs, particularly in
woven osteoid may be seen histologically.

smaller breeds such as Miniature Schnau

Severe hypercalcemia, hyperphosphatemia,
zers, but other breeds may be affected.

and high concentrations of

Various pathogenic mechanisms can

PTH seen in
advanced disease may cause osteosclerosis.

result in inadequate secretion of PTH.

Parathyroid glands may be dan1aged or
inadvertently removed during thyroid

Diagnosis: Renal secondary hyperparsurgery. After daniage to the glands or their athyroidism is diagnosed by laboratory
vascular supply, adequate functional
abnormalities consistent with renal
parenchyn1a often regenerates, and clinical
insufficiency accompanied by an increase in signs subsequently disappear.

serum PTH. Radioirnmunoassay of PTH that Idiopathic hypoparathyroidism in
must be species specific is commercially
adult dogs usually is the result of diffuse
available for most companion aninrnl
lymphocytic parathyroiditis that causes
species and horses. Assays that measure
extensive degeneration of chief cells and
fragments of the PTH molecule should not
replacement by fibrous connective tissue.

be used, because the concentration of

Other possible causes of hypoparathybiologically inactive metabolites of PTH
roidism include destruction of parathyroids
increases with renal failure.

by primary or metastatic neoplasms in the
anterior cervical area, and atrophy of

Treatment: Treatment options for renal
parathyroids associated with chronic
secondary hyperparathyroidism include
hypercalcemia. The presence of numerous
dietary modification, administration of
distemper virus particles in chief cells of the
calcitriol (the bioactive metabolite of
parathyroid gland may contribute to the low
vitamin D3) in combination with oral
blood calcium in certain dogs with this
supplementation of phosphate binders,
disease. Agenesis of the parathyroids is a
and management of the underlying renal
rare cause of congenital hypoparathydisease. Prescription diets with restricted roidism in pups. Certain cases of idiopathic
dietary phosphorus are available. Oral
hypopa.rathyroidism in animals (including
calcitriol (1.5-3.5 ng/kglday) has reversed
people) with histologically nom1al
hyperparathyroidism of chronic renal
parathyroids may be due to lack of the
failure, but calcitriol therapy is contraspecific enzyme in chief cells that converts indicated with hyperphosphatemia or
the pro-PTH molecule to the biologically
hypercalcemia. (Special compounding of
active PTH secreted by the gland. In other
calcitriol is needed, because the dosages
cases, an inunune-mediated mechanism
currently available conunercially are much
may be involved, because a similar
larger than tl1ose needed clinically.) Dietary
destruction of secretory parenchyma and
phosphorus binders are used to decrease
lymphocytic infiltration has been produced
the amount of phosphorus available for
experimentally in dogs by repeated
absorption in the intestines and should be
ir\jections of parathyroid tissue emulsions.

administered with meals. This therapy is

Pseudohypoparathyroidism is a variant
especially important during calcitriol
seen in people, but it is uncertain whether it
supplementation, because calcitriol
is seen in other animals. Target cells in
increases the absorption of phosphorus
kidney and bone are unable to respond to
and calcium.

normal or increased amounts of PTH, and

1058

DYSTROPHIES ASSOCIATED WITH CALCIUM, PHOSPHORUS, AND VITAMIN D
severe hypocalcemia develops even though
hypocalcemia usually is accompanied by
the parathyroid glands are hyperplastic.

hypophosphatemia and a low-normal or
subnormal blood glucose concentration as

Clinical Findings and Lesions: The
a result of the associated intense muscular

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functional disturbances and clinical
activity.

manifestations of hypoparathyroidism
primarily are the result of increased

Treatment: The neuromuscular tetany
neuromuscular excitability and tetany. Bone should be treated initially by restoring resorption is decreased because of the lack
blood calciun1 levels to near normal by IV
of PTH, and blood calciwn levels diminish
administration of calciwn gluconate. One
progressively (4---6 mg/dL). Affected dogs
recommended therapeutic regimen is 10 mL
are restless, nervous, and ataxic, with
of lO"A, calciwn gluconate in 250 mL of
weakness and intem1ittent tremors of

0.9"A, saline administered at 2.5 ml/kg/hr individual muscle groups that progress to
for S-12 hr. Care must be taken not to
generalized tetany and convulsions. Blood
administer the calciun1 too rapidly because
phosphorus levels are increased substanof its cardiotoxic properties. Longtenn tially, owing to increased renal tubular
maintenance of blood calciwn levels in the
reabsorption. Calcification of microvasculaabsence of nom1al PTH secretion should be ture, intracerebral calcification, decreased
attempted by feeding diets high in calciwn
mental function, cataracts, osteopenia, and
and low in phosphorus and that are
ligan1entous ossification have been
supplemented with calciwn (gluconate or
associated with chronic hypoparathylactate) and vitamin 03.

roidism.

Large doses of vitamin 03 (�25,000-50,000

In the early stages of immune-mediated

U/day, depending on the weight of the dog)

lymphocytic parathyroiditis in dogs, there is
may be required initially to increase the
infiltration of the gland with lymphocytes
blood calciwn level in hypoparathyroid
and plasma cells and nodular regenerative
animals, because the lack of PTH din1inhyperplasia of remaining chief cells. Later, ishes the rate of formation of the biologithe parathyroid gland is replaced by cally active vitamin O metabolite in the
lymphocytes, fibroblasts, and capillaries,
kidney. To prevent hypercalcemia and
with only an occasional viable chief cell.

extensive soft-tissue mineralization, the
dosage of vitaniin O should be carefully

Diagnosis: Diagnosis of hypoparathyacljusted after frequent determination of the roidism is based on clinical signs of
serum calciwn level. After acljusting the
increased neuromuscular excitability,
dosage of vitamin 0, a 4- to 5-day interval
severe hypocalcemia, and often moderate
should precede the next blood calciwn
hyperphosphatemia in a nonparturient
determination. Once the blood calciwn level
animal, as well as on the response to
has returned to normal, substantially lower
therapy. Some of the signs ( eg, tetany) and
dosages ofvitaniin Oare indicated for
laboratory data (eg, hypocalcemia) are
longtenn maintenance; in some dogs, only
similar to those of puerperal hypocalcedietaly calciwn supplementation is required mia (seep 992). However, puerperal
for longterm stabilization.

SARCOCYSTOSIS

In sarcocystosis, the endotheliun1 and
centimeters, depending on tl1e host and
muscles and other soft tissues are invaded
species. Most Sarcocystis spp infections
by Apicomplexan protozoans of the genus
are distributed worldwide.

SarcoC'lJStis. As the name implies, Sarcocystis spp (from Greek sarkos: muscle and Etiology, Transmission, and Pathokystis: cysts) form cysts in muscles of genesis: Sarcocystis spp normally
various intem1ediate hosts-people, horses, develop in two-host cycles consisting of an cattle, sheep, goats, pigs, birds, rodents,
intermediate host (prey) and the final host
can1elids, wildlife, and reptiles. The cysts

(predator). Species-specific prey-predator
vary in size from a few micrometers to
life cycles have been demonstrated for

SARCOCYSTOSIS

1059
cattle-dog (S cruzi), cattle-cat (S hirsuta), induced infection with S cruzi sporocysts
cattle-human (S hominis), sheep-dog
from canine feces, which may ca.use acute

(S capracanis, S hirc'icanis), sheep-cat
disease in calves; eosinophilic myositis in

(S gigantea, S medusiformis), goat-dog
cattle; and abortions, stillbirths, and deaths

(S capracanis, S hircicanis), goat-cat
in pregnant cows. Two cases of necrotic

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(S moulei), pig-dog (S meischeriana ), encephalitis in heifers have been reported.

pig-human (S suihominis ), pig-cat

Similar pathogenicity has been demon

(S porcifelis ), horse-dog (S Jayeri), strated for S tenella in lambs and ewes and llama-dog (S aucheniae), pigeon-hawk (S
for S miescheriana in pigs. An outbreak of
calchasi), and others. S sinensis has been myositis affecting 20 ewes with flaccid
detected affecting muscles of buffalo and
paralysis was a result of hea.yy Sarcocystis
cattle, but its final host remains unknown.

infection. In1mune status of the host and the

Some wildlife may serve as intermediate
dose of sporocysts may be the most
hosts (such as raccoons, rodents, birds, etc)

important factors for the development of
or final hosts ( coyotes, opossums, snakes,
clinical disease. Pathologic changes in
etc) for some species of Sarcocystis.

myocardium and skeletal muscles were

About 1-2 wk after ingesting muscle
more pronounced in cows with lymphatic
tissue that contains Sarcocystis cysts
leukemia. "lnu11uniza.tion" using small doses (sarcocysts), the final host begins to shed
of sporocysts appears to prevent developinfective sporocysts in the feces; shedding ment or reduce severity of clinical disease
continues for several months. After
in sheep when challenged with large doses
ingestion of sporocysts by a suitable
later (premunitive inU11unity). In dogs, a
intermediate host, sporozoites a.re liberated
longer prepa.tent period and shortened
and initiate development of schizonts in
patent period resulted after repeated
vascular endothelia of mesenteric arterioles infection. Pigs can also have persistent and mesenteric lymph nodes. Merozoites
acquired inununity after immunization
are liberated from the mature schizonts and
infections.

produce a second generation of endothelial

People may also serve as intem1edia.te
schizonts in capillaries from several organs.

hosts and suffer myositis and vasculitis,

Merozoites from this second generation
but tllis tissue phase is rare, and the source
subsequently invade the muscle fibers and
of such hw11an infection has never been
develop into the typical sarcocysts. Initially,
determined. Hw11an intestinal illness as
sarcocysts contain only a few metrocytesfinal host, with clinical signs of nausea, round, noninfective parasites that give rise
abdominal pain, loss of appetite, vomiting,
to the banana-shaped infective bra.dyzoites
and diarrhea that lasted as long as 48 hr,
found in mature cysts beginning 2-3 mo
has followed ingestion of sarcocysts of
after infection. Sarcocysts of some species

S suihominis in uncooked pork and
are easily visible with the unaided eye (S

S hominis in uncooked beef. Differentia
aucheniae, S hirsuta, S gigantea). The
tion between cysts of S sinensis and
presence of such sarcocysts as well as those S hominis in beef is extremely important of zoonotic species can cause condemnato avoid unjustified rejections.

tion of the carcass during meat inspection.

Sarcocysts of other species remain

Clinical Findings: Sarcocystis spp
microscopic, even though tremendous
infections are quite prevalent in farm
numbers of cysts may be present in the
animals; however, there have been few
muscles. The identification of different
outbreaks of clinical disease. Most animals
species could be achieved by molecular
a.re asymptomatic, and the parasite is
studies and cyst wall morphology (mainly
discovered only at slaughter. In cattle
ultrastructure).

severely affected by S ciuzi, the signs

S cruzi produce microscopic cysts,
include fever, anorexia., ca.chexia, decreased
principally in myocardium, and can affect
milk yield, diarrhea., muscle spasms,

1000/o of some cattle populations. S hirsuta
anemia, loss of ta.ii hair, hyperexcitability,
has been prin1arily responsible for cattle
weakness, prostration, and death. Cows
condemnation for visible sarcocysts. S
infected in the last trimester of pregnancy
meischeriana is the most important species may a.bmt. After recovery from a.cute affecting pigs and may affect meat quality.

illness, calves failed to grow well and

Macroscopic cysts of S aucheniae are an
eventually died in a ca.chectic state. Anemia,
in1portant cause of condemnation of llama
hepatitis, and myocarditis were the primary
meat. Sarcocysts are easily recovered from
lesions in a.cute ovine sarcocystosis after
esophagus, diaphragm, and heart muscle.

experimental challenge with S tenella

In general, Sarcocystis spp infections are
sporocysts. Cases of encepha.lomyelitis in
considered of low pathogenicity except
sheep were associated with a.Sarcocystis

1060

SARCOCYSTOSIS
sp infection. After recovery from acute
produce pigeon protozoal encephalitis with
illness, some sheep may lose their wool.

severe brain lesions and muscle cysts at the

S teneUa may also induce abortion in sheep.

san1e time.

At necropsy, acutely affected animals have

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hemon-hage of the serous membranes of the Control: Livestock become infected by viscera and myocardium. Sarcocystis spp
sporocysts from the feces of carnivores.

infections are probably most in1portant in

Because most adulL cattle, sheep, and many
growing ruminants and swine, in which they pigs harbor cysts in their muscles, dogs and can result in subclinical anemia and
other carnivores should not be allowed to
reduced weight gain.

eat raw meat, offal, or dead animals.

Equine protozoal myeloencephalitis

Supplies of grain and feed should be kept

(EPM, see p 1309) is caused principally by
covered; dogs and cats should not be

S neurona in American horses. Only asexual allowed in buildings used to store feed or stages of this parasite have been fom1d in
house animals. Amprolimn (100 mg/kg/day
horses, and they may be located in neurons
for 30 days), fed prophylactically, reduced
and leukocytes of the brain and spinal cord.

illness in cattle inoculated with S cruzi. Pro

Opossmns (Didelphis virginiana and
phylactic administration of amproli tun or

D albiventris) are its definitive hosts.

salinomycin also protected experimentally

Clinical signs in horses include gait
infected sheep. Therapeutic treatment of
abnormalities sucll as ataxia, knuckling,
the chronic stage (tissue cysts) has been
and crossing over. Muscle atrophy of the
ineffective. Vaccines are not available.

hi.ndlimb, which is usually LUlilateral, is

Experimental work demonstrated that
frequent. The lesions are typically focal,
infected pork and beef could be made safe
and brain-stem involvement is common.

for constunption by cooking at 70°C (158°F)

Depression, wealmess, head tilt, and
for 15 min or by freezing at -4 °C (24.8°F) for
dysphagia are other possible signs. EPM can

2 days or -20°C ( -4 OF) fof l day.

mimic many neurologic diseases. Horses may

Pyrirnethan1ine and sulfadiazine
also develop a myopathy. Multifocal myositis

(1 mg/kg/day and 20 mg/kg/day, respectively,
has been reported and is possibly due to
for 120 days or longer) is the traditional
another Sarcocystis species with horses as
therapy to treat horses with EPM. Diclazuril
the intermediate host, S Jayeii. PCR is an
and toltrazuril (5 mg/kg) are potentially
important diagnostic method. S calchasi can useful prophylactic agents againstS neurona.

ARTHROPATHIES IN LARGE ANIMALS

See also I..AMENE.SS [N CATI'LE, p 1066; HORSES, involving periarticular and intra-articular
p 1096; SHEEP, p 1166; GOATS, p 1092; and PIGS, ligan1ents, meniscal tears, and osteoarthrip 1151.

tis. Tramnatic arthritis is.seen in all breeds
of horses worldwide.

ARTHRITIS

Atthritis is a nonspecific term denoting
inflammation of ajoint. All joint diseases

Clinical Findings and Diagnosis: Trauof large animals have an inflammatory matic synovitis and capsulitis is inflammacomponent to varying degrees. Arthritic tion of the synovial membrane and fibrous
entities of inlportance include tramnatic
joint capsule associated with trauma.

arthritis, osteochondtitis dissecans,

Typically, the horse is an athlete and
subchondral cystic lesions, septic ( or
presents with synovial effusion in the
infective) arthritis, and osteoarthritis
acute stage, along with general Lhickening

(also called degenerative joint disease).

and fibrosis in the more chronic stage.

Lameness varies from a mild gait change

Traumatic Arthritis
to severe lameness. Tramnatic synovitis
and capsulitis is differentiated from other

Tramnatic arthritis includes traumatic
tramnatic entities by use of radiography to
synovitis and capsulitis, intra-articular chip
exclude osteochondral fractures or disease.

fractures, liga.mentous tears (sprains)

Tearing of ligaments or menisci (in

ARTHROPATHIES IN LARGE ANIMALS

1061
femorotibialjoints) can often be excluded
that cause degenerative changes in the
only by diagnostic arthroscopy. Osteochonarticular cartilage. Intra-articular sodium dral fractures are diagnosed with radiohyaluronate has been used effectively for graphs. Osteoatthritis is the progressive
mild to moderate synovitis and has a

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loss of articular cartilage and can be the
chondroprotective effect, but it is less
consequence of any or all of these traumatic
effective in severe synovitis or when
entities (see also p 1063). Osteoarthritis is intra-articular fractures are present. Use
diagnosed with radiographs when the
of an IV fonnulation of hyaluronic acid
changes ai·e sufficiently severe to demon

(systemic dose 40 mg) in clinical cases
strate loss of joint space ( associated with
appeai·s to be effective, and this is
articular cartilage loss), subchondral
supported by research data in a controlled
sclerosis, and osteophyte or enthesophyte
model of arthritis in horses. Polysulfated
formation. Lesser degrees of osteoarthritis
glycosatninoglycans (PSGAGs) are also
can be defined only with diagnostic
used frequently for traun1atic atthritis
arthroscopy. Clinical signs of osteochondral entities. PSGAG is effective for synovitis fractures are similar to those of synovitis
and can help prevent ongoing degeneration
and capsulitis, as well as those of osteoarof articular cartilage. Although effectivethtitis; differential diagnosis of these ness of PSGAG when used intra-articulai·ly
entities is based on radiographs and, in

(250 mg) has scientific support, effectivesome cases, arthroscopy.

ness when used IM (500 mg) is less certain.

Arthritis generally results in pain and

The use of pentosan polysulfate (PPS) at 3
altered function of the joint. If the process is
mg/kg, IM, has been shown to be effective as
active or acute, there is usually synovial
a disease-modifying drug with experimental
effusion, and the sunounding tissues are
equine osteoaithritis and has been
swollen and warm. In more severe cases,
extensively used in clinical cases outside
manipulation of the joint causes pain. In
the USA. Biologic therapies such as
more subtle cases, flexion tests are required
autologous conditioned serum are also
to elicit lameness. As the disease process
becoming more conm1only used.

becomes chronic, the range of motion is

Horses with osteochondral chip
reduced with fibrous thickening of the joint
fragmentation (most commonly seen in the
capsule. Radiographic evaluation is
cai·pus and fetlock joints) are treated with
necessary for positive confirmation of a
arthroscopic surgery to minimize tl1e
nun1ber of disease entities. Arthroscopy
ongoing development of osteoarthtitis.

is used to accurately assess the amount

Fragn1ents are removed, and defective bone
of damage to the articular cartilage and
and cartilage debrided. Rest periods of
to establish a prognosis.

2-4 mo follow, and physical therapy
regimens are instituted in the convalescent

Treatment: Treatment of acute traumatic
period. The success rate in returning horses
synovitis and capsulitis includes rest and
to previous performance level is high when
physical therapy regimens such as cold
secondary osteoarthritic changes are
water treatment, ice, passive flexion, and
minimal at the time of surgery. Osteochonswimming. NSAIDs (usually phenylbutadral chip fragments that are amenable to zone) are used routinely. In more severe
arthroscopic surgery and have successful
cases, the joint is lavaged to remove
results include those associated with the
inflanunatory products produced by the
distal radius or caival bones; dorsoproximal
synovial membrane, as well as articular
first phalanx; proximal palrnar/plantar first
cartilage debris that exacerbates the
phalanx; apical, abaxial, and basilar
synovitis. Joint drainage alone, without
fragments of the proximal sesamoid bones;
lavage or irtjection of medication, provides
fragmentation of the distal patella in tl1e
only short-term relief.

femoropatellar joint; chip fragments of tl1e

Various intra-articular medications have
tibiotarsaljoint; and fragments of the
been used. Corticosteroids are the most
extensor process of the distal phalanx
potent anti-inflanunatory agents and are

(coffinjoint).

effective in acute traumatic arthritis.

However, there are differences in the
adverse effects between various cortico

Osteochondritis Dissecans
steroids and various dosages. Betametha

For a complete discussion of equine
sone products and triamcinolone acetonide
osteochondrosis, seep 1148.

are effective with no deleterious adverse

In osteochondritis dissecans (OCD),
effects. Methylprednisolone acetate is more
a focal area of the immature articular
potent and longer acting than the other two
cartilage is retained, and the matrix in
drugs but has significant adverse effects
the basal area of this region becomes

1062

ARTHROPATHIES IN LARGE ANIMALS
chondromalacic and acellular. The

(sagittal) ridge of the tibia, lateral trochleai.·
immature articular cartilage separates
ridge of the talus, medial malleolus of the
from the underlying trabecular bone. The
tibia, and medial trochlear ridge of the talus.

chondral fracture extends horizontally and

All lesions are ai.nenable to ai.throscopic
vertically until a flap is formed. Synovial
surgery, and the prognosis is usually good.

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fluid gains entrance to the underlying

Surgery is reconunended when synovial
medullary space, and subchondral cysts
effusion is present. Lesions without
may fonn ( usually only in larger animals).

fragmentation in the metacarpophalangeal

The flap of immature ai.ticular cartilage may
or metatarsophalangealjoints can be
stay sepai.·ated and loose, break away
treated conservatively, and most affected
completely (''.joint mice"), or reattach by
animals recover well. U a fragment is
endochondral ossification to the underlying
present, arthroscopic surgery is recombone, especially in pigs, and result in a mended. In the shoulder, sw·gery is usually
wrinkled articulai.· surface. The latter occurs recommended, although milder cases have only if the joint is rested or protected, which
been managed conservatively with success.

permits reestablishment of the circulation

The prognosis with ai.throscopic surgery
necessary for endochondral ossification. U
is generally less favorable in the shoulder
the flap is tom free by joint motion, it may
tllan in other joints.

be ground into smaller pieces dwfag
locomotion and disappear, whereas the

Subchondral Cystic Lesions
larger plaques may become attached to the
synovial membrane, become vasculai.ized,

Subchondral cystic lesions ai.·e seen in the
and ossify. The resultant ai.ticulai.· defect, in
femorotibialjoint ai.1d in the fetlock, pastern,
time, fills with fibrocartilage.

elbow, shoulder, ai.1d distal phalanx. The
diagnosis is usually made on the basis of

Etiology: The exact cause of OCD is
localization of lan1eness with intra-articular
unknown but is asswned to be multifactoanalgesia ( synovial effusion is variable) and rial. Factors include genetic predisposition,
confim1ed with radiographs.

fast growth, high caloric intake, low copper

Subchondral cystic lesions are most
and high zinc levels, and endocrine factors.

frequent in the femorotibialjoint, followed
by the fetlock joint. Surgery (arthroscopic)

Clinical Findings: The most common
is currently reconm1ended in the femorosites of OCD, which usually is seen in young tibial joint whenever a complete cystic
animals, ai.·e the femoropatellar joint,
lesion is present. Smaller, dome-shaped
tibiotarsal (tai.-socrural)joint, fetlock
or flattened lesions are usually treated

(metacarpophalangeal and metatarconservatively in the initial period. Athletic sophalangeal) joints, and the shoulder.

soundness is achieved in 65%---7()0A, of these

Animals with OCD of the shoulder usually horses. Intralesional irtjection of corticopresent when< 1 yr old with severe forelimb steroids tmder arthroscopic visualization,
lai.neness and possibly some muscular
in preference to debridement as done
atrophy. Animals with OCD in.the other
previously, achieves supe1ior results. In
joints usually present with synovial effusion
cases with collapsed edges to tl1e cystic
and varying degrees of lan1eness. Diagnosis
lesion at arthroscopic surge1y, or in cases
is con.fumed with radiographs.

unresponsive to therapy, ai.throscopic
debridement with augmentation with fibrin,

Diagnosis: The history, age, breed, sex,
growth factors, and mesenchyn1al stern
and clinical signs provide useful infonnacells have been used. Surgery is usually tion; however, radiographs are required to
recommended for subchondral cystic
substantiate a diagnosis of OCD.

lesions of the distal metacarpus in the
fetlock but not as consistently as in the

Treatment: Treatment of OCD depends
femorotibialjoint. Single lesions associated
on the location and degree of involvement.

with the pastern and elbow joint are treated

Femoropatellar joint lesions are associated
conservatively and have a fair prognosis. U
with the lateral trochlear ridge of the femur,
possible, surgery is recommended for cystic
medial trochlear ridge of the femur, or distal
lesions of the distal phalanx (results with
patella. They are ai.nenable to ai.throscopic
conservative treatment are very poor).

surgery, which is reconunended in all cases
except early lesions chai.·acterized by

Septic Arthritis
flattening (without fragmentation) <2 cm

(Infective arthritis)

long on the lateral trochlear ridge. In the
tarsocruraljoint, OCD lesions are seen in

Etiology and Epidemiology: Septic or
decreasing frequency on the intem1ediate
infective arthritis results from sequestration

ARTHROPATHIES IN LARGE ANIMALS

1063
of bacterial infection in a joint. Infection

Treatment: Septic arthritis requires
of a joint develops in three main ways:

prompt treatment to avoid irreparable

1) hematogenous infection, which is
dan1age. Systemic broad-spectrwn
common in foals, calves, and lambs
antibiotics are indicated; the initial choice

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( commonly referred to as navel ill);
is based on the most likely pathogen but is

2) trawnatic injury with local introduction
subject to change based on cultme and
of infection; or 3) iatrogenic infection
sensitivity tests. Systemic antibiotic
associated with joint injection or smgery
treatment is often combined with intra

( usually in horses). Navel ill is only one
articular antibiotics (to achieve more
example of a hematogenous route of
effective sterilization of the joint) and
infection, which can also be gained from
other local therapy, including joint lavage

GI or pulmonary somces.

(initially) ai.1d arthroscopic debridement
and drainage. Adjunctive treabnent with

Clinical Findings and Diagnosis: Septic NSAIDs (eg, phenylbutazone) is also done.

arthritis is usually characterized by severe

The effectiveness of treab11ent is monitored
lameness and distention of the joint with
carefully with clinical signs and repeat
cloudy, tmbid synovial fluid that contains
synovial fluid analyses.

>30,000 WBC/mm3 and a total protein level
of>4g/dL.

Osteoarthritis

In foals, hematogenous osteomyelitis
often accomparues septic arthtitis. Septic

(Degenerative joint disease)

arthritis in foals has been classified into
type S (septic joint only), type P (involving

Etiology and Epidemiology: Osteoosteomyelitis of the adjacent growth plate arthritis is a progressive degradation of
as well), or type E (involving osteomyelitis
articulai· caitilage and represents the
of the epiphyseal and subchondral bone).

end stage of most of the other diseases

Vaiious organisms may be involved.

discussed above if treatment is ineffective

In young lainbs, Actinobacillus seminis
or the initial problem is too severe. For this
causes polyartht·itis, as do Chlamydia
reason, prompt diagnosis ai.1d correct
psittaci and E1ysipelothrix insidiosa. The management of traun1atic synovitis and
latter can follow docking, castration, or
capsulitis, intra-aiticulai· fractmes or
navel infection. Viruses and mycoplasma
traw11atic cartilage damage, osteochond1itis
may also be etiologic agents in food-producdissecans, subchondral cystic lesions, and ing anin1als.

septic arthritis are critical.

In mature goats, caprine arthritis
and encephalitis virus ( see p 7 4 7) is an Clinical Findings and Diagnosis: Lameinlportant cause of infective arthritis. In ness can be localized with analgesia to.the
young goats, C psittaci and Mycoplasma
affected joint. There ai·e varying degrees of
mycoides are frequent causes.

synovial effusion,joint capsule fibrosis, and

Bacte1ial (includingMycoplasma)

restricted motion ( decreased flexion ).

arthritides are seen in young pigs. In

Radiographic signs of osteoarthritis include
newborn pigs, septic artluitis usually is
decreased joint space, osteophytosis,
due to intraute1ine or navel infection with
enthesitis, ai.1d subchondral sclerosis. In

Escherichia coli, ConJnebacterium, Stre'[J
less severe cases, articular degradation
tococcus, or Staphylococcus spp. Control is requires definition with arthroscopy.

best directed toward reducing the possibility
of infection from the environment. Older

Treatment: Treatment of osteoarthritis is
pigs sometimes develop arthritis as a
most commonly palliative and includes the
sequela of infection with Haemophilus,
use ofNSAIDs, polysulfated intra-aiticular

Erysipelothrix, or Mycoplasma spp.

glycosaniinoglycans, intra-articulai·

Although diagnosis in the early stages is
corticosteroids, IV hyaluronic acid, and
not difficult, the more chronic stages can

IM pentosan polysulfate. The use of intrabe confused with articulai· lesions produced articular autologous conditioned serwn
by dietaiy hypervitarninosis A
has also been validated. Physical therapy

Trawnatic injury to joints with contamiregin1ens may prove useful. Artht·oscopy nation and progression to infection is
is conunonly performed to diagnose the
common in horses, and various species of
extent of articular cartilage loss, as well as
bacteria are involved. Infection associated
to treat p1irnary conditions such as articulai·
with intra-articulai· injection or smgery
cartilage separation, meniscal tears, and
occms in horses and is usually associated
ligan1entous injury. In advanced cases of
with Staphylococcus aureus or S e'[Jider
osteoarthritis, smgical fusion (arthrodesis)

midis.

may be performed on selected joints.

1064

ARTHROPATHIES IN LARGE ANIMALS

Surgical fusion of the proximal interphalan

(acquired bursitis) located over the
geal joint (pastern) or distal tarsal joints can
olecranon process and tuber calcaneus,
effect athletic soundness. Fetlock arthrorespectively, of horses. Frequent causes desis is also done in valuable animals and
include trauma from lying on poorly bedded

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makes them comfortable and capable of
hard floors, kicks, falls, riding the tailgate of
breeding. Treatment is usually unsuccessful
trailers, iron shoes projecting beyond the
in chronic cases in bulls and cows, but
heels, and prolonged recumbency.

restricted exercise and careful feeding
and nursing prolong the life of and can be

Clinical Findings and Diagnosis: Cirworthwhile for valuable breeding animals.

cw11scribed edematous swelling develops
over and around the affected bursa. Lame

BURSITIS
ness is rare in either case. The affected
bursa may be fluctuating and soft at first

Bursitis is an inflanm1at01y reaction within
but, in a short tin1e, a fim1 fibrous capsule
a bw-sa that can range from mild inflammaforms, especially if there is a recmTence of tion to sepsis. It is more common and
an old injmy. Initial bursa! swellings may be
in1portant in horses. It can be classified as
hardly noticeable or quite sizable. Chronic
true or acquired. True bursitis is inflammacases may progress to abscessation.

tion in a congenital or natural bursa ( deeper
than the deep fascia), eg, trochanteric

Treatment: Acute early cases may
bursitis and supraspinous bursitis (fistulous
respond well to applications of cold water,
withers, see below). Acquired bursitis is
followed in a few days by aseptic aspiration
development of a subcutaneous bursa
and injection of a corticosteroid. The bursa
where one was not previously present or
may also be reduced in size by application
inflammation of that bursa, eg, capped
of a counterirritant or by ultrasonic or
elbow over the olecranon process, shoe boil
radiation therapy. Older encapsulated
over the point of the elbow, and capped
bursae are more refractory. Surgical
hock over the tuber calcaneus.

treatment (usually cmettage and drainage)

Bursitis may manifest as an acute or
is reconm1ended for advanced chronic
chronic inflanunation. Examples of acute
cases or for tl1ose that become infected.

bursitis include bicipital bursitis and

A shoe-boil roll should be used to prevent
trochanteric bursitis in the early stages. It is
recmTence of a capped elbow if the
generally characterized by swelling, local
condition has been caused by the heel or
heat, and pain. Chronic bursitis usually
the shoe. With capped hock, behavioral
develops in association with repeated
modification so the horse does not kick the
traun1a, fibrosis, and other chronic changes
stall offers the only hope of pem1anently

( eg, capped elbow, capped hock, and carpal
resolving the problem.

hygroma). Excess bursa! fluid accumulates,
and the wall of the bursa is thickened by

Fistulous Withers and Poll Evil
fibrous tissue. Fibrous bands or a septun1
may form within the bursa! cavity, and

Fistulous withers and poll evil are rare,
generalized subcutaneous thickening
inflammato1y conditions of horses that
usually develops. These bursa! enlargediffer essentially only in their location in the ments develop as cold, painless swellings
respective supraspinous or supra-atlantal
and, unless greatly enlarged, do not severely bursae. Th.is discussion is of fistulous interfere with function. Septic bursitis is
witl1ers but, except for anatomic details,
more serious and is associated with pain
also applies to poll evil. In the early stage of
and lan1eness. Infection of a bw-sa may be
the disease, a fistula is not present. When
hematogenous or follow direct penetration.

the bursa! sac ruptures or when it is opened

The pain in acute bursitis may be relieved
for surgical drainage, and secondary
by application of cold packs, aspiration of
infection with pyogenic bacteria occurs, it
the contents, and intrabursal medication.

usually assumes a true fistulous character.

Repeated ir\jections may result in infection.

Treatment of chronic bmsitis is sw-gical

Etiology: The condition may be t.rawnatic

(and is done arthroscopically (bursoscopy).

or infectious in origin. Agglutination titers

In infected bursitis, systemic antibiotics as
suppmt an infectious etiology. Brucella
well as local drainage are required.

abortus can sometimes be isolated from the
fluid aspirated from the unopened bursa.

Capped Elbow and Hock

Clinical Findings: The inflanm1ation

Capped elbow and hock are inflanm1atory
leads to considerable thickening of the
swellings of the subcutaneous bursae
bursa wall. The bursa! sacs are distended

ARTHROPATHIES IN LARGE ANIMALS

1065
and may rupture when the sac has little
urine and transmitted via ingestion or, in
covering support. In more chronic,
some cases, inhalation.

advanced cases, the ligament and the dorsal
ve1tebral spines are affected, an.ct occasion

Clinical Findings: Chlamydia! polyarthrially these structures necrose.

tis is seen in lambs on range, on fa.nns, and

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In the early stage, the supraspinous bursa
in feedlots. Morbidity may be 5%---75%.

distends with a clear, straw-colored, viscid

Rectal temperatures are 102° -107°F
exudate. The swelling may be dorsal,

(39°-41.5°C). Varying degrees of stiffness,
unilateral, or bilateral, depending on the
lameness, anorexia., and a concurrent
arrangement of the bmsal sacs between the
conjunctivitis ( see p 506) mity be seen.

tissue layers. It is an exudative process from Affected sheep are depressed, reluctant to the beginning, but no true suppmation or
move, and often hesitate to stand and bear
secondary infection occurs until the bursa
weight on one or more limbs, but they may
ruptures or is opened.

"warm out" of stiffness and lameness after forced exercise. Incidence of the disease

Treatment and Prevention: The earlier
in sheep on range is highest between late
treatment is instituted, the better the
swnmer and early winter.

prognosis. The most successful treatment

The disease affects cattle of all ages, but
is complete dissection and removal of the
calves 4----30 days old a.re affected more
infected bursa. The expense of the
severely. Calves may have fever, are
protracted treatment required in chronic
moderately alert, and usually nurse if carried
cases often exceeds the value of the animal.

to the dam and supported while sucking.

Brucella vaccines have not proved helpful.

They invariably also have diarrhea., which can

Sodium iodide therapy is of limited value.

be severe. Affected calves a.sswne a hunched
position while standing; their joints usually

CHLAMYDIAL POLYARTHRITIS
are swollen, and palpation ca.uses pain. Navel

SEROSITIS
involvement and nervous signs are not seen.

Chlamydia] polyarthritis has been

(Transmissible serositis)

recognized in older pigs as well as in young
piglets. The affected piglets become febrile

Chlamydia! polyarthritis-serositis is an
and anorectic and may develop nasal
infectious disease that affects sheep, calves,
cata.n·h, difficulties in breathing, and
goats, and pigs. Chlan1ydial polyarthritis of
conjunctivitis. This condition has not been
sheep was first described in Wisconsin and
clearly differentiated from other infections
has since been recognized in the western
that lea.cl to polyserositis and arthritis in pigs.

USA, Australia., and New Zealand. The
disease was identified in calves from the

Lesions: The most striking tissue changes

USA, Australia., and Austria, and in pigs
are in the joints. In lambs, enlargement of the
from Austria, Bulgaria., and the USA.

joints is not often noticed, but in chronic·
advanced cases, the stifle, hock, and elbow

Etiology and Epidemiology: Strains
may be slightly enlarged. In calves,
of the causal a.gent, Chlamydia psitlaci,
peliarticular subcutaneous edema along
isolated from affected joints of sheep and
tendon shea.tl1s and fluid-filled, fluctuating
calves, are identical, but strain-specific
synovial sacs contribute to enlargement of
antigens in their cell walls distinguish them
the joints. Most affected joints of lambs or
from those that ca.use abortions in sheep
calves contain excessive, grayish yellow,
and cattle (seep 1332).

turbid synovial fluid. Fibrin flakes and

The GI tract is of prime importance in the
plaques in the recesses of the affected joints
pathogenesis of chlan1ydial polyarthritis
may adhere firmly to the synovial mem

(seep 598). The disease has been reprobranes. Joint capsules a.re thickened.

duced experimentally by oral inoculation.

Articular cartilage is smooth, and erosions

Because chlan1ydia.e can be recovered from
or evidence of marginal compensatory
the feces of clinically healthy calves and
changes are not present. Tendon sheaths
lambs, it is most likely the GI tract wherein
of severely affected lambs and calves may
the host and parasite stay frequently in
be distended and contain creamy, grayish
balance. If there is a shift in favor of the
yellow exudate. Surrotmding muscles are
chlan1ydia.e, then a systemic infection and
hyperemic and edematous, with petechia.e
chlamydemia. ensues; the ultimate site of
in their associated fascia! planes.

replication is the synovial membrane. The

GI tract also has been infected after

Diagnosis: The history and careful
experimental intra-articular inoculations.

exanlination of the pathologic changes in

Chlamydiae are excreted in the feces and
the joints and other organs can be of

1066

ARTHROPATHIES IN LARGE ANIMALS
diagnostic value. Cytologic examination
layer of the tendon sheath, is characterized
of synovial fluids or tissues may reveal
by distention of the tendon sheath due to
chlamydia! elementary bodies or cytoplassynovial effusion. It has a mUTiber of mic inclusions. Isolation and identification
possible causes and clinical manifestations.

of the causative agent from affected joints

The various types of tenosynovitis include

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confirms the diagnosis. Bacteriologic
idiopathic, acute, chronic, and septic
cultmes of affected joints a.re usually

(infectious). Idiopathic synovitis refers to
negative, but Escherichia coli or streptosynovial distention of tendon sheaths in cocci occasionally may be isolated. If the
yow1g ailin1als, in which the cause is
joints of young calves a.re arthritic, and if
uncertain. Acute and chronic tenosynovitis
navel lesions are absent, chlamydia!

a.re due to trawna. Septic tenosynovitis may
polya.rthritis should be considered.

be associated with penetrating wounds,

Clinical and pathologic features distinlocal extension of infection, or a hematogguish chlamydia! polyaithritis from most enous infection.

other conditions that cause stiffness and
lai11eness in lambs. Lambs with mineral
deficiency or osteomalacia usually a.re not

Clinical Findings and Diagnosis: There
febrile. The abnormal osteogenesis in these
a.re varying degrees of synovial distention of
two conditions ai1d the distinct lesions of
the tendon sheath ai1d laineness, depending
white muscle disease a.re virtually pathognoon the severity. Horses are markedly Jaine in monic. In arthritis ca.used by E1ysipelothri..'"C
septic tenosynovitis. Chronic tenosynovitis
rhusiopa.thiae, there a.re deposits on and
is common in horses in the tai·saJ sheath of
pitting of articular surfaces, peria.rticula.r
the hock (thoroughpin) and in the digital
fibrosis, and osteophyte fonnation. Larninitis sheath (tendinous windpuffs). These two due to bluetongue virus infection (seep 738) entities must be differentiated from synovial
can be differentiated clinically and etiologieffusion of the tarsocnrral ai1d fetlock cally. Detailed microbiologic investigations
joints, respectively.

a.re required to differentiate chlamydia!

arthritis from mycoplasmal artluitis.

Treatment: In idiopathic cases, no

Treatment and Prevention: If begun
treatment is initially recommended. Acute
early, therapy with long-acting penicillin,
cases with clinical signs may be treated
tetracyclines, or tylosin appears to be
symptomatically with cold packs,
beneficial. More advanced lesions do not

NSAIDs, and rest. Tenoscopic surgery is
respond satisfactorily. Feeding chlortetraoften used to treat specific conditions cycline at 150-200 mg/day to affected lai11bs
within the tendon sheath that give rise to
in feedlots reduces the incidence of
tenosynovitis symptoms. Application of
chlamydia! polyarthtitis. No approved
counterirritants ai1d bandaging has been
vaccines a.re available.

used in more chronic cases. Septic
tenosynovitis requires systemic antibiot

TENOSYNOVITIS
ics and drainage. If adhesions develop
between the tendon sheath and the

Tenosynovitis, an inflanl.lllation of the
tendon, persistent effusion and lameness
synovial membrane and usually the fibrous
is the rule.

LAMENESS IN CATTLE

Loss of milk of 1. 7-3 Uday for up to 1 mo
before and 1 mo after treatment (because

The lesions that cause lameness in dairy
of pain) plus milk discarded because of
cows result in intense pain and a.re a major
antibiotic therapy must also be considered.

aninlal welfare issue. Lameness also causes

Lame cows a.re more reluctai1t to use
stress, which debilitates and reduces
automatic milking systems and show visible
productivity. The financial impact of
signs of stress when forced to do so.

lan1eness includes losses from decreased

At least 10% of cows in a herd are culled
production, cost of treatment, prolonged
for reasons related to lan1eness. Rea.ring
calving interval, ai1d possibly nmsing labor.

replacement heifers is expensive, and

LAMENESS IN CATILE

1067
replacement animals are not initially as
posture cru1 be confused witl1 a conformaproductive as mature cows. Cows in poor tional defect referred to as "sickle hock,"

condition have a greater predisposition to
in which the angle of the hock is <160°.

lameness. Cows that are lame before

5) When the angle of the hock is <180°,
breeding have a reduced ability to conceive,
the posture is referred to as "post leg," an VetBooks.ir
and cystic ovaries are much more common
undesirable confom1ational characteristic
in lame cows. Lame cows are less aggresassociated with arthritis. 6) When the hind sive in their struggle for feed and are more
feet are held closer together than normal
likely to die early or be culled.

(adducted), pain in the medial claw is

Considerable funds are being invested in
indicated. The cow is said to be "stancling
bovine lameness research; within the next
narrow." This posture is often confused with
decade, national databases detailing bovine
a trait of confomiation called "bow leg."

lameness are expected to become

Standing narrow can be a sign of laminiticincreasingly available as a management related lesions in the medial claw .

tool. Although the lameness data are being

These principles of abnom1al posture can
collected primarily by hoof tlimmers,
be used to deduce tile region of the foot in
veterinruians should be familiar with this
which the seat of lameness is located. Use
information to continue to play a leading
of hoof testers may be one way to confirm
role in management of bovine lru11eness.

tl1e observation. For exan1ple, if there is
pain in the toe, the retraction phase of the

PHYSICAL EXAMINATION OF A
stlide (when tile foot passes behind the

LAME COW
phase of vertical weight-bearing) is reduced
considerably. ln contrast, if there is pain in

Visual Appearance of the Standing
the heel, the protraction phase of the stride

Animal: Abrasions or swellings on the
is reduced, or the foot is not cfillied as far
limbs suggest a prior traumatic event.

forward as nonnal. Usually, the gait of one

Decubital lesions (to the knee or more often
limb can be compared with that of the
the hock) might indicate prolonged periods
contralateral limb when viewed from the
of recwnbency or difficulty when rising.

side. However, lameness sin1ultaneously

Cubicle design should be reviewed.

present in contralateral limbs tends to

Muscular atrophy, particularly noticeable in
appear less severe tllan is actually the case.

the gluteal region, can be associated with a

It is not unusual in cases of subacute
painful condition such as arthritis. Cows
lanlinitis for all limbs to be affected more or
experiencing exti·eme pain can Jose body
less equally. In these cases, no specific gait
condition rapidly.

change is seen, but tile cows tend to place

Stance or posture can change as the
their feet carefully with each step, ie, tlley
bearing surface of the claw wears or there

"plod" or have a stilted gait.

is a painful lesion in the foot. In a nom1al
stance, the point of the hock (tuber

Examination of the Claw: In cows
calcanei) lies directly beneath the pin bone
exposed to concrete surfaces for a

(ischial tuber) when viewed either from tl1e
prolonged period, the sole of the lateral
side or from behind. Approximately 6096 of
claw is likely to be worn flat and become
the body weight is borne by the forelimbs.

much wider than that of tile medial claw.

A Jame anin1al adjusts its posture to relieve

Such soles are highly subject to traunia.

pain.

To facilitate exanlination of a completely

The following principles illustrate
flat claw, the surface of the sole should be
specific exru11ples of changes in stance or
washed and exanlined carefully for black
posture related to lameness: 1) A painful
marks by exploring with a hoof knife. If the
abscess in a lateral hind claw causes the
sole is heavily caked with mud or manure
cow to abduct that limb. 2) Pain in the heel

( eg, cows at pasture or confined in corrals
of the hind foot forces the cow to hold its
or straw yards), it is quicker and easier to
foot to tl1e rear, a posture known as
cut off a layer of superficial horn together

"camping back" or retraction. 3) After a cow with tile caked material to expose fresh
has spent much time walking on concrete,
horn beneath. Particular attention should be
the lateral hind claw may become overburpaid to the abaxial white line area. Removal dened (excessive buildup of solear horn).

of large runounts of sole horn is contra

This forces the hock to tum inwru·d, a
indicated in the diagnostic phase of an
posture referred to as "cow hocked."

examination. The interdigital space should

4) Pain in the toe, which occurs in laminitis,
be evaluated by separating tl1e claws and
causes the cow to hold its hind feet further
examining carefully for evidence of a
forward than nom1al, a posture referred to
foreign body, fibroma, footi·ot, interdigital
as "camping forward" or protraction. This
dermatitis, or digital dermatitis.

1068

LAMENESS IN CATTLE

LOCOMOTION SCORING
foot abnormality is considered a risk factor.

When a risk factor has been identified,

Locomotion scoring is a useful tool as part
control measures can be instituted before
of a routine herd health evaluation or in a
the problem becomes difficult to control.

detailed herd lameness investigation.

Lan1eness in cattle is a clinical sign of pain

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Most farmers will detect between only
with many possible causes that require

25% and 400Ai of truly lame cows; this
investigation. Methods to record lesions and
underestimation of lameness prevalence
rating severity are not yet standardized, but
means that the economic consequences of
computer programs are available. In many
lame cows are less obvious to farmers than
countries, as many as one-third of hoof
those caused by mastitis (loss of milk) and
trin1mers can provide this service and
fertility problems. Cows in the early stages
accurately identify and describe the severity
of sole ulcer, white line disease, and toe
of foot lesions.

necrosis syndrome show only slight signs of

In one survey, 86% of lesions recorded
lameness; if these lesions can be identified
were found in the lateral claw of hindlimbs
in their early stages, they can be treated and
and 14% in the forelimbs; 73% of forelimb
preventive measures instituted.

lesions were observed in the medial claw.

Locomotion scoring identifies slightly lame

The National Database in Denmark also
cows as well as those more obviously lame.

contains information about milk yield,

Therefore, use of locomotion scoring can
reproductive status, health, etc. The
demonstrate the real extent of the problem.

prevalence of lesions must be interpreted

Herd assessments should be done when
carefully, because not every cow with a
the cows are walking on level, unobstructed
lesion will show signs of lameness. However,
walkways that give the observer a clear view.

an abnonnally high incidence of lesions may

Locomotion scoring is frequently performed
forecast lan1eness to come. The findings
when the cows are leaving the milking parlor.

would indicate the urgency with which

In addition, milkers should note any cow
preventive measures should be implemented.

standing in the milking parlor with an arched

The incidence of lesions varies considerably
back, because it is highly probable that such
between countries and between regions of
cows are lame. Any cow lying down for an
the same country. Lesion incidence also
abnormally long time(> 70----80 min/bout)

changes with different management system
should also be noted for special attention.

practices ( eg, tie stall and free stall) as well as Locomotion scoring is a 5-point system
with variations during seasons of the year.

based on both gait and posture: 1) Normal:

The armual herd incidence of lameness

The cow is not lame; the back is flat.

can be extremely high; in unique cases as

2) Mildly lame: The back is slightly arched
many as 600Ai of the cows are affected at least
when walking. 3) Moderately lan1e: The back once. However, even a 100/er-15% incidence is arched when both standing and walking.

represents a significant economic loss.

The cow walks with short strides in one or
more legs. 4) Lan1e: The lame cow can still
bear some weight on the affected foot.

DISTAL DIGITAL ANESTHESIA FOR

5) Severely lame: The back is ai-ched; the

DIAGNOSTIC AND SURGICAL
cow refuses to bear weight on the affected

PROCEDURES
foot and remains recun1bent. (Some
observers use a 4-point scoring system,

For distal digital analgesia ( used for surgical
referring to normal as zero.) The repeatabilor diagnostic procedures), !;he dorsal site is ity of locomotion scoring is acceptably high
located on the dorsal axis proximal to the
among experienced observers.

interdigital space close to the metacarpal or

As the locomotion score increases, milk
metatarsal phalangealjoint. The needle
yield decreases; however, the composition
should be placed with care (because the
of the milk (fat, protein) remains unaffected.

proper digital artery can be found at the
dorsal site), and 10 mL of 2% lidocaine
injected. If the needle is inserted deep into COMPUTERIZED RECORDING OF
the interdigital space, the nerves of the

DIGITAL LESIONS
flexor surface can be reached. This obviates
the necessity of a flexor site block for

Recording foot lesions by hooftrinrn1ers is
simple procedures. The distribution of the
one of the most valuable advances in hoof
nerve supply to the axial face of the digits of
health care and can be used to demonstrate
the forelimb is not constant, which makes
the seriousness of the problem. In many
this technique unreliable for digital
cases, the data indicate the risk factors to
analgesia of the forelimb.

be investigated. Any defect in the animal's

The preferred flex or site is a little lower
environment that leads to some stress or
tl1an the dorsal site because it is difficult to

LAMENESS IN CADLE

1069
pass a needle through the partially cartilagiand rotated backward at a 45° angle. Because nous palmar/plantar ligament. The medial
cattle have two digits that overlap one
and lateral sites are located at the level of the
another when viewed radiographically from
dewclaws, and the needle is inserted dorsally the side, an abnom1ality may be unclear or (horizontal in the standing animal) from a
obscured. The oblique view allows the digit

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point 2.5 cm slightly proximal to the dewto be viewed from such an angle that one claws. For the flexor site and the medial
claw appears to be behind the other, which
and lateral sites, -5-8 mL of 2% lidocaine
gives a much clearer picture than can be
is i!\iected. For surgery of tl1e digit ( eg,
obtained when the digits a.re superin1posed.

amputation), the dorsal, palmar/plantar, and

Because each digit is projected differently
medial or lateral sites are used, depending
on an oblique view, it is best to compare two
on the claw. For interdigital surgery ( eg,
radiographs of oblique views taken at
removal of corns), botl1 the dorsal and
comparable but opposite angles.

palma.r/plantar sites are used. Differential

The lateromedial or mediolateral
diagnosis can be aided by selective
projection is generally of much less value
anestliesia of the nerves of the digit.

than the oblique view. However, because

The diagrams above illustrate the sites for positioning is relatively easy, this view is four regional nerve blocks in the front and
useful to evaluate fractures, fracture
hind feet. The site selected should be
repairs, and luxations.

perfused with 10 mL of 2% lidocaine using

In the axial projection, a lateromedial
an 18-20 gauge needle.

or mediolateral view of a single claw is

Intravenous regional analgesia is frequently accomplished by placing a nonscreen film used for lengthy surgical procedures such as

( eg, a paper "cassette") between the digits.

arthrodesis. Sedation and restraint is advised.

This view produces a good image of the

A tourniquet is applied just below the hock
affected distal phalanx and, if interdigital
or knee, the hair is clipped, and the skin
soft-tissue swelling is not too great, the
ste1ilized from a site over a vein. Lidocaine
distal interphalangeal joint.

(10--30 mL) without epinepluine is i!\iected
to produce analgesia witllin -10 min. The

Radiographic Analysis and Interpre
tourniquet should never be kept in place for
tation: A number of factors should be

>60 min. When surgery is complete, the
considered in radiographic analysis and
tourniquet should be loosened gradually to
interpretation. Age differences can be seen
prevent a flood of anesthetic suddenly
radiographically as differences in skeletal
entering the general circulation. Concurrent
development. In calves, physes are present
i!\iection of antibiotic may be helpful.

in the distal metacarpus and metatarsus and
at the proximal ends of the proximal and

RADIOGRAPHY
middle phalanges. In a very young calf, ).he
distal phalanges may be incompletely

Radiography of the Digital Region:

ossified so that the bones appear small, and

Radiography can help identify the site of
their distal ends are rounded and indistinct.

lameness and provide information about

The subchondral bone may appear
the stage to which the pathology has
indistinct and finely irregular; this should
progressed. This helps to determine the
not be mistaken for the subchondral bone
most advantageous treatment. When
lysis seen in septic arthropathy.

pathologic changes are seen in the region

Diseases stimulating periosteal new bone
of the distal interphalangeal joint, tissue
in cattle (such as corkscrew claw and
dan1age is often rapid and severe.

postrecovery septic arthritis) can cause

Before a radiograph is taken, the
marked changes in bone contour and
interdigital space and both claws should be
increased bone opacity.

cleansed thoroughly, and both claws lightly

Slight bony changes at articular margins
trimmed. If this is not done, false images or
and musculotendinous attachments are
shadows may mask abnormalities present
conunonly seen on radiographs of older
in the claws. The digits can be viewed
cattle. Roughening of the distal surface of
radiographically using four angles or
the distal digit is a normal sign of aging.

projections.

Changes that occur during the normal aging

In the dorsopalmar/plantar projection, the
process should not be confused with active
image produced shows all of the major bones
bony changes.

and joints without overlap. This view allows

Reactive new bone ( osteophyte,
diagnosis of many diseases of tlie bovine foot. enthesiophyte, or exostosis) that has been In the oblique projection, tl1e plate is
present for some tin1e has a distinct border
positioned beneath the claw, and the head of
and a rough outline, and the opacity is
the machine is placed dorsad to the digits
normally even. Active new bone has an

1070

LAMENESS IN CADLE
indistinct border and a rough outline, and
surgical purposes. Arthrocentesis is a
the opacity is uneven.

procedure by which synovial fluid may be

Diffuse loss of bone opacity occurs in
removed from ajoint for exan'lination. Local
subacute laminitis, nutritional bone disease,
anesthetic can be introduced to asce1tain
and after limb immobilization. Focal or
whether painful lesions are present in the

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localized loss of bone opacity occurs in
joint. Intra-articular therapy permits
bone infection (osteomyelitis) or inflammamedication to be deposited into the joint.

tion (osteitis), ea.rlyfracture healing, and

Because this procedure may be painful, a
with defects in endochondral ossification
nerve block at a higher level is recommended.

( osteochondrosis ).

For the distal interphalangeal joint, the

Increase in joint width is caused by the
needle is inserted lateral to the common or
presence of increased fluid in the joint.

long extensor tendon, which inserts into the

However, this is less evident if the animal is
extensor process of the distal phalanx. The
bearing weight at the time the radiograph is
entry point is just proxin1al to the coronruy
taken. To confirm that the joint is in fact
band. For the pastern joint (proxin1al
wider than normal, it may be compared
interphalangealjoint), the needle is inserted
with the contralateral joint.

lateral to the extensor tendon. For the fetlock

Indistinctness and loss of opacity of the
joint ( metacru-pophalru1geal or metatarsubchondral bone are often associated with sophalru1gealjoint), the needle is directed
joint infections. Loss of opacity is often
downwru·d close to the bone ru1d between it
irregular. For this reason, a single radioand the interosseous (suspenso1y) ligru11ent.

graph is unlikely to detect this pathology;

The joint can also be entered from the dorsal
therefore, several radiographs taken from
surface in a sinillar manner to the distal
different angles are usually advised.

joints; however, the flexor poucl1 is more

Compruison between suspect and known
capacious than the dorsal one. For the digital
nom1al joints is recommended. Subchondral synovial sheatl1 (sheath of the deep flexor bone may be indistinct in a young animal.

tendon), the needle is directed downward

Radiography is important to evaluate the
behind the interosseous ligan1ent.

progress of a fracture repair. A radiograph

For tl1e stifle joint, it is advisable to use
taken in1rnediately after a fracture has been
two sites because in some ru1irnals the
realigned is the basis for future evaluations,
lateral femorotibial compartn1ent may not
and subsequent radiographs are essential if
communicate with the rest of the joint. The
nonunion or bone infection is suspected.

first site is close behind the lateral patellar

Loss of bone opacity is difficult to
ligament (lateral femorotibial compartrecognize with certainty in metabolic and ment), and the needle should be directed
nutritional diseases. Because all of the bones caudally. The needle is inserted in the in the body may be equally affected, it is not
second site between the medial and middle
helpful to compru·e one bone with another.

patellar ligan1ents and directed slightly

In an adult animal, cancellous regions in the
down ru1d toward the large medial lip of the
bone ends may become coarser or "granular" trochJea (femoropatellar and medial in appearance as smaller bone trabeculae
femorotibial compartn1ents ).

are resorbed. In the diaphysis of'a normal
bone in both inm1ature and adult animals,
the cortex is thickest at midshaft and
becomes thinner towru·d both ends. If the
cortex at midshaft approaches the thinness
of the proxin1al and distal diaphyses,
generalized osteopenia must be suspected.

Lameness is a clinical sign of different

Soft-tissue swelling can be demonstrated
diseases or disorders. For each condition,
on radiographs only in the eru·Jy stages of a
the range of causal risk factors ru1d tl1eir
septic disease. The characteristics of a
severity varies; therefore, each condition
soft-tissue swelling may indicate the
has its own epidemiologic study. The
location of a lesion and the tissues involved,
importance of each factor differs depending
muscle or tendon disease, cellulitis or
on tl1e system of mru1agement, be it total
edema, or dark gas shadows ( eg, a sinus
confinement, less restrictive systems, or
or a cap of an abscess).

totally pastoral. Management factors can
usually be controlled, whereas factors such

ARTHROCENTESIS AND
as ambient temperatw·e, huntldity, and

ARTHROSCOPY
rainfall must be taken into consideration
but crumot be controlled entirely.

Arthroscopy enables visualization of the

The diseases and disorders that affect
inte1ior surfaces of ajoint for diagnostic or
the feet of dairy cows fall into two broad

LAMENESS IN CADLE

1071
categories: those caused by infectious agents increased by more than 0.25 kg/day for and those attributable to management.

multiparous cows and by 0.20 kg/day for

The following variables can be controlled: prirniparous cows to a maximum of nutrition/water, walking surfaces, resting

14--16 kg (30--36 lb).

and stress ( cow comfo1t, social confronta

The quality and quantity of fiber fed could

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tion, stocking density), cleanliness/hygiene
be more important than the carbohydrate

(prevalence of infectious agents/moisture/
component of the diet. Fiber can, depending
irritants), human care (hoof trimming,
on its physical characteristics, stimulate
footbathing, lesion recording, farmer
nmtination. If the carbohydrate:fiber ratio is
education), and genetic considerations.

>500A, carbohydrate, the animal is increas

If lameness has become a significant
ingly at risk of ruminal acidosis. If the
problem on a farm, it is invariably too late
percentage of acid detergent fiber for the
for a quick resolution. The first step is to
complete ration is <200A,, risk of runtinal
immediately obtain the services of a
acidosis also increases. If the particle length
competent hoof trimmer who preferably
of silage is cut too short (25% cut <5 cm long),
uses a chute side computerized lesion
the contribution of effective fiber is reduced.

recording system (seep 1068).

If a nutritional problem is suspected, a

Objective methods to assess risk factors

"walk around" should be done. Feed storage have been developed; progress is needed to
facilities should be evaluated for clues. For
develop more objective methods to assess
example, different batches of feed may be of
human care, farmer awareness, facility
different textures or colors. Changing from
hygiene, and the stressors to which cows
one silage storage unit to another can
are subjected.

indicate a possible sudden change in diet
characteristics. Sometimes feed is

Heritability: Correlations between
purchased off-farm even from several
genetics and lameness are being investidifferent suppliers.

gated in several European countries. It is

The manure should not contain fiber
thought that different lesions may have
particles d cm of undigested grain. This
different degrees of heritable susceptibility.

can be checked by placing 2 cups of manure

There is even some proof that the benefits of in a fine mesh kitchen sieve and waslting the hoof tlimming have a heritable component.

material through with water from a hose.

In Sweden a "Bull Index" has been

Feces should not contain mucin/fibrin casts,
created so that fanners may select sires
be foamy, or contain gas bubbles. The feces
whose progeny have a low predisposition
in the same feeding group should not vary
for lameness.

from fim1 to diarrhea. Run1enocentesis can
be perfom1ed as a last resort.

Nutrition: Subacute runtinal acidosis

There should be a drinking station for

(SARA) is a common problem in high-proevery 15 cows. The water supply should oe ducing dairy herds. Volatile fatty acids
clean and free of static electlicity. A high

(VFAs) produced by microorganisms in the
level of iron in drinking water can affect
rumen are absorbed by rumen papillae. The
palatability.

papillae shrink during the dry period and
need to be developed by lead feeding. If the

Walking Surfaces: Walking surfaces are
surface of the papillae is inadequate, the pH
another important contributing cause of
of the rumen contents drops.

lameness. The Nordic countries have

Successfully managing SARA depends on
pioneered the use of rubber matting. One
the quantity and digestibility of the carbohy

UK study showed that cows enter and exit
drate fed. The more rapidly carbohydrate is
the milking parlor more rapidly on rubber
digested, the more rapidly rumen acidosis
matting than on concrete. In addition, sole
will develop. Finely ground or moist grains
horn wears less on rubber than on concrete.

are more digestible than dry, cracked grain.

Of course, rubber is fully effective only if

Com silage is frequently used in dairy
kept free of slurry. Installing rubber matting
production. Sometimes tl1e energy content of is expensive but a reasonable recommendathe silage is completely underestimated, with tion. The best flooring system from tl1e disastrous results. Slug feeding once a day is
perspective of lameness is slats with rubber
contraindicated, and the more frequently
caps, but this is reasonable only for new
concentrates are fed the better. Sudden
installations or major upgrades.

changes in the diet or fomrnlation of the diet
are extremely dangerous. Component-fed

Resting, Stress, Cow Comfort, Social
cows should be given up to 7.5% of their

Confrontation, Stocking Density:

body wt in concentrates around calving.

These risk factors together with other

After calving, it is safest if rations are not
physical stressors have been referred to as

1072

LAMENESS IN CADLE
ecopathologic factors or an Animal

Stress is a factor that can and has been

Suitability Index. TI1ese tenns refer to an
measw-ed in cows. Stress may play a role in
assessment tool for housing conditions
causing lameness, and lameness itself is a
based on seven spheres of influence: walking, cause of stress. Stress may also be an feeding, socializing, resting and comfort,
etiologic factor in both reproductive failure

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behavior, hygiene, and care. Ecopathology,
and in some types of mastitis infections.

therefore, is evaluation of space allowance,

Social confrontation may be a surprising
cubicle dimensions, stall base, bedding, stall
cause of stress. The matriarch cows
and pen measurements, type of flooring,
dominate the pecking order. Presumably, a
slipperiness, stocking density, cleanliness,
submissive animal is somewhat stressed
hoof trimming and footbathing, feed bunk
when confronted by a dominant animal in a
space, water supply, walking surlace
narrow alley. Prolonged standing, waiting
conditions, and mobility locomotion score.

in line to drink, or spending >3 hr in the

Under nonnal conditions, a healthy cow
holding yard each day are commonly
rests 10-11 hr/day. Resting periods usually
overlooked factors. Overstocking increases
last just longer than l hr, during which tin1e
the occasions on which cows of signifithe cows ruminate and thus digest their cantly different dominance will face one
feed. Lameness, depending on its seve1ity,
another. This is particularly noticeable
tends to increase both the lying time and
when heifers are first admitted to the
the number of lying bouts.

milking herd. This may also be the first time

Anything that inhibits a cow from lying
heifers ever encounter concrete. Heifers
down is of particular concern. This can be
should always be given l mo to adapt to
assessed rapidly by use of the Cow Comfort
concrete before the added stress of facing

Index (CCI), which should be calculated 1
dominant cows. Alleys should never be
hr before milking. The number of cows lying <12 ft wide, feed alleys 13 feet wide, and in a stall should be divided by the number of
loafing alleys 14 feet. There must be more
cows standing or in any way touching the
cubicle stalls and feeding standings than
stall. It is assumed that cows standing and
there are cows. All too commonly, a building
touching the stall are showing a desire to
built to hold 50 cows is modified to take
rest; thus, the higher the CCI, the more

100-150 cows, with resulting catastrophic
probable there is a problem. If the incidence overstocking.

of noninfectious lameness is also high, then
cow comfort is a risk factor to be dealt with.

Cleanliness and Hygiene: When the

Cows not involved in calculating the CCI are prevalence of digital dermatitis is unacceptthose drinking, eating, or just walking.

ably high, contamination should be reduced,

Unwillingness to lie down because of
especially if the hind ends of the cows are
remembered discomfort is another reason
caked in muck. Possibly the most comfor prolonged standing·. However, inability monly used slw-ry removal system is the
to exercise reduces the amount of oxygen
scraper fixed to the front of a tractor.

and nutrition delivered to the claw.

Although this system is acceptable, it is

Stall size is important but varies
conm1only not done often enough. Autodepending on the frame size Of the cows matic scrapers are costly to install and
in a herd. The partitions must be of spacesubject to mechanical breakdowns. The sharing design. If the overall slope of the stalls overall effectiveness of flushing systems is adequate, the cows will lie with their
remains questionable.

hindlinlbs all running in the same direction.

The presence of any slurry during a

Cows prefer sand stalls above all other
clinician visit should evoke comment.

surfaces. The sand keeps cows cool and
provides good footing to rise. Mattresses

Farmer Education: P1iority must be
filled with rubber crumbs are acceptable;
given to improving faimers' knowledge and
concrete covered with straw or sawdust
increasing their willingness to implement
and hard rubber mats are less desirable.

recommendations, including routine

When a cow rises, she is forced to lunge
exainination (by the fanner) of the herd for
forward; anything that makes that difficult
lan1e cows. However, in the UK and France,
should be corrected. Neck rails (never
lack of tin1e and labor are reported as the
cables) should be 37-43 in. above the stall.

most important bai-riers to detecting and

A brisket board is important, and flexible
treating lameness.

structures are available to reduce the risk

Special efforts should be made to
of hematomas of U1e brisket. Loose house
help farmers understand the gravity
stalls built facing a wall are a poor conand complexity of an increasing herd figuration. Cows should not be forced to
lameness problem. Worrnation pamphlets,
lie or stand with their hindlinlbs in the alley.

regional seminars, and hands-on on-farm

LAMENESS IN CADLE

1073
demonstrations with a hoof trimmer and
phlegmon (footrot). Some cows will refuse
nutritionist involved can all be useful.

to enter a formalin footbath if the solution
is stronger than 4%. Formalin has been found
of value to control digital dem1atitis. The

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solution should be changed after the passage
of -200 cows, more frequently if the bath is

FOOTBATHS
heavily contaminated with manure. Formalin
has good bacteriostatic activity and some

Dry cows (and infected heifers) should
potential to harden the epidennis. However,
be included in the footbathing routine.

it is ineffective at temperatures < 13°C.

Pennanent, concrete footbaths may

Fom1alin generates strong fmnes that
measure 3 m (10 ft) long and 0.2-0.6 m
irritate the lungs of milkers and can taint

(8---24 in.) wide. The sides of the bath should
milk. It should never be used in baths
not slope inward and should be 15---25 cm
located near the milking parlor.

(6--9 in.) deep. Cows prefer to use footbaths

The stronger the formalin solution used,
that have a bottom close to floor level;
the more effective it is, but the danger of a
therefore, a built-up block "rounded lip"

chemical burn on the cow's skin is also
could be considered in the design. The
greater. If the hair on the foot appears to be
medicated solution should be a minimwn of
standing on end or the skin is pink, bathing

8---10 cm (3--4 in.) deep. Drainage from the
should be suspended. Normally, cows can
bath should be provided to ensure the foot
tolerate twice daily baths for 3 days using
can be properly cleansed. To avoid blockage,
a 3% solution. The treatment should be
the drain hole should be 10-20 cm in diameter repeated every 3 wk. Higher concentrations and located at the lowest point of the bath.

should only be used for the most resistant

Footbaths should be located in relation
conditions.

to the exit from the milking parlor in a

Formalin is regarded as a hazardous
frost-free environment with, ideally, an area
waste, and land disposal restrictions should
suitable to drain chemicals from the feet to
be checked and followed. Fom1alin must
avoid contaminating the bedding. At all
never be released into sewer systems,
costs, deviation from the normal free flow
because sewer treatment plants may have
of cow progression should be avoided.

problems and contaminated drinking water

Prewashing the feet before entering the
could be released. However, formalin is said
footbath has been increasing in popularity.

to break down in 7 days in sludge or slurry;

Ideally, the wash bath should be located
even then, it is wise to wait until it is diluted
before the cows enter the milking parlor.

to one pa.it formalin in three parts sludge

This allows time for washing fluid to drain
before spreading it on arable land.

before cows enter the chemical bath. The

Preferably, the land selected should not
dimensions should be similar to those of
have a high water table. Unused fom1aldethe medication bath.

hyde concentrate should be returned to the

Use of a footbath is not a substitute for
vendor.

either good hygiene or claw trimming.

Footbathing with a 5% solution of copper

However, if digital dermatitis is endemic
or zinc sulfate controls interdigital
on a farm, regular use of a footbath is
dennatitis and is of some value in controlmandat01y.

ling footrot (interdigital phlegmon). There

Plastic, fiberglass, or metal portable
are two grades of copper sulfate, and the
footbaths should be avoided. A hoof mat,
pentahydrate grade should be used. The
consisting of a sheet of foam plastic encased solution must be prepared 5 hours before in a perforated plastic cover, is also
use. Prewashing of the cow's feet is advised,
available. The foam is soaked in medication
and the solution should be changed after the
that squirts up between the claws when the
passage of -200 cows.

cow walks on the mat. There are no recent

Copper has a strong affinity to be bound
reports on the effectiveness of this device.

by soil, the organic matter in manure, and

Fully automated power spray washers are soil minerals. Hence, much of the copper claimed to be extremely economical in the
found in soil is unavailable for plant uptake.

use of water, and they require no operator.

Once the copper reaches a high level in the

They deliver soapy water, and some users
soil, the process caimot be reversed.

believe this device alone reduces the

Therefore, plants stunted by high levels of
incidence of foot disease.

copper have a lower nutritional value to
cattle. Copper sulfate footbath solutions

Chemical Agents for Footbaths:

may be tagged to slurry at the highest

Formalin 4% is the least expensive footpractical dilution and spread widely on bath solution for the control of interdigital
the land.

1074

LAMENESS IN CADLE

The sulfates are quite rapidly deactivated
surfaces, the lateral hind claw tends to wear
by combining with the proteins in manure.

less than the medial.

The use of antibiotics in footbaths has

If claws are routinely correctly trimmed,
been a popular past strategy for the
longevity of the herd may be extended.

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treatment, control, and prevention of digital

Trimming can be expected to decrease milk
dermatitis. Few reports on the use of
yield by up to 2 lb/day for 2 clays but should
antibiotics in footbaths appear in the
be restored or even increase in a similar
current literature. Antibiotics are expensive
period. Decrease in milk yield is partly due
and deteriorate in contaminated solutions.

to disrnption in the cow's feeding routine

The type of antibiotic used in footbaths
and handling. To some extent, variations
should be changed at intervals of -6 mo to
in milk yield reflect on the skill of the
avoid development of resistant strains of
trimmer. Trimming should be avoided in
the causal organisms. However, treatment
any location close to the milking parlor,
may be given for 2--3 days and repeated
and individuals handling the cows should
once after 7 days. Formalin footbaths may
never attempt trimming. Unskilled claw
be used alternately if more aggressive
trimming will negatively affect the claw
treatment is necessary. Antibiotics used in
health of a herd and should be avoided.

footbaths do not result in detectable levels

All claws should be evaluated before
of drng in the bloodstream or milk.

trimming. On average, the front ( dorsal

Antibiotic sprays or powders are still used
surface) wall of a hind claw measures
for topical treatments.

-7.5 cm long from apex to hair line. When

A new generation of chemical agents has
the dorsal wall increases in length, the
been developed for use in footbaths, but
dorsal surface of the claw tends to become
claims of effectiveness have not yet been
concave (buckles like the instep of a
adequately substantiated in controlled
hun1an shoe). This causes greater
trials. Foan1s are also available but the cost
weight-bearing to be transferred to the
of associated equipment is considerable.

posterior aspect of the claw, increasing

Foan1s keep the chemical agent in contact
pressure on the flex or process of the distal
with lesions better than liquid products.

phalanx, the point beneath which sole
ulcers develop. The longer the toe, the

FUNCTIONAL CLAW TRIMMING
greater the stress on the flexor system.

When the claws are short and the dorsal

The role of the professional claw trimmer
wall is> 7.5 cm, there is considerable risk
has changed significantly during the past
that the thickness of the sole at the apex
decade. The introduction of chute-side
will be less than the desirable 7 mm.

computerized data collection is providing

Thinning of the apex of the sole of
valuable data; however, it also requires
shmt-clawecl animals should be avoided.

additional training in lesion identification.

Foot trin111ting of every cow in a

Close collaboration between trimmer and
high-production, intensively managed herd
vete1inarian is beneficial for both as well as
is reconunended every 5 mo. Recording and
for the dairy industry overall.

reporting (to the veterinarian) the types of

Over time, the claws of cows wear,
lesions observed will prompt early
changing the shape of the sole, which in
treatment and timely introduction of
tum makes the foot unstable. The two claws preventive measures.

become unbalanced both longitudinally and
laterally. As changes develop in the lateral
claw, it becomes "overloaded," the heel
horn may become thicker ( overburdened),
and posture is compromised. Therefore, the
objective of trimming is to reduce excessive
weight bearing on load-bearing claws.

Although there are many in1po1tant lesions,

Under nmmal circumstances, horn
most lameness protocols are based on data
growth keeps pace with wear. The growth/
from digital dermatitis, sole ulcer, white line
wear rate at the heel is greater than at the
disease, toe necrosis/apical syndrome, and
toe. Hom that is dry tends to be extremely
sole hemorrhage. Early identification of
resistant to wear and may grow longer than
lesions pennits early treatment, which
nonnal. Thus, tl1e claws of cattle maintained significantly reduces the recovery period.

in straw yards tend to become overgrown.

The incidence of lameness in pastured

Conversely, the claws of cattle maintained
dairy cattle in New Zealand is extremely
in extremely wet conditions are softer than
low; the risk factors associated with
normal and more prone to wear and
housing do not exist in that country. Pasture
dan1age. If the cows are housed on concrete
management is also conunon in Chile.

LAMENESS IN CADLE

1075

DIGITAL DERMATITIS
vary considerably in size and appearance
both within a herd and in different parts of

(Hairy warts)

the world.

Digital dem1atitis is the most common

The following system has been developed

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disease of the feet of mature dairy cattle and to classify the stages of tllis disease: MO =
is endemic in intensively managed dairy
nom1al skin; M l = early, small circumoperations worldwide. It tends to mask or scribed red to gray epithelial defects of <2
overshadow other more painful lesions
cm in dian1eter preceding the acute stage,
present concurrently. Incidence is low in
appeanng between acute episodes or within
pastoral settings such as in New Zealand
the margins of a chronic M4 lesion; M2 =
and Chile. The presence of the disease in
acute, active ulcerative ("strawberry -like") beef cattle appears to be rnininlal.

or granulomatous (red-gray) lesions >2 cm
in dian1eter and sometimes surrounded by

Clinical Findings: Two main types of
wllite halo-like tissues, which may be
lesions are seen. The erosive/reactive fonn
slightly papillomatous; M3 = tl1e healing
is seen more conunonly in Europe, whereas
stage occurring within 1-2 days after topical
the proliferative or wart-like fonn is more
therapy, with the lesion covered with finn
prevalent in North America. Both fonns
scab-like material; M4 = the chronic stage'in
cause varying degrees of discomfort and
which the epithelium is thickened and/or
may give rise to severe lan1eness. Both
proliferative (filan1entous or scab-like) and
forms can be seen in the san1e animal. The
several centimeters in dian1eter.

two forms likely represent different stages
of the san1e disease process.

Treatment: Acute lesions are initially

Explosive outbreaks can occur when
treated topically. The lesion should be
affected cows are introduced to previously
scrubbed clean witl1 a stiff brush and soapy
unaffected herds.

water, rinsed, and d1ied. An antibiotic

1)·eponema-like organisms can be
powder such as oxytetracycline is applied
observed in microscopic san1ples isolated
and protected by a gauze pad or a small
from most lesions. However, the number of
feminine hygiene pad held in place by a
strains of TI·eponema affecting cattle can be waterproof bandage or a reinforced nylon as high as 80, some of which may be oral or
device (booties) that can be affixed with
rectal. It would be wise not to incriminate
hook-and-loop-tape closures. Multiple
just one strain as the cause because of the
treatments are usually necessary. Oxytetranumerous manifestations of digital cycline treatment has not resulted in
dermatitis. Digital dermatitis is likely to
detectable residual levels of the antibiotic in
be polytreponemal (eg, Tphagedenis,
blood or milk. Extremely high parenteral

T vincentii, and T denticola ).

antibiotic dosages have been reported to

Digital dermatitis is much more prevalent
help resolve severe lesions.

if hygiene is poor and the feet are exposed

Once a lesion has started to heal, topical
frequently to slurry. It is widely believed that dressings may be sprayed on with a a number of predisposing bacteria are
pressurized backpack spray unit. Soluble
involved. It has been postulated that the
oxytetracycline or lincomycin-spectinomyonce ubiquitous Dichelobacter nodosus cin (66 g and 132 g/L of water, respectively)

may be an important synergizing agent;
produces the best results. Contamination of

Campylobacter spp and PrevoteUa spp may the lesion must be avoided at this stage.

also be involved in the etiology.

Although apparent resolution can be

Skin maceration and the presence of a
achieved, recun·ence seems almost
semi-anaerobic environment are important
inevitable, and fanners should be so
predisposing factors. Many treponemes are
advised.

found in the deeper layers of the epidemlis,
some of which are believed to reach these

Control: There are no effective vaccines.

layers of the epidemlis via hair follicles.

The following methods are used in control:

A relatively weak immune response has

1) Automatic power washing of the feet
been detected in naive cattle.

with soapy water before ente1ing the
milking parlor. 2) Passage through a

Lesions: Lesions are most common in the
medicated footbath after passing through
region of the flex or commissure of the
the milking parlor with a 30-min drainage
interdigital space. Less typically, lesions
period. 3) Diligence in ensuring the
have been seen on the dorsal surface of the
environment is regularly freed from slurry
foot as well as arow1d the dewclaws. One or
and liquid contamination. 4) If digital
both hind feet are most commonly involved,
dermatitis is not present, replacement
although forefeet can be affected. Lesions
animals should not be introduced and the

1076

LAMENESS IN CADLE
herd should not be exposed to vectors such

Clinical Findings: The progress and
as unsterilized instruments or visitors' dirty
severity of lameness are variable and often
boots.

masked in bilateral cases, depending on the
size of the lesion and extent of the second

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PODODERMATITIS
ary infection. Because the lateral hind digit

CIRCUMSCRIPTA
is usually involved, the limb is often held
slightly abducted with weight-bea.iing on

(Sole ulcer)

the unaffected medial digit. In tie stalls,

Sole ulcer is generally regarded as the most
the hind toes may be rested on the edge
in1portant, prevalent, and costly of the
of a curb in an attempt to relieve pressure
noninfectious lesions. All too frequently, it is on the heel-sole junction. On flat surfaces, the cause of culling. Sole ulcers commonly
an affected cow stands with the hindlirnbs
affect one or both lateral hind claws,
camped back. Some cows may shake the
predominantly in heavy, high-yielding dairy
affected foot frequently, whereas those
cattle kept under confined conditions. A
with bilateral lesions may continually shift
sole ulcer is a circumscribed lesion located
weight from limb to limb and frequently lie
in the region of the sole/bulb junction,
down.

usually nearer the axial than abaxial margin.

The earliest stages of this lesion may be

Damage to the demtis is associated witl1 a
discovered during routine claw trimming.

circumscribed zone of localized hemor

As sole horn is removed from over the
rhage and necrosis. The incidence is
typical site, a hemorrhagic lesion may be
variable, but in some herds up to 40% of
exposed. The clinical lesion varies from a
mature cows can be affected.

soft, slightly discolored area that may be

Recently, Treponema-like organisms
painful under pressure to a distinct bright
have been identified in these lesions.

red knob of granulation tissue. This is often
the stage at which lameness becomes

Etiology and Pathogenesis:

severe enough to be noticed. Once the

Sinking
cori..um is exposed, infection can invade the
of the claw due to activation of matrix
deeper structures of the claw and spread
metalloproteinase, which is a feature of
proxinlally to involve the navicular bursa,
subclinical larnirtitis, is the major predisposing factor. As the space between the flexor process of the pedal bone narrows, the
coriurn is crushed, causing ischernic
necrosis and compromising horn production. This results in a hole forming in the sole. As the damaged corium undergoes
repair, granulation tissues erupt through the
hole in the sole. Because this condition is
strongly associated with subclinical
lan'linitis, some softening of the sole horn
will occur. This increases the rate of horn
wear. The sole horn also softens under very
unllygienic conditions when horn is
exposed to the fluid component in slurry.

Iatrogenic forms of the lesion are produced
when inexperienced claw trimmers remove
too much horn from beneath the heel ( and/or
the posterior region of the abaxial wall),
resulting in abnonnal pressure on the demtis.

Excessive wear of the softened sole horn
flattens and thins the sole.

Heel erosion is another potential
contributing cause of a sole ulcer. N onnally,
weight is borne by the anticoncussive
qualities of tl1e bulb of the heel, but if heel
erosion occurs, weight-bearing may be
transferred forward to the region beneath
the flexor process. Sometimes, a displaced
pad of horn slips over to the vulnerable

Sole ulcer over flexor process of distal phalanx.

area, causing abnormal pressure over the

The heel has been lost due to heel erosion.

flexor process of the distal phalanx.

Courtesy of Dr. Paul Greenough.

LAMENESS IN CATILE

1077
resulting in necrosis of the flexor tendon

The corium becomes infected through this
and ligaments of the navicular bone. A
lesion.

retroarticular abscess may develop, which

White line disease is often referred to as
may be further complicated by infection of
also being present in the apical region.

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the distal interphalangealjoint (seep 1088). Technically, this is true, but this type of Rupture of the flexor tendon leads to
lesion will be described as a component of
dorsal rotation (upward) of the toe
the toe necrosis syndrome (see below).

("cocked toe"). In complicated cases,
infection may progress up the deep flexor

Clinical Findings: The affected cow may
tendon sheath.

adduct its hindlimb(s). The abax:ial wall
may seem a little longer than normal, and

Treatment: Treatment must be aimed at
occasionally there may be slight swelling
removing pressure from the affected area.

and erythema of the coronary band above

Skillful therapeutic claw trimming is highly the heels.

effective. This procedure lowers the entire

The lateral claw of the hind foot ( often
bearing surface of the lateral claw, which
both) is usually involved. If bilateral, the
transfers loading to the sound medial claw.

disease may remain unnoticed W1til

Applying a "lift" has become the accepted
lat11eness is more pronounced in one limb
treatment for this condition. The simplest
than the other. Because the outer hind claw
form of lift is a wooden or rubber block
is affected, the limb is swung away from the
glued or nailed to the unaffected medial
body during each stride. The cow may stand
claw, thereby removing all weight-bearing
with the medial claw bearing weight. White
from the ulcer region. Recently, various
line separation without complications is
models of easier-to-apply plastic slippers
frequently seen at claw trimming. The
have been developed. Care must be taken
degree of pain and lameness depends on
when applying either a block or a slipper
the rate of development and extent of the
to avoid the sharp, hard, rear edge of the
subsolar abscess. Routine examination
device from causing pressure under the
of the sole must include the complete
sole. Blocks should be removed after -1
exploration of the abax:ial white line region.

mo to avoid causing damage to the sole.

Black marks must be explored with the tip

Protruding granulation tissue need not be
of a hoof knife as potential sites for track
excised and must not be treated with any
fonnation. Discharge of pus from the skin/
caustic agent, because this can retard
homjW1ction above the abax:ial wall is
healing. Bandages should not be applied,
always reason to suspect a white line lesion.

because this results in continued weight

In these cases, the white line must always
beating at the ulcer site. Furthermore,
be exanlined very carefully.

covering the lesion causes it to remain moist
and promotes maceration and bacterial

Etiology and Pathogenesis: The
infection.

lamellar/latninar atTangement is longest

Many ulcers never fully resolve, and
behind the wall on the dorsal side of the
affected cows may have chronic, low-grade
hoof. This an·angement gets shorter toward
lameness and need corrective foot trimming the heel and more or less disappears at the 3-4 times/yr for their productive lives.

abax:ial groove. That is not to say that the
collagenous fibers cease to exist in the other

Prevention and Control: Because the
regions of the dennis; it can be postulated
development of sole ulcers is intimately
that adhesion between wall and corium
related to subclinical laminitis, the latter
could be less intense. At the san1e time,
should be investigated and appropriate
beneath the bulbar region is the structure
control measures instituted (seep 1083).

known as the digital cushion. During
locomotion, the digital cushion is com

WHITE LINE DISEASE
pressed and expands toward the abax:ial
wall. Thus, this region is not only structur

White line disease is almost as prevalent as
ally weaker than more dorsal areas but is
sole ulcer and can be just as difficult to treat
also subjected to a different set of pressure
satisfacto1i.ly. Together with sole ulcers,
and mechanical stresses. The white line is
white line disease commonly affects one or
composed of very soft horn, which fills the
both lateral hind claws, predominantly in
spaces between the lan1ella at the most
heavy, high-yielding dairy cattle kept w1der
distal extremity of the wall. It is postulated
confined conditions. White line disease is
that stretching of collagen fibers, combined
characterized by hemorrhage into or
with sinking of the pedal bone, accounts for
separation ( avulsion) of the abax:ial wall,
the hemorrhage into the white line so
most commonly at the heel-sole junction.

frequently seen.

1078

LAMENESSINCATILE

Solid foreign bodies may lodge in the
understood. However, Treponema-like
softened, widened white zone. They may
organisms have been isolated from all of
push through to the corium beneath and
these lesions.

introduce infection; however, the presence

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of a foreign body is not essential for the

Etiology and Pathogenesis: Lesion
lesion to develop.

1-As subclinical Jantinitis progresses, in

There are three possible sequelae of localsome cases the distal phalanx will rotate.

ized infection: 1) a localized abscess may

Movement of the apex of the pedal bone
develop; 2) infection may be forced
will cause tearing of tissues, with resultant
proximally to form a track that may
hemorrhage. In extreme instances, the tip of
discharge at the coronary band; and 3) the
the bone will prolapse tlu·ough the apex of
infected track may, as it forces its way
the sole. Many cows witl1 a rotated digit also
proximally, infect other structures,
have a ridge (the reaction 1idge) running
depending on the site of the initial infection.

around the wall. The 1idge is sin1ilar in

An anterior track can infect the distal
location to a hardship groove and is
interphalangealjoint directly. Tracks
displaced distally in a sin1ilar manner.

fom1ing closer to the heel are likely to cause

Osteomyelitis of the distal phalanx can
infection of the bursa of the deep flexor
be seen in complicated cases.

tendon. Invariably, the bursa ruptures into

Lesion 2-Many cases have been reported
the retroarticular space, and an abscess
anecdotally in which the anterior half of the
develops in this location. Infection of the
sole has been worn down almost paper thin.

distal interphalangealjoint and the tendon

Hemorrhage from brnising is seen tl1rough
sheath of tl1e deep flexor tendon may follow. the thin horn at the apex. Breakdown of the Necrosis and avulsion of tl1e insertion of the
horn and forn1ation of an abscess have been
deep flexor tendon into the distal phalanx
reported. One probable cause is a painful
are frequent complications. These cases are
lesion in the heel, which forces the cow to
easily detected as the apex of the pedal
throw most of its weight onto the anterior
bone unrestricted by the flexor tendon
part of the sole.

tips up.

Lesion 3-The incidence of apical necrosis

Swelling of tl1e heel bulb represents the
can be quite high in young feedlot cattle,
most advanced fom1 of white line disease; it
many of which become recwnbent and die
is frequently misdiagnosed as footrot ( often
of pneumonia. The condition is sporadically
presented as a case of footrot resistant to
repo1ted in mature cows.

treatment). Footrot causes the whole foot

The main blood supply to the digit is the
to swell evenly to the fetlock; in contrast, a
very large axial digital artery, which is
retroarticular abscess leads to enlargement
vulnerable to pressure from the sharp
of only one heel bulb.

proximal edge of the axial wall. This artery
connects with the teffilinal arch that

Treatment: During a claw exanunation,
penetrates across the bone. Necropsy
any black mark in the white line must be
reveals that necrosis occurs distal to this
cut out until healthy horn is expooed. For
artery, and radiographs tend to suggest the
a local abscess, removal of an elliptical
same thing. The teffilinal aitery marks tl1e
segment of the wall adjacent to the lesion
margin at which patl1ologic fractures of tl1e
aids free drainage by providing a self-cleansdistal digit can be seen.

ing abaxial opening. Cream-colored pus

Necrosis of tl1e apex of tl1e pedal bone is
may indicate a corporeal response to tissues extremely conunon in yeai·ling beef calves tearing as collagen fibers stretch and the
after transportation over long distances. In
pedal bone sinks. In contrast, if tl1e pus is
either case, it is suspected tl1at standing for
black, it is likely that infection has
long periods is tl1e cause. Current laws in
penetrated from the outside.

Nortl1 America require tl1at cattle be

Abscessation at the coronary band is
unloaded and watered every 40-52 hr.

usually indicative that white line disease is

It is thought tl1at long periods of standing
present. The same applies to a retroarticular without exercise allow the blood to pool in abscess. Cases of nonhealing white line
the feet and damage tl1e tissues. During
disease have been reported.

locomotion, tl1e coronary cushion with tl1e
aid of venous valvules functions as a pump

TOE NECROSIS SYNDROME
to return blood to the general circulation.

The tern1 toe necrosis syndrome covers

Treatment and Control: Treatment
three different etiologies for a condition
is cost effective only in animals witl1 no
having a similar appearance. The three
obvious complication. The cavity should
different etiopatl10logies are not completely
be cleansed, dried, and packed witl1 an

LAMENESS IN CADLE

1079
antibiotic powder. If no changes occur after
thoroughly dried. Next, a fast-setting
a few days, the lesion may be covered with
adhesive is applied along the border of the
methyl methacrylate. If the bottom of the
axial and abaxial wall. The objective is to
lesion is black, a probe should be inserted; if
create a ridge on the wall that does not

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necrotic tissue can be detected, 1 -2 cm of the involve either the white line or sole. This apex of the toe should be removed under
layer is allowed to dry and harden before a
regional anesthesia with hoof cutters. The
second application of fast-acting adhesive is
condition of the pedal bone should be visible.

made. The block is set in place and held by a

If necrosis of the bone is confumed, a further
self-adhesive bandage until the fixative has

1-2 cm of toe should be removed. If the
fully set. Sufficient soft setting material is
wound bleeds profusely, it is likely that
then ir\jected through the hole in the block
necrosis is not extensive. When hemorrhage
to entirely fill the space and exert very
is minimal, it is probable that necrosis of the
gentle pressure on the dermis.

bone is extensive or a physiologic fracture is
present. There are several reports of the toe

HEEL EROSION

(not the claw) having been amputated with
satisfactory recovery. Systemic antibiotics

(Slurry heel)

and application of a lift to the sound claw is
advised. If the wound is obviously contami

Heel horn erosion is seen as a change in the
nated, the lesion should be packed with a
appearance of the surface of the bulb of the
hygroscopic mixture (500Ai magnesiwn
heel. Because heel horn erosion alone does
sulfate and 50% glycerin) and bandaged for
not always cause lameness, the true
a maximwn of24 hr, after which the lesion
incidence is unknown. However, subjective
should be thoroughly dried, dressed with
observations suggest that once cows have
antibiotic powder, and closed with methyl
been exposed to copious slurry, the
methacrylate.

incidence of heel erosion rapidly approaches
l OOOAi. In some cows, heel horn erosion
advances to a point at which complications

SOLE HEMORRHAGE
develop and lameness may be apparent.

Sole hemorrhage is by far the most conunon

Etiology and Pathogenesis: The etiology
noninfectious lesion in lan1e cows. It is
is unknown. Heel horn erosion is perhaps
regarded as a typical sign of laminitis but is
more conunonly seen in herds in which
frequently overshadowed by bmising of the
subclinical lanunitis has been diagnosed and
sole. Blood stains in the sole of the hoof are
in herds affected by digital dermatitis. It is
the most commonly seen abnormality of the
also more commonly seen during the winter,
sole. When subclinical lan1initis was first
particularly when the claws are exposed to
described, sole hemorrhage was considered
an w1hygienic, moist environment ( eg,
to be an invariable clinical sign. It was
intensively managed dairy units).

thought that the arteriovenous shunts in the
solear papillae were compromised, allowing

Clinical Findings: The first lesions seen
blood to perfuse down the tubules, giving a
are small circular erosions <0.5 cm in
bmsh-like appearance. Since then, solear
diameter. As the condition advances, these
hemorrhages have increased in prevalence.

lesions merge, and ridges form parallel to

This may be due to cows being forced to
the hair line on the axial surface of the bulb.

stand on concrete for longer periods than

Invariably, the color of the roughened area
previously. Bmising/trauma is more likely to is black. At this stage, the cow is not lame.

occur if the horn is softened by moisture, or

In the secondary phase, the appearance
if the quality of the horn is reduced because
of the heel varies. In some cases, there is a
of some nutritional error or because the
buildup of horn beneath the heel. Simultathickness of the sole is reduced too much neously, there may be a loss of horn under
during hoof trimming. Interpreting the tme
the axial part of the bulbs. The excessive
cause of solear hemorrhages can be
accwnulation of horn is often more
important.

pronounced in the lateral claw and causes
the hock to tum in (cow-hocked stance).

THIN SOLE

This stance resolves after therapeutic claw
trimming. Generally, the condition is

As the term "thin sole" in1plies, the anterior progressive wuess corrected. The
region of the sole has worn very thin due to
disturbance interferes with shock
excessive weight bearing on that region. An
absorption, and the animal throws more and
innovative method to treat "thin sole" begins more weight forward. A common concurby drilling a 1 O-nu11 hole through the center rent lesion is a sole ulcer. In other cases,
of a wooden block. The claw to be treated is
erosion completely denudes the heel of

1080

LAMENESS IN CADLE
organism of interdigital dermatitis may
be in1plicated in the etiology of digital
dermatitis.

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Etiology and Pathogenesis: Interdigital
dem1atitis is caused by a mixed bacterial
infection, butDichelobacternodosus has
been considered to be the most active
component. D nodosus is an anaerobe and
exceptionally proteolytic. The source of the
infection is the cow itself, and the .infection
spreads from infected to noninfected cows
through the environment. D nodosus cannot
survive for >4 days on the ground but can
persist in filth caked onto the claws, creating
an anaerobic environment. The bacteria first
invade the epidernlis of the skin between
the claws but do not penetrate to the dermal
layers. As the condition progresses, the
border between the skin and soft heel horn
at the posterior conunisure disintegrates,
producing lesions similar to ulcers or

Heel erosion with a wide claw and black
erosions. At this stage, the lesions cause
necrotic horn. Part of the sole over-reaching
discomfort. In tied systems, the hindlimbs
the interdigital space. Courtesy of Dr. Paul
are affected more often than the forelimbs.

Greenough.

In loose housing systems, the distribution
between fore- and hindlimbs is about equal.

horn-a process that also interferes with

Animals on slatted floors are affected less
shock absorption and can be associated
often than anin1als on solid floors.

with a sole ulcer. Treponema-like organisms have been observed in microscopic samples

Clinical Findings: The early stages of the
of heel horn.

condition appear as an exudative dermati

Heel horn erosion must not be confused
tis. The exudate oozes to the conmlissures
with separation of the heel, which is the
of the interdigital space and forms a crust or
result of the escape of pus from an abscess
scab, which may be observed occasionally
close to the heel.

on the dorsal surface of the digits. As the
condition progresses, the animal shows

Treatment and Control: Both heels
discomfo1t by "paddling," or constantly
should be reduced to the same height by
moving from one foot to the other. If the
paring away excess horn. Careful attention
heels of tl1e hind feet are especially painful,
must be paid to maintaining the bearing
the limbs are held further back than normal.

function of the abaxial wall and sloping the

True lameness does not develop until a
sole toward the axial border.

complicating lesion is present. After a

Attention to hygiene and reduction of
prolonged period, during which the animal
slurry are essential. The claws of dairy cows
has avoided bearing weight on the heel, the
should be trimmed twice each year. A weekly horn beneath the heel increases in thickness foot�ath (where pennitted, 3%-5%fo1malin), and some aberrations of gait result. In dairy starting no later than October m the northern cows, interdigital hyperplasia ( corns, hemisphere, should be provided.

fibroma) may be caused by the chronic
irritation of the interdigital space. Often,
the fibroma develops on one side of the

OTHER DISORDERS OF THE
interdigital space.

Foot-and-mouth disease can be confused

INTERDIGITAL SPACE
with interdigital dennatitis if the interdigital
space is not always examined carefully.

INTERDIGITAL DERMATITIS

Treatment: Systemic therapy, including the
use of antibiotics, is not cost effective. In

(Stable footrot, Slurry heel, Scald)

severe cases, the lesions should be cleaned

Since the widespread appearance of digital
and dried, after which a topical bacteriostatic
dern1atitis, interdigital de1matitis is rarely
agent is applied, eg, a 500/o mixture of
reported. This may in1ply that the causal
sulfamethazine powder and anhydrous

LAMENESS IN CA

TILE

1081
copper sulfate. Alternatively, an animal can be
week. The fore- or, more commonly, the
confined in a footbath for 1 hr, bid for 3 days.

hindlimbs can be affected, but more than
one foot is rarely involved at the same time

Control: Good management and housing
in mature cows. However, footrot can

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systems that keep claws dry and clean are
occasionally develop in several feet in
most important. Regular foot trimming
calves. The first sign is swelling and
helps avoid complications. Footbathing,
erythema of the soft tissues of the interdigibeginning in late fall and before clinical tal space and the adjacent coronary band.

cases can be identified during high-risk

The inflan1.lllation extends to the pastern
periods, is essential in herds known to be
and fetlock. Typically, the claws are
infected. Weekly footbathing may be
markedly separated, and the inflammatory
sufficient in the late fall, but the frequency
edema is uniformly distributed between the
may have to be increased in late winter.

two digits. The onset of the disease is rapid,
and the extreme pain leads to increasing

INTERDIGITAL PHLEGMON
lameness. In severe cases, the animal is
reluctant to bear weight on the affected foot.

(Footrot, Foul in the foot)

Fever and anorexia are seen. The skin of the

Footrot is a subacute or acute necrotic
interdigital space first appears discolored;
infection that originates in the interdigital
later, it fragments with exudate production.

skin, leading to cellulitis in the digital region. As necrosis of the skin progresses, Footrot has a worldwide distribution and is
sloughing of tissue is likely to follow.

usually sporadic. It may be endemic in

A characteristic foul odor is produced.

intensive beef units or in cattle at pasture.

If the disease proceeds unchecked,

The incidence varies according to weather,
weight loss is severe and milk yield is
season of year, grazing periods, and housing
significantly reduced. Milk production may
system. Footrot is presented less commonly
not recover during the current lactation.

today than decades ago, partly because

Open lesions can be infected with secondmore cases are treated by farmers and partly ary invaders. If the necrotic lesion is located because dairy cows spend much less tin1e at
in the anterior region of the interdigital
pasture. However, on average, footrot
space, the distal interphalangealjoint can
accounts for up to 15% of foot diseases.

become infected.

The appearance offootrot in loose

Hematogenous infection of the tissues
housing systems has been reported.

of the interdigital space may account for
peracute cases of footrot, which are

Etiology and Pathogenesis: Injury to
referred to as either "blind" or "super foul."

the interdigital skin provides a portal of

This form of footrot is characterized by the
entry for infection. Maceration of the skin
initial absence of a skin lesion, extreme
by water, feces, and urine may predispose
pain, and the tendency to progress despite
to injuries.

aggressive tl1erapy.

Pusobaclerium necropfwrum is
considered the major cause of footrot. It

Treatment: Most treated animals recover
can be isolated from feces, in which it may
in a few days. Good results are obtained
survive as a saprophyte, which may explain
with penicillin G, IM, for 3 days. Treatment
why control is difficult. It can also survive in
should be administered as soon as signs are
moist soil.

observed. However, the label dosage may be

F necrophorum is a gram-negative,
inadequate to effect a rapid resolution, and
nonspore-fornling, nonflagellated, non.moincreased dosages may be needed, requiring tile, pleomorphic anaerobic bacteria It has
increased withdrawal times. Treatment of
alipopolysaccharide endotoxin capable of

"super foul" must be particularly aggressive.

necrotizing activity. There are three sub

Early cases respond well to single doses of
species and a nun1ber of genotypes, each of
long-acting oxytetracycline.

which targets different tissues. When PCR

Sodium sulfadimidine solution IV or
assays become more widely available, the
trimethoprirn/sulfadoxine, IV or IM, bid
genotypes will be more readily identifiable.

for 3 days, can also be used. A single oral

Other organisms, such as Dichelobacler
administration of a long-acting bolus
nodosus, Staphylococcus aureus,
containing baquiiop1im/sulfadirnidine

Escherichia coli, Trueperella pyogenes,
may be suitable to treat beef cattle.

and possibly Bacl.eroides melaninogenicus

High concentration of an agent in the
can also be involved.

target tissues can be achieved by a regional

IV injection (seep 1068). Positive results

Clinical Findings: Research suggests that
have been obtained with penicillin or
the incubation period of footrot can be a
oxytetracycline.

1082

LAMENESS IN CADLE

Local treatment is essential for some
the distal interphalangeal ligament. The
longstanding cases and in all instances in
claws splay, and the interdigital skin is
which the anterior region of the interdigital
stretched. When not involved in weight
space has been compromised. The lesion
bearing, the skin folds outward and

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must be thoroughly cleansed, but it is
subcutaneous scar tissue develops. In these
inadvisable to curette or otherwise remove
cases, a mass tends to develop in the axis of
necrotic tissue surgically. The dorsal pouch of the interdigital space. The mass may the distal phalangealjoint is very superficial
become so large that it touches the ground
at this point. A nonirritant bacteriostatic
and may become necrotic. There may be a
agent (such as nitrofurazone or a sulfa
heritable disposition in some breeds such
preparation) should be applied as a topical
as Herefords.

dressing. The application of gauze, cotton

Corns are reported frequently in dairy
batting, or bandages is contraindicated.

cows when their feet are continually

However, the lesion can be protected and
exposed to slurry, chronic irritation, or have
immobilized by binding the digits together
interdigital dermatitis. Organization of areas
with a bandage. The entire digital region can
of irritated skin on one side or other of the
be protected from contamination if it is
dorsal conunisure accounts for developenclosed in a plastic bag fixed in place with ment of corns in dairy cows.

an adhesive bandage. However, prolonged

Interdigital hyperplasia affects forelimbs.

protection is not advocated, because the

Lameness results more often than not. As
enclosed lesion tends to macerate further.

the lesion becomes larger, its surface may

Bandages, if used, should be replaced daily.

become excoriated, sore, and infected.

Prevention and Control: Animals

Treatment: In simple cases, treatment
actively shedding infectious organisms
may be unnecessary. For surgical removal,
should be isolated until signs of lan1eness
the animal should be sedated, and dorsal
have disappeared. If this is not possible, a
and flexor regional nerve blocks adminiswaterproof dressing or protective boot tered (seep 1068). Surgery can be perfonned should be applied; however, animals wearwith the animal standing or in lateral ing protective boots should be monitored
recumbency. After preparation of the
carefully to avoid additional dan1age. Boots
surgical site, a tourniquet is applied and the
should be disinfected between use.

claws separated manually or with retrac

Because busy traffic areas are invariably
tors. The mass is removed, leaving as much
heavily contanlinated, steps should be taken of the interdigital skin as possible. If any fat to ensure that areas around drinking
protrudes when the claws are pressed
troughs, gateways, and tracks are adetogether, it should be removed. Care must quately drained. Animals at pasture might
be taken to avoid cutting deep structures
be moved to a clean, dry area, or possibly
such as the distal interphalangeal ligan1ent.

housed during periods of heavy rainfall.

After surgery, the wound should be dressed

Contanlinated concrete must be frequently
with an antibiotic powder and the claws
cleaned and scraped free of n1anure.

bandaged closely together. Some field

Preventive use of a footbath with an
reports suggest considerable success with
antiseptic and astringent solution ( eg,
wiring the toe together. Movement of the
copper or zinc sulfate [7%---100/o in water])

wound or separation of the claws must
has given beneficial results. Fonnaldehyde
be avoided until ---10 days after surgery.

solution (3%---5% in water) can also be used.

Cryosurgery is also an option.

Ethylenedianiine dihydroiodide has been
used as a feed supplement for prevention,
but the results are extremely uncertain.

Vaccines against F necrophorum have failed
because of the weak immune response to the
bacterium. High levels of zinc fed as a

The genetic relationships between what are
supplement have a beneficial effect by
now considered to be lamanitic-related
improving epidermal resistance to bacterial
claw disorders have been found to be
invaders.

moderate to high.

INTERDIGITAL HYPERPLASIA

LAMI.NITIS

Equine and bovine laniinitis are distinctly

(Corns)

different. Although acute lanlinitis occurs in

Etiology and Pathogenesis: In heavy
both species and can be caused by grain
beef breeds, the condition is thought to
overload, other etiologies can affect the
result from stretching of the insertions of
equine laniinae. A major difference between

LAMENESS IN CATILE

1083
the two species is anatomic, in that the
in this case is any physical insult causing
lan1ellar/lam.inar surface of the equine hoof
stress. This probably leads to the release of
is considerably more extensive than that of
bioactive messengers into the bloodstream.

the cow.

One important risk factor is traun1a; many

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For chronic laminitis, seep 1086.

clinicians are convinced that hard flooring is

Subclinical laminitis is almost certainly
equal in importance to nuttitional problems.

an incorrect desc1iptor for the disorder( s)

Care must be taken when dry cows and
observed. The condition has been referred
heifers are introduced to concrete after
to as claw horn disruption, but use of this
being accustomed to soft flooring.

term is misleading.

Subclinical lall1initis is of considerable

Pathogenesis: Although the release of
economic importance to the dairy industry,
biologic messengers into the bloodstream is
because it predisposes mature anin1als to
known, identification of the agents tl1at play
sole ulcer, white line disease, or the toe
a part in lan1initis is ongoing. Epidermal
necrosis syndrome. It has been seen in most
growth factor (EGF) recepto1s are present
developed countries and is of greatest
in the basement membrane of the corium. of
concern in high-production, intensively
the claw. EGF is liberated in large quantities
managed herds.

from the GI tract when it is damaged ( eg,
nunenitis) and could be involved in the

Clinical Findings: There are no definitive
pathogenesis of lall1initis. In addition to its
clinical signs of subclinical laminitis.

mitogenic effect, EGF can inhibit the

However, in any group of cows presented
differentiation of keratinocytes in vitro.

with the same set of insults, a few cows may

Inhibited differentiation of keratinocytes of
show slight signs of the subacute forn1 of
the hoof matrix is a dominant morphologic
the disorder. Some cows with subacute
feature in the early stages of laminitis. This
lall1initis may walk in a deliberate, careful
supports the hypothesis tl1at lan1initic
manner with the legs canied beneath the
histopathologic changes result from an
animal when walking. When standing, such
inadequate regulation of gelatinase activity,
animals tend to draw all four feet under the
resulting in selective degradation of
body. Erythema and edema (puffy foot) of
basement membrane components due to

U1e skin above the coronary band and
failure of the basement membrane-epideraround the dewclaws in freshly calved cows mis attachment.

may indicate a transitory la.mini.tis-like

More recent investigations have studied
insult and that the cows are being introthe role of matrix metalloproteinase (MMP) duced to concentrate too rapidly. Hoof
activity in the pathophysiology of lall1initis.

testers may evoke some response.

It is not known which endotoxins are

Sole hemorrhages are an invariable
involved in releasing MMPs. It is know11 tl1at
clinical sign of clinical lanunitis, but such

MMPs play some pait in allowing collagen
hemorrhages due to trauma are more
fiber supp01ting the distal phalanx to
common; therefore, this sign must be
stretch. During ilie periparturn period,
interpreted carefully (seep 1079).

hormones such as relaxin are generated.

Correct management of nutrition around

Etiology: The etiology of subclinical
calving is critical. In early calving heifers, it
lall1initis in cattle is not understood. The
is possible growth hormones could have a
classic hypothesis suggests that high levels
complicating role.

of carbohydrate in the diet (seep 225) invoke

Whatever the biologic messengers, they
an increase of Streptococcus bovis and
appear to affect two different types of

Lactobacillus spp, which induce a state of
tissues: the papillary or sol ear dermis and
acidosis in the rum.en. This causes gram.the collagen fibers of the lan1inae. This negative organisms to die and release vasoacresults in two distinctly different patholotive endotoxins. Rum.enitis is frequently gies. The first is disruption of nom1al
associated with ruminal acidosis. High levels keratogenesis, and the second, abnormal of histamine in the blood have been fow1d in

MMP activity, results in sinkage and/or
the early stages of the disorder. It is probable rotation of the digit.

that subacute ruminal acidosis is one key

The pathophysiologic process associated
factor in development of lall1initis, because
with compromised horn production statts
managing subacute rwninal acidosis (SARA) when vasoactive toxins or other biologic helps control the incidence of subclinical
agents reach the coriun1. Arte1iovenous
lam.initis.

shW1ts may be paralyzed, pressure inside the

Contemporary thinking is tl1at as
claw rises, and the walls of the vessels are
production levels increase, cows become
damaged. Blood or blood fluids escape and
more sensitive to risk factors. A risk factor
soak into the claw horn, staining it either

1084

LAMENESS IN CADLE
pink or yellow. Hemorrhagic staining of the

Etiology and Pathogenesis: A new sole
horn tubules of the sole give a "brush mark"

grows beneath an existing one when fluid
appearance. Mural thrombi form, reducing
forms between the dermis and epidermis.

blood flow and causing oxygen deprivation

This fluid can result from bruising of the

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and an insufficient nutrient supply to the
sole under conditions such as prolonged
keratin-producing cells. Thrombus formation walking on rough roads. The fluid may be is a characteristic feature of laminitis. The
pus from a subsolar abscess. Double sole
resulting horn is soft and prone to damage,
has been seen in cattle suddenly changed
infection, and scar formation.

from a mainly forage diet to one rich in

The second pathophysiologic process
concentrates. Double sole can be confused
involves MMP release and stretching of the
with underrunning of the heel, which is a
collagen fibers of the suspensory apparatus
frequent sequela of white line disease.

of the digit. Collagen fibers originate in

Double sole has also been seen after feeding
horny corrugations (lamellae) on the inner
moldy hay.

surface of the hoof wall and insert into
those areas of the distal phalanx that have

Treatment and Control: Treatment is
no periosteum. Thus, the pedal bone is
simple unless mismanaged. The abaxial wall

"suspended" from the wall of the hoof.

must remain completely intact and only a

The lamellae are arranged to increase the
portion of the sole covering the bulb cut
surface area from which the fibers originate. away. The sole beneatl1 is extremely soft The vascular tissue and germinal layer, the
and vulnerable to damage; therefore, the
laminae, are interleafed between the
animal should be confined to a well-strawed
lamellae. In areas of the wall and sole where
stall until the new horn has hardened, after
there are no lan1ellae, the tissues of the
which more of the sole may be removed.

demlis are referred to as corium. Whether

Sudden changes in the quality of the
laminitis is truly an inflan1matory process
forage should be avoided.

could be questionable.

As the collagen fibers stretch, the pedal
bone is displaced. Occasionally, the pedal

FOREIGN BODY IN SOLE
bone will rotate and the apex of the bone
will prolapse through the apex of the sole.

A stone or fragment of glass or metal

Perhaps more frequently, the whole bone
penetrating almost through the sole will
will "sink," causing the space between the cause pain due to pressure on the coriun1
flex or process and the sole of the claw to
and, if not removed, will lead to infective
narrow and increasing the possibility of a
c01iitis.

sole ulcer developing.

If the foreign body penetrates through to

Frequently, young aninlals appear to
the corium, infection is introduced to the
recover from laminitis. This may be bedermal level, and an abscess develops.

cause new blood vessels develop to form

The rapidity of onset and severity of the
collateral circulation and take over the
lameness depends to some extent on the
function of those that have been dllITlaged.

location of the sole penetration. In the

Nevertheless, each time an animal has a
apical and subapical region, the lesion is
bout of laminitis, more scar tissue is formed
located between the distal phalanx and the
and the animal is less able to recover from
nonresilient sole. As the abscess develops,
the next insult.

interungular pressure increases rapidly.

Thus, the onset of lameness is rapid, and

Treatment and Control: Treatment for
pain is severe. Acute lameness may cause
subclinical laminitis is impractical, because
the aninlal to stand with the foot off the
diagnosis in an individual aninlal is not
ground or with the toe lightly touching.

possible at the time of the causative

A differential diagnosis is fracture of the
insult(s).

distal phalanx.

Controlling subclinical laminitis ( see

In the sub-bulbar region, the coriun1 is
p 1083) in a high-production, intensively
located between the digital cushion ( a flexible
managed dairy herd requires a systematic
structure) and the soft, resilient horn of the
epidemiologic study.

bulb. TI1e onset oflan1eness is relatively slow,
and the pain is significant but not severe. The

DOUBLE SOLE
pus in the abscess tends to spread over a wide
area through the fascia! plane and to cause

In double sole, one sole is present while
separation of the skin-horn junction at the
a new sole grows beneath, ie, there is
heel. A moist discharge from this area may
complete shut-down of horn production
be the first indication of the lesion. TI1is is
for an undetermined short period of time.

referred to as "underrunning of the heel," a

LAMENESS IN CADLE

1085
condition that can be confused with double

Treatment: Most sandcracks are not
sole (see above).

painful and require no treatment. However, if
the origin of tl1e lameness can be traced to a

Treatment: The foreign body should be
claw in which a sandcrack is present, routine

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removed and the track cored out to the
treatment of the crack is appropriate.

corium with a fine-pointed hoof knife.

A crack at the coronary band can split

Creating a large hole is inappropriate. Pus is
open, allowing infectious organisms to
often released under considerable pressure.

enter. The protrusion of granulation tissue

Antibiotic should be squeezed into the
through such a lesion can be quite
cavity, which closes rapidly. The opening
troublesome. The dorsal pouch of the distal
should not be plugged but covered with
interphalangeal joint is extremely superfielastic waterproof material to prevent cial at this point. The joint is very vulnerblockage with mud or manure.

able, and lesions at this location should

Treatment consists of removing the
never be ignored. Superficial horn should
foreign body if still present. The detached
be pared away and an astringent dressing
horn should not be stripped off in its
applied (5()0A, mixture of a sulfa powder and
entirety. Part of the detached horn may be
anhydrous copper sulfate). Pressure should
removed, but the abaxial wall must be left
be applied using cotton batten held tightly in
intact to bear weight and spare the exposed,
place by a narrow, adhesive elastic bandage
newly forming sole. Bandaging may not be
encircling the entire coronary band.

required, but the animal should be housed

The fissures often have ragged edges that
in a well-strawed area for a few days.

may be twisted and gape open. Sometimes,
the edges move and pick up a foreign body.

Cosmetic treatment may be requested in tile

VERTICAL FISSURES
case of show animals. The axial wall at tl1e
tip of the claw should be cut back so that the

(Sandcrack)

weight is borne only by tile abaxial portion

Sandcracks are vertical fissures or cracks in
of the wall. The ragged edges of the fissure
the wall of the claw. They account for -0.2%
should be trimmed, ideally with the cutting
of lesions of the claws of dairy cows. In
disk of a grinding tool. In selected cases, a
western Canada, the average incidence in
fissure can be inlrnobilized with an
mature beef cows is -200Ai. In individual
application of methyl methacrylate after the
herds, the incidence can be as high as 60%.

two edges of the fissure have been laced

No breed differences have been recorded.

together with steel wire.

The lesion is extremely unsightly, which can
be a considerable drawback for beef cattle
producers who wish to sell their animals.

HORIZONTAL FISSURES

Horizontal fissures result from disruption of

Clinical Findings: Vertical fissures occur
horn production at the dermis beneath tile
almost exclusively in the lateral fore claw.

coronary band, leading to a defect in the

In dairy cows, fissures are usually small and
integrity of the wall. These fissures run
confined to the proximity of the coronary
parallel to the coronary band. The defect
band. In beef cattle, they are more
varies in severity from a shallow groove
extensive, mostly starting at the coronary

(hardship groove) to a complete fracture
band and/or running part or all of the way

(fissure) of the wall. A comparable anomaly
to tl1e bearing surface. In herds with the
is seen as a band of horn differing in
highest incidence of this disorder, lesions
appearance from the remainder of the claw.

are also observed to start from a horizontal

One form of the band is seen in animals
groove in the middle of tl1e claw.

stressed after weaning ( weaning groove) or
during a period of nutritional deprivation.

The fissure moves distally as the claw

Etiology: The etiology remains uncertain.

The incidence is highest in mature, heavy
grows, and the distal portion becomes
cows. Bending or buckling of the claw
progressively more mobile (tllin1ble) until it
around one or several horizontal grooves
fractures, leaving a "broken toe." A series of probably creates mechanical stresses that
grooves can destabilize tile vertical strengtll
cause rupture of the claw wall.

of the dorsal wall, causing it to bend

In beef cattle in the prairies, it is theorized

(buckled toe).

that the most probable cause is a rapid
change from a winter diet low in protein and

Etiology: Fissures are believed to be
high in fiber to one high in protein and low in caused by a wide variety of stressors, fiber.

including a difficult calving, an acute febrile

1086

LAMENESS IN CADLE
disease, or a sudden, relatively shmt-term
from strain of the distal abaxial collateral
but significant change in nutrition. A 1idge
ligament. Pressure from the exostosis on the
may indicate an event such as compensadennis of the wall probably accounts for the tory growth.

excessive growth of the abaxial wall.

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Clinical Findings: The horizontal groove

Treatment: Correctly trimming a
or fissure is an in1portant indicator of
corkscrew claw requires much skill. The
metabolic disturbance. The date on which
horn forn1ation is extremely hard and
the causal insult occurred can be calculated
difficult to cut. The abnonnally naiTow
by measuring the distance from the hair line
shape of the distal phalanx makes it difficult
to the fissure and dividing that number by the
to pare the claw without causing bleeding at
growth rate of the claw. In mature dairy
the toe. The strategy is to sho1ten the claw
cows, the rate of growth of the wall
as much as possible without causing
measured along the dorsal flexure of the claw bleeding. Next, the horn wall that is is -0.5 cm/mo. Growth rates are more rapid
displaced beneath the claw is cut away.

in young anin1als, in anin1als on intensive

Then, so fai· as is possible, the horn is
feed, and during the sununer months.

shaped to approxin1ate norn1al. Trinuning
helps the anin1al get around for a while but

Treatment: No treatment is possible
does not "cure" the condition. Affected
except when very deep fissures form a
animals should ultimately be culled.

thimble, which is extremely painful. In these
cases, the loose horn should be removed

SLIPPER FOOT
with pincers; regional anesthesia may be
needed.

A slipper foot is nained for its alleged
likeness to a Persian slipper. The claw is flat

CORKSCREW CLAW
and curled upward to fonn a squai·e end.

The horn is heavily ridged and has lost its

A corkscrew claw is twisted throughout its
shine, and the coronary bai1d is rougher and
length in a configuration that displaces the
dai·ker than normal. Although tl1ere is no
abax:ial wall by up to 360°. One or both
objective evidence to suppmt the theory, the
lateral hind claws may be affected in cows
slipper foot is probably synonymous with

>4 yr old. Although corkscrew claws are
chronic laininitis and may be a sequela of
rarely seen in bulls, many believe there is
either acute or subclinical larninitis.

a heritable component.

Treatment is always disappointing. The claw
can be shaped to approximate nonnal, but

Pathogenesis: Bone molding is seen in the invaiiably it collapses and serious sequelae distal phalanx, but it is not known whether
follow. Animals with slipper foot should be
this is a matter of cause or effect. Periarticuculled as soon as economically appropriate.

lar exostoses develop around the distal
interphalangeal joint, possibly resulting

ANKYLOSING SPONDYLOSIS

In ankylosing spondylosis, exostoses
develop on the ligan1ent of the ventral
aspect of the lumbar vertebrae, primarily in
older bulls. Fracture of the exostosis and
associated ve1tebrae causes pressure on the
spinal cord, which results in severe ataxia
or paralysis. There is no treatment.

DEGENERATIVE ARTHROPATHY

This nonspecific condition affecting mainly
the hip and stifle is characterized by
degeneration of articular cartilage and
ebumation of subchondral bone,joint
effusion, and fibrosis with calcification of

Corkscrew claw. Courtesy of Dr. Paul Greenough.

tl1e joint capsule.

LAMENESS IN CATILE

1087

Etiology: Many causes and predisposing
and, when trying to walk, the anin1al appears
factors influence the development of
to be dragging one foot behind the other.

degenerative joint lesions. There is almost
certainly an inherited predisposition to the

Treatment: Resolution is possible,

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condition. Certain confonnations, eg,
provided that the head of the femur or
straight hocks in beef bulls, are also
the rim of the acetabulum has not been
incriminated. Joint instability after trauma
fractured. The animal should be deeply
is a common cause. Nutritional factors
sedated to the level of recumbency. A rope
involved in some cases, such as rations high
should be looped around the groin of the
in phosphorus and low in calcium, influence
affected limb, which should be uppennost.

the strength of subchondral bone. Copper

The free ends of the rope should be tied
deficiency or fluoride poisoning also may act arotmd a tree or some other fixed object, sinillarly. Forced traction of a calf in breech
and traction should be applied to forcibly
presentation can impede the blood supply to extend the limb. Downward pressure the hip joint, and arthritis may result. The
should then be applied to the hock, which
role of infection is unclear. Infectious
should be strongly rotated outward
arthritis in calves usually produces severe

(upward) until the head of the femur slips
changes in the hock, but degenerative
back into the acetabulun1. Traction should
arthropathy rarely involves this joint.

be applied at several angles until the head of

Bulls fed high-grain diets for show may
the femur clicks back into the acetabulum.

become lame when as young as 6-12 mo,

If the head of the femur or the rim of the
but most cases are first noticed at 1-2 yr.

acetabultm1 is fractured, there will be
considerable crepitation, and the head of

Clinical Findings: Onset is gradual (later
the great trocanter will displace as soon as
in bulls), and both hip joints are usually
traction is stopped.

affected; stifle involvement is rare.

Lameness to the point of incapacitation,

PATELLAR LUXATION
with crepitation of degenerate joints, may
develop in a few months; however,
lntennittent fixation of the patella on the
correlation between pathologic changes
upper part of the femoral trochlea results in
and clinical signs is poor. The earliest
a characteristic jerky action of one or both
changes occur in the acetabulum and on the
hindlimbs. The limb remains in caudal
dorsomedial surface of the femoral head.

extension for a longer period than normal

In the stifle, the medial condyle of the
and may even be dragged for a few steps
femur shows the earliest changes. Because
before clicking forward to a normal posture.

degenerative arthropathy may result from

In young anin1als, the condition may resolve
any of several initiating factors, a specific
spontaneously. For luxations that do not.

diagnosis may be difficult.

resolve, medial patellar desmotomy should

Radiographic, cytologic, and microbiobe performed.

logic evaluation of the synovial fluid are
useful diagnostic aids. Arthroscopy of

FETLOCK DISLOCATION
articular surfaces and ligan1ents may help
attain a definitive diagnosis and prognosis.

Fetlock dislocation is seen in young cattle
when they cross cattle guards (grillwork laid

Treatment: Changes in the joints are
over a pit as a gate substitute). T.ranquilizausually irreversible by the time of diagnosis.

tion or light anesthesia facilitates replace

Palliative treatment of valuable breeding
ment of dislocated structures. A padded,
anin1als should be undertaken with the
fiberglass cast maintained in place for 3 wk
knowledge that the condition or predisposusually promotes a satisfactory recovery.

ing factors may be inherited. The diet
should be carefully analyzed and, if

HIP DYSPLASIA
necessary, corrected. This is especially
important in fast-growing anin1als, in

Hip dysplasia, a bilateral malformation
which adequate exercise is indicated
of the hip joint, is often associated with
and overfinishing should be avoided.

secondary osteoarthritis. It may be present
at bi.1th. However, abnonnal gait may

COXOFEMORAL LUXATION
develop in rapidly growing animals. Usually,
it is possible to rock the hindquarter to

Luxation of the coxofemoral joint is usually
produce a click as the head of the femur
upward. It is seen in cows riding each other.

pops in or out. Radiography may confinn

The affected limb appears shorter than the
the diagnosis in young anin1als. There is no
contralateral limb. The hock is turned inward treatment.

1088

LAMENESS IN CATILE

FRACTURES
mon); 2) sandcracks; or 3) white line disease
or retroarticular abscess.

Bone fractures occur in cattle of all ages,
but they are most common in those <l yr

Treatment: Digital amputation is
old. Corrective procedures may be justified
indicated in animals that have a limited life

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economically in this age group, provided
expectancy, eg, old or poor-producing
that joints are not involved. External
animals. The procedure is simple, quick, can
fixation techniques or Thomas splints have
be perfom1ed in standing animals under
been used successfully. In selected cases,
regional analgesia, and in most cases,
percutaneous transfixation or internal
produces rapid relief. Amputation is
fixation may be attempted.

performed llirough the skin with an

Fractures of major long bones in adult
embryotomy wire placed as close to the
cattle usually are not treated. The tuber
skin-horn junction as possible. Hemorrhage
coxae may fracture when cattle are hurried
is arrested by means of a tight bandage.

through narrow doorways. In these cases,

Alternatively, in the case of valuable
spicules of bone may penetrate the skin, or
animals, arllirodesis to fuse the distal and
unsightly distortions of the flank can result.

middle phalanges may be attempted.

Fractures of the proximal and intermediate

General anesthesia is reconunended. A 1-cm
phalanges may be considered for treatment
canal is drilled through the abaxial wall into
in tractable, young adult cattle.

tl1e joint, and a second canal is drilled from

Fracture of the distal phalanx is relatively
the causal lesion into the joint. The joint
common in adult cattle. Onset of lameness is cavity is enlarged by curettage, and a rapid, and the pain is usually severe. If the
drainage tube drawn through. Continuous
medial digit is involved, the animal may seek irrigation witl1 sterile saline should be relief from the pain by crossing its legs.

performed for 2-3 days. A wooden block

Natural recovery is prolonged, and because
is then applied to the sound claw and the
most such fractures extend into the distal
affected digit immobilized by fixing it to the
interphalangealjoint, a debilitating arthritis
block with methyl methacrylate. Immobilimay develop at the fracture site. If treatment zation is further facilitated by encasing the is undertaken, the sound digit should be
digital region in a cast. The cast is removed
elevated on a wooden block and the affected after4wk.

digit inunobilized in a flexed position to the
block using methyl methacrylate adhesive.

SEROUS TARSITIS

SEPTIC ARTHRITIS OF THE DISTAL (Bog spavin, Puffy hock) INTERPHALANGEAL JOINT

Serous tarsitis is characterized by lliree soft,

Most frequently, one of the causal lesions is
fluctuating swellings between the ligaments
present and tl1e transition from the initial
of the femorotarsaljoint. In some instances,
lesion to the joint infection is readily
this condition is heritable. It does not cause
apparent. However, when a swollen foot is
pain or lameness. In later life, there may be
treated before the cause has been estaba predisposition to arthritis. Serous tarsitis lished, ajoint infection may have been
is diagnosed by depressing the swelling of
ongoing for weeks before the true nature of
the joint capsule at one location and
the condition is diagnosed. If aggressive
palpating tl1e fluctuation that is seen at
treatment of a footrot case does not lead
another. There is no successful treatment.

toward resolution within 3 days, septic
arthritis should be suspected. Increased pain,
together with swelling of the anterior region
of the coronary band in cases of sand crack
and white line disease, is suggestive of joint
infection. Using regional analgesia and strict
aseptic technique, an aspirate of the joint can

SUPRASCAPULAR PARALYSIS
be collected and exanlined for infection. A
radiograph may indicate an abnormal

This rare condition results from paralysis
separation of the joint surfaces.

of the supraspinatus and infraspinatus
muscles caused by damage to the sixth and

Etiology: Infection enters the distal interseventh cervical nerves. Acute trauma to phalangeal joint via three possible main
the prescapular area ( eg, struggling into a
sites: 1) the dorsal commissure of the
head gate) produces a nonspecific ataxia
interdigital space, via penetrating trauma
immediately after the iajury. Several days
or complicated footrot (interdigital phleg-
after ilie iajury, the muscles may show signs

LAMENESS IN CA

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1089
of wasting, indicating the possibility of
prognosis is guarded. When the condition
permanent damage.

persists for �2 wk, damage is likely

Chronic injury to the neIVes causes
pennanent and the prognosis is grave.

marked wasting of the muscles within
weeks. A specific gait aberration develops.

ISCHIATIC PARALYSIS

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The stride is shorter than normal; when
weight is borne on the limb, it tends to

(Sciatic paralysis)

swivel. In some cases, the cause may be

Damage to the ischiatic and obturator
neIVe compression in or around the
neIVes after intrapelvic parturient trauma
vertebrae (eg, an abscess or fracture),
may cause recumbency after calving. It
which may be identified on radiographs.

may be a component of ilie downer cow

If the trauma is complicated, primary
syndrome. The tibial and peroneal nerves
treatment must be directed toward
are branches of the ischiatic neIVe that can
resolving the inunediate problem. However,
be damaged at extrapelvic sites.

if the clinical presentation suggests that the
injury is localized to the neIVe, inunediate
treatment with steroids or other anti-inflam

OBTURATOR PARALYSIS
matory agents is appropriate.

Passage of a calf tlu·ough the pelvis exerts
pressure on tl1e obturator neIVe. The close

RADIAL PARALYSIS
association of the obturator neIVe with the
origin ofilie ischiatic nerve can complicate

Distal radial paralysis results in an inability
interpretation of clinical signs.

to extend the carpus and digit. Proximal
radial paralysis prevents the animal from

Clinical Findings: Because the adcluctors
extending the elbow, carpus, and fetlock to
are inneIVated by ilie obturator nerve, an
bear weight.

animal adopts a base-wide stance or, in
recurnbency, a sitting position with both

Etiology: The proximal radial neIVe may
hindlirnbs extended forward. There is
be injured by stretching close to the brachial considerable risk iliat the adductor muscles plexus, in which case the triceps muscles as
will be damaged and iliat pem1anent
well as the extensors of the carpus and
recumbency will result. In addition to ilie
digits may be compromised. The damage is
base-wide stance, knuckling of the fetlock
frequently associated with casting an animal may be present. This indicates injury of ilie with ropes or with any situation in which
ischiatic neIVe. Both conditions may
the forelimb is accidentally restrained and
contribute to downer cow syndrome ( see
the animal stmggles violently to free itself.

p 1188).

Either distal or proximal radial paralysis
can result from prolonged recumbency in

Treatment: If obturator paralysis is
very heaVY animals.

recognized early enough, vigorous measures

The distal radial neIVe is vulnerable to
should be adopted to prevent complications
injury in tl1e musculospiral groove of the
involving the adductor muscles. The animal
htunerus, either from fractures or deep,
should be inm1ediately transferred to a site
soft-tissue trauma. A lesion of the neIVe
where there is good footing ( eg, a base of
proxirnal to ilie sulcus for tl1e brachial
tenacious manure over which clean straw
muscle causes proximal radial paralysis.

has been spread) to prevent slippage during
attempts to rise. The hindlirnbs can be tied

Clinical Findings and Diagnosis: In
together with a soft nylon strap fixed below
proximal radial paralysis, the elbow drops,
the hocks. The limbs are restrained from
the carpus and fetlock are in partial flexion,

"spreading" >3
and ilie limb is usually dragged. In distal
ft (1 m) apart.

radial paralysis, because the triceps muscles

FEMORAL PARALYSIS
remain functional, dropping of ilie elbow is
minimal. However, paresis affecting carpal

In femoral paralysis, paralysis of the
and fetlock position is present.

quadriceps muscles, which extend the stifle,
and partial paralysis of the psoas major

Treatment: Rapid in1provement can be
muscle, which flexes the hip, are seen.

expected in most cases. Animals should
be confined in a generously bedded stall.

Clinical Findings and Diagnosis:

Anti-inflammatory dmgs may be helpful,

Femoral neIVe paralysis is seen in large,
particularly in ilie early hours after ilie
newborn calves (eg, Charolais, Sinunental)

initial trauma. If skin sensation in the
after the use of mechanical force dming an
forelimb has been completely lost, the
assisted birth. Reduced quadriceps tonicity

1090

LAMENESS IN CADLE
reduces tension on the patella, with the
beneath the tendon of the gastrocnemius
result that a lateral patellar luxation may
muscle and can be damaged when the
develop. Atrophy of the quadriceps soon
tendon is traun1atized.

becomes obvious and, although the patella
can be replaced easily, the animal has

Clinical Findings: The hock joint is

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extreme difficulty walking. The condition
overflexed ( dropped hock syndrome) and
may affect one or both limbs. Prognosis is
the fetlock is partially flexed. The gastrocnerelated to the severity of the clinical signs.

nlius appears to be longer than normal and
gives the inlpression that it or its tendon

Treatment: Despite a fair or good
could be ruptured. The fetlock tends to be
prognosis, the animal may be unable to
buckled, but the animal can walk and bear
suckle unaided. The animal should be
weight, although its attempts to do so are
maintained in a well-bedded area, and
awkward. Compared with that seen in
colostrnm given as soon as possible after
peroneal nerve injury, tl1e gait disturbance
birth. A radiographic study should be done
is mild, but the postural disturbance could
to exclude fractures. The administration of
be pern1anent.

anti-inflanunatory drugs may be useful.

Treatment: The use of anti-inflammatory

PERONEAL PARALYSIS
drugs may be of value in the early stages.

However, the prinlary efforts should be

Peroneal paralysis results in paralysis of the
directed toward ensuring tl1at the animal
muscles that flex the hock and extend the
does not injure itself further, by maintaining
digits.

it on swiaces witl1 good footing.

Clinical Findings: The peroneal nerve is

SPASTIC SYNDROME
the cranial division of the ischiatic nerve. It
passes superficially over the lateral femoral

Episodic, involuntary muscle contractions
condyle and the head of the fibula, which
or spasms involving the hindlimbs are
makes it vulnerable to external trauma or
associated with postural and locomotor
pressure from recumbency. An affected
disturbances as well as spasticity. The
animal stands with the digit knuckled over
condition may progress to posterior paresis
onto the dorsal swiace of the pastern and
or hindlimb paralysis. It is seen most
fetlock. The hock may appear to be
frequently in Holstein and Guernsey cattle
overextended. In mild cases, the fetlock

3-7 yr old. Spastic syndrome is regarded
tends to knuckle over intermittently during
as a genetic disease, possibly due to an
ambulation; however, this may also occur if
autosomal donlinant gene with incomplete
the animal is expe1ienci,ng pain in the heels.

penetrance. The pathology and pathophysi

In severe cases, the dorsal swiace of the
ology remain obscure.

hoof may be dragged along the ground, and
sensation to the dorsun1 of the fetlock is

Clinical Findings: Clinical signs may vary
often decreased. Testing of reflexes may
in severity, duration, and frequency. Usually,
demonstrate that hock flexiori is absent, but
some stinmlus provokes the onset of
stifle and hip flexion are norn1al. This would
clinical signs, such as the effort associated
not be the case if the ischiatic nerve was
with rising or any factor that induces a
involved.

significant emotional reaction. Pain,
particularly in the feet or joints, may precipi

Treatment: Most cases resolve naturally.

tate an attack. During an attack, the animal

However, if the condition is associated with
may be unable to move forward, stands
long periods of recumbency, care must be
trembling, and characteristically extends its
taken to avoid exacerbation of the initial
hindlimbs backward. Between episodes, the
injury.

animal can ambulate nom1ally.

TIBIAL PARALYSIS

Treatment: Spastic syndrome is
progressive, and because of the possibility of

In tibial paralysis, there is paralysis of the
genetic transmission, rulimals (pruticularly
extensors of the hock and flexors of the
bulls used for artificial insenlination) are best
digits.

eliminated as soon as a positive diagnosis is
made. Palliative treatment for animals in the

Etiology: The tibial nerve is the caudal
peak of production may be helpful.

branch of the ischiatic nerve, which, in its

Mephenesin (30-40 mg/kg, PO, for 2-3 days)

proximal course, is well protected by the
may be given during an episode. Phenylbutagluteal muscles. Distally, it progresses zone may also have beneficial effects.

LAMENESS IN CA

TILE

1091

SPASTIC PARESIS
tent mild trauma to the precarpal area
caused by lack of bedding or a poorly

(Elso heel)

designed manger. B1'ucella abortus may be .

Spastic paresis is a progtessive unilateral or
isolated from the false bursa of some cases m

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bilateral hyperextension of the hindlirnb(s).

countries where this orgarusm has not been

It is seen sporadically in most breeds of
controlled. The lesion is a fim1 swelling,
cattle. Post-legged cattle are most
possibly fluctuating and up to several inches
frequently affected. Attempts to move
in diarneter, located over tl1e dorsal aspect of
are believed to simultan�ously trigger
the carpus. The hygroma is a lesion tl1at is
contractions of both ext�nsors and flexors
very difficult to resolve. The fust step is to
of the limb. Spastic pare�is is currently
ascertain radiographically whether there IS
considered to be inhelitl!d via a recessive
more than one cavity. Each cavity should be
gene( s) witl1 incomplete penetrance.

drained and infiltrated witl1 a long-acting
corticosteroid preparation. Surgical removal

Clinical Findings: The disease may be
is messy, witl1 little guarantee of a successful
seen within the first 6 111() of life. As the
outcome. Introducing initant matenals mto
animal ages, the gastroctiemius muscles
ilie cavity has had tmcertain results. If ilie
gradually contract. The l\ock and stifle
anin1al is milking and eating well, hygromas
become increasingly extended. Over a
should be left untreated.

period of months, tl1e hutdlimbs become
so stiff that the anin1al Walks with short,

RUPTURE OF THE
pendulum-like steps. If On]y one limb is
affected, the animal stands with the affected GASTROCNEMIUS MUSCLE
limb camped back and tl\e sound limb held

Rupture of the gastrocnemius muscle or
toward the midline to 111<1.intain balance. If
tendon is relatively rar·e. It is most likely to
both hindlimbs are affected, the animal
be associated wiili deficiencies of calciwn,
may attempt to bear more weight on the
phosphorus, and vitarnin D. Prolonged
forelimbs by holding the1i1 well back and
simultaneously arching i
recw11bency, with resulting myositis and
ts back.

struggling to rise, occasionally precipitates

The quadriceps muscl� has been
rupture of iliese muscles. Occasionally, the
implicated in the pathology of this disorder
condition has been associated wiili
and can be distinguished from the form of
pyeloneph1itis, which preswnably causes
the disorder affecting th1, gastrocnemius
a myositis, weakening the muscle enough
through use of a femoral nerve block.

to pennit rupture. II\iections of initating
medicaments into the gastrocnemius

Treatment: There is no successful medimuscle may cause necrosis and rupture.

cal treatment. Because St)astic paresis is

The hock remains flexed. When ilie niuscle
heritable, affected ani.rna\s ( especially
is completely ruptured, ilie standing arumal
breeding bulls) should be eliminated from
rests ilie hock and distal po1tion of ilie limb
the herd. Palliative surgicaJ treatment may
on tl1e ground or walking surface, which is
be attempted, although el.hical issues should
diagnostic, although rupture of ilie Achilles
be considered when breeding stock is
tendon may produce an identical gait.

involved. The procedures, usually performed

Successful treatment is extremely
on calves, include compl1,te tenotomy of the
unlikely in heavy adult arumals. A leg cast or
gastrocnemius tendon, Which results in a
splint iliat maintains the hock in extension,
dropped hock; complete 1:ibial neurectomy,
supplying adequate vitan1ins and minerals,
which results in sufficient relief to permit a
and proper nursing may be successful, but
steer to be finished for sla.ughter; and partial
a long recovery period is required.

tenectomy of the two insl:!rtions of tl1e
gastrocnemius muscle and the calcanean
tendon sheath, which overcomes the

RUPTURE OF THE PERONEUS
problem of the dropped hock.

TERTIUS MUSCLE

The peroneus tertius muscle can be forcibly
avulsed from its insertion by accidents
associated wiili mounting or, more
frequently, by ilie inexpe1ienced use

CARPAL HYGROMA,
of ropes to restrain a hindlimb.

.

The hock is abnormally extended, while

Carpal hygroma is a loca!:i.zed swelling of
ilie stifle remains flexed. The anin1al carmot
tissues, including the pre<;:arpal bursa, dorsal
advance ilie limb nom1ally, ilie calcanean
to the carpal joint. It results from intenni t -
tendon is flaccid, and the hooves may be

1092

LAMENESS IN CADLE
dragged. The site of avulsion may be painful
of the hock that has little effect on joint
to the touch. A specific iliagnostic feature
mobility. It can include the formation of a
is that the limb can be pulled backward
false bursa. The condition is caused by
without any resistance from the animal.

severe abrasion of the skin and subcutane

The conilition may improve slowly if the
ous tissue overlying bony prominences.

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animal is confined in a stall (loose) for

The skin may be excmiated by contact with
several months.

concrete and particularly sharp curbs.

Superficial abscesses must be drained

TARSAL CELLULITIS
extremely cautiously, because tl1ere is
considerable danger of entering the joint.

(Concrete hock)

Padding and bandages should always be

Tarsal cellulitis is characterized by a firm,
applied. Poultices rapidly reduce acute
subcutaneous swelling on the lateral aspect
swelling.

LAMENESS IN GOATS

Abno1mality of gait is a sign common to
wounds, foreign bodies such as stones or
many diseases and conilitions. A complete
clover burrs caught in tl1e interiligital space,
history is important for iliagnosis and should
or pus from a ilischarging abscess.

include incidence and duration in the herd,

Inspection should include the coronary
nutrition, feed changes, method of rearing,
band or coronet.

and recent introductions to the herd. (See

The rest of the leg should be palpated
also HEALTH-MANAGEMENT INTERACTION: GOATS,
carefully, including the bones, tendons, and
p 2147.)

muscles. Any muscle atrophy or restriction

Some causes of lameness may be
of movement should be noted, and
associated with systemic ilisease. Therecontralateral limb structures should be fore, a thorough physical exanlination
compared for signs of asymmetry. The joints
should always be performed, followed by a
also should be checked for heat, swelling, or
detailed exanlination of all four limbs, with
pain.

a specific assessment of gait and mobility in

If the clinical examination suggests joint
an attempt to localize locomotor problems.

involvement, it may be necessaiy to

In goats, as in other species, locomotor
aseptically sainple fluid from an affected
difficulties usually involve the musculoskeljoint for visual examination, cytology, Grain etal system directly, but conilitions of tl1e
stain, and culture and sensitivity tests. Joint
nervous system can minu'c musculoskeletal
fluid containing pus alone, or with
ilisease and should be considered during the Gran1-stained bacteria, inilicatesjoint-ill; clinical exanlination.

fibrin and pus combined suggestMyco

The hoof of the affected leg(s) should be plasma spp; clear or cloudy joint fluid with exanlined, and excess horn material removed many mononuclear ce'ils suggests caprine to leave a level, weight-bearing surface. If
arlliritis-encephalitis virus (CAE, seep 747).

the feet have not been trimmed recently,

A blood or serum san1ple may also be
or the goats have been on soft ground or
useful to establish the underlying cause
bedding, excess horn commonly overgrows
of lan1eness. In joint-ill, the WBC count is
from the walls, toes, and heels, and folds
high due to neutrophilia. Blood calcium,
over the sole. With severe neglect,
phosphorus, and vitamin D levels may

"sled-runner" or "Turkish slipper"-type help diagnose epiphysitis or rickets,
hooves with elongated toes may cause the
although blood levels often return to
goat to walk on its heels. The following
normal before the affected goat is
should be noted during foot trimming:

exainined. If CAE is suspected, the
any portion of the horn that is abnormally
presence of antibody can be checked;
thickened, any underrunning of the heel
however, false negatives may be seen
or sole, any abnormal wear of one claw,
during severe stress, and positive tests
or any abnormal or necrotic smell.

may be coincidental to another cause of

After trimming, the feet should be
laineness if seroprevalence of the CAE
scrubbed clean and inspected for puncture
virus is high in the herd of origin.

LAMENESS IN GOATS

1093

Radiography may be helpful. In epiphysi

A usually bilateral, congenital condition
tis, the growth plates should be checked;
that is a genetic defect is seen in Angoras in
there is also lateral deviation of the radii and Australasia. It is due to a recessive occasionally thinness of the bone. In CAE
autosomal allele that must reach a certain
virus infection, the initial swelling of the
level before affected animals appear; the

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soft tissue surrounding the affected joint
time between purchase of a carrier buck
may be followed by calciun1 deposits in the
and appearance of affected kids may be 5-6
swollen periarticular tissue, joint capsule,
generations. Either the fore- or hindlimbs
ligan1ents, tendons, and tendon sheaths.

are affected. In rare cases, only one forelimb

Later changes may include mild periarticuis twisted. In severe cases, the kid is either lar osteophyte production, "joint mice," and unable to stand or walks on its fetlocks.

rough extensions of the periarticular bone

In less severe cases, the kid may move
proximally and distally.

relatively easily with fetlocks that are

Some of the more important conditions
permanently partly flexed. In mild cases, the
that cause lameness in goats are discussed
lin1bs may gradually be splinted straighter
below, listed in alphabetical order. The
and straighter until the kid is able to bear
differential diagnosis in any case of
weight on its feet.

lameness is influenced by geographic

Anglo-Nubians in tl1e USA, Canada,
location, herd history, management

Australia, and New Zealand can have a rare
practices, and other relevant factors.

genetic condition called 13-mannosidosis. At
birth, affected kids have varying degrees of

CAPRINE ARTHRITIS AND
fixed flexion of the forelimbs and fixed
extension of the hindlimbs. They can see,

ENCEPHALITIS
bleat, and suckle if held up to tl1e teat.

Caprine arthritis and encephalitis (CAE)

Their withdrawal reflexes are norn1al or
virus infection has emerged during the
depressed, and there is intention tremor,
past 35 yr as a major cause of disease,
especially of the head. There may be
primarily in European breeds of dairy
nystagmus, deafness, and facial abnonnaligoats under intensive management. All ties. At necropsy, cutting the tendons allows
breeds of goats are susceptible to this
free movement of the limbs. Histologic
retrovirus, and prevalence of infection is
examination reveals typical lesions of
related to exposure to virus. Two distinct
lysosomal storage disease characterized by
forms of locomotor problems are seen. A
cellular vacuolation. Affected kids have no
neurologic form of the disease is seen in
plasma levels of 13-mannosidase, and both
young goats, usually 2-4 mo old but as old
parents have levels half the normal range.

as 1 yr. It is characterized by a progressive
paresis with incoordination leading to

COPPER DEFICIENCY
paralysis, usually involving the hindlimbs
and later the forelimbs. In older, adult

Copper deficiency may cause locomotor
goats, the virus infection manifests as a
difficulties in goats in two distinct ways.

chronic, progressive arthritis involving

Abnorn1al bone growth with increased bone
one or more joints and usually involving
fragility can predispose to fractures of long
the carpal joints. The initial sign is usually
bones. Independently, a neurologic
swelling of the affectedjoint(s), followed
condition known as enzootic ataxia or
by progressive degeneration of articular
swayback develops, in which copper
and periarticular tissues with calcificadeficiency of kids in utero or after birtl1
tion, leading to decreased range of
results in pern1anent myelin degeneration
motion, ankylosis, and overt loss of
in the spinal cord, leading to progressive
mobility.

incoordination and paralysis with failure of

For a more detailed discussion, see
mobility. Clinically, this appears similar to
p747.

tile neurologic form of caprine arthritisencephalitis virus (seep 747) infection in young kids. Copper status of the ration

CONTRACTED TENDONS IN KIDS
needs to be evaluated, and copper

Contracted tendons in newborn kids are
supplementation provided as necessary.

seen sporadically in goats of all breeds
throughout the world, usually with

EPIPHYSITIS
unexplained causation. However, there are
two specific, inherited conditions of goats

(Bent leg, Windswept)

that result in contracted tendons of

Epiphysitis may result from imbalance in
newborns.

the calcium:phosphorus ratio. It is seen

1094

LAMENESS IN GOATS
in young, rapidly growing kids (more often

JOINT-ILL
in males than in females) and in young
does in late pregnancy or in the early

Several joints of kids can be involved in
stages of their first lactation. These does
joint-ill, a nonspecific bacterial infection.

are young (eg, 12 mo), extremely heavy

Bacteria that have been incriminated are

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milkers, or carrying twins or triplets.

mainly gran1-positive and include staphylo

Epiphysitis is sometimes compounded by
cocci, streptococci, Corynebacteriiim spp,
rickets (seep 1051).

Aclinomyces spp, andErysipelolhrix
rhusiopalhiae, as well as gram-negative

Clinical Findings and Diagnosis: Epicolifonns.

physitis starts with lateral or medial bowing

Environmental bacteria gain entry to
of one or both radii. Later changes may
the neonate's circulation, usually via the
consist of lateral deviation of the digits
umbilical cord. Other methods of entry
on the fore- or hindfeet; lameness and
include contamination of breaks in the
reluctance to walk; an arched back; and soft
skin or via the GI or respiratory tract.

swelling and pain in the carpal, metacarpo

Predisposing factors include lack of
phalangeal, tarsal, and metatarsophalangeal
routine dipping of the umbilical cord;
joints. Diagnosis of epiphysitis can be
poor sanitation in the kidding pens; or
confirmed with radiography.

does kidding in overcrowded, dirty

Conditions that have been implicated
conditions. E rhusiopalhiae are
in its cause include an excess of dietary
soil-living bacteria that may persist
calcium with a calcium:phosphorus ratio
on farms or in pens used by sheep or pigs.

of>l.4:1 (generally >1.8:1), excess

Mycoplasma infection is also a differenprotein intake, excess dietary iron, indoor tial diagnosis (seep 1095).

housing of kids, or lack of vitamin D
caused by prolonged overcast weather

Clinical Findings: Withjoint-ill, more
and low vitamin D levels in the feed.

than one joint is hot, swollen, and painful.

Carotene has an antivitamin D effect.

Often, the affected limb(s) crumot bear

Vitamin D has poor stability in prepared
weight, and kids with more than one leg
feed, especially when mixed with
affected may be unable to stand. The more
minerals. Alfalfa is high in calcium ( 1.4%
commonly affected joints include the
calcium to 0.2% phosphorus) and protein.

cru'l)us, shoulder, hock, and stifle. Generally,

Owners frequently feed kids milk for
there is a fever but no reduction in appetite.

prolonged periods because of a lack of

Sometimes the navel area is inflan1ed, but
commercial outlets for milk.

often there is no visible abnonnality. An
abscess may fonn on the navel long after the

Treatment and Control: Once the
kid has recovered. The WBC count may be
probable cause(s) is identified, the diet
increased with a left shift.

should be corrected and the appropriate

If the condition becomes chronic,
supplement given-usually injectable
the limbs are stiff, some joints may be
vitamin D ancl/or phosphorus or oral
ankylosed, ru1d overall growth is poor. At
balanced calcium/phosphorus supplements. this stage the temperature is nonnal.

Predisposing factors also must be
corrected. The diet of growing kids should

Treatment: To be successful, treatment
be changed to slow growth rate. The mating
must be given early and, when possible,
of young does <7 mo of age should be
antibiotic selection should be based on
discouraged, and buck kids should be
culture and sensitivity testing. Frequent
separated from doe kids by 3 mo of age to
injections of high doses of parenteral
avoid unplanned matings. The diet for
antibiotics given for -1 wk may effect a cure
young does in milk with limb deformities
if combined with careful nursing. Joint
should be corrected to allow for nonnal
lavage with saline and antibiotic solutions
bone growth. Proper nutritional managemay enhance therapeutic outcome in select ment stops limb deformities from worsencases. Complications should be prevented ing, and such defomlities self-correct over
by providing soft bedding, frequently
time in most does.

turning any kid unable to stand, and massaging the affected joints. If ru1kylosis struts to FOOTROT AND FOOT SCALD
develop, the kid should be supported in a
sling for sh01t periods as frequently as

Footrot and foot scald are serious problems
possible.

of sheep and can also have a major adverse

In large, commercial herds, treating
impact on goats under certain management
severely affected kids may not be economiconditions (seep 2147).

cally justified, and hun1ane euthanasia

LAMENESS IN GOATS

1095
should be considered. Many that do recover
mycoides (la.i·ge colony variant) or other
remain unthrifty for the rest of their lives.

Mycoplasma spp may show severe
laineness with multiple hot swollen joints,

Control: Hygiene at parturition is essential.

weight loss, pyrexia, and poor coats. Some

A deep bed of clean sawdust, wood shavings, have diaiThea, and some have increased VetBooks.ir
or straw should be provided; it is often better lung sounds and respiratory rates. Affected to allow the doe to kid on fresh pasture if the
kids are generally 2-4 wk old. Morbidity
weather is wai111.

and mortality rates of 90% and 30%,

The umbilical cords of newborn kids
respectively, have been reported. Adult
should be dipped several times in strong, 7%
does with Mycoplasma infection may have
tincture of iodine. Cords should be dipped
mastitis and polyarthritis. Treatment is
each time the kid is handled in the first
with tetracycline, tylosin, or tiai11ulin, but

24-48 hr. Owners should clean their
prognosis for complete recovery is
footwear before entering kidding pens. Kids
guarded.

must receive adequate colostrnm at birth.

LAMINITIS

TRAUMA

(Founder)

Goats, in general, are agile creatures, but if
fiightened they may attempt inlpossible

Laminitis in goats is seen worldwide, but the jumps, with resultant fractures or other incidence is lower thai1 that in dairy cattle
irtjwies. Yai·ds designed for goats that ai·e
and horses. Predisposing causes include
infrequently handled should have a visual as
overeating or sudden access to concenwell as physical bai1ier. Chain-link fences trates, high-grain and low-roughage diets,
ai·e often associated witll limb fractures
or high-protein diets. Laminitis can also
when used for goat enclosw·es. Fortwiately,
develop as a complication of acute
most fractures of the lower linlbs heal
infections such as mastitis, metritis, or
rapidly with norn1al casting. Shearing of
pneumonia, especially after kidding.

Angoras is a source of potential problems

When laininitis is severe, the affected
when the shearer's comb cuts into or
goat is lan1e and reluctant to move; there is a through tile Achilles tendon. 01thopedic fever, and all four feet are hot to the touch.

procedures suitable for large dogs can be

Touching the coronary band elicits a severe
used. If goats are attacked by dogs or wild
pain reaction. In less severe cases, only the
canines and survive, they often have multiple
forefeet are affected. Laminitis can become
traumatic injwies that can include fractures.

chronic if the initial phase is not diagnosed

Some IM irtjections can cause problems.

or treated successfully. The onset is

For exainple, mixed clostridial vaccines can
insidious, but eventually the goat is seen
cause severe soft-tissue swelling and
walking on its knees, with "sled-rnnner"

laineness for �48 hr. Irritant drugs can
deformities of its hooves.

dainage nearby nerves and cause laineness,

In acute laminitis, the predisposing
particularly when thin or young goats are
condition, if identifiable, must be
injected in the thigh muscles and t11e sciatic
corrected promptly. The lan1initis is
ne1ve is affected. In some cases of severe
treated with analgesics such as daily
mastitis, especially gangrenous, there is a
parenteral flunixin meglumine, and hosing
hindlinlb lan1eness on the affected side as
or soaking the affected feet is also useful.

tile doe changes her gait because of swelling

Although antihistan1ines are frequently
and pain in the udder.

used, their effectiveness in treatment of
laminitis in goats remains unproved.

WHITE MUSCLE DISEASE

Simi!ai·ly, the use of corticosteroids is
controversial because they may contribute See also NUTRITIONAL MYODEGENERATION, to laminitis in horses, and they should not
p 1172. Most kids affected by white muscle
be used in pregnant does because of the
disease have been in good condition and are
risk of abortion. Chronic larninitis with

2-3mo old(range, 1 wk to 4 mo). Commonly,
deformed hooves is treated by routine,
sudden death is associated with cai·diac
vigorous foot trimming.

muscle dainage. Other kids ai·e depressed,
reluctant to move, and appear stiff, witl1 a

MYCOPLASMOSIS

"sawhorse" stance, or become recumbent.

Muscles, especially of the hindlin1bs, ai·e

See also CONTAGIOUS AGALACTIA, p 1352, atld furn and painful to the touch. Treatment is

CONTAGIOUS CAPRI E PLEUROPNEUMONIA, p 1474.

with selenium and vitanlin E iitjection in

Kids infected with Mycoplasma mycoides
acute cases.

1096

LAMENESS IN HORSES

LAMENESS IN HORSES

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Lameness is defined as an abnormal stance
clinical signs of lameness are the head nod
or gait caused by either a structural or a
associated with forelimb lameness and the
functional disorder of the locomotor
sacral rise, also called a pelvic rise or hip
system. The horse is either unwilling or
hike, associated with hindlirnb lan1eness.

unable to stand or move nonnally.

Hindlimb lameness should be assessed

Lan1eness is the most common cause of loss
from the side as well as from bellind,
of use in horses. It can be caused by trauma,
because tllis provides an opportunity to
congenital or acquired disorders, infection,
assess arc of foot flight, duration of
metabolic disorders, or nervous and
protraction and retraction phases, lengtll of
circulatory system disease.

weight-bearing phase, and the presence or

Lameness is not a disease per se but a
absence of a sacral rise. Forelimb lameness
clinical sign. It is a manifestation of pain,
should be observed from the front and side.

mechanical restrictions causing alteration

Hindlimb and forelimb lameness in many
of stance or gait, or neuromuscular disease.

horses will be accentuated when the horse

Pain is the most common cause of lameness
is worked in a circle with the affected limb
in all horses. Mechanical lan1eness is best
on the inside.

typified by complete upward fixation of the

Factors that predispose horses to
patella with its characteristic gait abnormallameness include physical immaturity, ity but can also be the result of fibrotic
which may occur in premature or dysmamyopathy of the semitendinosus muscle or ture foals, and training older foals before
of restrictions caused by annular ligaments,
maturity. Other factors include preexisting
adhesions, or severe fibrosis.

developmental mthopedic disease ( eg,

It is critical to con-ectly detemline the
osteochondrosis, flexural limb and angular
cause of tl1e lameness, because treatment
limb defoffnities); poor conformation;
varies greatly depending on the cause. For
improper hoof balance or shoeing; failure
example, the mechanical lameness of
to adequately condition perfom1ance
complete upward fixation of the patella
horses; monotonous repetitive stresses on
will not respond to analgesics, whereas
bones, tendons, ligan1ents, and joints in
lameness caused by pain often responds to
performance horses; hard, slippery, or
systemic or local analgesics and anti-inflamrocky surfaces upon which horses work; matory drugs. Some causes of lameness
and extremely athletic activities. Inciting
produce very characteristic and classically
factors in lameness include direct or
described gaits. In fibrotic myopathy, a
indirect trauma, fatigue resulting in
mechanical lan1eness, the affected limb is
incoordination of muscles (which often
pulled back and down quickly before the
occurs in racehorses at the end of races),
end of the protraction phase, giving the
inflanunation, infection, and failure to
impression that the foot "slaps down" on the recognize early disease before it creates ground. The signs are most obvious at the
significant pain.

walk. In stringhalt, a neuromuscular

Lameness in one part of a limb often
disorder, tl1e affected limb is hyperflexed
results in secondary soreness in another
during the cranial or swing phase, while tile
area of the san1e limb and may result in
stepwise caudal jerking movement before
lameness of the contralateral forelimb or
foot contact does not occur. Unfortunately,
hindlimb from overuse due to compensamany causes of lameness do not produce a tion. The entire horse should be evaluated
characteristic gait abnormality, making
for secondary lan1eness even when the
diagnosis a challenge.

cause of the primary problem is obvious.

Pain-related lameness can be classified

Secondary lamenesses are very common in
as weight bearing (supporting leg) or
perfom1ance horses but may occur in all
nonweight bearing (swinging leg) lameness. types of horses. A dramatic exan1ple of Altllough lameness is most often observed
a secondary lan1eness occurs when
as a weigh t -bearing deficit, it may be
biomechanical laminitis develops in the
composed of both. A supporting leg
normal contralateral limb of a horse with
lan1eness is seen when the horse reduces
limited weight bearing from a severe
the amount of time or reduces the amount
orthopedic problem causing shifting of
of force applied to the weight-bearing limb.

weight from the injured limb to the normal

The most consistent and easily recognized
limb.

LAMENESS IN HORSES

1097

THE LAMENESS
any exercise needed for diagnosis has been

EXAMINATION
completed.

The back and neck should be t110roughly

A systematic investigation of a lame horse
exan1ined with the horse restrained and

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may be time conswTling when the cause is
standing square on a level surface.

not obvious. The examination benefits from

Flexibility and extensibility of the back can
standardized facilities such as a level, firm,
be checked by alternately pinching the
nonslip surface to walk and trot the horse
midline in the mid thoracic and sacrococcyand a soft support area to lunge and ride the geal regions, whereas lateral flexion can be
horse. The examiner must be knowledgechecked by turning the horse short around able in equine anatomy, normal confom1aits own axis.

tion and gaits, regional anesthesia, and

Examination during exercise is often
imaging techniques and be able to recognize required to localize the lameness to a forelin1b and hindlimb lameness.

specific limb or site and to evaluate the

The exan1ination begins with a compreresponse to diagnostic regional anesthesia.

hensive medical history; type, age, and train

If lameness is major and acute and a
ing regin1en may give in1portant clues to the
fractw-e is suspected, exercise should not
lameness, as will the tin1e since onset of
be undertaken or a catastrophic breakdown
lan1eness, interim management, and any
may result. Similarly, diagnostic regional
suggestions that the lan1eness may improve
anesthesia should not be perfom1ed when
with either rest or exercise. The interval
a fractw-e is suspected. It is in1portant to
since the last shoeing should also be noted.

determine whether the horse may have been

Response to anti-inflammatory or analgesic
given analgesic medication before the
medications may provide useful informalameness exan1ination.

tion. Results of hematologic and biochemi

Recognition of lameness is a key skill to
cal analyses may shed light on other
successful diagnosis. The most consistent
problems that influence overall perforsign of a unilateral forelimb lameness is the mance.

head nod. The head and neck of the horse

Although valuable, modem diagnostic
rise when ilie lame forelimb strikes the
in1aging techniques are no substitute for
ground and is weightbearing, and fall when
detailed visual inspection and thorough
the sotmd limb strikes the ground. The
manual palpation of the limbs in weightbearsacral (pelvic) rise is the most consistent ing and nonweightbearing positions.

and easily observed sign of hindlimb

Confom1ation should be evaluated and the
lan1eness. The entire pelvis and sacrwn rise
horse visually checked for symmetry,
when the lame limb strikes ilie ground and
swellings, muscle loss, abnormal stance, and is weight bearing, and fall when ilie sound obvious irtjuries. The trnnk and limbs should limb strikes the ground. Both head nod and be palpated for heat, pain, swellings, and
sacral rise serve to reduce concussion on
joint effusion. The high degree of variation
the lame limb. A computerized, handheld
between horses should be remembered, and
gait analysis system tl1at objectively
comparison with the contralateral limb
measw-es ilie head nod and sacral rise is
should always be done, although the latter
available to detect lameness and is being
may not necessarily be a useful control. The
used by some veterina.tians.

reaction of the horse to palpation and the

The horse should initially be exan1ined by
range of flexion and extension of all joints
walking and jogging in hand wiili a loose
should be noted. The feet should be
line to the halter so that the movement of
thoroughly exan1ined, including compresilie horse is not restricted. A firm, nonslipsion of the walls and sole with hoof testers.

pery surface ( eg, hardpack fine gravel) is

Wear patterns of shoes and feet should be
ideal to trot on a straight line and to lunge
noted. A nwnber of abnormalities such as
on a firm surface. It also provides an
broken toe/pastern axis; mismatched hoof
opportw1ity to listen to ilie footfall and
angles; under-rw1, contracted, and sheared
consider this infom1ation along with the
heels; and disproportionate hoof size are
visual appraisal. However, feet of different
seen more frequently in lame than in sound
sizes and shapes and different shoes make
horses. Shoes should be left on during the
slightly different impact sounds, often
initial stages of the exan1ination, because
rendering these sotmds of little diagnostic
removing them might make the horse
value. Frequently, lan1eness is more
footsore and preclude further exan1ination
pronounced when the horse is worked in a
with the horse being trotted or ridden. Shoes circle. Circling can be done on a lunge line, should be removed for complete and
free exercise in a large round pen, in ha.t1d,
thorough examination of the foot when the
or under saddle. Lungeing on asphalt or conlameness has been localized to the foot and crete predisposes the horse to slipping and

1098

LAMENESS IN HORSES
injury but may be done in selected cases to
are training problems. If improvement on
accentuate a very subtle hoof or lower limb
medication occurs, the medication should
lameness. Both forelimb and hindlin1b
be witl1drawn and diagnostic anesthesia
lameness may become worse when the
used beginning in an arbitra.iy limb, most
horse is circled; most of the time, the
often a forelimb. In this way, multiple-limb

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lameness is accentuated when the affected
la.inenesses (as many as four), often
limb is on the inside of the circle.

min1icking the clinical picture associated

Flexion tests are useful diagnostic tools.

witl1 back pain, can be evaluated and

The range of movement and response to
treated.

passive Hexion, along with any suggestion

Diagnostic regional a.t1esthesia (see
of increased lameness or onset of lameness
p 1101) should be used to determine tl1e
after Hexion, should be obse1ved. The distal
a.i·ea of pain in all lan1e horses in which the
phalanges in both forelimbs anti hindlimbs
la.tneness can be localized to a specific limb
should be flexed independently of the
but not to a specific site on the limb. A
carpus and hock to obtain maximal infom1aconsistently obse1vable la.ineness must tion. Bending pressure should be fim1 but
be present for tl1e clinician to evaluate
not excessive, which can create false-posiresponse to anesthesia.

tive responses. All tests should be done on

Because la.tneness may be caused by
both sound and lame limbs for comparison.

neuromuscula.i· disorders, a complete

Consistency should always be applied, and
neurologic exa.tnination should be pa.it of
individual experience used. A single
the lameness exan"lination whenever a.tl
positive flexion test without associated
obvious painful or mechanical cause has
lameness may not be of significance.

not been found. The exa.inination should

To establish consistency, tl1e entire
include evaluation of cra.t"lial ne1ve and
exan1ination should involve the same
upper and lower motor neuron function.

handler, the same bitting when the horse is

Observing the horse execute movements
under saddle, and the same surfaces under
such as turning sho1t, backing, "hopping" on foot. The horse should be controlled so that
one forelimb ( with the other forelimb held
it is trotting at a useful, repeatable pace to
up), negotiating a curb, turning in tight
evaluate the lan1eness. Very slight sedation
circles, a.t1d walking uphill and downl"lill
of ne1vous or fractious horses with 3 mg
should be done. These tests help detennine
romifictine or 100 mg xylazine may result in
whether reduced proprioception, weaka horse with a more relaxed outline and ness, or spasticity may be the cause of the
allow a better assessment without
gait abnormality.

seemingly influencing the degree of
lameness. Slowing down tl1e pace at the trot

IMAGING TECHNIQUES
often illustrates a subtle lameness better,
because the horse loses its momentun1 and

Imaging techniques provide important
struggles with suspension in the affected
pathologic and physiologic information
limb(s).

necPssary to treat specific conditions.

A ridden assessment of the lJorse may

Imaging can be divided into anatomic and
be necessary, pa.tticularly with a subtle
physiologic methods. Anatomic imaging
la.tneness that can only be observed under
methods include radiology, ultrasonograsaddle. A multiple-limb la.tneness without a.tl phy, CT, and MRI. Physiologic imaging obvious single-limb la.tneness may also be
methods include scintigraphy and
detected. The clinical signs may be minor
thermography. When diagnostic analgesia

( eg, tl1e horse refusing ce,tain movements
has failed to eliminate the lameness, the
or activities, slight head tilts, or tail
lameness is too subtle for localization by
swishing). However, a good rider can, often
diagnostic analgesia, or the horse is not
inadvertently, hide a problem by his or her
amenable to handling or injection,
inherent expe1tise and ability to "correct"

physiologic imaging techniques may help
difficulties.

narrow the problem to a specific region.

Occasionally, a horse appea.i·s to be sow1ct Anatomic imaging methods can then be when lunged and ridden, but the 1ider feels
used to evaluate those areas. Imaging
that tl1e pe1iormance is impairect. ln such
may also help prevent injury. This
cases, it may be wotth working the horse on
requires early detection of the physioconcomitant analgesic or anti-infla.tnmatory logic changes associated with injury.

medication at therapeutic levels for an

Although frequent use of an anatomic
adequate period (eg, phenylbutazone
imaging method can detect change in

2-3 glday, PO, for 7-14 days) to assess
one region, physiologic imaging allows
whether improvement occurs. Some clinical assessment of the entire horse on a signs purpo1tect to be caused by la.t11eness
routine basis.

LAMENESS IN HORSES

1099

Anatomic Imaging Techniques
lin1bs of the horse require fewer projections.

Radiologic techniques are the methods

This is not because these are less complex
most commonly used to evaluate lameness
areas· rather the size of the horse makes it
in horses. Plain film radiography used to be
diffici'ut to g�t more projections. 1\vo views
the standard but it has been replaced by
can usually be ma.de of the elbow and tl1e

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computed r;diography in equine practice.

stifle. For the shoulder joint, usually only

Computed radiography can be divided into
one view is possible. For the hip, anesthesia.

indirect and direct. Indirect uses a special
is usually required. However, digital
plate instead of film. The plate stores energy radiography has ma.de it possible to take that is then read by a computer to produce
sta.i1ding hip projections on young horses
the iniage. Direct digital radiography also
and those with smaller muscle mass.

uses a special plate, but the radiation is

Production of good radiogra.phs requires
converted to a digital signal and sent
the correct exposure of the film. Proper kVp
directly to a computer. Direct digital
and mA settings, as well as proper focal fihn
radiography produces in1ages faster, but
distance are critical. Unfortunately, these
both share the advantages of fewer retakes,
factors ;a.ry and depend on the pa.iticular
a lower radiation requirement, and post
x-ra.y ma.chine and tl1e fihn or electronic
processing techniques that elin1inate
system used. For an1bula.tory equine

.

contrast problems. Radiography reqwres
practitioners, another factor that must be
multiple projections to evaluate any area.

considered is the electricity output m the

It allows assessment of bony tissues and
ba.i'l1 where the iniages a.i·e ta.ken-older
reflects both acute and chronic changes.

barns may not have sufficient electrical

Occasionally, radiographic techniques that
output for the x-ray genera.tor to make
provide more inforn1ation a.re needed.

the desired exposme. New computed

.

Contrast radiography provides mforma.t1on
radiography systems that a.i·e battery
a.bout articular ca.itilage and surfaces and 1s
operated can a.void these types of elecof pa.iticular value in determining whether trical problems.

subchondral cysts communicate with the

Ultrasonogra.phic exan1ina.tion can
joint and in delineating subcutaneous tracts. be used to assess any soft tissues. Like More recently, these techniques have been
radiography, the a.i·ea. to be exan1ined should
used to delineate cha.i1ges in the na.vicular
be evaluated in two planes go0 apa.it.

bursa and have produced 60% more

Selection of a probe should take into
inforn1a.tion than plain radiography.

account the depth, contour, and location of

Pathologic diagnoses are usually ma.de by
the tissue to be exan1ined. The deeper the
radiography in conjunction with clinical
tissue to be evaluated, the lower the
examination.

wavelength of the probe used. The higher

The goal of radiology, regardless of
the wavelength, the greater the detail that
system used, is to exa.inine the region
can be achieved. For examination of

.

sufficiently to fully evaluate the anatomic
superficial and deep flexor tendons or the
strncture. Dia.gnostic fihns require
suspensory ligament, a 7.5-10 MHz linear
preparation, positioning, and production.

probe is best. Exa.inina.tion of complex.

Preparation involves readying the object
anatomic areas such as the foot or pelVIc
to be radiogra.phed. In most cases, this
region requires a convex linear probe.

requires the object to be clean and all

Exa.inina.tion of the pelvic region internally
foreign materials removed ( eg, any
requires a rectal linear probe.

iodine-based products on the limb will

Ultrasonography is most useful in the
ca.use a.iii.facts on the ra.diogra.ph). For
evaluation of tendons and ligaments but
ra.diographs of the hoof, the shoe may need
can also be used to evaluate muscle and
to be removed a.i1d the sulci packed, in
ca.itila.ge. In all cases, tissue fiber
addition to cleaning.

alignment and echogenicity are the �actors

Positioning is critical; the object must
used to determine anatomic d1srupt1on.

be evaluated from a sufficient number of

Generally speaking, loss of fiber alignment
angles to ensme adequate evaluation.

and decreased echogenicity are signs of

Minimally, this means two ra.diogra.phs gQ0
a.cute injury; increased echogenicity is
a.pa.it. Many of the limbs require more VI
generally thought to indicate chrome

�ws
for adequate evaluation. Exammat10n of
conditions. However, if any questions a.nse
those projections may necessitate fmther
dming the exa.i11ina.tion, the opposite limb
views to better assess any areas of interest.

or area can be examined to compare

For instance, the equine foot, fetlock, and
changes. For the novice ultrasonogra.pher,
carpus require five projections, whereas the
it is a good idea to compare the right and
pastern and hock require four. The upper
left sides before making an ultrasonographic diagnosis.

1100

LAMENESS IN HORSES

Assessment of anatomic changes serves

Physiologic Imaging Techniques
as the basis for any pathologic diagnosis, as
well as being important in detennining

These techniques provide images that
prognosis. For these purposes, radiography
reflect physiologic processes. Unlike

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and ultrasonography are complementary.

anatomic imaging, which reflects structure,

Radiography provides infonnation
physiologic imaging techniques assess
regarding bony tissues, whereas ultrasonogmetabolism or circulation. Thermography raphy provides information about the soft
and scintigraphy allow examination of the
tissues that connect bone or provide
entire horse. When combined with a
supp01t.

thorough clinical examination, these

MRI and CT are high-detail anatomic
methods help identify irtjuries that may
in1aging tools. Their use is becoming
otherwise go undetected.

_ more
common in equine lameness evaluations.

Thennography is the pictorial representa

MRI in particular has become quite popular. tion of the surface temperature of an object.

Two types of MRI are available: low-field

It is a noninvasive technique that measures
and high-field magnets. High-field scanners
emitted heat in the form of infrared radiation
produce a stronger signal and higher resoluand helps detect inflammatory changes that tion pictures in a shorter tin1e than low-field may contribute to lameness. Relative blood scarmers. However, some low-field
flow dictates the thermal pattern; normal
scarmers can be used to exan1ine the
thennal patterns can be predicted based on
standing, sedated horse, whereas high-field
vascularity and surface contour. Skin
scanners require the horse to be anestheoverlying muscle is also subject to

. .

tized.

temperature increase dwing muscle actiV1ty.

The standing units can only be used
to evaluate from the carpus and hock

Circulation is invariably altered in irtjured or
distally. Because of the slower in1age
diseased tissues. Thern10graphically, the
acquisition with the low-field scarmers,

"hot spot" associated with the localized
motion can be a problem. MRI proV1des
inflanunation generally is seen in the skin
sliced images of the anatomic region of
directly overlying the irtjury. However,
interest. The slices are usually in three
diseased tissues may have a reduced blood
different planes: axial (transverse), sagittal
supply due to swelling, vessel tJu·ombosis, or

Oongitudinal), and dorsal. MRI of orthopetissue infarction. With such lesions, the area dic disease is performed in several
of decreased heat is usually swTounded by
acquisition sequences. Each sequence
increased thermal emissions, probably due
displays different anatomic, physiologic,
to shunting of blood. The American
and pathologic information.

Academy ofThern10logy has published

The most
common sequences are the proton density
guidelines for the use of infrared thermograand the Tl-weighted and phy in veterinary medicine. The purpose of

T2-weighted
images. Proton density provides the most
the guidelines is to provide criteria for tl1e
anatomic detail. Tl-weighted images
production of reliable and repeatable
highlight the structural characteristics of
thermal images.

bone and soft tissues, whereas.

During scintigraphy, polyphosphonate

T2-we1ghted
images emphasize the fluid character
radiopharmaceuticals are given IV. Therr

)stics
of tissues and are sensitive for detectmg
distribution is then measured by a ganm1a
synovial effusions, cysts, and edema
camera, which measures the radiation

Special sequences can further clarify or
emitted from the radiophannaceutical after
highlight a lesion. For instance, fat-supit is distributed through the body. The pressed sequences are used to evaluate
polyphosphonates bind rapidly to_ exposed
edema in high-fat signal areas such as the
hydroxyapatite crystal, generally m areas
bone marrow.

where bone is actively remodelling. Because

C
inflammation causes an increase in blood

T is a technology that uses very small
x-ray bean1s from many different angles
flow, capillary pern1eability, and extracelluaround the body (called a slice) that are lar fluid volwne, inflamed tissues accwnureconstructed by computer to produce an late high levels of radiopharmaceut(cal
in1age. Because the images are in slices,
during the soft-tissue phase of scmtigraphy,

.

there is less interference from sun-oundmg
allowing evaluation of soft-tissue iajuries.

anatomy. Therefore, the C

During the bone phase, the radiopham1a

T scarmer
provides the clearest images possible of the
ceutical accwnulates in areas of increased
limbs,joints, nasal passages, skull, smus
remodelling or vascularity. Because irtjured
cavities, and neck
bone is remodelled more rapidly, scintigra

These images improve
the clinician's ability to accurately define
phy helps detect lesions in bone and
and identify the extent of abnormalities of
ligaments, particularly to identify enthesopthese regions.

athy ( dan1age to the insertions of tendons
and ligaments on bone).

LAMENESS IN HORSES

1101

ARTHROSCOPY
ment of hand instrwnents for intra-a.tticular
procedures. A video can1era and video

(Tenoscopy, Bursoscopy)

screen a.i·e highly recommended to decrease

Arthroscopy is the accepted way to perform
the 1isk of contan1ination, to improve visuali

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joint surgery in horses and is a valuable tool
zation and depth perception, and to allow
in the diagnosis of joint disease. Arthrocapture of in1ages and videos. Triangulation scopic surgery can be used to remove bone
techniques are used to optimize ma.ttipulaand cartilage fragments, debride damaged tion of intra-articular instruments.

ligaments and menisci, assist the repair of

Arthroscopy, bursoscopy, and tenosarticular fractures with internal fixation, copy are often used to evaluate and treat
debride or inject subchondral bone cysts,
contan1inated synovial cavities. The
repair cartilage, and debride and flush
techniques facilitate wound debridement,
contaminated or septic synovial cavities.

removal of fibrin and foreign deb1is, a.t1d

Arthroscopy is a valuable method to
copious flushing of the cavities without
evaluate intrasynovial structures and is
inducing more trauma from a major
particularly useful to evaluate soft-tissue
incision. The nom1al intrasynovial
structures such as ligaments, cartilage,
environment can recover quickly. Bursosmenisci, and synovial membranes. It should copy of the navicular bursa has greatly
be used in concert with other diagnostic
reduced the need for the streetnail
methods, including high-quality radioprocedure to treat punctures of the navicular graphs, ultrasonography, and CT and MRI
bursa and has reduced the morbidity of
when available. Diagnostic arthroscopy
calcaneal infections after injury to the hock.

is the most sensitive and specific tool

Tenoscopy has improved the recovery rate
for intra-articular evaluation in horses.

of septic tenosynovitis in horses.

Athroscopes of2.5-5 mm diameter can be
placed in alljoints of the equine limbs;

REGIONAL ANESTHESIA
however, not all areas of every joint can be
examined. The a.tthroscope has also been

Regional anesthesia is a valuable diagnostic
used to examine, diagnose, and perform
aid used to localize lameness when, after a
surgery on structures within the digital,
thorough clinical exan1ination, the site of
carpal, and tarsal tendon sheaths (tenospain remains uncertain. Localizing pain copy) and in the navicular, calcaneal, and
allows other diagnostic procedures, such as
bicipital bursas (bursoscopy).

anesthesia of ajoint, radiography, ultrasonog

Advantages of arthroscopy compared
raphy, CT, scintigraphy, or MRI to be used
with standard surgical procedures include
more effectively and economically to identify
the use of small stab incisions for placement the cause of lameness. Additionally, use of of the arthroscope and instruments, the
regional anesthesia allows some surgical
ability to view numerous areas of the joint,
procedures to be performed without the need
easy operations on more than one joint
for general anesthesia, and it can be used to
during the same surgical procedure, less
provide temporary, humane relief of pain.

trauma to periarticular soft tissues, less

Lidocaine HCl (2%) and mepivacaine HCl
pain, reduced convalescent times, and

(2%) a.i·e the local anesthetic agents most
reduced complications.

commonly used to induce regional

Diagnostic and surgical arthroscopy
anesthesia during the la.tneness exa.tninais technically demanding, and extensive tion. Mepivacaine HCI is preferred by most
experience is necessary to become
clinicians, because it causes less tissue
proficient. Good lrnowledge of joint
reaction than lidocaine HCL Bupivacaine
anatomy and good hand-eye coordination

HCl is used to induce regional anesthesia
and spatial awareness are essential
for humane relief of pain, because it
characteristics of successful surgeons.

provides anesthesia that lasts 4--6 hr.

Most arthroscopic procedures are

The choice of anesthetic agent may
performed with the horse under general
depend on its duration of action. The
anesthesia. Many surgeons prefer dorsal
anesthetic effect of mepivacaine HCI, which
recumbency to allow surgical access to
lasts 90-120 min, makes this agent valuable
all sides of the joint, to allow surgery on
for examining a horse with lameness in
multiple joints and limbs, and to control
multiple limbs or if multiple sites of pain on
hemorrhage. Routine aseptic surgical
a limb are suspected. Lidocaine HCl, which
preparation and draping is necessary. Basic
has an anesthetic effect of only 30-45 min,
equipment required for arthroscopy includes n1ight be the preferred local anesthetic an arthroscope and insertion sleeve, light
agent when different techniques of diagsource and cable, fluid pwnp for joint nostic analgesia are likely to be used
distention, egress cannula, and an assort-
during the lameness examination.

1102

LAMENESS IN HORSES

Most nerves below the carpus or hock
proximally may result in proximal migration
a.re anesthetized using a 25-ga.uge, 5/8-in.

of anesthetic solution and unintended

(1.59-cm) needle. A 1 Y2-in. (3.8-cm),
anesthesia. of more proximal branches of
larger-gauge needle ( eg, 22- or 20-ga.uge) is
the nerve, thus confusing the results of the
used to anesthetize nerves located more
examination.

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proximally on the limb. If a relatively

When the goal of regional anesthesia. is to
large-gauge needle is to be used, SC
identify a. site of pain below the carpus or
deposition of a small a.mount of local
hock, only the smallest effective volume of
anesthetic solution, using a 25-ga.uge needle, anesthetic solution should be administered may a.void resentment by the horse when
to a.void inadvertent anesthesia. of a.<lja.cent
the larger-gauge needle is inserted.

nerves. When the nerve can be palpated

To a.void broken or bent needles during
subcutaneously, a very small volume of local
perineural administration of local anesanalgesic solution can be used because the thetic solution, the needle should always be
solution can be placed more accurately into
inserted detached from the syringe. Spinal
the fascia surrounding the nerve.

needles a.re flexible and more likely to bend

Before regional anesthesia. is performed,
than break and, thus, safer to use if there is
the horse should be consistently and
a possibility the horse may move the limb.

sufficiently la.me so that any improvement in

Using a flexible needle is especially
gait can be detected. Lungeing or riding the
important when the difference in range of
horse may ex.acerbate a subtle lameness.

movement between skin and deeper tissues

The lameness of some horses in1proves or
is large, in case the horse moves during
resolves during exercise; for these horses,
injection. Luer-lock syringes should not be
a false-positive response to regional
used because they a.re difficult to attach to
anesthesia. may result if the horse has not
the needle after it is inserted, and this type
been sufficiently exercised before it is
of syringe cannot be detached quickly from
ex.a.mined. If a horse is subtly la.me, using
the needle to prevent the needle from being
a wireless, inertial sensor-based system
pulled out, bent, or broken if the horse
designed to evaluate lameness allows
moves during the procedure. The needle
objective interpretation of results of
should be directed distally during insertion
diagnostic analgesia..

when anesthetizing nerves in the distal

Relief of pain and resolution of lameness
portion of the limb. Directing the needle
after local anesthetic solution is
common tendon
sheath of the
superficial a11d

/the deep digital
flexor tendons
ruticular pouc
within the
h
of t
carpal cru1al
he fetlock

--- superficial dig.

lateral digi taJ
flexor tendon
extensor tendon

� deep dig.

�
fu,xor tendon
common digi� �
extensor tendon ""'- I
interosseous
extensor tendon of
medms m
intersosseous medius -------
proximal pouch

� � of d1g1tal
entry site for the pastern joint
tendon

�try site for the coffin joint

"'-.;j'

collateral hg fetlock

�

X{ � ����: he
ie���n !:;ath
distal pouch of d1g1tal
lateral aspect
tendon sheath

,, lig chond1 ocompedalia
lig. chondrocoronalia

Arthroscopy and arthrocentesis joint entry sites in the digit, lateral aspect, horse. Illustration
by Dr. Gheorghe Constantinescu.

LAMENESS IN HORSES

1103
administered into the fascia surrounding a

Opinions vary concerning the amount of
nerve in the distal portion of the limb
skin preparation necessary before adminisusually occurs within 5 min, but anesthesia tering regional anesthesia. For short-haired
of larger nerves in the proximal portion of
horses, the site of iJ\iection is often prepared

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the lin1b may take 20-40 min. Results of a
by wiping the site with cotton pledgets or
regional nerve block can be misinterpreted
gauze sponges soaked in 700/o isopropyl
if the horse's gait is assessed before the
alcohol until a pledget or sponge appears
onset of pain relief. When assessing the
clean. If the site of injection is particularly
effects of anesthesia of nerves in the distal
dirty, it should be scrubbed with antiseptic
portion of the limb, the clinician should
soap. The consequences of a n'onsterile, SC
keep in mind that anesthetic solution might
iI\iection are usually minimal, but inadvertmigrate up the nerve to anesthetize more ent, nonsterile ir\jection of a tendon sheath
proximal structures, thus confusing the
or joint could result in septic synovitis.

results of the examination. To avoid this

Regional anesthesia of the distal portion
complication, the gait should be evaluated
of the limb can be accomplished in most
within 15 min after administering a regional
horses using minimal restraint, but for
nerve bock in the distal portion of the limb.

fractious horses or for horses previously

When a regional nerve block is administered subjected to regional anesthesia, using a lip in the proximal portion of the limb, the
twitch or lip chain is prudent. The twitch
horse may develop a gait abnom1ality or
works best when applied in1mediately
stwnble because of altered proprioception.

before placing the needle. If this does

When nerves above the hock or carpus are
not provide sufficient restraint, xylazine
anesthetized, it may be prudent to assess

(0.2 mg/kg) or detomidine (10 mcg/kg) can
the horse's gait on a soft surface or after
be given IV. Acepromazine has no analgesic
bandaging the distal portion of the limb so
effect and, therefore, is less likely to
that abrasion to skin over the dorswn of the
ameliorate lan1eness than is a sedative, such
fetlock is avoided if the horse stwnbles.

as xylazine or detomidine, which provides

If the gait is unchanged after regional
some analgesia. In fact, some clinicians
anesthesia, the effectiveness of the nerve
claim that acepromazine accentuates subtle
block should be detem1ined by checking
lameness, possibly by making the horse less
for skin sensation within the dem1atome
aware of its environment and, therefore,
expected to be desensitized. Skin sensation
more aware of pain in the lame limb. The
is assessed by pressing the tip of a ballpoint
degree to which sedation or tranquilization
pen, key, or sinillar instrwnent over the skin
interferes with assessment of gait depends
covering the region intended to be
on the severity of lan1eness and the skill of
desensitized. For a fractious horse, skin
the clinician performing the examination.

sensation is more safely checked with the

Restraining the horse in stocks to
limb held or from a distance using a blunt
administer regional anesthesia of the distal
instrwnent taped to a 3-ft pole. A wellportion of the limb increases the likelihood behaved, stoic horse may not react to
of iJ\iury to the clinician. Regional
stimulation of skin even though regional
anesthesia of the distal portion of the limb
anesthesia was ineffective. For such a horse,
usually requires multiple iI\iections, which
reaction to cutaneous stimulation should be
is most safely accomplished with the limb
assessed before regional anesthesia is
held. When a nerve block is performed
performed, or reaction to cutaneous
with the horse's limb on the ground, the
stimulation of the same dermatome on the
contralateral limb can be lifted off the
contralateral limb should be assessed.

ground to enhance the safety of the

When performing regional anesthesia,
procedure for the clinician.

especially in the distal portion of the limb,

When anesthetizing the foot of a forelimb,
local anesthetic solution can be adminismost clinicians prefer to hold the limb while tered inadvertently into a blood vessel,
facing in the opposite direction as the horse;
joint, tendon sheath, or bursa. Aspiration
however, some clinicians prefer to
before injection may indicate that the
anesthetize the foot while facing the same
needle has been placed within a blood
direction as the horse. When facing the
vessel. Administering the anesthetic
same direction as the horse, the foot can be
solution as the needle is withdrawn
held between the clinician's knees to free
decreases the likelihood of depositing the
both hands for the procedure, but the
solution in an unintended structure and
clinician is at risk of injury if the horse
results in deposition of the solution in more
swings its limb caudally. When the clinician
than one tissue plane, which increases the
faces the opposite direction as the horse,
likelihood of the solution contacting the
the procedure is performed using one hand
nerve.

because the other hand must hold the limb.

1104

LAMENESS IN HORSES

Nerve blocks performed distal to the
anesthetize a portion of the fetlock joint.

fetlock of the pelvic limb are most safely

Positive response to a basisesamoid nerve
perfonned with tl1e pelvic limb stretched
block, perforn1ed after a PDN block has
caudally and held on the thigh of tl1e
failed to ameliorate lameness, localizes the
clinician performing the block.

site of pain causing lameness to the pastern.

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Complications of regional nerve blocks

The low palmar nerve block, or low
are rare but include a broken needle shaft,

4-point block, is performed after a negative

SC infection, and infection of a synovial
response to the abaxial sesarnoid nerve
strncture adjacent to the nerve anestheblock. TI1is nerve block is usually performed tized. Local anesthetic solution is detectable with the horse bearing weight on the limb, systemically, which could create a problem
but it can also be pe1fo1med with the limb
for a horse participating in a competition if
held. The medial and lateral palmar nerves
the horse's serum is examined for the
are anesllietized, using a 25-gauge, 5/8-in.

presence of drugs.

needle, by depositing 2 mL of local anesthetic
solution over each palrnar nerve where it lies

Regional Anesthesia of the Forelimb
subcutaneously at the dorsal border of the
deep digital flexor tendon. The palmar ne1ves

Because perineural analgesia should start
should be blocked at llie level of the
distally and progress proximally, the palmar metacarpus to avoid the possibility of digital nerve (PDN) block is the most
misdirecting a needle into the digital flexor
commonly performed regional nerve block
sheath, which often extends proximally to
of the forelimb. The PDN block is perfo1med the level of the end of llie splint bones. When with tl1e limb held. The needle is inserted
fue palrnar nerves are blocked at tl1e level of
directly over the palpable neurovascular
the middle of fue metacarpus, tl1e communibuncUe -1 cm proximal to tl1e cartilage of cating branch lliat connects fuem, fue ramus
the foot. The needle is directed distally,
conununicans, should also be blocked witl1
and 1.5 mL of local anesthetic solution is

1 mL of local anesthetic solution. Blocking
deposited near tl1ejunction of the nerve and
one palmar nerve proxin1al to fue ran1us
the cartilage of the foot. The PDN block is
comrnunicans and the other distal to it allows
sometimes called a "heel block," but this
sensory impulses to propagate tJu·ough fue
tenninology is erroneous because the block
ran1us from fue side blocked proximal to the
anesthetizes the entire foot, including the
ramus and fuen proximally tl1rough fue
distal interphalangeal (coffin) joint. For a
pal.mar ne1ve blocked distal to llie ramus.

few horses, the PDN block may also cause at Though easily palpated on fue forelimb, tl1e least partial anesthesia of the proximal interramus comrnunicans is often nonexistent or phalangeal (pastern)joint, especially if a
impossible to palpate on fue pelvic limb.

large volume of local anesthetic solution

To complete the 4-point block, 1-2 mL of

( eg, >3 mL) is injected.

local anesllietic solution is deposited SC at

If the horse's gait does not improve
the distal end of each splint bone, where llie
after a PDN block, some clinicians next
palmar metacarpal ne1ve lies next to tl1e
administer a semi-ring block at the
periosteurn of fue third metacarpal bone.

pastern to anesthetize the dorsal branches

A positive response to a low 4-point block,
of the digital nerve that supply the foot.

perforn1ed after a negative response to an

Because the dorsal branches of the digital
abaxial sesamoid nerve block, localizes fue
nerve contribute little to sensation within
site of pain causing lameness to the fetlock.

the foot, a semi-ring block at the pastern is

The high palmar nerve block, or high
unlikely to improve tl1e gait if aPDN block

4-point block, can be pe1fonned when tl1e
failed to improve it.

low 4-point block fails to improve lan1eness.

Most clinicians proceed to a basisesa

Willi fue limb bearing weight, fue medial and
moid nerve block if the horse's lameness
lateral palmar and palmar metacarpal nerves
is not reduced with a PDN block. With this
are anesfuetized slightly distal to llie level of
regional nerve block, the palrnar nerves are
the carpometacarpaljoint. To anesthetize a
anestl1etized at the level of the base of the
palrnar ne1ve, a 25-gauge, 5/8-in. needle is
proximal sesan1oid bones, before tl1e nerve
inse1ted tJu·ough fascia to where fue nerve
branches into the dorsal and palmar digital
lies near the dorsal border offue deep digital
nerves. When performing an abaxial
flexor tendon, and 3-5 mL of anesfuetic
sesan1oid nerve block, 2.5--3 mL of local
solution is deposited over tl1e nerve.

anesthetic solution is deposited at the base

Anesthetizing the medial and lateral
of the proximal sesamoid bones over the
palrnar nerves alone desensitizes llie flexor
neurovascular bundle, which is easily
tendons and inferior check ligament. Willi
palpated at this location. More proxin1al
tl1e limb held or bearing weight, the palmar
deposition of local anesthetic solution may
metacarpal nerves are anesthetized slightly

LAMENESS IN HORSES 1105

VetBooks.ir

\ L--- caudal
r I cutaneous
antebrachial n.

ulnar n.

of ulnar n.

deep
br. of
palmar

Ydorsalbr.

'

paln1ar m1.

br. of �
lateral
medial
median n.,
ulnar
distal approach
ll.

�neti�ru;� 1111.

lateral
medial

0mar digital �

;------ lateral
medial --\
paln1ar br. of palmar

�
digital nn.

/
lateral
medial

Thoracic limb, lateral aspect

Thoracic limb, medial aspect

Landmarks for nerve block of the forelimb, horse. Illustration by Dr. Gheorghe Constantinescu.

distal to the level of the carpometacarpal
lateral palmar nerve distal to this site,
joint by inserting a 20- to 22-gauge, l \.2-in.

the structures they innervate, such as
needle into the angle formed by the junction the proxinlal aspect of the suspensory ligaof the third metacarpal bone and the second ment, are desensitized.

or fourth metacarpal bone. Anesthetizing

If the site of pain causing lan1eness
the medial and lateral palmar metacarpal
cannot be localized by performing the
nerves alone desensitizes the splint bones
previously discussed nerve blocks, most
and their interosseous ligan1ents and the
clinicians perform joint blocks of the carpus,
proximal aspect of the suspensory ligament. elbow, or shoulder. The order in which these An easier alternative to the high palmar
synovial structures are desensitized is not
nerve block, when the site of pain causing
important. The median and ulnar nerves are
lameness is suspected to be in the proxinlal
sometimes anesthetized simultaneously as
pmtion of suspensory ligan1ent, is the
part of a lan1eness evaluation to exclude pain
lateral palmar nerve block, which is
below the elbow as the cause of lameness,
performed, with the limb bearing weight, by
but more commonly, they are anesthetized
inserting a 25-gauge, 5/8-in. needle over the
along with the medial cutaneous a.ntebralateral palmar nerve where it courses over cheal nerve to allow surgery of the limb
the medial aspect of the accessory carpal
without the need for general anesthesia.

bone. The needle is inserted in a medial to
lateral direction at the distal third of a
palpable groove, and 2 mL of local

Regional Anesthesia of the Pelvic
anesthetic solution is deposited. Because

Limb
the medial and lateral palmar metacarpal

Techniques to ad.minister regional anesthenerves arise from the deep branch of the sia of the distal portion of the pelvic limb are

1106

LAMENESS IN HORSES

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common fibular

(peroneal) n.

caudal cutaneous

,

\
s

7
br.

v
saphenous n. ,,<f1\. "'!:.�'

:�:eous brr.

cranial br. -----------.i, , _
of superficial and
deep fibular
caudal hr --4

(peroneal) n.

tibial n.

dorsal

1 / deep br. of
metatarsal 11_ II -----------
r lateral plantar n.

medial

·- _
plantar n.

----; /J
dorsal metatarsal n III

----------
medial plantar metatarsal n.

�

_

_ _ ______-;!

> lateral plantar n

}

lateral plantar
medial plantar chg1tal n.

<, I{

_' �� metatarsal n.

/ -- �{
lateral plantar digital n.

plantar brr. of plantar digital nn.

Landmarks for nerve block of the horse pelvic limb. Illustration by Dr. Gheorghe Constantinescu.

slightly different than the teclmiques to
through a 20- to 23-gauge, 1-in. needle, axial
administer regional anesthesia of the
to the lateral splint bone and -1 cm distal to
forelimb, because branches of the deep perothe tarsometatarsaljoint, between the neal (fibular) neive of the pelvic limb supply
tendon of the deep digital flexor muscle and
additional inneivation to this region. These
the suspensory ligament. The solution
branches, the medial and lateral dorsal
diffuses to anesthetize the deep branch of
metatarsal neives, col.ITTle adjacent to the
the lateral plantar neive, which branches
extensor tendon and inneivate the dorsal
into the medial and lateral plantar metaaspect of the laminar coriwn. After tarsal neives that supply the proximal
depositing local anesthetic solution for a low
aspect of the suspensory ligament.

4-point neive block at the level of the distal

Depending on results of flexion tests or
aspect of the splint bones, the needle is
causes oflameness typical for the particular
redirected dorsolaterally or dorsomedially,
athletic function of the horse, the clinician
parallel to the bearing surface of the foot,
may proceed to joint blocks or to more
and an additional 2 mL oflocal anesthetic
proximal regional nerve blocks. The
solution is deposited SC to anesthetize the
peroneal and tibial neives can be blocked
medial or lateral dorsal metatarsal neives.

simultaneously to exclude pain in the hock

Most lan1enesses of the pelvic limb, however, or regions distal to the hock as a cause of can be evaluated accurately without
lameness, or the blocks can be perfom1ed
anesthetizing the dorsal meta tarsal neives.

separately to gain added insight as to the

The high plantar nerve block is
possible site of pain. Iflan1eness is
administered, using techniques similar to
ameliorated after a tibial neive block, but
those used to administer the high palrnar
not after a low 4- or 6-- point block, t11e
neive block, -1 cm distal to the tarsometasuspensory ligament is a likely source of tarsal joint. When the proximal aspect of the pain. Iflan1eness is an1eliorated after a suspensory ligan1ent is suspected to be the
peroneal (fibular) neive block, but not after
site of pain causing lameness, 3-4 mL of
a low 4- or 6- point block, one or more of the
local anesthetic solution can be deposited
tarsal joints are the likely source of pain.

LAMENESS IN HORSES

1107

The tibial nerve is blocked -10 cm
shoe. Horses with flat feet or either thin or
above the point of the hock on the medial
dropped soles are predisposed to bruising,
aspect of the limb, where it lies in fascia on
usually at the toe or around the periphery of
caudal surface of the deep flexor muscle,
tl1e sole. Bruising in the caudal sole at tl1e
cranial to the Achilles tendon. Twenty mL
buttress (the angle between the wall and tl1e

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of mepivacaine HCl is deposited through
bar) is termed a com. Bruising commonly
a 20-gauge, 1 Y2- in. (3.8-cm) needle at this
occurs with no abnorn1alities present on the
site, in at least several planes in the fascia
keratinized sole, although solar changes may
surrounding the nerve. The deep peroneal
be present ranging from some red staining of
nerve can be blocked on the lateral aspect
the inner solar epidermis ( due to minor
of the limb -4 in. above the point of the hock hemorrhage) to the palpable presence of in the groove formed by the lateral and Jong
serum either under tl1e solar epidennis or
digital extensor muscles. A 20-gauge, 1 Y2-in.

seeping through it. If untrcated, the affected
needle is directed slightly caudally until it
area can become infected (ie, a subsola.r
contacts tl1e caudal edge of the tibia, and
abscess). Persistent, nonresponsive bruised

20 mL of mepivacaine H Cl is deposited.

sole dorsal to the apex of the frog suggests
possible distal displacement of the distal
phalanx secondary to laminitis.

A "com" is most conunon in the forefeet on OSSEOUS CYST-LIKE LESIONS IN
the inner buttress and can be caused by 1) the

THE DISTAL PHALANX
heel of a shoe improperly placed (heel of
branch bent excessively toward frog); 2) a

Osseous cyst-like lesions in the distal phalanx
shoe left on too long, causing pressure on the
can result in a lameness that varies from mild
buttress; or 3) shoes fitted too closely at the
to severe and may be unresponsive to
quarters or too small for tl1e foot. Corns are
anti-inflan1TI1.atory medication. There is no
described as dry ( only mild bruising), moist
apparent breed or sex predisposition. The

( serous exudate present), or suppurative
cysts are commonly first diagnosed in young

(infected or abscessed). Bruising may be
horses (1--3 yr old) but may be diagnosed in
associated with lameness, depending on the
older horses. It is unknown whether the cysts
severity. When the foot is raised and the solar
have a developmental or tratm1atic origin.

surface freed of dirt and loose horn, a

They are most commonly located in tl1e
discoloration, either red or reddish yellow,
subchondral bone either in the extensor
may be noted. Pressure on the affected area
process or along the joint surface close to the
with hoof testers usually causes varying
rnidline; the cysts may communicate with the
degrees of discomfort, again depending on
distal interphalangealjoint. The lameness
the severity of the lesion.

may be exacerbated with distal limb tlexion,

Treatment of sole bruising is int1:nded to
and it usually responds to intra-articular
remove pressure and protect the bruised
anesthesia of the distal interphalangeal joint
area In horses predisposed to corns, proper
if the cysts communicate with thejoint. The
shoeing with branches that fit well on the
lameness may respond to palmar digital nerve hoof wall at the quarters and heels ( and anesthesia but more commonly requires a
extend to the caudal aspect of the buttress)

more proximal nerve block ( eg, abaxial
will decrease tl1e incidence of lesions. In
sesamoid) for resolution of the lan1eness.

horses predisposed to bruising due to

Diagnosis is confinned by radiography and/or dropped soles, application of a wide-webbed CT. Differential diagnoses include keratoma,
shoe beveled on the solar surface (ma.de
navicular disease, and prin1ary degenerative
concave relative to the solar surface) to avoid
joint disease of the distal interphalangeal
solar pressure will help protect the sole.

joint. Surgical treatment includes arthro

Additionally, a pad can be placed on the foot
scopic debridement; extracapsular (through
to protect the sole. In horses with painful
the hoof wall) approaches to the cysts have
corns, the affected heel can be unweighted
been used in less accessible lesions.

by trinuning the wall and insensitive sole to

Secondary fracture of the extensor process
minimize contact with the shoe until healed;
has been reported to occur due to a cyst in
a bar shoe can also help disperse pressure
that region. Some horses return to perforaway from tl1e trinm1ed area.

mance status, whereas others are used for

If the bruise/com is suppurating, ventral
alternative purposes such as breeding.

solar drainage, usually established with a
hoof knife, is usually adequate to allow

BRUISED SOLE AND CORNS
healing. If the affected subsolar area is
large, the abscess can usually be addressed

Bruising on the solar surface of the foot
by establishing small areas of drainage
usually is caused by direct iltjury from

( -1 cm in diameter) at opposite sides of the
stones, irregular ground, or a poorly fitting
affected area ( established by probing),

1108

LAMENESS IN HORSES
followed by lavage with saturated Epsom
markedly improved by palmar digital nerve
salt solution via either a 14-gauge catheter
block (which blocks both the navicular
or teat cannula attached to a 60-rnL syringe,
region and the coffinjoint). Radiography
repeated daily or every other day w1til
confirms the diagnosis, in which a sagittal
healed. This is usually more effective than
fracture is usually foW1d medial or lateral to

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foot baths or application of poultices. The
the midline; care must be taken to pack the
sole should be covered until the solar
sulci of the frog to avoid artifacts that
smface is covered by tough epithelium
appear as navicular bone fractures.

(horn). Parenteral antibacterial therapy is

Conservative treatment is prolonged rest
of questionable value unless cellulitis is
with corrective shoeing to apply a dramatipresent proximal to the coronary band.

cally raised heel (up to 12°); however, a
bony union at the fracture site is seldom

CANKER
satisfactory, and the prognosis is guarded to
poor. Surgical repair by lag screw has been

Canker is a chronic hypertrophy and apparent described to have a better prognosis.

suppuration of the horn-producing tissues of
the foot, involving the frog and the sole. The
cause is unlrnown. Although frequently

FRACTURE OF DISTAL PHALANX
desc1ibed as a disease seen in aninlals kept in
moist or unsanitary environments, it is also

(Fracture of third phalanx, os pedis, or
encoW1tered in well-erred-for aninlals. The
coffin bone)

disease can be observed in both front- and

Fracture of the distal phalanx is a fairly
hindfeet. It most commonly starts in the
common irtjury that occurs most commonly
caudal frog, where tlle affected area consists
at high speed (ie, during a race) or less
of an inflamed granulation tissue with
commonly from kicking a firm object ( eg,
proliferative epitheliW11, often appearing as
a stall wall). The fracture is caused by
fronds. The affected tissue is commonly
concussion and produces a sudden onset of
covered by caseous exudate, which may be
lan1eness. The lameness is severe if the
foul smelling. The surface of the lesion is
fracture is intra-articular but may be less
irregular, with a characteristic, cauliflowersevere if only a wing ( or solar margin of the like vegetative growth. The disease process
distal phalanx) is fractured with no articular
may extend to the sole and even to the wall,
component. Distal phalangeal fractures
showing no tendency to heal.

occur more frequently in the forelimb but are

Treatment requires sharp debridement
also common in the hindlinlb. Intra-articular
down to normal tissue, attempting to
fractures may be easily isolated to the foot;
maintain any normal epithelium. All loose
lameness is commonly associated with joint
horn and affected tissue should be removed.

effusion. Nonarticular fractures may require

After debridement, an antiseptic or
compression of the foot with hoof testers and
antibiotic dressing should be applied daily;
possibly Wlilateral palmar digital nerve
good results have been reported using a
anesthesia for localization. Lameness is
solution of lO"A, benzoyl peroxide dissolved
exacerbated by turning the horse or making it
in acetone. Metronidazole is corrtmonly
pivot on the affected leg. If the fracture does
applied topically with the benzoyl peroxide/
not extend into the joint, the lameness may
acetone treatment. A clean, dry woW1d
inlprove considerably after 48 hr of stall rest.

environment must be maintained to allow

The clinical sigris may be S{!ggestive, but
healing, which may take weeks or months.

the diagnosis is confinned by palmar digital

Close attention is required over the healing
nerve block and radiographic imaging.

period; if any questionable areas appear,

Radiographic confinnation may be difficult
they must be aggressively addressed.

inlmediately after the irtjury, because the
fracture is only a hairline at this stage.

FRACTURE OF NAVICULAR BONE

Often, more than two views are required
before the fracture line is evident. Repeating

Navicular bone fractures are usually a result
the radiography several days or weeks later
of tramna or excessive concussion to the

(to allow bone resorption) and using
foot, but the cause is not always known. It is
oblique views may be necessary to confum
much less common than distal phalanx
tl1e presence and exact site of the fracture.

fracture and is more commonly seen in the

Additionally, if the suspected fracture is in a
forelimb. Although pain is variable, hoof
wing of the distal phalanx, Wlilateral palmar
testers usually induce a painful response
digital nerve anestl1esia may be performed
over the frog. Lameness is severe with acute
to localize the lameness to that side.

fractures, but it may be less in a chronic

Detem1ining whether the fi·actw·e extends
fracture in which a fibrous union has
into the distal phalangealjoint is important.

presW11ably failed. The lameness usually is

Scintigraphy and MRI are other in1aging

LAMENESS IN HORSES 1109
options if a definitive diagnosis is not
the distal phalanx. Because the laminae are
possible by radiographs.

responsible for suspending the distal

Conservative treatment of &-9 mo rest
phalanx within the hoof wall, laminar failure
is usually all that is required for fractures not
in combination with the downward forces
involving the joint. Fractures often heal with
of the weight of the horse and distracting

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a fibrous union, so that, even though the
forces such as the tension from the deep
horse returns to soundness, radiographic
digital flexor tendon commonly results in
evidence of the fracture remains. A straight
a catastrophic displacement of the distal
bar shoe with a clip well back on each
phalanx, resulting in severe lameness.

quarter can be applied to limit expansion

Laminitis affects all breeds of horses.

and contraction of the heels. In young horses

( <3 yr old), fractures into the joint may heal

Etiology and Pathogenesis: Three
satisfacto1ily, provided a 12-mo rest petiod is
ma.in disease states are thought to be
given. Older horses (>3 yr old) have a much
associated wiili laminitis: 1) diseases
less favorable prognosis, and insertion of a
associated with sepsis or endotoxemia,
cortical bone screw using interfragmentary

2) endocrinopathic laminitis encompassing
compression across the fracture site is
boili equine metabolic syndrome (including
indicated; however, infection is a frequent
pasture-associated lan1initis, see p 1006 and complication, because an extracapsular
pituitary adenoma ), and 3) supporting limb
approach is required. Many fractures heal in
lanlinitis. The pathogenesis of lami.Jlitis
the presence of infection, but the screw must remains controversial and most likely varies be removed at a second surgery to restore
widely between iliese three primary causes.

the horse to complete working soundness.

A fourth, less common cause is ingestion of

Unilateral palmar digital neurectomy of
shavings (someti.Jnes inadvertently used for
racehorses with nonarticular wing fractures
bedding) from black walnut heartwood; the
has been used to allow return to competition
pathophysiology of tllis type of laminitis
without the delay for complete healing.

appears sinillar to that of sepsis-related
laminitis. The diseases causing systemic

KERATOMA
sepsis in sepsis-related laminitis are
diseases commonly associated with

(Keraphyllocele)

gram-negative bacterial ( or polynlicrobial)

A keratoma is a benign mass made up of
sepsis and include ingestion of excess
keratin tl1at is situated between the hoof
carbohydrate (grain overload), acute
wall and distal phalanx. The cause is
postpa.rturient metritis (retained fetal
unknown. Although keratomas originate at
membranes), colic (anterior enteritis, large
the level of the coronary band, the condition colon volvulus), and enterocolitis. Laminitis may be difficult to detect until the growth is
secondary to equine metabolic syndrome
well advanced and located in the wall far
most commonly occurs m overweight
distal to the coronary band. There is
horses and ponies and is commonly
commonly bulging of either the coronary
exacerbated when grazing lush pastures. It
band or the hoof wall over the keratoma,
is possible that lanlinitis occurring from an
depending on its position within the foot.

acute intake of lush pasture may be a combi

Pressure from the keratoma causes
nation of sepsis-related laminitis ( similar to
well-demarcated bone resorption of the
grain overload) and metabolic syndrome.

distal phalanx (usually appears that a "bite"

Supporting li.Jnb lan1initis can occur any
has been taken out of the solar margin in
time ilie horse places excessive weight
most cases), which can usually be
on one li.Jnb for an extended period because
visualized best via tl1e 65° dorsopalmar
of mability to use the oilier limb ( eg, postradiographic view of the distal phalanx.

operative orthopedic procedures, radial

Surgical removal of the mass is indicated.

nerve paralysis, or a septicjomt or tendon

Once localized, it is best to resect the mass
sheaili).

through an approach through the hoof wall

The basic cause of laminar failure m
versus from a solar approach.

laminitis is a failure of attachment of ilie
laminar basal epiilielial cells (LBECs) of ilie

LAMINITIS
epidennal laminae to ilie underlying dermal
lanlinae. Aliliough this failure was thought

(Founder)

to be primarily due to breakdown of ilie
matrix molecules in the basement

Equine laminitis is a crippling disease in
membrane and dennis (to which the LBECs
which there is a failure of attachment of the
attach) by matrix metalloproteases, studies
epide1mal laminae cormected to the hoof
have questioned ilie i.Jnportance of matrix
wall from the detmal lanlinae attached to
metalloproteases. It appears that the LBECs

1110

LAMENESS IN HORSES
may primarily be losing attachment to the
depending on which opposite limb has
underlying dermal laminae due to dysreguthe weight-bearing problem.

lation of the hemidesmosomes (the
adhesion complexes on the basal side of the

Clinical Findings: Classically, laminitis

LBECs that attach the cells to the underlyis considered acute, subacute, or chronic.

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ing mat1ix molecules of the basement

Acute laminitis is classically defi.ned as the
membrane) and possibly the associated
initial few days of clinical signs of laminitis
cytoskeleton. Inflammatory mediators and

( usually <3 days) in a horse in which the
enzymes ( eg, proinflammatory cytokines,
distal phalanx has not undergone displacecyclooxygenase-2) are markedly increased ment. Subacute laminitis is commonly used
in the laminae in the early stages of
to define laminitis in which clinical signs
sepsis-related laminitis and may injure the
have continued >3 days, but the horse still

LBECs or cause cellular dysregulation,
has no dist.al phalangeal displacement.

leading to loss of attachment. Hypoxia and

Chronic lan1i.nitis is classically defined as the
ischemia due to aberrant vascular flow is
case in which distal phalanx displacement
also likely to play a role in LBEC dysfunchas occurred regardless of the duration of tion in sepsis-related laminitis but appears
the disease. Early in laminitis, the horse
to occur later in the disease process.

is depressed and anorectic and stands

The pathophysiology behind laminitis
reluctantly. Resistance to any exercise is
associated with equine metabolic syndrome
marked, and the nonnal stance is altered in
is not as well researched as sepsis-related
attempts to relieve the weight borne by the
laminitis, but work indicates that inflammaaffected feet. If only the forelimbs are tory signaling does not play a major role and
affected, the horse will stand with the
that dysregulation of the LBECs is likely to
forelimbs placed far forward (to decrease
result from insulin-related signaling,
the weight on the front digits); tl1e llindlirnbs
possibly through growth factor receptors
also are placed more fo1ward to support
such as IGF-1 receptor. The pathogenesis of
more of the weight of tile horse. If forced to
supporting limb laminitis is only now being
walk, the horse shows a slow, crouching,
intensively investigated. These studies
short-striding gait. If all four limbs are
indicate that the central pathophysiologic
affected, the animal will appear "camped
factor in supporting limb laminitis is
out," with the forelimbs placed more
decreased laminar blood flow due to a
forward than usual and the hindlirnbs placed
lack of movement of the supporting limb
more caudally than usual. Each foot, once
because of pain in the opposite limb.

lifted, is set down as quickly as possible.

After loss of integrity of the laminar

In the acute stage of laminitis, tile entire
attachments, the distal phalanx can undergo
hoof wall may be warm. An exaggerated and
three types of displacement depending on the bounding pulse can be palpated and may be forces placed on the foot and the pattern of
visible in the digital arteries. Pain can cause
laminar injury. Symmetrical distal displacemuscular trembling, and a fairly u.niforn1
ment of the entire phalanx ( usually tenned
tenderness can be detected when pressure is

"sinking") occurs when there is circunlferapplied to the sole (most commonly in tile ential loss of laminar attachrnents, most
toe region). The pulse rate (60-120/rni.n) and
commonly seen in severe cases of sepsis but
respiratory rate (80-100/nlin) are commonly
also seen in equine metabolic syndrome.

increased, prirnatily because of pain.

Palmar rotation of the distal margin of the

Lameness is usually moderate to severe at
distal phalanx (usually tern1ed "rotation") is this time. In exceptionally severe cases, for
the most common displacement seen, and
which the prognosis is unfavorable, a
most likely occurs due to a combination of
blood-stained exudate may seep from the
loss of the dorsal lanlinar attachments (while
coronary bands. These clinical signs do not
maintaining some laminar integrity in the
always occur in endocrinopathic laminitis
quarters and heels) and tension on the deep
because of tile insidious nature of the disease
digital flexor tendon. Rarely, u.niaxial/
process, which can occur over months or
unilateral distal displacement of the distal
years; the first clinical sign in many of these
phalanx occurs, most commonly to the
horses is toe bruising due to solar compresmedial side in the forelimb; this displacement sion by the slowly displacing distal phalanx.

can only be visualized on an anterio1°posterior Radiographic evidence of displacement of radiograph of the foot. In laminitis related to
the distal phalanx can be present as early as
sepsis and equine metabolic syndrome, the
the third day after the onset of disease in
forelimbs are most commonly affected,
horses with sepsis/endotoxemia However,
although the hindlinlbs can also be affected
an MRI study has shown tl1at, in the acute
in severe cases. In supporting limb laminitis,
case, tl1e horse may have normal-appearing
either a front or rear foot is affected
distal phalanx on radiographs, despite

LAMENESS IN HORSES

1111
destruction of the entire dorsal laminar
the foot without severe duress to the horse.

attachment that is visible on MRI.

Lidocaine should be used for the nerve

Subacute cases may exhibit any or all of
block, because it will last only a short time
the above clinical signs but to a lesser degree.

(ie, not long enough for the anin1al to move

Often, there is only a mild change in stance,
excessively and further damage the

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with reluctance to walk and some increased
lan1inae); applying a temporary pad to the
sensitivity to concussion on the soles of the
foot not being radiographed (to protect
affected feet. TI1ere may be no demonstrable
that foot) is also reconunended. Gross
heat in the coronary band or increase in
observation and distinct measurements of
digital pulse. The acute and subacute forms
the hoof wall and sole thicknesses from the
of laminitis tend to recur at varying intervals
radiographs allow determination of whether
and may develop into the chronic form.

distal displacement, rotation, both distal

During and inunediately after displacedisplacement and rotation, or unilateral ment of the distal phalanx ( classically termed sinking has occurred. Depending on the chronic laminitis once displacement occurs,
radiographic diagnosis of the type of phalanregard.less of the temporal aspect of the geal displacement present, there is usually
disease course), the horse is usually
time while the nerve block is still effective
extremely lame and may spend a great deal
to apply a temporary type of pad or shoe.

of time recumbent. In severe cases, the foot
may prolapse through the sole cranial to the

Treatment: Acute laminitis constitutes
frog, or the coronary band may separate;
a medical emergency, because phalangeal
both occurrences gravely affect the
displacement can occur rapidly. Despite
prognosis. Longtem1 cases of chronic
prompt therapy, the prognosis is guarded
laminitis are characterized by changes in the
until recovery is complete and it is evident
shape of tl1e hoof and usually follow one or
that the hoof architecture is not altered. Most
more attacks of the acute form. Especially
anin1als should be administered NSAIDs,
with cases of rotation of the distal phalanx,
with flunixin meglun1ine being the drug of
bands of irregular horn growth (lan1i.ni.tic
choice if the horse is still systemically ill (ie,
rings) may be seen in the hoof, close at the
enterocolitis). Phenylbutazone is usually
toe and diverging at the heel ( due to minimal
used in the early chronic stage when the
hoof growth from the dorsal coronary band).

horse is lame but does not have signs of

The hoof itself becomes narrow and
systemic disease such as sepsis/endotoxelongated, with "dishing" of the dorsal emia. Close attention to the potential
surface of the hoof wall with a steep angle to
toxicities of NSAID therapy, particularly
the hoof wall proximally and a much more
with phenylbutazone, is required. Because
horizontally oriented wall distally.

phenylbutazone accumulates in the tissue

As the displacement of the distal phalanx

( unlike flunixin or most other NSAIDs ), it is
progresses in longterm cases, the sole
best to skip a day every 5-7 days to "clear the becomes flattened or somewhat convex in
system" (flunixin can be administered that
outline on the ground surface inunediately
day). NSAIDs should be used according to
cranial to the apex of the frog. The gait is
label instructions and, if used in combination,
similar to that already described, and when
the dosage of each drug should be reduced
standing, the body weight is continually
accordingly. Another option for treatment of
shifted from one foot to the other. Radiograchronic laminitis in horses at risk of renal or phy conunonly reveals rotation and some

GI complications is the COX-2-selective
bony resorption of the dorsal solar margin

NSAID firocoxib. Other options for analgesia
of the distal phalanx in longer term cases.

include detomidine, butorphanol, morphine,
or a constant-rate infusion of a "cocktail" of Diagnosis: In acute laminitis, diagnosis is
sedatives and analgesics.

usually straightforward and is based on the

For treatment of possible ongoing
history ( eg, grain overload) and posture of
ischemia, acepromazine is the only drug
the horse, increased temperature of the
found to effectively increase digital blood
hooves, a hard pulse in the digital arteries,
flow in some studies; however, this has been
and reluctance to move. Abaxial sesan1oid
questioned again by a study using lanlinar
nerve blocks of the forelin1b digits in the
microdialysis catheters in which urea
very lan1e horse allow assessment of
clearance ( an indicator of blood flow) was not
possible involvement of the hindfeet (by
changed in horses administered acepromawalking the anin1al a few steps) and enable zine. In a horse at risk of or in the early stages
full assessment of the soles of both feet (for
of sepsis-related lan1i.ni.tis, digital hypothersolar prolapse, etc). These nerve blocks also mia ( cooling of the foot by placing it directly make it possible to obtain good quality
in ice water) has been popularized again by
lateral and anterior-posterior radiographs of
several experimental studies consistently

1112

LAMENESS IN HORSES
demonstrating efficacy in protection of the
clogs in cases of rotation of the distal
structural integrity of the lamella.r tissue; in
phalanx.

one clinical study of enterocolitis cases in two

Surgical options include deep digital
hospitals, risk of developing laminitis was
flex or Leno to my, to neutralize the pull of the

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decreased 10-fold in septidendotoxemic
deep digital flexor tendon, and dorsal hoof
horses in which continuous digital hypotherwall resections. Deep digital flexor mia was pe1formed.

tenotomy is most conm10nly pe1fonned

During the first 2-3 wk, it is important
in cases of chronic rotation that do not
to remove standard shoes, because shoes
respond to the above shoeing techniques;
place the majority of stress on the hoof wall
it should always be accompanied by
and therefore the laminae. The feet should
aggressive derotation via rasping of the
be padded with a soft, resilient substance
caudal foot. The farrier and veterinarian
such as a 1- to 2-in. thick piece of closed-cell
must address subluxation of the coffin joint
foan1 cut to the diameter of the foot. Pads to
subsequent to deep digital flexor tenotomy
provide sole support can also be made from
in most cases (usually by applying adequate
different putties available to farriers.

heel wedging to neutralize the subluxation).

Decreasing padding ( or beveling the pad) in

Hoof wall resections are perfonned much
the region dorsal to the apex of the frog
less frequently than in the past. Generally,
decreases the stress on the dorsal laminae.

only a partial hoof wall resection is

Styrofoam insulation (2 in. thick) can be
performed (usually on the distal hoof wall)

used in small equids but usually provides
because of the severe digital instability
minin1al support in larger animals. Other
caused by removing the entire dorsal wall in
temporary shoes ( eg, Redden Ultimate and
an extensive hoof wall resection.

wooden or EVA clog) that can be applied
with out severe concussion can provide
different physical properties depending on

NAVICULAR DISEASE
the type of displacement (and veterinarian/
fan-ier preference) in the first few weeks.

(Palmar foot pain, Podotrochlosis,

Shoeing laminitic horses with metal shoes

Podotrochlitis)

is usually not a good option until -3-4 wk

Navicular disease is one of the most
after the onset of laminitis, when the laminar
common causes of chronic forelimb
structure may be stabilizing. The type of
lameness in the athletic horse but is
shoeing depends on the type of displacement.

essentially unknown in ponies and donkeys.

In a horse with distal phalangeal rotation, an

Navicular disease is a chronic degenerative
attempt is made to begin realigning the
condition of the navicular bone that
palmar surface of the distal phalanx to the
involves l ) focal loss of fue medullary
sole, while not allowing excessive forces on
architecture ( wifu subsequent synovial
the lan1inae. The breakover of the shoe is
invagination), 2) medullary sclerosis
moved as far caudally as possible, and some
combined with damage to the fibroca.rtilage
of the caudal hoof (from the frog apex
on fue flexor surface of fue bone, 3) traumatic
caudally) is removed to allow realignment to
fibrillation of the deep digital flexor tendon
the sole. This may have to be perfom1eo in
from contact with the damaged flexor
combination with raising of the heel ( with
surface of fue bone with adhesion
wedge pads, etc), which still allows alignment formation between the tendon and bone, of the distal phalanx to the solar surface while and 4) enfuesiophyte fom1ation OIJ the avoiding excessive changes in relation to the
proxin1al and distal borders of fue bone.

ground surface, thus preventing excessive
tension on the deep digital flexor tendon and

Etiology: The pafuophysiology of navicular
therefore the dorsal laminae. It may be
disease is unknown. The syndrome is likely
appropriate to place some type of resilient
due to a complex pafuogenesis rather tl1an a
putty on the solar surface to provide support
specific disease entity, alfuough fue greatest
to the distal phalanx in horses in which some
consensus appears to support a biomechanidegree of lan1ina.r instability is still suspected.

cal component ( causing increased bone

Multiple types of shoes can be used, including medullary pressure) and possibly a vascular heart bar shoes, egg bar shoes, and natural
component. There appears to be a hereditary
balance shoes. Steward clogs are an
predisposition, indicated by the sharp
important option for treating horses with
decrease in incidence of fue disease in Dutch
distal displacement of the distal phalanx;

Wann bloods after certification of stallions
these allow the horse to maximize comfort
wifu severe navicular changes for breeding
because of being beveled in multiple
was disallowed. It is considered to be a
directions ( and therefore minimizing lan1ina.r
disease of fue more mature riding horse,
stress). Some farriers/clinicians also use
commonly not appearing until 8--10 yr of age.

LAMENESS IN HORSES

1113

Navicular disease is overrepresented in some
under radiographic guidance). Radiographic
breeds ( eg, Waimblood horses, Quaiter
changes are variable and do not always
horses, and Thoroughbreds) and rare in
correlate with tl1e severity of latlleness. Thus,
others ( eg, Arabians, Friesians ). It is usually a
they may not be as important in the diagnosis
progressively deteriorating condition after
as the latlleness exatnination ( although they

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onset. Conformation of the distal limb is likely can be). Radiographs may demonstrate a to play a large role in the disease process and
range of degenerative changes involving the
degree of lan1eness. Excessive pressure on
navicular bone: marginal enthesiophytes,
the navicular bone occurs with a "broken
enlarged synovial fossae ( so-called vascular
back" hoof-pastern axis, usually accompachatIDels) of vaiiable size and cysts due to nied by an underrun heel and excessively long loss of medullary trabecular bone, general toe. This conformation, leading to excessive
sclerosis of the medullary cavity, and flex or
concussion between the flex or tendon and
surface changes ( observed on "skyline"

the navicular bone, may also cause navicular
radiographic view), including erosions and
bursitis, with direct datllage to the fibrocattiloss of a defined cortex.

lage of the flexor surface and the collagenous
surface of the flexor tendon itself.

Treatment: Because the condition is
both chronic and degenerative, it can be

Clinical Findings and Diagnosis: The
managed in some horses but not cured. The
disease is usually insidious in onset. An
most common effective treatments include
intennittent lan1eness is manifest early in the NSAID administration and corrective course of the disease. Because disease is
shoeing. Phenylbutazone is the most
bilateral, there may be no obvious head nod
commonly used NSAID, but it must be used
to the latlleness when the horse is trotted in
with caution because of adverse effects
a straight line, with only a shortened stride

(renal and GI injury). If used daily, it may be
present. Lameness is usually exacerbated
best to take the horse off the drug one day a
by lungeing the horse in a circle in both
week to allow the body to clear some of the
directions, with the inside foot usually exhibaccumulated drug; the horse can be given iting the greatest lan1eness. In early stages of
flunixin for that day. Another option in
the disease, the latlleness may not be visible
horses at increased risk of NSAID comeven at a lunge until a nerve block is perplications is the COX-2-selective NSAID
fonned on one of the two digits (ie, the two
firocoxib, which is fairly effective for
latlle feet cancel each other out). A flexion
orthopedic and atticular pain. With severe
test of the distal forelimb may produce a
latlleness, rest is indicated.

transient exacerbation of 18.llleness.

Foot care should include trimming and

Clinical diagnosis is mainly based on
shoeing that restores normal phalangeal
presentation of the horse ( age, breed
aligr1ment and balance; response to corrective
commonly at risk) and, importantly, on the
shoeing commonly takes -2 wk The principal

18.llleness exatllination, including a characobject of shoeing is to decrease the pressure teristic response to palrnar digital nerve
on the navicular bone. The shoeing technique
anesthesia. These horses are rarely positive
that most effectively decreases pressure on
to hoof testers (11 % positive in one study).

the naviculai· area is raising the heel ( usually

The lan1eness can be eliminated by palmar
performed with wedge pads or a wedged
digital ne1ve block, except in some horses
shoe). Rolling tl1e toe of the shoe further
with extensive secondary moderate to severe
relieves the pressure on the navicular bone.

datllage to tl1e deep digital flexor tendon

The egg bar shoe does not decrease navicular

(pain can radiate proximal to the palmer
pressure in sound horses on a hard surface
digital nerve block witl1 this pathology).

but has been reported to effectively decrease

However, because this ne1ve block
forces on the navicular bone in some horses
anesthetizes the entire sole and coffin joint in
with navicular disease or collapsed heels.

addition to the heel, response to the block

Additionally, egg bar shoes are likely to more
itself is not diagnostic. A transfer of 18.llleness
effectively decrease forces on the navicular
to the other forelimb, which also is elimiarea on soft surfaces (that horses are nated by a palmar digital nerve block, is
normally worked on); they are purported
necessary for a tentative diagnosis of
to work so!'newhat like a snowshoe by not
navicular disease. Anesthesia of the navicular allowing the heel to sink as deeply into a soft bursa is much more specific but is not as
surface as a foot with a standard shoe would.

commonly pe1forn1ed during a lan1eness

Natural balance shoes are ineffective at
exanlination because of the pain involved in
decreasing navicular pressure.

perfornling the irtjection (needle passes
lr\iection of the coffin joint with corticothrough the deep digital flexor tendon) and steroids will markedly improve soundness
the complexity of the irtjection (usually done
in -1/, of horses (for an average of2 mo),

1114

LAMENESS IN HORSES
whereas injection of corticosteroid into the
subsolar sepsis). Because the bone resorption
navicular bursa is reported to resolve the
is usually permanent, the radiographic finding
lameness for an average of 4 mo in 800/o of
does not indicate current pathology and may
horses that do not respond to standard
be due to a pathologic state that occurred
treatments (phenylbutazone, shoeing, and
years ago. Therefore, it is essential that a

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coffin joint injection). Increased incidence of
thorough exan1ination be performed,
rupture of the deep digital flex or tendon has
including application of hoof testers to the
been reported with multiple intrabursal injecentire solar margin of the foot and a lameness tions. Isoxsuprine hydrochloride is ineffecexanlination with nerve blocks if lameness tive as a vasodilator when administered
exists. (The entire solar surface, including the
orally and has little therapeutic value.

toe, will be anesthetized with a palmar digital

Palmar digital neurectomy may provide
nerve block)

pain relief and prolong the usefulness of

Navicular disease is an important
the horse, but no neurectomy should be
differential diagnosis to pedal osteitisconsidered curative. Digital neurectomy has associated toe bruising, because toe a high incidence of severe complications
bruising is also commonly bilateral and both
such as painful neuroma formation and
conditions respond to a palmar digital nerve
rupture of the deep digital flexor tendon.

block Radiography is helpful in diagnosis

Catastrophic injury to the distal limb in
and in differentiation from navicular
horses brought back to a high level of
disease. Pedal osteitis associated with
athletics after neurectomy has resulted in
chronic subsolar abscess is usually aseptic,
death of the rider. Other surgical procedures with the sepsis isolated to the soft tissue.

for navicular disease are unproved.

Radiographic signs of sequestration or

Although the prognosis is guarded to poor, severe focal lucency in the same region as a carefully designed therapeutic regin1en,
the subsolar sepsis may indicate septic
including corrective shoeing, NSAID therpedal osteitis, but lucency can also be an apy, and navicular bursa injections (and/or
artifact caused by subsolar gas once an
possibly coffin joint injections), can prolong
abscess is drained (an unopened abscess
the usefulness of most horses and the
usually has a tissue density). Curettage of
competitive status of many. Over months or
the affected distal phalanx should be
years, most affected horses reach a point of
avoided tmless it is docmnented to be septic.

nonresponsiveness to treatment.

Local treatment (ie, curettage of the
affected area) is necessary only if there is an

PEDAL OSTEITIS
active septic process associated with the
radiographic changes of pedal osteitis.

Pedal osteitis is a radiographic finding of

General treatment of nonseptic cases
demineralization of the solar margin of the
should be directed at the primary disease
distal phalanx, commonly associated with
that caused the resorption ( eg, corrective
widening of vascular channels near the solar
shoeing for chronic laminitis cases with
margin, which is best observed on a 65°
distal phalanx displacement that predisproxi.rnal-<listal dorsopalmar radiographic poses to solar margin bruising).

view. Although the term is usually used to
describe changes in the dorsal distal (toe)

solar margin, it can be used to describe bone

PUNCTURE WOUNDS OF THE
resorption of any aspect of the solar margin

FOOT
of the distal phalanx. The bony resorption
usually occurs due to chronic or repeated

(Subsolar abscess, Septic navicular bursitis)

pressure and/or inflan1rnation of the affected

Puncture wounds are common in horses
region. The resorption can be focal due to a
and are the most common cause of subsolar
focal lesion such as a keratoma, or it can be
sepsis. Most puncture wounds result only
more diffuse in states such as chronic toe
in sepsis of the subsolar soft tissue (ie,
bruising, in which the entire distal margin of
subsolar abscess) but can be catastrophic
the toe may appear "moth-€aten" due to
when the puncture is in the frog and travels
extensive bone resorption at the solar margin.

deep enough to enter synovial structures

Resorption in the toe region commonly
such as the navicular bursa, the distal
occurs in chronic lanlinitis cases in which
interphalangealjoint, or possibly the deep
displacement of the distal phalanx results in
digital flexor tendon sheath.

inadequate sole depth between the ground

Puncture of the sole by a foreign body
surface and solar margin of the distal phalanx, is associated with introduction of pathoresulting in chronic trauma and inflammation genic microorganisms that lead to subsolar
of that region of the phalanx and surrounding
abscess formation. Lameness is usually
soft tissue (ie, sole bruising or chronic
severe; the degree of lameness may be

LAMENESS IN HORSES

1115
similar to that of a fracture. The horse may
full healingtepithelialization of the solar
stand pointing the affected foot. There is
region entered; healing appears to be much
commonly a prominent digital pulse in the
more rapid and is easier to treat if the
affected limb. If allowed to progress, the
abscess is entered through the wall instead
abscess may travel proximally to rupture
of the sole. All horses with puncture wounds

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at the coronary band; there will usually
should be i.nununized against tetanus. Local
be edematous swelling proximal to the
and systemic antibiotic therapy are not
coronary band before rupture. Diagnosis
necessary for a sole abscess but should
is made by confirming the site of pain by
be considered with swelling above the
pulling the shoe, using hoof testers, and
coronary band (indicating septic eellulitis)

picking or paring the suspect area to locate
and must be used aggressively if sepsis of a
the foreign body or its dark tract. If a foreign synovial structure is present.

body is found in the frog, it may be best
to obtain a lateral radiograph of the foot

PYRAMIDAL DISEASE
to assess the structures penetrated before
removing the offending object. If a tract is

(Extensor process fracture, Buttress foot)

found in the frog, it should be probed and a
radiograph taken with the probe in place.

Fragmentation of the extensor process of

Because puncture wounds in or near the
the distal phalanx is thought to occur due to
frog commonly enter a synovial structure,
trauma, osteochondrosis, or presence of
they constitute a serious problem requiring
separate centers of ossification. Forelimbs
rapid, aggressive diagnosis and therapy. If a
are mo.re conunonly affected than
synovial structure is entered, the horse
hindlimbs. The fracture fragments are
should be placed on broad-spectrum
usually intra-articular but are conunonly
antibiotics and transported to a facility
nondisplaced; they may be adhered to the
capable of advanced surgical and medical
extensor tendon. The fragments may be
techniques; the affected synovial structure
incidental fmdings, but they may also cause
should be lavaged with sterile polyionic
lameness. The close association of the
solution as soon as possible (within hours).

extensor process with the distal inter

If a puncture wom1d is noted in the solar
phalangeal joint can result in secondary
area, ensuring adequate drainage from the
aithritis if the fragments are not removed.

site helps prevent abscess fom1ation. If

Fractures can be removed either via
there is a suspected abscess but no tract
arthroscopy or arthrotomy; arthroscopic
is found, the foot can be poulticed in an
removal of small fragments carries a good
attempt to promote organization of the
prognosis. With large, untreated fractures,
abscess for localization. If a tract is found
an enlargement of the toe region just above
that leads to a subsolar abscess, adequate
the coronary band is usually present, which
drainage should be established with a hoof
results in the "buttress foot" or pyran1idal knife; the drainage hole should be kept as
appearance to the foot. Systemic antismall as possible (-0.5-1 cm diameter) to inflammatory medication may be beneficial.

avoid a prolapse of sensitive coriun1. Some
farriers and veterinarians prefer to drain the

QUITTOR
abscess through the hoof wall (instead of the
sole) if possible. Once the abscess has been

(Coronary sinus)

entered, it should be probed to deteffiline its

Quittor is a chronic, septic condition of one
extent; a palmar digital ne1ve block will
of the collateral caitilages of the distal
usually be necessary before probing and
phalanx characterized by necrosis of the
lavage of the area. If the abscess underruns a cartilage and one or more sinus tracts large area of the foot, another small ingress/
extending from the diseased cartilage
egress hole can be made at the farthest
through the skin in the coronary band
extent of the abscess from the original entry
region. It is seldom encountered today but
point, and lavage can be performed by
was common in working draft horses in the
placing a 14-gauge catheter or teat carmula
past. Quittor usually follows injury to the
into the affected subsolar space and flushing
limb on the medial or lateral aspect of the
with saturated Epsom salt solution (made by lower pastern (immediately proximal to the adding Epsom salts to boiling water or saline coronary band, over the proximal extent of until some salt crystals sit on the bottom of
the cartilage), by means of which infection
the container and will not go into solution).

is introduced into the traumatized collateral

If a chronic subsolar abscess has developed,
cartilage. This leads to localized sepsis or
this treatment may have to be repeated daily
abscessation of the cartilage. The cartilage
to every other day for several treatments.

may also become infected through a quarter

The foot should be protected until there is
crack (see below). The first sign is an

1116

LAMENESS IN HORSES
inflammatory swelling over the region of the crack is dry. Multiple wires are then applied collateral cartilage, which is followed by
across the crack to stabilize it. The wires can
sinus forn1ation and intern1ittent drainage.

be placed either around sheet metal screws

During the acute stage, lameness occurs.

placed in the hoof wall on either side of the

Surgery to remove the diseased tissue
crack or through small holes drilled through

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is required, but care must be taken not to
the horn of the hoof wall on each side and
enter the distal interphalangealjoint. Local
exiting through the crack. The crack can be
or parenteral antibiotic therapy ( or both)

filled with either a resilient acrylic or putty,
without surgery is likely to fail. In the
but it is critical that there be no moisture or
absence of any therapy, poor drainage,
sepsis present. Fenestrated tubing can be
cartilage necrosis, and recurrent abscessaplaced between the deepest aspect of the tion lead to chronic lameness and extension
crack and the acrylic to allow for drainage.

to deep structures. The prognosis is

The hoof is then bandaged until new horn
unfavorable if the disease progresses to
formation is evident.

involve the distal interphalangealjoint.

SCRATCHES

QUARTER CRACK

(Greasy heel, Dermatitis verrucosa)

(Sandcrack)

Scratches is a chronic, seborrheic

Cracks in the hoof wall are thought to occur
dern1atitis characterized by hypertrophy
prin1arily because of excessive forces placed
and exudation on the caudal surface of the
on the hoof wall and the gemiinal tissue of the pastern and fetlock. It often is associated coronary band. It is proposed that shoeing
with poor stable hygiene, but no specific
does not allow the hoof wall to expand
cause is known. Heavy horses ( eg, draft
normally with weight bearing and that quarter horses) are particularly susceptible, and the cracks commonly fonn at the placement of
hindlimbs are affected more commonly.

the caudal nail, because the hoof wall will

Standardbreds can be affected in the spring
deform caudal to the nail but not cranial to it.

when tracks are wet.

This would place abnormal forces on the

Scratches may go unnoticed if hidden by
laniinar tissue and the gemiinal tissue of the
the "feather" at the back of the pastern. The coronary band at that point, resulting in a
skin is itchy, sensitive, and swollen during
defect in horn growth that appears as a crack.

the acute stages; later, it becomes thickened

The same excessive force on a quarter can
and most of the hair is lost. Only the shorter
occur with a shoe in which the branch is too
hairs remain, and these stand erect. The
short ( either due to placement of a shoe that
surface of the skin is soft, and the grayish
is too small or to an inappropriate interval
exudate commonly has a fetid odor. The
between resetting the shoe), resulting in
condition can become chronic, with
excessive pressure and wall stress at the
vegetative granulomas. Lameness may or
point where the shoe ends on the quarter. Toe
may not be present; it can be severe and
cracks are also thought to occur in shod
associated with generalized cellulitis of the
horses due to the fact that the toe expands
limb. As the condition progresses, there is
abnormally between the cranial-most medial
thickening and hardening of the skin of the
and lateral nails, leading to disruption of
affected regions, with rapid hypertrophy of
tubule formation at the coronary band.

subcutaneous fibrous tissue.

A crack in the horn emanating distally from

Persistent and aggressive treatment is usuthe coronary band is the most obvious sign.

ally successful. This consists of removing the

Lan1eness may be present, depending on the
hair, regular washing and cleansing with
degree of wall instability or the presence of
warm water and soap to remove all soft
sub mural sepsis. If infection is established,
exudate, drying, and applying an astringent
there may be a purulent discharge and signs
dressing. If granulomas appear, they can be
of inflammation and lameness.

cauterized. Cellulitis requires systemic

Therapy first involves proper trinuning of
antibiotic therapy and tetanus prophylaxis.

the foot to remove abnormal forces on the
coronary band and wall. Once the farrier and

WHITE LINE DISEASE
veterinarian are satisfied that the foot is
responding to the corrective trinuning and

(Hollow wall, Seedy toe, Onychomycosis)

shoeing (including the application of a bar

In white line disease, the hoof wall separates
shoe), the crack should be debrided (usually
from the underlying laniinae (stratum
with a rotary tool), and any moisture or sepsis internun1) at the level of the stratun1 medium treated with appropriate antiseptic and/or

(tubular horn). The separation likely starts as
astringent agents ( eg, 2"/o iodine) until the
a result of abnorn1al wall stress due to poor

LAMENESSINHORSES

1117
foot conformation or trimming ( eg, long toe,
in horses with abnormal limb or foot
underrun heels) and can start at the toes,
confom1ation on the affected foot or feet.

quarters, or heel. Opportunistic bacteria and

Corrective trinuning and shoeing, in an
fungi may be present in the fissures in the
attempt to restore proper heel aligrunent
hoof wall. The outer surface of the wall may
and foot balance, are required and entail

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appear sound, but on dressing the foot from
floating the heel on the higher heel. A full bar
the solar surface, there is commonly a
shoe to increase ground surface area while
separation of the hoof wall from the
protecting the affected quarter and heel
underlying laminae. Tapping on the outside
is used. Several shoe resettings may be
of the wall at the toe elicits a hollow sound
required before improvement is evident. The
over the affected portion. Lameness may be
prognosis is good in uncomplicated cases if
present in severe cases, in which loss of
the corrective measures are consistently
support of the distal phalanx results in
applied until new hoof growtil occurs.

displacement similar to that seen in laminitis.

The iliagnostic evaluation includes a
thorough physical examination and lateral

SIDEBONE
and dorsopalmar radiographs to assess the
extent of separation of the hoof wall and any

(Ossification of the collateral cartilages)

ilisplacement of the distal phalanx. For

Sidebone is ossification of the collateral
treatment, corrective trinuning is critical to
cartilages of the distal phalanx; it occurs
remove abnormal stresses on the hoof wall,
most often in the lateral cartilage. It is most
followed by removal of the entire extent of
common in the forefeet of heavy horses
the separated hoof wall to the point that
working on hard surfaces. Repeated
finn, healthy adhesion of the hoof wall to the concussion to the quarters of the feet is underlying stratum intemum can be seen.

purported to be the cause. Some cases arise

This hoof wall debridement is perfom1ed
from direct trauma. Sidebone is usually an
with a combination of hoof nippers, hoof
incidental radiographic finding and rarely
lmives, and possibly a rotary tool. With
causes lameness. If sidebone is a cause of
proper debridement, there may be no need
lameness, the lameness should entirely
for antiseptic or astringent treatment.

subside with a unilateral pahnar digital

However, topical treatment with tincture of
nerve block on the affected side.

iodine is commonly performed daily for at

When lameness is present, corrective
least a week. Adilitionally, commercial
shoeing to promote expansion of the
equine foot formulations that produce
quarters and to protect the foot from concuschlorine ilioxide can also be used. Correcsion may be of value. Grooving the hoof wall tive shoeing is critical to provide adequate
on the affected side has been reported to
support to the remaining foot, while
help reduce lameness. If sidebone is
removing stress from the affected regions;
documented as a cause of lameness,
a heart bar or egg bar shoe in combination
unilateral palmar digital neurectomy may
with a resilient putty in the caudal twobe inilicated if the horse does not respond thi.rds of the sole (to provide ilistal phalanx
to corrective shoeing and trinlming.

support) may be necessary if displacement
of the distal phalanx is a concern.

THRUSH

SHEARED HEELS

Thrush is a degeneration of the frog with
secondary anaerobic bacterial infection that

In sheared heels, there is severe acquired
begins in the central and collateral sulci. The
imbalance of the foot with asymmetry of the central sulcus is more commonly involved if heels. When viewing the caudal aspect of
the horse has sheared heels; the lateral sulci
the foot, one heel is higher than the other
are primarily involved in most cases of
side; the higher side commonly has a more
thrush ( without sheared heels). The affected
vertical hoof wall. When viewed from the
sulci are moist and contain a black, thick
side, the coronary band does not gradually
discharge with a characteristic foul odor; the
angle toward the ground surface in a
borders of the frog are commonly necrotic.

cranial-to-caudal direction (the normal

These signs alone are sufficient to make the
appearance) on the higher side. Some
diagnosis. Although many describe the
horses with sheared heels are lame. Hoof
primary etiology as a moist environment
cracks, deep fissuring between the bulbs of
with poor hygiene, it is more likely caused
the heel, and thrush frequently accompany
by poor foot conformation or trimming and
the problem. Sheared heels are most likely
lack of exercise (thought to help "clean out"

caused by abnormal forces being placed on
the sulci when the weight of the horse
one side of the foot and are seen frequently
pushes down on the frog and surrounding

1118

LAMENESSINHORSES
structures) than from lack of hygiene in the
are generally associated with lameness at
stall. However, a moist environment should
speed with clinical signs similar to those of
be avoided in anin1als with thrush.

dorsoproxirnaJ Pl fractures. These fractures

Treatment should begin by providing dry,
are more common in the hindlirnb, and
clean flooring and thorough debridement of
intra-articular diagnostic analgesia is often

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the frog and sulci. Additionally, the foot
needed to implicate these fractures as a
needs to be balanced, and affected horses
cause of lan1eness.

placed on a regular exercise schedule in a

Diagnosis is confin11ed by radiography. A
d1y area. An astringent solution ( eg, copper
number of oblique radiographic views may
sulfate solution) may be applied with daily
be necessary to ensure visibility of the
hoof cleaning. Commercial equine foot
fractures. For pal.mar or plantar osteochonformulations that produce chlorine dioxide dral fractures, oblique radiographic views
can also be used. If granulation tissue or
witl1 tl1e bean1 raised -20° from horizontal
sensitive tissue is exposed, astringent
may be more helpful for identification. The
solutions should be avoided; a paste made
diagnosis of sagittal or com.minuted
of metronidazole tablets can be applied
fractures of P 1 is typically straightforward,
instead to the affected areas in combination
with mar·ked Jar11eness and swelling.

with foot bandaging. The prognosis is

Incomplete, sho1t sagittaJ fractures can be
usually favorable with appropriate changes
more difficult to diagnose and may require
in shoeing and exercise.

special radiographic views off of dorsopalmar/plantar· and/or nuclear scintigraphy in the initial stages, because U,e fracture line
may be difficult to detect radiographicaJly.

Osteochondral "chip" fractures can be
removed arthroscopically with an excellent

FRACTURES OF THE FIRST AND
prognosis if no other abnom1alities within

SECOND PHALANX

U1e joint exist. Routine, nondisplaced
sagittaJ P 1 fractures can be repaired by

Fractures of the first/proximal phalanx (Pl)

internal fixation using screws placed in Jag
may occur in any type of horse used for
fashion via stab incisions. More complex Pl
perfonnance. They may be small osteochonfractures typically require open reduction draJ "chip" fractures along the dorsal margin and repair via lag screws to allow accurate of the proxin1aJ joint surface, sagittal
realignment of the articular surface of the

( complete or incomplete), or comminuted.

fetlock to limit postoperative arthritis.

Another category involves fragn1ents of the

Careful attention should be paid to tl1e
paJmar or plantar proximal aspect of P 1,
fracture configuration to ensure tl1at all
which may be associate.cl with osteochoncomponents ar·e incorporated in ilie repair.

drosis.

In some circumstances, CT may aid an

"Chip" fractures of the dorsoproxirnaJ
aspect of Pl typically involve the medial
aspect of the joint and occur in horses that
exercise at speed. These fractures are
nonnally traumatic in origin and result from
hyperextension of the fetlock joint. Acute

Jan1eness and increased effusion in the
fetlock joint along with sensitivity to firm
flexion of the fetlock are clinical signs that a
fracture may be present and radiographic
examination indicated. In nonracing breeds,
a chip fracture may be present on radiographs, but its clinical significance should be detem1ined with diagnostic analgesia before
being implicated as a source of lameness.

The cause of proxirnopalmar and
proxirnoplantar osteochondraJ fractures is
questionable; one thought is that they are
from osteochondrosis, the other is that they
are fractures. Axial fractures are classified
as type I fractures and are generally
articular. Type Il fractures are located
abaxiaJly and typically have minin1aJ

Comminuted fracture of the second phalanx
articular cartilage present. Type I fractures
in a horse. Courtesy of Dr. Matthew T. Brokken.

LAMENESS IN HORSES

1119
accrnate diagnosis and reconstruction of the removal. The presence of suspensory fractrne. Conservative treatment of severely
desmitis (seep 1122) in the affected limb
conuninuted fractures involves inunobilizaalso decreases the prognosis after srngery.

tion with a plaster or fiberglass cast for up to

Horses with apical sesainoid fractures in the

12 wk, with or without the use of transfixaforelimbs are less likely to race than those VetBooks.ir
tion pins through the third metacarpal/tarsal
with fractrnes in the hindlimbs (55% vs
bone. Complications of P l fractrne repair

86%). Size and shape of apical sesainoid
include implant failrne, poor alignment at
fractures does not appear to affect racing
the fractrne site leading to secondary
performance. Mid-body fractrnes typically
aithritis, and contralateral limb Jaminitis.

require reduction using lag screw( s)

Fractures of the second/middle phalanx
fixation with a prognosis of 75% ( 44% in

(P2) are most common in Quarter horses
another study) to return to racing. The
and typically affect the hindlimbs. Whereas
prognosis for basilar fractrnes involving a
osteochondral "chip" fractrnes are common
portion of the sesan1oid is fair compared
off of proximal Pl, osteochondral fractrnes
with that for fractrne of most of the base or
are relatively unconunon off of P2. The most in horses with associated articular disease common fractures of P2 are either palmar/

(poor prognosis). Complete disruption of
plantar eminence fractures of proximal P2
the suspensory apparatus, including
or comrninuted fractrnes. Treatment of
fractures of both sesainoid bones, is a
most P2 fractures is either with internal fixacatastrophic iitjury that may be accompation with a combination of plate(s) and nied by vascular compromise; however,
screws and/or a transfixation pin cast.

some horses can be salvaged for breeding

Residual laineness typically is present and
by surgical arthrodesis of the fetlock joint.

depends on the degree of osteoarthritis that
develops in the distal interphalangealjoint

OSTEOARTHRITIS OF THE
and, to a lesser extent, the proximal
interphalangeal joint (if not arthrodesed in

PROXIMAL INTERPHALANGEAL
the fracture repair). Prognosis depends on

JOINT
how comfortable the horse will be after
fracture stabilization to limit the risk of

Osteoarthritis of the proximal interphalancontralateral limb laininitis.

gealjoint (high ringbone) is a common cause
of lan1eness in many types of horses used for
a variety of disciplines. The osteoarthritic

FRACTURES OF THE PROXIMAL
process can start as a single traumatic

SESAMOID BONES
episode or as a result of "weai· and teai-,"

or overuse. Other causes of osteoarthritis of

Fractures of the proximal sesainoid bones
this joint are infection and developmental
are classified according to their location in
orthopedic disease. The proxin1al inter-
the bone. The most common sesainoid
phalangealjoint is a lower motion joint that
fractrnes in Standardbreds and Thoroughis somewhat unforgiving to high loads placed breds ai·e apical. They are caused by overupon it. Osteoarthritis is characterized by extension and often are associated with
cartilage loss and periarticular new bone
suspensory ligainent dainage. The lateral
formation. In the chronic, progressive
proximal sesainoid in the hindlirnb of
osteoarthritic pastern, laineness is typically

Standardbreds may be fractured as a result
subtle at first and becomes more noticeable
of torque forces induced by shoeing with a
as the disease progresses. Radiographic
trailer-type shoe. Other fractures include
findings may include periarticular new
mid-body, basilar, abaxial, axial, or
bone formation, subchondral Jysis and/or
conuninuted, and they may involve one or
sclerosis, and Joss of joint space (typically
both sesan1oids. Most, apart from some
the medial aspect of the joint). In the early
abaxial and base fractures, are articular.

stages of disease, diagnostic analgesia is

Clinical signs include heat, pain, and acute
typically required to localize the lan1eness.

Jaineness, which is exacerbated by flexion

In addition, a positive response may be seen
of the fetlock. There is often hemarthrosis
on lower lin1b flexion. Oral or intra-articular
and synovial effusion of the metacarpal/
anti-inflanunatory medication may relieve
tarsophalangealjoint. Diagnosis is
the signs of laineness temporarily. The use
confim1ed radiographically. Of Thoroughof intra-articular ethanol iitjection into the bred racehorses 2'2 yr old, 82% of horses
proximal interphalangealjoint has been
with apical sesan10id fractrnes removed
described. If srngical fusion is not an option,
arthroscopically ran at the san1e or at an
multiple irtjections were successful in
improved level. Horses with apical fractrnes some horses for facilitated ailkyloses.

of the forelimb medial proximal sesainoid

Srngical arthrodesis of the pastern joint is
are less likely to race after fragment
frequently required to successfully restore

1120

LAMENESS IN HORSES
performance. Typically, this involves a
fast exercise, the aba.xial portion of the
combination of plate(s) and screw(s). In a
proximal sesamoid bones is susceptible
retrospective study of 53 horses that had a
to stress-related ir\jury. Sesamoiditis is a
proximal interphalangealjoint arthrodesis
clinically distinctive condition; however,
using a combination plate-screw technique
it is poorly characterized pathologically.

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(81% forelimb, 95%hindlimb), 87%of horses

The clinical signs are sinillar to, but less
with follow-up were used as intended.

severe than, those resulting from sesamoid

Deterioration of articular cartilage within
fracture. Depending on the extent of the damthe metacarpal/tarsophalangealjoint is a age, there a.re varying degrees of lameness
common ir\jury in racehorses and can lead
and swelling. Pain and heat are evident on
to development of periarticular osteophytes,
palpation and flexion of the fetlock joint.

enthesophytes, and joint space collapse.

Radiographic evidence of sesamoiditis

In young, training horses, periosteal bone
involves periarticular osteophytes,
can form on the dorsal aspect of the distal
entheseophytes, focal osteolysis, and
metacarpus and the proximal aspect of the
enlarged vascular channels ( or linear defects
proximal phalanx, often involving the joint
in the aba.xial margin of the proximal
capsule ( osselets). Osteoarthritis is often
sesamoid bones). Grading scales for
secondary to a primary abnom1ality such
sesamoiditis exist and particularly note the
as a chip fracture or osteochondrosis ( see
vascular channels on radiographs. Severity of
p 1140). Treatment typically has two goals:

sesamoiditis on radiographs has been linked
reducing pain and minimizing further joint
to a decrease in racing performance in one
deterioration. The judicious use of antistudy. In another study, when radiographic inflammatories ( eg, NSAIDs, corticosteroids) signs of significant sesamoiditis were can provide pain relief. Newer biologic
present, horses had a 5 times greater risk
therapies (platelet-rich plasma, stem-cell
of developing clinical signs of suspensory
therapy, interleukin-! receptor antagonist
ligament branch ir\jury with onset of training.

protein) may help slow down or arrest the

The recommended treatment is enforced
progression of osteoarthritis. In severe,
rest and symptomatic treatment to combat
advanced cases, arthrodesis of the joint is
inflammation and soreness. The insertion
necessary to provide pain relief.

of the suspensory ligaments should also be
carefully evaluated by ultrasonography for

PALMAR/PLANTAR METACARPAL/ concurrent lesions.

METATARSAL NONADAPTIVE

CHRONIC PROLIFERATIVE

BONE REMODELING

SYNOVITIS

This condition affects the subchondral bone
of the palmar/plantar aspects of the distal

(Villonodular synovitis)

metacarpal/metatarsal condyles and is a

Proliferative synovitis is the enlargement of
conunon cause of performance-limiting
the fibrocartilaginous pad on the dorsoproxlameness in Standa.rdbred and Thoroughirnal aspect of the joint capsule attachment bred racehorses. It is thought ta be a stress
of the fetlockjoint. The cause of this
remodeling response to high-level activity in in.flanm1ation is thought to be from young racehorses and is associated with
repetitive trauma from exercise. Typically,
lameness referable to the fetlock region.

this condition is found most frequently in

Typically, the lameness improves with a
racing Thoroughbreds, but it may also
block of the palmar/plantar metacarpal/
develop in Standardbreds and nonracing
metatarsal nerves proximal to the fetlock.

breeds. Clinical signs include fetlock joint

Intra-articular analgesia of the fetlock joint
effusion, furn swelling over the dorsoproxican have varying results and is less reliable mal aspect of the fetlock joint, lameness, and
to improve lameness. Radiographic signs
decreased range of motion and a positive
may be minimal, and the changes are
response to fim1 flexion of the fetlock.

identified earliest using nuclear scintigra

Diagnosis can be suspected by palpation.

phy, CT, or MRI. Treatment consists of

Radiography can be used to identify
controlled exercise.

associated osteolysis at the proximal aspect
of the dorsal mid-sagittal ridge of the distal

SESAMOIDITIS
third metacarpal bone on the lateromedial
projection. The radiolucency is a result of

The sesamoid bones are maintained in
the dan1age to the cortical bone from the
position by the branches of the suspensory
overlying fibrous mass. Ultrasound
ligament proximally and by a number of
examination can also be performed, and the
sesamoidean ligaments distally. Because of
synovial pad is considered abnonnal if it is
the great stress placed on the fetlock during

>4 mm thick, has rounded distal margins, or

LAMENESS IN HORSES

1121
if hyperechoic regions are found within the
digital flexor tendon, superficial digital
pad. Treatment is surgical excision via
flexor tendon, and the distal digital armular
arthroscopy.

ligrunent. Any of these conditions can result
in tenosynovitis of the digital sheath and

DIGITAL SHEATH TENOSYNOVITIS can typically be diagnosed using ultra

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sonography or MRI.

Tenosynovitis of the digital flex or tendon
sheath is co nun on in all types of working
horses. Chronic digital sheath tenosynovitis
may be bilaterally synunetiic in the hindlimbs
in horses witl1 minimal clinical significance

("windpuffs"). The digital sheatl1 encom

TENDINITIS
passes ilie superficial and deep digital flexor
tendons and extends from tl1e distal one-iliird (Bowed tendon) of ilie metacarpus/metatarsus distally to just

Inflan1mation of a tendon can be acute or
proxin1al to ilie navicular bursa. Asynm1etric
chronic, with varying degrees of tendon
tendon sheatl1 effusion typically indicates a
fibril disrnption. Tendinitis is most conunon
problem. Lameness degree is vruiable,
in horses used at fast work, particulru·ly
depending on ilie structure( s) involved, and
racehorses. The problem is seen in ilie
may increase witl1 exercise. Horses are
digital flexor tendons and is more common
typically sore on finn flexion of tl1e distal
in ilie forelimb ilian in ilie hindlimb. In
limb. Aliliough some cases of tenosynovitis
racehorses, the superficial digital flexor is
are prin1ary and respond to conservative
involved most frequently. The primruy
ilierapy witl1 or without treatment of ilie
lesion is a central rnpture of tendon fibers
sheatl1 witl1 corticosteroids and/or hyalwith associated hemorrhage and edema.

uronic acid, otl1ers are secondruy to lesions
of structures contained wiiliin ilie sheath.

Etiology: Tendinitis usually appears

Ultrasonographic exrunination of ilie entire
after fast exercise and is associated with
digital flexor tendon sheath, including the
overextension and poor conditioning,
intersesrunoidean ligament and distal
fatigue, poor raceti·ack conditions, and
sesrunoidean ligan1ents, is recommended
persistent training when inflanm1atory proband typically leads to a diagnosis. However, lems in ilie tendon al.ready exist. Improper
marginal tears of ilie deep digital flexor
shoeing may also predispose to tendinitis.

tendon (typically dorsolateral in the pastern)

Poor conformation and poor training also
and tears of ilie manica flexoria can be
have been implicated.

difficult to diagnose via ultrasound but are
confirmed ilirough tenoscopic examination

Clinical Findings and Diagnosis: D1w
of ilie sheatl1. Verification of site of lan1eness
ing the acute stage, ilie horse is severely
should be confirmed via intrailiecal injection
lan1e and ilie involved strnctures are hot,
of analgesia
painful, and swollen. In chronic cases, iliere

Palmar/plantar armulru· ligament
is fibrosis with thickening and adhesions in
constriction can be primal)' due to desmitis
ilie peritendinous area. The horse witl1
of the ligrunent or secondruy to longstanding
chronic tendinitis may go sound while
tenosynovitis or enlargement of ilie flexor
walking or trotting, but lruneness may recur
tendons contained wiiliin ilie fetlock canal.

under hard work. Ultrasonography

Clinical signs are sin1ilar to iliose of oilier
delineates the cross-sectional and
causes of tenosynovitis and include pain on
longitudinal extent of the tendinitis.

palpation, swelling, and lruneness, especially
after forced flexion of ilie distal limb. Careful

Treatment: Tendinitis is best treated in
ultrasonographic exan1ination is recomilie early, acute stage. The horse should be mended to assess accompanying pailiology.

stall-rested, and the swelling and inflrunma

Treatment can be eiilier conservative (ie,
tion treated aggressively witl1 cold packs
steroids) or surgical (pal.mar/plantar armula.r
and systemic anti-inflanunato1y agents.

ligrunent desmotomy ). Surgery is best

Some degree of support or immobilization
pe.rfonned tenoscopically, which allows
should be used, depending on ilie runount
visualization of ilie remainder of ilie sheatl1
of drunage to ilie tendon. Inti·atendinous
for prirnruy pathology and assessment of the
corticosteroid injections are contraindidegree of constiiction.

cated. When a distinct hypoechoic or

Other common causes of tendon or
anechoic core lesion is present on ultraligrunent pathology distal to ilie fetlock sound exrunination, tendon splitting has
include desmitis of the distal sesrunoidean
been recommended (ilie rationale is to
ligrunents ( oblique and straight), deep
decrease intratendinous pressure due to

1122

LAMENESS IN HORSES
sernrn or hemorrhage). Cases also have been lameness to be localized to Lllis region. There treated with shock wave therapy, intraare multiple techniques to desensitize the lesional irtjection of fat-derived strornal cells
proximal aspect of the palrnar metacarpus.

or cultured bone rnarrow-de1ived rnesen

However, there is confusion interpreting the
chyrnal stern cells, or platelet-rich plasma
results of subcarpal analgesia because of

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products. The levels of evidence for these
the lack of specificity oflocal analgesic
modalities are variable. TI1e horse should be
teclmiques. After lameness has been
rehabilitated using a regimen of increasing
localized, radiographs as well as ultrasonoexercise. Supe1ior check ligament desrnotgraphic examination of the region should orny has been used as an acljunctive treatment be pe1formed. Ultrasow1d of the proximal to rninintize recurrence of the problem before
suspensory should be critically compared
the horse is returned to training.

with that of the other limb, remembering

Other treatments for chronic tendinitis
that bilateral lesions do exist. Nuclear
have included superficial point firing ( of quesscintigraphy can help detect osseous injwy tionable benefit) and percutaneous tendon
at the proximal suspensory attachment, but
splitting. Annular ligament desrnotomy is
negative scintigraphic images do not
also used when tendinitis occurs within the
exclude the presence of PSD. MRI is also
confines of the digital tendon sheath.

extremely useful to detect subtle changes in

The prognosis for a flat-racing Thoroughthe proxinlal suspensory ligament that may bred racehorse to return to racing after a
not be visible or conclusive with ultrasonogbowed tendon is guarded, regardless of raphy. In addition, MRI allows accurate
treatment. However, increasing success is
examination of the osseous structures
seen with eventers, show jumpers and show
acljacent to the suspensory ligament
hunters, and dressage horses, respectively.

( metacarpal bones and distal carpal bones).

In contrast to hindlimb PSD, most horses

SUSPENSORY DESMITIS
with acute forelimb PSD respond well to
rest and a controlled exercise program for
l.ajuries of the suspensory ligan1ent (interos3-6 mo ( -900/o retwn to function). Premaseous muscle) are common in forelin1bs and ture return to work typically results in
hindlimbs of horses. Lesions are typically
recurrence/persistence of lan1eness. Horses
classified as affecting the proxinlal, body, or
with chronic PSD may require a longer
branches of Ll1e suspensory ligan1ent.

rehabilitation program or acljunct therapy

(NSAIDs, shockwave, regenerative

Proximal Suspensory Desmitis: The
therapies) to return to consistent work.

te1111 proxin1al suspensory desmitis (PSD)

is restricted to lesions confined Lo the

Desmitis of the Body of the Suspen
proxinlal one-third of the metacarpus. PSD
sory Ligament: This is principally an
can occur unilaterally or bilaterally and is a
irtjwy ofracehorses. l.ajtuies usually affect
common irtjwy in all types of athletic horses. the f orelimbs of Thoroughbreds and the l.ajwy to the proxinlal suspensory ligan1ent
forelimbs and hind limbs in Standardbreds.

and/or its attachment to Ll1e proxinlal palmar Soreness on palpation of the forelimb aspect of the third metacarpal bone typically suspensory ligament is quite common in results in sudden onset lameness that seems
horses with lameness associated with a
to improve within a few days. Lameness
more distal limb problem; however,
varies from mild to moderate and is typically
strnctural abnormality of the ligaments is
not severe unless there is substantial
only rarely identifiable ultrisonographically.

involvement oftl1e ligament and its

Clinical signs vary and involve enlargement
attachment ( avulsion of the palmar cmtex).

of the ligan1ent, local heat, swelling, and

If Ll1e horse has bilateral PSD, there may be
pain. Diagnosis is usually based on clinical
less overt lameness but more loss of action
sigrts and can be confumed ultrasonographof the horse. Lameness is typically more ically. Treatment is aimed at reducing
noticeable on soft ground and with the
inflammation by systemic SA.IDs,
affected leg on the outside of the circle.

hydrotherapy, and controlled exercise.

Response to distal limb and/or carpal Hexion Shockwave therapy, platelet-rich plasma, tests is variable. Pressure applied to the
and stem-cell Ll1erapy have also been used
proximal palmar metacarpal region may
for suspensory body lesions.

elicit pain; however, this response/reaction
should be compared with that of the other

Desmitis of the Branches of the
limb to detemune significance.

Suspensory Ligament: This relatively

Diagnosis of PSD usually requires
common injury is seen in all types of horses
localization with diagnostic analgesia,
in forelimbs and hindlimbs. Usually only a
because typically horses do not have clinical
single branch in a single lin1b is affected,
signs ( eg, heat, pain, swelling) that allow
although both branches may be affected,

LAMENESS IN HORSES

1123
especially in hindlimbs. Foot imbalance is
one-third of tl1e metacarpus dorsal to the
often recognized in affected horses, and this
superficial digital flexor tendon. Ultrasonomay be a predisposing factor.

graphic examination is typically confinna

Clinical signs depend on the degree of
tory, with areas of enlargement, fiber pattern
damage and the chronicity of the lesion(s)

ilisruption, and loss of the normal border of

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and include localized heat and swelling.

the ligament. lr\jury to the ICL is usually

Swelling is often due to local edema of the
treated witl1 rest and controlled exercise,
affected branch. Effusion can be present in
along with possible shockwave and/or
the acljacent palmar/plantar fetlock joint
intralesional irtjection of platelet-rich
and/or the iligital flexor tendon sheath. Pain
plasma or stern cells. Desmatomy of tl1e ICL
is usually elicited either by direct pressure
has also been perfonned in horses that have
applied to the i.rtjured branch or by flexion of
not responded to conservative therapy.

the fetlock. Lameness is variable and may be
absent.

BUCKED SHINS

Diagnosis is based on clinical signs and
ultrasonographic examination. Radio

"Bucked shins" are pa.it of tl1e clisease
graphic examination should also be
complex known as dorsal metacat1)al
performed to evaluate the attachment of
disease. Bucked shins is a painful, acute
the suspensory branch on the proximal
periostitis on the dorsal surface of the third
sesamoid bones. Low 4-point iliagnostic
metacarpal bone. It is seen most often in the
analgesia as well as intra-articular analgesia
forelimbs of young Thoroughbreds
of the fetlockjoint (varying degrees based

(2-yr-olds) in training and racing, and less
on the location of tl1e branch irtjury)

commonly in Standai·dbreds and Quatter
improves lameness. Ultrasonography can
horses. This ir\jury can occw-bilaterally and
detect a range of abnormalities, including
usually occurs sequentially, with the left leg
enlargement, alteration of shape, and
being affected first because horses are
alterations in echodensity.

trained at1d raced in North America in a

Management depends on the severity of
cow1terclockwise direction. Bucked shins
the signs and on the breed and use of the
may be the result of high-strain cyclic
horse. Shockwave therapy, local anti-inflan1-
fatigue caused by excessive compression on
matories, ligament splitting, and regeneraa bone tl1at has not remodeled enough to tive therapy have all been used with varying
tolerate the stress placed on it. Stressed
results. Strict attention to foot balance is
bone forms a new layer of bone at the point
also critical in management of these lesions.

of stress. This new bone is weaker at1d, in

Clinical signs may take �6 mo to improve,
the process of rapid bone formation, the
and the condition may recur. Prognosis for
periosteum becomes elevated at1d inflamed.

reirtjury or persistence of lameness is worse

Diagnosis is typically by clinical
in horses that are hyperextended in their
examination at1d history ( soreness over the
fetlocks at rest or in horses with marked
dorsal aspect of the cat1non bone, soreness
periligan1entous fibrosis around the branch
after high-speed work or the first race, or
on ultrasound.

soreness the day after). Radiography is
beneficial to determine the amount of
periosteal reaction at1d if actual stress

INFERIOR CHECK DESMITIS
fracture( s) are present in the dorsal c01tex.

The accessory ligament of the deep iligital

Treatment typically consists of altering the
flexor tendon (inferior check ligament
training schedule to short bw-sts of speed

[ICL]) is a strong fibrous band that is the
work 2-3 times a week Rest from training
direct continuation of the common palmar
is also importatlt until the soreness at1d
ligament of the carpus. Desmitis of the ICL
inflatnrnation resolve. The acute inflat1llllamay be seen alone or develop secondarily to tion may be relieved by at1ti-inflatnrnatory
irtjury to the superficial digital flexor tendon. at1algesics ai1d application of cold packs.

In horses with severe ICL damage, the deep

Screw fixation with or without osteostixis is
flexor tendon may also be affected. lr\jury to
the method of choice to treat radiographithe ICL appears to be more common in adult cally demonstrated stress fractures.

or aged horses, affinning that degenerative
aging changes may predispose the ligament

EXOSTOSES OF THE SECOND
to injury. Ir\jury is relatively uncommon in

AND FOURTH METACARPAL
racehorses and is common in ponies and

BONES

Warm bloods ( show jumpers and dressage).

lr\jury of the ICL is usually unilateral. Diag

(Splints)

nosis is typically from clinical examina

Splints ptimarily involve the interosseous
tion, with swelling in the proximal
ligat11ent between the large (third) at1d small

1124

LAMENESS IN HORSES

( second) metacarpal (less frequently the
metatarsal) bones. The reaction is a periostitis with production of new bone ( exostoses) along the involved splint bone. Possible
contributory factors include trauma from

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concussion or injwy, strain from excess
training (especially in the inunature horse),
faulty confom1ation, imbalanced or
ovemutrition, or improper shoeing.

Splints most commonly involve the
second metacarpal bone. Lameness is seen
only when splints are forming and is seen
most frequently in young horses. Lameness
is more pronounced after the horse has been
worked. In tl1e early stages, there is no visible
enlargement, but deep palpation may reveal
local, painful, subperiosteal swelling. In the
later stages, a calcified growth appears. After
ossification, lan1eness disappears, except in
rare cases in which the growth encroaches
on the suspensory ligament or carpometacarpal articulation. Radiography is necessary to differentiate splints from fractured splint
bones.

Complete rest and anti-inflanunatory

Lateral condylar fracture of the distal third
therapy is indicated. lntralesional corticometacarpal bone (arrow) in a horse. Courtesy steroids may reduce inflan1mation and
of Dr. Matthew T. Brok ken.

prevent excessive bone growth. Their use
should be accompanied by counterpressure
associated suspensory desmitis, which has
bandaging. If the exostoses inlpinge against
a greater bearing on future performance
the suspensory ligan1ent, surgical removal
than the splint fracture itself.

may be necessary.

FRACTURE OF THE THIRD

FRACTURES OF THE SMALL

METACARPAL {CANNON) BONE

METACARPAL {SPLINT) BONES

The most common site of.major fracture of

Fractures of the second and fourth
the tllird metacarpal bone is in the distal
metacarpal (splint) bones are not uncomarticulation ( condylar fractures). Vertical mon. The cause may be from direct trauma,
fractures in the sagittal plane of the distal
such as interference by the contralateral leg
cannon bone ( condylar fractures) occur
or a kick, but often accompany or follow
predominately in young racehorses. Most
suspensory desrnitis and the resulting
condylar fractures are in the lateral condyle.

fibrous tissue buildup and encapsulation of

In Thoroughbreds, condylar fractw·es of the
the distal, free end of the bone. The usual site third metacarpus are at least twice as of these fractures is through the distal end,
conunon as third metatarsal fractures, but

-2 in. (5 cm) from tl1e tip. ln1mediately after
in Standardbreds, the ratio <if metacarpal to
the fracture occurs, acute inflanunation is
metatarsal fractures is nearly equal. Nearly
present, usually involving the suspensory
all lateral condylar fractw·es 01iginate from
ligament. Lameness is typically noted ( may
the mid to midaxial po1tion of tl1e lateral
be severe initially), which may recede after
condyle and traverse toward the lateral
several days rest and recur only after work.

cortex. In contrast to medial condylar

Diagnosis is confirmed by radiography.

fractures, lateral condylar fractures rarely

Ultrasound exaniination of the suspensory
spiral into the diaphysis of tl1e cannon bone.

ligament may also be beneficial to deter

Medial condylar fractures nearly always
mine a more accurate prognosis as well as
extend toward the axial aspect of the
guide a rehabilitation program. Surgical
cannon bone. Clinical signs are straightfo1�
removal of the fractured tip and callus is the
ward, with acute lan1eness after exercise
treatment of choice. Fractures involving tl1e

( or race) with marked effusion in the fetlock
proximal one-tllird of tl1e bone may require
joint. Radiographic exaniination should
surgical stabilization of tile bone to prevent
include a full series of the fetlock as well as
carpal instability, particularly if the fracture
a flexed dorsopalmar view. For medial
involves the second metacarpal bone.

fractures, complete exaniination of tl1e

Prognosis is based on severity of the
entire cannon bone should be perfonned.

LAMENESS IN HORSES

1125

Lateral condylar fractures can be treated
conservatively by casting, but the treatment
of choice is compression of the fracture,
with screws placed in lag fashion to
minimize or avoid osteoarthritis. For medial

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condylar fractures, in addition to lag screw
fixation distaJly, a plate is placed up the
remaining metacarpus.

The most conunon major long bone
fracture in horses is fracture of the
diaphyseal cannon bone. Typically, these
fractures result from trauma incurred while
the horse is pastured with other horses.

Open reduction and internal fixation is the
preferred treatment choice, because the lack
of soft-tissue coverage over an unstable
fracture typically causes these types of
fractures to become open when simply cast
or with a coaptation splint.

DISORDERS OF THE CARPUS

Flexed lateral radiograph of a horse with a
slab fracture of the third carpal bone (arrow).

The carpus involves three articulations:

Courtesy of Dr. Matthew T. Brokken.

the radiocarpal (antebrachiocarpal),
intercarpal (middle carpal), and carpometacarpaljoints. Problems are localized to the cause of lameness in racehorses. The
carpal area based on lameness, swelling,
primary etiologic factor is traun1a, usually
synovial effusion and pain on palpation,
associated with fast exercise. Chips typically
and responses to flexion and diagnostic
occur on the dorsal aspect of the joint. In the
analgesia. Visualization and palpation are
middle carpal joint, the most frequent sites
important to determine the site of swelling
are the distal radial carpal bone, proximal
in the carpus ( eg, synovial tluid in the
third carpal bone, and the distal intennedijoint or tendon sheath or swelling in the ate carpal bone. In the radiocarpaljoint, the
subcutaneous space). Light palpation with
most common locations are the proxin1al
fingers with the horse standing and with
inte1mediate carpal bone, distal lateral
the leg raised is beneficial in determining
radius, proxin1al radial carpal bone, and the
the specific area of fluid accumulation.

distal medial radius. Diagnosis is based on

Knowledge of the normal anatomic
clinical signs of synovitis and capsul.itis and
boundaries of the structures is in1portant.

radiographic demonstration of osteochon

Diagnostic analgesia of the carpaljoints is
dral chip fragment(s). Arthroscopic surgery
usually done intra-articularly. The antebrais the treatment of choice. The overall chiocarpal and middle carpal joints can be
prognosis is highly dependent on the degree
ir\jected easily. The carpometacarpal joint
of articular cartilage damage within the joint
communicates with the middle carpal joint;
identified on arthroscopy.

therefore, local analgesia in the middle
carpal joint provides analgesia of the

Carpal Slab Fractures
carpometacarpaljoint. There is considerable
distal palmar outpouching of the carpometa

Slab fractures extend from one articular
carpaljoint; with time, analgesia will diffuse
swface to another articular surface. In the
into the area of the proximal suspensory
carpus, slab fractures occur in both frontal
ligament, thus leading to confusing results.

and sagittal planes. The most common

Radiography of the carpus is critical for
fracture is a frontal slab fracture of the radial
specific diagnoses and should include
facet of the third carpal bone, followed by
flexed lateral as well as skyline views of
fractures of the intermediate facet and both
the distal row of carpal bones ( as well as
facets of this bone. The treatment of choice
proxin1al row/distal radius in some horses).

is lag screw fixation for fractures > 10 mm or
removal of the fracture fragments if they are

FRACTURE OF THE CARPAL
thin or not an1enable to lag screw fixation.

BONES

Accessory Carpal Bone Fractures

Osteochondral fractures ( carpal chip

These are less common than other fractures
fractures) of the carpal bones are a common
in the carpus. Lameness is typically acute

1126

LAMENESS IN HORSES
and severe, and there may be synovial
effusion in the carpal sheath and, less
commonly, the radiocarpaljoint. Radiographs confum the diagnosis. These fractures are typically treated conserva

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tively; however, if the fracture is articular
and fragmented, surgical removal of the
fragments has been perfom1ed. Fibrous
union may enable a horse to return to
athletic activity.

SUBCHONDRAL BONE DISEASE

OF THE THIRD CARPAL BONE

Degeneration and necrosis of the subchondral bone is common in racehorses and may precede slab fractures of the third carpal
bone. The condition was initially identified
in the proximal articular surface of the third
carpal bone and is considered to be a
consequence of cyclic trauma. Clinical signs
include lameness, reduced perfom1ance,
and effusion of the middle carpal joint.

Horses typically in1prove with intra-articular analgesia of the middle carpal joint. A skyline view radiograph is critical for
diagnosis and typically shows lysis and
sclerosis in the third carpal bone (typically

Marked new bone proliferation (arrow) in a
radial facet). Arthroscopic examination is
horse with osteoarthritis of the carpometathe treatment of choice, with removal of the carpal joint. Courtesy of Dr. Matthew I Brokken.

abnormal cartilage and subchondral bone.

of severe osteoa.rtluitis is largely palliative.

TEARING OF THE MEDIAL

Osteoarthritis of the carpometacai-pal joint

PALMAR INTERCARPAL
has been described ma.inly in Arabian and

LIGAMENT

Quarter horses. This condition typically
affects the medial aspect of the joint and is

This il\iury, first describ"ed in 1990, most
characterized by lan1eness ( minimal at first),
commonly involves the medial palrnar
fu111 swelling over the medial aspect of tl1e
intercarpal ligament but may involve the
distal carpus, and response to intra-articula.i·
lateral palma.r interca.rpal ligament. A
analgesia of tl1e middle carpal joint.

typical presentation is synovias and

Radiographs typically show periarticular
capsulitis unresponsive to therapy or the
new bone proliferation ( sometimes marked)

presence of carpal chip fragments with an
over tl1e proximal second a.i1d/or third
untoward amount of lan1eness. Diagnosis
metacarpal bone, lysis and/or sclerosis of tl1e
is made aithroscopically, and treatment is
bones surrounding tl1e medial carpometacarartlu·oscopic debridement of the tom fibers.

paljoint, and possible loss oftl1e medial joint

Prognosis depends on the degree of teai·ing,
space. Treatment consists of conservative
as well as lack or presence of concuITent
tl1erapy (systemic and/or intra-articular
subchondral bone damage.

anti-inflanunatories) and possible facilitated
artlu·odesis witl1 use of passage of drill bits
across the joint. (See also OSTEOARTIIRms,

OSTEOARTHRITIS OF THE CARPUS p 1063.)

Radiocarpal and/or middle carpal osteoa.i0
thritis typically appears with clu·onic

DISTAL RADIAL EXOSTOSIS AND
thickening of the joint capsule and usually

OSTEOCHONDROMA OF THE
associated decreased range of motion.

DISTAL RADIUS

Radiographic changes develop slowly, and
usually the degree of articular cartilage

Exostosis of the caudal aspect of the distal
compromise is severe. Cases that can
radial physis can cause tenosynovitis of tl1e
possibly lead to osteoarthritis should be
carpal sheath and da.tnage to the deep digital
treated aggressively and correctly. Treatment
flexor tendon. Exostosis is differentiated

LAMENESS IN HORSES

1127
from an osteochondroma based on its
location and histologic appearance.

Osteochondromas are present on the caudal
aspect of the distal radius metaphysis

Shoulder lameness in horses is less
normally 2-4 cm proximal to the distal radial common than many owners expect. Although VetBooks.ir
physis. Osteochondromas also have hyaline
cases are often described as having a typical
cartilage remnants present on histologic
gait (reduced protraction/cranial phase,
examination ( exostosis do not have hyaline
wearing of the toe, a swinging lameness), they
caitilage ). ltTespective of origin, these two
are still difficult to diagnose sin1ply from
conditions can cause lameness (swinging
analysis of tl1e animal's walk or trot. However,
leg) and carpal sheath tenosynovitis.

almost all cases have atrophy of the proximal

Diagnosis is generally made by radiogralin1b muscles ( especially supraspinatus, phy, but ultrasonic examination may be
infraspinatus, the cranial shoulder muscles,
helpful to define the presence of soft-tissue
and muscles of the cranial antebrachium)

injury. The condition can be treated
beyond that which would nonnally be
successfully via tenoscopy of the carpal
expected for lameness caused by distal lin1b
sheath with removal of the protruding mass
disease. This is associated not with shoulder
and identification and debridement of any
pat110logy per se, but is a general feature of
concomitant damage to the deep flexor
proximal limb lan1eness. mtra-articular
tendon. The prognosis is good and depends
anesthesia, medication, and centesis can be
on the degree of soft-tissue danrnge.

accomplished by passing a 90-mm spinal
needle between tl1e cranial and caudal parts

CARPAL HYGROMA
of the lateral tuberosity of the humerus,
angling caudodistally, from above; an

A carpal hygroma is a subcutaneous swelling ultrasound-guided teclmi.que is also over the cranial/dorsal aspect of the carpus.

described. Radiography is limited to the me

Typically, a history of trauma to the carpus is
diolateral projection, with the limb extended,
noted. The swelling is typically aseptic, but
and in some cases oblique projections
risk of infection can develop after drainage

( usually caudolateral-craniomedial or
or injection. Typically, a hygroma is a
proximocranial-proximodistal). Ul trasonogcosmetic blemish, and lameness is not raphy is essential for full assessment of thP
usually present. The diagnosis is made by
shoulder region, particularly the soft tissues.

palpation and visualization. Irtjection of
contrast material into the hygroma and

DEVELOPMENTAL DISEASES
subsequent radiographic examination
outlines the extent of the hygroma.

Developmental orthopedic disease

Communication between joint and hygroma
manifests in the scapulohurneral (shoulder)

is confirmed or excluded through fluid
joint principally as subchondral cyst-lil<e
injection into the cai-pal joints. Hygromas
lesions (bone cysts) affecting the glenoid of
can be treated in the early stage with
the scapula or as osteochondritis dissecans
drainage, steroid i.ajections, and bandaging.

of the hun1eral head. Also, a condition

When infection is present, surgical resection
almost exclusive to miniature ponies, caused
of the infected tissue is recommended.

by dysplasia of t11e joint and attributable to
hypoplasia of the joint surfaces, results in

RUPTURE OF THE COMMON
instability and secondary arthritis.

DIGITAL EXTENSOR TENDON

Subchondral Cyst-like Lesions: Bone

This condition occurs in foals and may be
cysts may develop in t11e glenoid, or socket,
present when the foal is born or develop in
of the shoulder joint. TI1ey may or may not
the first weeks of life. It can be primary or
conm1Unicate with tl1e shoulder joint and
secondary to carpal or fetlock flexural
respond variably to intra-articular anestl1esia.

deformities (seep 1150). Affected foals have Altl10ugh part of tl1e developmental a characteristic soft/fluid swelling over the
orthopedic disease complex, signs may not
dorsolateral aspect of the carpus and distal
be apparent until the anin1al is mature. m
radius. Ultrasound exan1ination is
common with other manifestations of this
confirmatory. Management involves stall
syndrome, lameness may not become a
rest and preventing secondary tendon
feature until tl1e animal begins work (typically
contracture with tl1e use of bandaging with
breaking in or early ridden exercise).

or without PVC splints to prevent knuck

Occasionally, bone cysts may be a cause of
ling, if appropriate. Prognosis is excellent in
lameness in an older horse, having remained
foals without concurrent flexural deformiquiescent for most of the animal's life; the ties or cuboidal bone abnormalities.

reason for these later onset cases is not clear.

1128

LAMENESS IN HORSES

Diagnosis is made by localization with
the scapulohumeral articulation. Oblique
intra-articular anesthesia, by exclusion
views may demonstrate deep erosion of the
of lower limb disease, or occasionally by
humeral head in severe cases. The generalgamma scintigraphy. Radiographs should ized destruction of the joint produces a "hot
document the lesion, although some cysts
spot" on a bone scan, if performed. There is

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are too small to be seen.

no simple treatment. Most cases present at

Treatment in young horses consists of
such an advanced stage that even palliative
rest in the hope the cyst will remodel to
care is impossible; euthanasia on humane
become non painful; however, this happens
grounds should be considered in such
only rarely. Intra-articular medication can
situations. Surgical arthrodesis has been
provide relief from lameness but usually
described but is rru·ely performed.

only transiently. Some disease-modifying
preparations show promise ( eg, autologous

FRACTURES
conditioned serwn), and some clinicians
favor the use of systemic glycosaminogly

Serious traun1a can result in fracture to any
cans. Surgical debridement is difficult in
part of tl1e shoulder region. However, the
most cases, because tl1e cyst location and
main sites affected are the supraglenoid
articular cartilage damage that causes
tuberosity of tl1e scapula ( which serves as
secondary osteoathritis may limit its
the origin of the biceps brachii muscle), the
effectiveness; however, it can be very
mid to distal scapula, and the proxin1al
successful. Injection of corticosteroids
humeral metaphysis.

directly into the cyst via an extra-articular

Supraglenoid tuberosity fractures, if
approach could be appropriate, but the lack
complete, invruiably displace in a crruliodisof 3-dimensional imaging of this region in tal direction, because of the pull of the biceps.

horses makes the approach hard to plan.

Large fractures can be surgically repaired.

However, this is not easy, because the

Osteochondritis Dissecans: Derangefragments are often difficult to reduce and ment of cartilage and bone development on
the in1plants ru·e both difficult to place and
the humeral head can result in weakness
prone to failure dwing recove1y from
within the ruticular cartilage that may lead
anesthesia or during convalescence. Smaller
to erosion or formation of a free flap of
fragn1ents can be removed, but the involvecartilage. Typically, the caudal part of the ment of the biceps tendon of origin has to be
head is affected, or at least it is the part most
resected. Very large fragments can involve
evident on radiographs. In other joints,
the joint surface. Cases usually present with
osteochondritis dissec3l1S often can be
severe lruneness and a history of trawna ( eg,
treated successfully with arthroscopic
a fall duringjumping or collision with a fixed
debridement. Unfortunately, access to the
object). On mrulipulation, tl1ere is often a
shoulder joint is severely restricted, and
sense of disarticulation between the lower
in most cases the full extent of the lesion
limb and shoulder as the biceps is disrupted.

cannot be seen or treated. Clinical resolution Crepitus may be felt. In most cases, because in all but the mildest cases in young horses is
the inciting cause is significant trauma, other
rare. Rest and various medi'tations have
signs such as soft-tissue abrasions or swelling
been tried, with little docwnented success.

will pinpoint the shoulder as the site of pain.

Radiographs will reveal the fracture, and

Scapulohumeral Dysplasia: Seemingly
ultrasonography can be very useful to assess
unique to the miniature breeds, this condition the biceps tendon. Management varies and ruises from a mismatch between the size of
depends on intended use, age, size of
the glenoid and humeral head. This causes
fragment, size of horse, etc. The prognosis for
instability of the joint and secondary arthritis. restoration of nom1al function is guru·ded.

Although undoubtedly a developmental

TI1e size of the fragment, degree of displaceproblem, probably with a significant degree ment, presence/absence of articular
of heritability, many cases do not present
involvement, degree of biceps disruption,
until the animal is an adult, and the history is
and intended use of the horse are probably
often of sudden onset lan1eness. On physical
the most important prognostic factors.

exanlination, proximal limb muscle atrophy

Mid to distal scapula fractures occur
is often profound and lruneness considerable. througl1 trauma or, in racehorses, as stress These factors, along with the breed
fractures associated with cun1ulative cyclical
disposition and the often-present sign of
fatigue. Trawna can result in complete or
resentment of proximal limb mrulipulation,

(presumably because of the flexibility of
make localization straigl1tforward.

the bone, especially in foals) incomplete

Radiographs reveal the presence of
fractures. Radiographs rarely help, because
osteoarthritis and vruiable subluxation of
of the difficulty in obtaining diagnostic

LAMENESS IN HORSES

1129
images of the area. Ultrasonography can

BICIPITAL BURSITIS
accurately assess the integrity of the bone
surface and is the technique of choice.

The biceps brachii tendon runs over the

Scintigraphy can also detect the injuries.

cranioproximal humerus, protected by

Comminuted fractures can occur, and the
a synovial bursa. Inflammation of this

VetBooks.ir
prognosis worsens with increased complexstructure can cause lameness and is usually ity of the fracture. Simple, nondisplaced, or
secondruy to a more serious inciting cause.

minimally displaced fractures usually heal

Trawna to the proximal hwnerus, cystic
well with rest alone.

lesions in the underlying bone, and injwy

Ultrasonography can be used to monitor
to the tendon itself will Gause secondruy
healing. Stress fractures are almost always
bursitis; it is important to recognize the
incomplete and heal very well, carrying an
prirnruy lesion and treat appropriately.

excellent prognosis for return to training.

Occasionally, idiopathic primruy bursitis

Very rarely, scapula fractures manifest as
arises and responds very well to medication
severe, unstable, conuninuted ir\juries
of the bursa with corticosteroids. Bacterial
necessitating euthanasia on humane grounds. contamination and, rarely, fungal infections The clinical appearance is key to making a
can cause bicipitai bursitis. In most cases, a
decision in these circun1Stances; although
wound in the vicinity of tl1e bursa alerts the
painful, scapula fractures with a good progclinician to this possibility but, very rarely, nosis cause no observable limb instability.

closed sepsis can occur. Treatment for

Deltoid tuberosity fractures are seen
septic bursitis follows the san1e pattern as
infrequently. They are usually the result of
for other synovial structures. Radiography
trauma, often a kick from another horse, and and ultrasonography complement each may involve a wound and vruiable amounts
other in the diagnosis and management of
of infection within the injury. Lesion-oriprimruy and secondruy bursitis. Repeat ented oblique radiographs and ultrasonograexanl.inations may be necessruy if a primruy phy define these injuries, and affected horses lesion cannot be detected, because it may usually recover fully with rest alone,
become obvious with time. Scintigraphy is
although surgical debridement of infected
useful in cases in which the prirnruy lesion
bone may be required in rare cases.

remains elusive, because small areas of

Stress fractures affect the proximal
bone damage or cavitation can go undehumerus also, almost exclusively in the tected radiographically.

caudal metaphyseal region. They are an
uncommon but important cause oflameness

INFECTION
in racehorses (the craniodistai metaphysis of
the humerus is also affected, seep 1051). The Sepsis of the shoulder joint occurs most
typical hist01y is one of sudden onset, often
commonly as a result of penetrating ir\jury.

moderate to marked lameness closely

Diagnosis and treatment proceed as for
associated with recent exercise, in an animal
other joints. In foals ( and rarely, weanlings
usually but not always in faster work
or yearlings) infection can spread hematog

Lameness is usually traJ1Sient, and the horse
enously and become established in the
generally becomes sound within a short time
growth plates or ends of the bones (physeal

( days to a week). If exercise resumes,
or epiphyseal infection). These infections,
lameness recurs. Localization is difficult;
provided they are not associated with
many are detected after the lower limb has
contamination of the synovial structures,
been eliminated as the source of pain, or with can be treated with high levels of antinl.icroscintigraphy. Radiographs can identify bials systemically before resorting to
periosteal and endosteal new bone at the site
surgical intervention. Metl10ds to provide
of ir\jury. Recovery is usually uncomplicated
high quantities of antinl.icrobials at the site of
and complete with a few weeks' rest.

infection exist ( eg, intraosseus perfusion).

Prolonged confinement may be counterproductive, and light exercise ( walking only) SUPRASCAPULAR NEUROPATHY
may be introduced surprisingly quickly once
the initial painful period has subsided. The

(Sweeney)

ir\jury remains evident on radiographs long

This syndrome describes the physical appearafter the bone is strong enough to witi1Stand ance of the horse's shoulder. It is not a diagnoexercise, but a gradual smoothing and sis in itself, because there are a number of
resolution of the callus will be seen as
potential causes. The most common cause is
remodelling proceeds. Undetected humeral
ir\jury to the suprascapular nerve.

stress fractures can result in failure of the

Ali cases have atrophy of the supraspinabone during exercise and complete tus and infraspinatus muscles that cover the
breakdown, necessitating euthanasia
scapula. This results in the scapular spine

1130

LAMENESS IN HORSES
becoming prominent; in severe cases, the
for rapid screening of the proximal limb and
muscles virtually disappear. The atrophy is
ce1vical and thoracic ve1tebra for dan1age
unusual in that it is often profound and very
that may have an adverse effect on prognosis.

localized, which are hallmarks of an injury
to a single lower motor nerve. The nerve

OSTEOARTHRITIS OF THE

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involved is the suprascapular. Although
the site of damage is rarely documented

SHOULDER
clinically, most cases involve trawna to the

Degenerative joint disease affecting tl1e
cranial shoulder at the point where the
shoulder joint poses the same problems here
nerve is exposed to potential compression
as it does elsewhere. If no primary cause is
as it courses over the cranial aspect of the
identified that is amenable to cmTection
scapula. The severity of dan1age determines
and if radiographic signs (periarticular
the degree of atrophy and the chances of
osteophytes, etc) are established, it is safe
recovery. If nerve function is severely
to assume that caitilage destruction is well
compromised, the shoulder joint becomes
w1derway. Signs can be an1eliorated, but
unstable (it is a synarthrosis with no true
not cured, with use of anti-inflanllllatory,
collateral ligaments, relying on the
ai1algesic, ai1d disease-modifying tl1erapies.

surrounding muscles to support it) and the
joint "pops out" sideways as the horse bears weight. This subluxation does not appear
overtly painful to the horse, but if the joint
cannot be stabilized, it may have significant

Elbow lameness is rare but should always be
implications for the longterm health of the
considered if tl1e source of pain cannot be
joint and the horse's athletic career.

isolated to the distal limb. Synoviocentesis is

Therapy is aimed at maintaining muscle
achieved via lateral approaches either close
health during the period of ne1ve recovery
to tl1e collateral ligai11ent or into the caudal
and maximizing neurogenesis. Horses should pouch. Radiography is limited to mediolatbe restricted to stable rest or a very small eral (limb extended) and craniocaudal
paddock. Complete inrn1obilization may
projections (weightbearing). Ultrasonogranegatively impact the nerve and muscles, but phy allows inspection of tile lateral joint
activity probably hastens joint degeneration.

margins and collateral ligament as well as

A surgical procedure to remove part of the
the medial collateral ligament (limb flexed
scapula over which the nerve courses has
and abducted). Lameness miginating from
been desc1ibed, aiming to provide optimal
the elbow is not generally considered to
conditions for nerve recovery. This should be
produce characteristic gait changes, but
considered, but its usefulness is open to
disuse muscle atrophy may be more evident
debate. Muscle stin1ulation, under tl1e
than expected with lower limb lesions.

guidance of a trained physiotherapist,

Occasionally, loss of definition or cliscomfort
will help to linlit muscle fibrosis and may
may be appreciable during careful palpation.

encourage nerve regeneration. The vast
majority of cases seem to be a result of neuro

DEVELOPMENTAL ORTHOPEDIC
praxia or axonotmesis (based orr clinical

DISEASE
obse1vations and rates of recovery), and
function is recovered with tin1e. However,

Cyst-like lesions occur in the proximal
tllis process can take many months, and
radius (usually medial) and less commonly
frequently some loss of muscle bulk will
tile distal hun1erus. They are·most
remain. The prognosis seems most affected
conunonly seen in young ailimals, similar
by duration of irtjury before diagnosis, degree to cysts in other locations, and the usual of atrophy at diagnosis, and willingness of the treatment regimens of rest, intra-articular owner to perform time-consuming physical
medication, and controlled exercise are
treatments for many months.

used. As with the shoulder, access

Other causes of sweeney include disuse
arthroscopically is limited. Extra-articular
atrophy ( wllich does not appear focal and is
approaches to the proximal radius have
rarely severe), bracllial plexus irtjury ( which
been tried but have the saine linlitations as
usually disrupts a number of ne1ves; atrophy
the shoulder, although in practice, when
is not focal but observable in a number of
mthogonal radiographic projections ca.ii be
muscle groups), and caudal cervical disease
obtained, there is more chance of building a
resulting in spinal ne1ve radiculopatily (in
tllfee-din1ensional in1pression of their size
which a nwnber of motor nerves are also
and location. Treatment options ai·e limited.

affected so tilat other muscles atrophy).

Other types of developmental orthopedic

Careful assessment of the muscles involved
disease in the elbow joint, seen commonly
and radiography of tile neck and shoulder
in other species, are rai·e or unrecognized in
will aid differentiation. Scintigraphy is useful
horses.

LAMENESS IN HORSES 1131

FRACTURES
periosteal and endosteal reaction at the
precWection site. This can also be docu

Significant trawna can result in breakage of
mented ultrasonographically. Scintigraphy is
any type, but the most commonly encouna sensitive method to detect fractures that tered fracture of the equine elbow affects
cannot be seen on radiographs. Management

VetBooks.ir
the olecranon of the ulna. Stress fractures
is tailored to tl1e comfort of tl1e horse and
affect the craniodistal metaphysis of the
severity of tl1e initial i.rtjury but proceeds as
humerns in racehorses.

for otl1er i.rtjuries of this type with a careful

Olecranon fractures in mature horses
retWTI to exercise, balancing structural
occur as a result of external trauma and may
integ1ity witl1 biomechanical requirements
be incomplete (rare), complete but non- or
for healing.

minin1ally displaced, or complete and significantly displaced. A nwnber of fractures are also open, as a result of tl1e trawna that

OSTEOARTHRITIS
caused tl1em. In cases of incomplete or

Degenerative joint disease of t11e elbow
nondisplaced fractures, conservative
joint, in tl1e absence of an inciting primary
therapy can be rewarding, altl1ough some
lesion, is managed as described for the
will displace during convalescence. Most
shoulder and otl1er joints (seep 1051). Some authorities recommend cross-tying tl1e
horses present witl1 lameness localized to
horse to prevent it from getting up and down
the elbow joint by diagnostic anestl1esia
during tl1e fu-st 6-8 wk of box stall rest. The
witl1 little or inconclusive abnormalities
use of splints and Robe1tJones bandages is
evident witl1 imaging. It has been reasonably
more controversial-a "pendulum effect"

proposed tl1at these horses may be suffe1ing
can result from increased weight on tl1e
from subchondral bone dan1age.

lower lin1b, possibly doing more harm than
good. Many olecranon fractures displace
undertl1e influence of the triceps muscle

COLLATERAL LIGAMENT INJURY
and require internal fixation to repair. The

Most commonly detected laterally, probably
use of a tension band plate is most common,
for biomechanical and imaging reasons,
witl1 reported success rates for return to
tl1ese ir\juries can be detected witl1
atl1letic function of -75%.

ultrasonography. Medial collateral liga

Fractures of the ulna in foals are less liable
ments are more difficult to image but can be
to displace and may therefore be treated more assessed. Radiographs may document new commonly with rest alone. If such fractures
bone ( enthesiophytes) associated witl1
are displaced, tension band plates can be
ir\jury. A nwnber are found by scintigraphy,
applied, but their use must be monitored
associated with a "hot spot" even in tl1e
carefully because they will interfere witl1
absence of radiographic changes. Prognosis
growth of tl1e lin1b (tl1e proxin1al radial
depends on tl1e severity of tl1e ir\jury. At tltis
physis fuses at 11-24 mo of age) and must be
time, no proven tl1erapies exist to augment
removed as soon as satisfactory healing has
ligament healing. A munber of treatments
been achieved. An unusual but potentially
have been tried, including intra-articular
difficult ir\jury to diagnose and treat occurs
medication, periligamentous i.rtjection of
when the proximal ulnar epiphysis is avulsed
biologics ( eg, platelet-rich plasma), systemic
due to Salter Harris type l or 2 i.rtjury of tl1e
disease-modifying drugs, and extracorporeal
physis, which fuses at 24---36 mo of age. In
shockwave tl1erapy.

some cases, tl1e epiphysis is retracted so far
proxin1ally tlmt it does not appear on tl1e
standard mediolateral radiograph and can be
missed. Less dramatic i.rtjuries of this type can
be managed conservatively, but significant
displacement requires surgical intervention.

BUCKED SHINS/DORSAL

Treatment and prognosis may be

CORTICAL FRACTURES OF THE
influenced by whetl1er the fracture enters
the elbow joint or not. To determine this,

THIRD METATARSAL BONE
careful assessment of high-quality

Modelling and stress remodelling of the
radiographs is needed.

dorsal cortex of the tl1ird metatarsal bone

Stress fractures at the craniodistal
occur in young racehorses but, unlike in tl1e
metaphysis of the hun1erus, just above tl1e
tl1i.rd metacarpal bone, it is rarely associated
elbow, occur in racehorses. The history is
with clinical signs of lameness. Dorsal
often sin1ilar to tl1at for fractures of tl1e
cortical fractures of the llii.rd metatarsal
proxin1al hwnerus and other stress fractures.

bone are rare but may occur in Thorough

Mediolateral radiographs will often detect
bred or Standardbred racehorses.

1132

LAMENESS IN HORSES

EXOSTOSES OF THE METATARSAL INCOMPLETE LONGITUDINAL

BONES

FRACTURES OF THE PLANTAR

Exostoses of the metatarsal bones

ASPECT OF THE THIRD

(splints) are common and may or may

METATARSAL BONE

VetBooks.ir
not be associated with lameness. Splint
exostoses may be caused by direct

Stress reaction and incomplete longitudinal
trauma or instability between metatarsal
fractures of the plantar aspect of the third
bones. Large exostoses on the proximal
metatarsal bone may occur due to stresslateral aspect of the second or fourth related bone irtjury at the origin of the
metatarsal bones are common and
suspensmy ligan1ent. These are usually
usually asymptomatic. Axially located
associated with increased uptake of
splint exostoses on the proximal end of
radionuclide on bone scintigraphy and
the second or fourth exostoses may
are clearly demonstrable on MRI.

impinge on the proximal end of the
suspensory ligament or on the lateral

FOCAL BONE REACTION AND
and medial plantar metatarsal nerves

AVULSION FRACTURES OF THE
and be associated with lameness.

THIRD METATARSAL BONE

Lameness is usually mild and can be
alleviated by infiltration of local anesthetic

Focal bone reaction and avulsion fractures
solution around the exostosis or by
of the third metatarsal bone at the site of the
perineural analgesia of the lateral and
proxin1al attachment of the suspensory
medial plantar metatarsal and lateral and
ligament are not unconunon. They may be
medial plantar nerves.

solitary irtjuries or, more frequently, are

Management of horses with symptoassociated witl1 proxin1al suspensory matic splint exostoses includes local cold
ligament desmitis. These irtjuries are
therapy (cold hosing, icing, etc), bandagfrequently found in sports horses. Severity ing, and administration ofNSAIDs.

oflameness is variable, and localizing signs

Infiltration of corticosteroids around the
are usually not evident. Diagnostic
exostosis may be beneficial in some cases.

analgesia is necessary to localize the pain.

Surgical excision of persistently painful

Some fractures may be evident radiologiexostoses by periostectomy, ostectomy of cally, whereas in other horses scintigraphy
exostosis without removing the parent
or MRI is necessary to confum the
splint bone, adhesiolysis, and fasciotomy
diagnosis. Conservative treatment with
can be performed successfully if exosrest and a controlled ascending exercise toses involve the axial aspect and
program is usually recommended. However,
encroach on or are adhered to the
recurrence of lameness is conunon,
suspensory ligament.

particularly in horses with concurrent
proxin1al suspensory desmitis; in these
horses, new·ectomy of the deep branch of

DIAPHYSEAL FRACTURE OF THE
the lateral plantar nerve may be the only

THIRD METATARSAL BONE'

chance to resume sustained athletic
perfonnance.

Diaphyseal fractures of the third metatarsal
bone usually result from direct trauma ( eg,

FRACTURES OF THE SECOND
kicks) or may result from propagation of

AND FOURTH METATARSAL
medial condylar fractures. Prognosis
depends on age and size of horse, configura

BONES
tion of fracture, integrity of the vascular

Fractures of the second and particularly the
supply, involvement of the metatarsofourth metatarsal bones are common and phalangeal or tarsometatarsaljoint, and
usually arise from direct trauma ( eg, kick
degree of contamination. Prognosis for
from another horse). Simple, comminuted,
adult horses with open, comminuted
and displaced fractures occur and are often
fractures of the third metatarsal bone is
associated with overlying wounds.

poor, but in those with closed, mildly

Diagnosis is confumed by radiography.

comminuted or oblique fractures, internal

Most second and fourth metatarsal bone
fixation may be possible (although often
fractures will heal with conservative
limited by financial constraints). Prognosis
treatment despite comminution and
in foals with simple or mildly comminuted
infectious osteitis with appropriate
fractures of the mid diaphyseal third
antinticrobial therapy, wound care
metatarsal bone after internal fixation
bandaging, and rest. Rest of 4-6 mo may be
with two plates is fair.

necessary in horses with open or infected

LAMENESS IN HORSES

1133
fractures. Segmental ostectomy may be

( and less co11U11only the proximal intertarindicated in horses with chronic dischargsal joint), colloquially known as "bone ing wounds and sequestrurn development.

spavin," is a common cause of lameness

Complete removal of severely comminuted
or poor performance in horses from all
foUith metatarsal bones has been reported
disciplines. La.tneness may be unilateral or

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as successful, although persistent lameness
bilateral, and pathology may develop in one
may result. Internal fixation of the fractures
joint only, or two or even three concurof the proximal end of the second metatarrently. Distal hock joint pain may be a sal bone may be indicated in some cases
sequela of incomplete ossification of tl1e
with marked displacement and instability of
central and third tarsal bones; certain
the fracture fragments. Open fractures of
conformational abnormalities (sickle hock,
the proximal end of the second and fourth
cow hocked, or excessively straight hock
metatarsal bones may result in sepsis of the
conformation) are also believed to be
tarsometatarsal joints, which requires
predisposing. It has been proposed that
aggressive antimicrobial therapy and
degenerative joint disease of the distal
appropriate treatment.

tarsal joints may be caused by excessive

Simple fractures of the distal encl of the
compression and rotation of these joints
second and fourth metatarsal bones,just
as tl1e horse jumps or stops. In Icelandic
above the "button of the splint bone," are horses, bone spavin is tl10ught to be
usually associated with desmitis of the
he1itable.

branches of the suspensory ligament.

In most horses, few clinical signs are
evident on physical exa.tnination, although

ENOSTOSIS-LIKE LESIONS OF
in horses with more chronic distal hock

THE THIRD METATARSAL BONE
pathology, the soft tissues over the medial
aspect of the distal hock joints may be

Enostosis-like lesions of the third metatarsal
appreciably tltlckened. La.tneness varies
bone appear as intense focal areas of
from subtle loss of perfom1ance without
increased uptake of radionuclide on
overt lameness to moderate or severe
scintigraphic exan1ination after injection of
lameness. A characteristic gait related to

99mTc-labelled methylene diphosphonate.

lan1eness from tl1e distal hock joints has

Radiologically, they appear as round or irregubeen described as adduction of the hindlin1b larly shaped areas of increased radiopacity
with an abrupt abduction occurring just
within the medullary cavity. They are usually
before the limb contacting the ground; tltls
asymptomatic and rarely cause lameness.

has been referred to as a "stabbing" gait, Lameness, if present, usually improves with
which, although frequently evident, is not
rest and administration ofNSAIDs.

pathognomonic. Horses can exhibit tltls
gait with lameness originating from other
causes, and distal hock pain may also
present with a different gait. Lan1eness may
be exacerbated when the horse is on a

FAILURE OF OSSIFICATION OF
circle, with some horses showing more

THE DISTAL TARSAL BONES
lameness with the affected limb on the
inside and some with the limb on the

Incomplete ossification of the central and
outside. A proxin1al Iin1b flexion test will
third tarsal bones is most common in
exacerbate lameness in some, but not all,
premature or twin foals and is characterized horses with distal hock joint pain.

by a "sickle-hock" appearance. It may occur Diagnostic analgesia should be used to
unilaterally or bilaterally. Radiologically, the localize the source of pain. Most, but not all, pa.itially ossified cuboidal bones appear
horses with degenerative joint disease of
smaller a.t1d more rounded than nom1al.

the distal tarsal joints will improve after

Early recognition and treatment are
intra-a.tticula.i· analgesia of the distal tarsal
important to prevent crushing of the bones
joints. A negative response to intra-a.iticular
and resultant progressive osteoarthritis.

analgesia of the distal tarsal joints does not

Cylinder tube casts can be used with good
preclude distal hock joint pain. Perineural
results to protect the in1.mature bones until
analgesia of the superficial and deep fibular
they have ossified.

and tibial nerves can be useful to confirm
hock pain.

OSTEOARTHRITIS OF THE DISTAL

Radiography is useful to confum the

TARSAL JOINTS
diagnosis. Radiologic changes may be
evident in only one or two projections;

Degenerative joint disease or osteoarthritis
therefore, a minimum of four standard
of the tarsometatarsal, distal intertarsal
orthogonal radiographic projections of

1134

LAMENESS IN HORSES
the hock should be taken. Radiographic
several yeat-s after treatment, the success
changes include narrowing or loss of joint
rate decreased and a significant nwnber of
space, sclerosis of the subchondral bone,
horses developed arthritis of the proximal
lysis of the subchondral bone, periarticular
intertat·sal and tat-socruraljoints. Other
osteophyte formation, and periosteal new
complications, including persistent

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bone fom1ation. The seve1ity of lameness
swelling, septic arthritis, skin sloughing,
and degree of radiologic change are poorly
and increased lan1eness, have been
correlated. In those horses in which distal
reported. Therefore, this technique is
hock joint pain is suspected but there is
difficult to recommend because of the inilittle radiologic change, scintigraphy of the tial severe pain and significant possible
tarsus may reveal an increased focal uptake complications. Intra-articular iajection of
of radionuclide in the distal tarsal bones.

ethyl alcohol to achieve arthrodesis has also

The ainl of treatment is to provide pain
been reported, although more longterm
relief so that the horse may remain in work.

follow-up studies are required to evaluate

It has been suggested that by maintaining
its usefulness and safety.

the horse in work, the distal hock joints will

In horses that do not respond to
eventually ankylose and the horse will
conservative treatment, a nwnber of
become pain free. However, progressive
surgical techniques have been reported.

radiologic ankylosis is rarely observed and

These include cunean tenectomy, subchonhas not occurred in lame horses without dral forage, neurectomy, and several
inte1vention.

different techniques of surgical atthrodesis.

Conservative treatment involves systemic

Cunean tenectomy may result in a

NSAIDs, intra-atticular medication with
tempora.Jy' improvement in lat11eness but is
corticosteroids, with or without hyaluronan,
w1likely to restore sow1d.ness. It is believed
remedial trimming and faniery, and
to reduce the pressure over the medial
adaptation of the work program. Systemic
aspect of the distal tat-sus and ctmean bw-sa
treatment with polysulfated glycosaniinoglyand to reduce the rotational and shear stress can (PSGAG), hyaluronan, or oral nutraceuover these joints during contraction of the ticals may be used as adjunctive therapy.

tibialis cranialis muscle.

Ti.ludronate, a bisphosphonate compound

The most common surgical technique
that inhibits osteoclastic activity, has been
used in treatment of distal tarsal osteoarthriadvocated for use in horses with distal hock tis is facilitation of fusion of the affected
pain. There are few controlled studies with
joints. Drilling across the distal intertat-sal
this medication and, in a small double-blind
and tarsometatarsaljoints is the most
clinical study, only one of eight horses
frequently used procedure to promote
improved with aclrninistration of tiludronate distal tarsal atthrodesis. Initial techniques for distal tarsal inflat_nmation or atthritis.

described a more aggressive procedure,

Extracorporeal shockwave treatment
with 600/o of the articular cartilage removed.

(ESWT) has also been used in treatment

Significant postoperative pain was
of distal tarsitis. Both focused and radial
associated with this procedure, and a more
portable units are available. In one
conservative approach using three drill
retrospective study of 7 4 horses with
tracts is currently recommended. Return to
osteoarthritis of the distal tarsaljoints
full athletic perfom1ance usually takes 10-12
treated with ESWT, 800/o of the horses
mo. Retrospective studies evaluating this
showed improvement in lameness but
technique report -600/o qf horses successfully only 18% of horses became sound.

return to their previous level of performat1ce.

Intra-articular ir\jection of sodiwn

Both neodymium:yttriwn alwniniwn
monoiodoacetate (MIA) has been used for
garnet (Nd:YAG) and 980-nm diode laser
chemical arthrodesis of the distal intertarsal have also been used to facilitate arthrodesis and tarsometatarsaljoints. MIA inhibits
of tl1e distal tarsal joints. Several studies
chondrocyte glycolysis and causes chonhave shown that horses treated with drocyte death. Contrast atthrography is
laser-facilitated arthrodesis are more
necessaty to ensure accurate needle
comfortable after the procedure than when
placement and that no communication with
surgical drilling or MIA is used. It has been
proximal joints is present before ir\jection
tl1eorized that the superheating that occw-s
of MIA. After injection, pain control is
with the laser may cause thermal dan1age to
important, because severe pain is often
ne1ve endings and diminish postoperative
present for 4-18 hr. Several studies have
pain. Intra-articular drilling with diode-laser
shown that 75o/<r-85% of horses have been
treatment has also been recommended,
free of latneness with radiographic evidence because the drilling should stimulate more of joint fusion at -6 mo after treatment.

bone production and fusion, whereas the

However, when horses were followed for
laser reduces the postoperative pain.

LAMENESS IN HORSES

1135

Surgical stabilization in addition to
capsule may occur due to osteochondrosis,
intra-articular drilling of the distal tarsal
degenerative joint disease, trauma, poor
joints has been proposed to have a superior
joint conformation, hemoaithrosis, or
clinical result versus intra-articular drilling
infection, or it may be idiopathic. Lameness
alone. Lag screws or a screw and plate
may or may not be present, depending on the

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combination have been used. One study
etiology. Diagnosis is based on clinical signs
repmted a success rate of 89"/o of horses
and a positive response to intra-articulai·
returning to soundness versus 60% with
ai1algesia of the tarsocmral joint if lan1eness
drilling alone; however, only a small number is present. Radiographs should be taken to of cases were repmted.

exclude OCD and other radiologically

Neurectomy of the deep fibular nerve and
evident pathology, and ultrasonography
a paitial neurectomy of the tibial nerves
should be clone to assess the periarticular
may be perfom1ed to relieve pain associated soft-tissue structures. Synoviocentesis of with the distal hockjoints, with -60% of
the tarsocruraljoint should be perfonned
horses undergoing surgery returning to full
if sepsis or hemoarthrosis is suspected.

athletic function.

Idiopathic synovitis may be diagnosed in the
absence of lai11eness or radiologic change.

OSTEOARTHRITIS OF THE

Idiopathic synovitis rai·ely interferes with

TALOCALCANEAL JOINT
use of the horse but may be considered an
wiacceptable cosmetic blemish. Idiopathic

Osteoarthritis of the talocalcanealjoint is
synovitis may be managed by draining the
rare. There are frequently no localizing
synovial fluid and medicating the joint with
signs. Lameness is usually paitially
intra-articular corticosteroids. Pressure
in1proved by intra-articular analgesia of the
bandages should be applied afterward to
tarsocruraljoint and alleviated by pe1ineural provide joint compression, and the horse analgesia of the fibular and tibial nerves.

stall rested for 2 wk. However, in approxi

Diagnosis is confirmed by radiography, with
mately half of horses, effusion will recur
radiologic changes of subchondral sclerosis,
and a persistent cosmetic blemish remains.

lysis, and joint narrowing evident within the

Intra-articular injection of atropine (8 mg)

talocalcanealjoint. The prognosis for return
may sometimes help.

to athletic soundness with conservative
management is poor. Surgical arthrodesis

OSTEOCHONDROSIS OF THE
has resulted in improvement in laineness but TARSOCRURAL JOINT
not complete resolution of signs.

Osteochondrosis dessicans (OCD) of the

OSTEOARTHRITIS OF THE
tarsocruraljoint is common in many breeds

TARSOCRURAL JOINT
of horses, especially Warm bloods an.d

Standardbreds. OCD of the tarsocrural

Osteoarthtitis of the tai·socrural joint may
joint may or may not be associated with
be seen as a primary disease or develop
laineness and is associated with variable
secondary to trauma, osteochondrosis, or
ainounts of joint effusion. Diagnosis is
osteoarthritis of the distal hock joints. It
confirmed by intra-articular analgesia of the
is usually associated with joint effusion.

tarsocruraljoint if lan1eness is present and

Lameness may vary from mild to severe
by demonstrating radiologic changes. Few
and is usually improved by intra-articular
of the common OCD lesions in the hock will
analgesia of the tarsocrural joint. In horses
heal spontaneously after 5 mo of age, so
with primary osteoarthritis of the tarsocruarthroscopic surgical removal is usually raljoint, often no radiologic abnorn1alities
advised. Prognosis for full return to athletic
are evident, and diagnosis is based on
fw1ction after surgery is good. If left
arthroscopic examination. Response to
untreated, fragments may come loose,
intra-articular medication with corticosteresulting in cartilage dainage and acute roids and hyaluronan is often disappointing,
signs of effusion and lan1eness.

and prognosis for return to athletic

OCD lesions in the tarsocrw·al joint
soundness is guarded to poor.

ai·e most commonly seen on the distal
intermediate ridge of the tibia. Lesions at

SYNOVITIS/CAPSULITIS OF THE
this site do not cause laineness unless

TARSOCRURAL JOINT
significant effusion occill'S or fragments
become loose. Dislodged fragments may

(Bog spavin)

become lodged in the dorsal part of the
proximal intertarsaljoint. Arthroscopic

Acute or chronic synovitis of tl1e tai-socrural
removal of the fragments is usually
joint resulting in distention of t11ejoint
associated with a good outcome.

1136

LAMENESS IN HORSES

OCD lesions of the distal end of the lateral after injury when fracture line bone trochlear ridge are most commonly seen in
resorption has occurred. CT or bone
heavy horses and Standardbreds. Lesions
scintigraphy can be useful for diagnosis
can be large and, if loose, cause acute onset
if fracture is suspected but not evident
of severe lameness and effusion. Large or
radiologically. Variable fracture configura

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loose lesions should be removed arthrotions can occur. Horses can be treated scopically, and even large lesions can be
surgically with lag screw fixation or
removed with a good prognosis. Prognosis
conservatively, depending on configuration
is determined by the proximal and axial
of fracture. Prognosis depends on fracture
extent of the lesion.

configuration.

Medial malleolar OCD lesions usually
cause more lameness and effusion than the

FRACTURE OF THE TALUS
more common OCD lesions on the distal
intermediate ridge of the tibia. They are

Sagittal fractures of the talus are rare and
usually seen on the axial aspect of the
have been most commonly reported in
medial malleolus and may be overlooked on
racehorses. Lan1eness is usually moderate
dorsoplantar radiographs. Early arthroscopic to severe and associated with tarsocrural removal of fragments is recommended to
joint distention. Fractures in racehorses
prevent erosive lesions from developing on
usually arise in the proximal aspect of the
the medial trochlea of the talus. Arthroscopic sagittal groove of the talus and are often surgery usually has a good prognosis for
incomplete. Fractures after traunm are
return to athletic function.

usually comminuted. Prognosis depends

Lateral malleolar fragments are usually
on fracture configuration.

traumatic and are only rarely (1 %) OCD
lesions.

FRACTURE OF THE FIBULAR

TARSAL BONE (CALCANEUS)

OSTEITIS OF THE CALCANEUS

Fractures of the fibular tarsal bone are

Osteitis of the end of the tuber calcanei may
uncommon and usually the result of traunm.

be seen after traumatic injury and subse

Small chip fractures may be successfully
quent infection. This most often occurs after removed. Complete body and physeal a kick from another horse or when the horse fractures are difficult to repair, although kicks a fixed object, such as a wall. Osteitis
they have been repaired with bone plates
causes moderate to severe lameness,
and tension band wiring. Horses with open,
cellulitis, and tarsal tenosynovitis.

comminuted fractures have a grave

Concurrent sepsis of the calcaneal bursae,
prognosis and warrant humane euthanasia.

tarsocrural joint, or tarnal sheath may occur.

Diagnosis is confirmed by radiography;
however, radiologic signs of focal osteolysis

FRACTURE OF THE LATERAL
may take days or weeks to develop and,

MALLEOLUS OF THE TIBIA
therefore, sequential radiographs are

Lateral malleolar fractures are usually
recommended. Treatment illvolves
traumatic. Small, well-rounded fragments
debridement of any bony lesions, endoare occasionally seen; they are considered scopic lavage of infected synovial cavities,
likely to be a form of OCD and are usually
and wound debridement combined with
asymptomatic. Small or minimally displaced
appropriate local and systemic antimicrofractures may be managed conservatively.

bial therapy.

Surgical removal of fragments may result in
a quicker recovery. Some fragments may be

FRACTURES OF THE DISTAL
removed arthroscopically, although some

TARSAL BONES
require an open approach through the
lateral collateral ligament of the tarsocrural

Fractures of the central and third tarsal
joint. Larger fragments may be successfully
bones occur most c01runonly in Standardrepaired by lag screw fixation.

bred or Thoroughbred racehorses. Fractures usually cause acute-onset severe hindlin1b lameness. Lameness is exacer

TARSAL JOINT LUXATION
bated by hock flexion. Acute fractures may

Complete luxation or subluxation of the
be associated with heat, swelling, and pain
tarsocrural, tal ocal caneal-centroquartal,
on palpation over the distal tarsal bones;
and tarsometatarsal joint may occur with
there may be tarsocrural joint effusion.

or without concurrent tarsal bone fracture

Diagnosis is made by radiography, but
as the result of severe trauma. Horses may
fractures may not be visible until 7-14 days
be salvaged for breeding or retirement to

LAMENESS IN HORSES

1137
pasture by reducing the luxation under
flexor muscles appear rather flaccid, and
general anesthesia and applying a full limb
there is a characteristic dimple on the
cast for 6----8 wk followed by a further 4-8
caudodistal aspect of the soft tissues of the
wk of immobilization in a heavily padded
crus. At trot, an obvious la.ineness is usually
bandage. Restricted range of motion of the
evident, with delayed protraction of the

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hock and progressive osteoarthritis means
limb due to overextension of the hock.

these horses are unlikely to return to

Diagnosis is usually based on clinical
athletic use.

signs and can be confirmed with ultrasonography.

DESMITIS OF THE COLLATERAL

Conservative treatment with 3-4 mo of
stall rest followed by slow and careful

LIGAMENTS OF THE TARSUS
reintroduction to exercise usually results

Collateral ligan1ent irtjury is usually the
in complete resolution of signs and return
result of trauma or a fall. Lameness va.iies
to athletic soundness.

from mild to severe, depending on the severity of irtjury. Flexion of the hock is usually STRING HALT
resented and will exacerbate lan1eness.

Effusion of the tarsocruraljoint and

Stringhalt is a gait abnormality characterperiarticula.i· swelling are evident. Lameized by exaggerated upward flexion of the ness may be improved by intra-articular
hindlimb that occurs at every stride at walk.

analgesia of the tarsocrural joint. Diag

The gait abnormality usually lessens at trot
nosis is confirmed with ultrasonography.

and is not evident at canter. It may occur

Increased uptake of radionuclide at the
unilaterally or bilaterally. All degrees of
proximal and distal attachments of the
hyperflexion are seen, from mild, spasda.inaged ligan1ent may be evident on modic lifting and grounding of the foot, to
scintigraphy, and enthesiopathy may be
extreme cases in which the foot is drawn
apparent radiologically in horses with
sharply up until it touches the belly and is
chronic irtjury. Conservative treatment is
then struck violently on the ground. In
recommended, with physical and chemical
severe cases, there is atrophy of the lateral
anti-inflanunatory treatments in the acute
thigh muscles. In Australian stringhalt and
stages and then a period of stall rest
lathyrism, the condition may be progressive

( 4-6 mo) followed by a controlled
and the gait abnormality may become so
ascending exercise progran1. Prognosis
severe that eutlumasia is warranted. Mild
depends on the severity of irtjury.

stringhalt may be intennittent. The signs are
most obvious when the horse is sharply
turned or backed. In some cases, the

RUPTURE OF THE FIBULARIS
condition is seen only on the first few.steps

(PERONEUS) TERTIUS
after moving the horse. The signs are often
less intense or even absent during warmer

The fibularis (peroneus) tertius is a
weather. Although it is regarded as
tendinous structure that originates from the
unsoundness, stringhalt may not materially
extensor fossa of the femur and runs over
hinder the horse's ability to work, except in
the craniolateral aspect of the tibia to insert
severe cases when the constant concussion
on the dorsoproximal aspect of the third
gives rise to secondary complications.

metatarsal bone, the calcaneus, and the

However, the condition may make the horse
third and fourth tarsal bones. It is part of the unsuitable for some equestrian disciplines reciprocal apparatus of the hindlin1b, which

(eg, dressage).

means there is concurrent flexion and

The etiology is unknown, but lesions of a
extension of the hock and stifle. Rupture of
peripheral neuropathy have been identified
the fibularis tertius may occur as a result of
in the sciatic, peroneal, and tibial nerves.

hyperextension of the limb and usually

Severe fomlS of the condition have been
occurs in the middle of the crus, or
attributed to lathyrism (sweet pea
laceration may occur on the dorsal aspect
poisoning) in the USA and possibly to
of the tarsus. Avulsion of the origin on the
flat weed intoxication in Australia.

fibularis tertius is rare in mature horses but

Diagnosis is based on clinical signs but
may occur in young aninlals.

can be confinned by electromyography. If

Clinical signs are pathognomonic,
the diagnosis is in doubt, the horse should
because rupture of the fibula.tis te1tius
be observed as it is backed out of the stall
means horses a.i·e able Lo extend the hock
after hard work for 1-2 days. False stringhalt
while the stifle is flexed. Horses are able to
sometimes appears as a result of some
bear weight on the affected limb. At walk,
temporary irritation to the lower pastern
the gastrocnemius and superficial digital
area or even a painful lesion in the foot.

1138

LAMENESS IN HORSES

When intoxication is suspected, removal
hemorrhage in the tai·sal sheath. This may
to another paddock may be all that is
occur with or without concurrent dainage
required. Many of these cases apparently
to the lateral digital flexor tendon.

recover spontaneously. In chronic cases,

Intrathecal hemorrhage results in pain and

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tenectomy of the lateral extensor of the
in.flanm,ation. Chronic in.flanm1ation may
digit, including removal of a portion of the
lead to synovial hype1trophy, fibrosis, and
muscle, has given best results. Improveintrathecal adhesions between the lateral ment may not be evident until 2-3 wk after
digital flexor tendon and paiietal lining of
smgery, and not all cases respond. This is
the sheath. Primaiy sprain injuries of the
not surprising, because the condition is a
lateral digital flexor tendon may also occur.

distal axonopathy. Other methods of

Infectious tenosynovitis after a penetrating
treatment include large doses of thian'line
injury and resulting in synovial sepsis may
and phenytoin.

also occur.

Treatment of thoroughpin depends on

CURB
the underlying cause. Treatment of acute
tenosynovitis, in the absence of tendinous

Cmb is a term used to describe a number of
or bony pathology, involves rest, systemic
soft-tissue injmies that cause swelling on
or local anti-inflammatory drugs, and cold
the distal plantar aspect of the tarsus.

therapy. Intrathecal medication with

Traditionally, the term "curb" is used to
hyaluronai1 and/or c01ticosteroids may be
describe enlargement of the Oong) plantar
useful in more severe cases. Intratl1ecal
ligament on the plantar aspect of the
corticosteroids ai·e contraindicated if there
calcaneus, but curb-like swelling may also
is tendon pathology. Horses with tenosynobe caused by peritendinous-periligamenvitis associated with bony fragments, tous inflan1mation, superficial or deep
intrathecal ossicles, teaiing or fraying of the
digital flexor tendinitis, or a combination
lateral digital extensor tendon, or adhesions
of injuries. Curb is primaiily an injury of
are candidates for tenoscopic surgery.

racehorses, particularly Standardbreds,

Horses with infectious tenosynovitis require
and confonnational abnormalities may be
lavage of the tai,;al sheath (best perfo1med
predisposing. Lameness vai·ies from absent
tenoscopically), plus appropriate systemic
to severe, depending on the structure
and local antimicrobial therapy.

involved and the extent of the injury.

Diagnosis of the exact nature of the injury
is confumed by ultrasonography. In most

FALSE THOROUGHPIN
cases, treatment involves local anti-inflammatory therapy and NSAIDs in the acute False thorough pin is a tern, used to describe
phase and then rest and a controlled
a nun1ber of swellings that may develop in
exercise program thereafter.

the distal region of the crus or tai·sus and
cranial to the gastrocnemius tendon. These

DISORDERS OF THE TARSAL
may be seen unilaterally or bilaterally and
ai·e more conm1on on the lateral aspect of

SHEATH
the Ii.nib. These discrete swellings do not

(Thoroughpin)

extend distal to the hock and caimot be
balloted from lateral to medial. The

The tarsal sheath is the synovial sheath of
swellings vaiy in size and may be acute or
the lateral digital flexor tendon at the level
insidious in onset and inay or may not be
of the hock. Tenosynovitis of the tarsal
associated witl1 laineness.

sheath (colloquially called thoroughpin)

The causes of false thoroughpin vaiy and
is common and can be caused by a wide
are not well understood. False thoroughpins
rai1ge of lesions.

are usually solitaiy, fluid-filled sacs; tl1ey

Idiopathic thorough pin results in mild to
may be multiloculated witl1 a wall of
moderate effusion of the tarsal sheath and
variable thickness ai1d may have fibrous
is most conunonly seen in young horses.

bands traversing them. They may develop

Effusion may arise from acute inflanm1ation
secondaiy to local hemorrhage or due to
in nearby tissues or edema in the distal limb
herniation of tl1e tarsal sheath, gastrocne

(sympathetic effusion). It is not usually
mius, or calcaneal bursae.

associated with lai11eness and tends to

Ultrasonography is useful to assess the
resolve spontaneously, although it may be
extent and nature of these swellings.

recurrent or persistent.

Positive-contrast radiography can be used

Thoroughpin may occur as a result of
to detennine whetl1er the swellings are
direct trauma ( eg, kick or hitting a fence),
discrete or conununicate witl1 other
leading to acute in.flaimnation and
structures.

LAMENESS IN HORSES

1139

In many horses, the lesions are not assoof the medial wall of the bursa creating ciated with lameness, so no treatment is
or establishing communication with an
required and the horses may stay in work.

acquired subcutaneous bursa. Treatment

In some animals, low-grade lameness may
is by radical resection of the disrupted
occm. Intrathecal medication with
fibrocartilage and division of remaining

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corticosteroids may improve lan1eness
attachments of the fibrocartilage or
in some horses, although swelling and
retinacular insertions with the unstable
lameness will often recur; in these cases,
main body of the superficial digital flexor
surgical excision may be cmative.

tendon, thereby creating a stable lateral
subluxation. Altl10ugh ·repair or reconstruction tecluuques have been reported, results LUXATION OF THE SUPERFICIAL
have been unreliable. Permanent stable

DIGITAL FLEXOR TENDON FROM
subluxation elinunates anxiety and usually

THE TUBER CALCANEI
results in a "sotmd" functional horse.

Luxation or subluxation of the superficial

GASTROCNEMIU S TENDINITIS
digital flex or tendon from the point of the
hock may occm after disruption to the

Tend.i.J.1itis of the gastrocnemius tendon is a
retinaculum that attaches the tendon to the
rare cause of hindlimb lameness in a horse.

calcaneus. Luxation or subluxation more

Iajury usually occms distally, although
commonly occms laterally but may occm
rarely at the musculotendinousjunction.

medially. Rarely, the superficial digital

Lan1eness may be sudden or gradual in
flexor tendon may split sagitally, and part
onset, and the severity of lan1eness varies
of the tendon luxates medially and part
depending on tl1e severity of injury.

laterally.

Distention of the calcaneal ( or intertendi

Lan1eness is usually acute and severe in
nous) and gastrocnemius bursa is common.

onset and associated with marked swelling

Lameness is usually exacerbated by a
over the point of the hock. Horses may
proximal limb flexion test.

become panic-stricken in the acute stages

Lameness is usually improved by periif the tendon is moving on and off the os nemal analgesia of the tibial nerve, and
calcis, and they may kick out frequently
diagnosis is confirmed with ultrasonograwith the affected limb. In some horses, the phy.

tendon will resume its normal position

Conservative treatment with stall rest and
when the horse is standing but luxate or
controlled exercise for 6-12 mo is usually
subluxate as the horse moves; in other
indicated. Horses with mild to moderate
horses, the tendon remains pem1anently
lesions have a reasonable prognosis for
displaced. Diagnosis is based on careful
return to athletic work, but the prognosis
observation and palpation and can be
for horses with more severe lesions is
confirmed by ultrasonography.

guarded.

In the acute stages, sedation and
analgesia are important. If the tendon

CALCANEAL BURSITIS
remains pennanently displaced laterally ( or
medially), treatment involves prolonged

The calcaneal (intertenclinous bursa) lies
stall rest ( 4-6 mo), possibly with the limb
between the tendons of the gastrocnenuus
immobilized in a heavily padded full limb
and superficial digital flexor muscles
bandage or cast. Lan1eness usually
proxin1al to the hock and extends on the
in1proves, but the horse may be left with
plantar aspect of the calcaneus to the level
a mechanical lameness causing a jerky
of the distal tarsus. In most horses, there is a
hincllimb action that may linut its use as a
communication between the calcaneal and
dressage horse, although horses may be
gastrocnenuus bursa and, in approximately
able to jump or race. Horses with a
a third of horses, with the subcutaneous
persistently medially displaced tendon
bursa.

usually have a greater degree of mechanical

Inflanunation and distention of the
lameness and a poorer prognosis for return
bursa may or may not be associated with
to athletic function.

lameness. It may be idiopatluc, secondary

In horses in which the tendon is unstable
to trauma or intrathecal hemorrhage, or
and subluxates on and offtl1e tuber
occur in association with gastrocnemius
calcanei, endoscopy of the calcaneal bmsa
tendinitis. Septic bursitis may occur
reveals disruption of both the medial
secondary to infectious osteitis of the
retinacular/calcaneal insertion of the
calcaneus or after a penetrating injury.

superficial digital flexor tendon and its

Horses with septic bursitis need to be
associated fibrocartilage, with disruption
treated aggressively with surgical debride-

1140

LAMENESS IN HORSES
ment and lavage and appropriate antimicro

SUBCHONDRAL CYSTIC LESIONS
bial therapy. Horses with aseptic bursitis may
be treated with rest, drainage, and intrathecal Subchondral cystic lesions most commonly medication with corticosteroids; results are
occur in the stifle in the medial femoral
variable.

condyle. Osseous cyst-like lesions may also

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occur in the proxin1al tibia. The pathogen

CAPPED HOCK
esis of these cysts is poorly understood,
but they may develop after trauma to the

Capped hock is due to distention of the
articular sUiface or as a result of osteochonsubcutaneous bursa or development of an drosis. Lesions often present in young
acquired bursa over the tuber calcanei. This
horses but can be seen at any age. The
usually results from repetitive trauma ( eg,
seve1ity of lameness varies from mild to
kicking or leaning on stable walls) and is
severe and may be acute in onset. Lameness
not usually associated with lan1eness.

may be intemlittent, particularly in older

Occasionally, a subcutaneous abscess may
horses. In some horses there is nlild
arise as the result of a penetrating injury
effusion of the medial femorotibial joint,
and lead to painful swelling and lan1eness.

but in many horses no localizing signs are

Treatment of an abscess requires surgical
evident. Intra-articular anesthesia of tl1e
excision and appropriate antinlicrobial
femorotibial joints may produce paitial
treatment.

improvement.

Diagnosis is usually confirmed by
radiography. Medial femoral subchondral
cystic lesions are most evident on caudocrailial projections and may appear as a OSTEOCHONDROSIS
variably sized round or oval radio lucent
defect in the subchondral bone. Some

Osteochondrosis (seep 1148) is a common
lesions are surrounded by an obvious
cause of stifle lameness in young horses.

sclerotic rim. In some horses, only a very

Lesions in the stifle most commonly occur
small defect is evident radiographically in
on the lateral trochlear ridge of the femur
tl1e medial femoral condyle; tllis may be a
but may also occur on the medial trochlear
precursor to subchondral cystic lesions.

ridge, in the intertrochlear groove, or on

Defects in the sUiface of the medial femoral
the patella. Lesions are often bilateral and
condyle may be evident ultrasonographiprobably develop in the first 6 mo of life.

cally in some horses. Subchondral cystic

In severe cases, joint effusion and
lesions in the proximal tibia are usually
lameness may be evident in foals or
smaller and most evident on lateral, lateral
yearlings. In less sev!=re cases, clinical
oblique, or caudocrailial radiographic
signs may not become evident until the
projections.

horse starts athletic work. In mild cases,

Nonarticular osseous cyst-like lesions or
clinical signs may be absent. The severity
small lesions may respond to conservative
of lameness varies from absent to severe
treatment, including rest, systenlic NSAIDs,
and is often acute in onset."Effusion of the
and intra-articular corticosteroids. If horses
femoropatellar joint is common. Diagnosis
do not respond to conservative treatment,
may be confirmed by demonstration of
surgery is indicated. Some surgeons advise
radiographic or ultrasonographic changes
injection of corticostero.ids into the lining of
or by arthroscopy.

the cyst under arthroscopic or ultrasono

Mild lesions in foals have been shown
graphic guidance to decrease the shedding
to heal with conservative treatment.

of inflammatory enzymes and mediators

More severe lesions in foals may require
into the joint; others advise arthroscopic
arthroscopic debridement, but care should
debridement of the cyst to remove the
be taken not to remove too much of the
contents and lining.

subchondral bone. In horses with larger

The prognosis for return to athletic
defects or fragmentation, arthroscopic
function in horses with subchondral
surgery is the treatment of choice to remove
cyst-like lesions of the medial femoral
osteochondral fragments and poorly
condyle after injection of the lining of tl1e
attached or loose cartilage and to debride
cyst under arthroscopic guidance has been
abnom1al subchondral bone.

reported to be fair, with 64% returning to

In adult horses, the prognosis after
athletic use in one study irrespective of the
surgery for return to athletic soundness is
age of the horse. The prognosis for return to
fair to good but depends on the severity of
athletic function after debridement of the
the lesions and the size of the defect in the
cyst seems to vary with the horse's age. The
subchondral bone.

prognosis for athletic soundness in horses

LAMENESSINHORSES

1141

<3 yr old was better ( -64%) than in horses
femorotibialjoints are sometimes present.

>3 yr old (35%) at the time of surgery in one

Lameness is usually improved by intralarge, multicenter retrospective study.

articular anesthesia of the femorotibial
joints. In some horses, radiographic

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MENISCUS AND MENISCAL
changes may be evident at the sites of

LIGAMENT INJURIES
attachment of the ligament with enthesiophyte formation or focal areas of radiolu

Injuries to the menisci and the meniscal
cency. Ultrasonography of the cruciate
ligaments are a conunon cause of stifle
ligaments is difficult but may demonstrate
lameness in adult horses. Lesions range
some lesions. However; in many horses,
from mild fibrillation of the meniscal
diagnosis is confirmed only by arthroscopic
ligaments and surface of the menisci,
examination.

causing low-grade, chronic lameness, to

Conservative treatment involving rest,
severe tears of the meniscal ligament and
systemic NSAIDs, and intra-articular
menisci, causing acute and severe lameness. corticosteroids is indicated in horses with The medial meniscus is more commonly
acute injuries. If horses do not respond to
affected.

conservative treatment, arthroscopic

Effusion of the femorotibialjoints is a
surgery is reconunended to debride loose
common, associated clinical sign. In most
and tom ligament fibers.

horses, lameness is significantly improved

The prognosis for return to athletic
by intra-articular anesthesia of the
function depends on the severity of injury.

femorotibial joints. Subtle radiographic

Horses with complete rupture have a grave
changes may be evident with enthesioprognosis. Horses with moderate to severe phytes or lytic areas at the site of attachinjuries have a poor prognosis for return to ment of the meniscal ligan1ent or dystrophic athletic function, whereas horses with mild mineralization within the meniscus.

injuries have a fair prognosis.

Osteoarthritic changes may be evident in
horses with chronic or severe injuries.

COLLATERAL LIGAMENT

Ultrasonographic examination may be
useful to demonstrate meniscal injury.

INJURIES

Arthroscopic examination is indicated in

Rupture or sprain of the medial or lateral
horses that do not respond to conservative
collateral ligaments of the stifle is usually
treatment (ie, rest and anti-inflanunatory
the result of an acute traumatic episode in
medication followed by controlled
which the distal limb is forced medially or
rehabilitation). Arthroscopy allows
laterally, thereby stressing the ligan1ents.

assessment of the extent and severity of

Rupture or sprain is more conunon in the
injury, although only the cranial and caudal
medial collateral ligament than in llie lateral
poles of the menisci are visible arthroscopicollateral ligament. Concunent injury of the cally. Arthroscopy also allows tom or
menisci or cruciate ligaments is common,
fibrillated fibers of the meniscal ligaments
particularly in severe injuries. Lameness
to be debrided and flaps of meniscus or
depends on the severity of the injury but
fibrillated meniscal tissue to be removed.

is usually quite severe initially. Localized

The prognosis for return to athletic
edema and joint effusion is seen, particufunction depends on the severity of injury.

larly in the acute stages. Flexion tests of the

Overall, -50% of horses with meniscal and
stifle usually exacerbate lameness. Clinical
meniscal ligament injury return to athletic
signs usually improve within a few days
use. However, in horses with severe tears
unless there is significant joint instability.

that extend beneath the femoral condyle

Intra-articular anesthesia of the ipsiaxial
and horses with concurrent osteoarthritis,
femorotibialjoint will not always alleviate
the prognosis is considerably poorer.

lameness. If the ligament rupture is
complete, stressed caudocranial radio

CRANIAL AND CAUDAL
graphs of the stifle may demonstrate joint

CRUCIATE LIGAMENT INJURIES
widening on the affected side. Enthesiophyte forn1ation at the origin or insertion of Complete rupture of a cruciate ligan1ent is
the ligament may be evident radiographiusually a catastrophic injury resulting in cally in chronic cases. Diagnosis is usually
severe lameness and joint instability. Strains confirmed by ultrasonographic examinaand partial rupture of the cranial and caudal tion.

cruciate ligaments may result in variable

Horses with mild sprains may be treated
lameness, depending on the severity of
conservatively with stable rest and
injury. Effusions of the femoropatellar or
anti-inflanunatory medication for� wk,

1142

LAMENESS IN HORSES
followed by a controlled, ascending
anthelmintic administration. Stable rest is
exercise rehabilitation program for a further contraindicated, and the horse should be 6---8 wk. Horses with mild sprains and no
turned out to pasture as much as possible.

joint instability have a fair prognosis for

Remedial foot trimming to ensure the foot

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return to athletic use. The prognosis for
is well balanced and shoeing with a bevelhorses with severe ir\jury is poor.

edged shoe with or without a lateral heel
wedge may be beneficial. A significant

INTERMITTENT UPWARD
proportion of horses will in1prove with

FIXATION OF THE PATELLA AND
maturity and conservative treatment,

DELAYED PATELLA RELEASE
although signs may recur if the horse
undergoes prolonged stall rest.

lntermjttent upward fixation of the patella

Medial patellar ligan1ent desmotomy is
occurs when the medjal patellar ligament
indicated in horses U1at do not respond to
remains hooked over the medial trochlear
conservative treatment or in horses with
ridge of the femur and locks the reciprocal
lan1eness caused by upward fixation of the
apparatus with the limb in extension. A
patella. Medial patellar ligainent desmothorse with upward fixation of the patella omy is most often perforn1ed in the sedated
stands with the hindlimb fixed in extension
horse w1der local anesthesia, although
with the fetlock flexed. The leg will usually
some surgeons prefer general anesthesia.

release with a sudden snap or jerking

After surgery, the horse should be restricted
movement.

to stable or small stall rest for 2 mo to

Some horses demonstrate a milder form
reduce the risk of complications. Fragmenof this condition. In these horses, there is tation of the apex of the patella is tl1e most
delayed release of the patella during limb
common complication after surgery ( see
protraction, most commonly evident as the
below); if it results in lameness, it may be
horse moves off or in downward transitions.

treated arthroscopically with good results.

Thls appears as a jerky movement of the

Other complications include lameness,
patella. Horses with recurrent upward
local swelling, or even patella fracture. The
fixation or delayed release of the patella may
prognosis after medial patellar ligament
develop chronk, low-grade lameness due to
desmotomy is generally considered to be
stifle soreness and may be reluctant to work
good, with recun·ence of the condition rare.

on soft, deep surfaces or up or down hllls.

Medial patella ligament splitting, whlch

Upward fixation or delayed release of the
involves making numerous small incisions
patella is most commonly seen in young
in the ligan1ent, has also been used
horses and porues, particularly if they are in
successfully to manage these horses.

poor body condition and poorly muscled.

Straight hlndlimb confohnation may

FRAGMENTATION OF THE
predispose to thls condition. It may also be

PATELLA
seen in older horses that have had trauma to
the stifle region, paiticularly if the horses

Fragmentation of the apex of the patella
are stabled or have been inactive.

usually occurs secondary to meclial patellai·

Diagnosis is based on recogrution of
desmotomy for management of upward
typical clirucal signs. In some horses,
fixation of the patella. Lesions ai·e believed
upwai·d fixation of the patella may be
to develop due to patellar instability as a
induced by pushlng the horse backwai·d or
result of the surgery. The seve1ity of lainemanually pushlng the patella proxin1ally.

ness varies from mild stiffness to moderate

Radiographs of the stifle should be taken in
laineness. A proxin1al limb flex.ion test
horses with femoropatellar joint effusion
usually exacerbates lameness, and
and laineness to establish concurrent or
femoropatellar joint effusion is usually
secondary pathology.

present. Lameness is localized by diagnostic

To release an upward fixated patella, the
anestl1esia of the femoropatellar joint, and
horse should be pushed backward while
diagnosis is confirmed by radiography.

simultaneously pushlng the patella medially

Arthroscopic debridement of the apex of
and distally. Alternatively, pulling the limb
the patella witl1 removal of tl1e osteochonforward with a rope ai·ound the pastern may dral fragments is the treatment of choice.

unlock tl1e patella If upward fixation of the

Prognosis is reasonable but depends on tl1e
patella is intermittent and not causing
severity of the condition.

lameness, a conditioning program should be
instituted. This involves daily lungeing or

PATELLAR LUXATION
riding of the horse, appropriate to its age
and type, as well as ensuring an adequate

Lateral luxation of the patella is a rai·e,
plane of nutrition, good dentistry, and
inherited condition in foals caused by a

LAMENESS IN HORSES

1143
recessive gene. Luxation of the patella in
causes of stifle lameness described and
adult horses is unusual and likely to be
usually results in persistent lameness of
traumatic in origin. Lateral luxation is more
varying severity. Diagnosis is confirmed
conunon than medial luxation and may be
with intra-articular anesthesia and
more likely in horses or foals with
radiography. Radiographic changes include

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hypoplasia of the lateral trochlear ridge of
periaiticular remodeling with osteophyte
the femur. The condition may be unilateral
fonnation and remodeling of the joint
or bilateral and varies in severity from
margins (paiticularly the medial tibial
intermittent luxation that readily reduces to
plateau), changes in the subchondral bone,
persistent luxation that cannot be reduced.

narrowing of the joint space; and dystrophic

Severely affected foals are unable to
mineralization of the soft tissues. The
extend the stifle and so adopt a characterisprognosis for athletic soundness in horses tic crouching position. If the condition is
with osteoarthritis of the stifle is poor, and
less severe, foals or horses may be reluctant
treatment is usually palliative. Newer
to flex the stifle and thus demonstrate a stiff
techniques for arthroscopy and regenerahindlimb gait. Diagnosis can be confirmed tive therapy may offer some hope for
by radiography.

severely affected joints.

Although a nun1ber of surgical treabnents
have been reported, the prognosis in adult
horses and in horses with concurrent

CHONDROMALACIA OF THE
osteoarthritis is poor. The prognosis for

FEMORAL CONDYLES
athletic function in foals may be slightly

Chondromalacia of the femoral condyles
better.

is being increasingly recognized in sports
horses. Horses typically present with poor

PATELLAR LIGAMENT INJURIES
perfonnance or low grade, often bilateral,
hindlirnb lan1eness with pain referable to the

Patellar ligament ir\juries are rare but may
stifle. Lameness or loss of perfom1ance
be seen in jumping horses. The middle patelusually becomes evident in younger horses lar ligament is tl1e most commonly affected.

as their work intensity increases. Frequently,

Lameness is variable but may be severe in
there are no localizing signs, although mild
acute cases. Clinical signs are often subtle;
effusion of the medial femorotibial and/or
femoropatellar joint effusion, periligamenfemoropatellar joints may be evident.

tous thickening, and edema are inconsistent

Typically there ai·e no radiologic or
findings. In many horses, lameness is
ultrasonographic signs evident. Arthroscopic
unchanged by intra-articular anesthesia
examination of the femorotibial joints reveals
of the femoropatellar joint; therefore,
abnom1ally soft, irregulai·, cracked, pitted,
diagnosis is confirmed by ultrasonography.

and poorly attached articulai· caitilage over

Treatment is prolonged rest (up to 6 mo).

all or part of the femoral condyles. Generally,

Lameness is often slow to resolve and may
tile prognosis for sustained return to athletic
recur.

soundness is guarded. More studies are
required to detemline tl1e best fonn of

GONITIS AND OSTEOARTHRITIS
surgical intervention in management of
tllese horses.

Mild to moderate inflanunation of the
femorotibial and femoropatellar joints of
unknown origin is common. Severity of

FRACTURES
lameness varies. Synovitis and capsulitis
may result from athletic sprain of the joints.

Fractures of the Patella

Mild trawna to tl1e articular cartilage,

Fractures of the patella usually result from
menisci, or any of the ligaments of the stifle
direct trawna, most commonly when a
may produce mild to moderate synovitis.

horse is kicked by anotller horse or hits

Mild synovitis usually responds to rest and
a fixed obstacle while jumping. Prognosis
intra-articular and systemic anti-inflanunadepends on fracture confom1ation. Sagittal tory drngs. If joint inflanunation and
fractures of tile medial pole of tile patella
lameness persist, further diagnostic
are most common. These fractures are
investigation and arthroscopic examination
usually intra-articular and involve tile
are advisable to assess concurrent or
attachment of tile parapatellar fibrocarticausative ir\juries and to prevent ongoing lage of tile medial patellar ligament.

degenerative joint disease and development

Complete horizontal fractures ai·e rare but
of osteoarthritis.

considered serious ir\juries because of

Osteoarthritis of the femorotibial or
fragment distraction due to the massive pull
femoropatellar joints may follow any of the
of tile extensor muscles. Complete sagittal

1144

LAMENESS IN HORSES
fractures may be more amenable to internal
are catastrophic and have a grave prognofixation, because there is less distractive sis. However, traumatic fragmentation of
force.

the femoral condyles or trochlear ridges can

Fracture of the patella usually results
also occur. Such injuries usually result in
in marked lameness initially, with swelling
acute onset, moderate to severe lameness

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and edema over the patella and effusion
with joint effusion. Diagnosis is confmned
of the femoropatellar joint. In less severe
by radiography. Treatment involves surgical
or nonarticular fractures, lameness may
removal of the fracture fragments to
improve within a few days. Diagnosis is
prevent development of osteoarthritis. This
con.fumed by radiography. Standard
is usually achieved arthroscopically but
radiographic projections of the stifle,
may require arthrotomy. The prognosis is
together with a cranioproximal-craniodistal
usually considered to be good after surgery,
oblique projection of the patella, are used to
so long as there is no significant concurrent
determine fracture configuration.

soft-tissue damage.

Management options depend on fracture
configuration. Horses with small, nondisplaced, nonarticular fractures may be treated conservatively with stable rest for

Disorders of the coxofemoraljoint are

6--8 wk and have a good prognosis for return relatively rare causes of lameness in horses.

to athletic function. Articular fractures of

Most cases are traw11atic in origin, secondary
the medial pole of the patella can be
to falls or being cast ( within a stall) in
removed arthroscopically or via an
recwnbency, although septic arthropathies
arthrotomy and are also considered to have
a good prognosis. Larger, mid-body sagittal
and developmental disorders of the joint
have been occasionally reported. Regardless
or horizontal fractures require repair by
of the etiology of the primary disease,
internal fixation. These injuries carry a
secondary osteoarthritis of the coxofemoral
risk of catastrophic breakdown during
joint is a common sequela, which will
anesthetic recovery but can have a favorafrequently result in permanent lan1eness.

ble outcome.

Lameness is the predominant presenting
clinical sign of any coxofemoral disease.

Fractures of the Tibial Tuberosity

Although the lameness can be subtle, more

Fractures of the tibial tuberosity are not
frequently a moderate to severe lameness
uncommon. There is little soft tissue

(non-weight-bearing) is seen at presentacovering this area, and fractures usually tion. In severe cases, the horse will often
result from direct trauma. Fracture
stand with the limb partially flexed. With
configuration may range from small
any degree of chronicity, atrophy of the
fragments off the cranial proximal part of
muscles of the hindquarters, such as the
the tuberosity to large fractures of the
gluteals and quadriceps, is often moderate
whole of the tuberosity extending into the
to marked. In cases of coxofemoral subluxafemorotibialjoints. Fracture of the tibial tion, the leg will be held in a semi-flexed
tuberosity usually results in marked
position with an obvious outward rotation
lameness initially with localized swelling
of the stifle and toe and an inward rotation
and edema. Lameness will often improve
of the point of the hock. In complete
within a few days. Diagnosis is confmned
coxofemoral luxations, the same rotational
by radiography.

abnormality in limb position is observed,

Small and nondisplaced fractures may
and additionally the leg will appear shorter,
heal with conservative treatment. Stable
which is best identified by the point of the
rest for 6--8 wk is advised. Dming the first
hock being displaced proximal to that of

2-3 wk, the horse should be prevented from
the contralateral limb. Most horses with
lying down by tying or the use of slings to
coxofemoral pathology show some pain on
prevent fragment displacement. Larger
proximal limb flexion or abduction. Rectal
intra-articular fractures should be repaired
examination is generally unrewarding,
by internal fixation. Fractures generally
although in some cases of acute fracture,
have a good prognosis for return to athletic
a hematoma or alteration in the bony
function if appropriately managed.

architecture is palpable per rectum.

Intra-articular local anesthesia of the

Fractures of the Femoral Condyles
coxofemoraljoint is frequently used to
and Femoral Trochlear Ridges
identify the joint as the cause of lameness,
particularly in cases of chronic lameness.

Fracture of the femoral condyles is usually

Although this technique can be technically
the result of direct trauma. Large, intrachallenging, ultrasonography can help guide articular, displaced fractures in adult horses
needle placement.

LAMENESS IN HORSES

1145

Definitive diagnosis of coxofemoral
reduction has aliowed animals to become
pathology usually requires some form of
comfortable pasture aninlals.

diagnostic imaging. Bone scanning

(nuclear scintigraphy) is commonly used

PELVIC FRACTURE
to identify the coxofemoral joint as the

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site of pathology. This technique is highly

Pelvic fractures are relatively common
sensitive for identification of the involvein horses and ponies and can occur as ment of the joint but has a low specificity
a consequence of trauma or stress from
for identification of the pathology within
athletic training. Fractures involving tl1e
the joint. Percutaneous ultrasonography
acetabulum almost always occur as a
can provide considerable information on
consequence of traun1a and usualiy present
the coxofemoraljoint, although its use
as a severe lan1eness, which is frequently
at this site is technically challenging.

non-weight-bearing at tl1e time of injury.

Radiography can be very rewarding,

Crepitus may be difficult to appreciate, even
especially in smaller horses and ponies,
dming passive flexion of the limb or rectal
although optimal views require general
examination. Radiography can be diagnosanesthesia. Because of the risk of using tic, but the difficulties of obtaining such
general anesthesia in horses with serious
inlages means that diagnosis is usualiy
limb injuries, such imaging is only rarely
achieved by a combination of nuclear
performed. A number of techniques are
scintigraphy and ultrasonography. In
available to radiograph the coxofemoral
particular, ultrasound diagnosis of pelvic
joint in the standing horse, using either a
fractures has advanced considerably and is
ventrodorsal or lateral oblique views.

now considered tl1e first-line method to

Arthroscopy of the coxofemoraljoint
assess pelvic fractures. Fractures of the
is possible, although it is technically
acetabulum, in contrast to other types of
challenging in most adult horses and
pelvic fractures, carry a poor prognosis for
ponies; acceptable joint visualization can
return to athletic function, because such
be obtained by most operators in foals.

fractures are frequently displaced and
invariably lead to osteoartluitis. The only

LUXATION OF THE
treatment is usually prolonged (6-9 mo) rest

COXOFEMORAL JOINT
followed by symptomatic therapy for any
resultant osteoartluitis.

Luxation of the coxofemoraljoint is
relatively rare in horses because of the

OSTEOARTHRITIS AND OTHER
strong ligamentous support provided to

COXOFEMORAL JOINT
the joint by the round ligament and the

DISEASES
accessory femoral ligament, as well as the
fibrocartilaginous lip that surrounds the

Osteoartluitis (OA) of the coxofemoraljoint
acetabulum. In horses, this injury is usually
is usualiy secondary to major traun1a such
secondary to trauma. Luxations are much
as luxation or fracture of the joint.

more common in smalI ponies, such as

Occasionally, idiopathic OA is diagnosed

Shetland ponies, in which luxation of the
as a cause of chronic lan1eness. Cases of
coxofemoraljoint has been frequently
osteochondrosis or bone cyst fonnation
described secondary to upward fixation of
within the coxofemoraljoint have been
the patella. Fracture of the dorsal acetabureported, which can lead to secondary OA.

lar rim may accompany the dislocation.

Septic aithritis of the coxofemoral joint is

Luxations are usually accompanied by a
seen occasionaliy in foals as a consequence
characteristic alteration in limb appearance. of hematogenous spread or idiopathicaliy in Luxations of tl1e coxofemoral joint arc best
adult aninlals.

managed by closed reduction under general

In cases of established OA, treatment
anesthesia, although this is likely to be
is usualiy symptomatic, using NSAIDs,
successful only if the reduction is perintra-aiticular corticosteroids, or other fom1ed soon after the injury. It can be
symptomatic treatments. In cases of septic
difficult to maintain the reduction in place
artluitis, treatment should consist of
through recovery from general anesthesia,
surgical debridement and lavage in
and although the use of surgical techniques
conjunction with local and systemic
or Ehmer slings has been advocated, no
antimicrobial therapy. In cases of OA, full
single technique has been shown to be
recovery is unusual. Successful treatment
successful. The prognosis for return to
of septic aithritis is possible in foals but
athletic function after coxofemoral luxation
unlikely in adult horses unless diagnosed
is very guarded. In small ponies, closed
quickly and treated aggressively.

1146

LAMENESS IN HORSES

Standardbreds, but when present, their
likelihood of causing pain seems higher.

Intenned.iate frequency and signs are seen

Back problems are a major cause of poor
in sport horses. Kissing spines can be found

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performance and gait abnormalities in sport
in perfonnance race and sport horses
and race horses. Although it is often
without back pain and even with normal
possible with the history and clinical
thoracolun1bar active and passive

(physical and dynamic) exantination to
mobilization. Thus, in each case, the clinical
suspect functional abnormalities of the
significance of these lesions must be
vertebral colwnn, definitive diagnosis of
carefully assessed. Diagnosis can be aided
the cause of the pain is a challenge. There
by injection of local anesthetic into the
is undoubtedly a complex relationship
affected interspinous spaces. Medical
between subtle ( usually bilateral) hindlirnb
management includes local injections of
lameness, back pain, and poor performance. steroids and/or shockwave therapy, as well It can be challenging practically to
as rehabilitation using tolerated exercises
differentiate and definitively deterntine the
after progressive wann-up at a slow canter.

relative importance of differing orthopedic

Surgical treatment has been advocated for
pathologies in such cases.

this condition, with surgical resection of the

Once back pain is suspected or estabaffected spinous processes being most lished in a horse, identification of the cause
commonly performed and being described
requires imaging procedures. This discipline as efficacious in managing this condition. A has seen major advances, particularly
nwnber of differing techniques have been
relating to integrating radiographic,
described for this surgical management.

ultrasonographic, and nuclear scintigraphic
findings. In addition, there is greater

Fractures
understanding of the relationships between
identification of specific in1aging findings

Multiple fractures of the spinous processes
and the possibly of such findings leading to
of T4--Tl0 are sometimes seen in horses that
pain.

have reared and fallen over backward. The
sun1mits and centers of ossification are

SPINAL PROCESSES AND
fractured and displaced laterally. After the
initial pain and local reaction have subsided,

ASSOCIATED LIGAMENTS
recovery is often satisfactory, with usually
no pern1anent effect on performance,
although a persistent deformation of tl1e

Kissing Spines
withers may require some adaptation of

The most common location of kissing
the saddle.

spines is the vertebral segment between TlO
and TlS, although these lesions are also

Desmopathies
identified between 11 and 16. Abnormal
findings can be seen in the dorsal part of the

(Supraspinal ligament injuries)

spinous processes where their identifica

Acute or subacute desmopathies can be
tion is easy; they include kissing and
identified ultrasonographically, because
overriding lesions. Different grades can
they demonstrate dorsoventral or transbe identified (grade 1: narrowing of the verse thickening of the ligan1ent, altered
interspinal space; grade 2: densification of
echogenicity, and obvious alteration of the
the margins; grade 3: bone lysis adjacent to
linear longitudinal pattern. They can be seen
the margins; grade 4: severe remodeling).

both in the median plane or asynm1etrically.

Abnormal findings can also be seen in the

In old or chronic injuries, the ligament often
ventral part of the spinous processes and
remains thicker, with a reduced echogenicmay involve the interspinal ligan1ents or ity and an irregular architectural pattern.

be associated with osteoartl1rosis of the

Hyperechogenic images with or without
articular processes. Their severity can be
acoustic shadows are compatible with
established using the san1e grading system;
mineralization or calcification of the
their clinical incidence seems higher.

supraspinous ligament. Alteration of the

The incidence of kissing spines seems to
bone surface of the top of the spinous
vary according to the discipline/use of the
processes indicates insertional desmopathy
horse and biomechanical effects of specific

( enthesopathy) of the supraspinous
gaits and exercises on the back. In general,
ligan1ent. The significance of findings can
these lesions are commonly found in racing
be difficult to definitively prove, because

Thoroughbreds and seem to be tolerated in
ultrasonographic abnormalities can be
many of them. They are quite rare in
seen in healthy as well as injured horses.

LAMENESS IN HORSES

1147

ARTICULAR PROCESS-SYNOVIAL
horses. This most commonly involves the

INTERVERTEBRAL ARTICULATION longissimus dorsi muscle, which acts to COMPLEXES
extend and laterally flex the vertebral
colwnn. All or part or the longissinrns

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The articular process-synovial inteivertebral
muscles usually arc strained dtuing ridden
articulation complex is located dorsally to
exercise, and clinical signs ru·e associated
the vertebral canal. It is composed of the
with altered performance and a.cute or
caudal articular process of one vertebra,
chronic back pa.in. The principal sites of
the synovial joint ( with articular cartilage,
datna.ge are the caudal withers at1d cranial
synovial fluid and membrane, and articular
lumbru· regions (just in front of and behind
capsule) located at the base of the interspinal the saddle area). Most of these inj w'ies space, and the cranial atticular process of the respond to rest and physiotl1erapy, although following vertebra. It is also known as the
several weeks may be needed for full
dorsal articular facetjoint. Osteoartluitis of
recovery. Abnom1alities of the thoracolumthis joint has been described radiographibar musculature are also frequently seen in cally, with a nwnber of different types
exertional rhabdomyolysis (tying-up
described, with sclerosis, periarticular
syndrome, seep 1178).

new bone, and narrowing of joint space
frequently being identified. Commonly two

LUMBOSACRAL JUNCTION
to five joints are affected, usually in the

ABNORMALITIES
caudal thoracic and cranial lumbar region. In
some cases, there will be abnormal nuclear

Abnormal findings of tl1e lumbosacral
scintigraphic uptake of the region, which can junction causing back pain are often aid with diagnosis. Further ultrasonographic
detected with ultrasonogra.phy and include
abnormalities can be identified, patticularly

1) congenital abnormalities such as
relating to pe1iarticulru· osteophytes and
lwnbosa.cral ankylosis (sa.cralization ofL6)

proliferation. Treatment and management
or inteivertebral ankylosis between L5 and
include periarticular ultrasonographic

L6; 2) disc degenerative lesions, especially
guided ir\jections of steroids, use of NSAIDs,
affecting the lw11bosacral disc (lesions
and rehabilitation using exercise protocols
include fissura.tion or cavitation of tl1e disc,
after progressive wann-up at a slow canter.

dystrophic mineralization, and ventral
herniation); 3) inteivertebral malalignment

VERTEBRAL BODIES AND DISCS

(spondylolisthesis) of tl1e lwnbosa.cral
joint or t11ejoint between L5 and L6; and

The most common lesion of vertebral bodies

4) intertransverse lwnbosacral osteoarthroand discs is ventral, ventrolateral, or lateral sis (periarticulru· osteophytes or remodeling
bony proliferation ( often called vertebral
at tl1e joint margins).

spondylosis); it is mainly found in the midthoracic area ( mostly between T l 1 and T l3) SACROILIAC JOINT
but can also be seen in the lumbar area They
can be found on asymptomatic horses but can ABNORMALITIES
also be responsible for acute pain or chronic

Acute and severe strain of tl1e sacroiliac
back stiffness. Spondylosis is a rare cause of
ligrunents is associated with a history of
back pain; in one smvey, only 3.4% of670
injury at1d severe pain in the pelvic or
horses with back pain demonstrated this
sacroiliac region, often with marked
abnom1ality. Congenital abnonnalities with
hindlimb lameness. Suba.cute or chronic
vertebral body deformation (triangular or
sacroiliac strain and osteoarthrosis of the
trapezoidal shape) are rru·e and usually found
sacroiliac joint cause typical back soreness.

in the thoracic vertebrae. Vertebral body

There is often a history of poor perforosteomyelitis, leading to neurologic signs, can mance, wiili an intemlittent, often shifting, be seen in the thoracolwnbar spine in foals.

hindlimb lan1eness. This may be associated

Vertebral body fractures occur in horses that
witl1 some restriction in hindlin1b action and
have had severe trawna or falls, particularly
dragging of the toes of the hindlimb(s).

in racehorses injun1ping races. Complete or

A diagnosis of sacroiliac pain and lesions
partial paraplegia results from drunage to tl1e
can be made in clinical practice witl1 a
spinal cord. The prognosis is usually grave.

combination of physical exan1ination and
exclusion of oilier ca.uses of lameness. A

MUSCLE STRAIN AND SORENESS
demonstration of in1provement in gait after
local anestl1etic infiltration of the sacroiliac

See also MYOPATHIES IN HORSES, p 1176.

joint region is occasionally perfonned to

Drunage to the muscles is probably the
confirm diagnosis. Ultrasonographic
most common cause of back soreness in
assessment of tl1e ventral aspect of tl1e

1148

LAMENESS IN HORSES
sacroiliac can be performed using a rectal
skeletal involvement includes vertebral
probe. Abnormal ultrasonographic findings
articular facets, which may be associated
seen at the ventral aspect of the sacroiliac
with stenosis of the vertebral canal and,
joint in clinical cases include bone modeling therefore, ataxia and proprioceptive deficits VetBooks.ir
of the sacrum and/or ilewn, narrowing of

(ie, wobbler syndrome), but the relationship
the joint space, remodeling or pe1iarticular
between these conditions is not clear.

osteophytes of the caudal border of the
articular surface of the sacrum and caudal

Clinical Findings: The clinical signs of
articular margin of the ileum, periarticular
equine osteochondrosis are difficult to
bone fragmentation, and ventral sacroiliac
characterize specifically because of the
ligament desmopathy and enthesopathy.

wide range of lesions and sites involved.

Treatment and management of sacroiliac

In young horses, many cases have no
disease is usually supportive and nonspedetectable clinical signs and are identified cific. Therapies include periarticular
only on presale radiographs. Furthermore,
ir\jections of steroids and rehabilitation
lesions of dyschondroplasia may not
using progressive warm-up at a slow canter
progress to osteochondrosis, and radioand exercises that develop the gluteal graphically observed osteochondrosis
muscles.

lesions may resolve over time without
producing clinical signs. In severe cases,
other signs of developmental orthopedic

DEVELOPMENTAL
disease also may be apparent.

ORTHOPEDIC DISEASE

The most common presenting sign of
osteochondrosis is a nonpainful distention

Developmental orthopedic diseases of
of an affected joint ( eg, gonitis, bog spavin).

horses constitute an important group of

The exceptions to this are joints in which
conditions that includes osteochondrosis,
swelling is difficult to detect ( eg, shoulder
physeal dysplasia, acquired angular limb
joint, medial femorotibialjoint), in which
deformities, flexural deformities, and
case lameness is more often the first sign
cuboidal bone malfom1ations.

observed. Clinical signs may be divided
broadly into two categories: t110se seen in
foals <6 mo old and those seen in older

OSTEOCHONDROSIS
animals. Often the first sign noted in foals is

(Osteochondritis dissecans, Dyschondroplasia) a tendency to spend more time lying down.

This is accompanied frequently by joint

Osteochondrosis is one of the most
swelling, stiffness, and difficulty keeping
in1portant and prevalent developmental
up witl1 other animals in the paddock. An

01thopedic diseases of horses. Although
accompanying sign may be the development
its specific etiology is not known, it is
of upright conformation of the lin1bs.

considered to arise from a focal disturbance

Fetlock osteochondrosis is particularly
in endochondral ossification, with subseseen in younger foals ( <6 mo old).

quent trauma or physiologic loading

Lameness is usually absent or mild except
resulting in lesion formation. The term osteofor those sites mentioned above for which chondrosis is currently used to describe the
the earlier sign of joint swelling is difficult to
clinical manifestation of the disorder;
detect. For example, lesions in the shoulder
however, the tenn dyschondroplasiais
frequently result in moderate to severe
preferred when refening to early lesions.

lameness, muscle atrophy, and pain on joint

Osteochondrosis has a multifactorial
flexion. In the stifle, some horses with
etiology that includes rapid growth, high
subchondral bone cysts in the medial
carbohydrate diet, mineral imbalance, and
femoral condyle present with lameness
biomechartics (ie, trawna to cartilage).

severe enough that a fracture may be

Genetics has been in1plicated, with some
suspected, and swelling may only be
breeds predisposed ( eg, Standardbred and
detected on careful examination. More

Swedish Wannblood). The condition mainly
severe signs are also observed when
affects articular growth cartilage, but tl1e
osteochondral fragments come loose within
metaphysis may also be involved. If the
the joint. This is often seen in yearlings or
physeal metaphyseal cartilage is affected,
older horses that present witl1 stiffness, flexbone contours and longitudinal growth are ion responses, and varying degrees of
disturbed (seep 1149). Dyschondroplasia at
lameness. These signs are usually associarticular surfaces may progress to formation ated with the onset of training.

of cartilage flaps or osteochondral fragments

( osteochondrosis ). At some sites, subchon

Diagnosis: Clinical diagnosis can often be
dral cysts may develop (seep 1062). Axial
made on the basis of signalment and signs.

LAMENESS IN HORSES

1149

More definitive diagnosis requires use of

In cases with more extensive osteochondral
some specific clinical aids. Radiographic
dan1age, prognosis depends on the extent of
examination has been the traditional way to
the joint surface that must be removed.

confinn diagnosis; however, early lesions

Prognosis is poor for cases with instability

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involving cartilage without significant
resulting from joint surface loss or in which
subchondral bone damage may not be
secondary osteoarthritis ( degenerative joint
visualized. In the distal limb, oblique views
disease) is advanced. This is often the case
may be helpful; in the hock, because the
witl1 shoulder osteochondrosis because
most common site of a lesion is the distal
of the difficulty in detecting early signs.

intermediate ridge of the tibia, the best view Cases involving subchondral cysts have is a plantarolateraVdnrsomedial oblique.

a guarded prognosis, because these cysts

·mtrasonographic exanlination of the
are often in important weightbearing areas
swollen joints can help delineate articular
of the joint, and restoration of the joint
damage and synovial inflammation and
surface is rarely possible.

detennine whether osteochondral
fragments are intra- or extra-articular. The

PHYSITIS
most accurate way to confinn diagnosis is
by arthroscopy, and most of the predilection

(Epiphysitis, Physeal dysplasia, Dysplasia of
sites are accessible.

the growth plate)

Scintigraphy has limitations in growing
horses because of nom1al high activity in

Physitis involves swelling around the growth
physes and sites of active endochondral
plates of ce,tain Jong bones in young horses.

ossification. It is a useful technique to detect Suggested causes include malnutrition, subchondral cysts and secondary degeneraconfom1ational defects, excessive exercise, tive changes in older horses. MRI is ideal for obesity, and toxicosis. The condition is seen diagnosis of both early and late lesions but
frequently in well-grown, fast-growing,
is usually not necessary. Also, sites that
heavy-topped foals during the smnmer when
are most diagnostically challenging are
the ground is dry and hard, and on stud
generally in the proximal limb, where
fanns where the calcitun:phosphorus ratio

, - ccess is difficult. Clinical pathology and the in the diet is imbalanced. This suggests that evaluation of synovial fluid is rarely helpful
it is a result of overload of the physeal area
but can be used to elinlinate inflammatory
due to excessive loading or weakened bone
causes of swollen joints.

and/or cartilage, or a combination of these
factors.

Treatment and Management: Management of osteochondrosis depends on the site and seve1ity of signs. Mild cases recover
spontaneously, and a conservative approach
may be appropriate. In young animals

( <12 mo old), this involves restricted
exercise for some weeks combined with
reduced feed intake to slow the growth rate.

Particular care should be taken to ensure
appropriate mineral supplementation ( eg, in
cases of suspected copper deficiency)- It is
controversial whether correcting the diet,
once signs have developed, will actually
assist resolution, but it may help limit or
prevent further cases on stud fam1s.

Intra-articular medication with hyaluronic
acid may be beneficial, but injection of
long-acting corticosteroids is not recommended in young, growing horses.

Cases considered for surgery are treated
arthroscopically_ This technique has been
successful in most affected sites, particularly the hock, stifle, and fetlock. Damaged cartilage, osteochondral fragments, and
compromised subchondral bone are
removed and the joint flushed extensively
with sterile fluid. Prognosis after removal of

Physitis in the distal tibia of a horse. Courtesy of discrete osteochondral fragments is good.

Dr. Chris Whitton.

1150

LAMENESS IN HORSES

Physitis most conunonly involves the
distal extremities of the radius, tibia, third
metacarpal or metatarsal bone, and the
proximal aspect of the first phalanx. It is
characterized by flaring at the level of the

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growth plate, giving a typical "boxy"

appearance to the affected joints. Radiographs aid clinical assessment.

Treatment consists of reducing food
intake to reduce body weight or at least
growth rate; confining exercise to a yard
or a large, weU-ventilated loose box with
a soft surface ( eg, peat moss, deep straw,
shavings, or sand); ensruing that the feet
are carefully and frequently t1immed; and
correcting the diet if necessary. The
calcium:phosphorus ratio should be
acljusted to 1.6: 1, and protein content
limited to < lO"A, of dry matter. ln general tern1s, bran should not be fed, and
dicalcirun phosphate or bone flour (10-30 g
daily) should be added to the diet. Vitamin D
supplements (PO or parenteral) are
indicated, but the dosage must be monitored closely to avoid hypervitaminosis D.

As a preventive measure, older foals or

Acquired flexural deformity of the distal
yearlings that are fat or heavy-topped
interphalangeal joint in a foal. Courtesy of Dr.

should be watched carefully for clinical

Chris Whitton.

signs, especiaUy when the groru1d is hard
and dry. When these conditions prevail, feed Clinical Findings: Signs vary widely rations and exercise should be restricted.

in newborn foals. Some carmot stand,
some attempt to walk on the dorsum of
their fetlocks, and others can stand but

FLEXURAL DEFORMITIES
knuckle in the fetlocks or carpi. One foal
may in1prove spontaneously, yet another,

(Contracted tendons, Club foot, Knuckling)

seemingly healthy at birth, may become
progressively worse. ln older foals, onset

Flexor tendon disorders are associated with tends to be rapid; such animals may walk postural and foot changes, lameness, and
around on their toes with their heels off
debility. They may be congenital and
the ground. A slower onset is charactertherefore identified in newborn foals or ized by an upright hoof with an elongated
acquired at an older age. Uterine malposiheel and concave toe. Physitis frequently tion, teratogenic insults (arthrogryposis),
is evident in these horses. Involvement of
and genetic defects have been either
botl1 forelimbs is common, with a tendency
implicated or proved to cause contracted
to be worse in one leg. Toe abscesses are
limbs in newborn foals. Chronic pain is the
a frequent complication of the hoof and
most common cause of acquired tendon
locomotion changes, and they add to the
contracture. Pain can arise from physitis,
pain and defomtity.

osteochondrosis, degenerative joint

Older horses (1-2 yr old) conunonly
disease, pedal bone fracture, or soft-tissue
knuckle in tl1e metacarpophalangealjoints.

wounds and infection. Pain induces reflex

Yearlings usuaUy are more severely affected
muscle contraction with shortening of the
and more difficult to treat than younger
flexor musculotendinous Ullits. The horse
animals. It is in1portant to attempt to
walks on its toes or knuckles in the fetlocks identify any underlying bone or joint
or occasionaUy the pastern joint. Nutritional disease, but tllis is often difficult and may errors referable to problems associated
have resolved.

with bone growth (ie, osteochondrosis and
physitis) are intimately associated with the

Treatment: Mild cases in newborn foals
syndrome and must be addressed as part of
often reqttire no treatment. More severe
treatment. (See also CONTRACTED PLEXOR
cases require suppo1tive therapy, and it

TENDONS, p 1042, and ANGULAR LIMB DEJ'ORMITIES,
is essential to correct failure of passive
p 1046.)

transfer of immUllity if the foal has not been

LAMENESS IN PIGS 1151
able to nurse adequately. Use of splints
procedure for flexural defonnity of the
necessitates careful fitting and managedistal lin1b and does not interfere with ment, because rubbing sores are common
future perfom1ance. Superior check
and can be severe. Casts are generally safer
ligament desmotomy may be included for
if used only for short periods (5--7 days).

horses with fetlock defomlities. For carpal

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High-dose oxytetracycline therapy is
defomlities, sectioning of the tendons of
commonly used ( 40-60 mg/kg).

insertion onto the ulnaris lateral.is and

Early acquired cases in older foals and
flexor carpi ulnaris is perfo1med. In
weanlings can be managed conservatively
hindlimbs, tenotomy of the medial head of
with nutritional c01Tection, proper hoof
the deep digital flexor is perfom1ed, because
trimming, and analgesia; however, once the
tl1e inferior check ligament is often vestigial.

deformity is present for> 1 wk, this is rarely

In severe cases, tenotomy of the deep digital
successful. Surgical treatment can be
flexor tendon can be used as a salvage
simple or complex, depending on the
procedure. Nutritional correction, proper
degree of involvement. Desmotomy of the
foot trimming, and analgesia are integral
accessory ligament of the deep digital flexor
to recovery when surgery is perfom1ed.

tendon (infe1ior check desmotomy) is the

The prognosis is fair to good for horses
most successful and commonly used
diagnosed early and managed properly.

LAMENESS IN PIGS

Lameness has been an issue in swine
remembered that some infectious agents
production for many years and continues
can affect and cause lameness in multiple
to be a problem worldwide. Although
species, so understanding the signalment of
lameness can be caused by congenital
not only the group of pigs under evaluation,
or developmental abnormalities, most
but also other pigs or species recently in
lameness in production animals is caused
contact or proxinlity with the affected
by pain associated with infections,
group, is part of the comprehensive
trauma-related il\iuries, or underlying
approach required for lameness investigametabolic diseases. As such, it has become tions.

an area of focus for swine fam1 audits of

In addition to the signalrnent of the
animal well-being. It is also an econonlic
individual pigs in a population, the
issue, because an increasing prevalence or
signalrnent of the composite group (ie,
incidence of lan1eness in a herd is likely to
demographics) is also an important
affect viability, growth, or reproduction of
consideration. Exan1ples of group
pigs. Pig flow may be affected if faITowing
signalrnent are tl1e proportion of gilts in
targets are not met because of high rates
farrowing groups because gilts are more
of breeding stock removal or if growth of
likely to pass pathogenic bacteria to their
grower/finisher pigs is slowed by high
progeny, or the herd immune status with
lameness incidence. As with diseases of
respect to a particular pathogen based on,
otl1er body systems, lameness problems
for example, time since tl1e most recent
in a swine herd require a comprehensive
vaccination against erysipelas. Even the
approach if a diagnosis ( or diagnoses) is to relative body condition of sows going into
be reached so that preventive or curative
a cold season can predispose populations
measures can be instituted.

to increased or decreased susceptibility
to herd health problems.

Signalment: The types and causes of
lameness can vary widely by age of the pig

History: History taking must be thorough
and, to a lesser extent, by gender and breed.

and should include information on age of

Traun1atic il\iury can obviously cause
onset, typical clinical signs, and progression
lameness in pigs at any age, but some types
of the lameness. Morbidity and mortality
of lameness arising from infectious or
associated with any lameness and the
physiologic causes can have a more linlited
number of groups, pens, rooms, or buildings
age range or set of circumstances under
with affected pigs are all relevant. Morbidity
which lameness develops. It should also be
infonnation should include treatments and

1152

LAMENESS IN PIGS
the responses observed. Culling rates can
keep pace with weight and nutrient density
also provide infom1ation on morbidity,
changes in the ration.

although recorded reasons for culling sows

Experiences with a series of lameness
are notoriously inaccurate. Condenmations
problems collectively referred to as
at slaughter can be another way to secure
metabolic bone disease-variably

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objective data on morbidity, when
concerning problems in calcium, phosphocondenmations for limb abnormalities or rus, and/or vitan1in D metabolism-have
fractures have a direct bearing on lameness
put more focus on the need to test feed
and for polyserositis or downer pigs, which
constituents more thoroughly before
have an indirect bearing on lameness.

inclusion in the diets, to test mixed feed

Mortality data can be evaluated as an
for adherence to the formulation, and to
absolute rate or, more usefully, as
monitor pigs more closely for serum vitan1in
incidence by stage or week of production.

D levels and bone densities so problems can

For sows, body condition score at the time
be detected earlier.

of death or euthanasia can help reveal

Farm staff have a large role in caring
underlying lameness conditions because
for pigs on farms and, therefore, are a
recorded reasons for cause of death are
key source of information and possible
also prone to inaccuracy, and lan1e sows
solutions to lameness problems. Personnel
tend to lose body condition before death
working with the pigs must also be
or euthanasia.

evaluated as possible contributors to

The investigation of a lameness problem
lan1eness problems. Pig handling and
on a farm also requires an understanding of
movement are obvious potential causes
the operation of the farm itself. The logistics of lameness, so understanding the level underlying the establishment of the group of of staffing and extent of staff training pigs under investigation should be explored: are important parts of the case history.

the source(s), transport, and placement of

Observing the interaction between the pigs
the pigs. The history of replacement
and the farm staff can help reveal the nature
breeding stock accessions is relevant,
of interactions likely to occur routinely on
especially if new herds of origin or different
the farm.

genetic lines were introduced.

Understanding the farm hygiene practices

Health progran1 and practices should be
is important to detennine risks of injury and
considered. It is important to detem1ine
disease from slippery surfaces or contamiwhether vaccination or medication nation from transport vehicles. If bedding
protocols were changed. If possible, it is
is used, determining the sources and
equally important to detem1ine whether
management of the bedding is also
protocols were followed correctly. Audits of significant to characterize disease risks.

product consumption or aptibody testing

Finally, the history of diagnostic results
for vaccine titers, if available, can be used
for the farm and the area are critically
as verification methods.

important to have a starting point for further

Investigating nutrition programs as a
investigation of lameness problems. If
possible contributor to lameness problems
possible, the disease history among
can become extensive. However, the
neighboring farms can help understand
fundamental questions can be reduced to
disease risks. At a minimum, a review of all
determining what rations were formulated,
the pe1tinent diagnostic testing results for
mixed, and delivered to the pigs. Problems
the specific herd is required ..

are relatively rare but possible during each
stage of the process. At the formulation

Clinical Evaluation: Diagnosis of
stage, lameness problems can result, for
lameness can be complex. At least three
example, when book values of phosphorus
body systems (musculoskeletal, nervous,
are different than actual amounts present
and integumentary) may be affected
in the product used, or vitamin D or
independently or in combination. Because
phytase activities are not at expected
of the different organ systems potentially
levels because of storage, processing, or
involved, a consistent and thorough
other issues, which can affect calcium and
approach to evaluate all components of
phosphorus metabolism. At the mixing
lameness is essential. When examining a
stage, mills can have time constraints that
herd with a locomotor problem, the focus
do not allow adequate mixing of feed
should not be solely on a group of affected
batches, so the feed composition can be
pigs. Younger pigs should be evaluated to
uneven. At the point of delivery, feed
identify potential underlying causes or
density differences in sow gestation feed
predispositions to the problem under
can result in over- or underfeeding when
investigation. Other groups of pigs of similar
volumetric feeders are not adjusted to
ages and older pigs housed in other pens or

LAMENESS IN PIGS

1153
buildings should also be evaluated to
challenge of managing recovery from
determine whether they have similar
anesthesia with other pigs present or in
or different problems. The conditions
facilities that may not be set up for such
potentially causing the problem should not
procedures.

be assrnned to be restricted to those most

Some farms may have lift chutes to

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often associated with one particular age
immobilize boai-s, sows, and gilts for foot
group.

trin11ning or other procedures. These chutes

When evaluating a population of pigs, it is
allow good restraint with full access to the
useful to first consider an inve1ted pyramid
feet and lower limbs, with none of the
approach of the entire room, followed by
disadvantages of chemical restraint.

pens of pigs and finally individual pig

However, availability of lift chutes on
evaluations. The entire room evaluation is
sow farms is limited.

intended to provide a general sense of the

A general physical examination of an
overall health, activity, and behavior of the
individual pig for laineness requires a
group. Pen-by-pen evaluations provide an
thorough, systematic, ai1d consistent
opportunity to make counts or estimates of
process by individual clinicians. One such
the prevalence and severity of the lan1eness.

approach is to proceed from the bottom up

The individual pig assessments ai·e intended
and front to back of the pig, ie, the feet are
to focus on the specific cause( s) of the
evaluated first, followed by the limbs and
lameness.

torso in a front-to-back progression.

The pen evaluation is intended to identify

The feet can be examined most easily
the lame pigs. Pigs should be made to move
when the pig is lying laterally rec.um bent or
around (in pens or into alleyways), to stand,
lifted (manually for small pigs or using a
and if housing allows, to walk, watching for
mechai1ical chute for sows). Standardized
behavior typical of Jaine pigs. The pen allead guides exist to score foot lesions by type.

and pen behind the last pigs to stand up and

Prevalence and severity of foot lesions in a
first pigs to lie down should be observed.

sow herd can be estimated by scoring the

Pigs that take advantage of the diversion
feet using statistical sainpling. Using a good
caused by the evaluation to access feed or
flashlight enhances scoring foot lesions.

water should be noted. Abnom1al gait and

Feet may need to be cleaned for pigs housed
posture, body condition (thin pigs are more
on non-slatted floors. Exploring lesions by
likely to be lame), and physical evidence
trinlnling with a hoof knife, clipper, or
of trauma, infection, or malformation
grinder requires adequate restraint and

(swelling, vesicles, etc) should be watched
safety protocols. Foot lesions have been
for in individual pigs.

well defined but do not always correlate

If an individual pig warrants a more
with lan1eness on ai1 individual pig basis,
extensive physical examination, some
because the pain associated with foot
degree of restraint may be required. If less
lesions depends on exposure or infection
restraint is sufficient, the pig can remain
of the sensitive tissues underlying the
free in a pen or stall, or a sorting panel can
claw, heel, and sole of the toes.

be used to prevent the pig from moving

Lin1b and joint palpation and manipulaaway. If more restraint is needed, small pigs tion should also be conducting using a
can be lifted or manually held for examinaconsistent approach. The ainount and type tion. Larger pigs can be snai·ed or cast using
of restraint again depends on age of the pig.

ropes. The advantage of this type of

Cardinal signs of inflammation, ie, heat,
restraint is that it inm10bilizes the pig.

swelling, pain, and redness, should be

Disadvantages are that the pig is placed in
noted. Strength, range of motion, crepitus,
an wmatural posture, excess muscle tone
and weight-bearing distribution should be
is normally stinlulated, and help from
evaluated. Joints embedded in muscle mass
additional people is usually required.

(eg, hip, stifle, shoulder) require deep

Anesthesia is another possible means of
palpation, which may not be possible on
greater restraint. The advantage is that
large, heavily muscled pigs. Fracture of the
muscles are relaxed, allowing manipulahead of the femur ( epiphysiolysis capitis tion of skeletal structures such as potential
femoris ), a common cause of downer sows,
fractures. Additionally, muscle mass can
is difficult to diagnose antemortem.

be assessed, joint taps or other diagnostic

Because it is buried under a large muscle
procedures can be performed, ai1d more
mass, even infectious arthritis in the stifle,
extensive evaluations such as radiography
a site commonly affected by Mycoplasma
or other scaiming are possible if war
hyosynoviae, can be missed on individual
ranted. Disadvantages are the management pigs on cursory exainination.

of controlled substances used as anesthet

The torso can be evaluated and palpated
ics, required withdrawal tinles, and the
for muscle mass, tone, and symmetry. Ribs

1154

LAMENESS IN PIGS
should be examined for evidence of
tic clinical signs, acutely affected, and
fractures or knobby thickening (rachitic
untreated (if available) are a reasonable
rosary), and the spine examined for
starting point. Alternatively, tliree freshly
kyphosis.

dead pigs can be exanlined and sanipled.

A neurologic exaniination is indicated in

Samples should be packaged and identified

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cases when neurologic disease is suspected
individually for each pig. Whole blood in
and should be pe1formed in a similar

EDTA and serum should be collected
fashion to that for dogs, cows, and horses
antemortem if possible. For small pigs,

(seep 1213).

postmortem samples can include intact

Postmortem exanlination of lanie pigs is
joints with the ski.Ji wiped clean and cooled
often required to reach a definitive diagnosis for transport. For larger pigs, two joint for a herd lameness problem. Field necropsy swabs of synovial membranes of affected of baby, nursery, and grower pigs is
joints should be collected, along witll
relatively easy to accomplish. However, for
chilled and fonnalin-fixed synovial
larger finisher pigs, gilts, sows, and boars,
membrane samples. Affected bones can
the process is laborious because of the size
also be submitted chilled.

of the animal and the need to examine

The bone of choice (based on tlie
numerous joints and bones, often including
recommendation of the laboratory) for
the spine if appropriate to tlie clinical
bone density deterniination should be
presentation. At a minimum, developing
submitted if warranted. Protocols to
expertise in opening joints on dead pigs tliat
evaluate bone density using front feet have
may not be ideal candidates for diagnostic
been developed and may be available in
sampling can help direct diagnostic efforts
some laboratories.

when more suitable pigs are available.

For suspected neurologic cases, one half

Exanlination of greater numbers of pigs
of tlie brain should be submitted chilled and
improves the odds of accurately charactertlle other half fixed in buffered lOOAi izing tlie cause( s) of lameness.

fornialin. Additionally, ve1tebral sections

Altliough on-farm necropsies are feasible,
from the cervicothoracic and lumbosacral
it may be better to submit entire or even live
region should be submitted chilled, witli
pigs to a full-service diagnostic laboratory.

5-cm segments of spinal cord also submitted

In particular, submitting Jive pigs to a
fixed in fonnalin. If muscle disease is
laboratory allows greater odds of successsuspected, a sample of diaphragm and fully cultwing Jive bacteria, which are
muscle from affected areas should be
needed for anti.microbial susceptibility
submitted fixed in formalin.

determination or production of autogenous

As pait of the postmortem exaiilination,
vaccines. Additionally, diagnostic laboratoa rib should be removed and maimally ries have the facilities and personnel to
snapped (like a twig) to gain an appreciape1fo1m more complete and careful tion of tlle bone mineral density. Depending
dissections of joints, tlle spine, and brain.

on the age of tlie pig, the rib should snap

This is particularly true of sow lameness
sharply. With practice, clinicians can
problems. For exaniple, an extensive
develop skill in evaluating bone mineralizadissection of the pelvis is required to reveal tion in tl1is m31111er.

an apophysiolysis of ischial tuberosity in

Evaluation of affected or cull pigs at a
young sows with characteristic dog-sitting
slaughter plant is not usually productive,
posture after farrowing. Likewise, vertebral
because processing lines run too fast .to
abscessation can be a common cause of
evaluate all tlie elements of tlie musculodowner sows, and the ve1tebral column skeletal system, and all joints c31111ot be
must be split sagittally to make a definitive
thoroughly exanlined. However, specific
diagnosis of tllis condition.

conditions can be evaluated even at line

If pigs are to be submitted to a diagnostic
speed. For exaniple, rachitic lesions may
laboratory, appropriate pigs must be
be apparent on ribs on hanging carcasses.

selected and delivered, accompanied by an

Condenuied carcass or euth3llized slow or
accurate history and a list of differential
down pigs can sometimes be made available
diagnoses. Adequate numbers of representfor exanlination. Some abattoirs are willing ative, acutely lame, untreated pigs are
to cooperate on specific projects to retrieve
essential.

lower Ii.nibs for investigative purposes if

If tissues are to be submitted for a
asked.

lameness evaluation, the diagnostic
laboratory should be contacted to

Environment and Management: Housdetennine what tests will be done and what ing ai1d the marmer in which pigs and their
tissues will be needed. In general, tissues
environment are mai1aged are central to
from tliree euthanized pigs with characte1is-
potential lameness problems, especially tl1e

LAMENESS IN PIGS

1155
interface between the pig and the floor.

ing expectations for rapid growth and muscle

F1001ing type is a major detenninant, and all development in modem hybrid pigs.

types have forms of lameness associated

Problems early in the production cycle may
with them. Dut and pasture lots can range
be reflected as abnormal bone growth in

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from too dry to too wet, leading to vertical
nursery or growing pigs, whereas recurrent
hoof wall cracks or foot infections,
deficiencies or those seen later in the
respectively. Bedding can serve as a source
fin ishing phase may result in weak bones in
of bacteria that cause infectious arthritis,
slaughter pigs or replacement breeding stock.

such as Erysipelothrix rhusiopathiae in

Druing the growing phase, the goal of the
straw bedding. Solid, partial slat, and fully
nutritional program should be to ens{u-e the
slatted floors also have relative advantages
development of a strong skeleton so that
and disadvantages in terms of associated
incidence of spontaneous bone fractures in
lameness conditions.

the finishing barn or during the slaughter

In addition to type offlooring, the
process is low, thus preventu1g large
acljustment and state of repair can have
numbers of culls or partial and complete
considerable influence on lan1eness. Holes,
condemnations of carcasses. Fractures of
gaps, and sharp edges on concrete floors can
the femur, humerus, ribs, or vertebrae may
traumatize the feet and lower legs. Abrasivebe induced by strong muscle contractions ness of the flooring surface may be too little,
during the slaughter process; however, if
which makes floors slippery and leads to
the problem is seen frequently, it may be
irtjuries, or too much, which can wear down
a reflection of tl1e overall integrity of the
the claws and promote heel overgrowth.

skeleton and warrant fru111er evaluation

Cleanliness and moisture are additional
of the minerals and vitamu1s in the ration.

factors to evaluate. Buildup of manure in

Clinical signs of hypocalcemia can develop
bedded areas can lead to foot infections,
before slaughter and can include lan1eness,
whereas excess moisture from misting
including spiral fracture of tl1e femur, leg
cooling systems rurming out of acljustment
weakness and posterior paresis, recumcan lead to softening of the claws, hoof wall bency and paddling, and even sudden death.

cracks, and excess wear.

In breedu1g aninlals especially, foot

Interactions among the pigs are also
lesions can cause lan1eness. Research has
important factors to evaluate. The sourcing
demonstrated tl1e need to balance diets careand mixing of discrete pig populations can fully for macro and trace minerals, as well as
influence whether infectious diseases are
key vitaniins such as vitamin D and biotin.

maintained as endemic within the

Excessive water hardness or high concenpopulation or can become epidemic trations of iron or heavy metals in water can
outbreaks as pigs become susceptible over
antagonize trace 1nineral absorption, leading
tinle with the loss of maternal in1munity and
to foot lesion development.

have commingling exposure. Stocking
density and space for aninlals to exhibit

Viruses: Some acute infectious causes of
social behaviors can influence how much
lameness in pigs can affect pigs of multiple
aggressive social behavior occurs within
ages. In particular, vesicular diseases
groups of pigs. Distance and conditions pigs
caused by several viruses can cause
are required to traverse to access feed and
lameness in breeding and growing swine:

water can affect wear on the feet and
foot-and-mouth disease, Seneca Valley
trauma to joints.

vints, swine vesicular disease, vesicular

Group size and stability also have an
stomatitis, and vesicular exanthema all fit
unpact on development of lameness. Sows
this clinical picture. Prevalence and clinical
housed in individual stalls are restricted in
severity among these viruses is variable, but
tenns of movement but tend to develop
because of the concern over foot-andfewer lan1eness problems than confined mouth, any episode of vesicular disease in
group-housed sows. Pigs kept in very large
pigs is cause for a full diagnostic investigagroup sizes have fewer aggressive tion involving regulatory personnel.

interactions than pigs housed in small
groups. Sorting growing pigs to allow for

Therapeutic Considerations: Theramore variation in size within pens can pies to treat or prevent lameness should,
reduce the time required for social
of course, be tailored to the presumed or
structures to become established at
confumed underlying cause of lameness but
weanu1g or regrouping tunes.

can also be symptomatic to reduce pain and
improve function. However, the regulatory

Nutrition: Skeletal development may
landscape for use of products to treat or
be affected by relatively short-term
prevent lan1eness in pigs is changing. This
nutritional deficiencies, especially consider-
is true not only for federal regulations

1156

LAMENESS IN PIGS
regarding use of antimicrobials and
in Canada but not in the USA. All these
analgesics but also for the patchwork of
products are administered by IM il\iection,
conunercial marketing programs that are
so treatment of large numbers of pigs is time
typically more restrictive on product use
conswning and potentially costly. Acetyl

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through contractual agreements. Thus, any
salicylic acid and sodiwn salicylate are
product type, dose, fom1, and use should be
allowed for analgesia in swine if manufaccarefully considered in light of pertinent tured under cGMP and may be a useful
regulations for the jurisdictions in which
acljunct therapy as a water treatment.

the pigs are being raised and marketed.

Additionally, meloxicam and ibuprofen

Production practices and conditions are
can be compounded from FDA-approved
also changing. In certain parts of the world,
hwnan products. An important considerapig farming is becoming more intensive, tion with use of any pharmaceuticals in pigs
whereas others are becoming more
near time of slaughter is observance of
extensive. These changes can alter the
withdrawal times recommended by the
epidemiology of diseases, posing both a
manufacturer.

challenge and an opportunity to intervene

Whenever feasible, introduction of a
more effectively to reduce lameness.

vaccination protocol to protect populations

Diagnostic regimens are becoming more
of pigs against a particular infectious agent
sensitive, increasing the likelihood of
is desirable. If a suitable vaccine is not
detecting and characterizing diseasecommercially available, an autogenous causing agents. Distinguishing between
product can be created for some pathogens
presence and significance of a diseasefor use in an individual herd and, provided it causing agent becomes more difficult, but
is cost-effective, can be used to prevent
a more precise understanding of exposure
regular outbreaks of disease. Regular
and transmission of agents should help
monitoring for causal organisms, serotype,
develop more effective control strategies.

etc, is essential for effective use of either

Pigs with acute diseases that may result
antibacterial agents or vaccines.

in death typically require parenteral therapy

Removing lan1e pigs from competitive
with a drug of choice (using approved
group housing environments to hospital
products first) based on tentative diagnosis
pens improves the chances of recove1y.

and the clinician's experience until results

Research is inconclusive as to the optimal
of a necropsy and antimicrobial sensitivity
flooring and husbandry conditions for
profiles are available. Virtually all the
recovery pens.

parenteral products available to treat
infections that cause lameness are given IM,

PIGS IN FARROWING HOUSES
with the site of choice behind the ear for all
age categories. It may be feasible to provide

Neonatal Polyarthritis (Joint-ill):

medication in the water or feed after the

Neonatal septic polyarthritis, which causes
initial parenteral treatment. Infectious
death in up to 1.5% of affected pigs, is
agents sensitive to a drug in vitro may not be caused by various facultative and specific sensitive in vivo, so clinical experience on

•
pathogens that cause localized infections
the farm is essential.

that precede septicemia. Healthy, suckling

In addition to antimicrobials to treat
pigs typically "paddle" with their legs,
infectious arthritides, the use of anti-inflamabrading the skin of the carpi or coronary matory agents to relieve pain can be useful
bands; an infection often becomes
and beneficial to the pig. Flunixin megluestablished under scabs that develop. Poor mine is approved for use in pigs for
hygiene at tail docking, ear notching, or
symptomatic treatment of fever in
castration, and careless clipping of needle
outbreaks of swine respiratory disease, but
teeth can also result in localized infections.

anti-inflammatory and analgesic qualities

If an infected wound leads to bacteremia,
can help relieve pain in a swollen joint or
organisms can cross the synovial membruised muscle (extra-label). Dexamethabrane, and polyarthritis is likely. Microsone has been recommended in pigs with organisms can also gain entry to the
streptococcosis and is labeled for glucocorcirculatory system via the tonsils or ticoid therapy in pigs. Another glucocmtioropharynx or as a result of an ascending coid, isoflupredone acetate, is specifically
omphalophlebitis. Pigs with exudative
approved for musculoskeletal pain that
epidemlitis (seep 860) are also prone to
causes lameness in pigs. In a controlled
polyartluitis, but tllis may be a reflection of
study in Europe, the COX-2 inhibitor
the san1e skin damage discussed above.

meloxicarn proved useful to alleviate

Affected pigs are lethargic and may fail
painful, noninfectious lameness in pigs.

to suckle. Joints are swollen, painful, and

This product is approved for use in swine
warm, and lameness affecting one or more

LAMENESS IN PIGS

1157
limbs is severe. With time, the soft, fluctuant
can lacerate the faces of other pigs,
swellings become firm. At necropsy, the
resulting in pyoderma Castration equipumbilicus should be examined to see ment must be kept sterile and sharp. If tail
whether it is hard and swollen. Typically,
stumps are infected, antiseptic solution may
cream or green pus is found in and around
be used as a spray to improve hygiene.

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swollen joints (particularly the elbows,

Litters from gilts are more prone to
carpi, stifles, and hocks), in the umbilical
neonatal polyarthritis. Colostral protection
stalk, and sometimes over the meninges or
against tJus syndrome and other infectious
in the fissure between the cerebrum and
diseases of baby pigs increases as a sow
cerebellum. Organisms isolated from baby
ages. Because pigs in large litters have to
pigs included streptococci (including
compete more to suckle and are, therefore,

Streptococcus suis), staphylococci,
more prone to lesions on their faces and

Actinoba.ciUus suis, 'I'ruepere/J.a pyogenes,
forelimbs, cross-fostering within 24 hr of

Escherichia coli, and occasionally,
birth to balance Jitter sizes may help. Piglets

Pasteurella mullocida, Erysipelothri,:x;
nursing sows with hypogalactia or agalactia
rhusiopathiae, or Haemophilus spp. If spend more ti.me nursing, leading to more
untreated, affected pigs become runts that
forelin1b lesions.

fail to thrive in the nursery.

Treatment must be based on bacterial

Diseases of the Foot: Neonatal foot
culture and antimicrobial sensitivity profiles lesions fall into two main categories: either and applicable regulations on product use.

the sole or heel is damaged by the floor, or

Antimicrobial therapy should be initiated
the hoof wall is traumatized by the sow
early in the course of the disease if it is to be
standing on a pig's foot or by entrapment
effective, and treating all pigs in the group at
in the flooring.

risk may be prudent, especially if S suis is Bruises or lacerations develop on either
implicated. Penicillins have been the drugs
the sole or heel. The lesions are associated
of choice, depending on the causal agent
with worn and rough floor surfaces and with
and sensitivity. However, a broader range
floors that have solid as well as perforated
of drugs is available, including lincomycin,
surfaces. Rough flooring can also cause
trimethoprirn/sulfonamide, and tylosin,
bruising in soft tissue below the hoof wall.

provided causal organisms are sensitive.

If spaces between slats are large, digits can

The range of suitable drugs is increased
be entrapped, and lameness results from
further if streptococcosis caused by S suis
bruising or infection at the coronary band.

develops (seep 731).

Pigs on expanded metal floors can incur

Regardless of the cause of a local
heel and wall injuries leading to loss of
infection, if there is an ongoing problem
accessory digits. Second and tJurd digits
with septic polyarthritis, it is important to
may be damaged as the pigs tJu·ust with
observe the practices used in farrowing
their feet during suckling and catch their
rooms and to look for opportunities for
toes against sharp metal edges. Sharp
improvement. An "all-in/all-out" flow of pigs spicules on woven wire cause lacerations
is in1portant, and scrupulous hygiene in
and predispose to infectious laminitis and
farrowing crates helps to reduce environpolyarthritis.

mental contanlination and incidence

Prevention is based on selecting floors
of neonatal polyarthritis. Prevention may
that minimally injure feet or skin. Because
be difficult because most types of floors,
of sinillarities with infectious polyarthritis,
including those bedded with straw, can
the approach to treatment and prevention is
cause skin abrasions. Plastic-covered
similar (see above). lmproved hygiene
woven wire provides a smooth, relatively
within the environment may help reduce
soft, self-cleaning floor and may help; plain
septic larninitis and allow injUiies to heal.

woven wire is similar if it is smooth. If
replacement of flooring is not economically

Muscular Disorders: Splayleg or
viable, sections of clean, soft carpeting may
spraddleleg (seep 1049) is precipitated by
help reduce skin abrasions.

weakness and immaturity of skeletal

Separate instrun1ents should be used for
muscles at birth because myotubular
teeth and tail clipping, and they should be
development is impaired. Forelimbs,
cleaned and disinfected between pigs,
hindlirnbs, or all four limbs may be affected
preferably using a dry paper towel. Soaking
so that the piglet either walks with difficulty
instruments in contanlinated disinfectant
or cannot stand. The disorder appears
solution between pigs or Jitters promotes
sporadically in litters, and only a few pigs
contamination and infection. If teeth are not in a Jitter are typically affected. There is clipped or if there are sharp remnants of
a hereditary component in European
clipped teeth, pigs that suckle aggressively

Landrace and, to a lesser extent, in Large

1158

LAMENESS IN PIGS

White pigs. Male, premature, and small
complaint. Congenital tremors cause pigs to
pigs, and pigs from older sows seem more
shake when awake and remain still when
susceptible. Deficiencies of choline,
sleeping. Either heredity or viral infections
methionine, and thiamine in the sow's
may cause the problem. ln the USA and
diet may precipitate the syndrome, and
other parts of the world, porcine circovirus

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zearalanone toxicity via the sow's milk has
has been implicated in congenital tremors.

been implicated, but there is controversy

The tremors usually are most severe during
as to the exact cause. To varying degrees,
the first week of life and make it difficult for
affected pigs are unable to move around and pigs to nurse. Affected pigs must be assisted die either because the sow crushes them or
with nursing until the tremors subside.

they become hypoglycemic because they
cannot feed. Alternatively, skin and foot

Hereditary and Congenital Disorders:

abrasions develop, predisposing to arthritis,

Mycotoxins in the sow's feed can cause
polyaithritis, or pododerrnatitis ai1d
arthrogryposis, which leads to deformity of
osteomyelitis of the digits.

limb bones, but the primary effect may be

Timely management practices ai·e
on neuromuscular function. Pigs affected
essential to ensure that pigs can feed and
by hereditary hyperostosis have thickened
avoid hypoglycemia and hypothennia. If
thoracic limbs and a domed forehead and
only the hincllimbs are affected, they can be
generally do not smvive. Polydactyly and
hobbled so that the pig can lever itself up
syndactyly are occasional abnormalities
using forelimbs and hop around to nurse.

that may affect locomotion of the baby pig;

Various hobbles, including a figure-8 tape or
syndactylous or mule-footed pigs have been
bai1clage, have been successful. Some
propagated and sold by some producers
recommend taping the pelvic limbs so they
with no obvious clisabilities for the pigs.

ai·e directed cranially on the belly. By using

When causal agents containinate the feed,
the limbs or pushing against a bellybancl, the sources of these products should be found pig potentially develops and strengthens
and avoided; if hereditary disease is
muscles, which can enable to pig to walk
suspected, the somce( s) of replacement
after a few days. Hobbles must be removed
stock must be investigated.

within a few clays of pigs walking, to avoid
ischemic necrosis of skin and other tissues

PIGS IN NURSERIES
as the pigs grow.

Pigs with splayleg may require assistai1ce

By the time pigs are weaned, diseases that
to suckle colostrum and milk for the first
affected the locomotor system during the
few clays of life. Some advocate the use of
nursing phase most likely will have resolved

"hot boxes" to nurture these and other ailing spontai1eously, responded to aggressive pigs, relying on milk replacers as the main
therapy, or resulted in death. Because pigs
source of food once the pig has had
that smvive episodes of polyarthritis
colostrum. Because slippery floors
generally remain Jaine, have one or more
exacerbate the condition, temporary use of
swollen "knotty" joints, and are in poor
sanitized mats may help. Any nutritional
condition, they should be culled.

deficiency or mycotoxin contamination of

In a swine producer smvey in the USA,
food should be addressed.

CNS and meningitis problems were

Iron toxicosis in piglets ( see p 3077) after considered the second most frequent cause
irtjection with iron preparations soon after
of death in weaned pigs, r�presenting
birth may be associated with muscle fiber

13o/1r-19% of losses. In this survey, Strepto
fragility, especially if there is a selenium
coccus siiis meningitis, Glasser's disease, deficiency in the sow and, therefore, the
and edema disease, respectively, were
piglet. Inadequate hygiene or technique
perceived to cause illness or death in one or
when baby pigs ai·e ir\jected with ai1 iron
more pigs in 50"/o, 17%, and 9% of surveyed
preparation can lead to bruising and septic
herds.

myositis. This problem can be resolved by
adequate training of fai-rowing room staff.

Infectious Arthritis or Polyarthritis:

Causes of polyarthritis in this group of pigs

Neurologic Disorders: Meningoencephusually includeMycoplasma hyorhinis, alocoele and cerebellar hypoplasia interfere flaemophiliis parasiiis, S siti,S, or Erysip
with locomotion in affected pigs, as can
elothri.x rhiisiopathiae, and less conunonly infections with Listeria monocytogenes

Streptococcus dysgalactiae subsp eqiiisimi
and Streptococcus siiis. Thus, S siiis can lis, Actinobacilliis eqmtli subsp eqiiiili, and cause locomotion problems as a result of
other bacteria prone to achieve bacterernia
meningitis and neurologic signs, or a

The bi.Ith canal and upper respiratory tract of
suppurative arthritis can be the primary
the sow are often the sources of the

LAMENESS IN PIGS

1159
organisms for the baby pig, which becomes
have developed. The initial, exudative
infected in the farrowing room. M hyorhinis
response is usually serous or serofibrinous
and H parasuis circulation in the sow herd
with a mycoplasmal infection; however, it is
can be predictive of infection levels in
fibri.nous or fibrinopurulent with G lasser's

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growing pigs. Alternatively, older pigs act as
disease. Hence, M hyorhinis causes a mild
caniers and are a source of infection for their
synovitis with villous hypertrophy and
peers. Pigs affected by E rhusiopathiae also hyperplasia; an excess of clear, yellow,
shed organisms in their feces and urine.

or brown synovia; and a serofibrinous

Essentially, all are systemic diseases with a
pericarditis, pleuri.tis, and peritonitis.

septicemic phase, and each may manifest

Otitis media has also been reported. With
as different clinical syndromes or as a mix

H parasuis, a fibri.nopurulent synovitis
of clinical signs.

with periarticular edema, polyserositis

As with many infectious diseases,
with pseudomembranes, and sometimes
management or environmental factors
fibri.nopwlllent meningitis are seen. The
that stress the pig or depress the immune
articular surfaces are usually unaffected
response can precipitate systemic disease
in either condition.

or an infectious arthritis. Moving and mixing

Diagnosis is based on clinical signs,
pigs (particularly if all-in, all-out managenecropsy findings, and detection of the ment is not used); overcrowding; cold,
organism. PCR tests are available to detect
damp, poorly ventilated, or cold, drafty

M hyorhinis and H parasuis. This is environments; and changing rations are all
in.1portant, because bacterial culture of both
major stresses that can lead to development
bacteria can be challenging if any treatment
of infectious arthritides or neurologic
has been instituted or if the pig has been
diseases that affect movement. It is also
dead more than a few hours. Treatment for
likely that active viral infections associated
either disease must be aggressive and start
with porcine reproductive and respiratory
soon after the onset of clinical signs if it is to
syndrome virus ( see p 729) or circovirus
be effective. The effectiveness of treating
may predispose groups of nursery pigs to

M hyorhinis infections with tylosin,
bacterial polyarthri.tis.

tetracycline, or lincomycin has been

Initially, shifting-leg lameness occurs, and variable. Organisms may be susceptible in joints can be warm, swollen, and painful. If
vitro and resistant in vivo. Treatment of
pigs are febrile, they may have no interest in

Glasser's disease is discussed in the relestanding and become inappetent. Chronic vant chapter (seep 720). With chronicity,
forn1s of polyarthri.tis with polyserositis
success in treating either disease is wilikely.

result in unthri.fty, runt pigs and, in the case

Appropriate changes in management to
of chronic erysipelas (seep 1160), mnt pigs reduce stress, strict all-in/all-out housing, and
may he lame with hard, swollen joints.

control of viral infections should all minin.1ize

The clinical signs seen in infections
the inlpact of Glasser's disease. Herds that
caused by M hyorhinis and H para.suis
maintain an SPF status may be free of both

(Glasser's disease, seep 720) are sin.mar,

M hyorhinis and H parasuis, but in herds because both cause painful polyartluitis
with documented outbreaks of Glasser's
and polyserositis. The conditions carmot be
disease, morbidity and mortality were high
differentiated grossly at necropsy. Infection
and productivity was decreased. Some 15
with M hyorhinis usually results in
serovars of H parasuis have been identified, lameness with moderate morbidity and
with much strain variation. Vaccination with
low mortality, but H parasuis can cause
conunercial or autogenous H parasuis
infection in 500/o--75% of pigs and mortality
bacteri.n may alleviate clinical disease in SPF
of up to 100/o. Outbreaks of Glasser's disease
herds. It is important to vaccinate SPF pigs
have been particularly severe in SPF and
that ai·e to be shipped to conventional herds
other naive herds. H parasuis may also play with vaccine effective against the serovars a part as a primary or concomitant agent in
present in the recipient herd. There is
swine respiratory disease complex and
cross-protection among some serovars.

cause disease in association with porcine

Vaccination of sows againstH parasuis
reproductive and respiratory syndrome
reduces the prevalence of the problem in
virus or influenza virus. Fever is associated
nursery pigs through passive in.UTiunity.

with mycoplasmosis but can be highest in

Glasser's disease (>107°F [41.7°C]) as pigs

Streptococcosis: The streptococcal
become anorexic and lan1e; sometimes
disease of main concern to the pig industry

H parasuis causes neurologic signs.

is caused by S suis (seep 731). Although

At necropsy, polyarthri.tis and polyserosithis organism can cause arthritis, CNS signs tis are seen with both mycoplasma infection and pneumonia are the most common and Glasser's disease, and pneumonia may
clinical presentations.

1160

LAMENESS IN PIGS

Erysipelas: Although acute erysipelas
and pigs exhibit pain in major joints ( eg,
can be seen in nursery pigs, it may be more
elbows, stifles, and hocks) that may develop
typical of growing/finishing pigs (seep 1160).

soft, fluctuant swellings. On necropsy,

If the acute form of the disease affects
lesions are restricted to the joints,

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nursery pigs and is not treated appropriespecially the stifles, and include an excess ately, the subsequent progression of the
of clear, yellow synovial fluid that may have
disease to the chronic form is seen in the
fibrin flakes, and yellow synovium with
grower/finisher pigs. Adequate vaccination
obvious villous hypertrophy. Articular
protocols are essential to controlling
surfaces and periarticular tissues usually
erysipelas. (See also SWINE ERYSIPELAS, p 626.) ai.·e unaffected. M hyosynoviae has been
isolated at slaughter or necropsy in pigs

Vertebral Deformities: Kyphosis or
with degenerative joint disease that is part
lorclosis and cuneiform deformities of
of the osteochondrosis syndrome, but it is
vertebrae have been seen in weaned pigs.

a secondai.y rather than a causal agent.

The condition has been reproduced

Diagnosis is based on the age of onset of
experiment.ally using gestation and nursery
clinical disease and clinical signs, including
diets deficient in calcium, phosphorus, and
lai.neness in one or more legs that may be
vitamin D. "Humpy back" pigs are seen
accompanied by fluctuating swelling and
sporadically in some herds; the spine is
puffiness around joints. Typically, pigs are
curved in the vertical plane such that the
afebrile and there is no evidence of
lwnbar vertebrae are higher than the
pneumonia, pleuritis, and peritonitis. If a
thoracic vertebrae, and there is a "kink"

definitive diagnosis is to be made based
between the two segments. Rickets is
on detection of the organism, sai.nples of
usually not seen clinically until the grower
synovium and synovial fluid should be
phase, but lesions must be initiated earlier,
collected from untreated pigs within
giving time for typical pathologic changes

3-4 clays of the onset of clinical signs.

to develop by -10 wk of age.

However, M hyosynoviae can be cultured
from healthy joints and is not always
recovered from affected joints.

PIGS IN GROWER/FINISHER

Lack of a response to penicillin in acute

AREAS
cases has been used to differentiate th.is
disease from erysipelas. Unlike polyarthritis

Lameness in pigs is of increasing interest
caused by M hyorhinis, response to
in North American swine production.

treatment with tylosin and lincomycin

Mycoplasma hyosynoviae in particular has
is generally good if administered promptly,
received more attention due, in patt, to
and tiatnulin or tetracycline may be
more intensive diagnostic efforts. Metabolic
effective where allowed. Mycoplasmal
bone disease has also been an area of focus
arthritis may exacerbate clinical signs
as problems have arisen after more complex associated with degenerative joint disease fonnulations for gestation and grow-finish
and osteoarthrosis and vice versa.

diets.

Erysipelas: Erysipelothrix rhusiop

Arthritis: Arthritis caused by Mycoathiae, the cause of erysipelas, is acquired plasma hyosynoviae and Erysipelothrix
from healthy carrier pigs or the environment,
rhusiopathiae emerge as important causes
in which the organism can survive for short
of lai.neness in pigs that have been moved to
periods. Erysipelas can be peracute, acute,
the grower/finisher areas. Again, mixing and or chronic. In the peracute form, pigs die moving groups of pigs; overcrowding; cold,
without clinical signs. In the acute form, pigs
drafty environments; or changes in
become febrile and may be lethargic and
management and feed may precipitate
anorectic and unwilling to rise because of
outbreaks of lai.neness.

pa.infuljoints and cyanosis of the extremi

In the case of M hyosynoviae, the upper
ties; the latter is associated with vasculitis in
respiratory tract of sows and older pigs in
peripheral vessels. After 2-3 days, the classic
peer groups is the likely source. As colostral

"dian1ond" skin lesions (focal urticaria)

immunity wanes at 4-8 wk of age, pigs
develop over the body surface. In some
become susceptible to infection. Generally,
outbreaks, lai.neness is seen without the
morbidity is low to moderate, but up to 500A,
skin lesions. In the chronic form, arthritis
of pigs may be affected; mortality is very
progresses such that the stifles and hocks
low. An acute lai.neness, lasting up to 10
become swollen and feel finn on palpation;
days, develops in groups of grower/finisher
skin necrosis can result in extensive
pigs or selected replacement stock. Artluitis sloughing of portions of the integun1ent. In may be exacerbated by trauma or stress,
chronic cases, discospondylosis also may

LAMENESS IN PIGS

1161
develop if intervertebraljoints are affected.

Osteomyelitis: Osteomyelitis can be

As the arthritis progresses and joints fuse,
seen in pigs of any age. If the integument is pain in the lumbar vertebrae may reduce
damaged, sepsis develops and a suppurative
boar libido. Cyanosis in the extremities in
lesion extends to ilie periosteun1 and bone.

chronic cases may be related to heart valve

Alternatively, organisms can invade bone

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failure. A presumptive diagnosis of acute
from the synoviwn of infected joints. Poor
disease is based on the clinical signs, of
processing or iJtjection techniques can
which the "diamond" skin lesions are most
initiate abscesses that can extend into
consistently useful. All three fom1s of the
adjacent bone. Disruption of the integrity
disease may be seen in the same herd if the
of the hoof wall initiates cellulitis and
problem has not been investigated and
osteomyelitis of a phalangeal bone. Ear
treatment has been delayed.

and flank biting wounds are other foci of

If the chronic fonn of erysipelas is
infection. Tail biting can result in local
investigated as a lameness problem and pigs infections that ascend the spinal canal and are necropsied, early changes in the disease
lead to epidural abscesses iliat can invade
process will have subsided ( eg, hemorand affect vertebral bodies. Lesions and rhages in lymph nodes, kidneys, and
clinical signs may develop slowly.

muscles). An excess of synovial fluid

Depending on ilie site of infection, the
accumulates during the acute phase, but in
pig may become ataxic and, ultimately,
chronically affected joints, there is villous
paralyzed in tl1e pelvic limbs. If bones or
hypertrophy and hyperplasia, hyperemia,
joints of a limb ai·e affected, the condition
and pe1iarticular fibrosis. If pannus has
is usually chronic and the pig becomes
formed, ilie aiticular surface becomes
three-legged lame. Young pigs cease to grow.

disrupted. Raised, focal skin lesions

At necropsy, creain or green caseous pus
progress to sloughed areas and, in extreme
is seen at ilie site of the lesion. If T,uecases, ilie ears and tail may have sloughed.

perella pyogenes is involved, there ai·e

Vegetative, valvular endocarditis is another
abundant pockets of green, semiliquid pus.

finding.

Other organisms isolated from these

Isolation of the causal organism is
abscesses may include streptococci,
important for a definitive diagnosis and
staphylococci, and enterobacte1ia.

is most successful if acutely affected,

Treatment is not usually feasible, and pigs
untreated pigs are necropsied and joint fluid
should be culled for humane reasons.

is cultured. PCR testing of chronic lesions

However, when applicable, hygiene can be

( eg, endocarditis) can be used to detect
in1proved, and problems such as tail biting
the bacteria in chronic cases. A bacterial
controlled or prevented.

culture with an antibiotic sensitivity profile
is useful during treatment of the herd.

Osteochondrosis and Osteoarthrosis:

Sometimes, a rapid response of the acute

Lameness associated witl1 these problems
condition to penicillin is a diagnostic aid.

may become clinically relevant by ilie tin1e

Provided ilie E rhitsiopathiae is sensitive t11e pigs are 4---6 mo old, but the major ranufito penicillin, this may still be an economic cations are in gilts, sows, and boars (see
choice for treatments. However, tylosin and
p 1158). Because there is a hereditary
lincomycin are also labeled for treatment of
component, ilie importance of these
erysipelas, and tetracycline may be
problems increases if affected replacement
successful if the organism is susceptible.

breeding stock is brought into a herd tl1at

Vaccination with either modified-live or
was previously free of eitl1er condition.

killed orgaJ1isms effectively controls
erysipelas in a herd, and outbreaks may be

Rickets: Although now uncommon, rickets
related to noncompliance witl1 vaccination

( see p 1051) is occasionally seen, usually protocols rather than to changes in the
associated with a feed formulation or mixing
virulence of the causal organism or the
error. Rickets affects rapidly growing, young
nature of the disease. Therefore, any
pigs with a clinical onset at -10 wk of age.

investigation of the problem should begin

Morbidity is high, and affected pigs become
with a detailed vaccination history to ensure crippled, anorectic, and unthlifty. Limbs are that sows are regularly vaccinated. Even
stunted and bowed,joints are swollen, and
with sow vaccination, infection is seen in
ilie head may seem disproportionately large.

grower/finisher pigs in some herds. On

Long bones of the limbs can spontaneously
these farms, growers must be vaccinated
fracture so that the pig becomes severely
in addition to ilie sows. In tl1e face of an
lame and unwilling to move. Ribs may
outbreak, concurrent use of killed vaccine
fracture. Some pigs develop poste1ior
and antibiotic is likely to be the most
pai·esis and sit on the ground if vertebral
effective control measure (seep 626).

bodies fracture and damage the spinal cord.

1162

LAMENESS IN PIGS

Absolute deficiencies of calcium,
makes hoof walls susceptible to cracking;
phosphorus, or vitamin D, or an imbalance
flaky skin accompanies hoof lesion and
of the calcium:phosphorus ratio causes
t11ere is generally poor reproductive
cessation of mineralization at the metaphyperformance in tile herd. As gilts are prepared sis and thickening of the growth plate and
for breeding, supplementing biotin may be

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epiphyseal growth cartilage.

helpful. Recommended inclusion rates of

On necropsy, bones should be dissected
biotin are 250-400 mcg/kg complete feed.

to determine whether there are any

Trace mineral deficiencies or in1balances
fractures or healing fractures, particularly
can also contribute to compromised hoof
in the ribs, humeruses, and femurs. The
wall and heel epidermis fo1mation.

costochondral junctions of most ribs are

Seleniwn toxicosis can cause coronary
enlarged to forn1 a rachitic rosary, and ribs
band swelling and necrosis in addition to
may bend with moderate manual force.

more generalized signs such as anorexia or

Bone remodeling is inadequate and,
even paralysis (seep 3085). Selenium and
radiographically, long bones and ribs are
ergot toxicity can result in hoof sloughing in
poorly mineralized. Failure of calcification
pigs.

and endochondral ossification results in
thickened, irregular growth plates and

Nutritional Myopathy (White
epiphyseal growth caitilages in which

Muscle Disease): In contemporary
hemorrhages may be seen grossly if slab
systems with adequate ration preparation
sections of the ends of long bones are cut
and storage, nutritional myopathy should
on a band saw. In chronic cases, bones can
not be problematic (seep 1174). Altl1ough
be cut with a knife. A sudden increase in
unexpected deaths are typical of seleniun1
cai·cass condemnations or paitial condemand/or vitamin E deficiency, sometimes pigs nations because of fractured limb bones,
are found recwnbent and unable to rise and
ribs, or vertebrae at slaughter should trigger
walk. At necropsy, a variety of pathologic
investigation of rations and their ability to
changes may be seen, including pale muscle
meet the nutritional needs of growing pigs,
masses, epicai·dial hemorrhages (mulberry
particularly with some of the fast-growing,
heart disease), and a pale, scan·ed liver with
lean contemporary hybrids. Ration analysis
an uneven surface (hepatosis dietetica).

is useful, but ctrrrent batches of feed may

Prevention includes supplementation
have been mixed correctly or with different
with selenite so that the total ration
lots of ingredients, thus making it difficult
concentration is 0.3 ppm selenium. lithe
to relate cause and effect. Keeping frozen
condition is diagnosed in a batch of pigs,
samples of each batch of feed for retrospecinjectable seleniwn/vitainin E can be given tive analysis is a good practice.

as a stopgap measure until supplemented

Although rations can be corrected and
feed is part of the nutrition prograin.

vitainin D given parenterally, thel"e is no
effective treatment, and attempts to reai·

BREEDING GILTS, SOWS, AND
large numbers of affected pigs have been
economically disastrous. Culling affected

BOARS
pigs may thus be the most cost-effecti\'e

After reproductive failure, lameness is
alternative.

typically the most important reason for
removal of breeding stock from tile herd.

Foot Disorders: On occasion, grower/

Lameness in breeding swine can result in
finisher pigs have overgrown claws or
the following: 1) higher rate of breeaing
bruises and cracks in the wall or sole of the
stock replacement with attendant increased
hoof. The floor type and condition is perhaps
risk of disease introduction; 2) an inability
the single greatest factor in detern1ining
to maintain a breeding schedule due to an
whether lesions develop or resolve. Floors
wu-eliable pool of breeding pigs and,
with wide slots enable digits to fall between
ultimately, an impact on pig flow in the
tile slats, causing damage. Floors kept too
grower/finisher area; 3) increased cost of
wet can soften tile hoof wall, making tllem
maintaining additional breeding stock;
more prone to trauma. Utile floor is too

4) poorer reproductive perforn1ance due to
smooth, the balance between growth and
regular replacement of la.me sows witll gilts;
wear of the horn is lost; if it is too rough, tile

5) poorer growth and feed efficiency in
hoof wall, coronary band, or skin above the
progeny pigs due to a higher proportion
hoof is damaged so tllat infectious agents
of pigs produced by first-parity sows;
can penetrate tile foot or adjacentjoints,

6) reduced pigs born alive because of higher
resulting in abscess forn1ation.

stillborn rates in lan1e sows and reduced

An absolute or intermittent deficiency
subsequent litter size due to poor lactation
of biotin results in weak, flaky keratin that
feed intake; 7) increased preweaning

LAMENESS IN PIGS

1163
mortality due to clumsy, lame sows that
established bone loses mineral and mass
tread or lie on baby pigs; 8) reduced
by a process of osteolysis, a different
weaning weights of pigs due to reduced feed
pathogenesis from that of either rickets
intake of sows in lactation; 9) reduced
or osteomalacia.

salvage value of cull sows due to increased

Gilts that have normal skeletal develop

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lactation weight loss and sow mortality; and
ment and are selected as breeding stock

10) reduced fertility in sound boars that are
must continue to have their nutritional
overworked while others are lan1e or being
needs met, both for their own growing
replaced. In sum, the impact of breeding
skeleton and, once pregnant, that of the
herd lan1eness on the biologic and economic
growing fetuses. This may precipitate as
perfom1ance of a f3.1.m can be substantial.

osteomalacia if amounts of calcium,

Many diseases that affect grower/finisher
phosphorus, or vitan1in Dare inadequate or,
pigs (seep 1160) can also affect young gilts in the case of the minerals, inappropriately
and boars selected as breeding stock.

balanced. The problem is fw-ther com

Arthritis caused by Mycoplasma hyosyno
pounded once the sow farrows, due
viae or acute or chronic erysipelas can
to secretion of calciwn in the milk. A
cause an incapacitating lameness. Polyfirst-parity sow may soon draw on her artlu·itis and polyserositis caused by
skeletal reserves and become osteoporotic.

M hyorhinis 3.1.·e seen occasionally in these Because sows C3.ll become pregnant within
older pigs. Susceptible, stressed adult

7 days of we3.11ing, there is little time for
pigs can succw11b to M hyorhinis with a
recovery of skeletal mass between one
higher fever and a more severe l3.111eness
breeding cycle and the next, so the skeleton
than is seen in nw-sery pigs. Likewise,
becomes progressively weaker. Lin1ited

Haemophilus parasuis can develop as an
exercise may also exacerbate calciun1
acute epidemic disease in gilts sow-ced from mobilization and bone loss. Consequently, herds free of the bacteria after entering a
in sows late in gestation, dw-ing lactation,
herd endemically infected. High morbidity
or soon after we3l1ing, bones that have
and even mortality that is quite refractory
become weak are susceptible to fractures. It
to treatment can result.

is not sw-prising that considerable nwnbers

If 1ickets or skeletal wealrness was a
of first- and second-litter sows are culled
problem in the growing phase, pigs that
because of fractures and 13.1.neness.

could have been affected should not be

Factors that may lead to bone fractures
retained as breeding stock. Ambulation
include entrapment of a limb in or under the
should be assessed as a component of
bars of a farrowing crate, activity as sows
breeding stock selection. Pigs with
are moved from their farrowing crates, and
conformational abnormalities of their limbs
fighting as new groups of weaned sows
or restricted or abnormal 3.1.nbulation
reestablish a social order in the breeding or
should be culled. Feet should be evaluated
gestation 3.1.·ea in group housing conditions.

for uniformity 3.1.nong and angulation of the

Sows mounted by other sows that are in
digits and for integrity of the wall, sole,
estrus are also prone to injury. The most
and heel. If any problems are identified,
frequent sites of fractures are femurs,
including abnormal traits such as overhwneruses, lwnbar vertebrae, and growth of the major or secondary digits
occasionally ribs. Whatever the factors that
in a particular line of pigs, these pigs also
precipitate the fractures, affected sows are
should be culled.

in pain and are either severely 13.1.ne and
unwilling to move or paraplegic.

Rickets, Osteomalacia, and Osteopo

Diagnosis is based on a histo1y of acute
rosis: These syndromes can affect older
lameness or paraplegia in pregnant,
age groups of pigs, with various clinical
lactating, or recently weaned gilts or sows.

outcomes. Most pigs, including breeding

Sometimes, crepitus can be detected in
stock, are slaughtered before their skeleton
affected limbs. A neurologic examination
has fully matw-ed; some growth plates are
can help locate spinal lesions if a sow is
functional up to 3.5 yr of age and, therefore,
paralyzed in the pelvic lin1bs. Affected sows
are susceptible to rachitic or other changes.

should be culled or euthanized after an early

Osteomalacia is characterized by an
diagnosis. Prevention through adequate
excess of unmineralized or poorly
nutrition and exercise for gilts and sows
mineralized osteoid that forms as bone
curtails the problem.

remodeling occw-s ( or does not occur).

Hence, osteomalacia is the component of

Osteomyelitis and Spinal Abscesses:

rickets (seep 1161) that affects the growth In addition to the causes discussed under
plate and is described in younger pigs. In
grower/finisher pigs, osteomyelitis may also
contrast, osteoporosis develops when
develop secondary to a vertebral fracture or

1164

LAMENESS IN PIGS
an epiphyseal separation. It is reasonable to
cial hybrid pigs. Dyschondroplasia results
assume that occasional "showering" with
in deformed long bones, particularly the
organisms from superficial wounds,
ulna. Pigs that have valgus deformity or
abscesses, or the respiratory or GI tracts
pem1anently flexed carpi tend to be
can be a source of infection. True'J)erella
unsuitable for sale as breeding stock and

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pyogenes seems to be a frequent cause
may be lame. In addition, epiphyseolysis
of the suppuration and abscessation.

and epiphyseal separation may be

Osteomyelitis of the ulnar epiphysis in
precipitated by weakening of underlying
young boars and sows has been reported.

growth plates and cause an incapacitating

Vertebral osteomyelitis and epidural
lameness.

abscesses can cause a variety of signs,

Although lesions that precede or develop
including nonspecific lameness, hypermeinto DJD or result in limb defonnities begin tria, ataxia, or bilateral flaccid paralysis of
to develop in younger pigs, clinical
the pelvic lin1bs. Except for the temporal
problems are not usually seen until pigs
nature of the infectious process, clinically it
are >4-8 mo old. Frequently, the fastest
is difficult to differentiate a destructive or
growing, most muscular, and heaviest pigs
space-occupying abscess from a fracture.

are affected. Given time, some pigs (if not

Regardless of underlying cause, recovery is
culled) recover from episodes of lameness,
unlikely, and the pigs should be culled.

but defonnities remain. Clinical signs vary
with the site and extent of lesions and can

Osteochondrosis and Leg Weakness
range from stiffness and a shortened stride

Syndrome (Degenerative Joint
or a stride affected by an angular lin1b

Disease, Dyschondroplasia):

defonnity to a three-legged lameness or an

Degenerative joint disease (DJD) and leg
inability to stand. Most commonly, tl1ese
weakness syndrome are generic tem1s for a
animals have a weight-bearing, shifting
clinical syndrome that is a major cause of
lameness because of bilateral lesions that
lameness and culling for lan1eness in swine
affect multiple joints in the same pig. Pigs
breeding stock. Although the conditions are
that "walk" on flexed carpi usually have
more often investigated in purebred stock,
severe DJD in the elbows, and pigs that tuck
they can cause major losses in commercial
their pelvic limbs under their abdomen in a
pig herds. Given the increased scale of
stance that resembles a "circus elephant
production in many herds and the shift
balancing on a ball" often have DJD that
toward pigs that grow faster, are more
affects stifles, tibial tarsal bones, or joints
muscular, and finish heavier, DJD and leg
on intervertebral processes.

weakness are critical issues.

If epiphyseal separation of the femoral

Osteochondrosis is a specific develophead has occurred, the pig has difficulty mental condition that represents the major
standing and initially will not use the
cause of DJD. Osteochondrosis is a defect in affected limb. A pig t11at has unilateral the development of cartilage of the growth
separation of the ischiatic tuberosity also
plates or articular cartilage in growing pigs.

has difficulty standing and a tendency to

The pathogenesis of osteochondrosis
slip; if both tuberosities are affected, the pig
is increasingly but still incompletely
has a hopping gait for a few steps after being
understood. In osteochondrosis, growth
lifted and then collapses. The severity of
plates are more prone to fracture because of clinical signs in any of these conditions areas of retained hypertrophic cartilage that
varies, and joints with less extensive lesions
focally thicken and weaken the cartilage.

appear to be protected by the gait if they are

Lesions develop when articular cartilage
more painful than other degenerating joints.

on the interior aspect of the joint surface

Severe joint lesions also have been seen in
becomes necrotic, ostensibly due to loss of
pigs that did not appear to be lame.

vascular supplies. The necrotic cartilage

In pigs that have limb defonnities ( eg,
interferes with the advancing ossification
dyschondroplasia affecting the distal ulnar
front, and the resulting irregular ossification
growth plate), thickened, irregular growth
underlying the weight-bearing cartilage
plates are seen on radiographs or at
surfaces is prone to clefting ( displaced
necropsy. In degenerating joints, there is an
cartilage "chips," or osteochondrosis
excess of yellow synovia, and synovial villi
dissecans), exposing the endochondral
may have proliferated. There are various
bone and causing pain and lameness. The
irregularities of the articular surface,
developmental lesions have a very high
including folds in the cartilage, clefts into
prevalence in young pigs but mostly resolve
the cartilage, flaps of cartilage, and in severe
with age and further development.

cases, craters and exposed subchondral

Osteochondrosis is apparently seen in all
bone. In chronic cases, osteophytes
the major breeds of purebred and comme1°
develop, detached fragments of cartilage

LAMENESS IN PIGS

1165
become embedded in the synovium and
skeleton, housing gilts in pens with �12 sq
start to ossify, and craters fill with
ft (1.1 sq m) per animal, and promoting
fibrocartilage. If vertebral joints are
exercise on nonslip floors. In problem
affected, vertebrae eventually fuse. Growth
herds, providing a "hardening off' period for
plates that are most severely affected by
gilts is encouraged. This includes purchas

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dyschondroplasia are those of the distal
ing gilts at <75 kg live weight, restricting
pa.it of the ulna and the ribs, whereas joints
their feed intake to slow their growth rate,
most often affected by DJD include the
providing � 1.1 sq rn per animal in pens with
elbow, stifle, and hock, or the intervertebral
solid or only paitially slatted floors, waiting
synovial joints.

to breed gilts w1til they are 8-10 mo old, and

Many potential causes of DJD or
housing gilts in pens until they fan-ow. If
osteochondrosis have been investigated.

replacements are purchased, suitable breed

There is evidence of a genetic component,
ing stock must be found and inferior pigs
because wiLhin breeds, specific boars have
rejected at the time of arrival at the farm.

been identified to have progeny with a
higher incidence of osteochondrosis.

Foot Disorders: Foot lesions can be quite

Breeds and lines of pigs that are heavy and
prevalent and severe among sows and boars
well muscled, particularly in the hams, are
and have been shown to cause laineness
commonly affected; therefore, crossbreedand reduce productivity and longevity of ing for hybrid vigor (ie, to create faster
breeding stock. Specific lesions paiticularly
growing, muscular hybrids) does not solve
associated with lameness include white line
the problem. The fastest growing pigs in a
lesions, heel-sole cracks, and heel overgroup seem to have a greater propensity for growth with erosions, but any of the lesions
lesions to develop in either growth plates or
can be significant in individual cases.

joints, but once slower-growing pigs reach

As with finishing pigs, floor type and
the body weight of their faster-growing
condition are important with respect to
peers, lesions ai·e comparable. Growth
lesion development. Housing type and
hon11one may affect chondrocyte metabomanagement are also important risk factors lism and thereby influence the onset of
for various types of foot lesions. Nutiition,
aiticulai· lesions.

including water quality, can affect the

Research into manipulating the energy,
growth rate and quality of the horn wall
protein, and mineral concentrations of
and heel epitheliw11.

the ration in an attempt to influence the

Bacterial inl'ections of the foot can
development of lesions has been inconcludevelop in any age pig but cause serious sive, even contradictory. None of the
losses in breeding pigs. Bacterial infections
imbalances or deficiencies of nutrients that
are often a sequelae of foot lesions that
typically are associated with lesions of
allow penetration of bacte1ia into underlycartilage or bone ( calcium, phosphorus, and ing sensitive foot structures. Foot infections vitamins A, C, and D) seemed to exacerbate
are seen in both confinement and semiconosteochondrosis. Deficient or excess zinc finement systems, with morbidity of
and manganese may be causal factors in

20%-68%. Often a single lin1b is affected,
osteochondrosis, but there is a paucity of
and the lameness progresses to the point
evidence from research.

that the pig is three-legged lame.

The stress of mixing pigs appears to have

Lesions usually develop gradually, and
little impact on the frequency of osteochonthe foot becomes swollen. Lesions vary in drosis, but trauma from handlil1g or housing
severity and can include heel erosions, sepaconditions have been found to affect clinical ration along the white line, toe erosions, osteochondrosis. The culling rate due to
sole erosions, vertical hoof wall cracks,
lai11eness for sows kept on solid floors is
deep necrotic ulcers, sinuses at the
less thai.1 that for those kept on slats, but the
coronary band, and chronic fibrosis. A mix
benefits of placing pigs with DJD on dirt lots
of organisms has been isolated from the
or pasture is equivocal. Although such pigs
lesions or identified in smears from lesions
usually become clinically sound within 6
and tissue sections. These included
wk, they are potential carriers of the

Trueperella pyogenes, Fusobaclerium
syndromes.

necrophorum, Borrelia suilla, and a

Because osteochondrosis and DJD
mixture of gram-negative and gram-positive
interfere with production efficiency, the
cocci and rods.

prognosis for affected pigs is poor. At best,

A diagnosis is made from the clinical
the following practices are recommended:

signs and a thorough evaluation of the feet.

selecting against replacement pigs that are

Ideally, the whole foot should be exan1ined
lame or have poor confom1ation, providing
in a recumbent or suitably restrained pig.

adequate rations for the growth of a strong

If there is a herd problem, all sows in crates

1166

LAMENESS IN PIGS
or pens should be examined. Whenever
muscle tendons and a proliferative osteitis
possible, feet of pigs from affected herds
on the medial hwneral epicondyle and the
should be evaluated at the slaughterhouse.

greater trochanter of the femur in sows.

Superficial examination of some less

Mixing gilts or sows before or after breeding
extensive lesions may lead to inappropriate
or at weaning conm1only results in pigs

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cause-effect conclusions. Therefore, to
becoming injured as they reestablish a
ensure that lesions are severe enough to be
social order. This can lead directly to
the cause of the lameness, some pigs can be
fractures of long bones or skin abrasions
culled for diagnosis of the problem and their tllat may cause secondary bacterial feet sectioned or claws removed after
infections.

immersing the foot in l 40°F water for 60

Traumatic injuries can also result from
min to determine whether the soft tissues
movement of groups to and from farrowing
and bones within the foot are infected.

facilities, especially movements of gilts into

Treatment of apparent foot infections
farrowing. Gilts typically are more anxious
with penicillin has been conm1only
and flighty than older sows. Carrying a
practiced (200,000 U into the lesion or
heavy, gravid uterus over potentially

600,000 U, IM), but effectiveness has not
slippery flooring over some distance poses
been proved and success decreases with
a high enough risk of injury without adding
chronicity of the lesion. Prevention is a more
other stressors. Movement should be cairn
productive longtenn strategy, and it involves
and deliberate, with small groups of gilts
in1proving the nature and cleanliness of the
and sows moved at a tinle to reduce
flooring, reducing moisture, resurfacing
potential injuries.

rough, abrasive areas, and ensuring

Sows housed in stalls with concrete slats
nutritional adequacy for hoof health. As
may tear their dewclaws when they attempt
replacement gilts mature, biotin and trace
to stand. Treatment with appropriate
mineral supplementation enhances the
antibiotics, protection of the wound with a
quality and strength of the hoof, and use
dressing, and isolation in a hospital pen that
in breeding sows is recommended.

has clean, deep bedding should enable a
lesion to heal. Prevention by trimming

Trauma: Trauma associated with
elongated dewclaws is a prudent and sinlple
overexe1tion can cause detachment of
management practice.

· LAMENESS IN SHEEP

Lameness in sheep may be caliSed by a
splinted and will heal within 3 wk. However,
nwnber of systemic diseases, some of which
leaving the limb splinted and unobserved
include naveVjoint ill (Escherichia coli and for too long may also lead to iatrogenic

E1ysipelothrix), tetanus, white muscle
laineness. The general principles of
disease, frostbite, chlan1ydial polyaithritis,
treatment and prevention·of these are
rickets, enzootic ataxia ( copper deficiency),
the same as in other species.

mastitis, orchitis, nutritional osteodystro

Lameness can be caused by a group of
phies, seleniwn toxicosis, laminitis,
infections specific to the feet. The most
dermatophilosis, bluetongue, ulcerative
well known of these is contagious footrot,
dennatosis, and in some countries, foot-anda mixed infection with Fusobacterium moutll disease. Weakness, ataxia, and
necrophorum and the obligate pathogen
neurologic problems may be misinterpreted

Dicheloba.cter nodosus. The skin between
as lameness in diseases such as scrapie,
the claws is the primary site of invasion;
listeriosis, and visna. Additional information
it is predisposed to infection by breaks in
on differential diagnosis, treatment, and
the epidermis from injury or maceration
prevention can be found wider tile specific
from prolonged exposure to moisture.

topics (seep 1039 and p 1209).

F necrophorum and T,ueperella pyogenes

Lamenesses are often due to injuries.

induce a transient condition called

Broken legs are common in young lainbs,
ovine interdigital dermatitis or foot
which are frequently injured inadvertently
scald, which may lead to more serious
by adults. Usually, tllese cari be easily
problems.

LAMENESS IN SHEEP

1167

INTERDIGITAL DERMATITIS
than in virulent footrot. The etiology and
pathogenesis are the san1e, but the strains

(Foot scald)

of D nodosus are less virulent and lack the Th
hoof-invasive properties of the strains that

_is necrotizing condition of the interdigital
skin usually precedes or accompanies
cause virulent footrot. D nodosus may also

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footrot. In Australia, it is considered to be
be isolated from cattle, but strains affecting
caused by less virulent strains of Dichelo
cattle usually cause only the benign form of
bacter nodosus and is termed benign
footrot in sheep. The economic effect of
footrot (see below). Wet weather, damp
benign footrot is much less than that of
pastures, and mud are predisposing factors.

virnlent footrot. Running the sheep through

In milder cases, the interdigital skin is red
foot baths containing l()OA, w/v zinc sulfate
hairless, swollen, and moist. In severely
once every 14 days during the wet season is
affected cases, the integrity of the interusually adequate for control. Since the digital skin is compromised, exposing
advent of long-acting antibiotics such as
subcutaneous tissues. Suppuration and
tetracycline, their use has been adopted
swelling of the deeper interdigital tissues
with good results.

may develop. Lameness can affect as many
as 9()0A, of sheep, and all four feet may be

Virulent Footrot
affected. The characteristic smell associated with virnlent D nodosits infections is Virulent footrot is a specific chronic
not present if D nodosus is not present.

necrotizing disease of the e�idermis �f the

Healing is rapid when conditions dry out,
interdigital skin and hoof matJ.ix that begins
but the disease may recur when conditions
as an mterdig1tal dem1atitis and extends
again become wet.

to involve large areas of the hoof matrix.

Because scald usually precedes a footrot

Because the sensitive lamina and its
outbreak, it is prudent to treat the condition
network of capillaries are destroyed by the
as if it were footrot. Other diseases to coninfect10n, the hoof wall (corium) loses its sider in the differential diagnosis include
blood supply and anchorage to the
dem1atophilosis (strawberry footrot, see
underlying tissue and becomes detached.

p 858), which affects the hairy skin of the

Footrot is extremely contagious and, under
coronet and pastern. Viral diseases such as
suitable conditions and susceptible
ulcerative demmtitis, contagious ecthyma,
genetics, morbidity may approach 10()0.A,.

and foot-and-mouth disease may be

The infection is also rarely found in goats,
exclud
deer, and cattle. The potential for genetic

�d by flock history, clinical signs, electron nucroscopy, and serology. Currently, selection for increased resistance to footrot
the treatment of choice consists of external
has been established.

application of l()OA, w/v zinc sulfate
disinfectants via a footbath or aerosol.

Etiology: Fusobacterium necrophorum,
a gran1-negat1ve anaerobic bacteria, is a

CONTAGIOUS FOOTROT
normal resident of manure-contaminated
environments. Under favorable environ

When there is concurrent invasion by
mental conditions, it colonizes the moist

Dichelobacternodosus of foot scald
macerated interdigital skin and provides'

contagious footrot results. The Australians
ideal conditions for invasion by D nodosus
separate footrot into two categories, benign
at tl1e skin/hoof interface. By action of
or virulent, depending on the strain of
proteases, D nodosus, also a gran1-negative D nodosus present. In tl1e USA however
anaerobe and obligate pathogen, liquefies
benign and virulent footrot are 'consider�d to
the cells of the stratun1 granulosun1 and
be the same ( due to the difficulty of differentistratum spinoswn, causing the separation of ating the two) and are treated accordingly.

tl1e hoof wall from the basal epitheliun1. It
works its way down the interdigital horn to

Benign Footrot
the heel, then to tl1e sole, and finally to the
lateral side of tl1e hoof. D nodosus has been The infection is confined largely to the
found to survive <3 wk outside the host but
interdigital skin, with only minimal
it can remain sequestered in cavities
underrunning of the adjacent horn.

cracks, or defomlities of the affected foot

Clinically, benign footrot appears similar to
for the life of the sheep. There are at least 20
ovine interdigital dern1atitis, butD nodosus
different strains of D nodosus, with varying is involved-a situation that is hard to assess pathogenicity. Transmission occurs most because culture of D nodosus is difficult and rapidly when conditions are wam1 and rarely done. The odor, however is charactermoist; however, cold, moist conditions istic. Lan1eness is common but iess severe
are also conducive to transmission.

1168

LAMENESS IN SHEEP

Clinical Findings: The most obvious sign
times, eg, during a wet season, temporary
is lameness, but the foot is seldom carried
control may be the only realistic goal.

or packed. In chronically infected sheep, the

Traditionally, treatment consisted of foot
hoof becomes gnarled and distorted. When
bathing using antibacterial solutions after
more than one foot is infected, some sheep
careful hoof trimming to remove all dead

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become recumbent or walk on their knees.

horn and expose infected tissue and

Brisket and knees tend to become hairless
bacteria to air. However, foot soaking for
and ulcerated. Affected sheep do not

30-60 min has been shown to be more
compete well for food, lose body condition,
effective even when trimming is not done.

and produce less wool. Rams with infected

In fact, Australian research has shown that
hindfeet may be unwilling to breed, and
trinuning may do more damage than good.

ewes with hindfeet lesions may be unable

The most effective solution is J()OA, w/v zinc
to bear the weight of a ram at service.

sulfate with 0.2% v/v of law1dry detergent

In early cases, examination of the feet
containing nonionic surfactants such as
generally reveals nothing more than
sodiwn lauryl sulfate. Aerosol sprays have
interdigital dermatitis. In slightly more
been used in lieu of foot bathing and include
advanced cases, in which the infection has
zinc sulfate, tincture of iodine, teti·acycline,
begun to extend into the hoof mat1ix, there
copper sulfate, fonnalin, chlorine bleach,
is slight detachment of the hoof wall at the
and other disinfectants. However, sprays
interface of tl1e interdigital skin and hoof.

are not as effective as foot bathing or

As the disease progresses, the separation of
soaking in zinc sulfate.

the horn spreads further under the heel and

The advent of long-acting antibiotics used
sole. Running one's thwnb between the wall
in combination with topical foot treatments
and the underlying tissue in the interdigital
has improved recovery and reduced carrier
space often detaches the wall from the heel
animals. Parenteral treatinent using a
and sole, revealing a white, slightly moist
long-acting oxytetracycline at 13.6 mg/lb

(but not purulent), odorous substance.

gives a duration of effect in cattle of 7-8

Finally, the outer wall is affected. The horny
days and probably a similar duration of
hoof may eventually be attached only at the
effect in sheep. However, sheep must be
toe and the coronet on the lateral side of the
placed in a "clean" area (ie, one in which foot. The odor of the necrotic tissue is
no sheep have been kept for at least 3 wk)

characteristic and helps to diagnose the
or in a completely dry lot after they are rw1
disease. Myiasis is a conu11on sequela
tlu·ough a foot bath and given the antibiotic.

during fly season; it may extend to the area

Sheep will become reinfected as soon as the
of the sheep where the infected feet come
antibiotic is cleared if returned to a contamiinto contact with the body when the sheep nated envirorunent. The feet of treated
is recun1bent. The clinical disease persists
sheep should be exan1ined once a week to
until the environment dries or the sheep are
identify those not responding to treatinent.

treated. After apparent healing, D nodosus

Sheep that do not respond should be
remains hidden in small pockets within
isolated and preferably culled. D nodosus
the foot, where it is detectable only by
is extremely difficult to eradicate from
extensive tlimming, and becomes active
a.t1in1als that have relapsed nwnerous times.

again when moist conditions recur. These

Fwthermore, subclinical or relapsing cases
sheep are carriers and generally remain
take valuable time to handle, identify, and
infected for life. lJ.m11w1ity to footrot after
isolate, and tl1ey remain a source of
infection does not seem to occur, because
infection for other anin1als.

relapses are the norn1.

Prevention and Control: Animals from

Diagnosis: In flocks with virulent footrot,
unknown premises or auction houses
tmderrunning and separation of the hard
should not be purchased. Any sheep to be
horn of the hoof of one or more feet,
added to the flock should be quarantined
complete with tl1e characteristic odor, is
for several weeks to prevent the spread of
diagnostic. If the problem is discovered
footrot and other chronic diseases. During
early when interdigital dermatitis is the
the quai·antine period, the animal's feet
only sign, it should be assun1ed that the
should be lightly trinuned and exan1ined
condition is an early stage of contagious
closely for pockets and other malformafooti·ot, and treatinent should be initiated tions that suggest a previous D nodosus
immediately.

infection. Vehicles ( eg, trucks, trailers) or
facilities in which unknown or infected

Treatment: Treatment efforts may be
sheep have been held should be thoroughly
directed toward temporary control of the
cleaned and disinfected before placing
disease or total eradication. At certain
wunfected sheep in them. If it is not

LAMENESS IN SHEEP 1169
possible to thoroughly disinfect transport
when the environment is dry; at other tin1es,
vehicles, zinc sulfate can be liberally
treatments should be directed more toward
scattered over the floor to reduce viable
control of transmission. Affected sheep
bacteria.

have to be identified by close exanlination

Because the incubation period of footrot
of all four feet; no other diagnostic tests are

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is -14 days, foot bathing at 10-day intervals
available (although some exciting European
will control spread of the organism in
research using PCR and interdigital swab
affected flocks during periods of the year
samples is showing great promise as a
when the sheep are in wet conditions.

diagnostic tool). Subclinical cases

Footrot has been controlled by placing foot
constitute a major problem. They will
baths with l()OA, w/v zinc sulfate solution
relapse as soon as they are placed in wet
around water troughs, forcing sheep to walk conditions and the infection spreads rapidly.

through them and stand in order to drink.

Other runiinants (goats, deer, cattle) are

Lame sheep should be separated for
potential sources of D nodosus. lf they are treatment and not returned to the flock
in contact with the sheep, they should be
until all evidence of footrot is gone.

considered in the eradication program.

D nodosus vaccines accelerate healing

To begin, the feet of all sheep should be
in affected sheep and aid in protecting
trimmed and carefully examined. The flock
unaffected sheep. They are recommended
should then be divided into affected and
as an additional tool to control or eradicate
unaffected groups. Sheep with no visible
the disease. However, their effectiveness
lesions are foot bathed, isolated, and placed
depends on the strain(s) causing the
on "clean," dry ground. (This group may
infection and those present in the vaccine.

have some degree of genetic resistance, and

No vaccine contains all the various strains
identifying them in some way is recom
ofDnodosus, and use of vaccination
mended. Retaining offspring from this
without other means of control will most
group could fmther help control the
likely select for strains not contained in the
disease.) This group should receive an
vaccine. Alum-precipitated vaccines require
irtjection of long-acting tetracycline at
two doses 4--6 wk apart to establish

13.6 mg/lb, and any lan1e sheep should be
effective immunity, which persists for 2-3
removed immediately. The group of sheep
mo. Lesions heal within 4--6 wk if immunity
with footrot lesions are culled or, after
is established. Oil-emulsion vaccines induce
careful hoof trimming, the feet are soaked
immunity within 3 wk of the initial dose and
for at least 30 min, and the animals are
may persist for 3-4 mo. In endemic areas,
treated with antibiotic and kept separated
revaccination is recommended at int1 .-vals
from the lesion-free group. This second
of 3-6 mo. Reaction to the vaccine is
group should undergo foot soaking once a
common, resulting in large granulomas and
week for a total of three times and/or be
occasional abscesses. Vaccines for F
medicated with long-acting oxytetracycline
necrophorum have not generally shown
at the time of soaking. At the end of this
much benefit in either treatment or
period, their feet should again be examined
prevention. Lately, the vaccine appears
and trimmed. Any sheep with an active case
to be unavailable in the USA.

of footrot should be culled. This group must

Addition of zinc to trace mineral salt,
be monitored closely during the next wet
reportedly effective in reducing hoof rot in
period to detect any carriers, which are
cattle, has not been shown to be particularly
usually the first animals to show lameness.

helpful for sheep footrot. However, zinc is

When no relapses have occun-ed for 1 mo or
important for immunity and skin/hoof
longer, this group may be placed with the
health. Providing it in a well-balanced trace
clean flock. However, placing a single active
mineral mix may be helpful in locations
or subclinical case in the clean flock can
deficient in zinc.

negate all of the previous hard work.

Australia has implemented an effective

Eradication: A successful eradication
eradication program involving many flocks.

program requires planning, commitment,

The program has three phases. The control
and an investment of time and money.

phase is used during periods of active

Eradication can be achieved only by
spread or to reduce the number infected.

eliminating all cases of D nodosus infection During this phase, vaccination, foot bathing,
in a flock and preventing its reintroduction.

and parenteral antibiotics can all be used.

This may be done by replacing affected

The eradication phase must take place
stock with footrot-free sheep or by
during the diy season and cannot begin until
rigorously treating all new infections and
several weeks after the use of all medicaculling affected sheep that do not respond tions has been stopped and 10-12 wk after
readily to treatment. Eradication is easiest
vaccination. Foot bathing and vaccination

1170

LAMENESSIN SHEEP
tend to mask the presence of infection.

Acute lameness with the sheep packing a

During this phase, all four feet of every
foot, swelling of one digit, and discharging
sheep are inspected every 3-4 wk. Infected
sinuses distinguish foot abscess from
sheep can be treated with parenteral
footrot.

antibiotics at the first inspection only. After

Early treatment with parenteral

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this, infected sheep are culled at each
long-acting antibiotics is sometin1es
inspection. This continues until there are
effective and may prevent joint infection.

two completely negative, consecutive flock

The therapy aims to maintain the integrity
examinations. In the surveillance phase,
of the joint ligan1ents by draining the
all lame sheep in the flock are examined
abscess and applying an antibacterial
immediately. If footrot is present, the flock
preparation and a self-adhesive bandage.

goes back to phase 1 or 2 again.

This reduces stress on the ligan1ents, keeps
the lesion out of the mud, and counters the
bacterial infection. Although the prognosis

FOOT ABSCESS
for complete recovery is poor, in most

(Infective bulbar necrosis, Heel abscess,
cases the foot heals sufficiently to allow

Bumblefoot)

adequate locomotion. Once the infection
becomes established in the joint, conserva

Bumblefoot is a necrotizing or purulent
tive treatment is not effective. However, a
infection involving the distal interphalantoe can be surgically removed (if the other geal soft tissues and sometimes the joint.

digit is healthy) with relatively good

The incidence is usually sporadic, but as
success.

much as 25% of the flock may be affected.

Control depends on early treatment and

The two organisms most consistently
moving the sheep to avoid conditions that
recovered from bumblefoot are Fusobacte
lead to ovine interdigital dennatitis or other
rium necrophorum and Trueperella
causes of abscess. Although F necrophopyogenes. Foot abscesses may develop as a nim vaccines are available, they have not
complication of ovine interdigital dem1atitis proved to be very effective.

by extension of the necrotic process into
the subcutis and then into the distal
interphalangeal joint. They also commonly

IMPACTED OR INFECTED OIL
develop after penetration of the interdigital

GLAND
skin by sharp objects ( eg, crusted snow,
frozen or stiff stubble of alfalfa and grain),

Sheep have a sebaceous ( oil) gland in the
bruising of the foot and injury of the skin
skin of the interdigital space. A thick, oily,
when slipping on frozen rocks, or even
translucent secretion is stored in a small
careless paring of the hoof. This joint is
pouch lying between the phalanges and is
vulnerable to infection on the iriterdigital
discharged to the skin surface through a
aspect where the joint capsule protrudes
duct in the skin. Occasionally, the gland and
above the coronary border as the dorsal and
its contents are mistaken for an abscess.

volar pouches. At these sites, the joint

However, the duct can become occluded,
capsule is protected only by the interdigital
causing distention of the oil pouch. It rarely
skin and a minimal an10unt of subcutaneous
causes lameness. The oil sac also may
tissue.

become infected, resulting in a local

Foot abscesses often develop when the
cellulitis or abscess that may be confused
soil and pastures are wet or frozen. The
with bun1blefoot. Expression of the
disease causes an acute lameness that is
contents by manual pressure relieves
usually restricted to one foot, which the
impaction. Infected glands can then be
sheep will not place on the ground. It may
treated with local or systemic antibiotics or
be possible to express necrotic material
both, depending on the extent and severity
through an opening in the interdigital skin
of the infectious process. Unlike bumblecaused by the bacterial invasion, but more foot, this condition generally responds
commonly the swollen sinuses break open
readily to treatment.

and drain at one or more points above the
coronet. If this does not occur, the swelling

INTERDIGITAL FIBROMA
will have to be lanced. In some instances,
movement of the affected digit is exagge1"

An interdigital fibroma is a mass of fibrous
ated, indicating that the ligaments about the
tissue between the toes that may resemble
distal interphalangeal joint have ruptured.

a papilloma. If not removed, it enlarges,

Displacement of the digit during locomotion spreading the toes. Tendrils grow upward and permanent defom1ity are likely in those
between the first phalanges, causing severe
cases.

lameness. If the fibroma is detected early,

MYOPATHIES IN RUMINANTS AND PIGS

1171
surgical removal (cryosurgery and
or other organisms. The organisms probably
electrocautery) may be successful;
enter through fissures between the wall and
however, by the time it causes lameness,
sole and through vertical and horizontal
the tendrils cannot be totally removed
fractures of wall horn. Sometimes, infection
from between the phalanges, and the
is enhanced by impaction with sand, mud,

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fibroma tends to recur.

or feces; by overgrowth of the hoof; or by
separation of the wall after laminitis.

SEPTIC LAMINITIS

Forefeet are affected more commonly.

Lameness is severe, and the affected

(Lamellar suppuration, Toe abscess)

digit may be hot and tender. There may be a

Septic laminitis is an acute bacterial
draining sinus above the lesion at the coroinfection of the laminar matrix of the hoof net, or the abscess may be found above the
that is usually restricted to the toe and
sole on the bottom of the foot. Applying
abaxial wall. The disease is sporadic and the pressure to vaiious sections of the sole with cause variable, but cases due to Pusobacte
the thumbs will elicit pain and help locate
rium necrophorum and True'J)erella
the pocket of infection. Affected sheep
pyogenes usually are more severe and
usually recover rapidly after paring of the
extensive than those involving streptococci
horn to provide dependent drainage.

MYOPATHIES IN RUMINANTS AND PIGS

INFECTIOUS MYOPATHIES
clostridial species, and myonecrosis caused
by this organism is fatal.

Clostridial Myonecrosis

Infections are characterized by a rapid

(Blackleg, Malignant edema, False blackleg,
clinical course, fever (104°-106°F

Gas gangrene, Gangrene)

[40°--41 °C]), lameness, systemic toxemia,
tremors, ataxia, and dyspnea, often

Clostridial infection of skeletal muscle is a
followed in 12-24 hr by recumbency, coma,
noncontagious cause of acute myonecrosis.

and death. Mortality may approach 100%.

Clostridium chauvoei, C Se'J)ticum,

Initially, the skin over the area may be

C sordellii, occasionally C novyi type B, swollen, hot, and discolored; however, as

C pm:fringens type A, C cam is, or mixed the disease progresses, the skin over the
infections involving several agents are
area may become cool and insensitive with
common (seep 601). Clostridia or their progressive sloughing. Crepitus may be
spores are ubiquitous in the environment,
detectable, indicating subcutaneous gas
feces, intestinal tract, and other internal
production. If a wound is present, malodororgans of a variety of species. Clostridial ous, serosanguineous discharge may be
myonecrosis may develop after introducseen. Hematology and serum biochemical tion of spores via an IM injection or
analyses usually reflect hemoconcentration
penetrating wound or through sporulation
and a stress/toxic leukograin with increased
of organisms already present in muscle
activities of serum CK and serum AST that
when suitable anaerobic conditions are
often do not reflect the toxicity of clostridial
created with muscle trauma. Any skeletal
myonecrosis. A definitive diagnosis is made
muscle group in the body can be involved,
from direct smear exainination, fluorescent
but most infections affect the limb or trunk
antibody testing, or anaerobic bacterial
muscles. Occasionally, muscles such as
culture of aspirates of affected tissues.

those around the vulva, tongue, and dia

Differential diagnoses include other
phragm can be involved, or the udder in a
fulrninant disease processes in which there
cow may be the primary site of sepsis. The
is rapid debilitation or death of the animal.

release of powerful exotoxins by multiply

Clostridial myonecrosis generally has
ing clostridia is responsible for the local
characteristic pathologic lesions that are
tissue damage, systemic toxemia, and
absent in most other conditions, making
widespread organ dysfunction. The toxins
diagnosis relatively straightforward.

of C sordelli are the most potent of all the Swelling and autolysis are rapid in animals

1172

MYOPATHIES IN RUMINANTS AND PIGS
that have died from clost1idial myonecrosis, S cruzi, S hirsuta, and S hominis are and the carcass usually has a foul odor
known to infect cattle, whereas S ovicanis
similar to that of rancid butter. This odor is
and S capracanis infect sheep and goats.

a characteristic of most cases of clostridial

The most conunon mechanism for natural
myonecrosis. C chauvoei infection is
infection in cattle is by ingestion of feeds

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characterized by engorgement of the
contaminated with infected carnivore feces.

subcutis and adjacent tissues with

(For complete discussion of sarcocystosis,
bloodstained fluids and gas bubbles. Cut
seep 1058.)

tissue from the affected area reveals moist,
dark-colored muscle in the periphery of the

NUTRITIONAL MYOPATHIES
lesion, with lighter-colored, drier muscle
with gas bubbles between the separate
bundles of muscle toward the center.

Nutritional Myodegeneration

Lesions are similar in sheep and cattle,

(White muscle disease, Stiff lamb disease,
except that there is usually less gas and the

Nutritional muscular dystrophy)

muscles are not as dry in affected sheep.

Myonecrosis resulting from

Nutritional myodegeneration (NMD) is an

C sordelli is
most often associated with lesions of the
acute, degenerative disease of cardiac and
neck or brisket area of cattle; death is
skeletal muscle caused by a dietary
frequently so rapid that subcutaneous gas
deficiency of selenium or vitanlin E in
accumulation is rare. ln addition to local
young, rapidly growing calves, lambs, and
myonecrosis, animals often have massive
kids. Dan1s usually consmned seleniun1-
subendocardial hemorrhages in the left
deficient diets dtui.ng gestation. Seleniw11
ventricle of the heart and hemorrhage in the
deficiency appears to be more important
trachea, bronchi, and thymus. Extensive
than vitamin E in preventing NMD. NMD
perirenal edema and hemorrhagic renal
occurs worldwide in areas where the soil
calyces and severe congestion of the lungs

(and therefore the derived grains and
are common findings.

forage) is deficient in seleniun1, and storage

Antibiotic therapy and aggressive surgical conditions do not preserve vitanlin E in debridement may be attempted in the
forages. Soil in the northeastern and eastern
individual animal; however, most cases
seaboards and northwestern regions of the
are usually fatal. Penicillin at a dosage of

USA are particularly deficient in selenimn.

44,000 U/kg, IV, every 2-4 hr is given until

Vitamin E deficiency occurs most comthe anin1al is stable (1-5 days). Use of monly when animals are fed poor-quality
specific antitoxins is recommended when
hay, straw, or root crops.

possible. Supportive fluid therapy and

Seleniun1 is an essential component of
use of analgesics and a.nti-inflan1rnatory
five antioxidant selenoproteins, and vitaagents for control of pain arid swelling are min E acts as an antioxidant within lipid
recommended. Short-acting corticosteroids
bilayers. Muscle degeneration is the result
may be used for initial therapy of sys-
of oxidant damage to cell membranes and
temic and toxic shock, but continued use is
proteins, leading to a loss of cellular
contraindicated in the face of overwhelming integrity. Young, rapidly growing animals sepsis.

usually ru·e affected, although the disease

Vaccination beginning at 4-6 mo in cattle
has also been reported in yearling and adult
with bacterins containing antigens against
cattle. When cardiac muscle is primarily
two or more clostridial species, including
affected, anin1als may be found in respira

C chauvoei, C septicum, C novy·i, C sordelli, tory distress, have cardiac arrhythmias, or and C perftingens is reconunended. For all
be found dead. ln such cases, the clinical
clostridial species except C chauvoei, two
course is frequently short, with death
doses of vaccine are necessary to establish
occurring conunonly in <24 hr despite
good protection. Booster vaccinations
medical therapy. When skeletal muscle
should be administered every 6----8 mo if
is primarily affected, signs of muscle
protection is to be maintained.

weakness, stiffness, and difficulty rising are
seen. Most affected animals are able to
remain standing only for short periods, and

Sarcocystosis
locomotor muscles may be firm and painful

Cysts of Sarcocystis are common in the
on palpation. If the respiratory muscles are
heart, esophageal, and skeletal muscle of
affected, the animal may show respiratory
cattle, sheep, goats, and other species but
distress and evidence of increased
rarely cause disease. Heavy infestations of
abdo1ninal effort when breathing. The
sarcocystis may cause fever, mild anemia,
muscles of the tongue may be involved,
chronic myositis, and muscle wasting.

resulting in dysphagia. Animals with

MYOPATHIES IN RUMINANTS AND PIGS

1173
skclr•tal NMD often respond favorably to
vitan1in E is insufficient for supplementatreatment and rest. Improvement is evident tion; it is present only as a preservative for
aJler a few days; within 3-5 days, animals
tl1e solution. Injectable vitamin E products
can often stand and walk
tl1at contain 300 and 500 IU vitanlin E per

Differential diagnoses include infectious
mL as o-cx-tocopherol are available. Oral

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diseases resulting in septicemia, pneumosupplementation is the general approach to nia, and toxemia; cardiac anomalies;
provide additional dietary levels of vitamin
cardiotoxic agents such as those found

E. Reconunended levels of supplementation
in plants ( oleander, senna, yew, white
for calves range from 15 to 60 mg of
snakeroot, and gossypol toxicity from

OL-cx-tocopherol acetate per kg of dry feed.

cottonseed); and the ionophore antibiotics.

Antibiotics may be indicated to combat

Other diseases causing stiffness of gait,
secondary pneumonia. Provision of
weakness, and recumbency with no change
adequate energy intake and attention to
in mental status include spinal cord
the fluid and electrolyte balance are critical
compression, cerebellar disease, suppuraif recovery is to be successful.

tive and nonsuppurative meningitis/

Under current federal regulations in the
myelitis, polyarthritis, neurotoxins such

USA, selenium can be incorporated into the
as organophosphates, tetanus, pelvic
total ration of rWllinants and other species
fractures, parasitic myositis, clostridial
to a level of 0.3 ppm. In salUmineral
myositis, and traun1atic injuries.

mixtures formulated for free-choice

Supportive evidence ofNMD includes
feeding, selenium can be incorporated at
increased levels of CK, AST, and LOH.

90 ppm for sheep and 120 ppm for cattle. In

Definitive diagnosis is based on demonstrace1tain areas or in herds, levels as high as tion of low whole blood selenium (normal

200 ppm selenium in salUmineral mixtures
range >0.1 ppm) or liver content (nom1al
may be necessaiy to maintain adequate selecattle 0.9-1. 75 mcg/g of dry matter, sheep nium levels. Federal regulations limit the

0.9-3.5 mcg/g dry matter). The critical
intake of supplemental selenium to
concentration of vitamin E (cx-tocopherol)

0. 7 mg/head/day in sheep and 3 mg/head/day
in plasma is 1.1-2 ppm in large animals.

in cattle. The use in ruminants ofrumenore

Vitanlin E deteriorates rapidly in plasma
ticular boluses, which release a precise
samples. Therefore, plasma samples for
amount of seleniun1 daily, is common in
cx-tocopherol analysis should be put on ice
many countries; however, under current
inlmediately, protected from light by

FDA guidelines such products are not
wrapping in foil, and stored at -21 °F ( -70°C)

available in the USA These slow-release
if analysis is to be delayed.

boluses cai1 replace supplementation by salt

Bilaterally symmetric myodegeneration
mixtures or by injections and are extremely
is a consistent finding in NMD. Skeletal
valuable in extensive grazing systems.

muscle degeneration is characterized by

Alternatively, individual animals can be
pale discoloration and a dry appearance
supplemented by periodic (30- to 60-day
of affected muscle, white streaks in muscle
intervals) injections of seleniurn/vitan1in E
bundles, calcification, and intramuscular
preparations to help maintain body
edema. The white streaks seen in cardiac
concentrations and assist in traI1Splacental
and skeletal muscle bundles represent
transfer of seleniun1.

bands of coagulation necrosis or, in chronic

Regardless of tile metllod of supplemencases, fibrosis and calcification. In calves, tation, periodic blood ( or tissue) sampling
the left ventricle and septwn are most
of aIU1nals at risk is reconunended to ensure
frequently involved, but both ventricles are
desired levels of selenium. Feeding animals
usually involved in lambs. Histologically,
properly prepared and stored hay and grain
affected muscle fibers may be hyperconor allowing access to high-q_uality, green tracted and fragmented, with some
forage should ensure adequate vitanlin E
mineralization of muscle fibers and others
intake.

Wldergoing macrophage infiltration.

The cardiac form ofNMD is often
incompatible with life, whereas the skeletal

Hypokalemic Myopathy
form may respond to injectable selenium

Hypokalemic myopathy in dairy cattle
products. The label dosage for selenium is
occurs when serW11 potassium concentra0.055-0.067 mg/kg (2.5-3 mg/45 kg), IM or tions ai·e <2.5 mmol/L, producing severe

SC. Dosage of these injectable products
signs of muscle weakness. Anorexia and
should not be greatly increased ahove that
enhanced potassium excretion due to the
on the label to prevent an inadvertent
administration of one or more doses of
selenium toxicosis. When using vitamin E/
isoflupredone acetate to ketotic cows are
selenium combinations, the amoW1t of
conrn1on causes of hypokalemia. Isoflupre-

1174

MYOPATHIES IN RUMINANTS AND PIGS
done acetate has both glucocorticoid and
tend to occur sporadically, and rapidly
mineralocorticoid activity, resulting in a
growing pigs 2-16 wk old are affected.

decrease in mean plasma potassium

Dea�h almost invariably occurs suddenly
conce_ntration by 25% 2 days after a single
and 1s often precipitated by exercise.

II\Ject10n (20 mg) and 46% in cows 3 days

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after two injections.

lesions: In mulberry heart disease, the
characteristic lesions are a pericardia! sac

. Clinical signs of hypokalemic myopathy
rnclude severe weakness, recumbency,
grossly distended with straw-colored fluid
abnom1al position of the head and neck
that contains fibrin strands, and extensive
rumen hypomotility or atony, abnormal'

hemorrhage tlu·oughout tile epicardiw11 and
feces, anorexia, and tachycardia. Cardiac
myocardiwn. Microscopically, the heait
dysrhytlunia is also common. Diagnosis is
shows both vascular and myocyte lesions·
based on clinical signs combined with

� addition to interstitial hemorrhage, t11e;e
serum potassiw11 of <2.5 nunol/1. Other

1s usually extensive rnyocai·dial necrosis
common clinical chemistry abnormalities
togetller with fibrin thrombi in capillai·ies.

include ketosis, metabolic alkalosis and
lf pigs survive for a few days, nervous signs
increased serum CK and AST activities.

may be seen as a result of focal encephalo

Muscle biopsies reveal a vacuolar
malacia.

myopathy.

In hepatosis dietetica, there is often

Restoration of whole-body potassium
subcutaneous edema ai1d varying amounts
balance can be difficult, and serum potassiw11 of transudate in serous cavities. Fibrin concentrations do not necessarily reflect
strands adhere to the liver, which has a
muscle potassiwn concentrations. Recomcharacteristic mottled appearance caused mended supplementation includes potassium by irregulai· foci of parenchymal necrosis chloride given IV (16 g/100 kg) and PO (26
and hemorrhage. Acute lesions may appear
g/100 kg) for approximately 5 days.

as scattered, red, swollen lobules and

Treatment should also be directed at
edema of the gallbladder wall. Focal
resolving the primary cause of ketosis and
lesions of myocardial necrosis and less
anorexia as well as providing supportive care. frequently, skeletal myonecrosis m'ay be Survival has been repmted to be 22"/o--79"Ai.

apparent.

Many pigs that die with seleniwn or
vitamin E deficiency have esophagogastric

Nutritional Myopathy of Pigs
ulceration or preulcerative changes.

(Hepatosis dietetica, Mulberry heart disease)

There are several specific diseases of pigs

Diagnosis: The history and gross
m which muscle degeneration may be
necropsy findings may be distinctive but
extensive ( eg, mulben-y heart disease)

histology to demonstrate specific c�diac
and others in which thE! degeneration is
and skeletal muscle lesions may be
f�equently less conspicuous ( eg, hepatosis
necessary. Differential diagnoses for
dietet1ca). Yellow fat disease (seep 1200)

mulben-y heart disease include acute
may be seen with accompanying rnyopathy.

septicemic diseases ( eg, salmonellosis,
erysipelas, and streptococcosis ), pericardi

Etiology: Mulberry heart disease and
t1s, polyserositis, and edema disease. For
hepatosis dietetica are associated with diets
hepatosis dietetica, pitch poisoning and
low in selenium or vitamin E. Adrninistragossypol toxicosis should also be considti ered, as should porcine stfess syndrome for

_on of iron dextran to piglets having low

Vltamrn E status may precipitate a severe
pigs with prominent skeletal muscle lesions.

myopathy (seep 3077) witll lesions identical Cases of seleniW11 or vitan1in E deficiency in to those of selenium or vitamin E deficiency.

pigs can be identified, as in other species, by

Other factors that may increase the
decreased levels of selenium vitamin E and
seleniW11 requirement include diets with
glutathione peroxidase in th� serW11 and
low concentrations of protein ( especially
tissues and by increased levels of CK and
sulfur-containing amino acids), diets with

AST in the serW11.

an excess of selenium antagonistic
compoWlds, and possibly genetic influences

Prevention and Treatment: Rations
on selenium metabolism. Vitan1in E may be
may be supplemented with seleniW11 or
less available in diets with high concentravitan1in E, or both (as for rW11inants).

tions of polyunsaturated fatty acids, vitan1in Affected pigs and their herdmates may be A, or mycotoxins.

given injections of selenium/vitamin E to
increase tissue levels rapidly. Injection of

Clinical Findings: These conditions have
sows in late gestation increases tissue levels
certain characteristics in common. Losses
in newborn piglets.

MYOPATHIES IN RUMINANTS AND PIGS

1175

TOXIC MYOPATHIES
membranosus muscles may arise as aninlals
weakened by hypocalcemia attempt to rise.

Plant Toxins

Additionally, the weight of a recumbent
animal on dependent muscle groups creates

Plant toxins affect both cardiac and skeletal
significant increases in intran1Uscular

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muscle. Clinical signs are not specific for
pressure, resulting in decreased perfusion
the toxin and include anorexia, cardiac
and ischemia of muscle and ne1ve. Muscle
failure with tachycardia, dyspnea, diarrhea,
traun1a leads to edema and inflammation,
stiffness, muscular weakness, recumbency,
both of which may exacerbate local tissue
and myoglobinuria. Myonecrosis may occur
degenerative changes. Mild !Jlcreases in
when gossypol is fed. Monogastrics,
serw11 CK can be expected in recumbent
including young calves, should not ingest
cows, but increases >5000 U/L usually
feed containing >200 ppm gossypol,
indicate traumatic muscle damage.

whereas mature ruminants may tolerate 20

Treatment requires correcting the
g of gossypoVhead/day. Senna obtusifolia
underlying cause of recun1bency, fluid

(sicklepod) is prevalent in the southeastern
therapy if renal datnage is evident, NSA!Ds,

USA, and ingestion of its seeds by swine
good nursing care, adequate footing and
or ruminants may cause a degenerative
bedding, and lifting or rolling the animal
skeletal and/or cardiomyopathy. Trematone
several times a day. Aquatherapy using float
is a toxic component of white snakeroot
tanks for cattle also appears to help relieve

(Eupatorium 1ugosum), which grows in
pressure on muscle groups.

shaded areas of the eastern and central

USA, as well as rayless goldenrod (Isocoma
wrightii), which is common in the

GENETIC MYOPATHIES

Southwest on open pastures. Ingestion of
these plants in quantities of -2% of body
weight can cause a fatal cardiomyopathy

Caprine Myotonia
and severe skeletal muscle degeneration.

Myotonia congenita in goats is due to an

Trematone remains active in hay and in the
autosomal dominant mutation that has
stalks of the dead plants on pasture.

incomplete penetrance in the skeletal
muscle chloride channel. Goats with this
lonophores
mutation have been selected for as a breed
and are commonly referred to as "fainting

Ionophores added to feeds in excess of
goats." Clinical signs ranging from stiffness
recommended levels can cause cardiac and
after rest to marked general rigidity after
skeletal muscle necrosis. Experimental
visual, tactile, or auditory stimulation
studies have indicated that LD5() values for
usually develop by 6 wk of age. These signs
monensin are 12, 17, 26, and 21-36, for
remain throughout the animal's life but are
sheep, pigs, goats, and cattle, respectively.

not progressive. A diagnosis of myotonia is

Feed concentrations of 100 g.,'ton and 400
made by identifying the characteristic "dive
g.,'ton have been fatal to sheep and cattle,
bomber" discharges in electromyography
respectively. Newborn calves dosed with
and/or by genetic testing.

100 mg lasalocid tid for cryptosporidiosis
experience muscle necrosis. Other
ionophores include naracin, salinomycin,

Congenital Muscular Dystonia in
and laidlomycin. At necropsy, pale areas

Belgian Blue Cattle
of myocardial necrosis and pulmonary

Congenital muscular dystonia in Belgian
congestion are usually prominent in cattle.

Blue calves is caused by an autosomal

Pigs and sheep tend to have mainly skeletal
recessive mutation in the gene encoding
muscle lesions that appear quite sin1ilar
the neuronal glycine transporter. Affected
grossly and histologically to those of
calves exhibit signs of lateral recumbency,
nutritional myodegeneration. Diagnosis
low head carriage, and trat1Sient muscle
requires history of exposure with developspasms after tactile or auditory stimulation.

ment of characteristic clinical and
pathologic alterations.

Phosphorylase Deficiency in

Charolais Cattle

TRAUMATIC MYOPATHIES

A mutation in the myophosphorylase gene
in Charolais cattle produces signs of

Muscle Crush Syndrome of Cattle
exercise intolerance and muscle necrosis

Muscle dan1age commonly accompanies
very sinlilar to nutritional myodegeneration.

bovine secondary recumbency (seep ll88).

The disease has been recognized in many

Tea.ting of adductor or semitendinosus/
countries, including the USA and New

1176

MYOPATHIES IN RUMINANTS AND PIGS

Zealand. Animals become exercise

Porcine RN(-) Glycogen Storage
intolerant, may collapse when forced to

Disease
exercise, and develop muscle necrosis
characterized by increased serum CK and

The RN(-) (rendement Napole) phenotype
prolonged recumbency. Supportive care
is common in Han1pshire pigs. It is due to an

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during episodes has allowed many young
autosomal dominant mutation in the protein
animals to survive and, unlrnowingly to the
kinase AMP-activated gan1ma 3 subunit
owner, enter the breeding herd.

gene (PRKAG3), which encodes the ganuna

3 isoform of AMP-activated protein kinase

Porcine Malignant Hyperthermia

(AMPK). Clinically, pigs appear healthy;
however, the 709u increase in glycogen

Malignant hypertherrnia in swine (seep 1027) content in skeletal muscle causes poor is due to an autosomal recessive genetic
meat quality at slaughter.

mutation in the skeletal muscle ryanodine
receptor 1 gene (RYRl) that causes
abnonnal meat quality in swine. Pie train,

Pseudomyotonia in Cattle

Poland China, and certain strains of

Bovine congenital pseudomyotonia is an

Landrace pigs are affected. During transpori.mpai.m1ent of muscle relaxation induced tation or anesthesia, pigs develop increased
by exercise that prevents animals from
body temperature, extreme rigidity of the
perfom1ing rapid movements. Different
skeletal muscles, and lactic acidosis. At
mutations in the ATP2Al gene that encodes
slaughter, affected muscles become pale,
the Ca2+-ATPase in skeletal muscle
soft, and exudativc, which diminishes meat
sarcoplasmic reticulum have been
quality. A genetic test is available to diagnose
identified in the Chiani.na, Belgian Blue,
affected and carrier ani.n1als.

and Romagnola breeds.

MYOPATHIES IN HORSES

Muscle disorders in horses present with a

Differential diagnoses for reluctance
variety of clinical signs ranging from muscle
to move, acute recmnbency, and discolored
stiffness and pain to muscle atrophy,
urine include lameness, colic, lan1initis,
wealrness, exercise intolerance, and muscle
fracture, pleuropneurnonia, tetanus,
fasciculations. The most common clinical
aorto-iliac thrombosis, neurologic diseases
presentation is muscle pain, stiffness, and
resulting in recLU11bency or reluctance to
reluctance to move due to rhabdomyolysis.

move, intravascula.r hemolysis, and

Rhabdomyolysis, defined as disruption of
bilirubinuria. Causes of non-exercisestriated skeletal muscle, can broadly be associated rhabdomyolysis include
grouped into causes associated with
infectious ( eg, Clostridiitm sp, influenza, exercise ( exertional rhabdomyolysis)

Stre'J)tococcus equi, Sarcocystis) and
and causes unrelated to exercise.

immune-mediated myopathies, nutritional
ltM•ii DIFFERENTIAL DIAGNOSES OF EQUINE MYOPATHIES

NON-EXERCISE-ASSOCIATED RHABDOMYOLYSIS

Inflammatory myopathies

Clostridial myositis

Influenza myositis

Sarcocystis myositis

Immune-mediated myopathy

Nutritional rnyopathy

Vitan1in E and selenium deficiency

MYOPATHIES IN HORSES

1177

•&H•J• DIFFERENTIAL DIAGNOSES OF EQUINE MYOPATHIES (continued)

Toxic myopathies

Ionophore toxicity

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Senna occidenlalis

Pasture myopathies

Rayless goldenrod/white snakeroot

Hypoglycin A in box elder and European sycamore trees Traumatic myopathies

Compressive anesthetic myopathy

Traw11a

Genetic myopathies

Glycogen branching enzyme deficiency in Quarter horses Polysaccharide storage myopathy types 1 and 2

Malignant hyperthennia in Quarter horses

EXERTIONAL RHABDOMYOLYSIS

Focal muscle strain

Sporadic tying-up (overexertion)

Chronic tying-up

Dietary imbalances, vitamins, minerals, electrolytes Polysaccharide storage myopathy types 1 and 2

Malignant hype1thennia

Recurrent exertional rhabdomyolysis

Idiopathic chronic exertional rhabdomyolysis

EXERTIONAL MYOPATHY WITH NORMAL CK

Mitochondrial myopathy

Polysaccharide storage myopathy type 2

MUSCLE ATROPHY

Myogenic atrophy

Severe rhabdomyolysis

Disuse

Cushing disease

Immune-mediated myositis (rapid atrophy)

Vitamin E----deficient myopathy

Homozygous polysaccharide storage myopathy type 1

Polysaccharide storage myopathy type 2

Neurogenic atrophy

Equine protozoa! myelitis

Local nerve trawna

Equine motor neuron disease

Idiopathic peripheral neuropathy

Toxic peripheral neuropathies

MUSCLE FASCICULATIONS

Pain, fear

Weakness (botulism, chronic debilitation)

Electrolyte abnormalities

Equine motor neuron disease

Hyperkalemic periodic paralysis

Hypokalemia

Otobius megnini ( ear tick) infestation

Myotonic dystrophy

Stiff horse syndrome

Shivers

1178

MYOPATHIES IN HORSES
myodegeneration (vitamin E or selenium
incidence of muscle stiffness also has been
deficiency), traumatic or compressive
found to increase during an outbreak of
myopathy, idiopathic pasture myopathy,
respiratory disease. Dietary deficiencies
and toxic muscle dan1age from the ingestion of sodiun1, vitarnin E, selenium, or a VetBooks.ir
of ionophores (eg, monensin, lasalocid,
calcium:phosphorus in1balance may
rumensin). Plants, including white snake
also be contributory factors.

root and vitamin D -stirnulating species,

A diagnosis of sporadic exertional
should also be considered (see TABLE 1).

rhabdomyolysis is made on the basis of a

Genetic causes of nonexertional rhabdomyhorse wiili no previous history, or a brief olysis include glJ ·cogen branching enzyme
history, of exertional rhabdomyolysis, signs
deficiency (foals), malignant hyperthem1ia
of muscle crarnping and stiffness after

(Quarter horses), and polysaccharide
exercise, ar1d moderate to marked increases
storage myopathy.

in serum CK and AST. Immediately on
detection of signs of exertional rhabdomy

EXERTIONAL MYOPATHIES
olysis, exercise should stop and the horse
should be moved to a well-bedded stall with

Exertional myopathy in horses is a
access to fresh water. The objectives of
syndrome of muscle fatigue, pain, or
treatment are to relieve anxiety and muscle
cramping associated with exercise. Less
pain and to correct fluid and acid-base
common exertional myopathies that cause
deficits. Tranquilizers or opioids may be
exercise intolerance without muscle
given. NSAIDs can be given to a wellnecrosis include mitochondrial myopathies hydrated horse. Most horses ar·e relatively
and forms of polysaccharide storage
pain free within 18--24 hr.

myopathy in Warmblood horses. Most

Severe rhabdomyolysis can lead to renal
commonly, exertional myopathies produce
compromise due to ischemia and the
necrosis of striated skeletal muscle and are
combined nephrotoxic effects of myoglotem1ed exertional rhabdomyolysis.

binuria, dehydration, and NSAID ilierapy. The

Although exertional rhabdomyolysis was
first p1iority in horses wiili hemoconcentrapreviously considered a single disease tion or myoglobinuria is to reestablish fluid
described as azoturia, tying-up, or cording
balance and induce diuresis. In severely
up, it is now known to comprise several
affected animals, regular monitoring of
different myopathies, which, despite

BUN and/or serum creatinine is advised to
sinillarities in clinical presentation, differ
assess the extent of renal damage. Diuretics
significantly in etiopathology.

are contraindicated in the absence of IV

Clinical signs usually are seen shortly
fluid therapy and are indicated if the horse
after onset of exercise. Excessive
is in oliguric renal failure.

sweating, tachypnea, tachycardia, muscle

Horses should be stall rested on a hay diet
fasciculations, reluctance or refusal to
with a dietary vitamin and mineral ration
move, and firm, painful lumbar and gluteal
balancer supplement for a few days. For
musculature are common signs. Episodes
horses with sporadic forms of exertional
range from subclinical to severe muscle
rhabdomyolysis, rest with regular access to
necrosis with recumbency and myoglobia paddock should continue until serun1
nuric renal failure. The severity varies
muscle enzy.n1e concentrations are normal.

extensively between individuals and to

Because ilie inciting cause is usually
some degree within the sar11e individual.

temporary, most horses respond to rest, a

A diagnosis of exertional rhabdomyolysis
gradual increase in training, and dietary
is based on demonstration of abnormal
adjustment. Endurance horses should be
increases in serum CK, lactate dehydrogeencouraged to drink electrolyte-supplenase, and AST.

mented water during an endw·ance ride ar1d

Exe1tional rhabdomyolysis can be either
monitored particularly closely during hot,
sporadic, wiili single or very infrequent
humid conditions.

episodes of exercise-induced muscle
necrosis, or chronic, with repeated episodes Chronic Exertional Rhabdomyolysis of rhabdomyolysis and increased serum CK
or AST with mild exe1tion.

Some horses µave recurrent episodes of
rhabdomyolysis, even wiili light exercise.

Sporadic Exertional Rhabdomyolysis Four fonns of chronic tying-up have been identified using muscle biopsies or genetic

All breeds of horses are susceptible to
testing: type 1 polysaccharide storage
sporadic exertional rhabdomyolysis. The
myopathy (PSSM), type 2 PSSM, malignant
most common cause is exercise tl1at
hyperthermia, and recurrent exertional
exceeds the horse's state of training. The
rhabdomyolysis.

MYOPATHIES IN HORSES

1179

Type 1 polysaccharide storage
horses. A diagnosis can be made by genetic
myopathy is seen frequently in Quarter
testing of blood or hair roots. Signs related
horse-related breeds ( especially halter and
to inhalation anesthesia include tachycardia,

Western pleasure horses), Morgans, and
tachypnea, hyperthemtia, muscle rigidity

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draft horses but is also present in at least
accompanied by a severe lactic acidosis,

20 other horse breeds. It is caused by a
increased serwn CK, and electrolyte
dominantly inherited mutation in the
derangements. Exe1tional rhabdomyolysis
glycogen synthase 1 (GYSJ) gene. A diagnoin Quarter horses witll malignant hypetthersis can be made by genetic testing of blood rnia can result in sudden death. Signs are
or hair san1ples. Quarter horse-related
preceded by excessive sweating, tachycarbreeds and other crossbred or light breeds dia, tachypnea, hyperthermia, and muscle
of horses with type l PSSM often develop
rigidity. Some Quarter horses have botll
episodes of rhabdomyolysis at a young age
malignant hyperthennia and PSSM, which
with little exercise. Rest for a few days
results in more severe signs of exertional
before exercise is a common triggering
rhabdomyolysis than tllose seen in horses
factor. Episodes are characterized by a
witl1 PSSM alone.

tucked-up abdomen, a camped-out stance,

Recurrent exertional rhabdomyolysis
muscle fasciculations, sweating, gait
is seen frequently in Thoroughbreds,
asymmetry, hindlimb stiffness, and

Standardbreds, and Arabian horses. It is
reluctance to move. Some horses paw or
likely due to abnorn1al regulation of
roll, resembling colic. Serun1 CK and AST
intracellular calcium in skeletal muscles. It
are increased during an episode (usually
appears tllere is intermittent disruption of

>l,000 U/L) and, unlike in other forms of
muscle contraction, particularly when
rhabdomyolysis, subclinical episodes
horses susceptible to the condition are
characterized by persistently abnormal CK
fit and have a nervous temperament. In
levels are common. Clinical signs in draft

Thoroughbreds, it is likely inherited as
horses may include loss of muscle mass,
an autosomal dominant trait.

progressive weakness, and recwnbency.

Diagnostic tests to detetmine tl1e cause

CK and AST may be normal in draft horses
of chronic tying-up include a CBC, serum
with this syndrome. When draft horses
chemistry panel, serwn vitamin E and
develop rhabdomyolysis, CK and AST may
seleniwn concentrations, urinalysis to
be markedly increased, and horses can
determine electrolyte balance, dietary
become myoglobinuric, weak, and
analysis, exercise testing, muscle biopsy,
reluctant to rise.

and genetic testing. An exercise challenge

Type 2 polysaccharide storage
test is useful to detect subclinical cases;
myopathy occurs in light breeds such as
serun1 CK is measured before and 4 hr after

Arabians, Morgans, Thoroughbreds, a
light exercise. In addition, quantifying the
variety of Warmblood breeds and some
extent of exertional rhabdomyolysis during

Quarter horses. A diagnosis is made by
mild exercise is helpful in deciding how
identifying an abnormal pattern of glycogen
rapidly to reinstate training.

storage in muscle biopsies in a horse with a

A diagnosis of type l PSSM is based on
negative GYSJ genetic test. In Quarter
identification of the GYSJ mutation and/or
horses < 1 yr old, it may cause difficulty
tl1e presence of muscle fibers with
rising from a recwnbent position and
subsarcolemmal vacuoles, dark periodic
increased serwn CK activity. Chronic
acid-Schiff (PAS) staining for glycogen, and
episodes of muscle stiffness, soreness, and
most notably, amylase-resistant abnormal
muscle atrophy with normal to modest
complex polysaccharide accwnulation. A
increases in semm CK are common in
diagnosis of type 2 PSSM is based on the
horses with type 2 PSSM. The most
absence of the G YSJ mutation and the
common presentation of this disorder in
presence of muscle fibers witll aggregates of

Warmbloods is a gait abnorn1ality, exercise
amylase-sensitive PAS-positive staining
intolerance, and loss of muscle mass when
glycogen and occasionally small amounts of
out of work that is not necessarily
amylase-resistant PAS-positive material. A
accompanied by a concomitant rise in
diagnosis of recurrent exertional rhabdomyserum CK.

olysis is based on history, clinical signs,

Malignant hyperthermia is caused by
increases in serwn CK and AST, and muscle
an autosomal dominant mutation in the
biopsy.

skeletal muscle ryanod.i.ne receptor gene

Horses with type 1 PSSM have constitu

(RYRJ). The mutation is responsible for
tively active glycogen synthase that is
both anestl1esia-related and non-anesthesiafurther stimulated by increased blood related causes of rhabdomyolysis in Quarter
insulin concentrations, resulting in high

1180

MYOPATHIES IN HORSES
muscle glycogen concentrations. When fed

INFECTIOUS MYOPATHIES
a starch meal, these horses take up a higher
proportion of the absorbed glucose in their

Virus-associated Myositis
muscles than healthy horses. Horses with

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type 2 PSSM also have abnormal glycogen

Necrosis of skeletal ai1d cai·dia.c muscle may
storage, but the cause of this myopathy is
occur in association with viral diseases such
unknown. Thus, the ideal diet for PSSM is
as equine influenza. and equine infectious
based on feeding forage at a rate of 1.5%-2%
ai1emia. In most situations, viral-induced
body wt, providing> 15% of digestible
muscle dai11age represents a component of
energy as fat and limiting starch to< lOOA, of
systentic multiple organ system involvedaily digestible energy by limiting grain or ment. Equine influenza. 2 has been found to
replacing it with a fat supplement. Caloric
cause severe rhabdomyolysis, a11d equine
needs should be assessed first to prevent
herpesvirus l has been reported to induce
horses becoming obese on a high-fat diet.

primaiy muscle stiffness and clinical signs

Improvement in signs of exertional
resembling exe1tional rha.bdornyolysis.

rhabdomyolysis for horses with PSSM
requires both dietary changes and gradual

Sarcocystis Myositis
increases in the amount of daily exercise

Cysts of the sporozoan pai·asite Sarcocystis
and turn-out.

a.re present in 90% of esophageal muscles

Horses with malignant hype1themtia. may
from horses >8 y:r of a.ge ai1d in 6% of gluteal
benefit from premedication with dantrolene
muscle biopsies from healthy horses.

( 4 mg/kg, PO) 60-90 min before exercise,

Occasionally, heavy infestations occur
paiticula.rly under hot conditions.

tlu·ough contamination of feed with canine

Management of recun-ent exertional
feces, resulting in signs of fever, ai1orexia.,
rha.bdomyolysis is aimed at decreasing the
stiffness, weight loss, muscle fasciculations,
triggering factors for excitement and
atrophy, and weakness. Diagnosis of
pha.m1a.cologic alteration of intra.cellulai·
sa.rcocystosis requires hist01y, clinical signs,
calcium flux with contraction. Management
laboratory evaluation, and the demonstrachanges that may decrease excitement tion of an i:nilanm1a.tory reaction to
include minimizing stall confinement by
immature cysts in muscle biopsies.

using tum-out or a hot walker, exercising

Treatment includes NSAIDs a11d drngs such
and feeding horses with recun-ent
as trin1etl10prim sulfa and py:rimethan1ine or
exe1tional rha.bdomyolysis before other
pona.zuril. (See also SARCOCYSTOSIS, p 1058.) horses, providing compatible equine
company, and the judicious use of low-dose

Anap/asma-associated
tranquilizers during training. A high-fat,
low-starch diet is beneficial, possibly by

Rhabdomyolysis
decreasing excitement. In contrast to horses Horses tl1a.t acquire Anaplasma phagocy
with PSSM, those with recwTent exertional
lophilum from tick i:ni"esta.tions can rai·ely rha.bdomyolysis often require ltigher calo1ic
develop clinical signs of severe muscle
intakes (>24 Meal/day). At these high caloric stiffness in addition to fever, malaise, ai1d intakes, specialized feeds designed for
limb edema. Hematologic findings include
exe1tional rhabdomyolysis a.re necessaiy,
ai1entia, tlu·ombocytopenia, neutropenia.,
because additional vegetable oil or rice bran
morula. visible in grai1ulocytes, and marked
cannot supply enough calories for equine
increases in serum CK and AST levels. A
athletes in intense training. Hay should
diagnosis is con.finned by PCR testing of
be fed at l.5o/o-2% body wt, and high-fat,
blood for A phagocytophilum. A direct toxic low-stai·ch concentrates should be selected
effect of A phagocytoph'ilum on muscle
that provide �20% of daily digestible energy
cells is postulated. Treatment should includP
as nonstructural carbohydrate and 20o/o-25% IV oxytetra.cycline ai1d supportive cai·e.

of digestible energy as fat.

Dantrolene ( 4 mg/kg, PO) given l hr

Streptococcus equi Rhabdomyolysis
before exercise may decrease the release of

Severe rha.bdomyolysis can occur in horses
calcium from the calcium release channel.

with Streptococcus equi equi submandibu

Phenytoi.n (1.4-2.7 mg/kg, PO, bid) has also
lai· lymphadenopa.thy and/or guttural pouch
been advocated as a treatment for horses
empyema. A stilf gait is the i.Jtitial clinical
with recurrent exertional rha.bdomyolysis.

sign, which progresses rapidly to severely

Therapeutic levels vai-y, so oral dosages a.re
pa.i.Jlful, finn, swollen epaxial and gluteal
adjusted by monitoring serum levels to
muscles. Many horses become rectm1bent
achieve 8-12 mcg/mL. However, longterm
with unrelenting pain that may warrant
treatment with dantrolene or phenytoin is
euthanasia. It is not clear whether myoexpensive.

necrosis is a direct toxic effect of S equi

MYOPATHIES IN HORSES

1181
on muscle cells or is due to profound
death may occur in the next 12-24 hr.

nonspecific T-cell stimulation by strepto

Myocardial damage occurs in some horses.

coccal superantigens and the release of

Hematology and serum biochemical
high levels of inflammatory cytokines.

analyses usually reflect a generalized state

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A diagnosis is based on hematologic
of debilitation and toxemia ( eg, hemoconabnormalities typical of S equi infection, centration and a stress/toxic leukogram
marked increases in CK(> 100,000 U/1), and
may be present). Serum CK and AST are

PCR or bacterial culture. Titers to the M
usually moderately increased; however,
protein of S equi are low in affected horses, they often do not reflect the toxicity of
unless they have recently been vacci-
clostridial myonecrosis ..

nated for strangles. At postmortem, large,

Ultrasonographic evaluation of swollen
pale areas of necrotic muscle are evident
areas may reveal fluid and characteristic
in hindlirnb and lumbar muscles. The
hyperechoic gas accw11ulation. Aspirates of
histopathologic lesions are characterized by affected tissues examined via direct smears severe acute myonecrosis with a degree of
or fluorescent antibody staining should
macrophage infiltration. Sublun1bar
show characteristic rod-shaped bacteria.

muscles often show the most severe and

Anaerobic bacterial culture of freshly
chronic necrosis, as indicated by greater
acquired samples may also be of value. Cut
macrophage infiltration of myofibers. The
tissue from tile affected area may reveal
prognosis becomes guarded if animals
abundant serosanguineous fluid with an
become recumbent.

odor of rancid butter. At postmortem,

Appropriate therapy includes IV penicillin swelling, crepitus, and autolysis are rapid, combined with an antimicrobial that
and bloodstained fluid is often seen
inhibits protein synthesis, such as rifampin.

discharging from body orifices.

Flushing infected guttural pouches and

Wound fenestration and aggressive
draining abscessed lymph nodes will
surgical debridement over tile entire
diminish the bacterial load. NSAlDs and
affected area is required for successful
possibly high doses of short-acting
treatment. Additional treatment includes
corticosteroids may diminish tile inflan1rnahigh doses of IV potassiun1 penicillin every tory response. Control of unrelenting pain

2-4 hr until the horse is stable (1 to 5 days),
is a major challenge in horses witll severe
combined with or followed by oral
rhabdomyolysis. Constant-rate infusion of
metronidazole along with supportive fluid
lidocaine, detomidine, or ketamine may
therapy and anti-inflammatory agents.

provide better anxiety and pain relief than

Extensive skin sloughing over the affected
periodic iltjections of tranquilizers. Horses
area is common in surviving horses.

should be placed in a deeply bedded stall
and moved from side to side every 4 hr if

Muscle Abscesses
tlley are unable to rise. Some horses may
benefit from a sling if they will bear weight

Staphylococcus aureus, Streptococcus
on their hindlirnbs when assisted to stand.

equi, and Corynebacte1ium pseudotuberculosis are common causes of skeletal Clostridial Myositis
muscle abscessation, which develops after
penetrating iltjuries or by hematogenous or

A variety of clostridial bacteria can
local spread of infection. Initially there is an
sporulate at tile site of an injection or deep
ill-defined cellulitis, which may heal or
wound, causing focal muscle swelling and
progress to a well-defined abscess. An
systemic toxemia in horses. Clostridium
abscess may heal, expand, or fistulate,
septicum, C chauvoei, C sporogenes, and
usually to tile skin surface witll potential for
mixed infections are associated with a high
a chronic granuloma with intennittent
fatality rate, whereas C perfringens type A discharge. Prognosis is usually good for
has a mortality rate of 20% with early and
superficial abscesses. Deep abscesses are
aggressive treatment. Clostridial spores
more difficult to manage successfully. The
may lie donnant in skeletal muscle, or spore
effect of an abscess on tile horse's gait
deposition directly into the tissue may
depends on its location and can vary from
occur in association with penetration. If
mild stiffness to severe lameness. Ultrasuitable necrotic conditions exist, tile sonography and culture of aspirated fluid
spores convert to the vegetative form,
are tile best means of diagnosis in superfireleasing powerful exotoxins. Within 48 hr, cial sites. Abscesses lying deep within
horses show depression, fever, toxemia,
muscles can be difficult to diagnose. There
tachypnea, and swelling and variable
may be an increased fibrinogen and
crepitus at the iltjection site. Tremors,
nucleated WBCs. The synergistic hemolysin
ataxia, dyspnea, recumbency, coma, and
inhibition test, which detects antibodies to

1182

MYOPATHIES IN HORSES

C pseudo tuberculosis, can be helpful for
abnormalities are usually restricted to mild
detection of internal abscesses. Treatment
to moderate increases in serun·1 CK and AST.

consists of poulticing, lancing, flushing, and

However, in some chronic cases serum
draining. Occasionally, surgical removal
muscle enzyme activities are normal.

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may be required for complete excision. If

Muscle biopsy of epaxial and gluteal
antimicrobial therapy is used, it should be
muscles shows lymphocytic vasculitis,
continued for several weeks.

anguloid atrophy, myofiber infiltration with
lymphocytes, fiber necrosis with mac

IMMU NE-MEDIATED MYOPATHIES rophage infiltration, and regeneration in acute stages. Biopsies of semitendinosus
or semimembranosus muscles may show
lnfarctive Hemorrhagic Purpura
some evidence of atrophy and vasculitis,

Pw1Jura hemorrhagica is often associated
but significant inflammatory infiltJ·ates may
with mild increases in serum CK activity;
be absent. The extent of the inflan1rnatory
however, horses vaccinated for, or exposed
infiltrates in epaxial muscles is such that a
to, Streptococcus equi within the last month diagnosis can often be established from rarely may develop extremely high semm
several fo1malin fixed-core needle biopsy

CK activity, variable edema, acute colic,
samples. The reason why specific muscle
finn swellings within muscle and under the
groups are affected is unclear.

skin, and unilateral lameness. Clinical signs

TreatJnent involves antibiotic therapy for
are due to painful infarctions of skeletal
horses with concurrent signs of infection
muscle, subcutaneous tissue, focal areas
and administration of dexamethasone
of the GI tract, and lungs resulting from a

(0.05 mg/kg for 3 clays), followed by
severe immune-mediated vasculopathy.

prednisolone (1 mg/kg for 7 -10 days)

Hematologic abno1111alities include
tapered by 100 mg/wk throughout 1 mo.

leukocytosis, hyperfibrinogenemia,

Sen.mi CK often normalizes after 7-10 days
hypoalbwninemia, and marked increases
of treatment. Generally, muscle mass
in serwn CK and AST. A diagnosis is often
gradually recovers throughout 2-3 mo even
established based on clinical signs, a
without corticosteroid tJ·eatment. Recurleukocytoclastic vaseulitis in skin and rence of atJ·ophy in susceptible horses is
affected tissues, and a very high S equi
common and may require reintroduction

M protein titer.

of corticosteroid therapy.

Successful treatment requires early
detection, penicillin for 14 days, and

MUSCLE CRAMPING
prolonged high doses of dexamethasone

(0.12-0.2 mg/kg) for at least 10 clays,

Muscle cramping is a painful condition that
followed by tapering doses of prednisolone
arises from hyperactivity of motor tmits
at an initial dosage of 2 mg/kg. Without
caused by repetitive firing of the peripheral
aggressive steroid treatment, the condition
and/or central ne,vous system. The origin of
progresses to intestinal infarction �d
tl1e cramp in most cases is believed to be the
death.

intramuscular portion of the motor nerve
temiinals. Most muscle cramps are also

Immune-mediated Polymyositis
accompanied by fasciculations in the san1e

Immune-mediated polymyositis is
muscle and normal serum CK activity.

characterized by rapidly developing atrophy Muscle cramps can be induced by forceful of the epaxial and gluteal muscles. It is seen
contJ·action of a shortened muscle, by
in Quarter horses, although other breeds
changes in the electrolyte composition
may be affected. The condition shows a
of extracellular fluid, and by ear tick
binlodal age di tribution, affecting horses
infestations. In contrast, muscle contrac

<8 yr or> 16 yr of age. In approxin1ately
tures, like those seen in exe1tional
one-third of affected horses, a niggering facrhabdomyolysis, are painful muscle spasms tor appears to have been exposure to S equi
that represent a state of rn uscle contracture
or a respiratory disease. Rapid onset of
unaccompanied by depolarization of the
atrophy of the back and croup muscles is
muscle membrane. Muscle contractures are
accompanied by stiffness and malaise.

invaiiably accompanied by markedly

Atrophy may progress to involve 500A, of the
increased serwn CK activity.

horses' muscle mass within a week and may
lead to generalized weakness. Focal

Electrolyte Disturbances
symmetric atrophy of cervical muscles has

Muscle cran1ping in endurance horses
been reported in a pony with immuneis most frequent in hot, hwnid weather.

mediated polymyositis. Hematologic

Horses may lose fluids at a rate of up to

MYOPATHIES IN HORSES

1183

15 Ulu in the fom1 of sweat and develop
recurring problem. The most consistently
remarkable deficits in sodium, potassium,
reported metabolic derangement is low
chloride magnesium, and calcium. Clinical
serwn ionized calciwn concentrations
signs of electrolyte derangements include
usually associated with hypochloremic

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muscle stiffness and periodic spasms of
metabolic alkalosis. Metabolic alkalosis
muscle groups. In addition, exhausted
may alter the ratio of free to bound calcium
horses are often dull, depressed, and

(increasing calciun1 binding to protein and
clinically dehydrated with increased heart
decreasing ionized calciun1), which possibly
and respiratory rates and persistently
induces diaphragmatic flutter.

increased body temperature. Synchronous

Most horses undergo rapid remission
diaphragmatic flutter may be seen in
of signs when given calciwn solutions IV.

association with cramping. Affected horses

Altl1ough hypomagnesernia is often present
do not generally develop myoglobinuria or
witl1 syncluonous diapluagmatic flutter,
have marked increases in serum CK and
horses do not respond to magnesiun1

AST levels.

supplementation wtless calcium is

Mild muscle cran1ping is self-limiting, and
administered concurrently. Response to
the signs abate with rest or light exercise.

tl1erapy is also reflected by improved mental

However, exhausted horses with metabolic
status, return of appetite, and gut motility.

derangements require inunediate treatment, For horses with chronic diaphragmatic including plasma volume expansion with
flutter, providing chloride, potassiwn,
oral or IV isotonic polyionic fluids and
sodiw11, calciwn, and magnesiun1 dwing
cooling ( using water and fans). Because
prolonged exercise may help reduce fluid
most horses with this condition are
losses and the metabolic alkalosis.

alkalotic, administration of solutions

Alternative approaches involve reducing
containing sodium bicarbonate is contradietary calciwn for a few days before indicated. Daily direct addition of2 oz of
competition in horses prone to diapluagsodium chloride and 1 oz of potassium matic flutter. Th.is reduction in dietary
chloride to the feed is recommended for
calcium may stin1ulate the endocrine
horses with recurrent cramping, in addition
homeostatic mechanisms and increase
to electrolyte supplementation before and
osteoclastic activity. Lintiting alfalfa hay,
after endurance rides.

which has a relatively high calciun1
concentration, may be indicated in

Hypocalcemia
chronically affected horses.

Hypocalcemia is a relatively rare disorder
in horses that has also been referred to as

Ear Tick-associated Muscle
lactation tetany, transport tetany, idiopathic

Cramping
hypocalcemia, and eclampsia. Clinical
signs, diagnosis, and treatment are

Otobius megnini infestations in tl1e ear
discussed elsewhere
canal can produce remarkably painful

(seep 987). In addition
to hypocalcemia, a metabolic alkalosis,
intemtittent muscle cramps not associated
hypomagnesemia/hypennagnesemia, and
with exercise tl1at last from minutes to a few
hyperphosphatemia/hypophosphatemia
hours and often resemble colic. Horses may
may be present and need correction before
fall over when stin1ulated. Between muscle
a return to normal function is seen.

cramps, horses appear to be nonnal.

Relapses do occur.

Percussion of triceps, pectoral, or
semitendinosus muscles results in a typical
myotonic cramp. Horses have increased

Synchronous Diaphragmatic Flutter
serum CK, ranging from 4,000 to 170,000

("Thumps")

IU/L. Nun1erous ear ticks can be identified

Synchronous diapluagmatic flutter is due
in tl1e external ear ca11al of affected horses.

to firing of the phrenic nerve in synchrony

O megnini is found in tl1e soutl1westem
with atrial depolaiization, causing the

USA. Without treatment, the spasms
diaphragm to contract with each heartbeat.

continue; however, local treatment of the

Th.is occasionally produces an audible
ear ticks using pyrethrins and piperonyl
thumping sound. Inciting causes include
butoxide results in recovery within 12-36
endurance exercise, hypocalcemia,
hr. Acepromazine may be helpful to relieve
hypoparathyroidism, digestive disturpainful cran1ping.

bances, and repeated administration of
calciun1-containi.ng fluids to performance

Shivers
horses. Synchrnnous diaphragmatic flutter

"Shivers" is a spastic condition of the ltindmay be a singular occurrence or a chronic and occasionally forelimbs of horses tl1at is

1184

MYOPATHIES IN HORSES
usually only evident when horses are backing

Foals witll myotonia dystrophica show a
or having their feet picked up. It is most
progression of signs in tile fu'st 1-2 yr of life
common in adult draft horse breeds,
to include areas of muscle atrophy fibrosis

Waimbloods, Warmblood crosses, and
and stiffness tl1at worsens witll exercise.

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Thoroughbreds > 16.3 hands tall. The

Retinal dysplasia, lenticular opacities, and
condition is characterized by periodic,
gonadal hypoplasia have been seen in
involuntary spasms of the muscles in the

Quarter horse, Appaloosa, and Italian-bred
pelvic region, pelvic limbs, and tail that are
foals with myotonic dystrophy.

exacerbated by backing or picking up the

A tentative diagnosis of myotonia can be
hindlimbs. The affected limb is elevated,
made on the basis of age and clinical signs
abducted, and may actually shake and shiver;
of stiff gait, muscle bulging, and prolonged
the tail head is usually elevated concurrently
contractions after muscle stimulation.

and trembles. When more severely affected

Definitive diagnosis of myotonia requires
animals are backed up, the hindlimb is
electromyographic examination. Affected
suddenly raised, semiflexed, and abducted
muscle mailifests pathognomonic, crewith the hoof held in the air for several scendo-decrescendo, high-frequency
seconds or minutes. The tail is elevated
repetitive bursts with a chai·acteristic "dive
simultaneously and trembles. After a variable bomber" sound. Myotonia dystrophica pe1iod of time the spasms subside, tl1e limb is shows dystrophic changes in muscle biopsies extended, and the foot is brought slowly to
not present in myotonia congenita.

tl1e ground. Some horses will refuse to pick

Dystrophic changes include ringed fibers,
up their hindlimbs and are very difficult to
numerous centrally displaced myonuclei,
shoe. Suggested causes include genetic,
sarcoplasmic masses, and an increase in
traumatic, infectious, and neurologic
endomysial and perimysial connective tissue.

diseases, although the exact etiology is

Fiber type grouping and atrophy of botl1 type
unknown. The condition in draft horses

I and type II muscle fibers may be present.

is usually progressive and eventually

Horses witll myotonia congenita or
debilitating; in Warmbloods and Thoroughdystrophica are rai·ely serviceable, and breds, it usually has less impact on perforeutllanasia is usually warranted in mai1ce and progresses more slowly. There
dystrophic foals because of the severity of
are no known treatments, but avoiding stall
stiffness and atrophy tllat develop over
rest and keeping horses fit appears helpful.

time. Conclusive evidence regarding tile
genetic basis of tl1is disorder in horses is

MYOTONIC DISORDERS
still not available.

Myotonic muscle disorders share the

Hyperkalemic Periodic Paralysis
feature of delayed relaxation of muscle
after mechanical stimulation or voltmtary

Hy PP is an autosomal dominant trait
contraction due to abnonnal muscle
affecting Quarter horses, American Paint
membrane conduction. Horses have tllree
horses, Appaloosas, and Qua1ter horse
known forms of myotonia: myotonia
crossbreeds worldwide. The point mutation
congenita, myotonia dystrophica, and
in tile voltage-dependent skeletal muscle
hyperkalemic periodic paralysis (Hy PP).

sodium chaimel alpha subunit occurs in -4%
of Quarter horses, but this percentage is

Myotonia Congenita and
much higher in halter and pleasure horse
performance types.

Dystrophica

Clinical signs range from asymptomatic

The initial signs of myotonia in foals are
to intennittent muscle fasciculations and
well-developed musculature and mild pelvic weakness and are first identified in foals to limb stiffness. Bilateral bulging ( dimpling)

horses 3 yr of age. Homozygous horses are
of the thigh and rump muscles is often
often more severely affected and may be
obvious and gives tl1e impression that tile
identified at a younger age tllan heterozyaninlal is very well developed. Percussion of gotes. A brief period of myotonia is often affected muscles exacerbates the muscle
seen initially, witll some horses showing
dimpling below a large ai·ea of tight
facial myotonia and prolapse of the tllird
contraction tllat can persist for a minute
eyelid. Muscle fasciculations beginning on
or more with subsequent slow relaxation.

the flanks, neck, and shoulders may become

Myotonia congenita usually does not
more generalized. Altllough most horses
show progression of clinical signs beyond
remain standing during mild attacks,

6-12 mo of age, and muscle stiffness
weakness witll swaying, staggering, dogmay improve with exercise. The cause sitting, or recmnbency may be seen, witll
has not been identified.

severe attacks lasting 15-60 min or longer.

MYOPATHIES IN HORSES

1185

Heart and respirato1y rates may be
wheat, and barley; and beet pulp should be
increased, but horses remain relatively bright fed in small meals several tin1es a day. Regular and alert. Respiratory distress occurs in
exercise and/or frequent access to a large
some horses as a result of upper respiratory
paddock or yard are also beneficial. Pasture is

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muscle paralysis. Once episodes subside,
ideal for horses with Hy PP, because the high
horses regain their feet and appear nonnal
water content of pasture grass makes it
with absent or minimal gait abnmmalities.

unlikely that ho1ses will consume large

Young horses that are homozygous for the
amounts of potassium in a short period of

Hy PP trait may have respiratory stlidor and
ti.me. Complete feeds for horses with Hy PP
pe1iodic obstruction of the upper respiratmy
are conrn1ercially available. For horses witl1
tract that can be fatal.

recurrent episodes even with dietary

Common factors that ttigger episodes
alterations, acetazolamide (2---4 mg/kg, PO,
include sudden dietary changes or ingestion
bid-tid) or hydrochlorothiazide (0.5-1 mg/kg,
of diets high in potassiw11 (>1.1%), such as

PO, bid) may be helpful. Breed registries and
those containing alfalfa hay, molasses,
other associations have restlictions on tl1e
electt·olyte supplements, and kelp-based
use of these drugs dwing competitions. Some
supplements. Fasting, anesthesia or heavy
hmses have both HyPP and polysaccharide
sedation, trailer rides, and stress may also
storage myopathy (PSSM) (seep 1178), which
precipitate clinical signs. TI1e onset of signs,
may result in an episode of rhabdornyolysis
however, is often unpredictable. Exercise per dming a hyperkalemic paralytic event with se does not appear to stimulate clinical signs;
subsequent increased serum CK activity and
serun1 CK shows no or minimal increases
prolonged recun1bency.

dwing episodic fasciculations and weakness.

Descent from the stallion Impressive in
a horse with episodic muscle tremors is

NUTRITIONAL MYOPATHIES
strongly suggestive ofHyPP. Hyperkalemia

(6-9 mEq/1), hemoconcentration, and

Nutritional Myodegeneration
hyponatremia are seen dwing clinical

Yow1g, rapidly growing foals born to dams
episodes, but a definitive diagnosis requires
that consun1ed selenium-deficient diets

DNA testing of mane or tail hair. Electrodwing gestation can develop nutlitional myographic examination of affected horses
myodegeneration (NMD; see p 1172).

between attacks reveals abnom1al

Seleniun1 deficiency has also been in1plicated
fibrillation potentials and complex
in rnasseter muscle myopathy and occasionrepetitive discharges, with occasional ally nonexertional rhabdomyolysis in adult
myotonic potentials and trains of doublets
hmses. Seleniw11 and vita.min E appear to be
between episodes. Differential diagnoses
synergistic in preventing NMD. Clinical signs
for hyperkalemia include delay before
in foals include dyspnea; a rapid, ilTegular
sernm centrifugation, hemolysis, chronic
heaitbeat; and sudden death in those witl1
renal failure, and severe rhabdomyolysis.

myocai·dial involvement. Dysphagia, muscle

Many horses recover spontaneously from
stiffness, trembling, finn muscles, difficulty

Hy PP episodes. Owners may abort early
rising, and myoglobinuria may also be seen.

mild episodes using low-grade exercise or

Aspiration pnewnonia is a frequent complicafeeding grain or com syrnp to stimulate tion. Diagnosis is based on finding moderate
insulin-mediated movement of potassium
to markedly increased serun1 CK and AST,
across cell membranes. In severe cases,
combined with low whole blood seleniw11
administration of calcim11 gluconate (0.2-0.4 concentt·ations ( <0.07 ppm) or vitan1in E
ml/kg of a 23% solution diluted in 1 L of 5%

( <2 ppm). Hyperkalemia, hyperphosdextrose) or IV dextrose (6 ml/kg of a 5%
phatemia, hyponatremia, hypochloremia,
solution), alone or combined with sodimn
and hypocalcernia can occur with severe
bicarbonate (1-2 mEq/kg), often provides
rhabdornyolysis when tl1e nom1al distinction
immediate in1provement. With severe
between extt·acellular and intracellular
respiratory obstrnction, a tracheostomy
compartments is destroyed by massive tissue
may be necessary. Acute death is common,
necrosis. Seleniwn-dependent glutathione
especially in homozygous anin1als.

peroxidase fom1ed in RBCs dming e1ythro

Prevention requires decreasing dietaty
poiesis also provides an index of body
potassium to 0.6%-l.1% total potassium
selenium status. Treatlnent includes IM
concentt·ation and increasing renal losses of
injection of selenimn (0.055-0.067 mg/kg)

potassiun1. High-potassium feeds such as
and either injectable or oral vitatnin E
alfalfa hay, first cutting hay, bro me hay, sugar

(0.5-1.5 IU/kg). Suppmtive therapy includes
molasses, and beet molasses should be
administering antibiotics to combat
avoided. Optin1ally, later cuts of timothy or
secondaiy pneumonia, feeding via nasogas

Bem1Uda grass hay; grains such as oats, com,
tlic tube, providing adequate energy intake,

1186

MYOPATHIES IN HORSES
and maintaining fluid and electrolyte

Affected horses are reluctant to move, have
balance.

muscle weakness and fasciculations, and
may become recumbent. Choke may be

PLANTS CAUSING MYOPATHIES
present, and gut sounds may be reduced,

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with reduction in feces production,

Horses ingesting 0.5%--2% body wt of
although appetite may be unaffected. Heart
trematone-containing plants are likely to die rates may be markedly increased, and from skeletal muscle and cardiac muscle
pulmonary edema may be present. The
necrosis. Horses present with marked
horses do not show signs of pain, despite
depression, weakness, low head posture,
evidence of widespread myopathy at
and increased cardiac and respiratory rates.

necropsy. Metabolic and respiratory

Serum AST and CK are often markedly
acidosis, increased cardiac troponin 1,
increased, and serwn electrolyte abnormalisubstantial increases in serwn CK and AST, ties such as hypocalcemia, hyponatremia,
and myoglobinuria also are common.

hypochloremia, hyperkalemia, and

Necropsy reveals widespread myodegenhyperphosphatemia may be present.

eration in postural and respiratory skeletal

Treatment is generally supportive.

muscles and the myocardiwn. A definitive

Trematone (seep 1175) has been identified
diagnosis can be made by identifying a
in white snakeroot (Eupatorium rugosum) pattern of accumulation of short- and and rayless goldenrod (lsocoma wrightii).

mediun1-chain serum acylca.rnitines and

Trematone remains active in the hay and in
specific urine organic acids and glycine
the stalks of the dead plants on pasture, so
conjugates typical of a deficiency in multiple
both the fresh and dried fom1s of the plants
a.cyl CoA dehydrogenases. Special stains for
should be kept from horses.

lipid reveal excessive lipid storage in the

Muscle necrosis may also occur in horses
heart, dia.phragnl, and other oxidative
ingesting Senna occidentalis seeds
postural muscles. Supportive therapy,
prevalent in the southeastern USA. Horses
including antioxidants ( eg, vita.min C,
develop incoordination, recumbency, and
vita.min E, riboflavin), and IV fluids
death. Gross skeletal muscle lesions are not
containing dextrose are recommended.

present, but histopathologic lesions include

Fewer than 75% of horses survive.

segmental myonecrosis.

One of 70 horses poisoned with blister

TOXIC MYOPATHIES
beetles (seep 3157) developed muscle
necrosis.

lonophores

Atypical Myoglobinuria

Ionophores are commonly added to rwninant
feeds for their growth promotion and coccid i

(Pasture myopathy)

osta.t properties. Horses, however, are 10

Atypical myoglobinuria occurs sporadically
times more sensitive to the toxic effects of
in horses kept on pasture, usually with no
ionophores in feed than cattle. When equine
supplemental feeding. It has been .recogfeeds are inadvertently contaminated witl1
nized most commonly in the UK and
ionophores or horses eat cattle feed, some

Europe, but a similar syndrome has been
anin1a.Js may die a.cutely with colic-like signs,
seen in North America. It occurs most often
myoglobinuria., hypokalemia., cardiac
in autumn but can occur in early spring; it
a.rrhytl11Tlia, and ta.chypnea Cardiomyopa.thy
often follows very windy or rainy weather
is the most common chronic sequela
and a cool spring. Ingestion of seeds of Acer
species trees such as the box elder (Acer

TRAUMATIC AND ANESTHETIC
negundo) in North America and European

MYOPATHIES
sycamore maple (Acer pseudoplatanus)

are implicated in the pathophysiology of

Postanesthetic Myopathy
this myopathy. These seeds contain the

After anesthesia., horses may develop severe
toxic nonproteogenic amino acid hypoglymuscle pain and weakness in one or more cin A, the toxic metabolite of which
muscle groups. Hypoperfusion of comirreversibly binds to multiple acyl CoA pressed muscle groups with resultant high
dehydrogenases, enzymes essential for
intra.compartmental pressure is the most
metabolism of short- and medium-chain
important causative factor for focal muscle
fatty acids and branched-chain amino acids.

involvement. The dependent triceps muscle

The clinical signs are sudden in onset and
is most commonly affected after anesthesia
rapidly progressive, frequently resulting in
in lateral recwnbency, whereas the
death. Several horses in a group may be
longissimus dorsi and gluteal muscles are
affected, although some may have no signs.

usually affected in horses that have been in

MYOPATHIES IN HORSES

1187
dorsal recumbency. Generalized myopathies of fibrotic myopathy. Affected muscles in may develop in horses that were hypotenacute cases are warm and painful on deep sive during anesthesia. The longer the
palpation. Chronically, hardened areas
duration of anesthesia, the higher the risk.

within the muscle may represent fibrosis and

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Signs are evident when horses try to stand
ossification. The associated gait abnom1ality
or may be delayed for up to 2 hr. A dropped
is usually most apparent at the walk and is
elbow stance typical of radial nerve
characterized by an abmpt cessation of the
paralysis characterizes triceps myopathy.

anterior phase of the stride of the affected

Gluteal myopathy results in unwillingness to limb, causing the leg to jerk suddenly to the bear weight on the hindlin1bs. Horses may
ground rather than continue its forward
appear distressed, with profuse sweating,
motion. The stride has a sho1't anterior phase
tachycardia, and tachypnea. The degree of
with a characteristic hoof-slapping gait. The
distress depends on the severity of muscle
gait reflects a mechanical hindlirnb lameness
damage. Affected muscles may feel very
that restricts normal function. Pain is usually
hard and show localized swelling. Semm CK
not a feature of chronic fibrotic myopathy.

may be nonnal immediately after the horse

Serum CK and AST are usually only mildly
stands but rise substantially and peak -4 hr
increased. In addition to palpation, diagnosis
after anesthesia. Pain relief is provided by
can be confirmed by ultrasonography,
sedation with detomidine, combined with
them10graphy, or scintigraphy. Light
opiate analgesics and NSAIDs. Constantnticroscopic evaluation of muscle biopsies rate infusions of detomidine or butorphanol
is frequently normal in acute cases. Chromay be beneficial for pain control in severe nically, fibrous replacement of muscle fibers
cases. Fluid therapy helps maintain renal
is apparent. Acute cases may benefit from
perfusion and urine output and ensures
rest and cold therapy followed by deep
adequate muscle perfusion. The prognosis
heating ultrasound and controlled stretchfor unilateral myopathy is usually good, ing. Clu·onic cases may require surgical
although with severe dan1age there may
excision or transection of the fibrotic part of
be residual muscle fibrosis, which may
tl1e muscle or tenotomy of the tibial insertion
compromise function. The prognosis for
of the senti.membranosus tendon.

generalized myopathy is more guarded.

Prevention requires minimizing the
time under general anesthesia, carefully

HEREDITARY AND CONGENITAL
positioning the horse on the operating table,

MYOPATHIES
and maintaining arterial blood pressure

>60 mmHg using fluid therapy and inotropic

Mitochondrial Myopathy
agents such as dobutanline (1-5 mcg/kg/min). A deficiency of Complex 1, the fu-st step in the mitochondrial respiratory chain, was

Malignant Hyperthermia
identified in a young Arabian filly with

The ryanodine receptor gene (RYRJ)

clinical signs similar to those of exertional
mutation in Quarter horses (seep 1178)

rhabdomyolisis. However, tltis horse
can cause fatal reactions under general
showed no changes in serum CK level
anesthesia that are characterized by
after exercise. A marked lactic acidosis
marked hyperthemtia, acidosis, electrolyte
developed even with light exercise, and
derangements, and muscle necrosis.

maximum oxygen consun1ption was

Unfortunately, once a fulminant episode is
drastically reduced, resulting in marked
underway it is difficult to prevent cardiac
exercise intolerance. Histopathologic
arrest. Diagnosis is by clinical signs and
evaluation of muscle biopsies showed an
genetic testing. Pretreatment with oral
abnormal increase in mitochondrial density,
dantrolene ( 4 mg/kg) 30--60 min before
and biochentical analyses revealed a
anesthesia is the only potential means to

Complex 1 deficiency. The horse has shown
prevent an episode.

slowly progressive signs of muscle atrophy
but has otherwise remained healthy at rest.

Fibrotic Myopathy

Fibrotic myopathy describes a classic gait

Glycogen Branching Enzyme
abnormality that develops when horses

Deficiency
iitjure their sentitendinosus and senti.mem

Glycogen branching enzyme deficiency
branosus muscles at the point of a tendinous

(GBED) is a glycogen storage disorder
insertion during exercise that requires
causing abortion, seizures, and muscle
abrupt turns and sliding stops. Trauma ( eg,
weakness in Quarter horse-related breeds
catching a foot in a fence), IM injections, and
caused by an autosomal recessive mutation
a congenital form are other potential causes
in the glycogen branching enzyme (GEE])

1188

MYOPATHIES IN HORSES
gene. The mutation is canied by goA, of
of affected foals. Gross lesions are not

Quarter horses and Paint horses, and at
evident, and routine H&E stains of tissues
least 3% of abortions are atttibuted to GBED may be nonnal or show basophilic in Quarter horses. Most foals diagnosed
inclusions in skeletal muscle and cardiac

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with GBED present at l day of age with
tissues. Frozen sections of muscle, heart,
hypothermia, weakness, and flexural
and liver show a notable lack of nonnal PAS
defo1mities of all limbs. Ventilatory failure
staining for glycogen as well as abnormal
may also be a presenting sign in addition to

PAS-positive globular or crystalline
recurrent hypoglycemia and collapse. All
intracellular inclusions. Branching enzyme
foals have died either from euthanasia
activity is mini.ma! in skeletal and cardiac
because of muscle weakness or suddenly
muscle as well as liver. A diagnosis is best
because of apparent cardiac arrhytJu11ia.

obtained by con.finning the presence of the

Persistent leukopenia, inte1mittent
genetic mutation in tissue samples or by
hypoglycemia, and high serum CK
identifying typical PAS-positive inclusions

(1,000-15,000 U/L), AST, and -y-glutamylin muscle or cardiac san1ples. There is no transferase activities are features
successful treatment.

BOVINE SECONDARY RECUMBENCY

(Downer cow syndrome)

Recrnnbency in cattle is caused by numerous tion of petiparturient hypocalcemia (milk metabolic, traumatic, infectious, degenerafever, see p 988) in cows that do not fully tive, and toxic disorders. lf treatmentof the
respond to calciw11 therapy. Calving

LU1derlying cause of recLUTibency is not
paralysis after clystocia may also result in
successful and cattle arf' unable to 1ise for
recrnnbency clue to traLUTiatic ir\jury to

>24 hr after initial recLUTibency, they may
tissues and nerves inside the pelvic cavity.

develop a secondary recwnbency from

Regardless of tl1e initial cause of recLU11-
pressure dan1age to muscles and nerves,
bency, all cattle develop pressure-induced
often tem1ed "downer cow syndrome." An
damage to muscles and nerves of ilie pelvic
alert downer cow does not show signs of
limbs, especially when lying on a hard
systemic illness or depression, is able to eat
surface. The hindlimb muscles of the leg the
and drink, and remains in sternal recLUTIanimal is lying on a.re compressed between bency for no apparent reason. A nonalert
tl1e bones and ilie skin by ilie physical
downer cow appears systemically sick and
pressure from ilie weight of the recLUTibent
depressed. Downer cow syndrome also
cow.

describes the pathology of pressure-induced

Wiili prolonged recumbency ( eg, if
muscle and nerve ir\jwies after prolonged
treatment of hypocalcemia is delayed), the
recLUTibency. The most inlportant patholyn1phatic and venous drainage to muscle is physiologic event that develops dwing
decreased because of sustaine\:I pressure
prolonged recLU11bency is a pressure-induced with no decrease in arterial blood flow. The ischemic necrosis of the thigh muscles that
net result of pressure-induced changes in
frequently affects both hindlegs.

blood flow is an increase in interstitial fluid
onambulatory disabled livestock are
voltm1e and presstu-e within the muscle,
those that cannot rise from a recLUTibent
because the fascia around each muscle
position or that cannot walk. This includes,
cannot expand sufficiently to accommodate
but is not limited to, those with broken
ilie increase in interstitial volLUTie. ln severe
appendages, severed tendons or ligaments,
and prolonged cases of recw11bency, the
nerve paralysis, a fractured vertebral
increase in intran1uscular pressure is visible
column, or metabolic conditions. Downer
as a finn swelling of the muscle. The
cows have been categorized according to
resulting compre�sion of muscles, nerves,
potential diseases of the C S into nonarnbuand blood vessels witlli.n an enclosed latory cows wiili progressive or nonprogrescompartment induces ischemic pressw-e sive neurologic findings.

dan1age of muscle and nerves, also named
compaitment syndrome. The sevetity of

Etiology and Pathogenesis: ln most
pressure dainage to tl1e muscles depends on
cases, downer cow syndrome is a complica-
regional anatomic factors (bones), duration

BOVINE SECONDARY RECUMBENCY

1189
of compression, and the surface on which

The positioning of the hindlimbs may
the animal is kept.

indicate the cause of the recumbency. Limbs

Pressure myopathy in downer cows
splayed out behind tl1e anin1al may indicate
is often complicated by damage to and
obturator neive paresis or paralysis, hip

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functional loss of the sciatic neive and its
dislocation, or fracture of the femur or tibia.

peroneal branch. The sciatic neive may be

Fracture should be suspected whenever the
damaged by direct compression against the
upper lin1b is extended sideways in such a
caudal femur, secondary swelling of the
maimer that a crease is formed in the skin.

sun-ounding muscles, or both. The degree of
dan1age to the sciatic neive is thought to be

Physical Examination: A thorough
a critical factor for recovery of downer
physical exan1ination should be pe1fonned
cows. Damage to the peroneal branch of the
when the cow is first presented. The rectal
sciatic neive results from direct pressure on
temperature should be wiU1in the normal
the neive as it crosses over the lateral
range. If it is lower than normal, some level
condyle of the femur.

of shock might be present. Recession of ilie

Experin1ental sternal recumbency in
eyes into tl1e orbit or persistence of a skin
halothane-anesthetized cattle for 6--12 hr,
fold for >2 sec indicates dehydration. Pallor
with the right hindlin1b positioned under the
of the mucous membranes suggests
body, resulted in a swollen and rigid limb and
toxen1ia, in which case a weak pulse and
pe1manent (tem1inal) recumbency in 500Ai of
tachycardia may be present. The respiration
the cases. Cattle able to stand after anestheof a recumbent cow may be labored by sia showed hyperflexion of the fetlock,
virtue of tl1e pressure of tl1e abdominal
indicating peroneal neive paralysis, and
contents on the diaptu·agm.

myoglobinuria with dark brown urine.

Vaginal exploration is mandatory in every

Necropsy of terminal downer cases revealed
peripartwn, recumbent cow and may lead to
extensive necrosis of the caudal tl1igh
discovery of a decomposing fetus. Damage
muscles and inflanrn1ation of the sciatic neive to and infection of tl1e wall of the vagina is caudal to tl1e proximal end of the femur.

conunon. Metritis and an associated

Additional complications of prolonged
toxemia can contribute to postpaitun1
recumbency include acute mastitis,
recun1bency.

decubital ulcers, and traumatic irtjuries to

Rectal exploration is essential for
the limbs ( eg, laceration and rupture of
differential diagnosis. The degree of uterine
muscle fibers in the thigh) from struggling
involution should be appropriate for the
and efforts to rise.

number of days postpartwn. Ballottement of
fluid in tl1e organ or lack of tonicity should

Clinical Findings: Periparturient cows
be noted. Unexpected anomalies may be
may be found in lateral recumbency, which
palpated. Adhesions, lwnps of necrotic fat,.

may indicate an unresolved metabolic
and enlargement or turgidity of tl1e ceIVix
problem such as hypocalcen1ia or
or vaginal wall are all sequelae of a difficult
hypomagnesen1ia Inquilies into the severity
birtl1. Hip dislocations and fractures of
and duration of parturition may suggest tl1at
tl1e pelvis may be palpated per rectum,
the recun1bency is at least partially due to
particularly if an assistant vigorously
exhaustion. In involuntary sternal recummanipulates the upper limb of a cow in bency, some cows may have a dull, listless
lateral recun1bency. Movement of the head
appearance. This may indicate hypocalceof tl1e femur in the obturator foran1en may n1ia in peripaiturient mature cows. The
also be detected in cattle witl1 caudoventral
second most likely cause of depression
hip dislocation. Craniodorsal dislocation of
is toxemia, the cause of wl1ich is most
the hip, tl1e most common direction for hip
commonly found in the genital tract or mamdislocation, or fracture of the femoral neck mary gland. Other cows found in involunor proximal femur should be suspected if tary sternal recun1bency may be bright and
the affected limb appears shorter than the
alert in appearance-the most typical
contralateral limb. Pelvic fractures can be
demeanor of the true problem downer cow.

associated with sciatic neive paralysis,

If the animal is young or not pregnant, the
whereas hip dislocation may be associated
cause is likely to be either physical damage
with some degree of obturator nerve
or a rare condition, either of which requires
paralysis. If eitl1er condition is suspected,
careful, detailed examination.

the sensory state of tl1e lin1 bs should be

The environment of the animal can have
evaluated by judicious and hw11ane
a bearing on the cause. If the footing is
application of an electric prod to the distal
slippery, physical damage to tl1e musculolimb. lnvoluntaiy sternal recun1bency may skeletal system should be suspected. This is
be associated with lyrnphosarcoma of the
much less likely among cows in open space
spinal canal, ve1tebral abscesses, or bizan·e
witl1 a dirt or well-bedded surface.

traun1atic irtjuries.

1190

BOVINE SECONDARY RECUMBENCY

Manunary gland examination should
treatments pending results of laboratory
always be performed on recumbent cows.

tests. Monitoring blood mineral status is an

A toxic infection of the udder with an
important part of downer cow management.

organism such as Escherichia coli can be
ln most cases, recovery depends on the

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a primary cause of recumbency. However,
quality of recumbency management and
such an infection may be precipitated by
nursing care. Lateral recW11bency must be
the recw11bency, especially if the udder is
corrected inu11ediately to avoid regurgitaengorged and remains wunilked.

tion and inspiration of stomach contents.

Blood samples are not usually taken

The anin1al should be rolled into sternal
when treating routine cases of hypocalcemia recumbency. However, if this posture is to However, hypocalcemia, hypophosphatemia, be maintained, the lin1b on which the animal and hypokalemia should be assumed to be
has been lying should be drawn from Wlder
present in all recwnbent cattle, and dete1°
tile body. In oilier words, if the animal was
mination of the biochemical status of cattle
presented in lateral recW11bency on its left
unresponsive to calcium therapy frequently
side, it should be rolled into sternal
helps guide treatment and prognosis.

recumbency on its right side. Suppo1t ( eg,

Hypokalemia and hypophosphatemia are
straw bale) placed Wlder the shoulder may
conunonly quoted causes of creeper cows
be required for some animals to maintain

( cows able to crawl but Wlable to stand).

sternal recW11bency.

Ale1t downer cows may have normal serW11

Attempting to stabilize a recW11bent cow
concentrations of calciw11, potassium,
on a concrete surface is highly undesirable
magnesiwn, and phosphorus. Downer cows
but sometimes unavoidable. Bedding the
have increased serwn CK, AST, and LDH;
area around and Wlder the cow with wet,
cows that do not recover have higher serum
sticky manure to a depth of >6 in. is a

AST and CK activities than cows that do
common practice. At least 10 in. of dry
recover. Increased serum CK activity is a
straw should be distributed over the wet
specific indicator of muscle damage;
mass. If the cow struggles and scrapes the
however, CK activity peaks shortly after
wet manure, exposing concrete, more
the stait of muscle damage and declines
manure must be added. The manure pack
noticeably within 4 hr. For this reason,
provides good footing but also may soil tl1e
increased serW11 AST activity is the best
skin with wine and manure. Dermatitis can
prognostic indicator in recwnbent cattle,
result, and cow comfort is reduced. More
with higher AST activities indicating a
seriously, the risk of mastitis resulting from
poorer prognosis. In cattle with severe
tile containinated environment is ve1y high.

muscle dan1age, the urine may contain

A bed of sand > 10 in. deep provides a more
myoglobin as well as higher than nonnal
effective method to house a recW11bent cow.

concentrations of protein. The age and

A sand bed usually drains well, and good
mean serum concentrations of phosphorus,
hygiene can be maintained if voided manure
magnesium, sodium, bilirubin, glucose, and
is removed several times a day.

urea are not significantly different between

Some recumbent cattle appear to lose
recovering and nonrecovering c;;ows.

interest in trying to stand; tllese cattle may

Lesions: Ischemic necrosis and ruptw·e
benefit from use of a specially designed
of muscles of the thigh region are co nun on
flotation tank that has a volume of
necropsy findings in downer cows. Hemor

-2,500-3,000 L. Cattle are loaded into tile
rhage and rupture of adductor muscles may
flotation tank by being dragged on a mat
be seen if the aninlal "spread-eagled" itself into the empty tank Doors are then put in
while stiuggling to rise on a slippery surface
place, and the tai1k is filled witll lukewan11
such as wet or icy concrete. Trawnatic and
water. Cold or hot water should be avoided,
inflanunatory irtjuries to sciatic and peroneal
because it can induce hypotl1er.n1ia or
ne1ves are also foWld in downer cows.

hyperthernua. Cattle should be encouraged

Damage to intra.pelvic nerves, such as the
to stand once the water reaches tile level of
sciatic and obturator nerves, accollilt for
the scapulohurneraljoint. When tile cow
most cases. Decubital ir\juries to the lateral
stands, the musculoskeletal and nervous
aspect of the stifle can be associated with
systems should be thoroughly examined
damage to the peroneal ne1ve.

to identify Wlderlying disease processes.

Cattle that can'support tlleir own weight
should be pern1itted to stand for 6-8 hr;

Treatment: Downer cows are often
however, tile water in tile tank should be
hypocalcemic. If an apparently hypocalceremoved as soon as cattle exhibit trembling.

mic cow does not respond to calcium

Cattle that remain standing should be
therapy, potassiw11, phosphorus, and
encouraged to walk slowly from the tank on
magnesiw11 should be given as additional
a nonslip surface. Cattle able to walk out of

BOVINE SECONDARY RECUMBENCY

1191
the tank after the first flotation treatment
become reestablished. The device is lifted
are 4.8 times more likely to smvive than
until the hindfeetjust touch the ground.

those that do not walk out of the tank. Cattle Often, the cow will hang with the limbs that stand on all fom limbs during the first
slightly flexed. This should not be confused
flotation treatment are 2.9 times more likely
with unilateral flexion, which indicates

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to smvive than those that had an asymmetperoneal paralysis. Next, one assistant on ric stance or were unable to stand. Reported each side of the cow presses a shoulder into success rates in retmning recumbent cattle
the paralun1bar fossa while facing the
to nonnal ambulation range from 37%-46%.

hindlimb. The device is slowly lowered

Hobbling may be considered in cows
as the assistants attempt to force each
suspected to have obturator or sciatic nerve
hindlimb into a weightbearing postme and
damage to prevent overabduction that can
to reduce the flexion by manipulating the
lead to muscular damage. Ropes should
stifle and hock. As soon as any weight is
never be used for this purpose. A soft nylon
supported by the two limbs, the device
strap may be wrapped twice around the
should be lowered 1-2 in. This process
middle of each metatarsus, alJowing a
may have to be repeated several times.

distance of at least 3 ft between the legs.

Even if the cow does not stand, the lifted

Assisting Cows to Rise: On every day of
position provides an opportw1ity to
the recw11bency, an attempt should be made
manipulate the limbs, auscultate for
to bring the cow to its feet. Several simple but
crepitation, and perfom1 vaginal and rectal
effective techniques can be tried. In one
examinations.

method, the clinician stands with feet pressed

Moving Recumbent Cows: The chances
under the cow at a point below the scapuloof resolution are considerably enhanced hwneraljoint. A sharp blow is delivered by
by moving the cow to a location with an
chiving the knees into the muscle mass below
earthen floor. In warm, relatively dry
and caudal to the scapula. This metl10d must
weather, the best location for a recumbent
not be used on the thoracic walJ unprotected
cow is grassy pastme, altl10ugh tl1is means
by the muscle mass to avoid fractming the
that a metl10d to lift the cow must be readily
ribs. If the anin1al struggles to rise, an
available. Otherwise, the location selected
assistant should grasp the root of the tail with
should have a roof and some protection
both hands and lift. Lifting on any other part
from the elements. These conditions often
of tl1e tail may cause damage. Recently calved exist in a hay barn or implement shed, cows can be motivated to rise if they hear
which may have the added benefit of
their own calf bawling with htmger. The calf
allowing installation of a pulley system
is best restrained close to the cow but out of
to lift the cow.

her sight. Some workers use electric goads

Moving the cow requires rolling her into
and various anecdotal or traditional methods
lateral recun1bency. The cow can then be
of inflicting pain to stimulate a cow to rise;
slid over clI-y straw for a short distance by
tl1ese measmes have a low success rate in
pulling on a rope attached to a lower
inexperienced hands and are not recomforelimb and a halter rope. Transportation mended.

over longer distances can be accomplished

The value of hip clamps is controversial.

using a suitably prepared frum gate hauled

Their proper use requires experience, skill,
by tractor. The longest dimension of the
and a delicate touch. Continual use causes
farm gate is closely applied to the back
trauma and pain that is counterproductive.

of the cow still in lateral recw11bency. A

The forelin1bs support 600Ai of a cow's weight
tarpaulin is placed on the gate to protect the
and, therefore, the use of a canvas sling
cow from contact with the ground. 01-y
under the stemun1 is almost mandatory for
straw is spread on the tarpaulin, and the
consistent success. A chest band is required
cow is rolled over onto the makeshift
to prevent the sling from slipping backward.

stretcher. The halter should be tied to the

If the sling is suspended from the tine at one
gate to minimize struggling, and a sack
end of a fork lift, and the hip clamps from a
placed over tl1e eyes to minin1ize alam1
tine at the other end, minimal trauma results.

while the cow is being moved. The tail is

If a fork lift is not available, a T-bar
best tied to the hock of the upper lin1b. Once
suspended by a pulley from an overhead
moved, the cow should be restored to
beam ( or a tripod for anin1als at pastme) will sternal recun1bency. A few cows, particuserve. The jaws of the clan1ps must be well larly if< 12 hr postpartum, will rise
protected with synthetic foam or rubber
i.nm1ediately after being moved to a location
secured in place with a wrap of duct tape.

with good footing.

Hip clamps should not be applied too

Recun1bent cattle should be examined
tightly and should lift the cow slowly to
daily to detemtine any change in ability to
allow time for the circulation of the lin1bs to
rise or bear weight. The chance of in1prove-

1192

BOVINE SECONDARY RECUMBENCY
ment is very low if the cow does not show
monitored closely around calving for early
any improvement within 5 days of moving to
signs of partwient paresis (seep 988).

a location with good footing and correction

Prophylactic administration of calciwn to all
of any serum electrolyte abnonnalities.

cows, beginning with cows entering their

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Supportive Care of Recumbent Cows:

second or later lactation, is beneficial in

It is vital that recumbent cows be provided
herds with a high incidence of milk fever,
with clean water at all times. A shallow
especially in smaller farms that cannot
rubber feed bowl prevents spillage. If the
implement feeding acidogenic salt diets.

cow does not drink, she must be given fluid

The critical issue seems to be the length
therapy either by drench or parenterally.

of time ( several hours) from when clinical

Every effort must be made to roll the cow
signs of milk fever begin until treatment.

from one side onto the other at least three

Every cow that has been successfully treated
times a day, with more frequent movement
for hypocalcernia should, if .necessary, be
being desired. If this is not done, the weight
moved to a location with a good footing and
of the cow results in continued ischemia of
remain there for 48 hr. Straw over sand
the muscles of the hindlin1b and exacerbaprovides good insulation and good footing.

tion of compartment syndrome.

Protection from the elements is essential.

Animal Welfare Considerations:

Rain and wind can reduce body tempera

Although a cow may rise after being
ture considerably and worsen shock if
recun1bent for >14 days, this does not in1ply
present. A windbreak of straw bales is vital.

that a cow should be unmonitored for this

Straw bedding should be provided to help
period. So long as the cow looks bright,
insulate the cow from the ground. A
occasionally struggles to rise, and continues
recumbent cow does not require a wann
to eat and drink, recovery is a possibility.

environment; however, in a cold environ

However, if the cow becomes listless shows
ment, an inactive animal can gradually
no interest in feed, or has decubital l�sions
succumb to hypothermia.

or starts to lose condition, euthanasia on

The downer cows most difficult to treat
hwnane grounds must be considered
are those that do not try to eat. A cow that
irrespective of how long she has been
salivates on its feed will not eat it later.

recumbent. A cow that has decubital

Rather than being offered large an10unts
lesions, a poor appetite, or shows signs of
of feed, the cow should be tempted with
wasting is unsuitable for salvage slaughter.

sweet hay. This should be cleared away

Attempting to send anin1als in this condition
eve1y 30 min if not accepted. Placing
to the slaughterhouse is considered an act
bitter-tasting weeds such as ivy or dandelion of cruelty in many countries.

in the mouth may provoke salivation and an

"Dragging" recumbent cows is illegal in
interest in eating. Lettuce a.nd'cabbage
some countries. Both veterinarians and
leaves are accepted by some cows. In
producers must be aware oftlle legal
extreme cases, the cow can be drenched
interpretation of the word "dragging." Access with rumen contents.

to some locations may be so restricted that
rolling the anin1al onto an in1provised sled
may be impossible. At all tin1es, even when

Prevention: Effective strategies to prevent
usmg a sled, great care must be taken to
milk fever are important to decrease downer
avoid injwy to dependent parts of tlle anin1al
cow syndrome. All dairy cows should be
such as tl1e udder, ears, and tail.

LAMENESS IN SMALL ANIMALS

Signs of musculoskeletal disorders include
endocrine, urinary, 'digestive, hemolyrnweakness, lameness, limb swelling, and phatic, and cardiopulmonary systems.

joint dysfunction. Motor or sensory

Evaluation of musculoskeletal disease
neurologic impairment may develop
is aimed at localizing and defming the
secondary to neuromuscular lesions.

lesion(s). Diagnosis requires accurate

Abnormalities of the musculoskeletal
revie
system may also affect other organs of tlle

.w of the signalment, history, and
physical status of the animal. A lan1eness

LAMENESS IN SMALL ANIMALS 1193
examination is critical to determine a
refeITal centers. N uclea.r scintigraphy
diagnosis. Useful ancillary tests include
involves IV irtjection of a radioactive
radiography, ultrasonography, arthrocentecompoW1d that localizes and highlights sis, arthroscopy, arthrography, electromyope1iosseous soft tissue and bone lesions. CT
graphy, and tissue biopsy and
imaging pennits high contrast and resolution

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histopathology. For subtle lesions,
of osseous structures, whereas MRI is
advanced in1aging techniques, including
helpful to delineate soft tissue ai1d joint
bone scans, CT, and MRI, a.re being used
irtjwies. Both can also be used to assess the
with greater frequency in specialty clinics
spinal colunm, although MRI is a better
and university hospitals.

standard to evaluate nervous tissues.

THE LAMENESS EXAMINATION

Arthroscopy: Althroscopy is a minin1ally
invasive tool used for diagnosis and therapy

The lameness exarnination is a key featw·e
of !rune ailimals. Advantages of the
to identify musculoskeletal lesions.

technique include improved visualization

Evaluation is performed with the animal at
and diagnosis of joint pathology, ability
rest, rising, and during locomotion on flat or
to treat irtjuries by removal of damaged
inclined surfaces. Single- or multiple-lin1b
cartilage or ligament, and reduced surgical
lameness is noted, with tl1e severity related
dissection. Disadvantages ai·e costs of
to the type of activity. With a forelimb
equipment and development of expertise in
lan1eness, the head is elevated during
its use. Common conditions that can be
weight bearing on the W1Sound limb. The
diagnosed or treated by arthroscopy include
stride is also shortened on the affected side.

osteochondrosis, bicipital tenosynovitis,

For hindlimb lan1eness, the head is dropped joint fractures, ai1d cranial cruciate during weight bearing on the affected limb.

ligai11ent and medial meniscal injuries.

Limbs should be assessed from a distal to
proximal manner, and bones,joints, and

PAIN MANAGEMENT
soft tissue should be palpated. Abnormalities to note include swelling, pain, Control of pain in Jaine or operative aili.mals
instability, crepitation, reduced range of
involves broad classes of compoW1ds such as
motion, and muscle atrophy. In evaluation

NSAIDs and opioids (see also PAIN ASSESSMENT
of a subtle or obscure lameness, serial

AND MANAGEMENT, p 2104). Analgesic agents
examinations before and after exercise
can be administered via oral, parenteral
may be necessaiy. For fractious animals,

(including constant-rate infusions),
sedation may be required; palpation,
epidural, local, or transdermal routes.

radiography, and arthrocentesis can often

Nonpham1acologic pain management
be perfom1ed while an anin1al is sedated
strategies include acupuncture therapy,
with IV butorphanol and acepromazine;
massage, physical therapy, and diet.

propofol; medetomidine (alone or

Commonly used NSAIDs include
combined with butorphanol or hydromorderacoxib ( 4 mg/kg/day, PO), firocoxib phone ); or a combination of ketamine,

(5 mg/kg/day, PO), meloxicam
diazepan1, and acepromazine.

(dogs: 0.1 mg/kg/day, IV, SC, PO; cats:

0.1 mg/kg/day, IV, SC, PO, for 1-3 days),

Imaging Techniques: Helpful imaging
carprofen (2.2 mg/kg, PO, bid), ketoprofen
procedures to diagnose laineness include

(1 mg/kg/day, PO, IV, SC, IM), etodolac
survey and contrast radiography, ultrasonog

(12.5 mg/kg/day, PO), tepoxalin
raphy, nucleai· scintigraphy, CT, and MRI.

(10 mg/kg/day, PO), and aspirin ( dogs:

Animals undergoing these evaluations

22 mg/kg, PO, bid; cats: 10 mg/kg, PO, every
should be heavily sedated or anesthetized.

48 hr). The use of NSAIDs is contraindicated

Swvey radiography of affected lin1bs or the
in animals with hepatic or renal insuffispine requires multiple, orthogonal views.

ciency, gastroenteritis, or coagulopathy, and

Subtle lesions a.re often identified after
in anin1als receiving conctment corticostecompaiison with the contralateral nonnal roid therapy.

limb. The most frequent contrast studies

Opioid analgesics bind toµ, K, and 8
used to evaluate lan1e animals ai·e arthroreceptors in the CNS to provide pain relief.

gran1s for joint diseases and myelography for Commonly used opioids include morphine spinal canal disorders. Ultrasonography is

(0.1 mg/kg, IV, IM, SC, every 3--4 hr),
useful to evaluate musculotendinous irtjuries oxyn10rphone (0.05 mg/kg, IV, IM, SC, every such as bicipital tenosynovitis, Achilles

3--4 hr), hydromorphone (0.1 mg/kg, IV, IM,
tendon rupture, and muscle contracture.

SC, every 2-4 hr), butorphanol (0.1 mg/kg,

Nuclear scintigraphy, CT, and MRI studies

IV, IM, SC, eve1y 2-4 hr in dogs and cats),
a.re usually available at private or academic
and buprenorplli..ne (0.01 mg/kg, IV, IM, SC,

1194

LAMENESS IN SMALL ANIMALS
tid in dogs and cats, also transmucosal
primary action as local anti-inflammatory
in cats). Opioid narcotics can be given
agents at the site of injury. Drugs used
with sedatives such as acepromazine
include preclnisone or preclnisolone

(0.5 mg/kg, IV, IM, SC, every 4-6 hr) for

( 1 -2 mg/kg/day, PO) or dexamethasone
enhanced efficacy of analgesia and

(1-2 mg/kg/day, IV). Their use is contraindi

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sedation. Oxymorphone, hydromorphone,
cated during concurrent NSAID treatment.

and butorphanol are more potent than

Gabapentin (10 mg/kg, PO, bid) is a
morphine. Buprenorphine has the longest
calcimn charmel blocker used to inhibit
duration of action. Another opioid, fentanyl,
neurons stimulated by pain; it is useful
is most frequently administered via
for treatment of anin1als with chronic
transdem1al patches applied for 3 days on
or neuropathic pain. Dexmedetomicline
shaved areas. Oral opioids used for pain

(5 mcg/kg/day, IM) and medetomicline
relief include tran1adol (5 mg/kg, tid),

(10 mcglkg/day, IM) are newer analgesicbutorphanol (1 mg/kg, tid), hydromorphone sedative, a2-receptor blocking agents useful

(0.5 mg/kg, tid), codeine (1 mg/kg, tid), and
to facilitate examinations or diagnostic
oxycodone (0.3 mg/kg, tid).

evaluations.

Local administration of analgesics

Joint fluid modifiers (glucosa.rnine,
involves joint ir\jections with morphine
chondroiton sulfate, hyaluronan, pentosan

(1 mg diluted in 5 mL of saline), bupivicaine
polysulfate, omega-3 fatty acids) have

(1 mU20 kg body wt), or lidocaine
received extensive attention in treating

(1 mU20 kg body wt) before joint surgery as
degenerative joint disease and alleviating
a preemptive block of intracapsular pain
discomfort. While contraindications and
receptors. Epidural morphine (0.1 mg/kg)

adverse effects are few, scientifically proven
in the lumbosacral space is also a useful
efficacy of these compotmds is linuted and
adjtmct for postoperative pain relief in the
most reports are regarded as anecdotal
hindlimbs and for reduced anesthetic
evidence. Stem cell therapy to alleviate pain
requirements. Corticosteroids are
and discomfort of diseased joints is also a
considered weak analgesic adjuncts,
newer modality for which scientific validity
because they indirectly reduce pain by their
is pending.

ARTHROPATHIES AND RELATED

DISORDERS IN SMALL ANIMALS

Many arthropathies are developmental,
followed by revascularization, resorption,
including aseptic necrosis of the femoral
and remodeling. The lesion is often
head, patellar luxation, osteochondrosis,
bilateral.

elbow dysplasia, and hip dysplasia. Other

Clinical signs include hindlimb lameness,
arthropathies are degenerative, infectious
atrophy of the thigh muscles, ·and pain
or septic, inunune-mediated, neoplastic,
during manipulation of the hip joint.

or traumatic.

Radiography reveals irregular bone density
of the femoral head and neck, collapse, and

ASEP TIC NECROSIS OF THE
fragmentation of the bone. Chronic cases

FEMORAL HEAD
have evidence of degenerative joint disease.

Treatment involves surgical excision of

(Legg-Calve-Perthes disease)

the affected femoral head and neck and
early postoperative physical therapy to

This deterioration of the femoral head seen
stimulate limb usage. Prognosis for
in y0tmg miniature and small breeds of dogs recovery is excel.lent.

is associated with ischemia and avascular
necrosis of the bone. The exact cause is
unknown, although there may be a

PATELLAR LUXATION
hereditary component in Manchester

Terriers. Infarction of the bone leads to

This hereditary disorder in dogs and cats is
collapse of tl1e femoral head and neck,
characterized by ectopic development of

ARTHROPATHIES AND RELATED DISORDERS IN SMALL ANIMALS

1195
the patella medial or lateral to the trochlear abnormal endochondral ossification of groove of the femur. Patellar luxation can
epiphyseal cartilage in the shoulder, elbow,
be associated with multiple deformities of
stifle, and hock joints. Although the exact
the hincllimh, involving the hip joint, femur,
cause is unknown, excessive nutrition,
and libia. Medial patellar luxations can be
rapid growth, trauma, and a hereditary

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involved with a reduced coxofemoral angle component are suspected to be contribut

(coxa vara), lateral bowing of the femur,
ing factors. As a result of abnormal
internal rotation of the tibia, shallow
maturation and vascularity, basal cartilage
trochlear groove, and hypoplasia of the
cells thicken and weaken, thus leading to
medial femoral condyle; lateral luxations
cartilage cracks, fissures, and flap
cause the reverse changes.

formation (osteochonclritis dissecans)

Clinical signs are variable and based on
after minor trauma or normal pressure to
the severity of luxation. Animals of any
the joint. Abnormal cartilage congruency
age may be affected. In general, cats and
and joint debris lead to a synovitis and
small and miniature breeds of dogs have
subsequent arthritis and continued
a medial luxation, and large dogs have a
cartilage breakdown. Cartilage flaps can
lateral luxation. Affected animals are lan1e
break loose and attach to the joint capsule
or ambulate with a skipping gait.

or migrate and deleteriously affect joint

Palpation of the stifle joint reveals
motion.

displacement of the patella. In Grade I,

Clinical signs are lan1eness, joint
clinical signs are mild and infrequent, and
effusion, and reduced range of motion in
the patella can be manually luxatecl but
affectecljoints or limbs. Locations of the
easily returns to the trochlear groove. In
lesions include tl1e head of the humerus

Grade II, the patella luxates during flexion

(shoulder joint), the medial aspect of the
of the joint and is repositioned during
humeral condyle (elbow joint), the femoral
extension, causing animals to have a
condyles (stifle joint), and the trochlear
resolvable skipping lameness. In Grade III, ridges of the talus 010ckjoint). Additionthe dislocated patella is more frequently ally, fragmented medial coronoid process
out of, instead of in, the trochlear groove,
and ununited anconeal process in the
and lameness is consistent. Bone
elbow joint may be related conditions.

deformities are evident in these animals.

Radiography is useful in identifyingjoint

In Grade IV, lameness and limb deformalesions; changes may include flattening of tions are most severe. Radiography of
joint surfaces, subchondral bone lucency
affected animals reveals various degrees
or sclerosis, osteophytosis, joint effusion,
of limb changes based on the grade of the
and "joint mice." Arthrography can be used luxation.

to delineate cartilage flaps, and arthros

The type of surgery is based on the
copy can also be perfonned to identify and
severity of the luxation and can include
treat crutilage or joint lesions. CT in1aging
both orthopedic and soft-tissue procedures. also helps identify subchondral bone Useful procedures involve fascia! releasing
changes.

incisions (on the side of the luxation),joint

Treatment involves surgical excision of
capsule and retinaculum imbrications (on
cartilage flaps or free-floating fragments
the side opposite the luxation), deepening
and curettage of subchondral bone to
of the trochlear groove, tibial crest
stimulate fibrocartilage forn1ation. Animals
transposition, and fabella to tibial
with degenerative joint disease may benefit
tuberosity derotation sutures. Severe
from NSA!Ds, eg, aspirin (10 mg/kg, PO, bid),
deforn1ations may require femoral or tibial

Catl)rofen (2.2 mg/kg, PO, bid), deracoxib
osteotomies, stifle joint arthrodesis, or limb

(4 mg/kg/day, PO), firocoxib (5 mg/kg/day,
an1putation.

PO), meloxican1 (0.1 mg/kg/day, PO),

Prognosis for recovery is good in mild
tepoxalin (10 mg/kg/day, PO), or etodolac
or moderately affected animals. Concur

(12.5 mg/kg/day, PO). Joint fluid modifiers
rent cranial cruciate ligament and medial
such as polysulfated glycosan1inoglycan
meniscal injuries should be identified and

(4.4 mg/kg, IM, twice a week for 4 wk)

treated. Cats are less severely affected than
may also help prevent cartilage degeneradogs and have an excellent prognosis.

tion. Prognosis for recovery is excellent
for the shoulders, good for the stifle joint,

OSTEOCHONDROSIS
and fair for the elbow and tarsal joints.

Concomitant signs of degenerative joint

Osteochondrosis is a developmental
disease, other joint conditions, or instadisorder of medium and large rapidly bility (hockjoint) deleteriously affect
growing clogs that is characterized by
recovery.

1196

ARTHROPATHIES AND RELATED DISORDERS IN SMALL ANIMALS

ELBOW DYSPLASIA
canine elbow. Bone fragments can be seen
by raruography, arthroscopy, or CT.

(Ununited anconeal process, Fragmented
medial coronoid process, Osteochondrosis

Osteochondrosis of the Medial
of the humeral condyle)

Humeral Condyle: This results from a

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Elbow dysplasia is a generalized incongrurusturbed endochoncl:ral fusion of the ency of the elbow joint in young, large,
epiphysis of the medial epicondyle with the
rapidly growing dogs that is related to
distal end of the hun1erus. The exact cause
abnonnal bone growth, joint stresses, or
is tmknown, but because the carpal and rugicartilage development. One or more of the tal flexors originate from the ventral aspect
following lesions may be present in the
of this structure, it may represent an
joint: an ununited anconeal process of the
epiphyseal avulsion. It results in pain
ulna, fragmentation of the merual coronoid
on flexion of the elbow or deep digital palpaprocess of the ulna, and osteochondrosis of tion and is accompanied by soft-tissue
the merual aspect of the humeral condyle.

swelling. Raruographically, raruodense

Railiographic grarung of dysplastic elbow
structures have been seen caudal and rustal
joints is performed by the Orthoperuc
to the ai·ea of the merual epicondyle.

Foundation for Animals in the USA and in

Scanrunavian and European kennel clubs.

Treatment: Early surgical treatment is
recommended before degenerative joint

Ununited Anconeal Process: This
disease develops. For fragmentation of
resu lt.s when there is separation of the
the merual coronoid process, a medial
ossification center of the anconeal process
arthrotomy or arthroscopy is performed
from the proximal ulnar metaphysis. Fusion
and the fragmented process removed. For
should be completed by 5--6 mo of age. The
ununited anconeal process, either a lateral
fracture is postulated to result from a
arthrotomy is perfom1ed and the unwlited
biomechanical imbalance of force and
process removed, or a nlidshaft ulnar
movement in the rapidly growing elbow.

osteotomy is perfom1ed to relieve

Initially, the anconeal process is connected
asynctu·onous growth and result in union of
to the ulna by a bridge of fibrous tissue,
the process. Reattactunent of the process by
which fragments to fom1 a pseudoarthrosis,
screw fixation is also an option. For
and the elbow becomes unstable. This joint
osteochondrosis, the subchondral bone
laxity continues to daniage the articular
lesion is curetted to stimulate fibrocartilage
cartilage, and secondary osteoarthritis
fom1ation. Prognosis after surgery is good
results. A hererutary basis has been
if degenerative joint disease has not
implicated but not proved.

developed in the joint. Aspirin or NSAJDs

Lameness develops insiruously between

(eg, carprofen, deracoxib, flrocoxib,

4 and 8 mo of age; however, some bilateral
etodolac, meloxicarn, tepoxalin) can be
cases may not be ruagnosed until dogs are
used to reduce pain and inflammation.

> 1 yr old. Affected elbows may deviate

Joint-fluid modifiers (glycosanlinoglycans,
laterally, and the range of motion is
hyaluronic aid) may be useful.

restricted. Advanced cases hav� osteoarthritis, joint effusion, and crepitus. Clinical HIP DYSPLASIA
signs are suggestive, and the ruagnosis is
confim1ed by radiography. A lateral

Hip dysplasia is a multifactorial abnom1al
radio graph of the elbow in the flexed
development of the coxofemoraljoint in
position allows visualization of the ununited dogs that is characterized by joint laxity and process. Both elbows should be exanlined
subsequent degenerative joint rusease. It is
because the condition can be bilateral.

most common in large breeds. Excessive
growth, exercise, nutrition, and hereclitary

Fragmentation of the Medial
factors affect the occurrence ofh.ip

Coronoid Process: In this condition
dysplasia. The pathophysiologic basis for
of the medial compartment of the canine
hip dysplasia is a dispaiity between hip joint
elbow, the coronoid process fails to unite,
muscle mass a11d rapid bone development.

either partially or totally, with the ulnar

As a result, coxofemoraljoint laxity or
diaphysis and, thus, does not become a pait
instability develops and subsequently leads
of the articular surface of the trochlear
to degenerative joint changes, eg, acetabunotch. Joint laxity, irritation, and finally lar bone sclerosis, osteophytosis, thickened
osteoarthritis result. This conrution and
femoral neck,joint capsule fibrosis, and
osteochondrosis of the merual humeral
subluxation or luxation of the femoral head.

condyle are considered to be the most

Clinical signs are variable and do not
common causes of osteoarthritis of the
always correlate with raruographic

ARTHROPATHIES AND RELATED DISORDERS IN SMALL ANIMALS

1197
abno1malities. Lameness may be mild,
formation. Joint degeneration can be
moderate, or severe and is pronounced
caused by tratm1a, infection, immuneafter exercise. A "bunny-hopping" gait is mcdiatccl diseases, or developmental malsometimes evident. Joint laxity (Ortolani f01111alions. The inciting cause initiates
sign), reduced range of motion, and
chonclrocyte necrosis, release of degrada

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crepitation and pain during full extension
tive enzymes, synovitis, and continued
and flexion may be present. Radiography is
cartilage destruction and inflanunation.

useful in delineating the degree of aithritis

Abnormal caitilage congruency and joint
and plaiming of medical and sw-gical
capsule anatomy can fwther lead to
treatments. Standard ventrodorsal views
alteration in normal joint biomechrulical
of sedated or anesthetized animals cai1 be
function. Pain and lameness develop
graded by the Orthopedic Foundation for
secondary to joint dysfunction or muscle

Animals, or stress radiographs performed
atrophy and to limb disuse. Although more
and joint laxity measw-ed (Penn Hip). A
common in clogs, joint degeneration may
dorsal acetabulai· 1irn view is used by some
also be seen in cats.

sw-geons to evaluate the acetabulum before

Clinical signs of degenerative joint disease
reconstructive surge1y. Modified ventrodorinclude laineness, joint swelling, muscle sal ai1cl dorsoventral projections have also
ati·ophy, pericapsular fibrosis, and crepitabeen proposed in an effort to minlic the tion. Radiographic changes in the joint
normal standing postw-e of clogs. Recent
include joint effusion, pe1iaiticular softreviews of American and international radiotissue swelling, osteophytosis, subchondral graphic screening programs have failed to
bone sclerosis, and possibly nano wed joint
identify a "gold standard." An evaluation
space. Althrocentesis may be unremai·kable
shift toward genome screening may yield
or yield minor changes in color, tw-bidity, or
more promising results in the future.

cell cow1ts of synovial fluid.

Treatments ai·e both medical and sw-gical.

Treatments can be medical or surgical.

Mild cases or nonsw-gical candidates

Nonsurgical therapies include weight

(because of health or owner constraints)

reduction, controlled exercise on soft
may benefit from weight reduction,
surfaces, and therapeutic application of
restiiction of exercise on hard surfaces,
warm compresses to affected joints.

conti·olled physical therapy to strengthen

NSAlDs ( eg, aspirin, etoclolac, cai-profen,
and maintain muscle tone, anti-inflanunatory deracoxib, meloxicrun, firocoxib, tepoxalin) drugs (eg, aspirin, cmticosteroids, NSAlDs),
reduce pain ai1d inflan1mation. Caution is
and possibly joint fluid modifiers. Sw-gical
advised with longtenn NSAlD usage in dogs.

treatments include pectineal myotenectomy

The most frequently cited adverse effects
to reduce pain, tliple pelvic osteotomy to
include GI problems such as inappetence,
prevent subluxation, pubic fusion to prevent
vonliting, and hemorrhagic gastroenteritis.

subluxation,joint capsule denervation to

A cai-profen-associated hepatopathy in
reduce pain, dorsal acetabulum reinforce

Labrador Retrievers has also been repmted.

ment to reduce subluxation, femoral head

C01ticosteroicls also suppress prostaglandin
and neck resection to reduce aithritis, and
synthesis and subsequent inflainmation, but
total !lip replacement for optimal restoration
sh01t-tem1 use is advised to prevent
of joint and limb functions. Additionally,
iatrogenic hyperadrenocorticism, caitilage
femoral corrective osteotonlies can be
degeneration, and intestinal perforation.

performed to reduce femoral head sub

Joint-fluid modifiers such as glycosanli.noluxation, although degenerative artluitis glycans or sodium hyalw-onate may prevent
may persist.

cartilage degradation. Sw-gical options

Prognosis is highly variable and depends
includejoint fusion (artlu·odesis), most
on the overall health and environment of the frequently pe1fom1ed on the cai-pus ai1d animal. In general, if sw·ge1y is indicated
tarsus; joint replacement, such as total hip
and pe1formed correctly, it is beneficial.

replacement; joint excision, such as femoral

Animals on wllich sw-gery is not performed
head and neck osteotomy; and amputation.

may require a change in lifestyle to live

Prognosis is variable and depends on the
comfortably.

location and severity of the ruthropathy.

DEGENERATIVE ARTHRITIS

SEPTIC ARTHRITIS

(Degenerative joint disease, Osteoarthritis)

Infectious arthritis is most frequently

Progressive deterioration of aiticular
associated with bacte1ial agents such as
cartilage in diarthrodialjoints is characterstaphylococci, streptococci, and colifonns.

ized by hyaline crutilage thinning, joint

Causes include hematogenous spread or
effusion, and periaiticular osteophyte
penetrating trauma, including surgery.

1198

ARTHROPATHIES AND RELATED DISORDERS IN SMALL ANIMALS

Other agents producing a septic arthritis
tumor arises from primitive mesenchymal
include 1ickettsia (Rocky Mountain spotted
cells outside the synovial membrane.

fever, ehrlichiosis) and spirochetes

Clinical signs include lat11eness and joint

(borreliosis).

sweJling. Radiography reveals soft-tissue

Clinical signs of septic arthritis include
swelling and a periosteal reaction.

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lan1eness, swelling, pain of affectedjoint(s),

Pulmonaiy metastasis is detected in -25%
and systemic signs of fever, malaise,
of animals at initial exat11ination. Biopsy
anorexia, and stiffness. Racliography may
reveals evidence of a soft-tissue tm11or.

reveal joint effusion in early cases and

Limb at11putation is the treatment of choice,
degenerativejointclisease in chronic
although palliative radiation may be
conditions. Arthrocentesis reveals increased
considered for cases with a low tLU11or
levels ofWBCs, especially neutrophils. The
burden not involving bone.

synovial fluid may be grossly purulent.

Bacterial culture and antimicrobial

POLYARTHRITIS
sensitivity testing may confim1 the diagnosis.

Serologic testing is used for nonbacte1ial

Polyarthritis involves inflanm1ation of
agents. Treatment is with appropriate IV and
multiple joints and is classified as infectious
oral antibiotics,joint lavage, and surgical

(septic artluitis, seep 1197) or noninfecdebridement in severe cases.

tious ( erosive or nonerosive [ immtme-mediated]). Nonerosive can be idiopathic or breed (Akita) associated, while erosive is

IMMUNE-MEDIATED ARTHRITIS
characteristic of feline progressive artluitis
and rheLU11atoid arthritis. Clinical signs of

Inflammatory polyarthritis secondary to
a polyarthritis include fever, lat11eness,
deposition of inunune complexes can
swollen joints, lethargy, and inappetence.

produce erosive ( destruction of articular

Diagnosis is by radiography Qoint effusion,
cartilage and subchondral bone) or
possible erosive bone destruction) and
nonerosive (periarticular inflanm1ation)

abnom1al (increased cell counts)joint fluid
fonns of joint diseases. Rhem11atoid
analyses. Treatments involve longtem1
aithritis, Greyhound polyarthritis, and
glucocorticoid therapy or other inununofeline progressive polyarthritis are suppressive medications such as azathioexat11ples of erosive arthritides. Systemic p1ine or cyclophosphatllide. Prognosis in
lupus erythematosus (SLE) is the most
most cases is guarded or poor, with relapses
conunon form of nonerosive arthritis.

conunon.

Clinical signs are lat11eness, multiple
joint pain, joint swelling, fever, malaise,

JOINT TRAUMA
and anorexia. Clinical signs conunonly
wax and wane.

Cranial Cruciate Ligament Rupture

Diagnosis is aided by radiography, biopsy,

Rupture of the crani.al cruciate ligan1ent is
arthrocentesis, and serologic testing.

most frequently due to excessive tramna

Radiography reveals periaiticular swelling,
ai1d a possibly weakened ligan1ent
effusion, and joint collapse plus subchonsecondaiy to degeneration, inlmune-mediclral bone destruction in erosive conditions.

ated diseases, or conformational defects

Althrocentesis reveals synovial fluid with

(straight-legged dogs). Plasmacytic-lymphoreduced viscosity and increased inflanunacytic synovitis is sometimes diagnosed tory cell counts. Biopsy of synovial tissue
concurrently with ligat11ent ir\jUI)', but it
reveals mild to severe inflanunation and
remains unclear whether it is a cause or
cellulai· infiltrates. Serologic testing is
effect of the joint instability. Stable
performed for rheumatoid factor and

( nonsurgical) joints with an early or mild antinuclear antibodies.

condition can be treated with steroids or an

Treatment involves anti-inflanm1atory

NSAID. Most irtjuries involve a midsubmedications ( eg, corticosteroids) and stance tear (mature dog), although bone
chemotherapeutic agents ( eg, cyclophosavulsion (immature dog) at the origin of the phai1lide, azathioprine, or methotrexate).

ligat11ent is possible. Instability of the stifle

Prognosis is guai·ded because of relapses
joint after rupture of the cranial cruciate
and inability to detemline the inciting cause
ligat11ent can lead to medial meniscal ir\jlU)',
of the autoinlmune reactions.

joint effusion, osteophytosis, and joint
capsule fibrosis.

NEOPLASTIC ARTHRITIS

Cllilical signs involve lat11eness, pain,
medial joint swelling, effusion, crepitation,

Synovial cell sarcoma is the most common
excessive cranial laxity of the proximal tibia
malignant tumor involving the joints. The
relative to the distal femur ( drawer sign, or

ARTHROPATHIES AND RELATED DISORDERS IN SMALL ANIMALS

1199
positive compression test), and increased
physis and joint. Specific conunon sites of
internal tibial rotation. Partial cranial
injury include the greater tubercle and
crlJCial ligament tears are characterized
condyle of the hun1erus, distal ulnar phys is,
by a reduced cranial laxity, usually more
and the head and condyles of the femur. The
pronounced in flexion. Medial meniscal
hwneral. condyle is also frequently injured in

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ir\jury may be identified by a clicking sound
mature Spaniel breeds and characterized by
during locomotion or flexion and extension.

Y or T fracture configurations. This may be

A tibial compression test (flexion of the
related to incomplete ossification and
hock and cranial displacement of the tibial
vascularity of the bone.

tuberosity) can also be used to demonstrate

Clinical signs of joint fractures include

1a.J(ity of the cranial cruciate ligament.

lameness, pain, and joint swelling. Chronic

Radiography reveals joint effusion and signs iitjuries may be characterized by angular of degenerative joint disease in chronic
limb deformities if the injury affected an
injuries. Arthrocentesis may reveal mild
open growth plate. Radiography and CT
cellular increases and hemarthrosis.

are useful in delineating the fracture.

Afthroscopy can confirm the diagnosis

The goal of joint fracture treatment is
but requires specialized equipment.

stable anatomic reconstruction to maintain

'Treatments include medical and surgical
joint congruency and joint and limb
therapies. Weight reduction, controlled
functions. Internal fixation wifu pins, wires,
physical therapy, and NSAIDs alleviate pain
or screws is performed to achieve stable
and discomfort from inflammation and
fixation. Prognosis for recovery is good if
degenerative joint disease. Surgical
proper surgical technique has been used
stabilization of the stifle joint is recomand joint trawna has not been excessive.

mended for active dogs. Extracapsular
techniques include fascial suturing, fabella
to tibial tuberosity imbrication sutures,

Palmar Carpal Breakdown
cranial transposition of the fibular head,

This hyperextension injury secondary to
leveling of the tibial plateau, tibial
falls or jumps produces excessive force
tuberosity advancement, and synthetic
on fue carpus, which leads to collapse of
grafts· lntracapsular techniques include
tl1e proximal, middle, and/or distal joints
fascia lata or patellar tendon grafts sutured
secondary to tearing of fue palrnar carpal
over the top of the lateral femoral condyle.

ligaments and fibrocartilage. Clinical signs

Medial meniscal iJ\iury requires removal of
include lameness, carpal swelling, and a
dar11aged avascular tissue. Postoperative
characteristic plantigrade stance. External
physical therapy is critical for clinical
splints or casts may be attempted in mild
recovery. Prognosis after surgery is good.

cases, alfuough surgical treatment is usually
required to restore limb function. Surgery

Joint Fractures
involves fusion ( arthrodesis) of fue affected

Trn.umatic fractures frequently involve the
joints using a bone plate and screws, pins
shoulder, elbow, carpal, hip, stifle, and tarsal and wires, or external skeletal fixation. A joints. In immature animals, the weakness
cancellous bone graft is used to enhance
of we physis compared with adjacent bones, bone wuon, and postoperative support is ligarnents, and joint capsule predisposes
necessary. Prognosis for recovery is good.

this area to ir\jury. A Salter-Harris classification scheme (l-V) is often used to describe Hip Luxation
the location of the fracture relative to the

Traumatic dislocation of the hip is most
frequently a craniodorsal displacement of
the femoral head relative to fue acetabulwn.

Clinical signs include lameness, pain during
manipulation of the hip joint, and a
shortened limb due to dorsal displacement
of the femur. Radiography is useful in
confinning fue luxation and delineating the
presence of oilier fractures in the femoral
head or acetabulum. Treatment involves
eifuer closed manipulation and postoperative slings to maintain the reduction or open surgical stabilization using sutures or toggle
pins. Femoral head and neck resection or
total hip replacement can be performed

Capital physeal fracture. Courtesy of Dr. Ronald after failed reductions. Prognosis for

Greefl·
recovery is usually excellent.

1200

MYOPATHIES IN SMALL ANIMALS

MYOPATHIES IN SMALL ANIMALS

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Myopathies can be congenital, hereditary,
least 30 mg daily for cats, or 15 mg daily
idiopathic, inflammatory, metabolic,
for mink, is necessruy. Antibiotics are of
neoplastic, traumatic, or due to nutritional
doubtful value, despite tile fever and
imbalances.

leukocytosis. Parenteral use of fluids is
not advisable wtless dehydration exists.

YELLOW FAT DISEASE

Because of associated pain, affected
ruli.mals should be handled as little as

(Nutritional steatitis, Nutritional panniculitis)

possible.

YelJow fat disease is characterized by a
marked in.tlanm1ation of adipose tissue and

LABRADOR RETRIEVER
deposition of "ceroid" pigment in fat cells. It MYOPATHY
may be seen alone in cats or with accompanying myopathy in rats, mink, foals, and (Centronuclear myopathy)

pigs.

This inhe1ited (autosomal recessive)

It is believed that an overabundance
condition is characterized by a type 2
of unsaturated fatty acids in the raLlon,
muscle fiber deficiency and is now called
together with a deficiency of vitanlin E
centronuclear myopathy. Clinical signs ru·e
or other antioxidants, results in lipid
seen at <5 mo of age and include skeletal
peroxidation and deposition of"ceroid"

muscle atrophy, stunted growtl1, ataxia, and
pigment in the adipose tissue. Most
weakness. Signs are progressive w1til the
natmally occuning and experimentally
animal reaches maturity, when tlley
induced cases have been in animals that
stabilize. Animals may have a normal life
have had fish or fish by-products as alJ or
span. Diagnosis is by creatinuria, muscle
prut of the diet. The specific cause is
biopsy, and electromyography. Histology
believed to be related jointly to the high
reveals increased connective tissue ru·ound
unsaturation of tl1e fish oil fatty acids and
muscle fibers and staining deficiency of
tl1eil" Jack of protection with vitru11in E or
type II fibers. Myotonic discharges are
otl1er antioxidants.

seen witll electromyography. There is no

Affected cats ru·e frequently obese,
effective treatment, altl1ough wru·m housing
usualJy young, and of either sex. They lose
and L-carnitine supplementation may make
agility, are unwilling to move, and resent
affected dogs more comfortable. This
palpation of tile back or abdomen. In
condition has different clinical features than
advanced disease, even a light touch causes
exercised-induced collapse in Labrador
pain. Fever is a constant finding, and

Retrievers.

anorexia may be present. •

In nlink, kits may be affected witll steatitis GREAT DANE MYOPATHY
shortly after weaning and, if untreated,
losses may continue until pelting tin1e. Signs
lnhe1ited myopatl1y of Great Danes is a
appear suddenly; the kits may refuse a night
noninflanm1atory condition of young Great
feeding and be dead by monling. Affected

Danes. Affected dogs have been identified
mink may refuse their feed and show a
in England, Australia, and Canada. An
peculiar, unsteady hop, folJowed by
autosomal recessive mode of inheritance is
complete impainnent of locomotion aml
suspected. Clinical signs include exercisecoma. At pelting, swvivors show yelJow induced tremors, weakness, and muscle
fat deposits and hemoglobinuria.

wasting. CK activity is usualJy increased,

The typical laboratory finding is an
fibrillation potentials are detected in
increased WBC count, with neutrophilia
skeletal muscles, and histopatllology
and sometimes eosi.nophilia. Biopsy of tl1e
reveals a central core myopathy. Treatment
subcutaneous fat shows it to be yellowish
is supportiv�, at best.

brown and finn. Histologic examination
reveals severe inflammato1y changes and

FIBROTIC MYOPATHY
associated ceroid pigment.

The offending excessive fat source must

Fibrotic myopatlly is a chronic, progressive,
be removed from the diet. Administration of
idiopathic, degenerative disorder affecting
vitan1in E, in tile fmm of a-tocopherol, at
tile senlitendinosus, gracilis, quad1iceps,

MYOPATHIES IN SMALL ANIMALS

1201
iniraspinatus, and supraspinatus muscles,
difficulty in opening the jaw, and muscle
primarily in dogs. The cause is unlrnown.

atrophy. Diagnostic hematologic values

Affected muscles are characterized by
include eosinophilia and increased levels of
contracture and fibrosis. Normal tissues are
globulin and muscle enzymes. Electromyoreplaced by dense collagenous connective graphy reveals abnom1al spontaneous

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tissue. Clinical signs include a nonpainful,
electrical activity in affected muscles. A
mechanical lameness. Neurologic function
biopsy sample of the temporalis muscle is
is nom1al. Surgical release of affected
usually taken; histologic changes include
tissues via tenotomy, myotenotomy,
lymphocytic-plasmacytic cellular infiltrates,

Z-plasty, or complete resection produces
muscle atrophy, and fibrosis. Although
inconsistent results. Prognosis is guarded
spontaneous regressioi;i can occur,
because of recurrence.

prednisone treatment, on a decreasing
dosage schedule (2 mg/kg/day for 2 wk, then

MYOSITIS OSSIFICANS

1 mg/kg/day for 2 wk, then 1 mg/kg/day for

1 mo) is usually effective. Relapses are

Myositis ossificans is an idiopathic
common, and long-term (6-8 mo) medicanon-neoplastic fom1 of heterotopic tion may be required.

ossification of fibrous connective tissue and
muscle that frequently affects tissues near

FELINE HYPOKALEMIC
the hip joint in Dobennan Pinschers. It may
be related to a bleeding disorder ( von

POLYMYOPATHY

Willebrand disease) in these dogs. Surgical

Feline hypokalemic polymyopathy is a
resection of the mineralized mass is usually
generalized metabolic muscle wealrness
rewarding.

disorder in cats secondary to hypokalemia
associated with excessive urinary depletion

POLYMYOSITIS
or inadequate dietary intake. Extracellular
hypokalemia causes muscle cell membrane

Polymyositis is a systemic, noninfectious,
hyperpolarization and secondary excessive
possibly immune-mediated, inflanunatory
permeability to sodium. This leads to
muscle disorder in adult dogs. It may be
hypopolarization of the muscle cell and
acute or chronic and progressive. Clinical
subsequent weakness.

signs include depression, lethargy,

Clinical signs include generalized
wealrness, weight loss, lameness, myalgia,
wealrness, ventroflexion of the neck,
and muscle atrophy. CK may be increased,
abnonnal gait, anorexia, and muscle pain.

and electromyography reveals abnormal

The neurologic exanunation is normal.

spontaneous muscle activity. Muscle biopsy

Serum chemistries reveal hypokalemia
reveals myonecrosis, lymphocytic-plasma

( <3.5 mEq/1) and increased creatini.ne and
cytic perimuscular infiltration, phagocyto

CK The urine has a low specific gravity, and
sis, and fiber regeneration. Polymyositis
potassium excretion is increased. Treatmay be associated with megaesophagus and ment is by potassium supplementation, immune-mediated disorders (myasthenia
given PO (5-8 mEqlday) or IV in cats with
gravis, lupus erythematosus, polyarthritis).

profound hypokalemia Prognosis is

Oral corticosteroids (1-2 mg/kg, bid for
excellent with early diagnosis and

3-4 wk) are the treatment of choice; other
treatment.

i.mmunosuppressive agents such as
azathioprine or cyclophosphamide can also
be used. Prognosis is favorable, although

MALIGNANT HYPERTHERMIA
relapses are not uncommon.

Malignant hyperthennia ( see p 1027) is a
hypermetabolic disorder of skeletal muscle

MASTICATORY MYOSITIS
characterized by catabolism and contracture, usually secondary to inhalant (Eosinophilic myositis)

anesthetic agents and stress. It is seen

Masticatory myositis is an immune-medimost frequently in heavily muscled dogs.

ated, inflarnmatory condition that affects

Abnormal calcium regulation, glycogenolythe muscles of mastication. The exact cause sis, and contractile protein activity result in
is unlrnown. Specific autoantibodies
production of heat, C02, and lactic acid.

directed against type II muscle fibers have

Clinical signs include tachycardia,
been detected in affected animals. In acute
tachypnea, pyrexia, muscle rigidity, and
cases, muscles are swollen, and there is
cardiopulmonary failure. Signs develop
difficulty in opening the jaw. In chronic

5-30 min after exposure to the anesthetic
cases, there is anorexia, weight loss,
agent. Treatment consists of in1mediate

1202

MYOPATHIES IN SMALL ANIMALS
cessation of anesthesia and hyperventilamechanism of if\iury can be direct, indirect, tion with oxygen. IV fluid therapy, corticooveruse, or migration of osteochondral steroids, and ice packs are also used.

fragments ("joint mice") from humeral

Dantrolene, a muscle relaxant, may be given
osteochondrosis lesions.

at 2-5 mg/kg, IV. Prognosis is poor in severe

Clinical signs include a progressive or

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cases. Urinary output, serum potassium
chronic, intermittent lameness that worsens
levels, and cardiac function should be
after exercise and improves with rest. The
monitored.

range of motion of the shoulder joint is
reduced, and atrophy of the shoulder

EXERTIONAL MYOPATHY
muscles may be apparent. Acute pain can be
elicited by applying digital pressure to the

(Rhabdomyolysis, Tying-up, Monday morning
biceps tendon dming flexion and extension
disease)

of the shoulder joint.

This acute exertional myopathy of racing

Diagnosis can be confim1ed by ultra

Greyhounds and working dogs is charactersonography or arthroscopy of the damaged ized by muscle ischemia secondary to
tendon. Radiography can reveal dystrophic
exercise or excitement. Avascularity and
calcification of the tendon, osteophytes in
lactic acidosis cause muscular lysis,
the intertubercular groove, or mineralized
myoglobin release, and a nephropathy.

fragments within the tendon sheath.

Clinical signs include muscle pain and

Contrast arthrography may demonstrate
swelling 24-72 hr after racing. Severe cases
filling defects and irregularities of the
are characterized by stiffness, hyperpnea,
synovial sheath. Arthrocentesis may be
collapse, myoglobinemia, and acute renal
inconclusive. Diagnosis can also be made by
failure. Urinalysis reveals myoglobinuria;
exploration of the tendon and associated
serum potassiun1, phosphorus, and muscle
sheath.

enzymes are increased. Treatment includes

Acute, mild cases can be treated with rest
supportive care such as IV fluids, bicarboand oral NSAID and opioids. Acute, severe nate, body cooling, rest, and muscle
cases can be treated with intralesional
relaxants (eg, diazepan1). Prognosis
irtjections of methylprednisolone acetate
depends on severity. (See also EXERTIONAL

(20-40 mg) and rest. Chronic cases

MYOPATHIES IN HORSES, p 1178.)

refractory to multiple corticosteroid
injections or cases involving identifiable

MUSCULAR TRAUMA
tendon defects or tears, or "joint mice,"

are treated by tenodesis (resection and
lnfraspinatus Contracture: Infraspinaattachment of the tendon to the proximal tus contracture is a uni- or bilateral fibrotic
hun1erus) and osteochondral fragment
myopathy of the infraspinatus muscle that is removal. Arthroscopic-guided tendon usually secondary to trauma in hunting or
resection has also been described.

working dogs. Clinical signs include an

Prognosis for recovery is good.

acute lameness, pain, and swelling in the
shoulder region. The lameness subsides, but Quadriceps Contracture (Quadriceps a gait abnormality develops 2-4 wk after

Tie-down, Stiff Stifle Disease): This
irtjury as muscle fibrosis and contracture
serious fibrosis and contracture of the
progress. Clinical signs include a characterquadriceps muscles develops secondary to istic adduction of the elbow, abduction of
distal femoral fractures, inadequate surgical
the foreleg, and external rotation of the
repair, and excessive dissection in young
carpus and paw. The limb is circumducted
dogs. Adhesions develop between the bone,
with each stride of the leg. Palpation of the
periosteal tissue, and quadriceps muscles,
shoulders reveals outward rotation of the
which lead to limb extension, disuse,
humerus as the elbow is flexed. Treatment
osteoporosis, degenerative joint disease,
consists of resection of the fibrous
and bone and joint deformations. Clinical
musculotendinous portion of the muscle,
signs include hyperextension and cranial
including tenotomy of the tendon of
displacement of the affected limb. Surgery
insertion. Limb and joint functions are
is usually required to resect fibrous tissues
in1mediately improved, and prognosis
and increase motion of the stifle joint. Bone
for full recovery is excellent.

and soft-tissue reconstructions along with
postoperative flexion bandages and

Tenosynovitis of the Biceps Brachii
physical therapy are required to recover

Tendon: This inflammation of the biceps
limb function. Prognosis is guarded.

brachii tendon of origin and associated

Prevention of the condition by accurate,
synovial sheath can be uni- or bilateral.

biologic stable repairs of bone fractures

It usually affects mature, large dogs. The
is preferred.

OSTEOPATHIES IN SMALL ANIMALS

1203

Achilles Tendon Disruption (Dropped
active dogs. Physical exanlination reveals

Hock): This acute, traumatic injury to the
focal pain at the proxinlal medial aspect of
common calcaneal tendon (gastrocnethe thigh (attachment of tendon to the lesser mius, superficial digital flexor, biceps
trochanter), especially dmi.ng simultaneous
femoris, semitendinosus, and gracilis
hip joint extension and internal rotation.

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muscle tendons) is seen primarily in

Ultrasonography reveals disruption of
mature working and athletic dogs. The
muscle fibers, and radiography may reveal
common tendon can be ruptured or
dystrophic calcifications at the region of
avulsed from the tuber calcanei of the
tendon insertion. Treatment with rest and
talus. Ruptures may be partial or complete, NSAIDs is helpful.

and the gastrocnemius tendon component
is most frequently affected. Clinical signs

MUSCLE TUMORS
include a severe non weight-bearing
lan1eness, tarsal hyperflexion, and a

Primary skeletal muscle tmnors can
plantigrade stance. Palpation reveals
be benign ( rhabdomyoma) or malignant
swelling, pain, and torn or fibrotic tendon

(rhabdomyosarcoma). Secondary tumors
ends. Radiography may reveal avulsed
involved with metastatic spread include
bone fragments. Treatment is by surgical
lymphosarcoma, hemangiosarcoma, and
repair of torn ends and reattachment of
adenocarcinomas. Local tumors (fibrosartendinous tissue to the tuber calcanei.

coma, osteosarcoma, mast cell tm11ors) can

External splints or fixators should be used
invade adjacent muscle. Lipomas can also
to protect the repair for 4 wk. Prognosis is
invade internmscular tissue spaces.

variable and based on chronicity of the

Clinical signs include localized swelling
in.jury, success of the surgery, and
and lameness. Diagnosis is confirnled by
expected performance of the dog.

biopsy and histologic evaluation of the
san1ples. Treatment is by surgical excision
lliopsoas Muscle Trauma: Trauma to the or lin1b amputation; chemotherapy and iliopsoas muscle or tendon of insertion can
radiation may be used depending on the
cause an acute or chronic lameness in
tumor type.

OSTEOPATHIES IN SMALL ANIMALS

Osteopathies can be developmental,
carpal joints. Radiography reveals the
infectious (osteomyelitis), idiopathic (eg,
bone deformations and closed physes.

hypertrophic osteopathy), nutritional,

Treatment is based on correcting
neoplastic, or tralllllatic.

angulation and length of the limb and
reestablisllingjoint congruity. Surgical

DEVELOPMENTAL OSTEOPATHIES procedures include corrective osteotomy and stabilization with internal or external

Angular Deformity of the Forelimb
implants and tension-releasing osteotomies.

(Radial and ulnar dysplasia)

Prognosis is good for aninlals without
severe limb deforn1ations.

Abnorn1al development of the radius and
ulna can occur secondary to distal (radial,
ulnar) or proximal (radial) physeal injm)' or

Craniomandibular Osteopathy
hereditary breed characteristics (Bulldogs,

Craniomandibular osteopathy is a

Pugs, Boston Terriers, Basset Hounds,
non-neoplastic, proliferative bone disorder

Dachshunds). Asynchronous growth of the
of growing dogs that affects the mandible
two bones leads to shortened limbs, cranial
and tympanic bullae ofTenier breeds. The
bowing of the bones, elbow joint subluxacause is unknown, but a genetic basis is tion, and valgus or varus deformities in the
suspected. The bone lesion is characterized
carpus.

by cyclical resorption of no1mal bone and

Clinical signs include lameness and
replacement by in1.111ature bone along
reduced painful motion in the elbow or
endosteal and periosteal surfaces.

1204

OSTEOPATHIES IN SMALL ANIMALS

Clinical signs vary in seve1ity and include
giant dogs that prin1arily affects the
oral discomfort, weight loss, fever, and
diaphyses and metaphyses of long bone.

painful palpable enlargement of the

The exact etiology is unknown, although
mandible. Radiography reveals bilateral
genetics (in German Shepherds), stress,
bone proliferation in the mandibles and
infection, and metabolic or autoimmune

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tympanic bullae.

causes have been suspected. The patho

Therapy is symptomatic and consists
physiology of the disease is characterized
of NSAIDs, opioids, or corticosteroids to
by intran1edullary fat necrosis, excessive
reduce inflammation and discomfort, along
osteoid production, and vascular congeswith a soft-food diet. Prognosis is good with tion. Endosteal and periosteal bone
mild bone proliferation and animal
reactions occur.

maturation.

Clinical signs are acute and cyclical and
involve single or multiple bone(s) in dogs

Hypertrophic Osteodystrophy

6--16 mo old. Animals a.re lame, febrile,

(Metaphyseal osteopathy)

ina.ppetent, and have palpable long bone
pain. Radiography reveals increased

Hypertrophic osteodystrophy is a developmultifocal intramedulla.ry densities and mental disorder of the metaphyses in long
irregular endosteal surfaces along long
bones of young, growing dogs, usually of a
bones. Therapy is ain1ed at relieving pain
large or giant breed. The exact etiology is
and discomfort; oral NSAIDs and opioids
unknown. The pathophysiology is based on
can be used during periods of illness.

met.aphyseal vascular in1pairment, leading

Excessive dietary supplementation in
to a failure in ossification and to trabecular
young, growing dogs should be avoided.

necrosis and inflammation.

Clinical signs include bilateral metaphy

Retained Ulnar Cartilage Cores
seal pain and swelling in the distal radius
and ulna, fever, anorexia, and depression.

Retained ulnar ca.itilage cores is a

Clinical signs may be periodic. Angular lin1b
developmental disorder of the distal ulnar
defomtities may develop in severely
physis in young, large, and giant dogs
affected dogs. Radiography reveals
characterized by abnom1al endochondral
metaphyseal bone lucencies and circumossification. As a result, progressive physeal ferential periosteal bone fonnation.

ca.lcification ceases, and forelin1b bone

Therapy is symptomatic and ain1ed at
growth is restrained. The exact etiology is
relieving pain ( eg, NSAIDs, opioids ),
unknown, although dietary ca.uses are
reducing dietary supplementation, and
suspected.

providing supportive fluid care. Treatment

Clinical signs include lameness and
with corticosteroids (prednisone 0.5 mg/lb,
angular lin1b deformities. Radiography

PO, bid for 5 days, then tapered as needed)

revea.ls a ra.diolucent cartilage core in the
may be superior to treatment with NSAIDs
center of the distal ulnar physis. Treatments
in Weirnaraners.

include cessation of dietary supplements
and osteotomy or ostectomies of the bone

Multiple Cartilaginous Exostoses
to reduce limb defom1ation. Prognosis is
based on severity of the condition.

(Osteochondromatosis)

Multiple cartilaginous exostoses is a

Scottish Fold Osteodystrophy
proliferative disease of young dogs and

This heritable condition ofScottish Fold
cats characterized by multiple ossified
cats is characterized by skeletal defom1a.protuberances arising from metaphyseal tions of the vertebrae, metaca.rpa.l and
cortical surfaces of the long bones,
metatarsa.l bones, and pha.langes secondary
vertebrae, and ribs. The exact etiology is
to abnonna.l endochondral ossification.

unlrnown, but hereditary (in dogs) and viral

Affected ca.ts are la.me, and affected bones

(in cats) causes are suspected. Animals
a.i·e deformed and swollen. Treatment is by
may be asymptomatic, and diagnosis is
removal of exostoses. Prognosis is guarded.

confirmed by palpation and radiography.

Surgical excision of the masses is recommended if clinical signs such as lameness OSTEOMYELITIS
or pain develop.

Inflanima.tion and infection of the medullary
cavity, co1tex, and periosteum of bone are

Panosteitis
most frequently associated witl1 bacteria.

Panosteitis is a spontaneous, self-limiting
such as Staphylococcus spp, Streptococcus disease of young, rapidly growing large and
spp, Escherichia, coli, Proteus spp,

OSTEOPATHIES IN SMALL ANIMALS

1205

Pasteurella spp, Pseudomonas spp, and NUTRITIONAL OSTEOPATHIES

Brucella canis. Anaerobic bacteria are less frequently isolated and may be part of a

See also DYSTROPHIES ASSOCIATED IVITII CALCIUM, polymicrobial infection. Ftmgal diseases

PHOSPHORUS, AND VITAMIN D, p 1050.

are based on geographic distributions and

Reduced bone mass, bone defonnities,

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include Coccidioides immitis (soutl1westexostoses, pathologic fractures, and loose em USA), Blastomyces dermatitidis
teeth (rubber jaw) a.i·e skeletal manifesta

(southeastern USA), Histoplasma
tions of nutritional derangements that affect
capsulatum (central USA), Cryptococcus
paratlly:roid hormone ftmction and calciun1
neoformans, and Aspergillus spp
and vitamin metabolism. Specific causes

(worldwide). Factors contributing to
such as secondary nutritional or renal
infection include ischemia, trauma, focal
hyperparatlly:roidism, hypovitaminosis D,
inflammation, bone necrosis, and hematogand hypervita.ininosis A can produce enous spread.

lameness. Diagnosis is by sernm chemistry

Clinical signs may be acute or chronic.

analyses, radiography, and identification

Animals may have lan1eness, pain,
of underlying nutritional deficiencies.

abscessation at the wound site, fever,

Treatment is aimed at reversing the specific
anorexia, and depression. Radiography can
etiology. Surgery is rarely indicated.

reveal bone lysis, sequestration, irregular
periosteal reaction, loosening of implants,

BONE TUMORS
and fistulous tracts. Deep fine-needle
aspiration, cytology, and blood cultures

Skeletal tun1ors ca.i1 be benign or malignant
may also reveal evidence of infection.

and primary or secondary to metastases or

Treatment includes botl1 medical and
adjacent soft-tissue strnctures. The most
surgical therapies. Long-term oral or
common primary bone tumor is osteosa.i·injectable antibiotics such as clavulanic coma tl1at affects the distal radius, proximal
acid/an1oxicilli.n (15 mg/kg, bid), cefazolin
humerus, distal femur, or proxin1al tibia.

(30 mg/kg, bid), clindan1ycin (11 mg/kg,

Clinical signs include lameness, bone
bid), enrofloxacin (15 mg/kg, bid),
swelling, and an acute, nontrawnatic
an1ikacin (15 mg/kg, bid), or oxacillin
patllologic fracture of tlle bone. Radiogra

(22 mg/kg, tid) are used. Additionally,
phy reveals osteolysis, proliferation, a.i1d
wOLmd debridement, lavage, and :removal
soft-tissue swelling; tlloracic radiographs
of loose implants are recommended. Open
should be performed to delineate metastatic
or closed wound drainage and delayed
masses. Bone biopsy using a Michelle bone
autogenous, cancellous bone grafting can
trephine or Jamshidi biopsy needle is
also be performed. In chronic, refractory
in1perative in confimling tlle diagnosis.

cases, limb amputation may be warranted.

Less frequently identified tun1ors inclw;!e

Prognosis is va.iiable and based on the
chondrosarcoma, fibrosa.i-coma, a.i1d
severity and chronicity of the infection.

hemangiosarcoma. Treatment includes limb

Appropriate antimicrobial therapy based
amputation and chemotl1erapy witll
on bacterial culture a.i1d antibiotic
carboplatin, cisplatin, or doxorubicin.

sensitivity testing is mandatory for

Palliative care to reduce pain and discomsuccessful results.

fort can be provided witll oral NSAlDs,
opioids, transde1mal patches, or radiation

HYPERTROPHIC OSTEOPATHY
tllerapy. Prognosis is gua.i·ded. Untreated
animals rarely live more than several

Hypertrophic osteopatlly is a diffuse
months. Amputation and chemotherapy
periosteal proliferative condition of long
may double tl1e survival tin1es. Median
bones in dogs secondary to neoplastic or
survival times after an1putation are 5 mo in
infectious masses in tl1e thoracic or
dogs and 4 yr in cats. Advanced procedures
abdominal cavity. The exact pathogenic
such as limb sparing a.i1d excision of
mechanism is unknown, but periosteal
metastases can also (infrequently) be
vascularity is reduced.

performed.

Clinical signs include lameness,
long-bone pain, and signs secondary to

BONE TRAUMA
body cavity masses. Radiography reveals
the primary masses and peripheral

Bone fractures are frequently caused
bone reactions.

by vehicula.i· accidents, firearms, fights, or

Treatment includes tlloracic or abdomifalls. Fractures can be open or closed and nal surgery to remove masses and unilateral
involve single or multiple bones. Charactervagotomy to block tlle neurovascular reflex istics of tlle fracture-such as simple,
associated with bone changes.

comminuted, oblique, transverse, or

1206

OSTEOPATHIES IN SMALL ANIMALS
spiral-are based on disruptive trauma

Antibiotics are given for open fractures or
forces (bending, compression, tension, and
prolonged repairs. Perioperative analgesics
rotation).

( eg, epidural morphine, narcotic skin

Clinical signs invariably include
patches, systemic narcotics [including
lameness, pain, and swelling. Railiography
constant-rate infusion], oral NSAIDs) are

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is useful in delineating the fracture pattern.

used to alleviate discomfort. Physical

Treatments are based on the type of
tllerapy or rehabilitation is critical to restore
fracture, age and health of the anin1al,
limb fwlction and overall well-being.

technical expertise of the surgeon, and

Prognosis for recovery is usually good,
owner finances.

depending on the nature of the injury and

Young, healthy dogs with incomplete
success of repairs; successful wound
fractures can be treated with external splints therapy and monitoring of cardiopulmoor casts. Other injwies are treated with nary and urologic fwlctions are essential.

external (fixators) or internal devices, such

Followup care includes railiographic and
as bone plates, screws, orthopeilic wires,
clinical assessments of fracture healing.

interlocking nails, and pins. Frequently,

Internal implants may not need to be
cancellous bone grafts are used to augment
removed unless complications such as
fracture healing in ill or aged patients.

stress protection, infection, or soft-tissue
irritation develop.

NERVOUS SYSTEM

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INTRODUCTION 1209

The Neurologic Evaluation 1213

History 1213

Physical and Neurologic Examinations 1213

Head 1214

Gait 1217

Neck and Thoracic Limbs 1217

Trunk, Pelvic Limbs, Anus, and Tail 1218

Clinical Pathology 1219

Cerebrospinal Fluid Analysis 1219

Imaging 1220

Electrodiagnosis 1220

Principles of Therapy 1220

CONGENITAL AND INHERITED ANOMALIES 1222

Cerebral Disorders 1222

Cerebellar Disorders 1225

Brain Stem Disorders 1226

Spinal Cord Disorders 1227

Neuromuscular Disorders 1231

Multifocal Disorders 1234

Miscellaneous Congenital Disorders 1236

DEMYELINATING DISORDERS 1236

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR

JUNCTION 1238

Degenerative Disorders 1238

Inflammatory Disorders 1239

Metabolic Disorders 1241

Neoplasia 1242

Nutritional Disorders 1242

Toxic Disorders 1242

Trauma 1243

Vascular Diseases 1244

DISEASES OF THE SPINAL COLUMN AND CORD 1245

Degenerative Diseases 1245

Inflammatory and Infectious Diseases 1249

Neoplasia 1252

Nutritional Disorders 1253

Trauma 1254

Toxic Disorders 1254

Vascular Diseases 1255

1208

NERVOUS SYSTEM

DYSAUTONOMIA 1255

Feline 1255

Canine 1256

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Leporine 1257

Equine 1257

FACIAL PARALYSIS 1258

NEONATAL ENCEPHALOPATHY 2094 (MGN)

LIMB PARALYSIS 1259

MENINGITIS, ENCEPHALITIS, AND ENCEPHALOMYELITIS 1262

MOTION SICKNESS 1267

NEOPLASIA 1267

PARANEOPLASTIC DISORDERS 1280

PHARYNGEAL PARALYSIS 186 (DIG)

POLIOENCEPHALOMALACIA 1281

PRION DISEASES

BOVINE SPONGIFORM ENCEPHALOPATHY 1284

CHRONIC WASTING DISEASE 1286

SCRAPIE 1288

VIRAL DISEASES

EQUINE ARBOVIRAl ENCEPHALOMYELITIS 1291

LOUPING ILL 1299

PSEUDORABIES 1300

RABIES 1302

TESCHOVIRUS ENCEPHALOMYELITIS 1307

BACTERIAL DISEASES

HISTOPHILOSIS 754 (GEN)

LISTERIOSIS 656 (GEN)

SPORADIC BOVINE ENCEPHALOMYELITIS 1308

PROTOZOAL DISEASES

EQUINE PROTOZOAL MYELOENCEPHALITIS 1309

NERVOUS SYSTEM INTRODUCTION

1209

PARASITIC DISEASES

CNS DISEASES CAUSED BY HELMINTHS AND ARTHROPODS 1310

Cestodes 1311

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Trematodes 1312

Nematodes 1312

Ascarids 1312

Filarids 1312

Metastrongyles 1313

Rhabditorids 1313

Miscellaneous Nematodes 1314

Arthropods 1314

TICK PARALYSIS 1314

NERVOUS SYSTEM INTRODUCTION

The neivous system is composed of billions
white matter and are an-anged into tracts.

of neurons with long, interconnecting

The tracts are usually nan1ed after their site
processes that form complex integrated
of origin and te1mination ( eg, the spinocerelectrochemical circuits. It is through these ebella.r tract begins in the spinal cord and
neuronal circuits that animals expe1ience
ends in the cerebellwn).

sensations and respond appropriately.

PNS sensory or afferent neurons carry

Neuronal processes that transmit
irlfonnation such as nociception, proprioelectrical alterations to the nemon cell ception, touch, temperature, taste, hearing,
body are called dendrites. Dendrites have
equilibrium, vision, and olfaction to the
receptor sites that receive stimulation or
spinal cord or brain stem. CNS sensory
inhibition from outside somces. If electrineurons carry irlfom1ation to the cerebel-cal stimulation of the cell body reaches a

I um, brain stem, and cerebrum forfW"ther.

critical threshold, an electrical discharge
interpretation. Important spinal cord and
called an action potential develops. The
brain-stem sensory tracts include several
action potential spontaneously travels away
spinocerebellar, spinothalamic, and
from the cell body along an outgoing
spinoreticular tract systems. The spinoreprocess called an axon. When the action ticular tracts begin in the spinal cord and
potential reaches the tenninal branches of
terminate in the reticular fom1ation of the
the axon, chemicals called neurotransmitmedulla. The dorsal fasciculi gracilis and ters are released. Neurotransmitters either
cuneatus of the spinal cord and the medial
stimulate or inhlbit receptor sites on other
and lateral lemniscus of the brain stem are
nemons, muscles, or glands. Although
also important sensory tracts. In animals,
neurons may have a vaiiety of shapes, each
these sensory tracts may carry fibers from
one has dendrites, a cell body, and an axon
many sensory modalities such as proprioand releases neurotransmitters.

ception, nociception (pain), and touch. An
alteration in sensation may be due to either

Basic Sensory and Motor Functions

CNS or PNS disease.

Reactions to sensory inputs are initi

The peripheral neivous system (PNS) is
ated by efferent or motor neurons in the
fom1ed by nemons of the cranial and spinal
cerebrnm and brain stem called upper
neives. The central neivous system (CNS) is motor neurons (UMNs). The UMN axons formed by neurons of the spinal cord, brain
descend to brain-stem and spinal cord
stem, cerebellum, and cerebrnm.

segments in tracts named after their site

Groups of nemonal cell bodies in the PNS
of origination and termination.

are called ganglia, whereas those in the CNS

The UMNs of the reticulospinal tracts
are called nuclei. Nuclei fom1 the CNS gray

(from midbrain, pons, and medulla
matter. Groups of axons in the CNS form the oblongata reticular fo1mation) and the

1210

NERVOUS SYSTEM INTRODUCTION
rubrospinal tract (from midbrain) are imporand PNS lesions to specific areas. If a reflex tant for voluntary movements of skeletal
is depressed or absent, a lesion must involve
muscles in domestic animals. The rubrospithe sensory nerve, intern uncial neuron, nal tract mainly functions to facilitate

LMN, or muscle at that particular site.

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flexors of the limbs, whereas the pontine

The autonomic nervous system is divided
and medullary reticulospinal tracts have
into syn1pathetic and parasyn1pathetic
either a facilitative (pontine) or inhibitory
portions and controls activity in smooth

(medullary) effect on the extensors. The
and cardiac muscles and glands. Visceral
corticospinal tracts ( cell bodies in the
afferent (sensory) neurons travel in cranial
cerebral cortex) are most important for
and spinal nerves and sensory spinal cord
voluntary movement in primates. Domestic
tracts to the thalarnic and hypothalamic
animals with severe cerebrocortical disease
regions of the brain stem. UMNs in the
may suffer only transient loss of voluntary
hypothalamus descend to LMN cell bodies
movements, because their corticospinal
of the brain-stem nuclei and sacral segtract has limited influence.

ments for parasympathetic control and to

The pontine reticulospinal (from the
the intennediolateral gray matter of
pons) and vestibulospinal (from vestibular
the spinal cord for syn1pathetic control.

nuclei of the medulla oblongata) tracts

LMNs of the syn1pathetic nervous system
facilitate extensor skeletal muscle activity
exit through thoracolun1bar spinal nerves
used to support the body. Knowledge of

(T l to IA) to affect smooth muscles
location and function of sensory and motor
associated with the pupils, eyelids, orbits,
brain-stem and spinal tracts is essential
hair follicles, blood vessels, and thoracic
to localize nervous system lesions and
and abdominal viscera. Horner syndrome
determine their severity. Mild spinal cord

(ptosis, miosis, and enophthalrnos) is a
compression affects the superficial spinal
common finding associated with loss
cord tracts (fasciculus gracilus, cuneatus,
of sympathetic innervation to the eye.

spinocerebella.r, and vestibulospinal tracts),

LMNs of the parasyn1pathetic nervous
so initial signs include ataxia and extensor
system exit via cranial nerve (CN) III to
weakness. Important voluntary motor tracts innervate smooth muscle of the pupils and are located in the lateral portions of the
eyelids, CN VII to the lacrimal and salivary
spinal cord deep to the spinocerebellar
glands, CN IX to salivary glands, and CN X
tracts, and paresis or paralysis develops
to cardiac muscles and glands and to
with moderate spinal cord compression.

smooth muscles of all the thoracic and

Because many tracts are involved, loss of
abdominal viscera to the level of the
nociception from the periosteum of the toes
transverse colon. LMNs of the parasyn1paand tail ( deep pain) occurs when spinal thetic nervous system also exit through the
cord lesions are bilateral and severe. This
sacral segments to all the viscera in the
loss of nociception is also an indicator of
caudal abdomen, including the bladder and
severe cord injury because those fibers that
colon. Sacral lesions commonly result in
transmit deep pain are typically nonmyeliloss of the urinary bladder ( detruser) reflex.

nated, slow-transmitting C type fibers,
which are very resistant to pressure.

Motor neurons with cell bodies in the

Divisions and Effects of Lesions
brain stem, and spinal cord gray matter and

See also THE NEUROLOGIC EVALUATION, p 1213.

axons that travel in the PNS cranial and

The PNS consists of 26 or more pairs of
spinal nerves, respectively, are referred to
spinal nerves that correspond to each spinal
as lower motor neurons (LMNs). Injury to
cord segment and 12 pairs of cranial nerves
either the UMNs or LMNs results in paresis
that correspond to specific brain and
or paralysis. Brain-stem and spinal cord
brain-stem segments.

reflexes are the phylogenetically oldest

The PNS spinal nerves fom1 the brachia!

responses of the nervous system. When the
plexus to the thoracic limb; the lumbosacral
eyelid is touched, it closes; when the toe is
plexus to the pelvic limb; and the cauda
pinched, the limb withdraws even before
equina to the bladder, anus, and tail.

conscious perception intervenes. Only a

Brachia! or lmnbosacral plexus lesions
sensory neuron in the PNS, a connector
cause paresis or paralysis of a thoracic or

(intern uncial) neuron in the CNS, and an
pelvic limb, respectively, with reduced or

LMN are necessary for a reflex to be
absent spinal reflexes and reduced or
present. In a monosynaptic reflex ( eg,
absent sensation of the limb. (See also
patellar reflex), only a sensory neuron and

LIMIJ PAHALYSIS, p 1259.) Cauda equina lesions

LMN are present. Du.ring the neurologic
result in an atonic bladder; a dilated,
exan1ination (seep 1213), testing brain-stem LU1.responsive anus; and a flaccid, paralyzed
and spinal reflexes is helpful to localize CNS tail.

NERVOUS SYSTEM INTRODUCTION

1211

Lesions of all spinal nerves ( eg, acute
hemiparesis or qua.driparesis with nom1al
polyradiculoneuritis) result in paresis or
or hyperactive limb reflexes, mental
paralysis of all four limbs ( quadriparesis or
depression from involvement of the
quadriplegia, respectively) with depressed or ascending reticular activating system absent spinal reflexes and altered sensation

CARAS), and CN V and IV deficits.

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of the limbs. Lesions restricted to PNS

The cerebellum is pa.rt of the metencephcranial nerves result in deficits associated a.lon and is attached to the dorsal surface of
with dysfunction of that particular nerve and
the pons and medulla by rostral, middle, and
no signs of dysfunction in the limbs or other
caudal cerebellar peduncles. The cerebelparts of the nervous system.

lum coordinates all muscle activity and

The spinal cord of dogs and cats is divided establishes muscle tone. The flocculonoduinto 8 cervical, 13 thoracic, 7 lumbar, 3
lar lobe of the cerebellum has equilibrimn
sacral, and 5 or more caudal segments.

functions and is considered pa.rt of the

Horses and cows have 6 lurnbar and 5 sacral
vestibular system. Unilateral lesions of the
segments, and pigs have 6--7 lurnbar and 4
cerebellum ca.use ipsilateral dysrnetria.

sacral segments. Spinal cord lesions from

(hypennetria or hypornetria) and a

L4 to S2 cause pelvic limb ataxia, conscious
contralatera.1 (paradoxical) head tilt.

proprioceptive deficits, and paresis or

Bilateral lesions of the cerebellum ca.use
paralysis with depressed or absent spinal
generalized incoorclination of the head and
reflexes and muscle tone (LMN signs).

limbs, head tremors (intention tremors),

Sensation may also be depressed or absent
and generalized dysequilibrium.

below the lesion. Lesions from T3 to

Midbra.in (mesencephalon) lesions ca.use

L3 cause pelvic limb ataxia, conscious
contralatera.1 conscious proprioceptive
proprioceptive deficits, and paresis and
deficits and hemiparesis. CN III nucleus
paralysis with nonnal or exaggerated spinal
involvement is present on the ipsilateral
reflexes (UMN signs). Pelvic limb sensation
side and localizes the lesion to the midbra.in.

caudal to the lesion may also be depressed

In large, mid brain lesions, the ARAS is
or absent. With spinal cord lesions
affected, and the animal will be stuporous
extending from C6 to T2, thoracic limb
or comatose. If the sympathetic UMNs and
spinal reflexes may be depressed or absent,
parasympathetic LMNs are both affected in
and severe lesions may ca.use quadriplegia.

the midbra.in, the pupils will be midrange

The spinal reflexes remain intact in the
size and tmresponsive to light.

pelvic limbs, but sensation may be affected.

Diencephalic lesions can be difficult to

Spinal cord lesions from C 1 to C5 cause
differentiate from cerebral cortical lesions,
hemipa.resis or hemiplegia (paresis or
because many tracts going to and from the
paralysis of the limbs on one side), or
cerebrum pass through the diencephalon by
quadriparesis. Spinal reflexes in all four
way of the internal capsule. The thalamus,
limbs a.re often preserved. Severe lesions
hypothalamus, and subthalamus of the
may ca.use respiratory distress or arrest due diencephalon have many important to involvement of the UMNs to respiratory
structures that alter feeding, drinking,
muscles in the C5 area.

breeding, sleeping, and other behaviors,

The bra.in stem is divided from caudal
as well as regulate body temperature.

to rostra.1 into four segments: the medulla

The pituitary gland, which controls
oblongata (myelencephalon), the pons
many hormonal functions of the body, is

(metencephalon), the midbra.in (mesenconnected to the hypothalamus. The ARAS
cephalon), and the thalamus and hypoprojects through the subthalanms area, in thalamus ( diencephalon).

which lesions also produce stupor or coma

Sin1i.lar to lesions of the cervical spinal

The telencephalon, also called the
cord, lesions of the medulla oblonga.ta cause cerebral cortex, is divided into the conscious proprioceptive deficits and
neocmtex, paleocortex, and archicortex.

wea.lrness on the same side (ipsilateral) or

The pa.leoc01tex and archicortex include the
both sides with nom1al or hyperactive limb
olfactory and limbic regions, which provide
reflexes. However, involvement of CN nuclei smell and emotional reactions to all stimuli.

IX, X, XI, or XII localizes the lesion to the

The neocortex is divided into the frontal,
caudal medulla oblongata. Involvement of
parietal, occipital, and temporal lobes. The

CN nuclei VI, VII, or VIII localizes the lesion
frontal cortex functions include intelligence
to the rostral medulla oblongata. It is rare to
and fine motor skills (corticospinal tract).

have a lesion of the medulla oblonga.ta that

Lesions in this area cause dementia., lack
does not affect one or more of the cranial
of recognition of the owner, difficulty in
ne1ves as well as sensory and motor tracts.

training, compulsive pacing, circling toward

Pon tine lesions cause ipsilatera.1
the side of the lesion (a.dversion syndrome),
conscious proprioceptive deficits,
and motor seizures with contra.lateral

1212

NERVOUS SYSTEM INTRODUCTION
involuntary muscle twitching. Contralateral

Infections of the nervous system are due
hopping and placing deficits are also found
to specific viruses, fungi, protozoa, bacteria,
with frontal Jobe lesions. Ascending and
rickettsia, prions, and algae. Noninfectious
descending tracts to and from the frontal
inflammations such as steroid-responsive
lobe form the internal capsule through the
meningoencephalomyelitis and meningoen

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region of the basal nuclei and diencephalon.

cephalomyelitis of unknown etiology

Lesions of the internal capsule can produce

(MUE), formerly called granulomatous
the same signs as frontal lobe lesions. The
meningoencephalomyelitis, Pug dog
parietal lobe (somesthetic cortex) is for
encephalitis, and other CNS inflammatory
interpretation of general perception,
diseases, may be immune-mediated. Until
nociception, temperature, and pressure;
there is a histologic diagnosis, the tem1
lesions result in proprioceptive deficits on

MUEis used.

the contralateral side of the body.

Toxicity of the nervous system is most

Occipital lobe and optic radiation lesions
frequently caused by organophosphates
result in blindness with pupils that respond

(seep 3064), pyrethrins (seep 3063), nmmally to light. Unilateral occipital lobe
carbamates (seep 3059), bromethalin (see
and optic radiation lesions result in some
p 3167), metaldehyde (seep 3070), ethylene
degree of visual loss in the contralateral eye,
glycol (seep 3046), metronidazole (see
depending on the percentage of crossover of
p 2696), theobromines (seep 2966), sedatives, the optic nerve fibers in the optic chiasm of
and anticonvulsants ( eg, phenobarbital,
the species (65% in cats; 75% in dogs; SOOh---90% bromide). Botulinum, tetanus, and tick in cattle, horses, pigs, and sheep). The pupils
toxins, as well as coral and certain other
still respond normally to light. Blindness
snake venom intoxications, cause
with pupils that do not respond to light is
neurologic signs.

associated with lesions of the retina, optic

Metabolic alterations of nervous system
nerve, optic chiasm, or rostral optic tract.

function most commonly result from

Difficulty in localizing sound is hard
hypoglycemia, hypoxia or anoxia, hepatic
to evaluate clinically. It may occur with
dysfunction, hypocalcemia, hypomagnetemporal lobe lesions, as may psychomotor semia, hypematremia, hypokalemia, and
seizures characterized by hysterical running. uremia. Hypothyroidism, hyperthyroidism,

"Fly-biting" or "star gazing" hallucinations hypoadrenocorticism, and hyperadrenocorare suspected to occur with lesions in the ticism are endocrine disorders that can
temporal-occipital region. Aggression
cause neurologic dysfunction.

occurs when the pyriform area (paleocor

Thian1ine deficiency results in ataxia,
tex) of the temporal lobe and the underlying
stupor, and coma or seizures in dogs, cats,
amygdaloid nucleus are affected. Aggression and cattle. Deficiency of vitamin B0 may can also occur with hypothalamic lesions.

cause seizures.

Lesions of the olfactory region may alter

Trawna to the PNS and CNS causes focal
feeding or breeding behavior. Slow-growing
and multifocal neurologic signs from
lesions of the cerebrum and diencephalon
physical dan1age, hemorrhage, edema, and
often result in few clinical signs because of
progressive fom1ation of oxygen-containing
the adaptability of functions in these-areas
free radicals and nervous system destrucin animals.

tion that is usually complete in 24--48 hr but
lasts as Jong as 4 days because of the slow

Mechanisms of Disease
influx of inflammatory cells.

Vascular lesions of anin1als are· usually

Disease processes affecting the nervous
due to septicemia and bacterial embolizasystem may be congenital or familial, tion of the CNS. Fibrocartilaginous
infectious or inflammatory, toxic, metaembolization of the spinal cord is common bolic, nutritional, traumatic, vascular,
in dogs. Arteriovenous malfom1ations occur
degenerative, neoplastic, or idiopathic.

occasionally and cause spontaneous

Congenital disorders may be obvious at
hemorrhages. Cerebrovascular disease
birth or sho1tly after ( eg, an enlarged head
from arteriosclerosis is rare in domestic
from hydrocephalus or an uncoordinated
animals but has been associated with
gait from an underdeveloped cerebellum).

hypothyroidism caused by hyperlipidemia.

Some familial disorders ( eg, Jysosomal

Cerebrovascular disease from hypertension
storage diseases) cause a progressive
is rare but may be seen as multiple cerebral
degeneration of neurons in the first year of
microbleeds with MRI.

life, whereas others ( eg, inherited epilepsy)

Familial degeneration of neurons occurs
may not manifest for 2--3 yr. (See also
in lysosomal storage disorders. Degenera

CONGENITAL AND INHERITED ANOMALIES OF THE
tion of intervertebral discs that subse

NERVOUS SYSTEM, p 1222.)

quently herniate into the vertebral canal

NERVOUS SYSTEM INTRODUCTION

1213
often produces paresis and paralysis in
more limbs. Information about the onset,
dogs.

course, and duration of the primary

Neoplasms of the CNS and PNS are most
complaint can be used to detemline the
common in dogs and cats. Astrocytes,
most probable disease mechanisms.

oligodendrocytes, and microglia can all

Congenital and familial disorders are most

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become neoplastic and fom1 astrocyconu11on in pw·ebred animals at birth or tomas, oligodendrogliomas, and gliomas.

within the first few years of life. lnflamma

Ependymal cells and the choroid plexus,
tory, infectious, metabolic, toxic, and
which line the internal cavities of the CNS
nutritional disorders can be seen in any
and produce CSF, also can become
species, breed, or age; tend to have an acute
neoplastic and form ependymomas and
or subacute onset; and are usually progreschoroid plexus papillomas. Meningeal cells sive. Vascular and traumatic disorders have
of the dura, arachnoid, and pial membranes
an acute onset and rarely progress after 24
fom1 meningiomas, which are common in
hr. Most degenerative and neoplastic
dogs and cats. Neurofibrosarcomas are
disorders tend to be seen in older animals
conunon tumors of the nerve sheaths of

( except for familial neuronal degeneration)

peripheral nerves in dogs. Lymphosarcoma
and have a clll'onic onset and progressive
is a common metastatic tumor of the PNS
course. Many idiopathic disorders begin
and CNS in dogs, cats, and cattle. Hemanacutely and in1prove throughout a short giosarcoma is the most common metastatic
time. Information about sin1ilar familial
twnor of the CNS in dogs. (See also
problems, concurrent or recent systemic

NEOPLAS!A OF'TflE NERVOUS SYSTEM, p 1267.)

disease, vaccination status, other affected

The idiopathic mechanism of disease is
aninlals, diet, possible exposure to toxins or
reserved for described syndromes with
trauma, and past neoplastic disorders may
characteristic clinical signs, predictable
be useful to fwil1er support certain
outcomes, and no known necropsy findings.

mechanisms of disease.

PHYSICAL AND NEUROLOGIC

EXAMINATIONS

EVALUATION

Evidence of disease in other body systems

An accurate history and thorough physical
may be associated with inflanu11atory,
and neurologic exanlinations are necessary
metabolic, toxic, or metastatic neoplastic
to evaluate a problem involving the nervous
disorders of the nervous system. Infections
system. An understanding of functional
of the CNS may not have any signs other
neuroanatomy, neurophysiologic concepts,
than neurologic. External signs of trauma
and mechanisms of disease is a prerequisite
or toxic exposure may support these
for accurate interpretation of clinical
mechanisms of disease.

findings. Based on the initial clinical

The neurologic examination consists of
assessment, 1) the anatomic location(s)

evaluation of the following: 1) the head,
of disease can be deteffilined, and 2) the

2) the gait, 3) the neck and thoracic limbs,
problem may be defined as diffuse,
and 4) the tJunk, pelvic limbs, anus, and tail.

multifocal, or focal; symmetric or asymlnitially, an attempt should be made to relate metric; painful or nonpainful; progressive,
all deficits to one focal anatomic lesion.

regressive, waxing and waning, or static;

If abnonnalities are found on evaluation
and mild, moderate, or severe. The potenof the head, then an initial attempt should tial mechanisms of disease must also be
be made to explain all limb abnom1alities by
considered to detemline differential
a lesion above the forarnen magnum. If no
diagnoses. Further diagnostic tests include
abnormalities are found on evaluation of the
clinicopathologic tests ( on serwn, blood,
head, but thoracic lin1b abnormalities are
urine, feces, and CSF), diagnostic imaging
present, then an attempt should be made

(including plain and contrast radiography,
to explain the abnom1alities by a cervical

CT, and MRI), and electrodiagnostic testing.

lesion (Cl to T2). Paralysis or paresis of all
four limbs with loss of all spinal reflexes

HISTORY

(with or without cranial nerve deficits) is
often associated with diffuse peripheral

Neurologic diseases tend to have a species,
nerve or neuromuscular junction disease
age, breed, and occasionally a sex predilec

(seep 1238).

tion. The primary complaints for neurologic

Knowledge of specific diseases within
problems often include behavioral changes,
a certain mechanism for a given species,
seizures, tremors, cranial nerve deficits,
age, breed, and sex of aninlal enables an
ataxia, and paresis or paralysis of one or
accurate list of differential diagnoses and

1214

NERVOUS SYSTEM INTRODUCTION
a diagnostic plan to be formulated after the
they are simple to test, and test results
history and physical and neurologic examcan help localize disease to that segment.

inations are completed. Toxic, metabolic,

Abnormal findings are produced by lesions
and nutritional mechanisms rarely produce
of the peripheral cranial neive or cranial
asymmetric neurologic deficits. The other
ne1ve nuclei. If a brain-stem lesion is

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mechanisms of disease may result in
present, abnonnalities are seen in tl1e gait,
symmeb.ic or asymmetric deficits.

thoracic or pelvic limbs, and at times mental
status. lf only a peripheral cranial neive is

Evaluation of the Head
affected, there are no changes in gait, the

Mentation, head posture and coordination,
thoracic or pelvic limbs, or mentation.

and cranial ne1ve functions are obseived

Cranial neive lesions of one side produce
during evaluation of the head. Abnonnal
ipsilateral deficits except for lesions of the
findings are due to lesions above the level of trnchlear neive (CN IV), which crosses in the foran1en magnum in the cerebrum, the
the mid brain.

brain stem ( diencephalon, midbrain, pons,
or medulla oblongata), or the cerebellum.

I. Olfactory: The olfactory neives trans

Dementia, compulsive pacing, or other
mit smell.

behavioral abnormalities and seizures are
frequently due to lesions in the cerebnm1

Tests: The anin1al's ability to find food
or diencephalon. Stupor, obtundation,
or the reaction to chemicals ( eg, cloves,
semicoma, or coma may be due to lesions of benzene, or xylene) should be obseived.

the cerebrum, diencephalon, or midbrain. A

Substances that initate the nasal mucosa
head turn or compulsive circling without a
and the trigerninal ne1ve endings ( eg,
head tilt is also associated with a cerebral
alcohol or phenol) should not be used.

or diencephalic lesion on the side toward

Signs of Dysfunction: lnability to find
which the animal turns. A head tilt is due to
food or respond to nonirritating chemicals
vestibular system disease (CN VIII, rostral
is found witl1 disease of the cribriform plate,
medulla oblongata, or cerebellum).

olfactory bulbs, and olfactory region.

Abnormal head coordination, bobbing, and
tJ.·emors result from cerebellar dysfunction.

II. Optic: The optic ne1ves are necessary

The cranial nerves consist of 12 pairs
for vision and also can-y the afferent fibers
located in specific brain-stem segments;
of the pupillary light reflex to the mid brain.

optic n.

maxillary, ophthalmic and
motor nn. of the eye
au1iculoinfratrochlear n.

palpebral n.

zygomaticofacial n.

infraorbital n.

infe,ior
mental n.

lactimal n.

Cranial nerves accessible for nerve block in a bovine head. Illustration by Dr. Gheorghe Constantinescu.

NERVOUS SYSTEM INTRODUCTION

1215
lacrimal n.

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suboccipital n.

mental n.

Cranial nerves accessible for nerve block in an equine head. Illustration by Dr. Gheorghe Constantinescu.

Visual Tests: Cotton balls can be dropped
stimulated with light. Unilateral lesions of
and the animal observed watching them fall
the optic tract, lateral geniculate nucleus,
to the floor. The menace response is tested
optic radiation, thalamus, or occipital
by making a threatening gesture toward
cortex usually produce a contralateral
each eye, causing the anin1al to blink The
visual deficit with no1mal pupillary light
animal sees the menacing motion (CN II)

reflexes (see above).

and blinks the eye (CN VII). In foals and
calves this reflex will be evident by 7 -10

Ill. Oculomotor: These nerves carry
days of age, whereas in puppies and kittens
efferent parasympathetic fibers from the
it may not be present until 10-12 wk
pupillary light reflex center of the mid brain

Excessive air cunents or touching the
to the fibers of the ciliary ganglion, which
eyelashes should be avoided, because this
innervate the const:tictor muscle of the
will test response to touch (CN V) rather
pupils. They are also efferent to the levator
than vision. Obstacle testing may be
palpebrae muscles; the dorsal, medial, and
necessary when visual acuity is in doubt.

ventral rectus muscles; and the ventral

It is useful to blindfold one eye at a ti.nle
oblique muscles of the eye.

to detect blindness of either eye.

Tests: The pupillary light reflex test

Pupillary Light Reflex: A bright focal
should be performed as described for the
light is directed into each pupil toward the
optic nerves, and const:tiction of the pupils
temporal retina, and the pupil is observed
to light should be observed. The presence or
for inunediate constriction. The opposite
absence of ptosis of the upper eyelid as well
pupil should constrict consensually ( a
as vent:t·olateral strabismus should be noted.

consensual or indirect response) (CN II
afferent and CN III efferent).

IV. Trochlear: These are the motor nerves

Ophthalmoscopic Examination: This
to the dorsal oblique muscles of the eye.

detects local eye diseases. Cho1ioreti.nitis or

Test: The eyeballs should be observed for
papilledema may be associated with central
a vertical misalignment ( easiest to see in
or pe1ipheral nervous system diseases.

species with a holizontal- or ve1tical-shaped

Papilledema is often seen with increased
pupil).

intra.cranial pressure.

Signs of Dysfunction: Trochlea.r nerve or

Signs of Dysfunction: Unilateral optic
midbrain lesions may result in the dorsal
nerve dysfunction results in a decrease or
aspect of the globe rotating laterally.

loss of vision and decreased pupillary light
reflexes on the affected side. Consensual

V. Trigeminal: These nerves have three
pupillary constriction of the affected eye
branches. The mandibular branch is the
should still occur when the other eye is
motor nerve to the muscles of mastication

1216

NERVOUS SYSTEM INTRODUCTION
and the sensory nerve to the floor of the oral

Signs of Dysfunction: A facial nerve
cavity, ventral dental arcade, and the skin of
lesion results in an inability to blink the
the ventrolateral head. The ophthalmic and
eyelid or move the lips or nose; acutely it
maxillary branches are sensory to the skin
produces a droopy face, and food accumuof the dorsolateral head; mucous memlates in the affected cheek. Tear and saliva VetBooks.ir
branes of the roof of the oral cavity, the
production may be reduced on the side of
dorsal arcade, and the nasal cavity; and the
the lesion. Later, facial muscle contractures
eyeball, including the cornea (pain).

are observed.

Tests: Jaw tone and masticatory

VIII. Vestibulocochlear: There are two
movements should be evaluated, and the
masseter and temporalis muscles should be
main divisions of these nerves. The first
palpated for atrophy to evaluate the motor
division, the cochlear nerve, transmits
component of the t1igeminal nerve. The
auditory stimuli. The second division, the
sensory function can be evaluated by
vestibular nerve, functions to maintain
touching the medial and lateral canthi of the
posture, muscle tone, and equilibrium.

eyelid, which elicits the palpebral reflex

Tests: Deafness is detected when loud
and closure of the eyelids (CN V afferent
noises do not evoke a response from an
and CN VII efferent). Stimulation of the
awake or sleeping aninlal. Unilateral
cornea results in globe retraction (CN V
deafness is best detected with electrodiagafferent and CN VII efferent). In stoic nostics, ie, a brain-stem auditory evoked
animals, sensation is tested by a pinprick to
response (BAER) test. (In puppies, this
the nasal mucosa (an avoidance response,
evaluation should not be perforn1ed before
turning the head away, will be seen).

6 wk of age, because results may be

Signs of Dysfunction: Lesions of the
erroneous.) Head tilt, dysequilib1ium, and
tiigeminal nerves or pons produce temporal
a tendency to circle, fall, or roll to one side
and masseter muscle atrophy and/or loss of
develop witl1 unilateral or asymmetric
sensation to the face, cornea, and nasal
vestibular lesions. The aninlal should be
mucosa. A bilateral lesion of the tligeminal
exaniined for tl1e presence of spontaneous
motor nerves produces a dropped jaw.

nystagmus with the head held in a nonnal
position and in a deviated position (positional nystagmus), as well as for abnormal VI. Abducent: These are the motor
eye position (ventral sti·abismus) on the
nerves to the lateral rectus and retractor
affected side when the nose is elevated.

bulbi muscles of the eye.

N onnal vestibular nystagmus (physiologic

Tests: The eyeballs should be observed
nystagmus) is seen as a few beats to the left
for medial strabismus. The corneal reflex
as the head is turned to the left, and to the
should be elicited with the 11yelids held open, 1ight as the head is turned to the right.

with the eyeball observed for retraction and

Signs of Dysfunction: Unilateral lesions
the third eyelid observed for prolapse.

of the vestibulocochlear nerves produce

Signs of Dysfunction: Lesions of the
dysequilibrium with a head tilt toward the
abducent nerves or rosti·al medulla
side of the lesion. A spontaneous posioblongata result in medial strabismus tional, horizontal, or rotary nystagmus is
and lack of globe retraction.

often present. A positional nystagmus ( one
in which the character of the nystagmus

VII. Facial: These are the motor nerves
changes with changes in the animal's
to the muscles of facial expression (ear,
position) or a vertical nystagmus are
eyelids, nose, and mouth). The sensory part
almost always seen with central vestibular
of CN VII is for taste on the rostral third of
disease. A bilateral vestibular lesion results
the tongue. The parasympathetic portion
in dysequilibriwn on both sides, wide
of CN VII innervates the tear glands.

side-to-side excursions of the head (often
with no head tilt), loss of normal vestibu

Tests: The menace and palpebral reflexes
lar nystagmus, and possible deafness.

should be elicited to test orbicularis oculi

Occasionally, a cerebellar or cerebellar
muscle function. The nose should be
peduncle lesion will result in a head tilt
examined for deviation ( with unilateral
away from the lesion (paradoxical head
lesions). The lip should be pinched to see
tilt), but conscious proprioceptive deficits
whether it retracts. The ear should be
and hemiparesis will be ipsilateral with
tickled to see whether it moves. Atropine or
hypermetria of limbs on the ipsilateral side.

another bitter substance may be placed on
the distal tongue to test taste. A Schirmer

IX. Glossopharyngeal and X. Vagus:

tear test should be perforn1ed to evaluate

The glossopharyngeal and vagus nerves
parasympathetic innervation of tear glands.

provide sensory and motor control of the

NERVOUS SYSTEM INTRODUCTION

1217
pharynx and larynx, and the vagus nerves
chronic lesions in the cerebral cortex and
provide sensory and motor control of the
diencephalon usually have a relatively
viscera.

normal gait but may circle compulsively.

Tests: The hyoid bones should be pinched Animals witl1 lesions of the midbrai.n, pons, VetBooks.ir
to elicit a gag reflex. The animal should be
and medulla oblongata have paresis or
observed for nonnal phonation and
paralysis of the limbs, with deficits often
respiratory sounds.

more severe on the side of the lesion.

Cerebellar lesions produce ataxia and

Signs of Dysfunction: Lesions of the
dysmet1ia. Vestibular dysfunction causes
glossopharyngeal and vagus nerves or
ipsilateral falling, rolling, or circling. If no
caudal medulla oblongata result in
abnonnalities a.re found on evaluation of
dysphagia, megaesophagus, or laryngeal
the head, but the gait is abnonnal, a lesion
paresis or paralysis. A change in phonation
most likely is located in the spinal cord,
also occurs with vagus nerve and nucleus
peripheral nerves, or muscles.

lesions.

Evaluation of the Neck and

XI. Spinal Accessory: These nerves

Thoracic Limbs
inne1vate the trapezius, stemocephalic,
and brachycephalic muscles.

The neck is examined for pain and, in large
animals, atrophy and desensitization to

Tests: The muscles should be palpated.

pinprick, which inclicate a lesion of tlle

Signs of Dysfunction: Lesions of the
ce1vical spinal cord. Wheelban-owing, tonic
cranial ce1vical spinal cord or caudal
neck and eye, conscious proprioceptive
medulla oblongata may result in muscle
positioning, placing, hopping, and 1ighting are
atrophy. This may be accompanied by
postural reactions tlmt detect subtle lesions.

weakness when the examiner turns the
head away from the side of the lesion.

Wheelbarrow: The pelvic limbs of small
animals a.re lifted slightly off U1e ground

XII. Hypoglossal: These a.re the motor
while keeping body posture as nom1al as
nerves to the tongue and geniohyoid
possible, and tl1e animal is evaluated while
muscles.

walking on tlle tlloracic limbs. This test is
used to detect sublle deficits of the tlloracic

Tests: The tongue should be observed for
limbs. Nonna! animals should not stunlble
muscular control during licking and lapping
or knuckle over on tlle toes as tlley walk.

of water. The tongue curls under to lap
water in dogs and cats. In large animals, the

Tonic Neck and Eye: Willi the dog or cat
tongue may be grasped and pulled side to
standing, tlle nose is elevated and the eyes
side to assess its strength.

obse1ved to see whetl1er tlley coordinately·

Signs of Dysfunction: Lesions of the
acljust to the center of tl1e palpebral fissures.

hypoglossal ne1ves or caudal medulla

In vestibular dysfunction, tlle eyeball on tlle
oblongata may result in deviation or atrophy affected side rotates downward (positional of the tongue. As with the facial nerve, this
strabisrnus or eye drop). Simultaneously,
deviation of the tongue is at first away
tlle thoracic lin1bs should extend witll no
from the affected side, then with muscle
tendency to knuckle or collapse, and the
contracture is toward the affected side.

pelvic limbs should flex.

Evaluation of the Gait

Conscious Proprioceptive Positioning:

Each foot is displaced by turning it onto its

The gait is observed while the animal walks,
dorstm1 or by abducting or adducting the
trots, gallops, turns, sidesteps, and backs
limb widely. The animal should in1mediately
up. In large animals, ambulation up and
replace the leg to a norn1al position. Lesions
down a grade, on and off a curb, and while
of tl1e nervous system often affect conscious
blindfolded may accentuate subtle gait
proprioception first.

deficits. Evaluation of gait is especially
important in ambulatory large animals

Placing: Small an.in1als may be carried
because postural reactions a.re difficult to
toward a table top; on seeing tl1e table, a
obtain because of size and because spinal
normal anin1al anticipates placing its
reflexes usually are not tested unless the
forepaws on tlle surface. If blindfolded, tlle
animals are recun1bent. In small anin1als,
animal should place tlle forepaws on tlle
subtle deficits may be detected by postural
table only when the limbs contact tlle edge
reaction testing of the limbs ( see below) and of tlle table. A loss of placing response may by hemistanding and hemiwalki.ng (standing be present in subtle dysfunction even when or walking on one side). Animals with
the gait is normal.

1218

NERVOUS SYSTEM INTRODUCTION

Hopping: In small animals, three legs can

Muscle Atrophy: Focal muscle atrophy
be held off the gronnd with normal posture
of the limbs or neck localizes the lesion to
maintained, and the animal forced to move
the cell body in the spinal cord, ventral
or hop (by being pushed laterally and
spinal nerve root, or peripheral axon of

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forward) on the fourth limb. For large dogs
the nerve that innervates that muscle.

and other large animals, one pelvic or
thoracic limb opposite the side to be tested

Sensation: Conscious perception of
is held off the ground. When the animal is
superficial (skin) or deep (osseous) pain is
pushed toward the side to be tested, it
tested by applying forceps to the skin or bone,
should hop on the limb. Animals will not
respectively, and observing a behavioral
hop when pushed in a medial direction.

response. Such a response indicates that the

Motor and proprioceptive loss, cerebellar
peripheral sensory nerve and spinal cord, as
incoordination, and cerebrocortical
well as the pathways through the brain stem
deficiency may be detected.

to the cortex, are intact.

If the evaluation of tl1e head is abnormal,

Righting: The animal is observed to see
an initial attempt should be made to explain
whether it can right itself from lateral
any thoracic limb abnonnalities by a lesion
recw11bency. A small animal suspended
above the foramen magnwn. If the thoracic
upside down by the hips attempts to hold its
limb abnonnalities carmot be explained by a
head up when the trnnk is rotated from side
lesion in the head, then a multifocal or diffuse
to side and extends its forelimbs to support
disease process (such as an inflanunatory,
weight when lowered to the ground. With
toxic, metabolic, nutritional, traumatic, or
vestibular dysfnnction, the animal twists
metastatic neoplastic disorder) must be
toward the side of the lesion or curls its
present.

head nnder (bilateral vestibular lesions).

If there are no abnormalities on
evaluation of the head, and the thoracic

Spinal Reflexes: The spinal reflexes are
tested with the animal in lateral recwnlimbs are abnormal, then a lesion of the bency and the limbs relaxed. When the
cervical spinal cord or brachia! plexus is
toes or skin of the distal thoracic lin1b are
present. In lesions of the cervical spinal
pinched, that limb should withdraw and the
cord, the gait of the thoracic and pelvic
opposite limb usually does not move. This
limbs is abnormal, and pelvic limb spinal
is the flexor or withdrawal reflex; it is
reflexes are nom1al or exaggerated.

present if spinal cord segments C6 to T2 and

If no abnormalities are fonnd on
nerves of the brachia! plexus are intact.

evaluation of the head and thoracic limbs,

Intramedullary spinal cord lesions at C6 to
then a lesion must be below the T2 spinal

T2 usually depress or abolish the reflex, but
cord segment.

mild extramedullary lesions may produce
no change. With lesions cranial to C6, a

Evaluation of the Trunk, Pelvic
simultaneous extension of the opposite

Limbs, Anus, and Tail
limb (the crossed extensor reflex) may

The trW1k of the animal is observed for abnoroccur when the tested limb flexes, The mal posture or deviation of the vertebral
crossed extensor is a nom1al reflex;
colnnm, pain, desensitization or hyperesthehowever, an exaggerated response is sia to light pinpricking, and focal muscle interpreted as an upper motor neuron
atrophy.

(UMN) sign indicating loss of inhibition
from the UMN. The Babinski reflex is

Cutaneous Trunci and Panniculus
elicited by stroking the palmar surface of

Reflex: Pinp1icks applied to tl1e skin of the the paw in either a carpus to toe or toe to
thorax and abdomen result in contraction of
carpus direction. A positive (abnormal)

the cutaneous trnnci muscle. This reflex arc
response would be dorsiflexion of the toes,
includes the afferent cutaneous branches of
which is interpreted as a UMN sign.

the lumbar and thoracic spinal nerves, a

Other tendons (biceps and triceps) and
spinal cord tract that ascends to T2, and the
muscles ( extensor carpi radialis) may be

LMNs in the lateral thoracic nerve to cutanetapped with a percussion hammer and the ous trnnci muscles. The reflex is used to
response evaluated to test C6 to C7, the
localize spinal cord lesions between the site
musculocutaneous nerve (biceps), and C7
of stimulation and T2.

to T2, the radial nerve (triceps, extensor
carpi). These reflexes can be difficult to

Postural Reactions: Wheelbarrowing,
obtain in normal animals, so a reduced
proprioceptive positioning, placing, and
response should be interpreted with
hopping are evaluated on the pelvic limbs
caution. All reflexes may be normal or
in a marmer similar to that used for the
exaggerated with lesions above C6.

thoracic limbs. As with the thoracic limbs,

NERVOUS SYSTEM INTRODUCTION

1219
these tests require complete integrity of the
metabolic dysfunctions. Serum cholinesterbrain, spinal cord, and peripheral nerves; ase is decreased in acute organophosphate
thus, they are useful to localize lesions and
toxicity, and serum lead detenninations are
to detect subtle deficits that support the
increased in lead toxicity. Senun thyroid and
presence of a neurologic lesion.

cortisol detemlinations and stimulation tests

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are useful to detect endocrinopathies. Serum

Spinal Reflexes: The pelvic limb spinal
titers or PCRs for viral, ftmgal, protozoa!,
reflexes are more reliable to localize
and rickettsial organisms can be evaluated.

thoracolurnbar lesions than are the thoracic

Serwn muscle enzymes, especially CK,
limb reflexes. Spinal reflexes are nonnal or
may be increased in myopathies. Serum
exaggerated with lesions above the reflex
acetylcho!ine receptor antibodies can be
arc (UMN) and are depressed or absent with detected in dogs and cats with myasthenia lesions at the level of the reflex (LMN).

gravis, and type II M muscle antibody titers

Percussion of the patellar tendon should
are used to confinn masticatory muscle
cause the stifle to extend if IA to L6 spinal
myositis. Muscle and nerve biopsies are
cord segments and the femoral nerve are
essential for diagnosis and characterization
intact. Percussion of the gastrocnemius and
of many neuromuscular disorders. In some
cranial tibial muscles causes the hock to
cases, brain biopsy is necessary to confinn
extend or flex, respectively, and tests the
and characterize an in.flan1rnatory or
tibial and peroneal nerves, lumbosacral
neoplastic process so that proper antimicroplexus, and L6 to 82 spinal cord segments. A bial therapy, chemotherapy, or radiation
crossed extensor reflex may be associated
therapy can be administered.

with lesions above L6 (UMN sign). When the
anus is pinched or pricked with a pin, the
sphincter tightens and tl1e tail pulls down

CEREBROSPINAL FLUID ANALYSIS
if Sl to 83 (anus) and caudal (Cd) tail

The analysis of CSF may further aid in detersegments and nerves are intact. An a.tonic nlining the mechanism of a CNS disorder

( areflexic) bladder, anus, and tail are seen

(especially in.flanunation). The technique of
with lesions affecting Sl to Cd5 or tl1e cauda collection is simple and safe with practice.

equina. As an incidental finding, the femoral

Analysis of CSF requires minimal special

(patellar tendon) reflex may be absent in
equipment. Cell counts and identification
some geriatric dogs.

should be perfonned witllin 30 min after

Muscle Atrophy:

collection, because cells begin to degener

Focal muscle atrophy
ate after that time. Several techniques are
of the tnmk or pelvic limb localizes a lesion
available to concentrate or stabilize cells so
to the nerve that innervates that muscle.

that a differential cell cotmt can be obtained

Sensation: In moderate to severe spinal
at a later time.

cord lesions, superficial sensation may be

CSF is collected from tl1e cerebellomedul'

absent from the cranial aspect of the lesion
lary cistern or the subarachnoid space in tl1e
caudally. In severe spinal cord lesions, deep
lwnbar region. An increase in protein is often
pain is absent from the periosteum of all
associated with encephalitis, meningitis, neotoes and the tail.

plasia, or spinal cord compression. Cellular
content increases most frequently witl1

Schiff-Sherrington Phenomenon: In
inflan1rnation of the CNS. Neutrophils are
some anin1als with acute, severe lesions
indicative of bacterial infections, subarachof the spinal cord between T2 and L3, the noid hemorrhage (RBCs are also present),
pelvic limb paralysis is accompanied by an
brain abscess or a steroid-responsive
extensor rigidity of tl1e thoracic limbs when
suppurative meningoencephalitis, or in some
the anin1al is in lateral recurnbency. This
cases, necrosis witllin a tunlor. Increased
occurs because of an interruption of an
nun1bers of lymphocytes, monocytes, and
ascending spinal cord tract from the lumbar
neutrophils are most conunon in steroidintw11escence, which inhibits extensors of responsive nonsuppurative meningoenthe forelimb. Although a severe lesion cephalitis, meningoencephalitis of unknown
produces tllis syndrome, the prognosis is
etiology (MUE) , fungal infections, toxoplasprobably not hopeless if deep pain sensation rnosis, and neosporosis. Cultures of CSF may can be elicited from the pelvic limbs.

demonstrate the causative agent in bacterial
and fungal infections. Paired senm1 and CSF

CLINICAL PATHOLOGY
imrnunoassays for canine distemper virus,
cryptococcosis, toxoplasmosis, neosporosis,

Abnormalities of serum glucose, liver

Rocky Mountain spotted fever, ehrlichiosis,
enzymes, BUN, bile acids, an1rnonia,
and borreliosis can assist in diagnosis of
electrolytes, or blood gases can occur with
these infections.

1220

NERVOUS SYSTEM INTRODUCTION

IMAGING
loss. Brain-stem disorders may also alter the

BAER; it may be abnormal in the Chiari

Plain radiographs of the skull and ve1temalformation of Cavalier King Charles bral column are useful to detect fractures,

Spaniels and may also be used as an
subluxation, infection, or neoplasia of
indicator in detennining brain death.

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osseous structures. In most infections or

Spinal cord evoked potentials can be
neoplastic processes of the brain and spiused to evaluate spinal cord integrity. These nal cord, plain racliographs are normal.

are elicited by stimulating a pe1ipheral

Myelography is used to detect compressive
nerve and recording the potential as it
or expansive spinal cord lesions, including
ascends the spinal cord.

herniated or protruded interve1tebral discs
and spinal cord tumors. CT and MRI scans
are useful to evaluate lesions of the brain
and spinal cord in small animals. CT scans

See a.lso SYSTEMIC PHARMACOTIIERAPEUTICS OF'

are helpful to detect changes in bone, acute

THE NERVOUS SYSTEM, p 2590.

hemon-hage, and CNS neoplasia. MRI scans
are the best to demonstrate soft-tissue

Seizure Control: Status epilepticus
changes, eg, neoplasia, abscesses,

( continuous or cluster seizures) in dogs and
inflammation, and hemon-hage. MRI is the
cats may be interrupted by diazepam, given
gold standard for evaluation of lumbosacral
at 0.5 mg/kg (not to exceed 10 mg at one
disease in small animals. Magnetic
time), IV. Sodium pentobarbital to effect,
resonance angiography can be used to
not to exceed 3-15 mg/kg, IV, may also be
evaluate vascular changes in the CNS.

used, followed by phenobarbital at 2-4 mg/
kg, IV, every 6 hr. A better alternative is to

ELECTRODIAGNOSIS
give propofol as a constant rate infusion at

0.1-0.6 mg/kg/min, followed by a loading

An electroencephalogran1 (EEG) is a
dose of phenobarbital (if the atlinlal is not
recording of the electrical activity of the
already on phenobarbital) of 2-4 mg/kg,
surface of the cerebral cortex, which is

IV, every 6 hr for a total of four doses.

influenced by subcortical stmctures. The

Diazepatn given at 0.5--1 mg/kg/hr as a

EEG is consistently abnonnal in hydrocephconstant-rate infusion may be used to alus, meningoencephalitis, head trauma,
control persistent status epilepticus. If the
and cerebral neoplasia. An EEG may
animal has a preexisting hepatic condition
detemline whether seizure discharges are
that precludes the use of phenobarbital,
focal or diffuse. The EEG is often normal in
then levetiracitam 40-60 mg/kg may be
idiopathic epilepsy, unless seizures are not
given IV, SC,or rectally, resulting in a
well controlled and inte1ictal spikes are
therapeutic blood level that will persist for
present.

9 hr. Oral anticonvulsants should be resumed

An electromyogram (EMG) is a recording
as soon as possible if cun-ently being given.

of the electrical activity of muscles and is

Recommended maintenance anticonvulused to evaluate the health of the motor sat1t therapy in clogs and cats is phenobarbiunit. The motor unit consists of the LMN, tal at 2-4 mg/kg, PO, bid, as needed to control
the nerve root, the peripheral nerve, the
seizures or to maintain senun levels at 15-40
neuromuscular junction, and skeletal
mcg/mL. Dogs can be treated with potassium
muscle. The peripheral nerve can be
bromide (KBr ), 22-44 mg/kg given with food
stimulated, and motor and sensory nerve
until the semm level is 1,500-3,000 mcg/mL.

conduction velocities calculated and

Because KBr has a long half-life, if stattecl
compared to known normal values to help
at maintanance levels, the steady state
define the neuropathy as an axonopathy or
therapeutic level will not be reached until 3
rnyelinopathy. Repetitive nerve stimulation
mo after initiation of therapy. Phenobarbital
may lead to a reduction of the evoked potenmay become clinically effective in 72 hr, tial in myasthenia gravis. Abnormalities of
whereas KBr may take several weeks. The
late waves (F and H) may be associated with longtenn efficacy of phenobarbital and KBr is disorders of the nerve roots.

about the srune. However, KBr bypasses the

The brain-stem auditory evoked response
liver, so it is prefen-ed in a.L1in1als with liver

(BAER) is a recording of electrical activity
disease. Animals taking phenobarbital often
in the auditory pathway from the inner ear
have increased liver enzymes ru1cl cholesterol
receptors through the brain stem to the
levels but decreased thyroid levels; these
cerebral cortex. The animal may or may not
should be expected at1d often do not require
be awake for this test. No response or a
treatment. KBr has also been linked with
clirninished response is seen in auditory
mega.esophagus and pancreatitis in clogs.

nerve disorders associated with hearing

Because KBr is not commercially available,

NERVOUS SYSTEM INTRODUCTION

1221
it may be prepared by a compmmding
the injury occWTed more thall 72 hr before
phannacist by mixing KBr crystals in water
treatment, ti1e benefit of PEG is questionto give a concentration of 250 mg/mL or by able. For maximal benefit, decompressive
packing the crystals in gelatin capsules. KBr
spinal surgery should be perfom1ed as soon
serum levels are affected by the salt content
as possible, usually witilin 24 hr, when

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of the diet, so ti1e diet should be consistent;
indicated.

the higher ti1e dietary salt content, the faster
the bromide is excreted via the kidneys. KBr

Anti-inflammatory Drugs: For control
has proved more efficacious tiian phenoba.t"

of CNS i.nflallunation in dogs a.i1d cats
bital in dogs witi1 cluster seizures and for
unassociated with a virus or other agent,
seizures that are difficult to control.

preclnisone at 2 mg/kg/day may be given PO.

Phenobarbital alld KBr may be given in

Oral fa.i11otidine at 0.5-1 mglkg, once or
combination. Diazepa.in is not all effective
twice daily; cin1etidine at 5-10 mg/kg, bid;
longtem1 oral allticonvulsallt in dogs because or misoprostol at 3 mcglkg, bid, is given to of its short half-life; however, a compounding
prevent GI initation. If GI ulcers develop
pham1acist Call prepa.i·e rectal suppositories
alld melena is detected, sucralfate (500 mg
containing diazepa.in 0.5-2 mg/kg for home
for cats a.i1d dogs <20 kg; 1 g for dogs >20
use in dogs with cluster seizures, or ti1e
kg), PO, tid-qid, is given 2 hr apart from
injectable fom1 Call be given rectally at
other drugs. NSAIDs should never be given

1 mg/kg to prevent trips to emergency clinics.

in conjunction with steroids, because GI

The tertiary allticonvulsallts, levetiracitam
ulceration is common. The dosages of all
alld zonisamide, are gaining greater favor.

steroids given should be slowly tapered;

Zonisamide especially has shown good
abrupt withdrawal should be avoided.

efficacy in controlling seizures in those

Prednisone Call be used as longtem1
anin1als with a poor response to phenoba.i·bimaintenallce therapy on alternate days to tal alld KBr.

avoid complete suppression of adrenal

KBr may cause asthma in cats, so its use in function. Oti1er chemotherapeutics used for cats is no longer recommended. Diazepall1
infla.i11matory CNS disease such as MUE a.i·e
at 0.5-1 mg/kg, PO, bid, may be used in cats
cyta.t·abine (50 mg/m2, SC, bid for 2 days,
with tmcontrolled seizures because of its
then repeated at3-4 wk intervals),
longer half-life in cats; however, in one
mycophenolate (10 mg/kg, PO, bid),
report diazepam was associated with fatal
alld cyclosporine (5 mg/kg, PO, bid).

hepatic necrosis in cats alld thus warrallts
close monitoring tiu·oughout ti1e first few

Antiedema Drugs: After cra.tlial surgery
weeks of ti1erapy. Phenobarbital is the
alld in a.tlinlals with brain tumors or head
allticonvulsallt of choice in cats; if seizures
injuries that cause a declining neurologic
are not well controlled, then levetiracita.t11 is
status, 20%ma.t1Jlitol, 0.5-1 glkg, may be
added. Acupuncture may be useful to
given slowly IV. Ma.tmitol is not given in
control seizures in all species.

spinal cord injuries. Use of methylprednisolone sodium succinate as described above Acute Spinal Cord Injury: Acute spinal
for acute spinal cord injury is no longer
cord injury from trauma, intervertebral disc
recommended for head injuries in people,
herniation, or fibrocartilaginous embolizaalld its use in the vete1inary field is tion resulting in paraplegia must be treated
declining. For palliative treatment of brain
aggressively in dogs to ensure the best
tumors, oral prednisone may be used.

challce for recovery. If the dog is seen within
the first 8 hr after injury, methylprednisolone

Muscle Relaxants: Diazepa.tn at 0.5
sodiun1 succinate or prednisolone sodium
mg/kg or methocarba.tnol at 40 mg/kg,
succinate is given at 30 mg/kg, IV, followed

PO, tid-qid, relieves muscle spasms from
by 15 mg/kg in 2 alld 6 hr, or a consta.tlt IV
intervertebral disc protrusion alld other
infusion to give a total dose of 60 mg/kg.

sources of nerve root initation.

Steroid use is not advised if it has been
longer thall 8 hr since the trauma occtuTed,

Antimicrobial Therapy: Refer to
because there may be more deleterious
discussions of specific infections for
effects tha.t1 beneficial ones. Dexall1ethasone alltimicrobial therapy reconm1endations.

is not used. Oral fa.inotidine at 0.5-1 mg/kg,
once or twice daily; cimetidine at 5-10 mg/

Nursing Care: Animals with paraplegia
kg, bid; or misoprostol at 3 mcglkg, bid, Call
alld quadriplegia need intensive nursing
be used to protect the GI tract. Polyethylene
care. The allimal should be maintained on
glycol (PEG) 309'osolution may be given IV at
padding alld turned every 4-6 hr to avoid

2.2 mIJkg, then repeated in 24 hr. PEG is a
decubital ulcers. The bladder must be
newer treatment that appears promising. If
expressed or catheterized every 6-8 hr.

1222

NERVOUS SYSTEM INTRODUCTION

In paraplegic animals, diazepam may be
feces to prevent dennatitis. Quadriplegic
given to facilitate relaxation of the urinary
animals may need to be hand fed nutritious
sphincter, making manual expression of
food and given plenty of water. Manual
the bladder easier. Urine must be moniextension and flexion of joints and muscle tored for evidence of cystitis. The skin
massage will help delay contractures and

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must be kept clean and free of urine and
muscle atrophy in paralyzed limbs.

CONGENITAL AND INHERITED

ANOMALIES OF THE NERVOUS SYSTEM

Congenital defects of the CNS are, by
limb. (See also DISEASES OF THE SPINAL COLUMN
definition, present at birth. Some congenital

AND CORD, p 1245.) Neuromuscular disorders
defects may be inherited, others may be
include diseases of the peripheral nerves,
caused by environmental factors ( eg, toxic
neuromuscular junction, or muscles.

plants, nutritional deficiencies, viral

Disorders of these systems can result in
infections); for many, the cause is unknown.

signs of weakness and ataxia sinillar to

In those animals born with a well-developed those seen in spinal cord disease. In nervous system (foals, calves, lambs, pigs),
addition, they often cause disturbance of
the clinical signs of a congenital neurologic
reflex function, pain sensation, or marked
disorder may be recognizable at birth.

muscle atrophy. In some cases, these

Kittens and puppies are born with a less
deficits are markedly episodic. Multifocal
well-developed nervous system, and in
disorders result in combinations of signs
those species, neurologic signs may not be
from more than one of these categories of
apparent until they begin to walk. In some
neurologic deficits.

inherited neurologic diseases, clinical signs
of the disorder are not seen until the animal
is an adult ( eg, caudal fossa malforn1ation

CEREBRAL DISORDERS
syndrome/syringomyelia, neuronal ceroid
lipofuscinosis), even though the defect has

Large Animals
obviously been present since birth.

Anencephaly means that the brain is

Congenital lesions can be categorized
largely absent at birth. It is a rare disorder
according to the primary region of the CNS
but is seen sporadically in calves; the cause
affected. Forebrain disorders (cerebrun1
is unknown. Because the pituitary gland
and thalamus) prin1arily result in clinical
may also be absent, prolonged gestation
signs such as visual disturbances, changes

(seep 1377) of affected calves can occur.

in mental status or behavior, abnonnal

Signs include profound lethargy, head
movements or postures, and seizures.

pressing, and blindness with norn1al

Cerebellar disorders usually result in an
pupillary reflexes. Cerebral.aplasia in calves
intention tremor, widebased stance, and
is usually associated with complete absence
incoordination (dysmetria) of the head,
of both cerebral hemispheres, and CSF may
trunk, and limbs. Brain stem disorders
leak out of a small opening on the midline
may result in cranial nerve dysfunction,
between the frontal bones.

postural disturbances, or vestibular

Exencephaly means that the brain is
dysfunction. In some cases, brain stem
exposed through a large defect in the skull
disorders may also result in weakness and

(craniwn bifida). The brain (encephaproprioceptive gait disturbances, with more locele), meninges (meningocele), or both
severely affected animals exhibiting

( meningoencephalocele) may protrude
impaired consciousness. Spinal cord
through this opening. Encephalocele and
disorders do not affect cerebral function
rneningocele are seen in many species and
or coordination of head movement but
are known to be inherited in pigs. Defects
may produce weakness, motor dysfunction,
may be closed or open in terms of communior proprioceptive deficits of the limbs, cation with the environment through skin
including either dysmetria or reduced
defects. Too little information exists to
proprioceptive placing in more than one
reliably predict outcome and resolution of

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1223
any deficits. Good surgical outcomes have
cephaly, but in hydrocephalus the ventricles
been achieved in rare case reports of closed
retain a complete ependyn1al lining. Clinical
meningoencephaloceles; however, safety
signs can vary from mild to severe and
and quality-of-life issues must be considinclude seizures, lethargy, or other forebra.in ered, as with any ataxic, seizming, or
abnom1alities. There may be extensive

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mentally inappropriate large anin1al. When
expansion of the lateral ventricles in the
the defects openly communicate externally,
frontal lobes. Hydrocephalus is seen

CNS infection should be presumed U11Jess
sporadically in all large a.ninlals, although
proved otherwise.

it is relatively conunon in calves, in which

In hydranencephaly, there is a marked
inheritance and vitamin A deficiency have
loss of cerebral cortical tissue (primarily the been implicated.

neocortex) within a cranial vault of nonnal

Cyclopia is characterized by a single
confonnation. The resultant cavity
orbital fossa. One cause in lambs is
communicates with the ventricular system,
ingestion by the gestating dam of plant
has an incomplete ependyrnal cell lining,
alkaloids from Veratrum californicum.

and is filled with CSF. Clinical signs may

This ma.lfom1ation also is seen in pigs.

include lethargy, propulsive circling, head

Idiopathic or familial epilepsy has been
pressing, and blindness. Hyclranencephaly
described in many species. Benign epilepsy
develops as a result of the destruction of
is seen in yoU11g foals, particularly Arabians,
developing neural tissues and is sometimes
up to 12 mo of age. The foal may present for
accompanied by cerebellar hypoplasia and
seizures, head injuries, or postictal blindness.

a.rthrogryposis. Hydranencephaly is seen

Foals usually recover spontaneously within
sporadically or as an epidemic in calves,
a few months, but anticonvulsa.nt therapy
lambs, and less commonly in piglets. Known (phenobarbital, 100--500 mg, PO, bid, for a causes include infection in utero with a

50-kg foal) is probably advisable for 1--3 mo,
nU111ber of viruses, including Aka.bane virus
followed by withdrawal over 2 wk. Epilepsy

( see p 620) in ruminants in Australia, Japan, beginning by 1 yr of age has been recorded
and Israel; bluetongue virus (seep 738) in
in Brown Swiss and Swedish Reel cattle.

sheep and cattle in North America; Rift Valley

Seizures are also seen in yoU11g Aberdeen
fever virus (seep 768) and the virus of

Angus calves; if these calves survive, tlley

Wesselsbron disease (seep 775) in sheep and show cerebellar signs but become clinically
cattie in Africa; the Cache Valley virus in
nonnal by 2 yr of age.

sheep in the USA; and the Chuzan virus in

Metabolic disorders and lysosomal
calves in Japan. Rarely, bovine viral diarrhea
storage disorders often cause signs of

(seep 1436) and border disease virus ( see fore brain dysfU11ction, along with other
p 622) produce hydranencephaly in lambs
neurologic deficits, and a.re discussed
and calves. Hydranencephaly and porencephfurther U11der multifocal disorders (see aly ( cystic cavities in the cerebrum) are seen
p 1234). Cerebral signs seem to be most
sometimes in lambs with in utero copper
prominent in citrullinemia.

deficiency (swayback). It also is seen in a

Citrullinemia. is a fatal hereditary
syndrome of prolonged gestation in sheep in
metabolic defect ofHolstein-Friesian calves

Scotland ( cause unknown).

(ma.inly in Australia. and New Zealand)

Hydrocephalus, an increase in volU111e of
associated with cerebral cortical edema.

the CSF, can appear similar to hydranen-

It is due to increased citrulline in plasma,
caused by deficiency of the urea cycle
enzyn1e argininosuccina.te synthetase.

Affected calves appear healthy at birth but
die of a.cute neurologic disease in 1-4 days.

Signs a.re sudden in onset and consist of
depression, aimless wandering, blindness,
seizures, opisthotonos, and recU111bency.

Narcolepsy, a disorder of sleep-wake
control (typically characterized by
excessive sleepiness or sudden paroxysmal
attacks of flaccid paralysis with conservation of consciousness), has been repo1ted in several equine breeds, particularly Shetland
ponies. The aninlal is otherwise healthy.

During narcoleptic episodes, rapid eye

Protrusion of tissue on the forehead of a foal
movements occur, and at the same time, the
with meningoencephalocele. CourtesyofDr.

anin1al may also show cataplexy or sudden

Rebecca Packer and Or. Paige Jackson, Purdue University.

loss of muscle tone with collapse.

1224

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

Small Animals
appear stunted and weak from birth and
begin seizuring at 4-5 wk of age. The disease

The same strnctural anomalies of the brain
is fatal. A genetic test is available for
as described for large animals (seep 1222)

diagnosis of this disease in Standard
a.re also found in small animals.

Poodles.

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Hydranencephaly has been described

Polymicrogyria. is an inherited disease
mainly in kittens after in utero exposure to
identified in Standard Poodles that results
feline panleukopenia virus/panrovirus (see
in focal areas of the brain having smaller
p 796). Brain stem malformations and
and more gyri than nonnal, resulting in
cerebellar hypoplasia may be seen
disrnption of function. The most common
concomitantly.

clinical signs are visual disturbances, but

Hydrocephalus is most common in
ataxia, behavioral problems, and hydrodogs, particularly in toy and brachycecephalus can also be seen. Clinical signs phalic breeds. It can be classified as
are attributable to the po1tion of tl1e brain
communicating (nonobstructive), in
affected by the abnormal gyri.

which CSF can flow freely into the

Idiopathic epilepsy may be inherited
subarachnoid space, or noncommunicatin certain breeds, including Beagles, ing (obstructive). Known causes of

Keeshonden, Irish Setters, Belgian
noncommunicating hydrocephalus include Tervurens, Siberian Huskies, Springer atresia of the mesencephalic aqueduct,

Spaniels, Labrador Retrievers, Golden
perinatal encephalitis, or adhesions

Retrievers, and German Shepherds. A
caused by intraventricular hemorrhage at
specific type of seizure known as temporal
bi1th. Clinical signs of hydrocephalus
lobe epilepsy appears to be familial in
usually indicate cerebral dysfunction and

Cavalier King Charles Spaniels and is
often progress, although some animals
characterized by behavioral manifestamay remain asymptomatic. The fontations such as "fly biting." The diagnosis of nelles are often patent, and affected
idiopathic epilepsy depends on eliminatanimals may have ventrolateral strabising other ca.uses of seizures, particularly mus. Blindness due to polymicrogyria
structural brain a.bnormali ties ( such

( excessive number of smaller gyri) and
as hydrocephalus or juvenile twnors),
asymmetric dilatations of the lateral
encephalitis,or metabolic causes(such
ventricles have been described in
as hepatic encephalopathy).

Standard Poodles. Hydrocephalus has

Hepatic encephalopathy is usually
been observed in Sa.int Berna.rd puppies
ca.used by a congenital portosystemic shunt.

in association with a.pha.kia. (absence of

The shunt may be a single large vessel, or
the lens) and multiple ocular defects.

there may be microscopic shunting of blood

Imaging by ultrasonogra.phy (through the
within the liver. Breeds often affected
fontanelle), CT, or MRI can provide the
include Mi.nia.tw·e Schnauzers, Yorkshire
diagnosis, and CSF analysis should

Terriers, Cairn Terriers, Australian Cattle
identify encephalitis. Treatment relies on

Dogs, Old English Sheepdogs, and Maltese
omepra.zole to reduce CSF production or,

Terriers. The clinical signs are usually
if necessary, corticosteroids, or sw,gery to
noticed before 6 mo of age and p1imarily
shunt CSF into the peritoneum.

reflect cerebral dysfunction, including

Lissencephaly, an absence or reduction
staring into space, inappropriate vocalizing,
of cerebral gyri, is a rare disorder seen in
aggression, and agitation. Advanced

Lhasa Apsos. It is also seen in association
neurologic alterations can ca.use depreswith cerebellar hypoplasia. in Irish Setters, sion, blindness, myoclonus, stupor, coma,

Wirehaired Fox Teniers, and Sa.moyeds and
or seizures. In ca.ts, these signs a.re often
in Kora.t cats with microencephaly. Clinical
accompanied by excessive salivation. A
signs consist of mild behavioral abnormalirare ca.use of hepatic encephalopathy is a ties and seizures.

deficiency of hepatic urea cycle enzymes.

Pug encephalitis is an ultimately fatal

Pre- and postprandial bile acid tests may
disease that may have a familial basis.

support the clia.gnosis. Definitive diagnosis

Affected Pugs show behavioral changes,
may be facilitated by use of radiographic
seizures, and CSF pleocytosis. A similar
imaging techniques, such as positive
nonsuppura.tive, necrotizing encephalitis
contrast portogra.phy, CT, transcolonic
has been reported in several other toy
portal scintigra.phy, or diagnostic gray-scale
breed dogs, including Yorkshire Terriers,
ultrasonogra.phy. Blood tests such as the

Chihuahuas, and Maltese Terriers.

ammonia tolerance test (seep 436) should

Neonatal encephalopathy is an
be used with caution in cases of suspected
inherited genetic disorder tl1a.t has been
hepatic encephalopathy because of 1isk of
described in Standard Poodles. Poodles
ca.using an encephalopa.thic c1isis. Resting

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1225
ammonia levels can be performed; however, cephaly and arthrogryposis may accompany ammonia levels have been poorly correlated the cerebellar disease. The pathologic with both the diagnosis and presence of
features include clestrnction or loss of one
clinical signs.

or more layers of the cerebellar cortex,

Lysosomal storage disorders that
particularly the granule and Purkinje cell

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commonly cause cerebral signs include
layers. Prophylactic vaccination of the dam
ceroid lipofuscinosis and fucosidosis,
before breeding can prevent the problem. A
although there are many other fonns of lysohereditary cerebellar hypoplasia/dysplasia somal storage disorders as well as other
is seen in Hereford, Shorthorn, Ayrshire,
inborn errors of metabolism (seep 1234).

and Angus calves. Cerebellar hypoplasia is

Genetic and enzymatic testing is available
present at birth and is nonprogressive, in
for some of these disorders. When specific
distinction to the abiotrophies.

tests are not available, organic acid screens

Cerebellar abiotrophies have been
may support the general diagnosis of
reported in many species. In abiotrophies,
metabolic error.

the cerebellar development proceeds

Puppy hypoglycemia is an idiopathic
normally, and the animal remains w1afsyndrome in toy breeds of dogs that is seen fectecl for a period of months or even years
in the first 6 mo of life. It seems to relate to
before cerebellar neurons begin to die off
a relative inm1aturity of the liver, which
prematurely. This is in contrast to the
affects glycogenolysis and can usually be
cerebellar hypoplasias, in which developing
managed by providing frequent meals of
cerebellar germinal cells and neurons are
a commercial puppy diet. The problem
destroyed in utero. In Aberdeen-Angus
usually resolves as the puppy matures.

calves, clinical signs of abiotrophy start

Narcolepsy or cataplexy is inhelited in
early and are accompanied initially by

Doberman Pinschers, Labrador Retrievers,
seizures. In Arabian foals and Swedish
and Dachshunds and has been desclibed in

Gottland ponies, the onset of signs is from
additional canine breeds. It is rare in cats.

birth to 9 mo; in Yorkshire and Large White

Attacks are often stimulated by excitement.

piglets, 1-3 mo; in Holstein calves, 3-8 mo;

It must be differentiated from valious types
and in Merino sheep, 3-6 yr. Most abiotroof syncope. Physostigmine (0.025-0.1
phies a.re probably inl1erited ( eg, recessive
mg/kg, IV) potentiates the frequency and
inheritance for affected Hereford cattle and
sevelity of cataleptic attacks. Imipramine

Welsh Motmtain and C01Tieclale sheep), but

(0.5-1 mg/kg, PO, tic!) can be used to control toxic causes should also be considered. The the sevelity of the cataplexy.

latter include locoweed, methylmercury,
and exposme to organophosphates in utero

(seep 3064). Use of trichlorfon cl ming

CEREBELLAR DISORDERS
pregnancy can cause a congenital tremor in

Large Animals
piglets due to both cerebellar hypoplasia
and hypomyelination.

Arnold-Chiari malformation is a

Hypomyelinogenesis congenita, in
complex malforn1ation of the caudal brain
which myelination is delayed throughout
stem and cerebellun1 and typically consists
the CNS, can resemble cerebellar disease
of herniation of cerebellar tissue through
due to the severe head and body tremor
the fora.men magnum into the cervical
that usually develops. In contrast to pme
spinal canal. It may be associated with spina cerebellar disease, a persistent fine tremor bifida, hydrocephalus, or meningomyeat rest is usually present as well as a marked locele. It is rare in domestic animals, and
intention tremor. Newborn lambs, piglets,
the cause is unknown. (A more co!lUllon
and occasionally calves are affected. The
variation of this disease is recognized in
condition can be associated with in utero
dogs and appears to be inherited, but this
infection by viruses such as the virus of
has not yet been proved.) In calves, it may

Border disease (seep 622) or swine fever
be seen with bilateral elongation and
virns (seep 713) or exposure to tlichlorfon
extension of the occipital lobes.

(seep 3067). Affected lambs are often called

Cerebellar hypoplasia has been

"hairy shakers." The condition is inherited described in many species. In utero viral
in Sacldleback and Lanclrace pigs and in
infection (bovine viral diarrhea [seep 1436],

Jersey and Shorthorn cattle. Signs are
bluetongue virns [seep 738], and swine
usually nonprogressive or may resolve
fever virus [seep 713]) during miclgestation
completely if myelination has only been
is the most conunon cause. Cerebellar
delayed.

lesions may also be seen with bovine fetuses

Swayback or enzootic ataxia is largely
infected with Aka.bane or Wesselsbron
due to copper deficiency, although there
virnses. Clinical or subclinical hydranen-
may be a familial predisposition. Hypomy-

1226

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM
elinogenesis can occur in utero and cause
available for this disease in the Coton de
obtundation, blindness/deafness, falling or

Tulear.

lying prostrate, and head tremor in lambs.

Congenital hypomyelination is seen

The condition can be prevented by treating
as a familial/inherited disorder in Sp1inger
affected ewes in pregnancy. Kids, piglets,

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Spaniels, Chow Chows, Weinlaraners, and
and perhaps calves may also be affected.

Bernese Mountain Dogs, usually with signs
developing around 2-8 wk of age. In the
latter three breeds, it is often tern1ed

Sm IIA.nlm Is
dysmyelination because the clinical signs

Cerebellar hypoplasia is seen in kittens
of whole body tremor usually resolve
after in utero infection with feline panleukospontaneously with tinle. The disorder is penia virus (seep 796). The condition is
rare in cats. The diagnosis can be c011.finned
nonprogressive, and affected cats may
using MRI. (See also DEMYEUNATING DISORDEllS, make suitable pets. Diagnosis can be
p 1236.)

obtained antemortem using MRI. Concomi

Caudal occipital malformation
tant hydrocephalus or hydranencephaly
syndrome and subsequent syringomyelia
may also be seen. Cerebellar hypoplasia has
has been conunonly reported in Cavalier
also been reported in Chow Chows and is

King Charles Spaniels and less commonly in
seen in association with lissencephaly in
other small breed dogs. The malforn1ation is

Irish Setters and Wirehaired Fox Terriers.

comparable to the Chiari type I malforma

A selective hypoplasia of the cerebellar
tion described in people and includes a
vermis is also seen in dogs, and when
congenital malfornrntion of the occipital
combined with hydrocephalus and cystbone, resulting in a crowded caudal fossa like dilatation of the fourth ventricle, the
and cerebellar herniation at the foramen
condition has been termed the Dandymagnum. The subsequent disruption of CSF

Walker syndrome, which may have a
flow results in fonnation of syringomyelia.

familial basis. The cerebellar vermis may

A large proportion of asyn1ptomatic
be partially or completely absent. Clinical

Cavalier King Charles Spaniels have the
signs are typical of a cerebellar disorder
caudal fossa malformation. Although the
and include tremors, ataxia, and hypermemalfo1mation is present at birth, clinical tria. Occasionally signs of head tilt and
signs often do not appear until later in life.

circling may also be present. Toy Fox

Clinical signs vary but conm1only include

Terrier dogs are predisposed to the
paresthesias ( eg, face rubbing, phantom

Dandy-Walker form.

scratching of the back of the head), ataxia,

Cerebellar abiotrophies have been
and weakness from syringomyelia. Medical
described in a number of breeds of dogs.

management is often not curative but can

In Samoyeds and Beagles, the signs are
be attempted with gabapentin (1 0 mg/kg,
apparent at the onset of ambulation; in

PO, tid) for paresthesias, omeprazole

Australian Kelpies, Rough-coated Collies,

(0. 7 mg/kg/day, PO) for reduction of CSF
and Kerry Blue Terriers, the clinical signs
production, and analgesics for pain
are seen in puppies from 4-16 wit of age; in
management. Surgical decompression via

Brittany Spaniels, Old English Sheepdogs,
caudal occipital craniectomy is preferred as
and Gordon Setters, the signs appear in
definitive treatment; however, recurrence
young or mature adults. Clinical signs
rates of25o/o-47%have been repo1ted.

include progressive cerebellar ataxia,
intention tremor, hypennetria, and possible

BRAIN STEM DISORDERS
loss of menace response due to cerebellar
involvement. Postural reactions remain

Small Animals
norn1al as with any pure cerebellar disease;

Congenital vestibular disease has been
however, affected animals may be
reported in German Shepherds, English
incoordinated when placing paws. Clinical

Cocker Spaniels, Doberman Pinschers, and
signs can be differentiated from cerebellar

Sian1ese and Bum1ese cats. Signs are
hypoplasia, above, by the onset. Hypoplasia
bilateral and may be accompanied by
is present since birth (apparent at time of
deafness. This is likely a peripheral
ambulation) and nonprogressive, whereas
syndrome affecting the vestibular apparaanin1als with abiotrophies are born nonnal tus, and labyrinthitis has been identified
and progress after onset.

histologically in some pups. The disorder

Bandera syndrome is seen in Coton de
appears inherited. There is no treatment.

Tulear dogs and manifests as a cerebellar

Deafness is permanent, although the clinical
ataxia from the tinle of birth. The cerebelsigns of vestibular dysfunction may improve lun1 is anatomically normal. A DNA test is
as the animal learns to compensate.

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1227

Canine multiple system degeneration
in all four lin1bs, and progressive pa.raparehas been identified in Kerry Blue Terriers sis; 3) norn1al spinal reflexes and cranial
and Chinese Crested dogs. Clinical signs
nerve function and absence of dramatic
reflect both cerebellar and brain stem
muscle atrophy; and 4) a familial relation

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dysfunction, including ataxia, dysmetria,
ship. The disease was initially described as
and festination. The disorder is inherited as

"weaver" because of the peculiar weaving
an autosomal recessive mutation. There is
gait. The histopathologic changes are
no treatment.

pri.maiily in the sensory ne,vous system, in
contrast to those of spinal muscular atrophy

SPINAL CORD DISORDERS

( see above). Spinal dysmyelination causes
congenital lateral recwnbency and

See also
opisthotonos, but spinal reflexes and

DISEASES OF THE SPINAL COLUMN AND
alertness are normal.

CORD, p 1245.

Sinlmental encephalomyelopathy,

Large Animals
which is seen in association with behavioral
change (eg, aggression or dullness), has ai1

Spinal muscular atrophy is an inherited
onset in Simmental and Simrnental-cross
disorder of Brown Swiss calves. The first
calves at 5--12 mo of age. The gait abnormalclinical sign of spinal muscular atrophy is ity progresses from pelvic limb ataxia to
weakness of the pelvic limbs at 2-6 wk of
recwnbency with opisthotonos, and death
age; calves (most are female) have difficulty
occurs within 6 mo. It has been reported in
getting up and then become recw11bcnt. The
the USA, UK, Australia, and New Zealand.

characteristic sign is severe muscle atrophy,

Characteristic lesions consist of SY1runetric
especially of the pelvic limbs. Histopathonecrosis in the caudate nuclei and in other logic exan1ination reveals degeneration and
areas of the brain and spinal cord. SirniJai·
loss of motor neurons in the ventral horns
multifocal lesions ai·e seen in 1- to 4-mo-old
of the spinal cord. Neurogenic atrophy of

Li.mousin and Limousin-cross calves (with
muscles is a consistent lesion. A sin1ilar
additional signs of blindness) in Australia
disorder is seen in red Danish calves of
and England and in Angus calves in

American Brown Swiss lines. It is possible

Australia and the USA
that spinal muscular atrophy and bovine

Progressive myelopathy of Murray
progressive degenerative myeloencepha

Grey cattle in Australia is inherited
lopathy (BPDME) are in some way related

( autosornal recessive), and calves usually
because they can be seen in the same blood
show spastic paraparesis and ataxia at birth.

lines, but the onset of BDPME occurs after

Neuronal degeneration is widespread in the

5 mo of age, and it causes ataxia and
brain and spinal cord; primary dernyelinadysrnetria rather than weakness and mustion also develops in the cord.

cle atrophy. A motor neuron disease with

Progressive ataxia of Charolais cattle
neurofilament accumulation is seen in
has been reported in the UK and North
horned Hereford cattle in Canada with

America. It causes clinical signs that are
signs appearing soon after birth that are
first noticed between 6 and 36 mo of age and
characterized by general tremors,
progress throughout 1-2 yr from slight
incoordination, difficulty standing, and
ataxia involving all four limbs to recun1-
hyperesthesia to tactile stin1ulation. A
bency. Female cattle typically rnailifest a
suspected hereditary lower motor neuron
rhythmic pulsatile pattern of wination.

disease with accwnulation of neurofila

Histologic lesions consist of eosinophilic
rnents also is seen in Yorkshire pigs around
plaques and rnyelin breakdown in the white

5 wk of age, characterized by pelvic limb
matter of the cerebellum and spinal cord.

paresis progressing to recun1bency. There

Neuraxonal dystrophy (NAD) appears
is degeneration and loss of motor new·ons
to be inherited in sheep and causes an
throughout the spinal cord and brain stern.

unsteady, stiff, and swaying gait that

A similar condition is seen in young
progresses to paraparesis and finally

Hampshire pigs.

tetraparesis. Suffolk and New Zealand

Bovine progressive degenerative

Coopworth sheep are affected as Jan1bs 1-6
myeloencephalopathy (BPDME, weaver
mo old; Romney sheep are affected at 6-18
syndrome) is a neurodegenerative disorder mo of age. Merinos develop a very sin1ilai·
of Brown Swiss cattle that is seen in the
disease at 1-4 yr of age. NAD has also been

USA, Canada, and Europe. Four basic
seen in 4- to 7-mo-old Merino Jambs. Axonal
criteria a.re required to establish a clinical
swellings (spheroids) ai·e typically found in
diagnosis: 1) onset of bilateral pelvic limb
gray matter of brain stern and spinal cord,
ataxia and dysmetria at 5-8 mo of age; 2)

although in the older Merino sheep, axonal
deficient proprioceptive responses, ataxia
spheroids mainly develop in large white

1228

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM
matter tracts of the CNS. NAD of Morgan
ment, with 46% regaining athletic function.

horses affecting the lateral (accessory)

Early treatment appears to be associated
cuneate nucleus usually develops at 6---12
with improved surgical outcome.

mo of age and causes spastic paraparesis

Occipitoatlantoaxial malformation is

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and pelvic limb ataxia. It is presumed to be
an inherited disorder (autosomal recessive)

inherited. NAD affecting several brain-stem
in Arabian foals and may also be seen in
nuclei and causing mild pelvic limb ataxia

Miniature horse foals, Holstein calves, and
has also been reported in 4-mo-old
lambs. Clinical signs are progressive ataxia,

Hafflinger horses in Gem1any.

tetraparesis, and an extended neck posture.

Equine degenerative encephalomy

Affected foals are usually tetrapa.retic at
elopathy has been mainly associated with
birth, although neurologic deficits may not
vitamin E deficiency, but it may have a famildevelop for several years. Diagnosis is by ial basis in Appaloosa horses and other
radiography. Laminectomy has been
breeds, based on occurrence of clusters of
reported to be successful in some cases.

cases. Degeneration of the spinocerebella.r

Spina bifida is seen in most species and
tracts results in a slowly progressive,
usually results in dysfunction of the tail and
symmetric ataxia and paresis of all four
anus, incontinence, and sometin1es pelvic
limbs that starts as early as 7 mo of age.

liinb weakness (seep 1230).

(See also DEGENERATIVE DISEASES OF'TIIE SPINAL

COLUMN AND COllD, p 1245.)

Pi-ogressive paresis in Angora goats

Small Animals
has been repo1ted in Australia and may have Spinal muscular atrophy is an inherited a heritable basis. Clinical signs of spastic
lower motor neuron (LMN) disorder in
paresis and ataxia appear from biith to 4 mo

Brittany Spaniels that can have an early (by
of age and progress to recumbency within a
l mo), intem1ediate (by 4-6 mo), or delayed
few weeks. Widespread (multisystem)

(> 1 yr old) onset. Rottweilers can also
neuronal degeneration is seen at necropsy.

develop an early fom1 of spinal muscular

Generalized glycogenosis in Shorthorn
atrophy that is referred to as a motor neu

(type ll) and Bral1man (type lib) cattle and
ron disease. Swedish Lapland puppies are
in Co1Tiedale sheep (resembling type II) is a
affected at 5-7 wk of age, Stockard parallysosomal storage disease that causes ill ysis (seen in Great Danes crossed with
th1ift, respiratory signs, paraparesis, ataxia,

Bloodhounds or Saint Bernards) has an
and muscle weakness at 3--9 mo of age.

onset at 11-14 wk, and English Pointers are

Cervical stenotic myelopathy
affected when -5 mo old. LMN disease also

(wobbler syndrome) is a compressive
is seen in puppies of other breeds, including
cervical spinal cord syndrome caused by

Dobem1an Pinschers and Briquet Griffon
ve1tebral canal stenosis, articular process

Vendeens; a focal form involving the
osteophyte proliferation, and vertebral body thoracic Jim b( s) is seen in German tipping that occurs in young, rapidly

Shepherds. Paraparesis or tetraparesis with
growing horses. Thoroughbreds, Tennessee
neurogenic muscle atrophy are the main

Walking Horses, and Warmbloods appear to
clinical features. The severe, generalized
be predisposed, with males being more

LMN disease in spinal muscular atrophy
commonly affected than females. Ovemutriclosely resembles the signs of a peripheral tion is an in1portant contributory factor, and
neuropathy. Loss of motor neurons in the
the clinical signs often can be reversed in
spinal cord is the most striking feature on
horses <9 mo old by reducing caloric intake
necropsy. There is no treatment.

and restricting exercise. Clinical signs

Demyelination of Miniature Poodles
typically become apparent from <6 mo up to is preswned to be an inherited disorder 4 yr of age and include cervical myelopathy,
involving primaiily the spinal cord. This rare
with the pelvic limbs usually affected more
condition causes paraparesis at 2--4 mo of
severely. Imaging ( eg, survey radiography,
age that rapidly progresses to tetraplegia.

myelography, CT, MRI) can be used to

There is no treatment.

identify stenotic or proliferative lesions,

Ataxia of Parson Russell and
causing spinal cord compression in the

Smooth-haired Fox Terriers can be
midcervical spine. Treatment usually
confusing, because several fom1s of disease
requires surgical decompression of the
exist. In general, the diseases affecting
spinal cord and, in some cases, ve1tebral
these breeds are a spinocerebellar ataxia.

stabilization. Interbody fusion with titaniwn The predominant clmical signs ai·e baskets ("Seattle Slew" implants) has
cerebellar ( cerebellar ataxia, intention
shown more success; however, the
tremor, hypennetria), but histopathologiprognosis remaiI1s guarded. In one study, cally at necropsy, spinal cord demyelination

77% of horses showed neurologic improve-
can be seen. Clinical signs begin to appear

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1229
at-2-6 mo of age. In one form of the

Degenerative myelopathy is a painless,
disease, seizures and myokymia (in which
slowly progressive myelopathy that occurs
the muscles appear to show verminous
commonly in dogs. Clinical signs are
movement) can occur. The disease is
typically consistent with a thoracolumbar

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progressive, although in some cases signs
spinal cord localization with pelvic lin1b
may stabilize but not regress, and some
paresis and ataxia, although progression
affected anin1als are able to live a relatively
may eventually involve the thoracic limbs.

normal life, despite the abnonnal move

Histopathologic changes include a
ments.

noninflammatory axonopathy and myelinop

Afghan Hound myelopathy is an
athy. Gennan Shepherds, Pembroke Welsh
inhe1ited disorder that causes both

Corgis, Boxers, Rhodesian Ridgebacks, and
demyelination and necrosis of the spinal

Chesapeake Bay Retrievers are predisposed.

cord. Paraparesis develops some time

There is no treatment. Physical therapy
during the first year of life and progresses to
slows the progression of clinical signs.

paraplegia within I wk. The thoracic limbs

A mutation has been identified that is
become involved over the next 1-2 wk. A
associated with increased risk of developing
similar condition is seen in young Kooiker
degenerative myelopathy, and a genetic test
dogs (Dutch Decoy dogs) of either sex, with
is available to identify those dogs at higher
signs beginning at 3-12 mo of age. Prognosis risk of developing the disease.

is poor in both breeds.

Progressive axonopathy of Boxer dogs

Neuraxonal dystrophy is described
is an autosomal recessive disorder that
in both cats and dogs but primarily in
causes patellar hyporeflexia, severe

Rottweiler dogs ( autosomal recessive
dysmetria, loss of paw position sense, and
inheritance). In Rottweilers, onset is
spastic paresis at 1-7 mo of age. Axonal
between 3-24 mo of age, and the disorder
spheroids are widespread in both the central
progresses slowly over several years.

and peripheral nervous system on necropsy.

Signs include cerebellar dysfunction and

Although this conclition causes loss of the
dysmetria in all four limbs, but with
patellar reflex, in general, tl1e signs are more
preservation of paw position sense, which
suggestive of spinal cord disease than of a
should distinguish it from leukoencephaloperipheral neuropathy. There is no treatmyelopathy (see below) and from advanced ment, but affected dogs can live relatively
motor neuron disease in the same breed.

comfortably for a considerable time.

Collie dogs in Australia and New Zealand

Breed-associated aseptic meningitis
develop similar clinical signs at 2-4 mo of

(steroid-responsive meningitis-arteritis) has
age. There is also early onset in Papillons
been reported in Beagles, Bernese Mountain
and Chihualmas and in cats ( autosomal

Dogs, Boxers, German Short-haired
recessive in domestic tricolored cats).

Pointers, and sporadically in other breeds ..

Axonal spheroids, often in specific regions

The main signs are neck pain, pyrexia, and
of the brain and spinal cord, are the
clraniatic pleocytosis in the CSF in young
characteristic pathologic finding of these
dogs. Prognosis is guarded to favorable,
conditions.

especially in dogs with acute disease that

Leukoencephalomyelopathy of
are treated promptly using immunosuppres

Rottweilers has a later onset than
sive closes of corticosteroids.

neuraxonal dystrophy (see above), usually

Congenital vertebral malformations
at -2-3 yr of age. It is possible that the
include hemivertebrae (shortened or
disorders have a sin1ilar basis, because
misshapen vertebrae), block (fused)

anin1als occasionally may show histopathovertebrae, and butterfly vertebrae (having logic features of both conditions. In
a sagittal cleft). Hemivertebrae are most
leukoencephalomyelopathy, there is no
common in screw-tailed dog breeds and are
head tremor, and paw position sense is
inherited in German Shorthaired Pointers.

delayed. Bilaterally symmetric areas of

Decompressive surgery can be very
spinal cord clemyelination are the predomisuccessful but sometimes needs to be nant findings on necropsy.

combined with spinal stabilization.

Calcium phosphate deposition in

Multiple cartilaginous exostosis is a

Great Danes causes mineralization of
benign proliferation of cartilage or bone
soft tissues and bone defom1ity, with
that can affect the ribs, long bones, or
dorsal displacement of C7. The resultant
vertebrae and may have a familial basis.

compressive myelopathy is seen in puppies Transitional vertebrae are often clinically 1-2 mo old. This condition is distinct from
associated with l mnbosacral stenosis.

caudal cervical spondylomyelopathy (see

Myelography or specialized in1aging
below).

techniques ( eg, CT, MRI) are usually

1230

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM
required to confirm spinal cord compres

Prognosis may be favorable after surgical
sion in these congenital conditions.

excision, although recurrence is possible.

Treatment consists of surgical removal.

Spinal dysraphism or myelodysplasia

Caudal cervical spondylomyelopathy
includes anomalies of the skin, vertebrae,

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( wobbler syndrome) may have a heritable
and spinal cord that are secondary to faulty
basis in Borzois (5-8 yr) and Basset Hounds
closure of the neural tube. Spinal dysraphism

( <8 mo) and probably also Doberman
is inherited in Wein1araners. Neurologic

Pinschers (<!2 yr) and Great Danes ( <2 yr).

deficits are evident by 4---6 wk of age and

Neurologic deficits range from mild ataxia
include paraparesis and a symmetlic
of the pelvic limbs to tetraplegia. Affected

"bunny-hopping" gait in the pelvic limbs.

dogs often keep their neck flexed ventrally,

There is a bilateral flexor reflex; pinching one
and there may be caudal cervical pain.

paw elicits flexion of both pelvic limbs. There

Spinal radiographs may show malalignment
may be scoliosis or abnormal hair streams on
or remodeling of the vertebrae, narrowing
the dorsal aspect of the neck. Diagnosis is
of one or more disk spaces, or spondylosis
based on clinical signs and imaging
deformans. CT/myelography or MRI usually
techniques such as myelography or MRI.

reveals a marked stenosis at the cranial

There is no treatment, but neurologic deficits
orifice of the mid cervical or caudal cervical
usually do not progress. Similar malfonnavertebrae. Several surgical techniques can tions have been seen in other breeds of dogs
provide stabilization of the vertebrae or
and in calves, foals, and lambs.

decompression of the spinal cord.

Syringomyelia is the development of one

Atlantoaxial subluxation is most
or more fluid-filled cavities within the spinal
commonly seen as a congenital disorder in
cord. Hydromyelia is accunmlation of fluid
young toy or miniature breeds of dogs and
within an enlarged central canal of the spinal
occasionally as a congenital disorder in
cord. It is often difficult to differentiate
several large breeds, including Rottweilers
between syringomyelia and hydromyelia, so
and Dobennan Pinschers. Signs usually
the tenn syringohydromyelia is often used.

develop within the first few years oflife and

Syringohydromyelia causes progressive
consist of an acute or slowly progressive
ataxia and paresis; scoliosis and spinal
onset of neck pain or gait dysfunction,
pain is possible. Causes include trauma,
ranging from ataxia to tetraplegia.

neoplasia, inflammatory conditions, and

Radiographic continuation of diagnosis
developmental malformations. The most
should be followed by stabilization using
common cause in dogs is caudal occipital
ventral fixation. The prognosis is guarded.

malfom1ation syndrome (seep 1226).

Arachnoid diverticuli ( arachnoid cysts,

Spina bifida occulta is a failure of the
arachnoid pseudocysts, meningeal cysts,
neural arch to fuse; if the spinal cord is also
leptomeningeal cysts, subarachnoid cysts)

involved, it is called spina bifida manicause accumulations of CSF and a focal festa. The most likely clinical signs of spina
myelopathy in young dogs. The cause is
bi.fida are LMN signs in the pelvic limbs and
unknown, but some cysts may have a
urinary or fecal incontinence. The prognosis
congenital origin. Signs consist pf progresfor animals with substantial neurologic sive ataxia and weakness. Diagnosis is
deficits is poor. Spina bi.fida can also
made by myelography and/or MRI.

accompany the sacrocaudal dysgenesis
that is inherited as an autosomal dominant
trait in Manx cats.

Pilonidal sinus ( dermoid sinus, dem1oid
cyst) is another consequence of faulty neural
tubulation that appears to be inherited

( autosomal recessive) in Rhodesian

Ridgeback dogs. The sinus is lined by skin
and may communicate with the subarachnoid space, causing possible meningitis or myelitis. Treatment consists of antibiotics
and surgical excision of the sinus.

Epidermoid cysts are rare lesions that
arise from entrapment of epithelial cells
during closure of the neural tube. Myelogra

Cervical spondylomyelo
phy or MRI will reveal an intramedullary
pathy (wobbler
syndrome) in a 6-yr-old Doberman Pinscher.

lesion in a young dog with progressive

Courtesy of Dr. Ronald Green.

neurologic deficits.

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1231

NEUROMUSCULAR DISORDERS
stilted gait. Electromyography is a useful aid
to diagnosis. This disease results from a

See also DISEASES OF THE PERIPHERAL NERVES AND
mutation in a chloride chaimel.

NEUROMUSCULAR JUNCTION, p 1238.

Muscular dystrophy is an inherited
d.isease in Merino sheep. It results in a

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Large Animals
slowly progressive stiffness that affects the

Spastic paresis is seen in many breeds of
lin1bs and neck from 3-4 wk of age onward.

cattle and has been referred to as "contrac

Clinically affected sheep have high resting
tion of the Achilles tendon," "straight hock," and postexercise concentrations of serum and "Elso heel." (See also LAMENESS IN

CK and lactate dehydrogenase.

CATTLE, p 1066.) It can be divided into two

Porcine stress syndrome or maligsyndromes, one that affects calves and one nant hyperthermia (seep 1027) is a
that affects adults. In calves, the condition
hypermetabolic and hypercontractile
appears to be familial and can be seen in
syndrome that, when triggered by anesthemany breeds, with signs beginning between sia or stress, produces a sustained increase

1 wk and 1 yr of age. It is characterized by
of intracellular calcium levels within
extension of the stifle and tarsus and by
skeletal muscle fibers. This in turn causes
spastic contracture of the muscles of one
muscle stiffness, hyperventilation,
or both pelvic limbs. Spasticity primarily
hyperthermia, and pale exudative pork. It
affects the gastrocnemius and superficial
results from a mutation in a calcium-chaimel
flexor muscles; in some cases, other
gene that is inherited as an autosomal
muscles of the pelvic limb are involved. The dominant trait, usually in Landracc pigs.

leg is usually held in extension behind the
calf and does not touch the ground during
walking. The disease is progressive but

Small Animals
usually responds to neurectomy of the

Hypertrophic neuropathy of Tibetan
tibial nerve. The cause is unknown. No

Mastiffs is an autosomal recessive disease
lesions are seen in peripheral nerves,
that has been recognized in the USA,
and the condition is thought to involve

Switzerland, and Australia. It causes pai·apaexcessive activity of the neuromuscular resis by 8 wk and may progress to tetrapai·espindle reflex arc. Adult cattle are affected sis. Hyporeflexia is marked, but senso1y
at 3--7 yr of age. Extensor muscles of the
function is preserved. Demyelination ai1d
back and pelvic limbs are affected, causing
remyelination are seen on nerve biopsy.

lwnbar lordosis and caudal extension of

Prognosis is guarded. Some puppies regain
the lin1bs. This condition is also thought
tl1e ability to walk but remain weak. There is
to be familial and is usually progressive.

no treatment.

Mephenesin (30-40 mg/kg, PO, for 2-3

Alaskan Malamute polyneuropathy'

days) may produce variable control of
affects Alaskan Malainutes 10-18 mo old.

signs. Quadriceps muscle hypoplasia as a

Clinical signs include exercise intolerance,
cause of congenital lameness has been
paraparesis progressing to tetraparesis,
described in Holstein calves. Reduced
muscle atrophy, hyporeflexia, and, in some
numbers of spinal cord motor neurons
cases, laryngeal paralysis. Electromyograsuggest that there is failure to innervate phy shows diffuse fibrillation potentials
the muscle on the affected side.

and positive sharp waves. On nerve biopsy,

Hyperkalemic periodic paralysis (see
there is axonal necrosis with demyelinap 104 7) is seen in Quaiter horses 2-3 yr old tion. There is no effective treatment,
and is due to an inherited mutation of the
although clinical signs stabilize in some
sod.iun1 chaimel. It causes episodes of
dogs. In most affected dogs, however,
muscle tremor and sometimes recumbency,
progressive disability leads to euthai1asia.

both of which may be precipitated by

Congenital laryngeal paralysis is seen
exercise. Hyperkalemia is usually present
in Bouvier des Flandres ( autosomal
during an attack, and electromyography can
dominant) and Siberian Huskies, Rottweilers,
also be helpful for d.iagnosis. Acetazolamide
and Bull Terriers < 1 yr old. It results in

(0.5---2.2 mg/kg, PO, bid) or hydrochlorothiexercise intolerance and inspiratoiy dyspnea.

azide (0.5 mg/kg, PO, bid) may lessen the

Diagnosis is confirmed by visualization on
frequency and severity of attacks.

laryngoscopy. Congenital laryngeal paralysis

Myotonia congenita is an inherited/
with diffuse peripheral neuropathy is seen
familial d.isorder in goats and Shropshire
in several breeds, including Dalrnatia.J1S,
lambs and is occasionally seen in horses. It

Rottweilers, and Pyrenean Mom1tain Dogs
causes muscle rigidity; marked dimpling on

(Great Pyrenees). Prognosis is guai·ded
percussion of the muscle belly; and a stiff,
to poor.

1232

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

Primary hyperoxaluria (l-glyceric
signs most prominently reflect muscle
aciduria) is a rare, inherited (autosomal
fibrosis and contractures. The resulting
recessive) neurofilament disorder of domesposture is that of the animal walking on its tic shorthaired cats that results in renal

"tip-toes." This is an inherited recessive disease and also produces weakness due to
disorder, reported in Beagles, for which the

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a pe1ipheral neuropathy. Signs develop at
genetic mutation has been identified. The

5-9 mo of age. A plantigrade stance is the
abnormal posture is present sho1tly after
most prominent sign, and spinal reflexes
birth. Other clinical signs include thickened
are sometimes reduced. Urine contains
cartilage of tl1e ear and wide-set eyes.

increased oxalate and 1-glycerate levels.

Seizw·es may occur concurrently. It is not

There is no treatment.

yet known whether the seizures are related

Neuropathy of hereditary hyperchy
to the primaiy disorder or are a concurrent
lomicronemia (hyperlipidemia) is a
disorder. There is no treatment. The human
suspected autosomal recessive disorder
counterpait to this disease is progressive
that causes a generalized peripheral
and frequently fatal; however, the disease
neuropathy in cats. Clinical signs do not
appeai·s to stabilize in dogs.

develop until at least 8 mo of age. The

Congenital myasthenia gravis
hyperlipidemia results in deposition of

(autosomal recessive) has been described
lipid granules within nerves, and there is
in Pai·son Russell Terrier, Smooth-ha.ired
evidence that the clinical signs can be

Fox Terrier, and Springer Spaiuel puppies. It
controlled by a low-fat diet. Blood samples
is due to either a deficiency or dysfw1ction
from affected cats have the appearance of
of the acetylcholine receptor, and there is

"cream of tomato soup."

none of the circulating antireceptor

Sensory neuropathy of longhaired
antibody seen in tl1e more common

Dachshunds (probably autosomal
acquired form of the disease. Clinical
recessive) causes pelvic limb ataxia at 8-12
signs usually start at 5-10 wk of age. The
wk of age. U1inary and GI function may also
characteristic finding is an exercise-induced
be disturbed. Paw position sense, spinal
wealmess, often associated with megareflexes, and pain sensation are depressed, esophagus. The prognosis is more guarded
and self-mutilation can occur. There is a loss than in acquired myasthenia gravis. The of myelinatecl fibers in sensory nerves and
congenital disease has also been described
in selected areas of the spinal cord. There is
in cats. A presynaptic fonn is seen in 12- to
no treatment, but affected dogs may have a

16-wk-old Gan1mel Dansk H0nsehund dogs
relatively nom1al quality of life, provided

( autosomal recessive). Treatment consists
self-mutilation does not occur.

of anticholinesterase drugs.

Sensory neuropathy of Border Collies

Scotty cramp (autosomal recessive)

manifests as ataxia, lack.of proprioception,
causes episodes of muscular hypertonicity
and abnonnal sensory testing. Onset is
in Scottish Terrier puppies. These episodes
usually at 5-7 mo of age and progresses
are exacerbated by excitement, exercise,
relentlessly. Euthanasia is the common
stress, and poor health and ai·e characte1°
endpoint. The genetics of this disease are
ized by a hypermetric gait and arching of
not yet known.

•
tl1e spine, which can cause tl1e clog to

Sensory neuropathy in Pointers is
somersault when it rw1s. The disorder
seen in English Pointers (autosomal
seems to be related to faulty serotonin
recessive) in the USA and Shorthairecl
metabolism. Diazepain and.promazines

Pointers in Europe. Self-mutilation of the
help to relieve signs.

digits is the main clinical sign, and disease

Congenital myoclonus of Labrador
onset is before 6 mo of age. Pain perception

Retrievers (fanulial reflex myoclonus)

is absent in the pelvic limbs and depressed
causes muscle spasms/hypertonicity from
in the thoracic limbs. There is neuronal Joss
an early age. Puppies may be unable to walk
in dorsal root ganglia. Prognosis is poor.

or even maintain a sternal position due to

There is no treatment.

extensor rigidity. The prognosis is very poor.

Inherited polyneuropathy of

Hypokalemic myopathy of Burmese

Leonberger dogs is a distal neuropathy,
cats ( autosomal recessive) causes periodic
with an age of onset of 1-9 yr in this breed.

pai·alysis or weakness with ventral flexion

Clinical signs include weakness, exercise
of the neck. Cats are affected at 3-4 mo of
intolerance, change in bark, and dyspnea.

age. Serwn CK is mai·keclly increased.

Pedigree analysis suggests an X-linked

Dietaiy supplementation of oral potassiun1
inheritance.

usually produces a favorable response ( eg,

Musladin-Lueke syndrome is a
potassiwn gluconate solution at 2-4 rnEq or
connective tissue disorder affecting
mrnol/cat/day, PO, until serw11 potassiwn
muscles, bone, heart, and skin. Clinical
levels ai·e stable).

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1233

Myotonia congenita is seen in Chow
may wax and wane and, in general, do not

Chows, Staffordshire Terriers, Great Danes,
become severely debilitating. Polymyosiand Miniature Schnauzers ( autosomal tis and dermatitis are evident on historecessive) and causes signs similar to those pathologic examination. This disorder has

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seen in myotonic goats. There is often a
also been seen in Beauceron Shepherds,
degree of muscle hypertrophy, and marked

Pembroke Welsh Corgis, Australian Cattle
stiffness is seen when dogs first rise.

Dogs, Lakeland Terriers, Chow Chows,

Dimpling is seen on percussion of several

German Shepherds, and Kuvasz dogs.

muscles, including the tongue. Diagnosis can

Glycogen storage diseases can cause
usually be confumed by electromyography
muscle weakness and exercise intolerance

( characteristic "dive bomber" sound); muscle in young dogs and cats. Examples include biopsy changes are mild and nonspecific.

glycogenosis types II (Lapland dogs), III

Prognosis is guarded, although membrane

(German Shepherds and Akitas), IV (autosostabilizing drugs (procainamide, mexiletine) mal recessive in Norwegian Forest cats),
result in significant improvement.

and VII (English Springer Spaniels).

X-linked muscular dystrophies have

Mitochondrial myopathy has been
been described in Irish Terriers, Golden
described in Clw11ber and Sussex Spaniels

Retrievers, Miniature Schnauzers, Rottweiland in Old English Sheepdogs. Mitochoners, Samoyeds, Gennan Shorthaired drial myopathies result in exercise

Pointers, Groenendaeler Belgian Shepherds,
intolerance and collapse, and blood lactate

Brittany Spaniels, Rat Terriers, Labrador
and pyrnvate levels are often increased after

Retrievers, Japanese Spitz dogs, and also
exercise. Ragged red fibers, indicating
in cats. All are due to mutations in the
increased nwnbers of mitochondria, may be
dystrophin gene. Males show muscle
seen on muscle biopsy. Inherited disorders
stiffness, dysphagia, and weakness at an
of carnitine metabolism are another cause
early age, along with a plantigrade stance
of mitochondrial myopathy; tlley may cause
and muscle atrophy as the animal gets older.

accwnulation of lipid vacuoles within

Initial muscle hypertrophy may be marked,
muscle fibers.

particularly in cats. Diagnosis is facilitated

Nemaline rod myopathy (probable
by the initial massive increases in serum
autosomal recessive) in cats causes
levels of CK and by demonstration of
weakness and later a hypem1etric gait at
hyalinized and mineralized muscle fibers

6-18 mo of age. Patellar reflexes are
on biopsy. Prognosis is guarded to poor.

depressed, and muscle atrophy develops

Currently, there is no treatment. A novel
progressively. Large nwnbers of nemaline
congenital muscular dystrophy has been
rods are found in skeletal muscle fibers. The
reported in cats associated with deficiency
prognosis is poor. A similar disorder is seen
of merosin (laminin o.2), in which degenerasporadically in young dogs.

tive changes occur in both muscles and

Central core myopathy has been
peripheral nerves.

described as a cause of weakness, muscle

Labrador Retriever myopathy
atrophy, and exercise intolerance/collapse

( autosomal recessive) causes a stiff gait and
in young Great Danes in the UK. Signs begin
marked muscle atrophy in puppies of both
at approximately 6 mo of age. Prognosis is
sexes. Signs worsen with cold, stress, or
poor.

exercise, and affected dogs may be unable

Congenital megaesophagus is
to keep their heads elevated in a normal
inherited in Wirehaired Fox Terriers and
position from as early as 3 mo of age.

Miniature Schnauzers and possibly also in

Tendon reflexes are usually absent. Signs

German Shepherds, Great Danes, Irish
stabilize by 6--8 mo of age, and the prognosis Setters, Newfow1dlands, Chinese Shar-Pei, is favorable, so affected dogs can make

Greyhounds, and Siamese cats. Clinical
good pets. There is preferential atrophy
signs include regurgitation and aspiration
of type II muscle fibers.

pneun1onia. Prognosis is guarded.

Dermatomyositis of Collies and

Devon Rex cat hereditary myopathy

Shetland Sheepdogs (inherited as a

( autosomal recessive) is seen in kittens
dominant trait with variable expressivity)

around 4-7 wk old and is characterized by
causes atrophy and weakness of the mastiexercise intolerance and passive ventroflexcatory and distal limb muscles from a few ion of the head and neck, which is especially
months of age, sometimes associated with
noticeable during locomotion, urination, or
trismus and megaesophagus. These signs
defecation. Some cats asswne a "dog-begare combined with a dermatitis over the ging" position. Megaesophagus is present.

face and extremities. The clinical signs

Prognosis is guarded.

1234

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

MULTIFOCAL DISORDERS

13-Mannosidosis causes recw11bency
and cerebellar signs in newborn Nubian

Large Animals
goats and Salers calves.

Hereditary neuraxial edema with

Ceroid lipofuscinosis is seen in sheep,

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inherited congenital myoclonus (probable cattle, and goats. Young Nubian goats show autosomal recessive) was fust reported in
cerebellar signs. Ran1bouillet sheep show
neonatal Polled Herefords and is the result of
blindness and decreased mentation from 8
decreased and/or defective glycine receptms, mo of age. South Hampshire lambs 9-12 mo which provide inhibitory neurotransmission.

old show blindness, depression, head and

The
thoracic limb tremor, and facial twitchi.t1g

_ calves are alert but unable to rise; they
are mcoordinated and have coarse, tonic
and die by 30 mo of age. Devon cattle
muscular contractions. Sudden stinmli cause
become blind and weak by 14 mo and die by
vigorous extension of the legs and neck.

4 yr of age. The genetic mutation has been

Shaker calf syndrome is a neurodegenidentified in some of these species (Devon erative disorder that is seen in Hereford
cattle, South Hampshire sheep).

calves. Affected animals show a marked

Globoid cell leukodystrophy has been
tremor within hows of bi.Ith, difficulty in
reported in polled Dorset sheep 4-18 mo
rising, a stiff gait, and loss of voice; signs
old. Exaggerated tendon reflexes, ascending
progress to spastic paraplegia. There is
paralysis, and cerebellar signs may be seen.

excessive accw11ulation of neurofilaments
within neurons of the central, peripheral,

Small Animals
and autonomic nervous systems.

Multisystemic chromatolytic neuronal

Vitamin A deficiency of sows can
degeneration in Cairn Terrie1s causes
cause incoordination, head tilt, pelvic li.tnb
para.paresis in young puppies that progresses
paralysis, paddling, and ocular lesions in
rapiclly to produce cerebellar involvement
piglets. Similar signs are seen in congenitally affected calves born from deficient

�th bouts of cataplectic collapse. Degeneration of neurons is widespread in the brain dams.

spinal cord, and sensory ganglia..

Multisystemic neuronal degeneration

Generalized Metabolic and Lysoso
has also been repmted in red-haired Cocker
mal Storage Disorders: Maple syrup

Spaniels and causes abnormal behavior and
urine disease is a genetic amino aciduria
cerebellar signs. Neuronal changes are

( consistent with a branched-chain ketoacid
found in various brain-stem nuclei. A similar
decarboxylase deficiency) in Hereford
condi�on i_s seen in Miniatme Poodles (3-4
calves. Affected calves are dull, become
wk) with signs chara.cte1ized by rolling from
recwnbent in 2-4 days, and tern1inally have
side to side, inability to stand or right into
opisthotonos. The histologic lesions are
sternal position, periodic opisthotonos
severe and consist of generalized status
intention tremors, and la.ck of a menac�
spongiosus in the CNS.

response associated with neuronal

GM
degeneration in tl1e cerebral cortex and

1 gangliosidosis is seen in inbred

F'liesian calves. Clinical signs become
cerebellwn.

evident during the first week of life and

Hydrocephalus in Bull Mastiffs is an
include depression, swaying of the
inherited disorder tl1at is also associated
hindquarters, reluctance to move and
with abnonnal myelin. It results in
stiffness. Death occms in 6--8 mo.'

blindness, a.bno1rnal behavior, a.nd

G M
cerebellar signs. Bilaterally symmetric

2 gangliosidosis causes hypermetria
and weakness in Yorkshire piglets within
spongiform lesions a.re found in the deep
the first 3 mo of life. Death occms in 4-6 mo.

cerebellar nuclei.

Dalmatian leukodystrophy is a rare

. a-Mannosidosis (autosomal recessive)

JS seen m Angus, Mun-ay Grey, and Galloway inherited condition that causes visual breeds. It produces ataxia, head tremor,
deficits with progressive ataxia and
aggression, and fail me to thrive. There may
tetraparesis at 3-6 mo of age. There is dilataalso be abortions and neonatal death. Most tion of ventricles, cavitation of cerebral
affected calves die within the fust year,
white matter, and widespread loss of
sometnnes shmtly after bi.Ith. Affected
myelin.

(homozygous) calves have an absolute

Fibrinoid leukodystrophy has been
deficiency of a-mannosidase, and heterozydesclibed in two 8-mo-old Labrador gotes are partially deficient. Mannosidosis

Retrievers, a 9-mo-old male Scottish Terrier
can be controlled by identifying and
a 6-mo-old female Miniature Poodle and a
eli.tninating heterozygotes on the basis

13-wk-old Bernese Mountain Dog. It results
of biochemical testing.

in progressive ataxia and tetraparesis with

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM

1235
personality changes starting at 6 mo of age.

Clinical signs are variable and multifocal,

Rosenthal fibers are found around blood
and eitller an ascending paralysis is seen
vessels of the CNS, and the cause seems to
by itself or combined with a cerebellar
be a disorder of astrocyte function.

disturbance. Death occurs 2-3 mo after tile

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Prognosis is poor.

onset of signs. Total protein content of CSF

Spongifonn degenerative conditions
may be increased. Large globoid cells are
have been described in young dogs and cats
distributed throughout the white matter of

(breeds include Labrador Retriever, Shetland the spinal cord and brain.

Sheepdog, Samoyed, Silky Terrier, Bull

GM, gangliosidosis is seen primarily in

Mastiff, Saluki, Cocker Spaniel, Malinoiscats, particularly Oriental breeds, and in Shepherd crosses, Rottweiler, and Egyptian

Beagles, Portuguese Water Dogs, English

Mau and Bunnese kittens) and are often

Springer Spaniels, Alaskan Huskies, and
associated with signs of ataxia/hypermetria,

Shi bas. Signs of cerebellar dysfunction
head tremors, intermittent contractures,
predominate, and corneal clouding may
postural abnorn1alities, and behavioral
develop.

changes. The underlying pathology relates to

GM2 gangliosidosis or familial
spongy degeneration of either white or gray
amaurotic idiocy (Derry disease) has been
matter. The pathogenesis of these disorders
seen in Gennan Shorthaired Pointers,
remains uncertain, although a genetic

Japanese Pointers, mixed-breed cats, and
mutation has been identified for a fanilly

Karat cats. Clinical signs seen at 6 mo of
of Australian Cattle Dogs and Shetland
age include behavioral change and visual

Sheepdogs. Prognosis is poor.

disturbances. Progressive ataxia and demen

Hereditary quadriplegia and
tia develop later. Clinical signs of ataxia,
amblyopia in Irish Setters produces
hypermetria, head tremor, and corneal
signs of head tremor, visual impairn1ent,
opacity develop in kittens at -3 mo of age.

nystagmus, inability to stand, and seizures

Niemann-Pick disease affects cats and
beginning at birth.

causes cerebellar dysfunction with an
associated abdominal enlargement due

Lysosomal Storage Disorders: This
to hepatosplenomegaly. The neurologic deficlinically rare group of conditions results cits tend to vary with the six subtypes of this
from deficiency of an enzyme that is
disease, ranging from severe cerebellar-like
essential for the metabolism of a protein,
signs (types A and C) to neuropathic signs
carbohydrate, or lipid substrate, or results

(type A variant).

from buildup of a byproduct that can be

Glucocerebrosidosis ( Gaucher
toxic to cells. Clinical signs usually appear
disease) is a rare disorder of Australian
early in life, although occasionally the onset

Silky Terriers tllat produces mainly
is delayed. Specific diseases have been
cerebellar signs at 4-6 mo of age.

associated with a particular breed, but in

Glycoproteinoses: Fucosidosis of
tlleory, any breed could develop any one

English Springer Spaniels has been
of these disorders, and many have been
reported in Australia, New Zealand, tile UK,
described in more than one breed.

and North America. It is characterized by

Considerable phenotypic variation should
clinical signs of ataxia, personality change,
be expected beyond the classic signs
dysphonia, dysphagia, hearing/visual
described below. Prognosis is poor for all of
deficits, and seizures. Signs tend to
these disorders, altllough gene replacement
progressively develop from 6 to >24 mo
therapies are being actively investigated.

of age. A high proportion of peripheral

Diagnostic testing is limited except for
lymphocytes may show cytoplasmic
tllose diseases in which the enzyme or
vacuolation. A DNA-based blood test is
mutation has been identified or tile pattern
available for diagnosis. Prognosis is poor,
or organic acids has been recognized.

and there is no effective treatment.

Testing often includes urine metabolic
oc-Mannosidosis has been seen mainly
screening, lysosomal enzyme screening,
in cats and may cause retinal and skeletal
histopathology for specific characteristics
abnormalities as well as neurologic deficits.

in tissue biopsy, or DNA testing for known

Cerebellar signs are the most consistent
mutations. Genetics laboratories should be
feature of the otherwise somewhat variable
checked for testing availability.

neurologic deficits.

Sphingolipidoses: Globoid cell

Mucopolysaccharidoses (Types I, II,
leukodystrophy (Krabbe disease) is

Ill, VI, VII): Mucopolysaccharidosis is
seen mainly in Cairn and West Highland
primarily a disorder of cats, although some

White Terriers. Several other breeds of
subtypes affect dogs. This disorder is
dogs, as well as cats, may be affected.

associated with a flattening of tile face,

1236

CONGENITAL AND INHERITED ANOMALIES OF THE NERVOUS SYSTEM
corneal clouding, and multiple bone dys

Hounds, Beagles, Poodles, and mixe d -breed
plasias. Plott hounds can also be affected.

dogs. It is most well known and genetically

Several types of this disease are reported;
understood in the miniature Wirehaired
type VI is often associated with progressive

Dachshund, and a genetic test is available

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paraparesis secondary to focal bony
for diagnosis in this breed. Clinical signs can
protrusions into the vertebral canal. The
include late-in-life onset myoclonic seizures
skeletal changes are nonprogressive after
that can in some cases be triggered by visual

9 mo of age, and decompressive surgery
or auditory stimuli. Other clinical examinamay in1prove the neurologic deficits.

tion findings are not commonly reported.

Glycogen Storage Disorders:

Glycogenosis (types II, III, IV, VII) and
mucolipidosis II arc not as well described.

MISCELLANEOUS CONGENITAL

English Springer Spaniels, Lapland dogs,

DISORDERS

German Shepherds, Akitas, and Norweigan

Forest cats are among those described.

Large Animals

Clinical signs generally include neuromus

Pendular nystagmus is seen in various
cular weakness, exercise intolerance,
breeds of dairy cattle but appears to have
muscle tremors, or dysphagia.

little clinical significance.

Mucolipidosis II affects domestic

Congenital deafness has been repo1ted
sho1thaired cats and generally causes
in horses.

skeletal malforn1ations.

Other Storage Disorders: Ceroid

Small Animals
lipofuscinosis is characterized by

Pendular nystagmus is seen in various
reduced vision, personality change, ataxia,
breed of Asian cats but appears to have
and seizures. Clinical signs typically appear little clinical significance. Compared with when animals are 12-24 mo old, although
pathologic fonns of nystagmus, in pendular
some can be older. The condition is an
nystagmus there is no fast or slow phase,
autosomal recessive trait in English
and the nystagmus arcs are similar to the

Setters, Tibetan Terriers, and Border
pendullllll movement of a clock.

Collies. It has been reported in many

Congenital deafness is primarily
additional breeds of dogs, as well as in
associated with Dalmatians but has also been

Siamese cats. The genetic mutation has
recorded in a nun1ber of breeds, including
been identified in some breeds of dogs. The Australian Blue Heelers and Shepherds, phenotype and age of onset are variable,

English Setters, Boston Terriers, and Old Engand signs tend to slowly evolve throughout lish Sheepdogs. It is linked to blue eye color
several years.

in white cats. The brain stem auditory evoked

La Fora disease occurs most commonly
response (BAER) is a useful diagnostic test
in miniature Wirehaired Dachshunds but
primarily used to identify carriers in a litter of
also can affect other breeds, such as Bassett
affected animals. (See also DEAFNESS, p 518.) DEMYELINATING DISORDERS

Hypomyelination and dysmyelination
ing disease, respectively, and are characare disorders of myelin development teristic of tl1e congenital rnyelin disorders
characterized by axons with thin myelin
seen in young animals. These pathologic
sheaths, or by axons that are nonmyelinchanges should not be confused with ated or have abnormal myelin. There are
dernyelination, in which there is a
two possible pathologic classifications:

breakdown and Joss of previously normal

1) thinly myelinated axons with predomimyelin. In general, these types of demyelinnantly normal myelin and occasional ating diseases do not present clinically as
nonmyelinated axons, or 2) thinly
congenital problems.

myelinated axons with predominantly
abnom1al myelin and mainly nonrnyelin

Etiology and Epidemiology: Demyeated axons. These categories have been linating disorders have been reported
called hypomyelinating and dysmyelinat-
worldwide in people, mice, pigs (British

DEMYELINATING DISORDERS

1237
saddleback, Landrace), cattle (Hereford,
ear·ly as 10-12 days of age and certainly by

Holstein-Friesian, Jersey, Murray grey,

U1e time of weaning. Signs include, most

Shorthorn), hamsters, rats, sheep, Siamese
notably, a gross whole body tremor that
kittens, and a number of dog breeds,
involves the limbs, trunk, head, and eyes.

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including Chow Chow, Springer Spaniel,

The tremor lessens or disappears when the

Dalmatian, Samoyed, Golden Retriever,
animal is resting or sleeping but reappears

Lurcher, Bernese Mountain Dog, Weimaon ar·ousal and increases with excitement.

raner, Australian Silky Ten-ier, and mixed

The tremors are very noticeable when the
breeds. This problem has also been
animal is eating and are a severe form of
documented in a litter ofVizslas and
intention tremor. In addition, some animals

Catal10ula Cur dogs.

may have difficulty standing ar1d arnbulating

In utero infect.ion and heredity are the
and may have weakness in the limbs.

general causes of hypomyelination. The

Secondary to this, postural test reactions
viruses of classical swine fever, border
may be deficient. Affected animals appear
disease, and bovine viral diarrhea have been
to have vision and other cranial nerve
incriminated, but mechanisms responsible
function, but occasionally a pendular·
for the hypomyelination have not been
nystagmus or a jerk nystagmus is seen when
defined; these tlu·ee pestiviruses are closely
the globes are voluntarily moved. These
related members of the family Togaviridae
nemologic deficits may be so severe in
and are transmitted both vertically and
some animals that euU1anasia is warranted.

horizontally. The inflanunatory neuraxial

In some breeds of dogs, such as Chow
disorders in domestic anin1als in which

Chows and Catal1oulas, the signs usually
demyelination is found are canine
dissipate over the first year of life, and the
distemper, visna, and caprine arthritis
dogs are nonnal by 12-18 mo of age. In
encephalitis syndrome. In none, though,
some dogs, the signs may disappear· as ear·ly
does CNS demyelination occm as the
as 12-16 wk of age.

predominant central featme of U1e disorder

In Golden Retrievers with PNS hypomyas it does in human multiple sclerosis. Most elination, the clinical signs include ataxia,
toxins that affect myelin cause demyelinaparesis, muscle atrophy, ar1d hyporeflexia tion. One in particular, trichlorfon, is an
to areflexia. There is no evidence of CNS
organophosphate (seep 3064) with a unique
hypomyelination in Uus breed, and tremors
toxicity that causes Type A-V porcine
ar·e not present.

congenital tremor syndrome. Pregnant
sows treated with trichlorfon dw-ing mid

Lesions: In CNS hypomyelination, gross
and late gestation ( days 4&--77) produce
pathology reveals pallor of the white matter
litters in which up to 900/o of the piglets
of the brain and spinal cord and possibly a
develop a marked tremor syndrome
gelatinous appearance. In PNS hypomyel.isecondary to cerebellar hypoplasia and nation, the gross char1ges are minimal a11d
hypomyelinogenesis. The mortality rate
there is no evidence of CNS involvement.

is high.

In CNS hypomyelination, the microscopic

Other disorders resulting in hypomyelinachanges include lack of myelin (which is tion are hereditary. Almost all of these
usually severe but not absolute), fewer
disorders result in CNS hypomyelination,
oligodendrocytes, astrocytes outnw11bering
except in Golden Retrievers, in which
oligodendrocytes, oligodendrocytes that
hypomyelination of the peripheral ne1vous
differ in appearance from those in healthy
system (PNS) has been reported. In CNS
animals, a11d abnonnal types of glial cells.

hypomyelination, the basic defect involves

In PNS hypomyelination, the microscopic
interference with the functional maturation
cha11ges consist of paucity of myelinated
of oligodendrocytes. The exacl mechanisms fibers, fibers with inappropriately thin for the defect are not known, but a point
myelin sheaths relative to the caliber of
mutation on a critical gene has been found

U1eir enclosed axons, occasional fibers
in Springer Spaniels. In PNS hypomyelinawith poorly compacted myelin, Schwarm tion, the defect involves Schwarm cells.

cells with larger than nonnal cytoplasmic

The genetic basis for the inherited
volw11e, and increased numbers of Schwarm
hypomyelination syndromes is not fully
cell nuclei.

defined, but in most instances, males are
affected more often and more severely than

Diagnosis: The diagnosis of CNS
females. This supports a sex- linked
hypomyelination is made primarily from the
recessive trait or mode of inheritance.

spectrum of nemologic deficits and signs
and the ear·ly age of onset. Unfortunately,

Clinical Findings: Clinical signs from
histopathology is the only definitive method
hypomyelination of the CNS can be seen as
to confim1 a diagnosis. In cases with a

1238

DEMYELINATING DISORDERS
heritable basis, pedigree evaluation may
organophosphates, chlorinated hydrocarbe helpful. In cases with a viral cause, bons, fluoroacetate, strychnine, hexachloroconfirmation may involve immunofluoresphene, bromethalin), and mycotoxins (eg, cent antibody-staining techniques or virus
penitrem-A).

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isolation from nervous tissue ( or both). In
cases of PNS hypomyelination, biopsy of

Treatment, Control, and Prevention:

peripheral nerves is beneficial.

There is no specific treatment for hypomy

Differential diagnoses include disorders
elination. The only means of control and
that could cause tremors in young animals.

prevention is selective breeding (for

The possibilities are numerous, but some of
heritable syndromes) and inununization
the more common include glycogen storage

(for viral-induced syndromes). If given time
disease, lysosomal storage disease,
to develop normal or fwther myelin, some
cerebellar hypoplasia, encephalitis,
animals with congenital hypomyelination
hypocalcemia, hypoglycemia, hyperamsyndromes become normal by the age of 12
monemia, toxins (eg, metaldehyde,
wk to 18 mo.

DISEASES OF THE PERIPHERAL NERVES

AND NEUROMUSCULAR JUNCTION

Diseases of the peripheral nerve and
disorder. Treatment of idiopathic laiynneuromuscular junction include degenerageal paralysis consists of surgery, such as tive diseases, ini1anunato1y diseases,
laryngeal tie back. Surgery does not restore
metabolic disorders, neoplasia, nutritional
nonnal laryngeal function but is usually
disorders, toxic disorders, trauma, and
successful in diminishing severe inspiratory
vascular diseases. For a discussion of
dyspnea. A potential complication of
congenital disorders, seep 1222.

surge1y is aspiration of food or liquid.

DEGENERATIVE DISORDERS

Canine Chronic Axonal Degeneration:

Canine chronic axonal degeneration,

Acquired Laryngeal Paralysis: Larynsometin1es called geriatric-onset laiyngeal geal paralysis (seep 1420) is co nun on in
paralysis polyneuropathy, affects middlemiddle-aged and older dogs. Large breeds, aged and older dogs and is characterized by
such as Labrador Retrievers, Golden
axonal degeneration of peripheral nerves.

Retrievers, and Saint Bernards, are

The cause is unknown. Affected dogs have
predisposed, but small-breed dogs and cats
a wide-based, shuffling gait with ataxia,
can be affected. In most cases, no underlytetraparesis, and generalized muscle ing cause is identified and the laryngeal
atrophy with decreased spinal reflexes.

paralysis is a component of a generalized

Laryngeal paralysis is often an early feature.

polyneuropathy, canine chronic axonal

Facial paralysis and dysphagia are also
degeneration. A few cases are due to trauma possible. Diagnosis is based on clinical or neoplasia affecting the neck or mediastifeatures, electrodiagnostic evaluation nurn. Hypothyroidism (seep 553) is also a
showing denervation and slowed motor
potential cause. Clinical signs consist of
conduction velocity, and nerve and muscle
voice change, laryngeal stridor, and a dry
biopsy showing loss of large-caliber nerve
cough. In severe cases, exercise intolerance
fibers with axonal degeneration and
and episodes of respirat01y---especially
neurogenic muscle atrophy, respectively. It
inspiratory---distress and cyanosis occur.

is important to exclude treatable metabolic

Some affected anin1als have signs of a more
causes such as hypothyroidism. The
generalized polyneuropathy, such as
neurologic deficits progress slowly over
weakness and proprioceptive deficits.

months. There is no specific treatment.

Diagnosis is based on laiyngoscopy with
the anin1al lightly anesthetized. There is a

Equine Laryngeal Paralysis: Seep 1458.

unilateral or bilateral lack of abduction of
the arytenoid caitilages and vocal folds

Dancing Doberman Disease: Dancing
during inspiration. Management consists

Doberman disease is a neuromuscular
of identifying and treating any underlying
disease that affects Doberman Pinschers

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR JUNCTION

1239
of either sex, 6 mo to 7 yr old, and is likely
results in unilateral or bilateral paresis or
inherited in an autosomal recessive pattern.

par·alysis of the facial muscles in dogs and

Initially, affected dogs intennittently flex
cats. Cocker Spaniels, Pembroke Welsh
the hip and stifle of one pelvic limb while

Corgis, Boxers, English Setters, and
standing. Within several months, most dogs
domestic longhaired cats are at increased

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alternately flex and extend both pelvic limbs risk. There is acute onset of unilateral or in a dance-like fashion. They often prefer to
bilateral inability to blink, drooping ear,
sit rather than stand. The condition slowly
drooping upper lip, and drooling from the
progresses to mild paraparesis, decreased
comer of the mouth. Facial sensation
proprioception, and atrophy of the

(mediated via the trigeminal nerve) remains
gastrocnemius muscles. The thoracic limbs
intact. Diagnosis is based on clinical
are not affected. Pathologic changes have
features and exclusion of other causes of
been reported in pelvic limb muscles as well
facial paralysis, including ear disease,
as peripheral ne,ves, and whether this is a
trauma, and brain-stem lesions. Pathoprimary muscle or nerve disease remains to logic findings consist of degeneration of
be clarified. There is no treatment, and signs
myelinated axons in the facial nerve. There
do not resolve. However, the disease usually is no inflammation. The cause is unknown, does not result in severe disability and does
and there is no specific treatment. Artificial
not appear to be painful.

tears often help prevent corneal dan1age.

Partial improvement may occur in a few

Distal Denervating Disease: Distal
weeks, but persistent dysfunction is
denervating disease is a common polyneucommon.

ropathy of dogs in the UK; it has not been
reported elsewhere. The cause is unknown.

Stringhalt: (See also p 1137.) Stringhalt in Any age and breed of dog may be affected.

horses is characterized by brisk, involtmtary

The onset of signs varies from a few days
flexion of one or both pelvic limbs during
to several weeks. There is progressive
the protraction phase of the gait. Severity
tetraparesis, hyporeflexia, ar1d atrophy of
ranges from a mild jerk in the limb to flexion
proxin1al skeletal muscles. Sensory deficits
so severe that the affected horse can hardly
are not apparent. Electrodiagnostic
walk. There may be atrophy of the muscles
evaluation typically shows dene1vatiun
in the distal aspect of the affected limb(s).

of lirnb muscles, relatively nonnal nerve

Stringhalt is seen in two forms. Ordinary
conduction velocity, ar1d markedly reduced
or classic stringhalt is seen sporadically
amplitude ofM waves. Peripheral nerve
throughout the world, usually as a tmilateral
biopsies are usually normal, but exan1ination
problem in individual horses. The cause is
of intramuscular nerves may be diagnostic;
unknown. Some cases resolve spontanedistal intran1uscular axons degenerate with ously, whereas long digital extensor
collateral axonal sprouting. Treatment is
tenectomy is effective in others.

supportive, and the prognosis is excellent,

Australian stringhalt is seen in outbreaks
with recovery in 4--0 wk. Relapse has not
that affect multiple horses in a region ar1d
been reported.

often affects both pelvic limbs. Horses in

Distal Polyneuropathy of Rottweilers: Australia, New Zealand, and the USA have been affected, usually in late sununer or

Distal polyneuropathy ofRottweilers is
autunm. Australian stringhalt is associated
characterized by paraparesis that slowly
with ingestion of Australian dandelion,
progresses to tetraparesis, hyporeflexia,

European dandelion, and mallow, perhaps
and muscle atrophy. The clinical course can
due to mycotoxins affecting these plants.

be progressive or can wax and wane. Male

Pathologically, the distal aspect of axons in
and female Rottweilers 1-4 yr old have been
affected. The cause is unknown. Electrodithe peroneal and tibial nerves degenerates.

Horses with Australian stringhalt usually
agnostic testing shows denervation in distal
recover spontaneously when removed from
muscles of the limbs and decreased motor
offending pastures.

nerve conduction velocity. Nerve biopsy
changes consist of axonal necrosis and
demyelination, often with infiltrates of

INFLAMMATORY DISORDERS
macrophages, most severe in distal ne1ve
fibers. Prognosis is poor, although some

Acquired Myasthenia Gravis: Acquired
dogs may temporarily improve with
myasthenia gravis is characterized by
corticosteroid treatment.

failure of neuromuscular conduction due to
reduction in the nun1ber of acetylcholine

Idiopathic Facial Paralysis: Idiopathic
receptors at the neuromuscular junction. It
facial paralysis is a common disorder that
is caused by the development of circulating

1240

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR JUNCTION
antibodies directed against the acetylchoa.re initially affected. Death from respiratory line receptors at the neuromuscular
paralysis can occur in severe cases. Spinal
junction. It is fairly common in mature clogs,
cord reflexes a.re weak to absent, and severe
especially German Shepherds, Golden
muscle a.trophy is evident witlun 10-14

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Retrievers, and Labrador Retrievers, but is
days. Pain perception is intact, and some
w1conunon in cats. Three clinical forms
dogs may appear hyperesthetic, showing
exist in anin1als. The generalized form,
signs of discomfort on palpation of the
which affects 57% of clogs with acquired
trunk or limbs. Menta.tion and appetite a.re
myasthenia, is characterized by exercisenot affected. Urination, defecation, and tail inclucecl stiffness, tremors, and weakness
movement usually remain normal.

that resolve with rest. However, weakness

Analysis of CSF collected from the
is not always associated with exercise.

lumbar suba.ra.chnoid space shows

Megaesophagus is conunon in the
increased protein with a normal cell count.

generalized fom1. Focal myasthenia ( 43% of

Electromyography shows denerva.tion, and
affected dogs) presents as facial, pharynnerve conduction studies show marked geal, or esophageal weakness without
dispersion and prolonged latency of
generalized weakness. Least common is

F-wa.ves, indicative of slowed conduction
folminant myasthenia, which presents as
in the ventral roots. There is no effective
acute, flaccid paralysis and megaesophagus, treatment other tlmn nursing ca.re, and c01uwhich rapidly progresses to respiratory costeroids are not helpful. Most a1Tected
paralysis and is usually fatal.

animals begin to in1prove spontaneously

Generalized weakness often resolves
wiU1in 3 wk, with complete recovery by 2-6
quickly after IV aclm inistration of edrophomo. Animals with severe signs and marked niw11 chloride (0.1-0.2 mg/kg), which is
muscle atrophy may recover incompletely.

often used as a diagnostic test. Definitive

Relapses can occur, especially in hunting
diagnosis is based on the detection of
clogs tl1a.t frequently encounter raccoons.

antibodies in serw11. Treatment consists of

Histopathologically, there is irtflan1mation,
anticholinesterase drugs, eg, pyridostignune
demyelina.tion, and varying degrees of

(1-3 mg/kg, PO, bid-tic!) or neostigrnine
a.xonal degeneration in the ventral nerve

(0.04 mg/kg, SC, qid). lnunw10suppressive
roots and peripheral nerves.

dosages of prednisone and other in1munomodulating drugs a.re reconunenclecl in Chronic Relapsing Idiopathic Poly
animals that do not respond to anticholinest
radiculoneuritis: Chronic relapsing
erase therapy. Megaesophagus is managed
idiopathic polyra.diculonewitis is a rare
with upright feeding and in some cases
disease associated with irtflamma.tion of the
gastrotomy tube placement for feeding and
nerves and ne1ve roots. lt affects mature
hydration. Aspiration pneumonia. is a
clogs and cats. Exercise intolerance, ataxia,
frequent complication of mega.esophagus
and weakness develop slowly throughout
and leads to death or euthanasia. in -500Ai of
several montl1s. Some animals have
affected dogs. The prognosis is generally
spontaneous temporary remissions. Spinal
good for animals withoutJ)newnonia., and
cord reflexes a.re decreased, and cranial

-85% of dogs will undergo spontaneous
nerves may be affected. In severe cases,
remission, evident by a decrease in antibody
decreased sensation is evident. Diagnosis is
titer, usually within 6 mo.

based on nerve biopsy. There is nonsuppura.tive irtfla.mma.tion; a.xonal degeneration; and Acute Idiopathic Polyradiculoneuritis:

demyelination of ne1ves, ne1ve roots, and, in

Acute idiopathic polyra.diculoneuritis
some cases, dorsal root ganglia. The ca.use is
primarily affects the ventral nerve roots and
unknown, altl10ugh irnrnune-mecliatecl
peripheral nerves. It is common in clogs and
mechanisms are suspected. Corticosteroids
rare in ca.ts. Clinical signs often develop
help in some cases, but the disease tends to

7-14 days after a raccoon bite or scratch
slowly wax and wane, gradually becoming

(Coonhouncl paralysis); however, other
more severe throughout months to yea.rs.

affected animals have not been exposed to
raccoons. A similar syndrome can develop

Chronic Inflammatory Demyelinating
in dogs and ca.ts witlun 1-2 wk of vaccina

Polyneuropathy: Chronic irtflanuna.tory
tion. An inrn1une-mediated reaction to
clemyelina.ting poly.neuropa.hy is a fairly
raccoon saliva or other antigen is suspected.

common disorder in adult clogs and cats. The

Initially, there is a short-stricled gait in the
ca.use is unknown. Onset of tetra.paresis with
pelvic limbs that progresses within 1-2 days
hyporeflexia. is insidious and sometimes
to flaccid tetra.paresis or tetraplegia. and,
accompanied by cranial ne1ve dysf1mction.

in some cases, to facial and laryngeal

Electromyography is usually nom1al, but
weakness. Occasionally, tl1e thoracic limbs
nerve conduction velocities a.re slowed with

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR JUNCTION

1241
temporal dispersion. N eive biopsy shows
effective. The prognosis is poor in dogs with
multifocal paranodal demyelination. Clinical
pelvic limb rigidity.

signs usually improve with ad.ministration of
corticosteroids (eg, prednisone 1-2 mg/kg/

Sensory Ganglioneuritis: Sensory
day), although signs may relapse when
ganglioneuritis affects dogs of any breed,

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therapy is stopped.

although Siberian Huskies are at increased

1isk. At 1-6 yr of age, there is ataxia of all

Polyneuritis Equi: Neuritis of the cauda
limbs with no paresis, dysphagia, regurequina (polyneuritis equi) is characterized gitation, and difficulty prehending food.

by inflammation of the sacrocaudal neives

Hyperesthesia and self-mutilation occur in
and occasionally other neives. It is seen in
some cases. There is decreased propriocepadult horses of all breeds in Europe and tive positioning, weak to absent patellar

North America. The cause is unknown,
reflexes, and decreased to absent pain
although an inlillunologic reaction incited
perception in the limbs and face. Diagnosis
by a viral infection is possible. Affected
is based on clinical signs, electrodiagnostic
horses have circulating antibodies against
testing that demonstrates slowed sensory

P2 myelin protein. The most consistent
neive conduction, and biopsy of a mixed or
clinical signs reflect involvement of the
sensory neive that shows loss of myelinated
sacrocaudal neives and include urinary and
axons and endoneural fibrosis. The cause is
fecal incontinence, tail paralysis, perineal
unknown, but loss of neurons in dorsal root
paresthesia or analgesia, atrophy of the
ganglia with infiltration of lymphocytes and
gluteal muscles, mild pelvic limb ataxia, and
macrophages is seen at necropsy. There is
in male horses, penile paralysis. Affected
no effective treatment; the disease typically
horses may rub the tail. The thoracic limbs
progresses and leads to euthanasia.

and cranial neives may also be affected.

Diagnosis can usually be based on clinical

Trigeminal Neuritis: Idiopathic
findings. CSF may be xanthochromic with
trigeminal neuropathy is conm1on in dogs
increased protein content and mononuclear
and unconlillon in cats. It is characterized by
pleocytosis. Sacral fracture should be
acute onset of flaccid jaw paralysis. Affected
excluded by rectal examination and
animals cannot close the mouth and have
radiography. There is no treatment, and the
difficulty eating and drinking. Homer
prognosis for recovery is poor. Histopathosyndrome, facial paresis, and decreased logically, there is granulomatous inflanunafacial sensation are also possible. The cause tion primarily affecting the extradural
is unknown. Histopathologically, there is
portions of the sacrocaudal neives.

bilateral nonsuppurative inflammation and
demyelination in the motor branches of the

Protozoa! Polyradiculoneuritis: Prototrigeminal neive. Affected animals u:,ually zoa] polyradiculoneuritis occurs in dogs,
recover spontaneously within 3---4 wk. Fluid
especially puppies, and is caused by
and nutritional support may be necessary.

infection with Toxoplasma gondii (seep

685) or Neospora caninum (seep 663).

METABOLIC DISORDERS

Transplacental infection is most conunon,
and multiple puppies in a litter can be

Diabetic Neuropathy: This unconm1on
affected. Affected puppies are normal at
complication of diabetes mellitus (see
birth but by 3---8 wk develop paraparesis and
p 579) is seen in cats and rarely dogs. Signs
a "bunny-hopping" gait with weak or absent include weakness, ataxia, and muscle
spinal ref exes. Over a pe1iod of several
atrophy. Affected cats often have unilateral
weeks, the pelvic limbs develop severe
or bilateral tibial neive dysfunction, evident
extensor rigidity and muscle atrophy.

as a plantigrade stance. There are several

Without treatment, the disease can progress
proposed pathophysiologic mechanisms,
to the thoracic limbs, eventually leading to
but prolonged hyperglycemia seems to be
dysphagia and fatal respiratory paralysis.

the important underlying factor. Pathologic

Serum CK concentration is often increased.

findings in neives consist of demyelination

Analysis of CSF usually shows increased prowith remyelination, axonal degeneration, or tein and leukocytes (neutrophils, mononuboth. Diagnosis is based on clinical findings, clear cells, and eosinophils ). Serum or CSF
laboratory evidence of diabetes mellitus,
antibodies or identification of the organism
and neive biopsy. The prognosis is guarded,
on muscle biopsy are helpful in diagnosis.

but partial or complete recovery can occur

Early treatment with clindamycin (15-20
with insulin therapy.

mg/kg, IM, PO, bid) or trimethoprim/
sulfadiazine ( 15 mg/kg, bid) and pyrirneth

Hypothyroid Neuropathy: This
an1.ine ( 1 mg/kg/day) for 4-6 wk may be
neuropathy is a potential complication of

1242

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR JUNCTION
hypothyroidism in dogs (seep 553). Mature
been associated with a valiety of tumors,
dogs, especially large-breed dogs, are
including bronchogenic carcinoma,
predisposed. Several syndromes have been
multiple myeloma, sarcoma, and adenoreported, including tetraparesis with carcinoma. The pathogenesis is not well

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proprioceptive deficits and hyporeflexia,
understood but may be related to an
vestibular dysfunction, megaesophagus,
inlmune response directed against the
and laryngeal paralysis. In some cases,
tun1or that cross-reacts with nerve
classic signs of hypothyroid.ism (eg, obecomponents. Clinically, there is paraparesis sity and dem1atopathy) are absent, and
or tetraparesis that progresses over several
neurologic dysfunction is the only sign of
weeks with decreased spinal reflexes and
illness. Pathologic findings in peripheral
muscle atrophy. Diagnosis is based on
nerves consist of demyelination or
identifying the underlying twnor, clinical
remyelination and axonal degeneration. The and electrodiagnostic findings of neuropapathophysiology is poorly understood and, thy, and in some cases, nerve biopsy. Signs
in some affected dogs with motor deficits, a
may improve with successful treatment of
myopathy may also be present. Diagnosis
the underlying tumor.

is based on clinical features, laboratory
assessment of thyroid function, and

NUTRITIONAL DISORDERS
response to thyroid supplementation.

In some, but not all, cases, signs resolve

Pantothenic Acid Deficiency: Pantowithin several months of starting thyroid thenic acid deficiency may develop in
replacement therapy.

animals (particularly pigs) on rations of com.

Clinical signs include pelvic limb ataxia and a

NEOPLASIA

"goose-stepping" gait in which the stifles remain extended and the hips flex to lift the

Nerve Sheath Tumors: Nerve sheath
limbs off the ground. Patl1ologic findings
tumors include schwarmomas, neurilemmoconsist of degeneration of myelinated fibers mas, and neurofibromas. They are seen in
in peripheral nerves and chromatolysis and
most domestic aninlals but are most common loss of sensory neurons in spinal ganglia in dogs and cattle. In dogs, tumors often arise
in the nerves of the brachial plexus, initially

Riboflavin Deficiency in Chickens:

causing unilateral thoracic limb lameness and Riboflavin deficiency ( curled toe paralysis, pain that may be confused with musculoskel
seep 2941) can develop if feed is not foretal disease. Pain may be elicited on palpation mulated properly. Affected chicks show of the axilla or abduction of the limb; large
poor growth, diarrhea, and weakness.

tumors can be palpated. Muscle atrophy and

There is inability to extend the hocks and
monoparesis eventually develop. The spinal
progressive inward curling of the toes, so
cord may become compressed by the
that chicks rest and walk on their hocks.

invasive tumor, causing neurologic deficits in

Mortality is high by the third week. At
other limbs. The trigeminal nerve is the most
necropsy the peripheral nerves, especially
frequently affected cranial ne.rve. This results
the sciatic nerves, are swollen. Histopatlloin unilateral atrophy of tile temporalis and logically, tllere is hypertrophy of Schwarm
masseter muscles and facial dysestl1esia or
cells, demyelination, and minimal axonal
anesthesia. Eventually, brain-stem compresdegeneration. Chickens often recover with sion can develop.

riboflavin supplementation unless tile

Early surgical excision may be curative,
curled-toe deformity is longstanding.

although recurrence at the proxin1al stump of
the resected nerve(s) is common. In cattle,

TOXIC DISORDERS
nerve sheath tumors are often recognized
incidentally in old aninlals at slaughter. Often,

Botulism: Botulism is intoxication with
multiple nerves, especially autonomic nerves
a neurotoxin produced by Clost1idium
and cranial ne,ve VIIl, are affected. Pelipheral botulinum. It is seen in horses, cattle, nerves may also be affected by other tumors,
sheep, and birds worldwide. It is uncommon
including lymphoma and leukemia (See al.so
in dogs and pigs. (For a complete discus

NEOPLASIA OF THE NERVOUS SYSl'EM, p 1267, and
sion, seep 605 and p 2889.)

PERIPl·IERAL NEllVE SHEATH TUMORS, p 126.)

lonophore Toxicity: (See al.so 10Nor1-10RES, Paraneoplastic Neuropathy: (See
p 1175.) Ionophore toxicity has been seen in
al.sop 1280.) Paraneoplastic neuropathy is
cattle, sheep, pigs, dogs, cats, and poultry;
associated with neoplasia unrelated to
horses are particularly susceptible.

tumor infiltration of nerves. It is most

Lasalocid-contaminated food has caused
common in dogs with insulinoma but has
flaccid tetraparesis witl1 hyporeflexia in

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR JUNCTION

1243
dogs. In 1995, cat food contaminated
horses, laryngeal paralysis has also been
with sialinomycin caused an outbreak
reported. There is no specific treatment.

of polyneuropathy in -850 cats in the

Netherlands and Switzerland. Affected cats

Tick Paralysis: Rapidly progressive
had acute onset of tetraparesis, hyporeparalysis may be caused by several species of VetBooks.ir
flexia, dysphagia, respiratory weakness, and ticks (seep 1314). Some female ticks produce eventual muscle atrophy. Histopathologic
a salivary toxin that interferes with acetylchofindings consisted of degeneration of distal line release at the neuromuscular junction. In
sensory and motor axons. Affected animals

North America, De1macentor variabilis and
usually recover with supportive care and

D andersoni may affect dogs, sheep, and
removal of the offending food.

cattle. In Australia, Ixodes lwloc-yclus causes an especially severe fom1 of tick paralysis in

Organophosphate Poisoning: Poisoning
dogs, cats, cattle, sheep, pigs, llamas, horses,
involving organophosphates (seep 3064)

and occasionally people. In Africa, the major
can cause three syndromes. The acute form tick associated with paralysis is I rubicun
is due to i.1Teversible inhibition of acetylcho
dus, with cattle, sheep, goats, and rarely dogs linesterase, resulting in increased acetylaffected. A wide va.tiety of ticks affect choline activation of the nicotinic and
aninlals in Europe and Asia.

muscarinic receptors in the parasympa

Clinical signs consist of paraparesis
thetic nervous system, nicotinic receptors
that progresses within 24-72 hr to flaccid
at the neuromuscular junction, nicotinic
tetraplegia, with weak to absent spinal cord
receptors of the syn1pathetic nervous
reflexes. Sensory perception and conscioussystem, and cholinergic pathways within the ness remain normal. Dysphagia, facial

CNS. Clinical signs of acute toxicity include
paralysis, masticatory muscle weakness,
muscarinic signs ( eg, vomiting, diarrhea,
and respiratory paralysis may develop in
salivation, bronchoconstriction, increased
severe cases. Treatment consists of removal
bronchial secretions), nicotinic signs ( eg,
of the tick and application of a topical
muscle tremor and twitching), and CNS
aca.ticide to kill any hidden ticks. For all
signs ( eg, behavioral change, seizures).

except I holocyclus paralysis, prognosis is The intermediate form is prinlarily
good, and recovery occurs within 1-2 days.

manifest as generalized muscle weakness

Tick antiserum is available for treatment of
due to accumulation of acetylcholine at the

I holocyclus paralysis, but prognosis is
nicotinic neuromuscular junction, causing a
guarded because death from respiratory
depolarizing block. Cats are especially prone
pa.i·alysis may occur despite treatment.

to this form of toxicity, most conunonly due
to chlorpyrifos. Affected cats often do not

TRAUMA
have obvious signs of acute toxicity, instead
developing tetraparesis and ventroflexion

The immediate effect of injury of a
of the neck several days after exposure.

peripheral nerve is a variable degree of

Mydriasis is conunon. Diagnosis is based on
dysfunction, depending on the severity of
a history of exposure and the presence of
the injury. The mildest form of injury is
typical clinical signs. Decreased cholinester neuropraxia, which temporarily disrupts ase activity in whole blood is supportive.

function with minimal morphologic

Treatment of acute or subacute toxicity
alterations in the nerve. Axonotmesis is
should include administration of atropine
disruption of axons without disruption of the

(0.2 mg/kg, IM) if dyspnea due to bronchial
surrounding connective tissue of the nerve.

secretions and bronchoconstJ.iction is

The most severe fom1 of injury is neurotmepresent. Atropine will not relieve the sis, which is complete severance of the
nicotinic signs of tremors and weakness,
nerve. With both axonotmesis and neurotmewhich should be treated with pralidoxime sis, there is subsequent degeneration of the
chloride (20 mg/kg, IM or SC, bid). Diphenaxons distal to the injury site and in a portion hydramine ( 4 mg/kg, IM or PO, bid) may help
of the nerve proximal to the i_l\jury site.

alleviate muscle weakness. Treatment for

Diagnosis of peripheral nerve injuries is
several weeks may be necessary.

based on the history and clinical assessment

The delayed form of toxicity is associof the motor and sensory function of the ated with degeneration of distal axons in the
affected nerve(s). Electromyography often
peripheral and central nervous systems. It is
helps identify denervated muscles 5-10
unrelated to inllibition of acetylcholinesterdays after injury. Nerve conduction studies ase and is seen only with certain organomay also be useful in diagnosis.

phosphates. Signs develop several weeks

Prognosis is guarded. With neuropraxia,
after exposure and are characterized by
complete recovery usually occurs within 3
weakness and ataxia of the pelvic limbs. In
wk. For function to return after axons are

1244

DISEASES OF THE PERIPHERAL NERVES AND NEUROMUSCULAR JUNCTION
disrupted (axonotmesis, neurotmesis), the
dorsal swface of the foot with the hock
nerve must regenerate from the point of
excessively flexed. There may be loss of
injury all the way to the innervated muscle.

sensation below the stifle except for the

The growth rate of regenerating axons in
medial aspect, which is innervated by a

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the distal stump is 1-3 nun/day. Recovery
branch of the femoral nerve.

is unlikely if the severed axons are
lr\jury to the tibial nerve results in inabilsubstantially separated or if scar tissue ity to extend the hock or flex the digits as
interferes with axonal growth. Although
well as reduced sensation over the plantar
vaiious anti-inflainmatory drugs have been
surface of the foot.

recorrunended for traumatic ne1ve ir\jw·ies,
lr\jury to the peroneal nerve results
there is little evidence of benefit. Surgery
in inability to flex the hock or extend the
to appose the nerve stumps should be
digits as well as decreased sensation over
performed promptly in cases in which the
the crai1iodorsal surface of the foot, hock,
nerve has been sharply transected. In
and stifle.

instances of blunt trawna, surgical

The femoral nerve may be injured in
exploration and excision of scar tissue may
calves ai1d foals during dystocia if excessive
help. Surgery is often successful in horses
traction stretches or otherwise dainages it.

with fibrous compression of the supra

This results in an inability to bear weight on
scapular nerve. Longterm management
the limb because of an inability to extend
consists of physical therapy to minimize
the stifle. The patellai· reflex is weak or
muscle atrophy and decreased mobility of
absent. Sensation is lost along the medial
joints. Bandages or splints may be
swface of the limb (saphenous nerve).

necessary to help protect the affected limb.

The suprascapular nerve is most
commonly injured in large aninlals

Brachia! Plexus Avulsion: Traumatic
secondaiy to trauma of tl1e shoulder region.

ir\jury to the C6 to T2 nerve roots that

This results in atrophy of the supraspinatus
innervate the thoracic limb can lead to
and infraspinatus muscles and instability of
brachia! plexus avulsion in dogs, cats, ai1d
the shoulder joint (sweeney, seep 1129). In birds. With severe extension or abduction of
horses, the nerve may be entrapped by
the limb, the nerve roots stretch or tear from
connective tissue that develops in the
their attachment to the spinal cord. Clinical
region of the supraspinous fossa.

signs vary with tl1e extent of root involvement. Complete avulsion results in flaccid Calving Paralysis: Calving paralysis is
pai·alysis of the limb, anesthesia distal to the
seen in heifers witl1 oversized fetuses. It has
elbow, ipsilateral Homer syndrome, and
previously been attributed to bilateral
ipsilateral loss of the cutai1eous trunci
compression of the obturator nerve, but

(panniculus) reflex. The injured ailinlal
damage to the sixth lwnbar ne1ve root,
bears little or no weight on the limb and
which contributes to the obturator and
drags the dorsal surface of the paw on the
sciatic nerve, probably accounts for most of
ground. Sensation to the ventral surface of
the paralysis. Ischernic necrosis of muscles
the paw is spared if only the cranial nerve
secondaiy to compression, and ruptures
roots are affected. Avulsion of the caudal
of muscles during attempts to 1ise, also
nerve roots causes loss of sensation on the
contribute to the parapai·esis. Additionally,
caudal surface of the limb with variable loss
metabolic derai1gements, such as hypocalceon the cranial surface.

mia, may complicate the syndrome. (See also

There is no treatment, and with complete

BOVINE SECONDARY RECUMBENCY, p 1188.)

avulsion, the prognosis is poor. Amputation
of the limb may be necessary because of

Facial Nerve Trauma: Facial nerve
danrnge from dragging or self-mutilation.

trauma is most common in large ailirnals

Recovery is possible in mild cases in which
that become recurnbent with subsequent
the roots are contused rather than avulsed.

compression of the side of the face. It can be
caused by pressure from a halter in horses

Peripheral Nerve Injuries: These ir\juries
during general anesthesia. There is ipsilaare some of the most common neuropathies teral lip paralysis, deviation of tl1e muzzle to
in aninlals. The sciatic nerve or its branches
the contra!ateral side, ai1d weak to absent
may be injured by pelvic fractures, during or
palpebral reflex. A drooping ear ca.ii result
after retrograde placement of intrainedullaiy
from injuries to the proxin1al aspect of the
pins in the femur, or by ir\jections of irritating
nerve.

substances in or near the nerve. Dainage to
the proxin1al aspect of the sciatic nerve

VASCULAR DISEASES
causes monopai·esis with inability to flex
tl1e stifle. The hock and digits cannot flex
lschemic Neuromyopathy: Ischenlic
or extend, ai1d weight is supported on the
neuromyopathy is most common in cats

DISEASES OF THE SPINAL COLUMN AND CORD

1245
with arterial thromboembolism secondary
lower thigh and are characterized as focal
to myocardial disease. It also is seen in dogs
muscle necrosis and degeneration of the
with a variety of underlying disorders,
central portions of the sciatic nerve and
including hyperadrenocorticism, hypothyits branches. Management consists of roidism, renal disease, cancer, and heart
analgesics, nursing care, and treatment of

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disease. Occlusion occurs most commonly
any underlying disease ( eg, cardiomyopaat the distal aortic trifurcation, resulting in thy ). Thrombolytic therapy with streptokiischemia of muscles and nerves in the pelvic nase or tissue plasminogen activator does limbs. There is acute, painful para.paresis
not improve survival. Anticoagulants,
and an inability to flex or extend the hock.

such as unfractionated heparin or low

The flexor reflex and, in some cases, the
molecula.r-weight heparin, are used to
patellar reflex are lost. Sensation distal to
reduce continued thrombus formation.

the hock is decreased. The gastrocnemius

Neurologic deficits may improve within
and cranial tibial muscles are often firm and

2-3 wk, but 6 mo may be requi.red for
painful. The nails may be cyanotic, and the
complete recovery. Permanent deficits are
femoral pulses are weak or absent.

possible. Approximately 60% of affected

Diagnosis can usually be made based
cats die or a.re euthanized during the initial
on clinical featmes. Serun1 CK is often
episode. In the cats that survive, the
increased. Doppler ultrasonography helps
longterm prognosis is guarded (median
evaluate blood flow in the distal aorta and

12 mo) because of the underlying heart
femoral arteries. Pathologic changes are
disease and high risk of recurrence of
present distal to the level of the middle to
thromboembolism.

DISEASES OF THE SPINAL COLUMN

AND CORD

Diseases of the spinal column and cord
congenital stenosis of the vertebral canal
include congenital disorders, degenerative
or hypertrophy of the liga.mentum flavum.

diseases, inflanunatory and infectious

Bony-associated compression affects young
diseases, neoplasia, nutritional diseases,

(several months to 4 yr), giant-breed dogs,
trauma, toxic disorders, and vascular
including Great Danes, Mastiffs, and
diseases. Many of these diseases are

Rottweilers. Spinal cord compression is
discussed in full in other chapters and are
due to bony proliferation of the articular
only b1iefly described here. For a discussion processes and pedicles, usually of the C4
of congenital disorders related to the spinal
to C7 vertebrae.

column and cord, seep 1222.

Clinical signs can be acute or slowly
progressive. Mild cases are characterized by

DEGENERATIVE DISEASES
subtle ataxia of all limbs, often evident as a
long, protracted stride in the pelvic limbs,

Cervical Spondylomyelopathy: Cerviwith short-strided gait in the thoracic limbs.

cal spondylomyelopathy, also called cervical

In severe cases, there is paresis or paralysis
vertebral malfom1ation-malarticulation and
of all limbs. Neck pain is variable. Differenwobbler syndrome, is compression of the tial iliagnoses include congenital anomalies,
spinal cord caused by abnmmal development trauma, meningomyelitis, discospondylitis, of the cervical ve1tebrae. Genetic factors and
and neoplasia. Survey radiographs cannot
possibly nutrition may be involved.

confinn a diagnosis of cervical spondylomy

In dogs, there are two fom1s of the
elopathy but are useful in excluding
disease, disc-associated wobbler syndrome
discospondylitis and bony neoplasia.

(DAWS) and bony-associated cervical

Definitive diagnosis requires myelography,
spondylomyelopathy. DAWS affects

CT,orMRI.

middle-aged (mean 7 yr), large-breed dogs,

Nonsurgical treatment is indicated for
especially Dobennan Pinschers. There is
dogs with mild signs and consists of
ventral compression of the spinal cord due
exercise restriction and prednisone
to protrusion of one or more caudal cervical

(0.5 mg/kg/day). Signs improve in -500/oof
discs, in some cases complicated by
dogs and remained unchanged in -25% of

1246

DISEASES OF THE SPINAL COLUMN AND CORD
dogs with nonsurgical treatment. Surgery
therapy or there a.i·e neurologic deficits. The
is indicated in animals with substantial
most conunon technique is dorsal la.tninecneurologic deficits and in those that do tomy with partial discectomy, but forarnenotnot respond adequately to nonsurgical omy or stabilization is indicated in certain
treatment. The specific technique is based
cases. Approximately 70%--95% of dogs

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on the changes evident on imaging and
improve with surgery, although preexisting
include ventral slot with pa.itial discectomy,
uri.na.ty incontinence may not resolve.

dorsal larninectomy, or distraction and
fusion of affected vertebrae. Overall, --800A,

Degenerative Myelopathy of Dogs:

of dogs do well with surgery.

Degenerative myelopathy of dogs, also

In horses, cervical spondylomyelopathy
called chronic degenerative radiculomyis the most common noninfectious disease elopathy, is a slowly progressive, noninflamof the spinal cord and occurs in ma.i1y matory degeneration of the axons and
breeds. Most horses present at <3 yr of age,
myelin primarily affecting the white matter
although they can be affected at any age.

of the spinal cord. It is most conunon in

The mid-cervical region is most commonly

German Shepherds, Pembroke Welsh
affected, and there is spinal ataxia and

Corgis, Boxers, Rhodesian Ridgebacks,
tetraparesis. Diagnosis is based on imaging
and Chesapeake Bay Retrievers, but is
and excluding other causes. Plain radiooccasionally recognized in many other graphs may show abnormal a.tticular facets
breeds. The cause is a mutation in the
and stenosis of the vertebral canal.

superoxide dismutasel (SOD!) gene,

Myelography is necessary for definitive
inherited in an autosomal recessive pattern
diagnosis and surgical pla.tU1ing. Nonsurgiwith incomplete penetra.t1ce. It is similar to cal treatment involves NSAIDs a.t1d dimethyl fa.tnilial arnyotrophic lateral sclerosis in sulfoxide to reduce inflanunation. ln
hwnan patients. Pathologically, there is
yearlings, diet modification can help.

noninfla.i1unato1-y degeneration of axons in

Surgery most commonly involves ventral
the white matter of the spinal cord, which
fusion of the affected vertebrae. Approxiis most severe in the thoracic region.

mately 8()0A, of affected horses in1prove with

Affected dogs are usually >8 yr old and
surgery. Owner!Iider safety is a major
develop an insidious onset of nonpainful
concern in horses with ataxia.

ataxia and weakness of the pelvic limbs.

Spinal reflexes are usually normal or

Degenerative Lumbosacral Stenosis:

exaggerated, but in adva.i1ced cases there

Narrowing of the lumbosacral vertebral
is flaccid tetraparesis a.t1d hyporeflexia
canal or inte1ve1tebral foramina results in
reflecting lower motor neuron involvecompression of the cauda equina or nerve ment. Early cases may be confused with
roots. It is most common in large breeds of
orthopedic disorders; however, propriodogs, especially German Shepherds, and is ceptive deficits are an early feature of
rare in cats. It results from degeneration and
degenerative myelopathy a.t1d are not seen
protrusion of the L 7-Sl disc, hypertrophy of
in orthopedic disease.

the ligarnentum flavum, or rarely subluxation

Myelography or MRI and CSF analysis
of the lwnbosacraljoint. The cause is
are essential to exclude compressive and
unlrnown, although Geiman Shepherds with
infla.tnrnato1-y diseases. A DNA test based on
congenital transitional vertebrae are at
the SOD l gene is available on the Orthopeincreased risk. Clinical signs typically begin dic Foundation for Animals Web site. Dogs
at 3--7 yr of age and may include difficulty
that are homozygous for the mutation are at
using the pelvic limbs, pelvic limb la.ineness,
risk of the disease and will pass one copy of
tail weakness, and incontinence. Pain on
the mutant allele to their offspring. Heterozypalpation or extension of the lumbosacral gotes are at low risk of the disease but have
joint is the most consistent finding. There
a 500A, chance of passing one copy of the
may be proprioceptive deficits, muscle
mutant allele to each offspring. Homozygous
atrophy, or a weak flexor reflex in the
normals are at low risk of the disease and
pelvic limbs. Plain radiographs may show
will not pass the mutation to offspring.

degenerative changes, but definitive

There is no specific treatment and no
diagnosis requires MRI, CT, or epidurograevidence that glucocorticoids, other drugs, phy. Dogs in which mild pain is the only sign
or supplements alter the course of the
may improve with 4-6 wk of rest. Epidural
disease. Most dogs are euthanized because
irtjection of methylprednisolone acetate
of disability within 1-3 yr of diagnosis.

(1 mg/kg on each of day 1, day 14, and day

42) is effective in --800A, of dogs with pain

Equine Degenerative Myeloencepha
a.t1d minimal neurologic deficits. Surgery is
lopathy: Equine degenerative myeloenindicated when pain is refractory to medical cephalopathy is a progressive neurologic

DISEASES OF THE SPINAL COLUMN AND CORD

1247
disorder of horses and zebras characterized
logic deficits, ranging from mild tetraparby diffuse degeneration of axons, myelin, esis to tetraplegia. In thoracolwnbar disc
and neurons in the spinal cord and, to a
herniation, there may be back pain, evident
lesser degree, the brain stem. It has been
as kyphosis and reluctance to move.

reported in many equine breeds in North

N eurologic deficits are usually more severe

Ametica, Australia, and England. The cause
than those seen in cervical disc disease and

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is incompletely understood, but a vitan1in E
range from pelvic limb ataxia to paraplegia
deficiency and genetic factors are susand incontinence. In paraplegic animals, pected. Clinical signs usually become
the most important prognostic finding is
apparent during the first year of life and
whether there is deep pain perception
consist of ataxia and weakness in all four
caudal to the lesion. This is assessed by
limbs, although the hindlimbs may be more
pinching the toe or tail and observing
severely affected. Clinical signs may
whether there is a behavioral response,
stabilize or slowly progress. There is no
such as a bark or turn of the head. It is
definitive diagnostic test. Clinical diagnosis
in1portant to pinch the bone to stimulate
is based on clinical features and excluding
deep pain receptors, not just the skin, which
other causes. Myelography and CSF
tests only superficial pain. Reflex flexion of
analysis are nonnal. Supplementation of
the limb must not be mistaken for a behavpregnant mares and newborn foals with ioral response.

vitamin E is preventive in predisposed

Definitive diagnosis of disc extrusion is
families, and affected horses may in1prove
based on in1aging studies. Spinal radiowith vitan1in E supplementation.

graphs may show narrowing of the affected
disc space, inte1ve1tebral foran1en or
lntervertebral Disc Disease: Degenarticular facets, or radiodense calcified eration and subsequent herniation of the
disc material within the ve1tebral canal.

intervettebral disc results in compression of However, radiographs are not sensitive or the spinal cord, spinal nerve, and/or nerve
specific enough for definitive diagnosis,
root. It is a common cause of spinal cord
which requires myelography, MRI, or CT.

disease in dogs, with a lifetime prevalence

Dogs witl1 pain and mininlal to moderate
of --3.5%. Clinical signs due to disc disease
neurologic deficits often recover with 2-3
are rare in cats and horses. Chondrodyswk of cage rest. A short course of predtrophoid breeds of dogs ( eg, Dachshw1d, nisone (0.5 mg/kg/clay for 3 days) is often

Beagle, Shih Tzu, Lhasa Apso, and
helpful in relieving pain. The use of

Pekingese) are most commonly affected,
anti-inflanimatory or analgesic medication
with Miniature Dachshunds having a
without concurrent cage rest is contraindilifetin1e prevalence of --200/o. In these breeds, cated, because an increase in the dog's there is chondroid degeneration of the discs
activity may lead to further disc extrusion
within the first few months of life. Disc
and worsening of spinal cord compression.

extrusion can occur as early as 1-2 yr of age, Clinical signs recur after conservative and clinical signs are often acute and
therapy in 300/o-40% of cases.

severe. In contrast, fibroid disk degenera

In animals with severe neurologic
tion typically occurs in large breeds of dogs
deficits, prompt surgery offers the best

>5 yr old and causes slowly progressive
chance of recovery ( see TABLE 1). Other clinical signs.

indications for surgery are failure of

The most common sites of disc herniation conservative therapy and recurrent are the cervical and tl1oracolwnbar regions.

episodes. Hemilanlinectomy with removal

The predominant sign of cervical disc
of the extruded disc material is the most
herniation is neck pain, manifested as
common procedure. Prophylactic
cervical rigidity and muscle spasms. There
fenestration of commonly affected disc
may be thoracic lin1b lan1eness or neuro-
spaces (eg, T l l tllrough IA) decreases
recurrence in small-breed dogs. Progressive
myelomalacia develops in 5%--100/o of dogs
with paraplegia and loss of deep pain
perception. In this syndrome, affected dogs
develop flaccid tetraplegia, the level of
anesthesia ascends cranially, and respiratory paralysis develops.

Diffuse Idiopathic Skeletal Hyperostosis: Also known as Forestier lntervertebral disc extrusion, L3-L4, in a dog.

disease in hun1an patients, diffuse

Courtesy of Dr. William Thomas.

idiopathic skeletal hyperostosis (DISH) is

1248

DISEASES OF THE SPINAL COLUMN AND CORD

RECOVERY RATES AFTER SURGERY FOR INTERVERTEBRAL DISC

DISEASE IN DOGS

Patient Type

Recovery Rate

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Nonambulatory small-breed dog with thoracolwnbar extrusion and 85%--95%
intact deep pain

Small-breed dog with thoracolW11bar extrusion and loss of deep 50%
pain<24hr

Small-breed dog with thoracolwnbar extrusion and loss of

<50%
deep pain >24 hr

Nonambulatory large-breed dog with chronic thoracolW11bar 25%--50%
protrusion

Ambulatory dog with cervical disc disease

95%

Nonambulatory dog with cervical disc disease

65o/o--95%
characterized by ossification of entheses,
factor. Adult horses of any age and breed can
the sites where a ligament, tendon, or joint
be affected, although Quarter horses are
capsule inserts into bone. Radiographic
affected most conunonly. Affected horses
criteria for diagnosis are flowing ossificatypically do not have access to pasture grass tion along the ventrolateral aspect of at least and are fed poor-quality grass hay.

four contiguous ve1tebrae with relative

Clinical signs consist of generalized
preservation of disc width and absence
synunetric weakness, trembling, and muscle
of facet joint ankylosis. Approximately
atrophy. Affected horses often stand with

4% of dogs > 1 yr old are affected, and the
their head held low and their feet camped
prevelance increases with age. As with
under their body, frequently shifting their
spondylosis deforrnans, Boxers are at
weight from one limb to another. Ataxia is
increased risk, with a prevelance of --400/o.

not a feature of this disease, in contrast to

The thoracic and lW11bar regions are most
most spinal cord diseases. Many affected
commonly affected. It is unclear how often
horses have retinal abnormalities, including

DISH causes clinical signs, and in many
a distinct reticulated pigment pattern and
cases the radiographic findings a.re
areas of hyperreflectivity. Electromyograincidental. However, spinal pain and phy and biopsy of the spinal accessory nerve
stiffness is possible and, in those cases,
or the sacrodorsalis caudalis muscle a.re
treatment is analgesics as needed.

useful in diagnosis.

There is no specific treatment, but some

Equine Motor Neuron Oise se:

horses improve partially after 2--3 mo of

Equine motor neuron disease is a progresillness. Horses that lack access to green sive, noninflammatory degeneration of
forage high in vitamin E for prolonged
motor neurons in the spinal cord and brain
periods should be supplemented with
stern of horses. It is most co nun on in the
vitaminE.

northeastern USA but has been reported in
several areas of North and South America,

Europe, and Japan. The cause is uncertain,

Degeneration of Motor Neurons:

but vitamin E deficiency is a strong risk

Degeneration of motor neurons is an
inherited or sporadic disease seen in

Brittany Spaniels, Pointers, German

Shepherds, Dobern1an Pinschers, and

Rottweilers; ca.ts; Hereford, Brown Swiss,
and red Danish cattle; Yorkshire pigs; and
goats. Also called spinal muscular atrophy, this disease is characterized by progressive
paresis, tremor, muscle a.trophy, and weak
spinal reflexes. The age of onset is typically
within the first 1-2 yr of life. Electromyography and muscle biopsy help docW11ent Diffuse idiopathic skeletal hyperostosis
muscle denervation, but definitive diagnosis

(DISH) in a dog. Courtesy of Dr. William Thomas.

is based on loss of motor neurons in the

DISEASES OF THE SPINAL COLUMN AND CORD

1249

Some of the more common infectious and
inflarrunatory diseases in which involvement of the spinal colmnn or cord is a prominent feature are discussed below.

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Bacterial Diseases

Discospondylitis is inflammation of the

Spondylosis deform ans in a dog. Courtesy of Dr.

intervertebral disc and adjacent vertebral

William Thomas.

bodies. Vertebral osteomyelitis is
inflan1mation of the vertebra without
ventral horn of the spinal cord and
concurrent disc infection. Both diseases are
brain-stem nuclei on necropsy.

usually caused by hematogenous spread of
bacterial or fungal infection. Immunosup

Metabolic Storage Disorders: Rare,
pression may play a role in some infections.

usually inherited, metabolic disorders can

Discospondylitis is most common in dogs,
affect the CNS, including the spinal cord.

especially larger breeds. Osteomyelitis of

(See also
the lumbar vertebrae can develop in dogs

CONGENITAL AND INHERITED ANOMALIES

OF'THE NERVOUS SYSTEM, p 1222.)

secondary to migration of plant awns. ln
cats, it is rare and usually due to direct

Spondylosis Deformans: Spondylosis
spread of infection from an adjacent wound.

defonnans is a noninflammatory condition

Discospondylitis and vertebral osteomyelicharacterized by formation of bony tis have also been reported in horses,
projections ( enthesophytes) at the location
ruminants, and pigs, especially neonates.

where the annulus fibrosus is attached to

Infection may be seen at any disc space,
the cortical surface of adjacent vertebrae.

and multiple lesions may be seen.

These bony growths vary from small spurs

1n canine discospondylitis, the most
located several millimeters from the
commonly isolated organisms are
junction between the disc and vertebra

Staphylococcus spp. Other organisms
to bony bridges that span the disc space
include Brucella canis, Streptococcus spp,
leaving at least part of the ventral surfa�e of

Escherichia coli, Proteus spp, Corynebac
the vertebra unaffected. The enthesophytes
terium .diphtheroides, Nocardia spp, and
typically expand laterally and ventrally but

Aspergillus spp. Spinal pain is the most
not dorsally and therefore rarely affect the
consistent clinical finding. Systemic signs,
spinal cord. The cause is breakdown of the
such as fever, depression, and weight loss,
outer fibers of the annulus fibrosis and
are less common. Neurologic deficits may
stretching of the longitudinal ligament. The
develop due to spinal cord compression
increased stress at the vertebral attachment
caused by proliferative tissue or rarely
of the longitudinal ligament incites bony
spread of infection to the spinal �ord o;
production.

pathologic fracture.

Spondylosis deformans is seen in dogs,
cats, and bulls, and the incidence increases
with age. It is uncommon in dogs <2 yr old;
by 9 yr of age, 25%- 709'o of all dogs are
affected. It is especially common in Boxers,
and a genetic predisposition has been
identified in this breed. It is typically an
incidental radiographic finding, and there

1s no correlation between the presence of
spondylosis and clinical signs. Rare cases
cause spinal hyperesthesia, which should
be treated with analgesics.

INFLAMMATORY AND

INFECTIOUS DISEASES

Infectious and inflammatory diseases of
the spinal column and spinal cord include
bacte1ial, rickettsial, viral, fungal, protozoa!,
and parasitic infections and idiopathic
inflammatory disease. Many of these

Spinal vertebral body abscess (cross-section).

diseases can also affect the brain (seep 1262). Courtesy of Dr. Sameeh M. Abutarbush.

1250

DISEASES OF THE SPINAL COLUMN AND CORD

Early radiographic findings consist of
poor for severely affected dogs. Vaccination
destruction of the adjacent vertebral end
is usually successful in preventing the
plates and collapse of the disc space. More
systemic form of distemper, but previously
advanced lesions also have variable degrees
vaccinated dogs can be affected by the
of osteophyte fom1ation. Blood and urine
neurologic form.

cultures often identify the causative

Caprine arthritis and encephalitis

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organism. Affected dogs should be tested

( see p 7 4 7) is caused by a lentivirus that can for brucellosis (seep 1402).

also cause pneumonitis and arthritis. CNS

Although clinical signs usually resolve
disease is most common in goats 2-4 mo
within 5 days of treatment with an
old, although older animals may also be
appropriate antibiotic, treatment should be
affected. There is an acute onset of slightly
continued for at least 8 wk. Amoxicillin/
asymmetric spastic paraparesis that may
clavulanic acid for presumed Staphylococ
progress to tetraplegia with exaggerated
cus spp infection is a good choice if cultures reflexes. A mononuclear pleocytosis and are negative.

increased protein in the CSF are present in

-500A, of the cases. Serologic testing is

Rickettsial Diseases
helpful in detecting infection, but false

Neurologic abnormalities, including signs
negatives can be seen. Histologically, there
of spinal cord dysfunction, are sometimes
is severe nonsuppurative inflammation
seen in dogs with rickettsial infection. Dogs
with demyelination or necrosis, most
with Rocky Mountain spotted fever
prominent in the white matter of the spinal

(Rickettsia rickettsii, seep 806) often have cord. There is no treatment, and recovery
thrombocytopenia, leukocytosis,
is unlikely.

and a neutrophilic pleocytosis and mildly

A related lentivirus is a rare cause of
increased protein on CSF analysis.

chronic encephalomyelitis in sheep (maedi,

Diagnosis is based on a 4-fold increase in
seep 1475). Affected sheep are usually >2 yr serwn antibody concentration. Dogs with
old and suffer an insidious onset of
ehrlichiosis (Ehrlichia canis, seep 803)

progressive ataxia, paraparesis, or
often have thrombocytopenia, anemia,
tetraparesis.

leukopenia, hyperglobulinemia, and

Equine infectious anemia (seep 699)

mononuclear pleocytosis and marked
occasionally produces encephalomyelitis
increase in protein on CSF analysis. A single in horses. Neurologic deficits are usually serum antibody titer is usually sufficient for
referable to spinal cord disease and include
diagnosis of E can is. Treatment of
ataxia and weakness in the hindlin1bs. The
rickettsial myelitis consists of doxycycline
protein concentration of and the number of
or chloramphenicol for 14--21 days.

lymphocytes in the CSF are often increased.

Prognosis is good with early treatment,

Diagnosis is by positive agar gel imrnunodifalthough neurologic deficits occasionally fusion testing. There is no treatment, and
progress despite treatment.

affected horses are usually euthanized to
prevent spread of the disease.

Equine herpesvirus 1 (EHV-1)

Viral Diseases
encephalomyelopathy is a neurologic

Canine distemper encephalomyelitis
disorder that affects horses worldwide. The

(seep 777), caused by a paramyxovirus,

EHV-1 virus infects vascular endothelial
remains one of the most conunon CNS
cells, particularly those within the CNS, and
disorders in dogs worldwide. Onset of
causes an immune-mediated vasculitis with
neurologic deficits may be acute or slowly
secondary infarction and hemorrhage
progressive, reflecting the location of the
throughout the brain and spinal cord. The
lesion(s) within the CNS. The brain stem

EHV-1 virus has also been associated with
and spinal cord are the regions most
meningoencephalitis in alpacas and llamas.

conm1only affected in mature dogs.

In horses, neurologic signs may be seen as

Neurologic signs are usually not preceded
the p1irnary disease or follow rhinopneumoby, nor coincident with, the systemic illness nitis or abortion. Any age animal may be
seen in young dogs.

affected.

Definitive antemortem diagnosis is

Neurologic deficits have an abrupt onset,
difficult. There may be active or inactive
vary from mild hindli.mb ataxia to paraplechorioretinitis on fundoscopy. A lymphogia, and usually do not progress after 24 hr.

cytic pleocytosis with increased protein

Urine dribbling, fecal retention, and sensory
concentration is the most conunon finding
deficits in the perineum and tail are
on CSF analysis. Reverse transcriptase-PCR
common. The CSF is often xanthochromic
on urine or CSF is useful in diagnosis. There
with increased protein content and nom1al
is no specific treatment, and the prognosis is numbers of cells. Diagnosis is based on

DISEASES OF THE SPINAL COLUMN AND CORD

1251
clinical findings and an increase in antibody

Older pigs may survive, but mortality is high
concentration in paired serum samples,
in young pigs.

isolation of virus from nasal or pharyngeal

Porcine hemagglutinating encephalo
secretions, or PCR testing. There is no
myelitis virus is a coronavirus that causes
specific treatment, but anti-inflammatory
both vomiting and wasting disease (see

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agents such as dimethyl sulfoxide,
p 728) and an encephalomyelitis. It is most
dexamethasone, and NSAIDs may help.

common in piglets <3 wk old, and there is

Supportive care is important to prevent
some overlap of these syndromes. The CNS
complications such as urine retention,
disease starts with several days of vomiting,
cystitis, and decubitus. Mildly affected
which is followed by hyperesthesia, muscle
horses often recover with supportive care.

tremors, ataxia, paresis, opisthotonos,

Even recumbent horses can eventually
coma, and death. Histopatl10logically, there
recover with meticulous nursing care.

is diffuse nonsuppurative encephalomyeli

Vaccination does not protect from the
tis, primarily involving gray matter.

neurologic form of this disease. (See

Diagnosis is based on necropsy or an
also EQUINE HERPESVlRUS INFECTION, p 1444.) increase in antibody titer in paired sera.

Feline infectious peritonitis (see

There is no treatment.

p 780) is a disease of domestic cats caused

Rabies (seep 1302) is caused by a
by an immune-mediated response to a
neurotropic rhabdovirus that reaches the
coronavirus. CNS involvement is common.

CNS via peripheral nerves. It produces

There are pyogranulomatous lesions
multifocal, nonsuppurative polioencephaloinvolving the neural parenchyma, choroid myelitis in all domestic mammals. Signs of
plexuses, ependyma, and leptomeninges.

spinal cord involvement include ataxia and

Clinical signs of spinal cord involvement
progressive paralysis, usually with absent
include spinal hyperesthesia and paraparereflexes. Affected animals typically, but not sis or tetraparesis. Hyperglobulinemia and
invariably, die with progressive neurologic
involvement of other organs, especially the
signs within 2-7 days of illness.

eyes, are common. Serum antibody tests
currently available are insensitive and

Fungal Diseases
nonspecific. A mixed ( neutrophilic and
mononuclear) pleocytosis with increased

Cryptococcus neoformans is the most
protein concentration is the most common
common fungus to involve the CNS in
finding on CSF analysis. There is no
animals. Infection is most common in dogs
effective treatment, and prognosis is poor.

and cats and occurs occasionally in horses.

Feline leukemia virus-associated

Other fungal organisms may invade the
myelopathy is seen in some cats infected

CNS, including Blastomyces de1malilidis,
with the feline leukemia virus (FeLV, see

Hisloplasma capsulalum, Coccidioides
p 790) for ;,,2 yr. Ataxia and weakness of the
immitis, Aspergillus spp, and phaeohyphopelvic limbs progresses to paraplegia within mycoses. Affected animals often have

1 yr. Other signs include diffuse spinal pain
involvement of other organs, such as the
and abnormal behavior. Diagnosis is based
lungs, eyes, skin, or bones. Signs of spinal
on clinical features, FeLV serology, and
cord involvement include paresis or
exclusion of other causes, such as spinal
paralysis and spinal hyperesthesia.

lymphoma and myelitis due to toxoplas

Diagnosis is based on serology, culture,
mosis or fungal infection. There is no
or identifying the organism in CSF or
treatment; affected cats are eventually
extraneural tissue. Fluconazole is often
euthanized because of disability. Pathologic
effective for cryptococcosis and coccidioifindings consist of white matter degeneradomycosis. Itraconazole or amphotericin B
tion, swollen axons, and dilation of myelin
is recommended for histoplasmosis and
sheaths in the spinal cord and brain stem.

blastomycosis, but the prognosis is guarded

FeLV antigen is present in the nervous
to poor. (See also FUNGAL INFECTIONS, p 632.) system, indicating that the lesions are due
to viral infection.

Protozoa! Diseases

Teschovirus encephalomyelitis (see

Equine protozoa! myeloencephalitis
p 1307), also called Teschen disease, Talfan

(seep 1309) is a conm10n disease of horses
disease, and porcine polioencephalomyelithat produces a nonsuppurative, often tis, is caused by a neurotropic teschovirus
necrotizing, meningoencephalomyelitis.

previously classified as an enterovirus.

Horses are likely an aberrant host for the

There is a peracute or subacute onset of
causative organism, usually Sarcocyslis
hindlin1b ataxia and paresis with hypore
neurona, but less commonly, other
flexia, depression, seizures, and death.

protozoa cause the disease. N eurologic

1252

DISEASES OF THE SPINAL COLUMN AND CORD
signs are extremely variable and often

An1erica, Europe, and Australia. The cause
asymmetlic, reflecting involvement
is Wlknown, but an infectious agent,
anywhere in the CNS. Ataxia and paresis
probably a virus, is strongly suspected. The
are common. Other potential signs include
disease causes neuronal degeneration,

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obscure lameness, focal muscle atrophy,
axonal loss, and demyelination with
and cranial nerve dysfunction. Approximononuclear inflammation, most severe in mately 75% of affected horses in1prove with
the thoracic segments of the spinal cord.

treatment, but pennanent neurologic

The clinical course is marked by progresdeficits are possible and relapse is not rare.

sive paraparesis of 1-2 mo duration, often

Neosporosis (seep 663) is caused by
with focal hyperesthesia, head tremor, and

Neospora caninum, a protozoan that can
behavioral changes. Antemo1tem diagnosis
cause a nonsuppw·ative encephalomyelitis,
is difficult. There is no treatlnent, and
most commonly in dogs. Infection in young
prognosis is poor.

puppies typically causes ascending

Granulomatous meningoencephaloparalysis with rigid contraction of the myelitis (GME) is an inflanm1atory disease
muscles of one or both pelvic limbs. Other
of the CNS in dogs worldwide. The cause is
organs, including muscle, liver, and lungs,
w1known, although an infectious agent,
can be affected. Diagnosis is based on
most likely a virus, is suspected. In the
detection of antibodies to the organism by
disseminated form, previously called inflamin1munohistochemistry or PCR. Early matory reticulosis, there are perivascular
treatment with clinda.mycin or sulfadiazine
accwnulations of mononuclear cells and
and pyrimethan1ine may be effective, but
neutrophils. In the focal fonn, previously
the prognosis is poor.

called neoplastic reticulosis, there are gran

Toxoplasmosis (seep 685) is caused by
ulomatous lesions containing primarily

Toxoplasma gondii and can occasionally
reticulohistiocytic cells. Adult dogs of
cause a nonsuppurative encephalomyelitis
any breed can be affected, but female,
in puppies, kittens, and piglets. Diagnosis is
small-breed dogs, especially Poodles, may
based on identifying the organism in tissue
be predisposed.

or a 4-fold increase in IgG antibody in paired

Clinical signs are variable and may
sera. In cats, a high concentration of IgM
indicate focal or multifocal brain or spinal
antibody in serwn or CSF supports the
cord dysfunction. Cervical pain and tetradiagnosis. Clindamycin or sulfadiazine paresis are the most conunon signs of
and pyrimethamine are recommended
spinal cord involvement. Signs are often
for treatlnent.

acute, but the focal fonn of GME can cause
neurologic deficits that slowly progress

Parasitic Diseases
over the course of several months. The CSF

Verminous myelitis is i.Rflanm1ation of the
usually has increased protein and pleocytospinal cord caused by parasite migration.

sis, with either mononuclear cells or

Organisms include Parelaphostrongylus
neutrophils predominating. MRI and CT
tenuis in sheep, goats, and llamas;
often show a single or multiple enhancing

Hypoderma bovis in cattle; Strongylus
masses. Tentative diagnosis is based on
vulgaris, Halicephalobus deletrix, and
clinical findings, inrnging, CSF analysis, and

Setaria spp in horses; Stephanurus
exclusion of other possible diseases. Dogs
dentatus in pigs; Cuterebra spp in cats; and often in1prove with immunosuppressive

Baylisascaris procyonis in dogs. Signs of
doses of corticosteroids and other
spinal cord involvement are usually acute,
immW1omodulating drugs such as
often asymmetric, and may be progressive.

cytarabine, cyclosporine, and procarbazine,

Antemo1tem diagnosis is difficult. Increased but relapse is possible, and many dogs eosinophils in the CSF is suggestive, but
eventually become refractory to treatlnent.

CSF findings are variable. Treat111ent with
fenbendazole, thiabendazole, or ive1mectin

NEOPLASIA
is recommended, but the prognosis is
guarded. (See also

See also

CNS DISEASES CAUSED BY

NEOPLASIA OF Tl IE NERVOUS SYSTEM,
p 1267.

HELMINTHS AND ARTHROPODS, p 1310.)

In dogs, neoplasms commonly affecting
the spinal cord include osteosarcoma,

Idiopathic Inflammatory Diseases
fibrosarcoma, meningioma, nerve sheath

Feline nonsuppurative meningoencephtumor, and metastatic neoplasia. A ttunor alomyelitis (feline polioencephalomyelilis,
resembling nephroblastoma is seen in
staggering disease) is a slowly progressive,
young dogs (5-36 mo of age), with German
inflammatory disease of the CNS in domes

Shepherds affected most commonly. This
tic cats. It has been repo1ted in North
tumor is consistently located within the

DISEASES OF THE SPINAL COLUMN AND CORD

1253
chemotherapy, such as prednisone,
vincristine, and cyclophosphan1ide.

Remission is possible in many cases, but
longtem1 prognosis is poor.

In cattle, lymphosarcoma may develop

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in the epidural space at any level, causing
spinal cord compression. Often, there is an
acute onset of paraparesis or recumbency.

Usually, there is other evidence of bovine
leukosis (seep 743). Definitive diagnosis is based on histopathologic examination.

N eoplasia is a rare cause of spinal cord
disease in horses, pigs, sheep, and goats.

NUTRITIONAL DISORDERS

Copper Deficiency: Deficiency of copper
causes CNS disease in sheep, goats, and
pigs. Swayback is the congenital fom1 in
lambs and is characterized by degeneration
and necrosis of the cerebrum. The acquired
form, enzootic ataxia, affects lambs, kids,
and pigs. Affected aninlals appear nom1al at
birth but develop progressive paraparesis
with hyporeflexia and muscle atrophy
within the first few months of life. Other
signs include diarrhea and unthriftiness
and, in lan1bs, abnormal fleece. Histologically, there is chromatolysis and loss of neurons and degeneration of axons,
primarily in the spinal cord and caudal
aspect of the brain stem. Animals may
improve with copper supplementation, but
permanent neurologic deficits are likely in
severely affected animals.

Hypervitaminosis A: Cats fed excess
vitamin A, usually from diets consisting

Spinal meningioma, T13, in a dog. Note
widening of the contrast column on the right
largely of liver, develop extensive exostoses,

("golf-tee sign") indicatin
most prominent in the cervical and thoracic
g a mass within the
subarachnoid space (myelogram). Courtesy of spine. Clinical signs include neck pain and

Dr. Wilfiam Thomas.

rigidity and forelimb lameness. Vertebral
lesions are evident on radiographs.

Reduction of dietary vitamin A prevents
dura mater between T lO and 12, causing
further exostosis but does not significantly
progressive paraparesis. Diagnosis of spinal
reduce the lesions already present.

neoplasia is based on radiography,
myelography, CT or MRI, and surgical

Thiamine Deficiency: Thiamine
biopsy. Surgical excision is possible in some
deficiency is most common in cats but has
cases, but in general, prognosis is poor.

also been reported in dogs. Causes include

In cats, lymphoma is the most common
inadequately formulated commercial diets,
neoplasia to affect the spinal cord. Adult
vegetarian diets, food preserved with sulfur
cats of any age can be affected. There is an
dioxide (which destroys thiamine), and raw
acute or slowly progressive onset of signs
fish diets (which contain thiarninase).

referable to a focal, often painful, lesion of

Affected cats typically exhibit brain
the spinal cord. Approximately 85% of
dysfunction characterized by vestibular
affected cats have positive test results for
signs, head tremor, ataxia, depression,
feline leukemia virus (seep 790), and many
severe ventroflexion of the head, seizures,
have leukemic bone marrow. Myelography,
and death. Clinical signs in dogs include

CT, or MRI shows extradural compression.

anorexia, depression, paraparesis, seizures,

Treatment consists of combination
coma, and death. Pathologic findings are

1254

DISEASES OF THE SPINAL COLUMN AND CORD
polioencephalomalacia, most prominent in
dysfunction. The prognosis is guarded for
the midbrain. Diagnosis is based on clinical
recwnbent horses and cattle. In animals
signs, dietary history, and response to
that have lost deep pain perception caudal
thiamine administration (thian1ine
to the lesion, the prognosis for return of
hydrochloride, 10-20 mg/day, IM, in
neurologic function is poor.

cats; 25-50 mg/day, IM, in dogs).

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TOXIC DISORDERS

TRAUMA

Arsenic Poisoning: Poisoning can

Acute spinal cord injuries are commonly
be seen in swine due to an overdose of
associated with spinal fracture or luxation.

organoarsenicals, which are often used as

Common causes in dogs and cats are
feed additives to promote growth and to
automobile accidents, bite wounds, and
control swine dysentery. With 3-nitro-4-
gw1shot woW1ds. Falls are common causes
hydroxyphenylarsonic acid ("3-nitro")

in horses. Cattle are susceptible to irtjuries
poisoning, there is degeneration of the
from breeding. Pathologic fractures are
spinal cord, optic nerve, and peripheral
common in cattle, sheep, and pigs with
nerves. Clinical signs consist of tremors and
malnutrition or vertebral osteomyelitis.

paraparesis. Mildly affected anin1als can

Damage to the spinal cord is caused not
recover after withdrawal of the offending
only by the primary mechanical injury but
feed. (See also ARSENIC POISONING, p 3071.) also as a result of secondary pathologic
changes, including edema, hemorrhage,

Delayed Organophosphate Intoxica
demyelination, and necrosis. These
tion: Intoxication can be seen after oral or secondary changes are due to biochemical
topical administration of organophosphatefactors, including the release of free containing insecticides or anthelrnintics,
radicals, leukotrienes, and prostaglandins
including haloxon. In addition to the acute
that cause further injury to nervous tissue
signs, delayed paralysis can develop 1-4 wk
and compromise blood flow to the spinal
after exposure. Suffolk sheep have an
cord.

inherited predisposition to this neurotoxic

Signs of spinal trauma are typically acute
ity, because they have low levels of plasma
and may progress in instances of W1stable
arylesterase activity. Affected animals have
fractures or luxations. Severe thoracolwnprogressive, symmetric paraparesis and bar spinal cord injury may cause paraplegia
occasionally become tetraplegic. Diagnosis
with increased extensor tone in the thoracic
is based on clinical signs and history of
lin1bs (Schiff-Sherrington phenomenon).

exposure. On histopathologic exanlination,

Radiographs usually demonstrate vertebral
there is Wallerian degeneration, most
fractures and luxations. However, in dogs
prominent in the spinal cord and brain stern.

with trawna, radiographs, compared with

The prognosis for severely affected animals

CT, reveal only -75% of spinal fractures, so
is poor. (See also ORGANOPIIOSPIIATES
advanced in1aging is indicated in animals

(TOXICITY), p 3064.)

with suspected spinal trawna and nonnal
radiographs. Treatm!!nt with methylpredni

Sorghum Poisoning: Sorghum spp, such solone may be helpful for animals with
as SorghW11, Sudan, and Jolmson grass, can
severe neurologic deficits if instituted
cause degeneration of the spinal cord in
within the first few hours of injury. One
horses and occasipnally in cattle and sheep.

protocol is 30 mg/kg, IV, followed 2 hr later

The pathogenesis may be related to the high
by 15 mg/kg, IV, followed 6 hr later by 15
content of hydrocyanide in these grasses.

mg/kg, IV, every 6 hr for a total of 24 hr of

There is ataxia and weakness of the pelvic
treatment. Dexamethasone is less effective
limbs and incontinence. Urine retention
and is associated with an increased risk of
often leads to cystitis and hematuria.

GI ulceration and pancreatitis. NSAIDs have Diagnosis is based on clinical features and minin1al benefit in acute spinal cord injury
a history of exposure. Signs may improve
and increase the risk of complications, espewith removal of the offending feed, although cially if used in cortjW1ction with corticopersistent deficits are possible. (See also steroids. DMSO (0.5-1 glkglday of a 10%---200Ai SORGHUM POISONING, p 3155.) solution, given slowly IV for 3 days) is
recommended in horses with acute spinal

Tetanus: Tetanus (seep 611) is caused by cord injury. Animals with mild neurologic
toxins produced by the vegetative form of
deficits often recover with 4--6 wk of cage or

Clostridiitm telani. Susceptibility varies
stall rest and analgesics. Surgical reduction
markedly among species; dogs and cats are
and stabilization is indicated for unstable
fairly resistant compared with horses.

vertebral irtjuries causing severe neurologic

Clinical signs usually develop within

DYSAUTONOMIA

1255
discs. It is seen primarily in adult dogs,
especially large and giant breeds. Miniature

Schnauzers and Shetland Sheepdogs also
may be predisposed. It is rare in cats,
horses, and pigs. Affected dogs have an

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abrupt onset of gait dysfunction, often
occurring during activities such as running
or jumping. Deficits are referable to a focal,
often asymmetric, lesion in the spinal cord
and rarely progress past 12 hr. Spinal pain is
typically absent.

Diagnosis is based on clinical findings and

MRI, which shows focal T2 hyperintensity

Fibrocartilagenous embolism in a dog, MRI.

Note T2 hyperintensity (bright) within the
within the spinal cord with no compressive
spinal cord dorsal to the L3-4 disc space.

lesion. In the acute stage, the CSF may have
a mild increase in neutrophils and protein

Courtesy of Dr. William Thomas.

concentration. Mildly affected dogs often
improve substantially within 1-2 wk

5-10 days of infection. These include

Prognosis is poor if deep pain perception is
localized or generalized muscle stiffness and
absent or if there is no improvement within
extensor rigidity, dysphagia, protrusion of
several weeks.

the third eyelid, and contracted masticatory

(lockjaw) and facial ( risus sa.rdonicus)

muscles. In severe cases, the animal may be

Postanesthetic Hemorrhagic Myelop
recumbent with opisthotonos and reflex
athy in Horses: Postanesthetic hemormuscle spasms. Diagnosis is based on raghic myelopathy is a rare complication
characteristic clinical features. Treatment
seen in horses positioned in dorsal
consists of wound care, antibiotics to kill
recumbency under general anesthesia. The
any remaining organisms, and tetanus
cause may be related to impaired venous
antitoxin. In mild cases, prognosis is good
drainage of the spinal cord due to compreswith early treatment. In severe cases, death sion of the caudal vena cava or azygous vein
may occur due to respiratory paralysis.

because of the weight of abdominal viscera.

There is paraplegia immediately after

VASCULAR DISEASES
recovery from anesthesia. Pathologic
findings consist of hemorrhagic necrosis of

Fibrocartilagenous Embolism: Infarcthe thoracolumbar spinal cord segments.

tion of the spinal cord can be caused by

The prognosis is poor. Positioning the horse
occlusion of spinal cord arteries or veins ( or
slightly tilted off the perpendicular and
both) with fragments of fibrocartilage,
maintaining adequate blood pressure may
believed to arise from the intervertebral
help prevent this complication.

DYSAUTONOMIA

FELINE DYSAUTONOMIA
cases have been seen in Dubai, New

Zealand, and Venezuela; and a few cases

Feline dysautonomia is characterized by
have been reported in the USA, in eastern
widespread dysfunction of the autonomic

Kansas and western Missouri. The etiology
nervous system. All breeds and age groups
is unknown. Dysautonomias in horses,
are susceptible, although the disease
dogs, rabbits, and hares share striking
appears to be more common in younger
similarities to the condition in cats.

cats. Feline dysautonomia was first
reported in 1982 and initially became

Clinical Findings: Affected cats initially
widespread in the UK (under the name
are anorectic and often have upper res

Key-Gaskell syndrome). The incidence has
piratory signs or transient diarrhea. The
declined considerably, but a few cases were
onset of more definite signs varies from
recorded in Europe in the 1990s; sporadic
peracute to chronic. Failure of the

1256

OYSAUTONOMIA
autonomic system of the GI and urinary
nasogastric tube feeding when regurgitation
tracts can cause esophageal distention and/
resolves. Maintaining an upright posture
or dysfunction, gastric and bowel distention
after oral intake is in1portant, because the
and hypomotility, and urinary bladder
main complication of this condition is
distention. Other common signs include
inhalation pneumonia. Thrice daily

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dilated, nonresponsive pupils, ptosis, and
evacuation of the bladder, provision of
third eyelid protrusion; a dry rhinariurn; and
warmth, use of artificial tea.rs and steam
reduced lacrirnal secretion. In addition, dry
inhalation, and assistance with grooming
oral mucous membranes, prolapse of the
are all important nursing considerations.

nictitating membrane, bradycardia, and

Liquid paraffin PO is helpful for constipation

U1inary or fecal incontinence may be seen.

but increases the risk of aspiration. Other

These signs reflect both sympathetic and
parasympathomirnetics, such as bethaneparasympathetic dysfunction, and there is chol (1-2.5 mg, PO, bid-tid), may be of use;
a wide range in the severity of presenting
however, their effect is crude, and overdossigns. A dilated anus is sometimes noted, age requires treatment with atropine. Metobut the underlying somatic lesion is clopramide (0.1 mg/kg, IV, or 0.3 mg/kg, SC,
undetermined. Clinical pathology findings
tid) may in1prove gastric emptying.

are nonspecific.

A small propo1tion of cats have recov

Lesions: Necropsy may show megaeered, and others are able to cope with sophagus, diphtheritic mucous membranes,
residual autonomic deficits. Such improvean atonic bladder, and retention of fecal ments often require up to 1 yr. In general, the
material. During the first few weeks after
prognosis is poor for severely affected cats.

onset, chromatolysis and neuronal
degeneration of pre- and postganglionic

CANINE DYSAUTONOMIA
sympathetic and parasympathetic neurons
is typical. A very specific distribution of

Canine dysautonomia is a degenerative
chromatolytic autonomic and somatic
polyneuropathy characterized by neurolower motor neurons is found in the brain nal degeneration within the autonomic,
stem and spinal cord. The central lesions
somatic, central, peripheral, and/or enteric
are identical to those found in the equivalent nervous system causing multisystemic disease in horses, dogs, rabbits, and hares.

effects sintilar, if not identical, to the

Chronic cases can be difficult to confirm
dysautonomia in horses, cats, rabbits, and
because surviving neurons appear normal,
hares. Canine dysautonomia was first
and diagnosis depends on an assessment
described in England in 1983, and there
of their numbers relative to surrounding
have been no new cases reported in the
stromal cells.

past decade. Although individual cases
have been reported in Scotland, Norway,

Diagnosis: Definitive diagnosis depends

Belgium, Germany, and Greece, canine
on histopathologic exanlination of
dysautonomia is less commonly reported
autonomic ganglia. Clinical confinnation
in Europe than in the USA, with higher
may be aided by contrast radiDgraphy
nun1bers primarily in the Midwest. In the

(including fluoroscopy) of the esophagus

USA, risk factors were reported to include a
and by reduced lacrirnal secretion ( <5 mm/
rural habitat and spending >509'o of the time
min when measured by the Schirmer tear
free outdoors.

test). Pilocarpine (0.1 %) applied to the
cornea causes profound miosis within

Clinical Findings: The most consistent

10-15 min due to denervation hypersensitivhistory and physical examination findings ity but has no effect on a healthy cat. Dilute
are acute-onset vomiting, diarrhea, mild

(0.5%) phenylephrine reverses the ptosis
obtundation, inappetence, reduced or
and protruding third eyelid. Although feline
absent anal tone, absence of pupillary light
leukemia virus (FeLV, seep 790) infection
responses and lacrimal secretion, mydriacan cause both anisocoria and urinary sis, and protrusion of the nictitating
incontinence, cats with dysautonomia
membrane. Secondary effects of autonomic
usually show other clinical signs and a.re
dysfunction, such as aspiration pneun10nia

FeLV-negative.

and lethargy, may develop. Weight loss is
often dramatic.

Treatment and Prognosis: The main

Laboratory findings are nonspecific.

aim of therapy is first to rehydrate the cat

Pharmacologic testing of the pupils is
and then to maintain adequate fluid balance.

probably the best single test for confirming

Total parenteral nutrition is useful initially
the diagnosis. Dilute pilocarpine (0.05%
but later can be replaced by gastrostomy or
ophthalmic solution) results in rapid

DYSAUTONOMIA

1257
pupillary constriction in dogs with
considered to indicate a poor prognosis.

dysautonomia because of supersensitivity

Affected horses often have dysphagia and
of the denervated muscle to cholinergic
esophageal dysfunction, which cause
drugs. The prognosis is grave.

drooling, difficulty passing a stomach
tube, nasal reflux of gastric contents, and

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LEPORINE DYSAUTONOMIA
pooling of barium contrast in the thoracic
esophagus. On rectal palpation, the

Leporine dysautonomia occurs in rabbits
mucosa is dry and tacky, and feces are
and wild hares, and fatal cases have been
scant and hard. Distended loops of small
reported in the UK. Gross lesions are similar intestine and an impacted large colon are to those of equine dysautonomia, including
seen in the more acute cases. Secondary
gastric distention, colonic impaction, and
ileal dilation/impaction and displacement
weight loss. Histopathologic changes in the
of the large colon can be confusing
central and peripheral nervous systems are
features. Cachexia can be profound
almost identical to those found in horses,
in chronic cases.

cats, and dogs.

Lesions: In acute cases, the stomach and
small intestine are markedly distended with

EQUINE DYSAUTONOMIA
fluid (which can result in gastric rupture),

(Grass sickness)

and tl1e large intestine is impacted. In
chronic cases, the GI tract is usually empty.

A fatal dysautonomia of unknown etiology,

All forms may show linear ulceration of the
equine grass siclrness causes marked
esophagus and hard, tan-y fecal balls.

reduction of GI motility due to widespread

Neuronal degeneration of pre-and postdegeneration within the autonomic nervous ganglionic sympathetic and parasympasystem. It is seen throughout northern thetic neurons is characteristic. A specific

Europe, and a few cases have been
distiibution of clu·omatolytic autonomic
diagnosed in the USA in the same geoand somatic lower motor neurons is found graphic area (Midwest) that has a high
in the brain stem and spinal cord.

prevalence of canine dysautonomia.

Grass sickness is seen at any age after

Diagnosis: No reliable in vivo diagnostic
weaning and at any time of year, but
test is available, but dysphagia, tachycarincidence is highest in spring and in horses dia despite few signs of pain, decreased GI

2-7 yr old. Although associated with
tract motility, a tucked-up stance ( chronic
recently acquired horses kept solely at
cases), and ptosis are useful features.

grass, the condition has very rarely been

Administration of dilute (0.5%) phenylseen in housed stock. All equidae appear ephrine to one eye should, within 20 min,
susceptible. Acute, subacute, and chronic
result in marked decrease in ptosis (111ost
fom1s are recognized, categorized by
easily seen as a decrease in the angle of
whether death occms within 24 hr, 7 days,
the eyelashes to the head when viewed
and 1 wk, respectively. However, chronic
from the front). Biopsies of ilea.I and rectal
cases can survive for weeks or months, and
tissue (1-cm long, formalin-fixed biopsies
a few cases have recovered. The exact
preferred) can confirm the diagnosis when
etiology is unknown, but the causal agent
examined by a pathologist experienced
is thought to be associated with grazing.

with grass sickness lesions. Postmortem

A Clostridium botulinum toxin may
confirmation of diagnosis depends on
be involved.

hjstopathologic examination of autonomic
ganglia. The cranial cervical ganglia are

Clinical Findings: Horses are a.febrile
the most accessible ganglia on postmorand show tachycardia, ileus, and colic.

tem examination and can be found in a

Patchy sweating and fine muscular
fold of mucosal tissue in the caudal wall of
fasciculations are often seen over the
the medial compartment of the guttural
shoulders and flanks, and penile prolapse
pouch.

may develop. Horses adopt a "tucked up"

stance, similar to that seen in equine motor Treatment: A proportion of mildly neuron disease (seep 1248). In contrast to
affected (chronic) cases can survive with
feline dysautonomia, pupillary light
dedicated nmsing care; a wide variety of
reflexes and tear production are normal.

feeds should be offered to encourage feed

Ptosis, with "droopy" eyelashes, tends to
intake. Acute and subacute cases have not
be prominent because of smooth muscle
survived and should be euthanized on
paresis. Rhinitis sicca ( dry nose) comhumane grounds. Stabling at-risk stock for monly develops in chronic cases and is
part of the day has been recommended.

1258

FACIAL PARALYSIS

FACIAL PARALYSIS

Asymmetry of facial expression is conunon
contracture, the ear carriage may be higher.

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with unilateral lesions of the facial nucleus

The fibrosis of the auricular muscles can be
or nerve in most species. Bilateral facial
palpated, and the ear becomes adhered in the
paralysis may be more difficult to recognize, abnormal position. In acute lesions, the lips but affected animals drool and have a dull
on the paralyzed side may hang loosely,
facial expression. Complete facial paralysis
exposing mucosa. When the animal eats or
is an inability to move the eyelids, ears, lips,
drinks, food and fluids may fall from the lips.

or nostrils. Facial paresis is reduced

The animal may drool excessively, and food
movement of the muscles of facial
may collect between the lips and teeth. In
expression and indicates milder nucleus or
chronic lesions, fibrosis of the lip muscles
nerve involvement. The nucleus of the facial can be palpated, and the lip on the affected nerve is located in the rostral medulla
side is higher than on the norn1al side. In
oblongata of the brain stem. The facial
acute, unilateral lesions, the nose deviates
nerve, cranial nerve VII, exits the brain stem
away from the side of the lesion, owing to a
near the vestibulocochlea.r nerve, passes
loss in muscle tone on the affected side. In
through the petrous temporal bone, and
horses, the affected nostril is unable to dilate
then exits the skull through the stylomason inspiration. In chronic lesions, muscle toid foramen and splits into auricular,
fibrosis and contracture cause the nose to
palpebral, and buccal branches.

deviate toward the lesion, and the muscles
feel finn and inflexible. Because the facial

Clinical Findings and Lesions: Clininerve provides sensory innervation to the cal signs of facial paralysis vary with the
distal tongue, a bitter substance such as
location, severity, and chronicity of the
atropine will not be recognized when placed
lesion. If a unilateral lesion is located in the
on the distal tongue.

facial nucleus or proximal portion of the

Often, the parasympathetic portion of the
facial nerve, paresis or paralysis of the
facial nerve is also affected, and tear and
eyelids, ears, lips, and nostrils on that side
saliva production on the side of the lesion is
are seen. A lesion of the auriculopalpebral
reduced or absent. Reduced or absent tear
branch of the facial nerve, near the
production, with eyelid paresis or paralysis,
zygomatic arch, results in paresis or
can result in corneal exposure with
paralysis of the eyelids and ear only. A
resultant ulceration. In cases of facial nerve
lesion of the palpebral branch of the facial
paralysis, a Schirmer tear test can be used
nerve, crossing the zygomatic arch, results
to detern1ine whether administration of
in paresis or paralysis of the eyelids only. A
artificial tears is needed. Reduced saliva
lesion of the buccal branch of the facial
production can result in dry mucous
nerve, as it courses along the surface of the
membranes, and food may collect in the
masseter muscles, results in paresis or
buccal folds. Dryness on the side of the
paralysis of the lips and nostrils only.

lesion can be detected by simultaneously

In small animals with facial paralysis, the
palpating the mucous membranes on both
palpebral fissure may be slightly larger on the sides and comparing the degree of moisture.

affected side; in horses and food animals, the

Other concomitant neurologic deficits
palpebral fissure is slightly smaller because
can further localize the facial nerve lesion.

of a loss of tone in the frontalis muscles

If the animal has ataxia, hemiparesis,
above the eyelid. When the medial or lateral
quadriparesis, or conscious propriocep-
can thus of the eyelids or cornea are touched,
tive deficits associated with facial nerve
the eyelids do not close, but the eyeball will
paralysis, a brain-stem lesion is probable.

retract into the orbit (if the trigeminal and

If the animal has facial paralysis with a
abducent nerves are functioning properly).

head tilt, nystagmus, or other evidence of

The third eyelid will passively elevate as
vestibular deficits, but no hemiparesis,
the globe retracts. If both eyes are tested
quadriparesis, or conscious propriocepsimultaneously, movement on each side can tive deficits, then a lesion of the facial nerve
be compared. When the animal is unable to
exists as it exits the brain stem or passes
blink the eye, corneal irritation may result
through the petrous temporal bone. If a
in excessive tear production. In acute
small animal has facial paralysis with ptosis,
denervation, the ear carriage is often lower
miosis, and enophthalmos (Homer
on the side of the lesion in all species, but in
syndrome), a lesion of the middle ear
chronic denervation with muscle fibrosis and is likely.

LIMB PARALYSIS

1259

Diagnosis and Treatment: Trauma is
the appropriate antibiotic, detem1ined by
a common cause of facial paralysis in all
culture and sensitivity on a saniple obtained
species. In horses, halter injuries and
via myringotomy. Corticosteroids should be
prolonged lateral recurnbency may injure
avoided because they may encourage
the buccal branches of the facial nerve on
osteomyelitis. The facial ne1ve paralysis can
the side of the jaw and cause unilateral or
be pem1anent, and longtenn adnlinistration

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bilateral paresis or paralysis of the lips and
of aitificial tears may be necessary.

nostrils. Cattle that struggle in stanchions

Guttural pouch infections (seep 1463) can
may injure the palpebral branch of the facial produce facial paralysis in horses. Lesions of nerve as it crosses the zygomatic arch,
the facial nerve nucleus can result in facial
causing unilateral or bilateral paresis or
nerve paralysis in equine protozoa] myeloenparalysis of the eyelid(s). Small anin1als may cephalitis (EPM, seep 1309). CSF analysis incur peripheral facial nerve injuries from
and titers for EPM are essential for diagnosis
rough handling, automobile accidents, or
and institution of appropriate therapy.

surge1y such as bulla osteotomy and total

Idiopathic facial nerve paralysis is
ear ablation. Electromyography, including
common in dogs and is diagnosed by
electrical stimulation of the facial nerve,
excluding other diseases. Otitis media must
can be used to determine the location and
be excluded with exan1ination and radioseverity of the injmy; however, changes will graphs. Because hypothyroidism (seep 553)

not be evident until 5-7 days after injmy.

can cause facial nerve paralysis, levels of

Therapy for injmy may include massage
thyroxine (T4) and thyroid-stimulating
and heat of denervated muscles for 15 min,
hormone should be determined in all dogs

2-3 times/day, to maintain their integrity
with facial paralysis. Thyroid replacement
while awaiting any nerve regeneration. Laser
therapy may not always resolve facial
therapy, also known as cold laser, low level
paralysis in hypothyroid dogs. If there is no
light therapy, or photobiomodulation, can
infection, thyroid function is nom1al, and
help nerve regeneration. The facial nerve can
there has been no known tralll11a, the
regenerate -1-4 nun/day, so serial neurologic
diagnosis of idiopatllic facial pai·aJysis is
examinations can also help determine the
made. There is no therapy. Artificial tear
prognosis. If there has been no improvement
adnlinistration may be necessary. Facial
after 6 mo, the chance of recovery is poor.

paralysis can be unilateral or bilateral and

Horses with collapsing nostrils may require
can resolve spontaneously or be pem1anent.

corrective surgery. Species that need the lips

It can occur on one side, resolve, and then
for drinking and prehending food must be
occur on the other side at a later time.

given deep water containers and wet bulky

Permanent paralysis may be disfiguring but
mashes.

does not affect the quality of life in dogs.

Otitis media is another common cause of

Primaiy neoplasia of the facial nerve
facial paralysis in all species, especially in
is rare, but dogs and cats can develop a
dogs with chronic dermatitis. Otitis extema
neoplastic process that affects nliddle
and a ruptured or diseased tympanic
ear structures, including the facial nerve.

membrane are often seen on otoscopic exanli

Squainous cell carcinoma and polyps of
nation under general anesthesia Despite an
the nliddle eai· are most common in cats.

intact tympanmn, 16% of animals with acute

Otoscopy of the external ear canal under
otitis extema may have otitis media, and as
anestl1esia with biopsy and histologic
many as 89% of anin1als with chronic otitis
exan1ination of abnormal tissue can assist
extema may have otitis media (See also OTms with the diagnosis. CT and MRI of the

E:XTERNA, p 527, and CfTITIS MEDIA AND INTERNA, p osseous bulla are necessaiy to determine

531). Skull radiographs, CT, and MRI may
the extent of the lesion before surgery. Early
be necessary to confinn otitis media The
radical excision of the tumor and radiation,
prognosis can be good if the diagnosis is made if indicated, may afford a good longtem1
early and the anin1al is treated for 4-6 wk with prognosis depending on tumor type.

LIMB PARALYSIS

Paralysis of one limb is referred to as
associated with a lesion of the C6 to T2 nerve
monoplegia and is most often associated
roots, the brachia] plexus, or musculocutawith diseases of the peripheral spinal nerves. neous, radial, median, or ulnar nerves.

Paralysis of the thoracic limb is usually

Paralysis of the pelvic limb is usually

1260

LIMB PARALYSIS
associated with a lesion of the IA to S2 nerve Deep pain is tested by applying
roots, the lrunbosacral plexus, or femoral,
hemostatic forceps to the bones of the digits
sciatic, peroneal (fibular), or tibial nerves.

or hoof testers to the hoof and observing a
behavioral response. The presence of deep

Clinical Findings and Lesions: Evaluapain from the fifth digit in small animals VetBooks.ir
tion of the posture and gait, spinal reflexes,
indicates integrity of the ulnar nerve. The
superficial and deep nociception, and
presence of deep pain from the other digits
muscle mass of the affected limb can
of the thoracic limb indicates integrity of the
localize the lesion to the nerve roots or
radial and median nerves.

plexus or to a specific nerve branch.

The eye on the side of the thoracic limb

Determining the exact location of the lesion
paralysis will show Homer syndrome
is important for an accurate prognosis

(ptosis, miosis, and enophthalmos) when
because the closer a nerve irtjury is to the
the lesion involves the T 1 to T2 nerve roots
muscle to be reinnervated, the better the
as they exit the spinal cord. Homer
prognosis for recovery. In general, nerve
syndrome is manifest in horses by ocular
root or plexus lesions have a poorer
changes and ipsilateral sweating of the face
prognosis than do peripheral nerve lesions.

and neck and in cattle by ocular changes

Muscle atrophy from denervation
and a unilateral loss of moistw·e on the
develops within a few days and is faster
muzzle.

to develop and more severe than disuse

Inability to extend tl1e stifle to support
atrophy. With disease of the suprascapular
weight in the pelvic limb is seen with IA to nerve, the supraspinatus and infraspinatus

L5 nerve root or femoral nerve disease; the
muscles are atrophied; generally, little gait
patellar reflex is reduced or absent, the
deficit is noted in small animals. However,
quadriceps muscle is atrophied, and
in horses, the shoulder drops ventrally and
sensation of the skin is reduced or absent on
rotates laterally, and the hoof may scuff or
tl1e medial surface of the lin1b. Inability to
drag the ground slightly. If the musculocutaactively flex the stifle, hock, and digits or neous nerve is affected, the animal is unable to extend the hock and digits is seen with to flex the elbow, and the biceps muscle is
lesions of the sciatic nerve, L6 to S2 nerve
atrophied. With radial nerve disease, the
roots. The animal will support some weight
elbow is dropped, the digits are knuckled
if the femoral nerve is spared but will stand
onto their dorsal surface, and the limb is
knuckled on the dorsrun of the paw or hoof
unable to bear weight. The thoracic limb
with the hock excessively flexed. If only the
flexor reflex (withdrawal reflex) is
peroneal branch of the sciatic nerve is
depressed or absent with lesions of the
affected, the hock will be overextended and
radial nerve (sensory portion), axillary
the digits knuckled. If only the tibial branch
nerve (shoulder flexio�), musculocutaneof the sciatic nerve is affected, the hock will ous nerve ( elbow flexion), or median and
be overflexed and the digits overextended.

ulnar ( carpal and digit flexion) nerves. The

The prognosis for tibial or peroneal nerve
triceps and extensor carpi muscles may also lesions may be better than that for sciatic atrophy in radial nerve disease. Superficial
lesions, so differentiation is imp01tant.

and deep digital flexor muscles atrophy with

The pelvic limb flexor reflex is diminished
lesions of the median and ulnar nerves.

or absent with sciatic nerve lesions. The

There is little gait abnormality with ulnar
gastrocnemius reflex is diminished or
nerve irtjury.

absent with lesions of the sciatic or tibial

Superficial sensation is tested by
nerve. The cranial tibial muscle reflex is
observing a behavioral response (such as
diminished or absent with lesions of the
looking, wincing, crying, or biting) when the sciatic or peroneal nerve. The distribution skin is pinched with hemostatic forceps or
of denervation muscle atrophy can indicate
pricked with a needle. Regions of skin
whether the sciatic or only one of its
sensation associated with specific nerves
branches is involved. Atrophy of gluteal,
are less distinct in equine and food animal
semimembranosus, semitendinosus, and all
species than in small animals. A loss of
muscles below the stifle indicates a lesion
sensation on the rostral skin surface of the
of the L6 to S2 nerve roots as they exit tl1e
thoracic limb from the elbows to the paws
spinal cord. If the gluteal muscles are
indicates radial nerve disease. The skin of
normal but the others are atrophied, then a
the caudal aspect of the limb, from the
lesion of the sciatic neive is located at the
elbow to the pads, is desensitized in median
sciatic notch or the proximal two-thirds of
and ulnar nerve disease, and the skin of the
the femur. Atrophy of the cranial tibial or
lateral aspect of the antebrachium and paw
gastrocnemius muscles alone indicates a
is desensitized with damage to the ulnar
lesion of the peroneal or tibial nerve,
nerve.

respectively. If superficial sensation is

LIMB PARALYSIS

1261
reduced or absent on the cranial and caudal

Electrical stimulation of a nerve with
aspects of the limb and in the perinea!

neurapraxia is usually nom1al, and the
region on the same side, then a lesion of the
prognosis is good, regardless of the findings

16 to 82 nerve roots is likely. With peroneal
of the initial neurologic exanunation. lithe
nerve lesions, superficial sensation on the
affected nerve does not respond to electrical

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cranial surface of the hock and tibia and on
stimulation distal to the site of the lesion <C3
the dorsal aspect of the foot is reduced or
days after injmy, the prognosis for recovery
absent. With tibial nerve lesions, superficial
is guarded. Serial neurologic exan1inations
sensation of the caudal surface of the hock
throughout a 6-mo period are necessary
and tibia and plantar surface of the paw is
if electromyographic evaluation is not
reduced or absent. Sciatic nerve lesions
perfonned.

cause a loss of superficial sensation in the

Injmy to the brachia! plexus or the C6 to
cranial, caudal, dorsal, and plantar regions.

T2 nerve roots is common in most species

A loss of deep pain may be associated with
due to direct shoulder traun1a or abnonnal
sciatic nerve lesions. Preservation of
shoulder abduction ( eg, in small animals hit
sensation on the medial aspect of the pelvic
by automobiles). Horses and cattle cast on
limb is attributable to preservation of the
hard surfaces for foot or other surgeries may
saphenous nerve.

develop a brachia! plexus injmy. If Homer

Electromyography can be used 7-10 days
syndrome is present on the same side as a
after a nerve insult to detect denervation in
thoracic lin1b that has lost sensation and is
muscles and to outline the distribution of
areflexic and paralyzed, a brachia! plexus
the nerve lesion. Denervation of limb and
avulsion is likely, and the prognosis for
paravertebral muscles indicates nerve root
recovery grave. With brachia! plexus
lesions. Denervation of a specific muscle
avulsion, tl1e nerve roots are tom from the
group indicates a lesion in its respective
spinal cord and cannot be repaired. If there
nerve. Electrical stimulation of the nerve
is also no response to radial nerve stimulacan be used to determine nerve integrity.

tion, recovery is hopeless. lithe limb drags

If some nerve integrity is present, the
on the ground, it can be held up with a neck
prognosis is better if motor nerve conducsling or amputated in small animals to avoid tion velocity is nonnal than if it is slowed.

laceration of the dorsal surface of the paw.

Three-legged dogs and cats generally have a

Diagnosis and Treatment: Trauma is the
good quality of life. lino Homer syndrome is
most common cause of acute monoplegia.

present with thoracic limb paralysis, the

Traumatic loss of nerve function may be due
prognosis for recove1y may be better.

to neurapraxia, axonotmesis, axonostenosis,

Lumbosacral plexus injuries are less
or neurotmesis. Neurapraxia is a tempocommon than brachia! plexus injuries but rary nerve conduction dysfunction that can
can be associated with automobile accidents
last several weeks, but recovery is complete.

or extreme limb abduction. Fractures of

Axonotmesis is rnpture of some axons

Jong bones can injure peripheral nerves
within the nerve but with an intact nerve
locally. Surgical intervention for pelvic and
sheath. Most closed nerve injuries from
hip disease and injection injuries are
stretch or compression are a combination of
common causes of sciatic nerve injuries.

neurapraxia and axonotmesis. Ruptured

Sustained pressure on the lateral aspect of
axons regenerate 1-4 mm/day, but functional the stifle can cause peroneal nerve injmy.

recovery depends on the integrity and

Heat application, massage, and stretching of
dian1eter of the nerve sheath and on the
tendons should be performed for 15 n1in 2-3
distance between injmy and reinnervation
times/day to keep muscles, tendons, and
sites. Nerves injured > 180 mm from their
joints healthy while the nerve is regeneratrespective muscles may be unable to make ing. A light bandage may prevent damage to
anatomic contact. If anatomic contact is
the foot from dragging, but reduction of
made, the nerve sheath contracture, which
circulation should be avoided. No specific
develops over time, may not leave enough
therapy is currently available to assist nerve
room to develop sufficient myelin to conduct regeneration, but recent studies with laser an effective electrical in1pulse. Axonoste
therapy, also known as cold laser, low level
nosis, or nan·owed nerve sheaths with
light therapy, or photobiomodulation, has
reduced nerve function, may be a sequela of
shown some promise in assisting nerve
nerve injmies. Neurotmesis is total nerve
regrowth. In traumatic injuries with
rnpture, and surgical reattachment is
accompanying swelling, small animals may
required for regeneration. If no nerve
be given NSAlDs or a short course of
function is found on the initial neurologic
anti-inflammatory oral prednisone at
examination, neurapraxia, axonotmesis, and 0.5 mg/kg/day for 5-7 days. This will help neurotmesis can be difficult to differentiate.

reduce edema, which can compromise

1262

LIMB PARALYSIS
circulation to the nerve. NSAIDs and
cral plexus is seen in dogs, cattle, and cats.

corticosteroids should not be used
lf the nerve roots within the spinal canal are
concurrently. NSAIDs can be given to horses
affected, an extramedullary mass may be
to reduce edema. lf volw1ta.ry movement,
visualized with a myelogran1, CT, or MRI in
nociception, and spinal reflexes improve
dogs and cats. Surgical exploration and

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within 1-2 mo, the prognosis is good. Limb
removal or biopsy are essential to determine
mutilation can be transient in recovering
diagnosis or prognosis. The longtem1
nerve injuries and may be prevented by
prognosis for nerve sheath twnors is poor,
temporary use of an elizabethan collar. lf
even after attempted surgical removal and
nerve iajury is suspected to be permanent
limb amputation. Nerve sheath twnors often
and the animal is mutilating the limb,
affect multiple nerve roots, and the tW11or is
an1putation is recommended in small
difficult to completely remove. lf appropriate
animals. Enough time should be allowed to
chemotherapy is instituted for lymphosarpass for possible regeneration of the nerve, coma, the length and quality of life may be
typically 3-6 mo, before amputation.

improved. Chemotherapy is not very helpful

Neoplasia of nerve roots and peripheral
to treat nerve sheath twnors, but radiation
nerves can cause a chronic, progressive,
therapy may have some benefit.

often painful paresis of a thoracic or pelvic

Horses with equine protozoa] myeloenlimb. (See also NEOPLASIA OF THE PERLPHERAL
cephalitis (EPM, seep 1309) may develop

NERVES AND NEUROMUSCULAR JUNCllON, p 1242,
monoparesis and focal muscle atrophy. CSF
and NEOPLASIA OF TILE NERVOUS SYSTEM, p 1267.) analysis and CSF and serwn EPM titers

Ne1ve sheath twnors are common in dogs.

should be evaluated so appropriate therapy

Lymphosarcoma of the brachia] or lwnbosa-
can be administered.

MENINGITIS, ENCEPHALITIS, AND

ENCEPHALOMYELITIS

Inflammation of the meninges (meningitis)

other causes of meningitis or encephalitis.

and inflan1rnation of the brain (encephalitis) In species other than 1uininants, especially are seen in animals and often manifest
adult animals, viruses, protozoa, rickettsia,
concurrently (rneningoencephalitis). Many
and fungi are as or more frequent causes of
of the inflammatory diseases of tl1e CNS of
meningitis or encephalitis than are bacteria.

animals are diffuse, involving both the brain

The appearance of many etiologic agents
and spinal cord ( encephalomyelitis and
such as arboviruses, certain rickettsia, and
meningoencephalomyelitis ). Because many
bacteria) are seasonal. Age is an important
inflanimatory processes are a.isseminated
consideration for bacterial meningitis
throughout the CNS at the time of clinical
associated with neonatal sepsis. Even witlli.n
observation, differentiation between
species ( eg, production animals), there can
meningeal-only inflan1mation vs extension
be a difference in risk factors. For instance,
of disease into the neuropil is often difficult
sporadic bovine encephalomyelitis ( see
to make antemortem. Thus, from a clinical
p 1308), caused by Chlamydia pecorum, and
standpoint, any one of these conditions may thromboembolic meningoencephalitis (see be the case in an animal with an inflanunap 754), caused by Histophilus somni, tory condition of the CNS.

usually occur in feeder beef cattle (6 mo to

In animals with meningoencephalitis or

2 yr old) and not replacement dairy calves
meningoencephalomyelitis, the clinical signs

Wlless managed on feedlots. Vaccine history
of meningitis often precede those of encephais also an essential factor in consideration of litis and may remain the predominant feature
differential diagnoses in animals with clinical
of the illness. This is especially apparent in
signs of inflanimation of the CNS, especially
meningitis involving neonates. Causes of
those caused by viruses.

meningitis, encephalitis, and meningoencephalitis include bacteria, viruses, fungi, Etiology and Pathogenesis: The
protozoa, rickettsia, parasite migrations,
incidence of meningitis, em;ephalitis, and
chemical agents, and idiopathic or irnmWleencephalomyelitis is fairly low compared mediated diseases. In rWllinants, generally
with that of infections of other organs.

bacterial infections are more common than

However, with the recent global expansion

MENINGITIS, ENCEPHALITIS, AND ENCEPHALOMYELITIS

1263
of the flaviviruses and tickbome Ana
disease of pigs (Haernophilus parasuis, see
plasma phagocytophilum and other
p 720), and Haernophilus agni septicemia in vectorborne diseases, the incidence and
feeder lambs.

risk of infectious brain and spinal cord

Streptococcus suis causes suppurative
infections of animals has likely increased.

meningitis of pigs in addition to other

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Bacterial Infections: When bacterial
syndromes such as pleuritis, epicarditis and
infections occur, they are more likely to be
arthritis. (See also STREPTOCOCCAL INFECTl�NS IN
sporadic than epidemic. The risk of hematog

PIGS, p 731.) Several species ofMycoplasma
enously dissemrnated CNS infections is
cause nonseptic encephalitis in their natural
likely to be low in adult animals because of
hosts such as goats (M mycoides), poultry
the blood-brain barrier. Many infections of

(M gallisepticum), cats (Mfelis), dogs the nervous system are the result of some

(M edwardii), and rodents (M pulmonis).

il'\iury to its protective barriers. In all species

Outbreaks of C pecorum occur in yearling
direct extension of bacterial or my co tic
cattle and cause spontaneous encephalomyinfections into the CNS can develop from elitis With polyserositis and peritonitis.

sinusitis, otitis media or intema, vertebral

Bacterial meningoencephalitis often affects
osteomyelitis, or discospondylitis. In calves
neonatal animals as a sequela of gram
withMycoplasma bovis otitis, meningitis
negative septicemia. Members of the
can occur. Infections can also be secondary

Enterobacteriaceae (E coli, Salmonella spp, to migrating grass awns or other foreign
and Kl.ebsiella pneumoniae) are the most
bodies, deep bite wounds, or traun1atic
commonly isolated pathogens, as well as
i.ajuries adjacent to the head or spine· this
streptococci ( conm1only Entervcoccus spp).

is common in hunting dogs. Iatrogenic

Actinobacillus equuli infection is an
infections are possible from diagnostic
in1portant cause of meningoencephalitis in
and surgical procedures.

foals. Failure of passive transfer of imrnuno

Brain abscesses also can arise from direct
globulins is the single most in1portant factor
infections or by septic embolism of cerebral
predisposing neonates to omphalophlebitis
vessels. Pituitary abscesses in fUlllinants are
or enteritis, with subsequent hernatogenous
thought to originate from bacterial invasion
spread of the infection to the CNS. Eliza
of the rete mirabile (intracranial carotid
bethkingia (formerly Chryseobacterium)

mirabile) surrounding the pituitary gland.

meriingosepticum is a bacteriun1 that can

In chronic brain abscesses, an adjacent or
cause meningitis in newborn and irnmunooccasionally diffuse fibrinous leptomeningicomprornised people and animals.

tis may develop. Streptococcus equi equi is

. Listeriosis (seep 2839), which is caused by
one of the most corrunon causes of brain

Listeria monoC'lJtogeries and is a conm1on
abscessation in horses, and Rhodococcus
infection in cattle, sheep, and goats and less
equi abscesses have been described in foals common in horses, is an example of a
both of which are secondary to primary

'

rnultifocal brain stern meningoencephalitis
infection of lymph or other tissues.

that ascends to the CNS via transaxonal

Spontaneous bacterial meningitis or
migration in cranial nerves. Mannheimia
meningoencephalitis develops in dogs rarely,
haernolytica and Pasteurella multocida
occurs more commonly in food animals and
although usually resulting in fibrinous '

is most corrunon in septic neonatal anin�als.

pneumonia and hemorrhagic septicemia in

Various aerobic bacteria (Pasteurella
ruminants, occasionally produce a localized
multocida, Staphylococcus spp, Escherichia fibrinopurulent leptomeningitis. Meningoen
coli, Streptococcus spp, Actinomyces spp, cephalitis due to M haernolytica has also
and Nocardia spp) and anaerobic bacteria
been reported in horses, donkeys, and mules.

(Bacteroides spp, Peptostreptococcus

Actinomyces, Kl.ebsiella, and Streptococcus a�aerobius, Fusobacterium spp, Eubacte
spp are sporadic causes of meningitis in adult
rium_spp, and Propionibacterium spp) have horses.

been isolated from animal infections.

Viral Infections: Viruses commonly

Bacterial endocarditis with associated
cause nonsuppurative meningitis,
septicemia is important in the etiopathogenencephalitis, and encephalornyelitis.

es1s of CNS infection in adult dogs. In Lyme

Several viruses are specifically neurotropic
enderruc ar�as, neurologic infection in dogs
or exhibit predilection for the CNS, causing

With Borrelia burgdorferi has been
a fulmrnate or fatal encephalitis, the most
in1plicated. Other non-neonatal hematognotonous being rabies virus infection (see enously derived infections are well-recogp 1302). Although rabies viruses primarily ruzed disease entities, such as thromboemspread to the CNS transaxonally, several bolic meningoencephalitis of cattle
other common DNA (adenoviruses,

(Histophilus somni, seep 754), Glasser's
herpesviruses, parvoviruses) and RNA

1264

MENINGITIS, ENCEPHALITIS, AND ENCEPHALOMYELITIS

(bunyavirus, lentiviruses, morbilliviruses,

Fungal Infections: Pathogenic fungi,
alpha viruses, flaviviruses) viruses are likely
including Coccidioides immitis,
spread via the bloodstream but exhibit high

Blastomyces dermatitidis, and Histo
neuropathogenesis once within the CNS.

plasma capsulatum, can cause menin

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Both hematogenous and transaxonal routes
goencephalitis. Opportunistic invasion
of spread are thought to occur in flavivirus
with Cryptococcus neoforrnans andAsper
infections. Recently, minute viruses
gillus spp has also been described in

(Parvoviridae) have been implicated in dogs several mammalian species. Rarely, other and nonhuman primates, respectively.

fungi, such as Candida spp, Cladosporium Reoviruses cause encephalitis in mice and
trichoides, Paecilomyces variotii,
nonhuman primates. Colorado tick virus, a

Geotrichum candidum, and dematiaceous

Coltivirus, has been implicated in infections
fungi (Bipolaris sp and Alternaria spp) in domestic species. Most animals have viral cause meningoencephalitis. Unicellular species-specific infections that exhibit
plants, Prnto/,heca wickerhamii and P
predilection for the CNS. Rarely, a
zopfii, can also produce an eosinophilic
postvaccination encephalomyelitis in dogs
meningoencephalomyelitis in dogs, cattle,
is associated with immwlizations against
and horses.

canine distemper virus, rabies virus, and
canine coronavirus-parvovirus vaccines.

Idiopathic/Immune Mediated: Several

Herpesviruses cause encephalomyelitis
idiopatllic meningoencephalitides are
syndromes in each of their respective hosts.

recognized in dogs. Granulomatous
meningoencephalomyelitis (seep 1252) is a

Infections Caused by Parasites: Many
relatively common CNS disease of dogs that
parasitic agents can cause meningoencephamost often affects yow1g to nliddle-aged, litis in both large and small anin1als.

small-breed females. A pyogranulomatous

Neuropathogenic protozoa include
meningoencephalomyelitis has been seen in

Toxoplasma gondii, Neospora caninum,
mature Pointer dogs. This acute, rapidly
and Encephalitozoon citnicitli in dogs and
progressive disorder is characterized by
cats. E citniculi can cause encephalomyeliextensive mononuclear cells and neutrotis in rabbits. Sarcocysti.s neurona and N
phils infiltrating the leptomeninges and
hughesii are important causes in horses,
pm·enchyma, especially in the cervical
with 'I'rypanosoma spp important in equids
spinal cord and brain stem. A necrotizing
outside of the USA. A wide variety of
meningoencephalitis of W1known etiology
protozoa can infect and cause severe CNS
has been reported in yoW1g, adult Pug dogs,
disease in adult cattle, including Babesia
as well as in Yorkshire Terriers and Maltese
bovis, Theileria parva (theileriosis), and
dogs. A steroid-responsive suppurative

'I'lypanosoma spp, whereasN caninitm and meningitis affecting mainly yoW1g ( <2 yr), T gondii can cause congenital encephalitis
large-breed dogs and a severe necrotizing
in calves. Free-living amoebae, Naegle'ria
vasculitis and meningitis syndrome has been
fowleria, Acanthamoeba spp, and
docwnented in Beagles, Bernese MoW1tain

Balamuthia mandrillaris are associated

Dogs, and German Shortl1aired Pointers,
with amoebic mening()encephalitis in dogs.

and both have been identified as possible

Aseptic suppurative or eosinophilic
immW1ologic disorders with a hereditary
meningoencephalitis associated with
predisposition. (See also CONGENITAL ANO
aberrant migration of parasites throughout

INI IERITEO ANOMALIES OF Tl-IE NERVOUS SYSTEM,
the CNS can develop in a number of animal
p 1222.) An eosinophilic meningoencephalihosts. In dogs and cats, CNS infections have tis that has been described in adult dogs
been reported with Dirqfilaria immitis,

(Golden Retrievers, Rottweilers, and South

Toxocarct canis, Ancylostoma caninum,

African Boerboels) and cats is also believed

Cuterebra spp larva, and Taenia spp. A wide to have an i.J11111W1ologic basis.

variety of nematodes have been rep01ted to
cause severe meningoencephalitis in horses, Clinical Findings: In the early stages including Setaria spp, Habronema spp, of inflammatory diseases of the CNS,

Strongylus spp, Halicephalobus gingivalis, nonlocalizing clinical signs are frequent. In
and Angiostrongylus cantonensis (the rat
dogs, for example, meningitis can easily be
lw1gworm). In cattle, nligrating Setaria and mistaken for interve1tebral disc extrusion,

Hypoderma, lmva are commonly implicated. polyarthritis, pleuritis, pancreatitis, or Recently, A cantonensis has been identified pyelonephritis. In horses, initial clinical
as a cause of eosinophilic; meningoencephasigns cm1 appear as lameness, myositis, litis in nonlmman primates. Parelaphostron
vertebral instability, or even colic. In foals,
gylus tenuis is especially important in goats extreme hyperexcitability and irritability
and llamas.

can be an early indication of sepsis in the

MENINGITIS, ENCEPHALITIS, AND ENCEPHALOMYELITIS

1265

CNS. Cattle can demonstrate anorexia,

Diagnosis: Often, there are no related
depression, and bizarre behavior.

changes in a CBC or serum biochemical

The usual signs of meningitis are fever,
profile to indicate CNS infection. The
hyperesthesia, neck rigidity, and painful
analysis of CSF is the most reliable and
paraspinal muscle spasms. Dogs and
accurate means to identify an encephalitis,

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occasionally horses display this syndrome
meningitis, or meningoencephalitis. CSF
acutely and sometimes chronically without
should be collected whenever history,
clinical signs of brain or spinal cord
species, or breed predisposition suggests
involvement. However, in diffuse meningoenmeningitis or encephalitis, or whenever cephalitis due to any agent, depression,
clinical signs indicate a disseminated or
blindness, progressive paresis, cerebellar or
multifocal CNS disorder. Without CSF
vestibular ataxia, opisthotonos, cranial ne1ve
analysis, an animal exhibiting back or neck
deficits, seizures, dementia, agitation, and
pain with an increase in rectal temperature
depressed consciousness (including coma)

may be misdiagnosed.

can develop, depending on the rapidity of

Adult large animals and dogs with
onset, pathology, and location of the lesions.

bacterial meningitis and encephalitis or with

Visual deficits, neck pain, seizures, behavsteroid-responsive suppmative meningitis ioral disturbances, ataxia, weakness, cranial
typically have a marked neutrophilic
nerve deficits, and depression may be seen in
pleocytosis in the CSF, with cell counts in
either focal or disseminated CNS disease.

t11e hundreds to thousands. The protein

In neonatal infections, omphalophlebitis,
content of the CSF is usually also signifipolyarthritis, and ophthalmitis with cantly increased(> 100 mg/dL), with an
hypopyon can accompany the CNS
increase in the globulin component of CSF
inflanm1ation. Because of its unusual

Rickettsial infections most often cause a
pathogenesis, listeriosis often causes
mild to moderate mononuclear pleocytosis,
asynm1etric vestibular dysfunction, with
although Rocky Motmtain spotted fever can
head tilt and circling, in addition to other
cause neutrophilic inflanm1ation secondary
cranial nerve deficits such as facial and
to vasculitis.

pharyngeal paralysis. In histophilosis of

In foals with meningitis, the CSF has an
cattle, the nervous signs tend to be peracute,
increased protein content, and even slight
with sudden collapse and profound
increases in WBCs in the CSF are significant
depression of consciousness (stupor or

(>10 WBC/µL). Any neutrophils obse1ved
coma); fever and lin1b stiffness may be the
on cytology in CSF from a foal warrant
only signs detectable in the prodromal
treatment with antimicrobials that can
stages. In sporadic bovine encephalomyelitis, obtain high therapeutic levels in the CNS.

calves demonstrate incoordination that can

Viral infections and listeriosis typically
progress to recumbency and opisthotonos.

produce a mild to moderate mononuclear
pleocytosis in CSF, with an associated

Lesions: Gross lesions are extremely variincrease in protein levels. However, tl1e CSF
able depending on cause and location and
is normal in rabies virus infections. Herpeswhether the disease is diffuse or multifocal.

virus infections cause markedly increased

Pathologic changes characteristic of
proteins and xanthochromia (yellow to
meningitis include diffuse infiltration of
reddish discoloration) without dramatic
leukocytes into the leptomeninges. This can
increase in cell count. Feline infectious
be mild if flaviviral, or florid if granulomaperitonitis (FJP) in cats and Eastern equine tous (thickened) or alphaviral (hemorencephalitis in horses are exceptions and rhagic). Frequently, the entire subarachnoid
can cause markedly high neutrophil counts.

space of the brain and spinal cord is

In FIP, a markedly high protein concentrainflamed. Vasculitis of meningeal vessels tion (>200 mg/dL) can also be seen.

and CNS arterioles may also be apparent.

Parasitic and fungal meningoencepha

In meningoencephalitis, the inflammation
litides cause eosinophilic or occasionally a
extends into the CNS parenchyma, resulting highly degenerate neutrophilic pleocytosis.

in leukocyte infiltration with large areas of

Granulomatous inflanunations usually
perivascular cuffing. Necrosis and malacia
induce moderate to high cell numbers and
of the CNS may be seen, with infiltrations of
increased protein in the CSF. The cell
macrophages, neutrophils, and plasma cells. population is predominantly mononuclear Grossly, this is seen as local areas of
or a mixed population of neutrophils and
discoloration. Listeriosis uniquely causes
mononuclear cells. Distinguishing a
microabscesses deep witllin the CNS
granulomatous infection due to a fungal or
parenchyma, which consist of accumulaprotozoa! organism from granulomatous tions of neutrophils and microglial cell
meningoencephalitis is often difficult. The
reaction with central liquefactive necrosis.

necrotizing encephalitides typically cause a

1266

MENINGITIS, ENCEPHALITIS, AND ENCEPHALOMYELITIS
mild increase in CSF mononuclear cells and tetracyclines, potentiated sulfonamides, protein concentration.

fluoroquinolones, and third-generation

Occasionally, bacteria are seen on
cephalosporins; higher than normal dosages
cytologic examination of the CSF and identimay be necessary to achieve and maintain fied with Gram stain. Successful culture of
adequate concentrations in the CNS. In farm
bacteria from CSF is more likely in large
animals, selection of drugs must be based

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animals than in dogs. In some cases, serial
not only on drug efficacy but also on
blood cultures are more successful,
whether the available drug is appropriate
especially in foals. Fungi and occasionally
for use in a food animal.

protozoa have been identified in CSF, but

For viral infections, the case-fatality rate
serology is usually necessary to confirm
varies. The most lethal viral infections are
mycotic and protozoa! infections in vivo.

rabies (100%) in all mammals, Eastern

Many of these diseases are fatal, and final
equine encephalomyelitis in horses
identification is made at postmortem with

(85%-100%), and distemper virus in dogs
in situ identification of the organism.

(50%). Availability of antivirals is limited,

For premortem etiologic identification,
and cost can be prohibitive. The most
agent-specific testing is recommended;
commonly treated viral infection of the
however, most agents, once in the CNS, are

CNS is Ii kely that of the neurotropic form
not detectable by direct testing through
of equine herpesvirus l; however, the
culture or nucleic acid-based testing of
prognosis is guarded in recumbent horses.

body fluids. Serologic testing is available for

Mycotic infections of the CNS have been
most viral encephalitides and, in particular,
treated successfully in people, but results
for arboviruses the most reliable test
in veterinary medicine are less rewarding.

exan1ines IgM in a single sample. Paired

Treatment with itraconazole or fluconazole
serum is required for IgG-based tests,
may be of benefit, but longtem1 therapy
especially those confounded by vaccinais required and relapses are frequent.

tion. Although CSF analysis is rewarding

Protozoa.I infections ( eg, toxoplasmosis,
in tenns of clinical pathology, detection
neosporosis, sarcocystosis) may respond to
of a pathogen within the CSF can also be
a potentiated sulfonamide (trimethoprim,
unreliable depending on the location and
pyrimethanline and sulfonamides). These
pathogen load within the CNS. Culture
are commonly used in combination with
of the CSF will often yield growth of the
clindamycin in small animals. However,
organism in bacterial meningitis; however,
relapse may occur because of the inability
the detection rate is often <4096 for many
to clear encysted organisms from the CNS.

viruses. Detection of antibody within the

Antiprotozoal medications have been

CNS can be nonspecific if there is leakage
approved for use in horses, such as the
through the blood-brain barrier. IgM
tliazine analogues, including diclazuril and
detection is likely a more reliable indication ponazuril. In balantidiasis, a disease in of intrathecal antibody production. Most
working donkeys, secnidozole has been
confinnatory testing is performed
shown to decrease fecal cyst counts, which
postmmtem if the animal dies.

should theoretically decrease the risk of
development of CNS disease.

Treatment: Other than for animals with

Glucocorticoids are usually contrathe probable immune-mediated, steroidindicated in anin1als with meningitis or responsive inflanl.ll1atory CNS diseases and
meningoencephalitis with an infectious
for animals with meningoencephalitis
etiology; however, a high-dose, short-term
caused by rickettsia and certain bacteria,
course of dexamethasone or methylprednithe prognosis is guarded. The case fatality solone may control life-threatening complirate in calves with bacte1ial meningitis has cations such as acute cerebral edema and
been reported to be 1 OOOA,; however, the case
impending brain herniation. Immunosupfatality rate in foals is much lower.

pressive doses of corticosteroids are

Appropriate use of antibiotics, according
required for successful therapy of the
to culture or serology results, is basic to sucidiopathic CNS inflammations seen in cessful therapy. Relapses are common, and
dogs.

prolonged therapy is often necessary.

Radiation therapy and immunomod

Correction of failure of passive transfer is
ulatory drugs have been used to treat
critical in neonatal large animals. Broadgranulomatous meningoencephalitis.

spectrum antibacterials that can penetrate

Supportive care should be specific for
the blood-brain barrier should be selected,
the needs of the individual animal and may
and bactericidal drugs are preferred over
include analgesics, anticonvulsants, fluids,
bacteriostatic agents. Recommended
nutritional supplementation, and physical
drugs include ampicillin, metronidazole,
therapy.

NEOPLASIA OF THE NERVOUS SYSTEM

1267

MOTION SICKNESS

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Motion sickness is characterized by signs
and promethazine hydrochloride) prevent
referable to stimulation of the autonomic
motion sickness, provide sedation, and
nervous system, including excessive
inhibit drooling. The centrally acting
salivation and vomiting. Affected animals
phenothiazine derivatives (such as chlormay also yawn, whine, or show signs of prornazine, prochlorperazine, and aceprornauneasiness and apprehension; severely zine rnaleate) have antiernetic as well as
affected animals may also develop diarrhea.

sedative effects. Cats have no histanline

Motion sickness is seen during travel by land, receptors in tl1e CRTZ; tl1erefore, antillistasea, or air, and signs usually disappear when rnines are ineffective in treating motion
vehicular motion ceases. The principal
sickness in this species. Motion sickness
causative mechanism involves stimulation
in cats probably is best treated with an
of the vestibular apparatus in the inner ear,
a-ad.renergic antagonist ( eg, chlorprornazine)

which has connections to the emetic center
instead of a pure H,-histarninergic antagonist.

in the brain stern. The chernoreceptor trigger

Maropitant, an NKl receptor antagonist, is
zone (CRTZ) and H,-histarninergic receptors
effective in treating motion sickness in dogs.

are involved in this pathway in dogs but

NKl receptors are located in the emetic
apparently are less important in cats. Recent
center of tl1e brain stern, which is the source
evidence has revealed that the neuroki.ni.n 1
most responsible for the vomiting and nausea
substance P receptors (NKl) in the emetic
of motion sickness. Blocking these receptors
center play a major role in motion sickness
is more effective t11an inhibiting the CRTZ.

in botl1 dogs and cats and are more

Therefore, rnaropitant is probably the drug of
important tl1an t11e receptors in the CRTZ.

choice to treat motion sickness in dogs.

Fear of the vehicle may also become a

Another benefit is that treatment is given
contributory factor in dogs and cats that
once daily. The drug is approved and available
develop a conditioned response to the event;
in tablet and iajectable fomis for use in dogs,
signs may be seen even in a stationary
while only the iajectable form is approved for
vehicle. In this situtation, behavioral
use in cats. Cats should be 16 wk old and dogs
modification may be needed to elinlinate

8 wk old before using maropitant.

this fear, or the use of drugs that provide a

Phenobarbital and diazepam can be used
sedative effect may be needed.

to produce a general sedative effect if

In some cases, motion sickness can be
anxiety is a problem. Oral administration
overcome by conditioning the animal to
of one of these drugs several hours before
travel. In others, ataractic and anti.nausea
departure should reduce or eliminate the
drugs can be used with good results.

signs of motion sickness. (See also DRUGS TO

A.ntillistanlines (such as diphenhyclranline

CONTROL Oil STIMULATE VOMITING (MONOGASTRIC),
hyd.rochlo1ide, dimenhyd.tinate, rnecli.zine,
p 2547.)

NEOPLASIA OF THE NERVOUS SYSTEM

Neoplasia of the nervous system has been
and muscle or from hernatogenous
reported in all domestic animal species.

metastasis of a pri.n1ary t1.unor in another

Nervous system tumors have been detected
organ. Trunor ernboli can lodge and grow
in 1 o/o--3"/o of necropsies in dogs. In cats,
anywhere in the brain, meninges, choroid
nervous system tumors are less common and plexus, or spinal cord. Dissemination or are mainly rneningiornas and lymphomas.

metastasis of CNS tumors is rare but may

Primary nervous system tumors originate
occur via the CSF patl1ways, especially if the
from neuroectoderrnal, ectodem1al, and/or
tu.n1ors are located close to the subarach.noid
mesoderrnal cells nonnally present in ( or
space or ventricular cavities ( eg, choroid
associated with) the brain, spinal cord, or
plexus papillorna, ependyrnorna, rnedulloperipheral nerves. Secondary tumors blastorna, neuroblastorna, pinealoblastorna),
affecting the nervous system may originate
or via a hernatogenous route such as the
from surrounding structures such as bone
dural sinus, with later development of

1268

NEOPLASIA OF THE NERVOUS SYSTEM
remote metastasis, most often in the lung.

Classification: Classification of nervous

Tumors may also spread by direct extension
system tumors in animals follows the
to surrounding tissues, especially bone. The
criteria used for tumors in people and is
osseous tentorium may be used as a
based primarily on the characteristics of
reference point to localize different areas
the constituent cell type, its pathologic

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of the brain within the cranial vault. Thus,
behavior, topographic pattern, and
tumors in the cerebral hemispheres are often secondary changes seen within and around referred to as supratentorial or anterior fossa the tun10r (see TABLE 2).

tumors, while those in the brain stem or

Immunocytochemical studies and
cerebellum are called i.nfratentorial or
imaging techniques may aid classification.

posterior fossa tumors.

Primary twnors typically grow slowly,

IH=iiil TUMORS OF THE NERVOUS SYSTEM IN DOGS AND CATS

Tumor Origin

Predilection Sites

Species

Incidence

PRIMARY TUMORS

Nerve cells

Ganglioneuroma

Variable, eg, cerebel-

Dogs

Rare

(gangliocytoma)

!um, cranial nerve

Ganglioneuroblastoma
roots, eye, cervical

Neuroblastoma
ganglion

P1imitive neuroectodermal
tumors

Neuroepithelium

Ependymoma

Third and lateral

Dogs, cats

Uncommon
ventricles

N ephroblastoma
l'vleninges,thoraco-

Dogs (German

Uncommon
lumbar spinal cord

Shepherd)

Choroid plexus papilloma

Fourth ventricle

Dogs

Common

Neuroglia

Astrocytoma (fibrilla.ry,

Pirifom1 area, convexity Dogs

Common
protoplasmic, gemistocytic, of cerebral hemispheres, (brachycephalic ), a.nap las tic)

thalamus, hypothalamus cats

Oligodendroglioma

·Cerebral hemispheres

Dogs

Common

(brachycephalic)

Glioblastoma

As for astrocytoma

Dogs

Unco1mnon

(brachycepha.lic)

Spongioblastoma

Variable, eg, ependymal Dogs

Rare
surfaces, cerebellum,

(brachycephalic)

optic nerve and tracts
l'vledulloblastoma

Cerebellun1

Dogs, cats

Uncommon

Gliomas (unclassified)

Periventricular areas, Dogs

Common
especially in cerebra.I
hemispheres

Peripheral nerves and nerve sheaths

Nerve sheath tumors

Peripheral nerves

Dogs, cats

Common

(schwa.nnoma, neurofibro-
sarcoma, neurofibroma,
neurinoma)

( continued)

NEOPLASIA OF THE NERVOUS SYSTEM

1269

•tJ:iifJ TUMORS OF THE NERVOUS SYSTEM IN DOGS AND CATS (continued) Tumor Origin

Predilection Sites

Species

Incidence

Meninges, vessels, and other mesenchymal structures

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Meningiomas (fibrous,

Convexities of cerebral Dogs

Common
transitional, psammomahemispheres and floor (dolicocephalic), tous, angiomatous,
of the vault
cats
papillary, granular cell,
myxoid, anaplastic)

Angioblastoma

Variable

Dogs, cats

Rare

Sarcoma

Variable

Dogs, cats

Common

Histiocytic sarcoma (focal Cerebral hemispheres Dogs, cats Rare
granulomatous meningoen- and brain stem

(in dogs)

cephalomyelitis reticulosis)

Pineal gland, pituitary gland, and craniopharyngeal duct Pinealoma

Pineal body

Dogs

Rare

Pituitary adenoma

Pituitary gland

Dogs (brachy

Common
cephalic ), cats

Craniopharyngioma

Hypophyseal

Dogs

Rare
infundibular areas

Heterotopic tissues

(malformation tumors)

Epidermoid, dermoid,

Variable (fourth

Dogs

Rare
teratoma, teratoid,
ventricle and cerebelintra-arachnoid cyst
lopontine angle for
epidermoid, quadri-
geminal cistern for
intra-arachnoid cyst)

Genn cell tumors

Base of brain above

Dogs

Rare
sella turcica

Hamartoma

Variable (eg, hypothala- Dogs

Rare
mus)

SECONDARY TUMORS

Metastatic tumors

Manm1ary gland adeno-

Variable

Dogs, cats

Relatively
carcinoma, pulmonary
common
carcinoma, prostatic
carcinoma, chemodectoma,
malignant melanoma,
lymphosarcoma, salivary
gland adenocarcinoma,
hemangiosarcoma, etc

Primary tumors from surrounding tissues

Osteosarcoma, lipoma,

Variable

Dogs, cats

Relatively
osteochondroma, chondro-
common
sarcoma, fibrosarcoma,
nasal adenocarcinoma,
hemangiosarcoma, multiple
myeloma, calcifying
aponeurotic fibromatosis,
epidennoid cyst, etc

1270

NEOPLASIA OF THE NERVOUS SYSTEM
whereas secondary, highly malignant,
tumors among domestic animals; glial
metastatic tumors and bone tumors
tumors, including unclassified gliomas, are
generally progress more rapidly. Many
the most nwnerous tumors in these breeds.

animal twnors have characte1istics

One study of 97 dogs indicated that Golden
analogous to corresponding hwnan

Retrievers also have a high incidence of
neoplasms; however, 15o/o-20% of neurobrain twnors ( especially meni.ngiomas ).

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ectodermal twnors (especially gliomas)

Secondary twnors extending into the
remain unclassified. Many of these are
cranial vault from the nasal sinuses are
related topographically to the ventricular
relatively common in dogs. ln some cases,
system and/or subependymal cell nests.

usually those involving caudal nasal tumors,

As many as 26% of neuroectodermal brain
the only clinical signs are neurologic
tumors are undifferentiated, as shown by
abnormalities such as behavioral changes,
immunocytochemical staining. Although
circling, paresis, seizures, or visual deficits.

brain tumors are occasionally reported in

Respiratory signs such as epistaxis, nasal
animals <l yr old, most are found in mature
discharge, sneezing, dyspnea, stertor, or
and aged animals. No sex predilection for
mouth breathing may develop after
nervous system tumors has been identified.

neurologic signs or may be absent. Nasal
twnor types include adenocarcinoma,

Incidence: The reported incidence of
anaplastic chondrosarcoma, epidermoid
nervous system neoplasia in animals varies.

carcinoma, esthesioneuroblastoma, neurofi

However, such tumors are reported more
brosarcoma, neuroendocrine carcinoma,
often in dogs than in other domestic
and squamous cell carcinoma. Unlike nasal
animals. ln one survey, 2.83% of 6, 175 dogs
cavity tumors, tumors that originate in
examined at necropsy had intra.cranial
middle or inner ear structures rarely extend
neop!asia. ln another report, incidence of
into the brain (see TABLE 2). Metastatic brain intra.cranial neoplasia was 14.5/100,000
tW11ors are also commonly recognized in
dogs at 1isk and 3.5/100,000 cats at risk A
dogs, with hemangiosarcoma being the
retrospective study of young dogs ( <6 mo
most common metastatic tumor type. ln
old) indicated that the three most common
cats, metastases most frequently originate
sites for neoplasia (in decreasing order)

from man1111ary carcinomas and lymphosarwere the hematopoietic system, brain, comas.

and skin. Brachycephalic breeds are at

Astrocytomas are probably the most
increased risk of some neuroectodermal
common neuroectodermal brain tumor in
twnors.

dogs. They are usually foWld in adult dogs,
but they have been reported in dogs <6 mo

Brain Tumors: ln dogs and cats, the brain
old. They are common in brachycephalic
is a. more common site of primary tumors of
breeds but can be seen in any breed.

the nervous system than the spinal cord or

Astrocytomas consist of relatively large,
pe1ipheral nerves. Meni.ngiomas, gliomas
protoplasmic-rich cells or smaller cells

(eg, astrocytomas, oligodendrogliomas),
with many processes. The cells tend to be
undifferentiated sarcomas, pituitary
arranged aroW1d blood vessels. There are
twnors, and ventricuiar twnors ( eg, choroid
several variants ( eg, anaplastic, fibrillary,
plexus papillomas, ependymomas) are
gemistocytic, protoplasmic, and pilocytic),
commonly reported primary brain tumors
most of which stain positively for glial
in dogs. Previously reported cases of
fibrillary acidic protein (GFAP), the
neoplastic reticulosis, gliomatosis,
chemical subunit of the intra.cytoplasmic
microgliomatosis, malignant histiocytosis,
intem1ediate filaments of astrocytes.

or the malignant fonn of granulomatous

Regressive changes found histologically
meni.ngoencephalomyelitis are now
include necrosis, mucinoid degeneration,
classified as histiocytic sarcomas or
cyst fom1ation, vascular proliferation ( often
lymphomas. Other primary brain twnors
in the form of glomeruloid nests), and

( eg, malformation twnors ), tumors of nerve
multinucleated giant cells. Hemorrhage
cells (eg, neuroblastoma, ganglioneuroblasis rare. Malignant astrocytomas display toma, and ganglioneuroma), pinealomas,
nuclear polymorphism, mitotic figures, and
craniopharyngiomas (a suprasellar
small cells with dense, hyperchromatic
ectoclem1al tun10r that may destroy the
nuclei. In one study using CT, astrocytomas
pituitary gland), spongioblastomas
and oligodendrogliomas appeared sinlilar

(embryonal glioma), and medulloblastomas
to one another, because both twnors had
are rare. Adult dogs of several brachycering-like, irregular enhancement and poorly phalic breeds-Boxers, English Bulldogs,
defined margins. Differentiating oligodenand Boston Teniers-are often cited as drogliomas from malignant astrocytomas
having the highest incidence of brain
with MRI has been difficult. ln some

NEOPLASIA OF THE NERVOUS SYSTEM

1271
instances, however, MRI is considered
only one of nine ependyrnornas was positive
superior to CT in defining diffuse leptofor GFAP. In a CT study of brain tumors, meningeal and low-grade cerebral astrocyependyrnornas had no definitive distinguishtomas. Astrocytomas are uncommon in ing features.

cats; in one report of four cats, the tumors

Gangliocytomas are rare intracranial

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invaded the third and lateral ventricles.

tumors reported in adult dogs of several

Choroid plexus papillomas are
breeds. Histologic findings include mature,
common tumors in dogs, with reported
neuronal-like cells with multiple processes,
frequency similar to that of glioblastomas
a central nucleus, and a nucleolus.

(-12% of neuroglial tumors). Developmen

Neuroblast-like immature cells may also
tally, the choroid plexus epithelium differbe seen, and occasionally, newly formed entiates from the ptimitive medullary
myelin sheaths. They seem to be seen most
epithelium and is related to the ependymal
often in the cerebellun1. Pure gangliocytocells. These tumors are reddish, papillary rnas have no glial elements and do not
growths that may bleed. Histologically, they
express GFAP. Mineralization and extenare well defined, grow by expansion, and sive necrosis accompanied by edema and
have a granular papillary appearance.

capillary proliferation may also develop.

Tumor papillae consist of vascular stroma

Suprasellar germ cell tumors are
lined by one layer of cuboidal or cylindrical
located dorsal to the sella turcica at the
epithelium. Immunocytochemical studies
base of the brain. They are often intimately
reveal that these tumors express epithelial
associated with the pituitary gland, which
but not glial differentiation, based on
may be trapped within or replaced by the
absence of staining with GFAP Keratin may
germ cell tumor. They are thought to result
be expressed from some of these tumors.

from extensive migration of germ cells

In both benign and malignant variants of
during embryogenesis. Neurologic signs
choroid plexus papillomas, dissemination
may be acute in onset and may include
to other areas of the brain or spinal cord
lethargy; depression; bradycardia; dilated,
via the CSF pathways may occur after
nonresponsive pupils; ptosis; visual deficits;
exfoliation. Obstructive hydrocephalus may
and blindness. Gem1 cell tumors may be
occur. Meningeal carcinomatosis may
larg-xtending from the olfactory
follow spread of the tumor in the subarachpeduncles to the pons and pyriform noid space. Choroid plexus tumors are seen
lobes-and may envelop other cranial
as well-defined, hyperdense masses with
nerves (eg, nerves III-VII). Histologically,
marked, uniform contrast enhancement on
the tumors usually contain a mixture of

CT scans. Marked enhancement, potentially primitive germ cells, cords resembling including hemorrhage and mineralization,
hepatocytes, and acini and tubules of tall
is also seen with MRI. Choroid plexus
colmnnar epithelial cells. They may stain
papillomas have no apparent predilection
positively for fetoprotein. Affected animals
for brachycephalic breeds and are rare in
are usually 3-5 yr old; Dobem1an Pinschers
cats.

may be at higher risk than other breeds.

Ependymomas originate from the

Some germ cell tumors have been
epithelium lining the ventricles and central
misdiagnosed as pituitary tumors or
canal of the spinal cord. They are rare but
craniopharyngiomas.

have been reported most frequently in

Glioblastoma multiforme, considered
brachycephalic breeds. The gray to reddish,
to be equated with the more malignant
soft, lobular masses tend to invade the
forms of astrocytornas, has been reported
ventricular system and meninges, which
with varying frequency in dogs. In one study,
may result in obstructive hydrocephalus.

the incidence was l2%of215 neuroglial

Mestastases within the CSF system may be
tun1ors. Most are large and found in the
seen. Ependymornas of the fourth ventricle
cerebrum. The tumor cells consist of
may encircle the brain stern. Both epithelial
medium-sized, round or fusiform cells with
and fibrillary varieties have been described.

isomorphic nuclei. Some glioblastomas

Histologically, cells are isomorphic, with
display considerable pleomorphism, with
pale or transparent cytoplasm and round,
small and large mononucleated and
chromatin-rich nuclei. Nucleus-free zones
multinucleated cells. They are locally
around blood vessels are characteristic.

invasive and destructive, well vascularized,

Some ependymornas appear hemorrhagic,
and often contain necrotic zones. Glioblaswith rnucinoid degenerative changes and tomas sometimes express GFAP and are
cyst formation. Malignant or anaplastic
most common in brachycephalic breeds.

ependyrnornas have moderate degrees of

Hamartomas are formed by disorderly
pleornorphisrn and necrosis and may merge
overgrowth of tissues normally present
into glioblastorna rnultiforme. In one study,
at a site. They are focal malformations

1272

NEOPLASIA OF THE NERVOUS SYSTEM
resembling neoplasms and have been
and are rare tumors in dogs. They typically
reported only rarely in dogs, usually as
lie close to embryonal lines of closure.

a subclinical finding.

Epidermoid and dermoid cysts result from

Hematogenous metastatic brain
inclusion of epithelial components of

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tumors commonly originate from
embryonal tissue at the time of closure of
extracranial sites. In dogs, they often
the neural tube. They reportedly have a
develop from carcinomas of the mammary
predilection for young dogs ( eg, 3-24 mo
glands, thyroid, bronchopulmonary
old), although cysts have been found in
epithelium, kidneys, chemoreceptor cells,
older dogs. They usually involve the cerebelnasal mucosa, squamous epithelium of the lopontine angle, fourth ventricle, or both.

skin, prostate, pancreas, adrenal cortex, and Cysts within the fourth ventricle may salivary glands. Brain metastasis from a
secondarily compress the medulla
transmissible venereal tumor has been
oblongata and cerebellum. Some epiderreported in a 5-yr-old male mixed breed dog.

moid cysts are incidental findings at

Common sarcoma metastases in dogs
necropsy.

include fibrosarcomas, hemangiosarcomas,

Histologically, epiderrnoid cysts may have
lymphosarcomas, and melanoblastomas.

a multilocular structure; most are lined by

Brain metastases may accompany intramedstratified squamous epithelium and contain ullary spinal cord metastasis in dogs with
keratinaceous debris, desquamated
lymphosarcomas or hemangiosarcomas.

epithelial cells, and occasional inflamma

In cats, metastases stem most often from
tory cells. In contrast, dermoid cysts
mammary carcinomas or lymphosarcomas.

contain adnexal structures such as hair

Most CNS lymphomas, Pspecially in dogs,
follicles, sebaceous glands, and sweat
are one part of a multicentric disease, with
glands. Cysts may measure as much as 2.5
extensive infiltration of the choroid plexus
cm in diameter. Because of the tumor's
and leptomeninges a common finding.

location, dogs may show signs of a

Neoplastic angioendotheliomatosis in dogs
pontomedullary syndrome ( eg, trigeminal,
is thought to be an angiotropic lymphoma,
facial, cerebellar, and/or vestibular
possibly of the B-cell line. Extraneural
dysfunction). Teratomas are well-differentitumor cells sometin1es localize in the ated germ cell tumors (see above) arising
meninges (eg, meningeal carcinomatosis),
from several embryonic gem1 cell layers.

often in association with intestinal

Medulloblastomas are highly malignant,
carcinoma or mammary adenocarcinoma.

uncommon neuroectodermal canine tumors

Histiocytic sarcomas (previously
that almost always develop in the cerebelnan1ed malignant histiocytosis or primary/
lum. The tun10rs tend to bulge into the
neoplastic reticulosis) are rarely reported in
fourth ventricle, often replacing part of the
dogs. Proliferation and/or infiltration of
cerebellar vennis and compressing the
neoplastic histiocytes in the basiarachnoimidbrain rostrally and the brain stem dal and ventricular areas (bilateral) is a
ventrally. They may infiltrate the meninges,
characteristic feature. These cells may also
metastasize within the CSF pathways, and
infiltrate the spinal dura mater, arachnoidal
cause obstructive hydrocephalus.

space, leptorneninges, and spinal nerve

Histologically, these tumors include sheets
roots. Histologically, the cells may have
of densely packed cells with pale cytoplasm
characteristic histiocytic morphology but
and oval or carrot-shaped nuclei with
exhibit moderate pleomorphism and numercoarse, granular chromatiR. Mitotic figures ous mitotic figures.

are common. Regressive changes include

Intracranial intra-arachnoid cysts
pyknosis and karyorrhexis. Although most
have been reported in dogs. These rare
cases are seen in young dogs, a cerebellar
malformation tumors seem to develop most
medulloblastoma with multiple differentiaoften in the quadrigeminal cistern. Of the six tion has been described in a 4-yr-old Border dogs in one report, three were <l yr old,

Collie.

four were males, and five of the six weighed

Meningioangiomatosis is a rare, benign

<11 kg. One dog had additional developmalformation of CNS blood vessels, charmental anomalies (abnormal corpus acterized by proliferation of the vessels and
calloswn and block vertebrae). On CT scans spindle-shaped, perivascular meningothelial and MRI, the cysts were extra-axial, had
cells in the cerebral cortex and brain stem
sharply defined margins, contained fluid
of juvenile and adult dogs. The meningotheisodense to CSF, and did not show contrast lial cells stain positively for vimentin, which,
enhancement.

along with the presence of mucopolysac

Malformation tumors, including
charides and collagen among proliferating
epidem10id and dennoid cysts and
cells, suggests a mesenchymal and
teratomas, originate from heterotopic tissue fibroblastic origin.

NEOPLASIA OF THE NERVOUS SYSTEM

1273

Meningiomas are extra-axial tumors.

The histologic classification of canine

They arise from elements of the dura within
meningiomas includes angioblastic,
the cranial and spinal spaces and are the
fibroblastic, meningothelial or syncytial,
most commonly reported brain tumors in
psarnmomatous, and transitional. Papillary

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cats. They are also one of the most common
and microcystic forn1s may also be seen.

intracranial tumors in dogs, with a reported

The tumors usually consist of large
incidence of 30%-39"Ai. In most studies,
meningothelial cells or fusifonn cells
meningiomas are seen in dogs > 7 yr old and
an·anged in whorls, nests, islands, or
in cats >9 yr old, although they have been
stream-like patterns. Cell boundaries are
seen in young cats ( <3 yr old) with mucotypically ill defined, and the nuclei contain polysaccharidosis type I and in dogs <6 mo
little chromatin. Canine meningiomas
old. They are often found in dolichocephalic
commonly have virnentin intermediate
breeds, especially Golden Retrievers. Canine
filaments. Regressive changes may include
and feline meningiomas have estrogen,
cavernous vascular formations, hemot"

progesterone, and androgen receptors.

rhage, hyaliniza.tion of connective tissue,

These usually benign tumors tend to grow
and deposits of fat, lipopigments, or
slowly under the dura mater, although direct
cholesterol. Many have evidence of focal
brain invasion has been repmted.

necrosis with suppuration. This is the likely

Pathologic findings include globular,
cause of the reported predominance of polyirregular, lobulated, nodular, ovoid, or morphonuclear cells in CSF in many dogs
plaque-like masses ranging in diameter from
with meningioma..

a few millimeters to several centimeters.

A grading system in human patients has

Meningiornas are typically discrete and
recently been adapted for dogs and may
often are firm, rubbery, and encapsulated.

predict twnor behavior. Grade I tumors are

They may contain granular calcifications
considered benign, grade II ttunors are

!mown as psarnmoma bodies. In addition,
considered atypical, and grade m twnors
there may be focal or massive calcification
are considered malignant.

of the tun1or. A substantial proportion of

Most feline epitheliomas are meningothebasal and plaque-like meningiomas involve liomatous or psa.mmomatous, often with
the floor of the cranial cavity, especially
cholesterol deposits.

when located near the optic chiasm or
ln meningeal sa.rcomatosis, sarcomas
suprasellar area. They also commonly are
cause diffuse thickening of tl1e meninges;
found over the convexities of the cerebral
extensive hemorrhages are common. These
hemispheres, less often in the cerebelloponrare tumors tend to infiltrate nervous tissue tomedullary region, and infrequently in the
and run along blood vessels. Cell types
retrobulbar space ( arising from the optic
include lymphoid, plasmacytoid, mature
nerve sheath). In cats, common locations
plasma. cells, immunoblastic cells, and·
include the tela choroidea of tl1e third
multi.nucleate giant cells.

ventiicle and the supratentorial meninges.

Oligodendroglioma.s are common

Cats also have a higher incidence (17%) of
tmnors in dogs, particularly in brachymultiple meningiomas. Hyperostosis, a cephalic breeds. In one report, they
thickening of bone acljacent to the meningicomprised 28% of neuroectodermal oma, may develop, especially in cats.

tumors. These tumors consist of chroma.

Meningiomas rarely metastasize outside
tin-rich, densely packed, round cells with
the brain, but may extend into paranasal
perinuclear halos. Most grow by infiltration
regions and lungs or be seen as primary
and destroy invaded tissue. Capillaries
extracranial masses as a result of embrytend to proliferate within these tumors, onic displacement of arachnoid cells or
producing glomerulus-like structures.

meningocytes. Those in extracranial

Regressive changes are similar to those
locations differ from intracranial meningiseen in astrocytomas (seep 1270). Necrosis omas primarily in their more aggressive
and extensive calcification are uncommon.

behavior and anaplastidmalignant nature.

These tumors do not stain with GFAP; in

Meningiomas may be distinguishable from
one study, 3 of 11 oligodendrogliomas
tun1ors within the brain parenchyrna on
reacted with myelin-associated glycoprocontrast CT scans by their appearance as tein, while none reacted with myelin basic
broad-based, peripherally located masses.

protein. Many canine oligodendrogliomas

Cystic and edematous meningiomas have
are mixed twnors with areas of astrocytic
been detected using CT scans and MRI.

and, in some cases, ependymal differentia

When a dural tail ( a linear enl1ancement
tion. The MRI features are similar to those
of thickened dura mater acljacent to an
seen with high-grade (malignant)

extra-axial mass) is detected by MRI, a
astrocytomas. Oligodendrogliomas are
meningioma is the most likely cause.

rare in ca.ts.

1274

NEOPLASIA OF THE NERVOUS SYSTEM

Pituitary tumors are corrunon in dogs,
lead to visual impairment, acute blindness
with an apparent predilection for brachyceand dilated, non.responsive pupils have phalic breeds. They are infrequent in cats.

been noted in seven dogs and one cat with

Tumors may be functional or nonfunctional.

pituitary masses that compressed the optic

Either type may cause hypopituitarism by
chiasm.

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mechanical or functional in1pairment of

Approximately 80% of cats diagnosed
remaining pituitary tissue, although this
with Cushing disease have PDH; tun10r
effect is uncommon. Nonfunctional canine
types include pituitary microadenomas,
pituitary tumors are corrunon and are
macroadenomas, and adenocarcinomas.

usually chromophobe adenomas, although

Pituitary acidophil adenomas, especially the
adenocarcinomas have also been reported.

large variety, have been associated with

Fw1ctional pituitary tumors associated with
acromegaly and nervous system signs ( eg,
the adenohypophysis are typically
circling, seizures) in cats, accompanied by
characterized by pituitary-dependent
insulin-resistant diabetes mellitus and high
hyperadrenoco1ticism (PDH). (See also
serw11 growth hormone concentrations.

HYPERADRENOCORTICISM, p 543.) Of the cases of l-listologically, pituitary tumors include
pituitary Cushing disease, �80% are
polygonal, round, and cylindrical cells
rep01tedly associated with a pituitary tumor. arranged in close contact with blood vessels In dogs, these tumors may stem from the
or fo1med into islands of cells divided by
pars distalis (80"A,) or the pars intermedia
connective tissue. The cell pattern may be

(20"Ai), because both regions contain cells
lllliform, resembling normal pituitary tissue.

that can produce adrenocorticotropic

Many pituitary tun10rs contain both
hormone. The tumors are generally
chromophobic and chromophilic cells.

chromophobic microadenomas ( < l cm in

Regressive changes include cyst formation,
diameter) that do not produce neurologic
necrosis, and hemorrhage. MRI with
signs. MRI studies suggest that as many as
contrast enhancement is extremely helpful

60"A, of dogs with PDH and no nemologic
to visualize microtumors (3-10 mm in
signs have pituitary tumors 4-12 nm1 in
diameter) and macrotumors (�24 rrun) in
dian1eter. As many as 50"A, of dogs with PDH
dogs with PDH, regardless of neurologic
and large chromophobic macroadenomas
signs. MRI and CT scans of pituitary tun1ors

(> 1 cm in diameter on MRI) may not show
reveal minimal peritumoral edema, LU1ifo1m
clinical signs related to an intracranial mass. contrast enhancement, and well-defined In one study, seven of eight dogs with
margins; however, tun10rs <3 mm in
pituitary neoplasia that had been treated for
dian1eter may not be visible. Adrenal and

PDH for varying periods of time (between
pituitary tun10rs may coexist in dogs with

1 and 2 yr) developed neurologic signs,
hyperadrenocorticism, complicating test
including abnormal behavigr ( eg, head
results and making diagnosis and treatment
pressing, lethargy, hiding, wandering,
more difficult.

pacing, tight circling, and trembling),

Primary skeletal tumors do not
seizures, and positional nystagmus. Most
typically cause neurologic signs. Multi lobupituitary tumors, especially those.derived lar osteochondroma originates in the flat
from the pars distalis, tend to grow
bones of the skull, usually in older,
dorsocaudally because the diaphragma
medium- or large-breed dogs and appears as
sella is incomplete. Chromophobic canine
a fin11, fixed mass. It may erode the craniun1
tumors from the pars inten11edia are smaller and compress, rather than infiltrate, and less destructive. Dorsal extension of
underlying brain tissues. Radiographically,
pituitary tumors may lead to compression
the tumor contains nodular or stippled
and obliteration of the infundibulm11,
areas of mineralization, resulting in a
ventral portion of the third ventricle,
characteristic "popcorn ball" appearance.

hypothalamus, and thalamus and may

Microscopically, the tumor contains
eventually inlpinge on the internal capsule
multiple lobules of osseous and chondroid
and optic tract. Hypothalamic or median
tissue. Local recurrence is common in
eminence involvement may cause central
high-grade tumors (78%) and occurs in 3()0A,
diabetes insipid us ( especially in middleand 4 7% of low- and intermediate-grade aged and older dogs with neurologic signs),
tumors, respectively. Metastasis frequently
manifesting as polymia, polydipsia, and
occurs (as many as 58%) but usually late in
isosthenuria or hyposthenuria. Alteration in
the disease course (> 1 yr) and also depends
water balance results from interference
on grade, with rates of 75% in high-grade
with the synthesis of antidiuretic hon11one
tumors and 60"A, in intermediate-grade

(ADH) in the supraoptic nucleus or release
tumors, as opposed to 30% in low-grade
of ADH into capillaries of the pars nervosa.

tumors. Vertebral osteochondroma is the

Although pituitary tumors generally do not
spinal cord counterpait.

NEOPLASIA OF THE NERVOUS SYSTEM

1275

Vascular malformations are considered
and its undifferentiated coW1terpait,
developmental lesions rather than true
ganglioneuroblastoma, have also been
neoplasms and are uncommon in both
reported in dogs.

dogs and cats. They may be located in the

Primal)' vertebral tW11ors are rare in
cingulate gyrus, pyrifonn-hippocampal
cats, with osteosarcoma being the most

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area of the temporal lobe, basal ganglia,
frequently reported. Metastatic, ex:tradural
cerebellum, occipital lobe, or septum
spinal cord twnors are unusual in dogs, but
pellucidum and fomix and comprise
ex:tradural lyn1phosarcoma is the most
variable combinations of arteries, veins, and common spinal tumor in cats. In most cases, capillaries. The vessels tend to be dilated,
these twnors are secondal)' to lyrnphosarsinusoidal in shape, and accompanied by corna elsewhere in the body, although
hemon-hages.

primal)' spinal cord lyn1phosarcomas have
been reported sporadically in dogs. In one

Spinal Cord Tumors: Spinal cord tun1ors
study in cats, ex:traneural involvement was
are relatively common in cats and dogs.

not foW1d in -500A, of tl1e cases, and the

They are generally classified according to
tumors were solitai)' in 22 of 23 cats. A
their relationship with the spinal cord and
predilection for the thoracic and lumbar
meninges as ex:tradural, intradural-ex:travertebral canal was seen, but the tumors medullai)', or intramedullaiy Depending on
may develop in any spinal region. Three of
tun10r location, any of the four spinal cord
tl1e tw11ors affected the brachial plexus
syndromes may be anticipated ( eg, cervical,
cervical roots (seep 1276). Spinal lymphocervicothoracic, thoracolumbar, or mas in cats may extend over multiple
lumbosacral syndromes). Regardless of
vertebral bodies and involve more than one
type, the mean age of most dogs with spinal
level of the spinal cord. Leptomeningeal
twnors is -6 yr, and tun10rs appear to be
spinal cord involvement is not common in
more common in medium and large breeds.

cats. A tumor tenned myxoma-myxosai�

Cats with lyn1phosarcoma tend to be
coma has been desc1ibed in four dogs.

younger (mean age of -3.5 yr), possibly

These malignant tumors resembled
because of the infectious etiology (ie, feline
soft-tissue myxomas, with polygonally
leukemia virus) of most cases. However, age shaped cells with gray, vacuolated alone does not preclude a diagnosis of
cytoplasm that stained positive for S-100
spinal tumor. The clinical course for the
protein antibody. The masses were
various twnor types and locations is not
extradural in three cases and intraduralclearly defined. In one study, the rate of extran1edullal)' in the oilier.

progression was fastest with intramedullal)'

Intradural-extramedullary tumors
tumors (1.7 wk), followed by ex:tradural
are f0tmd in tl1e subarachnoid space and are
tumors (3.4 wk) and intradural-extran1edulestimated to accOLmt for -35% of all spinal.

lal)' tumors (5.7 wk).

cord tw11ors. They are most commonly men

Extradural tumors are found outside
ingiomas or nerve sheaili tumors ( eg,
the dura mater and cause spinal cord
neurofibromas, neurilemmomas, and
compression. They are the most c01ru11on
schwarmomas) that grow into the vertebral
spinal tumors in both cats and dogs. The
canal and compress the spinal cord.

most frequent types of ca.11ine spinal cord

Approximately 14% of CNS meningiomas in
tun1ors are primal)', malignant bone tun1ors
dogs (but only 4% in cats) reportedly involve

( chondrosarcoma, fibrosarcoma, hemangiothe spinal cord. TW11ors may be seen in the sarcoma, hemangioendothelioma, multiple
cervical, lumbar, or thoracic cord regions.

myeloma, osteochondromas or multiple

In a report of spinal cord tun10rs in 29 dogs,
cartilaginous exostoses, and osteosarcoma)

nerve sheath twnors were the second most
and tumors metastatic to bone and soft
common type after ve1tebral tumors. In
tissue. Reports of secondal)' vertebral
a.11other review of ca.11ine spinal twnors, 39
tumors in dogs include anaplastic tun1ors,
of 60 nerve sheath tumors involved the
aortic body tumors, bronchogenic carspinal cord. Nerve sheath twnors often cinoma, chemodectoma, fibrosarcoma,
affect the brachial plexus (see below).

ganglioneuroma, hemangiosarcoma,

A primal)' intradural-ex:tramedullal)'

lyn1phosarcoma, malignant melanoma,
tumor with a predilection for Tl0-L2 spinal
mailUTial)' carcinoma, osteosarcoma,
cord segments in yoW1g dogs, particularly
pancreatic adenocarcinoma, perianal gland
retrievers and German Shepherds, has been
carcinoma, prostatic carcinoma, rhabdovariously diagnosed as ependymoma, myosarcoma, Sertoli cell carcinoma,
medulloepithelioma, nephroblastoma, or
squan10us cell carcinoma, transitional cell
neuroepithelioma. The origin of this tumor is
carcinoma, thyroid carcinoma, a.11d tonsillar

W1certain, and in1mW1ocytochernical studies
carcinoma. An ex:tradural ganglioneuroma
have not supported a neuroectodermal

1276

NEOPLASIA OF THE NERVOUS SYSTEM
origin. Monoclonal antibody studies suggest
on cytologic criteria), and determining the
it may be a nephroblastoma. Most cases are
cell of origin is usually impossible. Mid to
seen in dogs 5---;36 mo old, with males and
caudal cervical and/or rostral thoracic nerve
females affected equally. Clinical signs
roots, especially ventral roots, are the most

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include a thoracolumbar syndrome. CSF is
conunon sites for MPNST. These tumors
usually normal, although the protein level
frequently involve nerves of the brachia]

was increased in one dog. The extramedulplexus, often appearing as bulbous or lary masses are a tan to grayish white color
fusiform thickenings of one or more nerves.

and 1-3 cm long. They are generally found

They can spread to other nerves once they
dorsal and lateral to the spinal cord, may
advance to the common brachia] plexus
entrap the spinal roots, and may be accompabundle. The tumors typically result in slow, nied by areas of hemorrhage and severe
progressive, unilateral thoracic limb
spinal cord compression. Histologic findings
lameness and muscle atrophy, often
include solid sheets of ovoid to fusi.fom1 cells involving the infraspinatus and supraspinainterspersed with areas of acinar and tubular tus muscles. Affected ani.n1als may display a
differentiation, rudimentary glomeruli, and
unilateral Homer syndrome, pain on leg
focal squamous metaplasia.

movement, axillary pain on palpation (an

Intramedullary tumors are the least
axillary mass may be palpable), and may
common of the three categories of spinal
lick or chew at tl1e foot or carpus of the
cord tumors, with a reported frequency
affected limb. Intradural-extramedullary
of 15o/o--24%. Primary glial tumors ( eg,
spinal cord compression is most common
astrocytoma, choroid plexus papilloma,
with tumors located at the spinal nerve
ependyn1oma,oligodendroglion1a,and
roots, although more peripherally located
undifferentiated sarcoma) are the most
tumors occasionally may invade the
commonly diagnosed. Intramedullary spinal vertebral canal. The trigeminal is the cranial cord metastasis is an uncommon complicanerve most often affected by MPNST, tion of systemic malignancy in dogs, and
producing signs of unilateral trigeminal
neurologic signs may be the first indication
nerve dysftmction ( eg, unilateral atrophy
of systemic malignancy. The mean age of
of the masseter and temporalis muscles).

affected dogs is -6 yr, any part of the spinal

Brain-stem compression and local vertebral
cord may be involved, and there may be
erosion have been reported.

accompanying brain metastasis.

Peripheral nerves may also be affected by

Malformation tumors rarely affect the
other tumor types ( eg, giant cell sarcoma
spinal cord. In one report, a 2-yr-old, female
with cervical involvement, a malignant

Rottweiler presenting with a thoracolumbar
tumor of the apocrine sweat glands, and
syndrome had an intran1edullary epidersarcoma extending into the brachia] plexus moid cyst. The gray to off.white cyst was
have been described in dogs). Peripheral

-2 cm long, 1 cm in diameter, and extended
tumors of neuronal origin, such as gangliofrom Tl3 to L2 spinal cord segments. The neuromas and tl1ei.r more undifferentiated
empty lumen was lined by sin1ple stratified
counterpart, ganglioneuroblast.omas, are
squan10us epithelium or, in a few regions,
extremely rare but have caused extradural
by desquamating keratinized epithelium
spinal cord compression in dogs. Sympacontaining keratohyaline granules. The thetic ganglia are thought to be the source
spinal cord was severely compressed. These of ganglioneuromas. Lymphosarcomas may cysts may arise from growth of p1imordial
involve cranial and spinal nerves and nerve
epithelial cells entrapped during closure of
roots in cats and dogs and may extend
the neural tube.

intracranially. Myelomonocytic neoplasia of
the trigeminal nerve and ganglia, leading to a

Peripheral Nerve Tumors: Tumors of
dropped mandible and synm1etric atrophy of
cranial and spinal nerves and nerve roots
masticatory muscles, has been reported in
are common in dogs, cattle, and horses
dogs. Tumors of the ear canal ( eg, cerumibut are rarely seen in cats. In one report, nous adenocarcinoma, fibrosarcoma, and
peripheral nerve tumors accounted for
squan1ous cell carcinoma), as well as

-27% of canine nervous system tumors.

osteosarcoma of the skull, may affect the

Differing opinions on the cell of origin have
facial nerve or one of its branches. Neurofiled to confusion over the terminology used bromas rarely involve the vestibulocochlear
to describe these tumors. While schwannerve. Cranial nerves may be compressed by noma, neurilemmoma, and neurofibroma
meningiomas located on the floor of the
are common, interchangeable designations,
cranial vault. The vagosympathetic trunk
the term malignant peripheral nerve sheath
may be compressed by aortic body tumors.

tumors (MPNST) is recommended because

See also DISEASES OF' THE PERIPJ IERAL NERVES
many of these tumors are malignant (based

AND NEUROMUSCULAR JUNCTION, p 1238.

NEOPLASIA OF THE NERVOUS SYSTEM

1277

Clinical Findings: Some of the clinical
level of the mesencephalic aqueduct, can
signs and syndromes associated with
create obstructive hydrocephalus. The
various CNS tumors have already been
increased intracranial pressure may lead to
mentioned. Cerebral, hypothalamid
ischemic necrosis of the herniated tissue.

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diencephalic, midbrain, cerebellar,

Initially, seizures and behavioral changes
pontomedullary, and vestibular syndromes
may be the only abnormalities associated
associated with focal discrete intracranial
with tumors involving the rostral cerebrum
masses might be expected, depending on

( eg, olfactory and frontal lobes). Lesions of
tumor location. Accurate anatomic
the frontal and prefrontal lobes may result
localization is possible in many cases,
in no clinical signs. Acute blindness may
especially in the early stages of tumor
be the initial clinical sign in animals with
growth. However, correlation of clinicotumors in the region of the optic chiasm ( eg, pathologic signs with tumor location may be pituitary tumors, paranasal sinus carciimpossible because tumor location may be noma, polycentric lymphosarcoma, and
masked by secondary changes ( eg, brain
suprasellar germ cell tumors). Papilledema
herniation, cerebral edema, hemorrhage,

( often bilateral) is thought to result from
obstructive hydrocephalus, tissue necrosis,
a generalized increase in intracranial
and tumor spread within the brain) that
pressure. A variety of causes ( eg, multiple,
independently cause clinical signs. Partial
small metastatic masses from extracranial
brain herniation may result from increased
tumors, especially with malignant melaintracranial pressure and/or shifts in the noma and hemangiosarcoma) may lead to
brain caused by the tumor. Care must be
multifocal clinical signs associated with
taken to maintain optimal oxygenation and

CNS tumors. Other tumors, such as caravoid intracranial hypertension during cinomas (pulmonary or mammary), tend to
diagnostic tests that involve anesthesia and
produce fewer, larger metastases. The

CSF sampling because of the increased risk
cerebrun1, hippocampus, and cerebellar
of herniation.

cortex are common sites for hematogenous

Several types of herniation have been
metastases. Extraneural tumor cells
described. Cingulate gyrus herniation
sometimes localize in the meninges ( eg,
under the falx cerebri toward the unaffected meningeal carcinomatosis associated with hemisphere leads to compression of the
mammary adenocarcinoma or intestinal
opposite cingulate gyrus. Occipital or
carcinoma). Multifocal syndromes may also
temporal lobe herniation (primarily
result from primary CNS tumors in multiple
the parahippocampal gyrus) under the
sites, extension of an original tumor to
tentorium cerebelli ( caudal transtentorial
another site, or metastasis via the CSF
herniation) often causes dorsoventral and

Choroid plexus papillomas and epenlateral compression of the midbrain at the dymomas tend to obstruct cerebrospinal
rostral colliculi and partial occlusion of the
pathways because of their ventricular
mesencephalic aqueduct. Caudal displaceorientation, especially when they arise in ment of the diencephalon and mid brain may
the fourth ventricle. Neurologic signs
also occur. Clinical signs include initial
associated with ventricular tumors result
pupillary constriction, often followed by
from the tumor location and the degree of
mydriasis, tetraplegia, and coma. Rostral
ventricular dilation caused by obstructive
cerebellar vermis herniation under the
hydrocephalus. Clinical signs often are
tentorium cerebelli ( rostral transtentorial
insidious with either of these tumors; the
herniation) may lead to flattening of the
clinical course generally is protracted,
rostral cerebellum, marked compression
ranging from months to years. Extraneural
and rostral displacement of the brain stem,
immunoproliferative diseases in dogs and
and compression of the temporal cortex.

cats ( eg, multiple myeloma and macroglob

Despite the gross pathology, clinical deficits
ulinemia-associated lymphocytic leukemia)

may be absent. Cerebellar herniation
may also result in a range of intemlittent

( especially the caudal lobe of the cerebellar
cranial neurologic signs, including
vermis) through the foramen magnum
disorientation, ataxia, intention tremor
compresses the underlying medulla
of the head, visual in1pairment, circling,
oblongata and may cause malacia and
and staggering or falling. lntravascular
hemorrhage. Apnea, hypoxia-induced coma, erythrocyte aggregation impairs blood flow and tetraplegia may be seen. Concurrent
in the affected areas and probably leads to
foramen magnum and caudal transtentorial
the transient signs.

herniation may cause dysfunction in both

Pituitary tumors are associated with
the midbrain and medulla oblongata.

various endocrine signs, including acromeg

Herniation combined with attenuation of
aly, abnormal hair coat, gonadal atrophy,
the ventricular system, especially at the
polydipsia, polyuria, and obesity. (See also

1278

NEOPLASIA OF THE NERVOUS SYSTEM

TIIE PITUITARY GLAND, p 542). Behavioral
tumor location in all dogs and bone
changes, circling, paresis, seizures, or visual
infiltration in all but one. Localization of
deficits may result from extension of primary tun1ors in the intradural-extramedullary nasal cavity tumors into the cranial vault.

space was not always possible, however.

Respiratory signs, such as dyspnea,

Myelographic interpretation of intramedul

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epistaxis, nasal discharge, sneezing, stertor,
lary spinal cord metastasis may be difficult;
or mouth breathing, may follow neurologic
intramedullary tumors must be differentisigns or may not occur at all.

ated from hemorrhage and spinal cord
edema. Classically, myelograms of

Diagnosis: A variety of diagnostic imagintramedullary masses reveal widening of ing aids, including plain-film radiography,
the spinal cord shadow and tapering and
contrast radiography (eg, myelography),
attenuation of contrast in both lateral and
and specialized radiographic techniques
ventrodorsal views.

such as radionuclide imaging (scintigra

Electrodiagnostic techniques (eg,
phy), CT scans, and MRI are used to
electromyography, nerve conduction
diagnose nervous system tumors. These
velocity deterrnination), in cortjunction with
techniques provide information ( eg, axial
myelography and imaging techniques, can
origin, location, shape, pattern of growth,
facilitate diagnosis of peripheral nerve
and edema) that can be in1portant when
tLUnors. Myelogran1s reportedly often are
dete1mining prognosis, therapy, and
negative in animals with cervical MPNST.

outcome. Bone neoplasia may be observed

Analysis of CSF may reveal moderate
with plain-film radiography. Intracranial
increases in total protein content, total
tumors are better evaluated with MRI. Some white cell count, and CSF pressure. There is indices of malignancy ( eg, edema, extension a low frequency of tumor cells in CSF from of growth across the midline, poor margin
anin1als with brain or spinal cord neoplasia,
definition, and tissue invasion) have been
but malignant cells have been repo1ted in
defined using MRI, and many tumor types
dogs and cats with intracranial and spinal
can be presumptively diagnosed based on
cord (extradural and intran1edullary)

location, appearance, and contrast-enlymphosarcomas.

hancement patterns. Caution must be
exercised, however, because presumptive

Prognosis and Treatment: The
diagnoses made after imaging are found to
prognosis for anin1als with nervous system
be incorrect in -300/o of patients after a
tumors is generally guarded to poor but
histopathologic diagnosis is obtained.

depends on the extent of tissue damage,

Signs of extradural, intradural-extramedtumor location, surgical accessibility, and ullary, and intramedullary tumors vary on
rate of tun1or growth. Recent improvements
myelography. Extradural lesions are located
in treatment have centered mainly on
outside the dura mater, resulting in
surgical resection, radiation therapy, and
attenuation of the dural tube and spinal
chemotherapy, based on more accurate
cord. Deflection of the contrast column
tumor localization and identification using
away from the ve1tebral canal,_resulting in
imaging techniques, such as CT scans and
a widened epidural space, confinns an extra

MRI. Better identification and characte1izadural lesion. Intramedullary-extramedullary tion of tun1ors from tissue biopsies obtained
lesions develop in the subarachnoid space,
via stereotactically guided biopsy devices
where they act as wedges, displacing the
may lead to additional impcovement.

dura mater toward the bony vertebral canal

Although success rates for different tumor
and the spinal cord toward the contralateral
types and locations are not currently
vertebral canal. Contrast material abuts the
lmown, cerebral tun1ors (including
cranial and caudal margins of the tun1or,
meningiomas and ependymomas) without
resulting in a characteristic cup or golf tee
brain-stem signs appear to have the best
appearance. In contrast, intramedullary
prognosis, especially in cats. Radiation
tun1ors displace the spinal cord material
therapy may be the most successful
from within, enlarging the circumference of
treatment for a range of intracranial tumors
the spinal cord and attenuating the contrast
and, if surgery is performed, postoperative
material in the subarachnoid space
radiation therapy may prolong survival
surrounding the tm11or.

times. Radiation therapy is beneficial for

Results from one study suggest that CT is
treatment of inoperable tumors and may be
better than survey radiographs to visualize
better than surgery for dogs with infiltrative
bony changes associated with extradural
masses. A retrospective study of 86 dogs
lesions but that myelography is better than
with brain tumors showed that dogs treated

CT to classify spinal cord lesions. In another with 60Co radiation, with or without other canine study, MRI was used to detemline
combinations of therapy, lived significantly

NEOPLASIA OF THE NERVOUS SYSTEM

1279
longer than dogs that underwent surgery
therapy. More invasive treatments, such as

( some with 12sr implants) or dogs that
surgery, should be reserved for animals in
received symptomatic treatment. Dogs with
which the primary tumor is well controlled
a solitary site of involvement had a better
and no other systemic metastases can be
prognosis. Longterm control of primary
docl.lll1ented.

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brain tumors using cytotoxic chemotherapy

Most extradural spinal tumors are
alone is poor; symptomatic treatment ( eg,
primary bone tumors, and removal often
use of anticonvulsants and/or anti-inflamcauses decreased spinal stability, pathologic matory doses of c01ticosteroids) is
fractw·es, or spinal subluxation. In a study
palliative at best, with survival time
of canine malignant extradural twnors,
generally measured in weeks. Corticostepostsurgical survival times were short. A roids may relieve signs by reducing edema
report of20 vertebral twnors (primary or
near the tun10r and by causing temporary
metastatic fibrosarcomas or osteosarcoregression of lymphoid and reticulohistiomas) in dogs treated with combinations cytic twnors.

of surgery, radiation, and chemotherapy

The treatment of choice for meningioma
supports a guarded prognosis for dogs with
in cats is surgery, because these tun1ors are
vertebral neoplasia. Median survival tin1e
usually removable in toto, with postoperawas 135 days, with a range of 15----600 days.

tive survival times preaching a median of

Survival time after surgical resection of

-2 yr. Recurrence is possible, with reports
spinal lymphoma and myxosarcoma in
of up to 2()0,6 and with a median disease-free
dogs was 560-1,080 days in another report,
interval of9 mo; however, second surgical
although some dogs received postsurgical
resections are also feasible. In dogs, the
radiotherapy and chemotherapy. Methods
ability to completely resect meningiomas
recommended to treat spinal lymphosaris more limited, because tissue invasion is coma in cats include focal radiotherapy,
more frequent. The use of surgical aspirator
surgical cytoreduction, and systemic
devices and intraoperative ultrasound or
chemotherapy, including L-asparaginase,
endoscopic imaging may improve the
cyclophosphamide, vinc1istine, and
surgeon's ability to perform complete
prednisone. Longterm results are poor,
removal. Recent reports of dogs with
partly associated with a positive feline
tlll11ors removed by a surgical aspirator and/
leukemia virus status in these patients.

or endoscopic-assisted removal yielded

Aninlals with MPNST have a generally
median survival times of >3-5 yr. In earlier
poor prognosis, because only a small
reports, surgical resection alone resulted
percentage of these twnors can be
in median survival times of -200 days.

completely resected, and their recurrence

Postoperative radiation therapy appears
rate is high. Metastasis, often to the lungs, is
beneficial in some studies, with median
another complication. Early diagnosis of
survival times increasing by -1 yr over

MPNST may lead to better results. Mean
surgery alone. Radiation therapy as a sole
survival of 180 days after surgical resection
treatment, either in standard fractionated
was reported in one study. Many intraduralcourses ( usually throughout 3-4 wk) or in extran1edullary tumors ( eg, lipomas and
stereotactic radiosurgery (SRS) approaches
meningiomas) can be successfully removed,

( usually one to four treatments), has also
with long postsurgical survival. However,
been attempted. Success rates are difficult
intradural-extramedullary tumors that
to determine, because confirmation of

1) involve spinal cord segments of an
tun1or type is rarely performed, and only
intumescence, 2) are ventrally located,
preliminary reports for SRS have been
or 3) invade adjacent neural parenchyma
published. Addition of cytotoxic drugs
have a poor prognosis.

( most commonly hydroxyurea or CCNU)

Surgical resection is rarely possible for
postoperatively or at recurrence may
intramedullary masses. However, there
lengthen survival time.

are successful reports of removal of a

Astrocytic tumors/gliomas are usually not thoracoll.lll1bar intran1edullary ependytreated surgically because of location but moma and a tumor resembling a nephromay be treated with radiation therapy, with blastoma (by exploratory laminectomy,
reported survival times of 6--11 mo.

followed by durotomy and myelotomy).

Additionally, newer drugs, such as

Prognosis for dogs with intramedullary
temozoloamide, which has shown some
spinal cord metastasis is poor because of
promise in people, may have some use in
the frequent presence of disseminated
the treatment of these tun10rs in dogs.

disease, although corticosteroid therapy

Metastatic brain lesions are usually
may lead to temporary improvement.

treated palliatively, with a combination

Peripheral nerve and nerve root twnors
of medical therapy, radiation, and/or chemo-
can be successfully resected but may

1280

NEOPLASIA OF THE NERVOUS SYSTEM
necessitate removal of the affected nerve
average time to recurrence of 5 mo in one
and nerve root. If atrophy of all muscle
report. Long-term survival times (18--42 mo)

groups is extreme-as may develop with
have been reported. Even untreated, dogs
tumors involving multiple nerves of the
with trigeminal nerve tun1ors can have
brachia! plexus-or if more than one root is
prolonged survival times (as much as 21 mo

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involved, complete an1putation of the limb
in seven dogs). In 45 cats, median survival
may be required. Recurrence is common
time was 21.5 mo, with a200A, local
after resection of peripheral tumors, with
recurrence rate.

PARANEOPLASTIC DISORDERS OF

THE NERVOUS SYSTEM

Paraneoplastic syndromes are norunetastatic associated lymphocytic leukemia. A 3-yr-old complications of cancer with effects distant

Doberman Pinscher developed diencefrom the primary tumor. They are unrelated phalic syndrome, associated with a
to neurologic complications secondary to
diencephalic tumor (an astrocytoma) that
metabolic or nutritional disorders, infection,
produced growth hormone, resulting in
cerebrovascular incidents, or adverse effects
extreme emaciation despite adequate or
of treatments. They can affect all parts of the
increased nutritional intake.

nervous system, including the brain, cranial

Paraneoplastic myasthenia gravis (MG)

nerves, spinal cord, dorsal root ganglia,
has been strongly associated with the
peripheral nerves, and the neuromuscular
presence ofthyntic disease. MG can
junction. Some are thought to be inlrnunomanifest as systemic weakness, or more logically mediated tlu·ough cross-reactivity
focally, especially as megaesophagus. In one
by inimune cells against antigens expressed
review of canine thymoma, 4 7% of the dogs
by twnors and neural tissues (molecular
had MG, 33% had concurrent nonthymic
minlicry ), whereas others are related to
cancer (including pheochromocytoma,
the production of circulating hom1ones,
mammary adenocarcinoma, or pulmonary
peptides, or other substances that exert
adenocarcinoma), and 200A, had concurrent
systemic effects. .

signs of polyn1yositis. Dogs with thymom a

Paraneoplastic syndromes affecting the
associated MG often have antibodies to

CNS are rarely recognized in animals, but
nicotinic acetylcholine receptors, which
lack of awareness may lead to a low
can be used to diagnose and/or monitor
detection rate. Sporadic. case reports
treatment response. These dogs may
suggest that brain and spinal cord effects
produce autoantibodies to several other
can result from various tumor types. An
neuromuscular antigens, including

8-yr-old, male German Shepherd with a

1yanodine (a skeletal muscle calciun1-
history of acute pelvic limb paralysis,
release charuiel receptor) and the muscle
progressive Joss of motor function,
protein titin. Other tumors that have rarely
conscious proprioceptive deficits, loss of
been reported to cause MG include
superficial and deep pain sensation over the
osteosarcoma, lyn1phoma, and bile duct
trunk and pelvic limbs, and Schiff-Shercarcinoma. MG can improve with inlrnunorington-like hyperextension in the thoracic suppression or treatment of the underlying
limbs was diagnosed with hepatocellular
tumor but may also be persistent or occur
carcinoma with metastasis to the lungs,
after removal of a thymoma.

liver, spleen, and lymph nodes at necropsy.

An association between myositis ( eg,

Severe necrotizing myelopathy was present
dermatomyositis and polymyositis) and
throughout the gray and white matter of the
malignant neoplasia in people has been well
thoracic spinal cord, including spongy
established. Dogs with malignant tumors
degeneration, gliosis, demyelination, axonal
such as bronchogenic carcinoma, myeloid
swelling and degeneration, and neuronal
leukemia, or tonsillar carcinoma may also
necrosis. In a second case, a range of
have muscular necrosis and low-grade
neurologic deficits in a 17-mo-old, male
myositis, but the frequency of this

Poodle was attributed to hyperviscosity
potentially paraneoplastic association is
syndrome secondary to macroglobulinemia-
unknown. 1\vo dogs with multicentric

POLIOENCEPHALOMALACIA

1281
lymphoma were found to have polymyomas, hemangiosarcomas, undifferentiated sitis, but the presence of lymphocyte
sarcomas, and mast cell tumor.

infiltration within the muscle makes

Clinical signs may include reduced or
differentiating between primary and
absent spinal or cranial reflexes, flaccid
paraneoplastic disease difficult.

weakness, reduced muscle tone, paralysis

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Peripheral neuropathy is commonly
of lin1b or head muscles, and, after 1-2 wk,
associated with neoplasia in people, and is
neurogenic muscle atrophy. Dysphonia may
likely so in animals, as well, although less
also be present.

recognized clinically. A large survey on

Dogs and cats with clinical signs of
dogs with various malignancies revealed
nervous system disease ( or with myositis
multiple histopathologic changes in the
or necrotizing myopathy confim1ed by
nerve fibers, including paranodal-segmental histopathology) that do not respond to demyelination, remyelination, axonal
therapy or that relapse should be carefully
degeneration, and myelin globules.

screened for mal.ignancy, because

Associated tumor types included insuparaneoplastic syndromes may be the first linoma, multiple myeloma, lymphoma,
clinical sign related to tumor presence.

bronchogenic carcinoma, man1mary

Blood tests or imaging may be indicated.

adenocarcinoma, malignant melanoma,

Such vigilance may detect tumors at a more
thyroid adenocarcinoma, leiomyosarco-
treatable stage.

POLIOENCEPHALOMALACIA

(Cerebrocortical necrosis)

Polioencephalomalacia (PEM) is an
tissues or blood and deficiency-induced
important neurologic disease of ruminants
alterations of thiamine-dependent
that is seen worldwide. Cattle, sheep, goats,
biochemical processes (decreased blood
deer, and camelids are affected. PEM is a
transketolase activity, increased thiamine
pathologic diagnosis and a common end
pyrophosphate effect on transketolase, and
point of several conditions. Historically,
increased senun lactate). Unfortunately,

PEM has been associated with altered
many of these biochemical features of
thiamine status, but more recently an
altered thiamine status are inconsistently
association witl1 high sulfur intake has been
observed in cases of PEM, and decreased
seen. Other toxic or metabolic diseases ( eg,
thiamine status has been obse1ved in
acute lead poisoning, sodium toxicosis/
diseases other than PEM.

water deprivation) can result in PEM as well.

Prenuninant animals depend on dietary
thiamine. ln adult nu1linants, thianline is

Etiology, Pathogenesis, and Epidemi
produced by nunen microbes. Thiamine
ology: Polioencephalomalacia is seen
inadequacy can be caused by decreased
sporadically in individual animals or as a
production by rumen nlicrobes or factors
herd outbreak. Younger anirnals are more
that interfere with the action of thiamine,
frequently affected tl1an adults. Pastured
eg, plant thiaminases or thiarnine analogues.

animals can develop PEM, but animals on

Thiaminases can be produced by gut
high-concentrate diets are at higher risk, as
bacte1ia or ingested as preformed plant
are cattle exposed to high levels of sulfur,
products. They can either destroy thiamine
whether in water, feed (rations with
or form antimetabolites that interfere with
byproducts of com or beets processing),
thian1ine function. Thiaminase 1, produced
or a combination. The patterns of PEM
by Bacillus lhiaminolyticus and Clostrid
occurrence depend on the etiologic factors
ium sporogenes, and thiaminase 11,
involved.

produced by B anewinolylicus, catalyze

PEM has been associated with two types
the cleavage of thianline. The latter microorof dietary risks: altered thiamine status and ganism proliferates under conditions of
high sulfur intake. Thiamine inadequacy in
high grain intake.

animals with PEM has been suggested by

A neurologic disorder in Austral.ia has
several types of observations, including
been associated with the Nardoo fem
decreased concentrations of thiamine in

(Marsilea drummondii), which may

1282

POLIOENCEPHALOMALACIA
contain high levels of a thiaminase I
greatly at high temperatures, leading to
enzyme. Other fems, such as bracken
increased sulfw· intake due to concurrent

(Pte1idium aquilinum) and rock fem
increases in water conswnption and sulfate

(Cheilanthes sieberi), contain a similar
concentrations in water. Alfalfa, by virtue of
thiantinase I. Although PEM has been
its high protein and sulfur-containing antino

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produced experimentally by feeding high
acid content, can serve as a significant
doses of extracts of such plants, field cases
source of sulfur. Although grasses tend to be
are tmcommon, because these plants are
low in sulfw·, some circwnstances can result
w1palatable (seep 3089).

in high sulfate concentrations. Certain

Overall, there is not a linear relation
weeds, including Canada thistle (Cirsium
among the presence of nmtinal and fecal
arvense ), kochia (Kochia scopa1ia), and thiaminase, decreased concentrations of
larnbsquarter (Chenopodium spp), can
tissue and blood thiamine, and development accumulate sulfate in high concentration.

of disease.

Cruciierous plants normally synthesize

A beneficial response to thiantine therapy
sulfur-rich products and serve as important
by PEM-affected animals is sometimes
sources of excess sulfur. These include
considered evidence of thiantine inadtwnips, rape, mustard, and oil seed meals.

equacy. This thiamine-responsiveness is

Byproducts of com, sugar cane, and sugar
often seen iI treatment is initiated early in beet processing commonly have a high
the cow"Se of the disease. However, the
sulfw· content, apparently clue to the
assumption that this response indicates that addition of sulfur-containing acidifying deficiency of thiantine is the true etiology
agents. PEM has been associated with tl1e
should be viewed with cautfon. Large doses
use of these types of byproducts as feed
of thiantine, beyond maintenance needs,
ingredients. Com-based ethanol production
may have nonspecific, beneficial effects in
has resulted in increased availability of com
the energy-impaired brain.

byproducts that may vary widely in sulfur

PEM associated with high sulfur intake is
content. Wet distillers grains plus solubles
recognized with increasing frequency. The
have been shown to have sulfur content
basis of sulfuHelated PEM appears to be
ranging from 0.44%-1. 7 4% sulfur as dry
the production of excessive runtinal sulfide
matter. A high molasses-urea diet has been
due to the nmtinal microbial reduction of
associated with a form of PEM that lacks
ingested sulfur. Hydrogen sulfide (H2S)

altered thiamine status.

gas, which has the odor of rotten eggs,
accumulates in the rw11en gas cap.

Concentrations can be demonstrated with

Clinical Findings: PEM may be acute
commercially available H2S detection tubes
or subacute. Animals with the acute form
via percutaneous gas sampling. Although
often manifest blindness followed by
nonreduced forms of sulfur, such as sulrecwi1bency, tonic-clonic seizures, and fate and elemental sulfur, are relatively
coma. Those witl1 a longer duration of
nontoxic, H,S and its various ionic fonns are acute signs have poorer responses to highly toxic.substances that in.terfere with
therapy and higher mortality. Aninlals with
cellular energy metabolism. The CNS, by
the subacute fom1 initially separate from
virtue of its dependence on a high and
tl1e group, stop eating, and display twitches
uninterrupted level of energy production, is
of the ears and face. The head is held in
likely to be significantly affected by energy
an elevated position. There is cortical
dep1ivation. When cattle widergo a
blindness with absent menace response
transition to high sulfur intake, nmtinal
but normal bilateral pupillary light reflex.

sulfide concentrations peak 1--4 wk after

Dorsomedial strabismus may develop.

the change. This pattern is probably due to

Animals may show ataxia and sometimes
alterations in ruminal microflora. The occura hypermetric gait. As tl1e disease rence of PEM peaks during tl1e time period
progresses, there is c01tical blindness
when ruminal sulfide concentrations are the
with a diminished menace response
highest. Aninlals with sulfur-associated
and unaltered palpebral and pupillary

PEM do not have altered tl1iantine status.

responses. Dorsomedial strabismus may

A variety of sulfur sources can result in
develop. Head pressing, opisthotonos, and
excessive sulfur intake, including water,
grinding of the teeth may also be seen.

feed ingredients, and forage. Many

The subacute form of PEM is frequently
geographic areas have swface and deep
followed by recovery with only minor
wate1'S high in sulfate. When evaporation
neurologic irnpainnent. However, in a few
occUl'S, water sulfate concentrations
cases, the subacute form may progress to a
increase. Water conswnption by cattle is
more severe fom1 with recwi1bency and
temperature dependent and increases
seizures. Animals that survive the acute

POLIOENCEPHALOMALACIA

1283
fonn or advanced subacute form often
blood and tissues, transketolase activity,
manifest significant neurologic impairment
or the thiamine pyrnphosphate effect on
that necessitates culling.

transketolase. Demonstration of clinical

Lesions: Gross lesions are inconsistent
improvement after thiamine therapy is not
and frequently subtle, especially early in
adequate evidence for a specific diagnosis.

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the disease. Acutely affected animals may

The possibility of sulfur-associated PEM
have brain swelling with gyra] flattening
can be assessed by measuring tl1e sulfur
and coning of the cerebellmn due to
content of the water and dietary ingredients
herniation into the fora.men magnmn.

and then estimating the total sulfur intake

Slight yellowish discoloration of the
on a dry-matter basis. The maximal
affected cortical tissue may be present. The tolerated concentration of sulfur for cattle brains of acutely affected animals may also
and sheep depends on the type of diet. For
have autofluorescent bands of necrotic
diets >85% concentrate, the maximal
cerebral cortex evident on meningeal and
tolerable level of total sulfur is 0.3% dry
cut surfaces of the brain when viewed with
matter. For diets �45% forage, the maximal
ultraviolet illmnination. As the pathologic
tolerable level of total sulfur is 0.5% dry
process progresses, the affected cerebromatter. Because multiple factors are cortical tissue has macroscopically evident
involved in detennining tl1e actual risk
cavitation, sometin1es sufficient to result in
of developing PEM, these should not be
apposition of the pia meninges to the white
considered as absolute maximal concentramatter.

tions. Many cattle adapt adequately to sulfur

The initial histologic lesions are necrosis
intake levels greater than the maximal
of cerebrocortical neurons. The neurons
tolerable level, although negative effects
are shrunken and have homogeneous,
on perfonnance may occur.

eosinophilic cytoplasm. Nuclei are pyknotic,
faded, or absent. Cortical spongiosis is

Treatment and Prevention: The
sometimes present in the early phases of the
treatment of choice for PEM regardless of
acute form. Vessel cells undergo hypertrocause is tllianline adnlinistration at a dosage phy and hyperplasia. At later stages, the
of 10 mg/kg, tid-qid, for cattle or small
affected cortical tissue undergoes cavitation ruminants. The first dose is administered as macrophages infiltrate and necrotic
slowly IV; otherwise, the animal may
tissue is removed. A pattern seen in brains
collapse. Subsequent doses are adminisof cattle with early, severe, acute sulfurtered IM for 3-5 days. Therapy must be related PEM features multifocal vascular
started early in the disease com'Se for
necrosis, hemorrhage, and parenchymal
benefits to be achieved. If brain lesions are
necrosis in deep gray matter, including the
pa.iticularly severe or treatment is delayed,
striatmn, thalamus, and midbrain.

full clinical recovery may not be possib)e.

Beneficial effects are usually seen witllin 24
hr and sometimes sooner; however, if there

Diagnosis: The pattern of clinical
is no initial improvement, treatment should
signs should arouse suspicion of PEM.

be continued for �3 days. Reduction of

At necropsy, macroscopically evident
cerebral edema can be attempted with
cerebrocortical autofluorescent areas under administration of dexamethasone at a ultraviolet illunlination provide a presmnpdosage of 1-2 mg/kg, IM or SC. Symptotive diagnosis of PEM. Characteristic matic therapy for convulsions may be
histologic lesions are confirmatory.

necessary.

Differential diagnoses for cattle include

Dietary supplementation of thia.i1line at
acute lead poisoning, water deprivation/

3-10 mg/kg feed has been recommended for
sodimn toxicosis, Histophilus meningoenprevention, but the efficacy of this approach cephalitis, rabies, coccidiosis with nervous
has not been carefully evaluated. During a
involvement, and vitamin A deficiency.

PEM outbreak, sufficient roughage should

Differential diagnoses for sheep include
be provided. When the problem could be
pregnancy toxemia, type D clostridial
associated with high sulfur intake, all
enterotoxemia (focal symmetric encephalopossible sources of sulfur, including water, malacia), and listeriosis.

should be analyzed and the total sulfur

Confirmation of etiology or pathogenesis
concentration of the consmned dry matter
requires laboratory testing of samples from
estimated. Dietary ingredients or water
affected animals or their environment.

witl1 high sulfur concentration should be

Assessment of thianline status is difficult,
avoided; if this is not possible, then more
and results should be interpreted with
gradual introduction to the new conditions
caution. Few laboratories are capable of
can improve the chances of successful
routinely measuring thiamine content of
adaptation.

1284

BOVINE SPONG I FORM ENCEPHALOPATHY

BOVINE SPONGIFORM ENCEPHALOPATHY

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Bovine spongifonn encephalopathy (BSE)

Transmission, Epidemiology, and
is a progressive, fatal, infectious, neurologic

Pathogenesis: Classic BSE develops as
disease of cattle that resembles scrapie of
a result of food borne exposure to prions
sheep and goats (seep 1288). It was first
via contaminated animal-source proteins
diagnosed in the UK in 1986. Approximately

(meat and bone meal [MBM]) in cattle

200,000 cases of BSE have been diagnosed
rations. Horizontal transmission is not a
in cattle, with 97% reported from the UK In
significant source of new BSE infections.

1992, at the peak of the UK outbreak, 37,280

Calves born to infected cows are at
cases were reported in a single year. Lower
greater risk of acquiring BSE than calves
incidences were found in cattle native to
born to noninfected cows; however, this
most European countries and to Israel,
mode of transmission is of minor

Japan, USA, Canada, and Brazil. The
importance relative to infections acquired
economic consequences of the BSE
through contaminated feed sources. BSE
epidemic are important. Countries with BSE is not transmitted horizontally by contact cases experienced a dramatic drop of
or aerosols. There is no sex or breed
consumer confidence in beef products and
predisposition. In the UK, clinical disease
trade restrictions of cattle commodities.

was more common in dairy cows,

Since effective control measures have been
probably because they were more likely
implemented, BSE incidence has decreased
to be fed animal-source protein suppleto single cases in 2013.

ments. Most cases are diagnosed in cattle

3-6 yr old. The incubation period after

Etiology: In the 1990s, there was
exposure is -2-8 yr, and animals as young
intensive debate on the nature of the
as 22 mo have been diagnosed with BSE.

BSE pathogen. To date, the most widely

The details of pathogenesis are unknown,
accepted hypothesis is that a proteinabut studies indicate that after oral ceous infectious particle (prion) causes
exposure the agent replicates in the
the disease. Prions are misfolded

Peyer's patches of the ileum followed by
conformational isoforms of host-encoded
migration, via peripheral nerves, to the
proteins that induce protein misfolding,

CNS. Atypical BSE cases have been
protein aggregation, and disease upon
described from countries with no
transmission to other organisms. This
apparent classic BSE epidemic. Morehypothesis is supported by the agent's over, animals affected with atypical BSE
apparent resistance to heat, freezing,
are relatively old, and the incidence rates
ultraviolet light, and chemical disinfectdo not follow the trends observed for ant procedures effective aga1nst bacteria
classic BSE. Together, these findings led
and viruses. Prions are also responsible
to the hypothesis that atypical BSE
for scrapie of sheep and goats (see
results from spontaneous prion protein
p 1288); chronic wasting disease of
misfolding and is not related to ingestion
cervidae (seep 1286); transmissible mink
of prion-contaminated feed. However, the
encephalopathy (seep 1874); and kuru,
mechanisms that induce the spontaneous

Creutzfeldt-Jakob disease, fatal familial
prion formation remain obscure. It has
insomnia, and similar disorders of people.

been postulated that atypical BSE was at

All these conditions are also termed prion
the origin of the BSE epidemic in the UK
diseases, and the related protein is the

BSE has been transmitted experimenprion protein (PrPd, in which d stands for tally to many animal species by intracere

"disease associated"). Based on the
bral inoculation. During the epidemic of
anticipated mechanisms that trigger

BSE in the UK and continental Europe, a
initial PrPci misfolding, prion diseases are
few cases were seen in several species
classified as infectious, sporadic, or
of captive-bred wild ungulates and in
genetic. The classic type of BSE is caused
domestic companion cats as well as in big
by infectious prions; however, in the past
cats in zoo logic gardens. BSE has also
decade, rare, so-called atypical BSE cases
been confirmed in two goats, one from
have been described. There is epidemio

France and another from Scotland, but
logic and experimental evidence that
there is no evidence that BSE infected the
classic and atypical BSE differ in their
small ruminant population on a broader
etiology.

scale.

BOVINE SPONG I FORM ENCEPHALOPATHY

1285

Clinical Findings: Initial clinical signs

Treatment and Control: There is no
are subtle and behavioral in nature. The
effective treatment or vaccine for BSE.

spectrum increases and progresses over

Euthanasia is advisable as soon as there is
weeks to months, wilh most animals
some certainty of the clinical diagnosis,
reaching a terminal state by 3 mo after clinibecause animals become unmanageable, VetBooks.ir
cal onset. Commonly observed clinical
and their welfare is at risk
signs include hyperesthesia, nervousness,

The most effective control measure is
difficulty negotiating obstacles, reluctance
prohibition of the feeding of MBM to cattle.

to be milked, aggression toward either fam1 MBM supplements for cattle have been personnel or other animals, low head
banned in many countries as a consequence
carriage, hypem1etria, ataxia, and tremors.

of the BSE epidemic. Because of the risk of

Weight loss and decreased milk production
cross-contamination in feed mills, control
are common. Yet, in a large portion of
has been effected in the UK and other
affected animals, clinical signs may be

European countries by sin1ilar statutory
nonspecific, and involvement of the
prohibitions of the use of MBM in all farm
nervous system is not obvious in every
animal diets.

case.

With the drastic decline of classic BSE
cases over the past yea.rs, there is an

Diagnosis: Clinical examinations do not
ongoing discussion on possible alleviations
provide a definitive diagnosis. In case of a
of the complete MBM ban from feed of
clinical suspicion of BSE, the animal
animals other then cattle, ie, of pigs and
should be euthanized and the brain
poultry. In this regard, it is important to
subjected to neuropathologic examination. remember that any reemergence of BSE will In most countries, BSE is a notifiable
remain unrecognized for years because of
disease, and a suspect case must be
the extraordinarily long incubation period
reported to the veterinary authorities.

of the disease. Moreover, with atypical BSE

The OIE has nominated OIE Reference
persisting in the cattle population, there is a

Laboratories to assist national authorities
constant risk of reintroduction of BSE in the
of OIE member states in the diagnosis of
population. This highlights the need to

BSE. Confirmatory diagnostic methods
maintain a high level of disease awareness
include PrPd immunohistochemistry and
as well as effective surveillance and control

Western inlffiunoblot in brain tissue. The
measures.

identification of characteristic vacuolar
changes by histopathology in specific

Zoonotic Risk: A novel variant of
target structures of the CNS alone is no

Creutzfeldt-Jakob disease (vCJD) in the
longer the method of choice for BSE
human population in Great Britain, initially
confinnation. In most countries with a BSE seen in 1996, has been associated with the case history, active surveillance programs
emergence of the BSE a.gent. Cases of vCJD
have been established. Approximately a
have also been seen outside the UK. A
dozen commercial BSE screening tests are
proportion of the affected individuals had
available for active disease surveillance:

been living in the UK, but cases have been

ELISA, Western immunoblot, and immunoseen in Italy and France among people who chromatographic test formats. All these
had not visited the UK. The single person
tests are based on the in1Inunologic
diagnosed with vCJD in the USA was a
detection of Pr Pei in medulla oblongata
recent immigrant from the UK, and it is
san1ples.

presumed that this person was exposed and

Differential diagnoses include nervous
infected while residing in the UK. Infection
ketosis, hypomagnesemia, polioencephaloof people is thought to result from eating malacia, lead poisoning, ingestion of plant
infected bovine tissues. As a result, many
or fungal tremoragens, rabies, listeriosis,
countries have introduced the statutory
and other viral and bacterial neuroinfecremoval of high-risk bovine tissues from the tious diseases. In contrast to these
human food chain and/or banned human
differential diagnoses, BSE typically has
consumption of cattle >24 mo old. No cases
a slow onset of clinical signs, with an
of vCJD have been seen in laboratory
extended and progressive clinical course.

workers, but appropriate safety precautions

Veterinarians considering BSE as a likely
for handling the BSE agent and conducting
differential diagnosis should contact
necropsies of cattle suspected of being
national veterinary authorities and ensure
infected are recommended. Safety
that definitive postmortem diagnostic tests
precautions should primarily be aimed
are performed.

at avoiding accidental exposures.

1286

CHRONIC WASTING DISEASE

CHRONIC WASTING DISEASE

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Chronic wasting disease (CWD) is a

Transmission efficiency to cattle varies
contagious disease of captive and freedepending on the ce1vid species from which ranging deer, elk, and moose that causes
the CWD-infected brain homogenate used
progressive, fatal neurodegenerative
for infection is derived. A large study to
disease in adult animals. It is a member of
investigate susceptibility of cattle by the
the transmissible spongiform encephalopamore natural route of oral or contact thy (TSE) family of diseases, or prion
exposure began in 1997, and there has been
diseases, that includes bovine spongiform
evidence of CWD in the experimentally
encephalopathy; scrapie of sheep and goats;
exposed cattle. Differences in species
transmissible mink encephalopathy; and
susceptibility to CWD probably relate to
kuru, Creutzfeldt-Jakob disease (CJD), and
sequence differences among normal host
variant CJD of people. CWD was first

PrP proteins.

identified as a clinical syndrome in the late

1960s among captive mule deer in Colorado;

Transmission, Epidemiology, and
a decade later, it was recognized to be a

Pathogenesis: CWD is transmitted
spongifonn encephalopathy with characterhorizontally. Because prions are highly istics similar to those of scrapie (seep 1288). resistant to environmental and chemical It is found in free-ranging populations of
inactivation, they may accumulate in the
mule deer, white-tailed deer, and elk
environment and thus be available to infect

(wapiti) in 18 states (USA) and 2 Canadian
susceptible cervids. Consequently, close
provinces. Recently, the first cases of CWD
confinement of fann-raised ce1vids will
in free-ranging moose were diagnosed in
likely potentiate the spread of CWD.

Colorado and in Alberta, Canada. CWD

Likewise, winter feeding of deer and elk will
has also been found in fanned elk and
concentrate cervid populations and likely
white-tailed deer in a munber of western
potentiate ho1izontal transmission.

states and Canadian provinces and a few

Foraging on feeding grounds contanlinated
midwestem states. CWD has been identified by urine or feces of infected animals or outside of North America only once; a few
contact with either infected anin1als or
elk imported into Korea from Canada had
decomposing carcasses of animals with

CWD. Many states and provinces have

CWD results in transmission of disease
developed regulations for control and
to other susceptible cervids. Vertical
management of CWD in fam1ed populatransmission has also been reported. The tions, and federal regulations are in place
agent probably enters a susceptible host via
in Canada and the USA. It is a reportable
ingestion and is taken up by lyn1phoid
disease in most jurisdictions .•
tissues associated with the GI tract. The
agent can be detected in lymphoid, nervous

Etiology: CWD is caused by prions. These tissues, muscle tissue, antler velvet, blood, unconventional pathogens consist solely of
saliva, urine, and feces. Prions can be
protein, namely the misfolded isoform Prf>& detected in the blood and �aliva of infected of the n01mal host-encoded cellular prion
animals as soon as 3 mo after infection. In
protein (Prpc), which is a cell surface
urine and feces, detection of prions is also
glycoprotein with highest expression levels
possible already at a preclinical stage of the
in the CNS. On direct binding of Prpc to
disease. The agent most likely anives in the

Prpsc, Prpc adopts the disease-associated
brain by retrograde movement up the vagus
confom1ation. In contrast to Prpc, PrPSc is
nerve to tl1e dorsal motor nucleus of the
partially resistant to protease digestion and
vagus at the obex region of the medulla
accumulates within neurons, which
oblongata. Spongifom1 lesions in the brain
eventually leads to neuronal death.

develop first in the vagal nucleus at about

CWD is known to naturally affect mule
the time of onset of clinical disease. This
deer, white-tailed deer, elk, and moose.

occurs naturally witl1 an incubation period

Transmission after oral inoculation of other
of -1.5--3 yr; however, incubation periods in
cervid species, eg, reindeer, has been
all species known to be affected by CWD
reported. Experimentally, CWD can be
are influenced by certain PrP polymortransmitted by intracerebral inoculation to phisms. Prevalence in captive herds of deer
cattle, sheep, goats, domestic feITets, mink,
and elk may reach nearly lO()OA, in heavily
mice, han1sters, and squiITel monkeys.

contanlinated facilities; prevalence in

CHRONIC WASTING DISEASE

1287
free-ranging cervids is extremely variable,
obvious; vacuolization occurs in neuronal
from <1%to 400Ai, in some hunting areas in
perika.rya. and neuronal processes. Along

Wyoming.

with neuronal degeneration, astrocytic

The movement of CWD in populations of
hyperplasia and hypertrophy may appear.

free-ranging deer and elk follows natural

H&E staining of brains of affected animals

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migration routes, often along waterways
reveals amyloid plaques that appear as pale,
and natural corridors. In the past, movefibrilla.r, eosinophilic areas of neuropil and ment of CWD in farmed deer and elk in
a.re sometimes surrounded by vacuoles
commerce was through human-facilitated

(fl01id plaques). Detection of PrPSc in brain
transportation of animals incubating CWD.

sections by immunohistochemistry (II-IC)

Now that programs and regulations are in
provides a very good way to visualize CWD
place in most jurisdictions, movement of
pathology while maintaining the structural

CWD in live animals should be curtailed.

context. A drawback of II-IC is that it is not

Surveillance, however, should continue,
useful in diagnosis of subclinical CWD
and submission of samples from hunterbecause spongiform encephalopathy harvested animals may be mandatory in
develops about the same time clinical
areas with a high prevalence of CWD.

features do. PrPSc is detected by II-IC or
inununoblot in a variety of tissues in cervids

Clinical Findings: Animals with clinical
showing clinical symptoms. Although PrPSc

CWD are > 16 mo old and show a spectrum
can be found in regions of the brain not
of signs. The earliest and most difficult to
exhibiting spongifom1 change, typically
appreciate are subtle changes in behavior
there is correlation between PrPSc
and weight loss. These changes are often
deposition and spongifonn appearance.

detectable only by animal caretakers
familiar with the individual animal. As the

Diagnosis: Diagnosis based on clinical
disease progresses, behavioral changes
signs is not reliable, because they a.re
may include alterations in how the animal
unspecific and mild at the beginning of
interacts with herdmates and caretakers,
disease. Therefore, it depends on detecting

Joss of wariness, somnolence, persistent
disease-associated PrPSc in CNS or lymphoid
walking, polydipsia and polyuria., and
tissues. In mule deer and white-tailed deer,
hyperexcitability when handled. Affected
the CWD PrP accumulates in the retroanimals may show variable locomotor signs, pha.ryngeal lymph node before arriving in including ataxia ( especially posterior
the brain; thus, it is considered to be the
ataxia) and head tremors. Late in the
most important tissue to collect for testing.

disease, animals may have a low head

Both brain and lymph node samples should
carriage, drooped ea.rs, and fixed staring
be collected from elk. The correct portion of
gaze; they may hypersalivate and grind
the brain (ie, the obex, at the caudal enq of
their teeth. Dea.th after routine chemical
the fourth ventricle below the cerebellum)

immobilization has been noted. Aspiration
must be collected for a meaningful test. The
pneumonia may be the only presenting
laboratory should be consulted to detennine
clinical sign and is often the ca.use of death.

whether the samples must be fixed in l()OA,

CWD should be suspected in any adult
buffered formalin, chilled or frozen, or if
cervid with aspiration pnewnonia.. Weight
portions of the samples should be sent both
loss is progressive throughout t11e course
fixed and frozen. San1ples should be, and in
of disease, even when adequate feed is
many jurisdictions a.re required to be,
present, but it is important to recognize that
submitted to certified laboratories to be

CWD may be present in cervids that are not
tested for evidence of CWD. It is good
emaciated. Dea.th of CWD-a.ffected animals
practice either to send the carcass to the
may be precipitated by cold weather or
diagnostic laboratory or to collect a wide
other acute stressors. Affected cervids are
variety of samples, so that if diseases other
more susceptible to hunting, predation,
than CWD a.re present they will be identified.

vehicle collisions, and other f01ms of death

At a n1inin1um, samples for CWD testing
by misadventure. Carcasses and offal
should include brain and retropha.iyngeal
should be disposed of in a manner that
lymph nodes. Many laboratories accept
limits the exposure of farm-raised and
whole heads from cervids for testing.

free-ranging cervids to any potentially

Surveillance progran1s for free-ranging
infectious material.

cervids va.iy depending on thejwisdiction
and are usually conducted by the local

Lesions: Lesions a.re seen in tJ1e gray
wildlife management agency, which should
matter of the CNS. Lesions a.re bilaterally
be consulted if CWD is suspected in a
symn1etrical and anatomically constant
free-ranging deer or elk. Surveillance
among anin1als. Spongiform appearance is
depends mainly on submission of heads

1288

CHRONIC WASTING DISEASE
from hunter-harvested animals. In some

Control of CWD in free-ranging populaareas, active stuveillance is done by taking tions is extremely difficult and varies
biopsies from tonsils, retropharyngeal
depending on the location. All jurisdictions
lymph nodes, and recto-anal mucosa-associhave banned movement oFlive cervicls from ated lymphoid tissue (RAMALT). Diagnostic
endemic areas for translocations, and many

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tests include detection of PrJ>Sc by IHC,
have regulations on movement of parts of

ELISA, or Western blot in brain and/or
hunted deer and elk. In areas where CWD
lymphoid tissues. In the USA, these tests are
occurs, attempts at control have included
run only at USDA-certified laboratories.

population reduction, test and removal, and

ELISA is used as a screening test, and IHC,
intensified surveillance.

which is considered the prefe1Ted test, is

Only a few clisinfectants and methods of
used to confirm positive ELISA.

disposal inactivate prions. Fresh household

Nevertheless, more sensitive in vivo
bleach at 50% concentration for 30-60 min
diagnostic tests are desirable. Using in vitro
or sodium hyclroxide (1 M) for 60 min will
conversion such as protein misfoldi.ng
inactivate the agent and is inexpensive and
cyclic amplification (PMCA) or real-time
reacilly available but may be corrosive to
quaking-induced conversion assay
some surfaces and instrtunents. Additional

(RT-QUiC), CWD prions are detectable
disinfectants are being considered for
already at a preclinical stage in specimen
general use but are not yet approved.

that can be obtained antemortem by

Incineration in a medical incinerator,
noninvasive methods, such as blood, urine,
alkaline digestion in specially designed
feces, or saliva. However, these newly develequipment, and disposal in certified oped assays are not yet certified.

municipal landfills are used for disposal of

Differential diagnoses for animals
tissues and carcasses of animals with CWD.

suspected of CWD include brain abscesses,
traumatic il\iuries, meningitis, encephalitis,

Zoonotic Risk: Although CWD has been
peritonitis, pneumonia, arthritis, statvation
present in htu1ted populations of deer and
and nutritional deficiencies, dental attrition,
elk for >30 yr, no case of hun1an CWD has
and anesthetic deaths.

been identified. The risk to people appears
to be minimal. The CWD agent has been

Treatment and Control: There are no
detected in the muscle tissue of infected
treatments available for any TSE. Control
cervids. Public health authorities and
in farmed cervids is by depopulation with
wildlife management agencies suggest the
indemnity and development of a National
following precautions for hunters and

CWD Herd Certification Program in the
people handling cervids in areas where

USA. This is designed to be a voluntary

CWD is found to further reduce risk of
federal-state-industry cooperative program
human exposure: do not harvest deer or elk
administered by the USDA Animal and Plant that appear to be sick or abnormal; wear Health Inspection Service. This plan
rnbber, plastic, or latex gloves when
typically requires 5 yr of monitoring to
clressing the carcass; avoid contact with
achieve the highest status. The bases for
brain, spinal cord, and lymphoid tissues;

CWD control programs in"the farmed cervid
debone the meat when processing; clisinfect
industry are individual animal identification, knives, saws, and tables with 500Ai bleach; CWD testing in all animals in the herd that
and have the anin1al tested for CWD. All
die over a certain age, and limiting new herd public health authorities recommend that additions to animals from herds of comparaanimals positive for ariy TSE not be ble or higher CWD status.

consumed by people or other anin1als.

SCRAPIE

Classic scrapie, a natural clisease of sheep
disease of deer and elk, all of which are
and goats, is seen worldwide except in
thought to result [rom the accumulation of

Australia and New Zealand. It is one of the
an abnonnal fom1 of a cellular protein in the
transmissible spongifonn encephalopathies
brain. Natural transmission of scrapie to

(TSE), related to bovine spongiform
other species has not been shown. In the
encephalopathy and chronic wasting

USA, scrapie primarily affects black-faced

SCRAPIE

1289
sheep breeds ( eg, Suffolk, Hampshire, and

Europe and the USA. The 171 RR genotype is
their crosses), accounting for -96% of cases. considered to be resistant to classic scrapie.

In other countries, the disease is commonly

Scrapie is also rare in sheep with the
seen in other breeds, including those with

136/171 AAQR genotype. However, at least

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white faces.

83 atypical cases of scrapie from more than

110,000 tested samples have been recorded

Etiology, Transmission, and Patho
by The Veterinary Laboratories Agency of
genesis: An abnormal protein designated

Great 81itain. These discordant cases, most
as PrPSc, found in all TSE, appears to
classified as Nor 98 (first found in Norway in
convert a normal cellular protein called

1998) usually involve only a single sheep in
p1ion protein (PrpC) to its abnormal form
a flock with no obvious contacts between

(Prpsc) in susceptible animals. In sheep,
affected flocks. Nor 98 has been seen in
the susceptibility is controlled genetically;
sheep with genotypes considered to be
however, genetic susceptibility has not been resistant, and many of them have one or two established in goats. As it accumulates
of the amino acid leucine (L) at codon 131.

within a cell, PrPSc is deposited as an

This has led to the belief that such cases
amyloid plaque in lymphoreticular and
represent a spontaneous prion disease,
nervous tissue, where its accun1ulation is
analogous to sporadic Creutzfeldt.Jakob
hypothesized to cause the nervous signs
disease in people, and that the prion is not
associated with the disease. Although some
transmitted by direct contact. It has been
researchers still do not believe that PrPSc
reported in almost every European country,
itself is the disease agent, its presence is a
the Falklands, Canada, and New Zealand,
reliable diagnostic test for prion disease.

even though classic scrapie has not been

When PrPC is induced to change to Prpsc,
reported from New Zealand. Eight such
the conformation of the protein's structure
cases have been reported in the USA since
is reconfigured. Although the chemical

2003; the World Health Organization has
composition of the molecule is the san1e, its
classified th.is as a separate disease and
chemical properties change. The normal
declared that it should not affect trade.

protein is soluble in denaturing detergents

The classic disease is naturally transmitand is digested by cellular proteases such as ted during lambing from infected dan1s via
proteinase K. However, PrJ>Sc (as well as the
ingestion of infected placenta or allantoic
infectivity) is not destroyed by detergents
fluids by flock mates and newborn lambs.

and is resistant to breakdown by rendering

Wected males are not believed to transmit
processes presently used, heat sterilization
the disease, although there is one report of
temperatures, ultraviolet light, ionizing

PrPSc detected in semen of several 131/171
radiation, and most disinfecting agents. It

VVQQ and AVQQ V-dependent scrapie
is only partially inactivated by protease K.

affected-ran1s. This occurred after apparent

The genetics of scrapie in sheep is located transmission of scrapie to some of their on chromosome 13, and three codons (136,
offspring from 131/171 VVQQ scrapie eyelid

154, and 171) seem to control most of the
and rectal mucosa-negative ewes. However,
susceptibility to scrapie. Codon 136 codes
because of the rarity of 136/171 VVQQ
for either valine (V), alanine (A), or
genotype in the USA at this time, it is
threonine (T); 154 codes for arginine (R)

unlikely that this should be of concern.

or histidine (H); and codon 171 codes for

The embryo or fetus is not exposed to
glutamine (Q), lysine (K), H, or R. Resisscrapie while in utero in a scrapie-infected tance to scrapie is correlated with 136A,
dam, because there is physical separation

154H, and l 71R. These small changes in the
from PrPSc-containing allantoic fluid and
amino acid components of PrpC apparently
chorioallantois by the anlnion, which
enable it to resist reconfiguration. Scrapie is
remains free of PrP8c even when the other
usually related to polymorphisms at codon
placental tissues are infected. Lambs

171. Among sheep in the USA, 91%of brain
delivered via cesarean section from infected
samples testing positive for scrapie
dams, kept separate from the allantoic fluid,
originated from sheep with the 136/154/17 l
and isolated from infected sheep remain

AARRQQ genotype. However, sheep with
disease free. Despite the wide distribution
codon 136V are at the highest risk of
of normal prion protein in reproductive,
developing scrapie, even when they also
placental, and fetal fluids, PrPSc has been
carry one R at codon 171. Recently, it was
detected only in the caruncula.r portion of
shown that these cases are actually affected
the endometritun and cotyledonary
by another strain of tl1e agent that at one
chorioallantois (the fetal-maternal
tin1e was referred to as the V-dependent
interface) of pregnant scrapie-infected
strain. It was first described in Cheviots by
ewes-but only if both the dan1 and fetus

Irish researchers and has been reported in
are of a susceptible genotype. Although

1290

SCRAPIE
tissues of the maternal side of the placenta
loss and signs of prmitus are often not seen.

carry a susceptible prion protein, it requires

This strain, found in the University of Idal10
susceptible prion-containing cells from the
research flock, made up of local flocks
fetal side of the placenta for conversion to
found to have scrapie, mainly infects

PrPSc. However, there can be partial or

131/171 VVQQ and 131/171 AVQR sheep.

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incomplete anastomosis between fetal

It is probably present whenever scrapie
blood supply to the cotyledons an1ong
and the 136AV and V V genetics a.re found
fetuses of different genotypes on the san1e
together. Most veterinarians or producers
side of the uterine horn, which in rare cases
would not recognize sheep with the
can result in PrPSc accumulation in

V-dependent gene as having scrapie.

cotyledons with resistant genotypes.

Previous contamination of premises is

Diagnosis: A complete necropsy should
believed to be another source of scrapie
be perfonned on any sheep dying mysteriinfection. Anecdotal accotmts abound of ously, including submission of the brain for
flock depopulation and premises deconimmunohistochemical (IHC) testing for tan1ination that are followed by reclllTence
scrapie. Differential diagnoses include
of disease in repopulated infection-free but
caseous lymphadenitis, abomasal emptying
susceptible sheep.

disease, Johne disease, ovine progressive
pneumonia (visna), dentition problems, and

Clinical Findings: Classic scrapie,
meningitis.

which results from ingestion of PrPSc

Cmrently, a.II diagnostic tests for TSE
by a genotypically susceptible sheep, is
require infected tissue and the use of
a longterm, progressive, and debilitating
antibody reactions. Because animals
nemologic illness believed to always be
generally do not produce antibodies against
fatal. Clinical signs may be noticed 18 mo to
self, antibodies a.re mostly monoclonal in

5 yr after exposme and include progressive
origin or a.re made in rodents bred to have
weight loss with no concmrent loss in
no prion protein. IHC and ELISA a.re used
appetite, progressive ataxia, fine head
for routine testing. In the EU, ELISA tests
tremors (most apparent in the ears), and
a.re used for slaughter surveillance, but they
cutaneous hypersensitivity. Pruritus
are not licensed for scrapie testing in the
develops in -7QOA, of cases. Sheep may

USA. However, several test kits are used for
assume a vacant, fixed stare or, less often,
diagnosis of chronic wasting in wild elk and
become suddenly aggressive. Signs of
deer. The IHC test is used as a coniinnatory
hypersensitivity a.re often elicited by
test and is considered to be the gold
nibbing or scratching the sheep's back,
standard worldwide.

which induces the sheep to throw its head

Detection of PrPSc in reticuloendothelial
back, make chew.mg motions and lick at the
organs (spleen, lymph nodes) before
air, or compulsively nibble at the lin1bs
appearance of clinical signs or PrPSc in the
below the carpus.

brain is possible. Detection of PrP5c has

Ataxia is first detected when sheep are
been reported in 76% of tonsils examined
running. The hindlin1bs appear to be
and 57% of lymphoid tissue specin1ens
uncoordinated with the.forelimbs, and
collected from the third eyelid of infected
affected a.nin1als adopt a bunny-hopping
sheep. A small percentage of sheep in which
gait. Sheep often have a high-stepping gait in the brain contains PrPSc do not have the forelimbs, resembling a prancing horse.

detectable PrpSc in the lymph nodes, which

As signs worsen, the hindquarters sway
may be influenced by genotype or scrapie
while standing.

strain. The atypical strains a.re not often

Clinical signs last from 1 to >3 mo; sheep
found in lymphoid tissues.

generally become recumbent because of

The palatine tonsil has been used for
weakness and in coordination. If helped up,
biopsy and diagnosis; biopsy of the lymph
an affected sheep may be able to remain
follicles of the third eyelid is sin1pler and is
standing for hours but cannot rise
validated in the USA as a diagnostic test.

unassisted if it falls or lies down. Death

It yields a high percentage of unreadable
follows 1-2 wk after a sheep can no longer
samples due to lack of follicles in the
right itself. Blindness, resembling that seen
sample in as many as 400/o-600A, of adult
with polioencephalomalacia, occasionally
sheep. Biopsy of the lymphoid ring in the
develops. The clinical signs of scrapie can
rectal mucosa has also been validated and
vary, depending on the sheep's genotype
yields positive diagnoses in -55%--65% of
and the strain of scrapie. The V-dependent
positive sheep. Use of the mandibular
strain has a substantially more rapid clinical
lymph nodes has not been validated;
course of3-30 days and death in 2-3 days
however, biopsy of that site may be useful
after recurnbency. In these cases, weight
diagnostically, because exan1ination of

EQUINE ARBOVIRAL ENCEPHALOMYELITIS

1291
several tissues improves the chances of a
lymphoid tissue of aged black-face and
positive diagnosis. It has not been estabblack-face crosses and sheep sold for lished in the course of the disease when the
slaughter with signs of scrapie ( ataxia, poor
agent will consistently appear in these
body condition scores, a.lopecia. from
tissues, but it may be as early as 14 mo after
rubbing) are tested for scrapie by IHC.

exposure. The interval likely depends on the Sheep found to be positive are traced back VetBooks.ir
age of the sheep at exposure and genotype
to the herd of origin, which is quarantined,
or strain of scrapie.

and all animals are tested. All positive sheep

The pathologic changes associated with
and those with the l 71QQ genotype are
scrapie are confined to the CNS and include
eutha.nized. Animals sold from the flock are
vacuolation, neuronal loss, astrocytosis,
also traced and tested. Since the program
and accumulation of amyloid plaques.

was initiated, the prevalence of scrapie has

However, because histologic changes are
decreased 900/o, from -0.5% to -0.015% as of
often lacking, diagnosis is made on the basis the end of 2013. The goal is to have the USA of IHC staining of the obex, other parts of
declared free of scrapie by 2017.

the brain, and/or lymphoid tissue for PrPSc.

Voluntary efforts to control and eliminate
the disease have been undertaken by

Control: For disinfection, instruments
producers in the USA by selecting sheep
should be soaked in 2.5N Na.OH or a
with at lea.st one l 71R codon and culling
disinfectant shown to be effective against
sheep with susceptible genotypes; the
a.bnom1al prions. Incineration or digestion
expectation is that the remaining sheep will
by sodium hydroxide are considered
be resistant t.o scrapie infection. However,
appropriate to adequately inactivate
some concern has been expressed that
infected carcasses.

reliance on genetics for elimination of the

Individual and premises identification are
disease may inadvertently select for the
required for all breeding sheep leaving their
atypical strain of scrapie that infects the
original premises as part of the USA

171 RR genotype. So far there are no data
mandatory Sera.pie Eradication Program.

to support that concern.

A scrapie slaughter surveillance program

Rules prohibiting rwninant-to-rurninant
initiated by the USDA/APHIS has been
protein feeding have been in place in many
underway since 2003 in which brains and
countries for > 10 yr.

EQUINE ARBOVIRAL ENCEPHALOMYEL:.ITIS

(Equine viral encephalitis)

Equine encephalitides can be clinically
arboviruses pathogenic to horses on
similar, usually ca.use diffuse encephalomyvirtually every continent.

elitis (seep 1262) and meningoencepha.lomyelitis, and are characterized by signs of CNS dysfunction and moderate to high

Etiology and Epidemiology of
mortality. Arboviruses are the most

Arboviral Encephalitides:

common ca.use of equine encephalitis, but

Alphaviruses: North America is home to
rabies virus, Sarcocystis neurona (see
some of the most pathogenic encephalitic
p 1309), Neospora hughesii (seep 663),
viruses because of the enduring endemic
equine herpesviruses, and several bacteria.

status of alpha.viruses of the fan1ily
and nematodes may also ca.use encephalitis. Toga.virida.e. Endemic species in North, Arboviruses a.re transmitted by mosquitoes

Central, or South America include Ea.stem
or other hema.topha.gous insects, infect a
equine encephalitis virus (EEEV), Western
variety of vertebrate hosts (including
equine encephalitis virus (WEEV),
people), and may ca.use serious disease.

Highlands J virus, Venezuelan equine

Most pathogenic arboviruses use a
encephalitis virus (VEEV), Everglades virus,
mosquito to bird or rodent cycle. Tickbome
and Una virus (see TABLE 3). Other alpha.viencephalitides a.re also a differential ca.use ruses associated with equine encephalitis
in the eastern hemisphere. A.rboviral
are Semliki Forest virus in Africa and Ross
diseases are ever emerging, and there are

River virus in Australia. and the South

1292

EQUINE ARBOVIRAL ENCEPHALOMYELITIS

ARBOVIRUSES THAT CAN CAUSE OR ARE LINKED TO EQUINE

ENCEPHALOMYELITIS

Virus Species

Most Important
or Variant

Geographic Location

Reservoir

VetBooks.ir

ALPHAVIRUSES

North American Eastern Eastern North America,

Birds
equine encephalitis virus primarily east of Mississippi river

Madariaga virus

South America, Caribbean

Rodents

Western equine

Western South America

Birds, rabbits, and snakes
encephalitis virus

Highlands J virus

Birds

Venezuelan equine

Central and South America,

Cotton rat and other
encephalitis virus

Caribbean
rodents

Everglades virus

South Florida (USA)

Rodents

Ross River virus

Australia, Papua New Guinea Marsupial and placental mammals

Sernliki Forest virus

East and West Africa

Unknown

Una virus

South America

Birds

FLAVlVlRUSES

Japanese encephalitis

Asia, India, Russia, Western

Birds, swine

Pacific

Murray Valley

Australia, Papua New Guinea Birds, marsupials, and foxes Klli\iin virus

Australia

Birds (herons and ibis)

St. Louis encephalitis

North, Central, and South

Birds

America

Usutu

Europe, Africa

Birds

West Nile

Africa, Middle East, Europe,

Passerine birds

North, Central, and South

America, Australia

Louping ill

Iberian Peninsula, UK

Sheep,grouse

Powassan

North America, Russia

Lagomorphs, rodents, mice,
skunks

Tickborne encephalitis

Asia, Europe, Finland, Russia Small rodents

Pacific. EEEV has two distinct antigenic

EEE and WEE viluses are separated in
vruiants that ru·e sepru·ated longitudinally.

North America primarily latitudinally;

The North Ame1ican variant is the most
however, WEEV is relatively heterogeneous,
pathogenic and is found in eastern Canada;
with several subtypes consisting of WEE,
all states within the USA east of the

Highlands J virus, Sindbis, Aura, Ft. Morgan,

Mississippi River and in Arkansas,
ll.lld Y 62-33. Several varill.llts have been

Minnesota, South Dakota, and Texas; and in
found in horses ( see TABLE 3). WEE is found
the Caribbean Islands. The South American
in western Canada, states in the USA west
variru1t is less pathogenic and confmed to
of the Mississippi, and in Mexico and South
central and South America and is now

America. WEE previously isolated in the
called Madariaga virus (MADY).

south and eastern USA has been shown to

EQUINE ARBOVIRAL ENCEPHALOMYELITIS

1293
belong to the Highlands J virus serogroup.

horses in southeastern habitats not

VEE has six antigenically related subtypes:

associated with sylvatic field ecology, so a
subtype I, Everglades, Mucambo, Pixuna,
full understanding of the epizootic cycle still

Cabassou, and AGS0-663. Subtype I
remains to be elucidated. Intense focal
serovars AB and C primaiily cause epiactivity has been reported in Michigan, VetBooks.ir
zootics; subtype I and serovar IE caused a

Wisconsin, Ohio, Massachusetts, and
large outbreak in Mexico in 1993. Epizootic

New Hampshire. In 2005, Massachusetts
strains are not generally found in the USA,
experienced a hun1an case affected rate
although there was an epizootic of VEE in
more than five times that of the preceding

1971. Sylvatic subtype Il (Everglades) has

10 yr; affected people resided within Y2 mile
been isolated from people and mosquitoes
of a cranberry bog or swamp associated
in Florida; subtype Ill has been isolated in
witl1 forest habitat.

the Rocky Mountains and northern plains

In Central and South America, the
states.

principal vectors of MADY belong to Culex

The general life cycle of alphavimses

(Melanoconion) spp. These vectors feed on
involves transmission between birds and/or
birds, rodents, marsupials, and reptiles,
rodents and mosquitoes. In North America,
with rodent reservoirs possibly featuring
theoretically, EEEY is perpetuated in a
more impo1tantly in this life cycle. Before
sylvatic cycle between avian hosts
the yeai· 2000, comparatively few epizootics

(passerine birds) and mosquitoes, with
of disease caused by MADY in horses were
primary transmission in this cycle via
recorded in South America, with minin1al

Culiseta melanura. Birds do not develop
disease repo1ted in people. Furthermore,
disease but develop sufficient virem.ia for
there are notable differences in vimlence
transmission to mosquitoes unless the bird
between EEEY strains in South America vs
belongs to an introduced species that in
in North America. In 2008 and 2009, larger

North America includes European starlings,
outbreaks occurred in Central and South
house sparrows, pheasants, ai1d emus. Field

America. In northeastern Brazil, 229 horses
work in Alabama indicates that the northern were affected, with a case fatality rate of cardinal is the primary target for C

73"/o and disease severity sintilar to that of
melanura feeding; however, other

EEEY in North America.

mosquitoes (C erraticus) are capable

WEE is transmitted primarily by C
of feeding on a wider variety of birds,
tarsalis, which is found just west of the
including robins, chickadees, owls, and

Mississippi river and throughout the West.

mockingbirds. M=aliai1 reservoirs may

This mosquito breeds in sunlit marshes and
also be important during years of high
in pools of inigation water in pastures.

EEEY transmission. Experimental infection

WEE can also be transmitted by the tick
of cotton rats, a marshland rat found

De1macentor ande1·soni. Epizootics of
throughout the Americas, resulted in

WEE are associated with increased rainfall
viremiajust being capable of transmitting
in early spring followed by warmer than

EEEY, with juvenile rats developing higher
norn1al temperatures.

titers and l 00% mortality to infection.

Sylvatic VEE viruses are found through

Horses and people are clinically affected
out North, Central, and South America in
but do not develop viremia sufficiently high
jungle or swampy areas, Two cycles occur
enough to transmit vims to mosquitoes and
with VEEY, the enzootic cycle and the
so are considered "dead-end" hosts.

epizootic cycle. The mosquitoes that serve

However, young animals are more
as the primaiy vectors for the bird- or
susceptible to EEEY, and it is not known
rodent-mosquito life cycle are members of
how important non-neural tissues are for
tl1e subgenusMelanoconion (C cedecci).

harboring high viral infection. Presumed

Epizootics ai·e associated with a mutation to
extraneural sites of infection include
a subtype I (AB, C, and possibly E), a chai1ge
cardiac tissue and bone marrow. During
in manl.lllalian pathogenesis, and a change
epizootics, alpacas, llamas, cattle, swine,
to several bridge vectors. The enzootic cycle
cats, and dogs can develop disease. Snakes
centers around sylvatic rodents such as
have been identified as a possible reservoir.

spiny and cotton rats, which have high

Freshwater hardwood swamps are the
natural infection rates and can develop
most associated enzootic niche for EEEV. In
viremia high enough to trat1S1nit VEEY to
the southern USA, which has the highest
mosquitoes. Opossums, bats, and shore
n un1ber of reported aimual cases, reeme1°
birds likely contribute to dispersal of the
gence within mammalian hosts is associenzootic virus so that constant cycling ated with "tree farms" that often function as occurs. When epizootics occur with
inland freshwater swan1ps. Nonetheless,
mutation of the virus and this change in

EEEY disease occurs frequently in naive
mosquito vectors, equine infection becomes

1294

EQUINE ARBOVIRAL ENCEPHALOMYELITIS
a predominant feature in the maintenance
involving 900 horses. Although multiple
of epizootic VEE. All mammalian hosts are
pathogens were detected, including KUN,
capable of developing a high-titer viremia of

Murray Valley encephalitis virus, and Ross

-106 plaque-fom1ing units/mL for up to 5

River virus, there was emergence of a new
days, but the horse is likely to be the most
strain of KUN. The le viruses are fairly

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important manunalian host in tem1s of
nonpathogenic and found in lndia. (This
vector capacity.

sub lineage may soon be designated as
lineage 5.) Lineage 2 strains, long consid

Flaviviruses: ln general, viruses
ered African based and inducing mild
belonging to the Flaviviridae and Bunyaviridisease in horses, is also expanding globally dae families are less pathogenic than the
with increased neuroinvasive activity.

Togaviridae; however, viral encephalomyeli

Neuroinvasive disease due to lineage 2 has
tis caused by any of these pathogens is a
emerged across Europe in Hungary, Austria,
potentially catastrophic illness for any

Italy, and Greece, which had at least four
vertebrate host. There are 53 species of
epizootic cycles with cases of neuroinvasive
flavivirus, and many are clinical pathogens
disease identified in horses.

for horses, including Japanese encephalitis,

Both wetland and terrestrial birds may be

West Nile virus (WNV) encephalitis, Kunjin
involved in the natural cycle of WNV, with
virus (KUN), and Murray Valley encephalitis
migratory birds thought to introduce the
virus. Overall, the diseases caused by the
virus into a geographic region. However, a

Japanese encephalitis serogroup are similar
wide range of infected birds ( -326) have

( see TABLE 3). All of these viruses are high, sustained viremia and little or no
transmitted by a mosquito vector, with
clinical disease (passe1ines ). Fatal

Culex spp usually the most efficient infections among corvids ( eg, crows, blue
transmitter. KUN is actually a strain of WNV jays, and magpies) have been the hallmark and is found in Australia, some southeast
of WNV infection in the USA. Ticks have

Asia countries, and New Guinea. Disease in
been demonstrated to be infected with
horses caused by Murray Valley fever is

WNV, but their role in natural transmission
geographically restricted to the South
is unknown. Experimentally, transmission

Pacific and is sporadic in occurrence.

has been documented between cohabitating

WNV has the widest geographic
birds and from oral exposure to WNV in
distribution of all of the flaviviruses. Prior
drinking water in birds. Oral transmission
to 1999, WNV was recognized in Africa,
has been demonstrated experimentally in
the Middle East, Asia, and occasionally in
several types of raptors.

European countries. ln 1999, WNV infection
ln people, other important routes of
was first recognized in North America.

infection include blood transfusions, organ

Since then, the virus hq.5 spread throughout
donation, breast milk, and across the
the USA and parts of Canada and Mexico.

placenta. Sporadic infections and illness

WNV isolated from the outbreak in New
have also occurred in several other

York in 1999 appears to be closely related to
manunalian species, including dogs, cats,
an isolate recovered from geese in Israel in
can1elids, sheep, and squirrels. Oral

1998.

transmission has been demonstrated

Since 2010, continued worldwide spread
experimentally in cats. Farmed alligators
and reemergence of many flaviviruses,
have demonstrated disease and mortality
especially WNV, has occurred. As of 2014,
due to WNV, and there has also been a

WNV is recognized as having seven lineages, report of WNV-induced disease in crocowith lineage 1 (sublineage la, lb, and le) diles. Alligators are susceptible to oral
and lineage 2 affecting people and horses.

infection. ln addition to birds, only alligators

Lineage la activity in the USA and Europe
have consistently demonstrated high
dominated much of the end of the 1990s
enough viremia ( 104-105 plaque-fanning
until the mid-2000s, causing neuroinvasive
units) to amplify virus, serve as reservoir
infections in people and horses in Africa,
hosts, and transmit virus back to mosqui

Europe, Australia, Asia, North and Central
toes.

America, and the Middle East. In 2012, a

Most equine-associated flaviviruses are
very large epizootic occurred in the USA,
maintained in an enzootic transmission
with 5,674 human and 690 equine cases
cycle between wild birds and mosquitoes,
reported. New emergences have occurred
although tickbome encephalitis found in
in Greece and Serbia, and the first lineage la Eurasia can cause disease in horses. Many case in lndia was detected in 2012. Lineage
species of mosquitoes can transmit the
lb viruses are primarily represented by
equine virulent viruses, although Culex spp KUN, with Australia undergoing the largest
are principal vectors to maintain enzootic
epizootic of arboviral disease in 2011,
activity. C pipiens complex and C tarsalis

EQUINE ARBOVIRAL ENCEPHALOMYELITIS

1295
are thought to play the largest role in natural characterized by periods of hyperesthesia, transmission in North America. In the
ranging from mild apprehension to overt
eastern and Midwestern regions of the USA,
hyperexcitability, wiili fractious reactions

C pipiens is one of the major vectors,
to aural, visual, and tactile stimuli. Fine
whereas in the western regions of the USA,
and coarse tremors of the face and neck

C tarsalis

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is thought to be one of the most
muscles are common, described in 600/o-90%
efficient vectors.

of horses. Some horses have periods of cata

Bunyaviruses: Cache Valley virus
plexy or narcolepsy that may render them

(transmitted by mosquitoes and
temporarily or permanently recwnbent.

Culicoides
sp an10ng rabbits), Main Drain virus

Cranial nerve deficits can be seen in all

(transmitted by
arbovirus infections of horses; these include

Culicoides vaiipennis
an10ng hares and rodents in the western
most cranial nerves with cell bodies located

USA), and snowshoe hare virus (transmitin ilie mid- and hindbrains. Weakness and/or ted by
paralysis of the face and tongue are most

Culiseta and Aedes mosquitoes
among rabbits in southern Canada and
frequent. Horses with facial and tongue
northern USA) have all been identified,
paresis can be dysphagic, and overt signs
although infrequently, as the cause of
of quidding or even esophageal choke can
encephalitis in horses.

develop. Many horses with severe mental
depression and facial paresis will keep their

Clinical Findings of Viral Encephalo
heads low, resulting in severe facial edema.

myelitis in Equids: The initial clinical

Occasionally, head tilt may be seen.

signs are similar for the arboviruses;

Infrequently in WNV disease, urinary
progression of clinical signs and severity
dysfunction ranging from mild straining
of disease are the differentiating features.

to stranguria has been reported, making

Initially, horses are quiet and depressed,
differentiation from equine herpesvirus 1
with clinical neu.rologic signs generally

(EHV-1) more challenging.

occurring 9-11 days after infection.

During ilie neurologic phase, horses

Compared with WEE and WNV disease,
frequently thrash and injure themselves.

clinical signs of EEEV (and VEEV)

Sepsis from traw1ia in recwnbent horses
encephalomyelitis more frequently include
also occurs. Prolonged recumbency leads
altered mentation, in1paired vision, ain1less
to pulmonary infections, especially in foals,
wandering, head pressing, circling, inability
in which a long du.ration of slinging and
to swallow, irregular ataxic gait, paresis and
treatment may be pursued more frequently
paralysis, seizures, and death. Spinal signs
than in large, recwnbent animals. Dysphaare often symmetric with ataxia in all limbs, gia leads to decreased water and food
rapidly progressing to quadriparesis, along
intake, with renal daniage due to concurrent
with intensification of fore brain signs. Many
use of anti-inflan1matory drngs. Skin and
horses progress to recumbence within
muscle .necrosis are common in recwnhe.nt

12-18 hr of onset of neu.rologic abnorn1alihorses. Life-threatening trauma can also ties. Most deaths occur within 2-3 days after occur, including a ruptured diaphragm and the onset of signs.

fractures.

The clinical signs and course of disease

Lesions: All necropsies on horses
are highly variable in WNV disease and
suspected of viral encephalitis should be
other flavivirus encephalomyelitis.

perfonned with all participants wearing

Presenting complaints most often include
personal protective gear (ie, waterproof
neu.rologic abnormalities; otl1er conunon
gown, boots, gloves, N-95 or N-99 mask,
initial complaints include colic, lameness,
face shield, and hair covering). Gross
anorexia, and fever. Initial systemic signs
lesions are most common with EEEV and
include a mild fever, feed refusal, and
severe VEEV disease and are characterized
depression. Neurologic signs are highly
by widespread and prominent congestion
variable, but spinal cord disease and
of the meninges. In oilier infections, gross
moderate mental aberrations are most
lesions are rarer and are limited to small
consistent. Spinal cord disease manifests as
multifocal areas of discoloration and hemasynunetric, multifocal or diffuse ataxia and orrhage throughout the brain and spinal paresis. Severe manifestations of WNV may
cord. The brain should be examined
occur independently in the fore- or
microscopically for the presence of
hindlirnbs, unilaterally, or in a single limb.

me.ningoencephalitis. In EEEV infection, a

In all clinical studies published to date, for
severe gliosis with necrosis of ilie .neuropil

WNV, >90"A, of affected horses developed
is seen in ilie cerebrwn and extending
some type of spinal cord signs, whereas
through the corona radiata through the

40"h-60"A, developed behavioral changes
hindbrain and cervical spinal cord.

1296

EQUINE ARBOVIRAL ENCEPHALOMYELITIS

Although mononuclear cells are present,
neurologic signs are seen, viremia has
neutrophils a.re widespread and diffusely
ended and detection of vitus in the plasma
distributed. The gliosis is less nodular than
of clinically affected horses is of no value.

in WNV, and when there are accumulations

Serology is the key to antemortem
of cells, there is extensive necrosis and
diagnosis of recent alphavirus and flavivirus

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often frank microscopic hemorrhage within
infection in horses showing clinical signs.

and around lesions. In milder cases and in
lgM antibody rises sharply and is increased

WNV infections, microscopically there is
in 85%--90% of horses with clinical a.rboviral
a non-necrotizing lyrnphohistiocytic
encephalitis. Thus, the lgM capture ELISA
poliomeningoencephalitis. Slight to severe
is the test of choice to detect recent
inflammation, characterized by perivascular exposure to these viruses. Neutralizing cuffing of lymphocytes and monocytes, is
antibody titers (primarily IgG) develop
usually present. In more severe cases, there
slowly during this titne and stay increased
can be extravasation of fluid and red blood
for several months. Although neutralizing
cells from vessels. Often the distribution
antibody tests will differentiate between
of lesions is rnultifocal, with more severe
subtypes of these viruses, and are thus
lesions present in grey matter. In the
considered the gold standard for confumaneuropil, dying neurons often are surtory serology, paired serum samples are rounded by microglial cells. The most
essential to detect recent exposure and to
severe gliosis and perivascula.r cuffing is
differentiate antibody response due to field
often in the mid brain (thalamus, hypothalainfection from vaccine responses for any of mus) and hindbrain (pons and medulla),
these viruses. Because virus-neutralizing
extending into the cerebellum. Lesions can
antibodies appear at tl1e end of viremia and
be multi.focal in the spinal cord and can be
may precede appearance of neurologic
more severe in the lumbar cord.

signs, paired samples may not show a 4-fold
increase in horses while demonstrating

Diagnosis: No consistent changes in
neurologic signs. In horses that succun1b
clinical pathology have been found in
witl10ut premortem and postmottem
equine viral encephalitis. With EEEV and
testing, paired san1ples from febrile

WNV in horses, peripheral lymphopenia is
herd mates may be necessary to confirm
common. Horses are frequently azotemic,
presence of arbovirus activity within a
likely from decreased food and water
locale. Maternal antibodies may interfere
intake.

with neutralizing responses in young foals.

In general, no pathognomonic signs

This response is confounded by recent
distinguish flavivirus infection in horses
vaccination. The most common neutralizfrom other CNS diseases, and a full diaging antibody test formats are the classic nostic evaluatio11 should be performed.

plaque reduction neutralization test

Confirmation of flavivirus infection with

(PRNT) and a rnicrowell format test.

encephalitis in horses begins with

Practical application of the micro well vs
assessment of 1) whether the horse meets
the PRNT indicates that the endpoint titer
the case definition based on clinical signs;
ill the rnicrowell test can be several logs

(2) whether the horse resides in an area in
higher than ill the PRNT, so results cannot
which flavivirus has been confirmed in the
be compared between samples.

cun-ent calendar year in mosquitoes, birds,

Several postmortem diagnostic assays
people, or horses; and (3) lack of appropriare available and, al\;hough specific, they ate vaccination.

vary in sensitivity, dependmg on the vims.

In terms of antemortem diagnostic

The midbrain and brain stern have the
testing, analysis of CSF can be a valuable
highest concentrations of encephalitic
acljunct to presun1ptive clinical assessment.

viruses, including rabies virus. In1munohis

CSF analyzed from horses with acute EEEV
tochemistry and PCR testing for EEEV and
infection typically shows a neutrophilic

EHV-1 are relatively straightforward
pleocytosis with markedly increased total
compared with that for WNV. Diagnostic
solids. Horses infected with EEEV that are
testillg continues to confirm the tmreliabilpartially itm11une may have predominantly ity of detection of virus, even by PCR,
mononuclear cells, but nondegenerate
because of the low viral load ill WNV
neutrophils are still present. Altl10ugh
mfection. Often, only a single neuron in one

WNV-infected horses can have normal CSF,
or two sections may yield positive virus
if the CSF is abnormal, there is a mononustaining ill the horse by in1munohistochernclear pleocytosis with moderately to istry. When tested by PCR, the limited viral
markedly increased total solids. In a few
load dictates accurate testing of approptiate
horses with acute infections, vi.Jus may
tissues consistillg of several locations,
be isolated from tl1e CSF. By the titne
includmg thalan1us, hypothalamus, rostral

EQUINE ARBOVIRAL ENCEPHALOMYELITIS

1297
colliculus, pons, medulla, and anatomically

WEEV 200/o--500/o, from VEEV 500/o--75%, and
identified spinal cord. Viral isolation is still
from flavivirus infections 35%45%. Horses
important for molecular epidemiology.

with clinical neurologic signs from

Infectious and noninfectious causes of
alphavirus infection that recover have

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brain and spinal cord diseases should be
a high incidence of residual neurologic
considered as differential diagnoses.

deficits, whereas many horses that recover

Infectious causes include alphaviruses,
from WNV disease have been reported to
rabies, equine protozoal myeloencephalitis
have no residual neurologic deficits. In

(seep 1309), and EHV-1; less likely causes are EEEV infection, death is frequently botulism and verminous meningoencephalospontaneous. With WNV disease, horses myelitis ( eg, Halicephalobus gingivalis,
are euthanized for humane reasons, but

Setaria spp, Strongylus vul.garis).

spontaneous death does occur. In EEEV,

Noninfectious causes include hypocalcemia,
most surviving horses exhibit longterm
tremorigenic toxicities, hepatoencephalopa nemologic signs. In WNV disease, overt thy, and leukoencephalomalacia.

clinical signs in horses that recover can last
from 1 day to several weeks; improvement

Treatment: Treatment of viral encephaliusually occurs within 7 days of onset of tis is supportive, because there are no
clinical signs. Although 800/o--900/o of owners
specific antiviral therapies. Management is
report that the horse returns to no1mal
focused on controlling pain and inflanunafunction 1-6 mo after disease, at least 10%
tion, preventing injuries associated with
of owners report longterm deficits that limit
ataxia or recumbency, and providing
athletic potential and resale value. Deficits
supportive care. Intervention does not
include residual weakness or ataxia in one
appear to significantly affect the outcome of
or more limbs, fatigue with exercise, focal
most fulminate EEEV infections. For WNV,
or generalized muscle atrophy, and changes
flunixin meglumine (1.1 mg/kg, IV, bid) early
in personality and behavioral aberrations.

in the course of the disease decreases the
severity of muscle tremors and fascicula

Prevention: Vaccination against
tions within a few hours of administration.

alphaviruses and flaviviruses as core annual

Recumbent horses that are mentally alert
vaccines are considered the standard of
frequently thrash, causing self-inflicted
care for all horses in the USA as endorsed
wounds and posing a risk to personnel.

by the American Association of Equine

Responses to tranquilizers and anticonvul

Practitioners. Formalin-inactivated whole
sant medications are variable, depending on
viral vaccines for EEEV, WEEV, and VEEV
the virus and severity of disease. A sling and
are commercially available in bi- and
hoist may be used to assist horses that are
trivalent forms, usually formulated with
recumbent and have difficulty rising;
tetanus toxoid; several now include WNV.

however, recumbent horses with EEEV

Nonvaccinated adult horses require the
generally are too comatose to sling.

label priming two injections. For adult

Dysphagic horses require fluid and
horses in temperate clin1ates, an annual
nutritional support.

vaccine within 1 mo before the start of

Until equine protozoal myeloencephalitis
the arbovirus season is recommended.

is excluded, prophylactic antiprotozoal

However, for horses that travel between
medications may be instituted. Other
northern and southern areas affected by the
supportive measures ( eg, oral and parental
virus, injections should be given two or even
fluids and nutrition for dehydrated and
three times yearly in active arbovirus
dysphagic horses) are also important.

seasons. Mares should be vaccinated 1 mo

Broad-spectrum antibiotics should be given
before foaling to induce colostral antibody.

for treatment of wounds, cellulitis, and

If a pregnant mare is naive, the full priming
pneumonia. Horses with intermittent or
series starting 2 mo before foaling is
focal neuropathies have a better prognosis
reconunended. However, some mares do
than those with complete flaccid paralysis
not produce colostral antibody if vaccinated
or that appear comatose. Efficacy of
for the first time during gestation.

specific antiviral agents for treatment of

In foals that have received adequate
naturally occurring WNV or EEEV infection
colostrum from vaccinated dan1s,
is unknown, even in people. Recent work
vaccination should begin at 5-6 mo of
with passive immunotherapy indicates
age; foals should receive two additional
possible benefit after the onset of clinical
vaccinations at 30 and 90 days after the
signs in WNV models.

first one. It is unclear whether maternal
antibody interferes with vaccine responses

Prognosis: Mortality of horses showing
in foals; however, epidemiologic evidence
clinical signs from EEEV is 50%--900/o, from
strongly indicates that horses between 4 mo

1298

EQUINE ARBOVIRAL ENCEPHALOMYELITIS
and 4 yr old are highly susceptible to EEEV.

however, exposure to EEEV and WNV is

If there is early spring (March) activity in
detected in both species dming arbovirus
the southeastern USA, horses may require
seasons. In active years, young dogs have
three injections throughout the year,
been reported to be susceptible to EEEV
especially in horses <5 yr old and in horses
infection.

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that have recently arrived in the southeast

Keeping dogs and cats indoors or in a
ern USA. In foals born to nonvaccinated or
screened area, especially during the time
minimally vaccinated mares, maternal
when mosquitoes are most active, reduces
immunity may wane, and vaccination
exposure. Disposal of dead birds or other
should be perforn1ed at 4, 5, and 6 mo of
small prey that might be eaten may reduce
age. In Florida, where the highest numbers
oral exposure.

of EEEV cases occur, horses of all ages

Clinical cases of botl1 of these diseases
should be vaccinated in January and again
have also been recorded in other domestic
in April before the peak of the season. A
and exotic animals during active seasons.

third vaccination should be administered

Emus are exceptionally susceptible to
late in the sununer if the season is

EEEV. These animals are used for the
particularly active. The frequency of
commercial food industry, and infection
vaccination may be minimized to once or
results in high viremia and high amounts
twice per year in climates that have short
of virus shedding rectally, orally, and in
mosquito seasons and in which limited
regurgitated material. Vaccination will
activity has historically been reported.

prevent viremia, shedding, and disease.

Currently, several whole inactivated

Can1elids are susceptible to WNV, and
virion vaccines, one recombinant inactinmnerous reports of disease and pathology vated vaccine, and a canarypox-vectored
were recorded as the virus spread across
vaccine are licensed for prevention of WNV

North America. The killed, adjuvanted
viremia in most of the Americas, including
vaccine marketed for use in horses has been
the USA and Canada, and Europe. An
used in camelids without any reports of
inactivated virus vaccine is readily available major adverse effects, and animals have against Japanese encephalitis virus. There is demonstrated production of neutralizing experimental evidence that the canarypox
antibody.

WNV lineage l vaccine provides crossprotection against WNV lineage 2 infection.

Zoonotic Risk: The reporting of these

WNV challenge studies indicate that -10% of diseases (or suspicion of such) on an properly immunized horses do not produce
international and national basis is a basic

.neutralizing antibodies to WNV and that
duty of all veterinarians to ensure the health

2.3o/c,-3"/o of equine WNV cases seen in tl1e
and safety of horses and people. As such,
field are in fully vaccinated horses. The
a thorough diagnostic investigation to
duration of immunity from vaccination
confirm these infections is imperative,
with the killed, adjuvanted WNV vaccine
irrespective of state resources available
is unknown.

for subsidized testing.

Protection of horses from arboviruses

People may be infected by most of the
must also include efforts to minimize
arboviruses that commonly cause viral
exposure to infected mosquitoes. Mosquito
encephalitis in horses. Clinical signs in
mitigation includes applying an insect
people vary from mild flu-like symptoms
repellent that contains permethrin on the
to death. Children, the elderly, and those
horses at least daily during vector season,
who are imrnunosuppressed are tl1e most
especially at times of day when mosquitoes
susceptible. People with neurologic disease
may be most active. Environmental managedue to arboviruses usually have pern1anent ment is also essential and includes keeping
neurologic in1pairment after recovery.

the barn area, paddocks, and pastures

Human disease is reported infrequently and
cleared of weeds and organic material, such
generally follows equine infections by -2
as feces, that might harbor adult mosquiwk. Veterinarians should be aware of the toes. Cleaning water tanks and buckets at
possibility of human infection and use
least weekly will reduce mosquito breeding
repellents and otl1er procedures to protect
areas. Removal of other containers such as
themselves from hematophagous insects
flower pots and used tires t11at may hold
when working in sylvatic virus habitats
stagnant water is essential for reducing the
or handling viremic horses. In addition,
mm1ber of mosquitoes in tl1e area.

waterproof clothing (gown, boots, gloves),

Options for control of arbovirus infection
respirator (N-95 or N-99 mask), face shield,
in other animals emphasize reduction of
and hair covering are reconU11ended during
exposure. Few arbovirus infections have
all necropsies perfonned on horses
been documented in dogs and cats;
suspected of having encephalomyelitis.

LOUPING ILL

1299

LOUPING ILL

(Ovine encephalomyelitis)

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L<mping ill is an acute, tick-transmitted viral
intensity of viremia and frequency with
disease of the CNS that primarily affects
which clinical signs develop. After
sheep, but cattle, goats, horses, dogs, pigs,
inoculation by an infected tick, virus

South American can1elids, red grouse, and
initially replicates in lymphoid tissues,
people also can be affected; people can be
which gives rise to viremia that lasts 1--5
infected by tick bites or exposure to tissues
days. Only animals that develop high titers
or instruments contaminated with virus. The
can transfer the virus to ticks. During
disease is seen throughout the rough hill
viremia, a febrile reaction may be present,
grazings of the British Isles wherever the
but overt clinical signs are generally absent
vector tick, Jxodes ricinus, is prevalent.

until the virus enters the CNS and begins

Diseases of sheep indistinguishable from
replication, even though the immune
louping ill and caused by sinlilar viruses have response has eliminated the virus from been repo1ted in Norway, Spain, Turkey, and
the extraneuronal tissues. The extent of

Bulgaria, which suggests that the condition
neuronal damage consequent to viral
may not be rest1icted to the British Isles.

replication determines the severity of signs,
from none (subclinical) through varying

Etiology and Transmission: The virus
degrees of neurologic dysfunction to
belongs to the Flaviviridae family and is part sudden death. Histologic lesions may be of an antigenically closely related complex
present whether or not signs develop. Signs
of viruses known as the tickbome
include fine muscular tremors, nervous
encephalitides, which are primarily
nibbling, ataxia (particularly of the
associated with disease in people and
hindlirnbs), weakness, and collapse; death
distributed throughout the northern
may occur 1--3 days after onset of signs.

tl·mperate regions. Infection is transmitted

Peracute deaths may also occur. In some
lransstadially by the tick vector; transorecovered aninlals, residual paresis or varial transmission of louping ill virns does
torticollis may persist. All recovered
not appear to occur. In sheep flocks,
aninlals are solidly inunune for life.

mortality ranges from 600/o in newly

The severity of clinical disease in animals
introduced stock to 5%--100/o in sheep
recently infected with Anaplasma
acclimatized to the pasture. On farms where phagocytophilum (the cause of tickbome the disease is endemic, losses are mainly
fever [seep 772]) is markedly increased,
confmed to animals <2 yr old; adults tend to
preswnably because of the immunosupbe inllllune as a result of previous infection, pressive effect of this organism. The
and lambs are protected in their first season
accompanying pathology may be complex
by colostral antibody. However, when the
and associated with secondary bacte1ial
disease appears for the first tinle, or after a
and mycotic infection, accounting for the
lapse of several years, all ages of sheep are
high mortality experienced when naive
susceptible. Mo1tality is variable in other
flocks are introduced to tick-infested
species but tends to be high in red grouse.

pasture.

All species of vertebrates that come in

No specific gross lesions are present,
contact with questing ticks may become
although secondary pneun1onia may
parasitized and infected with louping ill
develop. Histologic examination of the CNS
virus, but only sheep and grouse develop
usually shows a nonsuppurative polioentiters of viremia sufficient to pass the cephalomyelitis with lesions predominantly
infection to the vector tick Infection also
in the brain stem.

can be spread through contact with
contaminated instrun1ents or tissues.

Diagnosis: The disease normally is seen

Infected lactating goats can excrete high
only in animals that have had access to
titers of virus in their milk, which may
tick-infested pasture; however, the
cause fatal infection of their kids and be
variable clinical picture necessitates
a potential hwnan health hazard.

differentiation from other conditions that
cause locomotor or neurologic dysfunc

Pathogenesis, Clinical Findings, and
tion. Confirmation is by histologic

Lesions: The course of infection in all
examination of the brain, virus detection
species is sinlilar, and varies only in the
in CNS tissue, and serology. As much of

1300

LOUPING ILL
the brain and brain stem as possible
provides protection for <2 yr. Colostrum
should be fixed in formaldehyde solution
from the vaccinated ewe prevents infection

(10% in saline), and sections examined for
of lambs in their first months. Generally, all
the characteristic lesions, which can be
animals to be retained for breeding are
useful in reaching a presumptive diagnovaccinated at 6-12 mo of age. Use of VetBooks.ir
sis. Diagnosis is confirmed by immunohisinsecticidal dips to protect against exposure tochemistry using an appropriate
to ticks generally is inadequate, although
monoclonal antibody. For routine
pour-on preparations reduce exposure, and
diagnosis, virus isolation is now seldom
their systematic use may effectively reduce
undertaken and has been replaced by
the abundance of ticks and prevalence of
reverse transcriptase PCR. This requires
virus infection.

a piece of brain stem to be collected into
virus transport medium and dispatched to

Zoonotic Risk: Louping ill virus infection a suitable diagnostic laboratory. Measureof people can cause severe encephalomyeliment of serum neutralizing and hemagglutis. Symptoms are biphasic; the initial, tination inhibition antibodies also can help flu-like symptoms are replaced 4-5 days reach a diagnosis and for surveys. The
later with signs of encephalitis. People
presence ofigM antibody in cattle and
become infected through the bite of
sheep serun1, detected by the hemagglutiinfected ticks or through contact with nation inhibition test, provides good
infected carcasses, sharp instruments,
evidence that the animal was infected
or aerosol. Only a few cases of natural
within the preceding 10 days.

transmission have been reported, most
occuning in laboratory workers. Those

Treatment and Control: No specific
engaged in the diagnosis or research of this
treatment is available, but nursing,
virus should be vaccinated with a human
hand-feeding, and sedation may be helpful.

vaccine against tickbome encephalitis

An inactivated, tissue culture-propagated
virus. Because goats can excrete high titers
vaccine is available and has successfully
of virus in their milk, goats kept for milk
protected sheep, cattle, and goats. A single
production in endemic areas must be
injection induces an antibody response that
vaccinated.

PSEUDORABIES

(Aujeszky disease, Mad itch)

Pseudorabies is an acut�, frequently fatal
rodents. Experimental studies in nonhuman
disease with a worldwide distribution that
primates indicate that rhesus monkeys and
affects swine primarily and other domestic
marmosets are susceptible but chimpanzees
and wild animals incidentally. The
are not. Reports of human infection are
pseudorabies virus has emerged as a
limited and are based on seroconversion
significant pathogen in the USA since the
rather than vims isolation. Infections in

1960s, probably because of the increase in
horses are rare. Only one serotype of
confinement swine housing or perhaps
pseudorabies virus is recognized, but strain
because of the emergence of more virulent
differences have been identified using
strains. Clinical signs in nonporcine animals
monoclonal antibody preparations,
are similar to those of rabies, hence the
restriction endonuclease assays, and heat
nan1e "mad itch" (pigs do not display this and trypsin inactivation markers.

sign). Pseudorabies is a reportable disease
and has been successfully eradicated from

Epidemiology: The vims can be transmitthe vast majority of the USA.

ted via nose-to-nose or fecal-oral contact.

Indirect transmission commonly occurs via

Etiology: Pseudorabies virus is a DNA
inhalation of aerosolized vims. Infectious
herpesvirus. The pig is the only reservoir
virus can persist for up to 7 hr in air with
host, but the virus can infect cattle, sheep,
a relative humidity of 2'55%. Data from
cats, dogs, and goats as well as wildlife,

England indicate that virus may travel via
including raccoons, opossums, sk1mks, and
aerosols for up to 2 km in certain weather

PSEUDORABIES

1301
conditions. Other studies have demonvirus is harbored in the trigeminal ganglia, strated that the virus can survive for up to 7
may exist. ln swine with latent infections,
hr in nonchlorinated well water; for 2 days
shedding may resume after periods of stress
in anaerobic lagoon effluent and in green
such as farrowing, crowding, or transpo1t.

grass, soil, feces, and shelled com; for 3

Experimentally, corticosteroid i.r\jections

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days in nasal washings on plastic and

( dexa.methasone, 2 mg/kg, IM) for 5
pelleted hog feed; and for 4 days in straw
consecutive days have induced recrudesbedding. The virus is enveloped and, cence.

therefore, inactivated by drying, sunlight,
and high temperatures (<!37°C [98.6°F]).

Lesions: Gross lesions of pseudorabies

Dead-end hosts, such as dogs, cats, or
virus infection are often undetectable.

wildlife, can transmit the virus between

Serous rhinitis, necrotic tonsillitis, or hemorfarms, but these animals survive only 2-3
rhagic pulmonary lymph nodes may be seen.

days after becoming infected. The potential

Pulmonary edema, as well as pneun1onic
role of insects as vectors is being investilesions of secondary bacterial pathogens, gated. Birds do not seem to play a role in
may be present. Necrotic foci (2-3 nun in
transmission.

diameter) may be scattered throughout the
liver. Such lesions are typically found in

Clinical Findings and Pathogenesis:

young ( <7 days old) piglets.

The clinical signs in pigs depend on the age

Microscopically, nonsuppurative
of the affected anin1al. Young swine are
meningoencephalitis is a characteristic
highly susceptible, and losses may reach
lesion that can be present in gray and white
lQ()OA, in piglets <7 days old. ln general, signs matter. Mononuclear perivascular cuffing
of CNS disease ( eg, tremors and paddling)

and neuronal necrosis may also be present.

are seen. If weaned pigs are infected,

The meninges are tl1ickenecl as a result of
respiratory disease is the prin1ary clinical
mononuclear cell infiltration. Necrotic tonproblem, especially if complicated by sillitis with the presence of intranuclear
secondary bacterial pathogens. Pseudorainclusion bodies, as well as necrotic bies virus has been reported to inhibit the
bronchitis, bronchiolitis, and alveoli tis, are
function of alveolar macrophages, thereby
conunonly seen. Focal areas of necrosis are
reducing the ability of these cells to process
often found in the liver, spleen, lymph
and destroy bacteria. A generalized febrile
nodes, and adrenal glands of macerated
response ( 41 ° -42°C [ 105.8° -107.6°F]),
fetuses.

anorexia, and weight loss are seen in
infected pigs of all ages. Mortality can be

Diagnosis: ln addition to the gross and
very low ( l o/o-2%) in grower and finisher
microscopic lesions, other diagnostic aids
pigs but may reach 5()0A, in nursery pigs.

include virus isolation, fluorescent antibody

Sneezing and dyspnea are frequently seen,
testing, and serologic testing. Brain, spleen,
and CNS involvement is reported occasionand lung are the organs of choice for virus ally. Clinical signs in nonporcine species,
isolation. Nasal swabs can be used for
such as cats, dogs, cattle, and small
isolation of virus from acutely infected

1wninants, include sudden death, intense
anin1als. The nasal specin1ens must be
local pruritus, CNS signs ( circling, maniacal
stored and transported in cold, sterile saline
behavior, paralysis), fever, and respiratory
with antibiotics to suppress bacterial
distress.

growth. The fluorescent antibody test can

After natural infection, the primary site
be performed using tonsil or brain.

of viral replication is nasal, pharyngeal, or

Many serologic tests are now available,
tonsillar epithelium. The virus spreads via
including se1wn neutralization, ELISA, and
the lymphatics to regional lymph nodes,
latex agglutination. Se1w11 neutralization,
where replication continues. Virus also
which is the standard test, requires 48 hr to
spreads via nervous tissue to the brain,
complete. An ELISA has been developed as
where it replicates, preferentially in
a screening assay for large volumes of sera;
neurons of the pons and medulla. In
however, specificity may be poor. Falseaddition, virus has been isolated from positive results are typically reassessed
alveolar macrophages, bronchial epitheusing the serum neutralization test. The lium, spleen, lymph nodes, trophoblasts,
latex agglutination test, although highly
embryos, and luteal cells.

sensitive and rapid, may also have poor

Viral excretion begins -2-5 days after
specificity. After infection, antibodies can
infection, and virus can be recovered from
be detected within 6-7 days using the latex
nasal secretions, tonsillar epithelium,
agglutination test, witllin 7-8 days using the
vaginal and preputial secretions, milk, or

ELISA, and within 8-10 days using the
urine for >2 wk. A latent state, in which
serum neutralization test.

1302

PSEUDORABIES

A differential ELISA has been used to
via feed and IM injection is recommended
differentiate antibodies produced as a result to control secondary bacterial pathogens.

of vaccination from those produced as a

Numerous programs have been
result of natural infection. The vaccines
developed for eradication of pseudorabies
used in swine are based on the deletion
virus. As of 2014, all 50 states in the USA are

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of certain genes (gI, gIII, or gX) from the
considered free of the disease in corrm1ervaccine virus. Swine vaccinated with a genecial pigs; however, the virus appears to be deleted vaccine do not mount an antibody
endemic in feral pig populations and has
response to the protein coded for by the
been identified on game ranches. Effective
deleted gene. In contrast, infection with
strategies for eradication of pseudorabies
field virus results in antibodies against these include whole-herd depopulation, a test and proteins.

removal strategy, and offspring segregation.

Colostral antibodies to pseudorabies

Although effective, whole-herd depopulavirus may be present until pigs are 4 mo old tion is costly and time consuming. Usually,

(similar to porcine paivovirus). Therefore,
problems other than pseudorabies virus ( eg,
paired samples or serologic profiles may be
genetic improvement) need to be resolved
necessary in grower and finisher pigs to
before whole-herd depopulation can be cost
assess decreasing levels of maternal
effective.

antibody and to ensure that pigs are

The test and removal strategy consists of
vaccinated at the appropriate time.

blood testing all breeding swine, culling all
positive animals, and repeating this

Treatment and Control: Although there
procedure until the population tests
is no specific treatment for acute infection
negative. Naturally infected animals can
with pseudorabies virus, vaccination can
be culled when such a strategy is used in
alleviate clinical signs in pigs of certain
conjunction with a differential vaccination
ages. Typically, mass vaccination of all pigs
program. A test and removal strategy can be
on the farm with a modified-live virus
effective, but it is laborious, and latently
vaccine is recommended. Intranasal
infected anin1als tliat do not exhibit an
vaccination of sows and neonatal piglets
antibody response on serologic testing may

1-7 days old, followed by IM vaccination
potentially resume shedding the virus at a
of all other swine on the premises, helps
later time.

reduce viral shedding and in1prove survival.

In an offspring segregation program,

The modified-live virus replicates at the site
young piglets (18--21 days old) are removed
of injection and in regional lymph nodes.

from vaccinated sows and raised to

Vaccine virus is shed in such low levels that
adulthood at another site. If enough gilts
mucous transmission to other animals is
and boars are raised in this manner, the
minimal. In gene-deleted vaccines, the
original breeding herd may be depopulated
thymidine kinase gene has also been
and subsequently repopulated with
deleted; thus, the virus cannot infect and
seronegative replacements. This method
replicate in neurons. It is recommended that
also allows seedstock producers to sell
breeding herds be vaccinated quarterly and
anin1als, even though the breeding herd is
that finisher pigs be vaccinated after levels
infected. In this case, however, all offspring
of maternal antibody decrease. Regular
must be individually tested using the serun1
vaccination results in excellent control of
neutralization test and have negative results
the disease. Concurrent antibiotic therapy
before being sold.

RABIES

Rabies is an acute, progressive viral
either successful elimination progran1s
encephalomyelitis that p1incipally affects
or their island status and enforcement of
carnivores and bats, although any mammal

1igorous quarantine regulations. Globally,
can be affected. The disease is fatal once
the dog is the most important reservoir,
clinical signs appear. Rabies is found
particularly in developing countries.

throughout the world, but a few countries

Integrated veterinary management of local
claim to be free of the disease because of
ailimal populations, by mass vaccination of

RABIES

1303
dogs and community promotion of
years, skunks were the most commonly
responsible pet ownership, is the most
reported rabid animal in the USA, but since
cost-effective, hwnane, long-term solution

1990, rabid raccoons have been the most
toward eliminating regional canine rabies
nwnerous. Canine rabies becan1e estabin a One Health context.

lished in dogs and coyotes ( Canis latrans)

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in southern Texas but was eliminated by the

Etiology and Epidemiology: Rabies is
end of the 20th century. Canine rabies exists
caused by lyssaviruses in the Rhabdovirus
in Mexico, with the potential to spread
family. Lyssaviruses are usually confined
throughout the USA if reintroduced. Skunk,
to one major reservoir species in a given
raccoon, and fox rabies are ea.ch found in
geographic area, although spillover to other
fairly distinct geographic regions of North
species is common. Identification of

America, although some overlap occurs.

different virus variants by laboratory

Bat rabies is distributed throughout the
procedures such as monoclonal antibody

Americas. The vampire bat is an important
analysis or genetic sequencing has greatly
reservoir in Latin An1erica and is the source
enhanced understanding of rabies
of multiple outbreaks in cattle, as well as in
epidemiology. Generally, each virus variant
people, particularly in parts of Amazonia.

is responsible for virus transmission

In western Europe, red fox rabies
between members of the same species in a
predominated before its elimination by oral
given geographic area. To date, > 15 different vaccination. In parts of eastern Europe, lyssaviruses have been described. Globally,
rabies in raccoon dogs is of increasing
rabies virus is the most important member
concern. Bat rabies, maintained by several
of the genus.

different lyssaviruses in insectivorous

From an epidemiologic perspective, the

Chiroptera, appears to be widely dist1ibuted
name of the mammalian species acting as
throughout Europe.

the reservoir and vector is used as an

Other wildlife play an important role in
adjective to describe involvement in the
the transmission of rabies in certain areas,
infection process. For exan1ple, rabies
including different species of mongooses in
maintained by dog-to-dog transmission is
the Caribbean, southern Africa, and parts of
tern1ed canine rabies, whereas rabies in a

Asia; jackals in parts of Africa; wolves in
dog as a result of infection with a variant
parts of northern Europe; marmosets in
from a different reservoir mammal, eg,

Brazil; and ferret badgers in China.

skunk ( or raccoon or fox), would be

All rabies reservoirs are also vectors of
referred to as skunk ( or raccoon or fox,
the virus, but not all vectors are reservoirs.

etc) rabies in a dog.

For example, cats can effectively transmit

In North America, distinct virus variants
the virus, but no cat-to-cat transmission of
are responsible for rabies perpetuation in
rabies perpetuates in lieu of a predominant
red and Arctic foxes in Canada and Alaska,
reservoir (such as infected dogs), and no
raccoons along the eastern sea.board from
unique feline rabies virus variant has been

Maine to Florida, and gray foxes in the
documented. However, cats are the most
southwest, including Arizona, Colorado,
commonly reported rabid domestic aninlal
and Texas. Two different variants are
in the USA. Virus is present in the saliva of
responsible for rabies in striped skunks, one rabid ca.ts, and people have developed in the south central states and the other in
rabies after being bitten by rabid ca.ts.

the north central states, which often

Reported cases in domestic cats have
extends into the Canadian prairies. Another
outnwnbered those in dogs in the USA
skunk rabies virus variant is found in
every year since 1990.

California. By comparison, the epidemiology of rabies in bats is complex. In general, Transmission and Pathogenesis: Lysea.ch variant found in bats may be charactersaviruses are highly neurotropic. Transmisized with a predominant bat species.

sion almost always occurs via introduction

Spillover from bats to terrestrial animals is
of virus-laden saliva into tissues, usually by
seen infrequently. Most hwnan cases of
the bite of a rabid animal. Although much
rabies in the USA in the past decade have
less likely, virus from saliva, salivary glands,
been ca.used by bat rabies virus variants
or brain can ca.use infection by entering the

( especially viruses associated with
body through fresh wounds or intact

Lasionycteris noctivagans, the silvermucous membranes. Usua.lly, saliva is haired bat, andPerimyotis subfiavus, the
infectious at the time clinical signs occur,
tricolored bat).

but domestic dogs, cats, and ferrets may

Rabies emergence may be affected by
shed virus for several days before onset of
changes in virus-host dynan1ics or human
clinical signs. Viral shedding in skunks has
transloca.tion of infected species. For many
been reported for up to 8 days before onset

1304

RABIES
of signs. Rabies virus has not been isolated
wild animals may lose tl1eir fear of people,
from skunk musk (spray).

and nom1ally nocturnal species may be seen

The incubation period is both prolonged
wandering about during the daytinle.

and variable. Typically, the virus remains at

The clinical course may be divided into
the inoculation site for a considerable time.

tlrree general phases-prodromal, acute

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The unusual length of the incubation period
excitative, and paralytic/endstage.

helps to explain the effective action of local

However, this division is of limited practical
infiltration of rabies immune globulin during
value because of the variability of signs and
hun1an postexposw-e prophylaxis, even clays the irregular lengths of the phases. During after exposw-e. Most rabies cases in dogs
the prodromal period, which lasts -1-3
develop within 21--SO days after exposure,
days, aninlals show only vague nonspecific
but the incubation pe1iod may be shorter or
signs, which intensify rapidly. The disease
considerably longer. One recorded case of
progresses rapidly after the onset of
rabies in a person in the USA had an
paralysis, and death is virtually certain a few
incubation period estinlated reliably of >8 yr.

days thereafter. Some animals die rapidly

The virus travels via the peripheral nerves
without marked clinical signs.

to the spinal cord and ascends to the brain.

The term "fwious rabies" refers to

After reaching the brain, the virus travels via
animals in which aggression (the acute
pe1ipheral ne1ves to the salivary glands. If an
neural excitative phase) is pronounced.

aninlal is capable of transmitting rabies via

"Dumb or paralytic rabies" refers to animals its saliva, virus will be detectable in the brain. in which the behavioral changes are Virus is shed intennittently in the saliva.

minimal, and the disease is .manifest

Hematogenous spread does not occw-.

principally by paralysis.

Under most circumstances, there is no
danger of aerosol transmission of rabies

Furious Form: This is the classic
virus. However, aerosol trans1nission has

"mad-dog syndrome," although it may be
occw-red under very specialized conditions
seen in all species. There is rarely evidence
in which the air contained a high concentraof paralysis during this stage. The aninlal tion of suspended particles or droplets
becomes irritable and, with the slightest
carrying viral particles. Such conditions
provocation, may viciously and aggressively
have been responsible for laboratory
use its teeth, claws, horns, or hooves. The
transmission under less than ideal
posture and expression is one of alertness
containment situations. There has been a
and anxiety, with pupils dilated. Noise may
suggestion of rare natural aerosol transmisinvite attack Such animals lose caution and sion in a cave inhabited by millions of bats.

fear of people and other anin1als. Carnivores

Oral and nasal secretions containing virus
with this form of rabies frequently roam
were probably aerosolized from tens of
extensively, attacking other aninlals,
thousands of rabid bats. Aerosol infection
including people, and any moving object.

may occur via direct attachment of the virus

They commonly swallow foreign objects,
to olfactory nerve endings.

eg, feces, straw, sticks, and stones. Rabid

Near the end of the clinical phase, after
dogs may chew the wire and frame of their
replication in the CNS, virus inay be found
cages, breaking their teeth, and will follow a
in nearly every inne1vated organ. Rabies has hand moved in front of the cage, attempting been transmitted by transplantation of
to bite. Young pups can seek human
tissues and organs from infected people.

companionship and are overly playful, but
bite even when petted, usually becoming

Clinical Findings: Clinical signs of rabies
vicious in a few hours. Rabid skunks may
are rarely definitive. Rabid animals of all
seek out and attack litters of puppies or
species usually exhibit typical signs of CNS
kittens. Rabid domestic cats and bobcats
disturbance, with minor variations among
can attack suddenly, biting and scratching
species. The most reliable signs, regardless
viciously. As the disease progresses,
of species, are acute behavioral changes
muscular incoordination and seizures are
and unexplained progressive paralysis.

common. Death results from progressive

Behavioral changes may include sudden
paralysis.

anorexia, signs of apprehension or

Paralytic Form: This is manifest by
nervousness, irritability, and hyperexcitabilataxia and paralysis of the tlrroat and ity (including priapism). The aninlal may
masseter muscles, often with profuse
seek solitude. Ataxia, altered phonation,
salivation and the inability to swallow.

and changes in temperan1ent are apparent.

Dropping of the lower jaw is common in

Uncharacteristic aggressiveness may
dogs. Owners frequently examine the mouth
develop-a nonnally docile anin1al may
of dogs and livestock searching for a foreign
suddenly become vicious. Commonly, rabid
body or administer medication with their

RABIES

1305
bare hands, thereby exposing themselves to
indicated. Suspect animals should be
rabies. These animals may not be vicious
euthanized, and tile head removed for
and rarely attempt to bite. The paralysis
laborat01y shipment.

progresses rapidly to all parts of the body,

Rabies diagnosis should be done by a
and coma and death follow in a few hours.

qualified laborato1y, designated by the local

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Species Variations: Cattle with furious
or state health department in accordance
rabies can be dangerous, attacking and
with established standardized national
pursuing people and other animals.

protocols for rabies testing. Inununofluores

Lactation ceases abruptly in dairy cattle.

cence microscopy on fresh brain tissue

The usual placid expression is replaced by
which allows direct visual obse1vation �f a
one of alertness. The eyes and ears follow
specific antigen-antibody reaction, is the
sounds and movement. A common clinical
current test of choice. When properly used
sign is a characteristic abnormal bellowing,
it can establish a highly specific diagnosis '

which may continue intermittently until
withm a few hours. Brain tissues examined
shortly before death.

must include medulla oblongata and

Horses and mules frequently show
cerebellum (and should be preserved by
evidence of distress and extreme agitation.

refrigeration with wet ice or cold packs).

These signs, especially when accompanied

Virus 1solat1on by the mouse inoculation
by rolling, may be interpreted as evidence of
test or tissue culture techniques using
colic. As in other species, horses may bite or mouse neuroblastoma cells may be used for strike viciously and, because of their size
confirmation of indetern1inate fluorescent
and strength, become unmanageable in a
antibody results, but it is no longer in
few hours. People have been killed outright
conm1on use in tile USA.

by such animals. These anin1als frequently
have self-inflicted wounds.

Prevention and Control: Comprehen

Rabid foxes and coyotes often invade
sive guidelines for control in dogs have been
yards or even houses, attacking dogs and
prepared internationally by the World
people. One abnormal behavior that can

Healtl1 Organization and in the USA by the
occur is demonstrated by an animal that

National Association of State Public Health
attacks a porcupine; finding a fox, or

Veterinarians (NASPHV). They include the
another animal, with porcupine quills can,
following: 1) notification of suspected
m many cases, support a diagnosis of rabies.

cases, and eutllanasia of dogs witll clinical

Rabid raccoons, foxes, and skunks
signs and dogs bitten by a suspected rabid
typically show no fear of people and are
animal; 2) reduction of contact rates
ataxic, frequently aggressive, and active
between susceptible dogs by leash laws,
during the day, despite their often crepuscudog movement control, and quarantine; 3) lar nature. In urban areas, they may attack
mass immunization of dogs by campaigns
domestic pets.

and by contmumg vaccmation of young

In general, rabies should be suspected in
dogs; 4) stray dog control and euthanasia
terrestrial wildlife acting abnormally. The
of unvaccinated dogs witl1 low levels of
same is true of bats that can be seen flying
dependency on, or restriction by, people;
in the daytime, resting on the dround
and 5) dog registration.

paralyzed and unable to fly, attacking

The Compendiwn of Animal Rabies
people or other animals, or fighting.

Control, compiled and updated regularly by

Rodents and lagomorphs rarely
the NASPHV, swnmarizes tile most current
constitute a risk of exposure to rabies virus.

reconunendations for the USA and lists all

However, each incident should be evaluated USDA-licensed animal rabies vaccines individually. Reports of laboratory-conmarketed in the USA. Many effective firmed rabies in woodchucks are not
vaccines, such as modified-live virus
uncommon in association with the raccoon
recombinant, and inactivated types, �e
rabies epizootic in the eastern USA.

available for use throughout the world; in
the USA, no modified-live rabies virus
vaccines are currently marketed (for any

Diagnosis: Clinical diagnosis is diffi-
species). Reconu11ended vaccination
cult, especially in areas where rabies is
frequency is every 3 yr, after an initial series
uncommon, and should not be relied on
of two vaccines 1 yr apart. Several vaccines
when making public health decisions. In the
ai·e also available for use in cats, and a few
early stages, rabies can easily be confused
for use in ferrets, horses, cattle, and sheep.

with other diseases or with normal

Because of tile increasing in1portance of
aggressive tendencies. Therefore when
rabies in cats, vaccination of cats is critical.

rabies is suspected and definitive'dia!!nosis

No pai·enteral vaccine is approved for use in
is required, laboratory confinnation i�
wildlife. Protective immunity from tl1e

1306

RABIES
commercially available vaccines for
bats, though small, can inflict wounds with
domestic species has not been definitively
their teeth and should never be caught or
demonstrated in wildlife species.

handled with bare hands. Bat bites may be

Until recently, the control of rabies in
ignored or go unnoticed, so direct contact
wildlife populations relied on population
with bats could be considered a risk of virus
reduction of wildlife in an attempt to reduce exposure. Any wild carnivore or bat VetBooks.ir
the contact rate between susceptible
suspected of exposing a person to rabies
animals; however, this proved difficult and
should be considered rabid unless proved
often not publicly acceptable, ecologically
otherwise by laboratory diagnosis; ideally,
sound, economically wananted, or prograrnthis includes bats in direct contact with matically effective. In Europe and Canada,
people, such as those found in rooms with
use of oral vaccines distributed in baits to
sleeping or otherwise tmaware persons.

control fox rabies has been widespread and

Wildlife, including wolf hybrids, should
effective. The disease in foxes has been
never be kept as pets; if one of those
elin1inated from most of western Europe
animals exposes a person or domestic
and curtailed significantly in Ontario. Use
animal, the wild animal should be managed
of a vaccinia-rabies glycoprotein recombilike free-ranging wildlife.

nant virus vaccine in the USA has success

Any healthy domestic dog, cat, or ferret,
fully eliminated coyote rabies in southern
whether vaccinated against rabies or not,

Texas and has lin1ited the western
that exposes (bites or deposits saliva in a
expansion of raccoon rabies from the
fresh wound or on a mucous membrane) a
eastern USA. The license limits use of the
person should be confmed for 10 days; if the
vaccine to state or federal rabies programs;
aninlal develops any signs of rabies during
it is not available to private veterinarians or
that period, it should be euthanized and
for individual animal use. Together with
its brain promptly submitted for rabies
other vaccines, it is also being used to assist
diagnosis. If the dog, cat, or ferret responsiin the control of dog rabies in developing ble for the exposure is stray or unwanted, it
countries.

may be euthanized as soon as possible and
submitted for rabies diagnosis. Since the

Management of Suspected Rabies
advent of testing by iJ1U11unofluorescence

Cases-Exposure of Pets: Where terresmicroscopy, there is no value in holding trial wildlife or bat rabies is known to occur,
such animals to "let the disease progress"

any animal bitten or otherwise exposed by a
as an aid to diagnosis.

wild, carnivorous mammal ( or a bat) not

Internationally, the World Health
available for testing should be regarded as

Organization reconm1ends several types
having been exposed to rabies. The NASPHV
of cell-culture vaccines for human groups
recommends that any unvaccinated dog, cat,
at 1isk. In the USA, guidelines for human
or ferret exposed to rabies be euthanized
rabies prevention follow recommendations
inlrnediately. If the owner is unwilling to do
prepared by the Advisory Council on
this, the animal should be placed in strict

In1.111unization Practices. Preexposure
isolation (ie, no human or animal contact)

iI1m1unization is strongly recon1.111ended
for 6 mo and vaccinated against rabies 1 mo
for people in high-risk groups, such as
before release. If an exposed domestic
veterinary staff, animal control officers,
aninlal is currently vaccinated, it should
rabies and diagnostic laboratory workers,
be revaccinated in1mediately and closely
and, under certain.circumstances, some
observed for 45 days.

travelers working in countries in which
canine rabies is enzootic. Preexposure

Zoonotic Risk: Rabies has the highest
vaccine is administered on days 0, 7, and 21
case fatality of any infectious disease. When
or 28. However, preexposure prophylaxis
a person is exposed to an animal suspected
alone carmot be relied on in the event of
of having rabies, the risk of rabies virus
subsequent rabies virus exposure and must
transmission should be evaluated carefully.

be supplemented by a limited postexposure

Risk assessment should include consideraregimen (two doses of vaccine, IM, on days tion of the species of animal involved, the

O and 3). For healthy, unvaccinated patients
prevalence of rabies in the area, whether
bitten by a rabid aniinal, postexposure
exposure sufficient to transmit rabies virus
prophylaxis consists of wound care, local
occurred, and the current status of the
infiltration of rabies inm1une globulin, and
animal and its availability for diagnostic
vaccine administration on days 0, 3, 7,
testing. Wild carnivores and bats present
and 14. When provided in a timely and
a considerable risk where the disease is
appropriate marmer, modem postexposure
found, regardless of whether abnormal
prophylaxis virtually assures hun1an
behavior has been observed. Insectivorous
survival.

TESCHOVIRUS ENCEPHALOMYELITIS

1307

TESCHOVI RUS ENCEPHALOMYELITIS

(Porcine polioencephalomyelitis, Teschen disease, Talfan disease) VetBooks.ir

Teschovirus encephalomyelitis (formerly
elsewhere. Conventional herds are usually

!mown as porcine enterovi.ral encephalomyendemically infected, and exclusion of elitis) is analogous to human poliomyelitis.

teschoviruses from SPF herds is difficult to

Severe disease is now rare; it is seen in
maintain. Wection is mainly inapparent,
eastern Europe and Madagascar but was
and pigs usually become infected at
last reported in western Europe from
weaning with the decline of passive

Austria in 1980. In other countries, sporadic
maternal immunity and mixing of groups.

mild disease is reported, or the disease is

Sporadic clinical cases of nervous disease
unrecognized.

are seen mainly around this time, although
disease is more conunon in unweaned

Etiology, Epidemiology, and Patho
piglets after introduction of a serotype
genesis: Until 1999, viruses causing this
to which the herd has not been exposed.

disease were classified within the genus

Ingested vims replicates in the GI tract

Enterovirus (family Picornaviridae).

and associated lymphoid tissue. There is no

However, analyses of their complete
destruction of gut epithelium, but virus is
genome sequences revealed them to be very
shed from multiplication sites into the feces
different from the enteroviruses, and they
for several weeks. In some pigs, especially
were reclassified in a new genus, Teschovi
those infected with virulent strains, virernia
rus, as the species Porcine teschovirus (the ensues and results in spread of infection to name was derived from Teschen disease). In the CNS.

2015, the species was renamed to Teschovirus A to remove reference to the host Clinical Findings: In acute virulent
species; however, the virus common name
infection, clinical signs appear 1-4 wk after
remains porcine teschovirus (PTV).

exposure in pigs of all ages. Ataxia is often

Originally, 11 porcine enterovirus (PEV)

seen first, followed by fever, lassitude, and
serotypes were defined by virus neutralizaanorexia. Seizures, nystagmus, opisthototion. Of these, PEV 1-7 and 11-13 have been nos, and coma may occur. Paralysis, initially
renamed PTV 1-10. Additional serotypes
evident as paraplegia but progressing to

(PTV 11-13) have also recently been
quadriplegia, is frequent in severe cases.

described, and it is likely more serotypes

Death is common within 3-4 days of onset
will be discovered in the future. PEV-8 has
of signs.

been reclassified as a member of a new

In mild disease, signs are essentially
picornavirus genus, Sapelovirus. PEV types
ataxia and paresis, the latter more rarely

9 and 10, which have not been associated
progressing to paralysis. Only young pigs
with neurologic disease, are distinct from

( unweaned or weaned) are susceptible, and
the teschoviruses and remain in the
recovery is frequent.

Enterovirus genus. PTVs are ubiquitous in

Lesions: There are no gross lesions.

swine populations throughout the world.

Microscopic changes are most prominent in

Many strains are nonpathogenic, but most
the gray matter of the brain stem, cerebelneurotropic strains belong to one of the first lum, and spinal cord. The nonsuppurative
three serotypes; serotype 1 includes not
encephalitis is characterized by neuronal
only the highly virulent but also many of the
necrosis, neuronophagia, glial foci, and
less virulent neurotropic strains. Although
perivascular lyrnphocytic cuffing. Meningiantigenic subtypes are recognized, they tis is often present over the cerebellum.

do not distinguish between more or less
virulent strains of virus. PTV can survive

Diagnosis: The clinical signs ( especially
in the envirorm1ent for months.

those of locomotor disturbance), epidemiol

Transmission is by direct or indirect
ogy, and absence of specific gross necropsy
contact with infected pigs. The virulent
findings offer a presumptive diagnosis. The
serotype 1 strain of classical Teschen
nature and distribution of histologic lesions
disease results in high morbidity and
provide supportive evidence. Acute and
mortality in all ages of pigs but apparently
convalescent serum samples, taken �2 wk
has remained confined to certain geoapart, may demonstrate a rise in neutralizgraphic areas. Mild, sporadic disease is seen ing or complement-fixing antibodies. Virus

1308

TESCHOVIRUS ENCEPHALOMYELITIS
isolation from the CNS is required to
the PTV serotypes, and molecular diagnosis
confirm the diagnosis. Differentiation of
by reverse transc1iptase-PCR (RT-PCR) and
severe and milder forms of the disease can
real-time RT-PCR has been described.

be based only on serologic, clinical, and
epidemiologic evidence.

Treatment and Control: There is no

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Differential diagnoses include the many
treatment. Live attenuated vaccine is used
other viral encephalitides of pigs, particufor control in areas expe1iencing severe larly classical swine fever, African swine
endemic disease. In the past, eradication
fever, pseudorabies, rabies, and the
measures in central Europe involved ring
encephalopathies of edema disease and
vaccination and slaughter and also
water dep1ivation/salt intoxication. The
restrictions on importation of pigs and pork
prominent locomotor signs in teschovirus
products. In many countries, suspected
encephalomyelitis also can be confused with disease must be reported to regulato1y several toxic and nutritional neuropathies.

authorities. In herds with endemic mild

The different serotypes are identified
clinical disease, introduction of new
either by virus neutralization, complement
breeding stock �1 mo before breeding
fixation, or ELISA using specific antisera.

should enhance passive immunity in

Genome sequence data is available for all
offspring.

SPORADIC BOVINE ENCEPHALOMYELITIS

(Chlamydia! encephalomyelitis, Buss disease, Transmissible serositis) Sporadic bovine encephalomyelitis (SEE) is
diarrhea, anorexia, and weight loss occur.

reported in various parts of the world. The

Nasal discharge and respiratory disease
disease affects cattle and buffalo, resulting
signs due to pleuritis may be seen. Early
in neurologic signs and polyserositis.

neurologic signs include stiffness and
knuckling at the fetlocks. Calves become

Etiology and Epidemiology: SEE
uncoordinated and stagger, circle, or fall
is caused by Chlamydia pecorum biotype
over objects. Head pressing and blindness

2. Genetically identical C pecorum isolates are not seen. In tl1e terminal stage, calves
have been identified from clinical cases
are frequently recumbent and may develop
in geographically different areas. The
opisthotonos. The course of the disease is

C pecorum isolates from clinical cases are
usually l 0-14 days.

distinct from tl1ose found in tl1e GI tract

Lesions: Lesions are not linlited to the
of asymptomatic animals. Based on these
brain; vascular damage can be seen in
findings, subclinical intestinal infections
several organs. Serofibrinous peritonitis,
in cattle and other animals may not be the
pleuritis, and pericarditis are common and
source of infection in SEE. The disease is
a.re especially pronounced in more chronic
most often seen in calves <6 mo old and less
cases. Microscopic lesions in the brain
commonly in older cattle. Sporadic cases
consist of perivascular cuffs and inflammaand outbreaks can occur within individual tory foci in the parenchyma composed
herds. Morbidity rates are most commonly
primatily of mononuclear cells.

<25%, but can reach 500/o. The mortality rate
can approach 300/o and is highest in calves.

Diagnosis: A tentative diagnosis can be

Many sick animals die if not treated at an
based on clinical signs and particularly on
early stage.

the presence of serofibrinous peritonitis
in the absence of other causes of

Clinical Findings: The incubation pe1iod
peritonitis such as intestinal volvulus,
in experimentally infected calves is 6--30
intussusception, traumatic perforation of
clays. The first sign in natural and experithe reticulum, perforated abomasal ulcer, mental cases is fever (104°-107°F
or displaced organs. Differential

[ 40° -41. 7°C]). Appetite remains good
diagnoses also include rabies, infectious
for the first 2-3 days despite the fever.

bovine rhinotracheitis with encephalitis,

Afterward, depression, excess salivation,
listeriosis, thromboembolic encephalo-

EQUINE PROTOZOAL MYELOENCEPHALITIS

1309
myelitis, polioencephalomalacia,
after Giemsa or immunofluorescent
pseudorabies, paramyxovirus encephalostaining.

myelitis, and malignant catarrhal fever.

SBE can be diagnosed by PCR detection

Treatment: The antibiotics of choice are
of C pecoriim DNA in brain tissue, pleural
tetracyclines, oxytetracyclines, and tylosin.

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fluid, pericardia! fluid, or peritoneal fluid

For treatment to be effective, it must be
of affected animals. Diagnosis can also be
given as early as possible in high doses ( eg,
confirmed by culture in either developing
oxytetracyclines at 10-20 mg/kg/day) and
chicken embryos or cell cultures, by
for ::Cl wk If treatment is effective, the fever
histologic changes in brain sections, or by
should drop significantly within 24 hr. No
evaluation of tissue impression smears
vaccines are available.

EQUINE PROTOZOAL

MYELOENCEPHALITIS

Equine protozoa] myeloencephalitis (EPM)

neurologic sign is possible. The disease
is a common neurologic disease of horses
usually begins insidiously but may present
in the Americas; it has been reported in
acutely and be severe at onset. Signs of
most of the contiguous 48 states of the
spinal cord involvement are more common

USA, southern Canada, Mexico, and several
than signs of brain disease. Horses with
countries in Central and South America. ln

EPM involving the spinal cord have
other countries, EPM is seen sporadically in
asymmetric or symmetric weakness and
horses that previously have spent time in the
ataxia of one to all limbs, sometimes with

Americas.

obvious muscle atrophy. When the
sacrocaudal spinal cord is involved, there

Etiology and Epidemiology: Most cases are signs of cauda equina syndrome. EPM
of EPM are caused by an Apicomplexan
lesions in the spinal cord also may result in
protozoan, Sarcocystis neurona. Horses
demarcated areas of spontaneous sweating
are infected by ingestion of S neurona
or loss of reflexes and cutaneous sensation.

sporocysts in contaminated feed or water.

The most common signs of brain disease in

The organism undergoes early asexual
horses with EPM are depression, head tilt,
multiplication (schizogony) in extraneural
and facial paralysis. Any cranial nerve
tissues before parasitizing the CNS. Because
nucleus may be involved, and the're may be
infectious sarcocysts are only rarely fmmed,
seizures, visual deficits including abnormal
the horse is considered an aberrant, dead-end menace responses, or behavioral abnorhost for S neurona. Like other Sarcocystis malities. Without treatment, EPM may
spp, S neurona has an obligate predator-prey progress to cause recumbency and death.

life cycle. The definitive (predator) host for

S neurona

Progression to recumbency occurs over
in the USA is the oposstun
hours to years and may occur steadily or

(Didelphis virginiana). Oposstuns are
in a stop-start fashion.

infected by eating sarcocyst-containing
muscle tissue from an infected intermediate

Lesions: There is focal discoloration,

(prey) host and, after a brief prepatent period
hemorrhage, and/or malacia of CNS tissue.

(probably 2-4 wk), infectious sporocysts are

Histologically, protozoa may be found in
passed in the feces. Nine-banded armadillos,
association with a mixed inflammatory
striped skunks, raccoons, sea otters, Pacific
cellular response and neuronal destruction.

harbor seals, and domestic cats have all been

Schizonts, in various stages of maturation,
implicated as intermediate hosts; however,
or free merozoites conunonly are seen in
the importance in nature of each of these
the cytoplasm of neurons or mononuclear
species is unknown. Sporadic cases of EPM
phagocytes. Also parasitized are intravascuare associated with Neospora hughesi, an lar and tissue neutrophils and eosinophils
organism closely related to S neurona. The
and, more rarely, capillary endothelial cells
natural host( s) of this organism have not yet
and myelinated axons. Merozoites may be
been identified.

found extracellularly, especially in areas of
necrosis. ln at least 75% of clinical cases,

Clinical Findings: Because the protozoa
protozoa are not seen on H&E-stained
may infect any part of the CNS, almost any
sections.

1310

EQUINE PROTOZOAL MYELOENCEPHALITIS

Diagnosis: Postmortem diagnosis is
days). The bioavailabilities of ponazU1il and
confirmed by demonstration of protozoa
diclazuril are improved by concurrent PO
in CNS lesions on the basis of distinctive
administration of com oil or DMSO. A
morphology or by irrununohistochemical
loading dose of ponazuril ( 15 mg/kg, PO)

staining. Testing for S neurona-specific
may be given on the first day of treatment to

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antibody is tl1e basis for presuniptive
rapidly attain therapeutic blood levels. The
antemortem diagnosis ofEPM. Serologic
sulfadiazine/pyrin1etha.mine product must
tests for specific antibodies against whole S
be given at least 1 hr before or after hay is
neurona ( eg, indirect fluorescent antibody
fed. Anemia may develop after prolonged
test) or S neurona surface antigens (snSAGs) treatment with sulfadiazine/pyrimetl1amine provide evidence of cmTent or recent
and is best prevented by providing
exposure to tl1e organism; thus, low or
folate-1ich green forage such as alfalfa hay
negative sermn titers tend to exclude the
or green pasture. Approximately 600/o of
diagnosis ofEPM. Conversely, positive or
horses improve witl1 each type of treathigh serum S neurona titers have limited ment, but <25% recover completely.

diagnostic utility in that such titers do not

Relapses occur commonly up to 2 yr after
clearly distinguish horses with subclinical
discontinuation of antiprotozoal therapy.

extraneural infections from those with EPM.

Because immunosuppression/immuno

In horses with neurologic signs, senun:CSF
deficiency may be a risk factor for EPM,
antibody titer ratios of <l: 100 or C-ratios > 1
i.tnmU11omodulators (eg, mycobacterial
are indicative of production of S neuron,a cell-wall derivative, levamisole, killed
antibody in the CNS and are highly supportparapox ovis, or transfer factor) are ive of tl1e diagnosis of EPM. In a few horses
someti.tl1es given as ancillary therapy.

witl1 EPM, CSF analysis reveals abnormalities such as mononuclear pleocytosis and Prevention and Control: No proven
increased protein concentration.

preventive is available. A conditionally

Depending on the clinical signs,
approved vaccine was marketed, but the
differential diagnoses may include cervical
license lapsed in 2008 and it is no longer
ve1tebral stenotic myelopathy, traunia, aberoffered. There is i.tlterest in usi.tlg antirant parasite migration, equine degenerative protozoal drngs for prevention; however, myeloencephalopathy, equine herpesvims 1
evidence-based protocols are not yet
myeloencephalopathy, equine motor neuron available. The source of infective sporodisease, cauda equina neuritis, arbovi.ral cysts is opossun1 feces, so it is pmdent to

(Eastern or Western equine, West Nile)

prevent access of opossmns to horse-feedencephalomyelitis, rabies, bacte1ial ing areas. Horse and pet feed should not be
meningitis, hepatoencephalopathy, and
left out; open feed bags and garbage should
leukoencephal9malacia.

be kept in closed galvanized metal
containers, bird feeders should be

Treatment: The FDA-approved treateliminated, and fallen ftuit should be ments for EPM are ponazuril (5 mg/kg/day,
removed. Opossunis can be trapped and

PO, for 28 days), diclazuril (1 mg/kg/day,
relocated. Because putative intem1ediate

PO, for 28 days), and a combination of
hosts carmot be directly infective for horses,
sulfadiazine and pyrimetl1amine (20 mg/kg
it is unlikely that control of these populaand 1 mg/kg, respectively, for at least 90
tions will be useful in EPM prevention.

CNS DISEASES CAUSED BY

HELMINTHS AND ARTHROPODS

A nun1ber of metazoan parasites (helmintl1s
likely to enhance transmission to the
and arthropods) are associated with
definitive host by means of predation. For
pathology in tile CNS and may be categoexample, Taenia multiceps multiceps is rized as described below.

acquired by the canine definitive host when

Immature (Larval) Stages of Parasites
tl1e dog i.t1gests the infective larval stages of
of Carnivorous Animals: These developtile tapewom1 Coenunts cerebralis in the mental stages may induce behavioral
brain and spi.tlal cord of the ovine i.tltem1edichanges in the i.tlterrnediate host tl1at are ate host. In sheep, C cerebralis causes

CNS DISEASES CAUSED BY HELMINTHS AND ARTHROPODS

1311
ataxia, which allows the dog (a carnivore)

dogs, foxes, and jackals) and occasionally
to more easily prey upon the infected sheep.

people. Its intermediate hosts include

Immature Stages of Parasites
sheep, goats, deer, antelope, chan1ois,

Exhibiting a Neurotropic Affinity: These
rabbits, hares, horses, and less commonly
developmental stages require conditions·
cattle, which acquire this ta.pewonn's eggs

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provided by the host's CNS for their growth
while grazing. After ingestion, some
and development. For example, Hypo
oncospheres hatch and reach the bra.in,
derma bovis in cattle can migrate through
developing by endogenous budding into
the spinal cord and adjacent tissues to reach a metacestode (larval) stage known as its predilection site, the dorsum of the back.

Coenurus cerebralis. Initial invasion and
development of the oncospheres may be

Erratic or Aberrant Parasites: These
responsible for acute suppurative meninparasites are n01mally found in non-neurogoencephalitis. The fully developed logic, predilection sites within the definitive
coenwus may be 5-6 cm in diameter and
host but, on occasion, may wander erratically cause increased intracra.nial pressure, into some portion of the CNS. For example,
which results in ataxia, hypermetria.,
larvae of Cuterebra spp are nom1ally found
blindness, head deviation, stun1bling,
in subcutaneous sites in dogs or cats but may
and paralysis. This clinical condition is
also aberrantly wander into the CNS and
colloquially known as gid, sturdy, or
localize on the cerebrum or cerebellun1.

staggers. In sheep, palpation of the skull

Incidental Parasites: These parasites are
caudal to the horn buds may reveal
found in a different host than that in which
refraction; surgery to remove the cyst,
they nonnally are found. For example,
including its wall, has a reasonable chance

Parelaphostrongylus tenuis nonnally
of success and is justified in valuable
is found in neurologic sites within the
animals. Dogs associated with sheep and
definitive host, white-tailed deer, in which
other livestock should not be fed the bra.in
the parasite is nonpathogenic. However,
or spinal cord from infected anin1als and
in an incidental host, such as moose, elk,
should be dewonned regularly.

or Ila.ma, the parasite migrates through
portions of the CNS and produces an often

Cysticercosis: Taenia solium is a
fatal neurologic disease.

tapewo1m found in the small intestine of
people. Its metacestode (larval) stage, a

Facultative Parasites: These parasites
cysticercus, is a large fluid-filled cavity or
are normally free-living within the animal's
vesicle or bladder found in the musculature
environment but, on occasion, can develop
of pigs. This larval stage was once regarded
into a parasitic existence. For exan1ple,
as a separate parasite, and it still retains the

Halicephalobus deletrix, a saprophytic soil scientific name Cysticercus cellulosae. In
nematode that is found free-living in nature,
people, this larval stage usually develops in
has been reported to produce pathology in
subcutaneous sites and musculature but
the CNS of horses.

may be found in nervous tissues, eg, the

Successful chemotherapeutic treatment
bra.in and ocular tissues. Infection in people
for cerebrospinal nematodiasis has been
stems from ingestion of tapewonn eggs in
reported with diethylcarbama.zine at 100
contaminated foods or from dirty hands.

mg/kg ( 45 mg/lb). Ivermectin and organo

In the bra.in, the parasite usually develops
phosphates kill larval bots and at least some
in the ventricles. Infection causes pa.in,
nematodes, but killing parasites in situ
paralysis, epileptiform seizures, locomotor
within the CNS may provoke additional
disturbances, and possibly death. The larval
tissue damage.

cysticerci commonly localize on the

Before implementing therapy for a
meninges and in the neuropil. Treatment of
pathogenic helrninth or arthropod, other
human cysticercosis is by surgical removal
possible causes of neuropathology should
of the lesion; however, the prognosis is
be carefully considered. In particular, rabies
poor.

(seep 1302) should always be included in
the differential diagnoses. The animal's age,

Echinococcosis: Echinococcus
vaccination status, exposure status, and
granulosus is a tapewom1 found in the
history are factors that should be considsmall intestine of the can id definitive host.

ered when rendering a diagnosis.

Its eggs are ingested by the intermediate
hosts, wild and domestic herbivores, eg,

CESTODES
sheep, cattle, and moose. People can also
serve as intermediate hosts. After hatching

Coenurosis: Taenia multiceps multiceps in the intestine of the intem1ediate host, the is an intestinal parasite of ca.nids ( especially
oncospheres invade the circulatory system

1312

CNS DISEASES CAUSED BY HELMINTHS AND ARTHROPODS
and lodge in various organs (the liver and
due to focal lesions in the CNS caused by
lungs), where they develop into large,
the death of aberrant arrested larvae of
thick-walled, unilocular hydatid cysts that

T canis. To::cocara larvae may also invade bud protoscolices endogenously. Hydatids
the eye and cause ocular larva migrans in
have been rarely reported in the CNS of
people.

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domestic anin1als and are rare in people, in

Baylisascmis procyon'is is the ascaiid
which they produce symptoms similar to
found in the small intestine of raccoons.

those of a brain tumor.

It causes larva migrans in both wild and

Foxes are the definitive host for a related
domestic animals in North America and is
species, Echinococcus multilocularis.

usually associated with the production of

Microtine rodents (such as voles) are the
clinical CNS disease. More than 90 species
intermediate hosts. This parasite has been
of wild and domesticated animals have been
rarely found in the brain of people, in which
identified as being capable of serving as
the invasive, thin-walled multilocular
pai·atenic (transport) hosts harboring B
hydatid cysts produce innumerable
procyon'is larvae. Some species, including
exogenous daughter cysts that bud
opossums, skunks, cats, pigs, sheep, and
protoscolices. Surgical intervention is more
goats, appear to be marginally susceptible
successful in removing unilocular hydatid
or resistant to the neurologic migration.

cysts of E granulosus.

The parasite has been associated with the
production of cerebrospinal nematodiasis

TREMATODES
in people, particularly children; it also has been implicated as a cause of ocular larva

Paragonimiasis: Paragonimus
migrans.

westermani and P kellicotti, the lung flukes, have been reported to migrate

Filarids
aberrantly and produce cysts in the brain
and spinal cord of pigs, dogs, cats, rats, and

Dirqfilaria immit'is is often referred to as people. Flukes in these extrapul
the canine heartwonn but can also infect
rnonic sites
in dead-end hosts do not produce patent
cats and ferrets. As adults, these parasites
infections.

usually infect the right ventricle and the
pulmonary artery and its fine branches. D

Schistosomiasis: Schistosomes, or blood

'i'rnm'ilis has been recovered from a variety
flukes, normally deposit their eggs in the
of aberrant sites, including the CNS of its
small vessels of the gut and urinary bladder,
definitive hosts and the anterior chan1ber of
from which they pass into the external
tl1e eye. (See also HEARTWORM DISEASE, p 127.) environment via the feces or urine. Some

Elaeophora schneideri, a filarid of the
eggs, however, may get into the general
carotid arteries and its branches, is conunon
circulation and reach the CNS, where they
in mule deer, prin1arily in western North
become encapsulated. This condition has

America Microfilariae accumulate in the
been noted in people and domestic anin1als.

skin of the head and face; intem1ediate hosts
are tabanid horseflies. Larvae develop in

Troglotremiasis: Troglotrema acutum
arteries of the leptomeninges before
inhabits the frontal and ethmoidal sinuses
migrating to the carotids. Infection is usually
of foxes and mustelids in Europe. Flukes
asymptomatic in nom1al definitive hosts.

live in pairs in cysts in these sinuses. These

In wapiti, moose, white-tailed deer, sheep,
parasites cause decalcification and atrophy
and goats, worms in the arteries cause
of the bony walls of the sinuses and
degeneration and loss of the endotheliun1
eventually result in perforation into the
and accunrnlation of plasma proteins
cranial cavity. Microorganisms enter the
and platelets on and within the inti.ma.

cranial vault, leading to fatal, purulent

Thrombosis, infiltration of the intima, and
meningitis. No treatment is available.

fibroblastic proliferation may eventually
result in occlusion and ischemic necrosis

NEMATODES
in associated tissues. Necrotic lesions
associated with occlusion of leptomeningeal
aiteries are conunonly found in the brain.

As ca rids

Neurologic signs include blindness, head

The larvae of some ascaiid roundworms,
deviation, circling, ataxia, and pai·alysis
including Toxocara spp of dogs and cats

(See also ELAEOPHO!lOSIS, p 904).

and Ba,ylisnscmis spp ofmustelids, can

Setaria digitala is fotmd in Asia and is a
cause CNS disease.

common parasite of the peritoneal cavity.

Nervous disorders, frequently associated

Microfilariae are found in the blood;
with ascaiid infection in young dogs, may be mosquitoes are intermediate hosts. Details

CNS DISEASES CAUSED BY HELMINTHS AND ARTHROPODS

1313
of development in the no1mal host are

Parnlaphostrongylus tenuis is found in
w1known. In cattle, clinical signs do not
the subdmal space and venous sinuses of
appear to develop. In horses, goats, and
the craniun1 of white-tailed deer in eastern
sheep, the developing wom1s invade the

North America Eggs reach the lungs in the

CNS and cause motor weakness, ataxia,
venous blood and develop into larvae,

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lameness, drooping eyelids or ears, and
which pass up the bronchial tree and out
lwnbar paralysis. Lesions include focal
with the feces. Wective lruvae, acquired
malacia and degeneration of axis cylinders
from terrestrial snails and slugs as the deer
and myelin sheath in all regions of the CNS.

feeds, invade the spinal cord ru1d develop

Setaria cervi has been reported on the
for several weeks in the dorsal horns of the
leptomeninges of deer in Emope and in the
gray matter; then, they invade and mature in
forn1er USSR, often in association with
the subdural space. The infection is usually

Elaphostrongylus cervi. Setaria spp have
asymptomatic in white-tailed deer.

also been found in the CNS of horses. The

However, P tenuis causes pathology in the
signilicance of these findings is unclear.

CNS of various ce1vids (moose, cruibou,

Filarids may also parasitize avian species.

wapiti) and antelope, llru11as, sheep, and

SplendidojUaria qiiiscula is found in the
goats. In these hosts, the parasite produces
cerebral hemispheres of grackles (Quis
considerable trauma in the CNS. In addition,
calus quiscua) and other birds in North
eggs deposited in the neural tissue provoke

America. Paronchocerca helicina is found
marked inflammatory reactions. Clinical
in the cranial leptomeninges of the snake
signs consist of ltm1bar weakness, ataxia,
bird (Anhinga anhinga) in the USA
lameness, stiffness, circling, abnonnal
positions of the head, and paralysis. Signs

Metastrongyles
vary in onset and chru·acter in individual

Angiostrongylus cantonensis is a common
ru1in1als. Temporary remissions are typical.

parasite of the pulmonary ruteries of rats in

Sk1jabingylus nasicola and S chit
southeast Asia and the south Pacific.

woodorum ru·e found in the frontal sinuses

Terrestrial, aquatic, and runphibious snails
of mustelids, especially mink, weasels, ru1d
and slugs ru·e intern1ediate hosts. Paratenic
skunks. Larvae acquired from terrestrial
hosts ru·e freshwater prawns, land crabs,
snails and slugs develop for a tin1e in the gut
coconut crabs, and planruians. Larvae
wall, then migrate to the spinal cord. They invade the cerebrun1 and develop in the
move on to the leptomeninges to the brain
new-al parenchymafor -2 wk, then enter
and along the olfactm-y tracts to the
the subarachnoid space and migrate, -1 mo
cribriform plate, which they penetrate to
after infection, to the pulmonru-y arteries via
reach the frontal sinuses. Their presence on
the venous system. Nemologic signs ru·e
the leptomeninges elicits hemorrhage and
rare in rats with light to moderate infecleptomeningitis. In heavy infections, some tions, but circling, crumibalism, and
subadult worn1s may invade the brain and
paraplegia may develop in heavy infections.

cause neurologic signs, including pru·alysis.

In endemic areas, people frequently acquire
infections by consuming raw or unde1�

Rhabditorids
cooked intern1ediate or paratenic hosts. In

Halice-phalobus deletrix is a free-living soil people, this parasite may produce a fatal
rhabditiform associated with soil ru1d decayeosinophilic meningoencephalitis. In ing vegetation in the host's environment.

Australia, A cantonensis has produced an

This nematode has been reported in the
ascending pru·alysis in puppies. It may be

CNS of horses ru1d people. It may reach tl1e
an incidental parasite in dogs.

CNS through wounds contru11inated by soil

Gurlita paralysans is found in the spinal
that contain these nematodes or through
veins of cats and has reportedly produced a
abscesses in tl1e oral and nasal cavities.

high incidence of pru·alysis. It may be an

The nematode multiplies in the CNS and
incidental parasite in cats.

is highly destrnctive of neural tissues.

Elaphostrongylus cervi is a common

Pathogenicity in the CNS can be attributed
pru·asite of the skeletal musculature of
to trauma caused by activities of the

Rangifer and Cervus spp (reindeer and elk) parasites; the role of excretory and
in the holarctic region, especially Eurasia. It
secretory products is tmknown. Also,
is transmitted through terrestrial snails and
tl1e parasites may transpo1t pathogenic
slugs and appru·ently develops for a time in
microorganisms to the CNS. Clinical signs
the CNS before migrating to the muscles.

are related to the location of and lesions

Wection is associated with lumbar
produced by the parasite. Signs resemble
weakness, pru·esis, and paralysis in cervids
viral encephalitis and include motor
in Sweden and in the former USSR.

weakness, ataxia, head deviation, circling,

1314

CNS DISEASES CAUSED BY HELMINTHS AND ARTHROPODS
depression, blindness, drooping of the ear
in the nostrils and paranasal sinuses. They
or eyelid, loss of the herding instinct, and
rarely penetrate the ethmoid bone and
paralysis. Lesions consist of vasculitis,
reach the forebrain. However, it is possible
hemorrhagic necrosis, and malacia.

that other factors facilitate entry of larvae
into the brain. The bones of the skull may

Miscellaneous Nematodes
erode. lf the brain is injured, clinical signs,

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Migrating larvae of strongyles (perhaps
such as a high-stepping gait and incoordina

Strongylus vulgaris) have been reported in
tion, may mimic infection with Coenurus
the CNS of horses. Larvae of Stephanurus
cerebralis. This condition is often referred dentatus rarely invade the CNS of pigs.

to as false gid. Smgical intervention may be

Larvae of 1'richinella spiralis were found
useful but can prove difficult if the laivae
in the brain in a fatal case of trichinosis in a
are difficult to reach.

person. Larvae of Strongyloides stercoralis

Larval Cuterebra spp, normally found in
may invade the brain of experin1entally
subcutaneous sites in dogs or cats, have
infected animals. Gnathostoma spini
been lrnown to wander into the CNS and
gerum has been found rarely in the CNS of
localize in the cerebrum or cerebellum (see
people. Euslrongylides ignotus in1planted
p 879). Intracranial migrations by larvae of
subcutaneously in rats and chickens
dipteran flies have been reported in people
migrated to the CNS and caused death

(Dermatobia hominis ), cattle (Hypoderma of the host.

bovis ), and horses (Hypoderma spp ).

Bots and warbles may move rapidly after

ARTHROPODS
death of the host and migrate into tissues far
from the site of oligin.

Myiasis is the development of larval

Treatment of intracranial rnyiasis is
dipteran flies (bots and warbles) within
currently experin1ental. Surgical and
the tissues or organs of people and other
medical therapies to alleviate intracrai1ial
domestic or wild anin1als. Myiasis that
myiases have been considered. The efficacy
involves the CNS is rather uncommon except of systemic organophosphates against for the laival stages of Hypodenna bovis, the migrating larvae of Hypoderma suggest that cattle heel fly. Its laivae nom1ally burrow
organophosphates may effectively eliminate
between the pe1iosteum and dura mater of
certain dipteran larvae from the nervous
the bovine spinal cord during migration to
system. Parenteral corticosteroids are also
the subcutaneous tissues of the back
recommended to prevent additional

Neurologic signs, varying from a transient,
inflammatory dan1age and intracranial
stiff, unsteady gait to paralysis, may be seen
pressure throughout the treatment pe1iod.

in cattle given systemic insecticides when

Ivermectin (300 mcg/kg on alternate days)

the laivae are present in the spinal canal. (See used in coajunction with corticosteroids also CATTLE GRUBS, p 876.)

should be considered experin1ental therapy

The larvae of Oestrus ovis, the nasal bot
for intracranial cuterebrosis in cats; it is not
fly of sheep (seep 1473), are nom1ally found approved by the FDA for this use.

TICK PARALYSIS

Tick paia.lysis (toxicity) is an acute, proand Amblyomma have been reported from gressive, symmetlical, ascending motor

Australia, Nortl1 Amelica, Europe, and
paralysis caused by salivary nemotoxin(s)

South Africa; these three plus Rhipicepha
produced by certain species of ticks. With
li1,S, Haemaphysalis, Otobius, andArgas
some species, other signs of systemic
have been associated with paralysis to

"single organ" toxicity ( eg, cardiac, airway, varying degrees in animals.

bladder, lung, esophagus, etc) may be seen

This toxicity is unique, because it is a
separate to or within tl1e classic pareticpulsed toxin flow associated with repeat paralysis presentation. People ( usually
tick feeding over a set period of tin1e.

children) and a wide valiety of other

Anin1als are generally affected by paralysis,
mai11mals, birds, and reptiles may be
but there are also very odd presentations of
affected. Hw11an cases of tick paralysis
associated toxicity. Deterioration cai1 be
caused by the genera/xodes, Dermacentor,
unpredictable and rapid in some cases, and

TICK PARALYSIS

1315
some animals may have prolonged and
tick exposure eventually is associated with
unexplainable recovery. Very severe cases
a decline in inununity, possibly due to
require intensive care, including artificial
toxin-neutralizing effects by the host. Tick
ventilation, to maximize recovery rates, and
factors include age, toxin absorption and
generally, only tick removal and use of tick
circulation dynamics, paralysis-inducing

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antitoxin serun1 (TAS) and antibiotics have
capability, other toxic effects, sexual
a major effect on overall mortality.

activity, rate and volume of secretions,
and the frequency of the sucking phase.

Etiology, Epidemiology, and Patho

The maximal prevalence of tick paralysis
genesis: The potential to induce paralysis
is associated with seasonal activity of
has been demonstrated, described, or
female ticks, mainly in spring and early
suspected in 64 species of ticks belonging

SUil1Iner, but in some areas ticks are active
to 7 ixodid and 8 argasid genera. On the
throughout the year. Environmental factors
eastern coast of Australia, the paralysis tick
such as temperature and hwnidity also play

I holocyclus ( and to a lesser extent I
a major role in tick morbidity and mortality
cornuatus and I hirstii, in which morpho

(ie, ticks are easily killed by both hoUdry
logic classification has been shown to be
and wet conditions). Modem rapid
unreliable) causes the most severe fonn of
transport of ticks attached to people,
tick paralysis, with a mortality of as much as animals, or plant material can give rise to I ()OA, in dogs ( usually 4%--5%), irrespective of
isolated cases of tick paralysis, far removed
therapy.

from the particular geographic area ( or

In North America, D andersoni (the
country) where the ticks are naturally

Rocky Mountain wood tick) and D
foW1d. The diagnosis may be delayed when
variabilis (the American dog tick) are the
such infested anin1als travel to areas where
most common causes. Sheep, cattle, and
such paralysis associated with reduced
people may be affected, as well as dogs. D
levels of acetylcholine is not typically seen.

albip'ictus, I scapularis, Amblyomma

Toxicity does not relate directly to tick
americanum, A maculatum, R san
size, number, or duration of attachment.

guineus, and O megnini may cause

The clinical signs produced in various hosts
paralysis. In fow1,Argas radiatus and A depend on several variables, including toxin
persicus have caused paralysis. In Africa, I secretion rate, local site responsiveness,
rubicundus (Karoo tick paralysis) and R
host inununity and susceptibility, and
punctatus in South Africa, R evertsi evertsi specific organ susceptibility.

and A rgas walkerae in sub-Sal1aran Africa, Systemic toxicity follows injection of
and R evertsi mimeticus in Namibia can
toxin( s) into the host, especially during pericause the disease. Cats appear to be ods of rapid engorgement, although large
resistant to the disease caused by these
numbers of larval or nymphal J;icks may also
ticks but are affected by I holocyclus.

cause the same paralysis of the neuromus

Toxicity is usually less severe (than in dogs), cular junction. The toxin is presun1ed to does not include chest complications, and
travel from the attaclunent site via the
has a better prognosis.

lymph to the systemic circulation and thus

I holocyclus in Australia causes a much
to all areas of the body, where it has a direct
more severe disease than that seen in North
effect on cellular potassium charmels and

America and elsewhere. Dogs and cats are
thus on intracellular calcium levels.

affected, as well as sheep, goats, calves,

However, primary hypoventilation is the
foals, horses, pigs, flying foxes, poultry,
main cause of death in most severe cases, in
birds (ostrich), reptiles (snakes and lizards), which alveolar disease may also be present.

and people. Both local (less common) and
systemic paresis and paralysis are seen.

Clinical Findings: In tick paralysis other

The natural hosts (bandicoots) are rarely
than that caused by I holocyclus, clinical
affected, presunmbly acquiring inununity at
signs are generally seen --5-9 days after tick
an early age. However, without exposure to
attachment and progress over the next
toxin, they too become susceptible.

24--72 hr. When I holocyclus is involved,

Host factors influencing epidemiology
clinical signs usually appear in 3-5 days
include species, sensitivity to toxin, age,

(rarely longer, eg, up to 18 days, possibly
acquired inununity, field behavior,
with virginal ticks) after attachment and
concurrent work demands, reaction to
usually progress rapidly throughout the
environmental factors, skin reactivity, and
next 24--48 hr. Tin1e periods can vary with
population density. Antitoxin inununity,

I holocyclus because of tick factors,
starting at least 2 wk after primary tick
environmental humidity, temperature
exposure and lasting a few weeks, can be

(microclirnate ), and host factors. Both
boosted by further infestations, but chronic

"shorter onset to severe" signs and delayed

1316

TICK PARALYSIS

"quiet" attaclunents with minimal signs may aspiration pnemnonia); such cases are
be seen. Removal of I holocycliis ticks does usually te1minal. Dogs with upper
not immediately halt progression of disease.

respiratory tract obstruction have a marked
ln severe cases, death from respiratory
expiratory stridor (not the classic inspiramuscle failure and other respiratory tory stridor of prin1ary laryngeal paralysis

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complications can occur within 1-2 days
of large breeds), often with the head and
of the onset of signs.

forelegs extended to maximize air flow and

Early signs may include change or loss
exchange. lf there is chest disease as well,
of voice ( due to laryngeal paresis); hindlimb
the animal is usually very dyspneic. A thrill
incoordination (preswned to be due to
can be felt at or just below the larynx in
weakness and not central CNS ataxia);
association with the obstructed expiratory
change in breathing rhytlun, rate, depth,
effort and stridor. The upper respirato1y
and effort; gagging, grunting, or coughing;
tract lesion can be easily missed, especially
regurgitation or vomiting; and pupillary
if the dog is paralyzed. Often the respiratory
dilation. Dogs with a grunt are believed to
rate is high and forced. In cats, the doll test
have increased airway resistance.

can be used to assess upper respiratory

Hindlimb paralysis begins as slight to
tract function. lf finger/thwnb compression
pronounced incoordination and weakness,
of the chest induces a stridor, then this
which is best observed with the animal
supports paresis or paralysis, irrespective of
turning or walking away from the observer
other respiratory tract defects. It is essential

(or when climbing stairs orjwnping up). As
that any upper respirat01y tract obstruction
paralysis progresses, the animal becomes
be cliagnosed, because the associated
unable to move its hindlimbs and forelimbs,
workload, anxiety, and resultant fatigue
to stand, to sit, to right, and finally to lift its
can quickly become terminal.

head.

Paralysis of esophageal muscles develops

A four-stage classification system based
in most dogs (but not cats), with or without
on systemic limb activity may enable
obvious esophageal dilation. Saliva and
clinical predictability. In stage 1, the dog's
ingested food or fluid pool in the esophagus
voice is changed ( usually noticed retrospecand may be regurgitated into the pharynx tively), and the dog is weakened but can still and mouth. Loss of pharyngeal function walk and stand. ln stage 2, the dog cannot
makes it difficult for the anin1al to clear
walk but can stand. ln stage 3, the dog
material from the upper respiratory tract,
cannot stand but can right. ln stage 4, the
which may then lead to aspiration
dog cannot right. Stages 3 and 4 ( -300Ai of
pnewnonia.

cases) indicate a poor prognosis. However,

Vomiting (with evidence of bile) may
some dogs show few signs because of low
occur in I holocyclm paralysis; a central
levels of toxin or high levels of protective
action of toxin on the vomiting center has
skin or systemic immw10logy, and some
been suggested. Most cases of vomiting
show signs in only one organ ( eg, esophareported by owners are probably regurgitageal paralysis). Sensation is usually tion, although drug-induced vomiting can be
preserved, but it is increasingly harder to
a complication. Dogs will gag and retch in
detect the clinical responses to stimuli due
an attempt to clear secretions and move
to lower motor neuron paralysis. (Visual
their head and jaw in an odd way, associated
analog scale scoring is also performed for
with a characteristic groan, to fwther
the neuromuscular junction, overall
attempt clearance of materials.

toxicity, and dyspnea, with highly predictive

Body temperature may be normal in the
results).

early stages; however, due to the toxin's

Breathing abnormalities include choke,
effect on arteriovenous anastomoses
upper respiratory tract obstruction,

(shunts), normal tl1ermoregulation is lost.

bronchoconstriction ( especially seen early

This can cause hyper- and hypothermia as
in cats), progressive fatigue of respiratory
animals are affected by local environ.mental
muscles, and aspiration of esophageal and/
factors. Shivering is also lost in severe
or gastric contents (due to loss of pharyncases. Profound hypo- and hyperthennia geal and laryngeal function), leading to
can occur suddenly and can be easily
aspiration pnewnonia. Aspiration can be
misdiagnosed; hypotl1ermia clinically
significant, and the lung severely affected
resembles tick paralysis in several ways.

before any obvious signs. It is possible to

When body temperatm·e is restored, the
have a silent (no crackles), severely
level of tick paralysis in some cases can be
pnewnonic lung if there is poor airflow into
mild.

the affected lobe. Some dogs have profound

Rarely in dogs, acute congestive herut
dyspnea, no crackles, and extensive
failure can present with extensive
pulmonary radiographic opacity ( due to
pulmonary edema due to diastolic

TICK PARALYSIS

1317
myocardial dysfunction (the myocardium is

Specific signs ( eg, congestive heart failure,
unable to correctly relax, reducing efficient
urethral obstruction) require routine
chamber filling and tl1erefore systolic
evaluation and treatment of that body area
cardiac output). Venous return may also be
or system.

reduced, and systemic venous pressure is

Botulism, polyradiculoneuritis, acute

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increased.

peripheral neuropathies, snakebite,

Some dogs have a prolonged QT interval
hypokalemia, and toadfish and ciguatera
on ECG, which can result in a lethal
toxicity are some differential diagnoses.

ventricular arrhytlmtia. The frequency of

In regions where ticks are endemic, tick
iliese unexplained deailis, which follow
paralysis is LLSually high on the list of
complete gross clinical recovery, is not
differential diagnoses for any flaccid,
known, but most veterinarians who treat
clinically ascending motor paralysis. It
many cases report such events.

should also be considered in the differential

Cats wiili moderate to severe toxicity can
diagnosis of megaesophagus, unexplained
be anxious. It is essential not to interfere
vomiting, acute left congestive heart failure
wiili these animals tmtil iliey have settled in

(dogs), or "astl1ma" (cats). The tick season ilieir cage. If procedures are forced on iliem, is usually well known for various areas ( eg, iliese animals can die from obstructive
a local creek) witltin ilie environment of a
dyspnea and the (presun1ed) associated
particular practice, and often most tick
hypoxentia, acidosis, and hypercapnea.

paralysis cases come from a few, well

Animals can dete1iorate if compromised by
defined, highly endemic areas.

excessive hospital stress ( eg, nursing

Blood and serwn values are unchanged
attention, noise, smell).

in the early stages. Increased PCV (with

Cats may present with an "astl1ma-like"

nonnal serum protein) indicates a fluid
ailway constriction, usually when they are
shift into the lungs and a more guarded
mildly paretic; expiratory wheeze on
prognosis. Other changes may include
aLLScultation, forced abdominal expiratory
increased levels of blood glucose, choleseffort, and very easily induced exercise terol, phosphate, and CK, and a decrease in
intolerance are classic signs at this time.

blood potassium levels, but none of these

These cats often have a positive doll test
changes are specific for tick paralysis or
and will, after a few steps, sit on their
indicate severity or prognosis.

hindquarters with ilie chest in a more

Echocardiography reveals boili diastolic
upright vertical position than normal, often
and secondary systolic myocardial
with an increased respiratory focus or
dysfunction associated witl1 reduced
effort. Feline "asthma" can be easily
ventricular filling, possibly due to boili
misdiagnosed at this stage if a tick is not
peripheral venous pooling and poor
found or suspected.

diastolic myocardial relaxatipn. Nonstressful radiography gives the best available Diagnosis: The presence of a tick in
prognostic support, and pulse oximetry the
conjunction wiili ilie sudden appearance of
best continuous assessment of oxygenation.

limb weakness and/or respiratory impair

Capnography helps assess the functional
ment is diagnostic. The offending tick may
level of ventilation. Artetial blood gas
no longer be attached, but a "skin crater" ( a analysis ( aliliough invasive) gives ilie best
hole 1-2 mm deep and 1-3 nun wide,
overall assessment of cardiopulmonary
surrounded by a variably raised and
function. However, the stress of any such
inflamed area) confirms the diagnosis.

testing should be considered; positioning

Sometimes neiilier tick nor crater can be
for chest radiographs ( eg, dorsoventral to
found (ticks attached deep in ilie ear,
lateral) can tip animals into a terminal
between toes, or in ilie mouth or anus may
hypoventilatory decline associated wiili
be missed). However, wiili ilie appropriate
acute respiratory or cardiac arrest.

clinical signs, in a known tick area wiiliout
another obvious cause of lower motor

Treatment: In most infestations ( except
neuron or neuromuscular disease, TAS

I holocyclus ), removal of all ticks usually treatment is still indicated. Recovery
results in improvement within 24 hr and
after treatment subjectively confirms
complete recovery within 72 hr. If ticks
the provisional diagnosis.

are not removed, death may occur from

Specific laboratory diagnostic techniques
respiratory paralysis in 1-5 days. Removal
are not available, but procedures that may
of I holocyclus ticks does not immediately
be generally helpful include a PCV, serum
halt progression of disease. Clinical signs
protein, and radiography to assess presence
can deteriorate for -24 hr and longer, but
and degree of pulmonary edema, megaesophmost dogs start to improve in 6-12 hr after agus, and pneun10nia due to aspiration.

TAS ilierapy. In any infestation, removal of

1318

TICK PARALYSIS
all ticks is absolutely necessary. The entire
weeks), and it will have no effect if tile toxin
integument should be searched, diligently
is already tissue bound and the animal is
and repeatedly, especially on long-haired
severely ill or about to become so (with
animals or those with thick coats. Most
toxin in the perivascular space).

ticks (SOOA,) are located around the head or

Minimization of stress and anxiety is

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neck, but they can be found anywhere on
essential. Acepromazine (0.03 mg/kg) may
the body. Plucking tl1e tick(s) yields the
be given SC before any other medication
best result (in dogs) and does not induce
or handling tllat may upset tile animal.

anaphylaxis.

However, high doses should be avoided,

Therapy for tick toxicity must address
especially if the animal is depressed,
primary tick toxemia and paralysis,
hypotensive, or hypotllermic. (Overdosage
secondary issues ( eg, esophageal reflux,
may induce hypotension and hypotl1ennia.)

aspiration pneumonia), and potential

Opiates are an alternative ( eg, metliadone,
te1tiary factors ( eg, chronic weakness,

0.3--0.5 mg/kg, SC, IM). Oxygen therapy
esophageal strictme ).

(nonstressful, usually nasal) is implemented

TAS is an immune sernm against the toxin (as indicated), but progressive disease (similar to tetanus antitoxin) and is the
requires more intensive therapy.

product of choice. It should be given as

General anesthesia is indicated in animals
early in the disease as possible; subsequent
that are severely fatigued and dyspneic, to

"top up" doses are not effective, because
allow for better administration of oxygen,
they are too late. For dogs, a minimal
esophageal drainage, and upper respiratory
dosage of 0.5-1 rnUkg, should be given
tract suction. Pentobarbit.one can be used as
slowly IV throughout at least 20 min to avoid a constant-rate infusion or given periodiany shock reaction. Rapid IV use can induce cally IV to induce light anestl1esia, witll
clinical reactions in >80% of dogs. Anaphyrepeat doses as needed. Anotller potential laxis can occm unpredictably (as with all
benefit of pentobarbitone may be control of
products), necessitating the use of highlong QT syndrome. The chief benefits of dose, soluble cortisol and rapid fluid
some form of anesthesia ( eg, profofol) are
loading, etc. Based on retrospective case
to reduce dyspnea, enable muscle rest, and
studies, cats are believed to be somewhat
help overcome primary muscle fatigue ar1d
more susceptible than dogs, presw11ably
general exhaustion. Periods of 6--8 hr of
with a second dose, a few weeks (not days)

light anesthesia ar·e best, with reassessment
after the first dose.

of clinical status after each period.

Aninlals with multiple ticks or in the early

Mechanical or manual ventilation may be
stages of paralysis should receive a higher
required but should be carefully assessed
dose, because these cases have tl1e most
because recovery can be delayed, especially
unbound toxin to n�utralize. However, there in brachycephalic animals. Longer-te1m are no data for the exact dosage rates
ventilation cases can have a 70% recove1y
required, and batch and brand levels of
rate. It is essential to assess pulmonary
protective irnmunoglobulin may vary.

(expired C02 levels) and alveolar (pulse

Severely affected dogs may have less
oxin1etry) ventilatory capacity and to be
remaining unbound circufating toxin for
aware of profound respiratory muscle

TAS to neutralize. However, debate persists
fatigue. Alveolar disease ( edema and/or
about the required (possibly less) dose of
pneun10nia) has a poor prognosis in such

TAS. It has been suggested that a standard
cases.

.

dose should be given, based on the amount

Atropine (repeated eve1y 6 hr, lowest
needed to neutralize the pulsed toxin flow
dose) can be used if GI and respiratory
from one tick rather than on a weight basis;
secretions ar·e excessive, but its effect on
a minimal dose of 10-20 mL is recomtear secretion (and the host's potential for mended for clogs (and 5-10 mLfor cats).

eyelid paralysis, reduced blink reflex, and

However, until the level of remaining
corneal d1ying) and cardiac rate and rhythm
unbotmd toxin in the affected animal and
char1ges should be considered.

the level of specific protective immuno

Antiemetic tllerapy should be used in
globulin can be better assessed, a set dose
animals that are vomiting, which is usually
rate cannot be established (tile level of
a poor prognostic sign. If tile animal is
disease is reflective of the level of bound
regurgitating, the esophagus should be
toxin, which is not affected by TAS).

aspirated along witl1 tile upper respiratory

TAS given IP is tile best alternative in
tract. Conect drainage positioning then
cats for which tile IV route is an issue ( eg,
becomes a vital factor in helping to avoid
respiratory distress, restraint dangers,
aspiration. Care is needed with gastroclyspnea). However, its clinically effective esophageal reflux cases regarding tlleir
half-life is believed to be sho1t ( days not
chronicity and tissue darnage.

TICK PARALYSIS

1319

Broad-spectrum bactericidal antibiotics
hypothem1ia.. Warmth applied at the lower
are indicated ( especially in severe cases)

limbs (especially the hindli.mbs) will be of
to help avoid development of aspiration
maximal benefit; direct application to the
pneumonia, but they must be given as soon
groin area may also potentially be useful.

as possible. Dogs with upper respiratory

Some animals may need wa.imed fluids, IV
tract obstruction require either tracheor rectally, to reverse a very cold presenta

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otomy or anesthesia and intubation to
tion (eg, s32°C). Sudden hyperthennia
overcome the potentially lethal effects

(>42°C) can be seen in hospitalized dogs.

of such obstruction.

They usually show exaggerated head and

Diuretics (eg, furosernide) with
possibly foreleg movements and signs of
maximally appropriate oxygen treatment
anxiousness. With cooling ( eg, wet towels,
are indicated to treat congestive heart
direct fan flow, high rate of air changes),
failure. Veraparnil (0.1 mg/kg, IV bolus) has
these signs a.bate.

been used to help relieve the basic toxic

Because the a.i1i.mal's condition is
myocardial effect of a failure to relax. The
expected to deteriorate after ticks a.i·e
toxin does unbind, so if the animal can be
re.moved and TAS is given, hospitalization
kept free of tenninal pulmonary edema ( or
with minimally invasive monitoring a.i1d
arrhythmia), the cardiac failure will reverse
good nursing care is necessary. The a.tli.mal
over a few days, provided routine suppo1t
should be kept in a quiet, dark, comfortable
is given. Esmolol has been used to treat
area of the hospital where it can be easily
affected animals that have a long QT
seen. It should be placed on the sternwn to
interval and the potential for a lethal,
maximize Jung function. Lateral recumunpredictable ventricular arrhytlunia bency, left side down with the shoulder (not

Fluid therapy should be used with great
the pharynx or neck) as the highest point, is
care, because pulmonary edema can be
the best position for drainage. If possible,
induced easily. Staying below maintenance
slight "head down" is also advised. Animals levels and ensuring the animal is assessed
should never be rotated unless it can be
for edema, both before and dilling IV fluid
done frequently (every 1-2 hr), day and
therapy, should be routine. Dehydration can
night.

occur in tick paralysis but not usually in

Because the animal ca1mot void,
routine cases until the second day of
catheterization is necessa.iy, with the
hospitalization, when increased PCV and
bladder expressed at least twice daily to
protein values may be evident. In small
avoid infection. As with other localized tick
patients, SC or IP fluids can be given if lung
toxicity effects, this may persist beyond
status is a concern. Exceptional cases may
the period when the a.ili.mal has generally
require extensive rehydration ( eg, paralyzed recovered. Eye protectants should be used in the sun with high hw11idity and temperato prevent corneal ulceration or dryness (lid ture for a day before presentation), but the
closure, artificial tears, contacts). Suction
extent of the underlying organ dysfunction
of the pharynx, la.iynx, and proximal
should be assessed before intensive fluids
esophagus minimizes upper respiratory
are given.

tract distress caused by saliva pooling and

The asthma-like disease in cats is hard to
regurgitation. An esophageal tube may be
reverse, because routine bronchodilators
slowly inserted to remove any pooled
do not seem to be effective.

matetial; in some cases, tllis is volwninous

Muscle fatigue can be reduced (with
and the tube may possibly prevent choke
recovery of some muscle strength) by short

(seen mostly in brachycephalic breeds with
periods (6-8 hr) of anesthesia. The animals
laryngeal blockage by foreign material).

remain hypercapneic but, with endotra

Fluid and oxygen therapy should be
cheal intubation and 02 therapy, can estabmonitored to a.void overhydra.tion or lish reasonable hemoglobin saturation
under-supply, respectively. Nut1itional
levels (>95%), provided there is no
support should be perforn1ed carefully to
significant alveolar disease.

ensw-e t11at GI and respiratory function can

Intoxicated animals lose their ability to
cope with any offered food and water.

regulate body temperature. Animals that

Repeated tick sea.i·ches should be
have fallen below 32°C (90°F) for a long
perfonned during hospitalization, especially
pe1iod may be ha.rd to resuscitate. Various
if the animal deteriorates unexpectedly or is
heating mechanisms are used (hot water
slow to recover. Long or matted hair should
bottles, blankets, hot air flow blankets), but
be clipped, especially a.bout the head and
peripheral heat absorption cam10t occur if
neck. Application of an a.ca.ricide may kill
arteriovenous anastomoses (shunts) are
any ticks missed in searching. However, the
shut due to the effect of the toxin and
stress of searching, clipping, or bathing can
the host's vasoconstrictive reaction to
be detrimental in severely affected or

1320

TICK PARALYSIS
nervous animals, in which sedation is
fore- and hindlegs) with unresolved tick
recommended.

paralysis often produces stridor, indicating
abnom1al laryngeal function. Aninlals

Prognosis: Appropriate and tin1ely
should be able to eat, drink, and walk

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treatment (TAS and antibiotics, especially
normally without any stridor before
in severe cases) saves -95% of affected
discharge.

animals, but -5% of animals are likely to die

Owners should be advised to continue
despite all treatment efforts, especially
searching recovered animals for ticks; use
those with aspiration, or advanced
appropriate preventive methods to avoid
respiratory paralysis and dyspnea. Most
reattachment of ticks; and avoid high
a.ilinlals (>800Ai) have only one tick and a
temperatures, stress, or strenuous exercise
large attachment crater. Prolonged recovery for at least the first month. Smaller, more and weight loss can be seen with various
frequent meals may also be indicated if
complications, and death can also occur
there was esophageal dysfunction. This rest
due to choke, respiratory muscle fatigue,
period especially applies to working farm
cardiac arrhythmias, congestive heart
clogs, in which early overexercise may lead
failure, and cardiopulmonary arrest. Older
to pem1a.i1ent muscle dan1age.

animals are at greater risk, as are very young
pups. Propo1tionally more severe cases are

Prevention and Control: Owners
seen at the start of the season, and a second
should not rely solely on chemical control

( close to the first) infestation will be more
to prevent tick infestation, because no
severe. Dyspnea, crackles, and wheezes are
product is totally effective, and a single
poor prognostic signs, as are high neuroattached tick can cause the disease. They muscular junction scores (3 and 4) or high
should be advised about when and where
visual analog scale scores (;:>75%) for
their pets will be at risk; encouraged to
toxicity or respiratory distress.

thoroughly search the coat daily; keep the

Before discharge, the drop test can be
coat as short as possible (to aid searching);
used in cats to assess neuromuscular
and understand the efficacy, appropriatefunction a.i1d three-dimensional gravitaness, safety, and lin1itations of available tional control. Cats should be able to
preventive products (sprays, topical
correct a fall from 10-20 cm above the top
spot-ons, tablets, and collars). Combination
of the table. Still-affected cats will not
therapy (eg, spray and collar) may give
con-ect in time and land more heavily,
better results by using two modes of action,
with the chin hitting the padded table top.

but there are no published data to support

Recovered cats land lightly with good head
this concept.

control. J un1ping up to and clown from the

Attempts to produce an effective vaccine
cage can also be used to.assess muscle
against the I holocyclus toxin have so far
strength in cats. In clogs, jumping down
been unsuccessful, as have been attempts at
from a cage can induce stridor, indicating

"in-field" tick control. Specific RNA studies unresolved respiratory paresis with forced
show that ticks vary geographically, and
expiratory air flow, because the unsupsuch genetic differences may explain why pmted abdominal mornentwn ·affects the
clinical signs of tick paralysis and visual
diaphragm and lung air flow, producing a
a.i1alog scale toxicity scores can vary
high-volun1e expiration. Lifting a dog ( with
between different areas at the san1e time
the holder's arms wrapped outside the
of the year in the same selliion.

REPRODUCTIVE SYSTEM

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INTRODUCTION 1323

The Gonads and Tubular Genital Tract 1323

Infertility 1328

Principles of Therapy 1328

CONGENITAL AND INHERITED ANOMALIES 1329

Intersex Conditions 1329

Male Genital Abnormalities 1330

Female Genital Abnormalities 1331

LARGE ANIMALS

ABORTION 1332

Cattle 1333

Sheep 1337

Goats 1340

Pigs 1341

Horses 1343

Camelids 1346

BOVINE GENITAL CAMPYLOBACTERIOSIS 1347

BRUCELLOSIS 1348

Cattle 1348

Goats 1350

Horses 1350

Pigs 1350

Sheep 1351

CONTAGIOUS AGALACTIA 1352

CYSTIC OVARY DISEASE 1354

Follicular Cystic Ovary Disease 1354

Luteal Cystic Ovary Disease 1356

Cystic Ovary Disease as a Herd Problem 1357

Cystic Ovary Disease in Mares 1357

EQUINE COITAL EXANTHEMA 1357

MASTITIS 1358

Cattle 1358

Subclinical Mastitis 1359

Clinical Mastitis 1362

Goats 1367

Ewes 1367

1322

REPRODUCTIVE SYSTEM

Mares 1368

Sows 1368

METRITIS 1368

Acute Puerperal Metritis 1368

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Metritis and Endometritis 1369

Pyometra 1370

Contagious Equine Metritis 1371

PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME 729 (GEN) POSTHITIS AND VULVITIS IN SHEEP AND GOATS 1372

Enzootic Posthitis and Vulvitis 1372

Ulcerative Balanoposthitis and Vulvitis 1373

POSTPARTUM DYSGALACTIA SYNDROME AND MASTITIS IN
sows 1373

Acute Multiglandular Mastitis 137 4

Acute Uniglandular Mastitis 1375

Chronic or Dry-Sow Mastitis 1375

Postpartum Dysgalactia Syndrome 1375

PROLONGED GESTATION IN CATTLE AND SHEEP 1377

PSEUDOPREGNANCY IN GOATS 1381

RETAINED FETAL MEMBRANES 1381

SEMINAL VESICULITIS IN BULLS 1383

TRICHOMONIASIS 1384

UDDER DISEASES 1385

Diseases of Bovine Teats and Skin 1385

Physiologic Disorders 1387

Pseudocowpox 868 (!Ta)

Traumatic and Structural Disorders 1388

UTERINE PROLAPSE AND EVERSION 1389

VAGINAL AND CERVICAL PROLAPSE 1390

VULVITIS AND VAGINITIS 1391

SMALL ANIMALS

REPRODUCTIVE DISEASES OF THE FEMALE 1393

Dystocia 1395

False Pregnancy 1395

Follicular Cysts 1395

Mammary Hypertrophy in Cats 1396

Mastitis 1396

Metritis 1397

REPRODUCTIVE SYSTEM INTRODUCTION

1323

Ovarian Remnant Syndrome 1397

Pyometra 1397

Subinvolution of Placental Sites 1399

Vaginal Hyperplasia 1399

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Vaginitis 1399

REPRODUCTIVE DISEASES OF THE MALE 1400

Orchitis and Epididymitis 1400

Balanoposthitis 1401

Paraphimosis 1401

Priapism 1402

Phimosis 1402

BRUCELLOSIS IN DOGS 1402

MAMMARY TUMORS 1403

PROSTATIC DISEASES 1405

Benign Prostatic Hyperplasia 1406

Prostatitis 1406

Prostatic and Paraprostatic Cysts 1407

Neoplasms 1407

Prostatic Calculi 1408

CANINE TRANSMISSIBLE VENEREAL TUMOR 1408

REPRODUCTIVE SYSTEM INTRODUCTION

The reproductive system provides the
organs in both sexes. The pituitary gland
mechanism for the recombination of
and the hypothalamus are the primary
genetic material that allows for change and
regulatory centers; thus, the regulatory
adaptation. Manipulation of this system in
function is, in part, neuroendocrine in
breeding management programs allows
nature. In pregnant females, the fetoplacenthe rapid and dramatic alteration of the tal unit has a significant role in maintaining
conformation and productivity of domestic
and terminating pregnancy.

animals. Theriogenology is the veterinary

For the temporal and physiologic features
clinical specialty that deals with reproducof the reproductive cycles of selected tion. The reproductive system is incredibly
species, see TABLES 1 -3.

complex in both its anatomy and physiology, and all aspects must be considered THE GONADS AND TUBULAR
when resolving reproductive problems.

The differences in the reproductive system

GENITAL TRACT
between the sexes and among species are

Both sexes have a pair of gonads ( ovaries
extensive. Both sexes have primary sex
or testes). However, in birds the right
organs and primary regulatory centers.

ovary does not develop; only the left ovary

Gonads and function-adapted, tubular
and oviduct are present in adult females.

genital organs constitute ptimary sex

The main functions of the gonads are

1324

REPRODUCTIVE SYSTEM INTRODUCTION
ll·HIII APPROXIMATE GESTATION PERIODS

Domestic Animals

Days

Wud Animals

Days

Cat

65

Bear (Black)

210

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Cattle•

Bison

280

Angus

281

Camel

365-400

Ayrshire

279

Chimpanzee

236

Brahman

292

Coyote

63

Brown Swiss

290

Deer (Mule and White-tailed)

200

Charolais

289

Elephant

660

Guernsey

283

Elk, Wapiti

255

Hereford

285

Giraffe

425

Holstein

279

Gorilla

270

Jersey

279

Hare

36

Limousin

289

Hippopotamus

240

Shorthorn

282

Leopard

95

Simmental

289

Lion

108

Dog

62-64b

Marmoset

150

Donkey

365

Monkey (Macaque)

180

Goat

150

Moose

235

Horsec

335-342

Muskox

255

Llama, Alpacac

335-365

Opossum

12

Pig

114

Panther

90

Sheep

150

Porcupine

210

Fur Animals

Days

Pronghorn

250

Chinchilla

111

Raccoon

63

Ferret

42

Reindeer

225

Fox

52

Rhinoceros (African)

480

Mink

Seal

330

European

41

Shrew

20

American

40-75

Skunk

63

Muskrat

29

Squirrel (Gray)

40

Nutria, Coypu

130

Tapir

390

Otter

270-300d Tiger

103

Rabbit

31

Walrus

450

Wolf

63

Whale (Sperm)

450

Woodchuck

31

See al.so SELECTED PllYSIOLOGJC DATA OP I.ABORATORY ANIMALS, p 1842.

a Individuals may range ±7-10 days from these averages.

b Gestation pe1iod is 58-72 days from breeding at unknown stage of estrus; from day of ovulation (which can be detennined by progesterone or LH monitoring), gestation period is 62-64 days.

c Individuals may range 20 days from these averages.

d 180+ days due to delayed implantation

REPRODUCTIVE SYSTEM INTRODUCTION

1325

•th•il APPROXIMATE INCUBATION PERIODS

Domestic Birds

Days

Caged and Game Birds

Days

Chicken

21

Budgerigar

18

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Duck

28

Finch

14

Muscovy duck

35

P3lTOt

26

Goose

28

Pheasant

24

Guinea.fowl

28

Pigeon

18

Turkey

28

Quail

16

Swan

35
gametogenesis ru1d steroidogenesis. Both
pregnancy and, in some species, by seafunctions are regulated primru·ily by son or lactation during the immediate
gonadotropins released by the ruiterior
postpartum period. Cycling may also be
pituitru-y gland under the influence of the
blocked by pathologic conditions of the
hypothalruirns. Hypothalamic control of
ovaries (eg, nutritional atrophy or ovru·irui
the pituitru-y is mediated by a peptide,
cysts) as well as by uterine disease (eg,
gonadotropin-releasing hormone (GnRH);
pyometra), which may result in persistent
the secretion ruid release of GnRH are
luteal function. Estrogens ruid progestergoverned by CNS stimuli and, through one act locally, affecting target organs
a feedback mechanism, by hormones
such as the tubulru· genital tract, and
produced by other endocrine organs such
distally, regulating gonadotropin release
as the gonads, pituitary, thyroid, ruid
by a feedback mechanism on both the
adrenal glruids. (See also ENDOCRINE SYSTEM, hypothalamus and anterior pituitary. In
p 538, et seq.)

addition, they play a prominent role in
sexual behaviors, lactation, ru1d the

The Ovaries: The size and location of the development of secondru·y sex characovaries vru-y with the species. The ovaries teristics.

crui be directly exrunined by ultrasonography or by palpation per rectum only in lru·ger ruiimals (eg, cows, mares, and

The Testes: The testes function in both
camelids). Once puberty is reached (see
spennatogenesis and secretion of steroid

TABLE 3), the size and form of the ovaries
hormones. Spennatogenesis is stimulated
are altered by cyclic functional structures,
by FSI-I and augmented by ruidrogens,
nrunely the corpus luteum (CL) and ovarian primarily testosterone. Interstitial cells of follicles. Follicle-stimulating hormone
the testes, under the influence of LH,

(FSH) is responsible for development of
produce testosterone. Testosterone ruid its
ovarirui follicles ruid synthesis of estrogens.

metabolites are required for development

Once a certain estrogen level is attained,
and function of accessory glands, copulaluteinizing hormone (LH) is released from tory organs, male sex characteristics, and
the ruiterior pituitru-y glruid in spontruiebehavior. For optinlal spennatogenesis, ously ovulating species. This LH release
mrunrnalirui testes must descend into the
triggers ovulation, which is followed by
scrotal cavity; however, steroidogenesis
development of a new CL. The increase of
occurs in testes that remain within the abdoluteal cells parallels rui increase in progestermen, ruid the libido of cryptorchid males is one output. In nonpregnruit polyestrous
usually not impaired. Photoperiod affects
a.nd seasonally polyestrous females, tl1e
both spenn cell fom1ation and steroidogenfunctional and morphologic life of the CL
esis in males of species that have a seasonal
is terminated by endogenous prostaglruireproductive pattern. Semen quality, libido, din (PG) F2a from the uterus. As the CL
ruid mating ability are reduced during the
regresses, a new ovulatory follicle(s)

seasonally anestrous period of females.

develops, which completes the estrous

Function of the testes can be assessed by
cycle. The hormonal changes during the
evaluation of representative semen srunples
estrous cycle can be monitored by
ruid hormone assays. Exaniination ruid
laboratory assay of hormones in blood,
measurement of the testes help predict
milk, or feces. Estrual cycling is continupotential spem1 output and may reveal ous after puberty unless interrupted by
pathologic conditions.

1326

REPRODUCTIVE SYSTEM INTRODUCTION
i@=i!ii FEATURES OF THE REPRODUCTIVE CYCLECycle Duration Species

Age at Puberty Cycle Type

Length
of Estrus

Cattle

10-12 mo,

Polyestrous all year

21 days

18hr

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usually first

(18-24)

(6-24)

bred-14- 15 mo

Sheep

6-9mo

Seasonally polyestrous, 17 days

24-36hr
early fall to winter

(14-20)

Goat

5-7mo

Seasonally polyestrous, 21 days

24-48hr
early fall to late winter

Pig

6-7mo

Polyestrous all year

21 days

40-60hr

(19-23)

Horse

10-24mo

Seasonally polyestrous, -21 days

5-7 days
early spring through

(19-23)

summer

Alpaca

12-18mo

Polyestrous all year in

Not

Up to 36days

N 01th America
applicable

Dog

6-24 mo; earlier Monestrous all year

6-7mo

9days
in smaller

(3-21)

breeds, later in
larger breeds

Cat

4-12mo

Seasonally polyestrous, 14-21 days 6-7days
spring through early fall

The Female Tubular Genital Tract:

female infertility. Applicability of diagnos

Except for the vestibule, which develops
tic methods for detection of uterine and
from the urogenital sinus, the female genicervical abnom1alities depends on species, tal tract is derived from the embryonic
size of the anin1al, and anatomy of the
paramesonephric ducts. Each of the
cervix. Clinical diagnosis is by transrectal
segments is adapted to fulfill its function.

and abdominal palpation, vagi.noscopy,

The oviduct acquires the egg(s ) and moves
hysteroscopy, radiography, and ultrasonogthe resulting zygote(s) into the uterns, while raphy. In small anin1als, laparotomy or its secretion provides a proper environment
laparoscopy may be necessary to assist with
for survival of gan1etes, fertilization, and the
diagnosis. Laboratory diagnostic aids
first few critical days of embryonic life.

include microbiologic and cytologic
interference with motility or secretion leads
examination of exudate or secretion,
to infe1tility. Species variation of the
histologic exan1ination of biopsies,
bicomual, Y-shaped uterus involves the size
endometrial cytology, and hom10ne assays.

of the body and length of horns, which are

The posterior tract, consisting of the
adapted to accommodate species -specific
vagina, vestibule, and vulva, serves as the
munber and form of fetuses and placentas.

copulatory organ and as the last segment of

The cervix provides a protective barrier that the birth canal. It also provides a pathway is relatively effective against ascending
for ascending infections, pai.ticularly when
infections. Morphologic and functional
effectiveness of the vestibulovaginal
integrity of the uterus and cervix are
sphincter or the vulvar labia is lost or
required to establish and maintain
reduced because of trauma, relaxation, or
pregnancy and for parturition. infections
defective confonnation of the perineal
contracted at mating or during parturition
region. Puerperal infections conunonly
and the puerperium are common causes of
involve the entire tubular tract. In addition,

REPRODUCTIVE SYSTEM INTRODUCTION

1327

•M:iifi FEATURES OF THE REPRODUCTIVE CYCLE (continued) First Estrus After

Best 'lime to Breed

Parturition

Comments

Insemination from

20-60days

Ovulation 10-12 hr after end of

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midestrus until 6 hr after
estrus.

end of estrus

18-20 hr after onset of estrus Next fall

Ovulation near end of estrus.

Daily during estrus

Next fall

Many intersexes born in
hornless strains.

Daily during estrus

4--10 days after

Ovulation usually -40 hr after
weaning
beginning of estrus.

Last few days of estrus, just

4--14 (9) days

Ovulation usually 1-2 days
before ovulation; should be
before end of estrus. Double
bred at 2-day intervals
ovulation occurs in -20% of
estrous periods, but twins rarely
progress to term.

When a large, viable follicle Fertile within

Alpacas are induced ovulators.

is present

15---20 days

Second day after ovulation

4-5mo

Proestrous bleeding 7-10 days.

Ovulation usually 1-3 days after
onset of estrus. Ova shed before
first polar body has been
extruded (primary oocyte).

Daily from day 2 of estrus

4--6wk

Induced ovulation 24--48 hr after
breeding.Pseudopregnancy
lasts 40 days. Infertile matings
delay onset of next cycle -45
days.

vestibulovaginal infection perpetuated by
morphologically and functionally to perform
urovagina and pneumovagina may sustain
additional specific functions. The epididychronic infection of the uterus. However, mides are involved in sperm cell maturation
the vestibule and vagina can be inflamed
and storage and in selective absorption of
even when the uterus is normal or pregnant.

abnormal spermatozoa. Ampullae and

Conversely, in closed-cervix pyometra in
accessory sex glands (ie, seminal vesicles,
cows and bitches, the vagina and vestibule
prostate, bulbourethral glands) contribute
may essentially be normal.

to the fonnation of seminal plasma The
size, fom1, and function of the accessory sex

The Male Tubular Genital Tract: In
glands vary among species. The seminal
males, the tubular tract provides a pathway
vesicles and the bulbourethral glands are
for spem1 cells and seminal fluid. It begins
absent in dogs. In bulls, the epididymides
in the testes as the rete testes and efferent
and seminal vesicles are common sites of
ductules, which exit the testes and merge
infection. Epididymitis is also common in
to become the head, body, and tail of the
rams. Prostatic infections, hypertrophy, and
epididymis; it then continues as the ductus
malignancy are found primarily in dogs.

deferens. In mammals, the ductus deferens

Pathologic conditions of the epididymides
ascends into the abdominal cavity via the
can be diagnosed by scrotal palpation or
inguinal ring and passes over the dorsal
ultrasonography in most anin1als. Other
aspect of the bladder to enter the pelvic
diseases or functional disturbances may
urethra. The testes in birds are permanently
require evaluation of one or several semen
retained in the abdominal cavity. The pelvic
samples. Common semen collection
and penile urethras are shared as an outlet
techniques used in veterinary medicine
for semen and urine. Along this pathway,
include artificial vagina, electroejaculation,
certain segments of the tract have evolved
and post-mating recovery from an estrual

1328

REPRODUCTIVE SYSTEM INTRODUCTION
female. The preferred technique varies with
exanlination, genetic testing, and semen
the species and operator preference. The
evaluation). The choice of diagnostic
pelvic accesso1y sex organs can be assessed
methods is detennined by the species as
by transrectal palpation and ultrasonograwell as by the size and temperrunent of the phy in large anin1als and by digital palpation
rulimal. Decisions with regru·d to type ru1cl

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or transabdominal ultrasonography in small
extent of laboratory tests ru·e based on
animals.

history ru1d inforn1ation gained during the
course of clinical exrunination. In each case

INFERTILITY
of reproductive failure, the diagnostic plan
should provide evidence to establish the

Interaction of the CNS, hypothalamus,
role of the female, the male, ru1d the
pituitary gland, gonads, and their target
breeding management progrrun.

organs results in finely coordinated

Reproductive problems arc seldom
sequences of physiologic events that lead to
accomprulied by alarming signs of disease.

estms and ovulation in females and to ejacu

Furthe,more, there is a time interval
lation of fe1tile semen by males. For optimal
between when a failure occms ru1d when it
results, ovulation and deposition of semen
becomes apparent. Examples are inte,vals
into the female genital tract must be closely
between unsuccessful service and return to
synchronized. Failure of any single
estrus or failure to give birth. This lag period
functional event in either sex leads to
may allow recovery, yielding negative results
infertility or sterility.

on exrunination. Interpretation of results

The ultimate manifestation of infertility is
also must account for species clifferences
failure to produce offspring. In polytocous
and, in species with a seasonal reproductive
species, a subnormal number of offspring
pattern, the fact that infertility may be
also con titutes infertility. In females,
physiologic during certain parts of the year.

infe1tility may be due to failure to cycle,
aberrations of the estrous cycle, failw·e to

PRINCIPLES OF THERAPY
conceive, or prenatal and perinatal death of
the conceptus. Major infe1tility problems in

See also SYSTEMIC Pl LARMACOTI IERAPEUTICS OF
males a.re caused by disturbances of the

THE REPRODUCTIVE SYSTEM, p 2606, and
production, transpo1t, or storage of

MANAGEMENT OF REPRODl.!CTION for the various
spennatozoa; aberration of libido; and
species, p 2171, et seq.

paitial or complete inability to mate.

The increasing demands for production

Most (if not all) major infertility problems
efficiency, along with changes in managehave a complex etiology, and several ment systems, have caused a shift in
factors, singly or in combination, can ca.use
therapeutic strategies in several domestic
reproductive failure. Pathogenesis may be
species. Especially for food and fiber
equally complex.

animals, the therapeutic approach of choice
often is a combination of phru-macologic

Diagnostic Approach: Because the
agents and c01Tection of management
female bears the offspring, she reflects
problems targeting the entire herd, with a
either success or failure or reproduction.

decreased emphasis on individual animals.

However, the first diagnostic step (regard

This trend is also reflected in the plioritizaless of the complaint) is to establish the tion of disease prevention and implementaetiologic role of the female and the male.

tion of biosecurity progran1s. The increased

Additionally, each point of hw11ru1
use of hmmonal pha.n11acologic agents for
involvement in the reproductive process,
reproductive management on a whole-herd
such as observation for estms, preservation
basis represents another aspect of this
of semen, and insemination methodology, is
change. Other therapeutic trends in food
a potential source of error. Such human
animals are the result of consumer
errors can be detected or excluded by
concerns regarding antimicrobial ru1d
assessment of performance, with the main
hormone residues in tissues and milk, as
emphasis on techniques and procedures
well as the increasing interest in organic
ru1d their adequacy and quality.

or natural foods.

Diagnostic methods have been developed

In small rulimals, therapeutic strategy has
to test the anatomic and functional
undergone a different but equally dran1atic
sounclness of both sexes. These include the
transfom1ation. The individual animal
signalrnent, a complete history, and clinical
remains the focus of therapeutic efforts, but
exrunination, supported by diagnostic aids
diagnostic techniques and treatments have
such as endoscopy, ultrasonography, and
become increasingly sopllisticated, often
laboratory tests ( eg, hormone assays, microreflecting or even presaging advances in biology, cytology, serology, cytogenetic
hw11an medicine.

CONGENITAL AND INHERITED ANOMALIES OF THE REPRODUCTIVE SYSTEM

1329

More effective therapy for reproductive
and accompanied by careful observation for
diseases comes with the risk of propagating
any problems that may develop with the dan1
a hereditary predisposition for lowered
or fetus.

fertility. However, the heritability of most

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reproductive traits is rather low, so selection

Assisted Reproductive Technologies:

programs aimed at improving fertility require Many of the assisted reproductive a longterm commitment to be successful.

technologies commonly used today had
their origin in veterinary species as either

Pharmacologic Control of Reproduc
research or commercial programs. Artificial
tion: Exogenous horn10ne therapy can be
insemination is commonly used to breed
used to regulate or control reproduction.

cattle, dogs, sheep, goats, pigs, and horses.

This control may take the fonn of suppres

Other technologies in use include embryo
sion or induction and synchronization of
transfer ( see p 2239) and in vitro fertilization reproductive activity. The same hormone
in cattle and horses. Somatic cell nuclear
may be used for both purposes. For example, transfer ( cloning, see p 2075) is more rarely progestogens are used to suppress estrus in
perforn1ed but has been reported for a
the mare, bitch, and queen but are also used
variety of anin1al species.

in the mare, cow, and sow to induce and
synchronize estrus for managed mating

Antimicrobial Treatment: Antimicrobial
programs. Steroid hormones with estroagents, most commonly antibiotics, are genic, androgenic, and progestational effects used for treatment of infections of the are used in a wide variety of applications.

male and female reproductive tracts in

The gonadotropins and GnRH are used to
all species (see also ANTIBACTERIAL AGENTS, alter gonadal function. Examples include
p 2652, et seq). Drug selection should be
superovulation of cattle with FSH, i.nducbased, whenever possible, on microbiologic tion of ovulation in mares with human
culture and sensitivity tests. The dosage,
chorionic gonadotropin (hCG), and stimuroute of administration, and interval lation of testosterone production with
between treatments vary among species.

GnRH for diagnosis of cryptorchidism

In food anin1als, proper withholding times
in dogs and stallions.

must be observed for meat and milk after

PGF2a is used primarily to terminate
antibiotic use.

luteal function. Clinical applications include
induction or synchronization of estrus in

Surgical Treatment: Surgical repair is
polyestrous species; treatment of pyometra
indicated for acquired confonna.tional
in dogs, cats, and cattle; and induction of
damage to the genital system of both sexes.

abortion in luteal-dependent species such

Examples include episioplasty, vestibuloas goats, alpacas, dogs, and cats.

vaginal or cervical cercla.ge, and cesarean

Depending on the species, glucocortisection in females and repair of preputial coids, prostaglandin, and oxytocin, alone or
i.rtjuries in males. Surgical sterilization is also
in combination, can be used to induce or
routinely done, either by gonadectomy in
manage labor. They should be used with
both sexes of most species or by ovariohyscaution at the appropriate ti.me and dosage terectomy in female ca.ts and dogs.

CONGENITAL AND INHERITED ANOMALIES

OF THE REPRODUCTIVE SYSTEM

INTERSEX CONDITIONS
induces downstream factors such as

SRY-box containing gene 9 (SOX9),

Sex detem1ination of the gonads is
anti-Miillerian horn1one, and glial cell lineimportant for development of the sex derived neurotrophic factor in Sertoli cells.

phenotype (internal and external genitalia,

Intersex conditions have been described
secondary characteristics) and sexual
in several domestic anin1al species. True
behavior. A sex chromosome genotype of
hermaphrodites are rare and have both

XY leads to the development of testes due
ova.iian and testicular tissue and exhibit
to the sex-determining region of the Y
anomalies of the external genitalia. The
chromosome (SRY) gene. The SRY gene chromosomal makeup is variable and may

1330

CONGENITAL AND INHERITED ANOMALIES OF THE REPRODUCTIVE SYSTEM
be a chimera, mosaic, or unknown.

have a short vagina that ends blindly

Pseudoherrnaphroditism, often referred to
without communication with the uterus.

as sex reversal syndrome, is more common.

The cervix is absent. The ovruies usually fail

Animals have one or the other type of gonad
to develop and remain small. Vascular
and external genitalia of the opposite sex.

anastomosis of the ch01ionic placentas

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Animals may be XY SRY negative or XX SRY of the two fetuses results in transfer of negative. In horses, the most common type
anti-M(Ulerian honnone from the male to
is 64XY SRY negative. Some cases of sex
the female fetus, which inhibits developreversal are believed to be due to a ment of the female tract.

recessive autosomal gene mutation.

N01mal ru1d freemrutin cattle can be

The most common intersex condition, the
differentiated based on length of the vagina
male pseudohern1aphrodite, has testicular
and on the presence or absence of a cervix.

tissue in the abdominal cavity or beneath

In calves 1-4 wk old, the normal vaginal
the skin in the scrotal region, and external
length is 13--15 cm, whereas in a freema.rtin
genital organs that resemble those of
vaginal length is 5---6 cm. Vaginal length is
females. Miniature Schnauzers, Basset
easily measured by gently inse1ting a

Hounds, and rarely, Persian cats may present
well-lubricated probe with a blunt end into
with pseudohennaphroditism when affected
the vagina. Cytogenetic exaniination can
by persistent paran1esonephric (Miillerian)

demonstrate XX and XY chromosome
duct syndrome. Undescended testes are
patterns in freema.rtins. The interchange of
attached to the uterine horns, and the vasa
cells that occurs in the placental circulation
deferentiaa.re located in the wall of the
between the fetuses can also be demonuterns. There are bilateral oviducts, a strated by detecting two different blood
complete uterus with a cervix, and a cranial
types in a single animal.

po1tion of the vagina. Bilateral scrotal testes
or unilateral or bilateral cryptorchidism may

Other Chromosomal Abnormalities:

be present. Affected anirnals can present

Chromosomal abn01ma.lities (XXY) have
clinically with pyometra, minary tract
been described in males with a.zoospermia
infection, prostate infection, or Sertoli cell
due to hypoplasia of tl1e testes, epididymis,
twnor. The diagnosis is confirmed by
ru1d vas deferens. To1toise-shell or calico
presence of a 78, XY chromosome constitumale cats possess two X chromosomes (XX/
tion, bilateral testes, and the presence of

XXY, XY IXXY, or other chirne1ic or mosaic
all paramesonephric (Miillerian) duct
combination) and are sterile.

derivatives. Androgen-dependent masculinization is that of a norn1al male. Treatment MALE GENITAL ABNORMALITIES
is limited to castration and hysterectomy.

The defect is inherited as an autosomal

Abnormalities of the Testis and
recessive trait in Miniature Schnauzers, and

Epididymis: Cryptorchidism is a failure
both females and males can be carriers.

of one or both testicles to descend into the

Homozygous affected dogs with a descended scrotum. It is seen in all domestic animals; it testis are generally fertile and capable of
is common in stallions and boru·s and is the
transmitting the trait to all offspring.

most common disorder of sexual develop

Polled intersex syndrome is well
ment in dogs (13%). Cryptorchidism is
described in goats. Polled homozygotic
caused by a combination of genetic,
males have decreased fertility due to
epigenetic, and enviromnental factors.

segmental aplasia of the epididymides.

Bilateral cryptorchidism results in sterility.

They are often XX SRY negative.

Unilateral cryptorchidism is more common,
and the male is usually fertile because of

Freemartinism: Freemartinism
spern1 production from the normally
syndrome is well known in cattle but has
descended testicle. The undescended
also been described in sheep, goats, and
testicle may be located anywhere from just
camelids. It causes sterility in females born
caudal of the kidney to within the inguinal
co-twin to males; -92% of all heifers born
canal and can be identified by transrectal or
co-twin to bull calves ru·e sterile. Single-born transabdominal ultrasonography. Abdomifreemartin females have been reported and nal testicles produce male honnones, and
ru·e believed to result from the in utero
cryptorchid animals have normal secondary
death of a male co-twin. These animals
sex chru·acte1istics and mating behavior.

exhibit varying degrees of female-to-male

C1yptorchidectomy is recommended for
sex reversal of the internal and external
all companion animals because of the
genitalia. The tubular genital organs in
suspected inherited nature of the condition
affected animals range from cord.like bands
and predisposition to testiculru· neoplasia
to near-norn1al uterine horns. Freemartins

(seminomas, interstitial cell tumors).

CONGENITAL AND INHERITED ANOMALIES OF THE REPRODUCTIVE SYSTEM

1331

Testicular hypoplasia has been

Hypospadias is an abnormal opening
described in several domestic species and is
of the urethra due to failure or incomplete
associated with chromosomal abnonnaliclosure of the embryonic urethral groove.

ties in some cases. It is common in some
fanilly lines in camelids.

FEMALE GENITAL

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Anorchism is the complete absence of

ABNORMALITIES
development of one or both testes. Unilateral
anarchism has been described in horses and

Ovarian Abnormalities: The most
camelids. In camelids, the kidney ipsilateral
conunon congenital abnormality of the
to the missing testis is also missing.

ovary is ovarian dysgenesis or ovarian

Partial or complete segmental aplasia hypoplasia. Ovarian dysgenesis has been of the structures originating from the
described in several domestic anin1al
mesonephric duct ( epididymis, ductus
species and has been associated "'ith
deferens, ampullae and seminal vesicles)

various chromosomal abnormalities
has been described in bulls. Bilateral

( monosomy X or 1\uner syndrome, trisomy
epididymal hypoplasia has been described

XXX, or Klinefelter syndrome XXY). The
in azoospermic stallions and camelids. In
ova.ties are very small and lack folliculai·
camelids, segmental aplasia of the
activity.

epididymis is often associated with
epididymal and rete testis cysts.

Segmental Aplasia of the Paramesonephric Ducts: The pai·ai11esonephric Abnormalities of the Penis and
ducts ai·e paired embryonic ducts that

Prepuce: Persistent penile frenulum is
develop into the anterior vagina, ce1vix,
not uncommon. Affected bulls are unable to
uterus, and ute1ine tube. Segmental aplasia
protrude the penis from the sheath and, in
of the pai·ai11esonephric ducts results in
most cases, cannot achieve intromission.

anomalies of those organs. The aplasia

Attachment can be minin1al ( eg, 0.5 cm), or

( obstruction) may be located in a segment
the preputial mucosa can be attached the
of the uterine tube, uterine horn, cervix, or
full length of the ventral rap he of the free
vagina. Ovarian development is norn1al.

part of the penis. Genetic association is

Accun1ulation of secretions proxin1al to the
suspected in some breeds. Surgical
obstruction occms secondatily (hydrosalcorrection should not be perforn1ed in bulls pinx, hydrometra, mucometra, colpometra).

intended for seedstock breeding. Many male

Segmental aplasia of the uterus may
foals may appear to have a persistent
involve one horn ( resulting in a condition
frenulum at birth, but the condition resolves
called uterus unicomis), both horns, or only
within a few days. If the condition persists,
part of one horn ( which may result in cystic
correction should not be attempted until
dilatation of the uterine horn anterior to the
the foal is at least 1 mo old.

area of dilatation). Uterus unicomis has

Preputial prolapse occurs due to a lack
been described in several domestic aitirnal
of or a weak preputial retractor muscle in
species. The condition seems to be relatively
polled breeds. The condition is exacerbated
conunon in camelids. These females can
when these breeds are crossed with
become pregnant and Catl}' the pregnancy

Brahman cattle.

to te1m. CeIVical aplasia has been described

Congenital short penis has been
in a few cases but is not as conu11on.

described in bulls and may be associated

Tme persistence of the hymen or
with short retractor penis muscles, which
imperforation of the hyn1en is the most
prevent full erection. Bulls may breed
conunonly reported paramesonephric duct
satisfactorily in the first season, but
anomaly in domestic animals. Fluid
copulation becomes impossible as their
accumulates in the vagina and uterus,
body size increases.

resulting in protmsion of the hymen at the

Short retractor penis muscle may occm vulva when the anin1al is lying down or congenitally or after injury to the penis or
straining. Hyn1enal defects are most
prepuce. Affected bulls have normal libido,
common in white Shorthorn cattle (white
but dming attempted seIVice the penis is only heifer disease).

partially protruded from the sheath and the
ejaculatory thrust does not occm. Failme

Cervical Abnormalities: Double external
of erection in bulls may be a congenital
os of the cervix is due to a failme of the
condition but is generally a sequela of tramna
paramesonepluic ducts to fuse. It may
and/or hematoma of the penis.

present as a band of tissue caudal to, or in,

Congenital vascular shunts have been
the external os of the cervix. In other cases,
described in bulls with partial erection or
there is a trne double external os opening
erection failme.

into a single caudal part of the ceIVical

1332

CONGENITAL AND INHERITED ANOMALIES OF THE REPRODUCTIVE SYSTEM
canal. Affected cows usually conceive
camelids. In extreme cases, the labia are
normally. Rarely, a true double cervix, with
completely fused. The condition is believed
a complete septum between the two cervito be due to an autosomal recessive gene.

cal canals, each opening into its respective

Rectovaginal constriction is a

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uterine horn (uterus didelphys), occurs.

connective tissue disorder of Jersey cattle
characterized by stenosis of the anus and/or

Vaginal and Vulvar Abnormalities:

vestibulovaginal sphincter. Bilateral

Vaginal stricture or vestibulovaginal
stenosis of the milk veins has also been
hypoplasia has been described in mares,
described and results in udder edema and
dogs, and camelids.

ischemic necrosis. It is a simple autosomal

Gartner's ducts, located beneath the
recessive defect. Anal stenosis renders
mucosa of the floor of the vagina, may
transrectal palpation difficult. Affected
develop multiple cysts, which are generally
females experience severe dystocia The
of no clinical significance.

prevalence of the disease has been

Vulvar atresia or hypoplasia ( atresia
substantially reduced because of idenvulvi) has been described primarily in tification of carrier bulls.

ABORTION IN LARGE ANIMALS

Abortion is the termination of pregnancy
in fresh condition, along with maternal
after organogenesis is complete but before
serum. The placenta and fetus should be
the expelled fetus can survive. If pregnancy
cleaned with water or saline, packed in
ends before organogenesis, it is called early
clean plastic bags, chilled (but not frozen),
embryonic death. A dead, full-term fetus is a
and rapidly transported to the diagnostic
stillbirth (its lungs are not inflated). Many
laboratory. In most cases, autolysis
etiologies of abortion also cause stillbirths,
proceeds at a much slower rate in fetuses
munmtification, and weak or deformed
than in carcasses of animals born alive. If
neonates.

chilled as soon as possible, most fetuses will

The etiologic diagnosis of abortion in
be suitable for exanlination, even if they do
livestock is a difficult and often frustrating
not reach the laboratory for 1 -2 days. Fetal
task. The diagnostic success rate is
pigs, sheep, and goats are usually small
relatively low and variable: 300/o-40% for
enough to transport or ship whole with the
bovine, 60%--65% for ovine, 35o/o-4()0,6 for
placenta. If there are multiple fetuses, three
porcine, and from <100,6 to 900,6in equine
to five should be submitted with their
abortion cases submitted to diagpostic
placentas. It is best to submit calves and
laboratories. The diagnostic success rate in
foals whole, but in many cases it is more
camelids is very low except in outbreaks.

convenient to perform a necropsy and

Nun1erous factors complicate diagnosis.

collect samples for submission.

Often, abortion follows initial infection by

The specimens routinely used for testing
weeks or months, so the causative agent is
vary somewhat between diagnostic
no longer apparent when abortion occurs.

laboratolies, but a basic set of samples that

Expulsion may follow fetal death by hours
will allow thorough exanlination includes
or days, with lesions obscured by autolysis.

stomach or abomasal contents; heart blood

Fetal membranes and the aborted fetus are
or fluid from a body cavity; unfixed lung,
usually contanlinated by environmental
liver, kidney, and spleen (some laboratories
agents before exanlination. Many sporadic
also request tissues such as thyroid glands,
abortions are likely the result of noninfecthymus, heart, brain, abomasurn, and tious (ie, toxic or genetic) causes, about
stomach); placenta (if available); and dam's
which much less is known than infectious
serum. These should be submitted in sterile
causes; many diagnostic laboratories are
containers to allow for microbiologic
not equipped or staffed to deal with these
cultures. Because they are always
causes of abortion.

contanlinated, placentas should not be

Another problem in detennining the cause mixed with other tissues.

of abortions is improper or inadequate

Representative samples of the
specimen selection and handling. The best
following should also be submitted in 10%
specimen is the complete fetoplacental unit
buffered formalin for histopathologic

ABORTION IN LARGE ANIMALS

1333
examination: lung, liver, heart, kidney,
abortion. Instead, veterinarians should
spleen, brain, skeletal muscle thyroid
become concerned if fetal loss is >3%--5%
adrenal glands, intestines, and placenta
per year or per month.

(seep 1584). In a large majority of cases

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grnss lesions other than signs of autoly;is Noninfectious Causes (mcreased pleural and peritoneal fluid
and blood-tinged subcutaneous edema)

The actual incidence of abortions in cows
are not present. However, if lesions are
due to genetic factors is unknown. Some
found, fresh and formalin-fixed samples
genetically caused abortions may not have
of affected tissues should be included.

phenotypically recognizable lesions. Most

Most agents, especially bacteria and
lethal genes cause early abortion or early
fungi, infect the placenta and thus gain entry embryonic death.

mto the anuuotic fluid, which is swallowed

Vitanlins A and E, selenimn, and iron have
by the fetus. Stomach contents can be
been implicated in bovine abortions but
obtained aseptically, making it the best
documentation based on experinlen'ts is
specimen for detection of fungi and most
available only for vitanlin A.

bacteria. Isolation from the stomach

Heat stress causes fetal hypotension
contents is much easier than from the
hypoxia, and acidosis. High maternal
placenta, which is always heavily contamitemperature due to pyrexia may be more nated. Lungs, liver, spleen, and kidneys are
important than environmentally induced

�so good for culture. Several agents ( eg,
heat stress.

fungi, Chlamydia, Coxiella) primarily

. Although severe trauma may rarely result
affect the placenta; failure to include
m abort10n (the bovine fetus is well
placenta decreases the probability they will
protected by the an1niotic fluid), fanners
be identified. Fetuses sometimes produce
undoubtedly blan1e too many abortions on
antibodies to certain agents ( eg, bovine viral the cow "getting bumped."

diarrhea vims, Neospora spp, Leptospira A nwnber of toxins can cause abortion in
spp ), and fetal semm or fluid from a body
cows. Ponderosa pine needles can cause
cavity can be tested for antibodies. The
abortion if ingested in the last trimester; the
presence of precolostral antibodies is
cows may become moribund after delivery
evidence of in utero exposure.

and hemorrhage excessively. The main

A single antibody titer in the dam rarely
abortifacient compounds in Ponderosa pine
provides evidence of ab01tion caused by a
needles are isocupressic acid and labdane
particular agent unless background herd
resin. Locoweed (Oxytropis or Astragalus titer levels are known. High maternal titers
sp) contains an indolizidine alkaloid that
may as likely be the reason an animal did
can affect the corpus lutewn, chorioallannot abo1t due to that agent, but absence of t01s, and neurons, resulting in abortion or
a titer can be used to exclude an agent.

defornlities. Broomweed (Guttierrezia

Antibody titers to agents with control
microcephala) ingestion can also cause
programs ( eg, Brucella abortus, pseudoraabortion, as can coumarins from rat poison, b1es VllUS) are always significant, even if the
many grasses, or moldy sweet clover.

abortion was caused by something else.

Sodiun1 iodide, IV, has been contraindicated

Demonstration of a 4-fold increase in
in pregnant cows, but no abortions or
antibody titer is required to prove active
adverse effects occurred in pregnant cows
infection by a specific agent. Often, abortion treated with a single high dose in some occms weeks or months after initial infection studies. Mycotoxins, especially those with of the dam, and her titer is stable or declining estrogenic activity, have been implicated in at the time of abortion. Paired semrn san1ples bovine abortions. Nitrates or nitrites have obtained 2 wk apart from l()OA, of the herd or
also been incriminated, but experimental
a minimum of 10 animals often demonstrate
evidence is controversial.

seroconversion and provide evidence of
active infection in the herd.

Infectious Causes

Neosporosis: Neospora caninum is

ABORTION IN CATTLE
found worldwide and is the most common
cause of abortion in dairy and beef cattle in

See ai,so MANAGEMENT OF REPRODUCTION: CATTLE, many parts of the USA. Dogs and coyotes
p 2171.

are definitive hosts for N caninum and can

Given the low diagnostic success rate, the
be the source of infection. Abortion can
high cost of laborat01y work, and the low
occur any time after 3 mo of gestation but is
profit margin in both the beef and dairy
most common between 4 and 6 mo of
industries, veterinarians should not attempt
gestation. Neospora can be associated with
to make an etiologic diagnosis in every
sporadic abortions or abortion stom1S, and

1334

ABORTION IN LARGE ANIMALS
repeat abortions in cows have been

Infectious Bovine Rhinotracheitis (IBR,
reported. Most infections result in an

Bovine Herpesvirus 1 ): Infectious bovine
asymptomatic congenitally infected calf.

rhinotracheitis (IBR) is a major cause of

Some infected calves are born with paralysis
viral a.bmtion in the world, with abortion
or proprioceptive deficits. Cows a.re not
rates of 5%---600/o in nonvaccinated herds. The

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clinically ill, and placental retention is not
virus is widespread, causes latent infections,
common. The fetus is usually autolyzed or,
and can recrudesce; therefore, any cow with
in a few cases, mununified and rarely has
a positive IBR titer is a possible carrier. The
gross lesions. Microscopically, nonsuppura virus is carried to the placenta in WBCs; over tive inflammation is common in the bra.in,
the next 2 wk to 4 mo, it causes a placentitis,
heart, and skeletal muscles. Organisms can
then infects the fetus and kills it in 24 hr.

be identified in these tissues and the kidneys

Abortion can occur any time but usually is
by imrnunohistochemical staining and PCR.

from 4 mo to tern1. Autolysis is consistently

Many late gestation fetuses have precolospresent. Occasionally, there are small foci of tral antibodies. They remain infected for
necrosis in the liver, but in a large majority
years and possibly for life. Vertical
of cases tl1ere are no gross lesions in the
transmission is common. During pregnancy,
placenta or fetus. Microscopically, small foci

Neospora organisms can become activated
of necrosis with minimal inflammation are
and infect the fetus. This is thought to be the
consistently present in the liver. Necrotizing
most common source of infection. There is
vasculitis is common in the placenta.

no treatment. Strict hygiene to prevent fecal

Diagnosis can be made by immunologic
contamination of feed by dogs or coyotes
staining of tl1e kidney, lung, liver, placenta,
may aid in prevention. A conunercial
and adrenal glands. IBR virus can be isolated
vaccine is available. (See also p 663.)

from -500/oof infected fetuses (most
successfully from the placenta). In most

Bovine Viral Diarrhea (BVD): In several
cases, maternal titers have peaked by the
surveys, BVD was the most commonly
time of abortion. In abortion storms, rising
diagnosed virus in bovine abortion cases.

titers can often be demonstrated in

The pathology of BVD in the developing
herdmates. Control is by herd vaccination;
fetus is complex. Infection before inseminaintra.nasal, modified-live virus, and killed tion or during the first 40 days of pregnancy
vaccines are available. (See also p 1434.)

results in infertility or embryonic death.

Infection between 40 and 125 days of

Leptospirosis: The pathogenic leptopregnancy results in birth of persistently spires were formerly classified as serovars
infected calves if tl1e fetus survives. Fetal
of Leptospira inte-rrogans, but they have
infection during the period of organogenesis been reclassified into 7 species with >200

(100-150 days) may result in-congenital
recognized serovars. Leptospira serovars
malforn1ations of the CNS ( cerebellar

Grippotyphosa, Pomona, Canicola, and
hypoplasia, hydrancephaly, hydrocephalus,
lcterohaemorrhagiae usually cause
microencephaly, and spinal cord hypoabortions in the last trimester, 2-6 wk after plasia). Congenital ocular defects have also
maternal infection. Serovar Hardjo is host
been seen ( cataracts, optic neuritis, retinal
adapted to cattle and can establish lifelong
degeneration, microphthalmia). After 125
infections in the kidneys and reproductive
days of gestation, BVD may cause abortion,
tracts. In addition to third trin1ester
or the fetal immune response may clear the
abortions, serovar Ha.rdjo reduces
virus. Diagnosis is by identification of BVD
conception rates in carrier cows and
virus by isolation, immunologic staining,
cows bred to carrier bulls.

PCR, or detection of precolostral antibodies

Although dams may show clinical signs
in aborted calves. The virus is present in a
of leptospirosis, most abortions are in otherwide variety of tissues, but the spleen is the wise healthy cattle. Abortion rates vary
tissue of choice. Rising antibody titers to
from 5o/<>-400/o or more. The leptospires

BVD in aborting animals or herdmates is
cause a diffuse placentitis with avascular,
diagnostic of recent infection. BVD virus is
light tan cotyledons and edematous,
immunosuppressive and is found in many
yellowish intercotyledona.ry areas. The
fetuses infected by other agents ( eg,
fetus usually dies 1-2 days before expulsion
bacteria., N canimim). Outbreaks of
and therefore is autolyzed. Occasionally,
abortions by organisms that normally cause
calves are born a.Jive but weak. Fetuses
sporadic abo1tion should raise suspicion of
infected with serovar Pomona may show
possible concurrent BVD virus infection.

icterus. There are no specific lesions, but

Prevention should focus on removal of
placenta and fetus should be submitted to
persistently infected cattle and herd
the laboratory for fluorescent antibody
vaccination. (See also p 267.)

staining or PCR testing for Leptospira.

ABORTION IN LARGE ANIMALS

1335

Although maternal titers are probably

Brucellosis is a serious zoonosis and a
waning by the time of abortion, an initial
reportable disease, and the appropriate
titer of> 1:800 may be suspicious. Approxiauth01ities should be contacted. (See mately one-third of cows aborting because
also p 1348.)

of serovar Hardjo have titers of <1:100 at the

VetBooks.ir
time of abortion. Cows infected with

Mycotic Abortion: Fungal placentitis
serovar Hardjo can shed the organism in
due toAspergillus sp (septated fungi,
urine throughout life. For other serovars,

600/o-80% of cases), or to Mucor sp, Absidia, the dam's urine can be cultured or examined Rhizopus sp, and a few other nonseptated for leptospires within 2 wk of abortion.

fungi, is an important cause of bovine

For control, sources of infection ( such as
sporadic abortion. Abortions occur from 4
feed or water contaminated by dogs, rats, or mo to term and are most common in winter.

wildlife) should be identified and elimi

It is believed the fungi gain entry through
nated. Vaccination with a five-way bacterin
the oral or respiratory tracts and travel
every 6 mo provides good protection against hematogenously to the placenta. Placentitis serovars Giippotyphosa, Pomona, Canicola,
is severe and necrotizing. Cotyledons are
and Icterohaemorrhagiae but does not
enlarged and necrotic with turned-in
protect against infection and renal shedding
margins. The intercotyledonary area is
by serovar Hardjo. New monovalent serovar thickened and leathery. Adventitious Hardjo vaccines that prevent infection, but
placentation is common. The fetus seldom
do not cure existing infections, are
is autolyzed, although it may be dehydrated;
available.

-300A, have gray ringworm-like skin lesions

The following treatments have been
principally involving the head and
found to eliminate the renal earner state:

shoulders. The diagnosis is based on the
a single injection of oxytetracycli.ne (20
presence of fungal hyphae associated with
mg/kg, IM), a single injection of tilmicosin
necrotizing placentitis, dennatitis, or

(10 mg/kg, SC), ceftiofur (5 mg/kg/day, IM,
pnewnonia. Fungi can also be isolated from
for 5 days or 20 mg/kg/day, IM, for 3 days),
the stomach contents, placenta, and skin
or amoxicilli.n ( 15 mg/kg, IM, two injections
lesions. Isolation must be correlated with

48 hr apart).

microscopic and gross lesions to exclude

Leptospirosis is zoonotic, and urine and
contamination after abortion.

milk of dams may be infective for up to

For control, moldy feed should be

3 mo, except for Hardjo, in which case cows
avoided. (See also p 3005.)

can be infective for life if not treated. (See
also p 646.)

Trueperella pyogenes: True'J)erella (Arcanobacterium) pyogenes causes sporadic Brucellosis: Brucellosis (Bang's disease)

abortion at any stage of pregnancy. Rarely,
is a threat in most count!ies where cattle are the incidence in a herd may reach epizootic raised. ln the USA, active control programs,
levels. The bacte!ium is present in the
including test, slaughter, and heifer
nasopharynx of many healthy cows and
vaccination, have greatly decreased its
in abscesses. It is not normally present,
incidence. Brucellosis causes abortions in
even as a contaminant, in fetuses or fetal
the second half of gestation (usually -7 mo), membranes, and isolation is almost always and -800A, of unvaccinated cows in later
significant, It gains entry to the bloodstream
gestation will abort if exposed to Brucella
and causes an endometritis and placentitis,
a,bortus. The organisms enter via mucous
which is diffuse with a reddish brown to
membranes and invade the udder, lymph
brown color. The fetus is usually autolyzed,
nodes, and uterus, causing a placentitis,
with fibrinous pericarditis, pleuritis, or
which may be acute or chronic. Abortion or
peritonitis possible.

stillbirth occurs 2 wk to 5 mo after initial

Bronchopnewnonia may be evident on
infection. Affected cotyledons may be
histopathology, but T pyogenes is best
nonnal to necrotic, and red or yellow. The
cultured from placenta or abomasal
intercotyledonary area is focally thickened
contents. Abortion is usually sporadic,
with a wet, leathery appearance. The fetus
and no effective bacterin is available.

may be n01mal or autolytic with bronchopneurnonia. Diagnosis can be made by Trichomoniasis: Tritriclwmonas foetus
maternal serology combined with
infection causes a venereal disease that
fluorescent antibody staining of placenta
usually results in infertility but occasionally
and fetus or isolation of B abortus from
causes abortion in the first half of gestation.

placenta, fetus (abomasal contents and

Placentitis is relatively mild, with hemorlung), or uterine discharge. Prevention is rhagic cotyledons and thickened intercotyby caJfhood vaccination of heifers.

ledonary areas covered with flocculent

1336

ABORTION IN LARGE ANIMALS
exudate. The placenta is often retained, and

Chlamydiosis: Chlamydia abortus, the there may be pyometra. The fetus has no
cause of enzootic abortion of ewes, causes
specific lesions, although T foetus can be
sporadic abortion in cattle. Most abortions
fow1d in abomasal contents, placental
occur near the end of the last trin1ester, but

VetBooks.ir
fluids, and uterine discharges. Wected cows they can occur earlier. Placental lesions typically clear the organism within 20 wk,
consist of thickening and yellow-brown
but bulls, especially those infected after 3 yr
exudate adhered to the cotyledons and
of age, can become lifelong carriers. There
intercotyledonary areas. I -Iistologically,
is no legal, effective treatment for individual
placentitis is consistently present, and
animals. Herd treatment is based on
pnewnonia and hepatitis can be found in
identifying and segregating pregnant
some cases. C abortus can be identified
females from "at-1isk" females for �5 mo and by exan1ination of stained smears of the
by identifying and culling all infected bulls.

placenta or by ELISA, fluorescent antibody

Prevention is by artificial insemination or
staining, PCR, or isolation in embryonated
natural insemination using noninfected
chicken eggs or cell culture. Organisms can
bulls. A killed, whole-cell vaccine is
often be identified in the lungs and liver but
available for use in cows. (See also p 1384.) not as consistently as in the placenta. There
are no vaccines for cattle, although they

Campylobacteriosis: Campylobacter
are produced for sheep (seep 1338). The
fetus venerealis causes venereal disease
bacte1iwn is zoonotic, occasionally
that usually results in infertility or early
producing life-threatening disease and
embryonic death but occasionally causes
abo1tion in pregnant women.

abortion between 4 and 8 mo of gestation.

C fetus fetus and C jejuni are transmitted by

Ureaplasma diversum Infection: Urea
ingestion and subsequent hematogenous
plasma diversmn is a common inhabitant
spread to the placenta. Both cause sporadic
of the vagina and prepuce of cattle that also
abortions, usually in the last half of gestation. causes abortions. Abortions are usually The fetus can be fresh with partially
single, but severe outbreaks occur on
expanded lungs or severely autolyzecl. Mild
occasion. The infection may also result in
fib1inous pletuitis and peritonitis may be
stillbirths and bilth of weak calves. Most
noted, as well as bronchopnewnonia.

fetuses are aborted in the third trimester

Placentitis is mild with hemotThagic
and are well prese1ved. The cows are not
cotyledons and an edematous intercotyleick, but retained placentas are conm10n.

donary area Campylobacter spp can be

Placentitis and a necrotic an1niotic membrane
identified by darkfield examination of
are common features. The intercotyledonabomasal contents or culture of placenta or ary areas are usually thickened and
abomasal contents. Isolation and identificasometimes contain areas of fibrin deposition of the species involved is in1portant if tion and hemorrhage. There are no gross
vaccination is to be instituted. Venereal
lesions in the fetus. Microscopically, there is
can1pylobacteriosis can be controlled by
nonsuppurative placentitis and pnewnonia
artificial insemination and vaccination.

characterized by accwnulations of lympho

Campylobacter spp are zoonotic, and
cytes around bronchi and by diffuse alveolitis.

C jejuni is an important cause of enteritis Diagnosis is by isolation of U diverswn
in people. (See also p 1347.)

from the placenta, lungs, and/or abomasal
contents.

Listeriosis: Listeria monocytogenes can cause placentitis and fetal septicemia.

Epizootic Bovine Abortion (Foothill

Abortions are usually sporadic but may

Abortion): Epizootic bovine abmtion is
affect 100/o--200A, of a herd. Abortion is at any
localized to the footl1ill region surrounding
stage of gestation, and the dam may have
the Sacran1ento/San Joaquin Valley and the
fever and anorexia before the abortion;

Eastern Sierra Nevada range of California.,
retained placenta is common. The fetus

Oregon, and Nevada. Epizootic bovine
is retained for 2-3 days after death, o
abortion usually causes a protracted
autolysis may be extensive. Fibrinous
abortion storm affecting primarily heifers or
polyserositis and white necrotic foci in
cows recently introduced to the geographic
the liver and/or cotyledons are common.

region; however, abortion can occur 3-5 mo

Diagnosis is by culture of Li leria from
after leaving tl1e endemic area. Abortion is
fetus or placenta. There is no available
usually in the last tJ.irnester, and rates may
bacterin. Listeri.osis is a repo1table disease
be as high as 600Ai. The animals abort
in many areas and is a serious zoonosis,
without illness, and the fetus is seldom
with spread possible through improperly
autolyzed. Although the etiologic agent
pastewized milk. (See also p 656.)

has not been definitively detern1ined, it is

ABORTION IN LARGE ANIMALS

1337
transmitted by the argasid tick Ornitho
causes abortion in experimentally
doros c01iaceus and is believed to be an
inoculated seronegative cattle, but is
unnamed bacterium in the Myxobacteria
seldom, if ever, diagnosed in field cases of

VetBooks.ir
family (order Myxococcales). The aborted
abortion. Occasionally, Salmonella spp
fetus may have hepatomegaly, splenomegcause abortion stonns. The cows are aly, and generalized lymphomegaly.

usually sick, and the fetuses and placentas

Microscopically, there is marked lymphoid
are autolyzed and emphysematous.

hyperplasia in the spleen and lymph nodes

Salmonellae can be isolated from the
and granulomatous inflammation in most
abomasal contents and fetal tissues and
organs. Fetal IgG is increased. Cows seldom
from ute1ine fluids and the dams' feces.

abort in subsequent pregnancies, and

Mycoplasma spp, Histophilus somni,
heifers are often exposed to endemic areas
and a wide variety of other bacteria can
before breeding age in an effort to prevent
also cause sporadic abortions in cattle.

abortions.

Schmallenberg virus, discovered in Europe
in 2011, belongs to the Sirnbu serogroup

Bluetongue: Bluetongue is caused
and has been associated with infertility,
by an Orbivirus with 24 serotypes and is
abortion, and fetal malfom1ation in several
transmitted by biting midges of the genus
nuninant species.

Culicoides. Historically, bluetongue
occun-ed from approximately latitude 35°8

ABORTION IN SHEEP
to 40°N, except in the western USA, where
it occurs to 45°N. After introduction of an

See also MANAGEMENT OF REPRODUCTION: SHEEP, attenuated, live virus serotype 10 vaccine
p 2212.

in the 1950s, abortion, mummification,

Abortion in ewes, as in cows, is not always
stillbirth, and the birth of live offspring with
easily diagnosed. Although many of the

CNS malfom1ations occun-ed in cattle and
toxins U1at cause abortion in cows also
sheep. Since then, multiple bluetongue
cause problems in ewes, others such as Vera
serotypes have been identified as causes
tium calfforniciim and kale seem unique
of similar reproductive losses in cattle and
to the ewe. Subten-anean clover (Trifolium
sheep. Attenuation of bluetongue virus can
subterraneum) is a co nun on cause of early increase its ability to cross the placenta.

embryonic death and abortion in sheep. The

There is evidence that before 2007,
major infectious agents ca.using abortions in
reproductive losses were caused by
sheep are Campylobactersp, Chlamydia sp,
attenuated bluetongue vaccine viruses,

Toxoplasma sp, Listeria sp, Brucella sp, either by vaccination of pregnant animals

Salmonella sp, border disease virus, and
or by spread of vaccine virus in nature by

Cache Valley virus.

Culicoides spp.

In 2006, serotype 8 bluetongue virus

Campylobacter spp Infection
appeared, spread, and became endemic

(Vibriosis): Infection with Campylobacter across northwestern Europe (north of
fetus fetus, C jejuni jejuni, and C lari 50°N), where bluetongue was previously
results in abortions in late pregnancy or
unknown. Beginning in 2007, abortions
stillbirths. The route of infection is oral.

and birth of "dummy" calves with brain

Ewes may develop metritis after expelling
malformations occurred in bluetongue

U1e fetus. Placentitis occurs with hemorinfected herds; affected calves were rhagic necrotic cotyledons and edematous
documented to have been infected in utero.

or leathery intercotyledona.ry areas. The

Since then, many such cases have been
fetus is usually autolyzed, with 400A, having
reported. Diagnosis is by identification of
orange-yellow necrotic foci ( 1 -2 cm
precolostral antibodies to bluetongue or
diameter) in the liver. Fetuses may have
identification of the virus by PCR. Brain,
accun1ulated serosanguineous fluid in the
spleen, and whole blood are the prefen-ed
thoracic and peritoneal cavities. Diagnosis
samples from fetuses and neonates for PCR.

relies on finding Campylobacter organisms

Control of bluetongue is by vaccination
in darkfield or fluorescent antibody
and management procedures to reduce
preparations or by isolation from fetal
exposure to biting midges. Modified-live and abomasal contents, liver, a.nd lungs, or from inactivated vaccines are available, but their
placental smears or in uterine discharge.

availability and use varies between

Identification of the species involved is
countries. (See also p 738.)

important, because in some areas C jejuni
is as common as C fetus, and some vaccines

Other Causes of Abortion: Aka.bane
do not include C jejuni. Strict hygiene is
virus (where present) causes abortion and
necessary to stop an outbreak. Use of
fetal anomalies. Parainfluenza-3 virus
tetracyclines may help prevent exposed

1338

ABORTION IN LARGE ANIMALS
ewes from aborting. However, many
dian·hea (BVD) virus and classical swine
isolates may be resistant to tetracycline.

fever (hog cholera) virus. Infection of

The disease tends to be cyclical, with
susceptible anjrnals occms after introducepizootics occurring every 4-5 yr; therefore, tion of persistently infected anin1als.

vaccination progran1s, which help prevent

Venereal trans1mssion from shedding rams

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outbreaks, should be consistently practiced. is possible. Abortion can occm at any stage C jejimi is zoonotic and is a common cause
of gestation. There are no clirucal signs in
of enteritis in people.

the dam, except for a mild fever and
leukoperua in a few cases. Live infected

Enzootic Abortion of Ewes (EAE):

fetuses usually are undersized, and tlley

Chlamydia, abortus is the cause of EAE,
often have congerutal tremors and an
which is characterized by late-tem1
abnormally hairy coat (hairy shaker lambs).

abortions, stillbirths, and weak lambs. C

Diagnosis is by identification of border
peco1urn is tile cause of chla.mydial artllritis disease virus in tile placenta or fetal tissues
and coajunctivitis of sheep. EAE occurs

(kjdneys, lungs, spleen, thyroid glands,
worldwide, except for in Australia and New
abomaswn) by fluorescent antibody

Zealand, and is most important in intenstaining, virus isolation, or demonstration sively managed sheep. Abortions occur
of precolostral antibodies. No vaccines are
dwing tile last 2-3 wk of gestation regardavailable. Inactivated BVD virus vaccines less of when infection occurs, and tile
are sometimes used in sheep, but their
fetuses are fresh witl1 mi.Illl\lal autolysis.

effectiveness is unproved. (See

Gross lesions in tile fetus are rare and may
also p 622.)

include ascites, lymphadenopatlly, and
liver congestion. There is placentitis witll

Cache Valley Virus: Cache Valley virus
necrotic, reddish brown cotyledons and
is a mosqwto-transmitted cause of inferthickened brown intercotyledonary areas tility, abortions, stillbirths, and multiple
covered by exudate. Chlan1ydial elementary
congerutal abnormalities in sheep. The
bodies can be found by exanlination of
virus is endentic in most parts of tile USA,

Gimenez- or Giemsa-stained smears of tile

Canada, and Mexko. Often, tllere are
placenta or vaginal discharge, but tl1e
epizootics affecting sheep over a wide
orgarusms cannot be differentiated from
geographic area tl1at can include several

Co.xiella burnetii, which occasionally
states. The most noticeable effects are
causes abortion in sheep.

stillborn lambs and the birth of live lambs

Definitive diagnosis is by identification of
witll congerutal abnormalities affecting

C abortus by ELISA, fluorescent antibody
tile CNS and musculoskeletal system.

staining, PCR, or isolation. Ewes seldom

Hydranencephaly, hydrocephalus, cerebral
abort more tllan once; but they remain
and cerebellar hypoplasia, arthrogryposis,
persistently infected and shed C abortus
scoliosis, torticollis, and hypoplasia of
from their reproductive tract for 2-3 days
skeletal muscles are common. Infection
before and after ovulation. Rams can be
before 32 days of pregnancy results in early
infected and transntit tile orgarusm
embryoruc deatl1. Infection between 32 and
venereally. Control consists of isolating

37 days of pregnancy results in musculoall affected ewes and lambs and treating skeletal and CNS lesions. Infection between
in-contact ewes witll long-acting oxytetra37 and 48 days results in primarily musculocycline or oral tetracycline. C abortus skeletal lesions. At tile time of abortion or
bacterins are available and reduce
birtl1, tile virus is usually no longer viable,
abortions. In parts of Europe, a modifiedand diagnosis is by demonstration of live vaccine is available for use.

antibodies in precolostral serun1 or body

C abortus is zoonotic, but hwnan cases
flwds. Vaccines are not available.

are rare. All have involved pregnant women,
who developed life-threatening illness.

Toxoplasmosis: Toxoplasma gondii is a Only in a few cases in which tile fetus was
major cause of abortion in small ruminants
delivered by cesarean section did tile infant
tllroughout tile world. Ingestion of
survive. Pregnant women should not work
sporulated coccidian oocytes early in
witll pregnant sheep, especially if abortions
gestation results in resorption or mun111illiare occmring.

cation; if ewes contract the disease late in
gestation, abortions or perinatal deatl1s

Border Disease: Border disease occurs
occur. Ewes do not usually appear sick. In
worldwide and is an important cause of
an outbreak, tllere is usually a wide range in
embryoruc and fetal deatl1S, weak lambs,
gestational age of aborted fetuses. In most
and congerutal abnonnalities. It is caused
cases tllere are no gross lesions, but in a few
by a pestivirus closely related to bovine viral cases there are distinct, small, white foci,

ABORTION IN LARGE ANIMALS

1339

1--3 mm in diameter, in some cotyledons.

Bluetongue: Bluetongue virus infection

The fetal brain often has focal areas of
is a cause of abortion, fetal mummification,
nonsuppurative inflammation on histology.

stillbirth, and congenital brain malfom1a

Fetal serology (indirect hemagglutination
tion in lambs. The clinical syndrome,
inhibition, latex agglutination, or fluoresserotypes involved, and diagnosis are the VetBooks.ir
cent antibody) may also be used. Once
san1e as for cattle (seep 1337). Most, if not infected, ewes are inm1une, so running
all, reproductive failure is caused by
unbred ewes with aborting ones may allow
attenuated vaccine viruses rather than field
them to develop immunity. 'l}ansplacental
viruses. Serotype 8 bluetongue virus has
transmission is possible. Preventing
been documented as a cause of abortions
contamination of feed by cat feces may
and congenital brain malformations in cattle
help reduce exposure. Toxoplasmosis
in northwestern Europe, and this is widely
is a zoonosis. (See also p 685.)

regarded as the first confinned outbreak of
transplacental transmission of wild-type

Listeriosis: Abortion caused by Listeria bluetongue virus in ruminants. Published
monocytogenes in ewes usually occurs in
studies from Europe have not found
late gestation. Aborting ewes show variable
evidence that serotype 8 is a significant
clinical signs, including fever, depression,
cause of fetal infection in sheep. However,
and anorexia, and some may succumb to
there are a few anecdotal reports of
septicemia. There is some necrosis of
abortions and congenital anomalies in
cotyledons and the intercotyledonary areas,
sheep attributed to serotype 8, and
and the fetus is usually autolyzed. Mummifiexperin1entally the virus has been cation is possible. The fetal liver ( and
demonstrated to be capable of crossing
possibly lung) may have necrotic foci, 0.&-1
the ovine placenta. The virus should be
mm in diameter. Diagnosis is by culture.

considered a potential problem in sheep

(See also p 656.)

until more is known.

Control of bluetongue is by management

Brucellosis: The major impo1tance of
procedures to reduce exposure to biting

Brucella ovis is as a cause of contagious
midges and vaccination. Inactivated and
epididymitis in rams. On a flock basis,
modified-live vaccines are available and
brucellosis results in infertility, but it also
widely used, but the availability of each
causes late-term abortions, stillbirths, and
varies between countries. Modified-live
birth of weak lambs. B melilensis is rare in vaccines are predominantly used in regions
the USA but causes abortion in areas where
with a long history of bluetongue, such as
it is found. B abortus occasionally causes
the USA and Africa, but their use is
abortion in sheep. Brucella abortions occur controversial. If used, the vaccine should
late in gestation, resulting in placentitis with not be given to pregnant ewes. Also, the edema and necrosis of the cotyledons and
vaccine should not be given when
thickened, leathery intercotyledonary areas. Culicoides spp are active, because tl1ey Many fetuses aborted due to B ovis are alive can and do transmit the vaccine virus to at the beginning of parturition, although
unvaccinated animals, including pregnant
fetuses can be mununified or autolyzed.

females. Bluetongue virus has a segmented

Most fetuses aborted due to B melilensis
genome, and reassortment viruses are
or B aborlit.S are autolytic. Culture of the readily produced in animals simultaneously
placenta, abomasal contents, and the dam's
infected or vaccinated with more than one
vaginal discharge are diagnostic. A vaccine
serotype. (See also p 738.)

for B melitensis is available in some
count1ies. B melilensis and B aborlus

Other Causes of Abortion: Aka.bane
are zoonotic. (See also p 1348.)

virus (where present) causes abortion and
congenital anomalies in sheep and is a

Salmonellosis: Salmonella, Abortusovis, differential diagnosis for Cache Valley

S Dublin, S Typhinmrium, and S Arizona virus infection. Coxiella burnetii causes
have caused abortions in sheep. S Abortusoccasional abortion storms in sheep, with ovis is endemic in England and Europe
the clinical syndrome and fetal pathology
but has not been reported in the USA. The
the san1e as for goats (see below). Neospora other serotypes occur worldwide. Most
caninum has been reported to cause
ewes are sick and febrile before aborting.

occasional abortions in sheep, with the

There are no specific placental lesions,
lesions resembling those of To.xoplasma
and U1e fetus is autolyzed. Diagnosis is
gondii. Fungal placentitis also occurs but
by culture of placenta, fetus, or ute1ine
is not as common in sheep as in cattle or
discharge. Salmonella spp are zoonotic.

horses. Other organisms associated with

(See also p 195.)

sheep abortion include Schrnallenberg

1340

ABORTION IN LARGE ANIMALS
virus, Rift Valley fever, Nairobi sheep

Toxoplasmosis: Toxoplasmosis is a
disease virus, Wesselsbron disease virus,
common cause of abortion in goats in the

Pmncisella tularensis, and Leptospira sp.

USA, and toxoplasmal abo1tion in goat.sis
sinlila.r to the syndrome in ewes. (See

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ABORTION IN GOATS
alsop 685.)

See also MANAGEMENT OP REPRODUCTION: GOATS, Leptospirosis: The most common
p 2182.

serovars of Leptospira inlerrogans

Noninfectious causes of abortion in goats
involved in caprine abortion a.re Grippotyinclude plant toxins, such as broomweed or phosa and Pomona. Although sheep a.re
locoweed poisoning; dietary deficiencies of
relatively resistant to leptospi.rosis, goats
copper, selenium, vitamin A, or magnesium;
are susceptible, with abo1tions occurring at
and certain drugs such as estrogen,
the ti.me of leptospirenlia. Some does have
glucocorticoids, phenothiazine, carbon
anemia, icterus, and hemoglobinenlia;
tetrachloride, or levanlisole (in late
others a.re a.febrile and a.re not icteric.

gestation).

Diagnosis is by serology or identification

Major infectious causes of ab01tion in
of Leptospira spp in the dam's urine, the
goats a.re chlanwdiosis, toxoplasmosis,
placenta., or fetal kidney. (See also p 646.) leptospi.rosis, brucellosis, Coxiella
burnetii, and listeriosis. Campylobacte-r Brucellosis: Brucella melilensis is the causes ab01tions but is not nearly as
principal organism involved in abortions
important in does as in ewes.

in anin1als with brucellosis; B abortus is
occasionally involved. Abortion may be

Chlamydiosis (Enzootic Abortion):

accomprulied by mastitis and lruneness and

Chlamydia abortus (the agent of enzootic
is most con1n10.n in the fourth month. The
abortion of ewes) is the most common
placenta is grossly nonnal, but does may
cause of ab01tion in goats in the USA. ln
develop chronic uterine lesions. lnfection in
naive herds, up to 600/o of pregnant does can
adults is lifelong, with organisms shed in the
abort or give birth to stillborn or weak kids.

nlilk (B melilensis is zoonotic but rare in Abortions can occur at any stage of
the USA). ln the USA, control is by test and
pregnancy, but most a.re in the last month.

slaughter. Tube agglutination and ca.rd tests

Reproductive failure is usually the only sign
can be used as screening tests. (See also
of C abortus infection, but occasionally
p 1348.)

there is concurrent respiratory disease,
polya.rthritis, conjunctivitis, and retained

Coxiella burnetii Infection: Coxiella
placentas in the flock. Aborted lambs a.re
bunietii is increasingly recognized as an
usually fresh with no gross pathology.

important cause of caprine abortion.

Placentitis is usually present and consists of

Occasional outbreaks also occur in sheep.

reddish brown exudate covering cotyledons Late-tenn abortions, stillbirths, and weak and intercotyledona.ry areas. Microscopilambs a.re the con1n1on presentations. Up cally, necrotizing vasculitis and neutrophilic
to 50% of the flock may be involved. The
inflammation a.re present in the placenta.

placenta is covered by gray-brown exu

Chlamydia! organisms can be visualized in
date and the intercotyledona.ry areas ru·e
appropriately stained placental smears, but
thickened. Microscopically, there is a
they cannot be differentiated from Coxiella
necrotizing vasculitis in the placenta,
burnetii. Fluorescent antibody or irnrnunoand many chorio11ic epithelial cells a.re histochenlical staining, ELISA, PCR, or
distended by small, coccobacilla.ry
culture can be used to definitively identify C
organisms <l µm in diameter. Infection
abortus. The placenta is the specimen of
involves only the placenta; without it,
choice, but sometimes the diagnosis can be
the diagnosis usually cannot be made.

made by testing liver, lung, and spleen.

Diagnosis is by identification of C burnetii

During an outbreak, aborting does should
by immunologic staining methods, PCR, or
be isolated, and tetracyclines given orally or
by isolation. Coxiella is zoonotic, ca.using parentally. There is no chlamydia! vaccine

Q fever in people. (See also p 623.)

for goats, but the vaccine for sheep is
relatively effective. Like sheep, goats that

Listeriosis: Listmia monocytogenes is abort a.re in1n1une. Sheep that abort due to
a common pathogen in goats and causes

C aborl'us remain infected for years, if not sporadic abortions. There a.re no specific
life, and shed the organism during ovulation; fetal lesions, and the fetus is often whether this occurs in goats is not known.

autolyzed. Does usually show no signs

C abortus is zoonotic, occasionally causing before abo1tion but may develop severe
serious disease in pregnant women.

metritis after abortion. Diagnosis is by

ABORTION IN LARGE ANIMALS

1341
isolation from the placenta, abomasal
and implantation, causing infertility,
contents, or uterine discharge. In the rare
embryonic death, and reduced litter size,
case of a herd outbreak, preventive
but rarely, if ever, abortion. Another class of
treatment with tetracycline is recommycotoxins, the fumonisins, causes acute VetBooks.ir
mended. (See also p 656.)

pulmonary edema in swine; sows tl1at
recover from the acute disease often abort

Caprine Herpesvirus 1 (CpHV 1 ):

2-3 days later.

CpHV 1 is closely related to infectious

Other toxic causes of abortions or
bovine rhinotracheitis virus of cattle and
stillborn pigs include cresol sprays ( used for
causes sporadic outbreaks of late-term
mange and louse control), dicumarol, and
abortions often unassociated with other
nitrates. Nutritional causes of reproductive
clinical signs. The virus also causes
failure are not well defined. Vitamin A
vulvovaginitis, balanoposthitis, and
deficiency can cause congenital anomalies
respiratory disease in adult goats and
and possibly abo1tions. Riboflavin
enteric and systemic diseases in neonatal
deficiency can cause early premature bitths
goats. Fetuses can be fresh or autolyzed and

(14-16 days), and calcium, iron, manganese,
do not contain diagnostic gross lesions.

and iodine deficiencies have been associ

Presumptive diagnosis is by microscopic
ated with stillbirths and weak pigs.

identification of necrosis with the presence

Carbon monoxide toxicity due to faulty
of intranuclear inclusion bodies in the liver,
propane heaters has been associated with
lungs, and other organs. Definitive diagnosis increased numbers of stillbirths and is by identification of CpHV 1 by isolation,
autolyzed full-term fetuses. Fetal tissues are

PCR, or inlillunologic staining methods.

cherry red; the sows do not appear affected.

Not all fetuses contain lesions or virus, so
multiple fetuses should be submitted.

Infected goats can become latently infected

Infectious Causes
and can shed the virus during times of

The major infectious causes of reproductive
stress. Vaccines are not commercially
failure in pigs include porcine reproductive
available in the USA.

and respiratory syndrome virus, porcine
parvovitus, pseudorabies virus, Japanese B
encephalitis virus, classical swine fever

ABORTION IN PIGS
virus, Leptospira spp, and Brucella suis.

See also MANAGEMENT OF REPRODUCTION: PIGS, p 2201.

Porcine Reproductive and Respira

Many agents that cause reproductive
tory Syndrome (PRRS): PRRS is caused
failure in sows produce a broad spectrum of
by an arterivirus. It is of major importance
sequelae, including abortions and weak neoin the USA and tl1roughout most of the nates, as well as stillbirth, mun1mification,
world. Most PRRS strains do not cross the
embryonic death, and infertility. Mummifiplacenta until after 90 days of gestation.

cation is seen more frequently in swine than

Consequently, most abortions are near the
in many other species because of the large
end of gestation. Affected litters contain
litter size. If only a few fetuses die, abortion
fresh and autolyzed dead pigs, weak
rarely occurs; instead, mummies are
infected pigs, and heal thy, uninfected pigs
delivered at term, along with live piglets
that often develop respiratory disease
or stillbirths.

within a few days of birth. The sows are
often anorectic and feverish a few days

Noninfectious Causes
before aborting. Concurrent respiratory
disease and increased munbers of bacterial

High ambient temperature (>32°C [>89.6°F]) infections in the herd are common.

is associated with increased returns to

Hemorrhage in the umbilical cord, when
estrus, increased embryonic mortality,
present, is the only gross lesion associated
decreased farrowing rates, and small litters.

with PRRS abortions. Not all fetuses are

The effect is greatest if heat stress occurs
infected, so multiple fetuses should be
at the time of breeding or implantation.

sampled. Viral antigen is most consistently

Increased embryonic mortality and
present in the fetal thynms and in fluid
increased irregular return to estrus are
collected from the fetal thoracic cavity. PCR
seen in pigs bred during the summer. High
testing of pooled thoracic fluid from three to
ambient temperature may play a role, but
five fetuses is the most reliable means of
there is evidence tl1at seasonal low
diagnosis. Herd management is important
progesterone levels are a major factor.

in control and prevention. Inactivated and

The estrogenic mycotoxins zearalenone
modified-live virus vaccines are available.

and zearalenol interfere with conception

(See also p 729.)

1342

ABORTION IN LARGE ANIMALS

Porcine Parvovirus: Porcine parvovirus

Japanese B Encephalitis Virus
is ubiquitous in pigs in the USA and most of

Infection: Japanese B encephalitis is
the world. Almost all females are naturally
an arthropod-borne disease that causes
infected before their second pregnancy, and
reproductive fail me in pigs and encephalitis
immunity is lifelong. Consequently, it is a
in people. The disease is reported p1imarily

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disease of first-parity pigs. Gilts that are
in southeast Asia, Indian subcontinent,
immunologically naive or have high passive

Indonesia, and Australasian regions.

antibody titers have the high.est risk of

Wected litters can contain dead pigs of varireproductive disorders caused by the vims.

ous sizes (including mw11.mies), stillborn

Wection before day 30 of pregnancy results
pigs, weak pigs, and pigs with CNS signs.

in early emb1yonic loss. Fetal infection

Hydrocephalus and subcutaneous edema
between 30 and 70 days of gestation can
are the most common gross lesions.

result in death of the fetus and sometimes

Diagnosis is confim1ed by viral isolation and
mwnmification. Not all fetuses are infected
immunohistochemistry. Viral nucleic acid
at the same time, and death at different
can be detected il1 tissue and blood samples
stages of pregnancy is typical. Some fetuses
using RT-PCR or nested RT-PCR. Pigs are
survive and are born alive but persistently
the primary amplifyil1g host for the virus
infected. Most fetuses infected after 70 days
and are vaccinated not only to prevent
of gestation mount an immune response,
reproductive fail me but also to prevent
clear the virus, and are healtl1y at birth.

hwnan infection.

Litters with dead fetuses of varying sizes,
including mwnmified fetuses, along with
stillborn and healthy pigs born to first-parity

Classical Swine Fever (Hog Cholera):

gilts, are the hallmark of porcine parvovirus. Classical swine fever is caused by a pesti

Diagnosis is by fluorescent antibody testing,
vilus eradicated from the USA but still a
virus isolation using lung from mwnmified
serious problem throughout much of the
fetuses, or demonstration of precolostral
world. With highly vil1.tlent strains that
antibody in stillborn pigs. Boars shed virus
cause se1ious maternal illness, ab01tion is
by varying routes, including semen, for a
common. Witl1 strains of moderate or low
couple of weeks after acute infection and
virulence, bilth of mummified and stillborn
can introduce the virus into a herd.

pigs, weak pigs, and persistently infected

Effective inactivated vaccines are available.

pigs are more common. Fluorescent
antibody staining, vims isolation, and PCR
are used for diagnosis. Both killed and modi

Pseudorabies (Aujeszky Disease,
fied-live vaccines are available, but their use

Porcine Herpesvirus 1 Infection):

in the USA is prohibited. (See also p 713.) Pseudorabies is a: cause of CNS and
respiratory diseases. Wection results in

Porcine Circovirus Infection: Porcine
latency, and seropositive animals are
circovirus type 2 (PCV2) is found worldconsidered infected. Wection early in wide, is ubiquitous in pigs, and is associated
pregnancy can result in.embryonic death
with several conditions, including sporadic
and resorption of the fetuses. Wection later
outbreaks of late-term ab01tions and tenn
in pregnancy can result il1 abortion and
litters with increased numbers of dead
birth of stillborn and weak pigs. Mununificapiglets. The dead piglets vaiy from small, tion can occm but is uncommon. There are
mwnmified fetuses to stillbirths. Nonmwnno gross lesions in most aborted pigs, but a mified fetuses typically have a large amount
few have pinpoint white foci of necrosis in
of serosanguineous fluid in their body
the liver and tonsils. Diagnosis is by virus
cavities. Microscopically, there is myocarisolation, PCR, or fluorescent antibody dial necrosis and/or fibrosis, and PCV2 is
staining. Effective gene-deleted vaccines
present in the heart and otl1er tissues. The
that allow serologic differentiation of
incidence of PCV2 reproductive fail me is
vaccinated and natW'ally infected pigs were
very low; when it occurs the problem soon
developed for the eradication program in
disappears, perhaps because most pigs are
the USA, but after eradication from
naturally exposed and immune before being
commercial pigs was completed in 2003,
bred. Diagnosis is based on presence of
vaccination was discontinued. Feral pigs in

PCV2 DNA or antigen in precolostral serun1
multiple states harbor the virus, and since
san1ples from live born piglets. Inununohis2003 there have been sporadic outbreaks of tochemistJ.y and m situ hybridization are
pseudorabies in herds that have contact
considered tl1e gold standard to detect the
with feral pigs. These outbreaks are
agent. Vaccines are available for grower and
cmrently controlled by herd depopulation.

finisher pigs, but their efficacy in preventing

(See also p 1300.)

reproductive failme is unlmown.

ABORTION IN LARGE ANIMALS

1343

Leptospirosis: Leptospira interrngans
reported to cause fetal losses in pigs, but

( especially serovar Pomona) is a major
they are not considered economically
cause of reproductive failure in swine
important. Blue eye paramyxovirus is an

(infertility, abortion, stillbirths, and the birth important cause of abortion, stillbirths, VetBooks.ir
of weak piglets). Although acute leptospiroand mummified fetuses in parts of Mexico.

sis occurs in adult swine, most cases are

Bacteria that cause sporadic abortions
asymptomatic. Pigs infected with serovars
include Staphylococcus aureus, Streptococ

Pomona and Bratislava can become chronic cus spp, Erysipelothrix rhusiopathiae, renal carriers. Abortion occurs 1--4 wk after

Salmonella spp, Pasteurella multocida,
infection, so the abortuses are autolyzed.

T1ueperella (Arcanobacterium) pyogenes,

Mummification, maceration, stillbirths, and

Listeria monocytogenes, and Eschm·ichia weak pigs are also seen. Diagnosis is based
coli.

on demonstration of leptospires in fetal
tissues or stomach contents. However,

ABORTION IN HORSES
severely autolyzed fetuses may result in
poor fluorescent antibody and inununohis

See also MANAGEMENT OF REPRODUCTION: HORSES, tochemistry results. PCR testing has better
p 2187.

sensitivity and specificity. Vaccination with
a multivalent bacterin every 6 mo helps

Noninfectious Causes
prevent the disease. Streptomycin was

The most common noninfectious cause
formerly used to elinlinate the carrier state
of abortion in horses is twinning. Most
and to treat pregnant sows during an outabo1tions related to twinning occur at 8-9
break, but it is no longer available for use in
mo of gestation and may be preceded by
food animals. Experimentally, high levels of
premature lactation. Placental insufficiency
injectable oxytetracycline, tylosin, and
ultimately causes abortion of twins.

erythromycin and high levels of tetracy

Umbilical cord abnormalities, such as
clines in the feed have elintinated the carrier torsion due to abnormal length (>100 cm), state. However, field results indicate that
are conunonly diagnosed as a noninfectious

Leptospira infection cannot be reliably
cause of abortion, particularly in Thoroughelintinated with antibiotics. Leptospirosis breds. Diagnosis of abortion due to cord
is zoonotic. (See also p 646.)

torsion requires evidence of localized
swelling or hemorrhage, because torsions

Brucellosis: Brucella suis infection in occur in some normal births. Signs of fetal
commercial swine has become rare in the
circulatory disturbances, such as subcuta

USA as a result of state and federal control
neous edema, a swollen, soft liver, and
programs. However, it is present in feral pigs microscopic mineralization of pl;i,centaJ
in multiple states; these represent a source
vessels, are also signs of un1bilical cord
of infection for conunercial pigs and people. obstruction.Various congenital fetal The route of infection is oral in most cases, abnormalities have been reported in cases
but venereal transmission is not uncommon. of noninfectious abortions.

Infected sows can abort at any stage of
gestation, and abmtions are not always

Mare Reproductive Loss Syndrome:

accompanied by illness. Abortion is

In spring of 2001, horse farms in Kentucky
probably due to endometritis and fetal
and neighboring states experienced an
infection. There are few fetal or placental
explosive outbreak of early abortions and
lesions, although some fetuses may be
late-term abortions, stillbirths, and weak
autolyzed. Diagnosis is by serology and
foals that died within a few days. Sinmlta.neisolation from the placenta and fetal tissues.

ously there was a large increase in fibrinous

No treatment has been uniformly effective.

pericarditis and unilateral uveitis in horses

Control is based on test and slaughter.

of all ages and both sexes. Together these

Brucellosis is one of the few venereal
conditions became known as mare
diseases recognized in swine. B suis causes reproductive loss syndrome (MRLS).

a serious zoonotic disease. (See also p 1348.) Analysis of records showed that MRLS had occurred in the area in earlier years. MRLS
has since been diagnosed in other states,

Other Infectious Causes of Abortion:

including New York ar1d F1orida An abortion

Pigs with foot-and-mouth disease ( see
storm with sinillar clinical signs and risk
p 629), African swine fever (seep 711), and factors was recently reported from AusLralia.

swine influenza (seep 1470) often abort, but Most early abortions occur at 40---80 days
they and their herdrnates also have clinical
of gestation, with some losses occurring as
signs of those diseases. Enteroviruses and
late as 140 days. A few affected mares have
encephalomyocarditis virus have been
colic, fever; ancVor purulent vulvar

1344

ABORTION IN LARGE ANIMALS
discharge, but most remain clinically
the infected fescue can be pasture, hay, or
nonnal. Typically, the first sign is abortion or
bedding. (See also p 3016.)

fincling a fetus dead in utero by ultrasound.

Most fetuses are expelled within 2 days to

Infectious Causes

VetBooks.ir

2 wk of dying and are autolytic. Neutrophilic

Infectious causes of abortion include viral
placentitis and metritis are usually present.

diseases (such as equine rhinopneumonitis

Most mares rebred during the same breecling
season do not become pregnant, but
and equine viral arteritis) as well as
bacterial and fungal infections.

conception is usually n01mal during the next
breecling season. Late-term losses generally

Equine Rhinopneumonitis (Equine
occur at 10 mo of gestation to term, and the

Herpesvirus 1 Infection): Equine
mare usually does not display signs of
rhinopneumonitis, specifically equine
impending parturition. Pathologic features
herpesvirus 1 (EHV-1) infection, is the most
of MRLS include the presence of amnionitis
important viral cause of abortion in horses,
and funisitis, with only the amniotic portion
although EHV-4 has also been isolated from
of the umbilical cord affected. The placenta
some cases. The principal mode of
and umbilical cord are thickened, edematransmission of the virus from horse to tous, and discolored light brown to yellow.

horse is by direct cont.act through nasal

Neutrophilic inflammation of the umbilical
secretions, reproductive tract discharge,
cord and placenta are usually present, with
placenta, or the abo1ted fetus. Short-disthe neutrophilic funisitis being characteristic tance airborne spread of infection is of the syndrome. A variety of bacteria can be
possible. Abortion is usually after 7 mo of
isolated from the fetuses, regardless of when
gestation and is not preceded by maternal
they abort, but are not considered causative.

illness. The placenta may be edematous

Pasture exposure to eastern tent caterpillars
or n01mal. Gross fetal lesions include

(Malacosoma americanum) is an in1portant
subcutaneous edema, jaundice, increased
risk factor, and both early and late-te1m
volume of thoracic fluid, and an enlarged
abortions have been reproduced by oral
liver with yellow-white lesions -1 mm in
administration of whole caterpillars or their
dian1eter. Histologically, these lesions
exoskeletons but not their digestive tract.

represent areas of necrosis containing

The mechanism causing abortion has not
intranuclear inclusions. Inclusion bodies
been confmned. It has been proposed that
are also found in necrotic lymphoid tissues.

an unidentified toxin associated with the

There is often a necrotizing bronchiolitis.

exoskeleton of these caterpillars is involved,

Diagnosis is by fluorescent antibody, PCR,
and that bacte1ial infections are secondary.

or virus isolation from fetal tissues.

Alternatively, caterpillar hairs (setae) may

Prevention is based on vaccinating at 5, 7,
penetrate the oral or intestinal mucosa and
and 9 mo of gestation as well as preventing
carry bacteria, resulting in bacteremia with
exposure of pregnant mares to horses
localization in the uterns and other organs.

attencling shows or other equine events.

(The horses in the Australian outbreak were

Abortion may occur despite regular
exposed to processionary caterpillers
vaccination. (See also p 1444.)

[ Ochragasf,er lunifer]).

Prevention consists of pasture manage

Equine Viral Arteritis (EVA): Abortion
ment to control the numbers of eastern tent
may follow clinical cases of EVA by 6---29
caterpillars and other procedures to prevent days. Abortion rates can approach 6QOA, in exposure of pregnant mares to eastern tent
a naive population as the result of direct
caterpillars.

impaiiment of placental ftmction and severe
fetal infection. Arteritis may be found in the

Fescue Grass Toxicosis: Ingestion of
fetal myocardium or placenta, but usually
fescue infected by the endophyte Neotypho
there are no fetal lesions. StaJlions can be
dium coenophialum causes prolonged
persistently infected, and EVA can spread
gestation, agalactia, edema and premature
venereally ( via natural cover or inseminaseparation of the placenta, and perinatal tion with shipped cooled or frozen semen)

death. Abortion may occur in the last 2 mo
or by aerosol. Diagnosis is by a history of
of pregnancy due to severe edema and

EVA shortly before abortion, virns isolation
premature placental separation. The
or PCR of placenta and/or fetal tissues, or
placenta is thickened and edematous and
by seroconversion of the dam. Prevention
does not rnpturc nonnally at the cervical
of EVA is by management to minimize viral
star. The chorioallantois precedes the foal
transmission in breeding populations and
through the birth canal instead of remaining
to prevent development of car1ier staJlions.

attached to the uterus (red bag), resulting in

In the USA, a licensed modified-live virns
anoxia and death of the fetus. The source of
vaccine is available for use in nonpregnant

ABORTION IN LARGE ANIMALS

1345
mares. Antibody titers resulting from
placentitis as a cause of abortion seems to
vaccination and natural infection cannot
be on the rise in Kentucky, Northern Ireland,
be clifferentiatecl, and the serologic status

En.gland, and South America. Several
of horses can affect their in1port status.

serovars of Leptospira inteirogans have

Therefore, the serologic status of breeding
been isolated from aborted equine fetuses

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horses should be determined before

(eg, Pomona, Grippotyphosa, Bratislava,
vaccination, and all subsequent vaccina

Pomona type kennewicki, and Hardjo type
tions should be recorded. (See also p 701.) hardjo-prajitno ). In North America, the most
conunon isolate is serovar Pomona type

Bacterial Abortion: Bacte1ial placentitis
kennewick.i, which is carried by several
is by far the most conunonly diagnosed
wilcllife species, including the striped
cause of ab01tion in many horse breeding
skunk, raccoon, whitetail deer, and
areas. PlacenLitis is a significant cause of
opossum. Most leptospiral abortions
equine late-term abortion, premature deli.very, occur between 6 and 9 mo of gestation.

and neonatal death. Except for Leptospira

The placenta is thick, heavy, edematous,
spp and nocardioforn1 infections, most
hemoIThagic, and occasionally covered
cases of bacterial placentitis are ascending.

with a brown mucoid mate1ial on the

Ascending placentitis is character.izecl by
chorion.le surface. Funisitis has also been
premature udder development, increased
described in leptospiral abortion. The fetus
uteroplacental thickness at the level of the
may have mild to moderate icterus and liver
cervical star, and mucopurulent vaginal
enlargement, and fetal histopathologic
discharge. If placentitis is untreated,
lesions may include various degrees of
placental function is comprorn.isecl and
nephritis and hepatitis. Diagnosis is by
placental separation ensues, resulting in
fluorescent antibody staining of placenta
fetal death and expulsion. In chronic
or fetal kidney, liver, or lung and by fetal
placentitis, the fetus may show intraute1ine
serology. (See also p 652.)

growth retardation. Streptococcus equi

Nocardiofonn placentitis is a distinct
subsp zooepidemicus, Escherichia coli,
type of equine placentitis first described in

Pseudomonas aeiuginosa, Enlembactei·
the USA in the late 1980s. Nocardioforn1
spp, and K/,ebsiella pneumoniae are the
placentitis may result in abortion, stillbirth,
most frequent isolates from the vaginal
or birth of weak foals at tenn. Some mares
discharge, uterus, placenta, and fetal
may exhibit prematlffe mammary gland
stomach contents. Other bacteria have also
development and lactation before abortion.

been rep01ted to cause ascending placentitis

Infection of the placenta is generally
in mares, including Streptococcus equisimi
thought to be a sequela of hematogenous
lis, Entei-obactei· agglomerans, a-hemolytic spread of microorganisms from a primary
streptococci, Staphylococcus aureus, and
port of entry. The lesion is an extensive and·

Actinobacillus spp. Exanlination of the
severe exudative, mucopurulent, and
placenta shows an edematous and thicken.eel necrotizing placentitis, frequently located ch01ioallantois with fibrinonecrotic exudate
at the base of the uterine horns or at the
at the level of the cervical star.

junction between the body and horns of the

Leptospira spp placentitis is characterplacenta. The affected area is thickened, ized by diffuse lesions secondary to
and its cho1ion.ic surface is covered with
hematogenous spread. Leptospiral
brown, necrotic, mucopurulent exudate
and dotted with white or yellow granular
structures. Underneath this mucoid
material, the chorionic surface is reddish
white, mottled, and roughened. Villous
necrosis and adenomatous hyperplasia of
the allantoic epithelium, and hyperplasia
with or without squamous metaplasia of the
chorionic epithelium are frequently seen.

Various groups of gram-positive, filan1entous, branching bacteria have been implicated as etiologic agents in mares
with nocardioform placentitis, including

Nocardia spp, Rhodococcits iubroperl'inctus, Amycolatopsis spp, and Cmssiella equi. The fetus is often severely underdevel

Ascending placentitis in a mare. Note the
oped as a result of placental insufficiency
congested and thick cervical star area.

and does not show any remarkable gross or

Courtesy of Dr. Ahmed Tibary.

histologic lesions.

1346

ABORTION IN LARGE ANIMALS

Potomac horse fever (seep 283), caused
iodine). Lactating and very young maiden
by Ehrlichia risticii, may be followed by
females may have an increased incidence
abortion in mid-to late gestation. There
of embryo and fetal losses.

is placentitis, and the placenta is often
retained. E risticii has been isolated from Infectious Causes

VetBooks.ir
fetal lymphoid tissues after abortion.

Histologically, there is fetal colitis. Identifica

Viruses: Viral causes of abortion are
tion of this colitis provides a preswnptive
dominated by bovine viral diruThea virus
diagnosis. There is a vaccine for Potomac

(BVDV). However, abortions due to equine
horse fever, but its efficacy in preventing
herpesvirus 1, equine ruteritis virus, and
abortion is not known.

bluetongue virus have been reported. The
most common BVDV serotype that affects

Equine Mycotic Placentitis: Mycotic
alpacas and llan1as is noncytopathic
placentitis in horses is also due to an

BVDV-lb. Abortion may occur at any stage of
ascending infection that causes placentitis
gestation, or a weak, persistently infected
with a thickened chorioallantois with

(PI) cria may be born prematurely. The birth
vruiable exudate. Causative agents include
of a PI anin1al can have significant effects on

Aspergillus spp, Mucor spp, Candida spp, a herd of anin1als. Diagnosis of BVDV

Histoplasma capsulatum, Coccidoides
infection is based on virus isolation from
spp, and CriJptococcus neofonnans.

fetal blood, fetal tissues (lymph nodes), ru1d

Fetuses abmted in late gestation may be
placenta. Immunohistochemistry may be
fresh, with evidence of growth retardation.

performed on forn1alin-fixed tissues. PCR on

A pale, enlarged liver or dermatitis may be
whole blood san1ples is commonly used to
found. Hyphae are found in the placenta,
screen newborn crias.

liver, lungs, or stomach contents.

Bacteria: The most commonly diagnosed
infectious causes of pregnancy losses ru·e

ABORTION IN CAMELIDS
chlru11ydiosis and brucellosis (in some parts

Pregnancy loss is a common complaint in
of tl1e world). Chlamydia spp have been
crunelid practice. The general approach to
identified as a cause of abortion and birth of
diagnosis is similar to that in other species.

weak crias in llrunas. C abortus has been

However, crunelids have several unique
associated with infertility and ovarian
features of placentation and pregnancy.

hydrobursitis in can1els.

In neru·ly all pregnancies, the fetal horn is

Brucellosis (Brucella abortus and B
the left uterine horn, and the placenta is
melitensis) is a common cause of abortion
epitheliochorial, microcotyledonary diffuse
in crunelids in some areas of the world.

(such as in the horse), but·the allantocho

Other reported bacterial causes of
rion adheres to the runniotic sac.

abortion in crunelids include leptospirosis

(Le'J)tospira interrogans serogroups

Icterohaemorrhagiae and Ballwn),

Noninfectious Causes
listeriosis (Listeria monocytogenes), and

Noninfectious causes of abortiort include
can1pylobacteriosis (Campylobactmfetus
fetal or placental abnormalities (twinning,
fetus). Coxiellosis (Coxiella burnetii) wnbilical cord torsion, severe deformities,
abortion is suspected to occur but has not
chromosomal abnormalities and placental
been diagnosed definitively.

insufficiency, uterine torsion), luteal

Nonspecific bacterial infections (Escheri
insufficiency (hypoluteidism), environmen
chia coli, Stre'J)lOCOCCUS equi ZOOe'J)ide'lni
tal stressors (severe disease process; long,
cus) are often isolated from cases of
stressful trip; heat stress), or iatrogenic
abortion that were due to placentitis.

causes ( administration of prostaglandin

F2a, corticosteroids, 8-way vaccines).

Protozoa: Reported protozoa! causes of

Recurrent loss due to luteal insufficiency
abortion in crunelids include toxoplasmosis
has been associated with obesity and

(Toxoplasma gondii), neosporosis
possibly hypothyroidism. Presence of large

(Neospora caninum ), and sarcocystosis
avillous areas suggest placental insuffi

(Sarcocystis aucheniae and S cruzi).

ciency. Twin conceptions are not rru·e, and

Trichomoniasis (Tritrichomonas foetus)

most are reduced to singleton or lost by
has been isolated from crunels, but there is
day 45. Abortion of twins is generally seen
no strong evidence it is involved in abortion.

between 5 ru1d 9 mo of pregnancy.

On a herd basis, severe losses may be

Fungi: Sporadic cases of abortion due to
seen with nutritional deficiencies (seleniwn, Ence'J)halitozoon cuniculi and Aspergillus vitamin A, iodine), or toxicosis ( copper,
spp have been reported.

BOVINE GENITAL CAMPYLOBACTERIOSIS

1347

BOVINE GENITAL CAMPYLOBACTERIOSIS

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Bovine genital campylobacteriosis is a
mucus in significant amounts in -50"A, of
venereal disease of cattle characterized
cows for several months after infection and
primarily by early embryonic death,
ai·e useful diagnostically. Although most of
infe1tility, a protracted calving season,
the genital tract may be free of infection
and occasionally abortion. Distribution
when a cow eventually conceives, the
is probably worldwide.

vagina may remain chronically infected

Uu·ough pregnancy.

Etiology and Epidemiology: The cause
is the motile, gram-negative, curved or

Clinical Findings: Cows are systemically
spiral, polar flagellated, microaerophilic
normal, but there is a variable degree of
bacteria Campylobacterfetus venerealis
mucopurulent endometritis that causes
or C fetus fetus. For many years, it was
early embryonic death, prolonged luteal
thought that C fetus fetus was generally
phases, i.ITegular estrous cycles, repeat
an intestinal organism, only occasionally
breeding, and, as a result, protracted calving
caused abortion in cattle, and was not a
periods, assuming the breeding season is
cause of infertility. However, C fetus fetus
long enough to allow for complete
can also be a.significant cause of the classic
clearance and a successful rebreeding.

infertility syndrome usually att1ibuted to C

Observed abortions ai·e not common. In
fetiis venerealis. There are several strains herds not managed intensively, disease may
of Cfetusfetus, and the only way to
be noticed only when pregnancy examinadetermine whether a strain is a cause of tions reveal low or marginally low
infertility is to test that possibility in a group
pregnancy rates but, more in1portantly,
of heifers. Campylobacter spp are very
great variations in gestation lengths,
labile and are destroyed quickly by heating,
especially when the disease has recently
drying, and exposure to the atmosphere.

been introduced to the herd. In subsequent

Unless cultured quickly after collection
yeai-s, infertility is usually confined to
from the animal and grown under microreplacement heifers and a few susceptible aerophilic or anaerobic conditions,
cows. Bulls are asymptomatic and produce

Campylobacter spp will not grow.

nom1al semen.

C fetus is transmitted venereally and also
by contaminated instruments, bedding, or

Diagnosis: Cai11pylobacteriosis and
by artificial insemination using contan1itrichomoniasis (seep 1384) are similai·
nated semen. Individual bulls vary in their
syndromes, and investigations should be
susceptibility to infection; some become
directed at both diseases. Systemic antipermanent carriers, while others appear to body responses ai·e not helpful, because
be resistant to infection. The primary factor
they are often due to nonpathogenic
associated with this variability seems to be

Campylobacterspp . A vaginal mucus
the age-related depth of the preputial and
agglutination test (VMAT) is useful, but
penile epithelial crypts. In young bulls
because of variability in individual

( <3-4 yr old), in which the crypts have
responses, at least l()OA, of the herd or at least
not yet developed, infection tends to be

10 cows should be sampled. An ELISA test
transient, with transn1ission apparently relyhas been developed for use on vaginal ing on sexual contact with a noninfected
mucus and is said to be more sensitive and
cow within a matter of n1inutes to days after
able to detect a wider range of antibody
the initial breeding of an infected cow.

responses than the VMAT. Vaginal culture

Spontaneous clearance in these younger
inm1ediately after abortion or infection can
bulls does not seem to be related to any
be used for diagnosis, but the number of
immune response, so reinfection can readily organisms may be low; in addition, because occur. In bulls >3-4 yr old, the deeper crypts C fetus is labile and requires special may provide the proper n1icroaerophilic
techniques for isolation, success is lin1ited.

environment required for chronic infections

An accurate diagnostic method is to
to establish.

test-breed heifers and then exaniine them

In cows, the duration of the carrier state
for infection, but tl1is is seldom practical.

is also vaiiable; some clear the infection

More often, the preputial cavity and fom.ix
rapidly, whereas otl1ers can carry C fetiis for are either scraped and aspirated with an

�2 yr. IgA antibodies are shed in cervical
infusion pipette or infused with buffered

1348

BOVINE GENITAL CAMPYLOBACTERIOSIS
sterile saline, and the prepuce is massaged
elimination of C fetus and, although cows
vigorously in the area of the fomix. The
may remain caniers, fertility is greatly
aspirate or sheath washing is then examined improved. In routine use, the vaccine should using a fluorescent antibody test and
be given once, -4 wk before breeding starts;

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culture. C fetus will survive for only 6-8 hr because antibody responses are sho1t-lived,
after collection, but inoculation into Clark's
cows should be revaccinated halfway
or similar media will allow survival for >48
tl1rough the breeding season. Bulls are
hr. For maximum accuracy, bulls should be
vaccinated for the san1e reason as cows (ie,
sampled twice, -1 wk apart.

for b·eatment as well as for prophylaxis) but

Caution should be exercised when
are given twice the dose used for cows, 3 wk

Cmnpylobacter spp are isolated from the
apart. The infection can also be eliminated
placenta because of the possibility of
in bulls by 1-2 treatments witl1 streptomycontamination by nonpathogenic fecal cin at 20 mg/kg, SC, together with 5 g of

Campylobacterspp. Conversely, failure
streptomycin in an oil-based suspension
to successfully isolate Cfetus from an
applied to the penis for 3 consecutive days.

infected aborted fetus or placenta often

For practical reasons, cows are not
results from overgrowth of the colonies by
usually b·eated for genital campylobactericontaminating organisms or the lethal osis. When practical, artificial insemination
effects of atmospheric oxygen.

is an excellent way to prevent or conb·ol
genital campylobacteriosis. Because C fetus

Treatment and Control: Vaccination
has been isolated from cows for >6 mo after
should start as soon as genital campylobacthe end of pregnancy, it has been suggested teriosis is diagnosed. Infected cows and
that artificial insemination should continue
cows at risk should be vaccinated.

until all the cows in a herd have been

Vaccination of infected cows hastens the
wough at least two pregnancies.

BRUCELLOSIS IN LARGE ANIMALS

Brucellosis is caused by bacteria of the
that caused by B abortus. B melitensis is
genus Brucella and is characterized by
not present in the USA.

abortion, retained placenta, and to a lesser

Wection spreads rapidly and causes
extent, orchitis and infection of the
many abortions in unvaccinated cattle. In
accessory sex glands in males. The disease a herd in which disease is endemic, an is prevalent in most countries of the
infected cow typically aborts only once
world. It primarily affects cattle, buffalo,
after exposure; subsequent gestations and
bison, pigs, sheep, goats, dogs (see
lactations appear normal. After exposure,
p 1402), elk, and occasionally horses. The
cattle become bacteremic for a short period
disease in people, sometimes referred to
and develop agglutinins and other
as undulant fever, is a serious public
antibodies; some cattle resist infection,
health problem, especially when caused
and a small percentage of infected cows
by B melitensis.

spontaneously recover. A positive serum
agglutination test usually precedes an

BRUCELLOSIS IN CATILE
abortion or a nom1al parturition but may be
delayed in -15% of cows. The incubation

(Contagious abortion, Bang's disease)

period may be variable and is inversely
related to stage of gestation at time of

Etiology and Epidemiology: The
exposure. Organisms are shed in milk and
disease in cattle, water buffalo, and bison
uterine discharges, and the cow may
is caused almost exclusively by Brucella
become temporarily infertile. Bacteria may
abortus; however, B suis occasionally is be found in the uterus during pregnancy,
isolated from seropositive cows but does
uterine involution, and infrequently, for a
not appear to cause clinical signs and is
prolonged time in the nongravid uterus.

not contagious from cow to cow. In some

Shedding from tl1e vagina largely disappears
countries, the disease in cattle is caused by
with the cessation of fluids after parturition.

B melitensis. The syndrome is similar to

Some infected cows that previously aborted

BRUCELLOSIS IN LARGE ANIMALS

1349
shed brucellae from the uterus at subseserum samples of nonvaccinated animals, quent normal parturitions. Organisms are
and of 1:200 of animals vaccinated at 4-12
shed in milk for a variable length of time-in mo of age, are considered positive, and the most cattle for life. B abortus can frequently animals are classified as reactors. Other be isolated from secretions of nonlactating
tests that may be used are complement

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udders.

fixation, rivanol precipitation, and acidified

Natural transmission occurs by ingestion
antigen procedures.

of organisms, which are present in large numbers in aborted fetuses, fetal membranes, and Screening Tests: In official eradication
ute1ine discharges. Cattle may ingest
programs on an area basis, the Bnicella
contaminated feed and water or may lick
milk ring test (BRT) has effectively located
contaminated genitals of other animals.

infected dairy herds, but there are many

Venereal transmission by infected bulls to
false-positive tests. The brucellosis status of
susceptible cows appears to be rare.

dairy herds in any area can be monitored by

Transmission may occur by artificial
implementing the BRT at 3- to 4-mo
insemination when Brucella-contaminated
intervals. Milk samples from individual
semen is deposited in the uterus but,
herds are collected at the farm or milk
reportedly, not when deposited in the midce1
processing plant. Cows in herds with a

°
vix. Brucellae may enter the body tJu·ough
positive BRT are individually blood tested,
mucous membranes, coajunctivae, wounds,
and seropositive cows are slaughtered to
or intact skin in both people and animals.

determine herd status.

Brucellae have been recovered from

Nondairy and dairy herds in an area may
fetuses and from manure that has remained
also be screened for brucellosis by testing in a cool environment for >2 mo. Exposure
serum san1ples collected from cattle
to direct sunlight kills the organisms within
destined for slaughter or replacements
a few hours.

through intermediate and tem1inal markets,
or at abattoirs. Reactors are traced to the

Clinical Findings: Abortion is the most
herd of origin, and the herd is tested. The
obvious manifestation. Infections may also
cost of identifying reactors by this method
cause stillborn or weak calves, retained
is mini.nlal compared with that of testing
placentas, and reduced milk yield. Usually,
cattle in all herds. Screening tests, including
general health is not in1paired in uncomplithe brucellosis card ( or rose bengal) test cated abortions.

and plate test, may be used in markets and

Seminal vesicles, ampullae, testicles, and
laboratories to identify presumptively
epididy.mides may be infected in bulls;
infected animals, thus reducing the number
therefore, organisms are present in the
of more expensive and laborious diagnostic
semen. Agglutinins may be demonstrated
tests.

in seminal plasma from infected bulls.

Brucellosis-free areas can be achieved

Testicular abscesses may occur. Longstandand maintained, effectively and economiing infections may result in artluitic joints in cally, by using the BRT on dairy herds and some cattle.

through market cattle testing. Adult cattle
are sampled at the time of slaughter.

Diagnosis: Diagnosis is based on bacteriol

Supplemental tests using sensitive
ogy or serology. B abortus can be recovered screening methods may be used in cattle in
from the placenta but more conveniently in
which the brucellosis status is unclear. Use
pure culture from the stomach and lungs of
of a battery of these tests improves the
an aborted fetus. Most cows cease shedding
probability of detecting infected cattle that
organisms from the genital tract when
have remained in some herds as possible
uterine involution is complete. Foci of
reservoirs of infection. Supplemental tests
infection remain in some parts of the
are also used to clarify the results of plate or reticuloendothelial system, especially
card tests, especially in serum samples from
supramanunary lymph nodes, and in the
vaccinated cattle. These tests, which
udder. Udder secretions are the preferred
include complement fixation and rivanol
specin1ens for culture from a live cow.

precipitation, are designed to detect

Senun agglutination tests have been the
prin1arily the antibodies specifically
standard diagnostic method. Agglutination
associated with Brucella infection. Another tests may also detect antibodies in milk,
supplemental diagnostic procedure is to
whey, and semen. An ELISA has been
test milk san1ples from individual udder
developed to detect antibodies in milk and
quaiters by serial dilution BRT, which can
serum. When the standard plate or tube
be used to detect chronic infection in
serum agglutination test is used, complete
udders of cows tl1at may have equivocal
agglutination at dilutions of 1:100 or more in
serum test reactions.

1350

BRUCELLOSIS IN LARGE ANIMALS

Control: Efforts are directed at detection
primarily through ingestion of the
and prevention, because no practical
organisms. The disease causes abortion
treatment is available. Eventual eradication
at approximately the fourtl1 mo.nth of
depends on testing and eliminating reactors. pregnancy. Arthritis and orchitis may occur.

The disease has been eradicated from many

Diagnosis is made by bacteriologic
individual herds and areas by this method.

examination of milk or an abo1ted fetus or

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Herds must be tested at regular intervals
by seru.n1 agglutination tests. The disease
tmtil two or three successive tests are
can be eliminated by slaughter of the herd.

negative.

ln most countiies where B melitensis is

Non.infected herds must be protected.

endemic, vaccination with the Rev. l strain

The greatest danger is from replacement
is common. Rev. l is an attenuated strain of
animals. Additions should be vaccinated

B melitensis and is administered by SC or
calves or nonpregnant heifers. If pregnant
intraconjunctival routes. B melitensis is
or fresh cows are added, they should
highly pathogenic for people.

originate from brucellosis-free areas or
herds and be seronegative. Replacements

BRUCELLOSIS IN HORSES
should be isolated for -30 days and retested
before being added to the herd.

Horses can be infected witl1 B1ucella

Vaccination of calves with Ba bortus
abortus or B suis. Suppurative bursitis, Strain 19 or RB51 increases resistance to
most commonly recognized as fistulous
infection. Resistance may not be complete,
withers or poll evil (seep 1064), is the most and some vaccinated calves may become
common condition associated with
infected, depending on severity of exposure. brucellosis in horses. Occasionally, abor

A small percentage of vaccinated calves
tion has been reported. It is unlikely that
develop antibodies to Strain 19 that may
infected horses are a source of tl1e disease
persist for years and can confuse diagnostic
for other horses, other animal species, or
test results. To minimize this problem,
people. Brucellosis in horses is very rare in
calves in the USA are mostly vaccinated
tl1e USA because of elimination of tl1e
witl1 a vaccine of Strain RB51. It is a rough
disease in cattle.

attenuated strain and does not cause
production of antibodies, which are

BRUCELLOSIS IN PIGS
detected by most serologic tests.

Whole-herd adult cattle vaccination using

Clinical martifestations of brucellosis in pigs

Strain 19 or RB5 l has been practiced in
vary but are sinular to those seen in cattle
certain high-incidence areas and selected
and goats. Altl10ugh the disease is often
herds in the USA with much success.

self-li..nuting, it remains in some herds for

Vaccination as tl1e sole means of disease
years. Brucellosis caused by Brucella suis
control has been effective. Reduction in the
rarely occurs in domestic anin1als other
munber of reactors in a herd is directly
than pigs. Epidemics of brucellosis in
related to the percentage of vaccinated
people have been reported among
anin1als. However, when proceeding from a
packing-house workers, and the usual
control to an eradication prograin, a test
source is infected pigs. The prevalence in
and slaughter program becomes necessary.

the USA is sometin1es high among feral pigs.

B a.bo1·t1is has been eradicated from cattle The incidence of swine brucellosis an1ong
herds in the USA, and all states are
domesticated animals in tl1e USA is very
considered free of brucellosis.

low. CU1Tently there are no known infected

Brucellosis is endemic in some nondodomestic swine herds.

mesticated bison and elk herds in the USA.

Transmission of B abortus to domestic cattle Etiology and Transmission: B suis herds is rare but has occuffed in several
is usually spread mainly by ingestion of
cattle herds commingli..ng with infected elk
infected tissues or fluids. Wected boars
in the greater Yellowstone Park area.

may ti·ansnut tl1e disease during service; the
orgaiusm can be recovered from semen.

BRUCELLOSIS IN GOATS

Pigs raised for breeding purposes are
sources of infection. Suckli..ng pigs may

The signs of brucellosis in goats are similar
become infected from sows but most reach
to those in cattle. The disease is prevalent in
weanling age without beconung infected.

most countries where goats are a significant
part of the anin1al industry, and milk is a

Clinical Findings: After eiqiosure to B
common source of hwnan brucellosis in
suis, pigs develop a bacteremia that may
many countries. The causal agent is
persist for as long as 90 days. During and

Brucella melitensis. Wection occurs
after the bacterenua, localization may occur

BRUCELLOSIS IN LARGE ANIMALS

1351
in various tissues. Signs depend considersimilar to tl1at in goats (see above).

ably on tl1e site(s) of localization. Common

However, B ovis produces a disease unique
manifestations are abortion, temporary or
to sheep, in which epididymitis and orchitis
pem1anent sterility, orchitis, lameness,
impair fertility-the principal economic
posterior paralysis, spondylitis, and
effect. Occasionally, placentitis and

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occasionally meb.itis and abscess formation. abortion are seen, and there may be The incidence of abortion may be 0-800/o.

perinatal mortality. The clisease was first

Abortions may also occur early in gestation
described in New Zealand and Australia
and be undetected. Usually, sows or gilts
and has since been reported from many
that abort early in gestation return to estrus
sheep-raising areas of tl1e world. B ovis
soon afterward and are rebred.

infection among sheep in tl1e USA is rare.

Ste1ility in sows, gilts, and boars is

There is no evidence that the disease is
common and may be tl1e only manifestation. present in any oilier animal species. Rare Before attempting treatment for other
natural and experimental infections in
diseases, it is logical to test for brncellosis
fai111ed red deer stags have been reported
in herds in which stelility is a problem.

in New Zealand.

Steruity in sows is more frequently

Rains as young as 8 wk have been
temporary but may be permanent. In boars,
infected expelimentally by various
orchitis, usually unilateral, may occur, and
nonvenereal routes. The disease can be
fertility appears to be reduced.

transmitted ainong rains by direct contact.

Active infection in ewes is unusual but has

Diagnosis: The p1incipal means of
developed after mating with naturally
diagnosis in pigs is tl1e brucellosis card
infected rains. Contaminated pastures do

(rose bengal) test; however, otl1er sernm
not appeai· to be important in spread of the
agglutination tests or complement fixation
disease. Infection frequently persists in
tests have been used. It is generally accepted ran1s, and a high percentage shed B ovis tl1at the tests have limitations in detecting
intermittently for several years.

brncellosis in individual pigs. Thus, entire

Primary maiufestations ai·c lesions of
herds or units of herds, ratl1er tl1an
the epididymis, tunica, and testis in rams;
individual pigs, must be tested in any control
placentitis and abortion in ewes; and
program. Low agglutinin titers are seen in
occasionally perinatal death in lambs.

almost any size herd, regardless of infection

Lesions may develop rapidly. In rams, the
status, and a few infected pigs may have no
first detectable abnormality may be a
detectable titer. The card test is usually more marked deterioration in semen quality accurate tl1an conventional agglutination
associated with the presence of inflamtests. Supplemental tests designed for cattle matory cells and organisms. An acute
may also be used for pigs.

systemic phase is rarely seen in naturally
occurring infections. After regression of

Prevention and Control: Caution
the acute phase-which may be so mild
should be practiced in tl1e purchase of
as to go unobse1ved-lesions may be
individual pigs tl1at exhibit a low agglutinin
palpated in the epididymis and scrotal
titer unless tl1e status of tl1e entire herd of
tunics. Epididymal enlai·gement may be
origin is known. Pigs should be isolated on
unilateral or bilateral. The tail of the
return from fairs or shows before reenterepididymis is involved more frequently ing the herd. Replacements should be
than the head or body, and the most
purchased from herds known to be free of
prominent lesion is spennatoceles of
brucellosis, or tl1ey should be tested and
variable size containing partially inspisisolated for 3 mo and retested before being sated spermatic fluid. The tunics freadded to tl1e herd.

quently become thickened and fibrous, and

There is no vaccine for brucellosis in
extensive adhesions develop between
swine, and no practical recommendations
them. The testes may show fibrous
can be made for treatment. Control is based
atrophy; these lesions are usually
on test and segregation as well as slaughter
permanent. In a few cases, palpable lesions
of infected breeding stock. Brucellosis
ai·e transient, while in others, organisms
remains a problem in feral swine and is a
may be present in semen over long periods
potential source of infection for domestiwithout clinically detectable lesions.

cated herds and people.

Because not all infected rams show
palpable abnormalities of scrotal tissues

BRUCELLOSIS IN SHEEP

(and not all cases of epicliclymitis ai·e clue
to brucellosis), tl1e remaining rams must

Brucella melitensis infection in certain
be exaininecl further. Rams shedding
breeds of sheep causes clinical disease
orgaiusms, but having no lesions, must

1352

BRUCELLOSIS IN LARGE ANIMALS
be identified by culture of semen. Repeated
noninfected ratns from older, possibly
examinations may be necessaty to identify
infected rams.

intennittent shedders. Microscopic

Immunization of weaner rams with
examination of stained semen smeat'S may
attenuated (Rev. 1) B melitensis has been
also be helpful; fluorescent antibody
recommended in some countries. Because

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exatnination is a highly specific diagnostic
infection in ewes apparently originates
aid. Serologic tests used for eradication of
almost exclusively from service by
disease and certification of anin1als include
infected rams, lamb losses through
indirect ELISA, complement fixation,
infection of ewes may be controlled
hemagglutination inhibition, indirect
economically by restricting vaccination to
agglutination, and gel diffusion.

ratns. There is no recommended vaccina

Incidence and spread of the disease may
tion in the USA.

be reduced by regular exan1ination of ran1s

Chlortetracycline and streptomycin used
before the breeding season and culling of
concurrently have effected bacteriologic
those with obvious genital abnormalities.

cw·es. However, treatment is not economic

Because susceptibility in rams increases
except in especially valuable ran1s, and even
markedly with age, it is advantageous to
if infection is eliminated, fertility may
keep a young ratn flock and isolaLe
remain impaired.

CONTAGIOUS AGALACTIA

First recognized in ltaly more than 200 yeat'S short distances and ingestion of contamiago, contagious agalactia is primarily a nated water.

disease of dairy sheep and goats and is

Sheep and goats are equally susceptible
characterized by an interstitial mastitis
to M aga.laetiae, but goats are additionally leading to a loss of milk production,
susceptible to Mee, Mrne, and M putrefa
atthritis, and infectious keratocortjunctivi
ciens. However these mycoplasmas may be
tis. It is more often seen on farms practicing
found in both ailin1al species in regions
traditional husbandry. Contagious agalactia
where they graze together. In general,
is principally caused by the wall-less
clinical disease is more pronounced in
bacteriwn Myeoplasma agalaetiae, but in
goats. Antibodies to Mee and Mme have recent years, M rnyeoides eapri (Mme;
been detected in South American can1elids,
fom1erly known as LC), and, to a lesser
but no mycoplasmas have yet been isolated.

extent, M eaprieolum eaprieolum (Mee)

Because alpacas, llatnas, and vicw1as
and M putrefaciens have also been isolated
develop polyarthr:itis, pnewnonia, and
from goats with mastitis, arthritis, and
pleuritis, it is likely that mycoplasmas may
occasionally, respiratory disease. The
eventually be found. Mme has also been
clinical signs of these infections are
isolated from cattle, although its role in
sufficiently sinlilar to those of contagious
disease in this species is hot clear·.

agalactiafor the OIE to include them as

Contagious agalactia has been reported in
causes of this listed disease.

many countries swTounding the Mediterranean, in particular Portugal, Spain, Greece, Etiology and Epidemiology: Mycoplas

Italy, France, Tw·key, Israel, and North
mas that cause contagious agalactia can

Africa, as well as in many parts of tl1e
persist for > 1 yr after clinical recovery of

Middle East, most notably Iran, India,
infected aninlals, wllich are the main

Mongolia, and parts of South America.

reservoir of the orgatlism. The introduction

Sporadic cases have been reported in the
of such carriers into a susceptible flock can

USA.

initially cause high morbidiLy and mortality.

Once established in a herd, young rumi

Clinical Findings and Lesions: The
nants become infected while suckling.

incubation period ranges from 1 wk to 2 mo

Adults are contanlinaLed via the milkers'

and can be followed by either an acute
hands, milking machines, or possibly by
disease with fever, neurologic signs, and
bedding. Other routes of transmission may
occasionally deatl1 or, more commonly, a
include aerosols of infective exudates over
subacute or chronic disease characterized

CONTAGIOUS AGALACTIA

1353
by mastitis, arthritis, and infectious
although rarely in the same animal.

keratoconjunctivitis. The infection begins

However, an acute forn1, in which there is
as an interstitial mastitis giving rise to a hot,
septicemia without specific local signs, can
swollen, and painful udder, followed by a
confound the diagnosis.

sudden drop in the quantity and quality

Laboratory diagnosis is the only means of

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of milk production. The milk may appear
confinnation. Preferred samples from living
discolored and granular, separating into
animals include milk and udder secretions,
watery and solid phases, or take on a thick,
joint fluid from arthritic cases, eye swabs
yellow consistency with milk clots
from cases of ocular disease, and serum for
obstructing the teat duct. After several
antibody detection. The ear canal is a rich
days, the affected udder shrinks because
source of pathogenic mycoplasmas.

of damage to secretory tissue. Abscesses

Isolation of mycoplasmas from the blood
within the udder and enlargement of the
during the brief mycoplasmaemia stage of
retromammary lymph nodes may also be
the disease is rarely successful. Samples
seen. Generally the clinical condition
from dead animals should include udder and
improves after a few weeks, with partial
associated lymph nodes, joint fluid, lung
restoration of udder function, but the
tissue ( at the interface between diseased and
quality of milk remains abnormal. In some
healthy tissue), and pleural or pericardia}

cases, atrophy and fibrosis lead to
fluid. Samples should be kept moist and cool
permanent loss of milk production.

and sent promptly to a diagnostic laboratory.

The acute syndrome may lead to abortion

PCR tests, which can be performed directly
and weak lambs as a result of ingestion of
on clinical samples, including milk, can be
infected milk or starvation brought about by used to confirm the diagnosis.

reduced milk production. Arthritis can be

Identification of the organism is usually
seen in adults and the young who find it
achieved by the growth inhibition or
difficult to keep up with the flock; affected
immunofluorescence tests using hyperimanimals may be seen limping or sitting on mune rabbit antiserum and, increasingly, by
their carpal joints because of the discom

PCR tests that can be pe1formed directly on
fort. In these animals, the joints are hot,
clinical samples, including milk, within
swollen, and painful. Conjunctivitis
hours. PCR, together with denaturing
presents as a discharge of clear exudates
gradient gel electrophoresis, which can
from the eyes, followed by corneal opacity,
detect all causative mycoplasmas in a single
keratitis, purulent exudation, and occasionreaction, has been described.

ally ulceration and panophthalmitis. Severe

Detection of antibodies in serum by
cases may result in irreversible blindness.

ELISA provides rapid diagnosis of disease

Necropsy often reveals generalized
but may not be very sensitive in chronically
peritonitis among anin1als that die during
affected herds and flocks. Indirect ELISA,
the acute stage. The infected udder is
some conunercially available, have been
grossly atrophic in either one or both
used routinely in control programs to
halves. Microscopically, the chronic
screen herds for M agalactia.e but less so
inflanlffiatory reaction in the stroma shows
for Mme and Mee. Immuno (Western)

increased fibrosis and a reduced number of
blotting can be used to confirm suspect
glandular acini. Infected joint capsules are

ELISA results and can distinguish field
edematous, and the synovium may contain
infection from vaccine antibody. In areas
clumps of fibrin. Articular surfaces may be
believed to be free of contagious agalactia,
eroded and occasionally ankylosed. In early
it is usually necessary to isolate and identify
stages of keratitis, the cornea is edematous
the causative organism to confinn infection.

and infiltrated with leukocytes; later,

Serologic tests are not widely available for
abundant purulent exudate infiltrates both

M putrefaciens.

the cornea and the ciliary body.

A number of other mycoplasmas such as

M putrefaciens is common in milking

M arginini, M bovigenitalium, and M
goat herds in western France. It can be
bovis have occasionally been isolated from
isolated from the milk of animals with or
mastitic milk and joint fluids, but their role
without clinical signs, and milk production
in disease is not known. M conjunctivae is a is usually severely affected. The milk of
common cause of keratoconjunctivitis but
affected animals has a characteristic smell
does not affect the udder or joints. Other
of putrefaction.

bacteria causing mastitis include staphylococci, streptococci, Escherichia coli, and Diagnosis: When a flock is severely

J(lebsiella; caprine arth!itic encephalomyaffected, clinical diagnosis is easy; the elitis virus and Erysipelothrix rhusiop
three major signs-mastitis, arthritis, and
athiae should also be considered in cases of keratoconjunctivitis-are generally present, arthritis.

1354

CONTAGIOUS AGALACTIA

Treatment, Control, and Prevention:

strains of M agalactiae. The use of

Regular laboratory monitoring of flocks/
erytlu-omycin and tylosin can destroy milkherds and replacement animals may help to producing tissue in small ruminants. In
prevent spread or introduction of disease
many disease-free countries and regions,
and can be done on serum and/or milk
a confirmed infected herd is always

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(including bulk tank milk) by serology,
slaughtered.

culture, or PCR. Culling or isolation of

In countries bordeting the Mediterrainfected animals is generally advised, nean, both attenuated and inactivated
because udder damage is considered
vaccines have been used with mixed
permanent. When this is not possible,
success. Some have provided protection
hygienic measures, such as improved
from clinical disease and have been useful
milking hygiene and pasteurizing milk
in endemic areas; however, they do not
before feeding to the young, should be
prevent transmission of the mycoplasmas.

implemented.

Generally, the duration of immunity,

Antibiotics that inhibit cell wall synthesis
particularly to the fonnalinized, inactivated

( eg, penicillins) are not effective against
vaccines that are used in Europe, is sho1t.

contagious agalactia. In vitro tests have

Vaccines containing two or three of the
shown that strains of M agalactiae are still causative agents are now available, but
sensitive to fluoroquinolones and macpublished data on their effectiveness is rolides. These can bring about clinical
scarce.

in1provement, paiticularly if given early in
the djsease, but there is always the danger

Zoonotic Risk: There is no evidence that
of promoting carrier animals. Resistance
contagious agalactia is transmitted to
to tetracyclines has been reported for some
people.

CYSTIC OVARY DISEASE

An10ng domestic animals, cystic ovary
cally related but differ clinically. Both
disease (COD) is most common in cattle,
are characterized by the presence of a
paiticularly the dairy breeds, but it occurs
fluid-filled structure >25 mm dian1eter,
sporadically in dogs (seep 1395), cats, pigs, persisting for > 7 days and associated with
and perhaps mares.

abnom1al reproductive perfonnance.

Cystic Ovary Disease and the Corpus

Luteum: Three ovarian structures in cattle
may include the tem1 "cyst": follicular cysts, FOLLICULAR CYSTIC OVARY
luteal cysts, and cystic corpus luteurn (CL).

DISEASE

However, in contrast to the other two, the
structure sometimes described as a cystic

(Cystic follicles, "Bulling")

CL (a CL with a cavity or "lacunae") actually Follicular cystic ovary disease may be
arises after normal ovulation. CL with a
defined on a number of levels. Essentially,
lacunae are a normal stage or variation of
all signs relate to the disruption of the

CL development ai1d ai·e found in nom1ally
nonnal endocrine events of the estrous
cycling and pregnant cows without
cycle, through the failure of ovulatory
concurrent abnonnal reproductive
events. Key features include the presence of
performance. The lacunae can be compared
a thin-walled, fluid-filled structure >25 mm
with the homogeneous, liver-like consistdiai11eter and present for> 7 days in the ency of the base of a typical CL.

absence of a CL on ultrasonographic

The CL may have an ovulation crown or
imaging of the ovary. Along with occasional
papilla at its apex; however, 10%-200;6 of
behavioral signs of nymphomania, such as
functional, nonnal CL fail to develop this
short inter-estrus intervals and excessive
feature.

heat behavior, ai·e endocrine changes,

The two pathologic forms of bovine cystic including a suboptimal luteinizing honnone ovary disease, follicular cysts and luteal

(LH) surge and persistently increased
cysts, are etiologically and pathophysiologi-
estradiol levels.

CYSTIC OVARY DISEASE

1355

Etiology and Pathogenesis:

signs, but others may be sexually quiescent;

A hereditary predisposition has been
anestrous or subestrous cows are a
implicated in dairy cattle. Cystic ovary
common presentation.

disease or syndrome (COD) is commonly

The affected ovaries generally are
considered to be associated with negative
enlarged and rounded, but their size vaiies,

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energy balance and stress factors in dairy
depending on the number a11d size of cysts.

cows that are high milk producers. Genetic

Their surface is smooth, elevated, and
predisposition to partition glucose to the
blister-like. Cysts frequently are multiple
udder to prioritize lactose synthesis and
and may approach 4-6 cm in diameter.

milk production is characterized by insulin

Under the influence of honnones produced
resistance in Holstein cattle. IGF-1 is a
by the cystic ovary or the lack of hom10nes
cytokine associated with metabolic

( especially progesterone) normally present
influences on reproduction and hence COD.

during estrous cycles, the uterus undergoes

Incidence increases with age. Most cases
palpable changes, which in turn vary with
occur within 3-8 wk of parturition at the
the duration of the cystic condition. Thus,
first attempted postpartum ovulation,
during tl1e first week, the uterine wall is
coinciding with peak daily milk production
thickened and edematous as an extension
and rapidly decreasing body condition. The
of the preceding estrus. Toward the end of
reported herd incidence is 5%-25% per
the first week, the uterine wall develops a
lactation, or higher in some problem herds.

sponge-like consistency. In chronic cases,

Dming normal proestrus, regression
atony and atrophy of the uterine wall are
of the CL coincides with development of a
common. Occasionally, the uterine horns
selected follicle, while the growth of any
become markedly shortened. Some degree
additional follicles is inhibited. In animals
of mucoid to mucopurulent vaginal
developing COD, ovulation fails to occur
discharge is common. Hydrometra, a
and the dominant follicle continues to
fluid-filled, extremely thin-walled uterus,
enlarge. An important component of the
is seen occasionally.

etiology is the failure of positive feedback of
follicular estrogen on the hypothalamus via

Diagnosis: Palpation of the uterus may
estrogen receptor ex to release sufficient
help differentiate a follicular cyst from a

GnRH during estrus to trigger an LH surge.

dominant preovulatory follicle; the estrous

The end result is a failure of ovulation at the
cow has a coiled, extremely turgid uterus
time of estrus. Moreover, other follicles
and a follicle. As noted earlier, cystic cows
may grow and form multiple cysts either
fail to ovulate a preovulatory follicle after
bilaterally or unilaterally.

undergoing CL regression and, on

Grossly, follicular cysts resemble
exainination of the reproductive tract, they
enlarged follicles, generally defined as
present with a large follicle, absence of a
varying in size from 25 mm to 50-60 mm in

CL, and absence of a turgid uterus.

dian1eter. The size and fom1 of an affected

Ultrasound technology per rectum can be
ovary depends on the number and size of
used to differentiate cysts from corpora
cysts present. The cystic ovary is capable, at
lutea and may help diagnose cyst type (ie,
least initially, of steroidogenesis, and its
follicular cyst wall diameter has been
products vary from estrogens to progesterdescribed as <3 nun vs luteal cyst wall one to androgens. The actions of the various diameter >3 nun). Larger, multiple cysts are hormones produced or the absence of the
easily identified by rectal palpation. History,
stabilizing action of high progesterone from
conformation, and uterine changes, when
the normal CL during -75% of the estrous
present, provide supplemental diagnostic
cycle (or both) are responsible for the
evidence.

changes seen in the genital tract, body
conformation, and general behavior.

Treatment: COD may be frustratingly
unresponsive to therapy. Some cysts

Clinical Findings: Behavioral aberrations
respond readily to an LH-type honnonal
range from frequent, intem1ittent estrus
treatment. In the past, human chorionic
with exaggerated monosexual drive to
gonadotropin (hCG) was commonly used.

bull-like behavior, including mounting,

It is most effective at 10,000 USP units IM,
pawing the ground, and bellowing. This
although success with lower doses given
behavior may be accompanied by

IM or IV has also been reported.

masculinization of the head and neck.

Hormone therapy with GnRH may be

Relaxation of the vulva, perineum, and the
effective at 100 mcg and less antigenic than
large pelvic ligaments, which causes the tail hCG. To hasten the onset of the first estrus head to be elevated, can occur in chronic
after treatment, prostaglandin (PG) F2cx
cases. Some affected cows show these
products can be given 7 days after hCG or

1356

CYSTIC OVARY DISEASE

GnRH. Ovulation synchronization protocols
tl1e srune as for follicular cysts. The release
combine GnRH and PGF2o: to control
of luteinizing honnone (LH) may be somefollicular dynamics, luteolysis, and what greater than that occurting when
ovulation. They allow for fixed timed
follicular cysts develop, and sufficient
artificial insemination (TAI) of cattle
to initiate luteinization of follicles but

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without the need for estrus detection and
inadequate to cause ovulation. Luteal cysts
have been successfully used to treat cows
may be an extension of follicular cysts such
with cystic ovaries. This protocol consists
that the nonovulatory follicle is partially
of giving GnRH, then prostaglandin 7 days
luteinized spontaneously or in response to
later, then a second administration of GnRH
honnonal therapy.

48 hr later, and finally TAI 0-24 hr later.

Breeding on the first estrus may reduce

Clinical Findings: Lu teal cysts are
recurrence by establishing pregnancy as
accompanied by nom1al conformation and
soon as possible. However, COD recurrence
anestrous behavior. Rectal palpation reveals
is a tisk.

a quiescent uterus charactetistic of tl1e

Manual rupture is used, but the potenluteal phase of tl1e estrous cycle. Luteal tial danger of traumatizing the ovruy ru1d
cysts are recognized as smooth, fluctuant
causing hemorrhage with subsequent local
domes protruding above the surface of the
adhesions should not be overlooked.

ovary. Usually, they are single structures.

Luteal cysts ru·e differentiated from

Prognosis: After therapy with an LH-type
follicular cysts on the basis of palpable charhonnone, a normal, fertile estrus can be acteristics of both the structurn and the
expected in 15-30 days. With GnRH therapy,
uterus and, to some extent, on the cow's

25% of cases required a second treatment,
behavior. Progesterone assay and ultraand 5% required a third. One-third of the sonography can help differentiate between
cases treated for the third ti.me did not
follicular and luteal cysts, although with
respond. Spontaneous recovery is possible
either method a final diagnostic decision
and is most conrn10n in cases arising during
remains somewhat subjective. On attempts
the first 50 days after calving. Likewise,
to manually rupture the cystic structure,
successful treatment encourages perpefollicular cysts burst or rupture under tuation of the disease in the herd if the
minimal pressure whereas luteal cysts
offspting ru·e used for breeding. Although
c3JU1ot be ruptured with reasonable force.

COD in cattle clearly has a genetic

Both types of cysts respond to LH or GnRH
component, it is unlikely that a single fann
therapy, but PGF,cx will lyse some luteal
using artificial insemination can significysts and generaily all diestrual CL
cantly influence the incidence. In Sweden,
structures.

progress has been made in reducing the
condition through culling and selection

Treatment and Control: The treatment
procedures for bulls used in artificial
of choice is luteolytic doses of PGF2cx if a
insemination, but affected cows are often
correct diagnosis can be asce1tained. A
still treated.

nom1al estrus is expected in 3-5 days. The
major limitation of this treatment is the

LUTEAL CYSTIC OVARY DISEASE
difficulty in accurately estin1ating the

3Jl1ount of luteal tissue present. If the

Luteal cystic ovary disease is charactetized
structure being diagnosed as a luteal cyst is
by enlarged ovru·ies with one or more cysts,
really a developing CL ( as discussed above,
the walls of which ru·e thicker than tl10se of
sometimes called a cystic CL), it may not
follicular cysts because of a lining of luteal
respond because dairy cows do not become
tissue. Incidence ratios of follicular versus
highly responsive to the luteolytic action of
luteal cysts vary greatly because of

PGF2o: until day 6 after estrus. Ultrasound
diagnostic tendencies of individual
ex3Jl1inati.on is increasingly conu11on and
vetetinarians. Classically, luteal COD is
facilitates diagnosis of ovarian structures.

defined as the presence of a fluid-filled

Luteal cysts also respond to htunan
ovarian structure >25 nrn1 di3Jl1eter
chorionic gonadotropin and GnRH therapy
persisting > 7 days in the absence of a CL
that is effective in the treatment of follicular
and with a wall diruneter >3 mm, usually
cysts, but the next estrus could occur 5-21
associated with abnormal reproductive
days after treatment. Mrumal rupture of
signs. Normal lacunae fonnation in CL may
luteal cysts is not recommended because of
be incorrectly classified as luteal COD.

the risk of tratuna and hemonhage. Because
of poor estrus detection practices on many

Etiology and Pathogenesis: The basic
dairy farms, the treatment of choice for both
causes of true luteal cysts ru·e believed to be
follicular and luteal cysts is intravaginal

EQUINE COITAL EXANTHEMA

1357
progesterone/prostaglandin ( a fixed
placenta, ketosis, etc) ai·e much more likely
timed artificial insemination protocol)

to develop cysts. Attempts to reduce these

( see p 1355). Application of this protocol in complications are indicated. 4) Have herd
affected cows promotes timely breeding
genetics been considered? It is well accepted
after treatment.

that ovarian cysts are more common in

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certain lines. 5) Has the nutritional program

CYSTIC OVARY DISEASE AS A
of the herd been evaluated? Nutritional

HERD PROBLEM
problems are frequently implicated as a risk
factor for COD. Proper nutlitional manage

Individual herds may experience excepment of da.Lty herds is always warranted.

tionally high rates ( -50%) of cystic ovary

Monitoring the effects of the nutritional
disease (COD) over a period of months.

prograin via a body condition scoring

Detemlining the cause of these multifacto-
prograi11 should be done as part of the effo1t

1ial episodes is not easy, but the following
to reduce ovaiian cysts in problem herds.

questions should be addressed: 1) Is the

6) Has management of cows around estrus
diagnosis accurate, ie, are the structures
changed? Social and environmental changes
being identified as cysts really cysts? This
may cause stresses associated witl1 COD.

can be established via second opinion
diagnoses, detemlination of milk or plasma

CYSTIC OVARY DISEASE IN
progesterone levels, ultrasound exanli.na

MARES
tion of the ovaries in suspected cases,
observing ovarian changes and time of

When diagnosing the reproductive status
estrous activity after treatment with
of mares, it must be remembered that
prostaglandin products, and/or improving
follicles during estrus are normally 4--6 cm
diagnostic skills by continuing education.

in diameter. Ovulation failure can also be

2) Has the palpation exanli.nation schedule
seen in mai·es having irregular estrous
for the herd changed? Initiating routine
cycles during the spring or fall transition
postpartum examinations for all cows and
phases of the reproductive cycle, but this
increasing frequency of herd visits can
state is not treated in the san1e way as the
result in an increased apparent incidence.

cystic ovary disease condition of cattle.

3) Has the herd incidence of peripaiturient

The granulosa cell tw110r condition in
complications and stress increased? Cows
mai·es causes marked enlai·gement of one
having problems around calving (such as
ovary but differs from cystic ovaiy disease
twins, milk fever, dystocia, retained
of cattle.

EQUINE COITAL EXANTHEMA

(Genital horsepox, Equine venereal balanitis in stallions) Etiology and Epidemiology: Equine coi

Equine coital exa.I1thema is probably
tal exanthema is a benign venereal disease
transmitted only in the acute phase of the
of horses tl1at probably occurs worldwide. It
disease; after the lesions have healed,
affects both sexes and is caused by equine
horses do not appeai· to shed the virus.

herpesvirus type 3 (EHV-3). Tlli.s virus has a

However, tile existence of a carrier state is
single antigenic type but also has small and
unclear: the scai-s tliat persist after healing
large plaque variants ill tissue culture,
may identify potential carriers, but such
indicating that variation may occur in the
asymptomatic carrie1-s have not been
severity of field outbreaks. Although the
identified. Immwli.ty is short-lived, but
pril11ary route of transmission is venereal,
evidence from stallions shows tllat
outbreaks have been docmnented m which
recurrence is not likely within a single
tra.I1Smission occurred via contanli.nated
breeding season.

supplies and instruments or by the use of a
single glove for rectal exainination of ma.Ily

Clinical Findings: Clinical signs in mares
mares. It is probably for this reason that
develop 4--8 days after sexual contact or

EHV-3 has also been isolated from horses
veterinary exainination a.Ild are ma.Ili.fest by
that have not been bred.

tile appeara.I1ce of multiple, circular, red

1358

EQUINE COITAL EXANTHEMA
nodules up to 2 mm in diameter on the

Diagnosis: A tentative diagnosis is
vulvar and vaginal mucosa, the clitoral
based on clinical signs and confirmed by
sinus, and perineal skin. These lesions
identifying ( using electron microscopy) the
develop into vesicles and then pustules and
virus in cells from the margin of ulcers.

eventually rupture, leaving shallow, painful,

Typical intranuclea.r herpesvirus inclusion

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ulcerated areas that may coalesce into
bodies can also be seen in cytologic or
larger lesions. Edema can develop in the
histologic preparations. Acute and
perineum and may extend to between the
convalescent samples for serum neutralizathighs. Occasionally, ulcers will be found on tion or complement fixation tests can also
the teats, lips, and nasal mucosa. Secondary
be diagnostic, but these tests must be
bacterial infection of the ulcers by
interpreted carefully because both EHV-1

Streptococcus spp is common, causing the
and EHV-4 have also been isolated from
ulcers to enlarge and exude a mucopurulent
genital lesions.

discharge. In such cases, the horse may
become febrile. Unless secondary bacterial

Treatment and Prevention: Sexual rest
infection occurs, skin healing is complete
is essential to allow ulcers to heal and
within 3 wk, but clitoral and vaginal ulcers
prevent spread of the disease. The use of
heal more slowly. Skin lesions persist for
antibiotic ointments to prevent secondary
long periods as unpigmented scars.

infections is also advisable. Affected horses

However, pregnancy rates are not reduced.

should be isolated until all lesions have

Lesions in stallions are similar to those in
healed, and disposable equipment should be
mares and are found on both the penis and
used for examinations. During the acute
prepuce. As a result, intromission is painful,
phase of the disease, mares should be bred
and the stallion may be reluctant to
only by attificial insemination. No vaccine is
copulate. If copulation does occur during
available. All horses should be examined
the ulcerative stage, the ulcers may
carefully before they are allowed to breed,
hemon-hage into the ejaculate, reducing
keeping in mind that the incubation period
sperm viability.

is up to 10 days.

MASTITIS IN LARGE ANIMALS

Mastitis, or inflammation of the mammary
primarily function as producers of milk for
gland, is predominantly due to the effects of
dairy products, particularly dairy cattle.

infection by bacterial pathogens, although

(See also UDDER DISEASES, p 1385.)

mycotic or algal microbes play-a role in
some cases. Pathologic changes to milk

MASTITIS IN CATTLE
secreting epithelial cells from the inflammatory process often bring about a decrease Almost any microbe that can oppottunistiin functional capacity. Depending on the cally invade tissue and cause infection can
pathogen, functional losses may continue
cause mastitis. However, most infections
into further lactations, which may reduce
are caused by various species of streptoproductivity and potential weight gain for cocci, staphylococci, and gran1-negative
suckling offspring. Although most infections rods, especially lactose-fennenting result in relatively mild clinical or subclinical orgatlisms of enteric origin, conunonly local inflanunation, more severe cases can
te1med coliforms. From an epidemiologic
lead to agalactia or even profound systemic
standpoint, the primary sources of infection
involvement, resulting in death. Mastitis
for most pathogens may be regarded as
has been reported in almost all domestic
contagious or environmental.

mammals and has a worldwide geographic

Except for Mycoplasma spp, which may
distribution. Climatic conditions, seasonal
spread from cow to cow through aerosol
variation, bedding, housing density of
transmission and invade the udder
livestock populations, and husbandry
subsequent to bacteremia, contagious
practices may affect the incidence and
pathogens are spread during milking by
etiology. However, it is of greatest frequency milkers' hands or the liners of the milking and economic importance in species that
unit. Species that use this mode of

MASTITIS IN LARGE ANIMALS

1359
transmission include Staphylococcus
referred to as mild or moderate. If the
aureus, Streptococcus agalactiae, and
inflanimatory response includes systemic

Corynebacterium bovis. Most other
involvement (fever, anorexia, shock), the
species are opportunistic invaders from the
case is termed severe. If the onset is very
cow's environment, although some other
rapid, as often occurs with severe clinical
streptococci and staphylococci may also
cases, it is termed an acute case of severe

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have a contagious component. Additionally,
mastitis. More severely affected cows tend
contagious transmission infrequently
to have more serous secretions in the
occurs for pathogens typically associated
affected quarter.

with environmental reservoirs, eg, through

Although any nun1ber of quaiters can
the development of host-adapted virulence
be infected simultaneously in subclinical
factors (Escherichia coli) or by shedding of mastitis, typically only one quarter at a time
overwhelming numbers of bacteria from
will display clinical mastitis. However, it is
infected udders (Trueperella [formerly
not unconm1on for clinical episodes caused

Arcanobacterium] pyogenes ).

by Mycoplasma to affect multiple quarters.

The bedding used to house cattle is the

Gangrenous mastitis can also occur,
primary source of environmental pathoparticularly when subclinical, chronic gens, but contaminated teat dips, intraman1-infections of S aurnus become severe
mary infusions, water used for udder
at tin1es of immunosuppression ( eg, at
preparation before milking, water ponds or
parturition). As with subclinical mastitis,
mud holes, skin lesions, teat trauma, and
culture of milk sainples collected from
flies have all been incriminated as sources
affected quarters is the only reliable method
of infection.

to determine the etiology of clinical cases.

Intramanimary infections are often
described as subclinical or clinical mastitis.

Subclinical mastitis is the presence of an

Subclinical Mastitis
infection without apparent signs of local

Epidemiology: All dairy herds have cows
inflanimation or systemic involvement.

with subclinical mastitis; however, the

Although transient episodes of abnormal
prevalence of infected cows varies from
milk or udder inflammation may appear,

5%-75%, and quarters from 2%-40%. Many
these infections are for the most part
different pathogens can establish a chronic
asymptomatic and, if the infection persists
infection in which clinical signs of mastitis
for at least 2 mo, are tem1ed chronic. Once
will manifest only occasionally. The primary
established, many of these infections persist focus of most sub clinical mas ti tis programs for entire lactations or the life of the cow.

is to reduce the prevalence of the conta

Detection is best done by examination of
gious pathogens S agalactiae and S aureus, milk for somatic cell counts (SCCs)

as well as other grain-positive cocci, most

(predominantly neutrophils) using either
notably Streptococcus dysgalactia.e ( which
the California Mastitis Test or automated
may also be contagious or an environmental
methods provided by dairy herd in1provepathogen), Streptococcus uberis, enteroment organizations. SCCs are positively cocci, and numerous other coagulase-negacorrelated with the presence of infection.

tive staphylococci, including Staphylococ

Inflanimatory changes and decreases in
cus hyicus, Staphylococcus epidermidis,
milk quality may start with secs as low

Staphylococcus x-ylosus, and Staphylococ
as 100,000 cells/mL. Although variable
cus intermedius. Herds have been

( especially if determined on a single
identified that have considerable subclinical
analysis), an sec of �280,000 cells/mL in
mastitis caused by gran1-negative rods such
a cow indicates a >85% chance of being
as Klebsiella sp, Serratia marcescens,
infected. Likewise, the higher the sec

Pseudomonas aeruginosa, and other
in a herd bulk tank, the higher the prevaatypical pathogens such as mycotic and lence of infection in the herd. Herd SCCs
algal microbes.

<200,000 cells/mL are considered desirable,

For contagious pathogens, adult lactating
and lower counts can be attained. Causative
cattle are most at risk of infection, either
agents must be identified by bacterial
while lactating or during the dry period.

culture of milk.

The prin1ary reservoir of infection is the

Clinical mastitis is an inflanimatory
manunary gland; transmission occurs at
response to infection causing visibly
milking with either milkers' hands or
abnom1al milk ( eg, color, fibrin clots). As
milking equipment acting as fomites.

the extent of the inflammation increases,

Primipai·ous heifers have been reported
changes in the udder ( swelling, heat, pain,
to be infected with staphylococci and
redness) may also be apparent. Clinical
streptococci before calving, although the
cases that include only local signs are
prevalence varies greatly ainong herds and

1360

MASTITIS IN LARGE ANIMALS
geographic regions. Teat-end dennatitis
cows not identified or cured during the
ca.used by the horn fly, H aematobia
initial therapy. Usually, 30-da.y monitoring
initans, which can harbor S aureus, has intervals are successful. A small percentage
been associated with increased risk of
of cows will not respond to therapy and are
infection in heifers, especially in wanner
best segregated or culled. In addition,

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clin1ates.

failure to use postmilking teat dipping and

For the contagious pathogens and
total d1y cow treatment to prevent new
coagulase-nega.tive staphylococci, there is
infections during the treatment period will
little or no seasonal variation in incidence
ultimately result in reinfection of the herd.

of infection.

Parenteral therapy is not likely to offer any
benefit over intra.i11an1rnary therapy.

Treatment: Therapy is given on the

Most other streptococci also display in
premise that treatment costs will be
vitro susceptibility to numerous antibacterioutweighed by production gains after als, especially 13-la.cta.in drugs. Despite this
elimination of infection. In the case of
apparent susceptibility, many streptococcal
contagious pathogens, elimination may also
infections are not as easily cured as those
result in a decrease of the reservoir of
ca.used by S agalactiae. Generally,
infection for previously noninfected cows.

subclinical infections caused by S uberis

No significant economic losses will occur as
and S dysgalactiae should be preferentially a result of delaying therapy until bacterial
treated at the end of lactation with
culture can be completed. However, many
intra.ina.inmary infusions of commercial d1y
subclini.cal cases selected as potential
cow products. Cure rates at this time may
therapy candidates have chronic infections;
exceed 75%.

pa.iticularly in the case of S aureus,

S aureus intra.ina.inrnary infections often prediction of therapeutic outcome by in
result in deep-seated abscesses. Therapy
vitro testing is unreliable. Drug distribution
is difficult, because resistance to antibacteafter int.ran1a.i11mary administration may not rials (paiticularly l3-la.ctan1s) is more be adequate because of extensive fibrosis
common tha.i1 with streptococcal infecand microa.bscess formation in the gland; it tions, and S au1·eus may survive intracelluis critical to assess the cow's inm1une status larly after phagocytosis when antibacterial
from a perspective of du.ration of infection,
concentrations a.i·e reduced. Int.ra.inanm1aiy
number of qua.rte.rs infected, and other
infusions may cure only 35o/o-400Ai of
variables.

infections; however, this number will be

Prevalence of S agalactiae infection can
substantially lower for chronic infections.

be rapidly .reduced by treating an entire

The success rate of therapy for chronic
herd-or more economically, all the
subclinical intra.ina.inmary infections
infected cows in a he.rd-with antibacterica.used by S aureus may be increased by als. All four quarters of infected cows
using both pai·enteral and intran1a.inmary
should be treated to ensure elinlina.tion
therapy. However, systemic therapy
of the pathogen and to prevent possible
involves extra-label drug use, and milk
cross-infection of a noninfected quarter.

and meat withholding periods must be

Cu.re rates can often be 75%--90%. Labeled
determined judiciously. Therapy should
use of conunercial int.ra.inan1ma.ry products
be administered for periods long enough
that contain a.inoxicilli.n, penicillin, and

(7--10 days) to allow effective killing of
e.rythromycin a.i·e as efficacious as procaine
the pathogen. It is most economical and
penicillin G infusions derived from
least likely to result in residues in milk if
multiple-dose vials. Consequently, use of
this therapy is applied to dry cows.

drugs originating from multiple-dose vials

Depending on susceptibility testing,

(labeled for systemic therapy) should not be lipophilic antibacterial drugs that used for intra.ina.inmary therapy, because
distribute well into mammary tissue,
conm1ercial intran1anm1a.iy preparations
such as oxytetracycline (11 mg/kg/day)

have superior quality control sta.i1dards for
a.re the best candidates for systemic
sterility and better reliability to predict withadministration, although several studies holding pe1iods for milk and meat after
have found oxytetra.cycline (administreatment. It is critical to apply strict aseptic tered for 4 days or less) to be ineffective.

techniques ( use of alcohol swabs for

Cure rates may not be much better than
teat-end prepa.i·a.tion) whenever any
those attained from spontaneous cure,
i.ntraman1rna.iy infusion product is
and cure must be defined critically.

administered.

Affected quarters should be monitored

Herds undergoing extensive therapy for S
ba.cteriologica.lly for ;;:30 days to
agalactiae must be monitored by SCCs a.i1d
encompass the refractory period when
bacteriology to further identify and treat
bacteria. may not be isolated.

MASTITIS IN LARGE ANIMALS

1361

Occasionally, premature agalactia will

Heifers: Many infections in calving
occur in chronically infected quarters,
heifers are caused by staphylococcal
particularly quarters infected with resistant
species other than S aureus, which have a
pathogens. Culling may be a practical
high rate of spontaneous cure. However,
option for these cows. Alternatively, it is
under some herd conditions, a substantial

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common to dry off the infected quarter and
portion of heifers are infected at calving;
continue to milk the cow. This may have
so.me of these infections are caused by
some benefit for genetically superior
pathogens such as S aureus. Potential anin1als within a herd or for cows that are to
sources include milk (fed to calves) and
be maintained until calving. Anecdotally, the body sites such as tonsils and skin. There overall milk production from such cows
is also a geographic risk factor: fly bite
may remain the san1e. The goal is to
dermatitis of the teat end, which
eliminate the infection by causing fibrosis of compromises this important physical the affected quarter, thus reducing the risk
barrier to infection, may play a role in
of frnther pathogenic change or systemic
the pathogenesis.

effects on the cow, as well as reducing risk

Intramammary infusions of 13-lactam
of infection for other cows.

antibacterial drugs 7-14 days before

D
expected calving dates have been reported
ry Cows: The dry period of the lactation
cycle is a critical time for the udder health of
to reduce the rate of intramammary
dairy cows. The man1mary gland undergoes
infections at calving. However, longterm
marked biochemical, cellular, and in1munobenefits on SCCs, milk production, and logic changes. Involution of the mammary
incidence of clinical mastitis during
parenchyma begins 1 -2 days after the end
lactation were found to be highly herd
of lactation and continues for 10-14 days.

variable and not consistent. Strict teat-end

During this time, the gland is particularly
antisepsis should be followed before
vulnerable to new intramammary infections.

infusion to prevent contamination; thus,

However, the involuted mammary gland
labor to handle animals for treatment can
offers the most hostile in1mune environment be extensive. This is not a recommended for bacterial pathogens. Consequently, the
management progran1 for many dairies.

dry period is an ideal tin1e to attain synergy

However, if herd records indicate that an
between antibacterial therapy and immune
tmdesirable proportion of first-lactation
function, without incurring the extensive
animals are infected at calving, particularly
costs typical of lactating cow therapy.

with staphylococci, this regimen may be

Intraman1mary administration of antibacteconsidered.

rials at the end of lactation has been a
standard of dairy mastitis management for

Prevention: New infections caused by

30 yr and continues to help reduce the

S agala.ctiae and S aureus can be prevented prevalence of mastitis in most dairy herds.

by focusing management efforts on milking

Nrnnerous commercial products are
technique and hygiene. Clean and dry
available and include penicillin, cloxacillin,
bedding, clean and dry udders at the tin1e of
cephapirin, ceftiofur, or novobiocin. One
milking, and lack of teat-end lesions all have
tube per quarter is sufficient and should be
a positive effect on control. The single most
administered immediately after the last
important management practice to prevent
milking of lactation. Therapy should not be
transmission of new infections is the use of
repeated by intraman1mary infusion; if there
an effective germicide as a postmilking teat
is a need to extend therapy, systemic
dip. These products should be applied as a
administration should be used as an adjunct
dip (rather than a spray) inu11ediately after
to the intran1an1mary infusion. In addition
milking. Other practices that augment teat
to eliminating existing subclinical
dipping include use of individual towels for
infections, one of the most critical roles
drying teats, gloves for milkers' hands, use
of dry cow therapy is to prevent new
of a premilking gem1icide (spray or dip),
infections. However, most conm1ercial dry
attachment of units at the proper time after
cow products have little or no activity
teat stimulation (60-120 sec), cleaning
against gram-negative pathogens, and their
milking units after an infected cow has been
administration at the start of the dry period
milked, or segregation of infected cows into
will not be effective against new infections
a separate milk group. This last option may
that begin during the periparturient period.

be unrealistic for cattle in free housing that

The anti.microbial therapy can be suppleare normally segregated for nutritional or mented by subsequent infusion of internal
reproductive reasons. Routine milking equipteat sealants that serve as a barrier to help ment evaluations should be conducted to
reduce new infections.

ensure that the teat-end vacurnn is operating

1362

MASTITIS IN LARGE ANIMALS
at a proper level and remains stable during

The standard metl10ds to monitor
milking. Proper pulsator function should be
subclinical mastitis, ie, routine somatic cell
maintained, and liners and rubber air hoses
counts (SCCs) and culture of cows with
should be replaced as needed.

increased SCCs, are poor predictors of herd

Proper milking hygiene also reduces
clinical mastitis episodes. Cows witl1 high

VetBooks.ir
the new infection rate of noncontagious

SCCs caused by chronic infections may
pathogens. More importantly for environoccasionally display clinical mastitis, mental pathogens, cows should be provided
although it is usually mild. However, cows
dry, clean housing. Emphasis should be
with low SCCs are also prone to develop
placed on bedding and any other practices
clinical mastitis. Herds with low SCCs may
that reduce the exposure of the teat end to
actually have a higher incidence of clinical
bacteria. Inorganic bedding suppo1ts less
cases caused by environmental organisms
bacterial growth than cellulose-based

(as high as 30-50 cases/100 cows/yr) than
material; thus, sand is preferred over
herds with higher SCCs. Similarly, routine
sawdust, straw, recycled paper, or manure.

culture of milk samples from a cow with a

In particular, higher incidence of infections
low SCC is a poor indicator of the probabilcaused by Klebsiella has been associated ity of developing clinical mastitis, especially
with sawdust bedding. Similarly, a higher
if the culture yielded no organisms.

incidence of infections caused by environ

Thus, tl1e incidence of clinical cases, and
mental streptococci has been associated
data from each case tl1at may determine risk
with straw bedding. However, the concenfactors ( eg, season, age, stage of lactation, trations of bacteria can vary greatly
and previous episodes), should be recorded
depending on moisture and presence of
as part of a mastitis control program. Milk
organic matter (such as in sand after
samples should be collected from affected
recycling). Thus, identification of reservoirs
quarters and, when feasible, antibacterial
of infection should not be based solely on
susceptibility testing perfonned. For welltl1e choice of bedding material. Regular managed herds in which mastitis caused
cleaning or changing of bedding, reducing
by contagious pathogens has been conheat stress, removing udder hair, preventing trolled, a goal for the incidence of clinical
teat traw11a, reducing udder edema in
mastitis should be 1-2 cases/100 cows
periparturient cows by nutritional
milking/mo. Severe mastitis cases should be
management of potassium and sodiwn
in the range of 1-2 cases/100 cows milking/yr.

intake, and preventing frostbite and fly

'Typically, 3%-400/o of milk samples
exposure all have a positive impact on
collected from clinical mastitis cases yield
environmental mastitis control.

no organisms on culture. However, of the
samples that do yield organisms, 900/o-95%

Clinical Mastitis
of the isolated bacteria include a wide
variety of streptococci, staphylococci,

When the balance between host defenses
or colifonns. lf this is not the case,
and invading pathogens causes a marked
especially if a single pathogen such as a
inflan1matory response, clinical signs
noncolifonn gram-negative rod or a mycotic
become apparent. Infectio'hs from any
or algal (Protolheca sp) predominates, a
patl10gen can be clinical or subclinical,
point source of infection should be
depending on the duration of infection, host
considered.

inunune status, and pathogen virulence.

Control of clinical mastitis usually focuses

Severe Clinical Mastitis: Colifonns
on prevention and elimination of pathogens

Qactose-fennenting gram-negative rods
that arise from an environmental reservoir.

of the fan1ily Enterobacteriaceae) are the

Thus, the epidemiology and prevention of
most conu11on cause of tltis fom1 of mastitis.

clinical mastitis is similar to previously

After infection, colifonu nun1bers in milk
discussed concepts regarding control of
increase rapidly, often attaining peak
subclinical mastitis.

bacterial concentrations within a few hours.

A subsequent decline (rapid in most cases

Epidemiology: Except for outbreaks
but may take several days in truly severe
of Mycoplasma, clinical mastitis in most
mastitis) in bacterial concentration follows
dairy herds is caused by environmental
neutrophil migration into the gland. Most
pathogens. In addition, many clinical mascoliform infections are cleared from the titis cases are transient, especially those
gland with few or mild clinical signs.

that are initial episodes for a cow and

However, if bacterial concentrations
quarter. Thus, from an epidemiologic
are increased enough to elicit an acute
perspective, assessment of clinical mastitis
inflammatory response, systemic involveis based on incidence and not prevalence.

ment is a frequent consequence.

MASTITIS IN LARGE ANIMALS

1363

Mastitis caused by colifonns results in a
dexan1ethasone (30 mg, IM) to dairy cows
higher incidence of cow death or agalactiaimmediately after introduction of E coli into related culling (30%--400,{,) than mastitis
the mammary gland has been reported to
caused by 0U1er pathogens (2%). Prognosis
reduce manunary gland swelling and
for cases of Klebsiella infection should be inhibition ofrwnen motility. Isoflupredone

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particularly guarded, because these cows

(10-20 mg, IM) has also been shown to
are twice as likely to be culled or die than
reduce local mammary swelling. Cattle are
those infected by other coliforms. Thus,
sensitive to glucocorticoid-induced in1.111une
primary therapy for severe clinical mastitis
suppression; however, it is unlikely that
should be directed against colifom1
one-time administration of a glucocorticoid
organisms, although secondary considerawill adversely affect cows witl1 endotoxintion must be given for other causative induced severe clinical mastitis. Temporaiy
agents. Supportive care, including fluids,
suppression of inflanunation as manifested
is indicated, and in the case of coliforn1
by reduced neutrophil migration may well
mastitis, may be the most beneficial
be beneficial. Care should be exercised in
component of the therapeutic regin1en.

administering these drugs to pregnant

Antibacterial therapy is ideally based on
animals; however, severe clinical mastitis
identification of the causative pathogen;
in and of itself may cause pregnancy loss
however, this is not attainable for some
in cattle.

hours after initial case recognition. In

There is little published research on the
addition, most antibacterial therapeutic
use of glucocorticoids for mastitis caused
regin1ens currently used for severe clinical
by gram-positive bacteria. It is reasonable to
mastitis in the USA are not approved by
expect that grain-positive infections would
the FDA.

be less likely to benefit from the anti-inflam

Many inflammatory and systemic changes matory activities of glucocorticoids a.11d seen in severe coliform mastitis result from
may even be adversely affected. Intra.IT1a.IT1-
the effects of release of lipopolysaccharide
mary glucocorticoid administration to

(LPS) endotoxin from the bacteria and
reduce local inflan1mation, without
subsequent activation of cytokine and
affecting the migration of neutrophils into
arachidonic acid-derived mediators of
the gland, is an attractive therapeutic
inflan1mation and the acute phase response.

option. Although products that combine

By the time therapy is initiated, maximal
antibacterial and glucocorticoid drugs for
release of LPS has likely occurred. Thus,
intran1an1rnary administration exist in
the primary therapeutic concern is the

Europe, it is not clear whether clinical
treatment of endotoxin-induced shock with
benefit is gained when compai·ed with
fluids, electrolytes, and anti-inflammatory
antibacterial therapy alone. As a general
drugs. The IV route is prefeITed as the initial
guideline, glucocorticoid treatment should
method of fluid administration. If isotonic
be reserved for severe cases of gram-negasaline is administered, 30--40 Lare tive mastitis, with a single dose ad.Ininisnecessary throughout a 4-hr period, which tered early in the disease course.

can be difficult under farm conditions. A

NSAIDs ai·e widely used in treatment
practical alternative is 2 L of 7% NaCl
of acute mastitis. Flunixin meglwnine,

(hypersaline) administered IV. This induces
flurbiprofen, carprofen, ibuprofen, and
rapid fluid uptake from the body compartketoprofen have been studied as treatment into tl1e circulation. Cows should then ments for experin1ental coliform rnastitis
be offered free-choice water to drink, and
or endotoxin-induced mastitis. Systemic
if at least 10 gal. is not consun1ed, 5--7 gal.

use of these drugs is prefen-ed over orally
should be pumped into the rumen. Many
administered aspirin, which is not likely to
cows with endotoxic shock are marginally
attain effective concentrations in tissue or
hypocalcemic; thus, 500 mL of calciw11
lead to beneficial results. Dipyrone use in
borogluconate should be administered SC
food aninlals is specifically prohibited by

(to avoid potential complications of IV
the FDA. Phenylbutazone is prohibited in
administration). Alternatively, rapid
dairy cattle >20 mo old; the tolerance level
absorption calcium gels, designed for
for phenylbutazone is zero, and detection
periparturient hypocalcemia, can be given.

of any concentration is an illegal residue.

If the cow remains in shock, continued fluid

Thus, these two drugs should not be used
therapy should be administered PO or IV as
for anti-inflan1matory therapy for mastitis
isotonic, not hypertonic, fluids.

in cattle.

If ad.Ininistered early in the course of

Treatment with ketoprofen in1proved
disease, glucocorticoids may be helpful in
recove1y of cows with acute clinical
cases of mastitis caused by endotoxinmastitis in a blinded, placebo-controlled producing coliforms. Administration of
study. Ketoprofen is available as a

1364

MASTITIS IN LARGE ANIMALS
veterinary product for use in horses, has
coli and treated with 500 mg of intran1an1-
a high therapeutic index, has favorable
mary gentamicin bid did not have lower
pharmacokinetics for use in lactating dairy
peak bacterial concentrations in ntilk,
cattle, and is approved for use in cattle in
duration of infection, convalescent SCCs

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France; however, it is not labeled for food
or serwn albwnin concentrations in ntilk,
animal use in the USA. The Food Animal
or rectal temperatures than untreated

Residue Avoidance Databank (FARAD)

challenged cows. In addition, gentamicin
recommends withdrawal intervals of 7 days
readily diffused through the milk-blood
for slaughter and 24 hr for milk, with IV or
barrier, resulting in drug residues in the

IM administration, for dosages up to 3.3
kidney that could extend beyond 18 mo.

mg/kg/day, for up to 3 days.

Because of zero tolerance for aminogylco

Flunixin meglumine is labeled for beef
side residues at slaughter, the use of this
and daily cattle. It is the only NSAID labeled
class of drugs in dairy cattle is not
for use in cattle in the USA and is therefore
recommended.

the most logical choice for treating clinical

Oxytetracycline (11 mg/kg/day, IV)

mastitis. In field studies, increased survival
improved outcome of cows with clinical
and improved milk production have not
coliform mastitis (not necessarily severe) as
been demonstrated after treatment of
compared with cows that did not receive
clinical acute mastitis with flunixin
systentic antibacterials. Ceftiofur sodiwn
meglwnine at a dosage of 1.1 mg/kg.

(2.2 mg/kg/day, IM ) decreased the mortality

However, in studies of experimental
and cull rates of cows with severe coliform
mastitis, flunixin meglw11ine reduced the
mastitis. This drug distributes poorly to the
severity of clinical signs such as fever,
man1111ary gland, supporting the emphasis
depression, heart and respiratory rates, and
on treating the cow rather than the
udder pain. The FDA-approved withdrawal
mar11111ary gland because of the risk of
intervals are 4 clays for slaughter and 36 hr
septicemia.

for milk when used as labeled by IV adminis

Intrarnarnmat'Y infusion of commercial
tration. Because of extensive and unpredictproducts that have good activity against able withdrawal periods, this drug should
gran1-positive orgartisms should be
not be administered by IM irtjection. As with adntinistered to any cow with severe the glucocorticoids, NSAIDs may provide
clinical mastitis. This treatment is not likely
symptomatic relief and promote well-being.

to affect the outcome of a case caused by

Administration early in the course of
coliforms but may provide some benefit for
infection is likely to increase clinical
cases caused by grain-positive cocci. The
benefit.

need for antibacterial therapy in cows with

Antibacterial therapy may be of
grossly abnormal milk, but with improved
secondary importance relative to immediate appetite, attitude, and milk production, supportive treatment of endotoxic shock,
should be evaluated critically. Unnecessary
but it remains an integral part of a therapeuextension of therapy in these instances tic regimen. Occasionally, coliform
results in increased discarded milk expense
infections do result in chronic mastitis.

for the dairy producer and risk of ar1tibacte

Research suggests that bacteremia may
rials in marketed ntilk.

occur in >4()0/o of severe colifom1 cases.

In addition, nwnerous other pathogens,

Mild Clinical Mastitis: No microincluding gran1-positive cocci, cause severe orgartisms are isolated from 3()0Ar--4()0/o of
clinical mastitis, which can be difficult to
bacteriologic cultures of milk san1ples
distinguish from cases caused by coliforms
collected from cows with clinical mastitis.

at initial presentation.

Many mild mastitis cases that fail to yield

Selection of an appropriate antibacte-
bacteria on culture are colifom1 intrarnarnrial for severe coliform mastitis depends mary infections that resolve before
primarily on the susceptibility of the
treatment is necessary. In addition,
organism to the selected drug and the ability munerous mild clinical mastitis cases ar·e to maintain effective concentrations at the
temporary setbacks in the balance between
primary pham1acologic target (which, in the pathogen and host defenses that occurs in case of colifonn mastitis, is the plasma
more chronic intrarnammary infections. A
compartment of the cow).

"no antibiotic" approach to mild clinical

In one study, IM gentanticin was not more
mastitis cases avoids costs of discarded
effective in preventing agalactia or death
milk and residue risks inherent in antibacteresulting from severe coliform mastitis, or rial therapy.

in improving other clinical outcomes, than

A comparison of cure rate in treated

IM erythromycin or no systentic antibacteriversus untreated cows in a study of three als. Cows experimentally challenged with E

Califot1Ua dairies found bacteriologic cure

MASTITIS IN LARGE ANIMALS

1365
assessed at 4 and 20 days after treatment
treated with intramammary infusions for up
with amoxicillin, cephapirin, or oxytocin
to 8 days as compared with 2 or 5 days. Care

(no antibacterial) did not differ for mild
should be especially exercised in teat
clinical mastitis cases caused by streptoasepsis for extended U1erapy because of the cocci and colifom1s. However, the rates of
increased risk of nosocomial infections.

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both relapses and recun-ing cases were
higher in untreated cows, especially an1ong

Unusual Pathogens: Pseudomonas
streptococcal cases. In a Colorado dairy
aeruginosa may cause outbreaks of clinical
study, a no-antibiotic approach also
mastitis. Generally, a persistent infection
increased the rate of relapses, with an
occurs, which may be characterized by
increase in the incidence of clinical mastitis, inten-nittent acute or subacute exacerbaprevalence of intra.manum,ry infections, tions. The organism is found in soil-water
and herd SCCs associated with streptococenvironments conunon to dairy frums.

cal infections. If bacterial cultw·e of affected Herd infections have been reported after quruters yields no organisms or coliforms,
extensive exposure to contaminated wash
therapy is not likely to be beneficial,
water, teat cup liners, or intramanunary
whereas if grrun-positive cocci are isolated,
treatments administered by milkers. Failure
therapy is reconunended.

to use aseptic techniques for udder therapy

Conunon sense and individual herd
or use of contanlinated milking equipment
history should determine the course of
may lead to establishment of P ae1uginosa
therapy for mild clinical masti.tis cases in
infections within the manunary glands.

dairy herds. Use of approved conm1ercial

Severe peracute mastitis with toxemia and
intramammary infusions is likely to be the
high mortality may follow inu11ediately in
best option. Assessment of success should
some cows, whereas subclinical infections
be based on bacteriologic cure but will be
may occur in others. The organism has
more practically based on return to nom1al
persisted in a gland for as long as five
milk. However, the frequency of relapsed
lactations, but spontaneous recovery may
cases should be monitored as the best
occur. Other than supportive cru·e for severe
mea.I1S to determine cures, because many
episodes, therapy is of little value. Culling is
cases will be deemed to have been
reconm1ended for cows.

successfully treated initially but relapse

Tl1leperella (fonnerly Arcanobacte
later in lactation. If mastitis recurs regulru·Jy
rium) pyogenes is common in suppurative
in affected quarters in the absence of
processes of cattle and pigs and produces a
systemic signs, repeated treatment of what
chru·acteristic mastiti.s in heifers and ciI-y
now has become chronic intrrunrunmary
cows. It is occasionally seen in mastitis of
infection is not warranted. Additionally,
lactating udders after teat injury, and it may
augmentation with parenteral therapy for
be a secondary invader. The inflru11mati.on
these cases has not been demonstrated to
is typified by the formation of profuse,
be effective and will not likely overcome the foul-smelling, purulent exudate. Mastitis expense of discarded milk, other related
due to T pyogenes is conm1on among dry
treatment costs, and the increased risk of
cows and heifers that are pastured during
residues in milk and meat. Previous history
the sununer months on fields and that have
of clinical cases ("repeat offenders"), long access to ponds or wet ru·eas. The vector for
duration of infection (as exhibited by high
anin1al-to-anin1al spread is the fly Hydro
individual SCCs or extended periods of
taea irritans. Control of infections is by
increased SCCs), and infections caused by
limiting the ability to stand udder-deep in
nonresponsive pathogens are the greatest
water and by controlling flies. Preventive
risk factors for poor therapeutic outcome.

treatment of heifers and dry cows in

Practitioners should develop a protocol
susceptible areas with long-acting penicillin
with dairy clients to reduce tumecessru-y
preparations has effectively reduced
treatment of poor risk cases as listed above
infections. Therapy is rru·ely successful,
and not rely on continued tmsuccessful
and the infected quarter is usually lost
therapy or seeking a "better drug."

to production. Infected cows may be

If standard regimens achieve less than
systemically ill, and cows with abscesses
desired results, it would be better to extend
usually should be slaughtered. (See also
initial therapy for a prolonged period rather

ACTINOMYCOSIS, p 590.)

than to change to other antibacterial drugs

Mycoplasma spp can cause a severe fonn
or increase the runount of each dose.

of mastitis that may spread rapidly tlu·ough

Studies have demonstrated improved cure
a herd with serious consequences. M bovis
rates for gran1-positive cocci, especially
is tl1e most conunon cause. Otl1er significant
coagulase-negative staphylococci and
species includeM californicum,
streptococci, when infected quarters were

M canadense, and M bovigenitalium.

1366

MASTITI S IN LARGE ANIMALS

Onset is rapid, and the source of infection is

Mastitis due to various mycotic organbelieved to be endogenous after outbreaks isms (yeasts) has appeared in dairy herds,
of respirat01y disease in heifers or cows.

especially after the use of penicillin in

The disease is often seen in herds undergoassociation with prolonged repetitive use ing expansion in which anin1als from
of antibiotic infusions in individual cows.

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outside sources have been added. 'Iypically,

Yeasts grow well in the presence of
introduced animals will be asymptomatic
penicillin and some other antibiotics; they
carriers and then shed the organism via
may be introduced during udder infusions
respiratory or intra.mammary transmission.

of antibiotics, multiply, and cause mastitis.

Some or all quarters become involved. Loss

Yet, heifers that have never received
of production is often dramatic, and the
intran1amrnary infusions may develop yeast
secretion is soon replaced by a serous or
mastitis. Signs may be severe, with a fever
pumlent exudate. Initially, a characteristic,
followed either by spontaneous recovery
fine granular or flaky sediment may be seen
in -2 wk or, more rarely, by a chronic
in the material removed from infected
destructive mastitis. Other yeast infections
glands. Despite the severe local effects on
cause nlininlal inflammation and are
udder tissue, cows usually do not manifest
self-limiting. If mastitis due to yeast is
signs of systemic involvement. The
suspected, antibiotic therapy should be
infection may persist through the dty
stopped inmlediately. Yeast or otl1er mastitis
period. Identification of infected cows
infections can be reduced if the tip of the
can be difficult because of the frequent
plastic infusion tube is only partially (rather
propensity of these cows to become
than completely) inserted through the teat
asymptomatic carriers and intennittently
canal during intramammary therapy.

shed the organism in milk.

A chronic, indurative mastitis similar to

Because there is no satisfactory
that caused by the tubercle bacillus has
treatment, affected cows should be
been reported to be caused by acid-fast
segregated during active outbreaks. Routine Mycobacterium spp derived from the soil, screening of tl1e bulk tank and milk strings
such as M fortuitum, M smegmalis,
may help identify the presence of infected

M vaccae, and M phlei when such organisms cows. However, culture of the manimary
are introduced into the gland along with
secretion of cows with clinical mastitis, or
antibiotics (especially penicillin) in oil or
recently calved cows, is the most reliable
ointment vehicles. The oil apparently
surveillance method. If cows continue to
enhances the invasiveness of these
display clinical mastitis or systemic signs,
organisms, and such therapy is contraindithey should be culled. Sanitary measures cated. These organisms otherwise tend to be
should be strictly enforced, especially at
saprophytic and to disappear from infected
milking and in hospital/treatment areas.

quarters, at least by the next lactation. In the

Milk from Mycoplasma-infected cows
meantime, mastitis is usually moderate.

should not be fed to calves, because this

Distinct outbreaks do occur and several
may result in respiratory and inner ear infechave been reported, especially with M
tions. Milk replacer or pasteurized milk,

Jortuitum and M smegmatis.

rather than discarded milk, should be fed

Prololheca sp are nonpigmented
to calves in herds with Mycoplasma.

unicellular algae conm1only found in wet

Nocardia asteroides causes a destmctive environments such as streams, stagnant mastitis characterized by acute onset, high
ponds, and marine waters, pa.iticularly in
temperature, anorexia, rapid wasting, and
hunlid habitats with organic matter in the
marked swelling of the udder. Response
soil. In daily fann environments, they are
in the udder is typical of a granulomatous
especially abundant in muddy or wet
inflammation and leads to extensive fibrosis
outdoor runs or lots, resting a.i·eas, paths
and formation of palpable nodules. Herd
where animals a.i·e driven, and pastures
histories suggest that infection of the udder
contaminated with slurry. Protothecal
may be associated with failure to ensure
mastitis in dairy cattle is often chronic and
asepsis in intramamrnary treatment of the
asymptomatic with increased SCCs,
conm1on forms of mastitis. Slaughter is
although sporadic severe infections occur.

recommended for infected cows.

Although some infections may spontane

Se-n·atia mastitis may arise from
ously resolve, longtenn caniage with
contamination of milk hoses, teat dips,
intem1ittent shedding is common. After
water supply, or other equipment used
initially causing clinical mastitis, infections
in the milking process. The organism is
may be undetectable by culture of milk for
resistant to disinfectants. Cows with this
several montl1s, only to recur during the
form of mastitis that continue to display
subsequent lactation, particularly soon after
clinical signs should be culled.

calving. Therapeutic interventions are

MASTITIS IN LARGE ANIMALS

1367
unrewarding. Thus, dairy producers have
in suckling kids. M capricolum has also
limited ability to predict the progression or
been reported to cause severe mastitis in
affect the outcome of protothecal mastitis
goats and infection in kids. Does usually
and are constrained to management options
recover in -4 wk.

similar to those used to manage chronic

As with cows, gram-negative organisms

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rnastitis caused by other pathogens.

cause intem1ittent infections that may be

T.herefore, the p1irnary management focus
severe but are usually self-linliting.

is prevention rather than mitigation of

Trueperella (fom1erly Arcanobacterium)

infections. To reduce pathogen exposure to
pyogenes sometimes produces multiple,
other noninfected cows in the herd, chronic
nodular abscesses.

rnastitic cows are often culled. The ptirnary

Does can also exhibit signs of mas ti tis
causative agent of protothecal mastitis in
from caprine arthritis and encephalitis (see
cattle has been identilled asP zopfti. Other p 747) and ovine progressive pnewnonia
reports have challenged the absolute

(seep 1475) secondary to systemic
exclusivity of P zopfii as the etiologic agent infection. Agalactia is common, as is a
of protothecal mas ti tis, but on a practical
hardening of the udder from fibrosis.

basis cows identified as having mastitis

Programs for diagnosis, control, and
caused by Prototheca sp are managed in
treatment of bacterial mastitis in goats
sin1ilar fashion, regardless of species or
are sinillar to those in cows. However,
genotype.

monitoring subclinical mastitis with
somatic cell coW1ts (SCCs) in does is

Prevention: Bacterins made using
difficult because of poor discrimination
core-antigen technology based on J5 mubetween infected and noninfected animals, tantE coli can help reduce the severity of
especially in the later stages of lactation.

clinical mastitis caused by coliforrns.

This is partially because a higher proportion

Vaccination programs using these bacof cells are epithelial in origin in goat milk terins should minimally include multiple
than in cow milk. As lactation progresses,
administration during the dry period to
shedding of epithelial cells into milk
reduce the incidence of clinical coliform
increases; thus, SCCs > 1,000,000 cells/mL
mastitis frequently associated with early
are common in uninfected does in late
lactation. Protocols for extended nwnbers
lactation. Proper milking procedures and
of immunizations of these bacterins may be
good environmental sanitation are needed
warranted in herds with high rates of severe
to reduce the prevalence and spread of
mastitis beyond 60 days in milk, because
infection. Chronically infected goats should
protection often wanes 50-60 days after the
be culled, as should goats with M mycoides
last immunization.

infections and those that do not recover
from M putrefaciens or M capricolum

MASTITIS IN GOATS
infections.

The organisms infecting the udder of goats

MASTITIS IN EWES
are sin1ilar to those in cows. Coagulasenegative staphylococci are generally the Mastitis can be an important disease in
most prevalent and can cause persistent
sheep, with an incidence >2%. In addition to
infections that result in increased cell
deaths from severe infections, the disease
coW1ts and low-grade mastitis with some
can be a cause of lamb mortality from
recurring clinical episodes. The level of
starvation or of depressed weaning weights
infection and incidence of mastitis due to
of lambs. Pera.cute, gangrenous (usually

Staphylococcus aureus tends to be low
due to Staphylococcus aureus ), acute,

( <5%) but can result in persistent infections
subacute, and probably subclinical types
that do not generally respond to tl1erapy.

occur. The organisms most commonly

Streptococcal intra.mammary infections can involved are S aureus, coagulase-negative occur in both subclinical and clinical cases
staphylococci, streptococci, Escherichia
but are usually much less frequent than in
coli, Mannheimia haemolytica, and True
cattle. Streptococcus agalactiae is not a
perella (formerly Arcanobacterium)

common pathogen of mastitis in does.

pyogenes.

Mycoplasma infections, ptirnarily M

The principles of diagnosis and treatment
mycoides (large colony type) and M
used in bovine mastitis can be applied to
putrefaciens, sometimes cause serious
ewes. Little is known about the control of
outbreaks of mastitis in goats (seep 1352).

ovine mastiti..s, but careful inspection of the

The latter also causes septicemia, polymammary glands of ewes before mating to arthritis, pnewnonia, and encephalitis,
detect and eliminate those with chronic
together with serious disease and mortality
mastitis should be beneficial.

1368

MASTITIS IN LARGE ANIMALS

MASTITIS IN MARES
severe toxemia. The saw's temperature
may increase to 107°F ( 42°C) or may be

Acute mastitis occurs occasionally in
subnormal. The affected glands a.re swollen,
lactating mares, most commonly in the
pw-ple, and have a watery secretion. Sow
drying-off period, in one or both glands.

mortality is high, and the piglets will die

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Streptococcus zooepidemicus is the most
wlless fostered or fed aitificially. Milk
frequent pathogen, but S equi, S equisimi
production of recovered sows may be
lis, S agalactiae, and S viridans are also impaired in the next lactation. The
found. A variety of gram-negative bacteria
treatment of peracute coliform mastitis in
has also been reported. Marked, painful
sows is similar to that in cows. Ampicillin,
swelling of the affected gland and acljacent
dihydrostreptomycin, or oxytetracycline
tissues develops, and the secretion is often
administered systemica!Jy have been used.

seroflocculent. Fever and depression may

Treatment of lactating sows requires considbe present. The mare may walk stiffly or eration of withholding periods, because
stand with hindJegs apart due to the
affected sows ai·e often culled after
discomfort.

weaning.

Treatment is similar to that in cows, but

Subacute mastitis may occur in older
when intramanunary infusions are used,
sows and lead to indw-ation of one or more
they should be inse1ted separately into both
glands, in1pairing the saw's ability to nurse
orifices of the teat. Systemic therapy has
a large litter. This form of mastitis is more
been suggested to include trimethoprimlikely to be associated with infection by sulfonamide (based on 5 mg/kg of
streptococci or staphylococci. Granulomatrimethoprim, PO, bid) or a combination tous lesions in the manunae of sows have
of penicillin (20,000 IU/kg, IM, bid) and
been associated withActinobacillus
gentamicin sulfate (2 mg/kg, IV, tid).

lignieresii, Actinomyces bovis, and

Therapy should be continued on the basis of

Staphylococcus aure-us infections.

culture and antibacterial sensitivity testing.

Fusobacterium necrnphorum and

Without prompt treatment, abscessation or

Trueperella (fmmerly Arcanobacterium)

induration of the gland can occw·. Little
pyogenes also have been incriminated in
is known about the frequency and
sow mastitis. A thorough examination and
persistence of subclinical intramanunary
culture of the rnanunaiy glands of the sow
infections in mares.

are important to diagnose ai1y of the above
peracute and subacute types of mastitis.

MASTITIS IN SOWS

(See also POSTPARTUM DYSGALACTLA SYNDROME,
p 1373.)

Mastitis can be important in swine-raising

The control of mastitis in sows has not
units. Peracute mastitis can affect sows and
been extensively investigated, but isolating
gilts and is most commonly associated with
sows in adequately disinfected pens
coli.form (Escherichia coli, Enterobacter
before, during, and for an adequate period
aerogenes, and Klebsiella) infections. It is after farrowing should help prevent the
most conunon at or just after partw·ition,
severe losses associated with coliform
and affected sows have"a moderate to
mastitis.

METRITIS IN LARGE ANIMALS

ACUTE PUERPERAL METRITIS
demonstrated the dominant role of
gran1-negative anaerobic bacteria.such as
ln all species, acute puerperal metritis

Prevotella me/.aninogenica and Pusobacte
occurs within the first 10-14 days postpar
iium necroplwrum. The condition is usually
t-w11. It results from containination of the
acute in onset. Affected cows, mares, ewes,
reproductive tract at paitulition and often,
does, or sows are depressed, febrile, and
but not inva.iiably, follows complicated
inappetent. A fetid, watery uterine discharge
parturition. ln1portant causative organisms
is characteristic of the condition in cows but
in cattle include Escherichia coli and
may not be conspicuous in other species.

Tlueperel/.a (Arcanobacterium) pyogenes,

Milk production is din1inished, and nursing
but cultw-e-independent studies have
young may show signs of food deprivation.

METRITIS IN LARGE ANIMALS

1369

Acute puerperal metritis responds well to
necrophonim or other gram-negative
systemic antimicrobial therapy combined,
anaerobic organisms. Signs of infection
if necessary, with NSAIDs and other
vary from obvious and persistent purulent
supportive measures such as fluid therapy.

exudate from tl1e uterus to inapparent

Cephalosporin antibiotics or penicillin are
infection. Changes in uterine consistency

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considered most approp1iate for systemic
may occur, but transrectal palpation alone
treatment of cows with metritis because
is an insensitive means of diagnosis. The
they are active against most common
presence of purulent exudate in the vagina
pathogens, reach therapeutic levels in
does not necessarily confum endometritis;
endometrial tissues, and may help prevent
the source of the exudate may be the cervix
some of the potential sequelae of metritis
or, occasionally, the vagina it.self. Manual
and endometritis, such as endocarditis or
vaginal examination or use of a device to
renal disease. Oxytetracycline requires
recover vaginal content may also allow
administration at high levels (11 mg/kg, bid)

evaluation of vaginal exudates for diagnosis
to maintain uterine tissue concentrations
of clinical endometlitis. Diagnosis of
of 5 mcg/g, which is below the minimal
subclinical (cytologic) endometritis
inhibitory concentration (MIC) for many
requires use of endometr·ial cytology,
strains of pathogenic Tpyogenes. Drainage
ultrasonography, or endometrial biopsy,
of the uterine content may be advantageous
because other signs are often absent.

but should be attempted only after initiation Cows with endometritis do not exhibit any of antimicrobial therapy; it should be done
systemic signs of illness, and appetite and
very carefully because the inflan1ed uterus
milk production are usually unimpaired.

may be friable, and manipulation of the

For decades, endometlitis in cows has
uterus may result in bacteremia.

been treated wit\1 intrauterine infusion.

Although infusion of antimicrobials may 1id

METRITIS AND ENDOMETRITIS
the uterus of bacteria, there is little evidence
that it elin1inates the endometrial inflanuna

Cows: Several specific diseases are
tion or restores fertility. Many preparations
associated with metritis or endomet1itis.

routinely administered into the bovine uterus

These include brucellosis (seep 1348),
are detrimental to ute1ine tissue. Increased
leptospirosis (seep 646), can1pylobactericoncern about milk and carcass residues, osis (seep 1347), and trichomoniasis (see along with poor or uncertain results, should
p 1384). More often, endometritis is the
discourage intrauterine therapy as a routine
result of nonspecific infections.

approach to management of bovine

The normal uterus is a sterile environendometlitis. Intrauterine infusion of ment, in contrast to the vagina, which hosts
cephapirin in a form specially fonnulaLed
numerous microorganisms. Opportunistic
for intrauterine use, and available in many
pathogens from the nonnal vaginal flora
countries (but not tl1e USA), has enhanced
or from the envirorunent may invade the
fertility in dairy cows with endometlitis.

uterus from time to time. A healthy uterus is

Systemic use of antimicrobials for treatr11ent
able to rid it.self of these transient infections
of clinical or subclinical endometritis has not
very efficiently; however, in the inunediate
been evaluated.

postpartum period, the uterus of cows is

Cows are more resistant to uterine
usually contaminated wit\1 a variety of organinfection during estrus, and as cows isms. Within days or weeks postpartum, the
undergo more estrous cycles after
sterile uterine envirorunent is reestablished
parturition, the prevalence of endometritis
in most aninlals. In those in which infection
diminishes. This has led to increased use of
persists, chronic or subacute endometritis
prostaglandin F2oc or it.s analogues, at usual
develops and has a detrimental effect on
luteolytic doses, for the management of
fertility. The prevalence of subclinical
endometritis, alt110ugh there is little
endometlial inflanunation in dairy cows
evidence that such use reduces the
seems to exceed the prevalence of uterine
incidence or effect of endometritis.

infection. The pathogenesis of this fo1m of
endometlitis is not yet understood, but it is

Mares: Aliliough profound endometritis
becoming increasingly clear that postpartwn accompanies contagious equine metritis uterine diseases, particularly in high-produc

(seep 1371) in mares, most breeding
ing dairy cows, are mediated by impaired
problems are related to endometritis caused
immune response, probably related to
by nonspecific infections. ln mares, the
negative energy balance.

most conunon etiologic agent of endomctri

In cows, the causative organisms are
tis is Streptococcus zooepidemicus, but
most often 1'rueperella pyogenes, alone
several otl1er organisms may be involved,
or in association with Pusobacterium
including Escherichia coli, Pseudomonas

1370

METRITIS IN LARGE ANIMALS
aeruginosa, and Klebsiella pneumoniae.

Infection may be of long duration, with

Yeasts and fungi are incriminated in some
signs recurring at each estrus. Some sows
cases, particularly in mares with reduced
recover spontaneously, but there does not
resistance, or as a sequela of exuberant
seem to be any effective treatment for those
antimicrobial therapy.

that do not. At necropsy, copious quantities

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Visible exudate is rarely a feature of
of purulent exudate may be found in the
endometritis in mares. (Contagious equine
uterus, making this condition more akin to
metritis is a notable exception.) Endometrial pyometra (see below).

inflammation is best confirmed by exan1ination of endometrial cytology or biopsy Other Species: Endometritis has been
samples. Additional support of the diagnosis
seen in sheep, goats, and camelids. In
is provided by ultrasonographic demonstracommercial sheep and goat flocks, diagnosis tion of intraluminal free fluid, especially
is seldom made antemortem, and treatment
during diestrus, or by isolation of potentially
is generally impractical. In animals with a
pathogenic bacteria from appropriately
persistent uterine discharge, renmants of a
guarded swabs of the endometrium. Because macerated fetus should be considered as a most causative organisms are common
nidus of chronic infection. Endometritis in
conunensals, isolation of bacteria alone
camelids is usually treated empirically based
is not sufficient evidence for diagnosis.

on treatments for cattle and horses.

Nevertheless, evidence suggests that fertility
of mares is impaired if either endometrial

PYOMETRA
cytology or culture is positive.

Intrauterine therapy is still commonly

Pyometra is characterized by accwnulation
used in mares. Many antinlicrobial drugs
of purulent or mucopurulent exudate in the
have been used, and effective doses
uterus. In cows, it is invariably accompadetermined mainly empirically. Some nied by persistence of an active corpus
examples include penicillin (5 million U;
luteum and interruption of the estrous
effective mainly against S zooepidemicus ),
cycle. In affected mares, the cervix is often
ticarcillin (6 g; broad spectrum), ampicillin
fibrotic, inelastic, affected with translunli

(3 g of soluble preparation), gentamicin
nal adhesions, or otherwise impaired. Mares

(2 g, buffered with bicarbonate; effective
may continue to cycle normally, or the cycle
especially against gram-negative agents),
may be interrupted. Discharge from the
and kanamycin (2 g; effective against
genital tract may be absent or intennittent
gram-negative bacteria). For fungal or yeast
and corresponding to periods of estrus. In
infections, 100 mg of amphotericin B or 500
general, affected animals do not exhibit any
mg of clotrimazole have been effective.

systemic signs of illness, but affected mares

Treatment should be continued for several
may be in poor condition. In both cows and
consecutive days, preferably during estrus.

mares, pyometra must be distinguished

Most of the above treatments constitute
carefully from pregnancy before treatment
extra-label drug use in the USA.

is undertaken.

Some mares appear particularly

The treatment of choice in cows is
susceptible to postbreeding endometritis.

administration of prostaglandin F2a or

These mares accumulate fluid in the uterine
its analogues at nom1al Iuteolytic doses.

lumen after mating or insemination. This is

Expulsion of exudate and bacteriologic
related to persistent endometrial inflamclearance of the uterus follows in -800/o of mation. In contrast, normal mares have
treated cases. Although first:service concepa vigorous, but transient, inflammatory tion rate after treatment may be low, most
response to mating, and the uterus rapidly
cows may be expected to conceive within
regains its sterile, noninflamed status.

three or four inseminations. The treatment

Postbreeding endo.metritis may be treated
may need to be repeated in -200/o of cows.

by uterine lavage or by use of oxytocic

No intrauterine treatment is reconunended
drugs to rid the uterus of fluid.

in conjunction with the prostaglandin.

In the face of cervical changes, drainage of

Sows: A fom1 of endometritis characterthe affected equine uterus may be virtually ized by profuse vaginal discharge at the
impossible. Lavage of the uterus using large
onset of estrus has been described in
volumes of fluid is recommended; however,

Europe and other regions. The causative
the condition frequently recurs, and
agent is usually Staphylococcus hyicus
permanent cure in these cases requires
or E coli, and the disease seems to be
hysterectomy or wedge resection of the
transmitted at mating or artificial inseminacervix to allow continual uterine drainage, a tion; signs are seen 15-25 days later during
salvage procedure that allows continued use
the subsequent proestrus or estrus.

of the mare but renders her infertile.

METRITIS IN LARGE ANIMALS

1371

Pyometra is seen in small ruminants,

Lesions: Lesions consist of edema
swine, and other species; diagnosis is
and hyperemia of the endometrium, the
rendered more difficult by animal size and
endocervix, and the vaginal mucosa. The
management practices. If pyometra is
microscopic lesions include invasion of the
diagnosed, evacuation of the uterus is
affected tissues by neutrophils during the
recommended.

acute stage, and by lymphocytes, mac

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rophages, and plasma cells later in the

CONTAGIOUS EQUINE METRITIS
course of the infection.

Contagious equine metritis (CEM) is an
acute, highly contagious venereal disease

Diagnosis: Diagnosis depends on
of horses ( and experimentally of donkeys)

isolation of the causative organism.

characterized by a profuse, mucopurulent

Although other bacterial infections of
vaginal discharge and early return to estrus
the genital tract of mares may produce
in most affected mares. Infected stallions
a conspicuous vaginal discharge, this
and chronically infected mares show no
is unconunon, and no other venereal
clinical signs. The disease is seen primarily
pathogen of the equine reproductive tract
in Europe, but technical challenges in
is as contagious. In mares, swabs for
propagation of the causative organism
culture should be taken from the endomeprevent accurate detem1ination of the trium (preferably during estrus) and from
precise distribution of the disease.

the clitoral fossa and sinuses. Swabs from
suspected stallions should be taken

Etiology and Transmission: CEM is
from the urethral fossa, the urethra, the
caused by the gram-negative, microaeropreputial cavity, the shaft of the penis, and, philic coccobacillus Taylorella equigeni
if possible, the preejaculatory fluid or
talis, also known as the contagious equine
ejaculate. Stallions should be sampled at
metiitis organism (CEMO). Important strain least three times before being declared free differences exist; some strains are resistant
of CEMO. Test-mating suspect stallions to
to streptomycin ( a fact that helps isolate
susceptible mares that are then screened
this fastidious, slow-growing organism from
bacteriologically constitutes a satisfactory
contaminants), whereas others are sensitive way to determine CEM status. All swabs to streptomycin. It is best cultured on
should be placed in a transpmt medium
chocolate Eugon agar at 37°C in an

(preferably A.mies with charcoal), kept on
atmosphere of 5%-l()OA, C0
ice or at 4 °C, and delivered to a qualified

2 in air. T equigenitalis is asaccharolytic but is positive laboratory within 24 hr ( or frozen if
for catalase, cytochrome oxidase, and
transport will take longer). A variety of
phosphatase and unreactive to other
serologic tests has been developed, but
conventional biochemical tests.

none is yet capable of reliably detecting.

CEM is transmitted primarily at mating,
the carrier status.

but infected fomites (instruments and
equipment) also play a role. Undetected

Treatment and Control: Stallions can be
infected mares and stallions are the source
treated by thoroughly cleaning the extended
of new outbreaks. Infected stallions show
penis with chlorhexidine surgical scrub and
no signs and harbor the organism in the
then applying nitrofurazone ointinent. This
smegnrn of the prepuce and the surface of
should be repeated daily for 5 days, and the
the penis, especially in the urethral fossa.

stallion retested at least 10 days after

The transmission rate is exceptionally high;
treatinent. Most mares rid themselves of
virtually every mare mated by an infected
uterine infection after a few weeks. Those
stallion becomes infected.

that become chronically infected harbor the

CEMO in the clitoral fossa or sinuses. They

Clinical Findings: In mares, a copious,
can be treated by thoroughly cleaning the
mucopurulent vaginal discharge is seen
clitoral area with chlorhexidine surgical

10-14 days after infected matings. Mares
scrub and then applying nitrofurazone
may return to estrus after a shortened
ointinent ( as for the stallion). 1n some mares,
estrous cycle. Although the discharge
surgical excision of the clitoral sinuses may
subsides after a few days, mares may
be required to rid them of infection.

remain infected for several months.

Control of CEM depends on identification

Chronically infected mares show no signs.

of infected carrier animals and on their

Most mares do not conceive at the tin1e of
treatinent or elimination from breeding
infected mating. If they do, they may infect
programs. Strict import regulations exist in
the foal at or shortly after birth. Foals so
many countries to avoid the introduction of
infected may become carriers of CEMO

CEM, and current prevalence of the disease
when they reach sexual maturity.

appears to be low.

1372

POSTHITIS AND VULVITIS IN SHEEP AND GOATS

POSTHITIS AND VULVITIS

IN SHEEP AND GOATS

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Two common and distinct fom1s of posmaterial from a preputial or vulvar ulcer.

thitis and vulvitis are recognized in small

Ulcerative posthitis or vulvitis has a
ruminants. The first, referred to as enzootic
seasonal occurrence that varies with local
posthitis and vulvitis, is associated with
animal husbandry methods. Peak incidence
high-protein diets, infection with
corresponds to the time when aninlals graze

Corynebaclerium renale or other
lush green pasture ( eg, spring and early
ureas e -producing organisms, locally high
swnmer in New Zealand or autunm and
concentrations of anunonia., and severe
winter in southern Brazil) or a.re fed or have
posthitis. The second is referred to as
access to high-protein feedstuffs.

necrotic or ulcerative balanoposthitis and
vulvitis. Its ca.use is unclear, but Myco

Clinical Findings: In mild cases, signs a.re plasma mycoides mycoides is implicated,
limited to swelling of the prepuce. In severe
as are other Mycoplasma spp organisms of
cases, swelling and inflan1ma.tion interfere
the Histophilus/Haemophilus group, and
with urination and result in straining, which
potentially viruses, such as ca.prine
needs to be differentiated from urolithiasis
herpesvirus l.

(seep 1502). Histologic characteristics are a.canthosis, parakera.tosis, and hyperkerato

ENZOOTIC POSTHITIS
sis, followed by leukocyte invasion and

AND VULVITIS
ulceration. Ulcers and scabs may be found
around the preputial orifice, on the lamina
intema. of the prepuce, and on the shaft of

(Sheath rot, Pizzle rot, Enzootic
the penis. Urine and exudate may accumubalanoposthitis) late in the prepuce. The condition may

Etiology and Epidemiology: This
ca.use severe discomfo1t. If the preputial
moderately contagious disease is ca.used
orifice or w·ethra is occluded, affected
by C renale, a gram-positive, diphtheroid
animals may die. Ulcerative vulvitis begins
bacterium capable of hydrolyzing urea.

with signs of vulvar inflammation, including

When protein intake is high, urinary urea
swelling and redness, and progresses to
concentration increases. Hydrolysis of urea
development of a yellow exudate with ulcerby C renale results in local production of ation and scab formation aroW1d the vulva,
large quantities of an1rnonia., which is
vestibule, and caudal vagina. The glans
believed to irritate the penis, lamina intema.

clitmidis may be swollen, red, and
of the prepuce, and skin surrounding the
ulcerated.

preputial orifice. The condition is more

Lesions of ulcerative posthitis or vulvitis
common in male castrates, probably
should be distinguished from those of
because of the hypoplastic nature of the
granular posthitis or vulvitis (associated
penis, exacerbated in some cases by failure
with Mycoplasma spp or Ureaplasma spp, of penile-preputial separation that leads to
seep 1391), herpesviral balanoposthitis or
pooling of urine in the prepuce. If preputial
vulvova.ginitis, ulcerative derrna.tosis ( see
hair is cut too short or becomes caked with
p 872 [sheep only]), or contagious ecthyrna.

mud or organic matter, drainage of urine

(orf, seep 866 [goats only]). Removal of the away from the preputial orifice (norn1ally
scabs of ulcerative posthitis or vulvitis
facilitated by this hair) is in1paired, and
characteristically results in little or no
ulcerative lesions may develop.

hemorrhage.

The incidence of ulcerative posthitis
is highest in Merino and Angora wethers,

Treatment and Control: If possible,
which is attributed to the long hair or wool
affected animals should be isolated from the
surrounding the prepuce in these animals,
rest of the herd and not fed a high-protein
allowing urine to soak the area, which in
diet. Lesions should be examined to ensure
turn is conducive to bacterial growth and
they do not interfere with urethral patency.

activity. It is also seen in show rams or rams

Clipping and cleaning hair around the
that have been fit for sale; in this case, the
prepuce may be beneficial. C renale is
condition is more associated with dietary
usually sensitive to penicillins and
protein levels. The condition can be
cepha.losporins, which may be beneficial if
transmitted experimentally by infective
practical. Ulcerative posthitis is controlled

POSTPARTUM DYSGALACTIA SYNDROME AND MASTITIS IN SOWS

1373
principally by limiting dietary protein to
flock to involve a considerable proportion
a level consistent with requirements. If
of the animals. The pregnancy rate in
untreated, scarring may be so severe that
affected flocks is depressed.

the penis cannot be extended.

The cause of ulcerative balanoposthitis
and vulvitis is not clear. Mycoplasma

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ULCERATIVE BALANOPOSTHITIS
mycoides mycoides has been isolated from
affected sheep. Trueperella (Arcanobacte

AND VULVITIS
rium) pyogenes is frequently present. In

(Pizzle disease, Knobrot, Peestersiekte)

some cases Histophilus ovis has been
isolated. Viruses, such as ovine herpesvirus

Ulcerative balanoposthitis and vulvitis is

2 or, in the case of goats, caprine herpesvicharacterized by ulceration and inflammarus 1, may be involved.

tion of the glans penis and the prepuce, as

Affected rams should be removed from
well as the vulva of affected ewes. The first
the flock and isolated. If practical, affected
signs observed may be swelling and
ewes should also be maintained separately.

bleeding of the prepuce or vulva. On

Rams should be treated witl1 antimicrobials;
exanlination, ulcers are seen; these bleed
ewes also respond well to antimicrobial
readily when manipulated. In ewes, the
treatment. Irrigation of the prepuce may
ventral aspect of the tail (where it contacts
help prevent preputial adhesions. Tulathrothe vulva) may be sin1ilarly affected. The mycin has been used successfully. Recovcondition may spread within a breeding ered animals appear to have normal fertility.

POSTPARTUM DYSGALACTIA SYNDROME

AND MASTITIS IN SOWS

Numerous etiologies or pathophysiologies and rapidly lead to piglet starvation.

can be involved in this syndrome, which is

Although the problem can be sporadic and
reflected by the use of several different
linlited to a few sows, sometimes it can
names-mastitis-metritis-aga.lactia (MMA) occur in a greater nwnber of sows and complex, a.galactia syndrome, dysgalactia
become nearly epidemic.

syndrome, mammary edema, periparturient

Differentiating acute multiglandulai:

hypogalactia. syndrome, agalactia toxemia, mastitis and hard udder syndrome can be and puerperal mastitis. However, these
difficult. For this reason, it is often reported
names are not synonyn10us and have
by producers as "acute mastitis."

often been misused. The syndrome can

PPDS is characterized by transitory
currently be classified according to the
hypogalactia. It can lead to acute multinumber of mammary glands affected, ie, glandular mastitis and should be considuniglandular or multiglandular mastitis ered as the general cause of lactation

(including postpartum dysgalactia
failure in the sow. MMA complex is a
syndrome [PPDS], MMA complex). (See
misnomer and is only part of the more
also MASTITIS IN LARGE ANIMALS, p 1358.) general PPDS. Although the mammary

Acute or chronic mastitis of only one or
glands are swollen and frequently warmer
two man1mary glands ( acute or chronic
than normal, grossly detectable prin1ary
uniglandular mastitis) in sows is present in
mastitis is uncommon. Likewise, metritis
nearly all herds. lf the entire udder is acutely (more commonly endometritis) is only an affected, it can be a primary or a secondary
occasional finding in some herds. Finally,
mastitis (acute multiglandular mastitis)

only rarely is there complete agalactia;
as well as ma.nunary edema ("hard udder
most sows continue to produce milk but at
syndrome"), which is common in primipaa greatly reduced rate (hypogalactia or rous sows.

more correctly dysgalactia). The primary

Due to bacterial effects, acute multiglanclinical signs of the sow's inability to dular mastitis is usually accompanied by
produce a sufficient an1ount of milk to
systemic signs and agalactia, whereas hard
meet the needs of the piglets are growth
udder syndrome is not. Both conditions
retardation and increased mortality in
occw· within the first 3 days after farrowing
piglets.

1374

POSTPARTUM DYSGALACTIA SYNDROME AND MASTITIS IN SOWS

Mammary glands of sows are anatomi

Major herd risk factors are the sow
cally different from those of cows. In sows,

(PPDS, see below), the piglets (uncommon
there are no well-identified gland cisterns
primary form), or the environment ( eg,

(gland sinus) in the mammary glands. There
some beddings such as wood shavings can
are usually two complete gland systems and
be contan1inated by Klebsiella pneu.mo
two teat orifices per teat. When three orifices niae ).

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are present, one sinus ends blindly at the

Some genetic lines of females are more
base of the teat and does not have glandular
resistant to coliforn1 mastitis than others.

tissue. There is no muscular sphincter

The heritability of this characteristic is
around the teat orifice. Therefore, intraman1-
believed to be -109u. Selection among the
mary treatment by way of the teat opening is
gilts to minimize or eliminate mastitis-prone
in1possible. Mammogenesis occurs almost
sows can provide longterm improvement of
exclusively during the last half of gestation
the herd.

and during the first days of lactation. New
glandular tissues are produced during each

Clinical Findings: Systemic signs such as
gestation. For this reason, feeding and
anorexia, constipation, fever, and depresnutrition are of major importance during sion are common. Local signs include acute
mammogenesis and the end of gestation,
induration of the mammary glands as well
and are less important at midgestation.

as severe edema and skin congestion of

Opinions differ as to whether the position
the mammary region. However, many sows
of the caudal manunary glands should be

( especially primiparous sows) develop
considered as a risk factor for mastitis
mammary edema without any signs of acute
development. Most recent findings seem
mastitis. Circun1stantial evidence suggests
to reject an increased incidence in caudal
that this is usually associated with
glands compared with cranial ones.

increasing milk production ( often the milk

Wection of a man1mary gland during one
drips during and right after farrowing) to
lactation has no consequences for the next.

such an extent that piglets are unable to

However, chronic lesions of the teat canal
consume all the available milk
may be present for multiple lactations.

Once acute multiglandular mastitis is
established, the secretion (with oxytocin) of
milk is no longer possible. Affected sows

ACUTE MULTIGLANDULAR
deny piglets access to the teats by lying on

MASTITIS
their mammary glands. General signs result
from bacterial multiplication and resorption

This syndrome is seen in all types of herds,
of toxins. Conunon consequences for the
including those with excellent hygiene and
litter include an economically significant
adequate disinfection practices. It occurs
increase in preweaning mortality caused by
mainly during the first 3 days after
weak piglets, neonatal diarrhea, starvation,
farrowing and has major consequences for
hypoglycemia-induced weakness, an
the piglets. Acute multiglandular mastitis
increased incidence of crushing by the
can also follow a specific systemic disease sow, and increased susceptibility to other
of the sow ( eg, septicemia, pseudorabies
diseases due to inadequate maternal

[seep 1300], porcine reproductive and
immunoglobulin transfer and other
respiratory syndrome [seep 7291).

problems ( eg, runt pigs).

Etiology and Pathogenesis: The

Diagnosis: Early cliagnosis is not always
etiology is multifactorial. Infections of the
easy. Most problem litters are thought to
mammary gland are more often secondary,
be due to early lactation problems. The
and many microorganisms have been
primary differential diagnoses are
identified, including Escherichia coli,
peripartum mammary edema, which is often

Klebsiella spp, Enterobacter spp, Citrobac
seen in primiparous sows without any
ter spp, Staphylococcus spp ( eg, S epider
systemic signs, and PPDS, which is less
midis ), and Pseudomonas aeru.ginosa. All spectacular but affects a greater number of
these microorganisms are common in the
sows. A thorough physical examination,
environment of sows.

including careful palpation of the mammary

Although many sows in a herd may be
glands, should be performed. However, it is
severely affected, this type of mastitis is not
necessary to be cautious in the interpretacontagious. After farrowing, the mammary tion-hard mammary glands without
gland is infected by environmental
systemic signs do not always indicate
opportunist bacteria. Very few bacteria
acute mastitis. Although frequently seen,

( often <100 organisms) are enough to
peripartun1 mammary edema is poorly
colonize the mammary gland.

documented. Sows often appear to be in

POSTPARTUM DYSGALACTIA SYNDROME AND MASTITIS IN SOWS

1375
discomfort and lay down, as do sows with

Diagnosis: The integrity of the manm1ary
mastitis. However, periparturn mammary
gland should be checked before each
edema can certainly lead to an acute
fanowing. Except for cases associated with
multiglandular mastitis. In contrast to the
inaccessible teats, risk factors involved in
situation in cows, interpretation of cellular
the development of blind teats should be
modifications in the milk is very difficult in
identified. Traumatic teat lesions can be the

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sows.

consequence of iitjuries induced by piglets
or other sows, or by slipping on slatted

Treatment and Control: Systemic
floors, etc. Unfortunately, these primary
antibiotic therapy should be started as soon
lesions often go unnoticed until several
as possible (seep 1376). Longterm control
weeks or months have passed. Size
of a herd problem also requires identificahomogeneity within a litter should also be tion and correction of risk factors. General
monitored. Any discrepancy or growth
antibiotic therapy as well as corticosteroids
retardation in a piglet compared with its
are useful to reduce the intensity of the
littem1ate could be indicative of mastitis
inflammatory reaction. Meloxican1 has also
in a mammary gland.

been shown to improve recovery of the
sows. Management techniques to improve

Treatment and Control: The affected
hygiene should be in1plemented as soon as
gland is lost for the cun-ent lactation and
possible. Cross-fostering is often the only
sometimes for the next lactation. During
effective way to save a litter.

subsequent lactations, the mm1ber of
nursing piglets should be limited, or the

ACUTE UNIGLANDULAR MASTITIS sow should be culled.

In lactating or weaned sows, inflammation
of a single mammary gland is common.

CHRONIC OR DRY-SOW MASTITIS

Such uniglandular inflammations are more
often noticed in old sows.

Postweaning or dry-sow mastitis is a
common type of mastitis that affects one or
a few glands. The prevalence among newly

Etiology and Pathogenesis: The
microorganisms involved are the same
weaned sows is 10%-200/o. Chronic mastitis
as those in acute multiglandular mastitis
is characterized by the formation of
abscesses and granulomas in the manm1ary

(see above). Sometimes only one or two
mammary glands are affected; the cause
tissue, which are often seen at weaning or
should be identified. Traumatic lesions or
sho1tly after. A primary pathogen has not
inaccessibility of teats to piglets a.re co nun on. been identified. Bacteria conunonly enter Piglets suckling inguinal mammary glands
the rnan1mary glands through teat wounds
caused by the piglets' sharp teeth during
of old sows are often unable to reach the
teat during the phase of milk ejection. Usually, suckling, fights among aggressive weaned sows grouped in the same pen, or traun1a
piglets have selected a specific gland by 24 hr
after birth. A piglet suckling a teat affected
associated with the particular anatomy of
by acute uniglandular mastitis will show
inguinal manunary glands of old sows.

growth retardation, while litter.mates remain
healthy. Milk secretion may be restricted by

POSTPARTUM DYSGALACTIA
acquired problems of mammary conforma

SYNDROME
tion (as in old sows), traumatic lesions, and
other teat abnormalities. Teat lesions may

Postpartum dysgalactia syndrome (PPDS)

have developed during the previous
is a primary cause of neonatal problems ( eg,
lactation, the previous weaning-to-estms
diarrhea, crushing, runting, inanition, poor
interval, or the previous gestation.

growth) but is challenging to characterize
because of its multiple manifestations and
the difficulty in making an etiologic
diagnosis. In a given herd, PPDS affects

-15%-200/o of the sows; a higher percentage
is unconunon. It is more common in young
sows in their first or second parity.

Etiology and Pathogenesis: There are
nun1erous rnultifactorial etiologies, which
complicate the diagnosis and clinical

Teat damage as a result of trauma in a sow.

evaluation. Classically perceived as a part

Courtesy of Dr. Glen Almond.

of the rnastitis-metritis-agalactia (MMA)

1376

POSTPARTUM DYSGALACTIA SYNDROME AND MASTITIS IN SOWS
complex, PPDS should instead be
large litter sizes, and a high postpartun1
considered a broader pathology. Thus, the
fever. Management practices reported in

MMA complex is essentially a subtype of
herds with a high incidence of PPDS include

PPDS, probably the most severe clinically
too much manual intervention during
but also the least conunon.

parturition or too many parenteral

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Evidence suggests that lipopolysacchainjections to sows (antibiotics, oxyto-tide (LPS) endotoxins, a po1tion of the cell
cin, prostaglandins) or piglets ( mainly
wall of all gram-negative bacteria, play a
antibiotics). Moving pregnant sows to
central role. Bacte1ial endotoxins can be
the farrowing facilities �4 days before the
absorbed from the uterus ( eg, endomettitis
expected farrowing, and feeding sows ad lib
or metritis), mammary glands ( eg, acute
during lactation also should be considered
multiglandular mastitis), or gut ( eg,

1isk factors. Piglet losses are due to
constipation as a consequence of feeding
emaciation or diarrhea ( or both), as a
finely ground feed to sows can result in
consequence of poor nuttition duting the
bactetial overgrowth and subsequent
first few days postpartun1.

absorption of endotoxins from the
intestines) and lead to endotoxemia.

Diagnosis: Diagnosis is difficult and

Identifying the source of the bacterial
based on clinical signs. Clinical examination
endotoxins is important to determine the
is best perfonned while piglets are nursing;
best preventive approach for the particular
milk ejection in affected sows is either
herd.

absent or of brief duration, which causes

The secretion of colostrum is detemlined
the piglets to actively nurse for an extended
by a complex honnonal balance (homeorhetime. During the initial stages, piglets sis ). LPS endotoxins exe1t their effects even
repeatedly attempt to nurse at frequent
before farrowing and act with the intervenintervals and do not settle after nursing. As tion of the innate immune system (maca result of vigorous nursing efforts, the teats rophage activation). These changes
may be traun1atized. As the energy reserves
adversely affect production and secretion
of the piglets are depleted, their attempts to
of colostrum and milk. In addition, the
nurse decrease, and they often migrate to
colostrum is as in1portant for its energy
the warmest portions of the farrowing crate.

content as it is for its immunoglobulin

Crushing by the sow is common. Therefore,
content. Any decrease in the amount of
litter behavior should be watched closely
ingested colostrum will result in consefor a prolonged time when trying to quences for the piglets such as diarrhea,
diagnose PPDS.

inanition, and poor growth.

Mammary tenderness, swelling, and teat

Other causes of general hypogalactia
damage are consistent with a diagnosis of
that should be considered include acute
lactational insufficiency. The man1mary
multiglandula.r mastitis, udder and teat
glands vary from grossly nonnal to swollen,
abnonnalities, hypocalcemia ( uncommon
firm, and warm to the touch, sometimes
in sows), and acute (agalactia) or chronic
with blotched purple skin. Pure bacterial

(hypogalactia) ergotism (uncommon in
cultures may be isolated from milk san1ples.

practice). Indeed, ergot detivatives

Rectal temperature of the sow vaties from
suppress prolactin release.

normal to markedly increased (>40.5°C

Risk factors are those associated with

[ 104.9°Fl). The concept that postpartum
stress of the sow and with conditions
rectal temperatures >39.5°C (103.1 °F)

that lead to bactetial multiplication and
predict early lactation problems must be
subsequent endotoxemia. Such factors are
questioned. Physiologic hyperthermia
numerous and are linked with different
observed in lactating sows should not be
entities ( eg, cystitis, mettitis, vaginitis,
confused with fever. Reduced appetite or
constipation, mastitis).

anorexia, constipation, and depression may

Genetics can also be a 1isk factor for
also be seen. Abnom1al and copious vaginal

PPDS; most recent studies identified
discharges may be seen in some sows ( eg,
susceptibility genes on chromosome 17.

cervicitis, endometritis ). Cystitis, mettitis,

Selection among genetic lines should
vaginitis, constipation, or mastitis in the
include this parameter.

sow and diarrhea in neonatal piglets should
be considered as a general syndrome

Clinical Findings: PPDS is seen almost

( requiring an overall diagnosis) rather than
exclusively within the first 3 days after
as individual problems.

farrowing. Associated signs are numerous
and vary from herd to herd, as well as within Treatment and Control: Systemic or herds. PPDS is commonly associated with
local therapeutic intervention (antibiotics,
fat sow syndrome, prolonged farrowings,

NSAIDs) can sometimes be helpful but only

PROLONGED GESTATION IN CA

TILE AND SHEEP

1377
on a short-term basis. Flunixin meglurnine
an10ng herds and depends on fann
may help to counteract the effects of
circumstances.

endotoxins. Antin1icrobial treatment is

As many risk factors as possible should
usually presc1ibed before susceptibility can
he identified and corrected or minimized.

be tested. A broad-spectrum antibiotic is

Systematic manual interventions during

VetBooks.ir
therefore recommended. However, if
farrowing or uterine washings should be
antibiotics are used longterm, a dependence
limited to only those that are necessary.

on them for puerperal fevers, acute mastitis,

There is no clear evidence that vaccines
vaginitis, endometritis, or neonatal diarrhea
have a beneficial effect. Good sanitation
can develop rapidly and lead to multiretends to decrease the incidence of mastitis sistant bacterial infections. Oxytocin or
in the sow and diarrhea in the piglets, but
prostaglandins ( or both) can be useful in

PPDS is also common in herds in overall
cases of prolonged farrowing or postpartum good health and with a high level of endomet1itis. By far the most effective
hygiene.

method is to cross-foster the piglets from

For clu·onic mastitis, use of partially
affected to healthy sows, as long as the
slatted fan·owing pens and cleaning with
health status of the litters are equivalent.

disinfectants between batches of sows in

Oxytocin (5-10 U/sow) is occasionally
the farrowing and breeding ai·eas may be
effective in reestablishing lactation if used
helpful. Cutting or grinding the piglets' teeth

4 or 5 times at 2- to 3-hr intervals. In herds
after farrowing is not considered a good
in which PPDS is a significant problem,
way to control chronic mastitis. Indeed, it
incidence may be reduced by inducing
can lead to a high prevalence of mastitis,
paiturition with prostaglandin F2ac; this
possibly ca.used by changes in the oral flora
results in rapid induction of labor and dilataof the piglets or the failure of piglets to tion of the teats for a shorter period of time.

suckle as a result of sore mouths from

However, the ainelioration is not constant
careless cutting of teeth.

PROLONGED GESTATION

IN CATTLE AND SHEEP

Paiturition is induced by the fetus in both
species, a slightly longer gestation length·
cattle and sheep. It is initiated by rising
is often seen ( eg, Zebu cattle have a mean
cortisol levels in the fetus that provoke a
gestation length of 296 days). Within breeds,
cascade of endocrine activity in the <lain.

individual bulls may sire calves witl1 longcr

Fetal cortisol increases as a result of
gestation length than nonnal, leading to a
increased adrenocorticotropic hom10ne
higher incidence of dystocia. In sheep, the

(ACTH) production by the maturing fetal
normal gestation length is 144-150 days.

pituitai-y ca.used by fetal stressors such as

In many cases, prolonged gestation is
hypoxia and hypercapnia. Gestation length
incorrectly diagnosed because of hun1an
is unique to each fetus, but approximate
error. The service elates of dairy cattle ai·e
gestation lengths can be ascribed to each
normally known. Hence tl1e date of
species (see TABLE 1, p 1324).

anticipated parturition is calculated and

In cattle, gestation length is influenced by
recorded once pregnancy is confirmed. In
factors such as the breed of the cow ai1d
beef cattle, in which cows often run with a
bull, calf gender, single vs multiple biith, the
bull, exact calving dates are not known, but
pai·ity of the cow, and the fetal genotype.

individual pregnant cows are expected to

Environmental factors, includiI1g nutrition,
calve witllin a recognized calving season.

ambient temperature, and the season of the

Individual aniinals tl1at have not calved at
yeai·, have a smaller influence. The breed
the anticipated time are checked to confirm
of cattle has the greatest influence on
tl1ey are still pregnant and tl1at their
gestation length. In European cattle of the
pregnancy appears to be normal.

Bos taurus species, considerable breed

In sheep, the exact lan1bing date is
vaifation is recognized ( eg, 279 days mean
seldom known unless ewes were served in
gestation in Holstein-Friesian to 287 days in
hand or by aitificial insemination. In most

Charolais). In breeds of the Bos indicus
flocks the ewes run with rams and, when

1378

PROLONGED GESTATION IN CATILE AND SHEEP
served, receive a raddle crayon mark on
the rumen while still within the uterus, so
their rumps to indicate that service has
that it carmot be palpated per rectum.

occurred. Crayon color is changed at 14- to

In some aninlals, prolonged gestation is

17-day intervals, and after later pregnancy
accompanied by development of excessive
confirmation, a lan1bing date within a 14- to
amounts of fetal fluid. The origin of

17-day period is calculated. Individual ewes
excessive fetal fluid can be assessed by

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that fail to lan1b are culled or further
analysis of sodiun1 and chloride levels in an
evaluated for pregnancy.

aspirated sample. Amniotic fluid contains

Miscalculation of the prospective calving
sodium at -120 mmol/L and chloride at -90
or lambing date, failure to record a subsemmol/L. Allantoic fluid contains sodium at quent service, faulty pregnancy diagnosis,

50 mmol/L and chloride at 20 mmol/L. The
and incorrect identification of aninlals may
correlation between hydrops amnion and
lead to a diagnosis of prolonged gestation in
hydrops allantois and prolonged gestation
an anin1al that has a nom1al pregnancy. True
is tenuous, however. Most fetal giants suffer
prolonged gestation is relatively uncommon;
from oligoamnios.

the common denominator is a defective

In true prolonged gestation, the fetus
hypothalamic-pituitary-adrenal axis.

is unlikely to be of any economic value.

Suspected cases should be investigated and

Treatment should be aimed at fetal delive1y
exanlined with care. In some cases, the fetus
with minimal damage to the dam. In cases of
is dead or severely defom1ed and is of little
fetal giantism, the dam may be distressed by
economic value. The life of the dan1 may be
the weight of the fetus and its associated
at risk if prolonged gestation is allowed to
fluids. Painful edema in front of the udder
continue, and teffilination of the abnormal
may indicate rupture or impending rupture
pregnancy is recommended.

of the prepubic tendon. A canvas sling
support can be placed around the abdomen

Diagnosis: When a number of cases of
to prevent further damage until the
prolonged gestation are seen in a herd
pregnancy is tem1inated. General health of
or flock, a full investigation should be
the dam should be assessed and economic
conducted in an attempt to identify the
considerations discussed with the owner
cause and possibly a preventive program. A
before treatment is attempted. Milk
genetic abnonnality may be detemlined by a
production may be compromised.

study of pedigrees or by finding an abnormal

Successful induction of parturition
karyotype in affected fetuses. Possible
requires an intact fetal hypothalamic-pituiexposure to toxic plants and viral infection tary-adrenal axis. Pregnancy is maintained
should be investigated. Tests for evidence of
in cases of prolonged gestation chiefly by
pathogenic viruses or serologic evidence of
continued production of progesterone by
exposure to them may lead to clear evidence the corpus luteum. Spontaneous induction of virus involvement. In some cases, the
of birth in cases of prolonged gestation fails
cause of prolonged gestation remains
as a result of insufficient production of fetal
unknown. Evidence of pituitary hypoplasia
cortisol and the failure of luteolysis to
or compromise may be found, but the
occur. Birth in both cows and sheep can be
underlying cause remains elusive.

successfully induced by administering both
prostaglandin F2a ( or its synthetic analogue

Treatment: In a case of suspected
cloprostenol) and the corticosteroid
prolonged gestation, the dam's breeding
dexamethasone by IM injection. Luteolysis
records, if available, should be checked to
is induced by the prostaglandin, and the
ensure that parturition truly is overdue.

maternal hormone cascade that precedes

Treatment of a case in which gestation is
parturition is initiated by the corticosteroid.

not genuinely prolonged may result in the

In cows, 500 mcg cloprostenol and 20 mg
delivery of a premature fetus that is unlikely
dexamethasone are given; in sheep 125 mcg
to survive. Once the true length of gestation
cloprostenol and 16 mg dexamethasone are
is established, a full clinical examination of
recommended. A single dose of these two
the dam should be conducted.

drugs is normally effective. Parturition

In cattle, rectal examination of the uterus
should begin in 24--72 hr.

and its contents is an important diagnostic

Induced parturition should be monitored
aid. Fetal parts may be palpable, and in
carefully. Assistance may be required if
some cases it is possible to detect an
there is evidence of uterine inertia or
abnormal cranium. An ultrasonographic
damage to the abdominal wall, either of
scan may confirm the presence of fetal
which might make expulsive efforts
abnormalities, including a thin-walled,
ineffective. Fetal malposition requiring
fluid-filled cranium. The weight of an
obstetric assistance may occur once birth
overdue fetus may cause it to pass under
begins. If the fetus is very large, dystocia

PROLONGED GESTATION IN CADLE AND SHEEP

1379
due to fetal-pelvic disproportion may occur,

PROLONGED GESTATION
and assisted delivery by careful traction

ASSOCIATED WITH FETAL
may be attempted. If this is not possible,
cesarean section may be required. If the

DEFORMITY
dam is seriously ill but considered well

Prolonged gestation associated with fetal
enough to withstand surgery, an elective
deformity cases usually occur as the result

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cesarean without an attempt at vaginal
of some compromise of the hypothalarnicdelivery may be considered. Fetal dysmatupituitary-adrenal axis of the fetus, which is rity can be a problem, especially in very
no longer able to initiate parturition. The
valuable cloned offspring, and intensive
affected fetus may either die and be aborted
care facilities may be needed.

or live on indefinitely in the utems. Genetic,

After fetal delivery, uterine involution
infectious, toxic, and m1lmown causes have
may be encouraged by administration of
been associated with this problem.

oxytocin. Retention of fetal membranes is
managed in the usual way (seep 1381).

Fluid therapy, antibiotics, and treatment

Genetic Abnormalities: Prolonged
with NSAIDs such as flunixin meglumine
gestation associated with fetal adrenal
may aid recovery and provide analgesia.

malfunction is a genetically determined
prolonged gestation caused by an
autosomal recessive gene of the fetus in

PROLONGED GESTATION

Holstein-Friesian cows. The fetal adrenal

ASSOCIATED WITH FETAL DEATH
glands fail to produce corticosteroids at
tenn, in response to fetal ACTH. As a

Fetal death may be followed by abortion,
result, the fetus continues to grow until it
fetal maceration, or fetal mummification. In
outgrows its blood supply. Induction with
cases of abortion and fetal maceration, the
dexamethasone does not induce normal
hormonal suppo1t of pregnancy is lost. The
labor and parturition because of insuffianimal nom1ally shows signs that pregcient preparation of the birth canal. A nancy has terminated. An aborted fetus may
cesarean section will save the darn, but
be found, the dam may show an abnormal
the fetus invariably dies due to adrenal
vaginal discharge, and she may return to
insufficiency.

estrus. Fetal bones may be trapped in the

Four further genetic abnormalities
uterus and compromise future breeding.

associated with prolonged gestation in

In cases of fetal mummification, fetal
various breeds of cattle involve fetal
death is often not in1rnediately apparent. In
pituitaly abnormalities. In one condition,
such cases, the corpus luteum persists in the severe fetal oversize (fetal giantism) is ovary, and there is no vaginal discharge and
present. In the second, the calf has severe
no signs of estrus. The abnormal pregnancy
craniofacial defects and is much smaller
in such anin1als continues indefinitely.

than normal. In the third condition, multiple

Affected animals are normally identified
skeletal abnormalities are present. In a
when owners notice that external signs of
fomth condition, genetic abnormalities
late pregnancy, including abdominal
may occur as a result of cloning.

enlargement, are less obvious than in other

Prolonged gestation and fetal
members of a group. Clinical examination
giantism has been reported in Holsteinreveals that the fetus is dead, although the Friesian, Ayrshire, and Swedish breeds of
dam is pregnant. Rectal examination reveals cattle. Gestation is prolonged by 21-150
an irregularly shaped, contracted uterus
days. Pronounced abdominal enlargement
with a fetal mass but no fetal fluid within it.

is seen in some cases. There is no attempted

There is no fremitus in the uterine artery.

parturition unless the fetus dies first after

Ultrasonographic exan1ination of accessible having outgrown its blood supply. Cervical parts of the uterus per rectum confirms the
relaxation is poor, and dystocia invaiiably
diagnosis. The abnormal pregnancy can be
results. The calf weighs 48-80 kg at birth
terminated by a single IM irtjection of
and shows signs of postmaturity. The coat
prostaglandin F2a. The fetus is expelled
and hooves are longer than normal, and
from the uterus and can be manually
prominent loose teeth are present in the
removed from the vagina 48 hr later.

gums. Breathing is difficult as a result of

In sheep, fetal mummification can
failure of surfactant release, and the calf
be diagnosed by abdominal palpation
may die from hypoglycemia. At necropsy,
supported by a transabdominal ultrasonohypoplasia of the anterior pituitai·y and graphic scan. Affected animals are normally
adrenal glands is seen.

culled on economic grounds. Treatment can

Prolonged gestation with craniofacial
be attempted ( see above).

defects in the fetus has been reported in

1380

PROLONGED GESTATION IN CATTLE AND SHEEP

Holstein-Friesian, Ayrshire, Guernsey, and
present, and the brain stem is smaller than

Jersey breeds of cattle and is thought to be
normal. Compromise of pituitary function
caused by a recessive gene. Affected fetuses
in the affected fetus can lead to prolonged
cease to grow at 7 mo gestation. There is no
gestation.

spontaneous parturition in affected cattle

Bluetongue virus (seep 738), found in

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because of the nonfunctional or absent

Africa, Australia, North and South America,
pituitary gland in the fetus. Calves are
and Europe, is also transmitted by insects;
usually dead when delivered. Some may
infection can occasionally cause prolonged
show evidence of severe abnormalities of
gestation. The fetuses of cows exposed to
the craniwn and face.

the virus at 60-120 days of pregnancy

Prolonged gestation associated with
developed hydranencephaly, whereas
multiple skeletal abnormalities has been fetuses exposed later in pregnancy reported in Hereford cattle. Affected calves
developed less severe CNS defects.

show evidence of pituitary aplasia or

Gestation lengths >200 days have been
hypoplasia. Arthrogryposis, torticollis,
recorded in ewes vaccinated during
kyphosis, and scoliosis are present, and
pregnancy with Rift Valley fever attenuated
some calves have cleft palates.

viral vaccine. Affected lambs developed

Prolonged gestation associated with
severe brain defects and skeletal abnonnalicloning has been reported in both fetal ties. Some ewes developed hydrops amnion
calves and lan1bs produced by somatic cell
by the fowth month of gestation. Ewes in
nuclear cloning. Early placental abnom1aliwhich pregnancy was not terminated ties have been detected in a high propordeveloped ketosis.

tion of such aninlals, and placentomegaly
may be seen in later pregnancy. The

Toxic Causes: Several plant toxins cause
abnormality may result in fetal death or, if
fetal deformity and prolonged gestation
the fetus survives, in the large offspring
when eaten accidentally or fed experimensyndrome. Spontaneous birth may not tally. When fed to sheep in early pregoccur, and prolonged gestation results.

nancy, Verat?"um californicum (skunk

Fetal lung and maternal manimary
cabbage) produces fetal deformities,
development is retarded and can comgiantism, and prolonged gestation. Cranial promise fetal survival.

defects and brain and eye abnormalities
were seen in fetuses of ewes fed this plant

Infectious Causes: Although bovine
at 14 days of gestation; pregnancy length
viral diarrhea virus (seep 267) can cause
in some cases was >230 days. The plant
abortion in cattle, it can also produce
contains the amine cyclopamine, which is
congenital defects in the fetus. These
believed to be responsible for the fetal
include cerebellar hypoplasia, anencephaly,
abnormalities. This plant also contains a
and hydrocephaly. Affected calves may be
number of toxic alkaloids that cause GI
born with severe defects of the CNS, but
disturbance, dyspnea, and convulsions in
prolonged gestation occasionally occurs if
sheep. Veratrum album has similarly
pituitary function is compromised. The
caused prolonged gestation and fetal
related pestivirus border disease virus (see
abnormalities in Holstein-Friesian cows
p 622) can produce severe brain and coat
in Japan.

abnormalities in fetal lambs. Pituitary

An tmidentified toxin in the plantSalsola
compromise in such lambs can lead to
tuberculatiformis ( cauliflower saltwort) is prolonged gestation.

thought to cause prolongea gestation in

Akabane virus (seep 620), found in
sheep. Pregnancy was extended >220 days,

Africa, Australia, the Middle East, and the
and affected lambs showed atrophy of the

Far East, can be transmitted by insects to
pituitary, adrenal, and thyroid glands.

both pregnant cattle and sheep. Bovine

Fetuses appear to be most susceptible to
fetuses exposed to the virus at 76-104
the toxin in the first and third trimesters of
days gestation may develop hydranenpregnancy. Amniotic fluid continues to cephaly (fluid-filled cavitation of the
increase in volume in cases of prolonged
brain). Exposure to the virus at 105-174
gestation associated with this plant.

days of pregnancy may cause both

Physical abnormalities such as cleft palate
hydranencephaly and arthrogryposis.

prevent normal swallowing of amniotic fluid

Affected fetuses may have severe brain
in affected fetuses. Excessive fetal weight
damage. The cerebral cortex may be
and the weight of accwnulated fetal fluids
absent and the cranial cavity filled with
may lead to rupture of the prepubic tendon
fluid. Cerebellar hypoplasia may be
in ewes.

RETAINED FETAL MEMBRANES IN LARGE ANIMALS

1381

PSEUDOPREGNANCY IN GOATS

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Pseudopregnancy is one of the major causes
variable size, separated by thin, double
of anestrus in dairy goats during the breeding layers of tissue that represent sections season. Older, parous does are most often
through the apposing walls of the distended,
affected. It is characterized by the persiscurved uterine horns. When an abundant tence of a corpus luteum in the absence of
amount of fluid is present, these tissue
a (viable) conceptus in the uterus.

layers can be seen undulating when the
examiner shakes the abdominal wall of the

Etiology and Pathogenesis: Failw-e
doe. During an early ultrasonographic
of luteal regression, either in nonmated
pregnancy diagnosis (20--30 days after
cycling animals or in mated does affected
mating or insemination), it can be difficult
by embryonic or fetal mortality, is the key
to discriminate between a normal pregfactor in the pathogenesis of the disorder.

nancy and a hydrometra because the

Pseudopregnancy can also spontaneously
embryo or placentomes can be difficult to
develop in urunated anin1als, even during
locate at that stage, and excess fluid may be
the nonbreeding season. A genetic predispomistaken for allantoic fluid.

sition has been postulated, but in a recent
study from the UK the incidence of

Treatment and Prognosis: Treatment
pseudopregnancy in the offspring of
with a luteolytic dose of prostaglandin F 2a
affected dan1s was not significantly different (or one of its synthetic analogues) induces from that in daughters of unaffected does.

luteal regression and discharge of the
ute1ine fluid within 1--2 days. If treated

Clinical Findings: Hydrometra(accwnu dw-ing the breeding season, the doe will lation of fluid in the uterus) is the primary
come into estrus within 2-3 days and can be
clinical feature of pseudopregnancy. It
mated or inseminated again. Sometimes a
develops during prolonged and continuous
second injection is necessary to accomexposw-e to progesterone from the corpus plish a complete emptying of the uterus.

luteum. When not diagnosed, pseudopreg

Pseudopregnancy also may end spontanenancy can persist for up to several months, ously when progesterone production by the
and the amount of fluid can reach a volume

(aging) corpus luteum stops. As a result,
of several liters. In such cases the distended
relaxation of the cervix and stimulation of
abdomen will give the false impression that
ute1ine contractility occur, followed by
the animal is pregnant; this can also be
discharge of the uterine fluid. This latter
accompanied by udder enlargement.

process has also been described as

"cloudburst." The fertility of does appears Diagnosis: Pseudopregnancy can be
to be nom1al after effective treatment with
diagnosed by ultrasonography. The fluid
prostaglandins, so culling of affected goats
is recognized as anechoic, black spots of
is generally not indicated.

RETAINED FETAL MEMBRANES

IN LARGE ANIMALS

(Retained placenta)

cows
whereas the incidence in beef cows is lower.

The incidence is increased by abortion

Retention of fetal membranes, or retained

(pa.iticularly with brucellosis or mycotic
placenta, usually is defined as failw-e to
abortion), dystocia, twin birth, stillbirth,
expel fetal membranes within 24 hr after
hypocalcemia, high environmental
parturition. Normally, expulsion occw-s
temperature, advancing age of the cow,
within 3--8 hr after calf delivery. The
premature birth or induction of pa.iturition,
incidence in healthy dairy cows is 5%--15%,
placentitis, and nutritional disturbances.

1382

RETAINED FETAL MEMBRANES IN LARGE ANIMALS

Cows with retained fetal membranes are

MARES
at increased risk of metritis, displaced
abomasum, and mastitis.

Equine fetal membranes are nonnally

Retention of fetal membranes is mediated
expelled within 3 hr after parturition, but
by impaired migration of neutrophils to the
expulsion may be delayed for 8-12 hr
placental interface in the periparturient
or even longer without signs of illness. The

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period. The impaired neutrophil function
cause of retention of fetal membranes often
extends into the postpartum period and
is not known, but the condition is associated
probably mediates the recognized complicawith infection, abortion, short or prolonged tions of retained fetal membranes. Cows with gestation, uterine atony, and dystocia. Mares retained fetal membranes have increased
that have retained their fetal membranes
cortisol and decreased estradiol concentraappear to be at increased risk of recurrence tions in late pregnancy. They may also have
of the condition, and Friesian mares are
an altered prostaglandin (PG) E
particularly predisposed. Retention of just

2:PGF2 ratio.

Uterine contractility is increased in affected
a portion of the fetal membranes entirely
cows. (Placental detachment, rather than
within the uterus (usually at the tip of the
uterine motility, is responsible for retention
previously nongravid uterine horn) is less
of fetal membranes.)

conspicuous but equally likely to result in

Diagnosis is usually straightforward as
complications. For this reason, the
degenerating, discolored, ultimately fetid
chorionic surface of the expelled memmembranes are seen hanging from the vulva branes should be examined carefully to

>24 hr after parturition. Occasionally, the
ensure they have been completely expelled.

retained membranes may remain within the

Retention of fetal membranes may
uterus and not be readily apparent, in which
mediate development of metritis or even
case their presence may be signalled by a
peritonitis. Laminitis is a potential sequela.

foul-smelling discharge. In most cases, there

For these reasons, it is common practice to
are no signs of systemic illness. When
administer oxytocin (5 U, IM, every 2-3 hr)

systemic signs are seen, they are related to
begirming 3-4 lu· after parturition if the memtoxemia. Uncomplicated retention of fetal branes have not yet been expelled. Calcium
membranes is unsightly and inconvenient for
supplementation may be beneficial. Manual
animal handlers and milkers but generally
removal of retained membranes carries the
not directly hannful to the cow. However,
risk of uterine danmge or prolapse and is not
cows with retained fetal membranes are at
reconunencled beyond gentle tugging to
increased risk of developing metritis, ketosis,
displace already loosened membranes. In
mastitis, and even abortion in a subsequent
cases of prolonged retention of fetal
pregnancy. Cows that have once had retained
membranes, antinlicrobials should be
fetal membranes are at increased risk of
administered prophylactically, along with
recurrence at a subsequent parturition.

other therapeutic strategies aimed at

Manual removal of the retained mempreventing lan1initis (seep 1109). Mares that branes is not recommended and is
have recovered from retention of fetal
potentially harmful. Trimming of excess
membranes do not generally have lower
tissue that is objectionable to animal
fertility.

handlers and contributes to gross contamination of the genital tract is pennissible.

DOES, EWES, AND SOWS

Untreated cows expel the membranes in

2-11 days. Routine use of intrauterine

In does and ewes, the incidence of retained
antimicrobials has not been found to be
fetal membranes increases with larger litter
beneficial and may be detrimental. Although
sizes and with assisted parturition. Systemic
advocated at various times, oxytocin,
treatment to guard against infection and
estradiol, PGF2u, and oral calcium
gentle traction on exposed membranes may
preparations have not been shown to hasten
be used. In sows, retained placentae are
expulsion of retained membranes or to
contained within the uterus and are not
prevent complications. When systemic
visible at the vulva. In this species, entire
signs of illness are present, systemic
fetuses may be retained. Usually, the fetus
treatment with antimicrobials is indicated.

or membranes decompose in situ. This may

In herds in which incidence of retained fetal
be accompanied by signs of systemic illness
membranes is unacceptably high, predisand a purulent vaginal discharge. Altl10ugh posing causes should be sought and
serious or fatal sequelae occasionally occur,
eliminated. Supplementation with vitan1in
the prognosis for recovery and future

E and selenium for herds in which these
fertility is surprisingly good. Antimicrobial
nutrients are deficient has been found to
treatment is indicated in anin1als with
be beneficial.

systemic signs of illness.

SEMINAL VESICULITIS IN BULLS

1383

SEMINAL VESICULITIS IN BULLS

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The seminal vesicles are paired accessory
arthritis, or pnetm1onia is considered more
sex glands located on the floor of the pelvis,
plausible.

lateral to the ampullae, and dorsal to the

Congenital malfonnation of tile excretory
neck of the urinary bladder. The vesicles
ducts of the vesicles where they open into
secrete a clear fluid that adds volume,
the urethra at the colliculus se.minalis has
nutrients, and buffers to semen. The tem1
been reported. A malformation of the

"seminal" vesicle is a misnomer, because the excretory duct orifice pennits reflux of
vesicles are not a reservoir for spem1atozoa.

spermatozoa or urine from the pelvic urethra

Seminal vesiculitis is an inflammation and into the vesicle. If the tubular lining of the often an infection of one or both vesicular
vesicle degenerates subsequent to irritation
glands. The pwulent material associated
from abnormal material in the ducts,
with vesiculitis is a contaminant of semen
significant local inflani.mation can result.

and is a cause for semen to be discarded

This noninfectious etiology may accoWlt for
from bulls collected at an artificial
the poor therapeutic response in some cases.

insemination center. Bulls foWld to have
vesiculitis during a breeding soW1dness

Clinical Findings: There are usually
examination are considered W1satisfactory
no external signs of disease. It has been
breeders. Bulls refractory to treatment
suggested that a bull with a severe acute
efforts should be culled.

case or vesicle abscessation may stand with
its back arched, have pain on defecation or

Epidemiology: Vesiculitis has been
rectal examination, and show hesitation
reported in bulls wherever breeding cattle
when moW1ting. However, such clinical
are raised. The repmted incidence of
signs are very WlCOm.mon.

vesiculitis in the general population of bulls
is 1o/<r-100/o. However, incidences of 200/o and

Diagnosis: Vesiculitis is usually first
even 49% have been reported for bulls
suspected after collection of a semen
housed in groups. Bulls of all ages can be
sample grossly contaminated with purnlent
affected, but vesiculitis is most frequently
matelial. If the bull has vesiculitis, the rectal
seen in yearling bulls presented for a
examination typically reveals an enlarged,
breeding soW1dness examination or
sometimes irregular, and often fibrotic
collected for the first time. Because many
vesicle. Vesiculitis may be tmilateral or
yearling bulls affected with vesiculitis are
bilateral. If vesiculitis is unilateral, there is
culled, it is seen less frequently in adult bulls. usually asynunetry in the size of the glands.

Infrequently, a vesicle will be abscessed; in

Etiology and Pathogenesis: Vesiculitis
such cases, the affected vesicle is markedly
is typically considered to be caused by
larger than the other and may be fluctuant
bacterial infection. The most commonly
on palpation.

identified bacteria are Trueperella pyogenes,

Purulent contamination of semen is not

Pseudomonas aeruginosa, streptococci,
pathognomonic for vesiculitis. A bull with
staphylococci, Proteus spp, and Escherichia epididymitis, orchitis, or posthitis may also coli. Other microbial agents implicated
have semen contaminated with purulent
include Mycoplasma bovigenitalium,
exudate. The entire genital tract must be

Chlamydia spp, and viruses.

examined to determine a possible cause for

Postulated pathogenic mechanisms
tl1e abnonnal semen. The prepuce may need
include infectious agents ascending the
to be douched with water or saline before
urethra to the vesicle, descending through
collection of semen to exclude postllitis as a
the ductus deferens from the testicles or
transient cause of pus in semen. Semen may
epididymides, or metastasis from another
be cultured but, wtless collected aseptically
tissue or organ hematogenously. The
after catheterization of the urethra, culture
ascending route of infection is considered
is usually unrewarding because of microbial
wilikely Wlless the bull has accompanying
contan1ination from the prepuce.

penile trauma or uretllritis. The descending
route would be considered if the vesiculitis

Treatment and Prognosis: Because
is ipsilateral to an infectious epididymitis or
vesiculitis may have a bacterial etiology,
orchitis. Vesiculi.tis subsequent to systemic
broad-spectrum antibiotics ad.ministered
infection, umbilical infection, infectious
at labeled therapeutic dosages are usually

1384

SEMINAL VESICULITIS IN BULLS
administered to affected bulls. There are no
cure is guarded to poor. This is particularly
published controlled studies that indicate
true for chronic cases. Spontaneous
preference of a specific antibiotic for
remission has been seen when vesiculitis
treatment. Prolonged-release antibiotics
was diagnosed in bulls< 1 yr old. Semen
are preferable because the bull, which can
contan1inated with purulent material is not

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become unruly, does not have to be handled
suitable for artificial insemination and
daily. Because vesiculitis is an inflan1TI1ation
should be discarded. Surgical removal of
as much as an infection, NSAIDs reduce the
affected vesicles has been done but is a
excretion of purulent material. Transient
difficult procedure. The prognosis after
alleviation of purulent contamination may
surgery is fair in yearling bulls; surgery has
be achieved during the treatment interval in
not been successful in adult bulls with
some bulls, but the prognosis for a longterm
chronic vesiculitis.

TRICHOMONIASIS

Trichomoniasis is a venereal disease of
along with poor pregnancy test results
cattle characterized primarily by early fetal

( eg, too many "nonpregnant normal'' and
death and infertility, resulting in extended
late-bred cows) is usually the presenting
calving intervals. Distribution is probably
complaint. In addition to a reduced number
worldwide.

of cows estimated to calve during the
regulai· calving season, an increased

Etiology and Epidemiology: The
number of cows with a "nonpregnant
causative protozoan, Tritrichomonas
abnorn1al" reproductive tract diagnosis is
foetus, is pyriforn1 and ordinarily 10---15 x seen. These include cows with pyometra,

5--10 µm, but there is considerable
endometritis, or a munilllified fetus.

pleomorphism. It may become spherical

Fetal death and abortions can also occur
when cultured in artificial media At its
but are not as common as losses earlier in
anterior end, there are three flagella
gestation. T foetus has been found in vaginal approximately the san1e length as the body
cultures taken as late as 8 mo of gestation
of the parasite. An undulating membrane
and, appai·ently, live calves can be born to
extends the length of the body and is
infected dams. Pyometra occasionally
bordered by a marginal filamerit that
develops after breeding.

continues beyond the membrane as
a posterior flagellum. Although T foetus can Diagnosis: History and clinical signs are
survive the process used for freezing semen, useful but are essentially the same as those it is killed by drying or high temperatnres.

of bovine genital campylobacteriosis (see

T foetus is found in the genital tracts of
p 134 7). Conf1m1ation depends on isolation
cattle. When cows are bred naturally by an
of T foetus, which may be difficult to
infected bull, 30%---9001,, become infected,
differentiate from other trichomonads
suggesting that strain differences exist.

resident in the digestive tract. Diagnostic

Variation in breed susceptibility to
efforts are directed at bulls, because they
trichomoniasis may also exist. Bulls of all
are the most likely caiTiers. Suction is
ages can remain infected indefinitely, but
applied to a pipette while it is used to
this is less likely in younger males. By
vigorously scrape the epitheliun1 in the
contrast, most cows are free of infection
preputial fornix. Alternatively, douching
within 3 mo after breeding. However,
with saline or lactated Ringer's solution
inununity is not longlasting and reinfection

( without prese1vatives) can be used.

does occur. Transmission can also occur

Aspirates or douches, concentrated by
when the semen from infected bulls is used
centrifugation, ai·e exainined using darkfield
for aitificial insemination.

contrast microscopy. This material is also
transferred immediately to the surface of a

Clinical Findings: The most conu11on sign liquid culture medium such as Diamond is infertility caused by embryonic death.

medium. Better success culturing the

This results in repeat breeding, and
orgatlism has been repo1ted when using
attending stock persons often note cows in
conunercially available media-filled
heat when they should be pregnant. This,
pouches. In addition, incubating the media

UDDER DISEASES

1385
beyond the standard 48 hr may also enhance susceptible to reinfection after successful the accuracy of the diagnosis. Sampling
treatment. Resistance to ipronidazole may
every 48 hr for 10 days from the bottom of
also be a concern. The biggest problem,
the tube and examining at 100-400x may
however, is that the success of treatment is
reveal the rolling jerky movements of
measured by repeated sampling, which may

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T foetus. Studies have examined the
mean the individual bull can never be
possibility of using PCR assays to identify
definitively called negative. Therefore, an

Tfoetus directly from the preputial samples unqualified recommendation for the bull's without an intervening culture. These tests
use cannot be given.

are being used by some laboratories to

Control consists of eliminating the
reduce the time required for a definitive
infection from the bull battery by culling all
diagnosis of trichomoniasis. Some
bulls and replacing them with virgin bulls
diagnostic laboratories are suggesting that
or by testing and culling positive bulls.

the scraping be placed in phosphate

Repeated testing in older bulls may be
buffered saline before transport to the
unsatisfactory, and it may be prudent to
diagnostic laboratory. A sample prepared in
cull them all. Reinfection is prevented by
this way can be effectively exan1ined for
exposing only the uninfected (clean) bulls
both trichomoniasis and can1pylobacterito uninfected ( clean) cows. Clean cows are osis by using a specific PCR application.

assmned to be those with calves at foot

Studies suggest that 90%--95% of infected

( even though some infected cows may
bulls will be positive on culture, and that
produce a live calf) and virgin heifers.

three successive cultures at weekly

In situations in which several herds are
intervals will detect --99.5% of infected bulls. commingled on the saine range, caution A vaginal discharge ( after treatment of
must be exercised to ensure that cows and
pyometra) or vaginal mucus ( obtained
heifers are not exposed to potentially
toward the end of a luteal phase) may also
infected bulls at the home ra1.1ch before they
be of diagnostic value.

are turned out on the common grazing

The number of times tl1e bull battery
pasture.

should be sampled and cultured to ensw·e

T foetus can be safely elinlinated from
tl1e bulls are negative depends on the
semen with dimet1idazole.

prevalence of fetal wastage in the cow

Vaccines developed some time ago for
herd. With more open and late cows, the
use in cows and evaluated in the field
frequency of testing should increase to
were not highly effective, especially in
improve the probability that bulls are
the absence of otl1er control measures.

negative for the protozoan.

However, the efficacy of whole-cell T foetus
vaccines has recently been critically

Treatment and Control: Vaiious
reviewed. Although there is some evidence
imidazoles have been used to treat bulls, but
to suggest that timely vaccination will
none is both safe ai1d effective. Ipronidazole
improve reproductive performance in
is probably most effective but, due to its low
heifers, there is a distinct lack of evidence
pH, frequently causes ste1ile abscesses at
that vaccination will reduce "bull-associiitjection sites. In addition, bulls are probably ated outcomes."

UDDER DISEASES

See a/,so MASTmS IN LARGE ANIMALS, p 1358, and udder skin of dairy cows that is often

PSEUDOCOWPOX, p 868.

referred to as bovine ulcerative rnanm1illitis.

BHV-II can occur sporadically or in
outbreaks that often have a seasonal

DISEASES OF BOVINE TEATS AND association with cold weather and may SKIN
result in reduced milk production and
increased susceptibility to bacterial

Bovine Ulcerative Mammillitis (Bovine mastitis.

Herpesvirus II and IV): Bovine herpes

Clinical signs range from relatively
virus II and IV (BHV-II, BHV-IV) can cause
mild, small plaques of edema to severe
an acute, ulcerative condition of teat a1.1d
ulceration. Early signs may vary, but the

1386

UDDER DISEASES
lesions often begin as one or more

Teat-end Hyperkeratosis: The
thickened, edematous plaques of varying
development of raised smooth or rough
size on the skin of one or more teats.

rings at the teat ends of lactating cows is a

Vesicles develop and may rapidly rupture,
common occurrence and is associated with
leaving a raw, ulcerated area that becomes the keratin dynan1ics of the streak canal.

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covered with a dark-colored scab. The

Teat ends affected with hyperkeratosis may
scabs tend to crack and bleed, especially if progress from smooth, doughnut-shaped milking is attempted. The lesions are of
lesions that do not affect milking to severely
variable size and can include much of the
hyperkeratotic rings with radial cracks.

teat wall and orifice. Teats are generally

When teats are severely affected, the ability
painful, and affected cows often resist
to properly sanitize teat ends before milking
milking, leading to development of
may be compromised. Diagnosis is usually
mastitis. The greatest incidence is often
made by clinical examination of affected
seen in first-lactation cows, but previously teats. The degree of hyperkeratosis is often unexposed cows of any age are suscepticharacterized by scoring teat ends using the ble. Severe lesions may take several
following scale: 1) no ring, 2) smooth ring,
weeks to heal.

3) rough ring, and 4) very rough, cracked 1ing.

Diagnosis is based on clinical signs and

The cause of hyperkeratosis is multifactoconfinned by histopathology or by virus rial; thus, prevention is directed toward a
isolation from early lesions. Treatment is
munber of potential risk factors. Hyperdirected toward supportive care, because keratosis is often associated with cold
there is no effective therapy for this virus.

weather, probably because of changes in

The use of iodophore-containing teat
peripheral circulation. Risk factors for
dips with added emollients may help to
development of hyperkeratosis include
inactivate the virus. It is important to isolate
incorrect use of teat sanitizers, exposure of
affected cows and to use separate milking
wet teats to cold weather, improper milking
equipment. Affected animals should be
machine settings leading to ovem1ilking,
segregated to prevent spread among all
inadequate massage phase during milking,
animals. The use of separate milking
and inadequate milk letdown. After
equipment; clean, single-use towels to dry
underlying risk factors are addressed,
udders; and clean gloves for milking
affected teats generally recover over
personnel help to prevent spread of the
several weeks or over a dry period.

agent to susceptible animals.

Dermatitis: Dermatitis of the udder has

Pseudocowpox: Pseudocowpox is a
a nwnber of causes, including chemical
condition of teat skin caused by a poxvirus
irritants, sunburn, and bacterial infection.

that results in a characteristic horseshoe

The udder can be exposed to chemical
shaped lesion or scab (seep 868).

irritants from bedding additives ( eg, some
types of limestone) or chemicals used

Bovine Warts (Bovine Papillomavirus):

during milking. The irritation usually

Several strains of bovine papillomavirus
resolves after removal of the offending

(BPV l, BPV5, BPV6, BPV9) cause the
substance, but gentle udder washes and
development of papillomas or fibropapillouse of emollient products can accelerate mas on teats. In some herds, pale, smooth,
healing. Udder impetigo (udder acne) is
raised lesions develop frequently on teat
a bacterial dermatitis characterized by
skin and may persist indefinitely without
development of small pustules on the skin
causing problems. In other instances,
of the udder and teats. Staphylococci
filamentous or frond-like lesions develop at
usually can be isolated from the pustules.

the teat orifice and interfere with milking.

Treatment of udder impetigo consists of

Bovine warts are spread by direct or
clipping hair from tl1e affected area and
indirect contact, and bovine papillomavirus
washing the skin thoroughly each day until

DNA has been identified in blood, milk,
the condition resolves.

urine, and other biologic fluids obtained
from infected animals. Diagnosis is usually

Frostbite: Teat skin can chap and crack
made preswnptively based on examination
when wet teats are exposed to cold winds
of the lesion and exclusion of other causes.

or frozen bedding areas. Exposure of wet

In many instances, treatment of warts is
skin to subfreezing temperatures may result
not necessary, but frond-like lesions that
in frostbite. Skin affected by frostbite
interfere with milking may require excision.

becomes swollen and discolored and

The use of autogenous vaccines and
ultimately develops a leathery texture.

virucidal teat dips may be recommended

In severe cases, the teat skin may slough.

in herd outbreaks.

Frostbite is best prevented by ensuring that

UDDER DISEASES

1387
teat skin is dry before allowing cows access
parturition. Positive effects of prenulking in
to housing areas or pastures during periods
heifers have been reported, but the practice
of temperatures <0°F. Care should be taken
may predispose older cows to parturient
to ensure that all bedding areas that contact
paresis (seep 988). Massage, repeated as
teat and udder skin are thoroughly dry. Teat
often as possible, and hot compresses

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disinfectant products ( eg, powder teat dips
stin1ulate circulation and promote edema
and other cold weather formulations)

reduction. Diuretics have proved highly
specifically designed for extremely cold
beneficial in reducing udder edema, and
weather are relatively successful at
corticosteroids may be helpful. Products
preventing frostbite after dipping. When
that combine diuretics and corticosteroids
liquid dips are used during periods of
are available for treatment of udder edema.

extremely low ambient temperatures, the
teats should be dried before the cows exit

Precocious Mammary Development:

the milking facility.

Initiation of nulk secretion in heifers before
calving is occasionally noted. Precocious

Udder Sores (Necrotic Dermatitis):

manm1ary development in a single gland

Moist, foul-smelling, necrotic lesions may
sometimes results from suckling by
develop in areas of tightly adjacent skin of
herdmates. Symmetric manmuuy developsome animals (such as the udder cleft).

ment has been occasionally associated with

In heifers, the lateral aspect of the udder
ovarian neoplasia or exposure to feedstuffs
and medial aspect of the tJ-tigh are often
containing estrogen or contanunated by
involved. In tJ-tis area, the udder is pressed
mycotoxins. Removal of contaminated
tightly against the leg, resulting in chafing,
feedstuffs generally results in resolution
dennatitis, and necrosis. Udder edema is a
of the problem.

risk factor for development of tlus condition
and must be treated concurrently. The

Failure of Milk Ejection (Milk Let
necrotic skin should be cleaned daily with
down): In rare instances, newly calved
an antiseptic solution and thoroughly dried.

heifers may have problems with milk

Mild astringents should be applied. A sinillar ejection. Fear of handling or unfa.nuliarity condition, which may be associated with
with the nulking facility or milking proceinfestation by Sarcoptes nutes, has been dures is tl1e usual cause. Care should be taken
seen at the anterior portion of the udder
to ensure that animals are handled calmly
between the two forequarters. Older cows
and gently and that the milking routine
have been reported to be at greater risk than provides for adequate stimulation (>20 sec) heifers. The swollen, necrotic area may be
before attaching the milking wut. Adnunistratreated topically with an approved nuticide; tion of oxytocin (20 IU, IM) may be necessruy
however, approp1iate milk withholding
in some instances, but doses should be
periods must be observed.

gradually reduced to avoid dependence on
admilustration of exogenous oxytocin.

PHYSIOLOGIC DISORDERS

Agalactia: Agalactia is seen occasionally

Udder Edema: Udder edema is common
in heifers and can be a primary endocrine
in high-producing dairy cattle ( especially
problem or a localized problem of the
heifers) before and after parturition.

manm1ruy gland. It is occasionally caused

Predisposing causes include age at first
by a severe systenuc disease or by mastitis
calving ( older heifers are at greater risk),
caused by Mycoplasma bovis. Agalactia has
gestation length, genetics, nutritional
also been associated with cows grazing or
management, obesity, and lack of exercise
eating endophyte-infested fescue.

during the precalving period. Prepartum
diets that contain excessive salt increase

"Blind" or Nonfunctional Quarters:

the severity of udder edema. Physiologic

Nonfunctional quarters are usually the
edema is not usually painful and occurs
result of a severe mastitis infection, which
when pitting edema develops symmetrically
may occur in dry or lactating cows or in
in the udder before parturition. Udder
heifers due to suckling by other heifers
edema is a risk factor for development
or calves. Some of these quarters may
of clinical mastitis and occasionally can
occasionally return to production in future
become a chronic condition that persists
lactations. Rarely, blind or nonfunctional
throughout lactation. Treatment should be
quarters may be congenital.

initiated if swelling threatens the udder
support apparatus or if edema interferes

Congenital Disorders: Congenital
with the ability to milk the cow. Edema
aben-ations include many structural defects,
can be treated by milking cows before
but the most significant disorder is

1388

UDDER DISEASES
supernumerary teats. These may be
during the dry period. These can be
located on the udder behind the posterior
recognized by intermittent disruptions in
teats, between the front and hind teats, or
milk flow. They may be removed by forced
attached to either the front or hind teats.

pressure downward on the teat cistern or

Removal of supernumerary teats from dairy
by use of specialized instrun1ents inserted

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heifers is desirable to improve appearance
tlu-ough the teat canal. Membranous
of the udder, to eliminate the possibility of
obstructions in the area of the armular
mastitis in the gland above the extra teats,
fold at the base of the gland cistern are
and to facilitate milking. Most are easily
sometimes seen in heifers. Treatment of
removed surgically when the heifer is from
these obstructions is generally unsuccessful.

1 wk to 1 yr old (best clone at 3--8 mo of age).

Complete teat obstruction may result

Supernmnerary teats may be surgically
when adhesions fill the teat cistern after
removed from preparturient heifers before
severe trauma. Treatment is similar to that
lactation begins. The incision should be
for stenosis (see below), but the prognosis sutured or stapled after excision of tl1e teat.

usually is more guarded. In instances of
severe irtjury, milking of the quarter should

TRAUMATIC AND STRUCTURAL
be pennanently discontinued.

DISORDERS

Teat stenosis is characterized by a
marked narrowing of the teat orifice or

Trauma and Laceration: Superficial
streak canal, which makes milking difficult.

wounds to the udder and teats may be

It usually results from a contusion or wound
cleaned with suitable antiseptic solutions
that produces swelling or formation of a
and treated as open wounds with frequent
blood clot or scab or from mastitis
application of antiseptic powders or sprays.

infections ( especially in prelactating

If the teats are involved, adhesive tape may
heifers). Teat obstructions can be diagnosed
hasten healing. W0tmds involving the teat
initially by careful palpation of the affected
orifice should be dressed with antiseptic
gland. Complex teat obstructions or
creams and bandaged after milking.

obstructions in valuable anin1als may

Affected quarters are at very high risk of
require diagnostic imaging such as
infection, and prophylactic treatment with
ultrasonography, contrast radiography,
intramanm1ary antibiotics is recommended
or theloscopy (endoscopy).

to prevent development of mastitis.

Treatment varies depending on severity.

Lacerations of the large milk vein should

Conservative treatment includes the use
be considered an emergency because of the
of teat cannulas and external pressure to
potential for severe hemorrhage; prompt
remove obstructions, whereas serious cases
compression and ligation of these
may require prompt referral to specialists for
lacerations is recommended.

thelotomy or theloscopy ( endoscopic

Deeper wounds of the udder and teats
surgery). All irtjuries to, or surgical proceshould be promptly (within 6 hr) cleansed dures on, the teat should be handled carefully
and sutured or stapled under local
to prevent infection. Prophylactic antibiotic
anesthesia with appropriate sedation and
infusions of tl1e quaiter are indicated when
restraint. When the wound involves· the teat
the teat or teat orifice is involved. Pennanent
cistern, it may be necessary to insert a
fistulas into the teat or gland cisterns are best
self-retaining teat cannula with removable
repaired during the dry period.

cap into tl1e teat for the first 24 hr to prevent
milk seeping through the wound ( which

Breakdown of Udder Support Appara
would delay or prevent healing) and to aid
tus: Rupture of the suspensory ligan1ents of in milking. The affected quarter should be
the udder ( usually tl1e medial suspensory
infused with antibiotic preparations.

ligament) occurs gradually in some older
cows and leads to a dropping of the udder

Teat Obstructions: Acquired teat
floor, resulting in lateral deviation of the
obstructions are usually the result of
teats. Occasionally, acute rupture can occur
proliferation of granulation tissue after the
at or just after paiimition. Animals with this
occurrence of an observed or unobserved
condition are at higl1 risk of developing
teat irtjury. Teat obstructions are usually
mastitis. There is no successful treatment;
recognized when they interfere witl1 milk
supportive trusses generally are not
flow. They can range from diffuse, tightly
satisfactory. The condition is suspected to
adherent lesions to highly mobile discrete
have a genetic basis, and these animals are
lesions tl1at float throughout the gland
often removed from the milking herd.

cistern. Some "floaters" are caused by
formation of small masses from butterfat,

Hematomas: Tramna ( often related to
minerals, and tissue in mammary ducts
inadequate housing) can result in contusions

UTERINE PROLAPSE AND EVERSION

1389
and hematomas of the udder. Hematomas
and can be attributed to rupture of tiny
usually appeai· as soft-tissue swellings
mammary blood vessels. Udder swelling
located anterior to the foreudder or
from edema or trawna is a potential
caudodorsal to the reai· udder. They may be
underlying cause. Bloody milk is not fit for
difficult to differentiate from abscesses.

conswnption. In most cases, it resolves

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Severe hematomas can result in anemia if
without treatment in 4--14 days, provided
not treated. In most instances, hematomas
the gland is milked out regularly. The
resolve after conservative treatment
occunence of fra11k blood in a single quarter
consisting of pressure wraps and rest.

is likely the result of severe, acute mastitis

Hematomas should not be incised or drained ( see p 1358) or trauma, and mil king should unless they become infected. Milking should
be discontinued until hemorrhage is
be pe1formed cautiously during the
controlled. lntramammary antibiotics
convalescent pe1iod. Hematornas that
should be administered if mastitis is
continue to enlarge should be considered
suspected.

an emergency because of the possibility
of excessive blood loss and shock.

Teat Sphincter Inadequacy ("Leakers"

or lncontinentia Lactis): High levels of

Abscesses: Subcutaneous abscesses of
intramammary pressure in high-producing
the udder (not involving the milk-producing
dairy cows may result in milk dripping from
tissue) can develop between the skin and
teats. Risk factors for milk leakage include
the supporting connective tissue of the
high peak milk flow rates, short teats, and
udder. Diagnosis is by needle aspiration.

inve1ted teat ends. Shorter inte1vals or more

Abscesses usually develop secondary
frequent milking may be recommended
to wounds, chronic mastitis, infected
when a large proportion of the herd is
hematomas, or severe contusions. They
affected. Occasionally, cows are observed
should be incised and drained when chronic
to leak milk continuously. These cows
and neai· the surface of the udder. The
usually have sustained a severe teat injury
wound should be flushed daily with an
or have a11 abnonnal streak canal. In
antiseptic solution or water under pressure
general, little ca11 be done to correct this
until healing is complete.

condition, and most of these cows will
develop mastitis; it is recommended that

Bloody Milk: The occurrence of pinkpersistent leakers be designated for removal or red-tinged milk is common after calving
from the herd.

UTERINE PROLAPSE AND EVERSION

Prolapse of the uterus may occur in any
organ. In sows, one horn may become
species; however, it is most conunon in
everted while unborn piglets in the other
dairy and beef cows and ewes and less
prevent further prolapse. In small animals,
frequent in sows. It is rai·e in mares, bitches,
complete prolapse of both uterine horns is
queens, and rabbits. lnvagination of the tip
usual. A contributory cause in sheep may
of the uterus, excessive traction to relieve
be grazing estrogenic pastures.

dystocia or retained fetal membranes,

In cows, treatment involves removing
uterine atony, hypocalcemia, and lack of
the placenta (if still attached), thoroughly
exercise have all been incriminated as
cleaning the endometrial surface, and
contributory causes.

repairing any lacerations. Rubbing the

Prolapse of the uterus invariably occurs
surface of the uterus with glycerol helps
immediately after or within several hours of
reduce edema and provides lubrication.

parturition, when the ce1vix is open and the

The uterus is then returned to its normal
uterus lacks tone. Prolapse of the postposition. An epidural anesthetic should be gravid uterine horn usually is complete in
administered first. If the cow is standing, the
cows, and the mass of uterus usually hangs
cleansed uterus should be elevated to the
below the hocks. The invagination of the
level of the vulva on a tray or hanunock
contralateral horn, which is prevented from
supported by assistants, and then replaced
exteriorization by the strong intercomual
by applying steady pressure begiiming at
ligainent, can be located by careful examthe ce1vical portion ( or at the level of the ination of the surface of the prolapsed
invagination of the nonprolapsed uteriI1e

1390

UTERINE PROLAPSE AND EVERSION
horn) and gradually working toward the
a means of increasing uterine tone. Caslick
apex. Once the uterus is replaced, a hand
sutures or other forn1s of vulvar closure are
should be inserted to the tip of both uterine
not useful, because the uterine prolapse
horns to be sure there is no remaining
begins at the apex of the uterine horn.

invagination that could incite abdominal

Prevention of recurrence depends on

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straining and another prolapse. Installation
complete and correct replacement of the
of warm, sterile saline solution is useful to
uterus and restoration of uterine tone.

ensure complete replacement of the tip

The prognosis depends on the amount
of the uterine horn without tramna. If
of ir\jury and contanlination of the uterus.

recmnbent, the cow should be positioned

The prognosis is favorable when a clean,
with the hindquarters elevated by placing
minimally tramnatized uterus is promptly
her in sternal recmnbency with the hind.legs
replaced. There is no tendency for the condiextended backward. When elevating the tion to recur at subsequent parturitions.

hindquarters of the cow, care should be

Complications tend to develop when
taken to lift the prolapsed uterus with the
laceration, necrosis, and infection occur,
hindquarters to prevent stretching and
or when treatment is delayed. Shock,
laceration of the uterine artery.

hemorrhage, and tJu·omboembolism are

Replacement of the prolapsed uterus in
potential sequelae of a prolonged prolapse.

mares is done in a similar way, usually with

In some instances, the bladder and
the mare sedated but standing, taking care
intestines may prolapse into the everted
not to perforate the uterus.

uterus. These require careful replacement

In sows and small animals, the uterus
before the uterus is replaced. The bladder
may be repositioned by simultaneously
may be drained with a catheter or need.le
manipulating it from outside with one hand
passed through the uterine wall. Elevation
and through an abdominal incision with the
of the hindquarters and pressure on the
other. Resection of the uterus is indicated in
uterus aid in replacement of bladder and
longstanding cases in which tissue necrosis
intestines. It may be necessary to incise the
has occurred. Once the uterus is in its
uterus carefully (in a longitudinal direction)

nonnal position, oxytocin (up to 5 IU, IV, or
to replace these organs. In cows, an1putaup to 20 IU depending on species, IM) is tion of a severely tramnatized or necrotic
administered to increase uterine tone.

uterus may be the only way to save the

Administration IV of calcimn-containing
animal. Supportive treatment and antibiotic
solutions is indicated in most cases, also as
therapy are indicated.

VAGINAL AND CERVICAL PROLAPSE

Eversion and prolapse of the vagina, with or
prolapse. Docking the tails of lambs may
without prolapse of the cervix, occurs most
dan1age structures that support the pelvic
commonly in cattle and sheep. A fom1 of
gird.le ( eg, coccygeus muscle) and predisvaginal prolapse, different in pathogenesis, pose to vaginal prolapse if the fail is docked
also occurs in dogs (seep 1399). In cattle and too short. The tail should be removed at tl1e sheep, the condition is usually seen in
level of tile ventral skin fold, leaving two or
mature females in the last trin1ester of
three coccygeal ve1tebrae intact.

pregnancy. Predisposing factors include

The prolapse begins as an intussuscepincreased intra-abdominal pressure tion-like folding of tile vaginal floor just
associated with increased size of the
cranial to tile vestibulovaginal junction.

pregnant uterus, intra-abdonlinal fat,

Discomfort caused by this eversion,
or rumen distention superinlposed upon
coupled with irritation and swelling of the
relaxation and softening of the pelvic gird.le
exposed mucosa, results in straining and
and associated soft-tissue structures in the
more extensive prolapse. Eventually the
pelvic canal and perinemn mediated by
entire vagina may be prolapsed, with the
increased circulating concentrations of
cervix conspicuous at the most caudal part
estrogens and relaxin during late pregnancy.

of the prolapsus. The bladder or loops of

Intra-abdominal pressure is increased in
intestine may be contained witllin the
recmnbent anin1als. Added to this, sheep
prolapsed vagina. As the bladder moves into
tend to face uphill when lying doW11, so
the prolapsed vagina, the urethra may be
gravity contributes to vaginal eversion and
occluded. The bladder then fills and

VULVITIS AND VAGINITIS IN LARGE ANIMALS

1391
enlarges, which hinders replacement of the

The Buhner suture has largely superseded
prolapsed vagina unless the bladder is first
earlier attempts to prevent prolapse by
drained. The bladder may even rupture with
various patterns of sutures in the vulvar lips
potentially fatal consequences. Vaginal

(which do not prevent the initial eversion
prolapse may be graded as I (intermittent
of the vagina into the vestibulum) or by

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prolapse, especially when recumbent), II
methods that relied on placement of a

(continuous prolapse), III (continuous
retention device within the vagina ( which
prolapse of vagina, bladder, and cervix), or
tend to cause discomfort and further

IV (grade II or III with tissue damage by
straining). Buhner sutures should generally
trauma, infection, or necrosis).

be removed before parturition to prevent

Although most common in mature animals
extensive laceration. Modification of the
in late pregnancy, vaginal prolapse can occur

Buhner suture to include an exposed,
in young, nonpregnant ewes and heifers,
horizontal mattress-like suture has the
especially in fat anin1als. Predisposing factors advantage of remaining in place even when include grazing estrogenic plants ( especially
vestibulovaginal tissues have little holding

Trifolium subterraneum) or exogenous
power, and a traditional Bulmer suture may
administration of estrogenic compounds
be prone to tear through the dorsal or

( usually in the form of growth-promotant
lateral vestibular wall. The Buhner suture
implants). Cervicovaginal prolapse is more
and its modifications attempt to replicate
common in stabled than in pastured animals,
the support normally provided by the
suggesting that lack of exercise may be a
constrictor vestibuli muscles that are
contributing factor. Vaginal prolapse may
lacking in cases of prolapse. Pern1anent
also be a problem in cows subjected to
fixation of the vagina can be achieved by
repeated superovulation for embryo recovery the Johnson button technique, whereby due to repeated exposure to supraphysiosutures are placed from the vagina, through logic concentrations of estrogens. A genetic
the sacrospinotuberal ligament and gluteal
component in the pathogenesis of cervicomuscles, and then anchored in the vagina vaginal prolapse is likely, because a breed
and on the skin with large, flat discs. This
predisposition exists in both cattle (Bra11-
can also be accomplished by anchoring tJ1e
man, Brahman crossbreds, Hereford) and
cervix to the prepubic tendon or iliopsoas
sheep (Kerry Hill, Romney Marsh). In pigs,
muscle. Although the cervical os may be
vaginal prolapse is often associated with
edematous and inflamed, cervicovaginal
estrogenic activity of mycotoxins.

prolapse seldom interrupts pregnancy and

For replacement of the prolapsed vagina,
does not specifically predispose to dystocia
an epidural anesthetic is first administered.

or postpartum uterine prolapse, which has

The organ is washed and rinsed, and the
a different etiology.

bladder emptied if necessary. Usually, this

Vaginal prolapse in sheep may occur
can be achieved by elevating the prolapsus
simultaneously in many ewes as a herd
to allow straightening of the urethra;
problem, making surgery impractical. In
occasionally, needle puncture through the
these cases, use of a commercially available
vaginal wall may be necessary. The vagina is
vaginal retention device ( a bearing retainer)

well lubricated (glycerol provides lubricamay be useful. Sheep may lamb without tion and reduces congestion and edema by
mishap with these devices in place.

osmotic action) and replaced and then held

Permanent fixation techniques ( cervicoin position until it feels warm again.

pexy or vaginopexy) have been described in

Retention is achieved by insertion of a
which the cervix or vaginal wall is anchored

Buhner suture-a deeply buried, circumferto other pelvic structures. They may be ential suture placed around the vestibulum
useful in individual cases of chronic or
to provide support at the point at which the
recurrent prolapse, but most cases are
initial eversion of the vaginal wall occurs.

resolved by a well-placed Buhner suture.

VULVITIS AND VAGINITIS IN LARGE ANIMALS

Contusion and hematoma of the vagina are
hemorrhage that can be controlled by
noted infrequently after parturition in all
ligation of the labial branch of the internal
species but particularly in mares and sows.

pudenda! artery. Necrotic vaginitis,

Occasionally, vaginal hematomas in sows
vestibulitis, and vulvitis may follow dystocia
may rupture and cause serious ( or fatal)

in all species. Onset of signs, consisting of

1392

VULVITIS AND VAGINITIS IN LARGE ANIMALS
arched back, elevated tail, anorexia,
yellow discharge develops. The infection
dysuria, straining, vulvai· and perivulvai·
spreads to tl1e uterns and uterine tubes, and
swelling, and possibly a fetid, serous
salpingitis and fi.mb1ial adhesions frequently
discharge, begins withln 1-4 days of
result in pern1anent infertility. Altllough

VetBooks.ir
paitmition and may persist for 2-4 wk. In
epivag has been transmitted experimentally
most cases, only gentle and conservative
by transferring exudate, the cause is
treatment is needed. Prophylactic antibiotic
unknown.

treatment is wise, because clost1idial or

Necrotic vulvitis has been observed as a
other organisms may proliferate in the
severe granulomatous and necrotic lesion
dainaged tissue and cause tetanus (see
centered on tl1e ventral commissure of the
p 611), blackleg (seep 602), or other forn1s vulva of cows, sometimes occurring in
of clostridial myositis. Possible conseoutbreak form. It is associated witll several quences of necrotic vaginitis include
pathogens, possibly acting sy:nergistically
pern1anent stricture of tl1e vagina,
and, in particular, Porphyromonas levii.

transvaginal adhesions, or perivaginal

Catarrhal bovine vaginitis has been
abscessation.

reported from mai1y countries. Altl1ough

Vestibular lymphocytic follicles, also
enterovirnses have been associated with this
called granular venereal disease, granulai·
condition, tl1e cause remains w1known. In
vulvitis, or granulai· vulvovaginitis, are seen
areas of tlle world where bovine tuberculoin cows and ai·e characterized by vestibular sis ( see p 687) is still endemic, vaginal
hyperemia and hyperplasia of tl1e lymphoid
lesions may be eitller a prin1aiy lesion after
nodules of tl1e vestibular mucosa. These
service by a bull witll genital infection or
lesions do not constitute a specific disease
evidence of uterine disease or of cervicitis.

but reflect irritation of the vestibulai·

One cause of vulvitis in sheep is
mucosa. They ca.ti be reproduced experiulcerative dennatosis (seep 872), charactermentally by topical application of Urea.

ized by crusted ulcers of the vulvar skin,
plasma ureolyticum or Mycoplasma spp penis, prepuce, and facial skin. Posthitis and
in goats and cattle.

vulvitis are also caused by

Infectious pustular vulvovaginitis of
tlle interaction of a high-protein diet and
cows is caused by bovine herpesvirus 1
infection witll urease-producing organisms,

(seep 1434) and is transmitted by natural
usually Corynebacterium renale. Demodex
service, nasogenital contact, or mechanimites have been seen in tlle vulvar skin of cally by insects such as flies. It is charactersheep; they usually are not associated witll ized by vaginal lesions. Affected cows show
lesions but may produce granulomas.

signs of vaginal discomfort ( raised tail,

Equine coital exanthema (seep 1357) is
frequent urination) and have numerous,
caused by equine herpesvirus 3. It is an
round, white, raised )esions of the
acute disease witl1out systemic signs. Red
vestibular mucosa. Within a sh01t time,
papules appear in tl1e vaginal and vestibular
these lesions progress to pustules and
mucosae 2-10 days after infection, which
erosions or ulcers. Mucopurnlent discharge
occurs as a result of mating witll an infected
may be prominent, even in pregnant
stallion. Lesions extend to the pe1ivulvar
animals in which pregnancy is uninte1�
skin. The lesions progress rapidly to
rupted. The histologic lesion consists
pustules, tl1en ulcerate, ai1d finally heal,
of necrosis of vestibulai· and vaginal
leaving depigmented scat'S. Stallions show
epitl1elium, witl1 intranuclear inclusion
sinillar lesions on tl1e penis and prepuce.

bodies typical of herpesvirns infection.

The disease causes discomfort and may

The virus may be secreted in the semen of
prevent mating but does not specifically
infected bulls (which have similar lesions
inhibit fertility.

of tl1e penis and prepuce). Intrauterine

Dourine (seep 38) is a venereal disease of
inoculation of the virus produces necrotizho1'Ses. Early signs are characte1ized by ing endometritis and cervicitis.

edematous swelling of the vulva and

A severe disease chai·acterized by
secondaiy vulvovaginitis of tlle swollen,
vaginitis in cows and epididyrnitis in bulls
initable tissue.

occurs sporadically in eastern and southern

Coital injmies of cows and mares may be

Africa, where it is referred to as epivag. The
attributable to tl1e relatively large size of tl1e
disease is spread by natural mating. In the
penis in tl1ese species compared witl1 tlle
early stages of infection, cows have intense
vagina. b:tjuries of the vulva and vagina may
vaginitis characterized by reddened
be caused by homed cattle. Vaginal injwies
mucosae witl1out ulcers, erosions, or
in a variety of species have also been
vesicular lesions. A thick, creatny, white to
inflicted maliciously.

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL

1393

REPRODUCTIVE DISEASES OF THE

FEMALE SMALL ANIMAL

VetBooks.ir

See a.lso MANAGEMENT OF REPRODUCTION: SMALL
and can be used in breeding management.

ANIMALS, p 2219.

The bitch ovulates -2-3 days after the LH

Most "infertile" dogs are healthy and
peak After ovulation, the follicles are
fertile. Breeding practices should be
replaced by corpora lutea (CLs), which
reviewed before engaging in diagnostic
produce progesterone. The production
testing for the less common causes of
of progesterone continues throughout
canine infertility. A basic understanding
diestrus, the phase of the estrous cycle after
of the reproductive cycle of the bitch is
estrus, regardless of whether the bitch is
essential to diagnose "infertility" problems pregnant. The duration of diestrus is the
related to breeding at the incorrect tin1e,
same as that of pregnancy, -62---{i3 days
artificial insemination, etc. Most bitches
from the LH peak. Unlike in other domestic
cycle twice a year, with an interestrous
species, in the bitch there is no production
interval of at least 4 mo. Bitches with <4 mo
of prostaglandin F2ac from the endometrium
between two cycles usually do not get
to cause luteolysis (CL regression). During
pregnant. Some large breeds (eg, Great
diestrus, many bitches go through

Danes) may cycle every 9-12 mo with
pseudopregnancy in which they may gain
normal fertility.

weight and have an enlarged abdomen;

The bitch is a spontaneous ovulator, ie,
other overt signs may be seen, including
ovulation occurs without any breeding
mammary gland enlargement, as well as
stimulus. The bitch starts cycling with the
prewhelping behavior such as nesting or
influence of hormones released from the

"adopting" toys and shoes. The pseudopreghypothalamus and pituitary glands.

nancy ( or di estrus) is considered a nonnal

Gonadotropin-releasing hormone (GnRH),
occurrence and may not need any
released from the hypothalamus, stimulates
treatment.

the release of follicle-stimulating hormone

(FSH) and luteinizing hormone (LH). FSH

Ovulation: The ova released during
has a primary responsibility for growth of
ovulation in the bitch are at the prirnm-y
follicles on the ovaries, whereas LH causes
oocyte stage, ie, the first polar body has not
ovulation of the follicles.

come out of the ovum and sperm are unable

The estrous cycle in the bitch is unique
to penetrate the ovmn. It takes -3 days for
and different from that of other domestic
the ovum to become a secondary oucyte,
animals. It starts with proestrus, which
which can be penetrated by sperm. Sperm
tnost breeders refer to as the start of the
can smvive as long as 10 days in the bitch's

''season," when spotting or bleeding from
reproductive tract. This can become a
the vagina is noticed. During proestrus, the
diagnostic challenge when a bitch's owner
bitch is attractive to males but does not
requests a cesarean section 62 days after
allow breeding. Estrogen produced by
breeding, because theoretically the
ovarian follicles causes changes in the
gestation pe1iod may be only 52 days.

epithelial cells of the vaginal mucosa, which A fairly reliable predictor of whelping can be examined by vaginal cytology ( see
is hypothennia or a decrease in rectal

J;J 1607). Estrus or time of receptivity follows temperature of2 °-3 °F, caused by a J;Jroestrus, when the bitch accepts the male
progesterone decrease 12--36 hr before.

for breeding. The duration of proestrus and

Vaginal cytology can also be used to predict
estrus is traditionally considered to be 9 days whelping by detennination of day 1 of each, on average, but each phase can range
di estrus.

from 2 or 3 to 21 days. During proestrus, the

Vulvar lips of the bitch are turgid or firm and

Reproductive Anatomy: Successful
become soft and "wrinkly" as the bitch nears vaginal swabbing technique requires the time of receptivity. In most bitches, the
knowledge of the unique reproductive
bloody discharge of proestrus also changes
anatomy of the bitch. The vagina of the
to a straw color as estrus nears, but some
bitch is ve1y long, -20 cm (9 in.) in a
rnay bleed all the way through estrus.

medimn-sized bitch. The cervix is located in

The production of progesterone is also
the abdominal cavity, whereas it is located

IJilique during the estrous cycle of the bitch.

in the pelvic inlet in other domestic animals

The early rise of progesterone dming estrus

(eg, cow, mare). Therefore, the cervix in the
is from the luteinized follicles of the ovaries
bitch cannot be visualized by an endoscope

1394

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL
or speculum; a flexible endoscope with a
than the parabasal cells, with small nuclei
light source is required. This is important to
and irregular/folded borders. Large
deposit semen transcervical in the uterus
nun1bers of these cells are seen dilling late
for aitificial insemination (AI). The size of
proestrus to early estrus. Superficial cells,
the uterus and ovaries vary considerably
also called cornified or anucleated, are the VetBooks.ir
with the breed.

Jai·gest of tl1e epithelial cells present during

Vaginal Cytology: A clean, cotton tip
estrus. Under a simple microscope, the
swab is commonly used to swab the vagina
nuclei of these cells appear faded or absent.

to obtain a cytology san1ple. An endoscope

The cells also appear "light in weight,"

cone or vaginal speculum can be used to
multi-layered, and with folded borders. The
guide the swab. A right-handed person can
appearance of 80%-900Ai of these cells in the
hold the bitch's vulva with a gloved left
smear is used to indicate that breeding can
hand, opening the vulvar lips with the
strut. A series of vaginal cytology sainples is
thumb and middle finger, while using the
needed to observe the progressive change in
index finger behind the vulva to support it.

epithelial cells; only one smear is unreliable.

The swab is moistened with warm tap water

Epithelial cells may remain the same for
and inse1ted al.most ve1tically into the
many days in some bitches, whereas they
vagina, avoiding the clitoral area, up and
may change witllin 24 hr in others. In
over the brim of the pelvis. It may be helpful
addition, many bitches reach 800/o-900Ai
to forward the swab, especially in small size
comification during estrus, but in others
bitches and bitches without serosanguinecornification never goes above 700Ai. In these ous discharge. If the swab feels "stuck" in bitches, waiting for 800/o-900Ai cornification
the vaginal folds, it may be pulled back
will result in loss of breeding during that
slightly and redirected before proceeding.

cycle. Anotl1er breeding management tool is

Once the swab is inserted to a depth of at
the progesterone assay, discussed below.

least6--10 cm (2-4 in.), it is rolled a few

The appeai·ance of neutrophils on the
times in one direction (if rotated back and
vaginal cytology sainple indicates the first
forth, the cotton may unroll and drop in the
day of di estrus, and whelping will occur
vagina) and withdrawn. Inserting the swab

57-58 days later. Daily vaginal cytology
as deep as possible to reach the cranial pait
sainples are recommended because in some
of the vagina ( versus tl1e caudal pait)

bitches, the cells change from cornified to
minimizes collection of extraneous debris.

superficial intennediate and neutrophils

Getting in a habit of reaching the cranial
appear witllin 24 holll"S.

vagina is also helpful to take san1ples for vaginal culture and for AL The swab is
rolled on a clean microscope slide, air-dried,

Progesterone Assay: Progesterone is
and stained; two slides are i"econrn1ended.

secreted not only from the CLs but also

Stains that can be used include Wrightfrom the early luteinized follicles of the Giemsa, RomanowskY, methylene blue,
ovaries. The eai·ly rise in progesterone can
eosin-nigrosin, Gran1 stain, etc. The slides
be used to determine ovulation in tl1e bitch,
with smeai-s are dipped 5--7 times-in each
which occlll"S -3 days after the LH peak. The
jar, rinsed witll tap water, air-dried, and

LH peak is very short. LH kits are available,
exainined under the microscope. Viewing
and LH should be checked every day dU1·ing
under 200 X magnification first is helpful to
the expected ovulation time. Progesterone
get an overall impression of the types and
assays ai·e conunonly used for. canine
distribution of cells before exainining more
breeding management. These ELISA-based
closely under 400X magnification.

qualitative test kits ai·e based on a color
change that corresponds to a range of

Vaginal Cytology Interpretation: Variprogesterone values. Many clinicians prefer ous theriogenologists, clinical pathologists,
to send the blood sainples to an endocrinoland other practitioners have interpreted ogy laboratory for progesterone detelTilinavaginal cytology of tl1e bitch a little tion by radioirnrnunoassay. Progesterone is
differently. One method is described here.

the saine hormone in all species, including

The vaginal mucosa is responsive pri.maiily
people; therefore, blood sainples can be
to estrogens, a11d so vaginal cytology is
analyzed for progesterone in veterinary or
useful only during the estrogenic phase of
hun1an diagnostic laboratories.

the cycle. Parabasal cells are small, round

The progesterone assay is an excellent
cells with large and distinct nuclei. The total
tool to detenni.ne ovulation ti.n1e for
area of the cytoplasm pait of the cell is
appropriate breeding. This becomes
smaller tha11 the nucleus. These cells (along
critical when using chilled transported or
with RBCs) are present during proestrus.

frozen-thawed semen for AI. As in vaginal

Superficial intermediate cells are larger
cytology, progesterone concentration is

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL

1395
monitored starting a few days after the

2-5 U in queens) given IM up to 3 tin1es at
start of proestrus, projecting ahead using

30-n1in intervals, with or without 10% calcium
progesterone concentrations of 2-10 ng/mL,
gluconate (3-5 mL, IV slowly) may promote
with 2-2.9 ng/mL indicative of ovulation in
uterine contractions. If no response follows,
approximately 2 days, 3-3.9 ng/mL in 1 day,
a cesarean section should be perfonned.

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and 4-10 ng/mL indicative of ovulation day.

Surgery is indicated for obstructive
dystocia, dystocia accompanied by shock or

DYSTOCIA
systemic illness, primary ute1ine inertia,
prolonged active labor, or if medical

Dystocia refers to abnormal or difficult
management has failed.

birth. Causes include maternal factors

( uterine inertia, inadequate size of birth
canal) and/or fetal factors ( oversized fetus,

FALSE PREGNANCY
abn01mal orientation as the fetus enters the

(Pseudopregnancy, Pseudocyesis)

birth canal). The condition occurs more
commonly in certain breeds. In one survey

False pregnancy is common in bitches and

(253 whelpings, 1,671 pups born), a high
uncommon in queens. It occurs at the end of
frequency of dystocia (32% of the individual
diestrus and is characterized by hyperplasia
bitches and 27. 7% of all the whelpings) in
of the man1mary glands, lactation, and

Boxers was reported, mainly due to uterine
behavioral changes. Some bitches behave as
inertia but also to fetal malpresentations.

if partuiition has occurred, "mothering" by Dystocia should be considered in any of
nesting inanimate objects and refusing to
the following situations: 1) animals with a
eat. The possibility of a true pregnancy
history of previous dystocia or reproductive
should be elin1inated by the history,
tract obstruction, 2) parturition that does
abdominal palpation, and abdominal
not occur within 24 tu· after a drop in rectal
radiographs and ultrasonography.

temperature to <100°F (37. 7°C), 3) strong

The falling progesterone and increasing
abdominal contractions lasting for 1-2 hr
prolactin concentrations associated witl1 late
without passage of a puppy or kitten, 4)

diestrus are believed to be responsible for the
active labor lasting for 1-2 hr without
clinical signs. No treatment is reconunended '

delivery of subsequent puppies or kittens,
because the condition resolves spontane-

5) a resting period during active labor
ously in 1-3 wk. In bitches with discomfort

>4-6 tu·, 6) a bitch or queen in obvious pain
secondary to mammary gland enlargement,

( eg, crying, licking, or biting the vulva), or
alternating cold and wann compresses on

7) abnormal vulvar discharge ( eg, frank
the engorged man1mae or wrapping the
blood, dark green discharge before any
abdomen with an elastic bandage may give
neonates are born [indicates placental
relief. Owners should be advised not to milk
separation]).

out the mammary glands, because doing so

To detem1ine the appropriate therapy, the
will only stimulate lactogenesis.

cause of dystocia ( obstructive vs nonob

Tranquilizers (eg, diazepan1, PO, up to
structive) must be detern1ined and the

4 days) may be considered for bitches with
condition of the animal assessed. A
significant behavioral changes. Estrogens
thorough history regarding breeding dates
should not be used because of the potential
previous parturitions, pelvic trauma, etc, i�
for bone marrow suppression. Megestrol
desirable. The anin1al should be exan1ined
acetate, a progestin (2.5 mg/kg/day, PO, for
for signs of systemic illness that if present '

8 days), is the only drug cun-ently approved
may necessitate immediate cesa'.rean
for treatment of false pregnancy in bitches
section. The normal vaginal discharge at
in the USA. Prolonged or repeated use of
parturition is a dark green color; abnormal
megestrol acetate may cause pyometra.

color or character warrants in1mediate

Androgens ( eg, mibolerone, 16 mcg/kg/day,
attention. A sterile digital vaginal exami

PO, for 5 days) may decrease clinical signs
nation should be pe1formed to evaluate
of false pregnancy in bitches. Mibolerone
patency of the birth canal and the position
is not approved for treatment of false pregand presentation of the fetus( es). Radiogranancy in bitches in the USA. lf owners phy or ultrasonography can detem1ine the
are distressed by repeated bouts of
presence and number of fetuses as

' well as
pseudopregnancy, the bitch should either
their size, position, and viability.

be bred or undergo ovariohysterectomy.

Medical management may be considered
when the condition of the dam and fetuses is

FOLLICULAR CYSTS
stable, when there is proper fetal position
and presentation, and when there is no

These fluid-filled structures develop within
obstruction. Oxytocin (3-20 U in bitches,
the ovary and result in prolonged secretion

1396

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL
of estrogen, continued signs of proestrus
commonly in postpartum queens. Rarely,
or estrus, and attractiveness to males.

mastitis is seen in lactating pseudopregnant

Ovulation may not occw· during this
bitches. Risk factors for developing mastitis
abnormal estrous cycle. Follicular cysts
include poor sanitary conditions, trauma

VetBooks.ir
should be suspected in any bitch showing
inflicted by offspring, and systemic
clinical manifestations of estrus for >21
infection. Mastitis may be acute or chronic.

days, or when proestrus plus estrus have

Mastitis may be localized ( eg, involving
lasted for >40 days. Estrous cycles due to
a single gland sinus), cliffuse in a single
follicular cysts in queens may be difficult to
gland, or diffuse within multiple glands. The
differentiate from normal, frequent cycles.

animal may be asymptomatic or critically

The primary differential diagnosis is
compromised. Milk from mastitic glands
functional ovarian granulosa cell tumor.

may appear normal grossly or may be

Assessment of vaginal cytology with
abnormal in color or consistency. In acute
presence of comified cells indicates
mastitis, the affected glands are hot and
increased serum estrogens.

painful. If acute mastitis progresses to

The treatment of choice is ovariohysterseptic mastitis, signs of systemic illness ectomy. If the animal is to be bred, induction such as fever, depression, anorexia, and of luteinization of the cystic follicles may be
lethargy may be seen, and the dam may
accomplished by using GnRH (25 mcg, IM)

neglect the neonates. In chronic or
or human chorionic gonadotropin
subclinical mastitis, the main complaint

(220 IU/kg, IV, or 1,000 IU, half IV, half IM).

may be failure of offspring to thrive.

Diagnosis is usually evident from

MAMMARY HYPERTROPHY IN
the history and physical examination.

Microscopic examination of milk may

CATS
reveal inflammatory cells. Milk from each
gland should be evaluated in any postpar

(Fibroadenoma complex, Mammary
tum bitch or queen with signs of systemic
fibroadenomatosis, Glandular mammary
illness. Before beginning therapy, a milk
hypertrophy)

sample should be collected ( or obtained by

This benign condition is characterized by
fine-needle aspiration) for bacterial culture
rapid abnormal growth of one or more
and sensitivity. Culture of milk or fluid
mammary glands. There are two basic types
expressed from the affected glands yields
of hyperplasia of the feline mammary
moderate to heavy growth of Escherichia
gland-lobular hyperplasia and fibro
coli or staphylococci.

epithelial hyperplasia. Lobular hyperplasia

Broad-spectrwn, bactericidal antibiotics
is seen as palpable masses in one or more
should be chosen based on sensitivity tests
mammary glands in intact cats 1-14 yr
and with the understanding they will be
old. Fibroepithelial hyperplasia occurs in
passed in the milk to the young. Antibiotics
young, cycling, or pregnant cats; in old,
such as tetracycline, chloran1phenicol, or
intact females and males; and in neutered
an1inoglycosides should be avoided during
males after treatment with pi:ogestins.

lactation unless the neonates are weaned.

Feline mammary hypertrophy is

Cephalexin (5-15 mg/kg, PO, tid) and
considered to be a hormone-dependent
amoxicillin/clavulanate (14 mg/kg, PO,
dysplastic change in the mammary gland.

bid-tid) are recommended as initial

Hyperplasia occurs within 1-2 wk after
therapeutic agents pending culture results.

estrus or 2 -6 wk after progestin treatment.

Hot-packing the affected gland encourages

The tremendously enlarged glands may
drainage and seems to relieve discomfort.

appear erythematous, and some of the skin

Fluid therapy is indicated in anin1als with
may be necrotic. Edema of the skin and
septic mastitis that are dehydrated or in
both hindlegs is common, and the condition
shock. An abscessed mammary gland
can easily be confused with acute mastitis.

should be lanced, drained, flushed, and

Ovariohysterectomy or mastectomy is
treated as an open wound.

curative, although spontaneous remissions

Nonseptic mastitis is seen most
occur. Ovariohysterectomy is followed by
commonly at weaning. The affected glands
regression of the glands and prevents
are wann, swollen, and painful to the touch,
recurrence.

but the anin1al is alert and healthy. Warm
compresses should be applied to the

MASTITIS
affected glands 4-6 times daily, and the
young should be encouraged to nurse from

Mastitis is inflammation of the mammary
these glands. When galactostasis occurs at
gland(s) associated with bacterial infection.

weaning, lactation can be din1inished by

It occurs in postpartwn bitches and less
reducing food and water intake of the dan1.

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL

1397

The mammary glands should not be
be used to distinguish ovariectornized
stimulated during this time. Appropriate
and sexually intact bitches.

food and water must be provided for the

Exploratory laparotomy to find and
young.

remove the ovarian remnant is the

VetBooks.ir
treatment of choice.

METRITIS

PYOMETRA

Metritis is postpartem infection of the
uterus. Predisposing causes include

Pyometra is a honnonally mediated
prolonged delivery, dystocia, and retained
diestrual disorder characterized by cystic
fetuses or placentas. Escherichia coli is the endometrial hyperplasia with seconclaiy
most common bacterium isolated from the
bacterial infection. Pyometra is reported
infected uterus; streptococci, staphyloprimaiily in older bitches (>5 yr old), 4-6 wk cocci, Proteus sp, and others are isolated
after estrus.

less frequently.

The primary clinical sign is purulent

Etiology: Factors associated with
vulvar discharge. Bitches or queens witl1
occurrence of pyometra include administrametritis are usually depressed, with signs of tion of longlasting progestational comfever, lethargy, and inappetence, and may pounds to delay or suppress estrus,
neglect their offspring. Pups may become
administration of estrogens to rnismated
restless and cry incessantly. Metritis should
bitches, and postinsemination or postcopube considered in any postpartum animal lation infections. Progesterone promotes
with signs of systemic illness or an
endometrial growth and glandular secretion
abnmmal vaginal discharge. A large, flaccid
while decreasing myometrial activity. Cystic
uterus may be palpable. Radiographs should endometlial hyperplasia and acclll11ulation be taken to detennine whether fetuses or
of uterine secretions ultimately develop and
placentas are retained. The hemogram may
provide ai1 excellent environment for
show leukocytosis with a left shift.

bacterial growth. Progesterone may also

Treatment includes stabilization with
inhjbit the WBC response to bacterial

IV fluids, supportive care, and antibiotic
infection. Bacteria from the nom1al vaginal
therapy based on culture and sensitivity
flora or subclinical urinary ti-act infections
testing of the vulvar discharge. Prostaglanai·e the most likely sources of uterine din F2a (O.l-0.25mg/kg, SC, for2--3 clays)

contai11ination. Escherichia coli is the most or oxytocin (5---20 U in bitches, 2-5 U in
corru11on bacterilll11 isolated in cases of
queens, IM) may help evacuate the uterine
pyometra, although Staphylococcus,
contents. Ova.riohysterectomy is recom

Streptococcus, Pseudomonas, Proteus spp,
mended after initial stabilization if the
and other bacteria also have been recovered.

animal is extremely ill or if future reproduc

Because queens require copulatmy
tion is unin1portant. Otl1erwise, it should be
stin1ulation to ovulate and produce
considered an elective procedure to be
progesterone from corpora lutea, pyometra
performed when lactation has ceased.

is less common in queens than in bitches.

Administration of rnedroxyprogesterone and

OVARIAN REMNANT SYNDROME other progestational cornpom1ds has been associated with development of pyometra in

Ovarian remnant syndrome refers to clinical bitches and queens. Pyometra can develop in signs indicating the presence of functional
ute1ine tissue left after ovariohysterectomy
ovarian tissue in a previously ovariohyster

(stun1p pyornetra). It can also occur
ectomizecl bitch or queen. It is not a
secondary to postpartlll11 metritis.

pathologic condition but a complication

By itself, estrogen does not contribute
of ovariohysterectomy. It occurs when a
to the development of cystic endornetlial
retained piece of ovarian tissue revasculai�
hyperplasia or pyornetra. However, it
izes and becomes functional. The most
does increase the stimulatory effects of
common presentation is recurrent estrus
progesterone on the uterus. Administra

( eg, vulvar swelling, flagging, standing to
tion of exogenous estrogens to prevent
be mounted) after ovariohysterectomy.

pregnancy (ie, "rnismate shots") during

Differential diagnoses include vaginitis,
diestlllS greatly increases the risk of
uterine stump pyometra, and exogenous
developing pyometra and should be
estrogen therapy. Presmnptive diagnosis
discouraged.

of ovarian remnant syndrome requires
demonstration of a comified vaginal

Clinical Findings: Clinical signs are seen
epithelimn in a spayed female. A commerduring diestrus (usually 4-8 wk after estrus) cially available luteinizing hormone test can
or after administration of exogenous

1398

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL
progestins. The signs are variable and
exclude other causes ofpolydipsia,
include lethargy, anorexia, polyuria, polypolyuria, and vomiting; they also evaluate dipsia, and vomiting. When the cervix is
renal function, acid-base status, and septiceopen, a purulent vulvar discharge, often mia. The uterine exudate should be cultured
containing blood, is present. When the
and sensitivity tests perfonned. Differential

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cervix is closed, there is no discharge and
diagnoses include pregnancy and other
the large uterus may cause abdominal
causes of vulvar discharge, polyuria and
distention. Signs can progress rapidly to
polydipsia, and vomiting.

shock and death.

Physical exan1ination reveals lethargy,

Treatment and Prognosis: Ovariohysdehydration, uterine enlargement, and if the terectomy is the treatment of choice for
cervix is patent, a sanguineous to mucopupyometra. Medical management could be rulent vaginal discharge. Only 200/o of
considered if preserving the reproductive
affected aninlals have a fever. Shock may
potential of the bitch or queen is desired.

be present.

F1uids (IV) and broad-spectrunl, bactericidal

The leukogram of anin1als with pyometra
antibiotics should be administered. F1uid,
is variable and may be normal; however,
electrolyte, and acid-base inlbalances should
leukocytosis characterized by a neutrobe corrected as quickly as possible, before philia with a left shift is usual. Leukopenia
ovariohysterectomy is performed. The bactemay be found in animals with sepsis. A mild, rial infection is responsible for the illness
normocytic, normochromic, nonregeneraand will not resolve until the uterine exudate tive anemia (PCV of28%-35%) may also
is removed. Oral antibiotics (based on the
develop. Hyperproteinemia due to hyperresults of the culture and sensitivity) should globulinemia may be f ound. Results of
be continued for 7 --10 days after surgery.

urinalysis are variable. With E coli uterine Medical therapy with prostaglandin F2a
infection, isosthenuria due to endotoxin

(PGF2a) can be used for aninlals to be bred
induced inlpairment ofrenal tubular
in the future, although prostaglandins are
function or to insensitivity to antidiuretic
not approved in the USA for use in cats or
hom10ne (or both) may develop. A
dogs. PGF2a causes luteolysis, contraction
glomerulonephropathy caused by
of the myometrium, relaxation of the cervix,
immune-complex deposition may result
and expulsion of the uterine exudate. They
in proteinuria. These renal lesions are
should probably not be used in aninlals >8
potentially reversible once the pyometra
yr old or in those not intended for breeding.

is resolved.

The delay before clinical inlprovement and
the many adverse effects of PGF2a preclude

Diagnosis: Pyometra should be suspected its use in a severely ill aninlal. PGF,a also in any ill, diestrual bitch or queen, especially should be used with caution in bitches or ifpolydipsia, polyuria, or vomiting is
queens with a closed-cervix pyometra
present. The diagnosis can be established
because of increased risk of uterine rupture.

from the history, physical exanlination,

Pregnancy must be excluded, because
abdominal radiography, and ultrasonograprostaglandins can induce abortion.

phy. Vaginal cytology often helps determine

Naturally occurring PGF2a (0.25 mg/kg/
the nature of the vulvar discharge. A CBC,
day, SC, for 5 days) is commonly used.

biochemical profile, and urinalysis help

Synthetic analogues ( eg, cloprostenol,
fluprostenol, and prostalene) are much
more potent than natural PGF2a and have
been used to treat pyometra in dogs.

Broad-spectrum, bactericidal antibiotics,
chosen on the basis of culture and
sensitivity tests, should be given for �2 wk.

The adverse effects of PGF2a include
restlessness, anxiety, panting, hypersalivation, pacing, tachycardia, vomiting, ruination, and defecation. In cats, vocalization and intense grooming behavior also may be seen. These reactions disappear
within 2 hr of the irtjection. The LD50 of

PGF2a in dogs is 5.13 mg/kg. Severe ataxia,
respiratory distress, and muscle tremors
may be seen in queens given 5 mg/kg. If

Pyometra in a 10-yr-old Norwegian Elkhound,
adverse effects are severe, IV fluids at rates
lateral projection. Courtesy of Dr. Ronald Green.

appropriate for treatment of shock are

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL

1399
indicated. Uterine evacuation after an
as a result of estrogenic stimulation.

injection is variable.

Occasionally, the prolapse continues

Other antiprogestins ( eg, aglepristone)

throughout pregnancy or recurs at
are available in some European countries.

parturition. The most conunon sign is a

Clinicians using aglepristone report
mass protmding from the vulva. Initially, the

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virtually no adverse effects as compared
surface is smooth and glistening, but with
with prostaglandins. Aglepristone is also
prolonged exposure it becomes dry and
used to treat bitches with closed-cervix
fissures develop. A slight vaginal discharge
pyometra. In one study, a dosage of 10 mg/
may be present. Although the hyperplastic
kg given on days 1, 2, and 8 in 15 bitches
tissue originates near the urethral orifice,
with closed pyometra led to opening of the
dysuria is uncommon. Vaginal hyperplasia
cervix after 26± 13 hr in all treated animals.

interferes with copulation. Reluctance to

Animals should be reexamined 2 wk after
breed or failure of intromission may be the
completion of medical therapy. If a sanguineonly clinical sign if the hyperplastic tissue is ous or mucopumlent vulvar discharge or
contained within the vaginal vault. Vaginal
uterine enlargement is still present, PGF2a
hyperplasia resolves spontaneously as soon
therapy, using the same protocol, may be
as estrogen declines.

repeated; however, the prognosis for

The diagnosis is made by the history
recovery is much worse. After medical

(stage of the estrous cycle) and examination
therapy, the prognosis for initial resolution
of the vagina. Estrogen.ic stimulation could
of the pyometra is good if the cervix is open
be confirmed by comification of the vaginal
but guarded to poor if closed. Of those
epithelial cells, the presence of the
animals that respond, as many as 90"A, of
characteristic serosanguineous estrous
bitches and 70"A, of queens with open-cervix
discharge, and the presence of estrous
pyometra may be fertile. Recurrence is
behavior. The differential diagnosis is
likely; 70"A, of bitches treated medically
vaginal neoplasia, which can be excluded
for pyometra had recurrence within 2 yr.

by biopsy of the protruding tissue.

Therefore, the animal should be bred on the

If the hyperplastic tissue is not causing
next and each subsequent cycle until the
problems, therapy is not indicated. However,
desired number of puppies or kittens has
if it protrudes from the vulva, it should be
been produced, and then spayed. Prostakept clean and moist and an antibiotic glandins should not be dispensed for owner
ointment applied. An Elizabethan collar may
administration because of the narrow safety
be necessary to prevent self-trauma These
index and the potential to trigger astlunatic
animals may be bred by artificial inseminaevents and pregnancy loss in people.

tion. The hyperplasia regresses as soon as
the follicular phase of the estrous cycle has

SUBINVOLUTION OF PLACENTAL
passed. Submucosal resection may be
necessary if the mass is extremely large or

SITES
if mucosal damage is extensive. Recurrence

Subinvolution of placental sites (SIPS)

is common even after surgical resection.

is abno1mal repair of the endometrial

Vaginal hyperplasia resolves within days of
placental sites. This disorder is most
removal of estrogen. Rarely, the hyperplasia
common in young bitches ( <3 yr old) after
recurs at paiturition, presumably associated
whelping a first litter. Bitches with SIPS are
with a burst of estrogen. Ovariohysterecnonnal except for hemorrhagic uterine tomy, the treatment of choice, pennanently
discharge passing from the vulva for several
corrects this condition by removing the
weeks postpartum. Diagnosis is by
gonadal source of estrogen, tlms preventing
exclusion; differentials include metritis,
recurrence.

vaginitis, and cystitis. Treatment is
supportive. Ovariohysterectomy is

VAGINITIS
recommended for bitches that become
anemic enough to require transfusion and

Inflarnrnation of the vagina may occur in
for bitches not intended for future breeding.

prepubertal or mature (intact or spayed)

bitches. It is rare in queens. Vaginitis usually
is due to bacterial infection, which may be

VAGINAL HYPERPLASIA
secondary to conformational abnom1al.ities
such as vestibulovaginal strictures. Viral

(Vaginal prolapse)

infection (eg, herpes), vaginal foreign

In vaginal hyperplasia, a proliferation of the
bodies, neoplasia, hyperplasia of the vagina,
vaginal mucosa, usually originating from the androgenic steroids (eg, rn.ibolerone), or floor of the vagina anterior to the urethral
intersex conditions also may cause
orifice, occurs during proestrus and estrus
vaginitis.

1400

REPRODUCTIVE DISEASES OF THE FEMALE SMALL ANIMAL

The most common clinical sign is a vulvar
therefore, culture results must be interpreted
discharge. Licking of the vulva, attraction of
cautiously. A heavy growth, especially of one
males, and frequent micturition also may
organism, is probably more significant than a
be seen. Signs of systemic illness are not
light growth of several organisms.

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present, and the hemogram and biochemical

Predisposing factors such as foreign
profile are nmmal. The absence of these
material or anatomic abnotmalities should
abnom1alities helps differentiate vaginitis
be coffected. Bacterial infection may
from open-ce1vix pyometra, the most
respond to local treatment (ie, vaginal
important differential diagnosis. The
douches). Systemic, broad-spectrum,
diagnostic evaluation should include a digital bactericidal antibiotics may be needed for examination of the vagina, vaginoscopy,
persistent infections. Prepubertal animals
cytology, and if necessary, culture of the
often do not require treatment, because the
exudate, as well as abdominal radiographs
vaginitis nearly always resolves with the
or ultrasonography to evaluate the uterus.

first estrus. Therefore, it may be wise to

An anterior vaginal culture may be obtained
delay elective ovariohysterectomy in
using a guarded ste1ile culture swab. The
affected animals until after their first
vagina contains nonnal bacterial flora;
estrous cycle.

REPRODUCTIVE DISEASES OF THE

MALE SMALL ANIMAL

See also MANAGEMENT OF' REPRODUCTION: S�W-L
culture may be obtained by fme-needle

ANIMALS, p 2219, and PROSTATIC DISEASES, p 1405.

aspiration. Testicular biopsy for histopathology and bacte1ial culture may be ORCHITIS AND EPIDIDYMITIS
performed, if needed, after less invasive
diagnostic tests have been completed.

Acute inflammation of the testis or

Because of the greater 1isk of granuloma
epididymis can be caused by trauma,
fom1ation, epididymal aspiration and biopsy
infection (fungal, bacterial, or viral), or
are rarely done. If future reproduction is not
testicular torsion. Infection can be
of in1portance, specimens can easily be
hematogenous or urologic in origin. Clinical
obtained during castration.

signs are pain and.swelling of the testes,

Treatment is difficult unless the
epididyrnides, and/or scrotum. There may
underlying cause can be identified. The
be wounds or other lesions in the scrotal
prognosis for maintaining fertility is
skin. Orchitis and epididymitis are rare in
guarded despite aggressive therapy because
cats unless due to trauma.

of the potential for irreversible dan1age to

The scrotal contents should be carefully
the gemunal epitheliun1, tubular degenerapalpated to identify which structures are tion, development of inrnnme-mediated
involved, including the epididymis and
orclutis, or obstruction of the duct system.

testis, but patient discomfo1t and edema

These sequelae may take months to occur.

can make palpation difficult. Ultrasonogra

Application of cool water packs may
phy ( with sedation or analgesia as needed)

decrease testicular damage caused by local
is helpful to further evaluate the affected
swelling and hyperthermia; care must be
structures and to confim1 the presence of
taken not to damage the scrotal skin. In
testicular torsion and focal ( eg, mass,
the case oftmilateral involvement, the
abscess) lesions in the testis or epididymis.

unaffected testis/epididynus must be

It can also identify less conunon causes of
protected from damage by heat, pressure,
scrotal enlargement such as scrotal hernia
and direct extension of the disease process.

or hematoma.

Hemicastration may be prudent. If bacterial

Diagnostic tests should always include
cultures are positive, appropriate systemic
evaluation for Brucella canis infection. (See antibiotics should be adnunistered for 3--4
also BRUCELWSIS IN DOGS, p 1402.) Cytologic wk. There is no completely successful
exan1ination of semen with bacterial and
treatment for B canis infection. All
mycoplasmal culture are also helpful, but
antifungal agents interfere with spermatosemen collection from animals that are ill genesis, either directly or indirectly. The
or in pain may be difficult. Testicular or
potential for involvement of the prostate
epididyrnal specimens for cytology and
by direct extension dictates the use of

REPRODUCTIVE DISEASES OF THE MALE SMALL ANIMAL

1401
antibiotics with good prostatic penetration
mature dogs, resolves spontaneously, and
once inflai1m1ation has subsided (fluoroquinis of little clinical significance. Diagnostic olones). Culture and sensitivities should
tests and treatment are not necessary,
refine therapy.

except as needed for reasonable hygiene.

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Histopathology may suggest an immune

Trauma, lacerations, neoplasia, foreign
mediated process ( eg, lymphocytic-plasmabodies, urinary tract infection, urolithiasis, cytic infiltration); treatment with immunoor phi.mosis may result in development of suppressive drugs has been attempted
more severe balanoposthitis. A mucopuruwithout success. Chronic B can is infection lent preputial discharge is the most
also causes lymphocytic-plasmacytic
common clinical sign. Excessive licking of
inflainmation. Furthem1ore, as a result
the prepuce may also be noted. Swelling of
of inhibitory effects on the hypothalainicthe prepuce and pain are rarely present pituitary-gonadal axis, glucocorticoids can
except in cases of trauma, snake bite, or
cause testicular atrophy and infertility. The
foreign bodies. If signs of systemic illness
ischemic dainage caused by testicular
ai·e present, the possibility of a more serious
torsion becomes in-eversible within hours.

concomitant disorder should be considered.

When maintaining fertility is not important,

Balanoposthitis is rare in cats.

castration is the treatment of choice for

The penis and prepuce should be
orchitis and epididy.mitis due to any cause.

thoroughly exai11ined, to the level of the

Lesions of the scrotal skin are treated the
fornix, for underlying predisposing factors.

saine as other skin lesions, keeping in mind

The use of saline infusion through a 1igid
that resection of scrotal skin can promote
endoscope facilitates this exainination, but
them1al dan1age to the testes.

an otoscope can be used if necessary.

Chronic orchiepididyrnitis may

Sedation or general anesthesia may be
develop as a sequela of the acute syndrome,
needed. Preputial cytology may be helpful.

or there may be no previous history of

Bacterial cultures of the preputial cavity,
testicu]ai· inflan1.mation. Possible causes
although sometin1es difficult to interpret
include those of acute orchiepididymitis,
because of the presence of norn1al preputial
immune-mediated orchitis and epididymitis, flora, may help identify unusual organisms neoplasia, and spem1atocele or granuloma
and determine antibiotic sensitivities for
formation. Most animals are asyn1ptomatic
refractory cases. Foreign bodies can be
except for infertility. Physical examination
submucosal and difficult to see, so tiny
often reveals testicular atrophy. Tunlors
tracts should be explored.

may be palpable. Palpation of the

Treatment includes con-ecti.ng any
epididymis may reveal induration or
predisposing factors, clipping long hair
enlargement, which may en-oneously be
away from the preputial orifice, and
interpreted as drainatic relative to the
thoroughly flushing the preputial·cavity
atrophic testis. Epididymal atrophy is
with a mild antiseptic ( eg, dilute povidoneuncommon. Ultrasonography can help iodine or chlorhexidine) or sterile saline
identify the lesions.

solution. If bacterial infection is suspected,

Other noni.nflanunatory causes of
an antibiotic ointment may be infused into
testicular atrophy include previous
the preputial cavity for 7-10 days. Recm0
exposure to excessive pressure, heat, cold,
rence of .mild balai1oposthitis is common
and cytotoxic agents. Hom1onal causes (eg,
i.JTespective of therapy. Castration may
glucocorticoids, estrogen from contralatdiminish genital secretions but will not eral Sertoli cell tumor, iatrogenic exposure
abolish them.

to human transdermal hom1one replacement therapy) are also possible.

PARAPHIMOSIS

The prognosis for return of normal
fertility in cases of chronic orchitis/

The inability to completely retract the pen.is
epididymitis is grave. If watTanted by the
into the preputial cavity usually occurs after
dog's value as a stud, the diagnostic and
erection. It is seen most often after semen
therapeutic plan is as described above for
collection or coitus. The ski.Ji at the
the acute condition.

preputial 01ifice becomes inverted, trapping
the extruded pen.is and in1pairing venous

BALANOPOSTHITIS
drainage. Other causes of pai·aphi.Jnosis
include a small preputial openi.J1g, priapism,

Inflanunation of the penile or preputial
foreign objects around the pen.is, a
mucosa is conm1on in dogs. The normal
constricting band of hair at the preputial
preputial secretions usually do not result in
orifice, or trauma. Paraphin1osis is easily
overt clinical signs. Mild balanoposthitis,
differentiated from priapism (persistent
resulting in a slight mucopurulent preputial
erection without sexual sti.J1mlation),
discharge, is present in many sexually
congenitally shortened prepuce, congenital

1402

REPRODUCTIVE DISEASES OF THE MALE SMALL ANIMAL
deformity of the os penis, or penile

PRIAPISM
neoplasia or hematoma on the basis of
physical examination and palpation.

Priapism is a persistent erection without

Paraphimosis warrants veterinary
sexual stimulation and is diagnosed by
intervention if not resolved quickly. The
physical examination. Partial paraphin1osis

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exposed penis quickly becomes edematous,
can also result. Priapism can be caused by
because its venous drainage is compromyelopathy, drugs, vascular abnonnalities, mised. With continued exposure, the
penile masses, or trauma, or it can be
mucosa becomes dry and painful. Selfidiopathic. It can be ischemic and a medical trauma exacerbates the condition. If
emergency. If nonischemic and no primary
recognized early, before severe edema and
cause is identified, therapy with gabapentin,
pain develop, paraphimosis is easily treated. ephedrine, or terbutaline can be attempted.

Treatment begins with gentle cleansing and

Castration is not helpful, because priapism
liberal lubrication of the exposed penis. The
is not testosterone mediated.

penis is then replaced inside the prepuce

If necrosis or gangrene is severe,
by first sliding the prepuce in a posterior
an1putation of the penis and prepuce and
direction, extruding the penis further. This
urethrostomy might be necessary.

everts the skin at the preputial orifice;
usually the prepuce then slides easily over

PHIMOSIS
the penis. The edema resolves promptly
once circulation is restored. Hypertonic

An abnonnally small preputial orifice,
solutions can be useful in difficult cases. If
resulting in inability to extrude the penis,
the everted prepuce does not slide over the
can be congenital, or acquired as a result of
edematous, exposed penis, a cold compress
neoplasia, edema, or fibrosis after trauma,
may be applied with gentle digital pressure
inflanrn1ation, or infection. Clinical signs
to act as a pressure bandage. A temporary
are variable. Usually, the problem is
purse string suture can be placed to keep
urmoticed until tile dog attempts to mate
the penis inside the prepuce.

and is unable to copulate. Urine can pool in

With paraphimosis due to other causes,
the prepuce and cause posthitis. Diagnosis
or of longer duration, sedation or general
is established by physical examination of
anesthesia can be required. It may be
the prepuce and penis. Treatment depends
necessary to incise the preputial skin to
on severity of the stenosis and intended
thoroughly examine the preputial cavity,
use of the dog. If the dog is not used for
remove restricting material, and relieve
breeding, therapy probably is not needed,
venous obstruction. The penis is then
although castration should be considered
replaced in the preputial cavity, and the
to prevent arousal. Surgical enlargement
incision is closed. If the urethra has been
of tile preputial orifice is indicated if the
damaged, temporary placement of a
animal is to be used for breeding, if tile
closed-system indwelling urinary catheter
phimosis contributes to balanoposthitis,
may be needed to prevent stricture
or in the unlikely event that phimosis
formation.

interferes witll normal micturition.

BRUCELLOSIS IN DOGS

Although dogs occasionally become
confined dogs, especially at time of
infected witllBrucella abortus, B silis, or breeding or when abortions occur.

B melitensis, these sporadic occurrences

Transmission occurs via ingestion of
typically are closely associated with
contaminated materials or venereal routes.

exposure to infected domestic livestock

Urine transmission has been reported but

(seep 1348).

seems to be unusual. Both sexes appear to

B can is is a cause of abortion at 45-55
be equally susceptible.

days of gestation in kenneled dogs. Dogs

Primary signs are abortion during the last
are the only definitive host of this orgatrimester of pregnancy without premonitory nism. Infection has caused a reduction
signs, stillbirths, and conception failures.

of75%in the nun1ber of pups weaned in

Prolonged vaginal discharge usually follows
some breeding kennels. The disease
abortion. Abortions may occur during
disseminates rapidly among closely
subsequent pregnancies. Infected dogs may

MAMMARYTUMORS

1403
develop generalized lyrnphadenitis and
or isolation of infected dogs identified
frequently epididymitis, periorchitis, and
by positive cultural or serologic tests at
prostatitis. Spondylitis and uveitis are
monthly intervals. Incidence of infection is
occasional complications. Bacteremia is
much lower in kennels where dogs are
frequent and persists for -18 mo after
caged individually. Longtem1 therapy, eg,

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exposure. Fever is not characteristic.

with a combination regin1en of streptomy

Diagnosis is based on isolation and
cin or gentarnicin and tetracycline, has been
identification of the causative agent or by
successful in many cases. Neutering of
serology. The organisms can usually be
infected dogs is sometimes an alternative
readily isolated from vaginal exudate,
to euthanasia.

aborted pups, blood, milk, or semen of

Prevention of canine brucellosis is done
infected dogs. The most widely used
by testing before entry and breeding. The
serologic test is an agglutination test by a
disease is reportable in some states. B
tube or slide method. Nonspecific agglutina
canis is zoonotic, although cases of human tion reactions occur in some dogs. To
infection are rare and less severe than
eliminate nonspecific antibody reactions,
those caused by the smooth species of the
tl1e serum is treated with 2-mercaptoethagenus. The true incidence is unknown.

nol and retested. An agar gel inm1Unodiffu

Diagnostic tests used for smooth species
sion test performed in some laboratories is
do not cross-react witl1 those for rough
quite specific. Other tests, such as immunospecies; this may result in a missed fluorescence and ELISA, have been used
diagnosis. In addition, signs of B canis
sometin1es.

infections may resemble those of other

Attempts at immunization have not been
diseases. Appropriate measures to prevent
successful. Control is based on elimination
exposure should be taken.

MAMMARY TUMORS

The frequency of man1mary neoplasia in

Genetic and nutritional effects on
different species varies tremendously. The
man1n1ary neoplasia have been identified in
dog is by far the most frequently affected
mice and some people but are still not as
domestic species, with a prevalence -3
well understood in dogs or cats. In people,
times that in women; -500Ai of all tw110rs in

BRCAl and BRCA2 are the most important
the bitch are manm1ary twnors. Mammary
genes significantly associated with
twnors are rare in cows, mares, goats, ewes,
mammary twnors. In dogs, one single
and sows. There are differences in both
nucleotide polymorphism (SNP) in exon 9
biologic behavior and histology of
ofBRCAl and one SNP in exon 24 of BRCA2
manm1ary tumors in dogs and cats.

were found to be significantly associated

Approxin1ately 45% of manm1ary twnors
with canine man1mary tw11ors. It has been
are malignant in dogs, whereas -90% are
demonstrated that the conswnption of red
malignant in cats, and dogs have a much
meat, obesity at l yr of age, and obesity a
higher nwnber of complex and mixed
year prior to diagnosis are associated with
tumors than do cats.

an increased risk of mammary gland tw11ors
in intact or ovariohysterectomized dogs.

Etiology: The cause of man1mary tw11ors

Obesity is thought to mediate breast cancer
is unknown in any species except mice, in
risk in postmenopausal women by
which an oncomavirus is causative in
increasing circulating free estrogen levels
certain inbred strains. Hormones play an
as well as through increased local estrogen
important role in the hyperplasia and
production by aromatases. It is possible that
neoplasia of manm1ary tissue, but the exact
obesity increases risk of manm1ary tumors
mechanism is unknown. Estrogen or
through sinillar mechanisms in dogs.

progesterone receptors ( or both) have

From a practical view, all man1mary
been repo1ted on manm1ary tumor cells in
twnors should be regarded as potentially
animals; these may influence the pathogenmalignant regardless of the size or nun1ber esis of hormone-induced man1mary
of glands involved. Spread of man1mary
neoplasia as well as the response to
carcinomas in both dogs and cats is
hom10ne therapy.

prin1arily to regional lymph nodes and

1404

MAMMARYTUMORS
lungs. In dogs, 5o/o-l 0% of mammary
glands are more frequently involved tl1an
carcinomas may produce skeletal
the posterior glands.

metastases, primarily in the axial ske

Histologically, most feline manunary
leton, but also in long bones.

tumors are a.denocarcinomas, with tubular

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or papillary types more common tl1an solid

Canine Mammary Tumors: Manm1ary
or mucoid types. Mixed mammary tumors
tumors in dogs are most frequent in intact
and sarcomas are less commonly diagnosed
bitches; they are extremely rare in male
than carcinomas. Benign tumors of the
dogs. Ovariectomy before the first estrns
feline manunary gland are relatively
reduces the risk of mammary neoplasia to
infrequent and account for only -100/o of

0.5% of the risk in intact bitches; ovariecthese tumors. The TNM clinical staging torny after one estrns reduces the Lisk to 8%
system is used for ma.nm1ary tumors in ca.ts
of that in intact bitches. Bitches neutered
as well as in dogs.

after maturity have generally been

A distinct entity called feline ma.nm1ary
considered to have the same Lisk as intact
hypertrophy has been noted in ca.ts (see
bitches. However, questions remain
p 1396). It affects primatily young, actively
regarding the impact of ovariohysterectomy cycling, or pregnant cats. It also has been at the tin1e of tumor excision. Questions
seen in neutered cats, including older males
also remain about the timing of such
given exogenous progestational drugs
surgery relative to survival. In one study,

( megestrol acetate). The disorder is marked
dogs spayed <2 yr before tumor excision
clinically by the rapid growth of one or more
lived 45% longer than either intact dogs or
manunary glat1ds.

those spayed >2 yr before tumor excision.

The two posterior mammary glands are

Diagnosis: A mammaty tumor is usually
involved more often than the three anterior
suspected on detection of a mass dw-ing
glands. Grossly, tumors appear as single
physical examination. The lengtl1 of time the
or multiple nodules (1-25 cm) in one or
mass has been present is usually W"Lknown,
more glands. The cut surface is usually
but the rate of growtl1 may be helpful in
lobulated, gray-tan, and firm, often with
determining prognosis. Palpation of the
fluid-filled cysts. Mixed rnanllllary tumors
regional lymph nodes can help detennine
may contain grossly recognizable bone or
the extent of spread. Thoracic ra.diographs,
cartilage on the cut surface.

preferably tllree views (a ventral-dorsal and

More than 500/o of canine man1mary
two laterals), should be taken to detect
tumors are benign mixed tumors; a smaller
pulmonary metastases. Fine-needle
percentage of malignant mixed tumors are
aspirates may differentiate between
seen. In the latter, epithelial or mesenchyinflatnmatory and neoplastic lesions but mal components, either singly or in
may lead to erroneous conclusions and
combination, may produce metastases.

delay of surgery. The diagnosis is deter

Histologically, ca.nine m=ary gland
mined by histopathology and is in1porta.nt
twnors have been classified by the World
in defining treatment and prognosis.

Health Organization as carcinm;nas (with
six types and additional subtypes),

Treatment and Prognosis: Mammary
sarcomas (four types), carcinosarcomas
tumors are treated surgically, although there

(mixed mammary tumors), or benign adenois no consensus as to the best procedure.

mas. This classification scheme is based on

Removal of the twnor alone.(Jun1pectomy),
the extent of the tumor, involvement of
simple mastectomy (removal of the affected
lymph nodes, and presence of metastatic
gland only), modified radical mastectomy
lesions (TNM system); it includes unclassi

( removal of the affected gland and those
fied tumors and apparently benign
that share lymphatic drainage and
dysplasias. In addition to tumor size and the
associated lymph nodes), and radical
status and timing of neutering, special stains mastectomy (removal of the entire (including those for the KIT receptor and
mammary chain and associated lymph

AgNOR) may have prognostic value.

nodes) all have their proponents. In dogs,
the more involved procedures have not

Feline Mammary Tumors: Manllllary
prolonged survival compared witl1 the
tumors in cats are most common in older
otl1ers, and the advantages of the simpler

(average 11 yr) intact females. Cats spayed
procedures are obvious. In ca.ts, radical
before 6 mo or 12 mo of age have a91%or an mastectomy has increased the diseas e -free 86% reduction, respectively, in tl1e risk of
interval but not survival time.

mammary carcinoma development than

In theory, the use of anticancer drugs to
intact cats. Parity does not affect feline
combat micrometastatic disease (adjuvant
mammary carcinoma development. Unlike
chemotherapy) is a reasonable considerain dogs, in ca.ts the two anterior or thoracic tion. However, chemotherapy has not been

PROSTATIC DISEASES

1405
shown to be an effective treatment for
difficult to manage by surgical or medical
mammary tumors in dogs. Part of the
means. This is in step with current interest
difficulty of evaluating the response to
in metronomic low-dose therapy in other
adjuvant chemotherapy relates to the fact
malignancies for an anti.tumor and

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that only about half of the canine mammary
anti.-angiogenic effect.

tumors diagnosed as malignant on

The prognosis is based on multiple
histopathologic examination actually
factors. In dogs, most mrum11ary tumors
behave that way. A combination of
that are going to cause death do so within
doxorubicin and cyclophosphamide has

1 yr. Sarcomas ru·e associated with shorter
been used with limited efficacy in cats.

survival times than carcinomas. Other

Neither radiation therapy nor antiestrogenic factors, including size of tumor, lymph node compounds have been effective.

involvement, and nuclear differentiation,

Use of the NSAID piroxicam (0.3
also affect the prognosis. In cats, tumor size
mgtkg/day, PO) as a single agent has
is important; cats with tumors >3 cm in
been beneficial in treating inflanunatory
diameter have a median survival time of 6
manunary carcinoma, a subtype of
mo, but cats with tumors <2 cm in diruneter
mammary tumor in dogs that has been very
have a median survival time of >4 yr.

PROSTATIC DISEASES

Disease of the prostate gland is relatively
only for ilie cranial aspects of the prostate
common in intact dogs but less conm10n in
to be palpated but also for better palpation
other domestic animal species. Benign
per rectum because the prostate can be
prostati.c hyperplasia is by far the most
pushed into or near ilie pelvic canal, which
common disease of the prostate in intact
is especially important in large-breed dogs
male dogs. Bacterial prostati.ti.s ( acute or
and in males wiili very enlarged prostates.

chronic), prostatic abscesses, prostatic and

Size, shape, symmetry, consistency,
paraprostatic cysts, and prostatic adenocarmobility, and ilie presence or absence of cinoma are seen much less frequently and
pain can be assessed by palpation. The
can be seen in castrated males. Depending
nom1al dorsal sulcus (depression) aids in
on the disorder, clinical signs may include
assessment of shape ru1d synunetry.

tenesmus during defecation, intermittent

Abdominal radiographs may help define
hematuria, recurrent urinary tract
the size, shape, and position of the prostate
infections, and caudal abdominal discomgland. The sublun1bar lymph nodes, lun1bar fort. However, many intact males with
vertebrae, and bony pelvis should be
benign prostatic hyperplasia ( with or
evaluated radiographically for evidence of
without chronic prostatitis) are asymptoperiosteal new bone and bony metastases.

matic or present with signs of hemospermia

A positive-contrast retrograde urefurograrn
and/or infertility only. Additional nonspecan be done when an abnormal prostate or cific signs, such as fever, malaise, anorexia,
paraprostatic cyst is difficult to differentiate
severe stiffness, and caudal abdominal pain,
from ilie bladder. However, transabdominal
can be seen wiili acute bacterial infections,
ultrasonography is tl1e best imaging modality
abscesses, and neoplasia. Prostatic
for evaluation of ilie prostate, because it
adenocarcinoma with bony involvement of
allows for evaluation of ilie prostatic
ilie pelvis and !um bar vertebrae may cause
parenchyma and adjacent soft-tissue
hindlimb gait abnormalities. Less comstructures. Increased echogenicity is monly, prostatic diseases may cause urinary
associated with benign prostatic hyperplasia,
incontinence. Prostatic adenocarcinoma
chronic bacterial prostatiti.s, and prostati.c
may cause complete urethral obstruction.

neoplasia, whereas areas of mineralization

Physical exanunation of the prostate
may be secondary to chronic bacterial
gland should include abdominal and rectal
prostatiti.s or prostatic neoplasia Mass
palpation. An enlarged prostate typically is
lesions wiiliin ilie prostatic urethra and
located further cranial ilian usual and can
discontinuity ofilie prostati.c urethral wall are
be found in ilie caudal abdomen rather ilian
both highly suggestive of prostatic neoplasia
wiiliin the pelvic canal. Simultaneous

If ilie dog will not ejaculate, mate1ial for
abdominal and rectal palpation allows not
cytologic and micro biologic exanunation

1406

PROSTATIC DISEASES
can be obtained by prostatic massage. Using usually evident within a few weeks and is aseptic technique, the bladder is catheteroften complete in several months.

ized, and all urine removed. The bladder is

For males intended for use in breeding,
flushed with saline, and this san1ple is saved. medical tl1erapy with finasteride is effective.

The catheter is then withdrawn so that the

Finasteride blocks the action of 5 ac-reduc

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end is caudal to the prostate. The prostate
tase, an enzyme that converts testosterone
is subsequently massaged per rectum for
to dihydrotestosterone. Dihydrotestosterabout 1 minute to release prostatic fluid into one is the biologically active ho1mone to the urethra, where it can be collected with
promote prostatic hyperplasia in both
the catheter. While occluding the urethral
people and dogs. Giving finasteride at
opening, saline is slowly ir\jected. The

1 mg/kg/day, PO, for 16-21 wk, to laboratory
catheter is then advanced into the bladder

Beagles resulted in a 50%-7(1'/o reduction in
as aspiration is performed and another
prostatic hypertrophy witl1 no negative
sample is collected. Results of cytologic
effect on semen quality. Lower dosages of
and microbiologic exan1ination from both
finasteride (0.1 mg/kg/day, PO, for 16 wk)

prostatic wash specin1ens should be
reduced hypertrophied prostate volume
compared. Prostatic massage may produce
by 43%, resolved clinical signs, reduced
septicemia in dogs with acute bacterial
dihydrotestosterone concentration by 58%,
prostatitis or a prostatic abscess. Neoplastic maintained nonnal testosterone levels, and cells are often not recovered in specimens
had no deleterious effect on semen quality,
obtained by ejaculation or prostatic
fertility, or libido in a group of nine dogs
massage.

with prostatic hypertrophy. However,

Fine-needle aspiration of the prostate
prostatic hypertrophy returns if finasteride
gland can be performed transrectally or
adn1inistration is discontinued. The low
percutaneously, with or without ultrasonodosage (0.1--0.5 mg/kg) of finasteride graphic guidance. While generally safe and
correlates to convenient dosing of one 5-mg
simple, this is not without some risk of
capsule/day for dogs weighing 10-50 kg.

penetration of surrounding structures.

Biopsy is the most definitive, but also the

PROSTATITIS
most invasive, diagnostic procedure to
differentiate prostatic diseases. To obtain

Inflammation of the canine prostate gland
diagnostic samples, prostatic biopsy should
usually is suppurative, and acute prostatitis
be perfom1ed via celiotomy or by a skilled
may result in abscesses. Chronic prostatitis
ultrasonographer.

occurs secondary to benign prostatic
hyperplasia ( see p 1406). Various organisms, BENIGN PROSTATIC
including Escherichia coli, Staphylococcus,

HYPERPLASIA

Streptococcus, andMycoplasmaspp, have
been incriminated. Infection may be

Benign prostatic hyperplasia (BPH) is the
hematogenous (acute prostatitis) or ascend
most common prostatic disorder and is
from the urethra ( chronic prostatitis).

found in most intact male dogs >6 yr old as a Because prostatic fluid nonnally refluxes result of androgenic stimulation or altered
into the bladder, a secondary urinary tract
androgen:estrogen ratio. It is not known
infection often accompanies prostatic
why some males are affected and others are
infection. Acute prostatitis and chronic
not. In some dogs, hyperplasia may begin as
prostatitis vary based on progression and
early as 2.5 yr of age and, after 4 yr of age,
severity of clinical signs.

cystic hyperplasia tends to develop. Clinical

Acute prostatitis is associated with
signs may be absent, or tenesmus,
malaise, pain, and fever. Dehydration,
persistent or intennittent hematuria, or
septicemia, and shock may occur in severe
hemorrhagic preputial discharge may occur. cases. Neutrophilia with a left shift, The diagnosis is suggested by physical and
monocytosis, and/or toxic WBCs may be
historical findings and by a nonpainful,
seen. Ultrasonography shows hypoechoic
synunetrically enlarged prostate. Radiology
areas consistent with small pockets of fluid.

can confirm prostatomegaly. Ultrasonogra

Ideally, prostatic material is obtained by
phy should show diffuse, relatively
prostatic massage for cytologic exan1ination
symmetric involvement with multiple,
and for culture and sensitivity testing.

diffuse, cystic structures. Cytologic

Massage of an acutely infected prostate may
exan1ination of massage or ejaculate
release organisms into the blood and cause
specin1ens reveals hemorrhage with mild
septicemia. Urinalysis shows hematuria,
inflan1rnation without evidence of sepsis
pyuria, and bacteriuria. The urine should be
or neoplasia. Definitive diagnosis is only
submitted for culture and sensitivity testing.

possible by biopsy. Castration is the

Often, the urine and prostatic material yield
treatment of choice; prostatic involution is
the san1e organisms.

PROSTATIC DISEASES

1407

IV fluid therapy is indicated when acute
to those seen with other types of prostatic
prostatitis is associated with dehydration
enlargement and usually become apparent
or shock. Because the prostate-blood
only when the cyst reaches a size sufficient
barrier is disrupted in acute prostatitis,
to cause pressure on adjacent organs. Large
antibiotics should be selected on the basis
cysts may result in abdominal distention

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of sensitivity testing and given for 3---4 wk.

and must be differentiated from the bladder

Enrofloxacin at a dosage of 5 mg/kg, bid,
and from prostatic abscesses.

orally is a good empiric treatment choice

Medical treatment is ineffective.

while awaiting results of microbiologic

Castration alone is unlikely to be of benefit
testing. After the infection is controlled,
but may be indicated after the cyst has been
castration should be considered. In some
removed. Total excision of the prostatic cyst
instances, multiple microabscesses within
is the treatment of choice. lf complete
an infected prostate gland may coalesce into excision of the cyst is not possible, the a solitary abscess. Large prostatic abscesses remaining portion of the cyst may be filled are best treated by surgical drainage and
with a leaf of omen tum secured with
intracapsular omentalization. Urine or
sutures. This "omentalization" of the cyst prostatic fluid ( or both) should be cultured
will provide internal drainage and lead to
again 2-4 wk after antibiotic therapy to be
resolution. Surgical excision is preferable
certain that infection has resolved.

to marsupialization, because clu·onic

Chronic bacterial prostatitis may
management of the marsupialization fistula
cause no clinical signs except recun-ent
is often problematic.

urinary tract infection. Physical abnom1alities may be lintited to the urinary tract.

NEOPLASMS

Rarely, prostatic size and shape may be
nonnal. Microbiologic exantination of the

The most common neoplasm of the prosthird (prostatic) fraction of the ejaculate is tate is carcinoma arising from ductal or
more accurate for assessment of chronic
urothelial tissue. Transitional cell carcibacterial prostatitis than exantination of noma aiising from the prostatic urethra
prostatic massage specimens. Dogs with
occasionally invades the prostate. Not only
clu·onic bacterial prostatitis are usually
does castration not protect against future
willing to ejaculate. Prostatic fluid and
development of prostatic neoplasia in dogs,
urine should be submitted for cytologic
but incidence of prostatic neoplasia is
and microbiologic exantination.

higher in castrated dogs.

Chro1tic bacterial prostatitis will not

The clinical signs of prostatic neoplasia
resolve without also treating for benign
may be sintilar to those of other prostatic
prostatic hyperplasia. In fact, most cases of
diseases. Pain and fever may be present. lf
chronic bacterial prostatitis will resolve
the neoplasm infiltrates the urethra,dysmia
with only treatment for benign prostatic
or urethral obstruction is likely. On rectal
hyperplasia, whether surgical (castration)

palpation, the prostate may be nom1al in size
or medical (finaste1ide). Antibiotic therapy
but feel asymmetiical and nodular. It may
alone is unrewarding. Many antibiotics
also be finnly adhered to the pelvic floor or
do not diffuse easily into the prostatic
adjacent structures. Ultrasonographic examparenchyma because of the presence of the ination may show an irregularly shaped
blood-prostate banier. The ntild inflanunaprostate gland with hyperechoic, heterogtion associated with chronic prostatitis may enous foci. Gross metastases are present at
not impair the blood-prostate barrier, so
the time of diagnosis in >8001,, of dogs with
antibiotics that are non-ionized at neutral
prostatic cai·cinoma. The most common
pH with high fat solubility ( eg, erythromysites of metastases are the regional lymph cin, clindamycin, trimethoprim-sulfamethnodes, ltunbar ve1tebrae, and bony pelvis.

oxazole, or enrofloxacin) are most effective. Spread to distant sites (such as the ltmgs) is lf antibiotic therapy is implemented, it
uncomn1on until late in the com-se of
should be continued for ?:4 wk.

disease. Urethral obstruction caused by
prostatic disease in dogs is ltighly suggestive

PROSTATIC AND PARAPROSTATIC of neoplasia, as is prostatomegaly in a CYSTS
previously castrated dog. Diagnosis is made
by biopsy. Prostatic tumor markern used for

Large cysts are occasionally found within
hmnan prostatic cancer, such as prostateor adjacent to (paraprostatic) the prostate specific antigen or prostatic acid phosgland. Paraprostatic cysts result from phatase, ai·e not present in caitine prostate
embryologic remnants of the female
glands.

reproductive tract found in males that

There is no effective curative ti·eatment
become fluid-filled. The signs are similar
for prostatic carcinoma in dogs. Because of

1408

PROSTATIC DISEASES
the high incidence of metastases at the time
offered some efficacy for dogs with
of iliagnosis, and the high incidence of
prostatic carcinoma in one study involving
urinary incontinence after prostatectomy in 32 dogs. Treatment with the cyclooxygendogs, total prostatectomy is not recomase inhibitors piroxicam (0.3 mg/kg/day, VetBooks.ir
mended as a treatment. Railiation therapy

PO) or carprofen (2.2 mg/kg, PO, bid)

for prostatic cancer often results in
significantly prolonged the median survival
incontinence due to radiation-induced
time of dogs with prostatic carcinoma
fibrosis of the urinary bladder. Alternative
compared with dogs receiving no treatment
means of ablating prostatic tissue such

(6.9 vs 0. 7 mo).

as transrectal high-intensity focused
ultrasound, transurethral intraprostatic

PROSTATIC CALCULI
absolute ethanol iitjections, transurethral
laser vaporization, or transurethral

When prostatic calculi occur (rarely), there
electrocoagulation have been successful
is usually some other prostatic disease as
in experimental studies but have not
well. Rarely, railiopaque prostatic calculi
been performed on dogs with prostatic
are incidental finilings on abdominal
carcinoma. A relatively simple treatment
railiographs.

CANINE TRANSMISSIBLE

VENEREAL TUMOR

Canine transmissible venereal twnors
biopsies. TVTs may be difficult to ilistinguish

(TVTs) are cauliflower-like, pedunculated,
from other round cell tumors, particularly
nodular, papillary, or multilobulated in
lymphosarcomas, when they occur in
appearance. They range in size from a small
extragenital locations. Although TVT has a
nodule (5 mm) to a large mass(> 10 cm) that
worldwide distribution, prevalence varies
is finn, though friable. The surface is often
from relatively high in some geographic
ulcerated and inflamed and bleeds easily.

regions ( eg, tropical and subtropical urban

TVTs may be solitary or multiple and are
environments) to rare in others.

almost always located on the genitalia. The

Although spontaneous regression can
tumor is transplanted from site to site and
occur, TVTs are usually progressive and
from dog to dog by' direct contact with the
treated accorilingly. Complete surgical
mass. They may be transplanted to acljacent
excision, radiation therapy, and chemoskin and oral, nasal, or conjunctiva!

therapy are effective treatments; however,
mucosae. The twnor may arise deep within
chemotherapy is considered the treatment
the preputial, vaginal, or nasal cavity and be
of choice. Vincristine sulfate (O.fHl. 7 mg/m2,
difficult to see drning cursory examination.

IV, once weekly for 3-6 wk) is reported to be

This may lead to misdiagnosis if bleeding
effective. The rate of tumor regression is
is incorrectly assumed to be hematuria or
negatively correlated with tun1or size, older
epistaxis from other causes. Initially, TVTs
age, and season. Usually, total remission can
grow rapidly, and more rapidly in neonatal
be expected by the sixth treatment.

and immunosuppressed dogs. Metastasis is

Adrian1ycin (30 mg/m2 for dogs weighing
uncommon (5%) and can occur without a

>10 kg; 1 mg/kg for dogs weighing slO kg; IV,
primary genital tumor present. When
once every 3 wk) and radiation therapy have
metastasis occurs, it is usually to tl1e
been effective for those aninlals that do not
regional lymph nodes, but kidney, spleen,
respond to vincristine.

eye, brain, pituitary, skin and subcutis,

The prognosis for total remission with
mesenteric lymph nodes, and peritoneum
chemotherapy or railiation therapy is good,
may also be sites.

unless there is metastatic involvement of

Because of their homogenous populaorgans other than skin. Complete surgical tions of large, round cells with distinctive
excision often cannot be achieved because
centrally located nucleoli, TVTs are usually
of the anatomic location of many of tllese
easily iliagnosed by cytologic examination
tumors. Recurrence is likely in such cases
of fine-needle aspirates or in1pression
unless acljunct radiation or chemotherapy
smears or by histopathologic evaluation of
is used.

RESPIRATORY SYSTEM

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INTRODUCTION 1411

Clinical Signs of Respiratory Malfunction 1412

Causes of Respiratory Malfunction 1413

Diagnostic Techniques 1415

Control of Respiratory Disease 1415

Principles of Therapy 1416

ASPIRATION PNEUMONIA 1417

DIAPHRAGMATIC HERNIA 1418

LARYNGEAL DISORDERS 1419

Laryngeal Paralysis 1420

LUNGWORM INFECTION 1421

MYCOTIC PNEUMONIA 1425

PHARYNGITIS 1426

Pharyngeal Trauma 1427

PULMONARY EMPHYSEMA 1428

RESPIRATORY DISEASES OF CATTLE 1429

Allergic Rhinitis and Enzootic Nasal Granuloma 1429

Sinusitis 1429

Necrotic Laryngitis 1429

Tracheal Edema Syndrome of Feeder Cattle 1430

Bovine Respiratory Disease Complex 1431

Enzootic Pneumonia of Calves and Shipping Fever Pneumonia 1431

Viral Respiratory Tract Infections 1433

Parainfluenza-3 Virus 1433

Bovine Respiratory Syncytial Virus 1433

Bovine Herpesvirus 1 1434

Bovine Viral Diarrhea Virus 1436

Other Bovine Respiratory Viruses 1436

Bacterial Pneumonia 1436

Mannheimia haemolytica-associated Bovine Respiratory Disease 1436

Mycoplasmal Pneumonia 1438

Chlamydial Pneumonia 1438

Contagious Bovine Pleuropneumonia 1438

Interstitial Pneumonia 1439

Acute Bovine Pulmonary Emphysema and Edema 1439

Anaphylaxis 1441

Hypersensitivity Pneumonitis 1441

Diffuse Fibrosing Alveoli tis 1442

Acute Respiratory Distress Syndrome of Feedlot Cattle 1442

1410

RESPIRATORY SYSTEM

4-lpomeanol Toxicity (Moldy Sweet Potato) and Perilla Ketone Toxicity (Purple Mint Toxicity) 1442

Toxic Gases 1442

Vena Caval Thrombosis and Metastatic Pneumonia 1442

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RESPIRATORY DISEASES OF HORSES 1443

Equine Herpesvirus Infection 1444

Equine Influenza 1447

Equine Viral Arteritis 1448

Hendra Virus Infection 1448

Pleuropneumonia 1449

Rhodococcus equi Pneumonia 1451

Acute Bronchointerstitial Pneumonia in Foals 1452

Strangles 1453

Recurrent Airway Obstruction (Heaves) 1455

Inflammatory Airway Disease 1456

Exercise-induced Pulmonary Hemorrhage 1457

Laryngeal Hemiplegia 1458

Pharyngeal Lymphoid Hyperplasia 1459

Dorsal Displacement of the Soft Palate 1459

Epiglottic Entrapment 1460

Subepiglottic Cyst 1460

Fourth Branchial Arch Defect 1461

Diseases of the Nasal Passages 1461

Nasal Septum 1461

Nasal Polyps 1461

Choanal Atresia 1462

Diseases of the Paranasal Sinuses 1462

Sinusitis 1462

Ethmoid Hematoma 1462

Sinus Cysts 1463

Guttural Pouch Disease 1463

Empyema 1463

Guttural Pouch Mycosis 1463

Guttural Pouch Tympany 1464

Rupture of the Longus Capitis Muscle 1464

RESPIRATORY DISEASES OF PIGS 1464

Atrophic Rhinitis 1465

Mycoplasmal Pneumonia 1467

Necrotic Rhinitis 1468

Pasteurellosis 1469

Pleuropneumonia 1469

Porcine Reproductive and Respiratory Syndrome 729 (GEN) Swine Influenza 1470

RESPIRATORY DISEASES OF SHEEP AND GOATS 1471

Sheep Nose Bot 1473

Contagious Caprine Pleuropneumonia 1474

RESPIRATORY SYSTEM INTRODUCTION

1411

Pasteurella andMannheimia Pneumonias 1474

Progressive Pneumonia 1475

Ovine Pulmonary Adenocarcinoma 14 77

RESPIRATORY DISEASES OF SMALL ANIMALS 1478

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Allergic Pneumonitis 14 78

Canine Influenza(F1u) 1479

Canine Nasal Mites 1480

Feline Respiratory Disease Complex 1481

Lung F1ukes 1483

Lung Nematodes 1483

Aelurostrongylus abstrusus 1483

Capillaria aerophila 1484

Filarids 1484

Neoplasia 1484

Tumors of the Nose and Paranasal Sinuses 1484

Tumors of the Larynx and Trachea 1485

Primary Lung Tumors 1485

Metastatic Tumors of the Lungs 1486

Pneumonia 1486

Pulmonary Thromboembolism 1487

Rhinitis and Sinusitis 1488

Tonsillitis 1490

Tracheobronchitis 1490

Infectious Tracheobronchitis of Dogs (Kennel Cough) 1491

RESPIRATORY SYSTEM INTRODUCTION.

The respiratory system perlorms several
particulate material. The upper airways also
functions. Most importantly, it delivers
provide for the sense of smell ( olfaction)

oxygen to the cardiovascular system for
and play a role in temperature regulation in
distribution to the body and it removes
panting animals.

carbon dioxide. Gas transfer occurs in the

Large, airborne particles are usually
alveoli of the lungs, where the air-blood
deposited on the mucous lining of the nasal
banier is a thin, permeable membrane.

passages, larynx, trachea, and bronchi, after

Failure or major dysfunction of gas transfer
which they are carried by the mucociliary
due to disease processes that compromise

"blanket" to the pharynx to be swallowed
this membrane or its air or blood supply
or expectorated. Small particles may be
have serious effects. In addition to gas
deposited as deep as the alveoli, where they
exchange, the respiratory system perlorms
are phagocytized by macrophages. Defense
nwnerous other functions, including
against invasion by microorganisms and
maintaining acid-base balance, acting as
other foreign particles is provided by anaa blood reservoir, filtering and probably tomic structures and by both nonspecific
destroying emboli, metabolizing some bioacand inununologic mechanisms (both tive substances ( eg, serotonin, prostaglancellular and humoral). These are the facdins, corticosteroids, and leukotrienes), and tors that determine species and individual
activating some substances ( eg, angiotensusceptibility to disease and that may be sin ). The respiratory system also protects
manipulated by using various management
its own delicate airways by wanning and
techniques, vaccines, antimicrobials, and
hwn.idifying inhaled air and by filtering out
other agents such as interferons and

1412

RESPIRATORY SYSTEM INTRODUCTION
lymphokines. Other mechanical factors
physiologic differences largely detemline
include the tortuosity of nasal passages;
why some pathogens affect only some
presence of hairs, cilia, and mucus; the
species ( eg, Mannheimia haemolyti,ea
cough reflex; and bronchoconstriction.

affects cattle but not pigs) and why

Cellular defenses include macrophages,
pneun1onia is very important in some species

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which phagocytize invaders and present

( cattle, pigs) but less so in others ( dogs, cats).

them ( or at least their important antigens) to

Hypoxia (lowered oxygenation, often
lymphocytes for stimulation of an inunune
termed anoxia) causes clinical signs of
response, and neutrophils, which often die
respiratory disease. It ca11 result from the
in their fight against invaders and must be
following: 1) reduced oxygen-carrying
removed along with their potentially
capacity of the blood (anemic anoxia, as
damaging enzymes. Secretory defenses
in carbon monoxide or nitrite poisoning,
include interferon for antiviral defense,
or true anemia due to various causes);
complement for lysis of invaders, surfactant

2) reduced blood flow (stagnai1t anoxia,
lining the alveoli to prevent their collapse
as in congestive heait failure or shock);
and to facilitate macrophage function,

3) insufficient alveolar ventilation,
fibronectin to modulate bacterial attachmismatching between ventilation ai1d ment, antibodies, and mucus.

perfusion, shw1t or diffusion impairment

The respiratory system must pe1fom1

(hypoxic anoxia, as in pneumonia,
many functions, preferably while expendpulmonai-y edema, chronic congestion, ing minimal energy. The required effmt is
pneumothorax, or paralysis of respirato1-y
increased by processes that oppose
muscles); or 4) inability of tissues to use
expansion of the lung (eg, fibrosis or hydro-,
available oxygen (eg, histotoxic anoxia,
chylo-, pneumo-, or hemothorax), impede
as in cyanide poisoning).

the flow of air ( eg, obstructive nasal disease,

Compensatory mechanisms for hypoxia
bronchiolitis, bronchoconst1iction,
include increased depth and rate of
laiyngeal pai·alysis, or pulmonary edema),
breathing, which is mediated by chemoreor thicken the air-blood interface ( eg, ceptors located in the cai·otid and aortic
interstitial pneumonia due to viruses or
bodies; contraction of the spleen, which
toxins, pulmonary edema).

forces more RBCs into the circulation; and

The anatomy of the respiratory tract
increased cardiac stroke volume and heart
differs mai·kedly among species in the
rate. If cerebral hypoxia develops,
following features: 1) shape of both the
respiratm-y function may be reduced even
upper and lower respiratory tract; 2) extent,
further due to depression of neuronal
shape, a11d pattern of the turbinate bones;
activity. Erythropoiesis is also stimulated

3) branching patterns of bronchi; 4) anatomy
with chronic hypoxia, although the degree
of tem1inal bronchioles, including collateral
of polycythemia is species dependent. In
ventilation; 5) lobatfon and lobulation;
addition, myocardial, renal, and hepatic

6) thickness of pleura; 7) completeness of the
functions may be reduced, as may motility
mediastinum; 8) relationship of pulmonary
a11d secretions of the intestine. If compenarteries to bronchial aiteries a11d bronchisatory mechanisms are inadequate, a oles; 9) presence of vascular'!3hunts;
vicious cycle may begin in which all

10) distJ.ibution of mast cells; a11d 11) blood
body tissues function less efficiently.

supply to the pleura Each vaiiation in
anatomic structure in1plies variation in
function, which can influence the pathogen

CLINICAL SIGNS OF RESPIRATORY
esis of respiratory disease in a particular

MALFUNCTION
species. The three main groups of species
that have sinillar subgross anatomy of the

Nasal discharge may be serous, catarrhal,
lung are 1) cattle, sheep, ai1d pigs; 2) dogs,
purulent, or hemorrhagic, depending on the
cats, monkeys, rats, rabbits, a11d guinea pigs;
degree of mucosa! or turbinate dan1age. It
and 3) horses and people.

indicates increased production of normal

Mai·ked physiologic variations also exist
secretions, sometimes supplemented by
between different species. For example,
neutrophils (purulent) or blood (hemorcattle ai·e prone to retrograde drainage from rhage). It probably also indicates decreased
the phaiynx, ai·e predisposed to pulmonary

"grooming" of the nostrils with the tongue hypertension ai1d reduced ventilation in a
when ailimals ai·e ill. Epistaxis (bleeding
cold environment, have relatively small lungs
from the nose) is often caused by vascular
witlt low tidal volw11e and functional residual
rupture, such as in mycotic infection of the
capacity, and are more sensitive to changes
guttural pouch or exercise-induced
in environmental temperatures than ai·e most pulmonary hemorrhage in horses, or by other species. These anatomic and
intranasal fungal infection or neoplasia,

RESPIRATORY SYSTEM INTRODUCTION

1413
systemic coagulopathy, vasculitis, thromas localized allergies and anaphylaxis (see bocytopenia (immune-mediated or a
p Sl l). Atrophy of the turbinates ( eg, in
result of rickettsial infection), hypervisatrophic rhinitis of pigs) removes a major cosity syndrome, hypertension, or nasal
filtration function and exposes the lungs to
trauma. Hemoptysis (the coughing up of
much heavier loads of dust and microorgan

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blood) occurs after rupture of pulmonary
isms. The nasal cavity may be obstructed by
aneurysms in the lungs of cattle with
tumors,granulon1as,abscesses,or foreign
chronic lung abscesses. Bleeding may also
bodies. Sinusitis can be a complication of
result from polyps, neoplasms, granuloupper respiratory infections, tooth root mas, trauma, thrombocytopenia, and
infection, or dehoming.

bracken fem or sweet clover toxicity.

Laryngitis, tracheitis, and bronchitis

Hyperpnea ( an increase in rate and depth
result in coughing and possibly inspiratory
of breathing) becomes dyspnea when the
or expiratory dyspnea. Coughing may be
breathing appears to be labored and causing
nonproductive if the ilTitation is caused by
distress. Hyperpnea, however, is not always a mucosa! erosion, or productive if caused sign of disease ( eg, labored breathing after
by copious exudate in the major airways.

vigorous exercise in an otherwise healthy

Severe pulmonaiy edema and emphysema
animal). Infectious respiratory diseases that
cause extreme respiratory insufficiency.

cause toxemia may further compromise the

The most common respiratory disease is
host, eg, bovine pneumonia due to M haemopneumonia, which is defined as inflamma
lytica. Dyspnea can be caused by disease
tion of the lungs. There are many systems to
of the respiratory tract itself ( eg, airway
classify the various types of pneun1onia.

obstruction, pneun10nia, bronchitis, or

One useful method is to classify according
alveolitis) or by other problems ( eg, heart
to the distribution of lesions in the lungs.

failure, acid-base imbalances, thoracic effu

Focal pneumonia has one or more discrete
sions, abnormal oxygen-carrying capacity
foci in a random pattern, eg, abscessation
of the blood, or disorders of neuromuscular
due to emboli from other sites, tuberculosis,
function). Labored inhalation seen with
or actinomycosis. Lobular pneumonia
obstructive diseases above the thoracic inlet
accentuates the anatomic pattern of

( eg, laryngeal paralysis, cervical tracheal
lobules, as in bronchopneumonia caused by
collapse) or with pleural effusions is termed

Pasteurella multocida. Lobar pneumonia
inspiratory dyspnea; labored expiration seen
covers large areas of lobes and is often
with obstructive diseases below the thoracic
severe ( eg, fib1inous pneumonic pasteurelinlet ( eg, diffuse bronchitis, principal losis of cattle). Diffuse or interstitial
bronchial collapse, or pulmonary edema) is
pneumonia often involves the entire lung,
te1med expiratory dyspnea. Fixed airway
as in maedi of sheep or in hypersensitivity
obstructions ( eg, tracheal neoplasia, foreign
reactions. The appearance or cause of a
body, or stenosis) or a combination of upper
particulai· pneumonia can be described
and lower obstructive airway diseases ( eg,
further, eg, gangrenous, parasitic (verminpleural effusion with congestive heart ous), aspiration, etc.

failure) result in both inspiratory and

Infection may develop as a result of one
expiratory dyspnea. Other responses include
or a combination of factors: 1) defense
coughing, clear exudates, and shallow
mechanisms are overwhelmed, 2) the
breathing with grunting, often associated
infectious agent is highly virulent, 3) the
with the pain of pleuritis.

size of the inoculum is large, and/or 4) the
animal's defense mechanisms are compromised. The initial problem in many CAUSES OF RESPIRATORY
pneumonias is thought to be a sudden

MALFUNCTION
change in the normal nasal bacterial flora,
which results in a sudden dran1atic increase

Congenital anomalies of the respiratory
in one or more species of bacteria. Bacterial
tract are rare but do occur. Examples
proliferation is usually caused by a breakinclude cysts in the sinuses and turbinates, down of the host defenses as a result of
tracheal hypoplasia, nasopharyngeal
stress ( eg, transportation, concurrent
turbinates, and accessory lungs. A common
illness) or cellular insult ( eg, viral infection,
cause of upper respiratory tract malfunctoxicity). These bacteria ai·e breathed into tion is rhinitis (which results in exudation
the lung in large numbers and may ovet"

of neutrophils, macrophages, and fluids),
whelm the n01mal defense mechanisms,
or erosion and ulceration ( or both) of the
localize, multiply, and initiate inflammation.

nasal mucosa. It may be caused by viral,

In addition, stress is often a precursor of
bacterial, fungal, or parasitic agents, as
viral respiratory infections, particularly in
well as by hypersensitivity reactions, such
groups of animals that have recently been

1414

RESPIRATORY SYSTEM INTRODUCTION
congregated and stressed by travel,
in cattle, causes edema, emphysema, and
handling, and mixing. Some respiratory viral
necrosis of alveolar epithelium, followed by
infections can cause temporary dysfunction
compensatory hyperplasia of these cells;
of phagocytic mechanisms of the alveolar
the effects on gas exchange result in severe
macrophages. This usually occurs several
hypoxia and dyspnea.

days after viral exposure. Inhaled bacteria

Although pneumonia is most important,

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proliferate and pneumonia ensues, often
several other thoracic conditions can cause
with an overwhelming infection and massive respiratory dysfunction. Pulmonary exudation into the alveoli.

edema, the abnormal accumulation of fluid

Pneumonia also can be caused by direct
in the interstitial tissue, airways, or alveoli
infection with viruses, bacteria, and fungi,
of the lungs, may occur in conjunction with
as well as by toxins arriving hematogcirculatory disorders, particularly left enously, by inhalation, or by aspiration of
ventricular failure or increased capillai-y
food or gastric contents.

permeability, occasionally in anaphylactic

Through natural processes, possibly aided
and allergic reactions, and in some
by appropriate therapy, the exudate may be
infectious diseases. Head trauma can cause
removed from the lungs, and the mucosa!

pulmonary edema in dogs. Dyspnea and
lesions of the air passages may heal.

open-mouth breathing may occur. Animals

However, serious sequelae can persist. Bron
stand in preference to lying down, lie only
chiectasis is a chronic lesion of the bronchi in sternal recun1bency, or may asswne a
and parenchyma characte1ized by irreverssitting position. Auscultation of the chest ible cylindrical or saccular dilatation, secondmay reveal wheezing and fluid sounds.

ary infection, and atelectasis. Ulceration of

Pleuritis (pleurisy) may be caused by
bronchioles caused by viral agents may lead
any pathogen that gains entrance to the
to organized plugs of connective tissue in
pleural cavity, but it is often an extension
small bronchioles, a lesion called bronchi
of pneumonia. Rapid shallow breathing,
olitis obliterans, which may cause
fever, and thoracic pain are suggestive of
permanent obstruction, atelectasis, and
pleuritis. Auscultation of the chest may
severe respiratory insufficiency. Constriction
reveal friction sounds.

of bronchi and bronchioles in chronic

Empyema (purulent exudate in the
allergic bronchitis and bronchiolitis results in pleural cavity) is caused by pyogenic similar clinical signs. However, administrabacteria or fungi reaching the thoracic tion of bronchodilators results in rapid relief
cavity via the blood or by extension of a
of airway obstruction in cases of allergic
pneun10nia, traun1atic reticulitis, or
bronchitis ( eg, heaves in horses). Some
penetrating wound of the chest. Cough,
chronic pneumonias ( eg, maedi in sheep) are
fever, pain, and dyspnea may be present.

characterized by firm diffuse lesions due to

Hemothorax (the accun1ulation of blood
hyperplasia of lymphoid follicles, hyperplasia in the pleural cavity) is usually caused by of smooth muscle around bronchioles,
trawna to the thorax, systemic coagulopadiffuse fibrosis, and diffuse lymphocytic thy, or thoracic neoplasia. Hydrothorax
infiltration. Aspiration pneumonia often

(the accumulation of transudate in the
leads to gangrene, with severe toxemia
pleural cavity) is usually due to interference
accompanying the acute inflammatory
with venous blood flow or lymph drainage.

reaction.

Chylothorax (the accumulation of chyle in

Most infectious pneun10nias develop in
the pleural cavity) is relatively rai·e and is
the anteroventral portions of the lungs.

seen most often in cats: It may be caused by

However, infectious agents, as well as
rupture of the thoracic duct but often is
neoplasms, can invade the lungs via the
idiopathic. The signs of all three conditions blood, which may extensively in1pair
include respiratory embarrassment ( eg,
pulmonaiy function, as can pulmonary
rapid shallow breathing with inspiratory
edema from chronic heart failure. Pleuritis,
dyspnea) and weakness.

empyema, hydrothorax, chylothorax,

Pneumothorax (air in the pleural
atelectasis, diaphragmatic hernia, or
cavity, seep 1664) may be of traumatic or pneumothorax can also seriously impair
spontaneous origin. Air can enter the
respiratory function. Pulmonary thrombosis pleural cavity through penetrating wounds leads to acute, often fulrninant, respiratory
of the thoracic wall or by extension from failure as a result of a lack of pulmonary
pulmonary emphysema or ruptured bullae.

arterial blood flow to ventilated regions of

The lung collapses if a large vol wne of air
the lung. Infarction of the lung can reduce
enters the pleural cavity. Bi.lateral pneumorespiratory function but is rare because of thorax may develop if the mediastinum is
the dual blood supply of the organ. Toxic
weak or incomplete. lnspiratory dyspnea
ir\jury, such as in 3-methylindole toxicity
or rapid, shallow breathing is evident.

RESPIRATORY SYSTEM INTRODUCTION

1415

DIAGNOSTIC TECHNIQUES

Acute nasal discharge, sneezing, or both,
may suggest the presence of infection (viral

Clinical history and physical exanlination
or bacterial) or a nasal foreign body.

should help to detemline the possible cause

Chronic nasal discharge warrants further
and site of respiratory disease. Lateral
investigation via radiography (nose,
ceIVical and thoracic radiographs may be
guttural pouches in horses), nasal CT,

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helpful when obstructive upper airway
rhinoscopy, nasopharyngoscopy, or nasal
disease or fixed airway obstruction is
biopsy. Rhinoscopy may be of limited value
suspected ( eg, tracheal foreign body,
if copious thick discharge or hemorrhage is
masses, foreign bodies, or stenosis ).

present. Bacterial cultures of nasal tissue

Thoracic radiographs are essential in any
may be of value if bacterial rhinitis is
animal exhlbiting lower respiratory signs
suspected; however, in some species (eg,

( eg, cough, rapid shallow breathing,
dogs and cats) primary bacterial rhinitis is
dyspnea), but diagnostic value may be
rare and typically occurs secondaiy to
linlited in animals that have a large thorax
other nasal conditions. Cytologic evalua

(eg, adult horses or cattle). Alterial blood
tion of nasal tissue may help diagnose nasal
gas analysis or pulse oxi.metry may help
fungal infections. Serologic testing for
assess the need for oxygen therapy in an
fungal respiratory infections may be
animal with severe dyspnea.

considered, but these findings should

When obstructive upper airway disease
correlate with the animal's clinical signs
is suspected, the diagnostic procedure of
and docun1entation of the presence of
choice is endoscopy of the respiratory tract, fungal organisms because false-positive preferably without sedation. Laryngeal
ai1d false-negative tests can occur.

function should be assessed, and the
presence of obstmctive lesions within the
nasopharynx, oropharynx, larynx, trachea,

CONTROL OF RESPIRATORY
or principal bronchi should be identified.

DISEASE

With diffuse or lobar lung disease,

Sudden dietary changes, weaning, cold,
diagnostic procedures include transtradrafts, dampness, dust, high levels of cheal wash, bronchoscopy with bronchoalainmonia, poor ventilation in general, and veolar lavage or endobronchial biopsy, and
the mixing of widely divergent age groups
transthoracic fine-needle aspirates of lung
all play a role in respiratory disease in
or lung biopsy. When bacterial pneu.monia
groups of animals. Stress and mixing of
is suspected, bacterial culture of transtraanimals from several sources should be cheal wash is recommended. Cytologic
avoided or minimized. Establishing individevaluation of transtracheal or bronchoalual animal identification, making accurate veolar lavage fluid may aid in the diagnosis
clinical and postmortem diagnose�, and
of fungal, parasitic, or allergic lw1g diseases. maintaining a record system of diagnosis Transthoracic fine-needle aspirates of lung
and treatment are important to minimize or
often are useful in the diagnosis of fungal
control outbreaks of pneumonia. Transporpneu.monia but have lower yields in the tation over long distances is another stress
definitive diagnosis of solitary pulmonary
factor that plays a major role in the patholesions. Solitary pulmonary masses often genesis of respiratory infections in large
require transthoracic Jung biopsy or
animals.

surgical excision for definitive diagnosis.

Immwlization can help control respira

Transthoracic ultrasonography is a
tory infection. However, control may be
sensitive diagnostic tool for pleural disease
compromised by improper tinling, use of

( eg, pleural effusion, pneu.mothorax) and
ineffective or inappropriate vaccines, or
for parenchymal lung disease when lesions
overwhelmingly negative management
are adjacent to the pleural surface.

practices. In most cases, severe insults to

In dogs or cats with pleural effusions,
the natural defenses cannot be reversed
thoracocentesis should be pe1formed for
later by therapeutic agents and biologicals.

cytologic and potentially nlicrobiologic

The mucosal surfaces of the respiratory
evaluation of fluid. In cats, pleural effusions tract contain lymphoid follicles that often occur with cardiac disease, so an
exchange cells with other parts of the body.

echocardiography should be perfom1ed.

However, most of the lymphocytes in the

In animals suspected to have a chylous
respiratory lining produce only IgA,
effusion, serum and fluid triglyceride levels
whereas the cells in the lymph nodes of the
should be dete1mined. Chylous effusions
respiratory tract produce IgM and IgG.

are associated with fluid triglyceride levels

Depending on the agent involved, various
greater than that in serum.

cell- and antibody-mecliated immune

1416

RESPIRATORY SYSTEM INTRODUCTION
responses occur in the respiratory tract
of tenacious ai1d viscid secretions by
and include opsonization, agglutination,
aspiration may be necessary in severe
in1mobilization, neutralization of toxins and
airway obstruction.

viruses, blockage of adherence to cells,

Antitussive agents are indicated to relieve
lysis, and chemotax:is. The type of inmmne
the discomfort associated with nonproduc

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response varies because of age, species, and
tive coughing but are contraindicated when
the means to respond to specific virulence
secretion of airway mucus is excessive.

mechanisms of the pathogens involved.

Products that contain atropine also are

Species vary in the type of in1rnune
contraindicated, at least in theory, because
response available at different sites in the
atropine increases the viscosity of airway
respiratory tract. Large antigen droplets
secretions.

may immunize the upper tract with IgA, but

Increased airway resistance caused by
small replicating particles may be necessary
bronchial smooth muscle contraction can
to immunize the lower tract. To develop
be alleviated with bronchodilators, which
adequate antibody levels to protect the
may be indicated in animals with asthm a. lungs, repeated doses of antigen plus like conditions and chronic respiratory
adjuvant, or a replicating antigen, are
disease. Methylxanthines, such as theooften necessary. These results are seldom phylline and antinophylline, are effective
achieved under field conditions ( eg, many
bronchodilators in species other than cattle
field trials using respiratory vaccines in

(and possibly dogs); however, the therapeucattle have not demonstrated statistically tic index is relatively narrow and they are
significant efficacy).

less efficacious than 132-agonists. Isoproter

Environmental management is an
enol, clenbuterol, and epinephrine are also
essential part of therapy in allergic
generally effective, and sodium cromoglyrespiratory diseases. For example, clinical cate may be used in horses with inflainmasigns in horses with heaves ( recurrent tory airway disease. Corticosteroids are
airway obstruction, seep 1455) or cattle with highly effective in allergic conditions, but hypersensitivity pneumonitis (seep 1441)

systentic use may result in adverse effects.

may be effectively controlled by preventing

Aerosolized corticosteroids are efficacious
exposure to molds present in hay.

and associated with few to no adverse
effects; however, they require an aerosol

PRINCIPLES OF THERAPY
delivery device ( eg, face mask) for proper
administration. Antihistantines can be used

See also SYSTEMIC PHARMACOTHERAPEUTICS OF
to alleviate the bronchoconstriction caused

THE RESPIRATORY SYSl'EM, p 2608.

by histantine release; however, they are of

Respiratory disease is often characterized
limited value in large animals. Bronchosby abnom1al production of secretions and pasm also can be reduced sig1tificantly by
exudates and by a reduced ability to remove
removing irritating factors, using mild
them. The primary goal of therapy is to
sedatives, or reducing periods of excitereduce the volun1e and viscosity of the secrement.

tions and to facilitate their removal. This can

In bacterial infection, antimicrobial
be accomplished by cantrolling infection
therapy should be instituted. The goal is to
and inflammation, modifying the secretions,
select either the most effective agent against
and when possible, improving postural
a specific organism or the least toxic agent of
drainage and mechanically removing the
several alternatives. Culture and sensitivity
material. Therapeutic methods include
testing of airway secretions provide a
altering the inspired air and administering
worthwhile, although not infallible, guide
expectorants, antitussives, bronchodilators,
to detemtining the appropriate antibiotic.

antimicrobials, diuretics, and other drugs.

Knowledge of tissue penetration and

However, expectorants have shown little
pharmacokinetic characteristics of the
or no beneficial effects in clinical trials.

antimicrobial agents is important as well.

Hydration should be maintained.

The following agents have proved effective

Inhalation of huntidified air may facilitate
in the listed species: cattle--oxytetracycline,
removal of airway secretions. Expectorants
cephalosporins, fluoroquinolones, macroare sometimes used with the intention of lides, florfenicol, penicillins, and sulfonaliquefying these secretions. However, they ntides; sheep and goats----oxytetracycline,
should be used in coajunction with ancillary cephalosporins, macrolides, penicillins, and respiratory therapy such as improved
sulfonamides; pigs-lincomycin, spectinopostural drainage, mild exercise, and mycin, penicillins, and sulfonamides; dogs
thoracic percussion, which (in addition to
and cats-cephalosporins, chlorainphenicoughing) encourages expectoration and col, ainoxicillin-clavulai1ate, antinoglycoremoval of secretions. Mechaitical removal sides, trimethoprirn-sulfainethoxazole,

ASPIRATION PNEUMONIA

1417
fluoroquinolones, macrolides, and
als is pennitted in some situations and is
tetracyclines; horses-penicillins, aminoglyregulated by the Anin1al Medicinal Drug cosides, cephalosporins, fluoroquinolones,

Use Clarification Act of 1994.

sulfonamides, and tetracyclines (the latter

The hypoxemia caused by most lung
with caution due to an occasional adverse
disorders usually can be corrected by

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effect of severe diaJ.Thea). Aminoglycosides
administering oxygen. However, continuare useful but can be nephrotoxic. Trimethoous administration of high concentrations prim, usually in combination with a sulfonincreases the tendency for regional amide, is useful for respiratory therapy in
resorption atelectasis, thus worsening the
most species but is not licensed for foodhypoxemia, and can cause pneumonitis on producing animals in the USA. Drugs such as its own. Hypoxemia is often accompanied enrofloxacin ( approved for small anin1als
by variable degrees of hypercapnia and
and cattle but not for horses in the USA)

acidemia. Endotracheal intubation and
and ceftiofur are effective for pneumonia.

mechanical ventilation may be necessary

Broad-spectrum antibiotics should
in animals with acute respiratory failure
be used if specific bacteria cannot be
or in animals that are comatose or apneic.

identified, and once begun, a full course

Arterial blood gas and pH determinations,
of therapy should be completed. Multiple
when practicable, are extremely valuable
antimicrobial agents should be used only
to monitor treatment.

with full lrnowledge of the potential drug

Diuretics are indicated in pulmonary
interactions. Because of residues in
edema. The osmotic diuretics have a
food-producing anin1als, veterinarians
minimal action on diuresis, carbonic
must use these products according to label
anhydrase inhibitors (eg, acetazolamide)

instructions and provide sound advice to
have a moderate effect, and loop diuretics
producers. Extra-label use of antimicrobi-

( eg, furosemide) have a profound effect.

ASPIRATION PNEUMONIA

(Foreign-body pneumonia, Inhalation pneumonia,

Gangrenous pneumonia)

Aspiration pneun10nia is a puhnonary
fine particulate food in dry environments
infection characterized by inflan1mation and
may inhale feed granules. Aspiration
necrosis due to in11alation of foreign material. pneumonia in cattle after treatinent for milk The severity of the inflan1matory response
fever is usually fatal. Cervids affected with
depends on the material aspirated, the type
clu·onic wasting disease may develop
of bacteria aspirated, and the distribution of
aspiration pneun10nia due to CNS dysfuncaspirated mate1ial in the lungs.

tion. In dogs and less frequently in cats,
aspiration pneun1onia is generally associated

Etiology: Inappropriate administration
with inhalation of oral ingesta, regurgitated
of therapeutic agents is a common cause
material, or vomitus. Common risk factors
of aspiration pneumonia in large animals
for dogs and cats include pharyngeal
and less common in dogs and cats. Liquids abnormalities ( cricopharyngeal motor given by drench or dose syringe should
dysfunction), esophageal diseases (megaenot be delivered faster than the animal sophagus, gasti·oesophageal reflux disease,
can swallow. Drenching is particularly
esophageal obstruction), weakened clinical
dangerous when the animal's tongue is
condition, and anesthesia or heavy sedation.

drawn out, when the head is held high, or

Bacteria in aspirated material may initiate
when the animal is coughing or bellowing.

acute infection or secondary infection later

In sheep, poor dipping technique with
in disease.

repeated in1mersion of the animal's head may
cause aspiration of fluid. Calves and lan1bs

Clinical Findings: A history suggesting
may inhale inflammatory debris if affected
recent foreign body aspiration within the
with diphtheritic stomatitis/laryngitis. The
past 1-2 days is of greatest value for a
muscles of deglutition may be affected in
diagnosis of aspiration pneumonia.

lambs with nutiitional myopathy. Pigs fed

Affected animals separate from the rest

1418

ASPIRATION PNEUMONIA
of the group and present with pyrexia
lw1g; it may be unilateral in animals in

104°-105°F (40°-40.5°C), a painful
which lateral recwnbency was the cause
expression, arched back, inappetance,
of aspiration, or bilateral and centered
depression, toxic mucous membranes,
on airways. In early stages, the lungs
and an increased respiratory rate (>40-60
are markedly congested with areas of
breaths/min) with a shallow abdominal
interlobular edema. Bronchi are hyperemic

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component. This is often associated with
and full of froth. The pneumonic areas tend
a purnlent nasal discharge that sometimes
to be cone-shaped, with tl1e base toward
is tinged reddish brown or green. Milk
the pleura. Suppuration and necrosis
yield is greatly reduced to zero in lactating
follow. The foci become soft or liquefied,
animals. Thoracic auscultation reveals
reddish brown, and foul smelling. There
reduced lung sounds over affected consoliusually is an acute fibrinous pleuritis, often dated lung, with increased breath sounds
with pleural exudate. Animals tl1at survive
over normal lung. In cows that aspirate
develop chronic abscesses and fibrous
ruminal contents as a consequence of
adhesions between the visceral and
becoming cast with hypocalcemia,
parietal pleura.

toxemia is usually fatal within 1-2 days.

Superficial consolidated lung and

Prevention and Treatment: Broadoverlying lesions of fibrous pleurisy can spectrum antibiotics should be used in
readily be identified on ultrasound
animals known to have inhaled a foreign
examination using either linear or sector
substance without waiting for signs of
probes connected to 5-MHz machines;
pneumonia to appear; however, this rarely
pleuritic friction rubs are not audible on
occurs in farm animals presented with
auscultation. In dogs and cats, clinical
severe clinical signs. A transtracheal wash
signs may be peracute, acute, or chronic.

can help identify the causative agent for

Cough, dyspnea, tachypnea, or exercise
which an antibiotic sensitivity can be
intolerance are seen most frequently.

obtained. Care and supportive treat-

Thoracic radiographs generally show
ment include NSAIDs such as flunixin
a bronchoalveolar pattern in gravitymeglumine. In small animals, oxygen dependent ventral lung lobes (right
therapy can be useful. Saline nebulization
cranial and middle and left cranial lobes);
and coupage may assist witl1 generating a
however, radiographic changes may not
productive cough to facilitate clearance
be seen until 24 hr after acute aspiration.

of the aspirated material. Despite all

Lesions: Aspiration pneumonia is
treatments, prognosis is poor, and efforts
usually in the anteroventral parts of the
must be directed at prevention.

DIAPHRAGMATIC HERNIA

A break in tl1e continuity of tl1e diaphragm
affected. Dogs and cats are characteristiallows protrusion of abdominal viscera into cally dyspneic in tl1e acute case. The degree
the tl1orax.

of dyspnea may vary from subclinical to
incompatible with life, depending on the

Etiology: In small animals, automobileamount of herniated viscera. If the stomach related trawna is a common cause of
is herniated, it may bloat and the animal
diaphragmatic hernia, altl1ough congenital
may deteriorate rapidly. In chronic cases,
defects of the diaphragm may also result in
systemic signs such as weight loss may be
herniation ( eg, peritoneopericardial hernia).

more prominent than respiratory signs.

In horses, diaphragmatic hernia may occur,

Physical examination findings may include
less commonly, congenitally or after trawna,
the absence of lw1g sounds and/or the
dystocia, or recent strenuous activity. Diapresence of GI sounds on auscultation of phragmatic hernias are extremely rare
the thorax. Congenital peritoneopericarin cattle.

dial hernia is most frequently an incidental
finding, although findings may be related

Clinical Findings: The signs vary,
to the respiratory or GI systems or due to
depending on the duration and species
compromised venous return to tl1e heart.

LARY NG EAL DISORDERS

1419

Horses most frequently present with acute,
or water-soluble contrast may be injected
severe colic secondary to displaced
intraperitoneally (celiogram). Radiointestines, or with respiratory signs and graphs may be difficult to obtain in horses
dyspnea. In cattle and water buffalo,
and cows; ultrasonography is useful.

diaphragmatic hernias may be associated

San1ples from abdominocentesis and
with traumatic reticulitis and herniation
thoracocentesis, electrocardiographs, and

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of the reticulum.

blood work may be obtained, and surgical
exploration of the abdominal cavity may

Diagnosis: Careful physical exan1inabe necessary for definitive diagnosis in tion, including auscultation and percusthese species.

sion, usually suggests the presence of
thoracic disease. The definitive diagnosis

Treatment: Surgical repair of the hernia
is most frequently made from radiographs.

is the preferred treatment. Other areas of

Loss of diaphragmatic contour, abdominal
trauma may be present. Optimally, the
viscera in the thorax, and displacement
animal should be stabilized before surgery.

of viscera from the abdomen may be

If the diaphragmatic tear is chronic, it is
apparent. Radiographic contrast studies
necessary to be especially careful with
may be necessary to make the diagnosis.

anesthesia, because reexpansion pulmo

Barium may be given by mouth (GI series),
nary edema is likely fatal.

LARYNGEAL DISORDERS

See a/,so LARYNGEAL f!EMJPLEGIA, p 1458.

In cattle, laryngeal edema has been seen

Laryngitis, an inflammation of the
in blackleg, urticaria, serum sickness,
mucosa or cartilages of the larynx, may
and anaphylaxis. In pigs, it may develop
result from upper respiratory tract infection
as a part of edema disease. In horses,
or by direct irritation from inhalation of dust, cattle, and sheep, laryngeal edema may smoke, or irritating gas; foreign bodies; or
lead to arytenoid chondropathy.

the trauma of intubation, excess vocaliza

Laryngeal chondropathy is a suppuration, or injury from roping or restraint tive condition of the cartilage matrix 1hat
devices (in livestock). Laryngitis may
principally affects the arytenoid cartilages; it
accompany infectious tracheobronchitis
is believed to result from microbial infection,
and distemper in dogs; infectious rhinotraoften as a sequela of inhalation of initants or cheitis and calicivirus infection in cats; infectrauma to the area In herbivores, trawna can tious rhinotracheitis and calf diphtheria in
occur when administering medications by
cattle; strangles, herpesvirus 1 infection,
bolus or drench or by ingestion of rough
viral arteritis, and infectious bronchitis in
foodstuffs; in dogs, trawna can occur from
horses; Fusobacterium necroplwium or
sticks or foreign bodies. Laryngeal chon

Trueperella pyogenes infections in sheep;
dropathy is characterized by necrosis and
and influenza in pigs.

ulceration of the laryngeal mucosa, over or

Edema of the mucosa and submucosa
just caudal to the vocal cords, and abscessais often an integral part of laryngitis and, tion within the arytenoid cartilage. Initially,
if severe, the rima glottidis may be
there is often acute laryngeal inflammation.

obstructed. Edema may also result from

Later, there is progressive enlargement of the
allergy, inhalation of irritants, or surgery
cartilages that co nun only results in a fixed
in the area. Intubation for anesthesia,
upper airway obstruction with stertorous
especially when attempted with inadbreathing and reduced exercise tolerance.

equate induction or poor technique, is

Laryngeal chondropathy is seen in horses,
likely to provoke laryngeal edema.

sheep, and cattle, most often young males.

Brachycephalic and obese dogs, and dogs There is a distinct breed predisposition with laryngeal paralysis (seep 1420)

in Texel sheep and Belgian Blue cattle.

develop laryngeal edema and laryngitis

Laryngeal contact ulcers are common
through severe panting or respiratory
in young feedlot cattle and often result in
effort during excitement or hyperthermia. necrotic laryngitis and chondropathy.

1420

LARYNGEAL DISORDERS

Clinical Findings: A cough is the principal
possible, airway patency may be estabsign of laryngitis when edema is slight and lished by passage of a pliable tube th.rough
the deeper tissues of the larynx are not
the glottis. Corticosteroids should be
involved. It is harsh, dry, and short at first,
administered to reduce the obstructive
but becomes soft and moist later and may
effect of the inflan1mato1y swellings.

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be very painful. It can be induced by

Concurrent administration of systemic
pressure on the larynx, exposure to cold or
ar1tibiotics is also necessary. In cases in
dusty air, swallowing coarse food or cold
which c01ticosteroids cannot be used,
water, or attempts to administer medicines.

NSAIDs can be given. Administration of

Vocal changes may be evident, especially
diuretic drugs, eg, furosemide, may be
in small animals. Stridor may result from
indicated to resolve laryngeal edema and,
swelling and reduced motion of the
if present, pulmonary edema. Identification
arytenoid cartilages in laryngeal chondropaand treatment of the primary disease thy. Halitosis and difficult, noisy breathing
is essential. Palliative procedures to
may be evident, and the animal may stand
speed recovery and give comfort include
with its head lowered and mouth open.

inhalation of humidified air; confinement in

Swallowing is difficult and painful. Systemic
a warm, clean environment; feeding of soft
signs ar·e usually attributable to the prin1ary
or liquid foods; and avoidance of dust. The
disease, as in infectious bovine rhinotracough may be suppressed with antitussive cheitis, in which temperatures of 105°F
preparations, and bacterial infections

( 40.5°C) may occur. Secondary systemic
controlled with antibiotics or sulfonasigns due to inappetance and dehydration mides. Control of pain with judicious use of
rapidly become apparent. Death due to
an arialgesic, especially in cats, allows the
asphyxiation may occur, especially if the
ar1inlal to eat, and thus speeds recovery.

animal is exerted.

Subtotal arytenoidectomy is an effective

Edema of the larynx may develop within remedy for laryngeal chondropathy of hours. It is characterized by increased
horses, although a return to full athletic
inspiratory effort and stridor arising from
capacity in competitive horses is unce1tain.

the larynx. Respiratory rate may slow as

Tracheolaryngostomies and permanent
the effort of breathing becomes exagge1°
tracheostomies have been used successated. Visible mucous membranes are fully to salvage cattle and sheep with
cyanotic, the pulse rate is increased, and
laryngeal chondropathy but carry
body temperature rises. Horses may sweat significant anesthetic risk. A medical profusely. Dogs with obstructions of the
alternative for rwninants is prolonged
conducting airways may show extreme
antibiotic therapy, 14-21 days of parenteral
disturbance of thermoregulation in hot
lincomycin (5-10 mg/kg), plus initial,
weather; marked hyperthermia is not
short-acting c01ticosteroids.

uncommon. Untreated animals with
marked obstruction eventually collapse

LARYNGEAL PARALYSIS
and often have signs of pulmonary edema.

Laryngeal par·alysis is common in clogs and

Diagnosis: A tentative diagnosis is
rare in cats. Signs include a c!J.y cough, voice
based on the clinical signs, auscultation
changes, noisy breathing that progresses to
of the laryngeal region, and exacerbation
marked difficulty in breathing with stress
of stridor by palpation of the larynx.

and exertion, stridor, and collapse. Regtuc

Definitive diagnosis requires laryngosgitation and vomiting may occur. Progrescopy. In conscious horses and cattle, sion of clinical signs is slow, usually taking
this can be achieved with a flexible
montlis to year-s before respiratory distress is
endoscope passed per nasum; in dogs and
evident. It is a common acquired problem in
cats, anesthesia or analgesia usually is
middle-aged to older, large and giar1t breeds
required. The history and signs usually
of dogs, eg, Labrador Retrievers, Irish
permit rapid identification of the primary

Setters, and Great Dar1es. It is seen less often
disease and the associated laryngeal
as a hereditary, congenital disease in Bouvier
involvement. Bilateral laryngeal paralysis, des Flandres, Leonbergers, Siberian Huskies, laryngeal abscess, pharyngeal trauma and

Bulldogs, and racing sled dogs.

cellulitis, and retropharyngeal abscesses

Diagnosis is based on clinical signs;
or masses can cause similar signs.

laryngoscopy under light anesthesia is
needed for confirmation. Laryngeal

Treatment: In laryngeal obstruction,
movements are absent or paradoxical
a tracheotomy tube should be placed
with respiration. Electromyography
immediately; if a tracheotomy is not
shows positive sharp waves, dene1vation

LUNGWORM INFECTION

1421
potentials, and sometimes myotonia.

therapy is surgical and directed at enlarging

Radiographs are not diagnostic. Denervathe glottic opening. Currently recomtion atrophy is seen on histologic sections mended techniques include arytenoid
of laryngeal muscles.

cartilage lateralization, ventriculocordec

Differential diagnoses include myositis,
tomy and partial arytenoidectomy,

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recurrent laryngeal or vagal nerve tumor,
castellated laryngofissure, or permanent
inflammation, myasthenia gravis, severe
tracheostomy. Studies have demonstrated
hypothyroidism, trauma, and more
that bilateral ventriculocordectomy
widespread generalized neurologic degenthrough a ventral median laryngotomy has eration. Therapy is directed at relieving
had good longterm treatment success for
signs of airway obstruction. Tranquilizasurgical treatment of idiopathic laryngeal tion and corticosteroids are effective
paralysis in dogs, and unilateral aryte-noid
temporarily in mild cases. Severe obstruclateralization appeared to be a suitable tion may require tracheotomy. Definitive
method to treat laryngeal paralysis in cats.

LUNGWORM INFECTION

(Verminous bronchitis, Verminous pneumonia)

An infection of the lower respiratory tract,

D viviparus is common in northwest
usually resulting in bronchitis or pneumo

Europe and is the cause of severe outnia, can be caused by any of several breaks of"husk" or "hoose" in young (and parasitic nematodes, including Dictyocau
more recently, older) grazing cattle. The
lus viviparus in cattle, llamas, and alpacas; lungwom1 of goats and sheep, D Jumia, is

D filaria in goats, sheep, llan1as, and
comparatively less pathogenic but does
alpacas; D eckerti in deer; D arnfieldi in cause losses, especially in Mediterranean
donkeys and horses; Protostrongylus rufe
countries, although it is also recognized as a
scens and Muellerius capillaris in sheep pathogen in Australia, Europe, and North
and goats; Metastrongylus apri, M puden

America. D fiJ,aria and D vivipmus are less dotectus, and M sal:mi in pigs; Oslerus pathogenic in alpacas and llamas, although
osleri, Crenosoma vulpis, and Eucoleus
severe infections can cause coughing,
aerophilus in dogs; andAelurostrongylus dyspnea, depression, and loss of condition.

abstrusus and E a.erophilus in cats. Other D arnjieldi can cause severe coughing in
lungworm infections occur but are less
horses and, because patency is unusual
common.

in horses (but not in donkeys), differential

Species of Dictyocaulus belong to the
diagnosis with disease due to other
superfamily Trichostrongyloidea and have
respiratory diseases can be difficult. M
direct life cycles. E aerophilus belongs to capillaris is prevalent worldwide and,
the Trichuroidea and is thought to have a
although usually nonpathogenic in sheep,
direct life cycle. The others belong to the
can cause severe signs in goats. Other

Metastrongyloidea and, except for O osleri,
lungworrn infections cause sporadic
have indirect life cycles.

infections in various animal species in

Some nematodes that inhabit the right
many countries.

ventricle and pulmonary circulation, eg,

Dictyocaulus spp: Adult females in the Angiostrongylus vasorum and Dirofilaria bronchi lay larvated eggs that hatch either
immitis, both found in dogs in certain areas of the world, may be associated with pulin the bronchi (D viviparus, D fiJ,aria) or monary disease. Clinical signs relating to
in host feces (D arnjieldi) after being
a cardiac or a pulmonary syndrome or to a
coughed up and swallowed. The infective
combination of both may occur.

third-stage larvae can develop on pasture
within 5-7 days in wann, moist conditions,
but typically in sununer in temperate

Epidemiology: Diseases caused by the
northern climates will require 2-3 wk. Once
rurninantDictyocaulus spp are of most
larvae are infective, transmission depends
economic importance. The cattle lungworrn on their dispersal away from the fecal pats.

1422

LUNGWORM INFECTION

Dispersal mechanisms are, primarily,
through ingestion of an infected terrestrial
mechanical and include rain or, in the case
snail or slug intermediate host. A abstrusus
of D viviparus and possibly D arnjieldi, by is normally acquired by cats after ingestion
the sporangia of the fungus Pilobolus. A
of a paratenic host such as a bird or rodent
proportion of infective larvae survive on
that has previously eaten the infected slug
pasture throughout the winter until the
or snail intermediate host. Adults of

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following year but, in very cold conditions,

O osleri live in nodules in the trachea of
most become nonviable. The principal
dogs, and larvated eggs laid by adults hatch
source of new infections each year is from
there. Larvae migrate up the bronchial tree
infected carrier animals, with overwintered
and may pass in the feces; however, these
larvae providing a secondary but not
are not active, are often dead or degeneratunin1portant contribution in some ing, and are not an important route of
countries. In the case of D arnjieldi,
transmission. Infection in domestic dogs is
donkeys are the prime source of pasture
mainly through saliva as the dam cleans her
contamination for horses. Clinical disease
pups. E aerophilus in dogs likely has a
in mminants usually develops on first
direct cycle, with larvated eggs being
exposure to sufficient infective larvae; the
ingested with food or water.

severity of disease and stin1ulation of an
immune response is related to the number
of larvae ingested. In cattle and sheep, this

Pathogenesis: The pathogenic effect
usually occurs during their first season at
of lungwom1s depends on their location
pasture; however, an increase in the number within the respiratory tract, the number of of older cattle affected has been reported
infective larvae ingested, and the animal's
and is attributed to the efficiency of some
immune state. During the prepatent phase
prophylactic anthelmintic regimens, which
of D viviparus infection, the main lesion is eliminates infection and prevents developblockage of bronchioles by an infiltrate of ment of a protective inm1une response.

eosinophils in response to the developing

Because transmission of infection to horses
larvae; this results in obstruction of the
requires infected donkeys (patent infections airways and collapse of alveoli distal to the rarely occur in adult horses but may occur
block. Clinical signs are moderate unless
in foals and yearlings), first infections can
large numbers of larvae are ingested, in
occur at any age in that species. Once
which case the animal may die in the
infected, adult mrninants generally become
prepatent phase with severe interstitial
immune to further disease, but a proportion
emphysema and pulmonary edema.

maintain subclinical infections during

In the patent phase, the adults in the
which they act as a source of further pasture segmental and lobar bronchi cause a contan1ination. Occasionally, when
bronchitis, with eosinophils, plasma cells,
previously infected adults or groups that
and lymphocytes in the bronchial wall; a
have not been exposed to reinfection for > 1
cellular exudate, frothy mucus, and adult
yr, and in which immunity may have waned,
nematodes are found in the lumen. The
are exposed to an overwhehning level of
bronchial irritation causes marked
infection, clinical disease may recur. In
coughing, and the entire reaction leads to
areas of Europe in which cattle are housed
increased airway resistance. A major
during winter and first grazing season calves component of the patent stage is developturned out in late April or May, the first ment of a chronic, nonsuppurative,
infections can be seen between mid June
eosinophilic, granulomatous pneumonia in
and late July, but most severe infections
response to eggs and first-stage larvae aspigenerally occur in previously unexposed rated into alveoli and bronchioles. This is
calves after development of the second
usually in the caudal lobes of the lungs and
generation of infective larvae on pasture
is severe when widespread; in combination
between August and early October.

with the bronchitis, death may result.

Interstitial emphysema, pulmonary edema,

Other Species: Metastrongylus spp in
and secondary bacterial infection are
pigs require an earthworm intermediate
complications that increase the likelillood
host; thus, infection is confined to pigs with of death. Survivors may suffer consideraccess to pasture and may become more able weight loss.

common in previously uncommon areas

If the animal survives until the end of
as a result of organic farming methods.

patency (2-3 mo for D viviparus ), most or

M capillaris andPrufescens in sheep and
even all of the adult worms are expelled,
goats require slugs or snails as intermediand the cellular exudate resolves over the ate hosts, which must be eaten for infection ensuing 4 wk. Most animals recover unless to occur. C vulpis is acquired by dogs
secondary infection develops in the

LUNGWORM INFECTION

1423
damaged lungs during the postpatent

In cats, A abstr1tsus produces nodular
phase. In a few animals, clinical signs are
areas of granulomatous pneumonia in the
exacerbated in the postpatent phase due
caudal lobes tl1at, if sufficiently generalized,
to development of a diffuse, proliferative
can be clinically significant and occasionally
alveoli tis characterized by hyperplasia of
fatal; a notable feature is the hypertrophy
the type II alveolar epithelial cells. The
and hyperplasia of the smooth muscle in tl1e

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cause is unlrnown, but it is seen much less
media of pulmonary arteries and arterioles.

often in cattle treated with anthelmintics

The nodules of O osleri, found in the
with a persistent action against D viviparus mucous membrane of the trachea and large such as the macrocyclic lactones ivennecbronchi, can produce extreme airway tin, doramectin, eprinomectin, and
irritation and persistent coughing. C vulpis
moxidectin.

infections result in chronic bronchitis and

D jUaria is similar to D viviparus, but bronchiolitis, which leads to chronic
interstitial emphysema is not a common
coughing. E aerophilus infections in dogs
complication. Bronchial lesions predomiare usually well tolerated but may ca.use nate in D arnfieldi infections; when an
chronic tracheitis and bronchitis.

alveolar reaction occurs, as in donkeys or

In adult animals not previously exposed
foals, there are lobular areas of overinflato infection, the lesions and pathogenesis tion due to intermittent obstruction of
are the same as in young animals. However,
small bronchi.

in adults with some degree of inmmnity,

The pathogenic effect of the other
reexposure to the parasite (eg, husk in
lungwonns has a similar basis, but
adult cattle) can result in different lesions.

frequently such severe clinical signs are

Despite the immune response, many larvae
not produced, perhaps because of a more
reach the lungs before they are killed in
restricted localization in the lungs and less
the tem1inal bronchioles and alveoli.

severe infections. The patent phase and the

Larvae not killed in the terminal bronchiassociated lesions last >4 mo for some oles may reach the bronchi and cause a
lungworms (M apri and A abstrusus) but bronchitis characterized by marked
can be >2 yr (M capillaris ). The lesions in eosinophilic infiltration of the bronchial
pigs with metastrongylosis are a combinawalls and greenish yellow exudate in the tion of localized bronchitis and bronchiolilumen comprising eosinophils, other tis with overinflation of related alveoli,
inflanm1atory cells, and parasitic debris.

usually at the tips and midway along the

The reaction associated with this process
diaphragmatic lobes. Associated with
can lead to severe clinical signs if the
the mass of nematodes in the lumen is
nodules are nwnerous and the eosinophilic
hypertrophy and hyperplasia of bronchibronchitis extensive; this is responsible for olar and alveolar duct smooth muscle with
the reinfection phenomenon.

marked mucous cell hyperplasia. Near the
end of the patent period (as adult worms

Clinical Findings: Signs of lungworm
are killed), gray-green lymphoid nodules
infection range from moderate coughing

(2-4 mm) are formed; fragments of dead
with slightly increased respiratory rates to
worms may be seen microscopically in
severe persistent coughing and respiratory
these nodules composed of lymphocytes
distress and even failure. Reduced weight
and plasma cells surrounding a central
gains, reduced milk yields, and weight loss
zone of eosinophils.

accompany many infections in cattle, sheep,

In M capillaris and P rufescens
and goats. Patent subclinical infections can
infections, chronic, eosinophilic, granuoccur in all species.

lomatous pneun10nia seems to predomi

The most consistent signs in cattle are
nate; the reaction is in the bronchioles
tachypnea and coughing. Initially, rapid,
and alveoli that contain the parasites, their
shallow breathing is accompanied by a
eggs, or larvae. They are surrounded by
cough that is exacerbated by exercise.

macrophages, giant cells, eosinophils, and

Respiratory difficulty may ensue, and heavother immunoinflammatory cells, which ily infected animals stand with their heads
produce gray or beige plaques (1-2 cm)

stretched forward and mouths open and
subpleurally in the dorsal border of the
drool. The animals become anorectic and
caudal lung lobes. Small (1-2 mm), greenish, rapidly lose condition. Lung sounds are nodular lesions may also develop. The effect particularly prominent at the bronchial of these lesions in sheep is minor, perhaps
bifurcation. In adult dairy cattle, milk yield
because of tl1e predominantly subpleural
drops severely, and abnormal lung sounds
location. This infection represents the
are heard over the caudal lobes. The
lower end of the pathogenic spectrunl for
reinfection phenomenon in adult dairy
lungworms.

cattle is usually seen in the fall; although

1424

LUNGWORM INFECTION
less severe than in initial infections, the
antibiotic therapy to ameliorate the condisigns are widespread coughing and tion. Adults of Dictyocaulus spp and M
tachypnea and a marked drop in milk yield.

apri ai·e readily visible in the bronchi

The signs in llamas, alpacas, sheep, and
during the patent phases of infection.

goats infected with D filaria are similar to However, examination of smears from

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those in cattle. Pulmonary signs usually
bronchial mucus or his to logic sections
are not associated with M capillaris or from lesions may be necessary to confirm

P rufescens in sheep, but the former
the diagnosis during other stages of
can affect goats similarly to D jilaria.

lungworm infection (and also for other

D arnfieldi is associated with coughing,
lungworms).

tachypnea, and unthriftiness in older

Bronchoscopy can be used to detect
horses but with few if any signs in foals
nodules of O oslmi or to collect tracheal
or donkeys.

washings ( dogs and horses) to exanline for

The main clinical sign of metastrongyloeggs, laivae, and eosinophils.

sis in pigs is a persistent cough that may

Necropsy should include examination of
become paroxysmal.

the trachea, particularly at the bifurcation,

Coughing and dyspnea occur with
for O osleri and the lesions they induce.

A abstrusus infections in cats and O osleri or C vulpis infections in dogs. Fatalities are Treatment: Several drugs are useful
relatively uncommon with these lw1gto treat lungworms (see TABLE 1). The wonns, although they do occur in kittens.

benzimidazoles (fenbendazole, oxfendazole, and albendazole) and macrocyclic Diagnosis: Diagnosis is based on
lactones (ivermectin, doramectin,
clinical signs, epidemiology, presence of
eprinomectin, and moxidectin) are
first-stage larvae in feces, and necropsy
frequently used in cattle and are effective
of animals in the same herd or flock.

against all stages of D v'iviparus. These

Bronchoscopy and radiography may be
drugs are also effective against lunghelpful. Larvae are not found in the feces worms in sheep, horses, and pigs.

of animals in the prepatent or postpatent

Levamisole is used in cattle, sheep, and
phases and usually not in the reinfection
goats, but treatment may need to be
phenomenon (D viviparus). ELISA tests
repeated 2 wk later because it is less
are available in some countries. The test
effective against laivae during the early
is mainly of use in detecting cattle that
stages. Topical fonnulations containing
have not been exposed, rather than as a
moxidectin, selamectin, or emodepside
differential diagnostic tool in acute
and oral fenbendazole have been used
respiratory disease. In the early stages
successfully in cats for A abstrusus.

of an outbreak, larvae may be few in

O osle1i in clogs is a problem, but there is number. First-stage larvae or laivatecl
evidence that fenbendazole and ivermeceggs can be recovered using most fecal tin ai·e effective if treatment is prolonged
flotation techniques with the appropriate

(fenbendazole). Injectible doramectin
salt solutions; however, larvae will
along with removal of as many nodules
crenate if allowed to-sit for a long time
as possible is the current treatment of
on the slide before examination, making
choice. E aerophilus in dogs and cats is
identification difficult. Bronchial lavage
similarly difficult to treat, but success has
can reveal D arnfieldi infections in
been reported with ivermectin, fenbendahorses. A convenient method to recover zole, or selamectin.

larvae is a modification of the Baermann

Animals at pasture should be moved off
technique, in which large fecal samples
infected pasture, and supportive therapy

(25-30 g) are wrapped in tissue paper or
may be needed for complications that can
cheese cloth and suspended or placed in
ai·ise in all species.

water contained in a beaker. The water at
the bottom of the beaker is examined for

Control: Lungworm infections in herds
larvae after 4 hr; in heavy infections,
or flocks are controlled primarily by
laivae may be present within 30 min.

vaccination or anthelmintics. Oral

In domestic pets, detection of firstvaccines are available in Europe for stage larvae in the feces, either on

D viviparus (northeastern areas) and
flotation or with the Baermann technique,

D jilaria (southeast). Two doses of
is still the diagnostic technique of choice.

irradiated infective larvae are given 4 wk

However, in dogs, cats, and horses,
apart, with the second dose given at least
because of the relative infrequency of

2 wk before the start of grazing or
infection in many areas, lungworms
exposure to probable infection. Used
may be considered only after failure of
properly, they prevent clinical disease,

MYCOTIC PNEUMONIA

1425

IH=i•il RECOMMENDED TREATMENTS FOR LUNGWORMS

Parasite

Host

'Ireatment8

Dictyocaulus

Cattle

Ivem1ectin, doramectin, moxidectin, eprino

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viviparus
mectin, fenbendazole, albendazole, levamisole

DfiJ,a

Ivermectin, doramectin, moxidectin, eprino
ria

Sheep, goat
mectin, fenbendazole, albendazole, levamisole

D arnjieldi

Horse, donkey Ivermectin, moxidectin

Metastrongylus spp

Pig

Ivem1ectin, doramectin, moxidectin,
fenbendazole, levamisole

Aelurostrongylus

Cat

Fenbendazole, emodepside, moxidectin,
abstrusus
selamectin

Oslerus osleri

Dog

Fenbendazole, ivermectin, doramectin

Eucoleus aerophilus

Dog, cat

Fenbendazole (dog), selamectin (cat)b

Crenosoma vulpis

Dog

Fe ban tel, fenbendazole, milbemycin oxin1e,
moxidectin
a In severe cases, NSAIDs may also be helpful.

b Anecdotal evidence for efficacy but no published evidence or label recommendations.

but some vaccinated animals may become
immunity to the parasite. The use of
mildly infected to the extent that larvae are multiple treatments may delay immunity excreted and perpetuate further infection.

to D viviparus until the animal is adult,

Anthelmintic prophylaxis has become
when infection (albeit usually less
feasible with the advent of anthelmintics
severe) can occur. However, these
with prolonged activity ( eg, ivermectin,
methods have become popular in that GI
doramectin, moxidectin, eprinomectin).

parasites are controlled simultaneously.

With persistent anthelmintics, two or

Other more sporadic infections can be
three treatments during the grazing
controlled more easily by man�gement, eg,
season, the timing of which depends on
avoidance of grazing horses with donkeys,
local grazing practice and epidemiology,
indoor husbandry of pigs, and by not
are effective and may, by disrupting
mixing sheep and goats on the same
developing infections, stimulate
grazing.

MYCOTIC PNEUMONIA

Fungal infection of the lung may result in an
agents of mycotic pneumonia in immunoacute to chronic active, pyogranulomatous compromised hosts (see also FUNGAL
pneumonia.

INFECTIONS, p 632). Infection is typically
caused by inhalation of spores, which can

Etiology: Cr1.Jptococcus neoformans,
lead to hemolymphatic dissemination.

Histoplasma capsulatum, Coccidioides

Pulmonary tissues and secretions are an
immitis, Blastomyces dermatiditis,
excellent environment for these organ

Pneumocystisjiroveci, Aspergillus spp,
isms. Aspergillosis is most commonly

Candida spp, and other less common
associated with sinonasal infection in
fungi have been identified as causative
dogs or sino-orbital infection in cats,

1426

MYCOTIC PNEUMONIA
with systemic infection being quite rare

Lesions: Multifocal to coalescing
and seen only in immunocompromised
lesions of granulomatous to pyogranuindividuals. Cryptococcosis most lomatous inflammation are present in the
commonly affects the nasal cavity in
lungs or other affected organs. Abscess
cats, with CNS infection less commonly
fom1ation and cavitation may be seen in
encountered in dogs and cats. The source
conjunction with yellow or gray areas of

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of most fungal infections is believed to be
necrosis. Causative organisms are present
soil-related rather than horizontal
within macrophages or areas of intense
transmission.

inflammation.

Clinical Findings: Mycotic pneumonia

Diagnosis: Thoracic radiographs often
is more commonly seen in small animals
disclose a diffuse pattern with tracheothan in large. The most common course bronchial lymphadenopathy in dogs or
of disease is chronic. A short, productive
large focal pulmonary granulomas in cats.

cough is often present. A thick, mucoid

If bone pain is present, skeletal radiograto mucopurulent nasal discharge may phy shows osteolysis with periosteal
be present. As the disease progresses,
proliferation and soft-tissue swelling at
dyspnea, emaciation, and generalized
infected sites. Abdominal radiography may
weakness become increasingly evident.

reveal granulomas or lymphadenopathy.

Respiration may become abdominal, with

The clinical diagnosis can be confinned
crackles on auscultation. Generalized
with impression smears of cutaneous
lymphadenopathy is common in dogs.

draining tracts, fine-needle aspirate of the

Multiple cutaneous and subcutaneous
lung, lymph node aspirates, or CSF tap
nodules with draining tracts may be seen

(cryptococcosis). Special stains can be
with blastomycosis in dogs. Blastomycoused to highlight the organisms.

sis is often associated with emaciation
and diarrhea in dogs, with skin lesions

Treatment: Treatment of mycotic
common in cats. Coccidiomycosis is often pnemnonia is often lengthy. Drugs of choice associated with severe bone pain due to
include itraconazole, fluconazole ( cryptococosteomyelitis in dogs, with skin lesions cosis), lipid-complexed amphotericin B, and
common in cats. Uveitis or granulomaterbinafine (aspergillosis). Newer generation tous chorioretinitis may accompany
azole antifungals such as voriconazole or
dimorphic fungal infections. (See also
posaconazole are more effective for resistant

FUNGAL INFECTIONS, p 632.)

infections or systemic aspergillosis.

PHARYNGITIS

Pharyngitis is an inflammatory condition
drink but may have difficulty swallowing
of the walls of the oro- or nasopharynx.

and appear dysphagic. Animals with

Pharyngitis may develop secondary to
secondary peripharyngeal cellulitis and
viral or bacterial infections of the upper
abscessation may be acutely dyspneic
respiratory tract, eg, strangles in horses
secondary to pharyngeal obstruction. For
and distemper in dogs.

example, foals affected with suppurative

In most species, a common pharynx is
pharyngitis secondary to abscessation
present at times other than deglutition.

of the retropharyngeal lyn1ph nodes can

The unique caudal pharyngeal-laryngeal
become acutely dyspneic and require an
anatomy of horses shows complete separaemergency tracheotomy.

tion of the pharynx into two components,
the nasopharynx and the oropharynx.

(See also PHARYNGEAL LYMPHOID HYPERPLASIA,

Diagnosis: The diagnosis of pharyngitis
p 1459.)

can be made with a complete physical
examination, radiography of the skull,

Clinical Findings: Animals affected with
endoscopic evaluation of the pharynx,
pharyngitis have a normal desire to eat and and microbial cultures of draining

PHARYNGITIS

1427
abscesses or nasopharyngeal swabs for
viral isolation. In small animals, oral pain
and resistance to having the mouth
opened may indicate retropharyngeal
abscessation and the presence of a
penetrating foreign body or oral or tonsil

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lar neoplasia. Abnormal pharyngeal tissue
should be biopsied and submitted for
histopathology to exclude pharyngeal
neoplasia. In small animals, oral examination and/or endoscopic examination is the best diagnostic tool for pharyngitis. In
large animals, the diagnosis of pharyngitis
is easily made by endoscopic examination
of the upper respiratory tract.

Treatment: Bacterial pharyngitis should

Stylohyoid fracture in a horse. Courtesy of Dr.

be treated with systemic antimicrobials

Sameeh M. Abutarbush.

based on microbial culture and sensitivity
testing. Abscesses should be drained and
lavaged when appropriate. Viral-induced
pharyngitis should be managed with antimicauses, such as incorrect passage of crobials to prevent secondary bacterial
balling guns or attempts to pass probangs
infections. Animals affected with either
per os. Affected cattle develop severe
bacterial or viral pharyngitis should be
swelling of the head and proximal neck
treated with NSAIDs. Pharyngitis secondsecondary to diffuse cellulitis caused by ary to foreign bodies should be resolved
penetration of the pharyngeal mucosa.

with removal of the offending object and

Feed frequently becomes impacted in
effective surgical drainage accompanied
these areas and can lead to acute
by excision of necrotic tissue.

dyspnea. Management of pharyngeal

Racehorses affected by pharyngeal
trauma in ruminants should include the
lymphoid hyperplasia can be treated with placement of a temporary rumen fistula to topical and systemic anti-inflammatory
provide extraoral alimentation while the
agents such as flunixin meglumine,
pharyngeal defect heals. Treatment
phenylbutazone, or dexamethasone. A
should also include systemic antimicrobicommonly used topical anti-inflammaals and anti-inflammatory agents. Some tory treatment includes prednisolone,
affected animals may also require surgical

DMSO, glycerin, and nitrofurazone. Large drainage of accumulated feed anct pharyngeal masses can also be treated
abscessation secondary to the foreign
with contact diode laser photoablation.

material.

Some veterinarians have also found

In small animals, oropharyngeal
hyperimmunization helpful in managing
foreign bodies are quite common in
pharyngeal lymphoid hyperplasia.

dogs but less so in cats. However, cats

Calicivirus infections in cats may cause are prone to ingestion of linear foreign mild, moderate, or severe ulceration of
bodies, which may become entangled
the oropharyngeal mucosa. Although
with the tongue and can be identified
specific antiviral therapies are not
with a careful oral examination under
available, affected cats should be treated
sedation or general anesthesia.

with systemic antimicrobials to prevent

Penetrating foreign bodies include
secondary bacterial infection. Animals
pins, needles, and pieces of stick or
that cannot maintain their own hydration
bone fragments. Small animals susbecause of severe mucosa! ulceration pected to have oropharyngeal foreign
may require nutritional and electrolyte
bodies should be evaluated with an oral
supplementation either intravenously or
examination while sedated or anestheby extraoral alimentation.

tized and with radiographs or ultrasound to identify all foreign material PHARYNGEAL TRAUMA
present. Once identified, pharyngeal
foreign bodies may be removed directly

Pharyngeal trauma in ruminants is not
via the oral cavity or approached
uncommon secondary to iatrogenic
externally.

1428

PULMONARY EMPHYSEMA

PULMONARY EMPHYSEMA

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Two major forms of pulmonary emphysusceptible to interstitial emphysema.

sema are generally recognized. Alveolar

Pulmonary diseases associated with airway
emphysema is abnom1al permanent
obstruction and dyspnea, such as bovine
enlargement of air spaces distal to the
respiratory syncytial virus infection, acute
terminal bronchiole and destruction of
respiratory disease syndromes, such as
alveolar septa! walls without apparent
acute pulmonary edema and emphysema
fibrosis. Interstitial emphysema is the

(seep 1439), and moldy sweet potato toxicity presence of air within the supporting

(seep 1442) are commonly associated with
connective tissue stroma of the lung
interstitial emphysema. Severe interstitial

(interlobular, subpleural, mediastinal,
emphysema can cause large gas bullae in
subcutaneous).

all parts of the lung and subcutaneous
emphysema as air dissects along fascial
planes from the lungs through the mediasti

Epidemiology and Pathogenesis:

mun and thoracic inlet to the subcutis of

Emphysema affects -10% of people with
the back.

chronic obstructive pulmonary disease;
the main risk factors are tobacco smoke
exposure and a,-antitrypsin deficiency. In

Clinical Findings and Diagnosis:

animals, it typically occurs secondary to

Clinical signs depend on the primary
a primary obstructive pulmonary disease
disease process. Often, affected animals
process. While the pathogenesis of
present with labored breathing, and
pulmonary emphysema is not fully
auscultation reveals abnormal breath
understood, at least three mechanisms
sounds such as wheezes and crackles due
have been suggested: 1) an in1balance
to airway disease. The area of thoracic
between protease secreted by neutrophils
auscultation is typically enlarged due to
and macrophages, and antiprotease
lung hyperinflation. At necropsy, the lungs
activity results in destruction of alveolar
do not collapse and stay overinflated.

walls and interstitial matrix; 2) inappropri

Histology is the only method to differenate maintenance of lung structure and tiate lung overinflation secondary to
repair follows injury; and 3) the condition
pulmonary emphysema from air trapping
develops secondary to obstruction of
due to airway obstruction from chronic
airways on expiration: due to chronic
bronchiolitis or bronchitis. Air bubbles
bronchitis/bronchiolitis or congenital

(bullae) of various sizes may be seen in the
abnormality of the airway wall. This
subpleural space and interstitium, as well
creaLes a "check valve" lesion, in which air as around the kidneys and pericardia! sac
is able to enter alveoli on inspiration or
in cattle with emphysema. Pulmonary
through collateral ventilation but is unable
emphysema affects a small percentage of
to leave freely and causes air trapping.

horses with recurrent airway obstruction

Recurrent airway obstruction, or

( -12%). Lesions may develop as subpleural

"heaves" in horses (seep 1455), is associbullae or emphysema localized to a lobe or ated with chronic bronchitis and bronchidiffused lesions.

olitis, resulting in alveolar hyperinflation

Minor degrees of emphysema may
by air trapping. The condition is partially
precede death if there was a prolonged
reversible with bronchodilators; however,
struggle or exaggerated respiration. These
a small subset of horses develop alveolar
agonal changes should be differentiated
emphysema presumably from chronic
from antemortem lesions.

overdistention of alveolar walls and
protease/antiprotease inlbalance associated with pulmonary inflammation.

Treatment: Emphysema is an irreversible

Congenital lobar emphysema of dogs (as
lung lesion; however, therapy directed
seen in the Pekingese breed) occurs secondtoward the prinlary disease process may ary to aplasia or hypoplasia of bronchiolar
result in significant improvement of clinical
cartilage that collapses during expiration,
signs, especially by targeting airway
leading to air trapping. Because of wellobstruction with administration of developed interlobular septa and lack of
bronchodilator and anti-inflan1matory
collateral ventilation, cattle are particularly
drugs.

RESPIRATORY DISEASES OF CATTLE

1429

RESPIRATORY DISEASES OF CATTLE

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Respiratory disease is among the most
bone lysis. Cytology of aspirated material
economically important diseases of cattle
from the affected sinus may reveal purulent
in production on a worldwide basis.

material.

Treatment: Sinusitis is treated by draining
the affected sinus. Trephine sites should be
selected carefully, using approptiate
anatomic landmarks. If an infected tooth is
the cause of maxillary sinusitis, the tooth

Allergic rhinitis is an uncommon disease of
can be repelled through a sinusotomy site
cattle that, when chronic, may lead to granucreated with a trephine. Once drainage has loma formation. The etiology is an allergic
been established, the sinus can be lavaged
reaction to pollen or fungal spores. Signs
daily with antiseptic solutions. Treatment
are seasonal and occur under warm, moist
with parenteral antibiotics is indicated if
conditions; they include rhinorrhea,
systemic signs are present. NSAIDs can
sneezing, and a sudden onset of dyspnea. In
be given for pain relief, if needed. The
the chronic stage, multiple granulomas may
prognosis is guarded.

fom1 on the mucosa.I surface of the nasal
cavity. Cytologic examination of nasal

Control: The best control method is to
discharges may reveal eosinophils.

dehom calves at a young age using a closed

Treatment should focus on removing the
dehoming technique. If this is not possible,
allergen or removing the animal from the
close attention should be paid to disinfecallergen. Treatment with cotticosteroids tion of surgical instruments between
to block tl1e hypersensitivity reaction is a
animals, dust control, and fly control.

consideration.

(Calf diphtheria, Laryngeal necrobacillosis)

Fusobacterium necrophorum, a gram

Etiology: Sinusitis in cattle typically
negative, nonsporefonning anaerobe, is
involves the frontal or maxillary sinus.

a nonnal inhabitant of the alimentary,

Frontal sinusitis is usually associated with
respiratory, and genital tract of animals. The
dehoming, and maxillary sinusitis with
organism is an opportwustic pathogen that
infected teeth. Numerous bacteria have
causes several necrotic conditions in
been isolated from sinusitis infections in
animals (ie, necrobacillosis ), including
cattle.

necrotic laryngitis.

Necrotic laryngitis is an acute or chronic

Clinical Findings: Frontal sinusitis may

Fnecrophorum infection of the laryngeal
occur immediately after dehoming while
mucosa and cartilage of young cattle,
the site is still open or months later after the
characterized by fever, cough, inspirato1y
dehoming site has healed. The condition is
dyspnea, and stridor. It occurs prin1arily in
most often unilateral. Signs may include
feedlot cattle 3--18 mo of age; however, cases
anorexia, pyrexia, unilateral or bilateral
have been documented in calves as young as
nasal discharge, changes in air flow through

5 wk and in cattle as old as 24 mo. Cases are
the nasal passages, and foul breath. Head
seen worldwide and year round but appear
carriage may be abnonnal. In longstanding
to be more prevalent in fall and winter.

cases of frontal sinusitis, there may be
distortion of the frontal bone, exophtha.1-

Etiology: Predisposing factors are
mos, and neurologic signs.

not fully understood. F necrophorum,
commonly isolated from laryngeal lesions

Diagnosis: Diagnosis can usually be made
of affected cattle, is unable to penetrate
on the basis of clinical signs. Percussion
intact mucous membranes. Laryngeal
may reveal a dull sound over the affected
contact ulcers, a common finding in
sinus. Radiographs may reveal fluid in the
slaughtered cattle, are thought to provide
sinus, the presence of dental disease, or
a portal of entry for F necrophorum.

1430

RESPIRATORY DISEASES OF CADLE

Transmission, Epidemiology, and
cartilage associated with a draining tract

Pathogenesis: Necrotic laryngitis is
swTounded by granulation tissue.

most common where cattle are closely
confined under unsanitary conditions or

Diagnosis: Clinical signs are usually
in feedlots. The prevalence in feedlot
sufficient to establish a diagnosis. However,

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calves is estimated to be 1 o/o-2%. Most
because numerous other conditions can
cases are sporadic and occur year round,
cause signs of upper airway obstruction,
but disease peaks in fall and winter.

the larynx should be visually inspected to

Mixed upper respiratory tract infections
confirm a diagnosis. This can be accom

( caused by infectious bovine rhinotraplished by means of an orally inse1ted cheitis virus and parainfluenza-3 virus;
speculum, laryngoscopy, endoscopy, or

Mycoplasma spp; and bacteria, including
radiography, but care must be exercised to

Pasteurella and Haemophilus), and the avoid fimher respiratory embarrassment.

coughing and swallowing associated with

A tracheostomy should be performed
these infections, may predispose feedlot
before laryngoscopic or endoscopic
cattle to develop laryngeal contact ulcers.

exan1ination in cattle with severe inspira

These ulcers on the vocal processes and
tory dyspnea. Differential diagnoses include
medial angles of arytenoid cartilages are
pharyngeal trauma; severe viral laryngitis
thought to provide a portal of entry for

( eg, infectious bovine rhinotracheitis);

F necrophorum.

actinobacillosis; and laryngeal edema,

F necrophorum causes inflammation,
abscesses, trauma, paralysis, or tumors.

necrosis, and edema in the laryngeal
mucosa, resulting in variable narrowing of

Treatment and Control: Oxytetracythe rin1a glottidis and inspiratory dyspnea cline (11 mg/kg, IV or SC, bid, or 20 mg/kg
and stridor. If infection extends into the
of long-acting tetracycline, SC, every 72 hr)

laryngeal cartilage, laryngeal chondritis
or procaine penicillin (22,000 U/kg, IM, bid)

develops, which may lead to a chronically
are the antin1icrobials of choice. NSAIDs
defo1med larynx. Pharyngeal invasion by

(aspirin, 100 mg/kg, PO, bid; flunixin,
the organism causes discomfort character1.1-2.2 mg/kg, IV, once daily or divided bid; ized by painful swallowing motions.

or ketoprofen, 3 mg/kg/day, IM or IV, for up

Systemic signs of illness have been
to 3 days) are used to decrease the fever and
attributed to the exotoxin produced by
laryngeal inflammation and edema. A single

F necrophorum.

dose of dexamethasone (0.2-0.5 mg/kg,

IV or IM) may be used to decrease laryngeal
edema in aninlals with severe respiratory

Clinical Findings: Initially, a moist,
distress. A tracheostomy is indicated in
painful cough is noticed. Severe inspiratory
cattle with severe inspiratory dyspnea.

dyspnea, characterized-by open-mouth

Good nursing care should be provided.

breathing with the head and neck extended,

Intravenous fluids may be required in dehyand loud inspiratory stridor are common drated animals. The prognosis is good for
findings. Ptyalism; frequent, painful
early cases treated aggressively; chronic
swallowing motions; bilateral, purulent
cases require surgery under general
nasal discharge; and a fetid odor to the
anesthesia to remove necrotic or granulabreath may also be present. Systemic tion tissue and to drain laryngeal abscesses.

signs may include fever (106°F [41.1 °Cl),

A 6()0A, success rate has been reported for
anorexia, depression, and hyperemia of the
surgical intervention in advanced cases.

mucous membranes. Untreated calves die

There are no specific control measures
in 2-7 days from toxemia and upper airway
for necrotic laryngitis; however, the
obstruction. Longterm sequelae include
proposed pathogenesis suggests that
aspiration pneumonia and permanent
control measures for common respiratory
distortion of the larynx, resulting in a
pathogens may be beneficial.

clU"onic harsh cough and inspiratory
dyspnea.

Lesions: Lesions are typically located
over the vocal processes and medial angles
of arytenoid cartilages. Acute lesions are
characterized by edema and hyperemia
surrounding a necrotic ulcer in the laryngeal Tracheal edema syndrome is characterized mucosa; lesions may spread along the vocal
by extensive edema of the mucosa and
folds and processes to involve the
submucosa in the dorsal membrane of the
cricoarytenoideus dorsalis muscle. In
lower trachea. The etiology is unknown.

chronic cases, lesions consist of necrotic

Proposed causes include respiratory viruses

RESPIRATORY DISEASES OF CATILE

1431
and bacteria, trauma to the trachea from
associated with BRO. An initial pathogen
feed bunks, passive congestion and edema

(eg, a virus) may alter the animal's
from excessive fat accumulation in the
defense mechanisms, allowing colonizathoracic inlet, hypersensitivity reactions, tion of the lower respiratory tract by
and mycotoxins.

bacteria..

The condition occurs in heavy feeder cat

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tle in the later two-thirds of the feeding

ENZOOTIC PNEUMONIA OF
period throughout North America but may
be most severe in the summer in southern

CALVES AND SHIPPING FEVER
plains (USA) feedlots. Onset is sudden and

PNEUMONIA
appears to be associated with an increase
in respirations stimulated by hot weather

Enzootic pneumonia and shipping fever
or exercise. The initial signs a.re a loud
pneumonia. share many similarities in their
inspiratory noise ( stridor) and the onset
respective etiologies and pa.thogeneses and
of dyspnea.. Forced movement ca.uses the
in general measures for control and
respiratory distress to worsen. The cattle
prevention.

become cyanotic and typically collapse and
die of asphyxiation in <24 hr. The disease is

Enzootic Pneumonia of Calves
usually very sporadic, with small numbers

(Dairy calf pneumonia, Summer pneumonia
of animals in the population affected.

of beef calves)

In the a.cute form, necropsy lesions

Enzootic pneumonia. of calves refers to
include edematous and/or hemorrhagic
infectious respiratory disease in calves.

thickening of the submucosa. and mucosa

The term "viral pneumonia. of calves" is
of the dorsal trachea extending from the
sometin1es used but is not preferred based
mid cervical area to the thoracic inlet.

on the current understanding of etiology

There is extensive hemorrhage in the
and pathogenesis. Enzootic pneumonia. is
trachea but no lung lesions. In the chronic
primarily a problem in calves <6 mo old
form, lesions consist of hyperemia. of the
with peak occurrence from 2-10 wk, but it
caudal third of the trachea with mucopumay be seen in calves up to 1 yr of age. It is rulent exudate in the trachea. In fatal
more common in dairy than in beef calves
cases, the lesion becomes completely
and is a common problem in veal calves. It is
obstructive.

also more common in housed dairy calves

Movement and handling of affected
than in those raised outside in hutches.

cattle should be limited. Antibiotics and

Peak incidence of disease may coincide
corticosteroids a.re recommended for the
with decline of passively acquired immunity.

a.cute form, although the efficacy of

Morbidity rates may approach 1000/o; case
treatment is not reported. Tra.cheostomy
fatality rates vary but can reach 20%.

may be required in severe cases. Providing
shade and cooling with fans or water

Etiology: The etiology is similar to
sprays is recommended. Animals that
that for BRD complex in genera.I (see
recover a.re prone to relapse and should
p 1431). The pathogenesis involves
be sent to slaughter.

environmental and management stressors
and possibly an initial respiratory viral
infection followed by a secondary
bacterial infection of the lower respiratory
tract. Stress results from environmental
and management factors, including

Bovine respiratory disease (BRO) has a
inadequate ventilation, mixing by adding
multifactoria.l etiology and develops as a
ca.Ives to an established group, crowding,
result of complex interactions between
and nutritional factors such as poorenvironmental factors, host factors, and qua.lity milk replacers. Partial or complete
pathogens. Environmental factors ( eg,
failure of passive transfer of maternal
weaning, transport, commingling,
antibodies is an important host factor
crowding, inclement weather, dust, and
related to development of disease. Any of
inadequate ventilation) serve as stressors several viruses may be involved, and a that adversely affect the immune and
variety of bacteria may be isolated from
nonimmune defense mechanisms of the
affected ca.Ives. Mycoplasmal and
host. In addition, certain environmental
bacterial agents, including Pasteurella
factors (eg, crowding and inadequate
multocida, Ma,nnheimia haemolytica,
ventilation) can enhance the transmisand Mycoplasma bovis, represent the sion of infectious agents among animals.

most frequently isolated pathogenic

Many infectious a.gents have been
organisms. The individual viral and

1432

RESPIRATORY DISEASES OF CADLE
bacterial etiologies, clinical signs, lesions,
into feedlots of large groups of calves from
and treatment are discussed under VIRAL
diverse geographic, nutritional, and genetic

RESPIRATORY TRACT INFECTIONS, below, and
backgrounds. Morbidity in feeder calves

BACTERIAL PNEUMONIA, p 1436.

often peaks within 7-10 days after assembly
in a feedlot. Morbidity can approach

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Control and Prevention: When calves

35o/c,-50%, and case fatality is 5o/c,-10%;
of varying ages are placed in communal
however, the level of morbidity and
pens, control of enzootic pneumonia is
mortality strongly depends on the array of
difficult. The severity of the pneumonia

1isk factors present in the cattle being fed.

may be decreased by improved husbandry,
proper housing, adequate ventilation, and

Etiology: The pathogenesis of shipping
good nursing care. Prevention begins with
fever pneumonia involves stress factors,
vaccinating the cows against specific
with or without viral infection, interacting
respiratory viruses and bacteria 3-4 wk
to suppress host defense mechanisms,
prepartum to improve the quality of
which allows the proliferation of conunencolostral antibodies. Calves should sal bacteria in the upper respiratory tract.

receive good-quality colostrum at 8o/<>-10%

Subsequently, these bacteria colonize the
of body wt in the first 6 hr after birth.

lower respirato1y tract and cause a broncho

Newborn dairy calves should be housed
pneumonia with a cranioventral distribution
individually in hutches or stalls and fed
in the lung. Multiple stress factors are
whole milk or a high-quality milk replacer
believed to contribute to suppression of
with a fiber content of <0.25% until 8-12
host defense mechanisms. Weaning is a
wk old. The use of calf hutches in dairy
significant stressor, and the incidence of this
herds is the preferred standard for calf
disease is highest in recently weaned calves.

housing and has been shown to signifi

Transp01tation over long distances serves
cantly improve calf respiratory health.

as a stressor; it may be associated with

However, delivering milk to a large
exhaustion, starvation, dehydration, chilling
number of hutches in cold weather
and overheating depending on weather
presents a significant challenge. Single
conditions, and exposw·e to vehicle exhaust
calf housing in naturally ventilated calf
fumes. Additional stressors include passage
barns is the next best alternative. Calves
through auction markets; commingling,
should be vaccinated against respiratory
processing, and surgical procedures on
viruses 3-4 wk before the first grouping,
anival at the feedlot; dusty environmental
although in some situations, the presence
conditions; and nutritional stress associated
of passive immunity may interfere with an
with a change to high-energy rations in the
active immune response. Calves should be
feedlot. The individual viral and bacterial
of similar age when assembled into
etiologies, clinical signs, lesions, and
groups, and a group should be limited to
treatment are discussed under VIRAL
slO. As calves mature, groups can become

RESPIRATORY TRACT INFECTIONS, below, and
larger as the size of the herd, facilities, and BACTEllIAI, PNEUMONIA, p 1436.

available labor dictate. An "all in/all out"

management style should be.practiced

Control and Prevention: Prevention
when establishing and terminating a
of shipping fever pneumonia should focus
group. Newborn beef calves and their
on reducing the stressors that contribute
dams should be moved from concentrated
to development of the disease. Cattle
calving areas as soon as the calf is nursing
should be assembled rapidly into groups,
well and strong enough to travel. The use
and new animals should not be introof screening systems such as the Calf duced to established groups. Mixing of

Respiratory Scoring Chart (University of
cattle from different sources should be

Wisconsin) may serve as an objective tool
avoided if possible; however, in the North
to evaluate calves for treatment.

American beef industry, this risk factor is
almost unavoidable for large intensive
feedlots. Transport time should be

Shipping Fever Pneumonia
minimized, and rest periods, with access

Shipping fever pnewnonia, or undifferentito feed and water, should be provided ated fever, is a respiratory disease of cattle
during prolonged transport. Ca.Ives
of multifactorial etiology with Mannheimia should ideally be weaned 2-3 wk before haemolytica and, less commonly,
shipment, and surgical procedures should

Pasteurnlla multoc-ida or Histoph'ilus
be performed in advance of transport;
somni (seep 754) being the impo1tant
however, the availability of these
bacterials agents involved. Shipping fever

"preconditioned" calves is quite limited.

pnewnonia is associated with the assembly

Cattle should be processed within 48 hr

RESPIRATORY DISEASES OF CATTLE

1433
after arrival at the feedlot. Adaptation to
fatal cases have a concurrent bacterial
high-energy rations should be gradual,
bronchopnemnonia.

because acidosis, indigestion, and anorexia
may inhibit the immune response. Vitamin

Diagnosis: Diagnostic procedures for PI-3
and mineral deficiencies should be
are similar to tllose for BOVINE RESPIRATOHY

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corrected. Dust control measures should

SYNCYTIAL \�RUS, see below.

be used.

Metaphylaxis with long-acting antibiot

Treatment and Prevention: Treatment
ics such as oxytetracycline, tilmicosin,
focuses on the antimicrobial tllerapy
florfenicol, gamithrornycin, tildipirosin, or
directed toward bacterial pneumonia
tulathromycin has been widely adopted as

(seep 1436). NSAIDs are also a therapeutic
a control measure given "on arrival" to
consideration.

cattle at high risk of developing shipping

PI-3 vaccines are available and are
fever pneumonia. Metaphylaxis on arrival
ahnost always combined witll bovine herhas been shown to significantly reduce pesvirns 1 (infectious bovine rhinotracheimorbidity and in1prove rate of gain and, tis). Modified-live and inactivated vaccines
in some cases, reduce mortality. Mass
are available for IM administration. Vaccines
medication in feed or water is of limited
containing temperature-sensitive mutants for
value because sick animals do not eat or
intranasal administration are also available.

drink enough to achieve inhibitory blood
levels of the antibiotic, and many of tllese
oral antibiotics are poorly absorbed in

Bovine Respiratory Syncytial Virus
ruminants.

Etiology: Bovine respiratory syncytial

On arrival, processing usually involves
virns (BRSV) is an RNA virns classified as a
administration of modified-live vaccines for
pneun10virus in the Paramyxovirns family.

viral antigens and for bacterial components

This virus was named for its characteristic
of shipping fever pneumonia. Because most
cytopathic effect-the fonnation of
cases of pneumonia occur dming the first 2
syncytial cells. In additional to cattle, sheep
wk after arrival, these on-arrival vaccines
and goats can also be infected by respiramay not have adequate time to stimulate tory syncytial virnses. Human respiratory
immunity. When possible, vaccinations for
syncytial virus (HRSV) is an in1portant
tile viral and bacterial components of
respiratory pathogen in infants and young
shipping fever pneumonia should be given
children. Antigenic subtypes are !mown to

2-3 wk before transport or earlier and can
exist for HRSV, and preliminary evidence
be repeated on entry to tile feedlot.

suggests there may be antigenic subtypes
of BRSV. BRSV is distributed worldwide,

VIRAL RESPIRATORY TRACT
and the virus is indigenous in the cattle
population.

INFECTIONS

BRSV infections associated witl1

Parainfluenza-3 Virus
respiratory disease occur predominantly in
young beef and dairy cattle. BRSV can be

Etiology: Parainfluenza-3 virus (PI-3) is
considered as a primary BRD patllogen and
an RNA virus classified in the Pararnyxoviis also a component of tile bovine respiratory rns family. Infections caused by PI-3 are
disease complex. Passively derived immmlity
common in cattle. Although PI-3 is capable
does not appear to prevent BRSV infections
of causing disease, it is usually associated
but reduces tl1e severity of disease. Initial
with mild to subclinical infections. The most exposures to tile virus are associated witll important role of PI-3 is to serve as an
severe respiratory disease; subsequent
initiator that can lead to development of
exposures result in mild to subclinical
secondary bacterial pnem11onia.

disease. BRSV is an important virns in tl1e
bovine respiratory disease complex because

Clinical Findings and Lesions: Clinical
of its frequency of occurrence, predilection
signs include pyrex.ia, cough, serous nasal
for tile lower respiratory tract, and ability to
and lacrimal discharge, increased respirapredispose the respiratory tract to secondary tory rate, and increased breath sounds. The
bacterial infection. In outbreaks, morbidity
severity of signs worsens with tl1e onset of
tends to be high, and the case fatality rate
bacterial pneumonia. Fatalities from
can be 0-20%.

uncomplicated PI-3 pneumonia are rare.

Lesions include cranioventral lung

Clinical Findings and Lesions: Fever
consolidation, bronchiolitis, and alveoli.tis

(104°-l08°F [40°-42°C]), depression,
witll marked congestion and hemorrhage.

decreased feed intake, increased

Inclusion bodies may be identified. Most
respiratory rate, cough, and nasal and

1434

RESPIRATORY DISEASES OF CADLE
lacrimal discharge are common. Dyspnea,

General control and prevention are
possibly with open-mouthed breathing,
discussed under ENZOOTIC PNEUMONIA OF
may become pronounced in the later

CALVES AND SIIIPPING FEVER PNEUMONIA, p 1431.

stages of the disease. Subcutaneous

Inactivated and modified-live vaccines
emphysema may occur. Secondary
are available and may serve to reduce
bacterial pneumonia is a frequent
losses associated with BRSV; however,

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occurrence. A biphasic disease pattern
there is a paucity of field trials to evaluate
has been described but is not consistent.

the efficacy of these vaccines.

Gross lesions include a diffuse interstitial pneumonia with subpleural and interstitial emphysema along with

Bovine Herpesvirus 1
interstitial edema. These lesions are similar (Infectious bovine rhinotracheitis virus, to and must be differentiated from other

Infectious pustular vulvovaginitis, and
causes of interstitial pneumonia (see al.so
associated diseases)

p 1439). Bronchopneumonia of bacterial
origin is usually present. Histologic

Etiology and Epidemiology: Bovine
examination reveals syncytial cells in
herpesvirus l (BHV-1) is associated with
bronchiolar epithelium and lung parenseveral diseases in cattle: infectious bovine chyma, intracytoplasmic inclusion bodies,
rhinotracheitis (IBR), infectious pustular
proliferation and/or degeneration of
vulvovaginitis (IPV), balanoposthitis,
bronchiolar epithelium, alveolar epitheconjunctivitis, abortion, encephalomyelitis, lialization, edema, and hyaline memand mastitis. Only a single serotype of
brane formation.

BHV-1 is recognized; however, three
subtypes of BHV-1 have been described on

Diagnosis: A diagnosis of BRSV requires
the basis of endonuclease cleavage patterns
laboratory confirmation. BRSV is a difficult
of viral DNA: BHV-1.l (respiratory subtype),
virus to detect, although chances of

BHV-1.2 (genital subtype), and BHV-1.3
isolation may in1prove when sampling

(encephalitic subtype). BHV-1.3 has been
animals in the incubation or acute phases
reclassified as a distinct herpesvirus
of infection. Although virus isolation is
designated BHV-5.

difficult, PCR is a useful and rapid method

BHV-1 infections are widespread in the
commonly used to detect the antigen.

cattle population. In feedlot cattle, the

Other procedures that have proved useful
respiratory form is most common. The
in detection of BRSV antigen are fluoresviral infection alone is not life-threatening cent antibody and inununoperoxidase
but predisposes to secondary bacterial
staining.

pneumonia, which may result in death.

Paired serum samples can be used to

In breeding cattle, abortion or genital
establish a diagnosis. However, the antibody infections are more common. Genital titer of animals with well-developed clinical
infections can occur in bulls (infectious
disease may be higher in the acute sample
pustular balanoposthitis) and cows (IPV)

than in the sample taken 2---3 wk later,
within 1-3 days of mating or close contact
because the antibodytesponse often
with an infected animal. Transmission
develops rapidly, and clinical signs follow
can occur in the absence of visible lesions
virus infection by up to 7-10 days. Single
and through artificial insemination with
serum samples with high antibody titers
semen from subclinically

.

infected bulls.

from a nw11ber of anin1als in a respiratory

Cattle with latent BHV-1 infections
outbreak may help diagnosis if coupled with generally show no clinical signs when the clinical signs. Calves that become infected
virus is reactivated, but they serve as a
with BRSV in the presence of passively
source of infection for other susceptible
derived antibody may not seroconvert.

animals.

Treatment and Prevention: Treatment

Clinical Findings: The incubation period
focuses on antimicrobial therapy to control
for the respiratory and genital fonns is 2-6
secondary bacterial pnewnonia (seep 1436).

days. In the respiratory fom1, clinical signs

There is no specific treatment for the viral
range from mild to severe, depending on the
interstitial pnewnonia. Supportive therapy
presence of secondary bacterial pnewnoand correction of dehydration may be nia. Clinical signs include high fever,
necessary. There are anecdotal reports of
anorexia, coughing, excessive salivation,
treatment with antihistamines and/or
nasal discharge that progresses from serous
corticosteroids being of benefit. Most
to mucopurulent, conjunctivitis with
animals will recover in several days without

Jacrirnal discharge, inflan1ed nares (I1ence
treatment.

the common name "red nose"), and dyspnea

RESPIRATORY DISEASES OF CATILE

1435
if the larynx becomes occluded with
esophagus, and forestomachs. In addipurulent material. Nasal lesions consist of tion, white foci may be found in the liver,
numerous clusters of grayish necrotic foci
kidney, spleen, and lymph nodes. Aborted
on the mucous membrane of the septal
fetuses may have pale, focal, necrotic
mucosa, just visible inside the external
lesions in all tissues, which are especially
nares. They may later be accompanied by
visible in the liver.

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pseudodiphtheritic yellowish plaques.

Conjunctivitis with corneal opacity may

Diagnosis: Uncomplicated BHV-1
occur as the only manifestation of BHV-1
infections can be diagnosed based on the
infection. In the absence of bacterial
characteristic signs and lesions. However,
pneumonia, recovery generally occurs
because the severity of disease can vary, it

4-5 days after the onset of signs.

is best to differentiate BHV-1 from other

Abortions may occur concurrently with
viral infections by viral isolation. Samples
respiratory disease but may be seen up to
should be taken early in the disease, and a

100 days after infection. They can occur
diagnosis should be possible in 2-3 days.

regardless of the severity of disease in the

A rise in serum antibody titer also can be
darn. Abortions generally occur during the
used to confirm a diagnosis. It is not
second half of pregnancy, but early
possible to detect a rising antibody titer in
embryonic death is possible.

abortions, because infection generally

In genital infections, the first signs are
occurs a considerable length of time
frequent urination, elevation of the tailhead,
before the abortion, and titers are already
and a mild vaginal discharge. The vulva is
maximal. BHV-1 abortion can be diagswollen, and small papules, then erosions nosed by identifying characteristic lesions
and ulcers, are present on the mucosal
and demonstrating the virus in fetal
surface. lf secondary bacterial infections do
tissues by PCR, virus isolation, immunonot occur, animals recover in 10-14 days.

peroxidase, or fluorescent antibody

With bacterial infection, there may be
staining. Gross and microscopic lesions
inflanunation of the uterus and transient
detected shortly after death may help to
infertility, with purulent vaginal discharge for establish a diagnosis. PCR methods can several weeks. In bulls, similar lesions occur
be used to identify antigen in a variety of
on the penis and prepuce. (See a1so p 1391.) tissues or exudates.

BHV-1 infection can be severe in young
calves and cause a generalized disease.

Pyrexia, ocular and nasal discharges,

Treatment and Control: Antimicrobial
respiratory distress, diarrhea, incoordinatherapy is indicated to prevent or treat tion, and eventually convulsions and death
secondary bacterial pneumonia. General
may occur in a short period after generalrecommendations for control are discussed ized viral infection.

under srnPPING FEVER PNEUMONIA, p 1432.

Immunization with modified-live or

Lesions: In uncomplicated IBR infecinactivated virus vaccines generally tions, most lesions are restricted to the
provides adequate protection against
upper respiratory tract and trachea.

clinical disease. Both IM and intranasal

Petechial to ecchymotic hemoIThages may
modified-live vaccines are available, but the
be found in the mucous membranes of

IM types may cause abortion in pregnant
the nasal cavity and the paranasal sinuses.

cattle. The intranasal vaccines can be used

Focal areas of necrosis develop in the nose,
in pregnant cattle. The IM vaccines are
pharynx, larynx, and trachea. The lesions
easier to use and often are the vaccines of
may coalesce to forn1 plaques.

choice in feedlots. Breeding and replace

The sinuses are often filled with a
ment heifers and bulls should be immunized
serous or serofibrinous exudate. As the
when 6-8 mo old, before breeding, and
disease progresses, the pharynx becomes
yearly thereafter. Some recommend that
covered with a serofibrinous exudate, and
young bulls not be vaccinated, because tl1ey
blood-tinged fluid may be found in the
may be discriminated against when sold for
trachea. The pharyngeal and pulmonary
breeding if they have antibody titers. Feeder
lymph nodes may be acutely swollen and
calves should be immunized 2-3 wk before
hemorrhagic. The tracheitis may extend
entry into the feedlot. A nun1ber of western
into the bronchi and bronchioles; when

European countries have eradicated or are
this occurs, epithelium is sloughed in the
attempting to eradicate BHV-1 from their
airways. The viral lesions are often
domestic cattle populations. Eradication of
masked by secondary bacterial infections.

the virus is possible by a combination of

In young animals with generalized BHV-1
serologic surveillance, culling of reactors,
infection, erosions and ulcers overlaid
biosecurity, and vaccination. To aid in
with debris may be found in the nose,
eradication, deletion mutant vaccines have

1436

RESPIRATORY DISEASES OF CADLE
been developed that pem1it discrimination
include bovine reovilus, enterovirus, and
between antibody produced in response to
coronavirus. Evidence is growing that
the vaccine and antibody produced in
bovine coronavil·us may have a more
response to natural exposure.

in1portant role in BRD than previously
recognized. Bovine coronavirus may play a

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Bovine Viral Diarrhea Virus
role in some outbreaks of calf pnewnonia
on pasture in beef cow-calf operations.

Bovine viral diarrhea virus (BVDV) is an

These viruses have a role similar to that of

RNA virus classified as a Pestivirus in
the other viruses previously discussed; ie, in
the family Flaviviridae (seep 267). The
combination with other stressors, they can
role of BVDV in BRD as a primary
serve as initiators of bacterial pnewnonia.

pathogen has been controversial but

Vaccines are not available for prevention of
appears to be that of a virus capable of
these vii·al respiratory diseases.

inducing immunosuppression, which
allows for development of secondary
bacterial pneumonia. Seroconversion

BACTERIAL PNEUMONIA
to BVDV after arriving in the feedlot has
been reported to be the occurrence of

Mannheimia haemolytica
respiratory disease in feedlot calves.

Calves that arrive at the feedlot with high
associated Bovine Respiratory
titers to BVDV have also been shown to

Disease
be less likely to develop respiratory

Etiology: Mannheimia haemolytica
disease, and BVDV has been reported to
serotype 1 is the bacteriwn most frequently
be the virus most frequently associated
isolated from the lungs of cattle with BRD.

with multiple viral infections of the

Although less frequently cultured, Pasteii1°
respiratory tract of calves. Some studies
ella multocida is also an important cause
have shown that the presence of a calf
of bacterial pnewnonia. Histophilus somni
persistently infected with BVDV in a
is being increasingly recognized as an
feedlot pen increases the risk of respiraimportant pathogen in BRD; these bacteria tory disease within that pen.

are nonnal inhabitants of the nasopharynx

Treatment for acute BVDV infection is
of cattle (seep 754). When pulmonary
supportive and includes antimicrobials to
abscessation occurs, generally in associaprevent or treat bacterial pneumonia.

tion with chronic pneumonia, Tiueperella

General principles of control are discussed
pyogenes is frequently isolated.

under ENZOOTJC PNEUMONIA OF CALVES ANO

Under n01mal conditions, M ha.emolytica

SIIIPPING FEVER PNEUMONIA, p 1431. Inactivated
remains confined to the upper respiratory
and modified-live vaccines are available for
tract, in particular the tonsillar crypts, and is

IM administration.' Recently, vaccines
difficult to culture from healthy cattle. After
containing both the type I and type II
stress or viral infection, tl1e replication rate of
genotypes have become available.

M haemolytica in tl1e upper respiratory tract Vaccination of cows before breeding witl1
increases rapidly, as does the likeW1ood of
modified-live vaccines is-an important
culturing the bacterium. The increased
strategy to prevent the occurrence of
bacterial growtl1 rate in the upper respiratory
persistently infected calves. Testing for
tract, followed by inhalation and colonization
persistently infected calves and removing
of the lungs, may occur because of suppresthem from the pen has been used as a sion of the host's defense mechanism related
strategy to reduce the risk of disease
to environmental stressors or viral infections.

within feedlots in high-risk groups.

It is during this log phase of growth of the
organism in the lungs that virulence factors

Other Bovine Respiratory Viruses
are elaborated by M haernol:yl'ica, such as an exotoxin that has been referred to as

Several other viruses may potentially be
leukotoxin. The interaction between the
involved in BRD. Bovine herpesvirus 4
virulence factors of the bacteria and host
has been implicated in several diseases,
defenses results in tissue damage with
including BRD. Bovine adenovirus has
characteristic necrosis, thrombosis, and
been associated with a wide spectrum of
exudation, and in the development of
diseases, with bovine adenovirus type 3
pnewnonia. TI1e pathogenesis of pnewnonia
being the serotype most often associated
caused by Pmultocida is poorly understood.

with BRD. Two serotypcs of bovine

This organism may opportunistically
rhinovims have been recognized to cause
colonize lungs with clu·onically damaged
respiratory tract infections in cattle. Other
respiratory defenses, such as occurs with
viruses reported to be associated with BRD
enzootic calf pnewnonia or existing lung

RESPIRATORY DISEASES OF CADLE

1437
lesions of feedlot cattle, and cause a purulent
encapsulated until 4 wk T pyogenes is
bronchopneumonia. H somni may invade
frequently cultured from these abscesses.

the lung and cause pneumonia after damage
to the respiratory defenses. This organism is

Diagnosis: Generally, neither serologic
capable of systemic spread from the lung to
testing nor direct bacterial detection are

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the brain, myocardium, synovium, and
performed, and diagnosis relies on gross
pleural and pericardia! surfaces; often, death
necropsy findings and bacterial culture.

can occur later in the feeding period ( 40--60

Because the bacteria involved are normal
days after arrival) from involvement of these
inhabitants of the upper respiratory tract,
additional organ systems.

the specificity of culture can be increased
by collecting antemortem specimens from

Clinical Findings: Clinical signs of
the lower respiratory tract by tracheal
bacterial pneumonia are often preceded by
swab, transtracheal wash, or bronchoalsigns of viral infection of the respiratory veolar lavage. Lung specimens can be
tract. With the onset of bacterial pneun10nia, collected for culture at necropsy. If clinical signs increase in severity and are
possible, specimens for cultw·e should be
characterized by depression and toxemia.

collected from animals that have not been

A combination of clinical signs of deprestreated with antibiotics to permit determision and fever (104°-l06°F [40°-41 °C]), nation of antin1icrobial sensitivity patterns.

without any signs attributable to other body

A multiplex PCR has been used to identify
systems, are the classic components of a
a number of bacterial agents in1plicated
case definition for early cases ofBRD.

with bovine respiratory disease, including

Serous to mucopurulent nasal discharge;

M hemolytica.

moist cough; and a rapid, shallow respiratory rate may be noted. Auscultation of the Treatment: Early recognition by trained
cranioventral lung field reveals increased
personnel skilled at detecting the early
bronchial sounds, crackles, and wheezes.

clinical signs of disease followed by

In severe cases, pleurisy may develop,
treatment with antibiotics is essential for
characterized by an irregular breathing
successful therapy. Treatment protocols
pattern and grunting on expiration. The
should be established so the producer has a
animal will become unthrifty in appearance
standardized approach to identifying and
if the pneumonia becomes chronic, which
treating cases. Long-acting antimicrobials
is usually associated with forn1ation of
such as tulathromycin, tilmicosin,
pulmonary abscesses.

florfenicol, and enrofloxacin have label
claims to treat BRD and are commonly

Lesions: M haemolytica causes a severe, used as first- or second-line treatment
acute, hemorrhagic fibrinonecrotic pneuoptions in feedlot calves. These long-acting monia. The pneumonia has a bronchopneuantimicrobials allow the feedlot pi·oducer monic pattern. Grossly, there are extensive
to avoid commingling sick animals in a
reddish black to grayish brown craniovenhospital pen, and treated anin1als can tral regions of consolidation with gelatinous return directly to the home pen. NSAIDs thickening of interlobular septa and fibrinous have been shown to be a beneficial pleuritis. There are extensive thromboses,
ancillary therapy in controlling fever in
foci of lung necrosis, and limited evidence
cases of BRD, but data are lacking in terms
of bronchitis and bronchiolitis.

of effect on relapse and mortality

P multocida is associated with a less
outcomes. If selection for treatment is late
fulminating fibrinous to fibrinopurulent
and pulmonary abscessation has occurred,
bronchopneumonia. In contrast to
it is dif-ficult to achieve resolution with

M haemolytica, P mullocida is associated
antimicrobials, and use of a convalescent
with only small an10unts of fibrin exudapen or culling of the animal should be tion, some thromboses, limited lung
considered.

necrosis, and suppurative bronchitis and
bronchiolitis.

Control: General principles of control

H somni infection of the lungs results in
are discussed under ENZOOTIC PNEUMONIA OF
purulent bronchopneumonia that may be

CALVES AND SHIPPING FEVER PNEUMONIA, p 1431.

followed by septicemia and infection of

The value of M lwemolylica and P mullocida multiple organs. H somni is associated
bacterins is questionable, and some reports
with extensive fibrinous pleuritis in feedlot
indicate they may even exacerbate the
calves.

disease. Newer vaccines, which include live

Pulmonary abscessation can occur as the
culture and subunit vaccines (leukotoxin ),
pnewnonia becomes chronic. Abscesses
show much more promise for disease
develop in -3 wk but do not become
prevention and may reduce morbidity in

1438

RESPIRATORY DISEASES OF CADLE
high-risk feedlot calves given one dose
bronchopneun1onia have been produced
of vaccine on anival by as much as 25%;
by experimental infections. A synergism
however, trials have not been consistent in
between Chlamydia and Mannheimia
all risk categories of feedlot cattle. Ideally,
haemolytica has been demonstrated
vaccination should be done 3 wk before
experimentally. Because this pathogen is
transport to the feedlot and can be repeated

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infrequently tested for, its overall in1poron anival. In dairy calves, vaccination of the tance remains undetermined. The organism
dam may be of benefit by providing passive
can be tested for by staining sections of lung
immuruty to the calf. H somni bacterins are lesions with Gimenez stain or by fluorescent
available, and there is some evidence they
antibody. Isolation requires inoculation of
are effective in control of BRD in feedlot
yolk sacs of embryonating chicks.

calves even when only one dose is given

Chlamydia! agents are sensitive to
on anival.

tetracyclines. (See also p 598.)

Mycoplasmal Pneumonia

Mycoplasma bovis is an emerging cause of

CONTAGIOUS BOVINE
respiratory disease and arthritis in feedlot

PLEUROPNEUMONIA
cattle and in young dairy and veal calves.

Experimental infections usually result in

Contagious bovine plueuropnewnonia is
inapparent to mild signs of respiratory
highly contagious and generally accompadisease, but virulent strains have been nied by pleurisy. It is present in Africa, with
identified that cause severe lung disease
minor outbreaks occurring in the Middle
in calves. However, this does not preclude

East. The USA has been free of the disease
a synergistic role for mycoplasmas in
since 1892, the UK since 1898, and Australia
conjunction with viruses and bacteria in
since 1973. The last outbreak of CBPP in

BRD. Mycoplasmas can be isolated from

Europe was seen in Portugal in 1999. Little is
the respiratory tract of nonpneumonic
known about the disease in Asia, but China
calves, but the frequency of isolation is
claims that its last outbreak was in 1995.

greater in those with respiratory tract
disease. M bovis has been associated

Etiology: The causal organism is
with otitis media in young calves and a

Mycoplasma mycoides mycoides small
syndrome involving chronic pneumonia
colony type. (See also p 14 7 4.) Susceptible and polyarthritis in feedlot cattle. These
cattle become infected by inhaling droplets
cattle invariably have a pneumonic lesion,
disseminated by coughing in affected cattle.

and 40%---60% may also develop a polyar

Small rwninants and wildlife are not
thritis and tenosynovitis that causes severe important in the epidemiology. Sheep and chronic lameness. The condition results
goats can be naturally infected but have no
in a chronic disease that does not respond
associated pathology. The organism can
to antimicrobial therapy. A significant
also be found in saliva, urine, fetal
proportion of these animals are euthanized membranes, and uterine discharges.

because of the chronic nature of the

Transplacental infection of the fetus can
disease. Lesions include chronic bronchooccur. Viability of the organism in the pneumonia with caseous and coagulative
environment is poor. The incubation period
necrosis. In severe cases, >80% of the I ung
varies, but most cases occur 3---8 wk after
tissue may be involved. Culture of these
exposure. In some localities, susceptible
organisms requires special media and
herds may show up to 700/o morbidity, but
conditions; growth of the organisms may
much lower infection rates ( ---100/o)

take up to a week. PCR tests are now
associated with clinical signs are more
available that can detect the mycoplasma
common. Mortality is likely to be ---500/o in
within hours, thus greatly speeding up
herds experiencing the disease for the first
diagnosis. Immunohistochemical tests can
time. Of recovered aninials, 25%may
also be done on fixed tissue that link the
become caniers with chronic lung lesions
mycoplasrna antigen directly with the
in the fom1 of sequestra of variable size.

lung lesion. Vaccines are commercially

Because caniers may not be detectable
available for M bovis, but their efficacy
clinically or serologically, they constitute a
has not been demonstrated conclusively.

serious problem in control programs. Breed
susceptibility, management systems, and
general health of the animal are important

Chlamydia! Pneumonia
factors that influence tile infection.

Chlamydia! agents have been implicated in
a number of diseases of cattle, including

Clinical Findings: In acute cases, signs
pneumonia. Clinical signs and lesions of
include fever up to 107°F (41.5°C);

RESPIRATORY DISEASES OF CADLE

1439
anorexia; and painful, difficult breathing.

made by in1munoblotting test. As soon as

In hot climates, the animal often stands
an outbreak is suspected, slaughter and
by itself in the shade, its head lowered
necropsy of preswnptively infected cattle
and extended, its back slightly arched,
is advisable.

and its elbows turned out. Percussion of
the chest is painful; respiration is rapid,

Control: The disease is reportable by law

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shallow, and abdominal. If the animal is
in many count1ies from which it has been
forced to move quickly, the breathing
eradicated by slaughter of all infected and
becomes more distressed and a soft,
exposed anin1als. In countries where cattle
moist cough may result. The disease
movement can readily be rest1icted, the
progresses rapidly, animals lose condidisease can be eradicated by quarantine, tion, and breathing becomes very
blood testing, and slaughter. Where cattle
labored, with a grunt at expiration. The
cannot be confined, the spread of infection
animal becomes recw11bent and dies after
can be limited by inunw1ization with

1--3 wk. Chronically affected cattle
attenuated vaccine (eg, Tl/44 strain).

usually exhibit signs of varying intensity

However, the vaccine is effective only if
for 3--4 wk, after which the lesions
herd coverage within a country is high.

gradually resolve and the animals appear

Tracing the source of infected cattle
to recover. Subclinical cases occur and
detected at abattoirs, blood testing, and
may be important as carriers. Infected
imposition of strict rules for cattle
calves may present primarily with
movement also can aid in control of the
polyarthritis that is seen as swelling
disease in such areas.

of joints and lameness.

Treatment is recommended only in

Lesions: The thoracic cavity may
endemic areas because the organ.isms may
contain up to 10 L of clear yellow or turbid
not be eliminated, and carriers may develop.

fluid mixed with fibrin flakes, and the

Tylosin (10 mg/kg, IM, bid, for six if\iections)

organs in the thorax are often covered
and danofloxacin 2.5% (2.5 mg/kg/day for
by thick deposits offibrin. The disease is

3 consecutive days) have been repo1ted to
largely unilateral, with more than 80%--90% be effective.

of cases affecting only one lung. The
affected portion is enlarged and solid.

On section of the lung, the typical marbled
appearance of pleuropneumonia is evident
because of the widened interlobular septa

This classification represents a group of
and subpleural tissue that encloses gray,
respiratory diseases characterized by an
yellow, or red consolidated Jung lobules.

acute onset of severe respiratory distress

Microscopically, this is a severe, acute,
and a combination of lung lesions that
fibrinous pneumonia with fibrinous
include pulmonary edema and congestion,
pleurisy, thrombosis of pulmonary blood
interstitial emphysema, alveolar epithelialivessels, and areas of necrosis of lung zation, and hyaline membrane fonnation.

tissue; the interstitial tissue is markedly

Lungwonn infection in cattle (seep 1421)

thickened by edema fluid containing much
can also result in an atypical interstitial
fibrin. In chronic cases, the lesion has a
pnewnonia .

necrotic center sequestered in a thick,
fibrous capsule, and there may be fibrous

ACUTE BOVINE PULMONARY
pleural adhesions. Organisms may survive

EMPHYSEMA AND EDEMA
only within the inner capsule of these
sequestra, and these animals may become

(Fog fever, Bovine atypical interstitial
carriers.

pneumonia)

Acute bovine pulmonary emphysema

Diagnosis: Diagnosis is based on clinical
and edema(ABPEE) is one of the more
signs and the characteristic gross pathocommon causes of acute respiratory logic lesions of the lungs. Complement
distress in cattle, particularly adult beef
fixation, latex agglutination, or competitive
cattle, and is characterized by sudden

ELISA tests can be used to aid definitive
onset, minimal coughing, and a course
diagnosis. Confirmation is often by isolation that ends fatally or improves dramatically of the mycoplasma followed by growth
within a few days. It is a disease involving
inhibition or inununofluorescence test using groups of cattle; morbidity may be >50%, hyperinunune rabbit sera against the
although usually only a small minority
mycoplasma, or increasingly by PCR.

develops severe respiratory distress.

Confirmation of serologic reactions can be

Typically, ABPEE occurs in the fall, 5--10

1440

RESPIRATORY DISEASES OF CADLE
days after change to a better, often lush,
bullae in interlobular and subpleural
pasture. A similar condition has been
regions. Submucosal hemorrhages are
reported when cattle are fed on a wide
often present on the larynx and in the
variety of grasses, alfalfa, rape, kale, and
trachea and larger bronchi. Histologi

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turnip tops.

cally, the lesion is characterized by
congestion, alveolar edema, hyaline

Etiology: Metabolites of the naturally
membrane formation, and areas of early
occurring amino acid L-tryptophan
alveolar epithelial hyperplasia of type
probably are responsible for many

II pneumocytes; occasionally, areas of
outbreaks. In the rumen, L-tryptophan is
bronchiolar necrosis may be found. The
degraded to indoleacetic acid, which can
emphysema is often dramatic and is
be converted to 3-methylindole by some
limited to interstitial fascia, where it is
ruminal microorganisms. 3-Methylindole
accompanied by edema.

is absorbed into the bloodstream and is

In animals slaughtered after 3 days of
the source of the pneumotoxicity after
illness, the lungs are still heavy and do not
metabolism by the mixed function
collapse normally. They are pinkish gray
oxidase system, which is very active
and of increased finnness; edema and
in the lungs. Apparently, the level of
emphysema are inconspicuous or absent.

L-tryptophan in crops is most likely to

Histologically, widespread alveolar
be high in lush, rapidly growing pastures,
epithelial hyperplasia characteristic of a
particularly (but not exclusively) in
diffuse, acute, proliferative alveolitis is
the fall.

seen.

Clinical Findings: ABPEE is most

Diagnosis: Diagnosis is based on history,
common in adult beef cows but may
signs, and lesions. Because the syndrome is
occur in either sex and in dairy or beef
not specific with regard to cause, evidence
cattle under similar management
must be obtained from history of manageconditions. Nursing calves are unaffected. ment factors such as change in pasture.

Outbreaks usually develop within 5-10
days of a change to better grazing and

Treatment: Severely affected animals
rarely occur in animals that have been
have so little pulmonary reserve that any
on a field >3 wk.

driving or handling must be done with

Mild cases may go unnoticed. Cattle are
caution to prevent immediate death.

subdued but still alert; there is tachypnea

Removal of cattle from the offending
and hyperpnea, but auscultation is usually pastures may not prevent the development unrewarding. Such cattle usually recover
of new cases for the next 4--7 days. No
spontaneously within days. Severely
treatment has been identified that will
affected cattle show extensive respiratory reverse the fully developed lesions of distress with mouth breathing, extension

ABPEE.

of the tongue, and drooling. A loud
expiratory grunt is common, but coughing Control: One approach to control is is unusual. In the early stages, auscultadietary management, including the tion reveals surprisingly soft respiratory
following options: 1) avoiding pastures
sounds. Mild exercise increases dyspnea
likely to induce ABPEE, 2) feeding hay
and may precipitate death. If death does
before turn out on pasture 3.!}d limiting
not occur, the animals improve dran1atiexposure time on suspect pastures, cally and resume eating by the third day.

3) limiting grazing time and gradually

At this stage, auscultation reveals harsh
increasing exposure to the pasture over
respiratory sounds and, in some animals,
time, 4) using pastures before they become
dorsal (emphysematous) crackles. Some
lush, 5) delaying use of lush pastures until
cattle have subcutaneous emphysema
after a hard frost, 6) initially grazing
extending along the back from the
pastures with less susceptible stock ( cattle
withers. Full clinical recovery may

<15 mo old or sheep), or 7) using strip
require 3 wk.

grazing.

A medical approach to control involves

Lesions: In affected cattle that have
feeding monensin or lasalocid which
died or been slaughtered in extremis, the
inhibit the bacteria that convert �-tryptophan
lungs are heavy and do not collapse
to 3-methylindole. Treatment with monensin
normally. They are widely affected, with
can be started 1 day before introduction to
vanous degrees of firmness; there is
pasture, whereas lasalocid requires a 6-day
extensive edema and emphysema, often
pretreatment period. These drugs are of no
with the formation of large, air-filled
benefit after onset of clinical signs.

RESPIRATORY DISEASES OF CADLE

1441

ANAPHYLAXIS
immunodiffusion) to M Jaeni are widespread among adult cattle by the end of Anaphylaxis or Type I hypersensitivity
each winter feeding period, and many
reactions in cattle can result in an atypical
apparently healthy cattle are seropositive.

interstitial pnewnonia. The lung is a major

By contrast, few adult cattle are seroposi

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target organ in cattle for Type I hypersensitive on other fanns on which "good" hay or tivity. Clinical signs are those of acute
grass silage is fed.

respiratory distress. Cattle that die of
anaphylaxis may have lesions consistent
with those described for atypical interstitial

Clinical Findings: Cattle may succumb
pnewnonia. Treatment is administration of
to the acute form of the disease over a
epinephrine; supportive treatment includes
period of weeks. Usually, only severe
anti-inflammatory therapy with corticosteacute cases are noticed. There is respiraroids or NSAJDs. IJ pharyngeal or laryngeal tory distress, anorexia, and agalactia in
edema is present, a tracheostomy may be
animals <!5 yr old; coughing and pyrexia
indicated.

also occur, and adventitious sounds are
occasionally heard on auscultation. Death
is rare.

HYPERSENSITIVITY PNEUMONITIS

The chronic disease usually has a
higher morbidity; in most instances, the

(Extrinsic allergic alveolitis, Farmer's lung
signs are weight loss, poor production,
disease)

and persistent coughing. Affected cattle

Hypersensitivity pneumonitis is a
are fairly bright and eat reasonably well,
condition that appears to be similar to
but tachypnea, hyperpnea, and coughing
farmer's lung disease in people and occurs
are widespread. Auscultation may reveal
in both acute and chronic forms in adult
cranioventral crackles and sometimes, in
cattle. The hw11an and bovine forms of the
more severe cases, scattered rhonchi.

disease may coexist on problem farms

Exercise intolerance may be seen, and
because of common exposure to dust from congestive cardiac failure can develop if moldy hay.

pulmonary fibrosis is widespread.

Lesions: The macroscopic lesions are

Etiology: The disease occurs when
often wu-emarkable; usually, there is mild
sensitized individuals inhale antigens
peripheral lobular overinflation with
from thermophilic actinomycetes,
diffusely scattered, small, gray, subpleural
commonly the spores of Micropolyspora
spots. Although transient pulmonary edema
faeni. The actinomycetes proliferate in
may be a feature of severe acute cases, tl1e
vast numbers in hay, grain, or other
hlstologic lesions consistently found are
vegetable material that has overheated
interalveolar cellular infiltration, epitl1elioid
to -150°F (65°C) after damp storage
granulomata, and bronchiolitis obliterans.

(30%--40% moisture content). Dust that

In some chronic cases, small foci of alveolar
contains large numbers of spores is
epithelial hyperplasia and metaplasia witl1
released when this moldy hay is shaken.

interstitial fibrosis are found. These areas

The small size (1 i1m) of the spores allows
may extend to include most, if not all, of the
them to reach the smallest airways and
lw1g substance to produce cases clinically
alveoli to provoke a reaction that has been indistinguishable from diffuse fibrosing termed a "hypersensitivity pneumonitis";
alveolitis (see below). Circwnstantial
this is considered to be predominantly a
evidence suggests that some cases of

Type III hypersensitivity reaction,
diffuse fib rosing alveoli tis are the encl
although a Type IV hypersensitivity
stage of hypersensitivity pneumonitis.

component is suspected (see IMMUNOLOGIC

DISEASES, p 817 et seq).

Treatment and Control: Because it is

Affected herds are found in areas where
often impossible to completely shield
rainfall is usually significant during the
cattle from further challenge, most
haymaking season, suggesting that a
recover only partially after dexamethaclinical problem may arise only after sone treatment (1 mg/5-10 kg body wt).

repeated sensitization and challenge from

However, improvement is usually marked
the spores. Clinical disease tends to arise
when cattle are turned out in the spring.

during the latter half of the winter feeding

Prevention is difficult in areas where hay is
period and usually only when moldy hay is
likely to be wet during the curing process
fed indoors. Under such circumstances,
and it is not possible to alter the feeding
serum antibodies (usually detected by
regimen.

1442

RESPIRATORY DISEASES OF CATTLE

DIFFUSE FIBROSING ALVEOLITIS

Fusarium solani, or the wild mint Perilla frutescens. Moldy sweet potato toxicity is

Diffuse fibrosing alveolitis is a chronic,
caused by the ingestion of a furanoterpeprogressive respiratory disease of undeternoid toxin produced by sweet potatoes mined cause and possibly of multiple

(Jpomoea batatus) in response to
etiologies. A proportion of affected cattle are

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infestation with the fungus F solani; the
seropositive for precipitating antibodies to
end result is production of the pneumo

Micropolysporafaeni, and this condition
toxin 4-ipomeanol. Perilla ketone toxicity
may represent the end stage of hypersensitivis caused by ingestion of the leaves and ity pneumonitis. Other than the respiratory
seeds of the plantP frutescens (purple
signs, the animals appear alert and maintain
mint), which contains a pneumotoxin and
a good appetite until the onset of heart
is found in the southeastern USA. The
failure in the terminal stages. Signs include
pathogeneses of both these conditions are
coughing, increased respiratory rate,
similar to that of ABPEE, as is approach to
dyspnea, and weight loss. Necropsy findings
treatment.

include right ventricular hypertrophy, interalveolar fibrosis, obliteration of the alveolar spaces, alveolar hyperplasia, bronchitis, and

TOXIC GASES
bronchiolitis. There is no treatment.

Nitrogen dioxide is a major component
of silo gas; in people, the disease associated

ACUTE RESPIRATORY DISTRESS
with exposure to N0

SYNDROME OF FEEDLOT CATTLE

2 is tenned silo filler's
disease. Exposure of cattle results in
respiratory distress and necropsy findings

An acute respiratory distress syndrome
of atypical interstitial pnewnonia. Treathas been described in feedlot cattle with ment is empirical and includes diuretics,
clinical signs and pathologic findings of
corticosteroids, and antibiotics to prevent
an atypical interstitial pneun1onia The
pneumonia.

syndrome occurs sporadically, and the

Zinc oxide is produced during oxyaetiology remains undefined. Feedlot heifers cetylene cutting or arc welding of galvaseem to be at higher risk of developing the nized pipes. These activities in closed
disease than feedlot steers. Bovine
facilities in which cattle are housed may
respiratory syncytial virus, abnormal
result in toxicity characterized by respiraproduction of3-methylindole in the rumen, tory distress. Lesions are similar to those
dusty conditions, and preexisting lesions of
described for atypical interstitial pnew110-
chronic cranioventral bacterial pneumonia
nia. Treatment is as described for nitrogen
have been suggested as causes or contributdioxide toxicity.

ing factors. Clinical signs include respiratory
distress characterized by tachypnea and
dyspnea, and affected cattle may be found
dead if clinical signs are unobserved. Lesions

VENA CAVAL THROMBOSIS
are those of atypical interstitial pneumonia

AND METASTATIC
with prominent emphysema and edema in

PNEUMONIA
the lungs. Treatment protocols have not been
defined; thus, treatment is syn1ptomatic and

Etiology: Vena caval thrombosis and
supportive. In many cases, emergency
metastatic pneumonia is associated with
slaughter is the most economical option.

multifocal abscesses in the-lung as the

Management strategies suggested include
result of septic embolism of the pulmonary
vaccinating for bovine respiratory syncytial
arterial vascular system arising from
virus, controlling dust in the feedlot, and
septic thrombi in the caudal vena cava.

avoiding abrupt dietary changes.

The most common cause of vena caval
thrombosis is ruminal acidosis leading to
rumenitis and subsequent liver abscessa

4-IPOMEANOL TOXICITY (MOLDY
tion, which may result in a thrombus in the

SWEET POTATO) AND PERILLA
caudal vena cava if the vessel wall is

KETONE TOXICITY (PURPLE MINT
infiltrated by the abscess. Bacteria most

TOXICITY)

frequently involved include Fusobaclerium necrophorum, Trueperella Clinicopathologic syndromes indistin
pyogenes, staphylococci, streptococci,
guishable from acute bovine pulmonary
and Escherichia coli.

emphysema and edema (AB PEE, see
p 1439) occur after ingestion of either

Clinical Findings: The condition usually
moldy sweet potatoes infested with
occurs in adult dairy cattle or in feedlot

RESPIRATORY DISEASES OF HORSES

1443
cattle on high-carbohydrate diets. Presentaneurysms, and blood clots from ruptured ing signs can be acute, manifested by resaneurysms found throughout the entire lung piratory distress, or chronic, manifested by
parenchyma. The generalized distribution
weight loss and chronic coughing.

of these lesions caused by hematogenous

A common presentation is tachypnea,
spread is characteristic of this condition.

tachycardia, hemic mummrs, coughing,

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pale mucous membranes, increased lung
sounds, hemoptysis, and epistaxis. Pyrexia

Treatment and Control: Because of the
and melena may also be present. The case
poor prognosis, treatment is not indicated.

fatality rate is essentially 100%.

lf attempted, treatment includes antibiotics
and supportive therapy. Control efforts

Lesions: A thrombus is found in the
should focus on reducing the incidence
vena cava, and hepatic abscesses may
ofrurninal acidosis, which can result in
be noted. A suppurative pneumonia is
rurnenitis and subsequent fom1ation of liver
present with pulmonary abscesses,
abscesses.

RESPIRATORY DISEASES OF HORSES

Viral respiratory infections are common
abnom1al lung sounds, hyperfibrinogenin horses; the most notable are equine emia, and leukocytosis. Secondary bacterial
herpesvirus infection, equine influenza, and
disease may result in mucosa! bacterial
equine viral arteritis. The clinical manifestainfections ( rhinitis and tracheitis) or may tions are similar and include pyrexia, serous produce more serious invasive disease such nasal discharge, submandibular lymphadas pneumonia and pleuropnewnonia.

enopathy, anorexia, and cough. In addition

Streptococcus equi zooepidemicus is the
to respiratory disease, equine herpesvirus
most conu11on oppo1tWlistic pathogen of
type 1 (EHV-1) can cause abortion and
the equine lung, although Actinobacillus
neurologic disease, and equine herpesvirus
equuli, Bordetella bronchiseptica,
type 5 (EHV-5) is a newly recognized cause

Escherichia coli, Pasteurella. spp, and
of multinodular pulmonary fibrosis. Equine

Pseudomonas aeruginosa are frequently
viral arteritis produces respiratory disease,
isolated. S equi equi, the causative agent of vasculitis, and abortion. Equine herpesvirus
strangles (seep 1453), is a prin1ary bacterial type 2 (EHV-2), equine rhinitis vims, and
pathogen of the upper respiratory tract and
reovirus are ubiquitous viral respiratory
is capable of mucosa! invasion without
pathogens, and infection results in minimal
predisposing factors. Rhodococcus eq·u·i is a clinical disease. Adenovirus pneun10nia is
primary pathogen of the lower respiratory
most often seen in association with severe
tract of foals and produces pulmonary
combined immunodeficiency in Arabian
consolidation and abscessation. R equi
foals. Hendra vims ( see p 1448) is a zoonotic pnewnonia has been reported in adult disease of horses identified in Australia; it is
horses with a compromised immune
rapidly fatal in horses, and close contact is
system.

necessary for disease transmission.

Noninfectious respiratory disease is a

Secondary bacterial respiratory
common, perfom1ance-li.rniting condition
infections are primarily initiated by viral
that affects adult horses of various ages.

disease, because viral respiratory infections Inflammatory airway disease is impair and/or destroy respiratory defense
characterized by excessive tracheal mucus,
mechanisms (ie, influenza destroys the
airway hyperreactivity, and poor exercise
mucociliary apparatus, EHV destroys
perfonnance in yow1g horses. The etiology
bronchial-associated lymphoid tissue).

is unclear, but viral respiratory infection

The most common organisms associated

(EHV-2), allergy, and environmental factors
with pneun1onia in horses are opportunistic may play a role in tl1e pathophysiology.

bacteria originating from the resident

Reactive airway disease (heaves) is
microflora of the upper respiratory tract.

triggered by exposure to organic dusts in

Clinical evidence of a secondary bacterial
older horses with a genetic predisposition
infection includes mucopurulent nasal
to allergic airway disease. Small airways are
discharge, depression, persistent fever,
obstructed by bronchoconstriction and

1444

RESPIRATORY DISEASES OF HORSES
excessive mucus production. The severity
procedures and perfom1ed only after other
of clinical signs ranges from exercise
diagnostic procedures have been exintolerance to dyspnea at rest.

hausted. Pulmonary neoplasia, pulmonary

The respiratory system is one of the
fibrosis, and interstitial diseases may
most accessible body systems to test
require lung biopsy to obtain a definitive

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diagnostically. Endoscopic exan1ination
diagnosis.

allows direct visualization of the upper

Vaccination does not always prevent
respiratory tract, guttural pouches,
respiratory infections in horses, but
trachea, and mainstem bronchi. Indicaduration and severity is usually lessened in tions for endoscopic examination include
horses that have been vaccinated regularly,
upper airway noise, inspiratory difficulty,
depending on factors such as the disease
poor exercise performance, and tmilateral
and specific vaccine. Vaccines are commeror bilateral nasal discharge. Radio graphs cially available for equine influenza, viral
of the skull are indicated to investigate
rhinopneumonitis, equine viral arteritis,
facial deformity, abnormalities of the sinus
and strangles. The cost and hazards of

(sinusitis, dental abnormalities, and sinus
each vaccination must be weighed against
cyst), guttural pouch ( empyema, tympany ), the probability of exposure and potential and soft-tissue structures ( epiglottis, soft
disease. Vaccination recommendations
palate). The most important techniques for
and schedules vary according to use of
evaluation of lower respiratory tract
the horse and its potential for exposure
secretions are transtracheal wash and
to contagious animals. The American
bronchoalveolar lavage. Transtracheal

Association of Equine Practitioners
wash is indicated to obtain secretions for

(AAEP) Infectious Disease Committee
bacterial and fungal culture of the lower
has developed guidelines for all core and
respiratory tract. Bronchoalveolar lavage
risk-based equine vaccinations; recomis indicated for cytologic evaluation of the mendations are posted on the AAEP
lower respiratory tract in animals with

Web site.

diffuse, noninfectious pulmonary disease.

Regardless of the type of respiratory

Nasal swab culture is inappropriate for
disease, environmental factors and
investigation of pulmonary infectious
supportive care are important to aid
disease but is indicated for horses with
recovery. A dust and ammonia-free stable
suspected strangles infection.

environment prevents further damage

Thoracic radiography and ultrasonograto the mucociliary apparatus. Highly palatphy are valuable for assessing lower able feeds are indicated to prevent weight
respiratory tract disease. Thoracic
loss and debilitation during the treatment
radiography is used to identify abnormaliand recovery period. Adequate hydration ties of the pulmonary parenchyma,
will decrease the viscosity of respiratory
mediastinum, and diaphragm. Pulmonary
secretions, facilitating their removal from
consolidation (pnewnonia), peribronchial
the lower respiratory tract. A comfortable,
disease, pulmonary abscessation, interstidry, temperature-appropriate environtial disease, and mediastinal masses ment will allow the horse to rest and

(neoplasia, abscess, granuloma) are most
minimize the role of the respiratory tract
easily identified via thoracic radiography.

in thermoregulation.

Thoracic ultrasonography is the most
appropriate technique to evaluate fluid in
the pleural space, peripheral pulmonary

EQUINE HERPESVIRUS
consolidation, and peripheral pulmonary

INFECTION
abscessation. Ultrasonographic examination can identify the volwne, location, and (Equine viral rhinopneumonitis, Equine
character of plemal fluid or air within the
abortion virus)

plemal space (pnewnothorax). Addition

Etiology and Epidemiology: Equine
ally, it can identify fibrin tags, gas echoes
herpesvirus 1 (EHV-1) and equine

(anaerobic infection), masses, and
herpesvirus 4 (EHV-4) comprise two
locttlated fluid pockets, and it allows the
antigenically distinct groups of viruses
clinician to determine the most appropriate
previously referred to as subtypes 1 and 2
site for centesis and to formulate a
of EHV-1. Both viruses are ubiquitous in
prognosis.

horse populations worldwide and produce

Plemocentesis is performed in anin1als
an acute febrile respiratory disease upon
with accwnulation of fluid in the plemal
primary infection, characterized by
space and should be conducted with
rhinopharyngitis and tracheobronchitis.

ultrasonographic guidance. Ltmg biopsy

Outbreaks of respiratory disease occm
and fine-needle aspiration are invasive
annually among foals in areas with

RESPIRATORY DISEASES OF HORSES

1445
concentrated horse populations. Most of
severe posterior paralysis with recumbency,
these outbreaks in weanlings are caused by
loss of bladder and tail function, and loss of
strains ofEHV-4. The age, seasonal, and
skin sensation in the perinea! and inguinal
geographic distributions vary and are
areas. In exceptional cases, the paralysis
determined by immune status and horse
may progress to quadriplegia and death.

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population. In individual horses, the

Prognosis depends on severity of signs
outcome of exposure is determined by viral and the period of recumbency.

strain, immune status, pregnancy status,
and possibly age. Infection of pregnant

Lesions: The pathogenetic mechamares with EHV-4 rarely results in nisms of EHV-1 and EHV-4 differ signifiabortion.

cantly. EHV-4 infection is restricted to

Mares may abort several weeks to
respiratory tract epithelium and associated
months after clinical or subclinical infection lymph nodes; EHV-1 strains develop with EHV-1. The neurologic form of EHV-1
cell-associated viremia and have a predilechas demonstrated increasing morbidity and tion for vascular endothelium, especially
mortality in the documented outbreaks
the nasal mucosa, lungs, placenta, adrenal,
since 2000 and appears to be evolving in
thyroid, and CNS. The neuropathic strain
virulence and behavior. Therefore, the
of EHV-1 produces a viremic load 10- to

USDA has designated neuropathic EHV-1 as

100-fold higher than that of non-neuropathic
a potentially emerging disease. The natural
strains.

reservoir of both EHV-1 and EHV-4 is the

Gross lesions of viral rhinopneumonitis
horse. Latent infections and carrier states
are hyperemia and ulceration of the
are seen with both virus types. Transmisrespiratory epitheliwn, and multiple, tiny, sion occurs by direct or indirect contact
plwn-colored foci in the lungs. Histologiwith infectious nasal secretions, aborted cally, there is evidence of inflammation,
fetuses, placentas, or placental fluids.

necrosis and intranuclear inclusions in the
respirat�ry epithelium and genninal centers

Clinical Findings: The incubation period
of the associated lymph nodes. Lung lesions
of ERV is 2-10 days. Susceptible horses
a.re characterized by neutrophilic infiltradevelop fever of 102° -107°F (38.9° -41. 7°C), tion of the tenninal bronchioles, peribronneutropenia and Jymphopenia, serous chiolar and perivascular mononuclear cell
nasal discharge, malaise, pharyngitis,
inflltration, and serofibrinous exudate in the
cough, inappetence, and/or submandibular
alveoli.

or retropharyngeal lymphadenopathy.

Typical lesions in EHV-1 abo1tion

Horses infected with EHV-1 strains often
include interlobular Jung edema and
develop a biphasic fever, with cellpleural fluid; multifocal areas of hepatic associated viremia coinciding with the
necrosis; petechiation of the myocardmm,
second temperature peak. Seconda
adrenal gland, and spleen; and thymic
ry
bacterial infections are common and
necrosis. Intra.nuclear inclusions are found
manifest with mucopurulent nasal exudate
in Jung, liver, adrenal, and lymphoreticular
and pulmonary disease. The infection is
tissues.

mild or inapparent in horses immunologi

Horses with EHV-1-associated neurologic
cally sensitized to the virus.

disease may have no gross lesions or only

Mares that abort after EHV-1 infection
minimal evidence of hemorrhage in the
seldom display premonitory signs.

meninges, brain, and spinal cord paren

Abortions occur 2 -12 wk after infection,
chyma. Histologica.lly, lesions are discrete
usually between months 7 and 11 of
and comprise vasculitis with endothelial cell
gestation. Aborted fetuses are fresh or
damage and perivascular cuffing, thrombus

.

minimally autolyzed, and the placenta JS
fonnation and hemorrhage, and in advanced
expelled shortly after abortion. There is no
cases, areas of malacia Lesions may occur
evidence of dan1age to the mare's reproducat any level of the brain or spinal cord.

tive tract, and subsequent conception is
unimpaired. Mares exposed late in gestation

Diagnosis: Equine viral rhinopneumonitis
may not ab01t but give birth to live foals
is difficult to clinically differentiate from
with fulminating viral pneun10nitis. Such
equine influenza (seep 1447), equine viral
foals are susceptible to secondary bacterial
a.rteritis (seep 701), or other equine
infections and usually die within hours or
respiratory infections solely on the basis
days.

of clinical signs. Definitive diagnosis is

Outbreaks with specific strains of EHV-1
determined by PCR or virus isolation from
infection result in neurologic disease (seep
samples obtained via nasopharyngeal swab

1245). Clinical signs vary from mild
and citrated blood sample (buffy coat) early
incoordination and posterior paresis to
in the course of the infection.

1446

RESPIRATORY DISEASES OF HORSES

In cases of suspected EHV-1 abortion,
viremia, which may result in transplacental
definitive diagnosis is based on PCR, virus
infection of the fetus.

isolation, and charactelistic gross and

For prevention and control of EHV-4- and
microscopic lesions in the aborted fetus.

EHV-1-related diseases, management

Lung, liver, adrenal, and lyrnphoreticular
practices that reduce viral spread are
tissues are productive sources of virus.

recommended. New horses ( or those

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Sero logic testing of mares after abortion
returning from other premises) should be
has little diagnostic value. Diagnosis of
isolated for 21 days before conuningling
neuropathic EHV-1 is detennined by
with resident horses, especially pregnant
real-time PCR on samples obtained from
mares. Management-related, stress-inducing
nasal secretions, CSF, or neural tissue to
circun1stances should be avoided to prevent
detect the neuropathic strain of EHV-1. A
recrudescence of latent virus. Pregnant
presun1ptive diagnosis can be based on
mares should be maintained in a group
clinical signs and CSF analysis (xanthochroaway from the weanlings, yearlings, and mia, albuminocytologic dissociation).

horses out of training. In an outbreak of

Necropsy reveals charactelistic pelivascurespiratory disease or abortion, affected lar cuffing and hemorrhage in the CNS.

horses should be isolated and appropliate
measures taken for disinfection of

Treatment: There is no specific treatment
contaminated premises. No horse should
for EHV infection. Rest and nursing care are
leave the premises for 3 wk after recovery
indicated to minimize secondary bacterial
of the last clinical case.

complications. Antipyretics are recom

Vaccination (EHV-4 and EHV-1) should
mended for horses with a fever > 104 °F
begin when foals are 4--0 mo old. A second

( 40°C). Antibiotic therapy is instituted upon
dose is given 4-6 wk later, and a third dose
suspicion of secondary bactelial infection
at 10-12 mo of age. Booster vaccinations
evidenced by purulent nasal discharge or
may be indicated as often as every
pulmonary disease. Most foals infected

6 mo through maturity (5 yr of age ). Vacprenatally with EHV-1 die shortly after birth cination programs against herpesvirnses
despite intensive nursing and antimicrobial
should include all horses that travel to
medication. If horses with neuropathic
high-risk destinations (racetrack, show

EHV-1 remain ambulatory or are recumbent
grounds) and all other horses on the
for only 2-3 days, the prognosis is usually
premises. A high-antigen load, inactivated
favorable. Valacyclovir (30 mg/kg, PO, bid)

EHV-1 vaccine is recommended to prevent
has shown promise in the treatment of

EHV-1 abortion. Vaccine should be
affected horses and in prophylaxis during
administered duling months 3, 5, 7, and 9 of

EHV-1 outbreaks. Intensive nursing care is
pregnancy. Mares are often vaccinated with
necessary to avoid pulmonary congestion,
inactivated EHV-1/EHV-4 at an interval 4--0
pneumonia, ruptured bladder, or bowel
wk before foaling. A modified-live EHV-1
atony. Recovery may be complete, but a
vaccine is available to help prevent
small percentage of cases have neurologic
respiratory disease caused by EHV-1.

sequelae.

Infection by other Herpesviruses:

Control: Immwlity after natural infection

Equine herpesvirus 2 (EHV-2) is ubiquitous
with either EHV-1 or EHV-4 involves a
in respiratory mucosa, conjunctiva, and
combination of humoral and cellular

WBCs of normal horses of all ages. The
immwlity. Whereas little cross-protection
pathogenic significance reinains obscure.

occurs between virus types after plimary

It has been suggested that EHV-2 is the
infection of inm1unologically naive foals,
cause of herpetic keratoconjunctivitis and
significant cross-protection develops in
inflan1Il1atory airway disease in young
horses after repeated infections with a
horses. Equine herpesvirus 3 (EHV-3) is
particular vilus type. Most adult horses are
the cause of equine coital exanthema (seep
latently infected with EHV-1 and EHV-4. The

1357), a benign, progenital exanthematous
infection remains dormant for most of the
disease.

horse's life, although stress or inm1unosup

Equine g=a herpesvirus 5 (EHV-5) has
pression may result in recrudescence of
emerged as the pathogen associated with
disease and shedding of infectious virus.

equine multinodular pulmonary fibrosis

Immw1ity to reinfection of the respiratory

(EMPF). The role of EHV-5 in EMPF is
tract may persist for as long as 3 mo, but
unclear (precipitating, causative, incidenmultiple infections result in a level of tal). Clinical signs include weight loss,
inmlwlity that prevents clinical signs of
cough, fever (valiable), and respiratory diffirespiratory disease. Diminished resistance culty. EMPF is seen plimalily in midd.lein pregnant mares allows cell-associated aged horses, although it has been reported

RESPIRATORY DISEASES OF HORSES

1447
in young horses. Physical examination

EQUINE INFLUENZA
findings include tachycardia, tachypnea,
increased respiratory effort (inspiratory),

Etiology and Epidemiology: Equine
and poor body condition. Wheezes and
influenza is highly contagious and spreads
crackles are often ausculted without a
rapidly among naive horses. Horses 1-5 yr
rebreathing procedure. In early cases,
old are the most susceptible to infection.

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EMPF may be mistaken as heaves. In

Orthomyxovirus Nequine-2 was first
addition to EMPF, EHV-5 has been
recognized in 1963 as a.cause of widespread
associated with lymphoproliferative disease epidemics and has subsequently become and lymphoma. One unusual case repo1t
endemic in many countries, except for New
describes a 21-yr-old horse with profound

Zealand and Iceland. China, Japan, and
pancytopenia and pulmonary fibrosis;

Australia experienced devastating

EHV-5 was isolated from the bone marrow
epidemics of equine influenza affecting tens
of this horse.

of thousands of horses in 2007. Equine

Diagnostic testing includes routine blood
influenza had not been reported in China
work, thoracic radiographs, and virussince 1993, in Japan since 1972, and had specific PCR testing on puhnonary secretions never been repo1ted in Australia.

(bronchoalveolar lavage) or percutaneous

Endem.icity is maintained by sporadic
lung biopsy sample. CBC reveals neutroclinical cases and by inapparent infection philic leukocytosis with or without
in susceptible horses introduced into the
hyperfibrinogenemia and anemia. Findings
population by birth, through waning
on thoracic radiographies range from a
immunity, or after movement from other
moderate interstitial pattern to a severe
areas or countries. A canier state is not
reticulonodular pattern. Differential
recognized for equine influenza. The clinical
diagnoses of radiographic images include
outcome after viral exposure largely
fungal pneumonia and metastatic neoplasia.

depends on immune status; clinical disease

Fungal pneumonia typically occurs after
varies from a mild, inapparent infection to
primary GI disease with neutropenia, and
severe disease in susceptible animals.

metastatic neoplasia is rare. The most

Influenza is rarely fatal except in don keys,
common antemortem diagnostic test is
zebras, and debilitated horses. Transmisvirus-specific PCR of bronchoalveolar sion occurs by inhalation of respiratory
lavage fluid. Percutaneous, ultrasoundsecretions. Epidemics arise when one or guided lung biopsy can be performed to
more acutely infected horses are introduced
confirm the diagnosis and establish a
into a susceptible group. The epidemiologic
prognosis. The procedure is not without risk outcome depends on the antigenic in dyspneic horses. Histopathology reveals
characteristics of the circulating virus and
multifocal granulomas, type II pneun10cyte
the inunune status of a given population of
hyperplasia, and intralun1inal cellular
horses at time of exposure. Frequent natural
accumulation. Advanced pulmonary fibrosis exposure or regular vaccination may indicates a poor prognosis for sutvival.

contribute to the degree of antigenic drift

The prognosis for survival is -500/o.

seen with specific strains of Nequine-2 virus

Horses with granulomatous inflammation
in some parts of the world.

have been successfully treated with
antiviral therapy. Valacyclovir (30 mg/kg,

Clinical Findings and Lesions: The

PO, tid) and/or acyclovir (10 mg/kg, IV, in
incubation period of influenza is -1-3 days.

1 L of isotonic crystalloid fluid as a constant

Clinical signs begin abruptly and include
rate infusion over 1 hr, bid x 2 days) appear
high fever (up to 106°F (41.1 °C]), serous
promising, although sensitivity of the
nasal discharge, submandibular lymphadvirus to these medications has not been enopathy, and coughing that is d1y, harsh,
documented. Doxycycline (5-10 mg/kg,
and nonproductive. Depression, anorexia,

PO, once to twice daily) is administered
and weakness are frequently seen. Clinical
to combat secondary bacterial infection
signs usually last <3 days in uncomplicated
and for its anti-inflanunatory properties.

cases. Influenza virus replicates within

Administration of corticosteroids is
respirato1y epithelial cells, resulting in
controversial, although they are commonly
destruction of tracheal and bronchial
used. Corticosteroids (0.08-0.1 mg/kg, IV,
epithelium and cilia. Cough develops early
every 24--48 hr) may improve disease
in the course of infection and may persist
outcome through reduction of pulmonary
for several weeks. Nasal discharge,
cytokines and inflanunatory mediators, but
although scant and serous initially, may
they may also cause irnrnunosuppression,
become mucopurulent due to secondary
which may enhance viral replication and
bacterial infection. Mildly affected horses
disease severity.

recover w1eventfully in 2-3 wk; severely

1448

RESPIRATORY DISEASES OF HORSES
affected horses may convalesce as long as 6
primarily for IM administration. A recombimo. Recovery may be hastened by complete nant canarypox-vectored influenza vaccine
restriction of strenuous physical activity.

has also been shown to be effective against

Respiratory tract epithelium takes -21 days
influenza challenge. Because the duration of
to regenerate; during this time, horses are
protection provided by current vaccines is

VetBooks.ir
susceptible to development of secondary
limited, booster iltjections for at-risk adult
bacterial complications such as pneumonia,
horses should be administered every 6 mo.

pleuropnew11onia, and chronic bronchitis.

Sedentary horses can be vaccinated

Complications are minimized by restricting
annually. Foals should be vaccinated with a
exercise, controlling dust, providing
single modified-live intranasal vaccine or a
superior ventilation, and practicing good
series of three inactivated vaccines
stable hygiene. P1imary complications of
beginnillg at 6 mo, with booster vaccination
vasculitis, myositis, and myocarditis are
in 3----6 wk and again between IO and 12 mo of
seen infrequently.

age. Broodmares should be vaccinated 4---6
wk before foaling.

Diagnosis: The presence of a rapidly
spreading respiratory infection in a group of
horses characterized by rapid onset, high

EQUINE VIRAL ARTERITIS
fever, depression, and cough is presumptive
evidence of equine influenza. Definitive

Equine viral arteritis (EVA) is caused by an
diagnosis can be detennined by virus

RNA togavirus and produces clinical signs
isolation, influenza A antigen detection
of respiratory disease, vasculitis, and ab01°

(patient-side kit), or paired serum samples
tion. Horses with EVA infection present

(hemagglutination inhibition). Nasopharynwith fever, anorexia, and depression. The geal swabs are obtained for virus isolation
clinical signs of respiratory infection due
and antigen detection. These samples
to EVA are serous nasal discharge, cough,
should be obtained soon after the onset of
conjunctivitis, lacrimation, and palpebral,
illness. Virus isolation in chick embryos
scrotal, and periorbital edema. Clinical
is highly specific but less sensitive for
signs of disease persist for 2-9 days.

detection of influenza because of bacterial

Treatment consists of supportive care
contamination of the san1ple. Antigen

(support bandages) and NSAIDs for fever
detection is perfom1ed using a hwnan
and inflanrn1ation. Antimicrobial therapy
influenza A kit, which provides immediate
is usually unnecessary. A carrier state
results that are not affected by bacterial
occurs in most stallions after natural
contamination.

infection and is primarily responsible for
persistence of the virus in the horse

Treatment and Prevention: Horses that
population through infectious seminal
do not develop complications require rest
fluids. Vaccination (modified-live virus) is
and supportive care. Horses should be
targeted toward prevention of venereal
rested 1 wk for every day of fever, with a
spread of EVA in breeding animals as
mini.Imun of3 wk rest (to allow regeneraopposed to prevention of respiratory tion of the mucociliary apparatus). NSAIDs
disease (seep 701).

are recommended for horses with a fever

>104°F (40°C). Antibiotics are indicated
when fever persists beyond 3-4 days or

HENDRA VIRUS INFECTION
when purulent nasal discharge or pneumonia is present.

(Equine morbillivirus)

Prevention of influenza requires hygienic

Hendra virus (HeV) is tl1e prototype species
management practices and vaccination.

of a new genus Henipavi1us within the

Exposure can be reduced by isolation of
subfamily Paramyxovirinae and was first
newly introduced horses for 2 wk. Numeridentified in Australia in 1994. The viral ous vaccines are commercially available for
agent is endemic in specific species of fruit
prevention of equine influenza. An intranasal bats (also called flying foxes), and close modified-live influenza vaccine, designed to
contact with these bats is suspected to have
induce mucosal (local) antibody protection,
facilitated transfer of the He V to horses.

has demonstrated protection against natural

Horses are infected by oronasal routes and
challenge. This vaccine is temperature
excrete HeV in urine, saliva, and respiratory
sensitive and is not capable of replicating
secretions.

beyond the nasal passages (ie, inactivated by

There have been multiple, sporadic
core body temperature). Most commercially
incidents of human and equine disease in
available influenza vaccines are inactivated,

Australia occurring in 1994, 1995, 1999,
acljuvanted vaccines recommended

2004, 2008, and 2009. The case fatality rate

RESPIRATORY DISEASES OF HORSES

1449
in horses and people is high, with reports
bacterial replication. Acute pulmonary
of 81 horses and 4 people succwubing to
infarction can be the inciting event for

Hendra virus infection, including an equine
equine pleuropneWllonia.

veterinarian investigating an outbreak.

Polymicrobial and mixed anaerobic

Very close contact is required to transmit
aerobic infections are common in horses

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the virus an1ong horses and from horses to
with pleuropneru11onia, with more than one
people, and the virus is not considered
organism isolated from transtracheal
highly contagious. Equine veterinarians
aspirates. The most common aerobic
are considered at occupational risk of
organisms are Streptococcus equi
contracting HeV. Infected horses develop
zooepidemicus, Esche1ichia. coli,
severe and often fatal respiratory disease,

Actinoba.cillus spp, Klebsiella. spp, characterized by dyspnea, vascular

Enteroba.cte1· spp, Staphylococcus aureus, endothelial dan1age, and pulmonary edema.

and Pasteurella spp. Anaerobic bacteria are Depression, anorexia, fever, respiratory
isolated from 400/o--700/o of horses with
difficulty, ataxia, tachycardia, and frothy,
plew·opneWllonia; Bacteroides spp,
nasal discharge are common clinical signs.

Clostridium spp, Peptostreptococcus spp, (See a.lso p 707.) A commercial HeV vaccine and Fusobacte1 .. ium spp are the most
for use in horses is available ru1der a Minor
common. The etiology of pleural infection

Use Pem1it for release to veterinarians who
in horses is usually bacterial, although
have completed an online training program.

Mycoplasmafelis and nocardial agents

Horses must have a microchip to be
have been isolated from pleural effusions.

vaccinated, and the infonuation must be
entered into the HeV Vaccine National

Clinical Findings and Lesions: Horses

Online Registry. The vaccine consists of
with pleuropneumonia present with fever,
soluble fom1s ofG glycoprotein ofHeV; it
depression, lethargy, and inappetence.

does not contain modified or inactivated

Clinical signs specific to pleuropneumonia
virus.

include pleural pain (pleurodynia) evident
as short strides, guarding, and flinching on
percussion of the chest; shallow respira

PLEUROPNEUMONIA
tion; and endotoxemia. Horses with pleural
pain have an anxious facial expression;

(Pleuritis, Pleurisy)

stand with their elbows abducted; and are

Pleuropnewuonia is defined as infection
reluctant to move, cough, or lie down. Gait
of the lru1gs and pleural space. In most
may be stiff or stilted, and some horses
instances, pleural infection develops
grunt in response to thoracic pressure,
secondary to bacterial pneumonia or
auscultation, or percussion. Nasal
penetrating tl10racic woru1ds. Spontaneous
discharge is a variable sign. Putrid breath
pleuritis (without accompanying pnellilloor fetid nasal discharge indicates anaerobic nia) is uncommon in horses. In the USA,
bacterial infection and necrotic pulmonary

-700/o of horses with pleural effusion have
tissue. The respiratory pattern is characterpleuropneWllonia. The prin1ary differential ized by rapid, shallow respiration due to
diagnoses for pleural effusion are neoplastic pleural pain and restricted pulmonary effusions, heart failure, and hydatidosis.

expansion from pleural effusion. A plaque
of sternal edema is seen in horses with a

Etiology and Pathogenesis: Viral
large volume of pleural effusion. Horses
respiratory infection, long-distance
with toxemia have injected mucous
transportation, general anesthesia, and
membranes, delayed capillary refill time
strenuous exercise are common predispos

(>2 sec), and tachycardia. Auscultation
ing factors that impair pulmonary defense
reveals a lack of breath sounds in the
mechanisms, allowing secondary bacterial
ventral lung fields and abnormal lung
invasion. Head restraint results in bacterial
sounds (often crackles) in dorsal lung
contan1ination and multiplication within the
fields. Cardiac soru1ds may be muffled or
lower respiratory tract within 12-24 hr and
absent or may radiate over a wider area.

may be tl1e single most important predispos

Although uncommon, pleural friction rubs
ing factor for development of pnew110nia
are most prominent at end-inspiration and
associated with long-distance transport.

early expiration and are detected after

Race and sport horses are particularly at
thoracic drainage.

risk. Most horses with pleuropneWllonia are
atl1letic horses <5 yr old. Exercise-induced

Diagnosis: In horses witl1 peracute
pulmonary hemorrhage may contribute to
pleuropnewuonia, laboratory findings
development of respiratory infection by
reflect bacterial sepsis or toxemia and
providing a favorable environment for
include abnormalities such as leukopenia,

1450

RESPIRATORY DISEASES OF HORSES
neutropenia, left shift, hemoconcentration,
initial antimicrobial therapy. Bacterial
and azotemia. Horses with more stable
culture and sensitivity should also be
disease have leukocytosis, mature
perfonned on transtracheal aspirate
neutrophilia, hyperfibrinogenemia,
san1ples, which yield positive bacterial
hyperglobulinemia ( chronic antigenic
cultures more frequently tl1an pleural fluid
stimulation), hypoalbuminemia (loss in
san1ples.

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pleural space), and anemia of chronic
disease.

Treatment: Management of horses with

Thoracic ultrasonography is ideal for
pleuropnewnonia includes daily ultrasound
investigation of pleural effusion and is
exanlination to monitor fluid production,
indicated in horses with regions of poor to
evaluate effective drainage, identify
absent breath sounds, thoracic pain, and/or
isolated fluid pockets, and assess periphdull thoracic percussion. Transudative eral pulmonary disease. The volume and
pleural fluid (neoplastic effusion) appears
character of pleural fluid will determine
anechoic, whereas more cellular exudate
whether single, intemtittent, or continual
appears echogenic. Gas echoes represent
drainage is indicated. Continual drainage
small air bubbles within pleural fluid, which
is preferable in cases with fibrinous,
may indicate an anaerobic pleural infection,
cellular, malodorous, and/or large volmne
a bronchopleural fistula, or iatrogenic
of effusion. A one-way (Heimlich) valve
introduction of air. Pulmonary atelectasis,
allows constant drainage of pleural fluid
consolidation, and abscessation can be
witl1 nlininlal risk of development of
identified if the lesions are located in periphpneumothorax. An indwelling chest tube eral lung fields. Ultrasonographic evidence
should remain in place as Jong as drainage
of a large area of pulmonary consolidation,
is productive. Medical therapy includes
in cor\junction with serosangui:neous suppubroad-spectrum antibiotics, NSAIDs, rative plew·aJ effusion, is consistent with
analgesics, and supportive care. Broadpulmonary infarction and necrotizing spectrum antimicrobial therapy targeting
pneumonia. Adhesions of the visceral to
common aerobic and anaerobic bacteria
parietal pleura can be visualized using

( eg, penicillin, gentanlicin, metronidazole)

thoracic ultrasonography, and these regions should be instituted pending results of should be avoided during thoracocentesis.

culture and sensitivity. Intrathoracic

Ultrasonography should be performed
fibrinolytic therapy has been reported to
before pleurocentesis to detennine the best
reduce fibrin deposition and pleural fluid
site for maximal drainage and to avoid
accunmlation. In some horses, the pleural
cardiac or diaphragmatic pw1cture.

infection does not resolve despite weeks

Thoracocentesis is perfom1ed for diagnosto montl1S of antimicrobial tl1erapy and tic and therapeutic purposes in horses with
drainage via indwelling chest tubes.

pleuropneun10nia. Pleural fluid should be

Thoracostomy allows manual removal of
drained relatively slowly to avoid hypotenorganized fibrinous material and necrotic sion. The hemithorax that appears to
ltmg; however, tllis technique should be
contain the most fluid is drained first.

limited to horses with chronic, stable,

Bilateral thoracocentesis is usually
tutilateral disease with resolving infection
necessary. The chest tube may be removed
in the contralateral henlithorax.

inunediately after drainage of the thoracic

Complications associated with pleurocavity or may be secured in place to allow pneun10nia include thrombophlebitis,
continual drainage. Thoracic radiography is
lami.Ilitis, bronchopleural· fistula, pulmoindicated after pleurocentesis to evaluate nary abscess, and cra.ilial thoracic mass.

pulmonary parenchyrnal lesions, mediasti

The prognosis for horses with pleuronal structures, and the presence/severity of pneumonia has greatly improved tlrroughpnewnolhorax.

out the past 20 yr because of early

Gross examination of pleural fluid
recognition, advancements in diagnostic
includes evaluation of color, odor, volwne,
testing, and aggressive therapy. The survival
and turbidity. Malodorous pleural fluid is
rate is reported to be as high as 900A, by some
associated with necrotic tissue and
investigators, with a 60% chance of return to
anaerobic infection and indicates a guarded
athletic performance. The duration of
prognosis. Cytologic evaluation of septic
hospitalization is not indicative of outcome;
pleural fluid reveals purulent exudate (>90% however, a delay in initiation of appropriate neutroph.ils) with increased cellularity
therapy by >48 hr promotes development of

(25,000-200,000 cells/µL) and increased
anaerobic infection and, ultimately, poor
total protein (>3 g/dL). Intracellular and
response to treatment. Placement of an
extracellular bacteria may be seen, and
indwelling chest tube does not limit the

Gram stain exanlination is used to direct
prognosis for return to athletic function.

RESPIRATORY DISEASES OF HORSES

1451

Horses with hemon-hagic necrotizing

Pulmonary regions with marked consolipneumonia respond poorly to conventional dation Jack breath sounds and exhibit dull
therapy and have a low survival rate.

resonance on thoracic percussion. In
foals with subclinical infections, small to

RHODOCOCCUS EOUI
moderate-sized abscesses ( < 10 cm) may

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PNEUMONIA
resolve spontaneously.

Immune-mediated polysynovitis ( eg, stifle

Rhodococcus equi is the most serious
and hock effusion) is often seen in affected
cause of pneumonia in foals 1-4 mo old.

foals at presentation. Intestinal and

It is not the most common cause of
mesenteric abscesses are the most common
pneumonia in this age group; however, it
extrapulmonary sites of infection. Foals
has significant economic consequences
with abdominal involvement often present
because of mortality, prolonged treatment,
with fever, depression, anorexia, weight
surveillance progran1s for early detection,
loss, colic, and dian-hea. Intestinal lesions
and relatively expensive prophylactic
are characterized by multifocal, ulcerative
strategies. Clinical disease is rare in horses
enterocolitis and typhlitis involving Peyer's

>8 mo old. Compelling epidemiologic data
patches with granulomatous or suppurative
indicate pulmonary infection probably
inflammation of the mesenteric and/or
originates within the first week of life. (See
colonic lymph nodes. The prognosis for
also p 679.)

foals with abdominal forms of R equi is less favorable than for those with pulmonary

Etiology and Pathogenesis: R equi is disease. Septic physitis and osteomyelitis
a gran1-positive, facultative intracellular
are Jess conm1on extrapulmonary sites of
pathogen that is nearly ubiquitous in soil.

infection. Vertebral osteomyelitis may result

Inhalation of dust particles laden with
in pathologic vertebral fracture and spinal
virulentR equi is the major route of
cord compression and is a devastating manipnemnonic infection. Development of festation of R equi osteomyelitis. Panophclinical disease is related to immunocompethalmitis, guttural pouch empyema, tency of individual foals; foals that produce
sinusitis, pericarditis, nephritis, nonseptic
little to no detectable 'I interferon (IFN-'I)

uveitis, and hepatic and renal abscessation
are at risk of developing pnemnonia.

with R equi have been reported.

Manure from pneurnonic foals is a major
source of virulent bacteria contaminating

Diagnosis: Routine laboratory evaluathe environment. Foals with pulmonary tion of CBC and serum chemistry reveals
infections swallow sputun1 laden with
nonspecific abnormalities consistent with

R equi, which readily replicates in their
infection and inflammation. Neutrophilic
intestinal tract. The pathogenicity of R equi
leukocytosis and hyperfibrinogenemia are
is linked to its ability to survive intracellucommon, and the severity of these fin rungs larly, which hinges on failure of phagosomerelates to prognosis. Thoracic radiographic lysosomal fusion in infected macrophages
evaluation may reveal a pattern of perihllar
and failure of functional respiratory burst
alveolization, consolidation, and abscessaupon phagocytosis of R equi.

tion. The presence of nodular lung lesions
and mediastinal lymphadenopathy in foals

Clinical Findings and Lesions: R equi

1-4 mo old is highly suggestive of R equi.

infection is slowly progressive, with acute

Bacterial culttu·e of transtracheal wash
to subacute clinical manifestations.

samples is required for definitive diagnosis.

Clinical signs of disease are difficult to

Cytologic evaluation of transtracheal wash
detect until pulmonary infection reaches a
samples reveals intracellular coccobacilli,
critical mass, resulting in decompensation
indicating that appropriate antimicrobial
of the foal. Pulmonary lesions are relatively therapy should be started pending culture consistent and include subacute to chronic
results.

suppurative bronchopnemnonia, pulmonary
abscessation, and suppurative lymphadeni

Treatment and Prognosis: The
tis. At the onset of clinical signs, most
combination of erythromycin (25 mg/kg,
foals are lethargic, febrile, and tachypneic.

PO, qid; esters or salts) and 1ifampin

Diarrhea is seen in one-third of foals with

(5-10 mg/kg, PO, bid) has historically been

R equi pnemnonia and may be caused
the treatment of choice for R equi infection by colonic microabscessation. Cough is
in foals. These antinticrobials may be
a variable clinical sign; purulent nasal
bacteriostatic, but their activity is synergisdischarge is less common. Thoracic tic, and the combination has markedly
auscultation reveals crackles and wheezes
in1proved survival of foals with R equi
with asymmetric/regional distribution.

pnetm1onia. Rifampin is lipid soluble (able

1452

RESPIRATORY DISEASES OF HORSES
to penetrate abscess material) and is

Prevention: There are several strategies
concentrated in phagocytic cells. Erythroto decrease the incidence of R equi mycin is concentrated in granulocytes and
pneumonia on endemic farms: early
alveolar macrophages; however, its antidetection of clinical cases, enhanced microbial activity is somewhat inhibited by
passive immunity for neonatal foals, and

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intracellular pH. Adverse reactions are
enhanced nonspecific immunity for
relatively common in foals treated with the
neonatal foals. Foals should be maintained
erythromycin-rifampiil combination.

in well-ventilated, dust-free areas, avoiding

Diarrhea, idiosyncratic hyperthemlia,
dirt paddocks and overcrowding. Pneutachypnea, anorexia, bruxism, and monic foals should be isolated and their
salivation can occur with erytlu·omycin
manure composted. Herd surveillance
administration, and antimicrobial resistpro grains for early detection of pneumonic ance of R equi to erythromycin-rifampin
foals on endenlic farms include twice
has been reported.

weekly physical exan1ination and auscul

Claritlu·omycin is the macrolide of choice
tation and monthly CBC and fibrinogen
for foals with severe disease, given the most
concentration. Foals witil a WBC count
favorable nlinimwn inhibitory concentra

> 14,000 cells/µL should be further
tion againstR equi isolates obtained from
evaluated via ultrasonographic examinapneumonic foals (900/o of isolates are tion for R equi. Administration of hyperiminhibited at 0.12, 0.25, lllld 1 mcg/rnL for mune plasma might reduce tile incidence
clarithromycin, erythromycin, and
and severity of R equi witilin the herd, but azithromycin, respectively). In foals with
it is not completely effective in preventing

R eqiLi pnewnonia, the combination of
disease. Hyperimmune plasma (1 L) is
claiithromycin (7.5 mg/kg, PO, bid) and
administered IV within the first week of life,
rifan1pin is superior to erythromycinfollowed by a second liter at -25 days of rifampin and azithromycin-rifampin. Foals
age. Foals with low IFN--y production in tile
treated with clarithromycin-rifampin have
first month of life appear more susceptible
improved survival rates and fewer febrile
to development of clinical disease. Adnlinisdays than foals treated with e1ythromycintration of a nonspecific inununostimulant rifampin and azithromycin-rifampin.

may enhance IFN--y production and protect

Reported adverse events of clarithromycinthis susceptible population. Mass treatment rifampin include diatThea in treated foals.

of foals witil subclinical infection has

The duration of antimicrobial therapy
resulted in marcolide- and rifampintypically is 3---8 wk.

resistant strains and should be avoided.

Supportive therapy includes provision of
a clean, comfortable environment and highly
palatable, dust-free feeds. Judicial IV fluid

ACUTE BRONCHOINTERSTITIAL
therapy and saline nebulization facilitates

PNEUMONIA IN FOALS
expectoration of pulmonaiy exudates.

NSAlDs should be administered as needed

Acute bronchointerstitial pnewnonia is a
to maintain rectal temperature <103.5°F
sporadic, rapidly progressive disease of

(39.7°C). Nasal insufflation witl1 oxygen is
foals characte1ized by acute respiratory
necessaiy in foals with severe respiratory
distress and high mortality.

compromise. Bronchodilator therapy may
or may not inlprove arterial oxygenation.

Etiology, Epidemiology, and Patho

Prophylactic antiulcer medication is
genesis: The etiology of acute bronchoinindicated in foals stressed by respiratory terstitial pneun1onia in foals is not clear. It
difficulty, pain, frequent handling, hospitalimay result from different insults ratiler than zation, and transportation.

a single factor, initiate a cascade of events,

The survival rate of R equi pnew11onia is
and result in a final common response of

-700/o-900/o with appropriate therapy. The
severe pulmonaiy damage and acute
case fatality rate without therapy ( or with
respiratory distress. Warm weather (>85°F
inappropriate antimicrobial therapy) is

[29.4 °C]) is a common epidemiologic factor.

-800/o. Paraineters for discontinuation of

Many foals have a history of antimicrobial
medical tilerapy include clinical signs, semm
therapy when clinical signs developed. No
fibrinogen concentration, and radiographic
virus is consistently isolated, and no
resolution of pulmonary consolidation and
bacterial agent has been consistently
abscessation. Life-threatening, antibioticidentified. Enteric gran1-negative organisms, induced enterocolitis, due to Clostridiiim

Rhodococcus equi, Pseudomonas
di.fficile, has been seen in tile dams of
aeruginosa, and Pneumocystis jiroveC'i
nursing foals treated witil all macrolide
have been cultured from the lungs of
prepai·ations.

affected foals.

RESPIRATORY DISEASES OF HORSES

1453

Clinical Findings and Lesions: The age
necrotizing bronchiolitis, alveolar septa!

of affected foals ranges from 1 wk to 8 mo.

necrosis, and neutrophilic alveolitis.

Acute bronchointerstitial pneumonia has an

Surviving foals develop a proliferative
acute or pcracute onset and is accompanied
epithelial and interstitial response, including
by high fever. The disease is rapidly
bronchiolar and alveolar epithelial hyperpla

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progressive and may result in sudden death
sia, type II cell hyperplasia, and hyaline
due to fulminant respiratory failure. Foals
membrane formation.

are unable or reluctant to move and are
usually cyanotic. Severe respiratory distress Treatment: Because the cause of is the most striking clinical sign. Clinicobronchointerstitial pneumonia is unknown, pathologic evaluation of foals with acute
therapy is symptomatic. Treatment includes
respiratory distress should include arterial
anti-inflan1matory therapy, broad-spectrum
blood gas, CBC, serum chemistry analysis,
antibiotics, thennoregulatory control,
and thoracic radiographs. Hypoxemia,
bronchoclilation, supplemental oxygen, and
hypercapnea, and respiratory acidosis are
supportive care. Anti-i.nflan1111atory therapy
consistent findings. These arterial blood gas
with corticosteroids ( eg, dexan1ethasone
findings quantify the severity of respiratory

0.1 mg/kg/clay, IV) appears to in1prove
in1pairment and are used to monitor
survival. An alcohol bath, an air-conditioned
response to therapy. The hypoxemia of
stall, and/or a fan are used in conjunction
bronchointerstitial pneumonia is relatively
with NSAlDs to maintain rectal temperature
resistant to supplemental oxygen therapy.

<103.5°F (39. 7°C). The suitability of an

Bronchointerstitial pneumonia is similar to
antibiotic regimen appears to have little
bacterial pneumonia in that hyperfibrinobearing on the outcome of bronchointergenemia and neutrophilic leukocytosis are stitial pneumonia. Nonetheless, broadseen in most foals.

spectrum antibiotic therapy should be
instituted to treat existing or impending

Diagnosis: Physical exan1ination and
secondary bacterial infections. Additional
clinicopathologic findings may appear
supportive therapy includes provision of a
sin1ilar to those of foals with severe R equi
clean, comfortable environment; highly
pneumonia (seep 1451), and thoracic radiopalatable, dust-free feeds; and ulcer graphic exan1ination may be the most
prophylaxis.

valuable diagnostic test to differentiate

R equi pneumonia from bronchointerstitial

Prognosis: Although mortality is high,
pneumonia. Interstitial pneumonia appears
affected foals that receive aggressive
as diffuse to caudodorsally distributed intermedical care have a reasonably favorable stitial and bronchointerstitial pulmonary
prognosis for survival (70%). The longtern1
opacities. With advanced disease, the radiopulmonary consequences after recovery graphic pattern progresses to include
from bronchointerstitial pneumonia are
patches of a coalescing alveolar nodular
variable, ranging from undetectable to
pattern with air bronchograms. Transtrapersistent exercise intolerance.

cheal aspiration may be prohibitively
dangerous to pe1forn1 on a dyspneic foal
but should be done when the foal becomes

STRANGLES
more stable to obtain samples for bacterial
culture/sensitivity, cytologic evaluation,

(Distemper)

and virus isolation. Cytologic evaluation

Strangles is an infectious, contagious
of tracheal aspirates reveals acute
disease ofEquidae characterized by
neutrophilic inflan1mation with or without
abscessation of the lymphoid tissue of the
evidence of sepsis. Bacterial organisms
upper respiratory tract. The causative
are often recovered from transtracheal
organism, Streptococcus equi equi, is highly aspiration samples or necropsy of foals with host-adapted and produces clinical disease bronchointerstitial pneumonia; however, no
only in horses, donkeys, and mules. It is a
single organism is consistently recovered.

gram-positive, capsulatecl 13-hemolytic

Necropsy examination reveals diffusely

Lancefield group C coccus, which is an
enlarged lungs that fail to deflate upon
obligate parasite and a primary pathogen.

opening of the thoracic cavity with rib
impressions on the visceral pleural surface.

Etiology and Pathogenesis: S equi

The cut surface of lung is mottled, with dark
equi is highly contagious and produces high red lung interspersed with more normalmorbidity and low mortality in susceptible appearing lung tissue and edematous
populations. Transmission occurs via
separation of lobules. The most prominent
fomites and direct contact with infectious
histopathologic findings are severe, diffuse,
exudates. Carrier anin1als are in1portant for

1454

RESPIRATORY DISEASES OF HORSES
exanlination of the retropharyngeal area,
or radiographic examination of the skull
to identify the location and extent of
retropharyngeal abscesses.

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Treatment: The environment for
clinically ill horses should be warm, dry, and
dust-free. Warm compresses are applied to
sites of lymphadenopathy to facilitate
maturation of abscesses. Facilitated
drainage of mature abscesses will speed
recovery. Ruptured abscesses should be
flushed with dilute (3%-5%) povidone-iodine

Strangles. Courtesy of Dr. Thomas Lane.

solution for several days until discharge
ceases. NSAlDs can be administered
judiciously to reduce pain and fever and to
maintenance of the bacteria between
improve appetite in horses with fulrni.nant
epizootics and initiation of outbreaks on
clinical disease. Tracheotomy may be
premises previously free of disease.

required in horses with retropharyngeal

Survival of the organism in the environment
abscessation and phatyngeal compression.

depends on temperature and humidity; it is

Anti.microbial therapy is controversial.

susceptible to desiccation, extreme heat,

Initiation of antibiotic therapy after abscess
and exposure to sunlight and must be
formation may provide temporaty clinical
protected within mucoid secretions to
improvement in fever and depression, but it
survive. Under ideal envirorm1ental
ultimately prolongs the course of disease by
circumstances, the organism can sruvive -4 delaying maturation of abscesses. Antibiotic wk outside the host. Under field conditions,
therapy is indicated in cases with dyspnea,
most organisms do not survive 96 hr.

dysphagia, prolonged high fever, and severe
lethargy/anorexia. Ad.ministration of

Clinical Findings: The incubation period
penicillin du.ring the early stage of infection
of strangles is 3-14 days, and the first sign of ( �24 hr of onset of fever) will usually arrest infection is fever(l03°-l06°F [39.4°-41.l °C]). abscess formation. The disadvantage of Within 24-48 hr of the initial fever spike, the
early anti.microbial treatment is failure to
horse will exhibit signs typical of strangles,
mount a protective in1mune response,
including mucoid to mucopurulent nasal
rendering horses susceptible to infection
discharge, depression, and submandibuafter cessation of therapy. If anti.microbial lar lymphadenopathy. Horses with
therapy is indicated, procaine penicillin
retropharyngeal lymph node involvement

(22,000 IU/kg, IM, bid) is the antibiotic of
have difficulty swallowing, inspiratory
choice. Untreated guttural pouch infections
respiratory noise ( compression of the
can result in persistent guttural pouch
dorsal pharyngeal wall), and extended head
empyerna with or without chond.roid
and neck Older aninlals with residual
fonnation.

inmrn.nity may develop an atypical or
catarrhal fonn of the disease with mucoid

Prevention: Postexposure immunity
nasal discharge, cough, and mild fever.

is prolonged after natm:al disease in

Metastatic strangles ("bastard strangles") most horses, and protection is associated
is characterized by abscessation in other
with local (nasal mucosa) production
lymph nodes of the body, particularly the
of antibody against the antiphagocytic
lymph nodes in the abdomen and, less

M protein. The clinical attack rate of
frequently, the thorax. S equi is the most strangles is reduced by 50% in horses
conm1on cause of brain abscess in horses,
vaccinated with IM products that do not
albeit rare.

induce mucosal immunity. Local (rnucosal)

production of antibody requires mucosa!

Diagnosis: Diagnosis is confirmed by
antigen stimulation. An intranasal vaccine
bacterial culture of exudate from abscesses
containing a live attenuated strain of S
or nasal swab samples. CBC reveals
equi equi was designed to elicit a mucosal
neutrophilic leu kocytosis and hyperfibrinoimmunologic response. This attenuated genernia. Se.rum biochemical analysis is
strain is not temperature sensitive
typically umemarkable. Complicated cases

(inactivated by core body temperature)

may require endoscopic examination of the
like the intranasal influenza vaccine.

upper respiratory tract (including the

Reported complications include S equi
guttural pouches), ultrasonographic
equi abscesses at subsequent IM iJ\iection

RESPIRATORY DISEASES OF HORSES

1455
sites (live bacteria on hands of administra

The pathophysiology involves smalltor), submandibular lymphadenopathy, airway inflammation (neutrophilic),
serous nasal discharge, and purpura
mucus production, and bronchoconstrichemorrhagica (seep 828).

tion in response to allergen exposure.

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Control: Clinically affected horses

Etiology: The average age at onset is 9 yr.

should be physically separated from the

Approximately 12% of mature horses have
herd and cared for by separate caretakers
some degree of allergen-induced lower
wearing protective clothing. The rectal
airway inflanrn1ation. There is no breed or
temperature of all horses exposed to
gender predilection; however, there does
strangles should be obtained twice daily,
appear to be a heritable component to
and horses developing fever should be
susceptibility.

isolated (and potentially treated with
penicillin). Contan1inated equipment

Clinical Findings: Horses present with
should be cleaned with detergent and
flared nostrils, tachypnea, cough, and a
disinfected using chlorhexidine gluconate
heave line. The typical breathing pattern
or glutaraldehyde. Flies can transmit
is characterized by a prolonged, labored
infection mechanically; therefore, efforts
expiratory phase of respiration. Cough
should be made to control the fly
may be productive and often occurs during
population during an outbreak. Farriers,
feeding or exercise. The abdominal
trainers, and veterinarians should wear
muscles respond by assisting with
protective clothing or change clothes
expiration, and hypertrophy of these
before traveling to the next equine facility. muscles produces the classic heave line.

Additions to the herd should be carefully

Characteristic auscultatory findings
scrutinized for evidence of disease or
include a prolonged expiratory phase of
shedding (nasopharyngeal culture) and
respiration, wheezes, tracheal rattle, and
quarantined for 14-21 days. Two negative
overexpanded !tmg fields. Wheezes are gennasal swab cultures should be obtained erated by airflow through narrowed
during the quarantine period.

airways and are most pronounced during

Most horses continue to shed S equi
expiration. Crackles may be present and
for -1 mo after recovery. Three negative
are associated with excessive mucus
nasopharyngeal swabs, at intervals of
production. Mild to moderately affected

4-7 days, should be obtained before
horses may present with minimal clinical
release from quarantine, and the minimal
signs at rest, but coughing and exercise
isolation period should be 1 mo. Prolonged
intolerance are noted during performance.

bacterial shedding (as long as 18 mo) has

Horses with RAO are not typically febrile
been identified in a small number of
unless secondary bacterial pneumo_nia has
horses. Guttural pouch empyema is the
developed.

source of infection in most prolonged

Horses from the southeastern USA may
carrier states. Bacterial culture of
demonstrate clinical signs on late-sunrn1er
nasopharyngeal swab and/or guttural
pasture, which likely reflects sensitivity to
pouch lavage is used to identify persismolds or grass pollens. This is referred to as tent carriers.

summer pasture-associated obstructive

RECURRENT AIRWAY

OBSTRUCTION

(Heaves, Chronic obstructive pulmonary
disease)

Recurrent airway obstruction (RAO) is
a common, performance-limiting, allergic
respiratory disease of horses characterized by chronic cough, nasal discharge, and respiratory difficulty. Episodes of
airway obstruction are seen when
susceptible horses are exposed to
common allergens. Most horses exhibit
clinical signs when stabled, bedded on
straw, and fed hay, whereas elimination
of these inciting factors results in

Chronic obstructive pulmonary disease with

"heave line"along the costal arch. Courtesy of remission or attenuation of clinical signs.

Dr. Thomas Lane.

1456

RESPIRATORY DISEASES OF HORSES
pulmonary disease. The management is
acceptable, low-allergen alternative
similar to that of a horse with heaves, with
sources of roughage and may be preferred
the addition of pasture avoidance.

by horses over the complete feeds.

Soaking hay with water before feeding

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Diagnosis: The diagnosis of RAO is
may control clinical signs in mildly
determined in most horses on the basis
affected horses but is unacceptable for
of history and characteristic physical
highly sensitive horses. Horses mainexamination findings. Hematology and tained in a stall should not be housed in
serum chemistry results are unremarkthe same building as an indoor arena, hay able. Radiographic findings in horses
should not be stored overhead, and straw
with RAO are peribronchial infiltration
bedding should be avoided. Horses with
and overexpanded pulmonary fields
summer pasture-associated obstructive

(flattening of the diaphragm). Thoracic
pulmonary disease should be maintained
radiographs are of little benefit in
in a dust-free, stable environment.

confirming the diagnosis of RAO and may

Medical treatment consists of a combinanot be necessary in horses with charaction of bronchodilating agents ( to provide teristic clinical signs, unless there is no
relief of airway obstruction) and corticoresponse to standard treatment after steroid preparations (to reduce pulmonary

14 days of therapy. However, they may
inflammation). Bronchodilator therapy
help identify the most important

(13 agonists and parasympatholytic agents)

differential diagnoses, including
will provide immediate relief of airway
interstitial pneumonia, pulmonary
obstruction until clinical signs of disease
fibrosis, or bacterial pneumonia.

are controlled by corticosteroids. Severely

Bronchoalveolar lavage is rarely
affected horses are ideally controlled with
required for diagnosis of fulminant RAO
aerosolized bronchodilators ( eg, albuterol,
and is not innocuous in horses that are
ipratropiurn) and systemic corticosteroids
dyspneic at rest. It is indicated in horses

( eg, dexan1ethasone 0.1 mg/kg/day, IV).

with mild to moderate disease with poor

Horses with mild to moderate airway inflamperformance and coughing during mation can be treated with aerosolized
exercise. Neutrophilic inflan1mation
corticosteroids and aerosolized or systemic

(20o/o-90% of total cell count) confirms the

( clenbuterol) bronchodilators. It is inappropresence of lower airway inflammation priate to treat RAO with bronchodilators as
and differentiates horses with eosinothe sole therapy. NSAlDs, antihistamines, philic pneumonitis, fungal pneumonia, or
and leukotriene-receptor antagonists have
lungworm infestation from horses with
not demonstrated therapeutic benefit.

heaves. Curschmann spirals may be seen
on cytologic evaluation ·and represent

INFLAMMATORY AIRWAY
inspissated mucus/cellular casts from

DISEASE
obstructed small airways.

(Lower respiratory tract inflammation, Small

Treatment: The single most ·important
airway inflammatory disease)

treatment is environmental management

Inflan1.111atory airway disease (IAD)

to reduce allergen exposure. Medication
describes a heterogeneous group of
will alleviate clinical signs of disease;
inflan1matory conditions of the lower
however, respiratory disease will return
respiratory tract that appear to be primarily
after medication is discontinued if the
noninfectious. IAD occurs in 22o/o-50% of
horse remains in the allergen-challenged
athletic horses and is a conunon cause of
environment. The most common culprits
impaired perforn1ance and interruption of
are organic dusts present in hay, which
training.

need not appear overtly musty to
precipitate an episode in a sensitive horse. Etiology and Pathophysiology: Horses should be maintained at pasture,

Proposed etiologies ofIAD include allergic
with fresh grass as the source of roughage, airway disease, recurrent pulmonary stress, supplemented with pelleted feed. Round
deep inhalation of dust, atmospheric
bale hay is particularly allergenic and a
pollutants, and/or persistent respiratory
common cause of treatment failure for
viral infections, most notably EHV-2. IAD
horses on pasture. Horses that remain
often develops after an overt viral respirastalled should be maintained in a clean, tory infection and may result from inability
controlled environment. Complete
of the in1.111une system to fully eliminate
commercial feeds eliminate the need for
viruses or bacteria from small airways.

roughage. Hay cubes and hay silage are

Streptococcus pneumoniae has been

RESPIRATORY DISEASES OF HORSES

1457
isolated from horses with IAD; however,
tivity response and may represent an
its role in the pathophysiology is unclear,
early form of recurrent airway obstrucbecause this population of horses is largely tion (seep 1455). In IAD-affected horses
unresponsive ( or transiently responsive) to
with increased mast cells in bronchoal

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antibiotic therapy.

veolar fluid, aerosol administration of
an inhaled corticosteroid preparation

Clinical Findings: The most common

(beclomethasone or fluticasone)

clinical signs are chronic cough and mucoid
improves clinical signs of respiratory
to mucopurulent nasal discharge. Fever and disease.

auscultable pulmonary abnormalities are
rarely seen. Horses with IAD demonstrate
poor exercise tolerance at maximal speed.

EXERCISE-INDUCED PULMONARY

Endoscopic examination reveals mucopu-

HEMORRHAGE

1ulent exudate in the pharynx, trachea, and
bronchi.

(Epistaxis, "Bleeder")

Diagnosis: Diagnosis of IAD is based on

Exercise-induced pulmonary hemorrhage
poor race performance and clinical signs.

(EIPH) is seen in most racehorses and in

Bronchoalveolar lavage is peifonned to
many other horses used in equine sports ( eg,
characterize tl1e type of pulmonary
polo, ban·el racing, 3-day events) that require
inflammation. Cytologic evaluation of
strenuous exercise for short periods of tinle.

bronchoalveolar fluid will reveal one of the

Epistaxis is seen in a small proportion ( -5%)

following inflammatory profiles: 1) mixed
of horses with EIPH. Blood in the tracheoinflan1mation with high total nucleated bronchial tree is identified in 45o/1r-75% of
cells, mild neutrophilia ( 15% of total
racehorses via endoscopic examination,
cells), lyrnphocytosis, and monocytosis;
and hemorrhage is detected by cytologic

2) increased metachromatic cells (mast
examination of bronchoalveolar lavage in
cells >2%of total cells); or3) eosinophilic

>90% of racehorses.

inflammation (5%-40% of total cells). The
mixed inflammatory profile likely results

Etiology: The proposed pathophysiologic
from environmental irritation or the
mechanism for pulmonary hemorrhage
consequences of a previous infectious
includes high pulmonary vascular pressures
disease.

dU1ing maximal exercise, with resultant
thickening of pulmonary vein walls and

Treatment: The type of inflan1mation
decreased lunlinal diameter and increased
in bronchoalveolar fluid will dictate
intravascular pressure at the level of the
the therapeutic plan. Regardless of the
pulmonary capillaries.

cytologic profile, all horses with IAD
should receive aerosolized bronchodilator Diagnosis: Endoscopic observation therapy before exercise to avert exerciseof blood in the airways 30-90 min after or irritant-induced bronchoconstriction.

exercise provides definitive evidence of

In horses with a mixed inflammatory

EIPH. Other sources of hemorrhage in
cytologic profile, administration of
the upper airway, particularly guttural
low-dose interferon-a is recommended
pouch mycosis (seep 1463) and ethmoid
for immunomodulation and antiviral
hematoma (seep 1462), must be excluded
activity. Interferon-a reduces tracheal
during endoscopic exanlination. If EIPH
exudate and improves cytologic profiles
is suspected and the horse cannot be
in horses with mixed inflanirnatory IAD.

exan1ined after exercise, cytologic

Eosinophilic bronchoalveolar fluid likely
examination of bronchoalveolar lavage
represents a Type I hypersensitivity
fluid for semiquantitative assessment of
reaction. In addition to tracheal exudates,
hemosiderophages is diagnostic. Stains
peripheral eosinophilia, miliary pulmothat highlight iron-containing pigments nary opacities, and eosinophilic pulmo

(Prussian blue) facilitate recognition of
nary granulomas may be seen in affected
these cells. Thoracic radiography
horses. If such fluid is identified, parasitic
demonstrates alveolar or mixed alveolarpulmonary disease should be considered interstitial opacities in the caudodorsal
in addition to hypersensitivity pneumonilung fields; however, radiographic tis. Systemic corticosteroid therapy is
examination of the thorax has little impact
recommended to reduce pulmonary
on the diagnosis or management of EIPH.

inflammation in horses with eosinophilic

IAD. Mast cell inflammation likely

Treatment and Control: Furosemide
represents a local pulmonary hypersensi-
reduces the incidence and severity of

1458

RESPIRATORY DISEASES OF HORSES

EIPH in Thoroughbred racehorses.

Loss of neuromuscular control of the

Horses with and without EIPH demonabductor muscle results in collapse of the strate equal improvements in race
arytenoid cartilage and vocal fold, which
performance after administration of
reduces the glottal cross-sectional area. The
furosemide, indicating that the drug may
resistance to airflow necessitates greater

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enhance performance via mechanisms
respiratory effort. Because of the pliable
unrelated to EIPH. Application of nasal
nature of the glottis, the exaggerated
dilator bands reduces RBC counts in
subatmosphe1ic pressure in the airway
bronchoalveolar fluid from affected
results in further collapse of the arytenoid
horses running on a treadmill by 33%.

cartilage and exacerbation of the imped

Alternative treatments, including
ance to airflow. Upon inspiration during
procoagulant agents ( eg, vitamin K,
strenuous exercise, the affected side is
conjugated estrogens, aminocaproic
drawn across the midline (by negative
acid), antihypertensive drugs, rheologic
pressure in the airway) until it abuts the
agents (pentoxyphylline), bronchodilaabducted normal arytenoid, effectively tors, prolonged rest, dietary supplements
occluding the airway ( dynamic collapse).

(hepseridin-citrus bioflavinoids), and

The characteristic inspiratory whistle
anti-inflammatory drugs, have not
results from resonance within the open
demonstrated therapeutic benefit.

ventricle on the affected side. The harsher
stridor, or roar, is produced by vortex

LARYNGEAL HEMIPLEGIA
shedding from the edges of the arytenoid
cartilage and vocal fold.

(Roaring, Left laryngeal hemiplegia)

Clinical Findings and Diagnosis: The

Left recurrent laryngeal hemiplegia is
principal clinical signs are inspiratory noise
characterized by paresis or paralysis of the
during exercise and exercise intolerance.

left arytenoid cartilage and vocal fold. It Affected horses are asyn1ptomatic at rest
manifests clinically as exercise intolerance
but may have an unusual whinny. Diagnosis
and inspiratory respiratory noise ("roaring") is confirmed by endoscopic observation of during exercise. Right-sided hemiplegia and
reduced or absent mobility of the arytenoid
bilateral (paraplegia) arytenoid dysfunction
cartilage and vocal fold. With laryngeal
are uncommon.

hemiplegia, the arytenoid cartilage and
vocal fold are located in a median posi-

Etiology and Pathogenesis: Progrestion within the laryngeal lumen and are sive loss of the large myelinated fibers in
in1111obile. Asynchronous movements of the
the distal portion of the recurrent
laryngeal cartilages occur commonly, with
laryngeal nerves results in neurogenic
variable clinical relevance. Horses with
atrophy of the intrinsic laryngeal muslaryngeal asynchrony, exercise intolerance, culature, the most crucial of which is
and respiratory noise during exercise
the cricoarytenoideus dorsalis muscle.

should have their laryngeal function

Axonal dystrophy of the left recurrent
evaluated endoscopically during treadmill
nerve occurs more commonly than the
exercise to confirm laryngeal dysfunction.

right, perhaps due to its extended length

Differential diagnoses include other
around the base of the heart. Left
pharyngeal conditions that produce upper
laryngeal hemiplegia is likely heritable.

Less common causes include direct
trauma to the recurrent laryngeal nerve,
accidental perivascular injection of
irritating substances, and plant (eg, Cicer
arietiniim [chick peas J and Lathyrus spp) and chemical intoxications. Lead toxicity
should be suspected in horses with
bilateral laryngeal paralysis. The peroneal
nerve (similar length to the left recurrent
laryngeal) may be affected with toxic
insults, and axonal dystrophy of the
peroneal nerve may manifest as stringhalt

(seep 1137). Although all breeds are
affected, prevalence is higher in males and Endoscopic image demonstrating grade IV
long-neckeclllarger breeds. The prevalence paralysis of the left arytenoid from a horse in young Thoroughbreds presented for
with left laryngeal hemiplegia at rest. Courtesy
sale is estimated to be ---3%---5%.

of Dr. Bonnie R. Rush.

RESPIRATORY DISEASES OF HORSES

1459
airway obstruction and exercise intolerance. Most of these conditions are easily differentiated from laryngeal hemiplegia
during endoscopic examination. Although
arytenoid chondritis may be confused

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with laryngeal hemiplegia, misdiagnosis
can be avoided by observation of the
shape and size of the arytenoid cartilages.

In arytenoid chondritis, the arytenoids
thicken transversely and lose their
characteristic "bean" shape. Abduction
and adduction are usually limited. The
axial (medial) surface of the arytenoid
cartilage may be distorted with granulation tissue protruding through the mucosa, and a contact (kissing) lesion
may be present on the contralateral
arytenoid cartilage. Arytenoid chondritis
should always be considered if motility of
the right arytenoid is reduced. Radiographic examination of the pharynx may Endoscopic photograph of grade 3.5/4
reveal mineralization within the arytenoid
pharyngeal lymphoid hyperplasia. Courtesy of
cartilages in cases of chondritis.

Dr. Jan Hawkins.

Treatment: Prosthetic laryngoplasty can
tissue and are unnoticeable. In yom1g,
stabilize the affected side of the larynx
matming horses, lymphoid follicles appear
during inspiration and prevent dynanlic
as prominent, raised nodules on the surface
collapse of the airway during exercise.

of the pharyngeal roof and extend down the

Laryngeal vent1iculectomy perfom1ed via
lateral walls of the pharynx and cranially
laryngotomy, or ventriculocordectomy
into the nasopharynx. Although PLH was
performed via transendoscopic laser,
once believed to be an important cause of
rm proves airflow and reduces the "roaring"

poor perfom1ance in racehorses, its clinical
sound during exercise. Prosthetic
significance is now questionable. Virtually
laryngoplasty is commonly done in racing
all young horses develop hyperplasia of
horses and is the only technique that
pharyngeal lymphoid follicles; in most
satisfactorily reduces the impedance to
cases, this represents a normal immunoinspiratory flow. Postoperative complicalogic event.

tions include chronic cough, chronic

Occasionally, follicles may enlarge and
aspiration of feed, implant failure, and
coalesce with surrounding follicles. In these
in1plant infection. Athletic performance will
situations, follicles may appear hyperenlic
improve after surgery; however, horses are
or inflamed and may exude mucoid or
more likely to experience inflan1matory
mucopurulent material. These cases likely
airway disease and exercise-induced pulmorepresent a mild or subclinical viral nary hemorrhage, have fewer race starts,
infection and may be associated with
and are unlikely to develop their predicted
in1paired performance. Signs of pharyngeal
perfom1ance potential.

pain include reduced appetite and frequent
swallowing. Treatment is not necessary in
the vast majority of cases; however, rest and

PHARYNGEAL LYMPHOID

NSAID administration are warranted in
horses demonstrating pharyngeal pain.

H YPERPLASIA

(Pharyngitis)

DORSAL DISPLACEMENT OF THE

Pharyngeal lymphoid hyperplasia is a

SOFT PALATE
common condition of the dorsal pharyngeal
wall seen in young horses (l--3 yr old).

Dorsal displacement of the soft palate

Horses do not have discrete masses of

(DDSP) is a performance-limiting condition
lymphoid tonsillar tissue; rather, they have
of the upper respiratory tract and is a
many small foci or follicles of lymphoid
relatively common cause of upper
tissue spread diffusely over the roof and
respiratory noise during exercise. Dwing
lateral walls of the pharynx. In mature

DDSP, the caudal free margin of the soft
horses, these follicles blend with mucosa!

palate moves dorsal to the epiglottis,

1460

RESPIRATORY DISEASES OF HORSES
creating a functional obstruction within
caudal edge of the soft palate to keep it
the airway. The cross-sectional area of the
ventral to the epiglottis. Palatal scleropharynx is reduced, and airflow resistance therapy via endoscopic-guided sodium
and turbulence are increased.

tetradecylally sulfate injection has

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demonstrated success in a small nwnber

Etiology and Pathogenesis: DDSP
of horses, resolving respiratory noise in
may result from several pathophysiologic

7 of 8 horses and improving performance
mechanisms. Inflammation of the upper
in 6 of 8 horses. A laryngeal tie-forward
respiratory tract due to infection may cause
procedure can be performed to alter the
neuropathy of the pharyngeal branch of the
position of the larynx with respect to the
vagus nerve as it traverses the floor of the
caudal edge of the soft palate.

medial compartment of the guttural pouch,
resulting in neuromuscular dysfunction of

EPIGLOTTIC ENTRAPMENT
the pharyngeal muscles that control the soft
palate. The retropharyngeal lymph nodes

Epiglottic entrapment is a less common
are in direct contact with the pharyngeal
cause of respiratory noise and exercise
branch of the vagus nerve, and retropharynintolerance. In this condition, the geal lymphadenopathy may result in
aryepiglottic fold completely envelops the
compression and irritation. Clinical signs
apex and lateral margins of the epiglottis.

can be induced by local anesthesia of this

The general shape of the epiglottis is
nerve. Congenital hypoplasia of the
visible, and the position ( dorsal to the soft
epiglottis may contribute to DDSP due to
palate) is appropriate. However, the
insufficient epiglottal tissue to maintain the
distinct serrated margins of the epiglottis
position of the caudal border of the soft
and the dorsal epiglottic vascular pattern
palate ventral to the epiglottis. Horses that
are obscured by a fold of aryepiglottic
have undergone laryngoplasty for left
mucosa. Clinical signs of epiglottic
laryngeal hemiplegia are more likely to
entrapment include inspiratory and expiradevelop DDSP.

tory respiratory noise during exercise and
poor exercise performance. Less common

Clinical Findings: DDSP creates a
signs include cough, nasal discharge, and
characteristic gurgling respiratory noise,
headshaking. In mature nonracehorses,
primarily during expiration, due to vibration cough is the most consistent presenting of the soft palate. Horses may make no
complaint. Diagnosis is determined by
noise at the onset of exercise but displace
endoscopic examination. Surgical
their palate during high-speed exercise,
correction of epiglottic entrapment is
causing them to "choke down." Head
axial division of the aryepiglottic fold to
position (flexed) may contribute to
free the epiglottis. Axial transection of
displacement.

the aryepiglottic fold may be performed
by transendoscopic contact Nd:YAG laser,

Treatment: The most effective
transnasal or transoral transection via
treatment for DDSP in young horses
curved bistoury, or direct excision

(2-yr-olds) and horses with evidence of
through a laryngotomy or pharyngotomy.

upper respiratory tract infection is rest

Surgical transection is generally curative,
and anti-inflammatory therapy. Caudal
with a relapse rate of 5%. Some affected
retraction of the tongue elevates the soft
horses can race successfully with the
palate and pushes the larynx caudally,
condition.

both of which may predispose to DDSP.

Placing a tongue tie during exercise

SUBEPIGLOTTIC CYST
reduces caudal retraction of the tongue.

Sternothyrohyoideus myectomy per

Subepiglottic cysts are an uncommon cause
formed in horses prone to DDSP to alter
of respiratory noise in young horses. They
the anatomy of the upper respiratory tract
are likely present from birth but remain
is successful in -50% of horses. Soft palate undetected until the horse begins exercise resection (staphylectomy) is frequently
training. These cysts are suspected to arise
performed in horses with DDSP and also
from remnants of the thyroglossal duct.

has a success rate of -50%; however, the

Clinical signs include respiratory noise and
mechanism of improvement after surgery
exercise intolerance. Large cysts may
is unclear. Success has been attributed
produce coughing, dysphagia, and aspiration
to reduction in the mass of soft palate
in foals. Diagnosis is determined by
obstructing the airway, easier replaceendoscopic examination of the upper ment of the shorter soft palate to the
respiratory tract. The cyst appears as a
subepiglottic position, and firming of the
smooth-walled, fluctuant mass that contains

RESPIRATORY DISEASES OF HORSES

1461
thick, yellow, mucoid material. Occasionally,
bridge of the nose as a juvenile can produce
the mass is not visible in the nasopharynx,
nasal septal deviation and thickening. Other
and oral examination under general
less common diseases of the nasal septum
anesthesia may be required to identify it.

include amyloidosis, fungal infection, and

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Histologically, subepiglottic cysts are lined
squamous cell carcinoma.

with a combination of stratified squamous

Thickening or deviation of the nasal
and pseudostratified columnar epithelium.

septum causes low-pitched stertorous

Treatment involves complete removal of the
breathing dwing exercise. Facial defonnity
secretory lining of the cyst. Rupture of the
may be seen. Septal abnonnalities may be
cyst results in immediate decompression,
detected by palpation, visual inspection,
but recurrence is common. The most
and endoscopic examination. Dimensions
common approach is ventral laryngotomy,
of the nasal cavity a.i·e difficult to appreciate
although transendoscopic Nd:YAG laser
via endoscopic exan1ination; however,
surgery has been used for complete excision. abnormalities of the mucosa are easily identified. Precise dorsoventral radiographs

FOURTH BRANCHIAL ARCH
of the skull provide definitive evidence of

DEFECT
septal defonnity, deviation, and thickening.

Histologic examination of any nodules or

(Rostral displacement of the
discrete lesions on the septum will identify
palatopharyngeal arch)

twnors, amyloidosis, or fungal infections.

The extrinsic structures of the larynx,

Surgical resection of the nasal septum is
such as the wing of the thyroid cartilage,
the only treatment option in most cases. The
cricothyroid muscle, and upper esophageal
entire diseased portion of the septum ca.ii be
sphincter, develop from the fourth branchial excised using obstetrical wire by transectarches. Aplasia or hypoplasia of one or more ing the septum on the dorsal, ventral, and of these structures may occur mtilaterally
caudal border. Hemorrhage is substantial
or bilaterally. Right-sided defects are more
dming tlus procedure (4-8 L), a.i1d the nasal
conunon than bilateral or left-sided defects.

passages are packed with sterile gauze

The severity of clinical manifestation ranges
soaked in saline or in 1: 100,000 epinephrine
broadly and is based on the degree of the
solution to minimize blood loss. Before the
defect. The most common clinical sign is
horse recovers from anesthesia, a tracherespiratory noise, although mild dysphagia, otomy is performed.

eructation, and cough have been reported.

Postoperative ca.i·e includes parenteral

Palpation of the larynx reveals absence of
antibiotics and NSA!Ds. The packing and
one or both wings of the thyroid cartilage,
tracheotomy tube should be removed 48--72
resulting in failure of the cricothyroid
hr after surgery. All incisions heal by second
articulation and a palpable space between
intention within 3 wk. Horses should be
the cricoid and thyroid cartilages. Radiorested for -2 mo before returning to nom1al graphic evidence of a fourth branchial arch
activity. After surgery, most horses make a
defect includes dilation of the cricopharynx
respiratory noise during work, although less
with a continuous column of air from the
than before surgery, and exercise tolerance
pharynx to the cervical esophagus. Rostral
is improved. Shortening of the upper jaw,
displacement of the palatopharyngeal
incisor malalignrnent, or nostril collapse
arch may or may not be detected during
can develop if the procedure is performed in
endoscopic examination. Endoscopic
inunature horses. Ideally, the surgery should
examination during treadmill exercise may
be delayed until maturity.

reveal dynamic collapse of the vocal folds.

Affected horses are unlikely to become

Nasal Polyps
effective athletes. Pa.itial arytenoidectomy

Nasal polyps are pedtmculated growths tl1at
may in1prove airway dynan1ics sufficiently
arise from the rn ucosa of the nasal cavity,
for pleasure riding.

nasal septum, or tooth alveolus. Polyps are
usually unilateral and single but can be bilat

DISEASES OF THE NASAL
eral and multiple. They form in response to

PASSAGES
chronic inflanunation by hype1trophy of the
mucous mernbra.i1e or exuberant prolifera

Nasal Septum
tion of fibrous connective tissue. There is no
age, breed, or gender predilection.

Diseases of the nasal septum are ra.i·e. Most

Clinical signs are poor airflow through the
nasal septal disorders are congenital abnoraffected nasal passage; inspiratory dyspnea; malities that remain undetected tmtil the
unilateral, malodorous, mucopurulent nasal
horse is exercised. Traumatic injury to the
discharge; and low-volume epistaxis. The

1462

RESPIRATORY DISEASES OF HORSES
mass may extend rostrally until it protrudes

On endoscopy, ptuulent material, a mass,
beyond the nostrils. Polyps are detected via
or blood can be seen in the nasal passage
endoscopic and radiographic exanlination,
originating from the nasomaxillary opening.

and histopathologic evaluation of biopsy

Lateral and dorsoventral radiographs of
samples provide a definitive diagnosis.

the skull may reveal fluid lines, sinus cysts,

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Stugical excision is perfom1ed via an incision solid masses, or lytic/proliferative changes in the false nostlil, a trephine opening, or a
associated with dental disease and neoplasia.

bone flap.

Oblique projections in a dorsal to ventral
direction may be required to improve

Choanal Atresia
views of the tooth roots. CT is useful,

Choanal atresia is caused by persistence of
particularly for ventral conchal sinus
the bucconasal membrane that separates the
disease. Centesis of the maxillary or frontal
primitive buccal or oral cavity from the nasal
sinuses is performed to obtain fluid for
pits dilling embryonic development. Bilateral bacterial culture, sensitivity testing, and and unilateral cases have been described in
cytologic examination. With sedation
horses. Clinical signs are evident immediand local anesthesia, the sinuses can be ately after birth in foals with bilateral disease, examined in the standing horse by insertion because dyspnea is severe and air cannot be
of an arthroscope ( 4 mm). A second portal
detected passing through the nostrils. An
could be used to insert an instrument into
endoscope or stomach tube passed through
the sinus to obtain specinlens, debride
the ventral meatus will be obstructed at the
tissue, and lavage the sinus cavity.

level of the medial canthus of the eye.

Bilateral complete choanal atresia is a

Sinusitis
life-threatening condition, and a trache

Primary sinusitis occurs subsequent to an
otomy must be performed immediately after upper respiratory tract infection that has birth. It may be possible to perforate a thin
involved the paranasal sinuses. It usually
membrane by electrocoagulation or laser or
involves all sinus cavities but can be
by excision through bilateral flaps centered
confined to the ventral conchal sinus. This
along the midline. Indwelling tube stents
cavity is difficult to detect radiographically
should be inserted through both choanae
and access stugically. Secondary sinusitis
and left in place for 6 wk.

can result from tooth root infection,
fracture, or sinus cyst. The first molar,

DISEASES OF THE PARANASAL
fotuth premolar, and third premolar (in
decreasing frequency) are the most likely to

SINUSES
develop tooth root abscesses. Clinical signs

The maxillary sinus is the largest paranasal
of secondary sinusitis closely resemble
sinus and is divided by a thin septun1 into
those of primary sinusitis, including
caudal and rostral parts. The frontal sinus
unilateral mucoptuulent nasal discharge
has a large communication with the dorsal
and facial defomlity. Tooth root abscesses
conchal sinus at its rostral end, thereby
typically produce a fetid nasal discharge.

fomling the conchofrontal sinus. The

Treatment of primary sinusitis involves
conchae or ttubinates are delicate scrolls of
lavage of the sinus cavity and systenlic
bone that are attached laterally in the nasal
antinlicrobial therapy based on culttue and
passage and contain the conchal sinuses.

sensitivity results. Second<!IY sinusitis

The caudal and rostral maxillary sinuses
requires removal of affected cheek teeth
have separate openings into the middle
or cystic material via sinusotomy.

nasal meatus, and the caudal maxillary
sinus communicates with the frontal sinus

Ethmoid Hematoma
through the large frontomaxillary opening.

Progressive ethmoid hematoma is a

Diseases that originate in one sinus cavity
locally destructive mass of nasal passages
may extend to and involve others.

and paranasal sinuses of uncertain

Most diseases of the paranasal sinuses
etiology. The mass resembles a tumor in
cause mucoptuulent or bloody nasal
appearance and development but is not
discharge. Drainage is unilateral, in conneoplastic. Large hematomas usually arise trast to disease of the lungs, pharynx, and
from the ethmoid labyrinth, and smaller
gutttual pouches, because the sotuce of
masses arise from the floor of the sinuses.

discharge is rostral to the caudal border of

Masses originating in the sinus extend into
the nasal septum. Unilateral facial swelling,
the nasal passage. An expanding hemaepiphora, dull percussion of the sinuses, toma can cause pressure necrosis of
and inspiratory noise are common
surrounding bone but rarely causes facial
manifestations of disorders of the sinuses.

distortion; it is primarily seen in horses

RESPIRATORY DISEASES OF HORSES

1463

>6 yr old. Low-grade, spontaneous,
intermittent, unilateral epistaxis is the
most common clinical sign. Horses with
extensive masses may have reduced
airflow through the affected nasal passage

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and fetid breath. In longstanding cases,
the mass may protrude from the nares.

In most instances, the lesion can be seen
extending into the nasal passages on
endoscopic examination, and the extent
of the mass can be determined radiographically. Conservative management includes intralesional injection of the mass with 4%
formaldehyde. Formalin is injected into
the mass using a guarded endoscopic

Empyema of guttural pouch, horse,
needle. The mass typically regresses
radiograph. Courtesy of Or. Ronald Green.

rapidly, but recurrence is common.

Neurologic signs have been reported after
depression, and anorexia may or may
intralesional formalin injection, associnot be seen. Diagnosis is determined by ated with communication of the hemaendoscopic examination of the guttural toma into the calvarium. Surgical excision
pouch. Radiographs of the pharynx
is achieved via frontonasal bone flap.

demonstrate a fluid line in the guttural
pouch and may allow identification of an

Sinus Cysts
associated retropharyngeal mass.

Sinus cysts are single or loculated

Systemic antimicrobial therapy alone
fluid-filled cavities with an epithelial lining.

rarely resolves the infection; guttural

They develop in the maxillary sinuses and
pouch lavage is necessary. Penicillin gel
ventral conchae and can extend into the

(prepared using sodium penicillin) can be
frontal sinus. A congenital form has been
administered directly into the guttural
described. Sinus cysts are typically found
pouch and may enhance bacterial
in horses <1 yr old but can also be seen in
clearance. Retropharyngeal abscesses can
those >9 yr old. The primary clinical signs
be resolved by rupturing the abscess into
are facial deformity, nasal discharge, and
the guttural pouch using an endoscopic
partial airway obstruction. Radiographs are
blade. If endoscopic rupture into the
more likely to identify a sinus cyst than
guttural pouch is unsuccessful, surgical
endoscopic exan1ination. Multiloculated
drainage is necessary for retropharyngeal
densities and fluid lines in the sin uses are
abscessation. Guttural pouch empyema
observed radiographically; occasionally,
may compress the dorsal pharynx and
dental distortion, flattening of tooth roots,
produce upper airway obstruction.

soft-tissue mineralization, and deviation

Tracheotomy may be necessary to provide
of the nasal septunl are seen. Treatment
a temporary alternative airway in these
involves radical surgical removal of the cyst
cases. If guttural pouch empyema is not
and associated conchal lining. Prognosis
treated, chondroid material may form in
for complete recovery is good, and the
the guttural pouch and serve as a source
recurrence is low. Some horses may have a
of chronic infectious exudate. A small
permanent, mild mucoid discharge after
number of chondroids can be removed
surgery.

endoscopically, but accumulations of
exudate, chondroid material, or unre

GUTTURAL POUCH DISEASE
solved retropharyngeal abscesses require
surgical drainage.

Empyema

Guttural pouch empyema is defined as the

Guttural Pouch Mycosis
accumulation of purulent, septic exudate

Mycotic plaques in the guttural pouch are
in the guttural pouch. The infection
typically located on the caudodorsal aspect
usually develops subsequent to a bacterial of the medial guttural pouch, over the (primarily Streptococcus spp) infection
internal carotid artery. In some instances,
of the upper respiratory tract. Clinical
fungal plaques may be multiple or diffuse.

signs include intermittent purulent nasal

The most common fungal organism
discharge, painful swelling in the parotid
associated with guttural pouch mycosis is
area, and in severe cases, stiff head

Aspergillus spp (seep 633). Clinical signs carriage and stertorous breathing. Fever,
arise from damage to the cranial nerves and

1464

RESPIRATORY DISEASES OF HORSES
the arteries within the mucosa! lining of the
signs and radiographic examination of the
guttural pouch. The most common sign is
skull. Severely affected ar1in1als may develop
epistaxis, due to fungal erosion of the wall
a secondary empyema. Tympany is usually
of either the internal carotid artery (most
unilateral, but bilateral cases have been

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cases) or branches of the external carotid
reported. Medical management with NSAIDs
artery. Hemorrhage is spontaneous and
and az1timicrobial therapy resolves most
severe, and repeated bouts may precede a
cases due to upper respiratory tract inflan1-
fatal hemorrhagic episode. Dysphagia,
mation. Surgical intervention is warranted

Homer syndrome, and dorsal displacement
in horses witl1 malformation of the guttural
of the soft palate may develop in response
pouch opening and involves fenestration of
to fungal damage to cranial ne1ves and the
the membraz1e that separates the affected
sympathetic nerve that superficially traverse
guttural pouch from the normal one. This
the guttural pouch. Dysphagia is a poor
provides a route for air in the abnormal
prognostic indicator and is highly correlated
guttural pouch to pass to the nonnal side
with nonsurvival. Diagnosis is detennined
and be expelled into the pharynx. The
by endoscopic examination of the guttural
postoperative prognosis is good.

pouch. Treatment consists of topical and
systemic antifungal therapy, based on
sensitivity testing. Topical antifungal therapy

Rupture of the Long us Capitis
is administered directly on the lesion via

Muscle
infusion through the biopsy channel of an

Traumatic rupture of the longus capitis is
endoscope. A fatal hemorrhagic event can be
the second most common cause (after
prevented by occluding the affected arteries
mycosis) of severe hemorrhage from the
along their course through the guttural
guttural pouch. The longus capitis muscle
pouch by means of a balloon-tipped catheter
is one of the ventral straight muscles of the
or a coil embolus. It is necessary to occlude
head. It inserts on the basisphenoid bone
the arteries proximal and distal to tl1e lesion
at the base of the skull. The point of
to prevent retrograde bleeding from the
rupture occurs at the inse1tion of the
circle of Willis.

muscle dorsal to the guttural pouch.

Rupture results from traumatic poll injury

Guttural Pouch Tympany

(rearing over backward) az1d produces
profuse hemorrhage. Hemorrhage into the

Guttural pouch tympany is seen in horses
retropharyngeal space can cause asphyxia
ranging from birth to 1 yr of age and is more az1d death. On endoscopic exaz11ination, common in fillies tl1an in colts. A genetic
swelling az1d hemorrhage caz1 be seen in
basis of disease has been identified in
the most rostral ar1d medial aspects of the

Arabian ar1d Gem1an warmblood breeds. In
guttural pouch by retroflexion of the
some cases, the condition is acquired due to
endoscope. On lateral radiographic
inflan1IDation of the upper respiratory tract.

exaz11ination, az1 avulsion fracture of the

The affected guttural pouch is distended with
basisphenoid bone may be seen overlying
air and fonns a characte1istic non painful
the guttural pouch region. Significaz1t
swelling in the parotid region. Breathing
neurologic deficits are often seen with this
may become ste1torous in severely affected
fracture. Treatment involves stall rest for
anin1als. Tympany may result from inflanrn1a4-6 wk; broad-spectrum az1tibiotics are tion or malfom1ation of the pharyngeal
given for 5-7 clays for az1y infection at the
orifice of the eustachian tube, which then
site of muscle rupture. Prognosis for full
acts as a one-way valve by allowing air to
recovery is good, but persistent neurologic
enter the pouch but preventing its return into
signs or recurrent hemorrhage worsens
the pharynx. Diagnosis is based on clinical
the prognosis.

RESPIRATORY DISEASES OF PIGS

Respiratory diseases of pigs can be
may be serious but of limited duration, ar1d
classified into two broad categories based
those that persist in a large number of pigs
on the extent az1d duration of overt disease:

for indefinite periods. Diseases in the first
those that affect lar,ge numbers of pigs az1d
category caz1 be costly, but tl1e losses are

RESPIRATORY DISEASES OF PIGS

1465
limited rather than ongoing. They include
the etiology of diseases in the second
swine influenza (seep 1470), classical swine category is complex, all the pigs should be
fever (seep 713), the pneumonic forms of
purchased from one source. This is also true
pseudorabies (seep 1300), porcine
when purchasing weaned pigs for feeder-pig

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circovirus-associated disease (seep 723),
units.

and porcine reproductive and respiratory

It is difficult to keep herds free of
syndrome (seep 729). The causal viruses
respiratory diseases. Aerosols have been
may persist in a herd, but outbreaks of overt
suspected as sources of pathogen entry
disease tend to be self-limiting.

onto naive farms. Organisms such as

The most impmtant syndromes in

Mycoplasma hyopneumoniae have been
the second category are mycoplasmal
postulated to be transmitted over distances
pneumonia and pleuropneumonia (see
of as far as 2 miles, depending on climate,
p 1467). Atrophic rhinitis, once considered
terrain, and density of pigs in the locality;
to be a significant cause of respiratory
however, this assun1ption is based on
disease in swine, has declined substanspeculation and use of mathematical tially as a result of eradication programs.

models rather than on experimental data.

Salmonellosis and Ha.emophilus pamsuis

Closed herds, ie, buying in no live animals
infections may be significant problems in

(using artificial insemination or embryo
some herds. Moderate levels of atrophic
transfer to bring in new genetic mate1ial),
rhinitis caused by Bordetella bronchisep
help establish in1munity to present
tica alone may not be too significant but,
organisms and avoid introduction of new
when coupled with toxigenic strains of
infections, strains, or serotypes. Multiple

Pas teurella, are an important cause of
site production or an "all-in/all-out" policy, economic loss due to decreased rate of
in which the entire barn or air space is
growth and reduced feed conversion in
emptied before refilling, can very effectively
young pigs. Enzootic pneumonia, when
minimize the potential effect of chronic
caused by mycoplasma alone, is of
pneun10nia.

little consequence; however, when it is

Respiratory disease is endemic in many
combined witl1 secondary infection, eg,
herds. The main control factors are stress

Pasteurella mullocida, the resulting
management, stocking density, ventilation,
condition may be severe. Actinobac'illw;
temperature control, and freedom from
pleuropneumoniae may be associated
mixing and moving. Multiple site production
with considerable losses in some herds.

or "all-in/all-out" and closed-herd manage

Migrating worm larvae or the infections
ment practices greatly decrease the need for
listed in the first category often lead to
preventive and therapeutic medication.

severe problems when they occur with
the infections in the second category.

ATROPHIC RHINITIS

The severity and economic importance
of diseases in tl1e second category also are

Atrophic rhinitis is characterized by sneezing,
related to population density and to the
followed by atrophy of the turbinate bones,
type and size of herd. They may be of little
which may be accompanied by distortion of
importance in weanling pig operations but
the nasal septum and shortening or twisting
become of major importance in high-density of the upper jaw. Its significance has feeder-pig units. Although mortality usually
declined substantially, and it is no longer
is low, economic damage results from an
considered a major health risk to swine
adverse and uneven effect on growth rate,
herds.

decreased feed efficiency, and additional
costs of drugs, particularly medicated feed.

Etiology: The etiology is complex and

However, when stress can be avoided by
involves at least two organisms. Various
proper management, such diseases may
infections ( eg, inclusion body rhinitis and
result in only minimal losses.

pseudorabies) and noninfectious agents

Finally, it must be stressed that respira

( eg, dust or high ammonia levels) cause
tory disease problems in pigs are frequently
sneezing and tear-staining, usually without
the result of multiple agents ( co-infection)

leading to atrophic rhinitis. Bordetell.a bron
and rarely due to the effects of a single
chiseptica has long been implicated as a
pathogen.

major cause. This bacterium is not

It is possible to set up herds free of
host-specific, although strains that cause
diseases in the second category by
atrophic rhinitis are generally isolated only
techniques such as SPF repopulation or
from pigs. Dogs, cats, rodents, and other
segregated early weaning, or by buying pigs
species may harbor B bronchise'J)lica for
from a pneumonia-free herd. The latter
long periods, but their role in the spread of
method is the least expensive, but because
atrophic rhinitis in pigs is unce1tain.

1466

RESPIRATORY DISEASES OF PIGS
appear below the medial canthi of tl1e eyes.

Some severely affected pigs may develop
lateral deviation or shortening of the upper
jaw, whereas others may suffer some degree
of turbinate atrophy with no apparent

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outward distoition. The degree of distortion
can be judged from the relationship of the
upper and lower incisors if breed variations
are considered. In addition to the above
clinical signs, outbreaks frequently impair
growth rate and feed conversion.

The severity of atrophic rhinitis in a
herd depends largely on tl1e presence of
toxigenic strains of P multocida, the level of management, and the in1mune status of
the herd. The latter is related to both
vaccination status and the parity distribution of the sow herd, because younger sows tend to shed more organisms and produce
less lactogenic in1rnunity for their nursing
piglets than do older multiparous sows.

Lesions: The degree of atrophy and
distortion is best assessed by examining a
transverse section at the level of the second

Atrophic rhinitis in a pig. The nasal turbinate
premolar tooth (the first cheek tooth, up to
bones have been completely destroyed after 7-9 mo of age); some recommend additional natural infection with type D toxigenic
parallel sections. In the active stages of

Pasteurefla multocida. Courtesy of the
inilan1rnation, the mucosa has a blanched

Department of Pathology, University of Guelph.

appearance, and purulent material may be
present on the surface. In later stages, the
nasal cavities may be clear, but there may be

Toxigenic strains of Pasteurella multocida
variable degrees of softening, atrophy, or

(type D), often acting withB bronchisep
grooving of the turbinates; deviation of the
tica, cause permanent turbinate atrophy
nasal septum; and asyrrunetric distortion of
and nasal distortion. Both organisms can
the surrounding bone structure.

cause clinical atrophic rhinitis.

The disease has been divided into two

Diagnosis: The signs and lesions are
forms: nonprogressive atrophic rhinitis,
commonly the basis for diagnosis; howdue Lo B bronchiseptica, is mild and ever, the presence of toxigenic strains of
transient and probably does not greatly

P multocida should be confirmed. Routine
affect the animal's growth and performance; monitoring is done in some breeding herds progressive atrophic rhinitis, due to
by measuring tl1e degree of turbinate
toxigenic P multocida, is severe, permaatrophy and giving the herd an atrophy nent, and usually accompanied by poor
score. Atrophic rhinitis. must be differentigrowth.

ated from necrotic rhinitis (seep 1468).

Outbreaks of disease usually follow either
the introduction of infected pigs or mixing

Control: It is rarely possible to keep
of pigs from different sources. Piglets may
herds entirely free from mild outbreaks
be affected at any age, especially with P
of sneezing, and a low level of aberrant
multocida, which also may infect mature
turbinates and nasal bones at necropsy is
animals. Crowding, inadequate ventilation,
con1rnon, even in herds that show no clinical
mixing and moving, and other concurrent
signs of rhinitis. When atrophic rhinitis rises
diseases are important contributory factors
to an unacceptable level in a herd, control
in intensification of the disease.

measures are usually strategic: chemoprophylaxis, vaccination, temporary closure Clinical Findings: Acute signs, which
of the herd to introduction of new pigs, and
usually appear at 3-8 wk of age, include
improved management ( eg, better ventilation
sneezing, coughing, and inflanm1ation of the
and hygiene, less dusty feed). Chemoprolacrin1al duct. In more severe cases, nasal phylaxis usually includes administration of
hemorrhage may occur. The lacrin1al ducts
antibacterial drugs to all sows, particularly
may become occluded, and tear stains then
before farrowing, as well as programs of

RESPIRATORY DISEASES OF PIGS

1467
repeated medications for newborn piglets
cases is difficult. It is rapidly inactivated
and sometimes for newly weaned pigs. Mediin the environment and by disinfectants, cation of weaner and grower rations, and
but it may survive longer in cold weather.

sometimes sow rations, is often helpful.

It appears to be host-specific.

Drngs commonly used are ceftiofur,

Mycoplasmal pneumonia is also

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sulfonamides, tylosin, and tetracyclines.

frequently complicated by other

Bacterins against toxigenic P multocida mycoplasmas, bacteria, and viruses, and B bronchiseptica have been develwhich affect the severity of the disease.

oped. Both toxoid vaccines and bacterin

Certain strains of M hyorhinis, and
toxoid mixtures are available againstP
perhaps some viruses, may themselves
multocida; although both give satisfactory act as primary agents to produce a results in most herds, infection can be best syndrome resembling the pneumonia prevented with bacterin-toxoid mixtures.

ca.used by M hyopneumoniae.

Typically, sows are vaccinated 4 and 2 wk

In most countries tl1a.t use modem
before farrowing, and the young pigs at
pig-farming methods, the lungs of30%-80%

1 and 4 wk of age. However, vaccination
of the pigs slaughtered show pneumonic
schedules recommended by the manufaclesions of the type associated with turer should be followed. A high level of
mycoplasmal infection. Pigs of all ages are
colostral immunity is acquired by piglets
susceptible, but within a herd, pigs become
nursing vaccinated sows. An intranasal
infected in the first few weeks of life either
vaccine using modified-live strains of
by their darn or by other young pigs after

B bronchiseptica is also available for
mixing. Transmission to lactating piglets
young pigs.

can occur from sows of all parities but is
most prevalent in first-parity (gilt) litters. In

MYCOPLASMAL PNEUMONIA
addition, witl1 the adaptation of segregated

(rnultisite) production, llie onset of the

(Enzootic pneumonia)

disease has been delayed and may be most

Mycoplasmal pneumonia is a chronic,
evident in the finishing stage at -18---20 wk
clinically mild, infectious pneumonia of
of age. The incidence of lung lesions is
pigs, characterized by its ability to become
highest in pigs 3-5 mo old. Immunity
endemic in a herd and to produce a
develops slowly, followed by regression of
persistent dry cough, retarded growth rate,
the lw1g lesions. Older growing and mature
sporadic "flare-ups" of overt respiratory
pigs may recover completely.

distress, and a high incidence of lung lesions
in slaughter pigs. It occurs worldwide.

Clinical Findings: In herds in which the

Clinical outbreaks of mycoplasmal
disease is endemic, morbidity is high, but
pneumonia may in1pair growth rate and
clinical signs may be minimal and mortality
feed conversion. This effect is enhanced
is low. Coughing is the most common sign
when large numbers of pigs are closely
and is most obvious when pigs are roused.

confined in poorly ventilated buildings

Individual pigs or groups sporadically
under poor husbandry conditions. The
develop severe pneumonia.. A conunon
effects of the disease are uneven and
predisposing factor is a change of weather,
unpredictable and place limits on the
but other stresses ( eg, transient viral
efficiency and flexibility of large production
infections, parasitic migration, and mixing
units. However, in swine units with good
pigs) may also ca.use outbreaks. The disease
disease control measures, mycoplasmal
is usually more severe when it first enters a
pneumonia may remain largely subclinical
naive herd.

and is of little economic importance.

Lesions: Affected lungs are gray or
purple, most commonly in the apical and

Etiology and Epidemiology: The
cardiac lobes. Old lesions become clearly
terms "viral pneumonia" and "enzootic demarcated. The associated lyn1ph nodes
pneumonia" are frequently used to
may be enlarged. Histologically, inflammadescribe a characteristic disease syntory cells are present in the bronchioles; drome now known to be caused primarily
there is pe1ivascular and peribronchiolar
by Mycoplasma hyopneumoniae. The
cuffing and extensive lyn1phoid hyperplasia
pleomorphic organism is fastidious,
smaller than most bacteria, and difficult to

Diagnosis: Clinical, pathologic, and episee clearly under ordinary light microdemiologic findings a.re usually adequate scopes. It can be cultured in specially
for diagnosis. M hyopneumoniae can be
prepared media, but isolation from field
demonstrated in impression smears of

1468

RESPIRATORY DISEASES OF PIGS
the cut surface of affected lung, identified herds that claim to be free of mycoplasby fluorescent antibody technique, and mal pneumonia. Hypotheses for these
sometimes isolated and identified in
outbreaks suggest that the organism may
culture. Serologic tests, principally the
never have been successfully eliminated

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complement fixation test, and ELISA are
in certain herds, but rather coexisted
occasionally used on a herd basis, but
within the population at an undetectable
results may be difficult to interpret. A
level for extended periods. Use of nasal

PCR test to detect M hyopneumoniae in
swab PCR technology has demonstrated
nasal and bronchial swabs has been
presence of the organism in pigs free of
developed and appears to be very
clinical signs, lesions, and antibodies.

sensitive and specific.

Analysis of tracheal sections from these
pigs by electron microscopy has
indicated presence of the organism

Control: When the disease first enters a
on the cilia.

herd, mass treatment with antibiotics ( eg,
tylosin, lincomycin, tiamulin, or a tetracycline) helps to control the severity of signs.

NECROTIC RHINITIS

When disease increases in endemic herds,
treatment of individual pigs with antibiotics

(Bullnose)

usually results in remission, presumably by

Necrotic rhinitis is an uncommon, sporadic
controUing secondary bacteria.

disease of young pigs characterized by

Inactivated mycoplasmal cultures have
suppmation and necrosis of the snout,
been developed as bacterins and consist of
arising from wounds of tl1e oral or nasal
whole-cell preparations as well as new
mucosa. Confusion exists in the literature
subunit bacterins. These induce exceUent
because of the use of the misnomer
protection against development of gross

"bullnose" to also describe atrophic rhinitis lesions and significantly reduce clinical

(seep 1465).

signs ( coughing) in growing pigs. Data
indicate that prefarrowing vaccination of

Etiology: Pusobacterium necrophorum
sows with M hyopneumoniae vaccines
is commonly isolated from the lesion and
significantly reduces colonization of
undoubtedly contributes to tl1e disease, but
suckling piglets.

other types of organisms are frequently

The economic effects of the disease can
present. They gain entry through damage to
be reduced, and sometimes eliminated, by
the roof of the mouth, often as a result of
improvements in housing and husbandry,
clipping the needle teeth too short or using
particularly ventilation and overcrowding,
blunt clippers.

along with medication and vaccination.

"All-in/all-out" management of pi.gs from

Clinical Findings and Lesions: Signs
birth to market is extremely effective at
include swelling and deformity of the face,
reducing negative effects of disease;
occasionally hemorrhage, snuffling,
following this practice improves growth
sneezing, foul-smelling nasal discharge,
performance and reduces lung lesions.

sometimes involvement of the eyes with

In large intensive units, starting with
lacrirnation and pw11lent discharge, loss of
foundation stock free of mycoplasmal
appetite, and emaciation. Generally, only
pnew11onia and adopting strict precautions one or two pigs in a herd are affected.

against direct and indirect contact witll

The facial swelling usually is hard, but
pigs from other herds is advisable. Unfortuincision reveals a mass of pinkish gray, nately, many herds set up in this way do not foul-smelling necrotic tissue, or greenish remain free of mycoplasmas for very long,
gray tissue debris, depending on the age
particularly in areas with a high density
of the lesion. The nasal and facial bones
of pigs. Field observations suggest that
become involved, and facial defonnity may
infection can be wind borne for at least
be marked.

a mile between large herds in cold, wet
weather.

Diagnosis: Necrotic rhinitis is readily

In the USA and parts of Europe, most
differentiated from atrophic rhinitis by the
herds free of mycoplasmal pneumonia
bulging type of facial distortion seen in the
were established by the pig repopulation
fom1er. The character of the exudate and its
technique. More recently, some have
location within the tissue of the snout or
been established by segregated early
face are also distinctive of necrotic rhinitis.

weaning. The biggest problems with
these herd programs are the breakdown

Prevention and Treatment: Prevention
rate and the difficulty of monitoring
is directed toward avoiding ir\juries to the

RESPIRATORY DISEASES OF PIGS

1469
mouth and snout, improving pig processing

PLEUROPNEUMONIA
techniques, and improving sanitation. When
the disease occurs repeatedly, needle teeth

Pleuropneumonia is a severe and contashould be clipped carefully.

gious respiratory disease, primarily of

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If the condition is advanced, treatment
young pigs ($;6 mo old), although in an initial
may not be advisable. Early surgical
outbreak, adults also may be affected. It has
intervention and packing the cavity with
a sudden onset, short course, and high
sulfonamide or tincture of iodine may be
morbidity and mortality. It occurs worlduseful. In young pigs, sulfamethazine given wide and appears to be increasing in

PO is of value.

incidence, although some reports suggest
that severity is declining in countries where

PASTEURELLOSIS
it has been long established.

Pasteurellosis is most commonly seen in

Etiology: The causal organism is
pigs as a complication of mycoplasmal

Actinobacillus pleuropneumonia.e. To
pneumonia (seep 1438), although swine
date, 15 serotypes have been identified; they
influenza, Aujeszky disease, Bordetella
vary widely in virulence and significance
bronchiseptica, or Haemophilus
across countries. Historically, serotypes 1,
parahaemolyticus may also cause

5, and 7 have been prevalent in the USA.

changes in the lungs that lead to disease

Transmission is mainly by nose-to-nose
caused by Pasteurella spp. The causative
contact, and many recovered pigs are
organism usually is P multocida. A
carriers. Clinical signs develop within
normal inhabitant of the porcine upper

4-12 hr in experimental infections.

respiratory tract, it produces an

Aerosol transmission is limited.

exudative bronchopneumonia, sometimes with pericarditis and pleuritis.

Primary, sporadic, fibrinous pneumonia

Clinical Findings: Onset is sudden, and
due to pasteurellae, with no epidemioin herds that have not been infected previlogic connection with mycoplasmal or ously, spread is rapid. Some pigs may be
other pneumonia, may also be seen in
found dead without having shown clinical
pigs. In both primary and secondary
signs. Respiratory distress is severe; there
forms, chronic thoracic lesions and
are "thumps," and sometimes open-mouth
polyarthritis tend to develop. Diagnosis is breathing with a blood-stained, frothy nasal based on necropsy findings and recovery
and oral discharge. Fever up to 107°F
of pasteurellae from the lesions.

(41.5°C), anorexia, and reluctance to move

Nontoxigenic strains of capsular type A
are typical signs.

are the predominant isolates from cases

Although primarily a disease of growing
of pneumonia. Toxigenic strains of
pigs, A pleuropneumoniae infection may

P multocida, in the presence of B
be fatal in adults or cause sows to abort. The
bronchiseptica, are now associated
course of the disease varies from peracute
with atrophic rhinitis (seep 1465).

to chronic. Morbidity may reach 50"Ai, and in

Septicemic pasteurellosis and meningiuntreated cases, mortality is high. Survivors tis occasionally occur in piglets. Mann
generally show reduced growth rates and
heimia haemolytica has been recovered
persistent cough.

from aborted fetuses, and septicemia may

Once established in a herd, the disease
also occur in adult pigs. There are no
may be evident only as a cause of reduced
distinctive lesions, and the pathogenesis
growth rate and pleurisy at the abattoir,
is obscure. Porcine strains of M haemo
although acute disease exacerbations may
lytica are often untypeable and do not
occur. However, severe lesions may not
belong to the common ovine and bovine
always be accompanied by equally severe
serotypes. However, some outbreaks in
clinical signs. Deaths in transit and carcass
the UK have been associated with close
condemnation may result. Concurrent
contact with sheep.

infection with mycoplasma, pasteurellae,

Control of the secondary, pneumonic
porcine reproductive and respiratory
form of the disease is generally based on
syndrome, or swine influenza virus is
prevention or control of mycoplasmal
common.

pneumonia. Early and vigorous therapy

Lesions: The pneumonia is usually
with antibiotics, or in combination with
bilateral. The characteristic lesion is a
sulfonamides, is indicated to prevent
severe fib1inonecrotic and hemorrhagic
chronic sequelae of all forms of the disease.

pneumonia with accompanying fibrinous

An increasing resistance to some antibiotics pleuritis. Fibrinous pleuritis and pericarditis has been noted among the pasteurellae.

may be severe. In acute cases, the lungs are

1470

RESPIRATORY DISEASES OF PIGS
dark and swollen and ooze bloody fluid
influenza virus. Field isolates of variable
from the cut surface; hemorrhagic, even
virulence exist, and clinical manifestanecrotic, bullae of various sizes may be tion may be determined by secondary
present. The trachea may contain bloodorganisms. Pigs are the principal hosts of stained froth. In chronic cases, the lesions
classic swine influenza virus. (Human

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are more organized and localized. Extra.thoinfections have been reported, but porcine racic lesions are uncommon.

strains of influenza A do not appear to
easily spread in the human population.

Diagnosis: An explosive disease onset

However, deaths have occurred in
is suggestive and, when combined with
immunocompromised people.) In 2009, a
clinical signs and gross lesions, often
pandemic strain of HIN 1 influenza A virus
justifies a tentative diagnosis. Concurrent
spread globally; it infected people, swine,
infections, eg, with pasteurellae, may
and poultry, as welt as a small number of
complicate diagnosis. In herds that have
dogs, cats, and other animals. The disease
been exposed and have developed at least a
in swine occurs commonly in the midwestdegree of immunity, the pattern may be less ern USA (and occasionally in other
distinctive. Many serologic tests, including
states), Mexico, Canada, South America,
complement fixation and ELISA, have been

Europe (including the UK, Sweden, and
used to confirm a herd diagnosis or detect

Italy), Kenya, China, Japan, Taiwan, and
carriers, but results are not always
other parts of eastern Asia.

straightforward. A definitive diagnosis
depends on isolation and identification of

Etiology: Swine influenza virus (SIV)

A pleuropneumoniae, a gram-negative
is an orthomyxovirus of the influenza A
coccobaciltus that requires V factor (NAD)

group with hemagglutinating antigen Hl
supplementation for growth. A Staphylo
and neurantlnidase antigen N 1 (ie, HlN 1 ).

coccus aureus nurse colony can provide

Recently, new subtypes of SIV have been
the necessary factor. PCR testing is also
reported (H3N2, H1N2, and H2N3). Influenza
available and provides better sensitivity

B and C viruses have been isolated from pigs
than direct culture.

but have not caused tlle classic disease.

The classic type A infection with isolates

Treatment and Control: Rapidity of
of mild virulence may favor replication of
onset and persistence in infected herds
pseudorabies virus (seep 1300), Haemophi
make treatment difficult. Ceftiofur,
lus parasuis (Glasser's disease, seep 720), tilmicosin, tetracyclines, synthetic

AclinobaciUus pleuropneumoniae ( see
penicillins, tylosin, and sulfonantldes have
above), and Mycoplasma hyopneumoniae
been used. The first treatment should be

(seep 1467), any of which may complicate
parenteral, followed by medication given
outbreaks. The ntlxing of carrier and
in water or feed, which also may protect
noninunune pigs is an important predisposcontact pigs.

ing factor. The virus is unlikely to survive

Because survivors frequently remain
outside living cells for >2 wk except in cold
carriers, control is difficult, afthough good
conditions. It is readily inactivated by
results are being claimed for some vaccines.

disinfectants.

Segregated early weaning, "all-in/all-out"

management, reduced stocking rates when

Transmission and Epidemiology:

possible, and in1proved ventilation are

In North America, outbreaks are most
recommended. In herds free of the disease,
common in fall or winter, often at tlle onset
replacements should be purchased from
of particularly cold weatller. In warmer
herds free of A pleuropneumoniae; if the
areas of the world, infection may occur at
disease proves difficult to control, herd
any time. Usually, an outbreak is preceded
depopulation and repopulation should be
by one or two individual cases and then
considered. Sero logic testing effectively
spreads rapidly witltln a herd, mainly by
detects previously infected herds but may
aerosolization and pig-to -pig contact. The
not identify carrier animals.

virus survives in carrier pigs for up to 3 mo
and can be recovered from clinically healthy

SWINE INFLUENZA
animals between outbreaks. In antibodypositive herds, outbreaks of infection recur (Hog flu, Pig flu)

as in1111unity wanes. Up to 40% of herds may
contain antibody-positive pigs. Carrier pigs

Swine influenza is an acute, highly
are usually responsible for the introduction
contagious, respiratory disease that
of SIV into previously uninfected herds and
results from infection with type A
countries.

RESPIRATORY DISEASES OF SHEEP AND GOATS

1471

Pathogenesis: The spectrum of infection
lungs but tend to be more extensive and
ranges from subclinical to acute. In the
confluent ventrally. Nonpnemnonic areas
classic acute form, the virus multiplies in
are pale and emphysematous. The ai.tways
bronchial epithelium within 16 hr of infection
contain a copious mucopurulent exudate,
and causes focal necrosis of the bronchial
and the bronchial and mediastinal lymph

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epithelium, focal atelectasis, and gross
nodes are edematous but rarely congested.

hyperemia of the lungs. Bronchial exudates

There may be severe pulmonary edema,
and widespread atelectasis, grossly
especially of interlobular septae, or a serous
appeaiing as plum-colored lesions affecting
or serofibrinous pleuritis. Histologically, the
individual lobules of apical ai1d intennediate
lesions, when fully developed, are prinlarily
lobes, are seen after 24 hr. The lesions
those of an exudative bronchiolitis with
continue to develop until 72 hr after infection, some interstitial pneumonia.

after which the virus becomes more difficult
to demonstrate. Losses in reproduction

Diagnosis: A presumptive diagnosis can
associated with prinlary outbreaks appear
be made on clinical and pathologic findings,
to be secondary, because vims has been
but confirmation depends on detection of
recovered only rarely from the fetus.

viral RNA via PCR, molecular sequencing, or
demonstration of vims-specific antibody.

Clinical Findings: A classic acute

Virus can be isolated from nasal secretions
outbreak is chai·acterized by sudden onset
in the febrile phase or from affected lung
a11d rapid spread through the entire herd,
tissue in the early acute stage. A retrospecoften within 1 -3 days. The main signs are tive diagnosis can be made by demonstrating
depression, fever (to l08°F [42°C]),
a rise in vims-specific antibodies in acute
anorexia, coughing, dyspnea, wealrness,
and convalescent serum sainples using the
prostration, and a mucous discharge from
hemagglutination inhibition test. Both H3
the eyes and nose. Mortality is generally
and H l subtype antigens should be included.

1 o/o -4%. The overt course of the disease is

This test is also used for herd surveys. To
usually 3-7 days in uncomplicated
diagnose uncomplicated influenza infection,
infections, with clinical recovery of the herd
conditions such as pasteurellosis, pseudoraalmost as sudden as the onset. However, bies, porcine reproductive and respiratory
vims may continue to cycle an10ng pigs
syndrome, and chlanwdial and Haemophi
when clinical signs are suppressed by
lus infections must be excluded.

immune responses. Some pigs may become
chronically affected. In herds that are in
good condition, the principal economic loss

Treatment and Control: There is no
is from sttmting and delay in reaching
effective treatment, although antimicrobials
market weight. Some increase in piglet
may reduce secondary bacterial infections.

mortality has been reported, and effects

Expectorants may help relieve signs in.

on herd fertility, including abortions in
severely affected herds. Vaccination and
late pregnancy, may follow outbreaks
strict in1port controls are the only specific
in nonirnmune herds.

preventive measures. Good management
practices and freedom from stress,

Lesions: In uncomplicated infections,
particularly due to crowding and dust, help
lesions usually are confined to the thoracic
reduce losses. Commercially available
cavity. The pnemnonic areas are clearly
killed vaccines that contain both HlN2 and
demarcated, collapsed, and purplish red.

H3N2 subtypes appear to induce a strong

They may be distributed ttu·oughout the
protective in1111une response.

RESPIRATORY DISEASES

OF SHEEP AND GOATS

Upper Respiratory Tract: Diseases of
sinusitis may include some or all of the
the upper respiratory tract of sheep and
following: tutilateral or bilateral, serous to
goats include sinusitis caused by the larvae
mucopurulent nasal discharge; decreased or
of Oestrus ovis, nasal foreign bodies, and
lack of ai.tilow through one or both nostrils;
nasal tun10rs. Clinical signs associated with
coughing; sneezing; and mild to severe

1472

RESPIRATORY DISEASES OF SHEEP AND GOATS
respiratory distress. The types of nasal
cartilages of the laiynx, resulting in
neoplasms reported include adenopapillonarrowing of the lumen. Affected sheep mas (nasal polyps), adenomas, adenocarcistand with the neck extended, head held nomas, lymphosarcomas (goats), and
lowered with flared nostrils, and mouth

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squamous cell carcinomas (sheep).

open; they are reluctant to move because

Enzootic nasal tumor is caused by an
of dyspnea. Delayed identification and/or
exogenous retrovirus referred to as
inadequate duration of antibiotic therapy
enzootic nasal tumor virus (ENTV). It can
may result in abscess formation within the
be transmitted experimentally by tumor
arytenoid cartilages.

homogenates, which would explain the
widespread occurrence of this condition

Lower Respiratory Tract: The most
within some flocks. This type of tumor
common problem associated with the lower
generally affects mature animals (2-4 yr
respiratory tract is pneumonia. Pneumonias
old), although it has been reported in
can be caused by viruses, bacteria, or
animals as young as 4 mo old. The lesion
parasites. They can be acute, chronic, or
may be unilateral or bilateral, resulting in
progressive.

either unilateral or bilateral serous, mucoid,

Viruses associated with acute pneuor mucopurulent nasal discharge. Advanced monia include pai·ainfluenza type 3 (PI-3), unilateral tumors may cause deviation of
adenovirus, and respiratory syncytial virus.

the nasal septum, resulting in bilateral nasal

These viral pneumonias most often affect
discharge. Affected animals show
lambs and kids.

progressive signs of dyspnea (inspiratory ),

Pl-3 is an enveloped RNA virus (family
including open-mouth breathing, decreased

Pai·amyxoviridae) that induces a mild
airflow as measured at the nares, dullness
interstitial pneumonia. Clinical signs may
on percussion over the turbinates, sneezing,
include coughing, serous nasal and/or
and head-shaking. Strid or may also be
ocular discharge, fever (104 ° -106°F
caused by compression of the larynx by

[40°-41 °C]), and an increased respiratory
enlarged retropharyngeal lymph nodes
rate. The single PI-3 serotype for sheep that
associated with abscessation of the head.

has been identified is distinct from the

Laryngeal chondritis also results in
bovine PI-3 serotype. Infection with this
inspiratory dyspnea of varying severity.

vims can be confirmed by its isolation from

With advancing tumor growth, exophthalnasal swabs from affected anin1als, or by mos and facial deformity may occur.

comparison of acute and convalescent

Metastatic spread is uncommon. Outcome
semm antibody levels. Treatment is usually
depends on the tumor type, condition of the
not warranted in mildly affected animals. In
animal, and extent of the lesion, but in most
severely affected animals in which
commercial situations the animal is culled
secondary pathogens are suspected,
for animal welfare and commercial reasons.

antimicrobial therapy is recommended

Surgical removal of a noninvasive tumor is
using dmgs with efficacy against the most
rarely undertaken.

likely organisms, such as P mullocida,

The most common probleIRs associated

M haemolytica, and Mycoplasma sp. There with the pharynx are trauma and abscessaare no PI-3 vaccines specifically designed tion. Pharyngeal trauma usually results
for use in small ruminants.

from overly aggressive use of equipment

Chronic, progressive viral pneumonia
used to administer boluses. Injuries may
is most common in adults and includes
result in the fom1ation of discrete abscesses
progressive interstitial retroviral
or extensive and diffuse cellulitis, both of
pneumonia (in sheep, ovine progressive
which can interfere with swallowing and
pneumonia or maedi [seep 1475]; in
possibly lead to respiratory difficulty or
goats, pneumonia induced by arthritis
distress. Bacteria commonly isolated after
encephalitis virus [seep 7 4 7]) and ovine
an incident of phaiyngeal trauma include
pulmonary adenocarcinoma (seep 14 77),

Trueperella, Pasteurella mullocida,
also known asjaagsiekte or the conta

Mannheimia haemolytica, and F'usobacte
gious lung tumor of sheep and, infre
rium.

quently, of goats.

Laryngeal chondritis is an obstructive

Chronic, progressive, proliferative
upper respiratory tract disease charactet"

changes in the lungs are usually associated
ized by severe dyspnea most commonly
with the lentiviruses (family Retroviridae),
encountered in meat-breed rai11s 18--24 mo
or so-called slow-virus infections. In both
old. Acute onset of severe respiratory
progressive pnewnonia and pulmonary
distress with marked inspiratory effort and
adenocarcinoma, the entire lung can change
stertor is caused by edema of the arytenoid
in a gradual process of abnormal cellular

RESPIRATORY DISEASES OF SHEEP AND GOATS

1473
proliferation. In affected sheep, the loss of

(See also p 1619). Treatment for lungwonn
functional lung tissue results in progressive
infection is rarely indicated; however, it is
dyspnea, anorexia, and weight loss.

likely that sheep with such infections will

M haemolytica, P rnullocida, Myco
also carry other nematodes that will cause

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plasrna spp, Chlarnydia pneurnoniae, and parasitic gastroenteritis and limit produc

Salrnonella spp are associated with either
tion.

primary or secondary bronchopneumonia
in sheep and goats. BothP rnultocida and

SHEEP NOSE BOT

M haemolytica, can be cultured from the
upper respiratory tract of nom1al sheep

The sheep nose bot fly, Oestrus ovis, is
and goats. Not all factors predisposing to
a cosmopolitan parasite that, in its larval
acute respiratory diseases are known, but
stages, inhabits the nasal passages and
acute viral infections in a susceptible
sinuses of sheep and goats. Its geographic
population can alter the protective
distribution is worldwide.

mechanisms in the respiratory tract so that

The adult fly is grayish brown and -12
certain bacteria may invade lung tissue,
mm long. The female deposits larvae in
multiply, and cause serious disease. An
and about the nostrils of sheep without
initial infection with PI-3 virus may
alighting. These small, clear-white larvae
predispose an animal to infection with

(initially <2 mm long) migrate into the
pathogenic M haemolytica. Also, Myco
nasal cavity; many spend at least some
plasrna ovipneurnoniae alone can cause
time in the paranasal sinuses. The larval
a mild bronchopneumonia; however, it is
period, which is usually shortest in young
often isolated along withM haernolytica
animals, lasts 1-10 mo. When mature, the
from sheep and goats with severe
larvae leave the nasal passages, drop to the
pneumonia, suggesting that the Myco
ground, burrow down a few inches, and
plasrna may predispose the lung to
pupate. The pupal period lasts 3-9 wk,
invasion by this organism. Additionally,
depending on the environmental condiintroduction of new animals, high-density tions, after which the fly emerges from the
stocking, poor ventilation, and a sudden
pupal case and pushes its way to the
change to a high plane of nutrition can act
surface. Mating soon occurs, and the
as stress factors that predispose to
female begins to deposit larvae.

development of pneumonia.

Caseous lymphadenitis (seep 63) caused

Clinical Findings: Once the larvae begin
by Corynebacteriurn pseudotuberC'ulosis
to move about in the nasal passages, a
may result in abscessation of the lungs and
profuse discharge occurs, at first clear and
mediastinal lymph nodes. This can result in
mucoid, but later mucopurulent and
a progressive debilitation in sheep and goats frequently tinged with fine streaks of hlood with or without obvious clinical signs of
emanating from minute hemorrhages
respiratory disease.

produced by the hooks and spines of tl1e

Parasitic or verminous pneumonias of
larvae. Paroxysms of sneezing accompany
sheep and goats are most commonly caused
migrations of the larger larvae. Larvae
by infection with Dictyocaulus.fua1ia,
present in the sinuses are sometimes unable

Muellmius capillmis, or Protostrongylus to escape; they die and may gradually
rufescens. (See also p 1421.) In contrast to become calcified or lead to a septic
the acute viral and bacterial pneumonias,
sinusitis. However, the principal effects are
which result in a bronchopneumonia
annoyance, witl1 a resulting reduction in
affecting the anterior ventral po1tion of the
grazing time, and loss of condition. Usually
lungs, vem1inous pneumonia affects the
only 4-15 larvae are found, although many
margins of the diaphragmatic lung lobes.

more may be present.

Dictyocauliis has a direct life cycle,

To avoid the fly's attempts at larval
whereas Protostrongylus and Muellerius
deposition, a sheep may mn from place to
have indirect life cycles and rely on a variety place, keeping its nose close to the ground, of snails and slugs to serve as intermediate
sneeze and stan1p its feet, or shake its head.

hosts. Adult forms of Dictyocaulus and

ConU11only, especially during the wanner

Protostrongylus live in bronchi but rarely
hours of the day when the flies are most
cause clinical signs. AdultMuellmius live in active, small groups of sheep gatl1er and
alveoli and lung parenchymal tissue and are
face the center of a circle, heads dow11 and
considered the least pathogenic of the three
close together.

lungwonns. Muellm"ius appears to cause more problems for goats than for sheep.

Treatment: Ivennectin at 200 mcg/kg, PO

Diagnosis of lungwonn infection requires
or SC, is highly effective against all stages of

Baem1ann exanlination of fecal material
the larvae.

1474

RESPIRATORY DISEASES OF SHEEP AND GOATS

CONTAGIOUS CAPRINE
fluid or affected lung, has greatly facilitated

PLEUROPNEUMONIA
the diagnosis of contagious caprine
pleuropneumonia. Serologic tests are

Contagious caprine pleuropneumonia is a
complement fixation, passive hemagglutinahighly fatal disease that occurs in goats in tion, and ELISA; the latex agglutination test
the Middle East, Africa, and Asia. It was
can be done in the field directly on whole

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seen for the first time on European soil in
blood as well as on serwn samples in the

Thrace, Turkey, in 2002, but does not appear
laboratory. Sero logic cross-reactions may
to have spread to neighboring countries,
occur with other members of the Myco

Greece and Bulgaria. Outbreaks have
plasma mycoides cluster.

recently been reported in sheep and captive
wildlife, including gazelles and small

Control: Quarantine of affected flocks is
ruminants.

desirable. Vaccines are available in some
countries, and good to excellent protection

Etiology: Mycoplasma capricolum
has been reported. Treatment with tylosin at
capripneumoniae (Mycoplasma biotype

10 mg/kg/day, IM, for 3 days, has been

F38) is the causative agent. It appears to be
effective, as has oxytetracycline (15 mg/kg).

transmitted by infective aerosol. Morbidity
can be 100%, and mortality 60%--10096. The

PASTEURELLA AND
disease is introduced into a new region by

MANNHEIMIA PNEUMONIAS
healthy carriers. Gathering or housing
animals together facilitates spread of the

Bronchopneumonia caused by Pasteur
disease.

ella multocida or Mannheimia haemo

Pneumonia and pleuropneumonia can be
lytica has a cranioventral lung distribution caused by other mycoplasmas, including
and affects sheep and goats of all ages

M mycoides capri. Taxonomic change
worldwide. It can be particularly
means this subspecies also includes
devastating in young animals around

M mycoides mycoides large colony type.

weaning. It is a common cause of

Morbidity and mortality rates are generally
morbidity and mortality in lambs and kids,
lower with M mycoides capri, and joint and
especially in those that have not received
udder infections may also be seen.

adequate colostrum or in which passive
colostral immunity is waning. The disease

Clinical Findings: Weakness, anorexia,
appears to occur most often in animals
cough, hyperpnea, and nasal discharge
that have undergone recent stress such as
accompanied by fever (104.5° -106°F
transportation, weaning, change of diet, or

[40.5°-41.5°C]) are often found. Exercise
commingling with animals from unrelated
intolerance progresses to respiratory
farms. Bibersteinia trehalosi (formerly
distress, with open-mouth breathing and

Pasteurella trehalosi) causes septicemia
frothy salivation. A septicemic form of the
in lambs 4--9 mo old (systemic pasteureldisease without specific respiratory tract losis). (See also PASTEURELLOSIS OF SHEEP AND
involvement has been described.

GOATS, p 765.)

Lesions: Typically, there is an excess of
straw-colored pleural exudate and acute

Etiology: P multocida and M haemo
fibrinous pneumonia. Consolidation is
lytica are commensals of the upper
sometimes confined to one lung. The
respiratory tract that can cause pneumonia
distention of interlobular septa by
either alone or in conjunction with other
serofibrinous fluid, commonly seen in
organisms. Primary infections with
infections caused by M mycoides capri,
respiratory pathogens such as parainfluenza
is rarely seen in contagious caprine
type 3, adenovirus, respiratory syncytial
pleuropneumonia. In antibiotic-treated or
virus, Bordetella parapertussis, or in
recovered animals, the predominant lesion
particular Mycoplasma ovipneumoniae
is a sequestrum similar to that seen in
appear to predispose to secondary infection
contagious bovine pleuropneumonia.

with Pasteurella and Mannheimia.

Diagnosis: The clinical signs, epidemiol

Pathogenesis: Stress appears to be an
ogy, and necropsy findings are used to
important factor that allows Pasteurella,
establish a diagnosis. The causative

Mannheimia, Mycoplasma ovipneumo
organism should be isolated and identified,
niae, other bacteria, and viruses to multiply but isolation may be difficult, and special
and impair the normal physical defense
media is required for culture. PCR, which
mechanisms, facilitating invasion oflung
can be perfom1ed directly on the pleural
tissue and development of pneumonia In

RESPIRATORY DISEASES OF SHEEP AND GOATS

1475
calves, alveolar macrophage function is

Trueperella pyogenes, a common causative
impaired after viral pneumonia. This results
agent of tung abscesses.

in decreased clearance of inhaled bacterial
pathogens, allowing them to become

Treatment and Control: Whenever
established. Pathogen-host interactions
possible, treatment should be based on

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result in tissue dan1age, especially because
bacterial culture and sensitivity, especially
of massive influx of neutrophils. As these
in herd or flock outbreaks, when valuable
neutrophils are lysed, enzymes are released
animals are involved, or in acute or
that cause more lung tissue damage. This
chronic cases when initial therapeutic
mechanism may be similar to that of
attempts have failed. Commonly recom

Pasleurella and Mannheimia pnewnonias mended antibiotics include oxytetracyin sheep and goats.

cline (10 mg/kg/day of non-long-acting
product, or 20 mg/kg once of the long

Clinical Findings: Acute respiratory
acting product), florfenicot (20 mg/kg,
disease caused by M haemolytica is
every 48 hr), and tylosin (10-20 mg/kg,
uncommon in adult sheep, unless there
once to twice daily). Therapy should
is a predisposing problem such as ovine
continue for at least 24-48 hr after body
pulmonary adenocarcinorna or other viral
temperature has returned to normal.

infection. Clinical signs include acute onset

Duration of treatment usually is 4-5 days.

depression, lethargy, and inappetance and

Tilmicosin and other macrolide antibiotics
are consistent with profound endotoxernia.

can also be used but are considerably

Sudden death may occur without clinical
more expensive than oxytctracycline.

signs having been observed. Affected sheep

Acute cases may also benefit from the use
are typically separated from the remainder
ofNSAIDs (eg, flunixin meglumine or
of the flock and are easily caught and
ketoprofen) in conjunction with antibiotic
restrained. On approach, they may show
therapy for control of endotoxernia and
an increased respiratory rate with an
inflammation.

abdominal component.

Inadequate ventilation, crowding,

Affected sheep are typically febrile
commingling of animals from various

(>40.5°C [104.9°F]). The mucous memfarms (feedlot or sale barn situations), branes are congested, and there may be
poor nutrition, failure of passive transfer
evidence of dehydration with sunken eyes
of antibodies, transportation, and other
and extended skin tent duration. Auscultastresses have all been associated with pneution often does not reveal significant monia outbreaks. Control and prevention
changes other than an increased respiratory lies with correction of the predisposing rate. Rumen contractions are reduced or
factors whenever practical.

absent. There may be evidence of diarrhea.

Prevention of pasteurellosis is best

Frothy fluid may be noted armmd the mouth attempted using vaccines incorporating during the terminal stages.

iron-regulated proteins; because these
proteins are antigenically similar, they

Lesions: There are subcutaneous
confer cross-protection against other
ecchymotic hemorrhages over the throat
serotypes. Breeding ewes require a primary
and ribs. The lungs are heavy, swollen, and
course of two injections 4-6 wk apart
purple-red in peracute cases, and the
followed by an annual booster 4-6 wk
airways contain blood-stained froth. Cases
before lan1bing. However, this vaccination
of longer duration show anteroventral
regimen provides only passive immunity
consolidation and fibrinous pleurisy.

to the lambs for up to 5 wk Lambs can
be protected by two doses of vaccine

Diagnosis: At necropsy, testing whether
administered from 10 days of age, because
lung tissue sinks (pneumonia) or floats
colostral antibody does not interfere with

( normal) remains a useful screening test. In
development of active immunity.

acute cases, cultures obtained from tracheal
swabs or washes or from !wig tissue or
associated lymph nodes are diagnostic.

PROGRESSIVE PNEUMONIA
llistopathologic examination is useful,
especially if other types of pnewnonia ( eg,

(Maedi, Zwoegersiekte, La bouhite, Graaffretrovirns interstitial pneumonia in adult Reinet disease)

sheep and goats) are also suspected. In

Ovine progressive pneumonia and
chronic cases, bacterial cultures may be less maedi-visna are chronic diseases of sheep rewarding; Pasteurella or Mannheimia
caused by lentiviruses (family Retrovirimay have been the initial problem, but dae) that are structurally and antigenically
results of cultures taken later may reveal
similar. Progressive pneumonia virus and

1476

RESPIRATORY DISEASES OF SHEEP AND GOATS
maedi (meaning "dyspnea") virus induce
and are abnormally firm and heavy ( -2 kg;
chronic progressive pneumonias that

2-4 times normal weight). Early lung
present with similar clinical signs. Visna
changes may be difficult to detect, but

(meaning "wasting") is the term used in
later in the disease, lungs are mottled by

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many parts of the world to refer to the
gray and brown areas of consolidation.

neurologic form of the disease in sheep,

The mediastinal and tracheobronchial
resulting initially in unilateral pelvic
lymph nodes are greatly enlarged and
paresis, progressing to paralysis. A closely
edematous. Interstitial pneumonia,
related lentivirus-induced disease in goats, perivascular and peribronchial lymphoid caprine aithritis and encephalitis (CAE,
hyperplasia, and hypertrophy of smooth
seep 74 7), affects the nervous system and
muscle are seen throughout the entire
joints. Reported seroprevalence for
lung. CNS lesions, when they occur, are
lentiviral infection in sheep varies widely,
those of meningolcukoenccphalitis with
ranging from 49% in the western USA to 9% secondary demyelination. All lesions are in the north Atlantic region. This variation
progressive and result from the cellular
has been reported in other countries as
immune response of the host, and not
well and may result from varied climatic
directly from viral damage.

conditions (ai·id vs more lush climates)

and management (range conditions vs
close confinement).

Diagnosis: Differential diagnoses of
progressive pneumonia include pulmonary adenocarcinorna, pleural abscesses, Etiology and Pathogenesis: The causal
and pulmonary caseous lyrnphadeni.tis.

lentivirus, which persists in lymphocytes,

Ultrasonographic exan1ination is very
monocytes, and macrophages of infected
useful to differentiate these various types of
sheep in the presence of a hun1oral and
pnewnonias in the live ailirnal. Listeriosis,
cell-mediated immune response, can
scrapie, cerebrospinal nernatodiasis, and
be detected by several serologic tests.

space-occupying lesions should be

Seropositive sheep and goats must be
considered when tl1e neurologic fom1
considered infected and capable of transmit

(visna) of the disease is seen.

ting the virus. Transmission occurs most

In the live animal, agar gel i.rnmtmodiffucommonly via the oral route, usually by sion and ELISA tests are used. The competiingestion of colostrum or milk that contains tive inhibition ELISA is reported to be highly
virus, or by inhalation of infected aerosol
sensitive and specific; it has been reported
droplets. Intrauterine infection is thought to
to produce false-negative results in animals
occur infrequently. All breeds of sheep and
very recently infected. Sero logic testing is
goats appear susceptible; however, some
considered a useful tool to detect infected
resistance to lentivirus infection may exist
sheep, especially if the disease has been
within breeds. Management practices can
confirmed in the flock by histopathologic
influence morbidity rates.

exan1ination or virus isolation. PCR and
virus isolation are sensitive ai1d specific
techniques to detect virus. However, both

Clinical Findings: Signs rarely occur in
are more expensive and time constm1ing
sheep <2 yr old and are most common in
than serologic testing.

sheep >4 yr old. The disease progresses
slowly, with wasting and increasing
respiratory distress as the main signs.

Control: Currently, there is no practical,

Coughing, bronchial exudate, depression,
effective treatment, and no vaccines are
and fever are seldom evident unless
available. Therefore, the only means for
secondary bacterial infection occurs. A
control and prevention is serologic
noninflammatory, indurative mastitis may
testing and removal of positive animals.

occur. The encephalitic form of visna

Because of the long incubation period
causes head tilt and circling, whereas the
and time to seroconversion, retesting
spinal form causes unilateral pelvic limb
animals once a year, or even twice a year,
proprioceptive deficits progressing to
is recommended. In addition to the test
paresis and eventually to complete
and cull approach, consideration should
paralysis.

be given to raising neonates in isolation
from their darns, especially if the dam

Lesions: Macroscopic lesions of
is seropositive. Lambs should be fed
progressive pneumonia are confined to
colostrum from �eronegative sheep, or
the lungs and associated lymph nodes.

heat-treated sheep colostrum, and raised

The lungs do not collapse when the thorax
on milk replacer, milk from seronegative

(with obvious rib indentations) is opened
ewes, or heat-treated sheep milk.

RESPIRATORY DISEASES OF SHEEP AND GOATS

1477

OVINE PULMONARY
in an adult sheep that is afebrile a.re highly

ADENOCARCINOMA
suggestive clliucal signs of OPA.

During the advanced stages of clinical

(Jaagsiekte, Sheep pulmonary adenomatosis) disease, several mL of a clear, frothy fluid VetBooks.ir

Ovine pulmonary adenocarcinoma (OPA) is
may flow freely from both nostrils when
a contagious, viral, neoplastic disease of the
the sheep's head is lowered during feeding;
lungs of sheep and more rarely of goats. It
this quantity may exceed 50 mL if the
has been repmted from Europe, Asia,
hindquarters a.re raised when the head is

Africa, and South and North America.

simultaneously lowered (colloquially
referred to as the "wheelbarrow test").

Etiology: OPA is an infectious neoplastic

This test causes affected sheep considerlung disease resulting from infection with a able distress and must be discontinued as
beta retrovirus called Jaagsiekte sheep
soon as some clear fluid appears at the
retrovirus (JSRV). The virus replicates
nostrils; euthanasia is warranted
predominantly in the ttm1or cells, is released immediately once this positive result is into the airways, and is found in respiratory
obtained. Not all cases of OPA produce
secretions. Transmission of JSRV occurs
this fluid in detectable amounts even in the
predominantly through the aerosol route by
advanced stages of disease. Therefore, a
inhalation of infected respiratory secrenegative wheelbarrow test should not be tions, although ilie virus may also be
considered conclusive, although a positive
transmitted via colostmm and milk.

wheelbarrow test is pathognomonic for

OPA.

Clinical Findings: The period of

There is presently no commercial
incubation after natural infection extends
confirmatory serologic test for OPA. The
over months, so clinical signs generally

PCR test has been used in research on OPA
become evident when sheep are 2-4 yr old. for several years. However, whereas the However, disease may be seen in lambs
test is highly sensitive in laboratory assays,

8-12 mo old that are progeny of infected
it fails to detect JSRV in most infected
darns. The tumors produce clinical signs
sheep other than ove1t clinical cases. This
when they become sufficiently large or
is because there a.re few infected cells in
numerous enough to interfere with
the blood during the early stages of disease
respiration. Affected sheep lose weight
progression. Bronchoalveola.r lavage has
and show increasing respiratory distress
been used on sedated sheep to collect cells
and panting. Crackles are audible over a
from ilie airways, followed by DNA
much larger area than the distribution of
extraction and PCR testing. Although this

OPA lesions determined ultrasonographimethod appears to offer better sensitivity cally. Coughing is not prominent, and
than the blood test, the sample collection
infected animals are afebrile unless
method does not lend itself to routine
secondary infection develops. During the
on-fa.rm large-scale testing.

advanced stages of clinical disease, the

Ultrasonography can be used to
tumor mass may occupy up to 60% of lung
differentiate chronic lung pathologies and
parenchyma. Clinical disease ends in
suppmt a diagnosis of OPA, including
death after many months but sometimes
superficial lung lesions as small as 1-2 cm in
within 1-2 days due to secondary
diameter. The first indication of changes in
pasteurellosis.

the superficial lung pa.renchyma caused by

OPA is tl1e abmpt loss of tl1e b1ight linear

Lesions: Tun1ors are confined to the
echo fonned by nonnal aerated lung tissue
lungs and, rarely, the associated lymph

(visceral or pulmonary pleura) to be
nodes. They vary from small nodules to
replaced by a hypoechoic area in the ventral
extensive solid areas iliat involve ilie
margins of the lung lobes at the fifth or sixtl1
ventral parts of one or more lobes and are
intercostal spaces.

firm, gray, flat, and sharply demarcated.

Copious an10unts of white, frothy fluid are

Control: No specific treatment or vaccine
present in the air passages. Histologic
is available. Affected sheep must be culled
changes are caused by uncontrolled
as soon as clinical suspicions are
proliferation of columnar-shaped type II
confirmed by ultrasonographic examinapneumonocytes and sinular cells in ilie tion of the chest. Antibiotic tl1erapy may
bronchioles (Clara cells).

temporarily improve the clinical appearance of those sheep with significant Diagnosis: Chronic weight loss, dyspnea,
secondary bacterial infection. Good
crackles, and copious amounts of serous
biosecurity is essential to nunimize the
nasal discharge from accumulated lung fluid risks of introducing OPA to unaffected

1478

RESPIRATORY DISEASES OF SHEEP AND GOATS
farms with purchased sheep. At this time,
subclinically infected sheep serve as a
the best that can be recommended once a
reservoir for the virus. Mruntaining sheep
diagnosis is confirmed is removal of all
in single-age groups is the most important
animals showing signs suggestive of
management factor to reduce clinical
pulmonary adenomatosis. However,
disease.

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RESPIRATORY DISEASES OF

SMALL ANIMALS

Respiratory diseases are common in dogs

(eg, overcrowding) are often associated
and cats. Although clinical signs such as
with poor hygienic and environmental
coughing and dyspnea are commonly
conditions, and the resultant stress
referable to primary problems of the
increases both the incidence and severity
respiratory tract, they may also occur
of infections. Conditions that favor the
secondary to disorders of other organ
spread of infections often occur in
systems (eg, congestive heart failure).

catteries, kennels, pet shops, boarding

Both young and aged animals are at
facilities, and humane shelters.

increased risk of developing respiratory

Congenital abnonnalities, such as
disease. At birth, the respiratory and
stenotic nares, elongation of the soft palate,
immune systems are incompletely
nasophruyngeal turbinates, and tracheal
developed; this facilitates the introduction stenosis, can cause respiratory dysfunction.

and spread of pathogens within the lungs,

Neoplastic masses, degenerative changes of
and alveolar flooding may occur. In aged
the airways, and tracheal collapse can result
animals, chronic degenerative changes
in dyspnea and other clinical manifestations
that disrupt normal mucociliary clearance
of respiratory disease.

and immunologic anergy may render the

Tracheal collapse is most common in
lungs more vulnerable to rurborne
toy and miniature breeds of dogs and rare
pathogens and toxic particulates.

in cats. The cause is unknown. Affected

A varying flora of indigenous commenanimals have a nonproductive, honking, sal organisms (including Pasteurella
chronic cough and inspiratory or expiratory
mullocida, Bordetella bronchiseptica,
dyspnea. Frequently tl1ey are obese and may
streptococci, staphylococci, pseudomonhave concurrent cardiovascular or other ads, and coliform bacteria) normally
pulmonary disease ( especially chronic
reside in the canine and feline nasal
bronchitis). Weight loss (if obese) is critical
passages, nasopharynx, and up.per
in management. Other measures include
trachea, and at least intermittently in the
exercise restriction, reduction of excitelungs, without causing clinical signs.

ment and stress, and medical tl1erapy, eg,

Opportunistic infections by these bacteria
wtitussives, ru1tibiotics, bronchodilators,
may occur when respiratory defense
and corticosteroids.

mechanisms are compromised by
infection with a primary pathogen ( eg,

ALLERGIC PNEUMONITIS
distemper, parainfluenza virus, or canine
type 2 adenovirus in dogs, and rhinotra

Allergic pneurnonitis is an acute or chronic
cheitis virus or calicivirus in cats), other
hypersensitivity reaction of the lungs ru1d
insults ( eg, inhalation of smoke or noxious small airways.

gases), or diseases such as congestive
heart failure and pulmonary neoplasia.

Etiology: An underlying cause is rarely

Secondary bacterial infections complicate
detennined in pulmonary hypersensitivity
the management of viral respiratory
reactions in dogs wd cats. Type I or
infections of both dogs and cats. Pathoin1mediate hypersensitivity is probably the gens may continue to reside in the
most COJmnon mechanism, although Type
respiratory tract of convalescent animals.

III and IV mechanisms may also be involved

When stressed, these animals may relapse; (see IMMUNOLOGIC DISEASES, p 817 et seq). The they can also act as a source of infection
celluiru· infiltrate is typically eosinophilic;
for others. Poor management practices
however, mixed inflru11111atory infiltrates

RESPIRATORY DISEASES OF SMALL ANIMALS

1479
consisting of mononuclear cells, eosino

Diagnosis: This is based largely on history
phils, and neutrophils, or predominantly
and on radiographic and clinicopatl10logic
lymphocytic infiltrates can be seen.

findings. Thoracic radiographs frequently

Eosinophilic bronchopneumopathy
show irregular patchy alveolar· infiltrates

(formerly pulmonary infiltration with and increased bronchial and interstitial VetBooks.ir
eosinophilia [PIE], seep 825) is a group markings. Radiographic evidence of
of diseases associated with both
heartworm disease or parasitic pulmonary
pulmonary-associated and peripheral
disease may suggest an underlying cause.

eosinophilia. Not all types of allergic

Typical hematologic changes are mild
pneumonitis, however, are associated
leukocytosis, variable peripheral eosinowith eosinophilic bronchopneumopathy.

philia ( 4%-500/o), and occasionally baso

Causes of eosinophilic bronchopneuphilia. Fecal analysis and an occult mopathy include migrating parasites,
heartworm test are indicated when lung
reaction to microfilariae of heartworms,
par·asitism or heartwo1m disease is
lungworms, chronic bacterial or fungal
suspected. Bronchoalveolar lavage for
infections (eg, histoplasmosis, aspergilcytologic analysis, culture, and detection losis), viruses, external antigens, and
of larval fom1s is often helpful. In allergic
unknown precipitating factors. Canine
pneumonitis, bronchoalveolar lavage
heartworm (seep 127) pneumonitis
cytology generally reveals a predominance
occurs when dogs become sensitized to
of eosinophils. Bacterial cultures of
microfilariae. A similar reaction may be
aseptically collected lavage specimens
seen in cat.s with heartworms. Migrating
ar·e commonly negative.

intestinal parasites and primary lung
parasites may induce either subclinical

Treatment: When an underlying cause
or mild signs of allergic pneumonitis.

can be found, elimination oftl1e offending

Pulmonary nodular eosinophilic
agent and a short-tem1 course of glucocorti
granulomatous syndrome is a rare, severe coids resolves the problem. Prednisolone eosinophilic bronchopneumopathy-like
begirming at 1 -2 mg/kg, PO, tapered over
syndrome that occurs in dogs and is

10-14 days is often sufficient. When
most often associated with heartworm
eosinophilic bronchopneurnopathy is
infection or possibly an uncontrollable
secondary to heartworm disease or
progressive form of eosinophilic
pulmonary parasites, treatment with
bronchopneumopathy. In this condition,
prednisolone before or during treatment for
a severe granulomatous hypersensitivity
the parasite controls the pulmonary signs.

reaction to microfilariae (or other antigen) When an underlying cause caimot be results in mixed alveolar and interstitial
determined, prolonged tl1erapy with
pulmonary infiltrates plus variably sized,
prednisolone for 3-12 wk is often required.

multiple pulmonary nodules scattered

When severe bronchoconstriction is
throughout the lung fields. Associated
suspected, bronchodilators or 13
pathology may include eosinophilic

2-agonists
may be helpful. Severely dyspneic animals
granulomatous lyrnphadenitis, tracheitis,
may require sho1t-tenn oxygen therapy.

tonsillitis, splenitis, enteritis, gastritis, and
pericholangitis. Pulmonary hypersensitiv

CANINE INFLUENZA (FLU)

ity also may be caused by drugs and
reactions to inhaled allergens; however,

Etiology, Epidemiology, and
this is poorly documented in small

Transmission: Two strains of the canine
animals.

influenza virus (CIV) have been identified,

H3N8 and H3N2. The H3N8 strain was fixst

Clinical Findings: Chronic cough is the
identified in the USA in 2004, and the H3N2
most common sign. lt may be mild or
strain was identified only in Asia until 2015,
severe, productive or nonproductive, and
when an outbreak occurred in the USA.

progressive or nonprogressive. Weight loss,

Outbreaks are most conunon when dogs
tachypnea, dyspnea, wheezing, exercise
are in close contact, eg, kennels, shelters,
intolerance, and occasionally hemoptysis
dog parks.

may be seen. Severely affected animals may

CIV is spread via respiratory secretions,
exhibit moderate to severe dyspnea and
contaminated objects ( eg, water bowls),
cyanosis at rest. Auscultation varies from
and people moving between infected and
unremarkable to increased breatl1 sounds,
unmfected dogs. The incubation period is
crackles, or wheezes. Fever is usually
usually 24 days from exposure to onset
absent. The degree of dyspnea and coughing of clinical signs, when dogs are most is related to the severity of inflammation
contagious; -200/o of infected dogs remain
within tl1e airways and alveoli.

asymptomatic but can still shed virus.

1480

RESPIRATORY DISEASES OF SMALL ANIMALS

Clinical Findings and Diagnosis: Most

The mites live in the nasal passages and
exposed dogs (800Ai) develop mild infection,
paranasal sinuses. The complete life cycle
with a cough that persists 1-3 wk and may
of P caninum is not known or understood.

be similar to the cough of canine infectious

Transmission is thought to be via direct and
tracheobronchitis (seep 1491). Other
indirect contact between dogs. There is no

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possible clinical signs include ocular and
evidence to suggest thatP caninum
nasal discharge, sneezing, fever, lethargy,
presents a zoonotic risk.

and anorexia. Some dogs become severely
ill, with high fever (104°-106°F), pnewnonia,

Clinical Findings: The most common
and secondary bacterial infection. The
clinical signs associated with nasal mite
mortality rate is< 10%.

infestation include epistaxis, sneezing,

There is no rapid test for specific
reverse sneezing, impaired scenting ability,
diagnosis. Nasal or pharyngeal swabs from
facial prmitus, nasal discharge, head
dogs ill for <3 days can be submitted for
shaking, and stridor. Other reported clinical

PCR testing. After 4 days of illness, PCR
signs include coughing, restlessness, and
testing may result in false-negatives, because collapse. These signs are not specific for the time of maximal virus shedding has
nasal mite infection and may indicate many
passed. Serwn antibodies to CIV may be
types of upper respi..rato1y disease.

detected as early as 7 days after onset of
clinical signs. The best method for confirma

Diagnosis: Differential diagnoses based on
tion of infection is serologic testing with
the clinical signs include many upper respiraacute and convalescent serwn samples.

tory diseases such as rhinitis (idiopathic,
secondary bacterial, parasitic, or fungal),

Treatment, Prevention, and Control:

oronasal neoplasia, dental disease ( oronasal

Treatment is largely supportive; most dogs
fistula), nasal foreign body, or nasopharynrecover in 2-3 wk. Additional treatment ( eg, geal disease (foreign body or mass lesions).

antimicrobials, NSAIDs) is warranted to

To exclude concuffent systemic disease, a
combat secondary bacterial infection,

CBC, sernm chemistry profile, and utinalysis
pnewnonia, and other complications.

should be perfonned. If epistaxis is present,

H3N8 canine influenza vaccines are
a one-stage prothrombin time, partial
available, but whether they protect against
thromboplastin time, and buccal mucosal
the H3N2 strain is unknown. Two vaccines
bleeding time should be considered in
for H3N2 canine influenza are available
addition to a platelet count.

under conditional license from the USDA.

Imaging of the nasal chambers via nasal/

Routine infection control practices and
dental radiographs should be considered.

good hygiene within facilities are key to

Alternative imaging modalities such as CT
preventing spread. CIV can persist in the
provide excellent images of the nasal cavity
environment for i-2 days but is readily killed and paranasal sinuses. More invasive by common disinfectants. There is no
diagnostic procedures such as rhinoscopy,
evidence of transmission of CIV from dogs
retroflex nasopharyngoscopy, nasal
to people.

flushing, and nasal biopsy must be delayed
until after in1aging, because iatrogenic
changes may be hard to distinguish from

CANINE NASAL MITES
primary disease.

Rhinoscopy and nasal flushing are the

The canine nasal mite, also known as
most useful diagnostic tools. Flexible

Pneumonyssoides caninum or Pneumo
rhinoscopes allow observation of the nasal
nyssus caninum, has been reported
choanae. This area is best visualized by
worldwide, including the USA, Canada,
putting a u-bend in the rhinoscope (retro

Japan, Australia, South Africa, Italy, France,
flexed view) and advancing it into the oral

Spain, Norway, Sweden, Finland, Denmark,
cavity until it can be hooked w1der the soft
and Iran.

palate. Gentle traction is applied, and the
endoscopist can view the nasal choanae or

Etiology and Epidemiology: The
the caudal nasal passages as they enter the
canine nasal mite has most commonly
nasopharynx. Flooding the nasal chambers
been rep01ted in dogs and has also been
witl1 anesthetic gas or oxygen to encourage
reported in a silver fox. There does not
the mites to migrate toward the nasopharynx
seem to be a breed, age, or sex predilection,
and the endoscope has been described.

although one report suggested that dogs

Nasal flushing may also help identify

>3 yr old were affected more often and that

P caninum. This is generally performed
large-breed dogs had a higher incidence
with the dog under general anesthesia with
than small-breed dogs.

a cuffed endotracheal tube in place. The

RESPIRATORY DISEASES OF SMALL ANIMALS

1481
oropharynx is packed with gauze, and saline in some populations. Dual infections with is flushed through the external nares with a
these viruses may occur. Other organisms

Foley catheter or a tight-fitting syringe to
such as C felis, Mycoplasma spp, and
collect fluid from the oropharynx. Retrograde reoviruses are believed to account for most flushing can be done by placing a modified
of the remaining infections or further

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catheter behind the soft palate, occluding
complicate FVR or FCV infection. Concurthe nasal pharynx, and flushing with saline.

rent Bartonella henselae also may further

TI1is allows fluid to be collected via the
complicate infection.

external nares. In both cases, the fluid

Natural transmission of these agents
should be evaluated using an illuminated
occurs via aerosol droplets and fomites,
magnifying lens to look for mites.

which can be carried to a susceptible cat by

The definitive diagnosis of nasal acariasis
a handler. Convalescent cats may harbor
can be made via endoscopy or nasal flushing virus for many months. Calicivims is shed if the mites are identified. This does not,
continually, while infectious FVR virus is
however, detemline whether the disease
released intermittently. Stress may
is primary or secondary.

precipitate a secondary comse of illness.

The incubation period is 2-6 days for FVR

Treatment: No drugs are currently
and FCV, and 5-10 days for pneumonitis.

approved for the treatment of P caninum;
however, ivermectin (200-400 mcg/kg,

Clinical Findings: The onset of FVR is

SC or PO), milbemycin oxime (1 mg/kg,
marked by fever, frequent sneezing, conjuncti

PO, three times at 10-day intervals), and
vitis, rhinitis, and often salivation. Excitement
selamectin (topical) have been suggested.

or movement may induce sneezing. The fever

The optimal treatment regimen has yet to
may reach 105°F ( 40.5°C) but subsides and
be detennined. Treatment has been reported
tends to fluctuate from nmmal to 103°F
to be effective in >85% of cases, and the

(39°C). Initially, a serous nasal and ocular
prognosis is excellent. However, treatment
discharge occurs; it soon becomes mucopu-
may not completely eliminate clinical signs,

1ulent and copious, at which time depression
particularly if infection is suspected rather
and anorexia are evident. Severely debilitated
than demonstrated. In these cases, it is
cats may develop ulcerative stomatitis, and
probable that the signs are the result of a
ulcerative keratitis develops in some. Signs
concurrent upper airway disease. Treatment
may persist for 5-10 days in milder cases and
is based on definitive diagnosis, but empirical as long as 6 wk in severe cases. Generally, the tl1erapy has also been performed based on a
mortality is low and prognosis good except
high index of suspicion.

for young kittens and aged cats. The illness
often is prolonged, and weight loss may be

FELINE RESPIRATORY DISEASE
marked. FVR often is complicated by second

COMPLEX
ary bacterial infections; abortions and
generalized infections also have been

Feline respiratory disease complex includes
associated witl1 disease.

those illnesses typified by rhinosinusitis,

There are many serologically related
conjunctivitis, lacri.mation, salivation, and
strains of feline caliciviruses. They appear
oral ulcerations. The principal diseases,
to have a predilection for the epithelium
feline viral rhinotracheitis (FVR; feline
of the oral cavity and the deep tissues of
herpesvirus type 1), feline calicivirus (FCV),
the lungs. Some caliciviruses are non

Chlamydiafelis, Mycoplmmiafelis, or
pathogenic. Some induce little more than
combinations of these infections, affect
salivation and ulceration of the tongue,
exotic as well as domestic species. Feline
hard palate, or nostrils; others produce
pneumonitis ( Chlamydia psittaci) and
pulmonary edema and interstitial pneumomycoplasmal infections appear to be of nia. Clinically, it is often impossible to
lesser importance. Feline infectious peritodifferentiate FVR from FCV infection. Two nitis (seep 780) typically causes a more
strains may produce a transient "lin1ping
generalized condition but may cause signs
syndrome" without signs of oral ulceration
of mild upper respiratory tract infection.

or pneumonia. These strains produce a

FVR and caliciviruses are host-specific
transient fever, alternating leg lameness,
and pose no known human risk. Human
and pain on palpation of affected joints.

conjunctivitis caused by the feline

Signs occur most often in 8- to 12-wk-old
chlamydia! agent has been reported.

kittens and usually resolve without
treatment. The syndrome may occur in

Etiology: Most acute feline upper
kittens vaccinated against FCV; no vaccine
respiratory infections are caused by FVR
protects against both of the strains that
virus, although FCV may be more prevalent
produce the "limping syndrome."

1482

RESPIRATORY DISEASES OF SMALL ANIMALS

Calicivirus has also been found in cats

Early in the clinical course of feline
with lyrnphocytic-plasrnacytic gingivitis
pneunionitis, the causative organism may
and stornatitis (seep 217). The superficial be identified in Giemsa-stained cortjunctival
lesions heal rapidly, and appetite returns
smears or scrapings. The elementary bodies

2--3 days after onset. The clinical course
are intracytoplasmic. Mycoplasmas occur as
usually is 7-10 days. An acute febrile
extracellular coccoid bodies often seen on

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response, inappetence, and depression
the swface of cortjunctival epitl1elial cells.

are common signs. Serous rhinitis and
conjunctivitis also can occur.

Diagnosis: The presuniptive diagnosis

C felis infections characteristically
is based on such typical signs as sneezing,
produce conjunctivitis (seep 506); infected conjunctivitis, rhinitis, lac1imation,
cats sneeze occasionally. Fever may develop
salivation, oral ulcers, and dyspnea. FVR
as the disease progresses beyond serous
tends to affect the cortjw1ctivae and nasal
lac1imal discharge to mucopu.rulent conjunpassages, caliciviruses the oral mucosa ctivitis, lymphoid infiltration, and epithelial
and lower respirat01y tract. Chlamydia]

hyperplasia. Convalescent cats may undergo infections result in chronic, low-grade relapses.

cortjunctivitis. These characteristics may

Mycoplasma spp may infect the eyes and
be obscured in mixed infections. Cytologic
upper respiratory passages, charactelistiexan1ination of Giemsa-stained conjunctival cally producing severe edema of the conscrapings is of value for the identification of junctiva and a less severe rhinitis.

chlamydiae and mycoplasmas. A definitive

The occurrence of severe viral upper
diagnosis is based on isolation and identifirespiratory disease is rare in adult, properly cation of tl1e agent. The orophaiyngeal vaccinated cats. These cats should be tested mucosa, external nares, and cor\junctival for other upper respiratory diseases and,
sacs are tl1e preferred sampling sites.

less commonly, concurrent immunodefi

However, diagnosis ofFVR may be difficult,
ciency diseases, including feline leukemia
because virus is shed intern1ittently and
virus and feline immunodeficiency 0.rus.

because seroprevalence and virus isolation
rates ai·e sinlilai· in ill and clinically nonnal

Lesions: Lesions generally are confined
cats. Sai11ples of ocular, nasal, or caudal
to the respiratory tract, conjunctivae, and
pharyngeal secretions for PCR may help
oral cavity. In FVR, the COf\junctivae and
establish a diagnosis and causative agent.

nasal mucous membranes are reddened,
swollen, and covered with a serous to

Treatment: Treatment is largely symptopurulent exudate. In severe cases, focal matic and supportive, but broad-spectruni
necrosis of these membranes may be seen.

antibiotics are useful against secondaiy

The larynx and trachea may be mildly
bacte1ial invaders ( eg, amoxicillin with
inflamed. The lungs may be congested, with
clavulanic acid, cephalospolins, trimethosmall areas of consolidation; however, prim-sulfa, fluoroquinolones, tetracyclines,
pulmonary changes are rarely remarkable
chloramphenicol) as well as directly against
in FVR except possibly in stressed, yow1g

C felis and M felis. Tetracyclines and kittens. The characteristic histologic lesion
fluoroquinolones are the most effective
of FVR is the acidophilic intrltnuclear
againstCJelis andMfelis. Nasal and ocular
inclusion body. Duling the early stage of
discharges should be removed frequently
illness, inclusions may be present in sites
for the comfort of the cat. Nebulization or
of epithelial necrosis on the tongue, nasal
saline nose drops may aid i)1 tl1e removal of
membranes, tonsils, epiglottis, trachea, and
tenacious secretions. Nose drops containing
nictitating membranes. Inclusion bodies are
a vasoconstrictor ( eg, two drops of ephedrine
transitory. Inclusions are not seen in
sulfate [0.25%solution] in each nostril, bid)

calicivirus infections.

and antibiotics may help reduce the amount

The characteristic lesion caused by FCV
of nasal exudate. Prolonged use of nasal
is ulceration of the oral mucosa. Lesions
decongestants, however, may result in
on the tongue or hard palate initially may
rebound nasal congestion and worsening of
appear as vesicles, which subsequently
clinical signs. A bland ophthalmic ointment
rupture. Ulcerations are occasionally found
containing antibiotics (tetracyclines in Cfelis
on the epitheliuni coveting the median nasal infections) is indicated 5---6 times daily to septun1. The more virulent caliciviruses
prevent corneal irritation produced by dried
destroy epithelial cells of the bronchioles
exudate. If corneal ulcers develop in FVR
and alveoli, which causes acute pulmonary
infections (herpetic keratitis), ophthalmic
edema that progresses through seropurupreparations containing idoxwidine or lent bronchiolar hyperplasia and interstitial
acyclovir are indicated in addition to other
pneunionia
antibiotic ophthalmic preparations. Lysine

RESPIRATORY DISEASES OF SMALL ANIMALS

1483

(250 mg, PO, bid-tid) interferes with herpetic
southeast Asia, and North America. P wes
viral replication and may reduce the severity
te1mani is a parasite of people and other
of FVR infection. If dyspnea is severe, the cat
animals in China and other countries in
can be placed in an oxygen tent. F1uids may
the Far East.

be indicated to correct dehydration, and

The adult flukes are fleshy, reddish
force-feeding may be necessary. Esophabrown, oval, and -14 x 7 mm. The eggs VetBooks.ir
gostomy and gavage may be appropriate for
are golden brown, oval, distinctly
alimentation in severely debilitated cats.

operculated, and -100 x 60 µm. The eggs

Antihistamines ( eg, chlorpheniramine
pass through the cyst wall, are coughed
maleate, PO, bid [8 mg for adults, 4 mg for
up, swallowed, and passed in the feces.

kittens]) may be beneficial early in the course The life cycle includes several snails as of the disease.

the first intermediate host, and crayfish
or crabs as the second. Dogs and cats

Prevention: 1\vo types of modified-live
become infected by eating raw crayfish or
virus FVR-FCV vaccines are available. The
crabs that contain the encysted cercariae.

first type is intended for parenteral adminis

After penetrating the intestinal wall and
tration; cats >9 wk old should be vaccinated
wandering in the peritoneal cavity, the
twice, with a3-wk interval. Kittens should be
young flukes pass through the diaphragm
vaccinated at intervals of3-4 wk until they
to the lungs, where they become
are 2!12 wk old. In adult cats, revaccination
established.

with a single dose every 1-3 yr is indicated.

Infected animals may have a chronic,

The second type of vaccine is administered
deep, intermittent cough and eventually
to healthy cats by instillation into the coqjuncbecome weak and lethargic, although tival cul de sacs and nasal passages. Owners
many infections pass unnoticed. Finding
should be advised that cats inoculated
the characteristic eggs in feces or sputum
oronasally may sneeze frequently for 4--7 days is diagnostic. The location in the lungs is after vaccination. Kittens vaccinated when
ascertained by radiography. Aberrant

< 12 wk old should be revaccinated when
infections can be identified serologically.

reaching this age. Annual revaccination with

Fenbendazole (50 mg/kg/day, PO, for
a single dose is recommended.

10-14 days) or less preferably albendazole

Modified-live virus FVR-FCV vaccines

(25 mg/kg, PO, bid for 14 days) reduce the
intended for parenteral administration
number of eggs deposited and eventually
are available in combination with either
kill the parasites. Praziquantel (25 mg/kg,
chemically inactivated or modified-live virus

PO, tid for 3 days) may also eliminate lung
feline panleukopenia vaccines. A parenterflukes in dogs.

ally administered vaccine composed entirely
of inactivated viruses also is available.

Vaccines containing either chick

LUNG NEMATODES
embryo- or cell-line-origin Cfelis are

See also
administered parenterally. A single dose

LUNG WORM INPECTION, p 1421.

is recommended for cats >12 wk old;
younger kittens should be revaccinated

Aelurostrongylus abstrusus
when they reach 16 wk. All should be

Aelurostrongylus abstrusus, the most
revaccinated annually. These vaccines
common lungwom1 of cats, is found in
are indicated in catteries or on premises
many parts of the world, including the USA,
where C Jelis infection has been confmned.

Europe, and Australia. They are small

The chlamydia! vaccines are available in
parasites (males 7 mm, females 10 mm),
combination with FVR-FCV and panleudeeply embedded in the lung tissues. The kopenia vaccines. Systematic vaccination
eggs are forced into alveolar ducts and
and control of environmental factors
adjacent alveoli, where they fom1 small

(such as exposure to sick cats, overcronodules and hatch. Once tl1e larvae escape, wding, and stress) provide good protecthey are coughed up, swallowed, and passed tion against upper respiratory disease.

in the feces. The larvae seen in the feces of
infected animals are tightly coiled, have an

LUNG FLUKES
undulating tail with a spine, and are <400
µm long. The life cycle includes snails or

Paragonimus kellicolli and P weste1mani slugs as first intermediate hosts, and frogs, usually are found in cysts, primarily in
lizards, birds, or rodents as transport hosts
the lungs of dogs, cats, and several other
of encysted larvae. When one of these
domestic and wild animals. They also have transport hosts is eaten, the larvae migrate been found rarely in other viscera or the
from the stomach to the lungs via the
brain. Infection is most common in China,
peritoneal and thoracic cavities. They reach

1484

RESPIRATORY DISEASES OF SMALL ANIMALS
the lungs within 24 hr and are seen in the
combined with administration of fenbenfeces in -1 mo.

dazole, levan1isole, or thlabendazole has

Although prevalence can be high, clinical
effectively treated infected dogs. Chemoand diagnostic signs are often lacking.

therapy alone can be successful but does

Chronic wasting, cough, dyspnea, and
not always result in a complete cure.

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pulmonary wheezes may be seen. The lungs

Pilaroides hirthi is similar to O osleri usually have solidified, gray, raised nodules
but is found in the lung parenchyma. The

1-10 mm in dian1eter; generalized alveolar
females are oviviparous. Adults are found in
disease has been seen in chronic cases.

nests in the lung parenchyma, where a focal

Treatment is difficult and not often necessary, granulomatous reaction occurs. Diagnosis but fenbendazole (50 mg/kg/day, PO, for
of low-grade infection can be difficult. Zinc

10-14 days) or ivermectin ( 400 mcg/kg, SC,
sulfate flotation is usually more successful
twice at a 3-wk interval) may be effective.

than using a Baermarm apparatus. Treatment with fenbendazole (50 mg/kg/day, PO,

Capillaria aerophila
for 10-14 days) or less preferably albenda

Although usually parasites of the frontal
zole (25 mg/kg, PO, bid for 5 days and
sinuses, trachea, bronchi, and rarely nasal
repeated in 2 wk) has reportedly been
cavities of foxes, C aerophila are found in effective. Ivermectin (200 mcg/kg, SC, twice
dogs and other carnivores. They are 25--35
at a 3-wk interval) may also be effective.

nun long. The females produce eggs with
bipolar plugs that resemble those of

NEOPLASIA
whipwonns; however, their shells are
colorless to greenish and pitted. The eggs

Tumors of the Nose and Paranasal
are laid in the lungs, coughed up and

Sinuses
swallowed, and passed in the feces. The
eggs can be identified from either tracheal

Tumors of the nose and paranasal sinuses
washes and bronchoalveolar lavage or fecal
account for 1 o/o--2% of all canine or feline
flotation. The life cycle is direct; dogs
twnors. The incidence in dogs is twice that
become infected through conswnption of
in cats; incidence is also higher in males of
feed or water contaminated with larvated
both species than in females. The mean age
eggs. After hatching in the intestine, the
at time of diagnosis is 9.5-10 yr for dogs and
larvae reach the lungs and bronchi via the

12 yr for cats. In dogs, nasal twnors are
circulatory system. They matw·e -40 days
nearly all malignant, and slightly >600/o are
after infection.

carcinomas, of which adenocarcinoma is

Clinical signs include coughing, sneezing,
the most common. In dogs, the ethmoturbiand nasal discharge. Treatment may be attnates tend to be the site of predilection.

empted using fenbendazole (50 mg/kg/day,

Dolichocephalic and mesocephalic breeds

PO, for 10-14 days) or ivermectin (200
appear to be at higher risk than brachycemcg/kg, SC, twice at a 3-wk interval).

phalic breeds. In cats, 2'90% of nasal twnors
are malignant, the most conunon being

Filarids
lymphoma and the second most common
being carcinomas. Tumors of the nose and

Oslerus osleri are tracheal worms of dogs,
paranasal sinuses typically are very invasive
usually found in thin-walled nodules around
locally and metastasize infrequently;
the bronchial bifurcation. They have been
metastasis is more likely in carcinomas and
found in the USA, South Africa, New
usually occurs late in the disease. Common

Zealand, India, Great Britain, France, and
sites of metastasis are regional lymph

Australia. The males are -5 mm long, and
nodes, lungs, and brain. Invasion of the
the females 10-15 mm. The life cycle is
paranasal sinuses tends to be greater in
direct, and an infected bitch can transfer
dogs than in cats. In general, survival of
larvae in her saliva to her pups while licking
untreated animals is 3--5 mo after diagnosis.

and cleaning them. On ingestion, the larvae

Chronic nasal discharge is the most
pass to the blood and are carried to the
corrunon clinical finding; it may be mucoid,
lw1gs and bronchi.

mucopurulent, or serosanguineous.

A persistent, dry cough is the most

Initially, discharge is unilateral but often
common clinical sign. Coughing may later
becomes bilateral. Periodic sneezing,
become severe, with respirato1y distress.

epistaxis, and respiratory stertor may

Finding larvae in the feces is diagnostic,
occur. Facial and oral deformities result
but because these larvae are lethargic and
from destruction of bony or soft-tissue
few in nwnber, bronchoscopy is a better
sinonasal structures. Retrobulbar extension
method. Surgical excision of the nodules
of these twnors results in exophthalrnos

RESPIRATORY DISEASES OF SMALL ANIMALS

1485
and exposure keratitis. Secondary epiphora

Diagnosis is made from the history and
may occur if the nasolacrimal duct is
clinical findings and by etinlinating other
blocked. Late in the disease, CNS signs (eg,
causes of upper airway obstruction or
disorientation, blindness, seizures, stupor,
coughing. The twnor mass may be seen
and coma) may develop if the tumor
radiographically or on laryngoscopy or

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extends into the cranial vault.

tracheoscopy. Definitive diagnosis is made

Diagnosis is based on history and clinical
on biopsy.

findings and elimination of other causes of

Surgical excision and resection is the
nasal discharge, sneezing, or facial
treatment of choice. Radiation therapy may
deformation. Nasal radiographs or CT
be palliative for radiosensitive tumors such
typically show increased density of the
as squamous cell carcinoma, mast cell
nasal cavity and frontal sinuses as well as
tumor, and lymphoma. Surgical resection of
evidence of bone destruction. CT is vastly
tracheal osteochondral dysplasia in dogs is
superior to plain radiography in diagnosis of cw·ative.

chronic nasal diseases. Definitive diagnosis
is based on biopsy of tumor tissue, either
with blind biopsy based on CT lesion

Primary Lung Tumors
localization or on rhinoscopic visualization

Primary tung tun1ors are rare in dogs and
with direct biopsy. Nasal hydropulsion
cats; however, tl1e reported incidence of
using a high-pressure saline infusion into
lung carcinomas has increased at least 100%
the nose often yields diagnostic samples
during the last 20 y.r. This is attributed to an
and, if large volumes oftwnor tissue break
increased average life span, better detection
free, nasal obstruction will be relieved
and awareness, or possibly increased
inunediately.

exposure to environmental carcinogens.

Treatment largely depends on tumor type

Most prin1ary lung tumors are diagnosed at
and extent of disease. The treatment of
a mean age of 10-12 y.r in dogs and 12 y.r in
choice for canine nasal adenocarcinoma is
cats. There is no consistent breed or sex
radiation therapy. Aggressive surgical
predilection in either species. Primary lung
excision, chemotherapy, radiation therapy,
tumors usually originate from t11e terminal
or combinations for other tumor types
bronchioles and alveoli; they occasionally
afford a more favorable prognosis when
develop as a second coincidental tmnor,
diagnosis is made early.

which may make differentiation between
primary and metastatic disease difficult.

Tumors of the Larynx and Trachea

Of the primary lung tumors in dogs and
cats, �8()0A, are malignant. Adenocarcinoma

Tumors of the larynx and trachea are rare in
and alveolar carcinoma are the most
dogs and cats. Tumors of the larynx most
common types. Primary lung sarcomas
frequently reported in dogs are oncocyand adenomas are rare in both species.

toma, squamous cell carcinoma, mast cell

Metastatic spread of primary tw1g twnors
twnor, melanoma, and osteosarcoma; in
is generally to other areas of the lungs,
cats, they are squamous cell carcinoma,
tracheobronchial lymph nodes, bone,
lymphosarcoma, and adenocarcinoma.

and brain. Intrapulmonary spread via

Benign inflanm1atory polyps of the larynx
the airways occurs in -500A, of dogs with
also are seen in dogs and cats. Tumors of the adenocarcinoma. Metastatic spread to the trachea are particularly rare. Osteochondral
pleurae, pericardium, heart, and diaphragm
dysplasia of the trachea ( osteochondroma)

may occur; miscellaneous extrathoracic
is a benign tumor of the trachea prin1a1ily
sites include liver, spleen, and kidney. Dogs
seen in dogs d y.r old. Other benign
with papillary (bronchoalveolar) adenocarmesenchymal tumors, carcinomas, and cinoma have a better prognosis than those
sarcomas are occasionally seen.

with other lung twnors; however, histologic

The most common signs of tumors of the
grade and detection of clinical signs are the
larynx include inspiratory dyspnea, stridor,
most important determinants of prognosis
voice change (hoarse bark or loss of voice),
and survival. Both recurrence and
coughing, and exertional dyspnea. Findings
metastasis tend to occur earlier and with
typically associated with tumors of the
greater frequency in dogs with moderately
trachea are coughing, dyspnea, stridor, and
or poorly differentiated tumors.

rarely hemoptysis. Laryngeal and tracheal
tumors may be associated with signs of

Clinical Findings: Primary lung tumors
fixed upper airway obstruction (inspiratory
have variable manifestations, which depend
and expiratory dyspnea). The degree of
on the location oftwnor, rapidity of tumor
dyspnea often relates to the degree of
growth, presence of previous or concurrent
luminal obstruction.

pulmonary disease, and awareness of the

1486

RESPIRATORY DISEASES OF SMALL ANIMALS
owner. Common signs include cough,

Metastatic Tumors of the Lungs
inappetence, weight loss, reduced exercise
tolerance, lethargy, tachypnea, dyspnea,

A localized tun1or may extend to the lungs
wheezing, vomiting or regurgitation,
by dissemination through hematogenous
pyrexia, and lameness. The most common
or lymphatic routes or by direct extension
clinical findings in dogs are cough, dyspnea,
of tumor cells. Certain primary tumors,

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lethargy, and weight loss, although 25% of
such as mammary adenocarcinoma, osteodogs with primary lung tumors have no sarcoma, hemangiosarcoma, and oral
clinical signs related to the tumor. Coughing melanoma, most commonly metastasize to is uncommon in cats; nonspecific signs,
the lungs. The lungs may be the only site of
such as inappetence, weight loss, and
metastasis, or there may be concurrent
tachypnea and dyspnea, are more common.

metastasis in other organs; in the forn1er,

In either species, tachypnea or dyspnea indithe diagnostic approach is to identify an cates massive tun1or burden or pleural
occult prinlaiy tumor or to cai·efully review
effusion. Pleural effusion is particularly
the medical history for disclosure of
common in cats with primary lung tumors.

previous tumor removal. Because pultno

Lameness may be due to hypertrophic
nary metastasis occurs late in the clinical
osteopathy (unusual in cats) or to metastacourse of a malignant tumor, prognosis is sis to bone or skeletal muscle. Thoracic
poor.

auscultation may be nonnal, reflect

The signs of metastatic pultnonary
increased breath sounds compatible with
disease are sinliiai· to those of prinlary
pulmonary airway disease, or be muffled

!wig twnors except that coughing is less
because of pulmonary consolidation or
common. Seve1ity of signs depends on the
pleural effusion.

anatomic location of the tun1or and whether
the lesions are solitary or multiple.

Establishing a diagnosis is sinlilar to that

Diagnosis: One-third or more of primary
for primary lung tumors. Because of the
lung tun1ors are recognized incidentally
limitations of routine radiography, small
during radiography for other problems, or
lesions (53 mm in diaineter), which are
at necropsy. Thoracic radiographs are
present in �4()0A, of cases with pultnonary
essential for a tentative diagnosis in those
metastasis, may not be seen. Thoracic CT
animals exhibiting compatible clinical signs. can identify lesions not seen radiographl

Prinlary lung tumors in dogs may occur as
cally.

single or multiple circun1scribed mass

Radiography of the chest should
lesions, as a diffuse lung pattern, or as
precede removal of tumors with a known
a lobar consolidation. In cats, single
high incidence of metastatic spread to the
circumscribed mass lesions are less
lungs. The major goal of cancer therapy
common, whereas a diffuse lung pattern
is prevention of metastasis rather than
or lobar consolidation is more frequent.

cancer eradication. Slow-growing or

Pleural fluid accunmlation is common in
solitary metastatic lesions are best treated
cats and less frequent in dogs. In either
by surgical excision. Chemotherapy or
species, chest wall involvem�nt and hilar
radiation therapy may be useful with certain
lymphadenopathy may be seen. Tentative
tumor types not an1enable to surgical
diagnosis can be made by excluding other
resection. Overall, the prognosis for
causes of pulmonary disease with similar
aninlals with pulmonary metastasis is
radiographic lung patterns. Definitive
poor.

diagnosis requires biopsy.

PNEUMONIA

Treatment: Surgical resection of tumor
via lobectomy of diseased lung lobes is the

Pnewnonia is an acute or chronic inflanimatreatment of choice. Inoperable lesions or tion of the lungs ai1d bronchi characterized
metastatic disease may be controlled with
by disturbance in respiration and hypoxchemotherapy. Overall median survival emia and complicated by the systemic
time for dogs having surgical treatment
effects of associated toxins. The usual
for primary lung tumor is 120 days. Mean
cause is primary viral infection of the
survival time for operable primary lung
lower respiratory tract.

tumors without node involvement in dogs is

Canine distemper virus, adenovirus

12 mo; if the lymph nodes are involved or
types 1 and 2, parainfluenza virus, and
multiple tumors are found at the tinle of
feline calicivirus cause lesions in the distal
diagnosis, survival time is only 2 mo.

airways and predispose to secondary bacte

Recurrence or metastasis of tumor is a
rial invasion of the lungs. Parasitic invasion
common cause of death.

of the bronchi, as by Filaroides, Aeluros-

RESPIRATORY DISEASES OF SMALL ANIMALS

1487
trongylus, or Paragonimus spp may result Treatment: The aninlal should be placed
in pneumonia. Protozoan involvement,
in a wam1, dry environment. Anemia, if
eg, by Toxoplasma gondii (seep 685) or
present, should be coITected. If cyanosis

Pneumocystis jiroveci, is rarely seen.

is severe, oxygen therapy may be used,

Tuberculous pneumonia, although
administered by means of an oxygen cage,
uncommon, is seen more often in dogs than
with a concentration of 30%--500/o. Empirical

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in cats. The incidence of mycotic granuantinlicrobial chemotherapy should be lomatous pneumonias is also higher in
i.Jlitiated and changed if needed based on
dogs than in cats. Cryptococcal pneumonia
results of culture of bronchoalveolar lavage
has been described in cats. Injury to
fluid. Supportive therapy should be
the bronchial mucosa and inhalation or
instituted as needed and may include
aspiration of irritants may cause pneumooxygen supplementation, pulmonary nia directly and predispose to secondary
physiotherapy (nebulization and coupage),
bacterial invasion. Aspiration pneun1onia
and bronchodilators. If no response is seen

(seep 1417) may result from persistent
after 48--72 hr of therapy, the treatment plan
vomiting, abnom1al esophageal motility, or
should be reassessed. Antimicrobial
improperly administered medications ( eg,
chemotherapy should be continued l wk
oil or barium) or food (forced feeding); it
after clinical and radiographic signs resolve.

may also follow suckling in a neonate with

Anin1als should be reexamined frea cleft palate.

quently. Chest radiographs should be
repeated at regul.ar intervals to monitor

Clinical Findings: The initial signs are
recurrence or note a primary underlying
usually those of the primary disease.

disease process and to detect complications

Lethargy and anorexia are conunon. A
such as lung consolidation, atelectasis, or
deep cough is noted. Progressive dyspnea,
abscessation.

"blowing" of the lips, and cyanosis may
be evident, especially on exercise. Body
temperature is increased moderately, and

PULMONARY
there may be leukocytosis. Auscultation

THROMBOEMBOLISM
usually reveals consolidation, which may
be patchy but more commonly is diffuse.

See also THROMBOSIS, EMBOLISM, AND ANEURYSM, In the later stages of pneumonia, the
p 141.

increased lung density and peribronchial

Pulmonary thromboembolism (PTE) is
consolidation caused by the inflanunatory
an obstruction of one or more pulmonary
process can be visualized radiographically.

vessels by a blood clot. The actual incidence

Complications such as pleuritis, mediastiniof PTE is uncertain, although in critically ill tis, or invasion by opportunistic organisms
aninlals or in tllose with certain disease
may occur.

states ( eg, immune-mediated hemolytic
anemia, corticosteroid administration,

Diagnosis: Analysis of bronchoalveolar
bacterial infections, protein-losing
lavage fluid is valuable for the diagnosis
enteropathy or nephropathy, neoplasia,
of bacterial infections. Cytologic examinatrauma, feline infectious peritonitis, tion can demonstrate the animal's immune
diabetes mellitus, hyperadrenocorticism,
response and indicate the intracellular or
hypothyroidism, dissenlinated intravascular
extracellular location of bacteria. Bacterial
coagulation, dirofilariasis) the incidence is
culture and sensitivity testing is required
considerable, and PTE is underdiagnosed.

and may include anaerobe and mycoplasma

Mortality rates of PTE in aninlals are
culture, especially in refractory cases. A
uncertain but probably significant. Survival
viral etiology generally results in an initial
depends on early diagnosis and early
body temperature of 104°-l06°F (40°-41 °C). appropriate therapy.

Leukopenia, often expected, may not be

Thromboemboli in the venous circulation
seen in many viral respiratory infections
become trapped in the pulmonary

( eg, canine infectious tracheobronchitis,
vasculature and, if occlusion is substantial,
feline calicivirus pneumonia, feline infecpulmonary and hemodynamic sequelae tious peritonitis pneun1onia). A history
result. Animals with preexisting cardiac or
of recent anesthesia or severe vomiting
respiratory compromise may be affected
indicates the possibility of aspiration
earlier or more severely. The acute
pneumonia. Acutely affected aninlals may
pulmonary consequences of PTE include
die within 24-48 hr of onset. Mycotic
ventilation-perfusion mismatch, hypoxpneun1onias are usually chronic in nature.

emia, hyperventilation, and bronchocon

Miliary nodules seen at necropsy may
striction. Hemodynamic consequences of
suggest protozoa! pneumonia.

PTE are related to the magnitude of the

1488

RESPIRATORY DISEASES OF SMALL ANIMALS
obstrnction and presence of coexisting

Treatment: Therapy should begin as
cardiopulmonary disease. Myocardial
soon as possible a.11d include suppo1t of
ischemia, a.rrhytlrn1ias, or right ventricular
respirato1y a.t1d cardiovascular systems,
failure may result. Decreased cardiac
prevention of thrombus development and
output may ensue with severe obstrnction
recurrence, a.11d possibly thrombolysis.

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to pulmonary arterial blood flow as a result

Oxygen supplementation a.t1d bronchodilaof decreased venous cardiac return.

tors are indicated when dyspnea is evident

In dogs, PTE is associated with proteinor when a.iterial oxygen saturation is <92%.

losing neph.ropathy, hea.itwonn disease,

Although a.11ticoagula.11ts such as warfarin or
endoca.i·ditis, cardiomyopathy, necrotizing
unfractionated or low-molecular-weight
pancreatitis, hypercortisolism, immunehepa.i·in do not lyse existing thrombi, their mediated hemolytic anemia, sepsis,
use is indicated to inhibit thrombus
diabetes mellitus, neoplasia, atherosclerop.ropagation a.11d prevent recurrent venous sis, trauma, and major surgical procedures.

thrombosis. Antiplatelet drngs such as

Cardiomyopathy a.t1d neoplasia are most
aspirin or clopidogrel ca.11 be given together
commonly associated with PTE in cats.

with, but not in lieu of, a.11ticoagula.11t
therapy. Sildenafil may benefit a.t1imals with

Clinical Findings: Clinical signs are
docw11ented pulmonary hypertension.

nonspecific a.t1d most often subclinical or

Thrombolytic therapy ca.11 rapidly cause clot
may be mild to profound, reflecting the
lysis a.t1d in1prove ca.i·diovascula.i· function
severity of cardiorespi.ratory compromise.

a.11d hemodyna.111ic stability, thereby

Dyspnea, tachypnea, a.11d depression are
reducing mo1tality in a.iumals with massive
commonly seen. Coughing, cyanosis,

PTE a.11d shock. Veterinary expe1ience with
hemoptysis, collapse, shock, a.11d sudden
thrombolytic agents such as strep to kinase
death ca.11 occur.

a.t1d tissue plasminogen activator is limited.

RHINITIS AND SINUSITIS

Diagnosis: Diagnosis is often difficult
because PTE ca.11 resemble many other

Inflammation of the mucous membra.11es
conditions, including pneumonia, pulmoof the nose a.t1d sinuses may be acute or nary edema or hemorrhage, neoplasia, or
chronic.

pleural effusion. Routine diagnostic tests
such as thoracic radiography or arterial

Etiology: Viral infection is the most
blood gas a.11alysis are nonspecific a.11d
common cause of acute rhinitis or
ra.i·ely confirm diagnosis. Arterial blood gas
sinusitis in dogs and cats. Feline viral
a.11alysis will identify hypoxemia present in
rhinotracheitis (FVR), feline calicivirus

800;6 of dogs, although response to oxygen is

(FCV), canine distemper, canine
variable. Thoracic radiographs ca.11 be
adenovirus types 1 and 2, and canine
normal in 9%-27% of dogs a.t1d in 9% of cats
para.influenza are most frequently
with PTE. Abnonnal radiographic findings
incriminated. Ch.ronic states exist for FVR
with PTE include alveola.i· or inLersLiLial
and FCV, with intermittent shedding
pulmona.iy infiltrates or regional ll.ypovasassociated with stress. Bacterial rhinitis cula.i· lung a.i·eas. However, thoracic
or sinusitis frequently is a secondary
radiographs that underestimate the degree
complication. Primary bacterial rhinitis is
of clinical respiratmy compromise should
extremely rare in dogs. It may result from
raise suspicion of PTE. Blood gas a.11alysis
infection with Bordelella bro·nchiseptica
may reveal hypoxemia and hypocapnia,
in dogs. Bacterial rhinitis appears to be a
indicating inefficient gas excha.11ge, but the
common complicating factor in cats with
presence of normal blood gas values does
chronic rhinosinusitis, although exposure
not exclude PTE. Echocardiography ca.11 aid to envi.ronmental aeroallergens may also in assessment, demonstrating cha.11ges
play a role. Allergic rhinitis or sinusitis is
suggestive of PTE a.11d pulmonary hypertena poorly defined atopy that may occur sion ( dilation of the right ventricle,
seasonally, possibly in association with
pulmonary artery, inferior vena cava; right
pollen production, or perennially,
ventricula.i· hypokinesis; tricuspid
probably in association with house dusts
regurgitation; abnormal septal wall motion). and molds. Smoke aspiration, inhalation A normal echoca.i·diogra.in does not exclude
of irritant gases and dusts, or foreign
diagnosis of PTE. Spiral CT a.11giography or
bodies lodged in the nasal passages also
selective pulmonary a.11giography remain
may cause acute rhinitis.

gold standards for diagnosis of PTE in

Ch.ronic rhinitis is commonly complipeople, but these adva.11ced imaging studies cated by secondary bacterial colo11ization
are available at few veterinary institutions.

or infection because the prin1ary nasal

RESPIRATORY DISEASES OF SMALL ANIMALS

1489
disease results in increased mucus
deep nasal tissue culture, and elin1ination
production and altered mucociliary
of other causes of nasal discharge and
clearance of debris within the nose.

sneezing. Advanced imaging studies and

Underlying causes of chronic rhinitis
biopsy may identify a specific etiologic
include idiopathic chronic inflammatory
diagnosis for nasal discharge ( eg, fungal

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disease (lymphoplasmacytic rhinitis),
rhinitis, neoplasia, foreign body) in as few
trauma, parasites (Cuterebra), foreign
as 36% of cats and 63% of dogs with chronic
bodies, neoplasia, or mycotic infection. In
nasal disease.

cats, chronic rhinosinusitis is a frequent

Serun1 titer for cryptococcal antigen is a
sequela of acute viral infections of the nasal
very specific and sensitive test for nasal
and sinus mucosa that result in hyperplastic
cryptococcosis. Serologic evaluation for
glandular and epithelial changes. Rhinitis or
aspergillosis is more problematic in that
sinusitis may result when an apical tooth
negative test results do not exclude
root abscess extends into the maxillary
infection. Nasal tissue culture for Aspergil
recess. Mycotic rhinosinusitis may be
lus may also result in false-positive results; caused by Cryptococcus neof01mans,
as many as 300A, of normal dogs and 400A, of

Aspergillus spp, and Penicilliitm spp. Cats dogs with nasal neoplasia have positive
are more often affected with Cryptococcus
culture results. The combination of
spp than dogs, whereas aspergillosis is
seropositivity for and culture identificafrequent in dogs but rare in cats.

tion of Aspergillus is highly suggestive of infection, although negative test results

Clinical Findings: Acute rhinitis is
do not exclude nasal aspergillosis. Direct
characterized by nasal discharge, sneezing,
sampling of visualized suspected fungal
pawing at the face, respiratory stertor,
plaques may potentially yield Aspergillus
open-mouth breathing, and/or inspiratory
hyphae in all cases.

dyspnea. Lacrirnation and conjunctivitis
often accompany inflanunation of the upper

Treatment: In mild or acute cases,
respiratory passages. Affected tissues are
supportive treatment may be effective.

often hyperemic and edematous. The nasal

Severe cases of rhinosinusitis in kittens or
discharge is serous but becomes mucoid as
adult cats may require parenteral fluids to
a result of secondary bacterial infection. If
prevent dehydration, and nutritional
inflanunatory cells infiltrate the mucosa, the
support via a nasogastric tube to maintain
discharge may become mucopurulent.

weight. Chronic secondary bacterial

Sneezing, in an attempt to clear the upper
rhinosinusitis may be treated with
airways of discharge or exudate, is seen
antin1icrobial chemotherapy for 3-6 wk.

most frequently in acute rhinitis and tends

Intennittent use of vasoconstrictive nasal
to be intermittent in chronic rhinitis.

decongestants usually provides only

Aspiration reflex ("reverse sneeze"), a short temporary relief of congestion.

paroxysmal episode of inspiratory effort in

Mycotic rhinosinusitis requires antifungal
an attempt to clear the nasopharynx of
therapy based on identification of a fungal
obstructing material, may also be seen.

etiologic agent. Fluconazole (50-100 mg/day,

Respiratory stertor, open-mouth

PO) or itraconazole (50-100 mg/day, PO)

breathing, and inspirato1y dyspnea occur
may be effective for treatment of nasal
when the nasal passages are narrowed
cryptococcosis in cats. Oral antifungal
from inflamed mucosa, glandular elements,
agents have variable efficacy in treatment
and secretions. An acute unilateral nasal
of dogs with nasal aspergillosis, although
discharge, possibly accompanied by
voriconazole ( 4 mg/kg, PO, bid) alone or
pawing at the face, suggests a foreign body.

in combination with terbinafine (15 mg/kg,

Neoplastic or mycotic disease is suggested

PO, bid for 1 mo) may be effective. Topical
by a chronic nasal discharge that was initially intranasal infusions of enilconazole or unilateral but becomes bilateral or that
clotrimazole or combined clotri.rnazole
changes in character from mucopurulent to
solution and crean1 depot therapy instilled
serosanguineous or hemorrhagic. Approxivia the frontal sinuses have success rates as mately 35% of cats with nasal cryptococcohigh as 5()0A, for the first treatment and 9()0A, sis have facial defonnity ( dorsal lump) of
with two treatments, although reinfection
the rostral aspect of the nose. Head shyness
or relapse may occur.

or facial pain is more commonly associated

Anin1als that do not respond to medical
with fungal rhinitis in dogs.

therapy may require surgery consisting of
sinusotomy or rhinotomy, lavage, and

Diagnosis: Diagnosis is based on history,
biopsy to reestablish definitive diagnosis.

physical examination, radiographic findings

Radiation therapy is the most viable

( especially CT), rhinoscopy, nasal biopsy,
treatment for intranasal neoplasia.

1490

RESPIRATORY DISEASES OF SMALL ANIMALS

TONSILLITIS
in refractory cases, culture and sensitivity
testing may be needed. Mild analgesics are

Etiology: Tonsillitis is common in dogs
appropriate for severe pharyngeal iITitation,
but rare in cats. In dogs, it seldom occurs
and a soft, palatable diet is reco1mnended
as a primary disease, but when present it
for a few days until the dyspha.gia. resolves.

is most frequently seen in small breeds.

Parenteral administration of fluids is

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It usually is secondary to nasal, oral, or
required for those animals unable to take
pharyngeal disorders ( eg, cleft palate);
food by mouth.

chronic vomiting or regurgitation ( eg, from

Tonsillectomy is rarely required for
megaesophagus ); or chronic coughing ( eg,
chronic prin1ary tonsillitis but provides
with bronchitis). Chronic tonsillitis may be
permanent relief. Other indications for
seen in brachycephalic dogs in association
tonsillectomy include tonsillar neoplasia
witl1 pharyngitis accompanying soft palate
and tonsilla.r enlargement that interferes
elongation and redundant pharyngeal
with airflow ( eg, in bra.chycephalic breeds).

mucosa. Chronic tonsillitis in young dogs
is thought to represent maturation of
pharyngeal defense mechanisms.

TRACHEOBRONCHITIS

Escherichia coli, Staphylococcus

Tracheobronchitis is an a.cute or chronic
aureus, and hemolytic streptococci a.re the inflan1mation of the trachea and bronchial
pathogenic bacteria. most often cultured
airways; it may be primary or secondary
from diseased tonsils. Plant fibers or other
depending on the etiologic agent. Bronchitis
foreign bodies that lodge in the tonsilla.r
may extend from the bronchioles to the lung
fossa. may produce a localized unilateral
parenchyn1a..

inflan1mation or a peritonsilla.r abscess.

Other physical and chemical agents may

Etiology: Canine infectious tra.cheobroncause irritation of the oropha.rynx and one chitis (kennel cough, see p 1491) is often
or both tonsils. Tonsillitis may also
secondary to viral infection of the respiraaccompany neoplastic tonsilla.r masses tory system. Other causes of tra.cheobronbecause of physical trauma or secondary chitis in dogs include parasites, eg,
bacterial infection.

Aelurostrongylus abslrusus (also in cats),

Capillaria aerophila, Crenosoma vulpis,

Clinical Findings and Diagnosis:

and Oslerus osleri.

Tonsillitis is not always accompanied by

Tra.cheitis may be secondary either to
obvious clinical signs. Fever and malaise
diseases of the oropharynx or to chronic
a.re uncommon unless consequent to
coughing related to heart disease or
systemic infection. Gagging, followed by
noncardia.c pulmonary disease. Other
retching or a short, soft cough, may result
causes include smoke aspiration and
in expulsion of small a.mounts of mucus.

exposure to noxious chemical fumes.

Inappetence, listlessness, salivation, and

Exacerbation of a chronic bronchitis
dyspha.gia. a.re seen in severe tonsillitis.

affecting middle-aged and older dogs may

Tonsillar enlargement may range from
follow sudden changes in the weather or
protrusion just out of the crypts to a mass
other environmental stresses. Feline
of sufficient size to ca.use dysphagia or
bronchial asthma (allergic bronchitis) is
inspiratory stridor. A septic, suppurative
a syndrome in ca.ts with similarities to
exudate may surround the tonsil, which
asthma in people. Young cats and Siamese
may be reddened with small necrotic foci
and Himalayan breeds a.re inost affected.

or plaques. Tonsillitis usually is a sign of

Feline asthma is associated with airway
generalized or regional inflammatory
hyperresponsiveness, airflow obstrucdisease; therefore, primary tonsillitis tion, airway remodeling, and eosinophilic
should be diagnosed only after underlying
airway inflammation. Asthma in cats is
diseases have been excluded. Squamous
induced by an aberrant immune response
cell carcinoma, malignant melanoma, and
with upregulation of cytokines, lea.ding to
lymphosarcoma. a.re conunon in canine

IgE production. Foreign bodies in the
tonsils and should be distinguished from
airway and developmental abnormalities
tonsillitis. Tonsillar lyn1phosa.rcoma
such as laryngeal deformities may
generally results in bilateral symmet1ic
predispose to bronchitis. Chronic
enlargement, whereas nonlyrnphoid
bronchitis most often affects small
neoplasia is usually unilateral.

breeds of dogs, although it is also seen
in large breeds. It is characterized by

Treatment: Prompt systemic administrapersistent cough for at least 2 mo in the tion of antibiotics is indicated for bacterial
absence of specific pulmonary disease.

tonsillitis. Penicillins are often effective, but

Bronchiectasis may occur as the end

RESPIRATORY DISEASES OF SMALL ANIMALS

1491
stage of chronic bronchitis in dogs.

inflarrunation in dogs with chronic

Recognition of tracheobronchitis as
bronchitis. Persistent, nonproductive
an often secondary disease syndrome
coughing is best controlled by antitussives
underlies the importance of diagnosis
that contain codeine. If conservative
and control of an associated primary
medical management is unsuccessful,
disease.

laboratory tests and radiographs of the

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thorax and cervical trachea should be

Clinical Findings: Spasms of coughing
evaluated to eliminate other differential
are the outstanding sign. These are most
diagnoses. Bronchoalveolar lavage or
severe after rest or a change of environtranstracheal wash for cytology and culture ment or at the beginning of exercise. On
sensitivity may be indicated to identify an
auscultation, respiratory sounds may be
etiologic agent and to determine appropriessentially normal. In advanced cases, ate antimicrobial chemotherapy. Puln1onary
inspiratory crackles and expiratory
physiotherapy consisting of sodium
wheezes are heard. Body temperature may
chloride nebulization and gentle coupage
be slightly increased. The acute stage of
may loosen secretions and stimulate
bronchitis passes in 2-3 days; the cough,
expectoration. A bathroom environment
however, may persist for 2-3 wk. Severe
with stean1 from a hot shower may be
bronchitis and pneun1onia are difficult to
substituted for nebulization.

differentiate; the fom1er often extends into

Oral (prednisolone, dexamethasone) or
the lung parenchyma and results in pneumoinhaled (fluticasone, budesonide) corticonia. Feline bronchial asthma may result in steroids are indicated for treatment of
cyanosis and dyspnea and may be
feline asthma. Bronchodilators (albuterol,
accompanied by eosinophilia.

terbutaline) may be considered for
adjunctive therapy in combination with

Lesions: During the acute and subacute
glucocorticoids but not as sole therapy for
inflammatory stages, the air passages are
feline asthma. Feline aerosol chambers
filled with frothy, serous, or mucopurulent
and inhaler therapy are available for
exudate. In chronic bronchitis, they contain
aerosol drug delivery in cats with feline
excessive viscid mucus. The epithelial
asthma. Cyprohepatidine, an antiserotonlinings are roughened and opaque, a result of diffuse fibrosis, edema, and mononuclear
ergic drug, has been suggested; however,
studies have failed to show significant
cell infiltration. There is hypertrophy and
reduction in eosinophilic airway inflamm a hyperplasia of the tracheobronchial mucous tion. Experimental studies suggest that glands and goblet cells. The act of coughing
cyclosporine A therapy may hold promise
is an attempt to remove the accumulations
to inhibit development of eosinophilic
of mucus and exudate from the respiratory
airway inflammation and airway remodpassages.

eling through inhibition ofT-cell activation
and cytokine synthesis. Avoidance of

Diagnosis: The diagnosis is made
environmental aeroallergens (eg, cigarette
from the history and clinical signs and by
smoke, perfumes, pollens, molds, dust)

elimination of other causes of coughing. In
must be considered in management of
chronic bronchitis, chest radiographs may
these cats.

show an increase in linear and peribronchial
markings. Bronchoscopy reveals inflamed

Infectious Tracheobronchitis of Dogs
epithelium and often mucopurulent mucus
in the bronchi. In addition, the procedure

(Kennel cough)

allows collection of biopsy and swab

Infectious tracheobronchitis results from
san1ples for in vitro assay. Bronchial
inflammation of the upper aiJways. It is a
washing is an additional diagnostic aid that
mild, self-limiting disease but may progress
may demonstrate causative agents or signifito fatal bronchopneumonia in puppies or to cant cellular responses ( eg, eosinophils ).

chronic bronchitis in debilitated adult or
aged dogs. The illness spreads rapidly

Treatment: In mild or acute cases,
among susceptible dogs housed in close
supportive therapy may be effective, but
confinement ( eg, veterinary hospitals or
treatment of concurrent disease is also
kennels).

indicated. Rest, wannth, and proper hygiene
are important. Broad-spectrum antimicro

Etiology: Canine parainfluenza virus,
bial chemotherapy is indicated for
canine adenovirus 2 (CAV-2), or canine
treatment of cough when infection is
distemper virus can be the primary or sole
docwnented. Corticosteroids are the
pathogen involved. Canine reoviruses
mainstay of therapy to reduce aiJway

(types 1, 2, and 3), canine herpesvirus,

1492

RESPIRATORY DISEASES OF SMALL ANIMALS
and canine adenovirus 1 (CAV-1) are of
and nursing care, as well as co1Tection of
questionable significance in this syndrome. predisposing environmental factors, hasten Bordetella bronchiseptica may act as a
recovery. Cough suppressants containing
primary pathogen, especially in dogs
codeine derivatives, such as hyclrocodone

<6 mo old; however, it and other bacte1ia

(0.25 mg/kg, PO, bid-qid) or butorphanol

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(usually gram-negative organisms such as

(0. 05-0.l mg/kg, PO or SC, bid-qid), should

Pseudomonas sp, Escherichia coli, and be used only as needed to control persistent

Klebsiella pneumoniae) may cause
nonproductive coughing. Antibiotics are
secondary infections after viral injury to
usually not needed except in severe chronic
the respiratory tract. Concurrent infeccases; cephalosporins, quinolones, tions with several of these agents are
chloramphenicol, and tetracycline are prefercommon. The role of Mycoplasma sp has able because tlley reach effective concentranot been clearly established. Stress and tions in tile traclleobronchial mucosa When
extremes of ventilation, temperature, and
needed, tile antibiotic should be selected by
humidity apparently increase susceptibilculture and sensitivity tests of specimens ity to, and severity of, the disease.

collected by transtracheal aspiration or
bronchoscopy. Antibiotics given PO or IM

Clinical Findings: The prominent clinical
may not significantly reduce the nUlllbers of
sign is paroxysms of harsh, dry coughing,

B lnvnchiseptica in the distal trachea or
which may be followed by retching and
major bronchi. Thus, in severely affected
gagging. The cough is easily induced by
dogs that are not responsive to parenteral
gentle palpation of the larynx or trachea.

antibiotics, kanan1ycin sulfate (250 mg) or

Affected dogs demonstrate few if any
gentamicin sulfate (50 mg) diluted in 3 mL of
additional clinical signs except for partial
saline may be administered by aerosolization
anorexia. Body temperature and WBC
bid for 3 clays. Aerosolization treatment
counts usually remain nom1al. Developshould be preceded by administration of ment of more severe signs, including fever,
bronchodilators. Endotracheal injection of
purulent nasal discharge, depression,
antibiotics ( eg, gentamicin) is a possible
anorexia, and a productive cough,
alternative to aerosolization. Corticosteroids
especially in puppies, indicates a complimay help alleviate clinical signs but should cating systemic infection such as distemper be used concmTently with an antibacterial or bronchopneumonia. Stress, particularly
agent; they are contraindicated in severely ill,
due to adverse environmental conditions
coughing dogs.

and improper nutrition, may contribute to
a relapse during convalescence.

Prevention: Dogs should be inllllmlized
with modified-live virus vaccines against

Diagnosis: Tracheobronchitis should be
distemper, parainfluenza, and CAV-2, which
suspected whenever ilie characteristic
also provides protection against CAV-1.

cough suddenly develops 5-10 days after

Commercial products frequently combine
exposure to other susceptible or affected
these agents and may include modified-live
dogs. Severity usually diminishes dming tile
parvovirus and leptospiral antigens. An initial
first 5 days, but tile disease persists for
vaccination should be given at 6-8 wk and

10-20 days. Tracheal tramna secondary
repeated twice at 3- to 4-wk intervals until
to intubation may produce a sinlilar but
the dog is 14-16 wk old. Revaccination
generally less severe syndrome. Thoracic
should be performed annually. When the risk

.

radiographs are essential to detennine the
ofB bronchiseptica infection is significant, severity of disease and to exclude oilier
a live, avirulent, intranasal vaccine or
causes of cough.

parenteral products containing subunit
bacterial extracts should be used. A

Treatment: Preferably, affected dogs
combination of an avirulent B bronchisep
should not be hospitalized because tile
tica and a modified-live parainfluenza
disease is usually highly contagious ( and also vaccine is available for intranasal use. One self-limiting). Appropriate management
inoculation is administered to puppies
practices, including good nutrition, hygiene,

>3 wk olcl.

URINARY SYSTEM

VetBooks.ir

INTRODUCTION 1494

Principles of Therapy 1496

CONGENITAL AND INHERITED ANOMALIES 1496

Renal Anomalies 1496

UreteralAnomalies 1498

Bladder Anomalies 1498

Urethral Anomalies 1498

LARGE ANIMALS

INFECTIOUS DISEASES 1499

Bovine Cystitis and Pyelonephritis 1499

Porcine Cystitis-Pyelonephritis Complex 1500

Swine Kidney Worm Infection 1502

NONINFECTIOUS DISEASES 1502

Urolithiasis 1502

Ruminants 1502

Horses 1505

Uroperitoneum in Foals 1506

Renal Tubular Acidosis in Horses 1507

Urethral Defects Causing Hematuria in Adult Male Horses 1507

SMALL ANIMALS

INFECTIOUS DISEASES 1508

Bacterial Cystitis 1508

Pyelonephritis 1510

Interstitial Nephritis, Glomerulonephritis, and Vasculitis 1511

Capillaria plica Infection 1511

Giant Kidney Worm Infection in Mink and Dogs 1511

NONINFECTIOUS DISEASES 1512

Renal Dysfunction 1512

Chronic Kidney Disease 1512

Acute Kidney Injury 1516

Glomerular Disease 1517

Renal Tubular Defects 1520

Renal Acidosis 1520

Fanconi Syndrome 1520

Renal Glucosuria 1521

Obstructive Uropathy 1521

Neoplasia 1522

Neoplasms of the Kidney 1522

Neoplasms of the Lower Urinary Tract 1523

1494

URINARY SYSTEM

Disorders of Micturition 1524

Urolithiasis 1525

Canine Urolithiasis 1527

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Feline Lower Urinary Tract Disease 1531

URINARY SYSTEM INTRODUCTION

Primary ftmctions of the W"inary system

Urinalysis: One of the most inlportant
include: 1) excretion of waste products of
diagnostic tests for evaluation of urinary
metabolism; 2) maintenance of a constant
tract disorders is a uiinalysis. (See also
extracellular environment through
p 1615.) Urine may be collected by one of
conservation and excretion of water and
foUl' methods: spontaneous mictuiition,
electrolytes; 3) production of the hormone
manual compression of the uiinary bladder,
erythropoietin, which regulates hematocatheterization, and cystocentesis. Each poiesis, 4) production of the enzyme renin,
method has advantages and disadvantages
which regulates blood pressUl'e and soditm1

(see TABLE 1). A urinalysis should include
reabsorption; and 5) metabolism of vitan1in
method of collection, urine specific gravity,

D to its active fon11 (1,25-dihydroxycholecolor, tmbidity, pH, glucose, ketones, bilicalciferol).

rubin ictotest, occult blood, protein, and

Many abnormalities of the urinary system
leukocytes ( uiine dipstick leukocyte tests
can be diagnosed from the signalment,
are Ullfeliable in cats). Urine specific gravity
history and physical examination findings,
should be obtained using a refractometer.

serum chemistry profile, W"inalysis, and

Microscopic exan1ination of urine sediment
aerobic bacterial urine cultUl'e. The history
should include RBCs, WBCs, epithelial cells,
should include infon11ation regarding
renal casts, bacteria, yeast, parasitic ova, fat,
changes in water consumption, frequency
sperm, and crystals. Delay in analyzing urine
of urination, volume of urine produced,
samples can result in artifacts ( eg, changes in
appearance of urine, and behavior of the
urine pH, fo1mation of crystals, etc), so it is
animal. It is also important to obtain
inlportant to note the time when the sample
information about historical and cUl'rent
was collected and the time when it was
drug administration, appetite, diet, changes
analyzed. If a sample will not be analyzed
in body weight, and previous illnesses or
il.m11ediately, it should be refrigerated.

il\iuries.

Protein in urine should be evaluated in

The physical examination should include
light of the specific gravity. Protein in a
palpation of the bladder and examination of
concentrated urine sample may not be
external genitalia. In dogs, rectal exan1inasignificant, whereas the same amount in tion should be performed to evaluate the
a dilute sample may be significant. Urine

Ul'ethra in both sexes and the prostate in
dipsticks provide a semiquantitative
male dogs. Rectal exanlination in cats may
assessment of protein and can be influenced
not be feasible because of their small size;
by Ul'ine pH. Therefore, they should be used
however, the kidneys are generally easier to
only as a screening test for protein, not as a
palpate in cats than in dogs. A full neurodefinitive diagnosis of proteinuria. A urine logic examination should be performed
protein:creatinine ratio from a single urine
on all animals with mictUl'ition disorders.

sample or from a 24-hr urine sample is

Additional diagnostic tests, such as CBC,
required to quantitate the amount of protein
blood gas analysis for acid-base status,
in urine. In dogs, the following International
blood pressUl'e, urine protein:creatinine

Renal Interest Society (IRIS) guidelines
ratio, iohexol clearance test, survey abdomishould be used for interpretation of urine nal radiography, abdominal ultrasonograprotein:creatinine ratios. In dogs, <0.2 =
phy, contrast studies of the upper and lower
nonprotemuric, 0.2--0.5 = borderline
urinary tract, cystoscopic examination of
protemuric, and >0.5 = proteinW"ic; m cats,
the urinary bladder, and renal biopsy may

<0.2 = nonprotemuric, 0.2--0.4 = borderline
also provide valuable information.

proteinuric, and >0.4 = protemuric. Urine

URINARY SYSTEM INTRODUCTION

1495

ADVANTAGES AND DISADVANTAGES OF URINE COLLECTION

METHODS

Method of Collection

Advantages

Disadvantages

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Spontaneous micturition No risk (eg, trauma,

May contain debris (eg, bacteria,
bacterial infection) to
exudate) from lower urinary and
animal. Avoids
genital tract. If bacterial growth
iatrogenic hematuria.

appears on urine culture, must
differentiate between urethral
contamination and urinary tract
infection. Quantitative urine
culture required.

Manual compression of Provides method to

May induce trauma to urinary
urinary bladder
obtain urine sample
tract, resulting in hematuria. May
when voluntary
be stressful for animal, especially
micturition has not
if bladder is painful. If bacterial
occurred.

growth appears on mine culture,
must differentiate between
urethral contamination and
urinary tract infection. Quantitative urine culture required.

Catheterization

Provides method to

Potential for trauma to urinary
obtain urine sample
tract, especially urethra. More
when other methods of
invasive than other methods;
collection have failed.

sedation may be required. Risk
of introducing bladder infection.

If bacterial growth appears on
urine culture, must differentiate
between urethral contamination
and urinary tract infection.

Quantitative urine culture
required. Least desirable method
of urine collection.

Cystocentesis

Preferred method of

Potential risk of trauma if
collection for urine
perfom1ed incorrectly or anin1al
culture. Avoids
moves during procedure.

contamination of sample Potential for iatrogenic hematufrom lower urinary tract. ria More invasive than spontaneous micturition. Potential for bacterial contamination of
sample if needle penetrates colon
during procedure.

protein:creatinine ratios must be inter25%-30% of all dogs with UTI have urine preted in the context of other information
bacterial counts below these figures at
from the urinalysis. Inflammation and
tile tin1e of specimen collection, so urine
hematuria can falsely increase urine
culture is in1portant to exclude a UTL
protein:creatinine ratios, although

Urine samples for bacterial culture may
hematuria generally has mininlal effects.

be obtained by the same methods used to
obtain samples for urinalysis; however, the

Bacterial Culture of Urine: A urinalypreferred method is cystocentesis. Urine sis is Ullfe!iable to exclude a urinary tract
obtained by cystocentesis should be sterile.

infection (UTI). Not all UTis are associated

If urine samples are collected by methods
with an inflammatory response. In addition,
other than cystocentesis, a quantitative urine

> 10,000 bacterial rods/mL and > 100,000
culture should be requested. If the sample is
bacterial cocci/mL of urine are required to
collected by spontaneous micturition or
consistently find bacteria in a urine sample
manual compression, significant numbers
using light microscopy. Approxinlately
of bacteria are present if� 100,000 colony

1496

URINARY SYSTEM INTRODUCTION
forming units (CFU)/mL of urine in dogs or
clearance test is a recently developed

�10,000 CFU/mL of wine in cats are detected.

alternative to detect renal dysfunction. It

Samples with> 10,000-90,000 CFU/mL in
entails recording an accw-ate body weight,
dogs and > 1,000-10,000 CFU/mL in cats
administering a precise amount of iohexol IV,
are suspicious for a UTI. If the sample is
and accurately timing the collection of blood

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collected by catheterization, �10,000
samples as directed after administration.

CFU/mL in dogs and �1,000 CFU/mL in cats

This test does not require timed collection of
is significant, whereas samples containing
urine samples or special equipment. Plasma

1,000-10,000 CFU/mL in dogs and 100-1,000
clearance of exogenous creatinine has also

CFU/mL in cats are suspicious for a UTI.

recently been validated for use in dogs.

Depending on the cause of the urinary

Serum Chemistry Profile: Evaluation
tract disorder, radiographic procedures,
of serwn chemistries, including BUN,
sonographic examination, and cystoscopic
creatinine, calciw11, phosphorus, bicarbonexamination of the bladder may provide ate, and serwn electrolytes, is useful in
additional valuable infom1ation. The kidmany winary tract disorders and can neys have a limited range of responses to
provide a crude indication of glomerular
disease; therefore, renal biopsies are rarely
filtration rate (GFR). Although increases in
useful when evaluating renal dysfunction.

BUN and creatinine are supportive of renal

An exception to this is in aninlals with
dysfunction, these tests are influenced
significant proteinuria.

by nonrenal factors as well. For example,

Blood gas analysis or serwn bicarbondehydration can cause increases in BUN and ate levels provide useful information on serun1 creatinine not associated with renal
acid-base status, especially in aninlals with
failw-e. BUN can also be influenced by diet
renal dysfunction. Metabolic acidosis is a
and GI bleeding and is considered inferior
common problem in chronic renal failure
to creatinine to evaluate GFR. Serun1
and can result in protein catabolism.

creatinine levels can be falsely decreased in
animals with severe muscle wasting and
falsely increased in aninlals with severe

PRINCIPLES OF THERAPY
muscle damage. Although BUN and serum
creatinine increase as GFR decreases, this

Diseases of the urinary system can result
relationship is not linear. Large changes in
from a variety of pathologic processes, and

GFR early in renal disease cause only small
appropriate therapy (as discussed in the
increases in BUN and serwn creatinine,
following chapters) depends on the
whereas small changes in GFR in advanced
location, severity, and cause of the problem.

renal disease may be associated with large

See also SYSTEMJC PHARMACOTHERAPElJTICS OF
changes in BUN and serwn creatinine.

THE URINARY SYSTEM, p 2617. If the condition is
not life threatening, appropriate diagnostic

Additional Diagnostic Tests: More
samples should be collected before
sensitive methods to detect renal dysfuncinitiating therapy. It is inlportant to tion include plasma clearance tests ( eg,
remember that some diagnostic tests and
inulin clearance), radionuclide techniques,
treatments have the potential to cause
endogenous creatinine clearance, and
significant harm. If the specific cause
exogenous creatinine clearance. However,
cannot be detennined, nonspecific and
these tests are impractical to perfonn
supportive therapy ( eg, monitoring fluids,
routinely in clinical practice. The iohexol
treating acidosis) should be instituted.

CONGENITAL AND INHERITED ANOMALIES

OF THE URINARY SYSTEM

Congenital and inherited anomalies of

RENAL ANOMALIES
the urinary system comprise a group of
anatomic defects that, although uncommon,

Renal Dysplasia and Hypoplasia:

may have subclinical to serious functional

These defects are most common in dogs
consequences.

and have been reported in many breeds,

CONGENITAL AND INHERITED ANOMALIES OF THE URINARY SYSTEM

1497
including Alaskan Malamutes, Bedlington
are an autosomal dominant inherited trait in

Terriers, Chow Chows, Cocker Spaniels,

Persian cats and domestic long-haired cats.

Doberman Pinschers, Keeshonden, Lhasa

Polycystic kidneys are also hereditary in

Apsos, Miniature Schnauzers, Norwegian
pigs and may alternatively be associated

Elkhounds, San1oyeds, Shih Tzus, Softwith avitaminosis A. Polycystic kidneys are VetBooks.ir
coated Wheaten Terriers, and Standard
rare in cattle and horses and very rare in

Poodles. Renal dysplasia is rare in cats,
sheep. Diagnosis is based on physical and
lambs, and horses. In pigs, renal dysplasia
radiographic findings, ultrasonic examinamay be idiopathic or associated with tion, or exploratory laparotomy. Pyelonenut1itional avitanli.nosis A.

phritis may be seen concurrently and

Renal dysplasia may be unilateral or
precipitate renal insufficiency.

bilateral. Animals affected bilaterally
generally die in the early neonatal pe1iod,
whereas animals affected unilaterally

Simple Renal Cysts: These solitary,
typically develop hypertrophy of the
unilocular cysts generally do not communicontralateral kidney. The kidneys are cate with the renal collecting system; the
usually small, firm, and pale; they may
rest of the kidney is nom1al. The origin of
have a unifonnly diminished renal cortex.

these cysts is unce1tain. They are usually an

Histologic examination reveals in1mature
incidental fmding in all domestic species.

glomeruli, primitive tubules, and secondary
in.flanl.11latory lesions, especially interstitial

Perirenal Pseudocysts: Perirenal
fibrous connective tissue.

pseudocysts are accumulations of fluid that

Polydipsia and polywia usually precede
develop external to the renal parenchyma.

signs of uremia. Dwarfing may be noticed

They have been identified in cats. Their
if the onset of renal failure occurs within

01igin is tmknown. The accumulated fluid
the first few months of life. Urinalysis,
may be located between the renal
hemogram, and blood chemistry changes
parenchyrna and the renal capsule or
are the same as in other chronic, progressive between the renal capsule and a thin-walled renal diseases. Uremia is usually identified
fibrous sac attached to the capsule. They
between 6 mo and 2 yr of age. The diagnosis
are termed pseudocysts rather than cysts
is suspected based on the breed and age of
because they are not lined by epithelitm1.

disease onset and is co1lfinned by renal

Because only a limited number have been
biopsy. 'Ireatment is aimed at managing
examined histologically, it is unknown
the associated chronic renal failure.

whether all perirenal fluid-filled strnctures

Renal Agenesis:

are pseudocysts. The fluid contained within

Renal agenesis, the
these stmctures is not urine or lymph but is
complete absence of one or both kidneys, is
described as a transudate. Clinical signs we
always accompanied by ureteral aplasia and
characterized by progressive abdominal
may be associated with aplastic reproductive enlargement. Abdominal palpation reveals tissues on the same side. The condition is
a large, firm, non painful mass located in the
typically an incidental finding so long as the
area of the kidneys. Renal function tests
other kidney functions nom1ally; frequently,
and urinalysis are typically normal;
the contralateral kidney undergoes
however, a mild azotemia may occur.

compensatory hypertrophy. Renal agenesis

Diagnosis is made by excretory urography
is believed to have fanlilial predisposition in
or ultrasonography. 'Ireatment involves

Beagles, Shetland Sheepdogs, and Doberexploratory surgery to confim1 the man Pinschers. Unilateral renal agenesis
diagnosis, drainage of the pseudocyst fluid,
is the most common congenital kidney
and resection of as much of the pseudocyst
condition in pigs; it is less conm1on in sheep,
wall as possible. The prognosis appears to
cattle, and goats. Bilateral agenesis results in
be good; however, only a limited nwnber of
early pe1i.na.tal death.

cases have been evaluated.

Polycystic Kidneys: Multiple cysts fonn
within the renal parenchyma, and such

Miscellaneous Renal Anomalies: Doukidneys are usually grossly enlarged on ble or multiple renal arteries are seen in -5%
palpation. This condition may be associated
of dogs. Other congenital defects include
with hepatic biliary cysts in both dogs and
renal malpositioning, renal fusion, and
cats. Polycystic kidneys may cause no
nephroblastoma. N ephroblastoma is an
clinical signs or lead to progressive renal
embryonal twnor and is rare in domestic
failure. This condition is familial in Beagles,
aninlals except pigs. It may cause no

Bull Terriers, Cairn Terriers, and West
problems but may be very large and cause

Highland White Teniers. Polycystic kidneys
abdominal distention.

1498

CONGENITAL AND INHERITED ANOMALIES OF THE URINARY SYSTEM

UR TERAL ANOMALIES

Incontinence occurs most often in cases of
bilateral ectopic ureters and may be due to

Ectopic Ureter: This defect is most
abnormal development of the bladder neck
commonly repo1ted in 3- to 6-mo-old dogs,
and uretllfa. An adrenergic agent such as
with female dogs affected 8 times more
phenylpropanolamine (0.5-1.5 mg/kg, PO,
frequently than male dogs. In dogs, ectopic

VetBooks.ir
bid-tid) may help minimize tl1e incontinence.

ureter has a repo1ted incidence of0.016%-

0.045%. In horses, ectopic ureter is the most

Miscellaneous Ureteral Anomalies:

common congenital anomaly affecting the

Less frequently recognized ureteral

Uiinary tract; as in dogs, it is significantly
anomalies include aplasia, duplication, and
more conunon in fillies than in colts. Ectopic ureterocele. Ureteroceles are characterized ureters are infrequently identified as a
by dilation of ilie submucosal ureter segclinical problem in cattle, sheep, or pigs.

ment within the bladder. Diagnosis is by

Other anomalies frequently associated with
excreto1y urography. Appropriate therapy is
ectopic ureter include hydroureter, hydroneureteronephrectomy if the lesion is lll1ilaphrosis, renal hypoplasia, bladder hypoteral with secondary hydronephrosis and plasia, and uretl1ral sphincter incompetence.

hydro ureter. If the proxin1al ureter and

Continual dripping of urine is the classic
kidney are nom1al, excision or incision of the
sign, although animals with unilateral
ureterocele, in addition to ligation of any
ectopic ureter may void normally; the
ectopic distal channel, has been successful.

inability to void normally suggests bilateral
ectopic UI"eters. A low-grade vaginitis or
vulvitis may also be present due to urine

BLADDER ANOMALIES
scalding. Involved UI·eters may open into tl1e

Urachal Remnants: Congenital
urethra, the uterus, or the vagina. Unilateral
anomalies resulting from incomplete
ectopic UI·eter is seen with equal frequency

UI·achal closure include patent urachus,
on right and left sides, and involvement is
urachal diverticulUin, U111bilical UI·achal
bilateral in -25% of cases. Ectopic ureters
sinus, and intra-abdominal urachal cyst.

generally result from disruption of

These conditions may be seen in any
development of the mesonephric and
domestic species but are most frequently a
metanephric duct systems. A genetic
clinical problem in cats, dogs, and horses.

component is suspected on the basis of

Clinical signs and appropriate therapy
identifying high-risk breeds (West Highland
depend on the type of anomaly. Patent

White Terriers, Fox Terriers, and Miniature
urachus is typically associated with continuand Toy Poodles) and a familial occurrence ous mi.nary incontinence, mine scalding of
in Siberian Huskies and Labrador Retrievthe ventral abdomen, and development of ers. Diagnosis is continued by IV UI·ography
bacterial mi.nary tract irtfections. Urachal
that traces the course of the ureter.

diverticula also predispose to urinary tract

Successful surgical treatments usually
irLfection by serving as a nidus for bacteria.

involve transplantation of affected ureters

Definitive diagnosis of boili disorders is by
into tl1e bladder, or ureteronephrectomy. A
positive contrast cystography. Treatment
recent review of surgically repaired ectopic
consists of surgical resection and 2-4 wk
ureters in female dogs indicated that factors
of appropriate antibiotic therapy when
including left- or right-sided ectopic ureter,
indicated. Surgical resection is the standard
unilateral or bilateral ectopic UI"eter,
treatment for U111bilical urachal sinuses and
presence of hydroureter, or presence of
intra-abdominal machal cysts.

tuinary tract infections were not significant
to influencing postoperative incontinence.

Miscellaneous Bladder Anomalies:

Another study showed that female dogs witl1 Bladder duplication, dysplasia, hypoplasia, ectopic ureters treated by cystoscopicagenesis, and exstrophy (congenital guided laser ablation had a 4 7% postoperaeversion) have been reported and are often tive success rate based on their maintaining
associated with other urinary tract defects.

urinary continence. Adclitional medical

Diagnosis is by physical examination,
management further improved the urinary
observation of micturition, and contrast
continence rate to 77%. Indications for
radiography. Clinical signs and therapy
ureteronephrectomy may include severe
depend on the type of anomaly.

ipsilateral renal disease such as hypoplasia,
hydronephrosis, or pyelonephritis in the
presence of a normally functioning

URETHRAL ANOMALIES
contralateral kidney. ln1portant postopera

Congenital or hereditary methral anomalies
tive complications are persistent incontiare unconu11on in all domestic species; they nence, hydroneplu·osis, and dysUiia.

include metllfal agenesis, imperforate

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

1499
uretlll'a, hypospadias, epispadias in
of the urethral meatus, a modification of the
combination with bladder exstrophy,
prescrotal urethrostomy is generally useful.

urethral duplication, urethral diverticula,
urethrorectal fistula, and urethral stenosis.

Urethrorectal and Rectovaginal

Fistulas: These congenital anomalies

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Hypospadias: This developmental defect
predominantly affect dogs, cats, and horses.

results from failure of the urettu·aJ grooves

The anomalies are more common in males
to fuse during phallus elongation. The
than females; males are more likely to
urethral opening is ventral and caudal to
develop urettll'orectal fistulas, whereas in
the tip of the penis and is classified on the
females the rectovaginaJ fistulas predomibasis of anatomic localization as glandular, nate. In dogs, English Bulldogs seem to
penile, scrotal, perinea], or anal. The penis
have a breed predisposition, possibly as
or scrotum may be tmderdeveloped as well.

a congenital defect clue to abnormal

This uncommon anomaly is most frequently
separation of the embryonaJ cloaca into the
seen in male dogs; the highest prevalence is
urettll'a and rectum. Clinical signs include
seen in Boston Terriers, suggesting a genetic hematuria and dysuria secondary to tLrinary basis. The condition is also rarely seen in
tract infection. Simultaneous passage of
bulls. Clinical signs depend on the site of the urine from the anus and urettll'a drning urettll'aJ meatus and include urine scalding
micturition may be noted. Appropriate
and complications of increased susceptibiltherapy consists of smgicaJ correction and ity to urinary tract infection. Although
concurrent management of urinary tract
surgical correction also depends on the site
infection.

INFECTIOUS DISEASES OF THE

URINARY SYSTEM IN LARGE ANIMALS

BOVINE CYSTITIS AND

The most common causative bacteria

PVELONEPHRITIS
are ubiquitous in the envirorm1ent and are
common inhabitants of the vagina and

(Contagious bovine pyelonephritis)

prepuce. Pyelonephritis develops from

Bovine cystitis is an inflammation of the
an ascending infection from the bladder.

urinary bladder of cattle that may ascend the

Cystitis may be present without involving
ureters to cause infection of the kidneys
the ureters or ascending to the kidney until

(pyelonephritis ). A sinillar condition is seen
some event occurs that compromises tl1e
in sheep. The condition is sporadic and
defense mechanism of the ureteraJ mucosa.

worldwide in distribution. Cystitis and

The organisms attack or colonize the
pyelonephritis are most often seen after
mucosaJ lining of the bladder and ureters
parturition (in one study, the average days
usually after some traumatic insult (such as
to onset after parturition was 83), with
parturition or abnormal defonnity of the
multiparous cows being at highest 1isk. In
vaginal tract). The stresses of parturition,
locations where tl1e disease has been studied, peak lactation, and a high-protein diet the prevalence is low ( d o/<r-2"Ai). Cystitis and (which increases the pH of the urine and
pyelonephritis are rare in male cattle.

is therefore conducive to colonization of the
urinary tract by C01ynebacterium spp) are

Etiology and Pathogenesis: Fonnerly,
all contributing factors. Routine catheterizatl1e most common causative agents were tion offue bladder with nonsterile catheters
tl1e Corynebaclerium renale group
may facilitate transmission of Corynebacle
of bacteria, including C renale, C cysl'ilidis, rium spp from cow to cow. The decrease in and C pilosum, as well as Escherichia coli; the frequency of urinary cathete1ization has
however, E coli and Trueperella (formerly been associated with a decreased preva

Arcanobacte,ium or Corynebacteriiim)

lence of Corynebacte,ium spp as a cause
pyoge,ies are now fue bacteria most
of pyelonephritis.

frequently isolated from cows wifu
pyelonephritis. Other opportunistic and

Clinical Findings and Lesions: The
environmental bacteria may be involved,
first sign observed may be the passage of
including staphylococci and streptococci.

blood-stained urine in an otherwise heaJtl1y

1500

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS
cow. As the infection proceeds up the
pyelonephritis confined to one kidney may
ureters, causing inflanunation and
benefit from unilateral nephrectomy.

subsequent involvement of the kidney, the

Even though the organisms are ubiquianimal exhibits discomfort manifest by tous in the environment, affected animals

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frequent attempts to urinate, anorexia, a
should be isolated from the herd to restrict
slight fever, loss of production, colic with
buildup of organisms. Because of suspicion
restlessness, tail switching, polyuria,
that bulls may act as mechanical vectors of
hematuria, or pyuria. In chronic cases, the

Corynebacterium spp, artificial inseminaanimal may show colic, dianhea, polyuria, tion in herds with multiple animals affected
polydipsia, stranguria, and anemia. As the
may be considered.

disease progresses, the bladder becomes
thickened and inflamed. The ureters become PORCINE CYSTITIS
thickened and dilated with a purulent

PYELONEPHRITIS COMPLEX
exudate. The involved kidneys develop
multiple small abscesses on the surface that

Porcine cystitis-pyelonephritis complex, a
may extend into the c01tex and medulla.

leading cause of m01tality in sows, has been
reported throughout the world. Increased

Diagnosis: Diagnosis is based on clinical
incidence appears to be correlated with
signs; hematuria; a history of recent
changes in management, particularly tlle
parturition; palpation of the left kidney for
adoption of confinement housing for
enlargement, loss of lobulation, and pain;
gestating sows. Distinguishing features of
ultrasonographic inspection of the kidneys,
endemic cystitis and pyelonephritis witllin a
ureters, and bladder; endoscopic inspection
herd include lack of a temporal relationship
of the bladder for detection of cystitis;
between tlle vulvar discharge and the estrous
microscopic examination of the urine for
cycle, minimal effect on herd fertility, low

WBCs and bacteria; dipstick screening for
morbidity, high mo1tality, and an increased
proteinuria and hematuria; and quantitative
frequency in advanced-paiity (6+) sows.

urine culture to identify the organism. The
right kidney cannot be palpated per rectum,

Etiology and Pathogenesis: A wide
except for the caudal pole in Jersey cows
variety of bacteria has been isolated from
and heifers. In early acute cases of
cases of porcine cystitis and pyelonephritis,
pyelonephritis, enlarged ureters and
including Escherichia coli, Arcanobacte
involvement of the kidney may not be
iium pyogenes, and Stre'J)tococcus and detectable on palpation per rectum.

Staphylococcus spp. These endogenous and

Typically, only one kidney is affected.

opportunistic organisms typically inllabit
tlle lower urinary tract and ai·e often referred

Treatment: Early diagnosis and prompt,
to as being responsible for nonspecific
sustained treatment are needed for a
ruinary tract infections. Act'inobaculum
successful recovery. A catheterized urine
suis, a specific urinary pafuogen, is an
san1Ple should be taken for culture and
important cause of a5cending infection in
antimicrobial susceptibility testing. The
swine. Formerly classified in tlle genera
treatment of choice for pyelonephritis due

Eubacterium and Actinomyces, A suis is a to Corynebacteriiim spp is penicillin
gram-positive, rod-shaped bacterium that

(22,000 IU/kg, IM, bid) or t1imethoprimgrows well under anaerobic conditions and sulfadoxine (16 mg combined/kg, IM, bid)

is a commensal organism of tlle porcine
for <!3 wk The dosage, frequency, and length urogenital tract. A suis is fimbriated, of administration for both of these drugs is
and the short, wide urethra of the sow
extra-label, and adequate precautions must
enhances accessibility to tl1e bladder.

be taken to prevent antibiotic residues from

Once within the bladder lumen, the
entering t11e human food supply. E coli
alkalinity of the environment increases due
infections require a broad-spectrum
to the cleavage of urea into atnmonia via the
antimicrobial. Ceftiofur (l.1-2.2 mg/kg/day,
urease enzyme. The increased pH enhances

IM or SC) or gentamicin (2.2 mg/kg, IM, bid)

bacterial proliferation at1d in.flames the
for <!3 wk have been used successfully in
mucosa! surface. The alkaline environment
some cases. Because of the extremely long
also inllibits the growth of competitive
tissue-depletion time, the an1inoglycosides
microflora at1d promotes precipitation of
may not be indicated in food-producing
urinary salts at1d crystals, particularly
animals. Manipulation of urine pH may tl1eostruvite. Such precipitates not only further retically be of value because E coli grow
increase inflatnmatory changes in the
best in acidic urine (pH <7), whereas
bladder mucosa but also provide a nidus

Corynebacterium spp grow best in alkaline
for bacterial growth at1d protection from
urine (pH> 7). Nonazotemic animals with
at1tibiotics at1d host defense mechanisms.

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

1501

Although the primary means of accessibil

Diagnosis: Cystitis and pyelonephritis
ity to the kidneys is not yet completely
in live aninlals can best be presumptively
understood, it is hypothesized that dan1age
diagnosed when frequent micturition of
to the urete1ic valves secondary to bacterial bloodstained and cloudy urine can be products (possibly originating from E coli)

observed. Examination of the urine

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may predispose affected aninlals to
sedin1ents may reveal the presence of
pyelonephritis.

inflanunatory cells, RBCs, granular renal
casts, bacte1ia, and crystals. Because of the

Epidemiology: Problems frequently
st1iking gross lesions, confirmation of the
encountered in confinement facilities
diagnosis is usually not difficult. To properly
that hasten the development of porcine
isolate the causative organism, care must be
cystitis are the reduced availability of water,
taken during sample collection to minimize
increased fecal contanlination of the
exposure to oxygen. In tl1e field, the bladder
perinea.I area, excessive weight gain, and leg should remain unopened, and the neck of i.njwies, all of which result in a reduced
the bladder should be sealed with wnbilical
frequency of urination and enhanced
tape. Sinlilar care should be taken witl1 renal
bacterial survival in the urogenital tract. The
tissue. Lesions of pyelonephtitis can be demproblem may not be as prevalent in outdoor, onstrated by examination of one kidney;
loose housed sows; however, data are
the other should remain unopened with
lacking. A suis has been isolated from the the ureter sealed as previously described.

preputial cavity of boars at slaughter, the

Cultures should be grown on colistin
vaginal tract of neonatal piglets san1pled
nalidixic acid agar at 37 °C (98.6°F) under
immediately after parturition, and the
anaerobic conditions for &--7 days. If the
vaginal tract of sows sampled throughout all
culture is to be done at a distant location,
stages of production. It may also be isolated
swabs can be placed into Kary Blair
from voided urine, contaminated parturianaerobic transport media for shipment. A tion sleeves of farrowing attendants, pen

PCR test for A suis has been described and floors of farrowing and nursery rooms, and
appeared to have better sensitivity than
the boots of stockpersons working in the
direct culture. Data indicate detection of
breeding area. The organism is ubiquitous,

1-2 CFU/rnL of urine, and the pathogen can
and the vaginal tract can become colonized
be successfully detected in samples of sow
anytin1e during the life of the pig.

urine and boar preputial cavity.

Clinical Findings: Clinical signs vary

Treatment and Prevention: Treatment
according to the severity and phase of the
of urinary tract infections may be successful
disease. In acute and severe cases, affected
if the coJTect antibiotic is administered
pigs may be found dead, probably from
early in the disease course. Penicillin and
acute renal failure. Symptomatic animals are
ampicillin are often the drugs of choice
usually a.febrile and may show anorexia,
because of their effectiveness in alkaline
hematuria, and pyuria. The urine is typically
conditions and their propensity for
reddish brown with a strong odor of
excretion through the urinary tract.

anunonia Urinary pH may increase from

Dosages of2.2 mg/kg are typically
nom1al values of 5.&--7 .5 up to 8- 9. Animals
administered IM for 3 days. Water-soluble
that survive the initial infection frequently
ampicillin can be adnlinistered at 2.3 mg/kg
experience weight loss and reduced
for 5 days, although bioavailability is
productivity secondary to end-stage renal
questionable and cost may become an issue.

disease, resulting in premature removal from Acidification of the urine through oral the breeding herd. Inflan1matory reaction
adnlinistration of feed-grade cib.ic acid has
on the mucosa.I surface of the bladder may
been reported. Results showed a reduced
be cataJThal, hemoJThagic, pw1.tlent, or
incidence of clinical urinary tract disease,
necrotic, and the bladder wall may be
as well as highly significant (P <.0001)

thickened. Struvites can also be found in the
differences in urinary pH and bacterial
lwnen. The ureters, often filled with exudate, concentration/mL of urine in medicated may increase to as much as 2.5 cm in
versus nonmedicated groups. A level of 70
diameter. Unilateral or bilateral pyelonephrimg of cib.ic acid was adnlinistered daily for tis or pyelitis is the prin1ary lesion in the

14 days with no palatability problems.

kidneys. The pelvic region of the kidney,

Maintaining excellent hygiene during
frequently distended with blood, pus, and
breeding and parturition, as well as
foul-smelling urine, often shows i.JTegular
throughout the gestation period, is critical
ulceration and necrosis of the papillae.

to prevent urinary tract disease. Facilities

In longstanding cases of pyelonephritis,
must be properly designed to reduce the
fibrosis ultimately replaces inflan1mation.

spread of pathogens within the breeding

1502

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS
herd and to allow for efficient removal of
some larvae errantly migrate to other
feces from the envirorunent. Free-choice
tissues and organs or to developing fetuses.

water should be available at all times,

Infections usually become patent in 9-16
because restricting water availability
mo but may be found as early as 6 mo.

through use of intennittent delivery systems
or poor husbandry results in an increase in

Clinical Findings and Diagnosis: When

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abnormal urine parameters in gestating
present in large numbers, kidney worms
sows, including decreased urine output,
may adversely affect growth. The principal
increased specific gravity(> 1.026), and
economic loss results from condemnation
increased creatirune concentration. Finally,
of organs and tissues affected by migrating
because a higher degree of urinary tract
larvae. The most severe lesions are usually
disease can be seen in older sows, proper
in the liver, which shows cilThosis, sca.i·
culling procedures are impo1tant to ensure
fonnation, extensive tlu·ombosis of the portal
that an optin1al pa.iity distribution is
vessels, and a variable amount of necrosis.

maintained within breeding herds.

Kidney and lung damage are also possible.

When worms are in the kidney or in cysts

SWINE KIDNEY WORM
that open into the ureter, eggs may be

INFECTION
recovered in the urine. Prepatent infections
are difficult to diagnose, and a definitive

Etiology: Stephanurus dentatus are
diagnosis depends on demonstration of
stout-bodied wom1s (2-4.5 cm long) found
the worms or lesions at necropsy.

encysted in pairs along the ureters in the
perirenal fat and in the kidney. The kidney

Control: Good control practices are
wonn is found worldwide, particularly in
indicated in areas where the worm is found.

tropical and subtropical areas. It is primarily Because of the long prepatent period, control a parasite of swine raised outdoors in the
may be achieved with a "gilts only" breeding southeastern and south central USA. The
program, which prevents patent infection
eggs hatch shortly after being passed in
from developing. Older boars are replaced
the urine and reach the infective stage in
with young boars from clean herds, and only

3--5 days. The larvae are susceptible to
gilts are bred and then sold after weaning.

temperature extremes, desiccation, and

Eradication is possible within 2 yr. More
sunlight. Infection is by skin penetration
comn10nly, antl1elmintics and sarutation
or ingestion of the infective larvae ( earth

(rearing on concrete or in confinement) are
worms may serve as parateruc hosts). The
used to control kidney worm.

larvae enter the liver, where they migrate

Ivem1ectin (in-feed for 7 days at 1.8 g/ton),
extensively for 3-9 mo. Larvae then
fenbendazole (in-feed for 3--12 days at
penetrate the capsule and migrate through

9 mg/kg/day), or levamisole (in-feed at 0.36
the peritoneal cavity to the perirenal area,
g/ton) are effective againstStephanurus sp.

where they find their way into the ureters,

Doramectm (single irtjection at300 mcg/kg)

kidney, and perirenal fat. Occasionally,
is also approved for use against this worm.

NONINFECTIOUS DISEASES OF THE

URINARY SYSTEM IN LARGE ANIMALS

UROLITHIASIS
leads to bladder distention, abdominal pain,
and eventual urethral perforation or bladder

For a more general introduction to
ruptme, with death from uremia or
urolithiasis, see p 1525.

septicemia. It is an in1portant disease of
feeder a.Jli.t11als but is also seen in mature
breeding a.Jli.tnals. Urolithiasis is seen most

Urolithiasis in Ruminants
often during winter in steers and wethers on

Uroliths in cattle, sheep, and goats are
full feed, or on range during severe weather
conm1on. Although moliths can be found
conditions with limited water intake,
anywhere within the urinary tract,
especially when the water has a high
methroliths are responsible for most
mineral content. Obstructive uroliths are
clinical problems. Obstruction induced by
comn10n in male goats, regardless of feed,
urethroliths causes urine retention and
season, or other risk factors. Urolithiasis

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

1503
has no specific geographic distribution,

Common sequelae of complete urethral
and the different urolith types reflect the
obstruction include urethral perforation,
mineral distribution of the feed. U roliths
hydronephrosis, or urinary bladder rupture.

occur in either sex, but obstructive

Bladder rupture often results in death from
urolithiasis develops primarily in males
uremia. The disease course may be 5--7

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because of anatomic differences.

days. Although urethral perforation may
also cause uremia and death, it is not

Etiology and Pathogenesis: Rwninant
uncommon for the ventral abdominal skin
urolithiasis is considered primarily a nutrito necrose and slough, allowing a pseudotional disease. The prevalence of urourethra to develop.

lithiasis in the USA is highest in calves,
lambs, and kids castrated at an early age

Diagnosis: Diagnosis based on the history,
and fed high-grain diets with roughly a l: 1
clinical signs, ai1d physical examination is
calcium:phosphorus ratio or a diet high in
usually straightforwai·d. Hypersensitivity in
magnesium. Rwninants fed high-grain diets
the region of the sigmoid flexure may be
with a low calcium:phosphorus ratio are at
evident. Palpation may identify abnom1al
increased risk of developing struvite
pulsations of the urethra and tissue swelling
uroliths, whereas ruminants grazing on
associated with the obstruction. Rectal
silica-rich soil are predisposed to fom1 silica
palpation may reveal an enlai·ged, distended
uroliths. Diets high in calcium ( eg, subterrabladder, or the bladder may be nonpalpable, nean clover) may result in calcium carbonate consistent with bladder rupture. Exan1inauroliths, while plants such as halogeton or tion of the urethral process in sheep and
tops from the common sugar beet may be a
goats may reveal the occluding urolith. ln
factor in calcium oxalate fonnation. The
small ruminants, the distended bladder can
mineral composition of water, in concert
be felt by abdominal palpation and visualized
with dietary mineral in1balances, probably
on ultrasow1d examination. Calcium
contributes more to initiating urolith
carbonate and calciw11 oxalate calculi can be
formation than does the Jack of water itself.

seen on radio graphs of the urethra in small

A definitive diagnosis of urolithiasis in a
rwninants; struvite calculi are not seen
single animal suggests that all males in the
on radiographs. If early clinical signs of
population are at risk of the disease. Struvite
obstructive uropathy are missed, the animal
calculi have the apperance of sand, whereas
may show only inappetence, depression,
calcium carbonate calculi and calcium
subcutaneous swelling along the penis, or
oxalate are distinct, round stones.

uroperitoneum; abdominal distention due to

The distal aspect of the sigmoid flexure of
uroperitoneum must be differentiated from
cattle and the sigmoid flexure and urethral
rwninal tympany, peritonitis, peritoneal
process of sheep and goats are the most
twnors, uterine hydrops, and GI tract
common sites for uroliths to lodge.

obstructions. Ballottement allows detection

Irritation at the site of lodging causes
of the fluid, and when viewing the animal
inflan1mation and swelling that contributes
from behind, the abdomen appears
to urethral occlusion. Castration of young
symmetrically enlarged and pear-shaped.

males also predisposes to urolith-induced

Ultrasound exarnination of the abdomen
urethral obstruction by removing honnonal
reveals a large arnount of hypoechoic fluid.

influences necessary for mature develop

Confirmation of ruptured bladder is
ment of the penis and urethra.

obtained by examining fluid collected by
abdominocentesis and finding that the

Clinical Findings: Clinical signs may be
amount of creatinine in peritoneal fluid is
associated with paitial or complete urethral
two times or more that in plasma. Subcutaocclusion. Animals with partial obstruction neous swellings along the prepuce and
dribble blood-tinged urine after prolonged,
ventral abdomen due to a perforated
painful (stranguria) attempts at urination;
urethra must be differentiated from
before complete occlusion occurs, urine
traumatic injury, subcutaneous abscesses,
may dry on the preputial hairs and leave
and umbilical or ventral hernias. ln breeding
detectable mineral deposits. Animals with
atlin1als, preputial lacerations with prolapse
complete urethral obstruction exhibit
and sheath infection, and hematoma of the
tenesmus, tail twitching, weight shifting,
penis must also be differentiated. In animals
and signs consistent with colic. lnappewith clinical signs of acute colic, other tence, bloat, depression, and rectal prolapse causes of abdominal pain must be also may be seen. Affected steers may
eliminated; these diseases include
elevate the tail and show urethral pulsaindigestion, stasis or obstruction of the GI tions just ventral to the rectw11. Goats may
tract, prin1ary enteritis, abomasal ulcers,
vocalize.

and coccidiosis.

1504

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

Treatment and Control: Treatment of
near the pe1ineal area may be necessary as
obstructive urolithiasis generally involves
a salvage procedure. Animals that develop
establishing a patent urethra and correcting
urethral perforation also require drainage
fluid and electrolyte imbalances. In many
of accumulated subcutaneous wine; this is

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instances, surgical management of the
accomplished by lancing the skin overlying
obstruction is all that is necessary; however,
the area of accumulated urine. Topical
severely uremic and depressed animals
antiseptics and fly repellents may be applied
require rehydration and correction of
to these ventral lacerations, and parenteral
acid-base and electrolyte abnonnalities,
antibiotics are recommended to prevent
especially hyperkalemia or hyperanunoneinfection.

mi.a. If a rupture of the urinary tract has

Cystotomy followed by dietary manageoccurred, hyponatremia, hypochloremi.a, ment is believed to be a more effective
hyperphosphatemia, and metabolic
longterm solution to urolithiasis in sheep
alkalosis with variable potassium concenand goats than is perinea! urethrostomy.

trations are found. Treatment with IV

Cystotomy allows removal of multiple
normal saline is indicated. The volume of
urocystoliths, permits bidirectional urethral
fluid administered should be calculated
flushing, and poses less risk of urethral
to correct clinical dehydration. Once the
stiicture. Tube cystotomy is generally
animal is rehydrated and any rupture
considered the treatment of choice,
repaired, fluid therapy may be continued
allowing time for the calculi to be expelled
to encourage diuresis.

spontaneously. An intact urethral process,

Animals with an intact urethra and
absence of abdominal fluid, and serum
bladder that have early clinical signs of
potassium concentration <5.2 mEq/L have
obstructive urethral disease may benefit
all been associated with improved survival
from conservative therapy using antispasafter tube cystotomy in small ruminants.

modics and tranquilizers. This is believed

If the bladder is ruptured, the ability
to relax the retractor penis muscles with
to urinate must be restored and uremia
straightening of the sigmoid flexure.

corrected. In aninials with substantial

However, conservative therapy is only
uroperitoneum, the peritoneal cavity
rarely beneficial in small ruminants and is
should be slowly drained using a teat tube
warranted only in cases of acute or partial
or trocar. Urine removal may also reduce
obstruction without evidence of urethral or
the severity of peritonitis and make the
bladder damage; it should not be used in
animal more comfortable. Fluid, electrocomplicated or advanced cases. Uroliths lyte, and acid-base homeostasis normally
trapped within the urethral process of sheep returns within 24 hr after restoration of a and goats may be removed by gentle
patent urinary system. Persistent uremia
manipulation or by amputation of the
indicates the possibility of hydronephrosis
urethral process. Proper restraint,
or ascending pyelonephritis or both. A
tranquilization, and a regional anesthetic
urethrostomy should be performed to
are necessary. The techniques vary, but the
provide unobstructed passage of urine.

typical procedure requires exteriorization

Attempts to surgically repair the ruptured
of the penis. Although an1putation may be
bladder have been largely unsuccessful
effective, relief is typically temporary ( <2
because of the chronic distention before
days) in most animals, because obstruction
the rupture. The bladder may heal
recurs due to the presence of multiple
spontaneously after urethrostomy and
uroliths.

removal of abdominal fluid; however, these

Perinea! urethrostomy has also been
animals are best salvaged within 3-4 mo
recommended as an effective surgical
to avoid further complications. Despite
technique in castrated males. Short-term
treatinent, some animals cannot pass w·ine
complications associated with pe1ineal
effectively, and the uroperitoneum recurs.

urethrostomy may include postoperative

These animals may be treated by performhemorrhage, surgical wound dehiscence, ing tube cystotomy followed by appropriand subcutaneous wine accwnulation.

ate antibiotic and fluid therapy.

Urethral stricture is a common longtem1

Several measures to prevent the
complication. Transection of penile
formation of urethral calculi have been
attachments to the pelvis may decrease risk
recommended. Most important for struvite
of postoperative stricture. In addition,
calculi prevention are to increase urinary
perinea! urethrostomy is associated with
chloride excretion, decrease urine pH, and
loss of breeding ability in intact males. In
provide a calciwn:phosphorus ratio of 2: 1
more complicated cases, such as those with
in the complete ration. Intensive concenurethral perforation, amputation of the trate feeding, such as in many finishing
penis proximal to the sigmoid flexure or
programs, frequently leads to urolith

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

1505
formation and urethral obstruction. Thus,

Etiology: The mechanism of urolith
any feeding program that incorporates
fonnation in horses is unknown, although
concentrate feeding must include
the alkaline pH and high mineral content
appropriate calcium supplementation.

of normal equine urine may favor crystal

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Adjunct measures to minimize the
formation and precipitation. Nonna! equine
formation of urethral calculi include
urine also contains large an10unts of
adding sodium chloride up to 4% of the
rn ucoproteins, which may seive as a
total ration. This promotes increased
cementing substance to adhere crystals.

sodium and chloride concentration in the

Consumption of feed and water high in
urine, water intake, and urine dilution,
mineral content may increase urinary solute
which increases the mineral solubility.

concentrations and thereby promote

Ammonium chloride can be used as a
crystallization and precipitation. Multiple
urinary acidifying agent (7-10 g/head/day
nephroliths may develop in horses with
for a 30-kg lamb or kid; 50-80 g/head/day
renal papillary necrosis (associated with
for a 240-kg steer). Complete rations with

NSAID administration while dehydrated)

dietary cation-anion difference (DCAD)

and mineralization of the papillae.

are also used to prevent struvite calculi;
these rations are high in chloride. Urine

Clinical Findings: Clinical signs depend
acidification antagonizes magnesiumon the urolith location. Most uroliths are a.mrnonium-phosphate crystal formation
located in tl1e bladder and cause dysuria,
and has been shown empirically to be a
pollakiuria, and hematuria. Hematuria is
useful preventive measure. Lower calciwn
most evident after exercise and toward
diets should be used if calcium carbonate
the end of a voided mine stream. Affected
or calcium oxalate is a concern.

horses frequently stretch out to urinate and

In operations with a significant problem
may maintain this posture for vaiiable
of urolith fonnation, evaluation of the ration periods before and after micturition.

is the most important measure that can be

Additional signs may include scalding of the
taken to reduce the incidence. Commercial
perineum in females or of the medial aspect
anionic dietary supplements are available
of the hindlin1bs in males. Geldings and
for small rwninants.

stallions may protrude tl1e penis flaccidly
for prolonged periods while intermittently

Urolithiasis in Horses
dribbling mine. Affected horses may
occasionally exhibit recurrent bouts of

Urolithiasis is a less common condition in
colic or an altered hindlin1b gait. Urethral
horses than in small rwninants or steers.

obstruction may also develop as the result

The disease can affect immature horses but
of a trapped urolith and is typically
is seen most frequently in adults. There is no accompanied by restlessness, sweating, breed predilection. Urolitl1iasis is seen more varying degrees of colic, and frequent frequently in males than in females, which
attempts to urinate. The bladder is
has been attributed to anatomic differences
distended on rectal exanlination. In most
between the male and female urethra.

fatal cases, a single large urolith, occasion

Equine urolitl1s have a dian1eter of
ally accompanied by smaller ones, is found

0.5-21 cm, weigh as much as 6.5 kg, and are in the bladder; less frequently, the urolith found most often within the bladder. Most
may be found lodged at tl1e bladder neck or
equine uroliths are composed of calcitu11
the ischial arch. Nephroliths are occasioncarbonate, in various hydrated forms, ally found via ultrasonography in horses
with either calcium phosphate or struvite
with cystic calculi; owners of such horses
uroliths occasionally noted. Calcium
should be informed that obstruction may
carbonate uroliths have two separate
recur.

clinical forms. The first form is a concre

Bilateral nephroliths are not tmconunon
tion of salts and rnucoproteins that varies
in adult horses that have been used for
in consistency from friable to finn. These
performance. Intern1ittent chronic
uroliths are usually yellow and oval or
obstruction of ureters will eventually cause
irregularly shaped; they frequently have
renal failure, resulting in weight loss and
a rough or spiculated surface and are
anorexia.

generally soft enough to be fragmented
during surgery. The second calcium

Diagnosis: Tentative diagnosis of
carbonate fonn is a firm concretion that is
urolithiasis is usually based on the history
hard and resistant to fragmentation and is
and clinical signs and confirmed most easily
typically smootl1 and white. There appears
by rectal palpation of a firm, ovoid, intrato be no difference in chemical composivesicular mass at or near the neck of the tion between these forms.

bladder. In most cases, urolith palpation is

1506

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS
not difficult, because clinical signs are rarely
case of a ruptured urachus, infection in the
evident until the stone is several centimeters
un1bilical stump can weaken the urachal
in diameter. Transrectal ultrasonography
wall and result in leakage of urine into the
with a 7.5 MHz linear probe allows
abdomen or subcutaneously near the
visualization of the stone. If ultrasound
umbilicus. Prematurity, neonatal encephaexantination cannot be performed, the lopathy, cystitis, ascending infection,

VetBooks.ir
distended bladder should be catheterized
abdominal trawna, failure of passive
to facilitate palpation and eliminate the
transfer, and sepsis may predispose the
possibility of urethroliths, urethral stricture,
foal to bladder rupture.

or smegma impaction of the urethral sinus.

Urinalysis frequently reveals RBCs,

Clinical Findings: Foals generally appear
neutrophils, calcium carbonate crystals, and
normal at birth but progressively become
proteinuria. Cystoscopy, ultrasonography,
lethargic, tachycardic, and tachypneic
and radiology are not essential for detection
throughout 24-48 hr. Signs may not appear
of urocystoliths in horses but may provide
for a longer period in foals with a ruptured
additional diagnostic or prognostic
urachus. As the condition progresses, the
information. Ultrasonography is necessary
abdomen becomes noticeably distended,
to identify nephroliths. Ureteroliths and
and ballottement may produce a fluid wave.

cystic calculi can usually be palpated during

Most foals attempt to urinate often, with
rectal examination.

small amounts of urine being produced.

This stranguria is often misinterpreted as

Treatment: Several surgical procedures
straining to defecate. Other foals may be
have been desc1ibed for urocystolith
an uric or urinate normally.

removal. Surgical options include midline
or paran1edian laparotomy and cystotomy,

Diagnosis: Ultrasonographic abdominal
pararectal cystotomy, subischial urethrosexamination and blood and peritoneal fluid tomy, urethral sphincterotomy, and laser
analysis can be helpful in diagnosis. Foals
or shock wave lithotripsy. Selection of a
usually have a neutrophilic leukocytosis.

procedure is dictated by the size, location,

Serum hyperkalemia combined with
and number of uroliths; the sex and
hyponatremia and hypochloremia are
physiologic status of the horse; and the
seen because of the high concentration
availability of surgical facilities. Bladder
of potassiwn and low levels of sodiun1
rupture, although uncommon in adult
and chloride in the urine, which rapidly
horses, may occur due to urethral obstrucequilibrate across the peritoneum. An ECG
tion or recumbency or after foaling in mares.

may show broad QRS complexes and very
tall T waves due to hyperkalemia. The

UROPERITONEUM IN FOALS
increased serun1 potassium predisposes the
foal to bradycardia and cardiac arrhythmias

Uroperitoneum is defined as urine leakage

(AV block, atrial standstill, and cardiac
into the peritoneal space. In foals, this most
arrest) if not corrected. Serum BUN and
commonly results from tearing of the
creatinine values can be nonnal but usually
bladder during parturition;prolonged
are increased. Blood gas analysis may also
recumbency while being treated for a
be nonnal or reveal a metabolic acidosis.

neonatal illness, or rupture of the urachus

Abdominal fluid is pale yellow and copious
secondary to umbilical abscessation.

and can easily be detected on ultrasono

Ureteral or urethral tears are rare. Some
graphic evaluation. The creatinine level in
studies indicate a higher incidence of
the peritoneal fluid is at least double that in
bladder rupture in males than in females,
the serum. This test is the most accurate
possibly because the narrower pelvis and
in diagnosing the problem. If laboratory
the longer, narrower uretlrra of colts is a
testing is not available, 10 mL of methylene
predisposing factor. Urachal rupture occurs
blue can be injected into the bladder via a
both in males and females. Traumatic
minary catheter. If the bladder is patent to
bladder rupture is thought to be caused by
the peritoneal space, dye should be seen in
uterine contractions on a full bladder as
the peritoneal fluid within 15 min.

the foal passes through the birth canal.

The clinical signs of progressive

Although most ruptured bladders at birth
depression and stranguria can confuse the
are thought to be traumatic, the presence of
diagnosis. Differential diagnoses include
smooth edges and absence of hemorrhage
septicemia (seep 2089), hypoxic ischemic around the tear in some foals might suggest
encephalopathy/neonatal encephalopathy
a congenital origin ( developmental defect

(seep 2094), persistent meconium
of the bladder wall). Most bladder tears are
impaction (seep 2096), or colic (seep 248) located on the dorsum of the bladder. In the
for other reasons.

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

1507

In the case of a urachal rnpture, abdominal Clinical Findings and Diagnosis: Signs ultrasonography may be helpful to establish
include acute onset of depresson, anorexia,
an etiologic diagnosis. Ultrasonography of
muscle trembling, and tachycardia and/or
the umbilical remnants may suggest the
an·hythmia. There are many differential
presence of infection or abscessation. A large diagnoses for these clinical signs, so selUlll VetBooks.ir
amount offluid in the abdomen is also seen.

chemistry testing and urinalysis are

Rarely, neonatal foals may become azotemic
necessary. There is a severe metabolic
because of rnpture of one or both ureters.

acidosis, marked hyperchloremia, and

Accumulation of urine in the retroperitoneal
hypokalemia with equine RTA. The urine
area can be seen via ultrasound.

pH is neutral to alkaline.

Treatment: Surgery is necessary to correct
the defect and, in uncomplicated cases, is

Treatment: Administration of sodiun1
very successful. The foal should be stabilized bicarbonate IV and PO is generally successbefore smgery. Potassium >6 mEq/L should ful in correcting the metabolic acidosis.

be lowered preoperatively by eitl1er 500 mL

Potassiwn supplementation may be critical
of nonnal saline, sodium bicarbonate plus
if the serwn potassitm1 concentration is

100/o dextrose throughout 30-40 min, or

<2.5 mEq/L or if the horse is trembling or has
sodium bicarbonate administration alone.

cardiac airhytlunias. Treatment throughout a

All of these treatments help drive potassiun1
few days may result in complete resolution
into cells. lf the potassiwn is >8 mEq/L or
in some horses, but others may require
the above treatments are unsuccessful,
continued supplementation witl1 soditm1
administration of insulin atO.l mg/kg, IV, in
bicarbonate administered PO.

dextrose and saline and/or peritoneal fluid
drainage can be considered.

The bladder should be repaired using
absorbable sutures. Because sw·gical

URETHRAL DEFECTS CAUSING
staples have migrated into the bladder and

HEMATURIA IN ADULT MALE
become the nidus for stone formation at a

HORSES
later date, they should not be used. lf the
un1bilical strnctures are enlarged (indicat

Etiology: The cause of the methral
ing infection), they should be removed at
defects is not proved, but they are believed
the time of surgery and cultured. After
to occur because of high pressure in the
surgical colTection of the bladder, an
corpus spongiostm1 at the end of urination
indwelling winary catheter may be placed
in geldings or during ejaculation in stallions.

for 48 hr to decrease bladder distention and
leakage of urine at the repair site; however,
this is rarely done on a first repair.

lf a bladder rnpture is recognized early
in an otherwise healthy foal and the foal is
stabilized appropriately before surgery, the
prognosis for recovery is good to excellent,
with success rates as high as 95%. In septic
or premature foals, in which complications
such as peritonitis, incisional complications, adhesions, and anesthetic death are encountered more frequently, the prognosis
is fair. All recumbent foals should be
considered at high risk of bladder rnptme
and may require prophylactic indwelling
catheterization.

RENAL TUBULAR ACIDOSIS IN

HORSES

Etiology: Type 1 renal tubular acidosis

(RTA) is a sporadic disorder in horses. The

RTA may be preceded by drug therapy for
another condition or renal injury, or there

Endoscopic examination of the urethra of
may be no predisposing cause. RTA may be
an adult Quarter horse gelding that had
hematuria at the end of urination. The defect
transient or recurring. Genetic predisposiin the urethra is dorsal and at the level of the tion is unproved but possible in some cases.

ischial arch. Courtesy of Dr. ThomasJ. Divers.

1508

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN LARGE ANIMALS

This high pressure may cause a "blow-out"

defect is seen in most cases on the dorsal
tear in the urethral mucosa.

convex surface of the urethra at the level
of the ischial arch.

Clinical Findings and Diagnosis:

Treatment: Some cases may heal

VetBooks.ir

The clinical signs are limited to hematuria
spontaneously, but most continue with
at the end of urination, associated with
intem1ittent hemorrhage; anemia is rare.

contractions of the bulbourethral muscle

Breeding rest is recommended for stallions.

in geldings or with hemospem1ia and

Subischial uretlu·ostomy or subischial
decreased fertility in stallions. All breeds
incision into the spongiosum penis reduces
may be affected, although the disorder
vascular pressme in the corpus spongioswn
seems more conunon in Quaiter horses.

during mination, allowing the defect to heal.

Diagnosis is based on clinical signs and

A buccal mucosa! graft was used to repair
urethral endoscopic findings. The urethral
the defect in a stallion.

INFECTIOUS DISEASES OF THE

URINARY SYSTEM IN SMALL ANIMALS

Most infectious diseases of the urinary
cause, such as idiopathic cystitis, interstitial
system in small aninlals are aerobic
cystitis, or urinary bladder stones. Geriatric
bacterial infections. Common organisms
cats, in1munosuppressed cats, or those with
include Escherichia coli, Staphylococcus,
systemic diseases ( eg, chronic kidney

Enterococcus, and Streptococcus. Less disease, hyperthyroidism) are more prone
common organisms causing infection
to bacterial urinary tract infections. Urinary
include Klebsiella, Proteus, and Pseu
tract pathogens, except for Leptospira
domonas. Pasteurella is more conunon in
interrogans, are not considered zoonotic.

cats than dogs. Mycoplasma is an U11com

However, the potential for multidrug-resistmon cause of urinary tract infection and is ant bacteria to localize in the urinary system
usually foU11d as a co infection with bacteria.

is a concern for both animal and human

Leptospirosis is a worldwide zoonotic
health. Subtherapeutic treatment regin1ens
disease caused by filatnentous bacteria that
and inapprop1iate antibiotic selection are
infect the kidney and many other organs.

contributing factors. Animals that receive

Fungi, yeast, and parasites U11commonly
chronic antibiotic treatment or are
infect the urinary system.

immunocompromised may (rarely) become

Bacterial infections or the urinary tract
infected with Candida spp. Systemic fungal
typically ascend from the methra into the
infections (eg, blastomycosis, aspergillosis,
bladder and in some cases into the kidneys.

protothecosis) can involve the urinary

Predisposing factors include abnomrnlities
system; the kidneys ;md prostate are the
of urine flow (eg, urine retention),
most likely sites.

decreased urothelial defense mechanisms,
decreased systemic inunU11e defense

BACTERIAL CYSTITIS
mechat1isms, or inadequate urine concentration. Female dogs are more susceptible Bacterial cystitis is infection and inilatnmato urinary tract infections than male dogs, tion of the urinary bladder. Clinical signs
except for bacterial prostatitis in older,
are pollakiuria, hematuria, dysmia, and

U11castrated male dogs. Dogs with
urinating in inappropriate places. Hematuconcurrent diseases ( eg, chronic kidney ria may be more noticeable at the end of the
disease or hyperadrenocorticism) are at
urine strean1. An anin1al may exhibit pain on
greater risk. Cats are relatively resistant to
palpation of the caudal abdomen, and the
bacterial cystitis compared with dogs. Less
bladder may feel thickened or irregular.

than 2% of cats 1-10 yr old with lower

Bacterial cystitis is occasionally diagnosed
urinaty tract signs have a positive culture
in an asymptomatic aninlal when a routine
for bacterial infection. Adults cats with
urinalysis is perfom1ed. Chronic glucocorticlinical signs of lower urinary tract pain and coid administration, hyperadrenocorticism,
inflatnmation typically have a noninfectious
chronic kidney disease, and diabetes

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1509
mellitus may be associated with asympto

SC, day one, which may be repeated once 7
matic urinary tract infections. Occasionally,
days later). A repeat urine culture 3-7 days
animals with no concurrent disease will
after oral therapy or on day 21 if cefovecin is
have bacteria in the urine without evidence
used is recommended. If positive, another
of a true infection (ie, bladder mucosa]

antibiotic based on the new susceptibility

VetBooks.ir
invasion and inflammation); this condition
test results is given for a longer treatment
is termed asymptomatic bacteriuria
period (eg, 3-4 wk). Very resistant or

Urinalysis often shows increased protein
recurrent infections should be treated for
and hemoglobin on the urine dipstick

4-6 wk. Every course of treatment should
analysis. The WBC part of the dipstick (ie,
be followed by a urine culture, even if the
nitrate) is inaccurate in dogs and cats and
signs have resolved. In animals that have a
should not be used. The w·ine pH may be
history of chronic or recun-ent infections, a
alkaline (7.5-9) if the bacteria are urease
urine culture should be done 3-7 days and 3
positive ( eg, Staphylococcus or Proteus).

mo after successful therapy. If both of these

However, an alkaline wine pH by itself
cultures are negative, then a urine culture
is not abnormal, because diet and other
should be repeated at 6 and 12 mo after
factors can affect wine pH. Urine sediment
therapy. Because resistance to antibiotics
should be exanlined microscopically.

can develop during therapy, antin1icrobial

Increased nwnbers of WBCs, RBCs, and/or
susceptibility testing should be perfonned
bacteria are consistent with cystitis.

on every positive wine culture.

Bacteria can be confused with stain

Animals with recwTent bacterial cystitis
precipitate; filtering the stain or evaluating
should be evaluated for an underlying
the sediment without staining is advised.

cause. A recurrent infection caused by the

Lack of visible bacteria in the sediment
same bacterial organism is termed a relapse
does not exclude uiinary tract infection.

and is essentially a treatment failure. This is

If clinical signs and/or urinalysis are
typically caused by inappropriate antibiotic
suggestive of infection, a urine culture and
therapy (ie, wrong drug, dosage, or
antimicrobial susceptibility test should be
treabnent duration) and often occurs
perfonned. Cystocentesis is the prefen-ed
because of an Ullfecognized complicating
method for sample collection, followed
factor ( eg, deep-seated bladder wall
by sterile urethral catheterization or a
infection, bladder polyps, renal or prostatic
midstream free catch into a sterile
involvement, concurrent disease). A
collection cup. A quantitative culture is
recurrent infection in which different
necessary to interpret the result, unless the
organisms are causative is termed a
san1ple was collected by cystocentesis.

reinfection and is usually caused by host

Ideally, the culture should be set up within 2
defense problems such as disorders of
hr of collection. If the laboratmy is off-site,
micturition (eg, urethral incompetence),
the sample should be refrigerated and
anatomic abnormalities ( eg, hooded vulva,
processed by the laboratory within 24 hr.

patent urachus, ectopic ureters, uroliths),

If the specimen cannot be refrigerated,
and/or concurrent disease ( eg, chronic
commercial collection kits that contain
kidney disease, hyperadrenocorticism,
preservatives can be used to maintain a
chronic glucocorticoid administration).

stable bacterial population at room

Abdominal radiographs are frequently
temperature for 24 hr. Laboratories that can
diagnostic for uroliths but negative survey
provide both quantitative culturing and a
films should be followed by ultrasonograminimwn inhibitory concentration-based phy, cystoscopy, and/or double-contrast
method for antimicrobial susceptibility
cystourethrography to exclude radiolucent
testing are prefen-ed.

urocystoliths, anatomic defects, polyps, and

Antibiotic regimens for infections
neoplasia. The history may reveal chronic
involving soft tissues, such as bacterial
glucocorticoid use. A serum biochemical
cystitis with prostatic involvement, should
profile, CBC, and complete urinalysis are
be similar to pyelonephritis (see below).

inlportant to exclude predisposing systemic

Sinlple bacterial cystitis is treated for
diseases, such as chronic kidney disease,

2 wk with a broad-spectrwn antibiotic
hyperadrenocorticism, and diabetes
that achieves a high concentration in the
mellitus. Other diagnostic considerations
urine. Appropriate initial choices include
include feline immunodeficiency vi.Ius,
amoxicillin (10-20 mg/kg, PO, bid-tid),
feline leukemia virus, and hyperthyroidism
cefadroxil (22-30 mg/kg, PO, bid),
in cats or hyperadrenocorticism in dogs.

cefpodoxime (5-10 mg/kg/day, FDA

In cases that respond to therapy but
approved for dogs only), ormetoprirn-sulcontinue to have frequent bouts of cystitis fadin1ethoxine (27 mg/kg, PO, day one, then
without an identifiable cause, low-dose

13.5 mg/kg/day, PO), or cefovecin (8 mg/kg,
prophylactic antibiotics can be used to

1510

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
prevent ascending bacteria from establishcasts may be present in fresh urine ing an infection according to the following
sediment. The urine culture is usually
protocol: l) a therapeutic course of an
positive; the CBC may show leukocytosis
antibiotic for the cuffent infection is
with a left shift. The biochemical profile
completed, 2) no antibiotics are given for
may be normal or show azotemia (prerenal

VetBooks.ir

3 days, to allow collection of urine for a
or renal) and/or hyperglobulinemia. The
culture after treatment, and 3) the
animal may be in kidney failure. Chronic
prophylactic protocol is immediately
pyelonephritis is more difficult to recognize,
statted. Prophylaxis consists of using a
because clinical signs may be subtle or
broad-spectrwn antibiotic ( eg, amoxicillin,
absent. Polyuria and polydipsia are
cefadroxil) at one-third of the total daily
frequent. In many cases, the disease goes
dose, given at bedtime, indefinitely. Every
m1recognized until kidney fail me occurs.

6-8 wk, the antibiotic should be stopped

Although abnonnalities in tl1e tuinalysis are
for 3-7 days to obtain a sample for repeat
present, they are often less dran1atic than
urinalysis and culture. Every new infection
with acute kidney infection. A single urine
should be treated with a therapeutic course
culture can be negative if bacterial numbers
of an antibiotic based on cultme and
are low. Other useful diagnostic tests
susceptibility results. The treatment
include abdominal ultrasonography and
antibiotic will likely be different than the

IV pyelography. Both studies may show
prophylactic antibiotic. Oral cranberry
dilation of one or both renal pelvises
extract and o-mannose may be useful
secondary to inflammation and partial
adjuncts. The most valuable therapeutic
obstruction. Asymmetric renal size and
antibiotics ( eg, fluoroquinolones, secondarchitectmal changes witl1 renal pelvic or third-generation cephalosporins) should
dilatation is highly suggestive of chronic
be reserved for resistant infections. lithe
pyelonephritis. In some cases, nephropyelorecllffent infection is resistant to the centesis via ultrasonographic guidance
prophylactic antibiotic, this antibiotic can
is useful to obtain a san1ple of urine from
still be used for future prophylaxis after
the dilated renal pelvis for analysis and
the infection is eradicated. Encouraging
culture.

frequent voicling during the daytime is

Pyelonephritis should be treated
helpful to prevent recmTent infections. The
aggressively with broad-spectrum
major disadvantage of using a prophylactic
antibiotics, based on urine culture and
antibiotic protocol is development of
antimicrobial susceptibility testing, for
multidrug-resistant bacteria.

4-8 wk. The infection may respond to the
same antibiotics recommended for cystitis,

PYELONEPHRITIS
but more frequent administration ( eg,
arnoxicillin tid rather tl1an bid) and/or

Kidney infection (pyelonephritis) is usuhigher dosages are indicated. A fluoroquinally due to ascending bacteria, although olone or a combination of a fluoroquinolone
hematogenous spread is possible. The
with a 13-lactatn antibiotic is often effective.

organisms and predisposing causes are

Dosages should be the san1e as for otl1er
similar to those of bacterial cystitis. •
soft-tissue infections. Animals that are

Renoliths and ureteroliths, which impede
febrile, anorectic, dehydrated, or azoternic
the normal flow of urine out of the renal
should be hospitalized to provide IV
pelvis, may be contributory. Animals at risk
antibiotics and fluid therapy. Fluid therapy
of pyelonephritis are the ve1y young, the
may prevent acute pyelonephritis from
ve1y old, the imrnunosuppressed, or those
progressing to azotemic acute kidney irtjwy
with inadequate urine-concentrating ability.

and will improve renal perfusion and uremic

In many instances, an underlying cause is
signs in animals already experiencing
not identified. Virulence factors associated
uremia. Animals with acute pyelonephritis
with specific bacte1ial strains play a role in
may recover n01mal renal function,
allowing colonization of the urotheliun1,
depending on the an10unt of damage that
especially with pyelonephritis caused by
occurred before treatment. In cases of

Escherichia coli. The fact that pyeloneptuictu·onic pyelonephritis witl1 a severely tis is usually ascending and bilateral
hydronephrotic, nonfunctional kidney, a
suggests that these virulence factors are
neplu·ectomy may be the treatment of
more in1portant than previously recognized.

choice once the aninlal has been stabilized.

Animals with acute pyelonephritis may

This will remove the source of infection and
exhibit kidney or flank pain, fever, malaise,
hopefully save the opposite kidney. IV
and sometimes vomiting, polyuria, and
pyelography and/or renal sci.ntigraphy are
polydipsia. Urinalysis shows proteinuria,
useful to assess the relative function of each
pyuria, bacterituia, and/or hematuria. WBC
kidney. lf both kidneys are severely

INFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1511
affected, medical management alone is the
include levamisole, fenbendazole,
only alternative. Recovery to chronic, stable
albendazole, and ivermectin. The treatment
renal failure is possible in many cases.

of choice is unknown, but a single dose of

The urine should be cultured during the
ivermectin at 0.2 mg/kg, SC, is likely to be
first 5-7 days of therapy to assess antibiotic
effective. It is not FDA approved for this use

VetBooks.ir
efficacy. A winalysis and culture should be
and is contraindicated in Collie breeds. The
repeated 3-7 days after therapy, and then
parasite may be self�limiting in the absence
monthly for 3 consecutive months. If all of
of reinfection.

these cultures are negative, the interval
between urine cultures may be gradually
lengthened. Animals with pyelonephritis are GIANT KIDNEY WORM
at high risk of persistence or recurrence of

INFECTION IN MINK AND DOGS
infection and for secondary infections at
other sites ( eg, bacterial endoca.rditis and

Mink are the most common definitive host
discospondylitis ).

for Dioctophyma renale, the largest known
nematode, which has a worldwide

INTERSTITIAL NEPHRITIS,
distribution. Many other species, including

GLOMERULONEPHRITIS,
dogs and people, can become infected. The
definitive host contracts the parasite by

AND VASCULITIS
ingesting encysted larvae in raw fish ( eg,
pike, bullhead) or frogs or by ingesting an

Acute interstitial nephritis in dogs is caused
infected annelid wom1. The larvae penetrate
most often by Leptospira inte-,rogans ( see the bowel wall and migrate first to the liver
p 650). Cats rarely de�lop leptospirosis, and
and later to the kidneys. In dogs, the
clinical signs are less severe than in dogs.

parasite often fails to reach the kidneys and

Other infectious causes of nephritis
may be found free in the abdominal cavity.

in dogs include Leishmania donovani

Kidney worn1s grow larger in dogs than in
and Bon-elia burgdorje-,·i. These systemic
mink, reaching up to 103 cm.

vectorborne diseases are endemic in specific

Female worms are larger than male
geographic areas. Glomerulonephritis is the
worms, and both are blood red. Both male
predominant renal pathology, so these are
and female worms must be present in the
considered inunune complex diseases rather
same kidney to complete the life cycle.

than true urinary tract infections. Toxoplas

Barrel-shaped, yellow-brown eggs with a
mosis can cause pyogranulomas in the
thick, pitted shell measuring 71-84 x 45-52
kidneys or elsewhere in the urinary system.

µm are shed into the urine.

Systemic infectious diseases that cause

In the kidneys, the wonn(s) cause
vasculitis in cats or dogs ( eg, feline infectious obstruction, hydronephrosis, and destrucperitonitis, Rocky Mountain spotted fever) tion of the renal parenchyma. The right
may also cause kidney disease.

kidney is most commonly affected. Kidney
failure can result if both kidneys are

CAPILLARIA PL/CA INFECTION
parasitized. Chronic peritonitis, adhesions,
and liver disease are also possible. Clinical

Capillaria plica may infect the urinary
signs are hematuria, pollakiuria, weight
bladder, and occasionally the ureters and
loss, and renal or abdominal pain. Urinalysis
renal pelvises, of dogs and cats. Distribution may reveal proteinuria, hematuria, and is worldwide, and wild animals appear to
pyuria. Ultrasonography or IV pyelography
be the primary hosts. A similar but less
shows the enlarged hydronephrotic
common organism, C felis cati, is also
kidney(s). The diagnosis is made by finding
found in cats. Dogs and cats become
the eggs in the urine sediment if both sexes
infected by eating earthworms that contain
of the nematode are present in the kidney
the first-stage larvae. Mature Capillaria are and the ureter is patent. Alternatively,
threadlike, yellowish, and 13-60 mm long.

exploratory laparotomy may reveal the

The eggs are colorless, operculated, have a
diagnosis. Worn1s may be found in the
slightly pitted shell, and are 63-68 x 24-27
peritoneal cavity, between the lobes of the
µm in size. Most dogs and cats are
liver, or within the affected kidney( s) via
asymptomatic. Some animals show signs
nephrotomy.

of pollakiuria, urinary incontinence, and

Unilateral nephrectomy is the treatment
urinating in abnormal places. The eggs are
of choice if the opposite kidney is unafshed in the urine and may be found in the fected. Preventing ingestion of raw fish or
urine sediment. Microscopic hematwfa and
other aquatic organisms is recommended in
increased nwnbers of epithelial cells may
areas where the parasite is known to infect
also be present. Reported treatments
wild animals.

1512

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

NONINFECTIOUS DISEASES OF THE

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URINARY SYSTEM IN SMALL ANIMALS

RENAL DYSFUNCTION
months or years before it becomes clinically
apparent, and it is invaiiably irreversible and

Failure of the filtration function of the
frequently progressive. Although congenital
kidneys leads to the development of
disease results in a transient increase in
azotemia (an excess of nitrogenous
prevalence in animals <3 yr old, the
compounds in the blood), which may be
prevalence increases with advancing age
classified as prerenal, renal, posh·enal, or of
from 5--6 yr. In geriatric populations at
mixed origin. Prerenal azotemia develops
referral institutions, CKD affects as many as
whenever mean systemic arterial blood

100/o of dogs and 35% of cats. The prevalence
pressure declines to values <60 mmHg and/or in the general small animal population is when dehydration causes plasma protein
likely to be lower, perhaps 1 %-3%. Several
concentration to increase. Conditions that
breeds of dogs and cats are associated witl1
may lead to development of prerenal
heritable CKD (seep 1496). There is no
azotemia include dehydration, congestive
apparent breed or sex predisposition
heart failure, and shock. Prerenal azotemia
for nonheritable CKD in dogs or cats.

generally resolves with appropriate

CKD is generally classified into vaiious
treatment, because kidney structure has not
stages ( see TABLE 2) based on laboratory been altered, which allows normal function
tests and clinical signs. In Stage 1, a process
to resume once renal perfusion has been
is dainaging the kidneys but azotemia and
restored. Renal azotemia refers to a
clinical signs have not developed. Unfortureduction in glomerular filtration rate nately, renal disease is tmcommonly

(GFR) of -75% during acute or chronic
detected at this stage. In Stage 2, the disease
primary renal ( or intrarenal) diseases.

has progressed, GFR has fallen to <25% of

Postrenal azotemia develops when the
nom1al, and azotemia is present, but clinical
integrity of the urinary tract is disrupted
signs are not yet seen. However, this stage

( eg, bladder rupture) or urine outflow is
may be associated with in1paired urineobstructed ( eg, urethral or bilateral ureteral concentrating ability and increased urine
obstruction). Once adequate urine flow is
volun1e. Stage 3 occurs when GFR has
restored, posh·enal azotemia will resolve.

declined further, azotemia is present, and
clinical signs are often seen. Stage 4 reflects

Chronic Kidney Disease
further progression and severe azotemia,

Chronic kidney disease (CKD) involves a loss with clinical signs present. This staging of functional renal tissue due to a prolonged
system applies to CKD only.

(�2 mo), usually progressive, process.

Dramatic changes in renal structure may be

Substaging Based on Blood Pressure:

seen, although structural and functional

Systemic hypertension is present in -200/o of
changes in the kidney are only loosely
dogs and cats with CKD and is associated
correlated. CKD often smolders for many
with target organ dainage in the kidneys,

IM=ii!J CLASSIFICATION OF STAGES OF KIDNEY DISEASE

1

2

3

4

Nonazotemic

Kidney

Mild Renal Moderate Renal Severe Renal

Disease

Azotemia

Azotemia

Azotemia

Creatinine (mg/dL)

Dogs

<1.4

1.4--2.0

2.1-5.0

>5.0

Cats

<1.6

1.6-2.8

2.9-5.0

>5.0
a Stages are as recommended by the International Renal Interest Society.

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1513

SUBSTAGES OF CHRONIC KIDNEY DISEASE BASED ON ARTERIAL

BLOOD PRESSURE (AP) MEASUREMENTS AND RISK OF TARGET

ORGAN DAMAGE

Substagea

APO

APl

AP2

AP3

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No or minimal

Low

Moderate

High
risk
risk
risk
risk

Blood pressure (mmHg)

Systolic

<150

150-159

160-179

>180

Diastolic

<95

95-99

100-119

>120

"Substages are as recommended by the International Renal Interest Society. Other modifiers that may be added to the AP substage: C = evidence of end organ damage or complications present; T = patient presently being treated.

eyes, CNS, and cardiovascular system. It
species-specific antibody test. Animals with
is recommended that animals with CKD be
microalburninuria frequently exhibit or
substaged on the basis of blood pressure
subsequently develop kidney disease, sysmeasurements (see TABLE 3).

temic inflammatory or metabolic disease,

In general, animals in substage AP3 and
neoplasia, or infectious diseases.

those in substage AP2 with preexisting

Proteinuria is an in1portant finding and is
target organ damage ( eg, retinal injury or
associated with a poor prognosis in aged

CKD) should be considered candidates
animals and in those with CKD. Changes in
for antihypertensive therapy.

the magnitude of proteinuria represent a
good marker for the efficacy of antihyper

Substaging Based on Proteinuria:

tensive therapy. Animals with CKD should

The routine dipstick evaluation of urine for
also be substaged on the basis of proteinprotein is not particularly specific, because uria ( see TABLE 4), using the protein:creatinine many of the positive reactions (1/, in dogs
ratio.

and 2/, in cats) are false-positives. Although
it is a useful screening test, a positive result

Etiology: Attempting to identify the
should be followed with a more specific
primary process causing the kidney disease,
test, such as the sulfosalicylic acid test, the
especially in Stages 1 and 2, is important
urine protein:creatinine ratio, or alburninto form a prognosis and treatment plan.

specific assays.

Known causes of CKD include diseases

Species-specific antibodies for albumin
of the macro vascular compartment ( eg,
have led to development of highly specific
systemic hypertension, coagulopathies,
and sensitive assays for the detection and
chronic hypoperfusion), microvascular
measurement of urine albumin concentracompartment ( eg, systemic and glomerular tions. Microalbuminuria is defined as a
hypertension, glomerulonephritis,
urine protein content that leads to a
developmental disorders, congenital
negative reaction for the routine urine
collagen defects, arnyloidosis), interstitial
dipstick and a positive reaction with a
compartment ( eg, pyelonephritis, neoplasia,

SUBSTAGES OF CHRONIC KIDNEY DISEASE BASED ON

PROTEINURIA

Substagea

N

BP
p

Non protein uric

Borderline

Protein uric

Dogs

0.2-0.5

Cats

0.2-0.4

" Substages are as recommended by the International Renal Interest Society.

b Urine protein:creatinine ratio

1514

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
obstructive uropathy, allergic and immunein Stages 3 and 4 usually reveal small, mediated nephritis), and tubular compartiJTegular kidneys, although nom1al to ment ( eg, tubular reabsorptive defects,
lai·ge kidneys can be seen in animals with
chronic low-grade ncphrotoxicity,
neoplasms, hyclronephrosis, or glomernloobstructive w-opathy). Many causes of neph1itis. Mucous membranes are pale in
chronic, generalized renal disease are
late Stage 3 and Stage 4, clue to the presence

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associated with progressive interstitial
of a nonregenerative, normocytic,
fibrosis. The severity of interstitial fibrosis
normochromic anemia.

is positively coJTelated with the magnitude
of decline of G FR and negatively correlated

Diagnosis: In Stages 1 ai1d 2, diagnosis
with the prognosis. The glomerular,
is often missed or made incidentally clW'ing
tubulointerstitial, and vascular lesions
imaging studies or willalyses conducted for
found in animals with generalized CKD are
other purposes. In Stages 3 and 4, the BUN,
often similar, regardless of the initiating
serun1 creatinine, and inorganic phosphorus
cause, paiticularly in Stage 4. At this point,
concentrations are increased. Potassiwn
renal histology may show only marked
depletion, clue to renal potassiwn wasting
interstitial fibrosis, which may be called
combined with inadequate intake and the
chronic interstitial nephritis or tubulointe1°
kaliw-etic effects of acidosis, is frequently
stitial fibrosis. This tem1 describes the
seen in cats and occasionally in dogs.

morphologic appearance of kidneys with

Hyperkalemia associated with oligw-ia and
end-stage chronic disease of any cause.

anuria may be noted in tenninal Stage 4

Because acute kidney iitjury may progress
or whenever marked prerenal azotemia is
to a chronic condition, any cause of acute
concunent with CKD. Systemic hypertenkidney iitjury is also a possible cause of sion ai1d associated complications develop

CKD.

in -20% of affected cats and dogs and can
occur at any stage. Osteoporosis may be

Clinical Findings: Generally, no clinical
seen radiographically, although this late
signs are seen as a direct result of disease
finding is generally not helpful for diagnosis.

tmtil ;,:75% of nephron function has been

The urine specific gravity may range from
in1paired (Stages 3 and 4). Exceptions are

1.001-1.060 in dogs and 1.005-1.080 in
chronic kidney diseases that develop as part cats, depending on body needs for water of a systemic disease with clinical signs
homeostasis; the normal rai1ge overlaps the
referable to involvement of other body
abnormal or inappropriate range. In animals
tissues ( eg, systemic lupus erythematosus,
witl1 dehydration and normal renal function,
systemic hypertension), chronic kidney
urine specific gravity should be > 1.030 in
diseases accompanied by nephrotic
clogs and > 1.035 in cats. The inability to
syndrome, or those associated with marked
produce concentrated mille when
renal inflarrm1ation and capsular swelling
challenged by dehydration is an early sign
leading to flank pain and occasionally to
of CKD; however, dogs witl1 primary
vomiting. Usually, the earliest clinical signs
glomerular disease, and some cats, may
conunonly attributable to renal dysfunction
become azotemic while retaining tl1e ability
ai·e polydipsia and polyuria, which are not
to concentrate W'ine to a specific gravity
seen until the function of approximately

> 1.035. Even so, concentrated W'ine is rarely
two-thirds of the nephrons has been
seen when the sernm creatinine is >4 mg/dL
impaired (late Stage 2 or eai·Jy Stage 3).

in an animal with azotemia of renal origin.

Ftuther destruction of renal tissue leads to

The polydipsia and pblyuria of CKD must
azotemia without new clinical signs in Stage be differentiated from diseases that cause 2, and finally to the clinically appai·ent
prin1aiy polydipsia ( eg, psychogenic
uremic syndrome in Stage 4. Initially, w-emia polydipsia, hypertl1yroidism) or interfere is associated with occasional vomiting and
directly with the wille-concentrating
lethargy. As the disease progresses within
mechanism. This includes conditions that

Stages 3 and 4 throughout months (dogs)

lead to retention of solute in tubular fluid
to years (cats), anorexia, weight loss,

( eg, diuretic administration, diabetes
dehydration, oral ulceration, vomiting, and
mellitus ), central diabetes insipiclus, and
diarrhea become fully marLifest. Loose
nephrogenic diabetes insipid us ( eg,
teeth, deformable maxilla and mandible, or
hyperadrenoco1ticism, hypercalcemia,
pathologic fractw-es may be seen with renal
pyometra, diseases causing septicemia).

secondary osteoclystrophy (seep 1056), but

Adrenal insufficiency leads to a tu·ine-conthese are uncommon and generally seen centrating defect and may tlms be confused
only in yow1g dogs with end-stage
witl1 Stage 2 and 3 renal disease, because
congenital renal disease. Physical
prerenal azotemia may be caused by the
examination and imaging studies of animals
vomiting, diatThea, and polydipsia

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1515
associated with hypoadrenocorticism.

daily in cats and bid in dogs) or an

Hyperkalemia, hyponatremia, and/or
angiotensin-receptor blocker (ARB) such as
reduced plasma Na+ to K+ ratio helps
telmisartan (1 mg/kg, once daily in cats and
establish a tentative diagnosis of adrenal
bid in dogs). lf an ACE inhibitor is used in
insufficiency, which must be confumed
conjw1ction with a renal diet, potassilUn

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by hom1onal assay(s). Also, animals with
should be carefully monitored. Hyperhypoadrenocorticism improve rapidly kalemia may develop, particularly in Stage
in response to proper therapy.

4, and dietary change or dosage acljustment

Combinations of survey radiography,
should be considered if semm potassitm1
abdominal ultrasonography, serial clinical
exceeds 6.5 mEq/L. While ACE inhibitors
pathology tests, including urinalyses and

( or ARBs) and calcilUn-channel blockers
illine cultures, and blood pressure
may be administered together, a calciun1-
measurements should be performed to
channel blocker is usually recommended as
evaluate the severity of disease, establish a
initial therapy in cats and an ACE inhibitor
prognosis, monitor the response to therapy,

( or ARB) in dogs. In addition to providing a
and identify complicating factors. Specific
continuous supply of fresh drinking water
renal function tests and renal biopsy may be
and encouraging ( and docwnenting)

helpful to identify the exact cause in Stages
adequate dietary intake, body condition

1-3, but the presence of advanced
scoring should be used routinely to assess
pathologic changes in Stage 4 is nonspecific
adequacy of intake. Animals in this stage
and often precludes identification of an
should be fed standard, conm1ercially
underlying cause by histologic studies. This
available maintenance diets, wlless they
condition in late Stage 4 is often described
are markedly proteinwic (see below). All
as end-stage renal failure clinically and as
affected aninlals should be reevaluated every
chronic, generalized nephritis pathologi6--12 mo, or sooner if problems develop.

cally. CKD should be distinguished from

In Stages 2 and 3, the principles for manthe more readily reversible acute disease.

agement of complications are the same,

Frequently, differentiation may be
except that the anin1al should be evaluated
accomplished with an appropriate history,
every 3--6 mo. These evaluations should
physical examination, and laboratory
include hematology, semm biochemistries,
findings, although a renal biopsy may be
and urinalysis. Because dogs and cats with
required. However, therapy for CKD caused

CKD are prone to development of bacterial
by a range of morphologic lesions is similar,
urinary tract infections, mine culture
so renal biopsies may not be wa.1Tanted
should be pe1fo1med annually and any tin1e
unless marked proteinuria is present or a
urinalysis suggests infection. The progrestreatable cause is suspected.

sive nature of this disease produces a
vicious cycle of progressive renal <jestruc

Treatment: With appropriate therapy,
tion. Measures that may slow this progresanimals can survive for long periods with sion include dietary phosphorus restriction,
only a small fraction of functional renal
dietary fish oil supplementation, antihypertissue, perhaps 5%--8% in dogs and cats.

tensive agents (for hypertensive clogs and

Recommended treatment varies with tl1e
cats), and administration of ACE inhibitors or
stage of the disease. In Stages 1 and 2,

ARBs (proteinuria substage P; see TABLE 4).

animals usually have minin1al clinical

Dietary restriction of phosphate and acid
abnom1alities. Efforts to identify and treat
load is essential in this stage, and specialthe primary cause of the disease should be ized diets for management of kidney disease
thorough. The identification and supportive
should be fed. Potassiun1 citrate or sodium
treatment of developing complications ( eg,
bicarbonate, given PO, may be indicated if
systemic hype1tension, potassium
the animal is severely aciclotic (plasma
homeostasis disorders, metabolic acidosis,
bicarbonate <15 mEq/L) or remains acidotic
bacte1ial urinary tract infection) should be

2-3 wk after diet change. If dietary
aggressively pursued. The systemic
restriction of phosphorus is unsuccessful
hype1tension seen in -20% of animals with
in maintaining a nonnal level of serum

CKD may be seen at any stage and is not
phosphorus within 2-3 mo, phosphateeffectively controlled by feeding a low-salt binding gels containing calcium acetate,
diet. The usual antihype1tensive medicacalcimn carbonate, calcitm1 carbonate tions for blood pressure substages AP2 and
plus chitosan, lanthanwn carbonate, or

AP3 (see TABLE 3) are a calciw11-channel
allll11inwn hydroxide should be adminisblocker such as amlodipine besylate tered with meals to achieve the desired

(0.25--0.5 mg/kg/day, PO) or an angiotensineffect. There is also a clear rationale for the converting enzyme (ACE) inhibitor such as
inclusion of dietary n-3 polytmsaturated
enalapril or benazepril (0.5 mg/kg, once
fatty acids in these stages.

1516

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

In late Stage 3 and Stage 4, all of the
most often presented to the veterinarian
principles of managing the preceding stages
when a sudden, major insult damages the
apply, except that the animal should be
kidneys. The principal causes are toxins ( eg,
evaluated every 1-3 mo. Dietary restriction
ethylene glycol, a.minoglycoside antibiotics,
of protein may relieve some of the signs of
hypercalcemia, hemoglobinuria, melaniine

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uremia. High-quality protein ( eg, egg
cyanuric acid, grapes or raisins, NSAIDs ),
protein) should be fed at a level of
ischemia ( eg, embolic showers from

2-2.8 g/kg/day for dogs and 2.8--3.8 g/kg/day
disseminated intravascular coagulation or
for cats. Commercial diets formulated for
severe prolonged hypoperfusion), and
cats and dogs with CKD generally meet this
infection ( eg, leptospirosis, borreliosis ).

recommendation. Administration of a
proton pump inhibitor such as omeprazole

Clinical Findings: Mild AKI often goes

(0.5-1 mg/kg/day, PO) or an H2-receptor
unrecognized; severe initial or repeated
antagonist such as fan1otidine (5 mg/kg, PO,
bouts may lead to CKD. Most often, AKI
tid-qid) decreases gastric acidity and
is recognized in advanced stages and is
vomiting. Anabolic steroids, such as
characterized clinically by anorexia,
oxymethalone or nandrolone, have been
depression, dehydration, oral ulceration,
administered to stimulate RBC production
vomiting and/or dia.iThea, or oliguria.

in anemic animals, but this is not effective.

Physical examination findings often reveal

Recombinant erythropoietin and other
dehydration but otherwise are usually not
erythropoiesis-stimulating agents ( eg,
rema.i·kable, although pain is occasionally
darbopoietin, continuous erythropoietin
elicited on palpation of the kidneys, which
receptor activator) may stimulate RBC
may be nmmal in size to slightly enlarged.

production, but antierythropoietin
antibodies develop in -5QOA, of animals

Diagnosis: A history of hypotension,
treated with the human recombinant
shock, or recent exposure to known
erythropoietin, epoetin alfa, and may result
nephrotoxins in an animal with suddenin refractory anemia. Darbopoietin may be onset uremia is the typical clinical picture
less likely to produce this effect and may be
of an animal with acute kidney disease.

preferred. Until species-specific products

The presence of poorly concentrated urine
become generally available, erythropoietin

( specific gravity 1.007-1.030) despite
administration is now recommended only
dehydration and/or azotemia suggests renal
for animals with clinically apparent signs of
dysfunction. Differentiating between chronic
anemia ( eg, weakness, marked lethargy not
and acute kidney disease ( and establishing
attributable to other factors), which
a specific cause in acute kidney disease)

generally occurs at a hematocrit <200Ai.

is important, because the prognosis and

Fluid therapy with polyionic solutions,
specific therapy may differ. Animals with AKI
given IV or SC in the hospital or SC by
usually have a compatible history and other
owners at home, is often beneficial in
urinalysis abnormalities; marked cylindruria
animals with intermittent signs of uremia.

is a frequent and definitive finding. Other

Oral vitamin D administration may reduce
urinalysis findings may include the presence
uremic signs and prolong survival,
of a large number of renal epithelial cells and
particularly in dogs. However, vitamin D
leukocytes in the urine sediment, glucosuria,
administration requires prior resolution
crystalluria, enzymuria, and/or myoglobinuof hyperphosphatemia (goal is serum rialhemoglobinuria. Anim� with AKI
phosphorus <6 mg/d.L), and it may induce
generally have increased serum urea
hypercalcemia. Probiotic medications and
nitrogen, creatinine, and inorganic phosphocertain dietary fibers may enhance gut rus concentrations and metabolic acidosis.

catabolism of nitrogenous compounds and

Oliguria or anuria after rehydration, which is
uremic toxins. Feeding tubes may help
often associated with hyperkalemia, is a poor
manage chronic anorexia. Euthanasia or
prognostic sign; in contrast, polyuric anin1als
renal replacement therapy (renal transplanhave a better prognosis, although they may tation and/or dialysis) should be carefully
become hypokalemic. The kidneys are
considered if therapy does not improve
typically normal in size and shape and an
renal function and alleviate signs of uremia.

anemia is often, but not al ways, absentfindings that may help differentiate acute from chronic kidney disease.

Acute Kidney Injury

After irtjury, the kidney has considerable

Because not all animals with acute kidney
potential for functional regeneration
irtjury (AKI) will be identifed or exhibit
through the process of compensatory
azotemia, AKI has replaced the older term,
hypertrophy and adaptive hyperfunction.

acute renal failure. Animals with AKI a.re

In animals with CKD, it is likely that most

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1517
of this regenerative process has occurred
osmotic diuresis (l()OA, or 200,6 mannitol or
before the initial diagnosis. In contrast,
dextrose, 0.5---1 g/kg, IV, as a slow bolus
animals with AKI have considerably more
throughout 15--- 30 min, alternated with
potential for improvement of renal ftmction,
infusion of lactated Ringer's solution,
if they can be sustained through a uremic

30 mllkg, IV, throughout 30 min). Subse

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episode. The duration of the uremic episode
quent measures generally include furosemay be substantial with some nephrotoxins nlide (2 mg/kg, IV, which can be doubled

( eg, 1-3 wk with aminoglycoside antibiotics
and then tripled at 2-hr intervals if mine
and 4---8 wk with ethylene glycol). A renal
production does not increase above the
biopsy may be of value in assessment of
target of 0. 5 mlJkg/hr). However, furosethe severity, extent, cause, and potential nlide may worsen the severity of AKI
reversibility of the disease.

caused by anlinoglycosides. Finally, renal

As a disease process, AKI is a spectrum,
vasodilators ( dopanline diluted in 5%
and the International Renal Interest Society
dextrose, IV, to provide 1-5 mcg/kg/min)

recommends that patients with AKI be
plus furosenlide (2 mg/kg, IV) may be tried
categorized primarily on the basis of serum
for 2 hr. Dopan1ine may lead to ventricular
creatinine. Animals with Grade I AKI have
arrhytluilias, and high closes of dopamine
nonazotemic AKI (serum creatinine
may cause renal vasoconstJiction.

�1.6 mg/dL). Animals with Grades II-V AKI

Dopanline produces minimal renal
exhibit varying degrees of azotemia, with
vasodilation in cats and calcium charmel
serum creatinine levels of 1. 7-2.5 mg/dL
blockade (eg, anllodipine besylate, 0.25---0.5
in Grade II, 2.6-5 mg/dL in Grade Ill,
mg/kg, or diltiazem, 1-3 mg/kg) may be

5.1-10 mg/dL in Grade IV, and >10 mg/dL
preferred. If attempts to restore urine flow
inGrade V.

fail, aggressive measures should be
discontinued to avoid overhydration. Daily

Treatment: Severe AKI that necessitates
fluid therapy based on maintenance and
medical intervention is a serious condition,
rehydration needs is continued until renal
with a survival rate of-500Ai. If the cause is function and clinical condition improve.

known, specific therapy should be instituted,

Feeding tube placement greatly facilitates
eg, 4-methylpyrazole or ethanol for ethylene
patient management at this stage and
glycol toxicity in dogs (seep 3046). Fluid
should be implemented for any animal with
therapy is indicated for all dehydrated and
marked renal azotemia (serun1 creatilline
inappetant animals. A polyionic fluid such

> 10 mg/dL after rehydration).

as lactated Ringer's solution is satisfactory

A second tl1erapeutic option, ratl1er than
unless hyperkalemia is present, in which
the aggressive measures discussed above,
case norn1al saline is recommended. Sodium
is to proceed directly to fluid therapy with
bicarbonate may be cautiously added to the
polyionic solutions while waiting for renal
fluids to correct acidosis.

regeneration. Again, feeding tube placement

In oligrnic or anuric animals, therapy to
for parenteral nutJition should be implepromote increased mine volume is often mented in anorectic animals with marked
recommended if the animal is well hydrated
azotemia. Peritoneal dialysis or hemodialyand mine production is <0.5 mlJkg/hr. This sis may be necessary if none of the above
approach has been questioned because
measures restores mine production.

urine flow may increase without corresponding increases in renal blood flow and GLOMERULAR DISEASE

GFR. Administration of excess fluid to an
animal in the maintenance phase of oliguric

Glomerular disease is a well-recognized
renal failure may result in life-threatening
cause of chronic kidney disease (CKD) in
pulmonary and cerebral edema. Nonethedogs, may produce acute kidney injury in less, efforts to increase renal blood flow and
dogs, and is also occasionally seen in cats

GFR may enhance mine production and do
with CKD. These animals should be staged
have a role in the management of these
and substaged as recommended above
animals. For this therapy, urine production

(see TABLE 2, TABLE 3, and TABLE 4). Animals must be quantitatively monitored closely via with primary glomerular disease as a cause an indwelling urethral catheter. Monitoring
of CKD may have somewhat different
central venous pressure is advised to
clinical and laboratory abnormalities
prevent overhydration. A sequential
than those with p1imary tubulointerstitial
approach generally includes an initial slight
disease. Although uncommon, urine
overhydration by administration of a test
specific gravity may be inappropriately
dosage of polyionic solution IV at 50 mIJkg.

high for the degree of renal dysfunction, a

If this fails to yield adequate mine flow
condition referred to as glomerulotubular
within 3 hr, further measures include
imbalance. Damage to the glomerular

1518

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
basement membrane results in albuminpeople such as Al port syndrome (hereditary uria, which may lead to hypoalbuminemia.

nephritis).

Animals may then exhibit signs related to

Most cases of an1yloidosis (seep 592) in
hypoalbuminemia ( eg, peripheral edema,
dogs and cats, including familial amyloidohypercoagulability with thrombosis, sis in Chinese Shar-Pei and Abyssinian

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hypercholesterolemia) instead of or in
cats, are reactive, or secondary, amyloidoaddition to uremia.

sis. In this form of the disease, an1yloid A

Secondary glomerulopathies, observed
protein is deposited in various tissues after
as sequelae of systemic or glomerular
serum levels increase as a result of chronic
hypertension in animals with Stage 3 or 4
inflanunation. When the kidneys are

CKD, are corrunon. Although the overall
affected, amyloid deposition
prevalence of a primary glomerulopathy
in the nonfamilial forms in dogs usually
as an inciting cause is not lrnown, it is
occurs in the glomerulus. However, in
apparently more common in dogs than cats.

Shar-Pei, at least 25% of Abyssinian cats,

Immune-mediated glomeruloneplrropathy
and in many domestic cats with the
is characterized by deposition or in situ
nonfa.milial form of this disease, amyloid
formation ofirrunune complexes in the
is found primarily in the medullary
glomerular capillary wall, which then incite
interstitiun1, where it interferes with the
inflanm1atory changes (seep 828). In one
renal concentrating mechanism and is
study of dogs, the mean age of presentation
more likely to produce nonproteinuric
for glomerulonephritis was 4--8 yr; 55% were

CKD than protein-losing glomerular
males, and there was no breed predilection.

amyloid deposition. In contrast, glomeru

Inm1une-mediated glomerulonepluitis has
lar amyloidosis usually leads to marked
been associated with neoplasia, rickettsial
proteinuria. The nonfa.milial form of
diseases, systemic lupus erythematosus
amyloidosis usually affects middle-aged

(SLE), heartworm disease, pyometra, clrronic to older dogs and cats. Beagles, Collies, septicemia, and adenovirus infection, but it is
and Walker Hounds are reported to be at
usually idiopathic. Althougll multifactorial in
increased risk. Animals with the familial
origin, the glomerular disease associated
form of the disease are usually diagnosed
with hyperadrenocorticism and diabetes
at a younger age.

mellitus in dogs is rarely attributable to
inm1une complex formation.

Clinical Findings: Glomerulopathy often

In one study of cats with glomeruloneleads to proteinwia (prin1arily albwninuria) phritis, the mean age at presentation was
and can produce hypoproteinemia, ascites,

3-4 yr; 75% were males, and there was no
dyspnea. ( due to pleural effusion or pulbreed predisposition. Primary glomerular monary edema), and/or peripheral edema,
disease in cats is mpst frequently associated
which may be referred to as the neplrrotic
with clrronic infection by feline leukemia
syndrome. Protein wasting can produce
virus (FeLV), feline inununodeficiency virus
preferential loss of lean body mass that may

(FIV), or feline infectious peritonitis (FIP)

be apparent on careful physical exanlination.

virus but has also been reported in

Severe or clrronic glomerular disease is a
association with neoplasia and systemic
cause of CKD; most dogs and many cats with
inflanmiatory diseases. The relatively young
glomerular disease eventually develop Stage
age and predilection for males reflects the

III or IV disease. Systemic hypertension may
high prevalence of FeLV infection as a cause be more prevalent in pi:oteinwic CKD and in reported feline cases.

may be seen at any stage.

Familial glomerulopathies as a primary

Proteinuria may result in loss of
cause of CKD have been reported in several
antithrombin ill tlrrougll the glomerular
breeds of dogs, including Bernese Mountain
basement membrane, leading to a hyper

Dogs, English Cocker Spaniels, English
coa.gulable state in dogs. Proteinuria also

Springer Spaniels, Doberman Pinschers,
contributes to mild thrombocytosis and

Greyhounds, LhasaApsos, Poodles,
platelet hypersensitivity, which contribute

Rottweilers, Samoyeds, Shih Tzus, and
to coagulation abnormalities in affected

Soft-coated Wheaten Terriers. These are not
dogs, generally when plasma albwnin levels
inunune complex diseases, although some
are 5: 1 g/dL. Severe dyspnea secondary to
are characterized by proteinuria and
pulmonary thromboembolism or other
associated clinical abnom1alities that
sequelae oftlu·ombotic disease may be
resemble those caused by immune-mediated
seen in dogs with glomerulonepluitis or
glomemloneplrropathy. Several of these
aniyloidosis. It is unclear whether a hyperbreeds of dogs have genetic defects in coagulable state also exists in protein uric
collagen stmcture and function (types ill or
cats, because clinical signs from hypercoag

IV), analogous to hereditary neplrropathies in
ulability have not been reported in cats.

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1519

Diagnosis: The BUN, creatinine, and
heartworm disease; in cats, tests for
phosphorus concentrations are usually
infection with FeLV, FIV, FIP, SLE, and
increased, although the degree varies with
heartworm disease should be included.

the stage of CKD at the time of diagnosis.

Animals should be staged and substaged on

Treatment: There ai·e six basic principles

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the basis of measurements of blood pressure
for treatment of glomemloneplu·opathies:

(see TABLE 3), proteinuria (see TABLE 4), and 1) If a cause of inunune complex disease can
serum creatinine ( see TABLE 2). Marked be identified, it should be treated. 2) Maniproteinuria with edema may be seen in the festations of the nephrotic syndrome, if
presence or absence of azotemia. Physical
present, should initially be managed by
findings are usually nonspecific except that
therapies designed to reduce proteinuria.

ascites, pleural effusion, and/or peripheral,

This includes a renal diet low in protein and
pitting, nonpainful, subcutaneous edema are
salt and subsequently, if needed,judicious
evident in some animals (75% of cats and 15% use of diuretics. 3) Antithrombotics ( eg, of dogs). Although uncommon, urine specific aspirin) should be considered for hypoalbugravity may be inappropriately high for nlinemic (plasma albunlin < l g/dL) dogs but
the degree of renal dysfunction. A urine
not cats, as well as for dogs with low serum
protein:creatinine ratio >2 suggests a glomerlevels of antithrombin ill ( <300A, of nom1al).

ular origin. If the sediment examination

In dogs with marked proteinuria and semm
eliminates inflanunatory urinary tract
albumin <2 g/dL, low-dose aspirin therapy
disease and hemorrhage as the source of

(2.5-5 mg/kg/day, PO) is appropriate, unless
proteinuria, then the degree of increase may
melena is present or gastlic ulceration is
help distinguish tubular proteinuria (typical
suspected. However, aspirin is bound to
ratio value of 0.5-2), glomerulonephritis
plasma proteins and is elin1inated via the

(typical ratio value of0.5-15), and glomerukidneys, so the lower end of the dosage lar amyloidosis (typical ratio value of0.5-40). rai1ge should be used in hypoalbuminemic However, substantial overlap exists in these
dogs. 4) Because proteinutia may promote
ranges, and a variety of glomerulopathies
interstitial fibrosis, treatinent to limit
such as focal segmental glomemlosclerosis
glomerular loss of protein is warranted and
in dogs have yet to be well characterized.

may include dietary protein restliction, n -3

Further, the ratio tends to be low in the
polyunsaturated fatty acid supplementation,
initial stages of a glomerulopathy, increases
and adnlinistration of an angiotensin-recepin severity as the disease progresses, and tor blocker ( eg, telmisartan 1 mg/kg/day, PO)

then decreases terminally as GFR falls to
or angiotensin-converting enzyme inhibitor
very low levels in late Stage 4 disease.

( eg, benazepril or enalapril, 0.5 mg/kg, PO,

Renal biopsy is required to detemline the
once daily in cats and bid in dogs). 5) Efforts
type of glomerular disease. Membranous
to reduce the magnitude and cons�quences
glomerulonephritis is reported most
of glomerular inunune complex deposition
frequently in cats; tl1ere is a roughly equal
should be considered, especially in animals
distribution of histologic findings in dogs,
with biopsy-confirmed glomerular
witl1 glomerular amyloidosis; focal segmental inflanm1ation and no known primary glomerulosclerosis; and membranous,
antigenic stin1ulus. Immunosuppressive
proliferative, and membranoproliferative
dmgs ( eg, mycophenolate, azathioprine,
glomerulonephritis all represented. The
cyclophosphainide, cyclosporine) can be
degree of proteinuria does not always
used in dogs with glomerulonephritis,
correlate with the severity of the histologic
although results are vaiiable. For ainyloidolesions or the degree of azotemia. Systemic sis, dimethylsulfoxide and colchicine have
hype1tension develops in an unusually large
been tlied, without consistent results.

proportion of anin1als with protein-losing

These anti-inflanunatory dmgs should be
glomerulonepluitis; tl1erefore, blood
adnlinistered only on a tlial basis with
pressure should be detemlined in all ailinlals
owner consent. Corticosteroids seem to be
with evidence of glomerular disease.

beneficial only in mild glomemlopathy; they

A careful search should be made for an
may worsen protei.nutia in other glorneminciting disease process. Abdominal and lopathies and should be avoided in animals
thoracic radiographs, ultrasonography, ai1d
witl1 ainyloidosis, because they are reported
specialized serologic tests can exclude
to enhance an1yloid deposition. 6) Maiufesvarious inflammatory, infectious, and tations of CKD should be monitored and
neoplastic diseases. In dogs with glomerulomanaged in accordance with the stage of nephritis, this includes tests for SLE ( eg,
disease (seep 1512).

antinuclear ai1tibody titer and LE prep) and
appropriate antigen or antibody screening

Prognosis: Although one study found that
tests for other infectious agents and
mean sutvival time of dogs witl1 glomerulo-

1520

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
nephritis was 87 days, the prognosis with
diagnosed by demonstrating increased
early diagnosis and appropriate therapy is
urinary fractional excretion of bicarbonate
much better. In a recent study of dogs with
when plasma bicarbonate levels are nom1al
glomerulonephritis, those receiving a
or decreased; this test is not practicable

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placebo medication swvived beyond the
in the clinical setting and diagnosis is
entire 6-mo duration of the study. The
presumptively based on history, signalprognosis for animals with amyloidosis is ment, and clinical pathology findings.

guarded but vaiiable, with reported mean

Therapy consists of oral administration of
survival times ranging from 49 days to 20 mo. an alkalinizing agent sufficient to maintain nom1al blood pH (1 mEq bicarbonate

RENAL TUBULAR DEFECTS
equivalentlkglclay for Type I and 1-6 mEq
bicarbonate equivalent/kg/day for Type II,

Renal Acidosis

PO). Therapy is more problematic in clogs

The fom1 of metabolic acidosis that occurs
with Type II renal tubular acidosis, because
in acute kidney injury and Stages 2-4 of
supplemental bicarbonate is readily lost in
chronic kidney disease, referred to as
the urine.

uremic acidosis, is due to reduced
urine-acidifying ability of diseased kidneys.

Fanconi Syndrome

In tffemic acidosis, although the ability of

Fanconi syndrome is a generalized proximal
individual tubular cells to reabsorb
tubulai· reabsorptive defect resulting in
bicarbonate and/or secrete hydrogen ions
excessive loss of many solutes in the wine.

may be normal, there is generally far less

It has been reported as an acquired
total cell mass present. Acid acctm1ulates
condition in clogs (chicken jerky treat
if the animal is under metabolic or dietary
ingestion, genta.nucin nephrotoxicosis,
acid pressure, which is common in
and an icliopathic form) and in a heritable
carnivores. This is particularly problematic
forn1 in a variety of breeds (most notably
in cats, which are often fed acidifying

Basenjis), in which it develops gradually
maintenance diets.

in adults of both sexes. There is excessive

Rare renal tubular defects in dogs and
urinary loss of glucose, sodiwn, potassium,
cats may result in hyperchloremic
phosphorus, mic acid, bicarbonate,
metabolic acidosis, referred to as renal
albumin, and anuno acids. Blood glucose
tubular acidosis. Two types of renal
concentrations are nom1al. Serum
tubular acidosis have been described in
electrolytes are normal eai·ly in the disease,
dogs and one in cats. In Type I ( distal),
but hypophosphatemia, hypokalemia, and
the ability of the distal tubule to secrete
metabolic acidosis are seen in the later
hydrogen ions against a concentration
stages.

gradient is defective; in Type II (proximal),

Clinical signs include polyclipsia,
the ability to reabsorb bicarbonate in the
polyuria, and weight loss. Signs of uremia
proxin1al tubule is reduced. Type I has been
may be present if the animal is in Stage III
reported in both species; Type II has also
or IV chronic kidney disease. Diagnosis is
been described in clogs in conjunction with
based on documentation of increased
other proximal tubular defects in acquired
urinary fractional excretion of glucose,

(gentanucin nephrotoxicosis and an
sodium, potassiun1, phosphorus, and
idiopathic fom1) and heritable (Fanconi
bicarbonate in the presence of normal
syndrome, seep 1520) forms.

plasma concentrations. Hypbalbununuria is

Type I renal tubular acidosis has been
likely to be present, because tl1e proximal
associated with dernineralization of the
tubule normally reabsorbs the small a!llow1t
skeleton ( clue to buffe1ing of excess
of albunun that traverses the glomerular
hydrogen ions) and nephrolitluasis ( due to
filtration barrier. Differential diagnoses
hypercalciuriafrom bone resorption) in
include simple renal glucosuria and chronic
dogs. Diagnosis is based on the presence of
kidney disease from other causes. The
hyperchloremic metabolic acidosis witl1 a
microscopic renal changes in the heritable
urinary pH that is inappropriately high for
fonn are not remarkable in tl1e early stages
the degree of systemic acidosis in tl1e
but progress to nonspecific findings
absence of bacte1ial urease modification of
characteristic of chronic kidney disease.

urine. Failure to produce acid urine in the

A genetic marker has been developed. A
face of metabolic acidosis or after oral
treatment regin1en to reverse the tubular
an1rnoniurn chloride loading is diagnostic;
defect has not been clesclibecl. The histohowever, tlus challenge test is contraindilogic appearance of tile acquired fonns of cated in animals that are already severely

Fanconi syndrome vary, depending on the
aciclotic. Type II renal tubular acidosis is
cause.

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1521

Oral supplementation of sodium chloride
develop. Hydroureter commonly develops

(5-10 mg/kg/day, PO), potassium (potaswhen the obstruction is located lower in the sium citrate 10-30 mg/kg/day, PO), and
tract. Increased hydrostatic pressure results
alkali (sodium bicarbonate 10-30 mg/kg/
in atrophy of functional renal parenchyma.

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day, PO) is indicated if the corresponding

The pseudodiverticula of the renal pelvis
serum concentration is low. Dogs with acute disappear first; later, even the cortex may or chronic kidney disease should be treated
atrophy. The affected kidneys eventually
symptomatically as appropriate. The
become grossly enlarged, functionless sacs,
heritable disease is slowly progressive
filled with mine or serous fluid that may
despite therapy and usually results in death
harbor bacteria.

from uremia.

Clinical Findings: Animals with urethral

Renal Glucosuria
obstruction frequently exhibit pollakiuria,

This is usually a congenital defect in
stranguria, and hematuria; abdominal pain
proximal tubular handling of glucose that
may be marked. Signs of uremia develop
results in glucosuria despite nonnal blood
rapidly and include vomiting, dehydration,
glucose concentration. Affected animals
hypothermia, and severe depression. The
may be asymptomatic, have polydipsia
bladder is distended and painful on
and polyuria, or have recurrent or severe
palpation, and a urethral catheter cannot
urinary tract infections due to bacterial
be readily passed. Bradycardia or cardiac
colonization in the presence of glucose.

arrhythmias due to hyperkalemia may be

Diagnosis is made by demonstrating
present, particularly if plasma potassiun1
persistent glucosuria despite a normal
is > 7 mEq/L. Because compensatory
blood glucose concentration and by
hypertrophy of the nonaffected kidney
identifying no other renal reabsorptive
results in a nonazotemic state, unilateral
abnormalities. This disease is so uncomureteral obstruction commonly is undiagmonly recognized that little is known about nosed, unless the animal has accompanying
its biologic behavior. The general consensus renal disease or the enlarged, hydroneis that it is not progressive and does not phrotic kidney is palpated during physical
require treatment, except that some animals examination and/or seen on radiologic or with heritable Fanconi syndrome may
ultrasonographic imaging studies.

initially exhibit glucosuria as the only
clinically apparent renal reabsorptive

Diagnosis: The history, clinical signs,
defect.

and physical examination usually provide
a straightforward diagnosis of urethral
obstruction. Ureteral obstruction should

OBSTRUCTIVE UROPATHY
be suspected in any acutely uremic cat,
including those with a history of chronic

Even though the kidneys would otherwise
kidney disease. Excretory urography or
be able to function normally, obstruction of
abdominal ultrasonography are necessary
urine flow at any point below the level of the to establish a diagnosis in animals with kidneys leads to accumulation of metabolic
bilateral or unilateral ureteral obstruction.

wastes and postrenal azotemia/uremia.

Serum potassium levels should be

Obstruction of the urethra by uroliths in
detennined immediately in animals with
dogs and by matrix-crystalline plugs in
cardiac an·hythmias. An ECG can provide
young male cats and obstruction of a ureter
presumptive evidence of hyperkalemia
by a urolith in geriatric cats are the three

(bra.dycardia; tall, peaked T waves;
most common causes, although uroliths,
increased PR interval; widened QRS
tumors, or blood clots may obstruct the
complex; atrial standstill) if laboratory
ureters ( or urethra) in either species.

results are delayed.

Hydronephrosis is characterized by
dilatation of the renal pelvis as the result of

Treatment: The urethral obstruction
partial or complete obstruction of outflow
should be relieved (seep 1525). Fluids given of urine from one or both kidneys. When

IV improve renal function and correct
the obstruction is acute, complete, and
electrolyte and acid-base abnormalities.

bilateral, morphologic changes in the

Normal saline is preferred but not required in
kidneys are less extensive, because the
hyperkalemic animals. Unless the animal is
period of survival is short. In unilateral
markedly hyperkalemic (serum potassium
or partial obstruction, the animal often

> 7 mEqlL ), has cardiac arrhythmias, or is
survives long enough for severe pressure
known to have preexisting kidney disease,
atrophy of the renal parenchyma and cystic
it is often best to avoid overcorrection by
enlargement of the affected kidney to
allowing plasma potassium and acid-base

1522

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
balance to return toward nonnal via
located at one pole of the kidney, and well
restoration of renal excretory function for
demarcated. Size varies from microscopic to

12 lu· before administering therapy specifiseveral times that of the nom1al kidney, and cally intended to correct these abnom1alities.

color may be yellow, white, or gray. Renal
ln anin1als with severe hyperkalemia and
ca.i-cinomas metastasize early to various

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cardiac a.iThytlunias, bicarbonate (0.5 mEq/
organs; the opposite kidney, lungs, liver, and
kg, given slowly IV over 5 min) or regular
adrenals a.i·e involved most commonly.

insulin and dextrose infusions can be given to

Nephroblastomas ( embryonal nephroma,
drive potassium intracellula.i-ly. Because of a

Wilms' tumor) arise from vestigial embryonic
postobstructive diuresis that lasts for 1-5
tissue. They are seen in young aninlals and,
days, hypokalemia and/or dehydration are
in dogs, are most commonly diagnosed at < l
often seen within 24-48 hr after correction of
yr of age. There is no breed predilection.

uretlu-al obstrnction. Plasma electrolytes,

Males a.i·e affected twice as conu11only as
body weight, urine output, hematocrit, and
females. Neplu-oblastomas are usually
plasma total solids should be monitored daily, urillateral but are occasionally bilateral. They with the type and quantity of fluid adminiscan grow to inm1ense size; it is not uncomtered acljusted approp1iately.

mon to have virtually the entire abdomen

Surgery is often necessary to conect
occupied by tumor. Metastasis may occur
complete ureteral obstrnction. When
to regional lymph nodes, liver, a.i1d lungs.

possible, the obstruction should be

Transitional cell ca.i·cinomas arise from
removed to reestablish urine flow. In some
transitional epitheliwn of the renal pelvis,
cases, tu-eteroliths will pass Uuough the
ureter, bladder, or urethra (seep 1523).

ureters, eliminating the need for surgery.

Other primary maligna.i1t renal neoplasms

This may require partial ureteral resection
a.i·e w1common and include hemangiosarcoand reimplantation, particularly in cats, mas, fibrosa.i·comas, leiomyosarcomas, and
which have very small and friable ureters.

squan1ous cell carcinomas.

In some cases, unilateral nephrectomy

The kidneys are a conunon site of
may be required, but a kidney should not
metastatic or multicentJic neoplasms.

be removed without clear evidence that the

Metastatic lesions may be urillateral or
contralateral kidney is capable of sustaining bilateral. Lyrnphosarcoma is the most life. Preferred evidence includes the
conunon multicentJic tumor involving the
estimation ofGFR in the contralateral
kidneys. As many as 50% of dogs and cats
kidney but could alternatively be based on
with lyrnphosarcoma have renal lesions and,
the following criteria: nom1al renal size,
in some cases, only the kidneys or kidneys
shape, and consistency on ultrasonography;
and brain are affected. Renal involvement
presence of nom1al vascular and excretory
is usually multifocal or diffuse, interstitial,
phases on excretory-urography; normal
a.i1d bilateral, and results in large, irregular
renal ultrasonographic exan1ination; and
kidneys. Lyrnphosarcoma in cats frequently
normal renal biopsy.

is associated with infection by feline
leukemia virus.

NEOPLASIA

Clinical Findings: Signs are nonspecific

Neoplasms of the Kidney
and may include weight loss, a.i1orexia,
depression, and fever. Bilateral neoplasms

Neoplasms of the kidney are uncommon
may unconunonly destJuy sufficient renal
and represent ---0.5%---1. 7% of all neoplasms
tissue to cause chronic kidney disease and
in dogs. Benign neoplasms are uncommon,
associated signs of uremia. Astute owners
usually incidental findings at necropsy, and
may notice "lwnps" in their animal's
generally of little clinical significance.

abdomen or abdominal enlargement.

Adenomas, lipomas, fibromas, and

Persistent hematuria, usually microscopic,
papillomas have been reported.

may occm. Rarely, renal tumors may

Primary malignant renal neoplasms
produce excessive erytluopoietin, which

( except nephroblastomas) are most
results in erythrocythemia (seep 43).

conrn1on in middle-aged to older animals. No
breed predilection has been found, except

Diagnosis: History and clinical signs may
for heritable predilection for the developindicate a mass in t11e area of the kidneys or ment of bilateral, multifocaJ cystoadenocarrenomegaly, which can be confinned by cinomas in Gennan Shepherds, generally
ultJ·asonography or radiography, although
between 5---11 yr of age. The most conrn1on
an excretory mogran1 or renal arteriogra.in
p1imary malignant renal neoplasm is
may be required. Radiographs of the tl1orax
carcinoma, which originates from the renal
may reveal metastatic disease. Neoplastic
tubular epithelium. Usually, it is urLilateraJ,
cells occasionally can be found in the urine

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1523
sediment. A tissue sample suitable for a
may be linked to exposure to herbicides and
diagnosis may be obtained via catheterizaolder-generation insecticides. Transitional tion. Cystoscopic biopsy can be an effective
cell tmnors are highly invasive and
method to obtain a diagnostic sample in
metastasize frequently, most commonly
dogs with transitional cell carcinoma of the
to the regional lymph nodes and lungs.

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bladder and urethra, especially females.

Ureteral and bladder neoplasms can cause

Percutaneous needle aspiration and
ch.ronic obstruction to urine flow with
cytologic examination may be sufficient for
secondary hyd.ronephrosis. Urethral tmnors
the diagnosis of lyrnphosa.rcoma in cats and
are more likely to cause acute obstructive
dogs, particularly when there is diffuse
uropathy. Intractable secondary bacterial
involvement or with ultrasonographic
urinary tract infections are commonly
guidance when multifocal disease occurs.

associated with neoplasms of the bladder

Histologic examination of tissue obtained
and urethra.

by cystoscopy, needle biopsy, or surgical
wedge biopsy is often necessary to

Clinical Findings: Hematuria, dysmia,
detem1ine the type of tumor.

strangmia, and pollakiuria are the most
common signs. Animals with ureteral

Treatment: illtrasound-guided endoobstruction and wlilateral hydronephrosis scopic diode laser ablation holds promise
may show signs of abdominal pain and
as a palliative treatment for dogs with
have a palpable, enlarged kidney. Signs of
transitional cell carcinoma of the urinary
uremia may be apparent in anin1als with
tract. Otherwise, treatment of all renal
bilateral ureteral obstruction and hydroneoplasms except lyrnphosarcoma involves nephrosis or with u.rethral obstruction.

su.rgical removal; unilateral nephrectomy is

The bladder wall may be thickened, and a
usually required. Lyrnphosarcoma is best
cord-like urethra or uretlu·al mass( es) may
managed by combination chemotherapy
be palpable rectally.

(seep 40). Chemotherapy is generally
ineffective against renal tmnors other
than lymphosarcoma.

Diagnosis: History and clinical signs are
highly suggestive of lower urinary tract
disease in anin1als witJ1 tumors of the

Neoplasms of the Lower Urinary
bladder or urethra Urinalysis frequently

Tract
reveals hematuria, and there may be

Neoplasms of the ureters, bladder, and
evidence of secondary infection. Chronic,
urethra are unconrn10n in dogs and rare in
uncomplicated urinary tract infections must
cats. The low incidence in cats may be due
be differentiated from tl10se associated with
to a difference in tryptophan metabolism
neoplasms. Neoplastic cells may be.found in
that results in low urinary concentrations of
tl1e sediment, particularly with transitional
carcinogenic tryptophan metabolites. The
cell carcinomas. For bladder tumors in dogs,
mean age of affected dogs and cats is 9 yr.

tl1e veterinary bladder tmnor antigen test

In the lower urinary tract, primary
may be helpful, although false-positives do
neoplasms are more likely to be malignant
occur. A cystourethrograrn, retrograde
than benign. Papillomas, leiomyomas,
urethrogra.rn, or ultrasonography is generally
fibromas, neurofibromas, hemangiomas,
necessary to detennine the location and
rhabdomyomas, and myxomas are found
infrequently.

Among primary malignant neoplasms
of tl1e lower urinary tract, transitional cell
carcinomas are diagnosed most frequently
in both species. Squan10us cell carcinomas,
adenocarcinomas, fibrosarcomas,
leiomyosarcomas, rhabdomyosa.rcomas,
hemangiosarcomas, and osteosarcomas
also are found. Transitional cell carcinomas
may be solitary or multiple papillary-like
projections from the mucosa or may
develop as a diffuse in.filtration of the ureter,
bladder, prostate, and/or urethra. Cystic
transitional cell tmnors are more common
in certain breeds of dogs, particularly

Scottish Terriers, have been associated witl1 Transitional cell carcinoma in trigone area of canine bladder, contrast radiograph.

prior therapy with cyclophosphamide, and

Courtesy
of Ontario Veterinary College.

1524

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
to deficiency of sex hormones in neutered
animals, particularly female dogs, and is
referred to as hom10nal-responsive urethral
incompetence. Idiopathic urethral sphincter

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incompetence also is seen. Urinary
incontinence associated with anatomic
defects may be detected in aninlals at an
early age. For example, an animal with a
unilateral congenital ectopic ureter may
void normally but "dribble" urine intemlittently, whereas animals with bilateral ectopic ureters are less likely to void

Transitional cell carcinoma in trigone area of
normally. Paradoxical urinary incontinence
canine bladder, pneumocystogram. Courtesy
may develop when there is a partial
of Ontario Veterinary College.

obstruction of the urethra leading to
bladder distention and overflow incontinence.

Failure of normal voiding is characterized
extent of the tumor. Biopsy of the tumor is
by frequent attempts to urinate with
required for definitive diagnosis.

stranguria and passage of only small
amounts of urine. Inability to urinate can

Treatment: Excision of the tumor, if
be due to mechanical obstruction of the
possible, is the most beneficial therapy.

urethra by calculi, neoplasms, or strictures;

Transitional cell carcinomas are frequently
detrusor atony from overdistention of the
located at the trigone of the bladder or in
bladder; or neurologic disease. Animals
the urethra and may necessitate radical
with abnormalities of the voiding phase
reconstructive surgery of the lower urinary
may develop overflow incontinence due to
tract. Prognosis is poor for these animals,
dribbling of urine associated with bladder
even with surgery, because recurrence and
overdistention.

metastasis occur rapidly. Radiation therapy

Neurologic causes of micturition
and/or chemotherapy with piroxicam,
disorders can be categorized as upper
cisplatin, doxorubicin, vinblastine,

(UMN) or lower motor neuron (LMN)

chlorambucil, or mitoxantrone will
lesions. Lesions in the sacral spinal cord,
generally prolong the life of affected
pelvic nerve, and detrusor atony lead to
anin1als. Dogs with transitional cell

LMN signs, which are often characterized
carcinoma, including those being treated for by a distended, easily expressed bladder.

the tumor, are predisposed to development

Dysautonomia in cats is a multisystemic
of bacterial urinary tract infections, and roudisease characterized by widespread tine urine cultures are indicated.

disruption of autonomic system functions,
including urinary incontinence ofLMN

DISORDERS OF MICTURITION
origin. Damage to the thoracolumbar spinal
cord or disease of the cerebrum, cerebel

Disorders of micturition result from a
lwn, or brain stem can lead to UMN signs,
dysfunction in the storage or voiding of
characterized by a distended bladder that is
urine and may be neurogenic or non-neurodifficult to express. Another neurologic genic in origin. Urinary incontinence is the
cause of inability to urinate is functional
failure of voluntary control of micturition,
obstruction ( detrusor-sphincter reflex
with constant or intermittent unconscious
dyssynergia), which occurs when there is
passage of urine. Incontinent aninlals may
incoordination of the normal micturition
leave a pool of urine where they have been
reflex; this is believed to result from
lying or may dtibble urine while walking.

overdischarge of syn1pathetic nerve

The coat around the vulva or prepuce may
inlpulses to the urethral sphincter, resulting
be wet, and perivulvar or peripreputial
in a failure of urethral relaxation during
dermatitis can result from urine scalding.

detrusor contraction. Animals with

Failure of urine storage is characterized
neurogenic incontinence may leak urine
by inappropriate leakage of urine due to

(LMN) and/or develop overflow incontifailure of bladder relaxation, urethral nence due to dribbling of wine associated
incompetence, anatomic defects, or
with bladder overdistension (any neurooverflow of stored urine. Urge incontinence genic cause).

is seen with detrusor irritability, usually
associated with cystitis. The most common

Diagnosis: Clinical signs are usually
non-neurogenic incontinence is attributed
suggestive of a micturition disorder. The his-

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1525
tory should include age of onset, whether
atony. Functional obstruction is treated
the animal is intact or neutered, age at
with sympatholytic drngs ( eg, phenoxybenneutering, current medication, and history zan1ine, 2.5-10 mg, 1-3 tin1es/day);
of previous winary tract disorders. A
cholinergic drngs may also be necessary.

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thorough physical and neurologic examina

Complete mechanical obstrnction of the
tion is indicated, and the act of voiding
urethra is a medical emergency and should
should be observed, including estimation
be relieved by catheterization and
of initial and final bladder volume.

retropulsion of the obstrncting material into

Animals with LMN lesions or an atonic
the bladder or by surgery. Animals with
bladder have a large, distended bladder that
detrnsor atony from overdistention but
can be expressed witl1 minin1al pressure.

without neurologic lesions benefit from

Animals with mechanical or functional
decompression of the bladder by placement
obstruction or with spinal lesions causing
of an indwelling urinru-y catl1eter for 3-7

UMN signs also have a large distended
days. This may be done continuously or
bladder, but urine cannot be readily
intemuttently. Those with neurogenic a.tony,
expressed. Caution must be exercised when
which usually does not respond to medical
attempting to express urine from these
management, may require manual
animals to avoid ruptming the bladder. Plain expression of the bladder or catheterization or contrast radiography, cystoscopy, or
several times daily.

ultrasonography are necessary to deterrnine
the type and location of mechanical

UROLITHIASIS
obstruction.

Anin1als witl1 functional obstrnction

Some mineral solutes precipitate to form

(reflex dyssynergia) generally exhibit
crystals in mine; these crystals may
pollakiwia with intenupted mine stream,
aggregate and grow to macroscopic size, at
distended urinary bladder, no identifiable
which time they are known as uroliths
structural cause of obstruction, and

( calculi or stones). Uroliths generally
overflow incontinence; the neurologic
contain an organic matrix that is believed
examination is generally abnormal. A
to vary minimally an10ng uroliths and tl1at
catheter can easily be passed into the
constitutes -2o/o-100Ai of the stone's chemical
bladder in anin1als with fw1ctional
composition. The remaining 900/o-98% of the
obstruction but will not pass in anin1als
urolifu is composed of minerals th� vary
wiili mechanical obstruction.

depending on the type of urolith. Urolithi
asis is a general tem1 referring to stones

Treatment: Accurate diagnosis or
located anywhere within the urinru-y tract.

localization of the lesion is essential for

Uroliths can develop in the kidney, ureter,
appropriate pharmacologic management.

bladder, or urethra and are referred to as

Animals with honnonal incontinence can be nephroliths, ureteroliths, urocystoliths, treated wiili the appropriate sex h01mone
and urethrolitl1s, respectively.

( eg, diethylstilbestrol in females and

Uroliilis in all animal species are
testosterone in males). The dosage should
composed of -10 different minerals.

be adjusted to the minimmn required to

Identification of fue minerals in uroliths by
maintain continence. Diethylstilbestrol
qualitative analysis is unreliable. The type of
may be difficult to obtain. Alternatively, an
minerals in uroliths can be readily identified
cx-adrenergic agonist drng ( eg, phenylproby optical crystallography, irLfrared panolamine, 2-4 mg/kg/day in divided
spectroscopy, and/or x-ray diffraction.

doses) can be given to anin1als with urethral

Minerals f0tmd in uroliths have a chemical
incompetence alone or in combination
name and often a nu.neral or crystal name
wiili an estrogenic compound. Alfuough

(see TABLE 5). Vruiation in urine characterisephedrine is another cx-agonist shown to tics over tin1e can result in more than one
be effective in tl1e treatment of tuinary
crystal type within a single urolith. In such
incontinence in female dogs, its use is more
instru1ces, the urolith core corresponds to
often associated with adverse effects of
conditions fuat were present when the
anxiety and excitability. Pseudoephedrine
urolith initially formed, and tl1e outer layers
is apparently not effective for this purpose.

correspond to more recent conditions.

Urge incontinence ( detrnsor instability) is

Mechanisms involved in stone formation
treated with anticholinergic drngs such as
are incompletely understood in dogs and
oxybutin chloride (0.5 mg/kg/day, PO) or
cats. However, three main contributing
propantheline ( dogs <20 kg, 7.5 mg/day;
factors are 1) matrix-the inorganic protein
dogs >20 kg, 15 mg/day; cats, 7.5 mg every
core may facilitate initial urolith formation,

72 hr). Cholinergic drngs such as bethane2) crystallization inhibitors-organic and chol are used in anin1als wifu detrusor
inorganic crystallization inhibitors may be

1526

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

•hi§f ii UROLITH NAMES

Mineral Name

Chemical Formula

Chemical Name

Struvite

MgNH4PO, • 6H20

Magnesium ammonium phosphate

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hexahydrate

Whewellite

CaC20, • H20

Calcium oxalate monohydrate

Weddellite

CaC20, • 2H20

Calcium oxalate dihydrate

Hydroxyapatite

Ca10(PO,MOH)2

Calcium phosphate (hydroxyl form)

Urate

C5H4N4Q3

Urate

Ammonium urate

NH, • C5H4N403

Ammonium urate

Sodium urate

Na• C5H4N403 x H20

Sodium urate monohydrate

Cystine

(SCH2CHNH2COOH)2

Cystine

Silica

Si02

Silica

Xanthine

C5H4N402

Xanthine
lacking or dysfunctional in animals with
a uremic crisis in cats witl1 previously
uroliths, and 3) pr·ecipitation crystallization
compensated clu·onic renal failure. Because
factors-a complex relationship among
clinical signs of renal dysfunction are
urine solutes and other chemical factors in
generally not apparent until two-thirds or
the urine can lead to conditions favoring
more of total functional renal parenchyrna
crystallization. Regardless of the underlying
is lost, clinical signs may not be seen except
mechanism(s ), uroliths are not produced
in the following situations: 1) both ureters
unless sufficiently high urine concentraare obstructed, 2) there is contralateral tions of urolith-forming constituents exist
chronic kidney disease, or 3) a renal
and transit time of crystals within the
infection develops. Unilateral ureterolitl1s
urinary tract is prolonged. For selected
may be identified serendipitously during
stones (eg, struvite, cystine, urate), other
abdominal imaging studies or surgery.

favorable conditions ( eg, proper pH) for

Abdominal palpation can help detect
crystallization must also exist. These
urocystoliths; the bladder wall may be
criteria can be affected by urinary tract
thickened, and a grating sensation may be
infection, diet, intestinal absorption, urine
felt when the bladder is palpated. Although
volume, frequency of urination, therapeutic
palpation may reveal a single large urolith
agents, and genetics.

or multiple uroliths by their crepitation, it

Clinical signs associated witb urolithiasis
cannot dependably identify all animals with
are seldom caused by microscopic crystals.

urolitl1s; urethral calculi may be detected by

However, fonnation of macroscopic
rectal palpation or located by passing a
uroliths in the lower urinary tract that
catheter. Because multiple w·oliths may be
interfere with the flow of urine and/or
present throughout the urinary tract, a
irritate the mucosal surface often results
complete radiographic exan1ination of the
in dysuria, hematuria, and stranguria.

tract is indicated; radiodense calculi >3 mm

Nephroliths often are asymptomatic unless
in dian1eter are usually visible on radiopyelonephritis exists concurrently or they graphs. Urate, and occasionally cystine,
pass into the ureter. Ureteral obstruction
urolitl1s may be radiolucent, requiring
may produce signs of vomiting, letl1argy,
contrast radiography or ultrasonography
and/or flank and renal pain, particularly
to confirm their presence. Urinalysis,
if there is acute total obstruction with
including identification of crystals on
distention of the renal capsule. The only
microscopic exan1ination of fresh, warm
clinical sign associated with unilateral
urine and bacterial culture and sensitivity
urethroliths may be pain, which can be
testing, is a critical pait of tl1e evaluation
difficult to detect in dogs and cats. If these
and may help determine the type of urolith
initial signs of ureteral obstruction do not
present. Ultrasonography and cystoscopy
lead to a diagnosis, unilateral ureteral
may also be useful.

obstruction may result in hydronephrosis
with loss of function of the ipsilateral

Urethral Obstruction: Urethral
kidney. Ureteroliths may also precipitate
obstruction is common in male dogs

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1527
and cats. It may occur suddenly or may

Canine Urolithiasis
develop throughout days or weeks. Initially,
the animal may frequently attempt to

The most common canine uroliths are

U1inate and produce only a fine stream, a
magnesium ammonium phosphate, calcium
few drops, or nothing. Animals may also
oxalate, or urate; less common uroliths

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exhibit extreme pain manifested by crying
include cystine, silica, calcium phosphate,
out when attempting to urinate. Complete
and xanthine. While general management
obstruction causes uremia within 36--48 hr,
includes surgical removal and medical
which leads to depression, anorexia,
management, the appropriate treatment
vomiting, diarrhea, dehydration, coma, and
protocol depends on the location of the
death within -72 hr. Urethral obstruction is
urolith and its chemical composition,
an emergency condition, and treatment
as well as on patient-specific factors.

should begin in1mediately.

N ephrolithiasis is generally not associated

If the bladder is intact, it is distended,
with an increase in the rate of progression
hard, and painful; care should be used when
of kidney injury; thus, it is recommended
palpating the bladder to avoid iatrogenic
that aninlals with nephrolithiasis be
rupture. If the bladder has ruptured, it
managed without surgery in most cases.

cannot be palpated and urine can sometinles, but not always, be obtained from the Struvite Stones: The most conunon
abdominal cavity by paracentesis. Animals
urinary stones in dogs are composed of
with spontaneous bladder rupture may
struvite. The mineral composition is mostly
appear temporarily improved because the
struvite (MgNH4P04 • 6H20), but frequently,
pain associated with bladder distention has
small an1ounts of carbonate-apatite and
been relieved; however, peritonitis and
ammoniU1n urate are present. In most cases,
absorption of uremic toxins and potassium
struvite uroliths form in association with
occur rapidly and lead to depression,
urinary tract infections with ureas e -producabdominal distention, cardiac arrhythmias, ing Staphylococcus or Proteus spp.

and death.

Although tl1ey are frequent in cats, sterile

Hyperkalemia and metabolic acidosis
struvite uroliths rarely fom1 in dogs. They
are life-tlireatening complications of urehave been detected in a family of English thral obstruction. An ECG (to record

Cocker Spaniels, suggesting a ;enetic
cardiac rhythm and rate) and a serum
predisposition.

potassium are indicated. Initial emergency

Medical management involves dissolucare involves inlrnediate relief of obstruction and prevention of stone fonnation. In tion by catheterization and fluid therapy
both instances, the aim of treatment is to
with normal saline. Occasionally, an
reduce the concentrations of NH..+, Mg2+,
obstruction at tile external urethral orifice
and P0,-3 in urine. For dissolution, urin�
can be dislodged by gentle massage.

should be extremely undersaturated for

Sometin1es, when a portion of the uretilfa is
struvite; for prevention, the degree of
dilated with fluid under pressure and then
struvite saturation should be sufficiently
suddenly released, uretilfal calculi can be
low to make crystallization unlikely. The
flushed out. The urolith nearly always can
choice between surgery, lithotripsy, and
be flushed back into the bladder by using
medical treatment may not be easy. Owner
the largest catheter that can be easily
compliance, the animal's acceptance of the
passed to the calculus, occluding the distal
diet, availability of lithotripsy, practice
end of the uretilfal lumen around the
philosophy, and knowledge of the indicacatheter, and infusing a sterile mixture of tions and contraindications are necessary
equal parts of isotonic saline solution and
to make a decision. If stone dissolution is
an aqueous lubricant. If the uretilfolith
prolonged or fails, it may be more costly
cannot be flushed back into the bladder,
than surgical treatment. Surgical removal
a uretilfotomy should be performed to
of uroliths is often incomplete, with small,
remove the obstructing stone(s). Depending hidden uroliths often inadvertently left in on the clinical circumstances, the uretilfotthe urinary tract serving as a nidus for omy site may be sutured or a permanent
recurrence.

urethrostomy created. Calculi flushed back

Before beginning stone dissolution by
into the bladder should be removed by
medical therapy, a physical exan1ination,
cystotomy to prevent recurrence, although

CBC, serun1 chemistry profile, U1inalysis,
in some cases they can be dissolved. The
urine culture and sensitivity, abdominal
stone should be sent for quantitative
radiographs to docun1ent stone size, and
analysis, with the animal managed
blood pressure measurement (if possible)

medically to prevent stone recurrence
should be perfom1ed. Contraindications
based on the results.

to stone dissolution include heart failure,

1528

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
edema, ascites, pleural effusion, hype1tenalthough failure could also result from poor sion, hepatic failure, renal failure, and
treatment compliance. Renal stones tend to
hypoalbuminemia. However, chronic
dissolve more slowly than bladder stones.

kidney disease is not always a contraindica

The recurrence rate after surgical

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tion for dissolution of struvite nephroliths.

treatment of struvite uroliths has been

Dissolution Protocol: While the use of
reported to be -20%-25%, witl1 most
urinary acidification to reduce urine pH
recurrences within 1 yr. When surge1y is
to <6 and other individualized dietary
perfonned to remove multiple small struvite
maneuvers may prove effective, a few
calculi, removing all stone material is often
commercially available diets that are
difficult. ln such cases, a4-wk dissolution
generally nutritionally balanced promote
protocol starting at the tin1e of suture
struvite stone dissolution. Dogs fed these
removal aids in preventing recurrence due
rations generally have reduced intake of
to residual crystalline material. Once the
protein, phosphate, and magnesium and
urinary tract is free of stones, prevention
a high intake of sodium. This results in
strategies are much more likely to be
osmotic diuresis, reduced daily urea output,
successful.

and enhanced urine volume. The low

Prevention Protocol: The key to
urinary urea concentration is one of the
prevention of recurrence in animals with a
most irnpo1tant features of such diets and
struvite stone associated with infection is to
also reduces ammonia production by the
achieve and maintain sterile urine. Routine
action of urease-producing bacteria. No
testing of wine pH by tl1e owner is
other food, including treats, should be
important. If fresh urine is alkaline, a
fed, and adequate fresh water should be
urinalysis and culture should be done, with
available at all times.

the dog treated appropriately if an infection

Urease-producing urinary tract infections
is present.

must be treated. The choice of antibacterial

Once stone dissolution is completed, a
should be based on sensitivity testing when
prevention program can be considered. The
possible. MostStaphylococcus and Proteus aim is to prevent urinaiy tract infections
infections are sensitive to levels of
witl1 urease-producing microbes. The
an1oxicillin or ampicillin achieved in the
concentration of major struvite solutes in
urine of healthy dogs. A urease inhibitor
wine should also be reduced. A conunercan be given but is not usually necessary.

cially available diet may be fed to lower

Concurrent treatment with a urease
minary phosphate and magnesium and to
inhibitor such as acetohydroxamic acid
maintain an acidic urine. Urease-producing
enhances the rate of struvite stone
infections should be elinlinated, after which
dissolution, particularly when antibiotic
owners should regularly check the pH of the
resistance precludes effective antibacterial
first voided urine in the morning after an
sterilization of the wine. A reasonably safe
overnight fast; in most dogs on a normal
dose of acetohydroxanlic acid appears to
diet, the urine will be acidic. Checking urine
be 12.5 mg/kg, PO, bid. A reversible, mild
pH weekly is sufficient.

hemolytic anemia has been see!\ in dogs
given higher dosages.

Calcium Oxalate Stones: CalciW11

After -4 wk of treatment, a physical
oxalate uroliths have been increasing in
exanlination, serum chenlistry profile,
frequency in dogs. Altl1ough_they may
urinalysis, and abdonlinal radiographs or
develop in any breed, Miniature Schnauzers,
ultrasonography should be repeated. The

Lhasa Apsos, Yorkshire Teniers, Bichon
stone dissolution protocol should be discon

Frises, Shil1 Tzus, and Miniature Poodles
tinued if severe adverse effects develop,
may be preclisposed. Most affected dogs
although a mild degree of hypoalbuminenlia
ai·e 2-10 yr old. Hypercalcilllia leading to
is to be expected and can be tolerated. With
calcium oxalate stone fom1ation can result
good compliance, the following results can
from increased renal clearance of calciW11
be anticipated: urine pH <6.5, urine specific
due to excessive intestinal absorption of
gravity <1.025, serum urea <10 mg/dL. The
calcium (absorptive hypercalcituia),
radiographic stone size should be compared impaired renal conservation of calcium with the size on previous radiographs.

(renal leak hypercalcilllfa), or excessive

Routine testing should be repeated every
skeletal mobilization of calcium (resorptive

4 wk Wltil 4 wk after the stone is no longer
hypercalciuria).

visible radiographically; tllis generally takes

Absorptive hypercalciuria is characte1°

8-12 wk but may take as long as 20 wk.

ized by increased urine calciW11 excretion,

Stones that fail to reduce in size after 8 wk
n01mal serum calcium concentration, and
of treatment are probably not composed of
n01mal or low se!'Wl1 parath01mone
struvite and should be treated another way,
concentration. Because absorptive

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1529
hypercalciuria depends on dietary calcium,
nucleic acid metabolites as relatively
the amount of calcium excreted in the urine
insoluble urate. The biologic mechanism
during fasting is normal or significantly
responsible for decreased hepatic
reduced when compared with nonfasting
conversion of urate to allantoin lies not in

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levels. Renal leak hypercalciuria has been
reduced uricase activity but in reduced
recognized in dogs less frequently than
hepatic transport of urate; the rate of urate
absorptive hypercalciuria. In dogs, renal
hepatic transport is approximately tlrree
leak hypercalciuria is characterized by
times faster in breeds other than Dalmanormal serum calcitun concentration, tians. The net result is that only 30%-400/o of
increased urine calcium excretion, and
urate is converted to allantoin in Dalmatians
increased serum parathom1one concentracompared with -900/o in other breeds.

tion. During fasting, these dogs do not show

Dalmatians fed a diet high in anin1al
a decline in urinary calcium loss. The
protein excrete a net acid load in the urine,
underlying cause of renal leak hypercaland urinary ammonium output is subseciuria in dogs is not known. Resorptive quently increased. The combined high
hypercalciuria is characterized by excessive concentration of ammoniun1 and urate in filtration and excretion of calcitun in urine
wine increases the risk of formation of
as a result of hypercalcemia. Hypercalcemic ammonium urate stones. The excretion of disorders have been associated only
acidic metabolites of an animal protein diet
infrequently with calcium oxalate uroliths
is believed to be important in this process,
in dogs.

because urinary aim11oniun1 excretion is

Routine laboratory detemiinations
enhanced and aimnonium urate is insoluble.

should include serum calcium, phosphate,

Urate output has been reported to be the
total C02, and chloride to eliminate the
sai11e in Dalmatiai1s that form stones and in
possibility of hyperparatl1yroidism and
those that do not, although in some studies
renal tubular acidosis. Dissolution of
tl1e methods used to detemline urine uric
calcium oxalate stones by medical means
acid concentrations were llllreliable. In
has not currently been established.

dogs with a portosystemic vasculai·

Treatment requires surgical removal
anastomosis, increased urinary ainmoniun1
or litl1otripsy followed by preventive
output may paitially be due to the increased
strategies.

filtered load of ainmonia, because plasma

Prevention Protocol: Recurrence is
levels of anunonia tend to be increased.

a major problem with calciw11 oxalate

Dissolution Protocol: Urine alkalinizauroliths. An "ideal" diet is considered to be tion minimizes renal a.I1Unonia production;
low oxalate, low protein, and low sodiwn
the goal is to achieve a urine pH > 7. If
and would maintain urine pH at 6.5--7.5
required, urine alkalinization can be
and urine specific gravity <1.020. A few
achieved by administering NaHC03,
commercially available canned foods

1 g ('A tsp )/5 kg, PO, tid, with food.

achieve these goals and may minimize tl1e

Potassium citrate, administered to effect

1isk of recurrence. Potassium citrate may be (25--50 mg/kg/clay) is an alternative, more added as needed to assure the urine pH is
palatable alkalinizing agent.

within the desired range; water may be used

U1inary urate output should be reduced.

to provide appropriate reduction in mine

This can be accomplished by feeding a
concentration. If t11ese urine conditions are
low-purine, low-protein commercial diet.

achieved and calcium oxalate crystals are

In addition, the xanthine oxidase inhibitor
still seen in warm, fresh urine, t.hen vitamin
allopurinol (15 mg/kg, PO, bid) may be

86 and/or thiazide diuretics can be
administered to ensure the nucleic acid
considered (although of unproven efficacy).

metabolite load is excreted as a combina

Effectiveness of therapy should be
tion of xantlline, hypoxanthine, uric acid,
reevaluated at 1- to 4--mo intervals by
and allantoin, rather than almost entirely
urinalysis. Chlorothiazide diuretics may
as urate. However, the effectiveness of
also be of value.

allopurinol in reducing urinaiy urate output
is variable, and urinary urate levels should

Urate Stones: Ammoniwn urate stones
be measured (although this may be
are most common in Dalmatians and in clogs difficult). Allopurino\ must be used with congenital portosystemic vascular
cautiously in dogs with hepatic disease
shunts. The fom1ation of ammoniun1 urate
or primary renal failure, because it is
calculi depends on the urine concentrations
metabolized to its active fom1 in the liver
of urate and anirnoniun1 and on other poorly and is excreted via the kidneys. It is understood factors. Dalmatians do not
important that diets high in purines not be
convert most of their metabolic urate to
fed to dogs receiving allopurinol because
allantoin and thus excrete the bulk of
xanthine uroliths may result.

1530

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

Urine volume should be increased to
understood reasons, not all cystinuric dogs
reduce the concentration of all dissolved
develop uroliths. However, the absence of
solutes in urine. This can be achieved by
uroliths does not preclude their future

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feeding canned diets restricted in protein. By development, and preventive measures reducing formation of urea, renal rnedullary
are indicated.

urea concentration declines, inte1fering

Cystinuria is thought to be inherited as
with the counterc111Tent system of urine
a sex-linked trait. However, in Newfoundconcentration. Adding salt, 1 g (\4 tsp )/5 kg, lands it is transmitted as a simple autosomal
daily to the diet, or rnbdng water with the
recessive trait. The defect has also been
food are additional methods. Salt should not
repo,ted in Dachshunds, Basset Horu1ds,
be given to animals with hypertension but

English Bulldogs, Chihualmas, Yorkshire
otherwise poses little risk in nom1otensive

Terriers, Irish Terriers, and mixed-breed
dogs without chronic kidney disease,
dogs. Cystinuria has been recognized
proteinuria, or hypoalbun1inernia.

almost exclusively in male dogs, except in

Newfoundlands. A ruine cystine concentra

Prevention Protocol: Prevention
strategies ain1 to reduce the concentration
tion of> 75 mg/g creatinine in nonfasted
of anunonium and urate in urine to levels
dogs is predictive of susceptibility to cystine
unlikely to induce flocculation.

urolith.iasis.

A low-protein, low-purine diet should be

Cystine solubility depends on urine pH,
fed to reduce ruinary urate output. Alkalinizawith solubility increasing rapidly when tion should be used as needed to ensure
urinary pH is > 7.5. Dogs fed meat-based
alkalinuria. Treatment with allopurinol
diets tend to excrete acidic urine, which

(10 mg/kg/day, PO) can be considered.

leads to urine cystine supersaturation.

Ideally, allopurinol is not needed as a

Cystinuria is a lifelong defect of tubular
supplement to dietary management;
reabsorption and cannot be cured. Cystine
however, ifurate crystals persist, a low-mainstones tend to recur within 1 yr without tenance dose of allopurinol is appropriate.

management to prevent recllffence, and

These dissolution and prevention
they often recur despite attempts at
strategies were developed for use in
prevention.

Dalmatians in which hepatic conversion of

Dissolution and Prevention Protocols:

urate to allantoin is reduced but the liver is

Urinary cystine output should be reduced.

otherwise normal. They may not be safe for

Protein-restricted alkalinizing diets have
use in dogs with portosystemic vascular
been associated with reducing the size of
shunts. Such dogs tend to develop
cystine urocystoliths. Urinary cystine
hypoalbru11inemia, edema, and ascites
concentration can also be reduced by
when fed a low-protein diet. The safety
administering N-(2-mercaptoproprionyl)of allopurinol in these dogs has not been glycine (2-MPG, tiopronin) or penicillamine.

established. In addition, alkalinization

2-MPG should be given at 15-20 mg/kg, PO,
can predispose to hepatic encephalopathy
bid, for dissolution, and at 10-15 mg/kg, PO,
because of increased GI absorption of

•
bid, for prevention. Penicillan1ine (15
dietary protein metabolites.

mg/kg, PO, bid) can be substituted for

2-MPG; unfortunately, -40% of dogs treated

Cystine Stones: Stones composed
with penicillamine exhibit anorexia and
almost entirely of cystine fom1 in dogs that
vomiting. The vomiting may b� partially
have a renal tubular amino acid reabsorpresolved by giving the medication with tion defect known as cystinuria. Healthy
meals; however, a severe reduction in
dogs demonstrate 97% fractional reabsorpdosage or complete withdrawal is often tion of cystine, whereas affected dogs
necessary.

excrete a much greater proportion of the

The urine should be alkalinized to a pH
filtered cystine load and may even exhibit

> 7.5. Sodium bicarbonate added to the diet
net cystine secretion. Cystine is a relatively
at 1 g (1A tsp )/5 kg, tid, readily accomplishes
insoluble amino acid; therefore, in high
this, but because sodium supplementation
concentration it may precipitate and form
may enhance cystinuria, potassium citrate
stones. Despite excessive 111inary loss of

(20-75 mg/kg, PO, bid) is preferred.

cystine in cystinuric dogs, plasma cystine

Urine volume can be increased by mixing
levels remain the same as in healthy dogs;
water with the food. Salt should not be
in fact, the only morbidity or mortality
added to the diet, because increased sodium
associated with the inherited defect of
excretion may cause increased cystine
cystine reabsorption is urolith formaexcretion. If urine vol rune is adequate and tion. Identification of cystine crystals
the urine pH is maintained above 7.5, most
by urinalysis indicates the dog is at risk
cystinuric dogs will pass urine that is only
of fom1ing cystine uroliths. For poorly
slightly supersaturated or undersaturated

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS

1531
for cystine. Under such conditions, only
with grossly observable stones composed
relatively small doses of 2-MPG or
primaiily of calcium oxalate has increased
penicillamine may be necessary to achieve
in cats. The most conunon feline uroliths

24-hr undersaturation.

are calcium oxalate, magnesium ainrnonium

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phosphate, and urate.

Silica Stones: Early reports indicated a

Urolithiasis is usually suspected based
predominance of silica stones in German
on clinical signs of hematuria, dysuria, or

Shepherds, but many breeds have now been urethral obstruction. Urinalysis, urine implicated. Urethral obstruction in males is
culture, radiography, and ultrasonography
the most common presenting problem, but
may be required to differentiate uroliths
signs similar to those associated with other
from urinary tract infection or neoplasia.

types of uroliths also may be noted. The

Radiography, cystoscopy, or ultrasonogramean age at occurrence is -6 yr. The stones phy are critically important to detect
are usually multiple and develop in the
uroliths, because only-100/oof feline urobladder and urethra. Silica uroliths are cystoliths can be detected by abdominal
radiopaque. They frequently, but not always, palpation. Uroliths with a diameter >3 mm have a characteristic "jackstone" appearare usually radiodense; however, because ance. Identification requires spectrographic
smaller uroliths are common, double-conanalysis and cannot be made with kits for trast radiography may be required for
qualitative stone analysis.

detection. Radiographic evidence of

The role of diet in spontaneously
uroliths is seen in -200/o of cats with
occurring silica urolithiasis has not been
hematuria or dysuria.

determined, although plants are often an

The usual clinical approach to grossly
abundant source of silica. If the diet of an
observable urocystoliths is surgical removal
affected dog is known to be high in silica, or
or lithotripsy where available, followed by
if silica urolithiasis has been recurrent, a
dietary therapy instituted as a preventive
dietary change should be recommended.

measure. For sterile struvite uroliths,

Only general management principles can be
medical dissolution is the preferred
suggested for silicate urolithiasis. Additreatment. Nephrolithiasis is not associated tional salt and/or water should be added to
with an increase in the rate of progression
the diet to induce diuresis and to lower the
of feline kidney injury, and cats with
urine solute concentration. When present,
nephrolithiasis are generally managed
urinary tract infections should be elimiwithout surgery.

nated. Diets high in plant proteins should
be avoided.

Calcium Oxalate Stones: Calciun1
oxalate uroliths are the most common feline

Feline Lower Urinary Tract Disease
uroliths and the most common nephrolith;

(Feline urologic syndrome)

although their underlying cause is
unknown. Conunon management schemes

Hematuria, pollakiuria, and stranguria are
that involve feeding urine-acidifying diets
the characteristic clinical signs of feline
with reduced magnesiun1 have reduced the
lower urinary tract disease (FLUTD) in cats. incidence of feline struvite urolithiasis.

Although the specific underlying cause

Magnesium has been reported to be an
of this common syndrome is often not
inhibitor of calcium oxalate formation
identified, associated conditions include
in rats and people; thus, the reduced
urinary tract infection, neoplasia, trauma,
magnesiun1 concentration in feline urine
urethral plugs, urolithiasis, and sterile
may partially explain the increase in
cystitis (feline interstitial cystitis).

calciun1 oxalate stones in cats.

Medical protocols that promote calcium

Feline Urolithiasis: Feline urolithiasis
oxalate dissolution are not known; therefore,
is a common disease seen with equal
surgery and lithotripsy are the primary
frequency in both sexes. Until recently, it
means for removal ( small bladder stones
was thought that most uroliths in cats
may be elinlinated by voiding urohydropulwere small and resembled sand or were sion). However, some calcium oxalate
gelatinous plugs that differed from typical
uroliths, especially those in the kidneys, may
uroliths in that they contained a greater
not cause clinical signs for months to years.

amount of organic matrix, giving them a

Because of the unavoidable destruction of
toothpaste-like consistency. Matrix-crystalnephrons during nephrotomy, iliis proceline plugs are most commonly found within dure is not recommended unless it can be
the urethra near the urethral orifice and are
established that the stones are a cause of
primarily responsible for urethral obstrucclinically significant disease. Recurrence tion. Recently, prevalence of urolithiasis
remains problematic. A variety of diets has

1532

NONINFECTIOUS DISEASES OF THE URINARY SYSTEM IN SMALL ANIMALS
been fonnulated to restrict the formation
is not complying with therapeutic recomof calcium oxalate uroliths and should be mendations.

considered appropriate for maintenance in
cats with nephroliths and after the removal

Other Feline Stones: Anunonium urate,
of urocystoliths. Diets that reduce the
uric acid, calcium phosphate, and cystine

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likelihood of formation of both struvite and
uroliths are less common in cats, but
calciwn oxalate stones are commercially
anunonium urate and uric acid account for
available. Eliminating any associated urinary

-6% of feline uroliths. Although a renal
tract infections, avoiding mineral and
tubular reabsorptive defect and portovascuvitamin C and D supplementation, and enlar anomalies have been incriminated as couraging water consumption are critical.

causes in a few cases, the cause of most
urate uroliths in cats has not been

Struvite Stones: Three distinct types
established. Nonetheless, formation
of struvite uroliths are recognized in cats:

of highly acidic and concentrated urine
amorphous urethral plugs with a large
associated with consumption of diets high
quantity of matrix, sterile struvite uroliths
in purine precursors ( especially liver)

( which fom1 perhaps as a result of certain
appears to be a risk factor.

dietary ingredients), and struvite uroliths

Medical protocols tl1at consistently
that form as a sequela of urinary tract
promote dissolution of anunoniun1 urate
infection with urease-producing bacteria.

uroliths in cats have not been developed,

Struvite uroliths induced by infection are
and surgery remains the most common
less common than sterile struvite uroliths.

method of removal. For small stones,

An additional type of struvite urolith in cats
voiding urohydropulsion may be effective.

consists of a sterile struvite nidus that

Prevention should include feeding a diet
predisposes to urinary tract infection with
low in purine precursors and promoting
urease-producing bacteria and subsequent
fonnation of less acidic mine that is not
formation of infected struvite laminations
highly concentrated. Although allopurinol
around the sterile nidus.

may reduce the fonnation of urate in cats,

Treatment of sterile struvite urolithiasis
studies of the efficacy and potential toxicity
focuses on reducing the urine pH to �6 and
of allopurinol in cats are required before
on reducing the urine magnesiwn concentrameaningful guidelines can be established.

tion by feeding magnesium-restricted diets.

Reducing urine pH and magnesium

Sterile Cystitis (Feline Interstitial
concentration is best accomplished by

Cystitis): Feline interstitial cystitis is
feeding a commercially available prescripgenerally taken to be synonymous with tion diet fom1ulated for this purpose. Some
sterile cystitis of w1known cause. The underdiets are formulated to reduce the formation lying cause of this disorder is unknown,
of both struvite and calciwn oxalate stones.

although anxiety and altered neuroh01mo

Generally, neither sodium chloride nor urine
nal factors have been implicated.

acidifiers should be given concurrently with

Diagnosis is by exclusion of other causes
these diets, because they are already
of lower urinary tract disease in cats, such
supplemented with sodiun1 chloride and
as obstruction by urethral plugs, bacterial
formulated to produce acidwia. In addition,
urinary tract infection, neoplasia or other
these diets should not be fed to cats that are
mass lesions, and urolithiasis. Diagnostic
acidemic, have azotemia of any cause, or
tests to exclude thes� conditions may
have cardiac dysfunction or hype1tension.

include radiographs, ultrasonography,

Urolith size should be monitored every 4 wk
urinalysis, urine culture, and cystoscopy.

by radiographs or ultrasonography, and

Because the cause of feline interstitial
crystalluria by winalysis. Struvite crystals
cystitis is unknown, the goal of treatment
should not form if therapy has been effective
is to reduce the severity and frequency of
in producing wine that is undersaturated
episodes of cystitis. Therapeutic considerawith magnesiun1, anm10nium, and phostions include reduction of stress through phate. Because small uroliths may not be
environmental changes, dietary adjustdetected radiographically, the calculolytic ments ( eg, use of canned preparations),
diet should be continued for �4 wk after
pheromones applied topically in the
radiographic docun1entation of urolith
environment, and analgesics ( eg, butordissolution. If treatment does not induce pha.nol, 0.2-0.4 mg/kg, PO, bid-tid).

complete dissolution of uroliths, it is likely

Other medications ( eg, anutriptyline,
that either the wrong mineral component

5--12.5 mg/cat, PO, once or twice daily;
was identified, the nucleus of the urolith is
clomiprarnine, 0.5 mg/kg/day, PO; fluoxcomposed of a different mineral than the etine, l mg/kg/day, PO) have yielded
outer portion of the urolith, or the owner
mixed results.

BEHAVIOR

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INTRODUCTION 1533

Integrating Behavioral Services into Veterinary Practice 1534

Glossary of Behavioral Terms 1534

Diagnosis of Behavioral Problems 1537

Prognosis of Behavioral Problems 1539

Treatment of Behavioral Problems 1539

Behavior Modification Principles 1540

Principles of Pharmacologic and Natural Treatment 1543

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS OF

DOMESTIC ANIMALS 1545

Horses 1545

Cattle 1551

Swine 1553

Sheep 1555

Goats 1556

Chickens 1557

Dogs 1557

Cats 1570

THE HUMAN-ANIMAL BOND 1575

Veterinary Family Practice 1575

Human Health Benefits of Pet Ownership 1577

Animal-assisted Interventions: Therapy, Activities, and Education 1578

Service or Assistance Dogs and Other Working Dogs 1578

Animal Welfare 1579

Euthanasia, Pet Loss, and Grief for Owners and Veterinarians 1580

Self-care for Veterinarians 1580

BEHAVIORAL MEDICINE INTRODUCTION

An animal's "behavior" is the product of its is outlined, followed by a description
genetic composition, the environment in
of common behavioral disorders.

which the animal functions, and the animal's

The minimum behavioral welfare
experience (particularly in the pre- and
requirements for the housing and enrichpostnatal environment through the primary ment of farm, zoo, and laboratory animals,
socialization period). This section focuses
known as the five freedoms, are equally
primarily on the diagnosis and treatn1ent of
important for family pets. These include
abnormal behavior of domestic animals.

freedom from hunger and thirst; discomfort;

For each species, normal social behavior
pain, injury, or disease; fear and distress;

1534

BEHAVIORAL MEDICINE INTRODUCTION
and freedom to express norn1al species
advice and preventive guidMce for new
behaviors. When these needs are not fully
pet owners. Veterinarians or staff with
addressed, welfare is compromised and
sufficient skills and training C3.!1 offer client
both health and behavior problems arise.

education about how to prevent and

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In companion animals, behavior
m3.11age undesirable behaviors Md classes
problems weaken the pet--0wner bond,
to help pet owners socialize and train their
resulting in a decreased owner commitment pets. A good set of resource mate1ials and to pet care. They are a prin1a.1y reason for
links to Web sites that provide appropriate
pet relinquishment and euthanasia. Yet
and sound behavioral guid3.!1ce cru1
studies show that many owners do not
supplement the advice provided.

report behavior changes to their veterinar

Veterinruy behavioral technicians can
ian, and most veterinarians neglect to
oversee the preventive counseling and
inquire about them. Thus, screening for any
training services offered by a vete1inruy
behavioral changes or emerging behavior
hospital. They can also play an integral role
problems should be done at each vete1inruy
during behavioral consultations by taking
visit to ensure that the behavioral health,
the history, demonstrating behavior
physical health, and welfare of the pet ru·e
modification techniques Md products, Md
being effectively and humanely managed.

conducting case followup and ongoing
support. lnfonnation sources for veterinarians, technicians, and staff interested in INTEGRATING BEHAVIORAL
veterinruy behavior ru·e listed in TABLE 1.

SERVICES INTO VETERINARY

Veterinarians also have a vested interest

PRAC TICE
in how clients train their pets. Trainers
should have a sound background on

Each veterinruy visit should include
species-typical behaviors, as well as how
screening questions to detem1ine whether
behaviors can be shaped and modified
there ru·e any behavior concerns or any
through the principles of learning that apply
ch3.11ge in behavior from previous visits.

to all species. The Association of Pet Dog

In addition to enabling the veterinari3.!1 to

Trainers, the American Hum3.!1e Associaassess the health and welfare of the pet, tion, and the Ame1ican Veterinruy Society of
this initiates a dialogue with clients about

Animal Behavior have published guidelines
behavior and lets them know that behavior
for approp1iate and hun1ane training and
is central to good veterinruy cru·e. Recordbehavior modification. Certified trainers ing responses to behavior questions at each
can be found at www.ccpdt.org Md www.

visit allows a baseline to be established for
karenpryoracademy.com, Md advocates of
future comparison.

force-free dog training at www.petprofes

A basic behavior-screening questionnaire
sionalguild.com. However, even with a
is a simple way to collect information.

certified trainer, veterinariru1s should

Questionnaires should be standardized so
observe Md talk with the trainer to ensure
no topic is left uncovered and so data C3.!1 be
that the methodologies used are humane,
compared from visit to visit. When used
effective, and appropriate for the individual
continually from the pet's first visit, these
owners Md pets. Having an active
tools allow for early detection Md
discussion about training with each dog
intervention. Addressing behavioral
owner CM help the owner to understand the
concerns early provides the best chance to
p1inciples of learning 3.!1d how to differentim3.11age the problem Md prevent a minor ate those trainers who use undesirable
issue from becoming more serious and
techniques from those who use humane,
deeply entrenched. If behavioral signs ( eg,
reward-based techniques.

barking, growling, lunging, housesoiling)

are identified during the visit, the vete1inari3.11 will need to detennine whether there GLOSSARY OF BEHAVIORAL
are underlying medical issues, whether the

TERMS
behaviors are norn1al and in context or
abnormal Md out of context, Md whether

Abnormal Behavior: These activities
they are manageable for the household,
show dysfunction in action 3.!1d behavior.

either to begin offe1ing behavior guidance

Alternatively, the tenns behavior problem,
or, when indicated, to refer the client for
behavior pathology, mental health disorder,
further counseling.

or emotional disorders might be used. By

Behavioral services should be offered
comparison, many behavioral complaints
using an integrated terun approach. Staff
are normal behaviors that are undesirable to

C3.!1 help with behavioral screening
owners ( eg, garbage raiding, jun1ping up,

(questionnaires) and provide pet selection
predation, herding, guarding).

BEHAVIORAL MEDICINE INTRODUCTION

1535

•h=i!i• BEHAVIOR RESOURCES FOR VETERINARIANS AND TECHNICIANS

Organization

Web Site

BEHAVIOR ASSOCIATIONS

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American Veterinary Society of Animal Behavior
www.avsabonline.org

Companion Animal Behaviour Therapy Study Group
www.bvba.org.uk

European Society of Veterinary Clinical Ethology
www.esvce.org

Society of Veterinary Behavioral Technicians
www.svbt.org

Australian Veterinary Behaviour Interest Group
www.ava.com.au/avbig

BEHAVIOR CERTIFICATION GROUPS

American College of Veterinary Behaviorists
www.dacvb.org

European College of Animal Welfare and Behavioural Medicine www.ecawbm.org Australian and New Zealand College of Veterinary Scientists www.anzcvs.org.au Academy of Veterinary Behavioral Technicians
www.avbt.net

Abnormal Repetitive Behaviors:

which may be accompanied by both

Abnormal repetitive behaviors are a
behavioral and somatic signs (vigilance
heterogenous group of behaviors that
and scanning, autonomic hyperactivity,
include both stereotypies and compulsive/
increased motor activity and tension).

in1pulsive behaviors (see below). Although
these two categories of behavior have

Compulsive or Obsessive-Compulsive
similarities in clinical presentation and

Disorders: Compulsive behaviors are
perhaps neurophysiology, they are not synonabnormal and repetitive, may be variable in Y1nous. In addition, underlying medical
form, and are often fixated on a goal. They
conditions might cause or contribute to
may be exaggerated, sustained, intense,
these signs. Thus, until a definitive diagnosis and difficult to interrupt or have an is made, the tem1 abnormal repetitive
element of dyscontrol in either the
behavior is a descriptive tenn for any of the
initiation or continuation of the behavior
behaviors that are maladaptive, repetitive
or the inhibition or switching between
or fixed, and pathologically abnonnal.

behaviors. They are generally derived from

Although categories overlap, clinical signs
normal behaviors such as grooming,
have
predation, ingestion, or locomotion.

been desclibed as oral/ingestive ( eg, pica,

Compulsive disorders might initially arise
polyphagia, licking, gulping), neurologic/
in situations of frustration or conflict but
hallucinatmy ( eg, fly snapping, light
become compulsive when they persist or
chasing), locomotory (eg, spinning,
arise outside the original context. There
pouncing), and self-directed ( eg, acral lick
appears to be a genetic predisposition to
dennatitis, psychogenic alopecia).

the development of certain compulsive
behaviors (eg, wool sucking in Oriental

Aggression: Aggression can be defined
breeds of cats, tail chasing in German
in a nan·ow sense (attack) or in a broader

Shepherds, flank sucking in Dobermans).

sense as agonistic behavior. In the latter

There is likely an alteration in serotonergic
case, aggression can be appropliate or
activity for most compulsive disorders in
inappropliate, in context or out of context,
dogs and cats. However, there can be a
inter- or intraspecific, or a challenge or
wide range of presentations, and multiple
contest that results in deference or in
neurotransmitters have been implicated
combat and resolution.

(eg, dopanline, opiates). This may indicate
an altered course of disease over time or

Anxiety: Anxiety is the apprehensive
that the diagnosis encompasses more than
anticipation of future danger or misfortune,
one disorder. Drugs that inhibit serotonin

1536

BEHAVIORAL MEDICINE INTRODUCTION
reuptake are generally most effective to
signaling of one individual in a pair ntight be
enhance serotonin transmission and inhibit described as dominant if the response of the dopamine activity. Brain areas of interest
second individual is deferent or subordinate.

include the prefrontal cortex and

However, domina.ntJsubordinate does not
amygdalae.

describe the relationship between the pair,

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unless tile response is consistent across

Conflict: Conflict arises when a pet has
resources and interactions. While this
competing motivations or is motivated to
temlinology applies to commwlication and
perfom1 more than one opposing behavior.

signaling between members of a species ( eg,

This might occur when a dog is motivated
dog-dog), it does not "translate" to communito greet but is fearful of approach, perhaps cation between species (eg, dog-hwna.n).

because of previous unpleasant experiences

( eg, yelling, hitting, piruting). The resultant

Fear: Fear is a feeling of apprehension
behavior might be either a displacement
associated with the presence or proxintity
behavior (see below) or aggression (when
of an object, individual, or social situation.

fear is an overriding factor).

Fear is part of nonnal behavior and can be
an adaptive response. The determination

Displacement Behavior: This type of
of whether the fear or fearful response
activity is generally a normal behavior that is
is abnormal or inappropriate must be
perfom1ed out of context, or is "displaced,"

determined by context. For example, fire
because the animal is unable-physically or
is a useful tool, but avoidance of fire is an
behaviorally-to execute another activity
adaptive response. If a pet is fearful of
or otherwise occupy itself. This is less
stimuli that a.re innocuous, such as walking
specific than redirected behavior ( see
on certain types of surfaces or going
below), in whlch tl1e intended behavior is
outdoors, such fear would be irrational and,
directed toward another target. When
if it were constant or recmTent, probably
displacement activity occurs, tl1e behavior
maladaptive. Fears usually occur as graded
may be out of context with the situation
responses, with the intensity of tile response

( eg, circling, air snapping, or even
proportional to the proxintity of the stimulus.

urination). Displacement behaviors may

A sudden, all-or-notlli.ng, profound, abnormal
arise from conflict or frustration or be a
response that results in extremely fearful
va.cuwn activity.

behaviors is usually called a phobia.

Dominance: Domina.nee is a concept

Frustration: This state arises when an
frequently ntisapplied. The ethological
aninlal is motivated to engage in a sequence
concept of dominance refers to competitive
of behaviors that it is unable to complete
control over a resource in a limited
because of physical or psychological
circumstance and to the ability of a higherobstacles in tile environment. When pets are ranking animal to displace a. loweHa.nking
frustrated-such as a cat that cannot gain
one from that resource. Rank is usually
access to an outdoor cat that it sees through
defined by an ability to control the resource
the window, or a dog that cannot get to a
or by access and ability to restrict matings;
stimulus on the other side of a door or
however, extra-pair copulation is almost
fence-the resultant behavior can be a
always more common when assessed by
redirected behavior ( eg, attack of another

DNA analysis than it was believed to be on
fa.nilly pet or owner), a displacement
the basis of behavioral observations.

behavior ( eg, stereotypic pacing), or signs

Domina.nee is not interchangeable with
associated with anxiety ( eg, whining or
hierarchical rank. Ranks, particularly those
howling). Another example of goal
that are linear and in which a "dominant"

frustration is the dog or cat that chases a
aninlal is identified, are largely artifacts of
laser light toy but is unable to finish the
experimental or manipulated situations. A
sequence or achieve any goal. This frustra

"dominant" a.nin1al is not the one engaged tion may lead to obsessive chasing of other
in the most fighting and combat. Most
lights and shadows.

high-ranking aninlals seldom have to contest
their right of access to a resource. Instead,

Phobia: Most fearful reactions are
high-ranking animals are usually better
learned and might be unlearned with
identified by the character and frequency
gradual exposure, although a lack of
of deferential behaviors exhibited by others
sufficient previous exposure, consequences
in their social group and by their ability to
of previous exposure, and genetic factors
respond appropriately to a variety of social
all play a role in how quickly or completely
and environmental circwnstances. Thus,
the unlearning ntight be achieved. Phobias
confident and assertive postures and
involve sudden, all-or-nothing, profound,

BEHAVIORAL MEDICINE INTRODUCTION

1537
abnormal responses that result in

Stereotypys nlight be associated with basal
extremely fearlul behaviors ( catatonia,
ganglia dysfunction and can be induced by
panic). Phobias may develop over tirnedopaminergic stimulation of the striatwn.

some animals develop increasingly more
intense fears with repeated exposure ( eg,

Vacuum Activity: When an animal is
storm phobias). However, once estabhighly motivated to perfom1 ai1 instinctive VetBooks.ir
lished, they are associated with immediate
behavior but there is no available outlet, a
and intense anxiety when the stimulus is
vacuwn activity may be exhibited (flank
presented. Once a phobic event has been
sucking, licking, etc). These activities have
experienced, any event associated with it
no apparent useful purpose.

or the memory of it is often sufficient to
generate the response ( eg, wind, rain,

DIAGNOSIS OF BEHAVIORAL
or darkening sky and stom1 phobias).

PROBLEMS

Although fears may diminish with repeated
exposure and no untoward consequences,

Veterinarians must have an understanding
phobias can remain at or exceed their
of the behavior ai1d development of the
fom1er high level for years even without
species, the principles of learning, and the
reexposure. The genesis for such events in
signs of fear ai1d anxiety to differentiate
dogs is usually either extremely frightening
normal behavior from abnormal behavior.

or traumatic, or the dog itself has profound

When presented with an animal with
internal problems with fear ( eg, genetic
undesirable behavior, the first step is to
predisposition) so that responses to
exclude any medical problems that might
unfanliliar stimuli are excessive. Owner
be causing or contributing to the behavresponses might inadvertently aggravate ioral signs. In addition, while it is common
the problem, either by further encouraging
to consider the effects of disease on
the behavior or by adding to the fearful
behavior, stress can cause alterations in
emotional state if the outcome for the pet
behavioral, physiologic, and immune
is tmpleasant ( eg, owner anger or punishresponses, which can have variable effects ment). Phobic situations are either avoided
on health and behavior with increasing
at all costs or, if unavoidable, are endured
chronicity. Stress leads to alterations in
with intense anxiety or distress.

the hypothalaniic-pituitai-y axis and in
levels of dopamine, serotonin, norepineph

Redirected Behavior: Redirected behavrine, and prolactin. In animals, stress can ior activities are directed away from the
cause or contribute to feline interstitial
principal target and toward another, less
cystitis; dermatologic, respiratory, and GI
appropriate target. When the anin1al is in a
disorders; and behavior problems such as
state of emotional arousal and is w1able to
compulsive disorders, exagg�rated fear
reach the appropriate target, the behavior
responses, and psychogenic polydipsia
can be redirected to an alternative target if
ai1d polyphagia.

the animal is interrupted.

Diagnosis of any behavioral problem
requires the identification of all behavioral

Stereotypic Behaviors: A stereotypy is
and medical signs, history taking, a physical
a perseverant repetition of behaviors that
and neurologic exanlination, and any
are unvaried in sequence and have no
diagnostic tests indicated to exclude
obvious purpose or function. They usually
underlying medical conditions that nlight
derive from contextually normal maintecause or contribute to the signs (see TABLE 2).

nance behaviors ( eg, grooming, eating,

If there is no underlying medical cause for
walking). The behaviors have been reported the behavioral signs, then a comprehensive commonly in farm, zoo, and laboratory
behavioral history is required to detemli.ne
animal species and arise in situations of
the diagnosis, prognosis, and treatment
conflict or frnstration related to confineoptions. The histo1-y should include: 1) sex, ment or husbandry practices. They may
breed, and age of anin1al (breed predisposiarise when the environment is barren or tions); 2) age at onset of condition or
stress evoking, when the animal lacks the
complaint; 3) duration of condition or
opportunity to display a full range of
complaint; 4) description of undesirable
species-typical behaviors, with maternal
behavior; 5) frequency (hourly, daily,
deprivation, and as a result of neurologic
weekly, monthly); 6) duration of bouts; 7) any
disorders. It is thought that some stereochanges in pattern, frequency, intensity, and typic behaviors, at least in their early stages,
duration of bouts; 8) corrective measures
may provide a mechanism for the pet to
tried and the response, if any; 9) any activities
cope. For example, non-nut1itive suckling
that stop the behavior ( eg, a11irnal colin calves may assist digestive processes.

lapses); 10) 24-hr schedule of ai1imal and

1538

BEHAVIORAL MEDICINE INTRODUCTION
ifM•fj MEDICAL CAUSES OF BEHAVIORAL SIGNS

Medical Condition

Behavioral Signs

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Illness or disease

Altered personality, lethargy, depression, withdrawal, anorexia, reduction in grooming, altered social relationships, altered response to stimuli NEUROLOGIC

Central ( affecting

Altered awareness and response to stimuli, loss of learned forebrain, limbidtemporal, behaviors, housesoiling, disorientation, confusion, altered and hypothalamic),
activity levels, temporal disorientation, vocalization, rapid-eye movement sleep change in temperament (fear, anxiety, aggression), altered disorders
appetite, altered sleep cycles, interrupted sleep ( aggression/waking/activity) Peripheral (neuropathy)

Self-mutilation, irritability, aggression, circling, hyperesthesia Focal seizures/temporal

Repetitive behaviors, self-trauma, chomping, staring, lobe seizures
altered temperament ( eg, intermittent states of fear or aggression), tremors, shaking, interrupted sleep

Sensory dysfunction

Altered response to stimuli, confusion, disorientation, altered sleep cycles, irritability, aggression, vocalization, housesoiling

METABOLIC I ENDOCRINE

Feline hyperthyroidism

Irritability, aggression, urine marking, increased activity, night waking

Canine hypothyroidism

Lethargy, decreased response to stimuli, irritability, aggression

Hyperadrenocorticism

Panting, night waking, housesoiling, irritability, polyphagia, anxiety Diabetes/hyperglycemia

Housesoiling, night waking

Functional ovarian and

Androgen-induced behaviors: males-aggression,
testicular tumors
roaming, marking, sexual attraction, mounting; femalesnesting or possessive aggression of objects Hepatic or renal

Signs associated with affected organ, anxiety, irritability, encephalopathy
aggression, altered sleep, housesoiling, mental dullness, decreased activity, restlessness, increased sleep, confusion Anemia or electrolyte

Pica
imbalances

Pain

Altered response to stimuli, decreased activity, restlessness/inability to settle, vocalization, housesoiling, aggression, irritability, self-trauma, waking at night Gastrointestinal

Licking, polyphagia, pica, coprophagia, housesoiling (fecal), wind sucking, tongue rolling, unsettled sleep, restlessness

Urogenital

Housesoiling ( w·ine ), polydipsia, waking at night

Dermatologic

Psychogenic alopecia (cats), acral lick dermatitis (dogs), nail biting, hyperesthesia, other self-trauma

BEHAVIORAL MEDICINE INTRODUCTION

1539
owner, as well as any day-to-day variability;
modify undesirable behavior requires that

11) environment and housing; 12) animal's
the owner be prepared and capable of
familial history; and 13) anything else the
identifying each situation and substituting
owner thinks is relevant. In farm anin1als,
a more desirable response, the initial
questions should be framed within the
approach should be to avoid or prevent the

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context of the problem so that housing,
provocative situation. The predictability of
management, group or herd behavior,
the problem, the ability of the owners to
production, and perhaps reproduction are
implement initial preventive strategies, the
addressed.

expectations as to what might be achieved,

For each behavior problem, the "ABC"

the pet's temperainent, how the pet's
should be considered, ie, the antecedent, or
behavior will need to be modified over tin1e,
what precedes the behavior; the behavior,
and the practicality of implementing the
or the description of the problem; and the
program considering the environment,
consequences, or what happens immedifainily, and pet should all be reviewed and ately after the behavior. With maturity and
must be both acceptable and practical for
learning, the animal's response to a stimulus the owners. In addition, special consideramay be modified; thus, the initial events may tion will need to be given in cases of be just as important to evaluate as the more
aggression to evaluate risk ai1d ensure
recent events.

safety. (For guidelines on risk factor

History might be collected in pait by
assessment, see www.esvce.org.)

having the owner complete a history
questionnaire before the visit, especially
with respect to data about the home and

TREATMENT OF BEHAVIORAL
housing, fainily, daily schedule, training,

PROBLEMS
husbandry, and background. However,
further interactive questioning and

In production animals, treatment focuses
discussion with those responsible for the
on group management, environn1ental or
animal's care, housing, and training are
housing modifications, and in some cases
required to further evaluate the progress
removing individual anin1als out of or to
and development of the problem from the
other groups. Specifics ai·e covered in the
initial event to the present time. Having the
relevant species discussions.

owners bring video clips of the behaviors

In companion animals, the treatment of
can further help provide insight as to the
behavior problems varies with diagnosis ai1d
diagnosis, prognosis, and how the problem
prognosis. In general, the program begins
might be managed or improved.

with prevention and avoidance of problems,

Additional infonnation about the pet's
while the owner develops effective strategies
personality, relationship with the owner,
to modify the pet's behavior so that it might
response to stimuli, and owner's response
gradually be reintroduced to the problem
might be gained during the visit by
situations while achieving a desirable
observation of the pet and how it interacts
outcome. Initially, prevention is necessary to
with the owners. Although provoking the
avoid fwther compromising the pet's welfai·e
pet is generally contraindicated because
ai1d to ensure safety in cases of aggression.

any further repetition of the problem is ill

Repetition of the behavior further aggraadvised for the pet and might lead to further vates the problem if the pet successfully
learning, a controlled interactive assessaccomplishes its intended goal ( eg, escape ment might include how the animal
or retreat from the stimulus), while each
responds to other anin1als ai1d people,
exposure in which the outcome is unpleasant
sounds, a child-like doll, or handling,

Cat1 condition further anxiety. Improvement
including physical exanunation, petting, or
is generally a slow and gradual process;
the application of products such as a head
therefore, owners must have realistic
halter, muzzle, or body harness. The pet's
expectations of what might be achieved.

response to commands can be assessed dur

Modifications to the environment may be
ing the visit, as well as the types of treats or
required, so that the pet can be kept away
toys most likely to positively affect the pet.

from the stinmli ( or the sights or sounds of
the stimuli) that incite the problem or from
the areas in which the problem occurs.

PROGNOSIS OF BEHAVIORAL

Modifying the pet's behavior is accomplished

PROBLEMS
by applying the p1inciples of learni.ng and
behavior modification, p1in1arily achieving

Client understanding and compliai1ce are
and rewai·ding desirable outcomes along
critical if animals with behavioral disorders
with use of products that improve safety,
are to improve. Because the strategy to
reduce anxiety, or help to achieve the

1540

BEHAVIORAL MEDICINE INTRODUCTION
desired response more effectively ( eg,
doorbell paired with the arrival of unfamilmuzzles, head halters, no-pull harnesses, iar people (for pets feai·fuJ of visitors), or
etc). Drugs and natural products may also be a doorbell paired with verbal or physical indicated for some pets and some problems.

discipline applied by the owner for barking
or jwnping up (pinning, leash corrections).

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Behavior Modification Principles

Similarly when a pet lunges or barks when
meeting new people on the street or at the

The most commonly used behavioral
front door, the use of positive punishment
techniques include habituation, extinction,
to inhibit the behavior (such as choke collars,
desensitization, counterconditioning,
prong collat'S, shock, pinning) may condition
response substitution, and shaping.

a new response in which unfamiliar people

Flooding is often talked about but seldom
become a fear-evoking conditioned stimulus.

used because it is likely to make most

A visit to the veterinai-y clinic tl1at may begin
animals worse. While punishment is
as a neutral situation may quickly become
frequently used with varying degrees of
feai· evoking if it is associated witl1 unpleassuccess, few people correctly use this ai1t outcomes or is further enhanced by
teclmique, and there are botl1 humane and
owner anxiety. In addition, all of the stimuli
safety issues with the use of positive punishassociated witl1 the event (sights, sounds, ment. For punishment to be successful, the
smells) also become conditioned stimuli for
aversive stimulus (eg, startling with a loud
fear. In much the same way, rain, wind,
noise, spraying compressed air) must occur
dai·kening skies, and lightning can quickly
sufficiently close to the onset of the
become conditioned fear-evoking stimuli
behavior that the probability of the behavior for pets fearful of thunder.

occurring in the future is lessened. Often,
pwushment is more about the owner's anger Counterconditioning and Desensitiza
than about changing the behavior. In
tion: Counterconditioning involves tl1e
addition, some dog owners have been ill
consistent and repeated pairing of a
advised by training advice that advocates
stimulus tl1at evokes ai1 unpleasant response
confrontation, with the intent of asserting
with sometl1ing that is emotionally positive
leadership (dominance). In fact, numerous

W1til a positive association is made. To be
studies have demonstrated that punishmentsuccessful, counterconditioning should be based training and confrontational
coupled with desensitization in which the
techniques are more likely to lead to fear,
stimulus is minimized or reduced to a level
avoidance, and increased aggression.

that does not evoke the fear response ( eg,

Most of the hwnane, passive, or positive
by reducing volwne, increasing distance,
techniques involved in behavior modificachanging the environment, or modifying tl1e tion are not hard to learn and together with
stimulus to sometl1ing less tl1reatening).

preventive strategies are very successful. In

Once a positive association is made,
fact, dogs trained with rewards have fewer
rewards cai1 be paired witl1 stimuli of
behavior problems, less fear, and Jess
gradually increasing intensity.

avoidance than dogs trained with punish

Desensitization and cow1terconditionment. The following is a short review of the ing are extremely time consuming. The
basic principles involved in the techniques
exercises must be constantly repeated, so
and their associated strategies.

tl1at the response is altered to a positive one.

All stimuli tl1at evoke fe:1r (sights, sounds,

Classical Conditioning: The pairing of
odors, tactile) must be considered. Clients
an unconditioned stimulus with a neutral
often want botl1 quicker fixes and less work.

stimulus results in a conditioned stimulus

However, moving too quickly provokes
and a conditioned response. Classical
anxiety and sabotages any behavior
conditioning can occur in both positive and
modification progran1.

negative ways. Examples of a positive conditioned emotional response are the pairing of Operant Conditioning: Operant
a clicker with favored treats (for clicker
conditioning is a method based on making
trairung) or a doorbell signaling visitors (for
an association between a behavior and
pets enthused about meeting new people).

consequences of that behavior. The results

Problems arise when a fearful condieither increase or decrease the likelihood tioned emotional response is established
of future responses. There are four types of
toward a previously neutral stin1ulus
behavior-consequence relations: positive

( visual, odor, auditory, anin1ate, inanin1ate)

and negative punishment and positive and
by repeated pairing with a feai0producing
negative reinforcement. Reinforcement
stimulus. Once tlus occurs, the stimulus
increases tl1e likelihood a behavior will
itself will elicit the fear response, eg, a
be repeated, and punishment leads to a

BEHAVIORAL MEDICINE INTRODUCTION

1541
reduction in behavior. Negative refers to
become fearful of repeating the behavior.

the removal of a stimulus, and positive

However, a potential consequence is that
refers to the application of a stimulus.

the pet becomes feaiful or defensive to the

Positive reinforcement training occurs
punisher or to an approaching hand.

if behavior is increased by something applied Relationships with people should always (generally something pleasant or appealremain positive' Also, if an tmpleasant VetBooks.ir
ing); negative reinforcement occurs if
consequence occurs only when the owner
behavior is increased by something removed is present, the behavior may continue in (generally something unpleasant). In positive the owner's absence. Another problem with reinforcement training, a reward should be
positive punishment is that punishment
given immediately and consistently until
paired with exposure to a stimulus
the behavior is reliably repeated. If the

(barking at cars, meeting other dogs on
behavior is to be trained on command or cue, walks) can result in a conditioned fear of a word or hand signal should then be added
the stimulus (see above).

before the behavior-reward sequence. Once

Punishment caimot be used to achieve
learned, behavior can be reinforced on a
desirable behaviors, only to stop what is
variable schedule, so that the period of time
undesirable. If the goal is to make the pet
or number of responses before the reward is fearful of repeating a behavior ( eg, garbage given is varied. Rewards are used for positive raiding, taking things from counters, chewing reinforcement, but a reward is not synonyplants) or to keep the pet away from an ai·ea mous with positive reinforcement. A reward (room, couch, bed), then environmental is anything desirable to the pet, from an
punishment or pet-activated punishment ( eg,
activity such as petting, walking, or play, to
motion detector alarms or sprays, upsidean item such as a toy, food, chew, or treat.

down carpet runners, aversive tastes,

However, unless there is a clear relationship
double-sided tape, or bai·k-activated sprays)

between the behavior and the reward
or remote punishment ( eg, spraying water

(timing, consistency, contiguity), then the
while out of sight, remote-activated alarm or
reward does not achieve the goal of
spray) might be most appropriate. However,
positively reinforcing behavior.

before focusing on how to stop what is

Negative reinforcement must not be
undesirable, the owner should first focus on
confused with punishment, because
providing a desirable alternative ( eg, where
punishment decreases behaviors and
to sleep, where to climb, what to chew).

reinforcement increases behaviors. One

Negative punishment is the reduction
example of negative reinforcement is
of a behavior by the removal of something
avoidance or escape behavior. For example,
pleasant. For exan1ple, if the pet is receiving
if an animal anticipates an unpleasant
affection or play when an undesirable
outcome (eg, meeting another dog,
behavior begins ( eg, play biting, mouthing,
veterinary visit), then the aversive outcome
mounting), the in1111ediate removal of the
will not occur if the anin1al retreats.

play or affection will "negatively" punish the Similarly, if the owner puts pressure on a
pet. However, unless the pet can detenni.ne
head halter until the desired behavior is
what behavior leads to the removal of play,
achieved ( eg, sit, back up), the release of
the behavior may actually intensify because
tension is negative reinforcement. One
of frustration at not receiving its reward.

potential consequence of negative reinforcement is that if a pet's threats or aggression Second-order Reinforcers: Signals
lead to removal of a stimulus ( eg, dog,
that can be used at a di.stance to convey
delivery person, owner), the behavior is
that the reward is coming are second-order
reinforced by the retreat of the stimulus.

reinforcers. Commonly used second-order

Positive punishment occurs when a
reinforcers are words (eg, "Good dog!"),
behavior decreases when something is
clickers, or whistles. By repeatedly and
applied (generally something unpleasant),
continuously pairing these with a primary
and negative punishment occurs when a
reward such as a toy or treat, second-order
behavior is decreased when something is
reinforcers can elicit the san1e response
removed (generally something pleasant
that the reward would, as long as the
or appealing). In positive punishment, if
pairing is repeatedly maintained. Clicker
behavior does not decrease after the first
training requires frequent practice and
few applications, tl1en the punishment is
excellent tinting, but once achieved the
not being appropriately timed or the
animal can be reinforced each time the
behavior is too strongly motivated to
desired behavior is observed. Clicker
be deterred by punishment. Positive
training is an excellent way to immediately
punishment applied by a person ( owner,

"mark" desirable responses, gradually
trainer) is intended to cause the pet to
shape new or more desirable behaviors

1542

BEHAVIORAL MEDICINE INTRODUCTION

(eg, longer, more relaxed), or associate
the animal learns that higher intensity
a positive emotional response with
behaviors achieve the desired outcome.

the stimulus. (A useful resource is
www.clickertraining.com.)

Habituation: Habituation is a gradual
lessening of a response to a stimulus.

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Premack Principle: When a more

Usually this occurs with repeated presentadesirable behavior is made contingent on a tion of a stirn ulus whereby the aninlal learns
less desirable behavior, the less desirable
that it does not signal anytlling important.

behavior is more likely to be repeated. Thus, For exan1ple, horses placed in a pasture the more desirable behavior serves as the
bordering a road may at first run away when
reinforcer. For example, if a pet wants to
traffic passes but eventually learn to ignore
go out or cross the street for its walk, the
it. Stimuli associated with potentially
owner can train a sit-stay before each of
adverse consequences are more difficult
these behaviors. A horse or dog that wants
to extinguish with habituation than other
to walk ahead can be taught that walking
stinluli. ln prey species, responses to
on a slack rein or leash will result in this
sounds associated with predators would
behavior.

be difficult to habituate, because they have
been selected for and generally are adap

Overlearning: Overleaming is the
tive. If the fear response is too intense,
repeated evocation and expression of an
instead of habituation the animal may
already learned response. It is a phenombecome increasingly more fearful of the enon frequently used in training for specific
stin1ulus. This is tenned sensitization.

events but may be underused in preventing

If an extended interval has occurred since
fearful responses in dogs. Overlearning
the time an aninlal last experienced a
accomplishes three things: it delays
stimulus to which it had habituated, the
forgetting, it increases the resistance to
aninlal may again react when reexposed to
extinction, and it increases the probability
the stimulus. This is tenned spontaneous
that the response will become a "knee-jerk"

recovery.

one, or response of first choice, when the
circumstances are similar.

Flooding: This is used to treat fears of
harmless stimuli by forcing the animal to

Shaping: Shaping works through gradual
stay in the presence of the stimuli until
approximations and allows the animal to be
the fear is extinguished. This procedure
rewarded initially for any behavior that
is seldom effective and has welfare
resembles the desired behavior. For
implications in dogs, because it initially
instance, when teaching a puppy to sit,
enhances fear and cannot be stopped until
providing a food reward for a slight squat
all physiologic and emotional signs of fear
will increase the probability that squatting
are gone. If done improperly, flooding may
will be repeated. This squatting behavior is
therefore increase problem behaviors. In
then rewarded only when it more closely
practice, a controlled level of flooding is
resembles a sit, and finally, when it becomes quite often used as a component of behavior a true sit. Shaping can algo be used to
modification, in which the stimulus is
reward an increase in duration of or
presented at a level that is low enough to
progressively more relaxed behaviors.

cause mild fear and the pet is not removed
until it habituates. This can then be combined

Extinction: The ending of a behavior once with reinforcement, ie, the pet is positively all reinforcement is removed is termed
reinforced or the stimulus removed (negative
extinction. For example, if people pet a dog
reinforcement) when the fear response
that jumps up on them for attention, the
subsides or abates.

behavior continues; if they stop, the dog will
eventually extinguish its response because

Response Substitution: This involves the
the reward is no longer there. However, any
replacement of an undesirable response with
f01m of intennittent reinforcement-even
a desirable one. For example, high-value
occasional petting of the dog in response to
rewards can be used to train desirable target
its jumping-will prolong the performance
behaviors that are alternatives to the undesirof the response. Valuable rewards, a long able behavior. However, if the behavior is
history of perforn1ance, and intemtittent
part of the pet's natural repertoire ( eg,
reinforcement all increase resistance to
greeting, barking), it can be particularly
extinction. Owners also must be prepared
difficult to train alternative behaviors.

for the intensity of the behavior to initially

Specific examples of response substitution
increase before it is extinguished. Giving in
include training a dog to sit or lie down as an
will make extinction even more difficult as
alternative to jun1ping up, mounting, or play

BEHAVIORAL MEDICINE INTRODUCTION

1543
biting; or to sit, walk on loose leash, or back
behavioral therapy are human drugs, very
up for dogs forging ahead or rurming out the
few of which have had pharmacokinetics
door. Training should begin in a variety of
established for animal species. This can
environments where success can be most
lead to inaccurate assumptions with
readily achieved. The desired endpoint for
respect to dosage, duration of effect,

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the new response is for the anin1al to be quiet
contraindications, and adverse effects.

and calm. Therefore, the owner must learn to In addition, there is a wide range of read the look in the eyes, body posture, facial published dosages based on the applicaexpressions, and breathing to be able to tion, individual variability, and desired
gradually shape the desired behavior.

outcome. Therefore, practitioners should

Training could then move to environments
remain current with the most recent
with increasing distractions and locations
veterinary behavior literature with respect
where the problem is most likely to arise.

to indications, recommended dosages,

Alternatively, the pet might be enticed to
evidence of efficacy, potential adverse
engage in a behavior tl1at is incompatible
effects, and contraindications before
with the undesirable behavior, eg, teaching
dispensing any of these medications. (For
tl1e dog to fetch a toy when visitors arrive
dosing guidelines, see TABLE 3). Depending
instead of jumping up.

on the drug and patient, compounding

To replace the undesirable behavior with
may be required to achieve an appropriate
one that is desirable, response substitution
dosage and formulation for administracan be coupled with desensitization by tion; however, reformulation may alter a
beginning training with stimuli of low
drug's pharmacokinetics, safety, efficacy,
enough intensity while training the target
and stability. Recent studies on the use of
behaviors (eg, relaxation) with high-value
transdermal preparations of behavioral
rewards. However, for pets that are fearful
drugs such as fluoxetine, an1itripyline,
or anxious, the focus should be on
and buspirone have found little to no
desensitization and counterconditioning to
absorption of transdermal preparations
change the pet's emotional state rather than
versus oral dosing.

the behavioral response.

A variety of natural products have been
used to treat anxiety; however, only a few
have demonstrated any evidence to

PRINCIPLES OF PHARMACOLOGIC support efficacy. Products that have AND NATURAL TREATMENT
published studies indicating potential
therapeutic effects to calm and reduce

Psychotropic drugs and natural products
underlying fear and anxiety include the
can be used to reestablish a more stable
canine appeasing pheromone (Adaptil®),
emotional state and improve trainability in
the feline cheek gland pheromones
animals that are anxious, fearful, or overly

(Feliway® and Felifriend®), a feline
reactive. Drugs might also be effective in
pheromone that might aid in scratching
the treatment of behavior that is abnormal, post training (Feliscratch®), L-theanine pathologic, or lacking impulse control.

(Anxitane®), a-casozepine (Zylkene®), a

In addition, drugs may be indicated to
diet supplemented with a-casozepine and
improve compromised welfare. However,

L-tryptophan (Royal Canin CalmTM Feline
whereas drugs can improve the animal's
and Canine), a product combining
emotional state and facilitate new

Magnolia ojficinalis and Phellodendron
learning, only with concurrent behavior
amurense (Harmonease®), aSouroubea
modification can new neuronal pathways
sp supplement (Sin Susto TM), as well as
be established, new behaviors learned,
perhaps melatonin, and lavender
and fearful responses to stimuli changed
aromatherapy.

to positive ones.

A physical examination and blood and

Evidence-based decision making is a
urine tests should be part of a minimum
way to provide the best information and
database before dispensing drugs to
treatment options. Treatment should be
ensure there are no underlying medical
selected using the evidence combined
problems that may be causing or
with the clinician's expertise regarding
contributing to the behavioral signs,
the animal, client, and problem. Very few
or that might have an impact on drug
drugs have been adequately tested in
selection and use. For tricyclic antiderigorous, randomized, controlled trials pressants and selective serotonin
for use in veterinary behavioral therapy.

rcuptake inhibitors, 4 wk may be required

In fact, most drugs used in veterinary
to achieve optimal therapeutic effect.

1544

BEHAVIORAL MEDICINE INTRODUCTION

DRUG DOSAGES FOR BEHAVIORAL THERAPY

IN DOGS AND CATS

Drug

Dog Dosage

Cat Dosage

TRANQUILIZER

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Acepromazine

0.5-2 mg/kg, prn" to tid

0.5-2 mg/kg, prn

BENZODIAZEPINES

Alprazolarn

0.01-0.1 mg/kg, prn to qid

0.125---0.25 mg/cat, prn to tid

Clonazeparn

0.1-1 mg/kg, bid-tid

0.05-0.2 mg/kg, one to three
times/day

Clorazepate

0.5---2 mg/kg, pm to tid

0.2-1 mg/kg, one to two
times/day

Diazepam

0.5---2 mg/kg, pm (eg, every4--6 hr) 0.2-1 mg/kg, pm to tidb Lorazeparn

0.025--0.2 mg/kg/day to pm

0.025--0.08 mg/kg, one to two
times/day

Oxazepam

0.2-1 mg/kg, one to two times/day

0.2--0.5 mg/kg, one to two
times/day

TRICYCLIC ANTIDEPRESSANTS

Amitriptyline

1-4 mg/kg, bid

0.5-2 mg/kg/day

Clomipraminc

1--3 mg/kg, bide

0.25-1 mg/kg/day<

Doxepin

3-5 mg/kg, bid-tid

0.5---1 mg/kg, one to two
times/day

Imiprarnine

1-4 mg/kg, one to two times/day

0.5-1 mg/kg, one to two
times/day

SELECTIVE SEROTONIN REUPTAKE INHIBITORS

Fluoxetine

1--3 mg!kfday<

0.5---1.5 mg/kg/day

Fluvoxamine

1-2 mg/kg, one to two times/day

0.25-0.5 mg/kg/day

Paroxetine

0.5---2 mg/kg/day

0.25---1 mg/kg/day

Sertraline

1 -3 mg/kg/day or divided bid

0.5---1.5 mg/kg/day

13-BLOCKER

Propranolol

0.2--3 mg/kg, pm to bid

0.2-1 mg/kg, tid
a2-AGONIST

Cioni.dine

0.01-0.05 mg/kg, pm to bid

AZAPIRONE

Buspirone

0.5---2 mg/kg, one to three times/day 0.5---1 mg/kg, one to three times/day

(continued)

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1545

DRUG DOSAGES FOR BEHAVIORAL THERAPY

IN DOGS AND CATS (continued)

Drug

Dog Dosage

Cat Dosage

VetBooks.ir

SEROTONIN ANTAGONIST REUPTAKE INHIBITOR

Trazodone

3-8 mg/kg, pm to tid

ANTICONVULSANTS

Carbarnazepine 4-8 mg/kg, bid-tid

2-6 mg/kg, one to two times/day

Gabapentin

5-30 mg/kg, bid-tid

3-10 mg/kg, bid-tic!

Levetiracetam

20 mg/kg, tid

10-20 mg/kg, tid

Phenobarbital ct 2-5 mg/kg, bid (to 10 mg/kg, pm

1-3 mg/kg, bid
for sedation)

Potassium

10--40 mg/kg/day, or divided bid

Not recommended
bromidect

GLIAL MODULATOR

Propentofylline• 2.5-5 mg/kg, bid

MONOAMINE OXIDASE INHIBITOR

Selegilinec,e

0.5-1 mg/kg/day (in morning)

0.5-1 mg/kg/day (in morning)

a pm = as needed
b Rare reports of hepatic necrosis with diazepam in cats and potentially with other benzodiazepines c Licensed and labeled for veterinary behavior use in some countries d Titrate upward if inadequate clinical improvement and serum levels not adequate e Licensed and labeled for cognitive dysfunction in some countries NORMAL SOCIAL BEHAVIOR AND

BEHAVIORAL PROBLEMS OF

DOMESTIC ANIMALS
even if the stallion leaves or dies. The group
size ranges from 2 to 21 horses; multiplemale bands are larger than single-male SOCIAL BEHAVIOR
bands. Groups are not limited to a specific
geographic area and will travel in search of

Horses are social animals that under feral
resources. Colts and fillies leave the group
conditions (or on pasture) live in bands
usually before 2 yr of age ( when they

(harems) that consist of several mares, their
become sexually mature), stay alone for a
offspring up to 2-3 yr of age, and at least 1
few months, and then join a different group
and as many as 6 adult males. The core of
or establish a new one. Some colts may
the group is the mares, which stay together
form a "bachelor band" with up to 16 males,

1546

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
and later join other groups in which the
have minimal contact with other horses.

stallion has died or been chased away.

They spend most of the time resting near

Hierarchy in horses appears to be linear
the dam. The socialization period is 2--3

(with occasional triangular relationships)

mo of age; the foal struts playing with other

VetBooks.ir
and not necessarily based on age, weight,
foals and explores its environment. It is
height, gender, or time in the group. These
important to provide gentle handling
are impo1tant factors when considering
during the first 42 days of life. At this time,
problems in stabled horses, and attentive
snapping (teeth clapping) peaks. This is a
management is required before introducing
behavior shown by foals toward adult
horses to each other. Offspring of highhorses, preswnably to reduce aggression.

ranking mares appear to be high-ranking

It may also be a displacement nursing
later in life, which might indicate both
behavior, such as air nursing. Snapping is
genetic and experience components.

not the sru11e behavior as smacking, which

Hierarchical rank in females is determined
is an aggressive behavior or threat.

by observing group behavior ( eg, seeking

Allogrooming also peaks at this time.

out resources such as water holes). Females

From 4 mo of age, the foal starts developmake the decision about whether to leave or ing independent relationships and spends to stay within a band based on factors such
more tin1e in adult ma.intenru1ce behaviors
as assessment of food resources or number
such as grazing and resting while standing.

of stallions in the group. High-ranking

There are sex differences in play; colts mount
females can successfully interfere with the
more and fight more tha.I1 fillies, who focus
nursing of foals by lower-ranking females.

on grooming ru1d nnming. Colts groom only

Mares have prefen-ed associates, are
fillies, while fillies groom botl1 sexes.

preferentially groomed, and will groom
certain individuals. As in many other species,
hierarchy in horses is based on deference by BEHAVIORAL PROBLEMS
lower-ranking artin1als, not fighting.

Mru1y behavioral problems ru·e associated

The highest-ranking stallion in a band
with confinement. Under free-rru1ging
does most of the breeding, because it is the
circwnstances, horses wru1cler and spend
firnt to secure access to a receptive female

>600A, of their clay foraging. The remainder of
and the first to displace a female from
their time is spent resting (standing or lying
another band. In the absence of conception,
down), grooming, or engaging in another
horses cycle every 21 clays during the spring
activity. This san1e pattern is seen under
and summer. There are three phases of
barn conditions; even with free choice of
sexual behavior in horses: courtship,
grain, horses will eat mru1y small meals a
mating, and postmating behavior. During
day. Horses are highly social ru1imals that
courtship the stallion will approach the
require contact with others for nom1al daily
mare, prance, sniff her, nuzzle her, and
ma.intenru1ce ru1d well-being. Isolating
groom her. The mare may squeal, kick, or
horses can lead to development of
move away to show the stallion she is not
problems. The ma.in goal of managing
ready, or she may stand still, deviate her tail,
behavior problems in horses is to identify
and urinate, leading the stallion to mount
the deviation from nom1al equine behavior
her. Pasture breeding can achieve lOOOA,
and con-ect it.

success rates, versus 500/o-6()0A, for "in hand"

or controlled breeding. This is probably
because of familiarity between the horses,

Aggression
higher fertility of the mare, and less

Aggression is a common problem in horses
aggression between horses.

and includes chasing, neck wrestling, kicks

Ovulation usually occurs 36 hr before
a.I1d bites, and other threats. Signs of aggresestrous behavior ends. Gestation lasts sion include eru·s flattened backwru·d,

315-365 days, with an average of340 days.

retracted lips, rapid tail movements,

Factors that affect gestation length include
snaking, pawing, head bowing, fecal pile
nutrition, time of year (shorter time for late
display, snoring, squealing, !evade (rearing
sun1mer breeding), and gender (slightly
with deeply flexed hindquarters), ru1cl
longer for colts). Mares usually deliver at
threats to kick. Submissive horses respond
night, even when provided with artificial
by avoiding, lowering the neck and head,
light. Bonding between mare and foal occurs
clan1ping tl1e tail, and turning away from the
in the first 24 hr. Most nursing behavior is
aggressor.

initiated by the foal and tenni.nated by the
mare, especially in the first month.

Aggression to People: This behavior is

Dwing the first month of life, foals show
seen mostly in stalls in which the horse feels
maximal dependence on their dams and
confined in a small space that is also easily

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1547
defended. The varieties of aggression
other people after delive1y. No treatment
toward people include fear, pain induced,
is required in most cases.

sexual (honnonal), learned, and dominance
related. Some horses, especially young

Aggression While Breeding: Stallions

VetBooks.ir
ones, play with each other while showing
that are aggressive when used for breeding
signs of aggression such as kicking and
are often overused or used out of season.

biting. Although benign to other horses, this

Stallions cai1 develop preferences for
can be dangerous to people.

mating and may not be compatible with the

The first step in managing equine
chosen mai·e; changing the mare may help.

aggression is identifying the cause, and if

If stallions were stabled with mares when
possible, removing it. Training and positive
they were colts, they may have some social
reinforcement to establish control over the
inhibition for mating, and forced mating can
horse are also used, along with desensitizaresult in aggression. The goal of treatment tion and counterconditioning. Dominanceis to treat the main cause of aggression; related aggression in horses is different
chai1ging the mare (because of preferences)

from canine status-related aggression ( also
or artificial breeding can also be attempted.

known as dominance aggression) in that it

Physical restraint ( eg, hobbles) and
is not context-dependent. Environmental
desensitization can help as well. Clicker
management is important as well; good
training has been used successfully to
management should include sufficient
desensitize stallions with this problem.

resources such as space, food, and water.

Some horses are considered to have

Stereotypic Behaviors
pathologic dominance aggression; they will
attack other horses and people that are near Compulsive behaviors in horses can be them. These horses should be separated
divided into movement-related behaviors
completely from other people or horses and
and oral behaviors. They can be called
have a poor prognosis.

stereotypic because they are repetitive,
occupy a large part of the daily activity, and

Aggression Toward Other Horses:

serve no function. Confmement and poor

Aggression toward other horses is mostly
management practices are the prinlaiy
associated with sexual competition, fear,
contributing factors. In addition, bedding,
dominance, or territory (protecting the
feed, and social contact influence stereogroup and resources). As with aggression typic behaviors. Horses that have more
toward people, some horses may be
social contacts, are fed more roughage and
pathologically aggressive toward other
more than one type, are fed two or more
horses. The first step is separation of
tin1es daily, and are bedded on straw are less
aggressive horses from other horses, and
prone to these behaviors. Cribbing and
keeping subordinate away from dominant
wood chewing are exainples of oral
horses. Separation is achieved by solid
behaviors, whereas weaving, stall walking,
walls or two fences to avoid kicks
and pawing are exan1ples of locomotor
through the fence. Horses should have
stereotypies. Horses with one stereotypic
sufficient resources, and desensitization
behavior are likely to exhibit another. In
and counterconditioning is the best

Thoroughbreds, these behaviors ai·e
treatment approach. In cases of sexually
conunonly seen in mares and 2-yr-old foals.

related aggression, castration and
progestins (eg, medroxyprogesterone

Cribbing {Aerophagia, Windsucking):

70-80 mg/300 kg/day) can help. Adverse

When cribbing, the horse usually grasps
effects of such treatment should be
an object in the stall (such as the water
weighed carefully, and the horse should
bucket) with its incisors, flexes its neck,
be monitored closely. Adding tryptophan
and sucks air into the pharynx. Some
to the daily ration or administering
horses will aspirate or swallow the air.

selective serotonin reuptake inhibitors

In some cases, horses will suck air with

(SSRis) may be helpful in some cases.

out grasping any object. Feeding highly

Punishment should be avoided.

palatable food (eg, grains, molasses) is
associated with cribbing. Lack of exercise

Maternal Aggression: Aggression by
is also associated with cribbing; endurance
mares toward people is normal during
horses are less likely to do it than race or
the first few days after paiturition. This
dressage horses. Thoroughbreds are more
behavior is hormonally driven and usually
prone to cribbing than other horses. The
wanes with time. Mares should be
rate of cribbing is higher in confined
fainiliarized with their caretakers before
horses; however, even if the horse is
delivery and have minimal contact with
turned to pasture once the behavior is

1548

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
established, it will persist. It is possible
and covering fence edges with wires and
that GI discomfort can lead to cribbing.

taste repellents can also help minimize

One of the major complications of cribbing
wood chewing.

is damage to the incisors. Other problems
include gastroduodenal ulcers and epiploic Geophagia (Pica): Most horses will VetBooks.ir
foran1en entrapment. In most cases,
ingest sand or dirt. Soil that is ingested is
cribbing is a benign behavior that does not
richer in iron and copper than other soils,
affect the horse's welfare and does not
and this may attract tile horse. Ingestion
require treatment. Close to 10% of foals 20
of stones can become a serious problem,
wk of age will start cribbing when weaned
because it can lead to intestinal obstrucand placed in stalls. Those kept on pasture tions. Management should include
will not start. It has been speculated that
increasing roughage and exercise and
horses can learn cribbing by watching
providing salt blocks and toys.

other horses; however, no clear evidence
exists.

Polydipsia: Polydipsia in horses is similar

Cribbing can be diagnosed by finding
to behavior seen in dogs (seep 1568). The

U-shaped pieces missing from fences and
most common presenting complaint is a
horizontal surfaces in the stall, and worn
wet stall due to frequent urination. It is
incisors and enlarged neck muscles in
important to exclude medical causes ( eg,
horses that crib. In some cases, the
diabetes insipidus).

caretaker may directly observe the
behavior. Management should include

Stall Walking and Weaving: These
more roughage, exercise, and social
behaviors are seen in confined horses,
contact. Turning confined horses to pasture
serve no purpose, are hard to interrupt,
may help, and providing toys and stimulaand are usually slower than other types of tion is also advocated. Placing a strap
movement. Horses that stall walk usually
around the horse's neck behind the poll will
walk in circles in the stall, and when
apply pressure each time the horse tries to
released to a larger space ( eg, pasture or
flex its neck. This essentially punishes the
barn) continue to circle in a small area.

horse for cribbing, with the punishment

Tying the horse to prevent walking will
associated with the behavior and not the
only transfonn the behavior into weaving,
caretaker. Alternatively, an open-end
ie, lifting the legs and shifting weight and
muzzle can be applied. This will allow the
head position from side to side in the same
horse to eat and drink but prevent it from
spot. Possible causes of stall walking
grasping objects to crib on. Some horses
include lack of exercise and social contact
find a way to crib with the muzzle ( eg,
and claustrophobia. Stress and anxiety
grasping a linear object, such as a stick),
appear to aggravate the problem. Treatand most horses seem to tolerate the strap ment should focus on increasing exercise
better than the muzzle. Keeping stalls free
and stimulation, providing social contact,
of horizontal surfaces and objects that tile
and turning the horse to pasture. Providing
horse can grasp can help minimize
tllick bedding and feeding more than twice
cribbing. A variety of surgeries have been
daily can help as well. In extreme cases,
suggested to manage cribbing; however,

SSRis might be necessary to control the
the varying success rates and negative
problem. Providing a large mirror in the
impact on animal welfare are significant
stall in front of the horse can help decrease
disadvantages.

weaving.

Wood Chewing (Lignophagia): Like a

Stall Kicking: Horses may kick the walls
horse that cribs, a wood-chewing horse will
of the stall because of boredom, aggression,
grasp pieces of wood with its incisors, but
or frustration. The horse may kick in
unlike in cribbing, it will swallow the pieces. anticipation when food is being prepared The definitive cause of wood chewing is
but is out of reach. When the horse is then
lack of roughage in tile diet. Confinement,
fed, the behavior is reinforced. The horse
high-concentrate diets, and lack of exercise
may also be frustrated when it cannot
and stimulation increase incidence of wood
achieve its goals ( eg, exercise, mating, or
chewing. Horses on pasture normally spend
social contact). It is possible tllat this

8-12 hr/day grazing, while confined horses
behavior is a fonn of self-mutilation. Many
spend <3-4 hr/day feeding. Wood chewing
horses that kick and make holes in the walls
increases in cold, wet weatller. Providing
of the stall also eat wood from these holes.

more roughage, exercise, stimulation, toys,

Treatment should be directed toward
or social contact can reduce incidence of
eliminating tile underlying cause. Treatthis behavior. Elinlinating exposed wood ment for aggressive kicking is discussed

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1549
earlier (seep 1546), and for most other
stimulation and exercise and increased
causes the treatment is similar to that for
social contact.

stall walking (see above). Owners should
never reinforce kicking by providing food

Fear and Phobia
when the horse kicks. Providing more

VetBooks.ir
social contact, exercise, and stimulation

Like dogs, horses can have fears and
can also help.

phobias. The two main presentations are
noise and location or envirorunent phobias.

Pawing: Similar to kicking but less

Horses have an innate fear of new things
dangerous, pawing or digging may be a

(neophobia) that explains some behavior
result of frustration and anticipation. This
issues such as trailer-related problems (see
could also be a displacement behavior.

below). The management is similar to that

Changing the floors to concrete may stop
in dogs and cats (seep 1565).

pawing; however, it will not change the
motivation to do so, and some horses

Trailer-related Problems: There are

( especially stallions) may rear up instead
two main presentations of trailer-related
of pawing. Treatment is similar to that for
problems: loading into the trailer and
kicking (see above).

travelling. Horses may be afraid to load into
a trailer because of innate factors ( eg,

Head Shaking: A head-shaking horse
neophobia, a dark interior, instability of
shakes or jerks its head uncontrollably,
the trailer, noise) and/or learned factors
without any apparent stimulus. Some

( eg, previous accident, motion sickness
horses will also snort, rub their head on
previous punishment while loading). A '

objects, and display an anxious expression.

horse may load into a trailer readily but

Most commonly, horses shake up and down. misbehave while inside. This could be There are five grades to this problem:

because the horse finds it difficult to keep

1) inte1mittent signs, mainly facial
its ?alance while the trailer is moving,
twitching; 2) moderate signs with noticeant1c1pates a stressful event such as a race able shaking such that can interfere with
after the trailer ride, or has motion sickness.

riding; 3) advanced stage, and difficult to

In a small nwnber of cases, horses are
control; 4) uncontrollable and unrideable
reluctant to leave the trailer. Heart rate and
horse; and 5) dangerous behavior with
salivary cortisol levels have been shown to
bizarre patterns. In most cases, the horse
increase during and after trailering.

looks as if it has nasal mites or is being

The best approach to managing trailering
attacked by biting flies. Many medical
problems 1s slow desensitization and
conditions can cause head shaking ( eg,
counterconditioning using food and treats.

seizures, respiratory tract diseases and

This may take a long time and may not be
parasites, ear and eye disease, GI disorders
suitable for an acute problem. Desensitizapain, trauma, nasal foreign bodies), and '

tion should be done long before the
these must be excluded. Behavioral causes
expected trailer ride. Punishment should

?f head shaking include an improper bit, an
be avoided, because it may aggravate the
mcompetent rider, fear and anxiety,
situation and be dangerous for both the
dressage leading to extreme cervical
horse and the caretaker. Some horses
flexion, and compulsive disorders. Geldings
prefer to see their environment and may
seem to be affected more frequently than
load better in a rear-facing trailer. Horses
stallions or mares. Management should
are herd animals and learn from each
include treating any underlying medical
other; having a horse with a trailer-related
problem, desensitization and countercondiproblem view another horse loading can tioning, and potentially use of SSRis.

facilitate learning. Foals should be loaded
with their mothers at an early age.

Self-mutilation: Some horses hurt

Sedatives such as xylazine can be used
themselves by biting or kicking the
in acute situations; however, the horse
abdomen with their hindlegs. Some of
may not learn to load or ride better while
these horses also vocalize. Underlying
drugged and may be less able to balance
causes include displacement behavior
itself for the ride and any performance
self-reinforced behavior, and redirected
after the ride.

behavior. Skin diseases and pain can also
lead to self-mutilation and must be excluded. Sexual Behavioral Problems This problem seems more common in young Silent Heat: Behavioral anestrus is males ( <2 yr old) and may possibly be
a common problem in young mares,
triggered by environmental stressors.

especially during the first cycle. The ovaries

Management should include sufficient
are normal on palpation, and ovulation

1550

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
occurs normally. However, the mare will
horse is masculinized before birth;
not accept the stallion. Causes include
therefore, some of these behaviors do
environmental stressors and mating
not require androgens to be expressed.

preference. Presenting several stallions may Some geldings may achieve erection and VetBooks.ir
help, and if the mare is still nursing a foal,
intromission while mounting the mare.

weaning may help.

In advanced cases, the horse should be
checked for pituitary adenoma. Nonnally,

Nymphomania: Medical conditions that
t11e testosterone level should be <0.2 ng/mL.

can cause excessive sexual behavior in

Treatment includes separation, progestins,
mares include granulosa cell tumor and
and SSRis.

persistent ovarian follicles. These conditions should be differentiated because a Eating Disorders
persistent follicle may resolve without
treatment (although it may require

Coprophagia: Eating feces is mainly seen
treatment with gonadotropins or luteinizing
in foals during the first8 wk of life. Foals
hormone or increasing daylight to <Cl6 hr),
usually consume fresh feces of their
whereas granulosa cell tumors require
mothers, and it is believed that maternal
surgical resection. Excessive estrous
pheromones play a role in this behavior.

behavior is manifested as squatting and

Deoxycholic acid is found in feces and
urinating frequently, receptiveness to males, may help protect against infantile enteritis and exposing the clitoris ("winking"). Some and aid in deposition of myelin. The
granulosa cell tumors produce testosterone,
behavior may also provide vitru.11in Band
leading to stallion-like behavior ( eg,
introduce nonnal intestinal flora. In adults,
aggression, mounting, flehmen, and urine
the behavior is mainly associated with a
marking). Management should be directed
low-roughage diet.

toward the underlying problem.

Obesity: Decreased exercise and

Psychic Estrus: Mares with psychic estrus overfeeding a palatable and highly show estrous behavior without any of the
concentrated diet can lead to obesity. On
physiologic correlates of heat. Treatment is
pasture, horses spend 8---12 hr grazing while
as for nymphomania (see above).

moving from place to place; confined horses
spend <3-4 hr. Increasing exercise, social

Poor Libido: Overused stallions, subcontact, and roughage can help maintain missive stallions presented to aggressive
appropriate body weight.

mares, and stallions with previous negative
experiences may be unwilling to mate.

Anorexia: Horses are herd animals, and

Masturbation is a n9rmal behavior in
any changes in social relationships or the
horses; colts will start mounting within the
environment can increase stress and lead to
first few weeks of their lives. Ejaculation is
anorexia. Appropriate weaning of foals is
rare, and fertility rates are unaffected. Some
also important to prevent anorexia. Submisowners use various devices to stop sive horses may not eat near aggressive
masturbation; these essentially punish the
horses if they have previously been
horse for masturbating and cause pain.

attacked. Management should be directed

They can cause fear while trying to breed
toward the underlying problem. Increasing
and predispose the stallion to poor libido.

social contact and separating affected

Management should be directed toward
animals from aggressive horses can help.

eliminating the underlying problems. The
stallion should be presented with teaser

Foal Rejection
mares, should be well rested and fed, and

There are three types of foal rejection:

have increased social contact with mares

1) avoidance, seen mainly in pri.Jnipru.·ous
on pasture. Using an ru.tificial vagina to
mares that appear fearful of the foal-the
desensitize the stallion can help, and
mare will not attack the foal but will not
treatment with anxiolytics such as
allow suckling; 2) intolerance of suckling,
diazepam may address underlying anxiety.

which is seen in primiparous mares or

Other cases may require semen collection
mares with a painful udder; and 3) agand artificial insemination.

gression toward the foal, in which mares
exhibit stallion-like behavior and may kick

Stallion-like Behavior in Geldings:

and bite t11e foal. There may be a genetic

Approximately 500/o of geldings show some
factor for this type of aggression in Arabians
stallion-like behavior, including courting
and Morgans. Some mares paw at the foal to
and mounting females, flehmen, fighting,
stimulate them to stand, and this should be
and attacking foals. The brain of the male
differentiated from aggression.

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1551

The most important aspect of treatment
and sniffing. Aggression and mounting also
is to protect the foal. In extreme cases, the
increase during the cycle. Heat detection is
foal should be supplied with colostrum
an important practice, especially in dairy
within the first 12 hr and then bottle fed or
cattle, in which aitificial insemination is
cross-nursed to another mare. Restraining
common. There are many methods to

VetBooks.ir
a primiparous mare and letting the foal
augment the detection of heat, including
suckle may teach the mare that nursing is
placement of dyes on cows' backs that
pleasurable and encourage her to let the
will stain the estrous cow's ventral torso
foal nurse without restraint. Avoiding any
and pedometers that record increased
disturbances while the mare is nursing the
movement. On some fanns, a teaser bull
foal is paramount for successful nursing.

is still in use. Bulls on pasture will graze

Any evidence of mas ti tis or retained
alongside proestrous cows; the bull will
placenta should be addressed. For an
stand head to head with the cow or may rest
aggressive mare, appropriate restraints
his head on her back. As estrus progresses
such as a barrier or tying should be
he will try to mount, licking her vulva and
considered. Feeding the mare treats while
showing flehrnen.

the foal nurses can help desensitize her. In

Parturition norn1ally occurs at night on
some cases, stimulating maternal behavior
pasture, ai1d the calf norn1ally starts suckling
by separating the mare from the foal or
in <3 hr. The newborn calf spends most of its
faking a threat to the foal ( eg, other horses,
time near the dan1 until it is -4-6 mo old,
dogs) can help. Medications such as
when it forms unstable groups with other
acepromazine, xylazine, diazepam, and
calves. Cows maintain bonds with their
progestins may help; however, these drugs
calves even when the next calf is born. On
can enter the milk and affect the foal.

pasture, heifers are weaned when -8 mo old
and bull calves when -11 mo old. Social
status increases with age, and social relationships are not stable until at least 1 yr of age.

SOCIAL BEHAVIOR

BEHAVIORAL PROBLEMS

Range cattle live in groups of cows and

Most behavioral problems in cattle involve
calves; males are often separated until
breeding or aggression and are related to
breeding season. Dominance in cattle is
poor management practices, confinement,
based on age, sex, weight, presence of
and lack of enrichment.

horns, and territoriality. Breed also seems
to play a role-heavier dairy cattle are
dominant to lighter breeds, while lighter

Breeding-related Problems
beef cattle are dominant to heavier breeds.

Silent Heat: Silent heat occurs most often

When a heavier and older cow is introduced
in heifers during the first cycle. Physical
into a group, it is usually subordinate to
signs of heat ( eg, vaginal discharge, vulvar
existing members of the group. In large
relaxation, and behavioral signs) are absent.

herds, triangular relationships between

Estrus detection methods (see above) can
cows exist. In dairy cattle, hierarchies
help identify cows in heat. In recent years,
change constantly as cows are added or
the use of free martins and dogs for
removed from the herd. Once a hierarchy is
detection of estrus has gained popularity.

established, overt aggression is reduced.

Very little is known about vocal

Nymphomania: Increased sexual
communication of cattle; most commonly
behavior occurs mainly in high-producing
noted are the moo, call, hoot, and roar. A
dairy cows that are 4--6 yr old and have had
distressed cow or calf will call or hoot, an

1--3 calves. These cows usually mount other
aggressive bull may roar, and a hungry calf
cows excessively, act like bulls, and have a
will give a high-intensity "menh."

significant decrease in milk production.

Under natural conditions, cows cycle

In most cases nyrnphornatlia is associated
throughout the year, with peak activity
with follicular cysts, and treatment with
between May and July and low activity
luteinizing hormone or chorionic gonadobetween December and February (northern tropin is useful.

hemisphere). The heat cycle is usually 18---24
hr and generally begins in the evening.

Masturbation: Masturbation in bulls

Common estrous behaviors include reduced normally does not affect fertility. The bull food intake, increased movement, flehmen,
will have a partial erection, ai·ch its back,
standing behind another cow and resting
and perfom1 pelvic thrusts. Because this
the chin on its back, and increased licking
does not lead to increased aggression or

1552

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
reduced fertility, no treatment is needed.

Aggression toward people usually includes

Increases in exercise and stimulation can
bunting, kicking, and crushing. Aggressive
reduce the frequency.

a.11d dangerous animals should be culled.

Poor Libido: Many diseases of bulls can

Aggression in Bulls: Bulls are notorious
lead to poor libido; therefore, the first step

VetBooks.ir
for their unpredictable aggression. Some
in managing impotence is excluding and
bulls may mount others, and these may
treating possible diseases. Bulls with poor
respond with aggression. Such fights can
libido may refuse to mount, avoid estrous
end with serious injuries and even death,
cows, and be unable to develop an erection.

especially if the bulls are homed. Dairy bulls

Behavioral causes for impotence include
are co nun only more aggressive ( and also
inexperience in young bulls that attempt
lai·ger and heavier) thall beef bulls. The bull
breeding an aggressive cow, bulls that are
may paw alld dig in the ground, and homed
used too frequently for semen collection,
bulls may kneel on the front legs alld dig
and the stress of a new environment. Using
using their horns. Because halld-reared bulls
a new teaser bull or, preferably, a teaser cow are more aggressive toward other bulls, it is in estrus can stimulate these bulls to breed.

thought that inadequate socialization may

Allowing the bull to watch other bulls
contribute to this behavior. Aggressive bulls
mounting may increase arousal. Food
should be sepai·ated from others alld
rewards ( eg, molasses) may help as well.

perhaps culled if dallgerous to people.

In many cases impotent bulls should be
eliminated from breeding programs, or
alternative ways of semen collection such

Kicking: Kicking is mainly a problem in
as electroejaculation should be used.

beef cattle alld is seen most commonly in
heifers. Beef cattle ai·e not selectively bred
for gentleness and are halldled minimally.

Buller Steer: Buller steers are steers

These allimals can be dangerous when
mounted by others. This problem is seen in
placed in pens or cages for exainination and

-3% of feedlot steers and seems related to
may cause severe injuries. Such al1inlals
both hormonal and crowding factors. Steers
should be handled carefully alld potentially
are usually in1planted with anabolic steroids, sedated. Food rewards Call be offered for most conunonly stilbesterol or estrogen,
calm behaviors.

which can lead them to mount others.

However, the level of these honnones in the
buller is usually lower. In large, overcrowded Nursing-related Behaviors groups of steers, the nun1ber of bullers is
lntersuckling: Non-nutritional suckling is
higher. This problem may also be related
a c01ru11on problem in calves; the suckling
to dominance; the more.dominant and
calf will suck on other calves or the cow on
aggressive steers mount otl1ers. Erection
ally available appendage or skin tag. This
and intromission rarely occur. Both tl1e
can lead to skin irritation alld even umbilical
buller and the m0tmting steer may fail to
hernias (if the suckling calf suckles on the
gain adequate weight because of psychologiwnbilical sheath of another calf). Poor nutrical stress and increased activity. Removing tion may infiuence development of this
the buller is the most common solution. Addbehavior (increasing roughage can minimize ing hiding places, placing overhead elect1ic
the problem). Penning or isolating suckling
wires, providing sufficient food and water
calves does not solve the pr,0blem; the calf
to avoid conflict, and painting odiferous
will continue to suckle on buckets or engage
mate1ial on the back of the buller also can
in self-suckling. The problem is more
help reduce incidence of this behavior.

conunon in calves wealled after 6 days of
age. Non-nutritional suckling occurs mostly

Aggression
after feeding; providing dry teats next to the
feeding area Call help reduce incidence of

Aggression in cattle is usually a result
this behavior. Other ways to minin1ize this
off ear, learning, and honnonal state.

behavior include placing a serrated nose

Aggression between cows is worse than
ring in the suckling calf, applying repellent
that between bulls. Homed cattle will bunt
materials to suckled areas, alld fitting a

(push or strike with the horns) and strike an
muzzle. These may prevent suckling but do
opponent on the side. Polled cows will use
not reduce the motivation to do so, alld calf
their head as a battering ram. Two cows can
welfai·e should be considered.

fight for a long period witl1 resting periods in
between. Each cow will rest while pushing

Cross-fostering: In some cases, it is
its muzzle between the udder and hindquais
necessary to cross-foster a calf. Dairy cows
ter of the other cow to inunobilize it.

are more likely to refuse a new or wlfainiliar

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1553
calf than beef cows. Bonding between the
typically consist of three sows and their
cow and calf is based on fetal fluid and
offspring. Boars are solitary. A hierarchy is
visual cues; therefore, covering the new calf
formed at social maturity. Sows in the same
with drapes soaked with anmiotic fluid or
group cycle at the same time and participate
the skin of the cow's own dead calf or
equally in group maternal behavior one sow
blindfolding the cow can help. Encouraging
will remain with the piglets while the others

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the cow with food rewards can also help.

forage. Communal nesting is also found
under free-ranging conditions. In confined

Miscellaneous Behavior Problems
pigs, a hierarchy is formed as early as 1 wk

Reluctance to Enter the Milking
of age. Piglets will fight newly introduced

Parlor: Reluctance to enter the milking
piglets in the pen. Piglets also fon11 a teat
parlor is a problem related mainly to
rank by the end of the first week of life· the
management. When dairy cows accustomed
dominant piglet suckles on the first p;ili of
to milking with sin1ultaneous feeding in a
teats and gains weight faster. Once the teat
stanchion barn are moved to free stalls and
order is forn1ed, the hierarchy remains
are not fed when milked, they may refuse
stable as long as the same piglets remain in
to enter the parlor. Previous negative
the same group. Normally, the heavier pig
experience ( eg, mastitis, aberrant electric
is more dominant. It appears that both
shock, punishment from the handler) can
geneUcs and experience play a role;
also play a role. In addition, changing the
dommant sows give birth to dominant
side from which the cow is normally milked
piglets. Once a hierarchy is fon11ed, fighting
can increase anxiety and even aggression.

1s mostly replaced with threats. Weaning

Providing more grain feeding, a cairn
takes place with.in the first 3--4 mo of the
environment, and possibly a preferred cow
piglet's life, but in mass production

"mate" can help minimize the problem. Simienvironments, it can take place as early lar problems can arise with the introduction
as 3-4 wk of age.

of electric squeeze gates.

Sows norn1ally have two estrous cycles
per year and fan·ow twice. Pheromones

Food Throwing: The underlying cause of
and the sight of a boar are major factors in
food throwing is not well understood. The
inducing cycles in gilts. In postfarrowing
affected animal grabs food with its mouth
sows, weaning helps induce estrus; boars
and throws it on its back. One possible
can be used to detect females in heat. The
explanation is maintenance behavior that is
boar is usually highly vocal ( courting song)

meant to reduce biting flies in the presence
and exhibits flehmen when an estrous
of docked tails. The diet mixture may also
female is present. Boars will nuzzle the
play a role; the problem is seen more
head, shoulders, flank, and anogenital area
commonly in cattle fed a total mixed ration.

of sows during comtship. Nonnally, boars
urinate several times and produce thick

Tongue Rolling: Tongue rolling occurs
saliva rich in pheromones. Boars raised
mainly in veal cattle and is most likely a
without the presence of other pigs show low
stereotypic behavior resulting from
sexual perforn1ance.

confinement. The affected calf flicks its

Communication in pigs is mainly vocal;
tongue outside and rolls it back inside the
there are -20 different recognized sounds.

mouth, followed by swallowing saliva. One

The grunt is one of the most conm10n sounds
study showed that veal calves that displayed given in response to familiar sounds or tongue rolling had no abomasal ulcers,
while looking for food (rooting). A short
while those that did not show this behavior
grunt is given when the pig is excited,
had ulcers. This may indicate that the behavwhereas a long grunt is a contact call and ior reduces stress. However, calves that
normally associated with pleasurable
showed tongue rolling as well as those that
stimuli. When pigs are aroused they may
did not had abomasal erosions. Increasing
squeal, and they may scream when hurt.

stimulation ( eg, adding sucking teats) may

Dominant pigs bark at subordinate pigs as
reduce incidence of this behavior.

a threat. Visual signals in pigs are not well
developed. The tail position indicates the
well-being of the pig. A tightly curled tail

SWINE
is an indication of a healthy pig, and a
twitching tail indicates skin irritation.

SOCIAL BEHAVIOR

In mass production environments, tails
are normally clipped to avoid tail biting

Pigs are social animals that under free

(see below). Olfactory signals are highly
ranging conditions live in groups of
developed in pigs. There are sex differences;
approximately eight individuals. The groups sows can detect lower concentrations of

1554

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
smell and pheromones than boars. When
sive than Durocs. Body fat percentage may
introducing a new pig into an existing
also be a factor; breeds with lower body fat
group, the resident pigs investigate the
a.re more aggressive when handled.

newcomer by nosing it. Pigs can form

Management includes slow introduction

VetBooks.ir
social ranks when they are blindfolded,
of new pigs into existing groups, provision
which indicates the importance of
of shelters where subordinate pigs can hide,
olfactory and vocal communication.

provision of sufficient resources and toys,

Socialization in piglets starts at -5 wk
and application of boar pheromones. Most
of age with consr,ecifics and at 14 wk of
producers keep lights dim in the pen to
age with other species. Pigs 14-17 wk old
reduce aggression. Using tranquilize1s such
are most sensitive, and any negative or
as azaperone (2.2 mg/kg) or amperozide
unpleasant experience during thls pe1iod

(1 mg/kg) can help reduce aggression but
can delay sexual maturity, leading to late
may not be economical. LithiWll (an
first farrowing. In free-ranging conditions,
antipsychotic) has been used successfully.

grouping promotes foraging, musing, and
protection against predators. Pigs under

Tail Biting: Tail biting is seen mostly in
free-range conditions will also choose one
confined pigs. Overcrowding and boredom
place to defecate. In commercial production, seem to be the main causes. Free-ranging the most noticeable group behavior is in
pigs spend 5-10 hr daily looking for food and
newborn piglets, which huddle when cold.

rooting, whereas pigs kept in pens consw11e
meals in a shmt time. Slatted floors witl1out

BEHAVIORAL PROBLEMS
bedding, low-salt diets, and low-iron soil
seem to predispose pigs to tail biting. Once

Many behavioral problems in swine are
the problem stalts, blood from the injmed
related to confinement or stress. The
tail seems to arouse the other pigs and can
treatment is usually directed toward
even lead to death of tl1e victim but rarely
managing social groups, establishing
advances to pme cannibalism. Most losses
nom1al conditions when possible, and
are due to secondary infections that result in
maintaining welfare.

culling. Management includes removing the
biting pigs (if there are only a few of them)

Aggression
and providing stimulation such as straw
bedding to root, toys, and com on tl1e cob

Aggression Toward Other Pigs: Piglets to chew. Most conunercial produce1s dock show aggression to other piglets within the
piglets' tails; however, this does not reduce
first week of life while forming a teat order.

the motivation for tail biting, and pigs may

Later, introducing new pigs into a group may bite the stwnp or ears instead.

lead to aggression as the.pigs establish
social ranks. Pi.gs may spend 1-2 min nosing

Cannibalism: Mostly seen in prin1iparous
each other, vocalizing, and then biting until
gilts, cannibalism accounts for4%of piglet
one of the pigs retreats. It may take several
deaths and is estin1a.ted to affect - lSoAi of
days to establish a hierarchy in older pigs.

litters. It is most common inunedia.tely after

Once the hierarchy is established, fights are
parturition when the sow is stressed.

rare and ranks are preserved mostly by

Usually, the sow will bark to warn piglets
threats from the dominant pig and subwalking by her head and then later attack missive gestures from subordinates ( eg,
them, biting them to deatl1. Fa.n·owing crates
twisting the head away). During estrous
have been used successfully to reduce the
cycles, sows may show severe aggression
incidence of cannibalism. Aza.perone (2.2
toward newly added sows. Submissive sows
mg/kg) has been used for treatment as well.

show the least estrous behavior, have small
litters, and lose weight (most likely due to

Crushing Piglets: Heavy sows may lie
low nourishment). Most aggression in pigs
on their piglets, killing tl1em. This nom1ally
seems to be related to resources such as
occurs when there are weak, underdevelfood. Crowding and limited amow1ts of food oped, or sick piglets that cannot move fast
increase aggression. Dwing breeding, boars
enough to a.void the sow. However, it is also
may fight and become very vocal; boars will
a breeding and management problemstrut shoulder to shoulder, cha.mp their jaws sows are na.tmally intensely protective

(producing pheromone-rich saliva), then
mothers that will prevent the handler from
finally face ea.ch otl1er and attack. Serious
attending to the piglets; selective breeding
injuries may result, especially among boars
for less-protective sows has resulted in
that still have their tusks. Breed likely plays
sows less devoted maternally. Management
a role; Large Whites a.re more aggressive
includes providing appropriate farrowing
than Hampshires, which are more a.ggres-
crates with slopes and bars on the sides that

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1555
allow the piglets to move away from the sow stereotypic behaviors include nibbing nasal and prevent the sow from rolling over on the secretions on the floor or another pig, bar piglets. In addition, heat lan1ps provide the
biting by confined sows, and polydipsia.

piglets with an alternative heat source and

Environmental enrichment in early stages
motivation to rest away from the sow.

is usually successful. Feeding smaller

VetBooks.ir
quantities more frequently and providing

Breeding-related Problems
toys, bedding to root, corn on the cob, and

Reproductive problems are usually
clean tires can be enriching and mentally
associated with management of boars and
stimulating for pigs.

sows and estrns synchronization. These
problems are fairly unusual in pigs because
of rigid genetic control of sexual behav10rs.

Mating preferences are an impoitant factor
in breeding management of pigs.

SOCIAL BEHAVIOR

Poor Libido: Poor libido in boars can be

Sheep ai·e a prey species, and tl1eir only
caused by nut1itional problems ( deficiendefense is to flee. Sheep display an intensely cies or overfeeding) and behavioral causes
gregarious social instinct that allows them
such as stress or fear. Exposing a boar to an
to bond closely to other sheep ai1d
aggressive female can result in low sex
preferentially to related flock members.

drive. Socialization, visual social contact

Flock mentality movements protect
with affiliative sows for a few days (in pens
individuals from predators. Flocks include
across from each other, not next to each
multiple females, offspring, and one or more
other), and appropriate nutrition are the
males. Ewes tend to stay in their maternal
keys to successful management.

groups for life, whereas rains may form
transient m1stable, and easily disbanded

Failure to Reproduce: This is seen
bachelor'herds. If most rains in a group die
mainly in confined gilts, and stress seems
because of fights or diseases, those
to play an important role. Regrouping or
remaining join another group. Under
overcrowding increases stress levels as
standard grazing situations, sheep graze
well. These two factors ( confinement and
together in casual affiliations; social
crowding) lead to chronic stress, delayed
hierai·chies are not as apparent as tl1ey ai·e
puberty, and failure to reproduce. In
for cattle.

contrast, acute and mild stress such as

Flock dynamics are apparent in groups of
transport and gentle handling accelerate
four or more as evidenced by willingness to
estrous cycles.

follow a leader or flee in llllison. When
escape is prevented, even a ewe may chai:ge

Refusal to Nurse: Nonnally, the sow lies
or threaten by hoof stomping. Separation
in lateral recun1bency and grunts to attract
from the flock can cause stress and panic.

the piglets to nurse. Mastitis is the most com

Isolation from other sheep can cause severe
mon reason sows refuse to nurse piglets.

stress and should be avoided. Min-ors can

A physical exanlination is necessary to
be used in the absence of other sheep.

exclude this and other medical conditions.

Males in rut will physically challenge one

The sow lies stemally, preventing the piglets
another for social rank and breecling
from accessing the teats. Mastitis is typically
privileges. Social rank depends on tl1e
seen during late phases of lactation when
presence and size of horns, body mass, and

.

the faiTowing crates are removed. Sows Wlth height at the withers and hocks. Age may postpartmn dysgalactia syndrome and
also play a role, because tl1e mortality of
mas ti tis (seep 1373) are usually too weak to Ian1bs from yeai·ling ewes is extremely high.

move and prevent the piglets from nursing.

Higher-ranking males concentrate on

However, these sows usually do not eat,
courting females when in rut and do not
and their piglets do not gain weight. Piglets
graze to the extent lower-ranking rains do.

of such sows should be transitioned to

Groups of 40-50 ewes/adult rain and 25-30
milk replacers ai1d solid food. This can be
ewes/juvenile rain are common manageencouraged by mixing sow's milk with the ment choices. Mortality in rains is five tin1es
food or sweetening the food.

that in ewes. Generally, subordinates ai1d

IoweHanking rains are excluded from
breeding, mlless lower-ranking ailimals

Stereotypic Behaviors
outnmnber the higher-ranking male and

Stereotypic behaviors are not common in
serve to distract or otherwise occupy him
pigs and mostly relate to management,

(this need not be cooperative). While the
boredom, and nutrition. The most common
higheHanking male usually has larger

1556

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
horns, the role of the demographic
tl1e ewe for individual lan1b recognition, as
environment (ie, the number of lowe r is the shape and color of the lamb's head.

ranking males in the group) prevents an

Ewes are more likely to accept Jambs that
extreme selection response for these
have fanli!iar head coloration.

secondary sex characteristics.

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In large groups of sheep or in sheep on

Lamb Rejection: Lamb rejection can be
large pastures, more subordinates are likely
associated with the social hierarchy or due
to mate. In tightly confined, relatively small
to behavioral, physiologic, or environmental
groups, the role the social order plays in
stresses ( eg, rain) at delivery. The smell of
mating is critical, and owners should
the wool is important to the ewe, and Jambs
understand that lower-ranking rams may
that smell unfan1iliar are more likely to be
not mate under such conditions.

rejected. Expe1imental results show that

Sheep are seasonally polyestrous and
lan1bs whose heads have been altered are at
reach puberty at 7-12 mo. Mating behavior
risk of rejection. Alteration of the tail does
includes nudging, kicking, or pawing with
not have the same effect. lfthe rejection is
the front legs, low stretching, and pushing.

noted sufficiently early, using a stanchion to

These same behaviors and head-to-head
confine the ewe with the lamb can address
banging with horn clashing occur in
the problem. Tranquilization may be
conflicts between males.

needed.

Artificial weaning occurs at 10 wk of age,
but these lambs recognize and will return to

Cross-fostering: Cross-fostering can be a
the ewes after a 2-mo separation. Sheep are
successful solution for abandoned, rejected,
naturally weaned at 6 mo of age, usually
or orphaned Jambs. Cross-fostering is best
when their mother again comes into heat.

addressed by fooling tl1e ewe, using cervical

Ewe Jan1bs continue to follow the dam, but
stimulation (using balloons that stimulate
ram lambs do not.

oxytocin release and maternal behavior).

Sheep are likely to be more intelligent

Cove1ing tl1e lamb to be fostered with a
than generally regarded. They respond
t-shirt that the ewe's own Jan1b has worn can
readily to food calls, may problem solve,
provide an appropriate olfactory cue, as can
learn their names, carry packs, and can even the skin of the ewe's own dead lamb.

be clicker trained. Sheep may be grazed on
open, unfenced areas and may heft (remain

Stereotypic Behaviors: In sheep,
in home field) to a limited area as a learned
stereotypic behaviors include wool-sucking,
behavior by Jan1bs from their ewes. Sheep
intersucking, and self-sucking (tails or
possess specialized neural mechanisms in
udder).

the right temporal and frontal lobes of the
brain and may recognize familiar human or
ovine faces for as long as 2 yr.

BEHAVIORAL PROBLEMS

SOCIAL BEHAVIOR

Homosexuality: Homosexuality is a

Social behavior in goats is similar to that in
normal behavior in sheep and is seen in up
sheep, and horns also play a major factor in
to 300/o of all rams. Incidence of homosexualcaprine social rankings. Goats also hide ity is decreased in rams raised in heteroearly in life but, unlike cows, spend more sexual groups and in rams that have
ti.me away from the nannies for the first
experience with ewes, but it still persists. It

6 wk than for the next 6 wk. The nanny
is unclear to what extent such behaviors are initiates early approaches, and the kid facilitated by a sex ratio that has been
initiates the later ones. Sexual behavior of
skewed for mating purposes.

goats differs slightly from that of sheep.

Billy goats tl1row their head up in the air and

Lamb Stealing: Ewes can steal the lambs
ventroflex their neck when they ejaculate.

of others before their own parturition and

They also frequently urinate on their front
then reject their own Jamb when it is born.

legs, which they then rub on the doe as part

Lambs seek out soft, warm, hairless areas
of the courtship ritual. The scent of female

( regardless of where they are), which can
urine is important and is transpo1ted into
help with raising orphaned lambs but render tl1e vomeronasal organ during flehrnen.

stealing easier. Individual pens or partial
barriers can usually prevent theft. Ewes will

BEHAVIORAL PROBLEMS
sequester the lambs at first, and providing
them a shelter where this can be done will

Behavioral problems are not commonly
help. The smell of tl1e wool is important to
reported in goats, perhaps because adult

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1557
males are expected to charge people
some cases by removing the instigator.

if their turf is traversed. Behavioral

Providing enrichment and changing the
problems may actually be more rare ( as
social structure by removing or adding
opposed to less frequently reported) in
individuals may help as well. In rare cases,
this group, because their maintenance
aggression can advance to cannibalism (see
conditions more closely mimic those in a
p 2873). Broilers and free-ranging chickens

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free-ranging situation. Domestication may are more likely to show these problems have had less of an impact on the social
because egg-laying chickens in mass
patterns of goats than is true for other
production are usually confined to small
species.

groups.

Aggression can manifest as pecking at the

Self-suckling: Goats that abort late in
head and face or as pecking at and pulling
pregnancy or those that have a second
feathers. Chickens have sharp and strong
pregnancy subsequent to nursing can
beaks that may lead to severe injuries.

self-suckle. The latter situation may be

Reducing daylight in battery conditions,
illuminating, because the behavior did not
adding tryptophan to the food, and beak
occur when the nanny was nursing.

trinuning can minimize aggression. Beak

Treatment involves behavioral and
trimming is a symptomatic treatment,
environmental enrichment, social
however, and may raise welfare concerns.

companionship that is stable before

Grooming and feather care are part of
pregnancy, and possibly some antianxiety
normal hygiene in chickens and can also be
medications.

social activities. Dust baths can help reduce
the incidence of feather picking.

Stereotypic Behaviors: Stereotypic
behaviors in goats are sintilar to those in
sheep (see above). Goats separated from a
group may develop competitive "rearing"

SOCIAL BEHAVIOR
or elevation.

The dog's social structure has been refeITed
to as a pack hierarchy, but this does not

CHICKENS
accurately or entirely describe the relationship of dogs with other dogs or with people.

SOCIAL BEHAVIOR

Scientific studies into the behavior of wild
wolves have established that the wolf pack

Free-ranging chickens are social animals. In is actually a family unit, with the adult these groups, hens and chicks are the core,
parents guiding the activities of the group.

while roosters live independently. Social

The dog likely originated from the grey wolf
maturity occurs at -1 yr of age, although

12,000-14,000 yr ago, although the origins of
most chickens are sent to slaughter before
domestication may extend back 30,000 yr.

this age. Free-ranging chickens show more

Conununication and relationships are estabaggressive behaviors than battery chickens lished through a language of visual signals
do. Rank is based on multiple factors ( eg,

(body postures, facial expressions, tail and
size, age, color, and social environment). A
ear carriage, and piloerection), vocalization,
new or foreign chicken is lower in rank than scents, and pheromones. However, a chicken on home ground. Both nesting
domestication and selective breeding have
and food intake are genetically controlled

Jed to extensive variation not only from wolf
behaviors, and chickens are selected for
to dog but also between breeds and
high food intake. Hens will form nests if
individuals in morphology, breed traits,
supplied with nesting material. An adult
temperan1ent, behavior problems, variation
chicken that has never used a nesting box
in behavioral neoteny, and social signaling.

will use one if provided.

In fact, Huskies retain most of the social
signaling repertoire of wolves, German

BEHAVIORAL PROBLEMS

Shepherds less than 2/,, and Cavalier King

Charles Spaniels the least. Thus, it may be

Aggression and feather pecking or plucking
difficult for dogs ( and people) to read and
are the two most common behavioral
interpret the signals of other dogs,
problems in chickens. They may be related
especially those of different breeds. Early
and possibly have sintilar underlying
and frequent socialization with a wide
components, including stress, overcrowdvariety of dogs is therefore an inlportant ing, and competition over resources such as
component of intraspecific communication.

food. Both conditions can be managed by

The tenn dominance (seep 1536) does
addressing the underlying problem and in
not describe the relationship between two

1558

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
individuals; it is a relative tern1 established
docosal1exaenoic acid during tl1e neonatal
by the value of the resource to each
and prenatal periods has been shown to
individual and the cumulative effects of
in1prove the puppy's brain and retinal
learning.

development and trainability.

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Hierarchy in dogs is neither static nor

Between the neonatal and socialization
linear, because the motivation to obtain and
period is a transition period, during which
retain a specific resource, together with
the eyes open and puppies begin to develop
previous learning, defines the relationship
motor skills. At this time, interactions with
between two individuals for each encounlittern1ates are in1portant for development ter. Stability is maintained by deference and
of social skills.

not by agonistic behaviors. Only in those

TI1e next petiod of development (socializarelationships in which one individual tion or sensitive period) extends from 3-4 wk
consistently defers to another across
to -12 wk of age. Owing this period, the
resources and interactions might a linear
puppy is most sociable and will most readily
hierarchical relationship between the
habituate to dogs, people, other animals, and
individuals be described. Although this
tl1e environment (sights, sounds, odor, touch,
tenninology applies to the intraspeci.fic
taste). Between 3 and 8 wk of age, puppies
communication and signaling between
start exploring their envirom11ent and
members of a species ( eg, dog-dog), it does
continue to refine social skills witl1 their
not "translate" to communication between
littennates and other dogs. Weaning is
species (eg, dogs-people).

non11ally completed at 7 wk of age, and at

Relationships witl1 people are not

-8 wk of' age puppies strut developing a
established by dominanUsubmissive social
preference for elimination locations.

signaling; they are a result of genetics, early

As the socialization period winds down,
handling, and socialization and shaped by
puppies make attachments Jess easily.

learning and consequences. In fact, dogs

Therefore, a lack of adequate socialization
have acquired an ability and readiness to
and enrichment during the sensitive
respond to hun1an behavior not found in
period can contribute to excessive
wolves, even if the wolf pup is hand raised
responses to stimuli, including fear and
and socialized. In tum, dog owners must
aggression. Spending the first 7-8 wk with
learn to read canine visual signaling and
the mother and littennates plays an
vocalization to understand when dogs want
important role in the development of
to engage and when they do not, as well as
social skills with other dogs. However, if
to train and reward relaxation and to safely
exposure to people, other pets, and new
and effectively modify fearful and
environments does not begin before the
aggressive behaviors.

end of the socialization period, the dog
may become socially maladjusted and

Canine Development
unable to cope and communicate. Proper
development of social skills can be

The first in1portant period of development is accomplished in part by adopting puppies the neonatal period, which extends into the
into the new home at -8 wk of age and
third week of life. Puppies are born with
enrolling in puppy socialization classes
closed eyes and lin1ited motor ability.

before 12 wk of age, so that the puppy can

Puppies are altricial; therefore, in the first
be exposed to a range of dogs, people, and
few weeks, maternal care is critical.

other stimuli (eg, novel s4rfaces, noises,

Grooming by the mother arouses the puppy
odors, moving objects, uniforms, and
to eat, stimulates elimination, and helps to
handling) in a controlled, instructional,
keep the puppies in the nest. Good maternal
and positive environment. Similarly, visits
care results in an increased ability to handle
to the veterinarian or groomer, car rides,
stress and increased maturation of the
visitors to the home, and the use of sound
nervous system. Sin1ilarly, mild stress in the
desensitization recordings provide
form of gentle hun1an handling during the
additional opportunities for exposure. Dog
first 2 wk of life can in1prove cardiovascular
appeasing pheromone and the presence of
performance and resistance to disease.

another dog may also ease adoption into a

Handled puppies also mature faster,
new home. If there are any signs of fear,
pe1fonn better in problem-solving tasks,
every effort should be made to overcome
and are better able to withstand stress as
the fear by finding the limits (threshold)

adults. In contrast, moderate to severe
the dog will tolerate and using food and
prenatal and neonatal stress as well as
treats or toys to try to ensure a positive
maternal separation can have a sensitizing
outcome. Continued exposure to a wide
effect on the hypothalamic-pituitary-adrenal variety of stinmli with positive outcomes axis. Feeding the bitch a diet eni1anced with
should be continued to adulthood.

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1559

The third Uuvenile) period extends

When the puppy caimot be effectively
from -3 mo to 1 yr of age. Domestic dogs
supervised, the household should be set
reach sexual maturity at 6-9 mo (later in
up to ensure success (and avoid failure).

some giant breeds) and social maturity at

Preventing undesirable behaviors while

12-36 mo of age. Social relationships are
providing the dog with options acceptable

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established to minimize conflicts within
to the owners and the dog gives the dog
the group. Although heredity and previous
control to make choices, reduces uncersocialization play important roles in the tainty and anxiety, and prevents undesirable
behavior of an individual, positive
behaviors. Of particular value to establish a
exposure to a wide range of animate and
safe haven is a crate, exercise pen, or room
inanimate stimuli during this period
to provide security and safety for the dog
should minimize development of fear and
when it caimot be supervised or wants to be
anxiety.

alone. A daily routine can be established

Domestic dogs are nonseasonal breeders
that provides stability and predictability for
and have on average two heat cycles/yr
the dog, beginning with meeting the dog's

(range one to four). If the female does not
social and physical needs, followed by
get pregnant, she will go through hormonal
sessions of inattention during which the dog
changes as if she were pregnant, known as
is given the opportunity to nap and rest or to
false pregnancy or pseudocyesis, which can
engage in exploratory play with its food and
be associated with overt physiologic and
chew toys. By confining the dog to a crate,
behavioral changes, including lactation,
pen, or room during these "inattention"

nesting, and protective aggression of
tin1es, the dog learns to spend tinle on its
objects such as toys.

own; this also may prevent dainage to
property, housesoiling, and even separation

Counseling to Prev nt Und alrable
anxiety. Undesirable behavior might

B h11vlor1
alternatively be prevented through
environmental mai1agement ( eg, child gate,

Veterinaiians and staff should work with
shutting doors, tie downs, deterrent
breeders, trainers, pet stores, and shelters
devices). Neutering males may also help to
to ensure that the newly adopted dog gets
prevent testosterone-influenced behaviors
off to the right start. For puppies, this
such as urine marking, mounting, and
includes advice on socialization, nom1al
roaining.

canine behaviors ( eg, jumping up, play
biting, elinlination) and how they can be

BEHAVIORAL PROBLEMS
managed, a household environment that
provides appealing but safe outlets for all of

When behavior of dogs is undesirable, there
the dog's behavioral needs ( eg, chewing,
are three levels of consideration: 1) Behaviors
social play, object play, rest), guidance on
within the nonnal range for the species, ·age,
canine communication, and learning
and breed. In these cases, the owners need
principles of reinforcement-based training.

guidance on how to effectively manage the

The goal should be to reinforce desirable
behaviors. 2) Behaviors more difficult
behaviors and to ignore or prevent
or challenging, because they might fall
undesirable behaviors. Clicker training can
within or just beyond the range of what is
be particularly useful to in1mediately mark
considered normal but are particularly
and reward desirable behavior and
intense or difficult to manage. Exainples
gradually shape behaviors that more closely
include mouthing, urine marking, mounting,
approximate the final outcome ( duration,
barking, chasing, predation, or overactivity.

relaxation).

Also in this category might be what could be

Oral behaviors are a common problem,
normal for the breed but unsuitable for the
because puppies have a behavioral need for
family and home (ie, mismatch). These
exploration and play. Therefore, providing
cases require behavior assessment and
constructive social activities that do not
counseling to ensure the owners have a
include mouthing or biting of people, such
realistic understanding of what might be
as tug gaines, retrieving, walking and
achieved and to implement treatment
running, chasing, hide and seek, playing
strategies, including environmental
with other dogs, and training for rewards,
management and behavior modification, to
gives the dog something positive on which
achieve an acceptable level of improvement
to focus. A head halter is also an option
for both the owners and the pet. 3) Behaviors
for better control of the head and muzzle.

that are abnormal or pathologic, as a result

Another way to manage oral stinmlation
of emotional disorders or mental health
and exploration is to provide chew toys,
issues. These may have developed as a
food-stuffed toys, and food-dispensing toys.

result of genetic factors, stressful perinatal

1560

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
environment (prenatal, neonatal),

While avoidance and escape is one strategy,
insufficient early socialization, medical
some dogs use aggression to remove the
conditions affecting brain health and
fear-evoking stimulus and are reinforced by
development, or particularly trawnatic
success (negative reinforcement).

environmental events. For these pets, the

Some of the more common presentations

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prognosis may be guarded, and owner
include the following: 1) fear of other dogs,
expectations altered to achieve an
especially those that are wlfamiliar, appear
acceptable outcome. Treatment generally
threatening to the clog, or with which the
requires both environmental management
clog has had an w1pleasant experience;
and behavioral modification, often in

2) fear of unfamiliar people, especially those
combination with medication (natural
who are novel or look, act, or smell different
products, diet, drugs) to improve underlying than those the clog is accustomed to ( eg, pathology and facilitate learning.

yotmg children); 3) feat· of inanimate stimuli

The process to diagnose behavior
such as loud or wlfanliliat· noises ( eg,
problems and their treatment with behavior
construction work, trucks, gunshot), visual
modification and drugs has been previously
stinmli (eg, un1brellas, hats, Wliforms),
described (seep 1539). If the problem is
envi.ronments ( eg, backyard, park, boarding
detenninecl to be a norn1al but undesirable
kennel), surfaces ( eg, grass, tile or wood
behavior, the owners will need counseling
floors, steps), or a combination of stimuli
on how to effectively provide for the

(eg, vacuwn cleaners, cat· rides); and 4) fear
pet's needs and how to reinforce what
of specific situations such as veterina.iy
is desirable while preventing what
clinics or grooming patfors. Some clogs have
is undesirable. For most canine behavior
a more generalized atudety, in which the
management problems, counseling from
fearful reaction is displayed in a wide range
veterinaty staff or trainers and quality
of situations to which a "normal" pet would resources are required, as well as hat1cls-on
be tmlikely to react. Although there can be
guidance from a trainer. Trainers should be
a genetic component to feat· and anxiety,
selected based on their credentials at1cl
prenatal and neonatal stressors, including
screened to ensure they use reinforcementmaternal separation, lack of socialization based training techniques. Positive

(ie, wlfanliliarity), or a previous unpleasant
punishment-based techniques should not
outcome clmi.ng encounters with the
be used in training, because at best they
stinmlus ( or similar stimuli), can also be
se1ve only to suppress undesirable behavior
causative factors.

and cat1 lead to fear, avoidance, and even

Phobic responses in clogs are generally
aggression. Management issues include
associated with loud noises ( eg, thunder,
inappropriate play ( eg, nipping or mouthing
fireworks, gunshots) and the stimuli
of people); unruly b_ehavior ( eg, pulling,
associated with these events, including rain,
lunging, jwnping up, mow1ting, overactivlightning, and perhaps even static or ity); and some forms of barking, destructive
pressure changes associated with a
behaviors, and housesoiling.

thunclerstom1. Some feat·s ( eg, veterinaty

If the problem is detem1ined to be an
clinics, going outdoors, entering certain
emotional disorder or abn"onnal behavior,
rooms, or walking on certain types of
resolution will require a combination of
flooring) may become so intense that they
behavior modification techniques,
meet the definition of a phobia.

modifications to the environment to prevent
fwther problems, and medications to help

Separation Anxietyi It is estimated that
reestablish a more nonnal mental state and

-14% of clogs have separation anxiety, or
facilitate new learning (seep 1539).

an inability of the pet to find comfort when
separated from fanilly members. The

Fears and Phobias
problem may be prima.iy ( eg, hyperattachment, dysfunctional attachment) as the Fear is a nom1al response to an actual
puppy ages and matures; in fact, the
or perceived threatening stimulus or
chat1ces of the problem developing can be
situation. Anxiety is a response to feat· at1cl
reduced by having puppies regularly spend
agitation, or apprehension when the animal
tinle during the clay on their own (preferably
anticipates a threat or fearful situation.

in a safe haven). In other cases, the anxiety

Phobia is an exaggerated fear response
about being left alone is seconcla.iy to an

(seep 1536). The fear response may include
event such as a change in the household or
panting at1d salivation, tucked tail, lowered
dog's daily routine, or associated with an
ears, gazing away, low body posture,
w1clerlying state of anxiety along with other
piloerection, vocalization, or displacement
behavioral issues such as noise phobias and
behaviors such as yawning or lip licking.

separation anxiety. Anxiety may lead to

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1561
destructive behavior (particularly at exits or Pinschers. The problem may first arise as a toward owner possessions), distress
displacement behavior when the dog is
vocalization, housesoiling, salivation,
frustrated, conflicted, or highly aroused.

pacing, restlessness, inability to settle,

Lack of predictability in the daily routine,
anorexia, and repetitive or compulsive
alterations in the environment, unpredictbehaviors. The behaviors are exhibited able consequences, lack of sufficient

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when the dog is left alone and generally
outlets for nonnal behaviors, and chronic
arise within the first 15-30 min after
or recurrent anxiety might be initiating
departure. A video recording can be an
factors. At this point, if the owners can
invaluable diagnostic aid to visualize the
teach appropriate acceptable alternative
behavior and determine whether there are
responses ( eg, sitting before greeting or
other concurrent signs of anxiety ( autoplay as an alternative to spinning) and nomic stimulation, increased motor activity, provide constructive alternatives ( eg, and increased vigilance and scarming). The
feeding from toys), the problem might be
diagnosis requires that other common
resolved. However, as the frequency or
causes of the signs be excluded ( eg,
intensity increases, the behavior may
incomplete housetraining, exploratory play
become compulsive. The diagnosis is
and scavenging, external stimuli leading to
considered to be a compulsive disorder
arousal and anxiety, noise aversion,
when the behavior interferes with norn1al
or confinement anxiety). Many pets with
function or when it becomes independent
separation anxiety begin to exhibit signs as
of ( or emancipated from) the inciting
the owner prepares to depart ( eg, putting on stimulus. There is likely altered serotonin shoes, getting keys, going to the door).

transmission.

When the owner is home, the dog may crave

Stereotypies are defined as repetitive
constant contact or proximity to the owner.

behaviors that are unvaried in sequence and

When the owner retwns, the welcoming
have no obvious purpose or function. They
responses are commonly exaggerated and
may arise when the environment lacks
the dog is hard to cairn down.

sufficient outlets for the dog to engage in
normal behaviors, or when caused by

Abnormal Repetitive Behaviors
maternal deprivation or as a result of a
neurologic disorder. It is possible tl1at

Abnormal repetitive behaviors may actually
stereotypic behaviors, at least in their early
comprise a nwnber of conditions with
stages, may provide a coping mechanism for
different pathogeneses, including compulthe pet. Stereotypies might be induced by sive disorders, stereotypies, neurologic
doparninergic stimulation.

disorders, and other forms of behavioral

Although most dogs respond to drugs that
pathology. Therefore, until a diagnosis is
inhibit serotonin reuptake including the
made, the term abnorn1al repetitive

SSRis and clomiprarnine, alterations in
behavior may better describe the clinical
other neurotransmitters may play a role, eg,
presentation.

dopamine, endorphins, N-metl1yl-o-aspartic

Compulsive disorders may be repetitive,
acid (NMDA). Because medical problems
stereotypic, locomotory, grooming,
might be the cause of the signs, these should
ingestive, or hallucinogenic behaviors that
first be excluded. In cases in which the
occur out of context to the tin1e and
physical examination, history, and
situation in which they take place, and
diagnostic testing do not clearly identify the
occur in a frequency or duration that is
cause, a therapeutic response trial might be
excessive. There may be lack of control
indicated ( eg, anticonvulsants to exclude
over onset or tern1ination. Although it can
focal seizures as a cause of fly snapping or
be debated whether animals can obsess,
light chasing; clomiprarnine or fluoxetine to
they do perceive and experience concern;
exclude compulsive disorders). See ai,so
therefore, the tenn obsessive-compulsive

TABLE 4.

has also been used to describe this
disorder. The diagnosis should start with
a description and observation of the

Aggression
behavior, including video recordings if

Aggression is the most common problem in
necessary. Because there is likely a genetic
referral practices across North America,
component for many compulsive disorders,
approximating 70% of the caseload. It is
the signalment and age of onset is also
also a major human concern, because at
important. For example, German Shepleast 5 million people are referred to the herds and Bull Terriers are known to spin
hospital each year in the USA alone for
or tail chase, while a genetic locus for flank
treatment of dog bites. Most forms of
sucking has been identified in Doberman
aggression, except for predation, are

1562

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

CLINICAL PRESENTATION AND MEDICAL DIFFERENTIALS FOR

COMPULSIVE DISORDERS

Diagnostic Tests I

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Compulsive Disorder Signs Medical Differentials

Therapeutic Trials

Ingestive: pica, licking, sucking, GI, food intolerance Endoscopy, food trial,
swallowing (glugging)

steroid trial, GI protectants

Polyphagia, polyuria,

Urogenital/renal, hepatic, Blood and urine testing, polydipsia
endocrine
hormonal assays, modified
water deprivation test

Dermatologidself-traurna: nail Atopic dermatitis,

Dermatologic tests ( eg,
biting, flank sucking, acral lick bacterial or parasitic skin scraping, trichograrn,
dermatitis, pyschogenic
hypersensitivity, adverse
fungal culture, biopsy),
alopecia, tail mutilation
food reaction, parasite,
therapeutic response tiial
infection, neuropathy, pain

Neurologic: spinning, star

Focal seizure, neuropathy Neurologic tests (eg,
gazing, pouncing, fly snapping,

MRI), therapeutic seizure
light or shadow chasing
therapy trial ( eg,
levetiracetam, potassi un1
bromide, phenobarbital)

distance-increasing behavior (ie, the dog is
aggression should be accurately identified
attempting to actively increase the distance to ensure initial safety. Predictability is a between itself and the stimulus). There are
critical issue in prognosis, both to prevent
many types of aggressive behaviors with
further incidents and to develop a stimulus
different motivations; however, fear,
gradient for treatment. The signalment,
anxiety, conflict (uncertainty), genetics,
environment, history, and target of the
and learned responses generally play a role
aggression also provide invaluable
in most cases; however, in some cases the
information as to whether the problem
behavior may be abnormal or pathologic.

might be safely and effectively managed.

The effects of early development (prenatal,

The type of aggression is an additional
postnatal), socialization, and previous
factor; some can be managed and
experience all play a role in development
improved, whereas others require
of aggression.

prevention. Finally, the clinician must

Aggression refers to threatening behavior
assess the ability of the owner to effecor harmful attacks and can range from tively and safely prevent the problem.

subtle changes in body -posture, facial

Aggression that is unpredictable, arises
expressions, and vocalization to biting.

during relatively benign interactions,

Dogs that are easily aroused are at high risk
involves targets that can.not realistically
of aggression, because their decision-making avoid exposure to the aggressive dog is affected by their physiologic state (ie, fligllt ( eg, young children, other household or fight). For treatinent to be effective, the
pets), or is performed by a large dog or
pet's anxiety and arousal must first be
in an uninhibited manner worsens the
managed by avoiding situations or staying
prognosis. Any medical condition that
below the threshold at which aggression
might cause or contribute to aggression
might arise. Some or all of a combination
must be identified, because they are
of reward-based training, behavior
important factors in diagnosis, prognosis,
products that can help to better manage
and treatment. (See www.esvce.org for risk the pet, and medications to help achieve a
assessment guidelines.)

behavioral state most conducive to new
learning is required to successfully modify

Fear-related Aggression: Fear is the
the behavior to achieve desirable outcomes
underlying cause of most forms of canine
and countercondition the pet to the stimuli
aggression. It is triggered by a stimulus
that incite aggression.

that is threatening to the dog. When the

Before treating aggression, the pracaggression is a direct response to a titioner must assess the potential risk of
challenge or confrontation, it might be
injury. All stimuli that might incite
referred to as defensive aggression. Fearful

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1563
dogs may try to avoid the stimulus but
possessive and by training the dog to give
become aggressive if they cannot escape
and drop on cue (beginning with items of

(eg, leashed, confined, cornered, or
low value for high-value rewards). If
physically grasped), are motivated to
safety is an issue (ie, the dog may hurt
maintain their place ( eg, on property,
itself by chewing on the item), it may be

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between the owner and stimulus, near
possible to trade the object for one of
food or toy), or if they learn that aggreshigher value. Providing more toys and sion is successful at removing the threat.

multiple small meals (eg, in feeding toys)

Inadequate socialization, learning, genetics
may reduce the value and novelty of the

(temperament), reinforcement of
resource.

aggressive behavior ( eg, retreat of the
stimulus), and associating a negative

Play Aggression: Aggressive play is a
outcome with the stimulus (eg, punishnom1al puppy behavior, which may persist ment) can all lead to the development of
into adulthood as a result of genetics,
feaHelated aggression. The diagnosis is
neotinization, and learning. When puppies
based on identifying signs of fear as well as
play aggressively with other puppies, they
the hist01y beginning with the first event,
may nip and bite but will generally resolve
because dogs can exhibit fear at the initial
the conflicts among themselves. However,
exposure but with time may display a more
if the problem becomes excessive, owner
offensive fom1 of aggression ( without
inte1vention may be required to redirect the
threats) when they learn it can be successdog's activities into other forms of play ( eg, ful. (For treatment of fear-related and other
feeding toys) or to interrupt the behavior
types of aggression, seep 1565.)

with commands or a leash and head halter.

If play with people escalates to biting, the

Possessive Aggression (Resource
interaction can be in1mediately stopped

Guarding): Possessive aggression is most

(negative ptmishment) and resumed when
likely to arise when a person or an aninlal
oral play ceases (positive reinforcement).

approaches the dog while it is in possession

Alternatively, a leash and head halter or
of something it wants to retain. Pets in the
verbal distraction ("off') can be used to
process of ingesting or chewing an object
intem1pt play biting. In all interactions, the
might be more likely to display aggression,
puppy should be taught to sit before given
but the behavior can also be seen in dogs
anything of value (eg, food, toys, affection).

near an object. Aggression is most commonly In addition, the puppy should be engaged in displayed when in possession of highly
regular alternative acceptable forn1s of play,
motivating food, treats, chew toys, stolen
including fetch, tug games, and manipulaitems, or even sleeping places. While genetics tion and chew toys. Punishment should not and early experience play a role in developbe used to stop play, because it can lead to ment, the relative value of the object to the
fear of the owner, defensive aggression, or
pet and the threat of losing the object to
conflict-induced aggression, or serve as
another dog or person determine whether
inadvertent reinforcement for some
the pet is likely to be possessive. Items that
puppies.

are novel or scarce may be more desirable.

Fear and defensive behavior also play a role

Redirected Aggression: Aggression is
if the owners threaten, punish, or confront
directed toward a third party when the dog
the pet when it takes an object or has it in its is prevented or unable to exhibit aggression mouth. The dog may also learn that it can
to its primary target. This type of aggression
successfully retain the object with
is most commonly described when the dog
aggression.

bites the owner as he or she grasps or

The problem might be prevented by
restrains the dog when trying to prevent or
tossing the puppy high-value treats
break up a dog fight. Similarly, dogs that
whenever the owner approaches or
might be aggressive toward a veterinarian
passes by the food bowl, and by offering
might bite the person restraining the dog.

a high-value treat or toy whenever the

Redirected aggression arises as a result of
puppy voluntarily gives up another toy
the frustration or interruption of other
or chew. Food bowls, toys, and chews
fonns of aggression or arousal.

should not be removed by confrontation,
because this can contribute to an increase Irritable/Conflict/Impulse Control in anxiety and aggression when approached. Aggression: Aggression directed toward In adult dogs, the problem should be
family members is often mislabeled as
managed by preventing access to these
dominance or status-related aggression.

items or confining the dog when it is

However, aggression toward family
given items over which it might be
members generally arises from fearful or

1564

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
defensive behaviors, resource guarding,

Dogs with impulse control aggression
redirected behavior, or situations of conflict
may respond with aggression to relatively

( competing emotional states and unpredictbenign interactions with family members. In able consequences). In some dogs, the
some lines of English Cocker Spaniels and
problem may be traced back to the owner's

English Springer Spaniels, this aggression is
attempts to inhibit excessive play aggresassociated with alterations in serotonin in VetBooks.ir
sion (see above).

blood san1ples or CSF

When a dog successfully uses aggression

When aggression is excessive, unpredictto achieve a goal ( retaining a resource) or able, and disproportionate to the level of
remove a threat, the pet learns that
threat, safety is a serious concern and the
aggression is successful (negative
prognosis generally guarded. However,
reinforcement). If the owner continues to
when behavior is abnonnal or pathologic,
threaten, confront, challenge, or punish the
substantial improvement might be achieved
pet, some dogs may inhibit their responses,
with a combination of drugs ( eg, SSR!s) and
but a large proportion become more
behavior modification.

aggressively defensive. When dogs are
resting or sleeping, chewing on a favored

Aggression Toward Other Dogs:

object, or no longer desirous of human

Dogs in the san1e group or household usually
affection, they may respond with either
avoid conflict without aggression. Communideferent displays or threats. However, if cation is based on dominant and submissive
the owner continues to approach, tries to
signals, with the deference of one of the
remove the resource, or attempts to pet the
two individuals to avoid escalation of
dog despite its signaling, aggression may
the encow1ter. Dominance is a relative
escalate and future signaling may be lost.

concept- the dog that displays deferent

The owne1°pet relationship can quickly
signaling may vary between resources and
deteriorate as the dog becomes more wary
situations. Aggression between individuals
and defensive while the owner becomes
living in the same household is generally
more fearful and/or confrontational.

an abnormal behavior caused by fear and

Genetic factors and early experience
anxiety, redirected aggression, impulse
likely also play a role; many of these dogs
dyscontrol, or poor intraspecific communiare easily aroused, excessively fearful, or cation skills as a result of genetics or lack
may have emotional disorders or behavioral
of early socialization and compounded
pathology (see below). Other cases are
by experience and learning. Redirected
primarily a result of learning. Aggression
aggression and competition over a valued
when grabbing the collar or during bathing,
resource may also lead to aggression
nail trinuning, or ear cleaning is a defensive
between dogs in the home.

response. Interrupting a pet that is aroused

Owners may play a role by inadvertently
may lead to redirected aggression. Theresupporting or encouraging a dog during an fore, when a dog is presented for aggression
encounter in which it would nom1ally defer.

toward family members, it can be difficult to Age or illness may also play a role, if tl1e way determine the dog's underlying motivation
in which one dog signals or responds to the
because each incident has added to prior
other is altered. Male-to-male aggression may
learning, fear conditioning, and underlying
have underlying hormonal factors that can
conflict. Dominance might refer to the
be improved by neutering; however, learning
relationship between two individuals of the
may play a role in maintaining aggression.

same species within a social group, as

If any situations arise in which the dogs
described by actions, interactions, and
are unable to resolve conflicts without
intraspecific communication/signaling.

aggression or injury, behavioral guidance

These relationships are not established by
should be sought. Aggression toward
aggression of the dominant individual but
unfamiliar dogs and those that are not
rather by the deferent signaling of others.

members of the family group are likely

Relationships between species, particularly
fearful, possessive, protective, or ten-itorial.

dogs and people, are established through
early socialization, the personality of the

Territorial/Protective Aggression:

individual, and what it learns from its

Aggression may be displayed when the dog
observations and interactions with family
is approached in its ten-itory. Territory can
members. Physical techniques intended to
be stationary ( eg, yard, home) or mobile ( eg,
assert dominance ( eg, pinning, rolling over)

car). What defines the behavior as territorial
and verbal discipline (yelling "no") are
is that the dog does not display fear to
therefore ill advised and can result in fear,
similar stimuli when outside its territory.

anxiety, and further aggression.

Fear, anxiety, defensive, and possessive

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1565
behaviors may all be components, because
aggression should resolve when tile
tl1e pet is most likely to display tile behavior
horn10nal state returns to no1mal and/or tile
toward unfamiliar stimuli, and the motivapuppies are weaned. The term maternal tion to escape or avoid (flight) is decreased
aggression has also been used to describe
or absent when tile pet is on its own property. tl1e aggression or cannibalism directed Learning (negative reinforcement when the
toward tile puppies by the bitch. Although

VetBooks.ir
stimulus retreats) and fear conditioning
tl1e problem may have a genetic component,

( unpleasant outcomes such as yelling,
it is reported to occur more frequently after
discipline, and confinement) can also play
a first litter. Ova.iiohysterectomy can
a role.

prevent further incidents.

Predatory Aggression: This is one of
tile most dangerous types of aggression,

Treatment of Fears, Phobias,
because tilere is usually no warning. The

Anxiety, and Aggression
attack is intended to kill prey, and tl1e bite is

Before implementing specific therapy to
uninhibited. The sequence of events may
manage, improve, or resolve a behavior
include stalking, chasing, biting, and killing.

problem, some conunon elements tilat

Y0tmg children and babies may be at risk
apply to most cases should be considered.

because tileir size and behaviors mimic

The initial discussion should focus on 1) an
tilose of prey. Although extensive socializaunderstanding of nonnal behavior as it tion to a species might reduce predation
relates to tile problem, 2) learning to read
toward that species, the behavior may be
canine body language and facial expresenhanced when predatory individuals are sions, 3) ensuring tl1at all of tile dog's needs
togetiler in a group. Predation is a nmmal
a.i·e adequately being met, 4) reviewing the
and dangerous canine behavior; tilus, any
principles of leaming and reinforcementdog tilat exhibits the behavior must be based training (predictable consequences),
prevented from opportunities to repeat it.

and 5) managing botil tile environment and
the dog to prevent further incidents. The

Pain-induced and Medical Causes of
cause, diagnosis, and motivation behind the

Aggression: Any disease tilat causes pain
behavior should be reviewed. Finally, the
or increases initability ( eg, dental disease,
owner should be given a prognosis witil
artllritis, trauma, allergies) can lead to
realistic expectations for botil short- and
aggression. The dog may become aggressive longterm outcomes.

when it is handled or anticipates handling.

ln most cases, treatment focuses on

Organ dysfunction (eg, renal, hepatic), CNS
changing tile dog's emotional response with
disease, and endocrinopathies ( eg, hype1�
the stin1ulus ( counterconditioning) and/or
adrenocorticism, functional testicular and
replacing tile undesirable response witil one
ovarian tumors, and tilyroid dysfunction)

tilat is desirable using reinforcement-based
might also contribute to initability and
techniques (response substitution).

aggression. (See al.so TABLE 2.) While However, dogs tilat are highly aroused
hypotilyroidism is more likely associated
respond witil autonomic fight-or-flight
witil lethargy, dermatologic signs, and heat
responses and tend to make reflexive
seeking in the early stages, it has been
responses. Therefore, arousal must be
suggested tilat dogs might display an
reduced before treatment can proceed. This
increase in aggression, particularly toward
can be achieved by training tile dog to settle
family members. Treatment should likely be
on cue, by mininlizing the intensity of tile
reserved for cases in which diagnostic tests
stimulus during exposure (desensitization),
are also consistent witil hypotilyroidism,
or by using management devices such as
because excessive supplementation could
head halters tilat can change the dog's focus
lead to a hyperthyroid state (with associand help it to settle, and witil drugs or ated medical and behavioral consequences). natural products that reduce anxiety and Treating tile medical problem may resolve
behavioral patilology. Early intervention
tile aggression, but the behavior, once
with medication may be necessary to
learned, may persist.

achieve success and can be in the best
interest of tile fearful, anxious, or phobic

Maternal Aggression: Maternal
dog.

aggression may be seen in intact females

There are common elements to the treatwith a litter of puppies or in females with ment of fear, anxiety, phobias, and most
pseudocyesis. It can be directed toward
types of aggression. The first step in the
people or otiler aninlals. Signs of aggression
treatment program is to identify each
arise when tile bitch's puppies or toys tilat
situation stimulus or interaction in which
mimic puppies are protected, and tile
tile problem might a.iise, so that a preventive

1566

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
program can first be implemented. Preven

By identifying a range (gradient) of the
tion ensures safety ( eg, in aggression cases),
dog's most favored rewards, the most
prevents further damage to the household
desirable can be used for training and
or injury to the dog, avoids further anxietyshaping new behaviors that approximate evoking situations for the dog, and ensures
the final goal; less-motivating rewards can

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no further aggravation of the problem
then be used to ensure in1mediacy and
through fear conditioning (ie, unpleasant
timing of previously learned commands. In
outcomes) and learning (ie, negative
addition, a way to minin1ize and control the
reinforcement if the stimulus retreats).

intensity of the stinrnlus will also need to be

Prevention can be most effectively
designed (eg, volume, distance, location).

achieved by identifying and avoiding any

Exposure exercises can then be implesituation in which the dog might be exposed mented by setting up situations in which
to the stimulus. A leash and head harness,
high-value rewards are used to reinforce
leash and body harness, or verbal comthe desired behavior and condition a mands (when effective) can also prevent
positive response during exposure to
access to the stimulus. If avoidance cannot
low-intensity stimuli and gradually
be ensured and aggression is a possibility,
proceeding through more intense stimuli.

then a basket muzzle might be the best

Setbacks can be avoided by determining
alternative.

the level of stinrnlus intensity at which a

A common starting point to begin to
cairn and positive outcome can be achieved
reduce anxiety, improve communication
and reinforced, and with the use of
and training, teach self-control, and allow
management devices such as a head halter
the dog to control its consequences/

(sit, reorient head, turn and walk away) or
outcomes is to establish a program of
front control body harness (turn away from
structured interactions in which the dog is
the situation) to ensure safety and success.

not given anything it values ( or wants) until

Drugs and natural therapeutics might be
it sits (or lies down). If the owners' response used concurrently in dogs with excessively is consistent and predictable by ensuring
intense or abnonnal behaviors to enable
the dog sits (or lies down) every time a treat
the successful implementation of behavior

(food or toy) is given, the leash is attached,
modification.

the dog goes in and out of the door or car, or

For noise phobias, controlled exposure
the dog wants affection, the dog will soon
can best be achieved through recordings
learn that the sit or down action is required
that can be gradually increased after each
to get the reward, at which point gradually
successful session of desensitization and
longer and more relaxed responses can be
counterconditioning. Concurrent behavtaught. This is sometimes tem1ed structured ioral management to reduce stimuli (with interactions, predictable consequences,
sound proofing, ear covers, eye covers,
learn to earn, or "saying please."

crate covers, or white noise) and develop a

Because the ultimate goal is to successsafe haven to help the dog settle might also fully expose the dog to controlled levels
help the dog to cope. For separation anxiety,
of the stimuli while achieving calm and
once a regular routine of play, exercise, and
positive outcornes,"it is necessary to
training is established, any additional
determine what behaviors need to be
reinforcement should focus on shaping
trained to achieve desirable outcomes
gradually longer inattention sessions when
during exposure training. For example,
the dog rests or occupies itself with favored
if problems arise indoors, the dog may
chew and food- o·r treat-filled toys, ideally in
first need to learn a focused sit, a relaxed
a comfortable safe haven (bed, crate, or
down, and a mat command ( or other
room) where the owners can house the dog
location such as room or crate). A drop
while gradually increasing their time away.

or give command and a come or recall

Any attention- or affection-soliciting
may also need to be trained. When
behavior should be ignored, unless the dog
problems arise outdoors, sit and focus or
is sitting or lying down calmly (sit for all
down and settle may also be useful, but
interactions) or resting on its bed or mat.

loose leash walking, backing up, or

Visual and auditory cues that signal
turning and walking away may be the
departure should be avoided if possible;
best options for stimulus exposure.

alternatively, they can be decoupled from

These behaviors should be learned
departw·e by exposing the dog while
reliably and consistently in a variety
remaining home, and associating with play
of environments with a minim urn of
and treats ( counterconditioning). In
distractions before the owners proceed
addition to preventive and environmental
to a graduated stimulus exposure (see
management strategies and behavior
p 1540 and p 1542).

modification, drugs or natural therapeutics

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1567
can be used to reduce underlying fear,

Buspirone, a nonsedating a.t1Xiolytic, is
anxiety, arousal, reactivity, or impulse
another option for ongoing use. Caution
dyscontrol to help facilitate learning; to
should be exercised when using anxiolytics,
improve underlying behavioral pathology;
because some may disinllibit fearful dogs,
and in many cases to improve the behavwhich could lead to increased confidence VetBooks.ir
ioral well-being of the dog.

and aggression.

For impulsivity, generalized anxiety diso1°

Selegiline, which is licensed in North
ders, excessive stimulus anxiety, and

America for treatment of cognitive
phobias, selective serotonin reuptake
dysfunction syndrome in dogs, is also
inhibitors (SSRis) and tricyclic antidepreslicensed for treatment of emotional sants (TCAs) are commonly used. Because
disorders or chronic anxiety in Europe.

fluoxetine has been evaluated in and

Natural products might be used alone
licensed for dogs, it is generally the first
or adjunctively with drugs or otl1er nahrral
choice of the SSRis, although fluvoxamine,
products to help calm or reduce anxiety,
se1traline, paroxetine, and citalopran1 might although evidence of efficacy is more be alternatives when fluoxeti.ne is insuffilinlited. A nun1ber of studies support the use ciently effective or adverse effects such as
of pheromone therapy. AdaptiJTM simulates
anorexia are an issue. SSRis are also used
the intern1anm1ary-appeasing pheromones
to treat compulsive disorders. Among the
produced by the lactating bitch and is

TCAs, clomipramine is licensed for use in
available as a spray, diffuser, or collar.

dogs and is an alternative to fluoxetine for

Pheromones have been used for anxiety
tl1e treatment of anxiety disorders and
associated with car rides, veterinary visits,
phobias. Because clomipran1ine is the most
separation anxiety, storn1 and fireworks
selective of the TCAs to inhibit serotonin
aversions, and to reduce the stress of
reuptake, it could be used for compulsive
adoption and aid socialization. A calming
disorders, as an alternative to SSRis. Other
or anxiety-modulating effect has been

TCAs might be selected for their more
reported for alpha-casozepine (Zylkene®, a
potent antihistaminic effects ( eg, doxepin,
milk protein hyd.rolysate ), Harmonease®
an1itriptyline ), whereas inlipramine has

(containing Magnolia officinalis and
been used as an aid in in1proving sphincter

Phellodendron amurense), 1.-theanine
control with behavioral incontinence.

(Anxitane®) and Sin-SustoTM (aSouroubea

Although the full effect might not be
plant blend), and aromatherapy (with
achieved for 3-4 wk, some effect might be
lavender). In addition, studies with
noted in the first week. For some compul

L-tryptophan in combination with a
sive disorders, especially those in which
low-protein diet have demonstrated a
there is a self-traumatic component,
possible reduction in some forms of
gabapentin or ca.rban1azepine might be used aggression. A commercial diet also has been concurrently, whereas in those cases in
developed that combines L-tryptophan and
which focal seizures might be causing the
alpha-casozepine (Royal Canin Calm®) that
behavioral signs, leveti.racetam, phenobai0
might aid in reducing stress and anxiety.

bital, or potassiwn bromide might be used
in a therapeutic response trial.

When an anxiety-evoking event can be

Hyperactivity
predicted (eg, thundersto1ms, fireworks,

Although hyperactivity or attention deficit
owner departure, visit to tl1e veterinarian,
disorder has been poorly docun1ented in
car ride, exposure to dogs or strangers on
dogs, there have been published case
a walk, visitors coming to the home), a
studies of dogs witl1 excessive motor
benzodiazepine can be given with the
activity and an altered ability to acquire new
antidepressant -1 hr before the event.

tasks Oea.t11), sometinles accompa.tlied by

Because benzodiazepines have variable
stereotypic behaviors. It may be patticularly
effects and relatively short half-lives, their
difficult to train such dogs to behaviorally
efficacy, dose, and duration should be
settle. There may also be signs of sympadeternlined in advance of their therapeutic thetic activity even at rest ( eg, increased
use. Clonidine, trazodone, or propranolol
heart and respiratory rate, vasodilation).

are other options that might be used

Affected dogs may respond to treatment
adjw1ctively with SSRis -1 hr before an
with methylphenidate. If no improvement
expected fear-evoking event ( eg, thunder,
with an initial dose of 0.25--0.5 mg/kg, bid,
fireworks, owner depaiture ). In some
the dosage can be gradually increased
refractory anxiety cases, trazodone,
eve1y few days Lo a maxin1wn of -2 mg/kg
clonidine, a benzodiazepine such as
until a measurable therapeutic response is
clonazepain, or perhaps gabapentin might
seen (reduced motor activity, heart rate,
be used concurrently with an SSRL
respirato1y rate, repetitive activities),

1568

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
provided no adverse effects develop.

compulsive disorders, many dogs,

Differential diagnoses include impulse
especially puppies, begin to chew and ingest
control disorders that might respond to
nonfood items as pa.rt of investigative and

SSRI therapy, and nonnal behaviors in dogs
exploratory behavior.

with behavioral needs that are not being

Dogs with hyporexia may have an anxiety
adequately met. In fact, it can be quite
disorder, and some may develop specific

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challenging to meet these needs in some
taste preferences and aversions that reduce
breeds and individuals, depending on the
what they will eat.

home and fan1ily.

Many feeding problems can be improved
tllrough a work-for-food progran1 in which

Destructive Behaviors
dogs a.re given food as reinforcers for

Many of the destructive behaviors,
training, witll the balance placed inside toys
including chewing, sLealing, garbage
that require chewing or manipulation to
raiding, and digging, a.re normal explorarelease tlle food. This encourages exploratory behaviors that arise when the dog is tion, makes feeding an eajoya.ble, timeunsupervised and not otherwise engaged in consUllling, and mentally challenging
more desirable activities. A regular daily
activity, and can limit the quantity conswned
routine with sufficient reward training,
and prevent gorging. As witll most behavior
exercise, and social eruichment can help
problems, correcting feeding problems
to ensure that these behaviors do not a.rise
needs to be accompanied by management
when the owners are home, although
strategies to prevent access to potential
varying degrees of supervision may be
targets at any tin1e the dog caruiot be
required. When the owners caruiot
supervised or actively engaged in other
supervise the dog, it should be provided
chew and play behaviors.

with adequate outlets for exploratory play
in the form of chews, food-stuffed toys, or

Elimination Behavioral Problems
manipulation toys, or in the case of outdoor
dogs, perhaps even a designated area for

Housesoiling: Dogs may soil in inapprodigging. These dogs may also need to be priate locations because of inadequate or
confined a.way from the areas in which
insufficient training, as a marking behavior,
problems might a.rise or housed in crates,
or as a result of fear or anxiety. However,
pens, or runs to prevent access to potential
pa.in, sensory decline, cerebrocortical
targets of destruction. Some dogs engage in
disease including cognitive dysfunction,
destructive behaviors because of anxiety
or any medical condition that leads to

( eg, separation anxiety, confinement, noise
increased volume, more frequent eliminaphobias). Together with the history, tion, pain on elimination, or lack of control,
videotaping or can1er.a. monitoring is
must first be excluded as potential causes
generally the best way to diagnose behavior
or contributing factors.

problems that occur when the owner is

A detailed behavioral history is
absent, as well as assess response to
necessary to detemline whether the dog has
treatment.

ever been housetrained. lf noL, a housetraining regin1en should be reviewed in which the focus is solely on reinforcement of

Eating Disorders
elimination in desirable locations rather

Behavioral problems related to ingestion
tllan punishment of elimination in inapproinclude those in which food intake is priate locations. This requires the owner to
excessive (polyphagia), inadequate
accompany the dog to its elinlination area

(hyporexia.), or too fast (gorging); water

(eg, outdoors), reinforce elinlination,
intake is excessive (polydipsia.); and
supervise tlle dog indoors to prevent or
nonfood items (pica) or feces ( coprophainterrupt any attempts at elimination gia) are ea.ten. Medical causes should be

(perhaps witll tlle a.id of a leash to ensure
excluded first. Some dogs that scavenge
continuous supervision), and return tlle
do so as a normal component of food
dog to its elimination site at appropriate
acquisition and are reinforced by success.

intervals or if tllere a.re signs that the dog is

Copropha.gia. may occasionally have a
ready to eliminate ( eg, sniffing, heading to
medical ca.use, but normal maternal
tlle door, sneaking away). When tlle owner
behavior includes consumption of feces and
is not able to supervise, a combination of
urine of young puppies. In addition, as pa.rt
scheduling ( ensuring that the dog eliminates
of exploratory behavior, many dogs are
before departure and having someone
attracted to and may ingest feces, compost,
return to take the clog to its elimination area
and prey ( dead or live). Similarly, although
before it must elinlinate) and confinement
some dogs with pica and polyphagia. have
training/prevention a.re required.

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1569

Dogs can either be confined away from
deferent postmes can be taught, such as a
areas where they might eliminate or kept in
relaxed sit, or any game or "trick" the pet an area where they will not eliminate, such
may have learned such as fetch or giving a
as a pen, room, or crate, where the dog eats,
paw. Phenylpropanolamine might increase
plays, or sleeps. Alternatively, the dog can
sphincter control, whereas imipramine may
be provided with an indoor elin1ination area
improve control and reduce anxiety.

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( eg, paper, indoor puppy potty) within its
confinement area where it can relieve itself

Other Elimination Disorders: Dogs
when the owner is gone. Puppies obtained
with separation anxiety or other fears and
from pet stores or any location where they
phobias ( eg, thunderstonn phobia, firework
have been extensively caged may be more
phobia) may soil during these times.

difficult to housetrain, because they have
never had to inhibit elimination and may
have learned to play with or eat feces.

Aging and Cognitive Dysfunction

The aging process is associated with

Marking Behavior: Although marking is
progressive and irreversible changes in
most often seen in intact males as a form of
body systems that can affect behavior
social and olfactory communication, it is

(see TABLE 2). In older dogs, these might
also seen in females ( especially when in
include hepatic or renal failure, endocrine
heat) and in neutered males and females,
disorders ( eg, Cushing disease), pa.in,
often as an ovennarking of other odors ( eg,
sensory decline, or any disease affecting
where other pets have urinated, or on items
the CNS ( eg, tun10rs) or circulation ( eg,
such as blankets with the residual odor of
anemia, hypertension). To diagnose the
other dogs, people, or cats). Some dogs will
cause of behavioral signs in a geriatric dog,
mark when they visit unfamiliar housea detailed history, physical examination, holds, especially when another dog's odor is
neurologic evaluation, and diagnostic tests
present. There is often a typical posture of
are required to exclude potential medical
a raised or partially raised leg when the
causes of the presenting signs. Many
surface to be marked is vertical. Fecal
owners do not report these signs, perhaps
marking is uncommon.

because the owners think they a.re

Although marking is likely a component
insignificant or assume little can be done.

of norn1al communication, it is unaccepta

Yet in one study, 30% of dogs 11-12 yr old
ble when it occurs indoors. Neutering intact
and nearly 70%of dogs 15-16yr old had
males will reduce the behavior, and good
signs consistent with cognitive dysfunction
supervision can prevent or inhibit most
syndrome (CDS). A more recent Internet
marking. As with housesoiling, dogs should
survey estimated CDS in 14.2%of dogs >10
be confined away from areas that might
yr old, with prevalence increasing with age,
be marked when owners are not able to
but >85% of these had not been diagnosed.

supervise. Marking that is related to anxiety

It is therefore essential that owners be
may be reduced by identifying and treating
informed of the importance of reporting
the cause, perhaps with the aid of drugs or
signs when they a.rise and for veterinarians
natural products that reduce anxiety.

to take a proactive approach in asking
owners about behavior at each visit. Early

Excitement, Submission, and
detection provides the best opportunity to

Conflict-related Elimination: Dogs may improve signs and slow the decline of eliminate when they are overly excited,
cognitive function.

such as when greeting people. Some dogs

Aging dogs may exhibit a decline in
will urinate when showing submissive
cognitive function (memory, learning,
postures ( eg, crouching to the ground or
perception, awareness) that manifests as
tmning over to expose the belly) or when
one or more of a group of clinical signs.

highly aroused. Because loss of urine

These are sometimes referred to by the
control may be associated with a concuracronyn1 DISHA and include disorientarent desire to both greet and show tion, interactions, sleep-wake cycles,
deferential behavior, many cases may be
housesoiling, and activity changes (which
due to conflicting behavioral motivations.

may be decreased or increased and

Treatment should focus on avoiding the
repetitive). In addition, anxiety, agitation,
stimuli (reaching, approach, eye contact)

and altered responses to stimuli are
that incite the behavior and avoiding any
frequently reported. The first and most
punishment during greeting, which would
prominent sign of brain aging is a decline
add to fear and conflict behaviors.

in learning or memory, which is generally

Acceptable alternative behaviors that are
impractical for pet owners to assess.

incompatible with excitable greeting or

However, neuropsychologic testing of

1570

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
older dogs has documented memory
range of differences in both physical and
decline beginning at 6-8 yr of age and
behavioral traits. Most cats are solitary
learning deficits by 9 yr of age. CDS in
hunters that prey on rodents and other
dogs is analogous to the early stages of
small animals, which is likely why their

Alzheimer disease in people, both in
coexistence with people is so successful.

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clinical signs and brain pathology. As with Kittens usually learn to prefer to hunt prey people, some dogs show minimal to no
that their mother hunted. Kittens may also
clinical impairment with age, whereas
develop lin1ited food preferences based on
others develop varying degrees of deficits. texture and taste if not given a variety of Treatment should first focus on environfoods when young.

mental enrichment (both physical and

In free-range conditions, multiple
mental stimulation), which has been shown
generations of related females can live
to slow cognitive decline and improve the
together, which also allows for communal
signs of CDS. Selegiline is a monoamine
rearing of kittens. Kittens may stay with the
oxidase B inhibitor that may improve the
social group until 12-18 mo old. Sexual
signs of CDS by enhancing dopamine and
maturity is reached by -6 mo of age. Queens
other catecholamines in the cortex and
are induced ovulators and generally cycle
hippocampus and by decreasing free radical seasonally ( most often from winter to load. Propentofylline, which is licensed in
swmner) about every 3 wk if not bred.

Europe and Australia for the treatment of

Weaning occurs at &-8 wk of age. Although
dullness, lethargy, and depressed demeanor
some kittens may suckle much later, this is
in old dogs, may increase blood flow and
more likely to be social than nutritional.

inhibit platelet aggregation and thrombus

Early weaning of kittens leads to earlier
formation.

onset of play and predation.

A number of natural products, including

The socialization period of cats is much
diets and supplements, have also been
shorter than that of dogs and may begin to
shown to have beneficial effects in
wane by 7 -9 wk of age. During this narrow
improving the signs and potentially slowing
window, exposure to cats, other animals,
cognitive decline. Two such diets are Canine people, and a variety of stimuli in the
bid®, which is supplemented with fatty environment is important for prevention of
acids, antioxidants, and DL-alpha-lipoic acid
fear. Kittens handled extensively by people
and L-carnitine to enhance mitochondrial
at 2-7 wk of age may be friendlier, more
function, and a specialized Purina One® diet
outgoing, and have fewer problems with
that uses botanic oils containing mediumaggression. Hand-reared kittens may lack chain triglycerides to provide ketone bodies feline social skills and may be hyperactive as an alternative source of energy for aging
in object and social play; however, if a kitten
neurons.

is reared with other cats in the home and

Other natural supplements that have
provided with play sessions with wand-type
demonstrated efficacy in improving cognitive toys, these problems may be prevented.

function include Senilife®, which contains a

Genetics, especially those of the father, also
combination of phosphatidylserine, Ginkgo
play a strong role in personality. Cats may
biloba, resveratrol, and vitanTins E and 86; be behaviorally categorized as active,

Activait®, which contains phosphatidylserplayful and aggressive, cairn and sociable, ine in combination with a-lipoic acid,
or timid and shy.

carnitine, fatty acids, glutathione, and other

Social play, including biting, chasing, and
antioxidants; S-adenosyl methionine
play fighting, begins arourid 4 wk of age,

(Novifit®); and apoaequorin (Neutricks®),
peaks at 6-9 wk, and declines at 12-14 wk.

a calcium-buffering protein found in

Social play may be directed at people,
jellyfish.

especially if there are no other cats with
which to play. Object play begins aroW1d

6-Swk and peaks at -18wk of age. Object

CATS
play simulates the predatory sequence
and includes stalking, chasing, pawing,

SOCIAL BEHAVIOR
pouncing, and biting and can be directed
at objects or social partners.

Cats are social animals that, in feral

Cats may develop preferences for
conditions, live in groups consisting mainly
particular elimination substrates. Many cats
of queens and their litters. The density of the dig before and after elimination (which may group depends partly on food resources.

be a visual mark or to bury urine and feces).

Because cats have been exposed to less

Cats are strongly influenced by scents and
selective breeding than dogs, there is far
may respond by marking with urine
less breed diversity and a much narrower

( spraying) or feces, scratching as both a

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1571
visual and scent mark, or rubbing sebaindoors. Although individual variability in ceous glands of the cheeks or body in the
expression can be extensive, a cat's primary
environment or on other cats. Urine
behavioral needs include eating (hunting),
marking, roan1ing, and fighting with other
drinking, elimination, security, play and
cats may be androgen influenced, in which
exploration, climbing, perching, and

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case these problems may be prevented or
scratching. Specifically, hunting and feeding
resolved by neutering.

needs might be better addressed by giving
food in small portions throughout the day

BEHAVIORAL PROBLEMS
and placing food or treats inside toys that
require some manipulation to release the

As with dogs, undesirable behavior might
food (batting, chasing, rolling, pawing). To
be 1) normal behavior but undesirable for add an element of hunting, the cat can be the owners (eg, climbing, scratching, and
given opportunities to chase, pounce on,
excessive nocturnal activity); 2) behaviors and bite toys the owner dangles or pulls in that fall within the range of normal but
front of the cat.

are at or near the limits, excessive in

Play appears to be motivated by two
intensity or frequency, and particularly
mechanisms: an initial interest if the toy
challenging or disturbing for the home
possesses appropriate characteristics
environment (eg, play biting, petting

(texture, small size) and rapid habituation.

induced aggression, overexuberant play,

Owners should find a nun1ber of toys that
play/predation, vocalization, asocial,
interest the cat and play with several
litter box avoidance); or 3) behaviors that different toys until the cat's interest wanes.

are abnormal, pathologic, or incompatible Cats may also be offered small toys for with living in the home ( eg, intercat
batting and chasing; boxes or containers to
aggression, fear and avoidance, urine
explore; appealing outlets to climb, perch,
marking). In most cases of normal but
and scratch; and perhaps an occasional
undesirable behaviors, the owners
catnip toy (to which 50%---750/oof cats
require guidance and resource material
respond).

on meeting the behavioral needs of cats

Teaching the basics of reinforcementand understanding learning principles based training allows owners to focus
to reinforce what is desirable while
on rewarding desirable behaviors ( eg,
preventing what is undesirable. When
where to eliminate, climb, scratch, or
behaviors are at or near the limits of
perch). Clicker training (seep 1540) can
normal, a more in-depth behavior
be particularly useful to immediately time
assessment is needed to discuss realistic

(mark) desirable behaviors and gradually
goals for what might be achieved, how
shape outcomes that more closely
the environment might be managed, and
approximate the final goal. Punishment
how the behavior might be modified. In
should be avoided, because it can cause
some households, it may be impractical
fear and anxiety toward the owners or
to make the changes necessary to achieve fear of handling and petting and, at best, an endpoint that meets the owner's
will stop the undesirable behavior only
needs. In cases when the behavior is
when the owner is present. Provided all
abnormal or incompatible with the home
of the cat's needs are adequately met, the
environment, a behavior consultation is
best approach to stop repetition of the
required to diagnose, determine the
undesirable behavior can be to prevent
prognosis, implement behavior and
access to areas where problems might
environmental modifications, and
arise. Another alternative is to teach
dispense drugs or supplements when
the cat to avoid the area by making it
indicated to achieve a sufficient level of
unpleasant with taste (eg, cayenne
improvement for the owner and the cat.

pepper), odor (eg, citrus), substrate (eg,

The most common behaviors seen by
upside-down carpet runner, double-sided
veterinary behaviorists are elimination
sticky tape), or perhaps a motion-activated

(undesirable toileting and marking) and
device (eg, alarm, air spray).

aggression. Because aggressive encounters in cats may be overt or subtle and passive, their frequency may be seriously

Diagnosis and Treatment
underestimated.

Assun1ing all possible medical causes

For both prevention and treatment, it is
have been excluded, a thorough history
in1portant to first ensure that the behavioral
is necessary to diagnose, detennine
needs of the cat are adequately met. This is a the prognosis, and develop an appropriate particularly important consideration for
treatment program. In cats, especially those
cats housed exclusively or primarily
with elimination and marking problems, it is

1572

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
particularly important to assess the
cats, is also available as a topical gel in some
environment either by visiting the home or
countries to reduce feai· of people or other
having the owners diagram the home so that cats. With intercat aggression, buspirone it can be determined how the environment
or a benzodiazepine might increase the
affects the problem and how it might be
confidence of the victim cat during
modified to improve the situation.

reintroductions. However, anxiolytic dmgs

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Response substitution (training an
could clisinhibit and increase aggression.

alternative desirable behavior) can be a
useful approach if the cat is reward trained
with food or favored toys to respond to one

Housesoiling
or more simple commands (eg, come, sit).

With housesoiling, the first step is always

A leash and harness can be used as an aid
to exclude meclical problems, because
in training as well as a way to prevent
any condition that affects urine volwne,
undesirable behaviors and ensure safety.

frequency, control, or ability to access

For fearful behavior, access to the stimuli
the litter box can cont1ibute to soiling.

should be prevented, at least in the short

Evaluating the behavioral history is then
term. For exan1ple, if cats are fearful or
the primai-y process to make the diagnosis,
aggressive with other cats or visitors,
determine the prognosis, and develop a
confinement away from the stimulus is an
treatment plai1. lnlportant aspects of the
essential first step to ensure safety as well
history include whether the elimination is
as to prevent further aggravation of the
wine or feces, whether urine deposits are
problem. This generally involves housing
vertical (spraying) or horizontal (soiling),
the cat in its own room with litter, toys,
duration ai1d frequency of the problem,
bedding, and food. When the cat is calm and
signalrnent and temperai11ent of the soiling
comfortable, it might then be possible to
cat, when and where the cat elin1inates,
gradually reintroduce the cat using favored
litter box details (nwnber, placement,
toys, treats, or food for cow1terconclitioning. cleaning, substrate, size), the cat's daily Dmgs for fearful behaviors that could be
routine, ai1d its home environment.

used on an ongoing basis include fluoxetine,
paroxetine, or clomipra.mine; buspirone or

Urine Marking (Spraying): Spraying is
other tricyclic antidepressants (TCAs) or
emission of a streain of urine onto vertical
selective serotonin reuptake inhibitors
surfaces, usually accompanied by elevation

(SSRis) might be an alternative. A benzocliai1d quivering of the tail and in some cases azepine such as alprazolam might be used
treading of the feet. Mai·king on horizontal
on an as-needed basis for situational anxiety surfaces ( eg, owner's clothing, bed cling, or such as car 1ides. Because of the range of
countertops) is less conunon. Spraying is
individual vaiiability in behavioral effects
much more commonly seen in male cats,
and adverse effects, trials with different
and neutering will reduce or eliminate it in
benzodiazepines should be done in advance most cats, although -lOOA, of neutered males to detem1ine which dmg and dose achieves
continue to mark. Marking may be due to
the desired effect ai1d for how long. Caution
ai1x:iety, such as might ai·ise wiU1 introducis necessary, paiticularly with the use of tion of a new cat; a change in schedule,
diazepain, for any indication of anorexia or
enviro1unent, or fan1ily (eg, renovations,
depression, because rare cases of acute and
new furnishings, new baby, rnaniage or
potentially fatal hepatic dysfunction have
divorce); or unfainiliar visual, auclitory,
been reported. In some situations, a
or olfactory stimuli.

benzodiazepine such as clonazepan1 might

Treatment can include a combination of
be considered on an ongoing basis for a
prevention, environmental modification,
more inunediate anxiety reduction and to
behavior modification, and medication.

enhai1ce appetite for counterconditioning.

Providing more litter boxes and more

Natural products including the F3 cheek
litter box locations, cleaning the soiled
gland pheromone (Feliway® [available as
areas with bacterial or enzymatic
cliffuser or spray]), L-theanine (A.nxitane®),
cleaners, and cleaning the litter box more
alpha-casozepine (Zylkene®), and a diet
frequently may reduce or eliminate
containing both alpha-casozepine and
marking in some cats. Punishment is

L-tryptophan (Royal Can.in Calm Feline TM)

contraindicated, because it increases fear
might also be used alone or adjunctively
and anxiety in an already anxious animal.

with drugs or other natural products to help

Unless the stimuli inciting marking or the
cairn, reduce anxiety, or reduce the stress
underlying factors contributing to the
associated with environmental change. The
marking can be effectively resolved, most

F4 cheek gland pheromone (Felifriend®),
cats are likely to require drug therapy
associated with social marking (bunting) of
with either fluoxetine or clomiprainine

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS

1573

(buspirone or other SSRis or TCAs might
area, making the area unpleasant (eg,
be an alternative). Feliway® feline
double-sided sticky tape, upside-down
pheromones in the form of a spray on

[nubs-up] carpet runner), or changing the
marked locations or a diffuser in the
function of the area (play, scratching,
environment might also effectively
feeding, sleeping).

reduce marking alone or in combination

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with drugs.

Aggression

Inappropriate Elimination: Soiling

Aggression Toward People: Aggreson horizontal surfaces with urine, feces, sion toward owners may be fear induced or
or both, can be a problem in males and
related to play or predation. Cats that bite
females. Cats that consistently return to
during petting may have a low tolerance for
the san1e location or substrate may have a
physical contact, and some cats bite to keep
location or substrate preference. Cats that
people from approaching or handling them
do not use their litter for urine, feces, or
when they ai·e resting, sleeping, or eating
both may be avoiding the litter itself, the

(which may be a learned, fear, or social
litter box, or its location. A conunon cause
issue). Aggression may be particularly
of avoidance is any medical problem that
intense if the cat is approached when it is
might cause painful elimination, increased
ai·oused. When the arousal is due to a
frequency, lack of control, or difficulty
stimulus to which the cat caimot gain
accessing the litter box. If medical problems access ( eg, another cat outside, loud noise), have been excluded or treated and the
the cat may redirect its aggression to any
problem persists, the focus should then be
person who approaches.

on the behavioral history. Avoidance might

Some cats display abnormal and
arise because of aspects of the substrate
out-of-context social responses, including

(texture, depth, scent, cleanliness), box
aggression, when approached or handled.

(size, shape, hood), or location that reduce

This may have a genetic component that is
appeal; unpleasant experiences at or near
compounded by insufficient socialization,
the box ( eg, insufficient cleaning, noises,
lack of adequate maternal care, inadequate
pain due to medical problems); or difficulty
early handling, and fear-evoking or
in gaining access to the box. Although
traumatic early experiences. However, at
anxiety may not be an inciting factor for
the time of presentation, most aggression
inappropriate elimination, cats may avoid
also has a learned component, because any
the litter or box if fearful (ie, personality) or
unpleasant response on the part of the
when there is conflict between cats in the
owner (eg, feai·, punishment) will cause
home (whether active or passive). Although
increased fear, whereas retreat of the
substrate, litter box, and location preferowner negatively reinforces the behavior.

ences may aiise secondary to avoidance,

Aggression toward strangers most Often
some cats may actually have a preference
has a fear component.

for a particular odor, texture, or location.

Treatment should focus on providing a

Aggression Toward Other Cats: Cats
litter, box, and site that is most appealing
may display aggression toward other cats
to the cat; reducing or preventing the use
due to play, predatory behavior, redirected
of the soiled location; and resolving the
behavior, fear, and perhaps as a statusunderlying factors contributing to the related behavior in which cats use
soiling. Appeal might be improved by idenaggression to retain control of sleeping tifying and resolving potential deterrents
areas, common areas, or possessions.

(eg, undesirable location, fear-evoking

Ultimately, the relationship that develops
stimuli such as furnace noise, or lin1ited
between any pair of cats will be affected
access such as a shared washroom),
by learning, because fearful responses
adding additional boxes or additional
by either cat can increase aggression, as
sites, finding a more appealing location for will retreat of one of the cats ( negative the litter, improving access to the litter
reinforcement). Aggression toward

(eg, larger box, ease of entry, ease of exit),
unfainiliar cats is most often a fear response
and finding out which litter (eg, sand,
but may have a territorial component.

clumping, clay, soft towel, scented) and
box type (eg, size, shape, height, covered,

Treatment: The first step is to ensure that
self-cleaning) is preferred by offering the
further irtjuries are prevented. Avoidance
cat choices to decide. Access to the soiled

(physical, visual, and preferably olfactory
location might be prevented by blocking
separation of cats that are fighting) is
access to the area, or the appeal reduced
parainount, and early intervention is best.

by using odor counteractants in the soiled

Although some cats will need to be

1574

NORMAL SOCIAL BEHAVIOR AND BEHAVIORAL PROBLEMS
separated at all times until they are calm
and string-may have a compulsive
enough to be reintroduced, if there are
disorder if the problem becomes sufficiently
particular times or situations when conflicts
frequent or intense; however, disease
arise, it might be necessary to separate the
processes, in particular those that might
cats only at these tin1es. Only after the cats
affect the GI tract, should first be excluded.

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are calm (which can take days to months)

Oriental breeds develop pica, particularly
can desensitization and counterconditionsucking of woolen objects, more frequently ing with favored rewards begin (ie, play
than other cats. Hallucinatory and
with toys, treats). Desensitization and
locomotory compulsive disorders are less
counterconditioning might first begin with
common than in dogs; however, painful
odors by grooming each cat with a brush or
conditions and any disease process
towel used on the other, and by feeding each affecting the neurologic system first cat separately in a common area on
need to be excluded.

opposite sides of a partition (glass, screen,

Cats often improve with modifications to
or solid door) and then in a common area at
tl1e environment that provide more control
sufficient distance that the cats can be calm
and predictability and increased enrichand take food or play with toys. Training ment, combined with medications that
one or both cats to wear a leash and harness
augment the an10unt of brain serotonin such
can help to ensure safety and distance
as fluoxetine and clomipranline.

during reintroductions, while a bell on the
aggressor can help the victim be aware of

Hyperesthesia
its whereabouts. Providing more threedinlensional space, including climbs and Hyperesthesia may not be a specific
perches, and ensuring sufficient resources
disorder but rather a sign of underlying
at sufficient distance to facilitate avoidance
medical or behavioral problems. Most
can fwiher decrease conflict. Reward
commonly, the skin along the lwnbosacral
training limited to a few selected verbal
area may twitch or ripple. There may be
cues ( eg, come, sit, go to your room) can
excessive self-grooming, hissing or biting
further aid in managing the cats during
at the back or flank, and intensive tail
introductions or in diffusing potentially
wagging. Some cats cry, dash away, and
aggressive situations. Punishment should
even defecate. These episodes arise when
be avoided, because it increases fear and
the cat is highly aroused and may be incited
anxiety in cats. Drugs might also be
by physical contact or external stimuli. A
indicated (seep 1565).

compulsive disorder is a consideration
when the intensity, frequency, and duration
of these problems is sufficiently severe.

Feline Compulsive Disorders

However, medical causes such as

Abnormal repetitive behaviors in cats are
neuropathic pain, dermatologic conditions,
derived from normal behaviors such as
myopathies, and focal seizures can also
stalking, chasing, grooming, etc. These may
present with similar signs. Therefore, a
be exacerbated by stress or anxiety such as
therapeutic response trial for neuropathic
alterations in relationships with people or
pain, seizures, pruritus, or compulsive
other cats, or may be inadvertently
disorders might be part of the diagnostic
aggravated by the owners either reinforcing
process.

or punishing the behavior (increasing conflict
and anxiety). If these behaviors occur out of

Fear
context or in a frequency or duration in

Fear may arise in cats as a result of genetic
excess of that needed to accomplish the task,
factors, lack of sufficient early socialization
a diagnosis of compulsive disorder should be
and exposure, or fear-evoking experiences.

considered. Medical problems must be

The fear may be oftmfamiliar people,
excluded, because they can be responsible
unfamiliar cats, dogs, noises, or places and
for many of the same signs. For example,
situations such as car rides, veterinary
self-mutilation, excessive grooming, and/or
visits, and unfamiliar environments. Some
self-directed aggression can be due to any
cats may also be fearful of fan1iliar people
condition that might cause neuropathic
and cats. This may be evidenced as
pain or pruritus such as adverse food
threatening displays and overt aggression
reactions, atopic dermatitis, and parasitic

(see above) or avoidance, withdrawal and
hypersensitivity.

hiding, and possibly spraying.

Cats that suck, Lick, chew, or even ingest

Treatment should begin with identificanon-nutritive substances-including natural tion and avoidance of any situation, materials such as wool or cotton, synthetic
stimulus, approach, or handling that might
fabrics, plastic, rubber, paper, cardboard,
lead to fear. When the cat is sufficiently

THE HUMAN-ANIMAL BOND

1575
calm, gradual improvement might be

Cognitive dysfunction syndrome (CDS)

achieved with desensitization and
is less commonly reported in cats than in
counterconditioning. Drugs might also
dogs. Yet in one study, -35% of cats >11 yr
be indicated (seep 1573).

old displayed at least one sign of CDS,
and 50% of cats > 15 yr old showed two or

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Aging and Cognitive Dysfunction
more signs. Brain changes are similar to
those seen in CDS in dogs (seep 1569).

Aging and younger cats have similar

Environmental enrichment and mental
behavior problems; however, the likelihood
stimulation is paramount to prevent and
of a pathophysiologic underlying condition
treat CDS. Medications, diets, and
is higher in older cats. Many diseases,
supplements might also improve the signs
including those affecting the CNS, metabolic of CDS or slow its progression. Although and endoctine systems ( eg, renal disorders,
no drugs or diets are licensed for feline
hyperthyroidism), sensory decline, and pain

CDS, selegiline and propentofylline have

( eg, arthtitis ), may present with behavioral
been used off-label. Both S-adenosyl
signs. Once medical problems have been
methione (Novifit®) and a commercial
excluded or treated, behavioral therapy may
diet containing antioxidants, arginine, B
be required. Behavior problems in senior
vitamins, and fish oil have demonstrated
pets may be more difficult to resolve
improvement in learning and memory in
because of a decline in cognitive function,
geriatric cats. Cognitive supplements
medical problems that cannot be entirely
containing antioxidants, vitamins, and
resolved, and drug contraindications or
phosphatidylserine (Senilfe®, Activait®)

adverse effects.

have also been developed for cats.

THE HUMAN-ANIMAL BOND

Companion animals are commonly
in1painnents. The dogs may also detect
considered to be family members, and
and alert people to impending seizures
the human-animal bond has become a
or abnormal blood glucose levels.

household tern1. More than half of all

The human-animal bond has also
households in the USA have at least one dog
increased focus on ensuring that animals
or cat, and most pet owners have more than
receive adequate consideration and care.

one pet. Cats outnumber dogs as compan

Albert Schweitzer's concept of "reverence
ion animals, and many veterinary practices
for life" has become a standard for
serve only cats. Yet, a 2008 study of the care
decision-making concerning animals.

pets receive reported that dogs were seen

Acknowledgment of the hun1an-anin1al
by a veterinarian more than twice as often
bond has become a cornerstone of
as cats, even in households with both
veterinary practice, and evidence suggests
species.

that practitioners who pay close attention to

Households with children are the most
the various aspects of the human-animal
likely to have pets. Most couples also have
bond will thrive both financially and in
pets, including retired couples, who have
te1ms of finding their work enjoyable and
recently shown a growth rate in pet
rewarding.

ownership. Currently, fewer than half of
single persons have a pet. In dealing with

VETERINARY FAMILY PRACTICE
owners, using approaches that incorporate
the entire family is an important feature of

The evolution of the role of pets in human
a successful veterinary practice.

affairs has opened new opportunities for

With the growing awareness of the
veterinarians, especially those in family
hun1an-animal bond, the roles of pets as
practice. Owners become deeply attached
service and therapy animals are expanding
to and ca.re about the health and wellinto new areas and fill many of the same being of their companion animals. Their
supp01t functions that people do. Service
expectations for veterinary care are
dogs assist people with various disabilities,
becoming similar to the care ideally
including mobility, visual, or hearing
provided in human medicine, particularly

1576

THE HUMAN-ANIMAL BOND
as high-tech medicine expands within
cation significantly affects the loyalty of the
veterinary specialties. In addition, the
pet owner to the veterinarian. Pet owners
current increased importance of animals
are more concerned with the health and
changes the nature of veterinary practice
well-being outcomes for the animal,
to include the entire family, and a sophistiwhereas veterinarians often emphasize cated level of family support is expected
time and services in their communica

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by many clients. The style and emphasis
tions. Clients value the genuine love and
of companion animal practices have
interest veterinarians show for the animals.

shifted, as reflected in the term "veteri

The veterinarian's empathetic concern
nary family practice."

expressed through effective communica

Practices that include the entire family
tion builds relationships with clients and
build lifelong relationships with families
enhances client satisfaction. Focus groups
and their animals. Clients look forward to
have revealed that clients expect veterinarconsistently seeing the san1e veterinarian.

ians to educate them, explaining in1portant

A new animal brought into the family is
information clearly and in various forn1ats.

the occasion to discuss the animal's life

Clients want to be provided options and
cycle with the family and provide an
offered a respectful partnership with
overview that can optimize the likelihood
the veterinarian in tl1e health care of their
of a positive human-animal relationship
pet. They expect interactive, two-way
with few behavioral problems. Veterinarconm1unication that includes listening and ians no longer just treat the animal;
asking relevant questions. Clear recomemotional needs of the family are mendations and effective communication
addressed along with the medical needs
of their rationale also lead to better
of the pet.

adherence to medical and treatment plans.

Many families with companion animals

A strong owner-animal bond is associated
have young children, particularly families
with greater attention to veterinary care.

that have both a dog and a cat. Animals are

Owners feel strongly about the quality of life
acknowledged to play a central and
of their pets, as revealed in studies involving
formative role in children's lives. In some
surgery or medical problems of pets.

studies, pet-owning preadolescents scored

Owners want effective pain management
higher on measures of self-esteem and
for the anin1al before, ct uring, and after
autonomy. Practitioners may consider
surgery, including spaying or neutering,
incorporating children into their communieven though they may not wish to adminiscations with the family and making it easy ter such medication at home. People feel
for families with children to be comfortable
that a good quality of life for their pets
during veterinary visits ( eg, providing a play
includes mobility, play or mental stimulaarea in the waiting room or planning for tion, health, and companionship. Owners of
children to be present in or visibly near the
dogs with heart disease expressed extreme
exanlination room). Hospitals providing
concern regarding their inability to
extended care for aninlals with complex
subjectively assess whether their pet is
diagnostic procedures and treatment plans
suffering. Teaching owners to assess and
that require hospitalization sometimes find
improve the animal's quality of life is an
entire fanlilies coming in to offer support to
important aspect of veterinary care and
the animal, perhaps spending hours with the client education. Veterinarians and owners pet; these hospitals may want to plan
can use a quality of life scale ( eg, the
accommodation for such families.

HHHHHMM Scale to monitor the pet's hurt,

Providing areas for relaxation, softer light hunger, hydration, hygiene, happiness, in public areas, and comfortable seating in
mobility, and more good days than bad) as
exam rooms without barriers from the
an aid in assessment. A strong majo1ity of
medical staff are some features that
owners indicate they would trade their pet's
in1prove client satisfaction. lnlpeccable
longevity for quality of life. Among variables
cleanliness also matters. Veterinary
of quality of life, the pet's ability to interact
practices that exhibit these values
with the owners was the most important.

demonstrate the understanding that

Good communication skills also build
medical interventions carry emotional
strong client-veterinarian bonds, and
consequences and that medical competence successful veterinarians pay close attention and providing emotional support go
to their nontechnical competencies,
hand-in-hand.

including interpersonal relationship

Studies have shown that communication
building skills. Such skills enable
has a key role in the owner-pet and
veterinarians and staff members to
client-veterinarian bond, because it affects
facilitate clients' understanding of medical
the care pets receive. Effective communi-
situations and preventive medicine

THE HUMAN-ANIMAL BOND

1577
throughout the animal's life, from encourag

(as measured by number of medical
ing clients to attend puppy socialization
visits) when they have a companion dog,
classes to prepaiing clients to provide
suggesting that a dog can be a stress
palliative care or deal with end-of-life
buffer that softens effects of adverse
issues. Follow-up communication can
events on the person. Of course, pets
also improve client adherence, which is
require caregiving, and the reciprocal

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generally lower than believed by veterinarcaregiving exchanged with the animal ians. Curricula for veterinary students
can also allow the person to nurture and
increasingly include opportunities to
feel needed, while also feeling nurtured.

develop communication skills, allowing

The animal's constancy bolsters courage
students to practice engaging clients, asking during setbacks, because the animal's open-ended questions, offering reflective
affection is unaffected by factors such as
listening and empathy, educating clients,
the person's physical capabilities or
meeting clients' and patients' needs, and
mood.

emphasizing support and partnership.

Companion animals facilitate social

Despite optimal communication skills,
interactions with other people and an
research has unfortunately shown that
overall positive social involvement. The
veterinarians inevitably encounter owners
socializing effects of dogs have been
who are inattentive, neglectful, over-involved., documented in public settings and also or completely cost-driven, as well as pets
among people with a variety of disabilities.

that are uncontrolled, dangerous, or dirty,

A companion animal provides a person who
adding to medical and emotional problems.

has few friends with an ally in making new

Almost all veterinarians feel they were not
human acquaintai1ces, while also creating a
prepared. by their education and training to
richer fanilly environment with enhanced
deal with such nonrnedical issues. Making
companionship. Even one person with an
plans in advance and developing specific
animal lives in a family unit and is greeted
protocols for interventions can prepare the
or recognized on arrival home.

veterinary staff with strategies for these

The motivating role of animals is a further
situations.

antidote to depression. Many people are
inspired to walk their dogs, volunteer to

HUMAN HEALTH BENEFITS OF
take animals into nursing homes for visits,

PET OWNERSHIP
or just actively nurture an animal, whereas
without the animal they may be less

Animal companionship both relaxes and
involved. and engaged in living or even
entertains people. Pets can provide both
depressed. Walking a dog and being
social support and status. In corning to
outdoors where other social contact arises

!mow their clients, veterinarians can assess
are two healthful effects of living with a
the importance of the pet to a family and the
canine compailion. Research project$ and
extent to which the fainily members benefit
community programs in many paits of the
from the potential psychosocial effects of

USA and elsewhere are seeking to raise the
living with an animal. The pet's contribution
popularity of dog walking as an approach
may be magnified for vulnerable people,
toward improving human health and
such as older adults who are facing
lessening hun1an disease, including diabetes
increasing disabilities and losses of close
and cai·diovascular problems.

companions and family. During stressful

The daily comfort, socialization, and
periods in people's lives, many studies have
relaxing motivation offered by an animal
reported. that pets offer meaningful comfort
also are associated with cardiovascular
that is protective against depression and
benefits. Blood pressure decreases
loneliness. Old.er women score more
transiently when a person relaxes with,
favorably on measures of mental health, and talks to, or just watches an animal. When college-aged women report Jess loneliness if human patients with increased blood living with a companion animal rather than
pressure were given medication and
alone.

randomly assigned. pets, those patients with

Similar comforting effects of animal
pets performed better on stressful tasks,
companions, whether cats or dogs, in
indicating a lower response to stress in this
warding off depression were reported for group; however, blood pressure scores did patients with Alzheimer disease. The
not differ in tl10se with pets and those
same is true for men with AIDS who had
without. Several studies show longterm
a companion animal and were cared for
health correlates with animal companionat home and whose social lives were ship, although the animals were not
shrinking. Older people experiencing
randomly assigned to the people but rather
typical life stresses are less affected
were chosen by them or their fan1ilies.

1578

THE HUMAN-ANIMAL BOND

Cardiovasculm· measures were better

SERVICE OR ASSISTANCE DOGS
among pet owners than nonowners in a

AND OTHER WORKING DOGS
large Australian study. 1\vo studies reported
that pet ownership was related to decreased If periodic exposure to an animal via mortality. Survival for 1 yr after heart attack
animal-assisted activities, therapy, or

VetBooks.ir
was found to be more likely among people
education is healthful for someone with
with companion dogs, along the lines of
special needs, more frequent or continual
human social support.

exposure may offer even greater benefits.

Service or assistance dogs are trained to
perform specific tasks in partnership with

ANIMAL-ASSISTED
people who have disabilities. In addition

INTERVENTIONS: THERAPY,
to guide dogs for people with visual

ACTIVITIES, AND EDUCATION
disabilities, hearing dogs for people with
hearing disabilities, and service dogs for

The field called animal-assisted therapy
people using wheelchairs, dogs can assist
originated when the public began to take
people with many other disabilities, such
animals into nursing homes and other
as detecting an impending seizure,
facilities to share them with residents.

detecting high or low blood glucose levels

Unless medically supervised, these
in a person with diabetes, or helping to
programs are termed "animal-assisted
stabilize a child with autism. A growing
activities," whereas those directed as part
role of service dogs is as psychiatric
of medical treatment are termed "anirnalservice dogs, assisting persons with assisted therapy." An emerging area is
mental illness such as post-traumatic
animal-assisted education, in which
stress disorders, schizophrenia, bipolar
animals m·e provided to help improve
disorder, agoraphobia (fear of open
classroom behavior or learning of children. spaces), or anxiety. Other working dogs Procedures to screen animals and provide
assist in law enforcement, agricultural
training for the people involved are offered or bomb sniffing, search and rescue, or and have been standardized by Pet
war tasks. Service and assistance dogs

Partners (formerly the Delta Society).

have legally protected special access to

However, progrmns that train and ce1tify
use public transportation through the

"therapy m1imals" (mainly dogs) are not

Department of Transportation and for
legislatively required as part of a certifihousing through the Department of cation process; likewise, there is no

Housing and Urban Development. Some
conventional educational process for
working dogs are kenneled in a facility
individuals seeking to work in this area.

when not working, although many police

Therapy dogs have no special rights of
dogs live with the families of their
public access and are not.granted special
handlers. Dogs range from being
privileges in housing or transportation.

purpose-bred with extensive training,

An accreditation process has been
to being shelter-sourced with minimal
developed for instructional programs
formalized training. Significant investserving health professionals thrqugh the ments of money and time are required for

International Association for Anirnalthe specialized training and development Assisted Therapy. The University of Denver
of working partnerships with these dogs.

offers social work students an emphasis in

As they forge working partnerships with
animal-assisted therapy. Some individuals
their dogs, the handlers inevitably
within human health professions, such as
become emotionally bonded. Formally
clinical psychology, social work, occupatrained assistance or service dogs can tional therapy, physical therapy, and/or
have several trainers or handlers in their
nursing, have incorporated animal-assisted
early lives, but after being placed,
activities and therapy with therapy dogs
typically spend the rest of their lives with
into their professional practice.

a single handler, providing assistance to

A much larger nwnber of people continue
the handler while also offering relief and
to volunteer to bring their animals into
comfo1t to other family members.

facilities, often with some screening

Also based on "equal accommodation"

process and training organized by local
for people with disabilities, "emotional
groups. Such groups often benefit from
support animals" (ESAs) m·e another
veterinary assistance and leadership in
category of animals assured legally
developing appropriate screening methods
protected special access to transportation
for selection and preparation of both
and housing if they provide a nexus of
animals and people participating in these
support for someone with a disability;
progrmns.

however, they lack the broader aspects of

THE HUMAN-ANIMAL BOND

1579
public access provided to service dogs.

ANIMAL WELFARE

Handlers ofESAs (and psychiatric service
dogs) may be asked by landlords or

Reducing or preventing the incidence of
transportation personnel to provide
animal pain or distress and promoting
documentation from their medical
animal well-being (and even pleasme) a.i·e
professionals that they have a disability
overall goals of animal welfare. These goals

VetBooks.ir
alleviated by the ESA. ESAs require no
pertain to animals on farms or in laborato-
special training; they naturally offer special 1ies as well as companion animals. Aversive support. ESAs are not limited to dogs but
handling, even if infrequent, can have
can be of various species so long as they
stressful consequences. Vete1inarians are
are helping the person who has the
often the first contacts when someone
disability.

seeks help for animals being badly treated

With limited oversight of service dogs and or receiving inadequate ca.i·e.

ESAs in the USA, pe1missive enforcement

Intentional, deliberate abuse of anin1als
of requirements, and an expanding array
is an extreme marker of a likely pattern of
of service dogs and ESAs, dogs of many
abuse elsewhere within a fa.tnily. Veterinardifferent breeds and body sizes are ians who report suspected animal abuse
providing meaningful support to people
sometin1es can avert similar abuse of other
with a va.iiety of disabilities. Smaller dogs
vulnerable fanilly members, especially
are easier to manage for people who are
children or older adults. Two studies
frail or live in small apartments, and they
reported that >900A, of vete1inarians would
may be sufficient for a person's needs, eg, in
report cases of suspected animal abuse to
their capacity to retlicve dropped items.

authorities. Most agreed that animal abuse

Wmmed veterinarians can offer wise
in fa.tnilies would tend to be linked with
counsel in these matters to people with
abuse or mistreatment of children or older
disabilities regarding the needed training,
adults.

medical care, and breed selection. This

Although occasionally seen by veterina.i�
service is valuable, because the growing
ians, outright abuse appears less common
demand for service dogs has resulted in
than the neglect, poor husbandry, or lack of
some cases of poorly trained dogs at high
essential medical ca.i·e of anin1als, some of
prices being presented for sale as purported
which may be inadvertent. A serious
service dogs.

problem occurs with animal hoarders who

Working dogs are extremely precious
may be mentally ill. The person, perhaps
and valuable to their handlers. When a
without awareness, acquires more animals
medical crisis arises with such a dog, the
tha.11 they can possibly care for properly.

veterinarian is often the closest profes

Some communities routinely combine
sional at hand and may need to provide
efforts of animal control and mental health
support to the handler as well as the
agencies when dealing with such cases ..

animal. Treatments that adversely affect

A major, widespread societal problem
performance, especially for an extended
of animal welfare is the abandoning and
period, disrupt functioning of both the
killing of companion animals. Relinquishdog and the person. If the individual has ment of animals that would be adoptable
a disability, special accommodation may
has decreased, yet the problem remains
be required for communication and
widespread. Many studies have shown
veterinary instructions. Treatments
that behavioral problems of animals and
not involving an emergency should be
owners' lack of knowledge of how to
planned well in advance, with consideraadequately care for an animal increase the tion of the handler's needs and schedule.

likelihood of relinquishment. Veterinary

Attentive listening and respect, although
tea.tns can provide leadership and
essential for all clients, assumes
education about more realistic expectaparticular importance in these relationtions of companion animals and can ships.

encourage earlier intervention if

Although no legal or regulatory process
problems arise.

certifies assistance dogs, Assistance Dogs

Despite the growing population of dogs

International is one organization engaged
and cats, the number of veterinary visits
in developing international standards.

has been decreasing, raising concerns

Curricula for professionals interested in
about whether pets a.i·e getting adequate
continuing education in this area are being
veterinary care. Cats receive less veterinary
offered by the Bergin University of Canine
care then dogs; a 2011 study found that 400Ai

Studies in Santa Rosa, California (formerly of cats had not been to a veterina.iian within the Assistance Dog Institute), leading to a
the past yea.i·, compa.i·ed with 15% of dogs.

Master of Science in Canine Life Sciences.

Most of these cat owners said their pet

1580

THE HUMAN-ANIMAL BOND

"hated" going to the veterinarian. A cat's As an alternative to euthanasia, it is
resistance to veterinary visits can be
inlportant to offer instruction in palliative
addressed by facilitating transport in
care for owners prepared to provide it.

carriers; making the visit, exan1ination, and

Procedures developed in hospice care can
treatment more comfortable for the cat and
assure high-quality, end-of-life care with
owner; or considering mobile veterinary
pain relief for anin1als, and help the fanilly

VetBooks.ir
services.

as well. The technical aspects of treatment

Some emotionally charged issues and
no longer override the compassionate care,
social conflicts pertaining to animals
as a specific approach is often offered to
reflect contrasting perspectives on animal
deal with the family's and pet's distress.

welfare. How best to deal with feral cats

Owners are also concerned about the
and their kittens can be a contentious
care of their pet's remains. Veterinarians
question when weighed against the impact
offer the available choices, with inforn1ation
on songbirds and other wildlife. Another
about the final disposition of the pet's
emerging concern is the possible adverse
remains. After a cremation, some owners
medical effect of early neutering for some
are concerned to know that the ashes they
breeds of dogs, such as a potentially
receive are, in fact, those of their own pet.

increased incidence of hip dysplasia or

Veterinarians' communication with clients
certain cancers. Although early neutering
concerning questions around euthanasia
curtails unwanted reproduction, other
and the care of pet remains is especially
options also could be offered to owners to
important, as is providing support during
manage reproduction. As contentious
the mourning process.

topics regarding animal welfare arise in

Compassionate veterinarians include
communities, veterinary professionals are
themselves in the circle of remembrance
those more prepared to offer reasoned and
of their clients' aninlals and respect the
informed leadership to address problems.

families' regard for the anin1al throughout
the relationship. Many grieving owners

EUTHANASIA, PET LOSS, AND
need a year of recovery to pass through

GRIEF FOR OWNERS AND
the holidays and family traditions before

VETERINARIANS
somewhat accepting a loss, and veterinarians may consider sending a remembrance When a beloved anin1al companion dies or
card to the fanilly after a year.

is ill, people are likely to feel stress, sorrow,
and grief. This may include the animal's

SELF-CARE FOR VETERINARIANS
fan1ily and neighbors in the community, as
well as the veterinary team that provided

Notwithstanding the anguish that pet
care. The significance of pets dying and the
owners experience, the process of animals
consequent emotional impact on owners is
dying, especially the act of performing
clearly profiled within the veterinary
euthanasia, poses an emotionally wearing
profession, and educational materials and
duty for veterinarians as well. A recent USA
support groups, hotlines, and counseling
sutvey found that a veterinarian typically
are available. The relatively short life span
euthanizes more than seven animals per
of dogs and cats means that owners face
month, sharply contrasting with a study of
losing several anin1als during a lifetime.

veterinarians in Japan, where the median

An extra burden comes in assuming
number of euthanasias in the previous year
responsibility for the moment of death by
was one, and 20% of Japanese veterinarians
euthanasia. The desire or perceived duty to
had not euthanized any pets that year. In
relieve pain and suffering may need to be
one study, euthanizing anin1als resulted in
weighed against the feeling of some owners
perpetration-induced traumatic stress for
about the wrongness of killing or a religious

11 % of the study sample of veterinarians,
argument for reverence for life. The
veterinary nurses/technicians, and
difficulty of this decision overlays the loss
research and animal shelter staff. Lower
with feelings of guilt and the thought that
levels of stress were reported an1ong those
there must have been some other step that
who were more satisfied with their social
could have been taken. Even with fanilly
support and had worked longer with
support, these feelings may not be
animals. Most veterinarians in another
assuaged. An1ong manied couples in one
study reported having been clinically
study, approximately half of the wives and
depressed. In one study, almost all
more than a quarter of husbands reported
veterinarians felt they were untrained in
they were quite or extremely disturbed by
explaining euthanasia to clients. Almost
the death of the family pet.

half regretted a specific occasion of

THE HUMAN-ANIMAL BOND

1581
euthanasia, and most private practitioners
into a helping profession, routine involvereported feeling guilty after performing ment with euthanasia and knowing the
euthanasia. After euthanizing their own
means to pe1forrn it, arid the contagion of
pets, a majority of veterinarians felt
emotional stress. This work becarne the
depressed, and 30% felt guilty. These
lynch pin for VetLife: Looking After the
figures were higher among female

Veterinary Profession (www.vetlife.org.uk/),

VetBooks.ir
veterinarians, suggesting that its impact
a Web site to support the well-being of
may have risen with the gender shift of
veterinarians and to address personal arid
the profession.

professional issues.

A major concern with regar·d to the

Increasingly, veterinary students and
mental welfare of veterinarians is the
practitioners realize the value of ongoing
suicide rate, which is higher than that of
monitoring of their own self-car·e and make
the general population. The suicide rate of
use of instmments such as a Self-Car·e
veterinarians in the UK is four tinies that of

Assessment Worksheet. This brief inventory
the general population; although precise
offers support to keep one's life in balance
figures ar·e not available, similar problems
with a detailed inventory of physical,
are arising in the USA. Risk factors
psychological, emotional, spLtitual, arid
mentioned in the UK include the initial entry professional self-care.

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CLINICAL PATHOLOGY

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AND PROCEDURES

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES 1584

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE

LABORATORY 1590

Clinical Biochemistry 1590

Clinical Microbiology 1595

Cytology 1597

Clinical Hematology 1610

Urinalysis 1615

Parasitology 1619

Serologic Test Kits 1621

DIAGNOSTIC IMAGING 1626

Radiography 1626

Ultrasonography 1632

Computed Tomography 1635

Magnetic Resonance Imaging 1636

Nuclear Medicine Imaging 1638

DISPOSAL OF CARCASSES AND DISINFECTION OF PREMISES 1639

EUTHANASIA 1641

MEAT INSPECTION 1644

PREPURCHASE EXAMINATION OF HORSES 1647

PREPURCHASE EXAMINATION OF RUMINANTS AND SWINE 1649

RADIATION THERAPY 1651

1584

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES

COLLECTION AND SUBMISSION

OF LABORATORY SAMPLES

VetBooks.ir

Each veterinary diagnostic laboratory
noted on the cardboard box label, and the
offers a unique set of diagnostic tests that is
stryofoam lid should not be sealed with
subject to frequent changes as better tests
tape. A "triple barrier" approach can be
become available. The increasing availabilapplied to most diagnostic specimens. One ity of tests based on newer molecular
bani er is the outer cardboard box; another
biology techniques is an excellent example
is the inner styrofoam container or perhaps
of this trend. The protocols for sample
sealable plastic bags (with adsorbent
collection and submission are therefore
material). Note that if air shipment of
also subject to change. The practitioner and san1ples is anticipated, tl1en International diagnostic laboratory staff miisl maintain

Air Transport Association (IATA) requiregood communication to complete their ments include specialized bags capable of
diagnostic efforts efficiently and provide
withstanding 95 kilo pascals of pressure.

optimal service to the client. Practitioners

The third barrier is around the san1ple itself.

must be specific and clear in their test

Liquid samples should not be shipped in
requests. The laboratory staff can provide
plastic bags; a sealable tube or jar should be
guidance when there are questions
used. The top of these fluid-filled containers
regarding sample collection and handling,
should be sealed with tape. The tube/jar is
as well as offering assistance in interpretathen placed in a sealable plastic bag with tion of test results. Most diagnostic
some adsorbent material in case of leakage.

laborato1ies publish user guidelines with

Fresh tissue samples are similarly placed
preferred protocols for sample collection
within a second bag (third barrier)

and submission, but the following broad
containing some adsorbent material. Use
recommendations are fairly standard.

of appropriate padding material within the

Regardless of the type of submission,
box will protect sample integrity while
a detailed case history should be included
preventing coolant packs from crushing
with the samples to assist laboratory
samples. Regulations regarding shipping of
personnel in detennining a diagnosis. The
biologic samples vary according to country
information should include owner, species,
but in the USA are mainly in the purview
breed, sex, age, animal identification,
of the Department of Transportation,
clinical signs, gross appearance (including

Hazardous Materials Regulations. Also,
size and location) of the lesion(s), previous

IATA restricts the volume of formalin that
treatment (if any), time of recurrence from
can be shipped in any single shipping
any previous treatment, and morbidity/
container to < 1 L in total and <30 mL per jar.

mortality in the group. If a zoonotic disease
is suspected, this should also be cl.early

Histology: Tissues for microscopic
indicated on the submission form to alert
examination collected either via biopsy or
laboratory personnel. The submission fonn
during necropsy can be critical to obtaining
should be placed in a waterproof bag to
a diagnosis. Use of this relatively rapid and
protect it from any fluids that might be
inexpensive diagnostic technique can often
present in the packaged materials.

result in substantial savings in time, money,

Waterproof markers should be used when
and animal life. The increasing number of
labeling specimen bags and containers.

immunohistochemical (IHC) tests that can

When packaging samples, the use of
be applied to fom1alin-fixed tissue has
breakable containers should be avoided,
further reinforced the utility of this
but properly padded glass tubes are
diagnostic technique.

commonly shipped. The basic principles of

Autolyzed tissues are generally useless
good shipping practices include the use of
for histopathologic exan1ination; prompt
sturdy containers, clearly labeled to contain
necropsy examination and organ sampling
biologic diagnostic specimens; ideally, this
are critical. Tissue should not be frozen
should be a styrofoan1 container within a
before fixation. Other than CNS tissues
cardboard box. Any coolant packs should

(see below), samples collected for
be sealed within plastic bags and accompahistology should never be > 1 cm thick nied by adsorbent material within the

(preferably 5-7 mm) and must be placed
container. If dry ice is used, this should be
immediately into ;;:10 times their volume of

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES

1585
phosphate-buffered lOOAi f01malin to ensure
artifact and should be avoided if possible;
adequate fixation. Tissues collected for
fixing the intact/halved brain in a large
histologic examination should be
volume of formalin for >24 hr is preferred.

representative of any lesions present and,
in the case of cutaneous punch biopsies

Microbiology: Any specific agents tl1at
and biopsies obtained via endoscopic
are of interest in tl1e diagnostic investiga

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collection, should be centered directly on
tion should be mentioned on the submission
the grossly visible lesions. Wedge biopsies
form; some agents have requirements ( eg,
or tissue samples collected at necropsy
anaerobic culture, special media) tl1at
should include some of the apparently
would not be used in most laboratories
normal surrounding tissue; the interface
unless the pathogen was cited as a
between norn1al and abnormal may
differential diagnosis. Laboratory techprovide key information. Excisional niques and capabilities for microbiologic
biopsies of small tumors ( <1.5 cm) may be
exan1ination vary; available tests include
cut in half. Larger tumors may be sliced like bacte1iologic culture, fungal culture, virus bread so that formalin can penetrate to the
isolation, in-situ hyb1idization, a variety of
face of each slice. Alternatively, several

PCR methods, fluorescent antibody tests,
representative samples (7 mm wide, includlatex agglutination tests, Western blotting, ing the interface of normal and abnormal)

ELISA, and many others. Most tests,
may be collected. The tissues should
including the newer molecular biology
remain in fixative for <!24 hr; after tl1is
techniques, rely on eitl1er tl1e growth/
initial fixation, the san1ples may be placed
visualization of intact viable organisms or
in a smaller volwne of fresh formalin for
the detection of tl1e nucleic acids and
shipment if necessary. Prolonged fixation
proteins of tl1ese patl1ogens. Therefore,
can adversely affect IHC testing, so
unfixed specimens (tissue, fluid, etc) should
samples should be shipped promptly if IHC
be collected aseptically and shipped
tests are anticipated. Histologic samples
promptly to avoid degradation. If PCR
should be shipped in unbreakable
testing is to be perfom1ed, it is particularly
containers and packed in a manner that
in1po1tant to avoid cross-contamination
prevents spillage during shipment. Fixed
between multiple animals in a submission;
tissues should be protected.from.freezing.

this applies to tissues, fluids, and even

Specific tissues collected at necropsy
dissection instnm1ents. Furthem10re, swabs
require additional attention. Because the GI
destined for PCR analysis should not be
mucosa decomposes rapidly, short sections
placed in agar or charcoal-based transport
of gut collected at necropsy must be opened
media. Calcium alginate swabs should be
lengthwise to allow adequate fixation. If
avoided. Instead, cotton or dacron swabs
spinal cord is to be submitted, the dura
should be shipped in a tube witl1 a few drops
mater should be carefully incised lengthof sterile saline or viral transport media.

wise to pe1mit more rapid penetration to

Some test protocols may permit pooling
the cord. Fixing tl1e brain poses a special
of organ specin1ens from an individual, but
dilemma, especially if a neuroanatomic
for the vast majority, it is preferable tl1at
location of the lesion(s) witl1in the organ
each tissue be collected into separate
could not be detern1ined antemortem.

sterile, clearly labeled bags or tubes for

Ideally, a whole, intact fixed brain is
shipping. Gut samples must never be pooled
required for complete histopathologic
in a container with oilier tissue san1ples. Tisanalysis. Immersion of the brain for many sues and fluids for most micro biologic
days in a very large volume of formalin is
assays may be frozen before shipment, but
required to adequately fix such a specimen,
generally freezing is undesirable if san1ples
so brains are commonly transported in an
can be chilled and delivered directly to the
only partially fixed state. If the specimen
laboratory within 24 hr. Exceptions to tl1is
can be shipped by overnight delivery, it may
rule include analysis for certain toxins, such
be acceptable to send a chilled, carefully
as those of Clostridium pe1:fringens and
packaged, W1fixed brain, which can tl1en

C botulimim, in which degradation of the
be processed at tl1e diagnostic laboratory.

toxin must be prevented by prompt freezing

Often, the brain is halved longitudinally
after collection. Adequate refrigerant
and one-half sent W1fixed (fresh), properly
should be provided so that samples remain
refrigerated, for microbiologic tests, while
chilled ( or frozen) until tl1ey reach tl1e
the other half partially fixes in transit. This
laboratory.

metl1od can prove W1Satisfactory if a
solitary unilateral lesion is involved. Slicing

Toxicology: If a known toxin is sustl1e brain into widths suitable for rapid pected, a specific analysis should always
fixation introduces considerable fixation
be requested-laboratories cannotjust

1586

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES

"check for poisoning." A complete
liver, kidney, whole blood, plasma/sernm,
description of clinical and epidemiologic
and urine, but exceptions exist, such as
findings may help differentiate poisoning
cerebral tissue for cholinesterase analysis.

from infectious diseases that can simulate

For some investigations, the diagnosis
poisoning. For a list of appropriate samples requires analysis of feed or water. If there VetBooks.ir
for many of the more common toxicities,
is doubt about sample submission
see TABLE 1. The most critical samples to be procedures, the laboratory should be
collected are generally stomach contents,
contacted.

GUIDELINES FOR SUBMITIING SAMPLES FOR TOXICOLOGIC

EXAMINATION

Suspected Poison
or Analysis

Specimen Required

Comments

Ammonia

Whole blood or serum

Frozen

Urine

Frozen

Rw11en contents

Frozen ( or may add 1-2 drops
saturated HgC13)

Anticoagulants (warfarin Whole blood

Heparin or EDTA
and related compounds) Liver

Refrigerated

Feed

Stomach contents

Arsenic

Liver

Kidney

Urine

Ing es ta

Feed

Chlo rates

Stomach contents

Frozen, in airtight container

Urine

Feed

Chlorinated hydro-

Cerebrum

Use only glass containers
carbons

Ing es ta

Avoid contamination

Body fat

Refrigerated or frozen

Liver

Kidney

Cholinesterase

Serum

Frozen

Cerebrum

Copper (and Ni, Fe, Co,

Kidney

Cr, and Tl)

Liver

Serum

Feed

Whole blood

Feces

Cyanide

Forage

Rush to laboratory or ship

Whole blood
promptly, frozen in airtight

Liver
container

Dicownarol

Forage

Liver

Ethylene glycol

Serum

Urine

Kidneys

Fresh plus fixed in fomialin

( continued)

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES

1587

GUIDELINES FOR SUBMITTING SAMPLES FOR TOXICOLOGIC

EXAMINATION (continued)

Suspected Poison
or Analysis

Specimen Required

Comments

VetBooks.ir

Fluorides

Bone

Best to send affected bone(s)

Water

Forage

Urine

Herbicides (many)

Treated weeds

Urine

Ing es ta

Liver or kidney

Ionophores

Feed

Rw11en contents

Heart

Fixed in formalin

Skeletal muscle

Fixed in formalin

Lead (also Hg, Mo, Ni,

Kidney
and Tl)

Whole blood

Heparinized blood preferred

Liver

Urine

Mercury and molyb

Kidney

See LEAD, above
denum

Whole blood

Liver

Feed

Mycotoxins

Grain, forages

Consult with laboratory

Liver, kidney
personnel on specific tests

Nitrate

Forage

Refrigerated

Water

Body fluids (eg, aqueous
humor)

Organophosphates

Feed

Also send urine, blood, and

(and carbamates)

Ing es ta
stomach contents from

Urine
clinically normal animals

Oxalates

Fresh forage

Do not macerate; freeze

Kidney

Fixed in formalin

Phenols

Gastric or mm.en contents In airtight container

Polychlorinated (and

Fat
polybrominated)

Cerebrum
biphenyls

Feed

Rumen pH

Ing es ta

Frozen

Selenium

Whole blood

Hepatinized

Feed

Liver

Hair clippings

Sodium (NaCl)

Brain

Other half fixed in formalin

Serum

CSF

Feed

Sodium fluoroacetate

Stomach contents

Frozen

(1080)

Liver

( continued)

1588

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES

GUIDELINES FOR SUBMITTING SAMPLES FOR TOXICOLOGIC

EXAMINATION (continued)

Suspected Poison
or Analysis

Specimen Required

Comments

VetBooks.ir

Strychnine (and some

Liver
other convulsants such

Kidney
as bromethalin)

Stomach contents

Sulfates

Water

Brain

Fixed in formalin

TDS (total dissolved

Water
solids)

Triaryl-P04

Ingesta

Feed

Urea

Feed

See AMMONIA, above

Vitamin A ( also D and E) Liver

Serum

Frozen

Vitamin 03 (rodenticides) Kidney

Zinc

Liver

Kidney

Serum

Use "trace minerals" tubes

Zinc phosphide

Liver

Frozen

Gastric contents

Tissues or fluids for chemical analysis
refrigerated; blood smears should not.

should be as fresh as possible and kept

EDTA is the anticoagulant of choice for a
refrigerated. For some analyses, freezing

CBC because it best preserves the cellular
is critical to prevent degradation of volatile
components of the blood and prevents
chemicals, and in rare i_nstances a chemical
platelet aggregation. Blood for coagulation
preservative is required.

testing should be collected into a blue top

If legal action is a possibility, all
tube, which contains sodium citrate. After
containers for shipment should be either
mixing, the sample should be centrifuged
sealed so that tampering can be detected or
for 5 min, and then plasma should be
hand-carried to the laboratory and a receipt
removed and transferred to a clean tube
obtained. The chain of custody must be
without anticoagulant. The plasma should
accurately documented.

be kept frozen until the tin1e of analysis.

If feed or water is suspected as the source

Whole blood should not be frozen because
of poisoning, samples of these and any
this causes cell lysis and gross hemolysis,
desc1iptive feed tag should accompany the
which interfere with testing.

tissue san1ples. If at all possible, a representative composite san1ple of the feed Clinical Chemistry: Most clinical
should be submitted from the suspect lot or
chemistry tests require serum, but an
shipment. In some instances, if an adequate
occasional test may require plasma.

amount of involved feed is available, some

Anticoagulants present in plasma may
of it may be fed to experimental animals in
interfere with tests; therefore, serum should
an effort to reproduce the signs and lesions
always be submitted unless plasma is
seen in the field cases.

specifically requested. Because lipemia can
interfere with a nwnber of chemistry tests,

Hematology: Routine studies require
dogs and cats should be fasted for 12 hr
anticoagulated whole blood and several
before san1ples are collected.

blood smears. Blood smears should be

For serun1 san1ples, the blood should be
prepared inunediately after the sample has
drawn into a red top tube or a separator
been collected to minimize cell deterioratube. The sample should be held at room tion. Anticoagulated blood should be kept
temperature for 20-30 min to allow

COLLECTION AND SUBMISSION OF LABORATORY SAMPLES

1589
complete clot formation and retraction.

Blood or cytologic smears should never

Incomplete clot fonnation may cause the
be mailed to the laboratory in the same
serum to gel due to latent fibrin fom1ation.

package with formalin-fixed tissues because

The clot should be separated from the glass
formalin vapors will produce artifacts in the
by gently running an applicator stick around
specinlen. Many laboratories now offer

VetBooks.ir
the tube walls ("rimming"). The sample
in1munocytochernical testing, and proper
should then be centrifuged at high speed
handling of cytologic submissions is

(-1,000 g; 2,200 rpm) for 10 min. Rough
required for reliable results. Usually
handling of tile san1ple or incomplete
air-dried, unfixed smears will suffice, but in
separation of erythrocytes from serum may
some instances shipping of samples in tubes
promote hemolysis, which can interfere
containing a transpo1t media is recomwith certain tests.

mended.

If the sample has been collected into a
serun1 separator tube, centrifugation will
cause a layer of silicon gel to lodge between

Fluid Analysis: Analysis of various
the packed cells and the serum. The gel layer effusions and fluids usually includes should be inspected to ensure the integrity
determination of protein content, total cell
of tile barrier, and re-centrifugation is
count, and cytologic exan1ination. Other
recommended if there is a visible crack in
tests may be performed depending on the
this layer. If a red top tube has been used, the source or appearance ( eg, chylous fluid) of serwn should be removed and transferred to the effusion. A sample of effusion/fluid a clean tube. Serum should be refrigerated
should be collected into an EDTA (purple
or frozen until analyzed.

top) tube for routine analysis. A second

Many commercial laboratories provide
sample should be collected into a serun1
sample containers and mailers.

( red top) tube if any biochemical analyses

( eg, triglyceride, cholesterol, lipase for

Serology: Serology generally requires
chylous effusions) are to be performed or if
serum, but plasma is often satisfactory.

a bacterial culture is desired ( eg,joint fluid).

San1ples should be collected as desc1ibed

These samples should be shipped chilled
for clinical chemistry tests and should
but not frozen. Smears for cytologic
always be free of hernolysis. In some
exanlination (see above) should be prepared instances, paired samples may be required
from a drop of the fluid immediately after
for an adequate diagnosis. The acute sample the sample has been collected to minimize should be collected early in the course of
cell deterioration and other in vitro artifacts.

the disease and frozen. The convalescent

Samples of CSF should be collected into
sample should be collected 10--14 days later, small EDTA tubes and shipped immedi
and both samples should be forwarded to
ately with high priority; the cytologic
tile laboratory at the same time.

value of CSF samples degrades rapidly and
the low cellularity makes examination of

Cytology: Air-dried smears are usually
direct smears wirewarding. If sufficient CSF
acceptable. Rapid air drying of smears
is available, tl1en a red top tube san1ple may
mininlizes cell distortion, thereby enhancbe useful for serology or culture attempts.

ing diagnostic quality. However, depending
on the method of staining used, some

Genetic Analysis: Tests based on the
laboratories prefer alcohol-fixed smears.

detection of specific genetic features range

San1ples can be obtained by fine-needle
from karyotype analysis to the identification
aspiration or by scraping. Imprints (touch
of specific genes. The laboratory offering
preparations) of external lesions can also be the test should be contacted to detemline used, although these tend to have a greater
tile specifics of sample collection and
degree of contamination. Aspirated material handling; required samples range from hair should always be smeared before air drying.

to skin or blood. Many blood-based analyses

Smears of fluid can be prepared using a
require collection into yellow-topped
traditional blood smearing technique.

acid-citrate-dextrose tubes and overnight

Highly cellular fluids may be smeared
shipment of the chilled tubes to tile
directly; fluids of low cellularity should be
laboratory. Tissue san1ples for genetic
centrifuged to concentrate the cells. Thick
analysis should be wlfixed and shipped
material or viscous fluid is more readily
inlmediately after collection. As with most
smeared using a squash technique in which
molecular techniques, aseptic collection
a second glass slide is placed over the
and tile prevention of cross-contamination
aspirated material and then slid rapidly and
between samples is critical for reliable test
smoothly down the lengtll of the lower slide. results.

1590

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

DIAGNOSTIC PROCEDURES FOR THE

VetBooks.ir

PRIVATE PRACTICE LABORATORY

Numerous laboratory tests can be done
evaluation of both together is essential for
in a private practice laboratory. Use of a
optin1al recognition of many of the most
commercial laboratory versus in-house
characteristic disease patterns (seep 1610).

testing should be evaluated to detennine

Before samples are collected, a list of
whether in-house testing is practical and
differential diagnoses should already be
economical. Because the availability of
established based on the history and
diagnostic laboratories and their reporting
clinical exan1ination. Then, additional
intervals may be problematic ( eg, nights and appropriate tests can be added to the basic holidays), performing some diagnostic
panel below.

screening tests in-house is often desirable.

Making a diagnosis entails establishing a

However, because the people performing
list of differential diagnoses based on the
these tests often have minimal technical
history and clinical exan1ination. Based on
training, quality control procedures must
this list, tests can be selected to include or
be rigorous. The time and care that must
exclude as many of the differentials as
be devoted to quality control issues may
possible. Yet more tests may be necessary
preclude in-house testing in many practices.

until only one of the original list remains

Errors may occur not only in testing
to determine the diagnosis. If all differenprocedures but also in sample collection tials are excluded, then the list must be
and handling and in recording results.

reevaluated. It is not good practice to order

Tests can be done using either manual or
tests without a sensible differential list
automated methods. Manual methods tend
unless the animal presents without
to be time consuming and are more subject
definitive clinical signs.

to human error. Automated and semiautomated systems are available but are more Basic Test Panel: Most veterinary
expensive. Factors to be considered include
laboratories offer a basic panel of tests,
instrument and reagent costs (including
which represents a minimal investigation
materials for calibration and quality control), applicable to most general situations. For availability of personnel training, technical
small animals, a typical panel includes total
support, and instrument maintenance and
protein, albumin, globulin ( calculated as the
service. Although service contracts can cost
difference between the first two analytes ),
up to 100/o of the purchase price of an
urea, creatinine, ALT, and alkaline
instrument, they are often cost-effective
phosphatase (ALP). In addition, a yellow
because of the expense of instrument
color seen in the plasma should be
repair.

•
considered an indication to measure
bilirubin. This panel may be modified as

CLINICAL BIOCHEMISTRY
appropriate for other species, eg, glutamate
dehydrogenase (GOH) and/or -y glutan1yl

Clinical biochemistry refers to the analysis
transferase (-yGT) are m"ore appropriate
of the blood plasma (or serum) for a wide

"liver enzymes" for horses and fam1
variety of substances-substrates, enzymes, anin1als, or it may be more appropriate to hom1ones, etc-and their use in diagnosis
concentrate prin1arily on muscle enzymes
and monitoring of disease. Analysis of other

(CK and AST) in athletic anin1als.

body fluids ( eg, urine, ascitic fluids, CSF)

Totalproteinlevel increases due to
is also included. One test is very seldom
dehydration, chronic inflammation, and
specific to one clinical condition, and basic
paraproteinemia. It decreases due to
checklists of factors affecting the most
overhydration, severe congestive heart
conunonly requested analytes are given
failure (with edema), protein-losing
below. Thus, rather than six tests that
nephropathy, protein-losing enteropathy,
merely confirm or deny six possibilities, a
hemorrhage, bums, dietary protein
well-chosen group of six tests can provide
deficiency, malabsorption, and some viral
information pointing to a wide variety of
conditions ( especially in horses).

different conditions by a process of pattern

Albumin level increases due to
recognition. Biochemistry tests should be
dehydration. It decreases due to the san1e
accompanied by full hematology, because
factors as total protein, plus liver failure.

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1591

Urea level increases due to excess

AST level increases in both muscle and
dietary protein, poor quality dietary protein,
liver damage but is of less value than ALT.

carbohydrate deficiency, catabolic states,

The half-life is 5 hr in dogs and 77 n1in in
dehydration, congestive heart failure, renal
cats. It is also reported to increase in
failure, blocked urethra, and ruptured
hypothyroidism.

VetBooks.ir
bladder. It decreases due to low dietary

Most of the above paran1eters are
protein, gross sepsis, anabolic hormonal
associated with liver function/dysfunction
effects, liver failure, portosystemic shunts
and are frequently overinterpreted. In small

( congenital or acquired), and inborn errors
animals, increases in ALT and ALP levels
of urea cycle metabolism. Urea measurecan reach four times normal and still be ment is used especially to indicate renal
associated only with fatty change, a
disease and to a lesser extent liver
nonspecific finding and not, in most cases,
dysfunction.

a primary liver problem. Some laboratories

Creatinine level increases due to renal
also frequently receive liver biopsies from
dysfunction, blocked urethra, and ruptured
dogs that have significant increases in liver
bladder. It decreases due to sample
enzymes and bile acids >80 but that have
deterioration. Animals with a high muscle
normal histologic morphology. The reason
mass have high-normal creatinine
for this is unknown.

concentrations, whereas animals with a low

In general, plasma enzyme levels
muscle mass have low-norn1al creatinine
decrease due to sample deterioration.

concentrations. Creatinine measurement is

Uncommonly, atrophy or fibrosis of an
used especially for renal disease.

organ may result in unusually low plasma

ALT is present in the cytoplasm and
activities of the relevant enzymes.

mitochondria of liver cells and, therefore,
increases due to hepatocellular damage. It

Additional Tests: Further tests may be
has a half life of 2-4 hr and rises higher than
added to the basic panel, according to the

AST but recovers quicker. There are minor
principal presenting signs, to create panels
increases with muscle dan1age and
for polydipsic animals, collapsing anin1als,
hyperthyroidism.

etc. These panels are structured so that the

ALP level increases due to increased
patterns of abnormalities typical of all the
bone deposition, liver damage, hyperthylikely differential diagnoses applicable to roidism, biliary tract disease, intestinal
the situation can be discerned. For example,
damage, hyperadrenocorticism, corticostea polydipsia panel may add calcium, roid administration, barbiturate administraglucose, and cholesterol. Calciw11 allows tion, and generalized tissue damage
recognition of hyperparathyroidism and

(including neoplasia). The most common
other causes of hypercalcemia (which
causes for an increase is raised levels of
causes polydipsia and renal insufficiency),
circulating steroids and biliary disease. The
glucose may indicate diabetes mellitus and
half-life is 72 hr in dogs but only 6 hr in cats.

contributes to the pattern characteristic of

Levels in the cat are generally much lower
hyperadrenocorticism, and cholesterol also
than in the dog, and any increase in cats is adds to the appreciation of the "Cushing
considered significant. In dogs, ALP levels
pattern." Renal failure is covered by the
in the thousands of units are usually
tests already included in the basic panel.

associated with increased steroid levels.

In contrast, in a panel for a "collapsing

ALP and ALT levels rarely rise above 1,000
aninlal," calcium and glucose may be added
units, even in severe liver disease.

to screen for hypocalcemia or hypoglyce

GDH level increases in hepatocellular
mia. Sodium and potassiWll are included to
dan1age, particularly hepatic necrosis,
screen for hypoadrenocorticism or
in horses and runlinants.

hypokalemia. Analytes that might be consid

-yGT increases in longer-term liver
ered for incorporation in such expanded
dan1age; it is particularly useful in horses
profiles are described below.

and ruminants.

Sodium level increases due to Conn

CK, the classic "muscle enzyme,"

syndrome (hyperaldosteronism), restricted
increases markedly in rhabdomyolysis and
water intake, vomiting, and most causes of
aortic thromboembolism. Slight level
dehydration. It decreases due to hypoadincreases are reported in hypothyroidism.

renocorticism, loss of any high-sodiun1 fluid

Only a very small an10unt of muscle damage
such as some fon11s of renal disease, and
such as bruising or IM injections can result
insufficient sodiWll provision during IV fluid
in high serum CK levels. In dogs and cats,
therapy.

unless investigating specific muscle disease,

Potassium level increases due to
increased levels are generally of no clinical
hypoadrenocorticism and severe renal
significance.

failure (especially ternlinal cases). It

1592

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
decreases due to Conn syndrome, chronic
monkeys, may be caused by hepatic
renal dysfunction, vomiting, diarrhea, and
lipidosis in cats), hemolytic disease (usually
insufficient potassium provision during JV
mild increase), liver dysfunction, and biliary
fluid therapy. Congenital hypokalemia
obstruction (intra-or extraliepatic).

occurs in Bunnese cats.

Theoretically, hemolysis is characterized by

Chloride level increases in acidosis,
an increase in uncoajugated (indirect)

VetBooks.ir
and in parallel with increases in sodiw11
bilirnbin, whereas hepatic and post-hepatic
concentration. It decreases in alkalosis,
disorders are characterized by an increase
vomiting ( especially after eating), and in
in conjugated ( direct) bilirubin; however, in
association with hyponatremia.

practice this differentiation is unsatisfac

Total C02 (bicarbonate) level increases tory. Better appreciation of the source of the in metabolic alkalosis and decreases in
jaundice is gained from bile acid measuremetabolic acidosis. It is less useful to assess ments.

respiratory acid/base disturbances.

Bile acid levels increase when hepatic

Calcium level increases due to dehydraanion transport is impaired, usually during tion (which is also associated with
liver dysfunction (bile acids are more
increased albwnin), primary hyperparathysensitive than bilirnbin to hepatic impairroidism (neoplasia of parathyroid gland), ment) and in the presence of a po1tosysprimary pseudohyperparathyroidism temic shunt ( congenital or acquired). The

(neoplasms producing parathonnonelatter condition is characterized by a related peptide [PRP], usually perianal
marked increase in bile acid concentration
adenocarcinoma or some fonn of lyrnphoafter feeding, from a fasting concentration sarcoma), bone invasion of malignant
that may be normal. It also increases in bile
neoplasms, thyrotoxicosis (uncommon),
duct obstruction; very little increase is seen
and overtreatment of part1.11ient paresis. It
in feline infectious pe1itonitis or mild cases
decreases due to hypoalbtuninemia,
of hepatic lipidosis. Very high levels can
parturient paresis, oxalate poisoning,
sometimes be seen without structural
clu·onic renal failure (secondary renal
histologic changes. The reason for this is
hyperparathyroidism), acute pancreatitis
not known.

(occasionally), surgical interference with

Cholesterol level increases due to fatty
parathyroid glands, and idiopathic
meals, hepatic or biliary disease, protein

(autoimrntme) hypoparathyroidism.

losing nephropathy (and other protein

Phosphate level increases due to renal
losing syndromes to some extent), diabetes
failure ( secondary renal hyperparathymellitus, hyperadrenocorticism, and roidism ). Decreases are seen in some
hypothyroidism. It decreases in some cases
downer cows and as part of the stress
of severe liver dysftmction and occasionally
pattern in horses and small anin1als.

in hype1thyroidism.

Magnesium level increases are rarely

Lactate dehydrogenase is a ubiquitous
seen, including dllling acute renal failure.

enzyn1e with a nwnber of isoenzymes;

It decreases in ruminants due to dietary
electrophoretic separation of isoenzymes is
deficiency, either acute (grass staggers)

necessary to locate the source of increased
or chronic, and diarrhea ( unconm1on ).

activity. It is therefore of very limited value

Glucose level increases due to highin general clinical practice.

carbohydrate meals, sprint exercise, stress

Sorbitol dehydrogenase level increases
or excitement (including handling and
in acute hepatocellular damage in horses
sampling stress), glucocorticoid therapy,
but is a very labile analyte.

hyperadrenocorticism, overi.nfusion with
ex-Amylase level increases in acute
glucose/dextrose-containing JV fluids, and
pancreatitis but in dogs is also increased in
diabetes meUitus. It decreases due to insulin chronic renal dysftmction. It is therefore of overdose, insulinoma, islet cell hyperplasia
limited use in the diagnosis of pancreatitis.

( unconm1on ), acetonemia/pregnancy

Pancreatic lipase inlmunoreactivity is now
toxemia, acute febrile illness, and idiopathithe test of choice for diagnosis of pancreatically (in certain dog breeds).

tis in dogs and cats. Amylase is not a useful

13-Hydroxybutyrate level increases in
indicator of pancreatitis in cats.

diabetes mellitus. It is a major component of

Lipase level increases in acute pancreatiketoacidosis and as such is also increased in tis in dogs (longer half-life than amylase) acetonemia/pregnancy toxemia and
and also occasionally in chronic renal
extreme starvation. It can be measured in
dysfunction. Lipase ( routine assay) is not a
both blood and urine.

useful indicator of pancreatitis in cats.

Bilirubin level increases due to fasting

Immunoreactive trypsin (trypsin

(benign effect in horses and squirrel
like immunoreactivity) level decreases

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1593
in exocrine pancreatic insufficiency in
and trypsin are quickly cleared by the
dogs. It will also increase (irregularly) in
kidneys. ln addition, any prematurely
pancreatitis.

activated trypsin is quickly removed by
prnte.inase inhibitors, such as a,-proteinase
mhib1tor and o:2-macroglobulin. In tum,

Tests for Pancreatic Disease:

VetBooks.ir

0:2-macroglobulin-trypsin complexes are

Pancreatitis: Serum amylase and
removed by the reticuloendothelial system.

lipase activities have been used for

Th us, the serum half-life for TLI is short and
several decades to diagnose pancreatitis
a significant degree of active inflanm1ation
in both people and dogs. Unfortunately,
is required to increase serum TLI concentraneither of these tests is botl1 sensitive and tion. Because of tl1e limited sensitivity of
specific for pancreatitis in dogs. In one
serum cTLI and ITLI concentrations for
study, significant serun1 amylase and lipase
canine and feline pa.ncreatitis, respectively,
activities remained after total pancreatecand because only a limited number of tomy, indicating there are somces of semm
laboratories measure these assays routinely,
amylase and lipase activity other tl1an the
serum TLI concentration is of limited
exocrine pancreas. Also, clinical data
usefulness for diagnosis of pancreatitis in
suggest a specificity for pancreatitis of only
dogs and cats.

-500/o for both of these markers. Many

Pancreatic lipase immunoreactivity
nonpancreatic diseases, such as renal

(PLI) concentration measmes the
hepatic, intestinal, and neoplastic dis�ases
concentration of classical pancreatic lipase
can lead to increases in sernm amylase anci
m the senun. This is in contrast to serum
lipase activities. Steroid administration can
lipase activity, which measures the
also increase serum lipase activity and
enzymatic activity of all triglyceridases
cause variable responses in serum an1ylase
present in the serum, regardless of their
act1V1ty. Thus, in dogs, measurement of
cellular origin. Assays to measure PLI in
serum amylase and lipase activities are
canine (cPLI) and feline (f'PLI) serum have
of lilnited usefulness for diagnosis of
been developed and validated and are
pancreatitis. Serum amylase and/or lipase
commercially available. Serum PL! is highly
activities that are 3-5 times the upper lilnit
specific for exocrine pancreatic function.

of the reference range, in animals with

Also, serum PLI is far more sensitive for
clinical signs consistent with pancreatitis
diagnosis of pancreatitis than any other
are suggestive of such a diagnosis. Howe�er, diagnostic test cmrently available .

it 1s important to note that -500/o of dogs that

. A pati.ent-side.selniqua.ntitative assay for
fulfill these criteria do not have pancreatitis.

diagnosis of canme pancreatitis is also
ln cats, serum amylase and lipase activities
available. A test spot that is lighter in color
are of no clinical value for diagnosis of
tl1an the reference spot suggests tl1at
pancreatitis. Altl10ugh cats with experin1enpancreatitis can be excluded. A test spot tal pancreatitis can show an increase in
darker in color than the reference spot
serum lipase activity and a decrease in
raises the suspicion of pancreatitis and
senun amylase activity, these changes are
should prompt the clinician to measme a
not consistent in cats with spontaneous
serum cPLI concentration in the laboratory.

pancreatitis. In one study of 12 cats with

Other tests for diagnosis of pancreatitis
severe forms of pancreatitis, not a single cat
in dogs and cats have been evaluated
had serum lipase or an1ylase activity above
including plasma trypsinogen activation
the upper limit of the reference range.

peptide (TAP) concentration, mine TAP

Serum trypsin-like immunoreactivity
concentration, mine TAP:creatini.ne ratio,

(TLI) concentration measmes mainly
serum o:1-proteinase inhibitor trypsin
trypsmogen, the only fonn of trypsin
complex concentration, and serum
circulating in the vascular space of healthy
armacroglobulin concentration. However,
md1V1duals. However, trypsin, if present in
none has been shown to be of clinical
the serun1, is also detected by these assays.

usefulness.

Senun TLI concentrations can be measmed

Exocrine Pancreatic Insufficiency: In the
by species-specific assays that have been
past, several fecal tests have been used to
developed and validated for both dogs and
diagnose exocrine pancreatic insufficiency
cats. ln healtl1y animals, senun TLI is low,

(EPI). Microscopic fecal examination for fat
but dming pancreatitis an increased amount and/or tmdigested starch or muscle fibers oft_rYPsinogen leaks into the vascular space, are at best useful to suggest maldigestion.

which can lead to an increase in serum TLI

However, in light of wide availability of
concentration. Trypsin that has been
tests to diagnose EPI, microscopic fecal
prematmely activated may also contribute
exan1ination is no longer justified. Fecal
to this increase. However, both trypsinogen
proteolytic activity had been used to

1594

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
diagnose EPI in small animals for several

Handling of Samples: Most biochemisdecades. Most of these methods, particutry tests can be performed on either serun1
larly the radiographic film clearance test,
or heparinized plasma. A few ( eg, insulin)

are unreliable. One method, which uses
require serum, whereas potassium is best
pre-made tablets to pour a gelatin agar, is
measured on heparin plasma separated

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considered most reliable. However,
immediately after collection. Glucose
false-positive as well as false-negative
measurement requires fluoride/oxalate
results have been reported. The clinical use
plasma. Suitable collection tubes with and
of fecal proteolytic activity is limited to
without anticoagulant are available
species for which more specific assays to
commercially. Plastic tubes are satisfactory
estimate pancreatic function are not
for blood in anticoagulant, but clotted blood
available and in areas where the more
must be collected either into glass tubes or
accurate and sophisticated tests are not
plastic tubes specially coated to prevent the
available.

clot from adhering to the vessel walls.

Serwn TLI concentration is the

San1ples for biochemical analysis should
diagnostic test of choice for EPI in both dogs
be separated as soon as possible after
and cats. Assays for TLI measure trypsinocollection to minimize artifacts caused by gen circulating in the vascular space. In
hemolysis and leakage of intracellular fluid
healthy animals, only a small amount of
components ( eg, potassium) out of the cells.

trypsinogen is present in serum. However,

San1ples in anticoagulant may be centriin dogs and cats with EPI, the number of fuged inlrnediately, but clotted samples
pancreatic acinar cells is severely decreased. need at least 30 min to allow the clot to Serum TLI concentration decreases
form. Fluoride/oxalate samples hemolyze
significantly and may even be undetectable.

very readily because the cells can no longer

The reference range for TLI in dogs is
respire, so timely separation is especially

5. 7-45.2 mcg/L with a cut-off value of <;;2.5
important. Proprietary gels or plastic beads
mcg/L considered diagnostic for EPI.

assist with separation, and these may be

Similarly, the reference range for TLI in cats
incorporated into the collection tube or
is 12-S2 mcg/L, with a cut-off value of .,;8
added before centrifugation.

mcg/L considered diagnostic. Rarely, anin1als

Larger bucket-type centrifuges will
with semm TLI concentrations below the
accept almost any type or size of tube, but
cut-off value for EPl do not have clinical
the rotors require careful balancing. They
signs of EPI. This is probably because of the
should be spun at 3,000 rpm for 10 min.

functional redundancy of the GI tract. At the

Dual-purpose, high-speed microhematosame time, many dogs and cats witl1 chronic crit centrifuges are favored for in-practice
diarrhea and weight Joss have mild decreases use, because they separate samples more in serum TLI concentration. Most of these
quickly and the san1e machine can be used
animals have chronic small-intestinal disease to measure PCV. However, they can handle and should be investigated accordingly.

only a limited range of small-volume

However, a small number of these dogs and
tubes.

cats may have EPI. lf there is no evidence of

Some "gel-tube" products may provide a
small-intestinal disease in such patients, a
permanent separation of serun1 or plasma;
trial therapy with pancreatic enzymes and
otherwise, this must be separated into a
reevaluation of serun1 TU concentration
fresh tube. The new tube must be adeafter 1 mo is indicated.

quately labeled. Samples may then be sent

PLI is also highly specific for exocrine
to a professional laboratory or analyzed in
pancreatic function and could be used to
the practice.

diagnose EPI. However, initial studies
showed there is a small degree of overlap in
semm PLI concentrations between healthy

Point-of-Care Tests: A number of
dogs and dogs with EPI, making the
biochemical analytes may be estimated in
measurement of PLI slightly inferior to that
the practice without the need for large
ofTLI for accurate diagnosis. In view of
analytical instruments.

these findings, PU assays for both dogs and

Total protein level is measured by
cats have been optimized toward higher
refractometry, using the same instrument as
concentrations, and the current assays are
is used to measure urine specific gravity,
no longer suitable for diagnosis of EPI in
provided the instrument has a total protein
dogs or cats.

scale. It is also valid for protein measure

A fecal canine elastase concentration
ment of ascitic and pleural fluids. The
assay has been developed and validated but
readout may be in g/dL, in which case
is inferior to the widely used TLI measuremultiplying the result by 10 will yield the ment.

SI unit of g/L.

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1595

Urea level may be estimated by
gency basics requires a dedicated instruchromatographic reaction strips, which ment capable of measwing multiple
correlate well with standard laboratory
analytes. Two types are available-those
methods. A rapid whole-blood color
based on transmission/absorbance
comparison strip is also available, but these
photometry (wet chemistry) and those

VetBooks.ir
read only up to -20 nunol/L and are thus of
based on reflectance photometiy ( d1ylimited use. A dedicated reflectance meter reagent chemistiy ). Transmission/
for urea estimation is not available.

absorbance photometiy is the reference

Glucose meters for use on whole blood
method on which all reference values and
are widely available for home use by human
interpretive guidelines are based. Reflecdiabetic patients. These yield acceptably tance photometry methods do not always
accurate results on animal blood, although
compare well with the reference method
an unexpected hypoglycemia should be
and are best confined to simpler tests such
confirmed by a professional laboratory.

as glucose and urea. For wider applications,

Fresh whole blood may be used, but fluoride such as enzyme analysis, wet chemistry blood or plasma is the prefen-ed sample if
instnunents are preferred.

analysis is not immediate.

In-clinic analysis is inevitably more

Ketone levels may be estimated on either expensive than the san1e investigations wine (preferred sample) or plasma/serwn.

clone by a professional laboratory, and the

This can be achieved by using the ketone
range of analytes available is more
patch of a wine dipstick, giving a qualitative
rest1icted. Additionally, the level of
result. However, there are a nw11ber of
accuracy or reliability is likely to be lower.

point-of-care instruments for measurement

Therefore, it is still best practice to regard of blood glucose and ketone levels,
in-practice analysis as an interim emergency
including specifically 13-hydroxybutyrate.

investigation, with the results to be

Triglyceride levels may be visualized in
confi1111ed as appropriate by a professional
a plasma or serwn san1ple as lipemia. If
laboratory. Detailed case laboratory
the milkiness rises to the top of the tube
evaluation of nonemergency patients is best
on storage, chylomicrons are present.

refen-ed to a professional laboratory from

Otherwise, the milkiness is caused by
the outset, for reasons of cost, accuracy,
triglycerides. This is a qualitative judgment
range of analytes available, and the
but is nevertheless useful, especially in
assistance of the clinical pathologist in
equine patients.

interpretation of the results.

Bilirubin level may also be appreciated

If in-clinic analysis is to be relied on
by eye in most species. Equine and bovine
for general case laboratory evaluation,
plasma is normally yellow, which makes
meticulous attention must be paid to quality
deternlination problematic, but in other
assurance. San1ples of known composition
species, any yellow color is abnormal and
must be ll.U1 at least daily for each analyte, in
indicates an increased bi.l.irubin level. Visual
both norn1al and pathologic ranges; unless
assessment of the depth and shade of color
these are within the tolerance limits, no
may provide additional information.

patient samples should be tested. Participa

Other point-of-care tests include
tion in an external quality assessment

C-reactive protein as a marker for
program is also strongly recommended.

inflan1rnation and cardiac troponin as a

Employing a trained technician will address
marker for cardiac muscle damage.

some of these issues but has implications

For emergency in-clinic use, the most
for availability of results dilling off hours
important analytes beyond these simple
and holidays. The veterinarian in charge
basics are sodiw11 and potassiw11. A
of the laboratory is responsible for all the
dedicated ion-specific electrode meter is the results issued and incurs a legal liability best way to measure these. lnstrun1ents are
to prove accuracy and reliability. If these
available that can analyze whole blood,
carmot be guaranteed to the san1e standard
although great care must be taken to avoid
as a referral laboratory, then results should
artifacts due to unappreciated hemolysis.

not be relied on without external confirma

Critical care meters are also available that
tion.

can estimate a variety of analytes, including
glucose, urea, and electrolytes; however,

CLINICAL MICROBIOLOGY
these have not been extensively validated
on nonhwnan blood, and results should be

In-house microbiology can be a valuable
interpreted with caution.

asset to practitioners, providing quick results
with nlinirnal investinent. Expensive

The Practice Laboratory: Extending
equipment and materials are not usually
in-practice analysis beyond these emer-
necessary for recovery of common aerobic or

1596

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
facultatively anaerobic bacterial pathogens,

Clinical specin1ens should be inoculated
such as Staphylococcus spp, Streplococcus onto both general purpose and selective
spp, and coliforms. Although microbiologic
media to maximize bacterial recovery.

media is not difficult to prepare, it may be

Plates containing trypticase/tryptic soy agar
more convenient to purchase from a
with 5% sheep blood are the most widely
scientific supply house. Most bacteria will
used types of general purpose media.

VetBooks.ir
grow readily on standard media (blood agar

Selective and/or differential media include
and MacConkey agar plates) when incubated

MacConkey agar (gran1-negative bacteria),
aerobically. Basic equipment should include
mannitol salt agar (staphylococci), and
an incubator, refrigerator, Bunsen burner or
phenyl ethyl alcohol agar (gram-positive
portable gas torch, and microscope with low,
bacteria). Microbiologic media should be
high, and oil immersion objective lenses.

stored in the refrigerator but allowed to

Materials should consist of inoculating loops,
warm to room temperature before
prepared microbiologic media, microscope
inoculation.

slides, Gram-stain reagents, 3"Ai hydrogen

Transfer of specin1ens to plated meclia
peroxide, oxidase reagent, microbial
depends on the type of specimen. Liquid
identification systems, and a current
specin1ens are inoculated by use of a sterile
veterinary microbiology textbook.

syringe or pipette. Swabs are generally
plated directly by rolling the swab over an

Specimen Selection and Collection:

area -2 cm in dian1eter. Feces are inocu

Although it is not always easy to obtain
lated by dipping a swab into the specimen.

optimal specimens when working with

Surgical biopsy specimens may be touched
animals, certain practices can ensure the
directly to the agar surface.

best possible specin1en under the circwn

Bacterial identification methods depend
sta.nces. Application of the following
on obtain.i.ng isolated colonies. The most
principles should result in acceptable
common technique to achieve isolation is to
specimens that produce high-<1ual.ity
streak plates using a wire loop. After the
microbiology results: 1) Specimens must
specimen has been inoculated onto a plate,
be obtained aseptically from a site that is
a wire loop is flamed, cooled, and passed at
representative of the disease process.

a go0 angle several times through the initial

2) Swabs are the most common specin1en
area of inoculation. The plate is rotated go0,
collected, but they are generally not the
the loop is flan1ed and cooled, and the
specin1ens of choice, because they may
process is repeated three more tin1es. This
become contan1inated with commensals
results in four quadrants on the plate, which
during the collection process and they
enable quantitation of the relative numbers
provide a small sample volwne. Swabs are
of bacteria present in a given sample after
most useful to obtain specimens from skin
colonies appear.

pustules, ears, coajunctiva, deep within

After inoculation, plates and tubes should
draining tracts or wounds, soft-tissue
be labeled and placed in an incubator set at
infections, or the reproductive tract. 3) A

35° -37°C. Plates are incubated with their
sufficient quantity of material should be
lids down to prevent condensed water from
collected to penmt adequate·examination.

dropping down from the lid onto the agar

4) Specin1ens must be collected at the
surface, which can result in confluent
proper time in the disease process and
bacterial growth.

before initiation of antimicrobial therapy to
maximize pathogen recovery. 5) If speci

Bacterial Identification: The first step in
mens are not immediately cultured after
culture evaluation is the visual examination
collection, they should be refrigerated.

of plated media. Most bacteria produce
visible colonies in 24 hr, although some

Specimen Processing: M.icrobiologic
require 48--72 hr. Inspection includes
testing should include both direct and
exanunation of colonial morphology, noting
microscopic examination and culture of the
both the types and numbers of colonies and
specimen. Gram-stained smears should be
any hemolytic reactions on blood-based
exan1ined using oil immersion to detem1ine
agar. Further classification is based on the
the correct reaction. Generally, both solid
presence or absence of growth on

(agar) and liquid (broth) media should be
differential or selective media.

inoculated. Solid media perm.it colony

After the evaluation of plated media,
isolation, rough bacte1ial quantitation, and
exan1ination of Gram stains made from each
selection or differentiation of nonnal flora
different colony type is perfo1111ed. Those
from potential pathogens, whereas broth
reactions, combined with colonial
media allow for recovery of small nun1bers
morphology, may allow for the presun1ptive
of organisms.

identification of organisms. If more than

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1597
one colony type is present, subcultures of
organism is standardized to a turbidity
each are made. A single colony is streaked
equivalent to 0.5 on the McFarland scale.

to a plate of nonselective medium. This will

Within 15 min of standardization, a sterile
ensure a pure culture of the unlrnown
swab is dipped into the bacterial suspension
organism, which is required for biochemical and a dry Mueller-Hinton agar plate is characterization and identification.

inoculated by streaking the swab over the

VetBooks.ir

Several microbial identification systems
entire surface three tin1es. To ensure an
are commercially available. Systems may
even distribution of the inoculum, tl1e plate
be manual or automated. Each usually
is rotated -60° each time. Antimicrobial
contains a complete package for identificadisks are placed on the plate and gently tion of a particular group of organisms.

pressed down to ensure their close contact

There are specific systems for staphylowith the agar surface. lnverted plates are cocci, streptococci, corynebacteria,
placed in an incubator at 35°C. Plates are
nonfermenting gram-negative rods, and
examined after 18 hr of incubation. Zones

Enterobacteriaceae. All are useful to
of complete inhibition are measured in
conduct a wide variety of biochemical tests
millimeters. The zone sizes around each
simultaneously. Most manual systems
drug are compared with tl10se published by
consist of plates or strips made up of a
the CLSI in document VET01-S2: Pe1for
series of wells or cups that contain test
mance Standards for Antimicrobial Disk
substrates. A pure culture of the unlrnown
and Dilution Susceptibility Tests for
organism in suspension is added to the test

Bacteria Isolated from Animals to make
wells. The strips are incubated aerobically
an interpretation of susceptible, intem1ediat 37°C for 24-48 hr. The wells are viewed ate, or resistant for each agent tested.

for colorimetric changes, and a biocode is

Reliable antimicrobial susceptibility
generated from scoring the test results. This
testing results can only be obtained by
numeric code is compared with those in the
following standardized procedures set forth
system database to obtain an identity for the in CLSI document VETO l-A4: Pe1formance test organism. Most systems are adequate

Standards for Antimicrobial Disk and
for identification of common, rapidly

Dilution Susceptibility Tests for Bacte1ia
growing aerobic to facultatively anaerobic

IsolatedfromAnimals, Second frtJ01ma
veterinary pathogens.

tional Supple1nent. Any procedural
deviation may lead to erroneous results. It is

Antimicrobial Susceptibility Testing:

imperative to properly store antimicrobial

Antimicrobial susceptibility testing is
susceptibility test disks and test media and
indicated when the susceptibility of a
to ensure quality control for each test. Any
pathogen cannot be reliably predicted
clinic that does not regularly perfom1
based on the clinician's experience or the
testing on a weekly basis may wish to use
identity of the pathogen, or if the antimicroa veterinary diagnostic laboratory fofthis bial agent of choice would not be acceptprocedure instead.

able for therapeutic use. There are two
common procedures to determine the

CYTOLOGY
antimicrobial susceptibility of bacteria that
are able to grow aerobically within 24 hr,

Cytology is a useful clinical tool for
and both have been accepted by the Clinical
investigation of disease processes, and the
and Laboratory Standards Institute (CLSI).

techniques and their interpretation have

The first procedure is qualitative and is
developed into an entire discipline. This
based on the agar disk diffusion method of
discussion is a brief guide to enable

Bauer and Kirby. The second procedure is
practitioners to prepare samples and
quantitative and involves dilutions of
undertake basic interpretation; it refers
antimicrobial agents, which are tested
mostly to small animals, but the basic
either in liquid or solid agar media. The
principles apply to all species.

latter is referred to as the minimal inhibitory

Cytology should be considered a guide.

concentration test.

Characteristics of the cells may not be

The agar disk diffusion method is more
sufficient in many instances to yield a
widely used to test the common, rapidly
definitive diagnosis or indicate the probable
growing aerobic to facultatively anaerobic
behavior of the lesion. These may require
pathogenic bacteria and lends itself better
exan1ination of the overall architecture
to in-house testing. The Bauer-Kirby method of tl1e tissue, for which cytology is not is based on the diffusion of an antimicrobial
appropriate. If complex, expensive, or
agent in1pregnated within a paper disk
life-threatening therapy is being considered,
through an agar medium. Briefly, a
then the diagnosis should if possible be
suspension of actively growing test
confim1ed by histology.

1598

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

Techniques
the syringe. Suction is released before

Full cytologic interpretation requires a good
withdrawing the needle. If suction is
quality sample. A substantial minority of
continued on withdrawal, the cell san1ple
samples collecled by practitioners are
is violently sucked into the barrel of the

VetBooks.ir
unsuitable for full interpretation. The
syringe, causing cell rnpture. Sample size is
technique appears to be simple, but
often very smaJJ and may be present only
consistently obtaining good-quality samples
within the lwnen of the needle and not in
requires practice. If samples are sent to a
the syringe. When the sample has been
laboratory for interpretation, sending more
obtained, the syringe is removed, filled with
than one is recommended. In addition,
air, reattached, and used to gently express
staining and exanl.ining one of the preparathe sample onto a clean, dry, glass slide.

tions in-house helps to monitor the quality

Expressing the sample forcefully will
of the samples taken and make a provisional rnpture cells. Another slide is placed on top diagnosis. This requires a good staining
of the sample and pulled lengthways to
technique and a good quality microscope
spread the sample to a monola.yer.

with a range of objectives, including oil

Additional pressure should not be applied,
immersion.

because this also may ca.use rnpture of the
cells. Thicker areas are not a concern; the
edges will often be thin enough to examine

Staining: The stains and techniques used
individual, nonoverla.pping cells. The
for cytology preparations in a practice
sample should be air dried as quickly as
setting are the same as those used for
possible to reduce t11e effects of shrinkage;
hematology preparations. The lraditional
a hair dryer can be used for this purpose,
stains for cytology preparations are
but heating tl1e sample must be a.voided.

modified Wright stain (Wright-Giemsa) and

This technique can be adapted to

May-Grunwald Giemsa. Over the past few
different situations. If blood contamination
years, good-quality rapid Romanowsky
is a problem, the size of the syringe and
stains have been developed for cytology
amotmt of suction can be reduced or the
and hematology and are often used by
syringe removed altogether. This is
veterinary diagnostic laboratories. Many
particularly a problem with bone marrow
different brands of rapid stain have been
aspiration but is common with aJl cytology
developed, so tiying a number of products
samples and is thought to be due to
to see which stain is best suited to a practice excessive suction on tl1e syringe. If blood is recommended. Poor preparations are not
contamination is unavoidable, the blood can
always the fault of the collection technique;
be centrifuged. However, if the sample is
the stain may be the problem. Stains
directly smeared, a featl1ered edge should
deteriorate with use and require regular
be examined, because th.is is where the
renewal. Many slides can be adjusted by
heavier cells from the tissue tend to
returning a finished stained slide to the stain congregate. Blood contamination can often for deeper color reaction, or if overstained,
be decreased with the use of a very fine
can have some color removed by placing the needle (25 gauge); this increases the chance slide in alcohol. ForrnaJin-tlxed cytology
of collecting enough cells for interpretation.

preparations must be stained with either

An alternative technique uses a needle

H&E or Papanicolaou stain. If samples are
without a syringe; no difference in the cell
sent to a laboratory for interpretation, the
harvest between these two techniques has
submission form should indicate whether
been shown. The needle is inserted without
fonnaJin has been added.

the syringe and repeatedly redirected to
san1ple different depths and directions

Fine-needle Aspiration: The aim of
within the lesion. The cells are detached by
fine-needle aspiration is to obtain a high cell
the cutting edge of the needle and enter tl1e
harvest with minimal artifactual damage or
needle lun1en by capillary action. After
blood contamination. The basic sampling
withdrawal of the needle, a syiinge
kit consists of 21- and 25-gauge needles and
containing air is reattached and used to

3-, 5-, and 10-mL syringes. Precise technique
gently express the sample. This technique
and choice of equipment depends on
is also particularly useful to sample fragile
physical characteristics of the lesion and
cells, such as lyinphoid cells from lymph
whether blood contanlination is a problem.

nodes. A far better cell harvest is obtained

The basic technique uses a 25-ga.uge
from splenic lesions with this technique
needle and a 10-mL syringe. The needle
than by applying suction. In addition, there
is inserted into the lesion and repeatedly
is greater sensitivity in placement of tl1e
redirected to sample a number of areas
needle, which is especiaJly useful for small
while applying a smaJJ amount of suction on
lesions.

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1599

Certain tissues tend to give a very low cell
during transit Severe bacterial overgrowtll
harvest. These are usually composed of
obscures the cells, and their metabolic
mesenchymal cells ( connective tissue) that
products tend to desti·oy cells in cytology
tightly adhere to each other and therefore
preparations. This is paiticularly useful for
do not exfoliate easily. For these lesions, a
bronchoalveolar lavage san1ples and urine,

VetBooks.ir
larger bore needle and increased suction
which often contain infectious agents and
may be necessary. However, a needle with
are prone to bacterial contamination at
a bore >21 gauge tends to provide a tissue
sai11pling. The laboratory must be advised of
core more suitable for histologic interpretathe presence of fonnalin, which excludes tion than cytology.

the use of Romanowsky stains. Adding

EDTA to help preserve cytology samples

Impression Smears: Impression smears
is often recommended, but the effect is
are often used for ulcerated SU1face lesions.

minimal.

They are of limited value, because they

Cells in CSF san1ples degenerate very
usually sample only the sillface inflammaquickly and are usually present in very low tory exudate and rarely include cells from
nU1nbers. Cytospin preparations are almost
deeper tissues. A better use of this
essential for CSF exanlination; this can
technique is at tl1e time of biopsy to allow an usually be achieved only in a reference inunediate assessment of the lesion before
laboratory. The addition of a few drops of
fixation and processing of the tissue sample.

l()OA, fonnalin preserves the cells in CSF very

The cut surface of the excised sample is
well dilling transit.

blotted a number of times to remove surface
blood and serilln, and the dried surface is
applied to a clean, dry slide with gentle

Interpretation of Cytology Samples
pressure. A nillnber of areas can be

Cytology interpretation can be guided by
prepared on a single slide. The preparations
an algorithm that also covers the common
should be quickly air dried and then stained.

questions asked by clinicians. From a
clinical viewpoint, it is often not necessary

Body Fluid Evaluation: Once a body
to complete all stages of this algoritlun. For
fluid (eg, urine, pleural or peritoneal fluid)

example, a sin1ple differentiation of
is obtained, a cytospin preparation is by
inflammation from neoplasia may be
far the best method of cell concentration.

sufficient to allow a decision on the next

However, few practices have access to
stage of case management. Full cytology
a cytospin, so centrifugation of the
interpretation may require the services of
preparation and san1pling of the centlifuged
a diagnostic laboratory, and a definitive
sediment is the usual method of cell
diagnosis often requires histopathology.

concentration. Once the slide has been

Some lesions caimot be definitively
prepared, it should be rapidly air d1ied
diagnosed by cytology. If in doubt or if the
before staining.

cytologic interpretation does not correlate

If the fluid is to be sent to a laboratory,
with the clinical picture, histology is
adding a few drops offonnalin (the
essential for full interpretation. Whenever
concentration is not critical) helps preserve
the diagnosis is in doubt, biopsy is
cells and prevent bacterial overgrowtll
indicated.

Cytology Sample

��

/�

Acute

Chronic

Granulomatous

/!

Epithelial

�

Mesenchymal

Round Cell

Algorithm to interpret cytology samples.

1600

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

Inflammation: Recognition of basic
vacuolated. They can look epithelial, and
inflammatory cells-neutrophils, eosinogreat care must be taken when interpreting phils, lymphocytes, macrophages, and
such cells. However, they do not normally
plasma cells---is essential for interpretation
form clusters, which is a key factor in
of cytology samples. Some tumors contain
differentiation from epithelial cells.

a large number of inflammatory cells, but

Macrophages are almost always seen in

VetBooks.ir
these are very uncommon, even when there
bronchoalveolar lavage fluid (they come
is tumor necrosis. The presence of only
from the alveoli) and body cavity fluids
inflammatory cells in a sample usually

(part of the modification process), joints
indicates a primary inflammatory lesion.

(a norn1al component but increased in

Ulceration produces inflammation on the
disease), and cyst contents (a nonspecific
surlace of neoplastic lesions, but even in
reaction).

this case the inflammatory cells typically

Eosinophils: Eosinophils have segdo not extend deeply into the underlying mented nuclei and eosinophilic cytoplasneoplasm. A small percentage of mast cell mic granules. They vary slightly between
tun1ors, however, are composed almost
species and are generally slightly larger than
entirely of inflan1rnation, hemorrhage, and
neutrophils. In cytology preparations, it can
edema with only a small nun1ber of mast
occasionally be difficult to distinguish
cells. These can be difficult to identify even
poorly stained eosinophils from neutroby histology.

phils, because the granules can become

Neutrophils: These are the first cells to
indistinct and the cytoplasm of degeneratarrive in an area of i.nflan1malion, and they ing ncutrophils become more acidic, giving
continue to be attracted to the site as long
a more eosinophilic staining reaction. They
as the inflammatory stin1ulus lasts. Large
are often seen in association with mast
nwnbers of neutrophils indicate acute
cells. Eosinophils are associated with
inflan1mation and often are accompanied
allergies and also are prominent in parasitic
by smaller nwnbers of macrophages. This
diseases, superficial cutaneous viral
pattern is most often ca.used by infection or
infection in cats, and fungal infections. They
foreign body reaction, including furu.ncuare the predominant cell type in specific lotic reactions directed against hair and
eosinophilic conditions such as eosinophilic
keratin embedded in the soft tissue. If fluids
granuloma in cats (rarely in dogs), canine
are not examined inllllediately, bacteria,
eosinophilic folliculitis and furu.nculosis,
if present, will begin to proliferate, but
and eosinophilic collagenolytic granuloma
phagocytosis of bacteria does not occur
in horses. Some cases of canine cutaneous
after sampling. Therefore, if the bacteria are
mast cell tumors have a very high proportruly pathogenic, they should be within the tion of eosinophils and very few mast cells
cytoplasm of the phagocytic cells. The cells'

(<5%of cases).

cytoplasm may contain RBCs, tissue debris,

Of the most commonly encountered
or foreign material.

veterinary species, rabbits and guinea pigs
have inflammatory cells equivalent to

Macrophages: Macrophages arrive at a
neutrophils in other species, but have
site of inflammation within 2-3"hr and are
eosinophilic cytoplasmic granules. These
not necessarily an indicator of chronicity,
are called heterophils. They can be difficult
although they often increase with time.

to distinguish from eosinophils. The cellular

They phagocytize bacteria and also larger
equivalent to neutrophils in.birds and
structures, such as fungi, cellular deb1is,
reptiles are also heterophils with eosinoand foreign mate1ial. These cells are often philic granules.

associated with tissue destruction.

Macrophages come from circulating

Lymphocytes: Lymphocytes are usually
monocytes and have variable morphology.

small with very little cytoplasm and

In the tissue, the cytoplasm greatly enlarges
smudged chromatin with no nucleoli. The
over tin1e and usually becomes vacuolated.

almost-round nuclei are similar in size to

The nuclei become rounded. If a macthose of red cells. RBCs are often present in rophage exhibits vacuolation or phagocytocytology preparations, where tlley can be sis, it is often described as activated. They
used as a comparative and absolute scale.

can be multinucleated, especially with

RBCs vary slightly with species; in dogs,
foreign body reactions and in longstanding

RBCs are -7 microns in diameter. Medium
lesions. Under certain circwnstances, they
and large lymphocytes, which have a
may become epithelioid. These cells have
slightly more open chromatin pattern and
oval or round nuclei and small, often
more cytoplasm, can also be seen in
indistinct, nucleoli. Their cytoplasm is
inflanl!llatory processes. Along with plasma
expanded but uniformly stained and not
cells, lymphocytes are part of tile chronic

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1601
inflanunatory response and tend to arrive in
populations. The presence of cells that are
tissue a few days after the acute inflammapredominantly of the same population tion has begun. However, they are not
indicates normal tissue, hyperplasia, or
specific for a particular stimulus and are
neoplasia. Ideally, the first stage in
mostly small lymphocytes. If mostly
evaluation of a cytologic sample for
mediwn to large cells are present,
neoplasia is to determine the tissue type

VetBooks.ir
lymphoma is a possibility. However, even
from which the cells have come. If this is
large lymphoblastic cells can be seen in
not possible, it is necessary to simply deterlow nwnbers in inflanunatory processes.

mine the likely behavior of the cells. This

Normal and reactive lymphocytes in body
can often be done without specifically
fluids often appear larger than the same
identifying the cell type. The following
cells from soft tissue.

checklist includes features that can be

Multinucleated Cells: These cells are
examined to determine tissue type and
large and have larger numbers of nuclei
likely behavior of the lesion: 1) cell
witl1 one to three small nucleoli and
numbers, 2) cell distribution within the
vacuolated cytoplasm. They develop from
smear, 3) cell shape, 4) nucleus:cytoplasm
macrophages (see above) and tend to
ratio, 5) pleomorphism (both nuclear and
appear late in the comse of inflanunation.

cytoplasmic), 6) number, shape, and size of

The cytoplasm should be examined for the
nucleoli, and 7) cytoplasmic content such
presence of fungal organisms and for
as melanin, metachromatic granules, fat,
foreign material. These cells are usually
etc. Classification of the cell type and likely
seen in small nwnbers mixed with other
behavior may require a tissue biopsy. With
inflanunatory cells as part of a granulomafew exceptions, histology will be necessary tous reaction. Multinucleated cells are
for a definitive diagnosis and is always
much less specific in birds and reptiles, in
necessary to assess mitotic index and to
which they are common in many focal
grade a tumor.

inflammatory lesions, iITespective of cause,

There are three basic tissue types:

and can appear quite early in the inflammaepithelial, mesenchymal (supporting or tory process.

connective tissue), and round cells.

Fibroblasts: Fibroblasts are not

Epithelial Cells: Epithelial cells are
inflammatory cells, but they are frequently
round, cuboidal, or polygonal and tend to
seen in association with inflanu11ation. They
aclhere tightly to each other and exfoliate
will proliferate as part of the repair reaction
in clusters or sheets. They have a sharp
associated with any tissue damage and
cytoplasmic outline and exfoliate in
appear in an inflanunatory lesion after -2
moderate nwnbers. Cells with more than
days. Classically, fibroblasts and fibrocytes
one nucleus are uncommon.

are elongated cells with pointed tails of

Mesenchymal Cells: Mesenchymal cells
cytoplasm. They have row1d or oval nuclei,
are tightly adl1erent and usually exfoliate in
indistinct nucleoli, and moderate an1ounts
low numbers as single cells or small
of Wlifonn, pale blue-staining cytoplasm.

aggregates. They are classically spindle

The cytoplasmic botmdaries are indistinct,
shaped but usually round up and become
giving a "wispy" appearance. When
fibroblasts are aspirated from tissue, the
cells often become round and lose their
spindle shape, but a small nun1ber,
especially cells in groups, retain their
elongated shape. Reactive fibroblasts
cannot be definitively distinguished
cytologically from low-grade spindle cell
tumors. If found in association with
inflanunatory cells, spindle cells are most
often reactive. If found in large clwnps with
no apparent stimulus, they are more often
neoplastic (but neoplasia cannot be
excluded). Because fibroblasts and
fibrocytes are the p1incipal connective
tissue cell, they are tightly adl1erent to each
other, and cell harvest tends to be low.

Within the usual blood contamination, there

Neoplasia: Inflan1matory lesions are
are cells that are well separated and
nonadherent; this is typical of round cell
characterized by cells from different
tumors. Courtesy of Abbey Veterinary Services.

1602

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
plwnp when removed from the body,

Unlike most malignant tumors, lymparticularly when they are lying singly phoma is commonly characterized by a
within the smear. The spindle shape is often

Wliform population of cells that are larger
more apparent in small aggregates. They
than norn1al lymphoid cells. Therefore,
tend to appear "wispy" because of indistinct variation in morphology is not necessary for

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cytoplasmic boundaries. Bi.nucleate cells
a diagnosis of malignancy with this tissue
are not unconunon.

type. If there is marked variation and small

Round Cells: Round cells have little or
lymphocytes are present, then that is more
no adherence in the body. They typically
typical of hyperplasia.

exfoliate in large numbers and lie individu

Some nonnal structures, such as hepatoid
ally in the smear without clwnping. Cells of
glands, have more than one cell type
this category include mast cells, lympho

(reserve and ternlinal cells) and can
cytes, histiocytes, plasma cells, and cells
therefore show variation in morphology,
of transmissible venereal twnors.

and benign tumors of hepatoid glands can
have a similar mixture. Nuclear morphology, however, maintains benign features.

Tumor Evaluation: To distinguish

Many mammary tumors can show
benign from malignant tumors, the
marked variation in cell morphology but
amount of variation in certain characterishistologically would be classified as benign.

tics within the cell population must be

Indicators of mammary tumor behavior are
assessed. In general, the more malignant
architectural features, such as local tissue
the cell, the less differentiated it becomes
invasion and invasion of vessels. These
and the more variation there is in the cell
cannot be assessed using cytology. These
morphology. Benign tumors have cells that exceptions often make cytologic interpretaare often uniform in size with a uniform tion Wlfeliable, particularly for these types
nucleus:cytoplasm ratio; they strongly
of tissues.

resemble or are identical to the cell of

Most spindle cell tumors do not
origin. The more malignant the cells
metastasize but are locally aggressive and
become, the more variation is seen in
often difficult to remove. The criteria for
these criteria. Nuclear criteria are the
malignancy are often less important with
major indicators of malignancy.

respect to the behavior of these tumors than

Criteria for malignancy include the
for the epithelial twnors.

following: variation in cell size and shape,
increased cell exfoliation, increased

Common Cytology Results: Some
nuclear size, increased nucleus:cytoplasm
specific features of cytology preparations
ratio, variation in nuclear size and an
can provide a more accurate interpretation
increase in multinucleated cells, increased
of the sample. Listed below are some
mitosis with abnormal mitotic figures, a
common results and their interpretation.

coarse and often clun1ped chromatin
pattern, altered shape of the nucleus due to

Mature Fat Cells: Mature fat cells are
close approximation of a nucleus from an
seen in benign lipomas and mature body fat.

adjacent cell (nuclear moulding), and large

It is not possible to differentiate these
and often multiple nucleoli0of irregular and
abnormal shape. There are a nun1ber of

"

exceptions to these indicators; in such
situations, histology is essential for full
interpretation.

The following are some exceptions to the
rules of interpretation:

Thyroid carcinomas usually have fairly

Wliform, well-differentiated cells. A
diagnosis of carcinoma can be made simply
on the size of the mass in dogs (tun10rs >3
cm are automatically considered malignant)

but not in cats. Major features of malignancy, such as capsular, soft-tissue invasion and vessel invasion, can only be identified
histologically. Other tissues in which it may
be impossible to differentiate benign from

These typical balloon-like fat cells are
malignant cells include apocrine gland
characteristic of benign lipoma and mature
body fat. Both involve the same cells and
carcinomas, basal cell tumors, melanocannot be distinguished on cytology. Courtesy mas, and proliferative lesions of the liver.

of Abbey Veterinary Services.

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1603
cytologically. Fat cells are mesenchymal
proliferation (including lipomas), because
cells, and because they tend not to exfoliate
these structural cells within the body are
well, they are usually present in low
tightly adherent cells that do not exfoliate
numbers. If a san1ple has come from the
well.

center of a nodular mass, fat cells are
diagnostic for lipoma. These clear-staining,

Cells with Cytoplasmic Granules:

VetBooks.ir
balloon-like cells are often in clusters,

The most important type among cells
folded, and overlapping.

with cytoplasmic granules is the mast
cell, given that mast cell tumors are

Spindle Cells: It is usually not possible
common in dogs. These are medium-sized
to differentiate reactive spindle cells from
cells with round nuclei. With Romanowthose of spindle cell neoplasia. Indicators sky stains, the granules are dark blue or
of neoplasia include absence of a reactive
purple, small (about the size of bacteria),
stimulus, such as inflammation or hemorand usually found in large numbers in the rhage, and a higher cell population with
cytoplasm. Less-differentiated mast cells
more numerous and larger clumps of cells.

have fewer granules. Cytology cannot be

Greater variation in cell morphology
used to grade mast cell tumors; grading
indicates more aggressive behavior. When
always requires histology, because it
removed from their tissue, they often round
does not depend on only cell morphology.

up and can be mistaken for round cells, but

The cells are fragile, and often there are
there are usually some distinctly spindle
large numbers of granules in the
cells in most preparations.

background that have been released from

Keratin: Keratin includes nucleated and
damaged cells. In dogs, eosinophils are
terminally differentiated non-nucleated
often present and very occasionally can
squamous epithelial cells. Keratin can be a
be the dominant cell type; however, they
contaminant from tl1e surface of the skin of
are less common in other species. Mast
tl1e animal or the skin of all handlers of the
cell tumors in horses have similar
san1ple and is a common artifact. It can also
cytology to those in clogs, but in cats the
be sampled from cutaneous keratin-filled
cells in mast cell tumors are often
cysts, which are always benign and very
smaller, more uniform, and have less
common, particularly in dog skin. Large,
distinct granulation.

densely packed clumps of keratin in

Thyroid cells can also have dark
restricted areas in the center of the slide
granules, usually blue or black. These
suggest that keratin is not an artifact but
tyrosine granules are very small, low in
has been sampled from the lesion.

number, and can be difficult to see. Larger

Blood: Blood is a common artifact of
black granules are associated with
fine-needle aspiration but can also come
melanomas. Cytology cannot differentifrom blood-filled spaces in tissue. These can ate benign from malignant melanomas;
be non-neoplastic, such as hematomas,
however, melanomas on haired skin in
aneurysms, or severe bruising, or neoplastic
dogs are usually benign and those on
lesions such as hemangiomas and
nonhaired areas, such as the lips, feet,
hemangiosarcomas. The presence of
and mouth, are usually malignant. Basal
spindle cells does not adequately differenticell tumors also often contain cells with ate neoplastic from non-neoplastic causes
melanin, especially in cats. These tumors
of hemorrhage (see above). Spindle cells
are usually benign and cytologically can
produce the neoplastic blood vessels in
sometimes be difficult to distinguish from
hemangiosarcomas, but especially in young
melanomas. Melanin can also be seen in
dogs, they can occasionally produce a very
macrophages (melanophages),
cellular capsule to a soft-tissue hematoma.

sometimes in large amounts, but it is

The capsule contains very active fibroblasts, usually in much larger clumps within the but they are not neoplastic. Blood that has
cytoplasm rather than fine granules that
come directly from the vascular system
are seen in melanocytes. Very fine
normally contains significant numbers of
magenta granules can sometimes be seen
platelets. Using a 25-gauge needle can help
in osteoblastic cells from osteosardecrease blood contan1ination. Blood is coma. Golden, granular material
almost always seen in aspiration from
accumulates in the cytoplasm of
parenchymatous organs, such as the liver,
macrophages when there has been
spleen, kidneys, and bone marrow.

hemorrhage into soft tissue (hernosiderophages ). Liver cells can sometimes No Cells: Lack of cells is a conunon
contain bile, which stains very dark, and
problem of fine-needle aspiration. If tl1e
occasionally long, thin strands of dark
technique is practiced properly, absence
material can be seen where canaliculi
of cells can indicate mesenchymal cell
have become filled with bile.

1604

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

Cells with Cytoplasmic Vacuoles:

show more marked pleomorphism and

A large, single vacuole is seen in fat cells. In
often differ markedly from normal plasma
normal or benign cells, the nuclei are small
cells. Many have a slightly histiocytic
and often indistinct, and the cells are often
appearance, and these can be difficult to
folded like a collapsed ball. Smaller cells
distinguish cytologically. These cells have
with larger, more prominent nuclei and
a round nucleus and a coarse chromatin

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some cytoplasm in addition to clear, often
pattern, which sometin1es becomes
small vacuoles are more suggestive of
cltunped ar0tmd the nuclear membrane.

malignancy.

The nucleus is often eccentric with an

Cells with multiple, small vacuoles with
intensely basophilic cytoplasm and
a foamy appearance include macrophages,
paranuclear pale Golgi zone.

sebaceous glandular cells, and salivary

Cells of transmissible venereal tumors
cells. It can be very difficult to differentiate
tend to have a moderate an101mt of
these; the site and other clinical features
cytoplasm ( more tl1an found in lymphocan be a deciding factor in interpretation.

blasts ), often with small vacuoles. Nuclear

Differentiation of Round Cell Tumors:

chromatin is coarse, with one or two fairly

Round cell tumors include mast cells,
prominent nucleoli. Mitotic figures a.re often
plasma cells, lymphocytes, histiocytic cells,
numerous. Unlike most cytology preparaand transmissible venereal tumor cells.

tions of neoplastic lesions, they tend to have

Mast cells have distinctive granules within
moderate variation in the
the cytoplasm and are usually easily
nucleus:cytoplasm ratio.

identified; if they are the dominant cell type,
this is diagnostic for a mast cell tumor. In

Cytology of Specific Sites:

rare cases, mast cells can have few or

Lymph Nodes: Normal, hyperpla.stic,
no granules in the cytoplasm. Lymphoid
and early neoplastic lymph nodes have a
cells classically have a very high nucleus:

mixed population of cells. Cells are
cytoplasm ratio; few other cells have this
predominantly small lymphocytes with
feature. Neoplastic, lymphoid cells are
variable nwnbers of mediwn and large
medium size to large, with a nucleus at least
lymphoid cells and some plasma cells.

1.5 times the size of an erythrocyte. Nucleoli A uniform population of cells indicates are often multiple, sometimes quite
neoplasia. Lymph node aspirates often have
prominent. However, the rare cases of
a population of cells that are much paler
small-cell lymphoma have cells indistinstaining and larger, with some cells guishable from normal lymphocytes.

completely losing their cytoplasm. These

Cells of a histiocytoma (Langerhans
cells are in varying stages of degeneration
cells) are not especially histiocytic
and should be ignored. Size in comparison
cytologically. They are round cells with a
with RBCs is useful. Normal mature
small to moderate amount of pale-staining
lymphocytes or small neoplastic lymphocytoplasm. They are fairly unifom1 and have cytes (rare) have nuclei the san1e size as
nuclei that are eccentric within the cell.

RBCs. However, neoplastic lymphoid cells

Nucleoli are indistinct. True histiocytic
have nuclei at least 1.5 times the diameter
cells are slightly more problematic to
of RBCs. Lymphomatous lymph nodes may
interpret. These are part of the cell line that
still contain a significant nun1ber of normal
includes the antigen-presenting cells, such
lymphoid cells. The proportion of smaller
as macrophages and Langerhans cells, but
mature lymphocytes must then be
can range from inflanmrntory and reactive
compared with the larger immature cells to
cells to highly malignant round cell tumors.

differentiate hyperplasia. from neoplasia.

They tend to be larger than the other round

The propo1tion considered significant
cells with more cytoplasm, sometimes are
varies, but in general, most cytologists
vacuolated, and can have oval or indented
consider a diagnosis of lymphoma when
nuclei. Infiltrates of histiocytic cells are
immature cells are >500Ai of the cell
often problematic, even with a full-tissue
population. Some cytologists require a
biopsy exan1ination, and always require
higher percentage of immature cells,
histologic examination to assess behavior.

particularly if there is only one lymph node

Neoplastic plasma cells include cells of
enlar·ged. If there is doubt, a biopsy should
myeloma. These are usually well differentibe perfom1ed. Histopathologic confirmation ated and have most of the characteristics of
of diagnosis is essential if tl1erapy for
nom1al plasma cells. When neoplastic, tl1ey
lymphoma is considered and is always
arc found in large numbers with few otl1cr
needed for full grading.

cell types present. Benign nodular prolifera

Submar1dibular· lymph nodes are often
tions of plasma cells, plasmacytomas,
difficult to assess. They drain the buccal and

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1605
nasal areas and are subject to strong
mesothelial cells from neoplastic cells
antigenic stimuli. They frequently undergo
within the body fluid. A small number of
hyperplasia, often histologically atypical,
these cells typically have a corona around
especially in cats. Cats also develop unusual the cytoplasmic envelope (giving a fuzzy neoplastic conditions affecting this node,
outline); this is a distinguishing feature of
such as the T cell-rich B-cell lymphoma and
mesothelial cells.

Hodgkin-like lymphoma, botl1 of which have

Mesothelial cells can be present in very

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a majority of normal lymph node cells. For
large numbers, especially in pericardia.I
these reasons, great care must be taken in
fluid. Malignant mesotl1eliomas are rare
the interpretation of lesions involving the
in domestic species, but it is not possible
submandibular lymph nodes, because
to differentiate neoplastic from reactive
false-negative and false-positive results
mesotl1elial cells on cytologic exan1ination.

for neoplasia are not unconunon.

The degree of polyploidy is not a distin

Aspirates from suspected enlarged
guishing feature.

submandibular lymph nodes often yield

Mixed inflan1rnatory cells increase in
only large foamy cells, which are salivary
number as a transudate becomes modified
cells. This result can be due either to
and are present in large nw11bers in an
sampling error or to hypertrophy of the
exudate. Mesothelial cells would be
salivary gland in cases of sialoadenosis. The
expected in this type of sample, and it can
cause of sialoadenosis is not understood,
tl1erefore be useful to look for a second
but a significant minority of submandibular
population when checking for neoplasia.

aspirates contain only these cells.

Smootl"tly demarcated aggregates of

Body Cavity Fluids: Meaningful analysis
atypical cells with no narrow spaces
of fluids from body cavities requires total
between the cells may indicate a second
protein (measured with a handheld
population of carcinoma cells.

refractometer), total cell count, and a

Tracheal or Bronchoalveolar Lavage
differential of cell types present (see TABLE

(BAL): Respiratory epithelial cells are

2). Pure transudates are rare, because they
seen in BAL from healtl1y and diseased
rapidly become modified by leakage of fluid
animals. The epitl1elial cells may retain their
from lymphatics or blood vessels and
original structure with a ciliated surface and
attraction of mixed inflan1rnatory cells.

basal nuclei, but they often appear round

Transudates attract activated macrophages
with indistinct cilia.

with varying nun1bers of non degenerate

Macrophages are usually the dominant
neutrophils. The lymphocytes tl1at may also
inflan1rnatory cell type in BAL from healthy
be present are classified as small, but most
anin1als. These come from deep in the
look slightly larger tl1an circulating
alveoli and are part of the normal defense
lymphocytes and are part of tl1e reactive
mechanisms. They greatly increase with
process of tl1e fluid in the body cavity. In
fluid accw11ulation in the lung ( eg,
addition, when fluid accumulates in the
cardiovascular insufficiency) and in
body cavity, the lining mesothelial cells
inflammatory conditions, where they are
proliferate and are shed into the fluid. These accompanied by other inflan1rnatory cells.

cells are large, often multinucleated, vary in

Debris, foreign material, hemosiderin,
appearance, and often are seen in groups

RBCs, and microorganisms can sometimes
with large nucleoli. They sometin1es form
be seen in the cytoplasm of these cells.

grape-like clusters with a narrow, pale space Macrophages containing hemosiderin in between the cells. These features are
people are called heart failure cells, but
usually considered to be associated with
their cause is less specific in domestic
malignancy, but in tl1is case, the cells are
species. There are increased numbers of
simply reactive and not neoplastic. Care
macrophages in many subacute and chronic
must be taken to differentiate these
ltmg disorders.

•t+litl CHARACTERISTICS OF TRANSUDATES AND EXUDATE

Total Protein (g/dL)

Cell Count (cells/mL)

Transudate

<2.5

<1,500

Modified transudate

2.5-7.5

1,000-7,000

Exudate

>3.0

>7,000

1606

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

In healthy dogs and cats, neutrophils
attached to the syiinge is slowly advanced
contribute <5% of cells in BAL preparations.

into the joint space and, taking care not to

Neutrophils are nonspecific inflammatory
scratch the articular surface, gentle suction
cells in the respiratory system and do not
is applied. Normal joint fluid is viscous and
necessarily indicate infection. They can
sticky and of small volun1e. The volwne of
be the most nw11erous cells in an inflan1mafluid, however, depends on the size of the VetBooks.ir
tory reaction, even in cases of allergy.

animal, the joint san1plecl, and the degree of

However, when neutrophils are present, the
effusion into tl1ejoint. When san1ple size is
cytoplasm should always be examined
sufficient, it is essential to release the
carefully for the presence of any infectious
suction on the syringe before withdrawing
agent. Bacteria can also sometimes be seen
the needle.

in the extracellular parts of the smear, but

Sample handling is critical; because
extracellular bacteria are often contamimany tests can be performed on synovial nants from the pharynx.

fluid and cytology is the most important,

Great care must be taken to differentiate
sometimes the sample volume is so small
eosinophils from neutrophils in BAL
that no other test is possible. Therefore, a
preparations because the granules are often
plain smear should always be made and
faint and difficult to identify. Eosinophils
quickly air dried as soon as the sample is
can comprise up to 5% of cells i.n BAL from
obtained. Most tests can be performed on
healthy clogs but may reach lOOAi in healthy
sainples without anticoagulant (a plain
cats. Eosinophils that comprise> 10% of
red-topped tube), or the san1ple can be
cells indicate an allergic respiratory disease, left in the san1pling syringe. However, although lungworms and heartworms can
blood contamination, hemarthrosis, and
also cause Lhis reaction. With lungworm
inflainmatory effusion introduce fihrin
infestation, laivae are sometimes present
into the joint, and the sample may clot.

as large coiled structures.

Placing part of the sample into an EDTA

Nucleated and nonnucleated squamous
tube can prevent this, but EDTA can
cells are commonly seen in BAL preparainterfere in the mucin clot test and, for tions and are often associated with bacteria
this reason, a heparinized san1ple may
on the cell surface. This indicates contanlinaalso be necessary.

tion from the pharynx. Bacteria are normal

Results of cytology preparations can
inhabitants of the pharynx, in particular
indicate the nwnber of cells present, the

Simonsiella, which ai·e very large, ladder-like type of cell and the differential, the organisms. Their presence confmns contamipresence of tumor cells, and the presence of nation from the pharynx. If bacteria are
bacteria. They can also give an indication of
present along with squan1ous epithelial cells,
viscosity. In fluid of normal or increased
it may not be possible to conclude whether
viscosity, cells tend to align in rows in the
the bacteria ai·e from the respiratory tree or
direction of the smearing; this is described
the pharynx. Bacteria in the cytoplasm of
as windrowing.

neutroph.ils confmns a significant infection.

In healthy aninlals, cell counts vary
widely (eg, 0-4,400/mL in dogs), but they ai·e

Synovial Fluid: Full exa.111ination of
usually very low. Counts >500/mL in dogs
synovial fluid should include protein
generally indicate a significant increase.

content, mucin clot formation, viscosity, cell Normal synovial fluid contains -2 cells/high

COWlt and differential, and direct cytologic
powered field (400X magnification). In the
exanlination. It is usually not feasible to
vast majority of cases where there is a.11
perform all of these tests in a practice
increased cell content, cell nun1bers are
setting, but cytologic exanlination ai1d
either low (up to 4 or 5 cells/high-powered
physical exainination can usually give a
field) in degenerative joint disease or very
good estin1ate of the results of most of these
high in septic or autoimmune arthritis. Intertests. Cytology, therefore, is the most useful mediate equivocal results ai·e extremely
single test in synovial fluid exanlination.

unconunon.

Sampling technique requires the follow

Cell types include joint mononuclear
ing equipment: a 3-mL syTinge, a 21- or
cells, which are a mixttll'e of circulating

25-gauge needle, clean glass slides, and
monocytes, tissue macrophages, and
various collection tubes (plain, EDTA, a.11cl
synovial lining cells. It is not possible, or heparin). This technique always requires a
even necessaiy, to differentiate these cells,
degree of sedation, and a sterile technique
because they all have a sinlilai· morphology
is essential. Each joint has a recommended
ai1d all react to sinillai· stimuli. Cytoplasmic
site for aspiration (beyond the scope of this
vacuolation of these cells, and especially the
discussion) and generally requires slight
presence of phagocytosis of debris or RBCs,
flexion or hyperextension. The needle
indicate activation, a feature not seen in

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1607
nom1al joint mononuclear cells. In

Neutrophi.ls a.re the most common
degenerative joint disease, synovial fluid
exudative cell but, as with BAL, often
usually contains only macrophages,
indicate secondary infection. In the case of
occasionally with extremely low nwnbers
intranasal neoplasia, cells with neoplastic
of neutrophils.

cha.racte1istics (seep 1601) may be present, Hemorrhage is common in synovial
but absence of these cells does not exclude

VetBooks.ir
preparations but is frequently an artifact.

neoplasia Only a minority of neoplastic

True hema.rthrosis provides a synovial fluid
processes erode the overlying respiratory
san1ple that is unifonnly contaniinated with
epitheliun1 and allow exfoliation of
blood at the time of sampling. If the blood
neoplastic cells.

contamination occurs at the very end of the

Similarly, absence of fungal hyphae
san1pling procedure with clear fluid initially,
within the preparation does not exclude
tllis is most likely artifact. In addition, in
fungal infection. Unless fungal plaques a.re
true hema.rtlu·osis, RBCs may be seen in the
sampled directly for both cytology and
cytoplasm of macrophages. Artifactual
culture, false-negative results are conu11on.

blood contanlination will also introduce

Viral inclusions are rarely seen.

WBCs, such as neutrophi.ls, making
interpretation of inflan1matory cells in the

Vaginal Cytology: This can be used to
san1ple difficult, although blood contanlinaidentify tile vrufous stages of the canine tion still gives only a low cell nwnber.

estrous cycle, but results must be inter

Neutrophils a.re present in large
preted in cortjw1ction with the animal's
nwnbers in both septic arthritis and
behavior. A sample of exfoliated cells is
autoimmune joint disease. These two
obtained from the vaginal vault crrulial to
conditions can usually be differentiated
the urethral 01ifice wiU1 a cotton-tipped
by the clinical llistory. In septic arthritis,
swab or glass rod. Cells ru·e gently rolled
bacteria a.re sometimes found within the
onto a glass slide, air dried, and stained.

cytoplasm of phagocytic cells. The absence

Features to be identified include neutroof bacteria, either within cytology phils, bacteria, RBCs, and the types of
preparations or by culture, does not exclude epithelial cells. Epithelial cells (in bacteria as a cause of a.rt1u;tis. False-negaincreasing order of differentiation) a.re tive results for bacteria a.re not uncommon.

pa.rabasal, small and Iru·ge intem1ediate

Lymphocytes a.re often present in very
cells, and superficial cells. Para.basal cells
small nwnbers in inflan1matory processes
are small, with central round nuclei,
but a.re not specific for a particular cause.

indistinct nucleoli, a relatively narrow band

Osteoclasts are very occasionally seen
of cytoplasm, and a nucleus:cytoplasm ratio
when there has been erosion of tl1e articular
of -1: l . Small intennediate cells have a
cartilage with exposure of the underlying
similar nucleus but a much larger an1ount of
bone.

cytoplasm. Large intem1ediate cells have a

Neoplastic cells in joint fluid a.re rare,
similar nucleus with very large amounts of
although joints can be the site of both
cytoplasm and an angular, irregular outline.

primary and secondary tumors.

Superficial cells also have large an1ounts

Macrophages increase with any damage
of cytoplasm, but their nuclei are pyknotic
to a joint, especially in cases of degenerative (small and contracted) or absent.

joint disease. Cytoplasnlic vacuolation of

The stages of the estrous cycle change
these cells, and especially the presence of
gradually. If a preparation does not conform
phagocytosis of debris or RBCs, indicate
exactly to a specific pa.rt of the cycle,
macrophage activation, a feature not seen
judgment must be made regarding what
in nom1al joint mononuclear cells. In
stages are present. In proestrus, all types
degenerative joint disease, synovial fluid
of epithelial cells ru·e present along with
often contains only macrophages.

neutrophils, RBCs, and mucus. As proestrus
progresses, the epithelial cells increasingly

Nasal Cavity: The cytology of nasal flush
approach temlinal differentiation (superfipreparations is similar to that seen with cial cells), and neutrophils slowly decrease.

BAL preparations. A small nwnber of

Bacteria a.re often present in lru·ge nwnbers.

respiratory epithelial cells a.re usually

In estrus, >900Ai of epithelial cells a.re
flushed out along witl1 exudate. A predomisuperficial cells, with no background nance of eosinophils may indicate i.nllaled
mucus. There ru·e large nwnbers of bacteria,
allergens, parasites, or fungi and may
but no neutrophils. In di.estrus, pa.rabasal
occasionally indicate bacteria or neoplasia.

and intermediate cells a.re >80% of the total

The presence of eosinophi.ls in the nasal
epithelial cells. Variable nun1bers of
cavity therefore is less indicative of a
neutrophils and bacteria ru·e present but
specific process than in some other sites,
usually fewer than in proestrns. It cru1 be
eg, the trachea or bronchi.

difficult to differentiate some stages of

1608

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
proestrus from diestrus. In anestrus

There are at least 10 common forms
parabasal and intermediate cells prectomiof urinaiy crystals. Identification is not nate. Neutrophils and bacteria are rare.

discussed here but may be readily

RBCs do not help differentiate the stages
accomplished by use of good reference
of estrus.

illustrations. (See also UROLITHIASIS, p 1525.) Because c

Cerebrospinal Fluid: Interpretation of

_ells in urine rapiclly degenerate,

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CSF cytology is difficult, because it can be
particularly if bacteria are present,
hard to obtain enough well-prese1vecl cells
centrifuged preparations of urine sai11ples
for exan1ination before the satnple
should be exanlined rapiclly after satnpling.

deteriorates. Cell counts in nom1al CSF are

If this 1s not possible, boric acid is often
low (0-5 cells/µL in dogs and 0 -8 cells/µL in
added to urine to prevent degeneration and
cats). However, there is a large variation in
bacterial overgrowth, although its effect
cell counts between individuals; counts can
may be very limited. If a delay between
also vaiy between cystemal and lumbar
satnpling ai1d exatnination is likely, a better
taps in the san1e individual. Because the
preservation method is the addition of a few
albunlin level of CSF is -20<>A, of that found drops of formalin; however, the traditional
in serum, the cells that are present rapiclly

Romanowsky stains caimot then be used.

degenerate. Cell counts should ideally be

H&E stain is a better alternative for
clone and morphology exanlined within 1 hr
formalin -fixed sainples.

of collection.

Nonna! urine usually has very few

Because of the low cell numbers, the use
nucleated cells. Single urothelial cells are
of an automated cell counter is usually not
occasionally present. Squatnous epithelial
appropriate. A hemocytometer cat1 be used
cells are also seen in urine and come from
for cell counts, and a cytocentrifuge for
the tem1inal urethra, vagina, vulva, and
cytology preparations. A simplified
preputial epitheliun1. Squatnous metaplasia
sedimentation technique ( description of
of bladder epitheliwn after chronic
which is beyond the scope of this discusinflammation is very rare.

sion) to concentrate cells onto a slide is

Neoplastic cells in urine sainples are
suitable for practice use. The presence of
almost always epithelial. They are rounded
more than one or two nucleated cells in a
polygonal cells, often clun1ped, with marked
plain smear of CSF should be considered
variation in morphology, especially the
potentially significai1t.

nucleus:cytoplasm ratio. Uniform cells are

In CSF, an increase in nucleated cells is
more likely to be nmmal. Mi.Icily pleomorcalled pleocytosis. There is tremendous P_hic cells can be associated with hyperplavariation ai1d overlap in both the degree of Sia ( eg,_ some cases of polypoid cystitis).

pleocytosis and the types of cells present

The inflainmatory cells seen in cystitis are
in both infectious and noninfectious
almost exclusively neutrophils. Eosinophils
conditions in the CNS. Interpretation
are seen in some rare, specific inil=atory
should be integrated with the other
conditions, but macrophages are very
clinical details of the case.

uncommon even in chronic conditions. By

If neutrophils
and/or macrophages are present, the
far the most common cause of inflan1IDation
cytoplasm of the cells should be searched
is infection, so the cytoplasm of the
for bacteria and fungi. The absence of
neutrophils should be exanlined carefully
organisms or pleocytosis does not exclude
for bacteria. It is very uncommon to see a
infection, and noninfectious conditions in
significant neutrophil component accompathe CNS can also produce a neutrophilic nying neoplasia or calculi. .

pleocytosis.

R�Cs are commonly seen with neoplastic

Apart from lymphoma, it is rare to find
and inflanm1atory diseases of the bladder
neoplastic cells in CSF. If noninflainmatory
but ai·e also often seen without an
cells are present in the CSF, they should
indication of other pathology. This can be
be interpreted using the basic principles
a sainpling artifact but is also a common
detailed above.

finding in cases of interstitial cystitis. In
cats, this tem1 is often used synonymously

Urine Cytology: U1ine can be exainined
with feline urologic syndrome but
as a wet preparation or as a dried cytology
interstitial cystitis also is seen 'in dogs
smear. Because of the absence of staining in
and people, suggesting other unknown
a wet preparation, these are better limited
pathogenic factors that can cause this
to exatnination for crystals and RBCs.

condition. Persistent hematuria without

Although nucleated cells may be seen, in
cytologic evidence of neoplasia or
most cases they caimot be identified and are inflainmation may indicate interstitial better exan1ined using a dried cytology
cystitis.

smear.

See also URINALYSIS, p 1615.

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1609
liver Cytology: Although cytology is a

Although the individual inflammatory cells
popular method to investigate liver disease,
can be recognized, it is not possible to
there is disagreement on its usefulness.

indicate which part of the liver is principally

Blood contamination is found in most
affected. Neutrophils can be seen in diffuse
samples and may overshadow inflammatory hepatitis and also in more focal cholangitis.

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infiltrates by introducing circulating WBCs.

Small, mature inflammatory lyn1phocytes

Diagnosis of many hepatic diseases relies
are usually seen in periportal inflammatory
on architectural features and the distribuconditions, such as lyrnphocytic pericholantion of the changes within the liver rather gitis in cats and chronic active hepatitis in
than on the morphology of individual cells.

dogs. Macrophages can also be seen in the

Finally, in some hepatic disorders,
chronic inflammatory conditions and also in
hepatocytes proliferate without significant
certain infections. Phagocytic cells should
changes in their individual morphology (see
be investigated for the presence of
below). These factors limit the amount of
organisms within the cytoplasm, but tlus is
information that can be obtained from
uncommon in liver disease.

cytology of liver tissue.

Primary proliferative nodular hepatocel

Sampling methods are similar to those
lular lesions include regenerative hyperplaused for other organs. San1pling is usually sia, nodular hyperplasia, adenoma
performed under guidance of ultrasound,

(hepatoma), and hepatocellular carcinoma.

but blind sampling can be performed at the

Biliary proliferations can appear as cysts,
tenth intercostal space at the level of the
adenomas, or carcinomas. Bile duct cells
connection of rib to rib cartilage. Bleeding
tend to be smaller than hepatocytes with
during this procedure is not a significant
less cytoplasm. They are cuboidal or low
risk
columnar cells that occasionally produce

In the healthy liver, hepatocytes are
tubular structures within cytology samples.

plun1p, polygonal rounded cells with a

The cytoplasm is also more uniformly pale
diameter of 25-30 microns. Nuclei are
staining and not significantly granular.

central and round with a single large,

Nucleoli are smaller and less distinct.

prominent nucleolus. A few cells are

Significant cell harvest from cystic bile
binucleated. There is a large amount of
ducts is uncommon because most of these
blue-staining cytoplasm that usually
lesions are sin1ply cystic space rather than
appears granular.

cellular. If a significant nwnber of biliary

Changes in the metabolism of liver cells
epithelial cells are obtained, neoplasia is
can be seen within the cytoplasm. The
most likely. However, malignant bile duct
presence of nun1erous small, discrete
cells are more commonly uniform in size
vacuoles or one large vacuole indicates
and shape and, therefore, do not always
accun1ulation of fat. This has several
show the morphologic features usually
potential causes and is prominent in feline
associated with malignancy.

hepatic lipidosis syndrome, starvation,

Hepatocellular proliferation is a difficult
pregnancy, and diabetes mellitus. Enlarged
area of interpretation, because hepatocytes
hepatocytes with a pale granular-staining
in benign proliferative lesions are very
cytoplasm but no discrete vacuoles are
similar to those in well-differentiated
characteristic of excess glycogen storage.

carcinomas and indeed often cannot be

This is most often caused by increased
differentiated even from normal hepatolevels of circulating steroids.

cytes. Only in cases with poorly differenti

Bile stasis and pigment accumulation ( eg,
ated pleomorpluc cells can an adequate
iron) can also be assessed by examination
interpretation of malignancy be made. The
of the cytoplasm. Hepatocytes nom1ally
benign and non-neoplastic proliferations
accumulate lipofuscin pigment, noted as
always have the same morphology as
small, fairly unifom1, dark-staining
nonnal hepatocytes. Therefore, false-negagranules, whereas bile and often hemosidtive results for proliferative lesions within erin tend to appear as slightly larger
the liver are common. Cytology is thus of
dark-staining bodies within the cytoplasm.

limited value for nodular hepatocellular

Bile accumulation within the canaliculae
lesions.

( canalicular plugs) can also occasionally be

Cytology can be a useful technique for
seen. These appear as black 1ibbons on the
diagnosis of round cell tumors in the liver.

surface of hepatocytes.

Even with severe inflarrm1atory lesions,

Cytologic interpretation of inflammation
lymphocytes are present in low numbers
is difficult because of the inevitable blood
and are generally small, mature lymphocontan1ination of samples. Inflan1mation cytes. A large population of medium and
should be considered significant only if it
large lymphoid cells indicates lymphoma.

is present wiiliin clusters of hepatocytes.

No other condition will give this result.

1610

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

The other common round cell tumor that
of neutrophils, along with an appropriate
can affect the liver (particularly in cats but
history, are typical of the disorder.

also occasionally in dogs) is mast cell
tumor. The granules within mast cells are

Mammary Cytology: Cytology is useful
metachromatic, facilitating diagnosis.

to differentiate inflan1111atory from

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Aspirates of normal liver may contain a few
neoplastic nodular lesions within mammary
mast cells, but in neoplasia they are usually
tissue. Man1111ary tumors are not commonly
present in large numbers. lf other cells are
inflamed. It is less useful to differentiate the
obtained from cytology preparations, they
neoplastic conditions.

should be interpreted using the principles

Neoplastic lesions must be interpreted
described above.

using the criteria listed above (seep 1601).

The criteria most useful to detem1ine the

Kidney Cytology: Normal renal aspirates behavior and prognosis of a man1111ary have almost a pure population of renal
tumor are local tissue and vessel invasion,
tubular cells. These are unifom1, mediun1-
not cell morphology. These are best assessed
sized cells of -17-20 microns with central
histologically rather than cytologically.

nuclei, small indistinct nucleoli, and a

Therefore, cellular morphology is not
moderate amount of pale-staining
necessarily a good guide to tumor behavior.

cytoplasm. In cats, lipid droplets within the

In cats, malignant cells are often uniform
cytoplasm are a common, nom1al feature.

and do not exhibit the normal malignant

The cells can be present either singly or in
features; the size of the malignant tun1or is
clusters and can occasionally be seen as
the most useful prognostic indicator.

tubular structures. They sometimes contain
small, dark granules within the cytoplasm.

CLINICAL HEMATOLOGY

Renal lymphoma is the most common
neoplastic disease of the kidney in cats and

Hematology refers to the study of the
dogs. Because the cells are usually widely
numbers and morphology of the cellular
distributed within the tissue, false-negative
elements of the blood-the RBCs (erythroresults with cytologic examination are cytes), WBCs (leukocytes), and platelets
uncommon. Diagnosis can be made using

(thrombocytes )-and the use of these
the criteria described above. Primary renal
results in the diagnosis and monitoring of
tumors are unconunon.

disease. (See also 1-IEMATOPOIETIC SYSJ'EM

Cystic lesions include renal cysts, most

INTllODUCTIO , p 4.)

commonly seen in cats but also occasionally
in dogs, and hydronephrosis. In both

Red Blood Cells: Three RBC measuredisorders, cell harvest is usually low, with ments are routinely done: packed cell
a large amount of fluid. The cellular
volume (PCV), the proportion of whole
component of the sample is.rarely helpful in blood volun1e occupied by RBCs; hemoidentifying further the nature of the cystic globin (Hgb) concentration of whole lysed
structure.

blood; and RBC count, the munber ofRBCs

Most inflan1111atory lesions in the kidney
per unit volun1e of whole blood. Although
are chronic and produce fibrous connective
these are separate estimations, they are in
tissue. Cell harvest from these lesions is
effect three ways to measure the same
usually exceedingly low, and cytology is not
thing, and it is incorrect to attempt to
typically a useful technique. Pyogenic
interpret them as separate variables.

inflanunation can sometimes be diagnosed.

Inasmuch as they do vary in rel.ation to each

Cytology may help diagnose feline
other, they allow calculation of two further
infectious peritonitis, although diagnosis
meaningful parameters, mean corpuscular
using serologic techniques is more
volume (MCV) and mean corpuscular hemocommon. Because of the usually severe and globin concentration (MCHC).

widespread nature of the inflammation, cell

MCV varies widely between manunalian
harvest is usually high. The wide mixture of
species, from -15 fL in goats to -90 fL in
inflanunatory cells present in feline
people. Avian and reptilian red cells are
infectious peritonitis, with a predominance
even larger, up to 300 fL. Nevertheless,

MCV (fL) = PCV(decimal fraction) x 1,000

RBC(x 1012/L)

MCHC (g/1) = whole blood hemoglobin concentration (g/1) PCV(decimal fraction)

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1611

MCHC varies little with species ( or
former is characterized by normal, mature
erythrocyte size), at -330 g/1.

RBCs and a norn1al ( or low) erythropoietin

Several artifacts can cause significant and
concentration, whereas the latter may show
potentially misleading alterations to
a regenerative RBC picture with high

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measured RBC paran1eters: 1) old samples
erytlrropoietin concentration. Relative
cause RBCs to swell, thus increasing PCV
polycythemia may also be associated with
and MCV and decreasing MCHC; 2) lipemia
very high PCV values, and norn1al, mature
causes a falsely high Hgb reading, and hence RBCs. Secondary polycythemia generally a falsely high MCHC; 3) hemolysis causes
shows a more modest increase in PCV, often

PCV to decrease while Hgb remains
with evidence of regeneration (more so
unchanged, again leading to a falsely high
when the cause is pulmonary or cardiac,

MCHC; 4) underfilling of the tube causes
less so when the cause is hormonal). It is

RBCs to shrink, causing PCV and MCV to
often possible to make the differential
decrease and MCHC to increase; 5) autodiagnosis of polycythemia on clinical agglutination causes a falsely low RBC
grounds.

cotmt, and hence a falsely high MCV.

Abnonnally low PCV (anemia) may be

Visual description of RBC morphology on
caused by loss of blood (hemorrhage),
a Romanowsky stain also provides useful
breakdown of RBCs in circulation
diagnostic infom1ation. The most common

(hemolysis ), or lack of production of RBCs
tenns include 1) nonnocytic--cells are of
by the bone marrow (hypoplasia or aplasia).

normal size; 2) macrocytes-abnormally

Presentation varies according to whether
large cells, usually polychromatophilic;
the condition is acute or chronic. Aplastic

3) microcytes-abnormally small cells,
anemia is always chronic in onset, because
usually caused by a lack of hemoglobin
anemia occurs gradually as existing cells
precursors; 4) anisocytosis-variation in
reach the end of their lifespan. (See also
size of cells due to macrocytes, microcytes,

ANEMIA, p 7.)

or both; 5) nonnochromic--cells are of

In acute hemorrhagic anemia, external
normal color; 6) polychromasia-variation
blood loss is easily appreciated clinically,
in color of the cells, which usually describes
but blood loss into a body cavity may be
the appearance of large, juvenile, bluishdetennined only on paracentesis. Initially, staining polychromatophilic macrocytes
all hematologic parameters may be normal,

(these broadly correspond to the "reticulobecause it may take 12 hr for fluid shifts to cyte" seen with new methylene blue
produce a decrease in the PCV. Within a few
staining, in which the reticulum represents
days, RBCs become regenerative, with
the remnants of the nucleus); 7) hypochrojuvenile fonns appearing in circulation masia-decrease in staining density of the

( except in horses, in which circulating
cells, usually due to a lack of hemoglobin
evidence of regeneration is not readily
precursors, especially iron; and 8)

appreciable). These consist of polychroannulocyte--extreme form of hypochromic matophilic macrocytes and normoblasts
cell with only a thin rin1 of hemoglobin.

(nucleated RBCs). Late normoblasts have a

PCV is the variable usually used to assess
small, nonviable nucleus and a moderate
the basic status of the erythron-increased
amount of cytoplasm colored sinillarly to
in polycythemia, decreased in anemiathat of the polychromatophilic macrocytes, although if a sample is too hemolyzed to
whereas early normoblasts have a larger,
allow measurement of PCV, a meaningful
viable nucleus and scanty cytoplasm. These

Hgb measurement may still be obtained.

are most easily distinguished from lympho

RBC count as such should not be intercytes by their more densely staining nucleus.

preted clinically.

If substantial amounts of blood have been

An abnormally high PCV (polycythemia)

lost from the body, the RBC picture may
may be relative, due to a change in the
become hypochrornic. Thus, this type of
proportion of circulating RBCs to blood
anemia shows an increase in MCV and a
plasma without any change in the size of the
decrease in MCHC. If bleeding is into a body
erythron, or absolute, due to a real increase
cavity, hypochromasia may not be evident
in erythron size. Absolute polycythemia
because hemoglobin precursors will be
may be prinlary ( eg, polycythemia vera or,
recycled. However, slight jaundice may be
rarely, erythropoietin-producing tumors) or
seen as the sequestered cells are broken
secondary ( a consequence of disease in
down. Some sequestered cells may also be
another organ system). (See also POLYreturned to the circulation intact, if CYTHEMIA, p 43.)

somewhat misshapen.

Polycythemia vera and erythropoietin

In acute hemolytic anemia, PCV will
producing tumors should be suspected only
decrease in1lllediately, and in the early
when PCV is very high, nmrnally >0. 7. The
stages some jaundice will be evident. In the

1612

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
very early stages, even a sample collected
produces a macrocytic RBC picture due to
with extreme care may be markedly
early maturation arrest of the erythrocytes.

hemolyzed. As with hemorrhagic anemia,

Neoplasia of the bone marrow may ca.use
the RBCs will become regenerative within
severe anemia as erythropoietic elements
a few days, with polychromatophilic
are crowded out, but some regeneration
macrocytes and nucleated RBCs evident.

may be seen as the remaining bone marrow

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Because hemoglobin precursors are not lost
attempts to compensate. In this case, other
from the body, true hypochromasia is not
bone marrow cell lines will also be affected.

seen.

True a.plastic anemia refers to a failure of

Chronic hemorrhagic anemia may be
the entire bone marrow. The shorter-lived
difficult to appreciate if blood is lost in the
granulocytes and platelets decrease first,
feces or urine, or due to bloodsucking
followed by a progressively severe anemia
ectoparasites. Anemia may be severe, and
that is nom1ocytic and nom10chromic.

the RBC picture will be regenerative on
presentation. Hypochromasia is usually

White Blood Cells: The WBCs consist
very marked. In very longstanding
of the granulocytes (neutrophils in most
conditions, depletion of iron and other
manunals, called heterophils in rabbits,
hemoglobin precursors can become so
reptiles, and birds [ and these look like
marked that most of the cells are microeosinophils in smears]; eosinophils; and cytic, and MCV may paradoxically decrease.

basophils) and the agranulocytes (lympho

Intermittent intra-abdominal hemorrhage
cytes and monocytes ). Although ea.ch type
leads to a somewhat different picture,
is traditionally counted by detennina.tion of
because blood shed into the peritoneal
its percentage of the total WBC population,
cavity can be returned to the circulation.

meaningful interpretation requires that the

PCV may therefore recover quickly (until
absolute nwnber of ea.ch type be calculated
the next episode), and signs of depletion of
by multiplying the total WBC count by the
hemoglobin constituents do not emerge.

fraction attributable to the individual cell

In chronic hemolytic anemia, RBCs a.re
type. Percentages of ea.ch cell type alone are
regenerative on presentation, except that
not helpful. An increased percentage that is
some cases of autoimmune hemolytic
due to an absolute decrease in another cell
anemia (AIHA) paradoxically show little or
type is not an increase at all.

no regeneration unW treatment has been

Mature neutrophils have a. lobula.ted
initiated. Hypochromasia. is less marked
nucleus, but when demand is high,
than in hemorrhagic conditions, and
immature cells witl1 an unlobulated band
misshapen RBCs (including target cells
nucleus (no constriction of the nucleus is
and folded cells) are more common. The
more than half the width of the nucleus)

spherocyte, in which the erythrocyte loses
may be released into circulation. They
its classic biconcave shape, is essentially
function as phagocytes and are important in
pathognomonic for AIHA. Jaundice may
infectious conditions and in inflammation.

be absent, because the products of the

Increased neutrophil counts (neutrophilia)

destruction of the RBCs may be cleared by
are caused by inflan1mation, bacterial
the reticuloendothelial system and the liver
infection, acute stress, steroid effects, and
as quickly as they are fom1ed.

neoplasia. of the granulocytic cell line

Hypoplastic and a.plastic anemia may be

(granulocytic leukemia can be difficult to
mild ifRBC production is merely depressed
differentiate from a simple neutrophilia.

secondary to some other disease. Protein,
without special stains or bone marrow
mineral, or vitamin deficiencies may cause
biopsy). Decreased neutrophil counts
hypoplastic anemia, but these are more

( neutropenia) are caused by viral infections,
likely to be secondary to another disease
toxin exposure (including foodbome

( eg, chronic hemorrhage or malabsorption)

toxins), certain drugs (eg, carbimazole and
than sin1ple dietary deficiency. Other
methimazole), autoirnmw1e destruction of
diseases may cause depression of erythroneutrophils, bone marrow neoplasia not poietin production, eg, renal failure,
involving the granulocytes, and bone
deficiencies of hormones that usually
marrow aplasia.

stimulate erythropoietin production ( eg,

Eosinophils a.re characterized by
hypothyroidism, hyperadrenocorticism),
prominent pink-staining granules on a
and chronic, debilitating conditions ( eg,

Romanowsky stain. They inactivate
chronic infections, chronic parasitism, and
histamine and inhibit edema fom1ation.

neoplasia.). RBC morphology is nonregen

Increased eosinophil counts ( eosinophilia)

erative and may be hypochromic if a
are ca.used by allergic/hypersensitivity
deficiency state is involved. Paradoxically,
reactions, parasitism, tissue ir\jwy, mast
vitan1in B,2 and/or folic acid deficiency
cell tumors, estrus, and pregnancy or

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1613
parturition in the bitch. Some large dog
days, but many are long-lived. The nwnbreeds ( eg, Gennan and Belgian Shepherds, ber in circulation is a balance between

Rottweilers) nonnally have a relatively high
populations in the blood, lymph, lymph
eosinophil count. Extremely high eosinonodes, and splenic follicles and does not phil counts (hypereosinophilic syndrome),
necessai·ily reflect changes in lymphopoiepossibly due to an out-of-control hypersensis. An increased lymphocyte coW1t VetBooks.ir
sitivity reaction, and eosinophil leukemia (a

(lymphocytosis) may occur for physiologic
form of chronic myeloid leukemia) are also
reasons, especially in cats, but significant
described. Decreased eosinophil count
increases usually indicate leukemia.

( eosinopenia) is almost always caused by

Immatw-e or bizarre cells may also be
the action of glucocorticoids, either
recognized. Decreased lymphocyte counts
endogenous or therapeutic.

(lymphopenia) are usually due to an effect

Basophils are rare in most species and
of corticosteroids, either endogenous
are characterized by blue-staining granules

( stress or Cushing disease) or therapeutic,
on a Romanowsky stain. They are more
and may also accompany neutropenia in
easily seen in cattle. They are closely related some viral infections, especially the to mast cells and, like them, initiate the
pai-vovimses. Lymphopenia may also be a
inflammatory response by releasing
feature of solid-organ lymphosarcomas,
histamine. An increased basophil count
when leukemia is absent.

(basophilia) accompanies eosinophilia in
some species as part of the hypersensitivity
reaction.

Platelets: Manu11alian platelets are pale

Monocytes are large cells with blue-gray
blue granular fragments (much smaller than
cytoplasm, which may be vacuolated, and a

RBCs) shed from multinucleate megakaryokidney bean-shaped or lobulated nucleus.

cytes in the bone marrow; avian and

Their main fw1ction is phagocytosis, and
reptilian platelets are true cells with nuclei.

they are essentially identical to tissue

They maintain the integrity of the endothemacrophages. An increased monocyte liwn and act as part of the clotting process
count (monocytosis) may occur in any
to repair dainaged endotheliwn, where they
chronic disease, especially chronic
ensure mechanical strength of the clot.

inflammation, and may be very marked in

Increased platelet cotmts (thrombocytoneoplasia. Monocytes also increase as pa.it sis) occur as a reaction to consW11ption
of the steroid response in dogs.

after injury, when large juvenile platelets

1¥mphocytes mainly develop outside the
may also appear; after splenectomy, as
bone marrow in the lymph nodes, spleen,
splenic stores are liberated to the circulaand gut-associated lymphoid tissue. They tion; after vincristine treatment, which
are the smallest of the WBCs, with a round,
increases platelet shedding from megakaryevenly staining nucleus and sparse ocytes; and in megakaryocytic leukemia.

cytoplasm. Larger, reactive lymphocytes

Decreased platelet counts (thrombocytocan be seen after antigenic stimulation, and penia) are caused by autoin1mW1e reactions,
care must be taken to differentiate them
thrombotidthrombocytopenic purpura,
from neoplastic lymphocytes. Their primary bone mairow suppression and aplasia, bone function is immunologic, including both
marrow neoplasia, and equine infectious
antibody production and cell-mediated
anemia. Signs ai·e petechiation and
inlmune responses. Some survive only a few ecchyrnosis more than frank hemorrhage, and little may be seen until the platelet
count is <20 x 109/L. Platelet functional
abnormalities present sinillai·ly, but platelet
numbers and morphology are normal.

Blood Sample Preparation and

Evaluation: In-house hematologic
investigations, with a rninin1W11 of specialist
equipment, can provide almost as much
information as a full laboratory analysis,
although some estinrntions are qualitative
rather than quantitative.

Blood for hematology should be collected
into tubes containing EDTA anticoagulant
and in1n1ediately mixed well to avoid

Ecchymotic lesions on the abdomen of a dog.

clotting. Larger (2.5 mL) tubes yield better

Courtesy of Ontario Veterinary College.

results than the smaller (1 mL) pediatric

1614

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
tubes and are less likely to clot. Neve1thediluent. An automatic pipette capable of less, it is essential to fill the tube exactly to
dispensing 0.95 mL and 0.05 mL (50 µL)

the mark, so smaller tubes may be
should be used to ensure an accurate
unavoidable for small patients. WBC
dilution. The sample should be mixed well

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morphology deteriorates most quickly,
and allowed to stand for 10 min while the
especially in equine blood, so if the sample
stain is taken up by the cells. The chamber
cannot be analyzed immediately, a thin
of the hemocytometer is then filled by
blood smear should be submitted to the
using a capillary (PCV) tube. The number
laboratory with the blood sample.

of cells in each of the four large comer

PCV is measured by microhematocrit,
squares of the grid are counted, and the
which is the reference method. A capillary
total divided by 20 to calculate the total
tube is filled% full with well-mixed blood

WBC count x 10 9fL.

and sealed at one end; heat-sealing is best if

Several hematologic instflllnents are
a Bunsen burner is available, otherwise a
available for in-practice use. Those based
proprietary clay pad is used. The tube is
on centrifugation, in which WBC measurespllll in a high-speed microhematocrit ments are made by spreading a stained
cent1ifuge for 6 min, and the PCV is read
buffy coat, are not true hematology
using a microhematocrit reader with a
analyzers, but give approximate counts.

sliding cursor. The appearance of the

Although a nlllllerical estimate of total
plasma ( eg, nom1al, icteric, hemolyzed,

WBC count is provided, the differential
lipemic) and the thickness of the buffy coat,

WBC count cannot distinguish between
which gives a very rough guide to total WBC
lymphocytes and monocytes, and results
count, should be noted.

do not always correlate well with standard

Further information is obtained from a
methods. This method is appropriate only
blood film. This is made by using one slide,
as an emergency approximation, and a
with a comer broken off as a spreader, to
blood film must always be examined in
pull a small drop of blood across a clean
addition. It is also wise to check the PCV
slide into a thin film. A suitable film is thin
by microhematocrit.

( one erythrocyte thick) and tapers to a

Impedance counters (Coulter principle)

feathered edge before the far end of the
are used by diagnostic laboratories and
slide. The broken comer of the spreader
perform well in experienced hands.

slide ensures two straight edges parallel to

However, it is difficult to achieve optimal
the long edges of the slide. Immediately
performance without trained technical staff.

after the film is spread, it is dried quickly by
lnstrun1ents not based on the Coulter
fanning the slide in the air. Air-dried smears
principle should be avoided for veterinary
can be sent to the laboratory in a slide
use, because their results do not necessamailer or stained and exanlined in the rily compare well on nonhun1an samples.

practice. Commercial rapid Romanowskylnstrunlents providing automated type stains merely require the slide to be
differential counts perform poorly on
dipped in tllree colored solutions in
nonhlllllan blood, and results must never
succession. Cell morphology is clear and
be accepted without also checking a blood
comparable to more pennanent stains such
film. No hematology laboratory should be
as Leishman or May-Gruenwald-Giemsa,
without the facility for examining blood
although quality dete1iorates after a few
films, and a blood film should be examined
days. The slide should be allowed to dry
for every patient sample. Quality assurance
naturally or dried with a hair dryer ( not
issues are the same as those for biochemiswiped dry), and exan1ined under oil try laboratories (seep 1590). If accuracy and
immersion.

reliability cannot be guaranteed to the same

Clinically useful information may be
standard as the referral laboratory, then
easily achieved in-house for all hematoresults should not be relied on without logic variables. The main deficiency is the
external confirmation.

absence of a numerical WBC count, and
hence of numerical values for the

Red Blood Cells: The size, uniformity of
differential WBC count. This may be
size, and presence of microcytes, macroacceptable for an interim emergency cytes, and abnormally shaped cells should
investigation, and a WBC count using a
be noted, along with cell color, unifonnity of
hemocytometer slide may be attempted.

color, and the presence of hypochromasia,

A mirrored slide with an Improved
polychromasia, and nucleated RBCs. An

Neubauer ruling may be used, with a
overall descriptive assessment of the RBC
cover slip fitted so that Newton rings are
picture should be made, including the
visible on both sides. The blood sample is
degree of regeneration or hypochromasia,
diluted 1:20 with Turck fluid or a similar
if any.

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1615

White Blood Cells: A qualitative
to the volume of urine collected and
estimate of numbers should be made (ie,
concentration of urine produced; therefore,
very low, low, normal, high, very high). This
it should be interpreted in context of urine
can be remarkably consistent with practice.

specific gravity. Significant disease may

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The proportions of each cell type can be
exist when urine color is nonnal. Abnonnal
estimated, or preferably, a formal differenurine color may be caused by presence of tial count of 100-200 cells performed.

endogenous or exogenous pigments, but it

Unusual or abnonnal WBC fom1s ( eg, band
does not provide specific infonnation.

or toxic neutrophils ), or pathologic cells

Interpretation of semiquantitative reagent

( eg, prolymphocytes, lymphoblasts, or mast
strips, which are colorimetric tests, requires
cells) should be noted.

knowledge of urine color because
discolored urine may result in a false-posi

Platelets: A qualitative estimate of platelet numbers, based on how many can be seen
tive result. Equine urine may turn brown
in a typical high-power field ( oil immersion)

after a period of time.

should be made. Several fields should be
exanlined, more if numbers appear low.

Clarity: Urine is typically clear but may

Results can be ranked as none seen ( on
become less transparent with pigmenturia,
entire slide), rare (very few on entire slide),
crystalluria, hematuria, pyuria, lipiduria, or
low in number ( <5 per high-power field),
when other compounds such as mucus are
adequate (5--20 per high-power field), or
present. Depending on the cause, increased
abundant (>20 per high-power field). Normal
turbidity may disappear with centrifugation
platelet numbers in the horse are about half
of the sample.

those of other species. ln a sample more than
a few hours old, platelets may clump into

Odor: Normal urine has a slight odor of
rafts, leaving areas of the slide apparently
anunonia; however, the odor depends on
devoid of platelets. Slides should be scanned
urine concentration. Some species, such as
for rafts before reporting platelet numbers as
cats and goats, have pungent urine odor
low. Enlarged or macroplatelets should also
because of urine composition. Bacterial
be noted.

infection may result in a strong odor due to
pyuria; a strong ammonia odor may occur if
the bacteria produce urease.

URINALYSIS

Urinalysis is an important laboratory test

Urine Chemistries
that can be readily performed in veterinary
practice and is considered part of a minimum Urine must be at room temperature for database. It is useful to docun1ent various
accurate measurement of urine specific
types of urinary tract diseases and may
gravity and for chemical analysis. These
provide information about other systemic
tests are usually done before centrifugatio!'I;
diseases, such as liver failure and hemolysis.

however, if urine is discolored or turbid, it

Urine may be collected by cystocentesis,
may be beneficial to perform these tests on
urethral catheterization, or voiding. Urine
supernatant (seep 1617).

should be evaluated within 30 min, but if this
is not possible, it may be refrigerated for up

Specific Gravity: Specific gravity is
to 24 hr or submitted to an outside diagnostic defined as the ratio of the weight of a laboratory; however, this may result in
volume of liquid to the weight of an equal
crystal precipitation. Refrigeration does not
volume of distilled water; therefore, it
alter urine pH or specific gravity. If cytologic
depends on the number, size, and weight of
evaluation is required and a delay in
particles in the liquid. It is different from
preparing the slides is anticipated, then a
osmolality, which depends only on the
preservative should be added. A few drops
nun1ber of particles in the liquid; measureof 100/o fonnalin ( exact concentration not ment of osmolality requires specialized
necessary) is better than boric acid.

instrun1entation.

However, the usual Romanowsky stains are

The urine specific gravity (SG) is
unsuitable with formalin; if submitting to an
determined using a refractometer designed
outside laboratory, it should be conununifor veterinary samples, which includes a cated that formalin has been added.

scale calibrated specifically for cat urine.

SG for species other than cats should be
determined using the scale for dogs. In

Urine Appearance
healthy animals, SG is highly variable,

Color: Normal urine is typically transpardepending on fluid and electrolyte balance ent and yellow or an1ber on visual inspecof the body. It is normally at least 1.015.

tion. The intensity of color is in part related

Interpretation of SG, therefore, depends

1616

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
on the clinical presentation and serum
sediment exan1ination. For example, a trace
chemistry findings. (See also URJNARY SYSTEM
amoru1t of protein in concentrated urine is

INTHODUCTION, p 1494.) An animal that is
less significant than a trace amoru1t of
dehydrated or has other causes of prerenal
protein in dilute urine. Alkaluria. will give a
azotemia will have hypersthenuric urine
false-positive reaction. Likewise, presence
with an SG >1.025--1.040 (depending on
of other proteins, such as Bence-Jones

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species). Dilute wine in a dehydrated or
proteins, will give false-negative results.

azotemic anin1al is abnormal and could be

Proteinmia. can be measured using sulfosalicaused by renal failure, hypo- or hypercylic acid precipitation, which detects adrenoco1ticism, hypercalcemia, diabetes
albwnin and globulins; however, it is not
mellitus, hyperthyroidism, and dimetic
accurate in dogs and cats. lf proteinU1ia is
therapy. In cases of diabetes insipid us,
present with an inactive w·ine sediment, its
values <1.010 can be expected. Glucosw'ia
significance can be verified and quantitated
increases the SG despite increased urine
by di.vi.ding the urine protein concentration
volwne.

by the Uline creatinine concentration ( urine
protein to urine creatinine ratio [UP:UC)).

Semiquantitative, Colorimetric

Interpretation of a UP:UC is as follows:

Reagent Strips: Reagent strips such as

<0.5:1 (dogs) and <0.4:1 (ca.ts) is normal,

Multistix® or ChemstJ.ip ® can be used to

0.4 or 0.5-1: 1 is questionable, and> 1: 1 is
pe1i01m several semiquantitative chemical
abnonnal. With primary renal azotemia, a
evaluations simultaneously. They are used

UP: UC >0.5: 1 in dogs and >0.4: 1 in cats is
routinely to dete1mine wine pH, protein,
considered abnom1al. A semiquantitative
glucose, ketones, bilirubinlmobilinogen, and
microalbwninuria test is available to detect
occult blood. Some reagent strips include
urinary albwnin in the range of 1-30 mg/dL.

test pads for leukocyte esterase (for

It uses ELISA technology specific for canine
detection ofWBCs), nitrite (for detection
or feline albwnin. Because of minor species
of bacteria), and SG; these are not valid in
differences in albru11in, there are different
animals and should not be used. Reagent
kits for dogs and cats. The microalbwninstrips a.re adversely affected by moistme and uria test detects lower concentrations of
have a limited shelf life. Bottles should be
albumin than a standard dipstick test pad.

kept tightly capped, and ru1used strips should Hematuria must be macroscopic to increase be discarded after their expiration date.

the microalbwninU1ia or UP:UC; however,
pyw'ia increases both.

Urine pH: Urine pH is typically acidic in
dogs and cats and alkaline in horses and

Glucose: Glucose is detected by a glucose
ruminants, but varies depending on diet,
oxidase enzymatic reaction that is specific
medications, or presence of disease. Reagent for glucose. Glucosuria is not present strip colorimetric test pads for pH detenninormally because the renal threshold for nation are accurate to within -0.5 pH units.

glucose is > 180 mg/dL in most species and

For example, a reacting of 6.5 means the

>240 mg/dL in cats. With euglycemia., the
actual pH is likely to be between 6.0 and 7.0.

a.mow1t of filtered glucose is less than the

Po1table pH meters are more acGurate than
renal threshold, and all of the filtered
pH colorimetric test pads. A bacterial urinary glucose is reabsorbed in the proximal renal tract infection with a urease-producing
tubules. Glucosuria can result from
microbe will result in alkalU1ia.. Urine pH will hyperglycemia ( clue to diabetes mellitus, affect crystalluria because some crystals,
excessive endogenous or exogenous
such as struvi.te, fonn in alkaline urine,
glucocorticoids, hepa.tocutaneous
whereas other c1ystals, such as cystine, form
syndrome, or stress) or from a proximal
in acidic urine.

renal tubular defect ( such as p1irnary renal
glucosuria. or Fanconi syndrome). If

Protein: The protein test pad uses a color
glucosuria is present, blood glucose
indicator (tetrabromophenol blue), which
concentration should be dete1mined.

detects primarily albru11in in urine. Results

False-negative results can occur with high
range from 10 mg/clL to 1,000 mg/dL.

urinary concentrations of ascorbic acid

Proteinuria can occur from prerenal (fever,

(vitamin C) or with formaldehyde (a
strenuous exercise, seizUI·es, extreme
metabolite of the urinary antiseptic,
envi.rorunental temperature, and hyperpromethena.mine, which may be used for teinemia), renal (primarily glomerular and
prevention of bacterial urinary tract
occasionally tubular disease), or postrenal
infections). False-positive results may occur

(inflammation, hemorrhage, and infection)

if the sample is contaminated with hydrogen
ca.uses. A positive reaction must be
peroxide, chlorine, or hypochlorite
interpreted in light of SG, pH, and urine

(bleach).

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1617

Ketones: Ketones are produced from
bin is rapidly cleared from plasma, resulting
fatty acid metabolism and include
in clear plasma. As with other colorimetric
acetoacetic acid, acetone, and
test pads, discolored urine may yield

13-hydroxybutyrate. The ketone test pad
false-positive results. A positive result
detects acetone and acetoacetic acid, but
should be interpreted with microscopic
not 13-hydroxybutyrate (which can be
exan1ination of urine sediment.

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measured in blood and urine using a
point-of-care instmment or a biochemistry
analyzer). The test pad contains nitroprus

Urine Sediment
side that reacts with acetoacetic acid and

Microscopic examination of urine sedin1ent
acetone to cause a purple color change; it
should be pa.rt of a routine urinalysis. For
is more sensitive to acetoacetic acid than
centrifugation, 3-5 mL of urine is transacetone. Ketonuria is associated with ferred to a conical centrifuge tube. Urine is
primary ketosis (ruminants), ketosis
centrifuged at 1,000-1,500 rpm for -3-5 min.

secondary to diabetes mellitus ( small

The supernatant is decanted, leaving -0.5
animals), consumption of low-carbohydrate
mL of urine and sediment in the tip of the
diets (especially in cats), and occasionally
conical tube. The sediment is resuspended
with prolonged fasting or starvation. A falseby tapping the tip of the conical tube against positive reaction can occur with presence of
the table several ti.mes. A few drops of the
reducing substances in urine.

sediment are transferred to a glass slide,
and a cover slip is applied. Examination of

Bilirubin/Urobilinogen: When
unstained urine is recommended for routine
hemoglobin is degraded, the heme portion
san1ples. Microscopic examination is
is converted to bilirubin, which is conjuperformed at lOOX (for crystals, casts, and gated in the liver and excreted in bile.

cells) and 400X (for cells and bacteria)

Some conjugated bili.rnbin is filtered by the
magnifications. Contrast of the san1ple is
glomerulus and excreted in urine. In dogs,
enhanced by closing the iris diaphragm and
but not cats, the kidney can metabolize
lowering the condenser of the microscope.

hemoglobin to bilirubin and secrete it.

Stains such as Sedistain® and new

Male dogs have a higher secretory ability
methylene blue can be used to aid in cell
than females. Dipstick reagent pads use
identification but may dilute the specin1en
diazoniurn salts to create a color change and and introduce artifacts such as stain are more sensitive to conjugated bilimbin
precipitate and crystals. Use of a modified
than unconjugated bilirubin. Bilirubinuria

Wright stain increases the sensitivity,
occurs when conjugated bilirubin exceeds
specificity, and positive and negative
the renal threshold as with liver disease or
predictive values for detection of bacteria.

hemolysis. 1n dogs with concentrated urine,

For some tests, air dried, stained smears are
a small amount of bilirubin can be normal.

necessary.

Pigmenturia and phenothiazine may result
in a false-positive reaction; false-negative

Red Blood Cells: 1n an unstained
reactions may occur with large amounts of
preparation, RBCs are small and round and
urinary ascorbic acid (vitamin C).

have a slight orange tint and a smooth

Urobilinogen, formed from bilirubin by
appearance. Nmmal urine should contain
intestinal microflora, is absorbed into the

<5 RBCs/field at400X magnification.

portal circulation and excreted renally. A

Increased RBCs in urine (hematuria)

small amount of urinary urobilinogen is
indicates hemorrhage somewhere in the
nom1al. Increased urinary urobilinogen
urogenital system; however, sample
occurs with hyperbilimbinemia; a negative
collection by cystocentesis or catheterizatest may be seen with biliary obstmction.

tion may induce hemorrhage.

However, the test is not specific enough to
be clinically useful.

White Blood Cells: WBCs are slightly
larger than RBCs and have grainy cyto

Occult Blood: The occult blood test pad
plasm. Normal urine should contain <5
uses a "pseudoperoxidase" method to

WBCs/field at 400 x magnification. Increased
detect intact RBCs, hemoglobin, and

WBCs (pyuria) can occur due to inflammamyoglobin. A positive reaction can be due tion, infection, trauma, or neoplasia.

to hemorrhage (hematuria), intravascular

Catheterization or collection of voided urine
hemolysis (hemoglobinuria), or myoglobinmay introduce a few WBCs from the uria. The latter two processes can be
urogenital tract.

distinguished by examination of plasma:

plasma will appear pink to red after

Epithelial Cells: Transitional epithelial
intravascular hemolysis, whereas myoglo-
cells, a common urine contaminant delived

1618

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
from the bladder and proximal urethra,
clinical disease. Parasitic ova observed
resemble WBCs but are larger. They have a
include those of Stephanurus dentalus,
greater amount of grainy cytoplasm and a

Capillm'ia plica, C felis, and Dioctophyma round, centrally located nucleus. In a voided 1·enale. Additionally, microfilatiae of urine sample, squan1ous epithelial cells may

Dirojilaria immilis may be seen in urine

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be seen. They are large, oval to cuboidal in
sediment.

shape, and may or may not contain a
nucleus. Occasionally, neoplastic transi

Crystals: Many urine sediments contain
tional cells may be seen in an aninlal with a
crystals. The type of crystal present
transitional cell carcinoma. Neoplastic
depends on urine pH, concentration of
squan1ous cells may be seen in an animal
crystallogenic materials, urine temperatw·e,
with a squamous cell carcinoma.

and length of time between urine collection
and exan1ination. Crystalluria is not

Cylindruria (Casts): Casts are elongated,
synonymous with urolithiasis at1d is not
cylindrical structures fonned by mucopronecessarily pathologic. Fw111em1ore, tein congealing within renal tubules and
uroliths may fo1m without observed
may contain cells. Hyaline casts are pure
crystalluria. Many urine sat11ples are
protein precipitates; they are transparent,
examined at room temperature, which may
have parallel sides and rounded ends, and
alter the nwnber of crystals present, and
are composed of mucoprotein. They may
the result may not represent the situation
occur with fever, exercise, and renal
in vivo.

disease. Epithelial cellular casts fonn from

Struvite crystals are commonly seen in
entrapment of sloughed tubular epithelial
canine and feline urine. Struvite crystalluria
cells in the mucoprotein; they may be seen
in dogs is not a problem wiless there is a
with renal tubular disease. Granular casts
concurrent bacterial w'inaty tract infection
are thought to represent degenerated
with a w·ease-producing microbe. Without
epithelial cellular casts. Waxy casts have
an infection, struvite crystals in dogs are not
a granular appearance and are thought to
associated with struvite urolith fonnation.

arise from degeneration of longstanding

However, some animals ( eg, cats) do form
granular casts. They typically have sharp
struvite uroliths without a bacterial urinaty
borders with broken ends. Other cellular
tract infection. In these aninlals, struvite
casts include RBC casts and WBC casts and
crystalluria may be pathologic. Struvite
are always abnonnal. RBC casts fom1
crystals appeai· typically as "coffin-lids" or because of renal hemorrhage. WBC casts

"prisms"; however, they may be an1orphous.

fonn because of renal inflan1mation, as with

Calciwn oxalate crystalluria occurs less
pyelonephritis. Fatty casts are not common
commonly in dogs and cats. If persistent, it
but can be seen with disorders of lipid
may indicate an increased risk of calciwn
metabolism, such as diabetes mellitus. A
oxalate urolith fotmation, which has been
few hyaline or granular casts are considered increasing in some countries throughout the nonnal. However, presence of cellular casts
past few yeai·s. (See also UROLITI-IIASIS, p 1502, or other casts in high numbers indicates
and p 1525.) However, calciwn oxalate and
renal damage, and may be one of the earliest calciw11 carbonate crystallwia is common laboratory abnormalities noted with toxic
in healthy horses and cattle. Calciw11
damage to renal epithelial cells ( eg,
oxalate diliydrate crystals appear as squares
gentamicin, amphotericin B).

with an "X" in the middle, or "envelopeshaped." Calcium oxalate monohydrate Infectious Organisms: The presence of
c1ystals are "dwnb-bell" shaped. An unusual bacteria in urine collected by cystocentesis
fonn of calciwn oxalate crystals is typically
indicates infection. Small nun1bers of
seen in association with ethylene glycol
bacteria from the lower urogenital tract may toxicity (seep 3046). These crystals are contaniinate voided samples or samples
found in neutral to acidic urine. They ai·e
collected by catheterization and do not
small, flat, and colorless and ai·e shaped like
indicate infection. Bacterial rods are most

"picket fence posts."

easily identified in urine sediment. Particles

Ammoniwn acid urate crystals suggest
of debris may be mistaken for bacteria.

liver disease ( eg, portosystemic shunt).

Suspected bacteria can be confirmed by

These crystals occur in acidic urine and ai·e
staining urine sediment with Gran1 stain;
yellow-brown spheres with irregular, spiny
however, aerobic culture is best to confinn
projections; however, they may also be
a bacterial urinary tract infection. Rarely,
atnorphous. Certain species, such as birds
yeast and fungal hyphae and parasitic ova
and reptiles, and certain breeds of dogs,
may be seen in urine sediment. Their
specifically Dalmatians, can nom1ally have
presence is not always associated with
atrunoniun1 acid urate crystalluria

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1619

Cystine crystals are six-sided and of
identification. Specimens should be fixed in
variable size. They are seen in acidic urine.

100/o formaldehyde solution or sent chilled.

Presence of cystine crystals represents a

Other preservative solutions ( eg, sodiun1
proximal tubular defect in amino acid
acetate forn1alin, polyvinyl alcohol,
reabsorption. Cystinuria has been reported
available in commercial mailer kits) better

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in many breeds of dogs and rarely in cats.

preserve protozoa and facilitate special

Dachshunds, Newfoundlands, English
staining (eg, trichrome, iron hematoxylin).

Bulldogs, and Scottish Terriers have a high

Routine exan1inations should be done by
incidence of cystine urolithiasis.

both direct fecal smear and fecal flotation.

Bilirubin crystals occur with bilirubinu

Direct smears are prepared by mixing feces
ria; however, they may be normal in small

( an amount of feces fitting on one-half the
numbers in dogs.

tip of a wooden applicator stick) with 1 drop
each of saline (for motile organisms) and

Lipids: Fat droplets are commonly present Lugol's iodine stain (to see internal in urine from dogs and cats and may be
morphologic structures, eg, those of
mistaken for RBCs. They often vary in size

Giardia), and covering with separate coverand tend to float on a different plane of slips on the same slide. Flotation methods
focus than the remainder of the sediment.

concentrate diagnostic stages and provide a

They are not considered to be pathologic.

cleaner final preparation, using -2 g of
feces. Sugar (specific gravity [SG] 1.27) and

Spermatozoa: Spermatozoa may be seen sodium nitrate (SG 1.39) are commonly norn1ally in urine collected from reproducused flotation media. Zinc sulfate flotation tively intact male dogs.

(SG 1.18), repeated on 3 consecutive days, is
the method of choice to reveal Giardia

Plant Material: Occasionally, plant
cysts, which are intennittently shed in
material may be seen in urine samples
feces. Motile nematode larvae may be
collected by voiding. When present, they
collected and concentrated by Baermann
indicate contamination of the urine san1ple
sedin1entation; a convenient method is to
and are not pathologic.

place -2 g of feces on several sheets of
cotton gauze in a tea strainer suspended in

Bladder Tumor Antigen Test
the wide end of a large, conical funnel fitted

The bladder tumor antigen test can be used
with a rubber tube and stopcock. The funnel
to screen for transitional cell carcinoma in
is filled with wam1 tap water or saline for
dogs. The results are not specific for

1 hr before sediment exan1ination. Larvae
transitional cell carcinoma, and non-neodescend within the funnel due to gravity and plastic disease ( eg, urinary tract infections,
are collected from the end of the stopcock
hematuria, etc) can give positive results. A
for microscopic examination. Special
negative test, however, is meaningful in that
procedures, such as fonnalin-ethyl acetate
a transitional cell carcinoma is not likely to
sedimentation, may be used for parasitic
be present. This test may be useful for
larval stages that do not float well.

routine screening of dogs at higher risk of

Sheather's sugar (SG 1.30) can be used to
developing transitional cell carcinoma ( eg,
detect small oocysts of Cryptosporidium

Scottish terriers) that do not have other

( 4-6 µ) or Toxoplasma ( 12 µ) by focusing
signs or laboratory findings of lower urinary just under the coverslip. Oocysts "float up"

tract disease. This tests for the presence of
to the under-surface of a coverslip placed on
basement membrane fragments and is a
the slide for 10 min before examination.

color reaction using a commercial test kit.

A direct smear using 1 drop of blood can
be used to detect motile microfilariae of

Dirojilaria immitis, but this should not be PARASITOLOGY
the sole means of detection. More accurate
exan1ination of blood may be done by a

Internal Parasite (Endoparasite)

modified Knotts' test: 1 mL blood is added to

Diagnosis in Small Animals: Diagnosis

9 mL of 2%formalin solution in a 15-mL tube
of internal parasites in small anin1als is
and centrifuged at 1,500 rpm. The supernatypically pe1formed by examination of feces tant is discarded and a drop of methylene for parasite eggs. Fecal samples should be
blue stain is mixed with the sediment
fresh, preferably collected from the animal

"button," which is pipetted onto a microduring the act of defecation or from the scope slide, covered with a coverslip, and
rectum using a fecal loop during the
examined to differentiate microfilariae of
physical examination. Specimens should be

D immiti,s from those of the nonpathogenic
submitted to a diagnostic laboratory in a

Dipetalonema reconditum. Commercial
sealed container, labeled with proper
filtration and staining procedures are

1620

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
effective alternatives to the modified Knotts' feces. Special slides containing chambers test. Animals on heartworrn preventive
with etched ru·eas of known volwne ru·e also
become amicrofilaremic, and an occult
used to estimate EPG, especially for small
heartworn1 test using a commercially
ruminants. Feces in a strained solution ( usuavailable ELISA for circulating uterine ally saturated salt) are introduced into each
antigen of adult female Dirqfila1'ia is the chrunber with a Pastew-pipette, and the

VetBooks.ir
method of choice for treated dogs. Feline
eggs are counted under low-power
dirofilariasis cannot be reliably diagnosed
magnification. A commonly used counting
by microfila.remia or antigenemia tests,
slide is the McMaster slide, which has two
because herutworn1 numbers ru·e typically
chan1bers, each with a volwne of 0.15 mL
too low; antibody titers to D immitis are
tmder the etched area. For example, if 3 g of
used to detect prior exposw·e and possible
feces are mixed with 42 mL of concentrate
cun-ent infection in cats.

solution, then each egg counted is
multiplied by 50 to yield the nwnber of EPG

Internal Parasite (Endoparasite)

in the fecal sample. Acceptable c01Telation

Diagnosis in Livestock: Fresh fecal
between the EPG and the relative worn1
samples from livestock should be collected burden is often possible in young animals, from pastw·e or, preferably, per recttun
although low ( <5 EPG) or negative counts
using plastic gloves. Samples should be
are typically found in adult animals. In
placed in a properly identified, sealed
young cattle, which generally have EPG
specin1enjru·. A representative munber of
counts 10 times that of adult animals, EPG
herd samples should be collected from a
counts >50 reflect a moderate infection, and
minin1wn of 10 animals to accow1t for the

EPG counts >500 indicate a heavy bmden
typical high individual vru"iation in munand a need for treatlnent.

bers of eggs shed. San1ples can be

Because fluke eggs do not float readily,
combined after thorough mixing to enable
quantitative fecal sedin1entation procedw-es
exrunination of a single herd composite
are usually used. Two gran1s of feces are
srunple.

mixed with 35 rnL soapy solution (2% liquid

Quantitative fecal egg counts by the
detergent) and strained tluough gauze into
modified Wisconsin centlifugal flotation
a 50-mL centrifuge tube. The tube is filled
procedme or similru· methods can be used
with soapy water ru1d allowed to stand for
to estimate relative infection burden for

3 min, after which Y.a of the supernatant is
nematodes of the "GI pru·asite complex" ( eg, discarded. This is repeated 2--3 times until
trichosti·ongylid larvae of cattle), while also
the supernatant is clean. All but 15 mL is
detecting coccidia ru1d other parasites such
pomed off, 2 drops of new methylene blue
as lungwonn larvae and tapeworms. Three
are added, and the eggs counted with a
grams of feces are placed in a container,
dissecting microscope in a gridded Petri
suspended in -15 mL water, strained
dish or by exru11ining several coverslipped
through a gauze squru·e into a 15-mL tube,
microscope slides. The eggs of the liver
and centrifuged (1,500 rpm for 3 min). The
fluke, Fasciola hepatica, can be differentisupernatant is decanted and the sediment ated from those of Paramphistomum spp,
mixed with saturated sugar sQ)ution, filling
the rumen fluke, by the golden color, more
the tube enough to fonn a positive meniscus bruTeled shape, and slightly larger size of before placing a 22 x 22 mm coverslip on the eggs of F hepatica versus t11e gray color, lip of the test tube. The tube is centrifuged
more pointed end, and smaller size of the
again at low speed (1,500 rpm for 5 min).

usually nonpathogenic rumen fluke.

The coverslip, with the surface film

Commercial sieve-sediment kits can reduce
containing eggs, is removed and ti·ansferred
sample preparation time by 50%. In cattle,
to a microscope slide for counting of

Fasciola EPG counts >3 suggest economic
trichostrongylid eggs in cattle feces or
losses; EPG > 10 may be associated with
strongylid eggs in horse feces. The total is
clinical signs.

divided by 3 to delive eggs.lg (EPG). Other
parasites are noted, if present, with a

External Parasite (Ectoparasite)

general abundance designation of + l (few),

Examination in Small Animals and

+2 (small nwnber), +3 (large nun1ber), or

Livestock: Animals with derrnatoses

+4 (too nwnerous to count).

should be evaluated by exrunining for

A saturated solution of table salt (SG
ectoparasites or evidence of their presence.

1.20) is an inexpensive alternative mediun1

For example, fleas may not be seen on a
for diagnosis of livestock parasites,
cat or dog, but small black flecks of flea
although salt may be highly corrosive to
excrement (flea frass or flea "dirt") that metal surfaces. Magnesiwn sulfate (SG
produce a reddish stain when placed on a

1.20) is the preferred mediwn for swine
moistened paper towel may be noted. Skin

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1621
must sometimes be scraped to diagnose

A negative result on a screening test is
parasites. A scalpel blade is used for the
very reliable; however, false-positive results
deep scrapings (until blood oozes) needed
may occur with the tests of soluble antigen,
to demonstrate parasites that live in
especially in a population of cats with a low
burrows ( eg, Sarcoples) or hair follicles
incidence of disease. A true positive result

(Demodex spp ). The scraped material is
may reflect either transient or persistent

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placed in a drop of mineral oil on a slide,
viremia, so clinical decisions should not be
and the entire area w1der the coverslip is
based on a single test result. Confirmation
scanned under low-power magnification.

of positive results, especially in asympto

A few drops of 100/o potassium hydroxide
matic cats, should be pursued by additional
solution may be added to clear deb1is and
testing such as soluble antigen testing using
allow better visualization.

a kit from a different manufacturer or
immunofluorescent antigen testing on blood

SEROLOGIC TEST KITS
or bone marrow. Cats witl1 discordant
results should be retested using both test

In-house serologic test kits continue to
methods in 60 days and should probably be
improve in reliability, ease of use, and types
considered potentially i.nfective until their
available. They include tests for infectious
status is clarified.

disease by measuring either antigens or

Some cats previously thought to have
antibodies. Antibody levels can also be
cleared infection have been identified using
measured to establish the presence of
real-time PCR, which is a ve1y sensitive
adequate protection to an infectious agent.

method to detect cell-associated FeLV

However, these levels are not an absolute
proviral DNA or viral RNA. These cats are
measure of protection. High serum antibody proviral DNA positive but FeLV antigen levels do not always confer protection, and
negative and are unlikely to shed virus or
low levels do not always indicate susceptidevelop clinical disease. However, proviral bility to infection. The level of cell-mediated

FeLV could be transmitted in blood
inununity is also in1porta.nt. Measurement of transfusions, so potential feline blood hormone levels also use serologic tests.

donors should be PCR negative for FeLV.

Many of these tests are ELISA that may be
microwell or membrane-based, but other

Feline Immunodeficiency Virus
types, including irnrnunornigration,

(FIV): Because the concentration of F1V
immunochromatography, and agglutination
antigen in tl1e blood of infected cats is often
tests, are also available. San1ple requireve1y low, in-house diagnostic tests are ments may be plasma, serun1, whole blood,
designed to detect anti-F1V antibodies
feces, or saliva, depending on the test
rather t11an antigen. Test kits yield a positive
format.

or negative result for antibody rather than a
titer. Antibodies usually develop within 60

Feline Leukemia Virus (FeLV):

days of infection, but this period is quite

Sero logic testing for FeLV is important to
variable, and a few infected cats do not
identify infected cats and prevent transmisdevelop detectable antibody levels. Once sion of the virus (seep 790). Testing is also present, antibodies appear to be present for
recommended before vaccination agai.nst

>2 yr, except for those transiently detect

FeLV, because vaccination of infected cats
able in kittens that have maternally derived
will not limit development or transmission
antibodies. A kitten <6 mo of age that tests
of disease. Most cun-ently available
positive should be retested after 6 mo of age
in-house diagnostic kits are designed to
for this reason. If the test is still positive, the
detect soluble FeLV-specific gag protein
kitten is most likely infected.

p 27, which is produced in large amounts

With the cun-ently available ELISA
during viremia. The time between infection
in-house test kits, sensitivity is high.

and the presence of detectable antigen

However, these tests cannot distinguish
varies but is likely to be within 28-30 days.

between antibodies produced in response

Vaccination agai.nst FeLV will not yield a
to vaccination with FIV vaccine and those
positive test result when antigen tests are
produced by natural infection. An ELISA
used, nor will the presence of maternally
test that appears to successfully discrimiderived antibodies in kittens. Testing sernm, nate between antibodies produced in
plasma, or whole blood is considered more
response to vaccination and t11ose produced
reliable than testing saliva or tears. Most
in natural infections has been developed but
test kits have positive and negative controls
is not available for commercial use. A
incorporated into the kit, so technical
reasonable approach is to use the in-house
problems with rnnning the test may be
test as a screening test. A negative result is a
detected.

fairly reliable indicator that the cat is not

1622

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY
infected. Positive results, especially in
present in puppies. They are less useful
asymptomatic cats, should be confirmed
for diagnosis of infection with CDV. An
by another test such as Western blot if
inununochromatography-based assay for
available. Kittens born to vaccinated queens

CDV antigen has been developed and has
are antibody-positive for a vruiable length of good sensitivity and specificity, especially VetBooks.ir
time.

when conjunctiva! swabs are the sa111ple
used; sensitivity and specificity are

Canine Parvovirus (CPV): Both ELISA
somewhat less for blood and nasal swabs.

and imrnunomigration test kits are available

This assay is not currently available as an
for detection of CPV antigen in feces. These
in-house test kit.

tests are fairly specific for the virus, but
dogs that have been recently vaccinated

Borrelia burgdorferi: Lyme disease
may transiently shed antigens detected by

(seep 659) is caused by the tickborne
the test kits. The sensitivity is somewhat
spirochete B burgdorferi. In general,
lower for several reasons. Fecal shedding
diagnostic tests for this infection have had
occurs for only -7-10 days, beginning on
several potential problems, including
day 3-5 after exposure, so virus is not
relatively high levels of positive results in
always detectable in dogs with clinical
clinically healthy animals, persistence of
signs. Blood in the feces as well as the
antibodies after appru·ent resolution of
formation of antigen-antibody complexes,
clinical disease, interpretation of antibody
with antibodies from the blood or exudate
titers in vaccinated dogs, and the fact that
present in the gut, may be associated with
detectable antibody may not be present
false-negative results. It appears that
until 4-6 wk after exposure. An in-clinic
in-house test kits may have decreased

ELISA test kit for detection of anti-B
sensitivity to the new CPV2c strain.

burgd01feri antibodies in serum or plasma

Although in-house test kits for diagnosis
minimizes some of these problems by using
of CPV are not licensed for use in cats,
a synthetic peptide (C6) based on a
several studies have shown they can be
conserved B burgd01feri-speciiic protein.

used to detect feline panleukopenia virus in

This protein is important in inducing a
cat feces. The specificity and sensitivity ru·e
hurnoral inu11une response by 3-5 wk after
not known. Some cats test positive after
natural infection in dogs. Vaccination does
vaccination, even when inactivated virus
not induce a cross-reactive immune
vaccines ru·e used.

response to this ru.1tigen, so assays using the

In-house tests for assay of anti-CPV

C6 protein are able to distinguish vaccineantibodies have become available to induced antibodies from those produced
evaluate the need for revaccination and the
in response to natural infections. C6-based
presence of possibly interfering maternal
assays ru·e also more specific than previous
antibodies. These tests are not intended to
tests, because there is no cross-reactivity
diagnose parvovirus infection and do not
with other tickborne agents or with
distinguish between natural exposure and
autoimmune antibodies.

vaccine-induced antibodies. Currently

A cwTently available in-house test assay
available test kits include.ELISA and
for anti-B burgdorfe1i antibodies is a
inununochromatographic tests. They ru·e
screening test that gives only a positive or
semiquantitative and use color changes in
negative result and is thus not quantitative.

positive control wells compared with color

Although licensed for dogs, this test kit also
changes in san1ples to determine relative
has been validated in cats and horses.

antibody levels. The level of anti-CPV

Quantitative assays, performed in reference
antibody protective against infection is not
laboratories, can be used to monitor
known, but results are interpreted based on
treatment efficacy (ie, detection of
protective titers measured by other
decreasing antibody titers), but these
methods. PCR is widely available for
results are not always conclusive.

detection of virus in feces.

Ehrlichia canis: Canine ehrlichiosis (see Canine Distemper Virus (CDV):

p 803) is a tickborne disease caused by one

In-house test kits for determination of
of several species of Ehrlichia. It can be
antibodies to CDV are available, usually
associated with thrombocytopenia, anemia,
in combination with canine parvovirus
and neutropenia as well as other nonspecific
antibody testing. These tests are semiquanclinical signs. Although identification of titative ELISA for anti-canine distemper IgG

Ehrlichia morulae in leukocytes can be
in serum or plasma. They may be used to
diagnostic for this infection, serologic assay
evaluate the need for revaccination and to
for detection of antibodies is more common
deten11ine tl1e level of maternal antibody
and has better sensitivity. In-house tests for

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1623
ehrlichiosis are either qualitative (giving
use. Batch testing and single sample testing
only a positive or negative result) or
are both available. All of the test kits have
semiquantitative tests for antibodies to E
very high specificity. False-positive results
canis. Those currently available are ELISA
are most often due to technical problems
to be performed on serum, plasma, or whole
such as inadequate washing or failure to

VetBooks.ir
blood. The test kits use either recombinant
read the results at the optimal time.

analogues of major outer membrane

Manufacturer's instructions should be
proteins of E canis or whole E canis
closely followed with any of the test
proteins as the antigen. The different
fonnats.

Ehrlichia species stimulate antibodies that Sensitivity varies from one test to another
appear to cross-react in tl1ese assays, for the
and is affected by worm load, worm gender
most part. Because anti-E canis antibodies

(a female antigen is detected, thus
may be very long-lived and may be present
male-only infections will not be detected),
in subclinical infections, detection of these
and maturity of female wmms. None of
antibodies does not distinguish between
these tests has 100% sensitivity. When
exposure and Ehrlichia-induced illness and
unexpected false results are obtained on an
cannot reliably indicate success of response
antigen test, additional testing, using a
to tl1erapy.

different fonnat, is recommended.

After adulticide treatment, antigenemia

Brucella canis: B canis is not a problem should become undetectable by 6 mo.

in some countries, and tests are not always

However, it can take more than a month for
readily available. However, infection may
some adult heartwonns to die, so a positive
be subclinical, or it may cause a variety of
antigen test at 5-6 mo after treatment does
clinical signs, including abortion, infertility,
not necessarily indicate treatment failure.

and discospondylitis (seep 1402). Infection The test should be repeated 2-3 mo later.

most often occurs during mating; thus,
testing of breeding anin1als is in1portant in

Heartworm Antibody and Antigen
disease prevention. A rapid slide agglutina

Cats: Heartwonn disease in cats is
tion test that includes a 2-mercaptoethanol
substantially different from the disease in

(2-ME) step to reduce false-positive results
dogs, and recommendations for serologic
by eliminating nonspecific IgM reactions is
testing are consequently different. Cats
available as an in-house diagnostic kit. This
tend to have a much lower worm burdenassay detects serum antibody to surface often only one or two wonns. Cats also
antigens of the bacteria. Reports of
have single-sex infections more frequently
sensitivity and specificity of this test vary
than do dogs. Circulating microfilaremia is
depending on the confinnatory test used.

rare in cats, and microfilariae have a shorter

ELISA and immunochromatographic assays
life span. These differences are often
have been developed for qualitative and
attributed to a more effective feline immune
semiquantitative tests for anti-B canis
response to heartwonn infection. However,
antibodies. Positive results obtained using
heartwonns can cause serious disease in
any of these test kits should be confirmed
cats.

with PCR or blood culture.

Heartwonn antigen tests are less
sensitive for detection of infection in

Heartworm Antigen-Dogs: Serologic
cats than they are in dogs, with a reported
testing for heartwonn antigen in dogs is
sensitivity of 50%-SOOA,. Therefore, a negative
more sensitive than screening for microantigen test does not exclude heartworm filaremia and, in addition, can detect occult
infection. Antibody testing is also available
infections. Heartwonn antigen is first
and can be useful as a screening test, but
detectable at -5 mo after infection and will
the presence of antibody does not confirm
usually precede microfilaremia by a few
feline heartworm disease. Transient
weeks; however, this time frame may be
exposure to larvae will stimulate producshifted later in anin1als on macrocyclic tion of antibody; many early infections are
lactone preventives and those with low
cleared spontaneously, and adult heartnumbers of wonns. Antigen test fonnats worms never develop. A combination of
available include ELISA and immunochrotesting for both heartwonn antigen and matographic assays. Serum or plasma may
anti-heartwonn antibody results in much
be used in all kits, and some may be
higher sensitivity and specificity than using
perfonned using whole blood. Some test
either test method alone. Combination
kits can be stored at room temperature,
testing is warranted in cats with clinical
whereas others must be stored refrigerated
signs of heartwonn disease when results
and brought to room temperature before
of a single test are not conclusive.

1624

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

Test kits for detection of heattwom1

A cwTently available in-clinic kit to
a.11tigen and anti-heartworm antibody in cats measure LI-I concentrations in serum is ai·e marketed in several fom1ats. These can
essentially qualitative, witil a serwn level of
use either plasma or sernrn and are

< 1 ng/mL bei.t1g read as negative and a level
qualitative or semiquantitative.

of> 1 ng/mL considered positive. The test is

311 immwiochromatographic assay.

VetBooks.ir

Canine and Feline Pregnancy

Ovariectomized bitches and queens have

Diagnosis-Relaxin: The only known
serum concentrations of LH > 1 ng/mL.

pregnancy-specific hom1one in the bitch

Because tl1is LH concentration is also seen
and queen is relax.in, which is produced by
in intact bitches about to ovulate, a single
the placenta when '-l fertilized egg is
high LH concentration does not confirm
implanted. Relax.in is first detectable in the
reproductive status, but a low LI-I concenplasma ai·otmd day 20-25 after fe1tilization.

tration indicates a nonovariectomized

It is not present i.t1 pseudopregnant or
alllillal.

non pregnant bitches or queens. Relaxin
levels peak by approximately day 40-50 of

Canine Ovulation Timing-Proges
gestation and drop at p31turition, but they
terone: Sernm progesterone begins to
may remai.t1 detectable for up to 50 days du1°
increase after the LI-I smge witil a modest
ing lactation. In-clinic test kits to measw·e
increase on tile day before ovulation and a
relaxin include microwell ELISA and
fwther increase to 4-10 ng/mL on the day
irnrnwiomigration qualitative tests requi.t·ing of ovulation. Progesterone conti.trnes to sernm, plasma, or whole blood. The assays
increase and stays increased throughout
appeai· to have very good specificity, ie, a
pregnancy or diestrus. As tile Jise i.t1
detectable level of relaxin is not fowid in
progesterone is more constant compared
non pregnant animals. False-negative results
with LH, daily testing is not necessaiy. It is
have been repo1ted in some bitches carrying reconm1ended tilat testing begin in late very small litters or in those with one or
proestrns and continue eve1y 2---3 days tmtil
more nonviable puppies.

a high range is reached, indicating ovulation.

The test kits for in-clinic progesterone

Canine and Feline Luteinizing
testing are senliquantitative ELISA with

Hormone-Ovulation Timing and
preovulato1y concentrations designated

Ovariectomy Status: In the bitch, senm1
according to the kit used. Some kits are
luteinizi.t1g ho1mone (LH) is no1mally
designed to give two additional progesterpresent in ve1y low levels except for a one ranges (intermediate and high),
dran1atic rise just before ovulation.

whereas others indicate only preovulatory

Ovulation occms 2 days after this LH smge,
and "ovulatory day or later" levels. In
alld the LH level returns to baseline within
comparison with other test methods, tile

2�0 hr of peaking. Serum progesterone
in-house test kits 31·e less accmate,
levels begin to rise at the tune of the LH
patticularly in the r311ge of roughly 1.5---10
smge. A bitch will be fe1tile between 4-7
ng/mL, which is tl1e range of i.t1terest for
days after the LH smge, with the most fe1tile eai·liest detection of ovulation. Accuracy is period on days 5 and 6. In addition, the LH
greater at higher progesterone levels. As
smge determines the gestation period, with
mentioned above, measurement of both LI-I
paitwition occurri.t1g between day 64 and 66 and progesterone is reconunended for most after the smge. The LH surge may occm
accmate breeding m311agement.

anywhere from 3 days before to 5 days after
the onset of estrous behavior, so it c31mot

Thyroxine: Assay of total serum tl1yroxine
be reliably predicted by behavior.

(T1) may be used as a screening test for

Ovulation tinting by measurement of LI-I
canine hypotilyroidism or as a diagnostic
requires daily testi.t1g, which usually begins
test for feline hyperthyroidism. (See also
when >500A, of vaginal epithelial cells 31·e

TIIE THYROID GLAND, p 552.) In addition,
cornified, based on vaginal cytology. There

T, concentrations are measmed when
is occasionally a false LH peak not followed
monitoiing therapy for hypo- or hypetthyby ovulation, but it will also not be followed roidism. An in-house ELISA test kit, which
by an increase i.t1 progesterone. For that
uses 311 additional instrwnent to read results,
reason, assays of both LH and progesterone
provides semiquantitative infmmation about
are reconunended for most accw·ate

T4 concentration in calline 311d feline sera.

ovulation detection. An i.t1creased LI-I

The assay is nm at one of two "dynatnic
concentration not followed hy increased
ranges," depending on tile predicted range
progesterone levels is considered a
of results. Published studies compai'ing this
proestrus fluctuation, and testing for
assay witil other test metilods for T4 vaty in
ovulation should continue.

tilei.t· conclusions. It is recommended that TI

DIAGNOSTIC PROCEDURES FOR THE PRIVATE PRACTICE LABORATORY

1625
concentrations be periodically measured

One quantitative handheld colorimetric
in stored pooled senun of cats and dogs to
in1mw1oassay is cun-ently available.

monitor whether assay performance is

Reports of sensitivity and specificity
consistent. It is probably still better to use
among these methods vary. In general,

VetBooks.ir
a commercial laboratory for thyroxine
sensitivity in identifying foals with IgG
measurement.

concentrations <400 mg/dL appears to be

Almost all (99"Ai) of total T4 is bound to acceptable for all methods. Thus, there are
protein in the blood and therefore not
few foals with total failure of passive
biologically accurate. Free T4 levels are a
transfer that would not be identified by any
more accw·ate test of thyroid function in
of these methods. Specificity is less
cats and dogs.

acceptable for some of the methods, and
treatment of some foals that did not need it

Foal lmmunoglobulin (lgG): Measuremight be instituted based on the results.

ment of foal serum IgG concentration
within the first 24 hr after birth can be useful

Calf lmmunoglobulin: Measurement of
in preventing disease related to failure of

IgG concentration in neonatal calf serum is
passive transfer of IgG in colostrum from
important for the same reasons described
mare to foal. Use of foal-side testing
for foals. However, IgG levels in calves are
procedures can facilitate prompt diagnosis
different from those in foals, with> 1,000
and treatment. A foal serum IgG level of
mg/dL considered evidence of adequate

>800 mg/dL is generally considered optimal,
passive transfer and < 1,000 mg/dL
with <200 mg/dL indicating failw·e of
indicating failure of passive transfer. Radial
passive transfer. Concentrations of 200-300
immunodiffusion is the gold standard for
mg/dL are considered evidence of partial
accurate measurement of serun1 IgG in
transfer.

calves (as in foals), but tl1e length of tirne

Although radial immunodiffusion is
required to complete this assay makes it
considered the most accurate test for IgG
less useful than other methods. Other
concentration, it takes much longer (5-24
methods include zinc sulfate and sodiw11
hr) than many of the other test methods and
sulfite tw·bidity tests, glutaraldehyde
thus is not as useful as an indicator of the
coagulation test, measurement of total
need for therapeutic intervention. More
senu11 solids by refractometry, and a lateral
rapid screening tests include the zinc sulfate flowthrough ELISA test kit.

turbidity test, glutaraldehyde clot test, and

The sodiwn sulfite and zinc sulfate

ELISA test kits.

turbidity tests are both based on the

The zinc sulfate test estimates lgG in
precipitation of high-molecular-weight
serun1 based on its precipitation when added proteins in these solutions. Serun1 is used as to a zinc-containing solution. Turbidity
the sample, and tests are read after 15--30
generally becomes visible when lgG levels
min of incubation. Results of these tests
are 400-500 mg/dL. This test takes -1 hr and
vary in sensitivity and specificity depending
may be pe1fo1med with zinc sulfate
on the endpoint chosen, and technical
solutions made in the clinic, or reagents for
difficulties with reagents can decrease test
the test may be purchased as a test kit.

performance. The glutaraldehyde clot test

The glutaraldehyde clot test requires the
is performed as in foals, with no clot
addition of 1 volwne of serum to 10 volwnes fom1ation at 60 min indicating failure of 10°'6 glutaraldehyde and examination of
of passive transfer.

the tubes at timed intervals up to 60 min.

Measw·ement of senun total protein by

The presence of lgG in the senun causes a
refractometer is a fairly reliable indicator
solid clot to form in the tube. Clot formation
of adequate passive transfer in healthy,
in <10 min generally con-elates to an IgG
well-hydrated calves. A level of 5.2 g/dL is
concentration of >800 mg/dL, whereas a
roughly equivalent to an lgG concentration
positive reaction within 60 min is interpreof 1,000 mg/dL.

ted as an IgG concentration of >400 rng/dL.

A commercially available ELISA test kit

Both of these test methods use senun,
uses serum as the sample and takes -20
rather than plasma, so time for the blood to
min. The assay is qualitative in that it
clot and separation of senun must be added
indicates an IgG concentration of> 1,000
to the time needed to perform the test.

mg/dL or <1,000 mg/dL. Sensitivity and

ELISA test kits for in-house or foal-side
specificity are reasonably good, and this test
testing can use either serum or whole blood
is less influenced by factors such as calf
as the sample and take -10 min. Most are
dehydration or reagent instability than some
semiquantitative, with color changes
other methods. Manufactw·er reconunendacorresponding to IgG concentrations of tions for storing and using the kits must be

<400 mg/dL, 400-300 mg/dL, or >800 mg/dL.

followed.

1626

DIAGNOSTIC IMAGING

DIAGNOSTIC IMAGING

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RADIOGRAPHY
essentially unchanged, as are the relative
numbers of x-ray photons penetrating

Radiography comprises the majority of
tissues of different densities such as bone,
diagnostic medical images generated in
soft tissue, and fat. However, the amount
veterinary practice, but other imaging
of darkening on the inlage is related to the
modalities such as ultrasonography, CT,
total number of photons reaching it.

MRI, and nuclear imaging are also very

Therefore, increasing mA increases in1age
impmtant and commonly available in
contrast. Changes in mA settings are
specialty practices and academic centers.

relatively linear; increased contrast is

Imaging provides a large amount of infonnadesirable when tissue densities are similar tion by noninvasive means. It does not alter

(eg, soft-tissue components of the
the disease process or cause unacceptable
musculoskeletal system). However,
discomfort to the animal. Although
increasing mA generally results in more
radiography itse!I is painless, sedation is
heat loading on x -ray tubes, thus lin1iting
often desirable to reduce anxiety and stress
exposure times and reducing tube life.

associated with the procedure, to promote

The third major parameter in mal<lng a
acquisition of good diagnostic studies with
radiographic exposure is exposure time.

minimal repeats, and to control pain

Increasing the exposure time increases the
associated with manipulation in anin1als
number of photons produced and hence the
with painful disorders such as fractures and
darkness of the inlage. For exposures in the
arthritis.

general diagnostic range, this is a linear
function; as is the case with increasing mA,

Equipment: Radiographs are made using
increasing exposure tin1e generally results
a specialized type of vacuum tube that
in greater heat loading of the x-ray tube than
produces x-rays. The tube cunent,
increasing kVp, once again potentially
measured in milliamperes (mA), and
shortening tube life.

voltage, measured in kilovolts (kV),

All three of the above parameters are
determine the strength and number of
interdependent, with exposure time and mA
x-rays produced and are two of the three
so much so that the term millian1pere-secexposure factors that can be set on most onds ( mAs) is usually used to indicate the
x-ray machines. Kilovoltage potential (kVp)

product of these two factors. Increasing the
is the highest potential voltage achieved at
mA and decreasing the exposure time by a
any given kV setting.

proportionate amount results in a radio

Higher kV settings produce more
graph less likely to be degraded by motion.

penetrating beams in which a higher

As a rule, it is best to minimize the exposure
percentage of the x-rays produced penetrate time but maintain an appropriate mAs and the subject being radiographed. There is
scale of contrast. Increasing kVp increases
also a decrease in the percentage difference
the number of photons penetrating the
in absorption between tissue types. This
subject and so darkens the iniage. This
results in decreased contrast (long-scale
effect can be used within limits to conect an
contrast) on the final image. High kVp
underexposure. The converse is likewise
techniques are most useful for studies of
tiue.

body regions with many different tissue

When correcting a previously unsatisfacdensities (eg, thorax). Higher kVp tory image, underexposure or overexposure
techniques are appropriate for larger and
should be corrected for by adjusting the
thicker animals with lin1itations. Increasing
mAs when exanuning areas of high contrast
kV is not a linear function, and small

(skeleton) or by adjusting the kVp when
increases in kVp settings may substantially
examining areas of low contrast (thorax).

increase the number of x-rays penetrating

This will maintain the same relative contrast
the animal. However, for a number of
for that anatomic area while adjusting the
reasons relating to the production and
film darkness.

absorption of x-rays, this effect is much less

Establishing a technique chart to take
dramatic above 85 kVp.

racliographs makes it easy for the operator

Increasing the mA setting on the machine
to arrive at a technique by simply correcting
increases the number of x-rays produced.

a standardized protocol for the size of the

The energy spectrw11 of the x-ray beam is
animal being examined and the anatomic

DIAGNOSTIC IMAGING

1627
area under consideration. It also ensures
the same number of lead lines per centithat radiographs of the same anatomic meter.

region will have a consistent appearance

Digital recording is rapidly increasing
from animal to animal. A technique chart
in usage, but radiographic images have
must be made for each machine. However,
traditionally, and still are, commonly stored

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some generalizations can be made.

on specially optimized fibn. However,

Exposure factors for the thorax should have even the best silver halide film is relatively mAs values �5 unless the animal is very
insensitive to x-rays. For that reason,
large. Values of 10 for the abdomen and
the x-ray film is usually placed between

15-20 for skeletal studies are appropriate. In
specially designed phosphorescent
many modem x-ray machines, the technique
screens-panels composed of microscopic
cha.it is built into the machine. The operator
phosphorescent crystals embedded in a
need only enter the species, body part, and
plastic matrix that directs propagation of
thickness, and the machine automatically
the phosphorescent light toward the film.

sets the technique. This is convenient and

These screens are much more sensitive to
reduces mistakes in technique, but the
x-rays than is film. When the x-ray strikes
settings may need to be altered to suit the
a crystal, it causes the crystal to phosphospecific equipment, film-screen ( detector) resce, and the light exposes the film
speed, and the viewer's preferences ( eg,
secondarily. This process of recording the
contrast level).

x-ray image is much more efficient than

Automatic exposure control (AEC) is a
using film alone and markedly reduces
system in which U1e operator sets the kVp
radiation exposure to the subject (someand m.A, and the machine terminates the times by a factor of 100 or more) and the
exposure at the appropriate time. If used
operator. It also reduces the amount of
properly, this system results in nea.i·Jy
scatter radiation recorded on the image.

identical image exposures between anin1als.

The screens and film a.i·e contained in a

However, appropriate kV settings are
lightproof cassette, which is transparent
needed, and consistent anin1al positioning
to x-rays.

is critical. Identical positioning between

Screens and film must be matched for
animals is required to achieve identical
spectral emission and sensitivity. Films
images. Placing the heart or lungs over the
produced by one company are generally

AEC sensor results in radically different
not optimally sensitive to screens made by
appea.iing radiographs. AEC is probably
another, and it is inadvisable to mix screen
most effective when large numbers of
and film brands. Screen and fibn combinaimages are being done of the san1e anatomic tions come in different speeds. The larger area by the same personnel.

the crystals in a screen are, the more likely it

X-ray machines are equipped with
is to interact with an x-ray and the greater
collimators that allow adjustment of the size the amount of light produced. Unfortuof the bea.tn to the size of the area being nately, larger crystals also produce larger
radiographed. This reduces the amount of
areas of light, which decreases the detail
scatter radiation generated, improving
of the fib11. Likewise, film with larger silver
image contrast and detail. Scatter radiation
halide grains is more sensitive to the light
is also the major source of radiation
creating the exposure but also reduces the
exposure to operators, so proper collimadetail or resolution of the final in1age.

tion is imp01tant to reduce this risk

Therefore, fine grain films are matched

When a radiograph is made, some of the
to fine crystal screens, resulting in very
x-rays are scattered. When the object being
detailed images that take more radiation
radiographed is ;,,10 cm thick (15 cm for
to produce. The converse is true for la.i·ge
digital systems), scattering becomes a
grain film and large crystal screens.

problem by causing unwanted exposure of

The speed of these combinations is
the x-ray film. A grid, which is a thin plate
designated by a rating of 100-1,600, with 100
made up of alternating thin strips of lead
being relatively slow but with very good
and plastic, can be placed between the
detail and 1,600 being very fast but with
animal and the film to reduce the scattered
limited detail. Film-screen combinations
x-rays from exposing the film. The ability of
with speeds of200-800 a.i·e generally used in
a grid to remove scattered radiation is
veterinary medicine; 200-speed systems are
measured by the grid ratio. The grid ratio is
used for small body parts and skeletal
determined by the height of the lead strips
imaging, whereas 800-speed systems are
divided by the distance between them. A
used for large abdomens in small animals
grid with an 8: 1 ratio will eliminate more
and thoracic radiography in large animals.

scattered radiation from exposing the film

Choice of the proper speed system for a
than will a grid witl1 a 6: 1 ratio if both have
specific use is based not only on the area

1628

DIAGNOSTIC IMAGING
being radiographed but also on the
developer solution with fixer inactivates it
capabilities of the machine. Small, portable
and requires replacement of the developer.

x-ray machines can be used for larger body

Improper har1dling of chemicals results in
parts with fast film-screen combinations,
mar1y artifacts on films as well as potential
substantially improving the utility of these
health hazards to the operators.

machines.

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Use of radiographic film is rapidly being

Film less Radiography: Image recording
phased out except for special purposes,
systems do not require the use of film,
with digital in1age capture likely leading to
screens, or processing chemicals. They
a cessation of film production for most
have several advantages over conventional
pmposes. As advances in digital detector
film radiography: 1) radiographs carmot be
systems continue, it is likely that images
lost if adequate data safeguards are used;
produced on digital detector plates will be

2) there is no need for film storage and its
indistinguishable in detail and quality from
attendant space and environmental requirethose acquired on film. It is already ments; 3) the process allows for matlipulabecoming difficult to find film cassettes and tion and enhancement after the image has
screens for medical radiography sold by
been recorded; 4) in1ages can be trat1smitprimary vendors.

ted electronically to a remote location for
immediate interpretation; 5) the images are

Darkroom: As digital image captme
generally available more quickly, usually
replaces radiographic film, darkrooms will
witllin 30 sec; arid 6) there is no need for a
no longer be required. However, because
darkroom.

radiographic film is still used by many

These systems can be divided into two
veterinary practices, a b1ief description of
categories: computed radiography (CR),
darkroom procedmes is provided.

in which a semiconductor plate contained

Once the film is exposed, it must be
in a cassette is exposed in the usual fasllion
processed in a darkroom to make the latent
at1d then read electronically inside a special
image recorded on the film visible and fixed
reader that detects the magnitude of
so that the image remains unchanged once
electrostatic charge on each of the
the film is brought into the light. Care should semiconductor elements within the plate; be taken to be sure no exterior light enters
and direct digital radiography (DR), in
the darkroom. Even very small amounts of
wllich a cesium iodide scintillator arTay
white light will markedly fog a film and
absorbs the x-rays, producing a light pulse
decrease its diagnostic quality. Safelights
detected by a large array (millions) of
used to illuminate darkrooms include filters
ar11orphous silicone photodiode/trat1sistor
that remove the frequencies of the light to
elements. In both systems, the electrical
which the film is sensitive, SQ the film will
output from each of the detector elements is
not be exposed. Films vary in their spectral
proportional to the nun1ber of x-rays that
sensitivity; therefore, when replacing a
stJ·ike the detector element at1d is mathsafelight filter, the spectral requirements of ematically quat1tifiable, hence the term
the filter must be specified.

"digital images." In both systems, the data Automatic processing systems improve
produced are processed by a computer,
processing quality and consistency and
which generates the iniage on a monitor
reduce the processing time compared with
according to a previously detennined
traditional hand fihn developing. Relatively
processing algorithm that is specific to the
few films processed per week can justify the region being radiographed. Processing purchase of an automated processing
algorithms are critical to the development
system. In any case, fih11 processing must be
of diagnostic images. In mat1y displaced
done in stiict accordance with the specified
systems, the algorithm Call be altered to
time and temperature requirements of the
provide enhat1cement of various features
fihn being used. These requirements have
of the image. The digital images ar·e then
been standardized for many years, and
stored electJ·onically at1d made available
automated systems are designed to meet
to at1y computer with access to the image
them.

arcllive.

Whether processing is manual or

The difference between the two systems
automated, the chemicals must be handled
lies in the intem1ediate step of exposing a
with care. Contamination of the darkroom
plate in CR, which is then placed in a reader.

with chemicals can ruin fih11, screens, and

These plates must be replaced periodically
clothes. Fumes from the chemicals may be
because of wear created during the reading
harmful, and some people may be more
process. There is also the issue of whether
sensitive than others, especially to the fixer
the latent image recorded by the reader is fill
solution. Cross contar1lination of the
accurate representation of the true in1age.

DIAGNOSTIC IMAGING

1629

The portability of the cassettes is an imporlocations and/or by copying the data files to tant benefit in practice situations in which
optical storage media that are then kept in a
radiographic images are produced in
safe location. Protection of the data from
multiple places. CR systems are also still
corruption is a more thorny issue. Because
considerably less expensive than all but the
images stored in a digital fom1at are easily

VetBooks.ir
simplest DR systems and generally still have
manipulated by various computer
higher resolution capabilities, which may be programs, it is possible that they could be important for imaging smaller anatomic
altered (accidentally or deliberately) to
parts.

reflect a different situation than the actual

DR systems are very complex electronione. For this reason, many electronic image cally and subject to the same insults as any
formats are not recognized as legal
complex electronic system. They are
documents and are not acceptable in a court
particularly sensitive to shock and
of law. Because of this potential for
electronic interference. However, when
alteration or abuse, a special medical image
properly cared for, DR systems are durable
f01mat has been developed and agreed on
and reliable. They do not require handling of
by the American College of Roentgenology,
the image recording plate, which reduces
the American College of Veterinary
wear and tear on the system. Their main

Radiology, and others as the standard
advantage over CR is image display speed.

format for medical image generation and

DR systems have been developed that do
storage. This is the Digital Imaging and
not require a cable to communicate

Conununication in Medicine (DICOM) III
between the detector and the computer
format. The key feature of this fonnat is the
processing the data into an image. The cable presence of a hidden header in the image file has been replaced by wireless communicathat records all manipulations of the in1age tion on specified electrical magnetic
or the header each tin1e the image is saved.

frequencies that are unlikely to be

The header also contains a large amount of
interfered with by other electromagnetic
information about the patient and
devices such as cell phones and electronic
production factors of the inmge, which must
equipment. Although they are still much
be specified before creation of the image.

more expensive than systems incorporating

This makes accidental or malicious
a cable connection between the detector
manipulation of the image much easier to
and computer, such systems are particularly trace. Another and even more in1portant suited for use in equine ambulatory
benefit of the DI COM III format is that it
practices. Images can also be sent to the
makes images easily transferable to other
storage system in a wireless manner in
sites for referral interpretation or patient
many areas.

referral. No digital imaging system should

The flexibility and reliability of digital
be purchased that does not conform to the
radiography systems, whether wireless or

DI COM III standard.

wired, have improved to the point that they

A common misconception associated
are almost universally used in hun1an
with digital radiography is that it results in
radiology departments as well as in many
decreased radiation requirements to
veterinary hospitals. As DR systems grow
provide a diagnostic image. Although there
in capability, reliability, ease of use, and
has been some progress in this direction,
resolution, and decrease in cost, it is
most current digital radiography systems
expected they will eventually replace both
require essentially the san1e amount of

CR and traditional film systems. Although
radiation to produce a diagnostic image as
currently DR still cannot match the spatial
with film. The computer system will attempt
resolution of either standard speed film or
to reconstruct the in1age with the proper

CR systems, newer systems are narrowing
level of contrast and edge enhancement;
the gap. This low spatial resolution is offset
however, data poor images will often lack
to a large degree by improved contrast
detail despite this enhancement.

resolution. Because of their inherent high
contrast, direct digital systems are also

Animal Restraint: Animals must be
becoming the choice in1aging device for
adequately restrained and positioned to
very large animals.

obtain quality radiographic images. People

The advent of digital imaging has led to
dressed in appropriate protective apparel
the development of special image storage
may manually restrain animals; however,
systems and fommts. The data stored on
manual restraint should be kept to a
computers must be protected from loss and
minimum. In some states, manual restraint
corruption. Loss of data can be guarded
is not allowed except under explicitly
against by storing identical sets of data on
defined circwnstances. Sedation or
different computers in different geographic
short-acting anesthesia is often necessary

1630

DIAGNOSTIC IMAGING
and usually desirable if medical circumlateral radiographic examination of the stances pennit it. Chemical restraint lessens abdomen than on a right lateral. Another the need for and intensity of manual
example of positioning affecting interprerestraint, which leads to fewer poor or tation is frequently encountered when
unacceptable radiographs and usually
evaluating the coxofemoral joints for hip

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shortens the time required to complete the
dysplasia in dogs. If the legs are excesexamination. In many instances, animals sively abducted, the femoral necks will
can be restrained and positioned using
appear thickened, mimicking the producsandbags, tape, and foam pads. With some tion of osteophytes and potentially leading
practice, it is often possible to complete the
to a misdiagnosis. Radiography of the spine
radiographic examination in essentially the
without the aid of anesthesia in an acutely
same time it could have been performed
paraparetic or paraplegic animal may
using manual restraint, with the added
result in inability to properly position the
benefit that the animal is less likely to injure
animal for optimal visibility of vertebral
personnel or itself.

structures because of the pain such

Animal motion may also be minimized by
positioning produces.

decreasing exposure time and maximizing
rnA to achieve the required .mAs for the

Radiation Safety: Radiographic exambody region examined. Other technical inations must be performed with proper
adjustments, such as increasing the kVp or
respect for radiation safety procedures.

shortening the film focus distance, may be

Diagnostic x-ray machines are potent
made in some cases. However, major
sources of radiation and can, if improperly
changes in film focus distance will likely
used, result in injurious exposure to
cause serious degradation of the image. In
personnel over tin1e. The exposure factors
most instances, it is preferable to chemiused in modem x-ray systems are substancally immobilize the animal as long as there tially lower than those used in the past but
is not a medical contraindication.

can still result in injury. It is never accept

Paradoxically, the development of DR
able to hold animals without the use of
systems that allow images to be viewed
lead-impregnated aprons and gloves to
within 30 sec of production has led to an
decrease exposure to the hands and body
increase in the number of radiographic
of personnel from scattered radiation.

images typically produced. Because the

Leaded gloves should not be used within the
images do not have to be processed in a
primaiy beam of the x-ray machine. These
darkroom or through secondary systems
gloves and aprons reduce exposure from
such as in CR, individuals making the
scatter radiation by a factor of -1,000 but
images often attempt to improve positionreduce exposure from the primaiy beam ing of the animal multiple times. Particularly by only a factor of -10. Thyroid shields in instances when the animal is being
are considered mandatory, and eye shields
manually restrained, there is a proportional
in the form of lead-impregnated plastic
increase in radiation exposure to both the

"glasses" are also recommended, especially animal and the holders. This can be avoided
when radiographing large animals, because
by taking a few extra seconds to properly
the exposures used are sometimes quite
position the anin1al for the first image.

high and the orientation of the beam is more

Proper positioning is also important to
likely to be horizontal. Upper limb, cervical
maximize the diagnostic content of the
spine, and skull studies in horses are
x-ray examination. In many cases,
particularly likely to result in substantial
improper positioning or radiographic
exposure to anyone holding the film/
examination can result in a misdiagnosis
detector or the horse.

or inability to appreciate major lesions.

Proper collimation of the x-ray beam is

Perhaps the best example of this is in
ai1 important ai1d integral part of radiation
thoracic radiography. Both right and
protection. If the x-ray bean1 extends
left lateral recumbent radiographs are
beyond the animal, then that radiation
recommended in dogs and cats. This is
contributes to increased scatter radiation
done because positioning of the animal on
and personnel exposure. Any image in
its side results in rapid relocation of fluids
which the entire field of the detector or film
to and atelectasis of the downside lung.

is exposed is probably under-collinlated,

The result is compression and increased
unless the animal extends to the limits
radiographic opacity of the dependent
of the detector. In addition, with digital
lung. Soft-tissue nodules, sometimes of
radiography systems, excessive amounts
considerable size, can be obscured by this
of exposure outside the subject can result
phenomenon. Similarly, lesions affecting
in false interpretation of the data by the
the pylorus may be more evident on a left
reconstruction algoritlun and substantially

DIAGNOSTIC IMAGING 1631
degrade image quality. If this occurs, the

Although interpretation is aided by
exposure must be repeated with proper
experience, conscious use of a systematic
collimation to achieve an acceptable image.

approach to evaluation of the image will

In most instances, Lhe x-ray beam should be
improve tile reading skill of even very
collimated to -1 cm outside the subject
experienced individuals and ensure tl1at

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limits to provide optimal image quality and
lesions in areas not of prin1ary interest or
radiation protection for personnel.

near tile edge of tile image are not missed.

Pregnant women and any personnel < 18

However, many studies have shown tllat
yr old should refrain from direct involveexperience is the best teacher with regard ment in taking radiographic images
to evaluation of radiographs. So, altllough
whenever possible. If a pregnant woman is
anyone will become more adept at in1age
directly involved in taking radiographs, she
interpretation with time, those individuals
should wear an apron that completely
who interpret large numbers of images will
encircles her abdomen.

be the most proficient. Even proficient

Although federal and state authorities
individuals can miss lesions tllat are
have set maximal limits for both extremiunfruniliar to tllem or so-called "lesions of ties and whole-body radiation exposure
omission." A lesion of omission is one in
for occupationally exposed personnel,
which a structure or organ generally
the principal of "as low as reasonably
depicted on tile image is missing. A good
achievable" (ALARA) should always be
example of tllis is tl1e absence of one kidney
adhered to. The currently set limits allow
or tile spleen on an abdominal radiograph.

occupational whole-body exposure to be

Therefore, particular attention to systemroughly the same as that which occurs atic evaluation of tile image is very
from environmental sources. However,
important. It is perhaps best to begin
in many veterinary teaching hospitals
interpretation of the image in an area tllat is
with large radiographic case loads, the
not of primary concern. For instance, when
occupational exposure is held to <10%
evaluating the tllorax of an fillin1al witll a
of the permitted values by use of proper
herut murmur, tile vertebral colmnn and
protective equipment and radiographic
skeleton should be evaluated first because
techniques. There is no reason for
if a substantial lesion is identified for tile
veterinarians or technicians in private
heart, it is possible that the skeletal
practice to ever receive exposures
strnctures may not be examined.

approximating the allowed limits unless

It is essentially in1possible to evaluate
they are heavily involved in specialized
radiographs without a preexisting bias as a
interventional radiography.

result of knowledge of tile history, physical

Individuals involved in taking radioexamination findings, and previously graphic images should be monitored for
pe1fon11ed laboratory results. This bias can
radiation exposure. This is essential to
easily promote under-evaluation of tlie
identify and correct conditions that can
image by focusing on only the ru·ea of
result in excessive radiation exposure to
interest associated with the bias.

personnel. Monitoring of exposure also

Interpretation of radiographic iniages
provides evidence of proper adherence to
depends on a pleural knowledge of fillatomy
radiation safety standards if questions
and m1derstanding of disease pathology.

ruise as to whether an employee's medical

Anatomic changes, such as in size, shape,
condition could be related to radiation
location/position, opacity, and margin
exposure. Several companies provide this
shrupness represent tile basis of radioservice for a relatively nominal fee.

graphic interpretation. In addition, the
degree of change, whetller generalized

Interpretation of Images:

tllroughout fill organ or associated with

Radiographic images are complex twoother abnormalities, must be evaluated. The din1ensional representations of threepresence of lesions tllat do not affect tile dimensional subjects that are generated
entirety of fill organ, such as focal enlargein a format unfamiliar to the average ment of the liver or focal opacification of the
individual. Substantial experience and
lung field, are strongly suggestive of
attention to detail is required to become
localized disease such as tumors or
proficient in interpretation. The start of
bacterial infections. Conversely, lesions
radiographic interpretation is a properly
causing generalized change throughout an
positioned and exposed study. Studies
orgfill such as tl1e liver or kidneys are most
that are poorly or inconsistently positioned
suggestive of a systemic disease such as
are difficult to interpret, and improper
viral infections or toxicities. Combinations
technique further decreases the an1ount of
of lesions in different locations or organs
information obtained from the radiograph.

also help narrow down the potential

1632

DIAGNOSTIC IMAGING
diagnosis. Careful attention to the basic
structures they are designed to evaluate and
principles of interpretation and use of a
should not be forgotten if modem imaging
careful systematic approach will often
procedures fall short. Many contrast
provide answers not readily apparent on
procedures do not require special equipinitial examination.

ment and can be perfom1ed in the average

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Once all of the lesions on the study are
veterinary practice, but interpretation is
identified, a rational cause for those lesions
best pe1fom1ed by someone with extensive
can be formulated. The maximum amount
experience and training in the interpretation
of information is derived from the
of radiographic images.

radiographic study when interpretation is
done in light of the clinical and clinicopatho

ULTRASONOGRAPHY
logic information available. In this way, the
most likely cause for the animal's condition

Ultrasonography is the second most
can be determined. However, many diseases commonly used imaging format in can cause similar radiographic lesions, and
veterinary practice. It uses ultrasonic sound
radiographs must be interpreted in light of
waves in the frequency range of l. 5-15
the entire gestalt of lesions present and not
megai1ertz (MHz) to create images of body
based on any single lesion if multiple
structures based on the pattern of echoes
abnormalities are present. In many cases,
reflected from the tissues and organs being
it is appropriate and advisable to seek the
imaged. Several types of image fonnats can
opinion of a radiologist for interpretation
be displayed. The most familiar one ( and the
of radiographic images, particularly as the
one that creates the actual image of
number of radiographic studies available
anatomy) is B-mode grayscale scfil1ning.

and potential diagnoses proliferate.

The sound bean1 is produced by a transducer placed in contact with and acousti

Contrast Procedures: Radiographic
cally coupled by means of a tra11Smission
exposure of film alone lacks sufficient
gel to the animal. An ultrashort pulse of
contrast to evaluate many structures;
sound is directed into the animal, after
therefore, contrast procedures are used to
which the transducer switches to the
increase the native contrast of organs and
receive mode. Echoes occur as the sound
lesions, to separate them from surrounding
beain changes velocity while passing from
tissues. Contrast media are radiopaque
a tissue of one density to one of another
compounds that have extremely low
density, even when the change occurs at
toxicity, although there are well-recognized
nearly microscopic levels. The greater the
hemodynamic alterations seen after
change in velocity, the greater the strength
administration of IV contrast agents. These
of the echo. A small percentage of these
consist of p1irnarily a refle:,c hypotension
echoes ai·e reflected back to the transducer,
followed by a rebound mild hypertension.

which then reconverts the energy of the

In extreme cases, the hypotension can lead
echoes into electrical impulses recorded by
to vascular collapse and even anaphylaxis.

the computer in the ultrasound machine.

This effect is thought to be primarily

The strength of the echo, the time required
associated with the hypertonic nature of
for the echo to return after the pulse, and
ionic contrast agents and is markedly less
the direction the sound bean1 that was sent
evident when nonionic agents are used. For
are all recorded. Using information from
this reason, nonionic agents have almost
multiple echoes, the machine.creates an
completely replaced the ionic agents as
image that represents the appearance of the

IV contrast material. IV and intra-arterial
tissues when cut in the same plane on an
contrast agents are generally iodine based
anatomic specimen. In modem scaiming
and increase the opacity of the blood,
systems, the sound beam is swept through
making vascular structures visible.

the body many tin1es per second, producing

Iodinated contrast agents are cleared
a dynamic, real-time image that changes as
primarily by the kidneys, making the collectthe tra11Sducer is moved across the body.

ing system of the urinary tract visible. Orally This real-time image is easier to interpret administered agents, primarily baiium
and allows the examiner to scan continusulfate-based compounds, outline the ously until a satisfactory in1age is obtained.

mucosa and lumen of the GI tract.

The image may then be frozen and recorded

Intrathecal contrast agents are also iodine
in a digital fom1at, which also allows for
based and allow evaluation of the spinal
recording of short segments of the real-time
cord and meninges. Many of these contrast
scan. As for radiography and all other
procedures have been largely supplanted by
medical imaging systems, the stai1dard,
modem imaging procedures, but many of
accepted, legal fonnat for digital images is
them are still the best way to image the
the DI COM Ill standard.

DIAGNOSTIC IMAGING

1633

Ultrasonography carmot be used to scan
yields information not available from standgas-filled or bony tissues. The sound beam is ard radiographic evaluation. Of course, totally reflected at soft tissue/gas interfaces
ultrasound carmot be used to evaluate the
and absorbed at soft tissue/bone interfaces.

bones themselves, so the two inrnging

Gas and bone also "shadow" any other
methods are complementary. In small
organs beyond them. Bowel gas can inhibit
animals, soft-tissue lesions of the liga

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imaging of adjacent abdominal organs, and
ments, tendons, joint capsule, and articular
the heart must be imaged from locations
cartilage of the shoulder and stifle joints
that do not require the sound bean1 to pass
are readily detectable by an experienced
through the lungs.

examiner. Mostjoints and muscles can

Sonographic imaging is also limited in
be evaluated by ultrasonography if the
regard to the depth of tissue that can be
operator is familiar with the normal
examined. Most scarmers will display
anatomy and the manner in which
tissues to a depth of -24 cm, but the image
pathology of those structures is manifest
is often quite noisy at that depth. This is
on the image.

because most tissue echoes do not return

Changes in the size and shape of organs,
directly to the transducer but are reflected
tissues, and structures are evident in most
in some other direction. By a depth of 24
cases, but evaluation of the echo pattern
cm, the loss of energy from the sound beam
is based on comparison with that of other
results in echoes so weak that the scarmer
organs and tissues the examiner has
carmot separate the returning echoes from
scarmed in other ani.n1als. The person
the background electronic noise. In
evaluating the scan must have a firm idea,
addition, some echoes that are not directly
developed from experience and comparireflected may return to the transducer by son with known normals, of the nonnal
reflection from a tissue outside the bean1
echo pattern for each organ scarmed with
path. Such echoes require longer to return
each transducer. The echo pattern will
to tl1e transducer and are depicted at a
change between transducers because of
spurious location, adding noise to the
changes in axial and transaxial resolution
image. Low-frequency transducers can scan
as well as transducer design. Comparison
deeper tl1an high-frequency transducers,
of the echogenicity of several tissues must
but resolution is decreased. There is much
be made, because any organ may have
less loss of bean1 intensity in fluid media
increases or decreases in the echogenicity
such as the urinary bladder, so if the bean1
of its parenchyma. Diseased organs may be
passes through such a fluid media, the
either uniformly altered in echogenicity or
maximum scarming depth may be increased
exhibit focal or multifocal changes. Focal
at the expense of temporal resolution.

changes are usually easier to detect than

Although ultrasound can be used to
uniform changes. Sonographic lesions are
evaluate most soft tissues, the heart and
sometimes quite characte1istic of a given'

abdominal organs still constitute the
disease process, but more often the
majority of examinations performed in
changes are nonspecific. Although
small animals. In scanning of the abdoultrasonography can be quite sensitive to men, the abdominal structures should be
detection of disease, the changes are not
systematically evaluated. Each sonograspecific for a given disease in most cases pher develops his or her own system of
unless a characteristic change in anatomic
completely evaluating the abdomen.

presentation is detected along with

Systematic evaluation ensures that all
changes in echogenicity.

structures are scanned. In the past, organs

Ultrasound technology has improved the
such as the adrenal glands and pancreas
ability of sonographic exal11i.nations to
were seen only if diseased and enlarged,
detect diseases previously not well
but modern ultrasound machines operated
characterized by sonographic evaluation.

by an experienced sonographer produce

Pancreatitis is a primary example, and in the
images of such quality that the normal
past 10 years, sonographic evaluation of the
adrenal glands, pancreas, and lymph nodes pancreas has become a mainstay of can be imaged.

assessing animals with suspected pancre

Ultrasonography also is widely used to
atic disease. However, it does not always
evaluate the soft tissues of the musculoagree with clinical pathologic evaluation or skeletal system. In Equidae, ultrasound is
physical examination. In some cases, the
used to detect and evaluate the presence of
physical examination and pathologic data
tears in the tendons and ligaments of the
will suggest pancreatitis, but it is not
legs. Examination of joints and the margins
detected on sonographic examination. This
of bones around the joints in both large and
is probably due to the great difficulty of
small animals is also widely performed and
interrogating the entire pancreas using

1634

DIAGNOSTIC IMAGING
ultrasound. In other cases, chronic
and add additional inforn1ation, such as
pancreatitis may be indicated by the
shape of the chan1ber.

sonographic examination but poorly

Ultrasonographic images are also used
characterized by clinical pathologic data
to acquire quantitative infonnation about

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because of the chronic status of the disease.

cardiac function. Measurement of specified

Cushing disease is also frequently difficttlt
parameters may be made on either the
to interpret on the basis of sonographic

M-mode scan or on the two-dimensional
examination or any other in1aging modality

B-mode in1age. Mathematical formulas are
because of the problems of benign
then applied to determine values for cardiac
adenomas that have no clinical significance
output, ventricular contractility, ejection
in the adrenal glands and because in true
fraction, ventricular wall stiffness, and

Cushing disease the adrenal glands are
other cardiac functions.

being overdriven by a pituitary adenoma

Doppler ultrasound makes use of the
and are not themselves structurally
familiar phenomenon that sound emitted
abnorn1al. Other instances of increased
from a moving object such as a train has a
usage of ultrasound are in the evaluation
different apparent frequency to someone
of other soft tissues such as muscle and
standing still relative to the moving object.

tendon injuries as well as cartilage injuries

If the object is moving away from the
in various joints such as the shoulder and
observer, the frequency of the sound is
stifle.

lower; conversely, if the emitter is moving

Ultrasonography can also be used to
toward the observer, the frequency of the
direct biopsy instrnments to acquire tissue
sound is higher. The same is true of
for a specific pathologic diagnosis. This
diagnostic ultrasound. Echoes from moving
obviates the need for an open surgical

RBCs change the frequency of the sound
exploration in many cases. Lesions buried
reflected back to the transducer. The
within large organs such as the liver and
amount by which the frequency is shifted is
kidneys that might not be detectable at
proportional to the velocity of the RBCs;
surgery may be detected and biopsied with
whether it is a positive or negative
ultrasonographic guidance. Presurgical
frequency shift is used to determine blood
diagnosis pennits more thorough and
flow direction. This is used to identify
specific planning of surgical procedures and valvular regurgitation (insufficiency), presurgical treatment of lesions. These
increased flow velocity (as in stenosis), or
procedures can frequently be safely
abnormal movement of the blood in the
perforn1ed under heavy sedation and
heart or vessels elsewhere in the body.

analgesia. Ultrasound-guided biopsy and

Doppler signals may be displayed in two
aspiration of lesions can also be performed
forn1ats. In the first, spectral Doppler, a
in large animals without the need for
sow1d beam is used to evaluate a specific
general anesthesia.

small volun1e within the vessel of interest.

This display resembles the M-mode display

Echocardiography: Echoca.rdiography
except that the frequency shift, or velocity,
is ultrasonic evaluation of the heart. In the
is substituted on the y-axis. It also shares
past, it was done using the M-mode format
high temporal resolution capabilities of the
of displaying ultrasound infonnation. A

M-mode fonnat. The second way to display
narrow beam of sound is projected into the

Doppler frequency shifts is to select a larger
heart, and the echo pattern and strength are
area of the scan and a real time B-mode
displayed onto a persistence screen with the image, encoding the velocities and direction x-axis of the display representing time
as a color spectrwn. The color ( usually red

(y-axis is depth), sin1ilar to the fan1iliar
or blue) depicts blood flow direction, and
fonnat of an ECG. The pattern and
the hue depicts mean flow velocity. This
amplitude of movement of the walls of the
allows evaluation of larger areas, but at the
chambers of the heart and valves can be
price of lower temporal resolution. For this
evaluated, as well as the size of the
reason, color-encoded B-mode flow studies
respective structures along the path of the
are used to guide placement of spectral
sound beam. The M-mode format has very
sample volwnes to acquire more accurate
high temporal resolution and thus is
and complete information. Thus, Doppler
especially excluded to evaluation of rapidly
studies complement and in1prove the
moving structures such as heart valve
accuracy and specificity of echocardioleaflets. Considerable experience is grams. Quantitative evaluation of spectral
required to obtain and interpret diagnostic

Doppler studies also allows the examiner to
studies. The M-mode examination has been
determine values such as pressure gradients
coupled with real-time B-mode studies to
across valves and stenotic areas or
improve the accuracy of beam placement
resistance to flow of blood entering an

DIAGNOSTIC IMAGING

1635
organ. In some cases, abnom1al blood flow
a slice, and each of the individual attenuapatterns can be detected before obvious tion points in the image is referred to as a
anatomic lesions are present.

voxel (volume element). The animal is then
moved a specified nwnber of millimeters,

Contrast Ultrasonography: Ultrasound
and the process repeated. By sequentially

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contrast agents increase the reflectivity of
scanning a body area, the entire volume of
blood and any tissue through which blood
interest can be imaged without any superimflows. Enhancement of blood reflectivity is position of structures. CT also has much
usually accomplished by ir\jection or
better contrast discrimination than
formation of transient microscopic bubbles
standard radiographs, so structures such as
in the plasma. The increase in echogenicity
individual parts of the brain or individual
is related to the amount of blood flowing
muscle bellies are seen as separate and
through the tissue. The bubbles are quickly
distinct on the CT scan. X-ray contrast
absorbed into the plasma and therefore do
media is frequently used to further enhance
not constitute an embolism hazard. The
the contrast between structures and help
ability to evaluate the vascularity of a tissue
characterize lesions.

provides additional information about the

Modern multislice CT scarmers can
type of lesion present. For instance,
acquire up to 620 cross-sectional images at
granulomas generally have poorer blood
once; each rotation may be as sho1t as\;,\
flow than normal tissue and do not enhance
sec. These systems are capable of continuas much as the sun-ounding tissue, whereas ous rotation (helical or spiral scanning), in
tumors may enhance more and retain the
which motion of the patient through the
contrast for a longer time than the surroundscarmer occurs in concert with the rotation ing tissue. Contrast agents hold great
of the scarmer. These systems can perform a
promise for improving both the sensitivity
complete scan of the abdomen or thorax in
and specificity of ultrasonographic
a person on a single breath hold ( -10 sec)

examinations. However, they are extremely
and with appropriate ECG-based control
expensive, which precludes their use in all
can provide CT images of a beating heart
but special instances or funded research.

during all p01tions of the cardiac cycle. The
image reconstruction time is short, and the

COMPUTED TOMOGRAPHY
entire study can be completed in less tin1e
than was required to acquire a single in1age

In computed tomography (CT), an x-ray

15 years ago. Some veterinary practices
tube moves arotmd the body and continunow have 8- to 64-slice scarmers installed, ously projects a thin fan of x-rays through
and the actual scan takes less tin1e than it
the body. Electronic detectors opposite the
takes to position the animal on the scanning
tube continuously monitor the nw11ber of
table. Even with such extraordinarily fast
x-rays passing through the body and the
systems, veterinary patients must still be
angle at which the beam is being projected.

anesthetized and in1rnobilized to perfon11

The number of x-rays reaching the detector
most studies, but the period of anesthesia
changes as the beam passes through
is short and the value of the inforn1ation
different tissues because of the tube
derived is great. Although studies have been
movement. A computer mathematically
published in which fully awake or minin1ally
evaluates the data and detem1ines the most
sedated anin1als were in1aged, scans
probable density of any point within the
performed in this marmer lack controlled
volW11e of tissue scarmed. The density is
positioning and reflect movement and are
generally measured in terms of HoW1sfield
therefore difficult to interpret. This type of
units, which divide the entire spectrum of
study should be reserved for instances in
possible densities into 4,000 levels
which the animal is severely obtunded by its
extending from a value of-1,000 to +3,000.

medical condition or for the rare instances

Air is considered to have a value of-1,000,
in which sedation would significantly alter
water is at 0, and lead or some other heavy
the status of the tissues ( such as an attempt
metal is at +3,000. Because these units
to evaluate the effect of drug intervention in
represent the degree to which the x-ray
an asthmatic cat).

bean1 is attenuated, the in1age generated is

As with conventional radiography, the use
really an attenuation map, which is what is
of nonionic contrast agents can markedly
displayed on the monitor and stored as a
improve tl1e diagnostic accuracy and
digital file by the computer. Together, all of
sensitivity of CT. For vascular studies, the
the attenuation points make an image of the
contrast dosage is also substantially less
cross-section of the portion of the body
than that used in conventional radiographic
through which the beam is passed. This
angiography. The utility of contrast
tomographic image is usually referred to as
enhancement on CT imaging is so in1portant

1636

DIAGNOSTIC IMAGING
that nearly all CT studies of soft-tissue
in1age-guided treatment obviates the need
structures such as the brain or abdominal
for a surgical procedure, reducing the
organs are contrast enhanced. Obtaining a
in1pact of treatment on the patient.

contrast-enhanced image after a nonen

CT scans are used to detect structw-al
hanced study allows comparison of the two
changes deep within the body, including
images to give insights into the hemodytwnors, abscesses, vascular abnormalities, VetBooks.ir
nan1ic and physiologic changes present.

occult fractures, and hematomas. Modern,

Modem reconstruction algorithms also
high-speed scanners are also used to
allow three-dimensional reconstruction of
evaluate dynamic physiologic processes
structures with a given density. Bones can
such as blood flow, changes in respiratmy
be depicted without the overlying soft
volwne, and intestinal dynamics. The
tissues, and vascular structures that have
radiologist must have a fin11 knowledge of
been contrast enhanced can be depicted
anatomy and physiology to ascertain the
without any overlying tissues. Newer
identity of structures in any plane through
scanners can produce images of vessels
the body and evaluate changes in its
that rival those obtained by conventional
anatomy or physiology. Knowledge of
contrast angiography.

physiology and artifacts are also important

In addition to some of the imaging
in evaluating CT scans. Extensive experiprocedures w1ique to CT, this modality is ence and training are required to become
replacing conventional radiography for
adept in perforn1ing CT procedw-es and
evaluation of some structures and diseases detiving the most infonnation from the traditionally assessed by radiography. CT
images. As the utility and availability of
scans of the skull in any species are far
scanners has increased, veterinary medicine
more informative and diagnostic than
has seen a great jump in the nwnber and
any conventional radiograph because
quality of instrwnents available for use in
the complex anatomy of the skull, which
veterinary patients.

results in a pattern of overlying structures
on a radiograph, is vastly simplified on

MAGNETIC RESONANCE
a CT scan, making the diagnosis much
more specific and accurate and improving

IMAGING
treatment results. CT scanning is also

Magnetic resonance in1aging (MRI) is the
rapidly replacing myelography for
newest forn1 of imaging in general use
evaluation of spinal cord disease because
today. In this imaging modality, a powerful
of its greater safety and speed as well as
magnet, up to 60,000 times as strong as the
being able to directly image the discs and
magnetic field of the earth, is used to
ve1tebrae. CT scanning is also receiving
transiently align the hydrogen atoms in the
much attention as a �creening procedure to
body with the magnetic field. All atoms
evaluate the lungs and other anatomic areas
with odd atomic numbers are affected, but
for evidence of distant metastasis in cancer
the effect on hydrogen overshadows the
patients. Metastatic lesions in the lung are
effect on other natural elements within the
far more evident at a smaller size on CT
body. If the hydrogen atoms are then
scans than on conventionaJradiographs. If
subjected to a radiofrequency (RF) pulse
a CT scan is perforn1ed after detection of
of the proper frequency, the alignment of
metastatic lesions on radiographs, the CT
these atoms is then deflected to one side
scan will almost always find more nodules
or reversed. Once the RF pulse is turned
than are evident on the radiographic images. off, the hydrogen atoms realign with the CT scans of the feet and legs of horses
magnetic field. The rate at which they do
can detect structural changes in bones and
this is restticted by ( and characteristic of)

hoof structures that are not readily evident
the molecule of which they are a part.

on even detailed radiographic images of the

During this relaxation or realignment
san1e body part. Unfortunately, no scanners
phase, the hydrogen atoms emit radio
currently can scan the abdomen or thorax in waves that can be detected by highly adult horses.

sensitive equipment. The frequency of

CT is also used to guide the acquisition
these waves depends on the strength of
of biopsy and aspirate of samples from
the magnetic field. By using a second set
many areas of the body, including the lungs
of magnets referred to as the gradients,
and brain, that cannot be approached using
the magnetic field of the scanner can be
ultrasow1d or other in1aging modalities.

arranged in such a way that each small

The san1e type of approach may be used to
discrete volume (voxel) has a different
perforn1 in1age-guided therapy of some
field strength. Because the RF emitted by
diseases such as radiofrequency ablation
the relaxing hydrogen atoms depends on
of twnor nodules in the liver. Such
the strength of the magnetic field in which

DIAGNOSTIC IMAGING

1637
it is located, each of these volumes can be
presence of even a single such pellet may
represented by a unique frequency. Then,
totally degrade the images. Another
by evaluating the signal strength and
potential source of such artifacts could
duration for each frequency, the chemical
be stainless steel sutures or hemoclips.

composition of each voxel can be

Depending on their chemical composition,

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estimated. In practice this is done by
such materials may or may not significantly
representing the signal strengths for each
alter the images.

volume on a monitor, much as is done with

MRI interpretation requires a finn

CT. The signal strength from each volume
knowledge of sectional anatomy as well as
element is very small, so many repetitions
knowledge of the physics of the imaging
or pulses of the RF field are required to
system. Because this type of imaging is
provide a statistically significant
based on chemical composition of the body
determination of the relative signal
rather than density, it provides exquisite
strength from the volume elements. Thus,
detail and contrast of body structures.

each scanning sequence may require

However, the duration of data acquisition
several minutes to perform. Sequential
limits its use in areas of substantial
examination of slices through the body is
movement, such as the chest and upper
done the same way CT exan1inations are
abdomen, although recent improvement in
performed. MRI differs from CT in that the
scanner technology has largely done away
data for all the slices in the volume being
with this limitation. MRI does not image
imaged are acquired simultaneously;
cortical bone well and therefore is of
however, previously only one set of planes
limited use in the evaluation of bony
is acquired at a tin1e, but recent developlesions, although it is quite applicable to ments in scanner technology allow
imaging of bone marrow and cartilage. Like
acquisition of volume data sets. Scans are

CT, MRI was initially used primarily for
typically acquired in more than one of the
neuroimaging and is still the mainstay of
three orthogonal planes, with different
imaging in that area. Another major area of
magnet pulsing sequences to highlight

MRI usage is in evaluation of blood vessels
different types of tissue. Also, unlike CT, deep within the body, particularly those of

MRI scans are seldom reformatted to
the legs, neck, and head. Because of its
project oblique planes, although threeexquisite sensitivity to the changes in dimensional rendering may be done either
tissue organization and composition as
on the scanner's computer or a standwell as density, MRI is also used frequently alone workstation.

for joint and muscle imaging, where it has

MRI does not use ionizing radiation and
become a valuable tool in assessment of
thus has gained rapid and wide use in
joint integrity because of its unique ability
pediatric imaging in human medicine.

to image cartilage and ligaments. This has

Although this is less of a concern in
led to great interest in developing and
veterinary medicine, the ability to obtain
promoting MRI in1aging of equine
diagnostic images without the use of
extremities if the issue of motion can be
ionizing radiation is desirable for veterinary
overcome.

personnel.

Contrast enhancement of MRI scans is

MRI scanners are extremely sensitive to
common when imaging the brain and other
the presence of certain metals such as iron
soft tissues. It can frequently permit the
and cobalt. The presence of such materials
radiologist to make a relatively specific
within the patient can markedly degrade
diagnosis regarding the etiology of
the quality of the image, even to the point
the lesions seen on the scan. In other
that it is not possible to develop an image at instances, the contrast images are the only all. Although surgical stainless steel now in
ones that reveal the presence of a lesion.

use has minimal ferromagnetic properties,

The agents used are specifically designed
it can still distort the in1age somewhat.

for use in MRI and are different from those

Even the small amount of iron present in
used in CT and radiography.

identity chips can produce significant

In the past, MRI systems were large and
artifacts on the images. For this reason,
expensive to purchase, install, and
animals to be subjected to MRI scanning
maintain, but many smaller, low-fieldshould have radiographs of the area of strength magnets are available, including
interest before being placed in the MRI
some specifically designed for use in
scanner. The presence of metallic foreign
veterinary medicine. Dedicated equine
material in the GI tract or soft tissues can
extremity scanners are available, and
easily result in a nondiagnostic study. An
although these instruments are relaexquisite example of this is the presence tively expensive, they are within financial
of a steel shotgun or BB gun pellets; the
reach of many large practices, especially

1638

DIAGNOSTIC IMAGING
those specializing in imaging and neurology.

NUCLEAR MEDICINE IMAGING

The use of lower field strengths will reduce
the construction requirements of MRI

(Nuclear scintigraphy)

facilities to house these instruments but
comes at the price of longer scan tin1es and

Although it has been around for >50 yr,

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decreased image resolution.

nuclear scintigraphy is still relatively
unused in veterinary medicine. The reason

The length of time required to complete
is because it uses radionuclides, which are

MRI scans and the exquisite sensitivity of
both expensive and heavily regulated. In

MRI to motion dictates that studies be
perfonned under general anesthesia.

addition, the images derived from the

Because powerful magnets are used,
studies are physiologic in nature and
tllerefore quite unfamiliar to most
ferromagnetic material may not be brought
into the room because of safety consideraveterinarians. This is unfortunate, because nuclear scintigraphy provides information
tions. For veterinary patients, injectable
on pathologic and physiologic processes
anesthesia may be used if special
that cannot be obtained by other means.

anesthesia machines, oxygen tanks, and

Nuclear medicine imaging involves
monitoring equipment are unavailable.

dosing the patient with a very small amotmt

Injectable anesthesia may not be appropriate for all patients, so facilities dedicated of a gamma ray-emitting radioisotope. The
location and distribution of the radioisotope
to veterinary patients are well advised to
have appropriate anesthetic equipment.

within the body is tllen detected with a

The cost of such equipment is minor
ganm1a camera, a device specifically
compared with that of developing the MRI
designed to collimate and detect gan1ma
rays. The isotope may be injected, ingested,
facility itself.

Because of their exquisite sensitivity to
or inllaled as appropriate for the study being
perfonned. The radioisotope is usually part
radiofrequency signals, MRI systems must
of a larger molecule that has a specific
be shielded from all extraneous signals
of this type. This requires installation of
affinity for the tissue or organ of interest.

For instance, some organic phosphonates
specialized shielding material in the walls
of the room in which the MRI is located.

have an affinity for bone, and isotopes
bound to sulfur colloids will localize in tile

Further, the larger, more advanced systems
liver and spleen. Very few radioisotopes
with higher field strength typically require
have direct affinity for a given tissue; iodine
liquid helium as a coolant to mininlize signal is the notable exception and localizes very noise from within the machine itself and to
strongly in the thyroid. Inllaled gases or
maintain a superconductive magnetic field.

The construction of an MRI facility must be
aerosols localize in the airways and lungs
and may or may not be absorbed into the
done under the direction of a qualified
bloodstream. In veterinary medicine, tile
architect and engineering' finn.

most conunonly used isotope is metastable

MRI scanners should be operated by
technologists specially trained in operation
technetiun1 99 (99111Tc), although radioactive of these instrun1ents. Many factors must
iodine, indium, and thallium are also used in
be taken into account when preparing an
specific instances.

anin1al for an MRI. This training is not part

The data collected by tl1e gamma camera
of either the veterinary curriculum or the
can be displayed directly on a monitor or
veterinary technical curriculum and must
projected onto a film or a digital file as a
be acquired by attending special training
pe1manent record. Most modem systems
sessions or preferably as part of the training
send the data to a computer system for
program in a school of radiologic technolanalysis, which allows enhancement of ogy. Having well-trained technologists to
count differences and detennination of
perform these studies will greatly in1prove
organ margins. The operator can select
the quality of tile scans and promote the use
regions of interest to analyze for isotope
of these instrun1ents for a wider variety of
content and rate for accumulation over
time. When the study uses a radiophaimaimaging applications.

Because of the expense of acquiring and
ceutical that is metabolized or has a limited
maintaining these instruments ( especially
residence time in an organ, organ function
those with field strength of 1 Tesla or
can be detennined. These dynainic studies
above), the technical complexity of MRI
can be used to evaluate tile function of
organs such as the lungs, kidneys, and heart.

in1aging, and the special training and
experience required to interpret tile in1ages,

Such studies may reveal abnormalities tllat

MRI scanning systems are generally found
static forms of anatomic imaging cannot
only in large private and academic referral
detect. Functional in1aging is tile great
specialty practices.

strength of nuclear medicine and allows
disease detection earlier and more readily

DISPOSAL OF CARCASSES AND DISINFECTION OF PREMISES

1639
than anatomic imaging systems. Advanced
sensitive and can often define the presence

MRI studies can emulate this functional
of or characterize the extent of some
aspect of scintigraphic imaging in some
disease processes long before they can be
cases, but those systems are much more
evaluated by anatomic imaging systems
limited in scope and availability, as well as
such as MRI or CT. When these images are

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costing an order of magnitude more.

combined with CT or MRI images,

Single photon emission computed
tremendous sensitivity for the detection
tomography (SPECT) and positron
of numerous diseases results.

emission tomography (PET) are advanced

The major issue with using nuclear
scintigraphic imaging techniques widely
medicine imaging in veterinary medicine is
used in human medicine for detection and
not the availability of ga.nuna can1eras or the
evaluation of many diseases. In both of
technical expertise required to operate
these techniques, a CT-like cross-sectional
them. Cameras are readily available on the
image based on the deposition of radionuused market, and training of teclmologists clides within the body is generated. Such
to operate them is not prohibitively
images have greater sensitivity than planar
complex. Rather, it is the regulations
inrnges and improved specificity as well.

surrotmding the acquisition and use of

PET imaging in particular has seen
radiopharmaceuticals. All use must be
tremendous growth in the last decade and
strictly docwnented and, wilike in human
is routinely used in the staging and
medicine, the veterinary patient generally
evaluation of many diseases, especially
must remain in the hospital after the study is
cancer. This technology, which is based on
perfonned to allow the agents to be mostly
the use of positron-emitting isotopes of
cleared from the body. A second reason for
lighter elements such as oxygen, nitrogen,
limited use is the physiologic nature of the
carbon, and fluorine, can evaluate the
lesions, which results in images of poor
metabolism and localization of these
spatial resolution even tl10ugh they are
elements with great sensitivity. PET
exquisitely sensitive to some disease
imaging is available at most academic
processes. The special training required for
centers, and its use exceeds that of
interpretation of tl1ese inrnges is provided as
traditional nuclear scintigraphy in some
part of a veterinary radiology residency
centers. These instruments are extremely
program available at only a few centers.

DISPOSAL OF CARCASSES AND

DISINFECTION OF PREMISES

When animals die or are slaughtered on

As general precautions, persons handling
farms, carcasses and parts that are u.n.fit for
carcasses and disinfectants should wear
use as food should be disposed of properly.

protective clothing and be properly

Safe and enviroru11entally responsible
equipped to complete the tasks of disposidisposal of animal carcasses, whether an tion and disinfection. The method of
individual death or during significant
disposal should preclude contan1ination of
mortality events, is an essential considerasoil, air, and water. Hides and other paits of tion. Premises should be promptly cleaned
a11imals that have succumbed to infectious
in a rnaru1er that prevents any infectious or
diseases or toxins should be safely disposed
toxic health hazard to domestic or wild
of a11d not retained for use.

animals or people. Information on the safe

There are restrictions on carcass
and lawful disposal of carcasses can be
disposal for cattle ;,,30 mo old because of
obtained from local envirorunental
specified risk materials (tissues in which
protection agencies. When the circumprions that cause bovine spongiform stances W1der which death has occw-red
encephalopathy [BSE] rnrH.:entrate).

suggest a transmissible disease or toxic

Sheep or cattle diagnosed with or
hazard, the nearest animal health official
suspected of being affected by scrapie (see
should be notified immediately.

p 1288) or BSE (seep 1284), respectively,

1640

DISPOSAL OF CARCASSES AND DISINFECTION OF PREMISES
must not be rendered. The preferred means
considered only when burial is not feasible.

of disposal for these animals is incinera

The bum site should be away from public
tion, although they may also be buried
view and on flat, open ground that is clear of

(see below).

buildings, hay or straw stacks, overhead
cables, and shallow underground pipes or

Rendering: Ordinarily, rendering is a safe,
cables. Locations upwind from houses, farm

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rapid, and economical method of disposal
buildings, roads, or populated areas, and
of carcasses. Renderers are required to use
those from which precipitation runoff may
equipment and methods that prevent health
contaminate the environment, should be
hazards. Local regulations specify
avoided.

requirements for transportation of

Carcasses must be placed on a quantity of
carcasses to rendering plants. During
combustible supporting materials sufficient
transportation, biosecurity must be
to reduce them completely to ashes. The
considered to avoid spreading infectious
material must also be arranged in a manner
agents into the environment.

to permit an adequate flow of air to the fire.

Gasoline or other highly volatile combusti

Burial: When a site acceptable to the
ble liquids should not be used.

local environmental protection agency is

To prepare the fire bed, an area of ground
available, burial is usually the preferred
should be staked out to accommodate the
method of disposal. In selecting a burial
nun1ber of carcasses to be burned: 8 x 3 ft
site, it is necessary to consider the
for each mature cow or horse, 5 mature pigs
adequacy of soil depth and to avoid
or sheep, 100 mature chickens, or 40 mature
underground electrical cables, water
turkeys. The fire bed bums best if at a right
pipes, gas pipes, septic tanks, and water
angle to the prevailing wind.

wells. The prevention of secondary

Under favorable conditions, burning
toxicosis or exposure to infectious agents
should be complete in 48 hr. Additional
to scavengers or groundwater must be
combustible material should be added
considered ( eg, the burial of a carcass
as needed. When the fire has died out,
infected with blastomycosis could
the ashes should be buried and the area
potentially contaminate the soil thereafcleaned, graded or plowed, and prepared ter). The burial pit or trench should be at
for seeding.

least 2.3 m wide and 3 m deep (7 x 9 ft).

The pit is a cave-in hazard and must not be

Other Disposal Methods: Composting,
entered without proper shoring, and any
fermentation, and dry extrusion methods
other appropriate precautions should be
have been developed to process certain
taken. At this depth, 1.3 m2 (15 ft2) offloor
dead aninlals and animal waste, destroy
space will accommodate a mature bovine
pathogenic organisms, reduce volume, and
or equine carcass, 5 mature pigs or sheep,
produce feedstuffs. Local environmental

100 mature chickens, or 40 mature turkeys. protection agencies and state agriculture For each additional meter (3 ft) in depth,
departments should be consulted concernthe number of animals per 1.3 m2 of floor ing the acceptability of these and other
space may be doubled. Conttlminated
possible alternative disposal methods.

litter, soil, manure, feed, milk, or other
material should be placed in the pit with

Disinfection of Premises: Removal and
the carcasses and covered with at least 2 m safe disposal of manure, feed, and debris by (6 ft) of soil. The covering soil should not
burial or burning, followed by thorough
be compacted. Decomposition and gas
scraping and cleaning of all buildings and
formation cause cracking, bubbling, and
equipment, must precede the application
leaking of fluids from a compacted burial
of chemical disinfectant. Except for steam
site. The soil should be mounded and
cleaning, cleaning with aqueous solutions is
neatly graded.

practical only at temperatures above
freezing. A cleaning agent such as trisodium

Burning: Burning in an incinerator that
phosphate or sodiwn carbonate dissolved in
is operated in compliance with local laws
hot water will facilitate cleaning. All traces
and ordinances is an excellent means to
of the cleaning agent must be rinsed away
dispose of one or a few carcasses and is the
with clear water before disinfectant is
preferred means for sheep with scrapie and
applied. Provision must be made to contain
cattle with BSE.

and safely dispose of cleaning solutions,

Burning carcasses in an open site should
rinse water, and disinfectant.

be done only when legally pem1itted.

Disinfectants recommended for general

Burning poultry carcasses should be
use on surfaces free of organic matter are

EUTHANASIA

1641
sodium or calcium hypochlorite (1,200 ppm
agents can be obtained from state or federal
available chlorine), iodine, phenol, and
animal health agencies. Disinfectants
quaternary ammonium compounds. Newer
should bear the approval statement of the
disinfectants use a combination of products

Envirorunental Protection Agency in the

( eg, quaternary ammonia and glutaralde

USA or of a similar agency in other
hyde) to enhance efficacy. Infonnation on
countries. Label instructions for application

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disinfectants for specific animal disease
must be followed.

EUTHANASIA

Euthanasia is the term used to describe
human abuse potential; 10) compatibility
ending the life of an animal in a way that
with species, age, and health status; 11)

eliminates or minimizes pain and distress.

ability to maintain equipment in proper

Animal slaughter, depopulation, and
working order; 12) safety for predators or
humane killing are distinguished from
scavengers should the animal's remains be
euthanasia, because they are performed for consumed; 13) legal requirements; and (14) reasons different than sparing an animal
envirorunental impacts of the method or
from unresolvable painful or distressful
disposition of the animal's remains.

conditions. Euthanasia of animals is a

To be able to understand and help others
common procedme performed by
to understand euthanasia, personnel
veterinary professionals, and because of
perf01ming euthanasia should be well
the seriousness of the action, it deserves
informed of established definitions of the
appropriate consideration. Some of the
more important physiologic and psychologimost difficult euthanasia decisions that cal states that may be observed dW'ing
veterinarians are required to make involve
euthanasia. The American Veterinary
the euthanasia of healthy animals when no

Medical Association Panel on Euthanasia
other alternative for their care can be
accepts the following important definitions:

identified. A veterinarian must be fully

1) anesthetic-induced unconsciousness is
prepared to speak frankly about the
the loss of the righting reflex; 2) pain is a
animal's condition and be knowledgeable
conscious experience; 3) distress is an
about all possible alternative care
animal's response to stimuli that interferes
resources when interacting with animal
with its well-being and comfort. Thus,
owners, caretakers, and control profesbiological functions (W'ination, defecation), sionals. Recognizing the importance of a
unintentional movements (limb paddling),

"good death" in the humane termination of
and vocalizations after administration of an
an animal's life, many countries and
appropriate euthanasia method, and
professional organizations have developed
subsequent recwnbency are not necessarily
guidelines and recommendations for
signs of perceived pain or distress. Loss of
animal euthanasia; some are more specific
physiologic function and death should
for certain species and envirorunental
occur in the following order to help prevent
settings. Most recommendations emphafear and distress: l) rapid loss of conscioussize certain factors that personnel ness, 2) loss of motor function, 3) arrest of
perfonning euthanasia should consider
respiratory and cardiac functions, and
when selecting the best method of
finally 4) pennanent loss of brain function.

euthanasia. These factors include: 1) ability lf loss of motor or respiratory and cardiac of the method to induce loss of consciousfunction precedes loss of consciousness, as ness and death with minimal pain and
might be the case if paralytic agents are
distress; 2) time required to induce loss of
used, animals may become fearful and
consciousness; 3) reliability; 4) safety of
experience distress. In some species,
personnel; 5) irreversibility; 6) compatibilparticularly rabbits and chickens, tonic ity with intended animal use and purpose;
immobility may be induced by fear, and care

7) documented emotional effect on
must be taken to not confuse this behavioral
observers or operators; 8) compatibility
response with loss of consciousness.

with subsequent evaluation, examination,

In addition to the selection of the
or use of tissue; 9) drug availability and
method of euthanasia, the euthanasia

1642

EUTHANASIA
administrator should consider the natural
owners, and caretakers have been
behavior of the species. For virtually all
considered.

species, being placed in a novel environ

Regardless of the method of euthanasia
ment before euthanasia is stressful.

selected, personnel perfom1ing euthanasia

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Therefore, a euthanasia approach that
must confom deatl1 and dispose of the
can be applied in familiar surroundings
carcass in a legal manner that does not
may help reduce distress. Gentle
contaminate food sources or the environrestraint, careful handling, and talking ment. Confo-ming death may best be
during euthanasia often have a calming
accomplished by an adjunctive method
effect on animals accustomed to human

(thoracotomy, decapitation) performed
contact. These techniques may also be
after the loss of consciousness. Using an
effective coping strategies with personnel adjunctive method may be especially and owners. In some species, sedation
important when euthanizing ectothem1ic
may assist in achieving the best condianimals, because their heartbeat and tions. The emotional attachment between
respiration are difficult to assess.

animals and their owners or caretakers

For a list of acceptable methods and
requires an additional layer of profesagents for euthanasia of different species of sional respect and care. Discussing
animals, see TABLE 3. The A VMA Guidelines
euthanasia openly with personnel allows
for Euthanasia 2013 provide additional
everyone the opportunity to understand
details, as well as references for specific
that the best interests of the animal,
technical and safety infonnation.

14H•il AGENTS AND METHODS OF EUTHANASIA BY SPECIES

Acceptable Methods with

Species

Acceptable Methodsa

Cond.itionsh

Aquatic

S 6.3c: Immersion in

S 6.3: Adjunctive methods (second
invertebrates
anesthetic solution
step) include 700,f, alcohol and

(magnesium salts, clove
neutral-buffered 10% formalin, pithing,
oil, eugenol, ethanol)

freezing, boiling

Amphibians

S 7.3: As appropriate by

S 7.3: As appropriate by speciesspecies:__injected barbituinhaled anesthetics as specified, C02, rates, dissociative agents,
penetrating captive bolt or fo-earm,
and anesthetics as specified, manually applied blunt force trauma to topical buffered tricaine
the head, rapid freezing
methanesulfonate or
benzocaine hydrochloride

Avian species

S 5: IV barbiturates

S 5: Inhaled anesthetics, C02, CO, N2,

(see ai,so

Ar, cervical dislocation (small birds

Poultry, below)

and poultry), decapitation (small
birds)

S 7.5: Gunshot (free-ranging birds)

Cats

S 1: IV barbiturates, injected S 1: Barbiturates (alternative routes of anesthetic overdose
administration), inhaled anesthetic
overdose, embutrarnide, T-61, coc,

CO{, gunshotc

Cattle

S 3.2: IV barbiturates

S 3.2: Gunshot, penetrating captive
bolt

Dogs

S l: IV barbiturates, irtjected S 1: Barbiturates (alternative routes of anesthetic overdose
administration), inhaled anesthetic
overdose, embutramide, T -61, COC,

CO{, gunshotc

( continued)

EUTHANASIA

1643

•&h•i• AGENTS AND METHODS OF EUTHANASIA BY SPECIES (continued) Acceptable Methods with

Species

Acceptable Methodsa

Conditionsb

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Finfish

S 6.2: Immersion in buffered S 6.2: Eugenol, isoeugenol, clove oil, benzocaine or benzocaine

C02-saturated water (aquarium-fish
hydrochloride, isoflmane,
facilities/fisheries), decapitation/
sevoflurane, metomidate,
cervical transection/manually applied
quinaldine sulfate, buffered blunt force trauma followed by tricaine methanesulfonate,
pithing, rapid chilling followed by

2-phenoxyethanol, irtjected
adjunctive method (aquarium-fish
pentobarbital, rapid chilling facilities), maceration (research ( appropriate zebrafish/
setting)

research setting)

Equids

S 4: IV barbiturates

S 4: Penetrating captive bolt, gunshot

Marine

S 7.4: Injected barbiturates

S 7.4: Inhaled anesthetics (captive)

mammals

(captive)

S 7.6: Gunshot, manually applied blunt
force trauma, implosive decerebration

(free ranging)

Nonhuman

S 2.3, S 7.4: lrtjected

S 2.3, S 7.4: Inhaled anesthetic, CO,
primates
barbiturates or anesthetic

C02 ( as appropriate by species)

overdose

Poultry

S 3.4: Injected barbiturates

S 3.4: C02, CO, N2, Ar, ce1vical dislocaand anesthetic overdose tion ( as anatomically approp1iate ),
decapitation, manual blunt force trawna,
electrocution, gunshot, captive bolt

Rabbits

S 2.4: IV barbiturates

S 2.4: Inhaled anesthetic overdose,

C02, cervical dislocation (as anatomically appropriate), penetrating captive bolt

Reptiles

S 7.3: As appropriate by

S 7.3: As appropriate by speciesspecies-injected barbituinhaled anesthetics as specified, C02, rates, dissociative agents,
penetrating captive bolt or firearm,
and anesthetics as specified; manually applied blunt force trauma topical buffered tricaine
to the head, rapid freezing
methanesulfonate or
benzocaine hydrochloride

Rodents

S 2.2: Irtjected barbiturates

S 2.2: Inhaled anesthetics, C02, CO,
and barbiturate combinatribromoethanol, ethanol, cervical tions, dissociative agent
dislocation, decapitation, focused
combinations
beam microwave irradiation

Small ruminants S 3.2: Irtjected barbiturates

S 3.2: Gunshot, penetrating captive
bolt

Swine

S 3.3: lrtjected barbiturates

S 3.3: C02, CO, N2, Ar, gunshot,
electrocution, nonpenetrating captive
bolt, manually applied blunt force
trauma

Reprinted, with permission, from the AVMA Guidelines on Euthanasia 2013 Edition. Note: Initial "S"

references with associated numbers in table entiies refer to specific areas of more detailed infonnation in the AVMA Guidelines, available at www.avma.org/KB/Policies/Documents/euthanasia.pdf.

• Acceptable methods are those that consistently produce a humane death when used as the sole means of euthanasia.

b Acceptable methods with conditions are those that may reqttire ceitain conditions to be met to consistently produce hmnane death, may have a greater potential for operator etTor or safety hazards, are not well documented in the scientific literature, or may require a secondary method to ensure death.

c Not recommended for routine use.

1644

MEAT INSPECTION

MEAT INSPECTION

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Inspection of meat by qualified individuals
substances that may make the edible
to eliminate unwholesome, adulterated, or
tissues unfit for human food should not be
mislabeled meat or meat products from the
slaughtered for such.

food supply protects consumers from the

Animals that have reacted to a test for
physical, infectious, and toxic hazards that
anaplasmosis, leptospirosis, or tuberculosis
may originate in food animals, the
are unacceptable as food. The temperature
environment, or people. The standard
of bovine tuberculosis reactors should be
procedures do not cover every possibility
taken on premortem inspection.

concerning the acceptability of carcasses,

Animals suspected of having a foreign
organs, or other anin1al parts; personal
disease or parasite should be held and
judgment is also required to ensure that
reported inu11ediately to the nearest federal
only wholesome, unadulterated product is
or state health official.

approved for food. (See also CHEMICAL

Animal welfare and humane slaughter

RESIDUES IN FOOD AND F'IBER, p 2518.)

concerns are increasingly important to the

Inspection activities are divided into
livestock industry. Slaughtering plants in the
premortem, postmmtem, and processing

USA are routinely observed to ensure full
inspection.

compliance with provisions of the Hun1ane

Methods of Slaughter Act of 1978 and

PREMORTEM INSPECTION
related regulations. Hun1ane handling of
livestock before slaughter is necessary and

Premortem inspection is conducted at the
includes methods of stimulation, nonabuse
abattoir on the day of slaughter to detect and by plant workers, provision of food and condemn animals that are unfit for slaughter water, safe pen construction, nonslip floors, and to note signs or lesions of disease that
and protection from adverse weather
may not be apparent after slaughter ( eg,
conditions.

rabies, listeriosis, or heavy metal poisoning).

Most large meat producers require

During inspection, aninlals should be
compliance with humane slaughter
confined in a lighted enclosure so that they
regulations. Therefore, these anin1als must
can be clearly observed at rest and in
be rendered insensible to pain by a single
motion. The aninlals must not be allowed to
blow, gunshot, or an electrical, chemical, or
enter into any area of th.e facility where
other method that is rapid and effective
slaughtering, dressing, or handling of edible
before shackling, hoisting, or cutting.

products is performed until they have been

Recognized ritual slaughter methods,
inspected and found to be acceptable
such as halal and kosher, are exempted
candidates for human consumption. Gates,
from these requirements.

chutes, and equipment must be available
to segregate abnon11al aninlals for closer

POSTMORTEM INSPECTION
exanlination and proper identification.

Seriously crippled animals, animals

Animals should be inspected immediately
commonly termed "downers," and disabled after slaughter and evisceration for or moribund animals are not acceptable
possible changes and lesions that indicate
candidates for slaughter as food. Rectal
unsuitability of the meat for food.

temperatures should be verified on any

Postmortem examination requires
animal suspected of being febrile. Body
observation of all parts of the carcass,
temperature should be <l 06°F ( 41 °C) for
dressing procedures, equipment, and
pigs and <105°F ( 40.5°C) for cattle, sheep,
facilities to prevent contamination of
goats, horses, and mules. Animals with
edible parts. The inspector must ensure
signs or lesions that do not warrant
that condemned carcasses and parts are
immediate condemnation can be identified
disposed of safely. The following are
as "suspects" so that their carcasses and
unacceptable for human food: lactating
viscera can be inspected separately.

mammary glands, laryngeal muscles,

Certain animals may be retained to allow
thyroid glands, and lungs. Brains, cheek
recovery from minor diseases or to permit
meat, and head trimmings from animals
depletion of residues of biologic subthat were stunned by lead, sponge iron, or stances and chemicals. Animals that may
frangible bullets, and carcasses suspected
have been treated with or exposed to
of containing antibiotics, sulfonamides,

MEAT INSPECTION

1645
or other residues are also unacceptable.

Pigs: Head: Exanline head and cervical CNS tissue and spinal cords must be
muscles. Incise mandibular lymph nodes.

discarded to eliminate the threat of

Viscera: Examine and palpate mesenteric
bovine spongiform encephalopathy in
lymph nodes and spleen. Palpate portal
the food supply.

lymph nodes. Exanline dorsal and ventral

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Routine postmortem inspection should
surfaces of the liver. Palpate left and right
include the following procedures.

bronchial and mediastinal lymph nodes.

Cattle: Head: Incise and visually examine Examine and palpate dorsal and ventral
tl1e left and 1ight atlantal, mandibular,
surfaces of the lungs. Examine and palpate
parotid, and suprapharyngeal lymph nodes.

heart. Carcass: Exanline external and

Exanline two incised layers of botil
internal surfaces and incise any suspected
masseter muscles. Exan1ine and palpate
abnormalities. Exanline and palpate
tongue. Viscera: Exanline abdonlinal
kidneys.

viscera and mesenteric lymph nodes.

Poultry: Exanline external surfaces for

Examine and palpate mminoreticular
dressing defects, bruises, and disease
junction. Examine esophagus and spleen.

lesions. Palpate ti.bias for bone diseases.

Incise and exanline anterior, middle, and

Examine internal surfaces, kidneys, and
posterior mediastinal lymph nodes and right lungs in place. Examine viscera and palpate and left bronchial lymph nodes. Exanline
heart, liver, and spleen.

and palpate costal and ventral surfaces of
the lungs. Incise heart from base to apex

Horses: Head: Exanline surfaces.

Palpate, incise, and examine mandibular,
tllrough interventricular septum, and
pharyngeal, and parotid lymph nodes;
examine and cut inner and outer surfaces.

guttural pouches; and tongue. Viscera:

Incise and examine hepatic lymph nodes.

Exanline and palpate lungs and bronchial

Incise bi.le duct in botil directions and
examine contents. Exanline and palpate
and mediastinal lymph nodes, and incise
any suspected abnonnalities. Exan1ine and
dorsal and ventral surfaces and renal
palpate spleen, liver, and portal lymph
impression of liver. Carcass: Exanline
nodes. Incise hepatic duct. Examine remaininternal and external surfaces. Palpate ing viscera. Carcass: Examine internal and
internal iliac and superficial inguinal or
supraman1mary lymph nodes. Exanline
external smfaces. Palpate superficial
inguinal or supra.manm1ary and internal
and palpate diaphragm and kidneys.

iliac lymph nodes. Exanline and palpate

Calves and Veal: Head: Incise and
kidneys and diaphragm. Examine and incise
examine suprapharyngeal lymph nodes.

the internal abdominal walls for possible

Viscera: Examine and palpate bronchial
parasitic cysts. Exanline spinous processes
and rnediastinal lymph nodes, heart, and
of thoracic vertebrae, supraspinous bursa,
lungs. Exanline spleen. Examine and
and first two cervical vertebrae for fistulous
palpate dorsal and ventral surfaces of tile
conditions. Exan1ine axillary and subscapuliver, and palpate hepatic lymph nodes.

lar tissues of white and gray horses for

Exanline abdominal viscera. Carcass:

melanosis.

Examine exposed inner and outer surfaces.

Palpate the kidneys and internal iliac lymph

GENERAL CONDEMNATIONS
nodes.

Livestock clearly showing at premortem

Sheep and Goats: Head and Carcass:

inspection any irreversible disease or

Examine body cavities and outer surfaces.

condition that justifies condemnation as

Palpate back and sides of carcass. Examine
unfit for use as food should be humanely
head, neck, and, shoulders. Palpate
destroyed and disposed of (seep 1639).

prescapular lymph nodes. Exanline and

Carcasses contan1inated by physical,
palpate kidneys. Palpate femoral, popliteal,
infectious, or toxic agents should not be
and superficial inguinal or supra.mammary
approved for use as food. Carcasses with
lymph nodes. Incise lymph nodes when
generalized conditions or diseases,
necessary to exclude caseous lymphadeniincluding cancers, that have so altered the tis. Viscera: Exanline abdonlinal viscera,
normal characteristics of the meat as to
esophagus, mesenteric lymph nodes,
cause it to be inedible or sufficiently
omental fat, and spleen. Exanline bile duct
abnormal to be reasonably considered unfit
and gallbladder and tl1eir contents. Exanline for food should not be approved. Localized and palpate liver and costal and ventral
conditions that do not affect the wholesurfaces of lungs. Palpate bronchial and someness of the entire carcass should be
mediastinal lymph nodes. Exanline and
removed by trimming so that tile remainder
palpate heart.

of the carcass can be used for food.

1646

MEAT INSPECTION

Special Considerations for Tuber
bruising, hemorrhage, or inflammation
culosis: The entire carcass should be
should be readily recognized. Odors from
condemned when there is evidence of tubercontaminating chemicals, fish, urine, or culosis. This includes when an active lesion
other sources are unacceptable. When

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is present; the anin1al is cachectic; a lesion
there is uncertainty about odors, a possible
is present in muscle, intermuscular tissue,
unwholesome odor can be enhanced by
bone, joint, abdominal organs other than the boiling or frying the meat.

GI tract, or in a lymph node associated with

Histologic examination may be used
these parts; extensive lesions are present in
to evaluate abnormalities caused by
the thoracic or abdominal cavity; lesions are physical, infectious, or toxic agents.

multiple, acute, and actively progressive;

Similarly, microbiologic examination may
and the nature or extent of lesions does not
be used to evaluate spoilage and deterindicate localization.

mine the presence of infectious organisms

An organ or part should be condenmed
capable of causing illness in consumers.

when it or its corresponding lymph nodes

Chemical and toxicologic examinations
contain lesions. When lesions in pigs are
should be done when the presence of adullocalized and are found at only one primary terative or toxic substances is suspected.

site of infection, such as the cervical lymph

It may be necessary to increase random
nodes, the unaffected parts are acceptable
microbial testing of meat products to
for food after condemnation of the affected
ensure their freedom from bacterial
organ or part. Even though certain
contamination.

carcasses minin1ally affected with
tuberculosis may be considered safe after
conm1ercial cooking, this procedure is not

ABATIOIR SANITATION
recommended for carcasses that are not
inspected in facilities inspected by federal

Abattoir buildings, equipment, personnel,
or state officials.

and operating procedures should assure
the continued wholesomeness and
freedom from adulteration of carcasses

DETECTION OF UNWHOLESOME
and meat. Floors, walls, and ceilings

MEAT
should be constructed of materials
and in a manner that allows sanitary

Meat for human consun1ption should be
operation and thorough cleaning. An
prepared from anin1als that were healthy
ample supply of hot and cold water and
and have been exsanguinated. Anin1als
cleaning materials should be convenihaving physical, infectious, or toxic agents ently available for slaughtering, cleaning,
that may be hazardous to human health or
and personal hygiene. Water of at least
that are otherwise unwholesome in their

180°F (82°C) should be available to
tissues should not be used for food. Fitness
sanitize equipment and tools after
for food can be detem1ined by a comprehencleaning. Equipment, knives, and utensils sive evaluation that may include chemical,
that have contacted diseased carcasses
histologic, microbiologic, organoleptic, and
should be cleaned and sterilized before
toxicologic examinations.

being used again. Waste-water drainage,

Meat should be examined under light of
with proper trapping and sewage
adequate intensity. Foreign objects on the
disposal, should be adeq1Jate to maintain
surface or visible within the tissue should
the abattoir in a sanitary condition.

be collected for further examination. Items Ventilation should be sufficient to such as feathers, fibers, hair, insect larvae,
assure that edible product areas are
or parasites may provide valuable data on
free of noxious odors. Access of flies,
the species, origin, and handling of the
rodents, and other vermin should be
meat. Color, odor, and texture should be
prevented. Lighting should be maintained
noted. Meat should be fim1, and cut
at an intensity adequate for cleaning and
surfaces should be glossy. Gray or green
inspection. Equipment should be of such
discoloration may indicate bacterial
material and so constructed as to be
action. Dark red meat may result from
readily and thoroughly cleaned and
postmortem retention of blood in animals
should be properly maintained. Separate,
that were not exsanguinated. A stable,
clean containers for edible and inedible
bright red color may indicate the unwholematerials should be provided at convenisome addition of sulfite. Ultraviolet light ent locations. Racks or tables should be
may be used to visualize rodent urine and
provided for heads. Personnel should
fluorescent substances produced by
wear clean garments and follow all
certain spoilage bacteria. Areas of
hygiene and sanitation procedures.

PREPURCHASE EXAMINATION OF HORSES

1647

PREPURCHASE EXAMINATION OF HORSES

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See also THE LAMENESS EXAMINATION, p 1097.

Through requests by the buyer or the buyer's

Prepurchase examinations are often
agent, the seller and/or the seller's veterinai0
requested by a potential buyer of a horse.

iai1 may agree to provide the horse's medical

The objective is to reduce the buyer's risks
history to the exain.ining veterinarian. These
in relationship to the general health and
medical records are returned at the end of
athletic soundness of the horse for sale. The
the examination. The potential examination
examination is not meant to guarantee
and its procedures should be thoroughly
soundness of the horse but is an attempt, on
reviewed with the buyer and seller verbally
the pa.it of the exainining veterinariai1, to
and with written explanato1y documents.

ascertain any preexisting problem or any

W1itten release fonns for riding the horse,
potential problem that may affect future
payment, and the seller's pemlission for any
soundness ( eg, degenerative joint disease).

interventional procedures, such as sedation

The exainining veterinariai1 should have
for radiographs, shoe removal, hair clipping,
experience with the specific breed and
etc, should be obtained before the examinadiscipline, as well as knowledge of the tion. Partial exanlinations should not be
purpose and level of exercise for which the
encouraged. Trial periods are often
horse is being purchased. Ideally, the
acceptable and encouraged, especially if the
examiner should also be aware of any related
seller can be assured of the horse's safety.

organizational regulations that may influence One option is to house the horse in a mutually the prepurchase examination. All notes
known, professionally managed barn. The
generated during the exanlination should be
seller may request that the horse be insured.

kept in the buyer's file, and a report should be

Traditionally, it is recommended that the
generated for the buyer. The examination
exanlining veterinariai1 have had no contact
should be conducted in a thorough and
with the horse or seller in a previous medical
organized maimer, because prepurchase
or personal role. However, this is often not
exanlinations ai·e a common cause of
possible when the horse is being sold witllin
litigation from dissatisfied buyers. The major
a small community or within the saine boardproblems related to litigation are lack of ing barn. In such situations, tl1e relationship
understanding of the prepurchase exai11inaof tile veterinarian to all parties involved tion process and the client's umealistic
should be clearly stated. The opposite
expectation of a secure investment.

situation can occur when the horse is ueing
purchased out of town and the exainining

Pre-examination Issues: At the onset, the
veterinarian is not the routine veterinarian
roles of all involved parties ( eg, buyer, trainer, for the buyer. The exanlining veterinarian legal agent) in the purchase of the particular
may want to have the buyer's routine
horse should be defined. Trainers may or may veterinarian review the exanlination report not have legal agent status. The trainer does
ai1d aiw ancillaiy information, such as
have the potential to be responsible for
radiographs, laboratory tests, etc. Also, if
assessing the buyer's expectations for the
any particular question arises dtuing the
horse's athletic future ai1d also whether the
exai11ination, an opinion from a board-certihorse is suitable for the buyer. If an agent is fied veterinaiy specialist might be indicated.

representing the buyer, the exanlining

If the veterinarian has working knowledge
veterinarian should encourage all infonnaof competition rules related to the discipline tion gathered to be communicated to the
in which the horse is being purchased ( eg,
buyer, along with the report. Buyers of horses height requirements), he or she should have different levels of experience and
explain how these rules may apply to the
practical expectations. The veterinarian
prepurchase exanlination. The veterinarian
should ascertain the particulai· buyer's expecshould counsel the buyer to learn the specific tations and define the limitations of the
mies and verify "cards" that belong to tl1e examination, emphasizing that the exai11inapony or horse. Having the buyer ve1ify any tion does not elinlinate risks.

rule requirements may help reduce future

The buyer is the owner of the information
problems.

but needs to maintain a level of confidential

State and international disease testing
ity so that the reputation of the horse is not
and other requirements should be reviewed
potentially altered because of inappropriate
with the buyer and complied with by the
dissemination of medical information.

exanlining veterinarian. Dmg testing should

1648

PREPURCHASE EXAMINATION OF HORSES
be offered to the buyer and its limitations
infonnation that may or may not have been
discussed. If the horse is purchased at a
known to the buyer, his or her agent, or tl1e
competition, or the seller is not !mown to
examining vete1inarian. A similar questionthe buyer, drug testing should be strongly naire can be devised for the buyer as to his or
recommended. Even when a buyer does not
her expectations, potential use, and previous
wish to have drug testing, exanliners often
experience with tl1e horse in question.

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collect blood at the time of the exanlination

Examples of such forms are readily available
and store the serum or plasma frozen. It
on the lntemet and may be modified as
would then be available if any questions
needed.

arose after the purchase.

Prepurchase exanlinations of perfor

Physical Examination: The examination
mance horses often are conducted under
for a perfonning horse can be divided into
several differenL conditions of training. The
four sections. The first part is observing the
ideal situation is that the horse is currently
horse in the stall. The second includes
active in the particular level of competition
observing the horse on a lead strap at a walk
for which it is being purchased. However,
and a trot on a straight line, doing flexion
prepurchase examinations can involve some
tests, and in a circle with a long line. The
inherent predictability, even though they are
tl'lird part of the exanlination involves
not classically meant for prediction of a
observation of the horse while it is being
horse's health. The following are examples of ridden. The fourth part includes diagnostic conditions an exanliner may face. Any of
procedures such as radiography and
these or other modifying conditions should
ultrasound.

be included in tl1e exanlination notes: 1) A
ln the UK, there is a standardized 5-stage
horse is currently in early training for a
vetting procedure: Stage 1, preliminary
specific athletic endeavor and the buyer is
exan'lination; Stage 2, trotting up in hand;
ultimately looking to have the horse compete Stage 3, strenuous exercise ridden or longed at a higher level. 2) A horse is coming off a
to evaluate conditioning, heait, breathing,
lay-off period and has been back in work for
and strains that might be expressed; Stage 4,
only a brief period of time. 3) An older horse
a period of rest for as long as 30 min to
that has some infirn'lities and is being
evaluate heart and lung recovery, during
purchased as a schoolmaster by a less
which tin1e paperwork such as identificaexperienced rider, in which case the physical tion can be completed; and Stage 5, a
demands will potentially decrease with the
second trot in hand and foot evaluation.

new buyer. 4) A horse is being purchased for

Phase 1 : The key to any successful
a financial investment. 5) A horse is being
prepurchase exanlination is having a
purchased as a pleasure or trail horse for a
systematic, consistent routine. At some
moderate or light workload but the horse's
point during the first part of the exai11inaattitude is extremely important. ln each of tion, a thorough identification of the horse
these conditions, different approaches are
should be recorded. This can be a written
needed, and different questions should be
description of its color and age verification
asked and understood by the exanliner.

with inspection of the teeth. Digital

Examinations of pre training and brood
photographs ai·e easily adapted ai1d helpful
stock present different issues to the
in prepurchase identification. Notations of
examining veterinarian. The examiner must
markings and any other permanent
be alert to potential lin'liting conditions of
peculiarities to tl1e horse's body arn also
the suckling, weanling, or yearling that
beneficial. The most common markings
would diminish its ability to perfonn its
include a star, stripe, blaze, or snip on the
potential future work. ln examining mares
face of the horse. Any white markings on
and stallions, experience witl1 reproductive
the legs should also be described. Other
examination procedures is needed. (See also
markings that are valuable to record include

BREEDING SOUNDNESS EXAMINATION OF THE MARE,
whorls on the face and neck, brands, and
p 2189, and BREEDING SOUNDNESS EXAMINATION OF
tattoos. The presence of any scai·s, splints,

THE MALE, p 2230.) ln all situations, thorough
or joint effusion should be noted. In some
knowledge of the rules of the specific breed
cases, brands or tattoos can give informaand any governmental disease regulations is tion, such as age ( eg, American Jockey Club
critical.

tattoos have an alphabet letter before the
number; "A" represents the years 1971 and

History: The simplest way for tl1e veterin1997, "B" 1998). The date, time, and place arian to accmnulate hi.story before the
of the examination should also be recorexanlination is to have the seller complete ded. The initial part of the exanlination
and sign a history form. This helps to legally
ideally should be done in a stall or area out
bind tl1e seller in tl1e transaction and gives
of direct smilight, dark enough for an

PREPURCHASE EXAMINATION OF RUMINANTS AND SWINE

1649
ophthalmologic examination. Temperature
can be longed. The horse is then monitored
and pulse recordings, auscultation of the
during recovery. Next, the jogging in hand is
heart and lungs, and oral examinations can
repeated so that any subtle lameness iliat
be done in the quiet and controlled confines
might have been accentuated during the
of the stall. It is also worth looking in the
exercise stage can be detected. All

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stall for wood chewing, the character of the
obseivations are duly recorded in the report.

manure and feed, and/or oral medication
remaining in the feed bucket.

Phase 4: The fourth part of the
examination should include any diagnos

Phase 2: The second phase of the
tic procedures necessary to determine
examination outside the stall can begin with
soundness, including radiographs
general body and skin condition. The body

(particularly of the feet, hocks, and
condition score ( 1 -9) can be assigned a
stifles), ultrasonography, and nuclear
nun1ber from thinness (1) to obesity (9).

scans. (See also THE LAMENESS EXAMINATION,

Scores of 4, 5, or 6 are considered nom1al.

p 1097.) Radiography is the most common

Each of the front and hind feet should be
diagnostic procedure performed. A recent
thoroughly examined; mismatching,
retrospective analysis of radiography in
abnormal foot conformations, flares,
equine prepurchase examinations
dishing, type of shoeing, and rings should be
suggests that higher radiographic grades
noted. Photographs that document body

(eg, 2-3) in the navicular bone and distal
condition sc01ing and feet can be part of the
phalanx are associated with lameness,
examination and may sin1plify a written
whereas similar grades in the tarsus were
description. Next, visual obseivation and
less likely to be associated with lameness.

palpation of the limbs, hoof examination

(including hoof testers), passive and active
flexion tests, and watching the horse move

Report of Findings: A summary report
on different surfaces on a straight line and
should be prepared and provided to the
in a circle should be done. It is also valuable
buyer. There are many published samples of
to perfom1 a basic neurologic examination.

iliese reports, available in letter or check-off
list form. The report should describe any

Phase 3: Many examiners feel it is helpful
abnom1al or undesirable findings and include
to watch the horse being ridden to exclude
an opinion as to the functional effect of these
any subtle unsoundness. It also gives the
findings. Tests that were recommended to
examiner some obseivations and insight into but declined by the buyer should be noted in ilie potential of the rider, if it is the buyer.

ilie final report. The American Association of

These obseivations are worth noting, even

Equine Practitioners publishes guidelines for
though it is the trainer's and buyer's responsireproduction, medications, sale issues such bility to deteffi1ine the suitability of ilie
as cryptorchidism, dental malocclusions,.

horse. It is in this portion of the examination
postsale examination of the upper respirailiat ilie British Equine Veterinary Associatory tract of horses intended for racing, radiotion recommends exerting the anin1al at a graph custody, and sale disclosure. Specific
level appropriate for its age and fitness.

guidelines to report prepurchase examina

Having the horse hand gallop for 5--10 min so
tions are also included. The British Equine
the examiner can evaluate breath sounds

Veterinary Association also publishes
and perform cardiac auscultation is
guidelines to conduct a prepurchase
recommended. Young or untrained horses
examination.

PREPURCHASE EXAMINATION OF

RUMINANTS AND SWINE

See also BIOSECURITY, p 2068.

sold or moved to other premises is

The buying and selling of cattle, sheep,
extremely important. The purchaser, ilie
goats, cervids, and swine are critical to the
seller, state and federal anin1al health
continuing vitality of the global livestock
officials, and others engaged in livestock
industry, and tl1e health of anin1als to be
transactions want assurance tl1at the

1650

PREPURCHASE EXAMINATION OF RUMINANTS AND SWINE
animals are healthy and will not introduce
established specific inlpo1tation requiredisease into the new herd or area.

ments in the USA. Global standards for the

Within the USA, every state has specific
movement of animals and animal products
animal health requirements that must be
are developed by the OIE.

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satisfied to legally move an animal into the The chief veterinary official (CVO) for
state. Because these requirements
each country is responsible for protecting
frequently change in response to a state's
the health of the animal populations in that
efforts to protect their animal populations,
country, as well as the public health in the
it is always recommended that the Office of
case of zoonotic diseases. Animal health
the State Vete1inarian in the destination
requirements for the destination cow1try
state be contacted before a move. Animals
can be obtained by contacting the CVO of
that arrive in a state without the proper
that country or more simply by contacting
health certification will likely be quaranthe office of tl1e USDA Area Veterinarian in tined w1til the proper tests and inspections

Charge (AVIC) located in nearly every state.

can be accomplished. In some rare

The AVIC has access to the animal health
instances, the animals may be destroyed
requirements for all foreign destinations.

because of the risk they pose to tl1e state's

Most of the CVI prepared for animals being
animal populations.

shipped to a foreign country must bear the

The state of destination may require
endorsement of the A VIC before the animals
additional statements about the animals in
leave the state of origin. Animals that are
the shipment. These statements, which
not accompanied by the proper docW11entagenerally provide addiLional information tion will be detained or refused at the
about the animals and their origin, are
border or point of debarkation.

added to the body of the certificate of

It is not unusual for an exhibition, sale, or
veterinary inspection (CVI). A pem1it
private treaty agreement to have requirenun1ber may also be required for some ments for animal movement tl1at exceed
species. Collectively, these additional
those of the state or country of destination.

docW11ents provide assurances that the

To detemli.ne tl1ese wlique requirements,
animals meet or exceed tl1e requirements
the host of the event or the buyer of the
o f tl1e state.

aninlal should be contacted.

Because of continuing progress in

The USDA veterinary accreditation
eradication programs for brucellosis,
program facilitates the movement of animals
tuberculosis, and pseudorabies in the USA,
by enlisting private veterinary practitioners.

many states have been declared free of

This system has reduced t11e need for state
these diseases by the USDA. Once a state is
and federal animal healtl1 agencies to
designated as "free," other states may waive provide these essential services to livestock
the requirement for an rndividual animal
producers. The accredited veterinarian is
test for these diseases and will instead
ultimately responsible for the completeness
receive the animals based on the state of
of any docwnent prepared and for certifying
origin's status. If a herd or flock has been
that the animals have been inspected and
declared free of a disease, incl11ding
are not showing signs of infectious,
classification as accredited-free, certifiedcontagious, or conunwlicable diseases.

free, or qualified-free, many states will

In the examination of any animal before
waive an individual animal test for the
sale, several points should be emphasized:

specific disease.

1) The vete1inaiian is working for the

Electronic CVI, especially when coupled
person paying the fee and reports only to
with radio frequency identification (RFID)

that person. The person responsible for
devices used as official identification,
compensating the veterinarian should be
reduce the time necessary to prepare and
infom1ed of tl1e cost before the inspection.

distribute the required paperwork. Although

2) The purpose for which the animal is to be

RF1D devices are not currently required for used should be clearly established before
interstate movement of animals, a recogthe examination. 3) The examining nized fom1 of official identification for each
veterinarian must be knowledgeable not
animal is required. If a state has specific
only in the care and treatment of animals
identification requirements, they can be
but also aware of the purpose for which
determined when contact is made with the
they will be used.

state of destination's animal health official.

Because legal action against the

Countries also have specific health
exanlining veterinarian is a possibility, a
regulations for inlported animals. These
veterinarian may choose not to provide a
regulations have been developed to protect
written report for prepurchase exanlinatheir animal populations for many of the tions. However, a written record of findings
same reasons individual states have
should be made, because it may be needed

RADIATION THERAPY

1651
at a future date. The responsibility of the
administration should be noted. The health
veterinarian is to supply information and
of the herd or flock of otigin and possible
identify abnormalities; the prospective
contacts with other animals before the sale
purchaser must make the decision whether
should be detennined, because animals so

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to purchase. The prospective purchaser
exposed could be in the incubation period
may also select a second veterinarian to
of disease. It should also be established
perfonn an additional inspection.

whether the animal received any drugs or

The examination is divided into three
medication that could alter its normal state.

parts: history, clinical examination, and

If this carmot be established in the history, it
special examinations or diagnostic
may be prudent to pe1iorm assays for
procedures.

suspected medication.

History: A complete history should be
obtained by questioning the seller,

Clinical Examination, Special Exami
examining the seller's records, and
nations, and Diagnostic Tests: All
observing the remainder of the herd or flock
areas of the body and their functions should
and the management conditions. The
be examined. The clinical exan1ination
animal's breed, sex, age, color, markings,
should establish the current state of the
tattoos, ear tags, brands, and other
anin1al's health and condition of each body
identification aids should be noted. If
system.

applicable, registration papers should be

As previously discussed, some diagnostic
checked and the animal's identity definitests are performed at the time of sale to tively established.

satisfy the requirements of the state or

For a breeding animal, the records of its
country of destination, but additional
sire and darn also should be considered,
diagnostic tests and special exanlinations
including their breeding ability, the
may be required by the seller, buyer, or
possibility of he1itable defects in the line to
others involved in the transaction. It may
which each belongs, and, if dead, the cause
also be necessary to conduct additional
of death. Also, breeding records of the
testing as indicated by the findings of the
animal itself should be reviewed to
clinical examination. When ce1tain diseases
detennine its fertility. Breeding records of
are not present in the seller's geographic
the herd of origin of the animal should be
area but are endemic in the purchaser's
examined for evidence of disorders that
area, vaccination (if available) for those spemay affect reproduction. If the animal is an cific diseases is frequently required before
adult female, the breeding dates and stage
movement. The CVI prepared after the
of pregnancy, if applicable, should be noted.

examination must accurately reflect the

Records should be examined to
findings of the accredited veterinarian ..

detemline whether the animal has had any

If a male is to be purchased for breeding
previous diseases, injuries ( and their
purposes, a complete breeding soundness
severity), or surgical procedures. Previous
examination (seep 2230) should be
vaccinations, their type, and date of
conducted.

RADIATION THERAPY

Radiation therapy has seen dramatic

Historically, radiation therapy was
increases in demand and sophistication in
delivered using orthovoltage x-ray
recent years, which has led to creation of
machines or very large activities of
a board specialty in radiation oncology,

64-cobalt and 137-cesium. Except for a few
granted by the Ametican College of
specialized instances, orthovoltage x-ray

Veterinary Radiology. The sophistication
machines have fallen from favor because
and scope of both veterinary imaging and
of the intensity of adverse radiation
radiation therapy has advanced to the point
reactions associated with their use and
that only a few radiologists now actively
their limited flexibility. Cobalt and cesium
practice in both the fields of imaging and
are no longer used because as long-lived
therapy.

isotopes they are extremely dangerous and

1652

RADIATION THERAPY

SELECTED COMMON NEOPLASMS THAT CAN BE TREATED WITH

RADIATION THERAPY

Tumor Type

Radiosensitivity

Comments

Nasal adenocarcinoma

Intermediate

Usually respond well but

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often recur

Nasal squamous cell

Low

Response is often minimal
carcinoma

Nasal chondrosarcoma

Intermediate to high

Some subtypes respond
better than others

Nasal osteosarcoma

Low

Response may be better if
after surgery

Oral melanoma

Low to intermediate

Poor response usually unless
after surgery

Oral squamous cell

Low

Especially poor in cats;
carcinoma
aggressive treatment
required

Osteosarcoma

Low

Metastatic disease in >900Ai;
pain palliation

Chondrosarcoma

Intermediate

Best when small; metastasis
a problem

Fibrosarcoma

Low to intermediate

Depends on tissue of origin

Injection-related

Low to intermediate

Best if done after first
fibrosarcoma
surgery, poor later

Thyroid carcinoma

Intermediate to high

Usually respond very well;

131 I possible

Thyroid adenoma

High

Treat with 131I(>95%cure)

Salivary adenocarcinoma

Intermediate

Usually respond well,
especially in cats

Brain tumor - meningioma Intermediate to high

Usually stabilizes mass; good
clinical result

Brain tumor - glioma

Low to intermediate

Depends on size, location,
and clinical signs

Brain tumor - lymphoma

High

Most effective treatment for

CNS lymphoma

Brain tumor - metastasis

Intermediate

Effective but short tem1 due
to other disease

Spinal cord mesenchymal Intermediate

Reasonable response but
tumor
dose limited by cord

Spinal neurofibrosarcoma Low to intennediate

Short-term response good
but commonly recur

Lymphosarcoma

High

Excellent response but can
only treat locally

Cutaneous lymphoma

High

Often curative

Nasal lymphoma

High

Good response, often very
durable

Thymoma

Low to high

Low for scirious form, high
for lymphocytic

( conti,nued)

RADIATION THERAPY

1653

SELECTED COMMON NEOPLASMS THAT CAN BE TREATED WITH

RADIATION THERAPY (continued)

Tumor'fype

Radiosensitivity

Comments

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Mediastinal chemo

Low

Large masses, dose limited by
dectoma
heait at1d lungs

Adrenal neoplasias

Low

Difficult to accurately
localize treatment

Transitional cell carcinoma Intermediate

May respond well initially but
recur

Prostatic adenocarcinoma Low to intermediate

Data available on response is
quite variable

Mast cell tumors

Intermediate to high

Very good for low grade, less
for high grade

Pedpheral nerve sheath

Intennediate to high

Strongly recommended after
tumor
surgery

Soft-tissue sarcoma

Low to high

Improves control after
surgery, not alone

Lick granuloma

Intem1ediate to high

Treatment of last resort,
often works well

Transmissible venereal

High

Very good control even for
tumor
large tumors

Equine sarcoid

High

Used in refractory twnors,
brachytherapy

Equine nasal carcinoma

Intermediate to high

Beam treatment effective,
very few sites

Equine ocular squamous

Intermediate to high

Best treatment when bone
cell carcinoma.

involved
heavily regulated in most of the world.

localization at1d distribution of the

Today, it is virtually impossible to purchase therapeutic beam within the patient. This these sources because of public safety
reduces the dose to healthy tissues relative
concerns.

to the dose to the neoplastic tissue being

Veterinary radiation therapy practices
treated, increasing cure or control rates and
today almost exclusively use linear
reducing the seve1ity of healthy tissue
accelerators as the source of the ionizing
complications. These programs are best
radiation used to treat neoplasia and
used in conjunction with CT or MRI in1ages,
occasionally specific benign diseases.

which determine the position and extent of

These machines produce powerful x-rays
the tumor within the body at1d its relative
and electron beains with energies of 4-20
position to healthy structures. Mat1y hours
million electron volts. The x-rays are used
of work may be required to generate a
to treat deep-seated tumors, whereas
treatment plat1 for a large, complex tumor.

electron bean1s are generally used to treat

Patients are then treated in precisely the
tumors of the skin at1d subcutis. Linear
san1e position as they were in for the CT or
accelerators ai·e complex machines that

MRI. Repeatability of positioning is of
require the support of a medical physicist
paran10unt imp01tance and cat1 be achieved
to maintain safe ai1d effective use. This
by using special positioning devices in
increased support load is offset by the
coajunction with careful landmarking.

machine's flexibility and speed, which is

Proper patient positioning is then confirmed
necessaiy as treatment techniques become
using at1 imaging system integrated with the
more sophisticated at1d complex.

lineai· accelerator. Once proper positioning

Computedzed treatment planning
is confin11ed, the treatment can be
systems are now used by vetednary
administered. Great attention to detail is
radiation oncologists to improve the
necessary during this pait of the treatment,

1654

RADIATION THERAPY
because even small changes in position can
the mediastinum and soft tissues of the skin
have profound effects on the distiibution of
and subcutis either before or after surgery.

the radiation dose delivered. This is

It is seldom used in the tream1ent of lung
especially true in CNS tun10rs, in which the
neoplasia or in the treat111ent of neoplastic

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lesion diameter may be only l cm.

disease of the abdominal cavity because of

Except in rare instances, all radiation
the mobility of tumors in these areas.

therapy treatinents using external sources

However, treatment of mediastinal tun10rs
of radiation must be delivered with the
and those of the pelvic canal, such as
patient immobilized by general anesthesia.

thymoma and prostatic carcinoma, are

Because the plane of anesthesia required is
possible and may well be indicated. As the
light and the procedures are typically of a
sophistication of radiotherapy techniques
relatively short duration, this repeated
increases, more and more types of
anesthesia is well tolerated, and complicaneoplasia are being treated at least in part tions are few with proper observation and
by radiation therapy.

monitoring. This requirement for anesthesia

In many instances, radiation therapy,
is rarely if ever a conti·aindication for
especially when combined with surgery and
implementing a course of radiation therapy.

chemotherapy, may be curative. However,

A typical course of radiation therapy
radiation therapy can delay the developconsists of multiple doses of radiation ment of disease or conti·ol its expansion in
delivered on different days. This is clone to
many instances. Radiation oncologists
allow healthy tissues to heal somewhat
typically talk in tem1s of control rate rather
between doses. Healthy tissues have a
than cure. Sometimes, the control may be
greater ability to repair radiation damage
relatively short lived, and recrudescence
than neoplastic tissues; therefore, use of
of the tumor occurs within months after
multiple small doses of radiation, although
completion of the treatment regimen. In
it has a cwnulative effect, favors survival of
other cases, control may last several years
healthy over neoplastic tissues. Most
or even until other disease processes
radiation therapy regimens designed with
supersede the neoplastic disease. Unfortucurative intent use 15-20 individual closes nately, it is seldom possible to predict even

(fractions) of radiation. Each dose of
within an individual tumor type which
radiation may be delivered using several
patients will experience good control and
different fractions of radiation of differing
which ones will not. Continual advances in
size, shape, and intensity. ln cases when the
the evaluation of genetic markers within
twnor is too advanced to be controlled by
tun1ors hold the promise of being able to
radiation, palliative therapy using larger
predict this in the future.

doses and fewer fractions of radiation may

Because of the lisk of serious and
be used to retard the tumor's growth or
potentially life-threatening complications
reduce associated pain. Such a palliative
associated with this treatment modality, the
approach may also be used when mandated
complexity of the equipment and sophistiby owner finances.

cation of the radiation therapy procedures

Whenever possible, removal.of a tumor
should only be presc1ibed by and adminisby surgery is preferred. However, in many tered under the supervision of a veterinarinstances, large neoplasms, or those in ian with special training, experience, and
critical areas such as the brain, are not
certification in the field of veterinary
amenable to complete or even partial
radiation oncology. A veterinary radiation
surgical removal. Even when a tun1or is
oncologist should also be consulted any
grossly removed, microscopic foci of
time further tream1ent is contemplated for
neoplastic cells often extend beyond the
neoplasia that has been treated by radiation
limits of the surgical field. This is more
therapy. This is particularly important if
common for some tun10r types than for
surgery within the radiation field is being
others. In all of these instances, radiation
considered.

therapy, often in combination with

Brachytherapy is the implantation of
chemotherapy, is useful in treating the
radioactive sources into the tumor to
remaining cancer. Radiation therapy is often achieve radiation therapy. It is seldom used the tream1ent of choice for brain tumors,
for treatment of cancers in animals because
nasal tumors, and other neoplasms of the
of the difficulties associated with maintehead and neck in which even partial nance of the sources and keeping the
resection may be extremely disfiguring or
sources in place within the tumor. The
carry a high risk of mortality. It may be the
notable exception to this is the use of
only ti·eatinent option for cancer of the
radioiocline to treat thyroid adenomas in
vertebral column and pelvic canal.

cats and adenocarcinomas in dogs.

Radiotherapy is also used to treat tumors in

Radioisotopes developed for tream1ent of

RADIATION THERAPY

1655
metastatic osseous neoplasia in people are
received widespread attention in vete1inary
also useful in the treatment of primary and
medicine because of tl1e cost of both tl1e
metastatic bone cancer in dogs and cats.

agents and the equipment required for their

Such "nuclear oncology" treatments are
in1plantation. However, in recent years
being continually developed for use in
there has been a marked upswing in the

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human medicine and are directly applicable
interest in such interventional radiology
to veterinary patients as well. In fact, tl1ese
procedures for both treatment and
treatments are typically developed in
diagnosis, not only of cancer but also of
veterinary patients before being introduced
many other conditions. Such teclmiques
into human medicine.

may well increase the interest in and

Implantable radiation sources that are so
availability of brachytherapy procedures.

small (microns or even nanometers) that

Because of the 1isk of excessive radiation
they are permanently in1planted within the
exposure and contanunation of the patient
body blur the margins between radiation
or hospital, these procedures should be
therapy and nuclear medicine. The
perfom1ed only by veterinarians with
in1plantation of such sources comes under
appropriate training, experience, and
the heading interventional radiology.

support in a properly licensed facility.

Interventional radiology procedures such as

A full list of appropriately trained and
catheter placement and CT guidance of
accredited veterinarians as well as a list of
source implantation are used to introduce
radiation therapy facilities can be obtained
both macroscopic and microscopic scale
through the American College of Veterinary
brachytl1erapy sources into neoplasms

Radiology or the American Vete1inary
located deep within the body. Targeting of

Medical Association.

such agents is accomplished either by using

The radiosensitivity of virtually any
sources of sufficient size to be locally
neoplasm is higher in minimal or microretained within the tissue or capillaries of scopic disease. Some neoplasms respond
the tumor or by targeting them specifically
well initially but tend to recur at some time
to twnor cells using monoclonal antibody
after radiation therapy. The time to
labeling. These teclmiques have been
recrudescence is highly variable between
around for many years but have not
and within tun1or types.

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EMERGENCY MEDICINE

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AND CRITICAL CARE

INTRODUCTION 1658

First Aid and Transport 1659

Ready Area 1660

EVALUATION AND INITIAL TREATMENT OF THE EMERGENCY

PATIENT 1660

Primary SUIVey (Triage) and Resuscitation 1660

Airway 1662

Breathing 1663

Circulation 1665

Secondary Survey 1667

SPECIFIC DIAGNOSTICS AND THERAPY 1668

Trauma 1668

Thoracic Trauma 1668

Abdominal Trauma 1669

Cardiopulmonary Resuscitation 1670

FLUID THERAPY 1675

Body Fluid Compartments and Fluid Dynamics 1675

The Fluid Resuscitation Plan 1676

Assessment of Resuscitation Efforts 1684

Maintenance Fluid Plan 1684

MONITORING THE CRITICALLY ILL ANIMAL 1685

The Rule of20 1685

OPHTHALMIC EMERGENCIES 1696

Traumatic Proptosis 1696

Traumatic Retrobulbar Hemorrhage 1696

Eyelid Lacerations 1696

Corneal Foreign Bodies 1697

Penetrating Intraocular Injuries 1697

Deep Stromal Corneal Ulcers, Descemetocele, and Iris Prolapse 1697

Corneal Lacerations 1698

Glaucoma 1698

Anterior Lens Luxation 1699

Anterior Uveitis 1699

Acute Vision Loss 1699

Optic Neuritis 1701

Sudden Acquired Retinal Degeneration 1701

Retinal Detachment 1701

1658

EMERGENCY MEDICINE AND CRITICAL CARE

WOUND MANAGEMENT 1701

General Principles of Wound Healing 1702

Initial Wound Management 1702

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Drains 1704

Bandages 1 705

Surgical Techniques 1705

Factors that Interfere with Wound Healing 1706

Management of Specific Wounds 1707

EQUINE EMERGENCY MEDICINE 1708

Equine Emergency Procedures 1708

Emergency Fluid Therapy 1708

Nasogastric Intubation 1710

Abdominocentesis 1711

Trocarization 1712

Tracheostomy 1713

Equine Trauma and First Aid 1 713

Fractures and Luxations 1 713

Guidelines for Safe Transportation 1716

Wounds and Lacerations 1716

Head Iajuries 1718

Ocular Iajuries 1718

Thermal Injuries 1719

Other Common Equine Emergencies 1720

Esophageal Obstruction 1720

Rectal Tears 1721

Postcastration Evisceration 1722

Neonatal Intensive Care and Emergencies 1723

Initial Assessment · 1723

Dystocia and Resuscitation 1724

Prematurity, Dysmaturity, and Postmaturity 1726

Neonatal Encephalopattw 1728

Sepsis 1728

EMERGENCY MEDICINE INTRODUCTION

Emergency patients present special

Problems can arise from an acute illness,
challenges because their underlying
toxicity, or injmy; from a chronic illness
disease processes can cause immediate,
that has decompensated; or from an
life-threatening problems that require rapid unexpected complication of a concurrent and aggressive intervention. In addition,
illness. The status of all postoperative
the full extent of the animal's illness,
patients should be considered critical until
injuries, or toxicity may not be evident for
life-threatening anesthetic or surgical

24-48 hr or more after initial presentation.

complications are excluded. The golden

EMERGENCY MEDICINE INTRODUCTION

1659
rule of emergency medicine is to treat
thick fabric can be used to provide support.

the most life-threatening problems first.

Radiographs can also be taken through

Variables that contribute to the overall
these materials without having to move the
success of emergency treatment include the
animal when it arrives at the hospital.

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severity of the primary illness or injury, the

Rapid detection of cardiopulmonary
amount of fluid or blood lost, age of the
arrest (CPA) in an unconscious animal can
animal, previous health problems, the
be difficult for owners. The pet's lack of
number and extent of associated condiresponse to external stimuli or presence of tions, time delay in instituting therapy, the
limp body tone are W1reliable indicators of
volume and rate of fluid administration, and

CPA. Instructing owners to feel for a pulse
the choice of fluids ( eg, crystalloid, blood
or heart rate can delay intervention. Instead,
components, or synthetic colloids). Therapy owners can be instructed to watch for chest must be done at the 1ight tin1e, in the right
excursions and to touch the cornea or
amount, and in the right order. Therapeutic
eyelids to elicit a corneal or palpebral reflex
failures are generally a result of failing to act in an tmconscious pet, with absence of one expeditiously at a crucial moment.

or both indicative of CPA.

Emergency care often begins with the

Mouth-to-nose resuscitation and chest
owner's initial telephone call. Instructing the
compressions (seep 1670) may provide
owner on first aid and transport procedures
enough respiratory and circulatory support
can be life-saving for the animal. The clinic
to maintain life during transport. If the
and staff must be in readiness, especially if
animal is cyanotic and collapsed (and
more than one anin1al in critical condition
was pawing at the face), an upper airway
arrives at the san1e time. The primary survey,
obstruction may be present; the owner
or triage (see below), requires a quick and should be instructed how to perform a
accurate assessment and decision regarding

Heinilich maneuver or sudden chest
the stability of the animal. As life-threatening compression to relieve the obstruction and airway, breathing, and circulation problems
then to manually clear the aiiway. If the
are identified, inlmediate treatment is
animal is unconscious and not breathing,
initiated. Once the anin1al has been stabilized, the owner should be instructed to close the a more systematic and organized approach
anin1al's mouth, place their lips over the
to the history and physical exanlination
animal's nostrils, and initially give 3-4 strong

( secondary survey) and more specific
breaths. If the animal's breathing does not
diagnostic and therapeutic procedures
become spontaneous, the owner should
aimed at the underlying cause can be done.

breathe for the aninlal at a rate of 10 breaths/
min. The owners can also be instructed to

FIRST AID AND TRANSPORT
compress the esophagus behind the
mandible on the left side so that most of the

Owners can provide significant medical
air will go down the airway instead of into
assistance at the scene of the injury. At the
the stomach. Chest compressions should
time of the initial telephone call, the owner
be initiated at a rate of 100-120/min. A
should be questioned about the level of
compression: ventilation ratio of30:2 can
consciousness, breathing pattern, type of
be perfonned. This necessitates another
injury or toxicity, and even some aspects of
person to drive during transport.

the aninlal's perfusion ( eg, gwn color, level

Owners should be asked whether
of responsiveness, heart rate). The first
hemorrhage is ongoing or whether bleeding
concern is for the safety of the owner.

was seen at the site of injury. Pulsating

Placing a light cloth over the head of the
arterial bleeding should be controlled
anin1al can lessen external stimuli that may
by direct digital pressure and then by a
cause fearful and aggressive reactions.

pressure bandage. Any long pieces of fabric

Owners can be instructed as to how to
or gauze can be used. Often, washcloths and
muzzle most dogs using a long strip of fabric hand towels are adequate when applied if there are no facial injuries or respiratory
with mild pressure. Additional material can
distress. Cats can be placed in dark boxes to be placed over the original bandage if it minimize stress during transport; the box
becomes soaked with blood. If the bleeding
should have holes large enough so that the
from a limb is venous ( dark, oozing), the
cat can be observed. It is vital that the
limb can be elevated above the heart.

owner adequately restrain the pet before

Tourniquets should be used only on
starting any first aid procedures to ensure
appendages ( eg, limbs, tail) when compresthe safety of the owner and pet.

sion wraps have failed to control bleeding.

When moving the aninlal, motion of the

The tension on the tourniquet must be
head, neck, and spine should be minimized.

relaxed to allow blood flow to the distal

A flat, firm board of wood, cardboard, or
limb and then retightened every 5-8 min.

1660

EMERGENCY MEDICINE INTRODUCTION

Penetrating foreign objects ( eg, sticks,

READY AREA
arrows) should be left in place during
transport; however, care should be taken

A central area of the clinic should be
to guard against movement of the object
designated as the "ready area," where
to prevent further irtjury. It is often
resuscitation therapeutics and equipment

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necessary to stabilize the shaft of the
are organized and available for in1mediate
penetrating object just outside the body
use. Front desk and triage staff should be
and, holding it firmly, cut off the shaft,
aware of presenting conditions that require
leaving a portion exposed so it can be
immediate evaluation by a vete1inarian. All
easily located.

members of the vete1inary tean1 must be

In dogs with fractures below the elbow or
fanilliar with the ready area and location of
stifle with significant displacement-and,
all necessary emergency equipment and
therefore, concern for movement causing
medications. Regular drills should be
damage to muscle, nerve, vessels, or
organized for emergency situations such as
bone-support can be provided during

CPA with subsequent cardiopulmonary
transport. Once the pet has been adequately
resuscitation efforts to ensure everyone
restrained, the owner can make a support
knows his or her role and to improve
splint from a rolled newspaper or magazine,
techniques. An emergency treatment or
which is secured in place by long pieces of

"crash" cart should contain endotracheal
fabric or duct tape.

tubes of various sizes, a laryngoscope,

Animals with altered mentation after
syringes of different sizes with 18- or
trauma should be transported with the head

20-gauge needles attached, and drugs for
level with the body or elevated 20°. There
carcliac resuscitation. Oxygen and a small
should not be any jerking or thrashing
and large bag-valve-mask apparatus or
motions, and manipulations of the neck or
other ready access to oxygen (such as
occlusion of the jugular veins should be
an anesthetic machine flushed free of
minimized.

anesthetic gas) should be inunediately

If a toxic ingestion is present, the owner
available, so positive-pressure ventilation
should be instructed to bring the anin1al
can be started. Other necessary mate1ials
inunediately to a vete1inarian. Instructing
include hair clippers, surgical scrub, tape,
an owner by phone to administer hydrogen
intravenous and intraosseous catheters
peroxide or other substances carries the
with Hushing solutions, intravenous
risk of further injury such as a vagal
isotonic crystalloids, pressure infusion
response (resulting in collapse and
bags, synthetic colloids, bandage material,
bradycardia), choking on vomitus,
and trauma transport materials. Additional
aspiration pneumonia, further toxic irtjury
beneficial equipment includes a defibrillafrom caustic substances, or mucosal irtjury tor, monitoring devices (ECG, Sp02, ETC02,
from hydrogen peroxide administration. If
and indirect blood pressure), a suction unit
possible, the container of the likely toxin
with Yankauer and whistle tip suction
should be brought in.

attachments, and warming devices.

EVALUATION AND INITIAL TREATMENT

OF THE EMERGENCY PATIENT

PRIMARY SURVEY (TRIAGE) AND
vomiting or diarrhea, urethral obstruction,

RESUSCITATION
labored breathing, cardiopulmonary
arrest, seizures, loss of consciousness,

Triage is the art of assigning priority to
severe alterations in mental state, acute
emergency patients and their problems
inability to walk, excessive bleeding,
based on rapid assessment of historical
prolapsed organs, potential snake bite,
and physical parameters (see TABLE 1).

heat prostration, open wounds exposing

Several historical or observed problems
extensive soft tissue or bone, anemia,
warrant transfer of the animal to the
burns, dystocia, shock, and disease that
treatment area regardless of physical
may rapidly decompensate such as gastric
findings. These problems include known
dilatation and volvulus and allergic
or suspected trauma, poisonings, profuse
reactions.

EVALUATION AND INITIAL TREATMENT

1661

IM:l!ii PARAMETERS TO EVALUATE DURING TRIAGE

Parameter

Evaluation

Significance

Mucous

Pink

Normal PCV and adequate perfusion

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membrane color

Pale or white

Anemia or shock

Cyanotic

Severe hypoxemia

Yellow

Increased serum bilirubin due to hepatic
disease or hemolysis

Capillary refill

1-2 sec

Normal perfusion and rapidity with
time
which capillaries refill with blood

>2sec

Poor perfusion or peripheral vasoconstriction

<l sec

Hyperdynamic states; could be
associated with fever, heat stroke,
distributive shock, or early compensatory stage of hypovolemic shock Heart rate

70-120 bpm (small dogs)

Nom1al heart rates; indicate that at least

60-120 bpm (large dogs)

one component of cardiac output is

120-200 bpm (cats)

normal

Bradycardia

Decreased cardiac output and subsequent
poor perfusion; cats in particular develop
bradycardia ( <120 bpm) in shock; an
irregular, slow heart beat can be
associated with in1Illinent cardiac arrest,
severe arrhythmias, or metabolic derangements ( hyperkalemia, hypocalcemia, etc) Tachycardia ( dogs > 180

Compromised diastolic filling; sinus
bpm, cats >220 bpm)

tachycardia often results from hypovolemic shock or pain; tachycardia that is irregular or associated with pulse
deficits usually indicates an arrhythmia,
and an ECG is indicated

Pulse rate and

Strong and synchronous

Normal; both femoral and digital pulses
quality
with each heart beat
should be palpated

Irregular

Usually indicative of a cardiac
arrhythmia

Bounding

Hyperdynamic (compensatory) state
of shock

Weak or absent

Decreased cardiac output, peripheral
vasoconstriction, decreased pulse
pressure, or thromboses

Level of

Alert and responsive to

Nonna! overall neurologic and metabolic
consciousness
surroundings
state

Depressed or obtunded

Can be caused by any illness or

(less responsive to visual decreased perfusion; may be mild, and tactile stimuli, sleepy moderate, or severe
appearance but still
arousable)

(continued)

1662

EVALUATION AND INITIAL TREATMENT

PARAMETERS TO EVALUATE DURING TRIAGE (continued) Parameter

Evaluation

Significance

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Stupor (arousable only

Severe neurologic or metabolic
with painful stimuli)

derangements

Comatose (unarousable

Abnormal cerebral electrical activity
with any stimuli) or
from primary neurologic disease or
seizures ( usually
secondary to metabolic derangements
associated with whole
seen in diseases such as diabetes,
body convulsions,
hepatic encephalopathy, hypoglycemia,
salivation, facial tremors, or toxin exposure; accurate history or possibly involuntary
prior health problems, current medicaurination and defecation) tions, and possible toxin exposure important

Level of pain

Vocalization, changes in

Clinical signs can be similar to those
behavior (avoidance,
seen in compensatory stage of shock;
aggression), or physical
pain delays healing and must be treated.

changes (tachycardia,
dilated pupils, etc)

Airway, breathing, and circulation are
expiratory stridor. Stertor is most common
evaluated sequentially, followed by
with pharyngeal disease. Possible causes of
examination for sources of hemorrhage,
large airway pathology include foreign
and determination of the level of conbodies, edema, laryngeal paralysis or paresis, sciousness and level of pain. The most
tracheal collapse, elongated soft palate,
common reasons for an animal in
aspiration of stomach contents, neoplasia,
catastrophic distress include 1) airwayand pharyngeal hematomas. Anin1als with airway obstruction or disruption; 2)

severe small airway obstruction have labored
breathing-cyanosis from tension
breathing witl1 an expiratory push of the
pneumothorax, alveolar flooding ( edema
diaphragm, cyanosis, and anxiety. Auscultafluid or blood), severe bronchoconstriction tion reveals high-pitched wheezes throughwith air trapping or brain-stem pathology out the lung field. In severe life-threatening
affecting ventilation; and 3) circulationsituations, the animal is cyanotic, shock (decreased perfusion), cardiopulmoopen-mouth breathing, collapsed, and nary arrest, extreme bradyarrhythrnias or
asphyxiating. Common causes include
tachyarrhythmias, cardiac tamponade, and
anaphylactic reactions; asthma (cats); and
acute intra vascular volun1e loss usually
bronchial obstruction from edema, mucus,
due to internal or external hemorrhage.

exudates, or foreign material.

Airway

Treatment: Unconscious, apneic animals

Life-threatening airway pathology
require immediate tracheal intubation. The

( catastrophic or severe) includes complete
clinician should be practiced in orotracheal
large airway obstruction and partial
intubation of animals in dorsal, lateral, and
obstruction of the large and small airways.

sternal recun1bency. lf an obstruction is
present, it must be inm1ediately relieved

Diagnosis: Animals with complete large

(with suction, manual removal, or the
airway obstruction are unconscious and

Heimlich maneuver) or bypassed via
apneic. Partial large airway obstruction
emergency tracheotomy. Once an airway
causes noisy breathing (stridor or stertor),
is established, confinned, and secured,
heard without the aid of a stethoscope.

ventilation is initiated with 100% oxygen

Cyanosis and anxiety are often present with
via a bag-valve-mask. Should auscultation
loud referred airway sounds heard throughduring ventilation detect absent or muffled out the thorax on auscultation. Compromise
lung sounds indicative of pleural fluid or air,
of the extrathoracic airway (nasal passages,
immediate thoracocentesis is warranted.

pharynx, larynx, or cervical trachea) causes

Heart sounds and pulses are checked and,
inspiratory striclor; compromise of the
when absent, cardiopulmonary resuscitaintrathoracic trachea or bronchi causes tion (seep 1670) is initiated.

EVALUATION AND INITIAL TREATMENT

1663

With partial large airway obstruction,
respiratory rate and effo1t, inunediately
flow-by oxygen is delivered through oxygen
followed by a change in the respiratory
tubing at a high flow rate aimed at the open,
pattern. Postural changes ( orthopnea)

panting mouth until an airway is secured or,
follow; clogs stand with the elbows abducted
if approp1iate, a transtracheal or nasotraand the back arched or high on the rear VetBooks.ir
cheal oxygen line is placed. Heavy sedation
haunches with the head and neck extended,
using a narcotidtranquilizer ( eg, butorphawhereas cats may sit crouched on aJJ four nol 0.2-0.4 mg/kg with or without aceprolimbs with the sternun1 slightly elevated.

mazine 0.01-0.05 mg/kg) combination may

Obvious labored, open-moutl1 breatlling, and
be used to relieve anxiety and struggling, to
changes in mucous membrane color (gray
allow a cursory examination of the pharynx
and/or blue [ cyanosis]) develop last and
and larynx, and to remove pharyngeal
indicate significant loss of pulmonary
foreign bodies. When tracheal intubation
fw1ction and in1pencling pulmonary arrest.

is necessary, general anesthesia should be

The location of the pathology-pleural
induced using rapid-acting IV anesthetics
space or parenchyrnal disease-can be
such as etomidate (0.5-3 mg/kg), ketamine/
cletemlined at presentation by car·eful
diazepan1 combination (5-20 mg/kg and
observation of tl1e breathing pattern and

0.1-0.4 mg/kg), or propofol (6-8 mg/kg to
auscultation of tl1e thorax. This will direct
effect). The ability of the laryngeal
resuscitative effmts. Taking racliographs or
cartilages to abduct dming inspiration
perfomling stressful diagnostic procedures
should be assessed during intubation and a
before the animal has been stabilized can
full oropha.ryngeal examination performed
lead to rapid decompensation.

when time allows. A tracheotomy is neces

Plemal space disease causes asynchrosary when pharyngeal, laryngeal, or tracheal nous breathing. The chest expands on pathology prevents orotracheal intubation
inspiration as the abdomen is pulled inward,
or when prolonged intubation is anticitllen the chest moves inward on expiration as pated. A transtracheal catheter can be used
tile abdomen expands. In cats, breatlling is
to provide oxygen suppmt during stabilizaslower and more deliberate than in dogs. The tion. When the airway pathology lies within
respiratmy pattern is the san1e whetl1er air,
the thoracic cavity, airway patency must be
fluid, or abdominal contents are in the plew·al
established down to the bifurcation of the
space. Thoracic auscultation reveals muffled
trachea Once the airway is established, it
lung sounds over tl1e affected regions.

should be secured with a tie and inflation of

Lw1g parenchyn1al disease causes quiet,
the cuff mechanism, as well as con.finned
smooth breathing, with the chest and
with at least two of the following methods:

abdominal wa!J moving in the sar11e
palpation of the tube within trachea in the
direction. Inspiration and expiration are
cervical region, ausculation of the lungs and
equa!Jy labored m1less concun-ent small
visualization of chest wa!J movement when
airway edema or constriction adds all
a breath is ad.ministered, visualization of the expiratory push. Cats demonstrate rapid, tube entering the airway, placement of an
shallow synchronous breathing, often with
end-tidal C02 monitor, or radiographs.

movement of the cupula. Thoracic

Cyanosis from sma!J airway obstructive
auscultation reveals louder than normal
disease is treated by providing oxygen by
lung sounds in early phases. As disease
flow-by, hood, or nasal cannula and sedation progresses, harsh ltmg sotmcls with moist with a narcotidtranquilizer combination.

crackles and rales are heard over the

Epinepluine is given for its bronchoclilatory
affected lungs. Pulmonary edema may be
effects both in anaphylaxis (0.01-0.02 mg/kg, car·diogenic, often accompanied by a IV) and in life-threatening asthma (0.02 mg/kg, mum1ur, gallop, or arThythmia noted on IM). Corticosteroids (preclnisone sodimn
auscultation and mild hypotl1ennia. Other
succinate, 15 mg/kg, IV, or clexamethasone,
differential diagnoses include CNS disease,

2-4 mg/kg, IM or IV) are given for a!Jergic
pnewnonia (viral, parasitic, fungal, or
bronchitis, asthma, or severe swelling of
bacterial), aspiration, pulmonary contuthe larynx or pharyngeal tissues. Other sions, or hemoglobin abnormalities.

bronchoclilators, such as arninophylline or

Noncarcliogenic pulmonary edema may be
terbutaline, are given IM, or albuterol can
caused by seizures, electrocution, after all
be given by nebulization in the case of an
acute airway obstruction (such as after
animal in crisis.

choking or near-drowning) and acute lung
irtjw-y, or respiratmy distress syndrome.

Thoracic radiography should be

Breathing
performed only when the arlinlal is able to

Diagnosis: Compromised breathing in both tolerate the procedure. Racliographs can clogs and cats manifests with an increased
help differentiate mally of these diseases;

1664

EVALUATION AND INITIAL TREATMENT
however, imaging should not delay therapy. the needle is inse1ted ventrally between the Some animals may be more tolerant of
sternum and costochondraljunction. When
ultrasonography. The thoracic focused
air is to be recovered, the needle is inserted
assessment with sonography (TFAST)

into the dorsal half of the thorax, above the
technique may be used to identify pleural
costochondraljunction. A local anesthetic

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fluid and air, exanlining both hemithoraces
is placed into the skin, subcutaneous tissue,
between the fifth and sixth ribs ventrally
and intercostal muscle at the site to be
and between the seventh and ninth ribs
tapped. After the needle is inserted just
dorsally. A pneumothorax may be present
through the skin, a drop of saline is placed
when the "slide sign" is absent; this is a in the hub of the needle. The needle is then
linear movement noted between the
gradually inserted straight into the thorax
visceral and paiietal pleura and requires

( with the needle perpendicular to the chest
practice to identify.

wall) until the saline in the needle hub
moves. The movement of the saline in the

Treatment: Oxygen is administered
hub indicates that the pleural space has
immediately via flow-by, mask, hood, or
been entered, although tllis may not always
oxygen cage techniques. Sedation with
occur. The needle is immediately directed
a narcotic/tranquilizer combination
so that it lies against the parietal pleura.

(butorphanol 0.2-0.4 mg/kg, IV or IM, with

This prevents laceration of the lung by the
or without acepromazine, 0.05 mg/kg, IV
needle as the lung reexpands. As soon as
or IM) can relieve struggling and anxiety.

the pleural space is entered, the evacuation

Longterm continuous supplemental oxygen
apparatus (an IV extension set, 3-way
is best provided by a nasal oxygen catheter.

stopcock, and syringe) is attached and

The intranasal oxygen catheter is placed
aspiration begins. In animals in which
after topical anesthetic has been instilled
the pleural space cannot be emptied ( eg,
into the nostril where the tube is to be
tension pneumothorax, ongoing hemorinserted. Humidified nasal oxygen flow rhage) or when repeated chest taps are
rates of 50---100 mUkg/min deliver 40o/o-60%
required within minutes to hours, an
inspired oxygen while allowing the ailimal
indwelling chest tube should be placed for
to be exanlined and the underlying disease
continuous closed suction until the problem
treated. Nasopharyngeal or nasotrachcal
resolves or futher therapy is perfonned.

catheters or bilateral nasal cannulas may

Lung parenchymal disease is primaiily
provide higher percentages of inspired
treated using oxygen supplementation, sedaoxygen. If cyanosis and decompensation tion to relieve anxiety, and therapy directed
persist or work of breathing is profound,
at the underlying cause. Cardiogenic edema
intubation and positive-pressure manual
is usually associated with a gallop, mum1ur
ventilation or mechailical ventilation with

(detemlined by auscultation), arrhythnlia,

1000/o oxygen is necessaiy
and/or nlild hypothernlia and responds well

Catastrophic pleural space disease
to furosenlide administration (1-4 mg/kg, IV,
with rapid cardiovascular decompensation,
every 1-2 hr) in all but the most severe of
absent lung sounds tlU'Qughout the thorax,
cases. Furosenlide is more effective when
and a barrel-shaped chest suggests tension
delivered as a constant-rate infusion
pneumothorax. A routine tl10racocentesis

( 1-2 mg/kg/hr). Cardiogenic edema can
is often inadequate for these anin1als, so
benefit from venodilation from nitroglycerin
an intercostal incision or placement of a
ointment (1A in. for cats and \!,, in. for larger large-bore catheter is necessary: lidocaine
dogs) applied topically to a shaved area of
is iajected for local anesthesia, a small skin
the abdomen, inguinal region, or directly to
incision is made between ribs (at the
a mucous membrane; severely affected
seventh to eighth intercostal space), and
animals with nom1al blood pressure may
hemostats ai·e used to enter the pleural
benefit from a balanced vasodilator
space, relieving the tension witllin the

(nitroprusside, 0.5-10 mcg/kg/min), tapered
thorax. This allows cardiovascular filling
up slowly and monitoring blood pressure
and lung reexpansion. The open pneumocontinuously to keep the mean aiterial thorax is then managed by placing a chest
pressure >85 mmHg. After initial stabilizatube and surgically closing the intercostal tion, further diagnostic procedures ( eg,
incision.

thoracic radiography and echocardiogra

When breathing is severely compromised
phy) aid in deternlining the cause and
by pleural air or fluid without tension
specific therapy. Animals with proteinapneumothorax, the pleural space should be ceous fluid ( such as occurs with noncardiodrained by thoracocentesis. The intended genic pulmonary edema, respiratory distress
site is clipped and aseptically prepared
syndrome, pneumonia, etc) will not respond

(when time pernlits). If fluid is expected,
to simple diuretic therapy. If oxygen

EVALUATION AND INITIAL TREATMENT

1665
supplementation does not maintain Pa02
approaches the tenninal stages, the hea.it

>60 mml-Ig (pulse oximetry or Sp02 >90"A,), rate slows in both dogs and cats, and aninlals
or if PaC02 �60 mmHg, or if there is
begin to lose consciousness. Clinical signs
moderate to severe increases in work of
in this tenninal stage include heart failure,
breathing despite oxygen therapy, then
pulmonary edema, severe hypotension,

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manual or mechanical positive-pressure
oligmia, and abnonnal respiratory pattems.

ventilation is required.

Cardiopulmona.iy arrest is a common

If respiratory failure is inuninent with
sequela.

pulmonary fluid visible in mouth or nares,
then intubation, airway suctioning, and

Treatment: The therapeutic goal is to
manual bag-valve-mask ventilation with
deliver oxygen and substrate to the tissues.

l OO"A, oxygen are required. Elevated or

This requires a heart that effectively pumps
postural pulmonary parenchyrnal evacuablood and adequate hemoglobin, intravastion (EPPE) can be performed with two or cular volllllle, vascula.i· tone and patency, as
more people elevating the pet vertically,
well as sufficient oxygen and substrate for
head down, while guarding the endotracellular metabolism. General guidelines for cheal tube. The thoracic cavity is manually
treatment of hypovolem.ic and distributive
compressed to assist airway and lung fluid
shock are described below, but modificadrainage. Manual ventilation with lOO"A, tions may be needed for specific animals
oxygen and suction of the airway should
or disease processes.

be performed between EPPE efforts.

Oxygen Supplementation: Oxygen

( at least 40"/er-60"A, inspired concentration) Circulation
should be administered by flow-by

Diagnosis: Animals with circulatory
technique, mask, hood, nasal carumla,
compromise have alterations in their
endotracheal tube, or transtracheal
physical perfusion parameters (ie, heart
catheter.

rate, mucous membrane color, capillary

Hemostasis: Control of ongoing
refill time [CRT], rectal temperature, pulse
hemorrhage is essential for stabilization
quality, and level of consciousness). Careful

3.Ild often required before restoration of
auscultation of the heart for a murmur,
circulation. The animal must be ca.i·efully
gallop, arrhythmia, or muffled heart sounds
a.i1d thoroughly exan1ined for any evidence
and of the lungs for evidence of fluid is
of external hemorrhage. Direct pressure
irnpmtant to help identify heart failure as
should be immediately placed over the
a cause of poor perfusion. Measurement
bleeding skin site, and bleeding arteries
of arterial blood pressure, central venous
clamped. When blood slowly oozes from a
pressure, central venous Pa02, and serun1
skin wound, a compression bandage should
lactate provide objective data for reaching
be placed. If more aggressive hemostasis is
resuscitation endpoints and monitoring
required, a blood pressure (pnelllllatic) cuff
trends of change after resuscitation.

or tourniquet can be tempora.iily placed until

In the early compensatory stages of
coagulation occurs or surgical intervention
hypovolernic shock in dogs, there is a rapid
is used to stop the bleecling. Tomniquets
heart rate, pink to red mucous membranes,
should not remain in place for> 10 min.

rapid CRT, and bom1cling pulses; the anin1al

Intrathoracic or abdominal hemon-hage
is most often alert and responsive. Anin1als
may be dfficult to detect and may be
with a significant amount of pain or anxiety
exacerbated when blood pressure and
may appear to be in compensatory shock;
circulation are restored. The focused
pain medications are warranted, and time for abdominal sonography for trauma (FAST) the anin1al to acclimate to the environment is technique may be used to rapidly identify helpful. This stage is rarely identified in cats.

free abdominal fluid, focusing tl1e probe on

Tachycardia is often the first and only sign,
tl1e ventral midline caudal to the xiphoid,
so persistent tachycardia must be considover tl1e urinary bladder, a.i1d on the right ered a sign of decreased perfusion and
and left dependent flank regions. A
addressed as such. As the pathology
fom0quadrant abclominocentesis C3.Il be
progresses, clogs begin to have pale mucous
pe1fom1ecl if ultrasound is not immediately
membranes, prolonged CRT, weak pulses,
available. The TFAST may be used to
tachycardia, and a decreased level of
identify pleural fluid as well.

responsiveness-the classic signs of the

Ongoing abdominal hemorrhage is
miclclle or early clecompensatory stage of
initially managed by small volume fluid
shock Cats have gray mucous membranes,
resuscitation to low-normal endpoints and
slow CRT, weak or absent pulses, hypotherabdominal counterpressure (seep 1667).

mia, and a nonnal or low heart rate. As shock Ongoing intrathoracic hemorrhage should

1666

EVALUATION AND INITIAL TREATMENT
be managed with thoracocentesis or a

Warming: Animals in shock should be
thoracostomy tube to evacuate the blood
warmed dwing fluid resuscitation until
and to allow measurement of the volume
rectal temperatures ai·e >98°F. This is best

Jost. Exploration of these body cavities
accomplished by increasing the environ

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may be required for assessment and
mental temperature using warm air blowers
definitive hemostasis if a coagulopathy is
or hot water bottles with blallkets, warm
not present. PCV of thoracic or abdominal
water blankets, and fV fluid line warmers.

fluid the same or higher than that of

Gastlic, pelitoneal, or urinary lavage may
peripheral blood confinns hemorrhage.

be needed for severe hypothermia. Surface

Significant volumes of cavitary hemorrhage wam1ing is instituted only after initial may be collected in sterile, empty fV bags
volun1e resuscitation has provided enough
or blood transfusion bags for autologous
intra.vascular volume to offset the
blood transfusion, if necessary.

peripheral vasodilation. Care must be taken
lntravascular Volume Replacement:

in animals with cardiogenic shock or

Intravenous or intraosseous catheters are
pericai·dial disease to avoid excessive
used, with multiple catheters placed for
peripheral vasodilation, because this may
rapid, large-volume infusion in dogs >30
exacerbate a relative hypovolemia ( due to
kg body wt. Isotonic crystalloids can be
decreased cardiac output).

administered by repeated Jow-volw11e

Corticosteroids: Corticosteroids
boluses (10-15 mLJkg) until desired
are administered when a deficiency is
endpoints of resuscitation are reached ( eg,
suspected (ie, Adclisonian crisis, critical
low-n01mal cardiovascular parameters).

illness-related corticosteroid insufficiency).

However, the interstitiwn is at risk of fluid

High-dose steroid administration has not
overload with crystalloids alone. The
been proved to reduce mortality in hypoconcurrent use of colloids and crystalloids volemic, septic, or cai·diogenic shock and
can reduce the an10unt of c1ystalloid
has been associated with increased
required, rapidly expand the intravascular
morbidity, so it is not reconunended.

space with a smaller volume of fluid infused,
and reduce the amount of fluid extravasat

Cardiovascular Support: Phannacoing into the interstitial spaces of vital organs Jogic agents (positive inotropes, systemic (eg, lung, brain). Isotonic crystalloids are
vasodilators, and vasopressors) can be used
given with hydroxyethylstarches (eg,
when fluid infusion has adequately replaced
hetastarch) or stroma-free hemoglobin.

intra.vascular volwne (ie, central venous

Whole blood, stroma-free hemoglobin, or
pressure >5-8 cm H20) but fails to restore
packed red cells are necessaiy during initial
blood pressure and perfusion, or when poor
volume resuscitation when hemorrhage has
cardiac contractility is thought to contribute
been significant.

to hypotension. A positive inotropic agent

Small volume resuscitation to lowcan be administered to increase cardiac normal endpoints (measured perfusion
contractility in diseases such as sepsis and
paraineters) is used to avoid volun1e
dilated cardiomyopathy ( eg, dobutarnine,
overload or hypertension and is ideal for
initially at 2-5 mcg/kg/rnin, and the dosage
aninlals with head irtjwy, pulmonaiy edema
titrated for optimal cardiac output).

or contusions, abdominal or intra.thoracic

Stroma-free hemoglobin ( dogs 5 mUkg; cats
hemorrhage, heart disease, and all cats in

1-3 rnL per cat, slowly) can be adminishypovolemic shock. Isotonic crystalloids tered, and repeated as indicated, for its
are given (10-15 mUkg, fV), followed by
colloid effect as well as its mild vasopressor
hetastarch or stroma-free hemoglobin
effect; it is particularly useful in animals

( dogs 5 mUkg, fV; cats 1-5 mUkg, fV,
with concurrent anemia. The initial
slowly), repeating the colloid infusion, to
resuscitation doses may be followed by
effect. The least an10unt of crystalloids and
a slow constant-rate infusion (dogs
colloids possible are used to obtain and

10-15 mLJkg/day; cats 1-3 rnllhr up to
maintain a systolic blood pressure of 90

5 mLJkg/day) to maintain perfusion if the
mrnHg, restore a normal heart rate, and
initial dose was successful and further
improve CRT and pulses. For an in-depth
support is anticipated. Pressor agents
explanation, seep 1675.

delivered as an fV constant-rate infusion
such as dopamine (5-20 mcg/kg/min),

Pain Control: Analgesia is provided
norepinephrine (0.05-2 mcg/kg/min) or
during initial fluid resuscitation for optimal
vasopressin ( extra-label, 1-4 m U/kg/rnin)

cai·diovascular response and relief of
are other options to support blood pressw·e;
anxiety. Narcotics are administered systemithey should be delivered in the smallest cally, and local anesthetics can be infiltrated
dosage needed to maintain arterial systolic
into the affected area. (See also p 2104.)

pressure >90 mmHg. The blood flow to the

EVALUATION AND INITIAL TREATMENT

1667
kidneys and GI tract, as well as other
information such as when the aninlal was
organs, may have been significantly
last completely normal. A chronology of the
impaired during shock. Urine output, heart
daily progression of abnormalities since the
rate, blood pressure, ECG, pulse intensity,
onset of signs can be useful. Background
and mucous membrane color should be
inforn1ation includes past medical

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closely monitored, because fmther vasoconproblems, toxicities, medications, drug striction can worsen organ blood flow and
and food sensitivities, blood transfusions
function. If organ function declines or if
the date of last vaccinations, and other
arrhythmias become a problem, the IV cl.tip
preventive care. Other organ systems
should be stopped.

not seemingly involved should also be

Hindlimb and Abdominal Binding:

historically evaluated. Details of the specific

When ongoing abdominal hemorrhage is
disease process are obtained and may help
suspected from trauma, hindlimb and
direct diagnostics and care.

abdominal counterpressure can improve

A complete physical examination should
perfusion. This procedure compresses the
be performed, working from head to tail.

arteries and arterioles within the bound

Particular attention is given to heait and
regions, increasing regional vascular
lung auscultation for abnom1alities, and to
resistance, and produces abdominal
abdominal, rectal, and joint palpation for
tamponade, thereby effectively slowing or
pain or enlargements. A complete neurologic
arrestmg hemorrhage and redirecting blood
and orthopedic exainination is often
flow from the venous capacitance vessels
warranted. Acute abdominal pain requires
in the caudal half of the body to the more
localization of tl1e pain and auscultation of
central (core) circulation. Hindlimb and
the abdomen for bowel sounds to localize
abdominal counterpressure can be
tl1e problem to the reticuloendothelial
perfonned by placing a rolled towel or
reproductive, urinary, or GI systems; the
rolled cotton between the legs and along
pentoneal space; or the muscle, skin, nerves,
the ventral midline of the abdomen. Th.is
or fat around the abdominal wall. Fever of
prevents the wrap from in1pairing ventilaunknown migin directs exanlination to tl1e tion or fracturing the spleen or liver. If time
peritoneal cavity and to the reproductive
pennits, a urinary catheter is placed. The
minary, pulmonary, and cardiovascular
h.indlimbs and abdomen are then fumly
systems.

wrapped with padded bandage material or

An initial minimum database should
towels, beginning at the toes of the hindlimb consist of a PCV, total solids, glucose, and and moving cranially toward the xiphoid,

BUN. Other important diagnostics include
taking care not to in1pede respiration. The
urinalysis (before fluid administration),
bandage should be secured with tape or
venous or arterial blood gas, an electrolyte
stretch bandage material wrapped in a
panel, a CBC, and a serum chemistry pan.el.

spiral pattern starting caudally and moving

When coagulation disorders are suspected
crarually. Abdominal binding should be
or surgery is anticipated, blood smears to
avoided in cases of intrathoracic or
estimate platelet number, buccal bleeding
intracranial hemorrhage. Once perfusion
time _to evaluate platelet ftmction, and a
has stabilized, the wrap is removed slowly
clottmg profile such as an activated clotting
by sections ( releasing one section every
tune or prothrombin time and activated

15 min) from the abdomen, starting at the
partial thromboplastin time are warranted.

most cranial portion and moving caudally.

A deficit in any of the first tlu·ee compo

Any signs of decompensation wan·ant rapid
nents of tile primary swvey (ie, airway,
rebinding of the region last unwrapped.

breatlling, circulation) will quickly result in
anaerobic metabolism due to poor oxygen
delivery to the tissues. This can rapidly

SECONDARY SURVEY
result in a type A lactic acidosis. Lactate can
be accurately, easily, and rapidly meas

The secondary survey of emergency
ured with several point-of-care analyzers.

patients is the process of obtaining

Nonna! lactate values in dogs and cats are
significant and thorough historical

<2 mmol/L. Lactate levels normalize rapidly
information, perfonning a complete
witl1 treatment of the underlying condition
physical examination, and collecting
of poor oxygen delivery to the tissues ai1d is
general diagnostic info1mation. These data
associated witll improved survival. Lactate
are used to direct the fo1mulation of a
can be used along with other paran1eters as
specific diagnostic, therapeutic, and
an endpoint of resuscitation in hypovolemic
monitoring plan.

aninlals. Initial increases in blood lactate

The history should be recorded in a
have been reported to be associated witll an
concise forn1at. The presenting complaint is
increase in complications and mortality in
obtained from the owner, who can provide
ce1tain diseases in small aninlals.

1668

SPECIFIC DIAGNOSTICS AND THERAPY

SPECIFIC DIAGNOSTICS AND THERAPY

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TRAUMA
occurs, the pe1ipheral blood PCV may be
nmmal or even increased with a normal or

Diagnostic and therapeutic efforts in
decreased relative total protein level; this is
emergency situations can be directed by
a clinical indication of hemorrhagic shock
the nature of the trauma. Blunt trauma is
in dogs and occurs because of splenic
commonly associated with thoracic and
contraction. This release of RBCs into
abdominal bleeding, organ rnpture,
circulation may occur faster than
fractures, and neurologic irtjmies.

interstitial to intravasculai· fluid shifts;

Penetrating trauma is typically localized to
therefore, serial PCV and total solid
the patl1 of the penetrating object, which is
measurements should be monitored after
rarely a straight line. Falling from a height
trauma. Both PCV and total solids will
causes long bone and facial bone fractures
decrease as hemorrhage and subsequent
as well as tl10racic and abdominal irtjuries.

crystalloid/colloid resuscitation continues.

A dog bitten by a larger dog can have

An extended initial database includes
deep-penetrating bite wounds, spinal
aiterial or venous blood gases, electrolyte
injmies, major abdominal and tl10racic
panel, blood lactate, and prothrombin time/
trauma ( even without penetrating wounds),
partial thromboplastin time. This baseline
and tracheal rupture from tl1e sheaiing
i.nfonnation is used to create the initial
forces sustained during thrashing motions.

treatment plan ai1d to provide the baseline

Resuscitation of the airway, breathing, and
for subsequent monitoring. Ionized
circulation; control of hemorrhage; and paiJ1 hypercalcemia has been associated with relief ai·e followed by a cai·eful evaluation
a poorer prognosis after traun1a ai1cl may
of the nervous system, chest, abdomen,
warrant more intensive monitoring. Survey
integument, and musculoskeletaJ system.

lateral racliographs of the chest and

The tratunatized animal should be
abdomen at presentation can demonstrate
approached as if multiple ir\ituies are
the initial changes resulting from thoracic
present. The neck and spine should be
and abdominal trauma. Orthogonal views
immobilized until a thorough exanunation
should be performed as the ai1imal's
for spinal fractures or luxations is made.

condition dictates. Ultrasound exainination

Thoracic auscultation for cardiac arrhythof the abdominal and thoracic cavities may mias and tl1e presence and quality of lung
provide additional information about
sounds should be done to identify chest
internal irtjuries and can often be perfmmed
injuries. The abdomen should be palpated
wlille fluid resuscitation is initiated.

for pain, fluid, or hernias. Extremity

Some scoring systems have been
fractures should be supported by bandeveloped for trauma, such as the animal dages or splinted to prevent further iajury.

trauma triage score; this system assigns

Significant swelling may indicate ongoing
a number from O (slight or no iajury) to
hemorrhage. Because many internal irtjtuies 3 (severe injury) in the following may not be apparent for a significant
categories: perfusion, cardiac, respiraainount of tin1e after tl1e initial traun1a tory, eye-muscle-integument, skeletal,
occurs (12-48 hr), close monitoring is
and neurologic. In one study assessing
essential to allow early detection of

>200 clogs evaluated after vehicular
potentially life-threatening problems. An
trauma, dogs that died or were euthaanin1al that appears nom1al and stable on nized had signficantly higher scores
initial exainination may have substantial

(median 6) than those that survived
underlying irtjury, making monitoring of at

(median 2); higher scores were also
least physical exanunation paraineters in
associated with higher cost of care.

the hospital ( eg, respiratory and heart rates,
mucous membrane color, and mentation)

appropriate.

Thoracic Trauma

Initial diagnostic evaluation should

Pulmonaiy contusions, pneumothorax,
include the minimum database before
cardiac arrhythmias, pleural hemorrhage,
fluids a.re administered, if possible.

peiicardial hemorrhage, 1ib fractures, flail

Point-of-care tests should nunimally
chest, and diaphragmatic hernia are some of
include a PCV, total solids, BUN test strip,
the potentially life-threatening complicaand blood glucose. When hemorrhage first tions that must be considered in thoracic

SPECIFIC DIAGNOSTICS AND THERAPY

1669
trauma. Oxygen supplementation and
cavity, and place a thoracostomy tube
analgesics allow careful physical examinabefore closure.

tion. An ECG, thoracic radiographs, blood

As the anin1al's condition allows, thoracic
gas analysis, and diagnostic or therapeutic
radiographs (two or three views) should be
centesis help detennine the extent and
performed to assess for injury to the lungs.

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seve1ity of the problems.

Many of the above-listed injuries may show

Severe pulmonary contusions cause
up on routine radiographs; however,
hypoxemia, labored breathing in a pattern
radiographic evidence of pulmonary
consistent with parenchymal disease, and
contusions may not appear until 12-24 hr
crackles and rales on pulmonary auscultaafter the initial injury.

tion. If the animal does not improve with

The heait should be ausculted and an
supplemental oxygen, pain medications,

ECG evaluated for arrhytlunias. A rrhythand fluid therapy, then tracheal intubation mias may not be present at the tinle of injury
and positive-pressure ventilation with 100%
but develop 12--48 hr after the event as
oxygen are indicated. The airway should be
myocardial contusions and hypoxemia affect
suctioned to evacuate blood and deb1is that
the cardiac conduction system. Common
are obstructing the flow of air.

ai-rhytlunias seen after thoracic trauma

Labored breathing with asynchronous
include sinus tachycardia, ventricular
movement of the chest and abdomen and
premature contractions, and ventricular
dull or quiet lung sounds is consistent with
tachycai·dia. Treatment with lidocaine or
plew·al air or fluid and warrants immediate
other anti arrhythmic medications is
thoracocentesis. Thoracocentesis should be warranted if the arrhythmias impair performed before taking radiographs in
perfusion, if the rate is rapid and sustained
animals with respiratory distress, because

(>180 bpm in dogs), if ventricular premature
animals may struggle and decompensate
contractions are multiform, or if there are
while radiographs are being taken;
prefibrillatory rhytluns (R on T phenomenon,
assessment with ultrasound may be less
torsades de pointes, ventriculai· flutter).

stressful but should not delay therapy. When
a negative pressure cannot be achieved,
repeated thoracocentesis or continuous

Abdominal Trauma
drainage of the pleural space by chest tube

The extent and severity of abdominal
is required. Large quantities of whole blood
injuries are often not initially apparent,
removed on thoracocentesis or ongoing
unless there is visceral herniation outside
leakage of air after 72 hr of pleural drainage
the body cavity. The abdominal surface
are indications for surgical exploration of
should be examined closely for evidence
the chest. Large volwnes of blood aspirated
of bruising, abrasions, lacerations,
dw"ing a centesis may be collected into an IV protrusions, localized swelling, hernfabag or blood transfusion bag, because they tions, distention, and pain. Animals with
may be used for autologous blood
evidence of abdominal pain that are in
transfusion.

shock are considered to have intra

The thoracic focused assessment with
abdominal hemorrhage until proved
sonography technique (TFAST) can help
otherwise. Rupture or laceration of the
diagnose pneumothorax, hemothorax, or
spleen or liver are the most common
thoracic wall trauma and provides an
sources of intra-abdominal hemorrhage.

alternative to radiographs when per

However, all abdominal organs are
formed by a skilled sonographer familiar
susceptible to the shearing forces from
with ultrasonographic changes associated
blunt trauma. Other common sources of
with these injuries. The chest cavity
abdominal bleeding include avulsed
should be palpated for 1ib fractures with
mesenteric vessels, dan1aged muscle,
displaced bone, flail segments, avulsion
or avulsion of the kidneys in the retroof ribs, torn intercostal muscles, and peritoneal space.

herniations. When flail segments impair

Approximately 40 mUkg Uust less than
ventilation, the segment is stabilized by
half of the circulating blood volume) is
securing it to an external fran1e or cast,
necessary before free blood in the
formed to the shape of the chest.

abdominal cavity will be evident by

Penetrating bite wounds over the chest
palpation or visual inspection; this volume
should be explored under anesthesia for
is associated with signs of poor perfusion
debridement and drain placement; if the

(shock). Smaller volumes of abdominal
wound is penetrating, the thorax may be
fluid may be apparent with radiographs,
surgically entered to inspect dan1age to
abdominocentesis, or ultrasound of the
underlying tissue, repair or deb ride that
abdomen. Abdominal distention from
tissue as necessary, lavage the thoracic
hemorrhage may become apparent if

1670

SPECIFIC DIAGNOSTICS AND THERAPY
aggressive fluid resuscitation increases

(body wall) hemorrhage or hemorrhage
blood pressure and disrupts one or more
into the GI system can be more challenging
blood clots that provided hemostasis.

to identify.

Small volume fluid resuscitation to

Criteria. for emergency exploratory

VetBooks.ir
achieve a low-normal blood pressure

Japa.rotomy include ongoing hemorrhage;
endpoint (90 mmHg systolic) is indicated
inability to stabilize shock; organ rotation,
to avoid sudden increases in arterial or
entrapment, or ischemia; diaphragmatic
venous pressures. When ongoing
hernia; and evidence of organ rupture or
abdominal hemorrhage is confirmed,
peritonitis. Some simple bladder ruptures
hindlimb and abdominal binding (see
may be amenable to medical management
p 1667) is indicated early to reduce the
and placement of a tuinary catheter. Surgery
amount of hemorrhage until hemostasis
to repair a diaphragmatic hernia should not
is accomplished.

be delayed, particularly with gastJic

After irtjury of any abdominal organ,
displacement into the thoracic cavity, respiraclinical signs of organ dysfunction or hollow tory compromise, or ongoing hemorrhage.

viscus rupture typically develop over a

Retroperitonea.l, severe fascia! compaitperiod of hours but may be longer or shorter ment hemorrhage (associated with pelvic depending on the nature of the irtjury. Acute
fractures), or hemorrhage into a hollow
abdominal pain is a key physical finding.

viscus is suspected in acutely t1·aun1a.tized

Survey abdominal radiographs can
animals that still have signs of a declining
demonstrate organ displacement, disten

PCV/tota.l solids, nonresponsive hemortion, rotation, or free abdominal gas or fluid.

rhagic shock, and no significant findings on

Fluid can be recovered by fow0quadrant
abdominocentesis, peritoneal lavage, or
abdominocentesis. Using the focused

FAST scan. Radiog:raphs typically show
assessment with sonography technique
expansion and loss of detail in the retJ·operi

(FAST, seep 1665), even small amounts of
toneal space. An IV pyelogran1 should be
free fluid in the abdomen can be identified
done to help delineate disruption in the
and aspirated using ultrasound guidance.

renal vasculai· supply or in the retroperito

When free fluid is not readily identified,
neal portion of the ureter before proceeding
a diagnostic pe1itoneal lavage can be done.

with exploratory surgery in this situation.

A fenestrated catheter is placed into the
peritoneal space, and warm isotonic saline

CARDIOPULMONARY

(20 milkg) is in.fused into the abdomen. The

RESUSCITATION
fluid is allowed to dwell for several minutes
and distribute throughout the abdomen; it is

The success of cardiopulmonary resuscitathen drained and evaluated.

tion (CPR) efforts depends on many factors,

Clear fluid indicates.that the possibility
including the underlying ca.use of the arrest,
of significant abdominal hemorrhage is
the timeliness and effectiveness of the
minimal. Fluid with a 1% PCV indicates mild intervention, and the preparedness of the abdominal hemorrhage, whereas fluid with
team adniinisteri.ng CPR. Overall prognosis
a PCV >5% indicates significapt abdominal
of recovery from cardiopulmonary arrest
hemorrhage that warrants careful

(CPA) with CPR effo1ts is as high as
monitoring.

35%-44%; however, only <100/oof anirnals

Fluid obtained from the abdomen
survive to dischai·ge. Aninlals with CPA
should be examined cytologically for
associated with anesthesia have a better
evidence of WBCs, plant or meat fibers,
prognosis. The An1e1ican College of
and free or intracellular bacteria.

Vete1inary Emergency and Critical Care

Biochemical evaluation for creatinine
developed the first set of guidelines for
and potassium, bilirubin, amylase, and
vete1inary CPR; this effort was tem1ed the
phosphorus help identify urinary system

Reassessment Campaign on Vete1inary
rupture, gallbladder rupture, pancreatic

Resuscitation (RECOVER) and is available
irtjury, or ischemic bowel, respectively.

at www.a.cvecc-recover.org. CPR is divided

Abdominal fluid glucose that is 20 mg/dL
into several sections: prevention and
or more below peripheral blood glucose
preparedness; basic cardiac life suppo1t
is characteristic of a septic peritonitis

(BCLS) promoting oxygenation, ventilation,
and warrants exploratory surgery. The
and circulation; advanced cai·diac life
a.bdominocentesis, peritoneal lavage, or
support (ACLS) using electrocardiogra.phic

FAST scan can be repeated in several
evaluation of cardiac rhythms, administrahours if fluid from the first assessment did tion of drugs, and defibrillation when
not indicate a significant problem but the
necessary; monitoring during CPR; and
clinical signs continue or progress.

postresuscitation management, which

Retroperitoneal, fascia!, or intramuscular
involves intensive monitoring of conunon

SPECIFIC DIAGNOSTICS AND THERAPY

1671
complications after anest as well as
fashion and should compress the chest wall
diagnosis and treatment of underlying condi

'h to \-\! of the width and allow full recoil of
tions that led to the cardiopulmonary anest.

the chest. When the cardiac pump
technique is used, direct compression of

Prevention and Preparedness
the ventricles of the heart contribute to

VetBooks.ir

In an effort to have the entire vete1inary
forward blood flow; in the thoracic pump
team prepared for CPR on any animal,
technique, changes in thoracic pressure are

RECOVER guidelines recommend standardthe important mechanism to generate ization and regular audit of resuscitation
forward blood flow. Simultaneous
equipment as well as immediate availability
ventilations and compressions should be
of cognitive aids and descriptive CPR
done in 2-min cycles; individuals perfonning
algorithms (eg, dose charts, checklists),
the ventilation and compressions should
which are available through the RECOVER
change functions every 2 min Lo prevent
website. Cognitive skill training and
fatigue and less-effective compressions.

didactics should be incorporated for all

Interruptions to chest compressions to
veterinary team members on a regular basis. assess ECG or auscult the heart should be Assigning a leader and having specific
minimal. Interposed abdominal compresleadership training, including deb1iefing sions may be added for animals without
after any CPR efforts, are reconunended as
abdominal disease if adequately trained
well. Each team member should be fanilliar
staff is available. This is performed by
with available medical equipment and his or
placing both hands on the abdomen and
her role during CPR.

compressing quickly, timing the
compression to be done between chest
compressions.

Basic Cardiac Life Support

The goal is to in1prove venous return to

When CPA is recognized, CPR efforts
the heart during the diastolic phase of the
should begin immediately. Early recognicompression cycle. Monitoring CPR (see tion and inte1vention is essential. Palpation
below) may necessitate a change in CPR
of pulses is not recommended before initiattechnique.

ing compressions, because this will delay
intervention. Mouth-to-nose resuscitation
should be performed until endotracheal

Advanced Cardiac Life Support
intubation and positive-pressure ventilation

In ACLS, an ECG is obtained to characte1ize
with 100% oxygen can be accomplished.

anhythmias, followed by drug administra

The compression to ventilation ratio should
tion or defib1illation as indicated. The
be 30:2. Once the airway is established, it is
purpose is to reestablish elect1ical and
imperative to confirm placement with
mechanical activity of the heart. The major
thoracic auscultation, visualization,
anesting rhythnis in veterinary medicine
palpation, and ETC02 monitoring, as well as include sinus bradycardia, asystole, to secure the tube with a tie-in. Ventilations
pulseless electrical activity (PEA, previshould be provided at a rate of 10 breaths/
ously termed electromechanical dissociamin, with a volume of 10 mUkg and an tion), and ventricular fibrillation or flutter.

inspiratory time of 1 sec. Ideally, these

Drugs are selected based on the an·hythnlia
breaths are provided with a portable
or known/suspected underlying disease
bag-valve-mask apparatus.

and can be administered by intravenous,

Simultaneous with ventilation, circulaintraosseous, or intratracheal routes (see tion should be promoted in small animals

TABLE 2). Drugs that can be administered
by compressing the chest externally.

intratracheally include naloxone, atropine,

Compressions should be performed with
vasopressin, epinephrine, and lidocaine
the animal in lateral recumbency ( or dorsal

(best remembered by the acronym NAVEL);
recumbency for barrel-chested animals,
the dosage for all drugs is usually doubled
such as Bulldogs). Compressions should
when administration is intratracheal.

be performed over the widest part of the

Intraca.rdiac administration of drugs is no
thorax using the "thoracic pump" technique. longer recommended, because arrhythmias, In keel-shaped animals (such as Greymyocardial hemorrhage, and myocardial hounds or cats), compressions may be
vessel laceration may occur.

perfonned directly over the heart (at the

If the anin1al is known or suspected to be
fourth and fifth intercostal space) using the
hypovolemic, isotonic balanced crystalloid

"cardiac pump" technique. The compressolutions should be rapidly infused to restore sion rate should be 100-120 compressions/
volw11e and promote perfusion. Synthetic
min regardless of size. Each compression
colloids such as hetastarch, hydroxyethyl
should be delivered quickly in a cough-like
starch, dextran 70, or stroma-free hemo-

1672

SPECIFIC DIAGNOSTICS AND THERAPY

DRUGS AND DEFIBRILLATION USED IN CARDIOPULMONARY

RESUSCITATION

Drug

Dosagea

Indications

Epinephrine

Low dose (0.01 mg/kg)

Asystole, ventricular

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every 3-5 min early in CPR; fibrillation, PEAb
high dose (0.1 mg/kg) after
prolonged CPR; 10 times
the dose may be required
when given .intratracheally

Atropine

0.1 ml/5 lb (0.5 mg/mL

Sinus bradycardia, asystole,
solution)

or PEA associated with high
vagal tone

Sodium bicarbonate

1 mEq/kg (1 mEq/mL

Severe metabolic acidemia
solution)

associated with prolonged

(> 10-15 min) cardiopulmonary resuscitation efforts (must be adequately
ventilated to be effective),
hyperkalemia

Calcium gluconate

1 ml/5-10 kg (2% solution Routine use not recommendwithout epinephrine) ed; treat cases with documented hypocalcemia ( or severe hyperkalemia)

Amiodarone

5 mg/kg

Refractory ventricular
fibrillation or pulseless
ventricular tachycardia

Magnesium sulfate

30 mg/kg

Hypomagnesemia, torsades
de pointes

Lidocaine

2-4mg/kg

Pulseless ventricular
tachycardia, ventricular
fibrillation resistant to
defibrillation

Vasopressin

0.4-0.9 U/kg

Combined with or as a
substitute for epinephrine
every 3-5 min (asystole,
bradycardia, PEA)

Naloxone

0.02-0.04 mg/kg

To reverse opioids

Defibrillation

4-6 joules/kg external

Single shock, resume CPR

(monophasic), 2-4joules/ efforts immediately after for kg external (biphasic),
one cycle (2 min), dose

0.2-1 joules/kg internal
escalation may occur
a Dosage should be doubled if given via intratracheal route.

b PEA= pulseless electrical activity
glob.in rapidly expand the intravascular
tered to euvolemic animals, because the
volume with much smaller infusion volumes
increase in central venous pressure may
required. Overzealous fluid administration
reduce myocardial and cerebral blood flow.

can result in fulm.inant pulmonary edema

Metabolic alterations such as hyperkalemia,
due to poor myocardial contractility and
hypocalcemia, and severe acidosis should be
arrhythmias. Fluids should not be adminis-
treated when evident but not otherwise.

SPECIFIC DIAGNOSTICS AND THERAPY

1673

Impedance threshold devices may be conof ventricular or supraventricular origin), sidered an adjuvant to therapy and used
but the heart has no muscular activity
only on animals weighing > 10 kg.

associated with the electrical activity, ie,

If closed chest BCLS is unsuccessful
no contractions and no cardiac output and,

(as detennined by lack of spontaneous
subsequently, no pulses. In this arrhytlunia,

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respiration or inability to generate
it is vital that thoracic auscultation be
detectable forward blood flow) after
perforn1ed in tandem with central pulse

5----10 min, open-chest CPR (see below) is

(femoral arterial) palpation and ECG
indicated. Instances when open-chest CPR
evaluation. There are no heart sounds or
is indicated dming initial BCLS include
pulse activity. However, severe hypovunwitnessed arrest, recent abdominal or olemia, pericardial effusion, and significant
thoracic surgery, suspected pleural or
accun1 ulation of fluid or air in the pleural
pericardial disease, traunm or pathology of
cavity can prevent detection of nonnal heart
the chest or abdominal wall with blood loss,
sounds. The ECG associated with these
diaphragmatic hernia, and in larger dogs in
conditions demonstrates tachyarrhytlunias,
which external compressions are unlikely
in contrast to the usually norn1al or slow
to generate an adequate forward blood flow. rate of PEA. Atropine and epinephrine or vasopressin may be given in an attempt to

Arrhythmias of Cardiac Arrest
correct this arrhytlunia. Defibrillation may
be attempted with pulseless ventricular

Asystole: Asystole appears as a flat line on tachycardia.

the ECG and suggests complete absence of
electrical activity. In arrest situations known
or suspected to be associated with

Sinus Bradycardia: Sinus bradycardia on
hyperkalemia, calcium gluconate should be
the ECG has P, QRS, and T waves that appear
administered. Regular insulin at 0.2 U/kg,
nonnal, except they occur at a much slower
followed by glucose at 1-2 g,'[J of insulin,
rate. This airesting rhytlun may be caused by
diluted to 25%, temporarily reduces senm1
many disease processes, such as high vagal
levels of potassium. Epinephrine or
tone due to GI, urinary, or thoracic disease,
vasopressin, with or without atropine can
and hyperkalemia due to urinary obstruction
be administered in an attempt to generate
or ruptme and prolonged CPA witl1 CPR
impulses. Fine ventricular fibrillation may
efforts. Treatment of known or suspected
look like asystole, and for this reason,
hyperkalemia with calcium gluconate,
open-chest heart massage and direct
insulin, and dextrose with or without sodium
observation of myocardial activity are
bicarbonate may be necessary. Atropine is
warranted early with this a.1.Thytlunia;
indicated in this an·hyt]unia.

if fibrillation is visualized, defibrillation is indicated.

If the CPA is believed to be associated
with drug administration, a reversal agent

Ventricular Flutter: This rhytlun is more
should be administered in addition to
chaotic than ventricular tachycardia and is
treating arrhythmias in ACLS. Benzodiazprefibrillatory. Lidocaine is the drng of epines such as diazepam and midazolam
choice to block the excited focus.

are reversed with flumazenil, opioid

If
lidocaine is ineffective after two boluses
medications such as fentanyl and
and pe1fusion is absent, defibrillation may
morphine-related drugs can be reversed
be required.

with naloxone or partially reversed with
butorphanol, xylazine can be reversed
with yohimbine, and dexmedetomidine

Ventricular Fibrillation: This rhytlun
can be reversed with atipamezole.

implies that multiple foci within the

If
inhalant anesthesia was used, it should be
ventricles are firing rapidly and independiscontinued and the anesthetic circuit dently, resulting in no coordinated mechaniflushed with fresh oxygen.

cal activity. There are no ventricular
contractions and no cardiac output. The goal
is to abruptly stop the electrical activity and

Open-Chest Cardiopulmonary
allow one strong (hopefully norn1al)

Resuscitation
electrical rhytlun to take over. Defibrillation
is more successful when there are few, strong (Emergency thoracotomy) foci ( coarse fibrillation) tl1an when there are

If possible, a quick clip of the hair along the multiple, weak foci (fine fibrillation).

intended incision site is helpful. Usually,
there is no time for a full aseptic preparation

Pulseless Electrical Activity (PEA):

of the ai·ea A scalpel blade or Mayo scissors

The ECG tracing can be no1mal or show an
are used to incise the skin and subcutaneous
arrhytlunia ( conunonly a bradyarrhytlunia
tissues along the cranial border of the fourth

1674

SPECIFIC DIAGNOSTICS AND THERAPY
or fifth rib from the spine to sternum. A
confirm endotracheal intubation. ETC02

Carrnalt forceps or Mayo scissors are used
may also be an early indicator of return
to bluntly dissect th.rough the underlying
of spontaneous circulation (ROSC) and
muscle tissues and push tlu-ough the pleura
effectiveness of CPR efforts ( when

Ventilations should be discontinued
minute ventilation is consistent). An

VetBooks.ir
momentarily, and the instrument should be

ETC02 of <10 mmHg indicates esophaguarded with a thw11b and forefinger as the geal intubation, ineffective CPR technique,
pleura is entered to prevent injury to the
incorrect placement of endotracheal tube,
heart or lungs. After the pleura is entered
or hyperventilation (if adequate perfusion
at the ventral aspect of the incision, Mayo
is established). An ETC02 reading of
scissors are used to incise the muscles

12-18 mmHg indicates an ROSC, and a
dorsally along the entire length of the
reading of >45 mmHg may indicate
intercostal space, along the cranial aspect
hypoventilation or increased C02 delivery
of the 1ib. Care should be taken to avoid
to the lungs after ROSC occurs.

incising the internal thoracic vessels running

Routine monitoring of ECG is essential
parallel and lateral to the sternun1. After the
during CPR to allow identification and
chest cavity is opened, manual ventilations
specific therapy of atThytlu11ias. Palpation of
should continue, and the pericardiodiapulses either to detect CPA or to monitor phragmatic ligament elevated and incised
effectiveness of CPR effotts is not recomwith scissors, extending the incision dorsally mended because of the insensitive nature of to just ventral to the plu·enic nerve. The heait this test. Use of Doppler monitoring ( on eyes is then lifted out of the pe1icardial sac and
or peripheral arteries) to detect CPA or moniobserved for any coordinated spontaneous tor effo1ts of CPR is also not reconunended.

contractions. If no cai·diac contractions are

Use of blood sainples may help guide
noted, the heait is grasped with one or both
therapy in some instances during CPR.

hands and compressed progressively from

Centrally collected sainples ai·e ideal;
the apex to the base. The compression is
however, most patients do not have a central
then released to allow the cardiac chai11bers
catheter. Peripheral blood sai11ples do not
to refill with blood. If fine or coai-se
necessarily reflect the central circulation but
fibrillation of the heart muscle is noted,
may help guide therapy in some instat1ces
internal defib1illation should be perfonned.

(such as hyperkalemia). lt is not recom

The descending aorta can be isolated and mended to monitor with arte1ial gas sainples temporarily cross-clainped to direct blood
or pulse oxin1etry; these require pulsatile
flow to the brain. Aortic cross-clainping
aiterial flow, which is inadequate during CPR.

can be pe1formed with atraumatic vascular

Close monitoring of an animal after
clan1ps or by using a modified Romm ell
arrest is vital, because significant
tourniquet, passing a ru_bber tube, latex
abnormalities of acid-base and electrotube, or umbilical tape ai·ound the ao1ta lytes (especially hyperkalemia) are
with the assistance of curved hemostats
common and may require additional
and then clainping on the tube to occlude
treatment. Paraineters such as ECG,
aortic flow. Ao1tic cross-clai11ping can be
blood pressure, neurologic status, pulse
performed for 10 min withoufserious
oximetry, ETC02, and venous blood gases
complications (from lack of blood flow
should be monitored closely. Blood
to the spinal cord).

pressure support with dopamine,

An ECG is evaluated and drugs given as
dobutamine, other pressqr agents, or
indicated during ACLS procedures. Return stroma-free hemoglobin, as indicated, may of spontaneous circulation allows lavage
be required to maintain cai·diac output.

of the thorax with large quantities of

Body temperature, glucose, and lactate
sterile, warm, isotonic saline; placement
may provide additional information.

of a thoracostomy tube; and surgical

With anaerobic metabolism that occlil'S
closure of the thorax. Cardiovascular
during shock and cardiopulmonary arrest,
support (seep 1665) is frequently required
blood lactate levels (seep 1686) rise
to maintain circulation while the underdramatically (no1111al levels are <2 mmol/L).

lying cause of the arrest is treated.

With ROSC, lactate levels may rise
drainatically and then resolve with

Monitoring
appropriate treatment.

End-tidal C02 (ETCOz) should be
measured in intubated patients at risk of

Postresuscitation Care
having CPR and is a useful monitoring

Routine use of large volumes of fluids is
tool during CPR efforts. Using an ETC02
not recommended and should be avoided
reading along with visualization,
in animals with congestive heart failure.

palpation, and auscultation can help

It is important to use resuscitation

FLUID THERAPY

1675
endpoints during post-CPA care to normalhypoxemic. Vasopressors and positive ize venous oxygen content, lactate, blood
inotropes are reasonable when needed.

pressure, central venous pressure, PCV,

Animals with open-chest CPR will require
and oxygen saturation. Medications to
control of hemorrhage, pleural lavage,
help reduce cerebral edema, such as
placement of a chest tube, perioperative

VetBooks.ir
mannitol and furosemide, can be
antibiotics, and closure of the thoracic
administered after CPA and are often
cavity. A large percentage of animals that
recommended to help decrease cerebral
sustain a CPA will have another episode
edema. Routine mechanical ventilation is
of CPA. Treatment of the underlying condinot routinely recommended but reasonable tion that led to the CPA is essential to help in animals that are hypercapneic or
prevent recurrence.

FLUID THERAPY

Cardiac function; intravascular volume; and
shock may have different hemodynamic
vascular tone, integrity, and patency are
profiles during the early and middle stages.

critical to normal circulation. An abnormal

Frequently, more than one type of shock is
ity in one or more of these components of
present, with hypovolemia likely to play a
circulation leads to stimulation of the
role in each fonn. Rapid and aggressive fluid
sympathetic ne1vous system, which results
resuscitation yields the best outcome, with
in compensatory changes to maintain
hemostasis used as required. ln veterinary
perfusion. The hemodynamic and cellular
patients, many stages and categories of
changes that develop as a result of these
shock will respond to fluid resuscitation
abnormalities are called shock. As shock
alone; medications such as antiaiThythrnics
progresses, oxygen and substrate delivery
and inotropes may be necessary for primary
to the tissues becomes insufficient to meet
cardiogenic shock, and vasopressor agents
energy requirements for cellular maintemay be necessary for distributive shock. The nance and repair. If shock progresses and
ability to create an effective fluid resuscitacellular energy demands cannot be met, the tion plan depends on an w1derstanding of the
ensuing organ failure leads to death. Early
different body fluid compartments and the
recognition of the type and stage of shock
dynan1ics of fluid movement and distiibution
is vital to establishing a successful fluid
between fluid compartments.

therapy plan; tin1ely intervention with
appropriate therapy will prevent or
decrease organ ir\jury and/or death.

BODY FLUID COMPARTMENTS

Shock is typically classified into three

AND FLUID DYNAMICS
categories: hypovolemic, cardiogenic, and
distributive. Hypovolemic shock develops

There are three major fluid cornpaitments;
when there is a blood volwne deficit <!15%;
intravascular, interstitial, and intracellular.

this may be from hemon-hage or other fluid

Fluid movement from the intravascular to
losses ( eg, as occurs with severe vomiting
interstitial and inti·acellular compaitments
and dian-hea). Cardiogenic shock results
occurs in tl1e capillaries. A capillary
when the heart fails as a pump; conunon

"membrane," which consists of the
causes include pulmonary emboli, cardiac
endothelial glycocalyx, endothelial cells,
tamponade, valvular insufficiency,
and the subendothelial cell matrix,
cardiomyopathy, and cardiac an-hythmias.

separates the capillai-y intravascular space

Distributive shock is caused by maldistribufrom the interstitial fluid compartment. This tion of blood flow away from the central
capillary "membrane" is freely permeable to circulation as a result of peripheral
water and small-molecular-weight particles
vasodilation; it can be caused by conditions
such as electrolytes, glucose, acetate,
such as anaphylaxis, corticosteroid
lactate, gluconate, and bicarbonate. Gases
deficiency (hypoadrenocorticism and critical such as oxygen and carbon dioxide diffuse illness-related corticosteroid insufficiency),
freely through this membrane to enter or
and systemic inflanunatory diseases that
exit the intravascular compartment.

lead to systemic inflammatory response

The interstitial compartment is the space
syndrome (SIRS). The different types of
between the capillaries and the cells. Fluids

1676

FLUIDTHERAPY
support the matrix and cells within tl1e
baroreceptors. This decreased rate of firing,
interstitial space. The intracellular
sent via the g.lossopharyngeal and vagus
compartment is separated from the
nerves to the medulla oblongata, results in
interstitial space by a cell membrane. This
decreased inhibition (stimulation) of the
membrane is freely permeable to water but
sympathetic system. Stimulation of the
not to small- or large-molecular-weight
sympatl1etic nervous system is manifested

VetBooks.ir
particles. Any particle movement between
by clinical changes in heart rate, pulse
the interstitium and the cell must occur
intensity, blood pressure, capillary refill time,
through some transport mechanism ( eg,
mucous membrane color, level of consciouschannel, ion pump, carrier mechanism).

ness, and rectal temperature. These physical

Fluids are in a constant state of flux
perfusion paran1eters, combined with blood
across the capillary endothelial membrane,
pressure, are used clinically to detect
tl1rough the interstitium, and into and out of
intravascular volume deficits. Most animals
the cell. The amount of fluid that moves
witl1 an intravascular deficit (poor perfuacross the capillary "membrane" depends sion) also have concurrent extra vascular
on a number of factors, including capillary

(interstitial and intracellular) deficits.

colloid oncotic pressure (COP), hydrostatic

Fluid deficit in the interstitial and
pressure, and pe1meability, which is
intracellular spaces causes clinical signs of
dictated by factors such as the endothelial
dehydration. Physical findings are used to
glycocalyx and pore sizes between the cells.

estimate the percentage of dehydration.

The natural particles in blood that create

Semidry oral mucous membranes, normal

COP are proteins: prin1arily albumin but
skin turgor, and eyes maintaining normal
also globulins, fibrinogen, and others. The
moisture indicate 4%---5% dehydration. Dry
hydrostatic pressure within the capillary
oral mucous membranes, mild loss of skin
is the pressure forcing outward on the
turgor, and eyes still moist indicate 6%---7%
capillary membrane generated by the blood
dehydration. As dehydration becomes more
pressure and cardiac output. Fluid moves
severe, significant quantities of fluid shift
into tl1e interstitial space when intravascufrom the intravascular space into the lar hydrostatic pressure is increased over
interstitium, causing concwTent perfusion

COP, when membrane pore size increases,
deficits with dehydration. Dry mucous
or when intravascular COP becomes lower
membranes, considerable loss of skin
than interstitial COP.

tw·gor, retracted eyes, acute weight loss, and
weak rapid pulses ( concurrent intravascular
deficit) indicate 8%---10% dehydration. Very

THE FLUID RESUSCITATION PLAN
dry oral mucous membranes, complete loss

In hypovolemic shock, compensatory
of skin turgor, severe retraction of the eyes,
neuroendocrine responses are initiated to
dull eyes, possible alteration of consciousrestore blood volume and meet metabolic ness, acute weight loss, and thready, weak
demands that occur during acutely
pulses indicate � 12% dehydration.

decreased cardiac output states, increasing

The physical guidelines to estimate

ATP demands. When perfusion continues to
dehydration are misleading in two cmmnon
be compromised despite these mechanisms, clinical situations. Chronically emaciated cells can no longer generate ATP, compensaand geriatric anin1als may have metabolized tory mechanisms become exhausted, and
the fat from around the eyes and the collagen
decompensatory shock ensues. An
in the skin, resulting in poor skin turgor and
adequate fluid resuscitation plan is
sunken eyes despite normal hydration.

necessary to optimize survival.

Animals with rapid fluid loss into a tl1ird

The fluid resuscitation plan should
body fluid space ( a space witl1in the body
include the following steps: 1) determine
cavity where fluid from the local interstitial
where the fluid deficit lies, 2) select fluid(s)

and intravascular spaces leak) have rapid
specific for the patient, 3) detennine
fluid shifts from the intravascular compartresuscitation endpoints, and 4) determine ments into these spaces before clinical
the resuscitation technique to be used.

evidence of interstitial fluid loss is seen. Both
situations require evaluation of mucous

Determination of the Fluid Deficit
membrane and eye moisture, PCV, and total
solids before dehydration can be estimated.

Loss of fluid volume from the intravascular
fluid compartment is manifested by poor
perfusion (shock) and inadequate tissue

Selection of Fluids
oxygenation. This volume deficit results in a

Fluids must be adn1inistered that will
lower vessel wall tension. Decreased wall
concentrate within the body fluid comtension in the amtic arch and carotid arteries partment where the volun1e deficit lies.

results in decreased stimulation of the

Crystalloids are water-based solutions with

FLUID THERAPY

1677
small-molecular-weight particles, freely
acetate, gluconate, and lactate) that are
penneable to the capillary membrane.

conve1ted. to bicarbonate in the liver,

Colloids are water-based solutions with a
equilibrating the pH of the fluid to normal
molecular weight too large to freely pass
blood pH (7.4). Normal saline (0.9%) is
across the capillary membrane. Colloids
isotonic but not buffered; it is used initially

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are thought of as intravascula.r volume
for specific clinical problems, including
replacement solutions, and crystalloids as
hyponatremia, hypematremia, hypercalceinterstitial volume replacement solutions.

mia, hypochloremic metabolic alkalosis,
head trauma, and oliguric renal fail me.

Crystalloids: The small-molecular-weight

Crystalloids are considered. balanced
particles in crystalloids are primarily
when they contain electrolytes in addition
electrolytes and buffers (see TABLE 3). When to Na and Cl (such as K, Mg, Ca), making
the sodium concentration of the solution is
them similar to plasma. Lactated Ringer's is
equivalent to that of the (red blood) cell, the
an example of a balanced solution; normal
solution is called isotonic. lntravascular
saline is not balanced.

administration of isotonic crystalloids ( eg,

The particular crystalloid. to administer is
lactated Ringer's, 0.9<>A,saline) will result
determined by the measmed or estimated
in interstitial volume replacement and
sodium and potassiurn concentrations and
minin1al intracellular fluid accumulation.

by tl1e osmolality of botl1 the animal's serum

More than 75% of the isotonic crystalloid
and the fluid to be administered ( see TABLE 3).

ad.ministered. IV can move into the

Most clinical problems will benefit from
extravascular space within 1 hr in a healthy
the use of buffered, balanced, isotonic
animal. This is because of the normal fluid
crystalloid.s ( eg, lactated Ringer's) as part
shifts between fluid compartments.

of the resuscitation fluid plan.

Hypotonic fluids ( eg, 5% dextrose in

Sodium Content: When serum
water, half-strength saline) will result in
sodium measurements are normal, a
intracellular water accumulation and
balanced. isotonic electrolyte solution
should not be used as resuscitation fluids.

can be used for volume replacement.

Hype1tonic solutions ( eg, 7% NaCl) contain

Serum sodium levels that are moderately
higher concentrations of sodiw11 and are
to severely decreased. ( <130 mEq/L)

best used when hydration is nonnal and
concurrently with other fluids.

or moderately to severely increased

(> 170 mEq/L) may contribute to serum

Crystalloid.s are considered. buffered
osmolality changes and result in
when they contain molecules (such as
neurologic abnormalities. Care must be
ltM•il CRYSTALLOIDS

Osmolality

Crystalloid

Toni city

Na•
c1-

K+

Ca•2 (mOsm/L) pH

Lactated. Ringer's Isotonic

130

109

4

3

273

6.7
solution

Plasmalyte-A ®

Isotonic

140

103

5

0

294

7.4

Normosol-R®

Isotonic

140

98

5

0

295

7.4

Normal saline

Isotonic

154

154

0

0

308

5.7

(0.9"Ai)

Dextrose (2.5% in Isotonic

77

77

0

0

280

4.5

0.45% saline)

Dextrose (5%) in Hypo tonic

0

0

0

0

253

5.0
water

Hype1tonic saline Hype1tonic 1,232 1,232

0

0

2,464

5.2

(7.5%)

Nonnosol-M®

Hypertonic

40

40

13

0

363

5.2
with 5% dextrose

Electrolyte units are mEq/L.

1678

FLUID THERAPY
taken not to increase or decrease the

In animals with decreased serum
sodium concentration too quickly, which
sodium content, volume replacement
may result in cerebral edema or dehydrashould be with isotonic saline (0.9%) tion (and can lead to intracranial
or other replacemenUisotonic fluids.

VetBooks.ir
hemorrhage). In general, sodium

Increased serum sodium values most
concentrations should not be altered by
commonly reflect a loss of solute-free

>0.5 mEq/llhr or 8-12 mEq/Uday. This
water. The animal should be perfused
allows for increased or decreased
and hydrated using isotonic saline or other
osmolality of neurons to adjust over time
replacemenUisotonic fluids. The free water
and avoids cerebral edema or dehydracan then be replaced, if necessary, using tion. Crystalloids are also classified as

2.5% dextrose in half-strength lactated
either replacement or maintenance fluids.

Ringer's, 2.5% dextrose in half-strength

Replacement fluids are intended to
saline, 0.45% saline, or 5% dextrose in
replace fluids lost from the body (such as
water when hypernatremia persists. This
through hemorrhage, vomiting, diarrhea,
must be done carefully, and the sodium
etc) and often contain a sodium concenconcentration lowered slowly. Desmoprestration near that of plasma (such as sin may be required if hypernatremia
lactated Ringer's or 0.9% saline); these
persists after appropriate fluid therapy,
fluids result in excessive concentrations
especially when the animal has hypostof sodium if given over prolonged periods henuria or head injury.

of time (>24-72 hr) or for animals with
free water loss; however, they are ideal

Potassium Content: When serum
resuscitation fluids for animals with
potassium estimates are normal, a
sodium-rich fluid losses. Maintenance
balanced electrolyte solution can be used.

fluids contain significantly less sodium

Unless severe, hypokalemia can be difficult

(such as half-strength saline or 5%
to recognize clinically. Few clinical
dextrose in water) and are intended for
situations warrant potassium supplementaanimals that have free water loss or tion beyond the content of lactated Ringer's
require prolonged fluid administration.

or Plasmalyte-A ® during initial volume

Replacement fluids given to an animal
replacement. Once the animal has been
with free water deficits or for prolonged
stabilized, potassium chloride should be
periods of time (without access to water)

added to the fluids, administered at ,s;0.5
will result in hypernatremia and
mEq/kg/hr. This rate may be increased
hyperosmolarity.

when severe hyperkalemia ( <2 mEq/1) is

Serum sodium alterations with fluid
associated with catastrophic clinical signs,
administration (MN a]) can be estimated

( eg, respiratory distress/hypoventilation
using the following formulit:

from paresis of the diaphragm or generalized lower motor paresis or paralysis). The serw11 potassium level must be closely

11[Na] = ([Na]11u;c1 - [NaJ,,uucnJ I (total
monitored with more rapid infusions. More
body water+ I), in which total body
commonly, potassium chloride is added to
water= 0.6 x body wt (kg)

•

1 L of balanced isotonic crystalloids

•••• GUIDELINE FOR POTASSIUM SUPPLEMENTATION IN DOGS

AND CATS

Serum Potassium
rnEq KCl to Add to

Concentration (rnEq/1)

1 L of Maintenance Fluids

<2.0

80

2.1-2.5

60

2.6-3.0

40

3.1-3.5

25-30

3.6-5.0

20

>5.0
none

FLUID THERAPY

1679
administered as maintenance fluids based
mia, diabetes, etc), administration of
on serum potassium concentration (see
hypertonic saline could result in severe

TABLE 4). Serum potassium concentration
hyperosmolality with neurologic
should be monitored closely during
complications. Because hypertonic
continued therapy. Potassium phosphates
crystalloid solution will leak into the

VetBooks.ir
may be used if a concurrent phosphorus
interstitium in < 1 hr, combining hypertonic
deficiency is present.

saline with a colloid is recommended to

In animals with hyperkalemia, fluids
offset the interstitial edema resulting from
should be selected carefully. When oliguric
interstitial extravasation.

renal failure is suspected as the cause of
the hyperkalemia, potassium-free

Colloids: When colloids are to be
solutions, such as 0.9% saline, are used for
administered, it must be decided whether a
volume replacement. Clinical conditions
natural colloid ( eg, plasma, albumin, or
requiring potassium-free solutions include
whole blood) or a synthetic colloid (see
oliguric renal failure, heat stroke, adrenal

TABLE 5) is to be used. When the animal
insufficiency (Addison disease), and
requires RBCs, clotting factors, antithrommassive muscle breakdown. After volume bin III, or albumin, blood products are the
replacement and fluid diuresis resolve the
colloids of choice.

hyperkalemia, a balanced electrolyte

When the initial goal is to rapidly in1prove
solution should be used. These solutions
perfusion in an anin1al with adequate RBCs,
have a normal pH and promote potassium
a synthetic colloid can achieve the desired
excretion. Recent evidence suggests that
voltune expansion rapidly. Choices of
with hyperkalemia secondary to feline
synthetic colloids include dextran, hydroxyurinary obstruction, any isotonic balanced ethyl starch (HES), and stroma-free
fluid can be used, with minimal concern for
hemoglobin.

increasing serum potassium as long as the

Dextrans are polysaccharides composed
underlying obstruction is treated.

of linear glucose residues. They are
produced by the enzyme dextran sucrase

Osmolality: Osmolality is defined as
the number of solute particles per unit of
during growth of various strains of
solvent. Serum osmolality can be calculated Leuconost.oc bacteria in media containing using the following formula:

sucrose. Dextrans are isotonic and can be
stored at room temperature. Dextran is

Osmolality (mOsmlkg) = 2([Na+J + [K+J)

broken down completely to C02 and H20 by

+ [glucose ]/18 + [BUN]/2.8
dextranase present in spleen, liver, lung,
kidney, brain, and muscle at a rate

Normal serun1 osmolality is 290-310
approaching 70 mg/kg every 24 hr. In nmmal
mOsm/L. Fluids that do not contribute
dogs, dextran 70 increases plasma volume
significantly to serum osmolality should

1.38 tin1es (138%) the volume infused.

be used for volume replacement.

Hemostatic changes in healthy

Hyperosmolar solutions include
experimental dogs given dextran 70
hypertonic saline, Nonnosol-M® with
include an increase in the buccal mucosa!

5% dextrose, or any isotonic fluid that has
bleeding time and partial thromboplastin
glucose or hypertonic saline added. Except
time and a decrease in von Willebrand
for hypertonic saline, the hyperosmolar
factor antigen and factor VIII coagulant
glucose-containing solutions are meant to
activity, without clinical bleeding. Dextran
be maintenance solutions used in anin1als in
copolymerizes with the fibrin monomer,
which fluids are not shifting rapidly from
destabilizing clot formation. Blood
the vascular compartment to a third body
glucose levels may be increased during
fluid space. They are usually not used as
dextran metabolism. Dextran 70 may
volume replacement solutions.

cause a change in the total solids value

Hypertonic saline provides a suprathat does not reflect actual protein content normal concentration of sodium and is
and may interfere with blood crossmatchgenerally given in a 3%, 7%, or 7.5% IV
ing. Moderate to life-threatening reactions
solution. The effect is to rapidly draw
in dogs have been rare. Dextran 70 is being
water from the interstitial space into the
used much less commonly in favor of
intravascular space, rapidly expanding the
other colloids, and dextran 40 is not
intravascular volume. Hypertonic saline
recommended because it is known to
may also decrease cellular swelling and
cause renal injury.

improve myocardial contractility. If the

Hydroxyethyl starch (HES) is the
animal has concurrent interstitial fluid
parent name of a polymeric molecule
deficits (dehydration) or a disease that
made from a waxy species of either corn
results in free water loss ( eg, hyperther-
or potatoes and is composed primarily of

1680

FLUID THERAPY
arnylopectin (98%). HES molecules vary in

Molar substitution rates vary from 0.35 to
size from ten thousand to several million

0. 7, and the higher the molar substitution,
daltons (average 70-670 thousand
the longer the hall�life in blood. The position
daltons). The disappearance of HES
of the molar substitution also impacts
molecules from the body depends
half-life; this can occur at the C2, C3, and C6
primarily on their rate of enzymatic
positions. Stereotactically, substitution at

VetBooks.ir
degradation by o:-amylase and subsequent
the C2 site impedes degradation by amylase,
renal excretion. Other methods of eliminaprolonging the half-life of HES; this is often tion include absorption by tissues (liver,
refen-ed to as the C2:C6 ratio. Higher ratios
spleen, kidney, and heart), uptake by the
imply impeded breakdown and therefore
reticuloendothelial system, and clearance
longer half-lives in blood. When hetastarch
through bile. Blood o:-amylase-mediated

(the most conm10n HES) is infused at 25
hydrolysis (primarily at the C6 position)

ml/kg in healthy dogs, the initial increase in
reduces the molecular weight to <72,000
plasma volume is 1.37 times (137%) the
daltons; these smaller particles are more
volume infused; most hetastarches will
osmotically active but eliminated at a
expand plasma volume lOOo/er-150%.

faster rate through the kidney. Metabolism Intra vascular persistence is significantly of HES retained in tissue is probably
greater than that of dextran 70, with 38% of
performed by cytoplasmic lysosomes.

hetastarch remaining, compared witl1 19"/o

An increase in serum amylase is to be
of dextran, 24 hr after infusion. Administraexpected without alteration in pancreatic tion by constant-rate infusion may provide
function.

a constant supply of larger molecular

Along with molecular weight, the degree
weight particles, perhaps maintaining and
of molar substitution, which is the number
augmenting plasma COP and intravascular
of glucose units on the starch molecule that
volume in animals with albumin loss or
have been replaced by hydroxyethyl units,
increased capillary permeability. Most
is the major determinant of how long the

HES molecules may persist in the body
different types of HES survive in the blood.

for 2-7 clays.

IHHIII SYNTHETIC COLLOIDS

Suggested

Colloid

Upper

In

Molecular

On co tic Limit

Concen-

Solution

Weight

C2:C6 Pressure (dose/kg/ tration

Colloid
with

(daltons)a Ratio (mmHg) day)

(%)

Dextran 70

0.9%NaCI

79,000

NA

59

20 mL

6

(10,000-

80,000)

HextendTM

Lactated

670,000

5:1

25-30

20rnL

6

(670/0.7)

electrolyte (20,000-
solution

2,500,000)

VetStarch TM/

0.9% saline 130,000

9:1

36

50 mL

6

VoluvenTM

(110,000-

(130/0.4)

150,000)

HESPAN®

0.9% saline 600,000

5:1

25-30

20 mL

6

(600/0.4)

(450,000-

800,000)

Stroma-free

Modified

65,000-

NA

20

See text

13
hemoglobin
lactated

130,000

(Oxyglobin®) Ringer's

(up to
solution

500,000)

NA = not applicable

3Average, followed by range in parentheses.

FLUID THERAPY

1681

Hydroxyethyl starches favor retention of
overload resulting from the colloidal and
intravascular fluid and prevent washout of
pressor properties of the solution. Oxyinterstitial proteins. In hypooncotic globin has also been used in cats as infusions
situations, HES infusion has a great

( 4-25 mllkg/24 hr) and/or rapid infusions
advantage over other colloids because the

(1-5 mUcat). Anecdotally, the pressor

VetBooks.ir
larger molecules remain intravascular,
effects in cats seem pronounced, and blood
limiting puhnonary fluid flux. It is nontoxic
pressure should be monitored. Oxyglobin
and nonallergenic in dosages as high as
has been associated with development of

100 mllkg in dogs. Many cats have a
pulmonary edema, pleural effusion, and
moderate reaction-nausea and occasional
respiratory distress, particularly in cats with
vomiting-with rapid infusion. However,
underlying heart disease.

when hetastarch is given slowly (through

Lyophilized canine albumin is available
out 5-15 min), this adverse effect is
as a 5% lypophilized solution that can be
minimal. Renal irtjury, reported to occur
reconstituted. It has been administered to
from an osmotic nephrosis in people, has
dogs with septic peritonitis and hypoalbubeen poorly documented in dogs and cats, minemia and has been demonstrated to
and allergic reactions are rare.

increase oncotic pressure, measured

Hetastarch is associated with minor
albumin levels, and Doppler-measured
alterations in laboratory coagulation
blood pressure, with increased albumin
measurements but not with clinical
levels persisting for as long as 24 hours.

bleeding unless daily minimal dosages

Minimal adverse effects have been noted.

(20-50 mllkg/day) are exceeded. Molecular

Replacement volume in mL of albumin 5%
weight seems to have the biggest impact on
solution (50 mg/mL) can be calculated using
coagulation, with larger molecular weight
tl1e following fomrnJa:

starches impacting coagulation to a greater
degree. The proposed mechanisms of
body wt (kg) x 90 mllkg x (target
impact on coagulation include "coating"

albumin level [eg, 2 mg/dL]- patient's
platelets or impeded platelet receptor
current albwnin level) x 0.2 g/dL
signalling, dilution of coagulation factors,
and interference with von Willebrand

It may also be administered as a more
factor/factor VIII interaction. Dilutional
concentrated solution (16%or 166 mg/mL)

effects on coagulation, cells, and proteins
for hypotensive patients, at a dosage of 800
are produced in response to the volume
mg/kg throughout 6 hr. Hwnan serwn
expansion of the plasma. Animals that
albwnin is available as well and has been
receive large volumes of HES solutions may
used with success in ctitically ill vetetinary
have more oozing if surgery is performed,
patients; however, when administered to
and diligent hemostasis is warranted.

healthy anin1als, severe adverse effects,

A variety of HES solutions are currently
including multiple organ failure, have been
available, each with its own advantages and
noted.

disadvantages based on its molecular

Blood products are important in many
composition.

situations (seep 17). Anin1als that need

Stroma-free hemoglobin (Oxyglobin®) clotting proteins may require frozen ( or is a polymerized bovine hemoglobin-based
fresh frozen) plasma or cryoprecipitate,
solution that increases plasma and total
which contains concentrated amounts of
hemoglobin concentration. This solution is
factor VIII and von Wtllebrand factor;
indicated for the treatment of anemia and
platelet-rich plasma may be necessary for
hypovolemia with tissue hypoxia It has
platelet deficiencies. Animals with severe
colloidal properties similar to those of
anemia or blood loss may require whole
hetastarch and exerts mild vasopressor
blood or packed red blood cells. Cavitary
activity, believed to be through scavenging
hemorrhage may allow collection of blood
of nitric oxide, a potent constitutive and
either with centesis or in surgery for
inducable vasodilator. The dark hue of the
autologous blood administration when
solution causes discoloration of the serum
banked blood is not available.

( and sometimes the urine) that can interfere
with some serum chemistry tests, depending

Fluid Selection: Interstitial and intracelluon the type of analyzer and reagents used.

lar volwne deficits ( dehydration) are

Bilirubinuria will be present. Dosages ,;30
replaced by the administration of crystalmllkg/day have been approved for dogs, loids. Intra.vascular volwne (perfusion)

with the rate of infusion < 10 mllkg/hr. When
deficits can also be replaced with crystalgiven to an animal with a nonnal blood loids alone. However, when large quantities
volume, administration must be slow and
of isotonic crystalloids are rapidly adminiscarefully monitored to avoid volume tered IV, there is an inunediate increase in

1682

FLUID THERAPY
intravascula.r hydrostatic pressure, a

Shock will deplete cellular energy
decrease in intravascula.r COP, and
stores, with subsequent cellular and
extravasation of large fluid quantities into
organ dysfunction. Restoring the
the interstitial spaces. By administering
circulation to "normal," with normal

VetBooks.ir
colloids in coajunction with crystaUoids
oxygenation and perfusion parameters,
du.ring fluid resuscitation of perfusion
may not be enough to allow sufficient ATP
deficits, less total fluid volume is required
production for repair as well as mainte

( crystaUoids reduced by 400/c,-600Ai), there is
nance. When an animal is suspected of
less tendency toward fluid overload, and
having a disease process related to SIRS,
resuscitation times a.re sho1ter.

such as vasoclilation, increased capillary

Many conditions can increase capillary
permeability, or depressed cardiac
permeability and cause systemic inflammaoutput, resuscitation endpoints are Lion (SIRS), including parvoviral dja.1Thea,
chosen for supranormal resuscitation (see
other severe GI rusease, pancreatitis, septic TABLE 6). The goal is to deliver oxygen and shock, massive trauma, heat stroke, cold
glucose to the cells in higher than normal
exposure, bums, snake bite, and systemic
concentrations to promote sufficient
neoplasia. Hetasta.rch or stroma-free
energy production for both repair and
hemoglobin a.re the colloids of choice for
maintenance of the cells.

intravascular volun1e resuscitation when

There a.re situations, however, when
there is increased capillary penneability
supranonnal resuscitation can be detriand loss of albumin through the capillary mental. Increased vessel wall tension can
membrane. Using crystalloids alone in
rusloclge a life-saving clot in the vasculature
animals that require large volumes for
of a traumatized anin1al, exacerbating
resuscitation or that have increased
hemorrhage. Brain and lung edema or
capillary permeability will result in
hemorrhage can be worsened by aggressive
significant interstitial edema.

ar1cl sudden increases in hydrostatic

Many of these animals also have
pressure. Hypotensive resuscitation
third-space fluid losses, most Hkely due to
provides endpoints that a.re at the lower
significant regional inflammation, that result lin1it of no1mal (see TABLE 6). The goal is to in massive flujd requirements and make it
administer the smallest volume of fluids
difficult to predict the volwne required to
possible to successfully resuscitate the
maintain fluid balance.

intravascula.r compartment while minimizing extravasation of fluids into the Determination of Resuscitation
interstitium (especially brain or hrngs),

Endpoints
titrating the arnow1t of preloacl to minimize
excess fluid load to a potentially rusabled

There a.re no "standa.r.d" formulas for
heart, and reducing the probability of
crystalloid or colloid infusion that will
dislodging clots. Small-volw11e resuscitaguar·antee complete volume resuscitation tion techniques should be used to reach
in a small animal. Variables such as renal
hypotensive resuscitation endpoints.

function, presence of a third body fluid
space, brain injury, lung injury, heart
disease or failure, continued losses, or

Determination of Appropriate
closed cavity hemorrhage require that fluid Resuscitation Technique resuscitation rate and volumes be individu

Large- and small-volume techniques are
alized for the patient. Sufficient volw11es
used to reach endpoints discussed above.

of fluid should be administered to reach

These closes of fluids should be adminisdesired endpoints of resuscitation. This tered throughout 10-15 min as a rapid IV
has also been termed ear·ly goal-directed
infusion, and then the animal should be
therapy. The endpoints typically reflect
reassessed for restoration of normal
perfusion status and include heart rate,
clinical perfusion parameters and
blood pressure, central venous pressure,
objective measurements of perfusion.

mucous membrane color, capillary refill

Continual reassessment and titration of
time, and pulse intensity. A resolution of
fluid doses will achieve resuscitation
an increased blood lactate to <2 mmol/dL
from shock in most cases (while the
supports adequate tissue oxygenation.

underlying disease is investigated and

More advanced endpoints, which car1 be
therapy instituted). Dogs in hypovolemic
used if additional instrwnentation is
shock that require supranormal endpoint
available, include a central venous
values can benefit from large-volume
pressure of 5-8 cm H20, central venous
resuscitation techniques. Typically,
oxygen saturation > 700Ai, and a urine
an initial infusion of 20-50 mUkg of
output of at least 1-2 ml/kg/hr.

buffered, balanced isotonic crystalloids

FLUID THERAPY

1683

14N•!I RESUSCITATION ENDPOINTS

Endpoints

"Supranormal"

"Hypotensive"

VetBooks.ir

Monitored

(high-end

(low-end

Parameter
resuscitation)

resuscitation)

Blood pressure

Systolic

90-120mmHg

80-90mmHg

Mean arterial

80-90mmHg

60-SOmmHg

Central venous pressure

6-Scm H20

3-5cm HP

Heart rate•

Dog

<140bpm

<140bpm

Cat

160-200 bpm

160-200 bpm

Capillary refill time

1-2 sec

1-2 sec

Pulse intensity (femoral)

Strong

Strong

Resuscitation technique

Dog

Large volume

Small volume

Cat

Small volume

Small volume

Clinical indications

SIRS diseases

Heart failure

Cortisol deficiency

Closed cavity hemorrhage

(hypoadrenocorticism,

Ongoing hemorrhage
critical illness-related

Brain disease
corticosteroid

Lung edema
insufficiency)

Oliguric renal failure

Anaphylaxis
a After appropriate analgesia
is given, followed by 5-15 ml/kg of a
dogs; 5-10 ml/kg for cats) is given.

hydroxyethyl starch solution. When

An HES solution can be administered
stroma-free hemoglobin is selected

(5 ml/kg in dogs; 2-5 ml/kg in cats)

as the colloid, the dosage is 5 ml/kg.

throughout 1-5 min as well. The

Additional colloids can be administered
perfusion parameters are reassessed,
using small-volume intravascular
and the initial bolus dose repeated as
resuscitation techniques if perfusion has
needed until the resuscitation endpoint
not improved to the desired supranormal
is reached. When stroma-free hemoglobin
endpoints after the initial large volume
is used as the colloid in dogs, the dosage
dose of fluids. Colloids should be added
is 2-5 ml/kg. Stroma-free hemoglobin is
immediately in any animal with proteinanot approved for use in cats, but it has ceous fluid losses (SIRS disease, GI fluid
been used successfully at a dosage of
losses, etc).

1-5 ml/cat (0.25-1 ml/kg) given slowly

Whole blood products can be administhroughout 5 min.

tered by large-volume resuscitation

Hypothermia, especially in cats, can
techniques in catastrophic hemorrhagic
significantly limit the cardiovascular
situations. However, initial administration
response to endogenous sympathetic
of stroma-free hemoglobin will allow for a
stimulus ( catecholan1ines) and to fluid
slower administration of whole blood and
resuscitation. Active external warming with
less chance for transfusion reaction from
circulating water blankets should be done
rapid whole blood administration.

once fluid resuscitation has been initiated.

Small-volume resuscitation techniques

Additional warming techniques such as
are recommended in hypovolemic cats
warm water bottles, fluid line wam1ers, and
and any dog with closed cavity hemorwann air blowers can be used to warm cats.

rhage, head injury, pulmonary contusions Aggressive volume administration without or edema, cardiogenic shock, or oliguric
active warming of hypothermic cats can
renal failure. An initial dosage of balanced result in pulmonaiy edema despite isotonic crystalloids (10-15 ml/kg for
continued hypotension.

1684

FLUIDTHERAPY

ASSESSMENT OF RESUSCITATION coagulation. The dosage is adjusted to EFFORTS
maintain an adequate mean arterial
pressure and CVP The ainount of crystal

Once the fluid therapy plan is underway,
loids administered with colloids must be
ongoing assessment is critical. If adequate
reduced by 4001<>-60% of what would be
fluids have been administered and
administered if crystalloids were used

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reasonable resuscitation endpoints have not alone. The maintenance fluid plan should been reached, several causes should be
address three ongoing requirements:

considered: inadequate volun1e administrareplacement of lost interstitial volume tion, ongoing hemorrhage, third body fluid

(rehydration), maintenance fluids (for
spacing, heart disease or pericardial fluid,
normal homeostasis), and replacement of
severe vasodilation, vasoconstriction, organ ongoing losses. The volume of rehydration ischemia, hypoglycemia, hypokalemia,
fluids required is determined by reassessing
arrhythmias, severe acidemia or alkalemia,
hydration paraineters after resuscitation,
decreased venous return, severe anemia,
using the following formula:% dehydration
endocrine disease (hypoadrenocorticism
x body wt (kg) x total body water (0.6).

or critical illness related to corticosteroid

This volume is commonly administered
insufficiency), hypothermia, or brain
throughout 4-12 hr with staildard isotonic,
pathology. These vaiiables should be
balanced electrolyte replacement fluids.

rapidly assessed and co1Tected. If a central

Maintenance fluid requirements
venous pressure (CVP) line is available, it

( 40 mUkg/day for larger animals and
should be checked to see whether CVP is

60 mUkg/day for smaller animals) are
near the endpoints assigned (TABLE 6). If not,
added to the rehydration rate. With
or if no CVP is available, a fluid challenge
prolonged parenteral fluid administration,
can be given. This typically consists of a
usually throughout a course of days, serum
bolus (10-15 mUkg) of crystalloids and
sodium may increase, and maintenance
a bolus (5 mUkg) of hetastarch. If the
fluids ( eg, half-strength saline or 5%
perfusion parameters improve with this
dextrose in water) may be needed to
challenge, then the likely cause of the
replace free water deficits.

nonresponsive shock is inadequate volume,

Ongoing or increased fluid losses vai-y
and coUoids are titrated to reach the desired substailtially and must be estimated and endpoints. Ultrasound, with an experienced
replaced. Ongoing losses can be estimated
ultrasonographer, may be useful to assess
by measuring mine and fecal output,
cai·diac function and/or volun1e status in
nasogastric tube suction, or vomitus
select patients.

volume. Insensible losses, which can be

If fluid volume appears adequate and
increased with fever, or higher metabolic
underlying etiologies have been addressed
demands can increase the maintenance rate
and treated and the animal is still hypotenby 15-20 mUkg/day.

sive, vasopressors can be used. Oxyglobin®
can be given at the dosages listed above if
it has not yet been used. If stroma-free

Monitoring Fluid Therapy
hemoglobin fails to increase the blood

All animals receiving fluids should
pressure, then dopainine is administered at
have a physical examination, including

2-15 mg/kg/min as a constant-rate infusion;
assessment of hydration and body
alternative vasopressors include norepiweight, with urine production checked at nephrine, vasopressin, and phenylephrine.

least twice per day, more frequently in

These medications are weaned once blood
the critically ill. Overzealous administrapressure has stabilized.

tion of crystalloids can manifest as
increased respiratory rate and effort,

MAINTENANCE FLUID PLAN
crackles or wheezes on auscultation,
serous discharge from the nares,

Maintaining intravascular fluids after
chemosis, jugular vein distention or
resuscitation from hypovolemic shock and
pulsations, shivering, edema, hypertenduring systemic inflanunatory response synsion (>140-150 mmHg systolic), drome disease conditions causing increased increased CVP (>8-10 cm H20), significapillai-y permeability cai1 be a challenge.

cant increase in body weight (>12%-15%),

Hydroxyethylstai·ch solutions or Oxyand rapid and/or dramatic decrease in globin® can be administered as a constailt

PCV and total solids. In animals with
rate infusion at 0.5-1 mUkg/hr in dogs, or
urinary catheters, urine output can be

0.25-1 mUkg/hr in cats. Newer HES
monitored and compared with fluid
solutions may be administered at higher
administration volumes. Monitoring CVP,
rates (2 mUkg/hr) without impacting
pulmonary capillary wedge pressures,

MONITORING THE CRITICALLY ILL ANIMAL

1685
and cardiac output variables may be
to maintain hydration by voluntary drinking
helpful in selected animals, although
and eating or tolerate enteral supplementapulmonary artery catheters are rarely tion (through a feeding tube) or subcutaneplaced. Monitoring electrolytes and ous fluid administration. Tape1ing the

PCV /total solids may provide an objective
volume infused IV tlU'oughout 24---48 hr

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measurement of fluid balance.

allows the renal medulla to reestablish

When parenteral fluid administration is to
the osmotic gradient and helps prevent
be discontinued, the animal should be able
excessive fluid loss through diuresis.

MONITORING THE CRITICALLY ILL ANIMAL

Anticipation, not reaction, is the key to
function, body fluid glucose levels, and
successful management of critically ill
ultrasonographic assessment techniques.

animals. Animals must be effectively treated Diagnostic tools that are cruTently being and actively monitored to detect or prevent
investigated and may apply to the Rule of 20
organ compromise before organ failure
in the future include biomarkers such as
occurs. This often requires aggressive and
cardiac troponins, C-reactive protein, etc.

repeated fluid resuscitation and support
throughout the course of definitive therapy.

Fluid Balance: The goal offluid therapy

Tissue hypoxia and organ compromise or

(seep 1675) is to provide adequate
failure can be a direct result of the primary
perfusion (intravascular volurne) and
disease or can be secondary to the disease
hydration (interstitial volrune) without
or its therapy. Organs frequently affected
overloading the interstitial space. Periphinclude the heart and blood vessels, eral perfusion can be assessed by physical
kidneys, lungs, GI tract, and liver. When the
parameters such as heart rate, mucous
disease process is multisystemic, problems
membrane color, pulse quality, and
such as malnutrition and coagulopathies
mentation, as well as by measured
must be anticipated. Optimal care requires
parameters such as blood pressure, central
a thorough and methodical approach to
venous pressru·e, urine output, and blood
diagnostic procedures, monitoring, specific
lactate measurements. Hydration can be
therapeutics, and supportive care.

assessed by physical parameters such as
mucous membrane and corneal moistness

THE RULE OF 20
and skin turgor, and by measured values
such as body weight. Animals with systemic

The Rule of 20 is a list of 20 critical
inflanunatory response syndrome (SIRS)

parameters that should be evaluated at least
diseases may require more fluid than
daily in all critically ill animals; many of
expected because of peripheral vasodilation
these should be assessed several times per
and loss of endothelial integrity, making the
day. Using the Rule of 20 ensures that the
administration of colloids with crystalloid
clinical status and therapeutic strategy for
solutions optimal. When treating fluid
each animal is comprehensive and meets
deficits, intravascular deficits should be
the animal's ongoing needs. Like any
addressed rapidly first; interstitial deficits
monitoring tool, the Rule of 20 is not a static
should be treated using standard calculaconcept but a dynantic one; the specifics of tions to correct dehydration and monitor
each parameter will change with advanceongoing losses.

ments in laboratory testing, understanding
of disease pathology, and current concepts

Oncotic Pull/Albumin: Albrunin
in critical care. In addition, the systems
provides the major intravascular oncotic
examined in the Rule of20 are not
pull in the normal vasculature. ln conditions
singularities; each is impacted by and can
in which there has been massive blood loss
impact other parameters, so each parameter or leakage of plasma proteins due to an should be assessed while considering the
exudative process, albun1in is lost from
patient as a whole. Some more recent
the intravascular space. This loss of intraapplications of the Rule of20 include vascular oncotic pressure combined with
monitoring of blood lactate levels, adrenal
increased capillary permeability associated

1686

MONITORING THE CRITICALLY ILL ANIMAL
with many SIRS diseases requires treatment
include inadequate nutrition, glycogen
using synthetic colloids that have a higher
storage diseases, heat stroke, young age,
molecular weight than that of albumin.

small size, severe liver disease or portosys

Colloid oncotic pull (COP) can be measured
temic vascular anomalies, certain neopla

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with colloid osmometry but is not comsias, hypoadrenocorticism, and iatrogenic monly available in veterinary practice.

insulin administration. Dextrose supple

Fom1ulas are available to calculate COP
mentation is warranted in any animal that is
based on plasma protein levels, but they are
hypoglycemic. Solutions with a dextrose
not reliable predictors of measured COP
concentration >5% are best administered

Normal COP in dogs is -20 nm1Hg. In
through a central line. Anin1als with clinical
patients with moderate to severe decreases
hypoglycemia despite administration of
in COP or in total proteins, natural and
solutions with high dextrose concentrations
synthetic colloids should be administered.

should be assessed for insulinoma and may

Examples of natural colloids include
benefit from glucagon infusions. A difplasma, concentrated human or canine ference of >20 mg/dL in blood glucose
albumin, and stroma-free hemoglobin.

values and abdominal fluid glucose values

Examples of synthetic colloids include
has high sensitivity and specificity for septic
dextrans and hydroxyethyl starches. Newer
peritonitis in aninlals who have not recently
understanding of the endothelial cell funchad surgery.

tion and the impact of the endothelial

Insulin treatment of hyperglycemia in
glycocalyx may present novel therapeutic
diabetic aninlals is important to offset
options in the future.

ketoacidosis or hyperosmolar complica

Part of the oncotic activity normally
tions. Constant-rate infusion (CRI) of
provided by albwnin can be provided by
regular insulin can result in the slow and
synthetic colloids, but only albwnin can
controlled lowering of blood glucose (to
pe1form other functions such as drug,
help avoid rapid changes of blood osmolalcation, and honnone transport, as well as ity); close monitoring of blood glucose
contribute to acid/base balance. Albumin
levels should be performed. Tight control
can be lost with a variety of diseases (GI,
of increased blood glucose has improved
renal, or SIRS); in addition, it is a negative
neurologic outcome after head trawna in
acute-phase protein, so production of
critical human surgical patients but not in
albumin drops during critical illness.

human medical patients; in addition,

Interstitial albwnin stores are drawn upon
increased incidences of hypoglycemia may
to replace serum albumin, and a low serum
occur with tight glucose control. Acutely
albumin reflects a total body deficit of
traumatized aninlals are prone to insulin
albwnin. Albumin levels <2 g/dL have been
resistance because of large an10unts of
associated with a poor prognosis; however,
circulating cortisol and epinephrine and
it is not known whether restoring albun1in
may develop hyperglycemia severe enough
levels improves survival. Plasma and
to require treatment with insulin. The
albumin transfusions are often adminisbenefit of tight blood glucose control has tered to supplement the albumin.to reach a
not been clearly demonstrated in veterinary
target of2 g/dL, but large volumes of plasma
medicine.

are required. Lyophilized canine serum albumin is now available in l 00-g vials, making Electrolytes and Acid-Base Balance:

replacement of albunlin more cost-effective

Hypokalemia can be a contributing factor in
and with lower total volumes than plasma
weakness and ileus of critically ill animals.

transfusions. Human albumin products

These aninlals commonly have reduced oral
have been used in critically ill dogs but may
intake and/or increased GI and urinary
result in severe organ dysfunction when
losses of potassium that require potassiwn
given to healthy dogs. Interstitial albumin
supplementation in the IV fluids. Hyperstores must be replenished as well as kalemia can be a life-tllreatening complicaintravascular levels, so multiple Wlits of tion of urinary tract rupture or obstruction,
plasma or albumin may be necessary to
renal failure, reperfusion injury, or massive
increase serum albumin levels.

cellular death. Hyperkalemia commonly
results in bradyarrhythmias and can be

Glucose: The goal is to maintain glucose
temporarily treated with calciw11 gluconate
between 80 and 120 mg/dL. Septic aninlals
and insulin, concurrently with dextrose
are at an increased risk of hypoglycemia
and/or sodiwn bicarbonate. The underlying
that can be severe enough to cause
pathology that led to hyperkalemia must be
hypotension or neurologic dysfunction
addressed. Other important electrolytes to
ranging from weakness to stupor or
monitor include sodium, ionized calciwn,
seizures. Other causes of hypoglycemia
phosphorus, magnesium, and chloride; all

MONITORING THE CRITICALLY ILL ANIMAL

1687
can be increased or decreased in critically ill prevent aspiration pnetunonia should be animals and may affect other body systems
used whenever appropriate. Arterial blood

(such as neurologic acid/base balance,
gas measurement is the "gold standard"

serum osmolality, the cardiovacular system,
method to detect hypoxemia or hypercarand RBCs). The anion gap (AG) can be bia. Pulse oximetry (Sp02) is a noninvasive

VetBooks.ir
calculated when blood electrolytes are
way to detemline the oxygen saturation of
measured: AG= [Na] + [K] -[HC03] - [Cl].

hemoglobin. Supplemental oxygen and/or

Nonnal AG values are between 12 and 24
therapeutic ventilation may be indicated
mEq/L. An increased AG indicates there is
with Sp02 values <96%. Hypercarbia can be
some unmeasured anion present in the
detected using end-tidal C02 through an
blood, which may include ketones, lactate,
endotracheal tube or nasal catheter and has
uremic compounds, or toxins ( eg,
been shown to corTelate with arterial CO.,
salicylates, ethylene glycol, ethanol,
levels in animals. Se1ial monitoring is
methanol, indomethacin, isoniazid,
recommended in the initial management
paraldehyde, propylene glycol). The most
of animals with respiratory compromise
common cause of metabolic acidosis is
to detem1ine the adequacy of oxygen
lactic acidosis caused by poor perfusion
supplementation and the need for
leading to anaerobic metabolism. Lactate
mechanical ventilation. If hypoxemia is
production results in an equimolar
unresponsive to oxygen supplementation
production of hydrogen ions and subse

(Pa02 <60 nunHg or Sp02 <900A,) or
quent alterations in blood gas values
hypercarbia is present (PaC02 >60 mmHg),

(metabolic acidosis). Lactate measureor if respiratory effort ( work of breathing) ments can be easily performed with
is substantially increased, manual or
handheld or benchtop analyzers. Resolution
mechanical ventilation is necessary.

of hyperlactatemia with adequate fluid

Ventilation should not be delayed until
resuscitation is often associated with
respiratory failure or arrest. Prognosis for
improved survival. Treatment involves
animals that require ventilation is variable;
maxin1izing blood flow and tissue oxygen
those with hypoxemia from congestive
delivery. Rarely is the administration of
heart failure or hypoventilation from
sodium bicarbonate (NaHC03) warranted
metabolic disease ( eg, hypokalemia) or
for perfusion-related acidosis. Once
cervical spinal disease have a better
perfusion and hydration are corrected,
prognosis than those that require ventilation
the acid-base status is reassessed.

for hypoxemia due to primary pulmonary

If severe metabolic acidosis ( as occurs
disease. Invasive (arterial san1pling) and
with ketosis or uremia) persists and HC03
noninvasive (ETCO/Sp02) blood gas
remains below -12 mEq/L after perfusion
measurements should be performed during
has been restored, slow administration of
mechanical ventilation to detennine need
fluids with NaHC03 supplementation is
for adjustment of the ventilator settings.

warranted, restoring serum values to > 15
mEq/L. The dosage of NaHC03 is calculated

Level of Consciousness/Mentation/
as follows:

Neurologic Status: A decline in an
animal's level of consciousness warrants
mEq NaHC03 = 0.3 x (target NaHC03 [ eg,
investigation to exclude metabolic causes,

15] -patient NaHC03) x body weight in kg
such as hypoglycemia, hyperglycemia,

Serun1 bicarbonate levels are carefully
hepatic encephalopathy, acidosis,
monitored to meet patient requirements.

electrolyte or osmotic derangements, or
sudden development of hypertension,
hypotension, or shock. An increase in

Oxygenation and Ventilation:

intracranial pressure can result from

Pulmonary function can be compromised
intracranial hemoIThage, fluid overload
in critical illness for a variety of reasons

( cerebral edema), primary brain/meningeal

(pneumonia, acute respiratory distress
disease, and/or ischemia. The drugs the
syndrome, thromboembolism, congestive
animal is receiving should be carefully
heart failure, etc). Early diagnostic tests ( eg, evaluated for adverse effects that can lead imaging, blood work, tracheal washes, urine to altered mentation or level of consciousblastomycosis antigen testing, etc) for ness. Cerebral edema may be responsive to
targeted therapeutics will help limit
medical management with furosemide and
extension of pulmonary disease. AspiraconctUTent mannitol therapy. Steroids may tion pneumonia is a particular challenge,
be indicated in certain inflan11Tiatory
because it is most commonly a "second hit"

diseases ( eg, meningitis, neoplasia), and
disease ( secondary to another systemic
antibiotics in infectious disease ( eg,
illness); therapeutics (such as antiemetics,
toxoplasmosis). Craniotomy may be needed
prokinetics, or use of nasogastric tubes) to
in animals not responsive to medical

1688

MONITORING THE CRITICALLY ILL ANIMAL
management. Cerebral perfusion pressure

Objective measurements of global

= mean arterial pressure - intracranial
perfusion may also include lactate
pressure. Elevating the head 15° and
monitoring; animals with a significantly
avoiding procedures that may increase
increased lactate concentration may have
venous pressure and subsequently
a poorer prognosis. Studies have demonintracranial pressure is essential. Maintainstrated that serial lactate monitoring as VetBooks.ir
ing normal oxygenation/ventilation, blood
pathology is treated is more useful than
pressure, glucose level, and serum
a single measurement. Central venous
osmolality is essential for animals with
oxygen measurement is another objective
brain disease. Neurologic status may be
measurement of global perfusion; nonnal
evaluated using a scoring system assessed
values are 70-80 mmHg, whereas lower
on a regular basis, such as the modified
values may indicate increased oxygen

Glasgow Coma Scale; lower scores are
extraction.

associated with a poorer prognosis.

Hypertension is a relatively uncommon

Spinal injury that is severe enough to
condition in veterinary medicine, but it can
cause paralysis (particularly with lack of
lead to catastrophic problems such as
deep pain sensation) and inability to
retinal cletaclunent or neurologic derangeventilate and ambulate, and that has not ments from intracranial hemorrhage.

responded to medical management ( such as

Hypertension can exacerbate proteinuria
anti-inflammatory medications) warrants
in animals with chronic kidney disease.

immediate imaging and surgical interven

Moderate to severe hypertension can be
tion. Loss of deep pain is associated with a
treated with oral antihypertensive agents
poor return to function. Serial neurologic
such as angiotensin-converting enzyme
exan1inations should be perf01med in any
inhibitors (eg, benazepril), calcium channel
animal with neurologic disease.

blockers ( eg, amlodipine ), direct arterial
dilators ( eg, hydralazine ), or systemic

Blood Pressure: Blood pressure should
injectable antihypertensive agents such as
be monitored via direct or indirect
nitroprusside (0.5-10 mcg!kg/min), titrated
methods. The goal is to maintain organ
to effect. Blood pressure must be monitored
perfusion by maintaining a minimum mean
constantly to assess response to therapy
arterial blood pressure >60 mmHg (systolic
with nitroprusside. Chronic hype1tension

>90 mmHg). In hypo tensive animals with
that is rapidly decreased may result in
adequate cardiac function, treatment
decreased renal perfusion.

consists of intravascular volume infusion

The A.nlerican College of Vete1inary

(seep 1675), oxygen administration, and

Internal Medicine classifies risk of
pain control. Hypotension unresponsive
target-organ dan1age from hype1tension into
to intravascular volume repl;icement can
four categories based on systolic blood
be due to one or more of the following:

pressure: I: <150 nunHg = minimal risk;
hypoglycemia, acidosis, alkalosis,

II: 150-159 mmHg = mild risk; Ill: 160-179
electrolyte disorders (eg, potassium,
nunHg = moderate risk; and IV: > 180 nunHg =
calcium, magnesium), brain-stem
severe risk.

pathology, cardiac arrhythmias, metabolic
toxins ( eg, hepatic, renal), ongoing fluid

Heart Rate, Rhythm, Contractility,
loss, relative hypoaclrenocorticism ( eg,
and Myocardial Injury: The electrical
cortisol deficiency), heart or pericardia!

and mechanical systems of the heart should
disease, excessive vasodilation, and
be evaluated separately. Specific antiarexcessive vasoconstriction. The need for rhythmic drug therapy should be instituted
cardiac support with positive inotropes
based on an accurate ECG diagnosis when
should be assessed. An experienced
perfusion is compromised by an ar-rhythmia
ultrasonographer may be able to assess
and the first-line therapy of oxygen
ventricular and/or capacitance vessel size
supplementation and analgesics has been
to provide an estimate of preloacl and
unsuccessful in controlling the atThythmia.

contractility. Once intravascular volwne

Arrhytlunias can occur for a variety of

( central venous pressure >8 cm H,0) and
reasons, such as SIRS diseases, splenic
cardiac function are assessed as adequate,
disease, organ torsion ( eg, gastric dilatationvasopressor therapy with CRI of dopamine volvulus ), and electrolyte abnormalities

(5-15 mcg!kg/rnin) or norepinephrine

(eg, hyperkalemia); the underlying

(0.05-2 mcg!kg/min), beginning at the
condition must be treated/investigated as
lower encl of the dosage range and
well. Some ventricular rhythms (such as
increasing by increments of 0.2-0.5 mcg, is
ventricular premature contractions and
recommended. Stroma-free hemoglobin
accelerated idioventricular atThythmias)

can be infused for its pressor effects.

may not necessarily require irnmediate

MONITORING THE CRITICALLY ILL ANIMAL

1689
therapy. Indications for treatment of a
marker in ca.ts with limb thromboembolism.

ventricular rhythm include tachycardia

Temperature is a vital parameter to monitor

(rates >160-180 bpm), clinical signs of poor
and treat in ca.ts with clinical signs of shock,
perfusion (low blood pressure, poor pulse
and active wa.m1ing is an essential
quality, etc), multifonn arrhytlunias, and
component of therapy. Therapeutic

R-on-T phenomenon. Other tachyarrhythhypothennia. may have some neuro-sparing VetBooks.ir
mias may respond to class I, II, III, or IV
effects in animals with trawnatic brain
antiarrhytlunics; bradyarrhythmias can
injw-y or in postresuscitation (CPR) care;
be challenging to treat medically and
however, fwther investigation is needed. In
may require pacemaker placement. An
animals with induced hypothermia, blood
echocardiogran1 can be perfom1ed to
flow to most organs can be significantly
evaluate cardiac contractility in SIRS
decreased, and coagulation may be affected.

diseases and to detect underlying cardiac

Altered body temperature is part of the
diseases. If cardiac contractility is
definition of SIRS-type diseases; oilier
decreased, dobutamine at 5-10 mcg/kg/rnin
paran1eters include an increased or

(dogs) or 2.5-5 mcg/kg/min (cats) should be
decreased heart rate, increased or
considered to provide inotropic support if
decreased WBC count, and an increased
there is evidence of poor cardiac output.

respirato1-y rate.

Recent studies have demonstrated that
dogs with mitral valve disease and dilated

Coagulation: Disseminated intravascula.r
cardiomyopathy have a poorer prognosis
coagulation (DIC) can develop in any aninlal
if their cardiac troponins ( cTnI) and/or
tl1at has w1dergone a period of relative
natriuretic peptide (NT-pro-BNP) is
vascular stasis as occurs during shock,
increased. However, these tests are not
severe tissue or capillary damage such as
available in all hospitals and do not
that whi::h occurs with trawna, exposure
necessarily direct therapy, or diagnose
of capillary endothelial cells to circulating
or differentiate disease processes.

inflammatory mediators as occurs during
sepsis or SIRS, or moderate to severe

Temperature: Body temperature is
alterations in body temperature. In the
considered part of the initial clinical
early stages of DIC, tllere may be few or no
database and should be measured regularly
clinical signs. However, as DIC progresses,
in every critically ill aninlal. A variety of
its effects are obvious and catastrophic. The
diseases can result in increased or
goal is to detect DIC in tl1e early stages and
decreased body temperature. Temperature
to slow or prevent its progression.

is measured most accurately and consis

Early DIC is characterized by a hypercotently with a rectal thennometer.

agulable stage in which serum antithrombin

Increased temperatures can be seen with

(AT) levels are decreased and tl1e coagulaenvironmental exposure (eg, heat stroke), tion cascade is activated by any of the
increased activity ( eg, exercise, exciteprecipitating causes. Activation of tlle ment), and infectious, inflammatory, or
coagulation cascade throughout the body
neoplastic diseases. Severe increases of
rapidly depletes the clotting factors and
temperature (>105.5° [40.8°C]), particularly
the blood platelet cow1t as platelets are
when prolonged, can lead to severe
incorporated into tl1e clots. At tllis stage, the
metabolic disease such as hemorrhagic
protlu-ombin time and partial thromboplasdiathesis, disseminated intravascular tin time may be decreased, but this is a
coagulation, and SIRS diseases, which may
challenging stage to identify and diagnose.

lead to multiorgan dysfunction. Effective

However, tllis rapidly progresses to a
means of cooling animals include fluid
hypocoagulable stage as the coagulation
therapy, using wet towels with fans, and
factors are conswned. In this late stage, the
placing alcohol in paw pads. Animals should prolhrombin time and partial tllromboplasnot be inunersed in cold water, because this tin tin1e ( or activated clotting time) are
causes peripheral vasocontriction and
prolonged, and fibrinogen degradation
decreases core heat dissipation. Fever
products a.re increased.

of unknown origin warrants a systemic

Treatment of DIC focuses on treating
evaluation (seep 1015).

the underlying disease and removing the

Hypothermia is most comnunonly
stimulus for continued activation of tlle
associated with anesthesia in small animals;
coagulation cascade. In tlle early hyperhowever, severe systemic disease (particucoagulable stages, treatment focuses on larly in cats) and environmental exposure
maximizing tlle function of AT, which is
may be contributing factors. Mild hypotherthe most abundant natural inhibitor of tlle mia can be a common sequela of severe
se1ine proteases of tlle coagulation cascade.

cardiovascular disease and is a prognostic

When AT levels a.re adequate, heparin can

1690

MONITORING THE CRITICALLY ILL ANIMAL
be administered SC (50-100 U/kg, tid). If
ing adequate Hgb levels is essential to

AT levels are <600A, of nonnal, then plasma
maintaining adequate oxygen delivery.

transfusions should also be given to

When anemia is associated with clinical
increase the level to ;i:S()OA,. In animals with
signs of tachycardia, increased respiratory

VetBooks.ir
diseases known to predispose to DIC,
rate, altered mentation, severe lethargy/
coagulation parameters and platelet counts
weakness, and hypotension, then packed
should be monitored. Thomboelastography

RBCs, whole blood, or stroma-free

(TEG) provides another means of global
hemoglobin should be administered to bring
assessment of the clotting cascade and may
the PCV to >200A, or the Hgb level to> 7 g/dL.

be a useful tool with suspected hypo- or

In some cases of hemolytic or chronic
hypercoagulable states; hypercoagulable
anemia, the PCV car1 be maintained at a
states are challenging to diagnose, and TEG
lower percentage before transfusion is
is one of the few methods that may provide
required if there are no corresponding
an accurate assessment.

clinical signs. In animals that require

Thrombosis occurs without DIC when
multiple blood san1pling (such as diabetic
there are alterations in Virchow's triad:

patients) or very small anin1als, blood
endothelial irtjury, blood stasis, and
san1pling should be minimized to prevent
hypercoagulable states. Abnormalities in
iatrogenic blood loss. Optimal hemoglobin
one or more of these components may be
levels have not been determined; however,
seen with vascular anomalies, atrial
conservative transfusion managment in
enlargement, severe systemic illness (SIRS,
people (Hgb goal of7 g/dL or PCV of200A,)

immune-mediated hemolytic anemia),
has in1proved survival benefit over more
trauma, neoplasia, renal disease, hyperliberal transfusion goals (Hgb of 10 g/dL
adrenocorticism, and as a primary disease
or PCV of 300A,).

in Greyhounds. The most common severe

Except in tl1e case of acute, life-threatenmanifestations of hypercoagulability are ing hemorrhage, before an RBC-containing
aortic and pulmonary thromboemboli.

blood product is administered, a crossmatch

Pulmonary thromboemboli should be
should be pe1formed to ensure a safely
suspected when significant hypoxemia is
administered transfusion. Even type-specific
present with minimal lung changes on
or "A-negative" blood may not be antigenithoracic radiographs. Anticoagulation cally appropriate for some dogs, because
therapy and oxygen support should be
many antigens are present on canine RBCs.

implemented, and oxygenation and

If multiple transfusions are anticipated,
ventilation monitored. Arterial thromboemblood typing should be perfonned as well.

bolism can occur in cats with underlying

Only type-specific blood should be
heart disease. Antithrombotics are
administered to cats. In dogs and cats with
warranted in these cases; options include
acute cavitary (pleural or peritoneal)

aspirin and/or clopidogre1; heparin (low
hemorrhage, blood may be salvaged from
molecular weight or unfractionated), or
the cavity with aspiration ( via centesis or
warfarin. Most of these drugs require close
exploratory surgery when indicated) and an
monitoring of clotting times to achieve
autologous blood transfusion administered
therapeutic goals. This disease can be
through a blood filter.

painful, and opioid medications ar·e often

Rarely, disease states may result in
warranted as well as monitoring for
altered hemoglobin (such as methemoreperfusion irtjury.

globinemia) or altered oxygen-carrying

Disease states that result in relative
capacity (such as carboxyhe1110globinehypocoagulability may include anticoagumia), often recognized by altered mucous lant rodenticide ingestion, fuln1inant liver
membrane color (muddy or brick-red,
failure, severe thombocytopenia, snake
respectively). Despite normal measured
bites, dilutional hypocoagulability from
hemoglobin concentrations, oxygen is not
fluid and colloid administration, and
being delivered to tissues in these animals,
congenital defects in the coagulation
and oxygen supplementation is necessary
cascade such as von Willebrand disease,
along with treatment of the underlying
hemophilia A or B platelet defects (Boxers),
disease.

or hyperfibrinolysis (Greyhounds). Therapy

An alternative means to increase
should be specific to the inciting cause;
oxygen-carrying capacity of the blood is a
plasma products are often necessary to
conm1ercial stroma-free hemoglobin-based
correct life-threatening coagulopathies.

oxygen carrier (HBOC) such as Oxyglobin®.

Monitoring PCV is not an adequate assess

Red Blood Cell and Hemoglobin
ment of oxygen delivery after use of HBOCs.

Concentration: Because Hgb carries

Animals with a PCV > 55% ( other than
most of the oxygen in the blood, maintain-
sight hounds and at high altitudes) may

MONITORING THE CRITICALLY ILL ANIMAL

1691
have microvascular sludging ( due to the
animal, etc). All vete1inary staff should
altered blood rheology) and hypertension
be encouraged to wash hands between

( which impairs microvascular delivery of
patients, treat wounds in a clean manner,
oxygen to the tissues). This occurs most
and administer IV injections only after
commonly with hemorrhagic gastroenteriswabbing an IV port with an alchohol swab.

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tis. Treatment with IV fluids, and phlebot

Educating hospital staff on appropriate
omy in cases of absolute polycythemia, are
patient handling techniques may help limit
performed to improve microvascular flow
development of nosocomi.al infections,
and oxygen delivery to the tissues.

which develop 48 hr after hospital
admission.

Renal Function: In animals that have

Ultimately, antibiotic selection should
had a hypotensive episode, are receiving
be based on the results of culture and
potentially nephrotoxic medications, or
susceptibility testing, but empiric treatment,
have primary renal compromise, renal
based on site of infection and suspected
function should be evaluated daily.

type of bacteria, is necessary pending these

Urinalysis perfom1ed on a sample collected
results. Empiric therapy may be based on
before fluid administration will help to
common organisms found at the affected
assess renal function. Nonna! urine output
site and/or Gran1 stain and cytologic
is 1-2 mIJkg/hr and can be closely
examination, which should be performed
monitored with an indwelling urinary
immediately. Repeat culture and suscepticatheter. Animals in polyuric renal failure bility testing may be necessary in animals
are most often managed medically;
not responding to therapy as expected or if
however, animals in oliguric ( <0.8 mIJkg/hr), prolonged antibiotic therapy is anticipated.

anuric ( <0.03 mIJkg/hr), or relative oliguric

In animals that have sustained a

(less than expected) renal failure may
hypotensive episode or have a GI disease
require peritoneal or hemodialysis to
that would allow bacterial translocation,
maintain fluid and electrolyte balance.

broad-spectrum bacterial coverage should

Serial measurement of serum BUN,
be provided until the results of culture are
creatinine, electrolytes, and phosphorus
available or the risk of systemic infection
will detect changes and help guide therapy.

has passed.

Serial urinalyses to detect glucosuria,

An antibiotic protocol should be
proteinuria, or renal tubular casts help
established for veterinary hospitals to
evaluate acute tubular injury before the
minimize the number of antibiotics
damage progresses to overt renal failure
administered empirically on a routine
and azotemia. If urine output monitoring
basis to reduce the development of
with a catheter is not possible, then
resistant organisms in the hospital
estimating urine output by measuring
environment and to improve their
absorbent pads or litterboxes is neccesary.

susceptibility patterns. Limiting use of

Body weights should be recorded regularly.

specific classes of antibiotics or having

Additional necessary diagnostics may
rotating schedules may help limit
include urine culture and susceptibility
development of microbial resistance.

testing, urine protein to creatinine ratio, or

Periodic environmental cultures and
specific testing for renal-specific disease
facility-based monitoring of culture and

(eg, ethylene glycol, leptospirosis). Animals
susceptibility results for evidence of
may also be monitored using a scoring
nosocomial infections and bacterial
system to provide additional "objective"

resistance patterns can help identify
monitoring: the International Renal Interest
and control sources of infection and

Society has a staging system to monitor
limit development of resistance. A
dogs and cats with chronic renal disease
first-generation cephalosporin ( eg,
based on serum creatinine, blood pressure,
cefazolin, 22 mg/kg, ti.ct) is useful for
and proteinuria.

gram-positive and gram-negative
infections; an alternative choice is an ami

Infection Identification/Prevention
nopencillin with a 13-lactamase inhibitor
and Treatment and Immune Status:

(such as clavulanic acid or sulbactam),

Strict aseptic technique should be observed
which has good gram-negative, gramwhen examining or treating animals that are positive, and anaerobic coverage at
neutropenic or receiving in1munosuppres20-30 mg/kg, ti.ct. If a resistant bacteria is si.ve drugs. These animals should be isolated suspected, gentamicin (3-5 mg/kg/day, from other animals and handled by a single

IV) can be given to more specifically
person who adheres to appropriate barrier
target gram-negative organisms after
nursing techniques (washes hands, wears
hydration and perfusion have normalized;
gloves and gown before handling the
a fluoroquinolone ( eg, enrofloxacin at

1692

MONITORING THE CRITICALLY ILL ANIMAL

5-10 mg/kg, IV, once or twice daily) is an
which helps prevent gastric ulceration
alternative. The once-daily dosage is less
and intestinal mucosa! compromise with
likely to cause toxicity and has the same
secondary bacterial translocation.

antibacterial effect as a divided dosage

Antiemetics are used in animals that
schedule. Metronidazole (7.5-15 mg/kg)

continue to vomit frequently despite
given slowly IV over 20 min every 6-8 hr is
placement of a nasogastric tube, thus

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used for suspected anaerobic infections.

improving patient comfort and reducing

If multiple antibiotics are started, the
the incidence of aspiration, vagal-inducecl
antimicrobial spectrum should be
collapse, and braclycardia that can
narrowed and antibiotic choice adjusted
accompany the vomiting reflex. Metoas soon as the organism's susceptibility clopramide blocks the dopaminergic
pattern is identified. Recurrent infections
receptors in the chemoreceptor trigger
should be investigated for an underlying
zone (CRTZ) and central vomiting center
pattern of resistance, nidus of infection,
and acts peripherally by promoting
or immune-compromising disease.

gastric emptying. Ondansetron and

Newer generations and classes of
clolasetron are potent antiemetics that
antibiotics, such as carbapenems ( eg,
block serotonin receptors and act at the
imipenim), third-generation cephalosporins

CRTZ and the central vomiting center;

(eg, ceftazidime), and vancomycin should
they are administered at 0.6-1 mg/kg/day.

be rese1ved for use in anin1als with bacterial

Maropitant is an NK, receptor antagonist
infections demonstrated to be resistant to
that blocks vomiting at the CRTZ, vomiting
other antibiotics.

center, ai1cl peripheral receptors, admin

WBC counts peliormed on a semireguistered at 1 mg/kg/clay, SC, or 2 mg/kg/day, lar basis ( every 48-72 hr) may indicate

PO. Vomiting refractory to all other
an appropriate response to infection/
treatments in an otherwise stable animal
inflan1mation or patient deterioration.

with normal blood pressure can be

Vaiious molecular or "bio" markers have
treated with chlorpromazine (dogs: 0.05-1
been investigated in SIRS-type diseases to
mg/kg, IV, every 4-8 hr; cats: 0.01-0.025
help understand and stratify disease. High
mg/kg, IV, every 4-8 hr). A combination of
mobility group box 1 protein and C-reactive
a11tiemetics that have different mechaprotein have been associated with poor nisms of action is often required to arrest
outcome or diagnosis of SIRS-type disease;
refractory emesis in severe illness; in
however, how that information affects
animals that require multiple antiemetics,
therapy has yet to be determined. Plasma
an obstructive disease should be
interleukin lB and IL-6 have been demonexcluded.

strated to have some prognostic value in

GI ulceration often accompanies
cats with sepsis.

critical diseases such as hypotension,
hypergastrinemia associated with liver and

GI Motility and Mucosal Integrity:

kidney disease, drug toxicities, neuro

Critically ill animals, even those without a
logic disease, and respiratory disorders
primary GI disease, are prone to gastric
requiring ventilation. Histamine2-receptor
atony, ileus, and gastric nlceration.

antagonists such as ranitidine and

Auscultation for bowel sow1ds should be
famotidine, and proton-pump inhibitors
pe1iom1ed three times a day. Metocloprasuch as omeprazole and pantoprazole mide ( 1 -2 mg/kg/day as a CRI) is useful
should be administered to treat gastric
because of its central antiemetic effects and
ulcers. However, changing the pH of the
its ability to increase progressive gastric
stomach ca11 change its microbial flora.

and intestinal motility. Other motility

Agents such as sucralfate and barium are
modifiers to consider include cisapride,
administered to bind to esophageal and
ranitidine, and erythromycin. Motility
gastric erosions and ulcers. Misoprostol
modifiers should be avoided if gastric or
may help prevent NSAID-induced
intestinal obstruction is suspected or has
ulceration when toxic levels ofNSAIDs
been confirmed.

are ingested.

Placement of a nasogastric tube to
allow removal of accumulated gas and

Drug Dosages and Metabolism: An
fluid reduces the possibility of aspiration
active medications list should be kept with
of refluxed gastric contents and allows
each a11imal's medical record and carefully
continuous decompression. The
reviewed daily for potential drug interacnasogastric tube also can be used to tions, drug dosages, and possible adverse
introduce small ainounts of a glucose and
effects. If renal or hepatic function is
electrolyte solution or a liquid diet to
compromised, or if protein (albumin)

provide nutrition directly to enterocytes,
binding capacity is decreased, some drug

MONITORING THE CRITICALLY ILL ANIMAL

1693
dosages should be decreased to account
ing or administering a liquid diet, the tube
for altered metabolism, elimination, or
should be flushed with saline. If this initial
protein binding. The daily review also
feeding is tolerated, the concentration is
should ensure that the dosage has been
increased to 2 parts liquid diet mixed with
calculated correctly and that it is appropri1 part water during the next 12---24 hr. If this ate for the animal's current weight and
is tolerated, then the undiluted diet can be

VetBooks.ir
body condition score. The sudden onset of
delivered to provide the full caloric
any new clinical signs should be investirequirements. As the animal recovers, bolus gated in light of the medications and their
feeding can be introduced by gradually
potential adverse effects.

decreasing feeding frequency and increasing volumes.

Nutrition: When nutritional needs

When nutritional needs cannot be met by
are not met, animals rapidly develop a
enteral feeding, parenteral feeding is used.

negative energy balance, which can result Partial parenteral nutrition, consisting of in GI dysfunction, organ dysfunction,
an1ino acid and carbohydrate solutions, can
poor wound healing, and even death.

be infused through a peripheral vein, provid

Direct enteral nutrition will improve the
ing part of the animal's caloric requirements
normal GI barrier, function, and motility.

in a readily metabolizable fom1. Total

Enteral feeding is always preferred, and
parenteral nutrition (including the lipid
most animals tolerate trickle flow feeding component) must be delivered through a techniques. Short-term options include
central venous catheter, because high osmosyringe or forced feeding; however, this larity of the solutions may cause phlebitis
can lead to food aversion and is not
and RBC lysis. In animals with prolonged
comfortable for most critically ill
anorexia, vitamin supplementation may
animals. Easy to place and well-tolerated, also be necessary.

short-term feeding tubes that allow

Appetite stimulants, such as the serotonin
trickle feeding include nasogastric,
antagonist cyproheptadine and the serotonin
nasoesophageal, and nasojejunal.

agonist mirtazapine, are commonly used but

Nasogastric tubes also allow gastric
with varying success. Oral benzodiazepines
suctioning to monitor GI function and
may cause hepatotoxicity in cats and are not
may limit continued vomiting and risk of
good alternatives; iitjectable benzodiazaspiration pneumonia; nasojejunal tubes epines may be used as a short-tenn solution
can be challenging to place. Long-term
for animals with rapidly resolving disease.

feeding tubes include esophagostomy,

The use of appetite stimulants provides
pharyngostomy, gastrotomy, or jejunosinconsistent food intake and is not tomy tubes. Each of these tubes are well
recommended as the primary way to
tolerated by most animals, and all require
administer nutrition in critically ill animals.

anesthesia to place; the esophagostomy
is a minor surgical procedure, and

Pain Control: Pain activates the stress
gastrostomy tubes can be placed with
hormone systems of the body and
endoscopic assistance.

contributes to morbidity and mortality.

Feeding by trickle flow is initiated with

Signs of pain are quite variable in animals;
small volumes of a dilute veterinary liquid
these may include decreased normal
diet solution. If an animal has been starved
behavior (decreased appetite, ambulafor an extended period of time, nutrition tion, grooming, etc), development of
should be increased slowly (by 25%---33% of
abnormal behaviors (vocalizing,
daily caloric requirements per day) to avoid
inappropriate urination, altered posture,
the hyperglycemia, hypokalemia, hypophossigns of agitation or aggression, etc), phatemia, and hypomagnesemia seen with
reaction to touch, and altered objective
refeeding syndrome.

physical parameters (increased heart rate,

For the first 12---24 hr, the diet should be
pale mucous membranes, dilated pupils,
calculated to provide 1A to '/, of the daily
etc), which can mimic signs of shock. (See
caloric requirement and is diluted 1 part
also SYSTEMIC Pl·IARMACOTl·IEllAPEUTICS OF THE
liquid diet to 2 parts water ( or electrolyte

NERVOUS SYSTEM, p 2590, and PAIN MANAGEsolution). This volume is delivered by CRI MENT, p 2104.) Animals that may not show
over 12---24 hr or divided into small boluses
obvious signs of pain but are known to
every 2--4 lu·. Before each bolus feeding and
have a painful condition should receive
every 6 hr during a CRI, the feeding tube
analgesics as part of their treatment (see
should be suctioned to dete1mine whether

TABLE 7). Preemptive administration of
any residual volume is present that would
analgesics is recommended, when
necessitate decreasing the volume infused
possible. Pain should be assessed using
or adding prokinetic agents. After suction-
a validated pain assessment tool and

1694

MONITORING THE CRITICALLY ILL ANIMAL
monitored on a regular basis during the
cardiovascular adverse effects, and their
course of hospitalization to ensure
actions are reversible with antagonists ( eg,
adequate analgesia.

naloxone ). Long-acting opioids are best

Analgesia in critically ill animals can
avoided in unstable animals. Reports of IV
safely be provided by opioids titrated to
morphine causing hypotension due to

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effect. Opioids provide potent analgesia
histan1ine release do not seem to be

(given IV, IM, or SC) with minimal
clinically significant if the drug is given

IH=iiii ANALGESICS USED IN EMERGENCY PRACTICE

Drug

Dosage

Comments

Morphine

Dogs: 0.05-0.4 mg/kg, IV, every

Incremental IV bolus technique:

1-4 hr; 0.2-1 mg/kg, IM or SC,
dogs-increments ofO.l mg/kg
every 2-6 hr; 0.1 mg/kg diluted
until analgesia appears adequate;
with 0.9% saline administered
cats-increments of 0.02 mg/kg.

epidurally at 0.23 mUkg, every

In dogs, this can be followed by

8-24 hr

CRI at 0.1 mg/kg/hr that can be
increased incrementally if

Cats: 0.05-0.2 mg/kg, IM or SC,
needed. Rapid IV injections may
every 2-6 hr
cause histamine release.

Oxymorphone/

Dogs: 0.02-0.l mg/kg, IV, every

Minimal cardiovascular effects;
hydromorphone 2-4 hr; 0.05-0.2 mg/kg, IM or SC, may cause panting or emesis every 2-6hr

Cats: 0.02-0.05 mg/kg, IV, every Can be given as a CRI with the 2-4 hr; 0.05-0.1 mg/kg, IM or SC, dose divided over 4 hr every 2-6hr

Fentanyl

Dogs: 2-10 mcg/kg, IV, every

With short half-life, fentanyl is

30-60 min; 2-20 mcg/kg/hr, IV as best administered as a CRI.

aCRI

Fentanyl

12.5 mcg/hr for animals <2.5 kg

The patches cannot be cut. More
transdermal
body wt; 25 mcg/hr for animals
than one patch may be used in
patch

2.5-10 kg body wt; 50 mcg/hr for larger anin1als. Injectable animals 10-20 kg body wt; 75
repository fentanyl solutions may
mcg/hr for animals 20-30 kg
be an alternative if available.

body wt; 106 mcg/hr for animals

>30 kg body wt

Butorphanol

Dogs: 0.2-0.5 mg/kg, IM, IV, or

Has a ceiling effect; s!1ort

SC, every 1 -3 hr
duration.of effect (1-2 hr) in
most dogs

Cats: 0.1-0.4 mg/kg, IM, IV, or

Can be given as a CRI with the

SC, every 1-6 hr
dose divided over 4 hr

Buprenorphine

Dogs: 0.005-0.02 mg/kg, IM or IV, May be more difficult to reverse every 1-6 hr

Cats: 0.005-0.01 mg/kg, IM, IV, or S ub lingual absorption reported to sub lingual, every 4-8 hr
be excellent in cats

Methadone

0.1-0.5 mg/kg IV, IM, or SC every Less vomiting than morphine, 4-6hr
less panting than hydromorphone

MONITORING THE CRITICALLY ILL ANIMAL

1695
over 5-10 min or as a CRI. Other medica

Nursing Care: Providing nursing care
tions such as hydromorphone, oxymorto critically ill animals requires a skilled, phone, and fentanyl can be given without
knowledgeable, attentive, and highly
this risk. CRI provides constant analgesia
trained nursing staff. Recumbent animals
and is often more convenient and less
should be turned from one side to the

VetBooks.ir
painful than inte1mittent IM or SC
other every 4 hr or maintained in
injections. In cats, injectable buprenorvariations of sternal recumbency to phine is absorbed systemically after
prevent decubital ulcers and atelectasis.

sublingual administration. Neuroleptanal

Physical therapy 3-4 times a day is
gesia can be provided by combination of an
important to maintain range of motion
opioid with a sedative ( eg, benzodiazepine)

and muscle tone and blood flow; this can
or tranquilizer ( eg, acepromazine) in
be provided through massage, passive
animals without contraindications to these
range of motion, encouraged activity, etc.

medications.

Activity may also improve GI motility and

For longtem1 control of pain, transdermal
provide a time when animals can urinate
fentanyl patches or repository fentanyl
and defecate outside of their kennel.

injections are used but require up to 12 hr to

Catheters should be labeled and marked
reach therapeutic blood levels; analgesia
with the date of placement, and catheter
must be provided by injection until
sites should be inspected on a routine
adequate blood levels have been reached.

basis for signs of infection or displace

If pain is not adequately controlled with
ment. When catheters are removed, the
opioids alone, then ketan1ine, an NMDA
entrance site should be inspected for
receptor antagonist, can be delivered by
inflammation/infection. Urine and fecal

CRI with the opioids. Ketamine may have
soiling should be immediately cleaned.

variable effects on the cardiovascular

Recumbent animals require regular
system, making patient selection crucial,
inspection and cleaning to prevent urine
and it should not be used as a sole agent
scalding of the skin; tail wraps minimize
for pain relief. Lidocaine, a local anescontan1ination from diarrhea. Nursing thetic, can be used as an adjunct for
care must be tailored to the specific
systemic pain relief when delivered as a
condition(s). A well-trained nursing staff

CRI and combined with ketamine and/or
can recognize deterioration or alterations
an opioid. Some investigation into using
in an animal often before the attending
maropitant as an adjunctive analgesic
clinician because of the substantial
agent is promising, because it decreased
amount of hands-on time with the
anesthetic requirements during noxious
patients.

stimuli in dogs.

Local pain relief can be provided
using local infiltrative or nerve blocks

Wound Care and Bandage Changes:

on extremities. Intermittent infusions

Bandages, essential to cover wounds,
of bupivicaine administered through
should be changed whenever they become
thoracotomy tubes or abdominal
soiled or wet. Distal limb edema can be
catheters can provide pleural and
improved by placing light compression
peritoneal analgesia. Epidural injections
wraps that are changed every clay. (See also
by needle or infusions by catheter can

WOUND MANAGEMENT, p 1701.) Open wounds
provide pain relief from pelvic, hindlin1b,
should be bandaged on arrival to prevent
and abdominal injuries or disease.

further contamination or nosocomial

NSAIDs are rarely used in critically ill
infection until surgical debridement can be
animals because of their effects on the GI
done. Areas of skin swelling or bruising
tract, kidney, and liver; however, they may
should be marked to detennine progresbe appropriate in animals with significant sion or resolution of the pathology.

fevers or orthopedic injury that are not
systemically ill. o:rAgonists (such as

Tender, Loving Care: Owner visits
dexmedetomidine) provide sedation as
should be encouraged. Animals should be
well, but case selection is critical because
handled and spoken to kindly to minimize
of the significant cardiovascular adverse
stress and anxiety. Having familiar items
effects. Other oral classes of medication
such as toys or blankets from home are
that are well tolerated for mild to moderate
helpful for some pets. Consolidating
pain include tramadol, an1antidine, and
several treatments at one time and
gabapentin. Adjuvant methods of pain
turning down the lights at night, when
relief may include placing ice packs on
the animal's condition permits, allow
regions of swelling, acupuncture, laser
the animal some time to rest and sleep
therapy, or massage.

undisturbed.

1696

OPHTHALMIC EMERGENCIES

OPHTHALMIC EMERGENCIES

VetBooks.ir

Ophthalmic emergencies require rapid
diagnosis and appropriate and often
aggressive therapy for maintenance of
vision.

TRAUMATIC PROPTOSIS

Traumatic proptosis may follow blunt
trauma ( eg, being hit by a car, fight with
another animal). During trauma, the globe is
luxated from the orbit, and eyelid spasms
prevent its retraction. Secondary orbital
hemorrhage and swelling displace the globe
further from the orbit. Comeocortjunctival

Traumatic retrobulbar hemorrhage, dog;
drying and malacia follow. Prognosis
hemorrhage displaces the globe forward
depends on pupil size and reflexes, duration
but not sufficiently to produce proptosis.

of exposure, other globe or orbital damage,

Courtesy of K. Ge/att.

breed (brachycephalics are predisposed),
and other systemic trauma. Approximately
ulcerative keratitis. Subcortjunctival and

40%--600/o of dogs, but very few cats, recover
intraocular hemorrhage may also be
vision. Treatment begins by providing
present, and the latter can prevent
moisture to lubricate the exposed
intraocular exan1ination. Corneal and
corneocortjunctiva General anesthesia
scleral lacerations should be excluded by
followed by a lateral canthotomy and
ophthalmic examination, and B-scan
complete temporary tarsorrhaphy with
ultrasonography to detect retinal detachusually two or three interrupted h01izontal ment is recommended in eyes with intraocumattress sutures (placed at one-half lar hemorrhage.

thickness of the eyelids) and stents should

Medical and surgical therapy consists
be followed by systemic antibiotics and
of topical and systemic antibiotics and
corticosteroids as well as topical antibiotics
corticosteroids, mydriatics if pupillary
and mydriatics (if miosis is present).

dilation is necessary, and a complete

Sutures and stents are reinoved only when
temporary tarsorrhaphy to protect the
a brisk blink reflex returns (usually 7 --21
cornea until a brisk blink reflex returns.

days), or more conservatively, a single

Prognosis is guarded, because secondary
suture every 2--3 days until all have been
glaucoma and phthisis bulbus are not
removed. Premature suture removal results
infrequent. lntraocular hemorrhage is
in lagophthalrnia and persistent and often
usually allowed to reabsorb.

progressive corneal ulceration. Complications include corneal ulceration, enophthalmia, optic nerve degeneration, keratocon

EYELID LACERATIONS
junctivitis sicca, and medial rectus muscle

Eyelid lacerations should be reapposed as
irtjury.

soon as possible. Lacerations involving the
lid margin require exact apposition to
prevent longterm v-shape defects and an

TRAUMATIC RETROBULBAR
in1paired lid function. Small dogs and cats

HEMORRHAGE
require a single layer of sutures ( usually
single interrupted 4-0 silk sutures), whereas

Orbital and ocular contusion can produce
large and giant breeds require a two-layer
retrobulbar hemorrhage sufficient to
closure; the deep layer involves the tarsus
damage the orbital vasculature and cause
and orbiculis oculi muscle ( single interexophthalrnos, iridocyclitis, and lagophthalrupted 4-0 absorbable sutures) and the mos. This occurs most often in dogs, horses,
superficial layer (skin) apposed with sinlple
and cats. The exophthalrnos and resultant
interrupted 4-0 silk sutures (remove after
lagophthalrnos are associated with an

7--10 days). Horses require double-layer
impaired blink reflex and acute exposure
closure. When skin sutures are in place, the

OPHTHALMIC EMERGENCIES

1697
lid must be protected from self-trauma by

Perforation of the lens can lead to rapid
either an Elizabethan collar (dogs and cats)

cataract formation, especially when the
or hard eye cup (horses). Because the blink
anterior Jens capsular tear is >2 mm Jong.

response is often impaired by the swollen

Vitreal and retinal hemorrhage and retinal
lid, a temporary tarsorrhaphy is necessary
detachments are likely. Ophthalmic
to protect the cornea. Postoperative therapy ultrasonography and orbital radiology are VetBooks.ir
often includes topical antibiotics and
most helpful to assess pellet location and
corticosteroids, as well as systemic
the integrity of the intra.ocular and orbital
antibiotics and NSAIDs.

tissues. Anterior Jens laceration and
rupture is also a common sequela of cat

CORNEAL FOREIGN BODIES
claw injuries in young dogs.

Penetration of the anterior lens cap

Corneal foreign bodies are seen most
sule (lacerations >2 mm) requires Jens
frequently in dogs, ca.ts, and horses. They
removal as soon as possible, because
are usually organic material, but sand,
escape of Jens material causes gradually
metal, and glass foreign bodies are also
intensifying lens-induced uveitis that
seen. Presenting signs include variable
often progresses to secondary glaucoma
blepharospasm, tearing, and a variable
and phthisis bulbus. The posterior
secondary iridocyclitis (aqueous flare,
segment changes usually resolve
miosis, iridal swelling, ocular hypotony,
provided the retina eventually reattaches.

and possible hypopyon). Ophthalmic

Focal retinal degeneration in the area of
examination reveals a foreign body on the
retinal penetration and detachment is
conjllllctival surface, in the posterior third
common. Prognosis is guarded and based,
eyelid fornix, or on or in the cornea.

in part, on the response to therapy and

Foreign bodies that adhere to the ocular
gradual clearing of the intraocular media.

surfaces are usually removed under topical

Therapy is directed at controlling the
anesthesia with either vigorous irrigation
post-traumatic inflammation and maintainor small serrated ophthalmic forceps. If the ing normal levels of intraocular pressure.

foreign body has embedded within the

Mydriatics and topical and systemic
deeper corneal layers or has penetrated
antibiotics and corticosteroids are
into the anterior chamber, general
administered to control the uveitis. Intraocanesthesia is required for careful removal ular hemorrhage is allowed to resolve, with
from either the anterior corneal surface or
anterior chamber hemorrhage usually
the anterior chamber. The corneal wound
disappearing in -1-2 wk and the vitreal
is apposed with simple interrupted 7-0 to
hemorrhage resolving in 3-6 mo.

8-0 absorbable sutures. Postoperative
therapy includes topical and systemic
broad-spectl'llJ11 antibiotics, myd1iatics,

DEEP STROMAL CORNEAL
systemic NSAIDs, and if necessary, drugs

ULCERS, DESCEMETOCELE, AND
to reduce intraocular pressure. Prognosis

IRIS PROLAPSE
for vision is usually good. Infrequent
complications include variable corneal

Most cornea.I ulcerations readily heal with
scar formation, septic endophthalmitis,
appropriate antibiotic, antiproteinase
cataract formation, and secondary

(often topical serum), and mydriatic
glaucoma.

therapy. However, cornea.I ulcers detected
late in the disease process, complicated by
other ocular diseases, or given inadequate

PENETRATING INTRAOCULAR
topical therapy can progress. These require

INJURIES
surgical intervention using a conjunctiva.I
graft or, more recently, the commercially

Penetrating intraocular injuries with
available porcine small-intestinal
retained foreign bodies are seen most
submucosa or experimental anmiotic
frequently in dogs and cats. They are often
membranes. Deep cornea.I ulcers,
associated with lead pellets and bullets that descemetocele, and iris prolapse are seen partially or totally traverse the ocular
with some frequency in dogs, cats, and
tunics, but splinters or spines ( eg, cactus)

horses. These conditions require immedican also cause a penetrating injury. Pellets ate surgical support of the weakened
or bullets usually cause self-sea.ling,
cornea, because they can threaten or
slightly tan corneal defects; may cause
seriously compromise corneal integrity.

intraocular hemorrhage; and may traverse

Brachycephalic breeds and dogs with
the lens and posterior segment wall.

keratoconjunctivitis sicca are most

1698

OPHTHALMIC EMERGENCIES
vulnerable. These corneal defects often
other systelnic irtjuries. If the entire eye
develop in the center of the cornea and
cannot be examined directly, B-scan
can markedly impair vision. Important
ultrasonography is used.

diagnostic aids are the Schirmer tear test

The corneal laceration is apposed with
to measure aqueous tear production and
simple interrupted 7-0 to 8-0 absorbable

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topical fluorescein to determine the extent
sutures. To provide additional protection
of the corneal ulcer. Corneal culture and
and support, the sutured laceration may
cytology can assist in choosing topical and
be covered with a third eyelid flap, bulbar
systemic antibiotics. Secondary anterior
cortjunctival graft, or partial temporary
uveitis with aqueous flare, miosis, ocular
tarsorrhaphy. Postoperative therapy to
hypotony, and hypopyon is common.

control the secondary iridocyclitis consists

Corneal ulcer depth must be accurately
of topical and systemic antibiotics, systemic
estimated using magnification, focal

NSAlDs, and mydriatics. Postoperative
illumination using a slit-beam, and topical
complications include variable and often
fluorescein. Central corneal ulcers are more
dense corneal scarring, cataract formation
vulnerable, because they require more time
with posterior synechiae, secondary
for the healing response and vascularizaglaucoma, phthisis bulbus, and bacterial tion. Adequate ulcer deb1idement is
endophthahnitis.

essential for successful adherence of a
cortjunctival graft. The corneal ulceration

GLAUCOMA

(stromal, descemetocele, or iris prolapse) is
covered with the bulbar cortjunctival graft

Animals are usually presented with

(360°, 180°, bridge, or pedicle) that appears
high-pressure glaucoma because
most appropriate.

intraocular pressure (IOP) >40-60 mmHg

For full-thickness corneal ulcers with
results in clinical signs of buphthalmia,
iris prolapse, cortjunctival grafts are also
mydriasis, corneal edema, episcleral
used, but the postoperative corneal opacity venous congestion, and variable ocular is usually larger and more dense. Postoppain. The underlying glaucoma may be erative therapy includes topical and
either open or narrow-closed angle, and
systemic broad-spectrum antibiotics,
either acute or chronic. Dog breeds most
systemic NSAlDs or corticosteroids, and
often affected with primary glaucoma
mydriatics. Treatments are gradually
include the American Cocker Spaniel,
tapered and administered for 4-8 wk.

Basset Hound, Chow Chow, Akita, Chinese

Postoperative complications include

Shar-Pei, Norwegian Elkhound, and
variable corneal scar and pigmentation,

San1oyed. In cats, glaucoma is often
anterior and/or posterior synechiae,
associated with anterior uveitis, whereas
secondary cataract formation, and rarely
in horses the risk factors are age > 10 yr
bacterial endophthalmitis.

old, anterior uveitis, and breed (Appaloosa). Although globe enlargement CORNEAL LACERATIONS

(buphthalmia) is detected fairly early in
dogs, buphthalmia in horses and cats is

Corneal lacerations are seim most
often missed until the glaucoma has
frequently in dogs and horses and infreprogressed.

quently in cats. Bites, self-inflicted trauma,

Diagnosis depends on clinical signs and
and other accidents can partially or totally
accurate tonometry. The Tono-Pen® and
penetrate the cornea. Partial-thickness

TonoVet® applanation tonometers are the
corneal lacerations are usually highly
most versatile. Gonioscopy and other
painful and require apposition with simple
diagnostic methods are used to evaluate the
interrupted absorbable sutures to the
anterior chamber angle and the posterior
healthy cornea. Excision of the lacerated
segment, including the optic neive head.

section is not recommended.

The goals of therapy are to rapidly lower

For full-thickness corneal lacerations,

IOP and to preseive as much vision as
signs usually include pain, blepharospasm,
possible. Immediate referral to a veteritearing, a corneal defect, and variable iris nary ophthalmologist is often helpful.

prolapse. Marked aqueous flare, hyphema,

Short-term treatment includes mannitol
miosis, and distortion of the pupil are

(1-2 g/kg, IV), topical 13-blockers and
common. Often, tl1e size of the iris prolapse
carbonic anhydrase inhibitors, systemic
is much larger than the underlying corneal
carbonic anhydrase inhibitors, and either
laceration. Prognosis depends on size and
prostaglandin analogues or miotics
position of the corneal laceration, other

(pilocarpine or demecariun1). The
ocular tissue involvement, gender (horse),
beneficial effects of the topical medicaage of the animal, duration of the irtjury, and tions are not usually apparent until IOP is

OPHTHALMIC EMERGENCIES

1699

<30 mm Hg. If mannitol treatment does not
confused with other inflammatory
lower IOP within 2-4 hr, anterior chamber
conditions of the cornea and/or conparacentesis under general anesthesia may junctiva. It presents clinically as acute be attempted. Longterm therapy usually
photophobia, pain, blepharospasm, a
includes topical and systemic ocular
congested and red conjunctiva, corneal

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hypotensive medications, laser cyclophoedema, reduced intraocular pressure, tocoagulation, cyclocryotherapy, and
miosis, aqueous flare (increased levels
anterior chamber shunts.

of proteins and inflammatory cells in
the aqueous humor) to frank hypopyon,

ANTERIOR LENS LUXATION
and/or hyphema. Chronic anterior uveitis,
in addition, may exhibit anterior and

Anterior lens luxation usually affects
posterior synechiae, irregular pupil
middle-aged dogs of the terrier breeds and
shape, cataract formation, and secondary
is seen most frequently in Smooth and Wire
glaucoma associated with peripheral

Haired Fox Terriers and Jack Russell
anterior synechiae and/or annular

Terriers. It is associated with zonular
posterior synechiae and iris bombe.

defects in the terrier breeds (associated

Anterior uveitis may be associated with
with the ADAMTSl 7 mutation), whereas
trauma, systematic diseases ( especially
in other breeds with inherited cataract
when bilateral), cataract formation, primary
formation it is associated with advanced
and metastatic neoplasia, and other causes.

cataract (hypermature) forn1ation. These

Prognosis and therapy depends on the
secondary glaucomas appear as acute
cause. Therapy usually includes myclriatics,
corneal edema, increased IOP, blepharotopical and systemic antibiotics, co1ticospasm, tearing, and ciliary flush. Often, the steroicls or NSAIDs, and other drugs to

Jens is in front of the pupil and often totally
target specific pathogens. Prognosis is
within the anterior chamber. Pupillary
usually favorable for acute anterior uveitis
blockage with vitreous adherent to the
but guarded for recurrent or chronic
posterior lens capsule and iridocorneal
anterior uveitis ( eg, uveoclermatologic
angle closure are common and can
syndrome in clogs, Golden Retriever uveitis,
markedly increase IOP within the posterior
or equine recurrent uveitis) because of the
segment. Applanation tonometry from the
high likelihood of developing secondary
central cornea may yield erroneous low
cataracts, refractory glaucoma, and phthisis

IOP levels. Direct examination of the
bulbus.

posterior segment is not usually possible,
and B-scan ultrasonography may be used
to evaluate the vitreous and retina.

ACUTE VISION LOSS

Treatment consists of lowering IOP
to normal levels (usually with mannitol,

Acute loss of vision may occur witl;t many

1-2 g/kg, IV); transpupillary aqueous humor
ophthalmic and CNS diseases, usually
flow may be reestablished with moderate
with abrupt onset of blindness, anisocodilation with lO"A,phenylephrinc. Lens ria, myclriasis, and Joss of both direct and
removal, preferably by phacoemulsification indirect pupillary light reflexes. Bilateral or intracapsular extraction, is performed as loss of vision is more common, but soon as possible. Postoperative treatment
unilateral vision loss can occur particuconsists of topical and systemic antibiotics larly when the other eye is blind. For
and cmticosteroids and maintenance of a
acute vision loss, large amounts of the
moderate but moving pupil. IOP is closely
retina must be involved; lesions of the
monitored and any increases treated with
optic nerve can cause blindness, because
topical f3-blockers, topical and systemic
the disease process can be quite localized.

carbonic anhydrase inhibitors, and

The rod or cone photoreceptors may be
prostaglandin analogues. Longtern1
preferentially affected initially and cause
postoperative complications include
either night or clay vision loss. Evaluation
anterior uveitis, secondary glaucoma, and
includes thorough ophthalmic and general
retinal detachment.

physical examinations, because many
systemic diseases may cause blindness.

ANTERIOR UVEITIS

Because visual field evaluations cannot be
performed in animals, subjective tests for

(Red eye)

vision are necessary and include the
menace test, dazzle reflex, maze test

Anterior uveitis or iridocyclitis is most
in both light and dark illumination,
common in dogs, cats, and horses but is
electroretinography, and visual evoked
uncommon in other species. It is often
potentials. See TABLES 8 and 9.

1700

OPHTHALMIC EMERGENCIES

•ih•J:• CLINICAL GUIDE FOR ACUTE BLINDNESS IN DOGS

Affected Visual

Diagnosis

Clinical Signs Pathway

Etiology

Sudden acute retinal

Acute-onset

Outer retinal

Unknown; Miniature

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degeneration
blindness,
layers

Schnauzer and
syndrome
dilated pupils,

Dachshw1d have

± PLR"

increased risk;
increased alkaline
phosphatase, ALT, and
cholesterol

Optic neuritis

Acute-onset

Optic nerve disc, Part of systemic disease
blindness, both retrobulbar

(eg, canine distemper,
eyes affected,
mycosis [ cryptococcodilated pupils,
sis, blastomycosis],

±PLR
protothecosis,
granulomatous
meningoencephalomyelitis), neoplasia,
trauma, orbital cellulitis

Retinal detaclunent

Acute

New·osensory

Systemic hypertension,
blindness,
retina
multiple intraocular
hemorrhage
myeloma

Intracranial disease

Nonna! eyes,

Optic chiasm

Pituitary masses, ± paraacute blindness
nasal masses, meningi

±PLR
omas, lymphosarcoma

Central blindness

Acute

Optic tracts,

Cardiac arrest during
blindness,
occipital cortex
anesthesia, seizures,
norma!PLR
severe head trauma

Slow vision loss

Progressive

Retrobulbar

Hydrocephalus, CNS
loss of vision/
visual tracts
neoplasia, granuloma

PLR
tous meningoencephalomyelitis

"Pupillruy light-induced reflexes

•th•!• CLINICAL GUID� FOR ACUTE BLINDNESS IN CATS

Affected Visual

Diagnosis

Clinical Signs

Pathway

Etiology

Retinal detach-

Acute blindness, Neurosensory retina

Systemic hyperten-
ment
hemorrhage
sion, intraocular

Intracranial

Normal eyes,

Optic chiasm

Pituitary masses,
diseases
acute blindness

± paranasal masses,

±PLR"

meningiomas,
lymphosarcoma

Central blindness Acute blindness, Optic tracts, occipital Cardiac arrest during
normal PLR
cortex
anesthesia, seizures,
severe head trauma

Slow vision loss

Progressive loss

Relrobulba.r visual

Hydrocephalus, CNS
ofvision/PLR
tracts
neoplasia

"Pupillruy light-induced reflexes

WOUND MANAGEMENT

1701

OPTIC NEURITIS
f-tmction; complete retinal and optic nerve
degeneration becomes apparent ophthal

Optic neuritis may be divided into papillitis
moscopically tJu·oughout several weeks.

(an inflamed optic nerve head visible with

There is no effective treatment.

an ophthalrnoscope) and retrobulbar optic

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newitis, which includes mydriasis, absence
of pupillary reflexes, and blindness without

RETINAL DETACHMENT
any ophthalrnoscopic abnormalities. Flash

Retinal detachment is being diagnosed more
electroretinography, combined with visual
commonly and is an important cause of
evoked potentials, and fluorescein angiogravision loss ( either Ul1ilateral or bilateral). It phy may be used to confirm optic neuritis.

is an important postoperative complication

A CBC, blood chemistry profile, neurologic
of cataract and lens surgery. Once retinal
examination, radiology, and vitreous and
detachment is detected, immediate medical

CSF analyses may be indicated.

and/or surgical treatment can reduce the

Papillitis is common in 1) granulomatous
resultant retinal degeneration and facilitate
meningoencephalitis in dogs; 2) systemic
restoration of vision. Contributing factors
viral, bacterial, and fungal infections in
include breed ( eg, Shili Tzu with vitreal
dogs, cats, horses, and cattle; and 3) trauma.

syneresis), previous cataract or lens

It appears as a swollen optic nerve head
removal, trauma ( dogs, horses, and cats),
with blurred margins, variable hemorsystemic hypertension ( cats and dogs), and rhages, and exudates. Peripapillary retinitis
systemic mycoses (dogs and cats). History,
is often present and appears as a translucent complete ophthalmic and systemic to opaque retina adjacent to the optic disk.

examinations, CBC, blood chemistry

Therapy is directed at the underlying
profile, and other diagnostic tests are
systemic disease. Systemic c01ticosteroids
important to deterrnine the w1derlying
may be used for the optic newitis. A positive cause. Ophthal.moscopy, B-scan ultrasonogresponse includes return of the pupillary raphy, electroretinography, and blood
reflexes and norrnal pupil size in several
pressure measurement are important
days, followed by vision a few days later.

diagnostic tests for retinal detachment.

Exudative nonrhegmatogenous retinal

SUDDEN ACQUIRED RETINAL
detachments may resolve with resolution of

DEGENERATION (SARO)

the inflammatory or hemorrhagic intra- and
subretinal exudates. Some retinal degenera

SARO occurs in dogs. Clinical findings
tion usually occurs, but vision may return.

include acute loss of vision (often occwTing

Retinal detachments secondar.y to Collie
throughout several days), widely dilated
eye anomaly ( see p 502) may be treated
and poorly responsive to nonresponsive
successfully by diode laser photocoagulapupils, and a norrnal-appearing ocular tion of the swTow1ding norrnal retina. Repair
fund us. Dogs affected most often are
of rhegmatogenous retinal detaclunents,
middle-aged and sometin1es have liver
characterized by retinal breaks (holes and
disease and hyperadrenocorticism with
tears), may be attempted using vitreoretinal
clinical signs of weight gain, polyuria,
techniques that are routine in people,
polydipsia, and polyphagia Electroretinogincluding intraocular gases, silicone oil, raphy indicates loss of outer retinal
scleral buckling, and laser or c1yoretinopexy.

WOUND MANAGEMENT

WoU11d healing is the restoration of the

Wounds may be classified as clean,
normal anatomic continuity to a disrupted
contaminated, or infected. Clean wounds
area of tissue. An understanding of the
are those created U11der aseptic conditions,
norrnal process of wotmd healing is
eg, surgical incisions. The nun1ber of
essential to make sound decisions in the
bacteria present can deterrnine the
management of wotmds. Correctly using the difference between contaminated and principles of wound management helps
infected wounds. As a guideline, > 1 ()-5
avoid premature wound closure and its
bacteria per gram of tissue is considered
potential complications.

adequate to cause infection. The level of

1702

WOUND MANAGEMENT
contamination, blood supply, and the cause

Migrating capillaries deliver a blood
of the wound all contribute to development
supply to the wound. 1l1e center of the
of the necessary conditions for infection,
wound is an area of low oxygen tension that
and each case must be assessed individually. attracts capillaries following the oxygen gradient. Because of the need for oxygen,

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GENERAL PRINCIPLES OF
fibroblast activity depends on the rate of

WOUND HEALING
capillary development. As capillaries and
fibroblasts proliferate, granulation tissue

Although there are many types of wounds,
is produced. Because of the extensive
most undergo similar stages in healing that
capillary invasion, granulation tissue is both
are mediated by cytokines and other chemovery friable and resistant to infection.

tactic factors within the tissue. The duration

Epithelial cell migration begins within
of each stage varies with the wound type,
hours of the initial wound. Basal epithelial
management, microbiologic, and other
cells flatten and migrate across the open
physiologic factors. There are three major
wound. The epithelial cells may slide across
stages of wound healing after a full-thiclrness the defect in small groups, or "leapfrog"

skin wotmd.

across one another to cover the defect.

Inflammation is the first stage of wound

Migrating epithelial cells secrete mediators,
healing. It can be divided into several
such as transforming growth factors ex and
phases, resulting in the control of bleeding

[3, which enhance wound closure. Although
and the resolution of infection. During the
epithelial cells migrate in random direcinitial phase, vasoconstriction occurs immetions, migration stops when contact is made diately to control hemon-hage, followed
with other epithelial cells on all sides (ie,
within minutes by vasodilation. During the
contact inhibition). Epithelial cells migrate
second phase, cells adhere to the vascular
across the open wound and can cover a
endotheliw11. Within 30 min, leukocytes
properly closed surgical incision within 48
migrate through the vascular basement
hr. In an open wound, epithelial cells must
membrane into the newly created wound.

have a healthy bed of granulation tissue to

Initially, neutrophils predominate (as in the
cross. Epithelialization is retarded in a
peripheral blood); later, the neutrophils die
desiccated wound.

off and monocytes become the predomi

Remodeling is the final stage of wound
nant cell type in the wotmd. Debridement is
healing. During this period, the newly laid
the next phase of wound healing. Although
collagen fibers and fibroblasts reorganize
neutrophils phagocytose bacteria,
along lines of tension. Fibers in a nonfuncmonocytes, rather than neutrophils, are tional orientation are replaced by functional
considered essential for wound healing.

fibers. This process allows wound strength

After migration out of the blood vessels,
to increase slowly over a long period ( as long
monocytes are considered macrophages,
as 2 yr). Most wounds remain 15%--200Ai
which then phagocytose necrotic debris.

weaker than the original tissue. However, the

Macrophages also attract mesenchymal
urinary bladder and bone regain I OOOA, of their
cells by an undefmed mechanism. Finally,
miginal strength after wounding and repair.

mononuclear cells coalesoe to form
multinucleated giant cells in chronic

INITIAL WOUND MANAGEMENT
inflammation. Lymphocytes may also be
present in the wound and contribute to the

The fu'st step in wound management is
inununologic response to foreign debris.

assessment of the overall stability of the

Proliferation is the second stage of
animal. Obvious open wounds can detract
wound healing. It consists offibroblast,
attention from more subtle but potentially
capillary, and epithelial proliferation
life-threatening problems. After initial
phases. During the proliferation stage,
assessment, the aninlal should be stabilized.

mesenchymal cells transform into

First aid for the wound should be perfom1ed
fibroblasts, which lay fibrin strands to act
as soon as safely possible. Active bleeding
as a.framework for cellular migration. In a
can be controlled with direct pressure. A
healthy wound, fibroblasts begin to appear
pneumatic cuff, instead of a tourniquet,

--3 days after the initial injury. These
should be used in cases of severe arterial
fibroblasts initially secrete ground
bleeding; the cuff should be inflated until
substance and later collagen. The early
hemon-hage is controlled. Use of a cuff
collagen secretion results in an initial rapid
avoids neurovascular complications that
increase in wound strength, which
can be associated with narrow tourniquets.

continues to increase more slowly as the

Treatment for any local wound should be
collagen fibers reorganize according to
guided by the fundamentals of debridement,
the stress on the wound.

infection or inflammation control, and

WOUND MANAGEMENT

1703
moisture balance. The wound must be
protected from further contamination or
trauma by covering it with a ste1ile, lint-free
dressing. The delay between examination
and definitive deb1idement should be
minimized to decrease bacte1ial contan1ina

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tion. If the wound is infected, a sample
should be collected for cul tme and
sensitivity testing. Antibiotic therapy should
be instituted in all cases of dirty, infected, or
puncture wounds. A broad-spectrum
bactericidal antibiotic, eg, a first-generation
cephalosporin, is generally reconunended
pending culture results. Analgesia is also
indicated for pain relief.

Thermal burn injury in a dog. Courtesy of Dr.

Kevin Winkler.

Wound Lavage: Irrigation of the wound
washes away both visible and microscopic
debris. This reduces the bacterial load in
the tissue, which helps decrease wound
complications. Assun1ing the solution is
nontoxic, the most important factor in
wound lavage is use of large volumes to
facilitate removal of debris. The recommended lavage is a moderate pressure system using a 35-mL syringe and a

19-gauge needle that delivers lavage fluid
at 8 lb/sq in. The use of antibiotics in the
lavage fluid is controversial.

The ideal lavage fluid would be antiseptic and nontoxic to the healing tissues.

Although isotonic saline is not antiseptic, it
is the least toxic to healing tissue. Smgical

Thermal burn injury after surgical debridescrub agents should not be used because ment in a dog. Courtesy of Dr. Kevin Winkler.

the detergent component is damaging to
tissue. Dilute antiseptics can be used safely.

Chlorhexidine diacetate 0.05% has sustained performed mechanically (with wet-to-dry residual activity against a broad spectrum of dressings), enzymatically, or biologically bacteria while causing minimal tissue

(maggot therapy).

inflammation. However, gram-negative

After initial inspection, lavage, and
bacteria may become resistant to chlorhexdeb1idement, a decision must be made idine. Stronger solutions of chlorhexidine
whether to close the wound or to manage it
are toxic to healing tissue. Povidone-iodine
as an open wound. Considerations include

1 % is an effective antiseptic, but it has
the availability of skin for closure and the
minimal residual activity and may be
level of contanlination or infection. If the
inactivated by plll"ulent debris. (See a/,so wound is left open, it should be managed

ANTISEPTICS AND DISINF"ECI"ANTS, p 2738.)

for optimal healing.

Debridement: After wound preparation

Wound Closure: Although primary
and hair removal, debridement can be
closure is the sinlplest method of wound
performed. Skin and local tissue viability
management, it should be used only in
should be assessed. Skin that is blue-black,
appropriate situations to avoid wound
leathery, thin, or white is associated with
complications. Wounds may be closed with
nonviability. Necrotic tissue should be
suture, staples, or cyanoacrylate. Clean
sharply excised. The debridement may be
wounds that are properly debrided usually
done in layers or as one complete section of
heal without complication. With a primary
tissue. Tissues that have questionable
closure, the layers should be individually
viability or are associated with essential
closed to minin1ize "dead space" that might structmes such as nemovascular bundles
contribute to seroma formation. The types
should be treated conservatively. Staged
of suture and suture patterns used depend
debridement may be indicated. In addition
on the size and location of the wound and
to sharp dissection, debridement may be
on the size of the animal.

1704

WOUND MANAGEMENT

Primary closure may not be appropriate
dressings is available. Alginate dressings a.re
for a grossly contaminated or infected
commonly used in the exudative wound to
wound. Therefore, if closure is a suitable
stimulate granulation tissue. Hydrogels a.re
goal, it may be delayed until the contaminaused to maintain moisture levels in drier tion or infection is controlled. The wound
wounds. Foam dressings may be used to
can be managed short-term as an open
absorb excessive exudate or protect

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wound until it appears healthy. At that time,
granulation beds. These newer dressings
the wound can be safely closed with
are changed only every 2-5 clays.

minimal risk of complications. The time
between initial deb1idement and final

Sugar Dressings: Sugar has been used
closure vary according to the degree of
as an inexpensive wound dressing for more
contamination or infection. Minimally
than three centuries to control odor and
contaminated wounds may be closed after
infection. The use of sugar is based on its

24-72 hr. Longer periods may be required
high osmolality drawing fluid out of the
for heavily infected wounds.

wound and inhibiting the growth of

Wounds that a.re closed >5 days after
bacteria. The use of sugar also aids in
the initial wounding a.re considered to be
the debridement of necrotic tissue while
secondary closure. This implies that
preserving viable tissue. Granulated sugar
granulation tissue has begun to fom1 in
is placed into the wound cavity in a layer
the wound before closure.

1-cm thick and covered with a thick
dressing to absorb fluid drawn from the

Open Wound Management: When a
wound. The sugar dressing should be
wound cannot or should not be closed, open changed once daily or more frequently wound management (ie, second-intention
whenever "strike-through" is seen on the
healing) may be appropriate. Such wounds
bandage. During the bandage change, the
include those in which there has been a loss
wound should be liberally lavaged with
of skin that makes closure in1possible or
wann saline or tap water. Sugar dressings
those that a.re too grossly infected to close.

may be used until granulation tissue is seen.

Longitudinal degloving i.Itjuries of the

Once all infection is resolved, the wound
extremities a.re especially amenable to open
may be closed or allowed to epithelialize.

wound management. Open wound

Because a large volume of fluid can be
management enables progressive deb1ideremoved from the wound, the animal's ment procedures and does not require
hemodynamic and hydration status must
specialized equipment ( such as may be
be monitored and treated accordingly.

needed with skin grafting). However, it

Hypovolemia and low colloid osmotic
increases cost, prolongs time for healing,
pressure a.re complications that may be
and may create complications from wound
associated with this therapy.

contracture.

Honey Dressings: Honey has also

Open wound management is based on
been used for wound dressings over the
repeated bandaging and debridement as
centuries. Honey's beneficial effects a.re
needed until the wound heals. Traditional
thought to be a result of hydrogen peroxide
therapy calls for wet-to-dry dressings
production from activity of the glucose
initially. The initial wide meshed gauze
oxidase enzyme. The low pH of honey also
dressings help with mechanical debridemay accelerate healing. Honey used for ment at every bandage change. Until a
wound healing must be unpasteurized, and
granulation bed f01ms, the bandage should
tl1e source of the honey appears to be a
be changed at least once daily. In the early
factor in its effectiveness. Manuka honey
stages of healing, the bandage may need to
may be the best option for wound ca.re. The
be changed as often as twice daily. After
contact layer wound dressings should be
granulation tissue develops, the bandage
soaked in honey before application. The
should be changed to a dry, nonstick
bandage should be changed daily or more
dressing so the granulation bed is not
frequently as needed.

disrupted. Both the granulation bed and the
early epithelium a.re easily damaged, and

DRAINS
disruption of the granulation bed delays
wound healing.

Drains a.re used to direct fluid out of a

With the concept of moist wound healing,
wound or body cavity. Passive drainage
bandaging is combined with autolytic
techniques require gravity or capillary
debridement to promote wound healing.

action to draw fluid from the wound or

The use of moist wound dressings keeps
cavity. Penrose drains a.re soft, flat,
white cells healthier, allowing them to aid
commonly used passive drains made from
in the deb1idement process. A variety of
latex. These drains must be placed in

WOUND MANAGEMENT

1705
gravity-dependent locations to ensure
tissue bed by keeping it too moist. Newer
proper function. A firmer drain can be
bandage materials may be in1pregnated with
constructed from a red rubber or silicone
various materials, such as silver, to help
tube. Active drains require some type of
control infection.

negative pressure to pull fluid from the

The secondary layer of a bandage absorbs

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wound. Red rubber or silicone drains can be
tissue fluid, pads the wound, and supports or
used with a closed system, and low-pressure inlmobilizes the limb. This layer is frequently suction maintained with the intennittent
composed of cast padding or roll cotton. The
use of low-pressure pumps or handheld
tertiary layer functions to hold the primary
rechargeable devices. Negative-pressure
and secondary layers in place, provide
wound therapy is based on this theory to
pressure, and keep the inner layers protected
remove purulent debris and speed closw·e
from tl1e environment. This layer is
of an open wow1d. The use of active,
composed of adhesive tape or elastic wraps.

closed-drain systems decreases the
likelihood of ascending infection that can

SURGICAL TECHNIQUES
be associated with passive drains. Drains
should be left in place until the draining

Advancement flaps can be used to move
fluid decreases in quantity and no longer
skin and relieve tension. The sin1plest type
appears purulent. The fluid can be
of advancement flap involves sliding skin to
evaluated by cytologic examination.

cover an adjacent defect. These flaps are
elevated without regard to their vascular

BANDAGES
supply. Flap survival depends on the subdermal vascular plexus from the flap base and The goals of bandaging include limiting
revasculaiization from tl1e recipient bed.

hemorrhage, immobilizing the area, prevent

Witl1 subdennal plexus flaps, the vascular
ing further trauma or conta.Jnination of the
supply is affected by the width of the flap
wound, preventing wound desiccation,
base. A high length/width ratio decreases
absorbing exudate, controlling infection,
the likelillood of survival, because blood
and aiding in mechanical debridement of
supply will not reach the distal end of the
the wound. When constructing bandages,
flap. Any flap placed in tension carries a
several principles must be followed to avoid
high risk of failure.

complications. The bandages should be

The basic advancement flap technique is
sufficiently padded, applied evenly and
known as the single pedicle advancement
snugly, composed of three layers (primary,
flap. Two slightly divergent incisions are
secondary, and tertiary), and placed to avoid made perpendicular to the defect. The traumatizing the newly fonned granulation
tissue is undennined, advanced, and
tissue or epitheliun1.

sutured to close the original defect. For

The first or primary layer directly
larger wounds, two single pedicle flaps are
contacts the wound to allow tissue fluid to
safer than one large flap. Two advancement
pass tlrrough to the secondary layer. The
flaps are combined to form the "H" plasty.

first layer may be adherent or nonadherent.

There are several other well-described flap

A nonadherent bandage is usually a fine
techniques, including the bipedicle advancemesh or foam, nonstick material and is ment flap and the "V-Y'' advancement flap.

indicated when a healthy granulation bed

In each of these techniques, the coverage
has developed. This layer prevents tissue
depends on stretching the skin over the
desiccation and causes minimal trauma.

defect. For this reason, tile use of these

An adherent bandage uses a wide mesh
techniques may be limited by vascular
material that allows tissue and debris to
supply or the regional anatomy, such as
become incorporated into the bandage. This tile area around the eyelids.

debris is then removed with the bandage

Flaps designed to incorporate a direct
change. Adherent bandages are classified as
cutaneous artery are known as axial
dry to dry, wet to dry, or wet to wet based on
pattern flaps (arterial pedicle grafts). The
the composition of the primary layer.

flaps can be used to cover a large area of

Dry-to-dry bandages consist of dry gauze
tissue and carry along a new blood supply to
applied to the wound. The bandages are
ensure flap survival. Muscle-based pattern
painful to remove but enable excellent
flaps can also be used to reconstruct a body
tissue debridement. Wet-to-dry bandages
wall defect in addition to covering a loss of
are made with saline-moistened gauze
skin. The surviving area of axial pattern
placed directly on the wound. They are also
flaps is 50"A, greater than a corresponding
painful to remove but result in less tissue
subdennal plexus flap and therefore allows
desiccation than dry-to-dry bandages.

coverage of a Jai·ger ai·ea. Because axial

Wet-to-wet bandages tend to damage the
pattern flaps are based on arteries, they

1706

WOUND MANAGEMENT
must have consistent landmarks and do
skin graft, creating graft edema. Anastomonot cover all regions of the body. The best sis with recipient bed vessels (inosculation)

described of the axial pattern flaps is based
begins within 48--72 hr of surgery. The
on the caudal superficial epigastJic artery.

edema may worsen immediately after

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Based in the caudal aspect of the abdominal
inoscuJation, because ruterial supply is
wall, this flap can extend cranially to
established before venous rettu11. The
include mammary glands 2 through 5. Other
edema should resolve as norn1al blood flow
commonly used flaps include the thoracorettul1s to the flap by day 4-6 after surgery.

dorsal, omocervical, and deep circumflex

All skin flaps and grafts require a clean,
iliac artery flaps.

healthy recipient bed for survival. This is

Free skin grafts are used for cases with
especially inlportant for subdern1al plexus
massive tissue loss such as large burns or
flaps and free tissue transfers, because they
degloving i.rtjuries. The grafts are best used
do not contain a direct cutaneous arterial
as a split mesh. This allows drainage and
supply. The recipient bed must be free of
helps prevent seroma formation. Skin grafts
debris, infection, and necrotic tissue.

will not remain viable if laid over squamous

Although flaps may have well-described
epithelium, denuded bone, cartilage, or
anatomic markers, determining their
tendon. The grafts must have a healthy,
viability may not be as easy. The simplest,
vascularized bed. Initially, nutJition for the
but least accurate, methods to assess a flap's
flap is maintained because capillary action
viability are subjective measures, including
pulls semm into the dilated capillaries of the the assessment of color, wrumth, sensation, and bleeding. Purple color cannot be used
as a predictor of viability. Contused, purple
skin is often viable. Progression from deep
purple to black indicates necrosis. Skin
temperature may be affected by the state
of vasoclilation and is therefore not an
accurate method to assess viability. Viable
flaps may bleed from a cut suiface, as may
nonviable flaps that still have some arterial
function but poor or no venous retUJ11. After
a flap is moved, it may develop edema for
the first few days ui1til venous vascuJarization is completed. Newer techniques and medications being developed for woui1d
care include platelet-tich plasma, extJ·acorporeal shock wave therapy, stem cell therapy, microcurrent stimulation, and a
variety of growth factors. Their efficacy has
not yet been completely demonstrated.

Appearance of a free skin mesh graft 24 hr
after surgery. Courtesy of Dr. Kevin Winkler.

FACTORS THAT INTERFERE WITH

WOUND HEALING

Factors that interfere with wound healing
may be divided by source into physical,
endogenous, and exogenous categories.

Physical factors that affect wound
healing include temperature and mechanical forces. Temperattrre affects the tensile strength of wounds. Ideal conditions allow
woW1d healing to occur at 30°C. Decreasing
the temperature to l2°C results in a 200A, loss
of tensile wound strength. Mechanical
forces include pressure ai.1d sheer force.

Pressui·e can compromise blood flow in the
region, decreasing oxygen levels in the
tissue. Sheer forces result in tearing of the
vessels. Because adequate oxygen levels ru·e

Appearance of a free skin mesh graft 3 wk
required for appropriate woW1d healing,
after surgery. Courtesy of Dr. Kevin Winkler.

anything that interferes with blood flow will

WOUND MANAGEMENT

1707
slow wound healing. Low levels of oxygen
according to the same p1inciples, depending
interfere with protein synthesis and
on the extent of the iitjwy. Damage to
fibroblast activity, causing a delay in wound
underlying structures ( eg, muscles, tendons,
healing. Oxygen levels may also be
and blood vessels) must be resolved before

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compromised by other physical factors,
closure. If a laceration is grossly contamiincluding hypovolemia, the presence of nated witl1 debris, primary closw-e of the
devitalized tissue, hematomas, and
wound may not be indicated. Contaminated
excessively tight bandages.

wounds may be closed with drains or treated

Endogenous factors typically reflect the
as an open wound.

overall condition of the anin1al. Anemia may
inte1fere with wound healing by creating

Bite Wounds: Bite wounds are a major
low tissue oxygen levels. Nub.ition has a
cause of injuries, especially in free-ranging
significant overall effect on the body.

animals. Cat bites tend to be small,

Although the ideal nub.itional level for wound penetrating wow1ds that frequently become healing is unknown, hypoproteinemia delays
infected and must be treated as an abscess
wound healing when the total senun protein
with culture, debridement, antibiotics, and
content is <2 gtdL. Because wound healing is
drainage. Dog bites have a more varied
a function of protein synthesis, malnub.ition
presentation. Because of tl1e slashing nature
can alter the healing process. The addition
of dog bite iitjwies, the major tissue damage
of DL-methionine or cysteine ( an important
is usually found beneath the surface of the
an1ino acid in wound repair) can reverse
wound. Although only small puncture marks
delayed wound healing. Uremia can interfere
or bruising may be evident on the surface,
with wound healing by slowing granulation
ribs may be broken or internal organs
tissue formation and inducing the synthesis
seriously dan1aged. The anin1al should be
of poor quality collagen. Obesity conb.ibutes
thoroughly exan1ined and stabilized before
to poor wound healing through decreased
definitive wound care is begun. The wow1d
blood supply and with poor suture holding
should be surgically extended as far as
in the subcutaneous fat layers.

necessary to allow a thorough exan1ination

Exogenous factors include any exterand detem1ination of its extent before a nal chemical tl1at alters wound healing.

decision on the repair can be made. After a

Cortisone is commonly implicated in wound proper assessment, debridement can be complications. Corticosteroids markedly
perfom1ed. Unless en bloc debridement is
inhibit capillary budding, fibroblast
perfmmed, complete wound closure is
proliferation, and rate of epithelialization.

usually not recommended because the sites

Similar to cortisone, vitan1in E adversely
are considered contan1inated. Closure can
affects wound healing by slowing collagen
be accomplished with drains, as a delayed
production. Vitan1in C is required for
closw·e, or by second intention depending·
hydroxylation of proline and lysine. Zinc
on the extent of the injury.

is required for epithelial and fibroblastic
proliferation; however, excessive zinc delays Degloving Injuries: Degloving iitjuries wound healing by inhibiting macrophage
result in loss of skin and a variable a.mount
function. Other factors that may slow
of deeper tissue. These injuries are a result
wound healing include radiation, alkylating
of a shear force on the skin. Sow-ces include
agents (eg, cyclophosphamide, melphalan),
fan belt iitjmies and loss of tissue dw-ing an
inapprop1iate concentrations of antiseptics,
accident with a motor vehicle. With a
and NSAIDs. Although most NSAIDs a.re
physiologic degloving injury, the skin is still
thought to be safe in wound healing, it has
present but completely freed from the
been suggested that agents selective for
tmderlying fascia lf the injury results in a

COX-2 inhibition may slow fracture healing.

loss of blood supply to the skin, necrosis
may develop later. In an anatomic degloving

MANAGEMENT OF SPECIFIC
injury, the skin is tom off the body.

WOUNDS

Degloving iitjuries frequently require
marked and repeated debridement.

Lacerations: Uncomplicated simple

Differentiating viable and nonviable tissue
lacerations are usually managed by complete may be a problem in the early w0tmd closme if they are not grossly contan1inated.

debridement process. An attempt should be

The wound should be thoroughly lavaged
made to salvage tissue in which viability is
and debrided as necessary before closure.

questionable. Subsequent debridement can

If tension is present on the wound edges, it
be used to remove any necrotic tissue. With
should be relieved by tension-relieving
orthopedic iitjuries that typically accompany
suture techniques, sliding tissue flaps, or
degloving iitjuries, final stabilization may be
grafts. Deep lacerations may be treated
delayed until local infection is under control.

1708

WOUND MANAGEMENT

Gunshot Injuries: In gunshot injuries,
fracture so that the soft tissues may be
most of the damage is not visible. As the
appropriately managed. Gunshot wounds
projectile penetrates, it drags skin, hair,
to the abdomen are an indication for
and dirt through the wound. If the
exploratory celiotomy. Gunshot wounds to
projectile exits the body, the exit wound
the thorax may require a thoracotomy if

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is larger than the entrance wound. The
hemotThage or pneurnothorax cannot be
amount of damage caused by the projectile
conservatively managed.

is a function of its shape, aerodynamic
stability, mass, and velocity. High-velocity

Pressure Wounds: Pressure wounds
projectiles tend to produce more dan1age
or decubital ulcers develop as a result
as a result of impact-induced shock waves
of pressure-induced necrosis. Pressure
that move through the tissue. The shock
wounds can be extremely difficult to treat
waves create blunt force trauma that
and are best prevented. Preventive
results in tissue and vascular dan1age.

measures include changing the position

Gunshot wounds are always considered
of the animal frequently, maintaining
to be contanlinated, and primary closure
adequate nutrition and cleanliness, and
is generally not recommended. These
providing a sufficiently padded bed.

wounds should be managed as open

Factors that predispose to pressure
wounds or by delayed primary closure.

wounds include paraplegia, tetraplegia,

After initial assessment and stabilization
improper coaptation, and immobility.

of the animal, the wound may be explored

Mild ulcers may be managed with
to evaluate the extent of damage and to
debridement and bandaging to prevent
determine a plan for repair. If the projectile further trauma to the affected site. More caused a fracture, the method of repair
severe wounds require extensive surgical
depends on the location and type of
management. After debridement and
fracture. External fixation, bone plates,
development of a granulation bed, an
and intramedullary nails are common
advancement flap or pedicle graft may
choices for rigid stabilization of the
be required for closure.

EQUINE EMERGENCY MEDICINE

Equine emergencies can be challenging for
physically not possible. Replacement fluids
veterinary practitioners and emotionally
are required when excessive losses have
charged for owners. There is also the
been incu1Ted or ongoing fluid losses
inherent possibility of injtu;' to the owner
anticipated.

and veterinarian because of the sheer size of

Design of a fluid therapy regin1en requires
the aninlal and the "fight or flight" reflexes of consideration of the volume required, the an injured horse. Problems can be reduced
type of fluids needed, and the route and rate
by educating owners about emergency
of adnlinistration. The volun1e to be
preparedness and first aid procedures. The
adnlinistered over 24 hr can be calculated
most common types of equine emergencies
using the following formula: volume to
are abdominal pain (colic), trauma,
adnlinister (L) = maintenance rate (60 mU
lacerations, and acutely ill foals.

kg/day)+ estimated fluid deficit (body wt

[kg] x estimate of dehydration)+ estimate

EQUINE EMERGENCY
of ongoing losses. Maintenance fluid
requirements are -1 Uhr for adult horses

PROCEDURES

( -450 kg) but are much lower if the aninlal
is not eating. Dehydration can be estimated

Emergency Fluid Therapy
by using clinical and laboratory parameters

Conditions that may require emergency

(see TABLE 10). These numbers should be fluid replacement include iajuries with
considered in relation to the horse's age and
concUtTent blood loss, exhaustion, acute
clinical condition and are only an estin1ate
rhabdomyolysis, hyperthenn.ia, and
of the deficit. For exan1ple, a nervous horse
circulatory shock secondary to systemic
may have a transiently high heart rate in
illness. Fluids may be needed for mainteresponse to excitement and an increased nance purposes when oral intake is

PCV because of splenic contraction.

EQUINE EMERGENCY MEDICINE

1709

PHYSICAL AND LABORATORY PARAMETERS FOR ESTIMATION

OF DEHYDRATION IN THE HORSE

Capillary

Plasma Skin

Estimated Heart Refill

Total

Creati- Elas-

Mucous

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Dehy-

Rate

Time

PCV Protein nine
ticity Sunken Membrane
dration

(bpm) (sec)

(%) (g/dL) (mg/dL) (sec) Eyes

Moisture/Color

6%

40-60

2

40

7

1.5-2

2

+!-

Moist/Pink

8%

61-80

3

45

7.5

2-3

2-3

+!-

Tacky/Pink

10%

81-100

4

50

8

3--4

3--4

+

D1y/Red

12%

>100

>4

>50

>8

>4

>4

++

Dry/Cyanotic

Ongoing losses are difficult to estimate,
are most commonly used for replacement
because losses from the GI tract are hard to
fluid therapy, whereas colloids are more
measure. The equine GI tract secretes and
often reserved for resuscitation pwvoses.

resorbs the equivalent of the extracellular

(See also FLUID THERAPY, p 1675.)

fluid volume (-30%of body wt) on a daily

Two general types of crystalloids are
basis. If small-intestinal ileus or obstruction
available: balanced electrolyte solutions
is present, the amount of gast1ic reflux

(BES), which are solutions of electrolytes in
obtained can be easily quantitated to gauge
concentrations similar to those in plasma,
losses. If the large intestine is not resorbing
and saline solutions, which contain only
water ( eg, diarrhea), fluid losses can be
sodium chloride. Although considered a
significant but difficult Lo measure. With
crystalloid, dextrose solutions are rarely
severe diarrhea, -500;6 of the extracellular
used alone, and are usually added as a
fluids can be I ost daily.

supplement to a BES when indicated by ilie

The formula to calculate volume of fluid
needs of the individual horse. The decision
to administer provides only a crude
to choose BES or saline can be based on a
estimate of needs; volumes administered
serum chemistry profile. Saline is chosen if
should be adjusted based on responses to
the sodium concentration is <125 rnEq/1, if
treatment, such as heart rate, pulse quality,
iliere is a metabolic alkalosis, or if ilie potascapillary refill time, urine production, PCV, sium is >5.9 mEq/L ( eg, acute hyperkalemic
serum total protein, creatinine, and lactate.

periodic paralysis, uroabdomen). ln most

Reassessment is required to adjust the daily
emergent cases, however, a BES is used.

fluid requirements for any horse receiving

The addition of colloids to a fluid therapy
supplemental fluids, and the timing should
regimen serves two purposes: it prevents
be dictated by the horse's clinical condition.

edema formation caused by hypoproteine

In horses in severe shock, cardiovascular
mia, and it maintains the intravascular fluid
parameters may need to be monitored
volume. Plasma products iliat contain
continually (eg, every 15 min) until
an ti.bodies to treat or prevent a variety
improvement is noted. In horses with severe of conditions (including endotoxemia, ongoing fluid losses ( eg, diarrhea, anterior

Rlwdococcus equi pneumonia, West Nile
enteritis), cardiovascular parameters
virus infection, clostridial diseases, and
should be reassessed every 4 hr and
snake envenomation) are also available.

laboratory paran1eters measured as

Colloid solutions are available in natural
frequently as 4 times a day until ilie horse
or synthetic forms. Natural colloids are
stabilizes.

plasma, serwn products, or albtuni.n. In

After determination of volwne required,
general, fresh or fresh frozen plasma is
the type of fluid to be administered should
selected when an increase in colloid
be selected. Fluid choices include
oncotic pressure is needed, and coagulacrystalloids (fluids containing substances tion factors or specific anticoagulants such
that freely cross the capillary membrane)

as antiilirombin III are required. Albwnin
and colloids (fluids retained in ilie vascular
solutions are not commonly administered
space for a certain number of hours because to horses, because the intravascular of their larger molecular size). Crystalloids
half-life of albumin in diseases witl1

1710

EQUINE EMERGENCY MEDICINE
compromised vascular permeability is
administration rates include cannulating
short. They also do not have the added
both jugular veins or using a pressure bag
benefits of whole plasma. Synthetic
system or peristaltic pwnp. Complications
colloids include dextran and hydroxyof pe1istaltic pwnps are endothelial damage VetBooks.ir
ethyl starch. The synthetic colloid most
and an increased 1isk of venous tl1rombosis.

commonly administered to horses is

An alternative route of fluid administrahydroxyethyl starch (hetastarch). It is used tion is use of an indwelling nasogastric tube.

to increase plasma oncotic pressure, and

Case selection is key, and horses that are in
its effect is best evaluated by clinical
shock, are >8% dehydrated, or have positive
response (decreased edema) or increased
net gastric reflux are not candidates for oral
oncotic pressure (measured by colloid
fluids. Equine electrolyte solutions are
osmometry). A refractometer that
prefen-ed, or a homemade mixture can be
measures total protein cannot be used
formulated using 5.27 g sodiun1 chloride,
to monitor the effect of synthetic colloid

0.37 g potassiwn chloride, and 3. 78 g
administration.

bicarbonate per liter of water. The daily

The goal of fluid therapy for treatment of
fluid rate is divided into boluses and
shock is to rapidly expand circulating blood
administered using a bilge pump. The
volwne to improve tissue pe1fusion and
horse should be checked for reflux before
oxygen delive1y. Isotonic crystalloids
administration. Volw11es <8 L every 2-4 hr
should be administered at a dosage of up to
are typically well accepted. lf a smaller

60-80 mUkg in the first hour ( equal to the
gauge feeding tube is in place, a continuous
circulating blood volwne) for maximal
delive1y system from a nonsterile IV set and
benefit. This fluid rate, the "shock dose,"

fluid bags or a carboy can be used, and the
should be given in boluses of 20 mllkg
rate should be determined in a manner

(approximately 10 Lat a time), and the
similar to that of an IV infusion rate.

horse should be reassessed between each
bolus to determine whether additional
boluses are needed. Because of the large

Nasogastric Intubation
volwnes of BES required, hypertonic fluids

Nasogastric intubation is an essential and
or colloids may be given first to immediately possibly life-saving procedure performed support the circulation until the shock dose
routinely in cases of equine colic to
of c1ystalloids can be administered. At a
decompress the stomach and to provide
dosage of 2-4 mllkg, hypertonic saline
therapy. After the horse is adequately

(7.5%) can rapidly expand the circulating
restrained, the nasogastric tube is passed
volwne by redistributing extravascular
into the ventral meatus, using the thwnb to
fluids into the vascular space. Because of
keep the tube directed con-ectly. lf a hard
redistribution, hypertonic solutions have a
structure is encountered ( eg, the ethmoid or
short duration of effect ( -45 min) in horses.

nasal turbinates) and the tube is difficult to

Colloid solutions can be used for a more
pass, the tube should be redirected more
sustained effect. Hydroxyethyl starch has
ventrally. Once the pharynx is reached, a
been reported to increased oncotic pressure soft resistance is felt when the tube contacts for up to 24--36 hr. However, dosages of
the larynx and/or esophageal opening. The
colloids >10 mllkg/day have caused
horse's head is flexed at the poll, and the
coagulopathies. For resuscitation, a
tube can be turned 180° so that the
combination of hypertonic saline ( 4 mVkg)

curvature of the tube is directed dorsally
and hetastarch ( 4 mllkg) may have the most toward the esophagus. Swallowing is beneficial and sustained effects.

stimulated with gentle pressure against the

The flow rate of fluids through an
esophageal opening or by blowing small
administration set is directly proportional
puffs of air into the tube, and tile tube is
to the diameter of the line and inversely
tllen passed into the esophagus by
proportional to the viscosity of the fluid and
coordinating with the swallow reflex.

the length of the infusion set. Polytetrafluor

Once the tube is in the esophagus, mouth
oethylene or polyw·ethane 14--gauge
suction on the tube will be met with
catheters are routinely used in horses. A
negative resistance. The tube may also be
rate of 7 llhr can be achieved when fluids
palpated in the proper position dorsal to the
are >2 feet above tl1ejugular vein, and faster larynx or on the left side of tlle neck above rates can be achieved through gravity flow
thejugular vein. lf the tube is in tlle trachea,
if the fluid bags are raised even higher. For
shaking the trachea will result in a "rattle."

more rapid flow, 10- or 12-gauge catheters
lf the horse coughs, or if air is noted when
with large-bore connection sets can be
suction is applied by mouth, tile tube should
used, but 10-gauge catheters are more
be witlldrawn into tlle pharynx and the
thrombogenic. Other ways to increase fluid
procedure repeated until tlle tube is

EQUINE EMERGENCY MEDICINE

1711
correctly positioned. Once the tube is

Because gastric outflow obstruction is rare
confirmed in the esophagus, intermittently
in horses, pH is usually not measured.

blowing into the tube will help to dilate the

Response to gastric decompression
esophagus and facilitate insertion into the
should be noted. Horses with functional

VetBooks.ir
stomach. The tube is advanced into the
ileus show signs of relief, and the heart rate
stomach until level with the twelfth rib. If
may decrease in response to decompresdifficulty is encountered in passing the tube sion. Horses with a mechanical obstruction
through the cardia, 60 mL of mepivicaine
usually remain in pain, although some do
may be injected into the tube and followed
respond. The rest of the physical examinawith air or water.

tion of horses with reflux should focus on

Once the tube is in place, if there is no
determining whether functional or mechanispontaneous reflux, the stomach should cal ileus is present. The amount of reflux
be lavaged. It should not be assun1ed that
obtained should be noted after each
any excess fluid in the stomach will drain
decompression, and the volun1e of fluids
spontaneously. Medications should never
given IV adjusted accordingly. Horses with
be administered by nasogastric tube
functional ileus generally need gastric
without checking first for net reflux. To do
decompression every 2--4 hr. The nasogasso, the tube is filled with -2 L of water using tric tube should be left in place only as long
a pump or funnel with gravity flow to
as required, because it can cause pharynestablish a siphon effect, the pump geal and laryngeal irritation. Esophageal
removed, and the end of the tube directed
rupture has been described in severe cases.

downward to verify the presence of gastric
contents. Subtracting the amount of water
pumped in from the amount of fluid

Abdominocentesis
obtained determines the "net" reflux.

Abdorninocentesis is important in the

Horses should be lavaged with at least 8 L of
evaluation of abdominal disease ( eg, weight
water to confirm lack of net reflux before
loss, colic, peritoneal effusions, or
any therapy is administered.

postoperative complications). Ultrasonog

Net nasogastric reflux is not normal.

raphy can be used to detem1ine the best

Occasionally, a small amount of reflux
location to obtain a fluid sample, which can

( < 1 L) is obtained if a horse has had an
be collected using an 18-gauge needle, a
indwelling nasogastric tube. In most horses
catheter, or a teat cannula through a stab
with colic, >2 L net reflux is abnonnal.

incision. Most commonly, the sample is

When reflux is obtained, the amount,
obtained just to the right of midline, caudal
character, and timing in relation to the onset to the descending pectoral muscle on the of colic should be noted, as well as any
dependent abdomen. This will prevent
clinical response to gastric decompression.

the site of the abdon1inocentesis froni

Typically, reflux accompanies smallinterfering with a surgical incision if an intestinal ileus, either functional or
exploratmy laparotomy is needed, and it
mechanical. Lesions of the proximal small
will also help to avoid the spleen. The body
intestine or pylorus produce large amounts
wall is much thicker off midline, and the
of reflux early in relation to the onset of
length of the instrwnent used to san1ple
colic. With lesions of the distal jejunum and
the fluid should be considered. A needle
ileum, there is initially no reflux, but
tap should be avoided with severe smallnasogastric reflux usually becomes intestinal distention to reduce the risk of
productive several hours after the onset of
bowel puncture and iatrogenic peritonitis.

colic. Occasionally, large-colon disorders

The fluid is collected using sterile technique
can be associated with net reflux if the
and placed in a tube with anticoagulant for
colonic distention exerts pressure on the
analysis and in a culture tube if peritonitis
duodenum as it courses over the base of
is suspected. It is useful to shake out the
the cecun1. Foul-smelling, fennented, or

EDTA from the tube before sampling,
copious bloody reflux is associated with
because EDTA will falsely increase the total
anterior enteritis and should be treated as a
protein.

biohazard because of the association of this

Normal values for abdominocentesis
disease with clostridial and Salmonella spp include a total protein <2.5 g/dL and WBC
organisms. With mechanical obstruction,
counts of <5,000 cells/µL. Repeated
including strangulating lesions and ileal
abdominocentesis will not significantly alter
impactions, the reflux is usually composed
these values above reference ranges. On
of fresh feed material and intestinal
cytology, neutrophils comprise most of the
secretions. Reflux originating from the
cells; the remainder are lymphocytes,
small intestine is alkaline, whereas reflux
macrophages, and peritoneal cells. With
composed of gastric secretions is acidic.

intestinal strangulation, protein increases in

1712

EQUINE EMERGENCY MEDICINE
the first 1-2 hr. After 3---4 hr of strangulation,
with bacterial infection ( eg, fever, depres

RBCs are present, and after �6 hr, WBCs
sion, anorexia, ileus, colic, endotoxemia).

increase gradually as intestinal necrosis

The WBC and total protein in the abdominoprogresses. Degenerate neutrophils will be centesis will be markedly increased. On
noted on cytology, and the gross appearance cytology, >9001<, of cells are neutrophils and VetBooks.ir
is serosanguinous. Peritoneal lactate is also
will appear degenerate. Free and phagocyincreased with intestinal ischemia (>4
tized bacteria are seen. A serum-pe1itoneal
mmol/L) or is found to increase over time if
glucose difference >50 mg/clL or a
serial abdominocenteses are performed.

peritoneal fluid pH <7.2 with a pe1itoneal

Enterocentesis sometimes occurs,
glucose <30 mg/clL is supportive of a
especially in cases of sand colic, and should
diagnosis of pe1itonitis.

be differentiated from intestinal rnpture.

With enterocentesis, cytology reveals plant
material, bacteria, and debris but few cells.

Trocarization

The horse's clinical condition is not

Trocarization is useful to decompress the
consistent with rupture, although in early
abdomen when abdominal compartment
rupture (-2-4 hr), clinical signs of
syndrome is suspected (increased intraendotoxemia ( eg, depression, tachycardia, abdominal pressure resulting in severe
congested mucous membranes, shock) may
abdominal distention, dyspnea, and
not be seen. Cytology of abdominal fluid
perfusion abnormalities). Trocarization is
compatible with intestinal rupture shows
perfmmed only for distention of the cecwn
a large nw11ber of toxic and degenerate
and large intestine, and never to decompress
neutrophils, in addition to bacterial
the small intestine or stomach. Thus, it is
organisms, plant material, and bacteria that
necessary to identify the segment of intestine
have been phagocytized by neutrophils.

involved before the procedure. In adult

Blood contamination that occurs during
horses, this is done by transrectal palpation
the procedure should be differentiated from
combined with transabclominal ultrasound.

internal hemorrhage or severely devitalized

Abdominal auscultation may note a "ping"

bowel. Blood from skin vessels or an
after percussion indicative of a gas-filled
abdominal vessel usually swirls in the
organ. In foals or small horses, radiographs
san1ple and spins down when centrifuged,
ancVor ultrasound can be used. The distended
leaving the san1ple clear. Fresh blood
segn1ent of large intestine must also be
contan1ination shows platelets, which are
against the body wall so it can be safely
not present in blood >12 hr old. If the spleen reached. The most common site for trocarizais accidentally punctured, centrifugation of tion is the upper right flank, just cranial to the
the sample reveals a PCV the san1e or higher greater trochanter at the location of the cecal than the peripheral PCV. In internal
base. Ultrasow1d is used to confim1 a
hemorrhage, the blood in the sample is
gas-filled structure at the chosen site, to
hemolyzed, there are no platelets, and
avoid other organs or large blood vessels.

erythrophagocytosis may be seen. When

In adult horses, a 14-gauge, 12.5-cm
centrifuged, the supernatant will remain
over-the-needle catheter is typically used,
reddish. Abdominal ultrasound will reveal
whereas in neonates, a 5-cm needle may
fluid swirling on the abdomen. If vascular
be adequate. The area is clipped, sterilely
compromise of the bowel occurs, hemolysis
prepared, and infiltrated with a local
of RBCs that leak from damaged capillaries
anesthetic. The catheter is inserted
will result in a serosanguineous fluid, with
aseptically and attached to a long
a reel supernatant after a spin.

extension set that is placed in a nonsterile

Abdominal surgery increases the total
cup of water to monitor progress. Gas
protein and WBCs in the abdominocentesis.

released will produce bubbles, and the

With a sterile peritonitis, the WBC cotmt will catheter may be repositioned as the bowel remain increased for up to 2 wk, and cell
decompresses. A successful trocarization
counts of 40,000 cells/clL have been reported may take >30 min to decompress the at 6 days after surgery. Neutrophils will
bowel. When removing the catheter, an
appear nondegenerate on cytology, and
antibiotic (usually -5 mL of gentamicin)

there are no bacteria The total protein
is infused as the catheter is withdrawn.

peaks at 6 g/dL 6 days after surgery and

Complications after trocaiization include
may remain increased for 1 mo. After an
pe1itonitis, hemorrhage, and a local
enterotomy, or resection and anastomosis,
subcutaneous abscess. The horse should be
degenerate neutrophils and occasional
observed for 48 hr for signs of peritonitis,
bacteria may be seen in the first 12-24 hr but including abdominal pain and fever. Peritonishould resolve in time. lf septic peritonitis is tis is confim1ed with abdominocentesis and present, clinical signs will be consistent
treated with systemic broad-spectrum

EQUINE EMERGENCY MEDICINE

1713
antibiotics until it is resolved. Hemorrhage is
synovial infections, and exertional
typically self-limiting, and local abscesses
rhabdomyolysis. Although many of these
can be drained percutaneously.

conditions cannot be treated in the field,
an accurate diagnosis and provision of

VetBooks.ir

Tracheostomy
appropriate emergency treatment are essen

Tracheostomy is used as an emergency
tial for the possibility of a successful
procedure for conditions resulting in acute
outcome.

upper airway obstruction ( eg, arytenoid
chondritis, snakebite). The incision site is

Fractures and Luxations
selected at the junction of the proximal and

A thorough physical examination is
middle third of the neck, above the "V"

warranted but may be complicated by the
formed by the paired stemomandibularis
severity of the i.rtjury and other factors ( eg,
muscles. If possible, the skin should be
pain, anxiety, exhaustion, dehydration,
clipped, aseptically prepared, and infiltrated owner/trainer anxiety). The goals of initial with a local anesthetic. In acute respiratory
coaptation of fractures are to relieve
distress, this may not be possible, and the
anxiety, prevent further i.rtjury, and allow for
procedure is performed without sterile
safe transportation for additional evaluation
preparation.

and possible treatment. Emergency

The incision (6--8 cm) is made on midline,
coaptation of unstable limbs is key and
through the skin and between the paired
should be perfonned before radiographic
stemothyrohyoideous muscles. The trachea
evaluation or transportation to a surgical
is exposed, and a transverse incision is
facility.

made between two tracheal rings, taking
care to avoid the tracheal cartilages. The

Initial Assessment: Fractures or
incision will extend to -300Ai of the
luxations should be suspected if a loud
circumference of the trachea. If the horse's
crack is heard, if there is acute, non-weighthead is elevated or extended, the tracheal bearing lameness, or if the limb has an
incision should be made caudal relative
to the skin incision, to avoid covering the
abnom1al angulation or is visibly unstable.

tracheostomy site when the head is lowered. The extent of the physical examination should be dictated by the situation, to avoid

AJ-type silicone tracheostomy tube may be
further i.rtjury to the horse or bystanders. If
used and secured in place to the mane with
the horse is recumbent, full assessment of
gauze. The cuff should not be inflated,
the limb should be completed before
unless the horse is to be ventilated, to
prevent tracheal necrosis. Alternatively, a
attempting to stand the horse. If the horse is
standing, examination of the limb should �e
self-retaining tube may be preferred because
of the tendency of J-tubes to fall out.

completed before attempting to move the
horse. With an unstable fracture, the limb

The tracheostomy tube should be
removed, cleaned, and replaced twice a
should be stabilized before any other
treatment.

day or more often if secretions occlude the
lumen. Petroleum jelly applied to the

Sedation or a twitch can be used to aid
restraint for the examination. For sedation,
surrounding skin will help to reduce skin
an az-agonist such as xylazine or detomidine
scalding. Complications are rare ( eg,
cartilage deformity, intraluminal granulacan be used. Because az-agonists often cause the horse to lean forward, which may
tion tissue, mucosa! structure) but can be
reduced by removing the tube as soon as
increase the weight on an ir\jured forelimb
possible. One method to determine when
or decrease the ability to manipulate the
the tube can be removed is to temporarily
limb, the minimal effective dose is preferred
occlude the lumen by hand and observe
to reduce ataxia. However, up to double the
whether the horse can breathe without it.

standard dose regin1en may be required to

After tube removal, the site is cleaned with
achieve effective sedation after maximal
saline twice daily and allowed to heal by
exercise or if the horse is excited. Butorphanol may be used for horses not well second intention. The trachea will
generally close in 10-14 days and heal
controlled by a2-agonists alone. Acepromacompletely in 3 wk.

zine should be reserved for euvolemic
horses because of its hypotensive effects. If
the horse is recun1bent and a serious i.rtjury

EQUINE TRAUMA AND FIRST AID
is suspected, general anesthesia can be
safely induced using sedation with xylazine

Common emergencies involving the
followed by induction with ketanline and
musculoskeletal system include fractures,
diazepam or tiletanline-zolazepam. Before
luxations, lacerations, puncture wounds,
sedation or anesthesia, the circulatory

1714

EQUINE EMERGENCY MEDICINE
system should be briefly assessed by
below and above the area of injury,
evaluating heart rate, mucous membrane
prevention of lateromedial and craniocaucolor, capillary refill time, and pulse quality.

dal motion, and never ending a splint in the

VetBooks.ir

A heart rate >80 bpm accompanied by a
middle of a long bone segment or at the end
delayed capillary refill time and poor
of a fracture line.

peripheral pulse quality indicate the need

Wounds should be carefully cleaned and
for IV fluid support. Laboratory detenninadebrided. A nonstick gauze bandage can be tion of biochemistry profile indices are
applied and held in place with confomung
becoming more commonly available in field
gauze. Cotton padding is applied to the
situations. lf available, parameters of
entire length of tl1e segment to be immobihydration and electrolyte balance are useful lized and held in place with gauze, followed
to dictate fluid volume and type.

by elastic bandage material. The bandage

For limb stabilization, it is useful to divide
should be snug, to avoid loosening with
the Jim bs into four levels, which help define
compression of the cotton material. Splints
the method of coaptation. Level 1 irtjuries
are then applied and held in place, ideally
involve the distal metacarpus/metatarsus
with fiberglass casting tape. This is
and phalanges and include the fetlock joint
paiticularly useful in stabilizing a luxation.

and extensor and flexor tendon irtjuries
lf casting tape is unavailable, heavy tape
located at the level of the metacarpus and

( duct tape or medical white tape) can be
metatarsus. Level 2 injuries involve the
used. The splints must be well padded to
mid-metacarpus to distal radius, the carpal
avoid the development of sores.

joint, and the mid- to proximal metatarsus.

Level 3 irtjuries involve tl1e mid- to proximal

Immobilization of Level 1 Injuries:

radius in the forelimb or the tarsus and tibia

Level 1 injuries include phalangeal fracin the hindlimb. Level 4 injmies are noted in tures, distal metacaipus and metatarsal
the forelimb proximal to and including the
fractures, sesamoid fractures, fetlock,
elbow joint, or in the hindlimb proxin1al to
pastern or coffin bone luxations, or
and including the stifle joint.

severance of one or more flexor tendons.

The presence of a fracture can be

Not included are fractures of tl1e coffin
detennined by instability, crepitus,
bone; tl1ey ai·e suppmted by the hoof
abnormal angulation, palpation of bone
capsule and do not require a splint.

fragments, or direct visualization of the

Although technically level 1 irtjuries,
fractured bone. Luxation should be
extensor tendon lacerations require a
suspected when there is abnormal
different mode of splint application and
lateral-to-medial motion at the level of a
are discussed separately.

joint. Radiographs are indjcated to confirm

Forelimb and hindlimb immobilization
the presence or absence of a fracture or
differ slightly because of the presence of the
luxation but only after coaptation has been
reciprocal apparatus in the hindlimb. In
applied. lf radiographic equipment is
forelimb irtjuries, immobilization is best
unavailable on site, the horse should be
accomplished by aligning the ca1U1on bone
transported to a referral facility for further
with tl1e phalanges to establish a straight,
examination. Hairline or stress fractures
weight-bearing colunm. The horse will bear
can be difficult to demonstrate radiographiweight, although not fully weight bearing, cally, particularly in field conditions.

on its toe. To bandage the lin1.b, an assistant

Therefore, in the presence of severe
holds the leg by the radius, allowing the
lan1eness with pain localized to a long bone,
limb distal to tl1e carpus to hang in a straight
external coaptation should be applied
line to facilitate bandaging. A modified
before moving the horse, to avoid cata

Robert-Jones bandage is placed using
strophic displacement of an incomplete
cotton combine bandage, brown gauze, and
fracture.

elastic bandaging material to form a light
bandage that will allow for soft-tissue

Emergency Treatment: Therapeutic
swelling. Each layer of bandaging material
aims of the initial management of tramnatic
is wrapped separately and in the same
injuries are to relieve anxiety, immobilize
direction to prevent shifting of the splint. A
the fracture or luxation for transportation,
splint is applied to the cranial aspect of the
prevent further damage, and provide safe
limb, extending from toe to caipus using 4-6
transportation. The principles of emergency
layers of overlapping, nonelastic tape ( eg,
coaptation of traumatic irtjuries in horses
white medical tape, duct tape). The splint
include appropriate wound care before
should be padded proxin1ally to prevent
application of external coaptation,
skin injury. lf lateral to medial instability provision of adequate padding to prevent
is noted, a lateral splint may be added or
skin abrasions, immobilization of the joint
casting tape applied over the splint.

EQUINE EMERGENCY MEDICINE

1715

In the hindlimb, the reciprocal apparatus
injuries, as in tl1e forelimb, the bandage
prevents extension of the distal limb if the
should be 3 times the diameter of the limb
horse is non-wcightbearing. Therefore, the
and extend from the floor to the stifle. Two

VetBooks.ir
limb is best immobilized by applying the
splints are needed. One splint will extend
splint on the caudal aspect of the limb, from
from the floor to the stifle laterally.

the toe, on the plantar aspect of the hoof, to

However, because of inte1ference with the
the point of the hock. Dorsal alignment of
reciprocal apparatus and the angulation of
the bony column will not be possible and is
the hock, tl1e caudal splint carmot extend to
not necessary for adequate coaptation.

the stifle but should stop at the point of the

Bandaging and splinting techniques are
hock.

otherwise sinlilar to those used for the
forelimb.

Immobilization of Level 3 Injuries:

A conunercially available splint (Kimsey

Level 3 injuries include fractures of the mid

Legsaver®) may be used for some level 1
to proximal radius, tarsus, or tibia. Because
fractures or tendon injmies; however, it
of the nature of the fracture, tl1e flexor
does not provide enough lateral-to-medial
muscles of the limb become abductors,
stability for joint luxations or severely
resulting in a valgus angulation. The medial
comminuted fractmes. The splint is readily
aspect of both the raili us and tibia does not
available in a munber of sizes, easy to apply,
have a sufficient muscle mass to help
and effective to achieve immeiliate
prevent penetration of the skin by fractured
in1111obilization. Two configurations are
bone, and open fractures are conunon. The
available: one with a slightly forward-angled goal of external coaptation is to prevent bar for a flexed position of the forelimb, and
abduction of the limb and soft-tissue irtjury.

one with a backward angle at the level of

On the forelimb, the splint is applied sinlilar
the fetlock to improve weight bearing. The
to that in level 2 injuries; however, the
forward angle is more effective for most
lateral splint must extend from the ground
fore- and hindlimb injmies, when weight
to tl1e withers. The caudal splint is the same,
bearing is not advantageous. Nonslip tape
extending up to the elbow. The lateral splint
should be placed on the foot plate after
above the bandage should be well padded to
application to make it less slippery,
improve fit and prevent skin injury. Once the
particularly on cement floors.

horse is stanili.ng on the trailer, the splint

Lacerations or rupture of the extensor
can be secured to the chest with nonelastic
tendons, mllike flexor tendons, require a
tape in a figure-8 configuration for further
different type of splint. When both extensor
stability, if.needed. On tl1e hindlimb, the
tendons are completely disrupted, the horse
splint is sin1ilar to that for a level 2 injury;
will knuckle over, which can lead to injury
however, the caudal splint is not needed,
of the dorsal aspect of the fetlock and
and the lateral splint should extend to the
further disrupt any associated wound. In
level of the tuber coxae. The splint can be a
this instance, external coaptation is needed
wide wooden board or a contoured metal
to prevent knuckling over at tl1e fetlock. A
splint made of electrical conduit. Adequate
splint is applied to the cranial aspect of the
padiling should be placed wherever the
fore- or hindlimb with the hoof flat on the
splint contacts skin above the bandage.

ground to prevent joint flexion.

Placing the hoof in extension can facilitate
splint application.

Immobilization of Level 2 Injuries:

Examples of level 2 injmies include mid to

Immobilization of Level 4 Injuries:

proximal carmon bone fractures, carpal

Level 4 injmies include fractures of the
bone fractures, distal radial fractures, and
scapula, hmnerus, femur, and pelvis. They
wounds of the carpus. The goal of
also include olecranon fractures and railial
coaptation is to prevent angulation and
nerve paralysis because these injuries
place the carpus in extension. In level 2
disrupt the passive stay apparatus in the
injuries of the forelin1b, a moderately thick
forelimb. The flexion of the carpus tliat

Robert-Jones bandage is applied up to the
results can cause injury to the dorsal aspect
elbow, wrapping each layer separately to
of the limb and eventually tendon contracprevent slipping. The bandage should be ture. For forelimb fractures and radial nerve

-3 times the diameter of the limb when
paralysis, a level 2 bandage and a caudal
finished, so that the entire splint lies flat
splint from the ground to the elbow is used
against tl1e bandage over its length. Two
to fix the carpus in extension. Although the
splints are applied, at a 90° angle, one lateral
fracture is not directly stabilized by tllis
and one caudal. The splints should extend
splint, it will prevent tendon contraction
from the floor to the elbow, and the hoof
and allows the horse to prop the leg, which
should be flat on the floor. In hindlimb
reduces anxiety. External coaptation is not

1716

EQUINE EMERGENCY MEDICINE
indicated for fractures of the hindlimb at

Wounds and Lacerations
this level. The joint above and below the
fracture cannot be immobilized, preventing

Wounds and lacerations are common in
fracture stabilization. Bandaging will only
horses. The steps involved in management

VetBooks.ir
distract the fracture and make it more
of these injw·ies include control of
awkward to move the horse. Hematoma and
hemoIThage, identification of all involved
soft-tissue swelling around the site of injury
structures, and evaluation of the need for
will provide functional immobilization. If
referral. Referral to a surgical facility is
tl1e pelvis is fractured, the need for
recommended if there are tendon injuries,
transportation and further diagnostics
penetration of a synovial structure,
should be discussed, because motion during extensive degloving injury, severe blood transit may displace fracture fragments,
loss, neurologic signs, or involvement of the
resulting in fatal hemorrhage.

thoracic or abdominal cavity. In addition to
wound management, tetanus prophylaxis,
analgesia, and appropriate antimicrobial

Guidelines for Safe Transportation
therapy are indicated. If severe blood Joss

Before loading an injured horse, proper
has occUITed, cardiovasculru· support
functioning of the vehicle should be
should be provided before and/or during
assessed, the horse stabilized, and the injury transportation.

immobilized as described. A low ramp
facilitates loading and unloading. The trailer Assessment: A brief physical exrunination ideally should be brought to tl1e horse if
should be completed before addressing the
possible for loading. Once loaded in the
p1imary problem. If the wound is located on
trailer, the horse will lean on the wall and
the limb, the presence and degree of
partitions to help balance and to reduce the
lameness should be noted as indicators of a
load on tl1e injured leg. It is never advised to
potentially more serious injury and the need
transport a horse loose in a trailer or in a
for coaptation. The following characteristics
makeshift stall. A sling can be placed under
ru·e then evaluated: location, hemoIThage,
the abdomen to help reduce the weight
configuration, penetration of a body cavity or
beruing on the lin1b. Many trailers have
synovial structure, and/or involvement of
standing stalls at 45° angles (slant load
tendons. Assessment should first include
trailers), which help horses balance during
application of a sterile, wate1°based
transport. If a regular, straight-load trailer
lubricant, clipping of the hair, sterile
is used, the horse should be loaded facing
preparation of the skin, and lavage of tl1e
backward for a forelin1b injury and forward
wound. Wounds over joints, tendon sheatl1s,
for a hindlin1b injury, to help cushion
or tendons (particularly flex or tendons),
sudden stops. The head should be loosely
puncture wotmds, and those tl1at expose
tied, in case the horse falls, and a hay net
or penetrate bone should be explored
provided to reduce anxiety. Frequent stops
tl10roughJy for injury to in1portant underlyshould be made to check on the status of ing structures. Hemorrhage may need to be
the horse and provide drinking water. If
controlled before furtl1er wound assessment
significant cardiovascular compromise
is possible. Pres.sure bandages may be
exists, IV fluids can be administered while
applied, and if tl1e ves.sel can be located, it
in transit.

should be temporruily clan1ped or ligated.

If the horse is severely injured and needs

Ce1tain wound configurations may
to remain recun1bent, it can be pulled onto
significantly damage tl1e blood supply to tl1e
the trailer after stabilizing the limb using a
skin and subcutaneous tis.sues and result in
large tarp or blankets as a glide. The horse
sloughing ( eg, an inverted "V" configuration, should be kept sedated dwing transport to
crushing injuries witl1 significant bruising).

avoid further injuries. A head protector, hay

Wounds over tl1e chest or abdomen may
bales, or a bandage can be used to protect
penetrate important organs. In tl1e case of
the head from self-trauma, and the down
tl1oracic wounds, development of an open or
eye should be padded with a towel or
closed pnewnotl1orax can lead to severe
blanket. The halter should be padded or
respiratory distress. Any horse with chest
removed to reduce the 1isk of facial nerve
traunra and dyspnea should have all open
paralysis, with lower limb bandages applied
wounds sealed witl1 plastic, airtight
to the remaining limbs to avoid traun1a
bandages and evaluated for a pneun1othorax.

caused by paddling. Foals can be trans

The potential involvement of a synovial
ported in recun1bency with the help of
structure should be immediately deterrestraint by a handler either in a trailer with mined. The horse should be restrained and
the mare or separated from the mare in the
sedated as needed for tl1e procedure. A site
vehicle with a handler.

of entry into tl1e joint or tendon sheath

EQUINE EMERGENCY MEDICINE

1717
remote from the wound is chosen, clipped,
be needed if there is injury to a supporting
and aseptically prepared. Using sterile
structure (bone, tendon) or significat1t
technique, saline or a balanced electrolyte
instability Ouxation).

solution is injected into the synovial

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compartment. The amount needed to

Pneumothorax: A penetrating chest
achieve distention and back-pressure can
wow1d can result in development of a
vary from a few milliliters, in the case of the
pnewnothorax and lead to respiratory
clistal tarsal joints, to >100 mL for the
distress. If untreated, pnewnomediastinwn
femoropatellar joint. All compartments of
can result, and tl1is or ilie prirnary pnewnothejoint should be assessed. Synovial thorax can be fatal. On exat11ination, a
structure involvement may be confirmed if
restrictive pattern to the respirations is
leakage of the injected solution is noted
noted. Auscultation of ilie thorax will reveal
from the wound. If communication is not
a lack of breaili sounds in the dorsal lung
noted, the solution is aspirated from the
fields. Because of the incomplete mediastijoint, and the structure is injected with a num in horses, a unilateral chest wound can
prophylactic dose of an antibiotic ( eg,
lead to bilateral pnewnothorax. An open
anukacin). ln chro11i.c wounds or injuries
pnew11othorax is managed by providing a
caused by a puncture, the communication
temporat)' seal over ilie chest wound. The
with the synovial cavity may have sealed.

wound is cleansed and bandaged with a

Horses should be reevaluated for increased
layer of aittight plastic wrap at1d sealed with
lameness, heat, or effusion over the next
elastic adhesive tape. The chest is then

3-5 days, which could be evidence of an
evacuated by inserting a 14-gauge catheter,
insidious infection. If there is significant
using aseptic technique, in the dorsal aspect
edema, swelling, or skin traun1a over all
of the 12th intercostal space. Aspiration can
points of entry, the synovial structure
be facilitated by use of a 3-way stopcock
should not be tapped to avoid the possibility
and 60-mL syringe or by negative suction.

of iatrogenic infection. ln these cases, close

A closed pneumothorax may require an
monitoring or direct probing of the wound
indwelling chest tube and Heimlich valve
with a sterile instrun1ent and radiographic
until the cause is resolved.

assessment may be diagnostic.

Extensor tendon injury of the distal limbs

Hemothorax: Hemothorax is a possible
results in the inability to appropriately place complication of a penetrating chest wound the hoof on the ground, and knuckling over.

at1d can lead to respiratory distress similar·

This suggests involvement of both extensor
to that seen in pnemnothorax. Auscultation
tendons in the proximal metacarpus or
of the thorax will reveal a lack of breath
metatat-sus, or the common digital extensor
sounds in ilie ventral lung fields, wiili
tendon more distally. Flexor tendon injuries
muffled heart sotmds. If dyspnea is noted,
result in hyperextension of the fetlock
the hemothorax should be drained;

(superficial digital flexor), lifting of the toe
however, if ventilation is adequate the chest

( deep digital flexor), or complete dropping
should not be tapped, and the blood will
of the fetlock to the ground (severance or
gradually resorb. To evacuate ilie chest,
rupture of the suspensory ligament). For
a 14-gauge catheter or thoracic trocar is
this to be seen, the horse must bear weight
placed using aseptic technique in the ventral
on the limb at least trat1Siently, but tl1i.s is
aspect of the 6th-8th intercostal space.

not advised. In complete suspensory

Ultrasound helps guide placement, to
breakdown, severe stretching of tl1e digital
prevent accidental penetration of vital
vessels can lead to thrombosis and
structures. Aspiration can be facilitated by
a vascular· injury and necrosis of the distal
use of a 3-way stopcock and 60-mL syringe
limb. It is important to support the fetlock
or provided by passive drainage with a
and not allow weight bearing until the limb

Heimlich valve. Complications of trocarizais stabilized in a flexed position.

tion can include pleuritis due to introduc

The goals of initial wow1d care are to
tion of bacteria, continued hemorrhage, and
decontanunate the wound as much as
hypovolemic shock if the fluid in the third
possible and prevent further contat11ination
space is removed too quickly. Conservative
during transportation. After clipping and
fluid therapy should be provided for
sterile preparation of the intact skin, the
cardiovascular suppmt, and a transfusion
injured tissue is lavaged with sterile saline
may be needed.

and cleaned by sharp debridement of gross
contamination. The wound should be

Penetrating Abdominal Wounds: Pendressed with a sterile, nonstick bandage etration of the abdominal cavity is a serious
and a support wrap or padded bandage.

and potentially fatal injury that can lead to

Immobilization of ilie limb (seep 1714) will hemorrhage, penetration of an abdominal

1718

EQUINE EMERGENCY MEDICINE
organ, or development of peritonitis. U a

Treatment: Treatment of head iitjuries is
penetrating wound is suspected, it should
mainly supportive to reduce secondary CNS
be sterilely prepared, cleansed with saline
damage. Horses with head injrnies can be
and low-pressure lavage, explored for the
severely ataxic and should be handled and

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presence of a foreign body, and debrided. A
moved with extreme caution. Uthe horse is
transabdominal ultrasound may reveal free
recU1Tibent, sho1t-tenn general anesthesia is
fluid. Abdominocentesis can be performed
best to transport the horse to a referral
to detect fecal contamination, indicating a
facility for further evaluation. Opioids
ruptured viscus, or internal hemorrhage.

should be avoided for sedation of horses

However, abdominocentesis may not be
with head traU1Tia because of the risk of
diagnostic initially, because indicators of
decreased cerebral perfusion pressure. The
peritonitis ( eg, increased total protein,
horse should be given IV fluids to maintain

WBCs, bacterial organisms) take several
normal blood pressure and reduce the 1isk
hours to develop. The wound should be
of cerebral ischemia Diuretics are
bandaged, and broad-spectrum systemic
contraindicated. U hypoventilation
antibiotics and pain management initiated.

develops, the horse should be intubated, and

In the presence of a large wound, or if the
ventilation assistance provided to prevent
abdominal musculatw·e is involved, the
hypercapnea. lithe blood-brain barrier has
abdomen can be supported with a
been breached by a fracture, broad-spectrrnn
compressive support bandage.

antibiotics should be started. NSAIDs are
administered to m.i.ninuze inflammation,

Head Injuries
and seizures should be managed with
diazepam (0.5----0.44 mg/kg, IV) or phenobar

Head iitjuries can result in severe CNS
bital (5---15 mg/kg, given slowly IV). Although
damage. lr\jwies can be primary ( eg,
controversial for traun1atic brain iitjury in
contusion, laceration, fracture, hemorhuman medicine, corticosteroids may be rhage) or secondary ( eg, subsequent edema, indicated in the a.cute phase of iitjury (eg, reperfusion iitjury, secondary necrosis).

dexamethasone, 40-100 mg, IV). DMSO

Therapy of head injury is designed to

(1 g/kg, IV, in 5 L balanced electrolyte solution
minimize secondary CNS dan1age.

every 12 hr) has also been used to rnininuze

Causes of head injury in horses include
secondary edema and decrease intracranial
direct trauma from a fall or blows to the
pressure. More effective for treatment and
head. A common cause of head injury is
prevention of edema is 20% mannitol
when the horse falls over backward onto

(1 mg/kg, IV, every 6---12 hr) or 7.5% hyperthe poll. Injuries associated with this fall tonic saline ( 4-6 rnUkg, IV, every 6---12 hr).

include basisphenoid fractures and

Ma.gnesiUlTI (0.05 mg/kg, IV, over 30 min) has
avulsion of the ventral straight muscles
also been proposed as a therapeutic agent to

(longus capitus and/or rectus capitus
reduce cerebral ischenua.

ventralis muscles) from the base of the
skull. Basisphenoid fractures can result in
acute optic nerve damage and·cerebral

Ocular Injuries
signs. Temporary or permanent blindness

Ocular iitjuries are usually trawnatic in
may result. Rupture of the ventral straight
origin and include periocular lacerations,
muscles may cause severe epistaxis,
corneal lacerations, foreign body penetratrequiring transfusion, and avulsion ing injuries, and direct blows to the eye,
fractures at the muscular insertion onto
causing retinal detaclrn1ent. (See also
the skull may contribute to additional

OPllTI-IALMIC EMERGENCIES, p 1696.) Evaluation CNS injury.

of acute ocular injury includes a thorough

The diagnosis is made by radiographs
evaluation of the structures of the eye
or CT to identify skull fractures, avulsion

(including the eyelids, conjunctiva, cornea,
fractures, or a soft-tissue opacity in the
and lens), a funclic examination, and
guttural pouch ( consistent with a hernaevaluation of cranial nerve function to toma from rupture of the ventral straight
assess the degree of dan1age. Vision can be
muscles). Endoscopy may show hemm0
assessed by the menace response and obstarhage from the guttural pouch originating cle course testing. Oculomotor, trochlear,
from the base of the stylohyoid bone or
and abducens nerve function a.re assessed
medial wall of the guttural pouch. Hematoby the position of the eye and pupillary light mas may be noted in the guttural pouch
responses. Facial nerve and sympathetic
septum where the ventral straight muscles
innervation to the eye are assessed by eyelid
lie. Hemorrhage caused by fractures may
tone and position of the eyelashes.

also be seen draining from the ethmoid

Treatment of a.cute ocular iitjuries
turbinates.

includes minimizing pain and inflammation,

EQUINE EMERGENCY MEDICINE

1719
preventing infection, and preventing further

Deep second-degree bum wounds may heal
injwies. If penetration by a foreign body is
spontaneously in� wk if care is taken to
suspected, rapid surgical intervention is
prevent further dermal ischemia that may

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indicated. Eyelid lacerations should be
lead to full-thickness necrosis.

sutured, with assistance of a palpebral

Third-degree bums are characterized by
nerve block and local infiltration of an
loss of the epidermal and dermal compoanesthetic. Sutures should be placed nents, including the adnexa. These bums,
carefully to prevent corneal abrasion, and
when fresh, range in color from white to
skin should be preserved during debrideblack. There is fluid loss and a marked ment. Anti-inflammatory medications
cellular response at the margins and deeper
administered to minimize pain and
tissue, eschar fonnation, lack of pain,
inflammation include NSAIDs and topical
shock, wound infection, and possible
osmotic agents. Pain from pupillary spasm
bacteremia and septicemia. Healing occurs
can be minimized by dilating the pupil with
by contraction and epithelialization from
atropine and covering the eye to prevent
the wound margins, or acceptance of an
myosis in bright sunlight. Acute injuries can
autograft. These bums are frequently
be associated with corneal ulceration and
complicated by infection.

secondary bacterial or fungal invasion. Use

Fourth-degree bums involve all of the
of broad-spectrwn topical antibiotic and
skin and underlying muscle, bone,
an antifungal medication may prevent
ligan1ents, fat, and fascia.

secondary infection of a corneal ulcer.

Horses that are acutely blind cannot move

Pathophysiology: After severe bums,
around their environment well. Further
there is a dramatic cardiovascular effect
ir\jury should be prevented by protecting
termed burn shock, which resembles hypothe blind eye and by careful handling.

volemic shock. Local and systemic capillary
permeability increases dramatically in

Thermal injuries
response to heat and the release of

Thermal injury to a horse is rare. Most cases
cytokines, prostaglandins, nitric oxide,
involve barn fires, lightning, electricity,
vasoactive leukotrienes, serotonin,
caustic chemicals, or friction. Most bums
histanline, and oxygen radicals. Because
are superficial, easily managed, inexpensive
heat is slow to dissipate from bum wounds,
to treat, and heal in a short time.

it is often difficult to accurately evaluate the
a.moUllt of tissue damage in the first 24--72 hr

Classification: Like those in people,
after injury. The extent of the bum depends
bums in horses are classified according
on the size of the area exposed, while the
to the depth of injury. First-degree burns
severity relates to the maximwn tempera.

involve only the most superficial layers of
ture the tissue attains and the duration of
the epidem1is. These bums are painful and
overheating. This explains why skin injury
characterized by erythema, edema, and
often extends beyond the boundaries of the
desquamation of the superficial layers of the original bum.

skin. The genninal layer of the epidennis is
spared, and the burns heal without

Management: Administration of isotonic
complication.

fluids, at a rate of 4 mllkgl'/o burn, in the first

Second-degree bums involve the

24 hr ( one-half of which is given in the first
epidennis and can be superficial or deep.

8 hr) is recommended, but fluid resuscita

Superficial second-degree bums involve the
tion is best titrated to maintain stable and
stratwn comeun1, stratun1 granulosun1, and
adequate blood pressure. An alternative is
a few cells of the basal layer. Tactile and
to use hypertonic saline solution ( 4 mllkg)

pain receptors remain intact. Because the
followed by administration of isotonic
basal layers remain relatively uninjured,
fluids. If there has been smoke or heat
superficial second-degree bums heal rapidly inhalation injury, crystalloid adnlinistration with rnininlal scarring, within 14-17 days.

should be limited to the amount that

Deep second-degree bums involve all layers
normalizes circulatory volwne and blood
of the epidennis, including the basal layers.

pressure. Continuing to administer

These burns are characterized by erythema
electrolyte solutions at the same rate after
and edema at the epidem1al-dennal
bum shock has resolved leads to edema,
junction, necrosis of the epidennis, accwnuwhich counters any in1provement in lation of WBCs at the base of the bum zone,
cardiovascular dynamics. During fluid
eschar ( slough produced by a thermal bum)

administration, hydration, lung sounds, and
formation, and rnininlal pain. The only
cardiovascular status should be monitored
gemlinal cells spared are those within the
carefully by clinical assessment and PCV
ducts of sweat glands and hair follicles.

and total protein measurement.

1720

EQUINE EMERGENCY MEDICINE

Flunixin meglwnine (0.25-1 mg/kg, IV,

The escha.r is sloughed by bacterial

1-2 times daily) is an effective analgesic.

collagenase activity within 4 wk. The

Firocoxib (0.1 mg/kg/day, PO) is a COX-2
exposed bed can then be grafted or allowed
inhibitor for horses. Although COX-2
to contra.ct.

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inhibitors would seem beneficial in the

Although bacterial colonization of la.rge
management of bwl"I patients, firocoxib
bUI1"1S in horses is not preventable, the
is approved only to alleviate musculowound should be cleansed 2-3 times daily, skeletal pain. Human studies have fow1d a
and a topical antibiotic reapplied to reduce
synergistic effect of keta.mine and morphine
the bacterial load to the wound. Occlusive
to a.meliorate pain of skin burn ir\juries.

dressings should be a.voided because of

Pentoxyfylline (8 mg/kg, IV, bid) is used to
their ability to produce a closed wound
improve the flow properlies of blood by
environment, which may both encourage
decreasing its viscosity. Administration of
bacterial proliferation and delay healing.

din1ethylsulfoxide (DMSO) at 1 g/kg, IV, for

Anmion can decrease the pain of the wound
the first 24 hr, may decrease inflammation
and is antibacterial. It is more useful in
and pulmonary edema. If pulmonary edema
areas of the body where it can be fimily
is present and is unresponsive to DMSO and
pressed into the wound, such as the distal
fw·osemide treatment, dexa.methasone can
limbs. Additionally, circulation to the
be administered once at 0.5 mg/kg, IV.

burned areas is often compromised, making

The cornerstones of therapy for smoke
it highly unlikely that parenteral a.dntinistra.inhalation injUiy a.re maintenance of ru1way tion of antibiotics can achieve therapeutic
patency, adequate oxygenation and
levels witltin the wound.

ventilation, and stabilization of hemody

The most commonly used topical
nan1ic status. Antibiotics and corticosterantibacterial for the treatment of bUI1"1s is oids do not influence swvival rates and
silver sulfadia.zine in a 1 % water miscible
should not be routinely administered.

crean1. It is a broacl-spectrnm, antibacterial

Systemic antimicrobials a.re indicated only
agent able to penetrate the escha.r. Silver
for proven infections, the incidence of which sulfadia.zine is active against gram-negative increases 2-3 days after smoke inhalation.

bacteria., especially Pseudomonas, witl1

Procaine penicillin IM is effective against
additional effectiveness against Staphylo
oral contaminants colonizing the airway.

coccus aureus, Escherichia coli, Proteus,

If signs of respiratory disease worsen, a

Enteroba.cteriacea.e, and Candida albicans.

transtracheal aspirate should be submitted

It causes minimal pain on application but
for culture and sensitivity testing, and the
must be used twice a day because it is
antibiotic regimen adapted accordingly.

inactivated by tissue secretions.

Horses with suspected significant smoke

Many bum patients suffer prmitus such
inhalation should be observed closely for
that measures must be ta.ken to prevent
several hours and hospitalized if b11I1"1s a.re self-mutilation of the wound. Reserpine
extensive. Successful treatment depends

(2.5 mg, PO, for7-10 clays), nom1ally used
on continual patient reassessment, as well
in horses as a long-acting tranquilizer, can
as early and aggressive ca.re.

effectively decrease tl1e urge to scratch by

First-degree bUI1"1s a.re generally not
successfully breaking the itch-scratch cycle.

life-threatening and thus simply managed.

Weight loss of 10%-15% during the course of

Second-degree bUI1"1s a.re associated with
illness is indicative of inadequate nutritional
vesicles and blisters. These vesicles should
intake. Gradually increasing concentrate,
be left intact, because blister fluid provides
adding fat in the f01m of vegetable oil, and
protection from infection and an intact
offering free-choice alfalfa hay increase
blister is less pru.nful than the denuded
caloric intake.

exposed surface. An antibacterial dressing
such as silver sulfa.dia.zine is applied to the
wounds while an escha.r is allowed to form.

OTHER COMMON EQUINE

Third-degree bums can be difficult to

EMERGENCIES
manage. The horse's systemic condition
should be stabilized as rapidly as possible

Esophageal Obstruction
before undertaking wound management.

Destruction of the demtis leaves a primary

(Choke)

collagenous structure called an escha.r. The

Intraluminal esophageal obstruction is a
escha.r does not prevent bacterial contamicommon emergency in horses and is caused nation or evaporation of heat or water. The
by in1paction of ingested feed material. The
escha.r should be covered with an antiba.cte-
most frequent sites of in1paction a.re the

1ial agent twice daily. Wow1d contraction
proximal esophagus and just cranial to the
does not occur while the escha.r is intact.

thoracic inlet. Predisposing factors include

EQUINE EMERGENCY MEDICINE

1721
bolting of feed, poor dentition, recent

After the obstruction has been relieved,
sedation, poor feed quality, recent feed
endoscopy can be used to assess the
changes, and dehydration. See also
esophageal mucosa. Circwnferential

ESOPHAGEALOBS'fRUCTION, p 215.

ulceration can lead to stJicture fom1ation

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with recUITence of obstruction. Horses tl1at

Diagnosis: Clinical signs of choke include have been choked are at risk of recurrence nasal discharge containing saliva and feed
in the 2-4 wk after the initial event, even
mate1ial, hypersalivation, coughing,
without visible esophageal damage. Feeding
retching, signs of colic, or frequent attempts
a slurried, pelleted diet or grass can prevent
to swallow. The horse may be observed
recutTence. When the esophagus has been
repeatedly stretching and extending the
damaged, narrowing is maximal 30 days
head and neck. Esophageal obstruction is
after the obstruction. Before attempts are
identified by palpation of a foreign body in
made to resolve a potential stricture, the
the neck, passage of a nasogastiic tube, or
horse should be managed medically with
esophageal endoscopy. In refractory cases,
dietary modification for 60 days to allow
radiography and contrast radiography may
for remodeling of the scar tissue. Broadbe used, particularly if a foreign body, spectnun antibiotics are administered to
stJicture, divetticulum, or esophageal
prevent or treat aspiration pnewnonia,
rupture is suspected. Ultrasonography may
along with anti-inflanunatory drugs and tetaidentify thoracic changes consistent with nus prophylaxis. Sucralfate (20--40 mg/kg,
aspiration of feed.

PO, tid--qid) has been advocated to facilitate
healing of esophageal ulceration.

Treatment: Once the presence of an
obstruction has been conilm1ed, the horse

Rectal Tears
should be muzzled, and feed and water with

Rectal tears are serious and possibly
held. Acute, simple obstructions may
life-threatening injuries in horse. Prevenresolve with sedation and consequent tion is key, but if a rectal tear occurs,
relaxation of the esophageal musculature.

appropriate and timely referral can result

An cx,-agonist such as xylazine or detomiin a successful outcome. Rectal tears are dine provides good muscle relaxation.

classified into four grades based on the

Oxytocin (0.11 mg/kg, IV) has been
number of layers involved. Grade I tears
demonstrated to provide good esophageal
involve the mucosa and submucosa only;
relaxation and has been used to resolve
grade II involve the muscularis only, with
esophageal obstructions. Adverse effects
a mucosal-submucosal hernia; grade III
may include mild signs of colic, and this
involve the mucosa, submucosa, a_od
drug should not be given to pregnant mares.

muscularis, leaving the serosal layer intact;

The obstruction should resolve within 1 hr
and grade IV involve all layers of the
after administration of a muscle relaxant. If
rectutn, including the serosa. In the case
the horse is dehydrated, IV fluids may also
of grade III tears, fwther classification is
help to resolve the obstruction.

made based on the location of the tear;

If the obstruction has not resolved within
grade Illa tears leave the visceral peritoneal

-1 how· after sedation, or if the choke is
intact, and grade IIIb tears are located
chronic (>3 hr duration), the horse should
dorsally in the mesentery. Most tears
be sedated again to allow the head to drop
resulting from rectal palpation are located
for lavage of the esophagus. A nasogastric
dorsally and extend into the mesocolon.

tube is passed, and gentle lavage with water

Retroperitoneal tears are rare but have
is performed to flush the esophagus.

been repotted. Fecal contamination often

Mineral oil should never be used because
occurs with grade IV tears, but bacterial
of the risk of aspiration pnewnonia. An
translocation and peritonitis is still possible
esophageal lavage tube (a nasogast1ic tube
with grade III tears. See al.so RECTAL TEARS, with a cuff) is useful to help resolve the
p 190.

obstruction and reduce feed aspiration.

Alternatively, a cuffed endotracheal tube

Diagnosis: A rectal tear is suspected
can be passed tlu·ough the nasal passages
when there is sudden loss of resistance
and into the esophagus, and a smaller
during palpation and when a copious
nasogastric tube used for lavage. These
amoWlt of fresh blood is present on the
procedures can be repeated internlittently
rectal sleeve. Blood-tinged mucus usually
and can be aided by general anestl1esia. If
indicates mucosa! irritation only. If a tear is
unsuccessful, an endoscope can be used
suspected, the severity should be immedito identify the obstruction and facilitate ately assessed and measures taken to
manual removal using endoscopic forceps.

initiate treatinent or referral.

1722

EQUINE EMERGENCY MEDICINE

The horse should be sedated for
horse should be monitored carefully for
assessment of the tear, and an epidural
development of a perirectal abscess, which
performed if there is any straining.

will require surgical drainage. For

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N-butylscopolammonium bromide
retroperitoneal tears with fecal contan1ina

(0.3 mg/kg, IV) may be given to decrease
tion, the tear can be packed with iodineperistalsis. A lidocaine enema may also soaked gauze and the cavity cleaned out
reduce straining. A speculum should not be
daily. In mares, the cavity can be drained
used, because it can worsen the tear. Digital
into the vagina, and the tear closed
palpation (preferably bare handed) is then
primarily. A laxative diet and analgesics are
carefully performed. A thin flap of tissue
provided to decrease the pain of defecation.

indicates a tear through only the mucosa.

The most serious complication of retroperi

If a large cavity with a thin membrane is
toneal tears is development of an abscess
noted, a grade III tear is present. If intestine
that migrates forward into the abdominal
can be palpated, the tear is a grade IV. Visual
cavity. This is prevented by ensuring
confirmation can be made carefully using
appropriate drainage into the rectum or
colonoscopy.

vagina.

For grade III or IV tears in a caudal

Treatment: Grade I and II tears can be
location, primary repair using sutures
medically managed with antibiotics, a
through a rectal approach can be attempted.

laxative diet (mineral oil, mashes of

A successful repair of a grade IV tear using a
complete pelleted feeds or alfalfa pellets,
linear stapling device has been reported.

fresh grass) and analgesics (flunixin

This approach requires that the abdomen
meglumine) to facilitate defecation. Select
has minimal to no contanlination. Alternagrade III tears can be managed similarly, if tively, these tears can be treated through a
necessary because of financial restrictions, ventral midline approach, followed by an but also require daily manual evacuation
antimesenteric incision in the caudal small
for up to 3 wk. Peritonitis is a risk, repeat
colon and repair through the lumen. A
epidurals are required, and the time
celiotomy has the advantage of a largecommitment is substantial. For the best colon enterotomy and lavage, thus reducing
outcome, grade III and IV tears should be
the fecal load on the suture line.

referred to a surgical facility. However, it

Grade III and IV tears can also be treated
is essential to prevent fecal contan1ination
by insertion of a rectal liner using a ventral
of the abdomen during transportation;
midline celiotomy. Rectal liners are made of
therefore, rectal packing is highly
a plastic ring glued to a rectal sleeve. The
recommended. The horse is sedated and
liner is introduced rectally by a nonsterile
an epidural performed using a combinaassistant and sutured to the small colon tion of xylazine and mepivicaine. A tampon using an external circumferential suture composed of a 7.5-cm stockinette filled
pattern that allows the ring to slough in -10
with moist, iodine-soaked cotton, coated
days, resulting in a small-colon anastomowith surgical lubricant is inserted until it is sis. The liner diverts the normal fecal
located at least 10 cm cranial to the tear.

passage until the tear has healed. In other

The stockinette should be inserted before
cases, a loop colostomy can be performed
filling it completely to avoid enlarging the
to maintain patency of the distal segment.

tear. The anus is then temporarily

The colostomy is perfqrmed as the first step;
occluded with a purse-string suture or
after the tear has healed, colonic continuity
towel clamp. The horse should be given
is reestablished using a second surgical
systemic, broad-spectrum antibiotics,
procedure. In all fecal diversion procedures,

NSAIDs, and appropriate tetanus
an attempt is made to close or approximate
prophylaxis. Prevention of fecal contamithe tear. Laparoscopic suturing of rectal nation by grade III and IV tears during
tears has been described experimentally.

referral has a direct influence on the
success of the outcome.

At the referral facility, the tear is

Postcastration Evisceration
reassessed to identify additional damage

Postcastration evisceration is always a
sustained during transportation. An abdomirisk after open castrations, but the risk is nocentesis is perfonned to check for
increased in draft horses, in Tennessee
peritonitis. After assessment, several

Walking horses and Standardbreds
treatment options are available. For grade II

(because of their larger inguinal rings),
tears with no fecal contanlination that are
or after castration of an adult stallion.

at risk of forming a diverticulum, primary

Evisceration typically occurs within 4 hr of
repair using a rectal approach can be
castration, but is a risk for up to 6 days after
attempted using one-handed sutures. The
surgery.

EQUINE EMERGENCY MEDICINE

1723

Diagnosis: Evisceration of omen tum
perforn1 a rectal examination before
or small intestine is first identified by a
removing the packing to ensure herniation
structure hanging out of the surgical
has not recurred and the intestine has not
incision. It is important to instruct the
adhered to the packing material.

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owner to keep the horse quiet and to
support the eviscerated structure(s) with a
towel to avoid further stretching or damage.

NEONATAL INTENSIVE CARE

Examination quickly reveals what structure

AND EMERGENCIES
is involved, so that treatment can be
initiated.

Initial Assessment

Early recognition of abnorn1alities is of

Treatment: For omental evisceration, the
utmost importance for successful managehorse is restrained, and rectal palpation ment of critically ill foals. (See also
performed to ensure that only the omentum

MANAGEMENT OF TllE NEONATE, p 2087.)

is involved. Prolapse of the omentum can

Immediately after birth, the cardiovascular
usually be managed by sedation and
and respiratory systems of the foal must
emasculating the omen tum as far proximal
adapt to extra-uterine life. These critical
as possible. For more severe cases, the
events can be undermined by factors such
horse is placed under short-term general
as inadequate lung development, SUlfactant
anesthesia, and the omentum and scrotum
deficiency (primary or secondary), viral or
cleaned and sterilely prepared. The
bacterial infection, placental abnormalities,
omentum is emasculated as proximal as
in utero hypoxia, and rneconium aspiration.

possible, and the scrotwn packed with

Spontaneous breathing should begin
gauze and closed. Systemic antibiotics and
within 1 min of birth, and many foals

NSAIDs are administered, and the packing
attempt to breathe as soon as the thorax
removed in 2 days. Barring complications,
clears the mare's pelvic canal. During the
antibiotics are discontinued on day 3.

first hour of life, the respiratory rate can be

If the small intestine is eviscerated, a

>60 breaths/min but should decrease to
short-term general anesthetic is given. The

30-40 breaths/nun within a few hours.

intestine is copiously lavaged and exanlined

Auscultation of the thorax shortly after
for damage. Avulsion of the mesenteric
birth reveals a cacophony of sounds as
vessels or intestinal compromise require
airways are gradually opened and fluid is
resection. The scrotun1 should be sutured
cleared. End-expiratory crackles are
closed over the eviscerated bowel, and the
consistently heard in the dependent lung
horse referred to a surgical facility. If the
during and after periods of lateral recun1-
intestine appears healthy, it is replaced in
bency. It is not unusual for a newborn foal
the abdomen, which often requires dilation
to appear slightly cyanotic during the
of the internal inguinal ring. Care should be
adaptation period, but this should resolve
taken to replace the intestine within the
within a few minutes of birth. Similarly, the
peritoneal cavity through the inguinal canal,
heart rate of a healthy newborn foal has a
and not through a separate, iatrogenic
regular rhytl1m and should be at least 60
opening. If the herniation cannot be reduced bpm after the first minute. Occasionally, confidently, the scrotun1 should be packed,
arrhythmias ( atrial fibrillation, wandering
sutured closed, and the case referred.

pacemaker, atrial or ventricular premature

If the herniation can be reduced, the
contractions) may be ausculted but should
inguinal canal and scrotum are packed
resolve within 15 min after birth. A
with sterile gauze, taking care to prevent
continuous holosystolic, or machinery,
introducing gauze into the abdomen, and
murn1ur heard for the first few days after
the scrotum is sutured closed. A short
birth over the left side of the heart is consistsegment of gauze is left exposed. Alternaent with patent ductus arteriosis. Various tively, the external inguinal ring and vaginal
other systolic murmurs, thought to be flow
tunic can be sutured closed primarily instead murmurs, may be heard during the first of packing. Systemic, broad-spectrum
week of life. Murmurs that persist beyond
antibiotics and NSAIDs are administered,
the first week of age, those that are loud
and the horse monitored closely for

(>2/6), or murmurs that cause exercise
development of colic or ileus, which may
intolerance or hypoxemia should be
indicate intestinal devitilization. Should
investigated more thoroughly.

that occur, the horse must be referred for

Foals are normally nonresponsive to
abdonlinal exploratory surgery. If the horse
stimulation while in the birth canal. This
progresses well, the packing can be
lack of responsiveness has led to the
removed in 48 hr, and antibiotics discontinpresumption of fetal death during ued 24 hr after removal. It is advised to
dystocia. Diagnostics, including palpation

1724

EQUINE EMERGENCY MEDICINE
of a pulse in the tongue, neck, or limb, or
fillies usually urinating before colts. It is
palpation and auscultation of the thorax
not unusual for colts not to "drop" their
for a heartbeat should be performed to
penis when urinating for the first few days
confirm the foal has died. If the foal's nose
of life because of the persistence of a
is accessible during parturition, nasotranorn1al tissue frenulum within the prepuce.

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cheal intubation will allow measurement

The penis should not be forced from the
of C02 tension in the expired gas. A long
prepuce; the frenulum will resolve without
endotracheal tube (size 7 -12 mm outer
treatment.

diameter) with an inflatable cuff should be

The gait of the newborn foal is hypermetused. The tube is passed blindly into the ric, with a wide-based stance. Extreme
ventral meatus using a finger to guide the
hypennetria of the forelimbs, usually
tube. Proper placement can be determined
bilateral but occasional unilateral, has been
by palpation of the throat. The cuff is
seen in some foals associated with perinatal
inflated, and manual ventilation is
hypoxia and ischemia, but this gait
peifom1ed with either 100% oxygen or
abnormality usually resolves without
room air. C02 tension is measured
specific therapy within a few days. Spinal
continuously with a capnograph or a
reflexes tend to be exaggerated in the
single-use end tidal C02 monitor. End-tidal neonate. Foals also exhibit an exaggerated C02 varies in foals during parturition,
response to external stinluli ( eg, noise,
depending on cardiac output and
sudden movement, touch) for the first few
ventilation frequency, but it should be
weeks of life.

consistently >20 mmHg and is usually
closer to 30 mmHg. Once manual
ventilation of a living foal is established, it

Dystocia and Resuscitation
must continue until the foal is delivered.

Most newborn foals make tl1e transition to

The righting reflex is present as the foal
extra-uterine life easily. However, for those
exits the birth canal, as is the withdrawal
with difficulties ( eg, dystocia, premature
reflex. Cranial ne1ve responses are intact at placental separation), it is of utmost birth, but the menace response may take as
importance to recognize and institute
long as 2 wk to fully develop. Absence of a
appropriate resuscitation procedures. A
menace reflex should not be considered
modified Apgar scoring system has been
diagnostic of visual deficits in newborn
developed as a guide to initiate resuscitafoals. The suckle reflex should be strong by tion and estimate the level of fetal

10 min of birth. Within 1 hr of birth, healthy
compromise (see TABLE 11). A brief physical foals demonstrate auditory orientation
examination should also be peiforn1ed
with unilateral pinna control. The normal
before starting resuscitation, because of
pupillary angle is ventromedial in the
humane issues concerning resuscitation of
newborn; this angle gradually becomes
foals with serious birth deforn1ities (such
dorsomedial throughout the first month of
as severe limb contracture and hydrocephlife. Foals may attempt to rise within 20
alus, among others).

min of birth; most should stand on their

The initial assessment begins during the
own within 1 hr and nurse by 2 hr. Some
presentation of the foal in the birth canal.

foals defecate shortly after standing, but

Although tl1e following applies primarily
many will not attempt to defecate until
to the birth of a foal froi:n a high-risk
after successfully suckling, about 3 hr after
pregnancy, quiet and rapid evaluation can
birth. First urination is more variable, with
be performed during any attended birth.

l&H•ill MODIFIED APGAR SCORE FOR EQUINE NEONATES

Clinical Evaluation

(first 20 sec of life)

Score:!

Score:2

Score:3

Heart rhythm and rate

Regular, >60 bpm Irregular, <60 bpm

Absent

Respiration

Regular

Irregular

Absent

Response to external

Sneeze, ear flick

Grimace, weak ear flick

Absent
stimulation (nose, ear)

Muscle tone

Active, sternal

Some ability to flex limbs Limp, lateral

EQUINE EMERGENCY MEDICINE

1725

The goal in the norn1al birth of a healthy
nasotracheal tubes or a bag-valve-mask is
foal is to minimally disturb the bonding
not readily available. Hyperventilation with
process between mare and foal. This also
lOOOA, oxygen is suggested to be the best
applies to a high-risk birth, although some
choice to reverse fetal circulation;
disruption of normal bonding is inevitable.

however, evidence from human medicine

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The strength and rate of any palpable
suggests there are no apparent disadvanperipheral pulse should be evaluated as the tages in using room air instead.

foal presents. The apical pulse should be

Almost 90% of foals requiring resuscitaassessed as soon as the thorax clears the tion respond to ventilation alone and
birth canal. Bradycardia (pulse <40 bpm) is
require no additional therapy. Nasotracheal
expected during forceful uterine contracintubation can be started while the foal is tions, but the pulse rate should rapidly
in the birth canal if the foal is not delivered
increase once the chest clears the birth
rapidly (eg, dystocia). This blind technique
canal. Persistent bradycardia is an
may require some practice but can be
indication for rapid intervention.

lifesaving. The nasotracheal tube also

The fetus is normally hypoxemic
provides a convenient site for administracompared with the newborn foal, and tion of intratracheal medications, such as
this hypoxia is largely responsible for
epinephrine. Once breathing is spontanethe maintenance of fetal circulation by ous, humidified oxygen should be provided
generation of pulmonary hypertension.

via nasal insufflation at 8-10 Ilmin.

During normal parturition, mild asphyxia

Chest compressions should be started
occurs and results in fetal responses that
if the foal remains bradycardic despite
lead to a successful transition to extraventilation or if a nonperfusing rhythm is uterine life. If more than mild asphyxia
palpated. The foal should be placed on a
occurs, the fetus is stimulated to breathe in
hard surface in right lateral recumbency
utero; this is known as primary asphyxia. If
with the topline against a wall or other
the initial breathing effort resulting from
support to keep the foal from sliding. The
the primary asphyxia is not effective, a
resuscitator's hands are placed over each
second gasping period occurs within
other either directly over the heart (the
several minutes known as secondary
cardiac method) or at the highest point
asphyxia. If asphyxia does not improve,
of the chest (the thoracic method). The
the foal enters a stage called "secondary
cardiac method is theorized to push blood
apnea," which is irreversible unless
forward by directly compressing the heart,
resuscitation is initiated. Therefore, the
whereas the thoracic method pulls blood
first priority of neonatal resuscitation is
forward by altering the intrathoracic
establishing an airway and breathing for
pressure; both methods are valid in the
the foal. Foals that are not spontaneously
foal. Compressions are provided at a rate
breathing are assumed to be in secondary
of 80-120 per min, depressing the thorax
apnea.

40% of its diameter, and allowing the chest

The airway should be cleared of the fetal
to fully recoil. The first round of compresmembrane as soon as the nose is presented. sions should last 30-60 sec to allow for If meconium staining is present, the airway
assessment of progress and addition of
should be suctioned before delivery of the
medications; after that, each round of
foal is complete, and before the foal
compressions should last 2-3 min,
breathes spontaneously to prevent
followed by a 10-sec break to allow for
aspiration. Suction should be continued to
assessment of heart rate, pulses, and
the level of the trachea if aspiration of the
rhythm. If the foal's heart does not start
nasopharynx is productive. Suctioning
immediately after compressions cease, the
should be brief and gentle; overzealous
resuscitator should switch out to prevent
suctioning worsens hypoxia, which causes
fatigue, and compressions are continued.

secondary bradycardia or cardiac arrest

Breaths should be provided by an assistant
through vagal reflexes. Suctioning should
at a rate of 8-10 per min during cardiac
stop once the foal begins to breathe
compressions, or 2 breaths for every 30
spontaneously.

compressions if the resuscitator is alone. If

If the foal does not breathe or move
the foal is not resuscitated after 10-15 min
spontaneously to right itself within seconds of compressions, cerebral hypoxia is likely of birth, tactile stimulation is necessary
to have made further resuscitation efforts

( eg, drying with a towel). If tactile
futile.

stimulation does not result in spontaneous

Because -5% of foals are born with
breathing, the foal should be intubated
fractured ribs, assessment for the presence
immediately and manually ventilated.

of rib fractures should be performed before

Mouth-to-nose ventilation can be used if
starting chest compressions. Some of these

1726

EQUINE EMERGENCY MEDICINE
fractures can be identified by palpation.

delivered, resuscitated, and managed, and

Fractures typically occur between ribs 3
care must be taken to ensure that cold
and 8, are usually multiple and consecutive, stress is minimized in newborn and and are located in a relatively straight line
critically ill foals. The foal should be dried

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along the part of the rib with the greatest
and placed on dry bedding once resuscitacurvature just dorsal to the costochondral tion is compete. Supplemental heat in the
junction. Unfortunately, their location over
form of radiant lamps or warm air
the heart can make chest compressions a
circulating blankets may be required.

potentially fatal exercise. Foals with rib

Fluid therapy should be used conservafractures should be placed in lateral tively in postpartum resuscitation. The neorecumbency with the fractured ribs down nate is not volume depleted unless
for compressions. After resuscitation,
excessive hemorrhage has occurred. Some
ultrasound can be used to identify rib
compromised newborns are actually
fractures that have escaped detection by
hypervolemic. Because the renal function
palpation, or new fractures caused by
of the equine neonate is substantially
compressions. Ultrasound is the most
different from that of adult horses, fluid
sensitive diagnostic tool to identify rib
therapy cannot simply be scaled down. If
fractures.

IV fluids are required for resuscitation and

Drug therapy should be started if a
blood loss is identified, administration of
nonperfusing rhythm persists for >30-60

20 ml/kg of a polyionic, isotonic, glucosesec in the face of chest compressions.

free fluid over 20 min (-1 L for a 50-kg foal)

Epinephrine remains the drug of choice at
can be effective. Indications for this shock
a dosage ofO.O 1-0.02 mg/kg, IV. If given
bolus include poor mentation, poorly
through the nasotracheal tube, the dosage
palpable peripheral pulses, and developshould be 0.05-0.1 mg/kg. Epinephrine ment of cold distal extremities compatible
can be repeated every 2 -3 min during
with hemorrhagic shock The foal should
compressions, coinciding with the 10-sec
be assessed after the initial bolus, and
assessments between rounds of compresadditional boluses (up to three) adminissions. Vasopressin (0.6 U/kg, every 10-20
tered as needed. Glucose-containing fluids
min) is gaining attention as a cardiovascucan be administered after resuscitation at a lar resuscitation drug, but experience in
rate of 4-8 mg of glucose/kg/min ( -120 milhr,
foals is limited. Atropine is not recom100/o dextrose in balanced electrolyte solution mended in bradycardic newborn foals,
to the average 50-kg foal), particularly in
because the bradycardia is usually
the obviously compromised foal. This
secondary to hypoxia. Atropine can also
therapy is indicated to maintain blood
increase myocardi� oxygen debt if hypoxia glucose levels, resolve metabolic acidosis, is not corrected. Doxapram is not
and support cardiac output, because
recommended for resuscitation of
myocardial oxygen stores have likely been
newborns, because it does not reverse
depleted.

secondary apnea.

Immediately after birth; the foal must
adapt to independent thermoregulation.

Prematurity, Dysmaturity, and

In response to the catecholamine surge

Postmaturity
associated with birth, uncoupling of

Traditionally, prematur;ity in horses is
oxidative phosphorylation occurs within
defined as a birth at <320 days gestation.

the mitochondria, releasing energy as

However, normal gestation length ranges
heat. This nonshivering thermogenesis is
from 310 days to >370 days in some mares,
impaired in newborns undergoing
which makes it difficult to define maturity
hypoxia or asphyxiation, and in those ill
based solely on gestational age. Premature
at birth. Human infants born to mothers
foals are small, with a fine, silky hair coat,
sedated by benzodiazepines are similarly
generalized muscle weakness, joint and
affected, a consideration in the choice of
tendon laxity, incomplete cuboidal bone
sedative and preanesthetic medications
ossification, a domed forehead, and floppy
in mares with dystocia or undergoing
ears. Foals born post-term, but small, are
cesarean section. In addition to nonshivtermed dysmature. These foals may also ering thermogenesis, thermoregulation
exhibit the characteristic signs of
in the healthy foal is supported by a high
prematurity. Dysmature foals may have
metabolic rate, a thick hair coat, fat
been classified in the past as "small for
stores, and the ability to shiver within
gestational age" and are thought to have
minutes of birth. Heat losses by convecsuffered from placental insufficiency. A tion, radiation, and evaporation are quite
postmature foal is a post-term foal that has
high in most areas where foals are
a normal axial skeletal size but is thin to

EQUINE EMERGENCY MEDICINE

1727
emaciated. The hair coat is generally long,
exan1ined frequently for signs consistent
and the teeth may have erupted in utero.

with early sepsis or nosocomial infection.

Postmature foals are usually healthy foals

The GI system of these foals is not
that have been retained too long in utero,
usually functionally mature because of a

VetBooks.ir
perhaps due to an abnormal signaling of
primary lack of maturity or secondary to
readiness for birth. Postmature foals
hypoxia. Dysmotility and varying degrees
become more abnormal the longer they
of necrotizing enterocolitis are common,
are maintained in utero, and they may
as are hyperglycemia and hypoglycemia.

suffer from placental insufficiency. They

Hyperglycemia is generally related to
are most commonly born to mares
stress, increased levels of circulating
ingesting endophyte-infested fescue (see
catecholamines, and a rapid progression
p3017).

to gluconeogenesis, whereas hypoglyce

Prematurity, dysmaturity, and postmatumia is associated with diminished rity may all be associated with high-risk
glycogen stores, the inability to engage
pregnancy. Iatrogenic causes include early
gluconeogenesis, sepsis, and hypoxic
elective induction of labor (based on
damage. Endocrine function may be
inaccurate breeding dates) or interpretaimmature, particularly regarding the tion of late-term colic or uterine bleeding
hypothalamic-pituitary-adrenal axis, and
as ineffective labor. Most often, the cause is contributes to metabolic derangements.

idiopathic. Even if undetermined, the cause If possible, enteral feeding should be may continue to affect the foal after birth.

delayed until metabolic and cardiorespira

All body systems may be affected by
tory parameters are stable, and parenteral
prematurity, dysmaturity, and postmaturity, nutrition provided. When enteral feeding and thorough evaluation is necessary.

is initiated, small volumes should be

Respiratory failure is conunon in these
provided first and slowly increased
foals and is related to immaturity of the
throughout several days.

respiratory tract, poor control of respira

Musculoskeletal problems are frequent,
tory vessel tone, and weak respiratory
particularly in premature foals, and include
muscles, combined with poorly compliant
significant flexor laxity, periarticular
lungs and a greatly compliant chest wall. It
ligament laxity, and decreased muscle tone.

is usually not due to a surfactant deficiency. Premature foals frequently exhibit flexor Most foals require oxygen supplementation laxity combined with decreased cuboidal and positional support for optimal
bone ossification that predisposes them to
oxygenation and ventilation. Effort must be crush injury of the carpal and tarsal bones expended to maintain these "floppy foals"

if weight bearing is not strictly controlled.

in sternal recumbency. Some may require

Physical therapy, in the form of assi;;ted
mechanical ventilation.

standing and controlled exercise, is

These foals also require cardiovascular
indicated in the management of these
support but are frequently unresponsive to
problems; however, care should be taken
commonly used pressors and inotropes,
to ensure that the foal does not become
including dopamine, dobutamine,
fatigued and stand in abnormal positions.

epinephrine, and vasopressin. Careful

Splints and casts only increase laxity in the
use of these drugs and judicious IV fluid
limbs, although light bandages over the
therapy are necessary. Renal function,
fetlock may be necessary to prevent injury
reflected in low urine output, is often
if flexor laxity is severe. Glue-on shoes may
initially poor because of a delay in making
help improve the weight-bearing axis. If
the transition from fetal to neonatal
tube casts are used, they should not extend
glomerular filtration rates. The delay can
below the fetlock to minimize laxity, and
be due to true failure of transition or
they should be changed regularly to
secondary to a hypoxic or ischemic insult.

prevent sores. These foals are also

Fluid therapy should be used cautiously in
predisposed to angular limb deforn1ities
these cases; an initial fluid restriction may
and must be closely monitored for
be required to avoid fluid overload.

development of this problem as they

Many premature, dysmature, or
mature. Postmature foals may be affected
postmature foals have suffered a hypoxic
by flexural contracture deformities, most
insult and present with all of the disorders
likely due to decreased intrauterine
associated with perinatal asphyxia
movement as they increase in size. (See
syndrome, inducing neonatal encephalopa
also F'LEXION DEFORMITIES IN HORSES, p 1150.) thy (seep 2094). Treatment is similar to

The overall prognosis for premature,
that of tern1 foals with these problems.

dysmature, and postmature foals remains

These foals are also predisposed to
good with intensive care and attention to
secondary bacterial infections and must be
detail. Many foals survive and become

1728

EQUINE EMERGENCY MEDICINE
productive athletes. Complications
event at the time of birth, maternal illness,
associated with sepsis and musculoskeletal or any abnormalities in the foal. Although abnormalities are the most significant
the umbilicus is frequently implicated as

VetBooks.ir
indicators of poor athletic outcome.

a major portal of entry for infectious
organisms, the GI tract may be the primary

Neonatal Encephalopathy
site of entry. Other portals of entry include

A wide spectrum of clinical signs is
the respiratory tract and wounds.

associated with neonatal encephalopathy,

Early signs of sepsis include depression,
ranging from mild depression with loss
decreased suckle reflex, increased
of suckle reflux to grand ma! seizures.

recumbency, fever, hypothermia, weak

Affected foals are typically healthy at birth
ness, dysphagia, failure to gain weight,
but show signs of CNS abnormalities
increased respiratory rate, tachycardia,
within a few hours. However, the timing of
bradycardia, injected mucous membranes,
onset of clinical signs varies; some foals
decreased capillary refill time, shivering,
are obviously abnormal at birth, and some
lan1eness, aural petechiae, and coronitis.

do not show clinical signs until 24 hr of

Survival rates of foals treated for sepsis
age. Neonatal encephalopathy is comhave improved, but infection must be monly associated with adverse peripartum
recognized early for the possibility of a
events, including dystocia, placentitis,
good outcome. The pathogen involved
twinning, and premature placental
can also affect survival. Gram-negative
separation. However, some foals have
species are more commonly diagnosed,
no known evidence for the cause of the
but gram-positive septicemia is being
hypoxic event, suggesting that unrecogrecognized more frequently, and multiple nized in utero hypoxia occurred. (See
organisms may be involved. It is important
also p 2094.)

to identify the organism early in the course

Therapy for the various manifestations
of the disease. Blood cultures should be
of hypoxia and ischemia involves control
obtained, as well as samples from synovial
of seizures and cerebral edema; support
fluid, CNS, peritoneal fluid, urine, and
of cerebral perfusion; correction of
tracheal aspirates if localized signs are
metabolic abnormalities; maintenance of
present. Until antimicrobial sensitivity
normal blood gas values, tissue perfusion,
patterns for the pathogen involved are
and renal function; treatment of GI
obtained, broad-spectrum antimicrobial
dysfunction; prevention, recognition, and
therapy should be started. IV amikacin
early treatment of secondary infections;

(25-30 mg/kg/day, IV) and penicillin
and general supportive care. Seizures must (22,000-44,000 U/kg, IV, qid) are good be controlled, because they increase
first-line choices, but renal function must
cerebral oxygen consumption by 5-fold.

be monitored closely. Other first-line

Diazepam (0.1-0.44 mg/kg, IV) and
antin1icrobials include high-dose ceftiofur
midazolam (0.04-0.1 mg/kg, IV slow) can
sodium (2-10 mg/kg, IV, tid-qid) or
be used for emergency therapy,but the
ticarcillin/clavulanic acid (50-100 mg/kg,
foal must be monitored for respiratory

IV, qid).

depression. For severe or persistent

Failure of passive transfer should be
seizures, phenobarbital (2-3 mg/kg, IV,
treated, if present, with hyperimmune
bid-tid) or a constant-rate infusion of
plasma. Intranasal oxygen in.sufflation at
midazolam (2-5 mg/hr for a 50-kg foal)

5-10 Ilmin should be provided even if
may be instituted.

hypoxemia is not present, to decrease the
work of breathing and provide support for
the increased oxygen demands associated

Sepsis
with sepsis. Mechanical ventilation may be

Sepsis in foals can be quite subtle initially,
necessary in cases of severe respiratory
and the onset of clinical signs is variable
involvement seen witll acute lung injury or
depending on the pathogen involved and
acute respiratory distress syndrome. If the
the immune status of the foal. Common
foal is hypotensive, pressor agents or
pathogens include gram-negative bacteria,
inotropes may be administered by
although gran1-positive infections have
constant-rate infusion. Inotrope and
been identified. Failure of passive transfer
pressure therapy is generally restricted to
of immunity can contribute to development referral centers, where the infusions and of sepsis in foals at risk. The current
tile foal's blood pressure can be closely
recommendation is that foals have an IgG
monitored. NSAIDs are used by some
level >800 mg/dL for passive transfer to be
practitioners, as are corticosteroids in
considered adequate. Other risk factors for
specific circumstances. Use of tllese drugs
development of sepsis include any adverse
should be judicious, because they may

EQUINE EMERGENCY MEDICINE

1729
have several negative consequences,
hyperglycemic on low glucose infusion
including, but not limited to, renal failure
rates. These foals may benefit from
and gastric or duodenal ulceration.

constant-rate infusions of insulin.

Anti ulcer medications are controversial,

Recumbent foals must be exan1ined

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because critically ill, recumbent foals
frequently for decubital ulcers, corneal
typically have an alkaline gastric pH but
ulcers, and for heat and swelling associmay be useful once the foal is ambulatory.

ated with the joints and physes. Physical

Supportive care is important in
tllerapy or passive range of motion exercises
treatment of septic foals. Foals should be
should be provided.

kept warm and dry, and turned at 2-hr

The prognosis for foals in the early
intervals if recumbent. Every attempt
stages of sepsis is fair to good. Once the
should be made to keep the foal sternal to
disease has progressed to septic shock,
improve respiratory function and reduce
the prognosis becomes less favorable,
atelectasis. Feeding septic foals can be a
although short-term smvival rates are
challenge if GI function is abnormal; total
similar to those seen in human patients.

parenteral nutrition may be needed. If at

Long-term smvival and athletic outcomes
all possible, foals should be weighed daily
are fair. Racing-breed foals that make it
and blood glucose levels monitored
to tile track perform similarly to their
frequently. Some foals become persistently age-matched siblings.

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EXOTIC AND

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LABORATORY ANIMALS

AMPHIBIANS 1734

Environment and Husbandry 1734

Clinical Techniques 1 735

Infectious Diseases 1737

Noninfectious Disorders 1741

Emergency Care 17 42

Amphibians as Laboratory Animals 17 43

AQUACULTURE 1743

Production Methods 1744

Production Medicine and Biosecurity 17 45

Necropsy and Diagnostic Techniques 17 46

The National Aquatic Animal Health Plan 17 4 7

Reportable Diseases and Regulatory Concerns 1747

Therapeutic Considerations 1748

Infectious Diseases 1753

Parasitic Diseases 1755

Bacterial Diseases 1757

Mycotic Diseases 1761

Viral Diseases 1761

AQUATIC SYSTEMS 1766

Types of Aquatic Systems 1766

Aquatic Life Support System Components 1767

Equipment Needed for Aquatic System and Water Analysis 1768

Environmental History 1769

Environmental Diseases 1769

Environmental Considerations for Selected Infectious Diseases of Fish 1778

AQUARIUM FISHES 1779

Fish Families 1781

Management 1784

Nutritional Diseases 1798

Parasitic Diseases 1799

Bacterial Diseases 1809

Mycotic Diseases 1811

Viral Diseases 1812

Neoplasia 1814

1732

EXOTIC AND LABORATORY ANIMALS

BACKYARD POULTRY 1815

Physical Examination 1815

Management 1816

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Laying and Reproduction 1818

Vaccination 1819

Common Management-related Diseases 1819

Common Infectious Diseases 1821

FERRETS 1824

Management 1824

Infectious Diseases 1824

Neoplasia 1826

Endocrine Disorders 1827

Other Noninfectious Diseases 1828

HEDGEHOGS 1828

Management 1829

Diseases 1831

LABORATORY ANIMALS 1836

Regulatory Requirements 1836

Animals Used in Research 1838

Management of Laboratory Animals 1839

Colony Monitoring 1841

LLAMAS AND ALPACAS 1844

Management 1844

Reproduction 1848

Herd Health 1850

Diseases 1851 .

MARINE MAMMALS 1856

Management 1856

Environmental Diseases 1857

Nutrition and Nutritional Diseases 1859

Bacterial Diseases 1861

Mycotic Diseases 1863

Parasitic Diseases 1865

Viral Diseases 1867

Neoplastic Diseases 1870

MINK 1870

Management 1870

Bacterial Diseases 1871

Viral Diseases 1872

Prion Disease 1874

Nutritional Diseases 1874

Poisoning 1875

Miscellaneous Diseases 1875

EXOTIC AND LABORATORY ANIMALS

1733

NONHUMAN PRIMATES 1876

Bacterial Diseases 1878

Mycotic Diseases 1880

Parasitic Diseases 1880

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Viral Diseases 1882

Nutritional Diseases 1883

Miscellaneous Conditions 1883

Psychological Well-being and Environmental Enrichment 1884

PET BIRDS 1885

Management 1885

Pediatric Diseases 1892

Bacterial Diseases 1896

Mycotic Diseases 1899

Parasitic Diseases 1904

Viral Diseases 1907

Geriatric Diseases 1912

Neoplastic Diseases 1915

Nutritional Diseases 1917

Reproductive Diseases 1920

Toxicoses 1924

Traumatic Injury 1925

Miscellaneous Diseases 1925

POTBELLIED PIGS 1929

Management 1929

Reproduction 1931

Feeding and Nutrition 1932

Diseases 1933

RABBITS 1937

Management 1937

Housing 1941

Nutrition 1943

Bacterial and Mycotic Diseases 1944

Viral Diseases 1950

Parasitic Diseases 1952

Noninfectious Diseases 1954

RATITES 1960

Management 1960

Reproduction 1962

Chick Management 1964

Infectious Diseases 1964

Parasitic Diseases 1965

Digestive System Disorders 1965

Musculoskeletal Disorders 1966

Toxicities 1966

Trauma 1966

1734

EXOTIC AND LABORATORY ANIMALS

REPTILES 1967

Management 1968

Bacterial Diseases 1991

Mycotic Diseases 1993

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Viral Diseases 1994

Parasitic Diseases 1996

Environmental Diseases and Traumatic Injuries 1999

Metabolic and Endocrine Diseases 2000

Reproductive Diseases 2001

Neoplastic Diseases 2002

RODENTS 2002

Chinchillas 2003

Gerbils 2011

GuineaPigs 2014

Hamsters 2021

Mice and Rats as Pets 2025

Mice and Rats as Laboratory Animals 2032

SUGAR GLIDERS 2035

TASMANIAN DEVILS 2043

ZOO ANIMALS 2046

Management Practices 2046

Preventive Medicine 2047

Clinical Care Programs 2048

Common Disorders and Procedures 2052

VACCINATION OF EXOTIC MAMMALS 2054

AMPHIBIANS

The class Amphibia is composed of
change, food availability, and habitat loss,
three orders: Anura (frogs and toads), the
combined with anthropogenic stressors,
largest with >3,500 species; Caudata
such as exposure to pesticides, fertilizers,

(salamanders, newts, and sirens) with -375
heavy metals, nitrogenous wastes, and
species; and Gymnophiona ( caecilians)

acidification, likely increase an1phibian
with -160 species.

susceptibility to disease, contributing to
the large population losses documented in

ENVIRONMENT AND
recent years. As ectotherms, amphibians

HUSBANDRY
them10regulate by shuttling back and fort.h
between different temperatures in their

Captive an1phibians require proper
environment. The range of temperatures
environmental conditions to remain healthy. necessary for proper metabolism, called Natural stressors, including temperature
the preferred optimal temperature zone

AMPHIBIANS

1735

(POTZ), varies among species. Metabolism,
emit biologically active ultraviolet-B
including the regulation of immune function

(280-320 nm) is recommended to prevent
and digestion, can be adversely affected if
metabolic bone disease. Bulbs must be
animals are kept at temperatures outside
chai1ged every 6--8 mo or according to the
of their POTZ. Infectious diseases and
manufacturer's specification.

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malnutrition are common problems in

Longte1m maiJ1tenai1ce of most captive
tropical amphibians kept at suboptimal
an1phibians requires live food. Although
temperatures.

most adult terrestrial and aquatic ainphib

Amphibians require moisture to prevent
ians feed on inve1tebrates, including
desiccation. Aquatic amphibians may be
eaithwonns, bloodwonns, black worms,
accommodated in aquariums with approwhite wonns, tubifex worms, springtails, priate areas for swimming. Terrestrial
fruit flies, fly larvae, mealwom1s, ai1d
amphibians need a shallow container of
crickets, some ai11phibians feed on
water in the enclosure. Moisture may also
vertebrates and require live minnows,
be provided by incorporating small streams,
guppies, goldfish, or neonatal mice or rats.

watelfalls, or ultrasonic humidifiers into

Vitan1in and mineral supplements are
enclosures, or by misting frequently witl1 a
necessary to prevent nutritional disease.

spray bottle. Because an1phibians have a

These ai·e commonly administered by
semipem1eable skin that readily absorbs

"gut loading" insects, using commercially
potentially ham1ful substances, the water
available diets high in calciw11 or by coating
must be clean and free of toxins such as
insects with powdered multiple-vitan1in
chlo1ine, anm1onia, nitrite, pesticides, and
preparations t11at include vitat11in 03 and
heavy metals. Chlorine can be removed
calcium (also known as "dusting").

from tap water by placing the water in a

Bleach (30 mL'L of water) can be used
barrel and circulating it through a carbon
to disinfect tools and housing materials.

filter for �24 hr before use. Some numicipal

A n1inin1w11 of 30 n1in of contact tune is
water supplies may include chloran1ines.

recommended, after which the tools should

The chloramine bond must be split with
be thoroughly rinsed with fresh water and
specific dechlo1inizing agents, after which
preferably dried before use. Several sets of
water can be filtered to remove the chlorine.

tools should be kept on hand when working

External canister filters or tmder-gravel
with more than one colony of a.J.1Unals.

filters help maintain water quality in tank

Hwnidifiers and spray bottles must be
waterfalls, strean1s, and ponds.

disinfected weekly to remove potentially

Substrates that can be used include
pathogenic bacteria, includingPseudo
gravel, soil, sphagnum moss, and mulch.

rnonas spp and Aerornonas spp.

Gravel should be either too large to be
swallowed or small enough to be easily

CLINICAL TECHNIQUES
passed in the feces. Soils with chemical
additives such as fungicides must not be

All possible routes of escape from the
used. Substrates such as sphagnum moss,
examination room, such as ventilation ducts
untreated hardwood mulches, and leaf litter
and sink drains, should be blocked before
can be used, but cedar and pine mulches
handling ainphibians. Recommended
have toxic oils and should be avoided. Some
supplies include a mist bottle containing
an1phibians cannot tolerate low pH and may
dechlorinated water, which can be used to
develop skin iJTitation if they come into
keep amphibians moist when handled, dip
contact with peat moss and sphagnun1
nets, a small aiJ· pump with airline and aiJ·
moss. Heating soils to 200°F for 30 n1in is
stone, a water quality test kit, a small room
reconu11ended to kill aithropods, such as
hwnidifier, tryptic soy broth blood culture
trombiculid mites, and heln1inth pai·asites.

vials, the anesthetic tricaine methane

Freezing substrates at <32°F also effectively sulfonate, and a microliter syringe.

removes many infectious organisms.

Fme-tipped culture swabs, glass slides,

Adequate ventilation (1-2 fresh air
coverslips, scalpel blades of vaiious sizes,
changes/11r) is needed to prevent disease in
ai.1 assortment of needles and syringes,
ainphibians. Live plants are recommended
sterile red-rnbber tubes, and ste1ile saline
furnishings for terrestrial an1phibians as
should also be readily accessible.

they purify the air, remove organic wastes in

The history should include a description
the soil, filter light, generate hurniclity, and
of the animal's diet and appetite; environprovide hiding and perching places. Aquatic mental conditions of the a.J.1Unal's habitat,
plants oxygenate the water, remove nitroincluding humidity, temperature, water genous waste, provide hiding places, and ai·e quality measures, and lighting regin1en; often a source of nutrition for larval amphibsocial structure and reproductive status; the ians. Full-spectrum lighting using bulbs that
recent introduction or loss of animals; and

1736

AMPHIBIANS
the use of medications. Problems noted
indicate respiratory disease. Rhabdias spp, by owners should be described in detail. A
a nematode that has a direct life cycle, is a
review of food and water quality records is
conunon cause of respiratory infections in
useful to identify important trends. A water
captive an1phibians. Eggs or larvae may

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san1ple from the animal's enclosure should
sometimes be detected in oropharyngeal
be analyzed for anm10nia, nitrite, pH,
mucus. Ocular lesions are often detected
hardness, alkalinity, and copper using a
and may include cor\jtmctival, corneal,
sin1ple test kit readily available from most
iridal, and lenticular changes. Corneal
pet stores. Owners must take and record air
diseases, including nonspecific keratitis
and water temperatures at the time of water
and lipid keratosis, are common. Corneal
collection.

scrapings are easily collected for cytologic

Before handling, the animal's body
exan1ination. Panophthalmitis and uveitis
condition, agility, posture, and behavior
are associated with systernic or localized
should be noted. Parasitic or microbial
infection. A sample of aqueous or vitreous
infections, malformation, or nutritional
humor can be collected with a small-gauge
deficiencies may cause asymmetry. Loss of
needle for cytology and for bacterial and
muscle mass commonly occurs as a result
ftmgal culture. Coelomic palpation may
of improper nutJ.ition, improper environdetect retained egg masses, bladder stones, mental temperatures, or chronic disease
foreign bodies, or neoplasms. Hydrocoelom

( eg, mycobacteriosis, chromomycosis,
and subcutaneous edema ( anasarca and
microsporidiosis). Neurologic impairment
ascites) are common and may be caused by
may be detected by first watching the
lymph heart failure; cardiac failure; renal,
animal move about its enclosure and then

GI, or hepatic disease; neoplasia; microbial
assessing its response to the introduction
infection; parasitism; toxicosis; improper
of stimuli. Neurologic in1pairment may
environmental conditions; or other
also be suspected if an an1phibian is unable unknown factors. Collection of fluid for
to maintain equilibrium or exhibits an
biochemical analysis, cytologic evaluation,
abno1mal swinuning pattern. When
and culture for bacteria and fungi is
handled, most normal an1phibians attempt
reconunended. Blood collected from the
to escape, withdrawing lin1bs that are
ventral abdmninal vein, lingual vein,
grasped. Placed upside down, most species
femoral vein, coccygeal vein, or by cardiac
will attempt to tight themselves. Touching
puncture and placed into lithium heparin
the eyes typically elicits a blink reflex or
can be used for hematologic evaluation. A
withdrawal of the globe.

vollllne equal to 1%of the body weight of a

A cool, bright light and magnification
healthy amphibian and 0.5% of the body
are required when perfon11ing a physical
weight of a sick amphibian may be taken.

examination. The mouth can be opened

Normal values have not been established for
using the edge of an index card, a plastic
most species of amphibians. Urine may be
card, or a rnbber spatula. The color of the
collected for analysis from those anurans
mucous membranes should be evaluated
that urinate when first restrained. Fecal
and any lesions noted ( eg, retrobulbar
samples uncontan1inated by environmental
ir\jllly, orogastric intussusception).

organisms may be collected from species

Ulcerations, erythema, hemorrhage, and
such as dart frogs by feeding the animal just
pigment loss in the skin may indicate poor
before placing it on a clean, moist paper
husbandry, tJ.·aun1a, or infections (microbial
towel. Direct and float exan1inations are
or parasitic). Improper substrate or
useful to identify protozoa and metazoa.

sanitation leading to bacterial and fungal

Treat111ents are administered orally,
infections can cause lesions on the feet.

topically, or by ir\jection. Oral acln1inistra

Touch preparations or skin scrapings of
tion requires furn restraint and opening the
affected areas are easily made and can be
mouth with a piece of waterproof paper or
stained with Wright-Giemsa and Gram
thin piece of plastic ( such as a credit card).

stains for cytologic evaluation. Heart rate

Guitar picks, which come in a variety of
can often be determined by watching the
thicknesses, work well. Small an1phibians
skin overlying the xiphoid or using a
can be dosed accurately using a microliter
hand-held 8-MHz transcutaneous Doppler
syringe. Many drugs may be administered
system. Because pulmonic respiration (if
topically; the skin of most amphibians will
present) depends on positive-pressure
absorb drugs directly. Some drugs, such
ventilation from buccal plllnping, respiraas eru·ofloxacin, may be irritating, and tory rate should be assessed by watching
alternative routes may be preferable.

the rapid movements of the intern1andi

Treatments may also be delivered topically
bular space. The nares should be free
by placing the amphibian in a medicated
of obst111ction from mucus, which may
bath. Bubble wrap or other nonabrasive

AMPHIBIANS

1737
material placed strategically over the
and recoveries are long. lntracoelomic
amphibian may be needed to keep it in
injections of propofol at a dosage of 35-45
contact with the solution. Injections are
mg/kg body wt will also provide sedation
typically given intracoelomically, into the
to anesthesia.

lymph sacs, or intravenously.

INFECTIOUS DISEASES

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Anesthesia: Anesthesia may be required
for further examination or for diagnostic

Bacterial Diseases: "Red-leg" syndrome and surgical procedures. Response to
commonly refers to the hyperemia of the
anethesthics depends on individual
ventral skin that accompanies systemic
health and species of the animal. Tricaine
infection in amphibians. Saprophytic,
methanesulfonate, ketamine hydrochlogran1-negative bacteria such as Aeromonas, ride, propofol, halothane, isoflurane,

Pseudomonas, Proteus, and Citrobacter
and sevoflurane may be used. Routes of
spp typically cause reel-leg. Viruses, fungi,
administration include immersion bath,
and other pathogens may cause similar
topically, or parentally. Inhalant anesthetlesions. Ventral hyperemia is a nonspecific ics are typically used topically or via an
sign and may also be seen with toxicosis.

immersion bath, because they are readily

Malnourished, newly acquired amphibians
absorbed through the skin. Larger an1phibthat are maintained in poor-quality water ians can be intubated and maintained on
or other inappropriate environmental
anesthetic gas. Parental anesthetics are
conditions are particularly susceptible.

typically injected IV, IM, intracoelomi

Clinical signs include lethargy; emaciation;
cally, or into the dorsal lymph sac. Injeculcerations of the skin, nose, and toes; tions into the rear limbs are avoided
and characteristic cutaneous pinpoint
because of the presence of a renal-portal
hemorrhages of the legs and abdomen.

system. Heart rate can be monitored in

HemotThages may also be seen in the
most an1phibians using an ultrasonic
skeletal muscles, tongue, and nictitating

Doppler positioned over the heart. A
membrane. In acute cases, these signs may
baseline heart rate should be established
be absent. Histologic evidence of systemic
before initiating anesthesia. Because
infection may include inflammatory or
amphibians can breathe through the
necrotic foci in the liver, spleen, and other
skin, observing gular movement is less
coelomic organs. Blood or, if present,
rewarding. Tricaine methanesulfonate is a
coelomic fluid, should be taken for culture
fine white crystal that is highly soluble in
before beginning therapy. Individuals
water. It can be prepared and stored as a
can be treated initially with enrofloxacin
l O g/L stock solution, which is diluted just
before use. Administration is by bath,
because most amphibians will absorb
tricaine through the skin. The dosage
used for many large amphibians is 2-3 g/L
for induction. For short procedures,
the amphibian should be immediately
removed and rinsed with fresh water. For
longer procedures, the amphibian may
be placed into a maintenance solution of

100-200 mg/L after it has been induced. In
smaller amphibians, an induction dosage
of 100-200 mg/L is safer. Aeration must
be provided in the anesthetic solution
to avoid hypoxia. Tricaine produces an
acidic solution that must be buffered to
a pH of -7 using sodium bicarbonate,
sodium hydroxide, or sodium hydrogen
phosphate. Isoflurane gas can also be
bubbled into an anesthetic bath placed in
a sealed container; this will allow both
percutaneous and inhalation absorption.

Ketamine hydrochloride injected
percutaneously or into the dorsal lymph
sac at a dosage of 75-125 mg/kg body wt

Red-leg syndrome in two leopard frogs. The
larger frog is more severely affected.

can be used; however, a surgical plane of

Courtesy
of Research Animal Diagnostic Laboratory, University of anesthesia can be difficult to maintain,

Missouri.

1738

AMPHIBIANS

(5-10 mg/kg/day, PO or IM), oxy1etracycline

Fungal Diseases: Many of the fungi that

(50 mg/kg, PO, bid), or chloramphenicol
infect amphibians are difficult to distinguish

(50 mg/kg, PO, bid) before receiving culture
grossly because they produce sinillar
and sensitivity results. If fungal infection
clinical effects, including lethargy and skin
is suspected, a 0.01% itraconazole bath
ulcerations. Some fungi can be identified via

(3.5 L fresh water mixed with 35 mL
the examination of a wet mount prepared
itraconazole solution; 5 min/day for 8 days)

from a skin scraping, whereas others

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may be effective.

require culture, histology, and special stains.

Mycobacteriosis, caused by acid-fast

Treatment includes proper hygiene and the
bacilli, including Mycobacteriumfo1·
use of topical or systemic anti.fungal agents
tuitum, M marinum, M chelonea.,
such as itraconazole. Other anti.fungal drugs

M abscessus, M avium, M szulgai, and
such as fluconazole may also be effective.

M xenopi, is found principally in debilitated ChytJ.idiomycosis is the most serious
amphibians. Although often an infection of
fungal infection in amphibians and has been
the integument, ingestion of infectious
implicated in tl1e decline of wild and captive
organisms may also lead to GI disease and
frog, toad, and salamander populations
systemic infection. Affected amphibians
around tl1e world. The causative agent,
may exhibit gray nodules in the skin, liver,

Batrachochytrium clendrobaticlis (Bd), is
kidneys, spleen, lungs, and other coelomic
a nonhyphal zoosporic fw1gus identified in
organs. Infected an1phibians may eat well
specin1ens preserved as far back as 1938,
but still lose weight. Acid-fast bacilli may be
yet it was not until tl1e 1990s that tl1e
detected in feces and oropharyngeal mucus.

organism was associated with large losses

A premortem diagnosis can be made by findof Australian frogs. Chytrids are typically ing acid-fast bacilli in animals with external
found in moist environments, where tl1ey
lesions. Culture of mycobacte1ia requires
feed on decomposing organic matter or are
special media such as Lowenstein-Jensen
parasitic to plants and inve1tebrates.

agar (cultured at 23°, 30°, and 37°C) but is

Amphibians are the only known vertebrate
frequently unsuccessful. In cases in which
host for chytrid fungi. Postmetamorphic
staining is inconclusive, confirmation using
anurans are affected far more than caudates

PCR is recommended. Treatment is not
or larval amphibians. Tadpoles are usually
recommended for this potentially zoonotic
subclinical, because Bel infects only tissues
disease, and euthanasia should be
tl1at contain keratin. Anuran larvae have
considered.

keratin only in their mouthparts, which

Chlamydiosis is a serious infection of
may become depigmented and sometimes
amphibians. Based on histologic lesions
damaged. Most caudate larvae do not have
and the presence of inclusion bodies, these
keratinized mouthparts. As larvae undergo
infections were originally attributed to
metamorphosis and their skin becomes

Chlamydia psittaci. Using molecular
keratinized, Bd can spread over the animal,
methods such as PCR, it has since been
infect tl1e stratun1 comeun1 of tl1e epidershown that other species of Chlamydia mis, and cause mortality. The "drink patch,"

have been associated with these infections,
specialized skin located in the ventral pelvic
including C pneumoniae, C abo1·tus, and
region lliat absorbs water, and tl1e digits are

C siiis. Chlamydia spp nave also been
especially affected. Diagnostic san1ples
found in apparently healthy frogs, which
are best taken from these regions for this
raises the question of whether these
reason. Because patl1ogenicity of Bd appears
animals are a reservoir or vector for these
to decline above 25° -27°C, it is speculated
infectious organisms. The disease was
that some amphibian populations living at
originally recognized in a mass mortality
higher elevations have disappeared because
of African clawed frogs (Xenopus laevis)

of tl1e cooler temperatures associated with
fed uncooked beef livers. Infected frogs
tl1e winter montl1s and possibly climate
may die peracutely or exhibit lethargy,
change. Altl1ough the exact mechanism
dysequilibriurn, cutaneous depigrnentaof infection is unknown, Bd causes skin tion, petechiae, and edema. Histologically,
hyperkeratosis and subsequent sloughing,
intracytoplasmic basophilic inclusion
osmoregulatory disruption, electrolyte
bodies can be identified in sinusoidal lining
disruption, and cardiac arrest. Infection
cells of the liver and spleen. Secondary
intensity (>10,000 zoospores) appears to be
bacterial infections are frequently present
associated witl1 mortality. Some amphibin affected an1phibians and must be treated ians, including tl1e bullfrog (Rana catesbei
appropriately. Antibiotic treatment, including ana) and the African clawed frog (Xenopus doxycycline (5-10 mg/kg/day, PO) or oxyte
laevis) are less susceptible to Bd and may
tracycline (50 mg/kg/day, PO), may be
serve as reservoirs for the disease. Mobile
effective against chlamydia! infection.

zoospores contribute to the loss of whole

AMPHIBIANS

1739
populations of amphibians. Clinical signs

Chromomycosis is caused by pign1ented
include abnormal posture, anorexia,
or black fu.ngi from several genera ( eg,
lethargy, dehydration, hyperemia, excessive Cladosporium, Fonsecaea, Phialophora, shedding of skin, pupillary miosis, and

Ochroconis, Rhinocladosporium, and
muscle incoordination. These signs may

Wangiella ). These fu.ngi may be fou.nd in
be mild to absent in infected caudates,
organic substrates such as topsoil and

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emphasizing the in1portance of performing
decayi.ng plant matter. Disease is either
diagnostic tests. Visualizing the spherical,
cuteaneous or disseminated systemic;
single-celled organisms in skin scrapings
both have been seen in captive and wild
stained with Wright-Giemsa or Gram stains
populations of an1phibians. Signs may
using a light microscope is diagnostic, but
include anorexia, weight loss, granulomathe organisms are not always readily seen.

tous skin lesions or ulcers, coelomic

Real-time PCR performed on swabs of the
distention, and neurologic disease.

i.ntegmnent or pieces of skin is diagnostic

Diagnosis is usually made postmortem by
and provides rapid assessment of presence
finding disseminated granulomas with
and quantity of zoospores. This is useful in
pigmented fu.ngal cells and hyphae. Culture
screening and management of amphibian
is frequently u.nsuccessful; histopathology
populations at risk, such as those tmdergomay be necessary to confirm tl1e diagnosis.

ing transp01t or quarantine. On histopathol

Treatment using itraconazole (10 mg/kg/day,
ogy, zoosporangia containing zoospores

PO, for 30 days) may be given, but the
are associated with hyperkeratosis and
prognosis is poor once the infection is
u.nderlying dermal infection. Treatment
disseminated.

includes the topical administration of

Zygomycosis, caused by fu.ngi of the
itraconazole (0.01% bath for 5 min/day for
class Zygomycetes (Mucor spp, Basidi

10-11 days) and maintaining animals well
obolus sp, and Rhizopus spp), affects within their normal them1al range. The use
both wild and captive populations of
of terbinafine (0.01% bath buffered using
anurans. Clinical signs include lethargy
bicarbonate to a pH of 7.2-7.4 for 5 min/day
and multifocal hyperemic nodules with
for 5 days) may also be effective. If approprifungal growth on the ventrum. Disease ate for the species, raising environmental
progresses rapidly and results in mortality
temperatm-es for captive populations to
within 2 wk. Zygomycetes are fou.nd in the

>23°C may help halt the i.nfection while
environment, especially soils and decaying
medicated baths are used to eliminate Bd.

matter, and are a normal component of the

Systemic antifungal drugs appear to be
an1phibian's GI tract. Successful treatment
ineffective in treating this infection of the
has not been reported, but advanced
epidermis. Bd is a World Organization for
antifungal agents may be tried.

Anin1al Health (OIE) notifiable disease.

Mesomycetozoans are fungus-like

Saprolegniasis refers to disease caused
microrganisms at the animal-furrgal
by several genera of opportunistic fungi
boundary. Those reported in the literature
or "water molds" that infect the gills and/or to infect amphibians include Amphibio
skin of aquatic and larval amphibians. When
lhecum (previously Dermosporidium),
in water, newly affected animals appear to

Amphibiocystidium, and Ichthyopho
have a whitish cotton-like growth on their
nus; however, continued molecular
skin. As the fu.ngal mat ages, it may become
characterization of these organisms is
greenish due to the presence of algae. Once
ongoing, resulting in nomenclature
removed from water, the fu.ngal mat
changes and taxonomic reorganization.

collapses and is difficult to see. Other signs

Amphibiothecum and Amphibiocyst
include lethargy, respiratory distress,
idium are spore-forming organisms that
anorexia, and weight loss. Skin ulcerations
typically produce a nonlethal infection in
may occm· as the infection progresses. A
anurans. Clinical signs include multifocal
diagnosis of saprolegniasis is made by
nodules and pustules, usually on the
finding hyphae and the thin-walled
ventrum, that resolve in 4-8 wk. Microzoospores in a skin scrape. Treatment with scopically encysted spores contain large
a malachite green dip (67 mg/L for 15 sec,
cytoplasmic vacuoles. Jchlhyophonus is
once daily for 2-3 days) or copper sulfate
pathogenic to salamanders and frogs

(500 mg/L for 2 min, once daily for 5 days,
living in the eastern half of the USA. Prethen once weekly u.ntil healed) may be and post-metamorphic life stages are
effective. Treatment of eggs with methylene
infected. Clinical signs include muscle
blue may be effective. Secondary bacterial
swelling in the thigh, rump, and tail
and parasitic infections may be present in
and may appear nodular, especially
animals with dermal ulcers. Poor water
in tadpoles. Debilitation may lead to
quality conditions should be c01Tected.

mortality, especially in adults. Diagnosis

1740

AMPHIBIANS
is based on histopathology or finding

Fecal samples collected by placing the
characteristic spores through microamphibian on clean, moist paper towels scopic examination of material from the
helps to prevent contamination from
lesions. There is no treatment other than
free-ranging protozoa. Cloacal wash, gill
supportive care.

clips, and skin scrapes are also diagnostic.

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Treatment using metronidazole is often

Parasitic Diseases: Many of the protozoa
effective for external and GI organisms.

and metazoa found in and on amphibians

Sporozoans such as coccidia (Eimeria and
are not associated with disease unless the

Isospora) and microsporidians (Micro
host amphibian is stressed or imrnunocom
sporidium, Pleistophora, and Alloglugea) promised. Recently caught or transported
may be incidental findings or parasitic.

an1phibians are particularly susceptible

Clinical signs are nonspecific and include
to parasitism, as are those kept in poor
poor body condition and wasting. Myxozoa
hygienic conditions and outside their
occasionally cause disease in an1phibians

POTZ. Parasites with indirect life cycles
and result in specific host/disease agent
tend to die out when wild-caught
lesions. Treatment efforts are focused on
amphibians are brought into captivity if the providing supportive care.

intermediate or final host is not present.

Metazoa parasites include myxozoa,

Conversely, infections by parasites with a
helminths, and arthropods. Myxozoa
direct life cycle may be magnified in a
infections in an1phibians generally do
closed environment. Excellent hygiene is
not cause mortality. Helminths that are
essential for parasite control and includes
pathogenic to amphibians include tremathe routine removal of sloughed skin, fecal todes (Ribeirola, Clinostomum) and
material, uneaten food, and carcasses from
nematodes (Rhabdias, Strongyloides,
animal enclosures.

Pseudocapillaroides ). Arthropods, such as

External parasites may be found by
the common fish parasitesArgulus and
close examination of an1phibians using

Lernaea, may infect amphibian aquatic life
magnification and a bright, cool light. A
cycle stages, whereas ticks and mites affect
skin scrape or biopsy may be required to
postmetamorphic terrestrial aninlals. Larval
identify parasites causing nodules or
dipterid flies may consume an1phibian eggs
epidermal lesions. Internal parasites are
and embryos and feed on the tissues of
often identified tluough examination of
adults. 'I\vo of the most significant
fresh fecal samples. Some small frogs are
metazoan infections in captive amphibians
translucent enough to allow the
are caused by Rhabdias sp and
visualization of nematodes using

Pseudocapillaroides xenopi.

transillumination. In some cases,

Rhabdiasis, caused by the lungworm
metazoan and protozoan parasites are

Rhabdias sp, commonly causes pulmonary
fom1d only at necropsy. Finding flagellates,
damage and secondary infections in
ciliates, and opalinids in the feces is
captive an1phibians. This nematode has a
nonnal and does not require treatment in
direct life cycle with free-living phases.

healthy amphibians. Although many larval

Adult worms live in the lungs, where they
nematodes found in the feces are
deposit larvated eggs that are coughed up,
nonpathogenic, treatment is reconunended swallowed, and then excreted into the because pathogenic and nonpathogenic
environment. Infective L
species cannot be readily distinguished.

3 larvae then
burrow through the skin of a new host,

Most protozoans found in the GI tract,
where they mature and migrate to the
including ciliates, opalinids, and flagellates, lungs. Affected animals may appear are commensals. The ciliate Tetrahymena,
anorectic, thin, and generally debilitated. A
although norn1ally nonpathogenic, has been premortem diagnosis may be made by associated with mortality of salamanders.

finding ova or worms in oral and nasal

Trichodinids may be found in the urinary
secretions. Infection should be suspected
bladder or on the skin of amphibians and
when nematode larva and larvated eggs are
require treatment. Hemoflagellates are
found in fresh feces from an animal with
occasionally found and generally
clinical signs. When rhabdiasis is suspected,
nonpathogenic but can result in anemia.

treatment using fenbendazole (100 mg/kg/

Greater-thannonnal loads of GI flagellates
day, PO, for2 days then repeated 12-14
and other protozoa may be found in
days later) or ivern1ectin (200-400 mcgfkg,
debilitated an1phibians and require

PO, once, repeated 12-14 days later) is
treatment aimed at restoring balance and
recommended. After the second of each
not eliminating the protozoa. External

2-day fenbendazole treatment or each dose
dinoflagellates
of ivermectin, the anin1als should be moved

( eg, Piscinoodinium) and flagellates
into a newly established environment to

( eg, I chthyobodo) can cause significant
mortality, especially in larval amphibians.

AMPHIBIANS

1741
prevent reinfection from free-living life
swimming behavior, swelling of the limbs
stages. Some reactions to fenbendazole
or body, edema, hydrocoelom, erythema,
have been reported, so animals should be
ventral skin hemorrhage ( especially in
monitored closely and treatment discontinthe hind region), and occasionally skin ued if necessary.

ulcerations. Lesions may appear very

The capillarid nematode Pseudocapillar
similar to those of bacterial dermatoseptice

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oides xenopi buffows into the skin and is
mias. The original viral lesions may be
known to affect colonies of the aquatic
overwhelmed by secondary invaders, and

African clawed frog. Signs include
many outbreaks of "red-leg" may have had
discoloration, roughening, pitting, and
underlying and undiagnosed viral infection.

ulceration of the skin. As the infection

Death typically results from multiple organ
progresses, lethargy, anorexia, and skin
failure. Amphibian larvae undergoing
sloughing occur. Diagnosis is made by
metamorphosis or recently metamorphosed
finding small, white nematodes beneath the
juveniles seem to be most susceptible to
mucus on the skin; skin scrapings may show infection. For this reason, mortality events larvae and ova. Treatment by adding
often occur in the spring/summer. Survivors
thiabendazole (0.1 g/L) to the water may be
appear to acquire some immunity to future
effective. Levamisole and other anthel.mininfections. Diagnosis is made using PCR, tics may also be effective. Frequent water
primary cell culture, and/or microscopy.

changes with removal of shed skin

Ranaviruses can persist in the aquatic
containing the parasite are required to
environment without a host for weeks,
prevent the amplification and spread of
which contributes to their ability to infect
infection to cage mates.

naive amphibian populations and emphasizes the need for biosecurity measures Viral Diseases: Renal adenocarcinomas
when transporting amphibians or working

(Lucke tumors), caused by ranid herpesviin envirorunents where the virus exists.

rus-1, are relatively common in leopard

Disinfection using bleach (1%) and
frogs (Rana pipiens) wild-caught in the
chlorhexidine (0. 75%) are effective.

northeastern and north central USA. Few

Ranavirus disease is notifiable to the World
frogs with tumors are seen in the summer,

Organization for Animal Health (OIE).

because viral replication is temperaturedependent. Virus particles and intranuclea.r NONINFECTIOUS DISORDERS
inclusion bodies are seen when frogs are in
hibernation, at 41 ° -50°F (5° -10°C).

Nutritional Diseases: Metabolic bone

Metastasis of the tumor to liver, lungs, and
disease is frequently seen in amphibians
other organs is common; both the primary
consuming nonsupplemented invertebrates.

and metastatic tumors can become very

Except for earthwmms, most invertebrates
large. There is no treatment. The neoplasm
used as food have an inverse
is a model of herpesvirus-induced cancer.

calciurn:phosphorus ratio. This results in

Ranaviruses, which are DNA-based
mandibular deformity, long bone fracture,
viruses in the genusRanavirus, family
scoliosis, and eventually tetany and
lridoviridae, have been identified as the
bloating. Diagnosis is made radiographically
cause of mass mortality in wild populations
by finding thinning cortices of long bones,
of anurans and caudates across the world.

mandibular and hyoid bone defonnities,

Environmental conditions, reservoir
pathologic fractures, and in severe cases, GI
species, persistence in the environment,
gas. Treatment includes correcting tl1e diet
direct and indirect transmission, stress, and
and administe1ing calcium glubionate
host immunity contribute to the impact of

1 mL/kg/day, PO, for 30 days. Full-spectrum
ranaviruses on amphibian populations.

lighting with biologically active ultraviolet

Species of Ranavi?'us that infect amphib

B light should be provided. Vitamin D3 can
ians include frog virus 3 (FV3) and FV3-like
also be administered in severe cases. Starvaviruses, Bohle iridovirus, andAmbysloma tion, resulting in weight loss, lethargy, and
tigrinum virus. These viruses are highly
dehydration, must be treated by providing
virulent and may produce 900/<r-lOOOA,
proper nutrition through assist feeding.

mortality in tadpoles and adults. Transmis

Thiamine deficiency is seen in amphibsion occurs through exposure to contamiians fed frozen fish containing thiaminase.

nated water or soil, contact with infected

Clinical signs include tremors, seizures,
individuals, and consumption of infected
and opisthotonos. Initial treatment is the
tissues. Fish and reptiles (especially turtles)

administration of thiamine at 25-100 mg/kg,
are reservoirs for ranaviruses. Clinical signs

IM or intracoelomic, followed by thiamine
are nonspecific, develop rapidly in a large

25 mg/kg body wt, PO, with each meal.

nwnber of cohorts, and include abnormal

Thiamine deficiency can be prevented by

1742

AMPHIBIANS

Neoplasia: Spontaneous neoplasia occurs
in most organ systems but is rare except
when caused by pollutants or an infectious
agent, such as the virally induced Lucke renal
carcinoma that affects populations of
northern leopard frogs (see above) or

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epidermal papillomata in the Japanese
firebelly newt. Witl1 increasing longevity in
captivity and better health care, it is likely that
more cases of neoplasia will be identified.

Trauma: Traumatic injuries are common in
captive an1phibians and include lacerations,
bone fractures, internal bleeding, desiccation, and the loss of digits, limbs, or tail.

Rapid assessment followed by supportive
care is required for a successful outcome.

Desiccation is common in an1phibians that
escape their enclosure or do not receive
proper care. For smaller amphibians

( <30 g), most fractures can be managed
conservatively with cage rest. For larger
amphibians, the use of external or internal
fixation may be beneficial. Pain management must be considered in traumatic cases.

The presence of opioid receptors suggests

As metabolic bone disease in amphibians
using opioids may be beneficial (buprenoradvances, pathologic fractures of the long phine, 0.02 mg/kg, IM, SC, or PO). NSAIDs
bones are readily seen on radiographs.

may also be used (meloxicam, 0.2 mg/kg)

Courtesy of the National Aquarium.

and appear to provide pain relief.

EMERGENCY CARE
routinely supplementing diets with 250 mg
thiamine/kg of fish fed.

Initial emergency support includes

The carotenoids, including vitamin A, are
providing fluid therapy, oxygen, and an
not synthesized by amphibians and must be
environment of proper temperature and
provided through diet. Excessive levels of
hwnidity. Placing the aninlal in a shallow
vitanlin A have been hypothesized to
bowl of isotonic or slightly hypotonic fluid
interfere with vitamin D metabolism and
enables transdermal uptake. Equal parts
contribute to metabolic bone disease,

2.5% dextrose in 0.45% sodiwn chloride and
whereas deficiency has been associated
lactated Ringer's solution is effective.

with lethargy, wasting, aRd inability to

Coelomic, IV, or interosseus fluids may be
use the tongue to catch prey due to the
given by bolus to larger animals at 5--10 mll
development of squamous metaplasia of the
kg. In the absence of known exposure to an
tongue (short tongue syndrome). Treatment
organophosphate, seizuring animals should
includes providing vitamin A supplementabe treated for hypocalcemia ( calcium tion and force feeding a proper diet.

gluconate, 100 mg/kg, IM, IV, SC, or

Obesity is a disease. Overfeeding is the
intracoelomic, once or twice daily),
primary cause of obesity; many amphibian
organophosphate toxicity (atropine, 0.1
species will continue to consume prey as
mg/kg, SC or IM as needed), and thiamine
long as it is available and without regard for
deficiency (vitamin B, 25--100 mg/kg, IM
their energy needs. The oversized fat bodies
or intracoelomic as needed). If sepsis is
may be palpated within the coelomic cavity;
suspected, antibiotic administration ( eg,
however, in females, ultrasound may be
enrofloxacin 5--10 mg/kg/day, PO, SC, IM,
necessary to differentiate enlarged fat bodies
or intracoelomic) should be initiated.

from egg masses. Treatment for active

Treatment for tramnatic injuries is directed
species includes enlarging the size of the
at minimizing blood loss, providing fluid
enclosure to allow increased activity.

therapy and respiratory support ( doxapram

Maintaining the amphibian at the upper end

5 mg/kg, IM or IV as needed), and reducing
of its POTZ will accelerate metabolic rate and pain (buprenorphine 0.02 mg/kg, IM, SC, or increase caloric use. Reducing caloric intake

PO, or meloxicam 0.2 mg/kg), followed by
also may be used to control weight.

corrective therapy.

AQUACULTURE

1743

AMPHIBIANS AS LABORATORY
after all ani.n1als appear satiated to avoid

ANIMALS
fouling the tank. Handling and research
protocols should be developed to minimize

Amphibians have long been used as
stress to the animals. Overcrowding must
laboratory animals. In an effort to enable
be avoided to maintain sanitation, prevent
scientific research while maintaining
disease transfer, and reduce social stress.

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humane and ethical principles, the 8th

Most aquatic species used for laboratory
edition of The Care a.nd Use of Laboratory
studies are kept in large, recirculating

Animal.s (National Research Council,
systems that have multiple tanks using a

National Academies Press, 2011) provides
common water supply. Water is filtered, sent
organizations conducting research on
to individual tanks, and then returned for
animals, including aquatic animals, with
filtration and disinfection. Proper water
information regarding environment,
quality is maintained using one or more
housing, management, and veterinary care.

types of filtration. These include a

This guide should be consulted when using
mechanical filter to remove suspended
amphibians in research. (See al.so LABORAwaste material, a biofilter to convert TORY ANIMAIB, p 1836.) Species that are captive
nitrogenous wastes to less toxic comborn and readily available from commercial pounds, and a chemical filter to remove
suppliers include the African clawed frog
dissolved organic compounds. The addition

(Xenopus laevis, X tropicalis ), the African of an ultraviolet sterilizer to inactivate
dwarf frog (Hymenochirus boettgeri), the
microorganisms is highly recommended.

fire-bellied toad (Bombina orientalis ), the Bulbs must be kept clean and changed every
axolotl (Ambystoma mexicanum), and the

&-8 mo for the ultraviolet sterilizer to
tiger salamander (A tigrinum ). Wild-caught remain effective. Ozone, a potent oxidant, species collected by researchers or vendors
may also be used with caution to remove
for use in the laboratory include tl1e
suspended organic material and potential
northern leopard frog (Rana pipiens, somepathogens from the water.

times called the grass frog), bullfrog (R

Anunonia toxicosis is common in systems
catesbeiana), cane toad (Bufo mminus,
that have not established a good biofilter.

sometimes called the marine toad), and the

Amphibians exposed to inappropriate levels
mud puppy (Necturus maculosus ). Other of ammonia typically produce excess

North American ranid frogs are sometimes
mucus, become dull in color, and attempt to
used. When collecting or importing
escape. Amphibians should be removed
amphibians, it is important to abide by state
from the contanli.nated water and rinsed
laws and obtain all required permits.

thoroughly with dechlorinated and well

Pelleted diets are available for some
oxygenated fresh water. A diagnosis can be
aquatic species, like African clawed frogs,
confirmed if the source water has anllllonia
bullfrogs, and axolotls, making it easier to
at levels >0.5 ppm, although toxicity can be
feed large groups. These foods must be
seen at levels >0.1 ppm for some species.

stored in a cool, dry location to maintain

Many tropical fish stores sell test kits that
freshness. Uneaten food should be removed
check for ammonia.

AQUACULTURE

Aquaculture is the production of marine and
and the USA's at $1 billion. Within the USA,
freshwater organisms under controlled
major commercial commodities include
conditions. Hundreds of different species of
channel catfish, centered around the
aquatic animals are raised in aquaculture

Mississippi Delta; rainbow trout in the
and include fish and aquatic invertebrates
north/northwest, including Hagennan
cultured for food, tl1e aquarium hobby, bait,

Valley, Idaho; Atlantic salmon in the Pacific
recreational fisheries, research, private
northwest and Atlantic northeast; aquaiiurn
ponds, and stock enhancement of wild
fish with production centered in Florida;
populations. Animal aquaculture was valued baitfish in Arkansas; and goldfish and koi at $137. 7 billion (USD) worldwide in 2012,
production scattered throughout the USA.

with China's production valued at $66 billion In addition, other public and private entities,

1744

AQUACULTURE
including research facilities, public aquaria,
aquaculturists who wish to include in-line
and hobbyists, are breeding nwnerous other
disinfection of system water. UV sterilizers
species.

act optin1ally at a wavelength of 254 nm and
disrupt pathogen DNA. Systems with tl1ese
components typically include a system

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PRODUCTION METHODS
bypass loop to feed a portion of total system
water into these disinfection tmits. UV

Aquaculture production methods vary
sterilizing wtits must be designed and rated
greatly, but regardless of method, a good
to deliver a specific "zap dose" to target a understanding of water quality and
specific pathogen or pathogen group.

chemistry, species requirements, and

Component maintenance, water clarity,
systems design and operation will facilitate
wattage, and water flow through the UV
good management. Production can be
sterilizer all contribute to the efficiency of
divided into two major categories:

the wtit. Although tl1ere are exceptions,
land-based and open-water systems.

in general the larger and more complex a

Land-based facilities use tanks and ponds
pathogen is, the greater the zap dose required
to house and raise fish. Tank systems can
to kill it. Ozone wtits use ltighly reactive 03
be flow-through, in which continuous
to break apart microorganisms. However,
replenishment of"new" water comes from a
because ozone can be very ha.imful to fish,
well, reservoir, or other central water body;
it must be removed from the water before
recirculating, with reuse of system water
it is retw11ed to the system. Ozone is also
after filtration to remove nitrogenous wastes a hwnan health hazard, so protocols to and dissolved and suspended particulates;
safeguard hwnan health should be impleor a combination of the two. Indoor, mented. See also AQUATIC SY&'TEMS, p 1766.

land-based tank systems afford much

Pond systems include ea.ithen and lined
greater control over water quality, predaponds typically filled from wells, aquifers, or tors, and pests than outdoor facilities, but
swiace water bodies. Ponds have minimal
often house fish at much higher densities.

water exchange and rely on good manage

Design and management of recirculating
ment of their more "natttral" systems to
aquaculture systems (RASs) requires
maintain acceptable water quality and
greater technical knowledge than for
control aquatic weeds, algae, and other pond
flow-through systems (see Southern
life. Nitti.fying bacte1ia a.i·e found on swiaces

Regional Aquaculture Center [SRAC]

in the pond. Important key water quality

Fact Sheet 4708 [https://srac.tamu.edu]).

pa.i·an1ete�xygen, carbon dioxide, and

Most RASs typically incorporate biologic
pH-can va.i-y widely throughout the day
filtration and mechanical filtration
in a pond because of photosynthesis by
components, although some also include
phytoplankton (algae) and otl1er plant life.

some type of chemkal filtration and in-line

During the day, photosynthesis increases
sterilization. Biologic filters rely on the
oxygen levels. However, during the evening,
establishment of two sets of nitrifying
when photosynthesis has ceased, oxygen is
bacteria on biofiltration surfaces to
conswned by all orga.Ilisms in the pond,
transform ammonia, a by-product of protein
including algae and higher plants, resulting
and nucleic acid metabolism by fish from
in lower levels. At the san1e time, increased
food, first into nitrite (a toxic intermediate),
production of ca.i·bon dioxide (without
and then into nitrate, considered a much
consun1ption through photosynthesis)

less toxic compound (although levels of
results in lowe1ing of pH. During the day,
nitrate may be problematic for inve1tebrates these trends are reversed. Any a.im11onia and, at higher levels, fish). More advanced
levels in a pond will have increased toxicity
systems include a denitrification compoas pH 1ises throughout the day. Other nent that transforms nitrate into nitrogen
challenges in pond production include pests
gas that is released into the atmosphere.

a11d predators, such as snails, otters, birds,

Mechanical filters remove particulates to
a.inphibians, and reptiles, as well as nontarget
reduce their negative effects on water
fish, all of which can also act as reservoirs or quality and fish health, and to improve water vectors for pathogens or intennediate hosts.

clarity, which facilitates observations.

See also AQUATIC SYSl'EMS, p 1766.

Chemical filtration is used to change the

Charmel catfish, tilapia, hybrid striped
concentration of specific ions or combass, shrimp, crawfish, baitfish, and pounds in the water ( eg, ion-exchange
orna.inental fish are raised in ponds, tanks,
resins such as those used in softeners
or a combination of the two. Some species,
to remove calciwn, or zeolite to bind
including rainbow trout, require higher
an1111onia). Ultr·aviolet (UV) sterilization
oxygen concentr·ations and a.re raised in
w1its and ozone are conunon choices for
land-based raceways.

AQUACULTURE

1745

Open-water aquaculture includes

Populations can vary from several individuals
production in net pens or sea cages placed
to mil.lions, with many facilities averaging
in oceans, bays, lakes, or reservoirs. Openthousands to hundreds of thousands within water systems rely on good flushing, dilution,
any given defined population.

and natural processes occurring within the

Biosecurity underlies critical fish health

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given water body to maintain acceptable
management practices for disease prevenculture parameters. In many cases, tion and management (see SRAC Fact Sheets
land-based systems are used for reproduction 4707, 4708, and 4712 [https://srac.tamu.edu/
and early life-stage growoutfor "open water
index.cfm/viewA!lSheets/]). Good biosecu-
aquaculture" species. Open-water systems do 1ity will minimize the risk of introduction have a number of challenges. Water quality in
and spread of an infectious disease into and
the main body of water cannot be controlled.

witl1in a facility, as well as n1inirnize the risk

Access (by boat in many cases) and logistics
that diseased animals or infectious agents
are more complex because of location within
will leave the facility and spread to other
a larger body of water. Biofouling (growth of
sites. Major biosecurity goals include good
algae, bacteria, other invertebrates) on nets
animal management, obtaining and
can reduce water exchange and degrade
maintaining healthy stocks through good
water quality with.in the net or cage. Pests
sourcing and husbandry, pathogen
and predators can be more difficult to
management, and people management
control, as can human theft or vandalism.

through education and awareness for staff

Disease management is also more complex
and visitors. See also mosEcumTY, p 2068.

because of increased environmental
restrictions in natural water bodies and

Animal Management: Eggs and animals
treatment logistics ( eg, modifications such as
should be from a reputable supplier, and

"tarping" (placing a large polyethylene liner anin1als should be screened for speciesover or under a net to hold water for specific health paran1eters and diseases of
temporary bath/in1mersion treatments).

concern. Previous testing and other relevant

Open-water systems are used for final
histo1ical and husbandry infomrntion should
grow-out stages of clams, oysters, mussels,
be obtained for any lots of fish entering a

Atlantic salmon, flounder, pompano, cobia,
facility. New fish should undergo quarantine
and other marine species. Production of
to prevent spread of disease. Water quality,
some freshwater species ( eg, tilapia) may
other environmental conditions ( such as
also use net pens set in lakes, ponds, or
choice of holding units, density, water flow,
reservoirs for growout.

lighting, and sound), and nutrition should be
optimized for the facility's goals and species.

PRODUCTION MEDICINE AND

Pathogen Management: Water source is

BIOSECURITY
a major risk factor for disease introduction,
with protected water sources (ie, sources

General veterinary approaches in aquaculthat do not have fish or other potential ture parallel those for other production
pathogen reservoirs) having low to zero risk
animals, such as large animals and poultry.

of carrying diseases of concern. Examples of

When working with fish, disease prevention
protected water sources include those from
is always more rewarding than treatment.

deep wells or disinfected municipal supplies.

Once fish are sick, accurately identifying

Protected water sources are preferable to
all present problems can be difficult, and
unprotected sources, such as surface waters
treatment must be administered early in
from a lake or river. Risks from unprotected
the course of an epizootic to be effective.

sources can be mitigated ( eg, through filtra

A comprehensive progran1 of fish health
tion, UV sterilization, chlorination, and/or
management should be based on tl1e
ozonation) to make them safer.

principles of good husbandry and biosecurity.

Efforts to maintain as clean an environ

Good husbandry practices, including water
ment as possible, including minin1al
quality, systems management, and nutrition,
accumulation of organic debris, proper disinfacilitate health and prevent disease.

fection of nets and equipment, and thorough

Consequences of poor husbandry are
disinfection of fish-holding units between
magnified in production aquaculture because groups of fish, help rnininuze disease of the greater size and density of populations
outbreaks by optimizing water quality and
in a production setting than in a hobbyist or
reducing pathogen loads and reservoirs (see
aquarium display system. Population health
below). Familiarity with common diseases
is the focus ( although valuable broodstock
for a given species, as well as potential
may warrant individual care), with prevendisease reservoirs and relevant diagnostics tive medicine of critical in1portance.

and control are important. Some pathogens,

1746

AQUACULTURE
such as the bacte1iaAeromonas hydrophila
products are strong oxidizers, and precauand the ciliated protist Trichodina, are tions listed on the label or relevant Material
considered ubiquitous and oppo1tunistic,

Safety Data Sheet should be followed when
whereas others may result in significant
handling them. A 1-hr contact time at 200
morbidity and mmtality ( eg, Streptococcus
mg/L will destroy most organisms of concern,
spp or Amyloodinium ), and/or have
including most viruses. Bleach should not be

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regulatory consequences ( eg, infectious
used in closed areas containing live fish,
salmon anem.ia or spring viremia of carp, a
because the volatile compound may get into
foreign animal disease in the USA).

the solution and kill fish in nearby tanks.

Quarantine of new fish at temperatures

My co bacteria are refractory to bleach
permissive for significant diseases will
disinfection because of their waxy cell wall.

facilitate detennination of presence of

Spraying equipment and contact smfaces
specific pathogens. Isolation of diseased
with alcohol after treatment with bleach
populations, use of equipment dedicated to
should etlectively eliminate mycobacteria,
a specific group, and system and equipment
although access to some smfaces ( eg, PVC
sanitation and disinfection are important
pipework) and associated biofilms may be
methods of pathogen management.

difficult. In these instances, it is understood
that major reduction in pathogen nm11bers

People Management: Important
is the key goal. Another commonly used
components of a good biosecurity program
aquacultme disinfectant, Virkon® Aquatic
include owner and staff education, aware

(active ingredient 21.4% potassiun1
ness, and commitment to p1inciples of
peroxymonosulfate and l.5% sodium
biosecurity. Written protocols and rules for
chloride), is highly effective at 1 o/o-2% concenworkers and facility visitors help solidify trations and considered much less toxic to
understanding and accountability. Increasfish (manufacttu-er directions must be ingly, facilities are making the effort to
followed). Quatemaiy ainmonimn comdevelop written biosecurity, health managepom1ds such as Rocca!® and benzalkoniwn ment, and disaster management plans.

chloride ai·e also excellent disinfectants and

Interested veterinarians should be familiar
can be used at concentrations of 500 mg/L for
with aquacultme systems and be able to
l hr, but residual films should be 1insed off
evaluate these protocols, as well as staff and
completely. Both Virkon Aquatic and
visitor adherence to them through general
quaternaiy ai1m1011iw11 compow1ds ai·e more
biosecmity audits.

suitable for net dips and net disinfection.

Cleaning and Disinfection: Proper

NECROPSY AND DIAGNOSTIC
cleaning and disinfection are critical

TECHNIQUES
components of a good fish health management program. There are a number of good For information on fish physiology, see
references for cleaning and disinfection in

AQUARIUM f1SHES, p 1779. General methods for
aquaculture settings (see SRAC Fact Sheet
clinical evaluation of aquacultmed species

4707: Biosecu1ity in Aquacultme, Part 1,
are similar to those used in aquai·ium fish.

Tables 1 and 2 [https://srac.tarnu.edu],

However, for more structmed smveillance
and Guide to Using Drugs, Biologics, and
and pathogen testing, more wufonn and

Other Chemicals in Aquacultme, Table 5
standard methods may be required.

[ www.fws.gov/fisheries ]).

OIE-accepted diagnostic methods for

Cleaning and disinfection of tanks and
reportable diseases are desc1ibed in The
equipment starts with general cleaning and

Manual of Diagnostic Tests for Aquatic
removal of dirt and organic debris. Organic

Animals (also known as the OIEAquatic
debris, including biofilms, and dirt can

Manual (www.oie.int]). Another good
shield pathogens from disinfection. Liquid
reference with standards for necropsy and
household bleach (3"/o-6% NaHClO) delivered diagnostics is The American Fisheries at 35 ml/gal. of water creates a concentration

Society Fish Health Section Blue Book (2014
of 200 mg/L. Granular bleach (HTH, calcium

Ed.) Suggested Procedures for the Detection
hypochlorite) is more stable than household
and Identification of Certain Finfish and
bleach and is often used on commercial

Shellfish Pathogens ( www.afs-fhs.org).

farms. It is available in three different concen

Depending on the specific goals for testing
trations: 15%, 50%, or 65% available chlorine.

( disease diagnostics, health certification,

The target dose of chlorine for disinfection is
smveillance) and on the ultimate recipient of

200 mg/L for at least 1 hr. This concentration
any testing results ( eg, another state agency
can be achieved by mixing 1.4 g of the 15%
vs another country), one or both provide
product/L of water, 0.4 g/L of the 50"A, product, excellent infonnation on methodology. Most or 0.32 g/L of the 65% product. These
veterinaiy practitioners will require

AQUACULTURE

1747
additional laboratory suppo1t for more
in state regulations regarding importation of
advanced diagnostics ( eg, virology,
aquatic animals. The State Veterinarian or
hlstopathology, bacte1iology). Therefore, it is

State Aninlal Health Officer is the ultin1ate
important that the laboratory is qualified and,
resource for inf01mation on state anin1al
for USDA-APHIS relevant documentation,
health regulations.

approved by the USDA-APHIS to run specific

Currently, USDA-APHIS has adopted the

VetBooks.ir
diagnostic tests for aquaculture species.

reportable disease list of tile OIE ( www.oie.

int) as reportable in the USA ( see TABLE 6, THE NATIONAL AQUATIC
p 1786). If a USDA-APHIS reportable disease

ANIMAL HEALTH PLAN
is suspected, appropriate samples should be
collected as per the OIE Aquatic Manual.

The U.S. National Aquatic Animal Health

Practitioners should stay informed of

Plan (NAAHP) (www.aph.is.usda.gov) was
changes in the status of diseases of regulatory
developed to facilitate the legal movement
concern, because they are liable if they have a
of all aquatic animals, their eggs, and
case that is not reported. Regulated fish
products in interstate and international
diseases of greatest concern to aquatic
commerce; protect the health and thereby
animal veterinarians in tl1e USA include koi
improve the quality and productivity of
herpesvirus, spring virernia of carp, and viral
fam1ed and wild aquatic animals; ensure the
hemorrhagic septicemia. Notification of
availability of diagnostic, inspection, and
reportable aquatic diseases should be made
ce1tification services; and minimize the
directly to the State Veterinarian and to the
in1pact of diseases when they occur in

USDA Area Veterinarian in Charge.

fanned or wild aquatic animals. The NAAHP
is a federal guidance document intended to

Health Certification: A major role of the
help direct federal, state, and tribal efforts
aquaculture veterinarian is health certificain the areas listed above. Work is ongoing to tion of many anin1als leaving a facility.

continue to refine and implement relevant

Movement of animals may be intrastate,
and urgent aspects of the NAAHP.

interstate, or international. Specific testing

USDA-APHIS is the lead federal agency
and general health requirements for aquaculfor commercial aquaculture and the proture exports vary according to region, state, tection of aquatic animal health. See the
country, and species. In some instances,
focus on fish health Web site (www.aphis.

only a visual inspection is required, whereas
usda.gov/focusonfish/) for useful links to
in others statistically determined sample
access additional information on the
sizes and more standardized diagnostic

USDA-APHIS aquaculture progran1.

methods are necessaiy. Level of required

The OIE sets the standards for members
oversight also varies. Some countries
of the World Trade Organization with regard
require only evaluation and signature by
to detemlination of internationally
a licensed veterinarian, whereas others
reportable diseases and their management,
require the oversight and acknowledgeand monitors these diseases with the ment of the national competent authority.

cooperation of member nations (see the

USDA-APHIS is the competent autl1ority for

Aquatic Anin1al Health Code [ www.oie.int]). commercial aquaculture in the USA and provides information on specific import/

REPORTABLE DISEASES AND
export requirements by country ( www.

REGULATORY CONCERNS
aphis.usda.gov). For importing countries
requiring USDA-APHIS oversight, veterinar

With increased regulation of ornamental
ians must be licensed to practice in the
and aquacultured fish in the USA, th.ere are

USA and obtain veterinary accreditation
additional needs for professional veterinary

(Category 2 accreditation is required for
services, including USDA health certificaaquaculture) through USDA-APHIS for tion (see below) for movement of animals.

evaluation of aquaculture species.

Implementation of the NAAHP should

USDA-APHIS is also tasked to protect
more clearly define the role of veterinary
aquaculture in the USA from foreign disease
practitioners in the future. USDA-APHIS
introduction. For facilities within the USA
provides voluntary training to practitionthat import fish, USDA-APHIS determines ers who wish to work in this area and is
health requirements for incoming shipdeveloping a special aquatic certificate for ments, with fish, crustacean, molluscan,
accredited veterinarians. Information on
and ainphibian diseases of concern listed
federal regulations pertaining to fish
by the OIE currently considered reportable
medicine is available at www.aphis. usda.

by USDA-APHIS; however, not all of these
gov. State law may be more restrictive than
are progran1 diseases with specific actions
federal law, and there is significant variation required for positive cases.

1748

AQUACULTURE

THERAPEUTIC CONSIDERATIONS
inforn1ation on the status of drugs and
chemicals, particularly those intended for

Although improvement of water quality,
aquaculture use. In addition, the FDA has
nutrition, and other general husbandry
listed several compounds as being of "low
factors may be enough to improve the health
regulatory concern." These compounds,

VetBooks.ir
of a population, chemotherapeutics al'e often although not fully approved, are considered required to ameliorate disease outbreaks.

innocuous enough for use in food fish. Of

Management of fish diseases is challenging
these, salt is the most important. A few
because of basic logistics, including the
compow1ds, including copper sulfate and
aquatic environment, numbers offish, and
potassiwn permanganate, are not FDA
routes of administration, and also because of
approved but ai·e legally available for limited
the pharmacologic and regulatory complexiuse in food fish as part of a supplementary ties of chemotherapeutic usage in fish.

FDA data collecting process as lnvestiga

One major point of confusion among
tional New Animal Drugs. For more
vete1inarians, more critical because of
infonnation, see https://srac.tainu.edu/
impacts on the aquatic environment, is the
index.cfm/eventlviewAIISheets/, specifically
difference between a drug and a pesticide.

the link for SRAC Fact Sheet 4 709 (lnvestiga

Drugs are regulated by the FDA, whereas
tional New Animal Dmg [lNAD] Exemptions
pesticides are regulated by the Envirorunental
and the National INAD Program [NIP]).

Protection Agency (EPA). According to the

Anotl1er category is drugs on the Index of

Federal Food Drug and Cosmetic Act

Legally Marketed Unapproved New Animal
definition, tl1e term "drug" can be defined four Dnigsfor Minor Species (tl1e Index). Fish ways: 1) articles recognized in tl1e official
are considered by the FDA to be a minor

United States Pharmacopoeia, official
species. The process of placing drugs on the

Homoeopathic Pharmacopoeia of tl1e United

Index involves the use of an expert panel

States, or official National Formulary, or any
and is intended to increase legal access
supplement to any of them; or 2) articles
to unapproved drugs intended for nonintended for use in tl1e diagnosis, cure, food-producing minor species (including
mitigation, treatment, or prevention of disease non-food fish) and non-food early life stages in man or other anin1als; 3) ai1icles ( other than of food-producing minor species ( www.fda.

food) intended to affect the structure or aiw
gov). Currently, the only two fish drugs on
function of the body of man or other animals;
the Index are AquacalmTM (metornidate),
and 4) ai1icles intended for use as a compoa fish sedative/anesthetic, and Ovaprirn®
nent of any of the aforementioned articles.

(GnRH + domperidone), a spawning aid also

The EPA regulates water and effluents and
used to "spawn out" egg-bound females
controls tl1e use of pesticides against "pests."

under some conditions. See TABLE 1 for

A "pest" is defined by the Federal Insecticide, a sun1rnary of the approval status and

Fungicide and R0denticide Act (FIFRA) as
withdrawal times of drugs used in aquacul

"any insect, rodent, nematode, fungus, weed" ture in the USA. Practitioners are encow0
or "any other fonn of ten-estrial or aquatic
aged to visit the FDA Web site frequently
plant or anin1al life or virus, bacteria, or otl1er for t.he most cun-ent information.

microorgal1ism ( except viruses, bacteria, or

Finally, a nwnber of compounds that are
other microorganisms on or in living man or
not FDA approved are used in pet fish
other living animals)."

practice under controlled conditions. These

Legally, a drug is a compound that works
drugs have no legal status and have no place
in or on the fish, whereas a pesticide works
in food anin1al praceice. A term forn1erly
in tl1e water. Challenges occur for one of
used by the FDA, "regulatory discretion,"

two reasons: 1) certain pathogens, and in
has fallen out of favor, but it does provide
particular some parasites, including tl1e
some explanation of the FDA:s current
fish louse A 1:gulus spp and anchorworm
approach to use of unapproved, non

Lernaea spp, have life stages off the host
lndexed drugs. The primai-y concerns are
and in the envirorunent; ai1d 2) certain
degree and magnitude of impact on human
compounds, such as copper and diquat, ai·e
and enviroru11ental safety, and regulatory
legal pesticides but are also drugs effective
action against any illegal use will be
against some patl1ogens.

weighed against tl10se two measmes (see
www.fda.gov for additional guidance).

FDA-approved Drugs, Indexed Drugs,

In addition to being aware of FDA
concerns, fish practitioners should be

Pesticides, and Regulatory Concerns
familiai· witl1 environmental regulations for

FDA-approved therapeutic options for fish
drugs and pesticides. Federal and state
ai·e limited but increasing. The FDA Web site
envirorunental regulations are of greatest

(www.fda.gov) is the best resomce for basic
importance when treating outdoor ponds.

AQUACULTURE

1749

Considerations include potential for entry

Antibiotics
of treated water into natural water bodies
or the water table and potential effects to

Aquaflor® is an approved medicated feed
nontarget species. Compounds labeled
containing florfenicol for use against
pesticides are regulated in the USA by the
specific pathogens in enteric septicemia

EPA and therefore cannot be used under

(Edwardsiella iclaluii) in channel catfish, VetBooks.ir
extra-label drug use provisions regulated by
coldwater disease (Flavobacteiium
the FDA (ie, these compounds cannot be
psychrophilum) in salrnonids, furunculosis
used in a manner beyond their specific label, (Aeromonas salmonicida) in freshwaters which would have to include an aquatic use
reared salmonids, streptococcal septicemia
section).

in freshwater-reai·ed warrnwater finfish,

Three FDA-approved antibiotics are
and colunmaris disease (Flavobacteiium
currently available for use in aquacultured
columnare) in freshwater-reared finfish.

food fish in the USA. Some of these

It is mai·keted as a VFD product. This
products can be useful in ornan1ental fish,
broad-spectrum antibiotic has excellent
especially koi; however, extra-label use
efficacy against many grat11-negative
of FDA-approved medicated feeds is not
bacteria and gran1-positive streptococci,
permitted under current law. Recognizing
although as a VFD drug extra-label use
the need to deliver some medications in
is forbidden. However, as discussed, for
a medicated food for fish, the FDA has

INAD data collection purposes, use may
indicated that it would not normally
be permitted in otller species and for other
consider regulatory action against a
indications in certain situations. The
veterinarian using medicated fish food in
witlldrawal time is 15 days.

an extra-label manner if the following

Oxytetracycline dihydrate (Teffaillycin®
criteria are met: 1) the extra-label use is

200 for Fish) is an in-feed medication
for treatment of a minor species as defined approved 1) to control mortality in freshby federal law; 2) in an aquatic species, the water-reared salrnonids due to cold water
use of medicated feed in an extra-label
disease associated withF psychrophilum,
manner is limited to products approved

2) to control mortality in freshwateHeai·ed
for use in other aquatic species; and 3) a
rainbow trout due to colwnnaris disease
valid veterinarian-client-patient relationassociated with F columnare, ai1d 3) to ship is clearly established.

mark skeletal tissue in Pacific salmon. All

Veterinaiians should also be fan1iliar with
approved uses require a21-day wiU1clrawal
tlle Veterinary Feed Directive (VFD). This is
period for haivest-size food fish species.

of particular interest to practitioners in rural

Onnetoprirn sulfadimethoxine (Romet-
ai·eas, who may be asked to write prescrip30®) is an in-feed treatment approved by tlle tions for aquacultured fish. For a veterinar

FDA to control furunculosis (A salmoni
ian to issue a VFD order, there must be a
cida) in salmonids, for which a42-day
valid veterinarian-client-patient relationwithdrawal period is required, and to ship, and tlle veterinai·ian must have
control enteric septicemia of catfish (E icta
exainined the fish ai1d identified a bacterial
luri) in channel catfish for which a 3-day
disease that would be treatable witll tlle
withdrawal period is required. Romet-30

VFD drug (eg, florfenicol). Extra-label use
can be used extra-label as long as there is a
of tlle VFD drug, including use for species
veterinarian-client-patient relationship and
or patllogens not indicated on tlle label, is
veterinary oversight.

prohibited by law. However, VFD drugs may

Hydrogen peroxide 35% (Perox-aid®) is
be legally accessible through enrollment in
administered by immersion and is FDA
the appropriate INAD (see above).

approved for use in finfish to control

A small group of compounds have been
bacterial gill disease (caused by F
designated by the FDA as "high regulatory
branchiophilum) in salmonids, external
priority," meaning their use is likely to
columnaris ( caused by F columnare) in
result in enforcement action. These drugs
freshwater-reared coolwater fmfish and
either have human or environmental safety
catfish, and fungal infection (saprolegniaconcerns or are related to compounds sis) of freshwater-reared finfish eggs.

considered critical for human health and

These are common external infections
disease. The most important of these
in fish that may follow handling or be
compounds are chlorainphenicol, the nitroassociated with high organic load or furans, fluoroquinolones and quinolones,
other water quality perturbations for the
steroid hormones, and malachite green.

affected species. Hydrogen peroxide is

These compounds should never be used in
used as a short-term, continuous-flow
food animals for any reason, and their use
bath. Treatments are administered daily
in nonfood species is discouraged.

or on consecutive alternate days for three

1750

AQUACULTURE

DRUGS USED IN AQUACULTURE IN THE US A - APPROVAL

S TATUS A ND WITHDRAWAL TIMES

Active Ingredient

Trade Name

Generic Use

Florfenicol

Aquaflor®

Antibiotic

VetBooks.ir

Oxytetracycline dihydrate

Terra.rnycin-200® Antibiotic

Onnetoprim sulfadimethoxine

Romet-30®

Antibiotic

Hydrogen peroxide (35%)

PEROX-AID®

Antimicrobial (gills and skin
only)

Chloramine-T

HALAMID Aqua® Antimicrobial (gills and skin
only)

Diquat

Reward®

Herbicide

Antibiotic (gills and skin
only)

Fom1alin

Fonnalin-f'l'M

Parasiticide (gills and skin

Fom1alin-B
only)

Parasite-S®

Copper sulfate (CuS04)

Parasiticide (gills and skin
only)

Potassium permanganate (KMn04)

Parasiticide (gills and skin
only)

Diflubenzuron

Di.rnilin®

Parasiticide ( external
crustaceans)

Tricaine methanesulfonate

Tricaine-S®

Anesthetic

Eugenol

Aqui-S20E®

Anesthetic

Metomidate

Aquacalrn®

Sedative

Chorionic gomidotropin

Chorulon®

Spawning aid
sGnRHa + domperidone

Ovaprim®

Spawning aid
treatments. An initial bioassay is

Other Chemotherapeutic Drugs
recommended before treating a large
group of fish. Paddlefish are sensitive, and

Formalin: Formalin is FDA approved
use of hydrogen peroxide is not recomfor use in finfish and penaeid (saltwater) mended. Other sensitive species include
shrimp. Several brands have received FDA
northern pike, pallid sturgeon, and in
approval for aquaculture use. Methanol may
some instances, walleye. Hydrogen
be added to formalin products as a preservaperoxide can be used extra-label, and tive. "Pure" JO()OA,formalin is, technically, experimental use has been attempted in
water saturated with -37%--4()0A, formaldeother species and for other indications, hyde gas. Formalin eliminates protistan
including as a parasiticide (see UF/IFAS
parasites and monogeneans from the

EDIS publication Use of Hydrogen
external surface of fish. It also has some

Peroxide in Finjish Aquacultiire [http://
efficacy against external fungal infections.

edis.ifas.ufl..edu/fal57]). There is no

It can be used as a prolonged bath at
required withdrawal ti.me after treatment
concentrations of 15-25 mg/L. The lower
with Perox-aid®.

concentration is recommended for pond

AQUACULTURE

1751

DRUGS USED IN AQUACULTURE IN THE USA - APPROVAL

STATUS AND WITHDRAWAL TIMES (continued) Application Method

Approval Statusa

Withdrawal 'lime

Medicated feed

FDA approved" (Veterinary 15 days

Feed Directive)

VetBooks.ir

Medicated feed

FDA approved

21 days

Medicated feed

FDA approved

42 days in salmonids; 3 days
in catfish

Immersion

FDA approved

None

Immersion

FDA approved

None

Immersion

EPA

5 days in channel catfish,

Immersion

INAD required
muskellunge, tiger
muskellunge, northern pike;

30 days in all others

Immersion

FDA approved

None

Immersion

INAD required

7days

Immersion

INAD required

7days

Immersion

EPA• (restricted use

Not for use in food fish
pesticide)

Immersion

FDA approved

21 days

Immersion

INAD required

72hours

Immersion

The Index

Not for use in food fish

Irtjection

FDA approved•

None (broodstock)

(prescription only)

Irtjection

The Index

Not for use in food fish

"Approval status is of January 8, 2015. Practitioners should check the FDA Web site (www.fda.gov) frequently for the most current information.

use, because formalin removes dissolved
treatment is essential because 250 mg/L may
oxygen from the water. Vigorous aeration
be lethal in some fish. At water temperaduiing formalin treatment is essential. When tures> 77°F ( 25°C), the concentration treating at s25 mg/L, a water change is not
should not exceed -170 mg/L. If adverse
necessary after chemical administration. At
reaction to the chemical becomes apparent,
this concentration, formalin has minimal
the fish should be in1mediately placed in
impact on biofiltration; however, if ammonia clean water. If formalin is allowed to chill to is tested using Nessler's reagent, a very high

<45°F, a white precipitate, paraformaldereading may be seen for several days. This hyde, will form. Because parafom1aldehyde
is an artifact caused by the interaction of
is highly toxic to fish, forn1alin should never
the two compounds. Use of the salicylate
be used if a precipitate or cloudiness is seen.

method to test ammonia is suggested when

Formalin is carcinogenic and potentially
formalin has been used in a system. Shorttoxic to workers; material safety data sheets tern1 baths with fonnalin can be provided at
should be on hand in businesses where the
concentrations up to 250 mg/L for 30 min,
chemical is used, and employees should be
but a bioassay and close observation dilling
informed of appropriate safety precautions.

1752

AQUACULTURE

There is no required withdrawal time after

In freshwater systems, the concentration
treatment with formalin.

of CuS0 is considered 1000/o active, and

4
application should be based on the total

Chloramine-T: Chloramine-T (HALAMID
alkalinity (TA) of tile water. If TA is <50

Aqua®), a biocide and mild disinfectant,
mg/L, copper sulfate cannot be used safely.

VetBooks.ir
has been approved by the FDA for three

If TA is 50-250 mg/L, a safe concentration of
indications: 1) to control mo1tality in

CuS0 can be determined by dividing the TA
freshwater-reared salmonids caused by

4
by 100. For example, if TA= 100 mg/L, a safe
bacterial gill disease associated with
concentration of CuSO, would be 1 mg/L. If

Flavobacteri:um spp, 2) to control mortality TA is >250 mg/L, the concentration of CuS0
in walleye due to external columnaris

4
should not exceed 2.5 mg/L. CuS0, also has
disease (F columnare ), and 3) to control

1
algicidal activity. Rapid death of an algal
mortality in freshwater-reared warm water
bloom can precipitate catastrophic o>.-ygen
finfish due to external columnaris disease
depletion. Use of CuS0 in ponds not

(F columnare). No withdrawal period is

4
equipped with supplemental aeration is
required before harvest.

risky. Use of CuS0, is hazardous if a pond

1
has a heavy algal bloom (secchi disk slS in.)

Hypersalinity and Hyposalinity:

or if the water is already deficient in oxygen

Hypersalinity (for freshwater systems) and
because of other factors ( eg, cloudy
hyposalinity (for marine systems) are often
weather, heavy stocking density, or high
used in aquaculture and can be effective
water temperature).

methods for control of some parasites.

Copper in marine systems, by contrast, is

Hypersalinity in freshwater typically
dosed according to level of free copper ion
involves use of sodium chloride, which is

(Cu2+). Therapeutic concentrations are
considered "low regulatory priority." In
based on maintaining a longterm dosage
some instances, dilution of seawater may be range of 0.15---0.2 mg/L of free Cu2+. As used. Sodium chloride effectively mitigates
discussed earlier, "blue" copper sulfate is nitrite toxicity (see AQUATIC SY5TEMS, p 1766) actually CuS0 •5HP, so for pwl)oses of
to reduce osmoregulatory stress in

4
marine systems, copper sulfate is considfreshwater fish and to control some ered 25% active ingredient (tile molecular
protistan and copepod parasite infestations.

weight of free copper is -25% of tile entire

In some instances, seawater may be used.

compound). Because copper is toxic and

Salt is not generally practical for use in
because treatment periods for susceptible
production ponds because of their large
marine pathogens often last for �2-4 wk,
volume, except for control or prevention of
copper should be added to a system slowly
nitrite toxicity, but it can be used in
at 0.05 ppm/day to reach the target range of
ornamental ponds that are not more than

0.15---0.2 mg/L over tl1e course of 3-4 days.

several thousand gallons. Salt is commonly

This allows the fish's body to acclimate and
used in recirculating aquaculture systems.

activate detoxifying pathways to reduce
toxic effects. Free copper levels should be

Copper Sulfate: Copper sulfate (CuSO,)

monitored daily. Copper is highly toxic to
is currently an INAD nQt yet approved by
many invertebrates, and even with slow
the FDA; however, a number of compounds
acclimation some saltwater species are still
containing CuS04 have been approved by
fairly sensitive. The following fommla can
the EPA as algicides for use in aquatic sites.

be used to calculate the grams of copper

Technically, the chemical form of the
sulfate required to treat a marine tank:

commonly used blue crystal copper sulfate
volume (in gal.) x 0.0038 x desired
is CuS0,1•5H20 (copper sulfate pentahyconcentration x 4 = g of CuS04•
drate ), but for purposes of brevity, the

Chelated copper compounds ( copper
fornmla CuS0. will be used here, and this
sulfate or copper ion chelated with anotiler

1
blue compow1d refen-ed to as "copper
chemical) have also been used in some
sulfate."

circumstances, but caution should be used

Copper sulfate is Cllffently designated as
for legal reasons and when dosing for

"of moderate regulatory concern" and is
treatment. Copper can be removed from a
used in food fish practice. CuS0 has been
system with water changes or by filtering

4
used for many years as a parasiticide and is
water tlu·ough activated carbon. Food fish
particularly useful in large production
must undergo a 7-day withdrawal pe1iod
ponds because of its relatively low cost.

after treatment before harvest.

Copper is highly toxic to fish, and safe use
depends on lrnowing both the volume of

Potassium Permanganate: Potassium
water to be treated and the total alkalinity,
permanganate (KMn0
as well as potential species sensitivities.

4) is an INAD, and

KMn0 is used as an external parasiticide,

4

AQUACULTURE

1753
fungicide, and bactericide. It is a strong
tion of fish, amphibians, and other aquatic,
oxidizing agent and "burns" organic
cold-blooded animals. In fish intended
material off the external surface of fish.

for human consumption, TMS can only

Overuse, particularly multiple uses within
be used in members of the Ictaluridae,
a short period of time (more than once a

Salmonidae, Esocidae, and Percidae, and

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week) will kill fish. The concentration of
water temperature should not exceed 10°C

KMn04 used varies with the pern1anganate

(50°F). Withdrawal period if used in these
demand of the water. In aquaria or ornamenspecies is 21 days.

tal ponds with very clear water, a concentration of 1-2 mg/L is usually safe and effective. Eugenol: Eugenol (Aqui-S20E®, active Permanganate demand is greater in water
ingredient J()OA, eugenol), one component of
with a high organic load. To detennine the
several found naturally in clove oil, is an
pe1manganate demand, a bioassay can be
lNAD intended for use as an anesthetic/
performed: the water to be treated is placed
sedative. Although eugenol is not approved,
in small containers, and KMn04 is added in
it is currently allowed for use in fresh water
incremental concentrations of 2 mg/L. The
fisheries work as a zero-withdrawal fish
correct concentration for therapeutic use
anesthetic. However, if used in aquaculture,
will be the lowest concentration that
the withdrawal tin1e is 72 hr. A related
maintains a pink color for 4-8 hr. If the
compound, isoeugenol (Aqui-S®), is not
concentration of KMn04 required is >6
allowed for use in tl1e USA because of
mg/L, then the organic load is excessive,
carcinogenicity concerns.

and sanitation practices should be
evaluated. KMn04 has little impact on

Metomidate: Metomidate hydrochlobiofilters when applied at s2 mg/L.

ride (Aquacalm®) is a fish sedative on the

Potassium permanganate is more toxic as

FDA-CVM Index of Legally Marketed
salinity of the water increases, and use in

Unapproved New Animal Drugs for Minor
marine systems is not recommended. Food

Species (the Index), labeled for the sedation fish must undergo a 7-day withdrawal
and anesthesia of ornamental finfish. It is
period after treatment before harvest.

not legal for use in food fish species.

Diquat: Diquat (Reward®), first registered

Spawning Compounds
as a contact herbicide (pesticide), has been
used for many years to control columnaris

Chorionic Gonadotro
disease (F columnare) in fish. Only recently gin: Chorionic
gonadotropin (Chorulon ) is FDA approved
has it come under greater FDA scrutiny and
for use as an aid to improve spawning
become an INAD for control of Flavobacte
function in male and female brood finfish.

rium species associated with bacterial gill This is the only spawning aid ap]i)roved by
disease and columnaris disease. Withdrawal the FDA for use in food fish species. There times for harvestable food fish species are 5
is no withdrawal time if used according to
days for channel catfish, muskellunge, tiger
label instructions on broodfish. Veterinarmuskellunge, and northern pike, and 30
ians may work as part of a team for fish
days for all other fish species.

hatcheries and may be asked to help obtain
spawning hormones. Cho1ionic gonadotro

Diflubenzuron: Diflubenzuron (Dimilin®),
pin is a prescription drug and is restiicted to
a chitinase inhibitor used to control
use by or on the order of a licensed
crustacean parasites, is a restricted use
veterinarian.

pesticide that can be applied only by
licensed pesticide applicators. Dimilin is

Gonadotropin-releasing Hormone
labeled for control of anchorworn1s on

(sGnRHa) + Domperidone: Salrnonid
ornamental fish and baitfish commercially

GnRH analogue + domperidone (Ovaprim®)

produced in ponds and tanks. Fish being
is on the Index and labeled for use as a
raised for hmnan consLUnption should not
spawning aid in ornamental finfish broodbe exposed to diflubenzuron.

stock. This product carmot be used in food
fish species.

Anesthetics/Sedatives

INFECTIOUS DISEASES

Tricaine Methanesulfonate

(MS-222, TMS): Tricaine methanesul

Some fish pathogens may be more common
fonate (approved product Tricaine-S®)

in or adapted to a given species, genus, or
is a benzocaine derivative and is the only
family; however, many are ubiquitous and

FDA-approved fish anesthetic. TMS is
have broad host ranges. Enviromnental
approved for the temporary immobiliza-
factors, including type of rearing system and

1754

AQUACULTURE
production method, influence pathogen
adversely affected when heavily infected
variety and prevalence within a given unit
with this organism. Other fish, reptiles, or
and facility. Many pathogens can infect fish
amphibians may serve as paratenic hosts
regardless of rearing system and production by feeding on infected fish and carry or method, but the following sections describe
transport the parasite.

pathogens that may be more problematic

Bactetial diseases, such as those caused

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under certain conditions.

by Edwardsiella ictalU1i and Streptococcus spp, as well as viral diseases may be Ponds: Most production ponds are
more difficult to control once they infect
outdoor and earthen ( dirt or clay lined) and,
a pond population because of logistical
over time, become high in organic loading
challenges with pond disinfection.

as a consequence of feeding, fish growth,
waste accumulation, and other related

Recirculating Aquaculture Systems:

processes. In Florida, smaller ponds

Recirculating aquaculture systems (RASs),
facilitate periodic cleaning, whereas much
by contrast, a.re situated within enclosed
larger catfish ponds in the southeast are
facilities with more limited access by
logistically much more difficult to clean.

potential final or intermediate hosts.

Although fish in production ponds are

Parasites with direct life cycles a.re more
ce1tainly susceptible to a wide spectrum
conunon and dangerous in an RAS, because
of parasites, high organics favor sessile

RASs used in production tend to have
ciliates, includingHeteropolmia/Epistylis,
greater fish densities and by definition

Apiosoma, andAmbiphyra, which attach
recycle water, which results in closer
to fish but feed on bacteria and other
fish-to-fish contact and greater buildup of
nutrients in the water column. Other protist
parasite nw11bers within the system. Once
parasites that thrive in 1ich, organic environa parasite infects a fish within an RAS, it ments include the trichodinids ( eg,
becomes magnified, and disease can spread

Trichoclina, Tripartiella), and Tetrahy
rapidly. Ichthyophthi?ius multifiliis
mena. Uronema, the marine counterpart to

("ich"), C1yptocaryon irritans ("salt water Tetrahymena, also thrives in highly organic ich"), and Amyloodinium (marine velvet
waters.

disease) can spread rapidly within an RAS.

Fish cultured in outdoor ponds are much

Similarly, egg-laying monogeneans such as
more susceptible to infection by melazoan

Dactylogyrus sp and Neobenedenia sp, the parasites with indirect life cycles because of
capillarid nematodes (which have direct life
the presence of final hosts and intermediate
cycles), and microsporidia also can spread
hosts that pennit completion of the life
rapidly within an RAS.

cycle. These include digeneans, myxozoa,

Bacterial and viral diseases a.re also much
nematodes, and cestodes. The presence of
more problematic in RASs, partly because
birds and snails facilitate infestations by
microbial flora can be much less diverse and
digeneans, requiring fish and snails as
skewed than in more natural pond systems.

intermediate hosts and aquatic birds as the

Mycobacteriosis and streptococcosis have
final host. Bolbophorus damnijicus is an
caused significant morbidity and mortality
important digenean parasite of channel
in RASs, which can favor their growth,
catfish, the final host of which is the
amplification, and fom1ation of reservoirs.

American white pelican, and the intennedi

Certain environmental conditions promote
ate hosts a.re the ram's horn snail and the
mycobacterial growth, including warm
fish. Centrocestusformosanus, another
water temperatures, low dissolved oxygen
in1portant digenean parasite infecting the
levels, acidic pH, high soluble zinc, high
gills of nun1erous fish species, uses a wading fulvic acid, and high hwnic acid. Many of bird, such as the green heron or great egret,
these conditions-especially the low
or the cone snail (Melanoides tuberculata)

dissolved oxygen, low pH, and an organito complete its life cycle.

cally tich environment-a.re present in

Oligochaetes, annelid worms, are also
intensive aquaculture systems. Closed
much more prevalent in highly organic
conditions and higher stocking densities
waters. H enneguya iclaluri, a myxozoan
enhance the potential for spread and
parasite and the causative agent of proliferaan1plification. Biofilms on the tanks, in tive gill disease in channel catfish, requires
pipework, and in filtration systems, as well
the oligochaete Dero digitata to complete
as organics, inaccessible or overlooked
its life cycle. Eustrongylides, a nematode
mortalities, and detritus, can serve as
parasite that infects wading birds as adults,
reservoirs.

has an indirect life cycle that may involve
either an oligochaete worm and a fish or just Net Pens/Cage Culture: Open ocean a fish. Juvenile, pond-reared fish can be
net pens, or cage culture systems within

AQUACULTURE

1755
large rese1voirs or lakes, have their own
these parasites can cause significant
unique challenges. Under ideal conditions,
epithelial damage, predisposing fish to

"open" access through the net or cage
opportunistic pathogens in the environstructures is intended to make use of the ment and compromising respiration and
vast surrounding water body and allow for
osmoregulation. Infested fish demonstrate
dilution of solid and dissolved wastes.

flashing, decreased appetite, loss of

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However, this "open" access also facilitates condition, and hyperplasia of infested
direct or indirect contact with pathogens
epithelial surfaces. Severe infestation of
endemic to the water body. Smaller wild fish the gills is particularly damaging. These or other organisms may directly enter and
organisms can be controlled with a single
intenningle with the farmed species, or
treatment of formalin, copper sulfate,
pathogens themselves may flow directly
potassium permanganate, or a salt dip.

into the stmcture tlu-ough the water or on

Excessive crowding and poor sanitation
otl1er vectors. The higher densities found in
are frequently associated with heavy
net pens and cages can then magnify the
infestations and should be corrected.

disease through close contact and facilitate

For identification of protists affecting
spread.

external surfaces of cultured fish, see

Salmonid producers, during marine
p 1799. Control strategies are detennined by
grow-out phases, can have significant
the species affected and their intended use,
losses caused by sea lice and infectious
the type of system the fish is housed in, cost
salmon anemia, among others. Neobened
of treatment, and environmental considera
enia and other monogeneans are a major
tions.

problem in warm water marine systems.

Bacterial diseases such as vibriosis are

Internal Protistan Parasites: For
common in net pens, and emerging viral
inforn1ation on flagellated parasites
diseases, including those caused by iridovi

( diplomonads such as Spironucleus, and
mses (including megalocytivinises) and
kinetoplastids such as C1yptobia iubilans ), betanodaviruses, are of increasing concern see INTERNAL PROTISTAN PARASITES, p 1803. These in marine open ocean systems because of
parasites are also conu-non in the GI tract of
potential for transmission from wild
susceptible aquaculture species. The use
populations.

of chemical treatment to control these
organisms is not feasible in food fish;

PARASITIC DISEASES
however, improvements in environmental
conditions and husbandry will decrease
morbidity and mortality.

Protists Infecting Gills and Skin: For

Opalinids, larger "cilate-like" parasites
infonnation on protists infecting the gills
commonly found in tl1e GI tract, may be
and skin offish, seep 1799. Wormation
found occasionally in kissing gourami,
presented here is relevant to fish reared in
discus, some catfishes, and other species.

intensively cultured systems. As previously

Considered commensal by some, these may
mentioned, trichodinids are indicators of
or may not be associated with disease.

poor sanitation and/or overcrowding. These
organisms are commonly found in cultured

Internal Metazoan Parasites: Myxofish, especially in systems with high sporean (Myxozoa) diseases significant in
stocking densities, high organic loads, and
aquaculture include whirling disease and
minin1al ( or no) in-line sanitation ( eg, UV
proliferative kidney disease (PKD) of salrnoor ozone). When fish are heavily infested, nids and proliferative gill disease ("han1-losses will occur. ln these cases, chemical
burger gill disease") of channel catfish.

treatment alone may not be adequate for

Whirling disease is caused by Myxobolus
complete control. Addressing management
cerebralis. Fish are infected as fingerlings problems that favor infestation should be
when the parasite infects cartilage in the
incorporated into the treatment plan.

vertebral colunm and skull, resulting in

Decreasing organic material is essential for
visible skeletal defonnities. Affected
treatment efficacy, because these organisms fingerlings typically show rapid tail-chasing can be protected from chemical treatment
behavior (whirling) when startled. The
by "hiding" within organic debris.

disease is also sometimes called "blacktail,"

Ambiphyra and Apiosoma are sessile because the peduncle and tail may darken
ciliates found on the skin, gills, and fins of
significantly. Recovered fish remain
fish. These are common in pond-reared fish carriers. Adults do not show behavioral and also have a predilection for organically signs, but skeletal defonnities associated rich environments. They are not generally
with infection do not resolve. The disease
found on marine fish. In high numbers,
can be prevented by purchasing uninfected

1756

AQUACULTURE
breeding stock and maintaining them in an
however, histology is required for
environment free of the inte1mediate hosts
confirmation. Quantitative PCR has

(tubifex wonns). A presumptive diagnosis
also been used diagnostically.

of whirling disease is made by detection of
spores from skulls of infected fish.

Platyhelminthes (Flatworms): Flat

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Diagnosis may be confirmed histologically
w01ms (Platyhelminthes: monogenea,
or serologically. Whirling disease is of
digenea, leeches, turbellaria, seep 1807)

regulatory concern in some states.

are also of concern in aquaculture.

PKO is one of the most economically

Monogeneans, including gyrodactylids,
important diseases affecting salrnonid
dactylogyrids, ancyrocephalids, and
industries of North Ame1ica and Ew·ope.

capsalids, have all been identified in

Rainbow trout are particularly susceptible.

nun1erous aquacultured species.

PKO is caused by Telracapsuloides

Ch.J1-odaclylus salaris is a rep01table
b1yosalmonae, a myxosporidian with four
disease of salrnonids but has not been
distinct polar capsules. It occurs most
repo1ted in tl1e USA. Any gyrodactylid
commonly in the swmner when water
found on a salmonid species should be
temperatures are> 12°C, and the parasite
identified well enough to determine
p1ima.rily infects yearling and yow1ger fish.

whetl1er it is G sala1is. Neobenedenia and

Clinical signs include lethargy, darkening,

Benedenia are in1portant monogeneans in
and fluid accumulation indicated by
marine aquaculture.

exophthalrnos, ascites, and lateral body

Although treatments will vaiy depending
swelling. Wected fish are frequently
on the aquaculture setting and species of
anemic, resulting in gill pallor. Grossly, the
parasite and fish host, formalin is approved
posterior kidney appears gray, mottled,
for use in food fish. Hyposalinity for marine
and significantly enlarged. Presumptive
species, including freshwater dips, can help
diagnosis can be based on obseivation of
reduce loading on fish, but environmental
suspect organisms, 10-20 µm in diameter,
reseivoirs (eg, eggs) will need to be
in Giemsa-stained wet mounts of kidney
controlled as well. Neobeneden'ia was
tissue. Histologic examination of infected
controlled in one study when salt levels
tissue, stained with H&E, and in1mw10histowere reduced to ,<;15 g/L for 5 days and ,:;18
chemistry are required for confirmation.

g/L for 7 days. Hydrogen peroxide is not

There is no treatment, but fish tl1at recover
approved for use against monogenean
from the infection are resistant to subseinfestations in food fish but can be used quent outbreaks. Wected stocks in
extra-label under the supervision of a
nonendemic areas should be depopulated,
veterinarian. Doses ai·e experin1ental (see
the premises sanitized, and disease-free

Use of Hydrogen Peroxide in Finjish
stock obtained for replacement. Avoidance

Aquaculture [http://edis.ifas.ufl.edu/fal57]

is the best preventive measure.

for some reported doses). Freshwater

Proliferative gill disease ("hamburger gill
monogenea can be treated with formalin
disease") is a myxosporean infection of
or saltwater dips to remove a majority of
channel catfish caused b:t Aurantiactino
parasites from fish, but environmental
my:1:on iclaluri. The organism has a
stages ( eg, eggs) will also require control.

complex life cycle, with the oligochaete

Digeneans have complicated life cycles,
worn1 Dero digitata serving as the
with several laival stages that infect one or
intennediate host. Channel catfish may
more hosts. As discussed above, fish raised
be aberrant hosts for A ictalU1i, and the
in outdoor aquaculture systems are more
disease usually occurs in new ponds or
likely to become infested by this group of
previously infected ponds tl1at have been
parasites. With rare exceptions, the first
drained and refilled. Although proliferative
intern1ediate host is a mollusc, witl1out
gill disease can cause catastrophic mortality which the life cycle generally cannot be approaching 1000/o, losses may be as low as
completed. The final host for many common

1 %. Disease occurs at water temperatures
freshwater aquacultured fish digenean
of 16° -26°C, and mortality is exacerbated
parasites is a wading bird. A diagnosis
by poor water quality, paiticularly low
usually can be established by gross or
dissolved oxygen or high levels of un-ionized microscopic examinations tl1at reveal the anunonia. Gills of affected fish are severely
cercarial, metacercarial, or adult worn1S in
swollen and bloody. A presun1ptive diagnosis any of the tissues or body cavities of tl1e can be made from a wet mount of infected
fish. Fish tend to fonn pigmented tissue
tissue, in which filai11ents appeai· swollen,
encapsulations tl1at encyst the parasites.

clubbed, and broken. Cartilaginous

Depending on tl1e color of the cysts in the
necrosis is strongly supportive of a
skin, the condition is called black, white, or
diagnosis of proliferative gill disease;
yellow grub disease. Heavily parasitized fish

AQUACULTURE

1757
often are weak, thin, inactive, and feed
stage, and the final hosts are aquatic reptiles
poorly. In many cases, low level infestations

(turtles, snakes, alligators). Under the
may not result in significant morbidity but
microscope, pentastome nymphs appear
will prevent sale of fish for aesthetic
as thick, stout, curved, and "segmented"

reasons. Treatment is not reconunended.

wonns (see Pentastomid Infections in

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Pond-reared, juvenile, tropical fish may

Fish [http:/ I edis. ifas. ufl. ed u/fa090]). Fish develop severe gill disease from metaceroften show no behavioral changes and may carial cysts of the digenean Centrocestus
have minimal morbidity or mortality, but
formosanus in gill tissue. Although acute
fish cannot be sold for aesthetic reasons.

death is occasionally seen, infected fish

Treatment is not reconunended, but
more commonly die during harvest or
management involves removal of final
shipping when they may be exposed to
hosts from the system.

suboptimal dissolved oxygen concentrations. If only a small percentage of gill tissue Crustacean Parasites: Crustacean
is infested, then fish may be clinically
parasites, includingArgulus,Le1naea, and
normal. Treatment of infected fish has not

Lepeophtheirius, can become significant
been successful; however, prevention of the
problems in aquaculture (seep 1808).

disease by elimination of the intermediate

Treatment of these organisms is not feasible
host, the freshwater snail Melanoides
for food fish species.

tuberculata ( common name, the redrimmed melania), has been effective.

BACTERIAL DISEASES

Bolbophorus corifusus is a digenean
trematode that causes morbidity and
mortality in channel catfish fingerlings in

Common Bacterial Pathogens
production ponds in Mississippi, Louisiana,

(Aeromonas, Vibrio, and Edward
and Alabama. The definitive host of B
siella): Common bacterial pathogens confusus is the white pelican, and the first (seep 1808),Aeromonas hydrophila,A
intermediate host is the ram's horn snail
salmonicida, Vibrio spp, Edwardsiella

(Heliosoma spp ). Cercariae released from
ictaluri, E tarda, Streptococcus spp, and
snails encyst in fish tissue, forming
other related gram-positive cocci, can also
metacercariae in any tissue, but most are
infect aquaculture species. Organisms that
found in skin and skeletal muscle of the
may have previously been identified as
peduncle of juvenile channel catfish. Severe

E tarda have now been recognized as new
disease (mortality up to 95%) occurs when
organisms with biochemical characteristics
metacercariae encyst in visceral organs,
very sin1ilar to those of E tarda. Two new
particularly the posterior kidney and liver.

groups are also recognized, E piscicida and Involvement of these organs can result in

E piscicida-like bacteria, which have been
a presentation similar to that of enteric
associated with disease in channel catfish
septicemia or channel vims disease,
and freshwater game fish (see below).

characterized by fluid accumulation in the

Treatments for food fish species are linuted
abdomen and exophthalmia. Skin and
to the species and disease indicated on the
muscle lesions typically result in raised
label of approved drngs, although approved
bumps that are white to reddish in color.

fonns of oxytetracycline and Romet® can

The presence of digenea in skeletal muscle
be used extra-label under the supervision
can result in condemnation of affected
of a veterinarian. Florfenicol (Aquaflor®)

carcasses by processing plants.

is the only drng approved for use against
streptococcal infections in freshwater

Other Vermiform Internal Parasites:

reared, warrnwater finfish; however,

Acanthocephalids (thorny-headed worms) extra-label use of this product is prohibited.

are common in wild fish as both larval tissue Enrollment in an INAD program may allow stages and adult intestinal parasites. They
limited use of florfenicol for indications and
are most common in salmonid and marine
species beyond the current label. See
fish. Arthropods are the first intermediate
https://srac.tamu.edu/index.cfm/event/
host. Adult acanthocephala are easily
view AllSheets/, SRAC 4 709 (Investigational
recognized by their protrnsible proboscis,

New Animal Drug [INADJ Exemptions and
armed with many recurrent hooks.

the National INAD Program [NIP]).

Pentastomids, which may present as

Appropriate withdrawal periods before
either "white grub"-like lesions externally harvest must be followed when used in food
or within the body cavity in numerous
fish species ( see TABLE 1, p 1750). Vaccines organs, have been identified in aquacultured are available for a number of bacterial aquarium fish species, including swordtails.

pathogens and species indications. Under

Fish are infected with the larval or "nymph"

supervision by a veterinarian, licensed

1758

AQUACULTURE
commercial vaccines can be used off-label

"hole-in-the-head" lesion. Fish affected

(see Use of Vaccines in FinfishAqiiaciil
with the meningeal. form may demonstrate
tiire [http://edis.ifas.ufl.edu/pdffiles/fa/
bizarTe behavior, including spirming, erratic
fa15600.pdf]).

swinu11ing, and general. disorientation.

Diagnosis is based on bacterial. culture

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Yersiniosis: Yersiniosis (enteric redrnouth
and isolation. Brain culture is indicated
disease) is a serious acute or chronic
whenever E ictaluri is suspected.

bacterial disease of intensively cultured

E ictaluri will grow on blood agar
salmonids. The etiologic agent is Yersinia
incubated at 25°C for 48 hr. Antibiotic
iuckeri. Signs are darkening and hemortherapy should be based on results of rhage of the mouth (red mouth), skin, anus,
sensitivity testing. Vaccination is available
and fins. Chronic signs are associated with
for charmel catfish fingerlings.

inappetence, exophthal.mos, swelling, and

There has been a significant change in
degenerative changes of internal organs.

understar1ding of fish diseases caused by an

Mo1tality rates are variable but are
orgar1ism historically identified as E tarda.

exacerbated by poor water quality and

This organism is the causative agent of
related stressors. Diagnosis is by isolation
emphasematous putrifactive disease of
and identification of pure cultures of the
catfish. The name is descriptive of the most
organism obtained from the internal. organs
conunon lesions, an ulcerative dermatitis
of infected fish. Fish that survive remain
associated with a malodorous, gas-produccarriers and may cyclically shed bacteria, ing bacteria. E tarda is an enteric bacteriun1
particularly when exposed to stressful
that is ubiquitous in terrestrial. and aquatic
conditions ar1d water temperatures of
enviromnents. It has been associated with

15° -18°C. Depopulation of infected fish and
enteric disease in marmnal.s, including
avoidance of introduction of infected fish
people, as well as birds, reptiles, and fish.

can be recommended, but preventive

Recent molecular work has demonstrated
vaccination is the usual procedure in
that several different organisms that may
endemic areas. Yersiniosis can be treated
have been previously identified as E tarda
successfully with ar1tibiotics, which should
ar·e likely causing many of the disease
be selected based on a sensitivity test.

outbreaks attributed to E tarda in fish.

Therapy should be continued for at least

These newly recognized taxa, E piscicida

14 days.

and E pi,scicida-like organisms, are
considered important emerging diseases in
the charrnel catfish industry. They can

Edwardsiella piscicida and E piscicida
present not only as an ulcerative dern1atitis
like Diseases: Edwards'iella ictaliiri
but al.so can cause a systemic granulomacauses enteric septicemia of catfish, the tous disease with gross and microscopic
most important infectious disease in the
lesions very sinillar to those seen in
charrnel catfish industry. Infection occurs
mycobacteriosis (seep 1760). Granulomain the spring and fall when water tempertous disease attributed to E piscicida tends atures are 22° -28°C, and mo�ty may be
to result in hepatic lesions, which are not
exacerbated by handling stress, chemical.

typical of mycobacteriosis. Histological.ly,
treatment, or poor water quality. The
the granulomas contain grain-negative and
disease occurs in two forms: the enteric ( or
acid-fast negative rods. Molecular testing
intestinal.) fom1 and the meningeal. form. In
is required to confirm a diagnosis of
the enteric form, infected fish may develop

E piscicida or E piscicida-like infection.

skin lesions characterized by massive

The disease will respond to antibiotics, but
petechial. hemorrhage around the mouth,
it is unclear whether fish can clear bacteria
operculun1, and eyes, or they may develop
sequestered in granulomas. These
measles-like, red, punctate lesions along the envir01m1ental. bacteria thrive in organically body wall. There is a hemorrhagic enteritis,
rich environments, so sanitation may need
and the intestine may be hemorrhagic and
to be addressed as part of the management
fluid- or gas-filled. Liver lesions are conunon strategy. For aquariums and recirculating and may be evident as multifocal. areas of
systems, UV filtration may help decrease
necrosis, abcessation, or hemorrhage. In
numbers of bacteria in the environment.

contrast, in the meningeal. fom1, few
external. signs may be seen in infected fish.

The bacteria enter the CNS through the

Columnaris and Related Diseases:

olfactory system, and affected fish develop

The taxonomic grouping of bacte1ia causing
severe meningitis. In fingerlings, the
colunmaris disease, cold water disease, and
inflarmnation may be severe enough to erode bacterial. gill disease has undergone the skull, resulting in the char·acte1istic
significant revision in recent years based on

AQUACULTURE

1759
genomic studies. The primary causative
may be affected. Disease is most severe at
agent of each of these important diseases
water temperatures of 4 ° -10°C, and signs
has been moved into the genus Flavobacte-
should not be seen at temperatures >l8°C.

1ium, although other genera have also been

Skin lesions usually begin on the dorsal
in1plicated. These gram-negative, rod or
and posterior surfaces of the fish but may
filamentous bacteria have a distinctive
be found on any part of the body. Advanced

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gliding motion. Skin or gill lesions have
cases show necrosis and ulceration of the
slin1y or cotton-like surface exudates, which peduncle, and underlying musculature will usually cover surface necrosis, ulcerations,
be exposed. As the disease progresses, the
and marginal hemorrhages.

infection becomes systemic, typically

Flavobacte1ium columnare, the most
involving the spleen, kidney, and liver.

prominent member of this group responsi

Confirmed diagnosis is possible after
ble for colmnnaris disease, is most
isolation of F psychrophilmn using
common in warm water species of fish. A
cytophage media (l5°-20°C for 3-6 days),
presumptive diagnosis can be made from
or by imrntmohistochemistry or PCR.

visualization of typical organisms on wet

Outbreaks can be controlled with
mounts of infected skin or gill tissue.

oxytetracycline.

Colunmaris disease can be confirmed by

Bacterial gill disease, caused by F
isolation of the organism on Ordal's or other
branchiophilum, is most frequently
cytophaga media. Sensitivity tests are
reported in young cultmed salrnonids or fish
difficult to perform, because F coliimnare
cultured under conditions of high organic
will not grow on Muller-Hinton media. lf the
loading. It has been seen occasionally in
disease is diagnosed early in the course of
aquar·iwn fish. It may be initiated by
infection, treatment with potassiwn
crowding and poor water quality, particupermanganate or hydrogen peroxide may be Jar·Jy high organic loads, high anunonia effective. lf the disease becomes chronic, it
levels, and silt. Gills appear· swollen and
may have become systemic, in which case
mottled, with patchy areas of bacterial
treatment with florfenicol or oxytetracygrowth that can be confirmed by microcline is recommended. Col=aris disease scopic exarnination of direct gill smears.

can be prevented by reducing organic

Hyperplasia, adhesions, and defom1ity of
loading and avoiding traun1atic irtjuries. A
the gill lamellae car1 be seen. In young fish
vaccine is currently available in the USA for
affected with the disease, mortality is high
use in channel catfish and largemouth bass.

and morbidity sustained. Prevention efforts

A similar organism affecting marine fish
include improving water quality a11d
was previously grouped with F columnare
avoiding overstocking. A single treatment
but has been given its own genus and is now
with potassium penrnmga11ate, followed by
named Te1iacibaculum maritimum.

addition of salt to the system (2-5 ppt) I'Qay

Potassimn pennanganate may not be a good help control losses, but sanitation is critical option in wannwater marine finfish because
for longterm resolution of the problem.

of its increased toxicity at higher salinities.

Antibiotic therapy may be used as needed

Flavobacterium psychrophilum causes
to control secondary bacterial problems.

coldwater (pedrmcle) disease, or
bacterial coldwater disease, in salmon ids

Bacterial Kidney Disease: Bacterial
and other coldwater species. Rarely, warmkidney disease is economically important in water fish exposed to cold temperatures
cultmed salmonids. The cause is Renibacte-

1ium salmoninarum, a11 obligate intracellular bacteria that is one of the relatively few grain-positive organisms that causes disease
in fish. Bacterial kidney disease is a ctu·onic
disease affecting juveniles (6-12 mo old)

a11d prespawning adults, with clinical signs
very similar to those of mycobacteriosis.

Clinically, infected fish appear lethargic and
darkened a11d may have coelomic distention, pale gills (a11emia), a11d vent hemorrhages. Typical lesions include grayish, localized, or conglomerate gra11ulomata in
the viscera, especially the kidney or body
wall; exophthalmos; blindness; cystic
cavities in musculatme; a11d emaciation.

Erosion typical of columnaris disease in a

A presumptive diagnosis ca11 be based on
silver dollar. Courtesy of Dr. Ruth Francis-Floyd.

visualization of small, gram-positive rods

1760

AQUACULTURE
in kidney imprints. Definitive diagnosis
anorexia, pale gills, and skin lesions.

requires isolation and identification of the

Internally, lesions are more typical, with
bacte1ia by using a selective medium that
granulomatous lesions possible throughout
contains cysteine and incubating at 15°C for
the viscera. The most characteristic lesions

3--6 wk. R salmoninarum is transmitted
may be found in liver and kidney tissue and

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both horizontally and vertically, and fish
appear as gray to yellow mottled areas with
that sU1vive an epizootic remain carriers.

ring-shaped foci. Visceral lesions are grossly

Infected female fish should be irtjected with
similar to those seen in advanced cases of
erytlu·omycin (11-20 mg/kg, IM) 14-60
mycobacteriosis, and differentiation is
days before spawning to prevent vertical
important. Histologically, intracellular
transmission. Eryt!u·omycin (100 mg/kg for
organisms may be seen in macrophages and

10-21 days) is effective when administered
hematopoietic tissue in the liver, spleen, and
in feed early in tl1e course of an outbreak;
kidney. Blood or tissue smears stained with
however, it is not FDA approved for this use.

Giemsa or acridine orange may reveal tl1e

Obtaining disease-free stock and preventing
intracellular organisms, often appearing
contamination by infected wild fish are the
as paired, curved, gram-negative rods in
best preventive measures.

macrophages or hepatocytes. Ricketlsia
like organisms can be isolated using a
variety of cell lines; however, confumation

Mycobacteriosis: Mycobacte1iosis (see
al.sop 1810) is an important disease in
of a suspect case may also be based on
aquaculture because of its typically chronic
serology.

nature (although acute and subacute

Transmission of rickettsial-like diseases
presentations can occur) and the lack of
in fish is not understood. In terrestrial
effective antibiotics. External or internal
species, a vector is often required; however,
masses, nodules, or granulomas are a

R salmonis has been demonstrated to
conunon presentation in aquaculture species.

smvive for 14 days in seawater, suggesting

Important differential diagnoses for a suspect that horizontal transmission in the absence case of mycobacteriosis, based on identificaof vectors may be possible in aquatic tion of granulomas in tissue, are Edward
species. Oxytetracycline is the treatment of
siella piscicida (seep 1758) and francisellosis choice, although it is unclear whether an ( see below). FUlther, although granulomaadvanced case can be completely resolved tous lesions are typical of mycobacteriosis,
with antibiotic treatment. Rickellsia-like
they are not always seen. In some species,
organisms do not appear to be a zoonotic
and under some conditions, granulomas may
threat, because they do not seem able to
not be present. Instead, caseous ("pus-like") survive at man1malian body temperatures.

lesions may tie seen, or histologically, only a
histiocytic infla.nunatory response (increased
macrophages/tissue phagocytes without

Francisellosis: Francisellosis, an
granuloma formation) may be apparent.

impmtant emerging bacterial disease

Acid-fast stains and/or culture are necessary
caused by Francisella noaticnensis, has
to exclude mycobacteriosis in cases with
been identified as the primary cause of
chronic morbidity/mortality and chronic
disease in a variety of aquacultured and
infla.nunation but no granulomas. In addition,
wild-caught species, including tilapia,
processing differences (including the
hybrid striped bass, Atlantic cod, Atlantic
decalcification method, if necessary, and the
salmon, various gnmt species, ornamental
type of acid-fast stain used) may affect
cichlids, fairy wrasses, and blue-green
staining characteristics of mycobacteria.

damselfish. In tilapia, francisellosis is often
associated witl1 environmental stressors,
especially cooler temperatures and poor

Rickettsia and Rickettsial-like
water quality, and so increasing tempera

Diseases: Rickettsial disease associated
tures (for indoor facilities) may help
with Piscirickettsia salmon is has been
mitigate the disease. Many signs and
described in salmonid species from Chile,
necropsy findings are grossly similar to

Norway, Ireland, and Canada. Rickettsialthose seen in mycobacteriosis. The disease like organisms have been reported in tilapia, can be acute, with few clinical signs and sea bass, and blue-eyed plecostomus.

high mortality, or subacute to chronic, wi.tl1

Rickettsial disease can result in acute
fish demonstrating erratic swimming,
mortality, affecting up to 95% of fish with
spiraling, buoyancy control problems,
few gross signs. In tilapia, acute mortality
anorexia, lethargy, exophthalmia, anemia,
may be triggered by sudden drops in
petechiation, and darkening. Severely
temperature. Chronic disease is manifest
infected fish may have necrotic or nodular
by nonspecific external lesions, including
gills with red and white patchiness, and

AQUACULTURE

1761
histologically, portions of the gill may also
hyphae, and positive confirmation was
be severely hyperplastic with consolidation
based on cultme characteristics and
of secondary lamellae. On necropsy, the
identification by PCR. The disease appears
spleen and kidney typically have a granular
to be linked to enviromnental stressors that
or nodular (granulomatous) appearance,
may include temperatme.

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and most other organs can also be affected.

In general, systemic fungal infections in

Francisellosis should be another differential aquacultured species do not respond well diagnosis for granulomatous disease in fish.

to treatments. External infections of

Identification is supported by history,

Saprolegnia may require environmental/
clinical signs, species affected, and
handling modifications in addition to
presence of non-acid-fast bacterial
chemotherapy. For food fish use, specific
organisms that are Giemsa positive and
commercial fo1111alin and hydrogen
weakly gran1 negative. Because F'rancisella
peroxide products are FDA approved for
does not grow on routinely used media
use against fungus on fish eggs. Use of these

(such as blood agar), confirmation requires
products on other life stages is extra-label

PCR of affected tissue and/or culture on
and requires veterinary oversight.

various special media, all of which include
increased levels of cysteine ( or cystine) and

Mycotoxins: See also p 1811. As in other glucose. Culture and sensitivity should be
species, mycotoxin contamination of feeds
performed by a microbiologist and
is associated with disease in aquacultme
laboratory with expertise in this pathogen
species. Specifically, expos me to aflatoxinfor identification and to determine contaminated feed causes serious disease
sensitivity patterns. Because F'rancisella is in rainbow trout. Aflatoxin is produced by
intracellular and causes granulomatous
fungi in the genusAspergillus and is
disease, chemotherapy may be less
commonly associated with use of oil-seed
effective, unless the disease outbreak is
crops such as com, cottonseed meal, and
identified very early in its course. Optimizapeanuts. Toxin production may be tion of husbandry, including increasing
associated with inlproper storage, with high
temperatures when possible, may help
hU111idity (>14%) and high temperatures
reduce morbidity and mortality.

(>27°C) being significant risk factors.

Affected trout may have a grossly distended

MYCOTIC DISEASES
abdomen, and necropsy findings reveal a
hepatoma or hepatic carcinoma. Liver

The "fungi" and "ftmgi-like organisms" (see lesions have been reported after exposure
p 1811) can affect aquacultured species. A
to concentrations as little as 1 mg/kg.

nwnber of these pathogens, previously

Disease has been induced experin1entally
lumped together as "fungi" based on
in tilapia at higher concentrations and/or
similarity in morphology and saprophytic
extended exposme periods. In one study,
lifestyle, are unrelated taxonomically. The
tilapia fed 10 mg/kg for 8 wk had liver
more common "water molds," including
pathology and when fed 100 mg/kg for 8 wk,

SaprolegniaandAphanomyces, are not
hepatic necrosis and mmtalities were seen.

tme fungi but members of the Oomycota

In another study, tilapia fed 0.245 mg/kg

(Oomycetes ). This distinction is in1portant,
over the course of 20 wk demonstrated
because a more precise tmderstanding of
reduced growth and liver pathology.

the biology of each group should lead to

Presence of the toxin can be confirmed
more targeted, effective management and
using high-performance liquid chromatograchemotherapy.

phy (HPLC) or ELISA. Commercial test kits

Another true pigmented fungus,
are also available.

Veronaea botryosa, has been identified and
described as the cause of a phaeohyphomy

VIRAL DISEASES
cosis in aquacultmed white sturgeon and

Siberian stmgeon. Affected fish had one

The identification and characterization of
or more of the following clinical signs:

previously undescribed viral diseases in
abnormal orientation, buoyancy control
aquaculture is increasing because ofrecent
problems, coelomic distention, reddening of technologic advances and increasing the skin, emaciation, and ulceration of the
expertise in the aquatic veterinary field.

skin or eye. Internal pathology included

Virnses (seep 1812) may also affect
hemorrhages throughout the coelom, the
susceptible species in aquacultme settings.

presence of serosanguineous fluid, and

Again, management options are linlited but
organomegaly with nodules or cysts in
vary depending on the type and pathogenicmultiple organs. Wet mounts of affected ity of the virus, species susceptibility,
tissues often revealed presence of fungal
reportability, and whether the virus is

1762

AQUACULTURE
considered endemic or exotic. In general,
epizootics have been attributed to importano approved or effective treatments exist tion of infected eggs or fry.

for viral diseases in aquaculture species.

Acute disease in fry <2 mo old may result in

Temperature manipulations are problematic, high mortality (>90'/o) with few external signs.

especially because of concerns over latency

Disease usually occurs at water temperatures
and potential recrudescence. Vaccine
of l ()0 -l2°C, although outbreaks occasionally

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development for economically important
occur at temperatures > l5°C. 1ypical signs
virnses is ongoing, and some vaccines exist
include lethargy witl1 sporadic hyperexcitfor some viruses either in the USA or internaability, including whirling. Sick fish may be tionally. Additional virnses of importance to
darkened with distended abdomens,
aquaculture are described below.

exophthalmia, pale gills, and mucoid fecal
casts. Important differential diagnoses

Herpesviruses (Alloherpesviruses)

include infectious pancreatic necrosis and

Herpesviruses ( alloherpesvirnses) are also
viral hemorrhagic septicemia Hematopoietic
important pathogens in aquaculture (see
tissue in the kidney and spleen are most
also p 1812). Herpesvirnses have been
severely affected by necrosis.

identified in a nW11ber of different

Risk factors include age (fish <2 mo old
aquacultured species, including cyprinids
are more susceptible), density, and water
and various cichlid species.

temperature. Hauling yoW1g fish aroW1d
dams in trncks may be a significant risk
factor because of crowding during transit.

Channel Catfish Virus Disease:

Although most disease outbreaks have been

Channel catfish virus (CCV) disease is an
reported in freshwater, active disease has
acute, virnlent herpesvirus infection of
occurred in Atlantic salmon housed in sea
fry and fingerling channel catfish that can
cages. Diagnosis is by viral isolation (from
cause mortality of >80% at water temperakidney and spleen of yoW1g fish and ovarian tures ;,,25°C in small fish (5:5 cm). As fish
fluid of broodstock), with confirmation by
age, mortality decreases, and clinical infecserum neutralization. Rapid serologic tests tion in fish > l yr old is rare. Acute infection
are becoming more available. A nonlethal
often includes a recent history of a stresstest involving viral isolation from mucus has ful event such as handling or transport, low
been repo1ted. The disease is transmitted
dissolved oxygen, or chemical treatment.

horizontally through the water, and vertical

Infected fish show signs of ascites, exophtransmission is suspected. Asymptomatic thalrnos, and hemorrhages in fins. The cell
carrier fish serve as reservoirs of infection.

line of choice for virus isolation is channel

A vaccine is available in the USA for use
catfish ovary, followed by serum neutralizaagainst this pathogen.

tion to confirm identification. Typical cytopathic effects include "cell fusion, syncytia Viral Hemorrhagic Septicemia: Viral
formation, and intranuclear inclusions.

hemorrhagic septicemia (VHS) is caused by

There is evidence for vertical transmission
a novirhabdovirns in the family Rhabdoviriof CCV; consequently, survivors of an epizodae and is a highly regulated disease in the otic should not be used for liroodstock.

USA VHS can be divided into several

Although CCV can cause severe mortality
different strains based on genotype: VHS
when an outbreak is in progress, the anstrain !Va is the predominant strain in USA nual number of cases of CCV in the catfish
aquaculture; strain lVb (see below) has been industry is relatively low.

identified in wild stocks only in the USA and

Canada; and strains I, II, and III are foW1d

Novirhabdoviruses
prin1arily in Europe and Asia. The disease
causes marked necrosis of hematopoietic

Infectious Hematopoietic Necrosis:

tissue in the kidney, particularly the anterior

Caused by a novirhabdovirus in the family
kidney, but largely spares excretory tubules

Rhabdoviridae, infectious hematopoietic
in the posterior kidney. Rainbow, brook, and
necrosis is listed as an OIE notifiable
lake trout (genus Salvelinus) and Atlantic
disease. It is endemic in salmonid ( Onco
salmon and brown and golden trout (genus
rhynchus spp) populations in the Pacific

Salmo) are susceptible. The virus also

Nortllwest and Alaska and has been reported causes disease in a variety of freshwater in Atlantic, chum, chinook, sockeye, and
and marine cold water fish, including pike,
kokanee salmon and in cutthroat, steelllead,
turbot, white fish, and sea bass. VHS also
and rainbow trout. Lake trout and Arctic
is foW1d in free-ranging marine fish in the
char, members of the genus Salvelinus,

Pacific nortllwest, including anadromous
appear resistant. The disease has also been
salmon (coho and chinook), as well as
reported in parts of Europe and Asia. Most
haddock and cod in the Nmth Sea.

AQUACULTURE

1763

The disease occurs in three forms: acute,
characterized by erythrocytic degeneration.

chronic, and nervous. Acute mortalities

Affected species include Pacific herring,
occur in rainbow trout fry <3 g and <30 days

Atlantic cod, and Pacific salmonids ( chum,
old. In these fish, the kidney is swollen and
pink, coho, and Chinook), steell1ead trout,
the anterior segment is necrotic and pale.

and cultured eels in Taiwan. The disease is

The liver may be pale with hemorrhagic
chronic, and external signs may be subtle or

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mottling, and systemic hemorrhage may be
nonexistent. Sick fish are anemic, which
visible in the eyes, skin, skeletal muscle,
may result in pale gills and internal organs.

and viscera. The most notable lesion is

Severity of the disease is related to age and
widespread hemorrhage in the liver,
species of fish, with juveniles <l g most
adipose tissue, and within skeletal muscle.

severely affected.

Moribund fish lie on the bottom of the tank

The characteristic lesion is a single
and may exhibit sporadic flashing and
eosinophilic cytoplasmic inclusion body in
corkscrew swinuning behavior. As fish
the circulating erythrocytes of anemic fish.

age, mortalities drop from 80%--lOOOA, to

The inclusions are best visualized from

100/o--500A,, The chronic forn1 is a persistent

Giemsa-stained fresh blood smears. 1b date,
infection with low RBC and WBC counts;
tl1e agent has not been successfully isolated.

virus can be isolated from all tissues.

. Histologically, increased hematopoietic

Chronically infected fish may exhibit few
activity may be evident in the kidney, and
visible external signs. The nervous form of
round cytoplasmic inclusions (0.8--4 µm)

the disease has been reported primarily in
are found in circulating RBCs. Inclusions
cultured freshwater fish but has also been
stain pink or magenta with Giemsa. Other
reported in marine fish.

degenerative changes may be evident in

The optimal temperature for active

RBCs, including cytoplasmic vacuolation
infection is 9° -12°C; the virus is unable to
and margination of nuclear chromatin.

replicate at temperatures> 15°C. The cell line

Hemolytic anemia with concmrent
of choice for virus isolation is bluegill fry
hemosiderosis and e1ythroblastosis has

(BF-2). Viral identification is confirmed by
been repo1ted in moribund Pacific herring.

serun1 neutralization. Newer diagnostic tests

Multinucleated giant e1ythroblasts may
include inm1unofluorescence, ELISA, and
occasionally be seen in peripheral blood,

PCR. VHS is a highly regulated disease, with
and macrophages may phagocytize
disease-free geographic regions defined in
abnonnal e1ythroblasts. A presumptive

Europe. No vaccine is commercially
diagnosis is based on the presence of typical
available. Veterinarians working with
cytoplasmic inclusions in circulating RBCs
zoologic collections must ensure that suscepof anemic fish. Confirmation requires tible species received from endemic areas
visualization of hexagonal virus particles
are properly tested and certified disease free.

in cytoplasm of affected RBCs using

In 2005, a new strain of VHS, VHS IVb, was transmission electron microscopy. A marine identified in the Great Lakes and caused
reservoir is suspected but has not been
widespread morbidity and mortality of only
identified. Vertical transmission is
wild stocks. Affected species included
suspected because of the high prevalence of
muskellunge, Chinook salmon, brown trout,
infection in fry from infected broodstock.

freshwater drun1, black crappie, bluntnose
minnow, gizzard shad, largemouth bass,

Epizootic Hematopoietic Necrosis:

smallrnouth bass, blue gill, yellow perch,

The ranaviruses are an important group
and channel catfish. Signs of VHS IVb can be
within the family lridoviridae and, as a
nonspecific. Some affected fish have no
group, include viruses that can infect fish,
clinical signs, but exophthalmia, ascites,
amphibians, and reptiles. One of these
hemorrhages (in the eyes, skin, gills, fin
causes epizootic hematopoietic necrosis
base), and behavioral changes may be seen.

(EHN), which so far has been repo1ted to

To date, no aquacultured specimens have
cause disease only in fish and is listed as a
been found to be infected with this strain,
notifiable disease by OIE. First reported in
but vete1inarians should be aware of it and
reclfin perch in Australia in the spring of
avoid introducing stocks or water from

1984, it has since been shown to cause
infected/unprotected systems.

disease, albeit less severe, in rainbow trout.

Similar viruses have been reported in
lridoviruses
sheatfish in Ge1many and black bullhead
catfish in France and Italy.

Viral Erythrocytic Necrosis: Viral

EHN is endotheliotropic, producing
erythrocytic necrosis has been reported in
necrotic lesions in the endotheliwn of

>20 species of marine and anadromous fish
blood vessels and some visceral lesions.

(both cultured and free ranging) and is

Behavioral signs include lethargy, darkening,

1764

AQUACULTURE
and erratic swimming. Mortality occurs
barrarnundi (Lates calcarifer), redfish
after 4-5 days. The most consistent lesion

(Sciaenops ocellatus), hybrid striped bass
associated with EHN is focal necrosis of

(Marone saxatilis x M chiysops), and gray hematopoietic tissue in the anterior kidney
mullet (Mugil cephalus).

and liver. Necrotic hematopoietic cells may

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Clinical signs are nonspecific but include
be visible within blood vessels. Presumptive
lethargy, anorexia, darkening, abnonnal
diagnosis is based on clinical signs and
swimming (including spinning) or position
isolation of the suspect agent in cell culture.

in the water, increased respiration, coelo

Bluegill fry (BF-2) is the cell line of choice.

mic distention, ulceration, hemorrhages/

Detection may also be accomplished using
petechiae, pale gills/anemia, fin erosion,

ELISA, immunofluorescence, or electron
white feces, and moderate to heavy
microscopy. Epizootics of EHN in redfin
mortalities. Higher temperatures may be
perch are most common in the spring and
associated with some outbreaks.

swnrner and almost exclusively involve

Diagnosis is based on clinical signs,
juvenile fish. Swvivors seem to be resistant
history, histopathology, and PCR identificato future infection. There is no evidence of tion (many of these viruses have not been
ve1tical transmission of EHN, and redfin
successfully cultured). Histopathology often
perch carriers have not been detected. An
includes areas of acute, diffuse, severe
unidentified reservoir and carrier host is
coagulative necrosis in some tissues, and/or
suspected. Fomite transmission of EHN has
variable amounts of necrosis and mild inflambeen demonstrated, and birds have also mation. Large, finely granular basophilic to
been shown to carry infected material.

amphophilic intracytoplasrnic inclusions are
most commonly identified in spleen and

Largemouth Bass Virus: This ranavirus
kidney, although in severe infections, liver,
was isolated from moribund largemouth
heart, oral cavity, thymus, bone, gills, skeletal
bass in South Carolina in 1995. It was
muscle, submucosa of the GI tract, and
previously isolated from largemouth bass
gonads are also affected.

in several Florida Jakes but had not been

There is currently no treatment for megadirectly associated with disease. It has been locytiviruses other than depopulation. A
found in largemouth bass in most southeastvaccine is available internationally but not ern and many midwestem states. The
yet available in tile USA.

disease is not well understood, because the
virus is commonly isolated from tissues of

Other Viruses
clinically normal fish. In the 1995 fish kill,

-1,000 fish died over a2- to 3- mo period in

Infectious Salmon Anemia: Infectious
an area that encompassed> 66,000 hectares.

salmon anemia is reportable to USDA

Lesions were nonspecific and are still poorly

APHIS and the OIE. The first report was
described. Fat-head minnow (FHM) is the
from fam1ed Atlantic salmon on the west
cell line of choice for isolation of virus.

coast of Norway in 1984. Affected fish were
lethargic and severely anemic (PCV <5% in
moribund fish). The causative agent is an

Megalocytiviruses: The megalocytiortl1omyxovirus. Acute outbreaks result in viruses are another very important and
high mortality. Initial signs include lethargic
emerging group of viruses within the family
fish hanging around the edges of the cage.

Iridoviridae (see MEGALOCYTMRUSES, p 1814).

As the disease progress�s, moribund fish lie

They have been associated with disease in
on the bottom.

freshwater angelfish and gourami species,

Diagnosis is based on clinical signs, with
as well as in numerous other aquacultured
emphasis on anemia (PCV < lOOA.), the gross
freshwater and marine food and aquariun1
appearance of a dark liver, and hepatic
fishes, including oscars and other cichlids
necrosis. Confumation can be by viral

(family Cichlidae ), swordtails, sailfin molisolation using the SHK-1 cell line. Virus lies, and other common live-bearers (family may be visualized in endothelial cells of Poeciliidae), and Banggai cardinalfish.

cardiac blood vessels using transmission

Numerous marine and freshwater food and
electron microscopy. The agent is envelgame finfish species are also naturally susoped, slightly pleomorphic, and -100 nm in ceptible to infection by megalocytiviruses,
size. Suspected cases can also be verified
including jacks and pompanos (several
using an inirnunofluorescent antibody
species, fan1ily Carangidae), mackerels and
technique on frozen tissue. Transmission is
tuna (several species, family Scombridae),
horizontal, and virus is shed in skin, mucus,
grouper ( several species, fanlily Serranifeces, and urine. Sea lice (Lepeophtheirus dae ), cobia (Rachycentron canadum),
salmonis) may be a vector; disease
largemouth bass (Micropterus salmoides),
outbreaks seem worse when sea lice are

AQUACULTURE

1765
present. There is no evidence of vertical
techniques. There is no treatment for
transmission. Sea trout have been proinfected fish, but avoidance can be posed as a possible reservoir of infection.

accomplished by purchase of SPF stocks,

Protective immunity has been demonquarantine, and disinfection of eggs with strated in salmon that survive an outbreak.

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iodophores (20-50 mg/L). Infectious

Vaccines are available internationally but
pancreatic necrosis is not regulated by the
may not confer complete protection. The

USDA, but state regulations exist in various
disease is heavily regulated in Norway and
parts of the country.

now in the USA, where the USDA should
be notified immediately of any suspected

Salmonid Alphaviruses: Salmonid
cases.

alphaviruses are the cause of pancreas
disease and sleeping disease in Atlantic

Infectious Pancreatic Necrosis:

salmon, rainbow trout, and brown trout. To

Infectious pancreatic necrosis is an acute,
date, reports have been from N01way and
systemic, contagious disease of salrnonid
parts of the UK, although farmed fish in
fry and fingerlings caused by a birnavirus.

other countries in Europe have also been

The virus is the archetype of the aquatic
affected. This suite of diseases and the
birnaviruses, which are further subdivided
etiologic agent are reportable to USDAinto two serotypes, A and B, that do not APHIS and the OIE, and this disease is
cross-react using serum neutralization. The
considered a foreign disease to t11e USA.

serotype B group currently consists of only

As the disease names suggest, pathology

10 isolates, all European in origin. In
involves necrosis and loss of exocrine
contrast, the A serotype contains >200
pancreatic tissue, as well as changes in
isolates that have been further subdivided
heart and skeletal muscle. Mortality rates
into 9 serotypes, Al-A9. Morbidity and
vary from minimal to >500A, in severe cases.

mortality occur only in young animals,

As a sequela, a percentage of surviving fish
usually <3 g; however, virus can be isolated
may become slender and Jong runts.

from survivors for the duration of their

Su.rvivors may also become ca.triers;

Jives, resulting in a persistent carrier state.

however, vertical transmission is still under

Recrudescence of disease in survivors has
debate, and horizontal transmission is
not been reported. The virus is vertically
considered the main route of infection. A
and horizontally transmitted, widespread,
vaccine is available in affected countries.

and reported worldwide, except in Iceland
and Australia. Rainbow trout are highly

Viral Nervous Necrosis (Betanodavi
susceptible to disease. In the USA, striped
ruses): The betanodaviruses are an
bass and their hybrids are recognized as
emerging group of viruses infecting >40
potential carriers. Other species affected
different species of primarily marine fish
include freshwater eels (Anguilla spp ), worldwide. Susceptible species include red
yellowtail, turbot, sea bass, and menhaden,
drum, cobia, barran1undi, tuna, groupers,
as well as aquatic invertebrates including
flatfishes, surgeonfishes, lemonpeel angelfish,
molluscs and crustaceans. Brook trout are
the orbicularis batfish, and tilapia. The
believed to be reservoirs of infection in the
resulting disease is also known as viral

USA.

nervous necrosis (VNN) and viral encepha

Clinical infection is nonspecific. Diseased
lopathy and retinopathy. A few freshwater
fish may be anorectic, ataxic, and display a
species have also been reported as suscepcorkscrew swimming pattern. Externally, tible. Betanodaviruses can infect tropical,
fish are darkened; exophtl1almia and
subtropical, or cold-temperate species,
external petechiation may be evident.

with species susceptibilities and optimal

Internally, petechiae may be visible on
temperature ranges varying depending
viscera; the gut is typically empty and may
on the strain of the virus. Four different
contain a yellow exudate. Fecal pseudogenotypes are currently recognized, and cysts may be evident in the water colunm.

VNN is reportable to USDA-APHIS and the

Histologically, focal areas of coagulative

OIE. As a group, betanodaviruses can infect
necrosis involve acina.r and islet cells of the
fish at temperatures ranging from approxipancreas and hematopoietic cells of the mately 15°-30°C.

kidney. Intracytoplasmic viral inclusions

Younger life stages (larvae, fry,
may be visible in pancreatic acinar cells.

fingerlings) are more frequently affected,

Infection should be confi.rmed with viral
although older, market-size fish may
isolation followed by serum neutralization.

become affected. Losses can range from

Most fish cell Jines are susceptible. The

15o/<r-100%. Betanodaviruses ai·e somewhat
virus can also be identified using fluorescent unique in that, as the disease name antibody, complement fixation, and ELISA
suggests, their target tissue is the CNS.

1766

AQUACULTURE

Consequently, clinical signs include
include wild invertebrates and contamiabnormal swimming or spinning, vertical nated water. Egg disinfection may help
position in the water, flexing of the body,
reduce impact of the disease. A commermuscular tremors, and darkening or cial vaccine may be available internationlightening of the skin. Hyperinflation of ally, but none is currently available in the
the swim bladder is also often seen, with

USA.

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affected fish positively buoyant and found

Histopathologically, in properly fixed
near the surface. Traumatic lesions
samples of affected CNS tissue (brain,
resulting from abnormal swimming may
spinal cord, retina of the eye), the presence
be secondary sequelae. Betanodaviruses
of severe vacuolation is a hallmark of the
can be spread horizontally and vertically,
disease. Disease and pathogen confirmation
and live or frozen fish fed to broodstock or is based on clinical signs, species, histopagrow-out stages may be a potential source thology, inununofluorescent antibody
of infection. Other sources of infection
techniques, and PCR.

AQUATIC SYSTEMS

A fundamental assessment in working

Basic housing units for fish may be
with aquatic species is exanlination and
outdoor ponds, raceways, cages, or
evaluation of the life support system
aquaiium systems (which may include
sustaining the animals. This is a critical step
recirculating system designs). The selection
in the clinical examination of any aquatic
of a housing unit will be dete1mined by
species, not just fish. The emphasis of this
available resources and facilities, as well
chapter is on aquariun1 and aquaculture
as the goals of the owner.

systems, but the principles may be applied

Outdoor ponds are typically constructed
to life-support designs for all aquatic
in clay-based soils, or they may have a type
organisms.

of plastic liner to retain water. In Florida,

Water quality management is a basic
there are also "water table ponds," which
component of successful maintenance of
have a certain an10unt of horizontal flow
aquatic organisms. Worn1ation is presented
of ground water into and out of the pond.

on normal parameters, as well as on

Production ponds vary greatly in size, but a
environmental diseases offish.

good design maximizes surface area while
minimizing depth (ideally <6 ft). This design

TYPES OF AQUATIC SYSTEMS
decreases the risk of stratification that can
result in catastrophic "turnover" events (see There are tl1ree basic types of aquatic
p 1771). Ideally, an aeration device should
systems, broadly defined as "open,"

be available for all outdoor ponds. In the

"semi-open," or "closed." An open system southeastern USA, most aquaculture
has inconling water from some source ( eg,
production ponds range from 0.1-20 surface
surface water, well water, or city water)

acres of water, whereas recreational fishing
flowing tllfough the culture facility one
ponds usually have a smaller swface area
time, then discharged. Raceway and cage
but may be quite deep, substantially
systems are examples of open systems.

increasing the risk of stratification and

Semi-open systems have some capacity to
turnover.

recirculate water, which requires some type

Ornamental ponds may vary from a few
of treatment, but fresh water from an
hundred gallons to many thousands. Larger
external source may be added as needed
ponds(> 10,000 gal.) are usually easier to
to supplement the treated water. Closed
manage from a water quality perspective
systems can be natural, such as.static
and are more forgiving of an owner who
outdoor ponds, or can be highly engineered;
may overstock or overfeed the fish. Most
intensive aquaculture systems depend on
larger ponds have water provided from a
extensive filtration of water before
well or city water source and are operated
recirculation. Aquariun1s are typically
as closed systems. Supplemental aeration is
considered closed systems; however, the
also very in1portant for these systems and is
complexity of design and carrying capacity
often provided by a waterfall, stream, or
of individual systems vary greatly.

other aesthetic means of moving water.

AQUATIC SYSTEMS

1767

Clinicians should not only test dissolved

Alternatively, new technologies allow cage
oxygen (DO) when evaluating an ornamensystems to be completely sunk in deep water, tal pond but also assess water movement.

decreasing the risk of damage from wind and

In poorly maintained systems, filters will
wave action. Advantages of cage production
become clogged and flow rates can
include tidal water exchange, which would
decrease dramatically. Poor flow rates
not require pretreatinent to be suitable for

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result in poor pe1iormance by biofilters and,
the fish. Disadvantages include potential
ultiniately, system failure with consequent
damage to equipment or escape of fish dilling
rises in total ammonia nitrogen concentrastonns, potential contamination in t11e event tions. Poor flow rates are also often
of a chemical spill or hannful algal bloom,
associated with low levels of DO and an
and concerns about adverse environmental
inability to maintain oxygen concentrations
impacts by the aquaculture operation itself.

near saturation. If the pond depends on a

Global use of cage cultlll·e technology is
waterfall as the primary source of aeration,
increasingly important as marine food fish
and flow rates decline, the aeration
are cultlll-ed more intensively.

capability is also compromised. Shade
may be an important consideration when
evaluating an ornamental pond. Lack of

AQUATIC LIFE SUPPORT SYSTEM
shade can result in rapid and extreme

COMPONENTS
heating of water, especially if the pond is
shallow. Hot water is not only detiimental

The basic components of a life suppo1t
in its own right, but it also does not hold
system are a vessel that houses the animals,
oxygen well, increasing tl1e risk of oxygen
and if water is to be recirculated, tl1e filtration
depletion. Shade trees around a koi pond
components, and a sU111p or reservoir ( area to
may contribute to leaf litter and organics in
collect water before and/or after treatinent).

the pond. Preventing predation is another

Understanding these component parts can
important consideration when designing an
help tl1e practitioner appreciate the basic
ornan1ental pond. Typically, fish housed in
design and how it may in1pact animal healtl1
these units are very colorful and may be
and disease management. Additional study is
very attractive to birds (including owls), as
required for clinicians who plan to develop
well as to mammalian predators such as
greater knowledge and skills for aquatic
raccoons or otters. In Florida, reptiles ( eg,
practice.

alligators) may also prey on ornamental

There are three basic types of filtration:

fish. Some type of visual barrier to mininuze
biologic, mechanical, and chemical. All
the detection of colorful fish by birds can
recirculating systems have biologic and
help, as can pond design features or other
mechanical components, and most also
structures tl1at linut the ability of wading
include a chemical component. Some types
birds to access the pond. An electric
of filters provide more than one of tl1ese
perimeter fence located 12-18 in. off the
functions and may be dual purposed in the
ground may keep small mammals or
design. Practitioners should fan1iliai.ize themcrocodilians out of an owner's yard, selves with basic filtration and more complex
protecting tl1e fish and other pets.

system designs as tl1eir experience grows.

Other types of systems, more typical of
aquaculture production, include cages and

Biologic Filtration: Biologic filters
raceways. A raceway system is typically a
remove nitrogenous waste from the system.

series of long, narrow, and relatively shallow

Fish excrete anm10nia directly from the
concrete or earthen tanks. Water enters the
bloodstreai.n via passive diffusion across
unit at one end and is discharged at another.

the gill epitheliun1. Biologic filters provide

Often, these use some source of surface
substrate and massive surface area for
water, such as a flowing river, for growout
nitrifying bacteria to live. These bacteria are
of the fish. Advantages of raceway systems
ubiquitous in the environment and grow well
include capacity for heavier stocking
when nitrogenous compounds ( ai.nmonia
densities than ponds of a corresponding
and nitiite) are present in tl1e water colunin.

volume. Disadvantages include concerns

These bacteria require both oxygen and a
about bringing pathogens or contaminants
carbonate source, which must be provided
onto the fam1 and discharging nutiient
by the water and filter design. Exan1ples of
waste, pathogens, or treatinent chemicals
biologic filters are plastic plenums placed in
in the effluent. Cage production is most
tl1e bottom of home aquaria, fluidized bed
common in open water, with t11e salmon
filters common in commercially designed
industry being a prime example. Typically,
systems, and an array of bead and sand
large cages are placed in protected bays
filters sold for use in ornamental pond ai.1d
for the grow-out phase of the operation.

aquaculture units.

1768

AQUATIC SYSTEMS

Aquatic vessel
housing fish

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Chemical

Filtration

(carbon
ultraviolet,
ozone, foam
fractionator)

Mechanical Filtration

Biological

(sand, foam, bead,

Filtration
filter, etc)

(requires 02
and CO,)

Settling Basin

Generic schematic of a basic aquatic life support system. Mechanical filtration should precede biofiltration. Mechanical filters help prevent channeling and anoxia in biofilters by removing large particulate matter. Biofilters must have a lot of surface area for nitrifying bacteria. Chemical filtration, although not required in all designs, polishes and cleans water before it is returned to the vessel housing the fish. Courtesy of Dr. Ruth Francis-Floyd.

Mechanical Filtration: Mechanical
the load on the biofilter); ultraviolet light,
filters a.re always placed before biologic
which removes potentially pathogenic
filters in the system design. Mechanical
organisms from the water column; and
filters typically receive water leaving the
ozone, which clrui.fies water and kills
vessel housing animals and remove large
microbes. Ozone is conunon in large
particulate matter before water comes into
commercial aquaria and requires a
contact with the biofilter. Large particles
de-gassing area before the treated water
can clog a biofilter, resulting in channeling
comes back into contact with fish.

and development of anoxic areas that

Malfunction of ozone units can be
greatly compromise function of the unit.

hazardous to people as well as animals

Mechanical filters can be as simple as floss
housed in aquarium system:,.

or foam pads receiving a stream of water, or
much more complex. Sand and bead filters

EQUIPMENT NEEDED FOR
a.re commonly used and have dual functions

SYSTEM AND WATER ANALYSIS
of mechanical ru1d biologic filtration.

To competently assess a system's design

Chemical Filtration: Chemical filters
takes some practice, but a basic understandprovide a way to treat the water. Activated ing and analysis can be accomplished by
carbon is very commonly used to remove
keeping in mind tile component pru·ls ru1d
toxins and colored compounds from
their functions. Site visits a.re essential to
aquarium water, which helps maintain
understanding how a system has been put
clarity. Activated carbon filters may also
together. In addition to assessing the design
be placed on inflowing water to remove
and functionality of a system, a site visit
chlorine and/or chlorrunine from city water.

allows tile oppo1tunity to assess mainte

Activated cru·bon filters can also be used to
nance and cleanliness, both c1itical aspects
remove treatment chemicals from water
of animal husbandry. The importance of a
before dischru·ge to city sewers. Other

DO meter cannot be overstated when
exrunples of chemical filters include protein
assessing an aquatic system. Oxygen
skimmers and forun fractionators, which
concentration should be measured in the
a.re commonly used in marine systems to
ru·ea housing the animals, and it should also
remove proteinaceous waste ( decreasing
be used to help identify areas prone to

AQUATIC SYSTEMS

1769
anoxia because of equipment problems,
affected and unaffected. If fish are brought
poor maintenance, or design flaws.

into the clinic for examination, a separate

Water quality testing equipment is a
water sainple should be provided in a
requirement for aquatic practice. Good
plastic bag or clean, plastic water bottle. If
quality testing kits are commercially
the source water is from a municipal water

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available at reasonable prices. Tests can
supply, a second sample should be collected
be run quickly, providing data in a timely
in a glass bottle for chlorine/chloramine
manner. Basic requirements include a
testing. Water samples collected by the
means to test temperature, DO, carbon
owner should be capped under the surface
dioxide (C02), chlorine, chloramine,
of the water without any gas bubbles visible.

anm1onia, nit1ite, nitrate, pH, total alkalinity, A mininlum of l quart of tank water should total hardness, and salinity. Testing for
be requested for regular analysis, and a
freshwater and marine systems is similar;
second smaller sample ( <100 mL) in a glass
however, the ammonia test often sold for
container for chlorine testing. If desired to
freshwater use requires the use ofNessler's
use for recovery after anesthesia of the
reagent, which has two distinct disadva.nai1imal, a lai·ger volume of tank water may tages: it contains mercury and therefore
be requested.

must be treated as hazardous waste, and it
does not work in maiine systems. Alterna

ENVIRONMENTAL DISEASES
tively, ai1 an1monia test using an ai11moniun1
salicylate reagent is rec0111mended.

Because poor water quality is the most

Chlorine test kits (free and total chlorine)

common cause of envirorunentally induced
are not included in many kits marketed to
diseases, some way to assess water quality
the aquaculture industry and need to be
is essential. Inexpensive test kits are easy to
ordered separately. Also, a copper test kit
use and provide reasonably accurate
and a refractometer (to measure salinity)

infom1ation. Professional aquacttlturists or
should be on hand for use in marine
advanced tropical fish hobbyists should be
systems. If a practice has enough cases to
encouraged to purchase and use their own
waiTant the investm!:!nt, an electronic
water-testing equipment. Pet fish owners
oxygen meter is strongly recommended.

often rely on pet stores to do the water

If working in a rw-al area where well water
testing; however, many pet stores have very
is con1monly used, test kits for iron and
limited capabilities in this area, use less
hydrogen sulfide should be considered. For
accurate tests, and may be unable to
true specialty practices, investment in a
accurately interpret results.

saturometer for detection of supersatura

Veterinariai1s practicing fish medicine
tion is also suggested.

should have a comprehensive understai1ding of the dynanlics and management of ENVIRONMENTAL HISTORY
water quality, including general guidelines
for acceptable water quality parameters

As with all aspects of medical analysis, a

(see TABLE 2). In addition to temperature,
good history is critical in establishi.ng a
basic paraineters of water quality can be
cliagnosis. Specific questions are important
grouped into four major categories:

te assess the environmental quality and may
dissolved gases, nitrogenous compounds,
play an important role in treatment
pH and carbonate compounds, and salinity.

recon1mendations. First, a thorough

The significance of water quality pai·ameters
description of animal housing should
varies with the type of system, species, and
include the volume, design of the system,
stocking density. Low DO ai1d high
and source of water. The number and size of
an1monia are the two water quality
animals stocked, species (fish and non-fish), paran1eters most likely to directly kill fish.

new additions, use of quarantine, decora

Water quality interactions are dynamic and
tions, plants, and previous medications ai·e
complex. Indirect relationsllips can lead to
pa.it of the case history and may also be
toxicity from otl1er pai·aineters, such as the
relevant to assessment of environmental
effect of rising pH on (increased) ai11mo1lia
quality and system design. Owners can be
toxicity, or there cai1 be indirect relationasked to bring fish and water samples to the ships between water quality and certain
clinic, or the practitioner may wish to visit
infectious agents. For exai11ple, low or
the site. Site visits allow the system to be
inappropriate temperature can be
more accurately evaluated and the behavior associated with fungal diseases of fish.

of fish to be readily observed. If a site visit is

A classic exainple is Fusariitm solani
not possible, the owner can be asked to
infection of bo1methead sharks, which has
provide a video and/or photos of the system
been managed by raising the envirorunental

(including filtration) and the fish, both
temperature to >80°F (27°C).

1770

AQUATIC SYSTEMS

"NORMAL" REFERENCE RANGES FOR ROUTINE WATER

QUALITY ANALYSIS

Parameter

Freshwater

Saltwater

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Dissolved oxygen

Saturation"

Saturation

Carbon dioxide

<12 mg/L

<12 mg/L
pH

6.5-9.0

7.8-8.3

TAN (total ammonia nitrogen)b

Omg/L

Omg/L

Toxic un-ionized ammonia (NH3)b

Omg/L

Omg/L

Nitrite

Omg/L

Omg/L

Nitrate

<20 mg/L

<70 mg/L

Total alkalinity (carbonate fraction)

> 100 mg/L CaC03 >250 mg/L CaC03

Total hardness (Ca and Mg primarily)

>20 mg/L CaC03 >250 mg/L CaC03

If source water is from municipal water supply:

Total chlorine (free chlo1ine + chloran1ines)

Omg/L

Omg/L

Free chlmine

Omg/L

Omg/L

• Dissolved oxygen in ponds will fluctuate on a diurnal basis. Concentrations <5 mg/Lare dangerous.

Mortality will be species-specific and related to time of exposw-e but may be obse,ved at s4 mg/L.

Oxygen sattu-ation at room temperature (25°C [77°F]) and sea level will be 8.27 mg/L in freshwater and 6. 75 mg/Lin seawater (35 ppt or chlorinity of 20 ppt).

"Under most circumstances, freshwater fish can tolerate total ammonia concentrations <l mg/L, whereas saltwater fish will usually tolerate TAN <0.5 mg/L. Un-ionized anm1onia concentrations

<0.05 mg/L ru·e not considered harmful.

See TABLE 3 for an overview of common
chlorine. Free chlorine measures hypochloenvironmental diseases of fish.

rous acid (HOC!) and the hypochlmite ion

(OCI-), which is the active property in

Chlorine, Chloramine, and Other
bleach. Total chlorine measures free chlorine

Toxicants: Aquatic organisms are sensitive
plus chlorine that is tied up as chlorru11ine.

to a wide variety of toxicants, particularly

Water treated with chloran1ines alone will
chlorine and chloramine, which are
test negative for free chlorine but have high
common additives to city water. Chlorine is
an10unts of total chlorine detectable;
also used to disinfect tanJ(s and equipment.

therefore, testing for both is important.

Chloran1ine is a fom1 of chlorine that has

When chloramines are treated with sodiun1
been stabilized by an1ination. When treated
thiosulfate to eliminate the chlorine,
for removal of the chlmine molecule,
an1monia is released into the system. In such
an1monia is released into the system. Both
an instance, repeated water changes ( each of
compounds are highly toxic to fish, with
which requires dechlorination, releasing
adverse effects seen at chlorine concentraadclitional ammonia) can result in high tions as low as 0.02 mg/Land mortality at 0.04 an1monia levels that also may be toxic. A mg/L. A simple colorin1etric test is available
properly conditioned biofilter should be able
to measure chlorine and chloran1ine in
to metabolize the rurnnonia as it is released,
aquatic systems. No chlorine or chloran1ine
but a new or dan1aged bacterial bed will not
should be detected at any time live ru1in1als
be able to mru1age the influx of an1monia
are present. Water san1ples for chlorine
from repeated deru11ination of chloran1ines.

testing should be tested onsite; however, if

This problem can be overcome by using a
that is not possible, they may be trru1Sported
dechlorinator specifically designed to deal
in glass bottles. The chemical can be
with chlora.mines by also binding the
tra.I1Sient and difficult to detect, so a negative
an1monia byproduct. Effective use of
test result may not completely exclude some
dechlorination products requires testing
contan1ination in the system being evaluated.

water for both free and total chlorine before

To test for chlorine and/or chlorru11ine, kits and after use. Following label instrnctions on are available that measure both free and total products sold from pet stores usually

AQUATIC SYSTEMS

1771
effectively removes these chemicals;

Dissolved Gases: Of the dissolved
however, in rare instances more chlorine/
gases, oxygen is the most important. In
chlorarnine than expected may be present
outdoor production ponds, photosynin mrnucipal water supplies. Treatment of thesis by algae is the primary source of
water supplies will vary, and boluses of
oxygen. A diurnal cycle is established,
chlorine or chloranune may be sent through
which coincides with photosynthetic

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water lines as part of maintenance protocols
activity. During daylight hours, when
in some circumstances. Further, inaccurate
photosynthesis occurs, oxygen levels rise
calculation of the volume to be treated can
and C02 levels fall. At night, respiration is
also lead to poor performance or failure of
the driving force, resulting in a decrease in
dechlorination products.

DO and an increase in C02• Most firtfish

Chronic exposure to sub lethal concenthrive when the DO concentration is >5
trations of chlorine is a surprisingly
mg/L. When DO is <5 mg.IL, fish become
frequent problem, even for experienced
stressed; depending on species, size,
aquarists. Veterinarians should test water
and duration of exposure, a fish kill may
for chlorine (free and total) every time a
result. Cardinal signs of a fish kill caused
sample is submitted from a tank that uses
by hypoxia include sudden, significant
a mlll1icipal water supply as source water.

mortality, usually noticed early in the

Clinical indications of sub lethal chlorine
morning (when oxygen levels ar·e lowest);
exposure are nonspecific but may include
often, large fish are affected more than
ragged fins, excess mucus on skin and gills, small fish. Fish that are hypoxic often cloudy corneas, behavioral signs such as
school near the surface of the water and
lethargy or irritation, and sometimes a
may be seen trying to gulp air, a behavior
history of low chlorine level and chronic
referred to as "piping." Differential
mortality.

diagnoses for piping includes low DO,

Other toxicants include hydrogen sulfide
high nitrite, and gill disease.

and heavy metals. Hydrogen sulfide

Altl10ugh low DO is most common early
usually is a problem in poorly maintained
in the morning in outdoor ponds, it car1 occur
tanks in wluch the sediments are not cleaned at any time. Other co11U11on causes of low frequently enough, allowing anoxic areas to

DO in ponds are cloudy weather, death of an
develop. Cleaning or other distmbance of
algal bloom, excessive feeding, overstocking,
these areas can release hydrogen sulfide into
and pond turnover. Unrecognized overstocktl1e water column, resulting in acute and ing can occur in koi ponds if fish spawn
catastrophic mortality. Another common
successfully and offspring survive and are
source of hydrogen sulfide is well water; if
retained in the system. Pond turnover is a
this is the case, a distinctive "rotten egg"

common cause of catastrophic mortality in
smell can sometimes be detected. Hydrogen
pond fish. It occurs most frequently in deep
sulfide is volatile and transient, so unless a
ponds (>6 ft) and involves a phenori1enon
water sample is collected at the time of the
refe1Ted to as stratification. Water at the
problem, a confumed diagnosis may not be
bottom of the pond cools, and a temperature
possible. Acute mortality has been rep01ted
gradient, called a tl1em1ocline, develops
at concentrations of 0.5 mg.IL, but any
between warm surface water and cool
detectable hydrogen sulfide should be
bottom water. The thermocline acts as a
considered a significant problem.

physical barrier between the surface water

Heavy metals in water can result in

( epilimnion) and bottom water (hypolimacute, or more often, chronic mo1tality.

nion). Because photosynthesis, and hence

If household plumbing includes copper
oxygen production, occw-s at the surface, the
piping, some copper may leach into the
hypolin1nion becomes hypoxic and develops
water. If released in sufficient volume, this
a biologic oxygen demand. When tl1e pond
may cause a fish kill. Problems are most
is nuxed, or "turns over," the oxygen is
likely when water has been allowed to stand removed as the biologic oxygen demand of in pipes. A copper test of suspect water
the hypolinuuon is satisfied. This sudden
should confirm the problem. Solutions
removal of oxygen can result in oxygen
include ruruung the water before it is placed depletion and a fish kill. The most common into the aquarium, or special filtration ( eg,
cause of pond turnover in the south em USA
activated carbon) to remove metals.

is a sW11mer tl1W1derstom1, in which energy

Zinc toxicity has been associated with
released from cold rain coupled with wind
use of stainless steel vessels to house fish. It
and wave action is sufficient to nux the pond.

has also been reported rarely from public

Fish kills in F1orida have occwTed after
exhibits in which coins were allowed to
hurricanes and have been attributed to pond
collect on the substrate or to be ingested by
turnover. Pond turnover can also be caused
fish.

by seining, aeration, or other management

1772

AQUATIC SYSTEMS

IM=Hii COMMON ENVIRONMENTAL DISEASES OF FISH

Disease

Problem

Behavioral Signs

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Low dissolved oxygen

Hypoxia

Piping at surface; large fish
affected more than small ones

Gas bubble disease

Supersaturation

Lethargy, buoyancy problems

(often N2 gas)

Carbon dioxide toxicity

C02 >40mg/L

Lethargy at surface

Ammonia toxicity (new

Un-ionized ammonia

Lethargy, anorexia, spinning,
tank syndrome)

>l mg/L
convulsive swimming
pH>8

Nitrite• toxicity

N02 >0.1 mg/La

Piping at surface

Low chloride (freshwater)

Nitrateb toxicity

N03 -N �70 mg/L

Lethargy

Low (no) iodine, 03

Old tank syndrome

Total alkalinity

Lethargy, poor appetite

(TA)-0 mg/L
pH <6, high total ammonia
nitrogen (TAN)

Lack of minerals

Total hardness <20 mg/L

Sudden death

Use of distilled water

Chlorine toxicity

Detectable chlorine

Acute: sudden death

Chronic: lethargy, irritation

Hydrogen sulfide toxicity Detectable H,S

Acute: sudden death

(rotten egg smell)

Chronic: lethargy, poor
appetite/growth

Copper toxicity

Cu2+ >0.2 mg/L

Sudden death

Low alkalinity

Zinc toxicity

Coins in exhibit

Lethargy, anorexia

Stainless steel, acidic pH

Stray voltage

Electrical short,

Irritation, mortality
mechanical problem

•There is tremendous species-specific variation to nitrite toxicity. Environmental conditions, especially chloride concentration, can mitigate the effects. Most test kits measw-e mg/L N02-N. To conve1t to N02 (mg/L) concentration, this value must be multiplied by 3.3.

b Most test kits measure mg/L N03-N. To conve1t to N03 (mg/L) concentration, this value must be multiplied by 4.4.

practices that result in mixing of the
lakes, ponds, and even rivers in the southern
epilimnion and hypolimnion. Fish kills

USA. Although rare, stratification-related
caused by pond turnover can be avoided by
phenomenon can occur in aquariums and
performing a weekly oxygen profile during
other aquatic systems. Under some
periods of greatest risk ( usually during hot,
conditions, flow rate, current patterns
summer weather). If stratification is

( related to tank design), and oxygen demand
detected, the pond should be aerated or
can cause layering (ie, stratification) and
mixed to break down stratified layers before
consequent focal areas of anoxia.

a significant oxygen demand layer can

When assessing DO and aeration in
develop. Turnover events resulting in
indoor systems or exhibits in which the
localized areas oflow DO are common
primary source of DO is an aeration device,
causes of wild fish kills during the sununer in
and water is clear, the percent saturation

AQUATIC SYSTEMS

1773

•t}iii• COMMON ENVIRONMENTAL DISEASES OF FISH (continued) Mortality

Physical Signs

Acute

Chronic

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Flared gills, dark

Catastrophic mortality

Ongoing

Gas bubbles in gill capillaries, fins,

Catastrophic mortality

Ongoing
and eyes; exophthalmos ("popeye")

None

Yes

Yes

Darkened

Catastrophic mortality

Ongoing

Gills and blood dark brown color

Yes

Yes

Swelling around throat ("goiter")

No

Yes

None

No

Yes

None

No

Yes

Acute: none

Catastrophic mo1tality

Ongoing

Chronic: excess mucus, cloudy eyes,
gill inflammation/ necrosis

None

Catastrophic mortality

Ongoing

None

Catastrophic mortality

Ongoing

None

Not usually

Yes

Enlarged abdomen (coins in GI tract)

Broken back

Yes

Yes
should be considered along with the total
anoxic, organic-rich areas within the

DO reading. The amount of oxygen that
system). In either case, an inability to
water can hold in saturation varies with
maintain a system at, or ve1y near, 100%
water temperature, salinity, and altitude. Of
oxygen saturation requires correction. Most
these three factors, water temperature is the fish do well if DO is >5 mg/L; however, the most important. As any of these variables
percent saturation should be considered
increase, the amount of oxygen in solution
an indicator of the system's health.

at saturation decreases. Saturation tables

Gas bubble disease is caused by
are available to determine percent
supersaturation of water with dissolved
saturation for a given DO if temperature,
gases. Although oxygen and/or C02 can
salinity, and altitude are known. Many
contribute to supersaturation, tl1e predomimodestly priced oxygen meters now nant gas contributing to the problem is
provide data on the concentration of DO
usually nitrogen. Gas bubble disease can

(mg/1) as well as the percent saturation. If
result in acute catastrophic or chronic
oxygen saturation is < lOOOA,, it may indicate
mortality. It may occm transiently and can
inadequate aeration for the bioload or
be difficult to confirm. Supersaturation
sanitation problems ( development of
should be considered when unexplained

1774

AQUATIC SYSTEMS
mortality is encountered in an aquarium
extensive granulomas developed. Treatsetting. One common source of supersaturament for C02 toxicity is increased and tion is the use of well water that contains
vigorous aeration. Stocking density should
high concentrations of nitrogen (gas) or C02• be assessed and may need to be decreased.

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Th.is problem is easily remedied by aerating
the water before it comes into contact with

Nitrogenous Compounds: Nitr�genous
the fish. Common causes of gas bubble
wastes enter the aquatic system directly
disease in public aquaria include the use of
from excretion by fish, decomposition of
cavitating pumps, leaks in plun1bing on the
organisms in the water, or degradation of
intake side ( allow for gas to enter and be
fish food. Fish foods are generally very
forced w1der pressure through the pwnp ),
high in protein, often >38%, and can add
and sometin1es excessive turbulence in cold
sigrtificant quai1tities of nitrogen to a
water exhibits. In these cases, the supersatusystem. Nitrogen is eliminated from fish by ration is caused by atmospheric nitrogen
passive diffusion of anm10n.ia (NH3) from
gas. Gas bubble disease is manifest by
gill capillaries. Once NH3 is released into tl1e
exophthalmos and the presence of tiny gas
water, it enters the nitrogen cycle, a natural
emboli within fins, corneas, or other tissue.

process in which bacterial populations

The presence of gas emboli within gill
chai1ge ainmonia to nitrite (N 02) and then
capillaries is diagnostic. Treatment of gas
to nitrate (N03). Nitrate is most commonly
bubble disease is vigorous aeration to
removed from aquariums by water changes.

volatilize excess gas and correction of

In large, commercial systems, discharge of
underlying mechanical problems. Consalt water to mtmicipal water supplies is not fimting a case of supersaturation can be
allowed, and nitrate accun1Ulates. It can be
extremely difficult, especially if mortality
removed by anaerobic filtration, which
was acute and gas emboli caimot be
converts N03 to nitrogen gas (N2), which
detected in tissue. Sometimes, tiny gas
is volatile and quickly leaves the system.

bubbles may be visible on the inside of the

These anaerobic filters are expensive
glass in an aquariun1, suggesting a lot of gas
and can be challenging from the design
is in the water col wnn. A saturometer will
perspective, so they are not conunon except
measure all dissolved gases and is the best
in very large exhibits. Plants or algae, if
tool for direct detection of the condition. If
present in a system, will use nitrogen

DO of the system is known, this equipment
products directly. Toxicity of each of these
can be used to calculate the concentration of paraineters is discussed below.

nitrogen gas present. Permanent correction

NH3 is highly toxic and frequently limits
of the problem includes identification and
fish production in intensive systems. It is also
correction of the sow-ce of the excess gas.

dynamic, and when it enters the aquatic

C02 can be toxic to fish a.t concentrations
system, an equilibrium is established between

> 12 mg/1. The concentration of C02 in

NH3 and anunon.iwn (NH/). Of the two, NH3
solution in ground water is typically <10
is fai· more toxic to fish, and its formation is
mg/1. Water from affected systems often
favored by high pH (> 7) and water temperais acidic (pH <7). A quick field test for ture. When pH exceeds -8.5, any NH3 present
excessive C02 involves vigorous aeration
can be dangerous. In general, a norn1ally
of a bucket of suspect water for 1 hr. A
functioning aquatic system should contain no
significant increase in pH (ie, > 1 tmit) over
measmable NH3 because as soon as it enters
the hour is indicative of excess CO,. Fish
the system, it should be remov�d by aerobic
exposed to high concentrations of C02 may
bacteria in the environment. Ammonia test
be quite lethargic and even disoriented.

kits do not typically measure NH3 directly but

Hybrid striped bass exposed to toxic levels
instead measure the combination of NH3 and
of C02 ( -40 mg/1) at the surface have been

NH,+, referred to as total anm10n.ia nitrogen
observed with their backs out of the water.

(TAN). A TAN <1 mg/Lis usually not cause for

These fish reacted drainatically to salt
concern wlless the pH is >8.5. However, if the
added to the affected tank by trying to jump
ainount of NH3 is increased, an explanation
out of the water. When C02 is high in the
should be sought. The ainount of toxic NH3
water colunm, fish are not able to release
present can be calculated using the TAN, pH,
it from the bloodstrean1, resulting in
and water temperature. When NH3 levels
hypercarbia and acidem.ia. The condition is
exceed 0 .05 mg/1, dan1age to gills becomes
exacerbated by low concentrations of DO.

apparent; levels of2 mg/Lare lethal for many

Nephrocalcinosis and visceral granuloma
fish. Fish exposed to an1mon.ia may be
were reported in salmon.ids exposed to a
lethargic and have poor appetites. Acute
high level of C02 in the water, leading to
toxicity may be suggested by neurologic signs
metabolic acidosis and urinary and tissue
such as spinning, disorientation, and
precipitation of calcium, around which
convulsions.

AQUATIC SYSTEMS

1775

Overfeeding or malfunction (death) of
improper management over a period of
a biologic filter are common causes of
months. Over time, the biofilter bacteria
increased NH3. If possible, a water change
acidify the water through the nitrifica-

(�500Ai) should be done as soon as high NH3
tion process. As the buffering capacity

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levels are detected. When changing water

(alkalinity) is exhausted, organic acids
to alleviate NH3 toxicity, it is in1perative to
that have accun1ulated drop the pH, and
consider whether source water contains
tl1e acidic environment kills the biofilter,
chloramines, because this can contribute
leading to an accwnulation of NH3. When
to increased NH,1 concentrations. If TAN
correcting such a situation, it is important to
is extremely high (ie, >5 mg/1) and pH is
eliminate as much "bad" water as possible
acidic (ie, <6), fish should be moved to
and avoid a shift in residual NHa-H to the
a clean system (tempered for pH and
toxic un-ionized state (NH3) as pH rises. A
temperature) to avoid a sudden shift from
simple water change under such circum

NH,+ to NH3 as the pH rises during the water stances can result in catastrophic mortality change. Feeding should be discontinued or
as pH rises above 7 and ammoniwn shifts to
significantly reduced until the problem has
un-ionized (toxic) ammonia. Over-the-counbeen corrected.

ter products that chemically remove or bind

Two conditions encountered in pet fish

NH3 can help prevent mortality, but the
medicine are characterized by high NH3
system must be thoroughly cleaned and
concentrations, appropriately called new
restarted. It will take several weeks for the
tank syndrome and old tank syndrome.

system to recover.

New tank syndrome occurs when NH3

The second breakdown product in the
levels rise during the first 2--3 wk after a new nitrogen cycle is nitrite (N02), which is system is set up, because the biofilter has
also toxic to fish. Most test kits actually
not had time to develop. In this situation,
measure nitrite-nitrogen rather than nitrite.

the NH3 concentration will be increased,

A conversion factor of 3.3 can be used to
but all other parameters should be within
calculate the actual nitrite concentration
nom1al limits. Beginning aquarists are likely

(3.3 x mg/L NOrN = mg/L N02). N0
to overstock and overfeed new systems,

2 can
enter the bloodstrean1 passively across the
resulting in significant NH3 spikes and,
gill epitheliwn. It complexes witl1 hemosubsequently, sick or dying fish. Daily globin to fonn methemoglobin, resulting
monitoring of TAN coupled with frequent
in methemoglobinemia, or brown blood
water changes to manage NH3 will be
disease. As in other species, RBCs
necessary until the biofilter cycles.

containing methemoglobin are w1able to

Maturation of the biofilter will be indicated
transport oxygen, resulting in a physiologic
by decreasing concentrations of TAN and
hypoxia regardless of oxygen content in the
increasing concentrations of N02 (which
water. There are species-specific differwill decrease as the filter conditioning ences in fishes' susceptibility to N02 toxicity
process is completed). Damage to a biofilter

(eg, centrarchids [bass, bluegill, etc] are
can be caused by use of antibiotics or other
refractory). Marine fish were thought to
chemicals and result in a sintilar situation.

be protected from N02 toxicity by salts in

It usually takes -6 wk for a new biofilter to
their environment; however, red drum
cycle. When tltis time frame is extended,
have developed brown blood disease in
there may be complications attributed to
the presence of N02. A tentative diagnosis
poor design, use of chemicals, or lack of
of brown blood disease can be made by
adequate oxygen and carbonate (alkalinity)

observing the characteristic chocolate
in the filter bed. To prevent new tank
brown color of the gills, although this
syndrome, aquarists use several "tricks"

change is not detectable until methemoto get biofilters started. These include globin levels are substantial. In severe
purchasing commercially available
cases, the color of blood san1ples will also
nitrifying bacteria from a reputable source,
be abnormally dark. Methemoglobin

"feeding" the bacteria with fish food or
concentrations in the blood can be
anm10niwn chloride before adding fish, or
detemtined, altl10ugh this is not necessary
adding fish slowly to the new system.

for clinical management. A water quality

Old tank syndrome is less frequently
test can confun1 the presence of N02• Fish
recognized. It is characterized by extremely
affected with methemoglobinemia typically
high NH3 levels (TAN may be >20 mg/1),
show signs of hypoxia, often manifest by
extremely low pH ( usually <6, may be <5 in
piping.

sev�re cases), and a complete absence of

The most rapid treatment for N0
alkalinity. The condition is caused by

2 toxicity
is a water change, but this is not feasible in
complete exhaustion of buffering capacity
large ponds. Increasing chloride (CJ-)

within a system, usually precipitated by
concentration in the water creates a

1776

AQUATIC SYSTEMS
competitive inhibition at the gill epitheliwn
factors include inadequate dietary iodine or
between Cl and N02• Many ornamental
environmental iodide, ozonation, and nitrate
ponds and aquaria are maintained with
exposure. Goiter is characterized by a ventral
residual chloride levels because of the
midline swelling in the cervical region of
addition of salt ( 1-3 ppt) as a relatively
elasmobranchs. Diagnosis can be confumed

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permanent treatment. In these cases, nitrite
by measuring T
is less likely to be a problem, because

4. In healtily (no clinical or
histologic evidence of goiter), captive, white
chloride levels are increased by the residual
spotted bamboo sharks housed in a natural
salt concentration. In freshwater production
seawater system, T, was 14. 77 ng/mL (range
ponds for channel catfish, a ratio of 6 parts
of 9.57-30.50 ng/mL in five anin1als). Lower

Cl to 1 part N02 has effectively prevented
levels have been reported in sharks with
or treated methemoglobinemia caused by
visual evidence of goiter. If an animal is
niLriLe exposure. The absorption of c1-
necropsied, thyrnid tissue can be evaluated
across the gill membrane reduces the
histologically to confinn tl1e diagnosis.

amount ofN02-entering the bloodstream;

Nitrate is well recognized as a goitrogenic
consequently, the percentage of hemoglobin
compow1d and may be present in fairly
converted to methemoglobin is decreased,
high concentrations(> 70 mg/L N03-N) in
resulting in irrunediate relief to the fish and a
recirculating aquariw11 and aquaculture
cessation of mortality usually witlun 24 hr.

systems. Nitrate blocks tl1e uptake of iodine

To detennine the amount of salt required to
by the thyroid gland, resulting in an inability
increase chloride levels in large ponds, the
to produce thyroid hormone and constant
concentrations of N02 and Cl present must
stimulation of tl1e glandular tissue. Fish and
be measured by commercial test kits. The
elasmobranchs absorb nucronutrients,
concentration of Cl needed (mg/1) = (6 x
including iodine, from tile water colwm1.

N02) - Cl present. Once the necessary

In an ozonated system, tile problem is
concentration of Cl- to be added is known,
exacerbated because iodine is converted
the volwne of water can be calculated in
to iodate (103), which is not biologically
acre-feet or gallons (1 acre foot= 1 surface
available. Dieta.Jy supplementation of iodine
acre, 1 foot deep or 325,850 gal.), and salt can at 10-30 mg/kg/wk is recommended for be added to achieve the desired Cl level ( 4.5
elasmobranchs to prevent development
lb of salt will add Cl at 1 mg/L to 1 acre-foot
of goiter. Environmental iodine should be
of water, or l lb of salt will add 1 mg/L Cl to
maintained witil concentrations of 0.15 µM

72,411 gal.). In aquariwns and garden ponds,

(0.01--0.02 mg/1) iodide (I-). Potassiwn
a water change and filter maintenance are
iodide (Lugol's solution) has been used to
recorrunended to cotTect nitrite problems;
increase enviromnental iodide concentrahowever, salt may still be used to halt tions in public aquaria. Goiter occurs in
mortality during a sudden increase in N02
teleosts and other aquatic species but is not
exposure for many freshwater fish.

as easily recognized. The body shape of many

Although considered less toxic than
elasmobranchs allows for easy recognition
anunonia or nitrite, chronic exposure to
of the problem dw;ng a visual exanunation.

nitrate (N03-N) has been 3§SOciated with
development of goiter in some species of
pH and Carbonate Compounds: The
elasmobranchs. As mentioned earlier for the
carbonate cycle is an important concept in
nitrite test kit, most test kits for nitrate
water quality management, and its complexactually measure NOrN. To convert to the ity is reflected in tile dyuamic interactions
actual N03 concentration, this nwnber must
between C02, pH, total alkalinity, and total
be multiplied by a cotTection factor of 4.4.

hardness. In aquatic systems containing

Practitioners should read the literature
algae or plants, C02 fluctuates on a diurnal
carefully to distinguish reports ofN03-N
basis, sinular but opposite to fluctuations in
versus N03 concentrations. Chronic

DO. As C02 concentration changes, the pH of
exposure to NOrN concentrations of70 mg/L the water also changes. As C02 concentraresulted in histologic evidence of goiter in tion decreases during daylight hours, pH
white spotted bamboo sharks within 29 days
rises, peaking in late afternoon. Conversely,
of exposure. Chronic exposure to NOrN of
as C02 concentration increases dwi.ng the

35 ± 5.12 mg/L resulted in development of
night, pH falls, reaching its lowest level just
ove1t goiter and 10091, mo1tality of brown
before daylight. A diurnal pH change from
spotted bamboo sharks and lSoA, mortality of

6.5 to 9 is not unusual in a freshwater fish
white spotted ban1boo sharks in a recirculatpond with a healtily algal bloom. Most ing system after ozone was added. Goiter is
freshwater fish can tolerate reasonable .

a complex disease, and tilere seem to be
fluctuations in pH, and the letilal limits for
species-specific differences in susceptibility
many species are approximately 4 and 10.

that are not well understood. Contributing

Marine fish are much less tolerant of pH

AQUATIC SYSTEMS

1777
fluctuations the marine environment is much
dolomite, or agricultural limestone can
more stable, with a pH of 8.2-8.3. For marine
be added to water to increase calcium
tanks, a pH in the range of7.8---8.5 is usually
concentration. For channel catfish, TH >20
considered nom1al.

mg/L is required for normal skeletal growth

Although fish kills caused by improper
and development. Fish absorb minerals from

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pH are rare, hydrated lime (Ca[OHb) is
the water column; therefore, use of water
sometimes added to freshwater ponds by
with very low TH, which can be caused by
mistake. Ca(OH)2 will rapidly increase the
use of deionized water, can result in poor
pH to > 10, killing all fish present. Correct
growth and mortality.

liming of ponds is mentioned briefly below.

C02 released into an aquatic system enters

Salinity: The salinity of seawater is
the carbonate cycle: H,O + C02 <-> H2C03 <-> detemlined by a complex array of salts.

H+ + HC03- <-> 2H+ + CO}-. The process is

Seawater is -3% salt, which is 30 ppt
driven by the presence of carbonate (CO}-)

(30 g/L). For marine fish, many of the
in the system, which is measured by testing
micronutrients present in seawater are
the total alkalinity (TA). For most fish, water
essential, so it is necessary to buy or make
should be of moderate alkalinity, 100--250

"sea salts." In freshwater, salinity may be mg/L. When TA is <50 mg/L, water is
increased using table or water softener salt
considered low in alkalinity, and buffering

(NaCl). Salt is often used in freshwater sysability will not be adequate to prevent major tems to reduce osmoregulatory stress or to
pH fluctuations. Toxicity of copper sulfate, an
eliminate certain ectoparasites. Salinity can
algicide and effective parasiticide, is closely
be measured with a clinical refractometer
associated with TA, and the compound
or with a hydrometer purchased from a
cannot be used safely if TA is <50 mg/L. To
pet store. It is important not to confuse the
raise alkalinity, dolomite (CaC03 and MgC03) chlmide (CJ-) test, which is used in assessor agricultural limestone (CaC03) may be ment of N02:Cl in freshwater systems with
added to the system. Dolomite is most
high nitrite, with salinity. The chloride test
convenient for small systems and can be
measures ppm chloride; if any salinity at
purchased in 50-lb bags and used to effect.

all is present in the water (ie, salt has been

Baking soda (NaHC0
added), the test will not work properly

3) can also be used to
increase alkalinity in small systems. To raise
because the amount of chloride present is
alkalinity in outdoor ponds, agricultural
so high. The easiest way to calculate the
limestone is commonly used; the method is
an1ount of salt needed to increase salinity
similar to "liming" a pasture. Soil samples can is to calculate the total volume in liters
be tested to determine how much lime needs

(3.8 L = 1 gal.). remembering that 1 g/L = 1
to be added, but in general 1 -2 tons per
ppt. Most non-pond freshwater systems can
surface acre works well. The limestone
be maintained with a residual salinity of
should be unloaded on the bank of the pond

1-3 ppt, whereas most saltwater systems
and then usually has to be moved into the
will have a salinity of 30--33 ppt. Some freshwater using a shovel and boat. It does not water species ( eg, wild-caught Amazonian
need to be distributed throughout the entire
fish) may not tolerate permanent exposure
surface area of the pond, but it takes several
to the low levels of salt mentioned above.

weeks to get into solution. Consequently, the
alkalinity will change slowly, so it should be

Temperature: Environmental temperamonitored for several days, or weeks if ture is extremely important to the health
necessary, after the addition of these
and well-being of fish and other aquatic
compounds. Lack of alkalinity can impair
species. As poiki.lothenns, fish have a very
biologic filtration, resulting in accumulation
linli.ted ability to control body temperature,
of an1monia in a system. Alkalinity should be
and physiologic systems are designed

�100 mg/L in freshwater systems and �250
to work optimally at species-specific
mg/L in saltwater systems.

temperature ranges. Sudden changes in

Total hardness (TH) should not be
temperature, of even just a few degrees, can
confused with TA. Both TH and TA are
result in compromise of inmmnity and
reported as mg/L of CaC03. The difference is
increased patl10genicity of some infectious
that the test for TA measures the HC03-,
agents. Some fish ( eg, channel catfish or

OH-, and CO}- fraction, and the test for TH
koi) are very tolerant of a wide range of
measures the calcium (Ca2+) fraction. The
environmental temperatures; however, this
test for TH also measures other divalent
does not imply that drastic temperature
cations in the system, including magnesium,
fluctuations are acceptable even for these
manganese, iron, and zinc. TH is important
species. Others, such as discus, thrive in
in detemlining the amount of calciun1
only a very narrow temperature window.

available to young fish. Calcium chloride,

When evaluating housing and husbandry,

1778

AQUATIC SYSTEMS
practitioners should know the temperature
the quality of an exhibit populated with
at which animals are being housed and
mycobacte1ia-positive fish. In this situation,
confirm that it is appropriate for the species.

tl1e exhibit should be clearly labeled as

Suboptimal environmental temperature is
mycobacteria-positive, a.Ild employees
an important component in some fungal
should be properly trained to minimize risk of

VetBooks.ir
infections. Many infectious agents,
disease tra.Ilsmi.ssion from the contanlinated
especially viruses, have specific temperaexhibit to personnel working in the area or to ture windows at which they cause clinical
other systems or a.Ilin1als.

disease and mortality. Fish infected but
maintained at temperatures above or below

Bacterial Gill Disease: Bacterial gill
these optimal ranges are more likely to
disease is an importa.Ilt disease of cultured
survive infection but may become carriers.

salmonids a.Ild has been reported in other

When handling or transporting fish,
species, including hybrid striped bass. It
moderating temperature change is essential. is rai·e in aquarium fish. It is caused by A general rule is 1 °F, or even 1 °C, per hour
bacteria in the genusFlavobacterium a.Ild
as a maximum change. Some fish may
other closely related genera a.Ild is ma.I1i.fest
tolerate more or less of a change over time.

by gill pathology (hyperplasia, clubbing of
gill filainents) and subsequent mOitality.

ENVIRONMENTAL

However, bacterial gill disease has aI1

CONSIDERATIONS FOR SELECTED importailt environmental component, a.Ild INFECTIOUS DISEASES
mechanical damage to gill epithelium,
which may be caused by excessive

A nun1ber of infectious diseases have
crowding a.Ild deb1is in the water column, is
specific environmental parameters that
believed to be an importailt predisposing
can substantially enhance the impact of
factor. Cleaning the environment, removing
an outbreak or make an outbreak more
debris, and decreasing stocking density all
difficult to control. A few of the more significontribute to a positive treatment outcome.

cant examples are mentioned below.

COITecting these Wlderlying problems also
prevents recw-rence of the condition.

Mycobacteria: Mycobacterium spp is an Potassium permanga.I1ate can be useful in
important infectious pathogen of fish and
removing orga.I1ic detritus from an affected
other aquatic organisms. There have been
freshwater system. However, caution is
many species of Mycobacterium identified
advised, because this treatment may cause
in fish; however, all are nontuberculous
mortality in fish already compromised with
and most are environmental. Typically,
significant gill dan1age.

environmental conditions common in
aquaculture favor growth of Mycobacterium. The Role of Temperature in Infectious These conditions include low DO concentra

Diseases: Many infectious diseases of fish
tions, accumulation of organic debris and
occur in a specific "temperature window,"

paiticularly biofihns, as well as acidic pH.

and adjusting temperature may be an

Mycobacteria are hydrophobic because of
importailt part of successful treatment. For
their thick, waxy cell walls and tend to adhere example, F'usarium solani is a filllgus that to swfaces a.Ild each other. Once infected fish
has been linked to suboptimal environmenai·e present in a system, these a.Ilimals may tal temperatures in bonnethead shai·ks.

continually shed the organism in feces

Infected sharks must have environmental
a.Ild cells released from external lesions.

temperatures raised above 80°F (27°C) to

Ultraviolet light (ie, UV filtration) may
control or prevent the infection. Saproleg
decrease the nun1ber of these bacteria in the
nia, a common fungus-like oomycete of
water column, which may help decrease
freshwater ai1d brackish water fish, is also
tra.Ilsmi.ssion; correction of these environoften associated with suboptimal environmental factors Ca.Il also enhance control mental temperatme. Raising water
efforts. In aquaculture, infected fish are
temperatme a few degrees may significa.I1tly
almost always culled. In display aquaria, howimprove response to treatment. Clinicians ever, the decision may be made to maintain
are encouraged to detennine optimal
infected fish. In these cases, environmental
environmental temperature when fish are
ma.I1agement can be aI1 importa.Ilt part of the
observed with this condition and to make
protocol developed for the care of affected
appropriate corrections if needed.

a.Ilimals. Maintaining oxygen concentration

Temperature is also critical in control of
near saturation a.Ild avoiding acidic a.Ild
most viral diseases of fish. Two importailt
organically rich environments in the
diseases of koi, spring viremia of carp (SVC)

presence of some type of disinfection on the
and koi herpes virus (KHV), have strong
system ( eg, UV or ozone) Ca.Il greatly enha.I1ce temperature predilections. This should

AQUARIUM FISHES

1779
always be kept in mind when working with

In these systems, a presenting disease
these popular pets. It should be remembered problem may be infestation of external that KHV is a warm water disease. Wected
surfaces of the fish with 'I'riclwdina, a
koi typically develop disease when water
common ciliate. 'Jhclwdina is often
temperatures are in the range of64°-8l °F
considered a bio-indicator of suboptimal

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(18° -27°C). Fish with KHV typically exhibit
conditions that may include overcrowding,
significant gill lesions and signs of hypoxia.

overfeeding, and excessive organic debris

In contrast, SVC is a cool water disease,

(ie, a dirty system). Thoroughly cleaning the
typically occurring at water temperatures of
system, removing detritus, and correcting

41 °--64°F (5°-l8°C). Both of these diseases
design flaws when possible are in1portant to
are reportable at the state and federal levels.

correct these problems. Treating the parasite

Although KHV is considered endemic in the
without co1Tecting system problems will

USA, SVC is a foreign animal disease, and
result in continual rectUTence and frustrathe USDA will impose quarantine and forced tion. Other infectious agents that may be destruction of fish if an infection is
observed in the presence of poor sanitation
confirmed. Consideration of water
include sessile ciliates such asEpistylis,
temperature is an in1portant first step when

Heteropolaria, Ambiphyra, and Apiosoma.

confronted with a disease in this species.

Saprophytic fungi and fungi-like diseases

Almost all viral diseases of fish have

( eg, tl1e oomycete Saprolegnia) may also
specific temperature ranges at which they
be seen when hygiene is a concern.

cause active disease. Clinicians must
familiarize themselves with diseases of

Infectious Sequelae of Environmental
concern and the temperatures at which

Disease: Fish that survive a severe environthey occur in the species at hand.

mental insult, such as an acute hypoxic
event, are at increased risk of opportunistic

Excessive Organic Load: Organic
bacterial infections. Common infections that
deb1is can accwnulate because of poor
may occur 1 -2 wk after ru1 insult could
husbandry or poor system design. Detection include infections withAernmonas of accumulated detritus can be surprisingly
hydrophila and Pseudomonasjluorescens
difficult when areas of "dead space" exist in in freshwater systems, ru1d Vibrio spp in
a system, because these areas are often not
marine systems. Given this possibility, it
directly visible. Environmental paran1eters
may be prudent to treat valuable fish with
that suggest tltis problem include an
a broad-spectrwn antibiotic with general
inability to maintain DO concentrations at
efficacy against gran1-negative organisms
or near saturation. Further, total alkalinity
after survival of a significant insult. In many
and pH may be lower than that in source
cases, good water and a quiet environment
water. All of these changes suggest a
will be sufficient for recovery, but when in
substantial an1ount of decomposition of
doubt, tl1e use of ru1tibiotics may be justified,
organic matter is occuning somewhere in
especially if they can be provided in feed.

tl1e system. Pet owners or aquarists may

Once fish start to break witl1 an infection,
need to break tl1e system down to locate
tl1ey often go off-feed, making treatment
and remove the accwnulated material.

much more difficult.

AQUARIUM FISHES

Aquatic medicine has emerged as a
zoologic collections, can be broadly divided
recognized specialty within the practice
into freshwater and marine species. Most
of zoologic medicine. Fish medicine, an
pet fishes are freshwater, and many are fann
important component of the aquatic
raised in the USA, Asia, or elsewhere. Many
specialty, is evolving, with distinct
fish sold tl1rough the pet trade are in1ported
subspecialties of aquaculture and producto the USA. Except for a small nwnber tion medicine (see AQUACULTURE, p 1743) as of species such as some clownfishes
well as pet and exhibit fish medicine that

(Amphiprion spp), dottybacks (Pseudo
focuses on individual animals. This chapter
chromis spp ), gobies (primarily Elacati
focuses on pet and exhibit fish medicine.

nus spp), blennies (primruily Meiacan

The business of omrunental fishes, which
lhus spp ), and seal10rses (Hippocampus includes specimens that may be added to
spp ), most marine fishes are wild caught.

1780

AQUARIUM FISHES

The trade in ornamental fishes is a global

Clinical management of individual
industry, and fishes are often moved
pet fish, exhibit aninlals, and valuable
through several dealers before reaching a
broodstock has changed dramatically in
wholesale or retail outlet. The source of
recent years. Advances include use of
these fishes is an in1portant consideration
nonlethal methods to diagnose disease and

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when designing quarantine protocols and
more sophisticated treatment options.

anticipating the types and severity of

Radiology and ultrasound are particularly
disease that may be seen in recently
well suited for use in aquatic species, as are
acquired animals. Some fish species,

CT and MRI. They are especially valuable for
whether marine or freshwater, are
evaluation of the gas bladder, investigation
particularly prone to parasitic and bacterial
of internal masses, and more. Development
infection during the quarantine period (first
of blood culture techniques to accurately

30 days), including the first few weeks after
identify bacterial agents and perform
arrival in a pet store or home aquarium.

susceptibility tests before starting antibiotic

Cyprinids such as koi and fancy goldfish
tl1erapy has been useful to decrease the
for ornamental ponds are popular pets and
need to euthanize, or surgically biopsy, an
typically respond well to veterinary care.

aninlal to achieve an accurate diagnosis.

Many of the highest quality are imported

Surgical advances, including use of
from Japan (koi) or China (fancy goldfish)

exploratory laparotomy and gas bladder
and may have significant value (up to several
repairs, have salvaged aninlals that
thousand dollars for show-quality koi). Many previously would have been euthanized.

are large enough for clinical manipulation,

The equipment needed to treat fish in a
are quite hardy, and often have significant
veterinary practice is modest. In addition to
emotional value to their owners. These fish
equipment already on hand ( eg, microscope,
are susceptible to several diseases of
glass slides and cover slips, basic surgical or
regulatory concern, most notably spring
dissecting tools), water quality parameter
vi.remia of carp and koi herpesvi.rus, which
testing equipment is needed ( see AQUATIC
are both reportable diseases.

SYSTEMS, p 1766).

COMMON PARASITIC DISEASES OF SELECTED FISH

FAMILIES

Parasite

Cyprinidae

Characidae

Ciliates

"Ich"

ChilodoneUa

Tetrahymena

"Flagellates"

Ichthyobodo
v

Piscinoodinium
v

Spironucleus

C1yptobia

Coccidia

Myxozoans

Cestodes

Monogeneans

Gyrodactylids

Ancyrocephalids

Dactylogyrids

Nematodes

Note: A table cell that is not marked does not mean the parasite is not seen in that fan1ily.

AQUARIUM FISHES

1781

In addition to these basic tools, a practice

Veterinarians who offer fish medicine
should have a few fish tanks for use as
should be aware of evolving regulatory
hospital systems. These can be 10- or 20-gal.

concerns, including the current USDA
tanks with simple foam filters and aeration
accreditation progran1s. In addition,
pwnps. A dechlorinator such as sodium
aquarium fishes are susceptible to several

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th.iosulfate should be on hand if the practice
reportable diseases, which include sp1ing
uses water that contains chlorine or
viremia of carp (seep 1813), koi herpesvirus chloramine. In addition, t1icaine methane

(seep 1812), epizootic ulcerative syndrome
sulfonate (MS-222) and baking soda should

(seep 1803), and red sea bream ilidovirus
be available for sedation or anesthesia.

(seep 1814).

Other useful equipment includes a 1-L
plastic graduated cylinder for measurement

FISH FAMILIES
of water volume, a balance to weigh out
anesthetic, and a battery-powered aeration

Th.is b1ief introduction to fish families is
pump if an anesthetized fish is to be moved
intended to provide veterinaiians new to
around the clinic for radiology, surgery, or
fish medicine with mforrnation on anatomy
other procedures. For surgery, a 10- to
and pathogens common to those fanillies.

20-gal. tank works well as a receptacle. An

Fishes can be first split into two major
egg crate lighting panel, or a plexiglass or
groups: the cartilaginous fishes such as
plastic cover with small holes drilled in it,
shai·ks ai1d stil1grays, ai1d the bony fishes.

can be placed over the tank to allow water to

To fwther divide them, bony fishes
flow over tl1e fish and back to the tank. The
conrn10nly kept as pets or display aiilinals
fish can be positioned in a v-shaped foam
usually belong to one of the two subcohorts

"bed," and a small, submersible aquarium
of Ostariophysi or Neoteleostei.

pump and flexible tubing can be used to

For an ove1view of common parasitic and
circulate anesthetic-treated, aerated water
viral diseases of aquaiitm1 fish, see TABLES 4
out of the tank and over the gills. Use of
and 5. Susceptibility of specific fa.111ilies of
equipment that can be sterilized after
fish to specific pathogens is implied;
each patient is advantageous.

however, the absence of mention of a

COMMON PARASITIC DISEASES OF SELECTED FISH

FAMILIES (continued)

Loricariidae

Cichlidae

Poeciliidae

Osphronemidae

1782

AQUARIUM FISHES

•ffi:iifl COMMON VIRAL DISEASES OF SELECTED FISH FAMILIES

Virus

Cyprinidae

Characidae

Rhabdovirus

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Spring viremia of carp

Kai, goldfish

Herpesviruses

Carp pox

Kai

Kai herpesvirus

Kai

Herpesviral hematopoietic necrosis

Goldfish

Iridoviruses

Megalocytivirus

Lymphocystivinis

Note: A table cell that is not mru·ked does not mean the virus is not seen in U,at frunily.

specific pathogen does not mean that other

The primary distinguishing anatomic
fanillies of fish are refractory.

features of this fanlily are the lack of a
stomach and a dual-lobed gas bladder. They

Ostariophysi
also often have a diffuse hepatopancreas,
and the posterior kidney is usually

Fishes that belong to this subcohort are
positioned between the two lobes of the gas
considered to be basal fishes; this does not
bladder. The absence of a stomach means
mean they are primitive. They have a unique attention must be given to feeding practices, chemical alarm system associated with
and the bioavailability of some oral drugs
their skin. If the epithelium is damaged, a
may be lower. Cyprinlds benefit from
material called schreckstoff is released by
several feedings per day. Related to feeding,
specialized club cells in the epidermis. It
buoyancy control is a common problem in
induces a flight response when detected by
fancy goldfish such as orandas, ryukins, etc,
nearby related fishes. These fish also have
due to aerophagia. This can be avoided by
cellular bone, which lends itself well to
feeding sinking feeds.

fracture stabilization techniques.

Mycobacterial disease is a frequent

Ostariophysians are physostomous,
problem in zebrafish ( dllllio) research
which means they have a pneumatic duct
colonies but can also be seen in other
that connects the anterior lobe of the gas
cyprinlds. Colunrnaris disease, caused by
bladder to the dorswn of the esophagus.

Flavobacterium columnare, is frequently

Another unique feature of ostariophya source of high mortality in koi and sians is the presence of a Webe1ian
zebrafish. Edwardsiella ictaluri is also
apparatus, which amplifies sound. This
a problem in zebrafish.

apparatus consists primarily of a small

Microspo1idia (Pseudoloma) is a fungal
series of auditory bones connected to the
parasite of concern in zebrafish.

gas bladder.

Ostariophysi includes popular aquariun1

Characiformes: The primary representafishes that belong to the families Cyp1inidae tives of this order are the tetras, such as
and Loricaridae and the order Characifom1es.

neon, cardinal, etc. Unlike the cyprinids,
characins have a stomach and pyloric

Cyprinidae: The fanlily Cyprinldae
caeca. They usually have a single-chan1-
contains more fish species than any other
bered gas bladder. Although they are similar
fanlily of freshwater fishes, and many are
to the smaller cyprinids externally, most
popular as pet fishes. Cyp1inids have a
members of Characiforn1es have a small
widespread distribution, including Asia and
arlipose fin.

North America. Representative cyprinlds

Mycobacteriosis and colunrnaris are
include goldfish, koi, barbs, danios, most of
conunon bacterial diseases of characins.

the freshwater sharks ( eg, redtail, rainbow,

Microsporidia (Pleistophora) is a fungal
and bala), and rasboras.

parasite of concern in tetras.

AQUARIUM FISHES

1783

COMMON VIRAL DISEASES OF SELECTED FISH FAMILIES (continued) Loricariidae

Cichlidae

Poeciliidae

Osphronemidae

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Loricariidae: Originating from South
epidermis. In addition, these fishes have

America, this family contains the popular
acellular bone and lack the Weberian
armored catfishes, the plecos ( short for
apparatus. Most have a single-chambered
plecostomus) and the small Otocinclus
gas bladder and are physoclistous, which
commonly kept in planted tanks. Their
means the gas bladder does not have a
scales are modified into plate-like scutes.

connection to the esophagus except at

They usually have a ventrally located
hatching.

mouth. Most are omnivorous, with some

Many popular aquarium fishes belong to
being herbivorous. Although some plecos
families in Neoteleostei, such as Cichlidae,
such as the genus Panaque are said to

Poeciliidae, and Osphronemidae.

be obligate wood-eaters in the hobby
literature, some sources indicate this is not

Cichlidae: This large family contains
true. Accordingly, these fishes have a long
many popular aquarium fishes, including the
intestine. Many of the plecos are able to
freshwater angelfish, discus, oscar, and
obtain oxygen through their stomach after
many more. Most cichlid species originate
swallowing air at the water surface.

from Central or South America or Africa

These fish are often very colorful, particu

Callichthyidae: Another group of popular larly those originating from the African Rift annored catfishes, including the genus

Lakes. Many cichlid species are aggressive

Corydoras, belongs to this family. Like the and tenitorial, requiring substantial cover
loricariids, the scales of these fishes are
to minimize injury caused by interspecific
modified into armor-like scutes. They have
aggression. Wild-caught An1azonian cichlids
small barbels on either side of the mouth.

( eg, freshwater angelfish and discus)

Axillary glands are located beneath the skin
generally prefer soft water and slightly
of the shoulder and are the source of the
acidic environments, whereas most African
venom that causes punctures by their

Rift Lake species thrive under hard water
pectoral fins to be painful. These fishes
and slightly basic conditions.

often scurry to the water surface to ingest

Cichlids have a single-chambered gas
air; oxygen is then absorbed via the
bladder, which often is severely reduced
intestine.

in riverine species from Africa.

C01ydoras spp appear to be very

Cichlids are usually hardy and well
susceptible to infection with F columnare.

adapted to aquariums. Many species are
prone to intestinal parasitism from the

Neoteleostei
flagellate Spironucleus. African cichlids
may be infected with Cryptobia iubilans,

This subcohort of fish families contains the
which causes a granulomatous gastritis, and
more advanced fishes. Unlike the ostariosome affected fish become extremely physians, the members of this superorder
emaciated. Monogeneans are common
do not have alarm signal cells in their
findings on the gills of tank-raised discus.

1784

AQUARIUM FISHES

Poeciliidae: This is another popular
posterior "caudal" kidney, which is
fanlily of aquarium fishes, which includes
retroperitoneal and ventral to tl1e verteguppies, swordtails, platies, and mollies.

bral column. Hematopoietic, renal, and

Some are euryhaline, such as the guppy and
endocrine tissues are found in tile kidney,

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the molly, whereas the swordtail and platy
witl1 hematopoietic tissue locat cl cranially
are stenohaline to freshwater. These fishes
and excretory tissue located caudally.

are adapted to feed primarily at the water

Divalent ions are excreted principally via
surface.

tile kidney, and monovalent ions and

Poeciliicls are susceptible to the bacterial
nitrogenous excretions via tile gills.

diseases F columnare and epitheliocystis.

Accordingly, lesions of the kidney and gills
may seriously interfere witll respiration,

Osphronemidae: This family, which
excretion, and fluid balance.

includes gouranli, paradise fish, and bettas,

The gas bladder (also known as the swim
is well-adapted to life in shallow, slow-movor air bladder) in bony fish, which originates ing to stagnant water. This group of fishes
as ai1 appendage of the fore gut, regulates
has a unique air-breathing apparatus often
body buoyancy and may also be used for
called a labyiinth organ that consists of
sound production. Physostomous fish have
plates covered in respiratory epithelium. It
an open connection between the swim
is located above the gills in the branchial
bladder and the GI tract, whereas physocliscavity and is deliberately filled with air tous fish do not. Although a single chamber
when these fishes rise to the air-water
in most fish, the gas bladder consists of dual
interface. The bulk of the oxygen required
chan1bers in cyprinids and tlrree chainbers
is obtained via the labyrinth organ, and if
in cod and suckers belonging to the genus
these fishes are held so they cannot reach

Moxostoma.

the air-water interface, they will drown.

A sensory lateral line system along tile

The endocommensalProtoopalina is
sides of the body and head receives stin1uli
often seen in the intestine.

from the aquatic environment and mediates

These fishes are susceptible to
adaptive responses tlrrough tile CNS.

F coliimnare.

Fish depend on increases in environ

For an overview of common parasitic and
mental temperature for efficient antibody
viral diseases of aquaiium fish, see TABLES 4
production dllling infections ( or after
and 5. Susceptibility of specific families of
vaccinations), when most pathogens are
fish to specific pathogens is implied;
replicating at a more rapid rate. The optimal
however, the absence of mention of a
temperature for antibody production varies
specific pathogen does not mean that the
with the species of fish (tropical, temperate,
other families of fish are refractory.

or coldwater). Extremes in environmental
temperature ( above or below that of the

MANAGEMENT
natural habitat) inhibit antibody production.

Like T lymphocytes in oilier vertebrates,

Many management p1inciples applied to
tllose in fish are responsible for cell-mediother species are equally rele�ant for fish, ated inm1llllity. Immunity is not as age
including taking a good history, considering
dependent in fish as it is in other animals;
approp1iate diagnostic techniques, and
young fish are usually immunocompetent
being cognizant of therapeutic options,
and can be vaccinated successfully.

water quality issues, and quarantine and

Antibodies are found in the mucus of
biosecurity procedures.

tile fish skin and GI tract.

Although vaccination of fish against

Physiology
specific diseases has been economically

Fish ai·e poikilothermic, and all physiologic
important in preventing losses, there is a
processes are greatly influenced by water
need for improved methodology. Advances
temperature. In freshwater, the internal
include increased use of autogenous
tissues of fish ai·e h
vaccines; several companies will work with
yperosmotic to the
envirorunent, whereas in saltwater they are
veterinarians and tlleir clients to develop
h
custom vaccines for specific situations. A
ypoosmotic. Stuface iajlllies to tl1e skin
make osmoregulation more difficult and may
few vaccines ( eg, for Aeromonas salmoni
be of serious consequence because of tl1e
cida) are available or in development for
loss of fluid balance and circulatory collapse.

pet fish, particularly koi.

The structure of the fish kidney varies
with tl1e species; generally it is divided into

History
an anterior "head" kidney, which is usually As with all species, a good history is critical
located anterior to the gas bladder, and a
to establish a diagnosis. Questions of

AQUARIUM FISHES

1785
particular interest for fish cases include the
that has died and been placed in a freezer has
number of animals affected, whether one
limited diagnostic value, but freshly dead
species or multiple, the chronicity of the
frozen fish may be useful for bacteriology,
problem, and a thorough description of
virology, or toxicology testing.

animal housing and care, including the

Fresh tissue san1ples of gill filaments,

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volume and design of the system (see
skin mucus, and fins should be collected,

AQUATIC SYSTEMS, p 1766), number and size of
prepared as a wet moW1t, and exanlined
animals stocked, species, new additions,

W1der a light microscope at40x, lOOx, and
use of quarantine, and previous medica400 x. Fresh water should be used to tions. Owners can be asked to bring fish
prepare wet moW1ts of external tissues from
and water samples into the clinic, or the
freshwater fish, and saltwater should be
practitioner may wish to visit the site.

used to prepare wet moW1ts from marine

Site visits allow the system to be more
fish. lf W1certain, water from the tank or
accurately evaluated and the behavior of
from the submitted water sample should be
fish readily observed. If fish are brought to
used. Ensuring that the salinity used to
the clinic, the owner should provide an
prepare moW1ts is sin1ilar to the salinity
animal showing the signs of concern. A live
present in the environment should allow
animal can be transported in a cooler with a
organisms to remain viable long enough for
battery-powered aerator. A separate water
identification. Distilled water should not be
sample should be provided in a plastic bag
used for tissue samples. Tissue should be
and transported on ice. A minimwn of 1
exan1ined for morphology and for the
quart of tank water should be requested
presence of parasites, bacte1ia, or fill1gal
for analysis. If desired for recovery after
elements. Microscopic examination of
anesthetizing the animal, a larger volume
internal organs is also recommended if
of tank water may be requested. Recently
the fish has been euthanized. Unstained
deceased specimens have diagnostic value
sections of stomach and intestine should be
and may be submitted to the veterinary
examined for presence of parasites, and the
clinic, or the owner may be directed to
lower intestine should be exanlined for
submit these to a laboratory experienced in
flagellates. Unstained sections of spleen,
fish necropsy and diagnostic testing ( see
anterior and posterior kidneys, and liver
below). Water samples should be submitted
should be exanlined for presence of
with necropsy specimens.

parasites, granulomas, or other anomalies.

Wet-moW1t exanlination offish tissues is

Necropsy and Diagnostic Techniques crncial for diagnosis of most parasites.

Blood can be collected from a number

Although the same principles are used in
of sites, and hematologic parameters
necropsy of fish as in other animals, great
measured. lnfish >25-100 g, depending on
emphasis is placed on an accurate and
species, the caudal vessels of the caudal
thorough history, premortem signs, fresh
pedW1cle, the duct of Cuvier ( common
necropsy material, and direct microscopic
cardinal vein), and the dorsal and ventral
exanlination of fresh tissue smears and
aortas are easily accessible. For smaller
squash preparations. Fish decompose
specimens that are to be euthanized, blood
quickly, and many saprophytic microorgancan be collected in a hematocrit tube isms reproduce rapidly in the decaying
immediately after euthanasia by severing
tissues, which complicates isolation of
the caudal pedW1cle and exposing the
pathogens unless samples are collected
caudal vessels. Use of hematology and
immediately after death. A general fish
sernm chemistry is limited, because normal
necropsy may include blood collection
values for many fish species are not readily

(premortem ); biopsy of gill, skin, and fin
available; however, the inforn1ation may still
tissues; bacterial or viral culture of internal
be clinically useful. Lithium heparin is the
organs; and histology. A veterinary clinic or
anticoagulant of choice for most fish
diagnostic facility fan1iliar with fish necropsy species, although EDTA is preferred for protocols and aquatic microbiology should
ictalmid catfishes, and plasma may be used
be used. Whenever possible, live fish should
for biochemistry tests. Serology may be
be submitted. If the fish has just died, the
diagnostic in certain cases ( eg, heavy metal
eyes should be clear and the gills normal in
toxicity). Whole blood (1-2 drops) can be
coloration and texture. There should be no
incubated in brain heart infusion broth at

"dead fish" smell; however, some m01ibW1d
room temperature on an electric rotator. If
fishes may have a strong odor. Freshly dead
cloudiness indicative of bacterial growth
fish should be placed in a sturdy plastic bag
develops, a loop of the blood-broth mix can
and submitted on ice. A water sample should be used to attempt primary isolation of a always be submitted with the fish. An animal
systemic bacterial pathogen.

1786

AQUARIUM FISHES

Fish should be euthanized and opened
for isolation of myxobacteria ( slime
under sterile conditions. A ste1ile swab of
bacteria, includi.ngFlavobacterium
posterior kidney, or other organ of interest,
columnare). Sabouraud agar is an excellent
may be shipped to a laboratory in transport
all-purpose media for isolation of fungal
media, but primary isolation directly onto
agents. Lowenstein-Jensen or Middlebrook
an enriched media ( eg, tryptic soya agar
media is recommended for isolation of

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enriched with 5% sheep blood) is preferable. Mycobacterium spp. Mueller-Hinton is the Altl1ough blood agar supplemented with salt media of choice for susceptibility testing of is helpful for ma.tine fish, it is not necessary
most common bacteria isolated from fish. U
if an eruiched blood agar is used. Ordal's or
abscesses or other obvious anomalies are
similar cytophaga media should be available visible, those sites should also be cultured.

IM:i!ii FISH DISEASES OF REGULATORY CONCERN IN THE USA Disease

Causative Agent

Susceptible Species

Viral hemorrhagic

Novirhabdovirus

Prin1ary: salmonids (Oncorhyn
septicemia (Egtved

Fan1ily: Rhabdoviridae
chus spp ), turbo, herring and
disease)

spat (Clupea spp ), Japanese
flounder

Secondary: grayling, whitefish,
pike, Atlantic and Pacific cod,
haddock, many freshwater,
marine, and estuarine species

Infectious hematopoietic Novirhabdovirus

Primary: cultured salmonids
necrosis

Fan1ily: Rhabdoviridae

( Oncorhynchus spp ); lake trout
and char (Salvelinus spp) are
resistant

Spring viremia of carp

Vesiculovirus

Primary: carp (including koi,

Fa.inily: Rhabdoviridae
goldfish), sheatfish (European
catfish), orfe, tench

Epizootic hematopoietic Rana virus

Primary: redfin perch
necrosis

Fan1ily:lridoviridae

Secondary: rainbow trout

(wild and farmed fish)

Red sea brea.in iridoviral Megalocytivirus

Red sea brean1, many
disease

Iridoviridae
other estua.i·ine species, other
marine species

AQUARIUM FISHES

1787

In general, bacte1ial or fungal cultures taken suggestive of Mycobacterium. If fish are from fish tissue should be incubated at
seen spinning or showing other behavioral
room temperature (25°C). Some agents of
indications of neurologic disease before
concern will not grow at all at 37°C, the
death, brain cultures are indicated.

standard temperature for incubation of

If viral disease is suspected, appropriate
cultures taken from mammals. Agents of
tissues may be collected. Specin1ens should

VetBooks.ir
zoonotic concern, such as Mycobacteriurri,,
include both fresh tissues placed in reagent
can be dual incubated at both 25°C and
ethanol and frozen tissues. Several viral

37°C. An acid-fast stain should be available
diseases are of regulatory concern to
for bench-top staining of granulomatous
veterinarians practicing fish medicine in
material which, when positive, is strongly
the USA (see TABLE 6).

FISH DISEASES OF REGULATORY CONCERN IN THE USA (continued) Clinical Signs and Pathology

Temperature Range

Status in USA

Acute form: nonspecific hemo,�

9°-12°c (48°-54°F)

Present in wild
rhaging (eyes, fins, skin),
optin1at
populations, sporadic,
darkening, exophthalmia, ascites
limited distribution;

Chronic forn1: few signs
endemic in Pacific

Neurologic form: spinning/

Northwest and Alaska
flashing

(wild salmonids,

Gross: enlarged spleen, ascites,
haddock, and cod);
necrotic kidney
emerging disease in

Histologic: focal necrosis of

Great Lakes region
kidney liver, spleen; hemorrhage
in muscle

Rapidly increasing mortality (fish 1 oo � l2°C (50° -54 °F) Present in western USA,

<l yr), lethargic but sporadic
optimal; rare >l5°C
sporadic, limited
bursts of rapid swin1ming occur,

(59"F)

dist1ibution; endemic in
protruding vent, fecal casts,

Pacific Northwest and
exophthalmic, pale gills, darken

Alaska ( wild salmo-
ing, abdominal distention/ascitic
nids ); also present in
fluid (possibly bloody)

parts of Europe ang Asia

Nonspecific: darkening, exoph12°�22°c (54°-72°F)

USA is free (last
thalmic, pale gills, distended
occurred in captive fish
abdomen, ascites, hemorrhage
in 2004, wild fish in

(gills,skin,eye),petechiae in

2007); occurs in eastern
organs (including swim bladder),

Europe, Russia, China,
protruding vent with thick mucoid
and Middle East
fecal cast

Coinfection with Aeromonas or
other bacteria common

Acute and high mortality of redfin Redfin perch: > l2°C

Has never occurred in
perch; darkening, ataxia, lethargy, (M°F)

USA; endemic in
hemorrhage around nares;

Rainbow trout: 11 ° -l 7°C Australia
morbidity and mortality of

(52°-63°F)

rainbow trout less severe

Experin1ental: 8° -21 °C

Histologic: necrosis, renal

(46°-70°F)

hematopoietic tissues

Severe anemia, lethargic, pate

Has never occurred in
gills, enlarged spleen

USA; occurs in Japan
and Taiwan

1788

AQUARIUM FISHES

FISH DISEASES OF REGULATORY CONCERN IN THE USA (continued) Disease

Causative Agent

Susceptible Species

Infection with HPR-

Isavirus

Atlantic salmon

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deleted or HPRO

Family: Orthomyxoviri-

Brown trout, sea trout, rainbow

Infectious salmon anemia dae
trout

Infection with salmonid Alphavirus

Atlantic salmon, rainbow trout,
alphavirus (pancreas

Family: Togaviridae
brown trout
disease or sleeping
disease)

Koi herpesvirus

Herpesviridae

Common carp and hybrids,

Cyprinid herpesvirus-3
including koi and ghost carp

Epizootic ulcerative

Aphanomyces invadans Atlantic menl1aden, striped syndrome (mycotic
mullet, many oilier freshwater
granulo�atosis)

and estuarine species;
snakeheads, barbs (Puntias
spp) sensitive; gouramis,
goldfish and oilier ornan1entals
susceptible; tilapia resistant

Gyrodactylus (Gyrodac Monogenea

Atlantic salmon, rainbow trout,
tylus salaris only)

Gyrodactylus salaris
brook trout, North American
only
lake trout, brown trout, grayling
arctic char

Tissue sections no larger ilian 1 cm3
calculated by multiplying measurements of
should be placed in 10% neutral buffered
the length, widili, and depili. Volwne of a
formalin for histopathology. After 24 hr of
circular tank is calculated by multiplying
fixation, iliey should be removed and placed 3.14 by the radius squared by ilie depth. To in reagent alcohol in case molecular diagcalculate directly into liters, measurements nostic techniques will be required.

should be in cm and multiplied by 0.001.

Therapeutic Considerations ·
lf the measurements are made in feet, the
result will be in cubic feet; cubic feet can

Therapy for pet and ornamental fish is often
be converted to gallons by multiplying by
based on environmental management

7.481. If ilie container is oddly shaped,
followed by ilie use of targeted ilierapy
volume may be calculated mathematically,
to control specific pailiogens. Use of
but it may be easier to purchase a flow
prophylactic medication in ilie absence of
meter to measure ilie volw11e required to
diagnostic testing is strongly discouraged
fill ilie tank. Alternatively, t11e volume
and may contribute to resistant bacte1ial
of inflowing water per minute can be
infection and oilier complications.

measured by detennining how long it takes

Drug ilierapy can be provided via several
to fill a 1-L graduated cylinder ( or 5-gal.

routes of administration, including expobucket). Using that inforn1ation, detenninsure by baili (adding medication to water), ing how long it takes to fill a tank or
medicated feed, irtjection, or topical
ornan1ental pond can provide a fairly
administration. Generally speaking, bath
accurate assessment of volume.

and topical treatments are most useful for

Some medicated feeds can be purchased
external infections, whereas medicated
commercially for aquaculture or pet fish.

food and irtjection are most appropriate

Custom-made medicated feeds can be
for internal infections.

prepared for use in ornamental fish. Flake,

Using a baili treatment requires accurate
pellet, or gel diets can be used as a base for
measurement of the volume of water to be
medicated food for pet fish. Cooking oil
treated. Volume of a rectangular tank is
spray is an effective binder for use wiili

AQUARIUM FISHES

1789

FISH DISEASES OF REGULATORY CONCERN IN THE USA (continued) Clinical Signs and Pathology

Temperature Range

Status in USA

Pale gills, severe anemia (PCV

In vitro:

Present in northeast

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<lO"Ai), swollen liver (black/brown Maximum replication USA, sporadic, limited
color), ascites, petechiae of

15°C (59°F)

distribution; endemic in
viscera, mesenteric fat, swim

No replication 25°C

Maine, New Brunswick,
bladder

(77°F)

Scotland, and Norway

Necrosis of exocrine pancreas,

12°-l5°C (54°-59°F)

Has not occurred in
heart and skeletal muscle changes

USA; detected in

Ireland, UK, France,

Germany, Italy, Spain,

Switzerland, Poland,
and Norway

Severe necrosis gill tissue

22°-25.5°C (72°-78°F)

Present in USA,
optimal•
sporadic, widely
distributed

Necrotizing deep ulcers (penetrate <25°C (77°F)

Present in USA,
body wall), granulomatous tissue ( reduced salinity also sporadic, limited
response; deep ulcers with red
contributes in brackish distribution
centers, white rims; invasive
systems)

nonseptate hyphae ( culture
possible but difficult)

Has never occurred in

USA
a Mmtalities stop at >30°C (86°F), but sutvivors remain carriers.

pelleted or flake foods for ornan1ental fish.

before returning the fish to the water.

The addition of medication to commercially

Repeated applications may be necessary.

available gel diets is easily done as the gel

Sunburn can occur in surface-swimming
cools. In general, medication should not be
fish or can be induced ( even in bottomadded when the gelatin is hot, because some dwelling species) by feeding photodynamic medications, particularly oxytetracycline,
drugs such as phenothiazine, although
are heat labile.

ultraviolet light penetrates water poorly.

Ir\jections can be given either IM or

Affected fish will have visible lesions along
intracoelomic (IC). IM injections are given
the dorsal surface. Providing shade solves
in the epaxial muscles, lateral to the dorsal
the problem.

fin. Ir\jection of some drugs can cause
muscle necrosis, so it is important to

FDA-approved Drugs and Regulatory
alternate injection sites and to limit

Concerns: FDA-approved therapeutic opinjections to every 3 days unless required tions in fish are limited; however, there has
more often. To administer IC injections, fish
been significant progress in approvals in the
should be placed head downward in dorsal
past few years, and this trend is expected to
recumbency to move internal organs away
continue. The FDA Web site (www.fdagov/
from the injection site, which should be
cvm/aqualibtoc.htm) is the best resource for
anterior to the anus, just off the ventral
current information on the status of drugs
midline. Topical treatments, usually in
and chemicals. In many cases, therapeutic
ointment forn1, should be applied directly
management of fish other than catfish or
to the external lesion(s). The fish can be
salmonids requires extra-label use of drugs.

manually restrained, usually without

A new mechanism called indexing is being
removing the entire animal from the water.

developed by the FDA to allow for legal use

The area to which the treatment is applied
of nonapproved drugs in ornamental fish.

should be held out of the water for several

The following information is intended for
seconds ( <l min) to allow some absorption
use in pet fish medicine.

1790

AQUARIUM FISHES

FDA-APPROVED DRUGS FOR AQUACULTURE USE IN

THE USA (2014)

Drug

Species

Indications

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IMMERSION

Formalin (Parasite-S®,

All fin.fish

Control external protozoa

Formalin-FTM, Formacide-B)

(Chilodonella, lchlhyobodo,

Epislylis, lchlhyophl,hirius,

Ambiphyra, Trichodina spp ),

Telrahymena spp and monogeneans (Cleidodiscus, Dactylogyrus, Gyrodactylus spp) All fin.fish eggs

Control fungi of the family

Saprolegniaceae

Penaeid shrimp

Control protozoan parasites

(Bodo, Epistylis, and Zoothamnium spp ) Salmon, trout, and

Control fungi of the family
esocid eggs
saprolegniaceae

Hydrogen peroxide (35%

Freshwater-reared

Control mortality due to

PE ROX-AID®)

finfish eggs
saprolegniasis

Freshwater-reared

Control mortality due to
salmonids
bacterial gill disease (Flavobacterium branchiophilum) Freshwater-reared

Control mortality due to

.cool water fin.fish and
external columnaris disease
channel catfish

(Flavobacterium columnare)

Oxytetracycline hydrochlo

Finfish fry and

Mark skeletal tissues, most
ride (OxyMarine, Oxytetrafinger lings
often otoliths, offinfish fry and
cycline HCI Soluble
fingerlings for identification

Powder-343®, Terramycin-343
purposes

Soluble Powder, PENNOX

343, TETROXY Aquatic)

Tricaine methanesulfonate

Fish, amphibians,

Temporary immobilization

(Tricaine-S®)

and other aquatic
poikilotherms

AQUARIUM FISHES

1791

FDA-APPROVED DRUGS FOR AQUACULTURE USE IN

THE USA (2014) (continued)

Dosage Regimen

Comments

VetBooks.ir

IMMERSION

Tanks and raceways: salmon and

Drug must not be subjected to temperature <40°F. Do trout: above 50°F: up to 170 µIJL
not apply to ponds when water is warmer than 80°F,
for up to 1 hr; below 50°F: up to
there is a heavy phytoplankton bloom, or dissolved

250 µIlL for up to 1 hr. All other
oxygen is <5 mg,'L. Ponds may be re-treated in 5-10
finfish: up to 250 µIJL for up to 1 hr days if needed. Do not treat ponds containing striped Earthen ponds: 15-25 µIlL
bass. Test on a small number from each lot to check for indefinitely
any unusual sensitivity to fom1alin before proceeding.

All fuuish eggs: 1,000-2,000 ppm

Prelin1inary bioassay should be conducted to
for 15 min; Acipenseriformes: up
determine species sensitivity.

to 1,500 ppm for 15 min

Tanks and raceways: 50-100 µIlL Drug must not be subjected to temperature <40°F.

for up to 4 hr daily

Do not apply to ponds when water is warmer than

Earthen ponds: 25 µIJL as single

80°F, when there is a heavy phytoplankton bloom,
treatment
or when dissolved oxygen is <5 mg/1. Ponds may
be re-treated in 5 -10 days if needed.

1,000-2,000 ppm for 15 min

Preliminary bioassay should be conducted to
determine species sensitivity.

Coldwater and coolwater:

Initial bioassay on a small number is recommended

500-1,000 mg/Lfor 15 min in a
before treating entire group.

continuous flow system daily on
consecutive or alternate days until
hatch

Wam1water: 750-1,000 mg/L for 15
min in a continuous flow system
daily on consecutive or alternative
days until hatch

100 mg/L (30 min) or 50-100 mg/L Initial bioassay on a small number is recommended (60 min) daily on alternate days for before treating entire group.

3 treatments

Fingerling and adults ( except

Use with caution on walleye.

northern pike and paddlefish):

Initial bioassay on a small number is recommended

50-75 mg/L (60 min) daily on
before treating entire group.

alternate days for 3 treatments

Fry ( except northern pike, pallid
sturgeon, and paddlefish): 50 mg/L

(60 min) daily on alternate days for

3 treatments

200-700 mg oxytetracycline hydrochloride (buffered) per liter of water for 2-6 hr

15-330 mg/L (fish)

Powder is added to water; concentration depends on

1: 1,000 to 1:20,000 ( other
desired degree of anesthesia, species, size, water
poikilotherms)

temperature and softness, stage of development.

Preliminary tests of solution should be made with
a few fish; 21-day withdrawal time (fish); laboratory or hatchery use only in other poikilotherms; water
temperature >50°F (10°C)

1792

AQUARIUM FISHES

FDA-APPROVED DRUGS FOR AQUACULTURE USE IN

THE USA (2014) (continued)

Drug

Species

Indications

VetBooks.ir

INJECTABLE

Chorionic gonadotropin

Male and female

Help improve spawning function

(Chorulon®)

brood finfish

MEDICATED ARTICLE/FEED

Florfenicol (Aquaflor®)

Freshwate!'-reared

Control of mortality due to enteric
finfish
septicemia of catfish associated
with Edwardsiella ictaluri,
streptococcal septicemia in
freshwater-reared warmwater
finfish, columnaris disease in
freshwater-reared finfish

Oxytetracycline dihydrate

Pacific salmon

Mark skeletal tissue, most often

(Terramycin-200® for Fish)

otoliths, of finfish fry and
fingerlings for identification
purposes

FreshwateHeared

Bacterial coldwater disease
salmonids

(Flavobacterium psychrophilum)

Scaled warm

Control bacterial hemorrhagic
freshwater-reared
septicemia (Aeromonas
finfish
liquefaciens) and pseudomonas
disease (Pseudomonas)

Cool freshwater

Control bacterial hemorrhagic
reared finfish
septicemia (Aeromonas
liquefaciens, furunculosis

(Aeromonas salmonicida), and
pseudomonas disease (Pseudomonas)

• Lobster

Control gaffkemia (Aeroccocus
viridans)

All freshwater-reared Control of columnaris disease finfish

Sulfadimethoxine-orme

Salrnonids

Control furunculosis (Aero
toprim (Romet-30®)

monas salmonicida)

Catfish

Control enteric septicemia

(Edwardsiella ictaluri)

Sulfamerazine

Rainbow, brook, and

Control furunculosis (Aero
brown trout
monas salmonicida)

Note: This is an abbreviated summary. For complete labeling, see the package inse,t. Approval applies only to the speciiic drug that is the subject of a new animal drug application (NADA); active ingredients from other sources ( eg, a bulk drug from a chemical company or similar compounds made by companies other than those speciiied in the NADA) are not approved new animal drugs. Approval applies only to use of the drug for the indications and manner specified on the label.

AQUARIUM FISHES

1793

FDA-APPROVED DRUGS F OR AQUACULTURE USE IN

THE USA (2014) (continued)

Dosage Regimen

Comments

VetBooks.ir

INJECTABLE

50-510 IU/lb males;

IM injection up to 3 doses; total dose not to exceed 67-1,816 IU/lb females

25,000 IU in fish intended for human conswnption;
restricted to use by or on the order of a licensed
veterinarian

MEDICATED ARTICLE/FEED

10 mg/kg/day for 10 consecutive

Veterinary Feed Directive drug; 12-day withdrawal
days
time

250 mg/kg/day for 4 days

Salmon <30 g; in feed as sole ration; 7-day
withdrawal time

2.5-3. 75 g/100 lb/day for 10 days

In mixed ration; water temperature not <48.2°F;

21-day withdrawal time

2.5-3. 75 g/100 lb/day for 10 days

In mixed ration; water temperature not <62°F;

21-day withdrawal time

1 g/lb medicated feed for 5 days

In feed as sole ration; 30-day withdrawal time

50 mg/kg/day for 5 days

In feed; 42-day withdrawal time

50 mg/kg/day for 5 days

In feed; 3-day withdrawal time

10 g/100 lb/day for up to 14 days

In feed; 21-day withdrawal time; not currently
available

Antibiotics: Antibiotics can be delivered

(in koi and exhibit fish). For approved
to pet fish through any of the treatment
dosages and withdrawal times, see TABLE
routes listed; however, medicated food is

7. Oxytetracycline (Terran1ycin® 200) can
most common and usually most effec-
be feel at a dosage of 55-83 mg/kg/day for
tive. Common antibiotics used in pet or

10 days to control many gran1-negative
ornamental fish include oxytetracycline,
bacterial infections, including colwnnaris
potentiated sulfa drugs, and enrofloxacin
disease. Because oxytetracycline has been

1794

AQUARIUM FISHES
on the market for many years, there may be

Use of topical ointments containing
significant resistance to it in some bacte1ial
antibiotics can be practical in pet fish. Some
isolates. Romet®-30 (sulfadi.rnethoxine and
seem to absorb fairly quickly, but if treating
ormetoprim) also is effective against many
a substantial wound, it may be appropriate
gram-negative organisms, with less resisto cover it with a waterproof 9ompound.

tance. Palatability can be a problem when

Frequent application of antibiotic ointment

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feeding medicated food to sick fish, which

(eg, twice a day) can work well to treat
may have a poor appetite.

superficial ulcers in pet fish.

F101fenicol is available as Aquaflor® for use
in medicated feed (see AQUACULTURE, p 1743).

Parasiticides: Several brands of formalin

Erythromycin is not FDA approved for

(37% forn1aldehyde in aqueous solution,
use in fish but is an excellent antibiotic for
not l()OA, forn1alin used for fixation of tisfish infected with gram-positive bacteria, sues for histology) are FDA approved as
particularly Streptococcus. Erythromycin
parasiticides for use in finfish and penaeid
can be fed at a dosage of 100 mg/kg/day, for

(saltwater) shrin1p ( see TABLE 7). These

14 days. Palatability may be a concern with
products are usually used as a prolonged
erythromycin-medicated feed. Erythromybath at concentrations of 15--25 mg/L. Vigcin has been used in management of orous aeration during fonnalin treatment
bacterial kidney disease of salmon.ids and
is essential. A concentration of 25 mg/L is
streptococcal infections in food and
equal to 2 drops/gal. or 1 mUlO gal. (useful
nonfood species. FDA permission is
for delivering formalin to aquarium fish).

required for use in food animals.

Salt is categorized as of "low regulatory

Delivery of antibiotics in a bath treatment
concern" by the FDA and has many uses in
is not generally recommended because of
fish medicine, including destruction of
unknown or linlited efficacy and damaging
single-celled protozoans and management
environmental effects (ie, antibiotics tend to
of osmoregulation. Salinity is typically
kill the biofilter). Oxytetracycline (100-400
measured as parts per thousand (ppt) or g/L
mg/L for 1 hr, daily for 10 days) has some

(1 ppt = 1 g/L). Seawater is typically 32-37
efficacy when delivered in a bath. Oxytetrappt salt. By increasing or decreasing the cycline in a bath treatment is chelated by
amount of salt to wllich a freshwater or
hard water and is therefore ineffective in
marine fish is exposed, osmoregulatory
marine systems. Enrofloxacin has been used stress can be mininlized and many parasites as a bath at 2.5--5 mg/L for 5 hr, daily for 7
elinlinated. For freshwater fish, a 30 ppt dip
days. Water changes are recommended after
for 0.5--10 min, depending on species, is an
the 5-hr contact time, and the drug may be
effective ectoparasiticide and is strongly
chelated by hard water. Kanamycin has also
recommended when moving fish. When fish
been used as a bath tr�atment at dosages of
show signs of distress, commonly mani50-100 mg/L for 5 hr, repeated every 3 days fested by rolling on their side, they should
for three treatments, with water changes
be removed from the bath. The use of salt is
recommended after the 5-hr contact time.

a quick and effective way to minin1ize the

N ephrotoxicity is a concern in fish treated
introduction of some protistans into a
with anlinoglycosides. Many "other options
system with new fish. A solution of 5--10 ppt
are discussed in the literature.

salt is recommended for transportation of

Injection is the most effective way to
freshwater fish; most species will tolerate
control the an1ount of antibiotic delivered to this concentration for se¥eral hours or days.

a fish. Enrofloxacin can be delivered IC at a

Pennanently increasing salinity to 2-3 ppt in
dosage of 5--10 mg/kg, and the higher dosage a freshwater system can minimize some can be repeated every third day, minimizing
parasitic protistans. Salt is not generally
handling. Three treatments are generally
practical for use in production ponds,
recommended. When using enrofloxacin,
except for control or prevention of nitrite
the less concentrated dose (22. 7 mg/mL) is
toxicity, because of their large volume, but
recommended, even for use in large fish,
it can be used in ornamental ponds that are
because of adverse tissue reactions with the not more than several thousand gal. Less concentrated dose. If iajection volume is
information is available on lowering salinity
excessive, more than one iajection site can
for marine fish; however, freshwater dips
be used. Other iajectable antibiotics include
adjusted for temperature and pH are often
arn.ikacin (5 mg/kg, IM, every 3 days for a
recommended when moving anin1als.

total of three treatments). As with other

Lowering salinity to 16-18 ppt can be very
aminoglycosides, nephrotoxicity may be a
useful when treating some parasitic
concern. Erythromycin (10 mg/kg/day, IM,
diseases, particularly Cryptocaryon.

for 3 days) can be used to treat gran1-posi

In saltwater systems, copper is sometive infections in large fish.

tin1es applied in a chelated form, because

AQUARIUM FISHES

1795
it stays in concentration longer. Chelated

Spironucleus spp, metronidazole does not
compounds may be difficult to use safely
seem to be effective against gastric infections
and require careful monitoring. Copper
with Ciyptobia iubilans. A concentration of sulfate (CuS04) can be used to txeat marine

-7 mg/L ( -250 mg metronidazole dissolved in
fishes, but the concentration of active

10 gal. of water) can be administered daily
copper (Cu2+) must be closely monitored
for 5 days. A daily water change a few hours

VetBooks.ir

(test kits are available) and should be
after treatment is recommended. Metronidamaintained at 0. 18-0.2 mg/L for up to 3 wk.

zole can be administered in medicated feed

When using over-the-counter products in
at 50 mg/kg, PO, for 5 days. Metronidazole
marine aquaria, label directions should be
may not be used in food fish in the USA.

followed. Cu2+ concentrations should be

Fenbendazole has been used to control
tested at least once a day.

intestinal helminths in fish. A dosage of 25

Copper is extremely toxic to invertemg/kg, delivered in food for 3 --5 days, has brates and plants, which must be removed
been commonly recommended, but efficacy
before the water is treated. Finally, copper
has not been evaluated in controlled trials.

will adversely impact the nitrifying bacteria

When fenbendazole has been used in a bath
in biofilters, and a transient increase in
treatment, high mortality has occurred.

anunonia and nitrite should be expected for

Consequently, this use is not recommended.

weeks to months after treatment. Monitor

Levamisole administered in a bath treatment
ing of anunonia and nitrite until measurable
at a concentration of 2 mg/L is also used by
concentrations subside is recommended.

some clinicians. These compounds may not

Organophosphates have been used in
be used in food fish in the USA.

nonfood fish practice for decades to control

Praziquantel is selective for flatwom1s, so
monogenea, parasitic crustaceans, and
consequently is used to control cestodes
leeches. Organophosphates can be used in
and external monogeneans. The most
freshwater systems, for ornamental fishes
common use of praziqua.ntel is as a
only, at concentrations of0.25 mg/Las an
prolonged bath in large maiine aquaria for
indefinite bath. Most compounds are sold as
control of capsalid monogeneans. It is

37.3% active ingredient liquid. Toxicity and
applied at a concentration of 5 mg/L and
efficacy are affected by pH, with more
may remain active for several weeks.

acidic pH resulting in increased toxicity.

Treated water should be run through an

For this reason, an increased dosage may
activated carbon filter before discharge.

be necessary in marine systems (pH 8-8.3 ),

Praziquantel can also be administered PO
with concentrations up to 1 mg/L used by
at a dosage of 35-125 mg/kg for up to 3
some facilities. Some veterinarians add
days or as a short-tern1 bath treatment at a
atropine (0. 1 mg/kg, PO, IM, or IC) to the
concentration of 10 mg!L for 3 hr. Efficacy
food of sensitive freshwater fishes and
has been demonstrated in yellowtail
marine exhibit fish before treatment with
ki.ngfish fed praziquantel at a dosage <lf
organophosphates. Because of environmen50 mg/kg/day, for 7 days. Use of praziquantel tal concerns, organophosphates should not
is not permitted in food fish in the USA.

be used in outdoor ponds, unless specific

Chloroquine has been used to control
provisions for such use exist in state law

Amyloodinium spp in ornan1ental marine
and are followed by the veterinarian. After
fish. It is applied as a prolonged bath at
treatment with organophosphates, most
concentrations of 10 mg/L. Efficacy in
facilities hold water for up to 96 hr before
recirculating systems seems to be very
allowing any discharge, and divers are
good; however, there are essentially no data
usually restricted from entering exhibit
on treatment intervals, effects on biofilters,
tanks for at least 48 hr. Organophosphates
or other basic husbandry effects. Weekly
may not be used in food fish in the USA.

exanlination of fish, including biopsy of

Diflubenzuron is a chitin synthesis
infected tissue, is recommended to assess
inhibitor effective against anchor worms
treatment efficacy. Some aquaiists have

(Lernaea), fish lice (Argulus), and other used chloroquine (10-15 mg/Lfor 7 days;
crustacean parasites in aquarium fish only.

follow-up with 10 mg/L may be required)

It is used as a prolonged bath at concentracoupled with decreased salinity (16--18 ppt) tions of0.03 mg/L. It has a fairly long
as a treatment for Cryptocaryon in marine
half-life(> 1 wk), and treated water should
fish. Results are mixed, but advantages
be retained for 28 days and then run ttu·ough include decreased labor, because intensive a carbon filter before discharge.

water testing is not required ( as is the case

Metronidazole is used to control intesfor Cu2+). Use of chloroquine is not tinal protozoans and can be delivered in a
pennitted in food fish in the USA. Treated
medicated food or as a bath when fish are
water should be run through a carbon filter
anorectic. Although very effective against
before discharge.

1796

AQUARIUM FISHES

Anesthetics: Tricaine methanesulfonate
before an invasive surgical procedure is

(MS-222) is the most commonly used anesrecommended.

thetic for fish. An FDA-approved product

Descriptions in the literature show how
is available. MS-222 is used to sedate,
a fish may be positioned for a surgical
anesthetize, or euthanize fish. It should alprocedure. For smaller animals, uch as koi, VetBooks.ir
ways be buffered with baking soda (sodium a foam "bed" is easily constructed and can bicarbonate) at a ratio of 2 parts baking
be covered witll sometlling as simple as
soda to 1 part MS-222. See also p 1753.

clear plastic wrap so that the fish does not

Eugenol and clove oil (an over-the-counlose skin, scales, or mucus from direct ter product, usually 84% eugenol) have
contact with the foam. The "bed" can be
become popular with pet fish enthusiasts as
positioned over an aquarium using a plastic
anesthetics. These products are not FDA
tray with holes to allow water drainage.

approved for use in fish in the USA, and use

A pump can move water containing an
in food animals is prohibited. When eugenol
anesthetic solution (usually MS-222) from
at concentrations of 50, 100, and 200 mg/L
the aquariwn through a small tube or
was compared with MS-222 in red pacu, it
catl1eter and across the fish's gills. Ideally,
resulted in effective immobilization of
dissolved oxygen, anunonia, and pH should
fish; however, there was concern about
be monitored in the anestlletic solution.

analgesia, prolonged recovery, and a nar

The fish can be covered witll a clear plastic
row margin of safety, especially at higher
surgical drape (avian drapes work well),
concentrations. Use of both MS-222 and
followed by fairly minin1al preparation of
eugenol resulted in hypoxemia, hypercapthe incision site. Plucking scales along the nia, respiratory acidosis, and hyperglycemia incision line and carefully cleaning the area in red pacu. Aqui-S® is a product approved
with a sterile swab soaked in sterile saline
for sedation of fish in other countries, and it
may be all tllat is required. Very dilute
is currently being investigated in the USA as
disinfectants such as povidone-iodine or
an anesthetic for non-food fish. The active
chlorhexidine can be used, but if the fish is
ingredient is isoeugenol, but evidence of
clean this is probably not necessary ( or
carcinogenicity in laboratory animals has
recommended) because the normal mucus
caused the use of this product in any food
has significant antibacterial properties.

fish to be strictly prohibited. The US Fish

Absorbable sutures are generally not
and Wildlife Service has an active INAD
recommended in fish, because they may
program assessing the potential use of
persist for significant periods of time (> 1 yr

Aqui-S in non-food fish.

in some cases). Monofilament material and
a needle with a cutting edge generally work

Euthanasia: Veterinarians should follow
well. The simple interrupted suture pattern
the A VMA Guidelines for-Eutl1anasia of
works well to close fish skin, but other

Animals (seep 1641). When using overdoses
techniques can be used successfully. Skin
ofMS-222 for euthanasia, the pH should be • sutures should be removed when the carefully ascertained before use; the sodiun1 incision site has healed, generally at 3-4 wk.

bicarbonate buffering can be variable

Surgical staples have been used successbecause of the type of water used to make fully in fish. Results using cyanoacrylate
up tile eutllanasia solution.

tissue adhesive have been mixed because of
a significant inflammatory reaction seen in

Surgical Considerations
some species. If postoperanve antibiotics
are used, enrofloxacin delivered via IC injec

Increasingly, surgery is an option for
tion at a dosage of 5 mg/kg is a good option
management of some medical problems in
but can only be given to non-food fish.

pet or exhibit fish, including neoplastic

Butorphanol given at 0.1-0.4 mg/kg, IM, and
disease, failure to ovulate (ie, "egg bound"

meloxican1 at 0.15 mg/kg, IM, have been
fish), and gas bladder repair for buoyancy
used for postoperative pain control in
problems. Fish skin does not have tl1e
non-food fish. Increasing the salinity in
subcutaneous tissue that provides flexibility freshwater systems to 1-3 ppt (g/1) is to domesticated animal tissue; therefore,
strongly recommended during tile recovery
wounds are not usually treated by surgical
and healing periods. Most freshwater fish
closure but instead allowed to heal by
should be able to tolerate a salinity of 3 ppt
second intention. The clinical evaluation

(3 g/L) on an almost indefinite basis.

before surgery is sinlilar to that in other
species, although tllere may be more
emphasis on imaging and less on blood

Quarantine and Biosecurity
work. Radiology and ultrasound work very

Quarantine is strongly recommended for
well in fish, and use of these techniques
pet fish and certainly for animals intended

AQUARIUM FISHES

1797
for display in public aquaria. A 30-day

Before purchasing new fish, the hobbyist
pe1iod is the minimum time for quarantine,
can 1un the previously disinfected sponge
but longer periods may be necessary.

filter in an established tank that is free of

Quarantined animals should be handled
disease to inoculate the sponge with
only when contact with all other animals is
nitiifying bacteria. This practice will help

VetBooks.ir
finished for the day. Quarantined animals
avoid the conunon water quality problems
should have their own designated equipthat occur in newly set up aquaria.

ment (ie, nets, buckets, siphons, etc) and
be kept separate from other animals.

Common Water Quality Problems in

Disinfectant should be used on equipment
and in footbaths at entry points to the

Hobbyist Aquaria
quarantine area.

New tank syndrome (seep 1775) usually When receiving fish, a thorough history
occurs within the first 6 wk after a new fish
should be obtained regarding previous
hobbyist sets up a tank. Owners may report
treatment or disease outbreaks. Fish
everytlling was fine for several weeks, and
should be examined early in the quarantine
then the fishes suddenly become lethargic,
period; a visual examination may suffice,
anorectic, and frequently die. Although
but for valuable specimens a full clinical
parasites may be present in newly purexamination, including recording the chased fishes, it is critical to perform a
weight of the animal and completing gill,
complete analysis on a water sample from
skin, and fin biopsies, is recommended.

the affected tank. Often total ammonia

Moribtmd fish should be exan1ined, and
nitrogen (TAN) or nitrite, or both, are high
dead fish necropsiecl. Prophylactic use
enough to result in toxicity. Treatment
of antibiotics may be warranted in some
should include decrease in feeding, water
shipments, especially recently imported
changes, tl1e addition of chloride for niti·ite
marine specimens. Treatment with
toxicity, and evaluation of adequate
praziquantel for monogeneans is often
biofiltration. It can take up to 8 wk for a
prudent with marine fish as well. Goldfish
biofilter in a tropical fish tank to become
commonly have significant monogenean
established. New tank syndrome can be
infestations, and treatment with formalin
avoided by several methods. One method,
or praziquantel may be appropriate. Koi
known as fishless cycling, is to completely
should be quarantined to prevent introducset up the tank but with no fish addition; tion of koi herpesvirus (KHV), a serious
anm1onia is added to achieve a concentraand reportable disease, to established tion of at least 1-5 mg.IL. This will initiate
populations. Koi should be quarantined for
the "cycling" process, which should be
a minimum of 30 days at a temperature of
monitored by regular testing for anm10nia,

75°F (24°C). Fish that become ill during
nitrite, and nitrate. Once no ammonia or
quarantine should be tested for KHV (see
nitrite is present, fish can be added safely.

p 1812).

Another method is to slowly acid several fish

Quarantine is not useful for some
to the tank over several months, although
pathogens, but that does not mean it should
this can result in high anunonia or nitrite
not be done. Examples are mycobacteria,
levels if not clone carefully.

which at this time carmot be detected with

Old tank syndrome (seep 1775) can
nonlethal tests, and many viruses, microoccur when water changes are small and sporidia, and myxozoans. These diseases
infrequent. In some cases, no water is
are usually detectable using necropsy
exchanged, and the practice of "topping
techniques if quarantined animals that die
off' is clone by adding water to the tank to
are thoroughly examined. Quarantine is
replace what has evaporated. Although tl1is
most useful for detection of external
can occur in any tartk, it is more frequent in
parasites and some internal parasites that
tanks that are inhabited by large, carnivocan be detected by examination of feces.

rous fishes. These fishes eat large, highprotein meals, frequently in the form of Biosecurity for the Home Aquarium:

other fish, and consequently excrete large

For a modest investment, a hobbyist can set
amounts of TAN. Consequently, the biofilter
up a quarantine tank using an inexpensive
uses up bicarbonate to ti·ansfonn TAN to

10-gal. tank, sponge filter, small aeration
nitrite and nitrate, and the bicarbonate
pump, and heater. Once fishes have cleared
depletion decreases total alkalinity. This
quarantine, the tank and equipment should
results in either a gradual or dramatic drop
be disinfected and stored dry until needed
in pH. If the former, the fishes will adapt to again. During the quarantine period,
the slow change often with no outward sign
separate nets and siphon hoses should be
of distress. If the pH decline is rapid, the
used exclusively for the quarantine tank.

result could be death for the resident fishes.

1798

AQUARIUM FISHES

The water quality parameters of total
thyroid hyperplasia, which has been seen
hardness, nitrate, total alkalinity, and pH are in botl1 elasmobranchs and teleosts. The often abnormal. Total hardness (TH) and
condition may be caused by an ove1t
nitrate are usually significantly higher than
nuttitional deficiency or may be associated
normal. TH of the tank water should be
with chronic nitrate exposure and/or the applicompared with TH of the water used for cation of ozone (see AQUATIC SYSTEMS, p 1766).

VetBooks.ir
water changes. Total alkalinity and pH are

Hepatic lipidosis is a conm1on problem
usually significantly lower. Often TAN will
seen in captive fishes and can occur for
be high because of inadequate bicarbonate
multiple reasons. Examples include
for the nitrogen cycle. lf the fish are still
starvation, a high percentage of carbohyalive, the water quality parameters should drates in the diet, a high an1ount of lipids,
be returned to norn1al by performing daily
and rancidity.

small water changes to avoid pH shock.

Fish require ascorbic acid, delivered in

From that point on, the tank should receive
tl1e feed. Most foodstuffs for fish should be
regular, large water changes to prevent a
supplemented with a stabilized form of
recurrence of the problem.

ascorbic acid. Inadequate dietary vitamin C
can result in a condition called "broken

NUTRITIONAL DISEASES
back disease" by some fanners and
hobbyists. Severely affected fish exhibit

With so many species of fishes kept in home
extt·eme scoliosis. Less obvious, but
and public aquaria, providing good nutrition
detectable on wet mount exa!11ination
is a challenge. (See al.�o p 2307.) A major ( 100 x) of gill tissue, is "bent" or deformed hurdle is that nutritional requirements are
cartilage, which may also indicate a history
known for only a handful of fish species.

of ascorbic acid deficiency.

Given the vast diversity in fishes, it is danger

Feeding a wide variety of feeds is
ous to assume what is good for one type of
one way to try to meet the nutritional
fish will be good for a sinillar but unrelated
requirements. Live feeds can be varied
fish. At t11e basic level, it can at least be
with diverse commercially prepared
detennined whether the fish is carnivorous,
feeds. This practice will also help prevent
omnivorous, or herbivorous. However,
animals from eating only one type of feed.

beyond that, the amount of protein and

Fishes that feed at the surface should be
lipids required is unknown. In general, many
fed feeds that float, whereas bottomfishes have a higher requirement for protein dwellers should be fed items that rapidly
t11an other vertebrates.

sink. The feed should be in particles easily

Inadequate nutrition can result in poor
ingested by the fish. Flaked feeds may be
growtl1, defonnities, a depressed inm1une
too large for a small-mouthed fish to easily
system, hepatic lipidosis, and impaired
ingest. Such feeds can be crushed to
metabolism. Iodine deficiency can result in • enable easy ingestion. In contrast, feeding

•M:i!j:• PROTISTAN PARASITES OF FISHES

Parasites

Tissue

Susceptible Species

External

Ichthyophthirius (FW),

Gills, skin,

All
ciliates (motile) Cryptocmyon (SW)

fins

'T'richodina (FW, SW),

Gills, skin,

All

Chilodonella (FW),
fins

Brooklynella (SW)

Tetrahyrnena (FW),

Skin, eye,

All ("guppy killer")

Uronema (SW)

muscle

External

Ambiphyra, Apiosoma,

Gills, skin,

Primarily pond fish

(sessile)

Epistylus
fins

External

Ichthyobodo, Cryptobia

Gills, skin,

All
flagellates

(see also Internal flagel-
fins

]ates)

AQUARIUM FISHES

1799
flaked feed to a large fish like an oscar or
tion, and rancidity. Many feeds can be
other cichlid will result in a messy tank,
frozen, which will prolong their shelf-life.

because larger fish cannot easily ingest

A feed container kept at room temperature
enough flaked feed to meet their requireshould be discarded after 2 mo of opening.

ments.

Commercial feeds stored in the freezer

When feeding a mixed population of
should be discarded after 6 mo. Commer

VetBooks.ir
fishes, as is typical in hobbyist tanks,
cial frozen feeds such as brine shrimp,
several types of feed items may be required
bloodwonns, mysids, glassworms, etc,
to meet the needs of the fishes. Often,
should be discarded after l yr. If thawed,
popular bottom-dwelling fishes such as
these feeds should not be refrozen.

loricariids and C01ydoras catfish are
expected to survive on the leftovers from
the other fish. This is not an acceptable

PARASITIC DISEASES
practice, and these fish should receive
targeted feeding.

All of the major groups of animal parasites

Another consideration is quantity of feed
are found in fish, and apparently healthy
fed. Ideally, adult fishes should be fed 3"A> of wild fish often carry heavy parasite bmdens.

their body weight daily for maintenance.

Parasites with direct life cycles can be

Fry and fingerlings can be fed up to 5% of
important pathogens of cultured fish;
their body weight daily. Various types of
parasites with indirect life cycles frequently
feeds have dramatically different weights.

use fish as intermediate hosts. Knowledge

For exan1ple, flaked feeds tend to be much
of specific fish hosts greatly facilitates
lighter than pelleted feeds. Pelleted feeds
identification of parasites with marked host
come in different sizes and can be floating
and tissue specificity, whereas others are
or sinking.

recognized because of their common

Most aquarium fishes should be fed at
occU1Tence and lack of host specificity.

least daily, except for carnivorous fish that

Examination of fresh smears that contain
ingest large meals. These may be fed once
living parasites is often diagnostic.

or twice a week.

The most common parasites of fish are

Careful attention must be paid to storage
protistans (see TABLE 8). These include of feeds. Fish feeds usually have a high
species found on external surfaces and
protein and oil content, which can
species found in specific organs. Most
dete1iorate rapidly. Dry feeds should be
protistans have direct life cycles.

kept in a pest-proof container and in an area
of low humidity and temperatme. High

Protistans Infecting Gills and Skin
humidity and high temperature result in

Ciliates: Ciliated protozoa are among the
degradation of the diet, promotion of mold
most common external parasites of fish.

growth and potential mycotoxin produc-

Most ciliates have a simple life cycle and

PROTISTAN PARASITES OF FISHES (continued) Signs

Diagnosis

Treatment

White spot disease; no spots Wet mount

FW-formalin, CuS04; SW-fonnalin,
visible if on gills only

Cu2+, decreased salinity, chloroquine

( efficacy not completely demonstrated)

High respiration rate, piping, Wet mount

FW-fonnalin, CuS04; SW-formalin,
excess mucus, flashing, loss

Cu2+
of condition

Mucus, flashing, intra-ocular Wet mount

External as above; improve sanitation
lesions, popeye

Internal: no treatment

Excess mucus, flashing,

Wet mount

Formalin, KMn04, CuSO, Managernentpiping, loss of condition decrease crowding, correct sanitation

Blue slime, flashing, piping,

Wet mount

Forn1alin, CuS04, KMn0
excess mucus, loss of

4, salt
condition

1800

AQUARIUM FISHES

PROTISTAN PARASITES OF FISHES (continued) Parasites

Tissue

Susceptible Species

External

Piscinoodinium (FW),

Gills, skin

Tiger barbs, many marine

VetBooks.ir
dinoflagellates Amyloodinium (SW)

fishes, inch.tding
clownfish and red drum

Internal

Spironucleus

Intestine

All cichlids, bettas,
flagellates
gouramis, other
aquarium fishes

Cryptobia iubilans

Stomach

African cichlids

Trypanosoma

Blood

Wild-caught Ioricariids

Coccidia

Various genera

Intestine

Multiple

Note: FW = freshwater; SW = saltwater
divide by binary fission. Ciliates can be
a rapid intensification of infection. Infected
motile, attached, or found within the
fish are extremely lethargic and covered
epithelium. The most well-known organism
with visible white dots. Mortality can be
in the latter group is lchthyophthirius
rapid and catastrophic. Infections confined
multijiliis, which has a more complex life
to gill tissue may not be recognized by
cycle than the other ciliates.

nonprofessionals (because white spots are

The infection caused by 1 multijiliis is
not grossly visible) but are easily diagnosed
referred to as "ich" or "white spot disease."

using gill biopsy techniques. The organism

I multijiliis is an obligate pathogen that
is identified using a light microscope at
cannot survive without the presence of
magnification of 40 x or 100 x. It is large
living fish. All fish are susceptible, and a

(0.5--1 mm), round, covered with cilia, and
similar appearing parasite, Cryptocaryon
has a characteristic horseshoe-shaped
irritans, is seen in marine species. I
macronucleus. Its characteristic movement
multijiliis is readily transmitted horizonvaries from constantly rotating to ameboidtally via direct exposure to infected fish like.

or via fomites ( nets, etc). Fish that survive

Ich infections require immediate and
an outbreak may be refractory in future
thorough medical treatment. Fonnalin or
outbreaks but may also serve as a source
copper are often drugs of choice. Over-theof infection to previously unexposed counter medications for pet fish often
individuals. The parasite invades epithelial
contain formalin and malachite green and
tissue of gills, skin, or fins, leaving a small
are effective but, because of regulatory
wound and visible white spot or nodule
concerns regarding the use of malachite
where each parasite encysts. The organism
green, should not be dispensed by the
causes substantial damage because of its
veterinarian. Multiple chemical treatments
unique life cycle (see below), which allows (with intervals detemUFted by water
temperature) are required for successful
treatment of 1 multijiliis. At wann
temperatures typical of home aquaiia ( eg,

>26°C), infected fish should be treated
every 2 -3 days. Constant chemical exposure
for at least 3 wk is generally recommended
to control Cryptoca.ryon in marine systems; lowering salinity to 16-18 ppt is often
helpful.

I multijiliis has a direct life cycle but has massive reproductive potential from each
adult parasite. Adults leave the fish host
and encyst in the environment, releasing
hundreds of immature parasites (tomites)

Typical white spots characteristic of "ich" on that must find a host within a specific time
gold sevrums. Courtesy of Dr. Ruth Francis-Floyd.

fraine ( days for warm water fish, weeks for

AQUARIUM FISHES

1801

PROTISTAN PARASITES OF FISHES (continued) Signs

Diagnosis

Treatment

Mortality, lethargy, piping;

Wet mount

Copper sulfate, chloroquine ( nonfood

VetBooks.ir

"velvet" (if on skin)

fish only); freshwater dips for marine
food fish

Weight loss (anorexia),

Wet mount

Metronidazole (nonfood fish only)

mortality of fry and juveniles

Extreme weight loss,

Wet mount,

None; management-correct sanitation,
anorexia
histology
feeding, stocking density, cull affected
fish

Anemia, mortality

Wet mount

Weight loss, mortality

Histology

Sulfamethazine ( efficacy questionable)

coldwater fish), determined by water
tissue and appear as little saucers or, from a
temperature. For this reason, leaving
lateral view, as little bubbles. The body of
a system fallow is one way to prevent
the organism may be cylindrical, hemispherreinfection. While encysted, parasitic life ical, or discoid. Trichodinids are characterstages are refractory to chemical treatment, ized by an attaching disc with a corona of
but cysts can be removed by thorough
denticles on the adoral sucker surface. For
cleaning and removal of debris from gravel
treatment of trichodinids, see TABLE 8.

substrates.

Infestations of Trichodina often indicate

Two important groups of ciliates are
poor sanitation and/or overcrowding, so
motile and move on the surface of skin and
chemical treatment alone may not be
gills of fish: Chilodonella spp ( which has a adequate for complete control.

marine counterpart, Brooklynella spp) and

Tetrahymena corlissi, another ciliate,
the trichodinids, which are found on both
may be motile and surface dwelling but is
freshwater and marine fish. Fish with
also occasionally found within tissue,
chilodonelliasis typically lose condition,
including skeletal muscle and ocular fluids.

and copious mucous secretions may be

Somewhat similar to Tetrahymena are the
noticed in areas where infestation is most
scuticociliates that affect marine fishes.

severe. If gills are heavily infested, the fish

Uronema and Miamiensis, like Tetrahy
may show signs of respiratory distress,
mena, are teardrop-shaped ciliates that,
including rapid breathing and coughing.

although prin1arily found on external

The gills may be visibly swollen and mucoid. tissues, can be very invasive. Tetrahymena Infected fish may be irritated as evidenced
spp are pear-shaped and 10-20 µm long,
by flashing (scratching) and decreased
with longitudinal rows of cilia and
appetite. Chilodonella can be easily
inconspicuous cytostomes. External
identified from fresh biopsies of infected
infestations of Tetrahymena spp are not
tissues. They are O.�O. 7 mm, are somewhat
uncommon on moribund fish removed from
heart-shaped with parallel bands of cilia,
the bottom of a tank or aquarium and are
and move in a characteristic slow spiral.

often associated with an environment rich

See TABLE 8 for treatment.

in organic material. As long as Tetrahy

Several genera of perit1ichous ciliates
mena spp are restricted to the external
have been grouped together and are
surface of the fish, they are easily elinlinated
collectively referred to as the trichodinids.

with chemical treatment and sanitation.

These include Trichodina, Trichodinella,

When they become established internally,

'Ihpartiella, and Vauchomia spp. Clinical they are not treatable and can cause
signs associated with trichodinid infestation significant mortality. Fish with intraocular are similar to those of chilodonelliasis,
infections of Tetrahymena spp develop
although secretion of mucus is not usually
extreme exophthalmos. The parasite is
as noticeable. Trichodinids are easily
readily identified by examining ocular fluids
identified from biopsies of infected gill or
with a light microscope.

skin tissue. They are readily visible using a

Ambiphyra, Apiosoma, and Epistylis
light microscope at 40 X-100 x. Trichodispp are sessile peritrichs that do not feed nids move along the surface of infested
on the fish host; instead, they attach to the

1802

AQUARIUM FISHES
fish, which is often debilitated, and use
copper sulfate, or potassiun1 pem1anganate
their cilia to filter and ingest bacteria and
baths. Because the parasite has a direct life
small microorganisms in the water column.

cycle, a single treatment should be

When seen in low numbers, they cause
adequate. lf reinfestation occurs, sanitalittle hann; however, in high numbers they tion and quarantine practices should be
can cause irritation. Their presence on a
evaluated.

'

VetBooks.ir
fish usually indicates a rich, organic

One of the most serious health problems
environment. Often, just performing large
of captive marine fish is the parasitic
water changes will diminish the popula
dinofl.agellateAmyloodinium spp. Its
tion. Salt can also be used to help control
freshwater counterprut, Piscinoodinium
the numbers. Ambiphyra and Apiosoma
spp, is less common but can also result in
are solitary but can be seen in large groups
high mortality. These parasites produce a
on a heavily infested fish. Epistylis,
disease that has been called "velvet," "n1st,"

Vorticella, and Carchesium are colonial

"gold-dust," and "coral disease" because of stalked peritrichs.

the brownish gold color they in1part to
infected fish. The pathogenic stages of the

Flagellates: Ichthyobodo spp are some of organism are pigmented, photosynthetic,
the most common and smallest (-15 x 5 µrn) nonflagellated, nonmotile algae that attach flagellated pro tis tan parasites of the skin
to ru1d invade the skin ru1d gills during their
and gills. A kinetoplastid protist, they are
parasitic existence. When mature, these
flattened, pear-shaped organisms with two
parasites give rise to cysts that contain
flagella of unequal lengths. These parasites
nwnerous flagellated, small, free-swin1ming
can be found on freshwater or marine fish
stages tl1at can initiate new infections.

from a broad geographic range. Ichthyo

Control of Amyloodinium is challenging,
bodo move in a jerky, spiral pattern, and
ru1d the prognosis is guru·ded. Copper
free-swimming organisms are fairly easy to
sulfate is the only therapeutic option for
identify in direct smear preparations. Once
food animals in the USA, and repeated
attached, the organism can be difficult to
treatments are necessary to break the life
see, but movement typical of a flickering
cycle. The disease is particularly problemflame may be seen under 400 x and is atic in clownfish. The treatment of choice in
characteristic. Affected skin often has a
omrunental fish is chloroquine, delivered at
steel-gray discoloration due to copious

10 mg.IL as an indefinite bath.

mucus production ("blue slime disease"),
and gills may appear swollen. Behavioral

Oomycota: Although the oomycetes
signs of infestation include lethargy,

(water molds) share some morphologic
anorexia, piping, and flashing. Ichthyobodo
traits with the true fungi, they are more
is readily controlled with salt, formalin,
closely related to diatoms, opalinids, and

1€N•ii COMMON METAZOAN PARASITES OF FISHES

Parasites

Tissue

Susceptible Species

Myxozoans

Myxosoma cerebralis Head, cartilage,

Rainbc;iw trout, salmonids

(IH)

(whirling disease)

backbone

Ceratomyxa shasta

Posterior

Salrnonids (Pacific NW)

intestine

Aurantiactinomyxon Gill

Chrumel catfish
ictaluri (PGD, HGD)

Henneguya

Gill

Chrurnel catfish, other

Sphaerospora

Kidney

Goldfish (pond-reared)

auratus (renal
dropsy)

Proliferative kidney

Kidney

Rainbow trout, all
disease
salrnonids

Monogeneans Gyrodactylus (Jive

Skin, fins

Goldfish, koi (predis-
bearer, except in
posed)

Loricaridae)

AQUARIUM FISHES

1803
labyrinthulomycetes. Of the many genera of
chite green. These dilute solutions should
water molds, Saprolegnia and Aphanomy
be effective in the home aquarium but
ces are the most frequently associated
should not be dispensed by the veterinarian
with disease in freshwater fishes. These
and should never be used on food animals.

primarily saprophytic organisms are

Use in zoologic collections is also discourconunon to freshwater fish around the aged.

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world. Saprolegnia conunonly infects fish

Epizootic ulcerative syndrome (EUS),
eggs and traumatized external tissues of
caused by Aphanomyces invadans, is a
live fishes. Gross signs are grayish white,
reportable disease and endemic to much
cotton-like growths on the skin, gills, eyes,
of the USA.

or fins that may invade deeper tissues of the
body. Fishes exposed to water temperatures
below their optimal range are especially

Internal Protistan Parasites
susceptible to Saprolegnia infection.

Flagellates: Spironucleus spp are

Microscopically, saprolegniasis can be
conunon, small ( -9 µm), bilaterally
recognized by making direct smears from
symmetric, flagellated (four pairs)

the infected tissues and observing the large
diplomonad protists most frequently found
nonseptate filaments. The sexual stages of
in the intestinal tract of finfish. Among
the organism can be seen only in cultures of
ornamental fishes, the cichlids are highly
the organism and are required for specific
susceptible. However, they are also
identification. Sabaroud's dextrose agar
frequently seen in the intestinal tract of
is acceptable for primary isolation of
gourami and some catfishes. Pathogenoomycetes, including the genus Saproleg
icity of these organisms is variable and
nia. Preventive measures include removal
correlated with the number present. If there
of predisposing causes, eg, improper
is a loss of condition, or> 15 organisms are
temperature, inadequate sanitation,
seen per low-power field on wet mounts
excessive chemical treatment, or the
of intestinal tissue or contents, then treatpresence of dead, infected fish and decayment is strongly recommended. The only ing organic material. If the environment is
treatment available for spironucleosis is
clean, the temperature is appropriate for
metronidazole (use only in ornamental
the species, and skin pathogens have been
species), which should be given orally but
eliminated, a single treatment with
can be administered as a bath if fish are
potassium permanganate, formalin, or
anorectic. Chronic infections have been
hydrogen peroxide is often adequate to
seen in fish maintained in unsanitary or
control external saprolegniasis. There are
crowded conditions.

some effective over-the-counter products

Cryptobia and Trypanosoma spp are
sold through the pet trade that contain mala-
slender, elongated (6-20 µm), actively

COMMON METAZOAN PARASITES OF FISHES (continued) Signs

Diagnosis

Treatment

Blacktail, skeletal deformity Histology, isolation of parasite None; regulatory
concern

Weight loss, distended and

Wet mount, histology

None; regulatory
hemorrhagic vent
concern

Mortality, piping

Wet mount, histology

None

None, severe hypoxia

Wet mount

None

Mortality, severely enlarged Histology

None
and cystic kidney

Lethargy, darkening, fluid

Wet mount, histology

None
accumulation, exophthalmia

Excess mucus, flashing,

Wet mount

Praziquantel in
weight loss
nonfood fishes,
formalin

1804

AQUARIUM FISHES

IH=HII COMMON METAZOAN PARASITES OF FISHES (continued) Parasites

'Ilssue

Susceptible Species

Family: Ancyrocephal- Gills

Goldfish, koi, angelfish,

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idae
discus (ptedisposed),

Family: Dactylogyri-
channel catfish
dae ( egg layers)

Capsalids; Benedenia, Cornea, gills,

Marine tropicals, other

Neobenedenia (egg
skin
marine species, marine
layer)

angelfish (predisposed)

Polyopisthocotylea

Gill

Striped bass

Trematodes

Heterophyidae

Gill

Red tail shark, black shark,

(IH usually
rainbow shark, angelfish
mollusc)

(FW), other pond-reared
fish, aquarium fish

Clinoslomum

Skeletal muscle Largemouth bass,
centrarchids, hybrid
striped bass

Bolbophorus confusus Skeletal muscle, Channel catfish viscera

Posthodiplostomum

Viscera, heart,

Largemouth bass, bluegill,
posterior kidney centrachids, salmonids,
other fish

Diplostomum

Eye (lens)

Fish are IH ( unspecified
species)

Cestodes

Diphyllobothrium

Viscera,

Salmonids, other FW
lat um
musculature
species

Corallobothrium

Intestine (adult) Channel catfish

Proteocephalus

Ovary (larval

Largemouth bass
ambloplitis
stage)

Bothriocephalus

Intestine (adult) Carp, aquarium fish
acheilognathi

Acantho-

Acanthocephalus

Intestine

Wild-caught salmonids,
cephalids
wild-caught marine fish

Nematodes

Capilla1'ia

Intestine

Angeliish, discus, other

(fish as DH)

aquarium fish

Camillanus

Posterior

Largemouth bass, other
intestine
centrarchids

Philometra

Posterior

Aquarium fish
intestine

Nematodes

Eustrongylides

Encysted in

Angelfish, other aquarium

(fish as IH)

coelom
species

Contracaecum

Encysted in

Largemouth bass,
viscera
centra.rchids

Leeches

Leech

Skin

FW gan1c fish, aquarium fish

Note: FW = freshwater; IH = intermediate host; DH = direct host; KMnO, = potassium permanganate

AQUARIUM FISHES

1805

COMMON METAZOAN PARASITES OF FISHES (continued) Signs

Diagnosis

Treatment

Piping, coughing, weight

Wet mount

Praziquantel in

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loss, skin lesions
nonfood fishes,
formalin

Eye lesions, flashing, weight Wet mount

Praziquantel in
loss, mortality
nonfood fishes,
formalin

Pale gills, piping, mortality

Wet mount

Praziquantel in
nonfood fishes,
fonnalin

Flared gills, hypoxia, piping, Wet mount
do not tolerate shipping and
handling

Yellow grub

Direct visualization, wet mount

None

Direct visualization, wet mount

None

Direct visualization, wet mount None

Cataracts, blindness

Direct visualization, histology

None

Adhesions, sterility

Direct visualization, wet mount Praziquantel in

(if gonads affected)

nonfood fishes

None

Direct visualization, wet mount Praziquantel in
nonfood fishes

Sterility

Direct visualization, wet mount Praziquantel in
nonfood fishes

Weight loss, enteritis,

Direct visualization

Praziquantel in
mortality
nonfood fishes

Enteritis, mortality

Direct visualization

Weight loss, pot belly

Direct visualization, wet mount Fenbendazole,
levamisole

Visualize worms protruding Direct visualization

Fenbendazole,
from anus
levamisole

Visualize worms protruding Direct visualization

Fenbendazole,
from anus
levamisole

Weight loss, pot belly

Direct visualization

Often none

Direct visualization

Anemia, weight loss

Direct visualization

None

1806

AQUARIUM FISHES
motile, biflagellated kinetoplastid protistans is used to treat food fish (21-day withdrawal easily detected in fresh blood and tissue
time) in some cotmtries. An FDA-approved
smears of both marine and freshwater
form of this drug is not currently available in
finfish. Hematozoic forms are generally
the USA. For aquaiium fish, 10 ppm sulfan1edescribed as Trypanosoma and have a thazine in the aquariwn water once a week
well-developed undulating membrane.

for 2-3 wk has been rep01tecl to be preven

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Trypanosomes can be transmitted by
tive, but safety and efficacy data are sparse.

leeches and have been associated with
anemia in blue-eyed plecostomus Panaque
sulloni and other wild-caught loricariids.

Metazoan Parasites

Cryp/,obia iubilans has been associated

Metazoan pai·asites include the myxozoans,
with granulomatous disease in African
helminths, and crustaceans, and ai·e common
cichlids and discus. Clinical disease is
in both wild and cultured fish ( see TABLE 9).

manifest by severe weight loss and

Fish frequently serve as intem1ediate or
cachexia. Clinically affected fish should be
transp01t hosts for larval parasites of many
culled. Prestm1ptive diagnosis can be made
animals, including people. Helminths with
from microscopic examination of fresh
direct life cycles are most imp01tant in dense
tissue. Typically, granulomas will be found
populations, and heavy parasite burdens ai·e
in the stomach, which may be visibly
sometimes found. In general, heavy pai·asite
thickened. Acid-fast positive material will
burdens seem to be more conunon in fish
not be found in granulomas caused by
originating from wild sources.

Cryplobia. Motile flagellates may be visible using magnification of 400 x or greater.

Myxozoans: Although originally thought
to be single-celled organisms, myxozoans ai·e

Sporozoans: Coccidiosis, although
multicellulai· and closely related to Cnidaria.

common in freshwater or marine finfish, is

They are conunon fish pai·asites and have life
rarely diagnosed in live fish. Many species
cycles that use inve1tebrates as definitive
of finfish are affected. Species of the genera
hosts and fishes for multiplication. Hence,

Cryptosporidium, Eimeria, and Goussia
myxozoan irtfections are often more
have been frequently repo1ted in both
conunon in wild fish or fish reai·ecl intensively
freshwater and marine fishes. The life
in outdoor fish ponds. The organisms tend to
cycles of many fish coccidia are unknown,
be host- and tissue-specific. Accordingly,
and some involve more than one host to
expression of the disease is related to the
complete their development. In addition
specific pathogen and host and location
to intestinal irtfection, the internal organs
within the host. For exainple, coelozoic
may be affected; sporulated Eimeria-like
myxozoans that reside in cavities typically
oocysts and sexual and asexual stages can
cause little pathology, wilike the histozoic
be found in direct sniears and histologic
forms that reside in tissues. Myxozoansections of the internal organs.

infected fish in captive display aquaria are

A mm1ber of Eimeria species are found
not able to transmit the irtfection illlless the
in skates and rays. Of these, E southwelli
necessaiy intermediate hosts are present.

has caused high mortality m cownose rays

Myxozoans are divided into two groups,

(Rhinoptera bonasus ), although it has been

Myxosporea and Malacosporea, and
reported in other species of rays. Infected
members of both groups are irtfective to
cownose rays often present with pale skin
fishes. Although a few qLSes of direct life
and loss of weight despite normal appetite.

cycle have been repo1ted, myxosporeans

F1uid obtained by aspiration of the coelomic
usually have an indirect life cycle, with
cavity should be examined for presence of
oligochaete or polychaete wo1ms used as a
coccidia Treatment with toltrazuril 10 mg/
definitive host. In contrast, bryozoans are
kg/day, PO, for 5 clays may help control but
used as a definitive host by tl1e malaconot eliminate irtfection. This parasite is highly sporeans.

prevalent in wild-caught cownose rays.

There are two important myxosporeai1

Heavy intestinal irtfection of Goussia spp
infections of ornan1ental fish. "Renal dropsy
has been associated with high mortality in
of goldfish" is caused by the myxosporean
comet goldfish (Carassius auratus ).

Sphaerospora aural'us. The disease is

Affected fish are lethargic, frequently lay on
characterized by renal degeneration and
their side, and have pale feces. Clumps of
ascites and is usually diagnosed by
cells in the intestine can be visualized on a
identification of spores in histologic
wet mount, but histopathology is required
sections of the kidney. Affected fish present
for diagnosis.

with extreme abdominal distention but may

Sulfamethazine, at 22-24 g/100 kg of fish
have few other clinical signs. Radiographs
wt/day in the feed for 50 days at 50°F (10°C),
may reveal a mass in the area of the

AQUARIUM FISHES

1807
posterior kidney; definitive diagnosis is
subject to a rapid buildup of parasites by
made at necropsy and confinned histologicontinual infection and worm transfer to cally. No practical treatment is available.

other fish in the tank or pond. Although

Henneguya, a myxosporean occasionally
many species are host specific, the more
found in ornamental fish, causes white
conunon types seen in aquaria are less
nodular lesions that are usually found in gill
selective. The two most common monoge

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tissue and may be grossly visible. Henne
neans in freshwater aquaria are gyrodactyl
guya is easily identified by the forked-tail ids and ancyrocephalids. Gyrodactylus,
appendage of the spore, seen microscopia common parasite of many ornan1ental cally. If ponds are dried and limed heavily,
fishes, primarily gives birth to live young
infection can be eliminated, apparently
and is usually found on skin; the ancyroby reduction of the intermediate hosts.

cephalids lay eggs and pai-asitize the gills.

Aquarium infection can be self-lin1iting in

Dactylogyrids are egg-laying gill monogenethe absence of intermediate hosts. Although ans commonly seen in cyprinid fishes,
an occasional cyst may be considered an
especially goldfish and koi. High nun1bers
incidental finding, severe damage has been
of any of these monogeneans can result in
associated with diffuse distribution of
catastrophic mo1tality of infested fishes.

interlamellar cysts.

The capsalids are a large group of

Myxosporean diseases significant in
monogeneans that affect brackish and
aquaculture include whirling disease and
marine fishes and include the genera
proliferative kidney disease of salmon.ids

Neobenedenia and Benedenia, which are and proliferative gill disease ("hamburger
important monogeneans in marine fishes.

gill disease") of channel catfish. Whirling

They attach and graze on skin and gill and tl1e
disease is caused by Myxobolus cerebralis.

cornea. The capsalids lay sticky eggs easily

Fish are infected as fingerlings when the
transmitted via fomites. Monogeneanparasite infects cartilage in the vertebral infected fish may show behavioral signs of
column and skull, resulting in visible
irtitation, including flashing and rubbing the
skeletal deformities. Affected fingerlings
sides of their bodies against objects in the
typically show rapid tail-chasing behavior
aquariwn. Fish become pale as colors fade.

(whirling) when startled. The disease is also

TI1ey breathe rapidly and distend their gill
sometimes called "blacktail," because the
covers, exposing swollen, pale gills. Localized
peduncle and tail may darken significantly.

skin lesions appear with scattered hemor

Recovered fish remain carriers. Adults do
rhages and ulcerations. Ulceration of the
not show behavioral signs, but skeletal
cornea may become evident if the eyes are
deformities associated with infection do not involved. Mortality may be high or chronic.

resolve. Whirling disease can be prevented

Praziquantel (5 mg/L, prolonged bath) is
by purchasing uninfected breeding stock
the treatment of choice for monogenean
and maintaining them in an environment
infection in freshwater and maiine oniamenfree of the definitive hosts (tubeficid tal fish. Formalin is the only treatment option
worms). A presumptive diagnosis of
for food fish. When using formalin, multiple
whirling disease is made by detection
treatments at weekly inteivals are recomof spores from skulls of infected fish.

mended for egg-laying monogeneans,

Diagnosis may be confinned histologically
because eggs are resistant to chemical
or serologically. Whirling disease is of
treatment. Organophosphates (0.25 mg/L,
regulatory concern in some states.

prolonged bath) have been used successfully
in ornamental fish in the past, but treatment

Monogeneans: Monogeneans have
with praziquantel is considered more
direct life cycles and are common, highly
effective. Organophosphates should be
pathogenic, and obligatory parasites most
avoided in systems containing elasmocommonly seen on skin and gills. The branchs and some characins and cichlids.

preferential location of some species is in

Many monogeneans on marine fish can be
internal organs such as the esophagus,
partially removed using freshwater dips for
stomach, posterior kidney, or urinary

1-5 min, depending on the tolerance of the
bladder. Freshwater parasites tend to
species; however, eggs will not be damaged or
be -0.1-0.Smrn long and are best seen
removed. To prevent the disease, introduction
microscopically; however, several
of infected fish should be avoided.

important species parasitizing marine fish
are significantly larger and may be visible

Trematodes: Trematodes belong to the
grossly. The worms can be identified by
phylwn Platyhelminthes, and this class
their characteristic hold-fast organ, the
contains two subclasses, Aspidogastrea and
haptor, which is armed with large and small

Dig en ea, both of which contain members
hooks. Aquarium and cultured fish are
that infect fishes. Also known as flukes, this

1808

AQUARIUM FISHES
group offlatwom1s has a complex life cycle
lvermectin can be highly toxic to aquarium
that includes a variety of host animals,
fish, particularly cichlids, and its use is
typically beginning with a mollusc. Fishes
discouraged.

can be a second intennediate or final host,
depending on the requirements of the

Leeches: Leeches are parasitic blood

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trematode species. Although adults may be
suckers of fish and also se1ve as vectors for
found in the intestine of infected fish, it is
blood parasites offish ( eg, Trypanosoma,
more common to see the metacercarial

Cryptobia, and haemogregaiines). They can
stage in fishes. This stage is usually
produce a debilitating anemia due to chronic
considered to cause little harm to the host
blood loss and disease. Leech infestations are
but much depends on the site of encystmost common in wild fish, but aquarium and ment. For exan1ple, large nun1bers of
pond infestations can occur by introduction
metacercariae encysted in gill tissue
of infested fish, plants, etc. Heavily infested
can be detrimental to nonnal function.

fishes have been observed to swim primai·iJy
at the water surface, often with their dorsum

Nematodes: Nematodes are common
exposed. Fishes exhibiting this behavior
in wild fish exposed to the intermediate
also suffer from ulcerative lesions of the
hosts. Fish may be definitive hosts for
exposed skin. Organophosphates (0.25 mg/L,
adult nematodes, or they may act as
prolonged bath) are somewhat effective but
transport or intem1ediate hosts for larval
not approved for use in food fish. Further,
nematode forms (anisakids, eustrongylids,
environmental regulations may restrict use in
and others) that infect higher vertebrate
outdoor ponds. Multiple treatments may be
predators, including people. Encysted or
required to control leeches, because eggs ai·e
free nematodes can be found in almost any
resilient and juveniles may continue to hatch.

tissue or body cavity of fish. Aquarium and

Preventive measures include avoiding
cultured pond fish may be heavily infected
leeches (ie, effective quarantine). Infestaif crustacean intermediate hosts are tions in recreational fishing ponds ai·e often
present. Cyclops and Daphnia spp are self-limiting.

common intermediate hosts for Philometra sp, a nematode that is pathogenic for Crustaceans: Pai·asitic crustaceat1S
guppies and other aquarium fish. These
include copepods and branchiurat1S. Some
blood-red worms can be seen in the
copepods, such as the anchor worm, ai·e
swollen abdominal cavity and protruding
obligatory parasites of finfish during specific
from the anus of affected fish (red worm
stages of their complicated life cycle. They
disease). Capillaria spp are commonly
lose their copepod f01m, including their
found in aquarium fish, particularly
appendages, and become rod-or sac-like
freshwater angelfish. Heavy infections in
structures specifically adapted for piercing,
juvenile angelfish have been associated
holding, feeding, and reproducing. Grossly,
with poor growth rates and an inability
they appear as barb-like attachments to the
to withstand shipping and handling.

skin or gills, where they feed on blood and

Treatment with fenbendazole (25 mg/kg for tissue fluids. They can cause hemorrhage, 3 days) is recommended, buf efficacy has
anemia, and tissue destruction, as well as
not been firmly established. Levamisole
provide a portal of entry for other pathogens.

(10 mg/L) administered as a bath treatment Many different species of these parasites can for 3 days has also been recommended.

be found on freshwater and marine fish. The
anchor worms, Lernaea spp, are conunonly
found in a wide variety of aquarium- and
pond-reared fish, including goldfish and
other cyprinids. Ergasilus spp infest the gills.

The branchiurans, often called lice,
have flattened bodies adapted for rapid
movement over the skin smiace. By means
of hooks and suckers, they pe1iodicaJly
attach for feeding by inserting the piercing
mouth pa.rt (sty let) into the skin. Sea lice

(Lepeophtheinis salmonis) are a significant disease problem of pen-reared salmonids. Consultation with a salmonid
health specialist is suggested if these

Small, gray speckled fish louse (Argu/us spp)

parasites are encountered, because
attached to the tail fin of a fancy goldfish.

treatment options ai·e limited and environ

Courtesy of Dr. Louise Bauck.

mental concerns are significant. Arguliis

AQUARIUM FISHES

1809
spp are commonly found on aquariwn,

Aeromonas salmonicida, a gram-negapond-reared, and wild freshwater fish.

tive, nonmotile rod, is the causative agent of

As a chitin synthesis inhibitor, diflubengoldfish ulcer disease and furunculosis zuron is the most effective treatment for
in salrnonids and is a very in1portant disease
crnstacean parasites. It is applied once at
of koi and goldfish. The disease also occurs

VetBooks.ir
the rate of 0.03 mg/L and has a long half-
in freshwater and marine species other than
life. Because of this and the toxicity of
the groups mentioned above. In the acute
diflubenzuron to all crustaceans, treated
form, hemorrhages are found in the fins, tail,
water must be retained for 28 days before
muscles, gills, and internal organs. In more
release. Organophosphates are somewhat
chronic forms, focal areas of swelling,
effective in controlling crustacean parasites,
hemorrhage, and tissue necrosis develop
but legal restrictions constrain clinical use
in the muscles. These lesions progress to

(seep 3064). Some success has been achieved deep crateriform abscesses that discharge in treating freshwater fish for parasitic
from the skin surface. Liquefactive necrosis
copepods by giving infected fish a 3% (30 ppt
develops in the spleen and kidney. Diagnosis

= 30 g/L) salt dip ( <10 min, remove fish when is made by isolating and identifying a pure it rolls) followed by 5 ppt (5 g/L) salt added
culture of the organism from infected tissue.

to the affected tank for 3 wk. The increased

Avoidance through use of good quarantine
salinity kills immature forms as they hatch.

practices, and vaccination when appropri

Diflubenzuron and organophosphates are
ate, is preferable to treatment. Successful
not approved for use in food fishes.

treatment is possible, based on appropriate
antibiotic therapy. Blood culture is an

BACTERIAL DISEASES
effective and nonlethal method for effective
identification and sensitivity testing of A

Epidemics of bacterial diseases are common salmonicida isolates from valuable koi.

in dense populations of cultured food or

Commercial vaccines are available for
aquariwn fish. Predisposition to such
prevention of A salmonicida in salmonids
outbreaks frequently is associated with poor and koi, but information on efficacy in koi water quality, organic loading of the aquatic
is limited.

environment, handling and transport of fish,

Vibriosis is a potentially serious, commarked temperature changes, hypoxia, or mon systemic disease of many cultured,
other stressful conditions. Most bacterial
aquaiiwn, and wild marine and estuarine
pathogens of fish are aerobic, gram-negative
fishes; it is less common in freshwater fish.

rods. Diagnosis is by isolation of the

Three genera of the fainily Vibrionaceae are
organism in pure culture from infected
frequently associated with infection in
tissues and identification of the bacterial
fishes: Vibrio, Listonella, and Photobacte
agent. Sensitivity testing before antibiotic
rium. These genera can result in hemoruse is recommended.

rhages and ulcerations of the skin, fin, and
tail; hemorrhagic and degenerative changes

Aeromonas, Pseudomonas, and
of internal organs; and other systemic

Vibriosis: A nwnber of bacteria produce a
changes. Diagnosis requires identification
similar syndrome, generically referred to as
of pure isolates from infected tissues.

hemorrhagic septicemia and character

Isolation of V cholerae from fish is not
ized by external reddening and hemorrhage
uncommon and should not cause alarm
in the peritonewn, body wall, and viscera
as Jong as the isolate is the non-0 type.

Morbidity and mortality are highly variable,

Preventive measures include mininuzing
depending on predisposing conditions such
stress and crowding. Coldwater vibriosis
as low dissolved oxygen, other water quality (Hitra disease), a serious problem in sea problems, handling stress, or trawna.

farming of salmonids, is characterized by

Ulcerative lesions are common as disease
high mortality, resistance to drug therapy,
progresses, and mortality can be significant
and stress mediation. The etiologic agent is
if stress is not controlled. Antibiotic therapy

Aliivibrio salmonicida. Because members
is recommended if fish are dying. Comm.on
of this fan1ily are ubiquitous in marine
bacterial isolates from affected fish include
environments, avoidance is difficult.

Aeromonas andPseudomonas spp, which

Preventive vaccination with formalin-killed
are more common in freshwater animals,

Vibrio is used in the salmonid industry.

and Vibrio spp, more commonly isolated

Antibiotic therapy should be based on
from marine fishes. Control is based on
results of sensitivity testing.

removal of predisposing factors. If
antibiotic therapy is warranted, drug

Edwardsiella: Edwardsiella ictaluri
selection should be based on sensitivity
is commonly associated with disease
testing when possible.

in chaimel catfish; however, it is also

1810

AQUARIUM FISHES
responsible for high m01tality in zebrafish,
weeks, with only a few fish dying each day.

both in research laboratories and aquarium Species known to be susceptible include fish. It is an obligate pathogen and can be
salmonids, assorted marine fish ( eg, mullet,
transmitted by direct contact with infected
sea bass), tilapia, sturgeon, and striped
fish, water, and feces. Clinical signs of
bass. Susceptible aquarium species include
disease in infected zebrafish include
rainbow sharks, red-tailed black sharks,

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hemorrhaging in the skin, pale gills,
rosy bai·bs, danios, and some tetras and
lethargy, and splenomegaly. On histopacichlids. In general, all fish should be thology, bacteria frequently can be found
considered susceptible. A characteristic
in high numbers in spleen, anterior and
matlifestation of Streptococcus infection
posterior kidneys, nares, and forebrain. It
is neurologic disease, often mailifest by
can be isolated on standard culture media,
spinning or spiraling in the water colUinn.

but it is slow-growing. Coinfections with

Brain ai1d kidney cultmes from suspect fish

Aeromonas spp are common; Aeromonas
should be incubated on blood agar at 25°C
spp are fast growers and can easily
for 24--48 hr. Gran1 stains of pinpoint
overgrow E ictaluri.

bacterial colonies reveal t-ypical chains

Although more commonly reported in
of gran1-positive cocci, which allow a
aquacultured fish species, epitheliocystis
presun1ptive diagnosis. Confumation
is seen in aquarium fishes and is frequently
requires definitive identification of tl1e
seen in discus (Symphysodon spp ), oscar
organism. Antibiotic therapy should be

(Astronotus ocellatus ), and occasionally
based on sensitivity testing. Erythromycin is
otl1er pet fishes. Epitheliocystis is caused
often the drug of choice, but it is not FDA
by an obligate intracellular bacteria in
approved for this use. Somces of infection
the order Chlamydiales. Infection most
may be environmental or include Jive foods,
frequently involves the gills and occasionsuch as tubeficid worms, amphibians, or ally the skin. Infections are more common
previously infected fish. Future epizootics
in freshwater-reared fish species. Epitheliocan be prevented if the source of infection cystis should be suspected if colorless
is identified and eliminated. Streptococcus
spherical structures (infected, hypertro
iniae has been isolated from tilapia and
phied cells) that have granular contents
aquarium fish and has zoonotic potential.

are seen on gill biopsy or skin scraping.

Autogenous vaccines ai·e available for use

Histopathologic exan1ination typically
in aquaculture facilities.

reveals basophilic hypertrophied cells.

The zoonotic gran1-positive bacterium

Clinical signs are variable and depend

E1ysipelothrix rhusiopat.hiae is frequently on severity of infection. Heavily infected
associated with rostral ulceration in
fish may be lethargic and dyspneic. Oral
cyprinids such as tiger barbs (Puntigrus
oxytetracycline has been used to success
tetrazona) and rosy barbs (Pethia
fully control infections.

conchonius ). It usually responds well
to treatment.

Flavobacterium: Flavobacterium
columnare, the member of this group

Mycobacteria: Mycobacteriosis is a
responsible for columnaris d.I');ease, is
chronic or acute, systemic, granulomamost common in warm water species of fish.

tous disease of aquarium fish and cultured

A presumptive diagnosis can be made from
food fish, paiticularly those reai·ed under
visualization of typical organisms on wet
intensive conditions. Predi�posing environmounts of infected skin or gill tissue. There mental factors include low dissolved
are several strains of this bacterium, which
oxygen, low pH, and high organic load,
range from low to high virulence. As yet
all found in recirculating aquaculture
unidentified water quality conditions
systems. Correct use of ultraviolet light as
predispose susceptible fishes to infection
a way to disinfect system water reduces
with the virulent strain. Mortality can be
bacterial counts and can be a useful tool to
acute, and by the time the condition is seen
control infection in exhibit ai1imals. The
it may be difficult to control.

causative bacteria can be any number of
species of Mycobacterium, including

Gram-positive Bacterial Infections:

M chelonae, M marinum, and M fortui

These infections of concern to fish
tum. Syngnathids (sea horses) are
cultUiists and aquaiists may be caused by
paiticularly susceptible, but the disease

Streptococcus and related generaLactococcan be seen in any fish. These weakly gram
cus, Enterococcus, and Vagococcus.

positive, acid-fast, nonmotile bacteria are

Infections are unconm10n but can cause
difficult to grow but can be isolated using
significant mortality (>50%) when they do

Lowenstein-Jensen or Middlebrook media
occur. Chronic infections may continue for
after incubation at 25°C for 3---4 wk. Signs

AQUARIUM FISHES

1811
as several species of maiine fish, including
angelfish and parrotfish. Disease is
associated with low water temperatures

( <80°F or 27°C). Bonnethead sharks are
particularly susceptible and develop
erosions and granulomatous lesions along

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the head. Resolution of lesions requires
warming the affected animals to a more
appropriate temperature for the species.

Closely related to true fungi, microsporidia are tiny, obligate intracellular, spore-forming parasites with single polar
filaments. They are common parasites of

Granulomatous lesions typical of Mycobacterium in a fancy goldfish.

finfish and are host- and tissue-specific;

Courtesy of Dr. Ruth
they can also infect helminth parasites of

Francis-Floyd.

fish. The spores are extremely resistant,
and microsporidia are considered
are variable and nonspecific; they can
non treatable. Microsporidia have a direct
include emaciation, ascites, skin ulceration
life cycle; therefore, horizontal transmisand hemorrhages, exophthalrnos, paleness, sion in an aquarium is likely. Some species
and skeletal defomtities. On necropsy, gross
of microsporidia cause the formation of
lesions of viscera consist of grayish white,
xenomas; a xenoma results in the
necrotic foci that sometimes coalesce to
hypertrophy of an infected cell and its
form tumor-like masses. Granulomas may
nucleus and is often surrounded by
not be grossly visible and are often found
fibrous connective tissue by the host.

first on wet mounts, especially of anterior

The spores are very hardy and can remain
kidney and spleen, or other viscera from
infective in water for many months. Ingestion
infected fish. A presumptive diagnosis is
of the spores is the primary route of infection,
based on visualization of acid-fast rods in
but entry through other portals, eg, damaged
granulomatous material from suspect
skin or gills, and transovarial transmission
lesions. Definitive diagnosis requires
are possible.

isolating and identifying the bacteria There

Recommendations for management of
are no effective treatments that eliminate
microsporidian disease include removal
mycobacteria in fish. Mycobacteria can
of older and moribund animals from a
cause zoonotic infections, and aquarists
population, ultraviolet sterilization, and
should be infonned of potential risks if
strict biosecurity. Depopulation and
handling or cleaning contaminated fish or
disinfection are reconunended for
exhibits. An infected aquarium should be
elin1ination of microsporidian infections.

disinfected before other fish are added.

Ovipleistophora ovariae infects ovarian

Bleach is not an effective disinfectant against tissue of golden shiners (bait fish), resulting mycobacteria; disinfection with alcohol or
in sterility. The organism has no intermediphenolic compounds is recommended.

ate host and is transmitted horizontally

(through ingestion of infective spores) or

MYCOTIC DISEASES
vertically (through infected ova). Fertility
declines as fish age, eventually resulting in

Aquatic fungi often are considered secondary sterility. Grossly, infected ovarian tissue tissue invaders that follow trauniatic irtjuries,
appears marbled. Diagnosis is confirmed
infectious agents, or environmental insults
by exan1ination of a wet mount of suspect
such as poor water quality or low water
tissue, revealing presence of microsporidian
temperatures. Because many fungi grow on
spores.

decaying organic matter, they are especially

Neon tetra disease is caused by Pleis
common in the aquatic environment.

tophora hyphessobryconis, which infects

For more info1mation on Saprolegnia
the skeletal musculature of a nun1ber of
and other members of the Oomycota, which
species of aquarium fish, including tetras,
are fungus-like protists, seep 1761.

angelfish, rasboras, barbs, and zebra.fish.

F'usmium solani is emerging as an impo1° Wected fish may exhibit abnormal tant cause of disease in captive marine fish,
locomotion caused by muscle dan1age,
particularly elasmobranchs. This organism
and muscle tissue may appear marbled or
is found in aquatic plants and soils in
necrotic at necropsy. The spores are readily
tropical and subtropical regions. Clinical
visualized in wet mounts of infected tissue.

disease has been reported in bonnethead

The microsporidiaPseudoloma
and scalloped hammerhead sharks, as well
neurophilia infects zebra.fish and can

1812

AQUARIUM FISHES
be problematic in research facilities and

Herpesviruses
the pet industry. The nervous system and
skeletal muscles are the most common sites

Carp Pox: One of the oldest recognized
of infections, but occasionally other organs
fish diseases, carp pox is caused by Cyprisuch as gonads are affected. A common nid herpesvirus-1 (CyHV-1). P,ox lesions

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presentation is lordosis, but some fish may
may be seen on other species of fish and
present with a grossly distended body with
are sometin1es referred to as fish pox. Lepale epaxial musculature caused by a sions typically are smooth and raised and
massive number of parasites. Often, fish
may have a milky appearance. They are
may be heavily infected yet show no clinical
benign, non-necrotizing areas of epidermal
signs of disease. Xenomas are not formed
hyperplasia. Severe cases may result in dewith this microsporidia. Fish are infected by velopment of papillomatous growtl1S, which ingesting spores from an infected fish or
may be a site of complicating bacterial
during spawning activity, when spores may
infection. Generally, lesi011S are self-limiting
be released from an infected ovary. It is
and of mininlal clinical significance. Carp
wumown whether this parasite can be
pox can be a significant problem in koi
transmitted vertically. An in1portant source
because their aesthetic quality, and hence
of infective spores is tank debris.

market value, is severely compromised.

A nwnber of microsporidia belonging

For the serious koi entlmsiast, fish affected
to the genus Glugea are associated with
with carp pox should be culled, preferably
disease in a disparate group of host fishes,
during quarantine. Surgical removal of the
including seahorses, flounder, and sticldelesions has not been rewarding.

backs. Wection with the members of this
genus results in xenoma fonnation.

Koi Herpesvirus: Koi herpesvirus (KHV),
caused by Cyprinid herpesvirus-3 (CyHV-3),

VIRAL DISEASES
was first recognized in 1996. It is widespread in the USA and considered endemic.

Descriptions of viral diseases of fish are

Confmned cases must be reported to the
rapidly expanding. Viruses are being reported State Veterinarian and the USDA Area in new species, and interpretation of the

Veterinarian in Charge. Because the disease
significance of findings is also changing.

is endemic, regulating bodies report its

Several viral diseases of ornamental fish are
occurrence to the OIE, but they do not
reportable ( see TABLE 6, p 1787).

require specific action, such as depopula

Although viruses of homeothemlic
tion, when the disease is reported.

aninlals are cultured at uniform tempera

KHV causes clinical disease in koi and
tures, fish viruses have wider, but specific,
common carp. Goldfish and grass carp are
temperature tolerancesin fish cell cultures
refractory to clinical disease but may serve
at lower temperatures. Because of this
as carriers. Koi that are exposed, but survive,
relatively defined temperature range,
may also serve as carriers. Clinical disease is
variation in temperature may enable control,
seen at water temperatures of 72°-81 °F
although often it merely induces latency.

(22° -27°C), with maximal mortality at

Because many viral diseases of fish are
temperatures of 72° -78°F (22° -25.5°C).

geographically linlited, regulatory agencies

Mortality rates can reach 80%-1000/o. Fish of
and fish farms in disease-free areas consider
any age are susceptible, but mortality rates
them exotic diseases and require certificamay be higher in younger fish, especially fry.

tion of introduced stocks. Many result in high The most obvious lesions are seen on gill mortality in young fish and little or no losses
tissues, which are severely affected and
in adults, which may become carriers. For
develop a mottled red and white appearance
these reasons, avoidance of carriers and
with obvious hemorrhage in some cases.

certification of SPF replacement stocks

Affected fish are lethargic, swim at the
are frequently required. Specific testing
surface, and may show behavioral signs of
procedures are available. Most vaccines used respiratory distress. The presence of severe for control of fish diseases are for bacte1ial
bacterial or parasitic disease may mask the
agents; however, use of vaccines to control
fact that KHV is the prin1ary cause of gill
some viral diseases is being introduced.

lesions. The disease is transmitted

Drugs are not effective; however, antibiotics
horizontally by exposure to sick or carrier
and other drugs may be used to control
fish and also by exposure to contaminated
secondary bacterial infections. Managewater, substrate, or equipment.

ment techniques that minimize stress and

When KHV is suspected, affected fish can
crowding, biosecurity measures, and temperbe shipped to a laboratory for confinnation.

ature manipulation hold the greatest pronlise Freshly dead specimens shipped on ice and for control of piscine viral diseases.

received within 24 hr should be adequate.

AQUARIUM FISHES

1813

PCR or virus isolation and identification can
exhibit clinical signs of disease if subjected
be used to confirn1 the infection in dead
to stressors. Water temperatures between
animals. Because of the value of koi, there

10° and 22°C will result in replication of the
is significant demand for nonlethal testing
virus that can be detected with quantitative
protocols. Blood, gill tissue from biopsy,

PCR. There is no treatment.

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feces, or mucus may be used to assess the
status of moribund fish. It is inlportant to

Herpesvirus of Angelfish: A herpesnote these tests can result in false-negatives virus of angelfish (Pterophyllum spp) has
if performed on clinically normal fish.

been detected by electron microscopy of

Indirect tests using blood samples, including
skin from moribund angelfish. Affected fish

ELISA or virus neutralization, are less
produce copious amounts of skin mucus
straightfoiward. Negative test results could
that gives affected fish a grey sheen. Often,
indicate a true negative or, alternatively, that
these fish have multiple parasitic infestathe infection is in its early stages and the fish tions and bacterial infections, sin1ilar to that
has not yet developed a measurable antibody of KHV in koi. It is suspected that sU1vivors response. A negative test result could
are carriers.

potentially be obtained from a previously
infected fish that has had a decrease in

Rhabdoviruses
circulating antibody; however, such a fish

Viral Hemorrhagic Septicemia (VHS):

could still function as a carrier. T11ere is a

This reportable disease is caused by a
misconception among some hobbyists that a

Novirhabdovirus and is a member of the
negative blood test is an adequate screening
fanlily Rhabdoviridac. This disease is listed
test to exclude canier status. Practitioners
by OIE as notifiable. Most of the reported
should communicate this clearly to owners,
hosts are not ornamental fishes, but koi
because it is easily misunderstood.

were shown to be susceptible experimen

IfKHV infection is confirmed in a
tally to genotype IVb. This genotype affects
population of koi, depopulation is strongly
a diverse group of fishes in the Great Lakes
recommended. Surviving fish are carriers
region of North America.

and can serve as a source of infection for
naive fish. Although mmtality decreases or

Spring Viremia of Carp (SVC): This
stops as water temperature approaches 86°F acute, virulent, usually hemorrhagic dis

(30°C), survivors will retain carrier status
ease of cultured carp is caused by a Vesicu,
and therefore put other populations at risk.

lovirus that, like VHS, is a member of the

P revention ofKHV is best accomplished

Rhabdoviridae family. The disease is listed
with careful quarantine protocols. A
as notifiable by the OIE. Historically, it was
minimum quarantine of 30 days at 75°F
reported in Europe and the former USSR;

(24 °C) is recommended to minimize the
however, several outbreaks have been
chance of introducing KHV to an estabrepo1ted in the USA between 2002-2001, in lished population of koi. If disease develops
both wild fish and cultured ornamental koi.

during the quarantine period, fish should be

SVC is considered a foreign aninlal disease
evaluated with special consideration for
in the USA and must be reported. It causes
excluding KHV. After quarantine, a new fish
disease in common carp, including koi, as
may be placed in an isolated area with a few
well as grass, bighead, silver, and crucian
fish from the established population and
carp. Linlited experience suggests that
monitored for signs of disease for at least 2
common goldfish may be susceptible.

wk as an added precaution. If koi are taken

Clinical signs are nonspecific and may
to shows, quarantine protocols should be
include darkening of the skin, exophthalmia,
followed every time they return. Koi
ascites, pale gills, hemorrhage, and a
enthusiasts should be strongly encouraged
protruding vent with thick mucoid fecal casts.

to attend English-style shows (versus

P inpoint hemorrhage in the swim bladder is

Japanese-style shows), where competing
indicative of SVC, if present. Co infection with
fish are not placed in a common container.

Aeromonas or other systemic bacteria may
obscUI·e the presence of the virus. The

Herpesviral Hematopoietic Necrosis:

bacterial component of the infection can

This condition of goldfish is caused by
be controlled with antibiotics; however,

Cyprinid herpesvirus-2 (CyHV-2). It is
depopulation of affected or exposed fish is
probably widespread throughout the USA,
required in the USA. The disease causes death
but it is not a reportable disease. Clinically
in both adult and young fish. Clinical disease
ill goldfish often are anorectic and exhibit
occurs at cool temperatures, 54° -72°F
pale gills and ascites. At necropsy, the

( 12° -22°C), an inlportant distinction from
spleen and kidneys (ante1ior and posterior)

KHV. The virus is readily isolated in comare often enlarged. As is typical for herpesmon fish cell lines and identified by sen.un viruses, survivors can be can·iers and
neutralization and fluorescent antibody tests.

1814

AQUARIUM FISHES
lridoviruses

Other Viruses:

Lymphocystis Disease: This typically

Koi sleepy disease is also known as carp
chronic, viral infection of wild or captive
edema virus. Ca.used by a poxvirus, it was
marine and freshwater fish is caused by
first seen in Japan in 1974 and has since
an icosahedral DNA virus of the Iridovirioccun-ed in other countlie , including the VetBooks.ir
dae family. Infection may be manifest by

USA. Affected fishes a.ppea.i· lethargic, lay on
benign, cauliflower-like lesions typically
theiJ· sides, and have thin body condition.

located on fins. The disease affects a wide

Mmtality is usually low but can be variable.

range of fish and is generally considered to

Gill hyperplasia. is a conunon histopa.tl10logic
have a global distribution. Within the aquarfinding. Infected koi can recover, but it is ium trade, painted glass fish and marine
unknown whether they retain a ca.iTier state.

tropical fishes such as the anemonefishes

(Pomacentiidae), marine angels (Pomacanthidae ), and butterflyfishes (Chaeto

NEOPLASIA
dontidae) are susceptible. Presmnptive

Neoplastic diseases sinlilar to those found
diagnosis is based on the presence of enin other aninlals a.i·e found in fish. Their larged fibroblasts (up to 1 mm), which are
incidence frequently is higher in some
easily visualized with a light microscope.

geographic areas and in certain species. Some

Microscopic examination typically reveals
tumors are genetically mediated, such as the
the appearance of grape-like clusters of
malignant melanoma. of the platy-swordtail
virus-la.den cells. Diagnosis is confirmed
cross, and possibly the pseudobra.nch ttm1or
histologically. Feulgen-positive cytoplasmic of cod, tllyroid tw110rs, malignant lymphosarinclusions and a hype1trophied nucleus are coma. of nortllem pike, and fibromas or
pa.thognornonic. The disease is usually selfsarcomas of goldfish. Liposa.i·comas have limiting but is of aesthetic concern.

been reported in captive-bred clownfish, and
pigmented tumors of unknown origin have

Megalocytiviruses: Several other ilidobeen seen in wild Hawaiian marine butterflyviruses have been described in ornan1ental fishes, Chaetodon mili.a1is and C multicinc
fish. Megalocytiviruses consist of two
tus. Both species a.i·e popular in the marine major groupings, red sea bream iridovirus
aquarium hobby. Altllough tile reported

(RSIV) and infectious spleen and kidney neincidence of twnors in sharks, skates, and crosis vilus (ISKNV). RSIV has been found
rays is low, neoplasia. does occur.

in >30 other marine fishes so far; many of

Gonadal ttunors a.i·e ilnportant neoplastic
the affected species include some ti·opical
disorders of fishes and have been repo1ted
fishes kept in aquaria. RSIV is a reportable
in koi and northern pike. Typically, fish
disease. ISKNV includes rnegalocytiviruses
present with a swollen abdomen, and,
that prin1a.iily affect ornamental freshwater
depending on the severity of disease, there
fishes. ISKNV is not cmrently reportable.

may be significant loss of condition. The

A megalocytivirus has been described
presence of a mass can be confirmed with
in freshwater angelfish (Pterophyllum
ulti·asotmd. Biopsy of tissue may not offer a
scalare), but the agent has !tot been
clea.i· diagnosis. La.parotomy of affected fish
isolated. It can result in high mortality. An
often reveals a circmnsclibed mass of
iridovirus has also been isolated in tl1e USA
gonadal tissue. Fish that are not excessively
from gouran1i in tl1e genus 'Jhchogaster
debilitated are excellent.surgical candidates
using a tila.pia heart cell line. This virus does
for removal of the mass.

not grow on FHM cells or other common

Viruses, especially retroviruses, have
cell lines used for isolation of fish viruses.

been associated with neoplasia. in fishes.

The gourami virus has been associated

Two examples of viral-induced neoplasia.

with systemic disease and mortality of
have occun-ed in tropical fishes. Viral

T trichopterus and T leeri goura.ini. Efforts particles have been found iii fibromas on
to fulfill River's postulates were supportive
tile lips of freshwater angelfish. Debulking
although not conclusive. Clillical disease
the tm11or can allow affected fish to feed
with the USA gourami megalocytivirus
norn1ally. Bicolor da.inselfish neurofibroma.appears to be more severe at water tosis, a fatal disease, was reported in 1991 in
temperatures �30°C, based on very linlited
wild Stegastes partitus found on the reefs
information. A megalocytivirus is known
of soutll FI01ida.; it is believed to be a
from dwarf gouran1i Trichogaster spp, but it viral-induced tun1or. Although not reported is not known whetl1er it b the same virus
in captive bicolor dan1selfish, it has the
that affects goura.ini in the USA.

potential to occur.

BACKYARDPOULTRY

1815

BACKYARD POULTRY

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Raising backyard poultry (Gallus domesti

Mixing birds of different species and from
cus) in mban environments is a growing
different sources increases the risk of
trend in the USA. In developing countries,
introducing disease, and it is preferable to
backyard poultry represent -800Ai of poultJy
keep only birds of similar ages and species
stock, often consisting of indigenous
together ("all in/all out"). If multiple ages unselected breeds of various ages, with
and/or species are kept on a property,
various species mixed in the same flock This
efforts should be made to minin1ize contact
serves to meet household food demands and
between groups by keeping them in
is an additional source of income. Modem
separate locations. Separating new or
day USA backyard poultry owners often view returning birds for at least 4-6 wk is their birds as companion animals, in contrast
necessary to monitor for signs of illness.

to poultry raised for commercial production.

Practicing good biosecruity (seep 2068) is

A 2010 USDA study in four cities (Los
also key for good poultry health.

Angeles, Denver, Miami, New York) found
that 0.8% of all households owned chlckens,

PHYSICAL EXAMINATION
and nearly 4% of households without
chlckens planned to have chlckens in the

Before conducting a physical exanlination,
next 5 yr. As backyard poultry ownershlp
the bird's appearance and behavior should
becomes increasingly popular, owners must
be observed from a distance and withln the
be properly educated about how to keep
flock A healthy bird should be bright, ale1t,
their flocks healthy; thus, more veterinarians
and interacting with the flock, with good
must be capable of providing this education.

appetite and free of abnonnal behavior.

All commercial and domestic chlckens

Chlckens and other domestic fowl can be
originate from the red jungle fowl (Gallus
restrained for examination by reaching over
gallus ), which was domesticated in
the back and holding the wings down. Then,

Southeast Asia many centuries ago. Today,
the bird should be picked up and the fingers
hundreds of different chlcken breeds are
inserted between the legs while supporting
bred for different purposes and are
the breast with the other hand. Restraining
characterized by meat-type, egg-laying type,
the bird upside down is not ideal, because it
and dual purpose. Meat-type chickens a.re
may increase it.s stress level and also cause
characterized by rapid growth rate and good regurgitation, as well as result in brok�n meat yield, versus egg-laying chlckens,
whlch are selected for good egg production.

Dual purpose chickens, such as Plymouth

Rock, New Hampshire, Rhode Island Red,

Wyandotte, and Orpington, are reasonably
good for both egg and meat production,
making them a suitable choice for backyard
chlckens for most owners. Purchasing
chlcks and other poultry from a reputable
hatchery or breeder is recommended to get
off to a good start and prevent future
problems. Purchasing from hatcheries or
breeders that participate in the National

Poultry Improvement Plan (NPIP) is
reconunended, because these flocks are
routinely tested for diseases such as

Salmonella Pullorum and S Gallinarum (seep 2865). A list of certified hatcheries and breeders can be found by contacting
official state poultry associations. In
addition, prospective owners are encouraged to physically visit the breeder f1ock or hatchery of purchase to ensure only healthy
birds are brought into the backyard flock

Many backyard flock owners have

Open mouth of a healthy chicken. Courtesy of
multiple ages and/or species of birds.

Dr. Patricia Wakeneff.

1816

BACKYARD POULTRY
bones if bones are brittle from low calcium.

smooth and free of cracks, and the tips

The bird should be kept as calm as possible
should come to a point.

to prevent injury to both the bird and the

4) Open the mouth and check for ulcers
handler. A chicken catcher, which is a wire
and mucosa! lesions on the tongue and
hook used to grab birds by the legs, can also
mucosa! membranes at the commissures

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be used. For larger birds such as turkeys,
of the beak.

'

the handler can fold his or her anns and

5) Check the color of the earlobes to
upper body over the wings and back of the
predict the color of the eggs the hens will
bird, hug firmly, and lift. It is important to
produce. Hens that have white earlobes
remain low to the ground when handling
generally produce white eggs, and hens that
bigger birds; grabbing these birds by their
have reel earlobes generally produce brown
wings or legs can be dangerous and easily
or other pigmented eggs.

cause ir\jury during struggling. For

6) Evaluate the feathers to check for
waterfowl such as ducks and geese, it is
feather loss and how they are clistiibuted.

easiest to use the neck as a catching handle;

Loss of feathers aroW1d the back and back of
however, once the bird is caught, it should
the neck may indicate mating behavior by
be picked up by grabbing the wings together roosters. Check feathers at the base of the behind the back and using the other hand to
feather shaft to look for parasites such as lice,
suppo1t the abdomen. Smaller flight birds,
mites, and nits (lice egg packets). Feathers
such as quail, chukar partridges, and
around the vent should be clear and free of
pheasants, can first be restrained by careful
blood or feces. Pasting of the vent with loose
use of a net or towel and then holding the
feces may indicate ente1ic disease. Check for
wings or legs. Catching birds on the first
scabs and blood aroW1d the vent, which are
attempt minimizes stress.

evidence of vent pecking and carulibalism.

Physical examinations should be

7) The two small bones at the sides of the
perfo1mecl using a systematic approach.

vent are the pubic bones. They should be
l ) Exan1ine the head and neck. The comb
flexible and have space in between. lf hens
should be bright red, slightly warm, tw·gid,
are in lay, this distance should be the width
and free of scabs and lesions. The bird
of three or four fingers. When the hen is not
should hold its head high and have good
laying, the pubic bones are usually stiff and
muscle tone.

close together ( distance between is one

2) Observe the eyes, and check for any
fi11ger width or less).

clischarge or cloucliness that may inclicate

8) Check the legs and feet. The scales
illness. The eyes of a healthy adult bird
should be smooth and closely adhered to
should be clear and btight and have a
each other. lf scales are raised and crusty,
coppeicred iris and a round pupil with
there may be a scaly leg mite infestation.

well-defined margins. Young chicks

Check the footpads for scratches, swellings,
generally have a blue-gray iris. The eyelids
or ulcers caused by footpad dennatitis or
should be free of swelling and opened wide.

pododermatitis (bumblefoot).

3) Check external nares for discharge,
crusts, and scratches. The beak should be

MANAGEMENT

Environment: Backyard poultry
ownership laws and regulations vary by city,

COW1ty, and neighborhoo9. Some cities and
homeowner's associations have specific
mies about chicken ownership, whereas
other cities pemlit chicken ownership with
no limitatio11s on the number or type of
chickens. It is important to know the
regulations and to keep peace with the
neighborhood about owning poultry.

It is cmcial to fence in backyard poultry
to keep them at home and to protect them.

Domestic chickens are easy prey for
predators such as cats, dogs, skW1ks, hawks,
and foxes. The fencing should extend into the
groW1d at least a foot to prevent predators
such as raccoons and foxes from cligging

Subacute pododermatitis (bumblefoot) in

W1der the fencing. Water holes and vegetation
a chicken with swelling of the footpads.

should be avoided aroW1d the coop, because

Courtesy of Dr. Patricia Wakene/1.

they encourage watetfowl, insects, rodents,

BACKYARD POULTRY

1817
and other vemrin to the area, which can harm

Wet litter ai1d high ai11monia levels can
poultry and spread disease. It is wise to cover
lead to se1ious welfai·e issues, including
the top of the enclosure to protect the birds
ammonia bums of the cornea, footpad
from predators that fly or climb, as well as Lo
dermatitis, breast blisters, and skin bwns.

prevent exposure to wild fowl that may

The US Environmental Protection Agency

VetBooks.ir
transnrit disease.

(EPA) reconunends that people and animals

Overcrowding should be avoided; space
not be exposed to 25 ppm of aimnonia for <!8
al.location must consider and allow for
hr. Adequate ventilation al.lows for moisture
growth of the birds. Enough indoor space
to be properly removed from the bedding.

should be available to prevent overcrowd

Chickens have a body temperature of
ing during inclement weather. The type of

105°-109°F ( 40°-43°C) and start to feel heat
bird will help detennine the type of housing.

stress at environmental temperatures> 75°F.

Most breeds of chickens are hardy, although In temperature extremes, poultry will modify meat-type birds are usually sturdier than
their behavior to stay in their thennoneutral
egg layers. Show breeds often do not have
zone (55°-75°F). The ideal temperature
hybrid vigor and require heated or cooled
range for poultry is 65° -75°F, with a relative
housing. Minimum space requirements
humidity of up to 400/o. 1b encourage good air
should be determined not only by size of
circulation, windows should be put up on the
bird but also for activity levels. However, in
south or east side of the bain, with a naiTow
general, laying hens and larger chickens
ledge on the windows to prevent birds from
need a minin1w11 of 1.5-2 sq ft of space
roosting a.Ild defecating in the area. Using
inside and 8--10 sq ft in outside runs. Ducks
misters and fans will help keep the poultry
and geese need much more space, 3-6 sq ft
cool during the hot swmner months, and a
inside and 15-18 in outside runs.

well-insulated bain will keep birds wan11

Floor type is an impo1tant consideration
during tl1e winter.

in building a coop, and owners need to be
cognizant about how to work with various

Nutrition: The biggest expense in raising
materials. Putting the birds on dirt is cheap
poultry is the cost of feed. However, good
and easy, but manure is hard to remove and
feed is a soW1d investment, because
can become a muddy mess without proper

W1bala.I1ced diets will reduce perforn1ai1ce
maintenance. When the soil gets wet or
levels a.Ild may result in nutritional diseases.

contaminated, the dirt must be tilled and

Conunon issues in backyai·d flocks ai·e insuffinew soil added after topdressing the old dirt cient water quality or ainoW1t, prolonged
with lime or bleach to prevent parasite and
storage and degradation of vitainins and
microbial overgrowth. Wood is another
minerals, dilution of balai1ced and complete
option, but it must be in good condition,
nutrition with scratch or supplemental feed,
because old wood may rot and harbor
and feeding diets for tl1e wrnng life stage,
pathogens, and exposed splinters can result

Poultry require 1.5-3.5 parts water for every
in injuries. In addition, wood should not be

1 pait of feed consumed ( up to 5-6 times for
treated, because chemicals such as lead can
waterfowl) and require more in hot weather.

be harmful to birds. Concrete flooring is the

Poultry will not consume feed if tl1e ai11otmt
best for pennanent coops, because it is easy
of water is inadequate, which can lead to
to clean, impervious to vennin, and a good
se1ious health problems. Poultry owners also
barrier to predators. However, it is the most
have to consider the possibility of bacteria
expensive and takes the most effo1t to

( eg, coliforrns) and otl1er contanlinants in the
maintain. It is also important to use good,
water, including arsenic, calciwn, chlorine,
absorbent litter material for bedding in the
copper, flu01ine, iron, lead, magnesiwn,
houses. The litter should be clean, dry, and
mercury, nitrates, nitrites, sodiW11, sul.l'ate,
free of mold. Good litter choices include
and zinc.

pine shavings, rice and nut hulls, chopped

Vitanlin and mineral deficiencies seen in
straw, and groW1d corncobs. Litter can get
poultry are discussed in more detail in the
very wet arow1d the drinkers, and proper
poultry section (seep 2936 and p 2930). The removal of caked litter is necessary. Wet
most conu11011 vitan1in deficiency problems
litter encourages growth of pathogens,
in backyai·d flocks are caused either by not
such as bacte1ia, fungi, and parasites, as
using a vitainin premix in the diet or by
well as leads to problems such as footpad
using a vitanlin premix beyond its shelf-life,
dennatitis. Dry litter creates a dusty
resulting in loss of efficacy. Typically,
environment and may cause tracheal
fat-soluble vita.I11it1 deficiencies, especially
irritation. Ideally, litter should contain
vitainin 03, will become clitlical.ly evident

200/er-25% moisture; a quick test is to grab a
before water-soluble vitainin deficiencies.

handful of litter and see whether the litter

The most conu11on presentation of birds
clwnps briefly and then CfWllbles apait.

with vitainin 03 deficiency is skeletal

1818

BACKYARD POULTRY
abnonnalities (tickets) that can present in
protein). It is critical to not feed layer diets
a flock as mortality, loss of condition, and
to nonlaying, growing birds, because the
birds that are lame or reluctant to move
inadequate protein levels and high calciwn
because of scoliosis, soft and pliable bones,
content (3.5%-6%) may result in irreversible
or lack of bone strength. Owners should be
renal dan1age. Thus, one of th� most

VetBooks.ir
advised to purchase quality feed, store it
common problems seen in mixed-age flocks
correctly (avoid temperature extremes
is urolithiasis (gout). Causes of gout include
to prevent vitan1ins and minerals from
infectious bronchitis virus, feeding excessive
denaturing), and use it within the expiration
levels of sodiw11 bicarbonate, mycotoxicodate. Feed should be stored in a dry, cool sis, and more often, feeding a high-calciwn
area to avoid vitamins from breaking down

(adult layer) diet to an in1rnature bird. Diets
and to prevent mold/fungal growth. Using a
for growing birds (pre-lay) are typically
black light to check for fluorescence in corn

O.Soi<>-1.2"Ai calci un1, whereas laying birds grains is a quick way to screen for hannful
require 3.5%--6% calciwn because of the
mycotoxins. If poultry owners wish to mix
nutritional demand for laying eggs (a typical
their own feed, the most common range
egg requires -2 g of calciwn). However, it is
of inclusion for a vitamin/mineral premix
important for adult layers to have adequate
would be 3-10 pounds of premix per ton of
calciwn to avoid osteoporosis ( cage-layer
feed. Most feed and premixes are available
fatigue) and thin-shelled eggs.

in large quantities and expire in 3-6 mo (as
short as 2 mo in the swnrner), and poult1y

LAYING AND REPRODUCTION
owners need to be aware of the dangers of
feeding old and improperly stored feed.

For laying hens, nest boxes just large enough

Backyard poult1y owners need to know
to fit one "seated" hen are desirable. If eggs how much feed each bird will conswne a
are to be collected for conswnption, efforts
day to predict when to order the next batch
need to be made to decrease broodiness in
of feed. A day-old chick will eat approxithe hens. The tenn "broody" refers to a hen mately the amount of feed that can fit on the
that stops laying eggs in order to sit on the
surface of a US quarter, and an adult laying
eggs, even when no eggs are present. As
hen should eat no more than a quarter of
soon as this behavior is noticed, the hen
pound of feed per day. In contrast, a
should be moved to a wire cage. Broody
meat-type bird may conswne close to twice
hens can have an aggressive temperament,
as much feed as an adult layer. However,
and caution must be taken during handling.

overfeeding or giving feed ad lib can result

Most hens put into cages become less
in musculoskeletal disorders. Using
broody in 2-3 days. Without intervention,
cmnrnercial broiler breeds in a backyard
hens may remain broody for 3--4 wk.

setting is strongly discouraged, because

Backyard flocks raised under natmal light
these birds need to be on very strict feed
will stop laying once hours of daylight
restriction to avoid metabolic disease. Birds
become shorter and undergo a molt period
with access to outdoors will supplement
lasting 3--4 mo or longer. Artificial lighting
their diet by foraging and eatipg insects. In
may be used for layers to lay eggs during the
addition, many poultry owners choose to
winter months, which will increase the
supplement their birds' diet with table
nun1ber of eggs laid during that period but
scraps and scratch grains. Scratch should
not the total munber of eggs laid by the hen.

not be ove1i"ed, because it may cause the

Light schedules are usually 13-hr days, or
birds not to eat a balanced diet. Fat scraps
lights on all night. Hens will be stimulated
should be avoided also, because they
to start laying again as hours of daylight
promote fatty liver and acute death from
increase, not with continuous lighting.

liver rupture. Signs of low or inadequate

Supplemented lighting increases the risk of
nutrient density include slow growth, slow
cannibalism in birds not individually caged.

or lack of egg production, and feather loss.

Chickens will lay eggs for -1 yr before going

Although foraging behavior may be desired,
into a molt. As long as feather loss is not
the birds should still receive most of their
associated with insect infestation, reddened
diet from a balanced, complete ration.

or abraded skin, poor nuttition, or open

The type of feed recommended vaties
wounds, an "unusual molt" can be asswned
with the species, age, and use of the bird. For for lengthy or bizarre-appearing feather loss.

some species of birds, finding the appropri

If desired, this is also the time hens can be
ate feed ingredients can be difficult. In
culled from the flock. In general, even the
general, garnebird owners who cannot find
best hens will approach only -70% of their
the appropriate gamebird sta.Iter feed can
former production level in their subsequent
substitute a turkey poult starter feed, which
production petiod. All hens should molt at
is typically high in protein (25%-28% crude
least once a year. If the hens do not naturally

BACKYARD POULTRY

1819
molt, molt can be induced by decreasing
temperature fluctuation), late deaths but
hours of light.

not pipped ( extreme temperature fluctuation, poor hwnidity), pipped but dried and Incubation and Hatching of Eggs:

stuck to the egg shell (generally poor humid

Probably the largest deternlinant in deciding
ity in late incubation, hatching period,
wheti1er to buy hatched chicks or hatch
weakened embryos from temperature

VetBooks.ir
within the backyard flock is the desired size
fluctuations), and pipped but drowned in
of the flock. For small flocks, inexpensive,
egg fluids or malpositioned embryos
easy-to-operate incubators/hatchers are

(turning malfunction during incubation).

available at fam1 stores or through mail order

Once the chicks are hatched, they should
catalogs. When first starting out, as many as
not be moved until dry and fluffed.

50"A, of tile eggs may not hatch, thus making

Occasionally, chicks will hatch that have not
egg space a concern if a large hatch is
completely absorbed their yolk sac and/or
needed. Most home incubators have good
intestines. These chicks have a poor chance
temperature control but inadequate humidity
of survival, and euthanasia is warranted. If
control. Chicken eggs can withstand changes
possible, all chicken chicks should be
in humidity during incubation; however,
vaccinated for Marek's disease (seep 2849).

other species such as turkeys are much more
sensitive to poor humidity control. Witil

VACCINATION
home incubators, temperature should be
regulated for at least 2-3 days before the eggs

For tile small flock owner, vaccination is
a.re placed. During incubation, the temperagenerally necessary only if U1e birds have had ture should be checked twice daily
disease problems in tile past, may possibly

(fluctuations between 98°F and 101 °F are
be exposed to other birds ( eg, at poultry
fine for chicken eggs; temperature requireshows, meat swaps, or wild bird access), or if ments for other species should be researched new birds are introduced to the flock ( open before incubation) and the water pan kept
flock). Birds should not be vaccinated for a
full. Eggs ( except dark shelled) should be
disease not present in their local area,
candled at least once during incubation,
because this will only introduce new
typically after the first mortality peak at 7-10
organisms into the flock. Also, a sick bird's
days of embryonation. Candling consists of
inunune system is compromised and tmable
shining a light through the egg to detemline
to withstand tile stress of vaccination.

embryo viability by detecting movement of

If certain diseases are a problem in a
the embryo and presence of blood vessels.

backyard flock, vaccination may be

Fertile eggs will candle dark except for the
recommended after veterinary consultation.

air cell ( air sac) with visible blood vessels

Ma.rek's disease is present in almost every
and a live embryo. lnfertiles or "yolker" eggs flock, and vaccination of chickens is stnmgly
will candle through with only a slight shadow
reconunended in all cases; vaccination is key
for the yolk and have no internal structures
for control and is inexpensive. Backyard
and no embryonic development. Embryos
poultry owners may pw·chase chicks from
tilat died with no positive development can
hatcheries and request their chicks be
also candle this way. Dead or nonviable
vaccinated at hatch witil serotype 3, or they
embryos may have a blood ring around the
can vaccinate their own chicks if hatched
embryo, caused by the movement of blood
onsite. Because the virus is ubiquitous and
away from the embryo after death.

spreads through feather dander, vaccinating

Dead eggs can be removed before
birds at hatch before they are most
possibly exploding. Eggs need to be turned
susceptible (2-7 mo) is critical to establish

-4 ti.mes/day until the last few days before
early inunWlity. There are three serotypes of
hatch ( embryonation day 18 for chicken

Marek's disease: 1, 2, and 3. Because most
eggs). It helps to know approxinlate
backyard chickens are vaccinated only for
incubation periods of the poultry of interest
serotype 3, they may not be fully protected.

to gauge when to provide adequate

Vaccination does not prevent infection or
interference for a successful hatch. For
shedding of the field virus.

example, the incubation period for chickens
is 21 days, for Bobwhite quail 23-24 days,

COMMON MANAGEMENT
for guinea fowl 27-28 days, for ducks 28
days, and for geese 28---33 days. If eggs do

RELATED DISEASES
not hatch, examination of the dead embryos

Birds are prey aninlals, so early signs of
can yield some clues as to the cause.

illness may be subtle and difficult to discern.

Conm1on problems include early deaths

Some early signs of illness include changes

(infertile eggs, too long or in1proper storage
in eating and drinking habits; dull featl1ers;
of eggs before incubation, extreme
soiling of the feathers around nares, vent,

1820

BACKYARD POULTRY
shoulders, or eyes; swelling around or
or males, fatty liver ( see p 2820) is characterdischarge around the eyes; discharge from ized by extreme fat deposition, sudden drop
the eyes or nares; abnormal feces; favoring
in egg production, and increased mortality.

or lameness in limbs; or decrease in activity.

The hens are often obese and have pale
combs, and the wattles and cqmbs may be

VetBooks.ir

Cannibalism: Pecking or cannibalism ( see covered with dandruff. The cause is thought p 2873) is one of the most frustrating and
to be a combination of fatty feed and
common problems to control in floor-reared
decreased exercise. Hens and poult1y fed
birds. Certain species such as pheasants
predominantly scratch diet (poultry treats,
and quail are notorious for cannibalism,
table scraps) are predisposed. Mortality is
often leading to individual cages as the only
clue to liver rupture and hemorrhaging, with
housing option. Certain breeds can be more
large blood clots found in the abdomen on
aggressive than others within specific
necropsy. Treatinent is by prevention; most
species. Cannibalism usually does not begin
backyard birds have adequate outdoor
in chicks <2-3 wk old, although in young
access for exercise, but the diet must be
chicks, it is generally the result of insufficontrolled. Lipotrophic agents and dieta.Iy cient feed or diarrhea (soiled or pasty
supplements (alfalfa, wheat bran, fish meal,
vents). In mature birds, methods to control
dried brewer's yeast, soybean mill feed,
cannibalism include reducing lighting,
vitamin E, and torula yeast) have been used
reducing bird density, increasing the
with inconsistent results.

nwnber of feeders, and trimming the beaks.

If an individual bird has been pecked

Cage Layer Fatigue (Osteoporosis):

severely on the skin and separate housing

Cage-layer fatigue (seep 2897) is common
is not available, spraying or painting the
in chickens, Coturnix quail, and Khaki
affected area with tree prwling tar (prwling

Campbell clucks. Birds are unable to sta.I1d
sealer) is a quick remedy. After the sealer
and have brittle bones. The ribs are often
has been sprayed or painted on the affected
deviated in a sign10id shape or fractured at
area, the bird should be restrained until the
the junction of the stemwn and vertebra.

sealant is dry. The tar protects the exposed

Paralyzed birds are ale1t and responsive
area from fluid loss, is nontoxic on open
unless dehydrated. Possible causes include
wounds, and has the advantage of
vitan1in 0

"identifying" the perpetrators by staining 3, calciwn, and phosphorus
deficiencies and/or imbalances. Birds may
their beaks black. If small munbers of birds
die acutely ( often from fractured spinal
are the aggressors, these birds can be given
vertebrae and severed spinal cords) or can
red spectacles that attach to their nares,
rapidly ( 4-7 days) recover after placement
red contact lenses, or have their beaks
on the floor with easy access to food and
retrirnmed to reduce trawna in other birds.

water. With backyard poultry, treatment
with vitamin 03 IM or calciun1 gluconate IV

Trauma: This is the most common
can be helpful. Oyster shells and other large
condition of backyard poultry and includes
particle calcium sources can be added to
predator injury, entrapment of limbs in cages the diet ad lib to prevent this condition. The or other equipment, cannibalism, crushing
oyster shell must not be ground so small
injuries (stepped on, trapped in doors, etc),
that it passes through the intestinal tract,
and self-mutilation (spurs, beak, nails). Most
because it is essential to have slow release
adult poultry are highly resilient and seem
of calciwn from larger particles being
able to recover from severe injuries if
ground in the gizzard. The strain of bird and
the wound has not penetrated into the
type of housing also affect incidence. The
respiratory or abdominal cavity. Supportive
key is to ensure good nutrition (and good
therapy includes providing warmth (via
cortical bone formation) just before onset
brooder lamp), adequate hydration, and
of lay. However, prolonged increase in
force-feeding warm molasses/sweetened
dietary calciun1 before production can
feed. Hydration can be encouraged by
result in urolithiasis and/or a permanent
offering a half concentration powdered milk
cessation of parathyroid gland activity.

instead of water. Superficial wounds can be
treated with antibiotic cream and parenteral
antibiotics. Most poultry will show evidence

Cloacal Prolapse or "Vent Blow-Out":

of recovery in 2-3 days. If there is no improve

The vent will prolapse temporarily during
ment after a few days, the prognosis for full
normal delivery of an egg. However, slow
recovery is generally poor.

retraction due to obesity or in poorly
developed hens (those that com� into lay

Fatty Liver: Although all laying birds
too early) will attract cannibalism, trawna,
retain more fat in their livers than non-layers and edema formation, which will often

BACKYARD POULTRY

1821
prevent retraction. Typically, these chickens
small, reddish-brown flecks. Red mites
are culled, and prevention is practiced by

(Dermanyssus gallinae) feed only at night,
controlling obesity, stocking density of
making daytime diagnosis difficult. They
cages, lighting schedules, precocious onset
can be found in cracks and seruns near
of lay, and proper beak trinuning. For
bedding areas and appear like flea dust or

VetBooks.ir
backyard poultry, stopping lay (reduced
salt and pepper-like deposits. Red mites
light, sharp reduction in feed), isolating
cause feather loss, ir1itation, and ru1emia.

from other birds, and keeping the vent clean

Several types of lice Jive on poultry, and
until retraction are sometimes effective in
lice or nits can be seen at the base of the
mild cases. If chicks are hatched in the fall,
feathers. In severe infestations, growth and
increasing light in the spring can induce
egg production can be affected. Insecticides
them to come into lay when they are
are available for treatment. Fowl ticks (see
physically inunature. Controlling light is
p 2876) comprise a group of soft ticks that
extremely in1portant in this circumstance.

pru·asitize many species of poultry and
wild birds. Ticks ru·e easily missed, because

Egg Binding: Egg binding is conm10n in
they spend relatively little time on the bird.

pullets brought into production too early or

Heavy infestations can cause anemia or
in obese hens. It can range from a temporary tick paralysis, and ticks can be vectors for egg-binding observed in pullets that lay large Borrelia an.serina (spirochetosis). Spraying eggs to complete obstruction of the oviduct.

of buildings with insecticide is the treatment

There can be eggs in the abdominal cavity
of choice.

(retropulsed); single or multiple eggs in the

Roundwonns and tapewonns are the
oviduct; or shell membranes, shells, and
most common internal poultry parasites and
yolk/albumin concretions in the oviduct.

are generally the result of soil contamination

The impaction can generally be identified on
and poor management. Unless infestations
abdominal palpation, ultrasound, and/or
are heavy, clinical disease is usually not
radiographic examination. Commercial
evident. A fecal examination should be
hens are culled. Backyard poultry can
pe1fonned before treatment to assess levels
sometimes be treated by external reduction
of infestation ( and monitor effectiveness of

( smashing) of the egg within the oviduct and
treatment), because most domestic poultry
natural elimination, or by sw-gical removal
will have some degree of internal parasitism.

of the entire oviduct (not ovary). Wrapping

Piperazine can be used for roundwonns,
the bird in a warm towel and massaging the
although its effectiveness can be minimal
abdomen toward the vent after use of
and drug resistance is a problem; off-label
generous amounts of lubrication around the
fenbendazole or levrunisole can be used for
cloaca can sometimes induce propulsion if
tapeworms. These compounds should
the binding is caught early enough. The
not be used in laying hens. Proper litter.

surgical approach is generally midline; care
management will reduce parasite loads
should be taken to minimize damage to the
ru1d reinfection. As in commercial poultry
air sacs. After removal of the oviduct, eggs
production, control of coccidia is one of the
deposited into the abdominal cavity will be
more costly problems in raising backyard
absorbed. Most hens will assume male
poultry. Coccidia are found pri.rnruily in the
characteristics ( crowing, aggression, spurs)

intestinal tract of most poultry but ru·e also
after surgery and are called "pollards"

found in the kidney in geese. Coccidiosis is

(genetically female, phenotypically male).

generally seen in young birds (1-4 mo old),
although it can be seen in any bird >10-14

COMMON INFECTIOUS DISEASES days old. Signs include diarrhea that is often bloody and frequently leads to loss in

The following list includes some of the
production, general malaise, and death.

more common conditions encountered

Coccidia thrive in moist, heavily soiled litter,
in backyard poultry practice.

and disease is often a result of too high a
density of birds. Prevention is by supplying

Parasitism
coccidiostats in the feed, which can be given

As in other species, the common parasites
to birds as early as in their starter diet. Outin poultry are mites, lice, ticks, worms, and breaks can be treated with treatment dose of
protozoa. Two common mites of poultry are
selected coccidiostats and extra-label sulfa
the N01thern fowl mite (Ornithonyssus
mugs. Sulfa mugs have a long withdrawal
sylviarum) and the red mite (see also
period and should not be used in laying
p 2877). The Northern fowl mite is most
hens. Routine yearly fecal exan1inations are
commonly found around the vent, tail, and
reconunended for all backyru·d flocks. (See
breast. These mites are easily observed as
also COCCIDIOSIS, p 2791).

1822

BACKYARD POULTRY

Viral Diseases
by respiratory disease and a drop in egg

Marek's Disease: Marek's disease (MD) is
production. Mortality is variable aJ1d
a co nun on viral disease of chickens, both in
depends on the strain of the vims. As witl1
conunercial production and backyard flocks
infectious bronchitis virus, vaccination is

(seep 2849). The primary lesions are tumors available but is generally givrn to backyard

VetBooks.ir
of the viscera, muscle, skin, and peripheral
poultry only if exposed to oilier birds.

nerves. Nerve lesions can be an early
indicator of the disease and result in a

Fowlpox: Fowlpoxvirns(seep 2824)

condition tenned "range paralysis." Birds
causes crusty and nodular lesions prilnaJily
with visceral tumors often have cachexia as
on the unfeatl1ered pmtions of the bird.

the only clinical sign.1\unors of the muscles

Occasionally, poxvirus caJ1 cause lesions in
and skin are frequently palpable. Tumors tl1at
tl1e mouth and trachea, causing death clue to
affect tl1e eyes ( ocular Mare k's) could be
suffocation (wet fom1). If the bird recovers,
seen as a grayish color change in the pupils or inununity is generally lifelong. Not all pox irregular margins of tl1e pupils, witl1 lack of
outbreaks are caused by fowl pox vims but
proper pupillary light reflex. MD cannot be
can be caused by related strains such as
treated but can be prevented by vaccination
turkey pox, psittacine pox, quail pox, etc.

at hatch. When backyard poultry are acquired Strains are usually species specific but can or hatched onsite, every attempt should be
occasionally affect other species ( eg, pigeon
made to vaccinate for MD. Vaccinations may
pox). One strain may not cross-protect witl1
not be effective if administered to birds > 1-2
another. Vaccination is available and should
wk old. Clinical MD generally affects birds
be given to flocks on premises with a

4-14 wk old; however, it is not unconunon in
previous history of pox or with presence of
older birds, and death loss 1s often sporadic
pox in nearby birds. Poxvirns is transmitted
ratl1er fuan explosive. If tumors are found m
through contact of infected lesions with .

fue viscera of deceased birds, carcasses
open wounds and by insect bites (mosqwshould be submitted to a diagnostic toes), 311d insect control is key to prevent
laboratmy for differential diagnosis between
spread.

MD and avian leukosis (seep 2851), anofuer
conunon lymphoid tumor disease. Avian

Avian Encephalomyelitis: Avian
leukosis is seen in birds >14 wk old, and
encephalomyelitis (AE; seep 2888) is seen in tumors are sinular to those found witl1
chickens, turkeys, pheasants, and quail. It

MD. Avian leukosis has no treatment or
prin1ari.Jy affects chicks 1-3 wk old. Nearly
vaccination.

all conunercial flocks are infected, but
clinical disease is low because of maternal
antibodies. AE can be transmitted vertically

Infectious Bronchitis: Infectious
in eggs laid between 5 and 13 days after
bronchitis vims (IBV; seep 2909) causes a
infection and is an enteric infection under
rapidly spreading respiratory disease in
natural conditions. The spread is more rapid
young chicks. Production is reduced and egg
shell abnonnalities are seen in laying hens.

in floor-raised birds tl1an in cage-raised birds.

There is no treatment, and vaccination of

Certain strains of IBV also clciuse kidney
breeders (both chicken and turkey) for
disease. Chicks infected early in life may
maternal antibodies to protect tl1e young
have pennanent damage to the oviduct, so
during early life is critical to prevention.

they do not produce eggs or become false

Because many specialty breeders, particulayers (seep 2897). IBV is highly transnuslarly those that sell stock to an intern1ediate sible but most birds recover with supportive supplier, do not vaccinate, AE is a fairly treabnent. Antibiotics can be adn1inistered
conunon viral disease in backyaJ·cl poultry.

in fue water to prevent secondaJy infection.

Vaccination should be given after 8 wk of

Vaccines are available; however, backyard
age but by at least 4 wk before production.

chickens are usually not vaccinated unless
they come in contact witl1 other chickens.

Bacterial Infections

Newcastle Disease: Newcastle disease

Salmonellosis: In general, Salmonella
vims (NDV; seep 2856) aifects numerous

Pullorw11 ( see p 2865) and S Gallinarum species of birds and is the reason for qu31·an

(fowl typhoid; seep 2866) cause the greatesli tine regulations for birds entering the USA.

problem for poultry, whereas STyphimu

Exotic NDV is highly fatal and is not present
riun1 S Enteritidis, S Heidelberg, and in the USA at this time. Past outbreaks have

S Ke�tucky are important in terms of public resulted in the slaughter of thousands of
healtl1. S Pullorum is egg transmitted, causes birds. Milder forms of NDV are present in
a diaJTheal disease in young chicks and
the USA and are primaJily characterized
poults, and results in high mortality. Adult

BACKYARD POULTRY

1823
birds are asymptomatic carriers. Diagnosis

(infectious synovitis) and M meleagridis
is based on disease history and isolation of

( venereal infection ru1d airsacculitis ).

the bacteria. Prevention is achieved by
pmchasing birds from a breeder flock that is

Fungal Diseases

NPIP certified (National Poultry Improvement Plan) clean of S Pullorum and typhoid.

Aspergillosis: Aspergillosis (see also

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Treatment is not recommended, because it
p 2901), or brooder pneumonia, is seen in
can cause birds to become carriers. Fowl
many poultry and other species of birds.

typhoid is seen in chickens, tmkeys, and

Birds <3 wk old are most conunonly
many other game and wild birds. Fowl
affected, and infection is obtained from
typhoid is similar in disease presentation and hatchers or brooders contanlinated with diagnosis to S Pullorum, although matme
fungal spores. Morbidity is variable, arid
birds can show clinical signs of fowl typhoid.

mortality can be high in clinically affected

Clinical signs are infrequently observed in
birds. Culturing the fungus or demonstratpoultry infected with S Ente1itidis and ing typical fungal hyphae in fresh prepara

S 'IyphimUiiUin, although most paratyphoid tions from lesions are used for diagnosis.

Salmonella infections are asymptomatic in

Prevention is accomplished by thoroughly
most poultry. Flocks can be monitored by
cleaning hatchers, incubators, waterers,
obtaining egg san1ples and environmental
feeders, and ventilation fans and by keeping
san1ples to cultme tl1e organism.

litter clean and dry. Treatment is expensive
and may not be effective. Ketaconazole and

Colibacillosis: Colibacillosis (see also nystatin have been used.

p 2814) is caused by Escherichia coli and is usually secondary to other infections such

Favus: Favus, or ringwo1m, also known as
as infectious bronchitis vims and mycoplaswhite comb, is a fungal disease caused by mosis. E coli is seen in most species and age Microsporum gallinae, which is of minor groups. A wide variety of clinical signs
importance in all fowl, especially chickens
affecting the respiratory, reproductive, and
and tUI·keys. Affected birds have small,
intestinal systems can be seen. Vigorous
white, chalky deposits on the comb, which
adherence to biosecUiity and sanitation
can enlarge and coalesce to form a dull
progratns can effectively prevent the
white, moldy layer that could be several
organism from causing disease. Many
millimeters tl1ick. The disease is self-linlitantibiotics can be used for treatment, and ing, and the comb heals after several
sensitivity to the antibiotic should be tested.

months. Typically, if the disease is limited

Treatment is usually successful if the
to the comb, the health of the bird is not
disease is in the early stages.

affected, but if feathered portions ru·e
involved, the bird may become emaciated

Mycoplasmosis {Chronic Respiratory
and die. Favus is a public healtl1 concern.

Disease): Chronic respiratory disease in
poultry (primruily chickens and tmkeys) is

Antibiotic Usage
generally caused by Mycoplasma gallisepti

Antibiotics are readily available in feed
cum infection (seep 2841 ). M gallisepticum stores and on.line poultry supply sites;
is a repmtable disease in tmkeys in select
however, use of antibiotics must be
states in the USA. Pathogenicity of
carefully considered. Each antibiotic is

M gallisepticum is enhanced by infection
labeled for different species and the use of
with other organisms. Clinical signs of
the poultry, and administe1ing the correct
respiratory disease develop slowly in a flock,
dosage may be difficult. In some instances,
and feed consumption drops. Infection of the antibiotics are useful to treat and control sinuses with pmulent exudate (swollen face) disease. Certain antibiotics such as ch Ioratnis common in tmkeys. Serology and isolation phenicol, glycopeptides, and fluoroquinoloand identification of the organism can be nes are prohibited for extra-label use in food
used for diagnosis. Prevention, as with the
aninlals, including backyard poultry. A
salmonellae, rests with establishment of a
veterinarian should be consulted; judicious
clean flock by eliminating the infected flock,
use of antibiotics may be recommended
completely sanitizing the premises, and
after appropriate diagnostics. However,
obtaining cleru1 stock. Vaccination is
vaccination, good biosecurity, good manageavailable on a state-by-state basis. Treatment ment, proper sanitation practices, and a
is expensive, and the disease often recurs
good plane of nutrition are key to control
after treatment is stopped. Other inlportant
of disease and are far more effective than
mycoplasmas in poultry include M synoviae
ru1tibiotic usage.

1824

FERRETS

FERRETS

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The domestic ferret (Mustela putorius
vaccinated at -8, 10, and 12 wk of age and
furn) is in the order Carnivora, family
then yearly. Vaccine reactions occur

Mustelidae, and has been in captivity for
frequently in ferrets; vaccinated anin1als
more than 2,000 years. Ferrets are used as
should be monitored for 20--30 min after
research anin1als, often in studies of the
vaccination, and only one vaccine (ie,
respiratory system and as a model for
rabies or distemper) should be given at a

Helicobacler sp infection. They have
time. Fen-ets raised commercially are of�
become popular pets in recent years in the
ten vaccinated for Clost1idium botulinum

USA. They are also used as hunting anin1als
type C at 6--8 wk old.

in Europe, Australia, and New Zealand.

MANAGEMENT

INFECTIOUS DISEASES

The male ferret (hob) can weigh as much as

2 kg when intact, with an average weight of

Bacterial Diseases: Helicobacter

1.2 kg when neutered. The female (jill) can
mustelae is found in the stomach and
weigh as much as 1.2 kg when intact, with
duodenun1 of all ferrets after weaning. It is
an average weight of 0.8 kg when spayed.

an oppo1tw1istic pathogen and can induce

Sexual maturity is reached at 4-8 mo and
chronic, persistent gastritis and ulcer
occurs in the first spring after birth. The vast fom1ation similar to the disease in people.

majority of ferrets are spayed or neutered

Gastric lymphoma may occw· in chronic
before 6 wk of age, primarily because
cases. Clinical signs include inappetence,
females are induced ovulators and can
vomiting, bruxism, diarrhea, melena, and
develop severe hyperestrogenemia if not
hypersalivation. Lethargy, weight loss, and
bred. Ferrets also have less of the musky
dehydration can also occur. These animals
smell that is characteristic ofMustelids if
may be painful on cranial abdominal
they are gonadectomized early in life. The
palpation because of the ulcers induced or
anal scent glands are usually removed at the
enhanced by tl1e presence of this bacteriwn.

time of the neuter or spay. Most physiologic

Definitive diagnosis requires examination of
data for ferrets are similar to those of the
tissue from surgical or endoscopic biopsy
domestic cat, except J;hat creatinine should
but is not commonly pe1fonned because
not be >0.9 mg/dL in ferrets. Ferrets require
of the ubiquitous nature of this organ-
high levels of fat and protein in the diet and
ism in the ferret GI tract. Silver stains
should be fed conunercial fen-et food or
and urease tests should be performed on
high-quality cat or kitten food. Most adult
the biopsy specimens when attempting to
ferrets have a large spleen. this is usually
determine a definitive diagosis. A moleccaused by extramedullary hematopoiesis ular assay is available for fecal samples.

and is nonpathogenic; ultrasonography and

Treatment is with multidrug regimens,
aspiration can be used for a definitive
including an10xicillin (2Q mg/kg, PO,
diagnosis.

bid), metronidazole (20 mg/kg, PO, bid),
and bismuth subsalicylate (1 mL/kg, PO,

Vaccination: Ferrets are vaccinated
annually for rabies and canine distemper.

bid). Clarithromycin (25 mg/kg/day, PO)

There is one FDA-approved rabies vaccine
and omeprazole (1 mg/kg/day, PO) can
for ferrets in the USA. It should be given to
be used for refractory cases. Treatment
ferrets >16wk old and repeated annually. If
is usually for 21 days. Because of the opthis vaccine is w1available, a recombinant portunistic nature of this pathogen, it is
vaccine should be substituted. Canine
in1portant to look for underlying problems
distemper vaccines for ferrets should be
such as gastroenteritis, foreign bodies, or
of chick embryo or recombinant origin.

stress. Treatment for H elicobacter is com

Vaccines of mink or ferret culture ( eg, most
monly initiated when gastroenteritis or
multivalent vaccines for dogs) should not be foreign bodies are diagnosed or when a used, because they may cause seroconve1°
gastrotomy is pefom1ed.

sion and disease. There is currently one

Lawsonia intracellularis can cause a

FDA-approved distemper vaccine in the
proliferative bowel disease, especially in

USA for fen-ets. Ferrets should be
younger ferrets. Signs include diarrhea,

FERRETS

1825
weight Joss, and rectal prolapse. Treatment
quent maldigestion and malabsorption.

is with chloramphenicol (25 mg/kg, PO, bid)

Definitive diagnosis is difficult, although
for 14-21 days.

scanning electron microscopy of the feces

Salmonellosis in fen-ets is rare but
may identify corona.virus. Increased ALT
associated with feeding raw or undercooked and alkaline phosphatase may occw·

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meat or unpasteurized milk. Signs include
secondary to hepatic lipidosis. Treatment is
bloody diarrhea, cof\iunctivitis, and anemia.

suppo1tive and includes fluids, nutritional

Salmonella Typhimurium, S Newport, and suppo1t, broad-spectrum antibiotics, and GI

S Choleraesuis may be involved. 'freatment protectants. Prevention is by quarantine of
is with aggressive supportive care and
new ferrets, thorough cleaning of new
antibiotics. Ferrets are susceptible to
bedding and toys, and washing hands and

Mycobacterium avium,M bovis, and
changing clothes after hanclling other

Mycobacterium tuberculosis. Intradermal
fen-ets.

testing is not reliable. Bacterial cystitis is

A second related corona.virus called
rare in ferrets and is usually associated with
ferret systemic corona virus causes a
urolithiasis and prostatomegaly. Escheri
systemic pyogranulomatous inflammato1y
chia coli, Staphylococcus aureus, and
disease resembling the dry form of feline

Proteus spp are most commonly identified.

infectious peritonitis. This disease is seen in

Bacterial pneumonias in ferrets are caused
young ferrets (average age 11 mo) and is
by Streptococcus zooepidemicus,
progressive throughout several weeks to

Mycobaclerium spp, and gram-negative
months. Clinical signs include anorexia,
bacteria such as E coli and Klebsiella
weigh loss, diarrhea, and enlarged
pneumoniae. Other bacterial infections are
intra-abdominal and, Jess commonly,
similar to those seen in other carnivores.

peripheral lymph nodes. Hypergammaglobulinemia, anemia, and CNS signs can be Viral Diseases: Fen-ets are susceptible to
seen as the disease progresses. This disease
canine distemper virus. Transmission is by was initially called disseminated idiopathic aerosol or exposure to infected secretions.

myofasciitis because of the white nodules

Clinical signs begin 7 -10 days after infection
found in many tissues on necropsy. These
and start as fever and dermatitis on the chin
nodules are pyogranulomatous inflanmiaand inguinal area, progressing to anorexia, tion and involve many organs, including
erythema of mucus membranes, and
peritonewn, adipose tissue, viscera, and
mucopurulent ocular and nasal discharge.

blood vessels. A pyogranulomatous

Brown crusts on the face and eyelids and
pnewnonia has also recently been reported.

hyperkeratosis of the footpads also occur.

Treatment is supportive with immunosup

Respiratory signs develop and progress
pressants such as prednisolone and
rapidly. Diagnosis is by history, clinical signs,
anecdotal reports of use of polyprenyl
and positive immunofluorescent antibody
il1m1w1ostin1ulants, which have resulted in
testing or histopathology. Mortality is close
some increase in swvival til11e. Average
to lO()OA, and typically occurs 12-14 days after
survival time is -2 mo.

infection.

Aleutian disease is a parvovirus

The human influenza virus causes fever,
originally seen in mink, but at least two
lethargy, anorexia, nasal discharge, sneezing,
distinct ferret strail1s of the virus have been
and depression in fen-ets. Treatment is
identified (seep 1872). The virus causes
supportive and includes antibiotics for
ilnmune complex deposition in organs,
secondary infections, antihistamines, and
which results in a variety of nonspecific
an1antadine (6 mg/kg, nasally, bid). Recovery
clinical signs such as progressive weight
is usually within 7 -14 days.

Joss, weakness, ataxia, hepatomegaly, and

Two coronaviruses cause disease in
splenomegaly. A severe hyperganm1aglobufeJTets. The fen-et enteric corona.virus lil1emia is tl1e most consistent finding on
causes epizootic catarrhal enteritis. This blood work. A preswnptive diagnosis is disease is highly transmissible and is often
based on clillical signs and hyperglobulinebrought into a group of fen-ets by an mia. The two most common tests for the
asymptomatic juvenile animal. Clinical
virus antibody are counterinummoelectrosigns begin 2-14 days after introduction of phoresis and inmlunofluorescent antibody
the new feJTet or exposure through fomites
tests. Definitive diagnosis is difficult,
and include anorexia, vomiting, green or
because many apparently nom1al feITets
mucoid diaJThea, melena, dehydration,
have positive titers. The organism has been
lethargy, and weight loss. The disease is
found in the urine, feces, and blood of
most severe in older fen-ets, which may take symptomatic and asymptomatic anin1als.

months to fully recover. The virus causes

Treatment with anti-inflammatories and
blunting of the intestinal villi and conse-
inmltmosuppresants such as prednisolone

1826 FERRETS
and cyclophosphamide can be considered
helpful in identification of the worms in the
and may have clinical benefit. Treatment of
right ventricle, pulmonary arteries, and vena
infected mink kits with gamma globulincavae. Peripheral microfilaremiais uncomcontaining Aleutian disease virus antibody mon in ferrets; therefore, antigen testing is
has decreased mortality rates, but this
more beneficial. Treatment using Jongtem1
treatment has not been attempted in ferrets.

antithrombotic drugs and adulticides can be

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There is currently no vaccine available for
done but may cause problems. Low-dose
this disease in ferrets.

ivennectin (0.05 mg/kg, SC, monthly until
clinical signs and microfilaremia resolve) is

Fungal Diseases: Ferrets are susceptible
the current reconunended treatment ( see
to Microsporurn canis and 1)'ichophyton I-IEARTWORM DISEASE, p 127).

mentagrophytes. Transmission is by direct

Coccidiosis can cause disease in young
contact or fomites and is often associated
ferrets including diarrhea, lethargy, and
with overcrowding and exposure to cats.

rectal prolapse. Diagnosis and treatment are

Infection is more conm1on in kits and young
similar to those in dogs. Rectal prolapse can
ferrets and is often seasonal and self-limitalso occur with coccidiosis and usually ing. A pyogranulomatous dermatitis and
resolves after treating tl1e underlying
fungal pododermatitis has been associated
disease. Topical hemorrhoidal creams may
with Microsporum nanum. Other fungal
be helpful.

diseases in ferrets include cryptococcal
meningitis and blastomycosis causing

NEOPLASIA
granulomatous meningoencephalitis.

Fungal pnew11onia is uncommon in ferrets

Cutaneous mast cell tumors are probably
but can be caused by Blastomyces
tl1e most conm1on nonendocrine tumor in
dermatitidis and Coccidioides immitis
ferrets. These twnors can appear anywhere
in endemic areas. Cryptococcosis from
on the body but typically affect the trunk

CryptococcitS bacillisporus and C neo
and neck. The tun1or appears as a raised,
j'(nmans var grubii has been diagnosed in·egular, and often scabbed mass. Systemic
in ferrets. Signs include pneumonia,
signs are rare, but the tumors may bleed
pleuritis, rhinitis, and regional lymph
when scratched. Treatment is by excision.

nude enlargement.

Local treatment with strontiun1 may also be
beneficial.

Parasitic Diseases: Ear mites are the

4'ffiphoma is common in ferrets and can
most conunon ectoparasite in ferrets and
affect many organ systems, including the
are caused by Otodectes cynotis. The same
lymph nodes, spleen, liver, heart, thymus,
ear mite is found in dogs and cats, and it can
and kidneys. Disease of the spine and CNS
be passed between species. Diagnosis and
has also been seen. Lymphoma of young
treatment are as for dogs and cats ( see
ferrets is often rapidly progressive, whereas
it is often a chronic disease in adults.

OTITIS EXTERNA, p 527). Fleas are also
common in ferrets and can be transmitted

Clusters of lymphoma have been seen in
between ferrets and other houscliold pets.

related or cohabitating ferrets, and a viral

Diagnosis is by visualization, and treatment
agent is suspected in those cases. Diagnosis the same as for dogs and cats (see FLEAS
tics should include a CBC, chemistry panel,
radiographs, ultrasonography, and aspirates

AND FLEA ALLERGY DERMATITIS, p 880). Many of
the long-acting topical treatments, such as
of any suspected tissues. Treatment
fipronil, last longer in ferrets because of the
protocols for ferrets have not been
increased sebwn in the coat. Mange in
standardized but can include removal of the
ferrets is caused by Sarcoptes scab'iei and neoplastic tissue if possible, chemotherapy,
can be seen as a generalized dermatitis or
and/or radiation therapy. Inununosupprescan be limited to the feet, toes, and pads in sion is a conunon problem witl1 chemothera pedal form unique to ferrets.

apy in ferrets, and frequent CBCs are

Heartworm disease, caused by DirojUaria
inlperative with any treatment protocol.

immitis, can be found in ferrets, especially Chordomas and chondrosarcomas
if given outdoor access in endemic areas.

have been repo1ted in ferrets. Chordomas

Disease can be caused by even a single wonn.

typically appear as firm masses on the tail.

Clinical signs include lethargy, coughing,

They may become ulcerated from dragging
dyspnea, and ascites. Ferrets are typically
on the ground but otherwise cause few
infected with a very small nun1ber of worms
problems. These tumors have also been

(1-20), making diagnosis difficult. Echocardireported at the cervical region, causing ography is warranted, because the parasites
paresis and ataxia. Surgical removal is
often obstruct blood flow and cause right-side suggested when possible. Chondrosarcoheart failure. Echocardiography may also be mas can develop anywhere along the spine,

FERRETS

1827
ribs, or sternum and tend to cause spinal
old. The most common clinical sign is hair
cord compression and associated clinical
loss beginning on the tail and rump and
signs. Treatment should include removal, if
progressing up the flank and head.

possible.

In females, a swollen vulva and enlarged

Splenomegaly is common in adult
marnillae may also be seen, whereas males

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ferrets and is usually caused by extran1edulmay develop aggression and stranguria lary hematopoiesis; however, lymphoma
secondary to prostatic enlargement. Bone
and hemangiosarcoma can occur. An
marrow suppression may be seen in either
irregular or firm spleen should be investisex, with severe hyperestrogenemia. A gated with ult:rasonography and aspiration.

presw11ptive diagnosis is made after history
and physical examination. The enlarged

ENDOCRINE DISORDERS
adrenal glands are often palpable cranial to
either kidney. CBCs and chemistry panels

Insulinomas are very common in ferrets
are typically nonnal. Radiographs are not

>2-3 yr old. These functional trunors of the
useful, because the masses do not calcify as
pancreatic (3 cells cause increased insulin
commonly as in other species. Ultrasonoglevels, resulting in hypoglycemia and its raphy can demonstrate enlargement of
associated clinical signs such as wealrness,
tl1e gland(s). Definitive diagnosis requires
lethargy, poste1ior paresis, hypersalivation,
measurement of the three sex honnones,
bruxism, and seizures. Diagnosis is based
which can be perfonned in a panel (at
on demonstration of hypoglycemia and

University of Tennessee).

corresponding nom1al or increased insulin

Medical and surgical treatments exist.

levels. Other blood tests are usually nom1al.

Sw·gical removal of the adrenal gland(s) is

Ultrasonography is only occasionally useful
more likely to be curative than medical
in demonstrating these pancreatic masses.

management, but there is still a recurrence

Medical and surgical treatments are possible,
rate of -4QOA, after surgery. The left gland is
but there is no cure, and owners should be
easier to remove, because the right gland is
made aware of the chronic and progressive
closely associated with the caudal vena
nature of this disease. Surgical treatment
cava. If both sides are affected, a subtotal
involves removing discrete tumors via
adrenalectomy can be pe1ionned. Histology
nodulectomies or partial pancreatectomy.

of these glands may reveal hyperplasia,

Microscopic tumors within the entire
adenoma, or adenoca.rcinoma. Functionally,
pancreas are common; therefore, removal
all three grades are similar, and metastasis is
of the entire tumor is unlikely. A period of
unlikely. Hypoadrenocorticism may develop
euglycemia occurs after surgery in some
if both adrenal glands are completely or
cases, but most cases require continued
partially removed. This may be treated with
medical treatment. Major benefits of surgery
rnineralocorticoid and glucocorticoid
are decreased severity of signs, ease of
supplementation. Medical management of
management, and moderately increased
hyperadrenocorticism is ainled at reducing
survival time. Medical management includes
the clinical signs but does not affect the
use of prednisone (0.&--2 mg/kg, PO, bid)

adrenal tw11or itself. Leuprolide acetate is the
and diazoxide (5-30 mg/kg, PO, bid) to
most common drug used. The mechanism is
counteract the effects of the tumor; however, not completely understood but is probably this does not affect the tumor directly.

related to down-regulation of peripheral

Prednisone increases resting blood glucose
honnone receptors. Leuprolide is a repositol
levels and down-regulates peripheral insulin
fonnulation of a GnRH agonist that is
receptors, whereas diazoxide decreases
fonnulated in 1-mo (100-400 mcg, IM) and
insulin release from the (3 cells and competes

4-mo (2-4 mg, IM) preparations. Owners
at peripheral insulin receptors. These drugs
should be advised that this is a lifelong
can be used independently or synergistically.

treatment to control the clinical signs of tlle

'Iypically, prednisone is used first until the
disease. Recently, some clinicians have
dosage approaches 2 mg/kg and then
treated hyperadrenocorticism medically only
diazoxide is added. Medical treatment is
during breeding montlls, typically November
lifelong, and glucose levels should be
to March. Deslorelin acetate, a sinillar GnRH
monitored &--7 days after changing doses
agonist, is also available. This is a longerand at least every 3 mo afterward.

acting inlplant that lasts 10---17 mo. This drug

Hyperadrenocorticisrn in ferrets is
is well tolerated by ferrets. Melatonin can
caused by excessive secretion of the sex
also be used at 1 mg per ferret per day, orally
honnones progesterone, testosterone (in
or in an injectable, repositol fonnulation,
the fonn of androstenedione), and estrogen
which is reported to last 4 mo. This drug
by the zona reticularis of the adrenal gland.

cow1teracts tl1e alopecia and may help witll

It can be seen in ferrets as young as 1.5 yr
oilier signs as well, but, like leuprolide, is

1828 FERRETS
only symptomatic treatment. Drugs used to

Dilated cardiomyopathy can occur in
control sex hormone levels in people are
ferrets, usually those> 4 yr old. Clinical
beginning to be used in fenets and show
signs can be similar to those of insulinoma,
promise in controlling clinical signs.

so both should be excluded when examining a ferret with lethargy, wea.kpess, ascites, VetBooks.ir

OTHER NONINFECTIOUS DISEASES increased respiratory effort, or exercise intolerance. Diagnosis is by radiography

Gastric foreign bodies are common in
and echocardiog:raphy. Treatlnent is based
ferrets because of the animal's inquisitive
on echocardiographic abnormalities and
nature. Foreign bodies are usually soft rubber includes furosemide, digoxin, enalapril, or plastic items but can also be tlichobezoars.

benazepril, and pimobendan. A fonnulary

Clinical signs include anorexia, bruxism,
should be consulted for dosing instructions.

hypersalivation, cranial abdominal pain,

Renal disease in ferrets is similar to that
dianhea, and melena. Vomiting is more
in other species. Renal cysts are common in
common with gastlitis than with foreign
adult ferrets and usually do not cause a
bodies. Diagnosis is with plain or contrast
problem unless present in large numbers.

radiography. Treatlnent involves surgical or

Uroliths can develop in ferrets fed diets high
endoscopic removal. Gastlitis should be
in plant proteins and are usually composed
ti·eated after removal of the foreign body.

of struvite.

HEDGEHOGS

Hedgehogs are in the family Erinaceidae,
and projects forward, and there is a gap
within the order lnsectivora. The centi·al
between the maxillary first incisors. The

African hedgehog (Atelerix albiventri.s ),
stomach is simple, and a vomiting reflex
also known as the white-bellied, four-toed,
is present. The male has a conspicuous
or African pygmy hedgehog, is native to dry,
prepuce that opens mid-abdomen. There is
open habitats in central and eastern Africa.

no scrotal sac; the testes are located in a

They are nocturnal and very active, jogging
para-anal recess surrounded by fat and can
for miles in search of inve1tebrate prey. In
be palpated in reproductively active males.

the USA, it is illegal to own a hedgehog as a

The female urogenital opening is a few
pet in some states and municipalities; in
millimeters cranial to the a.nus. The uterus
other states, a permit is required. Additionis bicornuate with a single cervix and no ally, a USDA permit is required to breed,
uterine body. Hedgehogs are polyestrous
transport, sell, or exhibit hedgehogs.

and breed throughout the year in captivity.

Ovulation is believed to be induced, and

Anatomy, Physiology, and ehavior:

sterile matings with pseudopregnancy may

The dorsum is covered in a dense coat of
occur. Hedgehogs are born hairless, with
keratin spines; each spine has a basal bulb
closed eyes and ea.rs; at birth the spines are
that firmly attaches it within the follicle,
covered by a membrane that is removed
with a nanowed po1tion at the skin surface.

within the fast few hours oflife.

Healthy spines are difficult to pull from the

Hedgehogs are a.dept at climbing, digging,
follicle without breakage. The spined skin
swimming, and jogging. While they have
has a thin and hairless epidern1is and a
sensitive olfaction and heaiing, their sense
thick, fibrous dermis wilh much fat and few
of vision is not as well developed. Foraging
blood vessels. A wary hedgehog will raise
hedgehogs norn1ally emit a variety of
the spines and crouch. If a hedgehog is
snuffling sounds; agitated hedgehogs make
frightened, contraction of the pa.nniculus
a loud hissing sound that may be punctumuscle pulls the loose spiny skin over the ated with various puffing and cough-like
entire body. The pa.nniculus is thickened at
sounds. With intense disti·ess, a screain may
the rim to fonn the orbicularis, a pursebe emitted. With patience, most hedgehogs string-like muscle that closes the spined
lea.111 to accept handling.

skin over the animal. For selected

Hedgehogs demonsti·a.te a unique behavior
physiologic data for Af1ica.n pygmy
called self-anointing, or anting. This behavior
hedgehogs, see TABLE 10.

may be elicited by a variety of substances,

Hedgehogs have brachydont teeth.

paiticulai·ly those with a strong odor. The

The fast incisor in each quadrant is large
hedgehog takes the material into the mouth,

HEDGEHOGS

1829

•t#=iii••• PHYSIOLOGIC DATA FOR AFRICAN PYGMY HEDGEHOGS

Average body weight

Male : 400-600 g

Female: 300-400g

Life span

Average 4-6 yr, may live to 8 yr

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Body temperature

95.7° -98.6°F ( 35.4° -37.0°C)

Adult dental formula

2 (I 3/2:C 1/1:P 312:M 3/3) = 36 (variations have been noted )

GI transit time

12-16 hr

Heart rate

18 0-28 0bpm

Respiratory rate

25-50bpm

Age at sexual maturity

2-3mo

Reproductive life span

Male: throughout life

Female: 2-3 yr

Gestation

34-37days

Litter size

3-4 (range 1-9)

Birth weight

10-lSg

Eyes open

14-lSdays

Deciduous teeth eruption

Begins on day 18; all deciduous teeth erupted by 9 wk Permanent teeth eruption

Begins at 7-9 wk

Age at weaning

5-6 wk (start eating solids at 3 wk )

mixes it with frothy saliva, and applies the

Ambient temperature should be 72° -90°F
mixture to its spines with the tongue. The

(22° -32°C); 75° -8 5°F ( 24 ° -29°C) is optimal.

purpose of this behavior is unknown.

Hedgehogs may go into a torpid state if too
cool or too wann; this is believed to be

MANAGEMENT
unhealthy for pet hedgehogs. A heating pad
placed UI1demeath the enclosure or a

Housing: Wild hedgehogs are solitary;
ceramic reptile heater may be used. Low
as pets they are usually maint.ained in
hUinidity ( <4096) is preferred. Hedgehogs
individual cages. Some fanciers successfully avoid bright light; however, a day cycle of house multiple animals together, but this

10-14 hr of mild light should be provided.

can lead to disproportionate feeding and

AJtllough some owners may attempt to
injUiies from fighting. Healthy hedgehogs
convert their pets to a diurnal schedule,
are very active; 2 x 3 ft are minimal floor
most remain nocturnal.

dimensions. Hedgehogs are able to climb

Some hedgehogs use a litter tray; natural
and can escape through small holes, so the
plant litters used for cats make the best
cage must be secure and lidded. Glass tanks

Jitter substrate. Clay, ciUinping-type litter, or
and plastic-bottomed cages with wire walls
sand may stick to tlle animal and should not
are suitable, provided that the wire spacing
be used. Many hedgehogs defecate in their
is sufficiently close. Widely spaced wires
hide boxes and exercise wheels, so daily
can lead to limb entrapment or death if the
spot cleaning is often necessary. Exercise
hedgehog's head becomes ensnared by its
wheels witll solid metal or plastic running
spines. A hiding place is essential. The cage
surfaces are highly recommended.

substrate should be soft and absorbent.

Hedgehog legs can become entrapped in

Recycled newspaper bedding is a good
wire wheels. Hedgehogs should be let out
choice; aspen shavings, alfalfa pellets, and
daily for exercise. Cardboard tubes, straw,
hay are other options. Wire, cedar, corncob,
safe climbing structures, swimming tubs,
and dusty or scented substrates are not
and other toys provide interest. Dirty
recommended, and cloth bedding poses
hedgehogs may be bathed with a mild pet
a risk of limb entrapment. The substrate
shan1poo and use of a soft-bristle vegetable
should be 3-4 in. deep to allow for digging.

brush.

1830

HEDGEHOGS

Diet: The ideal diet is a commercially
exainination room. Healthy, untroubled
prepared hedgehog food. If hedgehog food
hedgehogs should be active and walk with
is not used, premium food for less active
the ventrun1 raised off the table, but weak or
cats or dog food are alternatives. Food
wary hedgehogs tend to crouch. The nose is
should be rationed to prevent obesity.

normally moist and active. !)espiration is

Depending on the animal's weight and
normally silent, except when the hedgehog

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activity, 3-4 tsp (15-20 mL) of the main diet
hisses in defense. No1mal feces are dark
is typically fed daily. Growing animals and
brown and ve1)' soft to pellet-like. The skin
reproductively active females may be fed
in the spiny areas may have a mildly ill)' or
ad lib, and calcium-rich foods are recomflaky appeai·ance, but excessive flaking, quill mended.

loss, erythema, and crusting ai·e abnmmal.

In addition to the main diet, -1-2 tsp

Once the hedgehog is sedated or

(5-10 mL) of varied moist foods and/or
anesU1eLized ( eg, with isoflurane at a light
invertebrate prey ( eg, canned cat or dog
plane), the remainder of the exainination
food, cooked meat or egg, low-fat cottage
can be perfonned. HydJ·ation may be
cheese, mealwo1ms, eaithworn1s, waxassessed by eyelid turgor. The eyes should wom1s, gut-loaded crickets) and -1 tsp
be cleai·, and the pinnal margins should

(5 mL) of vegetable/fruit mix ( eg, beans,
be free of crusting or ragged edges. The
cooked carrots, squash, peas, tomatoes,
teeth should be white and the gingiva a
leafy greens, banana, grape, apple, pear,
uniform pink. The oral cavity and tongue
berries) should also be provided daily.

should be inspected for ulcers, foreign
lnve1tebrate prey and dry food items may be material, and masses. Normal lymph nodes hidden in the bedding to promote foraging.

are difficult to palpate, but they may

Hedgehogs should not be fed raw meat or
become enlarged in cases of neoplasia or
eggs, which may harbor Salmonella. Milk
infection. The heait should have a regulai·
can cause diarrhea. Vitan1in or mineral
rhythm and no murrnms, and a femoral
supplementation is not necessary for
pulse should be palpable. The abdominal
hedgehogs fed a commercial diet. Hedgecontour should be flat but may be distended hogs are often slow to accept new foods,
by obesity, organomegaly, masses, or fluid.

and diet changes must be made with cai·e.

The prepuce or vulva should be checked for

Fresh water should be available at all times.

inflai11mation, discharge, or adherent debris.

Most hedgehogs can learn to drink from

Testicles may be palpable in the para-anal
water bottles.

area. The toes should be inspected for
encircling fibers and overgrown nails.

Breeding and Neonatal Care: Females
should be at least 6 mo old before breeding.

Clinical Techniques: The jugular vein

A weight gain of�50 g within 3 wk of
can be used to collect blood sainples; its
breeding suggests pregnancy. At 30 days,
anatomic location is similar to that in other
abdominal and man11Ua.J)' enlargement may
small mainmals. Alternatively, the cranial
be detected. Infanticide and cannibalism of
vena cava may be used, but there is a
the young can occur; the feJJ1ale needs strict
greater risk of cardiac puncture because
privacy from other hedgehogs and people
of the relatively cranial position of the
starting -5 days before delivery and
hedgehog heart. The femoral, lateral
continuing 5-14 days after parturition.

saphenous, or cephalic veins may be used

In cases of lactation failure or abandonfor injections or to collect small samples ment, fostering of the pups (or "hoglets") ( up to 0.5 mL).

to another dain with similarly aged pups

SC injections can be given in the spiny
is usually successful. If a surrogate dai11 is
or furred areas; the furred skin is more
unavailable, a canine milk replacer may
elastic and vascular but less accessible.

be fed through a feeding tube or syringe;

The dell11is under the spiny skin is poorly
however, hai1d-reaiing of hedgehogs is
vascularized, so drugs or fluid given in this
associated with high mortality. Weaning
location may not be absorbed for several
generally occurs at 5-6 wk, and the young
hours. The junction of furred and spined
may be moved to separate cages at 8 wk.

skin provides aJ1 accessible and reliable site.

Daily handling staiting at 3 wk will result

IM injections may be given in the triceps,
in hedgehogs that remain tan1e.

quadriceps, gluteal, or orbicularis muscles.

IV catheters are usually dislodged if the

Restraint and Examination: Because
animal curls. An intraosseous catheter may
most hedgehogs roll up when restrained,
be placed in the tibial crest using a 22- or
a thorough exainination usually requires

25-gauge needle or 1-in. spinal needle; the
chemical restraint. Before sedation, the
catheter remains accessible even when the
hedgehog should be observed in the
animal is curled.

HEDGEHOGS

1831

Radiography may be useful, but the

Preventive Medicine: Hedgehogs have a
hedgehog's spines can obscure detail. For
sh01t life span and often hide signs of
lateral views, the spines can be pulled away
illness; therefore, examinations (under
from the chest and abdomen and secured
isoflurane anesthesia) every 6 mo with
with a large plastic clip. Anesthesia is
blood testing are recommended. A 2-yi·-old
generally required for proper positioning.

hedgehog should be considered geriatric.

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Oral medication may be difficult to

There are currently no vaccines labeled for
administer. Some anin1als accept liquid
use in hedgehogs. Because hedgehogs are
medications that have been compounded
not usually housed in mixed gender groups,
with fruit flavor. Alternatively, medication
castration and ovariohysterectomy are not
may be injected into mealwonns or mixed
generally requested or recommended. The
with a favorite food. Applying topical
incidence of uterine and mammary tumors
medications is complicated by the presence
is a concern; however, tl1e effect of early age
of spines and self-grooming, and some
ovariohysterectomy on tumor reduction is
odors may initiate anting behavior (see
w1known.

p 1828).

A cage temperature of 80° -85°F (27° -

DISEASES

29°C) is recommended for ill hedgehogs.

Voluntary feeding is facilitated by providing

Sick hedgehogs with a variety of illnesses,
the animal's customary diet and by offering
including acariasis, dental problems,
live invertebrates. Anorectic anin1als should
pneumonia, gastric ulceration, neoplasia,
be fed a high-calorie canine or feline diet via
and hepatic disease, often present with
syiinge or tube. For ongoing assisted feeding, nonspecific clinical signs such as lethargy, a pharyngostomy or esophagostomy tube
weakness, and anorexia. This frequent
can be placed.

presentation serves to emphasize the

Hedgehogs are not bacterial fermenters,
importance of diagnostic testing, even if
and there are no particular concerns
anesthesia is required.

regarding antibiotic use. For appropriate
drngs and dosages in this species, consult

Cardiovascular and Hematologic
the Exotic Animal Formulm-y (2013) or

Diseases: Dilated cardiomyopathy (see
other sources.

p 115) is a common postmortem finding,
with an incidence of 38% in captive African

Anesthesia and Surgery: A 4- to 6-hr
hedgehogs. The etiology is not known;
fast is recommended before anesthetic
however, genetic and nutritional causes have
procedures longer than 20 min. Isoflurane
been suggested. Affected hedgehogs are typiis commonly used for induction and cally;:, 3 yr old, although it may be seen in
maintenance. Hypersalivation may occur,
animals as young as l yi· of age. Males are
and premedication with atropine is advised.

slightly overrepresented. Signs include

Ketamine, diazepam, midazolam, xylazine,
dyspnea, decreased activity, weight loss, an
and toletamine/zolazepam have also been
auscultable murmur, ascites, and acute
used but may prolong recovery. Tracheal
death. Radiographs typically demonstrate
intubation may be indicated for longer or
varying degrees of cardiac enlargement,
oral procedures and is accomplished with
pulmonary edema, pleural effusion, hepatic
a 1.0-1.5 mm endotracheal tube, Teflon IV
congestion, and abdominal fluid. Common
catheter, or feeding tube.

gross necropsy findings associated with

Spines are removed by clipping or with
cardiovascular disease in hedgehogs include
steady traction. Hedgehogs may self-muticardiomegaly, hepatomegaly, pulmonary late traumatic or surgical wounds; prompt
edema and/or congestion, hydrothorax,
primary closure with subcuticular sutures
a.scites, and pulmonary or renal infarcts.

should be used whenever possible.

Norn1al echocardiographic measmements

Bandages and dilute chlorhexidine baths
have been published for the African pygn1y
are well tolerated. If the cutaneous muscle
hedgehog. These reference intervals, along
is damaged, it must be closed in a separate
with subjective evaluation of wall motion
layer. Contraction of the rolling-up
and chan1ber size, can be used to confim1 the
musculature can cause wound dehiscence.

diagnosis of dilated cardiomyopathy.

Elizabethan collars are not practical.

Hematologic and biochemical testing are

Ovariohysterectomy is similar to the
useful to screen for concurrent problems
procedure in other mammals, although
and to monitor the effects of tl1erapeutic
substantial fat surrounds the ovaries and
agents. Therapy with furosemide, enalapril,
mesosalpinx. Castration is performed
and digoxin may be helpful. Alternatively,
through a para-anal skin incision over each
furosemide, pin1obendan, and supplementatesticle; a closed technique is preferred.

tion with oral carnitine have been used. The

1832

HEDGEHOGS
longterm prognosis for hedgehogs with

Hepatic lipidosis is relatively common
congestive heart failure is poor.

and may be a sequela of cardiomyopathy,

Saddle thrombus and pulmonary
neoplasia, starvation, obesity, toxicosis,
thromboemboli have been seen. Myocardial
pregnancy, or infectious disease. Signs may
mineralization and splenic extramedullary
include lethargy, inappetenc�, icterus,

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hematopoiesis may exist in pet hedgehogs
diarrhea, and signs of hepatic encephalopawith concurrent diseases; the clinical signifithy. Diagnosis is supported by testing for cance of these lesions is unknown.

hepatic enzymes, plasma bilirubin, and bile

Congenital erythropoietic porphyria was
acids. Radiography and ultrasound-guided
reported in a 6-mo-old male inbred pet
liver aspirates may also be performed.

African hedgehog.

'Ireatment for hepatic lipidosis is similar
to that in other species. Other important

Gastrointestinal and Hepatic Diseases:

causes of liver failure include primary and

GI obstructions are most often caused by
metastatic hepatic neoplasia. Hepatic
ingestion of mbber, hair, or carpet fibers.

necrosis caused by human herpes simplex

Signs include acute anorexia, lethargy, and
virus 1 was reported in a hedgehog that
collapse. Vomiting may be present but often
received dexamethasone.

is not. Diagnosis of obstruction is complicated by the fact that gaseous dilation of the lntegumentary Diseases: Acariasis

GI tract can be a nonspecific finding in ill
caused by Caparinia spp (psoroptic mite)

hedgehogs. A fatal intestinal mesenteric
is very common. Infestation with Notoedres
torsion has also been reported. Alimentary
spp ( sarcoptic mite) has also been reported
inflammation, including esophagi tis, gastritis, in hedgehogs. Signs include lethargy, enteritis, colitis, and gastric ulceration with
decreased appetite, hyperkeratosis,
perforation, has also been seen. Most of these seborrhea, quill loss, loose quills, and white hedgehogs had nonspecific signs such as
or brownish crusts (mite droppings) at the
decreased appetite and weight loss; vomiting
base of the quills and around the eyes.

and diarrhea were not seen. A case of

Hedgehogs may scratch or rub themselves,
gastroesophageal intussusception and
but many individuals do not have obvious
megaesophagus has been reported in a
pruritus. Some animals have subclinical
hedgehog. This animal's clinical signs
infestations. Diagnosis is confirmed by
included dyspnea, vocalization, and
identifying mites and eggs (nits) via skin
salivation; vomiting ensued before death.

scraping. Treatment consists of ivermectin

Enteritis may be caused by Salmonella or
or a combination of iven11ectin and amitraz.

other bacteria Salmonellosis in hedgehogs

All bedding must be removed, and cage
may be clinically silent or may cause diarrhea, furnishings disinfected or discarded. During weight loss, decreased appetite, dehydration,
treatment, the cage is lined with paper that
lethargy, and death. Diagnosis should be
must be changed daily. All hedgehogs in the
confirmed with fecal culture, using Salmo
home should be treated concurrently.

nella-enriching medium. Although treatment

Pet hedgehogs may be infested with fleas;
is indicated in hedgehogs with clinical signs
however, cat and dog fleas generally do not
of disease, owners should be advised of the
infest African pygmy hedgehogs. This is
zoonotic potential and the risks of creating
likely because of the hedgehog's low body
antibiotic resistance. Alimentary candidiasis
temperature. 'Ireatment consists of topical

( Candida albicans) and cryptosporidiosis
or systemic flea control agents. Shampoo
are other reported infectious diseases.

and powder products that are safe for

Although numerous species of nematodes,
kittens appear to be safe for hedgehogs.

cestodes, and protozoa have been identified

'Iropical rat mites, Omithonyssus bacoti,
in wild hedgehogs, their significance in pets
may also cause flaky skin and loss of spines;
appears to be minimal.

fipronil spray is an effective treatment.

Diarrhea also can be associated with

Dermatophytosis is a common clinical
some commercial diets or inappropriate
disease in African pygmy hedgehogs;
foods such as milk. GI neoplasia, particuhowever, infection without significant larly lymphosarcoma, is relatively conunon.

clinical signs is also possible. Dermato

Other considerations for GI signs include
phytes (Triclwphyton erinacei,
dietary change, toxins, hepatic disease, and

T mentagrophytes, Microsporum spp, and
malnutrition. Hedgehog digestion does not

Arthroderma benhamiae) cause crusting
rely on bacterial fermentation, and there is
dem1atitis, especially around the face and
no evidence of antibiotic sensitivity as is
pinnae. Quill loss may also be noted.

seen in herbivorous marnmals. Hematoche

Although some animals may scratch with
zia should be clearly differentiated from
the hindlin1bs or mb against stationary
urinary or vaginal bloody discharge.

objects, many individuals do not display

HEDGEHOGS

1833
signs of pruritus. Some infections are
systems. The most common tun10rs are
secondary to other dermatopathies, such as
mrunmary gland tumors, lymphosarcoma,
acariasis or trauma. Diagnosis is confirmed
and oral squrunous cell carcinoma. The
by cultwing spines in dermatophyte test
median age at tin1e of diagnosis is 3.5 yr,
mediwn. Treatment consists of topical

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antifungal agents, with systemic griseofulalthough tumors may be seen in aninlals vin or ketoconazole if needed. Lime-sulfur
as young as 2 yr old. In one survey, > SOOA,
dips may also be used. Other hedgehogs in
of the twnors were malignant. Proliferathe home may be subclinically infected, and tive uterine tun1ors or polyps ru·e common
treatment of all animals is recommended.

and ru·e associated with vaginal bleeding,

Contact dermatitis may result from
hematuria, and weight loss. Ovariohysunsanitary bedding. Cellulitis has been terectomy allows prolonged survival of
linked to secondary myositis and sepsis; the
hedgehogs with uterine twnors. Some
primary cause in most of these cases was
sarcomas have been associated with retrotrawna. Staphylococcus simulans was viral infection.

reported to cause de1matitis characterized

Signs depend on the location and severity
by a broad, well-circwnscribed area of hyperof disease and may include palpable masses, keratosis and alopecia on the back of a
weight loss, anorexia, lethru·gy, diarrhea,
hedgehog. Allergic dermatitis has been
dyspnea, and ascites. Diagnosis is based
anecdotally desctibed; restricted antigen
on cytology or h.istopathology. Diagnostic
diets, antihistamines, and glucocorticoids
imaging and blood testing may help
may be helpful. Pruritus may be observed
detemline the extent of the disease and
with development of new spines, as occurs in establish a prognosis. Treatment generally young hedgehogs. Pemphigus foliaceus has
includes surgical excision and supportive
been reported; loss of spines, flaking skin,
cru·e, although other treatment modalities
moist erythema, and epidermal collarettes
may be helpful. Not eve1y mass in pet
were seen. Dexamethasone ir\jections were
hedgehogs is neoplastic; for exrunple,
reported to be an effective treatment.

abscesses, bone cysts, papillomas, and

Skin neoplasia is common. Squan10us cell
ute1ine polyps are seen.

carcinoma, lyrnphosarcoma, and sebaceous
gland carcinoma have been described.

Neurologic Diseases: New-ologic signs

Papillomas of suspected viral etiology have

(particularly ataxia) may be caused by
been reported; recurrence in other sites
torpor, hepatic encephalopathy, postprutwn
after excision is common. Cutaneous and
eclrunpsia, malnutrition, traun1a, interve1tesubcutaneous nodules may also be caused bral disc disease, toxins, infarcts, infectious
by abscesses, mycobacteriosis, and
causes ( eg, parasitic migration, rabies),

Cuterebra larvae.

otitis media, demyelination, polioencepha-
lomalacia, or neoplasia.

Musculoskeletal Diseases: Myositis

Hedgehogs kept in cold ( or sometimes
secondary to cellulitis has been reported.

excessively high) temperatures may enter

Osteoartluitis has also been seen. Bone cysts
a state of torpor or dormancy. In this state,
should be considered as a differential for
the hedgehog has a greatly dinlinished
mandibular masses, along with neoplasia and response to stimulation, decreased heart trawna. Fractw·es can occur when a limb
and respiratory rates, and possibly
becomes entrapped in a wire cage or exerincreased susceptibility to infection.

cise wheel. Splinting can be perf01n1ed for

Do1n1ancy cru1 last for several weeks,
distal limb fractures. Surgical correction may
during which the hedgehog may have
also be performed, but any fixation device
periods of activity with ataxia.

must be able to withstand the hedgehog's

Hypocalcemia may result from poststrong rolling-up mechanism. Lameness may pattw11 eclrunpsia, malnutrition, or for
be caused by ingrown toenails, rutluitis,
unknown reasons, and usually responds
nutritional deficiencies, pododem1atitis,
to calciwn supplementation.

constriction of a foot or digit by fibrous

Inte1vertebral disc disease has been
material, neurologic disease, or neoplasia
repo1ted. Both cervical and lwnbar lesions
have been identified; multiple discs were

Neoplasia: Neoplasia in hedgehogs is
affected in each of these hedgehogs.

very conm1on in both sexes. A vruiety of

Radiographic findings included spondylosis,
twnor types affecting every body system
disc-space natTowing, and disc mineralizahas been reported. According to one survey, tion. Necropsy findings included degenerathe body systems in which most tumors tion of the nucleus pulposus and armulus
were found were the integwnentary, hefibrosus, dorsal extrusion of disc material, molymphatic, alimentary, and endocrine
and mineralization of the nucleus pulposus.

1834

HEDGEHOGS

One case had evidence of fibrocartilaginous
although administration of topical medicaembolism. Temporary improvement with tion can be difficult. Blind hedgehogs
corticosteroids has been described in two
navigate their captive environments with
cases of intervertcbral disc disease.

minimal detriment to their quality of life.

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Vestibular signs may be caused by otitis

According to one report, ocular proptosis
media/internal or central neurologic disease.

is relatively common and carries A poor

Demyelinating paralysis (wobbly
prognosis for viability of the eye. Hedgehogs
hedgehog syndrome) occurs in as many as
have a shallow orbit that may predispose

100/o of pet hedgehogs. Onset can occur at
them to proptosis, especially if excessive
any age but is more common in animals <2 yr
fat accwnulation or orbital inflammation
old. An early sign is the inability to close the
is present. Concurrent neurologic disease
hood. This progresses to mild, intemtittent
may result in ocular trawna
ataxia. The signs gradually increase
in severity and include falling, tremors,

Oral and Dental Diseases: Oral neoplasia,
exophthalmos, scoliosis, seizures, muscle
particularly squamous cell carcinoma, is
atrophy, self-mutilation, and severe weight
conunon in hedgehogs. Dental disease,
loss. The paralysis usually ascends from
including calculus, gingivitis, and periodontihindlimbs to forelimbs and usually leads to tis, is also common. Periodontal disease is
complete paralysis within 9-15 mo after the
often associated with a bacterial component.

onset of signs. Death occurs within 18-25

The addition of abrasive items to the diet
mo. Appetite is usually norn1al until the

( eg, hard kibble, charcoal, or bone) and
ten11inal stages, when most hedgehogs
antibiotics are reconm1ended for prevention
become dysphagic. The diagnosis is
and treatment of periodontal disease,
confirmed at necropsy. Histopathologic
respectively. Dental prophylaxis, periprocelesions include vacuolization of white matter dural antibiotics, and tooth extraction may (cerebnrm, cerebellwn, brainstem, and
be necessary to treat severe dental disease.

spinal cord), axonal swelling, degeneration

If advanced periodontal disease requires
of spinal cord ventral tracts, and axonal and
extraction of all the teeth, hedgehogs can be
myelin degeneration in brain white matter.

maintained on soft food. Tooth fractures and

Peripheral nerves may also be involved.

dental abscesses are also seen. Actinomyces

Inflammation of the CNS is not associated
infection has been reported; anaerobic
with wobbly hedgehog syndrome. The
culture and treatment should be considered
etiology is unlrnown, but a hereditary basis
for dental abscesses in hedgehogs.

is suspected. Ntrmerous treatments have

Excessive tooth wear occurs in older
been attempted without success. Euthanasia hedgehogs, and hedgehogs with this is warranted when the quality of life is
condition should be fed a soft diet.

compromised. A single case of pnewnonia

Hedgehog teeth do not grow continuously
virus of mice in an African hedgehog with
and should not be trimmed. Hedgehogs are
suspected wobbly hedgehog syndrome,
susceptible to wedging of hard items (eg,
resulting in nonsuppurative encephalitis
peanuts) against the palate. Stomatitis may
with vacuolization of the white matter, has
develop in males that bite their mates;
been reported.

treatment is with soft food and antibiotics.

Nutritional Disorders: Obesity is

Otic Diseases: Pi.1U1al dermatitis is
common. Healthy hedgehogs should be able
common; skin crusts, accwnulated
to roll up completely, without any fat deposits secretions, and a ragged pinnai margin may protruding. Treatment includes reducing
be seen. Dermatophytes and acariasis are
high-fat foods, rationing the main diet, and
in1portant causes; other possibilities include
increasing exercise. Weight reduction should
nutritional deficiencies, dry skin, seborrhea
be gradual to prevent hepatic lipidosis, and
with hyperkeratosis, and extension of ear
owners should monitor their pet's weight.

canal disease. Ear mites (Notoedres cati)

Nutritional excess or deficiency may occur
are occasionally seen; signs, diagnosis,
with unbalanced diets; for example, calciW11
and treatment are as for cats (seep 921).

deficiency may result from a diet consisting

Bacterial or yeast otitis externa is also seen;
mainly of invertebrates. Moist diets may
these infections are often secondary to acariapredispose hedgehogs to periodontal sis or another cause of chronic inflanunation.

disease. Other nutritional diseases are

Signs include ptmtlent discharge, odor, and

W1common.

sensitivity of the face and ear. Otic cytology,
skin scrapings, cleansing, and topical

Ocular Diseases: Hedgehogs are prone to
antimicrobial/anti-inflanunatory therapy are
corneal ulcers and other ocular il\iuries. Diagused as for other species. Otitis media/interna nosis and treatment are as for other species,
can also be seen.

HEDGEHOGS

1835

Reproductive Diseases: Posthitis may
factors may contribute to the high prevabe caused by substrate entrapment in the lence. Nephritis, tubular necrosis, nephroprepuce. Hemorrhagic vulvar discharge calcinosis, glomerulosclerosis, renal
is often caused by uterine neoplasia or
infarcts, polycystic kidneys, neoplasia,
endometrial polyps. Pyometra and metritis
and various glomerulonephropathies have

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have been repo1ted. Dystocia also is seen
been identified. Signs associated with renal
and treated as in other small mammals.

disease tend to be nonspecific, although

Premature births occasionally occur; the
polyuria and/or polydipsia may be noted.

prognosis for young without a suckling

Diagnosis should be based on urinalysis and
reflex is poor. Agalactia may be suspected
serum chemistry panels. Treatment consists
if neonates lose condition within 72 hr
of correcting the underlying cause, fluid
after birth. Diagnosis may be confurned by
therapy, and supportive care.

attempting to express the mammary glands;
however, this usually requires anesthesia
and may cause the dam to abandon or

Zoonoses: Several strains of Salmonella
cannibalize her yow1g. Causes of agalactia
are found in pet hedgehogs, including S
include malnutrition, stress, lack of

Tilene, S Typhimurium, and S Enteritidis.

oxytocin, inadequate manunary develop

Many cases of transmission to people have
ment in young females, and mastitis.

been docwnented, particularly in young

Supportive care for weak neonates includes
children. It should be assun1ed that all
wanning to nonnal body temperature over
pet hedgehogs can carry and transmit

1-3 hr, fluid support, and caloric support

Salmonella. Because infected animals
once nonnothen11ia has been achieved.

may shed intermittently, a negative culture
cannot exclude the carrier state. Treatment
aimed at eliminating the carrier state is

Respiratory Diseases: Predisposing
unlikely to be successful and may lead to
factors for upper and lower respiratory tract
antibiotic resistance.

infection are suboptimal environmental

Human de1matophytosis from pet
temperature; aromatic, dusty, or W1Sanitary
hedgehogs is also well docwnented. African
bedding; concurrent disease causing
pygmy hedgehogs can be subclinical caniers
inullunocompromise; and aspiration of
of T'richophyton menla.grophytes var
material from an oral infection. Signs include erinacei, Microsporum spp, andArt.hrn
nasal discharge, increased respiratory noise,
derma benhamiae. In addition, some people
dyspnea, lethargy, inappetence, and sudden
are extremely sensitive to contact with
death. Radiographs, hematologic testing,

African hedgehog spines and develop
and culture of tracheal or lung lobe aspirates
transient, markedly pruritic urticaria after
are useful in diagnosis. Treatment includes
handling a hedgehog.

antibiotics, nebulization, supportive care,

Wild African hedgehogs are susceptible
and correction of underlying problems.

to foot-and-mouth disease. To prevent

Differential diagnoses for dyspnea are
introduction of this disease to the USA,
pulmonary neoplasia and cardiac disease.

importation of African hedgehogs was

A case of fatal corynebacte1ial bronchobanned by the USDA in 1991.

pnewnonia has been reported in a pet African

Rabies has not been reported in wild or
hedgehog. Pasteurella spp and Bordetella captive African hedgehogs, but the salivation
bronchise'[Jlica can cause respiratory
that occurs during anting is occasionally
infections in European hedgehogs and are
mistaken as a sign of rabies. A single report
possibly important in Atelerix as well.

of rabies in a wild European hedgehog

Lungwonns can also cause pnewnonia, but
exists.

this is unlikely in indoor pets. The existence

Human herpes simplex virus 1 was
of cytomegalovirus in African hedgehogs has
recovered from the liver of a pet African
been questioned; in any case, it is highly
hedgehog that died acutely after glucocortiunlikely in domestically raised pets.

coid treatment for intervertebral disc disease.

Monkeypox virus DNA was recovered from
an African hedgehog housed with many other

Urinary Diseases: Cystitis and urolithiexotic species at a pet distributor facility in asis cause changes in urine color, stranguria, Illinois. Candida infection of the footpads pollakiuria, inappetence, and lethargy.

and intestine of the African pygmy hedgehog

Urinalysis with culture and radiographs
has been reported. Acute intestinal cryptoshould be obtained. Renal disease is also sporidiosis has been reported. A single case
common (500/o prevalence in a necropsy
ofChagas' disease (T'rypanosoma crnzi)

survey) and in many cases may be secondwas reported in a captive African hedgehog ary to systemic disease. Genetic or dietary
housed outdoors in Texas.

1836

HEDGEHOGS

African pygmy hedgehogs are considered

(Q fever), and Leptospira spp. Possible
susceptible to a variety of infectious agents,
viral zoonoses include Crimean-Congo
based on susceptibility observed in other
hemorrhagic fever, arboviral tickbome
hedgehog species. Possible bacterial
encephalitides, and pararnyxovi.ruses of the
zoonoses include Yersinia pseudotubercu

Morbillivirus group. Chlamydia psittaci

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losis, Y pestis, Mycobacterium marinum,
and Toxoplasma gondii have been isolated

M avium intracellulare, Coxiella burnelii
from wild European hedgehogs.

LABORATORY ANIMALS

REGULATORY REQUIREMENTS
vertebrate animals, not just those that are
warm-blooded. Regulatory compliance is

Most American laboratories must adhere to
based on a system of self-regulation whereby
two main sets of animal welfare regulations:

institutions must provide the following to
the Animal Welfare Act (AWA; created in
federal officials: a written Animal Welfare

1966) and the Public Health Service Policy

Assurance that describes their compliance
on Humane Care and Use of Laboratory
with the PHS Policy, updates via an annual

Animals (PHS Policy; originally enacted in
report, timely repmting of all incidents of

1985).

noncompliance, and site visits for-cause or

The Animal and Plant Health Inspection
other purposes. Failure to adhere to PHS

Service (APHIS) of the USDA oversees

Policy can result in revocation of federal
enforcement of the AWA, which covers the
funding for some or all research projects
care of research animals and includes
at the instit1.1tion.

guidelines for the oversight and conduct

The 8th edition of the Guide for the Care
of studies intended to minimize or prevent
and Use of Laboratory Animals, released in
pain or distress of laboratory animals. The

2011, at 220 pages represented a 76% increase

AWA also regulates zoos, exhibitors, animal
in information, guidance, and prescribed
dealers, and those who transport animals in
action from the content of the 7th edition
commerce. All warm-blooded species are

(1996). It is organized into five chapters that
regulated by the AWA, whether alive or
cover the subject areas of 1) key defining
dead, except for domestic mice and rats
concepts, including applicability, a brief
bred for scientific purposes, birds, and farm
review of the ethical principles in the humane
animals used in agricwtural research.

care and use of anin1als in research, and

Provisions for veterinary care have existed
clarifying definitions; 2) articulation of the
under the AWA since 1970; requirements for
basics of an animal care and use progran1,
exercise for dogs and ensuring the
most prominently oversight structure, salient
psychological well-being of p.onhurnan
aspects of safety, and requirements for
primates were added in 1985. The AWA is
training; 3) the environment, housing,
enforced through a self-reporting mechaand management of research animals; nism along with routine, unannounced

4) veterinary care; and 5) animal research
inspections by APHIS. Failure to meet the
facility design and physical plant operation.

requirements

While tl1ere were abundant changes in the
of the AWA can result in fines, citations,

Guide from the 7tl1 to 8th edition, most
criminal proceedings, or revoked registramomentous were the unprecedented respontion with disqualification to use AWA-regusibility delegated to the attending veterinarlated species in research.

ian (AV) for the welfare of any animal in

The PHS Policy is based on a set of
research at all times during experimentation
research animal care standards, the Guide
and in all phases of the animal's life and in
for the Care and Use of Laboratory
establishing the unambiguous and absolute

Animals, first published in 1963. The PHS
authority of the AV to prescribe treatment

Policy requires institutions to use this guide
and other interventions, including removal
as a basis for developing and in1plementing
of subjects from experimentation. Other
institutional progran1s for research involving significant additions addressed the animals. The PHS Policy has been modified
accordance of cage space allocated to
only once, in 2002, while the Guide, now in
breeding rodents, the genetic management
its 8th edition, was last revised in 2011. The
of rodent breeding colonies to ensure authenpolicy applies to all research institutions ticity, the care of aquatic species, and an
awarded federal grants and covers all
enhanced emphasis on the training of person-

LABORATORY ANIMALS

1837
nel when applicable in proper animal care
these general responsibilities, the AV is
and methods of use, particularly in aseptic
responsible for reviewing the facility's PVC
surgery and hwnane euthanasia technique.

at least once a year to ensure that the
following meet contemporary standards of

Program Accreditation: The Associa-
vete1inary care for each species: vaccina

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tion for Assessment and Accreditation of
tions, handling of biologics and drugs,

Laboratory Animal Care International
product safety assurance, parasite control,

(MALAC), a p1ivate, nonprofit organization
emergency care, euthanasia methodology,
that promotes the hwnane treatment of
nutiition, pest control and product safety,
anin1als in science through voluntary
quarantine procedures, exercise ( dogs
accreditation and assessment programs,
only), environmental and social enrichment
was incorporated in 1965. More than 890

(nonhuman prin1ates only), water quality
companies, lllliversities, hospitals, govern

(when marine mammals are involved), and,
ment agencies, and other research institufor wild or exotic animals, capture and tions in 37 corn1tiies have voluntatily earned
restraint methods.

MALAC accreditation as of 2013. Institutions
that seek MALAC accreditation are subject

Institutional Animal Care and Use
to comprehensive peer review of their anin1al

Committee: Since 1985, the AWA and
care and use progran1 every 3 years; this

PHS Policy have required that Instituaccreditation is given credence by the tional Animal Care and Use Committees

National Institutes of Health as a means of

(IA CUC) oversee not only the care, but
demonstrating compliance with PHS Policy.

also the use, of animals in research.

The responsibilities of the IACUC are

Veterinary Care: Under provisions of
delineated in these laws and the associthe A WA, all persons who use animals in ated federal policy and regulations.

research or for exhibition, sell them at

According to the AWA, the IACUC must
the wholesale level, or transport them in
consist of at least one veterinarian with
commerce must have established programs
training in laboratory animal science and
of veterinary care and animal husbandry.

expertise in the species under considera

APHIS requires the owner of each licensed
tion, at least one practicing research
and registered facility to define a progran1
scientist, and at least one person not
of veterinary care (PVC), including the
affiliated with the institution. The PI-IS
employment of an AV. In cases in which the

Policy requires a minimum of five

AV is not a full-time employee, the facil-
members, including at least one of each
ity owner must prepare a written PVC
of the following: veterinarian, scientist,
and schedule an appropriate frequency of
nonscientist, and nonaffiliated member.

visits by the AV. These visits must be on

Each IACUC has three main areas of
at least an annual basis. Whatever the emresponsibility: review of research protocols; ployment arrangement, the facility owner
semiannual evaluations of the institution's
must give the AV sufficient authority to
animal care and use, which includes
inspections of anin1aJ housing areas and
ensure adequate veterinary care. The PVC
laboratories where animal procedures are
must incorporate appropriate facilities,
pe1formed; and judiciary activities such as
personnel, equipment, and services to
investigating anin1al welfare concerns and
meet this standard; ensure the availabil-
acljudicating disagreements. Review of
ity of emergency, weekend, and holiday
research protocols by the IA CUC involves
care for animals; include the requirement
considering the merits of the anin1al study in
for the daily observation of all animals by
the context of a broad range of complex,
employees to assess the animals' health and
scientific, anin1al welfare, and veterinary
well-being; and define channels for the
topics. The IACUC also has the responsibility
direct and frequent comm llllication
to monitor the compliance of ongoing studies
between facility personnel and the AV.

and the authority to suspend research not

Responsibilities of the AV include using
performed in accordance with the conditions
suitable methods to prevent, control,
or with unforeseen negative consequences.

diagnose, and treat diseases and injuries;

Since 1985, the IA CUC has been the primary
providing adequate guidance and training of
means of anin1al welfare oversight within
personnel who care for animals regarding
research institutions in the USA.

handling, in1mobilization, anesthesia,
analgesia, tranquilization, and euthanasia;

Emergency Preparedness: History
and ensuring that the pre-procedural and
shows that animal research facilities are
post-procedural care of animals is in
regularly and often tmpredictably subject
accordance with established vete1inary
to the effects of natural events, manmade
medical and nursing procedures. Beyond
actions, or failures of technology that

1838

LABORATORY ANIMALS
imperil animals, experiments, and facilities.

leading to what are known as "knockout"

While principles of disaster preparedness
mice, profoundly increased the use of mice
and response have been integral to the
as research subjects. Since these advances,

Guide since its 7th edition, in 2013 the
countless mutant genotypes of mice have

USDA instituted requirements for emerbeen developed, ranging from subtle defects gency and disaster preparedness and
in i.nm1une function to full-fledged, inherited

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response plans and mandated training
diseases viltually homologous with those of
programs for appropriate personnel.

higher manunals.

As such, the Guide and USDA policy in

Among other rodents, the domestic
conjunction make it mandatory that each

Norway rat (Raltus norvegicus) is second
institution craft and train personnel in a
only to the mouse as a research subject. Rats
comprehensive emergency operations and

(seep 2032) share many of the attlibutes of disaster responsiveness plan.

mice that make them attractive for use in
research, but because they are larger than

ANIMALS USED IN RESEARCH
mice, they are suited for a greater variety
of manipulations. Nun1erous mutant and

Research institutions registered under the
inbred strains and outbred stocks of rats are

AWA are required to submit an annual report
used in a broad aiTay of studies, including
to APIDS that details, among other specificatopics such as aging, cancer, reproductive tions, a listing of the common names and the
physiology, drug effects, behavior, addiction,
numbers of reportable species used. In 2010,
alcoholism/cirrhosis, artluitis, brain and
there were 1,104 research institutions in the
nerve in.jury, hypertension, embryology,

USA registered under the requirements of
teratology, endocrine diseases, neurophysithe AWA. These institutions repo1ted the ology, infectious disease, stroke, organ
total use of 1, 134,693 regulated animals. The
transplantation, and surgically induced
most abundant species used were guinea
disease. The genetic engineering of mutant
pigs (213,629), rabbits (210,172), and the
rat types, however, has lagged behind mice
combination of several species of hamsters
and is only beginning to show effect.

(145,895) of which >90% were estimated to

Excluding mice and rats, guinea pigs and
be of the Syiian variety. Other animals used
rabbits are the most corrunon mairunals used
included nonhuman primates (71,317), dogs
in research, although tl1eir numbers have

(64,930), pigs (53,260), domestic cats
declined from peaks in the 1980s. Although

(21,578), sheep (13,271), and a combination
the guinea pig ( Gavia porcellus) was ainong of marine mammals, otl1er farm animals, and the first animals to be used in medical other species not identified (341,214). There
research, its popularity has din1inished
is no federal reporting requirement for mice,
relative to that of mice and rats because of
rats, birds, an1phibians, or fish, making
its long gestation pe1iod (59-72 days), small
precise numbers difficult to determine.

litter size (2-5), poor vascular access, and

Research subjects of these species, for the
difficulties in anesthesia. Guinea pigs are still
most part, are obtained via a combination
used in notable ways in u1m1unology, in
of in-house breeding colonies and from
vaccine and infectious disease research, and
commercial vendors, with production and
as hearing models. Rabbits are used most
sales data from the latter being proprietary
often in product safety testing; for polyclonal
and not disclosed publicly. Wild-caught birds antibody production; and in studies of vision, and aquatic species sometimes may be
orthopedics, and cardiology.

captured for experimental purposes. Since

In addition to the Syrian hamster

2000, the estimated total number of mice

(Mesocricetus auratus ), a few other species and rats used for research purposes
of hamsters are used in research, including
annually in the USA has ranged fairly
the Armenian, Siberian (Djungarian),
consistently from 20 to 30 million. There

Chinese, Europeai1, ai1d Turkish species.

are millions of zebra fish and thousands

Hamsters are readily available, reproduce
of amphibians, likewise, used annually.

easily, ai1d are relatively free of spontaneous

The domestic mouse, Mus musculus and
diseases but susceptible to many induced
related subspecies ( see MICE AND RATS AS
viral diseases. They are used for studies of

LABORATORY ANIMALS, p 2032), is popular as a
obesity, induced cai·cinogenesis, prostatic
mammalian research model because of
disease, toxicity, infectious diseases
its small size, adaptability, docility, low

(including slow viruses), dental caries,
husbandry costs, fecundity, well-defined
chronic bronchi.tis, and teratogenesis.

healtl1 and genetic backgrounds, and relative

Other rodent species used in research
ease of genetic manipulation. The developinclude gerbils, deer mice, chinchillas, ment of genetic engineering techniques of
cotton rats, rice rats, multimammate rats,
inserting foreign genes (transgenes) into tl1e

Egyptian spiny mice, degus, voles, and
mouse genome and the ability to delete genes, woodchucks, among others.

LABORATORY ANIMALS

1839

While rodent models are unarguably the
conscientiously applied programs of anin1al
most common for scientific use, larger
care and use, tl1e best possible conditions for
animal models provide unique opportunities conducting research are provided. TI1e Guide for biomedical research. Dogs are used
for the Care and Use of Laboratory Animals
in studies of cardiology, endocrinology,
is still the primary reference for information
orthopedics, prosthetic devices, surgical
on basic principles and standards for

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techniques, pharrnacokinetics, and product
laboratory animal management.

safety. Since use of dogs began declining in

Laboratory rodents that are disease- and

1984, livestock have been used more
pathogen-free and tl1at do not possess
frequently. This has been a consequence
antibodies indicative of past infection are
of regulatory and public pressure related
readily available from commercial vendors.

to the use of dogs, but it is also due to

Procuring such animals from high-quality
attributes of comparative anatomy and
sources, transporting them in filtered
physiology that make livestock more
shipping containers, and maintaining
conducive to particular investigations. For
them in facilities with both physical and
example, swine are used for cardiovascular
procedural baniers to the introduction of
research (particularly atherosclerosis), in
infectious agents are effective measures to
studies of digestive physiology, as surgical
prevent disease within a colony that may
models, and for xenotransplantation. Sheep
confound or ruin expe1iments.

are used for studies of neonatal develop

Although there are colonies of some
ment, hun1an vaccine improvement, astl1n1a
species of primates that are free of most
pathogenesis and treatment, drug delivery,
agents that cause infectious disease in these
circadian rhythms, and surgical techniques.

species, many primates used are of feral or

Nonhuman primates remain critical in studwild origin. For this reason, appropriate ies of vision, the neurosciences, infectious
quarantine, isolation, and conditioning
diseases, vaccines, and product safety testing.

programs should be implemented in

In recent years, they have become increasaddition to tl1e progran1 followed in tl1e ingly valuable as models of immunodefiimporters' facilities.

ciency virus infection and the neurodegenerative diseases associated with aging.

Housing: Cages, pens, or runs should

Although the absolute number of cats
provide adequate space to allow for nonnal
used in research has been in steady decline
physiologic needs, pennit postural acijustsince 1980, cats are still in1portant models ments, and meet requirements for speciesin the neurosciences and in the study of speci.fic behavior. When possible, compatible
infectious diseases.

groups of social animals should be housed

The most important aquatic species used
together. Primary enclosures should be
in research are the zebra fish and the
constructed of durable materials, easjly

African clawed frog.

cleaned and sanitized, and designed for

Other species used in scientific research
comfort and safety. Static microisolation
include goats, calves, horses, ferrets,

(filter top) cages and more advanced
annadillos, opossums, domestic and wild
individually ventilated caging systems have
birds, reptiles, amphibians, other species
been used widely for rodent housing to
of fish, and invertebrates.

impede cage-to-cage transmission of
infectious agents. However, infection can be

MANAGEMENT
transmitted horizontally or vertically from
parents to progeny in breeding colonies;

Consistently delivered quality programs of
naive mice introduced for cross-breeding and
husbandry and veterinary care provide the
back-crossing can perpetuate infection; and
foundation that enables valid scientific
experimental mice potentially can be
research. For proper management of
exposed to pathogens via a contanlinated
research aninlals, the animal care and
environment, shared watering valves,
research staff must be responsible, sensitive
research devices, or when taken to laboratoto the anin1als' health and well-being, well ries. Individual ventilation of cages serves to
trained in the humane care and use of
delay deterioration of the environment within
laboratmy animals, highly motivated,
the cage and maintain a more consistent and
experienced, and diligent in perfonning
wholesome microenvironment; it also saves
their duties and responsibilities. Standard
space in the facility and can be engineered to
operating procedures must be established,
minimize odors, allergens, dust, and heat
and training and supervision provided to
exhausted into the macroenvironment. A
assure a consistently applied and uni.fomtly
potential drawback of ventilated cages is
higil level of aninlal care. Within research
that hairless genotypes and neonates may
facilities, environmental conditions must be
be prone to chilling. TI1is risk can be reduced
carefully controlled so that, along with
by providing nesting material.

1840

LABORATORY ANIMALS

Federal law in the USA requires that
mental and social conditions for each
laborato1y dogs have an oppmtunity to
species or group of species at the cage level.

exercise regularly and have sensmy con-tact with other dogs w1Jess restricted by Bedding: Bedcting materials should be
experimental or behavioral considerations.

nonirritating, absorbent, free of chemical

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Housing for nonhwnan primates must
contamination and pathogen's, and
provide social and envirorm1ental enrichunpalatable. Adequate quantities should ment to promote psychological well-being
be used to dilute and limit contact with
compatible with the experimental and
excreta, promote air quality and other
practical constraints of the housing
environn1ental factors by suppressing
situation. Successful enrichment strategies
microbial growth, and keep ani.n1als dry
for nonhtm1an p1imates have included pair
and clean between changes of bedding or
or group housing; variation in the ctietary
caging. The major types of contact bedding
content and method of presentation;
used are derived from ground corncobs,
diversification of the internal cage environhardwood chips, recycled paper, heat-ment with ancillary apparatus ( eg, perches, treated softwood shavings, and virgin
swings, or ladders); provision of devices
cellulose. Untreated softwoods are not
to enhar1ce visual, auditory, or tactile
reconm1ended because they contain volatile
stimulation; and participation in challenging,
oils that may alter hepatic enzyme systems
nonaversive behavioral laboratory stucties.

and affect certain kinds of research.

Efforts to extend and adapt envirom11ental

Depencting on research requirements,
enrichment practices to other laboratory
bedding may be steri.lized by autoclaving
animal species warrant consideration and
or irradiation before use or used as is.

have been in1plemented in mar1y institutions.

Temperature, relative humidity, ventila

Feeding: Feed should be of adequate
tion rates, lighting conctitions ( spectrwn,
quantity, palatable, free of contaminants,
intensity, and photope1iod), gaseous
nutritionally adequate, easily accessible,
pollutants ( eg, arnrnonia), and noise should
and provided using mea.J1S that meet
be carefully controlled at all times and
behavioral needs accorcting to specific
monitored as approp1iate. Unstable
species requirements. Feeds specifically
enviromnental conctitions can have a
manufactured for research ani.n1al use are
profound effect on the comfort, well-being,
preferred, because they are more likely to
ar1d metabolism of anin1als and therefore on
be urti.fonnly constituted, free of contamithe quality of experimental data derived. In nants, of known shelf life, and mill dated.

general, temperature should be maintained

Feed should be manufactured, transported,
at 68° -79°F (20° -26°C) for most rodents;
stored, and used in ways that minimize its

61 ° -72°F (16° -22°C) for rabbits; 59° -64 °F
deterioration, contamination, or irlfestation.

(15° -l8°C) for ferrets; 64 ° -84°F (18° -29°C)

Most small animals consume food in relation
for prin1ates, clogs, and cats; and 61 °-81 °F
to their energy requirements as influenced

( 16° -27°C) for most farm animals and
by the envirorunent and ctictated by their
poultry. Within these ranges, optimal
genotype ar1d ar·e fed ad lib; rabbits,
systems should maintain temperatures
laboratory carnivores, swine, aquatic
within ±1 °F of the set point. Relative
arnphibia.J1S, and prin1ates may be restricted
hurnictity should be maintained at30%-70%
to measured quantities of feed each day. As a
for most species and preferably within lO"A,
general rule, laboratory a.rµmals minimally
of the set point. Ventilation rates should be
conswne 4%----6% of their body weight in food

10---15 fresh air changes/hr. Air should not be
daily. In addition to conm1ercially prepared
recirculated unless it has been treated to
and usually pelleted natural ingredient ctiets
remove particulate and gaseous contamiof varying specification ( eg, quality control nants. Lighting should be ctistributed evenly
and assurance of ingrectients), semi.synthetic
and sufficiently intense to promote ani.n1al
or completely synthetic ctiets and all-liquid
well-being and to allow personnel to observe preparations can be fom1ulated for use in the animals and to perform all husbandry
certain kinds of research. Autoclavable or
and sanitation duties safely and effectively.

irractiated ctiets are available for rodents and

Diw11al or day-night cycles, as detenni.ned
can be used when sterilization of feed is
by species' requirements, should be
desired.

controlled by automatic tin1ers to maintain
circactian and neuroendocrine regulation.

Water: Potable, uncontarninated water

The microenviromnent within certain types
should be provided in adequate quantities to
of caging may be very different from that
meet specific species requiTements. Quality
of the macroenvironn1ent of the room.

assurance progran15 that measure pH,

Carefully conducted research is needed to
hardness, chemical content, ar1d microbial
more precisely define the optimal environ--
load are recommended. Highly pwilled,

LABORATORY ANIMALS

1841
deionized, acidified, chlorinated, or sterile
suspended cages over excreta pans and for
water may be required under certain
mice in ventilated caging systems, cage
experimental or husbandry conditions. Water changes every other week should be is usually provided ad lib in manually filled or
adequate. For larger anin1als, excreta and

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automated watering devices. Particularly in
soiled bedding should be removed daily, and
the housing of rodents, an automated water
ptimary enclosures cleaned and sanitized
supply enhances the advantages of ventilated
daily, or at minimmn every other week. Water
caging systems and reduces operational
bottles and oilier watering or feeding devices
costs'expenses, increases safety for anin1al
should be cleaned and sanitized at least
care technicians, saves labor, reduces
weekly. Automated watering devices on
disruptions of the mice by caretakers, and
cages, racks, or in rooms should be designed
provides consistently high water quality. The
and programmed to flush continually or regudrawback of the use of automated drinking larly or tlley should be manually drained,
water supply for rodents is the risk of
rinsed, and sanitized at regular, frequent
hypothemtia, drowning, or dehydration of
intervals. Heating cages and other equipment
cage inhabitants as a consequence of failure
to 180°F (82.2°C) or using appropriate chemiof the in-cage water delivery valve.

cal disinfection ( eg, hypochlorite solutions)

Water quality is the most important
kills nonspore-fomting pathogenic bacteria
environmental variable for aquatic species
and viruses. All caging and other equipment
and a key detemtinant of health. Inadequate
should be rinsed tl1oroughly after treatment
water quality or fluctuations of water tempwith detergents or disinfectants. The erature are physiologic stressors that impact
effectiveness of tile programs of sanitation
the intake, digestion, and use of food; alter
should be evaluated regularly using approprithe immune system; and predispose to oppate nticrobiologic, organic matetial detection ortunistic infection. Water for aquatic vertesystems or other means.

brates should be free of nitrite, anunonia, and
chlorine, with total coliform counts not

Vermin Control: Professionally directed
exceeding 200/mL. The pH should be 6.5---8.5.

programs to prevent, identify, and eradicate

Although aquatic amphibians may be mainor control insects or escaped, feral, or wild tained in small containers of standing water,
rodents must be instituted, regularly
water recirculation with biologic filtration
scheduled, and consistently docmnented.

and periodic partial replenislunent with

The use of pesticides should be as a last
fresh water, just as with fish, are helpful in
resort and generally be confined to areas
suppressing bacterial counts and preventing
not used for animals or for storage of feed
the build-up of toxic chemicals. The ideal
or bedding. If these agents are used in
water temperature range for maintaining the
proximity to animals or their food and
aquatic amphibians used most popularly in
bedding, researchers should be informed of
research, the tetraploid South African clawed the use. Relatively inert substances, such frog (Xenopus wevis) and the axolotl
as silica aerogel or boric acid powder, are

(Ambyst.oma mexican'Um ), is 65° -72°F
reconunended and are useful for control

(18°-22°C). For X tropicalis, a smaller, more of crawling insects, eg, cockroaches.

rapidly maturing, diploid species of clawed
frog from forested west Africa, water
temperature should be 70° ---S5°F (21 ° -29°C).

COLONY MONITORING

(See also AMPHIBIANS, p 1734.) Zebrafish and other tropical species used in research are

While most corrunercially reared rodents,
best maintained at a consistent water
some rabbits, and relatively fewer dogs,
temperature witltin the range 80° -90°F
cats, and p1imates can be obtained as SPF

(27°-32°C).

anin1als, resident animal colonies must be
monitored for naturally occurring disease

Sanitation: A mliformly high level of
as a measure of the effectiveness of the
animal enclosure and facility sanitation is
prevention and control program. Investigamandatory to ensure that animals are clean tors should be infonned regularly as to the
and dry, air quality is adequate ( witllout using health status of their research animals. In masking agents), and primary enclosure
addition to monit01ing for infectious
surfaces and accessories are clean. Housing
disease, a quality assurance progran1 should
rooms and ancillary support space should be
monitor for genetic integtity, especially for
cleaned and sanitized as often as necessary
inbred mouse strains that are bred and
to keep them free of dht, debris, and
maintained in the research facility, as well as
potentially harmful contantination. For
for environmental factors ( quality of feed,
rodents in solid-bottom cages, usually 1-3
water, and bedding; efficacy of sanitation
changes per week will suffice; for rodents,
programs; air handling and quality; lighting;
rabbits, and nonhmnan primates in
noise; etc) tllat can affect colony health.

1842

LABORATORY ANIMALS

Colony health monitoring consists of

For colony-bred rats and mice, programs
a defined program of regular physical and
for disease monitoiing can consist of any or
laboratory evaluations of animals within a
all of the following: vendor swveillance,
unit, as well as a morbidity and mortality
quarantine and isolation evaluation, ongoing
reporting system that enables timely
clinical and postmortem evaluation during

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identification of potential problems.

the course of studies, sentinel aninlal

Thorough investigations of illnesses, deaths, programs, and evaluation at tennination of and unusual experimental outcomes in a
the study. In addition, all transplantable
colony are essential components of such a
tumors, cells, or other biologic products
progran1. For selected physiologic data of
destined for animal passage should either be
some laboratory animals, see TABLE 11.

screened for murine and zoonotic pathogens

While certain general principles apply,
or colony management practices used to
a health monitoring program must be
appropriately isolate animals receiving these
specifically developed for each species
materials. Of particular concern to colony
maintained in a facility. For example,
health is the occasional and justifiable need
generally, all primates are quarantined and
to obtain aninlals from less well-defined
isolated on arrival. Physical examinations,
sources, such as an investigator's colony at
tuberculin testing, and baseline hematoanother institution or other nonapproved logic and other clinical pathologic tests
source. The presence of infectious agents
should be perfonned. In addition, serologic
either in transplantable tumors or noncomevaluation for Macacine herpesvirus type mercial aninlal sources can pose a substan1 (fom1erly Cercopithecine herpesvirus tial threat to resident colonies and personnel.

type 1, Herpervirus simiae, B vims), simian

Colony monitoring of rodents is typically
retroviruses, and other specific agents may
based on serology, bacteriologic, and
be pe1iom1ed, depending on the species of
parasitic evaluations supported by the
primate. Primates should be released from
evaluation of environmental, fecal, and fur
quarantine only when both the health status san1ples through the use of molecular and suitability for use are detennined.

biologic techniques such as PCR.

Furthennore, primates should have regular

Although the use of filter top caging
health surveillance screens, each consisting technology to in1pede cage-to-cage of defined elements. Depending on the
transmission of infectious agents in ronature and value of the colony and research dent colonies has resulted in a dramatic use, screenings may range from quarterly to reduction in enzootic disease transmission semiannual or annual in frequency. (See
and protection of naive aninlals from

Q.{,SO NONHUMAN PRIMATES, p 1876.)

epizootics, it has created challenges for
iM:i•ili SELECTED PHYSIOLOGIC DATA OF LABORATORY ANIMALS•

Gestation

Age and Body Weight

Species

Period (days)

Litter Size
at Sexual Maturity

Mice

19-21

6-10

6 wk (20-30 g)

Rats

21-23

6-14

2-3 mo (0.2-0.3 kg)

Guinea pigs

59-72

1-4

3-4 mo (0.4-0.5 kg)

Han1sters, golden

15-18

4-10

2 mo (85-110 g)

Gerbils

25

2-9

3 mo (60-100 g)

Rabbits

30-33

4-12

5-6 mo (3-4 kg)

Squirrel monkeys

150

3-5 yr(0.6-l.l kg)

Rhesus monkeys

164

1-2

3-4 yr (5-11 kg)

Chimpanzees

227-235

7-10 yr (40-50 kg)

Baboons

164-186

4-7 yr (11-30 kg)

a See also TABLE 3, FEATURES OF TIIE REPRODUCTIVE CYCLE, p 1326.

b Typical of an average adult; varies with body mass index, number of animals per cage, moisture in feed, temperature, etc.

" Results obtained under anesthesia.

LABORATORY ANIMALS

1843
sentinel programs. Because most diseases
themselves may add confounding influences
of laboratory rodents do not cause clinical
if their age or genetic background makes
signs and there can be high and unpredictthem relatively resistant to infection.

able turnover of research rodents, health

The primary contemporary challenges
surveillance programs are traditionally
to the health of research rodents-particubased on the premise that infectious agents larly mice-are the noroviruses, parvo

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can be transmitted to sentinels, which can
viruses, Helicobacler spp, pin worms, and
then be tested for a variety of pathogens.

fur mites that infect or infest colonies,

This provides assurance that the research
perturbing biologic processes and
colonies are free of specific pathogens
introducing variation into research data.

and alerts persormel to the presence of

For the most part, these agents, along
infection. Before the widespread use of
with mouse hepatitis virus , are thought
filter top caging, dedicated sentinels in open
to have gained entry to research colonies
cages were readily exposed to airborne
largely via the trading of live mice of
fomite particles and true aerosols from
unique genotypes between institutions.

infected animals in the colony.

The situation has been complicated by

The san1e filter tops that protect colony
the inability of quarantine progran1s to
anin1als from contagion, however, also hinder reliably detect these agents. However, the exposure of sentinels to these same
there is a body of substantial, compelling,
agents. For many reasons, dedicated
anecdotal evidence that nonsterilized
sentinels are preferred over the alternative of
diets may be a source of introduction for
monitoring colony rodents. State-of-the-art
some pathogens ( eg, mouse pa.rvovirus ).

sentinel programs have thus come to rely on

Murine norovirus has been shown to be
the regular exposure of sentinels to soiled
the most widespread virus in domestic
bedding as the means of exposure to colony
mouse colonies. The virus likely existed in
animals. This indirect exposure has been
research mice for decades, but it was not
found to be suboptimal for the detection of
described until 2003. Mouse parvovirus
many bacterial pathogens, agents transmitted was definitively discovered 10 years by true aerosol, and fur mites. Agents that are
earlier. These viruses may persist for
shed intermittently, those with a self-linlited,
lengthy periods in mice and can consingle window of shedding, those tl1at require taminate and remain infectious in the
a high dose to be infective, and those that
environment for months, ma.king them
may deteriorate rapidly are difficult to detect
ideally suited to persevere in colonies
by exposure to soiled bedding. The sentinels
kept in filter top cage systems.

SELECTED PHYSIOLOGIC DATA OF LABORATORY ANIMALS• (continued) Usual Life Span Average Body

Heart Rate

Water Consumption

(yr)

Temperature (°C) (bpm)

(per day)h

1-3

37

310-840

4-7mL

2-3

37.5

300-500

30mL

3-4

38

230-380

150mL

2-3

37

280-410

30mL

3-4

39

250-360

4rnL

5-7

39

200-300

300-700mL

16-20

39

300-380C

70-110 mL

15-30

38

120-180C

0.2-1 L

20-30 ( ma! es)

37

60-120C

2.2-2.71

30-40 (females)

30-40

39

95-145c

1-1.5 L

1844

LLAMAS AND ALPACAS

LLAMAS AND ALPACAS

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The four members of the South American
length and crimp have emerged. A
camelids (SACs) are the llama, alpaca,

"suri-style" llama has recently been
guanaco, and vicuiia. Although their
introduced into the North American market.

progenitors originated in North America,

In contrast, there are two morphologithese species evolved in the South American cally distinct types of alpacas: the Huacaya Andes, with the wild guanaco and vicuiia
and Suri. The more conunon Huacayas have
se1ving as the foundation stock for the
a lofted fiber coat with variable coverage
domesticated llama and alpaca, respecdown the legs and around tl1e face. Suri tively.

have a flat-lying corded fiber structure

Mature, average alpacas weigh 60----80 kg

("dreadlocks") with less coverage on the
and stand 76---97 cm at the withers. Alpacas
head. Alpacas have shorter "spear-shaped"

are primarily used as fiber-producing
ears, a lower tail set, slightly more humping
animals. The fiber grows rapidly and ideally
to the back, and a sloping rear end that
requires shearing every 12--24 mo. Mature
results in a slight sickle hock appearance.

llamas are significantly larger animals,

SA Cs ai·e most closely related to the Old
weighing an average of 120-200 kg and

World camelids (Bactriarl and Dromedary),
standing 102-127 cm at the withers. Llamas
having the same number of chromosomes,
were primaiily developed as pack animals
similar anatomy and physiology, and
and can carry loads of 25---40 kg. Both domesgeneral patterns of disease susceptibility.

tic SA Cs are meat staples for indigenous

Altl1ough conventional runlinants are
peoples. Males and females of both species
frequently used as reference points for drug
have approximately similar mature weights.

dosage extrapolation, disease susceptibility,

Guanacos are similar in size to llamas but
and management decisions, it is important
weigh somewhat less. Unlike llamas and
to remember that SA Cs and common
alpacas, in which coloration patterns vary
domestic ruminants are not the same.

markedly, guanacos and vicuiia have a "wild
pattern" characterized by a light brown or
tan coat over tl1e neck, back, ai1d outside of

MANAGEMENT
the legs, with white on the underbelly and
medial surface of the legs. Vicuiias are

Llamas and alpacas are adaptable to a wide
slightly taller than alpacas, with a longer
climatic range and have been successfuily
neck, much shorter fiber, and a characterisraised in regions with winter temperatures tic "bib" of long fibers in tl1e chest region.

as low as -20°C ( -4 ° F) if reasonable wind

Vicuiias have extremely fine fiber and are
shelter is provided. Heat stress is a signifimanaged and protected in much of South

-
cant problem if aninlals have moderate to

America.

heavy fiber coats and are subjected to high

All SA Cs have 7 4 chromosomes ai1d can
temperature and hunlidity. Shearing, leaving
interbreed, producing fertile F l progeny.

remaining fiber at least 2 cm long to prevent

The most common, natmally occurring
sunburns, and providing access to shade and
cross is a llan1a-alpaca mating, producing a
sufficient water usually allow SACs to handle

"huarizo" that is intern1ediate in size, body moderately high temperature and humidity.

characteristics, and fiber quality. Recent

Air conditioning, misters, ai1d dainp sand pits
attempts to increase fiber quality and
are helpful to maintain heavy fiber coats in
quantity have involved alpaca-vicuiia
warm, humid climates. Llamas and alpacas
crosses resulting in paco-vicuiias. Intact
can adapt well to damp climates as long as
male llainas and alpacas are called studs
the temperature does not get too high, and

(machos in Spanish), whereas castrated
few problems of either footrot or "rain scald"

males are referred to as geldings. Females
are encountered.

are called females (hembras in Spanish).

Llamas and alpacas can be housed witl1

The neonates and young up to 6 mo of age
other species, including sheep, goats, and
are called crias, whereas juveniles are called
horses. Individual llainas (ideally geldings)

tuis in the local Quechua language.

have been successfuily used as guard

Most llamas have characteristic
animals with sheep flocks and goat herds.

"banana-shaped" ears, a level back, and a

Llainas and alpacas are herd animals and
high tail set. There are no distinct llama
do poorly if isolated from cohorts or other
breeds, but several types based on fiber
animals; ill animals should be housed with

LLAMAS AND ALPACAS

1845

14N!ifi SELECTED DRUGS USED IN LLAMAS AND ALPACAS

Drug

Dosage

Comment

SEDATION/ ANESTHESIA

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Xylazine

0.1-0.2 mg/kg, IV

For sedation

0.3-0.4 mg/kg, IV

For recumbency

Butorphanol

0.1-0.2 mg/kg, IM or IV

For sedation

KXB: ketamine

1 mll22.5 kg, IM (llan1as)

Mix 1,000 mg ketarnine with

( 4 mg/kg), xylazine

1 mlll8 kg, IM (alpacas)

100 mg xylazine and 10 mg

(0.4 mg/kg), and
butorphanol; if needed to
butorphanol
maintain anesthesia, Y., initial

(0.04 mg/kg)

dose can be given rv in the
medial saphenous vein

ANTIBIOTICS

Aqueous procaine

20-40,000 units/kg, SC
penicillin

Long-acting tetracycline 18-20 mg/kg, SC, every 2-3
days

Ceftiofur

2.2 mg/kg, IM or IV, bid

Trimethoprirn/

3/15 mg/kg, IV, bid
sulfarnethoxazole

Arnpicillin sodium

6 mg/kg, IM or rv, bid

Enrofloxacin

5 mg/kg, rv, bid

Gentan1icin

0. 75 mg/kg, rv, tid

4-5 mg/kg/day, rv

Tobrarnycin

4 mg/kg/day, IV

Arnikacin

12 mg/kg/day, rv

REPRODUCTIVE
hCG•

5,000IU

GnRH

1 mcg/kg

Cloprostenol

100-150 mcg, IM, repeated
in 24 hr

Dinoprost trometh5 mg, SC, repeated in 24 hr
amine

ANTHELMINTICS

I vermectin

0.2 mg/kg

Pyrantel pan1oate

18 mg/kg

Fenbendazole

5-lOmg/kg

Clorsulon

7-14 mg/kg

Albendazole
lOmg/kg

1846

LLAMAS AND ALPACAS

•tli!iti SELECTED DRUGS USED IN LLAMAS AND ALPACAS (continued) Drug

Dosage

Comment

COCCI DIAL

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Ponazmilb

20 mg/kg/day for 3 days

Ideally should be followed by
sulfadimethoxine, 55 mg/kg,

SC on day 1, then 27.5 mg/kg,

SC, for 2 additional days

GASTRIC

Omeprazole

0.4 mg/kg, bid

MANGE, LOCAL THERAPY

Mixtme of:

Shake before use and apply
mixtme to local lesions with a
paint brush every 5 days for 5
treatments

Mineral oil

2 oz

DMSO, 10%

2 oz

Ivem1ectin, injectable 4 mL

Gentan1icin
l g
a Human chorionic gonadotropin

� For treatment of Eim.eria. mae11san'iensis
herdrnates if appropriate. If sufficient space
food. An arm around the base of the neck
is available, large groups of males (or
and another arm holding the tail or flank
females) can be pastured togetl1er. In the
region on tl1e opposite side can restrain
presence of nonpregnant females, however,
many anin1als. Halter-trained SA Cs can be
intact males and recently castrated geldings
easily led into a smaller area for exan1inawill commonly spend much of tl1eir time tion and treatment. Specially designed llama
fighting, typically biting at the ears, neck,
chutes should be used for reproductive
and scrotum. Llamas and alpacas generally
examinations and other potentially
do not destroy fences and can usually be
uncomfortable procedmes. In contrast,
confined behind a 1.5-m or 1.2-m fence,
alpacas respond better to most procedmes
respectively. Barbed wire is not needed for
if assistants, and not restraint chutes, are
containment, and electric fences have been
used to hold the anin1als. Witl1 both llan1as
successfully used.

and alpacas, it is particularly" in1portant to

A somewhat unique behavioral charactermaintain control of the anin1al's head. The istic of SA Cs is the use of communal dung
neck is very muscular and can move witl1
piles. Anin1als urinate and defecate on the
amazing speed. Sedation is not needed
same pile, with favorite sites being in the
for most procedures. A small catch pen
depths of barns and other inconvenient
crowded with anin1als will afford adequate
locations. Normal feces are pelleted and
control to administer injections and
finn. Unless forage becomes very limited,
perfom1 body condition scoring.

animals will not graze in areas around or
downstream from dung piles. The uretl1ral

Feeding and Nutrition: Mature males,
dian1eter in both males and females is
and most females during midgestation, will
relatively small, and the process of urination maintain appropriate body condition on takes much longer than in other species of

10%-14% crude protein grass hay with total
comparable size.

digestible nutrients (TDN) of 50%-55%. Late
gestation and heavily lactating females

Handling: Llan1as and alpacas are highly
require a slightly higher percentage of crude
trainable, and most animals can be easily
protein and TDN of 60%-65%. Under basal
taught to come into a barn or corral for
conditions, most can1elids eat l.So/tr-2% of

LLAMAS AND ALPACAS

1847
body wt/day on a dry-matter basis. Legumes
administration of xylazine, ketaniine, and
are usually not needed and may contribute
butorphanol usually provides 20-30 min
to obesity. Palpating the amount of tissue
of recwnbent restraint. Butorphanol can
over the lumbar ve1tebrae and ribs can best
provide sedation of short duration and is
assess body condition. Body condition is
especially useful for head, ear, and dental

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generally scored from 1 (thin) to 9 (fat),
procedures.

with 5 being ideal.

Llamas and alpacas tolerate general

Seasonal vitamin D deficiency, characteranesthesia well and usually do not require ized by diminished growth, angular limb
tranquilization before induction. Induction
deformities, kyphosis, and a reluctance to
and maintenance of anesthesia is similar to
move, can be a problem in heavily fibered
that in other domestic species; however,
animals raised in regions with poor sun
tracheal intubation requires some practice.

exposure during winter months. The
problem is most severe in rapidly growing,
fall-born c1ias. Serum phosphorus of <3

Clinical Pathology: Hematology and
mg/dL, a calciun1:phosphorus ratio of >3: 1,
cHnical chemistries are similar to those
and vitaniin D concentrations of <15 rm101/L
in other species, with a few significant
in crias <6 mo old are diagnostic. Nonna]

differences. Camelid RBCs are relatively
phosphorus and vitaniin D concentrations
small and elliptical and may produce
in this age group are 6.5-9 mg/dL and
anomalous results when evaluated using

>50 nmol/L, respectively.

an automated cell counter. Normal PCV

To date, there does not appear to be
is 27%-45%, normal RBC counts are
a nutritional justification for routinely

10.1-17.3 x 106/µL, and normal WBC counts
incorporating ionophores into the diet of
are 8,000-21,400/µL.

camelids. However, because pelleted or

Basal glucose concentrations in llamas
mixed-grain feeds intended for cameHd
and alpacas are more typical of monogastric
consumption may be forn1ulated in the
species than runlinants. Basal levels are
same facilities that handle ionophores,

82-160 mg/dL, but glucose levels >300 mg/dL
cameHd feed has been accidentally
are common after stressful events. For
contaminated. Such an incident resulted in
additional hematologic and serum biochemia high incidence of death, and other health cal reference ranges, see TABLF..S 6 and 7, p 3176.

compromises to animals exposed during the
period of consumption are not fully known.

Drug Use: No drugs are currently

Routine and effective purging of feed
approved for use in llan1as and alpacas, so
milling facilities should allow for producall use is extra-label. SA Cs in North America tion of cameHd feed without contamination;
have the potential to be food animals,
however, human error and equipment
making drug withdrawal tin1e a considerafailure can still compromise any feed tion. See TABLE 12 for antibiotics that have product.

been used for treatment of sensitive

Copper toxicity is a much greater conbacteria in SACs.

cern than copper deficiency in cameHds.

Although drug use in exotic species is

Although there is a requirement for copper
commonly based on approaches used in
in camelid diets, mistakes in formulation
other species and often has favorable
and use of multiple supplements without
results, adverse outcomes have prevailed
full knowledge of total copper intake has
with numerous drugs in carnelids.

resulted in toxicity. Most reported cases of

Ca.melids are prone to lidocaine toxicity,
toxicity have been due to chronic intake
so its use should be minimized. lf deemed
rather than acute deaths.

necessary, lidocaine should be diluted to

0.5% and used sparingly; the total dose

Anesthesia: There are several options for
should not exceed 4 mg/kg (1 mL of 2%
sedation and anesthesia of camelids ( see
lidocaine/5 kg). Lidocaine toxicity is

TABLE 12). Generally, alpacas require more
characte1ized by lethargy, ataxia, slow and
drug than llamas to achieve the same
labored breathing, weakness, hypotension,
results. For short procedures, it is usually
and diminished response to stimuli.

not necessary to withhold food and water;

Diazepan1 should be available and
however, when deemed necessary, both
administered at 0.1--0.5 mg/kg in case
should be withheld at the same time,
of lidocaine toxicity.

reducing the tendency to regurgitate.

Although dexametl1asone is used in other

Xylazine can be used for sedation without
animals to stin1ulate surfactant activity in
recumbency. Higher dosages will result in
fetal lungs, as little as 0.5 mg in pregnant
recumbency and provide a light plane of
camelids has consistently caused fetal death
anesthesia for 20-30 min. Simultaneous
and complications, including retained

1848

LLAMAS AND ALPACAS
placenta and ute1ine prolapse. Virtually any

Commonly and inlmediately after
steroid-containing product that a female
ca.melids are injected with B-complex
camelid comes in contact with, especially
vitamins or leva.rnisole, they demonstrate
dming the third trimester, will cause
signs of hyperexcitement and itching. In the

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abortion. Even a c1ia with steroid cream
case of multiple procedures or'adnlinistraon the muzzle nursing a dan1 has caused tion of several injections, those anticipated
abo1tion.

to sting should be done last.

TI!micosin has caused enough deaths in
camelids to warrant the recommendation

REPRODUCTION
that it should not be used in these species.

The cardiovascular system is the target of

Reproductive Physiology
toxicity, which may be due to calcilllll
channel blockade.

Females: Relative to body size, tile

The prolonged-release form of ceftiofur
nonpregnant reproductive tract of SA Cs is
has produced neurologic changes, including relatively small. Uterine morphology is blindness. IV administration should be
sinlilar to that of a mare, witll relatively
avoided. However, many came lids have
short horns and uterine body. The cervix
been successfully treated SC without
can be felt on rectal palpation and has two
problems.

or tlu·ee ca.itilagenous rings. The urethra

Normally used to reverse xyla.zine
opens onto the floor of tile vagina. A·
sedation, tola.zoline has produced severe
suburethral diverticulwn is present.

signs, including initially anxiety, hyperes

Ovarian activity typically begins at 10-12
thesia, profuse salivation, and tachypnea.

mo of age. Ca.melicls are induced ovula.tors.

Convulsions, hypotension, and GI hyper

At the onset of puberty, follicular waves
motility resulting in diarrhea also develop.

occur, with a dominant follicle developing

Doses >2 mg/kg a.re incriminated, as well as
every 12-14 days. Because of the small size
too rapid IV administration. Because death
of females and tile potential for dystocia.

has also resulted after a.cl.ministration of
associated with early breeding, females are
tola.zoline, use of yohimbine is likely a better
usually not bred until they a.i·e > 18 mo old
approach.

and weigh 40 kg (alpaca) or 90 kg (llama).

Dinoprost tromethamine (prostaglandin

When a female is truly receptive, she will

F2a) use in ca.melids has often resulted in
usually assume a position of sternal
rapid death, likely due to bronchiolar
reclllllbency ( cushing) witllin seconds to
constriction and pulmonary edema.

a few minutes after introduction of a

Leptospirosis 5--wa.y killed vaccine has
male and allow the male to breed. While
ca.used type 2 hypersensiµvity and ana.phymounting, the male will typically begin a la.xis in camelids. Sinlilar reactions have been vocalization described as "orgling." The repmtecl occasionally in cattle and swine, so
voltune of tile ejaculate is relatively small
it is likely that sensitivity will increase in

(2-5 mL) and is mostly deposited directly
camelicl herds in which vaccination against
into the body of the uterus after cervical
leptospirosis is indicated.

•
dilation. Ejaculation occurs over an

Atropine, whether administered locally
extended period of time. An ovulation
in the eye or pa.renterally, has resulted in
induction factor in the semen stin1ulates
pupillary dilation observed to persist in
reflex ovulation -24-30 hr after ma.ting. A
camelicls for as long as a week. Treated
functional corpus lutetun (CL) is present
a.nin1als must be kept out of direct sunlight

2-3 days after ovulation. The fertilized
until pupillary response is normal.

oocyte is usually found in the uterus by day

Ca.melicls have relatively thin skin, and

7 after ma.ting, with in1pla.ntation occurring
use of topical eprinomectin can result in
by -30 days of gestation. The type of
clern1a.titis and blisters.

placentation is diffuse epitheliochorial,

After a llan1a. herd was treated for biting
developing in both horns. Altl1ough
lice with topical permetluin lOOAi, some
ovulation occurs from eitller ovary,
animals were observed to be breathing hard
uniquely, -95% or more of the pregnancies
and drooling; recovery was uneventful.

are carried in tl1e left horn. Live birtl1s of

Although nUlllerous potential adverse
twins are extremely uncommon, with most
effects from therapeutic use of trimethotwin pregnancies being resorbecl or aborted prim-sulfametlloxa.zole have been rep01tecl
early in gestation.

in the literature, it appears that acute death

A female with a fw1ctional CL will
after IV administration is rare. The rate of
aggressively refuse tile male's efforts to
administration or existing condition being
mount. An indication of pregnancy is the
treated may be a predisposing factor in tl1e
female's rejection of the male if he is
outcome.

reintroduced > 15 days after tile initial

LLAMAS AND ALPACAS

1849
breeding. Progesterone concentrations
prognosis because of the small urethral
of > 1 ng/mL are typical in females with a
dian1eter (3.5-5 French).

functional CL and can be used for confirma

Although androgen production may begin
tion of both ovulation at 6--9 days after
at <8 mo of age, and some spem1 can be

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mating and of pregnancy at >21 days after
collected by vaginal retlieval as early as 14
mating. Persistent CL are periodically seen
mo of age, nonnal preputial adhesions
and account for most false-positive results
prevent full penile extension and copulation
when using serum progesterone for
until �18-24 mo of age. Most males enter
pregnancy confinnation. Rectal palpation
breeding programs when 18-24 mo old, and
for pregnancy diagnosis is practical in
most are fertile by 30 mo of age. Sexual
llamas at >45 days of gestation. It is usually
maturity may be later in alpacas than in
not possible to safely perform rectal
llan1as.

palpation in alpacas, unless the palpator has

Semen evaluation is difficult in camelids
small hands. Pregnancy can positively be
because of the small total volwne of semen
diagnosed by transrectal ultrasound from
and the dribble ejaculation. Although males

-28 days of gestation, although it is possible
can be trained to mount a phantom or
to be suspicious as early as 10-12 days
dummy equipped with an artificial vagina,
based on presence of fluid and to be
semen collection usually requires heavy
reasonably sure by day 21 when a hypersedation or anesthesia and electroejaculaechoic "embryo" is seen. Ultrasonographic tion. Semen collection, even from males of
transabdominal approach from 45-60 days
known fertility, is inconsistent. The most
can be expected to produce positive results.

reliable semen evaluation is afforded by

Nom1al gestation in camelids is -342 ± 10
postbreeding retrieval from the vagina of a
days, with alpacas being somewhat shorter.

receptive dam.

Most normal birtl1s (> 70%) occur in the
morning. Dystocias due to excessively large
c1ias are rare. There are few reliable

Management of Reproductive
indications of pending delivery. Stage I labor Problems typically lasts 1-6 hr and may be accompa

Fertility problems are relatively common
nied by increased frequency of urination,
in llamas and alpacas. Although most
increased "hwnming," and separation from
problems plimalily involve females,
the herd. Stage II labor is rapid (typically
problems with males include hypoplastic

<30 min), with delivery of a cria weighing
testes, penile injuries, and heat stress,

5.5--8 kg (alpaca) or 11-16 kg (llama). Stage
which is characterized by scrotal edema,

III should be complete within 4-6 hr. All
decreased activity, and reluctance to breed.

stages are usually longer in a first-time

After heat stress, fertility can be permadelivery. Retained placentas are rare.

nently impaired or reduced for up to 6 wk.

Uterine involution begins shortly after birth,

Shearing, adequate shade, and sufficient
and most females can conceive within 14-21 water help prevent the problem. When days after delivery. Females have four teats
working with inexperienced males, vaginal
and do not exhibit significant mammary
intromission should be visually confirmed.

enlargement during the prepartunl peliod.

Because of the relatively high incidence

Mastitis is rare.

of congenital anomalies, anatomic problems
must be considered as causes of infertility

Males: Both testicles should be fully
in nulliparous animals. In multiparous
descended at birth. Testes should be at least
aninlals, vaginal strictures, uterine

2 x 4 cm and 3 x 6 cm in mature alpacas and
infections, and cervical damage are also
llamas, respectively. Relative to body size,
relatively common. Complete uterine
the testes are smaller than those of many
strictures are possible sequelae of dystocia.

other domestic livestock species and are

The diagnostic approach to all these
held close to the body wall. The urethra is
conditions is sinular to that used in mares,
relatively small and contains a urethral
except that rectal palpation cannot usually
diverticulum at the level of the ischial arch,
be safely done in alpacas unless sedated. If
making retrograde catheterization difficult
uterine biopsies or cultures are appropriate,
to impossible. The unstin1ulated prepuce
they should be performed when the dam has
points backward, accounting for the
a dominant follicle, which relaxes the
rear-directed urination, while the forwardcervix.

pointing penis is fibrous, with a sigmoid

Ruptw·e of a mature follicle (>7 mm) can
flexure. A cartilaginous process is present at reliably be induced with hun1an chorionic the tip of the penis, and the urethra opens
gonadotropin or GnRH. Increased

1-2 cm back from the tip. Urinary calculi
progesterone concentration (>l ng/mL)

are relatively uncommon and have a poor

7 days after copulation or hormonal

1850

LLAMAS AND ALPACAS
treatment is indicative of CL formation.

pe1fringens type C and D vaccinations and

Although persistent CL have been identified, tetanus toxoid. In regions where liver they are relatively rare. Prostaglandin
fluke (Fasciola hepatica) infections or
treatment will result in regression of a
snake envenomations are a problem, use
persistent CL and abortion throughout
of polyvalent vaccines against C novyi,

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gestation. Induction of parturition with

C septicum, C sordellii, and C chauvoei prostaglandins or glucocorticoids is not
reconunended. Rapid death of llamas and
are warranted. One successful approach
alpacas has occurred after prostaglandin
has been to give an initial vaccination at
therapy, especially at high doses and when

3 mo of age, a booster 30 days later, and
administered by other than SC route.

annual boosters thereafter. Llamas and alpacas are inununocompetent at birth, so HERD HEALTH
neonatal vaccination can begin in the first
week of life, followed by two boosters at

3-wk intervals.

Neonatal Care: Crias should be on their

Abortions secondary to Leptospira spp
feet and attempting to nurse within 2 hr
infections are regionally a problem and can
after birth and every 1-2 hr thereafter for
usually be prevented using an initial
the first few days. While weight gain for the
vaccination, followed by boosters twice
first 24 hr postpartum may be minimal,
a year. Killed rabies vaccines have been
thereafter llamas should gain 250-500 g/day
used with unknown efficacy in endemic
and alpacas 100-250 g/day. Healthy crias
areas. Any attempt to control other viral
should approximately double their birth
diseases (including West Nile virus
weight by 1 mo of age.

infection) should only involve use of

Routine cria care should include
killed vaccines.

weighing and single dipping the navel in 7%
tincture of iodine or 0.5% chJorhexidine

Dental Development and Care: The
three times during the first 24 hr after birth.

dental pad of llamas and alpacas is similar

If appropriate for the area, supplemental
to that of a cow. At birth, the first two pairs
seleniw11 could be provided by injection (0.5 of lower incisors are nonnally through the mg for alpacas, 1 mg for llamas). At birth is
gum line; lack of eruption is one indication
an ideal time to take a blood sample if there
of prematurity. The central, middle, and
is any concern of failure of passive transfer
lateral mandibular deciduous incisors are
of colostral antibodies. Having a baseline
replaced at -2-2Y2, 3-3Y2, and 4--6 yr,
sample to measure PCV and total proteins
respectively, although determining age by
to compare with a subsequent sample at
the teeth is notoriously inaccurate in these

24 hr will provide valuable infom1ation
species.

regarding failure of passive transfer and

A unique feature of SA Cs is the develophydration.

ment of the upper 13 and upper and lower
canine teeth on both sides into "fighting"

Parasite Control: Parasite control proteeth that may grow to >3 cm long. The grams vary according to climatic conditeeth can cause serious damage to other tions, population density, and parasite load,
males during fights and usually need to be
and should be developed according to local
cut flush to the gum with obstetrical wire or
conditions.

a grinder beginning with eruption at 18-24

No drugs have been approved for use in
mo of age and repeated as needed in intact

SACs. However, anthelmintics that are
males. If castration is to be performed,
generally recognized as safe and effective
eruption of the fighting teeth signals an ideal
include ivem1ectin, pyrantel pamoate, and
time to schedule both procedures. Growth
fenbendazole. Parasite resistance has
of fighting teeth usually stops after
developed in all ruminant species, making it
castration. Fighting teeth in most females
necessary to develop a strategic dewom1ing
barely penetrate the gurnline and seldom,
program, particularly in locations where the if ever, need to be cut. Tooth extraction meningeal wom1 is present. Liver flukes can
to avoid periodic trimming is impractical
be a significant problem. Control with
because of very deep, curved roots.

clorsulon or albendazole is usually

The incisors are open-rooted in alpacas
effective, although repeated clorsulon
and continue to grow throughout life. Poor
treatment every 6-8 wk may be necessary.

occlusion of the incisors and dental pad
necessitate periodic tooth trimming and

Vaccinations: Most vaccination protocols
appears to be more of a problem in alpacas
for SA Cs have been empirically derived.

than in llan1as. Cheek teeth are rooted,

Most aninlals should receive Clostridium
normally sharp, and do not require regular

LLAMAS AND ALPACAS

1851
floating. Premolar and molar occlusion
the maxilla The mandible may or may
should be checked and problems corrected
not have a similar deviation. When severe,
in older animals exhibiting difficulty in
occlusion of the nares and lack of apposichewing or weight loss.

tion of the incisors and dental pad usually

Abscessed lower second premolar and
necessitate euthanasia of the cria. There
first and second molars are seen as a hard,

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appears to be a relationship of this defect to
well-developed swelling on the lateral
choanal atresia, in that they occasionally
surlace of the mandible over the affected
occur together.

teeth. A draining tract may or may not be

Ocular and ear conditions include
present. The area is usually not painful on
juvenile cataracts (seen occasionally),
palpation, and most animals maintain body
blocked nasolacrimal ducts, and an
condition. No bacterial agent has been
association between blue eyes and deafness
consistently isolated from the abscesses.

in some lines of white anin1als. Fused (tip or

Prolonged antibiotic therapy is palliative,
base) and short ("gopher") ears are
although rarely curative. Tooth extraction
recognized heritable defects, the latter
usually requires making a lateral incision
appearing to be a dominant trait.

over the affected teeth, splitting the tooth

Cardiac defects are relatively common,
because of the divergent roots and repelling
with ventricular septa! defects heading the
the tooth into the oral cavity. Care should be list.

taken during extraction to avoid mandibular

Numerous musculoskeletal defects
fracture.

have been identified, including syndactyly
and polydactyly. Arthrogryposis, rotated

Nail Trimming: Some animals rarely need talus, angular lin1b deformities of the front foot care, whereas others require nail
limbs, and tendon laxity are also seen.

trimming every 2--3 mo. Diet, genetics, and

Other congenital anomalies identified in
environment likely play a role. The nails
llamas and alpacas include atresia ani,
should be trimmed flush with the bottom of
atresia coli, umbilical hernias, and
the pad. Occasionally and especially with
several different types of tail defects,
overgrown toes, "quicking" may occur but
including a pronounced lateral deviation
generally is inconsequential.

of the tail at the base.

Urogenital defects are much more

DISEASES
common in SACs than in other species.

Significant defects in females include uterus
unicornis, hypoplastic ovaries, double

Congenital and Inherited Anomalies
cervices, segmental aplasia of the vagina or

Although few congenital anomalies have
uterus, and clitoral hypertrophy suggesting
conclusively been shown to be genetic in
intersex conditions. Unilateral absence of a
origin, it is assumed that defects inherited
kidney is periodically seen, commonly in
in other species are probably inherited in
association with choanal atresia. Total

SACs as well. Accordingly, this should be
absence of kidneys has also been seen.

considered in breeding decisions. Facial

Congenital conditions in males include
and cardiac defects are reported to be the
hypospadia, retained testicles, testicular
most frequent inherited anomalies. A
hypoplasia, persistent frenulum, ectopic
historically narrow gene pool is likely the
testicles, and corkscrew penis.

reason that congenital defects are relatively
common in SACs. Affected individuals

Bacterial Diseases
commonly have more than one defect.

Brucellosis, tuberculosis, and Johne's

Choanal atresia, a condition caused
disease (paratuberculosis) have been
by failure of the inner nares ( choanae) to
identified in SA Cs, although the naturally
open during embryologic development, is
occurring incidence of these infections is
the most widespread congenital defect. It
low. There are reported cases of both type C
can be unilateral or bilateral and may result
and D Clostridium perfringens, which has
in complete or partial blockage. Accordprompted the use of toxoid vaccination as a ingly, the primary clinical presentation is
routine measure in most herds. Although
a variable degree of respiratory distress

SA Cs are not apparently highly susceptible
in the neonate. Distress becomes more
to tetanus, most herd vaccinations using the
apparent during nursing, and crias com

CID toxoid include tetanus toxoid.

monly gasp as milk is inhaled. Surgical

C perfringens type A is a very important
correction is not recommended.

pathogen under stressful circumstances,

Wry face is characterized by a slight
especially in Soutl1 America, and results in a

( <5°) to severe (>60°) lateral deviation of
high death rate in crias <4 wk old. Entero-

1852

LLAMAS AND ALPACAS
toxogenic strains of C perfringens type A

Mycop/asma Infection
are believed to be particularly lethal.

Clinical signs are similar to those of type

A common condition that was formerly

A infections in other species, with a rapid
referred to as eperythrozoonosis is now

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onset of neurologic changes followed
known to be caused by Mycoplasma
shortly by death.

lwemolamae. A high percentage' of the SAC

Anthrax has been diagnosed in SA Cs, but
population has been exposed by insect
vaccination should only be done in endemic
vectors, contan1inated needles, or transplaareas using a killed product.

centally. Animals with a healthy in1mune

Respiratory infections in North An1erica
system develop a state of premunity (infected
caused by bacteria remain relatively rare, but
but inunune ); they demonstrate the organism
in South America the condition referred to as
in RBCs only when stressed or truly
alpaca fever is caused by Strept.ococcus
inm1unosuppressed. PCR diagnostic tests are
zooepidemicus. The onset of this condition
available. 'Ireatment of clinically affected
is often preceded by stressful conditions.

anemic animals with long-acting tetracy

Individual cases and herd problems with
clines does not entirely clear the infection
abscesses caused by Corynebacterium
but improves the anemia.

pseudotuberculosis have been reported.

Contact with sheep and shearing wounds

Fungal infections
are likely contributing factors.

As with most animals, ubiquitous contact
with fungal organisms in SACs will

Viral Diseases
occasionally lead to clinical disease.

Notable clinical possibilities include

Most can1elids are seropositive for a
coccidioidomycosis, candidiasis, aspergilpresumptively nonpathogenic adenovirus losis, cryptococcomycosis, muconnycosis,
that is specific to llamas. Occasionally, an
and mycotoxins. The most significant fungal
anin1al will develop a titer to bovine viral diarinfection in SA Cs is coccidioidomycosis; it rhea virus, and a few anin1als have developed
is an endemic problem in the southwest
a mild diarrhea, respiratory disease, and even

USA, potentially affecting all resident
abortion presun1ably in response to the virus.

animals (as well as the human population).

Exposure during pregnancy also can lead to

An in1portant consideration is that SACs
persistent infection in c1ias. Equine
showing chronic respiratory signs even
herpesvirus 1 infections with associated
in nonendemic locales may have been
neurologic signs and blindness have been
exposed during shows or breeding time
seen in a small number of SA Cs, particularly
while in endemic areas.

when cohabitating with equids. Growing
numbers of neurologic cases in SACs have

Gastrointestinal Diseases
been found to be due to Eastern equine
encephalomyelitis virus. Bluetongue virus

The oral cavity and esophagus of SA Cs are
likely will emerge as a clinical entity in SA Cs
unremarkable. The stomach has three
as it evolves with greater distribueion and
distinct compartments (C-1, 2, and 3) that do
pathogenicity. An outbreak in 2007 of
not correlate directly with the four chambers
respiratory disease, principally in alpacas,
of the ruminant stomach. Although not
was found to be due to what is referred to
classed as ruminants, they do eructate,
as alpaca respiratory coronavirus. Stress
regurgitate, and remasticate and would be
conditions often predispose to the onset of
clinical presentations that vary from mild
upper respiratory tract disease to severe
respiratory disease and death.

During the spread of West Nile vims
across North An1erica, SACs were found to
be susceptible, with most developing a titer
consistent with exposure. Some became
severely affected and died. Naive and
immunosuppressed animals are most likely
to be at risk. West Nile virus vaccines
approved for horses have been found to
produce a good inunune response. SACs
can also contract foot and mouth disease,
although clinical disease is usually relatively
mild; the carrier status of infected animals is Mycoplasma infection in llama RBCs. Courtesy presun1ed to be of short duration.

of Dr. LaRue Johnson.

LLAMAS AND ALPACAS

1853
considered as foregut ferrnenters in C-1 and

Hepatic Disease: The visceral surface

2. Only the distal fifth of C-3 is analogous to
of the liver nom1ally has multiple fissures,
the acid-secreting monogastric stomach. The
whereas the parietal surface is smooth and
spiral colon is generally a flat, single spiral
lobation is indistinct. There is no gallbladprone to blockage when the centripetal loop der. SACs appear to be particularly

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turns to become centrifugal.

susceptible to Fasciola hepatica, with
fecal shedding beginning 10-12 wk after

Megaesophagus: Moderate to severe
infection. Clinical signs can include ill thrift,
dilatation of the esophagus is relatively
diminished growth, and acute death. Icterus
conunon in llamas and alpacas, especially
is rarely seen. Increased serum bile acids
after instances of choking. Signs include

(>25 µmol/L) and enzyme concentrations
chronic weight loss frequently associ-

(no1mal, alkaline phosphatase 15-121 nJ/L
ated with postprandial regurgitation or
and AST 66-235 nJ/1) are also diagnosti

"frothing" of food. There is no identified age cally useful.

or sex predilection, and no consistent cause

Hepatic lipidosis is a relatively conunon
has been established. A suspected case of
problem in SA Cs. Clinical signs associated
megaesophagus should be confirmed witl1
witl1 liver failure in other species are
barium contrast radiography. No treatments frequently seen, altl10ugh acute death ( surgical or changes in feeding practices)

without prior indication of pending
have been consistently successful. The
problems also has been reported. The cause
longterm prognosis is fair to poor, with
is not clearly established, but stress and/or
some animals maintaining condition for an
abrupt decrease or change in food
extended period and others continuing to
consumption appear to play a role.

lose weight.

Treatment is symptomatic. Mortality in
untreated animals is frequently high.

Stomach A tony: Gastric atony is an
occasional problem of unknown cause.

Small- and Large-intestinal Diseases:

Signs include decreased or complete

Diarrhea is relatively tmcommon in llamas
cessation of food consumption, loss of
and alpacas. Shortly after birth, SAC crias
body condition, and depression. Other GI
may experience a mild diarrhea due to
problems, including diarrhea, may be
abundant dam nillk production, essentially
present. Supportive therapy, including
a substrate purge. The primary recognized
fluids, is frequently helpful. Lack of food for
infectious causes of diarrhea in neonates

3---5 days also usually causes the death of
include rotavirus, coronavirus, cryptobacteria and protozoa in C-1 and C-2.

sporidia, and enteropathogenic strains of

Transfaunation (0.5-1 L) of camelid C-1 or

Escherichia coli. Some crias also have a
strained rumen contents (sheep or cow),
transitory diarrhea 2-3 wk after birth, at
administered by gavage, frequently results
about the time they experience new food
in a dramatic improvement in appetite and
matter. At this same time, some crias
reestablishment of appropriate flora.

develop colic signs due to blockage in tl1e
spiral colon. Diarrhea in older neonates is

Ulcers: Partial and complete thickness
more likely associated withEimeria spp
erosions of the acid-secreting distal portion
infection, especially associated with the
of C-3 and most proxin1al portion of the
stress of weaning. Identified causes of
duodenun1 occur. Signs may include
diarrhea in older animals include Yersinia
decreased food consmnption, intemlittent to pseudotuberculosis, Salmonella spp, severe colic, and depression. Although the

Giardia spp, and Cryptosporidium
cause has not been clearly established, stress parvum. Treatment options are the same as appears to be a significant component, witl1
for other species (ie, fluid and electrolyte
problems often developing 3---5 days after
replacement and appropriate antibacterichange of environment affecting social als).

structure, serious injuries, and illnesses.

Diarrhea in adult SACs is relatively rare

No reliable premortem diagnostic
but often accompanies a change of feed.

procedures are available; treatment is usually Serious conditions characterized by based on history and clinical signs. Theoretidiarrhea include eosinophilic enteritis, cally beneficial oral medications have not
infection with Eimeria macusaniensis or
proved effective. Parenteral administration

Mycobacterium paratuberculosis, or
of omeprazole reduces acid production.

severe nematode parasitism. Compared

Stress reduction, including clinical housing
with that in cattle with Johne's disease, the
with a coh01t anin1al, parenteral antibiotics,
clinical course in SA Cs tends to be short and
and supportive therapy, are helpful.

fatal. When diagnosed by fecal examination,

1854

LLAMAS AND ALPACAS

E macusaniensis must be promptly
exposure and applicatil<ln of aloe vera lotion
treated, because infection can cause
have proved useful. Lat;er appearance of
marked debilitation. Although variable,
sunburned sites varies !from mild peeling
current therapy recommendations include
to ulcers.

oral ponazuril followed by parenteral

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sulfadimethoxine.

Lymphosarcoma is the only neoplasia

Ulcerative Pododerirnatitis: Llamas
found with significant frequency in SACs.

and alpacas kept in moiist conditions

It can occur as either a juvenile lymphoma
develop "in1mersion focOt," characterized
or a primitive malignant round cell tumor.

by footpad blistering ar'ld sloughing, with

Clinical signs and course vary depending
variations depending rnn infection by
on organ involvement.

anaerobic bacteria. De!Pridement,
antiseptics, and foot pr,otection may be

Respiratory Diseases
required for prolonged pe1iods to facilitate
resolution. Treatment \With penicillin is

Auscultation of llamas and alpacas is
always indicated unlest.l tmique bacterial
difficult and frequently unrewarding. Little
isolates are involved. T'.hese cases require
air movement is heard under nom1al
a relatively long healini;s period.

conditions, and identification of areas of
infection, congestion, or consolidation is
typically difficult. Lateral radiographs may

Mange, Lice, and Tic:ks: All four genera
be required for diagnosis of pneumonia.

of mange mites (ie, Sai·coptes, Psoroptes,

Bacterial infections of the I ung are relatively Ch01ioptes, andDemoclex) have been rare, with Streptococcus and Corynebacte-diagnosed in camelids. Alopecia, hyperkera

1ium spp being the most common isolates.

tosis, and scaling acc01r1panied by pruritus

Chronic obstructive pulmonary disease
tend to charactetize all (l>pecies. The clinical
appears to be increasing in frequency.

signs may resemble t110ise of zinc deficiency.

Animals allowed to live to their expected

Deep skin scrapings or ibiopsies are ideal to
life span is a factor, but feeding practices
make a definitive diagnosis. Although various
can contribute to onset as well as exacerbaoptions for tl1erapy exist, most mange cases tion of clinical signs---coughing, shortness
will respond to routine J?arenteral doses of
of breath, and expiratory dyspnea. Therapy
ivermectin repeated every l� 14 days. Oral
includes changing the feeding regimen to
therapy does not appeaf to be as effective.

reduce dust, molds, and pollen. Bronchodi

Chorioptes infestation t11ay require higher lators and steroids may be helpful but
doses repeated every 14--21 days and local
remain unproved.

therapy. Refractory Sai-coptes cases
involving the lower legs have benefited from

Skin Diseases
the same topical treatment.

With louse infestatio:n, it is in1portant to

Unique features of normal can1elid skin
detennine whether pediculosis is due to
histologically include a marked vascularity
biting (Damalinia breviceps) or sucking
and significant presence of eosinophils.

(Microthoraci11s cameli) lice. This can be

Several skin conditions are shared with
accomplished with tl1e aid of a hand lens or
sheep and goats, including ringwmm,
microscope. Use of trai1sparent t.ape to
contagious ecthyma, dem1atophilosis,
retrieve lice for diagnosis from within the
and occasionally pizzle rot.

depths of wool can be :oittempted. Sucking
lice can be treated witi1 injectable ivem1ec

Shearing Injury and Sunburn:

tin as per routine mange therapy. However,

Complications associated with shearing are
biting lice are not affected by parenteral
common. Lacerations may occur where
ivermectin. Topical application of synthetic
there are loose folds of skin, eg, near tl1e
pyrethrin preparations has been effective,
axilla. These often heal uneventfully with
but ctitical doses for t11ese species have not
or without suturing. Hot shears may cause
been established. Preventive measures for
bums that lead to thick scabs, usually on
lice and mange include toutine treatment
the dorsum of the back, that may resemble
of new herd additions .,swell as animals

"wool rot." A history of shearing by a novice visiting and returning for breeding purposes often helps confinn the diagnosis. Antibiotic or from shows. Ticks have caused tick ointment is generally beneficial for these
paralysis as is seen in other species. In
iatrogenic lesions.

addition, ticks gaining :Lccess to ears have

Sunburn also can occur after shearing,
caused inner ear afflictions resulting in
especially in light-skinned animals. If found

Homer syndrome as well as encephalitic
in the acute stage, protection from further
death.

LLAMAS AND ALPACAS

1855

Copper Deficiency: Copper deficiency
tion. Systemic or topical steroids produce
is characterized by depigmentation of fiber
some transient response, but steroids may
with a wiry or steely teid;ure. Juveniles grow
cause abortion in can1elids. Tn northern
poorly and are predisposed to infections.

climates, the condition tends to spontane

Confirmation of deficiency is best based
ously improve during winter months.

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on comparison of liver copper levels with

Alopecia of the ears has also been seen,
species nonnals. Therapy requires dietary
particularly in black alpacas.

supplementation. However, excessive
supplementation will cause copper toxicity,

Idiopathic Hyperkeratosis (Zinc
which has been diagnosed more commonly
responsive Dermatosis): Onset of
than deficiency.

idiopathic hyperkeratosis is possible at any
age. The lesions appear as nonpruritic

Dorsal Nasal Alopecia (Dark Nose
papules with a tightly adherent crust.

Syndrome): The most common clinical

Papules progress to plaques and then large
sign of dorsal nasal alopecia is usually
areas of thickening and crusting. Lesions
alopecia over the bridge of the nose. The
are most common in the less densely haired
skin is nom1al or variably scaly, hyperareas of the perineum, ventral abdomen, pigmented, and thickened. Dark-haired
inguinal region, medial thighs, axilla, and
animals are predisposed, presumably
medial foream1s, but the face may also be
because insects prefer the warmer surface
involved. The signs may wax and wane.

of a dark background. In some animals, the

Diagnosis is by skin biopsy. Treatment is 1 g
condition may be secondary to rubbing the
zinc sulfate or 2-4 g zinc methionine per
nose; in others, it may be a fly bite exacerba-
day. Calcium supplementation should be
minimized and alfalfa hay discontinued.

Affected animals may be zinc responsive
but not deficient.

Idiopathic Nasal/Perioral Hyperkeratotic Dermatosis (Munge): Most animals with munge are 6 mo to 2 yr old at
onset. Variable degrees of hyperkeratosis

(heavy, adherent crusts) in paranasal and
perioral regions are seen. Less commonly,
the bridge of the nose and periocular and
periaural regions are affected. Inflammatory lesions may wax and wane. Qifferential diagnoses include viral contagious pustular dermatitis, dermatophilosis,
dermatophytosis, bacterial dermatitis,
and autoimmune/immune-mediated
disease. Treatment is directed at resolving secondary bacterial infections (ie, daily 10% povidone iodine scrubs plus
application of 7% tincture of iodine).

If lesions do not respond to antibiotics,
adding topical glucocorticoid preparations or intralesional triamcinolone acetonide (2 mg/mL) may be beneficial.

Some animals do not respond to any of
the described therapies, including those
with juvenile llama deficiency syndrome,
which has been shown to affect both
llamas and alpacas; in these cases, an

Perinasal munge in a llama. Courtesy of
evaluation of the immune response is

Dr. LaRue

Johnson.

indicated.

1856

MARINE MAMMALS

MARINE MAMMALS

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Marine mammals are a diverse group of

Good air quality, especially in indoor
species that include cetaceans, pinnipeds,
facilities (10-20 air changes/hr) is as
sirenians, sea otters, and polar bears. The
important as good water quality. Photopericetaceans consist of two major groups with ods, light spectral and intensity requiredifferent physiology and anatomy: toothed ments, sound tolerances, and flight distance
whales (Odontocetes) and baleen whales
requirements are not well established for

(Mysticetes ). The pinnipeds consist of three
any cetacean. Extremes in any of these
major groups: true seals (Phocidae ), eared
factors should be considered detrimental
seals (Otariidae), and walrnses (Odobeniin the absence of specific data.

dae). Sirenians (Sirenidae) are of a single

Environmental requirements of pinnipeds
fanlily that includes manatees and dugongs.

are similar to those of cetaceans except that

The sea otter (Enhydra lutris) is a marine
pinnipeds can "haul out" on land. Although member of the Mustelidae, and the polar
captive pinnipeds can be kept in freshwater,
bear (Ursus maritimus) is the only member saltwater pools that meet the specifications of the U rsidae that is considered marine.

listed above for cetaceans are preferred.

Few pharmaceuticals or vaccines are

Most pinnipeds obtain their metabolic
approved for use in marine mammals. Many
water requirements in food and do not
recommendations can be made based on
require access to freshwater if provided
personal experience or published reports,
fish with a high fat content. However, it is
but clinicians should be cautious in their
common practice to allow pinnipeds
application.

access to potable water.

Pools for captive pinnipeds should

MANAGEMENT
provide shelter from wind and some shade.

Haul out requirements are different for each

The general rule in maintaining marine
species, and some pinnipeds ( eg, the
mammals in captivity is to duplicate their

N orthem fur seal [ Callorhinus ursinus])

natural environment as closely as possible.

require very specific timing of access to land

Most live in marine habitats, although some

( eg, only at the pupping season).

species migrate into freshwater; Baikal

Sirenians are warmwater species with
seals (Phoca sibirica) and five species of
water requirements sinlilar to those of
river dolphins have adapted completely to
cetaceans, although the most common
freshwater habitats. Manatee subspecies
sirenian in the USA, the Florida manatee
vary in the time they spend in freshwater,

(Trichechus manatus /,atirostris), migrates but the dugong (Dugong dugong) is
between marine and freshwater environcompletely marine.

ments seasonally. Manatees do better in

Marine cetaceans sht>uld be kept in water
captivity if salinity is changed seasonally
with a salinity of 2&-35 g/L, preferably using
to match migration in the wild.

balanced sea salts. Water for captive marine

In captivity, the sea otter thrives best in
cetaceans should be maintained as close to
a cold marine water system. Because the
the pH of mid-ocean waters (8-8.3) as
fur of the sea otter is its major protection
possible. Freshwater cetaceans and seals
against hypothermia, the water must be
require water sinlilar to that of their natural
kept free of oils and organic material that
habitat. In the USA, the Marine Mammal
could mat or damage the coat.

Protection Act of 1972 specifies that

The polar bear naturally lives on arctic
colifonn bacte1ial counts of water for
and subarctic ice. It has successfully
captive marine man1TI1als must be 51,000
adapted to subtropical climates in captivity

MPN (most probable number/100 mL).

but is more susceptible to dennatologic

Marine mammals kept in the extremes of
disease in warm climates. Polar bears
their temperature tolerance range are more
traditionally have been provided with
susceptible to environmental and infectious
freshwater in captivity. Proper attention to
disease. In general, cetaceans and pinnipeds
filtration and water quality is beneficial.

are better adapted to cold than to heat, but
species-specific tolerances differ. Inappropri

Restraint: Marine mammals must be
ately combining different species for display
restrained for thorough examinations.

purposes can result in compromises that

Trained cetaceans and pinnipeds can be
jeopardize the well-being of some species.

taught behaviors to facilitate examination

MARINE MAMMALS

1857
and collection of diagnostic samples. For
eral anesthesia of cetaceans and pinnipeds
these animals, the presence of familiar atdifficult. Anesthetic drugs conunonly used tendants is important.

in other animals often have narrow margins

For complex procedures or tmtrained
of safety or cause tmexpected reactions in
animals, the safest approach to restraining
marine mammals. Tranquilizers, sedatives,

VetBooks.ir
a cetacean is to remove it from the water.

and anesthetics should be administered

Captive enclosures should allow water
to marine mammals only by personnel
drainage so that cetaceans can be stranded
experienced in their use. Specialized aneswithout the use of nets. As the animal begins thetic machines and respirators (apneustic to lose buoyancy in the draining water, it
plateau) are required for cetaceans. Sireshould be positioned over thick foam pads nians rarely require general anesthesia or
to minimize struggling and injury. Nets are
tranquilization for treatment. Sea otters can
an alternative for corralling small cetaceans
be sedated with diazepan1 (0.2 mg/kg body
kept in sea pens or encountered in the wild;
wt) or tiletan1ine-zolazeparn (1 mg/kg). A
however, experienced personnel are
combination of fentanyl (0.22 mg/kg) and
required to minimize the risk of drowning
diazepam (0.07 mg/kg) has been successor iajury to the animal or staff. Netted ful for sample collection in wild sea otters.

cetaceans are placed on foam or specially

Narcotic recycling has been seen. Surgical
designed stretchers or floats that can
anesthesia can be obtained with higher dossuspend the animal above water level.

ages of fentanyl-diazepam (0.33 mg/kg/0.11

Small cetaceans (dolphins) can often be
mg/kg); tiletan1ine-zolazepam (2 mg/kg);
restrained by the weight of three or four
or halothane, isoflurane, or sevoflurane,
attendants-one person controls the
with or without nitrous oxide. Polar bears
peduncle of the tail fluke and the others
are routinely immobilized with etorphine,
apply weight to the animal's body. The
tiletamine-zolazepam with or without
pectoral fins should be folded alongside the
medetomidine, ketamine with xylazi.ne,
animal in a natural position to avoid
or a variety of other agents used IM. The
permanent damage. In larger cetaceans
required dose is highly dependent on the

(whales), the powerful tail fluke may be
individual animal and environment.

secured with mechanical restraints.

Capturing pimlipeds is generally easier on
dry ground, although small animals can be

ENVIRONMENTAL DISEASES
captured in the water with end-release hoop
nets. Larger animals should not be netted in
water but should be coaxed or driven from

Corneal Edema: Corneal opacity is
the water or have the water drained from
frequent in captive pinnipeds kept in either
their pool. On land, hoop nets can be used
freshwater or saltwater; it is also seen in
on larger animals. Cargo nets, baffle boards,
captive cetaceans but is rare in .wild
and "come-along" poles also can be helpful.

animals. It can be due to various environ

Once captured, small seals can be
mental problems. Transient cases can be
restrained for some procedures by an
caused by sin1ply moving an animal to
experienced handler sitting on the seal's
freshwater from saltwater or vice versa.

back and holding the head. Larger pinnipeds Lack of shade and excessive bright light or more complex procedures require an
have been implicated. Poor water condiappropriately designed squeeze cage.

tions ( eg, high bacterial loads or overuse of

Sirenians are relatively docile; problems
oxidative disinfectants in the water) also
in restraint are generally due to their bulk
have been associated with the disease.

and weight, and caution is recommended

Nutritional deficiencies have been
because they tend to roll. They can be
suggested as causes, but response to
handled in much the same way as
supplementation with vitamin C or A has
cetaceans. Sea otters can be restrained like
not been dramatic. Feeding other oral anmost other large mustelids. Hoop nets can tioxidants (leuti.n, grape seed extract) as
be used to remove them from pools. Once
a preventive measure is being evaluated.

they are out of the water, restraint bags,

The condition is usually self-limiting if
squeeze boxes, or other restraint devices
the underlying insult to the cornea is
for small wild carnivores can be used. Polar removed early enough in the pathogenesis.

bears are large and dangerous, and manual
restraint is not advised.

Corneal Ulcers: Corneal ulcers are
conunon in captive pinnipeds and
cetaceans. They can be the result of direct

Anesthesia: Physiologic adaptations to
trauma or the sequelae of unresolved or
diving and marine environn1ents make gen-
tmtreated cases of corneal edema.

1858

MARINE MAMMALS

Diagnosis is by observation of epithelial
parasitic damage and increased histamine
defects on corneas stained with fluorescein.

content of spoiled fish, may be involved in

Culture of the lesion (bacterial, fungal)

the cause of a GI ulcer, but the disease in
before therapy can help direct treatment
captive animals should be considered
of nomesponsive cases with associated
associated with environmental or stressinfections. In trained animals, small lesions related conditions. Dramatic environmental

VetBooks.ir
can be treated topically. In untrained
changes, including changes of personnel or
animals, subcor\junctival ir\jections of
companion animals, can precipitate se1ious
antibiotics and steroid are required. Oral

GI ulceration in cetaceans or pinnipeds.

docycyline is being used in some pin.niped

Clinical signs include lethargy, partial
cases to stabilize the cornea, and topical
anorexia, abdominal splinting, pallor, and
cyclospo1ine or tacrolirnus is being used in
occasionally regurgitation. Animals with
tractable animals with some success in
bleeding ulcers show anemia and possibly
reducing recurrence. Extensive lesions
leukocytosis. Diagnosis generally is based
benefit from protection by suturing tl1e
on identification of man1.111alian RBCs in
eyelids. Deep ulcers or lacerations in danger
gastric washes; confirmation is by endoof eroding Descemet membrane should be scopic visualization of the lesions. Palliative
stabilized with a thin methylacrylate patch.

treatment of nonpe1forating ulcers usually

As in corneal edema, successful resolution
consists of administration of histamine
and prevention of recurrence depend on
blockers and alW11ina gel-based antacids
removal of the underlying cause.

with or without sin1ethicone, along with
frequent small meals. The w1derlying cause

Foreign Bodies: Many captive marine
must be identified and corrected for successmammals develop tl1e habit of swallowing ful resolution. Management of perforating
objects dropped into tl1eir pools. In
ulcers with resulting peritonitis includes
cetaceans, the opening to the second
intensive broad-spectrU.111 antibiotic and
compartment of the stomach is small, and
fluid therapy. As in people, stress-induced GI
foreign objects remain in the first compartulcers are more likely to develop in marine ment. In pinnipeds, the small pylorus
mammals that have previously had an ulcer.

prevents passage of most foreign bodies.

Frequently, no clinical signs are evident. On

Trauma: Traumatic lesions (eg, cuts,
occasion, anorexia, regurgitation, or lethargy
wounds from gunshots or propeller blades)

may be seen. Diagnosis is often made by
are common in marine mammals. Propeller
having witnessed tl1e anin1al swallow an
ir\juries are a major problem in manatees,
object. Smaller anin1als can be radiographed;
which commonly enter heavily navigated
in small cetaceans, the esophagus can be
recreational waters in Florida. Traumatic
palpated to establish the presence of foreign
wounds should be cleaned, debrided, and
bodies. Animals occasionally regurgitate
generally allowed to heal as open wounds
foreign bodies; however, assisted removal is
unless body cavities are breached.

usually indicated. Removal is usually best

Antibiotics should be administered during
performed by gastroscopy, whlch is also used convalescence to prevent gross infection.

as a method of diagnostic confim1ation. All

Maintenance of good water quality and a
efforts should be made to prevent ingestion
high plane of nutrition is beneficial to the
of foreign bodies. Training anin1als to retrieve healing process. Large wounds frequently for reward as a displacement to swallowing
heal uneventfully.

foreign objects is thought to be beneficial.

Oil Exposure: Exposure of marine

Gastrointestinal Ulcers: GI ulcers are
mammals to spills of petroleum hydrocara significant problem in captive marine bons is a major concern. Sea otters are
mammals and are also found in free-ranging
paiticularly susceptible to such exposure
marine mammals. Ulcers of the first
because of their natural grooming habits
compartn1ent of the cetacean stomach are
and their lack of an insulating blubber
a common necropsy finding and pose less
layer. Hepatotoxicity, renal toxicity, GI
severe clinical problems than do ulcers of
damage, and loss of horneothermic ability
the pyloric region or proximal duodenwn.

are irnportai1t effects of exposure to

Gastric ulcers in pinnipeds frequently
petroleum hydrocarbons; however, the
progress to perforation, whlch results in
most devastating effects are due to direct
peritonitis and subsequent deatl1. Gastric
pulmonary danrnge from inhalation of
ulcers also are found in sirenia.ns. Altl10ugh
volatile hydrocarbons.

ulcers in cetaceans perforate less frequently

Experimental evidence suggests cetaceans
than in pinnipeds, they should be treated as
and pinnipeds will avoid petroleum spills if
a serious problem. Various causes, including possible ( unlike sea otters) and are relatively

MARINE MAMMALS

1859
resistant to toxicities from direct skin
wt for maintenance. Larger species (whales,
contact. Ingestion of large quantities of oil by
elephant seals) generally require less food
these species is unlikely, and although baleen
per unit body weight (2o/<r-5% of body wt) as
fouling occurs in mysticete whales, it usually
adults.

resolves within 24-36 hr. Pinnipeds and

Sirenians thrive on a diet of hydroponic
cetaceans are susceptible to severe
grass and various lettuces and vegetables,

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puhnonary dan1age due to inhalation of
supplemented with high-protein monkey
volatile hydrocarbons as are other mammals,
chow, carrots, bananas, and multivitarninincluding people. Efforts to reduce human mineral supplements used particularly to
exposure to hydrocarbons when dealing with
balance calcium to phosphorus ratios. It is
oil-contan1inated anin1als is a top priority.

thought that sirenians ingest considerable

Treatment of exposed anin1als includes
anin1al protein incidentally cl ming grazing in
removal of oil from both the skin ( using mild
the wild. Intake requirements have been
detergents, eg, 2% New Dawn) and the GI
estimated at 7o/<r-9"Ai of body wt daily.

system ( activated carbon gavage ), along with

Sirenians are generally fed several times a
physiologic supportive therapy. For sea
clay to accommodate their grazing feeding
otters, use of warm wash water and provision pattern.

of soft freshwater reduces recovery time. It is

Sea otters are usually fed diets consisting
critical to recognize that capture, transport,
of vaiious invertebrates ( echinoderms,
and holding stresses appear to lower the
molluscs, occasional crustaceans) ai1d fish.

threshold of hydrocarbon toxicity in these

Adult anin1als require -25%-30% of their
animals.

body wt in food each day.

Polar bears in the wild have high-lipid

NUTRITION AND NUTRITIONAL
diets, particularly in winter when they

DISEASES
subsist heavily on seals. They are considered to have an exceptional dietary Generally, captive anin1als fed a diet that is
requirement for vitan1m A, ai1d some
solely or primarily fish are provided dead
clennatologic conditions respond to daily
fish that have been frozen. The logistics and
supplementation of 20,000-l,000,000 JU in
difficulty in providing this diet can lead to
the diet. Polar bears ai·e commonly feel lai·ge
some special nutritional concerns. All fish
amounts of fish in captivity.

are not of equal nutritional value; diets
consisting of a single species of fish are

Neonatal Nutrition: Young, unweaned
unlikely to provide balanced nutrition for
marine marnmals are frequently encounany animal. Sinularly, one diet will not serve tered in stranclings and must be fed a diet
all piscivores equally. Only fish suitable for
resembling their dam's milk In captivity,
human consumption should be fed. (See ai,so neonates may be abandoned by their NUTRITION: EXOTIC AND ZOO ANIMALS, p 2297.)

parents and require artificial rearing. The

Storage and thawing of frozen fish must
milk of marine man1111als has a high lipid
be monitored carefully. Feed fish should be
content. Most species are carbohydrate
held at or below -l9°F ( -28°C) to slow
intolerant, and neonates fed formulas with
deterioration of their nutiitional value
cai·bohydrates develop severe, life-threatenthrough oxidation of an1ino acids and ing bacterial gastroenteritis. Most neonatal
unsaturated lipids. Dehydration of frozen
marine man1111als also require in1111ense
fish can also be a problem for animals that
caloric density in replacement milks. Milk
obtain their water from food. Fatty fish
replacement formulas based on commercial
should not be stored >6 mo. Few fish, with
component-based milk replacers ( eg,
the possible exception of capelin, should

Zoologic® Milk Matrix) have begun to
be stored > 1 yr. To retain optimal vitamin
supplant some of the very complex
content and reduce moisture loss, frozen
scratch-made formulas used in the past.

fish should be thawed in air under

When confronted with a marine man1111al
refrigeration. Thawing in water leaches
neonate to raise, contacting one of the
away water-soluble vitamins. Thawing at
major marine mainmal rescue centers for
room temperature encourages bacte1ial
advice is recon1111ended.

growth and spoilage.

Phocid and otaricl seals can be reared

The energy requirements of marine
on the saine milk replacer-based formulas.

mammals vary with age, environmental

Pinniped pups should be feel every 4 hr in
temperatures, and condition. Young,
their first week of life; gradually, the an10unt
growing bottlenosed dolphins and smaller
of fonnula fed should be increased and the
pinnipecls generally require 9o/<r-15% of their
feedings dropped to five per clay. Harbor
body wt in high-quality fish per clay. Older
seal (Phoca vituli7W) pups should be tube
anin1als may need only 4o/<r-9"Ai of their body fed until 2-3 wk old, when they cai1 be

1860

MARINE MAMMALS
weaned to small pieces offish. Elephant
hydrochloride (up to 1 mg/kg body wt),
seal pups require tube feeding until they
followed by oral supplementation. Control
are 4 wk old, when weaning can begin.

usually involves supplemental thian1ine at

California sea lion (Zalophus califor

25 mg/kg food, preferably administered 2 hr
nianiis) pups can be force fed fish as early before a main feeding.

VetBooks.ir
as 4 wk of age and be free feeding by 6 wk.

Neonatal walruses (Odobenus rosrnarus) Vitamin E Deficiency (Steatitis, White have been reared on milk replacer-based

Fat Disease): The antioxidant properties
formulas, as well as on whipping-cream
of vitan1in E are believed to play an in1portant
base extended with ground molluscs (clams) role in maintaining the integrity of cellular rather than fish. They also seem to tolerate
membranes. Oxidative processes during the
carbohydrates reasonably well. Walruses
storage of fish destroy vitai11in E and other
have a much longer nursing pe1iod than
ai1tioxidants. Steatitis has been induced
other pinnipeds.

experimentally in phocid seals, and rela

Neonatal cetaceans have longer nursing
tionships between vitan1in E deficiency
periods than pinnipeds. Success at bottle
and hyponatren1ia are suspected. Captive
rearing has improved with experience,
piscivores commonly are supplemented PO
and individuals from species ranging from
with vitai11in E at a rate ofas much as 100
common dolphins (Delphinus delphis) to
mg/kg of feed, which generally maintains
gray whales (Escrichtiiis robustus) have
high serum levels of the vitan1in. This does
been reared successfully. The fat content
not appear necessary if feeder fish are
of cetacean milks varies considerably;
properly stored and thawed.

bottlenose dolphin (Tursiops spp) milk
is -17% fat (half that of most pinniped

Hyponatremia (Salt Deficiency,
milks); beluga whale (Delphinapterns leu

Addison Disease): Hyponatremia
cas) milk, 27%; harbour porpoise (Pho
in pinnipeds is closely related to adrenal
coena phocoena) milk, 46%; and mysticete
exhaustion and development of Addison
blue whale (Baleanoptera musculus)

disease, which links the syndrome to
milk, 42%. Formulas based on commercial
environmental stressors rather than to a
component milk replacers supplemented
simple primary salt deficiency. It is most
with ground fish and oils have been fed
common in pinnipeds maintained in
successfully to bottlenose dolphins and
freshwater exhibits but can be seen in
harbour porpoises using a lamb's nipple
animals kept in saltwater. It is more
or stomach tubing.

common in phocid seals but occurs in

Neonatal sirenians begin to nibble sea
otarids and other marine man1mals. Signs
grasses shortly after birtl1 but may continue
include periodic weakness, anorexia,
to nurse up to 18 mo. They can be reared on
lethai·gy, incoordination, tremor, and
aitificial milks with early weaning. Neonatal
convulsions. Serum sodium levels can fall
sea otters also have been reared successto <140 mEq/1. Severely affected animals fully from birtl1 on artificial formulas.

may collapse in an Addisonian crisis,

Neonatal polar beai-s are extremely altricial
which can be fatal.

and are a challenge because of an appar

Emergency therapy consists of sodium
ently irnmature immune system. Polai·
chloride infusion and replacement corticobear milk is high in fat (31 %) and contains steroids. Longterm management of advanced
minimal lactose. Polar bears have been
cases requires n1ineralocorticoid supplesuccessfully reared on fmmulas with a mentation in cortjunction with oral sodium
whipping-creain or oil base.

chloride supplements and periodic monitoring of serum sodium levels. Provision Thiamine Deficiency: This can be seen in
of saltwater pools and supplementation of
any piscivorous animal. Thian1ine in the food sodium chloride (3 g/kg food) in the diet of is destroyed by the activity of thian1inase
captive pinnipeds maintained in freshwater
enzymes or antithian1ine substances in the
pools should be considered a poor second
fish being fed. These active enzymes can also choice. Animals on salt supplementation destroy supplemental thian1ine placed in fish should have continuous access to if the fish sits for long periods before feeding. freshwater.

Clinical signs of thian1ine deficiency ai·e
primarily of CNS disturbances. Affected

Histamine Toxicity (Scombroid
anin1als may show anorexia, regurgitation,

Poisoning, Mackerel Poisoning):

or ataxia. The condition can progress to

Scombroid fish (mackerel, tuna) and other
seizures, coma, and death.

dai·k-fleshed fish have a short shelf life, even

Animals with signs of thian1ine deficiency
when frozen at low temperatures. A complex
respond rapidly to IM injection ofthian1ine
of substances, including histamine formed

MARINE MAMMALS

1861
by bacterial decarboxylation of the large
cephalitis, and hepatic and splenic necrosis.

amount of histidine found in the flesh of the

Transmission may be horizontal and
fish, is responsible for the signs seen in
vertical.

affected marine mammals. The toxicity can

The bacteria possess the same surface
also occur with nonscombroid fishes,
antigens commonly used for diagnosis in

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including poorly handled herring, ancholivestock. The prevalences of marine vies, or pilchard. It is most common in
mammal brucellosis are not known, but
pinnipeds but is seen in other marine
cases appear to be widespread. The role of
mammals. Clinical signs include anorexia;
environmental factors in the emergence of
lethargy; a red, inflamed mouth or throat;
ma.iine mammal disease is unknown.

and conjunctivitis and increased lacrirna

There is some evidence of potential for
tion. Occasionally, vomiting, diarrhea,
zoonotic infections, and there have been a
pruritus, urticaria, or postures indicative of
few cases of hun1an infections from marine
abdominal pain are seen. Antihistamines,
ma.inmals in those with contact with tissues.

including cimetidine, may provide

In one case, the cultured organism from the
symptomatic relief, but the condition is
blood of a laboratory worker matched a
generally sel f -limiting, and the animal
marine mammal strain she was working
begins feeding within 2 -3 days. In more
with. Three other human cases in which
severe or acute cases, epinephrine is
marine man1rnal-associated Brucella
effective in counteracting the histamine
strains were isolated had no documented
reaction. Cortisone and diphenhydramine
contact with marine man1mals but histories
hydrochloride can be beneficial in the face
of eating raw shellilsh or fish and contact
of respiratory difficulty. Control consists of
with raw fish bait.

avoiding scombroid fish in the diet or paying
careful attention to their quality, storage,

Clostridial Myositis: Severe myositis
and handling when used.

due to infections with Clost1idium spp has
been diagnosed in captive killer whales,

BACTERIAL DISEASES
pilot whales, bottlenose dolphins, California
sea lions, and manatees. All marine
mammals are probably susceptible. The

Actinomycetes: Nocardiosis (seep 666) disease is characterized by acute swelling,
is commonly reported in debilitated marine
muscle necrosis, and accumulations of gas
mammals. Several species of Nocardia have in affected tissues, accompanied by a severe been described from both captive and
leukocytosis. Untreated, it can be fatal.

free-ranging marine mammals of many

Diagnosis is based on detection of
species, both pinniped and cetacean.

gram-positive bacilli in aspirates of the

Diagnosis is usually postmortem, and most
lesions and is confirmed by anaerobic
affected animals present with a systemic
culture and identification of the organism:

form of disease. Infections due to Actino

Treatment includes systemic and local
myces or Arcanobacterium spp are receiving antibiotics, surgical drainage of abscessed considerable attention and have also have
areas, and flushing with hydrogen peroxide.

been diagnosed in many marine mammal

Commercially available inactivated
species. A rcanobacterium phocae has
clostridial bacterins are used routinely in
been in1plicated in pathology in stranded
some facilities, although efficacy in marine

California sea lion, common dolphin, gray
man1rnals has not been studied. Botulism
seal, harbor seal, northern elephant seal,
has been reported in captive California sea
and sea otter. A rcanobacterium anima
lions during an endemic outbreak of the
lium has been isolated from harbour
disease in waterfowl. Affected animals
porpoise, To date, most cases are diagnosed
stopped eating and appeared unable to
postmortem, but the infection may be
swallow several days before dying.

underreported.

Pneumonia: The chief cause of death in

Brucellosis: Since the 1990s, previously
captive marine mammals ( other than polar
unknown strains of Brucella have been
bears) is believed to be pneumonia. Most
found in free-ranging pinnipeds and
cases of marine mammal pneumonia have
cetaceans from many countries. 1\vo
significant bacterial involvement, and most
species have been classified: B ceti
organisms cultured from terrestrial species

(cetaceans) and B pinnipedialis (seals).

have been identified in marine ma111rnals.

There appears to be host preferences.

Pneumonia often can be considered the

Pathologic findings include placentitis,
result of mismanagement, although even
orchitis, abortion, mastitis, pneun1onia,
in carefully managed captive animals
subcutaneous lesions, artluitis, meningoen-
pneumonia-associated mortality is

1862

MARINE MAMMALS
common. Marine mammals require good
versial, and vaccine breaks can occur.

air quality, including high rates of air

Vials of killed erysipelas bacterin should
exchange at the water surface in indoor
be cultured for surviving organisms before
facilities. Tempered air or acclimation to
use in marine mainmals. Modified-live
cold temperatures is also important to
bacterins should be avoided for the initial
prevent lung disease, even in polar species.

vaccination. Fatal ai1aphylaxis can occur

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Animals acclimated to cold temperatures
on revaccination. For this reason, some
are usually quite hardy; however, sudden
vaccination prograins have been reduced
transition from warm environments to cold to one-time administration even though air, even with warmer water, can precipiantibody titers fall below the presumed tate fulminating pneumonias, particularly
effective level.

in nutritionally or otherwise compromised

If cetaceans are to be revaccinated,
animals. Clinical signs include lethargy,
sensitivity tests should be performed by
anorexia, severe halitosis, dyspnea,
injecting a small ainount of bacterin
pyrexia, and marked leukocytosis. The
submucosally on the lower surface of the
disease can progress rapidly. Diagnosis
tongue. Hypersensitive animals develop
is usually based on clinical signs and
swelling and redness at the injection site
confirmed by response to therapy,
within 30 min. Because the vaccine is
although bronchoscopy and fine-needle
extremely initating, no more than 3-5 mL
aspirates are being used more extensively
should be used at any one site, even in
to establish the cause of pneumonic
nonsensitive mammals. A long needle (<!2 in.

disease in marine mammals. Treatment

[5 cm]) should be used to assure that the
consists of correction of environmental
vaccine is deposited in the muscle and not
factors and appropriate intensive
between muscle and blubber, or a sterile
antibiotic and supportive therapy.

abscess can result. Bacterin should be
administered in the dorsal musculature

Erysipelas (Diamond Skin Disease):

anterior and lateral to the dorsal fin.

Erysipelas can be a serious infectious

Administration posterior to the dorsal fin
disease of captive cetaceans and pinnipeds
can result in a severe tissue reaction,
and has been recognized in wild harbour
inm10bilizing the a.J.1imal for several days.

porpoises, bottlenose dolphins, and harbor

To maintain high antibody titers, a booster
seals. The organism, Erysipelothrix
after 6 mo and annual revaccination are
rhusiopathiae, which causes erysipelas
required.

in pigs and other domestic species, is a
common contaminant of fish. A septicemic

Leptospirosis: This has been diagform of the disease in maiine mammals can nosed in otarid pinnipeds and bears. In be peracute or .acute; affected animals die
seals, the disease is characterized by
suddenly either with no prodromal signs or
depression, reluctance to move, polydipwith sudden depression, inappetence, or sia, and pyrexia. It may also cause abortions
fever. A cutaneous form that causes typical
and neonatal deaths in California sea
rhomboidal skin lesions is a more chronic
lions and Northern fur seals. Lesions
form of the disease. Ani1nals with this fom1
include a severe, diffuse, interstitial
usually recover with timely antibiotic
nephritis, with renal tubules packed with
treatment.

spirochetes. The gallbladder may contain

Necropsy of peracute cases generally
inspissated black bile, but hepatitis may
fails to reveal grossly discernible lesions
not be apparent grossly. Hyperplasia of
other than widespread petechiation.

Kupffer cells, erythrophagocytosis, and

Diagnosis is based on culture of the
hemosiderosis are seen histologically.

organism from the blood, spleen, or body

Gastroenteritis can be a feature. Antibodcavities. Arthritis has been found in anin1als ies to various Leptospira serovars (includthat have died with the chronic fom1.

ing£ Caiucola, L Icterohaemorrhagiae, Treatment of the peracute and acute

L Autumnalis, and L Pomona) have been forms has rarely been attempted, because
identified in many species, including
the absence of prodromal signs obscures
sea otters and manatee. Treatment in
the diagnosis. Animals with the dermatopinnipeds is similar to that in dogs (see logic fonn usually recover with administrap 650). Control in captive animals tion of penicillins, tetracyclines, or
requires serologic examination of new
chlorainphenicol and supportive treatanimals during quarantine. Captive ment.

animals can be vaccinated in endemic

Control seems primarily related to proareas. Leptospirosis is zoonotic, and vision of high-quality fish that is properly
appropriate precautions should be
stored and handled. Vaccination is contro-
taken.

MARINE MAMMALS

1863

Streptothricosis {Dolphin Pseudopox,
and is possibly of public health significance.

Cutaneous Dermatophilosis): Strepto

(See also TUBERCULOSIS AND OTHER MYCOBACTE
thricosis, a subcutaneous bacterial infection

R!AL INFECTIONS, p 687.)

withDermatophilus congolensis, has been
reported in pimlipeds and polar bears. It must Mycoplasmosis: Mycoplasma spp have be distinguished from sealpox. Simultaneous
been isolated from the teeth, wounds, and

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infections of streptotluicosis and pox have
respiratory tracts of seals. They have been
been recorded in sea lions. Cutaneous
associated with respiratory disease
streptothricosis usually manifests as sharply
historically but can be found in healthy
delineated nodules distributed over the entire animals. They are frequently cultured from body and usually progresses to death.

animals concurrently infected with

Diagnosis is based on demonstration of the
respiratory vi.ruses.

organism in biopsies or culture. Treatment
with prolonged high dosages of systemic

Miscellaneous Bacterial Diseases:

antibiotics can be successful.

Marine mammals are probably susceptible

Sporothrix schenckii, the cause of a
to the entire range of pathogenic bacteiia.

subcutaneous mycosis, has been reported in Pasteurella mitltocida has caused several Pacific white-sided dolphins (Laegenorhyn
outbreaks of hemorrhagic enteritis with
chus obliquidens).

depression and abdominal distress, leading
to acute death in dolphins and pinnipeds. It

Mycobacteriosis: Marine mammals
has also been reported to cause pneumonia
are susceptible to various mycobacteria.

in pinn.ipeds. In dolphins, Mannheimia

Evidence points to mycobacterial disease
haemolytica has been incriminated in
being possibly endemic in free-ranging
hemorrhagic tracheitis that responded to
otarids off the coast of Australia. Originally
chloramphenicol therapy.

thought to be caused by Mycobacterium

Plesiomonas shigelloides has been
bovis, subsequent molecular assessment
responsible for gastroenteritis in harbor
places the isolates from free-ranging
seals. Burkholderia, pseudomallei has
southern hemisphere pinnipeds in a unique
caused serious fatal outbreaks of disease
cluster assigned its own species in the M
in various marine mammals in captivity in
tuberculosis complex. Subantarctic fur
t.he Far East. Salmonella spp have caused
seals (Arctoce'J)halus tropicalis) are
fatal gastroenteritis in manatees and
thought to be the common link in the spread beluga whales. Staphylococcal septicemia of M pinnipedii to other piruliped species
has caused the death of a dolphin with
because they cohabit with the other !mown
osteomyelitis of the spine (pyogenic
affected species, Australian sea lions
spondylitis ). Another case of intradiscal

(Neophoca cinerea) and New Zealand fur
osteomyelitis, due to Staphyloc.occus
seals (Arctoce'J)halusforsteri). Otherwise, aureus, was treated successfully with a
mycobacteriosis has been a disease of
prolonged course of cefazolin sodium
captivity. Pinnipeds, cetaceans, and
and cephalexin. S aureus also has been
sirenians have developed disease due to M
incriminated in a fatal pneumonia in
bovis, M smegmatis, M chitae, M fortui
a killer whale. Vibrfo spp infect slow
tum, M chelonae, and M marinum.

healing wounds of cetaceans managed

Cutaneous and systemic forms are seen.

in open sea pens.

There are strong indications that immunosuppression may be involved in develop

MYCOTIC DISEASES
ment of infections by the atypical
mycobacte1ia.

Captive marine mammals seem particularly

Intradermal testing with high concentraprone to fungal infections (seep 632). Most tions of bovine or avian purified protein
appear to be secondary to stress, environderivative tuberculin can be used to screen mental compromise, or other infectious
exposed animals; however, anergy occurs
disease. Some systemic mycoses have
and the usefulness is controversial. In
distinct geographic distributions. Diagnosis
pinn.ipeds, iitjections in the webbing of the
is based on clinical signs and confirmed by
rear flippers should be read at 48 and 72 hr.

identification of the organism in biopsy or,

ELISA screening has identified antibodies in
preferably, culture. Wet mounts in lactoseals but requires further evaluation before phenol or cotton blue may render an
it can be considered a screening test.

immediate diagnosis witl1 some of the

Diagnosis is made by culture and identificamorphologically distinct fungi. Tissue tion of the organism from lesion biopsies,
smears cleared in warm l()OA, potassium
tracheal washes, or feces. Mycobacteriosis
hydroxide can be examined to identify
in marine mammals is an emerging disease
characteristic fruiting bodies or hyphae.

1864

MARINE MAMMALS

Topical medication of pinnipeds for
ineffective despite serun1 drug levels above
dennatophytosis is feasible. Smaller
the suggested therapeutic range.

cetaceans can be kept out of water in a sling
for 2-24 hr, if areas of the body not being

Dermatophytosis: Mycotic dermatitis
treated are kept moist. Otherwise, systemic
due to Trichophyton spp or Microsporum

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therapy is used.

can is generally responds to topical
povidone-iodi.ne, oral griseofulvin, or both.

Aspergillosis: Fatal pulmonary
aspergillosis has been diagnosed in

Lobomycosis: This disfiguring cutaneous
several species of cetaceans, including
disease is caused by infection with Lacazia
bottlenose dolphins and killer whales, and
loboi. The disease has been reported only in in several pinnipeds, including Antarctic
people and in Atlantic bottlenose Sota.lia
fur seals (Arctocephaliis gazella ), harbor

(Sotalia,ftuviatilis) dolphins. Culture of
seals, and California sea lions. In addition
the organism has not been possible. Exto disseminated aspergillosis, case reports cisional therapy and systemic antifungal of aspergillomas of the inner ear have
drugs have been used with varying sucbeen reported in free-ranging harbour cess. Zoonotic transmission is strongly
porpoise, and cutaneous aspergillosis has
suspected in a case of a European han-
been seen in gray seals (Halichoerus
dler of an infected dolphin. Most human
grypus) with concomitant mycobactericases have no history of marine mammal osis. The respiratory form has been a
contact. Differential diagnoses include
postmortem diagnosis. Cutaneous lesions
sporotrichosis, chromomycosis, paracochave responded to topical povidonecidiodomycosis, and other fungal diseas-iodine with ketoconazole therapy
es characterized by extensive granuloma

(10 mg/kg/day, PO).

formation.

Candidiasis: This common mycotic

Systemic Mycoses: The systemic
disease in captive cetaceans occurs
mycoses of marine manm1als are a zoonotic
secondary to stress, unbalanced water
risk, and precautions should be taken to
disinfection with chlorines, or indiscrimiprevent infection when handling dead and nate antibiotic therapy. Ca.ndidiasis is also
diseased animals. Cystofilobasidiales has
reported in pinnipecls and has been found in
caused fatal disease in a California sea lion.

cultures of wild cetacean blow holes and

Blastomycosis has caused fatal disease in
stomachs. In clinical disease in cetaceans,
bottlenose dolphins, California sea lions, a
the lesions usually are found around body

Stellar sea lion (Eumetopiasjubatus ),
orifices. At necropsy, esophageal ulcers are

Northern fur seals, and polar bears. Fatal
often found, particularly in the area of the
systemic histoplasmosis has been repmted
gastroesophagealjunction. In phocid
in a captive harp seal (Pagophilus
pinnipeds, inflammation at the mucocutane
groenlandicus ), a bottlenose dolphin, and a ousjunctions, particularly at the comrnis

Pacific white-sided dolphin. Coccidioidomysures of the mouth and around the eyes, cosis has been found in bottlenose dolphins,
anus, and vulva, is the common presenta

California sea lions, and sea otters. Blastion. Diagnosis is based on identification of tomycosis has been successfully treated
the yeast in cultures or biopsy. Canclidiasis
with intensive management, including 70
generally responds well to ketoconazole (6
days of itraconazole (3.5 mg/kg/day, PO)

mg/kg/day, PO) along with correction of any
combined with antibiotic and supportive
enviromnental deficits. Supplementation
therapy when indicated.

with-preclnisolone (0.01 mg/kg) may be
appropriate to compensate for ketoconazole inhibition of glucocorticoicl production. Zygomycetes: Dennatologic conditions caused by variousPusarium spp have been

Fluconazole (2 mg/kg, bid) has also been
used successfully. One anecdotal report sugreported in pygmy sperm whales (Kogia, gests a possible toxic reaction to ketocona
breviceps ), Atlantic white-sided dolphins
zole in a northern elephant seal (Mirounga

(Laegenorhynchus acutiis ), harbor seals,
angustirostris). Early detection and treatgray seals, California sea lions, and northment is usually successful. Another opportunern elephant seals. Diagnosis is based on istic yeast, Cryptococcus neoformans, has
culture or organism identification from
been diagnosed in fatal advanced pulmobiopsy. Cases have responded to ketonary disease in a bottlenose dolphin.

conazole (5 mg/kg/day for 10 days), flu

Prolonged treatment with itraconazole
conazole (0.5 mg/kg, bid for21 days), or

(120 days) at routine manm1alian doses was
itraconazole ( 1 mg/kg/day for 120 clays).

MARINE MAMMALS

1865

Mucor spp and Entomophthora spp have Mites have been associated with large,
caused fatal disease in bottlenose dolphins,
roughened lesions of the laryngeal area of
harbour porpoises, and harp seals. Other
cetaceans, but their overall significance or
zygomycetes have been diagnosed as a
treatment is unknown.

cause of fatal disseminated disease in

Demodectic mange has been diagnosed

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various species of marine mammals.

in California sea lions. Nonpruritic, alopecic

Localized fusariomycosis has been suclesions with hyperkeratosis, scaling, and cessfully treated in a captive beluga whale
excoriation develop on the flippers and

(Delphinapterus leucas) using voriconother body surfaces that contact the azole after surgical debridement. These
substrate. Diagnosis is made by deep skin
infections should be considered diseases
scrapings and identification of the mite.

of debilitated animals; the underlying

Secondary bacterial infection that results
cause of the low host resistance to these
in pyodem1a is seen in chronic cases.

opportunistic infections must be corrected

Treatment is the same as in dogs ( see
if therapy is to be successful. Amphoterp 920). Predisposing factors in pinnipeds icin B has been the therapy of choice for
are unknown. The mites are not readily
zygomycete infections, but newer imidatransmitted among contact animals.

zoles warrant consideration and may have

Heavy infestations of sucking lice are
clinical efficacy despite laboratory tests of
common in wild pinnipeds and can cause
resistance.

severe anemia. The lice can be seen grossly
and are readily transmitted. They are highly
sensitive to ivem1ectin as well as to

PARASITIC DISEASES
chlorinated hydrocarbon insecticides.

Rotenone powder is also effective. The

Marine mammals are susceptible to all of
affected animal must be removed from the
the major groups of parasites, including
water, allowed to dry before being dusted,
various nematodes, trematodes, cestodes,
and kept out of the water for � 12 hr.

mites, lice, and acanthocephalans. Clinical

Treatments must be repeated in 10-12 days.

experience with many of these is limited,

Animals in captivity can be freed of
whereas others are commonly seen in
parasites if no new sources of infestation
recently captured specin1ens.

are introduced.

Acanthocephalans: Cetaceans are

Lungworm: Lungwonns are common in
the primary host of Bolbosoma spp but
all pinnipeds. Sea lions have ParajUaroides
can be infested with parasites of the genus
decorus, whereas true seals are usually

Corynosoma, which have pinnipeds and sea parasitized by Otostrongylus circumli
otters as primary hosts. Bolbosoma spp
tus. The latter parasite is also found.in
have been reported in pinnipeds. C enhydra
the hearts of some phocids; however, it
has only been reported from sea otters.

does not produce a microfilaremia. Both

Diagnosis is by detection of eggs in feces,
of these parasites use fish as intennediate
but clinical disease and therapy are not well
hosts. There are at least four species of
documented. Three species of ProjUicoUis
lungwonns in various cetacean hosts, in

(also found in birds) are reported to cause
cluding Halocercus lagenorhynchi, which
peritonitis associated with intestinal
has caused prenatal infections in Atlantic
perforation in sea otters. Mortality usually
bottlenose dolphins.

occurs before the parasite produces ova.

Lungwonn infection can be diagnosed by

Premortem diagnosis is problematic. No
exan1ination of feces or bronchial mucus.

successful treatment has been reported.

Anorexia, coughing, and sometimes
blood-flecked mucus are the first signs of

Acariasis: Nasal and lung mites are found
pulmonary parasitism. Treatment of P
in phocid and otarid seals. Lung mites cause
decorus infection consists of mucolytic
rattling coughs. Nasal mites cause nasal
agents administered intratracheally,
discharge but apparently little discomfort.

antibiotics to treat any concomitant

Diagnosis is made by identifying the mite in
bactelial pneumonia, ivennectin, and
nasal secretions or sputum. The life cycles
concurrent prednisone or dexamethasone.

of these mites are not completely known.

Diagnosis of O circumlitus in elephant

Infections have been cleared rapidly with
seals is complicated by mortality occurring

Lwo i.ajecLions of ivennecti.n at 200 mcg/kg,
after generalized clinical signs of depres2 wk apart. Treatment of infected anin1als sion, dehydration, and neutrophilia before
elin1inates the problem in captive enclothe parasites become patent and first-stage sures without environmental treatment.

larvae can be detected in sputum or feces.

1866

MARINE MAMMALS

Some treatment success has been reported
the advantage of oral administration. Prevenusing intratracheal administration of tion in endemic areas has been successful
levamisole phosphate (5 mg/kg/day for 5
with oral administration of ivem1ectin
days); however, combined therapy with

( canine dosages) monthly or diethylcarivermectin and fenbendazole given 3 days bamazine (3.3 mg/kg) weekly in food during
after initiation of therapy with dexamethathe mosquito season (see also p 127).

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sone, antibiotics, and mucolytic agents may
be more effective. Cetacean lungworms

Other Nematodes: The Anasakidae are
probably are also susceptible to levamisole
pathogenic nematodes found in the stomach
and ivennectin; however, the sudden deaths
of marine mammals. Granulomas fmm at
of two beluga whales irtjected IM with
their attachment sites and can lead to blood
levamisole phosphate suggest this drug
loss, ulceration, and ultimately perforation
administered by that route may be
and peritonitis. Raw fish is most often
contraindicated. A percentage of pinnipeds
incrinlinated as the source of infection.

also show neurologic reactions to IM

Infections with Contracaecum spp are
injection of levamisole; PO or SC adminiscommon in wild cetaceans and pinnipeds.

tration has been recommended.

Polar bears in captivity are prone to heayy

Lungworm infections often remain
ascarid infection. Gastric nematodes can be
asymptomatic for long periods, with clinisuccessfully treated with oral dichlorvos cal signs appearing only when an animal

(30 mg/kg), fenbendazole (11 mg/kg), or
becomes debilitated for other reasons. In
mebendazole (9 mg/kg) given twice, 10 days
captivity, lungworm infections are usually
apart. Ivem1ectin may be considered.

self-limiting if larvae are not introduced in

Hookworms ( Uncinaiia spp) are found
fresh fish intermediate hosts. Feeding
in pinnipeds. Severe infections are known
frozen fish prevents reinfection.

in fur seals. Newborn fur seal pups are
infected via colostrum. Disophenol

Heartworm: Heartworms of the genus

(12.5 mg/kg) or ivermectin (100 mcg/kg)

Acanthocheilonema are a common
injected SC have been effective against
necropsy finding in pinn.ipeds. Phocid seals
these parasites.

are affected by A spirocauda, and otarids

Many species of a large spirurid
are infected subcutaneously by A odendhali. nematode ( Crassicauda spp) infect the Transmission of A spirocauda is thought to
cranial sinuses, major vessels, kidneys,
be by the seal louse (Echinophthirius
and man1mary gland ducts of cetaceans.

lwrridus ). Both groups of pinnipeds can

Successful treatments are not docun1ented
be infected with the canine heartworm,
but are potentially possible with systemic

Dirofuaria immitis, in endemic areas;
parasiticides. The dual intermediate host
however, phocid seals are abnom1al hosts.

requirement of these species in captivity

Dirofilariasis is diagnosed by identifying
usually means these infections are
microfilariae in the blood. Transmission is
self-limiting.

thought to be by the san1e mosquitoes that
bite dogs. A graded regimen of levamisole

Cestodiasis: Diphyllobothrium
phosphate progressing to a fugh dosage
pacijicum is commonly found in sea lions,

( 40 mg/kg/day for 1 wk) has successfully
and heayy infection is thought to cause
cleared infection in captive pinnipeds, with
intestinal obstmction. Praziquantel

(10 mg/kg) is an effectiv� treatment.

(

Other cestodes commonly seen include

D lanceolatum in phocid seals, Diplogonoporus tetrapterous in all pimlipeds, and Tetrabothriumforsteri and Strobilocephalus triangularis in cetaceans. Cetaceans are also commonly infected with subcutaneous tapeworm cysts throughout the blubber.

These usually are the larval fom1s of
tapeworms of sharks. Several species of
cestodes are reported in sea otters and polar
bears but are not known to have clinical
significance.

Trematodiasis: Fluke infections are
common in pinnipeds and cetaceans;

Acanthocheilonema microfilariae. Courtesy of Nasitrema spp are found in the nasal

Dr. James McBain.

passages and sinuses of cetaceans. Ova

MARINE MAMMALS

1867
of these trematodes have been associated
cetacean, otarid, and phocid species and are
with necrotic foci in the brains of animals
often not associated with any recognized
showing behavioral aberrations and have
clinical signs. Successful treatment has
been incriminated as a cause of localized
been reported in an adult California sea lion
pneumonia in cetaceans. Infections are
with myositis using ponazuril (10 mg/kg/
often accompanied by halitosis and brown
day, PO) for 28 days and prednisolone in the

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mucus around the blowhole and occasionfirst 5 days of therapy.

ally by coughing. Diagnosis is based on demonstration of typical operculated trematode Toxoplasmosis: Toxoplasma gondii is ova in blowhole swabs or feces. Oral
known to infect the California population of
praziquantel (10 mg/kg, two treatments 1
sea otters, causing disease that ranges from
wk apart) is usually effective. Reinfection
asymptomatic infection to severe encephalican be prevented by not feeding fresh or live tis. Fatal meningoencephalitis due to T
fish.

gondii has also been reported in a Florida

Zalophotrema he-paticum is an
manatee and disseminated disease in
important hepatic trematode of California

Antillean manatees. Toxoplasma spp
sea lions; it causes biliary hypertrophy and
encephalitis is also reported in harbor seals
fibrosis of the liver. Signs are usually seen
and Northern fur seals. Disseminated
in adults and include icterus, lethargy, and
toxoplasmosis is reported in California sea
anorexia. Bilirubinemia and increased
lions. T gondii is reported from Atlantic
serum hepatic enzymes are common.

bottlenose, Risso's (G'rampus griseus),

Diagnosis is based on identification of
striped (Stenella coeruleoalba), and spinner trematode ova in the feces. Treatment with
dolphins, and serologic evidence of
praziquantel ( 10 mg/kg) or with bithional
toxoplasmosis is being discovered in an

(20 mg/kg) has been successful.

ever0widening arTay of marine manm1al

Various other trematodes infect the
hosts, including polar bears. No successful
stomach, intestines, liver, pancreas, and
treatment has been repmted. n·ansplacenother abdominal organs of marine tal transmission has been reported in a
mammals. Pancreatic fibrosis due to

Risso's dolphin.

trematodiasis is a common necropsy
finding.

VIRAL DISEASES

Coccidiosis: Coccidia (Eimeria phocae)

have been found in harbor seals with a fatal,

Adenovirus: Adenovirus has been
bloody diarrhea. Clinical disease with this
isolated from a sei whale (Balaenoptera
parasite is thought to be rar·e unless the host
borealis), beluga whale, and bowhead
is stressed through capture, handling, or
whales (Balaena mysticetus ). A novel
husbandry changes. At least two new
otarine adenovims 1 has been isolated from
species of intestinal coccidia have been

California sea lions affected with hepatic
identified in California sea lions. A
disease, and adenovirus particles have been
coccidian, Cystoisospora delphini, has
reported in walms and fur seals. Fatal
been repo1ted as the cause of enteritis in
disease associated with adenovitus
bottlenose dolphins; however, some
infection has been reported in California sea
consider the parasite to have been a fish
lions, South African fur seals, and South
coccidia not associated with the disease.

American sea lions. No disease was noted in

E trichechi reported from the Amazonian
the cetaceans.

manatee (Trichechus inunguis ), and

The most prominent histologic lesion in

E nodulosa repo1ted from the Florida
all cases was hepatic necrosis. Massive
manatee, are also not associated with
coagulation necrosis without apparent
disease. These coccidia are probably
zonal distribution was seen in some
susceptible to ar1ticoccidial drugs used
animals. Basophilic intranuclear inclusions
against other species, eg, an1prolium. (See
in hepatocytes or granular an1phophilic
also p 203.)

intranuclear inclusions in Kupffer cells were
seen. No evidence of adenovirus was

Sarcocystis: Sarcocystis neurona is detected in the lungs. Adenovirus from
found in high prevalence in the California

California sea lions is not known to cause
population of sea otters. Infection can be
disease in people.

asymptomatic or cause severe encephalitis
characterized by generalized neurologic

Caliciviruses (San Miguel Sea Lion
signs. No successful treatment of neuro

Virus): Calicivimses have been isolated
logic cases has been reported. Sarcocystis
from otar·id seals, walms, Atlantic
spp have been found in the muscles of many
bottlenose dolphins, and opaleye fish

1868

MARINE MAMMALS

(GireUa nigricans). The marine calicivi

PhHV-2 has been associated with
ruses appear to be serotypes of vesicular
recurring circumscribed areas of alopecia
exanthema of swine virus (VESV, see

-0.5 cm in diameter in gray seals. Herpetic
p 738). Several species of mysticete
lesions in beluga whales are generally
cetaceans have antibodies to different
circular, as much as 2 cm in diameter, and

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serotypes of VESV. By 4 mo of age, most
may appear slightly depressed with a target

California sea lions have neutralizing
appearance or be raised and proliferative.

antibodies to one or more of the serotypes.

The centers of some lesions are necrotic or

Opaleye fish are probably responsible for
may contain verrucous growths. Systemic
the endemic status of caliciviruses in
infections have not been documented in the
marine manunals that inhabit the coastal
cetaceans.

waters of California. To date, infections

Diagnosis is often made at necropsy or
have not been diagnosed in marine
by clinical signs and observation of charmanUt1als in the Atlantic Ocean.

acteristic intranuclear inclusion bodies

The most consistent lesion in marine
in biopsies of early skin lesions. In seals,
manunals is skin vesicles. In pinnipecls, the
interstitial pneumonia caused by herpesvivesicles are most prevalent on tl1e dorsal rus must be distinguished from bronchial
surfaces of the fore flippers. In dolphins,
pneumonia caused by influenza virus.

vesicular lesions have been seen in associa

In systemic herpesvi.rus infection, therapy
tion with "tattoo" lesions and old scars.

is supportive. In a documented epidemic,

Vesicles are 1 mm to 3 cm in diameter. They
oral acyclovir did not eliminate tl1e infection
usually erode and leave shallow, fast-healing
but appeared to significantly shorten clinical
ulcers, but occasionally vesicles regress and
signs in primary infections. Vaccination
leave plaque-like lesions. Treatment is
with 1 mL of trivalent poliovirus vaccine
supportive only; skin lesions usually resolve
to control recrudescence of suspected
without treatment Infection may cause
herpesvirus lesions has been used with
premature parturition in pirmipecls. Affected
some success; although it reduced the
pups have interstitial pneumonitis and
severity of recrudescence in seals, there is
encephalitis and fail to thrive.

a potential public health risk because live

Inoculation of marine caliciviruses into
poliovi.rus may be shed after vaccination.

pigs causes vesicular lesions identical to

Stress and immunosuppression are assothose seen in vesicular exantl1ema. In ciated with recrudescence of latent
people, heavy exposure to marine
infections. There is no evidence that the
caliciviruses can result in neutralizing
herpesviruses of pinnipeds or cetaceans
antibodies. Localized lesions in an
are zoonotic.

accidental laboratory exposure as well as
isolation of calicivirus from a clinically ill

Influenza Virus: Four different
primate indicate that these viruses should
influenza A viruses have been isolated
be handled carefully.

from harbor seals and two other subtypes
from a stranded pilot whale. HIN 1 has

Herpesvirus: Herpesviruses isolated
been isolated from a northern elephant
from pinnipecls include phocitl herpesvirus
seal. Serologic evidence of exposure to

1 (PhHV-1), an alpha herpesvirus, and four
influenza virus exists for a wide range of
ganm1a herpesviruses, phocid herpesvirus 2
marine mammals. Infection is probably

(PhHV-2), Hawaiian monk seal herpesvirus,
common. Only nonspecific clinical signs

Otarid herpesvirus 1, and Northern elephant were reported in the stranded pilot whale, seal herpesvirus. Herpesviruses have been
which had difficulty maneuvering, was
identified in a wide range of cetaceans,

\ emaciated, and was sloughing skin.

some associated with encephalitis and

Disease due to influenza virus in seals is
others with various skin lesions.

better characterized. Even well-fed

Young harbor seals from Atlantic waters
captive animals become weak, incoordiinfected with PhHV-1 develop nasal nated, and dyspneic. Swollen necks due
discharge, inflanunation of the oral mucosa,
to fascia! trapping of air escaping through
vomiting, diarrhea, and fever, followed by
the thoracic inlet is reported. Occasioncoughing, pneumonia, anorexia, and ally, white or bloody nasal discharge is
lethargy that can result in death in 1-6 days.

evident. The incubation period during

Morbidity can approach 100% in stressed
epidemics in harbor seals is ,,;3 clays.

seals in crowded conditions; mortality is

Many factors probably contribute to

-500/o. The incubation period appears to
the explosive nature of the reported
be 10-14 days. Pacific harbor seals witl1
epidemics. High population densities and

PhHV-1 tend to develop signs related to
unseasonably warm temperatures
adrenal and hepatic dysfunction.

contribute to high mortality.

MARINE MAMMALS

1869

In harbor seals, influenza pneumonia is

America, in large part due to Jack of
characterized by necrotizing bronchitis and
availability of the appropriate vaccine.

bronchiolitis and hemorrhagic alveoli tis. In
the pilot whale, the lungs were hemorrhagic
and a hilar node was greatly enlarged. For

Poxvirus: Poxvirus has been identified

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differential diagnosis, see HERPEsvrnus,
morphologically in skin lesions of both
above.

captive and free-ranging pinnipeds and

The virulence of epidemics has precluded cetaceans of a wide range of species.

attempts at intensive supportive care.

Lesions in California sea lions, harbor seals,

People whose eyes were contaminated
and gray seals are probably due to parapoxwhile doing necropsies, or by being sneezed viruses; lesions in South American sea lions
on by affected seals, have developed kerato

(Otaria byrnnia) and Northern fur seals are cortjunctivitis within 2-3 days, and identical
probably not. An orthopox virus has been
virus has been recovered. All affected
isolated from pox-like lesions on a gray seal.

people have recovered completely within

Poxvirus has also been associated with skin

7 days without developing any antibody
lesions in Atlantic bottlenose dolphins,
titers, which suggests that the reaction is

Atlantic white-sided dolphins, killer whales,
local, as occurs with Newcastle disease
dusky dolphins, long-beaked common
vims.

dolphins (Delphinus capensis ), Hector's
dolphins (Cephalorhynchus hectori),
and Bunneister's porpoises (Phocoena.

Morbillivirus: Phocid seals are susceptible
spinipinnis ), among others.

to canine distemper virus ( see p 777) and to a Outbreaks typically occur in postweanling
closely related but distinct morbillivilus
pinnipeds recently introduced into captivity.

(phocine distemper vims [POV]). Generally,

The incubation period is 3-5 wk A break in
young seals are affected and show depresthe epitl1elial surface may be required to sion, anorexia, crusting conjw1ctivitis,
start an infection. Lesions can recur. Small,
nasal discharge, and dyspnea. Pnewnonia
cutaneous, raised nodules (0.5--1 cm in diamdevelops, and mortality can be high in eter) occur on the head, neck, and flippers of
previously unexposed animals. Outbreaks in
affected pinnipeds. These may increase to
wild harbor seals have been extensive in the

1.5--3 cm in dian1eter dwing the first week

North Sea. Seals vaccinated witl1 canine
and may ulcerate or develop satellite lesions
distemper vaccine have been rendered
during the second week After the fourth
immune to challenge with the virus
week, lesions begin to regress, although

( suspension of organ material) obtained
nodules are reported to persist as long as
from dead wild seals.

15--18 wk Areas of alopecia and scar tissue

A delphinoid distemper virus ( cetacean
may remain after resolution.

morbillivirus [CMV]), closely related to

Cutaneous poxvirns infections in
rinderpest (seep 771) and peste des petits
cetaceans can develop on any part of the
ruminants (seep 766), has been implicated body, but lesions are most common on the in the deaths of harbour porpoises and
head, pectoral flippers, dorsal fin, and tail
common dolphins off the coast of the UK,
fluke. They range from ring or pinl1ole
striped dolphins in the Mediterranean, and
lesions to black, punctiform, stippled
bottlenose dolphins in the western
patterns ("tattoo" lesions). Ring or pinhole Atlantic and Gulf of Mexico. Pilot whale
lesions appear as solitary, 0.5--3 cm, round
calves, white-beaked dolphins (Laegeno
or elliptical blemishes, which sometimes
rhynchus albirostris), harp seals, hooded coalesce. They are usually light gray and seals (Cystophora cristata), and
may have a dark gray border, although the

Mediterranean monk seals (Monachus
reverse color pattern is also seen. Lesions
monachus) have been affected by POV
may persist for months or years without
and/or CMV infections. In the wild, harp
apparent ill effects.

seals and pilot whales have been incrimi

Major differential diagnoses include
nated as apparent reservoirs of POV and
cutaneous streptotlrricosis and calicivirus.

CMV, respectively.

Diagnosis is based on the presence of

Therapy is supportive. Mortality in naive
eosinophilic, intracytoplasmic inclusion
populations is high, often due to secondary
bodies in lesion biopsies and is confirmed
infections facilitated by the immunosupby identification of typical poxvirus pressive impact of active morbillivirus
paiticles by electron microscopy.

infection. Vaccination with a subunit

Poxvirnses of marine mai11111als do
vaccine is practiced in European rescue
not appear to cause systemic infections.

centers and appears to be protective, but

Although animals witl1 cutaneous poxvirus
this approach has not been applied in North
lesions have died, other factors were

1870

MARINE MAMMALS
responsible. Therapy to control secondary
common dolphin, Risso's dolphin, harbour
bacterial infections is indicated only when
porpoise, and white-beaked dolphin. The
skin lesions suppurate. The pa.rapoxviruses
only retrovims cultured and characterized
of pinnipeds can cause isolated lesions on
to date in a marine mammal was a spumavi

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the hands of people not wearing gloves
rus isolated from recurring skin lesions in a
during contact with infected animals.

California sea lion that subsequently died
of Pasteurella pneumonia complicated

Miscellaneous Viral Diseases: A 1inged
with herpesvirus.

seal (Phoca hispida) in Norway was diag

Coronavirus infections have been
nosed with rabies, which was confinned by
associated witl1 pneumonia epizootics in
inmmnofluorescent examination of the
wild Pacific harbor seals. A coronavilus has
brain. At the time, there was an epidemic of
also been identified in a beluga whale.

rabies in foxes in the area Other rhabdovi

An entcrovims of unknown pathogenicity
mses isolated from cetaceans, which are not isolated from a rectal swab of a California recognized by antisera to representatives
gray whale has been reclassified as a
of the Lyssavirus, Ephemerovirus, or
calicivims. Antibodies, unassociated with

Vesiculovirus genera, may be related to
disease, against human i.niluenza vims
rhabdovimses of fish.

(after challenge) and poliomyelitis virus

Papillomavims infections have been
were found in bottlenose dolphins.

reported in a wide range of cetaceans,

Enterovirns has been found associated with
including narwals (Monodon monoceros)

tongue lesions in bottlenose dolphins.

and several species of mysticete whale.

Severe enteritis and vomiting that rapidly

Lesions are typical of those found in
led to death in a captive beluga whale were
terrestlial species. No therapy is !mown.

suggestive of parvovirns entelitis, but no

Lesions are usually self-limiting.

viJ·us was isolated.

Hepadnavirus infection with a hepatitis

B-like agent has been documented in a

Pacific white-sided dolphin with a long

NEOPLASTIC DISEASES
history of recurrent illness in captivity.

No evidence of zoonotic transmission

Tumors in marine mammals are infrequent,
was identified.

although a wide valiety has been reported.

Endogenous gamma retroviruses have

They are of little consequence except for
been identified in the genome of killer
malignant lymphoma in harbor seals, in
whale, bottlenose dolphin, Atlantic
which holizontal transmission can occur
white-sided dolphin, long-finned pilot
in a closed population, and transmissible
whale, striped dolphin, short-beaked
venereal twnor of California sea lions.

MINK

MANAGEMENT

&ir circulation and shade in the waimer
months.

Mink (Mustela vison) are housed individu

Mink feed may be supplied as a wet gruel
ally in raised, wire mesh pens. A nest box
placed on top of the wire mesh or as a
with a hole for entry is attached outside or
conm1ercially prepai·ed, dJy, pelleted ration
placed within the pen. Wood used for the
placed in feed hoppers. During the weaning
nest box should not be painted or treated
and postweaning peliods, food is supplied on
with wood preservatives. Soft, awn-free
feeding trays or placed on an acljustable wire
marsh hay, clean straw, untreated dry wood
nest box cover for small kits that Call.llot
shavings, or fine wood-wool make suitable
reach the top of the pen. Fresh water should
nest matelial. Nest boxes should be cleaned
always be available. Wateling cups fastened
and nest mate1ial replaced as required,
to the outside of the pen with a lip protruding
especially before whelping. Sheds are used
inside are used. Automatic, heated, recirculatthroughout the year and should admit ing wateli.ng systems with individual nipples
natural daylight. There should be plenty of
are most commonly used in sheds.

MINK

1871

Cold storage facilities are necessary to
for the hun1ane treatment of animals by the
freeze and store the meat portion of the

Fur Commission USA.

ration. A day's supply of fish and meat
by-products is thawed, commercial cereal

BACTERIAL DISEASES

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and vitan1ins added, and the combined
ration mixed with water to a consistency
that will remain on the wire of the pen

Botulism: Botulism (seep 605) occasionwithout dropping through. Ready-mixed ally causes heavy losses in unvaccinated
feeds may be delivered daily, either ready to
mink that constm1e feed containing type C
feed or in frozen blocks that are thawed as
toxin. Usually, many mink are found dead
required. Dry pelleted diets are used on
within 24 hr of exposure to the toxin, while
some ranches for part or all of the year.

others show varying degrees of paralysis

Ranchers usually keep one male for each
and dyspnea. Necropsy findings are
five female breeders. Mink are seasonal
nonspecific and related to death from
breeders, with reproductive activity
respiratory paralysis. Diagnosis is
controlled by increasing periods of daylight.

confirmed by inoculation of serum or

Artificial lights in the sheds must be used
filtered tissue from affected mink into mice.

with caution, because they may adversely

The immw1otype of the botulism toxin is
affect photoperiod and interfere with the
type C in almost all outbreaks.

normal reproductive cycle. In the northern

Toxic feed should be removed and
hemisphere, the breeding season begins in
sampled for testing, and stored feed or
late February or early March and lasts -4
ingredients tested for the toxin. Recovered
wk. Mating should occur within 1 hr after
mink are not in1mune to further challenge.

the female is placed in the male's pen. If

Annual vaccination of kits (at 6-8 wk) and
fighting ensues, they should be separated.

breeders with vaccines containing type C

Ovulation is induced by mating. Females
botulism toxoid, Pseudomonas bacterin,
mated before mid-March are usually mated
distemper, and mink virus enteritis vaccines
again after 7-8 days, often with an additional is highly recon1mended.

mating the following day; thus, individual
females may be mated two or three times.

Hemorrhagic Pneumonia: Pseudo

Ova from two matings have been known to
monas aeruginosa may result in serious
develop in the same litter. Implantation of
losses. Mink of all ages are affected,
the fertilized ova is delayed, so the apparent
particularly during the stress of fal! molt.

gestation period is 40--75 days. The implanta

Mink are usually found dead with no
tion period can be altered by using artificial
prodromal signs. A bloody nasal exudate
light after breeding.

may be seen at the time of death. Gross

Mink have one annual litter of 1 to 12 kits
lesions include a severe hemorrhagic

(average 5). Most kits are born during the
pneumonia with swelling and consolidation
last week in April and the first 2 wk in May.

of one or more lung lobes. Treatment

Kits are blind, hairless, and weigh -10 g
involves inunediate vaccination of the entire
when born but grow rapidly throughout the
herd. APseudomonas bacterin is included
summer to reach a weight of -1,200 g
in the recommended 3-way vaccine (see

(females) or 2,600 g (males) by October.

above).

Kits are weaned at -6-8 wk of age and may

Escherichia coli has become the more
be separated shortly thereafter and housed
common cause of hemorrhagic pnew11onia
in single pens. Adult mink are extremely
in mink as a result of vaccination against
agile, strong, and vicious. Handling requires

Pseudomonas. Gross and clinical signs are
the use of special leather gloves or wire
indistinguishable from those of Pseudo
catching cages.

monas. Bacterial culture is the only way to Mink kits are vaccinated when at least
determine which pathogen is present.

6-8 wk old with a 3-way vaccine containing

Exposure to E coli most frequently comes

Pseudomonas bacterin, botulism, and mink
from contaminated water, but it may also
enteritis virus, and again when at least 10
be feedborne. Underlying viral infections
wk old with a modified-live distemper
such as influenza, Aleutian disease, and
vaccine. Breeders should be revaccinated in
distemper must be excluded. Antibiotic

December or January before the breeding
sensitivities are a must to assist with
season.

treatment selection, because sensitivity

Pelt collection usually is done in
patterns for E coli in mink vary greatly.

November or December. The most humane
way to kill mink is with pure cooled carbon

Urinary Infections and Urolithiasis:

monoxide in cylinders. In the USA, mink

Urinary tract infections, commonly called
farms are certified under the strict criteria

"plum bladders," cause serious losses in

1872

MINK
females in late spring ( during pregnancy

Treatment should be based on antibacand lactation) and in males in late swnmer terial sensitivity tests. Drugs may be
and autumn ( during the rapid growth and
administered parenterally or in the feed or
furring period). Several predisposing
water. Dosage can be estin1ated on the basis
factors have been suggested, including
of body wt; female mink weigh -2-3 lb

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contamination of food, cages, or nest boxes

(0.9-1.4 kg), and males -5-6 lb (2.3----2.8 kg).

by pathogenic bacteria; decreased water

Dosages recommended for cats should be
intake; or increased ash intake.

used and adjusted for weight. However,

Mink may die without showing signs, but
some sulfonan1ides ( eg, sulfaquinoxaline
a large, distended bladder can be palpated
and sulfainethazine) ai1d streptomycin
grossly, or they may have difficulty in
should not be used in mink. TI·imethoprim/
urinating or dribble urine. Occasionally,
sulfadiazine causes abortions in pregnant
hematuda may be seen. Necropsy findings
female mink.

include acute hemorrhagic cystitis or

The source of infection should be
pyelonephritis, usually associated with
detennined and eliminated. Enteritis often
calculi (magnesium ammonium phosphate)

is caused by containinated or spoiled feed
in the bladder or kidneys. Various organand dirty nest boxes. Abscesses are often isms, including staphylococci, coliforms,
caused by if\iury from wire or splintered
and Proleus sp, have been isolated.

wood in the pens, awns in hay or straw used

In severe outbreaks, culture and
for bedding, or spicules of bone in the feed.

antibiotic sensitivity tests should be done,

Outbreaks of tularemia, anthrax, brucelloand medication added to the feed. Good sis, tuberculosis, and clostridial infections
sanitation to reduce environmental
have been caused by feed contan1inated
contamination and increasing the water
with tissue of animals that have died or
supply help prevent the condition. When a
are carriers of these infections. Cai·efuJ
continual problem exists (with magnesium
selection of feed ingredients and disinfecarnmoniwn phosphate calculi), feed-grade tion of equipment and pens are impo1tant in

(75%) phosphoric acid may be added to the
prevention and control of many infections.

feed (0.8 lb/100 lb [8 g/kg] of wet mixed

Dead stock should not be used as mink feed.

feed), from March to early June and from
mid-July to October, to reduce the urine pH.

VIRAL DISEASES

Feed and urine pH should be monitored
to keep urine pH at �6. Feed pH should not
be <5.1.

Aleutian Disease (Plasmacytosis):

Aleutiai1 disease is a parvovirus infection

Mastitis: A variety of bacteria, mainly
characterized by poor reproduction, gradual
staphylococci, streptococci, and Escheri
weight loss, oral and GI bleeding, renal
chia coli, are involved in mastitis in mink.

failure and uremia, and high mortality. All

Staphylococcal mastitis typically results in
color phases of mink may be infected, but
abscessation of affected glands or subclinilight color phases genetically derived from cal disease evidenced only by mild diarrhea
the Aleutiai1 color phase are most susceptiin the kits. E coli causes a peracute, •
ble. The causative parvovirus is not related
necrotizing mastitis similar to that seen in
to mink viral enteritis (see below).

dairy cattle. Predisposing factors include

TI·ansmission occurs in utero ai1d by direct
poor nest box and cage sanitation, rough or
or indirect contact witl1 infected rµink.

sharp edges to the entrance of nestboxes,

After infection, immunoglobulin levels
and high bacterial contamination of feed.

frequently increq.5e markedly. Inununoglob

Treatment and prevention involve improving ulins ai·e tmable to neutralize the virus; management and treating individual animals
inunune complexes form and deposit in
or the herd with appropriate antibiotics
various tissues, resulting in inuntme-combased on sensitivity testing.

plex glomerulonepluitis and aite1itis. Gross
pathologic changes include splenomegaly,

Miscellaneous Bacterial Diseases:

renal changes ( varying from swelling and

Vaiious diseases or signs of disease,
petechiation to atrophy and pitting), and
including septicemia, pnewnonia, purulent
enlai·gement of mesenteric lymph nodes.

pleuritis, abortions, abscesses, cellulitis,

Histologic lesions include plasma cell
and enteritis, occur sporadically; occasioninfiltration in the kidneys, liver, spleen, ally, they may become herd problems. Many
lymph nodes, ai1d bone matTow; bile duct
bacteria, incluilingProleus, Klebs'iella, and proliferation; membranous glomerulone

Campylobaclerspp, coliforms, streptophritis; and fibrinoid aiteritis. Kits from cocci, staphylococci, and salmonellae, have

<la.ins negative for Aleutian disease virus
been isolated.

may die from acute interstitial pnetU11onia.

MINK

1873

Aleutian disease is controlled through a
and ventral abdominal wall; neurologic
test and slaughter program. Positive mink
signs ( convulsions and "screanling fits"); or are identified by blood testing for specific
a combination of these. Histologic ELISA,
antibody by counterirnmunoelectrophoresis inununohistochemistry, or fluorescent or lateral flow ELISA. All positive mink
antibody examination may reveal intra

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should be culled. Mink to be kept for
cytoplasmic or intranuclear inclusions or
breeding stock should be tested in late fall
distemper antigen in epithelial cells of the

(before selection of breeding stock and
bladder, kidneys, bile ducts, intestine, lungs,
pelting) and in January or February (before
trachea, and occasionally brain. Recent
breeding). New introductions to the herd
outbreaks have required PCR confirmation,
should be tested.

because imrnw1ohistochemistry testing was

Genetic selection of resistant mink
negative.

using a quantitative ELISA and/or iodine

In outbreaks, affected mink should
agglutination test is being used to increase
be culled, and the balance of the herd
smvivability and reproduction. These tests
vaccinated as soon as possible. Deaths from
identify mink with hypergammaglobulineneurotropic distemper may occur W1til 12
mia for culling. The quantitative ELISA
wk after vaccination. Kits should be
identifies overall antibody levels to Aleutian
vaccinated prophylactically when 11-12 wk
virus, allowing mink with lower antibody
old with a modified-live vaccine. Ordinarily,
levels to be selected for breeding.

adults are vaccinated at the san1e time.

There is no vaccination or effective
treatment. The virus is present in the saliva,
urine, feces, and blood of infected mink.

Mink Viral Enteritis: Mink viral enteritis

Pens should be steam cleaned and dipped
is a highly contagious disease caused by a
in or sprayed with 2% sodiun1 hydroxide.

parvovirus related to, but not identical with,

Equipment should be disinfected after
that of feline panleukopenia ( see p 796). All handling, vaccinating, or testing mink on
ages are susceptible, but the disease is most
infected farms. Raccoons and flies may
serious in kits. Transmission usually occurs
serve as vectors, and their control is
by the fecal/oral route; the incubation
essential.

period is 4-8 days.

Clinical signs include sudden anorexia;
depression; watery, mucoid, blood-tinged

Distemper: Mink of all ages are susceptible to canine distemper virus (seep 777).

diaiThea; dehydration; and death. Charac

The incubation period is 9 -14 days. The
teristic gross lesions include a flaccid,
virus may be recovered from infected
dilated, hyperemic small intestine with
mink 5 days before clinical signs appear.

liquid fetid contents. Some mink may die

Recovered mink may continue to shed the
suddenly with no gross lesions. Intestinal
virus for several weeks. Transmission may
lesions are characterized by erosion of
be direct (through contact or aerosol) or

SUiface mucosa, blunting and attenuation
indirect.

of villi, and dilation of crypts. Ballooned

Clinical signs include nasal and ocular
epithelial cells may contain inclusion bodies
discharge; hyperemia, thickening, and
simi!ai· to those of feline panleukopenia. A
crustiness of the skin on the muzzle, feet,
fluorescent antibody procedure is used to
confirm the diagnosis. Splenic and lymph
node lesions include lymphoid depletion
and necrosis.

Early in an outbreak, all mink showing
signs should be culled or isolated, and all
clinically healthy mink should be vaccinated
immediately. Affected mink can be treated

PO with a mixture of kaolin, pectin, and
neomycin. Mink viral enteritis can be
prevented by vaccination. All mink should
be vaccinated when they reach at least 6-8
wk old with a combination 3-way vaccine
containing mink viral enteritis, botulism,
andPseudomonas. Annual vaccination is

�
recommended.

Mink kit showing signs of canine distemper,
includin

Influenza: The first case of influenza
g heavy nasal and ocular discharge
with eyelids that are swollen and sealed shut.

was identified in the USA in mink in

Courtesy of Dr. John Gorham.

October 2010. Since then, it has become a

1874

MINK
frequent cause of disease on mink ranches.

disease virus. There are no corrunercially

Influenza usually presents with coughing
available vaccines. Treatment is sympand sneezing heard in areas of the ranch.

tomatic and of questionable value. It is

Losses usually increase due to second-
ary bacterial infections. Influenza has
important to differentiate this condition
also affected newborn kits, presenting as
from mink viral enteritis.

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increased respiration and significant death
losses. Exposure to influenza can come

PRION DISEASE
from multiple sources. Raw pork, poultry
products, and sick employees may all be

Transmissible Mink Encephalopathy:

avenues for vims introduction. Treatment

This progressive neurologic disease of mink
consists of treating secondary infections
is rare, but mortality may reach 60"/o-90"A, of to mitigate losses. Spread across the ranch
the ranch population. The incubation period
usually takes 2-6 wk. After the disease runs is 8-12 mo. Mink usually bite compulsively, its course, >90"A, of mink have been shown
are incoordinated and somnolent, scatter
to be antibody positive.

feces in the pen, and flip their tails up over
their backs (like squirrels). Histologic
lesions of the brain are spongiform changes

Aujeszky Disease (Pseudorabies):

of the gray matter, astrocytosis, and

Aujeszky disease occurs occasionally in .

neuronal vacuolation. The demonstration
mink fed pork products contammated with
of disease-specific prion protein in nervous
pseudorabies virus (seep 1300). Mortality
tissues aids in the diagnosis. Although the
may be high, and clinical signs are referable
means of transmission is tmknown,
to the CNS (tonic and clonic convulsions,

"downer" cattle are suspected to be the
excitement alternating with depression, and source of the agent. There are no vaccines sell�mutilation in some cases). Diagnosis is
or treatment.

confirmed by virus isolation or serology.

Because contaminated pork is the usual
source of infection, all pork products should NUTRITIONAL DISEASES
be cooked before being fed to mink.

Steatitis or myositis (yellow fat disease,

Astrovirus (Shaky Mink Syndrome):

see p 1200) occurs in young, rapidly growing Astrovirus infection is a self-limiting
mink as a result of excessive, rancid, unsatuneurologic disease seen sporadically in rated fatty acids and a deficiency of vitamin
mink kits from mid June to mid July.

E in the diet. Affected mink may be found

Usually, the condition is lin1ited to one kit
dead, or they may exhibit slight locomotor
per litter, with an incidence ofO. l o/o-2%.

disturbances followed by death. Necropsy

Higher incidence has been reported on a
fmdings include yellow, edematous internal

European ranch. Kits have tremors, and
or subcutaneous fat that contains an acidhistopathology shows meningoencephalitis.

fast pigment. It is more common to fmd

Mmtality is low and appears to be caused by myoglobinuria and dark red bladders inability of the mink to eat or drink because

(resembling plum bladder). Histopathology
of the shaking. Early in the disease,
shows myositis and cardiomyopathy. Hepatic
astrovirus can be identified, but later the
vitamin E levels <15 mcg/g can lead to acute
mink clear the virus and are negative.

death. Control consists of removal of the

Lesions and clinical signs do not improve,
source of the rancid fats and polyunsatuand euthanasia of affected mink is rated oils and proper storage of feed.

warranted for welfare concerns.

Stabilized vitaniin E may be administered in
the feed (15 mg/mink) for 4 wk, and affected

Epizootic Catarrhal Gastroenteritis:

kits should be irtjected parenterally with

Millions of mink have been affected by an

10-20 mg of vitamin E for several days.

agent ( most likely a coronavirus) that

Feeding a nutritionally sound diet with
causes an acute catarrhal gastroenteritis.

added vitamin E is preventive.

The disease usually occurs in adult dark

Chastek paralysis (thianiine deficiency)

mink. Outbreaks occur most frequently
results from feeding certain raw fish that
during tin1es of stress, eg, early fall moltcontain the enzyme thiaminase. These include whitefish, freshwater smelt, carp,
ing, spring mating, and whelping seasons.

goldfish, creek chub, fathead minnow,

Clinical signs (mucus in the feces and
buckeye shiner, sucker, charmel catfish,
partial anorexia) rarely last longer than
bullllead, minnow, white bass, sauger pike,

5--6 days. Death may occur if the affected
burbot, and saltwater herring. Affected
mink are immunosuppressed by Aleutian
mink gradually become anorectic, lose

MINK

1875
weight, and die after terminal convulsions
within 1-2 mo with clinical signs consistent
and paralysis. Fish that contain high levels
with either gastroenteritis or CNS disturof thiaminase should be thoroughly cooked bance. Individual mink may be treated with
at 181 °F (83°C) for 2!5 min, or fed raw as a
calcium edetate as a chelating agent. All
portion of the diet only on alternate days.

sources of lead should be removed.

Mink injected with thiamine hydrochloride,

Insecticides other than pyreth:turn,

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50 mg, SC, recover rapidly. Adequate
piperonyl butoxide, and rotenone may be
thiamine (brewer's yeast) should be
highly toxic to mink. Even these insecticides
included in the ration.

should not be used on mink <8 wk old, or

Rickets occurs due to the rapid growth
where such mink can contact them ( eg, nest
rate of kits when rations are deficient in
boxes). Other insecticides should be avoided
vitamin D, calcium, or phosphorus. Affected whenever possible. (See also p 3058.) kits usually crawl unsteadily in a frog-like

Wood preservatives ( chlorinated
posture, have rubbery bones, and are
phenols, cresols) can cause death of kits in
smaller than normal. The diet should be
the first 3 wk of life and occasionally of older
supplemented as required, and severely
mink. They should not be used where mink
affected kits may be treated individually.

can chew on treated wood (pens, nest boxes,

(See also p 1051.)

or nest litter). Shavings used as nest-box

Nursing disease is a metabolic disease
litter should not contain wood preservatives.

that affects lactating mink -40 days after

Diethylstilbestrol causes reproductive
whelping. It is characterized by rapid
failure and a high incidence of urinary tract
dehydration, serum electrolyte imbalances,
infections in mink and should not be
renal shutdown, and death. Treatment can be
included in the ration. Similarly, thyroid
successful if affected females are identified
and parathyroid glands included in meat
as soon as they begin refusing feed and
trimmings fed to mink may result in
rehydrated with IP or SC sterile fluids. The
reproductive failure if present at high levels.

disease is multifactorial; although there

Chlorinated hydrocarbons and
appears to be a genetic predisposition in
polychlorinated biphenyls contained in
certain light color mutations, it is more
the ration can cause reproductive failw·e.

severe in females with large litters and during Mink appear to be exquisitely sensitive to hot weather. Often, affected females have
polybrominated biphenyls; 1 ppm in the
concurrent subclinical mastitis. Adequate
ration has caused litter size and offspring
water, environmental cooling systems,
viability to decrease. (See also p 3056.)

fostering kits from large litters to make litter

Dimethylnitrosamine (DMNA) is
size more manageable for the female, and
hepatotoxic in mink. In the past, addition of
early weaning help prevent this condition.

sodium nitrate as a preservative to herring

Cotton underfur usually indicates
meal resulted in fonnation ofDMNA, wl;lich
anemia and may be caused by feeding
causes hepatic degeneration, ascites, and
certain fish (Pacific hake, coalfish, whiting)

extensive internal hemorrhage.

that interfere with iron metabolism in mink,

Sulfaquinoxaline upsets normal
which affects melanin pigment formation.

blood-clotting mechanisms of mink and

Thoroughly cooking the offending fish at
causes extensive internal hemorrhage.

181 °F (83°C) for 2!5 min or feeding it on

Streptomycin is toxic to mink.

alternate days prevents the condition.

Salt toxicity is seen in young kits

Biotin deficiency, which can cause gray
starting on solid food. Affected kits become
underfur and loss of guard hair, is seen
dehydrated and show CNS signs such as
when high levels of uncooked eggs,
tremors or seizures. The most common
particularly turkey eggs, are fed. Avidin, a
cause is increased salt levels in feedstuffs.

factor present in eggs, inactivates biotin, a

By-product from the cheese, poultry, fish,
vitamin required for pigmentation and hair
and processed sandwich meat industries
growth. Affected mink may be injected with
contain higher than expected salt concen1 mg biotin twice weekly for 4 wk, and trations. Prevention is accomplished by
biotin may be added to the ration. Biotin
testing feed and ingredients for salt levels
deficiency can be prevented by cooking
and removing ingredients with high salt
eggs at 196°F (91 °C) for 5 min.

concentrations and supplemental salt.

POISONING

MISCELLANEOUS DISEASES

Lead poisoning (seep 3078) may be seen

Fur clipping and tail biting are common
in mink that have ingested lead-containing
in mink and may be caused by captivity. Fur
paint from wire or other equipment.

clipping decreases the value of the pelt,

Affected mink gradually lose weight and die
and tail biting frequently results in fatal

1876

MINK
hemorrhage. There is no effective treat

Gastric ulcers and hepatic and renal
ment. All mink demonstrating these
lipidosis are common in mink and usually
behaviors should be culled.

are associated with high levels of dietary fat

Urinary incontinence (wet belly
or with other diseases or stresses that result
disease) is a nonfatal condition that usually
in several days of ina.ppetence ( eg, during

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affects obese males in the late summer and
late gestation, the period of weaning kits, or
autumn. It is characterized by dribbling of
the fall period of funing up). Renal lipidosis
urine and staining of the pelt around the
is commonly seen in mink implanted with
winary orifice. Because affected areas of
melatonin. Treatment involves B vitamins
the pelt must be discarded, the condition

( either feeding or via injection) and
is of economic importance. The cause is
increasing the protein quality of the feed.

unknown, but genetic strain, high dietary

Hereditary diseases such as hydrocephfat lPvel, and obesity appear to have the alus, hairlessness, "screw neck," "bobbed greatest influence on incidence. Affected
tails," Ehlers-Danlos syndrome, hemivertemink should have an ample water supply.

brae, and tyrosinemia. occur occasionally.

Starvation and chilling cause death in

Culling the sire, dam, and littem1ates of
mink fed inadequate fat or provided with
affected mink is necessary for control.

too little feed during the winter and early

Coccidiosis (seep 203) occasionally
spring. Affected mink are thin and may run
causes losses in young mink Affected
until they collapse and die, or they may be
mink have dia.1Thea, blood-tinged feces,
found dead in their cages. Such deaths
dehydration, and weight loss. Coccidiousually occur after the environmental stats may be used to control outbreaks.

temperature decreases suddenly, especially

Coccidiosis can be prevented through good
in the early spring when mink are being
sanitation and regular manure removal.

brought into breeding condition. Necropsy

Myiasis develops in mink when flies
reveals emaciation and an absence of body
of Wohifahrtia spp lay maggots directly
fat, in some cases accompanied by hepatic
on the skin of kits. The larvae penetrate
lipidosis and gastric ulceration. This results
the skin and produce inflammation and
from improper management and must be
lesions that resemble abscesses. Affected
differentiated from infectious diseases.

kits become restless, lose condition, and

Gray diarrhea in mink clinically
may die. Malathion dust (5%) placed
resembles clu·onic pancreatic necrosis in
beneath the litter in the nest boxes
dogs and is characterized by a ravenous
beginning a few days before the flies
appetite and passage of large a.mounts of
appear may help prevent infestation. It
gray, fetid feces. Affected mink appear to
should not be used before whelping or
die of starvation. No pancreatic abnormaliuntil the kits are 1 wk old. Treatment may ties, viruses, bacteria., or parasites have
be repeated once after a 2-wk interval.

been demonstrated to be causes. Treatment

(See also CUTEREBRA INFESTATION IN SMALL
is of questionable value.

ANIMALS, p 879.)

NONHUMAN PRIMATES

This overview presents a working

(pig-tailed monkey); some African species,
knowledge of the common fan1ilies of
p1in1arily Chlorocebus aeth-iops (African
nonhun1an prin1ates maintained in captivity.

green monkey, vervet) andPapio spp

More species than ever are now promul

(baboons); and some of South American
gated and maintained in captivity, and many
origin, Saimiri sciureus (squirrel monkey)

are kept in private facilities. Prosimians
and Aolus t1ivirgatus ( owl monkey).

such as Lemur catta (ring-tailed lemur)

Sagilinus spp (ma.nnosets) and CaUithrix and New World monkeys such as Cebus
spp (ta.marins, ma.nnosets), also of South
albifrons (white-fronted capuchin) are

American origin, have had more limited use
commonly encountered in practice. The
in research but are common in the pet trade.

nonhwnan primate species most widely

Increased restrictions on exportation or
used in research a.re the macaques, Macaca
reduced availability of nonhun1an primates
mulatta (rhesus monkey), M fascicularis
from countries of origin have led to

( cynomolgus monkey), and M nemestrina
decreased importation. Importation of

NONHUMAN PRIMATES

1877
nonhuman primates into the USA is
in a facility registered with the CDC.

prohibited except for scientific, educa

Imported animals that die or become
tional, and exhibition purposes.

severely ill and require euthanasia during

Nonhw11an primates are natural hosts
this quarantine period must be necropsied
for a variety of infectious agents, many of
and the deaths reported to tl1e CDC,

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which are zoonoses, and are also suscepti

Division of Quarantine. In clinical practice,
ble to many human infectious diseases,
any new nonhuman primate should be
such as measles and tuberculosis.

tested for tuberculosis, and a routine fecal

Consequently, newly acquired nonhuman
examination and trichrome stain should be
primates should be quarantined for 1-3 mo
done. Depending on the species, routine
before research use or introduction into
tests such as tl10se for cytomegalovirus,
established colonies, to pennit adequate
herpes simiae, and herpes simplex (1, 2, etc)

evaluation of their health status and to allow also can be run at this time. Many of tl1e adaptation to the laboratory environment.

nonhw11an primates seen in clinical practice

The basic principle of quarantine is to
are infants and are irnmunocompromised;
completely isolate each group of animals
they are highly susceptible to common cold
and not mix animals from different
and influenza viruses as well as streptococshipments or sources without restarting the cal infections and should be isolated from
quarantine period. Nonhuman primates
people witl1 upper respiratory signs.

imported into the USA must undergo a

For nonhuman primate therapeutics,

31-day minimtll11 primary import quarantine
see TABLE 13.

•th•if• NONHUMAN PRIMATE THERAPEUTICS•

ANTIBIOTICS

Amoxicillin

11 mg/kg/day, IM or SC; 11 mg/kg, PO, bid; 62.5 mg, PO, bid (lemurs)

Metronidazole

25-50 mg/kg, PO, bid for 10 days (gastroenteritis and inflammatory bowel disease)

Azithromycin

40 mg/kg, PO, once, then 20 mg/kg/day, PO, for 5 days Cefazoli.n

25 mg/kg, IM or IV, bid for 10 days

Ceftriaxone

50-100 mg/kg, IM or IV, bid

Doxycycline

2.5 mg/kg, PO, bid for one day, tl1en 2.5 mg/kg/day, PO

Minocycline

2-15 mg/kg/day, PO

Enrofloxacin

5 mg/kg, IM or PO, once to twice daily for 10 days

Erythromycin

30-50 mg/kg, IM or PO, bicl-tid

Gentamicin

3-5 mg/kg, IM or IV, bid for 5-7 days

Penicillin G potassiw11 + 20,000-60,000 U/kg, IM, once to twice daily (higher dosage in penicillin G benzathine
lemurs)

Trimethoprim15-50 mg/kg, PO or IM, bid; sulfarnethoxazole at 20 mg/kg, sulfarnethoxazole

PO, bid (higher dosages for lemurs)

PARASITICIDES

Fenbendazole

50 mg/kg/day, PO, for 5 days, repeated in 2 wk

Ivem1ectin

200-300 mcg/kg, SC, IM, or PO, repeated in 14 days

Mebendazole

22 mg/kg/clay, PO, for 3 days, repeated in 14 days (for Giardia sp)

Metronidazole

30-50 mg/kg, PO, bid for 5-10 days

1878

NONHUMAN PRIMATES

NONHUMAN PRIMATE THERAPEUTICS• (continued) Praziquantel

5 mg/kg, IM, PO, or SC, once (15-20 mg/kg, PO or IM, for some cestodes; 40 mg/kg, PO or IM, for trematodes)

Thiabendazole

100 mg/kg, PO, once, repeated in 14 days (owl monkeys); 50

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mg/kg/day, PO, for 2 days (Strongyloides ); 75-100 mg/kg/day, PO, for 10 days (Entamoeba, Balantidium) in great apes ANESTHETICS AND ANALGESICS

Ketamine hydrochloride 10-15 mg/kg, IM, for restraint only; ketamine (15 mg/kg) with diazepam (1 mg/kg), IM, or ketamine (8 mg/kg) with
midazolarn (0.2-1 mg/kg), IM, for additional muscle
relaxation

Ketoprofen

2 mg/kg/day, IV or IM

Inhalant gas (isoflurane, l %-2%; maintenance of surgical plane of anesthesia halothane)

Flw1ixin meglumine

0.5-2 mg/kg, IV, IM, or SC, bid

(analgesic)

Buprenorphine

0.005-0.01 mg/kg, SC, IM, or IV, bid-qid (great apes) 0.015-0.02 mg/kg, IM, SC, tid-qid (New World primates) Butorphanol tartrate

0.02 mg/kg, SC, qid (New World primates); 0.02 mg/kg (not to exceed 0.3 mg total), IM (chimpanzees); may cause profound respiratory depression

Dexrnedetomidine

40 mcg/kg, IM, for anesthesia in combination with ketamine at 20-30 mcg/kg, IM (lemurs) or at 2-6 mg/kg, IM (macaques and baboons)

Midazolan1

0.05-0.l mg/kg, IV (slow) or IM: 0.1-0.5 mg/kg, IM (with ketamine helps prevent seizures in lemurs); 5 mg/anin1al, IM

(chimpanzees)

Oxymorphone (opioid

0.025-0.075 mg/kg, IM or IV, every 4-6 hr (New World analgesic)

p1imates); 0.15 mg/kg, SC, IM, or IV, every 4-6 hr (Old World primates); 1-1.5 mg/animal, SC or IM, every 4 hr (chimpanzees) Pro po fol

2.5-5 mg/kg, IV bolus induction, 0.3-0.4 mg/kg/min constantrate infusion (baboons and macaques); 7-8 mg/kg, IV bolus

• (marmosets, larger nonhuman prin1ates); 1-2 mg/kg, IV bolus (chin1panzees), followed by infusion to effect; oxygen support always available

Tiletamine-zolazepam

3-5 mg/kg, IM, for restraint only (great apes), severe ataxia noted during recovery: 1-2.5 mg/kg, IM (New World
prinlates); 1.5-3 mg/kg, IM (macaques)

a All are extra-label uses.

BACTERIAL DISEASES
hydrophila are implicated. Nonlmrnan
primates may be intennittent, asympto

Gastrointestinal Diseases: The bacteria matic carriers of any of these organisms.

most commonly associated with GI disease

Helicobacter spp have been implicated as
in nonlmman primates are Campylobacler
a cause of gastritis, anorexia, and vomiting.

jejuni and Shigella spp. Occasionally, GI diseases may be major problems in
enterotoxigenic Escherichia coli, Pseudo
captive nonhuman primates. Clinical signs
monas aeruginosa, Yersinia spp, Lawso
include watery or mucoid, blood-tinged
nia intracellularis, Salmonella spp,
feces, rapid dehydration, emaciation, and

Aerobacter aerogenes, and Aerobacler
prostration. Smaller primates will dehydrate

NONHUMAN PRIMATES

1879
and become hypoglycemic very rapidly. In
respiratory viral infection). Clinical signs
many privately owned nonhuman primates,
may include coughing, sneezing, dyspnea,
dietary indiscretion is common, and the
mucoid or mucopurulent nasal discharge,
owner should be asked about irregular
pyrexia, lethargy, anorexia, and weight loss.

feeding habits. Rectal prolapse is an

The principal lesions seen at necropsy a.re
occasional sequela. Helrninths or pathothose of bronchopnetmionia or lobar VetBooks.ir
genic protozoa may be a complicating factor. pneumonia. Empiric antibiotic therapy with Fecal assays and trichrome stains should
azithromycin, tiimethoprim/sulfamethoxabe done, and appropriate anthelrnintics zole, penicillin, or cephalospmin ( either of
administered. Mortality can be extremely
the latter two in combination witl1 an
high in acute outbreaks unless treatment is
aminoglycoside) generally is indicated.

instituted promptly to restore and maintain

Cultures from pharyngeal swabs or
nom1al fluid and electrolyte balance. The
transtracheal lavage are useful to isolate the
most common lesions at necropsy a.re
causative agent and determine the specific
hemorrhagic enteritis, enterocolitis, colonic
antibiotic sensitivity. Intensive nursing and
ulcers, or sin1ply colitis.

other supportive therapy, such as fluid and

Severe clinical signs and death a.re
oxygen administration, may also aid
generally due to dehydration, hypokalemia,
recovery in select cases.

and metabolic acidosis. Hydration should
be restored and maintained with parenteral

Tuberculosis: All nonhtmian primates a.re
electrolyte solutions. Although medications
susceptible to tuberculosis, although major
may often be easily administered pa.renterdifferences exist in the prevalence of cases ally, potassium, B vitamins, electrolytes,
in different species. Most cases of tuberbismuth subsalicylate, and antibacterial culosis in nonhwna.n primates have been
agents can be administered PO or by
reported in Old World primate species such
nasogast1ic tube in most nonhuman
as rhesus monkeys. Reports in New World
primates. Culture and identification of the
species such as squirrel monkeys are much
infecting organisms and assessment of
less frequent. The incidence of tuberculosis
antibiotic sensitivity may be needed for
is d % among quarantined Old World
effective therapy. Metronidazole at 25-50
primates, but 45% of cases ( especially
mg/kg, PO, bid, may be instituted tmtil
cynomolgus monkeys) may not be
culture results a.re obtained. Enrofloxacin (5 diagnosed until after the fast 30 days of mg/kg/day) or the combination oftrirnethoquarantine. Clinical signs a.re not a reliable prim ( 4 mg/kg) and sulfan1ethoxazole (20
indication of the severity of tuberculosis in
mg/kg), administered as a total daily oral
monkeys. A monkey that appears healthy
dosage for 10 days, is useful to treat
may have extensive miliary disease involving
shigellosis. Azithromycin (30-50 mg/kg, IM,
thoracic and abdominal organs; signs of
bid for 7-14 days) is recommended to treat
debilitation may appear only sh01tly oefore

Campylobacter-associated diarrhea.

death. However, advanced tuberculosis
should be suspected in animals that cough;

Pneumonia: Upper respiratory diseases
lose appetite or weight; and/or have enlarged
of bacterial origin can cause widespread
or draining lymph nodes, ski11 wounds that
illness, and bacterial pneumonia is
fa.ii to heal, or abdominal masses. A testing
associated with increased mortality,
progran1 is mandato1y; a tuberculin skin test
particularly in newly imported or immature

(intra.dermal tuberculin skin test), using
nonhuman primates. Causative agents
manimalian old tuberculin (MOT) is the
include Streptococcus pneumoniae,
only USDA-approved tuberculin test for

Klebsiella pneumoniae, Bord.etella
nonhwnan primates and is the primary
bronchise-ptica, Haemophilus injluenzae,
diagnostic method for routine surveillance.

and various species of streptococci,

Intra.dermal injection ofO.l mL of MOT using
staphylococci, and pasteurellae. Both New
a 26-gauge needle in the palpebrae is an

World and Old World infant primates a.re
approved USDA method; 0.5 mL may be
highly susceptible to cross-species transfer
used in mannosets and tan1arins. The
from people. Many tin1es, caretakers have
injection sites a.re observed at 24, 48, and 72
had a history of an upper respiratory
hr after injection. Grading systems can be
infection, so adequate history on presentafound in the Guidelines for the Prevention tion is important. Infants that a.re handrea.red and Control of Tuberculosis in Nonhwnan frequently present with aspiration pnewno

Primates on the National Institutes of Health
nia from bottle feeding, and approp1iate

Web site. J.f palpebral swelling is present
cultures and radiographs will be needed.

with a lid droop, this may be interpreted as

Pneumonia may accompany or follow
positive. Tuberculin tests should be done on
other primary diseases ( eg, dysentery or
all nonhwnan primates on aITival at the

1880

NONHUMAN PRIMATES
facility and at 2-wk intervals thereafter until
owned non.hLUllan primates, it is more
at least three consecutive negative tests have conunon. Topical treabnent of ringwonn been recorded for the entire group. The last
with undecylenic acid oinbnent or 1%
test should be administered within 14 days
tolnaftate cream, bid for 2--3 wk, may help,
of the release from quarantine and
but nonh wna.n primates often orally remove

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introduction into an established colony.

any topical medications, making treabnent

The time from initial infection to skin-test
ineffective. Administration of griseofulvin
conversion depends on the route of exposure, at 25 mg/kg/day, PO; ketoconazole at the infecting inocu1Lm1, and the strain of

5-10 mg/kg, PO, bid for 30 days; or
organism, but usually occurs within 3---4 wk in fluconazole at 2--3 mg/kg/day, PO, for 30 days rhesus monkeys. Late in the disease, anergy
is also very effective. Candida spp are
can result in a negative skin test. Anergy may
conllllon saprophytes of the skin, GI tract,
also be induced by concuJTent viral infection,
and reproductive tract; they act as
such as measles, or inllllunosuppressive
facultative pathogens in debilitated
disease. Wected nonhuman primates may
nonhlUllan prin1ates. Ulcers or white, raised
also develop latent tuberculosis. These
plaques may be seen on the tongue or
animals appear healthy, are not infectious,
mouth; the fungus may also attack
and are often skin-test negative. Latent
fingernails. Oral lesions must be differentituberculosis may be reactivated in response ated from those of traLUlla, monkeypox, or
to environmental su-essors or other in1mune
herpesvirus infections. A topical crean1
modulation, leading to active disease and
containing nystatin is effective in superficial
potential b-ansmission.

infections. Oral nystatin (200,000 U, qid,

After their release from quarantine, all
continued for 48 hr after clinical recovery)

nonhwrnm primates should be skin-tested
is effective for candidiasis of the GI tract.

at least semiannually, and quarterly testing

Dermatophilus congolensis infection has
is reconllllended for research animals.

been reported in owl monkeys. Papilloma

Captive animals in private settings and New
tous lesions are seen on the face and

World primates may be tested annually.

extremities. The infection is transmissible

Radiographic examination of the chest may
to people. Aspergi.llosis may develop in
aid diagnosis in well-established cases but is various nonl1LUllan primate species, and the LUlfeliable because lesions rarely calcify or
organism usually is a facultative pathogen in
cavitate as they do in people. Additional
immunocompromised hosts. Treabnent
diagnostic tests, such as cultlll'e, PCR, and
with voriconazole or terbinafine is
staining of a gastric lavage or transtracheal
empirical. In endemic regions of the
wash sample, ELISA, and comparative
western and southwestern USA, Coccidi
abdominal skin testing with avian and
oides immitis has been associated with
atypical tuberculins, may aid in diagnosis.

fungal pneumonia and disseminated

Biopsies of positive or suspicious abdomimycosis ("valley fever") in monkeys and nal tests may be useful in identifying true
apes after exposlll'e to airborne spores of
delayed-type hypersensitivity reactions.

this soil fungus.

Because of the public health risk, euthanasia is recommended for all positive reactors.

PARASITIC DISEASES

Tuberculosis should then be confirmed at
necropsy. When a positive case is identified,

Newly imported nonhwnan prin1ates harbor
the entire group of exposed nonhlLillan
nun1erous parasites. Some are conunensal;
p1irnates in a maintenance colony should be
others can be made seif-limiting by stx;_ict
quarantined, and skin testing at 2-wk
sanitation and good husbandry. However,
intervals inlplemented. Privately owned
some can cause serious diseases or
animals should be quarantined away from
debilitation and should be removed by
small children and untrained personnel. For
specific treatment. Captive-raised New
anin1als in quarantine, the pe1iod should be

World prin1ates housed indoors (ie, with
restarted and testing should be continued.

their caretakers) are rarely f0tmd to have

All personnel working with any notlhLUllan
intestinal parasites; however, this may not
primates or in primate facilities should have
be the case when they associate with
regular skin tests.

sandboxes and various outdoor enclosUl'es.

Fecal examinations should be part of the

MYCOTIC DISEASES
routine clinical annual examination.

See also FUNGAL INFECTIONS, p 632.

Arthropods: Pulmonary acariasi�

Microsporum spp and Trichophyton

(Pneumonyssus spp) is conunon in
spp rarely infect institutional nonhun1an
wild-caught Asian and African primates,
primates. In clinical practice with privately
particularly rhesus monkeys and baboons.

NONHUMAN PRIMATES

1881

Infection is rare in laboratory-raised or

Tetrapelalonema are filarid worms found in
captive, privately raised nonhuman
the peritoneal cavity of ew World species;
primates. The life cycle of Pneumonyssus
large numbers may be present with ve1-y
spp is not well understood. Infestations
lin1ited host reaction. Lungwo1ms such as
usually do not produce se1ious sympto

Filaroides are commonly found in many

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matic disease, although they may cause

South American monkeys.

sneezing and coughing. Lesions include
dilation and focal chronic inflammation of

Cestodes: Bertiella sluderi and other terminal bronchioles. The gross lesions
enteric cestodes may be found in animals
may occasionally be confused with
of feral 01igin and are treated effectively
tuberculous granulomas. Ivermectin (200
with praziquantel (5 mg/kg, IM, PO, or SC,
mcg/kg, SC, PO, IM, repeated in 14 days)

once). For some cestodes, 15-20 mg/kg, PO
has been used for treatment in closed
or IM, once, will be needed. Somatic larval
breeding colonies.

(cystic) cestodiasis has been repo1ted.

Mange mites (Psorergates spp, Sarcop

Flukes may cause respirato1-y, GI, and
tes scabiei) or sucking lice (Pedicinus hematologic signs. Schislosoma sp is a
obtusus) are seen occasionally, particublood fluke, whereas Fasciola sp infect the larly in feral animals, and may produce
liver and may cause hepatic disease ai1d
dem1atoses. Systemic treatment with
abscessation (more common in Old World
ivennectin, 200 mcg/kg, PO, SC, IM,
prin1ates ). The intermediate hosts ai·e
repeated every 3 wk, or topical treatment
snails and crustaceans, which are ingested
with pyrethrin, repeated after 3 days if
through contan1inated water or food. This
necessai-y, is recommended. Use of more
is of zoonotic concern. Praziquantel at 40
toxic topical parasiticides should be
mg/kg, PO or IM, in a single dose has been
avoided because of the possibility of
effective.

ingestion during grooming. Fleas are
commonly seen in New World primates

Protozoa: Nonhuman primates may serve
that are associated with dogs or cats in the
as hosts of various intestinal amebae.

environment. Premise control measures

Enlamoeba hislolytica is the principal
must be instituted, and baths with a
pathogenic form in nonhuman priniates (as
pyTethrin-based shan1poo will temporarily
in people). It has only rarely been reported
remove fleas from the anin1al's haircoat.

as pathogenic in monkeys, mostly in South

American spider and woolly monkeys.

However, it can be a serious infection in

Helminths: Oesophagostommn may
mannosets and has caused serious enteritis
cause characteristic granulomatous
in great apes. In a heavy infection, it may
nodules in the large bowel associated with
cause severe enteritis and diatThea, and
development of the wonns and with an
cysts may be demonstrated in the feces in
immune reaction of the host. The nodules
large numbers. The fecal t1ichrome stain
may rupture and cause peritonitis.

is a useful tool to diagnose these types of

Strnngyloides and 'I'richostrongylus are infections, which are often overlooked
invasive-adults may cause enteritis and
in a direct or flotation fecal exan1ination.

diarrhea, larvae may cause pulrnonai-y

Giardia inhabit the upper small intestine
lesions during migration. These helminths,
and may cause wate1-y diatThea. Treatment
as well as 'I'richuris, can be treated
with metronidazole (50 mg/kg/day, PO, for
effectively with thiabendazole at 100 mg/kg,

5---10 days) is reconunended. C?yplosporid
administered PO at intervals of 2--4 wk;
ium parvum may also cause diarrhea in
ivermectin at 200 mcg/kg, SC, repeated in 14 nonh un1an primates, mainly in young days; or febendazole at 50 mg/kg/day, PO,
ailimals. Successful treatment in maimosets
for 3 days ai1d repeated in 14 days. The
with pai·omomycin has been reported. This
effectiveness of anthelmintic treatment is
infection is usually self-limiting in inummoenhanced by aggressive environmental competent hosts.

hygiene practices. Prosthenorchis is an

Blood parasites, such as Plasmodiitm,
acanthocephalan, common in Central and

Leishmania, and Tlypanosoma spp, are South American nonhuman primates, that
also found. Generally, there is an equilib-
burrows into the mucosa of the ileocecal

1iwn between the parasite and the natural
junction and sometin1es pe1forates the
host, with infections rarely causing overt
bowel or causes obstruction when present
clinical disease. Trai1smission of sinliai1
in large numbers. Cockroaches are
malarias to people, although rai·e, has
intermediate hosts, and their elin1ination,
occun-ed in ai·eas where the appropriate
along with strict sanitation, is essential for
mosquito vectors are present. Some
control of infection. Dipetalonema and
nonhuman primate species ( eg, owl

1882

NONHUMAN PRIMATES
monkeys) are excellent models for malarial
in chimpanzees (Pan troglodytes) and
research.

monkeys. lncreased AST and ALT values are

Naturally occurring toxoplasmosis
of diagnostic significance in nonhwnan

(Toxopi,asma gondii) has been reported
primates. Hwnan infections have been
in Central and South American p1imates.

contracted from chin1panzees.

Clinical signs of infection tend to be

Because some vaccines are not available

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nonspecific (lethargy, anorexia, diarrhea).

to protect nonhuman primate colony

Hepatic focal necrosis and fibrinous
personnel or the primates against herpes
pnewnonia with edema are common
and some viral hepatitis infections,
histologic findings. Toxoplasma can be
exposure should be prevented. This is
demonstrated in blood smears in acute
best accomplished by carefully training
cases. (See also p 685.)

personnel in the handling of nonhuman
primates, using personal protective

VIRAL DISEASES
equipment ( clothing, face masks, gog-
gles or shields, and gloves), separating

A number of herpesviruses affect
primates in species-specific rooms,
nonhuman primates; many exist as latent
and paying strict attention to hygienic
or subclinical infections in reservoir hosts
standards. In private facilities, prescreenbut cause severe disease or death when ing the primates by serologic and PCR
transmitted naturally to other hosts. All
testing is recommended.

macaques are considered to be potential

Several other viruses commonly produce
shedders of Cercopithecine herpesvirus
clinical disease in newly imported primates.

type 1 (Herpesvirus simiae, B virus). The

Rubeo la infection (measles) acquired via
infection is generally subclinical or mild
hwnan contact can asswne epizootic

( conjunctivitis or oral vesicles) in Macaca
proportions. The virus causes a nonprwitic,
spp but usually causes a fatal encephalitis
exantllematous rash on tile face, chest, and
and encephalomyelitis in people. Translower portions of tile body; it may also cause mission may occur via a bite, scratch, or
interstitial giant-cell pnewnonia, rhinitis,
contamination of a superficial wound or
conjunctivitis, and, paiticularly in New
mucous membranes (eg, conjunctiva) with

World monkeys, gastroenteritis. Marmosets
infectious saliva, conjunctiva) secretion, or
are extremely susceptible, and children,
genitourinary secretions. Human fatalities
especially, should not be encouraged to
due to B virus encephalitis illustrate the
interact witll this species. There is no specific
importance of using appropriate precautreatment. Vaccination of infant rhesus tions and personal protective equipment
monkeys and oilier macaques witll hwnan
to prevent direct or indirect contact with
measles vaccine is recommended. Modifiedmacaque secretions and body fluids.

live measles vaccine can cause disease

Captive-born and raised animals should
in marmosets and is not recommended.

still be screened when first presented in

Monkeypox and oilier poxvirus infections
a clinical setting and subsequently every
may be seen in primate colonies. Monkeypox
year afterward in a private facility.

is a reportable, zoonotic disease character

Sairniriine herpesvirus type 1 (herpesviized by a maculopapular rash and variolous rus T) causes mild herpetic lingual ulcers
pustules (seep 2419). Affected monkeys
and stomatitis in squirrel monkeys, but fatal
usually survive; after recovery, tlley are
epizootics have followed natural transmisinlmune to challenge.

sion to owl monkeys and marmosets. The

Immunosuppressive dfsease in
hw11an herpesvirus, herpes sin1plex virus
nonhuman primates may be caused by a \
type 1, causes a mild infection in people and
number of retroviruses, including several
certain other primates, but owl monkeys,
orthoretroviruses formerly called type C
gibbons, capuchins, and tree shrews
and type D oncomaviruses, and several

(Tupaia glis) are highly susceptible and
simian immunodeficiency viruses (SIVs ).

may die; signs may include ulcerations of

The SIVs are lentiviruses closely related to
the mucous membrane or skin, conjunctivihuman immunodeficiency virus 1 (HIV-1) tis, meningitis, or encephalitis. Hwnan
and HIV-2. Unique isolates have been
caretakers witil oral lesions should be
found in different species of nonhuman
replaced until tile infection regresses, and
primates. SIVs are of low pathogenicity in
any interaction witll tile public should be
the natural hosts, African species, and
discouraged.

infections are often clinically silent but

Naturally occurring, clinically silent
may cause devastating disease similar to
infections of hepatitis A virus ( enterically

AIDS in macaques after cross-species
transmitted hepatitis virus) have been seen
transmission. SIV has been demonstrated

NON HUMAN PRIMATES

1883
to infect people, although the longterm

Central and South American primates (New
consequences of infection are unknown.

World) cannot and require provitanlin D,1.

Infection with orthoretroviruses in the

Commercial diets specifically formulated
genus Betaretrovirus (formerly the type D
for New World primates should be the main
retroviruses SRV, 5 serotypes) may cause
component of the diet of these animals.

an immunodeficiency predisposing to a

Fish-liver oils provide an adequate source

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complex of diseases such as fibromatosis,
of 03, or as little as 1.25 IU/g of diet can be
atypical mycobacteriosis, intestinal
added to the ration. Exposure of monkeys
cryptosporidiosis, pneumocystic
to sunlight facilitates conversion of vitan1in
pneumonia, disseminated cytomegalovi

D to active fonns. Without adequate 03,
rus infection, and candidiasis in colonies

New World primates may develop
of macaques. Infection with oncornavisecondary nutritional hyperparathyroidism ruses in the genus Dellaretroviius

(seep 1054).

(formerly type C retrovirus) results
primarily in lyrnphoproliferative disease,

MISCELLANEOUS CONDITIONS
and rarely T -cell lymphoma, in Old World
monkeys and apes. There is great
host-interspecies variation in clinical

Diabetes: Diabetes is frequently seen
signs and susceptibility from virus to
in clinical practice. The genus Cebus is
virus. Transmission between nonhuman
overrepresented. Causes of diabetes vary
primates is via direct or indirect contact
from obesity ( carbohydrate overload),
with infected blood and other body fluids
genetic predisposition, and overall poor
or from darn to offspring.

dietary choices. The animal should be

Hemorrhagic viral zoonoses, such as
brought to the hospital fasting; laboratory

Ebola, Marburg, and mosquitoborne yellow
tests should include a CBC, serum
fever, are risks with wild-caught animals. An chemistries, a urinalysis, levels of insulin important differential diagnosis for these
and fructosan1ine, and a glycosylated
zoonoses is simian hemorrhagic fever. This
hemoglobin. The caretaker should be

Arterivirus infection is subclinical in
educated on dietary restrictions and the

African monkeys but is highly contagious
availability of newer commercial diets for
and fatal for Asian species. Hemorrhagic
these animals. Blood glucose readings can
necrosis of the proxin1al duodenum is a
be obtained at home by the caretaker, and
pathognomonic lesion. Captive populations
both oral and parental medications
that ultimately are housed in private
administered with little effort.

facilities are a low risk.

Acute Gastric Dilatation: Life-threatening bloat occurs sporadically in captive NUTRITIONAL DISEASES
nonhuman primates and may be assocfated
with feeding after a prolonged fast or periods

See also NUTRITION: EXOTIC AND zoo ANIMALS, of water restriction or accidental overfeed p22 87.

ing. Etiologic factors include intragastric

All laboratory nonhuman primates are
fe1mentation associated with Clostridium
susceptible to vitamin C deficiency.

peifringens and abnom1al gastric function.

Hypovitaminosis C may cause immunosup

Monkeys become acutely ill, with clinical
pression and increase susceptibility to
findings sinlilar to those seen in small
infectious diseases before clinical signs of
animals ( see p 384 ). Acute gastric dilatation the deficiency appear. Commercial monkey
is often fatal without emergency treatment.

diets contain vitamin C that is stable for 3

The stomach must be evacuated and fluids
mo after the diet is milled and packaged, if
replaced, in like volume, with electrolyte
properly stored. Supplemental sources are
solution given parenterally. Shock and
green leafy vegetables and citrus fruits.

dehydration usually occur and require

Orally ad.ministered human pediatric
prompt treatment. Periodic evacuation of
vitamin preparations that contain ascorbic
the stomach may be necessary for several
acid are readily accepted. Daily intake of
days until GI function is nom1al. Metabolic
vitamin C at 3-6 mg/kg prevents scurvy.

alkalosis may result from continued loss

Scurvy should be treated with ascorbic acid
of hydrochloric acid. Adequate sodium,
at dosages of 25--50 mg/kg/day until clinical
chloride, and potassium must be provided
signs resolve and dietary consumption of
via parenteral fluid therapy.

adequate vitamin C is restored. Primates
require vitamin D to prevent rickets and

Tetanus: Infection with Clostridium
osteomalacia. Asian and African primates
tetani is a risk with free-ranging and
can use provita.min 02 (in plant materials);
outdoor-housed monkeys, pruticularly as

1884

NONHUMAN PRIMATES
a consequence of fighting, partmition,
shutdown; antibiotics should be given to
frostbite, and other fo1ms of skin trauma.

prevent infection and sepsis. Measures

Immunization with tetanus toxoid should
should be taken to enhance the psychologic
be considered for populations at risk.

well-being of nonhuman prinrntes ( eg, group

Marmosets are routinely vaccinated with
housing, exercise pens, shelters, foraging

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adsorbed human product or equine product
activities, and cage toys), and animals in
at 0.25 mg, IM, every 5 yr. (See also TETANUS, social groups should also be provided
p611.)

facilities for refuge and escape.

Intestinal Adenocarcinoma: The
number of aged nonhmnan primates

PSYCHOLOGICAL WELL-BEING
maintained in captivity has increased in

AND ENVIRONMENTAL
recent years, primarily due to improvements in husbandry, nutrition, and ENRICHMENT
veterinary care, but also because of an

Providing for the psychological as well
emphasis on animal models for aging
as the physical well-being of nonhuman
research. This increase in the aged
primates maintained in captivity is a
nonhmnan primate population, particuhigh priority. Psychological well-being is larly macaques, has been associated with
enhanced by appropriate social companan increase in the incidence of intestinal ionship (ie, compatible conspecifics);
adenocarcinoma, which may exceed 20%
opportunities to engage in behavior
in animals >30 yr old in some colonies.

related to foraging, exploration, and other

Decreased appetite, weight loss, anemia,
activities appropriate to the species, age,
and a palpable abdominal mass are
gender, and physical condition of the
common clinical findings. Tests for fecal
animal; and housing that allows typical
occult blood are often positive. Radiomovement and resting postures. When graphic examination may show changes
home cages are of the minimum legal size,
associated with partial obstruction.

enlargements or added exercise areas

Surgical biopsy is diagnostic for adenocarshould be encouraged. Interactions with cinoma. The location of these tumors is
human caretakers should be generally
most commonly the ileocecocolic junction, positive and not a source of undue stress.

rarely in the small intestine. Histologic

Well-designed and implemented environlesions include a thickened intestinal wall mental enrichment programs should
and constriction of the lumen (so-called
meet these basic requirements, with the

"napkin ring" lesion), with variable signs objective of minimizing traumatic injuries
of hemorrhage and ulceration. Metastatic
due to aggressive interactions, reducing
lesions are uncommon, and some animals
the incidence of stereotypic and selfrespond favorably to.surgical excision.

injurious behaviors, and ameliorating
preexisting abnormal behaviors. Results

Trauma: Trauma from cagemate
of attempts to manage self-injurious
aggression or self�mutilation (biting or hair
behavior ( eg, self-biting, hair plucking)

pulling) may occur occasionally, as may
with drugs such as benzodiazepines
thinning of the hair due to self-induced
or haloperidol have been inconsistent,
alopecia. Trauma is also very common in
and longterm management is generally
captive nonhuman primates in clinical
unrewarding. Socializa�ion, which may
practice. Animals that live with other
involve visual and auditory stimuli as well
species in the domestic environment may
as physical contact, appears to provide
be subjected to wounds inflicted by dogs
substantial benefit to most species of
and cats. Massive soft-tissue injury, such as
nonhuman primates, and should be
that which occurs from these attacks, may
provided within the constraints of research
cause increased loads of bacteria into the
protocols and daily management practices.

bloodstrean1, as well as acute blood loss and Additional enrichment options include shock causing coagulopathy and endotheforage boards or other food-related lial disruption. This complicated chain of
enrichment devices, manipulation mirrors,
events causes hypothermia, acidemia, and
and a variety of cage toys provided on a
inflan1mation and should be treated as a
rotating schedule to maintain novelty.

life-threatening emergency. Rapid control of Animal behavioral assessments as well hemorrhage, correcting the hypothem1ia,
as periodic review and evaluation of the
early blood component administration, and
effectiveness of enrichment program
high-volume fluid therapy are indicated to
components should be performed by
avett continued ischemia and renal
appropriately trained individuals.

PET BIRDS

1885

PET BIRDS

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Advances in avian medicine have changed
possible (considering space and cost), while
the emphasis from infectious diseases and
following mininlum size reconunendations
emergency medicine to wellness care.

(TABLE 14). Cages must be large enough to

Nutrition and behavior are important
accommodate multiple perches and ensure
components of the health of psittacine birds
that birds will have adequate room to move
and play a major role in pet bird wellness
around and exercise.

programs. Mass in1portation of wild-caught
psittacine birds was curtailed in the
mid-1980s, and the current pet bird

MANAGEMENT
population is comprised primarily of
captive-bred parrots. This has resulted

Managing pet birds in the clinical setting
in novel medical concerns and unique
can be challenging. The ability to "mask"

behavioral challenges. The knowledge base
clinical signs of illness until late in the
regarding psittacine and other pet bird diets
disease process often results in birds
and husbandry continues to increase, as
presenting much sicker than owners
does the importance of providing a
realize. Because of this, birds are also
psychologically suitable environment for
riskier patients to evaluate. Birds have a
these complex aninlals. Pet birds are
much higher metabolism than mammals,
intelligent and social animals adapted for
and oxygen deprivation can occur during
flight. Keeping solitary pet birds in small
restraint, treatment, or diagnostic
indoor cages, with limited opportunity for
sampling. Owners should be informed of
exercise, has both physical and psychologithe risks of handling and sampling and the cal consequences.

need for a step-by-step approach through

Veterinarians have a responsibility not
the physical examination and diagnostic
only to diagnose and treat disease but also
testing. Placing severely debilitated birds
to educate bird owners on how to provide
in a warm oxygen incubator or cage while
the best care for and prevent disease in their obtaining the history and before physical bird. Preventing disease entails providing a
examination may be warranted. In all
proper diet, an appropriate size cage and
avian examinations and diagnostic
perches, proper sanitation, and environprocedures, being prepared with all mental eruichment (ie, toys, foraging
needed items for examination, sample
opportunities, social interaction).

collection, and treatments before

A cage provides living space as well as
restraining the bird is important. This
protection and security. It should be large
includes a light source, oral speculum,
enough to not only house the bird and
gram scale, stethoscope, syringe and
provide ample room for climbing and
needle for venipuncture, blood tubes,
playing but also to accommodate toys,
and fluids for administration. If a bird is
foraging opportunities, and multiple
extremely stressed, in pain, or not used
perches of different sizes and textures.

to handling, sedation before diagnostic

Owners should purchase the largest cage
testing may be warranted.

•M:i•il• MINIMUM CAGE SIZE AND BAR SPACING RECOMMENDATIONS

Cage Size (inches

Bar Spacing

Bird

[length x width x height])

(inches)

Budgerigar, cockatiel, lovebird,

20 x 20 x 30

0.5
parrotlet

Conure, Poicephalus spp, caique,

36x24x48

0.75
miniature ma.caw

African grey parrot, Amazon

40x30x60

0.751
parrot, small cockatoo

Ma.caw, large cockatoo

48x36x66

1.5

1886

PET BIRDS

History: Having the owners bring a pet bird

Physical Examination: The bird should be
in its own cage for examination is desirable
observed in the cage or carrier before manual
but often impractical. Alternatively, owners
restraint. Observation should be done from a
can be asked to bring photos or videos of the
nonthreatening distance (several feet away).

cage set-up, as well as recent papers from the

The bird's stance and breathing pattern
cage floor so the droppings can be examined.

should be noted. Is it perching and standing

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The history should include the type and size
on both legs? Is it alert? Al:e the eyes open or
of cage, cage bar size and spacing, type of
closed? Al:e the feathers fluffed or sleek? Is
substrate and how often it is changed,
there a wing droop? Is the tail bobbing up
frequency of cleaning food and water bowls,
ar1d down (a sign of increased respiratory
where the cage is located in the home, and
effort)? Is the bird open-mouth breathing?

temperature and hwnidity of the cage

A respiratory rate should be obtained at this
environment. The diet that is offered, the
tin1e. The nonnal resting respirato1y rate for
foods that are actually eaten, and any recent
pet birds varies with size and species, with
changes in diet or appetite should be noted.

the rate ranging in smaller birds ( <300 g)

A complete history also should include the
from 30-60 beats/min and in larger birds
source of the bird and whether it was hand or

( 400-1,000 g) from 15-30 beats/min. If the
parent raised; exposure to other birds or pets, bird is showing signs of respiratory distress, including client-owned birds and birds
it should be placed in a warm, oxygenated
outside the home; length of ownership and
incubator before restraint.

history of previous owners; how much tin1e

Birds should be restrained in a marmer
the bird is outside of its cage and if it is
that minimizes stress and does not cause
monitored dwing this tin1e; exposure to
undue fear. If the bird is used to being
outdoors; and ti.me spent in interaction with
handled, often a towel can be slowly and
people or other birds in the household.

gently placed over the bird. If an owner has

The length of time a bird has been in the
worked with the bird at home with a towel,
household is usually inversely proportional
the veterinariar1 may ask the owner to
to the probability that illness will be caused
towel the bird and then hand it off for
by a primary infectious disease. Newly
exan1ination or testing. Minimizing
acquired birds or those exposed to other
restraint ti.me, talking to the bird in a quiet
birds outside the household via bird shows
voice, and moving slowly can help with
or pet store visits are most likely to be
many birds. Baby birds or hand-raised
affected by contagious diseases. Chronic
cockatoos often can be exan1ined with
malnutrition ar1d secondary infections are
minimal to no restraint. Many pet birds will
more common in birds without recent
step out of the cage or on to a hand arid can
exposure to potentially infectious birds.

be gently toweled. Some nervous birds may

Malnutrition is a major cause of subclinical
benefit from sedation for exan1ination and
disease in birds, which often becomes
diagnostic testing. Birds that are not
clinical when a secondary infection occurs.

handled routinely (breeding or aviary

Clinical signs of illness can be difficult to
birds) may have to be gently toweled
detect in birds. However, astute owners may directly from the cage or carrier.

recognize minor behavioral i:lifferences in

Restraint of psittacine birds involves
their bird, such as not vocalizing in the
immobilizing the head, generally with a
morning or decreased interaction with
thwnb on one side of the mandible and the
farnily members. These char1ges should
be considered potential signs of illness.

Owners with less experience or less
interaction with their birds are less likely
to notice these early signs. Feathers can
effectively mask even severe emaciation
or abdominal distention. Owne1s may
also notice other signs of illness, such as
changes in droppings or vocalizations,
or if the bird appears to be sleeping more.

Veterinar·ians who see avian patients should
be able to identify common species of pet
birds ( cockatoos, Amazon parrots, macaws,
conures, etc) and be familiar with nonnal
species-specific behaviors. For example,
parrots of Pionus spp often make rapid
sniffing noises when stressed that can be

Restrained Quaker parakeet. Courtes
mistaken for respiratory distress.

y of the

Schubot Exotic Bird Health Center.

PET BIRDS

1887

----skull

)

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::::::,� , 7:,,,;::me,as

""" I//,,,, scapula
clavicle

, , 1 ' � thoracic

----------

- - v

�
e1tebrae
metacarpal bone

�

...

nbs

�\
sternum--/)\
le
v

�::�::

phalanges

I.lit'

\

Z ve1tebrae

/
patella

�
phalanges

/

""' pygostyle
t1b1a � femur
r

• \ fibula

Skeleton of a budgerigar. Illustration by Dr. Gheorghe Constantinescu.

index or middle finger on the other. The feet

Exudate around the nares can indicate
and the distal reminges (primary wing
respiratory or sinus infection, and debris on
feathers), if not trimmed, a.re held by the
the feathers of the head or face can indicate
opposite hand in medium to large parrots.

vomiting or regurgitation. The condition of

This leaves the thorax and abdomen free to
the feathers and skin should be noted,
expand with respiration. If the primary wing including the symmetry and integrity of the feathers have been trimmed, a towel may be
beak and nails. Overgrown beak and nails
useful to prevent the wings from flapping
can indicate poor husbandry, nutrition, or
during restraint. Birds should be observed
liver disease. The integument of the feet
closely during restraint; all birds can
should be intact, without excessive wear,
become stressed, and obese birds can
callous, or ulceration. Excessive wear of
overheat, especially when held in a towel. If
the plantar surface of the feet can indicate
respirations become increased or labored,
inadequate perching or poor nutrition. Excesor if the bird becomes weak, the bird should sive wear or callous unilaterally may indicate
be returned to its cage.

a problem with the contralateral foot.

As soon as the bird has been restrained,

Body condition can be detennined by
the crop should be palpated to detennine
palpating the pectoral muscles. A keel
whether food or fluids are present. If the
scoring system from 1-5 is often used,
crop is full, the holder should monitor for
with 1 as very thin, 5 as obese, and 3 as
any signs of regurgitation during restraint.

an appropriate score for most pet birds.

Diagnostic procedmes may need to be

Severely obese birds may deposit fat over
delayed until the crop empties. An accmate
the neck, thighs, and abdominal cavity.

weight is critical to monitor health, body

Wings and legs should extend and flex fully,
condition, and recovery from illness and to
and grip strength should be symmetrical.

detennine fluid therapy, nutritional needs,

Respiratmy rate should be monitored
and medication dosages. Ears, eyes, nares,
throughout the examination; respirations
and oral cavity should all be examined and
may increase with hyperthem1ia, stress,
appear clean, with no exudate, masses, or
or obesity. Respirations should nom1alize
swellings. The choana on the roof of the oral
within 3-4 min after the bird has been
cavity should have intact sharp papilla.

released. Heart rate is rapid in restrained

1888

PET BIRDS
birds; typically, a large parrot will have
mended. Some smaller birds are able to
a heart rate of >250 beats/min when
compensate by holding their tails to the
restrained. Arrhythmias may occur but can
side and are still able to fly even with all
be difficult to categorize because of the
primary reminges trinuned.

rapid heart rate. The cloaca should have

Excessively aggressive wing trims,

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sufficient tone to provide tight closure, the
especially when performed at ilie same tin1e
skin should be moist, and the feathers
as a nail trim, can cause boili physical and
around the vent should be clean.

psychological damage to birds. The sudden
lack of stability and lift can cause birds to fall,

Routine Grooming Procedures: Wing
possibly irtjuring either ilie carina of ilie keel
clipping is frequently requested by owners.

or ilie beak. This lack of stability can lead to

Conununication with owners about wing
serious behavioral problems, especially when
trims is vital and should include the degree
it occurs in a young bird iliat is learning to fly.

and purpose of the wing trim. Owners may

Nail trimming is often requested,
assume that a wing trim is required at
frequently for the owner's comfort and not
regular intervals. In captivity, however, the
because of true overgrowth of the nails.

frequency at which feathers are molted

However, nail trinm1ing decreases the
varies widely based on nutrition, exposure
bird's stability and increases the chance
to natural sunlight, photopeliod, and
it will fall from its perch. Generally, a
hun1idity. The fact that a wing trim is a
compromise can be reached by blunting
deterrent to flight, but not a guarantee,
the needle-like tip while still leaving
should be emphasized. A bird that can only
sufficient nail to allow a stable grip.

glide to the ground indoors may be able to

Various types of equipment can be used
fly outdoors on a windy day. The basic types
for nail trims, depending on the size of the
of wing trims are: 1) Removing 4-7 of ilie
bird. Human fingernail trimmers work well
distal prin1ary flight feathers from both
to remove the tips of the nails from very
wings, below the level of the coverts. The
small birds. Cat claw trimmers, White's nail
number of feathers that must be removed is
trimmers, and hobby drills with sanding
inversely proportional to the bird's weight.

bits are all useful. Sanding tools are also

2) Leaving 1-4 distal plimary feathers and
excellent to remove excess keratin that can
removing the remainder of the plirnaries
accumulate on the lateral surfaces of the
from boili wings. This clip has fallen out of
beak. Beak trimming is sometimes
favor, but some owners have used it for
necessary because of an overgrown upper
many years. If it has worked well for their
or lower beak. Birds with beak deformities
bird, it may be wise to continue its use. 3)

often have underlying nutritional deficien

Removing a variable number of primary
cies, disease, or previous trauma. Healthy
feathers from just one wing. This clip
birds provided adequate environmental
is unnecessarily severe and not recom-
abrasive surfaces rarely require beak trims.

esophagus

\
ad.renal gland
lung
crop----

I ovary kidney

�
ureter
glandular stomach --

<l ,, _ I t%t large intestine
spleen ---....

_ 4 '-\ /
muscular stomach-----,,+.-;--

I/ bursaof

Fabriclus

..

1·
liver
clewn/

""

\
cloac
urodeum / '

vent
proctocleum

I
jejunum

Viscera, budgerigar. Illustration by Dr. Gheorghe Constantinescu.

PET BIRDS

1889

Concrete (cement) perches are available
but can cause artifacts in the blood smear,
in various sizes and textures. These can
affecting the differential cell count.

work well for medium-sized psittacine birds

The nom1al PCV varies between psitta

( -250-700 g) when a suitable size is selected
cine species. For exan1ple, cockatiels
and properly placed in the cage. These
normally have a higher PCV than many

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perches can eliminate the need for both nail
other species, averaging 500/o-55%.

trimming and removal of excess keratin

Cockatoos (Cacatua spp), however, often
from the beak. The perch should be placed
have a PCV in the 400/o-45% range.

where the bird is forced to stand for b1ief

Anemia can be a result of blood loss or
pe1iods ( eg, in front of a food bowl or treat
decreased production. Blood loss can occur
cup). To avoid irritation to the plantar
in cases of trawna or severe organ disease or
surfaces of the feet, the concrete perch
in idiopathic cases such as conure bleeding
should not be the main perch on which the
syndrome. Response to blood loss anemia
bird sits to preen or sleep.

may include the presence of inunature

In previous decades when parrots were
erythrocytes and anisocytosis along with
widely imported, open-rolled steel bands
increased polyclu·omasia. Decreased RBC
were used to identify the location at which
production can occur with any chronic
they were quarantined. Now most birds are
disease, and the anemia is often nonregenera
leg banded ( using closed bands) as chicks
tive. Toxins such as lead or oil ingestion can
for individual identification. Bands present
result in hemolytic anemia.

certain hazards to the bi.rd, but removal also

Polycythemia is rare in birds and is
entails some risk if the proper equipment is
defined as a PCV > 700Ai. lt has been reported
not available. The open (gap present), rolled,
in birds with chronic respiratory diseases
steel quarantine bands are extremely strong
and in macaws with pulmonary hypersensiand require removal by a full-size bolt cutter tivity syndrome, a condition that occurs in
with sharp edges. The closed alurninwn
macaws housed in poorly ventilated areas
bands placed on young, captive-raised birds
with birds that produce large amounts of
must be stabilized to prevent twisting while
powder clown such as cockatoos, cockabeing cut. These bands require two cuts tiels, and Af1ican grey parrots.

to remove; a sharp, properly designed

Avian RBCs are nucleated, so traditional
instrun1ent for removal decreases the danger
mammalian methods of WBC determination
of leg trauma Full-circle plastic bands can be
are not adequate. Various diluents ( eg,
removed in the same manner. Microchipping Eosinophil Unopette®, Natt-Herricks®
is replacing or augn1enting banding as a
solution) are available to enable accurate
means of identification. The standard for

WBC detenninations. Estimated WBC
placement of these chips in psittacine birds is
counts are less accurate but can be useful
in the left pectoral muscles. Adverse reactions when the individual perfom1ing the estin1ate or failures in birds have been infrequent; the
produces blood smears of consistent quality
intramuscular placement reduces the risk of
and thickness. Normal total WBC counts
microchip migration. Although microchipvary with species and age (see TABLE 15).

ping is relatively safe in large parrots with

Adult cockatiels often have total WBC
good breast muscle (> 150 g), it is riskier in
counts of 4,000-7,000 x 103/µL. Adult
smaller birds. Microchipping small birds
macaws are usually at the high end of the

( <150 g) has resulted in bleeding and death.

normal avian range (12,000-15,000 x 103/µL).

For many avian species, reference values

Clinical Pathology: Hematologic
for WBC counts are still being determined. A
testing and plasma biochemical analysis leukocytosis, and the differential or type(s) are especially in1portant in birds, because
of WBCs that are increased, can identify
physical examination tends to be less
underlying disease and give an indication
revealing than in other anin1als. The
of the most likely ca.uses. The differential
quantity of blood that can be drawn
count in birds can be affected by bacterial,
depends on the weight and health of the
fungal, and viral diseases, as well as toxins.

bird. Blood collection should be limited to

The types of avian WBCs are the heterophil,

1 % of body wt. Blood is usually collected
eosinophil, monocyte, and basophil.

from the 1ightjugular vein, which is larger

Heterophils are equivalent to manunalian
than the left. The basilic (wing) vein can
neutrophils, with much the same function.

also be used but is prone to hematoma

Avian heteropl1ils contain lysosomal
fom1ation. In medium to large psittacine
enzymes and are bactericidal and phagocytic.

birds, seabirds, and poultry, the medial

They are the first cells Lo respond to any
metatarsal vein can also be used. Coating
infectious or inflammatory disease process.

a syringe with an anticoagulant before

Instead offomung a Ii.quid pwulent material,
collection may be helpful in smaller species
avian heterophils form an inspissated,
in which san1ple collection may take longer
caseous mate1ial. This caseous material is

1890

PET BIRDS
then walled off by macrophages and fibrous

No reliable biochemical indicator is currently
tissue to fonn a granuloma Heterophilia can
available to detect early renal inlpairment.

occur during infection or from stress.

Serum or plasma glucose is higher in

Heteropenia is often associated with an
birds than in mammals, with levels of
overwhelming infection or viral disease.

250-400 g/dL common, depending on

Lymphocytes function in antibody and
species. Levels that indicate diabetes also

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antigen production and cellular and hurnoral vary with species and individuals but often immune reactions. Lymphocytosis may
are >700-800 g/dL (seep 1925).

occur in chronic infections ( chlamydia!,

Hepatic enzymes measured commonly
fungal, mycobacterial) or with lymphoid
include AST and LOH, which have normal
neoplasia. In some species ( eg, canaries and
values several times those of mammals (AST,

Amazon parrots), up to 70%of the WBCs are

10-400 U/L; LOH, 75-450 U/L). Measurement
normally lymphocytes. Lyrnphopenia is
of CK is often performed concurrently to
often associated with viral diseases ( eg,
differentiate increased values of AST due to
circovirus or polyomavirus) or sepsis.

muscle necrosis from those due to hepatic

Monocytosis is often associated with
damage. LOH is a short-lived enzyme of
chronic granulomatous diseases such as
limited usefulness in detection of hepatic
chlamydia!, fungal, or mycobacterial
necrosis. ALT levels are very low compared
infection. Eosinophilia has been reported
with those in man1mals (5-15 U/L); however,
with parasitic diseases and has also been
increased levels can indicate hepatocellular
associated with delayed hypersensitivity
necrosis. Birds have low bilirubin reductase
reactions. Basophilia can occur during inflamlevels; therefore, total bilirubin is normally matory conditions and chronic infection.

also very low, and increases with hepatic

Physiologic differences in birds create
disease are not consistent (total bilirubin
variations from accepted mammalian nom1al
range 0-0. l rng/dL). Birds also do not
values for many biochemical measurebecome icteric with hepatic disease as do ments. Because of the excretion of uric acid
mammals; they excrete biliverdin through
rather than urea as the primary product of
their kidneys, resulting in yellow or limeprotein metabolism, uric acid levels are green urates. Bile acid measurements are
significantly higher in birds than in mammals,
useful indicators of hepatic function, with
whereas BUN is significantly lower. Uric acid
levels < 100 µrnol/L considered normal for
may be increased in severe renal disease or
most avian species ( depending on the
with articular gout (seep 1926). Severe
laboratory). Establishing reference values
dehydration may increase uric acid levels,
for different avian species will enhance the
but levels return to normal with rehydration.

usefulness of bile acid assays.

lftNll�I NORMAL HEMATOLOGIC VALUES IN SELECTED PET BIRD SPECIES

Sample

Bird

Size (n)

WBC x 103/µL

PCV

African grey parrots (Psittacus erithacus)

176

8-11

42-50

Amazon parrots (Amazona spp)

155

7.5-12.5

44-49

Budgerigars (Melopsittacus undulates)

57

2.5-6.5

42-53

\

Cockatiels (Nymphicus hollandicus)

212

3.0-7.8

45-57

Cockatoos, umbrella (Cactua alba)

115

5-13

38-48

Conures (Aratinga spp)

62

7.5-11.5

42-49

Eclectus parrots (Eclectus roratus)

44

7.0-11.7

41-49

Lovebirds (Agapornis spp)

31

4.5-9.0

39-51

Macaws (Ara spp)

146

8.5-15.5

41-52

Pion us parrots (Pionus spp)

28

7.0-11.5

44-51

Quaker/monk parrots (Myiopsitta monachus)

62

5.5-12.5

38-48

Senegal parrots (Poicephalus senegalus)

26

6.5-12.0

37-49

Note: Samples were obtamed at wellness examination. No other concurrent disease was detected or treated, except for behavioral concerns.

PET BIRDS

1891

Calcium and phosphorus values are
warmed to 102° -106°F Sites of administra similar to those found in mammals. These tion are the lateral flank, the inguinal web,
levels may increase up to 3-fold in hens in
and the back. Maintenance fluids are
preparation for egg laying (ie, calcium -30
estimated at 50 ml/kg divided bid-tid. In
mg/dL and phosphorus> 10 mg/dL), usually
dehydrated birds, 500Ai of the total daily
with a relatively normal ratio of these minermaintenance can be administered SC (25

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als. Total solids as measured via refractommllkg) and repeated every 6-8 hr until eter are significantly lower in birds than in
hydration is reestablished.

mammals, with levels of 3--5.5 g/dL normal

IM injections are given into the pectoral
for most species. Total solids can also
muscles in most pet birds; leg muscles are
increase in reproductively active hens.

also used in some species, particularly

Cholesterol and triglyceride reference
raptors. The muscle fibers of birds are more
ranges are still being evaluated, but
vascular and tightly packed than those of
reference values are -180-250 mg/dL for
man1rnals, making both muscle necrosis
cholesterol and 51-200 mg/dL for triglycerand inadvertent IV ir\jection more likely.

ides. Increased levels of both triglycerides

IV ir\jections are occasionally indicated in
and cholesterol have been reported in birds
birds. Con1rnon medications administered
fed a high-fat diet. High levels can also be

IV are some antibiotics, amphotericin B,
seen in reproductively active females and
chemotherapeutic drugs, contrast media,
may be a risk factor in birds that develop
and fluids.

atherosclerosis. Omega-3 fatty acids added

Indwelling catheters can be placed in
to the diet as well as dietary restriction and
the jugular, basilic, or medial metatarsal
conversion to a pelleted diet have been
veins for constant-rate infusions or
shown to reduce hypertriglyceridemia and
intem1ittent fluid administration. Intraossehypercholesterolemia.

ous (IO) catheters can also be inserted,

Hematology and Plasma Biochemistry
generally in the proximal tibiotarsal bone or
of the Neonate: Neonates have some
distal ulna. A standard hypodermic needle
in1portant differences from mature birds
may be used ( usually 25-gauge for initial
in their hematologic and biochemical
entry, followed by a second 22-gauge needle
parameters. Neonates have a lower PCV
sutured in place), or a spinal needle with

(20%-300Ai). The normal adult range is
stylet may be used for large birds. Without
present beginning at 10-12 wk in most
a stylet or second needle, a bone plug may
species. Neonates have a lower total protein
obstruct the needle. The IO or IV catheter

( 1-3 mg/dL) and concomitant lower plasma
is intermittently flushed with wann saline
albumin concentrations than adults. A high
whenever fluids are not being infused.

WBC count (20,000-40,000 cells/uL) is

Maintaining an IV catheter in an avian
common in neonates; the nom1al adult
patient can be challenging, and IO catheters
range is present at 9-11 wk of age. Neonates
are often preferable for longte1m fluid
also have lower uric acid values and higher
therapy. However, fluid tllerapy via IO
alkaline phosphatase and CK concentracatheters can be painful to the bird, tions than adults.

especially after 1-2 days.

Crop (gavage) feeding may be used
to meet caloric needs in anorectic birds.

Routine Medical Procedures: Injec

Con1rnercial formulas are available and
tions can be given by several routes. SC
convenient to use. Adequate hydration and
injections are used for fluid administration,
normal body temperature (103° -l06°F
some vaccinations, and many routine

[39°-41 °Cl) must be established before
medications such as antibiotics. Preliminary initiating crop feeding to prevent desiccastudies show that the SC route may be as tion of the crop food and GI stasis. In adult
effective as IM injections for most medicabirds, generally 30 mVkg can be administions, without the associated muscle tered tid-qid. Baby birds have a much more
necrosis. To ensure that the medication or
distensible crop and will hold -lOOAi of their
fluid being injected is actually deposited
body weight per feeding ( 100 mllkg). Oral
subcutaneously, the skin must be clearly
medications may be added to the crop
visualized; use of alcohol to wet the skin
feeding or given directly by mouth. The
and feathers is recommended to aid in
technique of holding tile bird so that the
visualization. Insulin syringes (50 U or 0.5
medication is administered into tile
mL) with 27-gauge needles are invaluable
con1rnissure of tile mouth and rolls onto
for accurate dosing when small quantities
tile tongue will minimize stress, loss of
must be administered. SC fluids are often
medication, and tile danger of aspiration.

used in birds. To maximize their absorption

Medicating birds can be quite difficult for
and minimize discomfort, fluids should be
owners; wrapping the bird in a towel for

1892

PET BIRDS
administration of medication can be
minimized. A small animal ventilator can
stressful for both the bird and the owner
be used for most birds as small as 100 g and
and, in some cases, adversely affect the
can greatly improve ventilation during
human-bird bond. Compounding medicaanesthesia. If a mechanical ventilator is not tions to make them more palatable and in a
available, manual intermittent positive

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smaller volume can be very helpful in using
pressure ventilation will increase oxygenaoral medications. Mixing the flavored tion in anesthetized birds. A capnograph,
medication with favorite foods, juice, or
pulse oximeter, and Doppler are also useful
baby food can also help ensure compliance.

for anesthetic monitoring. The normal

Medications administered in the water are
body temperature of most psittacines is
indicated only in special circumstances

103°-l06°F (39°-41 °C). Birds tend to lose
such as small flocks of birds or aviary birds
body heat rapidly when anesthetized, and
not used to handling and would require
maintaining body temperature drning
daily netting and restraint, or in special
prolonged anesthesia or surgery is crucial
cases in which an owner cannot handle a
for recovery. Birds with feather loss ru·e
bird. Enrofloxacin and doxycycline in
more at risk of hypothennia. Water warming
drinking water generally provide adequate
blankets under the bird or Bair HuggersTM
blood levels for efficacy. However, lack of
can be used effectively to maintain body
accurate dosing, stability of the medication,
temperature. An emergency drug sheet and
and palatability make this route undesirable
emergency drugs should be readily available
in most cases.

whenever a bird is anesthetized.

Sedation is sometimes desirable for

Environmental management is very
diagnostic or treatment procedures to reduce in1portant; severely ill birds benefit greatly stress and minimize fear. Midazolam adminfrom increased environmental temperature istered at 0.5--1 mg/kg, IM, or 1-2 mg/kg
and hun1idity ( eg, use of commercial
intranasally (IN) is a safe and effective
incubators with temperature ru1d hrnnidity
sedation protocol in most pet birds;
controls). For at-home emergencies, a
flumazenil (0.02-0.1 mg/kg, IM or IN) may
warm environment cru1 be created by
be given to reverse the effects. If the bird
wrapping clear plastic wrap ru·ound three
is thought to be in pain or discomfort,
sides of the cage and placing an electric
butorphanol (0.5--3 mg/kg, IM or IN,
heating pad on the remaining side, being
depending on species) may be given alone
sure the bird cannot reach the pad. Digital
or with midazolan1. Amazon parrots often
thennometers with remote probes can
require the higher dosage (2--3 mg/kg) of
provide accurate monitoring of environbutorphanol, whereas raptors require the mental temperatures. A quiet location, away
lower dosage (0.5 mg/kg). lsoflurane or
from the sound of barking dogs and other
sevoflurane anesthesia delivered by face
excessive activity, will decrease stress.

mask can also be used alone or in conjunc

The cage arrangement cru1 be critical for
tion with sedation for more prolonged
ill birds. If a perch is supplied, tl1e food and
procedures or painful treatments.

water must be elevated so that the bird has

Intubation in birds is relatively easy,
ready access without having to climb down
because the absence of an epiglottis
from the perch. Often, it is best to remove
facilitates visibility of the tracheal opening
perches entirely from the cage of an ill bird
and arytenoids. Fasting before anesthesia
and place the food and water container on
should be of minimal duration; fasts of 4-6
the cage floor so that the bird has easy
hr are typical. Regardless of the duration of
access and does not expend energy simply
the fast, the crop should be palpated for the
trying to maintain a perched position.

presence of food or fluid before anesthesia.

Delayed crop emptying is cmm11on in

PEDIATRIC DISEASES
clinically ill birds. If anesthesia must be
administered to a bird with food or water

Birds are classified by their maturity level at
still in the crop, fluid should be removed by
hatching. Parrots, doves, and fmches ru·e
a feeding tube if possible, and the head
altricial, hatched without feathers, with
should be elevated for the duration of
eyes closed, and helpless. Poultry, ratites,
anesthesia, regardless of whether the bird
and waterfowl are born precocial, with
is intubated. Endotracheal tubes should be
down feathers, open eyes, and the ability
uncuffed, because the absence of a tracheal
to walk and feed themselves at hatching.

ligament increases the risk of tracheal

Psittacine .neonates are completely
necrosis if a cuff is overinflated. Even an
dependent on tl1e pru·ent birds for wam1tl1
uncuffed tube can cause tracheal damage
and food; they also lack a functional
or necrosis; therefore, after the bird is
inunrn1e system and are more susceptible to
intubated, head movement should be
disease. Because of these characteristics,

PET BIRDS

1893
proper husbandry and nutrition of the chick
their keel bone; therefore, the muscle and
and parents is critical for their health and
subcutaneous fat over the hips, elbows, and
survival.

toes should be evaluated. It should be

Today, chicks are either parent raised
detennined whether the ea.rs and eyes are

(most small parrots such as budgerigars and open, or when they opened, if known.

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lovebirds) or hand raised (large parrots).

The skin, feather quality, and distribution

There are advantages and disadvantages
of the feathers should be exainined. Healthy
with both methods. Most aviculturists
chicks have yellowish pink skin, and
believe that hand-raised parrots make better feathers first appear on the head, wing, and pets and that incubator hatching and hand
tail. Abnormal feather growth or delayed or
raising reduces the incidence of some
abnom1al opening of eyes can be a sign of
infectious diseases. Disadvantages of hand
stunting. Stress bars (lucent areas a.cross
raising can include stunting and an increase
the vane of the feathers) indicate a period of
in husbandry-related diseases such as crop
stress when that portion of the feather was
stasis or aspiration pnewnonia Many avian
fonning. These are common during
veterinarians and behaviorists also believe
weaning, so a few stress bars are not
that hand raising may lead to behavioral
uncommon. A large nwnber of stress bars
issues because chicks cannot learn speciesmay indicate an underlying illness or speci.fic behaviors from parent birds and
condition.

become in1p1inted on people.

The oral cavity should be moist with no

The health of a chick depends on many
plaques or lesions, and the choana should be
factors, such as the health of the parents,
exaniined for blunting of the choanal papilla,
genetics, the incubation process, nutrition
which can indicate hypovitanlinosis A or

(type of food, temperature, and consischronic respiratory disease. The crop may tency), environment (hwnidity, warmth, and be quite full in a neonate. The veterinarian cleanliness), and exposure to infectious
should observe for crop contractions and
diseases. When an ill neonate is presented,
ask when the chick was last fed and how
the history of not only the chick, but also of
much was fed, to detemline whether the
its parents, the avia1y, and the nursery a.re
crop is emptying nonnally. Nestlings have a
in1portant. Is the chick being hand fed or
nom1ally distended abdomen because of an
parent fed? Is the chick incubator hatched?

enlarged proventriculus and ventriculus

How old is the chick? Is the nursery closed,
from being fed lai·ge ainounts of fom1ula.

or are chicks taken in from other facilities?

Chicks should be handled carefully to avoid

What is the temperature and hwnidity of the
placing excess pressure over their abdomen.

nursery? What is the type of food fed, its

The spine, neck, wings, legs, and feet
consistency, temperature, amount fed, and
should be exanlined for abnonnal curvature
frequency of feedings? What are the
or weakness and evaluated for npm1al
cleaning practices?

posture. The vent should be clean of debris.

General environmental temperature
guidelines are for newly hatched psitta.cine
chicks, 92°-94°F; Wlfeathered chicks,

Aspiration Pneumonia: Aspiration

90 ° -92°F; pin-feathered chicks, 85° -90 °F;
pnewnonia is one of the most common
and fully-feathered and weaned chicks,
causes of respiratory disease in hand-fed

75° ---80 °F.

psittacine birds. Chicks can aspirate while

A diet of25o/e>-30% solids should be fed to
being fed large quantities of liquid formula,
chicks >2 days old (more dilute fonnula for
especially when being fed by ai1 inexperinewly hatched), with the environmental enced person. Aspiration often occurs as
temperature between 102°-l06°F Most
birds begin to wean.

medical issues aiise in young birds in the

Clinical signs include increased respirafirst week of life, at fledging, or at weaning.

tion, respiratory distress, poor feeding

Physical exainination of the chick can
response, and depression. Depending on
typically be done with minimal restraint,
the age and size of the chick, a CBC and
and the chick should be kept warm
radiographs may aid in the diagnosis;
throughout the exainination. The crop
however, diagnosis is often based on history
should be palpated at the beginning of the
and physical exainination findings.

exan1ination. Birds with food in their crop

Treatment consists of oxygen therapy,
should be handled carefully to reduce the
nebulization, antibiotics, antifungals,
risk of regurgitation and/or aspiration.

wa.nnth, supplemental fluids, ai1d anti

Menta.tion and body weight ( a growth cha.rt
inflanll1latory drugs. Prognosis is guarded.

should be requested from the breeder if
possible) should be noted. Before they

Bacterial Disease: The nonnal gut microfledge, chicks have little musculature over flora in chicks is primarily grain-positive

1894

PET BIRDS
bacteria. The presence of large nwnbers of
older birds, a rigid endoscope may be
gram-negative bacteria or budding yeast
necessary to visualize and extract upper GI
indicates infection. Bacterial infections can
foreign bodies. The endoscope may be used
occur from multiple sow·ces: an unsanitary
either orally or through an ingluviotomy
envirorunent, inappropriate storage of
incision, depending on the accessibility of
formula, and use of unclean feeding utensils.

the foreign body.

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Clinical signs can include crop stasis, poor
feeding response, regurgitation, depression,

Crop Stasis: Crop stasis, defined as the
and dehydration. Diagnosis is based on
inability of the crop to empty in a normal
clinical signs and results of a fecal or crop
time frame, is a common condition in

Gram stain, CBC (leukocytosis, monocytohand-fed chicks. Crop stasis can occur due sis ), and culture and sensitivity testing.

to poor husbandry and nutritional practices

Treatment is with antibiotics, based on
or p1imary disease. Envirorunental
cultme and sensitivity results if available,
temperatures that are too cold or inadand supportive care. Neonates on antibiotequate humidity can lead to crop stasis, as ics often develop secondary yeast infeccan feeding formula that is too cold or thick.

tions; therefore, prophylactic treatment

All aspects of the nursery and feeding
with an antifungal drug such as nystatin or
practices should be evaluated.

fluconazole may be warranted (see TABLE 18, Clinical signs include a distended crop,
p 1901).

dehydration, poor feeding response,
regw·gitation, and depression. Diagnosis is

Yeast Infection: Candida albicans can based on physical examination findings,
be present in low nun1bers in a healthy
palpation of the crop, and cytology and/or
chick but may proliferate in the presence of
culture of the crop contents.

antibiotic treatment, malnutrition, stress, or

Treat111ent may include physically
immunosuppression. It is the most common
emptying the crop, fluid therapy, antibiotics
fungal infection in young birds and can result and /or antifungals, and providing smaller, in thickening of the crop mucosa, which
more dilute, and more frequent feedings
may be palpable externally and has been
once the crop is emptying.

described as "Turkish towel in appearance."

Clinical signs are crop stasis, poor

Crop Burns: Crop bwns result from
feeding response, and depression. There
feeding baby bird formula that is too hot. This
may be lesions or plaques in the oral cavity.

can occur when a microwave oven is used to
intestinal or gasbic candidiasis can result in
heat the forn1ula (not recommended because
malabsorption. Diagnosis is with fecal or
of the formation of hot spots within the
crop cytology revealing large numbers of
fom1ula). Mild cases may result in red
budding yeasts.

and inflamed skin in the area of the crop.

Treabnent is with antifungal medications.

Second- and third-degree bwns will be

Antifungals should be given to baby birds
acutely inflamed and blistered and may lead
prophylactically when on antibiotic therapy
to tissue necrosis and fistula forn1ation. In
to prevent yeast overgrowtl,1 (seep 1899).

subacute cases, birds may be presented with
food draining from a fistula tlu·ough the crop

Viral Disease: The most common viral
wall and skin. Diagnosis is based on history,
diseases in psittacine chicks are polyoma
clinical signs, and physical examination
virus, avian bomavirus, proventricular
findings. Treab11ent includes antibiotics,
dilatation disease and circovirus, and
supplemental fluids, anti-inflanu11atory cl.tugs,
psittacine beak and feather disease (see
and nutritional suppmt. Surgical repair is
p 1908).

often required but should be postponed until
the burned area is well demarcated ( usually

Foreign Bodies: Foreign bodies can be
several days); repair involves debriding
found in young birds, including ingestion of
devitalized tissues, separating the crop wall
substrate, toys, or feeding tubes. Diagnosis
from overlying skin, and closing the two
is based on clinical signs, history, and
layers separately. Prognosis is good if tl1e
radiographs or CAT scan results. Treabnent
remaining crop wall is sufficient for closure
may require an ingluviotomy to gain access
and the esophagus is intact.

to the mucosa! swface and lumen of the
crop, provenbiculus, or ventriculus.

Esophageal and Pharyngeal Trauma:

Removal of a foreign body, such as a feeding Esophageal and pharyngeal traun1a occurs tube, is the most common indication for this from improper hand-feeding teclmique, procedure in pediatric birds. In larger or
either with the syringe tip or a rigid feeding

PET BIRDS

1895
tube. This leads to tissue trauma, cellulitis,
because of handlers inexpe1ienced at
and distribution of food into subcutaneous
hand feeding. Inappropriate quantities of
tissues. Birds may present depressed,
han d -feeding fonnula, incorrect temperaanorexic, cold, and dehydrated, with poor ture, and incorrect consistency of the
feeding response. Swelling may be palpable
fonnula cause reduced feeding response
in the neck area. Diagnosis is based on
and/or GI stasis. Birds purchased soon after

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the history of hand feeding and oral or
arriving at the pet store are often mistakenly
endoscopic examination to identify the
labeled as "weaned." In nature, these birds puncture site.

would be eating paitially on their own but

Surgically opening the pockets, flushing
still receiving supplementation from their
the wounds, and allowing for drainage is
parents. When such a bird is sold to an
important in treatment, along with
uninforn1ed owner, it usually takes a few
antibiotics, analgesics, anti-inflammatory
days to a few weeks for the bird's insuffidrugs, and supportive care. Prognosis cient food intake to create noticeable
depends on severity of the lesion, an1ount
debilitation and weakness. These birds
of food deposited in the tissues, and how
may also have underlying problems, eg,
quickly the lesion is detected and treated.

decreased hepatic function or inm1unosup

In severely trawnatized cases, prognosis
pression.

is guarded to poor.

Diagnosis is based on the history and
physical exai1li..nation findings. Treatment is

Hepatic Lipidosis: The liver relative
supportive (fluids, nutritional support, and
to total body weight is typically larger in
wanntl1). Antibiotics or antifungal drugs
neonates than in adult birds, so some
may or may not be needed, based on
degree of hepatomegaly is nmmal in chicks.

diagnostic test results. Some of these birds

However, neonates with hepatic lipidosis
will survive, but many will not.

typically have the following characteristics:

1) they are usually still being hand fed, often

Splayleg or Rotational Leg Deformity:

with a commercial formula to which the

The term splay leg is a catchall for deformiowners have added peanut butter, oil, or ties of the legs in young birds. Often, there
some other high-fat food, and 2) they are
are laxities of the ligai11ents of the stifle
usually heavy for their age and exhibit
and/or angular deforn1ities of the femur,
severe respiratory distress. These birds
tibiotarsus, and tai'Sometatarsus. Causes
must be handled gently and minimally. Cool
are poorly documented, but risk factors
oxygenation is the best first step. They have
include nutritional deficiencies ( consistent
virtually no air sac capacity, and tl1e stress
with those of metabolic bone disease, see
of feeding and breatlli..ng at the same tin1e
p 1917) and insufficient support or substrate
may exceed their oxygen reserves.

in the enclosure.

Drastically reducing the quantity of crop

Various methods of external coaptation
food per feeding, adjusting the content of
have been devised ai1d are most successful
the formula, and adding lactulose to the
when the bird is young. Placing tl1e chick in
fo1mula are the general nutritional changes
a deep enclosure with a suspensory device
required. Parenteral fluid supplementation
or cloth that allows the leg to be directed
will help keep the initially hyperthennic
vertically or taping the legs together in a
bird hydrated. When possible, blood

"hobble" may be cmTective if implemented
san1ples should be submitted to check for
early. Stifle subluxation can develop
concurrent infection or other diseases.

because of disruption of the cruciate and /or
collateral ligainents. Surgery ( osteotomy

Failure to Thrive: Hereditary, congenital,
and external skeletal fixator) may be used
and husbandry issues may affect the growth
for rotational deformities.

of young birds. Stunted chicks are thin, and
the head is dispropo1tionately large. Toes,

Beak Deformities: Mandibular
wings, and hips are thin; eye and ear
prognathism commonly occurs in several
openings may be delayed. The skin may be
birds from the san1e clutch and is seen most
dry and without adequate subcutaneous fat.

commonly in cockatoos. If detected early,

Abnonnal feather patterns (swirls) may
tl1e hand feeder may be able to correct
develop on the head of a stm1ted chick.

prognathism by pulling the beak upward

Stunting can develop early, in the frrst 30
and out for several minutes, several tin1es a
days, or shortly after purchase from the
day. In older chicks, the condition may
breeder. Usually stunting is caused by
require a prosthetic that pulls the upper
husbandry and nutritional issues, often
beak out and over the lower beak. This can

1896

PET BIRDS
be cumbersome and painful, and the
correction is needed or recommended.

prosthetic often needs to be reapplied.

Extending the palpebral fissure by

Trans-sinus pinning is a more recent and
cortjunctival eversion can be performed
more reliable method of correction but
with modest success when the palpebral
carries some risk.

ape1ture is absent or reduced and functional

Scissor beak is a lateral deviation of the
vision is compromised.

'

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upper or lower beak. This may be caused
by improper incubation temperature or

"Lockjaw": Bordetella avium is the possibly genetic factors in some chicks.

causative agent of a syndrome that can

If detected early, mild scissor beak can be
appear in clutch mates, most commonly in
corrected by manually placing a counter
cockatiels. Bacterial invasion from the
force on the beak for several minutes 2-3
sinuses progresses to the skeletal muscle of
times daily. More severe defects may require the mandible, resulting in a myositis and placing a beak prosthetic.

"locltjaw." Treatment is antibiotics and
supportive care. Manually opening the beak

Constricted Toe Syndrome: Concan be difficult, so feeding and medicating stricted toe syndrome is fairly common in
the bird can be challenging. Prognosis is
neonates, often affecting more than one
guarded to grave.

digit. An annular band of fibrous tissue
forms at a joint of the digit, impeding
circulation. The cause is unknown, although Choanal Atresia: Choa.i1al atresia is seen either excessively low or high htunidity and
most commonly in African grey parrots but
septicemia have been proposed. This
has also been documented in other species.

syndrome is most common in Eclectus

With choanal atresia, the conununication
pa.tTOts a.i1d macaws, usually in chicks
between the nares, infraorbital sinus, a.i1d
housed in environments with inadequate
the choana is incomplete or absent. Clinical
humidity.

signs are increased mucus accumulation

When detected early, debriding the
a.i1d possible infection in the nares and
annular ba.i1d and applying a moist dressing
sinuses. Blunted choa.i1al papilla may be
is often effective. In more severe cases,
detected on oral exa.inination. Diagnosis is
small longitudinal incisions can be made
by endoscopic exa.inination of the choana.

on the medial and lateral surfaces of the

Atresia can be treated by creating an
affected toe to allow for swelling and to
opening in the choana through the na.i·es
promote circulation. If circulation Joss is
with an intra.inedullary pin. A red rubber
severe and necrosis is appa.i·ent, a.inputation
feeding tube is then threaded through the
may be necessary. NSAIDs can be used to
nares, out the choana, and back behind the
reduce inflan1mation and pain. A bandage
head of the bird and is left in place for 2-3
will protect the site from contan1ination a.i1d wk This procedure is usually performed in secondary infection. Early detection a.i1d
stages, beginning with a small tube first and
intervention is c1itical in successful
following with a larger tube.

treatment.

BACTERIAL DISEASES

Toe Mal position: Toe malposition
usually involves the lateral or fourth toe,

Bacterial diseases a.i·e common in pet birds
which points forwa.i·d instead of backwa.i·d.

and should be considered j.n the differential

If discovered early, malposition is easily
list of any sick bird. Inappropriate husbancorrected by taping the toe in a normal dry and nutiition are often contributing
position. In young birds, the foot can be
factors. Neonates and young birds a.i·e
bandaged with the toe pointing backwa.i·d in
especially susceptible. GI and respiratory
the nom1al position for several days. Older
infections are most common a.i1d can lead
chicks may need prolonged bandaging.

to systemic disease.

Normal bacterial flora of companion

Cryptophthalmia (Eyelid Atresia):

birds include Lactobacillus, Corynebacte

Cryptophthalmia is most commonly seen in
rium, nonhemolytic Streptococcus,
cockatiels and is often observed in clutch

Micrococcus spp, and Staphylococcus
mates. The condition is usually bilateral.

epidermidis.

The eyelids, if present, are generally normal

The most commonly repmted pathogens
in conformation but greatly reduced in
are grain-negative bacteria (Klebsiella,
length, leading to small to nonexistent

Pseudomonas, Aeromonas, Enterobacter,
palpebral fissures. If the palpebral fissure is

Proteus, and Citrobacter spp, Escherichia sufficient to allow functional vision, no
coli, and Serratia marcescens ). Pasteurella

PET BIRDS

1897
spp have been repo1ted as possible

Diagnosis is based on clinical signs and
septicemic agents in birds attacked by pet
results of cytologic examination and culture
cats or rats. Mycobacterium and Chla
of tissue or swab san1ples. A Gram stain is
mydia are common intracellular bacterial
used to identify normal flora, yeast, and
pathogens. Infections with Salmonella spp
spore-forming bacteria. Culture is needed
are occasionally seen.

to identify specific organisms and their

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The most common gram-positive
sensitivity to antibiotics. Sainples can be
bacterial pathogens are Staphylococcus
obtained from the respiratory, GI, urinary,
aureus, S intermedius, Clostridium,
and reproductive tracts. Sample sites for

Enterococcus, Streptococcus, and other
culture and cytology include the choanal

Staphylococcus spp. Methicillin-resistant
slit, sinus, cloaca, wounds, conjw1ctiva,

S aureus (MRSA) is rare but has been
internal organs (via ultrasound-guided
documented. Mycoplasma spp have been
fine-needle aspirates, endoscopic exan1inain1plicated in chronic sinusitis, often found tion, or surge1y), and blood.

in cockatiels. This organism is difficult to

Treatment is based on location of
culture, and the true incidence is unknown.

infection and results of culture and

Staphylococci and streptococci ( especially
sensitivity testing. See TABLE 16 for a hemolytic strains) and Bacillus spp are
paitial list of frequently reconunencled
thought to be responsible for several
antimicrobials.

dem1atologic conditions in psittacine birds.

Staphylococci are often isolated from

Chlamydiosis
lesions of pododermatitis (bumblefoot) in
many avian species.

(Psittacosis, Ornithosis)

Clostridial organisms are conunon

Chlamydia psittaci is an obligate
secondaiy invaders of dainaged cloacal
intracellular bacterium tl1at can infect all
tissue in birds with cloacal prolapse or
companion birds but is especially common
papillomatosis. Several specific syndromes
in cockatiels, budgerigars, and parrots.

of birds cai1 aiise from various species of

Cu1Tent state and federal regulations
clostridia. A Grain stain or anaerobic
governing the testing, reporting, treatment,
culture is necessaiy to identify these
and quarantine for Chlamydia should be
organisms.

followed.

•M:iif rj ANTIMICROBIALS USED IN PET BIRDS

Antimicrobiala

Dose, Route, and Frequencyb

Amikacin sulfate

15 mg/kg, IM, bid

Amoxicillin/clavulanate

125 mg/kg, PO, tid

Azithromycin

50 mg/kg/clay, PO

Ceftazidime sodium

75 mg/kg, IM, tid

Ciprofloxacin

25 mg/kg, PO, bid

Clindan1ycin

100 mg/kg, PO, bid for 5 days to treat Clostridium Doxycycline

25 mg/kg, PO, bid for 45 daysc

Doxycycline injectable, 20 mg/mL

75-100 mg/kg, IM or SC, every 5 days, then weekly
for six treatments0

Enrofloxacin

15-20 mg/kg, PO or IM, bid

Metronidazole

25 mg/kg, PO, bid for 14 days for Giardia,

Clostridium

Marbofloxacin

2.5 mg/kg/day, PO

Trimethoprim/sulfamethoxazole

50-100 mg/kg, PO, bid
a Most are unapproved for use in birds, and caution is indicated.

b May vary with etiology and species treated
c Duration and dosage for treatment of Chlamydia

1898

PET BIRDS

The incubation period of C psittaci is from chl01tetracycline-in1pregnated seeds or 3 days to several weeks. The organism is
other foods are available or can be
excreted in the feces and in nasal and ocular
manufactured to treat infected flocks. A
discharge of infected birds. Although labile in doxycycline-medicated feed for budgerigars the environment, the organism can remain
can be created by combining 300 mg of

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infectious in organic debris for > 1 mo.

doxycycline hyclate (froni capsules) with

Clinical signs range from asymptomatic

1 kg of a mixture of oats, millet, and
carriers to severe disease and may include
sunflower oil ( 1 part cracked steel oats is
ocular, nasal, or cor\junctival irritation and
mixed with 3 parts hulled millet; add 5-6 mL
discharge; anorexia; dyspnea; depression;
of sunflower oil per kg of the oat/seed
dehydration; polyuria; biliverdi.nuria; and
mixture). Fresh medicated mix should be
diarrhea. Clinically ill birds may have a
made daily and feel as the sole diet for 30
leukocytosis, monocytosis, and increased
days. Doxycycli.ne may also be added to the

AST and bile acid concentrations. Radiowater for cockatiels (200-400 mg doxycygraphs may reveal hepatomegaly, splenocline hyclate/L of water), Goffin's cockatoos megaly, or airsacculitis.

( 400-600 mg/L ), and African grey paiTots

Diagnosis of C psiltaci can be challeng

(800 mg/L ). A doxycycli.ne syrup, using a
ing, especially in the absence of clinical
monohydrate- or calcitm1-syrup formulasigns. Few laboratories will culture the tion, can be given at 40-50 mg/kg/day, PO,
organism. Various antibody and antigen
to cockatiels, Senegal paiTots, and bluetests are available, but these have limitafronted and orange-winged Amazon paITots; tions. Serologic tests available include
in African grey paITots, Goffin's cockatoos,
indirect fluorescent antibody, complement
blue and gold macaws, and green-winged
fixation, ELISA, and fluorescent antibody.

macaws, the recommended dosage is 25

A positive serologic test result is evidence
mg/kg/day, PO. These indirect modes
that a bird has been infected but might
of antibiotic administration depend on
not indicate active infection. Exposed
ingesting sufficient quantities of antibiotics
but clinically normal birds may produce
to maintain effective blood levels, which
appreciable antibody titers. Acutely ill birds
may not always occur. Only certain
may not mount an antibody response, also
forrn ulations of doxycycline can be given
yielding false-nPgative results. These factors IM or SC. Doxycycli.ne i.rtjectable has been make an antibody test an insufficient
successful at 75-100 mg/kg every 5-7 days
screening tool for chlamydiosis in birds
for 6 wk.

when used alone. Because of the intracel

Because C psillaci is transmissible to
lular nature of Chlamydia and the
people, the zoonotic risk must be considered
reduction in numbers of organisms that
when designing the diagnostic and theraaccompanies antibiotic use, false-negative peutic plan. Current state and federal
results of antigen tests are conm1on. With
regulations governing the testing, reporting,
the advent of PCR testing, diagnosis of
treatment, and quarantine for birds infected

Chla.mydia is more readily accomplished,
with Chlamydia should be followed. A
and attempts to culture the organism
compendiw11 of control measures is available
or identify elementary bodie·s in tissue
at www.nasphv.org/docurnentsCompendia specimens are rarely done. Laboratories Psittacosis.html.

should be consulted before shipment to
identify appropriate samples and shipping
methods. Because of the difficulty in

Avian Mycobacterioi:is
diagnosing Chlamydia, a single test method Avian mycobacteriosis infections are may not be adequate, and a PCR assay of
usually caused by Mycobaclerium aviiim
a combined cor\junctival, choanal, and
and M genavense. Mycobacterium inlrncel
cloacal swab sample, in cor\junction with
lulare, M bovis, and M tuberculosis are less a serologic test, is recommended.

commonly reported. Psittacine birds most

Doxycycline is commonly used for
commonly infected are brotogeris
treatment of Chlamydia infection. Because
parakeets and Amazon paJTots. Avian
the treatment pe1iod required to eliminate
mycobacteriosis is a chronic progressive
the organism is uncertain, treatment for
disease affecting the liver and GI tract.

45 days is reconm1ended. Dietary calcium

Clinical signs include anorexia, weight loss,
sources should be reduced if doxycycli.ne
depression, and diaiThea. Birds with eai·ly
is administered orally. Clinically ill birds
infections may show few clinical signs.

should be treated with oral or injectable

Diagnosis of mycobacterial infection can
doxycycli.ne initially to establish therapeube challenging and is most reliably done by tic drug levels quickly. Fonnulations of
acid-fast staining, culture, and/or DNA
doxycycline in the food or water and
probe of a biopsy specin1en. Biopsy of the

PET Bl RDS

1899
liver, intestines, spleen, or a suspected mass
which commonly affects the GI tract.

is recommended; however, PCR testing of

Although C albicans is the most common
ultrasound-guided fine-needle aspirates of
isolate, others including C tropicalis,
the liver may be diagnostic. Avian mycobac

C parapsilosis, C glabrata, and H a,nse

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teria are difficult to culture, so a negative
nula spp may also be found and may be
culture result does not exclude infection. A
refractory to treatment.

fecal acid-fast stain has poor sensitivity but

C albicans is not generally considered
may identify birds shedding large numbers
a primary pathogen. Small nun1bers of
of organisms; PCR testing of a fecal sample

Candida are commonly found in the GI
is a more sensitive test method. Most birds
tract of birds and may become pathologic
will have a significant leukocytosis with a
when normal digestive flora are disrupted
monocytosis. Radiographs may reveal
by in1munosuppression. (See also CANDIDI
hepatomegaly and splenomegaly. Granulo

ASIS, p 2791.)

mas may occur that may be confused with

Candidiasis most conunonly affects
tun10rs.

unweaned chicks. Those on broad-spec

If infected birds are in a multiple bird
trum antibiotics are most at risk. Neonatal
collection, determining whether other birds
cockatiels are considered most susceptible.

are infected can be difficult. Husbandry and

Infection may be endogenous, because
sanitation should be assessed. High-risk
of yeast overgrowth, or caused by oral
birds should be isolated and monitored by
inoculation of large numbers of Candida,
serial examinations (weights), CBCs, and
either by parental feeding or by hand
fecal acid-fast stains or PCR testing.

feeding with utensils that are inadequately

Treatment involves combination
cleaned.

antibiotic therapy for 6-12 mo or longer.

Clinical signs in adult birds are typically

Owner compliance is critical and should
mild and may include mild weight loss,
be discussed at length before beginning
lethargy, and dull plumage. Young birds may
treatment. Use of multiple antibiotics
have more severe disease, especially if they

(typically three) is recommended, because
are immunocompromised. Clinical signs in
mycobacterial organisms are prone to
juvenile birds include anorexia, crop stasis,
developing antibiotic resistance. Antibiotics white plaques in the oral cavity, regurgitain differing combinations that have been tion, and weight loss. Localized infections
used successfully are rifabutin ( 45 mg/kg),
in the oral cavity can lead to difficulty
clarithromycin (60---85 mg/kg), ethambutol
swallowing or halitosis. With severe

(30 mg/kg), and enrofloxacin (20-30 mg/kg).

infections, there may be complete crop

All combinations are used daily.

and GI stasis. Thickening of the crop may

Birds with advanced disease and
develop (Turkish-towel appearance).

granuloma formation have a poor progno

Infection of the proventriculus and ventricusis. Although human infection has not been lus can also occur and may lead to more
associated with exposure to birds,
severe clinical signs such as weight loss,
precautions should be taken for zoonotic
regurgitation, diarrhea, and depression.

risk, especially in immunocompromised

See TABLE 17 for differential diagnoses for people.

regurgitation in birds.

Diagnosis of candidiasis is by identifying

MYCOTIC DISEASES

Candida spp on a Gram, Romanowsky-type,
or new methylene blue stain of the feces,

Fungal diseases are conunon in companion
crop contents, or regurgitated material.

birds. Often, they are a secondary infection

Scrapings or impression smears may also
in an already ill or immunocompromised
be performed to diagnose suspected yeast
bird. The most common fungal diseases are
infections of the skin. In severe cases, when
respiratory tract infections caused by
tissue invasion has occurred, the budding

Aspergillus spp and GI tract infections
yeast will produce hyphae that can be seen
caused by Candida spp. Macrorhabdus is in scrapings obtained from the crop or
an unusual fungus that affects the GI tract
pharynx, or from the feces.

and occurs most commonly in small pet

Often candidiasis is secondary to poor
birds (budgerigars, lovebirds, finches,
husbandry and an unclean environment.

parrotlets, and cockatiels).

If a reservoir of exogenous Candida is
present ( eg, poor nest box or feeding tube

Candidiasis
hygiene), then eliminating the source of the

Candida is critical. In neonates with crop

Candidiasis is a common fungal disease
stasis, the crop must be emptied and
seen in pet birds. The etiologic agent is the
smaller amounts fed until the crop stasis
opportunistic yeast Candida albicans,
has resolved. Metoclopramide may help

1900

PET BIRDS
lffl:11111 DIFFERENTIAL DIAGNOSES FOR REGURGITATION IN PET BIRDS

Species

Commonly

Common Agents

Problem

Affected

(if known)

Typical Signs

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Toxicosis

Various

Lead, zinc,

Vomiting, abnormal
pesticides,
droppings, lethargy,
medications
possible CNS signs

Oral upper GI

Cockatiels, various Plants (Pathos,

Lethargy, ptyalism,
irritation

Philodendron),
passive regurgitation
various medica-
of water, erythema of
tions, other caustic tongue and pharynx
materials

Proventricular

Macaws, miniature Avian bornavirus

Weight loss, vomiting,
dilatation syndrome macaws, African
seeds in feces,
grey parrots,
possible CNS signs
cockatoos, others

Bacterial GI

Various

Gram-negative

Vomiting, watery
infections
bacteria
droppings, lethargy

Candidiasis

Cockatiels,

Ca.ndida, spp

Regurgitation, crop
lovebirds, others
distention, oropharyn-
geal and crop lesions

Trichomoniasis

Budgerigars,

Trichomonas spp

Regurgitation, mouth
cockatiels, doves,
and crop lesions
others

(white matter), mucus
in crop

Ventricular,

Cockatoos,

Wood shavings,

Vomiting, depres-
proventricular, or
macaws, Eclectus
corncob bedding,
sion, weight loss
crop obstruction
parrots, cockatiels, other bedding,
others
fibers, foreign
bodies, ascarids

Proventricular

Various

Neoplasm

Vomiting, weight
adenocarcinoma
loss, lethargy, severe
pain, sudden death

Internal papilloma-

Amazons, macaws

Psittacine

Vomiting, straining to
tosis
herpesvirus 1
defecate, secondary
cloaca! and choanal
infections

Abdominal mass

Budgerigars

Renal or gonadal

Weight loss,
mass-usually
lameness, vomiting
neoplasia

Behavioral

Various

Courtship behavior Regurgitation on
mirror, owner, toy,
or cagemate
crop motility and prevent regurgitation.

from the GI tract, it is only effective when

After identifying and resolving any
in direct contact with infected tissue, so it
predisposing factors, treatment with
is often administered tid before feeding. If
nystatin or fluconazole should be initiated.

the yeast is resistant to nystatin or the bird

Nystatin (300,000 IU/kg, PO, bid) is
is difficult to medicate, then fluconazole
commonly used for treatment because of

(20 mg/kg, PO, every 48 hr) is available for
its low cost and low toxicity. Disadvantages systemic treatment are poor taste and large volume required.

Flock treatment has historically been

Because it is fungistatic and not absorbed
accomplished with use of chlorhexidine at

PET BIRDS

1901

10 mlJgal. of drinking water for 1-3 wk.

exposed to large numbers of aerosolized

Because chlorhexidine is a disinfectant, its
spores. It is not transmitted bird-to-bird.

use will also deplete the normal digestive

Aspergillusfumigatus is the most common
flora. Acidification of the upper GI tract by
species isolated; A.flavus and A niger are use of apple cider vinegar has also been
also found. Rhizopus, Penicillium, Miicor,

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reported to resolve Candida overgrowth.

and Scedosporium apiosper-mimi can

See TABLE 18 for some antifungal drngs
cause similar signs and are more difficult to
used in pet birds.

diagnose and treat. Predisposing factors
for developing infection include species
predilection (African grey parrots, Amazon

Aspergillosis
parrots, cockatiels, and macaws), aspiration

Aspergillosis is an opportunistic infection
of food or medications, immm1osuppresthat typically occurs in inm1unocomprosion (underlying disease), moldy bedding misecl hosts (malnutrition, especially
or feed, and use of corticosteroids. Poor
vitamin A deficiency) or when birds are
hygiene and inadequate ventilation,

•tti=i•f 1:• ANTIFUNGALS USED IN PET BIRDS

Antifungala

Dosage

Route, Frequency

Amphotericin B

1 mg/kg intratrachcal;

Given intratracheally once daily;

0.25-1 mg/mL sterile
nebulizecl 10-20 min, bid
water for nebulization

1.5 mg/kg

IV, tic!

Arnphotericin B
lOO mg/kg

PO, bid x 30 clays
suspension

Clotrimazole

2 mg/kg

Given intratracheally, once
daily x 5 days

10 mg/mL (1%)

Nasal flush; nebulized for

30 min bid

Enilconazole

1 mg (0.05 mIJkg of a

Given intratracheally, once

1:10 dilution)

daily x 7-14 clays

0.1 mIJkg in 5 mL sterile Nebulize for 30 min, 5 days water
on, 2 days off

Fluconazole

5-15 mg/kg

PO,bid

20 mg/kg

PO, every 48 hr x 3 treatments

Griseofulvin

10 mg/kg

PO,bid

5-Flucytosine

20-75 mg/kg

PO,bid

F- lOb (quaternary

1.5/400 mL distilled

Nebulization for cutaneous and
ammoniun1 disinfectant)

water
possibly respiratory fungus

Itraconazole

5-10 mg/kg

PO, once to twice daily Oower
dosage, and use cautiously in

African grey parrots)

Ketoconazole

10-30 mg/kg

PO,bicl

Terbinafine

10-15 mg/kg

PO,bid

1 mg/mL solution

Nebulization for 30 min

Nystatin oral suspension 300,000-600,000 U/kg

PO,bid

(100,000 U/mL)

Voriconazole

12-18 mg/kg

PO,bid
a Most are w1approved for use in birds, and caution is indicated.

b Quaternary ammonium and biguanidine compound; nontoxic, an1pholytic swfactant

1902

PET BIRDS
especially in warm, hw11id climates, can
sion, so consultation with the laboratory
also increase the incidence of disease.

regarding interpretation is important. PCR
testing to detect specific Aspergillus DNA is Clinical Findings: Clinical signs depend
a much more sensitive method to confirm
on the site of infection. Most infections
infection and is more suitable for immuno

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occur in the upper respiratory tract, air
compromised birds because detection of
sacs, lungs, trachea, and syrinx. Systemic
antibodies is not involved. Plasma protein
infections occur when the infection spreads
electrophoresis showing increased
to internal organs, including bone, liver,

13-globulin levels is consistent with
kidneys, or brain. Eye and ski11 infections
aspergillosis. Definitive diagnosis may
can also occur. Anorexia and weight loss
require direct visualization of lesions either
are often present. Respiratory signs may
by surgery or endoscopy and confirmation
include dyspnea, tail bobbing, exercise
by biopsy, cytology, and/or fimgal culture of
intolerance, and voice change. Rhinitis
lesions. Low fimgal viability may yield a
caused by Aspergillus appears similar to
negative culture despite confinnation by
bacte1ial rhinitis or sinusitis. A Gran1 stain
cytologic results.

or modified Wright's stain of lesions or
deb1is often demonstrates fungal hyphae.

Treatment: Treatment vaiies depending

Infraorbital sinusitis caused by aspergillosis
on the site of infection. An acute tracheal
often must be surgically debrided before
infection with obstruction by an aspergiltherapy is effective. Extensive or chronic loma is an emergency that may require
fimgal sinusitis may lead to osseous
placing an air sac tube. After tube placechanges and pem1anent malformation ment, syiingeal or tracheal plaques ai·e
of the upper respiratory architecture.

removed with a rigid endoscope. Arnpho

Extension of infection to the brain can
tericin B can then be instilled intratrachecause CNS signs.

ally at 1 mg/kg through the glottis, and

Tracheitis due to aspergillosis can occur
treatment with systemic antifimgals and
in immunocompromised birds. Aspergillus
nebulization should be started. Amphogranulomas often fom1 in the syrinx of tericin B is the only fimgicidal agent
psittacine birds and raptors and are
available and can be used in nebulization,
particularly challenging to treat. Changes in
as a nasal flush, intratracheally, ai1d in IV
vocalization may occur before dyspnea is
administration. For nebulization, a
observed, and often these birds will stretch
concentration of 0.25-1 mg/mL of sterile
out their necks while breathing. Lower
water can be used. Nasal and sinus flushes
respiratory disease, including airsacculitis,
are generally more dilute at 0.05 mg/mL of
often involves invasion by Aspergillus spp.

ste1ile water. Arnphotericin should not be

Granulomas of the air sacs or the coelom.ic
diluted with saline, because th.is decreases
cavity are also common, usually in the
its potency.

caudal thoracic or abdominal air sacs.

Flushing the nares and sinus with

These lesions may require surgical

Wl11ledicated sterile water or saline before
resection.

medicating may allow saniples to be obtained
for cytologic exanlination and culture.

Diagnosis: Diagnosis can be challenging

Several flushes ofunmedicated warm
but should be pursued because treatment is
isotonic saline or sterile water should be
longtem1 and costly. Aspergillosis should be
done before a final infusion of the medicated
considered in any pet bird presenting with
mixture. Care must be exercised to maintain
signs of upper or lower respiratory disease,
the bird's head in a downward position to
wasting disease, or marked leukocytosis/
avoid the potential for aspiration of the
monocytosis. A leukocytosis/monocytosis
infected debris into the lower respiratory
combined with clinical signs and radiotract.

graphic findings can provide a strong

Itraconazole (5-10 mg/kg, PO, once to
presw11ptive diagnosis in suspect cases.

twice daily) is the most commonly used

Often birds with chronic disease will be
azole for systemic infection. African grey
anemic. A radiograph may reveal airsacculiparrots are more sensitive to adverse tis, granulomas, or severe pulmonary
effects of itraconazole, especially
disease. A CT scan or MRI is more likely
regurgitation and anorexia, and should
to reveal more subtle or diffuse disease.

be dosed at 5 mg/kg/day, PO. Terbinafine

Serologic testing is of limited use; antibody

(10-15 mg/kg, PO, bid) can be used in lieu
and antigen titers, including galactoma.nnan
of or in conjunction with itraconazole.

antigen testing, often result in false-negative

Clotrimazole can be used for nebulization
or false-positive results. A false-negative
in conjunction with systemic therapy
often occurs because of immunosuppres-

(10 mg/mL, nebulized 15-30 min

PET BIRDS

1903

2-4 times/day). Voriconazole (12-18 mg/kg,
n\llllbers of organisms, whereas sick birds

PO, bid) is being used for resistant strains
tend to shed large nun1bers. Birds may shed
of Aspergillus.

the organism intennittently, so a negative

If fungal granulomas are identified and
fecal examination does not exclude
the lesions are accessible, debulking
infection. Wet mount, modified Wright's, or

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endosurgically or treating the lesions

Gram stain of a fecal sample often reveal
topically with amphotericin B may in1prove
organisms. M ornithogaster appears as a
the outcome. Birds undergoing treatment
large, gram-positive rod, with mottling or
should be monitored closely for adverse
stippling throughout its length. Although
effects of many antifungal drugs, which can
the size and length may vary, organisms
include depression, anorexia, and liver
recovered from the droppings are generally
dysfunction. Hepatic enzyme, bile acids,
several magnitudes larger than the normal
and uric acid concentrations should be
digestive bacilli found in birds. Selected
monitored every 4 wk druing treatment.

veterinary laboratories offer both visual

Treatment success may be difficult to
identification and PCR testing. M orni
detennine, but serial CBCs and radiographs
lhogaster does not grow on conventional
may be helpful. Treatment with oral drugs
fungal media. Radiographs may reveal a
should be continued for 2-4 wk after
dilated proventriculus. Necropsy lesions
clinical signs have resolved. Birds with
may include thinning of the isthmus,
aspergillosis often have underlying disease
proventricular dilation and ulceration,
problems and may be inlmunocomprothickening of the proventricular wall, mised, which may affect treatment and
mucus production, and softening of the
recovery. Thickened and scarred air sacs
koilin layer of the ventriculus.

that develop during and persist after
infection can provide an ideal environment

Treatment and Control: The goals
for disease recurrence.

of treatment are to reduce the mm1ber of
organisms and improve the general health

Macrorhabdus ornithogaster
and inlmunocompetence of the bird. Ampho

Infection
tericin (100 mg/kg, PO, bid for 30 days) has
had the highest treatment success rate, but

(Macrorhabdosis, Megabacteria, Avian
failures are common, especially with a
gastric yeast)

shorter duration of treatment. Acidification

Macrorhabdus ornithogaster most often
of the proventriculus (apple cider vinegar,
affects the proventriculus and ventriculus of
vitamin C) has been reported to create an
smaller companion birds ( eg, budgerigars,
environment less conducive to proliferation
parrotlets, lovebirds, cockatiels, and finches). ofMacrorhabdus. Voriconazole has been Previously described as a bacteriUlll, this
successful (anecdotal) at 10 mg/kg, PO,,bid.

organism has a worldwide distribution and

Treatment with sodiUlll benzoate in the
varies widely in pathogenicity.

drinking water has been anecdotally
reported to be successful but still experi

Clinical Findings and Diagnosis:

mental. SodiUlll benzoate at 1 tsp/L water

Clinical signs of infection are weight
for 5 wk cleared the infection in nonbreedloss, regurgitation, lethargy, passage of ing budgerigars, but in budgerigars that
undigested food, and diarrhea. These
were rearing chicks in high environmental
clinical signs may minlic proventricular
temperatures >90°F, treatment with Y2 tsp/L
dilatation disease. Mortality may be high,
water resulted in neurologic signs and death
but birds may recover. In birds that recovof the adult budgerigars because of their er, relapses and potential shedding of the
increased water intake. The current
organism in the feces are likely. This disreconunendation for treatment of Mac
ease is often seen in conjunction with im
rorhabdus with sodiUlll benzoate is Y2 tsp

(2.5 g) of sodiun1 benzoate powder/L of
munosuppression ( eg, polyomavirus and
water ( used as only water source and made
ci.rcovirus infection, or associated with
fresh daily). If the birds are not d1inking
poor husbandry). Asymptomatic infection
the medicated water, the dose should be
is common.

decreased to 1/.1 tsp (1.25 g)/1 of water, and Diagnosis is made by examining a wet
slowly increased back to Y2 tsp over the next
mount of a fresh dropping at 10-50 x
few days. Feces should be rechecked at 14
magnification with the stage condenser
days; if Macrorhabdus organisms are still
mostly closed to increase contrast. The
present, the dose should be increased over
large, rod-shaped organisms are approxiseveral days to 1 tsp (5 g)/1. Feces should be mately 2-4 µm wide and 60-90 µm long.

rechecked at 30 days. The lower dose of 1/.1

Many birds are asymptomatic and shed low
to Y2 tsp powder/L of water should be used

1904

PETBIRDS
in birds housed outdoors in summer

Rhodotorula mucilaginosis

(temperatures >90°F [32.2°C]) and in
birds feeding chicks. Gloves should be

Rhodotorula nwcilaginosis is a yeast
worn when handling medication.

occasionally seen in skin infection in raptors

Asymptomatic carriers are common.

(falcons). It causes yellowish brown ctusty

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Artificial incubation of eggs and hand
areas of the skin in the axillary or inguinal
feeding nestlings can help establish a
areas. Untreated lesions may develop into
pathogen-free flock.

hyperkeratotic proliferative growtl1s. Diagnosis is based on physical exan1ination findings and results of cytologic or histopathologic

Malassezia spp
examination and culture of infected tissues.

Mala.ssezia spp have been reported in birds Treatment involves excision of proliferawith feather picking and dermatologic tive lesions and topical antifimgal tl1erapy.

conditions. In suspect cases, biopsy or

Antibiotics may be necessary to prevent
cytology should be performed. Culture is
secondary irlfections, and analgesics or
often unrewarding. The recommended
anti-inflammatory drugs may be warranted
treatment is fluconazole at 5-10 mg/kg, PO,
for pain.

once to twice daily. Topical therapy with
either dilute chlorhexidine 0. 1 % spray or

Miscellaneous Mycoses
clotrimazole may be used alone or in
conjunction with systemic treatment.

Dermatophytosis, including Trichophyton
and Microsporum spp is occasionally
reported in pet birds. Treatment protocols

Cryptococcus neoformans
for dogs and cats are used (seep 874).

Cryptococcosis is worldwide in occurrence

Histoplasmosis and mucormycosis are also
and caused by a saprophytic fungus,
occasionally reported in pet birds.

C1yptococcus neofonnans. This fungus is
tmcommon in avian species, but it has been
isolated from the fecal droppings of wild

PARASITIC DISEASES
birds, particularly pigeons, and from feces
of canaries and psittacine birds. C neo

See also roui:rnv, p 2780 et seq.

fonnans infection has been reported in

Parasitic disease has become less conm1on

Columbiformes, a Moluccan cockatoo, a
in captive parrots throughout the past 20 yr
thick-billed parrot, a green-wing macaw,
with the restrictions against in1portation of
and an African grey parrot. Veterinarians
wild-caught birds; many pet birds now are
should be aware that not only can birds be
incubator hatched, hand raised, and have
carriers of the disease and become ill but
little to no access to the outdoors or to other
also that C neoformans is zoonotic. Most
birds. Commonly reported parasitic diseases
hun1an irLfections with C neoformans occur
include protozoa.I irLfections such as giardiain irnrnunocompromised individuals and are sis in cockatiels, sarcocystis in larger associated with environmental exposure,
parrots, and mites in budgerigars and
although cases have been reportecLin which
passerines.

contact with a pet bird appeared to be the
source of irLfection.

Parasites of the Circulatory System

Clinical signs of Cryptococcus irLfection

See also BLOOD BORNE ORGANISMS, POUl:rRY,
include weakness, lethargy, anorexia,
p2780.

diarrhea, and dyspnea. With CNS involvement, neurologic signs such as blindness Protozoa: Haemoproteus was previously and paralysis may occur. Clinical diagnosis
documented with great frequency in
can be difficult. A definitive diagnosis
imp01ted Cacatua spp. Leucocytozoon,
requires demonstrating the organism on

P/.asmodium, and Atoxoplasma spp are all cytologic or histologic examination or
seen occasionally in various species, most
culture. The organism is a round to oval
commonly in rap tors, canaries, and
yeast with a mucopolysaccharide capsule.

Columbifonnes, and are currently not of

A mucoid gelatinous exudate may be noted
major significance in psittacines. Atoxowithin the respiratory tract, coelomic plasmosis is still diagnosed in canaries.

cavity, sinuses, brain, or within the Jong
bones.

Treatment recommendations for birds

Parasites of the Gastrointestinal
include amphotericin B, itraconazole,

System
ketoconazole, fluconazole, or voriconazole.

Giardiasis: Giardiasis has been reported in

Fluconazole or voriconazole are the drugs
many species of birds but is most commonly
of choice for CNS or ocular irLfections.

seen in cockatiels. Adult birds may be latent

PETBIRDS

1905
carriers. Transmission is presumably direct

Cryptosporidiosis has been seen in a

(ingestion of infective cysts). Affected
variety of avian species but is thought to be
cockatiels occasionally exhibit feather
a secondary rather than a primary pathogen.

pulling in the axillary and inner thigh regions,

Transmission of Cryptosporidium spp is
along with vocalization. A true causal
through ingestion or inhalation of sporu

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relationship between giardiasis and these
lated oocysts. Because of the small size and
clinical signs has not been proved. Droppings low shedding rate of Cryptosporidium spp, of affected cockatiels may be voluminous
diagnosis can be difficult, but a Sheather's
and aerated (a "popcorn" appearance).

sugar flotation test is best. An acid-fast stain

There are several ways to diagnose
can also be used to detect the organism.

Giardia spp infection: the zinc sulfate

Clinical signs may involve the GI, respiraflotation test of feces to detect cysts, the tory, or urinary tract, especially in
direct saline smear of fresh feces to detect
immunosuppressed birds. Treatment for
motile trophozoites, and an ELISA test for
cryptosporidiosis in birds is not described.

Giardia spp antigen in feces. Because the

Plasmodium spp infection (malaria) is presence of cysts is variable, serial tests
highly pathogenic in gyrfalcons, canaries,
may be needed. The accuracy of the
and penguins. Plasmodium is spread by

Giardia. spp SNAP test designed for people
mosquitoes. Clinical signs may be none to
is unknown.

weakness and death. Treatment for malaria,

Metronidazole (50 mg/kg/day, for 5--7
if needed, is with chloroquine.

days) or carnidazole (20 mg/kg/day, PO, for

Atoxoplasmosis is a highly pathogenic

1-2 days) is the recommended treatment.

protozoa! disease that causes hepatomegaly

In cockatiels, treatment of giardiasis with
and splenomegaly in canaries, with coccidiafenbendazole at dosages extrapolated from like oocysts shed in the feces. The host
dogs has been anecdotally reported to cause
becomes infected by ingesting the oocysts.

death.

Infected birds may be asymptomatic or
exhibit anorexia, weight loss, diarrhea, and

Trichomoniasis: Trichomoniasis has been
depression. Clinical disease is typically
reported in many orders of birds, including
more severe in fledgling birds, whereas

Colurnbifom1es, Galliformes, Falconiadults are often asymptomatic. Diagnosis formes, Psittacifom1es, and Passe1ifom1es.

is made by fecal flotation (best in adults),

Trichomonas gallinae ( called frounce in
buffy coat smear with Romanowsky stain,
birds of prey and canker in Columbifom1es)

liver impression smear, or PCR testing of
is occasionally seen in pet birds, notably
feces. Treatment options are toltrazuril
budgerigars. Clinical signs may include

(12.5 mg/kg/day, PO, x 14 days) or sulfaanorexia, dysphagia, weight loss, and chlorpyridazine (150-300 mg/L drinking
dyspnea. Whitish yellow, caseous lesions
water, 5 days/wk x 2-3 wk).

adherent to the mucosa of the oropharynx,

Other protozoan parasites such as
crop, and esophagus may be seen in raptors
coccidia are much more common in
and Colurnbifom1es. Budgerigars generally
gallinaceous or Co!umbiforme birds,
do not have grossly visible oral lesions but
although coccidial oocysts are seen
do have increased salivation and regurgitaoccasionally in psittacine and passerine tion. Transmission is by direct (parents
birds.

feeding young) or indirect (ingestion of
contaminated food and water) contact;

Roundworms: Various genera and
raptors may become infected by ingesting
species of roundworms infect pet birds,
infected pigeons or doves.

and wild birds may transmit nematodes to

Microscopic examination of a warm
captive parrots housed outdoors. Transmissaline mount of material from the oral sion is direct by ingestion of embryonated
cavity may reveal the flagellated organism.

ova. Clinical findings include loss of

Treatment protocols include carnidazole
condition, weakness, emaciation, and

(20 mg/kg, PO, once), ronidazole (&--10
death; intestinal obstruction is common in
mg/kg/day, PO, for 14 days), or metronidaheavy infections. Diagnosis of intestinal zole (50 mg/kg/day, PO, for 5 days).

nematode infection is by fecal flotation,
although shedding of ova may be intermittent. Ivermectin (0.2 mg/kg, PO, SC, or IM, Other Protozoa! Diseases: Other
repeated in 10-14 days), pyrantel pamoate
protozoan parasites such as coccidia are

(4.5 mg/kg, PO, repeated in 10-14 days), or
much more common in gallinaceous or
fenbendazole (20-50 mg/kg, PO, repeated in

Colurnbifonne birds, although coccidial

14 days) are generally effective. In warm
oocysts are seen occasionally in psittacine
climates where exposure via outdoor
and passerine birds.

aviruies is likely, routine deworming

1906

PET BIRDS

(every 6 mo) with one of these anthelrnin

Parasites of the Respiratory System
tics is often practiced.

Air Sac Mites: Ste1'nostoma. tra.chea.

Cestodes: Cestodes are uncommon in
colum parasitizes the entire respiratory

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domestically bred birds. The most common
tract, most frequently of canaries and
pet birds infected with tapewom1s are
gouldian finches. The mites aie found in
cockatoos, African grey parrots, and
the trachea, syrinx, lungs, and air sacs.

finches. Intennediate hosts are most likely

All stages of the mite are found within
insects and arachnids of various types,
the respiratory tissues. The life cycle is
earthwom1s, and slugs. Infected birds are
poorly understood.

asymptomatic or are unthrifty, with or

In mild infections, birds are usually asympwithout diarrhea. Diagnosis is based on tomatic; in heavy infections, audible dyspnea
visualization of eggs on a fecal flotation.

(high-pitched noises and clicking), sneezing,

Praziquantel (5--10 mg/kg, PO or IM,
tail bobbing, and open-mouthed breatlling
once) is the recommended treatment.

are noted. Copious amounts of saliva are

Recurrence is rare in cases in which the
seen in the oropharynx, and ptyalism may be
intermediate host is not indigenous to the
present. Signs are exacerbated by handling,
area where the bird is housed.

exercise, and other stresses. Mortality can be
high. Transillumination oftl1e trachea in a
darkened room occasionally reveals the

Parasites of the lntegumentary
mite. Response to treatment can help reach

System
a diagnosis.

Scaly Face (Leg) Mite:

When the recovery of an individual bird is

Knemidocoptes
paran10unt, treatment should be adminis
pila.e ( also Cnemidocoptes pila.e) is common in budgerigars and rare in all other
tered quickly and with minimal handling.

psittacine species. In budgerigars, white,

Ivermectin (0.2-0.4 mg/kg, PO or IM)

porous, proliferative encrustations involving
repeated in 2 wk or moxidectin (0.2 mg/kg,
the comers of the mouth, cere, beak, and

PO or topically) repeated in 2 wk may be
occasionally the periorbital area, legs, or
administered.

vent are typical. In passerine birds (particularly canaries and European goldfinches), Sarcocystosis: Sarcocystosis is a major
crusts fom1 on the legs and surfaces of the
cause of mortality in parrots housed
digits ("tassel foot"). The mites can be
outdoors in the southern USA. In severely
recovered from facial scrapings of budgeriaffected areas, even indoor birds can gars, although the clinical appearance is
be infected via contaminated food. The
generally pathognomonic. In passerines
oocysts of this protozoan parasite are
affected with Knemidocoptes, skin scrapings passed from infected opossum feces by of tl1e legs often result in hemorrhage and are insects (eg, flies, cockroaches) or mice generally not recommended. Ivennectin
and rats into the feed cups or enclosure

(0.2 mg/kg, PO or IM) or moxidectin
of the birds. The feces of these transport

(0.2 mg/kg, PO or topically) is generally
hosts are then consumed by the birds, and
effective. The treatment is repeated in 2 wk.

a rapidly fatal disease can develop. Old

World species are immunologically naive

Feather Mites: Psittacine birds are
to this disease, and a high mortality rate is
seldom affected by feather mites. Occasionobserved in untreated birds such as cocka\ ally, infestation with the red mite (Derma.n
toos, African grey parrots, and Eclectus
yssus ga.llina.e) may be found in outdoor
parrots. Cockatiels are also susceptible,
aviaries, especially in nest boxes. A causative
and renal as well as pneumonic lesions are
relationship between mites and feather
often noted at necropsy in this species.

picking is often assumed by owners of

Although not contagious, cases tend to
feather-picking birds, although this is rarely
occur in clusters because the infected
the case. More commonly, behavioral,
opossum feces are spread via insects
husbandry, and/or systemic factors are
around the aviary grounds. Large die-offs
linked to feather loss ( see p 1927).

have been documented.

Mite-infested birds may be treated with

Clinical signs are lethargy, passive
pyrethrin sprays, 5% carbaryl powder, or
regurgitation of water, respiratory distress,
ivermectin (0.2 mg/kg, PO or IM) repeated in
weakness, ataxia, and anemia. In Old World

2 wk. Nest box treatment includes mixing 5% paiTots ( eg, cockatoos, Afric3.11 grey parrots), carbaryl powder into the nest box substrate.

disease occurs in the early stages of infection

Cages should be cleaned thoroughly, and
as the parasite is undergoing schizogony or
wooden nest boxes should be discarded and
merogony (asexual reproduction) in the lung.

replaced.

This causes lung dainage, 3.lld the birds die

PETBIRDS

1907
acutely with or without signs of respiratory

The typical presentation of budgerigar
distress. In New World parrots ( eg, macaws,
fledging disease is a well-fleshed juvenile,
con mes), the organism encysts in the muscle
just before fledgling age, with acute onset
or CNS, causing weakness, ataxia, or nemoof lethargy, crop stasis, and death within logic signs. The disease can manifest as

24-48 hr. Other clinical signs are cutaneous

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an asymptomatic or clinically apparent
hemorrhage, abdominal distention, and
muscular disease, cardiac disease, acute
feather abnormalities. Surviving budgeripulmonary disease, or encephalitis.

gars >3 wk old often exhibit feather

Encephalitis (paresis, intention tremors, and
dystrophy (French molt or feather dusters).

head tilt) has been seen in psittacines and

In other species of psittacines <4 mo old,
rap tors.

the infection is also often fatal. Older

No specific diagnostic test is available,
nonbuclgerigar psittacines may have
although results of plasma protein
subclinical disease or hemorrhages and
electrophoresis may indicate infection
coagulopathies. Prevalence of the vims in

(marked increase in 13-globulin concentraadult psittacines, including budgerigars, is tions with or without a marked increase in
thought to be high.

gamma globulin concentrations). An

Antemortem diagnosis is accomplished
indirect immunofluorescence antibody
with DNA probes of cloaca! swab and blood

(IFA) test has been developed that may aid
samples and virus-neutralizing antibody
in antemortem diagnosis of the nonperacute tests of blood samples to identify birds with form of sarcocystosis in psittacine birds.

previous viral exposme. Diagnosis in a flock

The sensitivity and specificity of the IFA test
setting is typically based on clinical signs,
ranges from 83%-86%. Results of muscle
signalment, and necropsy findings.

biopsy may be conclusive for the encysted

Gross necropsy findings in deceased
stages but is not commonly perfom1ed.

chicks often include pale skeletal

When a muscle biopsy is done, the
musculature and subcutaneous ecchyquadriceps muscle has been reported to motic hemorrhages. The kidneys and liver
be a better biopsy site than the pectoral
are enlarged and may be pale, congested,
muscle. Increases in enzyme activities of
and mottled, or have pinpoint, white foci.

LDH, AST, and CK have been reported.

Petechial or ecchymotic hemorrhages

Protracted treatment with trimethoprim/
may also be present on viscera, particusulfa (30 mg/kg, bid) and pyrimethamine larly the heart. The heart is sometimes

(0.5 mg/kg, PO, bid) has had linlited sucenlarged and may show hydropericarcess. Response to treatment is generally clium. Intranuclear inclusion bodies are
monitored by serial PCV san1pling. Newer
often seen in the liver, kidneys, heart,
drngs used to treat infection by the related
spleen, bone marrow, uropygial gland,
protozoa, Sarcocystis neurona, that affects skin, feather follicles, etc.

horses have not yet been evaluated for

Aviary control methods include
treatment in birds.

avoiding the housing of budgerigars or

Gross necropsy findings include
lovebirds on premises where other species
increased lung density, hemorrhage, and
are bred, adhering to standard hygiene
renal lesions. Clinical signs may also reflect
procedures, preventing access to the

CNS involvement. Histopathologic san1ples
nursery by visitors, and not introducing
should include lung, kidney, muscle, and
birds into the aviary without 90 clays

CNS tissue if neurologic signs are apparent.

quarantine and testing. Eliminating APV
infection from an infected budgerigar

VIRAL DISEASES
aviary is challenging. First, all breeding
must be stopped for 6 mo. The presence of

Avian Polyomavirus
infected neonates, fledglings, and adults
propagates the disease. During this time,

(Papovavirus, Budgerigar fledgling disease,
adult birds are moved to a noninfected

Psittacine polyomavirus)

area while the entire aviary is disinfected.

Avian polyomavirus (APV) primarily affects

Nest boxes should be disinfected or
young birds. There are two primary fonns
discarded and replaced. After 6 mo, adult
of the disease based on species affected:

breeding birds can be returned to a clean
budgerigar fledgling disease and a nonbudgaviary and breeding resumed.

erigar polyoma infection. Both are character

Pet store prevention should include
ized by peracute to acute death of preweaned separating neonates from different somces, neonates. Adult birds typically are resistant
purchasing birds from somces where
to infection; they will seroconvert and shed
polyomavirus testing and vaccination are
the virus for up to 90 days, then clear the
perfom1ed, and ideally, not pmchasing or
infection. The incubationpe1iod is 7-10 clays.

selling unweaned birds.

1908

PETBIRDS

Treatment is supportive care. A vaccine is

Diagnosis is based on clinical appearavailable. For breeding birds, two doses of ance; results of PCR testing of feces, feather
the vaccine are administered at a 2-wk
dander, or blood; and biopsy of affected
interval; this should be done off-season. The featl1er follicles showing basophilic intracymanufacturer recommends administration toplasmic inclusions.,Testing by PCR may

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of the first dose when the chick is >35 days
detect infection in birds tl1at still appear
old, with a booster vaccination in 2-3 wk.

healthy. These birds may subsequently
become ill or may mount an effective response
to the virus. Because of tl1e stability of the

Psittacine Beak and Feather Disease
virus, PCR analysis can also be used for

Psittacine beak and feather disease (PBFD)

environmental testing. Quarantine and
is caused by a psittacine circovirus. The
retesting are recommended for PCR-posivirus was first recognized in the 1970s in tive, asymptomatic birds. At necropsy,
cockatoos with beak and feather lesions.

affected birds often have no gross lesions

Since then, it has been recognized in most
internally, but intranuclear or intra.cytoplasspecies of parrots and also in Passeri.f01mes mic inclusions may be seen histologically in and Columbi.fom1es. Infected birds shed
the feathers, bursa, thymus, liver, or other
virus in their feathers, feather dander, feces,
organs.

and oral secretions. Transmission occurs by

There is no specific treatment for PBFD,
inhalation and/or ingestion of the virus and
and treatment of infected birds is supportcan occur vertically. The virus is very stable ive. The contagious nature of PBFD and its
in the environment, so fomites can be a
generally tem1inal outcome in clinically
signillcant source of infection. The nan1e is
affected birds warrant isolation and
not as representative of the current typical
eventual euthanasia in most clinical cases.

clinical presentation, which often does not

Strict hygiene with attention to dust control,
include beak abnom1alities and is less likely
screening protocols including PCR testing
to have the severe, classic feather abnorof both birds and tile environment, and malities seen in cockatoos when the disease lengthy quarantines are highly recomwas first documented. Use of screening mended in breeding facilities with

PCR tests has greatly decreased the
susceptible species. All new susceptible
prevalence of the virus in captive bred
birds should be tested before introduction

Cacatua spp. However, disease is still seen to the aviary. In infected breeding colonies,
in African grey parrots, Eclectus parrots,
removing all eggs for cleaning and artificial
lovebirds (Agapornis), lorikeets, and other incubation may also be required. Since the
species, but is rare. The natural infection
development of a PCR-based assay,
appears to occur primarily in juvenile birds,
prevalence of the disease has decreased.

with few instances of clinical infection seen
in birds >3 yr old.

Pacheco's Disease

In the classic PBFD infection, the first
indication of the presence of disease is a

(Pacheco's herpesvirus)

lack of powder down on the beak. The virus

Psittacine herpesvirus is an alpha herpesvicauses abnormal formation of growing rus that is the causative agent of Pacheco's
feathers and inlmunosuppression. Feathers
disease and internal papiUomatosis in
are pinched or clubbed at tl1eir base and
parrots. Pacheco's disease causes a viral
may have hemon-hage within the developing hepatitis seen predoh1inantly in N�w World shaft. The feathers fall out easily and grow
species (Amazon parrots, macaws, and
back slowly or not at all. The distribution of
conures). Internal papillomatosis occurs in
affected feathers depends on the age of the
parrots that have survived Pacheco's
bird and the stage of the molt when infected. disease. Papillomatosis is most commonly Pigment loss may occur in colored feathers.

observed in macaws, Amazon parrots,

The bi.rd may live with these lesions for
conures, and hawk-headed parrots. Disease
months to years. As the disease progresses,
is associated with stress, which can cause
the inlmune system is affected, and most
clinically healthy carriers to shed virus and
birds die of secondary infections. A peracute initiate infection in susceptible birds, as f01m of the disease occurs in young birds,
often occurs during introduction of new
which develop enteritis and pneumonia,
birds, relocation, or in those with underlylose weight, and die. African grey pan-ots ing illness or during breeding. It is spread by
may develop a pancytopenia, because the
direct contact, aerosol, or fecal contaminavirus attacks the bone marrow. These birds tion of food or water, with an incubation
die suddenly with viral inclusions in the
period of3-14 days. The outcome of tl1e
thymus, bursa, and bone marrow.

infection depends on the genotype of the

PETBIRDS

1909
vims, the species of bird infected, and the

The lesions of pa.pilloma.tosis are
bird's overall health. Wected birds become
predominantly present in the oral and
chronic carriers and will remain persistently cloaca! mucosa but may also be folllld infected and intem1ittently shed tl1e virus
internally in the intestinal tract, or less
tlu·oughout their lives. Old World species
commonly, in the conjunctiva or bursa.

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a.re Jess likely to be either ina.ppa.rent

Owners usually first notice blood from a
carriers or clinically susceptible. Patagopapilloma. in the droppings, ancVor the nian species and some Aratinga spp may
pa.pilloma prolapses tlirough tl1e cloaca.

be natural hosts in the wild, and some

Lesions may be mild or severe ( ulcerated
individuals of these species may a.symptoand bleeding) and often wax and wane.

matically shed vims when stressed. Other

Ulcerated lesions may need to be cauterized
species can also a.ct as carriers.

or surgically removed, although they

Ten11inal signs include a.cute death in
typically recur. Treatment is supportive,
well-fleshed birds and bright yellow ura.tes
such as analgesics, cautery, and antibiotics

�itl1 scant feces. Other clinical signs a.re
to prevent secondary infection. Antiherpesdia.ffhea., green ura.tes, lethargy, regurgitavit·al drugs a.re not curative and do not tion, weakness, and depression. Diagnosis
appear to in1pa.ct tl1e course of disease.

in the live bird can be done by DNA probes
of combined oral and cloaca! swabs or

Other Herpesvirus Infections:

blood samples. Increases in plasma.AST

Amazon tracheitis is also caused by a
activity and marked Jeukopenia. have been
herpesvirus, although the incidence of this
reported.

infection is low. Other clinically significant

Because of the a.cute nature of the disease,
herpesvimses include the strain responsible
gross histologic lesions may not be evident.

for papillomatous foot lesions in Cacatua

However, most affected birds will have
spp and the depigmentation lesions noted
hepa.tomegaly, splenomegaly, and renomegon tl1e feet of macaws.

aly. The liver may be mottled or grossly
discolored. Ecchymotic and petech.ial
hemoffha.ges may be present on the

Avian Bornavirus/Proventricular
pe1ica.rdium and within the mesente1ic fat.

Dilatation Disease

Intra.nuclear inclusions a.re seen histologica.Jly in tl1e liver, spleen, intestinal epithe

(Macaw wasting disease)

lium, and pancreas. Primary differential

Proventricula.r dilatation disease (PDD),
diagnoses for Pacheco's disease include
also known as macaw wasting disease,
a.cute salmonellosis, polyoma.virus, and
neuropathic ganglioneuritis, lymphopsitta.cine reovitus. Acyclovir (80 mg/kg, tid, pla.smacytic ganglioneuritis, psitta.cine
or 400 mg/kg in feed) can be used dilling an
encephalomyelitis, and most recently avian
outbreak; however, the risk of increased
bomavirus (ABV), was first recognized in
transmission because of hanclling is great.

the late 1970s in ma.caws imported into the

Autogenous vaccines have been developed

USA and Gem1any. The disease p1ima.rily
during outbreaks and have effectively
affects ma.caws, conures, and African grey
decreased morbidity and mortality. An
parrots, although all pa.iTots a.re probably
inactivated vaccine is available.

susceptible. The causative agent of this
disease is avian boma.virus.

The common presentation of affected
birds is chronic weight loss ( often following
an initial increase in appetite), passage of
tmdigested food ( most easily recognized
when whole seeds are found in the
droppings), and regurgitation. A dilated
proventriculus may be seen ra.diographically. Neurologic signs ( convulsions, tremors, weakness, ataxia, blindness) may
occur in some species, with or without
concuffent GI signs. Clinical signs may be
slowly progressive or develop a.cutely.

Outbreaks a.re sporadic, with a low
morbidity a.i1d a high mortality.

Cloacal papilloma, gross lesion, in a blue·

Before the discovery of ABV as the
fronted Amazon parrot. A red proliferative
mass commonl
causative a.gent of PDD, the only antey originates from just inside the rim of the cloaca I opening. Courtesy of
mortem diagnosis was identification of

Dr. Louise Bauck.

lymphopla.sma.cytic infiltrates in the tissues

1910

PET BIRDS
of affected birds, most commonly with a
birds are rarely exposed to a susceptible
crop biopsy. Histopathologic lesions can be
strain. Because of import restlictions,
present in the brain, spinal cord, pelipheral
poxvirus in blue-fronted Amazon parrots
nerves, nerves of the GI tract, heart, adrenal
is no longer commonly seen. In pet bird

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gland, lungs, and kidneys. Transmission is
practice, vetelinalians will generally
fecal/oral, and positive results of PCR
encotmter only canary, lovebird, and pigeon
testing of choanal, cloaca!, or fecal swabs
poxviruses and fowlpox (seep 2824), which
confirms the presence of ABV. Serologic
have specific host ranges. Poxviruses are
assays such as ELISA can also confirm
environmentally stable, increasing the
exposure. Although the presence of ABV in
likelihood that a viable orgaiusm will come
the droppings indicates shedding, many
into contact with a susceptible host.

birds are positive for ABV with no clinical

Poxviruses cairnot penetrate intact skin,
signs of PDD. If or when these birds may
and a break in the skin or mucous memdevelop disease is unknown.

brane must be present for infection to

Because shedding of the virus is
occur.

intennittent, one negative result of fecal

Poxvirus infection may cause cutaneous,
or cloaca! PCR testing does not exclude
diphthelitic, or systemic infections based
disease. Testing at least three times at
on the strain of virus, route of exposure,
weekly intervals, with all three tests being
affected species, and age and health of
negative, is best before declaling a bird
the bird. The cutaneous fonn appears as
negative for ABV. Differential diagnoses
nodular proliferations or wartlike lesions on
are heavy metal toxicosis, foreign body
the unfeathered skin around the eyes, beak,
intestinal obstruction, internal papillomatonares, and legs. The diphthelitic forn1 is sis, internal neoplasia, and GI infections
characterized by lesions on the mucosa,

(including bactelial and fungal proventlicutongue, pharynx, and larynx. The septicenuc lar infections).

fo1m is characterized by a ruffled appear

Clinicopathologic findings vaiy, but
ance, depression, cyanosis, anorexia, and
increased plasma CK activity and mild
wartlike tumors of the skin. The cutaneous
lyrnphocytosis, monocytosis, or heterofonn is most commonly seen in psittacines philia may be seen. Proventiicular biopsies
and raptors.

in affected birds are prone to dehiscence

Clinical signs depend on the fonn of
and are not done routinely. Crop biopsy is
disease, location of the lesions ( eye, oral,
a less invasive diagnostic tool and may
ear), and overall health of the bird and may
be useful if the collected sainple contains
include lethargy, respiratory distress, partial
sufficient innervation to be diagnostic;
blindness, difficulty eating, weight loss,
however, a negative crop biopsy does not
emaciation, and skin lesions. Diagnosis of
exclude the presence of PDD.

poxvirus infection is typically confim1ed

Treatment for PDD includes providing
through history, physical exainination
easily digestible foods and may be aided by
findings, and histologic findings of Bollinger
adn1inistration of an NSAID ( eg, meloxicain, bodies in affected tissues.

celecoxib ). Isolation of positive"birds is

Treatinent is usually nonspecific and may
in1portant in disease prevention. Testing
include supportive care, fluids, parenteral
by PCR ( a minimun1 of three tests) and
vitanun A, ophthalmic ointinents for eye
separating positive birds from negative
infections, assisted feedings, and antibiotics
birds is a recommended control measure,
to prevent or treat secondary ir)fections.

although the number of false-negative tests

Lesions on the skin may need daily cleaiung.

( due to intemtittent shedding) makes this a

Transntission is via insect vectors ( mosquito
long and potentially difficult task. ABV is
bites) or other entry through breaks in the
not a long-lived virus in the environment;
skin. Therefore, mosquito conti·ol and
therefore, good hygiene and ultraviolet light
indoor housing are vital to prevent
can help to linut spread of disease in a home
outbreaks. Vaccines for canarypox,
or aviary setting.

fowlpox, and pigeonpox are available but
are specific for their host species.

Poxvirus Infections

Viscerotropic Velogenic Newcastle

Poxviruses are large DNA viruses that

Disease
induce intracytoplasmic, lipoplulic
inclusion bodies (Bollinger bodies) in the

(Exotic Newcastle disease)

epithelial cells of the integument, respira

Viscerotropic velogenic Newcastle disease
tory tract, and oral cavity. All birds are

(VVND, seep 2856), caused by a parainyxoconsidered susceptible to poxvirus virus group 1, affects most avian species
infection, but many compaiuon and aviary
and is a significant threat to the poultry

PET BIRDS

1911
industry. Transmission is by respiratory
has been reported in >320 species of birds.

aerosols, fecal contamination of food or

The American crow ( Corvus brachy1un
water, direct contact with infected birds,
chus) and other corvids have suffered
and fomites.

particularly high morbidity and mortality.

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Birds may be asymptomatic or die

Other affected species include canaries,
acutely. Clinical signs include depression,
psittacines, and raptors. Although
anorexia, weight loss, sneezing, nasal
psittacines appear to be somewhat
discharge, dyspnea, coajunctivitis, bright
resistant, the disease has been reported in
yellow-green diarrhea, ataxia, head
parakeets, cockatoos, conures, rosellas,
bobbing, and opisthotonos. In prolonged
caiques, lorikeets, and a King pan·ot.

cases, unilateral or bilateral wing and leg

Affected parrots have been adults housed
paralysis, chorea, torticollis, and dilated
outdoors with docwnentation of mosquito
pupils also may be seen. Primary differential populations present. Mosquitoes (Culex diagnoses include other paran1yxoviruses
spp) are the p1incipal vectors of disease.

(non-Newcastle), psittacine proventricular

Clinical signs include depression,
dilatation syndrome, and heavy metal
anorexia, weight loss, head tremors, ataxia,
toxicosis. Lesions include hepatomegaly,
blindness, seizures, and death. Juvenile
splenomegaly, petechial or ecchyrnotic
birds are the most commonly affected.

hemorrhages on serosal surfaces of all

Ophthalmologic findings in raptors are
viscera and air sacs, airsacculitis, and
anterior uveitis, exudative chorioretinal
excess straw-colored peritoneal fluid.

lesions, and chorioretinal scarring.

Diagnosis is traditionally via viral isolation,

Antemortwn diagnosis can be difficult.

but agar gel inununodiffusion tests that can

Initial diagnosis may be based on clinical
be performed on whole blood or serum are
signs, species, and age; however, many
available.

diseases may cause similar clinical signs.

Only symptomatic treatment is possible

Serologic tests (serum neutralization) may
and thus not advised. If suspected, VVND
indicate antibody response to infection.

must be reported to appropriate federal and

Paired samples submitted 2 wk apart may
state authorities. Vaccination is prohibited
reveal a rise in antibody levels and give a
in birds entering the USA, because it does
more definitive diagnosis. Adult birds may
not eliminate the carrier state and hampers
have high circulating antibody levels in
viral detection during quarantine.

endemic areas. Diagnosis is often determined at necropsy. The brain and kidney Other Paramyxovirus Infections:

are the preferred tissues to submit for

There are several less pathogenic strains of
histopathologic exan1ination.

paramyxovirus. Paramyxovirus groups 2

There is no specific treatment for WNV
and 3 are endemic in aviculture. Parain birds. Some birds may improve witl1
myxovirus group 2 causes mild illness in
supportive care (fluids, feeding, antibiotics/
passerines and a more serious disease in
antifungals as needed) and time. A vacpsittacines. Clinical signs in psittacines cination protocol using a recombinant
include tracheitis, pnewnonia, and enteritis.

vaccine has been successful in some birds.

Paramyxovirus group 3 is reported most

The recommendation is vaccination of
frequently in Neophema spp, lovebirds, and
captive birds 2-4 wk before mosquito
gouldian finches and typically causes mild
season, with a booster 3 wk after the initial
disease. Clinical signs may be absent, and
dose.

disease results in acute death. In disease

During the mosquito season, birds should
of longer duration, respiratory signs,
be housed indoors or in completely covered
pancreatitis, and torticollis may occur.

outdoor facilities. Mosquito netting and

Diagnosis is the san1e as for para.myxovimosquito traps should be used, and any rus group 1. Treatment for paramyxovirus
standing or stagnant water sources
groups 2 and 3 infections is supportive care.

eliminated.

The vaccine for paramyxovirus group 1
should not be used in psittacines, because

Avian Influenza
it can cause fatal reactions.

Avian influenza is caused by an orthomyxo

West Nile Virus
virus. Because of the zoonotic potential of
some strains and the recent discovery of

West Nile virus (WNV) infection is an arthronew mutations, this virus may become a podbome virus in the genus Flavivirus
more significant pathogen. Both the

(fanilly Flaviviridae ). WNV was first
zoonotic potential and the economic effects
reported in birds in the USA in August 1999.

on the poultry industry are causes for

Many species of birds can be infected, and it
concern. (See also AVIAN INF'LUENZA, p 2902.)

1912

PET BIRDS

GERIATRIC DISEASES

Arthritis

Until recently, geriatric medicine has been a

Septic and traumatic aithritis may occur at
neglected area of avian medicine. Infectious
any age. Septic art11ritis is most common in
diseases, inadequate diets, and poor
tl1e digits. Osteoartlu;itis is also common in

VetBooks.ir
husbandry meant that most pet birds did
getiatric birds and can lead to oilier issues
not live long enough to develop geriatric
such as pododennatitis if not caught early
conclitions. As the knowledge base of avian
and treated. The weight of t11e bird, its
medicine, nutrition, and proper husbandry
general physical condition, previous
has grown, so has the life span of pet birds
injuries, and any concurrent medical
increased. Most pet birds have tl1e potential
conditions can all cont:tibute to the onset
to live 20-80 yT, depending on tlleir size
and seve1ity of artll.titis. Concurrent

( with smaller birds having a sho1ter life
pododern1atitis is often present and may
span and larger birds a longer life span).

be botll a cause ai1d result of decreased

Witl1 pet birds living longer, tile incidence
activity. Malnutrition, which decreases tl1e
of ge1iat:tic-onset diseases, including
integtity of tile plantar epitllelium, and
cataracts, neoplasia, arthritis, and
concurrent obesity are often present in
cardiovascular disease, has increased.

affected birds. The cage environment,
especially tl1e vaiiety, diaineter, ai1d texture
of perches, can be important in providing

Cataracts
comfort ai1d stability for artluitic birds

Cataracts occur in many species of
while preventing or rnininlizing pododermapsittacine birds as they age, notably titis. If possible, the nails should be left witl1
macaws, Amazon parrots, and cockatiels.

sharp points to add st:t·ength and stability to

These species may be prone to cataracts or
the grip. Wings should not be clipped, to
may be overrepresented in t11e older pet
help witll balance.

bird population. If tile onset of cataracts is

Clinical signs vary, depending on tile
gradual, adaptation to decreased vision
location of the arthtitis and tile severity of
usually occurs; if not, clinical signs can be
disease. Birds may exhibit lan1eness or be
depression, inactivity, and reluctance to
less active. A flighted bird may not want to
come out of or move around in t11e cage.

fly or may not fly as well. The bird may not

The eyes of older birds should be
be perching nonnally or may fall off
examined annually to detect early changes
perches. Oilier signs of artluitis are swollen
in lens opacity. Because of tile small size of
or warm joints, decreased range of motion,
the exposed cornea and pupil in psittacines,
feather picking or mutilation, or excessive
and tl1e nun1erous acquired diseases that
vocalization.

can occur, screening by an ophtllalmologist

Diagnosis is based on clinical signs, physiis rec01runended. Cataracts often develop cal exanlination findings, and imaging
secondary to infection or trauma or may be

(radiographs or CT scan). Radiographic
age related. Uveitis may also be present.

lesions include narrowing of the joint space,

Additional ophthalmic <:onditions tllat may
sclerosis of tile subchondral bone,
be encountered in geriatric birds are
misalignment of the joint, ai1d osteophyte
keratoconjtmctivitis sicca, corneal
formation. CT scai1s help detemline tile
ulcerations, third eyelid abnormalities,
severity of tile bony changes. Commonly
hypopyon, anterior uveitis, conjtmctival
affected joints are tile tarsus, stifle, and
granulomas, infection of tl1e conjunctiva
phalangealjoints. The joints of the tlloracic

( eg, Chlamydia, Mycoplasma, poxvirus),
limb appear to be less conunonly affected.

Hardetian gland adenoma, and lymphoma.

A multimodal treatment plan is recom

In large psittacine birds, surgical removal
mended, incorporating both medical and
of cataracts is successful in many cases. The nonmedical modalities. Medical treat111ent bird's general health and the degree to
includes tile use ofNSAIDs, chondroprowhich tl1e cataracts affect its quality of life tectants, and possibly opioids. The most
should be evaluated before surgery.

common NSAID used in avian medicine is

Conunonly used mydriatics are not useful in
meloxicai11 (0.5-1 mg/kg, PO, once to twice
birds because of the skeletal (as opposed to
daily), a COX-2 inhibitor. Potential adverse
smooth) muscle found in tile iris. In any bird
effects of NSAIDs ai·e renal ischenlia, so
with decreased vision, minimal alteration of
tlley should be used witll caution longtern1
tile home environment is ctitical. Early
and at tl1e lowest tllerapeutic dose possible.

cataracts, especially if uveitis is present,

Anecdotally, glucosai11ine (20 mg/kg, PO,
may be painful. NSAIDs, eitller ocular drops
bid, or 35 mg/kg, PO, once daily or every

(fturbiprofen) or systemic (meloxican1,
oilier day) or polysulfated glycosanlinoglycelecoxib ), or botll, can be used to reduce can (5 mg/kg, IM, once weekly for 4 wk tl1en
inflanunation and pain.

monthly) has been used successfully. The

PET BIRDS

1913
latter should be used carefully, because
arthritis. Bumblefoot is often a sequela
some birds have had fatal coagulopathies
of osteoarthritis. Pododermatitis is a
from the injections.

progressive disease. A localized hyper

Opioids may be necessary for acute
emic lesion develops, followed by
exacerbations of a chronic arthritic
ulceration and, if untreated, abscess

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condition or for conditions not responding
formation and osteomyelitis. Initially, the
initially to NSAIDs. Tra.madol (15-30 mg/kg,
skin on the metatarsal and digital pads

PO, bid-q_id) or butorphanol (0.5-3 mg/kg,
becomes f1attened and smooth. The skin

IM, every 4 hr ( depending on species of
may become proliferative and then ulcerate,
bird), may be used until the NSAIDs take
allowing bacterial access, which leads
effect.

to inflammation and infection. As the

Additional management includes
infection progresses, tendon sheaths
husbandry changes, a weight loss and exercise become affected, and osteomyelitis and plan, a healthier diet ( rich in omega-3 fatty
septic arthritis develop.

acids), and physical therapy. Encouraging

Birds may present with lameness, depresflighted birds ( without clipped wings) to fly sion, and anorexia due to the inf\an1.mation,
in a safe environment is the best fom1 of
pain, and infection. Diagnosis is based
exercise. If a safe environment is not possible,
on clinical signs, physical examination
encouraging climbing, walking, or even
findings, radiographs, and culture results.

stepping up multiple times can be exercise for Affected birds should be exanlined parrots. Foraging for food, by putting multiple thoroughly for predisposing ir\juries or foraging boxes on opposite sides of the cage
illness.

or enclosure, promotes exercise. If the bird

Treatment includes correcting inapprois overweight, then weight loss is essential, priate husbandry (adding padded perches
because studies have shown that obesity is a
or perches covered with artificial grass)

risk factor for osteoarthritis in many species.

and conversion to a healthier, preferably

This may involve converting the bird slowly
formulated diet. Weight Joss and exercise
to a pelleted diet with added essential fatty
should be encouraged in obese birds (flying,
acids. Fatty acids may have an anti-inflammaclimbing, or walking). In early cases, this tory effect and be renal protective. Flax seed
may be all that is necessary.

oil ( 0.1--0.2 mIJkg,'day, PO) is reconunended

As the disease progresses, a bandage may
as the best source of fatty acid supplementabe necessary to relieve the pressure on the tion for birds. Other husbandry changes, such
lesion. The lesions should be kept clean.

as changes in perch texture or diameter or

Strict sanitation of the perches and feet is
padding perches, can be helpful in birds with
important to prevent bacterial infections. If
weak or painful legs or feet.

a scab is present, it should be softened and

Articular gout is also common in older
removed or surgically debrided'. Antibiotic
birds (seep 1926). Differentiation between
use should be based on results of culture
arthritis and articular gout is critical
and sensitivity testing. Staphylococcus spp because of the vast differences in progresis most commonly identified; other reported sion, quality of life, and prognosis.

bacte1ia include Escherichia coli and

Proteus spp. Effective antibiotics are

Pododermatitis
amoxicillin/clavulanate (125 mg/kg, PO,

Pododermatitis, or bumblefoot, is a
tid), enrofloxacin (10-15 mg/kg, PO, bid),
relatively common condition of older
and marbofloxacin (5 mg/kg,'day) for 10-14
pet birds. It is a general term for any
days. Pain management is important and
inflammatory or degenerative condition
includes a combination ofNSAIDs and/or
of the avian foot and can range from mild
opioids, depending on the severity of
redness to bony changes. Bumblefoot
disease and after any surgical debridement.

develops most commonly when birds are

One regimen is meloxican1 (0.5-1 mg/kg,
either housed with inappropriate perching once to twice daily) along with tramadol or secondarily to an injury in one leg,

(15-30 mg/kg, PO, bid-tid), and, in severe
which causes the bird to shift its weight to cases or after surgery, butorphanol (0.5-3
the other (good) leg and creates increased mg/kg, IM, every 4 hr, depending on pressure and potential ulceration on the
species). Local anesthetics may be helpful
plantar surface of the foot. Birds most at
after surgery.

risk are birds with leg fractures; arthritis
of a hip, stifle, or tarsal joint; and obese

Renal Disease
birds or birds on a poor diet ( eg, vitamin

Renal disease may be seen at any age, but

A deficiency). These are the same
older birds are more likely to develop renal
conditions that can predispose a bird to
insufficiency. Causes are multiple and

1914

PETBIRDS
include glomerulonephropathies, renal
function, 100 frames/sec mininlmn speed,
tubular gout, and chronic bacterial
and microcurved or phased a.tTay probes
nephritis.

with a minimmn 7.5 MHz frequency.

Clinical signs include weight loss,

Anatomic constraints in birds also limit

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depression, polyuria, polydipsia, and articthe ecl10cardiograph windows available.

ular gout. Diagnosis is made based on a

Para.ineters for chan1ber sizes, blood flow
persistent hypermicemia before and after
velocities, functional contractility, and
fluid therapy. Imaging (radiographs or CT
valvular insufficiency have been detemlined
scan) may demonstrate small or large
for several species, and studies are ongoing
kidneys with or without mineralization.

in this area.

Occasionally, urethroliths may be seen.

Reported therapies include enalapril

Renal biopsy is necessary for definitive

(0.25-0.5 mg/kg/day, PO), furosemide
diagnosis.

(0.15-2 mg/kg, PO, SC, or IM, once to twice

Treatment includes supportive care (fluid
daily), pimobendan (6 mg/kg, PO, bid), and
therapy) and antibiotics as needed based on
digoxin (0.01-0.02 mg/kg, PO, bid).

diagnostics. Colchicine (0.04 mg/kg, PO,

Although most avian therapeutic regimens
bid) and allopurinol (10-30 mg/kg, PO, bid)

are still extrapolated from those used in
have successfully treated certain disease
mammals, nmnerous reports indicate that
processes. After stabilization, conversion
cardiac drug therapy can improve cardiac
to an appropriate diet should be initiated.

function, thereby increasing the quality and

Essential fatty acids (omega3) at 0.1-0.22
length of life.

mllkg/day, PO, have been used anecdotally
to manage renal disease in birds.

Pulmonary Hypertension: The
ca.i·diovascular system of birds differs

Cardiac Disease
anatomically and physiologically from that

As birds live longer and diagnostic
of ma.inmals. The right at1ioventricular
techniques improve, cardiac disease is
valve is a single, muscular valve with no
being diagnosed more frequently. It can be
chordae tendinae. The physiologic
difficult to detect and may min1ic other
responses that maintain low pulmonary
problems, such as respiratory disease.

vascular resistance (both vascular

Cardiac disease has been associated with
distensibility and vasculature recruitment)

atl1erosclerosis in pet birds, and potential
a.i·e absent in birds, resulting in the inability
risk factors are a sedentary lifestyle, a
of the pulmonary vasculature to accommohigh-fat diet, and hypercholesterolemia.

date increased cardiac output by either

Clinical signs are weakness, depression
altering vascular diameter or changing the
or lethargy, increased respiratory rate and
percentage of vascular cha.imels being used.

effort, or tachycardia. With right-side heart

This may be, at least in part, responsible for
disease, hepatomegaly and ascites are
the high incidence of pulmonary hypertencommon. Disease also may be subclinical, sion syndrome in poultry (seep 2871) as
then present acutely, with the bir.d a.tTesting
well as right-side heart disease in psittawhen diagnostic tests or treatments are cines. Studies on the impact of pulmona.i-y
attempted. In birds, right-side cardiac
hypertension in broiler hens have
disease is more prevalent than left-side.

demonstrated that the response to

Consultation with a cardiologist on any
pulmonary arterial hypertension in
avian patient with suspected cardiac
chickens involves an increase in two
disease is advised. Diagnosis of the
vasoactive substances: a vasodilator and
ca.i·diovascula.i· abnormality and fom1ing
a vasoconstrictor. The vasoconstrictor
a therapeutic plan requires knowledge
predominates over the vasodilator in
of avian anatomy and physiology and
broiler hens susceptible to pulmonary
a cardiologist's diagnostic skills and
hypertension. For geriatric psittacine
pharmacologic recommendations.

patients witl1 puhnonary hypertension,

Radiographs and cardiac ultrasound
vasodilator therapy should be explored.

ca.i1 aid in the diagnosis.

Macaw asthma may theoretically cause

The stress of handling can increase
pulmonary hypertension, both from chronic
intracardiac blood flow velocity 300% in avian capilla.i-y hypoxia and subsequent patients; therefore, inhalant anesthesia or
polycythemia.

sedation is prefe1Ted over manual restraint
for perfom1ance of echocardiogra.ins in all

Atherosclerosis: Atherosclerosis is a
but the most docile birds. The equipment
proliferative lesion of the tunica media
necessary for echocarcliology in birds
and tunica inti.ma of elastic and muscular
includes an ultrasound unit with Doppler
arteries. Atherosclerotic plaques cause

PET BIRDS

1915
abnorn1al vascular flow and loss of

Treatment involves supportive care
endothelial integrity. These changes in

(fluid therapy), antibiotics as needed, and
vessel walls can initiate tlu-ombosis. In
medications to support hepatic function
birds, lesions are primarily in the aorta and
such as silymarin (milk thistle) (100-150

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brachiocephalic arteries. Atherosclerosis is
mg/kg, PO, bid) and ursodeoxycholic acid
common in psittacine birds. It is generally a

(10-15 mg/kg/day, PO).

geriatric condition, except in African grey
parrots, in which this disease has been
observed in very young birds. Amazon

NEOPLASTIC DISEASES
parrots, macaws, and African grey parrots

Neoplasia occurs with some frequency in
seem to be particularly susceptible.

pet birds of all ages and includes cancer of

Predisposing factors appear to include
the skin, sinuses, oral cavity, GI tract, lungs,
age (most affected birds are 10-15 yr old),
air sacs, liver, spleen, kidneys, reproductive
sedentary lifestyle, and a high-fat diet.

tract, bone, vascular and connective tissue,

Clinical signs are rarely reported in birds,
and brain. The incidence of cancer is likely
and the condition is often associated with
to rise as pet birds age. Often, external
sudden death. Clinical signs that may be
tumors can be seen on physical examination
seen are exercise intolerance, dyspnea,
and diagnosed by fine-needle aspirate and
episodic weakness, and neurologic signs
cytology or biopsy. Internal neoplasia often

( eg, seizures, tremors, paresis). At necropsy,
requires imaging (radiographs, ultrasound,
grossly thickened arterial walls are seen.

or CT scan), endoscopic examination, or

Diagnosis can be difficult. Radiographiexploratory surgery to detem1ine tl1e type cally, the right aortic arch may be enlarged,
and extent of the neoplasia Treatment
with increased density. Lipemia is often
protocols are becoming more successful
present, and marked increases in cholesbut are still extrapolated from other species terol and triglyceride concentrations may
and often have been perfom1ed in only one
be seen. Unfortunately, definitive antemoror two birds. More information ( clinical tem tests are lacking.

studies and research) is needed on

Medical treatment is anecdotal. A variety
diagnostic tests, treatments (including
of treatments have been advocated to lower
adverse effects), and prognosis of neoplasia
cholesterol levels, but none appears to be
in companion birds.

consistent in its efficacy. Isoxsuprine (10
mg/kg/day, PO) has been used anecdotally
with some success. Essential fatty acids

Pseudoneoplastic Skin Conditions

(flax seed oil at 0.1-0.2 mUkg/day, PO)

Xanthomas are not neoplasms but locally
have been advocated and used to reduce
invasive subcutaneous, yellow, fatty mass�s
cholesterol and inflan1mation.

in the skin. Xanthomas are rarely found in
internal organs. The distal wing, keel, and

Liver Disease
the sternopubic area are common locations,
although xanthomas may be found

Liver disease can affect birds of any age but
anywhere. Cockatiels and budgerigars are
is more common in geriatric birds. Hepatic
overrepresented, although xanthomas are
lipidosis is most common, possibly resulting seen in most psittacine species. The lesions from longterm feeding of an inappropriate
may be pruritic and may be associated with

(high-fat) diet. Chronic liver disease can
lipomas or sites of chronic irritation. The
result in fibrosis of the liver and decreased
cause is unknown; however, dietary
liver function and failure.

improvement, including sufficient vitan1in

Clinical signs of liver disease are anorexia, A, has been curative in less advanced cases.

lethargy, overgrown beak and nails with

Xanthomas tend to be vascular. Therapy
bruising, biliverdinuria, discolored feathers,
includes surgical resection, although in
and, in later stages, ascites. Birds often are
large masses closure may be difficult, and
overweight or have a history of being obese.

strict attention to hemostasis must be

Clinical pathology may reveal high liver
observed. Amputation is reconu-nended
enzyme levels (AST) and bile acids, a
for xanthomas on the wing tip.

nonregenerative anemia, and high triglycer

Lipomas occur most frequently in
ide and cholesterol concentrations. In1aging
budgerigars, rose-breasted cockatoos,

(radiographs or CT scan and/or ultrasound)

Amazon parrots, and cockatiels. These
may reveal hepatomegaly or rnicrohepatica.

benign, soft, yellowish, encapsulated

Liver biopsy may be necessary to confin11
subcutaneous masses are most often
the diagnosis and detern1ine etiology and
located on the keel or in the sternopubic
prognosis.

area If traumatized, they may become

1916

PET BIRDS
inflamed or necrotic. Lipomas can grow
and fu1e-needle aspirate and cytology or
rapidly and result in ulceration of the overbiopsy of the lesion.

lying skin. Treatment includes conversion

Reconrn1ended treatment is surgical
to a low-fat diet, weight loss in obese birds,
excision with or without radiation therapy.

and surgical excision. Recurrence is

Cobalt-60 radiation therapy and intrale

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common with incomplete removal.

sional carboplatin and cisplatin have had
limited success in treatment of SCCs.

Cutaneous,Subcutaneous,and

Radiation therapy with a strontiurn-90

Other Neoplasms
probe has had some success in treatment of

SCCs of the uropygial gland after surgical

Fibrosarcomas may be lobular, subcutaneexcision or debulking.

ous masses without skin involvement or

Musculoskeletal neoplasms reported
may be seen as erythemic skin lesions. They
in psittacines include osteosarcoma,
may also develop in the oral cavity, bone, or
chondroma, chondrosarcoma, hemanabdominal cavity. Fibrosarcomas tend to be gioma, and leiomyosarcoma. Wide surgical
locally invasive and recurrent. Surgical
resection is the suggested treatment.

excision followed by radiation and

Internal carcinomas include ovarian
chemotherapy has shown some success.

neoplasia (vaiious cell origins), renal

Liposarcomas are malignant tumors of
carcinoma, hepatic adenocarcinoma,
the lipocytes and have rarely been reported
and hepatobiliary adenocarcinoma
in pet birds. They have been described in

(related to papillomas in Amazon patTots ).

cockatiels, budgerigars, a conure, an

Clinical signs of coelomic twnors include

African grey parrot, and a quaker parakeet.

anorexia, weight loss, depression, and/or

They are similar in appearance to lipomas
dyspnea (from organ enlai·gement and

(yellowish, gray mass) but are fumer, more
compression of air sacs). Gastric carcinoinfiltrative, and vascular. Cytologic exan1mas, generally diagnosed at necropsy, are
ination may not differentiate between a
often found at the proventricular-ventriculipoma and liposarcoma, so surgical biopsy lar junction. Death from gastric neoplasia
is recommended. Therapy includes surgical
may be caused by hemorrhage, gastric
excision, although recunence is common
perforation and sepsis, endotoxic shock,
with incomplete removal.

or inanition and subsequent wasting.

Squamous cell carcinoma (SCC) is a

Diagnostic tests include radiographs with
malignant tumor comprised of moderately
or without barium contrast, CT scan, or
undifferentiated to poorly differentiated
ultrasound with fu1e-needle aspirate and
squan1ous cells. SCCs are most conunon on
cytology or biopsy.

the skin and beak, in the oral cavity,

Both carboplatin and cisplatin have been
esophagus, or crop, arid on the distal wing
used successfully in various forms of internal
and phalanges. These tumors tend to be
carcinoma. Toxicity studies with cisplatin in
locally invasive. Cutaneous SCCs often
cockatoos indicate that psittacine tolerance
appear as proliferative masses or woundlike for this drug may be greater than that of ulcers. Tumors often develop at sites of
manunals. Several cases of ovarian neoplasia
chronic irritation. It has been expe1imenhave been treated with GnRH agonists tally demonstrated that inflammation can

(leuprolide or deslorelin implant) witl1 some
promote neoplastic proliferation. SCCs of
success.

the uropygial gland can occur and result in

Pituitary adenomas are most prevalent
enlargement of the gland and ulceration.

in budgerigars and cockatiels but have been

SCCs of the beak result in overgrowth and
observed in other psittacine species. Tumors
defom1ation of the beak. Tumors involving
may cause acute neurologic conditions ( eg,
the sinuses or oral cavity t-ypically have
seizures, opisthotonos, ataxia, blindness,
poorly defu1ed borders and are associated
ai1d difficulty flying). Affected birds may
with necrosis and hemorrhage.

also show signs related to the pituitat'Y

Clinical signs of SSCs of the sinus or oral
hormone(s) affected (eg, adrenocorticocavity are dyspnea, dysphagia, anorexia, tropic hormone [ACTH] associated with
exophthalmos, and nasal discharge. Clinical
polydipsia and polyuria). Diagnostic tests
signs of birds with SSCs of the crop or
are of lin1ited use. Pituitary tumors are
esophagus include anorexia, regurgitation,
t-ypically diagnosed based on species and
and depression. Cutaneous SCCs tend to be
clinical signs and ai·e confirmed at necropsy.

locally aggressive and recur, but there are

Thymoma and thyroid adenocarcino
few reports of metastasis. Tun1ors are often
mas have been reported in several
associated with chronic (secondary) bacpsittacine species. P1imat')' pancreatic terial and fungal infections. Diagnosis is
neoplasias of variable cell origins have
based on imaging (radiographs, CT scan)

been repo1ted.

PET BIRDS

1917

IQmphoma/lymphosarcoma is the most
research reports are available for chemocommon lymphoid neoplasia in psittacine therapy or radiation therapy protocols in
and passerine birds. Multicentric lyrnphobirds. Because very little is known about sarcoma is most common, whereas
chemotherapy and radiation in birds, a
lymphocytic leukemias occur rarely.

cw-rent literature search and consultation

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Lymphoma can involve the spleen, liver,
with a veterinary oncologist are recomkidneys, GI tract, skin, bone, oviduct, lungs, mended before treatment of a pet bird
sinuses, thymus, testes, brain, mesente1y,
diagnosed with cancer. In addition to the
trachea, and pancreas. The liver is most
antineoplastic drugs that have been used in
commonly affected, followed by the
birds discussed below, see ANTINEOPLASTJC
spleen and kidneys. Nw11erous reports of

AGENTS, p 2722.

exophthalmos in psittacines, particularly

Vincristine was used in the chemotherayoung African grey parrots, have been peutic regimen of an African grey pai-rot
diagnosed as retrobulbar lymphoma.

with malignant lymphoreticular neoplasia, a

Cutaneous lymphoma often occurs on the

Moluccan cockatoo with lymphoma, and a
head or neck. Lesions are grayish yellow,

Pekin duck with lymphoma and leukemia.

diffuse or multifocal, and may resemble

Cisplatin/carboplatin was evaluated in
xanthoma or inflanlrnation. Clinical signs
eight sulfur-crested cockatoos. A dose of l
vary based on location of the twnor but may
mg/kg infused over l lu- was tolerated well,
include depression, anorexia, weight loss,
and plasma levels were in a therapeutic
coelomic distention, paresis, lameness,
range. Adverse effects were weight loss,
blindness, regurgitation, or dyspnea.

regurgitation, and bone mai-row suppres

Canaries often present for having stopped
sion. Intratun1oral cisplatin and radiation
singing.

therapy were used to treat fibrosarcoma in

Diagnosis is based on physical exan1inaa macaw. Intralesional cisplatin was used tion findings, imaging (radiographs with or
unsuccessfully in treatment of SCC in a
without contrast, ultrasound, or CT scan)

Buffon's macaw. Carboplatin was used
and fine-needle aspirate or biopsy of
successfully to treat a bile duct carcinoma
affected organs, masses, or bone maITow.

in a yellow-naped Amazon pan·ot ai1d

A CBC often reveals leukocytosis or
pancreatic duct adenocarcinoma in a
lymphocytosis rather than a leukopenia.

green-winged macaw.

Anemia (PCV <35%) is conlrnonly reported.

L-.A.spai·aginase was used to treat

No evidence of retroviral activity has been
lymphoma in a Moluccan cockatoo.

associated with psittacine lymphoma.

Adverse effects associated with treatment

Treatment has included surgical excision
were weight loss, lethargy, ai1orexia, and
with or without chemotherapy. Chemotherregurgitation. Doxorubicin was used apy regimens have included one or more of
successfully in a blue-fronted .A.mazofl
the following: corticosteroids, orthovoltage
parrot with osteosarcoma. Doxorubicin in
x-ray, chlorambucil, doxorubicin, L -asparacombination therapy was unsuccessful in ginase, cyclophosphanlide, a-interferon,
treating lymphoma in a Moluccan cockatoo.

and/or vincristine sulfate. Diphenhydramine

Chlorainbuci.l was used successfully in
and dexamethasone have been used to
treatment of cutaneous pseudolymphoma
reduce the incidence of allergic reaction or
in a blue and gold macaw. Cyclophosphaanaphylaxis. Although chemotherapy and mide has been used to treat lymphoma in a
radiation therapy have been successful,

Moluccan cockatoo.

treatment success overall has been variable.

Radiation therapy has been used in

Primary respiratory neoplasia is
birds with variable results (seep 1651).

unconm1on in psittacines, except for a
mixed pulmonary tumor reported in

NUTRITIONAL DISEASES
cockatiels. Metastatic pulmonary neoplasia
may occur.

Proper nutrition for compailion birds
hist01ically has been and continues to be a

Chemotherapy and Radiation
concern for avian veterinarians, avicultw�

Therapy Agents
ists, and owners. Although avian nutrition
has greatly improved in the past decades,

Most reports of chemotherapy in birds have
nutritional disease is still conm1on in pet
demonstrated both higher tolerance for
birds. The availability of fonnulated diets
chemotherapeutic agents than expected and and hand-feeding formulas have been less tunior response than desired. Anecdotal
pivotal in improving avian nutritional health,
reports indicate that neoplasia in birds is
but many birds are still fed inadequate diets.

more resistant to radiation than that in man1-

The two most conunon reasons for
mals. Very few case reports and even fewer
malnutrition in companion birds ai·e feeding

1918

PET Bl RDS
diets that allow the birds to choose what

Vitamin A Deficiency: Vitamin A plays
they want to eat ( either mixtures of seeds/
an in1portant role in avian health and is
nut and pellets, or table foods the owner
cmcial for a healthy inunune system.

considers healthy) and feeding pure seed or

Hypovitaminosis A causes squamous

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seed-based diets. Feeding a mixture of
metaplasia of epithelium within the
pellets and seeds is also common, resulting
oropharynx, choana, sinuses, GI tract,
in selective eating and consequently
urogenital tact, reproductive tract, and
inadequate nutrient consumption.

uropygial gland as well as hyperkeratosis of

Many of the illnesses seen in pet birds
the feet. All-seed diets and even mixed diets
have their basis in malnutrition. This
of Y2 seeds and Y2 pellets are deficient in
includes hepatic disease, renal insufficiency, vitamin A.

respiratory impainnent, musculoskeletal

Clinical signs are nasal discharge,
disease, and reproductive problems. For
sneezing, periorbital swelling, conjunctiviadditional information on nutrition in pet tis, dyspnea, polyuria, polydipsia, poor
birds, see p 2288.

feather quality, feather picking, and
anorexia. Birds may have absent or blunted

Obesity: Obesity is common in companpapilla of the choanal slit. White plaques ion birds. High-fat diets (seeds, nuts, and

(hyperkeratosis) may develop in and
many table foods), overabundance of food,
around the mouth, eyes, and sinuses. In
and a sedentary lifestyle are all contributchronic epithelial conditions ( eg, pododering factors. Obesity is typically defined as matitis, sinusitis, and conjunctivitis) that
a bird being 20% over ideal weight, with
have been refractory or recurrent, often
a body condition or keel score of 4 out of
vitamin A deficiency is the primary cause.

5 (seep 1887). Galahs, macaws, Amazon

Birds with reproductive disease on poor
parrots, and quaker parrots are prone to
diets should be considered deficient.

obesity. Clinical signs may not be evident

Treatment involves treating secondary
but include lameness (pododermatitis and/
infections, supplementing with vitan1in A,
or arthritis) and respiratory issues from
and converting the bird to a good quality
excessive abdominal fat.

pelleted diet. Parenteral vitamin A can be

Obese birds should be converted to a
given (100,000 U/kg, IM). Vitamin A
pelleted diet with portion control. Exercise
precursors, such as spirolina, sprinkled
should be encouraged by providing a larger
daily over the food are a safe way to
cage with multiple food bowls around the
supplement diets deficient in vitamin A.

cage to encourage movement. Rope or

The diets of all pet birds should be evaluated
spiral rope perches will encourage climbing
for vitamin A content.

and balance. A flight cage outdoors should
be provided for flighted birds, and walking

Iodine Deficiency: Goiter, or thyroid
or climbing stairs encouraged for nonhyperplasia, occurs in budge1igars on all-seed flighted birds. Obese birds are more prone
diets deficient in iodine. This condition is no
to arthritis, fatty liver disease (hepatic
longer common because of the availability of
lipidosis), atherosclerosis, and cardiac
pelleted and fortified diets. Classic signs are
disease.

respiratory stridor, wheezing, or clicking due
to the pressure of the thyroid on the syrinx.

Lugol's iodine (1 drop/250 mL.of drinking
water) can be used until conversion to a
pellet or fortified seed diet is accomplished
and clinical signs have subsided.

Calcium, Phosphorus, and Vitamin 03

Imbalance: Seed-based diets are well
known for their calcium:phosphoms
in1balance and an1ino acid deficiencies.

Sunflower seeds, which tend to be selected
preferentially by many psittacines, are low
in calcium, deficient in essential an1ino
acids, and high in fat. Safflower seeds are

Fatty liver disease (hepatic li
actually hjgher in fat content than sunflower
pidosis), gross
lesions, in a cockatiel. A pale liver is located
seeds, contrary to popular belief, and also
beneath the heart, nestled in a pad of
contain inadequate an1ino acids and
abdominal body fat. Courtesy of Dr. Louise Bauck.

calcium.

PET BIRDS

1919

Metabolic Bone Disease (Nutritional

Hemachromatosis is reserved for cases

Secondary Hyperparathyroidism):

associated with actual pathology. As iron

Nutritional secondary hyperparathyroidism
levels within the liver increase, hepatic
can occur in young and older pet birds.

lysosomes are dan1aged and release ionic

Because the calcium to phosphorus ratio in
iron, resulting in oxidative dan1age to

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most seeds is poor (high phosphorus and
membranes and proteins. Iron storage
low calcium), birds on a seed diet become
disease is common in mynalls and toucans,
seriously depleted. The effects of a calciumand in certain zoo birds such as birds of deficient diet are often compounded by
paradise; it has been occasionally rep01ted
inadequate exposure to unfiltered sunlight
in pet psittacine species, particularly lories.

in birds housed indoors, resulting in vitamin

Iron storage disease is associated with

03 deficiency as well. In young birds,
excessive intake of dietary iron. However,
especially African grey parrots, hypocalcenot all birds are affected when fed similar mia may present as osteodystrophy, with
diets, and stress or genetic factors may also
cmvature and deformation of the long
play a role. Certain foods rich in vitamin C,
bones and vertebrae. African grey parrots
such as citrus fruits, increase dietary iron
are also prone to an acute hypocalcemia
uptake. Current dietary iron recommendasyndrome that is associated with both tions for toucans and mynalls are <50-100
hypocalcemia and hypovitaminosis 03.

ppm.

Clinical signs include weakness, ataxia,

Clinical signs are anorexia, weight loss,
tremors, depression, seizures, and pathodepression, distended abdomen with logic fractures. In reproducing birds, eggs
ascites, dyspnea, and biliverdinmia. The
are often thin-shelled, egg production and
liver, spleen, and heart are the most
hatchability are decreased, and embryonic
commonly affected organs. Circulatory
death occurs. Calcium deficiency can lead
failure, ascites, and hypoalbunlinemia are
to cessation of egg laying, egg binding, or
often seen clinically. Diagnosis is by liver
cloacal prolapse. Diagnosis is based on
biopsy.

decreased total and ionized plasma calcium

Treatment includes periodic phlebotomy,
levels and radiographic evidence of
iron chelation, and dietary modification.

decreased bone density or pathologic

Recommending low-iron diets routinely
fractures. Serum 25-hydroxycholecalciferol
for pet mynalls and toucans is prudent
levels can also be measured and are usually

( commercial formulas are available).

low.

Foods high in vitan1in C should be avoided.

Treatment is supportive care, calcium

Supplementation with chelators such as
and vitanlin D supplementation, conversion
tannins, fiber, and phytates has been
to an appropriate diet, and exposure to
suggested.

ultraviolet light, preferably natural sunlight.

If pathologic fractures are present, splinting

Additional Nutritional Concerns: In
or bandaging may be necessary, along with
addition to the well-documented nutritional
cage rest, NSAIDs, or analgesics. Initial
deficiencies in diets designed for psittatreatment should consist of calcium cines, described above, the following
gluconate (100 mg/kg, IM).

dietary concerns should also be noted:

Pet birds should have exposure to natural

1) the potential sensitivity of individual
sunlight when possible. Owners should
birds to dyes and preservatives added to
provide an outdoor cage that provides
some seed and pelleted foods; 2) the high
opportunities for climbing and/or flight and
incidence of hepatic lipidosis, atheroscleroaccess to direct sunlight. Birds should be sis, and right-side heart failure in sedentary
monitored closely when outdoors, even in a
captive birds consuming primarily seed
cage, because many predators can injure a
diets; 3) the occurrence of hepatic fibrosis
pet bird through cage bars.

and cirrhosis secondary to aflatoxicosis

Vitamin D Toxicosis: Although excessive
from improperly stored seed and pet-grade
oral calcium intake is not thought to cause
peanuts; 4) the difference between food
clinical problems in most cases, excessive
provided by well-meaning owners for their
oral vitamin 0
birds to eat (table foods, fonnu]ated

3 can cause harmful calciun1
accun1ulation in tissues such as the kidneys. pelleted diet, vegetables, etc) and what the Supplements should be used carefully, espebirds actually consume (seed); and 6) the cially in susceptible species (eg, macaws).

low palatability of most vitamin and mineral
supplements added to water, which are not
only ineffectual but can lead to decreased

Iron Storage Disease: Iron storage
water consumption and dehydration.

disease refers to disease that occurs with

Foods that owners should be advised to
excessive iron accumulation in the liver.

avoid feeding their birds at any time are

1920

PET BIRDS
chocolate, caffeinated beverages, alcohol,

Common reproductive problems in pet
junk food (salt, sweets), milk products,
birds include behavioral issues, failure to
onions, avocados, and apple seeds.

reproduce, excessive egg production,

Wild birds spend many hours a day
dystocia ( egg binding), impacted oviduct,
foraging for food. Captive and pet birds
egg yolk peritonitis, cloaoal prolapse, and

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usually consume all of their caloric needs at
neoplasia.

one food bowl, with very little time or
energy expended. To promote a healthier

Behavioral Problems: Behavioral
lifestyle for companion birds, foraging
problems that can be related to reproopportunities should be provided that ductive issues include feather picking,
increase activity, promote a healthier diet,
mutilation, and excessive screanting. These
and stimulate birds intellectually. Owners
behaviors can also occur for other reasons,
need to provide a cage large enough for the
so a full evaluation must be done to
bird to climb and play in, with rope or other
detemtine tl1e cause. Behavioral problems
perches that stimulate activity and balance.

are most common in hand-raised paiTots

Multiple small food bowls should be placed
overly bonded to their owners. Psittacines
throughout the cage to encourage
are intelligent, social a11in1als. In the wild,
movement. Foraging toys with food bits
most live in flocks, have a set breeding
promote activity as well. An outdoor flight
season (based on temperature, photopecage that allows natural sunlight and riod, humidity), ai1d raise chicks with their
increased activity is ideal.

mate. In captivity, most pet birds are kept
all year at stable temperatures and ai·e

REPRODUCTIVE DISEASES
provided adequate food, which is often high
in fat. This can promote breeding behavior

Birds are oviparous, meaning they lay and
year round.

incubate eggs. Chicks may be precocial

Many hand-raised parrots are overly

(hatched with downy feathers and able to
bonded to their owner at sexual maturity,
eat on their own soon after hatching) or
resulting in sexual frustration that may lead
altricial (featherless and completely
to over-gromning behaviors and excessive
dependent on being fed by parent birds until contact calls (screanling) when the owner weaned). Passerine and psittacine birds are
leaves tl1e room or house. Some of these
altricial. Sexual maturity occurs from 6 mo
over-stimulated ( excessively handled and
of age in smaller birds to 3--5 yr in larger
petted) birds begin laying eggs or masturparrots. Most hens have only a left ovary bating early, leading to egg binding or
and oviduct and are heterogarnetic (the
cloacal prolapse (seep 1922) along with
female determines the sex of tl1e chick).

feather destructive behavior or screanling.

The male has two testes located internally

Significant behavior modifications may
cranial to the cranial pole of the kidney.

need to be implemented (seep 1927) along

Most wild birds have a specific breeding
with conversion to a pelleted diet. In some
season. Captive and pet birds breed at any
cases, a GnRH agonist may be necessary to
time based on environment{photoperiod),
decrease production of reproductive
nutritional status, and absence or presence
hormones. This should ideally only be done
of a mate (bird) or perceived mate (human)

along with in1plementing necessai-y
and/or nest box. Females store calcium in
behavioral modifications.

their bones (hyperostosis), which is later
used in egg shell production. Ovulation

Excessive or Chronic Egg Laying:

occurs in response to increasing levels of

Excessive egg laying is when a bird has
estrogen and luteinizing hormone. The
repeat clutches, lays more eggs than
oviduct is composed of four segments: the
no1mal, or produces more eggs than is
infundibulum, where fe1tilization occurs;
normal. It is common in small birds, eg,
the magnum, where albumen is deposited;
budgerigars, lovebirds, and especially
the isthmus, where tl1e inner and outer shell
cockatiels. Affected birds typically are on a
membrane is added; and the uterus ( shell
high-fat and high-calo1ie diet. Other birds
gland), where calcification of the shell
typically are housed either in the same cage
occurs. The entire period of egg formation
or close by, or birds are overly bonded to the
takes -24 hr. Most pet birds lay 2 to 4 eggs in
owner. They often have an extended photoa clutch, altl10ugh indetenninate layers such period (> 12 hr). In some color mutations, as cockatiels and budgerigars can produce
there may be a genetic predisposition.

much larger clutches.

Clinical signs may not be evident, with

Most pet birds are not sexually dimoronly a history of excessive egg laying, or the phic, so dete1mining the sex requires
bird may present nonperching, weak,
endoscopic exan1ination or DNA sexing.

depressed, and tail bobbing (indicating

PET Bl RDS

1921
dyspnea), with decreased defecation or
may be distended. An egg is not always
voluminous droppings. Birds often have a
palpable. Diagnostic tests may need to wait
wide-based stance, are broody, and may
until the bird is stable; they include a CBC,
have pathologic fractures from hypocalceplasma biochemical profile (including mia. Excessive egg laying, if untreated,
ionized and total calcium), and radiographs.

often leads to more serious reproductive

These tests may need to be done stepwise in

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issues such as dystocia, impacted oviduct,
a critical patient.

egg-yolk peritonitis, or cloaca! prolapse.

Medical treatment includes fluid therapy,

Diagnosis is based on the history, physical parenteral calcium supplementation, exanlination findings, high plasma calcium
analgesics, and/or NSAIDs, and continued
levels, and radiographic findings of
maintenance in a warm humid incubator.

hyperostosis and/or evidence of an egg.

Oxytocin and the avian equivalent arginine

Reproductively active birds often have high
vasotocin both cause uterine contractions
cholesterol, t1iglyceride, and total protein
and induce oviposition, as can prostaglanconcentrations.

dins F or E. If the egg is adherent to the

Treatment involves decreasing day length
uterine wall or unable to be passed ( often
to 8 hr of daylight, conversion to a pelleted
due to swelling, adhesions, or collection of
diet, removal of nest boxes and any toys the
feces and mates), administration of these
bird may be overly bonded to, removal of
drugs could tl1eoretically lead to uterine
any mate, and discussion with the owner of
ruptme, but this has rarely been repmted.

appropriate handling of their bird. Calciwn

If medical management fails, then
supplementation and a GnRH agonist may
sedation, inhalant anesthesia, and manual
be needed to reduce the production of
extraction may be required. With the bird
reproductive hormones. Usually, leuprolide
under anesthesia, the cloaca is lubricated
acetate (800 mcg/kg, IM, every 3 wk for
with sterile jelly. Barring adherence of the
three injections, then pm) is administered.

egg to the uterus, steady digital pressure

If the above changes and medications are
applied between the end of the sternum and
unsuccessful, then a salpingohysterectomy
tl1e egg will cause the slow descent of the
may be necessary. This will prevent egg
egg. At this point, the uterus will often evert
laying but not always ovulation, because it
and reveal the white pinhole where the
is impossible in birds to remove all ovarian
uterine opening is located. This opening
tissue. Prognosis is good with early cases
will gradually dilate. Very seldom will any
that respond to management, dietary
additional pressure or manipulation be
changes, and GnRH agonists.

required. After the egg is delivered, tl1e
uterus typically will normally involute. If

Egg Binding: Dystocia ( egg binding) is a
oviposition does not occur with digital
common occurrence in captive hens, most
pressure or because of a soft-shelled egg,
notably in cockatiels, budgerigars, and
ovocentesis is indicated. After aspiration,
lovebirds. Usually, these birds are chronic
finner shells are collapsed and carefully
egg layers, and calcium deficiency
removed or allowed to pass. Postoperative

( resulting in misshapen or soft-shelled
care includes antibiotics, NSAIDs, and a
eggs) is a factor. Other causes include

GnRH agonist to reduce further egg laying.

vitanlin A deficiency, oviductal disease or

After egg extraction, the hen may continue
neoplasia, abdominal wall herniation, being
to be depressed, witl1 labored breathing,
a first-time layer, and genetic factors. An
and often will not appear clinically normal
inappropriate environment and lack of a
for up to 24 hr. A second egg may be produced
nest box can be contributing factors for
by the following day, so repeated palpation
some birds. Egg binding may also be seen in is indicated.

large psittacines, although excessive egg

Surgical intervention (salpingohystereclaying is not as commonly associated with tomy) is warranted if the egg is severely
the condition in these birds. Obesity,
adhered to the oviduct, multiple eggs are
general nutritional inadequacy, behavioral
present, or the egg is ectopic. Prognosis
factors, and husbandry conditions may be
for egg binding is fair to good if medical
involved. Egg-bound birds often present as
treatment or manual extraction of the egg
emergencies. These birds should receive
is effective. Husbandry, nutritional, and
supportive care (ie, rehydration, parenteral
behavioral issues as discussed m1der
calcium, increased humidity, and warmth)

excessive egg laying ( see above) need to
before attempting extraction of the egg.

be addressed.

Clinical signs include a bird on the
bottom of the cage, depression, closed eyes,

Impacted Oviduct: An impacted oviduct
bobbing tail, and dyspnea. The abdomen
is often a sequela of dystocia or salpingitis.

1922

PET BIRDS

The oviduct becomes impacted with excess
yolk, along with bacteria ( eg, Escherichia
mucin, albumen, and soft-shelled or mal
coli, Staphylococcus) in the coelomic cavity fom1ed eggs. These mate1ials often become
results in infection. Egg yolk coelomitis
adhered to the oviduct wall and become
causes a severe inflammatory reaction and
inspissated. Clinical signs are depression,
can lead to an egg-related pancreatitis or a

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anorexia, distended abdomen, and possibly
yolk emboli (which can resemble a stroke).

dyspnea.

This occurs most commonly in cockatiels.

Diagnosis is based on a history of chronic

Clinical signs are similar to other reproegg laying or dystocia. Imaging (radioductive disorders, but typically abdominal graphs, CT scan, or ultrasound) may reveal
distention and ascites are present. Birds
an enlarged oviduct. Hyperostosis may be
often present severely compromised and
present. The bird may have a leukocytosis
require supportive care before diagnostic
and high total protein, cholesterol, and
testing. A leukocytosis and monocytosis
triglyceride concentrations. Treatment is
may be present. Imaging ( radiographs or
supportive (fluids, analgesics, NSAIDs, and
ultrasound) may reveal an enlarged oviduct
antibiotics). Surgery is recommended but is
or a fluid-filled abdomen. Endoscopic
high risk.

examination may be diagnostic but should
be done only by an experienced clinician in

Cystic Ovarian Disease: Birds with
a bird with ascites. Abdominocentesis may
cystic ovarian disease often present with
need to be performed to relieve dyspnea.

a history of previous egg production, but

Other treatments include fluids, antibiotics,
egg laying may not have occurred for
analgesics, anti-inflammatories, a warm
several years. Cystic ovarian disease is
incubator, and oxygen as needed. Many
most commonly seen in budgerigars
birds will in1prove with supportive care and
and canaries.

antibiotics, but some may require salpingo

Clinical signs may include depression,
hysterectomy. Prognosis is fair with medical
inactivity, abdominal distention, ascites,
management and becomes guarded to grave
and often dyspnea. Abdominal palpation
with surgical intervention.

often reveals distention with ascitic fluid.

Diagnosis is similar to other reproductive
diseases. The fluid is usually a transudate,

Cloaca! Prolapse: Cloacal prolapse can
although it should be examined for evidence occur in any bird that strains frequently.

of secondary infection or egg-yolk

It is seen in egg-bound hens and in adult
peritonitis. Careful aspiration of fluid from
cockatoos, typically males. The exact cause
the ventral midline may relieve respiratory
is not known, but the following characterisdistress. Imaging (radiographs or ultratics have been associated with most cases: sound) when the bird is stable will often

1) hand-raised birds, 2) delayed weaning
demonstrate hyperostosis of the femurs and or continued begging for food, 3) close other long bones. On the lateral view, the
attachment to at least one person, 4) signs
ventriculus will be displaced cranially, and a
of either a child/parent or a mate/mate
space-occupying mass will be noted in the
relationship with the owner, who may not
renal and gonadal area. Ultrasonography
be aware of these signs, and 5) a tendency
can often detect cystic follicles, in addition
to hold the feces in the vent for prolonged
to normal follicular development.

periods (eg, overnight), rather than

Treatment is supportive care, abdominodefecating in the cage or when the bird has centesis if ascites is present, antibiotics, and been taught to defecate on command.

GnRH agonists to reduce reproductive

Cockatoos independent of people do not
hom10ne production, stimulate atresia of
have this medical problem.

the follicles, and decrease cyst size and

If detected and treated early, surgery
production. Surgery may not be needed if
combined with behavioral modification may
there is no concurrent infection or
correct the problem and prevent secondary
neoplasia.

infections and other complications.

Treatment includes cleaning exposed tissue,

Egg Yolk Coelomitis: Egg yolk
carefully debriding any necrotic or infected
coelomitis is another common sequela of
tissue, using hyperosmotic fluids to reduce
chronic reproductive disease. It can occur
swelling, and gently replacing the tissue.

after salpingohysterectomy because of the

Stay or transcutaneous sutures may be
inability to completely remove the ovary
required for several days and are more
and the potential for ovulation to occur into
effective if combined with GnRH agonists
the coelomic cavity. Other causes are
and changes in management ( eg, reduced
ectopic ovulation, salpingitis, neoplasia,
handling of pet cockatoos by owners).

cystic hyperplasia, or ruptured oviduct. Egg

Owners may be unwilling to alter their

PET BIRDS

1923
behavior, because often their attraction to
endoscopic examination (to evaluate
the bird is because the bird is willing to
health and status of reproductive organs)

allow stroking and cuddling. If the bird still is important. Common findings during
perceives its owner as either a parent or
endoscopy include same-sex pairings,
mate, it will continue to strain and the
immature birds, and reproductive disease.

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problem will likely recur. Behaviors that

Physical examination, hematologic
should be avoided include stroking the bird,
testing, and biochemical profiles are
especially on the back (ie, petting); feeding
recommended to determine overall health.

the bird warm foods or food by hand or

Treatment will depend on the examination
mouth; and cuddling the bird close to the
and diagnostic findings and may include
body. If an owner is serious about trying to
alterations in the environment or medical
change their bird's behavioral patterns,
therapy if indicated.

consultation with a board-certified veterinary behaviorist who is experienced with Medical and Surgical Management:

psittacines is advisable.

In many cases of reproductive disease,

In severe cases, where the vent is flaccid,
birds with moderate to severe disease
vent reduction and/or cloacopexy may need
require intensive nursing and suppo1tive
to be perforn1ed but should only be done
care. Often, physical examination and
with behavior modification. Females may
diagnostic tests must be postponed until
require salpingohysterectomy, because the
the bird is stabilized in a warm (85°-90°F)

vent reduction and cloacopexy may not
oxygen incubator with supportive care.

allow passage of an egg.

Procedures may need to be done in a
stepwise fashion over time to minimize

Reproductive Failure: Most owners do stress. Treatments may include warm not breed their pet birds, but reproductive
parenteral fluid therapy, nutritional
failure is an issue for aviculturists who
support, analgesics, anti-inflammatories,
do. When evaluating a pair of birds for
and antimicrobials (based on results of a
reproductive failure, a complete history is

Gram stain or culture and sensitivity
important. Is this a bonded pair ( do they
testing). Some birds may require surgery.

sit close to each other and allopreen, etc)?

Reproductive surgery in birds is compli

How long have they been together? Have
cated by the difficulty in removing the
they had a successful clutch in the past?

ovary. Because of the position of the ovary

What is their diet? Are the cage size, nest
cranial to the kidney, near the left adrenal
box, and perches appropriate for the
gland and major vasculature, removing
species of bird? Most pet birds prefer an
the entire ovary is not possible. The
enclosed nest box and a stable perch for
standard approach to the avian reproducbreeding. Is the owner certain of the sex?

tive tract is a left coeliotomy. Endoscopic

One of the most common reasons birds
orchidectomy and salpingohysterectomy
do not reproduce is same-sex pairs.

have been described but require special

Con.firming the sex by DNA testing or
ized training.

•ih•itl DRUGS USED IN AVIAN REPRODUCTIVE DISEASE

Drug

Type/Class

Dosage

Calcium gluconate (1()0;6) Calcium supplement

50-100 mg/kg, SC, TM

Calcium glubionate

Calcium supplement

25 mg/kg, PO, bid

Leuprolide acetate

GnRH agonist

700-800 mcg!kg, IM, every 2-3 wk

Deslorelin acetate

GnRH agonist

4.7-mg and 9.5-mg implants SC,
dorsal back between scapulas every

3--61110

Oxytocin

Honnone

5-10 U/kg, IM; may repeat once

Dinoprostone

Prostaglandin E2

0.02-0. l mg/kg, topically to
uterovaginal sphincter

Dinoprost tromethamine Prostaglandin F2

0.02-1 mg/kg, IM, intracloacal once

1924

PET BIRDS

TOXICOSES
galvanized toys, chains, mesh, bells, keys,
ai1d pennies (post 1982). Galvanized wire

Heavy Metal Toxicosis: Lead toxicosis
contains mainly zinc, but some may also
is commonly reported in companion birds
contair1 lead.

as well as in free-ranging avian species,

Clinical signs of zinc toxicosis include
especially waterfowl. In pet birds, toxicosis
ai1orexia, GI clisease: weakness, regmgita

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often occurs from ingestion of metal in the
tion, polyclipsia, ai1d polymia. Diagnosis is
home, such as blinds, costume jewelry,
based on history ai1d clinical signs and ai1
mirrnr backings, bir·d toys, hardware cloth,
increased blood zinc level. Radiographs may
and curtain weights. Ingested lead degrades
reveal metallic densities within the GI tract.

in the ventriculus and then is slowly released Blood sainples for zinc ai1alysis should be into the GI tract and blood. The lead is
collected in glass or all-plastic syringes ai1d
stored in soft tissues and bone and is slowly
tubes. Rubber stoppers on serum tubes
excreted over time. Lead toxicosis affects
ai1d the grommets on some plastic may
numerous biochemical processes in birds.

ai-tifactually increase the zinc levels in the

Clinical signs vary depending on the
collected sai11ple. Blood zinc levels >2 ppm
amount of lead ingested and may include
ai·e cliagnostic for zinc toxicosis.

anorexia, weight loss, regmgitation,

Treatment of zinc toxicosis is similar to
diaiThea, depression, ataxia, weakness,
lead toxicosis with supportive cai·e, Ca
seizures, blindness, polymia, and polydip

EDTA, DMSA, ai1d o-penicillainine. The
sia. Amazona spp, Ara tinga spp, Eclectus source of zinc should be determined if
paiTots, ai1d some other species may
possible ai1d removed from the environdevelop hemoglobinmia.

ment. Zinc is not stored in the bone like

Diagnosis is based on clinical signs,
lead, so it chelates faster thai1 lead.

biochemical analysis, hematologic finclings,
blood lead levels, and cliagnostic in1aging.

Polytetrafluoroethylene Toxicosis:

Hematologic testing may reveal a microcytic, Polytetrafluoroethylene (PTFE) gas hypochrom.ic anemia. Increased concentrapoisoning occms commonly in pet birds tions of AST, total protein, wic acid, ai1d CK
housed in or near kitchens. The gas is
may be present. Racliographs may reveal
released from nonstick cookware such as
metallic densities within the GI t.ract.

Teflon® when the pai1s are overheated, at

However, the absence of metal in the GI tract
temperatmes reaching 280°C (536°F). Other
does not exclude toxicosis. A blood level >50
somces of PTFE include irons, i.roni.ng board
mcgldL (0.5 ppm) is considered cliagnostic of
covers, some self-clea.J1ing ovens, heating
lead toxicosis. Blood lead levels >20 mcg/dL
elements from some reverse cycle heat

(0.2 ppm) with clinical signs is considered
pumps, ai1d some heat lainps. See also
consistent with lead toxicosis. Lead levels of

POLYTETRAFLUOROETHYLENE (POISONINGS IN

3-6 ppm or higher are considered significai1t

POULTRY), p 2862, a.J1d SMOKE INHAf""flON, p 3022.

in tissue (kidney, liver, brain, or bone).

Often, the only clinical sign is acute death.

Treatment includes supportive cai·e (fluids,

Other signs depend on the level of exposme
nutrition, etc) ai1d chelating therapy with
and size of tl1e bird. Small birds often clie
calcium edetate clisodium (Ca EDTA) (30-35
suddenly with minirnal exposure. Larger
mg/kg, SC or IM, bid) for 3-5 days W1tiJ
birds may present with dyspnea, wheezing,
asymptomatic ( with fluid therapy), followed
ataxia, weakness, in respiratory clistress, or
by oral treatment with climercaptosuccinic
seizming. Witl1 a large enough exposme,
acid (DMSA) (25--35 mg/kg, PO, bid) or, less
large birds can clie acutely. Diagnosis is based
commonly, D-penicilla.J11ine (30-50 mg/kg,
on a history of exposure ai1d sudden death, or

PO, bid). Midazolam or cliazepam may be
a hist01y ai1d clinical signs consistent with
necessaiy for control of seizmes. Bulk cliets
expos me.

( with psylliW11, peai1ut butter) may assist in

Treatment is supportive witl1 a warm,
removal of lead from the GI tract. In severe
oxygenated incubator, fluids, NSAlDs,
cases, flushing of the GI tract W1der general
broad-spectrum ai1tibiotics, ai1d diuretics.

anesthesia may be necessary. Somces of lead

Prognosis is guai·ded. Necropsy often
in the environment must be removed.

reveals severe hemorrhage ai1d congestion

Lesions associated with lead toxicosis
of the lW1gs.

seen on postmortem exai11ination include
demyelination of peripheral nerves,

Tobacco: Passive inhalation of tobacco
vasculai· necrosis, renal nephrosis,
smoke (second-hai1d smoke inhalation) or
hemosiderosis in multiple orgai1s, ai1d focal
contact with tobacco on hai1ds, fingers, hair,
areas of vascular dai11age in the cerebellum.

or clothes of smokers cai1 lead to chronic

Zinc toxicosis is frequently reported in
respiratory clisease ai1d dennatologic
pet birds. Somces of zinc include ai1y
problems on tl1e face ai1d feet of pet birds.

PET BIRDS

1925

Clinical signs may include coughing,
becomes stressed or weak at any point
sneezing, nasal and ocular discharge,
during handling or treatments. Emergency
dyspnea, cortjunctivitis, or feather destructreatments include warm fluids (SC, IV, or tive behavior and mutilation. Ingestion of
intraosseous ), analgesics, anti-inflammatotobacco products has led to hyperexcitabilries, and antibiotics. Maintenance fluids are ity, seizures, and death. Diagnosis is based
estin1ated at 50 ml/kg divided bid-tid. In

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on history, clinical signs, and response to
dehydrated birds, 500;6 of the total daily
treatment.

maintenance can be administered SC (25

Treatment will depend on severity of
ml/kg) and repeated every 6-8 hr w1til
clinical signs. For birds that are dyspneic or
hydration is reestablished. Often, birds are
showing neurologic signs, supportive care
stressed and in pain and may benefit from
and oxygen may be needed. If the bird has
sedation for diagnostic testing and
ingested tobacco, activated charcoal may be treatments. In stressed birds, midazolan1
warranted. Treatment involves removing

(0.5-1 mg/kg, IM, or 1-2 mg/kg, intranathe bird from the exposure and placing it in sally), with or without butorphanol (0.5-1
a smoke-free environment. Owners who
mg/kg, IM or intranasally) can be used.

smoke should wash their hands before

Often with trawna cases, diagnostic tests
handling their birds.

or extensive treatments or surgery should

Other aerosols, including some carpet
be postponed w1til the bird is stable, which
fresheners, plastics either melted or burned
may take 12-48 hr. All birds with trawna
in a microwave oven, perfumes, deodorizshould be treated with the goal of the bird's ers, votive candles, and new heating duct
survival first and treatment of traumatized
systems may also be irritating or toxic to
tissue second. For example, a bird that has
caged birds.

been struggling for hours with its leg band
caught, with possibly a fractured tibiotarsal

TRAUMATIC INJURY
bone, is in more danger of dying from stress
related to the prolonged struggling than

Trauma is a common presentation for avian
from the fracture.

patients. Cat or dog bite wounds or large birds

Diagnostic tests should be based on
attacking smaller birds all occur frequently.

physical exan1ination finclings and may

Pet birds allowed to roan1 or fly freely in the
include radiographs to determine whetl1er
house can become irtjured flying into walls,
fractures or luxations are present.

windows, or ceiling fans, or falling off

With predator bite wounds, antibiotic
shoulders, play gyms, or the top of their cage.

fuerapy consisting of treatment for both

Birds can also be irtjured in fueir cage. A foot
anaerobic and aerobic bacteria is crucial to
or band may get caught in a toy or in tl1e bars.

increase the chances of a successful case

Other common traumatic irtjuries include
outcome.

puncture wounds, lacerations, fractures, limb
amputations, and crushing injuries.

MISCELLANEOUS DISEASES

Stabilization is paramount; birds
presenting with traun1a are often cold and

Diabetes Mellitus: Diabetes mellitus (DM)

stressed and have suffered blood loss. The
is an W1common disease of pet birds and can
bird should be placed in a warm, oxygenbe challenging to diagnose. Notmal glucose ated incubator inunediately after presentalevels in birds are significantly higher fuan tion and observed from a distance. Is there
those in man1mals (200-400 mg/dL). Birds
respiratory distress (tail bobbing) or
often have a significant hyperglycemia with
open-mouth breafuing? Is there active
stress, which can occur when handled or
bleeding? Is the bird able to perch? Is it
restrained. Glucosuria can occur at 600 mg/dL
using both legs? Is there a wing droop?

in birds, so birds wifu a stress hyperglycemia

After the initial assessment, the clinician
can also have glucosuria witl10ut a diagnosis
must decide whether to maintain the bird in
ofDM. Therefore, a persistent hyperglycemia
the incubator or oxygen, perform a brief
and glucosuria need to be documented for a
physical exan1ination and begin in1mediate
diagnosis ofDM in birds.

supportive treatments, or perform a more

Controlling blood glucose levels is a
thorough physical exan1ination with or withbalance between the activity of glucagon and out diagnostic tests. Before picking up the
insulin witl1in the pancreas. In man1mals,
bird, a detailed plan must be determined,
pancreatic disease often leads to DM and is
and then all items set up al1ead of tin1e for
due to a lack of or resistance to insulin,
anticipated treatments and diagnostics.

which causes the blood glucose to rise. The

Examination and treatments may need to
cause of hyperglycemia and DM in birds is
be done in steps, placing the bird back in the less clear. Blood glucose levels in some birds oxygenated incubator to recover if it

(granivorous birds) seem much more resp on-

1926

PET Bl RDS
sive to glucagon levels than to insulin levels,
rarely diagnosed antemortem and is typically
whereas other bird species may be more
found at necropsy. Acute death is often the
responsive to insulin. It is still debatable and
only clinical sign. The serosal surface of
may depend on the species as to whether DM various organs and the renal tubules are the in birds is caused by abnormalities with
locations of uric acid deposition. Diagnosis

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insulin, glucagon, or both.

of articular gout is by identifying gout

Clinical signs of DM in pet birds include
tophi-whitish yellow, subcutaneous, and
polyuria, polydipsia, increased glucose
intra-articular deposits that demonstrate uric
levels in the blood and urine, and weight
acid crystals on staining. Uric acid levels
loss. DM is often seen in conjunction with
commonly are increased.

obesity or pancreatic or reproductive

Treatment includes fluid therapy to reduce
problems and may be transient in such
uric acid levels and analgesics for pain.

cases. A persistent hyperglycemia and

Articular gout tends to be severely painful.

glucosuria need to be documented for a
lf effective pain control cannot be accomdiagnosis ofDM. Diagnosis is based on plished, euthanasia should be considered.

persistent increases in blood glucose

Surgical removal of these top hi is not

(> 700-800 mg/dL) and glucosuria, along
practical in most cases, because they are
with clinical signs of disease.

extremely vascular and the risk of fatal

Treatment includes converting the bird to
hemorrhage is high. Additionally, unless the
a healthier (pelleted) diet and limiting treats. underlying condition can be identified and Response of birds to mammalian insulin is
corrected or controlled, new tophi will
variable, and insulin treatment is generally
appear very rapidly. Allopurinol (10-30
less effective in birds than in mammals.

mg/kg/day, PO) and colchicine (0.04 mg/kg,

Regular insulin at 0.1--0.2 U/kg has been

PO, once to twice daily) may be useful in
used successfully to stabilize birds.

control of articular gout. The genetic,

Longer-acting insulins (NPH or ultra-Lente)

nutritional, or environmental factors that
at 0.067-3.3 U/kg, once to twice daily, have
predispose a bird to gout are not fully
been used for longtem1 control. Bird owners understood. However, current treatment of are often reluctant to give injections to their
birds with increased uric acid levels include
birds, so often oral antidiabetic medications
conversion to an appropriate diet (this may
are used. Glipizide (0.5 mg/kg, PO, bid, or
be a pelleted diet in some species) or a diet

1.25 mg/kg/day, PO) and metfonnin
change to whole grains, seeds, fruits, and

( 100-500 mg/L of drinking water) have been
vegetables for some smaller birds such as
used anecdotally. Water intake, urine output, cockatiels and budgerigars (for whom a weight, and glucosuria should be monitored
pelleted diet may be a factor in renal
to deteffi1ine whether the treatment
disease). Essential fatty acids ( omega 3) at
protocol is effective. Il} some cases, dietary

0.1--0.22 mllkg/day, PO, have been used
conversion and weight loss can result in
anecdotally to manage renal disease in birds.

resolution of the clinical signs, reducing or
eliminating the need for oral medications or
insulin.

Gout: Gout is the abnom1al deposition of
uric acid in the body. Uric acid is the major
end product of protein breakdown in birds.

It is produced and secreted primarily in the
kidneys and liver and eliminated by tubular
secretion. Elimination is independent of
glomerular filtration rate. Hydration has
only a minimal effect on plasma uric acid
levels; therefore, hyperuricemia can be an
indicator of renal disease in birds. Gout
typically occurs secondarily from increased
plasma uric acid levels. Articular gout
occurs in the joints (most often the
metatarsal and phalangealjoints) of birds,
and visceral gout occurs on the serosa of
various organs and is commonly found on
the pericardium, liver, and spleen.

Clinical signs of articular gout are pain,

This macaw has a single, large ingrown
lameness, swelling in the joints, depression,
feather or feather cyst. Canaries are
commonly affected with multiple feather
anorexia, and dehydration. Visceral gout is
cysts. Courtesy of Dr. Louise Bauck.

PET Bl RDS

1927

Feather Cysts: Feather cysts are ingrown

Malnutrition is likely a more common
feathers that result in a granulomatous mass.

contributing factor to feather plucking than

Recurrence is common unless the extensive
the medical conditions listed above. Basic
dissection of the feather follicle is accomseed and table food diets often create plished. In birds witl1 multiple affected
multiple nutritional deficiencies. These

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feathers, such as the genetically predisposed
deficiencies cause abnormal skin and

Norwich canary, this is not practical.

feather development resulting in plucking
behavior, as well as myriad other medical
problems that may occur. The dyes and

Feather Destructive Behavior: The
preservatives added to seeds and most
phrase "feather plucking" is commonly
pelleted diets may be a factor for some
used to describe behavior that ranges
birds. The relatively low humidity in most
from mildly excessive preening to selfhouseholds also has a drying effect on the mutilation. Management of this condition
skin. Being deprived of natural sunlight,
is frequently challenging. Feather plucking
fresh air, humidity, and the nom1al light/
seldom has a single etiology, and it is
dark cycle has negative physiologic and
prudent to thoroughly explore all possible
psychologic effects on birds.

contributing factors, including underlying

A diagnostic evaluation for a bird with
medical problems. Good communication
feather destructive behavior may include a
concerning feather plucking in birds at the

CBC, biochemical profile, viral testing, skin
onset will help owners realize that this is
biopsy, radiographs, and/or endoscopic
a complicated behavior that is difficult to
examination. Behavioral feather picking
stop. The goal should be to improve tl1e
should be detem1ined only after a complete
health of the bird and to reduce (or elimievaluation that excludes as many medical nate) the plucking behavior if possible.

causes as possible.

Possible medical causes for feather

Treatment is based on the findings of the
plucking include: 1) Endo parasites ( espediagnostic evaluation. A hom10nal bird may cially giardiasis in cockatiels) and, rarely,
need an injection of leupolide acetate, a
tapeworms or roundwom1S. 2) Ectoparasites

GnRH agonist, to reduce reproductive

(rarely). 3) Hepatic disease, with associated
behavior, along with environmental changes
pruritus. 4) Coelomic cavity granuloma or

(seep 1920).

mass. 5) Neoplasia, which typically causes

Altl10ugh treatment of medical and
localized plucking of the area associated
environmental factors may reduce tl1e
with an underlying mass. 6) Folliculitis or
severity of feather plucking, a strong
dennatitis that is primary, or secondary to
behavioral component is often involved.

excessive plucking and/or mutilation.

Treatment of some of the above-mentioned

Bacteria, viruses, fungi, or yeasts may be
problems may lead to initial improvement,
involved. 7) Allergies. Although difficult to
followed by a relapse. Psychologic stressors
confirm, a change in environment or diet
can lead to feather plucking as a displacewhen allergens are suspected may lead to a ment behavior. Unfortunately, once the stress
decrease in plucking and a tentative diagnosis has been relieved, the habit may still remain.

by elimination. 8) Endocrine abnormalities,

Feather plucking does not occur in the wild,
the most likely being hypothyroidism.

where birds are occupied with finding food,

However, hypothyrnidism is overdiagnosed
maintaining their social status in the flock,
in part because of the lack of established
seeking a mate, avoiding predators, and
normal values for avian thyroid levels, the
breeding and raising young. Therefore, often
low range for baseline T4 noted in birds, and
the best-kept birds, which have all tl1eir
difficulty in obtaining a reliable thyroidapparent needs met, will pluck feathers for stimulating hormone (TSH) response test.

behavioral reasons. Psychologic conditions

Nevertheless, some obese birds that demothat may cause featl1er plucking in birds vary.

nstrate a lack of weight loss after aligid diet,

Overstirnulation may cause plucking in a
accompanied by poor quality featl1ers and
nervous bird. Another bird that plucks from
infrequent molts, may be thyroid deficient.

boredom may feel both stimulated and

The plucking exhibited by these birds is often
slightly threatened by increased activity in
an attempt to rid themselves of old, damaged
the home and stop plucking to pay attention
feathers. 9) Heavy metal toxicosis, notably
to the environment and guard itself against
zinc. Barbering and feather plucking from
potential predators. Birds that reach sexual
zinc ingestion have been hypothesized. Many
maturity may begin to pluck as an outlet for
of these cases lack radiographic evidence of
their increased energy and agitation. Owners
heavy metal and require a blood zinc analysis
of these birds often report that tl1eir birds
for diagnosis.

show more cage territoriality, more

1928

PET BIRDS
aggression toward family members, and
multiple food dishes throughout the cage
potentially, sexual behavior toward a
or hide food inside foraging toys to
perceived human mate or inanimate objects.

stimulate normal foraging behavior.

All feather destructive behavioral issues

Enrichment can be provided in the form of
require a multimodal treatment approach
natural branches, toys, wood to chew on,
that involves proper nutrition, eruichment,
multiple play gyms throughout the house,

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providing foraging opportunities and, in
natural sunlight, and ideally a flight cage to
some cases, psychotropic medications ( see
encourage activity. Exercise should be

TABLE 20). Neither of these catego1ies of drugs
encouraged, either through flight or
tends to produce longtenn positive results,
walking and climbing activities. Rope and
and adverse effects may be seen. As is true of
boing perches stimulate activity and
most medications administered to pet birds,
balance. Teaching birds tricks such as
these drugs are not approved by the FDA
waving, dancing, and recall can provide

Psychotropic drugs should not be used
intellectual stimulation and positive
alone but only in conjunction with dietary
interaction between the owner and bird.

modifications, enrichment, and foraging

In addition to traditional medical
opportunities. In addition, changes may
therapies, acupuncture has been reported to
need to be made in the owner/bird
be helpful in some cases. Dietary suppleinteractions. Dietary modifications include mentation with omega fatty acids has been
both conversion to a healthier fomrnlated
repmted to be helpful. Whether this is due
diet and providing foraging opportunities
to the antiprostaglandin effect or a true fatty
for the bird. Owners can place food in
acid deficiency is not certain.

PSYCHOTROPIC MEDICATIONS USED FOR FEATHER PLUCKING IN

PET BIRDS

Medication a

Dosage

Comments

PSYCHOTROPIC MEDICATIONS

Arnitriptyline

1-2 mg/kg, PO, once to

Maximal effects may require treatment for
twice daily
several weeks.

Clomipramine
l mg/kg/day, PO

Effects similar to those of amitriptyline but
may be effective in some cases in which
amitriptyline is not.

Diazepan1

2.5-4 mg/kg, PO, as

Limited usefulness; most birds require a
needed
close that causes sedation to inhibit
plucking.

Haloperidol

0.15 mg/kg, PO, once to

Serious adverse effects, including
twice daily for larger
anorexia, hepatic dysfunction, and CNS
birds; 0.2 mg/kg, PO, bid signs have been reported; most often used for smaller species
in cockatoos.

Fluoxetine

2 mg/kg/day, PO, once to Effectiveness reported to vary; maximal twice daily
effects may require treatment for several
weeks.

HORMONES

Medroxypro

Decreases sexual behavior; not recomgesterone
mended because of serious adverse
acetate
effects, including weight gain, polyuria,
polydipsia, lethargy, hepatopathy, diabetes
mellitus, and death.

GnRH agonist, 300-800 mcg/kg, IM

Decreases sexual behavior by negative
eg, leuprolide
feedback, reducing production of sex
acetate
hormones.

a All are extra-label usages.

POTBELLIED PIGS

1929

An ideal medical treatment is not likely
respiratory distress, and cyanosis of the
to be found for feather plucking in captive
facial skin.

birds. Environmental manipulation,

Diagnosis is based on a history of being
ensuring quality nutrition, and psychologic
housed with feather down-producing birds
adaptations suited to the species and
in poor ventilation with respiratory disease
temperament of the bird offer the best hope
and often polycythemia (>600/<>-700A,). Pulmo

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to reduce this syndrome. Consultation with
nary biopsy is diagnostic. Histopathologic
a board-certified behaviorist fan1iliar with
lesions are confined to the lower respiratory
psittacines may be indicated.

tract. The most prominent lesion is atrial
smooth muscle hypertrophy and some atrial

Hypersensitivity Pneumonitis:

loss due to fusion and epithelial bridging.

A respiratory condition sinlilar to chronic

Treatment is supportive care and
obstructive pulmonary disease (COPD) has
removal of the bird from the offending
been reported in macaws (prinlarily Blue
environment. Improved ventilation and
and Gold macaws). These birds often have
separation from birds that produce powder
a history of being housed with birds that
down is critical. NSAIDs such as meloxiproduce large amounts of powder down, cam (0.5--1 mg/kg, PO, once to twice daily)

such as cockatiels and cockatoos in poorly
may help reduce inflan1mation. AJbuterol
ventilated environments. The birds may

(0.05 mg/kg, PO, bid) has been used anecdoalso have secondary bacterial or fungal tally. Birds should be housed to reduce
infections.

stress and minimize exertion. Often, birds

Clinical signs include increased respiwith confirmed pulmonary hypersensitivity rations, exercise intolerance, dyspnea,
will not have a normal life expectancy.

POTBELLIED PIGS

Potbellied pigs (PBPs) have a short to

MANAGEMENT
meclium wrinkled snout, small erect ears,
large jowls in proportion to the head, short

Environment: PBPs are sensitive to
neck, pronounced potbelly, swayed back,
extremes of heat and cold and should be
and straight tail with a switch at the end.

provided a clean, dry, draft-free environ

The CON and LEA lines of PBPs at l yr of
ment. Adults are usually comfortable in a
age should not be> 18 in. at the withers
temperature range of 65-75°F (18.3-23.9°C).

(ideal height �14 in.) or weigh> 95 lb (ideal

Because pigs do not sweat, temperatures
weight �50 lb). The life span of PBPs is

�85°F (29.4°C) are stressful to adults.

probablyS--20 yTwith -10-15 yr typical.

Extended exposure to high temperatures

Very small or obese PBPs may have a
combined with high hwnidity may be
shortened life span. For hematologic and
fatal to PBPs not acclimated to such an
senun biochemical reference ranges, see
environment. Cooling methods for adult

TABLES 6 and 7, pp 3176 and 3178.

PBPs include moving air across the body,

The term "teacup" pigs has no strict
wetting the skin for evaporative cooling
definition, and it is difficult to make an

(more efficient as hwnidity decreases),
educated guess of mature size without
providing shade, and resting on cool
seeing the parents and grandparents, which
surfaces.

is rarely possible. Mature size is also heavily

Newborn pigs are very susceptible to
influenced by adequate nutrition. ln general,
drafts and chilling and require an environwhen pigs are "selected for smaller size," in mental temperature of -90°F (32°C). Chilled
addition to nutritional stunting, many other
pigs will pile on each other and shiver, and
possible problems of miniature pigs may be
their hair will stand on end. A poor environmagnified. These include hypoglycemia, ment may cause neonates to become
idiopathic seizures, musculoskeletal
moribw1d and hypoglycemic (see MANAGEMENT
defom1ities, heart disease, cleft palate,

OF'THE NEONATE IN LARGE ANIMALS, p 2088) within
atresia ani, and reproductive problems

24--36 hr. Heat lamps or pads can be used to
such as dystocia and agalactia.

provide supplemental wam1th, but their use

1930

POTBELLIED PIGS
should be monitored closely because of the
and challenge other PBPs or people for
electrocution risk from chewed cords; pigs
status. Such challenges need to be addressed,
tl1at become too hot will spread out and pant.

or the pet may leru11 to use aggression to get
what it wants. A combination of aversive

Housing: PBPs may be housed outdoors
techniques ( eg, hand clapping, grnff

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or indoors (or both) but must be approprivocalizations, stomping) and rewarding the ately acclimated to the specific environmen

PBP for positive behavior may help manage
tal situation.

the problem. Failure to deter this unwanted

PBPs housed outdoors should have a
behavior is a common reason why PBPs are
large pen (�50 sq ft/pig) with a structure
placed in rescue operations or abandoned.

within to provide sleeping, feeding, and
watering areas. Pigs will use dirt for
elimination, and daily removal of feces and

Vaccinations: Neutered PBPs should be
addition of fresh dirt to cover and absorb
vaccinated against erysipelas and tetanus.

urine is required. Hay or straw may be

Tetanus toxoid is especially important in
added to prutially satisfy the need to root.

PBPs housed outside in contact with other

However, "rooted-up" pen ground should be
species ( eg, petting zoos). Leptospirosis
filled in with fresh dirt from time to time.

vaccine (6-way) may also be considered, but

Fencing should be well secured in the
there is a substantial risk of high fever after
ground to prevent it from being rooted up,
use. Vaccines are not specifically approved
but it should also be portable so that the
for PBPs, so those commercially available
entire pen can be moved periodically, giving
for domestic swine are substituted. Two
access to fresh, clean dirt. The old pen dirt
initial vaccinations 3---4 wk apart ru·e
should then be smoothed out and left
followed by boosters every 6 mo for
wmsed for several montl1s before being
erysipelas and every year for tetanus, or
used again. If pens are maintained on solid
both boostered yeru·ly at the time of armual
surfaces ( eg, concrete pads), feces and
physical exan1ination. Breeding PBPs should
urine should be removed daily, and fresh
be minimally vaccinated against erysipelas,
hay or straw provided as needed. Water
leptospirosis (6-way ), and pruvovirus; tl1ey
dispensers must be secured to keep pigs
should be vaccinated twice, 3---4 wk apart,
from spilling the water by rooting or
before breeding and before rebreeding or
dru11aging the device by chewing.

every 6--12 mo. Other vaccines should be

PBPs housed indoors should have a
used as exposure risk indicates. Routine
particular area ( eg, a laundry room), with an
vaccination against various pathogens not
elimination area in one comer and a sleeping only minimizes sickness but helps prevent and eating area in another corner. A litter
zoonotic disease and may satisfy requirebox with the side cut down to accommoments for pet licensure. Safety and efficacy date easy entry and exit may be used for
are concerns when using conunercial
elimination. Nontoxic material should be
domestic swine vaccines in PBPs. Considused for litter because pigs are curious and eration should always be given to the
tend to chew on everything. A blanket may
an1ount of antigen per body weight that is
be provided to allow the pig to burrow under
injected, especially in small pigs. Excessive
and partially satisfy the need to root while
antigen administration may cause adverse
indoors; a box of dirt is another alternative.

reactions. No rabies vaccine is approved for
use in PBPs because of tl1e extremely low

Exercise: PBPs should be exercised
incidence of rabies in swine in the USA.

whether kept outside or indoors. They may
be trained to walk on a leash or released

Parasite Control: External and internal
into exercise areas. Daily exercise is
parasites are possible health problems in
important not only for physical health but

PBPs, and the zoonotic potential of
also to relieve boredom that may otherwise
sarcoptic mange and roundwonns should be
manifest as destructive chewing or rooting
considered when counseling owners. Fecal
or as aggression. Even if the PBP does not
san1ples via fecal flotation may be evaluated
exercise much when given the oppo1tunity,
in PBPs as early as 6 and 10 wk old for
the various stinmli from an outside
whipwonns and roundworms, respectively.

environment appear to be beneficial to

Dewonners, such as oral fenbendazole at
overall temperan1ent. Many household and

3 mg/kg/day for 3 days; ivennectin at 300
garden plants are toxic to PBPs, which are
mcg/kg, SC; or doran1ectin at 300 mcg/kg,
adventw·ous eaters (seep 3103).

IM, should be used as indicated. Iajectable
ivennectin and dorrunectin are highly

Temperament: As healthy, neutered PBPs
effective against sarcoptic mange, the
mature, they may become more aggressive
most conunon external parasite in PBPs.

POTBELLIED PIGS

1931

Dental Care: The eight needle teeth

Dystocia is of special concern in PBPs.

(four deciduous lateral incisors and four

Because the birth canal is too small to
deciduous canines) of newborn PBPs
inspect for unborn pigs via palpation,
should be trimmed to prevent injury to
radiography or ultrasonography may be
littermates and laceration of the sow's
indicated to reveal undelivered piglets.

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underline. Four pennanent canine teeth

Oxytocin (5-10 U) may be used to aid
erupt at -5-7 mo of age and are first
delivery if the vaginal canal is patent. The
trimmed at or after l yr of age. Elongated
decision to perform a cesarean section, if
permanent canine teeth may cause discomindicated, should be made promptly, before fort, malocclusion, and persistent chewing
the sow becomes toxic and has friable
motion and salivation. In PBPs, the canine
uterine tissue and vessels. Cesarean
teeth grow continually and should be cut
section may be performed by several
about once a year using obstetrical wire,
approaches, but the right flank approach
mechanical saws, or other instruments.

has two advantages: the piglets nurse away

Sedation or anesthesia is required. Teeth
from tl1e incision, and gravity pulls the
should be cut as close as possible to the
incision shut, minimizing the chance of
gum line without cutting the oral mucosa
dehiscence. Regardless of surgical
or lips; there should be no exposed root
approach, surviving piglets will probably
canal after cutting the canine teeth of any
require hand-raising.

type of swine. Tetanus antitoxin (500-1,500

Ovariohysterectomy in PBPs at 4-6 mo

U, depending on PBP size) and antibacteriof age is ideal. Older female PBPs generally als are usually administered. In PBPs
display irritable behavior for 2-3 days of
properly vaccinated with tetanus toxoid, a
estrus out of every 21 days of the estrous
tetanus antitoxin injection is unnecessary.

cycle. Perforn1ing an ovariohysterectomy

Tartar buildup can be removed manually
during estrus in older PBPs is a formidable
by instmment scraping at the same time
task because of the tremendous vasculature
the canine teeth are cut. Dental cleaners
in the broad ligan1ents of the horns of the
for small animals may be used with care,
uterus; surgery should be delayed until
positioning the head of the PBP downward

-7-10 days after estrus. A distal midJine
during use to prevent water aspiration.

approach, as if perforn1ing a cystolomy, is

Geriatric PBPs may have abscessed and/
routinely used for ovariohysterectomy. The
or exposed tooth roots; sedation (tiletamineuterine horns fold back and are located zolazepam 2.2 mg/kg, IM, in ham) and examibeside the body of the uterus witll the nation of the oral cavity with or without
ovaries. No ovarian ligament teruing is
endoscopy is indicated if anorexia and/or
necessary as in dogs and cats. Penetration
bruxism are reported. Radiographs may be
of the cervix by sutures should be avoided
necessary to diagnose tooth root abscessawhen ligating the uterine stump to prevent tion. Swelling followed by a draining tract
intermittent postsurgical hemorrhage from
at the angle of the mandible, especially in
the vulva. A right flank approach may be
geriatric PBPs, indicates canine tooth
used in extremely obese PBPs, in which
abscessation. Removal is challenging
wound dehiscence could be a complication.

even for skilled surgeons and may result

Isoflw·ane or sevoflurane anestllesia
in mandibular fractures. However, PBPs
provides excellent muscle relaxation.

seem to recover well after tooth extraction

(Malignant hyperthennia [seep 1027] has
followed by antibiotics and tetanus
been reported only once in a PBP under
prophylaxis.

isoflurane gas anesthesia, so it is thought to
be rare in PBPs.) Hypothermia during and
after surgery is an important concern. A

REPRODUCTION
baseline rectal temperature should be
recorded at anesthesia induction, and
normal body temperature should be

Females: First estrus occurs as early as
maintained until recovery is complete.

3 mo of age in gilt piglets. The lack of estrus

Injectable anestlletics such as xylazine plus
or a distended abdomen in a young gilt may
tiletanline-zolazepam can delay normal
be due to pregnancy if she has been exposed tl1ermoregulation for 5-6 hr after anestlleto littermate boars. If the female does not sia. Because some PBPs may become
cycle, the abo1tifacient prostaglandin F2o:,
apneic when placed in prolonged dorsal
given as two injections (8 mg and 5 mg in a
recwnbency, intubation is preferred to

25-kg pig) 12 hr apart, can be administered
masking; however, PBPs may be difficult lo
when corpora lutea have become susceptiintubate, and prolonged efforts at intubable to luteolysis after day 13 after estrus.

tion may cause laryngeal edema and

Estrus should occur 3-7 days later.

postsurgical complications.

1932

POTBELLIED PIGS

Early spaying also reduces the risk of
available in meal, crumble, or pellets, may
ovarian cysts, uterine tumors, and cystic
also be used with professional veterinary
endometrial hyperplasia. An obviously
guidance. Green leafy vegetables, alfalfa,
distended abdomen is seen with large
and green grasses (but not weeds, because
ovaiian or uterine masses (;:,,20-30 lb).

some are toxic) can be added to the ration to

Vulvar hemorrhage may be a sign of uterine
satisfy appetite. Fruits such as apples and

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tumor and can be life-threatening. Although
grapes may be given in litnited an10unts.

most ovarian or uterine masses can be

High-energy treats should be avoided
surgically removed, some are so extensive
because PBPs tend to become overweight.

and invasive that euthanasia is required.

Even when calorie intake is restricted,
weight loss is difficult because the minitnal

Males: PBP boars retained for breeding
ainount of exercise possible in obese PBPs
should be kept in secure pens; they should
burns few calories. Laineness is another
not be kept as pets because of the unpreconunon factor litniting exercise capacity.

dictable behavior of boars around other

Maintaining nonnal hoof length via
animals or people. Neutering is usually
tritnming is itnportant for mobility.

performed at 8-12 wk of age, using

Swimming is an alternative form of exercise
it\jectable or gas anesthesia. One protocol
for obese, lame PBPs, but acclitnation and
for it\jectable anesthesia is xylazine at 2.2
supervision is necessary.

mg/kg, IM, followed by tiletamine-zolaze

Young weaned PBPs thrive best if
pan1 at 6.6 mg/kg, IM, both injections in the
adequate colostrum was conswned within
ha.ins. Detennining whether both testicles
the first 24 lu· of life. PBPs deprived of
ai·e descended before surgery is itnportant
colostrum easily succumb to diarrheal and
because cryptorchidism is seen in PBPs.

septicemic disease. For early nutrition,

An inguinal hernia is another possible
commercial milk replacers are available, but
complicating factor. The midline skin

2%-3% pasteurized milk or powdered milk
incision is made craiual to the scrotum, and
also can be used successfully. Approxistructures such as the vas deferens and mately 1 oz every 4--6 hr should be fed from
blood vessels ai·e ligated a.11d excised similar a bottle with a nipple until the pig is trained to the procedure in dogs. Both inguinal ring
to drink the milk from a shallow bowl or
areas should be closed to prevent herniapan; usually, this can be done in <24 hr. The tion. Removal of tunic, cremaster muscle,
volwne fed should be increased as the pig
a.11d extraneous subcutaneous tissue,
grows but decreased if diarrhea occurs.

followed by closure to obliterate empty

Overeating dian·hea may be controlled with
space, help prevent seroma fom1ation.

kaolin/pectin preparations given every 4 hr.

At the titne of castration, the preputial

Infectious diarrhea that may be from
diverticulum or "scent gland" may be
grain-negative bacteria ( eg, Escherichia
removed by eversion and excision to
coli) should respond to parenteral or oral
minimize the pooling and discharge of
gentan1icin or oral spectinomycin. The diet
foul-smelling preputial fluid. Umbilical
can be converted to solid feed by mixing a
hernia may complicate removal. Early
small a.111ount with milk to make a gruel and
castration may interfere with the developgradually increasing the ratio of feed to milk ment of the preputial diverticulun1, making

( conversion to all feed in -14 days).

its removal urmecessary, especially in PBPs

Increasing ainounts of fresh water should
kept outside. Tetanus antitoxin (if no
be provided as the diet is converted.

current tetanus toxoid vaccination) and

Urolithiasis from triple phosphate
antibacterial injection are given after
crystalluria may occur in PBPs but can be
surgery of the reproductive tract.

prevented through addition of urinaiy acidifiers to the ration. At least one conunercial PBP feed contains anunoniwn chloride,

FEEDING AND NUTRITION
and feed additives containing anunonium
chloride or citric acid are available. Owners

Fresh water should be available at all titnes
may feed fruits or vitamin C in an attempt
to prevent dehydration and salt toxicity
to acidify the urine. A constant source

( water deprivation). Balanced diets are
of clean, fresh water is also in1portant
essential to provide proper daily nutrients
to prevent the accumulation of triple
and prevent obesity. Starter, grower, and
phosphate crystals. Additlg fruit juice to
maintenance rations for PBPs are commerwater may increase water consumption cially available as crumbles or pellets. The
and help acidify the urine. Inadequate
recommended an1ount per body weight
water consumption by sedentary PBPs in
should be fed divided into at least two meals/
cool weather has been associated with
day. Rations for commercial domestic swine, urolithiasis.

POTBELLIED PIGS

1933

DISEASES

Saiutation to minimize infective closes of
pathogenic coliforrns in the environment

Furnishing adequate housing, nutrition, and
of young, nursing PBPs is important for
care will minimize disease in PBPs, as in
prevention. Conunercial swine vaccines to
other species. Many diseases of PBPs are
prevent colibacillosis are available but must
similar to those of domestic commercial
be given to sows before farrowing to

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swine, although some are more common
stimulate il11rnw1ity and secretion of IgA
in PBPs.

into the milk. Treatment is based on in vitro
ai1tibacterial sensitivity testing, but

Gastrointestinal System
ai1tibiotics such as oral or irtjectable
gentarnicin or injectable ceftiofur are

Gastritis and gastric foreign bodies
usually effective.

arc common in PBPs because they are

Enterocolitis from Salmonella
omnivorous and prone to ingest many types

Typhi.murium infection can affect PBPs of
of objects. Keeping PBPs indoors where
any age, but it usually occurs after weaning.

they are tmable to root and restricting

Sources of salmonellae include waste food
calo1ie intake to prevent obesity probably
from overturned gai·bage cans, exposure to
contiibute to this continual search for food.

carrier swine (such as the dan1), or fecal

Dividing the daily ration into two or more
material from other animal species. Mild to
portions and furnishing low-calorie foods
severe diairhea with mucus and blood can

(eg, lettuce, cabbage, celery, carrots, or
result. Diagnosis is tJu·ough signalment,
green grasses) may help satisfy appetite. If
histmy, and fecal culture or PCR. Salmo
an ingested foreign body is small or pliable
nella spp are characteristically resistant to enough, it may pass through the GI tract and
many antibiotics, so in vitro antibacte1ial
cause mild gastritis that is self-limiting or
sensitivity testing is i.rnpo1tant. Parenteral
only requires antibiotic therapy. Larger
gentarnicin at 2.2 mg/kg/clay for 3 days may
objects may remain in the stomach or
be effective in ilie interim. Untreated PBPs
partially pass into the duodenum or a more
may die. Some recovered PBPs may develop
distal pait of the small intestine. Clinical
rectal st1icture after enterocolitis, resulting
signs such as vomiting ai1d colic can be
in megacolon and a clistenclecl abdomen.

acute but may be more subtle and increase

Subsequent straining to defecate cai1 cause
in intensity over several days or weeks.

rectal prolapse. Surgical correction of the

Radiographs may reveal obvious foreign
rectal prolapse will not correct the
material or delayed gastric emptying. CBCs
underlying problem. Owners should be
may indicate infection but are usually not
advised that mai1y Salmonella spp,
infommtive; sen.m1 enzyme and electrolyte
including S Typhimurium, are zoonotic.

panels may only reflect dehydration.

Healthy PBPs may be tested via fecal

Surgical correction is indicated but may not
culture or PCR to cletennine their salmobe successful if extensive necrosis of GI nella status. Multiple tests are more
tissue is present. Fluid replacement and
accurate predictors than single tests.

nutritional supplementation plus antibacte

Vaccines available for conunercial swine
rial therapy and tetanus prophylaxis are
have not been used much in PBPs.

indicated in convalescing PBPs.

Bacteremia or septicenua after S

Lower GI obstruction clue to bowel

Choleraesuis infection may also affect
stricture occurs in geriatric PBPs. Anorexia,

PBPs, usually after weaning. Somces of
scant fecal production, and a bloated
infection ai·e similar to those of S Typhi.muabdomen with massively distended rium. Mild to inappai·ent diarrhea followed
intestines seen radiographically are typical.

by fever, lethargy, anorexia, cyanosis of

Sedation and endoscopic exainination of
extremities, recun1bency, and cleaili may
the oral cavity, esophagus, and stomach
ensue. Diagnosis, treatment, prevention,
ai·e indicated to exclude other problems.

and zoonotic potential ai·e similar to those

Exploratory laparotomy ai1d anastomosis
of S Typhimuriun1; zoonosis is mainly a with or without bowel resection is usually
threat in inununocompromisecl people.

remedial.

Constipation may be seen in PBPs;

Colibacillosis or Escherichia coli
however, each nonnal bowel movement of
diarrhea is generally an important disease
a PBP is typically composed of one or more
in young PBPs. Mortality may be high in
cylindrical formations made up of smaller,
piglets that have not ingested adequate
multiple fecal balls iliat may give tl1e
colostn.m1 in their first 24 hr of life. Older
impression that the PBP is constipated.

PBPs apparently develop resistance to

True constipation may occm clue to low
colibacillosis. Diagnosis is tlu·ough
water intake in sedentary PBPs or to an
signalrnent, history, and fecal cultme.

actual disease. Careful evaluation is

1934

POTBELLIED PIGS
warranted before treatment is adminismite populations increase sufficiently to tered. Enemas may be contraindicated if
make the condition obvious. Treatment
there is pathology such as colitis. In simple
with ivermectin (300 mcg/kg, SC, repeated
constipation, fecal softeners or mild
in 2 wk) or doramectin (300 mcg/kg, IM,
laxatives such as sodium sulfate or
repeated in 3 wk) is indicated. Recently

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magnesium sulfate may be used. These
acquired young PBPs shquld be given a
should be given with food, if possible,
routine preventive injection of either
because forced PO administration can
parasiticide when first presented for
result in aspiration pneumonia and death,
exan1ination.

especially with mineral oil. Encouraging

Melanoma is an important skin twnor in
increased water intake by flavoring with
swine. Tumor removal and evaluation of
fruit juice or liquid gelatin may be helpful.

metastatic potential through histopathology

Regular exercise is also beneficial to
is important for prognosis. Spontaneous
promote normal feces.

regression of melanomas, with subsequent

Rectal prolapse occurs due to straining
depigrnentation of the hair, skin, and iris, is
from bowel irritation from diarrheal
occasionally seen in PBPs; affected swine
disease, rectal stricture after S Typhimuusually have nom1al life spans.

rium enterocolitis or previous rectal

Sunburn may develop in PBPs exposed
prolapse repair, cystitis or urolithiasis,
to sudden, high-intensity sunlight. Skin
persistent coughing, dystocia, or possibly
lesions may or may not be obvious, but
genetic predisposition. Small, uncompliaffected PBPs appear painful and seem to cated, recent rectal prolapses may be
have hindlimb weakness or paresis. A
repaired via anesthesia and purse-string
sunburned PBP may be "down in the back
closure of the rectum that allows for
legs" and show intense pain with vocalizaminimal passage of feces. Larger, complition. A thorough history is in1portant for the cated prolapses require surgical excision.

diagnosis. Exposure to further sunlight

Recurrence is less likely after surgery but
should be prevented. Symptomatic
is possible regardless of method of repair.

treatment is remedial.

Lymphosarcoma, lymphoma, and

Bleeding back syndrome ( dippity pig
carcinoma of the intestines occur in aged
syndrome) is of unknown etiology. Signs are

PBPs. Signs are vomiting, anorexia, melena,
almost identical to those of sunburn (pigs
anemia, and chronic weight loss followed
dip their backs, vocalize, and show signs of
by death ( or euthanasia). Confirmation is
extreme pain) but with no history of sun
by postmortem histopathology.

exposure. Circular, serum-oozing lesions
of various sizes are seen on lumbar skin
lntegumentary System
surfaces. Affected PBPs recover in several

Dry, flaky skin with _minimal to severe
days with restricted activity with or without
pruritus is seen in virtually all PBPs. Wiping
symptomatic treatment. The condition may
down the skin with wet towels each week
recur in some animals.

will remove the flakes. Moisturizing lotions

Erysipelas, caused by Erysipelothrix

( eg, aloe vera) also temporarily alleviate
rhusiopathiae, is a generalized bacterial
this problem. Fatty acid supplementation
infection that affects swine. For details on
can be used as a more longtem1 remedy, but
clinical signs, diagnosis, and treatment, see
caution must be exercised not to promote
p626.

obesity.

Sarcoptic mange is the most important

Musculoskeletal System
ectoparasitic disease of PBPs. Intense

Lameness due to lower back, hindlimb,
pruritus and dennatitis are the basis for a
or forelimb weakness is common in PBPs.

presun1ptive diagnosis. In many cases, the

Because of their conformation, PBPs are
owners have pruritic skin lesions on the
susceptible to muscle pulls, ligament
anns or abdomen. Examination of skin
damage, and fractures of the back and
scrapings ( deep enough to contain some
limbs. Because PBPs usually struggle
blood) from several sites usually confirms
against manual restraint (predisposing
the diagnosis in advanced cases but may be
to injury), sedation or anesthesia is often
negative in less advanced cases if very few
used for procedures such as prolonged
mites are present. In young PBPs, the
exan1ination, radiography, foot trimming,
source of infestation is usually the dani;
blood collection, and dental work.

in older PBPs, the source is usually other

Tiletamine-zolazepam at 2 .2 mg/kg body
infested pigs. Young PBPs isolated from
weight, IM (in the ham), provides excellent
other pigs and kept as pets may harbor
analgesia and chemical restraint for these
mange mites as a subclinical problem until
minor procedures; recovery, although

POTBELLIED PIGS

1935
smooth, is prolonged and requires careful
additionally require antiseptic cleaning with
monitoring. Gas anesthesia is also used
tan1ed iodine and systemic antimicrobial
and has the advantage of rapid recovery
therapy ( ceftiofur at 4.4 mg/kg/day for 3-10
time. Fasting for 24 hr and withholding
days, or ampicillin at 11 mg/kg, PO, bid for
water for 4-6 hr before sedation or

7 -lOdays).

anesthesia is recommended.

Zygomycosis from M1tcor spp infection

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PBPs with injuries to the back or limbs
has occurred in the distal hindJimb of a PBP.

are usually treated with anti-inflammatory

The large growth that encompassed the
drugs, such as buffered aspirin with antacid,
entire foot was composed of infected/
flunixin meglumine, or glucocorticoids ( eg,
abscessed tissue that involved bone.

dexamethasone). Polysulfated glycosami

Amputation was remedial.

noglycan and/or glucosan1ine/chondroitin

Tetanus may occur after wound contarnisulfate products may be tried in nonresponnation from dog bites, skin abrasions, oral sive cases.

cavity abrasions, or surgical procedures.

Fractures of the distal humerus and

Tetanus toxoid should be part of the routine
elbow area and femur are common. These
vaccination schedule of PBPs at high risk of
occur fromjun1ps off furniture (distal
exposure. If there is no current tetanus
hw11erus), dog bites (elbow area), restraint
toxoid vaccination, tetanus antitoxin

(elbow area and femur), equine kicks

(500-1,500 U, depending on body weight)

(femur), and other traw11a. Repair via
should be administered IM in the neck
pins, screws, plates, and external devices
after recovery from ar1y surgery or dental
successfully restores some range of motion
procedure ( eg, trimming of canine teeth).

if fractures are in1mobilized properly and

Treatment for tetanus is by massive doses of
any sepsis is controlled.

tetanus at1titoxin and penicillin early in the

Infectious arthritis may affect the very
disease, along with tranquilizers, isolation
young to older PBPs. Lameness with or
to mininlize external stimuli, and suppo1tive
without joint swelling in one or more limbs
therapy.

is the usual clinical finding. E1ysipelothri.x
rhusiopathiae, Streptococcus spp,

Mycoplasma hyosynoviae, M hyorhinis,

Nervous System

Staphylococcus spp, and Haemophilus

Systemic bacterial infection can be
parasuis are possible causes. Treatment
caused by (in approxin1ate decreasing
early in the disease course with an effective
order of in1portance) Streptococcus suis
antimicrobial ( eg, lincomycin at 11 mg/kg,
type 2, other Streptococcus spp, Salmonella bid for 3 days) may be effective. Treatment

Choleraesuis, Haemophilus parasuis,
after chronic changes have occurred,

Escherichia coli, other gram-negative
antimicrobial ineffectiveness against the
bacteria, and Listeria monocytogenes.

etiologic agent, or misdiagnosis are reasons

CNS signs may include fever, depression,
for treatment failure and persistence of
incoordination, staggering, postural
lameness. In chronic cases, pain manageabnormality, head tilt, circling, nystag-ment with anti-inflan1IDatory drugs should
mus, seizures, and death. PBPs are most
be considered. Polyarthritis from neonatal
commonly affected from birth through 4--6
infection of the navel may be due to various
mo of age. Treatment with the appropriate
environmental bacteria, including Pseudo
antibacterial therapy ( eg, extra-label
monas spp. If degenerative arthritis and
florfenicol, which penetrates the bloodjoint fusion from chronic inflanm1ation are brain barrier) in the early stages of infection
present after polyarthritis, euthanasia may
is most effective; however, death may be the
be warranted. Osteochondrosis may also be
first clinical sign. Because S suis type 2 is a considered in shoulder, elbow, hip, and stifle zoonotic disease agent, care should be lar11eness, but this condition is not common
exercised to prevent human infection when
in slow-growing, light-muscled anin1als
performing necropsies on pigs dying from
such as PBPs.

suspected CNS disease.

Overgrown and/or cracked hooves

Overheated PBPs may be depressed,
are a common cause of lameness. Regular·
inactive, and recumbent and show
exercise on abrasive surfaces ( eg, concrete)

open-mouth breathing or panting with an
will wear hoof ends and help keep them the
initial fever followed by a subnormal and
appropriate length. In PBPs with overdecreasing temperature. The prognosis is grown, elongated hooves, normal yearly
grave, but some overheated PBPs may
length can be maintained by routine yearly
respond to resting on a cool surface and
trimming W1der sedation or anesthesia.

cooling only the head with water for 10-15

Hoof cracks can be caused by overgrown
min followed by packing ice bags aroW1d
hooves. PBPs with cracked hooves may
the head. If the temperature is still not

1936

POTBELLIED PIGS
controlled, cold-water enemas can be used

Aclinobacillus pleuropneumoniae (see
while additional areas of the skin surface
p 1469) causes a life-threatening pneumonia
are packed in ice. Symptomatic treatment
that may occur after infection from the sow
is continued as indicated.

or exposure to carrier animals. Signs range

Salt toxicity occurs after water
from coughing, fever, and lethargy to

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deprivation for� 36 hr followed by sudden
sudden death, depending or, the serotype of
rehydration or, less commonly, after

A pleuropneumonia.e. Prompt a.i1tibiotic
prolonged consumption of high-salt foods.

treatment with penicillin or ceftiofur is

Affected PBPs may have seizures, walk
indicated. Recovered PBPs usually have
aimlessly, or show other CNS signs such
permanent tissue loss in affected Jung
as blindness or postural abn01malities.

a.i·eas and may have recurrent respiratory

Diagnosis in the affected live animal is
problems. Vaccines available for domestic
confirmed by high levels of serum sodium,
commercial swine may be used in PBPs if
usually 1 60-183 mEq/dL ( normal range
there is an exposure risk.

142-153 mEq/dL). Gradual rehydration and

Swine influenza (seep 1470) is an
symptomatic treatment to counteract
important viral pnewnonia in PBPs that a.i·e
cerebral edema is indicated, but severely
taken to fairs, exhibitions, wd petting zoos
affected PBPs may only be stabilized to a
and exposed to other pig populations. It is
vegetative and blind status. The histopathousually self-limiting after 7 -10 days but can logic finding of eosinophilic infiltration into
be fatal. HIN 1, H3N2, HlN2, and H2N3 are
brain tissue is also diagnostic.

the most common strains in domestic

Seizure from unknown cause occurs
swine. Multivalent vaccines available for
in PBPs. Animals < l yr old seem most
domestic swine could be used in PBPs if
susceptible. Frequency may range from
indicated. Swine influenza is a zoonotic

1-2 seizures per month to several per
disease.

day. Infrequent seizures may require no
preventive medication. Diazepam is used to

Urinary System
control more frequent episodes. Phenobarbital in addition to diazepam may be required Cystitis and urolithiasis a.i·e common
to control the most severe cases. Seizures
in PBPs. Signs include frequent urination
may cease as the affected PBP ages.

or straining to urinate. Urinalysis, urine
culture, CBC, serum chemistry, radiography, and ultrasonography a.i·e in1portant Respiratory System
diagnostic aids. A sterile urine sample for

Atrophic rhinitis is an infectious disease
culture can be obtained via cystocentesis.

of swine that initially causes sneezing, nasal

Cystitis without tliple phosphate crystalludischarge, tea.iing, a.i1d growth retardation.

ria should respond to extended wtibacte

Younger PBPs a.i·e more c_ommonly affected. rial therapy based on in vitro sensitivity For details on clinical signs, diagnosis, and
testing. Acidification of the urine may
treatment, seep 1465.

minimize recurrence of infection. Nephritis

Pneumonia can be a very serious
can occur after cystitis as an ascending
disease in PBPs because of their
infection. Leptospirosis may be a primary
relatively small lung capacity. 'The most
cause of nephritis. Increased BUN wd
common cause of pneumonia is from
creatinine values may aid in tl1e diagnosis
initial Mycoplasma hyopneumoniae
of neplu·itis and kidney failure. A 6-way
infection (seep 1467), which immunovaccine for leptospirosis is routinely given compromises the lungs, followed by
to breeding PBPs (seep 1930) but may also

Pasleurella mullocida infection. Young
be considered for routine use in rescue
pigs contract these infectious agents from operations where many PBPs are housed their dams or from mixing with infected
in close contact. Vaccination may possibly
pigs after weaning. Antibiotic treatment
reduce renal shedding of leptospires should
may be more effective if directed against

PBPs become chronically infected and,

P mullocida, because this bacterium
tl1erefore, minin1ize transmission of this
becomes the most important pathogen
zoonotic disease.

once coughing is present for several days.

In a PBP that is straining wd unable to

Vaccines available for M hyopneumoniae
urinate, the bladder size should be reduced
in domestic commercial swine have been
immediately by cystocentesis after sedation
used in young PBPs to prevent mycoplaswd radiography (plain or contrast) or mal pneumonia and subsequent Pasleur
ultrasonography to evaluate the location of
ella pneumonia. Vaccination in older
urethral and bladder stones. If the blockage

PBPs is probably unnecessary unless risk
is in the uretlu·a, cystotomy is recomof exposure warrants continued use.

mended (both sexes) to identify and remove

RABBITS

1937
calculi in all possible locations. Calculi in
described to conect failed perinea!

the urethra of males may be removed by
urethrostomies in PBPs. Rupture of the
cutting through the sheath to expose the
bladder is a grave complication because
distal penis, catheterizing the urethra, and
normal bladder tone may not return even
backflushing into the bladder. Calculi that
after stones have been removed and the

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cannot be removed by this method must be
bladder has been surgically repaired. Laser
surgically removed by incising the urethra
lithotripsy has been used to fracture
at the location of the blockage. However,
urethral calculi not removable by flushing.

scar tissue at the healed incision may also

Routine urinalysis as part of an annual
cause urethral obstruction. Suturing of the
examination may enable early diagnosis and
urethra is followed by cystotomy and
prevention of serious urinary tract disease
bladder flushing to minimize recunence and in PBPs.

then by inspection for more calculi. The

Psychogenic water consumption
bladder is then closed, and a Foley catheter
should be considered in PBPs ( especially
is inserted into the bladder, tunneled
young PBPs) with polydipsia and polyuria.

through the abdominal muscles, and

PBPs may develop a habit of drinking water
sutured to the skin. Several days later, the
and urinating frequently because of possible

Foley catheter is occluded, and the urethra
boredom or unknown causes. Cystitis and
is inspected to determine patency and urine
crystalluria should be eliminated as
flow; if not patent, the Foley catheter is
differential diagnoses. Measuring urine
opened again, and the process is repeated
specific gravity before and after a 12-hr
several days later. When the urethra
water fast will demonstrate whether the
becomes patent, the Foley catheter is
affected PBP is able to concentrate urine.

removed. Although the urethra in females

Ability to concentrate mine indicates
is short, blockage can still occur. Because
normal kidney function and helps exclude
urethral catheterization is difficult without
diabetes insipidus. Estimating the daily
endoscopy, a Foley catheter is inserted into
water intake and urine output will further
the vagina and inflated, and a purse-string
aid the diagnosis of psychogenic water
suture is placed at the vulva. Retrograde
intake or establish that water consumption
flushing through the urethral opening in the
and urination are, in fact, normal. Relieving
vaginal floor is attempted. A cystotomy is
boredom may be helpful to change this
then performed to remove all possible
behavior. Affected young PBPs typically
calculi, followed by routine closure of the
outgrow this condition. If water is restricted
bladder. Foley catheter placement into the
and offered only with meals, care must be
bladder may not be necessary. Further
taken to prevent salt toxicity.

treatment includes antibiotic therapy and

Chronic kidney failure is a common
acidification of the urine. Despite these
cause of death in geriatric PBPs. Lethargy,
efforts, some affected PBPs do not recover
anorexia, dehydration, azotemia, anm1onia
and require euthanasia. Perinea! urethrostobreath odor, and low temperature are mies are usually only temporarily successful possible presenting signs. Symptomatic because the surgical site becomes occluded
treatment such as rehydration and
by amorphous material or urethral polyps,
antibiotics (procaine penicillin 22,000
and patency cannot be reestablished.

IU/kg/day, lM, for 3 days) may be at least

However, surgical methods have been
temporarily helpful in less severe cases.

RABBITS

The European or Old World rabbit
in cold climates such as the Rocky

( Oryctolagus cuniculus) is the only genus

Mountains. Rabbits are not rodents.

of domestic rabbits. Wild rabbits and hares
include cottontail rabbits (Sylvilagus) and MANAGEMENT
the "true" hares or jackrabbits (Lepus). Rabbits have been bred for fur, meat, wool, Management of rabbits for meat, fur, or
exhibition, and for use as laboratory
wool production is quite different from
anin1als. The closest relative to the rabbit is
maintenance of a pet or house rabbit. The
the pika (Ochotona p1inceps), which lives

Ame1ican Rabbit Breeders Association

1938

RABBITS

(www.arba.net) provides guidance for both
at least having the eai· wann) and applying a
production and pet rabbit care. The House
topical anesthetic cream greatly facilitate

Rabbit Society (www.rabbit.org) is another
tl1ese procedures.

resource regarding pet rabbit care.

Clinical Pathology: Clinical pathology in

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Restraint: Proper handling and restraint is
rabbits vaiies from that in other domestic
i.rnpo1tant. Rabbits have powerful hindlimbs, animals. The n01mal neutrophil:lymphocyte which can kick out and lead to broken
ratio is 1: 1. The rabbit neutrophil is called
backs. Rabbits should never be held by the
a "pseudoeosinophil" or heterophil because ears; they should be scruffed at the neck,
of its red-staining cytoplasmic granules.

and the body finnly supported at the nm1p.

Both the heterophil and the granules are

If they are not held properly and securely,
smaller tl1an the eosinophil and eosinophil
fractures or luxations of lumbar vertebrae
red granules. Rabbits do not usually
can easily follow struggling. If a rabbit
respond with a leukocytosis to an active
appears to be very stressed or excited, a
infection. In case of stress, tl1e ratio of the
sedative may be indicated to avoid if\iuries
heterophils and lymphocytes changes
caused by handling. Midazolarn at 0.5---1
toward a relative heterophilia without
mg/kg, IM, is often enough to adequately
increasing the total WBC count. Many sick
sedate the rabbit for a thorough physical
rabbits have hemoglobin and PCV values
examination.

much lower than nonnal; this makes the

PCV one of the best indicators of healthy or

Ph
sick animals. Calcium metabolism in rabbits
ysical Examination and Sample

Collection: Most techniques for physical
results in higher norn1al blood calcium
examination suitable for dogs and cats may
levels (up to 16 mg/dL) and a wider range
be applied to rabbits. A thorough oral
than in other animals, which can lead to an
examination, including palpation of the face
e1Toneous diagnosis of hypercalcemia.

and bottom of the jaw, should be perfonned

Rabbit urine ranges from yellow to brown
to evaluate dental health. An otoscope or a
or reddish. A dipstick can quickly differentipediatiic nasal speculum can assist visualizaate norn1al rabbit urinary pigments from tion of the molars. Conscious rabbits will
hematuria. Traces of glucose and protein
usually resist a full dental examination, and
are normal in rabbit U1ine.

sedation or anesthesia is required. Sex can
be detennined by depressing the external

Therapeutics: Very few products are
genitalia to reveal a slit-like vulva in females
licensed for use in rabbits, leading to
or the penis in males. The testicles descend
exti·a-label use of drug therapies approved
at 10--12 wk. Normal body temperature is
for use in other species. Paiticulai· caution

103.3°-104°F(39.6°-40°C). Body temperamust be exercised in use of antibiotics that ture <100.4 °For > 105°F is cause for concern. suppress norn1al GI microflora and result in Blood can be collected from the cephalic
enteric dysbiosis and/or enterotoxemia.

vein, lateral saphenous vein, and the jugular

This has been called "antibiotic toxicity."

vein. The lateral saphenous vein is easy to

Antibiotics contraindicated in rabbits
access when the rabbit is held and resting
include clindan1ycin, lincomycin, erythroon someone's forearm, with the resti·ainer mycin, arnpicillin, arnoxicillin/clavulanic
holding the leg above the stifle joint. The
acid, and cephalosporins. The flea treat111ent
lateral saphenous vein runs across the
fipronil is contraindicated in rabbits
lateral aspect of the tibia at the middle of the because of severe toxic reactions in some length of the bone. In larger rabbits (>3 kg),
individuals. Supportive care for rabbits
the ear veins can also be used. The auricular
often includes aggressive IV fluid support.

or marginal ear vein provides a site for

The maintenance fluid rate for rabbits ( 120
venous administration or catheterization.

mUkglday) is much higher that1 that for

Drugs should not be if\iected through the
dogs and cats. Hospitalized rabbits often
ear veins, because this can lead to phlebitis
require doubling of maintenat1ce rates, or 10
and subsequent ear sloughing. Only
mllkglhr. In addition to fluid support, pain
physiologic crystalloid fluids should be
control is also commonly needed. NSAIDs
administered via the ear vein. The centi·al
and opioids are often used in synergy. The
aitery can be accessed for direct blood
dosage of meloxicain in rabbits is 1 mg/kg/
pressure monitoring during anesthesia; no
day, which is also signi.ficat1tly higher that1
drugs should be injected into the central
tl1at in dogs at1d cats. Opioids such as
aitery. The auricular vasculature is sensitive
oxyrnorphone or hydromorphine cat1
to temperature; having the rabbit wann ( or
readily be used at1d have not been shown

RABBITS

1939
to cause GI stasis. In most cases, additional
cally. If breeding is delayed several weeks
force feeding is not required, and the rabbit
and the doe is given full feed, weight is
should be offered food after fluid and pain
quickly regained.

management has been initiated. Syringe

The gestation period is -31-33 days.

assisted feeding can be offered to see

Does with a small litter ( usually S4) seem to

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whether the rabbit is interested in food
have a longer gestation period than does
intake. In rare cases in which the rabbit
that produce larger litters. If a doe has not
refuses to eat, eg, cases of severe hepatic
kindled by day 32 of gestation, oxytocin
lipidosis, active feeding is necessary;

(1-2 IlJ) should be given to induce parturitreatment may require aggressive nutritional tion; otherwise, a dead litter is almost always suppmt via syringe feeding, nasogastric tube delivered sometime after day 34. Occasion

(3-5 French), or pharyngostomy tube ( soft
ally, pregnant does abmt or resorb the fetuses
esophagostomy tube designed for cats).

because of nutritional deficiencies or disease.

The least invasive method is often the most

Nest boxes should be added to the
successful approach. Vaiious commercial
cages 28-29 days after breeding. If boxes
products for assisted feeding of rabbits
are added too soon, the does foul the nests
are available. Products are available for
with urine and feces. A day or two before
immediate c1itical care ( eg, Emeraid®) as
kindling, the doe pulls fur from her body
well as for longterm assisted feeding and to
and builds a nest in the nest box. The young
meet the needs of the recovering rabbit ( eg,
are born naked, blind, and deaf. They begin

Recovery®, Recovery Plus®, Critical Care®).

to show hair on day 2-3 after bi.Jth, and their
eyes and ears are open by day 10. Neonatal

Reproduction: Rabbit breeds of
rabbits are unable to them1oregulate until
medium size are sexually mature at 4-4.5
about day 7. Rebreeding can occur any time
mo, giant breeds at 6-9 mo, and small
after parturition, because the doe can
breeds (eg, the Polish Dwarf and Dutch) at conceive 24 hr after kindling. Some 3.5-4 mo of age. The rabbit is an induced
commercial growers use accelerated
ovulator and, contrary to popular belief,
breeding schedules and rebreed 7-21 days
has a cycle of mating receptivity; rabbits
after parturition, whereas most people
are receptive to mating -14 of every 16
raising rabbits for show or home use
days. The degree of mating receptivity
rebreed 35-42 days after parturition.

is indicated by the color of the vaginal

Most mediun1-sized female rabbits have
orifice and by the an10unt of moisture on

8-10 nipples, and many kinclle 12-15 yOLmg. lf
the labia. A doe is most receptive when
a doe is unable to nurse all the kits effectively,
the vagina is red and moist. Does that are
kits may be fostered by removi.J1g them from
not receptive have a whitish pink vaginal
the nest box during the first 3 days and giving
color with little or no moisture. Many
them to a doe of approxinlately the same age
breeders test mate the doe 10-16 days
with a smaller litter. lf the fostered kits are
after breeding as a way to detect pregmixed witl1 the doe's own kits and covered nancy, but this is unreliable. Palpation
with hair of the doe, they are generally
of the doe's abdomen for "grape-sized"

accepted. Moving the larger kits to the new
embryos in the uterus is a much better
litter instead of the smaller kits increases the
technique to detect pregnancy. The best
chance of success. Does nurse only once or
time to palpate is 12 days after breeding.

twice daily. Kits nurse <3 min. Kits are

Pseudopregnancy is common in rabbits
weaned at -4-5 wk of age.

and can follow any induced ovulation,
the introduction of a male rabbit in the

Rearing Orphaned Kits: Kits can be
environment, or other stimuli.

hand-reared, but mortality is high. They

A ratio of l buck to 10 does is common
should be kept warm, dry, and quiet. Kitten
practice, but many commercial growers find milk or goat milk replacer or a fom1ula of Ye that l buck to 20-25 does is more economicup evaporated milk, Vz cup water, l egg cal. Bucks can be used daily without
yolk, and l tbsp com syrup can be used.

decreasing fertility; more frequent use

Feedings vary from Ye tsp to 2 tbsp,
requires periods of rest. The doe should
depending on the age of the kits. Kits should
always be taken to the buck's cage for
be fed only every 12 hr to avoid overfeeding
breeding. The breeding program should
and to mimic the natural feeding behavior of
continue year round. Does that experience
the doe. Cottontail kits start eating greens
long periods of rest between litters tend to
around day 15-18, whereas domestic rabbit
become obese and difficult to breed. Docs
kits are weaned when -6 wk old.

constantly in gestation and lactation may
become underweight, and their receptivity

Surgery: Preoperative fasting is not
to the buck and fertility decrease dramati-
required or recommended. Rabbits carmot

1940

RABBITS
vomit. Additionally, rabbit stomachs are
larger-size tube. If no visual aid is available,
never empty, even after prolonged fasting.

the rabbit can be intubated blindly, but this

However, a short fast ( 1-2 hr) should be
procedure requires much skill and has the
done to assure that the oral cavity is free of
potential for iatrogenic trauma if not
food. Premedication with butorphanol or
performed properly. In the classic blind
diazepam/midazolam will reduce stress
teclmique, the rabbit is placed in a sternal

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from preoperative handling. Premedication
position with the head held and tl1e nose
with atropine will be useful for only a short
pointing at the ceiling. The ET is guided
time, because many rabbits have an
behind the incisors and to the larynx. The
atropinase that clears the drug from the
operator listens for the sounds of inspiration
system rapidly. Instead, glycopynolate may
and expiration and times the advancement
be used to reduce bradycardia and upper
of the ET witl1 maximal inspiration. A
airway and salivary secretions (0.01-0.1
second technique involves placing the
mg/kg, IM or SC, or 0.01 mg/kg, IV). Isoflurane rabbit in lateral recwnbency with the head is reconunended for general anesthesia, but
dorsi.flexed. The ET is advanced along the
premedication with a combination of an
hard palate to the back of the throat until

NSAID and an opiate (such as meloxicam at
condensation can be seen within tl1e lwnen

1 mg/kg, PO, and butorphanol at 0.4 mg/kg,
of the ET. The condensation is used to judge

IV) can reduce the minimwn alveolar
the cycles of inspiration and expiration, and
concentration (MAC) of isoflurane from
the ET is advanced at maximal inspiration.

2.5% to 2.3%. Lidocaine administered as a

Proper ET placement should be confinned
constant-rate infusion has also been shown
regardless of placement method. An
to reduce the MAC of isoflurane (lidocaine
alternative to intubation is a supraglottic
can be given at a loading dose of 2 mg/kg, IV,
airway device (V-gel®). A species-specific
followed by 100 mcg/kg/min).

phaiyngeal device is placed in tl1e oral cavity

The long and narrow pharynx and large
and advanced caudally until it sets in place
tongue make rabbits difficult to intubate.

automatically. The device sits on top of the

Laryngospasm can be minimized by
glottis and seals the surrounding structures,
application of lidocaine on the epiglottis.

creating ai1 airtight connection between the

There are several repo1ted techniques to
trachea and tl1e tube.

intubate rabbits; all require selection of the

Adequate general anesthesia can be
appropriate tube size and length to avoid
achieved for a shmt procedure with
tracheal iajury. A pediatric laryngeal mask,
iJ'\iectable ketainine (25-50 mg/kg) in
uncuffed Cole, or cuffed Murphy eye type
combination with a tranquilizer such as
endotracheal tube (ET) can be used, but
xylazine (5-10 mg/kg, IM). The combinaselecting the appropriate size (2-4 mm) tion of ketarnine (10-20 mg/kg, IM) and
is critical. The risk of tracheal iajury
dexmedetomidine (0.125-0.25 mg/kg, IM)

increases with repeated intubation
provides adequate anesthesia; - 1 13 of the
attempts, but ET cuff pressure, prolonged
original dose can be repeated if anesthesia
duration of intubation, and movement of
needs to be prolonged. Atipamezole can be
the ET during mechanical ventilation and
given IM in equal volwne to dexmedetomianimal positioning for anesthesia-seem to dine volume for reversal.

be more critical because of the vascular

It is critical for rabbits to start eating
anatomy of the rabbit trachea. Rabbits are
postoperatively, and analgesic treatment for
best intubated with visualization, using an

1-2 days will help prevent inappetence. A
endoscope or similar technology. Direct
rabbit in pain may chatter or grind its teeth
visualization of the epiglottis and ET
while sitting in a hunched position. Analgesic
placement can also be accomplished by
treatment may include opioid drugs such as
using a laiyngoscope with a Miller O blade,
buprenorphine (0.01--0.05 mg/kg, SC, IM, or
a rabbit oral specula, and cheek dilators.

IV, bid-tid) or butorphanol (0.05--0.4 mg/kg,

The glottis should be visualized using

SC or IM, bid-tid), or NSAIDs such as carpthe endoscope, and the tube cai·efully rofen ( 1. 5 mg/kg, PO or SC, bid), flunixin
advanced toward the glottis. The natural

(0.5-2 mg/kg/day, PO, deep IM, or IV, for no
position of the epiglottis is behind the soft
more than 3 days), or meloxicain (1 mg/kg/
palate. The ET can be used to disengage
day, PO or SC). Trainadol used at 11 mg/kg,
the glottis from the soft palate, and then

PO, causes no adverse effects and has been
introduced into the glottis and down the
reported empirically to be effective in
trachea. Care must be taken to not dainage
rabbits. However, a study showed that this
the arytcnoid cartilages when inserting
dose does not achieve plasma levels that
the tube into the trachea, because these
would be considered adequate in people.

caitilages reduce the diameter of the glottis

Prolonged opiate exposure has not been
significantly and can be easily damaged by a
associated with GI stasis.

RABBITS

1941

Postoperative supportive care is critical
incorporate, but not penetrate, the gastric
to a successful surgical outcome. Hay and
mucosa. Pre- and postsurgical care should
water should be offered as soon as possible
include fluids and antibiotic therapy.

after surgery. Alfalfa hay can be used to

Rabbits can chew out skin sutures;
improve appetite. Banana is favored as a
therefore, skin closure should be performed
treat by many rabbits. Hand feeding or
with a4-0 absorbable synthetic suture with

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syringe-assisted feeding is necessary if the
a cuticulai0cuticular pattern. Tissue glue
rabbit does not eat on its own soon after the
may be added to finish this closure. Rabbits
surgery. If the rabbit does not eat within 2-3
tolerate staples.

hr after surgery, the analgesic protocol
should be reevaluated. The rabbit should

Euthanasia: Rabbits may jwnp or scream
be assisted feel until it refuses further food
when the traditional overdose of barbiturate
intake in each session.

is given in the marginal eai· vein. Sedation

Castration can reduce aggressive
with midazolan1 (5 mg/kg, IM or IV) or
behavior and is suggested for house
propofol (10 mg/kg, IV) is recommended
rabbits and group-housed rabbits. It has
before administration of the barbiturate.

no advantage for meat-type rabbits. The

As a further precaution, euthanasia solution
testicles are lateral and anterior to the
may be diluted 1: 1 with saline to prevent
penis, as in marsupials and not as in most
a negative reaction ai1d to reduce viscos-
other placental man1mals. Castration is
ity of the solution to facilitate a faster and
performed using a closed technique or
smoother ir\jection.

by an open technique with closure of the
large superficial inguinal ring to prevent

Other Management Techniques: Toeherniation.

nails on the hindlimbs may severely scratch

Female pet rabbits should be spayed
w1protected arms of handlers. Nails should
because of the high risk of uterine cancer.

be trimmed every 1 -2 mo. Declawing is not

Rabbits have two uterine horns connected
recommended, but some rabbits tolerate
to the vagina by two separate ce1vices. The
application of adhesive nail caps.

oviduct loops around and is much longer

Some breeders tattoo or place ear tags on
than in cats or clogs. Ovariohysterectomy is
their rabbits for identification purposes. For
more complicated in older or multiparous
show purposes, the right ear is reserved for
rabbits because of the large amount of fat in
registration marks applied by registrars of
the mesometrium. Postoperative adhesions
the American Rabbit Breeders Association.

are a common complication, which may be

A tag placed in the anterior cartilaginous
reduced by calciun1-blocker treatment
pa.rt of the eai·, nearer to the head, is less

(verapamil, 200 mcglkg, SC, tid for3 days).

likely to be pulled out.

To avoid adhesions, all blood clots should
be removed before closing the abdomen,
and the GI tract should not be handled at all.

HOUSING

The use of spay hooks is not recommended
in rabbits, because the intestinal loops a.re

Pet Rabbits: A rabbit hutch placed in the
easily damaged; tissue forceps ( eg,
back yard, basement, or garage has been

Aclson-Brown) a.re a better choice.

and continues to be traditional housing for

Although the vast majority of trichorabbits. The hutch should be conveniently bezoars can be managed medically with
accessed for proper care of the rabbit,
aggressive fluid therapy (10-12 mUkg/hr)

because diseases of neglect are common in
and appropriate pain medication (eg,
rabbits abandoned in a hutch at the back of
oxymorphone ), a small percentage of GI
the yard. Care must be taken to prevent the
cases need to be surgically corrected.

hutch from being exposed to severe heat,

Surgery should usually be considered if
because rabbits are prone to heat stroke.

the condition has not improved after 24 hr

The flooring of the hutch should be covered
of aggressive medical therapy. When
with some type of soft padding to provide a
gastrotomies are performed, the stomach
comfortable resting spot. Sore hocks can
is elevated by stay sutures through a
lead to more problems if the rabbits ai·e
cranial celiotomy incision. An incision
housed on wire or wooden flooring for
is made through the greater curvature
long pe1iods. Keeping the area ai·ow1d the
of the stomach. It is important to remove
hutch cleai1 is important to avoid a large
stomach contents from the pyloric
population of flies, which often lead to fly
sphincter and to examine the stomach
strike ( myiasis) that is often fatal. There
lining for abnormalities. A fine, absorbshould be adequate ventilation and able monofila.ment suture should be used
protection from dogs or other predators
for closure of the stomach wall and
such as raccoons.

1942

RABBITS

House Rabbits: In the natural setting,
between litters. Disinfecting the nest box
rabbits use a latJ.ine system. This behavior
after cleaning and again just before placing
can easily be exploited by providing a litter
it in the cage helps reduce incidence of
box. Rabbits usually readily accept a
disease. The box should be large enough to
litterbox with little training. Rabbits have
prevent crowding but small enough to keep

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continuously growing teeth and need to
the kits warm. A standai·d size nest box for
chew on things to appropriately wear down
mediun1-sized rabbits is 16 x 10 x 8 in.

the teeth. If no appropriate food material that Wooden, metal, or plastic nest boxes with requires significant chewing efforts ( eg, hay)

nesting material ( eg, straw, hardwood
is offered, rabbits are likely to gnaw on
shavings, CareFresh® bedding) serve well in
vaiious objects in the environment, such as
either wann or cold weather. Rough edges
furniture, curtains, carpeting, or electrical
such as splinte1ing wood should be avoided,
wiring, which is dangerous for the rabbit ai1d
because they contribute to mastitis when
creates a fire hazai·d. Rabbits should be
does hop in and out of the nest box.

confined to safe quaiters when unsupe1vised. Pens: Pens should have a nonslip floor and Cages and Ancillary Equipment:

may be bedded with stJ.·aw or shredded pa

Rabbits can gnaw, and caging should be
per covered with straw or hay to increase
constructed of durable materials. Cages
absorbency. Shavings or sawdust ai·e not
should be easily sanitized and allow easy
the best, because the scent is too power-
cleaning. All-wire cages with a minimun1
ful. Pen sides should be at least 4 ft high
of 12-gauge wire (16-gauge recommendor high enough to allow the rabbit to stand ed for cage floor to support the weight of
erect on the hindlimbs.

the rabbit) are preferred. Aquariun1s are
not appropriate housing for rabbits ( or

Group Housing: When setting up group
other small manunals) because of inadhousing, compatibility is a major factor.

equate air circulation. The size of the cage

Personalities should be evaluated for docility
depends on the size of the rabbit. Giant
and aggressiveness. Strain influences
breeds (>12 lb) require a minitnw11 of30
personality. Rabbits that have grown up
x 36 in. to 36 x 48 in. Mediwn breeds
together are best, although adults may be

(7-12 lb) require 24 x 30 in. to 30 x 36
so aggressive toward each other that serious
in. Smaller breeds can be accommodated
fights occur. Neutering will in1prove compatibility. A period of acljacent proximity is by 18 x 24 in. The cage should be tall
prudent before group housing rabbits.

enough to allow the rabbit to stand on its

Another factor to consider is stocking density.

hindlin1bs. The cage should be equipped

Floor space recommendations vary from 3.5
with a feed hopper and a watering system.

to 10 sq ft/rabbit to allow territory establish

Feed hoppers are best constructed of sheet
ment. Others reconunend 3.5 hop lengths per
metal with holes or a screen in the bottom
rabbit as a general rule. Regardless, groupfor removal of"fines" (small, broken feed housed rabbits should be provided escape
particles). Rabbits drink more than other
and hiding places and should be frequently
animals of similai· size, and.they should
monitored.

be offered ad lib potable water. Rabbits
will conswne significantly more water

Production Housing: Housing
when water is offered from a dish versus
requirements for rabbits depend on climate.

a sipper bottle. Rabbits often chew on the

Minin1al housing ( an A-fran1e roof without
watering valve and may eventually desides) can be used in moderate climates, stroy it wuess it is made of stainless steel
whereas a climate-controlled rabbitry
or has a stainless centeipiece. If a water
may be necessary in hot or cold climates.

dish caimot be offered, water bottles with

Rabbitries should be located on neai·ly
level ground and use well-drained soil or
sipper tubes are a good alternative. Howtile-drained pits for manure. Shade should ever, food dishes ai·e easily contan1inated
be provided over as much of the rabbi try as
and should be washed and disinfected
possible. Rabbits are prone to heat stress.

daily. A barren cage is inadequate; the

Although rabbits tolerate subzero temperacage environment should be enriched ( eg, tures when provided proper shelter, the
cage furniture, toys) to provide stimulaoptimal rabbit environment is 61 ° -72°F.

tion. Optimally, rabbits should be given

Increased hwnidity levels should also be
run time outside of the cage daily.

avoided, because they will increase the

Nest boxes should be constructed so that
likelihood of heat stress and potentially
they can be easily placed in the cage and
de1matopathies. Good ventilation at all
later removed for cleaning and disinfecting
times is imperative.

RABBITS

1943

Sanitation: Cleaning frequency depends

Separation of dig es ta on the basis of particle
of the type of facility or caging system.

size occurs in the hindgut. Pe1istaltic action

Rabbits typically choose a preferred latrine
rapidly moves large particles (>0.5 mm),
site, such as a comer of the cage. This
primarily lignocellulose, through the colon
nonnal behavior can be exploited during
and excretes them as hard fecal pellets. This

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litterbox training. A strategically placed
is the "indigestible fiber" component of the litterbox is readily accepted by most pet
diet. The clinical importance of a diet high
rabbits. Sanitation is especially important in
in long particle length is to maintain the
rabbit production. Poor sanitation leads to
motility of the cecwn and colon. This is why
disease and deaths; therefore, cleaning and
these fibers are sometimes referred to as
sanitizing must be constant. Nest boxes

"scratch factor," because they mechanically must be disinfected between uses. Cages,
stimulate GI motility. Antiperistaltic action
feeders, and watering equipment should be
moves smaller particles ( <0.3 mm) and
sanitized periodically with an effective and
soluble material into the cecum, where they
inexpensive sanitizing solution such as
undergo fermentation. This component of
diluted household chlorine bleach (1 oz/1
the diet is known as "digestible" or
quart water) or other less corrosive

"fem1entable" fiber. At intervals, t11e cecal disinfectants. Complete cleaning should
contents are expelled as "soft feces" or
be perfonned before housing new stock.

cecotrophs and consun1ed by the rabbit

An active rabbitry constantly experiences
directly from the anus. Cecotroph ingestion
a loose hair problem. Does pull hair from
is highest when rabbits are fed a diet high in
their bodies to make nests, and some of this
nondigestible fiber. This reingested material
hair becomes airborne. It sticks to almost
provides microbial protein, vitamins
any surface, including cages, ceilings, and

(including all the B vitantins needed), and
lights, and must be removed periodically.

small quantities of volatile fatty acids, which

The most effective ways to remove hair
are essential in rabbit nutrition. However,
from cages are washing or using a propane
because amino acids obtained in this
torch or flame. Washing, brushing,
manner make only a minor contribution
sweeping, and vacuuming also ru·e effective
to the rabbits' protein needs (particularly
in other parts of the rabbi try. Pens or
young, growing rabbits), the diet must
wire-floored cages should be brushed or
supply the additional amino acids, altl1ough
hosed every 2 wk. An acid wash may be
the requirements for essential amino acids
required to descale rabbit urine from solid
in rabbits have not yet been defined.

floor pans.

Rabbits digest fiber poorly because of the

Frequent manure removal is essential.

selective separation and rapid excretion of

Excess manure leads to unacceptable levels
large particles in the hindgut. A generous
of ammonia in the air, which predisposes to
amount of dietary fiber (--15%crude fiber) is
respiratory disease. The manure can be
needed to promote intestinal motility'a.Ild
composted in an efficient pit system.

mininlize intestinal disease. High-fiber
intake can be provided by use of ad lib

NUTRITION
timothy hay (--30%--35%fiber). Fiber may
also absorb bacte1ial toxins and eliminate

Rabbits are small herbivores with specialthem via the hard feces. Diets low in fiber ized feeding needs and digestive systems.

promote an increased incidence of

They ru·e selective eaters and choose
intestinal problems, eg, enterotoxemia.

nutrient-rich leaves and new plant shoots

Carbohydrates will actually inhibit motilin
over mature plant material that is higher in
release. Motilin is a polypeptide honnone
fiber. Rabbits are therefore considered
secreted by cells of the duodenum and
concentrate selectors, because they
jejunum, which stimulates the GI smooth
naturally pick and choose foods higher in
muscle. Excess starch can also be substrate
energy density, which predisposes them to
for the proliferation of pathogenic bacteria
obesity in captivity. Anatomically, rabbits
such as Clostridium spirofonne, which
are nonruminant herbivores with an
produce a potent toxin. Cecwn fe1mentaenlarged hindgut. The large cecum supports tion produces volatile fatty acids, which are
a population of microorganisms that uses
responsible for 400/o of the rabbits' calorie
nutrients not digested in the small intestine.

requirement. Volatile fatty acids also aid in

Most of the bacterial population in the
the control of pathogenic organisms by
cecum is made up of the gram-positive
helping to maintain the nom1al pH (6--7) in

Bacteroides sp. This makes the rabbit very
the cecwn.

sensitive to oral antibiotics; administration

A dietary supply of vitan1ins A, D, and E
of oral antibiotics can disturb the Bacteroi
is necessary. Bacteria in the gut synthesize
des population and lead to fatal GI upsets.

B vitamins and vitamin Kin adequate

1944

RABBITS
quantities; thus, dietary supplements are
pelleted diets with a tin1othy hay base. Adult
unnecessary. Disease and stress may
pet rabbits not intended for breeding should
increase the daily vitamin requirements.

be fed a high-fiber pelleted diet, restricted to

Feed preparation and storage must be done

\/,; cup/5 lb body wt/day to prevent obesity
in a manner that will reduce losses from
and maintain GI health.

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oxidation, which destroys vitamins A and E

.

more readily than other vitamins. Diets

Production Rabbit Nutrition: Rabbits
containing 2:3QOA, of alfalfa meal generally
are efficient conve1ters of poorly digestible
provide sufficient vitamin A. Levels of
materials to meat. Therefore, it is easy to
vitan1in A in the diet must be >5,000 IU/kg
overfeed or w1derfeed does and growing,
and <75,000 IU/kg. Levels out of this range
adolescent rabbits (fryers). The amoW1t to
may cause abortion, resorbed litters, and
feed depends on the age of the fryers or on
fetal hydrocephalus. Vitamin E deficiency
the stage of pregnancy or lactation of the
has been associated with infe1tility,
does. A general rule in feeding fryers is to
muscular dystrophy, and fetal and neonatal
feed all that can be conswned in 20 hr, with
death. Pet rabbit diets sold in pet stores or
the feed hopper empty -4 hr/day. Does are
even in bulk at feed stores may not have
usually fed ad lib once they kinclle. The
adequate turnover, which may result in
general practice is to bring does from
nutritional deficiency. Hay packaged for
restricted to full feed slowly dw"i..ng the first small manm1als may have been sitting on
week of lactation. Does bred to kinclle five
the shelf for an extended period.

times dw·ing the year generally have their

All the components of the basic diet (ie,
feed restiicted between litters; those bred
protein, fiber, fat, and energy) should be
intensively should be on full feed continumanaged in consideration of the life stage ally once they begin the first lactation.

(growth, gestation, lactation, maintenance),
breed, condition, and lifestyle of the rabbit.

Ratios should meet the nutrient require

BACTERIAL AND MYCOTIC
ments of the National Research Cotmcil (see DISEASES

TABLE 21). Pelleted rabbit feeds provide good
nutrition at reasonable cost. Fresh, clean

Pasteurellosis
water should always be available. Pro

Pasteurellosis is common in domestic
longed intake of typical commercial diets
rabbits. It is highly contagious and
containing alfalfa meal by laboratory or pet
ti·ansmitted primarily by direct contact,
rabbits kept for extended periods under
although aerosol transmission may also
maintenance conditions may lead to kidney
occur. The etiologic agent isPasleurella
damage and calciW11 carbonate deposits in
mullocida, a gran1-negative, nonrnotile
the urinary tract. Ad lib timothy hay is
coccobacillus. In conventional colonies,
usually recommended for the maintenance

300/o--900/o of apparently healtl1y rabbits may
diet of adult rabbits. Reducing the calcimn
be asymptomatic carriers. This is in1porlevel to 0.4o/<r-0.5% of the diet for nonlactattant to consider when nasal cultures are ing rabbits helps reduce these problems.

collected, because not every positive result

This can be accomplished by fe.eding
indicates a pathologic condition. To get a
itM•fj• NUTRIENT REQUIREMENTS OF RABBITS Digestible Total Carbo-Digestible

Protein

Protein(%) Fat

Fiber hydrates

Nutrients

(%) Total Digestible

(%)

(%)

(NFE,%)a (%)

Maintenance

12

9

1.5-2

14-20

40-45

50-60

Growth and

16

12

2-4

14-16

45-50

60-70
finishing

Gestation

15

11

2-3

14-16

45-50

55-65

Lactation

17

13

2.5-3.5 12-14

45-50

65-75

(with litter of

7-8)

a NFE = nitrogen-free extract

RABBITS

1945
true representative culture of the nasal
into the nostril can also be beneficial.

bacterial fauna, the rabbit needs to be

Necropsy reveals bronchopnewnonia,
heavily sedated or anesthetized and a deep
pleuritis, pyothorax, or pe1icai·dial
nasal culture obtained by introducing the
petechiae.

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culture tip relatively far into the nasal

Otitis media or interna ("wry neck"

opening. Several barrier colonies of
or head tilt) results from infections with
laboratory rabbits have been established
vai'ious agents. Pasteurella multocida was
as Pasteurella-free.

reported to be isolated from 97% of cases of
otitis media, including clinical a.11d

Clinical Findings: Pasteurellosis presubclinical cases. Bordetella bronchisep
sents with a vaiiety of clinical symptoms,
tica and staphylococci were also found in
including rhinitis, pneumonia, abscesses,

5%-lOOA, of cases. An accun1ulation of pus or
reproductive tract infections, torticollis,
fluid in the middle or inner ear causes the
and septicemia. Rabbits may develop
rabbit to twist its head, eg, "wi-y neck" or Pasteurella septicemia and die acutely
torticollis. However, not all rabbits with
without any clinical signs. Septicemia
middle ear infections show torticollis.

necropsy findings may reveal only

Longterm antibiotic treatment is required
congestion and petechial hemorrhages
for drug penetration into the affected
in multiple organs.

area. Antibiotic therapy may only prevent

Rhinitis ( snuffles or nasal catarrh) is an
worsening of clinical signs, and the
acute, subacute, or chronic inflanunation of
prognosis is guarded with medical therapy
the mucous membranes of the air passages
alone. Total ear canal ablation and bulla
and lungs, induced primarily by Pasteurella, osteotomy are often indicated when but Pseudomonas, Bordetella bronchisep
medical ma.11agement of otitis media and
tica, Staphylococcus, and Streptococcus intema fails. Proper imaging of the ear
have also been isolated. The initial sign is
lesions is indicated before surge1-y. Often, a
a thin, serous exudate from the nose and

CT scan of the head will help to identify the
eyes that later becomes purulent. The fur on
lesion and potentially help to differentiate
the inside of the front legs just above the
otitis media/interna from intracranial
paws may be matted and caked with dried
disease in cases of torticollis ( eg, Encepha
exudate, or this area may be clean with
l'itozoon c:urt'iculi infection).

thinned fur as a result of pawing at the nose.

Conjunctivitis and dacryocystitis

Infected rabbits usually sneeze and cough.

( weepy eye) is a co nun on problem in
ln general, snuffles occurs when the
rabbits. Predisposing factors include
resistance of the rabbit is low. Recovered
mecha.11ical irritation, eyelid diseases, and
rabbits are likely carriers. Pneun1onia can
dental disease. Conjw1ctivitis in rabbits may
ensue.

be associated with other disease processes,

Pneumonia is common in domestic
especially dacryocystitis. The most
rabbits. Frequently, it is a secondary a.11d
incriminated cause of conjunctivitis is
complicating factor in the enteritis complex. P multocida; however, this may be only a The cause is typically Pasteurella multo
secondary infection. Primary infections are
cida, but other bacteria such as Klebsiella less conunon than oppo1tunistic infections.

pneumoniae, Bordetella bronchiseptica,

Transmission is by direct contact or fomites.

StaphylococC'US aureus, and pneumococci

Affected rabbits rub their eyes with their
may be involved. Upper respiratory disease
front feet. Bacterial conjunctivitis can be

( snuffles, see above) is often a precursor of treated with topical chlorainphenicol,
pneun1onia. Inadequate ventilation, sanitaciprofloxacin, or gentan1icin combined with tion, and nesting material are predisposing
systemic broad-spectrw11 antibiotic therapy
factors. The number of cases of pneun1onia
if topical treatment alone is ineffective.

is directly proportional to the level of

Dacryocystitis and acquired nasal duct
ammonia in the cage, hutch, or rabbitry.

obstruction may arise from chronic rhinitis

Ventilation is of utmost importance to
that travels up the nasolacrimal duct to the
provide good air quality. Affected rabbits ai·e eye or occasionally from dental disease anorectic, listless, dyspneic, and might have
such as tooth root inflanunation or
a fever. Treatment should include systemic
abscessation. Treatment includes gentle
antibiotics, optimally based on a culture and flushing with saline of the duct through sensitivity, because of possible resistance to
the nasolacrirnal puncturn, but care is
common pathogens. The rabbits are usually
warranted to not dainage the nasolacrimal
dehydrated, and supportive care with
duct during flushing. Dacryocystorhinograhydration and syringe feeding is often phy or injection of contrast material into
necessary as well. Topically administered
the lacrimal punctwn will provide good
ophthalmologic antibiotic products instilled radiographic detail of the duct throughout

1946

RABBITS
its course and show the site of obstruction.

reproductive organs in cortjunction with

In long-standing cases of dacryocystitis and
antibiotic therapy is indicated for pet
cortjunctivitis, the puncturn and segments
rabbits. The contan1inated hutch and its
of the nasolacrirnal duct may progressively
equipment should be thoroughly disin

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narrow and be replaced with scar tissue
fected.

until they are irreversibly obstructed. This
results in pe1manent epiphora, and owners

Diagnosis: Diagnosis of pasteurellosis
should be advised accordingly. To relieve
is based on clinical signs and isolation of
discomfort and inflammation associated

P multocida. Carriers can be identified by
with these conditions, the use of topical
an indirect fluorescent antibody test on
nonsteroidal anti-inflanunatory ophthalmic
nasal swabs. A technique that uses small,
preparations such as flurbiprofen can be
saline-moistened, pediatric nasopharyngeal
considered. Systemic NSAIDs such as
swabs has proved superior to tl1e standard,
meloxicam should also be used.

larger nasal swab. The swab is directed

Cortjunctivitis also accompanies
medially tllfough the external nares past the
rabbitpox (seep 1951) and myxomatosis
turbinates and onto the dorsal smface of the

(seep 1950).

soft palate; sedation is recommended. The

Subcutaneous and visceral abscesses
swab is then retracted and can be used in
caused by Pasteurella may be clinically
tl1e fluorescent antibody test or plated
silent for long periods and spontaneously
onto a culture medium. An ELISA test
rupture. When bucks penned together fight,
to detect antibodies againstP multocida
their wounds frequently develop abscesses.

may also help detect carriers. PCR can

Abscesses in rabbits are treated differently
than abscesses in cats; rupture or drainage
discriminate between different isolates,
via Penrose is not the recommended course.

but it is not conunercially available. It is

Thick-walled abscesses should be surgically
important to remember that Pasteurella
excised en bloc if possible. Open wounds
can be sampled from a large percentage
should be debrided or curetted, marsupialof clinically normal rabbits, and culture ized, and left to heal by second intention.

results must be interpreted carefully and

Facial abscesses are often related to dental
in combination with the clinical signs and
disease (seep 1954). Drainage of the
the antibiogram from sensitivity testing.

abscess accompanied by systemic antibiotic Not every strain of Pasteurella is pathotherapy based on culture and sensitivity genic.

tests has been successful, although
recurrence can be common.

Treatment and Control: Treatment is

Pasteurella can cause genital infec
difficult and will most likely not eradicate
tions, but several other organisms also may
the organism. Antibiotics seem to provide
be involved. The spirochete Treponema
only temporary remission, and the next
para,luiscuniculi is the causative agent
stress ( eg, kindling) may cause relapse.

of rabbit syphilis. Genital infections are

Prolonged treatment for 6-8 wk is often
manifest by an acute or subacute inflammaneeded. Many of the newer antibiotics are tion of the reproductive tract and most
already ineffective because of an increase
frequently are found in adults, more often in
in resistant strains. Before treatment, a
does than bucks. In the case of Treponoma,
culture and sensitivity should be done to
a severe cortjunctivitis or dermatosis
determine the best antibiotic to use. Very
between the toes can also be a key clinical
often, systemic antibiotic therapy can be
sign. If both horns of the uterus are affected,
augmented by local antibiotic therapy.

the does often become sterile; if only one

Gentamicin ophthalmologic drugs instilled
horn is involved, a norn1al litter may
into the nostrils can be a significant aid to
develop in the other. The only sign of
treat upper respiratory tract problems with
pyometra may be a thick, yellowish gray
systemic antibiotics. Fluoroquinolones are
vaginal discharge. If bloody discharge from
usually good drugs if no resistance has built
the vulva is observed and a large uterine
up. Oral medication is usually well tolerated
horn can be palpated, uterine adenocarciand without adverse effects. In case of noma should be included in the differential
unsatisfactory results, doxycycline can be
diagnosis. Bucks may discharge pus from
added, because both drugs appear to have
the uretl1ra or have an enlarged testicle.

a synergistic effect. Sometimes, amikacin

Chronic infection of the prostate and
or azitllfomycin must be used based on
seminal vesicles is likely, and because
culture results. Although medication in
venereal transmission may ensue, it is best
the drinking water is not recommended
to cull the animal in a production rabbitry
because of the tainting of the flavor and
colony. Surgical removal of the infected
potential underdosing, tllis is sometimes the

RABBITS

1947
only possible route to treat animals on a

Enterotoxemia: Enterotoxemia is a
larger scale. Enrofloxacin (200 mg.IL of
severe diarrheal disease, primarily of
drinking water for 30 days) can be effective
rabbits 4-8 wk old when naturally infected;
for upper respiratory P multocida
it also can affect rabbits at all life stages if
infections. Procaine penicillin (60,000 IU/
an inappropriate antibiotic is given orally.

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kg/day, SC, for 10-14 days) is also recom

Signs are lethargy, rough coat, greenish
mended for individual rabbits, but caution is brown fecal material covering the perineal warranted, because deaths from enterotoxarea, and death within 48 hr. Often, a rabbit emia can follow if the dmg is accidentally
looks healthy in the evening and is dead
given orally.

the next morning. Necropsy reveals the

An effective intranasal vaccine is in
typical lesions of enterotoxemia, ie, a
development but not conu11ercially
fluid-distended intestine with hemorrhagavailable; therefore, the best method of control in large rabbitries is strict culling.

ic petechiae on the serosal surface. The

1\vo methods to free a production colony
primary causative agent is Clost1idium
of Pasteurella have been reported. The
spirnforme, which produces an iota toxin.

first involves culture and culling of positive

Little is known about transmission of the
animals; once the colony isPasteurella
organism; it is assun1ed to be a conu11enfree, it must be maintained in isolation. ln sal normally present in low numbers. The
the second method, pregnant does past
type of diet seems to be a factor in develkindling are treated with enrofloxacin.

opment of the disease; enterotoxemia is

While does remain Pasteurella-culture
seen less often when high-fiber diets are
positive, the kits remainPasleurella-culture fed. Because most 13-lactams, lincomycin, negative. Carriers can be identified by an
clindamycin, and erythromycin induce
indirect fluorescent antibody test on nasal

Clost1idium-related (eg, Clostridium
swabs.

diffic'ile) enterotoxemia because of their
selective effect on normal, gram-positive

Listeriosis
bacteria, their oral use is contraindicated

Listeriosis, a sporadic septicemic disease
in rabbits. Enterotoxemia is a conside1°
characterized by sudden deaths or aboration for these antibiotic therapies. These tions, is most common in does in advanced
diarrheas are remarkably similar to those
pregnancy. Poor husbandry and stress may
that occur naturally ( described above as
be important in initiating the disease.

enterotoxemia). Treatment of colony rab

Clinical signs are variable and nonspecific
bits is seldom attempted because of the
and include anorexia, depression, and
rapidity of death. However, when popuweight loss. ln contrast to the disease in lation size permits, cholestyramine has
cattle and sheep, listeriosis seldom affects
been used with promising results, both
the CNS in rabbits. The causal agent,
as a preventive and a treatment. Reduc-

Listeria monocytogenes, spreads via the
ing stress of the young rabbits (weaning,
blood to the liver, spleen, and gravid uterus.

etc) and ad lib feeding of hay or straw are

At necropsy, the liver consistently contains
helpful in prevention. Adding 250 ppm of
multiple, pinpoint, gray-white foci. Because
copper sulfate to the diet of young rabbits
diagnosis is rarely made premortem,
treatment is seldom attempted. L monocy
also helps prevent enterotoxemia. Indi
togenes can infect many animals, including
vidual animal treatment for enterotoxemia
people. It is difficult to isolate witl1 nonnal
should include aggressive fluid therapy
methods, and special techniques are often
and intensive supportive care. Monitor-
required.

ing of hydration status, body temperature,
and heart rates is extremely important.

Intestinal Diseases

There is little evidence that antibiotics are
helpful. Prognosis for advanced cases is

Intestinal disease is a major cause of death
often poor. Diagnosis depends on history,
in young rabbits. Although most diarrheal
diseases were once lumped together (as the
signs, lesions, and demonstration of C spi
enteritis complex) or simply called mucoid
roforme. Centrifugation of intestinal conenteritis, specific diseases are being tents at 20,000 g for 15 min followed by
delineated. Diet, antibiotic treatment, and
culture of the supernatant-pellet interface
other factors create disturbances of the GI
will reveal the organism. For a definitive
microflora and may predispose rabbits to
diagnosis, the presence of iota toxin in the
dysbiosis and intestinal disease. For
supernatant of centrifuged cecal contents
discussion of GI stasis due to hairballs,
can be demonstrated by in vivo or in vitro
seep 1956.

assays.

1948

RABBITS

Tyzzer Disease: Tyzzer disease (see
blood agar and then having the isolate
p 199), caused by Clostridiurn pil�fo1me, is biotyped or serotyped. Electron nli.crographs
charactenzed by profuse watery diarThea,
of E coli attached to the mucosa are also
anorexia, dehydration, lethar·gy, staining of
helpful. ln severe cases, treatment is not
the hindquarters, and death within 1-3 days
successful; in mild cases, antibiotics may be

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in weanling rabbits 6---12 wk old. Acute
effective. Severely affected rabbits should be
outbreaks have been associated with >90"A,
culled, and facilities thoroughly sarutized.

mortality. Some rabbits may develop

High-fiber diets appear to help prevent the
chrome infections that present clirucally as
disease in weaned rabbits.

a wasting disease. Infection occurs by
ingestion and is associated with poor

Proliferative Enteropathy: Proliferasarutation and stress. The lesions consist of necrotic enteritis along with multifocal
tive enteropathy caused by Lawsonia
intrncellularis
necrosis in the liver and heart. Diagnosis is
has been reported to cause
diarrhea in weanling rabbits. Clirucal
made histologically; special stains ( eg,

G1emsa or Warthin-StarTY silver) show the
symptoms include diarThea, depression, and
characteristic intracellular· bacterium.

dehydration, which resolve over 1-2 wk.

Culturing is impractical, because the

Disease does not cause death unless
associated with a dual infection with
bacterium does not grow on artificial media.

Serologic tests are available from animal
another enteropathogeruc agent. Diagnosis
is based on necropsy fmdings of a thickened
diagnostic laboratories. Tyzzer disease
affects a wide spectrum of other species but
and corrugated ilewn and histologic
has not been repo1ted in people, although
identification of the rod-shaped to curved or
titers have been documented in pregnant
spiral silver-stairung organism in crypt
women. Although antibiotics used in
enterocytes. The organism requires
treatment of other arli.mals have not been
cell-contairung media ( enterocytes) for
effective in rabbits, oxytetracycline has
culture. Immunohistochemistly and PCR
been of some value in limiting an outbreak.

may be useful to identify L intrncellularis.

Isolation of sick animals and symptomatic

No vaccine is available. Aggressive
disinfection and decontamination of the
treatment is advised. Chlorarnphenicol or
housing facility to reduce the presence of
flotfenicol is the treatment of choice but
hardy spores is indicated with either 1%
some rabbits appear sensitive to the�e
peracetic acid or 3% hypochlorite.

antibiotics when given orally, so careful

GI monitoring is required.

Colibacillosis: Escherichia coli as a cause of rabbit diarrhea has been confused

Mucoid Enteropathy: Mucoid enteropaby the circumstance thatE' coli often thy is a distinct diarTheal disease of rabbits
proliferate when rabbits develop diarrhea
characterized by minimal inflammation
for any reason. Enteropathogeruc strains of
hypersecretion, and accwnulation of m�1cus

E coli (serotype 0103) conunonly express
in the small and large intestines. The cause
the eae gene, which codes for intlrnin an
is unknown, and it may occur concurrent
outer membrane protein associated �th the with other enteric diseases. Predisposing attaching and effacing lesions. Serotypes
factors include dietary changes, dietary

015:H, 0109:H2, 0103:H2, 0128, and 0132
fiber <6% or >22%, aritibiotic treatments
are also impo1tant. Healthy rabbits do not
environmental stress, and challenges with
have E coli of any strain associated with
other bacteria. Clinical signs ar·e gelatinous
their GI tract.

or mucus-covered feces, anorexia, lethargy,

Two types of colibacillosis ar·e seen in
subnormal temperature, dehydration,
rabbits, depending on age. Rabbits 1-2 wk
rough coat, arid often a bloated abdomen
old develop a severe yellowish diarThea that
due to excess water in the stomach. A fimi,
results in high mortality. It is common for
impacted cecwii may be palpable. The
entire litters to succumb to this disease. ln
perinea! ar·ea is often covered with mucus
weaned rabbits 4-6 wk old, a dian·heal
and feces. Diagnosis is based on clinical
disease very similar· to that described for
signs arid necropsy findings of gelatinous
enterotoxenli.a is seen. The intestines are
mucus in the colon. Rabbits may live for
fluid filled, with petechial hemoffhages on

-1 wk. Treatlnent is difficult and often
the sernsal sutface, sinlilar to the pathology
wirewar·ding in severe cases, but intense
tlescnbed for both Tyzzer disease and enterofluid therapy, antibiotics, and analgesics toxernia ( see above). Death occurs in 5-14
should be tiied. Prevention is the sarne as
days, or rabbits ar·e left stunted and wittuifty.

for ariy rabbit enteropathy by focusing on

D1agnos1s 1s made by isolatingE coli on
an adequate, fiber-rich diet.

RABBITS

1949

Mastitis
widely available and can be used to diag

(Blue breasts)

nose Tparaluiscuniculi. Hutch burn is a
differential diagnosis.

Mastitis is common in commercial

Benzathine penicillin G, 42,000 IU/kg, SC,
rabbi tries and is occasionally seen in
at weekly intervals for 3 wk, is necessary to

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smaller units but rarely in pet rabbits. Poor
eradicate treponematosis from a herd.

sanitation enhances spread throughout the

Procaine penicillin (60,000 IU/kg/day, SC, for
rabbitry. Mastitis affects lactating does and

7 days) is also reconunended for individual
may progress to a septicemia that rapidly
rabbits. All rabbits must be treated even if no
kills the doe. Generally, it is caused by
lesions are present. Lesions usually heal
staphylococci, but streptococci and other
within 10-14 days, and recovered rabbits
bacteria have been isolated. Initially, the
can be bred without danger of transmitting
manunary glands become hot, reddened,
the infection.

and swollen. Later, they may become
cyanotic, hence the common name, "blue

Dermatophytosis
bag." The doe will not eat but may crave
water. Fever �105°F ( 40.5°C) is often noted.

(Ringworm)

If antibiotic treatment is sl.alted early (the

Clinical dennatophytosis commonly affects
first day the doe goes off feed), the rabbit
individual rabbits, but epizootics can also
may be saved and damage limited to one or
occur. Ringworm is generally associated
two manunary glands. If more than two
with poor husbandry, poor nutrition, and
glands are lost, keeping the doe may not be
other environ.mental stressors. The cause is
economical. Because penicillin often causes most conrn10nly 'I'richophyton mentagro
diarrhea in rabbits, does should be treated
phyles and occasionally Microsporum
only after the pelleted ration has been
canis. Transmission is by direct contact.

replaced with hay or some other high-fiber

Fomites, such as hair brushes, that evade
diet (seep 1947). Kits should not be fostered proper disinfection can play a significant to another doe, because they will spread the
role in spreading infection. Asymptomatic
infection to the foster mother. Handrearing
cruTiers ru·e very conrn1on. The lesions
of infected young may be attempted but is
usually appear first on the head and may
difficult. The incidence of mastitis can be
spread to any area of the skin. Affected
reduced if nest boxes are maintained
areas are circulru·, raised, reddened, and
without rough edges to the entrance, which
capped with white, bran-like, flaky material.

can traumatize the teats when the doe

A negative result with a Wood's lamp
jumps in and out of the nest box. It is
illumination does not exclude dermatophyessential for the nest box to be sanitized tosis, because all agents do not fluoresce.

before and after use. Vaccines have not

Hair plucked from the edge of the lesion
proved to be beneficial to prevent mastitis.

may be cultured on special media, such as
dem,atophyte test media or Sabouraud's

Treponematosis
agar. A KOH skin scraping taken from the

(Vent disease, Syphilis, Spirochetosis)

pe1iphery of the lesion that reveals fungal
forms confirms the diagnosis. Because

Treponematosis, a specific venereal disease
rabbits with active infections ru·e infectious
of domestic rabbits, is caused by the
for people and other aninlals, they should be
spirochete Tre-ponema paraluiscuniculi.

either isolated and treated or euthanized.

It is seen in both sexes and is transmitted

Griseofulvin at an individual dosage of 25
by breeding and from the doe to offspring.

mg/kg body wt/day, PO, for 4 wk, or in the

Although closely related to the organism that
feed at 825 mg/kg of feed, is effective but
causes hw11an syphilis (T pallidum ), T
not approved for use in rabbits; it should
paraluiscuniculi is not transmissible to
not be used in rabbits intended for human
other domestic animals or people. The
consumption. Griseofulvin may be
incubation period is 3---6 wk. Small vesicles or teratogenic and should not be used in ulcers are formed, which ultimately become
pregnant does. Topical antifungal creams
covered with a heavy scab. These lesions
containing itraconazole (5 mg/kg/clay, PO,
usually are confined to the genital region, but
for 4--6 wk), clotrinlazole, or miconazole
the lips and eyelids may be involved. Infected
may be effective extra-label treatments. For
rabbits should not be bred. Diagnosis is
rabbitries, treatment with either 1% copper
based on the lesions and observation of
sulfate as a dip or 8 oz of MECA (metabothe spirochete's corkscrew motility under lized chlorous acid/chlorine dioxide
darkfield microscopy. Serologic tests used to
compound, 1: 1: 10 mix of base:activator:

diagnose T pall:idum, such as the VDRL slide water) sprayed on six tin1es in a 26-day
test and the rapid-plasma regain card test, are period was shown to be effective.

1950

RABBITS

Tularemia
of the California brush rabbit (S bachmani),

Tularemia is rare in domestic rabbits, but wild the reservoir of tile infection. Losses in rabbits and rodents are highly susceptible
rabbitries may be 25o/<r-900/o. Transmission
and have been involved in most epizootics.

occurs via mosquitoes, fleas, biting flies,

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Up to 900/o of human cases of tularemia are
and direct contact. •
linked to wild lagomorph exposure. The

The initial sign is conjrn1ctivitis that
etiologic agent, Prancisella tularensis, is an rapidly becomes more marked and is
aerobic nonmotile, gram-negative, pleomoraccompatlied by a milky ocular discharge.

phic, bipolar coccobacillus prevalent in the

The rabbit is listless and anorectic, with a
south central USA. It is highly infectious
fever tllat frequently reaches 108°F ( 42°C).

and passed through the skin, through the

In acute outbreaks, some rabbits may die
respiratory tract via aerosols, by ingestion,
within 48 hr after signs appear. Those that
and via bloodsucking aithropods. Tularemia
survive become progressively depressed
causes an acute fatal septicemia. Diagnosis
at1d develop a rough coat. The eyelids, nose,
is based on necropsy findings of septicemic
lips, at1d ears become edematous, which
bacterial disease with nrn11erous small,
gives a swollen appearance to the head. In
bright-white hepatic foci, congestion,
females, the vulva becomes inflat11ed at1d
and enlargement of the liver and spleen.

edematous; in males, the scrotum swells. A

Treatment of the animal is not indicated.

characteristic sign at this stage is drooping

Tularemia is a reportable disease. See also
of tile edematous ears. A purulent nasal
p692.

discharge invariably appears, breathing
becomes labored, at1d the rabbit goes into
a coma just before death, which usually

VIRAL DISEASES
occurs within 1 -2 wk after clinical signs

Viruses are not in1portailt causes of clinical
appear. Occasionally, a rabbit survives for
disease of rabbits in the USA but include
several weeks; in tllese cases, fibrotic
the infectious fibromas, papillomatosis,
nodules appear on the nose, ears, at1d
rabbitpox, myxomatosis, and a herpesvirus
forefeet. Rabbits inoculated experimeninfection (virus 3). Rotaviral enteritis also tally witll laboratory strains of the virus
has been diagnosed in the USA and seems
invaiiably develop small nodules at the
to contribute to the overall problem of
point of injection after several days; similar
intestinal disease in rabbits. Viral hemornodules develop later on other parts of the rhagic disease is forn1d in almost every
body, particularly the ears.

corn1try that raises rabbits except the USA.

Few characteristic gross lesions are

In April 2000, the USDA diagnosed rabbit
forn1d at necropsy in the acute forn1 of the
calicivirus in a backyard facility in Iowa.

disease. The spleen is occasionally enlarged

Rapid response at1d cooperation between
and is almost always devoid of lymphocytes
federal at1d state agencies contained this
when exat11ined histologically. In rabbits
outbreak and eliminated the source of
that survive longer, subcutaileous edema
infection. The USA is cur.rently considered
at1d nodular skin tumors are seen. The
free of rabbit hemorrhagic disease.

seasonal incidence of the disease, clinical
signs ( especially the swollen genitalia),

Myxomatosis
and high mortality are all of diagnostic
significat1ce. Large, eosinophilic, cytoplas

Myxomatosis is a fatal disease of all breeds
mic inclusion bodies in the conjrn1ctival
of domesticated rabbits caused by myxoma
epitllelial cells are also helpful in diagnosis.

virus, a member of the poxvirus group.

Outside the USA, vaccination is an option

Myxornatosis is called "big head" and is
and highly recommended in endemic areas.

chai·acterized by mucinous skin lesions or

An attenuated vaccine prepai·ed from a
myxedema of tl1e head. Wild rabbits such as
myxomatosis virus has protected rabbits
the cottontail (Sylvilagits) and jackrabbits infected rn1der both field at1d laboratory

(Lepus) are quite resistat1t. Myxoma virusconditions. This vaccine is not available in infected Sylvilagus develop fibroma-like
the USA, and because there is no effective
lesions similar to tllose caused by rabbit
treatment, euthanasia and burying or
fibroma virus. All oilier m=als are
burning of affected rabbits is indicated.

refractory to the virus. Myxomatosis

Preventive measures include protecting
has a worldwide distribution. In the USA,
rabbits from exposure to arthropod vectors.

myxomatosis is restricted largely to the
coastal area of California and Oregon,
where epidemics occur infrequently but

Rabbit (Shope} Fibroma Virus
sporadic cases are common. These areas

Shope fibromas are forn1d under natural
correspond to tile geographic distribution
conditions only in cottontails, although

RABBITS

1951
domestic rabbits can be infected by

Shope papillomavims; therefore, arthropod
inoculation of vims-containing material.

control could be used as means of disease

Fibromas may be found in domestic rabbits
prevention. The oral papillomavirus is
in areas where they are endemic in wild
distinct from the Shope papillomavims

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rabbits and where husbandry practices

(which is also distinct from the Shope
allow contact with artlu·opod vectors.

fibroma vims). Skin tun1ors caused by the

A fibroma vims, a member of the

Shope papillomavirus never occur in the
pox-vims group, causes this tumor, which is
mouth. Neither type of papillomatosis is
found on the legs, feet, and ears. The earliest treated, and the condition usually resolves lesion is a slight thickening of the subcutaspontaneously over time.

neous tissues, followed by development of
a clearly demarcated soft swelling. These

Rotaviral Infection
tmnors may persist for several months
before regressing, leaving the rabbit

Rotavims has been isolated from rabbits
essentially nonnal. Intracytoplasmic
with diarrhea in many different countries. In
inclusion bodies are seen when sections
serologic studies of rabbit colonies around
of the tumor are exanlined histologically.

the world, almost lOO"A, of tl1e adult rabbits

Because Shope fibromas are of little sigin some rabbitries were positive for nificance in domestic rabbits, no control
rotavims, demonstrating its widespread
measures have been developed.

nature. Rotavirus is shed in the feces of
infected rabbits and, therefore, is probably

Rabbitpox
transmitted by the fecal-oral route. Yom1g
rabbits of wea11ing age are most susceptible.

Rabbitpox is an acute, generalized disease

It is probable that rotavirus is only mildly
of laboratory rabbits ( Oryctolagus) that
pathogenic, but most rotavims infections
apparently has not been recognized in wild
are complicated with pathogenic bacteria
rabbits (Sylvilagus). A few outbreaks have
such as Clostridium spp or E coli. The been repo1ted in the USA since 1930. The
mixed infection results in a much more
causative vims is closely related to vaccinia
deadly syndrome. There is no treatment, but
virus, and some outbreaks may have been
the infection appeai-s to be self-limiting if
caused by a virulent strain of vaccinia. Pox
susceptible rabbits are not continually introlesions may be present on the skin. Most duced into the population. Expe1imentaJly,
rabbits develop a fever and nasal discharge.

the vims is shed for only 1 wk after

The mortality rate varies but is always high.

inoculation. Therefore, cessation of

The most characteristic lesions seen at
breeding for 4-6 wk seems to allow the
necropsy are a skin rash, subcutaneous
disease to flll1 its comse, because seroposiedema, and edema of the mouth and other tive does do not infect their offspring.

body openings. Because of the edematous
condition, "poxless" rabbitpox may be
confused with myxomatosis. The virus may

Rabbit Calicivirus Disease
be isolated or the infection diagnosed

(Viral hemorrhagic disease)

serologically by methods appropriate to
vaccinia. (See also rox

Rabbit caJicivims disease was first reported

DISEASES, p 867.)

Spread through a rabbitry is rapid, but
in 1984 in tl1e People's Republic of China,
rabbits inoculated with smallpox vaccine
from whence it spread through the domestic

(vaccinia vims) are immune. Rabbitpox
and wild rabbit populations in continental
vims does not infect people.

Emope. The first report of the vims in the

Western hemisphere was in Mexico City in

Papillomatosis

1988. Mexico successfully eradicated
the vims by 1992. Outbreaks of rabbit

Two types of infectious papillomas occur
caJicivims disease have since occurred in
infrequently in domestic rabbits. The oral

Australia (1995), New Zealand (1997), and
papilloma, caused by the rabbit oral

Cuba (1997). In 1995, as a result of a
papillomavims, is the most important
laboratory accident in southern Australia,
clinically. The lesions consist of small,
the virus escaped from quarantine and
grayish white, pedunculated nodules or
killed 10 million rabbits in 8 wk. Rabbit
waits on tl1e undersurface of the tongue or
caJicivims disease was confirmed in a group
floor of the mouth. The second type, caused
of 27 rabbits in Iowa in April 2000 in the
by tl1e cottontail (Shope) papillomavims, is

USA. The source of infection was not
characterized by horny warts on the neck,
determined. The outbreak was contained,
shoulders, eai-s, or abdomen and is
tl1e vims eradicated, and the USA remains
p1imarily a natural disease of cottontail
disease free. Rabbit caJicivims is a
rabbits. Arthropod vectors transmit the
reportable disease in the USA.

1952

RABBITS

Rabbit calicivirus disease is highly
oocysts may also be demonstrated by feinfectious in European rabbits (Oryctola
cal flotation. It is important not to confuse
gus ), but cottontail rabbits and jackrabbits the oocysts with the nom1al yeast (Cyniclo
are not susceptible. People and other
myces guttulatus ), which is commonly
mammals are not affected. The calicivirus is
seen in fecal exantinations.

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highly contagious and can be transmitted by

Treatment is difficult, and control rather
direct contact with infected rabbits or
than cure is expected. Sulfaquinoxaline
indirectly by fomites. Infection results in a
administered continuously in the drinking
peracute feb1ile disease causing hepatic
water (0.04% for 30 days) prevents clin.ical
necrosis, enteritis, and lymphoid necrosis,
signs of hepatic coccidiosis in rabbits
followed by massive coagulopathy and
heavily exposed to E stiedae. However, it
hemorrhages in multiple organs. Rabbits
may not prevent the lesions. Sulfaquinoxashow few clinical signs and die within 6--24
line may also be given in the feed at 0.025%
tu· of fever onset. Morbidity rate is often
for 20 days, or for 2 days out of every 8 days.

lOOOAi, and mortality 600/<r-900Ai. A killed

A single oral dose of sulfadin1ethoxine at 50
vaccine effectively reduced the incidence of
mg/kg, followed by its inclusion in drinking
rabbit calicivirus in Europe in the late 1980s. water at 1 g/4 L for 9 days, was found to Rabbits are vaccinated at 10 wk, and annual
significantly reduce fecal oocyst count.

boosters are recommended.

Because feed-grade sulfaquinoxaline can be
difficult to obtain, liquid sulfaquinoxaline is

PARASITIC DISEASES
used more commonly. Withdrawal time is

10 days for rabbits used for food. Other

Coccidiosis
coccidiostats that may prove to be effective

Coccidiosis is a common and worldwide
include a.mproliun1 (9.6% in water or 0.5
protozoal disease of rabbits. Rabbits that
mU500 mL), salinomycin, diclazuril, and
recover frequently become carriers. There
toltrazuril. A single oral dose of toltrazuril at
are two anatomic fonns: hepatic, caused by

2.5 mg/kg or 5 mg/kg has also significantly

Eimeria stiedae, and intestinal, caused by
reduced oocyst count. Treatment is best

E magna, E irresidua, E media, E per
adntinistered for a mini.mw11 of 5 days and
forans, Eflavescens, E intestinalis, or
repeated after 5 days. Rabbits treated
other Eime1ia spp. Transmission of botl1 the successfully are in1mune to subsequent hepatic and intestinal fo1ms is by ingestion
infections.

of tl1e spornlated oocysts, usually in

Treatment will not be successful unless a
contaminated feed or water.

sanitation progran1 is instituted simultaneously. Elimination of fecal-oral transmis

Hepatic Coccidiosis: Severity of disease
sion of infective oocysts is achieved by
depends on the munber of oocysts ingested.

preventing feed hoppers and water crocks

Young rabbits are most susceptible.

from becoming contaminated with feces.

Affected rabbits may be anorectic and have

Hutches should be kept dry and the
a rough coat. Hepatic coccidiosis is nJost
accwnulated feces removed frequently.

often subclinical, but growing rabbits may

Wire cage bottoms should be brushed daily
not make normal gains. Infrequently, death
with a wire brnsh to help break the life cycle
may follow a short course. Rabbits usu-
of the protozoa. Anunonia ( 1 (JOA,) solution is
lethal to oocysts and is the best choice to
ally succumb within 1 mo after a severe
disinfect cages or ancillary equip1i1ent
experimental exposure. At necropsy,
exposed to fecal mate1ial.

small, yellowish white nodules are found
ttu·oughout the hepatic parenchyma. In
the early stages, they may be sharply de

Intestinal Coccidiosis: This fonn of
marcated, whereas in the later stages they
coccidiosis can occur in rabbits receiving
coalesce. The early lesions have a milky
the best of care, as well as in rabbits raised
content; older lesions may have a more
under unsanitary conditions. Typically,
cheese-like consistency. Microscopically,
infections are mild, and often no clinical
signs are seen. In early infections, there are
the nodules are composed of hypertrofew lesions; later, the intestine may be phied bile ducts or gallbladder. Diagno-thickened and pale. Good sanitation
sis of this form of coccidiosis is based
programs that can eliminate hepatic
on the gross and microscopic changes,
coccidiosis do not seem to eliminate
along with demonstration of the oocysts
intestinal coccidiosis. Intestinal coccidiosis
in the bile ducts. An impression smear of
is generally diagnosed by fecal flotation and
a lesion in tl1e liver examined under light
microscopic identification of tl1e oocysts
microscopy often reveals oocysts. The

(species). It is important to distinguish

RABBITS

1953
coccidian oocysts from the nonpathogenic
dan1age the inner ear, reach the CNS, and
yeast Cyniclomyces giiltulatus that can
result in torticollis (seep 1945). The brown also be found in large numbers. Treatment is crwnbly exudate should never be removed similar to that for hepatic coccidiosis
in a conscious rabbit, because this is very
except that sulfaquinoxaline is given for 7
painful. The crusts will slowly slough off as
days and repeated after a 7-day interval.

the mites die and the tissue underneath

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heals. The incidence is much lower when

Larval Worm Infection
rabbits are housed in wire cages instead of

Although adult tapeworm infections are
solid cages. The mite is readily transmitted
rare in domestic rabbits, the discovery
by direct contact. Rabbits should be treated
of larval tapeworm cysts on the serosal
systemically with any of the miticides
peritoneum is common. Rabbits are
approved for use in dogs and cats. A variety
intem1ediate hosts for two species of canine of injectable ivennectin treatment regimens tapeworm, Taenia serialis and T pisi
effective against both fur and ear mites have
formis. Although T se1ialis is rare in been reported, with the dosage of ivennecdomestic rabbits, it is somewhat more tin 200-400 mcg/kg, SC, two or three
common in wild ones. The larval stage of T
treatments 10-21 days apart. Mites may also
pisiformis, a cysticercus, is found attached be treated with selamectin (20 mg topically
to the mesenteries. Before forming these
every 7 days has been effective).

fluid-filled cysts, the young larvae migrate

Fur mite infestations are common, and
through the liver, where they leave white,
two genera, Cheyletiella andListrophorus,
tortuous subcapsular tracts. Generally,
are found worldwide. A nwnber of different
there are no clinical signs, and diagnosis
species of the genus Cheyletiella are found on occurs at necropsy. Treatment is usually not
rabbits. The most conunon in North Ame1ica
attempted, but control is accomplished by
is C parasitovorax. The genus Listrophorns restricting access of dogs (the final host of
has but one species, L gibbus. TI1ese mites the tapewonn) to the area in which food
live on the surface of the skin and do not
and nesting material are stored. Mebendacause the intense pnuitus seen with sarcoptic zole at lg/kg of feed (50 mg/kg) for 14 days
mange. Fm mite infestations usually are
is reported to be an effective treatment.

asymptomatic unless the rabbit becomes

Baylisascmis procyonis has been
debilitated. Cheyletiella may be noticed as reported in rabbits. Signs are similar to

"dandruff." Scraping the dandruff onto a dark those induced by Encephalitozoon
paper or background will demonstrate the
cun'iciili. No treatment is available.

"walking dandruff," as Cheyleti,ella is called.

Transmission is by direct contact. Diagnosis
is accomplished by skin scraping and light

Ectoparasites
microscopy. Cheyletiella mites may cause a

The ear mite Psoroptes cuniculi is a
mild dermatitis in people, especially on the
common parasite of ra.bbits worldwide.

anns. Weekly dusting of animals and bedding

Mites irritate the lining of the ear and cause
with pennethrin powder can control
serun1 and thick brown crusts to accumu

Cheyletiella mites.

late, creating an "ear canker." Infested

Rabbits are rarely infested with either
rabbits scratch at and shake their head and

Sarcoptes scabiei or Notoedres cati. These ears. They lose weight, fail to produce, and
mites burrow into the skin and lay eggs.

suffer secondary infections, which may

The rabbits are extremely pruritic, and
the parasites are difficult to eliminate
on domestic rabbits. The condition is
extremely contagious and can be transmitted to people.

Fleas of the Ctenocephalides Jelis,

C can is, and Pulex irritans species can affect rabbits and many other animals.

Imidacloprid is a flea a.dulticide; the feline
dose should be divided in two or three
spots to treat rabbits infested with fleas.

Fipronil is contraindicated for use in
rabbits because of potential toxicity. Flea
collars a.re also not recommended. It is
important to also treat every cat and dog in

Gross lesions of Psoroptes cuniculi in a rabbit.

the house, because the original host is not

Courtesy of Dr. Louise Bauck.

usually the rabbit.

1954

RABBITS

Encephalitozoonosis
examination of the feces. Single treatments

Encephalitozoon cuniculi is a widespread
are not very effective, because the life cycle
protozoa! (microsporidian) infection of
is direct and reinfection is common.

rabbits and occasionally of mice, gwnea

Piperazine citrates in the water (3 g/L) for
pigs, rats, and dogs. Usually, no clinical
alternating 2-wk periods or fenbendazole

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signs are seen, but a few rabbits develop

(50 ppm in feed for 5 days) are effective
mild chronic renal disease. Some develop
treatments. Rabbit pinworms are not
bra� lesions that may result in convulsions,
transmissible to people.

tremors, or head tilt. Head tilt is often caused
by bacterial infection with Pasteurella

NONINFECTIOUS DISEASES
multocida; this can be difficult to distinguish from head tilt associated with E

Broken Back
cuniculi infection, because both infect10ns are common and can occur together. The

Fracture or dislocation of lumbar vertebrae
mode of transmission is not definitively
with compression or severing of the spinal

!mown but the organism is shed in the
cord is common in both pet and commercial
urine �d potentially can infect the fetus in
rabbits. The predisposition to a fractured
utero. It seems to be mildly contagious in a
back highlights the in1portance of adequate
rabbit1y. At necropsy, the most significant
and proper restraint skills by the handler. If
macroscopic lesion is pitting of the kidneys.

a rabbit struggles during restraint, it is often

Microscopic lesions consist of focal
best to carefully release the grip and relax
granulomas and pseudocysts in the brain
the rabbit instead of fighting against the
and kidneys. Sometin1es a severe, focal,
forceful movements of the scared animal.

interstitial nephritis is seen. In some cases,

Common signs include posterior paresis or
an ocular manifestation is a key clinical
paralysis and urinary and fecal incontinence
presentation, and lesions range from
due to loss of sphincter control. Irnt1al signs
phacoclastic uveitis to mature cataracts.

of paralysis may resolve within 3-5 days as

Diagnosis is made by histologically
swelling around the cord diminishes.

identifying the lesions (pseudocysts) and

Supportive therapy includes anti-inflanunaobserving the organisms when stained tory medication to reduce dan1age from
with Giemsa, Gram, or Goodpasture carbol
swelling. In acute cases, methylprednisofuchsin stains. Several serologic and skin lone sodium succinate might be beneficial.

tests are helpful in screening rabbits for

The rabbit should be hospitalized and
antibodies to the organism, but positive
medical treatment, including pain
serology only indicates past infection and
management, IV fluid therapy, nutritional
does not confirm a diagnosis. Effective
support, and cage rest should be initiated;
treatment has not been established. Some
with this approach, the severe clinical signs
evidence suggests that oxibendazole or
of paraplegia can gradually resolve over 3
albendazole (20-30 mg/kg/day, PO, for 7-14
mo of conservative therapy. Although these
days, then 15 mg/kg/day, PO, for 30-60 days) cases may appear "hopeless," rabbits can or fenbendazole (20 mg/kg/day, f'.O, for 28
in1prove to the point of being able to
days) may be effective. Prevention entails
voluntarily move both hindlin1bs and to
good sanitation and possibly serologic
ambulate by walking and hopping. Intense
screening of breeding stock WI th ehmmanursing and management are required.

tion of positive reactors. A differential
diagnosis in rabbits with outdoor access is

Cannibalism
an aberrant migration of Baylisascaris spp

Young does may kill and eat their young for
into the nervous system. Encephalitozoonoseveral reasons, including nervousness, sis is an emerging disease of in1munodefineglect (failure to nurse), and severe cold.

cient people.

Dogs or predators entering a rabbitry often
cause nervous does to kill and eat the

Pinworms
young. Cannibalism of the dead young

Passalurus ambiguus, the rabbit pinwom1, occurs as a natural, nest-cleaning instinct.

usually is not clinically significant but often

If all management practices are proper
is upsetting to owners. It is common in
and the doe kills two litters in a row, she
many rabbitries and is distributed
should be culled.

worldwide. Transmission is by ingestion
of contaminated food or water. The adult

Dental Disease
worm lives in the cecum or anterior colon.

Dental disease may present as excess

Diagnosis is made by observing the adults at salivation (slobbers), teeth grinding, or necropsy or by fmding the eggs during
anorexia. Oral examination and palpation

RABBITS

1955
along the ventral surface of the jaw should

Extraction of cheek teeth involves
be a part of routine physical examinations
delicate elevation and luxation if the dental
of rabbits. Dental abscesses may develop as
anatomy is nom1al. Extraction of multiple
a consequence of foreign bodies (eg, plant
cheek teeth carries a very poor prognosis
material embedded between the tooth and
for recovery, although some pet rabbits do

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gum), pulp exposure after tooth trimming,
well with very few molars if the diet is
inappropriate diet, or other diseases. Dental
suitably modified. Continued monitoring
abscesses also may appear as retrobulbar
of the occlusal smiace and followup
abscesses. Hence, a rabbit that presents for
adjustment is expected. Pain management
primarily ophthalmologic signs such as
and extended-duration ( 4 wk to months)

epiphora or exophthalrnus should receive a
systemic antibiotic therapy based on culture
fuJJ dental examination. Rabbit incisors may and sensitivity are indicated.

wear differently depending on diet, and a
pelleted diet may predispose the rabbit to

Dental Malocclusion: The incisors,
dental disease. Multiple teeth are commonly premolars, and molars of rabbits grow affected. A thorough oral examination
throughout life. The normal length is
under heavy sedation or full anesthesia and
maintained by the wearing action of
diagnostic radiographs are indicated. Often,
opposing teeth. Malocclusion (mandibular
a skull CT provides significantly more
prognathism, brachygnathism) probably is
infonnation because of the complexity of
the most common inherited disease in
the lesions and the 30 structure of the head
rabbits and leads to overgrowth of incisors

( which is difficult to fully image with plain
witl1 resultant difficulty in eating and
radio graphs).

drinking. Dental trinlming is often done

Dental extractions may be accomplished
witl1 combined anesthesia of diazeparn (1-5
using a fine-tipped dental elevator worked
mg/kg, IM) followed by or in combination
along the root to free the tooth. Incisors are
with ketanune (10--20 mg/kg, IM), or a
curved and require use of a specialized
combination of ketamine and dexrneditomirabbit incisor luxator or similar curved dine (seep 1939).

instrument for removal. Curettage of the

Occasionally, the cheek teeth overgrow
alveolus to destroy the apical genninal
and cause severe tongue or buccal lesions.

tissue is required to prevent regrowth of

Because malocclusion is generally consithe tooth. Regrowth is unlikely if the pulp dered to be inherited, rabbits with this
remains in the extracted tooth, but followcondition should not be bred. However, up radiographs in 2-3 mo will confinn
young rabbits can damage their incisor
successful extraction. After lavage, infected
teeth by pulling on the cage wire, which
sockets can be filled with doxycycline
results in misalignment and possibly
periceutical gel or antibiotic-impregnated
malocclusion as the teeth grow. This
polymethyl methacrylate (PMMA) beads.

condition is difficult to differentiate from

PMMA beads are sometimes available
genetic malocclusion, and these rabbits
from compounding pharmacies or can be
should also be culled. Genetic malocclusion
self-manufactured. Care has to be taken to
generally can be detected in rabbits 3-8 wk
choose an antibiotic that is heat stabile ( eg,
gentanucin) in the beads. Other treatment
options include leaving the surgical site
open and marsupializing the skin to allow
healing by secondary intention and to
facilitate local antibiotic therapy. Antibiotics
can be instilled into the open wound by eye
drops or by packing the wound with
antibiotic-impregnated gauze. Gingival
tissues can be sutured closed if needed or
can remain open to avoid development of an
anaerobic environment. It is important to
avoid any cutting of the teeth with wire
cutters or even dental pliers. The pressure of
such cutters can be transnutted through the
tooth and fracture the whole tooth, which
will result in further problems. An elongated
tooth should always be drilled down by a

Severely overgrown incisor teeth in a rabbit.

dedicated dental burr. Defect treatment witl1

If younger animals, the cause (eg, brachygcalcium hydroxide paste results in tissue nathia) is often genetic. In older animals, the
cheek teeth are often part of the problem.

necrosis and is contraindicated.

Courtesy of Dr. Joerg Mayer.

1956

RABBITS
old. If incisors are suddenly overgrown in
the fiber or feeding hay along with the
an adult rabbit, it is not enough to trim the
pellets. Adding magnesium oxide to the diet
incisors down. The problem commonly
at 0.25% also may be helpful. In some cases,
originates in the back of the mouth, and
hair chewing is a result of boredom because
a full assessment of the cheek teeth is
of lack of fiber or chew substrate. Providing
warranted. The dental procedure needs to
environmental enrichmertt often halts this

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be done under full anesthesia and with
behavior.

special equipment. Rabbit dentistry is very

The hair becomes a problem only if
different from that in dogs and cats because
excess an10unts are consw11ed or if it
of the differences in anatomy and physiolaccw11ulates in the stomach and blocks the ogy. Special training and literature about
pylorus. If this happens, the rabbit becomes
rabbit dentistry is readily available, and
anorectic, loses weight, and dies within
dental procedures in rabbits should be

3-4 wk. Premortem diagnosis of pyloric
perfmrned only by those with specific
obstruction can be difficult, because
training.

palpable hairballs can be an incidental
finding and radiography is often nondiag

Gastric Stasis, Hair Chewing, and
nostic.

Hairballs

Once GI stasis affects the emptying of the
stomach, gas accLm1ulation creates further

The GI tract of the rabbit is similar to that of
visceral distention and pain. The resulting
the horse, with an anatomy and physiology
decreased food intake and GI hypomotility
that often leads to clinical complications.

cause an increased cecal pH and altered

One of the most frequent presentations is
cecal microflora, creating cecal dysbiosis.

gastric stasis, which has a variety of causes,

Alterations in water and electrolyte balance
including stress and/or pain. The initial
result in systemic ketoacidosis and hepatic
phase of the problem commonly goes
lipidosis. Gastric ulceration and even
unrecognized by the owner or untrained
gastric rupture may occur.

veterinarian. Because they are a prey

The goals of treatment are to remove
species, rabbits do not overtly show signs
the obstruction, stimulate motility, restore
of discomfort or pain and remain quiet and

GI microorganism balance, and relieve
inactive. Rabbits are commonly presented
dehydration and anorexia. Most cases can
in an advanced state of stasis that has
be managed by aggressive fluid managealready led to dehydration, pain, and hepatic ment (maintenance is 100-120 rnllkg/24 hr), lipidosis. Decreased food intake has a large
with affected rabbits receiving double the
impact on the health of rabbits and affects
rate of maintenance fluids (10 mllkg/hr)

many other factors of homeostasis. When

IV. Pain medication ( eg, oxymorphone
food intake is decreased, water intake is

0.2 mg/kg every 4-6 hr) is essential to
also conunonly decreased. The GI contents
relieve the GI discomfort. With aggressive
lose the typical slurry-like consistency and
fluid and pain management, the rabbits
become pasty. As the rabbit becomes
usually feel better within 24 hr. Because
dehydrated, water is absorbed from the GI
the GI tract is either full or distended with
tract into the vascular space, which masks
contents, oral force feeding should be
the typical hematologic signs of dehydration
discouraged. Energy can be provided by

( eg, no increase in PCV). A decrease in
adding dextrose to the IV fluids. Food
energy uptake will produce hepatic lipidosis should be ava.i.lable at all times and in relatively quickly in rabbits, which in turn
different forms c eg, hay, vegetable matter,
decreases food intake. It is of utmost
supportive care formula). Rabbits often
importance to realize the seriousness of the
start to eat on their own after they are
condition and to counteract the downward
properly hydrated and received analgesia
spiral.

for visceral pain. If the rabbit does not eat

Rabbits groom themselves constantly,
because of advanced stages of hepatic
so the stomach contents often contain
lipidosis, assist syringe feeding should
hair. When the GI contents are of normal,
be started. Once a true GI obstruction has
slurry-like consistency, the hair nom1ally
been excluded, treatment can then include
passes through the GI tract and is excreted
a motility stimulant such as metocloprawith the fecal pellets. A high-fiber di.et helps mide (0.5 mg/kg, PO or SC, tid-qi.d) or
to create a fiber mesh that prevents the GI
cisapride (0.5 mg/kg, PO, bid-ti.cl); however,
contents from becoming too dense so that
this should not be started before hydration
hair can more easily pass through the upper
and pain management. Reestablishment of

GI tract along with the mesh of fiber. Hair

GI microflora may be assisted by probiotic
chewing is generally a result of low fiber in
treatment or cecotrophs from healthy
the diet and can be corrected by increasing
rabbits.

RABBITS

1957

Mineral oil and laxatives do not effecadequate sphincter control of the bladder tively remove the hair mass. Roughage Q1ay
constantly dribble urine and may be
or straw) should be fed during the treatment affected. The membranes of fue anus to help carry the hair fibers through the GI
and genital region become intlamed and
tract and out with the feces. Surgical
chapped. The area soon becomes secondartreatment should be considered only if ily infected with opporttmistic pathogenic

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medical management has not resulted in
bacteria. Brownish crusts cover the area,
improvement.

and a hemorrhagic, purulent exudate may be

Prevention of GI stasis is the best option
present. Keeping hutch floors clean and dry
and can be accomplished by providing a
and applying nitrofurazone or an antibiotic
high-fiber diet, avoiding stress and obesity,
ointment to fue lesions hastens recovery.

providing environmental enrichment, and
combing daily to remove loose hair. Rabbits

Ketosis
also consume significantly more water
when offered by bowl vs sipper bottle. Clini

(Pregnancy toxemia)

cal research does not support routine doses Ketosis is a rare disorder in rabbits that of mineral oil, wetting agents, or proteolytic
may result in death of does at or 1 -2 days
enzymes as effective preventives.

before kindling. The disease is more common
in first-litter does. Predisposing factors

Heat Exhaustion
include obesity and lack of exercise. The

Rabbits are sensitive to heat. Hot, humid
probable cause is starvation. Oilier signs are
weather, along with poorly ventilated
dullness of eyes, sluggishness, respiratory
hutches or transport in poorly ventilated
distress, prostration, and death. The most
vehicles, may lead to the death of many
significant lesions are fatty liver and kidneys.

rabbits, particularly pregnant does.

The body mobilizes fat and transports it

Affected rabbits stretch out and breathe
to fue liver to be broken down for energy,
rapidly. Hutches should be constructed so
tlms fue fatty liver. Diagnosis depends on a
that they can be sprinkled in hot, humid
detailed history and physical examination
weather. Free access to cool water should
and clinical signs. A key clinical sign is clear
be provided. When the environment can
urine; the urine of healthy rabbits is usually
be controlled, optimal conditions are a
cloudy. Injection of fluids that contain
temperature of 50° -70°F (15.5° -21 °C) and
glucose and assisted syiinge feeding may
a relative hwnidity of 40%-60%, with 10-20
help correct the disease. Breeding young
air changes/hr. Wire cages are preferable
does early, before they become too fat, is
to solid hutches. Treatment consists of
also helpful. Hairballs in fue stomach are
immersing rabbits in cold water during the
often a factor in ketosis.

heat of the day, especially those that will
kindle in the next day or two. Breeding

Moist Dermatitis
bucks may lose a majority of viable sperm

(Wet dewlap)

and might not breed successfully for
several weeks until new sperm production

Female rabbits have a heavy fold of skin on
replaces the sperm killed by thermal
tl1e ventral aspect of fue neck. As fue rabbit
stress.

drinks, tl1is skin may become wet and soggy

("slobbers"), which leads to inflan1mation.

Contributing factors include dental malocclu

Hutch Burn
sion, open water crocks, and clamp bedding.

(Urine burn)

The hair may slip, and fue area may become

Prolonged irritation of the bladder mucosa
infected or flyblown. The area often twns
wifu calciwn sediment can cause a cystitis
green if infected wifu Pseudomonas spp.

fuat can manifest in incontinence and soiled

Automatic watering systems wifu drinking
fur (seep 1959). A wet perianal area often
valves generally prevent wet dewlaps. lf open
causes additional problems such as fly strike water receptacles are used, fuey should have and dennatitis. This condition is often
small openings or be elevated. Once fue area
referred to as hutch bum, Hutch bum is
is infected, fue hair should be clipped and
often confused with treponematosis and can antiseptic dusting powder applied. In severe be truly differentiated only by the absence of cases, parenteral antibiotics and analgesics spirochetes on darkfield microscopy and by
are necessary.

the lack of antibodies to Treponema
paraluiscunicul'i. It is caused by wet and

Ophthalmologic Disease
dirty hutch floors and affects the anus and

Corneal ulceration is fue most common
external genitalia. Also, rabbits fuat lack
ophfualmic problem of rabbits. Rabbits

1958

RABBITS
appear predisposed to this condition for
organisms on histopathology of excised
two main reasons: 1) the globe and surface
tissue or DNA probe on removed lens
of the cornea are significantly larger in
material. Treatment involves lens removal
rabbits than in most other domesticated
by phacoemulsification or enucleation.

pets, and 2) rabbits do not blink as

Spontaneous lens regeneration may occur.

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frequently as other species, which leaves

Prosthetic lens insertion is not recomthe cornea less moist. Many potential mended. The prognosis is guarded without
underlying issues should be excluded,
smgery; glaucoma develops in most
although environmental causes and trauma
affected rabbits. Topical treatment includes
are the most frequent causes. The cornea

NSAlDs and mydriatic and antibiotic
should be carefully protected dw'ing
medications. After starting topical
anesthetic procedures. The lack of tear
medications, progress and intraocular
production associated with keratocortjuncpressw·e should be checked in 5--7 days.

tivitis sicca or dry eye may further increase

Monitoring should continue eve1y 2--3 wk
the risk of corneal damage. Exophthalmia
for the next 2 mo. Systemic therapy for
as a result of orbital or dental disease or

Encephalilozoon should be sta.Jted.

facial paralysis associated with encephalito

I.nherited glaucoma is discussed below
cytozoonosis can make blinking difficult

(see below).

and lead to corneal damage. Superficial
ulcers can be treated with broad-spectrun1

Ulcerative Pododermatitis
ophthalmic antibiotic solutions. Treatment
progress should be assessed in 1-2 days.

(Sore hocks)

Epithelial "lips" indicate a nonhealing ulcer.

Ulcerative pododermatitis does not involve

Such ulcers should be debrided after
the hock but the plantar surface of the
application of a topical anesthetic, followed
metatarsals and, less commonly, the volar
by the same treatment as for a superficial
surface of the metacarpal-phalangeal region.

ulcer. If the ulcer does not respond to

The cause is either pressure on the skin from
topical treatment, collagen shields or even
bearing the body weight on wire-floored
contact lenses have been used successfully.

cages or trawna to the skin from stamping,
ln severe cases, surgery and placement of a
with secondary infection of the necrotic
co11junctival pedicle graft may be required.

skin. Several factors, including accumula

Differential diagnoses of corneal lesions in
tion of urine-soaked feces, ne1vousness,
rabbits include corneal occlusion (overposterior paralysis after a spinal cord iajury, growth of coajunctival tissue) and limbic
and the type of wire used, may influence
or corneal dermoid ( skin-like tissue in an
development. Genetics are also involved.

abnormal location over the cornea). Hair

The Rex appears to be predisposed because
may protrude from a limbic dermoid. These
of the lack of the longer guard hairs that
growths do not appear painful.

usually act as a cushion over the predis

Pseudopterygium, an aberrant growth
posed area of the hock. Heavy-breed rabbits
of cor\junctival membrane tissue, is
such as the F1emish Giant and the Checksometin1es seen in rabbits. The cause is ered Giant are also susceptible. Affected
not known, and tl1e condition is slbwly
rabbits sit in a peculiar position with their
progressive. The coajunctival membrane
weight on their front feet; if all four feet are
extends from the bulbar cortjunctiva and
affected, they tiptoe when walking. Various
slowly grows onto the cornea, giving the eye debridi.ng agents can be used t9 clean the an opaque appearance. Sw·gical removal of
lesion, followed by topical antibiotic
the overgrown cortjunctiva is straightfortreatment along with parenteral antibiotics.

ward but leads to recurrence. Daily

Radiographs exclude osteomyelitis witl1
administration of topical cyclosporine 0.2%
severe lesions. The rabbit must be removed
in the affected eye might help slow down
from the cage or given a solid tloor (board or
recuJTence.

mat) on which to sit or rest. Treatment is

Phacoclastic uveitis secondary to
often difficult and time consuming, with

Encephalilozoon cuniculi (seep 1954) has
application of bandages that need frequent
been recognized to present as iridal swelling changing. Low-level laser therapy has shown and white or pink nodules on the iris. The
some benefits and is encouraged. Husnodules are bacterial iridal or corneal bandry in1provement should focus on
stromal abscesses and give tl1e typical
providing soft, dust-free bedding. ln many
appearance of cotton candy in the anterior
cases, weight management is also indicated.

chamber. Spores replicating in tl1e lens may

Because large feet and thick footpads are
result in cataract forn1ation and even lens
hereditary, selection of breeding stock for
rupture, leading to a painful uveitis.

these traits has reduced the incidence of

Diagnosis is confumed by presence of the
pododermatitis.

RABBITS

1959

Urolithiasis
also is seen in the breeding herd. A correct

Urolithiasis is seen routinely in pet rabbits
assessment of vitamin A becomes critical in
and occasionally in commercial rabbitries.

treatment, and both serum and liver should

It is generally suspected when hematuria is
be analyzed. In deficiency, tile serum level of

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seen. (A dipstick can quickly exclude
vitamin A is below normal (2.6-4.2 lU/mL).

normal pigment causes of red urine.) The
ln tox.icosis, the serw11 level can be normal
rabbit
but the concentration of vitamin A in the '

's calcium metabolism is significantly
different from that in other vertebrates.

liver is ve1y high (>4,000 lU/g). Treatment

Rabbits do not require vitan1in 0
of the deficiency involves increasing tile

3 to absorb
calciw11 from the gut into the bloodstream.

carotene content of the diet or adding a

The vast majority of dietary calciWll is

VItanlin A supplement. Treatment of
readily absorbed into the bloodstream
hypervitanlinosis A requires reducing
leading to relatively higher blood calci�
vitamin A i.n the diet. However, reducing t11e
levels (up to 16 rng/dL [4 mmol/L] can be
amount of vitamin A stored in tl1e liver i.s
normal). Renal elimination of calciWll is
extremely di.fficult. If tile doe's reproduction
much higher in rabbits (as high as 600A,) than
has been in1paired, replacing the doe is
in other ve1tebrates (2%-5%). This often
probably more cost-effective tilan ttying
gives the wine a cloudy appearance which
to decrease the vitanlin A level. Because
is non11al. Feeding a calciw11-rich di�t for a
genetic hydrocephalus appears to be
prolonged time to a metabolically inactive
inhe1ited recessively, conb·ol requires
rabbit (ie, not growing, pregnant, or
culling both parents.

lactating) can lead to an abnom1al
hypercalciuria, and calcium can precipitate

Bupht.halmia (Blue Eye, Moon Eye,
out as bladder sludge or form uroliths. Small Infantile Glaucoma): BuphthaJmia is an stones are often voided, but surgery is
autosornal trait witil incomplete peneb·ance
frequently needed to remove larger tuinary
that results in variable clinical severity.

stones. Urolitlls are caused by calciWll

Intraocular pressures begin to rise as early
carbonate and triple phosphate crystals
as 3 mo. One or both eyes may be affected.

precipitating out of normal wine when the

Glaucoma can be treated medically
pH increases to 8.5-9.5. Normal rabbit Uiine

( dorzolanlide 2%; l drop tid) or by surgical
has an average pH of8.2. Several factors
enucleation. Affected rabbi.ts should not be
have been incriminated in urolithiasis
bred.

including nutritional imbalance ( espe�ially
the calciU111:phosphorus ratio), genetic

Splayleg: Splayleg is presW11ed to be
predisposition, infection, inadequate water
an inherited disorder presenting with
intake, and metabolic disorders. Short-ten11
abduction of one or more legs as early as
treatment involves surgically removing the

3-4 wk of age. The right rear limb is most
uroliths, whereas longterm treatment
commonly affected, although tile conditioi1
focuses on reducing dietary calciWll intake.

may be unilateral or bilateral. Hip dysplasia

Because alfalfa is high in calcium and one
can occur during posblatal development
of til
among rabbi.ts housed on slick nest boxes

� main dietary components of regular
rabbit pellets, switching to tin1othy-based
orfloming.

pellets and to grass or timothy hay and
rolled oats helps to prevent recurrence.

Neoplasia

By far, tile most common tWllor in rabbits is

Heritable Diseases
uterine adenocarcinorna. The incidence can

Hydroce_phalus: Hydrocephalus,
be as high as 60% in intact does >3 yr old.

characterized by an enlarged head , is

The disease may present witil multicentlic
occasionally seen in neonatal rabbits. The
tt.m1ors tl1at involve both horns of tile
top of the skull appears dome-shaped, and
uterus. The masses can often be palpated as
tile fontanelle is wider tilan normal. Most
globular polypoid structures. The tW11or
affected rabbits are born dead; occasionally
often metastasizes to tl1e liver lungs and
tiley live for several weeks but generally
other organs; cystic rnastitis n;ay de;elop
exhibit neurologic sigllS. At necropsy, the
concurrently. This disease is tile primary
brain is enlarged; on cut section, the
reason to recommend spaying of nonbreedventricles are greatly enlarged and filled ing female rabbits at the age of 4-6 mo.

witl1 CSF. The cause can eitiler be genetic or

Lymphoma and otl1er neoplastic disorders
result from dietary deficiency or excess of
of lymphoid tissue are common tw110rs tl1at
vitamin A. ln tile case of a dietary deficiency
occur in all ages of pet rabbits. Malignant
or hypervitanlinosis, poor reproduction
lymphomas (lyrnphosarcorna) are relatively

(low fettility, small litter size, abortion, etc)

common and may occur in rabbits <2 yr old.

1960

RABBITS

The manifestation can be extremely vaiied,
or permanent exophthalmos. Because of
ranging from ocuJai· lesions, to skin, to
the impaired venous return from the head
leukemic fo1ms. Lymphosarcoma presents
through the chest, the venous sinuses
with a tetrad of lesions, including enlarged
behind the globe expand and cause the
kidneys, splenomegaly, hepatomegaly, and
exophthalmos. A chest radiograph to scan
lymphadenopathy. Treatment of lymphoma
for masses should be perfoqned in all
can be attempted by chemotherapy, but
rabbits with exophthalmos. The thyrnoma

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prognosis is often poor due to the often
can sometin1es be removed surgically
aggressive form of the disease. Rabbits
relatively easily, because it does not involve
can be treated with "typical" chemotheraother major structures in the chest cavity.

peutic agents, ai1d adverse effects to these

In the case of thyrnic lymphoma, surgery is
drugs appear less common than in other
often less successful, because the structure
domesticated pets. Thyrnoma and thymic
is often not possible to be removed in toto.

lymphoma are the most common mediasti

Radiation of the thorax has been desc1ibed
nal masses in rabbits. Differentiation
as an effective therapy, and animals have
between the two is difficult and usually
smvived for yeai-s after the treatment. If
requires a fine-needle aspirate or a biopsy
no advanced therapy is an option, oral
of the chest mass. The typical clinical sign
prednisolone has been used in a few cases
for a chest mass in rabbits is intermittent
with moderate success.

RATITES

Twelve species of birds ai·e grouped as

Greater Rheas (Rhea americana) include
ratites, not including the order Tinantifive subspecies, and the Lesser Rheas (Rhea formes. These include the ostrich, emu,
pennata) include three subspecies. Sin1ilai·
rhea, cassowary, and kiwi. The ostrich, emu, to emus, rheas have brown to gray-brown and rhea ai·e the ratite species primarily
feathers.

raised in production facilities, whereas all
may be fom1d in zoo collections. The ostrich

MANAGEMENT

01iginated in Africa and has been commercially raised since 1850 for feathers, meat, Physical restraint of ratites is different for
and hide products. The emu is native to
each. The ostrich's head can be caught by

Australia and has been raised for meat, oil,
hand or hook, and a hood can be placed
and leather in many countries around the
over the head. Once hooded, the ostrich's
world, including the USA. The �outh
head should be maintained below the level

American rhea has been produced prin1arily
of its body to restrict it from kicking its legs
for feathers.

forwai·d. An ostrich kick cai1 seriously

Ostriches (Strulhio camelus) are the
injure a handler and, once captured, the
largest members of the ratite group. Mature
bird will quickly try to back.up and kick
ostriches may stand 2.4-2.8 m tall and weigh anyone in front of its body. Because an up to 160 kg, although most ai·e 65-130 kg.

ostrich will back up when its head is held,

Males are black and white, females ai·e
an assistant should be positioned behind
brown.

the bird to push as the person holding its

Emus (Drnmaius novaehollandiae) are
head leads the ostrich forward. Emus must
second only to ostriches in size, measuring
be handled from behind, grasping the
up to 2 m tall and weighing 18--48 kg. Female wings and lifting the bird slightly upward emus are typically larger than males. Both
and back. The front of the bird should be
females and males have brown to grayavoided to prevent being injured by the brown plumage with black feather shafts
claws on the feet, because, as with all
and tips. Emus are flightless but travel at a
ratites, emus will kick forward to try to
quick trot and can sprint at speeds up to 51
escape. Rheas are handled much like emus.

km/hr.

Some handlers use hoods to facilitate

Rheas can reach l. 7 m in height and 40 kg
handling emus and rheas, although this
in weight. They are native to South America
technique is not as effective as it is with
and are divided into two species: the
ostriches.

RATITES

1961

Juvenile birds from 4 mo to yearlings are
side of the wings and the medial metatarsal
best handled by slowly and calmly herding
veins. In emus, the jugular vein and medial
them into an enclosed barn. If they cannot
metatarsal vein are the blood collection
see out of an enclosure and are crowded into sites of choice. Venipuncture of the jugular·
a comer, they will often sit if not startled.

vein is more difficult in ostiiches because of

When calmly herded into a confined area,
their size and because sudden movement
young birds can easily be sexed, banded,
by the bird can result in lacerations and

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and administered antiparasitic medication,
exsanguination. In debilitated ratites,
and diagnostic samples ( eg, blood) can be
catheterization (adults, 14-gauge, 13-cm
collected. If there is no enclosed area,
catheter) of the jugular vein is easy and
p01table panels with plywood or plastic
provides a readily accessible port to the
applied can be used to herd the birds into
vascular system. The right jugular vein is
the desired space.

more developed than the left.

Physical and Laboratory Examination:

Anesthesia: Chemical restraint for

Before the bird is restrained, it should be
handling and surgical procedures in
examined from a distance while walking/
ratites use typical veterinary drugs.

running in its enclosure for conformation,

Anesthesia may be induced in younger
gait, body condition, respiration rate and
birds with isoflurane or sevoflurane using
character, and behavior-related problems.

the same procedures as with small

The enclosure should be inspected for
animals. Intubation for maintenance is
fresh droppings and urine. Green urates
recommended, but the cuff should not
may be an indication of hepatitis, whereas
be inflated because of the possibility of
dry, hard fecal material is common in birds
pressure necrosis (birds have complete
that are dehydrated or suffering from GI
tracheal rings that do not expand with
impaction. The droppings should be
the tracheal cuff). Xylazine and ketar11ine
examined for tapewom1 segments and
combinations are commonly used for
collected for fecal flotation and direct
short procedures on induction, followed
parasite evaluation.

by intubation and gas anesthesia. Xylazine

The eyes and sinuses are exarnined for
administered at 2.5 mg/kg, IV, followed,
any discharge or swelling, and the beak and
after sedative effect is noticed, by keta
oral cavity exanlined for any lesions. The
mine at 1 mg/kg, is an effective protocol.

neck is palpated, especially in the area of

However, xylazine has significant cardiothe thoracic inlet, for any swellings. Overall respiratory depressant effects and should
body condition should be noted and is
not be used in severely ill birds. Also, xylazine
detemlined by the epaxial muscle mass,
is not recommended as a premedication
rated on a.scale of 1-5, with 1 being
for inhalation anesthesia, because it may
emaciated and 5 obese. The feathers and
greatly enhance the cardiodepressant.

skin are exar1lined for lesions and parasites.

effects of gas anesthetic agents. Recovery

The thorax is auscultated, and heart rhythm
may be smoother if diazepam is given at
and rate are detemlined. The abdomen is

0.2 mg/kg, IV or TM. Tiletamine/zolazepam
palpated from the ventriculus, which lies
is an induction alternative for ratites,
immediately caudal to the breastplate, to
closed at2-10 mg/kg, IM, or 1 -3 mg/kg,
the proventriculus, located between the

IV, with the higher end of the dose range
legs. The caudal abdomen is palpated and
recommended for emus and rheas. Once
balloted for any evidence of coelomic
the bird has been induced, padding should
fluid or retained eggs. Finally, a cloacal
be placed under the body during the entire
examination is performed to verify normal
procedure to minimize neuropathy and
ar1atomy. When indicated, samples for
myositis. Ostriches may develop peroneal
microbial culture can be collected from the
nerve paralysis when placed in lateral
trachea, cloaca, and caudal oviduct, arid
recumbency, without padding, for <l hr.

blood can be collected for a CBC and serum

Sternal recumbency does not appear to
chemistry panel. (For hematologic and
interfere with respiration while anestheserum biochemical reference ranges for tized, but the large body size of ratites may
ostriches, see TABLES 6 and 7, pp 3176 and restrict their ability to breathe. Therefore,

3178). Sodiun1 heparin is the preferred
manual or mechanical respiration is recoar1ticoagulant for both the CBC and serum mmended during general anesthesia to
chemistry panel. A slide should be prepared
reduce the cardiorespiratory depressant
in1mediately for cytologic evaluation.

effects of both gas anesthetic agents and

Recommended sites for venipuncture and physical compression of air sac volume.

catheterization in ostriches and rheas are

The neck should be straight and the head
the cutaneous ulnar veins on the ventral
elevated slightly above the body during

1962

RATITES
general anesthesia. Vital signs of ratites
health and production results, appropriate
should be monitored while under anestheratite feed formulated for ostriches, emus, sia along with body temperature ( esophaand rheas is recommended. Ostriches, geal) to maintain nom1othermia; intravenous emus, and rheas have significantly different access should be established for drug and
digestive systems and specific nutritional

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fluid administration. During recovery, the
requirements for optimal growth, reproducbird should be placed in a dark, quiet, tion, and health. High-quality grass can be
preferably padded enclosure in sternal
used as a grazing supplement for ostriches
recumbency. Wrapping the body with the
and rheas. Chicks allowed to hatch in the
legs immobilized under the animal while in nest are coprophagous, eating feces from sternal recumbency will often allow the
the parents for the first few weeks of life.

bird to recover with minimal struggle.

Vaccination: When indicated in a

Surgical Procedures: Surgical
specific flock, autogenous bacterins for
procedures in ratites generally are related

Salmonella, Escherichia coli, and
to the GI tract, orthopedics, and trauma
clostridial diseases have been used;
repair. Proventriculotomy for foreign body however, this is not a common practice, removal and impactions in ratite species is and these products may be difficult to a common surgical procedure. In young
obtain. For emus, equine encephalitis
birds, incisions should be made carefully,
vaccination is recommended. Tissuebecause the abdominal wall is very thin.

culture propagated, inactivated bivalent

To perform a proventriculotomy, the bird

Eastern and Western equine encephalomyis positioned in right lateral recumbency elitis (EEE, WEE) vaccine prepared and
with the left pelvic limb abducted and
licensed for use in horses, and that may
supported caudally in a stand. In ostriches, contain equine tetanus antitoxin, has the ventriculus is located caudal to the
effectively protected emus against EEE
proventriculus in the coelomic cavity;
and WEE infection. A vaccination protocol
therefore, the surgical incision to access
is to administer IM an initial full equine
this part of the GI tract should be through
dose at 6 wk of age, followed by booster
a left paramedian approach beginning -15
vaccinations at 10 wk of age and at 5- and
cm caudal to the keel. Yolk sac removal

6-mo intervals thereafter and before and
due to nonabsorption and/or infection
after breeding season (April and Septemis common. Egg retention in hens is ber). A booster should be administered
addressed surgically, and often multiple
when EEE or WEE is identified within 10
eggs are removed. Orthopedic surgeries
miles of the production facility or before
are addressed as in other species with
transfer to an endemic area. The recompins, plates, and transfixation casting as mended vaccine protocol (emus) for
needed for fracture repair. Laceration

Clostridium chauvoei (blackleg) using
repair is performed as in other species.

the ruminant vaccine with or without

Upper esophageal tears from attempted
tetanus antitoxin is to administer an initial
hooking (capture) will often heal by
vaccine at 2 mo of age, followed by a
second intention and, unless se�ere,
booster vaccination at 3 mo and then
do not require surgical repair.

annually after the end of breeding season

As in all production anin1als, the cost
in April.

of surgical correction of many conditions
might be greater than the commercial
value of the individual animal presented.

REPRODUCTION

Producers should be made aware of cost
considerations.

Anatomy: All female ratites have a single
left ovary and oviduct. The oviduct consists
of 1) the infundibulum, where fertilization

Nutrition: To date, there has been little
occurs; 2) the magnun1, where the thick
reliable research on ratite nutrition. The
albumin is put on; 3) the isthmus, where the
formulations of commercial diets available
inner and outer shell membranes are added;
are based on studies in Africa and Australia,

4) the uterus, where the shell is added; and
as well as extrapolations from available

5) the vagina. The opening of the vagina into
poultry infom1ation. Current trends are to
the cloaca is on the left side of the cloaca at
feed 14o/o-200/o protein from the time chicks
the ten o'clock position.

hatch to 3 mo of age, reducing the protein

The male ratite has two intra-abdominal
level after 3 mo of age. Ostriches and rheas
testicles located near the kidneys. During
are hindgut fem1enters and have the ability
the breeding season, the testicles increase
to digest fiber from a young age. For optimal

2000/o-3000/o in size. The rooster does not pro-

RATITES

1963

If eggs are wet or dirty, they should be
washed in a warm l l0°F ( 43.3°C) disinfectant solution ( eg, chlorhexidine, sodimn hypochlorite, quaternary anirnonia) before cooling.

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Commercial incubation of eggs is
performed in forced air incubators.

Ostrich eggs generally are incubated at

97°F (36.1 °C) for 40-42 clays and moved to
the hatcher at 40 days or when the chick

"pips" (breaks the egg). Emu eggs are
incubated at 97° -98°F (36.1 ° -36. 7°C) for

Ostrich semen. Courtesy of Dr. Karen Hicks·

54-58 days and moved to the hatcher at

Alldredge.

50-52 days or at "pipping." Rhea eggs are
incubated at 98°F (36. 7°C) for 40 days and
moved to the hatcher at 38 days or at
duce spenn when not in season. Roosters

"pipping." While temperature in the
in the ratite family all have a phallus that
hatcher is the same as incubation, the
serves to transport semen from the
humidity should be higher.

ejaculatory ducts in the cloaca of the male

For optimal perfom1ance of hatchery
to the cloaca of the female. The phallus is
operations, excellent basic management
shaped differently in ostriches, emus, and
and biosecurity practices must be followed,
rheas; however, the function is sinillar. All
including "all-in /all-out" management.

ratite phalluses have a dorsal groove

Groups of newly hatched birds should be
through which the semen travels.

placed in an area of adequate space (to run
and exercise their rapidly growing legs and

Breeding: Ostriches and rheas are long
bodies), heat, and ventilation, with fresh
day breeders. The season is controlled by
water and feed. Mixing groups of young
the photoperiod Oength of daylight) as well
birds should be avoided (to reduce stress)

as the an1bient temperature; in North
until chicks are at least 3 mo old.

America, the breeding season is spring and
summer. The emu is a short day breeder and

Reproductive Diseases: Many

Jays in the late fall and winter. Once tl1e
diseases can result in reproductive failure,
breeding season has started, the cock and
either through failure to produce eggs
hen become reproductively active. The
or through production of abnormal or
ostrich cock develops external "breeding"

contaminated eggs. Bacterial salpingitis or
colors and begins to display; the hen bemetritis is common. The etiologic agents gins to flutter. This behavior continues for
vary, as does the severity of the infection.

days to weeks before egg laying begins.

In mild cases, only the uterus or shell gland

In general, females become reproduc-
is affected (metritis), and clinical signs
tively active before the males. Therefore,
range from abnormal shells to no egg
early eggs are often infertile. This is also
production at all. Infection may result
trne for emus and rheas. Ostrich hens lay
from retrograde bacterial invasion (from
every other day during the proper season
breeding or uterine fatigue), extension
if the eggs are collected daily. In the wild,
of an airsacculitis, or perforation of the
normal clutch sizes for ratites are 15 to 25
abdominal cavity by a foreign body.

eggs, whereas 30 is average in a captive

Affected hens generally have a history
production facility. The range is from Oto
of erratic egg production, malformed or

167 consecutive eggs.

odoriferous eggs, or a sudden stop in
production. On physical examination,

Hatching:

temperature and respiration are variable,

If eggs are gathered and stored
for "batch setting," they should be cooled, if there may be a discharge below the cloaca,
possible, to 60°F (15.6°C). Physiologic
and hens may have a fetid odor. Affected
zero-or the point at which the emb1yo
hens have WBC counts ranging from 8,000
to >100,000/µL. Ultrasonography and
stops developing-is 72°F (22.2°C). The
radiology are useful to assess the an1ount
egg is laid with the embryo in the 60,000
and consistency of exudates in the oviduct.

cell stage, and cooling the egg before

If a bacterial salpingitis is diagnosed
incubation ensures that all cells develop
through a caudal oviductal (vaginal)

in synchrony. In general, hatching eggs
culture, subsequent treatment is based
should not be washed if they are clean.

on organism isolation and sensitivity.

1964

RATITES

CHICK MANAGEMENT

INFECTIOUS DISEASES

The basic principles of animal husbandry
lnfectious diseases are primarily a problem
and aviary management, including an
in chicks <6 mo old. lnfective agents

"all-in/all-out" system of management,
associated with disease in chicks include
biosecurity of the flock and facility, and a
bacterial, fungal, viral, and parasitic agents.

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stress-free environment, are inherent to

However, the isolation of disease agents in a
successful ratite production. Generally, the
sick chick must be considered in conjunclevel of identifiable infectious or contation with a review of nutritional, environgious disease among chicks is low, and mental, management, and genetic factors.

most clinical signs are produced by stress

Diarrhea is the most common clinical
factors such as poor ventilation, oversign in ratite chicks. Many chicks will have crowding, excessively high an1bient
diarrhea when the yolk sac is absorbed and
temperatures, overuse of antibiotics,
the chick starts eating well, at 8--12 days of
improper incubation or hatching proceage. lf the chicks are alert and active, no dures, improper nut1ition, and other
treatment is needed. Chicks will also
management-related disease. When
develop diarrhea after a sudden change in
considering the sick chick, it is important
diet for which treatment with probiotics is
to evaluate the population at risk and take
indicated. Bacterial causes of diarrhea
appropriate steps to prevent spread of
include Escherichia coli, Salmonella spp,
disease. This often means elimination

Pseudomonas spp, Campylobacler jejuni,
of clinically ill chicks by appropriate

Klebsiella spp, Clostridium pmjringens, quarantine or euthanasia. If an infectious

Clostri,dium colinum, Mycobacterium spp
disease is involved, treating the individual

(adults), Streptococcus spp, and Staphylo
chick in its environment places the other
coccus spp. The appropriate antibiotic
birds within the group at risk.

should be determined by culture and

Ratite chicks do well on a wide range of
subsequent microorganism isolation and
substrates (including sand, grass, alfalfa, or
sensitivity, and the source of bacteria
native pasture) if they are introduced to the
identified (eg, barn, hatcher, inadequate
substrate at hatch and have adequate space,
hygiene, airborne vectors). Viral agents
ventilation, and sufficient feeders and

( suspected pathogens) that may cause
waterers. Ostrich chicks up to 3 mo old
diarrhea include paran1yxovirus, reovirus,
grow best and have the fewest managementherpesvirus, bima-like virus, enterovirus, related diseases ( eg, proventricular
adenovirus, and corona virus. Treatment for
impaction, leg problems, and feather
viral dianhea is supportive only, and any
picking) if 100-133 sq ft of pen space per
potential source of the virus ( eg, wild birds,
bird is available. Ostrich chicks do not do
infected hens, people) should be eliminated.

well when confined to concrete floored

GI obstruction is another cause of diarrhea;
housing. Adequate exercise is an important
treatment is surgical, and any changes in
consideration for nOimal leg growth and
environment or feed should be made slowly
digestive function.

to prevent recU1Tence. In cases of fungal

Musculoskeletal abnonnalitiesofthe
candidiasis, antibiotic treatment should
coxofemoraljoint, stifle joint, femur, and
be discontinued and a dry environment
tibiotarsus are common physical problems
maintained. Although the pathogenicity of
of ratite chicks. Spraddle leg is an abnormalprotozoa relating to diarrhea diagnosed in ity of the coxofemoraljoints that prevents
ostrich chicks is unknown, metronidazole
normal adduction of the limbs. Lack of
is considered the treatment of choice.

exercise and excess weight due to edema at

Enteritis may also be caused by managehatch or overfeeding are the main underlyment enors, including ovem1edication and ing causes of spraddle leg and progressive
excess electrolyte supplementation in
lateral rotation of the tibiotarsus and the
drinking water during hot weather.

tarsometatarsus. Limb musculoskeletal

The incidence of yolk sac infection and
abnormalities are progressive and have an
retention generally is low in naturally
extremely poor prognosis; management
hatched chicks. However, this condition
practices must be in place to prevent their
often occurs when owners assist to hatch
occurrence, including maintenance of an
a chick or tie off the omphalomesenteric
appropriate growth rate and provision of
vessels and bandage the abdomen. The yolk
acceptable substrate and opportunity to
sac may also be contaminated through the
exercise. Rolled toes are diagnosed more
ostium at the ilea! opening when absorpoften in young ostriches and can be treated tion of the yolk material by the vitelline
by splinting the affected toe( s) in a nonnal
membrane (yolk sac lining) is delayed.

position.

Bacteria commonly isolated from the yolk

RATITES

1965
sac are gram-negative; however, yolk sac
trichostrongyloid-type eggs in the feces.

retention secondary to noninfectious

The recommended treatment for the ostrich
causes also occurs.

wireworm is ivermectin at 0.2 mg/kg or

Poxvirus infections are more frequent
fenbendazole at 15 mg/kg. Another
in ostrich chicks and produce typical, crusty
nematode with clinical significance for
granulomatous lesions on the face, ears, and ratite species is Baylisascaris spp, which VetBooks.ir
neck. Poxvirus is transmitted by insect
is transmitted from skunks or raccoons
vectors, primaiily mosquitoes. The disease
through feed. This neurotropic pai·asite
is self-lin1iting, and mortality is low. Vaccinacauses CNS lesions and signs. Restricting tion of a flock during an outbreak with
exposure to raccoon and skunk feces is the
fowlpox vaccine may stop the spread of
best prevention. Chandlerella quiscali is a disease. The vaccine is a cutaneous fowlpox nematode identified in emus that results in vaccine administered by dipping a large
cerebral larval migrai1s. The common
needle with reservoirs near the tip that
grackle is the definitive host for C quiscali,
allow inoculation when a puncture is made
and emus are exposed to the parasite through
through the propatagiun1. Staphylococcal
the bite of Culicoides crepiisciilaris. Birds dermatitis occurs as a secondary problem in infected with C quiscali develop profound debilitated chicks, especially when external
torticollis and incoordination that leads to
parasites disrupt the epithelial integrity.

emaciation, scoliosis, and death. Ivermectin

Eastern equine encephalomyelitis can is the treatment of choice for C qiiiscali cause death in ostrich chicks as a fading
infections in emus.

chick syndrome and as a violent and fatal
gastroenteritis in emus of all ages.

Vaccination of emus for this disease is

Arthropods: Three types of arthropods
can affect ratites: lice, ticks, and quill mites.

necessary in areas where the virus exists.

Lice can be a problem, especially in

Avian influenza has been diagnosed in
ostriches. Biting lice (Stru thioliperurus
rheas and other ratite species. Routine
stiuthionis) cause skin and feather
testing for avian influenza is required for
damage. Treatment with permethrin spray
most intrastate shipments of ratites.

(poultry concentration) is effective, as is
if\iectable ivennectin at 1 mL/110 lb, IM.

Parasitic Diseases

Several species of ticks have been identified

Protozoa: A number of intestinal
on ratite species; their main significance is
protozoa, includingHexamita, Giardia,
as vectors of disease. Feather mites live in

Trichomonas spp, Cryptosporidium, and the vein on the underside of the feather and

Toxoplasma spp, have been isolated from
feed on blood. Ratite feather mites can be
ratite chicks. The pathogenicity of these
visualized as small, reddish, dust-like
parasites in all ratite species is unknown,
particles in the feather vein. Treatment for
ai1d immtmosuppression may be required
ticks aild mites is ivetmectin at 0.2 mg/kg at
for disease to develop. Metronidazole at

30-day inte1vals.

10 mg/kg, PO, bid, is recommended for
protozoa! pai·asite infections diagnosed in

DIGESTIVE SYSTEM DISORDERS
ratite species. Coccidiosis is common, and
although not believed to be pathogenic, it

Impaction of the proventriculus ai1d
can be treated with sulfa drugs. If coccidiingestion of foreign bodies are maI1agementosis is causing clinical signs (eg, diarrhea), related problems. Chicks are at high risk of
the underlying inlmunosuppressive disease
impaction for the first 2 wk after movement
condition( s) must be diagnosed to
to a new environment, with or without a
effectively treat the protozoa! disease.

chaI1ge in substrate or diet. Proventricular
inlpactions are also diagnosed as a sequela

Cestodes: The tapewormHoiittuynia
of diseases involving ileus of tl1e GI tract.

struthionis is common in Africa but rarely

Impactions with sand aild concentrated feed
diagnosed in the USA. The intermediate

Cail be maI1aged medically with psyllium
host is not known. Treatment is fenbendalaxatives aI1d supportive therapy. Impaczole, PO, at 15 mg/kg/day for 5 days, used at tions witl1 forages or ingestions of foreign
regular intervals.

material ( eg, hardware, rocks, jewelry, etc)

require proventriculotomy surgery for

Nematodes: The wireworm Libostron
removal and subsequent resolution of the
gylus douglassii is the most economically
problem.

significant GI parasite of ostriches. Mature

Cloaca! prolapses are common in young
worms and late larval stages live in the
chicks. Frequently, the chick has dian·hea or
crypts of the glandular portion of the

311 impaction within the GI tract that causes
stomach. Diagnosis is based on finding
straining and subsequent prolapse of the

1966

RATITES
cloaca The prolapse is easily reduced and a
eat and are stw1g in the oral cavity by red
purse-string suture is placed for 24-48 hr,
ants or wasps. Nicotine from cigarette butts
making sure there is adequate room for the
has resulted in CNS signs. Toxic plants that
bird to defecate/urinate while the suture is
contain solanine ( eg, silverleaf, nightshade)

in place.

result in vomiting and diarrhea, whereas

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Intestinal torsion or volvulus, primru·iJy
plants that contain high levels of'nitrates
involving the colon, occurs in ostriches of
result in dyspnea and CNS signs. Anunonia
all ages. It can present as a flock problem
toxicity is seen in birds housed in poorly
when the diet is suddenly changed,
ventilated barns and results in clinical signs
especially if the new diet has a high fiber
of corneal edema, epiphora, and dyspnea.

content. Clinical signs include scant to no
feces, slight diarrhea, abdominal enlarge

TRAUMA
ment, and vomiting. Abdominocentesis and
radiographic imaging of the coelom are

Wing luxations and fractures can result
diagnostic. When an early diagnosis is
from hauling or breeding accidents. Most
achieved, surgical intervention is corrective
cases of wing luxation are actually a radial
but often not economically feasible.

paralysis rather than a true luxation of the
joint. However, a true hun1eral luxation

MUSCULOSKELETAL DISORDERS
from the shoulder can occur. Treatment for
botl1 irtjuries is the saJne and involves taping

Exertional myopathy results from capture,
the wings up over the back. Maintaining the
transport, attack by predators, or fighting; it
wings in this position for 1-2 wk generally
can occur in birds of all ages. Borderline
resolves the problem. Fractured wings,
nutritional deficiencies may exacerbate
depending on the location of the fracture,
stress-related myopathy. Clinically, birds ru·e can be repaired with a half-Kirschner often unable to stand but ru·e otherwise
apparatus or splints ( or both). Occasionally,
bright, alert, and responsive. Fluid therapy
intraJnedullary pinning is required. With
to correct metabolic acidosis and to effect
minor wing fractures in emus, taping may
diuresis, combined with anti-inflarnmatory
be sufficient to treat the irtjury.

and antibiotic therapy to prevent clostridial

Lacerations of the neck skin and
disease, are indicated. Administration of
musculature may involve the trachea and
vitaJnin E at 5 mg/kg, with or without
esophagus of ratites that are i.t"\iured due to selenium at 0.06 mg/kg, is recommended.

contact witl1 fences. Prinlary closure of the

If nutritional deficiencies are expected,
trachea and esophagus in acute i.J"\iuries is
correcting the diet by adding oral vitrunin E
recommended. If the esophageal i.J"\iury is
to the diet or drinking water is indicated.

old, the esophagus will often heal tlrrough

Vruious treatments, including slinging the
secondary intention. With severe neck
bird to exercise the legs and swimming,
irtjuries, an esophagotomy tube, placed in
have been tried for myositis secondary to
the distal third of the cervical portion of the
overexertion or trauma. However, handling
esophagus, may be required for alimentation.

the bird in this manner is very stressful; it is

Lower leg irtjuries commonly occur in
preferable to allow the bird to sit until it can
ratites that contact cable fencmg at a high
stand on its own, which may take up to 90
rate of speed. Standard principles of wound
days. The prognosis remains guarded, even
management ( see p 170 l) should be applied, if the bird is alert and has a good appetite.

including debriding and bandaging the
wound. If bone is exposed in a lower leg

TOXICITIES
injury, radiographic imagmg of the affected
area, at weekly mtervals, is recommended,

Many different disease toxicoses have
because stress fractures and sequestra can
been documented in ratites. Exogenously
occur. Often, tlle soft-tissue irtjury shows
administered seleniun1 has resulted in acute
nom1al heali.J1g 3 wk after trawna, but
selenium toxicity in ostriches, leading to
tlle bird may still have a fracture of the
pulmonary edema and congestion. The feed
tarsometatarsus. Luxation of the phalanges
additive monensin has been associated with
is common, especially if the bird's enclosure
myositis and malabsorption syndrome in
has icy or muddy areas. If tlle luxation is not
ostriches and emus. Gossypol in conunertreated promptly, casting the foot in a cial ostrich feed contruninated with cattle
nonnal flexed position for 5-6 wk generally
feed resulted in a malabsorption syndrome.

allows enough soft-tissue fibrosis and repair

Cantharidin from blister beetles has resulted to maintain the luxatedjoi.J1t ill place. When in hemorrhagic gastritis and enteritis in
casting alone is unsuccessful, artlrroclesis of
emus. Young chicks are sensitive to insect
thejomt according to standard equine
stings, and death is common when chicks
procedures can be perfom1ecl.

REPTILES

1967

REPTILES

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The class Reptilia includes >8,000 species,
membranes that divide the coelom
b.ut only a few dozen are likely to be encouninto compartments. Snakes' organs are tered in general practice. All the Crocodilia,
distributed in a longitudinal arrangement.

front-fanged poisonous snakes (but not all

Boas and pythons are printitive snakes and
backed-fanged poisonous species) and both
have both left and right lungs; however,
species of poisonous lizard (Heloderma
other snakes lack a developed left lung.

spp) are considered to be dangerous ani

Squan1ates have incomplete tracheal rings,
mals and are usually covered by federal
and males have paired copulatory organs
and/or state legislation. These species are

(llemipenes).

not generally kept as pets and will therefore

The chelonians are characterized by their
not be discussed here. The class Reptilia
shell, which comprises a dorsal carapace
includes four orders: Crocodyla ( crocoand ventral plastron. The internal organs diles, alligators, gharials), Testudines
are separated by two thin membranes. The

(turtles and tortoises), Squamata (lizards
heait is located within a cardiac membrane,
and snakes), and Rhynchocephalia
while the lungs are dorsad and separated

(tuataras).

from the remaining viscera by a postpulmo

Reptiles are vertebrates with organ sysnary membrane ( or septum horizontale ).

tems similar to those of mammals. How

Chelonians have complete tracheal rings,
ever, they are ectothermic and rely on
and males have a single copulatory phallus.

environmental temperature and behavior
to control their core body temperature.

Physiology: Reptiles rely on environmen

They possess both renal and hepatic portal
tal temperature and behavior to maintain
circulations, and predominantly excrete
their body temperature within their preferred
anrn10nia, w·ea, or uric acid depending on
optimal temperature zone (POTZ). Within
their evolutionary adaptations. Their RBCs
tltis species-specific POTZ, a reptile is able
are nucleated, and their metabolic rates are
to achieve the preferred body temperature
lower than those of mammals. All reptiles
for specific metabolic activities, which may
exhlbit ecdysis-a normal process by which vary diurnally and seasonally and by age the outer skin is periodically shed. Diurnal
and gender. The metabolic rate of reptiles
species require broad-spectrum light for
is lower than that of mammals and birds.

vitamin 03 synthesis and calcium homeosta

Consequently the K constant to detemtine
sis. Fertilization is internal, and females
energy expenditure, nutiitional requiremay produce eggs (oviparous) or live young ments, and allometric drng doses is given by

(ovoviviparous).

the equation BMR = K(body wt [in kg]0.75), in

Reptiles are not considered highly social
which BMR = basal metabolic rate in Kcal/
creatures, and multiple-male groups can
day and K = 10 (the energy constant for
lead to intraspecies aggression. Single-male,
reptiles).

multiple-female groupings can work well

All snakes, lizards, and chelonians have
for certain species, but the solitary reptile
a three-chambered heart (two atria and
is often the healthiest pet. The life span of
one ventricle), whereas crocodilians have
many reptiles can exceed 10--20 yr, requiring a four-chambered heart. All reptiles have a longterm commitment from owners.

both pulmonary and systemic circulations

(sin1ilar to mammals). In noncrocodilian

Anatomy: Reptiles possess a common
reptiles, functional separation of venous
cloaca, which receives the lower GI,
and arterial blood is largely maintained
reproductive, and urinary tracts. In
via a muscular ridge within the ventricle.

addition, lungs are simpler and composed

Peripheral blood cell types include erythroof vascular pockets, more like a cavitated cytes, heterophils, eosinophils, basophils,
sponge than alveoli.

lymphocytes, monocytes (including

Lizards and chelonians are quadrnpeds
azurophils), and thrombocytes. Renal and
and have a familiar pentadactyl limb
hepatic p01tal circulations exist, and
arrangement. Reptiles lack a true diaintra- and extracardiac vascular shunts phragm; in many species, all organs are
may be present, especially in aquatic
contained within a single coelomic cavity.

species.

Some lizards (eg, tegus and monitors) have

Reptilian skin is usually heavily keratithin postpulmonary and/or post-hepatic nized and protected by scales. The chelonian

1968

REPTILES
shell is composed of both dennal bone plates
and keratinized epithelial scutes. Reptiles do
not have extensive skin glands, and their
skin is essentially dry. However, many male
lizards have a series of pre-anal or femoral

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pores located cranial to the vent or along the
craniomedial aspect of the hind.limbs. In
some species, both sexes have these glands,
but they are more pronounced in the male.

Clu·omatophores are conm1on and enable
many species, most notably the Charnaeleonidae, to change color. Bony skin strnctures, osteoderms, are found in the crocodilians
and some lizards. These strnctures may

Green iguanas, male (left) displaying a larger
inte1fere with radiographic interpretations
dewlap and jowls than the female (right).

Courtesy of Dr. Stephen Divers.

and surgery. Certain species of snakes have
heat-sensitive receptors located around U1e
maxilla U1at are used to locate prey. Skin
characteristics ( eg, crests, spines, dewlaps)

females it enters a cloacal gland only to a
are often used for species or gender
depth of 3-6 scales. Sexual dimorphism
identification in those species that exhibit
in chelonians is usually obvious in adults;
din1orphic variation.

males often have a concave plastron and a

All reptiles shed their skin. The
longer tail. Many reptiles, especially lizards
frequency of ecdysis depends on species,
and chelonians, are territorial and will fight
age, nutritional status, environmental
conspecific males, causing severe injuries.

temperature and humidity, reproductive

In addition, overzealous and unrelenting
status, parasite load, hormonal balance,
males may ardently pursue females,
bacterial/fungal skin disease, and skin damcausing repeated harassment. Fertilization age. The entire process can take 7-14 clays.

is internal, and reproduction is either
oviparous ( egg production) or ovovivipa

Reproduction: Most species require
rous (live bearing). Gender determination
some form of conditioning before breedmay be genetic (most snakes, many lizards) ing (eg, hibernation, seasonal noctwnal
or related to incubation temperature (most
cooling). Many species are sexually
chelonians, some lizards).

dimorphic. Male lizards are generally
larger, have pre-anal or pre-femoral pores,

MANAGEMENT
have hemipenal bulges at the tail base,
and often are more brightly colored. The

Veterinarians must not only be familiar
gender of snakes is dete1minecl by probing
with common reptile species and their
for the hemipenes with a blunt, lubricated
management but also be able to extract
probe. In males, U1e probe will enter to a
clinically relevant husbandry information
depth of 6-14 subcaudal scales, wliereas in
from U1e owner in a timely manner. The

•M:iiffi RECOMMENDED MINIMUM SPACE REQUIREMENTS FOR REPTILES

Reptile Group

Minimum Space Requirement

Tortoises and terrapins

0.4 m2/0. l m carapace length

Purely aquatic chelonians

0.25 1113/0. l m carapace length

Terrestrial lizards

0.2 m2/0. l m total length

Arboreal lizards

0.4 m3/0. l m total length

Boas and pythons

0.6 m2hneter of snake

Kingsnakes and rat snakes

0.6 m2/meter of snake

Whipsnakes and racers

1.2 m2/meter of snake

Arboreal snakes

0.8 m3/meter of snake

REPTILES

1969
use of a history form can greatly facilitate
desirable, although theft, predators, 3.11d
this process and ensure that nothing is
wildlife carriers of disease should be
overlooked.

considered.

VetBooks.ir

Species: Different species from different

Heating: A variety of heaters can be used,
locations must not be mixed. Ideally, only
including incandescent bulbs, infrared
a single species should be kept in any
cera.irucs, heating pads or mats, warnling
enclosure, and care must be exercised to
cables, tubular heaters, radiators, convector
avoid competition for resources such as
heaters, a.i1d natural sunlight radiation.

food, basking areas, and retreats. In general,

Heaters of an appropriate size should be
tl1e solitary reptile pet is often the healtllithern10stat controlled, screened from the est. Most nonbreeding pet snakes and
animals, and positioned toward one end of
aquatic turtles are best maintained as a
the enclosure to provide a thern1al gradient.

single pet, because trauma while feeding is

"Hot rocks" frequently result in burns in
common in groups. Some lizards, notably
la.i·ger a.ilimals a.i1d should be avoided. Light
the chameleons (Chameleo spp), are so
bulbs ca.imot be used to provide nocturnal
territorial that isolation is often essential
heat.

for longterm survival in captivity.

Environmental Lighting: All reptiles
benefit from broad-spectn.un lighting.

Enclosure: The size of the enclosure is

However, UVB light (290-300 run) is
important, and although many breeders
especially important for most diurnal lizards
and retailers may be able to intensively
and chelonians for vitamin D3 synthesis a.i1d
manage stock, pet owners should be
calcium regulation. The best source of
advised on minimum enclosure sizes (see
lighting is unfiltered sunlight. However,

TABLE 22), the importance of providing the
m3.11y artificial fluorescent strip-lights,
largest enclosure possible, and correct
compact fluorescent, and mercury halide
cage furniture. The type of enclosure
bulbs are available. Almost every light

(arboreal, terrestrial, subterranean, or
ma.i·keted for reptiles has tl1e tenn "broad"

aquatic) should be appropriate for the
or "full" or "natural" on its packaging, species (see TABLE 23).

creating confusion for veterinarians and

Glass aqua.iia are conunonly used, but
owners alike. Appropriate lights must be
the greater visualization perceived as an
labeled as providing UVB or, better still, be
advantage to the owner may be stressful to
exanlined 3.11d tested using a spectrometer.

the reptile. Glass is also a poor insulator,

Even suitable fluorescent lights must be
and greater heat Joss may lead to dra.inatic
placed relatively close to the reptile a.i1d
temperature fluctuations. Even if the entire
replaced every 9-12 mo. Most transparent
top of the enclosure is covered by mesh,
plastic 3.11d glass barriers filter out UVB
ventilation may be severely ha.inpered.

wavelengtl1s. A photoperiod of 12 hr/day

Plastic or fiberglass enclosm·es are more
is suitable for general maintena.i1ce.

expensive but more versatile.

Newspaper, a.itificial turf, and orga.ilic

Humidity: Hunlidity that is too lligh or low pa.iticulates ( eg, bark chips) are suitable
can create se1ious problems. Hunlidity is
materials to line cages and vivaria, but they
seldom directly controlled, although the
must be completely replaced regularly. Soil,
advent of dedicated hmnidifiers and sp1inkler
sand, and natural leaf litter can also be used,
systems makes this practical. Decreasing
but oven baking is reconunended to sterilize
ventilation to maintain temperature and
before use. Gravel and pebbles are not
hunlidity is ill advised and frequently causes
reconunended for terrestrial species,
skin and respiratory disease.

because they are difficult to clean and often
ingested by reptiles. Other essential items

Quarantine and Record Keeping:

include a water bowl (large enough for the

Although the incubation period of m3.11y
reptile to bathe) and various retreats ( eg,
reptile disorders is unknown, quar3.11tine
cardboard boxes, cork ba.i·k, shredded
periods of 3 -6 mo are reconm1ended.

paper). Cle3.11, secure branches are required

Owners should also be encouraged to
for arboreal species. Soap 3.11d water is
keep detailed records of a.i1y ch3.11ges in
generally all that is required to clean cages,
husbandry or nutrition, breeding activity,
but bleach can be used as long as rinsing is
in-contact animals, disease outbreaks,
tl10rough. Some cleansers ( eg, phenolic
health issues, and previous treatments.

disinfectants) are toxic. In certain areas,
the climate may pernlit keeping reptiles

Nutrition: Species identification is
in outdoor enclosures, which is highly
essential to critically appraise captive

1970

REPTILES

IMPORTANT HUSBANDRY REQUIREMENTS FOR SELECTED

REPTILES

Species

Habitat/Vivarium '[ype

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Corn/rat snake

Terrestrial, scrubland

Boa constrictor

Terrestrial, rain forest (semi-arboreal/aquatic)

Ball python

Terrestrial, scrubland

Leopard gecko

Terrestrial, arid scrub

Green iguana

Arboreal, rain forest

Bearded dragon

Terrestrial, desert

Water dragon

Arboreal, rain forest

Savannah monitor

Terrestrial, arid scrub

Greek tortoise

Terrestrial, temperate to subtropical

Box tortoise

Terrestrial, temperate to subtropical

Leopard tortoise

Terrestrial, tropical

Red-footed to1toise

Terrestrial, tropical

Red-eared slider

Temperate to subtropical gravel bottom or bare,
water depth 30 cm min, land area 113 of tank

" POTZ = preferred optimal temperature zone. Temperature requirements shown are air temperature gradients. In general, basking temperatures should be 5°C warmer, whereas at night these tempera

! ures should fall by 5°C.

h BS = broad-spectrum lighting (UVB 290-300 nm) essential, NS = no special lighting requirements

" I or i = insectivorous, H or h = herbivorous, C or c = carnivorous; upper case indicates major food preference, lower case minor food preference.

" Humidity requirements are significantly greater clming ecdysis.

diets (see TABLES 24 and 25). Rodent-eating http://ndb.nal.usda.gov for the USDA
carnivores such as most snakes present few National Nutrient Database for Standard problems as long as the rodent is recogniz

Reference). Calciwn or vitanlin 03 deficiency
able to the snake as food. Obese rodents

(generally due to poor quality lighting
that have been frozen for prolonged periods
and low-calcium diets) leads to secondmay contain fewer nutrients. Feeding live ary nutritional hyperparathyroidism in
rodents is not advised ( and is illegal in some insectivores and herbivores. A variety countries) because of the dangers of preyof commercially available .foods are induced trauma to sedate reptiles and the
available in moist, canned, and dry
welfare in1plications for the live prey.

pellet forms. These may help provide a

Insectivorous reptiles can be well catered
balanced diet, but they have not been
for with a variety of commercially available
critically evaluated.

crickets, waxworms, tebos, locusts, meal

Although some species will drink from a
worms, cockroaches, and flies. Feeding
water bowl, others will only imbibe water
insects a nutritional diet high in calcium
droplets on plants and decor. Poor water
and dusting the insects with a high-calcium
quality has been implicated as a cause of
reptile supplement immediately before
stomatitis in snakes. Lack of appropriate
feeding is required to prevent deficiencies.

water delivery has been implicated as a

Providing herbivorous reptiles with a
predisposing cause of renal disease in green
varied and nutritious diet can be difficult.

iguanas. The advent of tinler-controlled

Foods with a high calcium:phosphorus
sprinkler systems makes regular water
ratio should be selected with due regard
provision possible for many of these more
given to the species-specific requirefastidious drinkers.

ments for vegetables and fruits. Human

See also 'UTRITIO : EXOTIC AND zoo ANIMAJ..5
nutrient databases can be useful (see

(REPTILES), p 2302.

REPTILES

1971

IMPORTANT HUSBANDRY REQUIREMENTS FOR SELECTED

REPTILES (continued)

POTza(°C)

Humidity%

Lightingb

Hibernation

Dietc

25-30

30-70d

NS

Yes
c

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28-31

70-95

NS

No
c

25-30

50--80

NS

No
c

25--30

20-30d

NS

No

I, c

29-33

60--85

BS

No

H

20-32

20-3oc1

BS

No

I, c, h

24-30

80-90

BS

No

I, c, h

25--32

20--40d

BS

No

C,i

20-26

30-50

BS

Yes

H,c

22-28

50--80

BS

Yes

H,I,c

25-30

30-50

BS

No

H,c

25-30

50-90

BS

No

H,c

24-28

Aquatic

BS

Possible

H,I,c

Physical Examination
longer to accomplish and cause unnecessary stress or discomfort to the animal. It is The successful diagnosis and treatment of
possible that sedatives and anesthetics may
reptile diseases requires proper restraint
affect clinical pathologic results, especially
and performance of a variety of clinical
hematology.

techniques. Although the principles are

The decision to examine a potentially
similar to those used for domestic animals,
dangerous reptile should be made witl1 due
there are a number of reptile-specific
regard to legislative and safety requirepeculiarities. It may be possible to observe ments. No species of Chelonia is legally_
calm specimens unrestrained, pemlitting an
considered dangerous, but several species
assessment of demeanor, locomotion, and

( eg, snapping turtles, Chelydra spp) have a obvious neurologic disorders such as
ferocious bite that makes them a formidable
lameness, paralysis, paresis, and head tilt.

opponent. In addition, the Convention on

Observation of reptiles within their usual
the International Trade of Endangered
environment is particularly valuable and

Species of Fauna and Flora (CITES) may
should be done whenever possible. Nervous also have implications for Appendix 1 and 2
or aggressive species are best restrained at
reptiles kept as pets. Even some common
all times using towels, snake hooks, clear
pet species ( eg, com snake) may be illegal
plastic containers, and restraint tubes.

in some endemic areas, whereas native

Gauntlets severely reduce the clinician's
venomous snakes may be freely collected
tactile sensation but may be required
because they are considered "vemlin."

when dealing witl1 large lizards or small

The risks of reptile-borne zoo noses are
to medium-sized aggressive crocodilians.

probably no greater than for other animal

Careful consideration should be given to the groups, and basic personal hygiene after safety of veterinary staff, zoo keepers, and
handling reptile patients will rnininlize
private owners when dealing with large or
these risks. The major zoonoses include
otherwise potentially dangerous reptiles. In

Salmonella, Pseudomonas, Mycobacte
many cases, chemical agents can expedite
rium, C1yptosp01idium, and Rickettsia
procedures and considerably reduce risks
spp and pentastomids (arachnid lung
to both the reptile and human handlers.

parasites). Major public concern centers on

Given the improvements in reptile
the commensal reptile Sa.lmonella spp, and
anesthesia, even manageable reptiles may
clinicians are advised to obtain a copy of the
be preferentially sedated or anesthetized
statement policy and client brochure on tllis
for procedures that would otherwise take
subject produced by the Association

1972

REPTILES
of Reptilian and Amphibian Veterinatians
ment, and disease progression or resolu

(www.arav.org/special-topics/).

tion. Relating body weight to length and

Every reptile must be accurately weighed; confom1ation gives an assessment of body an accurate weight is important to avoid
condition. The snout-vent length of lizards
deaths associated with drng overdose,
and especially snakes is worth noting,
particulai·ly anesthetics and aminoglycobecause organ position and growth can VetBooks.ir
sides. In addition, serial weight measurebe calculated as a result. Chelonian body ments pemtit an appraisal of growth and
condition relies on relating total weight to
captive management, response to treat-
straight carapace length or body volume.

COMPOSITION OF ANIMAL FOODS THAT MAY BE OFFERED

TO REPTILES

Food Item

Dry Matter(%)

Protein(%)

Fat(%)

Mealworms (Tenibri.o)

42.2

52.8

35

Superworms (Zophoba)

40.6

17.4

17.9

Locusts

31.2

61.7

19.4

Crickets

38.2

55.3

30.2

Earthworms

22

49.9

5.8

Waxwom1s

38.3

15.5

22.2

Chicken muscle

25.6

20.5

4.3

Egg, whole

25.2

12.3

10.9

Mice, 1-2 days old

Mice, adult

19.86

8.81

COMPOSITION OF PLANT FOODS THAT MAY BE OFFERED

TO REPHLES

Food Item

Dry Matter(%)

Protein(%)

Fat(%)

Alfalfa

15.5

37.1

Apple"

0.2

0.6

Banana•

29.3

1.1

0.3

Black currants

Blackberry

Broccoli

3.6

0.3

Cabbage

1.3

0.2

Carrots

10.1

0.7

Clover hay

11

1.9

Collard

Cranberries

Damsons

Dandelions

Endive

1.7

0.1

REPTILES

1973

Transillumination of the coelom using a
with moistened gauze between the shell or
cold light source can be used to visualize
scales and the stethoscope diaphragm can
the internal structures of small lizards and
be helpful. Doppler ultrasound is particusnakes and is particularly useful to confirm larly useful to detennine heart rates.

suspected impactions and foreign bodies.

Care must be exercised if a hot light source

Snakes: The head of an aggressive snake

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( eg, incandescent spotlight) is used,
or a snake of unknown disposition should
because of the possibility of bums.

be identified and restrained before opening

Auscultation of reptiles is difficult and
the transportation bag to remove the
often unrewarding. Electronic stethoscopes
animal. In general, the head of the snake is

COMPOSITION OF ANIMAL FOODS THAT MAY BE OFFERED

TO REPTILES (continued)

Energy (KcaVg)

Calcium(%)

Phosphorus (%)

Ca:PRatio

6.53

0.06

0.53

0.11

0.01

0.02

0.43

0.1

0.75

0.13

0.23

0.74

0.31

0.59

0.85

0.69

0.03

0.22

0.13

1.21

0.01

0.2

0.05

1.47

0.05

0.22

0.02

1.6

1.8

0.88

2.07

0.84

0.61

1.37

COMPOSITION OF PLANT FOODS THAT MAY BE OFFERED

TO REPTILES (cont'inued)

Energy (KcaVg)

Calcium(%)

Phosphorus (%)

Ca:PRatio

3.94

1.29

0.21

6.14

0.57

0

0

0.57

0.79

0

0.02

0.25

0.06

0.04

1.4

0.06

0.02

2.62

0.1

0.06

1.49

0.04

0.03

1.22

0.23

0.04

0.02

2.29

0.2

5.0

0.2

0.07

2.76

0.01

0.01

1.36

0.02

0.01

1.5

0.18

0.07

2.4

0.08

0.03

2.67

1974

REPTILES

COMPOSITION OF PLANT FOODS THAT MAY BE OFFERED

TO REPTILES (continued)

Food Item

Dry Matter (%)

Protein(%)

Fat(%)

VetBooks.ir

Fennel

2.8

, 0.4

Fig

Grass (lawn)

33

2.4

1.2

Iceberg lettuce

1.2

2.5

Kale

Lemon

Lettuce"

4.1

0.4

Mustard cress

Orange

13.9

0.8

Parsley

Radish

Raspberry

Red currants

Spinach

3

0.3

Tomatoa

6.6

0.9
trace

Turnip

1.1

0.9

Watercress

2.2

0.3

White grapea

20.7

0.6
trace
a The poor Ca:P ratio of these con:unonly used items may make them less suitable as a staple component of a reptile diet.

held behind the occiput using the thumb
body posture, cloaca! tone, proprioception,
and middle finger to support the lateral
skin pinch, withdrawal, and papillary and
aspects of the cranium. The index finger is
righting reflexes can be used to assess
placed on top of the head. The other hand is
neurologic function.

used to support the body. Restraining the

The entire integument, particularly
snake's head in this manner supports the
the head and ventral scales, should be
cranial-cervical junction, which, having only thoroughly examined for evidence of a single occiput, is prone to dislocation.

dysecdysis (poor shedding), trauma,

When dealing with large boids, a second,
parasitism ( especially the conunon snake
third, or even fourth handler is required to
mite, Ophionyssus natricis, and ticks), and support the body during the examination.

microbiologic infection. Any recently shed

It is usually safer and more convenient to
skin should also be examined, if available,
sedate a large, pugnacious snake than to
for evidence of retained spectacles. Skin
risk injwy to the snake, owner, or staff.

tenting and ridges may indicate cachexia

Nonvenomous species should be

("poverty lines") or dehydration; ticks and supported using one or two hands,
mites may congregate in skin folds,
depending on size. Nervous or aggressive
infraorbital pits, nostrils, and corneal rims.

snakes can be restrained using plexiglass

The infraorbital pits ( where present) and
tubes or sedated before examination. The
the nostrils should be free from discharges
clinician should attempt to gauge muscle
or retained skin. The eyes should be clear,
tone, proprioception, and mobility. Systemiunless ecdysis is imminent. The spectacles cally ill serpents will often be limp, lack
covering the eyes should be smooth; any
strength, and be less mobile. Head carriage,
wrinkles usually indicate the presence of

REPTILES

1975

COMPOSITION OF PLANT FOODS THAT MAY BE OFFERED

TO REPTILES (ro11ti1111<·d)

Energy (Kcal/g)

Calcium(%)

Phosphorus(%)

Ca:PRatio

0.1

0.05

1.96

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0.28

0.09

3.04

1.58

0.1

0.09

1.1

0.14

0.03

0.02

1.34

0.17

0.06

2.9

0.11

0.01

9.17

0.12

0.02

0.02

0.85

.. 0.06

0.06

1

0.35

0.04

0.02

1.71

0.2

0.13

1.53

0.04

0.02

1.63

0.04

0.02

1.41

0.03

0.03

1.2

· 0.09

0.05

1.69

0.14

0.01

0.02

0.62

0.05

0.01

2.89

0.22

0.05

4.23

0.63

0.01

0.02

0.86
a retained spectacle. Tiie spect.acle repreenlarged organs, and masses may be sents the transparent fused eyelids, and
palpable. The cloaca can be examined using
therefore the cornea is not normally
a dedicated otoscope or by digital palpation.

exposed. The subspectacular fluid drains

Examination of the oral cavity is often left
through a duct to the cranial roof of the
until last, because many snakes object to
maxilla When blocked, the buildup offluid
such manipulation. However, even before
causes a subspectacular swelling that often
the mouth is opened, the tongue should be
becomes infected. Damage to the underlyseen flicking in and out of the labial notch ing cornea can result in panophthalrnitis
with regularity. The mouth can be gently
and ocular swelling. Retrobulbar abscessaopened using a plastic or wooden spatula to tion results in protrusion of a normal-sized
permit an assessment of mucous membrane
globe. Other ocular pathologies can include
color and the buccal cavity for evidence of
uveitis, corneal lipidosis, and spectacular
mucosa! edema, ptyalism, hemorrhage,
foreign bodies, including slivers of wood or
necrosis, and inspissated exudates. White
other vivarium materials.

deposits may indicate uric acid deposition

Working from cranial to caudal, the head
due to visceral gout. The pharynx and glottis
and body are palpated for swellings, wounds, should be examined for hemorrhage, foreign

'.1hd other abnormalities. The position of any
bodies, parasites, and discharges. Openmternal anomalies, noted as a distance from mouth breathing is a reliable indicator
the snout and interpreted as a percentage of
of severe respiratory compromise. The
snou�-vent length, enables an assessment of
patency of the internal nares and the state of

Possible organ involvement. Recently fed
the polyphyodontic teeth should be noted.

�akes have a midbody swelling associated

With the prey within the stomach; handling
s

Lizards: Lizards vary considerably in size,

_uch individuals may well lead to regurgitation.

strength, and temperament; therefore, a

Pre ovulatory follicles, eggs, feces,
variety of handling techniques are required.

1976

REPTILES

Thl' tl'g11s and monitors :tr() r<'IIO\\'IH'd !'or i-wal<'H should IH' clp;m and fn•1• of distlwir pmn'rful hilt's, wlH'rt':ts ot hPr spc'cic's, dwrgPs. Tiu• pn�se11c<· of' dry, white! material
pm1kularlv tlw grec'n ig11a11a, an' much
around I.he nostrils of'smrw ig11ani<I lizards
mor0 likl'lv to us0 their claws and tail. The
is normal, hccausc some specic�s excrnte
main prnhic'm wlwn handling small lizards
snit through specialized rmc;al glands. The
is restraining tll('rn lH'forl' they flee. The
rostrum should he examined for trauma,

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lizard should be transpo1tcd in a securely
often caused by repeated at.t.empLc; to
tied cloth bag, so that the position oft.he
escape from a poorly designed vivarium or
lizard can be identified and the lizard held
to evade cagemat.es. The head, body, and
before the bag is opened. Large lizards are
limbs should be palpated for masses or
best restrained with the forelimbs held
swellings, which can be abscesses or
laterally against their coelom and the
metabolic bone disorders. Lizards suffering
hindlimbs held laterally against the tail base. from severe hypocalcemia and hyperphos

The lin1bs should never be held over the
phatemia may exhibit periodic tremors and
spine, because fractures and dislocations
muscle fasciculations. The coelomic body
can occur. Nervous lizards can be wrapped
cavity of most lizards can be gently
in a towel to aid restraint. Smaller lizards
palpated. Food and fecal material within
can be restrained around the pectoral girdle, the GI tract, fat bodies, liver, ova, and eggs holding the forelimbs against the coelom,
are usually appreciable. Cystic calculi,
although care is required not to in1pair
fecoliths, enlarged kidneys, impactions,
respiratory movements. A lizard should
retained eggs or ova, and unusual coelomic
never be grasped by the tail, because many
masses may also be noted.

species can drop the tail ( autotomy) in an

The cloaca should be free from fecal
attempt to evade capture. Restricting the
staining, with visual and digital examination
vision of a lizard ( eg, a towel placed over the considered routine. In the green iguana, head) is often the simplest way to facilitate
renomegaly can be appreciated by digital
handling and examination. A useful
cloaca! palpation. The high incidence of
restraint technique for iguanid or monitor
dystocia necessitates a need to identify
lizards uses the vasovagal response: gentle
gender during examination. Many species
digital pressure applied to both orbits
of lizards are sexually dimorphic, although
causes many lizards to enter a state of
sexing juveniles can be difficult.

stupor for up to 45 min ( or until a painful or
noisy stimulus is applied). This technique

Tortoises, Turtles, and Terrapins:

enables the mouth to be gently opened

Small to medium-sized tortoises are not
without the need for excessive force. If
difficult to handle, although their strength
possible, the lizard should be observed
and uncooperative nature can hinder
unrestrained to check for neurologic
examination. Patiently holding the tortoise
problems. Calm lizards may be permitted to
with its head. down will often persuade a shy
walk around the examination table or on the individual to protrude the head from the floor. However, if in any doubt, the lizard
shell. Placing the thumb and middle finger
should be placed in a large plastic enclosure
behind the occipital condyles prevents
to prevent escape during observation.

retraction of the head. However, with larger

The integument should be examined for
species, it may be physically impossible to
parasites ( essentially mites and ticks) and
prevent a strong individual from pulling
trauma due to fighting, mating, and burns.

free. In such cases, sedation or use of a

Lizards tend to shed their skin in stages.

neuromuscular blocking agent may be

Classically, dysecdysis and skin retention
necessary. The more aggressive aquatic
occurs around the digits and tail, causing
species should be held at the rear of the
ischemic necrosis. Extensive skin folding
carapace. Some species ( eg, snapping
and tenting may indicate cachexia and
turtles) have long necks and an extremely
dehydration.

powerful bite, necessitating great care.

The head should be examined for

Certain species also have functional hinges
abnormal conformation. The mouth can be
at the front and/or back of the plastron, and
opened using a blunt spatula or, in iguanas,
care should be exercised not to trap a finger
by gently applying pressure to the dewlap.

when the hinge closes.

The buccal cavity and glottis should be

Examination of the head should include
examined thoroughly for evidence of
the nostrils for any discharges and the beak
trauma, infection, neoplasia, and edema,
for damage and overgrowth. The eyelids
especially pharyngeal edema. The internal
should be open and not obviously distended
extent of any rostral abrasions should be
or inflan1ed, and the eyes should be clear
evaluated. The nostrils, eyes, and tyrnpanic
and bright. Cortjunctivitis, corneal

REPTILES

1977
ulceration, and opacities are frequent
hyperparathyroidism resulting from dietary
presentations. The tyrnpanic scales should
deficiencies of calcium, excess phosphorus,
be examined for signs of swelling associor a lack of full-spectrum lighting.

ated with aural abscessation. Applying

Pyramiding of the shell appears to be more
steady distractive pressme to the maxilla
associated with inappropriate hwnidity

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and mandible can open the mouth, and a
than dietary imbalances. Shell infection may
mouth gag can be inserted to prevent
present as loosening and softening of the
closure. Aggressive chelonians, generally
scutes with erythema, petechiae, purulent
aquatic species, often threaten by openor caseous discharges, and a foul odor.

mouth displays, which provide a good

Prolapses through the vent are obvious,
opportunity to examine the buccal cavity
but it is necessary to determine the
with minimal handling. Mucus membrane
structme(s) involved. Prolapses may
coloration is nonnally pale; hyperemia may
include cloaca! tissue, shell gland, colon,
be associated with septicemia or toxemia.

bladder, or phallus. Internal examination

Icterus is rare but may occur with biliverusing digital palpation and an endoscope is dinemia due to severe liver disease. Pale
recommended.

deposits within the oral membranes may
represent infection or mate tophi associated with visceral gout. The glottis is Anesthesia and Analgesia
positioned at the back of the fleshy tongue

For some minor procedures ( eg, blood
and may be difficult to visualize; however, it
sampling), simple restraint may be all that is
is in1portant to check for any inflammation
required. This can be enhanced by temporary
and glottal discharges consistent with
immobilization techniques such as dorsal
respiratory disease.

recmnbency, reduced light intensity, or gentle

The integument should be free of damocular pressure ( vasovagal response). For age. Subcutaneous swellings are usually
more invasive and painful procedmes,
abscesses. Aquatic species appear more
general anesthesia must be used. Although
susceptible to superficial and deep mycotic
considerable anatomic, physiologic, and
clern1atitis, especially around the head,
phat111acologic differences exist between
neck, and limbs. The withdrawn limbs can
reptiles, some general guidelines are
be extended from the shell of small to
applicable. The following is therefore
medium-sized chelonians by applying
intended as a practical approach, ratl1er
steady traction. Because the coelomic space tl1at1 an exhaustive review of reptile within the shell is restricted, gently forcing
anesthesia
the hindlimbs into the shell will often lead to
partial protrusion of tl1e forelimbs and head,

Preanesthetic Assessment and
and vice versa. A wedge or mouth gag can

Stabilization: All reptiles should be
be used to prevent complete closure of a
hospitalized and mruntained at their
hinge. No chelonian will close a hinge on an
preferred optimal temperature zone at all
extended limb. The integument should be
times to minimize physiologic disturexan1inecl for parasites (particularly ticks bance, facilitate recovery, and mruntrun
and flies), dysecdysis, trauma, and infection
immunocompetence. Although hypotherthat may arise clue to predator attacks.

mia will reduce movement, it does not

Aggressive conflicts and courting trauma
provide analgesia and is therefore
must also be considered in tl1e communal
unacceptable as a means of anesthesia on
environment. Limb fractmes are less
welfare grounds. It can also dran1atically
common in chelonians tl1an in other
affect the pharmacokinetics of any drugs
reptiles, but when they do occm they are
administered and greatly prolong
often associated with rough handling and
recovery.

secondary nutritional hyperparathyroidism.

A full clinical examination should be

Focal subcutaneous swellings are usually
performed and tl1e anin1al accurately
abscesses, but grossly swollen joints or
weighed, although this may not be practical
limbs are more often cases of fracture,
or possible in some cases. The hydration
osteomyelitis, or septic arthritis.

status of all reptiles should be assessed,

The prefemoral fossae should be palpated especially if debilitated or post-hibernation.

with the chelonian held head-up. Gently

For elective procedures ( eg, neutering),
rocking the animal may enable palpation
underweight, dehydrated, or debilitated
of eggs, cystic calculi, or other coelomic
anin1als should be nursed for days, weeks,
masses. The shell should be exan1inecl for
or months LU1til their condition improves.

hardness, poor conforn1ation, trawna, or

For nonelective surgery, dehydration should
infection. Soft, poorly mineralized shells are be corrected before anesthesia. Even the usually a result of secondary nutritional
most rnoribLU1d egg-bound reptile will

1978

REPTILES
usually benefit from stabilization for 24-48

Reptiles should be fasted before all
hr before surgery is perfom1ed. Reptiles that elective surgery to avoid the compression have not been stabilized before surgery tend of lw1g(s) associated with large meals and to succumb intra- or postoperaLlvely.

potential regurgitation. Fasting depends on

Although oral fluids are least invasive to
tl1e feeding regimen of ilie reptile, but in
administer and provide the most physiologigeneral one feeding cyt:le should be skipped VetBooks.ir
cally normal method of rehydration, they
before surgery. Premedication wiili sedatives
are sufficient only for mildly dehydrated
such as acepromazine and atropine is
anin1als and are contraindicated immedigenerally rare in reptiles, aliliough midaately before surgery because of the risks zolam has been advocated in large cheloniassociated with regurgitation. Intracoeans. However, presurgical administration lomic fluids are more suitable, but uptake
of analgesics should be considered routine
can take many hours and their use is

(see TABLE 26).

problematic if coeliotomy or coelioscopy
is plarmed. For dehydrated surgical candi

Anesthetic Induction: IV or intraossedates, IV or intraosseous fluid therapy ous propofol provides a rapid, controlled
should be administered before, during,
mode of induction. It is relatively nontoxic,
and after surgery as necessary.

and iliere is reduced risk of ilirombophlebi-

ANALGESICS, SEDATIVES, AND ANESTHETICS USED IN

REPTILES

Drug

Dose and Route

Comments

Morphine

1.5 mg/kg, IM, SC

Chelonians (red-eared sliders)

IO mg/kg, IM, SC

Lizards (bearded dragons)

Not analgesic for snakes. Causes
pronounced respiratory depression
in turtles.

Hydromorphone

0.5 mg/kg, IM, SC

Chelonians: appears to cause less
respiratory depression tl1an morphine

Tramadol

5 mg/kg/day, PO, SC;

Chelonians (red-eared sliders); less

IO mg/kg, PO, every 4 respiratory depression than morphine days

Butorphanol

20 mg/kg, SC

Snakes ( comsnakes) at high doses. Not
analgesic for bearded dragons or redeared sliders. May cause respiratory depression, and high-dose volun1e may
be unpractical. May be able to partially
antagonize opiate agonists like morphine.

Meloxicam

0.2 mg/kg, IV, IM, SC,
every 24-48 hr

Ketamine

I 0-40 mg/kg, IM

Sedation, prolonged hangover effects

40-60 mg/kg, IM

Deeper sedation but not sufficient for
painful procedures and care in debilitated
individuals

Ketamine IO mg/kg,

Deep sedation/anesiliesia in many
combined with
chelonians. Reversed using atipan1ezole
medetornidine 0.1--0.2 (0.5 mg/kg, IM) and, if necessary, naloxone mg/kg ( or dexmedeto (0.2 mg/kg, IM)

midine 0.05--0.1 mg/kg)

and morphine 1.5 mg/
kg or hydromorphone

0.5 mg/kg, IM ( or 50%
dose, IV)

REPTILES

1979

ANALGESICS, SEDATIVES, AND ANESTHETICS USED IN

REPTILES (continued)

Drug

Dose and Route

Comments

Midazolam

2mgfkg, IM

Premedication, or can be given with

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ketamine to increase sedative effects or
promote similar effects at lower ketamine
doses.

Dexrnedetomidine 0.05---0.1 mg/kg, IV or

Often used in combination with ketan1ine

IM
and opiates as a sedative to light
anesthetic. Useful when IV access is
difficult.

Atiparnezole

10 x mg dose of

Used to reverse dexmedetomidine
dexrnedetomidine, IM

Tiletamine/

3-12 mg/kg, IM

Tortoises, lizards, snakes. Low dose useful
zolazeparn
to facilitate intubation. Higher doses
associated with prolonged recoveries.

Propofol

3-10 mg/kg, IV,

Low dose rate for larger reptiles.

intra.osseous

Subanesthetic doses produce variable
short-term sedation.

Alfaxalone

5---10 mg/kg, IV

Sinlilar effects to those of propofol IV, but

10-20 mg/kg, IM
higher doses effective IM. Larger IM dose
volumes may warrant dividing into two or
more irtjections.

Isoflurane

1%-5%

Routine gaseous agent; subanesthetic
levels provide short-term sedation. Mask
down or conscious (sedated) intubation
possible in some species.

Sevoflurane

2%--7%

Very similar effects to those of isoflurane
but recoveries appear to be faster.

Preferred agent for critical or large
reptiles.

tis if it is irtjected perivascularly. This is of
or by mask. However, breath holding tends
particular concern, because IV access may
to occur in turtles and crocodilians, which
be relatively difficult, especially in active
can respire anaerobically for prolonged
animals undergoing elective procedures.

periods. Induction may take 10-30 min in

Alfaxalone has been licensed in the USA; it
cooperative lizards and snakes. Intubation
is an excellent IV induction agent and is also
of conscious patients has been suggested
effective when used IM.

after local lidocaine spray, but the adverse

If IV access is impractical or dangerous to effects of increased stress and catecholaattempt, IM agents can be used to induce mine release should always be considered.

sufficient chemical restraint for intubation.

There is also the potential danger of being For IM irtjections in lizards and chelonians,
bitten.

the forelimb muscles are preferred, whereas
for snakes, the epaxial muscles are used. An

Maintenance of Anesthesia: Isoflurane

IM combination of ketanline, medetomidine
or sevoflurane are the agents of choice for

(or dexmedetomidine), and morphine or
maintenance of anesthesia. These volatile
hydromorphone has proved effective for a
inhalation agents have faster modes of
variety of chelonians; this can be readily
action, are more controllable, and facilitate
reversed using atipan1ezole and, if
faster recoveries than most alternatives.

necessary, naloxone or naltrexone.

Furthem1ore, their lack of reliance on

Squan1ates can also be induced by
hepatic metabolism or renal excretion
inhalation agents in an induction chan1ber
reduces the anestl1etic risk to debilitated

1980

REPTILES
reptiles or those with questionable renal
intracardiac or pulmonary shunts, especially
or hepatic function.

in aquatic species. However, end-tidal

Intubation of reptiles is relatively siJncapnography has proved effective.

ple. Small-gauge endotrachcal tubes or

Toward the end of surgery, the anesthetic
catheters are easily inserted through the
gas should be discontinued while maintain

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glottis immediately caudal to the tongue;
ing ventilation for anothet 5-10 min to
this may be aided by forcing the tongue up
facilitate excretion. At this point, oxygen
and forward by pressing a finger into the
should be discontinued in favor of room ail'

intermandibular space from under the jaw.

delivered by bag-valve mask to encourage

The reptilian glottis is actively dilated, and
spontaneous respiration.

therefore its movement will often be
abolished in anesthetized aniJnals; a guiding

Postoperative Support: Once it is
stylet can be useful to facilitate endotrabreathing spontaneously, the reptile can be cheal tube placement. The bifurcation of
returned to an incubator or vivruiurn to fully
the trachea may be far craniad in some
recover. Continued monit01fag is essential
chelonians, and gaseous exchange has also
until righting reflexes return ru1d the ru1in1al
been reported within the tracheal lung of
is an1bulatory. Additional analgesia, fluid,
some snakes; care should be taken to use
and nutritional support should be provided
a short endotracheal tube that is securely
as indicated.

taped in position.

Noncrocodilian reptiles lack a dia

Diagnostic Techniques
phragm; skeletal intercostal muscles

(Squamata) or limb movements (Chelonia)

Radiology: Several anatomic differences
control breathing. The action of these
make it difficult to obtaiJ1 quality radiomuscles is abolished at a surgical pla.ne of graphs rn reptiles. The relatively small size
anesthesia, and intermittent positive-presof most pet reptiles and the lack of diffuse sure ventilation is required. Ventilation rates body fat often produce iJnages of poor should initially mirror preanesthesia
contrast. Thick, highly keratinized scales,
evaluations and then be acljusted to
osteoderms, or shells cru1 severely hinder
maintain end-tidal capnography readings of
the x-ray bean1, necessitating greater power

15-25 mmHg. Electrical ventilators enable
and a subsequent loss of fine soft-tissue
precise control of ventilation rates and
detail.

pressures.

Despite these difficulties, most high

Monitoring anesthesia in reptiles differs
capacity units can be set to produce quality
considerably from doing so in mammals.

radiographs of reptiles. High-detailed

Palpebral and corneal reflexes are reliable
screen/film combrnations ( eg, mrunmograin those species in which they can be phy film) are essential to obtain sufficient
elicited (ie, all chelonians, all crocodilians,
detail and contrast, especially in smaller
most lizards, but no snakes). However,
aniJ11als. Various agents can be used to
corneal reflexes are abolished at toxic
in1prove contrast. Barium sulfate (300/o) can
doses, and pupillary diameter may bear little be used for GI studies. Water-soluble iodine relation to the depth of anestltesia (unless
compounds such as iohexol can be used for
fixed and dilated, which indicates excessive

GI, urogenital, ru1d IV techniques. The
anesthetic depth or brain anoxia and death). injection of air rnto the coelom of a lizru·d Jaw tone and withdrawal reflexes (tongue,
can greatly frnprove the appreciation of
limb, or tail) are abolished only at a surgical
preovulatory follicles.

plane of anesthesia. This also correlates

Snakes: Snakes can be difficult to position
with full loss of the righting reflex, loss of and restrain for radiographic exrunrnations
spontaneous movement, and complete
unless ru1esthetized. If tl1e purpose of the
muscle relaxation.

exan1rnation is sfrnply to exclude radiodense

Heart rate may be monitored by auscultaforeign bodies, tl1e snake may be allowed tion or by visualization or palpation of the
to coil in its natural position. If detailed
heart beat in most snakes and some lizards.

exan1rnation of the skeletal, respfratory, and

Pulse oxin1etry, using either an esophageal
digestive system is desfred, the snake must
or cloacal reflectance probe, is useful to
be extended. A plastic restraiJ1t tube can be
monitor pulse rate and strength. Although
used for this purpose; however, tlus may
the blood oxygen saturation (Sp02) reaclings
produce some radiographic artifact. In
are often low and have not been validated for larger snakes, several films will be needed to repLlles, monitoring the trend in Sp02 is often racliograph the entire length of the body.

helpful. Doppler ultrasonography can also be Lateral views are best taken using hotizontal used over peripheral arteries or the heart.

beams to avoid displacement rutifact of the

Blood gas estinmtions are often affected by
viscera. However, standru·d laterals with the

REPTILES

1981
snake taped in lateral recumbency can be

Chelonians: Most chelonians are fairly
useful, especially when horizontal beams
easy to position and restrain. For vertical
are not possible or safe to undertake. The
beam dorsoventral radiographs, most
interpretation of dorsoventral views are
conscious animals will remain motionless
hindered by the spine and ribs but can still
long enough to pennit exposure. Ideally, the

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be useful when dealing with obvious lesions
head and limbs should be extended from the
including eggs and mineralized masses.

shell to reduce superimposition of the limb

Lizards: Small lizards can often be
musculature on the coelomic viscera More
restrained by taping them to the radiography
active anin1als can be restrained by taping
film or table for a dorsoventral view. Placing
them to the cassette or by placing them in a
cotton balls over the eyes, and wrapping
racliolucent container, although this should
them with self-adhesive tape will often
be avoided with smaller specimens ( and
produce a calm, motionless lizard. A
lower exposures), because material artifacts
dorsoventral view can help identify foreign
may appear. For lateral horizontal beam
bodies, intestinal impaction, or coelornic
radiographs, the chelonian is best placed
masses. A horizontal x-ray bean1 provides
on a central plastron stand to encourage
the best lateral imaging in lizards, especially
extension of the lin1bs and head while the
when evaluating the respiratory system. The
tortoise remains in1mobile. Both left and right
positioning for this view involves rotating the lateral projections should be taken with the x-ray tube 90° and placing the film vertically
lateral edge of the shell touching ( or as close
behind the lizard. Elevating the body of the
as possible to) the cassette. The third basic
lizard on rolled towels or foam pads helps
coelomic view is the horizontal craniocaudal
prevent supe1irnposition of the limbs with

( or anterior-poste1ior) view. The chelonian is
the coelornic cavity. The positioning for, and
positioned on a central plastron stand, with
mterpretation of, crocodilian racliographs
the caudal edge of the carapace touching ( or
are sinillar to those used for lizards.

as close as possible to) the cassette; the head
should be facing the x-ray tube and the beam
centered on the midline of the cranial rim
of the carapace. Radiology of the head and
lin1bs requires exteriorization from the shell
usually under general anesthesia. The use
of sandbags, foan1, and tape aid positioning.

Standard interpretation requires that both
true lateral and dorsoventral views should be
taken-€ven slight rotation makes interpretation more difficult Ultrasonography: A useful and often
underrated teclmique, ultrasonography has
gained popularity as a diagnostic technique
for reptiles. It is particularly useful for
exrunining tissue pru·enchyrna, guiding
biopsy needles, and, with color flow

Doppler, investigating cardiac disease.

Unfortunately, the equipment tends to be
expensive, and several probes with small
footprints are required, given the variation
in reptile size ru1d ultrasotmd applications.

Ultrasound waves crumot penetrate through
mineralized tissue or air ru1d therefore
ultrasonography has obviou� llinitatio1�s to
investigate respiratory ru1d GI diseases.

The giru1t species require a 5-MHz probe,
whereas a 7.5-MHz probe suffices for most
reptiles. When exrunining very small
specimens ( or for ultrasonography of eyes),
a 10-20 MHz probe is more appropriate.

Good contact ru1d in1aging generally require

Radiograph of a Greek tortoise demonstrating
several abnormal eggs, including one within
copious quru1tities of gel or a water bath. It
the bladde'. and encased by uric acid, forming
is helpful to maintain the animal in a nom1al
a large urolith. Courtesy of Dr. Stephen Divers.

position or, failing that, at least appreciate

1982

REPTILES
the complications associated with organ
exanlinations ( eg, buccal cavity and cloaca)

displacement. Ultrasonography can be a
may be possible in a conscious or sedated
useful adjunct to radiography, especially to
aninlal using a mouth gag or other approp1iassess the reproductive tract ( evaluating ate restraint, but complete inlmobilization
ovarian activity and distinguishing between
is preferred to avoid risking dan1age to
pre- and postovulatory egg stasis), liver and
patient, staff, or equipment. Anesthesia is

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gallbladder, urinary system, soft-tissue
mandatory for coelioscopy.

masses, and heart. Ultrasonography has
been used to guide liver biopsy, although
iatrogenic traw11a has been reported in

Blood Collection: Venipuncture is
snakes.

generally a blind technique in reptiles. Up to

0.5 mUlOO g may be safely collected from

CT and MRI: CT offers excellent,
healthy reptiles, less in debilitated animals.

high-resolution, detailed inlages. Pote n

There is a relative lack of hematologic or
tially, it would be the diagnostic inlaging
biochemical data for most reptiles. In
technique of choice for the respiratory
addition, blood values can vary dramatically
system and skeleton of reptiles. MRI
with species, environment, nutrition, age,
produces prinlarily high-detailed inlages
breeding, and hibernation. Given this
of soft-tissue structures and is useful to
variability, published ranges may be of
diagnose neurologic, hepatic, renal, and
limited value. More reliance should be
reproductive diseases in reptiles. Disadvanplaced on establishing an individual's tages of these techniques are the need for
observed range and using serial sampling to
general anesthesia to completely eliminate
monitor the progress of hematologic and
motion, equipment availability, and cost.

biochemical changes. The use of a toenail
clip to obtain blood may result in fecal or

Endoscopy: Endoscopy has proved to
urate contanlination, increased tissue
be a most useful diagnostic tool in reptile
enzymes, and hemogram and electrolyte
medicine, and given the small and delicate
changes due to the peripheral nature of
nature of many species, continued
the sample and the crushing aitifact of
development of minimally invasive
collection. Of even greater concern are the
techniques is likely. Flexible endoscopes
ethical and welfare issues associated with
are useful for respiratory endoscopy in
toenail clipping.

snakes or GI endoscopy in many species.

The two common sites for venipuncture

The main disadvantage of the flexible,
in snakes are the caudal vein and the heart.

fiberoptic endoscope is the poorer in1age

The caudal vein is accessed caudal to the
quality than for those obtained using rigid
cloaca, between 25% and 500/o down the tail,
scopes of a sinlilar dian1eter. However,
and avoiding the paired hemipenes of
the continued develop·ment of smaller
males. In lizards, the most clinically useful
videoscopes looks likely to redefine flexible
vessel is the ventral midline caudal vein,
endoscopy in reptiles. The compact body
best accessed 200/o-800/o down the tail. The
size of most pet reptiles, coupled with
most clinically useful vessels in chelonians
their coelomic body design, makes rigid
appear to be the jugulars, subcarapacial
endoscopy useful in many situations.

sinus, and dorsal coccygeal veins. The left

Although equipment must be matched to
and right jugular veins are preferred
size of the reptile, in general the 1.9-mm and
because of the reduced risk of lymphatic

2. 7-mm telescope and sheath systems work
contanlination.

well for most pet species, enabling gas
insufflation, fluid irrigation, and biopsy

Necropsy: A detailed necropsy should be
capability.

undertaken whenever possible, because it

Insufflation is essential to provide the
often provides a definitive diagnosis. When
lens-organ distance required for visualizamanaging a disease outbreak in a population. For GI endoscopy, air and/or saline is tion, elective euthanasia and necropsy of
used; for coelioscopy, medical grade C02
one or more individuals is often the most
or saline is preferred. Coelomic pressures
efficient and cost-effective means of
seldom need to be >5 mmHg. When perdiagnosis. Fresh necropsies can provide fornling endoscopy in small neonates or
organ biopsies, blood, and other bodily
within a hollow viscus ( eg, bladder, oviduct,
fluids for laboratory exanlination. The
cloaca, stomach), warmed sterile saline
submission of microbiology samples,
inigation often provides better clarity than
especially bacteriology, from reptiles that
gas insufflation.

have died and remained within a heated

General anesthesia is recommended
enclosure must, however, be interpreted
for all endoscopy procedures. Certain
with caution.

REPTILES

1983

Surgery
samples may have been collected before
surgery. Therefore, the amount of blood a

In general, pe1forming surgery on a reptile
reptile can afford to lose during surgery may
patient should be approached with the same be considerably less. Careful consideration principles as those used for domestic
must be given to minimizing hemorrhage
animals. However, there are some specific
using cotton-tipped spears or applicators,

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anatomic considerations, as well as unique
vascular clips, and radiosurgery.

aspects of patient preparation, positioning,

Patient positioning will depend on the
and equipment. Only a basic discussion
species and the nature of the surgery.

follows here, and consulting other sources

Consideration should be given to ensuring
on reptile anatomy, physiology, husbandry,
that head and neck position does not
anesthesia, and surgery, as well as domestic
interfere with ventilation; avoiding
animal surgery literature, is essential before
excessive compression of the head, limbs,
perfornting surgery on any reptile.

or coelorn to prevent pressure necrosis,

For truly giant reptiles, such as giant
visceral rupture, or hypoventilation of the
tortoises, the use of stronger, large animal
lW1gs; avoiding extreme and prolonged
instruments is recommended. For reptiles
hyperextension or hyperflexion of any joint;
weighing 5-50 kg, most instruments
and ensuring that the surgical site is easily
used for small anin1als are appropriate.

accessible and does not require surgeon

However, most pet reptiles weigh < 1 kg,
positioning that will result in fatigue.

and microsurgical instruments are often

Sand-bags, bean-bags, foam supports, and
required. These instruments are not miniaadhesive tapes can be used to maintain turized versions of standard instruments
patient position.

but rather balanced instruments with fine,

When reptile skin is incised, it tends to
small tips. Because microinstruments
invert. Therefore, everting suture patterns
can be costly, ophthalmologic instruments ( eg, horizontal mattress) are recommended can be useful alternatives. Plastic, selfto ensure opposition of tissue without future retaining retractors can be adjusted to
dysecdysis. The skin suture materials should
fit different sizes of incisions and do not
be rnonofilament. Wire suture may be
compromise ventilation. Smaller versions
required for repairs involving shell or thickly
of standard abdominal retractors can also
keratinized skin containing osteoderms.

be used but are significantly heavier.

Staples have also been advocated, because

Eyelid retractors can be useful to retract
they cause mild eversion of the skin. Given
coelomic incisions in small lizards and
the length of time it takes for reptile wounds
snakes. Epoxy resins or low-temperature
to heal, sutures should not be removed until
veterinary acrylics are used for many

6--8 wk after surgery.

chelonian plastron closures and shell

The primary factors to consider
repairs.

postoperatively are analgesia and continued

Rapidly absorbable suture materials are
vigilance concerning hydration, temperarecommended for internal soft-tissue ture, nutrition, and hygiene. It is widely
applications. For prolonged internal
understood and accepted that reptiles can
durability, polydioxanone or nylon are
feel pain. Pain slows the healing process
preferred. Poliglecaprone, monofilament
and depresses the normal filllction of the
nylon, and polydioxanone are favored for
immune system in manunals. There is no
skin suturing, although wire may be
evidence to suggest this process would not
necessary for giant to1toises or monitor
be similar in reptiles. Clinically, reptiles that
lizards.

receive postoperative analgesia appear to

Because most reptile patients that require recover better than those that do not. The surgery are significantly smaller than
continuation of preemptive analgesia using
man1111alian patients, some degree of
opioids and/or NSA!Ds should be a routine
magnification is generally recommended.

part of postoperative care.

Headband or frame-mounted operating

Few drugs are approved by the FDA for
loupes (2-4 x magnification) with a
use in reptiles. Medications can be given by
dedicated halogen or xenon light source
a variety of routes, including PO, SC, IM, IV,
are affordable, versatile, comfortable, and
intracardiac, intracoelomic, intraosseous,
simple to use. While operating, microscopy
intrasynovial, or intratracheal irtjection.

telescopes can provide magnification with

Certain drugs can be applied topically, given
selected 1igid endoscopy systems.

per cloaca, by inhalation (nebulization),

A healthy reptile can generally tolerate
or by direct intralesional administration.

0.4-0.8 mUlOO g body wt of blood loss.

Because reptiles are ectotherrns, tempera

Reptiles in need of surgery are often
tures outside the preferred optimal
compromised, and diagnostic blood
temperature zone (POTZ) can have

1984

REPTILES
profound influences on drug distribution,

Antimicrobials: Many bacterial infections
metabolism, excretion, and elimination
in reptiles are caused by gram-negative
half-life. Some therapeutic regimens state
bacteria, particularly Pseudomonas,
a fixed temperature at which the reptile

Aeromonas, Citrobacter, Klebsielta, and
should be held during treatment. lithere are Proteus spp. Bacterial resistance to many VetBooks.ir
pharmacokinetic data on the drug, then the
commonly used antibacterials is seen, and
elimination of the drug will be known and
many gram-negative bacteria can have
constant. However, if this stated temperaunexpected sensitivity to particular antiture is below or above the POTZ for the bacterials; therefore, sampling for Gram
species being treated, then stress and
stain, cytology, culture, and sensitivity
debilitation may ensue. Even when the
testing should be done before starting
stated therapeutic temperature is within the tl1erapy. Antibacterial therapy must usually POTZ for the species being treated, constant be given while awaiting the results of exposure to a fixed temperature is likely to
bacterial sensitivity tests. In these circun1-
be stressful.

stances, an1ikacin, ceftazidime, and

Reptiles have a well-developed renal
enrofloxacin or ciprofloxacin are often
portal system; blood from the caudal half of
preferred (see TABLE 27). In severe infecthe body passes through the kidneys before tions, anlikacin may be combined with
reaching the systemic venous circulation.

ampicillin or amoxicillin for respiratory

Drugs injected into the caudal half of the
tract infections or with ceftazidime for
body may have a significantly reduced
generalized or systenlic infections.

half-life if excreted via tubular secretion.

Chloramphenicol in combination with

However, studies have demonstrated that
neomycin may be given for GI infections.

these effects are unlikely to be clinically

Penicillin, metronidazole, lincomycin, or
significant. Of potential concern is the
clindamycin can be used for anaerobic
caudal injection of nephrotoxic drugs that
infections.

may reach renal tissue in high concentration.

Fungal and yeast infections commonly

Also, the large bladder of chelonians may act
occur in reptiles. GI and skin mycoses are
as a drug reservoir and lead to a secondary
particularly common in reptiles maintained
therapeutic peak many hours after drug
on inappropriately longterm broad-specadministration. The shell of tortoises, turtles, trum antibacterials. Cutaneous mycoses and te1rnpins is largely living tissue;
can often be treated by debridement and
therefore, all chelonian medication should
topical application of antifungals. GI
be based on total body weight.

infections can be treated with nystatin,
whereas systemic infections may require

Drug Dosage and Allometric Scaling:

itraconazole or ftuconazole. In cases of

Numerous pharmacokinetic studies have
pulmonary mycoses, antifungal medication
been published for reptiles, and tl1ese
may be given by nebulization or intratrashould be considered tl1e most reliable cheal or intrapulmonary injection.

source for information on drug dosages.

Herpesviruses can cause severe morbidity

When species-specific inforn1ation is not
and mortality in chelonians. Acyclovir has
available, it is possible to extrapolate from
been used witl1 some success during the
closely related species. If there are no
early stages.

pharmacokinetic data or reliable clinical
experience for a particular species, it may
be necessary to extrapolate pharmacoki

Parasiticides: Parasititides used
netic data from other aninlals. Allometric
commonly in reptiles are listed in TABLE 28.

scaling calculates the drug dose and dosing

Parasiticide overdosage may lead to drug
frequency using metabolic rate rather than
toxicity, which may be seen as neurologic
body weight. The basic allometric equations signs, including seizures. Ivermectin is are shown below, in which W = body weight
contraindicated in chelonians, and adverse

(kg) and K = energy constant, which is 10
reactions have been reported in some
for reptiles. These equations can be used to
iguanid lizards, skinks, and indigo snakes.

calculate a dose and dose frequency for a

Milbemycin has been successfully used
species for which no data are available, by
in box tortoises and terrapins, but it is
using pharmacokinetic data from a known
recommended that ivermectins and
species ( control), whether another reptile
milbemycins be avoided in all chelonians
or man11Tlal or bird:

because safer alternatives are available.

Permethrin is licensed for use in reptiles

Minin1un1 energy cost= K (W0.75)

and appears safe and effective against

Specific minimum energy cost = K (W·0.25)

mites and ticks.

REPTILES

1985
itiN!ffl ANTIMICROBIAL DRUGS USED IN REPTILES

Drug

Dosage

Comments

Acyclovir

80 mg/kg/day, PO; topical cream 12 times Antiviral VetBooks.ir
daily

Amikacin

Com snake: loading dose 1. 7 mg/kg, IM, Maintain hydration followed by 26 mcglkg/hr via osmotic
infusion-pump implant

Gopher snake: initial dose 5 mg/kg, IM,
then 2.5 mg/kg, IM, every 3 days

Gopher tortoise: 5 mg/kg, IM, on
alternate days

American alligator Uuvenile):

2.25 mg/kg, IM, every 3--4 days

Ball python: 3.5 mg/kg, IM, every 4-5 days

50 mg/10 mL saline x 30 min nebulization
bid

Amoxicillin

22 mg/kg, PO, bid

Often ineffective unless

10 mg/kg/day, IM
given in combination
with aminoglycosides

Amphotericin B 0.5- 1 mg/kg, intracoelomic, IV, 1-3 days Aspergillosis; fluid for 14-28 days
therapy recommended

Tortoise: 0. 1 mg/kg/day, intrapulmonary, Pulmonary candidiasis for28 days

5 mg/150 mL saline for 1 hr of nebulization, bid for 7 days Ampicillin

Most species: 10-20 mg/kg, SC, IM,

1-2 times/day

Tmtoises: 50 mg/kg, IM, bid

Azithromycin

Ball python: 10 mg/kg, PO, every 3-7 days

(3 days for skin infections, 5 days for
respiratory tract, 7 days for liver and
kidneys)

Carbenicillin

200--400 mg/kg/day, IM

Cephalexin

20--40 mg/kg, PO, bid

Ceftazidirne

20--40 mg/kg, SC, IM, IV, every 2-3 days

Ceftiofur

Tortoises: 2.2--4 mg/kg/day, IM

Snakes: 2.2 mg/kg, IM, on alternate days

Lizards: 5 mg/kg/day, IM, SC

Cefuroxirne

100 mg/kg/day, IM, for 10 days at 30 °C

Chloramphenicol Indigo snake: 50 mg/kg, IM, bid

Midland water snakes: 50 mg/kg, IM,
every4 days

Most species: 20--40 mg/kg, IM, once to
twice daily

Ciprofloxacin

10 mg/kg, PO, on alternate days

Clarithromycin

Desert tortoise: 15 mg/kg, PO,

Mycoplasma
every 2-3 days

Clindamycin

5 mg/kg, PO, bid

Clotrirnazole

Topical

Fungal dermatitis

1986

REPTILES

ANTIMICROBIAL DRUGS USED IN REPTILES (continued) Drug

Dosage

Comments

Doxycycline

Most species: 5-10 mg/kg/day, PO

VetBooks.ir

Hermann's tortoise: 50 mg/kg, IM, then

25 mg/kg, every 3 days

Enrofloxacin

Most species: 5-10 mg/kg/day, IM, PO

IM injection likely causes
necrosis, and consideration should be given to
single injection followed
by oral administration

Nasal flush 50 mg/250 mL sterile water;

1-3 mUnares daily to every other day

Burmese python Guvenile): 10 mg/kg,

IM injection likely causes

IM, initial dosage, then 5 mg/kg, IM,
necrosis, and consideraevery 48 hr. Pseudomonas: 10 mg/kg, IM, tion should be given to every 48hr
single injection followed
by oral administration

Hermann's tortoise: 10 mg/kg/day, IM

IM injection likely causes
necrosis, and consideration should be given to
single injection followed
by oral administration

Monitor lizards: 10 mg/kg, IM, every 5
days

Indian star tortoise: 5 mg/kg, IM, once to IM injection likely causes twice daily
necrosis, and consideration should be given to
single injection followed
by oral administration

Crocodilians: 5 mg/kg IV every 2-3 days

Fluconazole

Lizai:ds: 5 mg/kg/day, PO

Sea turtles: 21 mg/kg, SC, once; then

10 mg/kg, SC, 5 days later

Gentamicin

American alligator: 1. 75 mg/kg, IM, every Maintain hydration, 3-4 days at22°C
nephrotoxicity reported

Painted turtle: 10 mg/kg, IM, on alternate Maintain hydration, days at 26°C
nephrotoxi«?ity reported

Red-eared terrapin: 6 mg/kg, IM, every

Maintain hydration,

25 days
nephrotoxicity reported

Gopher snake: 2.5 mg/kg, IM, every 3

Maintain hydration,
days at 24 °C
nephrotoxicity reported

Itraconazole

Chameleon: 5 mg/kg/day, PO

Fungal dermatitis

Spiny lizard: 23.5 mg/kg/day, PO, for 3
days, with persistent drug concentration
for 6 days

Snakes: 10 mg/kg/day, PO

Sea turtles: 5 mg/kg/day, PO, or 15 mg/kg,

PO, every 72 hr

Kanamycin

10 mg/kg/day, IM, at 24 °C

Fluid therapy recommended

REPTILES

1987

ANTIMICROBIAL DRUGS USED IN REPTILES (continued) Drug

Dosage

Comments

Ketoconazole

Crocodilians: 50 mg/kg/day, PO

VetBooks.ir

Most species: 15-30 mg/kg/day, PO, for

14--28 days

Lincomycin

10 mg/kg/day, PO; 5 mg/kg, IM, once to
twice daily

Marbofloxacin

Ball python: 10 mg/kg, PO, every 48 lu-

Metronidazole

Bacterial infections, 20-50 mg/kg, PO,

Maximal dose for tricolor
every 1-2 days
snake, king snake, indigo
snake, or Uracoan
rattlesnake, is 40 mg/kg

Neomycin

10 mg/kg/day, PO

Oral only, not to be given
systemically

Nystatin

Enteric fungal conditions in turtles:

100,000 U/kglday, PO, for 10 days

Oxytetracycline

Most species: 5-10 mg/kg/day, IM, PO

Pain, irritation, and
inflammation at injection
site

American alligator: 10 mg/kg, IV, IM,

Mycoplasmosis
every 4--5 days

Piperacillin

50-100 mg/kg, IM, every 12 days

Fluid therapy recom-
mended

Polyrnixin B

Topical

Abrasions, wow1ds

Silver sulfa-

Topical every 24--72 hr

Broad spectrum for skin
diazine
infections

Sulfamethoxy-

80 mg/kg, SC, IM, then 40 mg/kg/day, for Coccidial infections diazine

5-7 days

Tobramycin

Chelonians: 10 mg/kg, IM, every 1-2 days Potentially nephrotoxic; Most species: 2.5 mg/kg, IM, every 1-3
fluid therapy recom-
days
mended

'fylosin

5 mg/kg/day, IM

Mycoplasmosis

Voriconazole
lOmg/kg,PO

•hh•fl• PARASITICIDES USED IN REPTILES

Drug

Dosage

Parasite

Comments

ENDOPARASITICIDES

Fenbendazole

25-100 mg/kg, PO every Roundwonns,

Can cause

14 days for up to 4

Hexamita
leukopenia
treatments

50 mg/kg/day, PO, for

3-5 days

Ivennectin

200 mcg/kg, PO, IM, SC,

Not in chelonians;
repeat after 14 days
care in skinks and
indigo snakes

1988

REPTILES

•tfiii.J:• PARASITICIDES USED IN REPTILES (continued) Drug

Dosage

Parasite

Comments

Levamisole

5 -10 mg/kg, SC,

Ltmgworms and Snakes, lizards,

VetBooks.ir
intracoelomic, repeat
other nematodes care in tortoises
after 14 days

(use 5 mg/kg)

Mebendazole

20-25 mg/kg, PO, repeat Strongyles and
after 14 days
ascarids

Metronidazole

20-40 mg/kg, PO, every Protozoa

1-2 days for 2-5
treatments

Oxfendazole

68 mg/kg, PO, as a

Nematodes
single dose

Paromomycin

35--100 mg/kg/day, PO,

Amoebas,

Does not eliminate
for 28days
cryptosporidia
cryptosporiclia

Ponazuril

Bearded dragons: 30

Coccidiosis
mg/kg, PO, every 2 days
for two treatments

Praziquantel

8 mg/kg, PO, SC, IM,

Tapeworms,
repeat after 14 days and flukes

28days

Pyrantel

5 mg/kg, PO, repeat in

Nematodes

14 days

Spirarnycin

160 mg/kg/day for 10

Snakes with

May reduce clinical
days, then twice weekly cryptosporidi-
signs but does not
for 3 mo
osis
clear infection

Toltrazuril

5--15 mg/kg, PO, repeat Bearded

Safety, efficacy, and
in 14 days
dragons,
pharmacokinetic

15 mg/kg, every 48 hr
coccidiosis
data lacking
for 10 days; discontinue
for 2 wk; repeat every

Tortoises,

48 hr for 10 days, and
intranuclear
repeat as necessary
coccidiosis

Trimethoprin1-sulfa

30 mg/kg/day, PO, for

Coccidia

10-28days

ECTOPARASITICIDES

Dichlorvos1 cm2 of strip/30 cm3

Toxic, vivariwn
irnpregnated strip
vivarium for 28 days or
should be emptied;

2.5 cm2 of strip/25 cm3
keep out of direct
vivarium for 2-3 days
contact of animals
every week

Fipronil

By spraying, every

Mites and ticks

7-lOdays

Iverrnectin

By spraying, 1 -2 mL/L

Mites and ticks

Should not be used

(lOmg/mL)

water every 7-10 days
in chelonians; use

200 mcg/kg, IM, every
care in skinks and

7 -14 days
indigo snakes

Permethrin (1Cl%)

Topical spray

Mites and ticks

Licensed product
available for
reptiles in the USA

REPTILES

1989

Other Medications: Dosages for
electrolyte losses through frequent vomiting
medications used for a variety of other
or dianhea. Water balance in reptiles differs
disorders of reptiles are listed in TABLE 29.

from that in mammals, because, per unit
body weight, reptiles have a higher

Fluid Therapy: Dehydration in reptiles
percentage of total body water (63.0 %--
is usually associated with prolonged

74.4%) and a higher percentage of intracel

VetBooks.ir
anorexia and water loss, deprivation, or
lular water ( 45.So/o-58.00Ai). These values
an inability to drink, rather than mixed
appear to be highest in freshwater species,

•th•ff• MISCELLANEOUS DRUGS FOR REPTILES

Drug

Dosage

Condition

Allopurinol

20--25 mg/kg/day, PO

Gout, reduces uric acid production

Aluminium

100 mg/kg, PO, every 12--24 hr

Reduces blood phosphorus levels
hydroxide

Aminophylline

2--4 mg/kg, IM

Respiratory disease when
bronchodiJation required

Argipressin

0.01--1 mcg/kg

Egg binding (more potent than

( vasopressin)

oxytocin)

Ascorbic acid

10--200 mg/kg, IM, as required

Ulcerative stornatitis

Calcito.ni.n

1.5 units/kg, SC, tid

Hypercalcemia, fluid therapy also

50 units/kg, IM, repeat
recommended
after2 wk

Secondary hyperparathyroidism

Calcium

100 mg/kg, lM, qid, or 400

Hypocalcernia in iguanas; high
gluconate
mg/kg, IV, intraosseous, given
phosphorus concentration may

(lOmg/mL)

over24hr
cause soft- tissue mineralization

Cimetidine

4 mg/kg, PO, tid-qid

Regurgitation, vomiting, gastritis,

GI ulceration

Cisapride

0.5--2 mg/kg/day, PO

GI motility modification; not
recommended to use with
clarithromycin in tortoises

Cholecalciferol 100--1 ,000 units/kg, IM, as a

Hypocalcemia, fibrous osteodystrosingle dose
phy in iguanas

Cyanocobalamin 50 mcg/kg, SC, IM

Appetite stimulation

Dexamethasone 30--150 mcg/kg, IM, IV,

Inflammation, shock, beware of
intraosseous
inmmnosuppression

Dinoprost

500 mcg/kg, IM, as a single dose Egg binding in snakes (prostaglandin)

Doxapram

5--10 mg/kg, IV, intraosseous

Respiratory stimulation

Fllll1ixin

100--500 rncg/kg, IM, IV, once to Inflammation, pain twice daily

Furosemide

2--5 mg/kg, IM, IV, once to twice Diuresis ( effective despite lack of daily
loop of Henle in reptiles)

Iodine

2--4 mg/kg, PO, every 7 days

Prophylaxis for goitrogenic diets

Iron

12 mg/kg, IM, every 7 days

Anemia in alligators

(alligators)

Levothyrox.ine

20 mcg/kg, PO, on alternate

Hypothyroidism in tortoises
days

1990

REPTILES

•M=i!ffj MISCELLANEOUS DRUGS FOR REPTILES (continued) Drug

Dosage

Condition

Metoclopramide 60 mcg/kg/day, PO, for 7 days

Stimulation of gastric emptying in
tortoises

VetBooks.ir

Prednisolone

1-2 mg/kg, PO

Anti-inflammatory, reduction of
nephrocalcinosis, beware of
immunosuppression

Selenium

25-500 mcg/kg, IM

Deficiency in lizards

Sucralfate

0.5-1 g/kg, PO, tid-q_id

Gastric irritation/ulceration

Thiamine

50-100 mg/kg, IM

Thiamine deficiency

Vitamin A

5,000 units/kg, PO, every 7 days Hypovitaminosis A (iatrogenic hypervitaminosis A may result
from repeated treatment)

lower in terrestrial reptiles, and lowest in
moderate to severe cases, intracoelomic, IV,
marine reptiles, with the concentration of
or intraosseous routes are favored.

isotonic saline in nonmarine reptiles being
lntracoelomic administration of fluids

0.8%. This has led to the conclusion that
is faster, less stressful, and allows delivery
nonnal 0.9% saline may be too concentrated
of a larger volume than stomach tubing.

for most reptiles. Balanced crystalloid fluids Large volumes of intracoelomic fluid could containing dextrose (260-290 mOsm/L)

compromise lung function and may be
appear to be effective. As a general guide,
slowly absorbed; however, IV catheterizamaintenance requirements are about tion is not easy, and cut-down procedures

5-15 ml/kg/day, and rehydration should
are often required. In emergencies with
proceed at 35-40 mlikg/day, although in
larger snakes, it is possible to place an
cases of shock, rates of 3-5 mlikg/hr can
intracardiac catheter. Fluid infusion is best
be used for several hours.

controlled by a syringe driver or infusion

In many instances, simply permitting
pump. If such devices are not available, the
a reptile to bathe in shaJlow, warm water
total daily fluid volun1e can be divided into
within a vivarium maintained at the
three or four bolus injections, each given
species-specific preferred optimal
slowly over 10-20 min. IV catheters can
temperature zone will promote drinking.

usuaJly be left in place for up to 72 hr;

Such a method is acceptable when reptiles
intracardiac catheters up to 24 hr. Intraosseare able and willing to drink voluntarily.

ous infusion is an easier technique in lizards,

However, in many cases oral fluids must
smaJI crocodilians, and chelonians. The
be delivered via a stomach tub�. For oral
needle is directed into the medullary cavity
rehydration, mammalian electrolyte
of a long bone, and aspiration of marrow or
solutions can be used but are best diluted
radiography can verify correct positioning.

by a further 100/o-15% to produce a slightly

Great care must be exercised when dealing
hypotonic solution. Significant amounts of
with osteodystrophic lizards to avoid
water may also be absorbed via the cloaca
limb fractures. Infusion rates for IV and
when chelonians (and possibly other
intraosseous administration are similar. As
species) bathe. Oral fluid therapy works
a general guide, 0.8--1.2 ml/kg/hr is suitable
well to provide maintenance requirements,
for rehydration purposes, but in cases of
rehydrate mildly dehydrated reptiles, and as
severe dehydration or shock or during
a vehicle to give oral medications and food.

surgery, 3-5 mlikg/hr can be given for

For alert and active reptiles, this method is

2-3 hr.

preferred because it facilitates GI activity,

Colloids are less frequently used in
and fluids are rapidly absorbed when the
reptiles because much of the water loss is
reptile is maintained at correct temperafrom the intracellular space rather than tures. Repeated stomach tubing is stressful
plasma, but they can be used in cases of
and can be difficult in strong chelonians;
acute hemorrhage. If severe hemorrhage
therefore, esophagostomy tubes are
occurs (ie, PCV <5%), whole blood may
recommended for longterm oral therapy.

be given by IV and intraosseous routes.

Small fluid volumes can be given SC, but in

Cross-matching does not appear necessary,

REPTILES

1991
at least for a single transfusion. Ideally the
antibiotics are recommended. Good
donor and recipient are of the same species.

sanitation is paramount for prevention.

Another shell disease of turtles is caused

BACTERIAL DISEASES
by Beneckea chitinovora, a common
infectious agent of crustaceans. Erythema

Bacte1ial diseases are common in reptiles,
and pitting of the shell with ulceration is

VetBooks.ir
with most infections caused by opportunisseen. Septicemia is unconu11on. Topical tic agents that infect imrnunosuppressed
iodine is recommended in addition to
hosts. A comprehensive approach is
antibiotics. The practice of feeding crayfish
required to ensure the success of a
is often implicated in this condition and
therapeutic plan. It is in1portant not only to
should be discouraged.

determine the causative agent but also to
con-ect predisposing factors. Appropriate

Ulcerative or Necrotic Dermatitis:

therapy in the absence of appropriate

Ulcerative dermatitis (scale rot) is seen
husbandry and nutrition will ultinmtely fail.

in snakes and lizards kept in unllygienic

Culture and sensitivity are recommended
conditions with excessive humidity and
to detem1ine appropriate therapy. Most
moisture. Moist, contan1inated bedding
bacterial infections involve gran1-negative
allows bacterial and fungal growth that,
bacteria, many of which are considered
when coupled with exposure to fecal
commensal. Anaerobic infections are not
degradation products, can predispose to
uncommon, but organisms can be difficult
small cutaneous erosions. Secondary
to culture. Gran1-positive bacteria on
infection with Aeromonas spp, Pseu
smears, in conjunction with a negative
domonas spp, and a nun1ber of other
culture, may indicate an anaerobic
bacteria may result in septicemia and death
infection. Alternatively, if a therapeutic
if untreated. Erythema, necrosis, and
choice was based on aerobic culture and
ulceration of the dermis, and an exudative
sensitivity and response is poor, then the
discharge are common. Although lesions
presence of an anaerobe should be
are often sequelae of skin injuries, they
considered.

more often develop from within, as is the
case with classic necrotic dermatitis in the

Septicemia: A number of infectious
ball python. The disease can develop even
conditions are similar in appearance,
when these anin1als are maintained under
regardless of species. Septicemia is a
pristine conditions, so it is not simply a
common cause of death. The systemic
matter of excessive moisture and poor
disease may be preceded by trauma, local
hygiene. The condition starts with
abscessation, parasitism, or environmental
hem01Thage into scales, followed by
stress. Aeromonas and Pseudomonas spp pustules that eventually lead to open and
are frequently isolated; the fom1er may be
ulcerated lesions. Treatment with systemic
transmitted by ectoparasites. Death may
antibiotics, topical antibiotic ointment, and
be peracute or follow a protracted course.

excellent hygiene and husbandry are

Conunon temunal signs are respiratory
essential.

distress, lethargy, convulsions, and

Blister disease has traditionally been
incoordination. Petechiae may be found
considered a separate entity but is sin1ply
on the ventrun1, and chelonians develop
an early stage of ulcerative (necrotic)

erythema of the plastron. Sanitation and
dermatitis. The cutaneous involvement is
husbandry can be significant factors in
characterized by pustules or blisters that
reducing outbreaks. Affected reptiles
may resolve without development of
should be isolated, and antibiotic therapy
ulcerative lesions if treatment is started
initiated.

early. A low-grade thermal injury may mimic
blister disease because of the potential

Septicemic Cutaneous Ulcerative
development of fluid-filled vesicles.

Disease (SCUD): Classically, SCUD is a
shell disease of aquatic turtles caused by

Abscesses: Focal infections caused by

Citrobacter freundii; however, various
traw11atic injuries, bite wounds, or poor
bacteria have been isolated from diseased
husbandry are seen in all orders of reptiles.

skin and shell. Serratia spp may act

Subcutaneous abscesses are seen as
synergistically by facilitating entry of
nodules or swellings. Differential diagnoses

C freundii. The scutes are pitted and
include parasitic nodules, tumors, and
may slough with an underlying purulent
hematomas. Isolates of the anaerobic
discharge. Anorexia, lethargy, and petechial
organism Pe'J)tostre'J)tococcus and of the
hemon-hages on the shell and skin are seen;
aero bes Pseudomonas, Aeromonas,
liver necrosis is also common. Systemic

Serratia, Salmonella., Micrococcus,

1992

REPTILES

E1ysipelotlni.-r:, Citrobacterfreimdii,
especially with vitan1ins A and C, has been

Morganella morganii, Proteiis, Staphylo
advocated but does not always affect the
coccus, Streptococcus, Escheiichia coli,
disease comse.

Klebsiella, and Dermatophilus have been recovered from reptilian abscesses, often in

Pneumonia: Respiratory infections are

VetBooks.ir
combinations. Small, localized abscesses
common; the incidence crui be influenced
should be completely excised to avoid
by respiratory or systemic parasitism,
recunence, which is frequent. Larger
unfavorable environmental temperatures,
abscesses should be marsupialized,
unsanitary conditions, concurrent disease,
followed by aggressive local wound
malnutrition, and hypovitaminosis A.

treatment. The lining of the abscess must

Open-mouth breathing, nasal discharge, and
be aggressively scraped to remove as much
dyspnea are frequent signs. Aeromonas and
material as possible. Appropriate systemic

Pseudomonas spp are frequently isolated,
antibiotics may also be indicated but are
but many respiratory infections are mixed.

seldom necessary after complete excision.

Septicemia may develop in severe or

Anaerobic bacteria are common in these
prolonged cases. Treatment consists
lesions, and an appropriate antimicrobial
of in1proving husbandly and initiating
agent ( eg, metronidazole, ceftazidirne, or a
systemic antibiotics. Nebulization therapy
potentiated penicillin product) may need
with antibiotics di.luted in saline, in
to be used or added to a current regin1en.

combination with acetylcysteine, has been

Visceral abscessation may occm as
used together with parenteral antibiotics.

a result of hematogenous infection.

Reptiles with respiratory infections should

Abscesses of the female reproductive
be maintained at the mid to upper end of
system are common and may result in
their preferred optimal temperatme zone.

coelomitis. Surgical intervention is

Increased temperatures are important not
indicated; systemic antibiotics alone are
only to stin1ulate the inmmne system but
rarely, if ever, successful.

also to help mobilize respiratory secretions.

Subspectacle abscessation is seen in

Turtles often have an underlying vitamin A
snakes, and conjunctivitis is seen in the
deficiency and require dietary correction.

other orders. Severity ranges from mild

Many turtles treated for pneumonia do not
inflan1111ation to panophthalrnitis and may
improve completely until after treatment for
occm as a result of ascending infectious
vitamin A deficiency.

stomatitis (see below). Topical antibiotic
ointments are used in turtles, lizards

Mycoplasmosis: Mycoplasmosis is
without spectacles, and crocodilians. In
a known cause of rhinitis and upper
snakes and lizards with spectacles, drainage respiratory tract disease in chelonians and is achieved by smgically removing a small
polyserositis in crocodilians. In chelonians,
wedge from the spectacle and flushing the
the disease has been associated with
subspectacular space and lacrirnal duct
population declines, and the disease is often
with an antibiotic solution (eg, gentamicin).

chronic and/or intermittent. In Ame1ican

Some affected reptiles, especially turtles,
alligators, mycoplasmosis results in severe
may need supplemental vitamiR A.

systemic disease and frequently death. A

Infectious Stomatitis: Infectious
stomatitis is reported in snakes, lizards, and
turtles and characterized early by petechiae
in tl1e oral cavity; caseous material develops
along the dental arcade as tl1e condition
worsens. In severe cases, infection extends
into the mandible and maxilla. Aeromonas
and Pseudomonas spp, common oral
inhabitants, are most frequently isolated,
along with a variety of other gram-negative
and gram-positive bacteria. Respiratory or

GI infection may develop in poorly managed
cases. Surgical debridement, irrigation with
antiseptics, systemic antibiotics, and
supportive therapy are indicated. In severe

Aural abscesses represent middle ear
cases with ulceration or granuloma
infections in turtles and chelonians. In box
formation, aggressive smgery may be
turtles, these abscesses are commonly
associated with vitamin A deficiencies.

indicated. Vitanlin supplementation,

Courtesy of Dr. Stephen Divers.

REPTILES

1993
variety of Mycoplasma species have been

Mycobacteriosis: Mycobacterial
isolated. PCR and serologic diagnostic aids
infections are often associated with clu·onic
have been developed, and treatment using
wasting in wild, imported reptiles and are
fluoroquinolones, clarithromycin, and
seen as granulomatous lesions at necropsy.

oxytetracyline has been advocated.

Chelonians generally exhibit pulmonary

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involvement, whereas lizards, snakes, and

Otitis: Ear infections occw- frequently in
crocodilians commonly show visceral
turtles, especially box turtles and aquatic
granulomas. The species isolated are
turtles. Marked swelling is seen at the

Mycobacterium ulcerans, M chelonae, M
tympanic membrane, and caseous material haemophilum, and M marinum. All are is present. Proteus spp, Pseudomonas
cultured at reduced temperatw·es and may
spp, Citrobacter spp, Morganella
require long periods for growth. Rifampin
morganii, Enterobacter spp, and other
and isoniazid are hepatotoxic, and the
bacteria have been isolated. The tympanic
longtenn administration required is unlikely
membrane must be incised, and aggressive to be safe. There are no reports of successcurettage of the area performed. Surgical ful treatment.

removal of the abscess is usually cw-ative
as long as all infection is removed and the

Salmonella Arizonae and Edwardsiella

Eustachian tube is patent. The open area

Infection: These bacteria have been
should be flushed with diluted povidoneisolated from clinically healthy reptiles.

iodine or a similar product for a few days

The zoonotic nature of these commensal
to prevent premature closure and to keep
organisms must be considered when
the area clean. Systemic antibiotics are
handling or treating reptiles. Attempts to
rarely required. Ear infections may be
eliminate these microorganisms from
secondary to hypovitaminosis A; dietary
reptiles and their eggs have been tmsuccesssupplementation of vitamin A may be ful and are not recommended. Vete1inarians
beneficial.

and reptile owners should be aware of the
infom1ational brochures available from the

Association of Reptile and Amphibian

Cloacitis: Often traumatic in 01igin,

Veterinarians.

infectious cloacitis is characterized by edema
and hemopwulent discharge. Cloacal calculi
may form in vitamin or mineral imbalances

MYCOTIC DISEASES
and should be manually removed and

Excessively high hw11idity, low environfollowed by dietary correction. In pericloacal mental temperature, concmrent disease, abscesses, the infection often migrates
malnutrition, and other stressors may
craniad. Ascending winary or genital tract
predispose reptiles to development of
infections are common sequelae. Aggressive
various mycoses. Little is known about
therapy, including sw-gical debridement,
the pathogenesis of systemic mycoses,
local wound treatment, and appropriate
which can develop over a long period, but
systemic antibiotics, is indicated. Fecal
maintaining good sanitation and husbandry
examinations should be perf01med to
reduces the frequency of infection.

identify potential parasitic causes.

Aspergillus, Candida, Cladosporium,

Metarh-izium, Mucor, Paecilomyces,

Spinal Osteopathy/Osteomyelitis:

Penicillium spp, and the Chrysosporium

Although previously repmted in the reptile
anan1orph of Nannizziopsis miesii are a
literature as Paget disease, this condition is
few of the organisms associated with
now thought to be a chronic bacterial
systemic disease. Reports of successful
osteomyelitis of the spine. Traditionally,
treatment of systemic mycoses in reptiles

Paget disease is characterized by repeated
are few. Suggested treatments for deep
episodes of osteoclastic bone resorption
fwlgal respiratory infections include
and deposition, leading to dense, brittle
amphotericin B, itraconazole, flucona-
bones. Commonly reported in snakes, these
zole, and voriconazole. For superficial or
proliferative and progressive spinal lesions
localized mycotic infections, sw-gical
have been investigated and are thought
removal of the granuloma with local wound
to be associated with chronic bacterial
treatment is advised. Basidiobolus spp,
infections, most conunonly involving
pathogenic for man1mals, are foWld in feces

Salmonella spp in snakes. Diagnosis is by
of healthy reptiles.

biopsy or blood culture. Longterm antibiotic

Demiatophytosis has been described
therapy may be helpful, but the prognosis is
in all orders of reptiles. Geot1ichum,
guarded to poor.

Fusa1ium, and Trichosporon are the

1994

REPTILES
genera most frequently isolated. In

As the disease becomes chronic, some boas
most cases, cutaneous injury precedes a
exhibit neurologic symptoms ranging from
secondary fungal infection. Chelonians with mild facial tics and abnormal tongue flicking fungal infections of the shell can be treated
to failure of ilie snake to right itself when
by local debridement and topical applicaplaced in dorsal recwnbency and severe tion of Lugo! solution or povi.done-iodine.

seizures.

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Exposure to ultraviolet light also may be

Pythons are thought to be a more
beneficial.

abnormal host for the IBO virus, because

Ulceration of GI tissues has been
t11e course of disease is more acute ai1d
associated with infections by Mucor and
new·ologic symptoms more profow1d. Most

Fusarium spp. Chronic visceral granupyilions present with severe neurologic lomatous disease of liver, kidneys, and
disease. Although the active disease can
spleen has been caused by Metarhizium
linger for months or more in boas, most
and Paecilomyces spp. Few signs other
pyilions die wiiliin days or weeks of the
than weight loss are seen before death.

onset of clinical signs.

Animals may continue to feed until a few

Exposure to this retrovirus/arenavirus
days before death.

appears to be due to a transfer of body

The most frequent sites of mycotic
fluids. Breeding, fight wounds, fecal/oral
infection are the skin and respiratory tract.

containination, and snake mites have been

Metarhizium, Mucor, and Paecilomyces
implicated as common ways of transfer. A
spp are frequent isolates. Aspergillus and
tentative diagnosis is based on history and

Candida spp have been isolated from
clinical signs. Blood work varies depending
pulmonary lesions of lizards and chelonion the stage of ilie disease, but few diseases ans. Most infections involve gran uloma or
in snakes will cause such increased WBC
plaque fonnation with resultant signs of
counts in the eai·ly stages. On blood smears,
respiratory distress before deatl1. Ca.ndidiinclusion bodies are frequently found in asis in large snakes has been treated with
the cytoplasm of leukocytes. A definitive
nystatin (100,000 U, PO, for 10 days).

diagnosis is obtained vi.a biopsy of internal
tissues in which ilie characteristic eosino

VIRAL DISEASES
philic inclusion bodies ai·e found, eg, the
liver, kidney, esophageal tonsils, and

Few viruses have been clearly proved as
stomach.

etiologic agents of disease in reptiles, but

IBO is not curable, and many owners
several have been linked strongly enough
choose euthanasia. However, individuals
for iliem to be considered ilie causative
may elect to isolate tl1eir snakes and treat
agent until proved otherwise. A nw11ber of
wiili supportive and palliative measures. It
viral PCR and serology _tests are available.

is essential to educate owners not to sell
infected specimens or their offspring,

Inclusion Body Disease (IBD) of Boid
because this has caused tl1e disease to

Snakes: Boa constrictors and several
spread worldwide.

species of pythons are most commonly
affected by IBO, which was originally

Retroviruses: Retroviruses have also
tl10ught to be caused by a retrovirus but
been found in Russell vipers, com snakes,
recently an arenavirus has been implicated.

and California kingsnakes in association

Boas are considered a more typical host
with malignant tun1ors. A �etrovi..tus isolated
because so many are infected, and they
from a sarcoma in a Russell viper was
can harbor the virus for years with few
designated as vi.per virus. A related vi..tus
to no clinical signs. Early signs, possibly
was isolated in a com snake from a
precipitated by any factor causing
rhabdomyosarcorna and designated
inununosuppression, include a history
comsnake retrovirus.

of untluiftiness, anorexia, weight loss,
secondary bacterial infections, poor wound

Adenoviruses: Adenoviruses have been
healing, dem1al necrosis, and regurgitation.

implicated in fatal hepatic or GI diseases

In essence, IBO should be considered in
in snakes (gaboon vipers, ball pythons, boa
every sick boa. Typical findings in the acute
constrictors, rosy boas, and rat snakes),
phase of ilie disease include leukocytosis
lizards (Jackson chaineleons, savarmal1
and a normal chemistry panel. As ilie
monitors, and beai·ded dragons), and
disease progresses, WBC counts tend
t:rocodilia11S.

to decline to subno1111al levels. Blood

In bearded dragons, the route of tra11Smischemistry results vaiy depending on sion appears to be fecal/oral contan1ination.

how debilitated and dehydrated the boa

Clinical signs are more commonly noted in
becomes, but organ dainage may occur.

juvenile dragons but can affect adults,

REPTILES

1995
usually to a lesser extent. Signs are vague

Buoyancy problems and high mortality are
and include lethargy, weakness, weight loss,
reported.

diarrhea, and sudden death. The morbidity

Fibropapillomatosis has been reported
is high in young bearded dragons, but
from free-ranging sea turtles, especially
survival is increased with supportive care.

around Hawaii. The route of transmission is

Fluid administration, force feeding, and
not known. The light gray to black masses

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antibiotics for secondary infections are
range in size up to 20 cm in diameter. The
useful.

location of the masses seems to dictate the

Because the signs of disease in bearded
severity of signs. Masses occurring on
dragons are vague and similar to those
periocular tissue can obscure vision.

caused by coccidia and nutritional

Growths on the flippers can interfere with
disorders, it is important to confirm the
swimming and the ability to forage for food.

diagnosis. Characteristic intranuclear

Internal masses also are seen, primarily
inclusion bodies are found in several
in the lungs, liver, kidneys, and GI tract.

internal organs, primarily the liver. When

Diagnosis is made by characteristic lesions
working with a large breeding group of
and histology. Treatment consists of surgical
lizards, it is practical to sacrifice a failing
removal, with wide margins to help reduce
specimen to make a diagnosis. Premortem
recurrence. Some turtles recover spontanediagnosis can be accomplished by liver ously, whereas those with internal lesions
biopsy. Identification of adenovirus from
usually perish. It is suspected that fibrofresh feces may be possible in the future.

papillomas are caused by a herpesvirus,

Recovered lizards should be quarantined
and infected specimens should be isolated
for at least 3 mo. Duration of viral shedding
from healthy turtles.

after recovery is unknown, so owners
should be discouraged from selling or
trading previously infected animals.

Paramyxovirus: Paramyxovirus
infections are more common in viperid

Herpesviruses: Herpesviruses have been
snakes but have been reported in nonisolated from freshwater turtles, tortoises, venomous snakes as well. This highly
and green sea turtles. In freshwater turtles,
contagious virus causes predominantly
the virus may be associated with hepatic
respiratory signs; transmission appears to
necrosis. In tortoises, the virus may cause
be from respiratory secretions. Secondary
necrosis of oral mucosa accompanied by
bacterial infections are common because
anorexia, regurgitation, and oral and ocular
of the severe inflammation initiated by the
discharge. Treatment in tortoises includes
virus, and it is not unusual to note nasal
isolation, supportive care, and application
discharge, open-mouth breathing, caseated
of 5% acyclovir to oral lesions. Oral acyclopus in the oral cavity, and labored breathing.

vir appeared to in1prove the lesions in a

Neurologic involvement, including tremors
desert tortoise. Herpesvirus is diagnosed
and opisthotonos, is occasionally noted.

by the presence of intranuclear inclusion

Paramyxovirus should be suspected
bodies and electron microscopic demonin any respiratory infection that does not stration of viral particles.

respond to treatment with supportive care,

Herpesvirus infection of fam1ed green sea antibiotics, and nebulization. Endoscopic turtles have been associated with gray patch biopsies and postmortem samples of lung disease and lung-eye-trachea disease,
can be submitted to detect viral particles
whereas fibropapillomas plague certain
by histology and electron microscopy. A
free-ranging populations. Gray patch
hemagglutination inhibition test is available
disease (chelonian herpesvirus 1) causes
to measure antibodies against ophidian
epizootics of small, circular papular skin
paramyxovirus in zoos and private
lesions that coalesce into patches and is
collections; a positive titer should be used
associated with young turtles maintained
as a screening tool to help eliminate
in crowded, warmer, stressful situations.

infected aninlals and prevent carriers from

Biopsies of the skin reveal basophilic
entering noninfected collections.

intranuclear inclusion bodies in epidermal

There is no specific treatment, but
cells; viral particles are noted in the
supportive care and antibiotics may prove
cytoplasm by electron microscopy. There
useful. Affected specimens should be
is no specific treatment, but reduction of
isolated and strict hygiene practices
crowding and stress appears to decrease the followed. Although a vaccine is under incidence. Lung-eye-trachea disease causes
development, it is currently not effective.

harsh respiratory sounds, with ulcerations
and caseous debris over the globe and

West Nile Virus: West Nile virus has
throughout the oropharynx and trachea.

resulted in epizootic outbreaks in farmed

1996

REPTILES
alligators, with the virus causing multi

PARASITIC DISEASES
organ necrosis, heterophilic granulomas,
heterophilic perivasculitis, and lymphoplas

Ectoparasites: A limited nun1ber of
macytic mengingoencephalitis. Very high
ectoparasites ai·e seen, except on wild and
viremia titers have been reported in various
newly acquired reptiles. Mites are distrib

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reptiles, suggesting that reptiles may play a
uted worldwide, and most reptiliat1 species
role as an an1plification host.

are affected. Reduced vitality and, in heavy
infestations, death due to anemia may

Papillomas: Viral particles appear to be
occur. Skin of affected reptiles appears
transmitted from one European green lizard
coai-se, and dysecdysis is frequent. The
to another via bite wounds. The resulting
common snake mite (Ophionyssus
papillomas are 2-20 mm in diameter and
nal1icis) and lizard mite (Hirsliella spp) may be single or multiple. Alt.hough there
are generally <1.5 mm long and ai·e often
are no signs in the initial phase, affected
fow1d around the eyes, gluttaJ folds, or any
lizards may become lethargic and anorectic
other indentation on the reptile. Mites may
and die. Diagnosis involves detection of
also be associated with mechanical
viral particles by electron microscopy.

transmission of Aeromonas hydrophila, a

Treabnent consists of surgical removal
variety of other bacteria, rickettsial agents,
of single masses, although regrowth is
at1d probably viruses. Mites ai·e visible to
conunon. Isolation of affected lizards is
the naked eye but ai·e hai·d to see in small
perhaps the only way to prevent spread.

numbers. If mites are suspected, gently

A papilloma-type virus also appears to
rubbing the reptile while it is standing over a
affect Bolivian side-neck turtles and
piece of white paper will allow the mites to appears as white, oval skin lesions
be seen after they have fallen off. Affected
distributed over the head. Ulcerative shell
reptiles often spend an inordinate ainorn1t
lesions are also seen, primarily on the
of time soaking to drown the mites.

plastron. Diagnosis is made by identifying

Exainination of the water dish can reveal
viral particles on electron microscopy.

the drowned remains of many mites. The

Treabnent is supportive and palliative, and
gluttaJ folds, involutions around the face,
affected animals should be isolated.

and the space between the eye and its orbit
ai·e favored areas and should be inspected
lridoviruses: Iridovimses have been
carefully.

repo1ted in various chelonians, snakes,

There are mai1y methods of treabnent;
and lizards. An iridovirus was fow1d in a
however, a pem1ethrin is specifically

Hem1ann's tortoise, which died without
licensed for use in reptiles, and ivem1ectin
prior signs of disease. Progressive anemia
is also frequently effective in squan1ates.

in Australian geckos has been linked to an

Ticks are conunon on reptiles, and heavy
iridovims. Clinical signs range from none to
infestations may result in anemia. Argasid
stomatitis, rhinitis, conjunctivitis, tracheitis, ticks may cause paralysis, with muscle edema, and cutaneous abscessation. In
degeneration at the site of the bite. The
some cases, the recovered iridoviruses
transmission of green-lizard papillomahave been closely related to amphibian associated virus, several hemogregaiines,
ranaviruses. Although the clinical in1po1�
and the filarid worm Macdonaldius oscheii
tance of several of these viruses remain
have been associated with ticks. Ticks cai1
unclear, iridoviruses deserve close
transmitEhrlichia rum'inantium, the
attention, especially in chelonians.

cause of heartwater, and consequently the
importation of African reptiles has been

Other Viruses: Many other viruses
controlled. Ticks can be removed manually
continue to be isolated from reptiles, but
or by using pennethrin spray. Systemic
little information exists regarding disease,
antibiotics are often indicated because
diagnosis, control, and treabnent. Two
of systemic infections associated with
nonpathogenic rhabdoviruses were isolated
multiple cutaneous bite worn1ds and,
fromAmeivasp lizards. In addition to
potentially, with transmission of pathogenic
herpesvimses and adenoviruses, paivovibacteria.

ruses and picomaviruses have been found

Leeches have been forn1d on the legs,
in the intestinal tract of snakes, but their
head, neck, ai1d in the oral cavity of a variety
exact role is unknown. A poxvirus-like virus
of turtles and crocodiliat1S.

has been isolated from circun1scribed

Cheloniat1S frequently have cutaneous
cutaneous lesions in a caiman ai1d from
myiasis. Bot flies (including Culerebra sp) dermal lesions in a tegu. A reovirus isolated
create a cutaneous worn1d in which to lay
from Chinese vipers was associated with
their eggs, which hatch into bots that live in
death without prior signs of illness.

cyst-like stmctw-es W1til mature enough to

REPTILES

1997
leave the wound. These lesions are
tllroughout tile body wall, suggesting that
characterized as a lump under the skin; on
the larvae may be able to penetrate the skin.

closer inspection, they have an opening

Overwhelming parasitism is common when
often lined by a black, crusted material.

poor hygiene results in highly contanlinated

Treatment consists of slightly expanding the environments. Rhabdias and related VetBooks.ir
natural opening and manually removing the
species have been found in tile lungs of a
bot with a forceps. The wound is then
variety of snakes; embryonated ova may
flushed with povidone-iodine, chlorhexbe found in the oral cavity and in lung idine, etc, and an antibiotic ointment is
aspirates. Embryonated ova and free larval
instilled. Systemic antibiotics are indicated
forms may be seen in tl1e feces. Larvae
in reptiles that have multiple lesions.

resembling Rhabdias also have been seen

Cutaneous myiasis also occurs secondary
in the gingiva of snakes witl1 stomatitis.

to existing wounds, and maggots must be

Infections often are subclinical but may be
manually removed and the underlying
associated with secondary bacterial
lesion treated with topical and systemic
pnew11onia. In severe cases, deatll may
antibiotics as needed. During heavy fly
result.

season, turtles often are housed indoors or

Stomach worms of tl1e genusPhysalop
with screens over their enclosures to offer

/,era are seen in lizards. Gastric ulceration some protection.

may occur in severe infections. Ova are

Ectoparasite infestations are best
elliptical and may be embryonated.

prevented by thorough screening and

Numerous snakes are infected by Kaliceph
quarantine of all new animals entering a
alus spp. This hookwom1, capable of
collection.

transcutaneous infestation, prefers the
upper GI tract and causes erosive lesions at

Helminths: The stress of captivity coupled sites of attachment. Ova are similar to tllose witl1 a closed environment predisposes to
of Physaloplera spp. Large granulomas
heavy burdens of parasites witll direct life
caused by the above species have also
cycles. Every effort must be taken to rid
caused GI obstruction in snakes.

reptiles of parasite burdens and the environ

Ascarids frequently infect reptiles.

ment of intem1ediate hosts.

Ova are sinlilar to those of asca.rids from

Pathogenic trematodes infect the vascular manll11alian hosts. Severe lesions and deatl1
system of turtles and infect the oral cavity,
may be seen in infected snakes. Clinically
respiratory system, renal tubules, and
infected snakes frequently regurgitate
ureters of snakes. Chemotl1erapeutic agents
partially digested food or adult nematodes
have not effectively eliminated these
and are anorectic. The major lesions are
parasites, although praziquantel has shown
large granuloma.tous masses in the GI tract;
some promise.

they may abscess and perforate the

Tapeworms are found in all orders of
intestinal wall.

reptiles but are rare in crocodilians. Rep

Many oilier nematode species may be
tiles may act as tile definitive, paratenic, or
fotmd in reptiles. Capilla.rid, trichurid, and
intermediate hosts for a large munber of speoxyurid ova may be found on fecal cies. Although most species of tapeworms
examination. The nonpathogenic larval and
are generally nonpatl1ogenic in wild reptiles,
oval fonns of parasites of prey items ( eg,
weight loss and death have been reported.

Syphacia obvelala, tile mouse pinw01m)

The complex life cycle of cestodes and
may be found when infected prey is
restricted geographic range of intermediate
consumed. Treatment should be attempted
hosts limit tl1e number of cases in captive
when evidence of parasitism is present.

reptiles. When present, proglottids may be

Some larval forms of nematodes are
found around tile cloaca, or typical cestode
suspected or confirmed to penetrate tile
ova may be isolated from feces. Treatment
skin ( eg, Strongyloides and Kalicephalus ), is with praziquantel, repeated in 2 wk.

bypassing the oral reinfection route. The

Plerocercoids of the genus Spiromelra may
subtle nature of reinfection by tllis route
be found as soft swellings in tl1e subcutis.

often goes wmoticed until the reptile is

These larval stages may be removed
overwhelmed by parasites. Close attention
surgically.

to tile inll11ediate removal of excreta and

Nematodes are found in all orders of
fastidious sanitation help reduce parasite
reptiles, and several genera are imp01tant.

burdens in captivity.

Strongyloides spp frequently inhabit the

Dermal lesions ca.used by tile spirurid
intestinal tract of reptiles; larvae are seen
worm Dracunculus spp may be seen.

in the respiratory tract and respiratory

Nun1erous species of spirurids infect the
exudate. In snakes, the larvae have been
mesentery, coelomic cavity, and blood
seen within granulomas distributed
vessels. These worms require a mechanical

1998

REPTILES
vector, so their incidence is reduced in
die can serve as carriers, including garter
captive-bred reptiles or in reptiles that have
snakes, northern black racers, and box
been in captivity longterm. Treatment
turtles. Although most turtles are resisconsists of increasing the environmental tant, the giant tortoises are susceptible.

temperature to 95° -98°F (35° -37°C) for

Other resistant groups include eastern king

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24-48 hr. However, some "cool-adapted"

snakes, crocodiles, and cobras (possibly
reptiles may not tolerate this treatment.

as an adaptation that allows them to eat
snakes). Most boas, colubrids, elapids,

Pentastomes: Pentastomes are found
vipers, and crotalids are highly susceptible.

in a wide variety of reptiles, with variable

Transmission is by direct contact with the
pathogenicity. Pentastomid infections are
cyst forn1. Hepatic abscesses containing
occasionally associated with pneumonic
numerous E invadens trophozoites are
signs, but these primitive arthropods can
common in chronic cases. At necropsy,
inhabit any tissue, and symptoms will vary
gross lesions may extend from the stomach
with their migration path and tissues reto the cloaca. The intestine shows areas of sponses. Pentastomes were initially found
ulceration that tend to coalesce, caseous
primarily in tropical poisonous snakes;
necrosis, edema, and hemorrhage. Multifohowever, as more necropsies on reptiles cal abscesses in a swollen, friable liver are
were perfonned, more were found. Necropseen in the hepatic forn1. Identification of sy results from 88 bearded dragons showed trophozoites or cysts in a wet preparation that 11 were infested with pentastomes. No of fresh feces or tissue impressions, or in truly effective treatment has been reported, histologic sections, is diagnostic. Turtles but praziquantel at dosages of 8 mg/kg and
and snakes should not be housed together.

ivern1ectin at 5-10 times normal dosages

E invadens is best treated with
have been shown to reduce ova numbers
metronidazole. Tetracycline and paromobeing shed but have not eliminated the rnycin have been used but are considered
worn1s. The most novel approach has been
ineffective against the hepatic form. Strict
to endoscopically locate and mechani-
sanitation and hygiene measures should be
cally remove all the adult pentastomes.

observed.

Recognition of pentastomal infestations

Flagellates, especially Hexamita spp,
is important, because these parasites are
have been reported to cause urinary tract
thought to present a zoonotic risk.

disease in chelonians and intestinal
disease in snakes. The "Giardia" seen in
some cases of enteritis in snakes may

Protozoa! Diseases: Numerous
actually be Hexamita or one of the
protozoans are found on reptiles; most
relatively nonpathogenic flagellates that
are hannless commensals. The most
inhabit the intestinal tract of snakes.

serious protozoa! pathogen of reptiles is

Enlamoeba invadens.

Differentiation between the species

Clinical signs are
requires expertise, and special preservaanorexia, weight loss, vomiting, mucoitives and stains are required to identify dal or hemorrhagic diarrhea, and death.

most of these organisms. Metronidazole

Enta.moebiasis mJly be epidemic in large
has been used to treat flagellates. Indigo
snake collections. Herbivores appear less
snakes, king snakes, and uracoan rattlers
susceptible than carnivores; a number of
should be treated at the low end of this
reptiles that seldom become affected or
dosage range. Early studies with benzimidazoles are very encouraglng and should also be considered as a viable therapy.

Several coccidial organisms have been
reported: Klossiella from the kidney,

Isospora from the gallbladder and intestine, and Eimeria from the gallbladder. The
severity of disease varies with the coccidia
and affected species. Because of their direct
life cycle, these parasites can increase
to tremendous nun1bers, especially in
irnmunosuppressed reptiles. Oocysts are
not fragile and can survive for weeks in a
dessicated condition. Fastidious, daily
cleanings are necessary to remove all feces
and feces-contan1inated food and water.

Entamoeba invadens trophozoite (left) and
cyst (right) (1,000X oil immersion).

Insects and other food items must be

Courtesy of

Dr. Stephen Divers.

removed on a daily basis, because they are

REPTILES

1999
another source of contamination ( eg,
leading to hypocalcemia, distortion of the
crickets may eat the oocysts while gathering skull, and abnormal occlusion and wear.

fluid from the feces). Persistent treatment

Increased levels of dietary protein may
using sulfadimethoxine is required until
contribute to accelerated growth of these
infection is resolved, often taking 2-4 wk;
tissues, while a lack of abrasive food items

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success should be measured by serial fecal
limits natural wear in captivity. Treatment
samples.

consists of trimming or grinding the beak

Trimethoprim-sulfa is another useful drug into a more normal conformation. The to treat coccidia. Care should be taken
condition usually recurs because of primary
when using sulfa in reptiles with dehydramalocclusion, and longtern1 maintenance tion or renal compromise. If in doubt, a
may be required.

balanced electrolyte solution should be

Males of many species can be highly
administered PO at appropriate dosages.

territorial and exhibit aggression toward

Even under the best conditions, treatment
other males or toward females dUiing
will eliminate coccidia in only 509'o of cases.

mating periods. lr\juries to cagemates can

Treatment resulting in a reduction of
be severe and are best avoided by separatcoccidia is still important, and cocci dial ing animals at feeding and reducing the
numbers should be periodically monitored.

number of aninlals allowed in a breeding

Plasmodial (malarial) organisms, as well
group. When separated individuals are
as other intracellular blood protozoans,
placed together for breeding, they should be
have been reported in reptiles. Their
carefully monitored. If reptiles must be kept
significance is unknown, and treatment
together, it is vital the enclosure is large
is not considered necessary.

enough to avoid competition for resources,

Cryptosporidiosis is frequently reported
especially basking areas, and retreats. Food
in association with postprandial regurgitaand water is best placed in multiple location (snakes, Cryptosporidium serpentes), tions to prevent dominant cohabitants from
diarrhea (lizards, Cryptosporidium
intimidating the others.

saurophilum ), marked weight loss, and

Fractures due to trauma are commonly
chronic debilitation. The organism affects
seen in all species. They are often associated
the GI mucosa, resulting in marked
with secondary nutritional hyperparathythickening of the gastric rugae and loss of roidism in chelonians and lizards. Long bones
segmented motility. A mass in the gastric
may be repaired with lightweight external
region is often, but not always, palpable
coaptation. A simple way of splinting the legs
in snakes, and contrast radiographs or
of lizarcls is to tape the injured leg to the body
endoscopic examination reveals rugal

(front legs) or tlle tail (rear legs). These
thickening. Many lizards, including Old
splints are tolerated well and protect the

World chameleons and savannah monitors,
injured limb from further injury.

are affected primarily in the intestine.

lr\jury to the spinal column must be

Mucosa! thickening develops as a result
assessed individually; when clear displaceof invasion by nun1erous cryptosporidial ment is not evident, radiographic evaluation
organisms. Diagnosis can be made using
should be performed. Spinal ir\juries caudal
acid-fast stains on fresh feces or on the
to the vent may be tolerated, but ir\juries
coating from regurgitated items or
cranial to the vent frequently result in
endoscopic gastric biopsies, which will
constipation and retention of mates, with
identify the tiny oocysts. Although several
variable limb movement. Environmental
treatments have been suggested, none
changes ( eg, low branches, shallow water

( except for hype1immune bovine colostrum) dish, nonabrasive substrates) and teaching have been consistently effective. Intensive
the owner how to empty the cloaca! content
supportive care will often stabilize and help
will allow the lizard to survive. Because
prolong tlle life of the affected reptile.

lliese fractures are often secondary to

Euthanasia is a valid option for infected
secondary nutritional hyperparathyroidism,
reptiles. Cryptosporidiosis was previously
a thorough history of the reptile's husbandry
considered a zoonotic disease; however, it
may also reveal the need for nutritional
now appears that the species commonly
changes.

found in reptiles do not affect m=als.

Aggressive iguanids may frequently lash
out with their tails and damage them against

ENVIRONMENTAL DISEASES AND the vivarium glass or other furniture.

TRAUMATIC INJURIES

Continual damage can lead to ischemic
necrosis of the tail. Secondary infection

Beak anomalies in chelonians inhibit
may follow and progress to osteomyelitis.

feeding and are often associated with

In some cases, septic emboli may lead to
secondary nutritional hyperparathyroidism
tail infection. In either scenario, tail

2000

REPTILES
amputation, in addition to investigation
function. Often, eyecaps or annular bands
and correction of predisposing factors, is
on the tail or digits are retained. Eyecaps are
required. Radiography should precede
best treated by application of an ophthalmic
surgery, because osteornyelitis may appear
ointment bid for several days until they
more cranial than the external lesion. Tail
either fall off or can be grasped with a pair

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amputation in iguanids should be perof fine forceps and carefully removed.

fom1ed under anesthesia, taking advantage

Patience is advised-eyecaps should never
of the lizard's ability to perform autotorny.

be forced off because of the possibility of

The tail is sin1ply bent and twisted sharply
damaging the spectacle.

to cause a fracture through a fractw·e plane.

Recalcitrant, retained sheds are best

Muscle fibers are trimmed, but the tail is left
treated by soaking tile reptile in warm
unsutured to encow·age regeneration. Clean (77°-85°F [25°-29°C]) water for several postoperative conditions are essential, but
hours and tilen pulling gently with a gauze
antibiotics are not. Tail necrosis in reptiles
sponge. A hwnidity chamber also works
that do not exhibit autotomy requires a
well and can be as sinlple as a 10-gal.

more traditional surgical amputation with
aquaritm1 with an undertank heater in which
primary closure of the wound.

wet batl1 towels are placed. The top can be

Burns are generally associated with
covered witil a light cloth to increase humidunscreened incandescent lights or other ity levels, but excessive heat must be
heat sources. Fluid loss, dehydration, and
avoided and can be relieved by allowing
septicemia are common sequelae. However,
more ventilation if needed.

many can be treated by cleansing the site,

Prey-induced trauma, caused by live,
applying antibiotic ointment, providing
uneaten invertebrate and vertebrate prey,
analgesics, and placing the reptile in a clean, can frequently cause severe trawna, witil dry environment. Silvadene cream is the
secondary infection and abscessation.

preferred topical dressing, because it is

Whenever possible, rodents tilat have been
water miscible and is effective against yeast
freshly killed or frozen and thawed should
and bacteria, includingPseudomonas spp.

be offered to prevent i..rtjwy to tl1e reptile

In w1infected burns, sterile skin protec

( dead prey should be discarded after 12 hr
tants can be applied to the area to act as a
if uneaten). The feeding of live prey is illegal

"second skin." These products allow access in many countries. Fresh bite wotmds may
to the water and help keep contaminants
be treated by cleansing witil povidoneout. In severe burn cases, fluids are given to iodine ( diluted 1: 10). Parenteral antibiotics,
offset fluid losses, and systemic antibiotics
based on results of culture and sensitivity
are required to prevent secondary infection.

tests, should be used. Untreated wounds

Pain management and assisted feeding
frequently abscess and are seen as a soft
techniques may also be applied.

or hard swelling. The abscess, including

Traumatic injuries tb turtles may result
the fibrous capsule, should be removed
in fractures to the plastron, the carapace, or
surgically, and the defect sutured. Open
both. Repairs should be delayed in anything
or draining abscesses should be curetted,
other than fresh wounds. Contaminated
flushed witil povidone-iodine, and parentissues should be gently debrided, flushed, teral antibiotics achninistered. Antibiotic
and appropriately bandaged using a
ointments witil proteolytic enzymes may
wet-to-chy technique. Holes in the bandages
be helpful. (See also ABSCESSES, p 1991.) can be created to allow the legs to remain
exposed. If obvious infection is present,

ME�BOLICANDENOOC�NE
samples should be submitted for microbiol

DISEASES
ogy before systemic antibiotics are started.

Once stable, the wow1ds should be cleaned

Gout: Gout is seen in all orders of reptiles; again, and tl1e fractures realigned under
visceral and articular fom1s have been
general anesthesia and repaired using zip
reported. Radiographs often reveal
ties. These irtjuries also can be repaired
mineralized tophi in affected organs
using epoxy resin or a quick-setting, epoxy
and joints. Primary visceral gout is the
glue layered over fiberglass screen. Dental
accwnulation of urate microcrystals in
and orthopedic cements have also been
organs secondary to a chronic hyperuriceused to stabilize fractured tissues. Healing is rnia and is generally caused by excessive slow and may require 4-6 mo or longer.

protein in tile diet. Secondary visceral gout

Dysecdysis, or incomplete or inadequate
is due to chronic hyperuricemia from such
skin shedding, may be caused by low hwnidcauses as dehydration and renal insuffiity, ectoparasitisrn, nutritional deficiencies, ciency. Gout can be ve1y debilitating,
infectious diseases, lack of suitable abrasive causing discomfort to the point that some surfaces, or even decreased thyroid
reptiles refuse to move, eat, or drink

REPTILES

2001

Primary visceral gout is treated by
try, although a definitive diagnosis requires
correcting the diet. Secondary visceral gout
demonstration of reduced renal function
is treated by attempting to correct the

( eg, iohexol clearance) and renal pathology
underlying problem, be it dehydration or

(eg, renal biopsy).

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renal disease. The prognosis is poor in

Reports ofhypertrophic osteopathy
advanced cases. Allopurinol is effective
are uncommon and currently appear to be
at reducing blood uric acid levels. Drug
limited to lizards with extensive periosteal
administration usually must be longterm,
proliferation beginning in the distal long
because signs typically recur if treatment
bones and progressing proximally. The
is discontinued. Euthanasia must be conpathogenesis is unknown, but theories sidered in reptiles in which movement is
include chronic anoxia, toxins, and vagal
painful and appetite becomes suppressed.

neurologic pathways.

Metabolic Bone Diseases: Secondary

Miscellaneous Endocrine Disorders:

nutritional hyperparathyroidism is the

Endoc1ine diseases are not often documost common bone disease seen in reptile mented in reptiles. Diabetes mellitus has
practice. It relates to poor diet (low calcium
been reported in chelonians; glucosuria and
to phosphorus ratio, vitamin D3 deficiency)

hyperglycemia are the primary findings, and
or poor husbandry (lack of UVB light, inadpolyphagia may or may not be apparent.

equate thermal provision). Affected reptiles

The etiology is often undetermined but has
are generally rapidly growing herbivorous
been associated witl1 gastric neuroendoand insectivorous lizards and chelonians.

crine carcinomas in bearded dragons.

Signs include anorexia; lethargy; an inability Pancreatectomy in lizards may result to walk normally; swollen/distorted
in hypoglycemia, in1plying that other
mandible, maxilla, and/or long bones; limb
hormones, such as glucagon or somatotroand spinal pathologic fractures; cloacal pin, may play a role in the pathogenesis of
prolapse; muscle fasciculations; and tetany.

diabetes mellitus in reptiles.

Diagnosis requires radiography to document

Hypothyroidism and thyroid hyperplageneralized demineralization of the skeleton sia have been reported in Galapagos
and low plasma levels of 25-dihydroxychole

Islands tortoises. It has been speculated
calciferol. Findings in the late stages include
that high amounts of dietary iodine in the
hyperphosphaternia and low total and ionized natural diet may play a significant role.

calcium. Treatment of c1itical cases requires

Feeding goitrogenic foods to tortoises has
fluid therapy, nutritional support, and
been incriminated in development of this
parenteral calciun1 therapy if hypocalcemic.

condition. The primary clinical sign is

Correction of the diet and husbandry are the
subcutaneous edema.

mainstays of successful therapy.

Hyperthyroidism has been reported iFt

Secondary renal hyperparathyroidism a female green iguana that presented with occurs in adult reptiles and is associated
polyphagia, loss of the dorsal spines, hyperwith hyperphosphatemia, soft-tissue calcifiactivity, increased aggression, tachycardia, cation, osteodystrophy, and hypocalcemia
and a bilobate mass palpable anterior to

Provisional diagnosis generally rests on
the thoracic inlet. Surgical thyroidectomy
history, radiography, and plasma biochemis-
returned the lizard to a euthyroid state.

REPRODUCTIVE DISEASES

Dystocia (Egg Retention): Sterilization
is rarely performed in reptiles, and therefore
reproductive disease remains a common
presentation. In oviparous reptiles, eggs

( demonstrating various degrees of shell
mineralization) may be retained, whereas
in ( ovo )viviparous species unfertilized
ova or fetuses may be seen. In some cases,
abnom1al and persistent preovulatory
follicles may also be diagnosed as spherical
masses that fail to ovulate or resorb. Dystocia
is generally not an acute presentation as in

Secondary nutritional hyperparathyroidism
m=als or birds, and reptiles may retain
in a green iguana. Note the swollen, fibrous
eggs/fetuses for weeks or even months after
long bones and maxilla (insert). Courtesy of Dr.

tile nonnal timing of laying/bi..rth. Coupled

Stephen Divers.

with imprecise details of copulation, this

2002

REPTILES
can often make the distinction between
cleaned, and the application of hyperosmotnormal gravidity and dystocia difficult in ics may help reduce swelling and facilitate
otherwise clinically healthy reptiles.

replacement. However, it is also in1portant

Certainly, severe metabolic disturbance and
to determine the cause to prevent recu1�

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infection can exacerbate the issue. In general, rence.

a presumptive diagnosis can be achieved

Prolapses of the hemipenes and phallus
tlu-ough palpation and diagnostic imaging,
can be amputated after induction of general
especially radiography and ultrasonography.

anesthesia or intrathecal ( caudal spinal)

Hematology and plasma biochemistry may
block; this will render the anin1al infertile.

also help identify inflammatory/infectious

If the prolapsed tissue is viable and can be
changes and metabolic disturbances,
replaced, purse-string sutures of the vent
especially hypercalcemia
should be avoided, because they tend to

Unless there is evidence of acute disease,
defonn the vent and may interfere with the
medical management may be tried, although urogenital openings. In such cases, it is it frequently fails. Improvements in
preferable to use a transcutaneous
husbandry ( especially provision of solitude
cloacopexy technique. If tl1e tissue is not
and a suitable substrate), corrections of any
viable, then careful and detailed surgery is
metabolic disturbances, subcutaneous
required when attempting debridement and
dilute oxytocin/vasotocin, and potentially
resection-anastomosis of the cloaca, colon,
prostaglandin (PGF2• and PGE) may be
or bladder and often necessitates both
helpful. In most cases, surgical ovariosalcloacal and coeliotomy approaches.

pingectomy is required (unless a valuable
breeding animal) after medical stabilization.

NEOPLASTIC DISEASES

Vent Prolapse: A variety of prolapses

Neoplasia is becoming increasingly common
may be seen emanating from the vent of
as captive reptile populations age, and it
reptiles, including cloaca, colon, oviduct,
should always be included in the differential
hemipenes/phallus, and (if present) bladder.

diagnosis of disease. In addition to spont

Common causes include dystocia, copulaaneously developing neoplastic diseases, tion trauma, cloacitis, bacterial/fungal/
tumors have been associated with paraparasitic infection, metabolic disease sitism and oncogenic viruses. Surgical or

( especially secondary hyperparathyroiendoscopic biopsies are prefeITed for dism), cystic calculi, renal disease, neoplasia, diagnosis. Techniques such as radiography, or any space-occupying lesion within the

CT, MRI, ultrasonography, endoscopy,
coelom causing tenesmus. It is important to
cytology, histopatl10logy (biopsy), and viral
identify the prolapsed organ, because some
isolation provide improved diagnostic

(eg, phalluslhemipenes) can be amputated,
capabilities. Once neoplasia is diagnosed,
whereas others (eg, cloaca, colon, bladder)

treatment protocols sin1ilar to those used
cannot. The prolapse should be gently
in other aninlals could be considered.

RODENTS

The order Rodentia, with -2,020 living
highly specialized, eating, for example, only
species placed in 28 fan1ilies ( approxia few species of invertebrates or fungi.

mately half of all manunalian species), is the

Despite their morphologic and ecologic
largest order of mammals. They are found
diversity, all rodents share one characterisworldwide except in Antarctica and on tic: a highly specialized dentition for
some oceanic islands. Ecologically, they are
gnawing. Rodents have a single pair of
remarkably diverse. Some species spend
upper and a single pair of lower incisors.

their entire lives above the ground in the

Between each incisor and the first cheek
canopy of rainforests; others rarely emerge
tooth is a toothless interval called the
from beneath tile ground. Some species
diastema. The incisors are rootless and
are aquatic, whereas others are equally
grow continuously. Enamel is deposited on
specialized for life in deserts. Many rodents
the anterior and lateral incisor surfaces; the
are to some degree omnivorous; others are
posterior incisor surface is dentin. During

RODENTS

2003
gnawing, as the incisors chisel against each
in husbandry, often rodents subjected to
other, they wear away the softer dentin,

"benign neglect" live long, healthy lives. The leaving a sharp enamel edge. This "selfadverse effects of overfeeding pet rodents sharpening" system is very effective and is
are seen in the early development of many

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one of the keys to the enormous ecologic
spontaneous twnors and degenerative
success of rodents.

diseases.

Using the incisors together to chisel away
at a surface requires muscle that forcefully

CHINCHILLAS
brings the lower jaw forward. The masseter
muscle does this in rodents. Rodents are

Chinchillas are slender-bodied, mediun1-
traditionally divided into three groups based size rodents with short forelimbs and Jong on how the masseter attachments evolved:

muscular hindlimbs that give the aninlal a
sciuromorphs (eg, squirrels, beavers),
rabbitlike appearance. The head, eyes, and
hystricomorphs (eg, New and Old World
ears are relatively large, and the bullae are
porcupines, guinea pigs, jerboas ), and
greatly expanded. Chinchillas have long
myomorphs (eg, New and Old World rats
gestation periods and deliver fully fun-ed
and mice, hamsters, gerbils, voles).

young with open eyes.

Most modem rodents have adapted to eat

In the wild, chinchillas live in relatively
seeds, which links them to the evolution of
barren areas of the Andes ofNorthem Chile
modem grasses. All rodents evolved from
at elevations of 3,000-5,000 m. Chinchillas
slu·ewlike carnivorous or insectivorous
live in bun-ows or rock crevices but are well
ancestors and have since diverged into
adapted for ruruling. They dust bathe, are
various families and subfamilies.

vegetarian, and are active throughout the

Despite the large nw11ber of rodents,
year. They are gregarious, living in groups
only a few species are owned as pets. The
of several hundred. All domestic (USA)

common pet rodents are chinchillas, gerbils, chinchillas are descendants of 13 individuguinea pigs, hamsters, mice, and rats. Less als brought to the USA in 1927.

common pet rodents are African giant
pouched rats, degus, prairie dogs, spiny
mice, and voles.

Biology

As prey aninlals, rodents do not show

Chinchillas come in a variety of colors. The
obvious signs of pain or disease until near
original chinchilla fur color in the wild was
death. Consequently, sick rodents are often
mottled yellow-gray. Through selective
presented late in disease progression when
breeding, the most common color seen is
the prognosis is more guarded. Dermatodark blue grey (the dominant fur color).

logic conditions make up 25% of rodent

Other colors have emerged and include the
cases presented for small aninlal consultadominant colors of beige, white, and ebony,·
tion. Trawnatic injuries are also frequent
and the recessive colors of sapphire, violet,
and seen in rodents of all ages. Although
charcoal, and velvet. Eye color may be
some diseases al'e caused by shmtcomings
black, pink, or red due to fur color genes.

1ti:1111·1 BIOLOGIC DATA OF PET RODENTS

Chinchilla

Gerbil

Guinea Pig Hamster Mouse

Life span" (yr)

4--15

2.5-4

4--8

1-2

1-2

Adult male body wt (g)

400-500

45-130

800-1,600

85-140

20-30

Adult female body wt (g) 400-600

55-135

700-1,300

95-120

18-35

Sexual maturity (wk)

32-36

9-12

10-12

4--7

6---8

Gestation (days)

111

24--26

63-69

16

19-21

Litter size (average)

2

1-12

3-4

6---10

5-12

Weaning (days)

42-56b

21

30b

21-30

21-23

•Life span data is for typical life span range in pet rodents. Life spans exceeding these times have been recorded for rodents in research studies.

b Guinea pigs and chinchillas have precocious young that can eat some solid food at 7-14 days. Early weaning results in lower body wt and social maladaptation in later life.

2004

RODENTS

Ten different sounds comprise the vocal
distance is greater. Extrusion of the penis
repertoire of chinchillas, depending on the
from the urethral orifice will confirm the sex
behavioral context. Different sounds are
of the chinchilla, as long as the clitoris is not
made during explorato1y behavior, predator mistaken for a penis. There are two major VetBooks.ir
avoidance, sexual behavior, and social
differentiating features: the penis is
behavior, including social contact and
significantly larger than the clitoris, and
agonistic (defensive and offensive)

the extruded penis can be separated and
behavior. In addition, chinchillas can raise
distinguished from the prepuce (whereas
and lower the tones of the calls they make.

the extruded clitoris tends to evagina.te,

All chinchillas have a similar cry that is used
and the clitoral prepuce is not apparent).

conunonly from birth.

The female chinchilla has an estrous
cycle of 38 days. Females are seasonally

Husbandry
polyestrous, and the breeding season is

Chinchillas are ve1y tolerant of cold but

November to May in the northern hemisensitive to heat. The ambient temperature sphere. The gestation period averages 111
range to which chinchillas are adapted is
days. Generally, the female will have two

65° -80°F (18.3° -26. 7°C). Exposure to higher
litters a year with 1 to 6 young ( average 2)

ambient temperatures, especially in the
per litter. Young become sexually mature
presence of high hun1idity, can result in
at 8 mo of age. Chinchillas have a long life
heatstroke. A good general rule is to add the
span, repo1ted to be up to 20 yr.

unit values of the temperature (Fallrenheit)

Sexing chinchillas ( and guinea pigs) can
and hwnidity, and consider any value > 150
be difficult. In females, a vaginal closure
to be dangerous. For exa.n1ple, 85°F + 65%
membrane seals the vagina.I orifice at all
hwnidity = 150. Chinchillas will develop
times except estrus and parturition. The
matted fur if kept in a warm (>80°F
vaginal orifice is U-shaped and situated

[26. 7°C]), humid environment.

between the a.nus and the mound-shaped

Chinchillas are easily housed in either
urethral orifice. It is difficult to distinguish
wire mesh-bottom or solid-bottom cages,
when closed and is indicated by a slightly
although solid-bottom cages are recomraised, semicircular area. When its closure mended for pregnant females a.bout to have
membrane covers the vaginal orifice, the
young. Wire mesh spacing in cages should
ureUiral orifice can be mistaken as a genital
be narrow, because tibial fractures
opening. The well-developed clitoris of
commonly occur in yow1g chinchillas that
female chinchillas (and guinea pigs) can be
catch a hindleg in wide floor mesh grating.

manually extruded wough the urewal

Chinchillas are shy animals and need a
orifice and mistaken for a penis. The vagina
place to hide when in captivity. In the wild,
is open during estrus. During these times,
chinchillas conceal themselves in rock
the vaginal closure membrane dissolves
crevices. Polyvinyl chloride (PVC)

and then repairs. During estrus, there is
plwnbing pipes, especially elbow, Y, and T
no vulval swelling. Instead, the perinew11
sections, make ideal hiding places. The
changes color, going from a dull pink to a
pipes should be 4-5 in. in diameter and are
deep red. The perineal color increases
easy to sanitize by placing in a dishwasher.

dramatically at the time of vaginal

Because chinchillas have a ha.bit of dust
pe1foration and remains intense throughout
bathing, a box containing a mixture of silver
most of the luteal phase of the estrous cycle. sand and Fuller's earth (9: 1 ), 2-4 in. deep Male chinchillas do not have a true
should be placed in the cage daily. Dust
scrotwn. The testes are contained within
baths should be provided for -30 min/day.

the inguinal canal or abdomen, and

If dust baths a.re left in tile cage for long
two small, moveable scrotal sacs arc next to
periods, they become soiled with feces.

tl1e a.nus, into which the caudal epididymis

When chinchillas do not have access to a
can drop. The external appearance of tl1e
dust batl1 in captivity, the fur becomes
scrotal sacs is similar to the nonpendulous
matted from oily secretions. Dust bathing
scrotwn of pigs and ca.ts. The penis is
often causes irritation of the eyes, resulting
readily apparent below the a.nus, from
in conjunctivitis without associated clinical
which it is separated by an expanse of bare
signs of upper respiratory infection.

skin. The penis can be manually extruded

Excessive dust bathing has been reported to

1-2 cm when flaccid. The tip of tl1e erect
result in pulmonruy epithelial hyperplasia.

penis extends to the level of tl1e a.xilla., a
and grru1ulomas.

distance of -11 cm.

Chinchillas have a high requirement for

As with other rodents, the a.nogenital
dietruy fiber. Their diet should ma.inly
distance gives the best initial indication of
consist of high-quality grass hay. Pelleted
tl1e animal's sex. In males, the a.nogenita.l
chinchilla diets ru·e conunercially available

RODENTS

2005
and should be used to supplement the diet.

large patch of fur, revealing smooth, clean

Guinea pig or rabbit pelleted diets have also
skin underneath. It may also occw- with
been used successfully to supplement the
improper handling, fighting, or situations
diet. Like rabbits and guinea pigs, chinchilthat overexcite a chinchilla. The fur can las produce two types of fecal pellets: one
take several montl1s to regrow and

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nitrogen-rich intended for cecotrophy, and
frequently is a different shade. To prevent
one nitrogen-poor delivered as fecal pellets.

fur slip, chinchillas should always be

Urinary calculi, urolithiasis, metastatic
handled gently with minimal stress.

renal calcification, and nephritis are reported
occasionally. Calculi are typically composed
of calcium carbonate. Such conditions are

Infectious Diseases
often associated with feeding a diet high in

Nearly all significant reports on infectious
calciw11 and low in phosphorus, such as
diseases of chinchillas over tile past 60 yr
alfalfa hay.

come from colonies of chinchillas raised for

Polygamous breeding colonies are
fur, and most reports of bacterial disease
common among chinchilla ranchers, and
in colonies are <!30 yr old. Reviews of
a system of individual female housing has
chinchilla disease often give the false
been devised that allows a single male to
impression that these animals are highly
serve 12 females. A variety of breeding techsusceptible to infectious disease. However, niques have been used successfully, and
the incidence of infectious disease in pet
mating is facilitated by observing changes
chinchillas is low.

in the vaginal closure membrane and
perf01ming vaginal cytology. Pregnant

Bacterial Infections: Historically,
females do not make a nest.

Pseudomonas aeruginosa infections,

Chinchillas possess well developed and
yersiniosis, and listeriosis occw-red
anatomically elaborate male accessory
frequently an1ong fur-ranched chinchillas.

reproductive glands. The secretions from

Estimates of fw0ranched chinchilla
these glands form a hard plug that remains
nwnbers in the USA in 1954 were> 100,000
in the female tract after copulation. In
animals. By the mid-1960s, these nw11bers
chinchillas, the vesicular gland provides
were reduced significantly to only a few
the bulk of the accessory gland secretions,
thousand. Reports since 1980 of yersiniosis
and the fluid hardens or gels when mixed
and listeriosis in chinchillas come almost
with prostatic secretions. A 2-3 in. long,
exclusively from fw--ranched chinchillas in

1-in. diameter, irregularly shaped, firm,

Hungary, Poland, Slovakia, and Croatia.

waxy plug is often found in the female's

These four European countJ.ies supply
cage after mating.

almost 50% of the 200,000 chinchilla pelts
produced annually worldwide.

Physical Examination

Opportunistic bacterial infections in
chinchillas can cause disease, localized

The chinchilla's overall appearance and
either to one organ or as septicemia.

behavior should be noted. Sick chinchillas

Affected animals usually are immunocommay show weight loss, hunched postw-e, promised by age, underlying disease,
abnormal gait, scruffy fur, or labored
nutJ.itional status, or husbandry-related
breathing. They may be lethargic or
factors ( eg, poor hygiene, poor ventilation,
unresponsive to stimulation. Chinchillas
contaminated feed). Members of the fanlily
should be handled calmly and gently to

Enterobacte1iaceae and P aeruginosa have
minin1ize stress. Docile, non pregnant
been associated with significant morbidity
animals can be removed from a cage by
and mortality in chinchillas. However,
grasping and lifting the base of the tail while

Enterobacteriaceae and P aeruginosa can
using the opposite hand to supp01t the body. also be isolated from clinically healthy Routine restraint can be accomplished by
animals. Therefore, most of these organwrapping a towel around the body. Small isms are not considered primary pathogens.

chinchillas may be grasped gently around

P aeruginosa infections in pet chincllillas the thorax, taking care not to restrict
and epizootic outbreaks in fur-ranched
breathing. Pregnant females should not be
chinchillas are the most frequent bacterial
handled unless necessary. Pregnancy is
diseases repo1ted. Initially, the infection is
detectable by palpation at 90 days gestation
usually localized to one organ and can be
and may be determined by regular weighing. associated with coajunctivitis, enteritis, By day 42 of gestation, weight gain in
pneumonia, otitis media and intema,
pregnant chinchillas will increase rapidly.

metritis, and abortion. As tile infection

A protective reaction in chinchillas
progresses, systemic spread is common. An
known as fur slip results in the release of a
acute generalized fonn witll septicemia and

2006

RODENTS
sudden death can occur. P aeruginosa can
tl1is claim is often repeated. L monocy
be part of the nom1al intestinal flora in healthy logenes is an environmental bacterium chinchillas and has been isolated from 40%
capable of existing both as an animal
of healthy chinchillas. Stress, concurrent
pathogen and plant saprophyte. Most cases
disease, or contaminated drinking water
of listeriosis in anin1als aris from ingestion

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predispose to infection and clinical disease.

of contan1inated food, and the disease is

Conjunctivitis is a common initial sign of
common in anin1als, including chinchillas,

Pseudomonas infection in chinchillas.

feel on silage. Listeriosis is a cecal disease in

Anorexia, lethargy, and decreased fecal
chinchillas with blood borne dissemination.

output often follow. Characteristic patho

The main target organ is the liver, where the
logic lesions are miliary necrosis in the
bacteria multiply inside hepatocytes. Early
internal parenchyrnal organs and a necrotirecruitment of polymorphonuclear cells zing typhlocolitis. Strains off' aeruginosa
lead to lysis of hepatocytes, bacte1ial
that are multidrug resistant have reduced
release, septicemia, and, in sUiviving hosts,
antibiotic susceptibility and are highly
development of lung, brain, spleen, lymph
virulent and widespread in chinchillas.

node, and liver abscesses.

Antimicrobial drug selection should be

Other recorded infections in chin-
based on cultw-e and susceptibility testing.

cl1illas include clostridial enterotoxemia,

Generally, P aeruginosa is susceptible to
salrnonellosis, and KlebsieUa infection.

fluoroquinolones, third-generation cepha

Affected anin1als display nonspecific
lospmi.ns, or aminoglycosides. Topical
septicemic signs such as loss of appetite,
polyrnyxi.n Band gentamicin-containi.ng
respiratmy distress, and dia.tThea ai1d die
formulations can be used for empiric
within a few days after onset of clinical
treatment because of the low prevalence of
signs. Salmonella epizootics characterized
isolates resistant to these drugs. Multicomby gastroenteritis and abmtion are repo1tecl ponent P aeruginosa vaccines (formalinin fUI0ranched chinchillas. Case repmts of killed bacteria, endotoxi.n-associated

Salmonella infection in pet chinchillas have protein and/or toxoids) have been used in
been linked to the presence of pet reptiles
fur-ranched chinchillas with some success.

or wild birds.

However, they are not suitable for pet
chinchillas because of their variable
immunity against differentPseudomonas

Viral Infections: There are no speciesstrains, limited in1mune response of 6----8 mo, speciiic viral diseases described for
and adverse reactions at the local injection
chinchillas. Clunchillas are susceptible to
site.

human herpesvims l (HSV-1) and may play

The causative agents of yersi.niosis,
a role as a temporaiy reservoir for hUinan

Yersinia pseudo tuberculosis and Y
infections. Two case reports exist that
enterncolitica occur worldwide in areas
describe spontaneous, herpeslike viral
of moderate and subtropical climate, and
infection in chinchillas. Affected animals
outbreaks in fur-ranched chinchillas are
displayed conjunctivitis and subsequently
described. Y enterocolitica is the species
showed neurologic signs of seizures,
most frequently isolated from chinchillas.

disorientation, recun1bency, and apathy.

Yersiniosis is an enteric disease that damages Nonsuppurative meningitis and polioenepithelium of the ileum, cecun1, and colon, cephalitis with neuronal necrosis and
resulting in mucosal hemorrhage and
intranuclear inclusion bodies were found on
ulceration. Lymphoid infiltration results
histologic examination. In addition, the eyes
in hypertrophy of Peyer's patches and
displayed ulcerative keratitis, uveitis,
mesenteric lymph nodes and necrotizing
retinitis ai1d retinal degeneration, and optic
granulomas. Systemic spread results in
neuritis. The clinical signs, distribution of
granulomatous lesions in the lungs, spleen,
lesions, and the viral antigen suggest HSV-1
and liver and death. A chinchilla-type strain
is a pri.maiy ocuJai· infection with subseof Y enterocolitica (biovar 3, antigens or quent spread to the CNS in chinchillas.

serovar 1, 2a, 3) persists enzootically an10ng
chinchilla stock worldwide.

Parasitic Infections: Protozoa:

Listeriosis is common in fur-ranched

Historically, group-housed chinchillas in fur
chinchillas but has not been reported in pet
rai1ches and research colonies had a high
chinchillas. The original scientists who
prevalence of giardiasis. However, tl1e
described listeriosis in chinchillas claimed
role of Giardia duodenalis (synonym G
that chinchillas are highly susceptible to
lamblia) in causing disease in clunchillas is infection with Listeria monocytogenes.

difficult to establish. Giardia is rai·ely found It has not been proved, but unfortunately,
in fecal samples from wild chincl1illas, and

RODENTS

2007
healthy chinchillas can harbor G duodena

Dermatophytosis is uncommon in chin
lis organisms in low numbers in the small
chillas. 'I'lichophyton mentagrophytes is
intestine. Experimental infection of healthy
the dermatophyte most commonly isolated,
chinchillas with Giardia cysts failed to
although Microsp01um canis and M
induce clinical disease. Predisposing
gypseum have been incriminated in
factors, such as stress and poor husbandry,
outbreaks of spontaneously occurring

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are believed to cause an increase in parasite
dennatophytosis. Wected chinchillas show
numbers, resulting in dian-hea and
small, scaly patches of alopecia on the nose,
potentially death. Recently weaned anin1als
behind ilie ears, or on the forefeet. Lesions
seem prone to developing clinical signs.

may appeai.· on any part of the body, and in

Signs of giardiasis in pet chinchillas can
advanced cases a large circumscribed area
include a cyclic sequence of appetite loss
of inflai.nmation with scab fonnation
and diarrhea, associated with declining
occurs. Aliliough most mycologic studies
body and fur condition. Chinchillas with
of chinchillas are based on animals with
giardiasis can be treated with metronidaclinical signs, fungal cultures of fur-ranched zole, albendazole, or fenbendazole. Whether chinchillas show a 5% incidence of T menta
these compounds eradicate Giardia cysts
grophytes in animals with nonnal skin and a completely or only inhibit cyst production is 300/o incidence in animals with fur damage.

unknown; therefore, treated anin1als may

Diagnosis of dermatophytosis is based on
remain a source of chronic cyst shedding.

appearance of lesions and isolation of ilie

To prevent reinfection, all anin1als in
causative agent by using dermatophyte test
contact with infected individuals should
medium (DTM). Wood's lan1p exan1ination
be treated, and the environment should
is rarely helpful, because most cases are
be thoroughly disinfected. Wooden cage
caused by T ment,agrophytes, which does
interior parts such as resting boards should
not fluoresce under ultraviolet light. Treatbe discarded. Giardia cysts remain ment consists of either itraconazole (10 mg/
infectious for up to several weeks in a cool,
kg/day, PO) or terbinafine (30-40 mg/kg/day,
hun1id environment.

PO) for 4-8 wk. Dem1atophytosis is

Toxoplasmosis was commonly found in
contagious to people and other animals.

fur-ranched chinchillas but is now rarely
seen. Necropsy lesions include hemon-hagic
lungs, an enlarged spleen, and enlarged

Metabolic and Nutritional Disorders
mesenteric lymph nodes. Chinchillas may

Systemic disease or painful conditions
also develop focal necrotic meningoenmay result in secondary GI problems with cephalitis due to Toxoplasma gondii.

nonspecific clinical signs such as anorexia,

Other protozoan infections include
decreased fecal production, and lethai.-gy.

Eimeria chinchilla, which is seen in

Identifying the underlying cause is critical.

fur-ranched chinchillas. Single case reports
to improve the outcome and reduce chance
described in pet chinchillas include hepatic
of recllffence. The initial diagnostic
sarcocystosis, Cryplosporidi'um spp
evaluation should consist of whole body
gastroenteritis, and Frenkelia spp
radiographs, fecal parasite exan1ination,
meningitis.

fecal cytology, and fecal culture for enteric

Cestodes and Nematodes: Pet chinchilopportunistic pathogens ( eg, E coli, P aeru
las have a low prevalence of nematode and
ginosa ). Urinalysis, plasma biochemical
cestode infections. Outbreaks of cerebral
analysis, and a CBC help to diagnose nonnematodiasis caused by the raccoon GI and coexisting metabolic disorders ( eg,
ascai.id Baylisascaris procyonis are
hepatic lipidosis, ketosis, renal disease)

reported in chinchillas housed outside in
to determine prognosis and therapy. In
high northern American climates. An orbital addition to specific treatment for the cyst due to Taenia coenurus has been
primary underlying GI disorder, general
reported in a pet chinchilla with exophthaltreatment guidelines include replacing mos.

fluid deficits and maintaining nom10-
volemia by parenteral and enteral fluid
therapy, nutritional and caloric support, and

Fungal Infections: There are two reports
analgesia (buprenorphine 0.03-0.05 mg/kg,
of Hisloplasma capsulatum infection in

SC, tid) if a painful condition is suspected.

chinchillas. At necropsy, there was pulmo

Cheek tooth crown and root abnormalinary hemon-hage, bronchopneumonia, ai.1d ties are common in chinchillas. Abnormalipyogranulomatous splenitis and hepatitis, ties related to subclinical dental disease
with the organism seen in nun1erous giant
have been reported in one-third of appcells. H capsulatum was cultured from arently healthy chinchillas presented for
timoiliy hay used for food.

routine physical exan1ination. Nutritional

2008

RODENTS

(eg, less abrasive diet in captivity) and
should be limited to severely diseased and
genetic causes have been proposed as
mobile cheek teeth. Analgesia is essential
predisposing factors for development of
after any dental procedure (buprenorphine
dental disease. Tooth elongation and its

0.03-0.05 mg/kg, SC, tic!; rneloxicarn
secondary complications, affecting the

0.3-0.5 mg/kg, PO or SC, once or twice

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reserve or the clinical crown or both, are
daily). Chinchillas in advanced stages of
the underlying cause of most clinical
dental disease should be fed soft, leafy
signs. Chinchillas are often able to eat and
grass hay, vegetables, moistened pellets,
maintain good body condition until severe
and "critical-care" formulas offered on a
complications such as soft-tissue trauma
dish.

from sharp dental spikes or periodontal

Chinchilla anatomy precludes the ability
abscessation have developed. A history
to vomit. Choking may be observed when
of reduced food intake, changed food
the entrance to the trachea is occluded
preferences toward more easily chewed
by a large piece of food or bedding or in
feed items, weight loss, reduced fecal
postpartwn females that eat their placentas.

output, saliva-stained skin and fur with

Aspiration of tiny particles from the foreign
crusting and alopecia of the perioral area,
body can irritate the lower respirato1y tract
wetting and crusting of the chin ("slobbers") and precipitate a suffocating, edematous and forefeet, epiphora, poor fur condition,
response leading to drooling, retching,
and fur chewing are indicative of dental
coughing, and dyspnea as the chinchilla
disease. On clinical examination, palpable
attempts to dislodge the foreign body. If
irregularities of the ventral borders of t.he
untreated, choking may lead to asphyxiamandible and overgrown or irregular tion and death. Megaesophagus, which
occlusal surfaces of the incisor teeth may
leads to regurgitation and aspiration pneube found.

monia, is desctibed. Affected chinchillas

A thorough examination of the oral
show recurting pneumonia despite treatcavity under general anesthesia is required, ment. Contrast radiographs are used for
because 5096of intraoral lesions can be
diagnosis.

missed when examining the mouth in a

Gasttic ulcers are conrn1on in young
conscious chinchilla. Endoscopic-guided
chinchillas and are frequently ca.used by
intraoral examination is the preferred
feeding coarse, fibrous roughage or moldy
method. Cheek teeth often show coronal
feeds. Clinica.lly affected animals may be
elongation, fom1ation of sharp spikes
anorectic or asymptomatic. Lesions may
buccally on the edges of the occlusal
only be noted at necropsy, with gastric
surfaces, and widened interproximal
mucosa! ulcers and erosions covered by
coronal spaces containing feed and fur. Los
thick, black f-luid. Prevention includes
of tooth substance or brown discoloration
decreasing dieta.ty roughage and feeding
of occlusal and interpi:oxinlal tooU1 surfaces a commercial pelleted diet.

is often seen. Erosions of the buccal

Bloat, or tympany, can result from sudden
mucosa, gingival hyperplasia, and gingival
dietary changes, especia.lly overeating.

pocketing are common secondary findings.

Bloat has been reported in lactating females

Radiography is a helpful tool to check tooth

2-3 wk postpartum and may be related to
position and overgrowth of the roots. CT
hypocalcemia Gas production from the
scans of the skull are useful in early
bacterial f-lora in static bowel loops rapidly
diagnosis of malocclusion.

a.ccunmJates within 2-4 lu·. Affected aninlals

The prognosis for chinchillas with
are letl1a.rgic and dyspneic, with a painful,
dental disease depends on the severity of
distended abdomen. They may roll or
disease, the animal's general condition,
stretch while attempting to relieve their
and owner compliance. Repeated intraoral
discomfo1t. Treatment may require passage
examinations and treatments w1der
of a stomach tube or pa.racentesis to relieve
general anesthesia are necessary to
gas build-up. Lactating females may
control complications and to maintain an
respond favorably to calciw11 gluconate
acceptable quality of life for the animal.

administered IV slowly to effect.

Treatment consists of removing spikes,

Diarrhea and soft feces a.re co1ru11on.

reducing elongated crowns, and removing

Besides infectious ca.uses ( eg, parasites,
impacted debris in gingival pockets.

bacteria.), inappropriate feeding of fresh

Instilling doxycycline gel in deep gingival
green feed high in simple carbohydrates
and periodontal pockets reduces periodonor sudden changes in diet will result in tal inflammation. Animals with significant
clysba.ctetiosis and ca.use soft feces. Owners
periodontal infection can be treated with
may desctibe feces smeared on tl1e cage
penicillin G benzathine (50,000 ru, SC,
resting board and the presence of fecalevery 5 days). Extraction of cheek teeth stained perianal fur. On clinical exa.mina.-

RODENTS

2009
tion, the chinchilla may show no signs or, in

Diagnosis is based on a history of polydipsia
severe cases, be anorectic, dehydrated, and
and polyuria, hyperglycemia (<!200 mg/dL),
depressed. Infectious causes are excluded
and glucosuria. Chinchillas and other
based on the history and by appropriate
hystricognath rod en ts ( eg, guinea pigs,
diagnostic testing. Systemic parenteral
degus, tuco-tucos) ai·e unusual in that their

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antimicrobial therapy ( enrofloxacin 10 mg/kg, insulins exhibit a ve1y low biologic potency SC, diluted bid) should be used to treat
relative to pig insulin, yet the recept01�bindpredominately gran1-negative opportunistic ing affinity is significantly higher, indicating
pathogens in chinchillas with severe dystl1at tile efficacy of their insulin on receptors bacteriosis, when an infectious cause is
is -2-fold lower t11an tllat of pig insulin.

suspected but unconfirmed, or when the

Hypoglycemia is always a great risk when
animal is in a compromised general
treating diabetes with recombinant hun1an
condition. Oral drug administration should
insulin or porcine insulin. Treatment
be avoided, because absorption and effecinvolves reducing obesity and feeding a tiveness of oral drugs are decreased when
diet high in protein, low in fat, ai1d high

GI function is abnormal. Once an animal is
in complex cai·bohydrates.

eating and GI function is improved, the oral
route can be used. Intestinal secondary
yeast overgrowth, caused by Cyniclomyces

Traumatic rnjuries
gullulatus (previously Saccharomycopsis

The predator avoidance mechai1ism known
gullulala) that lines the stomach, is often as fur slip, in which a chinchilla releases a
seen in chinchillas with soft feces. However, lai·ge patch of fur, thus enabling it to escape, increased nun1bers of this yeast in chinshould not be confused with tl1e vice of fur chillas is considered secondaiy, rather
chewing. Chinchillas may chew each
than a cause, promoted by an underlying
other's fur, resulting in a motll-eaten coat.

gastroenteric disease process.

Clinically, hair loss is seen along the

Constipation is more common than diarshoulders, flanks, sides, and paws. The rhea. Chinchillas may strain to defecate
affected ai·eas appeai· dai·ker because the
and produce no fecal pellets or have a
underfur is exposed. Mothers often transmit
reduced output of smaller, thin, hard fecal
the vice to offspring. The higher incidence
pellets that may be stained with blood.

of fur chewing in commercial herds may be

Abdominal palpation reveals firm cecal
evidence of maladapted displacement
ingesta and a tense abdomen. Intestinal
behavior. Some clinicians claim affected
intussusception is a critical differential
chinchillas suffer from malnutrition ai1d
diagnosis for absence of fecal pellets. A
chew their fur for dietary requirements.

sudden change in diet, an inappropriate diet

Multiple food factors are probably involved
of insufficient dietary fiber and roughage, or
in this type of malnut1ition, and the ex.act
infectious causes can result in dysbactericause requires further dietary studies.

osis, gastroenteritis, ileus, and consequently

Dming breeding, bite wounds that
constipation. Dehydration, anorexia, dental
abscess are often seen in group-housed
disease, and uterine compression in gravid
ailin1als. Culture of the abscesses often
females may also result in constipation.

yi.eldsStaphylococC'us spp. Female

Chronic cases may lead to rectal prolapse,
chinchillas ai·e larger tllan males and more
intestinal torsion, cecal impaction, or
aggressive. They are highly selective in tlleir
colonic flexure. To provide relief, the GI
choice of males for mating and will keep
tract should be rehydrated. Enteral fluid

"unsuitable" males at bay by mination,
therapy (100 ml/kg/day, PO, divided into
kicking, and biting. Bite wounds often result

4--5 doses) will stimulate the gastrocecal
in the loss of pieces of ears and toes. Older
reflex and rehydrate dehydrated ingesta.

females commonly kill a young male housed

Chinchillas with abdominal pain may resist
in the same cage.

enteral fluid therapy, and buprenorphine

The chinchilla's lai·ge, delicate ear pinnae

(0.03-0.05 mg/kg, SC, tid) and parenteral
ai·e easily traun1atized, most often from bite
fluid therapy will be required.

wounds. Therapy includes cleaning the trau

Pathologists often see fatty liver without
matized area and applying topical antibiotclinical signs or other histologic lesions in ics. Suturing large eai· lacerations is usually
routine necropsies of chinchillas. This
not effective and not recommended. lf
is most likely due to prolonged anorexia
dainage is severe, ear tissue may require
before death.

significant debridement or paitial surgical

A few cases of apparent type II diabetes
removal. n·auma can result in rapid
mellitus have been described in overweight
hematoma development, with blood and
chinchillas. Clinical signs may include poor
serun1 filling the space between skin and
appetite, lethargy, ai1d weight loss.

cartilage. Hematomas should be lanced, and

2010

RODENTS
contents gently removed to avoid further
severe cases, an engorged penis is seen
damage to the ear. The skin over the
protruding 4-5 cm from the prepuce,
hematoma must remain in contact with
resulting in paraphin1osis. This painful
the underlying cartilage and should be
condition may cause urethral constriction
immobilized by sutures if necessary.

and acute urinary retention. CJµ·onic

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Traun1atic fractures of the tibia are
paraphirnosis may culminate in infection
commonly seen and associated with the
and severe damage to the penis, affecting
animal catching its hindlimb in a cage bar.

breeding ability. Getting fur from a female

The tibia is a straight bone longer than the
during copulation is the most conu11on
femur, with little soft-tissue covering; the
cause of fur ring. However, the fur may
fibula is virtually nonexistent. Tibial
come from other males or the same animal,
fractures are either transverse or short
because the condition is also seen in
spiral and generally are associated with
group-housed and single-housed males
bony fragments. Tibias of chinchillas are
not exposed to females. Males should be
thin and fragile, and surgical repair can be
examined for fur 1ings at least four times a
difficult; complications are common. Soft,
year; active stud males should be examined
padded bandages and lateral splints usually
every few days. In some male chinchillas,
do not provide adequate stability for tibial
the penis will hang out of the prepuce all the fractures to heal. External fixation and
tin1e and is not engorged. In these cases, the
intramedullary pins, alone or in combinacondition is not caused by fur-ring but by tion, have been recommended for surgical
excitement brought on by separation from
stabilization of tibial fractures in chinchila mate or exhaustion because of too many las. Restricted exercise in a single-level
females in the same cage. Fur rings can
enclosure, ideally without cage bars, is
be cut or gently rolled off the penis after
necessary. The prognosis for tibial fractures
applying a sterile lub1;cant. Occasionally,
is guarded, and complications after surgical
sedation or anesthesia may be required to
fixation are common and include bone-pin
remove the fur ring.

loosening and infection, nonunion, necrosis
of the distal lin1b, and self-mutilation.

Neoplastic Disorders

Hindlimb amputation should be considered
if surgical fracture stabilization fails or is

Despite a life span reported up to 20 years,
not indicated. Chinchillas usually adapt very references on neoplasia in chinchillas are well after an1putation.

rare. Post.mortem exan1inations of 1,005
fur-ranched chinchillas before 1949 and
another 1,000 fur-ranched chinchillas

Reproductive and Iatrogenic
ranging in age from <6 mo to 11 yr between

Disorders

1949 and 1952 did not list neoplasia as a

In chinchillas, the fine structure of the
cause of death. Between 1994 and 2003,
interhemal membrane of the placental

325 chinchillas were presented for clinical
labyrinth is hemomonochorial, consisting
investigation at a major university
of a single layer of syncytial trophoblasts.

veterinary hospital. Tumors were diagnosed

In this respect, the placental labyrinth is
in only three anin1als (1 %). During the same
sin1ilar to that of the guinea pig, another
period, the incidence of neoplasia was
hystricognath rodent. Female chinchillas
higher in rabbits and rodents than in
may experience an unusual puerperal
chinchillas (guinea pigs, 7%; ra�, 34%; and
disorder of trophoblastic emboli, resulting
rabbits, 6%). Single reports of tumors in
in pulmonary embolism.

chinchillas include neuroblastoma,

Chinchillas usually give birth early in the
carcinoma, lipoma, hemangioma, malignant
morning and only rarely after midnight.

lyn1phoma, hepatic carcinoma, and lw11bar

Dystocia is usually associated with the
osteosarcoma.

presentation of a single, oversized fetus
or malpresentation of one or more kits.

Miscellaneous Disorders

Uterine ine1tia has also been reported as a
cause of dystocia. Chinchillas respond well

Age-related Disorders: Aged chinchilto cesarean section.

las may develop posterior cortical cataracts

Male chinchillas that groom excessively
and asteroid hyalosis.

frequently produce small amounts of urine
or strain to urinate; repeated cleaning of the

Cardiac Disease: Heart murmurs ranging
penis may mean the animal has a fur ring.

from mild to moderate are often heard in

This is a ring of hair around the penis and
young chinchillas. Reports of cardiac
under the prepuce that eventually stops the
disease in chinchillas are scarce, and the
penis from going back into the prepuce. In
significance of heart murmurs in young,

RODENTS

2011
clinically healthy chinchillas remains

Mongolian gerbils construct simple bun-ows
unlrnown. There have been anecdotal

(2-3 ft long) in soft soil where they spend
reports of cardiomyopathy, ventricular
most of their time.

septa! defect, and mitral and tricuspid valve
insufficiencies. Echocard.iography is used

Biology

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to differentiate innocent from pathologic
murmurs.

Mongolian gerbils have several coat
colors. The wild coat color is agouti and is

Foot Disorders: Foot disorders
controlled by an autosomal dominant gene.

predominantly affect the hind feet. Lesions

Sandy gerbils have a recessive color gene
can include hyperkeratosis and erythema;
and show a yellow to ginger color on the
less commonly, deep infections or open
dorsum and the typical creamy white belly
lesions of the plantar aspect of the feet can
of a wild-type Mongolian gerbil. The dorsal
develop. In mild cases, environmental
yellow hairs have short black tips and a
improvements and application of glycerin
light olive green base. A clear demarcation
or petroleum-based ointment often resolve
line between dorsal and ventral color is
the hyperkeratosis and erythema. In severe
present. Black gerbils have an autosomal
cases, lesions are surgically debrided,
recessive gene; white albino gerbils with
followed by open-wound management and
red eyes also have an autosomal recessive
bandaging until healing is complete.

gene.

Gerbils have a large, ventral abdominal
marking gland that is androgen dependent.

Zoonotic Risk

It attains greater size in males and develops

The major zoonotic risk from chinchillas is
at an earlier age. The gland is used for
potential transmission of Giardia. Studies
te1Titorial marking. Females mark their
have indicated the existence of seven
territory after partmition and become more
genetic groups ( or assemblages) within
aggressive.

Giardia, two of which (A and B) are found

The adrenal cortex produces nearly equal
in both people and animals, whereas tl1e
an10unts of c01ticosterone and 19-hydroxyremaining five (C-G) are host-specific. Most corticosterone. When the gland weight is
chinchilla infections occur with assemblage
compared with body weight, the adrenal

B. However, genotyping within assemblages
gland is -3 times larger in gerbils than in

A and B of animal species Giardia to
rats. Gerbils have a high proportion of RBCs
determine zoonotic potential has not
with polychromasia, basophilic stippling,
been done. Therefore, Giardia-infected
and reticulocytosis.

chinchillas could be a potential reservoir

Male gerbils attain sexual maturity by
of zoonotic transmission.

70-84 days. Vaginal opening in females
occurs between 40-60 days, followed by 30

GERBILS
days before sexual matwity occurs. Gerbils
tend to pair bond, and when older females

Gerbils are also lrnown as jirds or sand rats.

lose their mate, getting them to accept

The pet and laboratory gerbil is Meriones
another is often impossible. Early-maturing
unguiculates, commonly lrnown as the
females are more likely to breed success

Mongolian gerbil. There are 14 species in
fully on first pairing, and the lifetime
the genusMeriones.

fecundity of early-maturing females is

Externally, gerbils are quite ratlike. The
more than twice that of their late-maturing
head and body lengtl1 is 9 5- 180 mm, and tail
littermates. Two-thirds of the early-maturing
length is 100-193 mm. The average weight is females that do not reproduce after a first 50-55 g for females and 60 g for males. The
pairing will become pregnant after a second
covering of fur on the tail is short near the
pairing, but only 10% of late-maturing
base and progressively longer toward the
females do so.

tip so that it is slightly bushy. Coloration of

The gestation period of nonlactating
upper parts varies from pale, clear yellowish gerbils is 24-26 days, but lactating females through sandy and gray. The sides of the
always have a prolonged gestation of27
body are generally lighter than the back.

days. If females are bred in the postpartun1

Wild Mongolian gerbils are found in
period, implantation is delayed, and

Mongolia, adjacent parts of southern Siberia gestation can be as long as 48 days. Mean and northern China, and Manchuria. Gerbils
litter size ranges from 3 to 7 animals. Young
inhabit clay and sandy deserts, bush
gerbils suckle for -21 days and begin to eat
country, and arid steppes. They have a high
solid foods at 16 days. In general, day 25 is
degree of resistance to heat stress and
considered suitable for weaning. The
dehydration. They are ten-estrial, and wild
normal life span of a gerbil is 2 -3 yr.

2012

RODENTS

Husband
a.re noted in the proximal collecting tubules
ry

The diet of wild Mongolian gerbils consists
and hepatocytes.

of green vegetation, roots, bulb seeds,
cereals, fruits, and insects. They hoard food

Physical Examination

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and are not normally coprophagic, unless

The gerbil's overall appearance and
diets lack adequate nutrient value. Gerbils
behavior, pa.iticularly in relation to its
thrive on commercially available pelleted
cagemates, should be noted. Sick animals
rodent diets with 18%-2()0A, protein but may
are often isolated from others a.i1d may
have deficiency problems when fed
demonstrate weight loss, hw1ched posture,
prin1arily homemade diets, sun.flower
letha.i·gy, rough fur, labored breathing, and a
seeds, or table scraps, which lack specific
loss of exploratory behavior. Early signs
nutrients. Sun.flower seeds are high in fat
of illness involve changes in the color,
and low in calciwn. Pelleted chow (5 g/day)

consistency, odor, and a.inount of urine and
has been recommended to avoid obesity.

feces. The perinea! area should be checked

Gerbils will develop high blood cholesterol for fecal or urine stains or discharges from
concentrations on diets containing >4% fat.

the vulva in females. Fecal sa.inples may be

This is manifest as Jipemia and is more
taken for parasite detection and bacterial
pronounced in males.

culture. The fw· and skin should be

Gerbils excrete little urine, and fecal
exa.inined for alopecia, fight wounds or
pellets are hard and dry. Their cages require
other trauma, ectopa.i·asites, and elasticity
less frequent cleaning than other pet and
for evidence of dehydration. The oral cavity
laboratory rodents. Gerbils adapt to a wide
should be checked for overgrown teetl1.

range of an1bient temperatures. Because

Ea.is and eyes should be exa.inined for
they have a propensity to develop nasal
discha.i·ges or inflammation. Feet should
dermatitis at relative hwnidities >500A,, a
be exa.inined for sores and overgrown or
low hun1idity is advisable.

broken nails. The abdomen should be

Gerbils require sandbathing to keep their
palpated for masses. Normal body
coats from becoming oily. The lipids have
temperature is 98° -102°F (37° -39°C).

two sources: Harderian gland nasal

Respiratory rate or signs of labored
excretions spread by autogrooming and
breath.ing should be noted. The thorax can
sebaceous exudates from the skin. The
be auscultated with a pediatric stethoscope.

consequences of lipid removal by sandbath

Gerbil tails are fragile, and only the base
ing a.re multiple; it not only cleans and
of the tail should be grasped during handling
grooms the pelage but also deposits lipids
to avoid injury.

on the substrate that a.ct as olfactoty
signals. Sandbathing is usually completed

Infectious Diseases
within 5 min. Additionally, it has homeostatic consequences. Hair color lightens in Bacterial, Mycoplasmal, and Rickett

Mongolian gerbils allowed to sand bathe.

sial Infections: "Facial eczema," "sore When sandba.thing is prevented, accumulatnose," and nasal dermatitis all describe a ing hair lipids mat the pelage;and behavior
common skin condition seen in gerbils.

changes. Sandbath-deprived gerbils

Clinical lesions next to the external nares
increase their frequency of "sand rolls"

appear e1ythematous initially, progress to

(rolling onto their side or back and
localized alopecia, and develop into an
returning to their feet within 1 second),
extensive moist dem1atitis. The cause is
decrease grooming, and increase territorial
believed to be increased Harderian gland
marking (especially males).

secretion of porphyrins ( simila.i· to

Gerbils often stand erect on their
chromodacryoIThea in rats), which act
hindlin1bs, so it is irnpmtant that cages have
as a primary skin irritant. Experimental
a solid bottom and that the floor-to-lid

Ha.i·deria.i1 gland-adenectornized gerbils do
height is tall enough to allow for this
not develop nasal or facial lesions. Various
behavior.

staphylococcal species (St,aphylococC'us

Pet gerbils kept in inferior cages painted
aureus and S xylosus) may act synergisti with lead pa.int or that use alloys containing ca!Iy to produce the dermatitis. Stress
lead have a high potential to develop
factors such as environmental humiclity
chronic lead toxicosis because of their

>50% or overcrowding cause excessive
gnawing behavior and the urine-concentrat

Harderian gland secretion. Nasal dennatitis
ing ability of their kidneys. Chronically,
infection may extend to tl1e maxilla.i-y
gerbils become emaciated, livers are small
sinuses. Affected gerbils develop anorexia,
and pigmented, and kidneys are small and
stop drinking water, lose weight, and die.

pitted. Microscopically, acid-fast inclusions

The distribution and nature of the lesions

RODENTS

2013
are useful in diagnosis. Accwnulated

Infections with dwa.rftapewonns,
porphyrins will fluoresce W1der ultraviolet

Hymenolepis diminuta and Rodentolepis
light (Wood's lamp). Routine bacte1iology

(fom1erly Hymenolepis) nana, are
yields isolation of pathogenic staphylococci.

reported in pet gerbils. Dehydration and

Treatment includes carefully cleaning the
mucoid diarrhea are often presenting signs.

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skin lesions and use of topical ( chloram

R nana has a direct life cycle and may
phenicol l % ophthalmic ointment, tid) or
potentially infect people if ingested.

parenteral antibiotics ( except streptomycin,

Recommended tream1ent is niclosarnide fed
which is fatal in gerbils). Prevention requires at 10 mg feed/100 g body wt for two 7-day reduction of environmental hwnidity below
periods separated by 1 wk Also effective

400,6, reduction of sources of stress such as
are thiabendazole (0.33% mixed in the feed
overcrowding, or sandbath deprivation.

for 7-14 days) or praziquantel (5-10 mg/kg,

Naturally occurring Tyzzer disease,

IM, SC, or PO, repeated in 10 days).

an enterohepatic disease caused by the

Historically, reports exist of pet gerbils
obligately intracellular bacteriwn Clost1id
infected with the tropical rat mite Ornithoium piliforme, is the most frequently nyssus bacoti (seep 2030).

described fatal infectious disease of gerbils.

Conunon clinical and pathologic findings

Fungal Infections: There have been no
are sudden death or death after a short
reports of naturally occuning or experiperiod of disease, and the presence of mental dermatophyte infections in the
multiple foci of hepatic necrosis. Diarrhea

Mongolian gerbil. Other fW1gal infections
and necrotic lesions in the intestinal tracts
in Meriones spp are exceedingly rare.

are variably present. The probable route of
infection in naturally occurring infection
is by mouth, because gerbils exposed to

Metabolic and Nutritional Disorders
infected bedding will contract Tyzzer

Gerbils develop spontaneous, insidious
disease. Supportive fluids and prophylactic
periodontal disease after 6 mo on standard
treatment with doxycycline (5 mg/kg, PO,
laboratory rodent diets. On the same diets,
bid for 7 -10 days) or metronidazole (20

-lO"Aiof the animals will become obese, and
mg/kg, PO, bid for 7-10 days) are recomsome will show decreased glucose tolerance, mended to reduce mortality in cagemates.

increased sefillll immwioreactive insulin,

Because the bacteria form spores, the
and diabetic changes in the pancreas and
housing environment should be thoroughly
other organs.

sanitized and disinfected.

The Mongolian gerbil is susceptible to

Traumatic Injuries
infection by Helicobacter pylori, which
causes severe gastritis, gastiic ulceration,

Thin skin covers the tail of the gerbil. Unlike
and intestinal metaplasia. Gastric adenocarrats or mice, if a gerbil is picked up by the cinoma develops in approxin1ately one-third tip of its tail, the skin will often slip off, of infected gerbils> 15 mo old. Clostridium
leaving a raw, exposed tail that eventually
dilficile-associated fatal enterotoxemia has becomes necrotic and will shed. If the tail been associated with treatrnent using
skin is lost, the bare tail must be surgically
nutritionally balanced triple-antibiotic
amputated where the skin ends.

wafers ( containing amoxicillin, metronidazole, and bismuth) to eliminate naturally Iatrogenic Conditions
occurring Helicobacter infections. Affected A fatal syndrome of acute toxicity is
animals are repo1ted to die within 7 days of
produced in Mongolian gerbils after
antibiotic treatment.

injection of penicillin-dillydrostreptomycinproca.ine combination. The toxicity is due to Viral Infections: Naturally occmring viral
the dillydrostreptomycin, and 50 mg will
infections of gerbils are not reported.

produce almost l OO"Aimortality in adult
gerbils. Approximately 20"/o-400,6 of gerbils

Parasitic Infections: Syphacia obvelata, develop reflex, stereotypic, epileptiform
the mouse pinwonn, and Dentostomella

(clonic-tonic) seizures from -2 mo of age.

translucida, an oxyurid, are found in

Animals seize in response to sensory

Mongolian gerbils. Pet store gerbils often
stimulation and forced exploratory
are infected with mouse pinworms. D
behavior, but t11e incidence and severity
translucida is commonly foW1d in the small of their seizures are variable; the seizures intestine of both research and pet gerbils.

generally pass in a few minutes, may be

There is an average of four parasites per
mild or severe, and have no lasting effects.

animal, but no clinical manifestations of

Although tile incidence and severity of
disease are associated with tl1e infection.

seizures often decrease with age, certain

2014

RODENTS
subsets of adult gerbils do not improve with
phropathy and focal myoca.i·dial degeneraage but progressively become more severe.

tion a.iid fibrosis, especially in older male

The susceptibility is seen in selectively bred
gerbils.

lines but may occur in pet gerbils. Seizures

Mongolian gerbils have a remarkable
can be suppressed in genetically predispropensity for development of aural posed gerbils if they are frequently
cholesteatoma. They occur in 500A, of gerbils

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stimulated by handling during the first 3 wk

> 2 yr old. Cholesteatomas in the ear canal
of life. Anticonvulsant therapy is unnecesdisplace the tympanum into the middle ear.

sa.iy.

Compression and seconda.iy infection result

Cystic ovaries occur frequently in
in bone necrosis and inner ear destruction.

Mongolian gerbils. Cysts range in size from

Clinical signs include head tilt.

1-50 nun in dia.i11eter. Removal of affected
ovaries does not sigruficantly affect

Zoonotic Risk
reproductive perfom1ance.

Females with one ova.iy are slightly

There are no specific reports of zoonotic
inferior in fertility compared with normal
disease transmitted by pet Mongolia.ii
females; a general decline in fertility may
gerbils, although pet gerbils infested with
be evident in older females.

Ornithonyssus sylvimum (tl1e nmthem
fowl mite) and Derma.nyssus gallinae (the
chicken mite) have been the source of avian

Neoplasia
mite den11atitis in children. Avian mite

Ma,jor surveys of spontaneous neoplasia in
infestation is a rare cause of pmritic
laboratory colonies of Mongolian gerbils
dem1atoses in people. The mites spend
have been reported. A 25%---4()0A, incidence of
most of their life cycle on the avia.i1 host but
neoplasia in gerbils usually occurs after 2-3
may be transmitted to people by direct or
yr of age. Squa.i11ous cell ca.i·cinoma of the
indirect contact. The scarcity of reports
sebaceous ventral marking gland in males
may be a true reflection of the absence of
and ova.i·ian granulosa cell tumor in females
zoonotic disease in gerbils or may reflect
account for SQOA, of tun1ors seen in animals
their low popularity as a pet rodent.

>3 yr old. The ventral marking gland tumors
invade locally a.iid can metastasize to lymph

GUINEA PIGS
nodes and lung. Adrenoco1tical tumors,
cutaneous squa.i11ous cell carcinoma,

Guinea pigs, like chinchillas, are hystJ.icogmaligna.iit mela.iioma, and renal a.iid splenic nath rodents. They belong to tl1e fa.i11ily
hema.iigiomas were the next most com

Cavidae, which contains 14 species of
monly repmted tumors. Numerous other
animals commonly known as cavies and
tumors, including duodenal and cecal

Patagonian hares ( or ma.i·as). Four digits
adenocarcinoma, hepatic lympha.iigioma,
on the forepaw and three on the hindfoot
hema.iigioma a.iid cholangiocarcinoma,
characterize Cavidae.

splenic and renal hema.iigioma, uterine

A stocky build, large head, short legs, and
leiomyoma mid hema.iigiopericytoma,
unfU1Ted, short ears characte1ize guinea
ovarian teratoma, testicular teratoma, and
pigs. Head and body length is 200-400 rru11,
maligna.iit mela.iioma, were also reported.

there is 110 external tail, and weight is

However, the total incidence of these tumors 500-1,500 g.

was<5%.

In South America, wild cavies inllabit

Case reports of spontaneously occurring
rocky areas, sava.imas, forest edges, and
tumors in pet gerbils include infiltrative
swan1ps from Colun1bia and Venezuela
craniopharyngiorna, histiocytic sarcoma,
southward to Brazil and northern Argentina.

systemic mastocytosis, malignant

They live in groups of up to 10 individuals
melanoma, a.i1d astrocytoma.

and inllabit burrows that they or other
animals dig. They are most active at night,

Miscellaneous Disorders
when they forage for a variety of plant
materials. Domestication of the guinea pig

Congenital Disorders: Ventricular
began at least by 900 BCE and may have
septa! hea.it disease is seen occasionally
begun as early as 5,000 BCE.

in newborn gerbils.

Biology

Age-related Disorders: In two separate

The An1erican Cavy Breeders Association
reviews, the pathologic findings in aging
recognizes 13 breeds that it divides into

Mongolian gerbil colonies have been
groups or varieties. The most conu11on
reported. Besides neoplasia, there was a
breed is the American cavy and was known
high incidence of chronic glomerulone-

01iginally as the English cavy. Self cavies are

RODENTS

2015
a group of solid-colored animals ( eg, black,
days. Guinea pigs have only a single pair of
cream, red, lilac, beige, saffron, and
inguinal nipples.

chocolate). Nonselfs are a group made up of

Male guinea pigs have pronounced penile
the coated breeds, the marked breeds, and
styles or spicules on the glans penis. Yotmg
the ticked or agouti breeds. The coated
male guinea pigs reach puberty at -3 mo of
cavies include the Abyssinian, Rex,
age and females at 2 mo. Guinea pigs live

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Longhaired varieties (Peruvians, Silkies,

6---8 yr.

Shelties, Coronets, and Texels), Crested,

Teddy, and Satins. The short, wire-haired_

Husbandry

Abyssinian may look unhealthy because its
coat is arranged in whorls or rosettes, giving As a species, guinea pigs are extremely it a rufl1ed, untidy appearance. An
adaptable to a great range of climates,
tmdercoat and projecting guard hairs make
although as individuals they are highly
up the normal fur coat of a cavy. The Rex
susceptible to vaiiations in local temperahas short guard hairs that do not appear ture and hmnidity. Guinea pigs are nervous
above the level of the undercoat, the Satin
animals and may refuse to drink or eat for a
breeds have an abnormal hair fiber that
period after any significant change in their
produces a sheen, and the Teddy breeds
location, feed, or husbandry. The effect of
have a kinked or bent hair shaft that causes
environmental changes on guinea pigs is
the coat to stand erect over the entire body.

minimal or nonexistent when two ailimals

The marked group contains Dalmatian,
are kept together. If a sick guinea pig must
tortoise shell, and Himalayan varieties. The
be kept in hospital, housing a cagemate with
tern1 "variety" describes a color ( eg, steel the sick animal reduces stress.

grey, tortoiseshell) that is not yet a

Guinea pigs live in fainily units centered
recognized breed.

on an alpha male. Mature males, and

Several researchers have analyzed guinea
especially strangers, will fight. However,
pig calls and distinguish between 7 and 11
two males raised together from a young age
distinct sound patterns. Although different
or a group of non breeding females will not
authors have given different nan1es to each
enc0tmter dominance problems. Social
unique sound, there is general agreement on problems are diminished with castration at least 7 sounds.

and ovariohysterectomy, but lea.111ed

Lymphocytes are the predominant WBC
behavior in adult males after castration may
in guinea pigs and range from 45%-809u of
still make them antisocial.

the WBC count. Many small lymphocytes

Guinea pigs require a constant source
are sinlilar in size to erythrocytes. Large
of water that must be changed daily. They
lymphocytes contain Kurloff bodies, large
dirty their water bowls or sipper tubes with
intracytoplasmic mucopolysaccharide
food when they drink They do not lick
inclusion bodies. Kurloff bodies are seen
sipper tubes without training, defecate·
under normal conditions in guinea pigs and
indiscriminately, and are prone to sit in and
are estrogen dependent. Pregnant females
soil their food bowls and sleeping areas.

may have 2%---5% lymphocytes with Kurloff

However, they are generally good eaters
bodies in their peripheral blood; they are
and not as fussy as rabbits.

present in large numbers in adult females,

Guinea pigs produce two types of fecal
and numbers fluctuate with the stage of
pellets: one nitrogen-rich intended for
estrous cycle. There are few Kurloff bodies
cecotrophy, and one nitrogen-poor
in adult males, and they are rarely seen in
delivered as fecal pellets. When food is
newborns.

continually available, -400/o of the feces are

Like chinchillas, guinea pigs share
reingested, and 900/o of this coprophagy
unusual reproductive physiologic characoccurs at night. However, when food is teristics of hystricomorph rodents. Female
limited, guinea pigs ingest feces during
guinea pigs ( or sows) have a pregnancy of
parts of the day when food is unavailable.

68 days ( range 59---72 days) and an average
estrous cycle length of 17 days ( range

Physical Examination

13-25 days). They have a vaginal closure

Guinea pigs are easy to hold and restrain.

membrane that is open at estrus and

Although they do not bite, very young
parturition but sealed during anestrus and
guinea pigs may nip. Healthy guinea pigs
pregnancy. Guinea pigs have an average of
feel "dense" and are alert. Fatigue, lack of 4 young per litter, with a range of 1---13. The
interest in surroundings, and light body
young ( of both species) are born fully furred
weight are often general signs of illness.

and well developed. Young guinea pigs

Sick guinea pigs may show evidence of
usually nurse for 21 days, although they
weight loss, hunched posture, abnormal
can smvive on solid food alone after 5
gait, drawn in abdomen, scruffy fur, or

2016

RODENTS
labored breathing. They may be lethargic
wheezy breathing, sneezing, nasal
or unresponsive to stimulation. Respiratory
discharge, and coughing. The affected
and GI conditions are most commonly
guinea pig becomes depressed and
encountered; thus, ocular or nasal disanorectic. S pneumoniae infections are charges or diarrhea may be present. Feet
nearly always associated with middle ear

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should be examined for sores or broken
infection and head tilt. Increased rndiodennails. Teeth may sometimes overgrow and sity of the affected tympanic bulla may be
should be checked. However, the mouth is
seen on radiographs. Because of limited
small, and examination of the oral cavity is
antimicrobial sensitivity, chloramphenicol
difficult. Ears and eyes should be examined

(50 mg/kg, PO, bid) is the recommended
for discharges or inflammation, and the
treatment. A major differential diagnosis for
submandibular area should be examined
pneumonia is Borclete/J.a bronchiseptica
for swellings.

infection.

Venipuncture can be difficult in guinea

Rabbits may harbor B bronchiseptica in
pigs because of the lack of obviously
their respiratory tracts without developing
accessible peripheral veins. The lateral
disease. However, this organism is an
saphenous vein and the cephalic vein are
aggressive pathogen in guinea pigs, causing
useful to draw small amounts of blood. For
pneumonia, conjunctivitis, otitis media,
large an1ounts of blood, the anterior vena
abortions, and stillbirths. The clinical signs
cava can be used, with the guinea pig under
include anorexia, inappetence, nasal and
anesthesia. This technique requires
ocular discharge, dyspnea, and often
practice. If performed incorrectly, there is a sudden death (this could also include
risk of death associated with intrathoracic,

S pneumoniae and S equi zooepidemicus ).

pericardia!, or pulmonary hemorrhage.

Rabbits and guinea pigs should not be
housed together as pets. Treatment is

Infectious Diseases
ciprofloxacin (10-20 mg/kg, PO, bid).

B bronchiseptica possesses a �-lactamase

Bacterial Infections: Streptococcus
and is resistant to many penicillins and
equi subsp zooep·idemicus (previously cephalosporins and mostly resistant to

S zooepidemicus) may be carried in
trimethoprim-sulfarnethoxazole. Most
the nasopharynx as a latent infection.

isolates are sensitive to doxycycline

Abrasions of the oral cavity ( eg, molar

(2.5--5 mg/kg, PO, bid) and fluoroquinolones
malocclusion) allow bacteria to be

(marbofloxacin, 4 mg/kg/day, PO; ciprotransported to draining lymph nodes of floxacin, 10-20 mg/kg, PO, bid; enrofloxathe head and neck, causing suppurative cin, 5--10 mg/kg, PO, bid for 14 days).

lymphadenitis. Clinically, guinea pigs

Salmonella infections were historically
present witl1 large, unilateral s�ellings in
common in guinea pigs in research colonies.

the neck. The affected aninlal is often in

With present standards of husbandry,
good flesh and shows no other signs of
rodent control, and good quality feed, the
disease. The differential diagnosis should
disease rarely occurs. It is most likely seen
always include cavian leukemia. Treatment
when guinea pigs are kept outside and wild
is surgical excision of the affected lyii1ph
rodents have access to their feed. Disease
nodes and systemic antibiotic treatment.

is more often seen in young or stressed

Bacterial culture and antibiotic sensitivity
animals. Wection may be subclinical, and
should always be recommended. Streptodiarrhea is rarely present. Clinical signs cocci are generally sensitive to chloran1-include conjunctivitis, fever, lethargy,
phenicol (50 mg/kg, PO, bid), and this
anorexia, rough fur, palpable hepatosplenoantibiotic is "safe" to give systemically to megaly, cervical lymphadenitis, and aborguinea pigs. Alternative "safe" antibiotics tion in pregnant sows. Mortality is often
are azithromycin (15-30 mg/kg/day, PO;
high in epizootic outbreaks. If aninlals
discontinue if soft feces) and fluoroquinorecover, organisms may be shed intermitlones; however, bacterial resistance to tently. Diagnosis is accomplished by
these antibiotics is now frequently seen.

isolating the organism from blood, ocular

StreptococC'Us pneumoniae may be
secretions, lymph nodes, or spleen. Because
carried in nares as an inapparent infection.

of zoonotic considerations and the potential

Predisposing factors for development of
for a carrier state, treatment is not
bacterial pneumonia are changes in
recommended.

environmental temperature, humidity, or

Chronic dermatitis ( especially of the
ventilation. This always occurs in winter in
forepaws) is a common condition usually
guinea pigs kept outside. The young, old,
seen in obese guinea pigs housed on wire
and pregnant are the most susceptible. Clinor abrasive floors. Poor sanitation is also a ical signs of pneumonia are dyspnea,
predisposing factor. The feet are swollen

RODENTS

2017
and hairless with ulcers and scabs 1-3 cm in

Other na.tttrally occurring viral infections
diameter on the plantar surface. Staphylo
of gui.J.1ea. pigs such as cytomegalovirus a.i1d
coccus aureus is the usual causative agent
parainfluenza. rarely ca.use detectable
and probably enters the foot through a
clinical disease. Sero logic surveys indicate
cutaneous w0tmd. Awns and straw in the
that guinea pigs will develop a.i1tibodies to

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bedding can also cause foot puncttU"es. The
rat and mouse pathogenic viruses but do not
inflanunation can progress to osteoa.ithritis
develop disease.

and systemic amyloidosis secondary to
chronic staphylococcal infection. Surgical

Parasitic Infestations: Ma.i1ge, ca.used
treatment is often tmsuccessful, because
by the sa.i·coptid mite 11-ixacarus ca.viae, is there is rarely an abscess to be excised or
a common disease. The clinical signs are
drained but rather a diffuse cellulitis that
dra.inatic: intense pruritus, widespread
infiltrates sw-rounding tissue. 'Treatment
alopecia., and hyperkeratosis. T caviae is
involves housing the affected guinea pig
tra.J1S1nitted through direct ani.J.nal-to-a.ilimal
on clean, dry, soft bedding, topical or
contact from sow to weanlings dwing
pa.i·enteral administration of antibiotics, and feeding, and tlu-ough contact witl1 infested foot ba.i1da.ges as needed. Unfortunately, the
cage mate1ial such as bedding. The mites
condition may not respond to therapy.

may be capable of existing subclinically,

Chlan1ydial coajunctivitis is one of
becoming active with stressors (such as
the most conunon causes of infectious
sllipping or pregnancy), i.J.mnunosupprescoajunctivitis in guinea pigs. It is caused by sion, or otl1er underlying diseases. In

Chlamydia caviae, an obligate intracellular affected ani.J.nals tl1a.t exhibit hematologic
ba.cteriwn. Clinical disease usually is found
cha.i1ges such as heterophilia., monocytosis,
in young aninlals 4-8 wk old. Rhinitis, lower
eosi.J.1ophilia., and ba.sophilia, vigorous
respiratory tract disease, and a.bo1tion ca.ii
scratching may ttigger convulsive seizures.

also occur. Concmrent ba.cte1ial infections

The seizw·es a.i·e controlled by diazepam
can contribute to the respiratory symptoms.

( 1-2 mg/kg, IM, as needed). The clinical

C caviae can rapidly spread through a breedprestm1ptive diagnosis should be confirmed ing or resea.i·ch colony. The orga.ilism infects
with several skm scrapings, usually
primarily the mucosal epitheliun1 of the
revealing a massive T caviae infestation.

coajunctiva. and, less frequently, the ge1lital

Treatment involves ivermectin (0.4-0.5
tract of guinea pigs. Asymptomatic infection
mg/kg, SC, repeated 2-3 tinles at inte1vals
can occur, but clinical disease most often
of 7-10 days), or spot-on dermal treatment
results in mild inflanmiatory coajunctivitis
with either selamectin (15 mg/kg for <800 g
with a slight, yellow-white discharge,
body wt; 30 mg/kg for >800 g body wt). The
co11iw1ctival hyperemia., chemosis, and even
guinea pig should also have a whole body
severe coajunctivitis with profuse, purulent
washing with fipronil repeated twice at
ocula.i· exudate. Demonstration of intra.cytointervals of7-10 days. Fipronil should not be plasmic inclusion bodies in Giemsa.-stained
used when open skm wow1ds are present.

coajtmctival epithelial cells often confirms

Other ectopara.sitic diseases are
the diagnosis. The most sensitive and
infrequent in guinea pigs. Westation with
reliable method of diagnosis of chlamydiosis
the fur mite Chirodiscoides caviae may
is PCR testing. Antichlamydial therapy with
result in pruritus and alopecia. along the
doXYcycline (5 mg/kg, PO, bid for 10 days) is
posterior trunk of the body, while underlythe treatment of choice and usually results ing skm is relatively Lma.ffected. SubclinicaJ
in complete recovery. Guinea pigs develop
cases may be a.symptomatic. Treatment is
short-lived inunwlity to C caviae and, after with sela.i11ectin (15 mg/kg for <800 g body
a short petiod, may be susceptible to
wt, 30 mg/kg for >800 g body wt) adminisreinfection.

tered twice at 2-wk intervals.

Lice infestation with either Gyropus
ovalis or Gliricola porcelli is usually Viral Infections: Adenovirus is speciesa.symptomatic but in severe cases may lead specific for guinea pigs and may ca.use a
to prwitus, alopecia, and flaky skin surfaces
prinla.ry respiratory pnewnonia. The
around the neck and ea.i·s. Lice may be
a.symptomatic carrier state is thought to
obsetved di.J."ectly on ha.i.J.· shafts with a
be common, but prevalence is Lmknown.

magnifying glass. A si.J.1gle application of

Clinical disease, while rare, can be initiated

0.05 rnL of a topical solution containing l()OA,
by stress or inhalation anesthesia. and
inlidacloprid and 1 % rnoxidectin is an
occurs more often in i.J.1unw1ocompromised,
effective treatment fur lice infestations
young, or aged animals. Morbidity is low,
i.J.1 guinea pigs. Prevention is a.i.J.ned at
but anin1als usually die suddenly without
i.J.11proving sanitary conditions in the
clinical signs.

aninlal's environment.

2018

RODENTS

Fungal Infections: Dennatophytosis

Treatment is systemic therapy with
is common in guinea pigs, and natural
or without topical treatment. Spot-on
infection is always associated with
treatment products should not be used

Trichophylon menlagrophyles var
alone, because they may predispose

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menlagrophyles. Lesions typically begin
individuals to chronic subclinical infection.

as broken hairs and circular, scaly alopecia Rather, whole-body shampooing, clipping, initially occurring at the tip of the nose,
or rinsing with topical antifungal agents
which spreads to the periocular, forehead,
in conjunction with systemic therapy is
and pinna! areas. In severe cases, the
preferred. For topical therapy, either
dorsal sacrolumbar area is also affected,
enilconazole (0.2% at a dilution of 1:70) or
but the lin1bs and ventrum are usually
miconazole shampoo (with or without
spared. Pruritus is usually minimal or
chlorhexidine ), once or twice weekly, can
absent. Some animals have more inflambe used. Enilconazole is licensed for use as matory lesions characterized by erythema,
an environmental disinfectant and is used
follicular papules, pustules, crusts,
off-label in treatment of dermatophytosis.

pruritus, and occasional scar1ing. High

Systenlic therapy is either itraconazole
temperature and humidity may contribute

(10 mg/kg/day, PO) or terbinafine (30-40
to a more severe infection.

mg/kg/day, PO) for 4-8 wk. Lesions may

Tmentagrophyles can be isolated from
resolve in 2-3 wk, but antifungal therapy
the skin and fur in up to 15% of clinically
should be continued until two DTM cultures
normal guinea pigs. Guinea pigs can be
a.re negative, with a 2-wk inte1val between
tested for dennatophytes by using a new
cultures. Often, dermatophyte infections
toothbrush to comb all parts of the hair coat
of the skin require 2-3 mo of therapy.

and impress the bristles onto dennatophyte
test medium (DTM) in several sites. In a
healthy animal, dermatophytosis is

Metabolic and Nutritional Disorders
generally a self-limiting disease, with full

Guinea pigs of all ages require a dietary
resolution after development of an
source of vitamin C. The stability of vitamin
appropriate cell-mediated immune

C in diets varies with composition of the
response. In inummocompetent animals,
diet, storage temperature, and hun1idity.

this usually takes 100 days. Nevertheless,

The feed content of vitamin C is reduced by
treatment is recommended because it will
dampness, heat, and light. In fortified diets,
accelerate resolution of lesions caused by
approximately ha.If of the initial vitamin C
dermatophytes, thereby minimizing the
may be oxidized and lost 90 days after the
tin1e course of the infection and mininlizing
diet has been mixed and stored at temperatile potential for spread to other animals or tures >22°C (71.6°F). Water in an open
people. Whenever possible, c_uring the
container may lose up to 500A, of its vitamin
infection in the pet, while simultaneously

C content in 24 hr. Aqueous solutions of
decontanlinating the environment, is
vitamin C will more rapidly deteriorate in
desirable. Environmental control should be
metal, hard water, or heat and are more
performed every 14 days with enilconazole
stable in neutral to alkaline solutions.

(0.2%) or concentrated chlorine laundry

Clinical signs of hypovitaminosis C
bleach (1: 10) solutions.

include diarrhea, alopecia, and pa.in (from
joints); animals are thin and unkempt.

Petechiae on mucous membranes a.re not
always seen, although hematuria may be
present. Guinea pigs will show signs of
vitamin C deficiency within 2 wk if it is not
provided. Serum hypercholesterolemia (>60
mg/dL) and hypertriglyceridemia (>30 mg/dL)

is seen in vitamin C--deficient guinea pigs
after an overnight fast. Guinea pigs need

-10 mg vitamin C/kg body wt daily for
maintenance and 30 mg vita.min C/kg body
wt daily for pregnancy. Vegetables high in
vitamin C include red or green capsicwns,
tomatoes, spinach, and asparagus.

Metastatic calcification occurs most often

Ringworm (Trichophyton) in a guinea pig.

in guinea pigs > 1 yr old. Clinically, anin1als

Dermatophyte infections on guinea pigs are
present with muscle stiffness and failure to
often located on the face, back, or front feet.

thrive. Mineralization may be confined to

Courtesy of Dr. Louise Bauck.

soft tissues a.round elbows and 1ibs. Mineral

RODENTS

2019
deposition may also be more widespread,
first or second pregnancy. The disease is
involving lungs, heart, aorta, liver, kidneys,
caused by a reduced carbohydrate intake
uterus, and sclera. Dietary factors such as a
and mobilization of fat as a source of energy.

low-magnesium and high-phosphorus diet,

Changes in feeding routine and stress may
and high calcium and/or high vitan1in D
precipitate the crisis. Clinically, the sow

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intake have been implicated. Feeding
stops eating and is initially depressed, then
conunercial, high-quality guinea pig diets
becomes comatose and usually dies within
has reduced the incidence seen in labora5----6 days. Treatment is rai·ely successful in tory colonies.

advanced cases. Aggressive treatment is

There are two other, similar syndromes
necessary and involves administration of
in guinea pigs that affect either the skeletal

5% glucose solution either IV or SC and/or
muscles (muscular dystrophy) or the myopropylene glycol orally, nub.itional ca.rdiun1 and skeletal muscles (muscular
supplementation, and cesarean section.

degeneration and mineralization). These

Sows in late pregnancy can be given water
two conditions are associated with a
within which a small ainount of glucose has
vitamin E/selenium deficiency. A separate,
been dissolved as a preventive measure.

incidental finding of multifocal mineraliza

The circulatory or preeclai11psia fom1 of
tion of individual muscle fibers may be seen
pregnancy toxemia is due to uteroplacental
in major muscles of hindlimbs. Affected
ischemia. The gravid uterus compresses the
anin1als are often asymptomatic.

aorta, resulting in significant reduction of

Spontaneous diabetes mellitus is common
blood flow to the uterine vessels. Placental
in guinea pigs. The clinical manifestations
necrosis, hemorrhage, ketosis, and death
are mild or variable. Guinea pigs show
follow. If suspected, emergency cesarean
polydipsia and weight loss while maintaining section and/or ovariohysterectomy are a good appetite. Hematology and urinalysis
required to save the sow's life.

show glycosuria, hyperglycemia, and high

Guinea pigs have a high perinatal
serum triglyceride levels; ketonemia and
mo1tality. Dystocia at1d stillbirths are
ketonuria are not seen. Exogenous insulin
related to large fetuses, subclinical ketosis,
is not required for survival.

and fusion of the symphysis pubis. If
females are first bred after 6 mo of age, the

Reproductive and Iatrogenic
symphysis pubis often fuses and does not

Disorders
separate during parturition. Many stillbirths
are often seen in prirniparous females.

Multiple cysts are often present on ovaries

Pregnancy lasts 59-72 days ( average 63
of females >l yr old. The cysts contain
days). If a female strains continually for >20
clear, serous fluid and may reach 2-4 cm
min or fails to produce young alter 2 hr of
in dian1eter. Cysts may be unilateral or
intermittent straining, dystocia may be
bilateral. Clinically, ovarian cysts are
occurring. Careful exainination of the
associated with reduced reproductive
cervix is necessary to assess how much
performance, cystic endometrial hyperplaseparation of the symphysis pubis is sia, mucometra, endometritis, and alopecia.

present. There should be at least the width

Radiography and ultrasonography should
of the index finger to permit passage of the
be performed, especially if an abdominal
fetus. If adequate separation has occurred,
mass is palpable. Diagnosis of the disease
oxytocin (1-2 units, IM) can be given. If the
by plain radiography is difficult because of
fetus is stuck, or parturition does not begin
the similar opacity of ovarian cysts and
within 15 min of giving oxytocin, performabdominal neoplasms. Abdominal ultraing a cesarean section is necessary. The sound allows differentiation by imaging
uterus should be opened close to the
the inner structure of the ovaiian cyst.

bifurcation of the horns. The guinea pig

Treatment is laparotomy and surgical
has a bicomuate uterus with one cervix.

removal of the ovary and cyst. Differential
diagnoses include splenic, uterine, and
ovarian tumors.

Neoplasia

Although the clinical signs ai·e sirnilai·,

Spontaneous tumors are relatively
there are two recognized forms of
unconm1on in guinea pigs and are usually
pregnancy toxemia: the fasting/metabolic
seen in anin1als >3 yr old. Trichofolliculoma,
form and the toxic fom1. Both occur in late
a benign twnor of the hair follicle epithepregnai1cy. Affected sows show depression, liwn, is the most common skin twnor of
acidosis, ketosis, proteinuria, ketonuria,
guinea pigs. The tumor presents as a
and a lowered urinary pH (from -9 to 5----6).

slow-growing, oval mass varying in

Metabolic pregnancy toxemia occurs
diaineter from 0.5----7 cm and located prein obese sows, especially females in their dominantly in the subcutis of the dorsal

2020

RODENTS
lumbar or sacral region, or in the lateral
mia/septicemia. Paradoxica!Jy, clostridiaJ
femoral and lateral thoracic area Males are
overgrowth (Clostridium difficile) has also affected twice as frequently as females. The
been identified. C difficile is a pathogenic average age of affected animals is 3 yr.

organism, not nonnally recoverable from

Epidennoid cysts arising from hair follicles
intestinal contents.

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are often associated with these tumors or

Treatment for antibiotic toxicity is
may arise independently. Ulcerating tumors
p1irnarily supportive. The antibiotics should
and ruptured cysts discharge caseous
be stopped imrnectiately, fiuid therapy (IV or
mate1i.al. Treatment of tJichofollicuJomas
intJ·aosseous) should be administered, and
and epidermoid cysts is surgical excision.

analgesics should be provided to prevent

Tumors of the reproductive tract
abdominal discomfmt. High-fiber diets
represent 25% of sponta.neolli? twnors in
should be syringe fed to prevent ileus.

guinea pigs. Most are ovarian and uterine

Cholestyrarnine (1 g in 10 mL water, tid, for
twnors, although manunary adenocarci5--10 days), an ion exchange resin, has been noma is seen in both male and female
used experimentally to bind clostlidial
guinea pigs. The prevalence of mammary
toxins in clindan1ycin-induced enterotoxtwnors in males is higher than in otber emia. If the enterotoxemia is severe, the
species.

condition is life-threatening and the
prognosis guarded.

Miscellaneous Disorders

Age-related Disorders: Urolithiasis is

Antibiotic Toxicity: The lethal sensitivity
a common problem in older guinea pigs,
of guinea pigs to antibiotic tl1erapy cannot
especially females, because of the proximity
be overemphasized. Antibiotics repo1ted
of the uretlu·al orifice to the anus and tl1e
to cause enterotoxemia are penicillin,
high risk of infection with fecal contan1iampicillin (amoxicillin), bacitJ·acin, nants likeE coli. However, it may be seen
erythromycin, spiramycin, stJ·eptomycin,
in guinea pigs of both sexes and alJ ages.

lincomycin, clinda.mycin, vancomyci.n, and

Clinical signs include dysuria, crying when
tetracycline. Topical antibiotics have also
attempting to urinate, and occasiona!Jy
caused fatal enterotoxemia. The following
hematwia. Diagnosis is by abdominal
tl1erapeutic dosages of antibiotics have been radiology. The calculi are radiopaque and used clinically in guinea pigs (see TABLE 31).

usually composed of calciwn carbonate

Trimethoprim-sulfamethoxazole,
or calciwn phosphate; calculi can also be
chJoran1phenicol, and enrofloxacin are safe
composed of calciwn oxalate. Obstructive
to use in guinea pigs. Narrow-spectrwn
urolithiasis, hydroureter, hydronephrosis,
antibiotics witl1 antibacterial activity
and possible concun-ent septicemia can
against gram-positive bacteria should be
develop if the problem is not treated.

avoided; the ca.use of deatli is a decreased
ln addition to sex and age, diet may
gram-positive bacterial fiora and increased
be related to urolithiasis. Foods high in
gram-negative fiora., with related bactere-
calcium, eg, alfalfa hay, may result in a high

IM=Hili ANTIBIOTIC DOSAGES FOR USE IN GUINEA PIGS

Antibiotic

Dosage

Azithromycin

15--30 mg/kg/day, PO ( discontinue if soft feces occur) Ceftiofur

1 mg/kg/day, IM (for pneumonia)

Cephaloridi.ne

12.5 mg/kg, IM, once to three times daily for 5--14 days Chlora.mphenicol

30-50 mg/kg, PO, SC, or IM, bid

Ciprofioxacin

10-20 mg/kg, PO, bid

Doxycycline

2.5-5 mg/kg, PO, bid

Enrofioxacin

5--10 mg/kg, PO or IM, bid

Gen tamicin

6 mg/kg/day, SC (use cautiously)

Metronidazole

10-40 mg/kg/day, PO

Trin1ethoprim-sulfamethoxazole 30-50 mg/kg, PO, bid

RODENTS

2021
dietary calciwn:phosphorns ratio. Urinary
a large accumulation of sebaceous glands.

ascorbate, if present at a high concentra

The sebaceous glands are testosterone
tion, increases stone fonnation in guinea
dependent, and in adult males, excessive
pigs given high-calciwn or high-oxalate
accwnulation of sebaceous secretions
diets. This may be both beneficial and
occurs in the skin arnund the base of the

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deleterious, ie, needing to give enough
spine and the folds of the circwnanal and
vitamin C to prevent scurvy but not increase
genital region. In areas covered by fur, the
stone forn1ation.

hair becomes thick, matted, and greasy.

Surgical removal is standard treatment.

These folds can be periodically cleaned with

However, it is often complicated by
surgical alcohol or a gel hand cleanser
exuberant inflanmiatory reactions to suture
to preclude infection and unpleasant smell.

material. Prophylactically, potassiwn citrate/
citric acid can be given as an inhibitor of

Zoonotic Risk
crystal formation in urine. Citrate is not
administered for its urine-acidifying effect as

Pet guinea pigs carrying derniatophytes are
it is in dogs and cats, but because of its ability a zoonotic risk for their owners, especially to bind calciwn into water-soluble calcium
children, who are often the only affected
citrate.

members of a household. Risk factors for
human dennatophytosis are young guinea

Dental Disease: The clinical signs and
pigs and recent acquisition of a new guinea
treatment of malocclusion in guinea pigs are pig. When treating ringworm in guinea pigs, almost identical to those in rabbits, except
environmental treatment should also be
premolar teeth are more commonly affected reconunended to the owners, with special (seep 1955).

attention given to the bedding and clothing
of people in contact with infected or carrier

Alopecia: Alopecia develops to a degree in
anin1als. Contagious material may persist in
all guinea pigs in late pregnancy (60---70 days) the owner's clothing and bedding and is a and during nursing. It results from reduced
common reason for a pet's relapse after an
anabolism of maternal skin associated with
initial response.

fetal growth. Hair loss usually begins on the
back and progresses bilaterally on the flanks

HAMSTERS
and ventral abdomen. Nursing guinea pigs
may worsen the condition by pulling hair

The most common pet and research
from their mothers. The alopecia resolves
hamster is the golden or Syrian hamster
slowly either after parturition or when the

(Mesocricetus auratus). All Syrian
sow stops nursing.

hamsters in captivity appear to have

Thinning hair is common in young anin1als originated from a litter of eight hamsters at weaning. It is associated with a period of
collected near Aleppo in Syria in 1930. Four
transition in which coarse guard hairs of the
of the animals escaped, a male killed one
adult coat are developing and neonatal fur is
female, and only one male and two females
being lost. Ear chewing and barbering are
remained. From these three anin1als, litters
seen in group-housed guinea pigs that
were raised that were distributed to Europe
develop a social hierarchy. Often younger
and the USA for research and subsequently
anin1als of lower rank develop hair loss from
as pets. In 1971, an additional 12 Syrian
fur chewing by dominant older members.

hamsters were captured in the field by

The hair loss is characterized by an in·egula.r,
fanners and imported to the USA.

almost stepwise pattern. Treatment involves

Syrian han1sters have a head and body
separation of the aggressive anin1al(s).

lengtl1 of 170---180 nun and tail length of

Single-housed guinea pigs that become

12 nun. They range in weight from 110---140
bored may inflict self-barbering. In these
g, and females are larger than males. Wild
cases, areas the anin1al cannot reach such as

Syrian hamsters have a light, reddish brown
the head, neck, and anterior shoulders are not dorsal coat, and the underparts are white.

affected. Changing the guinea pig's environ

The skin of Syrian han1sters is very loose.

ment and providing large amounts of fresh

Other species now COilll11on as pets are
hay often prevent boredom and stop this vice.

the dwarf hamsters such as tl1e Djungarian

Bilateral, symmetric alopecia may be

(Plwdopus sungorus) and Roborovsky (P
seen in older females with ovarian cysts.

roborovskii) hamsters. They are small

Other differential diagnoses for alopecia are

( <100 g body wt), have a docile disposition,
mite infections and dermatophytosis.

do not attempt to bite or run away, th.rive

Sebaceous glands are abundant along the
in captivity, and make good pets. This
dorsal surface of guinea pigs and around the discussion primatily deals with diseases anal orifice. The circumanal region contains
of the Syrian hamster.

2022

RODENTS

Biology
shallow bwrnws. Deep bedding that is

At least 20 mutations affecting coat color in
appropriate for bun·owing is recommended.

Syrian

Cages with at least 40-80 cm of bedding

.hamsters are !mown. Most are sin1ple
recessive traits, four are dominant and two
enhance the welfare of Syria.11 hainsters.

are sex-linked. Five mutations aff�ct the fur

Wild Syrian hainsters are omnivorous
giving rise to long hair (also !mown as "tedd� eating many kinds of green vegetation VetBooks.ir
bear''. hamsters), rex, and satin coats. Length seeds, fruit, and meat. Exposure to cold of hair m the longhaired Syrian hamster is
stimulates hamsters to gather food and
influenced by testosterone. Longhaired
tl1ey will often hibernate at temper;tures
males from the age of sexual maturity have

<5°C (41°F). Syrian hainsters do not fatten
significantly longer hair than females or
before hibernation ai1d will starve unless
castrated males, which display fluffy,
they waken periodically to eat. Hibernating
shorter hair.

an!l11als remain sensitive to external stin111li

Syrian hainsters possess paired, flank
and are usually a.roused if handled. Syrian
organs m the costovertebral area that ai·e
hamsters have prominent depositions of
androgen dependent and consist of
brown fat beneath and between the
sebaceous glands, pigmented cells and
shoulder blades, in the axilla, and in the
tem1inal hairs. They are larger and.heavily
neck and perirenal areas.

pigmented in males ai1d used for territorial

Syrian hamsters are active chewers ai1d
marking. All hamsters possess enorn1ous
skillful at escaping from their cages. Glass
cheek pouches that open inside the lips,
water tubes a.re contraindicated for Syria.11
extend well back of the shoulders and
ha.111sters, because they will readily bite
when filled with food more than d�uble the
through glass. Stainless steel sipper tubes
width of the animal's head and shoulders.

close to the floor are recon1111ended. Because

Adult male Syrian hainsters develop large

Syrian hamsters have broad muzzles that
adrenal glands due to enlargement of tl1e
often prevent tl1em eating from feed hoppers,
zona reticularis, which is three times the
feed pellets are placed on tl1e floor of tl1eir
size of that in female hainsters. Like gerbils,
cage. Han1sters are naturally coprophagic.

Synan hamsters have a high proportion of
erythrocytes with polychromasia.

Physical Examination

Female Syrian hainsters ai·e heavier fuan
males and generally are aggressive toward

The animal's overall appearance and
other hamsters. Nonestrous females can
behavior, particularly in relation to its
behave especially aggressively towai·d young
cagemates, should be noted. Sick animals
males and may kill them. The 4-day estrous
are often isolated from others and may
cycle is characterized by a copious
show weight loss, hunched posture,
postovulatory discharge on the last day.

lethargy, rough fur, labored breathing, and a

The discharge is creamy white and has a
l�ss of exploratory behavior. Early signs of
distinctive odor; it fills the vagina and usually
disease mvolve changes in the color
extrudes through the vaginal orifice. Its
consistency, odor, and volwne of urine and
stringy nature is distinctive, and if touched it
feces. The perineal area should be checked
can be drawn out as a tlu·ead of about 4--6 in.

for fecal or wine stains or discharges from
length. Estrus lasts -1 day, and the gestation
the vulva in females. Fecal sainples may be
pe1iod is 16-19 days. The litter size ranges
taken for parasite detection and bacterial
from 2 to 16, with an average of 9. Cannibalculture. The fur and skin should be ism of yow1g accounts for nearly all preexai11ined for alopecia, fight wounds or weaning mortality. Cold ambient temperaoilier trawna, and ectopa.rasites. The oral tur
cavity should be checked for overgrown

�s ( <10°.c [50°F]), lean diets, and low body
weight dwmg pregnancy increase cannibalteeth or impacted cheek pouches. Ears ism. Disturbing the mother by handling the
should be exainined for discharges or
young or nest, and not providing adequate
mflan1matmn ai1d eyes for discharges or
nesting material, warmth, food, or water,

COI\Junct1vit1s. Feet should be exai11ined for
often results in cannibalism. Syrian hainsters
sores and overgrown or broken nails. The
are prolific breeders, and there may be 3-5
abdomen should be palpated for masses.

litters/yr. The young are weaned at 20 days

Syrian hamsters a.re not normally
and capable of reproducing at 7-8 wk. The
aggressive but can be provoked if suddenly
life span of Syrian hamsters is 2-3 yr.

startled, awakened, or roughly handled. It
may be easier to scoop Syria.11 han1sters up

Husbandry
m a small container rather than pick them
up directly. Their highly elastic skin should

In the wild, Syrian hamsters live on dry rocky be grasped sufficiently to prevent the anin1al steppes or brushy slopes. They construct
from biting.

RODENTS

2023

Infectious Diseases

Bacterial Infections: Diarrhea may
occur in Syrian hamsters of any age and is
known as "wet tail," although this euphemism is frequently used to describe the disease in young hamsters. Proliferative

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ileitis is the most significant intestinal
disease of 3 - to 10-wk old Syrian hamsters
and results in high mortality. It is caused by
the intracellular bacteliurn Lawsonia
intracellularis. Treatment involves
correcting life-threatening electrolyte
imbalance and dehydration, administering

Gross lesions of Demodex infection in a
antibiotics, and force feeding. Several
hamster. Note the characteristic hair loss on
antibiotic treatments are recommended,
the head and neck. Courtesy of Dr. Louise Bauck.

including doxycycline (5--10 mg/kg, PO, bid
for 5--7 days), enrofloxacin (10 mg/kg, PO or

IM, bid for5--7 days), and trimethoprimsulfamethoxazole (30 mg/kg, PO, bid for 5--7
declines to a much lower level. Enzootically
clays). Symptomatic treatment with bismuth
infected Syrian hamsters develop HaPV skin
subsalicylate may be given if diarrhea
tumors rather than lyinphoma. HaPV
persists. Replacement electrolyte and
lymphoma-affected Syrian hatnsters appear
glucose solutions should be given orally,
thin, often with palpable masses in the
and electrolyte fluid replacement such as
abdomen. Often, they have demodectic
saline or lactated Ringer's solution should
mange due to either Demodex criceti or
be given at a dosage of 20 mIJlOO g body wt

Daurati.

once daily. Sequelae of proliferative ileitis
in surviving Syrian hamsters may include

Parasitic Infections: Fecal smea.i-s of
eventual obstruction, intussusception, or

Syrian hamste1-s are abundant in protozoan
rectal prolapse.

organisms. However, tl1eir role in enteric

Diarrhea in adult Syrian hamsters is
disease is speculative, because similar
associated with Clostr idium difficile
protozoa are found in comparable nwnbers
enterotoxemia and, as in guinea pigs, may
in both healthy and diseased anin1als.

occm 3-5 days after administration of

Demodex C1iceti and D aurati are
antibiotics such as penicillin, lincomycin,
occasionally found on han1ste1-s. Clinical
or bacitracin.

signs consist of mild to moderate alopecia,

'Iyzzer disease due to Clostridium
pruritus, and erythema generally on the
piliforrne is seen in Syrian hamsters and
dorsal region of the body, the hindlimbs, anti
is usually precipitated by stress such
face. Additionally, crusts and scaling may
as overcrowding, high environmental
be found on physical exan1ination. Skin
temperatme and hwnidity, heavy internal
scrapings confirm the presence of a large
and external parasite load, and nutritionally
mm1ber of Demodex spp in valious stages
inadequate diets. C piliforrne is opportunisof development. Treatment consists of tic in i.nununosuppressed animals and not
a combination of l% seleniun1 sulfide
seen in inununocompetent anin1als.

shampoo and topical application of

Bacterial pseudomycetoma has been
selamectin (15 mg/kg, applied once).

described in several dwarf hamsters. The

Han1sters that do not respond to treatment
treatment is excision.

or relapse often have serious underlying
disease and typically die within 3 mo.

Viral Infections: Hamster polyoma virus

Histolically, reports exist of pet hamsters

(HaPV) is the cause of epizootic lymphoma
infected with the tropical rat mite Oniitlw
in young Syiian hamsters and epitheliomas
nyssus bacoti (seep 2030).

in older enzootically infected hamsters.

When first introduced into a naive

Fungal Infections: Spontaneously
population of breeding Syrian han1sters,
occmring derniatophytosis is extremely

HaPV results in an epizootic of lymphoma,
rare in Syrian ha.i11sters.

with an incidence as high as 80%. Lymphomas often alise in the mesentery but can Neoplasia
atise in the axillary and cervical lymph
ln older Syrian ha.insters, lymphoma is the
nodes. Once enzootic in a hamster popmost frequently observed neoplasm of the ulation, tl1e occurrence of lyi11phoma
hematopoietic system. It is multicentlic and

2024

RODENTS
conunonly affects lymphatic organs.

hamsters. Not surprisingly, it is infrequently

Cutaneous lymphoma, resembling mycoreported in pet Syrian hamsters, in which sis fungoides (an epidermotropic T-cell
overcrowding is not a problem.

lymphoma in people), is seen occasionally

Degenerative renal disease also occurs
in adult Syrian hamsters. Affected animals
more frequently in older female Syrian

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show anorexia, weight loss, and patchy
hamsters. Affected kidneys are pale and
alopecia. Cutaneous lymphoma can be
granular. Microscopically, glome.rular
misdiagnosed as hyperadrenocorticism
changes vary from thickening of the

(Cushing disease), because affected
basement membrane to glomernlar
hamsters initially show patchy alopecia
obliteration. Arnyloid deposition occw·s
and dermal hyperpigmentation. However,
frequently as a concmrent event.

cutaneous lymphoma shows rapid progre

Polycystic liver disease is seen in Syrian
ssion of the disease, with mean time from
hamsters> l yr old. The lesions are due to
presentation to euthanasia-10 wk. Adenodevelopmental defects of the bile duct and mas of the adrenal gland are common in
are not associated witl1 clinical signs. At

Syrian hamsters, but few reports exist of
necropsy, nwnerous thin-walled cysts may
confirmed clinical Cushing disease in
be seen.

hamsters.

Melanomas, not only of the flank organ

Zoonotic Risk
but also of the skin, are frequently reported
in Syrian hamsters. There is a striking 10: l

Syrian hamsters have a reputation as
male:female melanoma ratio.

carriers of lymphocytic choriomeningitis

Djungarian han1sters showed a high
virus (LMCV), a rodent-borne virns that
prevalence of neoplastic disease (5 times
can cause substantial neurologic disease,
greater than Syrian hamsters), and most
particularly among prenatal and inmrnnotun1ors are integumental ( eg, mammary compromised people. The conunon house
tumors, atypical fibromas, and papillomas).

mouse, Mus musculus, is the natural host
and principal reservoir of LCMV. People are
typically infected through close proximity

Miscellaneous Disorders
to wild mice and their droppings. However,

Age-related Disorders: Atrial thromthree of the largest outbreaks of LCMV
bosis occurs in aging Syrian hamsters with
infection in the USA were attributable to
an incidence of up to 7(YYo. Most thromboses
hamsters obtained from a single supplier
develop in the left atrium secondary to heart in the late 1970s. More recently, individual failure and lead to a consumptive coagucases of LCMV infection have been lopathy. Although the incidence does not
epidemiologically linked to han1sters
differ between the sexes near the end of
among organ transplant recipients.

tl1eir respective life spans, att:i,al thrombosis

Although the risk of hamsters transmitting
occurs on average at a younger age in

LCMV to the general population may be
females (13.5 mo) than in males (21.5 mo).

overstated, a Gennan swvey of persons in

Aged Syrian hamsters present with clinical
contact with pet hamsters confinned an
signs of cardiomyopathy such as hyperpnea, increased risk of LCMV infection, especially tachycardia, and cyanosis. In tmtreated
in city dwellers, younger age groups, and

Syrian hamsters, death usually follows within females. Transplacental infection occurs in a week after these signs are evident. The
the fetus of women who develop viremia
incidence of atrial thrombosis is influenced
during the first and second trimesters. The
by the endocrine status of the animal,
virus acts as a nemoteratogen, causing
especially by the amount of circulating
chorioretinopathy, hydrocephalus,
androgens. Thus, the castration of male
microcephalus, lissencephaly, and

Syrian hamsters is linked to an increase in
potentially fetal death. The relative risk
the prevalence of at1ial thrombosis.

posed by hamsters should be considered

Weight loss is seen in older Syrian
among transplant recipients and pregnant
hamsters and often associated with hepatic
women, because infected animals may
and renal amyloidosis. It is the principal
remain clinically unaffected by LCMV and
cause of death in longterm research studies.

can transmit the virns for at least 8 mo.

Females have a higher incidence (80%

When apparent, LCMV infection in
among han1sters > 18 mo old), increased
hamsters is characterized by wasting. Early
severity, and earlier age of onset of an1yloisigns are decreased activity and appetite dosis than males. There is a correlation
and unkempt coat. Later signs include
between social stress induced by crowding
weight loss, hunched posture, blepharitis,
and amyloidosis in laboratory Syrian
convulsions, and eventually deatl1.

RODENTS

2025

MICE AND RATS AS PETS

Husbandry

Mice and rats are not as corrm10n as pets as

The best cages are made of a material
other rodents. They are used extensively in
that is easy to clean and deodorize and is
research and, consequently, a separate
indestructible to rodent chewing or digging

VetBooks.ir
section on mice and rats as laboratory
in the comers. The cage floor can be solid
animals follows below (seep 2032).

but should be waterproof and easy to clean.

Although a great deal of information has

Wire mesh floors should be avoided,
been accumulated on wild and laboratory
because rats and mice can trap their feet
rodents, very little of this infom1ation
and especially hincllimbs in tl1e openings,
pertains to pet rodents.

resulting in fractures and il\iulies.

The prevalence and type of mouse and rat

Animal cage bedding is described based
diseases seen in clinical practice are quite
on its use ( eg, contact, noncontact, and
different from those seen in a research
enlichment bedding) or the material from
setting. The diagnosis and treatment of pet
which it is made ( eg, wood-based [ chips,
mice and rats involves evaluation and care
shavings, peelings, wood-wool and
of an individual animal from a household,
sawdust], paper-based [ cotton and pulp
not the healtl1 management of rodents from
fiber, recycled paper], com [husks and cobs],
a research colony. Most problems in mice
cellulose, and vermiculite). The purpose of
and rats a.re dermatopathies, respiratory
bedding is to keep animals dry and clean. Pet
infections, and neoplasia.

owners generally choose bedding based on
cost and availability, whereas laboratory
vetelinarians choose bedding based on

Biology
cost and water-holding capacity. Some pet
bedding con ta.ins lemon and chlorophyll to

Male rats are sexually mature by
give it a pleasant scent. This type of bedding

6-10 wk; female rats are sexually mature
iffitates pet rodents, and the cololing agents
by 8-12 wk. The breeding life of both male
can stain the coat of white rats or mice.

and female rats is 9-12 mo. Estrous cycle

Traditionally, owners prefer paper and
length in female rats is 4-5 days, and
softwood chips, such as pine or aspen, to
estrus lasts 10-20 hr. Female rats ovulate
straw because it requires fewer bedding

-10-20 eggs. Gestation lasts 21-23 days;
changes. Cedar and other wood chip
pseudopregnancy from sterile matings
shavings reduce ectoparasite problems
lasts 12 days. Rats have an average litter
and have a pleasant scent. However, such
size of 8-18 pups. Weaning takes place
bedding is not recommended, because it
at-21 days.

emits toxic aromatic hydrocarbons that

Both male and female mice are sexually
increase the incidence of cancer in anin1als
mature by 6--8 wk and have a breeding life of and cause mouse and rat pup mortality.

9 mo. Estrous cycle length in female mice is

Owners must combine frequent bedding

4---5 days, and estrus lasts 10-20 hr. Female
changes with good husbandry such as
mice ovulate -6--10 eggs. Gestation lasts
regular cage cleaning, low anin1al density,

19-21 days; pseudopregnancy from sterile
and low environmental temperature and
matings lasts 12 days. Mice have an average
hwnidity. This will reduce toxic or odorlitter size of 5-12 pups. Weaning takes place causing gases such as ammonia from
at-21 days.

building up, because urease-positive

Male mice and rats produce a small
bacteria in the feces act to break down urea
amount of sperm daily at puberty ( eg,
in the uline. Aquariwns are not suitable

40-50 days in a rat). It is not until 75-100
cages for rats and mice because of
clays (10-14 wk) in rats that optimal sperm
inadequate air circulation and subsequent
production and reserve occur. Male
buildup of ammonia. Environmental
rodents show a constant libido after sexual
temperature and relative hwnidity can
maturity; in contrast, females are receptive
depend on husbandry and housing design
to copulation only during estrus. Males
and can differ considerably between tl1e
cannot fertilize females until 6--8 wk after
cage and room. Factors that contribute to
reaching puberty.

variation in temperature and hwnidity

The average life span of mice is 18-24 mo
include cage matelial and construction,
and of rats 18-36 mo. Restricting dietary
number of animals per cage, frequency of
calories without compromising overall
bedding changes, and bedding type.

nutrition results in increased life span.

Size and manipulability of bedding

Obesity in pet rats and mice is corrm10n, and
material are the main detem1inants of1nice
calorie-restlicted pets live significantly
and rats' choices. Mice and rats avoid
longer lives.

bedding consisting of small particles,

2026

RODENTS
whereas they prefer bedding consisting of

Most rodent en.riclunent studies focus
large, fibrous particles. When exposed to
on modifying the area inside the enclosure
different types of nesting materials such as
rather than the size of an enclosure.

paper strips, comhusks, sawdust, and wood

However, rats prefer larger cages, and

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materials ( shavings, peelings, and chips),
experimental studies suggest rats should
rats choose long strips of soft paper. Rats
have a larger space that allows shaiing of
also select opaque or semi opaque nest
tl1e environment witl1 up to four other rats.

boxes to transparent nest boxes. Mice show

The minimum recommended height of
no preference between paper and woodcages should take into account typical derived materials but show a clear
postures of rats and 1nice. This includes the
preference for materials that they can
animal standing fully erect on its hindlegs,
manipulate such as paper tissues, ·string,
and vertical movements such as stretching
and wood materials (shavings, peelings,
upward and possibly climbing. Conseand chips). Many mice will combine two quently, minimal cage heights of 12-15 in.

prefen-ed nesting materials to make

(30-38 cm) for rats and 7--8 in. (18--20 cm)

complex nests. Mice typically dislike
for mice are recommended.

wire-bottomed cages; however, both male

Environn1ental enrichment is important
and female mice will spend more ti.me in a
for both mice and rats. For example,
wire-bottomed cage with nesting material,
suspended cloth han1mocks are popular
despite the grid floor that they usually avoid.

with rats, and suspended (plastic or

In environ.mentally enriched cages with
stainless steel) shower hooks fitted into one
hollow tubes, mice have no overwhelming
another can make a swinging chain. Rats
group preference for shape, opacity, or
will use more eruiclunent devices than
openness of tubes and prefer to sleep in
mice, but they usually stop using the devices
sawdust when it is available. Mice will sleep
after 3-4 days. Rotation of enrichment toys
in hollow tubes only after the sawdust is
and introduction of novel devices excite
removed; they use short, wide tubes more
their cwiosity. Food treats are also valuable
frequently tl1an long or short nan-ow tubes.

en.riclunent items. These can range from

Mice and rats are optimally maintained at
simple, inexpensive treats such as a daily
temperatures of 64°-79°F (18°-26°C).

piece of a breakfast cereal to formulated

Relative hwnidity should also be controlled
nutritious or calorie-free treats. Rats also
but not nearly as nan-owly as temperature.

love chocolate, and it is not toxic when fed

An acceptable range of relative humidity is
in small an10unts. Pet rodents accustomed

300/o-700Ai. Both temperature and hwnidity
to handling will eat food treats out of the
regulation are important to prevent ringtail
owner's hand. This daily routine can allow
and exacerbation of respiratory disease.

owners to detect subtle changes in the pet's

Avascular necrosis of the tail, or ringtail,
behavior. Sick rodents effectively hide signs
occurs primarily in young rats in low-hun1idof disease. Sick rats do not show the same ity environments. Excess heat and hun1idity
interest in their daily treat, and this can alert
cause heat stroke and indirectly cause
the owner early to disease when it is still
decompensation of chronic respiratory
treatable and/or reversible.

disease, resulting in death.

Housing male and female rodents

Mouse and rat owners should check
together will result in mating and
water bottles daily. 1f mice are deprived of
subsequent litters. Mice and rats experiwater for only a short ti.me and experience ence postpaiturient estrus, and fertilizadramatic fluctuations in the suJTounding tion can occur. However, in1plantation of
temperature, especially >99°F (37°C), they
the resulting blastocysts is delayed during
die. In contrast, healthy rats tolerate water
lactation and occurs at weaning, ensuring
deprivation and temperature fluctuations
that the next litter is not born until the
better. They can live for 7 days without
earlier one has been weaned. Female mice
water, in temperatures between 64 ° -79°F
become sexually mature at 6--8 wk of age,

(18° -26°C), although they may lose up to
and female rats are sexually mature by 10

65% of their body weight.

wk of age. Unless opposite-sex rodents

Minimal space allocations of 23 sq in. (58
housed together are separated or neutered,
sq cm) are recommended for individual rats
having a new litter every 3-5 wk is
weighings200 g, and 60 sq in. (152 sq cm) for
possible.

rats weighing<! 500 g. For mice, minin1al

Rats and mice are omnivores and will eat
space allocations of 15 sq in (38 sq cm)

food of both plant and ailimal origin. In the
for individual mice weighing >25 g are
wild, rats ai1d mice will eat a wide variety of
reconm1ended. These are small surface
seeds, grains, ai1d other plant material as
areas, and veterinarians should advocate that well as inve1tebrates, small vertebrates, and owners provide larger space for their pets.

carrion. Their ability to scavenge paitly

RODENTS

2027
accounts for their successful colonization
contact and environmental enrichment.

of diverse geographic regions.

Isolation-reared rats will experience

Fonnulated pelleted diets for laboratory
fighting, physical irtjuries, and weight loss
rodents are convenient and nutritionally
when placed into a colony of socially
balanced diets for early life and reproducexperienced rats. Young rats should VetBooks.ir
tion. However, laboratory rodent diets are
be housed together to develop social
relatively high in fat and low in fiber, and
affiliation. Singly housed rats should not be
when provided ad libitun1, they cause
put together. Owners should be advised to
obesity. Consequently, the amount of
encourage enrichment and human contact
pelleted diet owners provide daily should be with pet rats.

limited. Diets fonnulated specifically for pet
rodents are now commercially available.

Owners should supplement their pet's diet

Physical Examination
with feeds high in fiber such as vegetables,

Observing the condition of the rodent's
limited amounts of fruit, and occasional
living quarters provides useful infonnation.

treats.

Wonnation obtained from a physical

Coprophagy is a normal behavior in rats
exan1ination is often limited because of
and mice. It is an inherent behavior, because the mouse or rat's size. Activity of the rat, it is seen in genn-free rodents purposely
condition of grooming, and the presence of
bred for research. Unlike rabbits, which eat
a head tilt or discharges in the cage should
cecal feces from their anus, mice and rats
be noted. If dyspnea or depression is seen,
eat fecal pellets on the floor of their caging.

extreme care should be used when handling

The amount of feces eaten varies between
the animal, because it is probably very sick
rodents, their age and physiologic status
and could die from the stress of a physical

( eg, coprophagy increases in pregnancy),
exan1ination.

and the diet fed. On a nutritionally complete

Pet rodents that have been frequently
diet, rats will eat -1 ()OA, of their feces. When
and gently handled usually require only
rats are housed together, they ingest each
minin1al restraint. Less cooperative anin1als
other's feces. The unique odor of a colony is
need to be more finnly restrained, and use
due in part to ingestion of feces, and the
of a towel or even heavy gloves may be
group scent enables distinction between
required. Weight measurement is essential
members and nonmembers. Mice engage in
to calculate appropriate dosages of medicoprophagy -6 tin1es/day. Growing mice cations and provides an opportunity to
show vigorous coprophagous activity,
gauge the rodent's temperament before
eating 13 pellets/day. However, it gradually
beginning tl1e actual physical examination.

decreases to 1 !h pellets at 2 yr of age.

The head, ears, eyes, and nose should be

Owners should house different species of
exan1ined for discharges, and the oral cavity
rodents separately to prevent interspecies
for dentition. Lymph nodes and glands of
disease transmission. For exan1ple, rats
the head can be observed for size and
carry Streplobacillus moniliforrnis (see
palpated for consistency. Assessment of the
p 2418), a cause of fatal septicemia in mice,
head is probably the most time-consuming
as part of the nonnal nasopharyngeal
part of the exan1ination. The abdomen
bacterial flora. Rodents of the same species
can be palpated for consistency and the
should be housed in such a way to protect
presence of unusual masses. Animals
vulnerable animals from more aggressive
should not be squeezed too vigorously,
members of their group. This includes
because overzealous palpation can result
separating young animals from older ones.

in visceral rupture. The anogenital region

Female rodents are generally compatible
should be exan1ined for discharges and
when housed in the same cage, unless one
staining of tl1e fur or skin. When a rodent
female has lived much of its life alone. Male
is picked up, it generally urinates and
rats are generally compatible, especially if
defecates. A dipstick should be ready to
raised together. However, owners should
perform an in1.rnediate urinalysis; feces can
never house strange male rats in the same
be caught in a small tube and exan1ined
cage together because they will fight. Male
later. The limbs should be palpated for
mice generally fight if housed together,
tenderness or fractures, with special
unless they are litte1mates raised together
attention given to the paws, noting the
without females present. Male mice are best lengtl1 of the nails and condition of the housed singly or with female mice.

footpads.

Rats are social animals, and grooming is

Respirations and heart rate in mice and
a socially affiliative behavior. Singly housed
rats are rapid and, therefore, difficult to
rats may develop isolated-rat stress
measure. Instead, signs of dyspnea should
syndrome if left alone without hun1an
be noted. Some respiratory infections, such

2028

RODENTS
as mycoplasmosis, are clinically silent.

mg/kg) and doxycycline (5-10 mg/kg) given

These diseases can be better heard than
orally bid for 14 days often alleviates severe
seen; abnormal sounds called "snuffling" in clinical signs. Additional treatments such as
rats and "chattering" in mice are noticeable daily nebulization therapy with 7% hyperwithout a stethoscope.

tonic saline to break down the mucus

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biofilrn in respiratory passages, broncho

Infectious Diseases
dilators (theophylline 10 mg/kg, bid) to
improve airway patency, and reducing

Bacterial Infections: Rats are the natural
ammonia levels in cages by daily removal
host of the bacte1ium Streptobacillus
of bedding and use of clean paper will
monilif01mis. It is a commensal organism
ameliorate the disease. Chronic low dose
of the nasopharyngeal flora and does not
doxycycline (5-10 mg/kg/day, PO) helps to
cause disease in rats. However, individuals
prevent acute relapses. The doxycycline
bitten by rats may become infected with
is both bactericidal for mycoplasma

S moniliformis and develop rat bite fever, a organisms and has a marked immunopotentially fatal disease (seep 2418). Mice modulatory effect on the chronic airway
housed with rats will become infected
inflarnmation.

with S moniliformis and develop fatal

The most important aspect of CRD for
septicemia characterized by polyarthritis,
clinicians is that respiratory mycoplasmosis
cervical lymphadenitis, pneun10nia, and
varies greatly in disease expression because
splenomegaly.

of environmental, host, and organism

Respiratory disease caused by infectious
factors tl1at influence the host-pathogen
agents is the most common health problem
relationship. Examples of such factors
in rats. Three major respiratory pathogens
include intracage ammonia levels;
cause overt clinical disease: Mycoplasma
concurrent Sendai virus, coronavirus
pulmonis, Streptococcus pneumoniae,

(sialodacryoadenitis vims), pneun10nia
and Corynebacterium kutscheri. Other
virus of mice, rat respiratory vims, and/or
organisms such as Sendai virus ( a para

CAR bacillus infection; the genetic
myxovirus ), pneumonia vims of mice (a
susceptibility of the host; the virulence of
paramyxovirns), rat respiratory vims (a
the Mycoplasma strain; and vitamin A or E
hantavirus), cilia-associated respiratory
deficiency. Although CRD is rarely seen in

(CAR) bacillus, andHaemophilus species
laboratmy rats, most pet rats have CRD to
are minor respiratory pathogens that rarely
some degree. One survey of pet ratteries in
cause overt clinical disease by themselves.

the northwest USA showed vi.ttually all

However, the minor respiratmy pathogens

(95%) were positive for CAR-bacillus and M
interact synergistically as copathogens with
pulmonis, and approxin1ately half were
the major respiratory pathogens to produce
positive for other viral respiratory agents.

two major clinical syndromes: "chronic

Bacterial pneumonia is nearly always
respiratory disease (CRD) and bacterial
caused by S pneumoniae, but seldom in the
pneumonia.

absence of some combination involving M

CRD is the best-understood multifactorial pulmonis, Sendai virus, or CAR bacillus.

respiratory infection in rats. M pulmoni s is Infection with C kutscheri also results in
the major component of CRD, and the
pneumonia but only in cortjunction with
disease is also !mown as murine respiratory
debilitation or inununosuppression. In pet
mycoplasmosis. Rats with CRD rarely live
rats, in1mtmosuppression can result from

>2 yr. Clinical signs are highly variable.

diabetes, neoplasia, or dietary deficiencies.

Initial infection commonly occurs without

C kutscheri pneun10nia is rare in pet rats.

any clinical signs; early signs involve both

Pneun1onia caused by S pneumoniae can
the upper and lower respiratory tracts and
be of sudden onset. Young rats are more
may include snuffling, nasal discharge,
severely affected t11an older ones, and often
polypnea, weight loss, hunched posture,
tl1e only sign tl1ey exhibit is sudden death.

ruffled coat, head tilt, and red tears.

Mature rats may demonstrate dyspnea,

Dyspnea, the primary presenting complaint,
snuffling, and abdominal breathing. A
is caused by ciliostasis, subsequent buildup
purulent exudate may be seen around the
of lysozyme-rich inflanunatory exudate in
nares and on the front paws from wiping of
airways, bronchiectasis, and bronchiolectathe nostJils. A tentative diagnosis is based sis from inflanunatory damage to bronchion identification of nwnerous gram-positive olar membranes. Chronic disease often
diplococci on a Gram stain of the exudate
includes middle ear infection ( via the
or in a san1ple submitted for cytologic
eustachian tube). Antibiotic therapy may
exanlination. Severe bacteremia is an
alleviate clinical signs but does not
important consequence of advanced disease
eliminate the infection. Enrofloxacin (10
and results in multiorga.n abscesses and

RODENTS

2029
infarction. Treatment is amoxicillin/
lesions such as conjunctivitis, keratitis,
clavulanic acid (13.75 mg/kg, PO, bid) or
corneal ulcers, synechia, and hyphema can
f3-lactamase-resistant penicillins such as
develop secondary to lacrimal dysfunccloxacillin, oxacillin, and dicloxacillin, tion. The eye lesions usually resolve but
which can all be administered orally or
occasionally progress to chronic keratitis

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parenterally.

and megaglobus.

Ulcerative dern1atitis caused by

Staphylococcus aureus infection results
from self-tratm1a associated with fur mite

Parasitic Infections:

infestation or, more commonly, from

Protozoa: Endoparasites are relatively
scratching of the skin over an inflamed
common in mice. However, only two
salivary gland. Rats have a remarkable
parasites regularly encountered in the digesability to resist infection with S aureus.

tive tract, the protozoan parasites Spironu

Treatment consists of clipping the toenails
cleus muris and Giai·dia muris, are of the hind paws, cleaning the ulcerated
considered patl1ogenic, even though they
skin, and applying a topical antibiotic.

are not associated witl1 clinical signs in

Systemic treatment is rarely necessary.

imrnw1ocompetent hosts. Diagnosis is

The two most common causes of clinical
based on demonstration of characteristic
respiratory disease in mice are Sendai virus
trophozoites in wet mow1ts of fresh
and M pulnionis infection. Sendai virus is
intestinal contents or feces. Treatment is
associated with an acute respiratory
metronidazole (10-40 mg/kg/day, PO, or
infection in which mice display chattering

0.04o/o--O. l % drinking water solution for 14
and mild respiratory distress. Neonates and
days), but it does not completely elinlinate
weanlings may die. Adults generally recover
the infection.

within 2 mo. When the disease expression
exceeds this pattern, the cause is most

Nematodes: Pinwonns are ubiquitous
likely conctuTent mycoplasmal infection.

and considered nonpathogenic in mice. Two

M pulmonis is the cause of chronic
are commonly encountered: Syphacia
pnemnonia, suppurative rhinitis, and
obvelata and Aspicularis letrnplera. Often, occasionally otitis media. Chatte1ing and
the only indication of pinworm infestation is
dyspnea are caused by accwnulations of
rectal prolapse due to straining. To establish
purulent exudate in inflamed and thickened
a diagnosis of S obvela.la infestation, a clear nasal passages. Survivors often develop
cellophane tape impression of the perianal
chronic bronchopneLU11onia, bronchiectaskin can be made. Adults obvelata females sis, and pulmonary abscesses. Antibiotic
deposit ova around tl1e anus. A letraptera
therapy may alleviate clinical signs but does
does not deposit its ova in tllis area, and fecal
not eliminate the infection.

smear or flotation is required to confirm a
diagnosis. Ivem1ectin (2 mg/kg, PO, given

Viral Infections: Viral diseases of mice
twice at a 10-day interval) elinlinates
and rats are common. However, most
pinwonns from nlice. The recommended
diseases are subclinical and important only
label dosage for nlice with ectoparasites
in laboratory animals in which they have the (0.2 mg/kg, given twice at a 10-day interval) potential to have a significant effect on
does not eliminate pinworms.

research.

Mites: Most infectious causes of alopecia

Sialodacryoadenitis virus, a coronavirus, and dennatitis in mice are associated with causes inflan1mation and edema of the
fur nlites. Generalized thinning of the hair,
cervical salivary glands in rats. Owners of
especially on difficult-to-groom areas such
infected rats often describe their pets as
as the head and trunk, is seen. The coat
having mLU11ps. Sialodacryoadenitis virus
often has a greasy appearance and, in cases
infection is highly contagious. It initially
of heavy infestation, noticeable pruritus and
causes rhinitis followed by epithelial
self-inflicted dennal ulceration may occur.

necrosis and inflammatory swelling of the

Three mites are commonly seen: Myobia
salivary and lacrimal glands. Cervical
musculi, Myocoples musculinus, and
lymph nodes also become enlarged. There

Radfordia affinis. M muscitli is tl1e most
is no treatment for this disease. Glandular
clinically significant mouse mite. Infestahealing follows within 7-10 days, and tions are usually caused by more than one
clinical signs subside within 30 days, with
species. Mites are spread by direct contact
minimal residual lesions remaining. During with infected mice or infested bedding.

acute inflammation, affected rats are at

Diagnosis is based on identification of adult
high risk of anesthesia-related mortality
mites, nymphs, or eggs on hair shafts with
because of the decreased diameter of the
the use of a hand lens or stereoscopic
upper respiratory tract ILU11en. Ocular
microscope. Adults and nymphs appear

2030

RODENTS
pearly whlte and elongate; eggs are oval and
have a scurfy appearance, with patchy
can be seen attached to the base of hairs or
areas of alopecia and va.iiable degrees of
inside mature females. Mite infestations are
erythema and crusting. Pruritus is usually
treated with ivermcctin (0.2 mg/kg, SC or
minimal to absent, and the lesions do not

PO, twice at 10-day intervals). Alternatively,
fluoresce under a Wood's la.inp. T menta
a few drops of ivem1ectin solution ( diluted
grophytes can be isolated from the fur of

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to 1:100 in equal parts of water and
clinically nom1al mice but is rare in rats.

propylene glycol for tlrree treatments) can
be placed on the mouse's head to allow
spread by grooming and ingestion.

Neoplasia

Ectoparasitic infestation is less common

The most common subcutaneous tumor
in rats than in mice. Occasionally, the fur
in rats is fibroadenoma of the manm1ary
mite Radfordia ensifera is seen. Although
glands. The distribution of the manunary

R ensifera infestation produces few ill
tissue is extensive, and the tumors can
effects, heavy infestation may lead to
develop anywhere from the neck to inguinal
self-trauma and ulcerative dennatitis.

region. Tumors can reach 8-10 cm in

Ornithonyssus bacoti, the tropical rat
dia.ineter and are seen in both males a.i1d
mite or red mite, is a bloodsucking parasitic
females. The surgical technique for twnor
mite prin1arily found in wild rats such as the
removal is straightforward, and survival
brown rat (Rattus noruegicus) or the black
after mastectomy has been reported to be
roof rat (Rattus rattus ). It has a wide host good if the tun10r is benign. The prevalence
range and occasionally infects pet han1Sters, of manunary tumors, as well as that of gerbils, rats, and mice living in very old
pituitary tumors, is significantly lower in
buildings or when building construction or
ovariectomized rats than in sexually intact
renovations disturb colonies of wild rodents rats. However, tl1e recurrence of fibroadthat had been on the premises and acting as enomas is common in W1involved ma.imna.i'Y
hosts. 0 bacol'i can survive for long periods tissue, and often several surge1ies are
in the environment and travel considerable
needed.

distances in search of new hosts. lf it does

In contrast, man1m3.!'Y tun10rs in mice are
not find a suitable rodent host, it will feed on nearly always malignant a.i1d often a.i·e not people. Its common nan1e is a misnomer,
amenable to surgical removal. The most
because it is found worldwide in tropical
common spontaneous tun1ors associated
and temperate climates. Mites appear whlte
with the skin are ma.i11ma.i'Y adenocarcinobefore feeding and become red-brown after mas, followed by fibrosarcomas. The
engorgement. Heavy infestations on pet
incidence of mamrna.i'Y tun1ors varies
rodents resemble fine sawdust within the
according to the mouse strain and the
fur. 0 bacoti typically does not cause
presence or absence of mouse ma.I11mary
clinical signs in pet rodents, but heavy
tumor viruses; the incidence is as high as
infestations cause anemia, debility, weakness, 700,6 in some strains. In wild and outbred pruritus, and death in small rodents. As well
ntice, the incidence of fibrosarcomas is
as causing discomfort, the mite is a vector
lo/o--6%.

for the rodent filarial nematode Litomo

Subcutaneous twnors are nearly always
soides carinii and a potential vector of
malignant and often have ulcerated by the
several human pathogens. Most infestations
time a diagnosis is made. Tumors can be
occur in late spring or early sU111mer when
treated by surgical excision, but the chance
fledglings are leaving the nest and the mites
of recwTence is hlgh and tl1e prognosis is
are searchlng for another food source.

poor.

Infestation of O bacoti is eliminated by a
combination of bathing and treating the
host anin1al with selamectin ( 15 mg/kg, one

Miscellaneous and Iatrogenic
topical treatment), elin1ination of commen

Disorders
sal rodent reservoirs, and insecticide

Dental Overgrowth: Dental problems
treatment of the pet's cage (pennetlrrinare cmmnonly seen in pet ntice and rats impregnated cotton balls 7.4% placed inside
because of their continually erupting
the cage weekly for 6 wk) and environment
teeth. Overgrown incisors are seen most

(fipronil spray or synthetic pyretlrroids).

frequently in rats and ntice, in contrast with
molar occlusion seen in guinea pigs and

Fungal Infections: Dem1atophytosis
chlnchlllas. Overgrowth is easily treated
is uncommon in pet mice and rats. It is
witl1 a high-speed drill that cuts through the
caused by Trichophyton mentagrophytes.

overgrown incisors without splitting or

Lesions, when present, are most common
splintering them, leaving a clean, smooth
on the face, head, neck, and tail. The lesions
surface. Cutting the teeth with rongeurs

RODENTS

2031
does not produce good longterm results,

There are no other lesions, and only one
and problems may arise. The incisor may
mouse, the dominant individual, retains all
fracture longitudinally; the fracture may
of its fur. Removal of the dominant mouse
reach the apex and cause the animal
stops barbering; frequently, however,
discomfort. Bacteria can enter the fractured
another mouse assw11es the dominant role.

tooth, track down to the apex, and cause an

Barbering is often seen in female mice

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apical abscess. Extraction of the incisors is
caged together. Male mice, except
an alternative to trimming; however, this
littennates raised together from bilth, are
procedure is difficult because of the
more likely to fight, often ve1y savagely, and
incisors' long roots.

inflict severe bite wounds on one another,
especially over the rump, tail, and shoul

Age-related Disorders: Chronic
ders.

progressive nephrosis is a common

Mechanical abrasion resulting from
age-related disease in rats. The kidneys are
self-trawna on cage equipment is a form of
enlarged, pale, and have a pitted, mottled
husbandry-related alopecia. Small patches
surface that often contains pinpoint cysts.

of alopecia appear on the lateral surfaces

Lesions consist of a progressive glomeruloof the muzzle. They result from chafing on sclerosis and widespread tubulointerstitial
metal feeders, poorly constructed watering
disease, primaiily involving the proxin1al
device openings, and metal cage tops.

convoluted tubule. Proteinuria often is> 10

Unlike barbering, dem1atitis may also be
mg/day. The disease occurs earlier and is of
associated with alopecia. Treatment
greater severity in males than in females.

consists of replacing the poorly constructed

Dietary factors appear to have an inlportant
equipment with nonabrading equipment.

role in the progression of renal disease.

Individually housed mice can display

Caloric restriction, the feeding of low-proaberrant stereotypic behavior such as tein diets ( 4%-7%), and limiting the source
polydipsia and bai· chewing that results in
of dietary protein reduce the incidence and
mechanical abrasion and alopecia. In these
severity of the disease. Treatment is
cases with one mouse, replacing the cage
supportive and involves feeding a lowequipment does not help. Instead, protein diet.

environmental enrichment toys such as

Avascular necrosis of the tail, or ringtail,
running wheels or hollow tubes should be
is seen primarily in young rats, and
provided. Nursing mice often have ventral
occasionally in young mice, kept in
abdominal and thoracic alopecia; this is
low-humidity environments. If ringtail is
nom1al and is nearly always associated with
diagnosed, treatment involves at11putation
the extensive distribution of mammaiy
of the tail below the necrotic annular
glands.

constriction.

Sometil11es a pet mouse presents with
clinical signs of mite infestation but no

Skin Disease in Mice: Most of the
evidence of 1nites or known history of
diseases seen in pet mice are associated
recent exposure to other aninlals. Biopsy
with the skin and represent >25% of all
sat11ples may be useful in these cases to
cases. Behavioral disorders, husbandrydistinguish active acariasis from dermal related problems, micro biologic/parasitic
hypersensitivity to mites or other allergens
infections, and idiopathic skin diseases are
such as tilnber chip bedding. Dem1al
seen. Behavioral, husbandry-related, and
hypersensitivity is well desc1ibed in certain
infectious causes of skin disease ai·e
inbred strains of mice and is characterized
relatively straightforward to diagnose
by severe pruritus, the presence of fine
and treat. However, many skin diseases
dandruff all over the body, and occasionally
characterized by chronic or ulcerated skin
ulcerative dermatitis.

( often secondarily colonized by bacteria)

Idiopathic skin disease is characterized
are diagnosed as idiopathic. This group is
by ulcerative dermatitis with pruritus in
commonly unresponsive to treatment,
mice that are negative for prin1aiy
topical or systemic, and affected mice are
ectoparasitic, bacterial, or mycotic
often euthanized.

infections. Histopathologic examination

Barbering and fighting are manifestations
and inununofluorescent microscopy of
of social dominance, a fonn of behavior
selected inbred strains of mice have
relating to the social rank and dominance
revealed an underlying vasculitis attributed
status of an individual mouse in a group.

to immune complex deposition on dermal

Barbering is a unique condition seen in
vessels. Dietary factors and dysregulated
group-housed mice in which the dominant
fatty acid metabolism have been inlplicated
mouse nibbles off the whiskers and hair
in the development of the ulcerative
around the muzzle and eyes of cagemates.

dem1atitis in these mice. This common

2032

RODENTS
disease of mice of a C57BL6 background is

The nonspecific initial presentation
caused by an underlying inun une-mediated
combined with difficulties in culturing
vasculitis, and the severity appears to be

Streptococcus moniliformis produce a
modulated by dietary fat and vitamin E
significant risk of delay or failure in
content. Topical treatment twice daily with
diagnosis. Rats are not reconunended as

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0.2% cyclosporine in 2% lidocaine gel
pets for children. Adults with pet;rats
supplemented with gentamicin at 50 mcg/mL
should practice regular hand washing and
results in either complete heafu1g or nearavoid hand-to-mouth contact when handling complete healing of the ulcerated skin,
rats or cleaning rat cages.

regardless of the size of the skin ulceration.

There are sporadic but persistent reports

Skin swellings in mice are usually tumors
of cases of Oniithonyssus bacoti
or abscesses. Needle biopsy often reveals
dermatitis from pet rodents that manifests
the nature of the contents and allows
as an erythematous papular rash. It often
diagnosis. Three opportmlistic pathogens,
excoriates because of intense pruritus.

Staphylococcus aureus, Pasteurella

Occasionally, vesicles, wi:icarial plaques,
pneumotropica, and Streptococcus
diffuse erythema, or hemorrhage are seen.

pyogenes, are isolated frequently and can

Affected areas of the skin are those usually
cause abscesses in other organs. Antibiotic
covered by clothing (such as arms and
therapy with penicillins or cephalosporins,
tnmk), with the face and webs of fingers
concurrent with drainage and debridement
usually spared. There is considerable
of the abscess, is effective.

evidence that O bacoti carry and have
the potential to transmit several human

Chromodacryorrhea in Rats: The
pathogens. Experiments have shown that

Harde1ian glands of rats are located behind

O bacoti transmits Rickettsia akari
the eyes and secrete porphyrins that are

(rickettsialpox), Yersinia pestis (plague),
increased in response to stress and disease,

Coxsackie virus, Francisella tularensis
coloring t11e tea.rs red. When porphyrin

(tularemia), and Trypanosoma cruzi
eruiched tear fluid d1ies around the eyes

(Chagas' disease). Researchers have also
and external nares, it resembles crusts of
documented O bacoti specimens with
blood. Owners often describe their rats as

Coxiella burnetii (Q fever), hantavirus,
hemorrhaging from the eyes and nose. The

Bon·elia spp (Lyme disease), Bartonella porphyrins can be readily differentiated
spp, and Rickettsia spp.

from blood witl1 a Wood's lan1p, because

Mice are inapparent carriers of dennatothey fluoresce under ultraviolet light.

phytes, and pet mice are a zoonotic risk for

Although chromodacryorrhea is not
their owners, especially children.

pathologic, it is a consequence of acuteonset stress such as that caused by pain, illness, or restraint. It usually indicates a

MICE AND RATS AS LABORATORY
chronic tmderlying disease.

ANIMALS

Rodents used for research arc maintained in

Zoonotic Risk
tightly controlled environments designed to

As rats have become popular as pets,
reduce tl1e impact of unwanted variables in
children now account for >50% of the cases
animal experiments. Many factors have the
of rat bite fever (RBF) in the USA; 14% of
potential to influence the rodent's biologic

RBF cases in children involved exposm·e
response in a laboratory test. Besides a
to a rat at school. RBF manifests as a
description of the experiment, research
bacteremia and septicemia characterized by journals often require a description of the fever, chills, myalgia, arthralgia, headache,
research rodent's source, nlicrobiologic
and vomiting. A petechial rash develops
status, and environment ( eg, feed, water,
over the extrenlities, in particular the palms
temperature, humidity, light exposure) in
and soles, but sometimes is present all over
the materials and methods section.

the body. The incubation period is 3-10 days Environmental conditions, husbandry (average 5 days). Wants and children may
procedures, and animals must be similar
experience severe diarrhea resulting in
if research data generated from one
weight loss. Mortality occurs in 7%-13%
laboratory is to be judged based on
of untreated patients. After infection, a
reproducibility and thus validation. If
polyarthritis develops in 50o/o-70% of
variables such as feed, housing, rodent
patients. Prognosis is good with treatment
genetic background and disease-free or
with parenteral penicillin early in the
microbiologic status are not properly
disease. Fatalities are associated witl1 late
controlled, then experin1ental results can be
reporting or late recognition of the disease.

of limited use or even worthless. Although

RODENTS

2033
complete elimination of vaiiables in animal
gem1-free environment and foster care. This
experiments is not possible, many factors
procedure was successful in eliminating
that contribute to variation cai1 be signifimany patliogens not transmissible in utero, cantly reduced or eliminated. One of tlie
eg, endoparasites, most bacteria, and some
most important variables is tlie effect of
viruses. The third period (1980-present)

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infectious agents on reseai·ch mice and rats.

has been one of eradicating indigenous

Few infectious agents found in laboratory rodent viruses. The reduction in known mice and rats today cause overt, clinical
viruses infecting rodents was accomplished
disease. Distinguishing between infection
tlu·ough serologic testing of animals for
and disease is critical to interpreting tlie
antibodies to specific pathogens. A.ntibodymicro biologic status of laboratory animals.

positive colonies were subsequently

Infection indicates the presence of
eliminated or cesarean-rederived.

microorgaiiisms, which may be patliogens,

Most modem reseai·ch animal facilities
opportunists, or commensals, of wliich the
incorporate some fom1 of health monitoring
last two are most numerous. Clinical
into tlieir animal care progran1 ( see TABLE 32).

disease does not need to be present for

Since the 1980s, it has been based on
microorgaiiisms to affect research. Animals
serology, although moleculai· metliods of
tliat appear normal and healtliy may be
detection ( eg, PCR) are rapidly increasing in
unsuitable as research subjects because of
use. The laboratories tliat perforrn serologic
the unobservable but significant local or
assays primarily test groups of reseai·ch
systemic effects of viruses, bacteria, and
rodents or tlieir sainples. The well-being of
parasites witli which tliey may be infected.

tlie animal colony is more important thai1

Knowledge of the varied and unwanted
the well-being of an individual animal, and
effects of natural patliogens in laboratory
laboratory animal medicine is effectively a
rodents has steadily increased over the past
type of "herd medicine." Although healtl1

130 yeai"S of conducting animal research.

monitoring is costly, it results in significant

The historic struggle against patliogens of
longtem1 savings, because researchers can
laboratory rodents is often divided into
use fewer animals and the animals' daily
three periods. The first (1880-1950) was
care is not as labor intensive. Health
when mice and rats becaine common
monitoring allows laborat01y animal
research animals. Many of these original
veterinariatlS to check tl1e health stat1.1s of a
stocks hai·bored a variety of natural, or
colony, inf01m researchers of their animals'

indigenous, patliogens. During tliis period,
patliogen status, prevent enb.y of patliogens
improvements were made in saiiitation,
into tlie facility by screening animals
nub.ition, environmental control, and oilier
received from unknown sources, and
aspects of animal husbandry. The result was promptly deal witli tlie presence of a great reduction in the range and prevaunexpected infectious agents in rodents.

lence of patliogens found in laboratory

Undetected infection makes laboratory
rodents. The second period (1950-1980)

aiiimals unfit for research and renders
was one of gnotobiotic derivation, when
experimental data unreliable. It is more
cesarean rederivation was used to replace
cost-effective to prevent enb.y of infec-
infected stock with uninfected offspring.

tious agents into a facility or to detect and

Full-term fetuses were removed from an
eliminate tliem early than to discard months
infected motlier and transferred to a
of research data.

INFECTIOUS AGENTS COMMONLY TESTED FOR IN LABORATORY

RODENTS

Test

Agent

Description

Species

PROTOZOA

E cun

Encephalilozoon cuniculi A sporozoan parasite of Mice, rats
rabbits and rodents

BACTERIA

C pil

Clostridium pilif01me

Agent ofTyzzer disease

Mice, rats

2034

RODENTS

INFECTIOUS AGENTS COMMONLY TESTED FOR IN LABORATORY

RODENTS (continued)

Test

Agent

Description

Species

CARB

Cilia-associated-

A bacterial respiratory ,

Mice, rats

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respiratory bacillus
pathogen of rodents and
rabbits

M pul

Mycoplasma pulmonis

Agent of mouse and rat

Mice, rats
pulmonary mycoplasmosis

VIRUSES

ECT

Ectromelia

A mouse poxvirus

Mice

TH-1

Toolan's H-1 virus

A rat parvovirus

Rats

Hantaan virus

A zoonotic hantavirus of rats; Rats
several types (HPS, NED)

exist throughout world

K -virus

Mouse pneumonitis virus

A mouse papovavirus

Mice

KRV

Kilham rat virus

A rat parvovirns

Rats

LCM

Lymphocytic choriomeni.n-

A zoonotic arenavirus

Mice, rats
gitis virus

LDEV

Lactate dehydrogenase-

A mouse arterivirus

Mice
elevating virus

MADI (FL)

Rodent adenovirus strain 1 Mouse adenovirus, rodent Mice, rats
adenovirus strain 1 (FL)

MAD2(K87) Rodent adenovirus strain 2 Mouse adenovirus, rodent Mice
adenovirus strain 2 (K87)

MCMV

Mouse cytomegalovirus

A mouse herpesvirus

Mice

MHV

Mouse hepatitis virus

A mouse coronavirus

Mice

MNV

MuriJ1e norovirus

A mouse calicivirus

Mice

MPV

Mouse parvovirus

A mouse parvovirus

Mice

MTV

Mouse thymic virus

A mouse herpesvirus

Mice

MVM(MMV) Minute virus of mice

A mouse parvovirus

Mice

PolyVM

Polyoma virus of mice

A mouse papovavirus

Mice

PVM

Pneumonia virus of mice

A rodent pneumovirus

Mice, rats

SDAV

Sialodacryoadenitis virus

A rat coronavirus

Rats

Reo3

Reovirus type 3

A rodent reovirus

Mice, rats

SenV

Sendai. virus

A type 1 paran1yxovirns

Mice,rats

RTV

Rat theilovitus

A rat picomavirus

Rats

TMEV

Theiler murine encephalo-

Mouse poliovirus, strain

Mice

(GDVII)

myelitis virus

GDVII

SUGAR GLIDERS

2035

SUGAR GLIDERS

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Sugar gliders (Petawus breviceps) are
on the frontal and sternal glands of postsmall, nocturnal marsupials native to pubescent males. These glands give both

Australia, Indonesia, and New Guinea that
sexes a musky odor.

live in eucalyptus and acacia forests. They

Sugar gliders have large, protmding,
belong to the family Petauridae, which
widely spaced eyes, giving them a wide
includes the wrist-winged gliders. Gliders
field of vision, especially at night. Their
in this family possess a gliding membrane
ears move independently and are highly

(patagiwn) that mns from the wrist of the
sensitive to sound. They also have a great
forelimb to the ankle of the hindlimb and
sense of smell to locate food, sense predathat allows them to glide as far as 50 m and tors, and recognize both their tenitory and
forage for food using less energy. They use
their colony-mates. Wild gliders have gray
their tails as stabilizing rudders that enable
fw- and a central black stripe dorsally on
them to change direction easily. The second
their heads; domesticated gliders may look
and third toes on their hindfeet are fused to
sinlilar to the wild type but also come in
form a "grooming comb" that helps them
several color variations. Sugar gliders are
clean their fur. Females are seasonally
polygamous, territorial, and live in colonies
polyestrous and have a double vagina, two
of 5 to 12 individuals with a donlinant male.

uteri, and a pouch containing four teats;

They sleep in tree hollows by day and
they often have twin births. After 16 days of
between foraging trips at night. They tolergestation, the young Uoeys), each weighing ate a wide range of environmental temponly 0.2 g, migrate to the pouch to develop eratw-es and go into torpor to conserve
further and finally leave the pouch after
energy in very cold conditions. Sugar gliders

70-7 4 days. They remain in the nest until
are omnivorous and feed on sugar-1ich plant

110-120 days of age, when they are weaned.

and insect exudates ( sap, gw-n, nectar, manna,

They stay with the colony until 7-10 mo old.

pollen) and invertebrates as a source of

Males have a forked pettis (to match the
protein. They a.re hindgut fermenters and
female's double vagina) and a pendulous
possess a well-developed cecum that
scrotun1 containing two testicles. Males do
utilizes bacterial fermentation to break
not urinate from the forked end of the penis
down complex polysaccha.tides contained
but from the proximal end. Both males and
in gwn. See also TABLE 33, which sw11ma.tizes females have paracloacal scent glands
important biologic a.i1d physiologic data
acljacent to the vent (the cloaca! opening or
for suga.i· gliders.

common opening of urinary, reproductive,
and GI tracts) with which they mark
territory and each other, and males also

Physical Examination: For a full clinical
have frontal scent glands on their foreheads
exanlination, anesthesia with isoflurane via
and glands on their throats and chests.

face mask may be required if gliders are

Sparse fur and an oily discharge are nonnal
very stressed or biting. More docile animals
may be exan1ined while wrapped in a small
towel and cupped in the palm of the hand.

Gliders inside fabric bags or pouches may
be pa.tiially exposed, one body pa.it at a
tin1e, for exa.nlina.tion. Because gliders are
nocturnal, it may be best to schedule
clinical exan1inations earlier in the day
when they are less active. If possible, the
animal should be first observed moving in
its cage to assess posture, coordination, and
demeanor. If the glider is anesthetized,
cloa.cal temperature, hea.it rate, and
respiration rate can be recorded, and the
heart and lungs assessed with a pediatric
stethoscope. The fur and skin should be
exa.t11ined for ectoparasites, tra.wna.tic
irtjury, fur loss, and degree of hydration;

Forked penis of a male sugar glider. Courtesy of the oral cavity for broken teeth, dental

Dr. Laurie Hess.

abscesses, or tartar build up; and the eyes

2036

SUGAR GLIDERS
ittN•ii SELECTED PHYSIOLOGIC DATA FOR SUGAR GLIDERS

Life span

9-12 yr

Adult male body wt

100-160 g

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Adult female body wt

80-135 g

Respiratory rate

16-40/min

Heart rate

200-300 bpm

Body temperature

97.3°F (36.3°C)

Thermoneutral zone

80° -88°F (27° -31 °C)

Food consumption

15%-20% body wt/day

Dentition

Diprotodont

Dental fommla

2(13/1-2 C 1/0 P 3/3 M4/4)

Puberty

8-12 mo in females, 12-15 mo in males

Estrous cycle

29 days

Gestation period

15-17 days

Litter size

2 (81%)

Birth weight

0.2 g

Pouch emergence

70-74 days

Weaning

110-120 days
and ears for any abnormalities. The cloaca!

Blood Collection, Hematology, and
area should be examined, and the penis

Biochemistry: Reference ranges for sugar
of males extruded. The abdomen should
gliders are presented in TABLE 34. Chemical
be palpated, and the pouch in females examrestraint, essential to allow blood collecined. Major joints should also be palpated, tion, is most safely achieved with isoflurane/
and digits and toenails checked for evidence oxygen administered via mask and T -piece.

of trauma.

To assist in making clinical diagnoses, blood
samples may be obtained from the cranial

Diagnostic and Treatment Techniques:

vena cava, jugular vein, medial tibial artery,

If animals are dehydrated, isotonic fluids up
or lateral tail vein. Blood volumes of up to
to l()OA, of body wt can be administered SC

1 % of body wt can be collected; typically
over the shoulder region. Care should be

0.5-1 mL is obtained. To access the cranial
taken not to induce edema to the patagium.

vena cava, a 27- or 25-gauge needle on an

Fluids also may be administered intraosseinsulin syringe may be inserted in the .

ously in the proximal femur or tibia. SC
thoracic inlet just lateral to the manubriurn,
injections may be given in the same area
with the needle directed at a 30° angle from
that SC fluids are administered. IM
midline toward the opposite hindleg. The
injections may be given in the epaxial
vena cava is not visualized directly during
muscles of the neck and dorsal thorax. IV
venipuncture but is accessed blindly using
injections are very difficult to perform but
the manubriurn as a palpable landmark. The
may be accomplished in cephalic or lateral
jugular vein can be visualized if the hair is
saphenous veins in an anesthetized glider.

clipped and the vein is forced to fill by apply

Radiographs generally require the glider
ing gentle digital pressure at the thoracic
be anesthetized for proper positioning.

inlet; it sits midway between the point of the

Pulmonary diseases are easiest to detect
shoulder and the mandibular ramus. The
with radiographs. Feces may be easily
needle can be bent at its base to facilitate
san1pled and checked annually with a fecal
venipuncture at this site. The medial tibial
float and direct smear for parasites; aninlals
artery, which runs very superficially just
with diarrhea should have their feces
distal and medial to the stifle joint, is easier
cultured and tested for appropriate
to access and can be sampled with a 27-or
antibiotic sensitivity.

25-gauge neeclle and 0.5-1 mL syringe.

SUGAR GLIDERS

2037

Pressure after sampling is required to prevent Gliders ideally should be fasted for at least hematoma fom1ation. The size of the lateral

4 hr preoperatively. Preoperative analgesics,
tail vein is most suited to skin prick and
sedatives to reduce preoperative stress, and
droplet collection into capillary tubes.

local and gas anesthetics all may be used.

Small blood samples (0.25 mL) may also

Care must be taken to keep gliders warm

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be obtained from the cephalic, lateral sapheduring surgery to ensure rapid recovery.

nous, femoral, and ventral coccygeal veins

Gliders undergoing surgeries that last> l hr
with a 27-gauge needle on an insulin syringe. or that require intra-abdominal access should be administered fluids intraosse

Anesthesia and Surgery: Anesthesia
ously (in the femur or tibia) throughout
in sugar gliders should be approached the
the procedure if IV access is impossible
san1e way it is in other small mammals.

because of small size. Shorter, sin1ple

SELECTED HEMATOLOGIC AND SERUM BIOCHEMICAL VALUES

FOR SUGAR GLIDERS

Conventional

(USA)Units

SI Units

HEMATOLOGY

Hemoglobin

13-15 g/dL

130-150 g/L

Hematocrit

45%-53%

0.45-0.53 UL

RB Cs

5.1-7.2 x lOG/µL

5.1-7.2 x 1012 /L

Mean corpuscular Hgb concentration

30-33 g/dL

300-330 g/L

Mean corpuscular Hgb

18.2-20.6 pg

18.2-20.6 pg

WBCs

5-12.2 x 103/µL

5-12.2 x 109/L

Neutrophils

1.5-3 x 103/µL

1.5-3 x lQ9fL

Lymphocytes

2.8-9.2 x 103/µL

2.8-9.2 x 109/L

Monocytes

0.06--0.2 x 103/µL

0.06--0.2 x 109/L

Eosinophils

0.02-0.14 x 103/µL

0.02-0.14 x 109/L

Basophils

0

0

Plasma proteins

5.6--6.9 g/dL

56-69 g/L

Albumin

3-3.5 g/dL

30-35 g/L

Globulin

2.2-3.6 g/dL

22-36 g/L

BIOCHEMISTRY

ALT

50-106 U/L

50-106 U/L

AST

46-179U/L

46-179U/L

Calcium

6.9-8.4 mg/dL

1. 7-2. l mmol/L

CK

210-589U/L

210-589U/L

Creatinine

0.2-0.5 mg/dL

17. 7-44.2 µmol/L

Glucose

130-183 mg/dL

7.2-10 mmol/L

Phosphorus

3.8-4.4 mg/dL

1.2-1.4 mmol/L

Potassium

3.3-5.9 mEq/L

3.3-5.9 mmol/L

Sodium

135-145 mEq/L

135-145 mmol/L

Urea

18-24 mg/dL

6.4-8.6 mmol/L

2038

SUGAR GLIDERS
procedures may necessitate only SC fluids,
ligated, as is the ute1us proxin1ally to the

Conunonly used preanesthetics include
lateral vaginal canals. After resection of
atropine or glycopyrrolate, midazolam, and
both ovaries and ute1i, the linea is closed,
either butorphanol or buprenorphine. Local
and the skin is sutured subcuticularly and
anesthetic injections of a 50:50 mixture of
closed with skin glue. Distal penile

2% lidocaine with 5% bupivicaine may be
amputation is another conunon surgery.

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used to infiltrate the incision site to help

Sexually frustrated males may self-mutilate
reduce the chance of postoperative
the distal end of their penises or develop
self-mutilation. To facilitate castration, this
paraphimosis. Because males urinate only
mixture may be diluted with sterile water
from the proximal end, the distal, forked
and infused into the base of the scrotal stalk
segment may be safely amputated. Other
nearest to the abdomen, while a low
surgeries performed in sugar gliders include
concentration of gas anesthetic is adminiscystotomy to remove uroliths, urethrostered. Both isoflurane and sevoflurane may tomy to alleviate urinary tract obstruction
be administered via small face mask or via
from uroliths in males, and surgical removal
a large face mask used as an induction
of impacted paracloacal glands. The skin
chamber. For surgery, gliders may be
over impacted glands is infiltrated with a
maintained on gas anesthesia with a face
small volume of local anesthetic and
mask or intubated with a 1-nun Cook
incised; the gland is bluntly dissected and
endotracheal tube tlu·eaded with a stylet.

removed without rupturing it. The blood

During surgery, blood loss should be
vessel supplying fue gland may be ligated
monitored carefully; use of radiosurgery
with 5-0 or 6-0 polydioxanone or cut and
may help minimize bleeding. Because
cauterized with radiosurgery. The skin is
sugar gliders tend to chew incisions after
closed with tissue glue.

surgery, ideally subcuticular sutures and
skin glue should be used to close skin

Drug Dosages: Very few phannacologic
incisions. Analgesics should be adminisstudies have been performed in sugar gliders, tered before surgery to minimize pain
and most published drug dosages have been
inunediately after surgery. Gliders should
extrapolated from those detern1ined for
recover from surgery in temperaturecats, fe1Tets, and hedgehogs. For drugs and controlled incubators.

dosages commonly used in sugar gliders,

Orchiectomy and scrotal ablation are
see TABLE 35.

conunonly performed on male sugar gliders
to prevent breeding and decrease sexual

Nutrition and Housing: Ideally, sugar
frustration. Hair is clipped around the base
gliders should be maintained as a group
of the scrotal sac and stalk, and the skin is
with one male and a number of females.

cleaned without alcol:)ol so as not to lower

If breeding occurs, the young should be
body temperature. A local anesthetic is
removed soon after weaning, or violent
administered at the base of the stalk, and
attempts to disperse them may occur.

with the glider under gas anesthesia, the

Because sugar gliders are arboreal
incision is made over the scrotal stalk -2--3

(tree-dwelling), a large cage (ideally of
mm from the body wall. The· spermatic

PVC-coated stainless steel) is best for
cords are exposed by blunt dissection and
nocturnal climbing. As large a cage as
are clan1ped and ligated with 5-0 polydioxpossible should be provided with a anone suture or cut and cauterized with
minimum size of36 x 24 x 36 in. Bar spacing
radiosurgery. The scrotal sac containing the
should not be more than ·1 x 0.5 in. wide, or
testicles and distal spern1atic cord is then
feet and heads may become entrapped.

removed, and the ligated stalk can be

Caging containing vertical bars should be
sutured to the abdominal wall fascia to
avoided, because vertical bars do not faciliprevent herniation. The skin is then closed tate climbing. A wooden nest box (made
with tissue glue. Standard ovariohysterecfor birds) or a fabric pouch positioned high tomy is not routinely perforn1ed because
up in the cage should be provided for
of the internal position of the female
hiding and sleeping. Cages should contain
reproductive organs, which are difficult to
numerous branches (commercially
access beneath the pouch. With ovariohysavailable for bird cages) and horizontal terectomy, the area around the pouch is
shelves to promote climbing. Swings and
clipped and scrubbed in a routine manner,
chew toys made for birds are ideal for
and a 1-2 nun incision is made paramedian
gliders to play with. Exercise wheels
to the pouch. The linea alba is bluntly
containing smooth interiors (so as not to
dissected and incised, and the bladder is
entrap toes) should be provided for physical
exteriorized from the incision to reveal the
and mental stimulation. The cage bottom
ovaries beneath. The ovarian arteries are
may be covered with newspaper or other

SUGAR GLIDERS

2039

IM=l!if i COMMONLY USED DRUGS IN SUGAR GLIDERS

Drug

Dosage

Considerations

ANTIBIOTICS

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Amoxicillin

30 mg/kg, PO or IM, once daily For dem1atitis
or divided bid

Amoxicillin-clavulanic

12.5 mg/kg/day, PO

Broad-spectrum against
acid
anaerobes and aerobes

Cephalexin

30 mg/kg/day, PO

Enrofloxacin

2.5-5 mg/kg, PO or IM, once

Potential tissue necrosis
or twice daily
when injected

Gentarnicin

1.5-2.5 mg/kg, SC, IM, IV, bid

Nephrotoxic

Metronidazole

25 mg/kg/day, PO

Penicillin

22,000-25,000 ill/kg, once or
twice daily

Sulfadin1ethoxine

5-10 mg/kg, PO, once or twice Ensure hydrated
daily

Trimethopri.rn/sulfa

10-20 mg/kg, PO, once or
twice daily

ANTI PARASITICS

Carbary! 5%powder

Topically or in cage

Use small amounts to treat
ectoparasites

Fenbendazole

20-50 mg/kg/day, PO, x 3 days For roundworms, hookworms, whipworms, tapeworms

Iverrnectin

0.2 mg/kg, PO, SC; repeat in

For roundworms, hook14days
worms, whipworms, mites

Metronidazole

25 mg/kg/day x 3 days; repeat For intestinal protozoa in 14 days

Piperazine

100 mg/kg, PO

Pyrethri.n powder

Topically

For ectoparasites

Selamectin

6-8 mg/kg, topically; repeat in For ectoparasites

30days

ANTI FUNGALS

Itraconazole

5-10 mg/kg, PO, bid

Nystatin

5,000 ill/kg, tid x 3 days

For Candida

ANALGESICS

Acepromazine/

1. 7 mg/kg/ 1. 7 mg/kg, PO

Postoperative analgesic
butorphanol
and sedative to decrease
self-mutilation of incision

Buprenorphine

0.01-0.03 mg/kg, PO or SC,
bid

Butorphanol

0.1-0.5 mg/kg, SC or IM,
every6-8hr

Meloxicam

0.1-0.2 mg/kg/day, PO or SC

Anti-inflammatory

2040

SUGAR GLIDERS

•t·Nii*i COMMONLY USED DRUGS IN SUGAR GLIDERS (continued) Drug

Dosage

Considerations

PREANESTHETICS

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Atropine

0.02-0.04 mg/kg, IM, SC, IV

To lessen intraoperative
secretions

Glycopyrrolate

0.01-0.02 mg/kg, IM, SC, IV

To lessen intraoperative
secretions

ANESTHETICS

Diazepam

0.5-2 mg/kg, PO, IM, IV

Sedative, anticonvulsant

Isoflurane

1%-5%

Via face mask or intubation

Ketamine

30-50 mg/kg, IM

Ketamine/medetomi2-3 mg/kg/0.05-0.1 mg/kg, IM Immobilization dine

Ketan1ine/midazolan1

10-20 mg/kg/0.35-0.5 mg/kg,

Give ketamine 10 min after

IM
midazolan1

Midazolam

0.25-0.5 mg/kg, IM or IV

Sedative, anxiolytic

Sevoflurane
lo/c,-5%

Via face mask or intubation;
possible toxicity, use cautiously

CARDIAC DRUGS

Enalapril

0.22-0.44 mg/kg/day, PO

Furosemide

1-4 mg/kg, SC or IM,

Diuretic
every 6-12 hr

GI DRUGS

Cisapride

0.25 mg/kg, PO, once to three GI motility enhancer
times a day

Metaclopramide
o'.05-0.l mg/kg, PO, bid-qid

GI motility enhancer

HORMONES

Calcitonin

50-lOOW/kg, SC or IM

Helps mobilize calcium

Prednisolone

0.1-0.2 mg/kg/day, PO, SC, IM Corticosteroid

VITAMINS

Calcium glubionate

150 mg/kg/day, PO

Calcium supplement

Vitamin A

500-5,000 IU/kg, IM, once

For dennatitis

Vitan1in E

25-100 ID/glider/day

Vitamin K

2 mg/kg, SC, every 1-3 days

Intestinal and liver disease
recycled paper product that is nontoxic
cockroaches, moths) to promote dental
if ingested. Several food and water bowls
health, as well as a daily nectar/sap substitute
should be provided throughout the cage,

( eg, fructose/sucrose/glucose or honey
with designated areas for eating, drinking,
diluted to lOOAiwith water). Nectar should
exercising, and hiding.

account for -500Ai of the diet. Several nectar

The recommended diet for captive sugar
substitutes are conrn1ercially available,
gliders includes calcium-loaded insects
including Gliderade nectar supplement

( c1ickets, mealwonns, waxwonns,

(Exotic Pet Nutrition Company, Newport

SUGAR GLIDERS

2041

News, VA), acacia gmn powder, and nectar
bacteria, including Pas teiirella miiUocida,
diets meant for Jory birds. Other protein

(conm1onJy contracted from pet rabbits),
sources in addition to insects include eggs,
staphylococci, streptococci, Mycobacte
lean meat, newborn mice, and commercial
rium sp ( especially in skin), Klebsiella sp, pelleted diets meant for sugar gliders.

and Clost1idium. Clinical signs may be

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Corrunercial diets or homemade insectivore
nonspecific, with depression, loss of
or omnivore mixes should be provided in
appetite, and weight loss being the most
addition to live food, with insects and
readily detected. Bacterial infections in
pelleted food accounting for nearly 50% of the gliders may present as opportunistic skin total diet. Fruits, nuts, and vegetables should
infections associated with trauma or may
be offered only in moderation ( <lOOA, of total
result in sepsis from other underlying
diet), because many fruits and vegetables
primary diseases. Although sugar gliders
lack essential vitamins, minerals, and protein
a.re hindgut fermenters, broad-spectrum
and contain mostly water. Several commerantibiotic therapy is well tolerated, probably cial diets and recipes for homemade diets are
because diets fed in captivity are digestible
available; no single diet studied has yet
without fermentation. Injectable, longproved to be ideal for captive sugar gliders.

a.cting penicillin with cla.vula.nic acid is an

Traditiona!Jy, before the availability of
appropriate first-line antibiotic. If indicated
conunercial pelleted diets, a homemade
by culture and sensitivity or by failure to
formula ca!Jed Leadbeater's mixture was fed
respond to first-line treatment, chJoran1-
successfully in addition to insects, fruits, and
phenicol and enrofloxacin are also well
vegetables. The mixture contains 150 mL of
tolerated in this species. Injections can be
wann water mixed with 150 mL of honey, one
given IM into the epa.xial muscles or SC over
hard-boiled shelled egg, one teaspoon of
the shoulders. Pala.table oral medications
multivitamin/mineral supplement, and 25 g
may also be administered.

of high-protein dry hun1an infant cereal. An
alternative to the homemade Leadbeater's

Protozoa I Disease: Toxoplasmosis is a
diet is commercia!Jy available High Protein
conunon and serious disease of marsupials,

Wombaroo Diet (Wombaroo Food Products,
typically presenting with neurologic signs.

Glen Osmond, South Australia), a powdered

Gliders may be infected with toxoplasmosis
protein supplement that is mixed with water
oocysts found in cat feces. Ca.re should be
before feeding. In addition, if not provided
taken to a.void cat feces corning in contact
in the diet, a multivitanlin and nlineral
with the bedding or food of sugar gliders.

supplement with calciun1 should be sprinkled Prevention is more successful tlla.n on food daily. Food should be offered in the
treatment. Coccidia. may also ca.use severe,
evening, when sugar gliders are active, on an
sometinles fatal diarrhea. in young gliders
elevated platform, because gliders feel more
a.nd may be contracted via fecal-oral
secure eating up high, as they would in trees
transmission from otller species.

in the wild. Sugar gliders are genera!Jy robust
in captivity when proper husbandry practices

Parasitic Diseases: Internal parasites
are followed; however, nutritional deficienrarely ca.use disease in captive gliders, but cies, especia!Jy of calcium and protein, are
giardiasis and cryptosporidiosis have been
commonly seen in captive gliders fed
seen in captive anin1als. Strongyle eggs also
inappropriately. Obesity also is conunon in
have been seen on fecal flotation. Internal
gliders fed excessive amounts of treats high
parasites reported to infect sugar gliders
in fat and protein and not provided with the
include nematodes of the genus Parastrnn
opportunity to exercise. Iron storage disease,
gyloides andParaustrostrongylus and a
in which excessive dietary iron accw11ula.tes
liver trematode of tile genusAthesmia. Wild in tl1e liver (hemochroma.tosis ), spleen, and
sugar glider nests genera!Jy contain a range
other tissues, has been reported in captive
of host-specific mites and fleas, but
gliders and may be associated with wild
ectoparasites are tmconm1on in captivity.

gliders' evolutionary adaptation to extract

Dusting with pyretllrin or carba.ryl powder
limited iron available in natural diets.

(50 g/kg) has controlled fleas and mites.

Hepa.tocellular toxic changes and cinhosis

Both the nest and the animal should be
from iron deposition may lead to death,
treated. Sela.mectin also has been used
unless the disease is caught and treated early
to treat ectoparasites on sugar gliders.

with chelation and supportive care.

Ivern1ectin and fenbendazole have been
used to treat GI parasites.

DISEASES AND SYNDROMES

Nutritional Osteodystrophy: Pet sugar

Bacterial Diseases: Sugar gliders are
gliders maintained on a mainly fruit diet
susceptible to infection with conm1on
witil few gut-loaded insects or other protein

2042

SUGAR GLIDERS
sources are very susceptible to nutritional
if present), and replaced once the glider is
osteodystrophy (nutritional secondary
anesthetized. Vertical mattress sutures may
hyperparathyroidism). This condition
be placed next to the vent to help prevent
results from an imbalance in dietary
recurrence, and the glider should be given

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calciwn, phosphorus, and vitamin D and
postoperative analgesics, antibiotics, and
manifests clinically as a posterior paresis

NSAIDs.

progressing to hindlimb paralysis, muscle
tremors, pathologic bone fractures, and

Urinary Tract Disorders: Sugar gliders
sometimes, in advanced cases, seizures.

can develop cystitis, crystalluria, and

Chronic malnutrition can lead to increased
urolithiasis. They may show hematuria,
liver and kidney values, hypoproteinemia,
stranguria, and dysuria. Affected gliders
and anemia. Radiography reveals osteoposhould have a urinalysis and urine culture rosis of the vertebral colwnn, pelvis, and
and sensitivity testing and should be
long bones in particular. Measurement of
properly hydrated. Antibiotics should be
ionized blood calcium typically demonadministered based on results of culture strates a low ionized calcium level.

and sensitivity testing. Cystotomy may be

Treatment involves cage rest; administrarequired to remove uroliths. Male gliders tion of calcium, vitamin 03, and fluids;
may develop urinary tract obstruction from
assisted feeding; and correction of the diet.

uroliths and require urethrostomy if

Seizuring gliders should be given diazepam
cystocentesis and flushing of the distal

IV, ideally, or if not possible, IM, intraosseurethra do not relieve the obstruction.

ously, or intrarectally, to stop seizures.

These gliders should receive analgesics,

Severely affected gliders may be given
antibiotics, fluids, and NSAIDs. Sugar
calcitonin to decrease calcium resorption
gliders with renal failure may show
from bone once calcium supplementation
weakness, polyuria, and polydypsia and
has nom1alized plasma calcium levels.

should be treated with standai·d treatment

Severe skeletal ( especially spinal)

used in other mainmals for renal disease.

defonnities may not be reversible.

Neurologic Disease: Causes of neuro

Dental Disease: Sugar gliders conswning
logic signs in pet sugar gliders include
large an1ounts of soft, sugary foods are
nutritional secondary hyperparathyroidprone to tartar buildup and periodontal ism, bacterial meningitis, toxoplasmosis,
disease. Tartar may be scaled off under
traumatic brain ll'\iury, otitis media/intema,
anesthesia. Advanced periodontal disease
encephalitis from aberrant CNS migration
or traumatic tooth fracture may lead to
of Baylisascaris procyonis, and encephatooth decay and exposed roots, necessitatlomalacia from hypovita.minosis E. Gliders ing extraction and treatment with antibiotexhibiting neurologic signs should undergo ics, analgesics, NSAIDs, and antiseptic
a full evaluation, including blood testing
mouthwash ( either made for cats and dogs

(CBC and chemistry), fecal testing for
or fruit-flavored for children). Unlike rodent
parasites, radiographs, and CT scanning
teeth, sugar glider teeth do not grow
plus CSF analysis, if indicated. Prognosis
continuously or require trinlrning.

in many of these cases is poor.

Diarrhea: Potential causes of diarrhea in

Neoplasia: Gliders are prone to
sugar gliders include bacterial infection
neoplastic disease in old age. Hepatocellu

(from Escherichia coli, Clostridium sp,
lar twnors and lymphoid neoplasia are
and other bacteria), GI parasites, malnutricommon, as is manimary gland adenocarcition, stress, and metabolic disease (such as noma. Cutaneous melanoma, scent gland
liver or kidney disorders). Sugar gliders
tllnlors, bronchogenic carcinoma, and
with diarrhea should have a fecal analysis
chondrosarcoma of the jaw also have been
for parasites, fecal bacterial culture and
reported. A soft-tissue carcinoma associ

Gran1 stain, blood testing (CBC and
ated with a microchip implant was reported
chemistry panel), and possibly radiographs.

in a mallogany glider (Petaurus gracilis ). A Gliders with diarrhea should be given
malignant testicular interstitial cell tllnlor
supportive care with fluids, supplemental
in a mallogany glider was managed by
feeding, and drug therapy, as dictated by the
hemicastration. Transitional cell carcinoma
cause of the GI signs. Rectal and cloaca!

with squainous differentiation was noted
prolapse can occur in gliders secondaiy to
pericloacally in a 10-yr-old male sugar glider.

diarrhea and straining and is more common
in malnourished aninlals. The prolapsed

Miscellaneous Disorders: Sugar gliders
tissue must be cleai1ed, checked for
may develop cardiomyopathy/myocarditis,
necrotic areas (which must be removed
cataracts in juveniles (possibly associated

TASMANIAN DEVILS

2043
with nutritionally imbalanced handfeeding
pacing are also seen in stressed gliders.

fonnula, hyperglycemia, and hypovita

Sexually mature male sugar gliders without
minosis A), cloacitis/vaginitis (females),
access to females may self-mutilate the tail
irregularity of ear margins/crusting of
base, limbs, scrottm1, penis, or perinew11

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pinnae from ear mite infections, and
and may develop paraphirnosis, in which the
retrobulbar abscesses associated with facial penis remains extruded from the cloaca and bite wounds in competing males. These
becomes trawnatized and devitalized,
syndromes are treated with medications
necessitating amputation. These gliders
and surgical procedures, when indicated,
should receive pain relievers, antibiotics,
sinillarly to those used in other man1mals
and possibly antidepressants, plus an
with these conditions.

Elizabethan collar, to enable healing. At
least 2 hr per day, preferentially at night,

Behavior: Sugar gliders live in colonies
when they are awake, must be spent with
in the wild and are very social. Thus, they
pet gliders for proper socialization.

should be kept in captivity in groups of two
or more. Gliders love to crawl into pockets

Zoonoses: Diseases that may infect sugar
or pouches, where they feel safe and more
gliders, such as salmonellosis, giardiasis,
relaxed. Behavioral disorders can develop in leptospirosis, clostridiosis, and toxoplasmosugar gliders housed alone, with incompatsis, are potentially zoonotic. Sugar gliders ible mates, or in inappropriate cages. When
are best handled wrapped in a small towel,
housed singly, not given enough social
because they may bite and scratch, and
stin1ulation, or not provided with a nest box
although they are small, their lower
or pouch in which to hide or enough room
incisors, which are designed to bite through
to exercise, they may self-mutilate their fur
tree bark, may inflict significant dan1age.

and skin, develop stereotypic behaviors, or

Biting and scratching can be avoided by
become aggressive. Anxious gliders will
gentle handling and proper socialization.

overgroom, causing fur loss, particularly

All ocular, nasal, GI, and genitourinary
at the tail base. Anorexia, polyphagia,
discharges should be treated as potentially
polydipsia, coprophagia, cannibalism, and
infectious.

TASMANIAN DEVILS

The Tasmanian devil is the largest
age. Wallabies, wombats, and sheep are the
marsupial carnivore in existence, currently
usual source of canion, but other dead
restricted to tl1e island-state of Tasmania,
domestic livestock, roadkill, and 1080-

Australia. Devils have black fur, and white
poisoned wildlife are also consun1ed. The
flashes on the chest and rump may be
proportion of hunting to scavenging is
present. They are sexually dimorphic, with
unknown. Female devils are facultative
males having a thicker neck and broader
polyestrus witl1 up to three estrous cycles
head than females. Males typically weigh
within a breeding season, each cycle -60

9-12 kg (up to 14 kg), and females 6-8 kg
days apart. They are polyovular (up to 114

(up to 9 kg). Devils are mainly nocturnal
oocytes per ovulation) and may give bi.Ith to
and hide during the day in rock dens, log
up to 40 embryos. Mating peaks over late
cavities, or underground burrows made

February to the end of March and, as is
by other aninlals. They live up to 6 yr in
typical for marsupials, females give birth
the wild and 9 yr in captivity. Devils are
to highly undeveloped yotmg -3 wk after
nonterritorial and generally live within an
mating. Females have a rear-facing pouch,
area of 10 krn2. They can occupy a wide
with fow· teats in tl1e pouch cavity, limiting
range of habitats, from dry sclerophyll
the maximwn total offspring raised per year
forest, open eucalypt environment, and
to four. The young are carried in the pouch
coastal woodland, to pasture and agriculuntil they are 4-5 mo old, weaned at 5--8 mo, tural areas where carrion (from domestic
and become independent at 10-12 mo.

livestock and macropod populations) is

Sexual maturity is reached at 2 yr of age for
abundant. Devils are specialist carrion
both females and males, although females
feeders but will hunt prey, particularly
have been confirmed to reproduce as young
those weakened by disease, irtjury, or old
as 1 yr old.

2044

TASMANIAN DEVILS

Physical Examination and General
monitor heart rate and pe1ipheral oxygen

Anesthesia: Wild Tasmanian devils can
saturation. For quick procedures such as
be restrained and exanuned in a hessian
physical exanunation and blood collection,
sack by an experienced handler. Devils have
a mask is sufficient to maintain anesthesia.

an exceptionally strong bite for their body

For longer procedures, an endotracheal

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size, and handling conscious animals must
tube (5--5.5 Fr) is indicated. Thedevil's
only be done by or attempted in the
larynx is narrow, and a laryngoscope is
presence of experienced personnel.

essential. Local anesthetic must be applied

The handler sits on the ground and
to prevent laryngospasm before intubation.

locates and holds the devil's muzzle closed

As the devil starts to recover from
from outside the sack. The devil is then
anestl1esia, it is placed back in the sack and
positioned between the handler's legs,
observed until it is fully awake and ready to
with the devil facing outward and head
be returned to its enclosure.

uppermost. The head and face are gently
revealed with one side of the sack left

Proliferative Lesions: Tasmanian
covering the devil's eyes. The handler then
devils are prone to developing proliferative
moves the free hand directly onto the
lesions, tile most conunon being devil facial
muzzle, continuing to hold it closed, and the
tumor disease (DFTD). Cell proliferations
teeth/mouth can be exan1ined to estimate

(benign and malignant) affecting skin and
age of the devil by lifting tile upper lip.

adnexa, and endocrine and lymphoreticular

The mouili can be opened for intraoral
tissues ( eg, squamous cell carcinomas,
examination. It is important to visualize all
lymphosarcomas, adenocarcinomas) are
aspects of the oral cavity, including under
commonly seen at necropsy in adult and
the tongue, for signs of tumors. N om1al
senile captive devils. ln older captive devils
lymph nodes are not palpable in devils;

(�5 yr old), man1mary and anal gland tumors
therefore, subcutaneous masses should be
are tile most common.

considered suspicious. If a blood sample

Devil Facial Tumor Disease: Devil facial
is required, the devil is positioned as
tumor disease (DFTD) is a malignant
described, ie, facing away from the handler.

infectious tumor first observed in 1996. As

An assistant can collect up to 12 mL of
a result of> 70% of the population having
blood from the jugular vein. Thejugular vein succumbed to DFTD, devils have been is not visible or palpable; to locate it, the
listed as an endangered species. The
index finger of one hand palpates the groove prevalent characteristic of DFTD, as tile immediately cranial to the clavicle and just
name suggests, is tile presence of tun10r( s)

lateral to the stemohyoideus muscle. The
on tile facial area. Tumors are also found
finger pulls the skin distally and, wiili the
inside tile mouili (gingival mucosa, hard
oilier hand, a 21-gauge needle_ is inserted
palate, lips) and on the head and neck.

0.2-0.5 cm into tile groove while applying

Rarely, D FTD tun10rs may be found on the
negative pressure to the syringe. Gentle digirump or other areas of the body, but these tal pressure is applied to tile venipuncture
are thought to be metastatic tun10rs rather
site after blood collection is complete. The
tl1an primary. More ilian one tumor is often
devil can then be placed back into tlie sack,
with the head facing up and away from the
handler, so tile tail, cloaca, and pouch can
be examined.

Devils bred in captivity or brought to
captivity before 2 yr of age are generally not
amenable to handling, so general anesthesia
is required for examination. These animals
can be trapped in ilieir enclosure and
transferred to a hessian sack or picked up
by the tail base and transferred to the sack.

Anesthesia can be induced by using a mask
on the devil through the sack. Isofluorane
has been used successfully. Ideally, the
devil's muzzle is positioned in a comer of
the sack to facilitate mask placement. The
sack should be secured around tile devil to
prevent excessive movement and escape

Tasmanian devil with extensive ulcerated
tumors on the muzzle and nose. Devil facial
from tile mask. Devils are induced in 2-3
tumor disease nodules can be seen also on
min and then removed from tile sack. A
the lower left gum and left cheek. Courtesy of
pulse oximeter can be attached to the ear to

Dr. Alexandre Kreiss.

TASMANIAN DEVILS

2045
seen, and tumors on the same devil often

DFTD; the tumor cells "down regulate"

vary considerably in size and appearance.

major histocompatibility complex (MHC)

The tumors often ulcerate and display
molecules on the cell surface, so that
epithelium break up, necrosis, exudation,
antigen presenting cells do not recognize
and bacterial contamination. Most devils
the tumor cells. In dogs, the immune

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affected with DFTD show signs of
system might overcome this by producing
metastases (65%of cases in a study of91
cytokines and "forcing" the tumor cells to affected devils), principally to the regional
express MHC and become targets for
lymph nodes but also to the lungs and
cytotoxic T cells.

spleen.

The most remarkable characteristic

Cutaneous Lymphoma: This lymphoid
of DFTD is its transmissible nature, a
skin tumor has been recently seen in both
concept supported by several independent captive and wild caught devils, affecting lines of research. The tumor is of Schwann predominantly older females. No etiologic cell origin and is transmitted by biting.

agent has been implicated. It can present

Devils with tumors in the oral cavity have
as a localized erythematous lesion, mainly
free tumor cells "coating" the canine teeth. in the limbs and ventral part of the body, or The tumor cells are transplanted when a
as a generalized alopecic and exudative
bite wound penetrates the subcutaneous
form. This condition progresses over
tissue or mucosa of the next devil. The
several months. There is no known
most common bite site in devils is the
treatment.

head, which, therefore, is where almost all

DFTD tumors are present. The incubation

Parasitic Diseases: Tasmanian devils
period is unknown but is estimated to be
are susceptible to both Demodex sp

3-15 mo. Most devils die within 6 mo of a
infection and tl1e sa.rcoptiform Diaboli
tumor becoming grossly visible. Death
coptes sarcophilus. The latter is common
results from starvation, depending on the
and can be treated with ivermectin 200
size and location of the tumor, or from
mcg/kg, SC, every 4 wk for 3-4 mo. Wild
metastatic disease. No evidence of this

Tasmanian devils often harbor the
disease in other species has been found.

dasyurid-specific flea Uropsylla tasman

No preclinical diagnostic test is available.

ica. This unusual flea has all stages of its The tumor cells have a characteristic and
life cycle on the host. The larva is comconsistent karyotype, showing loss of three monly found embedded in the subcutis of
autosomes, loss of both sex chromosomes,
the tail, limbs, or ventral area. Adult fleas
and addition of four marker chromosomes.

are less common.

Histologically, DFTD tumors share the same

The two most common GI parasites a.re
morphologic features as a high-grade
the nematode Baylisa semis I asmaniensis

.malignant tumor composed of diffuse sheets and the cestode Anoplotaenia dasymi. If of small, row1ded to polygonal shaped cells
the cestode burden appears excessive in
with ovoid hyperchromatic nuclei. Mitotic
captive devils (visible proglottids on feces),
figures are frequent, and eccentrically
they can be treated with pra.ziquantel
located nuclei result in a plasmacytoid

(5 mg/kg, SC).

appearance.Tumor cellsrnight appear
cohesive and epithelioid in appearance and

Spinal Cord Degeneration: A comfom1 elongated trabecular and solid alveolar mon condition in aged (<!5 yr old), captive
structures. The gold standard diagnostic test Tasmanian devils has been described as a for DFTD tumors is immune-staining with
degenerative leukoencephalopa.thy and
periaxin. It is common for devils to develop
myelopa.thy. It manifests by a progressive
other cell proliferations, which must be
swaying of the hindlegs, eventually
differentiated from DFTD.

worsening to paresis and paralysis in

There is currently no known treatment
several months. Histologically, it is
for DFTD; vincristine and doxorubicin have
characterized by a.xonopa.thy and vacuolabeen tried without twnor reduction, and to tion of the spinal cord. Intervertebral disc
date surgery has not been successful.

disease is a common finding. There is no

Radiation therapy has not been assessed.

known treatment.

Research into a vaccine is underway.

The only other tumor transmitted by

Zoonotic Concerns: Trichinella
direct cell implantation is the canine
pseudospiralis appears to be endemic in
transmissible venereal tumor (CTVT,
the Tasmanian devil population, with no
see p 1408) of dogs. Although CTVT is
known hun1an cases to date derived from
generally a benign tumor, it shares the
devils. Devils also harbor Salmonella
same immune-escape mechanism as
species in the feces.

2046

ZOO ANIMALS

ZOO ANIMALS

The physical health as well as the social
anin1al and results in a better display. Food

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and behavioral well-being of zoo animals
can also be used to attract an animal to an
depends on enclosure design, nutrition,
area where it can be more easily and safely
husbandry, management, group social
exanl.ined or treated.

structure, behavioral enrichment, and good
medical and surgical care. Naturalistic

Reproduction: The biology and social
enclosures with soil and vegetation are
behavior of animals must be w1derstood
appealing to the public and inore stimulatto promote reproduction. Species should ing for the animals, but they present
be maintained alone, in pairs, or in groups,
challenges for both sanitation and parasite
depending on their established social
control programs and may complicate
systems. For exan1ple, in mixed species
restraint procedures. Mixed species
groups of Artiodactyla, it is possible to
exhibits may increase risk of disease
establish species estrous cycles through
transmission between species and can
a variety of techniques, including monitorresult in interspecific aggression if approing hormone levels in the urine and feces.

priate choices are not made.

Monitoring reproductive cycles may be

This chapter provides a general discus-
used to determine when to introduce and
sion of management practices, preventive
remove breeding males, with males of otl1er
medicine, clinical care programs, and some of
species rotated to coincide with the estrous
the more commonly encountered disorders in
periods of the females of each species. This
zoo animals. For more specific information,
may also reduce injuries from interaction
refer to other chapters within this section ( eg,
between breeding males. At parturition, the
see AMPl·UB!ANS, p 1734; MARINE MAMMALS, p 1856; males of some species should be removed

LLAMAS AND ALPACAS, p 1844; RATITES, p 1960;
for several weeks to prevent attacks on the

NONJ-IUMAN PRlMATES, p 1876; llEPTILES, p 1967; and
postpartwn females or their offspring. In

VACCINATION OF EXCYl1C MAMMALS, p 2054). For
colder climates, males should be introduced
more information on nutrition, see NUfRlTION: at a time that will allow births to occur

EXCYl1C AND ZOO ANIMALS, p 2287.

during warm weather.

Artificial reproductive technologies such

MANAGEMENT
as artificial insemination, in vitro fertilization, and embryo transfer have been Husbandry: The animal's exhibit should
successfully used in diverse zoo species.

approximate its natural environment and

These efforts have made a significant
enhance the visual experience for zoo
difference in some endangered species
visitors. Many healthy man1mals and birds
breeding programs ( eg, black-footed ferret).

can tolerate a fairly wide temperamre range

However, success requires substantial
if given access to shade and water in hot
investment of resources (financial,
weather and to a dry, draft-free shelter with a personnel, etc) to deteml.ine basic wann spot and ample food to meet increased paran1eters of reproductive cycles and energy requirements in cold weather. It is
responses to pharmacologic manipulation.

essential to ensure that each animal has

An emerging management priority in
access to the protected environment and
maintenance of zoologic collections is the
that one dominant individual does not
need for selective reproduction. Indiscrinl.iexclude others from shelter, food, or water; nate reproduction is unethical and carries
such exclusion can result in frostbite or even
the potential for overproduction that
death due to exposure. Feed receptacles
exceeds the capacity of the exhibit, the zoo,
should be designed to avoid fecal contanl.ior other zoos to approp1iately house the nation and be easy to clean.

progeny. Overly successful breeding

With large munbers of birds or mammals,
programs carry a risk of limiting resources
and especially in mixed species exhibits,
that could compronl.ise other captive
several watering and feeding stations
propagation progran1s. Regional cooperashould be established at appropriate heights tive breeding programs such as Species to reduce territorial conflicts that may result Survival Plans should be followed.

in injuries or deaths. The timing of feedings

Management is aimed at ensuring genetic
is important. In many species, it is best to
diversity of the species into the future.

feed small amounts throughout the day to

Contraceptive efforts in zoos are multifacstimulate activity; this is beneficial for the eted and include pem1anent techniques

ZOO ANIMALS

2047

( castration, vasectomy, ovariohysterecapprop1iate to ensure that infectious tomy, tubal ligation), as well as reversible
diseases are not introduced into the
ones such as separation of the sexes,
pennanent collection when the quarantined
administration of birth control pills,
animals are released to exhibits. Quarantine
hmmonal implants, gonadotropin-releasing
facilities should follow the "all-in/all-out"

hom1one agonists, and oral or iajectable
principle, ie, if additional animals are added

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progestins. Reversible contraception can
to an ongoing quarantine, tl1e quarantine
also be used to control timing of reproducperiod should be restarted.

tive cycles. There is ongoing work with

During quarantine, animals should
immunocontraception through administrareceive appropriate vaccinations and tion of porcine zona pellucida vaccines. The
diagnostic testing ( eg, tuberculosis,

Association of Zoos and Aquaria Wildlife
heartworm). They should be exan1ined and

Contraception Center is a good source of
treated for ecto- and endoparasites and
up-to-date information on contraception
screened for ente1ic bacte1ial patl10gens.

teclmiques.

Before release, animals should receive
physical and laboratory exanunations,

PREVENTIVE MEDICINE
which may include radiographs, serology,
hematology, and clinical chemistries. Serum

The foundation of a medical program
should be frozen for future reference and
for zoo animals is preventive medicine.

possible epidemiologic studies. All

Preventive medical programs should be
procedures and results should be recorded
adaptive and include attention to individual
in each individual aninial's medical record,
specimens as well as the herd, troop, or
which is an essential component of the
flock. Components of the progran1 include
medical progran1. Each animal should also
quarantine of new arrivals, periodic fecal
be identified by some permanent method
examinations and treatments for parasites,

(eg, tattoo, tag, band, eartag, transponder)

booster vaccinations, health screening
to ensure future identification.

procedures, nutrition evaluation, necropsy

When new animals are introduced to
exanunation of deceased specimens, and
enclosures, caution and forethought are
a comprehensive pest control program.

necessary to prevent self-induced trauma.

Animals should be evaluated to ensure

Visual barriers, eg, suspending canvasses
their health complies with local, state,
from fences or enclosure walls or obscuring
and federal health requirements before
glass with soap to provide a visual cue, are
shipment to other zoos or before release
standard management steps to protect
in managed reintroduction programs.

newly introduced specimens from accidents

Preshipment evaluations can also be used
dUiing acclimation to a new exhibit.

as an opportunity to assess the overall
health status of the group in which the

Parasite Control: Like domestic animals,
animal has been living.

zoo animals are vulnerable to a wide variety
of ecto- and endoparasites, and sinular

Quarantine: Animals entering a
drugs are used for treatment. Care must
collection must undergo quarantine.

be exercised in tl1e choice of medications

Quarantine facilities should be designed
because of species-specific sensitivities
to allow handling of animals and proper
to some drugs. Young animals and those
cleaning and sanitizing of enclosures.

stressed by shipment, disease, or iajury are

Shipping crates should be cleaned and disinthe most likely to be adversely affected by fected before they leave the quarantine area,
parasites. At these times, commensal
and the crates' contents disposed of
parasites ( especially protozoa) can cause
appropriately. Quarantine facilities require
disease. Acute dia1Thea can result from
barriers against ingress of potential vectors
massive infections of coccidia, Tricho
and vermin. Separate keepers who are
monas, Giardia, or Balantidiiim spp.

skilled at recognizing signs of stress and

Arnebiasis, which is fairly common in
disease and who will carefully monitor feed
primates and reptiles, can be fatal in a
intake and fecal characte1istics should care
compromised animal. Intestinal parasites
for quarantined animals.

may be a major, continuous problem in

Quarantine entry should be strictly
species kept in naturalistic exhibits or on
controlled. Only essential personnel should
di.J.t substrate or pasture, especially in
be allowed into the quarantine facility.

young, newly introduced, or stressed

Individuals leaving the quarantine facility
individuals. Of most concern are parasites
should not return to other animal areas
witl1 di.J.·ect life cycles. Incorporating
without showering and changing clothing.

anthelmintics directly into the feed is

The duration of quarantine should be
helpful. As in domestic species, antheln1in-

2048

ZOO ANIMALS
tic resistance may develop and necessitate
the use of mechanical and chemical control
rotating medication. Parasites with indirect
methods. Choice of agent, method of use,
life cycles are less frequently a problem if
and storage may minimize zoo animals'

the exhibit area is free of intennediate
access to pesticides and the risk of
hosts.

secondai-y poisoning. Common zoo pests

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may serve as important disease ve�tors. For

Vaccination: Vaccination programs for
exainple, cockroaches are intermediate
carnivores, nonhuman primates, equids,
hosts for GI parasites of p1imates and birds;
artiodactylids, and birds should be
rodents can harbor and spread Listeria,
developed. Vaccination of zoo carnivores is

Salmonella, and Leptospira spp 3.lld essential because of their susceptibility to

F'rancisella tula.rensis. Wild and feral
vaiious diseases such as feline panleukopecarnivores such as foxes, raccoons, 3.lld nia, feline rhinotracheitis, feline calicivirus,
domestic dogs and cats can devastate
rabies, canine distemper, and canine
anin1al collections through predatory
paivovirus. (See al.so VACCINATION OF 8XOTIC
attacks and may be in1portant vectors for

MAMMAIB, p 2054). Previously, only killed
viral diseases such as rabies, paivovirus,
virus vaccines were recommended, but
and canine distemper. Raccoons may also
recent studies have shown that some
transmitBaylisascaris parasites, which
modified-live vaccines are safe for use in
can cause laival migration, resulting in fatal
select species. Further studies ai·e required,
neuropathy in some species. Pigeons, geese,
because some modified-Jive vaccines
ducks, and starlings are potential reser

( especially canine distemper) can result in
voirs for avian diseases; they consume or
fatal disease in certain species. A canarypoxcontaminate animal food and deposit vectored recombinant canine distemper
droppings everywhere. Arthropod vectors
vaccine has proved safe for use in those
can transmit pathogens such as West Nile
species susceptible to modified-live virus
virus.

vaccine-induced disease. Appropriateness of
rabies vaccination depends on the circum

Nutrition: Some zoos have either a staff
stances of each collection. If indicated in
nutritionist or a nutritional consultant on
rabies-endemic areas for protection of
contract. Zoos that do not should have some
individual animals, only a killed rabies
degree of veterinary oversight of diets and
vaccine should be used. The decision to
diet ch3.11ges. This is especially true for
vaccinate zoo animals for less common
addition of native or exotic plant species to
diseases for which a vaccine is available
the diet as browse for eitl1er enrichment or
should be made on an individual basis.

as an integral pa.it of the diet. Protocols

Recombinant and subunit vaccines are being should be developed for diet fom1ulation, developed for a variety of infectio.us diseases diet changes, and addition of plant material for domestic animals. Extra-label use of
to the diet.

vaccines should be done with caution until
safety and efficacy studies have been

CLINICAL CARE PROGRAMS
completed for zoologic species.

The mainstay of the zoo medical progran1 is

Necropsy: All dead animals should be
a qualified and dedicated keeper staff. The
necropsied. This should include gross and
keepers know tl1e individual animals under
histopathologic evaluation of tissue and
their care and observe them daily. Tbey ai·e
viral, bacterial, or fungal cultures when
the first to recognize abnormalities such as
appropriate. Tissues should also be saved
anorexia, inactivity, abnormal feces, or
for potential future exanlinations. A
changes in behavior that may reflect early
thorough pathology exan1ination allows
medical problems. Overzealous repmting of
evaluation of medical, management, and
observations is preferable to indifference.

nutritional prograins. It is also valuable in

Because many zoo animals, especially prey
identifying problems requiring immediate
species, instinctively conceal overt signs of
action to safeguard the healtl1 of tl1e
ilh1ess until tl1e disease process is well
collection. Variations in anatomy should be
advanced, it is necessary to make keepers
recorded, because such observations may
aware of the significance of what may seem
aid in future diagnostic procedures or
to be trivial changes. Past associations with
therapy in the species.

the veterinarian may arouse some animals'

responses to the veterinarian's presence,

Pest Control: A successful control
which will mask subtle changes noticeable
prograin is continual and requires a
to keepers.

concerted effmt by zoo staff to mininlize

Once a diagnosis is made, the treatment
harborage and food for pests, in addition to
of zoo animals is sinillar to that of domestic

ZOOANIMALS

2049
species except in the method of drng
restraint. Struggling with an animal to
administration and restraint. A comparaadminister treatment may do more hat-:tn tive medical approach is generally most
than can be offset by treatment. Physical
successful and involves application of
restraint is indicated in some species for
medical or surgical information about
minor manipulation or close observation.

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diseases affecting free-ranging animals,

Restraint devices (squeeze cages) or chute
related domestic animals, or people.

systems are frequently used for species that

Frequently, other vete1inaty experts or
ai·e large, dangerous, or difficult to handle.

human medical or dental specialists are

Many procedures can be perfonned on
consulted for advice or assistance with
unanesthetized animals so confined,
complicated medical or surgical cases.

including limited physical examinations,

Knowledge of compai·ative anatomy,
tuberculin testing, administration of
physiology, behavior, nuttition, pathology,
injections or anesthetics, collection of
and taxonomy is useful. Attention must be
blood sainples, ttimming malfom1ed claws
paid to both individual and population
or overgrown hooves, and application of
health.

topical medications.

Unless medical conditions dictate

Altl1ough the dimensions and constl'Ucotherwise, it is often preferable to leave ai1
tion of these devices vaiy, some operate by
ai1imal under treatment at its home exhibit
movement of one wall to restrain the animal
where it can maintain contact with its
against the otl1er. Openings are provided to
conspecifics and keepers. This can also
allow safe access to the animal. Many
prevent disruptions in social hierarchies,
restraint devices for hoofstock are designe<I
which may cause difficulties with reintrowith a "V" shape; once the animal enters, the ductions to an established group.

floor is lowered and the animal's body is
restrained by the "V" with its feet suspended Behavioral Training: An active
off the ground. Whenever possible, animals
behavioral training prograin enables
should be trained to enter or be enticed,
in1proved health cai·e. Through positive
rather than forced, into the restraint device.

reinforcement, ainphibians, reptiles, birds,

Ideally, these facilities should be designed
and man1111als in zoo settings have been
as part of the animal's regular quarters and
trained to perform behaviors on command
located in an ai·ea where the animal is
that facilitate accomplislunent of vatious
nonnally shifted as part of the daily routine.

management or medical procedures.

Exhibits should contain nest boxes or

Management behaviors include shifting
restraint pens equipped with doors that
on and off exhibit, onto scales, and into
operate remotely to confine the animal.

restraint devices or shipping containers.

From these areas, the animal can be

Medical procedures include urine collectransfen-ed to a restraint device, anesthetic tion, venipuncture, IM injection, tuberculin
chamber, or shipping container. Weighing
testing, ultrasonographic exainination, and
facilities are essential.

rectal or vaginal exainination. Often, these

Small mammals and birds may be caught
behaviors are incorporated into behavioral
and restrained in long-handled hoop nets.

and environmental enrichment prograins.

These nets must be deep enough that the

Enriclu11ent prograins ai·e designed to
animal can be confined in the blind encl,
encourage animals to display more of their
with the upper part of the net twisted to
normal behavioral repertoire, eg, increasing
prevent escape.

opportunities for foraging or social

Persormel participating in capture or
interaction, which allows animals to spend
restraint procedures must w1clerstand
their tin1e more as they would in nature.

their role and be aware of the behavioral

Protected contact, a management system
characteristics at1cl physical abilities of
for elephants, uses positive reinforcement
animals. This is essential to ensure safety of
to encourage the elephant to present
botl1 animals and personnel. Heavy gloves
appropriate body parts through openings in
protect handlers from teetl1 and claws when
a wall. Procedures such as venipuncture
animals are manually held after capture.

from the ear, foot trimming, reproductive

Cai·e must be used to avoid excessive
evaluation, artificial insemination, and
pressure on animals, because gloves hinder
tl'llnk washes are routinely performed using
both dexterity and the perception of the
protected contact. This system provides
ainount of pressure being exerted. Gloves
safety for personnel working with elephants are also difficult to clean and can be a fomite and gives the elephant a degree of choice.

for transmitting infectious agents.

Physical Restraint: Most zoo animals

Diagnostic Techniques: The fundatnenresent being handled and resist manual tal diagnostic technique is a good history

2050

ZOO ANIMALS
and thorough visual and physical examina

However, these injections may be painful
tion ( often requiring anesthesia). Ease of
and add the trauma of dart il.npact and
sample collection for laboratory testing
injection, especially when delivering large

(CBC, biochemical profile, serology,
volumes ( eg, 10 mL) over long distances (50
cytology); fecal examination for parasites;
m). Problems can be minimized through
urine for urinalysis; and aerobic, anaerobic,
careful selection of the most apprqpriate

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fungal, and viral culture depends on species
drug and drug concentration, as well as the
anatomic differences. Radiography and
type of dart gun for the intended use. In
ultrasonography are commonly done.

addition, practice with projectile darts is

Endoscopy, laparoscopy, and minin1ally
mandatory before their use. Marksmanship
invasive surgery are used when indicated,
and fan1iliarity with the weapon are
with use of CT and MRI becoming more
essential-such weapons in the hands of a
common. Vil.tually any technique used for
novice can be fatal. Other less traumatic
other species can be modified for use in zoo
methods of IM injection, over shorter
species.

distance, include syringe poles or blow
guns. Through behavioral training, it is also

Drug Administration: Few drugs are
possible to administer IM injections through
approved for use in zoo species, but
volunta.J.y participation of the aninlal. IV
extra-label drug use laws allow drugs to be
therapy is generally restricted to anesthelegally used in species for which they are tized anil.nals or those maintained in
not licensed. Providing quality medical care
restraint devices or small enclosures for
to zoo animals requires that medications
the duration of treatment.

be used without documented therapeutic
benefit, dosage, treatment schedule,

Anesthesia: Safe anesthesia of zoo
contraindication, and toxicity data in these
aninlals is of special concern. Many
species. Whenever possible, drug adminisprocedures routinely accomplished on tration should be based on pharmacokinetic domestic aninlals with minin1al restraint data. If appropriate data are not available,
require anesthesia of zoologic species for
extrapolation from what is lrnown about
the welfare and safety of both zoo aninlals
these para.meters in other species using
a.i1d personnel. Before anesthesia of a zoo
metabolic scaling is necessary. Appropriate
animal, the veterinarian should be fan1iliar
dosage is necessary if therapy is to be
with the species and choice of anesthetic
beneficial, especially with drugs that have
agent. Anesthesia records for the individual,
the potential for organ toxicity. Antibiotic,
other specimens of the same species in the
antifungal, and analgesic treatments, as well collection, or published references for the as anesthetic dosages, are becoming less
species should be reviewed. Consultation
empirical because of increasing specieswith someone lmowledgeable in the field is specific !mow ledge resulting from
advised, because there are large differences
pha.nnacok.inetics studies in zoo species.

in effective drugs and dosages in the

When using a drug on a group of anin1als
diversity of species in a zoo logic practice.

for the first time, it is often wise to initially

An anesthetic plan should be developed for
administer it to just one or two indiviooals.

each anesthetic episode; the plan should

If no adverse effects are seen, the rest of the
include the anesthetic drugs and doses to be
group can then be treated.

used, other needed pharmaceuticals ( eg,

Drug administration can be challenging.

emergency drugs, analgesics, anthelmintics,

Oral medication has the advantage of
vaccines), monitoring equipment, and any
minimal disturbance to the aninlal, but
other special equipment to perfom1 the
ensuring adequate individual intake may
procedure at hand.

be a problem, especially when aninlals are

Many factors influence an anin1al's
housed in a group. Mixing the medication
response to anesthetic drugs, including age,
with favorite foods or treats is helpful. Oral
sex, stage of reproductive cycle, general
antibiotics in hoofstock and other species
nutritional status, and most especially
can disrupt nmmal bacterial flora and lead
mental state before drug administration.

to GI problems. Oral sedative or anesthetic

Variations may be marked between species
administration can result in variable onset,
as well as individuals and between different
duration, and depth of effect because of
collections of the same species. An excited
inadequate consumption or delayed
aninlal usually requires more drug and, once
absorption. IM injections with a hand
anesthetized, has a greater tendency to
syringe can be difficult unless a restraint
develop capture myopathy secondary to
device or other means of physical restraint
hypertherm.ia, respiratory depression, and
is used. Remote IM injections may be made
acidosis. Capture myopathy can also occur
by fuing a projectile syringe from a da.it gun.

in manually restrained anin1als and is more

ZOO ANIMALS

2051
common in ungulates or long-legged birds
rapid reversal after the procedure has been

(seep 2884). Monitoring of anesthetized
completed.

animals may include heart and respiratory

Tiletarnine-zolazepam, a dissociative
rates, temperature, ECG, oxygenation
anestl1etic-tranquilizer combination, is

( measured by blood gas determination or
relatively safe in most species, has a rapid
pulse oximetry), ventilation (measured by
induction, and can be concentrated to

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blood gas determination or end-tidal C02),

200 mg/mL to allow a small delivery volwne.

and blood pressure (measured directly or by It is conunonly used for anesthesia of oscillometric techniques). Attention must
carnivores and primates. However, a
be paid at all times to appropriate positiondisadvantage of this drug combination ing and padding of anesthetized animals and is that no complete antagonist exists; extremes of environmental conditions to
therefore, recoveries can be longer than
prevent secondary complications.

with other combinations that can be

The nature of an enclosure in which
completely reversed.

animals are to be anesthetized should be

The rapid onset and shmt duration of
carefully considered before initiation of an
anesthesia induced by the sedative-hypnotic
anesthetic episode to minimize complicapropofol renders it particularly attractive tions. For example, prey species that are
for use in zoo species. However, because of
darted may startle and hit fences or other
the necessity for IV administration, its use is
barriers. In herd situations, the herd
limited to species such as reptiles, birds,
members may attack and irtjure or kill the
and small manunals that can safely be
darted animal as anesthetic induction
manually restrained for drug administrabegins ( eg, ataxia).

tion. It is also useful as an acljunct anes

Xylazine, detornidine, or medetomidine
thetic agent in large mammals first

( aradrenoreceptor agonists) used alone
immobilized with another drug combinaproduce adequate sedation in some tion.

ungulates, mainly bovids, to allow some

The potent opioids etorphine, carfentanil,
manipulative procedures. The sedative
and thiofentanil, alone or in combination
effects can be antagonized by administrawith other agents ( eg, azaparone, acepromtion of yohirnbine, tolazoline, or atipamazine, xylazine, detomidine), have been ezole. arAgonists should not be used as
userl extensively for anesthesia of
the sole anesthetic agent in dangerous
ungulates, elephants, and rhinoceros. The
carnivores, because the animals may appear antagonist of choice for these opioids is sedated but can respond aggressively when
naltrexone, a pure narcotic antagonist,
stimulated. Peripheral vasoconstriction
which induces complete reversal when
caused by these agents alone or in
given at 100 mg of naltrexone per mg of
combination witl1 other drugs can lead to
opioid. The reversal dosage of naltrexone
significant hypertension, so blood pressure
can be given IV or IM, and in species prone
should be monitored. Peripheral vasoconto renarcotization after reversal, additional striction may also interfere with monitoring
naltrexone may be administered SC. It can
pulse oximetry and can make venipuncture
also be given IM 6-8 hr later by remote
more difficult.

delivery to prevent renarcotization when

The cyclohexanline ketanline ( either
the animal is not being observed. Accidental
alone or in combination with tranquilizers
exposure of people to ultrapotent narcotic
or sedatives such as xylazine or medetomianalgesics is quite dangerous. Therefore, dine) is a common anesthetic for small to
they should be used only by trained,
medium-sized man1mals, especially
experienced personnel, and only after
carnivores, p1irnates, and some ungulates.

development of accidental exposure

A concentrated ketarnine preparation (200
protocols.

mg/mL) can be obtained from compounding

Various drug combinations ( using
pharmacies, with a resultant decrease in the ketarnine, telazol, medetomidine, detomirequired irtjection volume. Combining dine, butorphanol, midazolan1, diazepam, or
ketamine with a sedative or tranquilizer
xylazine) have been developed for specific
speeds induction, minimizes excitement,
species and purposes. Administration to
increases muscle relaxation, and provides
novel species should be undertaken with
a smoother anesthetic induction and
care.

recovery than using ketamine alone. The

Isoflurane has become the inllalation
ability to reverse the sedative effects of
anesthetic of choice for small man1mals,
xylazine or medetomidine with the
birds, and reptiles. It is also used as a
antagonists yohimbine, tolazoline, or
supplement to an irtjectable anesthetic or as
atipan1ezole enables the use of a lower
an anesthetic maintenance agent to prolong
ketarnine dosage and a more complete and
anesthesia in virtually all species. Isoflurane

2052

ZOO ANIMALS
is safe and potent and has minimal adverse

Baylisasca.ris, etc. Recognition of these
effects, short induction, and quick recovery
zoonotic diseases and institution of
periods. Sevoflurane has the advantage of
procedures to minimize the disease risk
even sho1ter induction and recovery
to zoo staff and the visiting public are
periods and may be preferred over
important components of a zoologic

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isoflurane in some species. Small animals
practice. An occupational health 19rogran1
can be induced with a face mask or placed
should be developed for personnel coming
in an anesthetic chamber. Inhalation
in contact with collection animals. Personal
anesthesia can be maintained or suppleprotective equipment ( eg, disposable mented using a face mask, nasal cannulae,
gowns, gloves, face shields) should be used
or intratracheal intubation, depending on
as required by zoo personnel. Frequent
the species and anesthetic plane.

hand washing is also recommended. (See
also ZOO NOSES, p 2414.)

Regulatory Issues: Collection, transport,
and exhibition of wild animals requires

COMMON DISORDERS AND
compliance with local, state, and federal
laws. Permits may be necessary to maintain

PROCEDURES
these species. Institutions in the USA must

In general, the disease processes and treatcomply with appropriate rules and ments of zoo species are similar to those
regulations such as those of the USDA,
of domestic pets, agricultural species,

United States Fish and Wildlife Service,
laboratory animals, or people. Commonly

National Oceanographic and Atmospheric
encountered medical problems include acute

Administration, and National Marine
or chronic gastroenteritis, traun1atic irtjuries

Fisheries Service. Some specific health

(bite or gore wounds, lacerations, fractures,
requirements in the USA include compliluxations), localized (abscess or cellulitis) or ance with the USDA's Animal Welfare Act
generalized (septicemia) bacterial infections,
and CDC regulations governing importation
parasitic infestations, obstetric problems,
of primates and maintenance of colonies of
lameness, aithritis, and GI foreign bodies.

captive bats. The Drug Enforcement Agency

AvianAspergillus infection generally governs the purchase and use of controlled
results in chronic respiratory tract disease
substances in the USA. Specific regulatory

(seep 1901). Affected birds may exhibit
rules and regulations may dictate manageweight loss, markedly increased WBC
ment of certain species. As an example, in
counts, ai1d in later stages, dyspnea. Death
the USA, the USDA requires that elephants
ca.J1 also occur peracutely if there is a
have three negative trunk wash cultures for
localized aspergilloma that occludes the
tuberculosis during a 12-mo period,
trachea or in cases of fungal septicemia.

collected on separate days, preferably

Necropsy generally demonstrates extensive
during a 7-day period.

fungal granulomas in the air sac and lungs.

Species that are more sensitive to Aspergil

Zoonoses: Many human infectious and
lus infections are penguins, pheasants,
parasitic diseases are of animal origin, ie,
and waterfowl. Treatment is generally
are zoonotic. Free-ranging and captive wild
unrewarding because of the advanced
animals may harbor zoonotic diseases that
state of infection when diagnosed but can
pose a potential health risk for those who
include oral (flucytosine or itraconazole), IV
work with these animals. Reptiles are

( ainphotericin B), or nebulized ( enjlconacommonly asymptomatic caniers of zole) 3.11tifungal medications.

Salmonella spp. Avian species may be

Infectious pododermatitis (bwnbleinfected with Chlamydia spp. Tuberculosis foot) is a common disorder of birds. It can
infections in manunals, especially primates,
be either willateral or bilateral and is
ungulates, and elephants, can be transmitcharacterized by lameness, inflainmation, ted from people or harbored and shed by
and swelling of the footpad due to localized
animals to infect zoo staff. Many enteric
bacterial infection. Sequelae of infection can
bacterial or parasitic pathogens of primates
include chronic pododennatitis, septicemia,
can be transmitted to people. Bats may be
or ai11yloidosis. It can occur due to irtjury,
a source of Histoplasma spp or rabies.

infection, inappropriate substrate, obesity,

Carnivorous species of reptiles, birds,
or unilateral linlb problems (trawna,
and mammals that consume uncooked
arthritis) that result in excess and abnonnal
meat-based commercial diets or whole prey
weight bearing on the contralateral foot.

may develop an asymptomatic Salmonella

Treatment includes correction of the
canier state. Numerous zoo species, as well
primary problem, local and systemic
as feral domestic or native species on zoo
antibiotic and symptomatic treatment, and
grounds, may harbor LeJ)tospira spp,
in more advai1ced cases, surgery.

ZOOANIMALS

2053

Avian mycobacteriosis is a chronic
tuberculosis; however other species,
problem in many bird collections, and
including M bovis, have caused clinical
control measures are difficult, because
disease in elephants. Asian elephants are
premortem tests are unreliable (see
more frequently infected than African

TUBERCULOSIS, p 2869). Aggressive sanitation
elephants. Clinical signs are nonspecific and

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of the infected enclosures and culling of
usually present only in advanced cases; tl1ey
infected and exposed birds may help limit
include chronic weight loss, anorexia,
disease dissemination but will not eliminate
weakness, exercise intolerance, discharge
it. Marsupials and young primates may also
from the trw1k, cough, and dyspnea.

develop infection when exposed to infected

Definitive diagnosis is by culture. Screening
birds or contaminated environments ( such
by serologic testing, including imrnunochroas in a mixed species exhibit). The disease matographic (lateral flow), multi-antigen
in marsupials can manifest by development
print in1rnunoassay, and dual patl1 platform
of lung or bone lesions and is resistant to
test, are not confimlatory and are not used
most therapies. The disease in prin1ates is
as definitive regulatory tests. The USDA has
often benign but may result in nonspecific
established testing and treatment protocols
tuberculin test responses.

for captive elephants in tlle USA.

Prevention of flight in birds is accom

Hoof and nail trims are necessary when
plished by amputating one wingjust distal
overgrowth occurs and are most often
to the radiocarpaljoint (pinion) or less
required in rwninants, equids, elephants,
commonly by perfomling a tenectomy and
rhinoceros, and larger carnivores. These
fusing the radiocarpaljoint. Pinioning of
procedures should be conducted on a
young birds soon after hatching is easier
regular basis to avoid excessive overand more successful. TI1e appropriateness growth. On occasion, the services of an
of perfomling this procedure on birds is
equine farrier are used for more complicontroversial. (See also ROUTINE GROOMING
cated cases such as when an equid has

PROCEDURES, p 1888 et seq.)

foundered. Elephant foot care is especially

Bone fractures are repaired with splints, important to prevent chronic musculoskelcasts, surgical fixation, or a combination of etal problems and can usually be accomthese methods. Because maintaining a plished in an awake elephant through
splint on a zoo animal can be difficult, rigid
training. Many other species require
internal fixation or an external fixater are
chemical immobilization for foot care.

preferable. For best results, fixation should

Mandibular osteomyelitis (lumpy jaw)

be rigid, strong, and require minin1al
is a common problem of small rwninants
postoperative care. Because casts must
and macropods ( wallabies and kangaroos).

be left in place for 6--8 wk, freedom of

It can occur secondary to coarse feed, oral
movement and a rnininlwn of discomfort
trauma, or dental disease. Animals generally
must be assured. Newer lightweight, strong,
present with localized facial swelling and a
waterproof, fiberglass casting material is
foul oral odor or discharge. Treatment
especially useful.

consists of lancing the abscess, debriding

Mammalian tuberculosis still
infected bone, removing affected teeth if
occasionally occurs in zoo collections, and
indicated by radiographs, and treating with
routine screening of primates, hoofstock,
systemic antibiotics.

elephants, and keeper staff is indicated ( see

Dentistry in zoo animals presents wlique
p 687). Interpretation of intradern1al
problems. The roots of canine teeth in
tuberculin tests can be problematic in
primates and carnivores are more extensive
nondomestic species because of the
tllan the exposed crown. Simple traction
occurrence of nonspecific responses. When
and rotation cannot remove such teeth
a test is suspicious or positive, a complete
intact; dislodging with a dental elevator
health evaluation should be performed,
is essential. A small electric drill or bone
including additional tests such as radiochisel is used to remove a section of graphs and gastric and bronchial lavage
alveolar bone around the root. Root canals
for mycobacterial cytology and culture.

are indicated when a large canine tooth is

Diagnostic immunologic tests are available
fractured and viable pulp exposure occurs.

for zoo bovids and cervids and include

Specialized long dental instruments are
lymphocyte stimulation tests and ELISA.

required to remove the nerve tissue from

Other tests under development include
these elongated canals. The incisor teeth of
antigen 85 and )'-interferon testing. The
rodents, such as beavers, porcupines, and
incidence of elephant-to-hwnan transmiscapybaras, grow continually; unless these sion of tuberculosis has increased in recent
animals are supplied with coarse feed or
years. Most cases of tuberculosis in

Jogs to gnaw on, their incisors grow
elephants is caused by Mycobacterium
excessively and interfere with their ability

2054

ZOO ANIMALS
to feed. Periodontal disease in zoo animals
head, neck, trunk, and thoracic limbs.

is treated by routine cleaning ( under general Cyanosis of the tip of the tongue that anesthesia) and by providing adequate
progresses caudally and hemorrhage of
chewing substances to supplement the soft,
the tongue and oral ulcers are also seen.

prepared diets fed to many zoo animals.

Antemortem diagnosis is cun-ently made

Because of excellent management,
by PCR analysis of whole blood. Early,

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husbandry, nutrition, and veterinary care,
aggressive treatment with antiviral agents
many zoo animals live to advanced ages.

(farnciclovir or ganciclovir) with good

Care of geriatric specimens is becoming
supportive care has decreased the mortality
increasingly common, including such
rate since 2009.

disorders as diabetes, heart failure, chronic

Since the emergence of West Nile virus
arthritis, and neoplasia. The same
in the USA in 1999, it has been detected in 22
diagnostic and therapeutic principles of
orders of birds, 8 orders of mammals, and 2
management of these disorders in people
orders of reptiles. Man1mals showing
or domestic anin1als may be successfully
clinical infections in zoos include alpacas,
applied to the care of affected zoo aninlals.

sheep, reindeer, harbor seals, Indian

Elephant endotheliotropic herpesrhinoceroses, a polar bear, a wolf and virus infection (EEHV) is one of the
several domestic canids, a Barbary
most significant disease threats to captive
macaque, white-tailed deer, and a killer
elephants. Several virus types that cause
whale. Clinical signs have also been seen
disease have been described, although viral
in alligators.

latency is common. EEHV primarily causes

Highly pathogenic avian influenza
acute hemon-hagic disease, mostly in young

(HPAI) is a threat to zoo bird collections.

Asian elephants (Elaphas maxim us) with a Zoos should develop HPAI response plans mortality rate of up to 85%. Clinical signs are and establish a dialogue with state and predominately nonspecific and include
national agricultural regulatory agencies
lethargy, anorexia, mild colic, and
to mitigate the impact of HPAI on zoo
tachycardia. There is often edema of the
collections.

VACCINATION OF EXOTIC MAMMALS

Exotic mammals are susceptible to many
fitness in critically endangered manunals.

of the san1e infectious diseases that affect

Certainly, infectious disease outbreaks in
domestic manunals. However, vaccination
small nwnbers of highly genetically valuable
of these species is often extra-label, because
individuals can disastrously affect conservavaccines are tested and approved for use tion projects. Unfortunately, the biology of
only in domestic species. Vaccination
many of tl1ese preventable diseases
protocols recommended for exotic

(incubation pe1iod, transrnissibility, etc) in
manunals are therefore based on limited
exotic mru.11mals is often Wlknown. Captivity
published infom1ation, anecdotal expe1imay enhance the risk of acquiring disease ence, and relative risk of disease to the
based on food sources, exposure to rodents
species from the infectious agent or
and otl1er disease hosts, and ru.1 unknown
vaccination itself. Reports of lack of serodegree of exposure of other zoo anin1als, conversion, antibody production, sustained
which is unlikely to occur in nature. Thus,
protection, and induction of the disease
due consideration of protection of captive
resulting in morbidity and mortality in a
nondomestic species, even those destined
vruiety of species, particularly for rabies ru.1d
for release to the wild, is warranted. Core
distemper, are common after vaccination of
vaccines ru·e designated as those that protect
exotic manunals. Regardless, vaccination
captive animals from li.fe-ttu·eatening,
should be considered in captive wildlife and
globally distributed diseases. The detemiinaconservation prograJ.11S based on a number tion of protection has largely been based on
of factors. Many diseases preventable by
studies in domestic species; nonetheless,
vaccination such as canine distemper virus,
based on cun-ent knowledge, these vaccines
canine parvovirus, feline calicivirus, feline
deserve full consideration for inclusion into
panleukopenia virus, and rabies virus have
vaccination reginlens for captive exotic
caused population declines or reduced host
mrunmals.

VACCINATION OF EXOTIC MAMMALS

2055

Individual animal safety dictates that
elsewhere in tl1e Manual, and the reader
inactivated or recombinant viral or bacterial should refer to the relevant chapters. In vaccines are preferable to modified-live
domestic mammals, young anin1als have
virus (MLV) vaccines, which have the
differing vaccine schedules than those
potential to cause disease in exotic
presented in TABLE 36 based on waning
mammals and abmtions in hoofstock.

maternal antibodies. Consideration of the

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However, in select species, especially Old
provided references and consultation with

World apes, MLV vaccines have received
experts in zoo medicine and exotic manm1al
sufficient use to wan·ant consideration
husbandry are reconunended to develop
based on the se1ious risk of morbidity and
vaccination protocols. Specific vaccine
mortality. Use ofMLV vaccines for rabies
protocols should be developed for
and distemper are generally contraindicated neonates. For apes, a yow1gster vaccination in exotic man1mals. In particular, use ofMLV schedule, based on tl1e hwnan schedule, distemper vaccines in exotic mammals may
should include tl1e killed polio se1ies and
result in postvaccinal myelitis or distemper.

Haemophilus vaccination (see www.

Recently developed canary pox-vectored
cdc.gov/vaccines/schedules/index.html).

vaccines are the current vaccine of choice

Although titer detem1inations may be
for distemper and appear botl1 safe and
useful for evaluation of vaccination in
efficacious. The following concepts should
exotic manunals, the la.ck of antibodies
be considered before extra-label use of a
does not equate to lack of immune
vaccine in an exotic anin1al. Possession
response. This method quantifies only
of the anin1al should be legal per state
tl1e Immoral immW1e response, not the
conununity and other applicable laws.

cell-mediated aspect, and protective titer

Infonned consent of the owner and
levels for exotic manunals have not been
discussion of the availability or lack of
evaluated or established. Examples of titers
safety and efficacy trials associated with the
that may be assessed include rabies,
use of this vaccine in the animal should be
distemper, parvovirus, and leptospires, as
documented in the medical record. Use of
well as the encephaJitjc viruses and many
product and vaccination procedures with
vii.uses affecting nonhuman primates that
record of previous success such as those
also affect people. Yearly and preshipment
used or recommended in zoo (Association
vi.J.·al titers, which vary based on species,
of Zoos and Aquariums or American
are recommended for all primates. Titers

Association of Zoo Veterinarians) protocols,
change based on natural disease exposure,
and those with publications supporting
independent of vaccination, may or may not
their safety and efficacy in the species,
confer protection from disease, and may
should be considered. Vaccination may be
also wane quickly, despite repeated
foregone in tl1e face of lack of data to
exposure.

support that a certain disease occw·s,
despite antibody presence, in some species.

Bovine Herpesvirus 1: Inactivated and

Vaccination protocols developed for
attenuated-live vaccines for infectious
exotic manmrnls should be detennined with
bovine rhinotracheitis and infectious
respect to number of anin1als, husbandry,
pustular vulvovaginitis are available.

relative value of anin1al and offspring,

Vaccines may not prevent infection but
pregnancy, species susceptibility to a
reduce clinical signs and significantly
disease, likelihood of encountering disease,
reduce shedding of field virus. Use of the
disease prevalence in the surroW1c!ing
inactivated vaccine in exotic hoofstock
locality, ability to obtain useful products,
may be preferred, because abortions and
infonnation of reported or anecdotal
initiation of disease in vaccinated hoofstock
benefits or disadvantages with usage of a
have not been adequately studied.

vaccine in that species, housing and vector
control programs, and zoonotic and

Canine Distemper: Most, if not all of the
infectious potential of the disease. As in

Carnivora, including canids, procyonids,
domestic species, animals that are feb1ile or
mustelids, and the vive1Tids, are considered
have other clinical signs of illness should
susceptible to canine distemper virus
not be vaccinated. Because a full vaccine

(CDV); the susceptibility of most Ursida.e
dose is required to elicit a satisfactory
and Hyenida.e is W1known. Giant and red
inunune response, remote vaccine
pandas are an important exception among
administration should be weighed against
the ursids and appear quite susceptible;
anesthetic and disease risk Some nondocanine distemper vaccination has been mestic mammals and their reconunended
specifically evaluated in and is recomvaccination protocols ( eg, cervids, rodents, mended for use in this species. Large felids,
lagomorphs, can1elids) are reviewed
particularly tigers and lions, also appear

2056

VACCINATION OF EXOTIC MAMMALS
susceptible to disease, which in exotic
canary pox-vectored subunit distemper
mammals manifests primarily in the
vaccine, which causes approp1iate serologic
neurologic fom1. CDV is considered a core
titers and appears safe and effective, is now
vaccination in captive canids and should
recommended for use in susceptible exotic
also be considered in captive exotic felids
mammals. Generally recorrunended

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with a history of disease in the collection.

vaccination regimens for young anin1als

Many species of small carnivores have
incorporate an initial vaccination after
developed vaccine-induced distemper after
weaning with a 1-mo booster followed by
receiving an MLV vaccine. The recombinant
yearly revaccination. Vaccination of

IH=lllil VACCINATIONS RECOMMENDED FOR EXOTIC MAMMALSVaccination Animal Group

Disease or Vaccine

Vaccine Typea

Frequency

Primates (especially

Poliomyelitis

MLV

Annual

Pongidae): monkey,

Measles

MLV

Annual
ape

Mun1ps

MLV

Annual

Rubella

MLV

Annual

DPTb or tetanus

K

Annual

Canidae: fox, wolf,

Canine distemper

Vectored, MLVd

Annual
coyote, wild dog

Canine adenovirus 2

MLV

Annual

Canine parvovirus

K

Annual

Canine parainfluenza

MLV

Annual

Leptospira bacterin-Clc

K

Annual

Felidae: exotic cats

Feline panleukopenia

K/MLVct

Annual

Feline rhinotracheitis

K/MLV

Annual

Feline caliciviruses

K/MLV

Annual

Mustelidae/Viverridae/ Canine distemper

K/MLV, Vectorectct Annual

Procyonidae: raccoon, Feline panleukopenia

K/MLV

Annual
skunk, ferret, coati,
genet, otter, weasel,

Canine adenovirus 2

K/MLV

Annual
mink, kinkajou
bacterin-CI

Leptospira bacterin-CI

K

Annual

Ursidae: bear

Canine adenovirus 2

K

Annual

Leptospira bacterin-CI

K

Annual

Hyaenidae: hyena,

Canine distemper"

K/MLV

Annual
aardwolf

Feline panleukopenia0

K/MLV

Annual

Artiodactyla/ Run1inan- BVDf (in endemic areas)

K

Annual
tia: deer, sheep, cattle, 8-way Clostridium bacterin K

Annual
goat, antelope,
can1elids

5-way Leptospira. bacterin

K

Annual or
every6mo

Parainfluenza 3

MLV

Annual

Perissodactyla

Tetanus

K

Annual

Equidae: ass, zebra

EEES

K

Annual

WEEh

K

Annual

VACCINATION OF EXOTIC MAMMALS

2057

VACCINATIONS RECOMMENDED FOR EXOTIC MAMMALS (continued) Vaccination

Animal Group

Disease or Vaccine

Vaccine Typea

Frequency

Equine rhinopneumonitis

K

Every4 mo

VetBooks.ir

West Nile virus

K,DNA

Annual

Iniluenza

K

Annual

Suidae!Tayassuidae:

5-way Leptospira bacterin

K

Annual
pigs, peccaries

Erysipelas bacterin

K

Annual
a MLV ; modified live virus; K ; killed
b Df'r; diptheria, peitussis, and tetanus
c Canicola or IcterohaemotThagiae
d Not ferret origin; recombinant canarypox origin preferred e Controversial; some believe hyaenids are not susceptible

'BYD ; bovine virnl diarrhea
g EEE ; Eastern equine encephalomyelitis
h WEE ; Western equine encephalomyelitis
free-living animals should be carefully
rhinotracheitis, and feline calicivirus is
considered, because vaccine efficacy is
preferred for use in exotic mammals.

unknown for many nontarget species, and
animals may have recovered from or be
incubating disease, rendering vaccination

Equine Encephalomyelitis: Because
a poor use of resources.

nondomestic equids are susceptible to
equine encephalomyelitis, vaccination

Canine Parvovirus and Feline
should follow guidelines for domestic

Panleukopenia: Canine parvovirus,
equids in endemic areas. lnactivated
raccoon parvovirus, and feline panleukopetrivalent (Eastern, Western, Venezuelan) or nia virus are closely related antigenically
bivalent (Eastern, Western) vaccine, or a
and pathogenetically. Canidae, Felidae,
combination of these with tetanus toxoid,
most Mustelidae, Procyonidae, and
are administered according to manufacturer

Viverridae are considered susceptjble
instructions. lnitial immunization is two
to one or more of these parvoviruses.

doses, 1-2 wk apart with armual revaccina

Binturongs are susceptible to feline
tion. Although susceptibility of tapir species
panleukopenia, and vaccination is
is unknown, a similar vaccination regimen
recommended. Vaccinations that protect
has been recorrunended in this species. The
from feline panleukopenia are considered
susceptibility of exotic equids to West Nile
core vaccines in exotic felids, while those
virus is unclear, but zebra, tapir, and related
that protect from canine parvovirus are core species are often vaccinated for West Nile vaccine for canids. Based on insufficient
virus; efficacy and safety of the inactivated
attenuation ofMLV vaccines for some
equine (more commonly used) or the DNA
species, only inactivated vaccines of tissue

West Nile virus vaccination in these species
or tissue-culture origin are recommended
is unknown.

for use in exotic mammals. Vaccine and
dosage regimen have been empirically

Equine Herpesvirus 1 Infection:

detem1ined but should adhere to label direc

Equine herpesvirus 1 (EHV-1) can cause
tions, with boosters recommended at 2 wk,
abortion in exotic equids; killed virus

6 mo, and then armually. Based on reports of vaccination is recommended, because vaccine reaction associated with MLV
adequacy of attenuation in MLV vaccines is
combinations of canine distemper, canine
unknown for nontarget species. Vaccination
adenovirus 2, canine parainfluenza, and
of foals should begin at 4 mo, with boosters
canine parvovirus, multivalent vaccination
at 4-mo intervals up to 1 yr. Mares must be
with killed feline panleukopenia, feline
vaccinated often to provide protection from

2058

VACCINATION OF EXOTIC MAMMALS
abortion, because EHV-1 natural protective

Infectious Canine Hepatitis (Canine
immunity after infection lasts only 4 mo.

Adenovirus 1 ): All Canidae and binturong, a viverrid, are susceptible; Ursidae Erysipelas: The bacte1iumErysipelo
may also be susceptible. In foxes, the

VetBooks.ir
lhri.x rhusiopalhiae is pathogenic for
disease is called fox encephalitis due to a
the Tayassuidae, nondomestic Suidae,
predominant neurotropism and neurologic
cetaceans, and pinnepeds. Erysipelas
signs. Canine adenovirus (CAV) is a'core
bacterin can be administered with the
vaccination for captive cru1ids. Because a
standard regimen to nondomestic swine and
killed vaccine is not conu11ercially available,
peccaries (seep 2817). Despite the impormultivalent MLV vaccines containing canine tance of preventing erysipelas in mruine
distemper and CAV-1 or CAV-2 ru·e often
mrurnnals, there is no bacte1in designed
administered. Based on the close antigenic
specifically for these animals. Vaccination of
relationship of CAV-1 and CAV-2, vaccinacetacerulS and pinnepeds is controversial, tion with either virns provides cross-protecbut a subunit vaccine has been investigated tion. CAV-2 is thought less likely to cause
in dolphins ( see also
postvaccinal reactions, such as corneal

BACTERIAL DISEASES OF

MARI 'E
opacity and hemorrhagic and necrotizing

MAMMALS, p 1861). In facilities where
captive cetaceans ru·e vaccinated, extra-label
hepatitis (vaccine-induced adenoviral
bacte1ins ru·e used to prevent erysipelas
hepatitis). However, administration of
outbreak. Based on vaccine breaks, the

CAV-2 MLV vaccine to a mru1ed wolf
necessity of bacterin culture ru1d sensitivity

(Ch1ysocyon brachywus) has resulted
testing before revaccination, and the risks of
in vaccine-induced adenoviral hepatitis.

fatal anaphyla.xis, sterile abscessation, tissue

Therefore, vaccination recommendations
reaction, and ruumal inunobilization, some
for this species ru·e lin1ited to canine
facilities have reduced vaccination to
distemper virns, cru1ine pru-vovirus, and
one-time administration, even though
rabies; vaccination with MLV CAV-2 is
antibody titers fall below the presumed
contraindicated in this species. For other
effective level. Booster at 6 mo and rumual
cru1ids, reconu11ended vaccine regimens are
revaccination are reconm1ended to maintain
a single dose of the multivalent vaccine at
protective antibody titers. Because disease
weru1ing, with monthly boosters w1til 4 mo
apperu-s less conm1on and vaccination is not
of age followed by rumual revaccination.

without significant tisk of morbidity and
mo1tality while protective efficacy remains

Canine Influenza Virus: Canine
unknown, vaccination is not routinely
influenza virus vaccination for domestic
recommended in pinnepeds.

crunivores is considered noncore. However,
if a collection has a history of canine
influenza or is located in an endemic ru·ea,

Feline Caliciviruses: Exotic felids
vaccination may be considered. Vaccination
are susceptible to feline caliciviruses, and
may also be considered for great apes, as
some strains may cause serious morbidity
well as for contact staff on a yeru·ly basis
and mortality. This is considered a core
before flu season. Equine influenza vaccine
vaccine in exotic felids. Vaccines are often
is administered to nondomestic equids in
combined into a multivalent fomrnlation,
some zoos.

and vaccine regimens ru·e as for feline
rhinotracheitis.

Leptospirosis: Leptospirosis occW"S
sporadically in exotic Cru1idae, Procyonidae,

Feline Herpesvirus Rhinotracheitis:

Viverridae, Ursidae, Mustelidae, Suidae,

Feline viral rhinotracheitis is a serious
primates, Tayassuidae, and in Cervidae and
disease threat in exotic Felidae and is
other rununants of the fantilies Bovidae,
considered a core vaccine. Available

Altiodactyla, Perisodactyla, Proboscidae,
vaccines, inactivated, subunit, and MLV, are

Crunelidae, Giraffidae, etc. Vaccination of
combined with feline calicivirns and are
domestic carnivores withLeplospira
usually in multivalent fmmulations with
bacterins is considered noncore. However,
other pathogens ( eg, feline panleukopenia).

if a collection has a history of or is in an

A single dose should be administered at
endemic ru·ea for leptospirosis, vaccination
weaning, with monthly boostern until 4 mo
should be considered with bacterins that
of age and rumually thereafter. In domestic
contain inm1unogens againstLeptospira
cats, vaccination provides reasonable
interrogans serovaJ"S Cru1icola and
disease protection but does prevent

Icterohaemorrhagiae. Carnivores are
infection or viral latency. Vaccinated cats
vaccinated with a 1- or 2-mL dose, lM or SC,
can be infected; however, clinical signs and
at6--8 wk of age, repeated in 14days.

viral shedding are reduced.

Boosters are given every 6 mo. Hoofed

VACCINATION OF EXOTIC MAMMALS

2059
animals are inmmnized with 5 mL of

Rabies: All exotic mrum11als ru·e susceppentavalent bacte1in IM; annual or preferably tible to rabies (seep 1302). Vaccination is semiannual boosters are recommended.

considered core for felids and canids in

Vaccination does not necessarily prevent
endemic areas at1d recommended for
shedding of the causal organism(s).

man1111als in zoos in areas where incidence

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Ruminants, pigs, and peccaries are
of rabies in free-living wildlife is high.

immunized with pentavalent bacterins that

However, the efficacy of parenteral rabies
contain the serovars Pomona, Hardjo,
vaccination of exotic matmnals has not

Icterohaemorrhagiae, Canicola, and
been established, at1d no commercially

Grippotyphosa. Hoofstock should have an
available vaccine is licensed for use in
initial vaccination with a booster 4-8 wk
free-living at1ilnals. Use of rabies vaccines
later (as per label instructions); booster
i.!1 these species is extra-label and is not
vaccination is essential, because leptospiroconsidered protective in the event of a bite.

sis vaccines are killed vaccines. At a

Based on the potential for hun1an rabies
minimwn, hoofstock should be revacciexposure, keeping wild-caught catnivores nated yearly approximately 6---8 wk before
as pets should be discouraged and is illegal
the breeding season. However, because
in many jurisdictions. Wild-caught aninials
protective titers can wane within a year, a
such as foxes, raccoons, and skunks may
semiannual vaccination schedule may be
have been exposed to the vii-us when quite
instituted if leptospirosis is an issue or
young at1d may incubate disease for a
occurs in valuable breeding stock.

prolonged period (>l yr), renderil1g a

Vaccination does not necessarily prevent
shott obsetvation period inadequate. The
shedding of the causal organism(s).

National Association of State Public Heal th

Veterinru·iat1s recommends that wild-caught

Measles, Mumps, and Rubella: Pongiat1ilnals with public contact ( eg, in zoos) dae are often ilmnwlized against measles,
should be quarantined for at least 180 days.

mwnps, and rubella at 2---3 mo of age and

When vaccination is considered
annually thereafter with 0.5 mL ofMLV
necessary, only kille d -virus vaccine should
human vaccine irtjected SC. This vaccination
be used, and it should be administered via
is also reco11U11ended for monkeys. New
deep IM injection. MLV rabies vaccine

World monkeys are more resistant than Old
licensed for use in domestic species should

World monkeys, but mortality is high when
never be used in exotic at1imals, because
infected. Vaccine administration in other
such vaccines are often insufficiently
prin1ates is optional, depending on colonyattenuated at1d may produce clinical rabies specific concerns. Vaccination of susceptlble
at1d death. Several inactivated vaccines
populations of nonhuman prin1ates (>6 mo
prepared of nervous tissue ( eg, mu1ine,
old) should be considered when contact with
ovine, or caprine) or tissue culture have
people cannot be adequately controlled ( eg,
been found satisfactory in terms of safety
nonhwnan primates as pets). Annual booster
at1d immunogenicity, the latter based on
doses are given.

limited tests that demonstrated adequate
at1tibody responses in some exotic

Parainfluenza 3: Exotic sheep and goats
carnivores. The humat1 diploid cell-line
are susceptible to pneumonia caused by
origin killed-virus vaccines appear to have
parainfluenza 3 (PI-3) and Mannheimia
the best ilnmunogenicity in domestic
haemolytica. Modified-live virus PI-3
species. Young animals are vaccinated at
vaccines, particularly those adnlinistered

3---4 mo of age, and vaccinations must be
intranasally are useful to reduce the
repeated annually. Vaccination for rabies of
incidence of pnewnonia in lambs. Vaccine
bats in captivity is done at some institutions;
is adnlinistered at 3---4 mo of age, 1 mL

MLV vaccination of bats incubating the
per nostril, and repeated 3---4 wk before
rabies virus may hasten the disease course
anticipated shipment and annually thereafter. at1d result in death (as occurs in people).

Use of oral bait vaccination for control of

Poliomyelitis: Pri.n1ates, particularly the
rabies in wildlife continues in several

Pongidae (great apes) are susceptible to
countries; this vaccination is not intended
poliomyelitis. Oral trivalent MLV poliomyelitis for use in captive, single animals.

vaccine is preferred to parenteral inactivated
vaccine because of ease of administration. A

Clostridial Diseases: Priniates, exotic
single human dose (0.5 mL) is given PO on a

Equidae, Proboscidae (elephants),
sugar cube after 6 mo of age and annually

Pongidae, Cervidae (deer), camelids, at1d
thereafter. Vaccinated anilnals should be
exotic sheep at1d goats should be ilnmuisolated from unvaccinated ptinlates nized against tetanus. Although the

(including people) for 1 mo after inoculation.

susceptibility of tapirs to tetanus has not

2060

VACCINATION OF EXOTIC MAMMALS
been docw11ented, vaccination is recomwidespread in zoos. Unfortunately, mended. Exotic Equidae and elephants
satisfactory vaccines for many infectious
are vaccinated on the same schedule as
diseases are not available for exotic
domestic horses; primary immunization at
animals. Inactivated BVD vaccines are

3-4 mo of age consists of two IM ir\jections
recommended in situations in which BVD

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of tetanus toxoid, 1 mo apait. A single
has been a problem. Annual vaccination
booster dose is given annually.

witl1 one sta.J.1dard bovine dose IM should

Pongidae are often vaccinated against
begin at 3 mo of age. Satisfactory vaccines
tetanus using the diphtheria, tetanus toxoid,
for bluetongue, epizootic hemorrhagic
ai1d phase 1 pertussis (DPT) vaccines
disease, malignant catarrhal fever, and
intended for use in human children or
encephalomyocarditis virus are not
monovalent hwnan tetanus toxoid.

currently available in the USA. In contrast,

Monovalent tetanus toxoid is preferred,
a nun1ber of vaccines are available for
because pertussis and dipthe1ia are not
extra-label use in exotic man1rnals, which
considered health risks for nonhw11an
may not be efficacious or necessary. These
prin1ates. However, susceptibility of these
noncore vaccines for domestic carnivores
diseases likely varies in primates, because
include feline leukemia virus, feline
olive baboons were recently found to
im1mmodeficiency virus, Chlamydiafelis,
develop clinical signs of pe1tussis and a
feline infectious peritonitis, feline Giardia
strong anamnestic response. Prin1ary
vaccine, coronavirus, and Lyme disease. If
immunization consists of 0.5 mL of vaccine
a collection has a history of these diseases
ir\jected IM on tl1ree occasions at 3-mo
or is in an ai·ea endemic for disease,
intervals, with a booster dose 1 yr alter
vaccination may be considered. Antlrrax
the third ir\jection. Thereafter, booster
vaccine has been administered to cheetal1
immunizations of 0.5 mL of diphtheria

(Acinonyx jubatus) and black rhinoceros
tetanus toxoid or tetanus toxoid alone

(D·ice1·os bicornis) without apparent ill
are given every 3-5 yr or after potential
effect, and conference of protective
exposure due to injury.

inm1unity in some with a single booster

In exotic hoofstock, tl1e need for
was recommended. Vaccination of valuable
clostridial vaccines depends on animal
animals could be considered in the event of
husbandry and density, environment, ai1d
an outbreak. Brucellosis affects both
local disease circw11stances. If vaccination
free-living and captive marine mammals,
is waiTanted, vaccines should be given
with minimal apparent zoonotic potential.

according to manufacturers' recommenda

No vaccination or oilier control methods
tions for hoofstock. Multivalent clostridial
for brucellosis are established for these or
vaccines are available for prophylaxis;
other exotic man1rnal species in captivity.

teta.J.1us antitoxin can be used if tetanus is

Vaccination programs for free-living bison
a concern. Pregnant animals she>Uld be
and cervi.ds are controversial. Although the
vaccinated 4-8 wk before paiturition to

MLV vaccine effectively prevents future
increase specific colostral immunoglobuabortions and the transmission of lins. Neonates can be vaccinated at4 and 8
brucellosis, it does not protect from
wk of age with Clostridium pe1fringe.:ns
infection or seroconversion, may induce
type C and D. Exotic sheep, goats, and
abortions in pregnant a.J.timals, and is
cervids ai·e sometimes vaccinated beginning infectious to people. The reemergence of at 10-12 wk of age with multivalent
brucellosis worldwide ai1d an increasing
clostridial bacterin-toxoids containing
incidence of hun1a.n disease underscore the
immunogens for Clostridium tetani, C
need for new and improved brucellosis vac
perf1ingens (types B, C, D), C septicum, cines. The vaccinia, cowpox, and smallpox

C chauvoei, C novyi, C sordellii, and C

(variola) viruses are closely related pox
hamnolyticum in areas of high exposw·e
viruses that may have all evolved from a
risk. The initial dose is 5 mL followed in 6
single ancestral virus. Cowpox virus has
wk by a 2-rnL dose, administered SC. A 2-mL
caused morbidity and mortality in canids,
booster dose should be given annually.

felids, equids, elephai1t, rhino, camelids,
viverrids, rodents, primates, and hoofs

Miscellaneous: A nwnber of infectious
tock; zoonotic disease has been reported.

diseases, including bovine viral diarrhea

Vaccinia titers have been docWllented in

(BVD), bluetongue, malignant cata.J.Thal
free-living nonhwnai1 primates in Soutl1
fever, epizootic hemorrhagic disease of

An1erica. The CDC currently limits distribudeer, anthrax, encephalomyocarditis virus, tion of vaccinia. vaccine to health care and
cowpox, ai1d brucellosis, may appear as
bioindust1ial laboratory workers witl1
serious local problems but are not
exposure risk.

MANAGEMENT AND

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NUTRITION

INTRODUCTION 2066

BIOSECURI TY 2068

Principles of Biosecurity 2069

The Three Levels of Biosecurity 2071

Developing a Biosecurity Program 2071

Bioexclusion 2071

Surveillance 2073

Biocontainment 2073

Handling Disease Outbreaks 2074

CLONING OF DOMESTIC ANIMALS 2075

Technical Aspects of Cloning 2075

Status of Cloning Domestic Animals 2076

Rationale for Cloning 2077

Controversies 2077

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE 2078

Acupuncture 2079

Manual Therapy 2081

Laser Therapy 2083

Herbal Medicine 2084

Nutraceuticals and Dietary Supplements 2086

Homeopathy 2087

MANAGEMENT OF THE NEONATE 2087

Large Animals 2087

Failure of Passive Transfer 2088

Sepsis in Foals 2089

Specific Clinical Manifestations of Sepsis 2092

Neonatal Pneumonia 2092

Omphalitis, Omphalophlebitis, and Patent Urachus 2092

Neonatal Uveitis 2093

Septic Arthritis 1062 (MUS)

Neonatal Encephalopathy 2094

Meconium Impaction 2096

Small Animals 2096

Care of Orphaned Native Birds and Mammals 2100

PAIN ASSESSMENT AND MANAGEMENT 2104

Pain Perception 2104

Recognition and Assessment of Pain in Animals 2105

2062

MANAGEMENT AND NUTRITION

PainAlleviation 2106

Analgesic Pharmacology 2107

Opioids 2107

Nonsteroidal Anti-inflammatory Drugs and Corticosteroids 2110
a2-Agonists 2110

Ketamine 2110

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Other Analgesic Agents 2111

Local and Regional Analgesic Techniques 2111

Chronic Pain 2112

Osteoarthritis Pain_ 2113

Cancer Pain 2113

STR AY V OLTAGE IN A NIMA L HOUSING 2113

VE NTILATION 2116

Air Quality 2116

The Dilution Effect of Ventilation 2117

Cold Weather Ventilation 2117

Wann Weather Ventilation 2119

HE ALTH-MANAGEMENT INTERACTION

AQUA C ULTURE and AQUATIC SYSTE MS 1743 (EXL) BEEF CATTLE 2119

Beef Cattle Breeding Herds 2119

Reproduction 2120

Cull Cow Selection and Management 2120

Nutritional Management 2121

Health and Production Management Program 2122

Vaccinations 2122 ·

CalfManagement 2122

Replacement Heifers 2125

General Health Managemeilt Considerations 2126

BeefFeedlots 2126

Economic Impact of Disease 2127

Implementing a Feedlot Medicine Program 2127

Feedlot Records 2128

Vaccination Protocols 2129

Nutritional Advice 2129

Disease Epidemics 2129

Control and Prevention of Disease 2130

Beef Quality Assurance and Beef Safety Programs 2133

Development of Antimicrobial-resistant Bacteria 2134

DAIRY CATTLE 2135

The Modem Dairy Industry 2135

Animal and Herd Productivity 2136

Interactions Between Health and Production 2139

The Health Management Program 2140

MANAGEMENT AND NUTRITION

2063

GOATS 2147

HORSES 2151

PIGS 2160

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SHEEP 2164

SMALL ANIMALS 2169

MANAGEMENT OF REPRODUCTION

CATTLE 2171

Nutrition 2171

Breeding Program for Heifer Replacements and Cows 2172

Bull Reproductive Management 2174

Breeding 2175

Artificial Insemination 2175

Pregnancy Determination 2176

Embryonic Death, Abortion, and Abnormal Fetal Development 2177

Calving Management 2178

Dystocia Management 2180

Cow-Calf PairManagement 2181

GOATS 2182

Puberty and Estrus 2182

Breeding Soundness Examination 2183

Breeding 2184

Induction of Estrus 2184

Pregnancy Determination 2185

Pregnancy 2186

Parturition 2186

HORSES 2187

Reproductive Cycle 2187

Breeding Soundness Examination of the Mare 2189

Pregnancy Determination 2194

Parasite Control During Pregnancy 2195

Vaccinations 2195

Abortion 2195

Parturition 2196

Dystocia 2198

Examination of the Fetal Membranes 2199

The Early Postpartum Period 2200

Breeding Soundness Examination of the Stallion 2200

Breeding 2201

PIGS 2201

Sow and Gilt Management 2202

Boar Management 2203

Breeding Management 2207

2064

MANAGEMENT AND NUTRITION

SHEEP 2212

Reproductive Physiology 2212

Measuring Reproductive Performance 2213

Factors Affecting Reproductive Performance 2214

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Breeding Programs 2215

Pregnancy Determination 2216

Prenatal Losses 2216

Ram Management 2217

Artificial Insemination 2218

SMALL ANIMALS 2219

Breeding Soundness Examination 2219

Breeding Management 2221

Manipulation of the Estrous Cycle 2225

Pregnancy Determination 2225

Prevention or Termination of Pregnancy 2226

Whelping and Queening 2227

Labor and Delivery 2227

Postpartum Care 2228

Periparturient Problems 2228

Infertility 2229

BREEDING SOUNDNESS EXAMINATION OF THE MALE 2230

Bulls 2231

Rams 2233

Bucks 2234

Stallions 2234

Boars 2237

Dogs 2237

EMBRYO TRANSFER IN FARM ANIMALS 2239

Cattle 2240

Sheep and Goats 2242

Pigs 2242

Horses 2242

HORMONAL CONTROL OF ESTRUS 2244

Horses 2245

Cattle 2245

Goats and Sheep 2246

Pigs 2247

Dogs 2247

Cats 2248

NUTRITION

BEEF CATTLE 2248

Nutritional Requirements 2248

Feeding and Nutritional Management 2263

The Breeding Herd 2263

MANAGEMENT AND NUTRITION

2065

Stocker Cattle 2263

Finishing Cattle 2264

Performance Modifiers 2264

DAIRY CATTLE 2265

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:Nutritional Requirements 2265

Feeding and Nutritional Management 2278

Feeding Young Calves 2280

Feeding Calves from Weaning Through Maturation 2282

Accelerated Calf-rearing Programs 2283

Feed Additives 2284

Nutrition and Disease 2284

EXOTIC AND ZOO ANIMALS 2287

Birds 2288

Psittacines 2288

Passerines 2290

Columbiformes 2290

Raptors 2291

Piscivorous Birds 2291

Waterfowl 2292

Gallinaceous Birds 2292

Ratites 2292

Mynahs 2293

Toucans 2293

Managing Avian Zoological Collections 2293

Mammals 2293

Handrearing Zoo Mammals 2293

Bats 2294

Carnivores 2296

Insectivores, Edentates, and Aardvarks 2297

Marine Mammals 2297

Marsupials 2298

Primates 2299

Rodents and Lagomorphs 2300

Subungulates and Ungulates 2301

Reptiles 2302

Crocodilians 2306

Snakes 2306

Turtles 2306

Tortoises 2307

Lizards 2307

Fish 2307

GOATS 2308

Nutritional Requirements 2308

Herbage and Browse Utilization 2310

Nutritional Diseases 2311

2066

MANAGEMENT AND NUTRITION INTRODUCTION

HORSES 2312

Nutritional Requirements 2313

Feeding Practices 2321

Nutritional Diseases 2323

Feeding the Sick Horse 2328

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Feeding the Aged Horse and the Orphan Foal 2329

PIGS 2329

Nutritional Requirements 2329

Feeding Levels and Practices 2340

Major Feed Ingredients 2341

Feeding Management of Sows and Litters 2342

Feeding Management of Weanling Pigs 2342

Growth Stimulants 2342

Nutritional Diseases 2343

RABBITS 1937 (EXL)

SHEEP 2345

Nutritional Requirements 2345

Feeding Practices 2348

Farm Sheep 2348

Ewes 2348

Lambs 2349

Mature Breeding Rams 2351

Range Sheep 2351

Nutritional Diseases 2353

SMALL ANIMALS 2354

Nutritional Requirements and Related Diseases 2354

Nutrient Classifications 2366

Dog and Cat Foods 2373

Pet Food Labels 2373

Pet Food Product Types 2374

Feeding Practices 2376

Nutrition in Disease Management 2379

MANAGEMENT AND NUTRITION

INTRODUCTION

Almost all domesticated animals rely on

Genetic advancement has led to continual
their caretakers to maintain their health and
increases in productivity that place similar
well-being, to provide appropriate nutrition,
continual pressure on animal husbandry
and to meet behavioral needs and any special management to ensure it does not limit physiologic requirements. The success
animal health, well-being, or productivity.

of proper management and nutrition is

Proper management and nutrition are
especially important to agricultural species
also central to the prevention and control
that must sustain growth and production.

of infectious and noninfectious diseases.

MANAGEMENT AND NUTRITION INTRODUCTION

2067

Infectious diseases occur after colonization
address risk factors unique to particular
of an animal by microbes ( eg, a bacterium,
pathogens and diseases.

virns, rickettsia, parasite), but simple

The need to identify and implement
infection by a microorganism is not usually
multifaceted management strategies
sufficient for disease to develop. Environthat will maintain health and enhance mental and host factors influence whether
productivity is likely to increase in animal

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the animal will develop clinical or subcliniagriculture. This need for new strategies is cal disease or have impaired productivity.

driven by competitive and economic forces

Management has a substantial impact on
within the industry and by pressure for
environmental and host conditions that
change from interested parties outside
contribute to disease susceptibility.

agriculture. Identifying and implementing

Eradication and exclusion of specific
these management changes requires
organism( s) that cause disease is the only
collaborative efforts of all groups working
certain way to prevent infectious disease.

in livestock production, including veterinar

This is usually impractical or impossible
ians, animal scientists, and nutritionists, with
for many conrn1on diseases of agricultural
consideration of economic and other forces
animals. As a result, it becomes necessary
acting on producers.

to control rather than to prevent infectious

All of agriculture, but particularly
disease by reducing circumstances that
animal agriculture, is under pressure from
favor the presence or the spread of the
consun1er and special interest groups to
infectious agent, by mitigating environmenaddress concerns arising from some industry tal circumstances that cont1ibute to developpractices. These concerns include potential ment of disease once animals have become
links between aglicultural practices and
infected, and by minimizing circumstances
antimicrobial resistance in hun1an pathothat increase host susceptibility. Circumgens, relationships between envirornnental stances that contribute to the development
contanlination and intensive animal
of a disease are called 1isk factors, and they
production, the role of agricultural
can be related to the microbe, the environmanagement practices in reducing the risks ment, or the host. Identifying and mitigating
of foodbome illnesses and risks of exposure
the impact of risk factors is the goal of a
to zoonotic pathogens, and the in1pact of
management strategy to prevent specific
ag1icultural practices on animal welfare.

diseases and to maintain productivity.

Even though there may be no conclusive

A multifaceted approach to disease
evidence linking livestock production to
prevention and control through management these public health and public interest issues, practices is particularly important when
livestock production management will likely
dealing with many of the common infectious
change in response to the perception of such
and noninfectious diseases seen in food
links. Any changes in current practices will
animal production systems ( eg, enzootic
require development of new approaches to
pneumonia in calves and piglets, neonatal
maintain anin1al health and production,
diarrhea, bovine respiratory disease complex which will require a substantial investment of feedlot cattle, infectious infertility in
in research and education.

swine and cattle, metabolic disease in dairy

Increasingly, livestock production must
cows) as well as in companion animals ( eg,
ensure that management practices are
respirato1y disease in cattelies, kennel cough implemented at the farm level as part of the in canine boarding facilities, infertility and
industry-wide system to maintain the safety
viral respiratory disease in horses). Many of
and wholesomeness of the food supply.

these diseases are difficult to control without

Validated on-frum food safety progrruns are
an integrated approach, because they either
often based on Hazard Analysis and Critical
have a complex etiology involving the

Control Point (HACCP) principles. They
interaction of multiple microbes or are
emphasize that all stages of the food
caused by pathogens for which there are
production chain have a role in ensuring food
no reliable treatments or effective specific
quality and safety. Developing, in1plementing,
preventive measures.

and auditing these management programs are

Prevention and control of these diseases
essential to maintain consun1er confidence.

is best achieved by implementing manage

These progranis require implementation and
ment practices to mitigate recognized risk
docU111entation of management practices that
factors for infection, disease development,
reduce the risk of physical, chemical, or micand impaired productivity. Often, these are robial hazards entering the hwnan food
general management reconrn1endations
supply ttu·ough production practices on farms.

that are not targeted at specific infectious

Animal agriculture is also under pressure
organisms. Effective control may also require
from within the industiy to better protect the
in1plementation of management practices to industry itself. Well-publicized outbreaks of

2068

MANAGEMENT AND NUTRITION INTRODUCTION
disease such as bluetongue, Schmallenberg

N utiitionally related diseases include
virus, avian influenza, and transmissible
diseases associated with a nutritional excess
spongiform encephalopathies in several

( eg, direct toxic effect, digestive upset),
species ( eg, bovine spongiform encephalopanutiitional deficiency ( either primary or thy, scrapie, chronic wasting disease) have
secondary), or nut1itional imbalance. In

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focused the industry's attention on biosecuanimal agriculture, health and production rity as a disease prevention and control
are also heavily influenced by feeding
strategy. Biosecurity is a set of management
management in addition to ration fom1ulapractices that aims to prevent the introduction. Feed preparation and delivery are tion of infectious or other disease-causing
often as in1portant in ensuring anin1al health
agents and/or to prevent the further spread
and productivity as the actual nut1itional
of agents that are introduced or are already
value of the ration itself. Inadequacies in
present (see ai,so below). Biosecurity
nutritional delivery can directly cause
programs can be implemented at a room,
disease ( eg, mminal acidosis, lan1initis)

building, farm, regional, or national level.

or increase susceptibility to disease ( eg,

Similar to disease prevention programs,

Clostridium perj'ringens enterotoxemia).

biosecurity programs often comprise a set of

Nutritionally related diseases in
general practices and sets of management
companion animals also include both
practices targeted at specific pathogens.

conditions of excess ( eg, developmental

Nutritional management is a subcategory
orthopedic disease in dogs related to excess
of animal management. Proper nutrition is
calcium and energy) and of deficiency ( eg,
essential to health and productivity. Nutrition blindness in cats related to taurine also plays a role in susceptibility to disease
deficiency).

( eg, feline lower urinary tract disease) as

Feeds and feeding management can also
well as in medical management of certain
influence animal health if feeding results in
diseases ( eg, diabetes in dogs and cats,
exposure to physical hazards ( eg, sharp
equine metabolic syndrome, ketosis and
objects), chemicals ( eg, mycotoxins, toxic
hypocalcemia in dairy cattle). Rations/diets
plants), allergens ( eg, dust mites, mold
must be formulated to provide for basic
spores), or microbes ( eg, molds, Salmonella
physiologic needs ( eg, energy, protein, fats,
spp ). Feeding and waste management
carbohydrates, vitamins, minerals) and to
practices are also important to prevent
ensure optimal growth and productivity.

and control infectious disease spread

Proper ration formulation considers age, sex, through fecal-oral transmission ( eg, breed, physical activity, and lactation and
salmonellosis, neosporosis, paratuberculosis,
gestational status.

toxoplasmosis).

BIOSECURITY

The tenets of biosecurity have been long
agent." This broad definition recognizes
recognized by veterinarians. However,
that disease is a complex interaction
throughout the past decades, interest in
between the host, the disease-causing
biosecurity as a scientific discipline has
agent, and the environment. Biosecurity
surged because of l ) disease outbreaks that
can be considered in terms of individual
have threatened to devastate agricultural
animals or populations of animals (flocks
economies, and 2) bioten-orism. In fact, the
or herds), economic entities (production
meaning of the tem1 biosecurity and the
facilities or companies), or geographic
stmcture and focus of biosecurity programs
regions ( counties, states, countries, or
have evolved throughout time to more
continents), thus facilitating compartmenaccurately reflect the scientific commutalization for trade purposes. Importantly, nity's evolving perception of disease as well
it addresses strategies for both disease
as the needs of the consumer, the veterinary
prevention (eradication) and control
profession, and producers and owners.

(limiting the consequence of infection).

In modern animal medicine, biosecurity

Benefits of an effective biosecurity
is probably best defined as "all procedures program include optimized animal health implemented to reduce the risk and conseand welfare and, in the case of food animal quence of infection with a disease-causing
medicine, improved productivity and

BIOSECURITY

2069
end-product value, as well as safe regional/
through slaughter, clean-out, and disinfecinternational trade. Although implementation; and preventing dissemination of the tion of a comprehensive biosecurity plan
disease-causing agent. Eradication is
or program has obvious benefits, allocareserved for t110se diseases that pose a dire tion of resources must be economically
public healtl1 threat, that have a devastating

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(food animals) or emotionally ( companion
effect on animal performance, or that
animals) justified. Unless a disease poses a
severely compromise end-product quality.

specific risk to human health or animal
welfare, its mere presence in an individual

Disease Control: In disease control
animal or population of animals is not
strategies, the emphasis shifts from
significant. Intervention strategies are
preventing disease to reducing its conseconsequently chosen based on both their quence or economic inlpact. Prevalence data
economic and biologic efficiency.

are now use<l primarily to assess tl1e level of

A dynamic and integrated epidemiologic
protection and challenge, not merely tl1e
and economic analysis is required to
presence or absence of disease. Although
determine and quantify the negative effect
biosecurity still relies on principles of
of a disease challenge, and the anticipated
prevention, disease-control progrruns focus
positive response to the proposed
more on lintiting the extent and consequence
intervention strategy. Such integrated
of exposure. Many biosecmity measures
analysis has become significantly more
ainled at preventing or eradicating epidemic
important in intensive production systems.

disease also produce beneficial by-products,

The economic impact of disease can be
such as establishment of a fim1 fom1dation
difficult to assess. This is particularly so in
for control of erosive/endemic diseases and
intensive production systems in which
enhancement of host resistance through
economic return is governed by not only
immmtization.

animal productivity but also product quality.

In addition, the consequential loss from

Disease Management and Disease
disease challenge is, at best, only prutially

Determinants: Disease-1isk management
recoverable. Using tl1e cost of disease to
must be an integral part of any animal
justify intervention overemphasizes the
management progran1. Economic ru1alysis
consequence of inaction, and it is useful
is a critical step in biosecurity plan design,
only in justifying intervention strategies
because resource allocation must be aligned
directed at preventing disease challenge.

with risk The success of a disease control
progrrun depends on the ability to identify

PRINCIPLES OF BIOSECURITY
and subsequently address risk of infection.

Disease risk in a population is chru-acterized

Disease control and prevention relies on
by the probability of point infection and
the interrelated processes of bioexclusion,
subsequent spread. Aggregate risk is the smn
surveillance, and biocontainment. Prevenof each individual risk of adverse health tion of disease is costly, difficult, ru1d time
effects in an exposed population. The
consuming and is primarily directed at
spread and consequence of point infection
preventing epidemic or exotic diseases. It
is influenced by several factors referred
invariably involves eradication of diseaseto as disease detemtinants.

causing agents from a population of animals

Because infectious disease is the result
or geographic area. In contrast, control
of a complex interaction between several
progrruns are less demanding and prin1arily
factors, any factor that influences the risk
focus on limiting endemic diseases to
and consequence of disease challenge is a
tolerable levels within a population of
disease deterntinant. Disease deterntinants
animals or geographic area. Although
have traditionally been classified as primary
preventing exposure to disease-causing
or secondary; intrinsic or extrinsic; and
agents remains an objective of control
host-, agent-, or environment associated.

strategies, strategies are primarily focused

In intensive production LU1its, the housing
on limiting the consequence of disease.

environment, agent, and host determinants
are largely under the control of the

Disease Prevention: Disease prevention
manager/caretaker, who thus has the
depends on 1) stringent bioexclusion to
greatest influence on disease detenninants.

avoid contact between tl1e disease-causing
agent and the host, 2) eru·ly detection of a

Risk Assessment: Risk assessment is
breach in biosecurity through vigilant
used to estimate the probability of exposure
smveillance, and 3) rapid implementation
to an agent, the probability that exposure
of a ruthless biocontainment policy. This is
will cause infection and disease, the
feasible only if there is an effective merulS of
probability that disease will spread, and the
detecting infection; containing the infection
consequence of such spread. Statistical

2070

BIOSECURl1Y
techniques such as the chi-square test can
represents more than a measure of disease
be used to assess whether a specific factor/
virulence. It is more factually the dose
process is correlated with disease, but these
required to infect the least resistant animal
provide no estimate of the degree of disease
within the population. This is because the
risk. The measure of association most
risk of a challenge exposw-e increases once
frequently used to assess risk magnitude is
one aninlal in a population becomes

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the risk ratio (probability of disease given
infected or diseased. Agent replication
exposw·e divided by the probability of
increases the risk of exposw·e by increasing
disease given no exposw-e ).

the dose and (possibly) virulence of the

Disease control begins with evaluating
agent, with each new infection escalating
each part of the production process as a risk
the risk further until even relatively
factor for infection. On a basic level, risk of
resistant animals become at risk.

infection equals the probability of each event
causing infection multiplied by the number

Epidemiology: See also BASIC PRINCIPLES
of times each event occurs. But estimating

OF EPIOEMJOLOGY, p 2397. Effective biosecwity
the degree of risk requires analysis of many
requires an understanding of the causal
other factors, including host resistance and
relations between exposw-e and disease,
the dose/virnlence of the organism.

because the prevalence and consequence of

As a first step to lin1it health risk, a
any infectious disease involves a complex
biosecurity program should critically assess
interaction between several disease
the necessity of all events or processes that
determinants. The epidemiology and
potentially carry risk, and only crucial ones
relative risk for each disease should be
should be allowed. Limiting the potential for assessed to detennine the best way to infection within crucial events is focused on
allocate resources for effective control
improving host resistance or reducing the
procedw-es. Furthe1more, epidemiologic
challenge dose or virulence of the infecting
statistics can be used to detennine the best
organism.

way to limit current and future financial
risk. Several important epidemiologic

Host Resistance: Inmmne efficiency is
factors need to be considered (below).

the key factor governing host resistance.

A healthy animal produces an appropriate

Source of Infection: In addition to
inunune response sufficient to combat
identifying those animals that have become
infection and its impact on productivity.

infected, other variables, which are asso

Conversely, a response that is either
ciated with the relative impmtance of
excessive or insufficient will adversely
a particular sow-ce, should be assessed,
affect well-being and performance.

including the shedding pattern, host range,

Resistance varies among individuals
mode of transmission, and farming practices.

primarily due to genetic differences that

Transmission: Disease transmission
typically follow a Poisson distribution.

within a population is influenced by direct
lmmunosuppression reduces both
contact with infected aninlals, as well as
individual and herd/flock in1munity. The
by indirect exposure from contan1inated
weakest members of a population will be
objects (fomites). These fo1ms of horizontal
most negatively impacted by individual
transmission influence the rate and extent
stressors ( eg, disease or poor nutrition),
of transmission within and among groups.

which have a cwnulative in1pact on

This is in contrast to vertical trarismission
inllllunity. Such highly susceptible animals
between parent and offspring. Vertical
tend to skew the resistance curve to the
transmission may result from direct
right, resulting in a dramatic decline in
contanlination or (in some cases) from
flock/herd in1munity.

transovarial transmission of disease-causing

Host resistance, challenge dose, and
agents within the embryo itself.

organism virulence detem1ine whether an
infectious challenge results in disease. Dose

Spread: Disease spread is influenced
is the nun1ber of organisms to which an
by factors such as incubation period,
individual animal is exposed, and virulence
replication rate, resilience, and virnlence of
is the inherent capability of the agent to
the disease agent. These factors influence
infect (infectivity) and cause disease
spread within the population as well as

(pathogenicity) within the host. The
disease course (acute, subacute, chronic)

traditional measw·e of infectivity is the
within individuals. For exan1ple, disease
infective dose 50 OD
spread is accelerated by a resilient orgarlism

50), which is defined
as the dose required to infect 500A, of the
with a short incubation period and high
animals in a specific population.

replication/shed rate.

When designing a health program, it

Susceptibility and Predisposition: For
is in1portant to remember that the ID50
ar1 effective control prograr11, it is important

BIOSECURITY

2071
to !mow the range (species, breed, type) of
changing rooms, and housing design.

susceptible hosts. Furthermore, host, agent,

Long-range planning and programming is
and environmental factors can predispose
important and should consider on-site
animals to infection or disease. For
movement of vehicles, equipment, and
example, environmental stress can
animals; traffic patterns; and feed

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compromise immune function.

delivery/storage.

Prevalence: Disease prevalence is
directly proportional to the risk of challenge.

Procedural Biosecurity: This tertiary

Endemic diseases are difficult to prevent,
level deals witl1 routine procedures to
whereas diseases that are exotic (ie, not
prevent introduction (bioexclusion) and
nom1ally present) or epidemic in nature are
spread (biocontainment) of infection
easier to track, contain, and eradicate.

within a facility. These activities should be
constantly reviewed and quickly adjusted

Morbidity and Mortality: Morbidity
as needed in response to emergencies.

refers to the animals in a population
showing signs of disease at particular times.

DEVELOPING A BIOSECURITY

Diseases that spread rapidly typically have a
high morbidity rate (percent). Mortality rate

PROGRAM
represents the percentage of anin1als in a

Biosecurity programs consist of bioexclupopulation expected to die during a sion, surveillance, and biocontainn1ent.

particular disease outbreak.

Recovery: Disease recovery is influenced

Bioexclusion
by many factors (ie, disease determinants).

The primary focus of bioexclusion is to limit
the level of exposw·e to disease-causing

THE THREE LEVELS OF
agents below tile threshold for infection or

BIOSECURITY
colonization. This requires a systematic
approach to preventing patllogen movement

A comprehensive biosecurity program
across physical or imaginary baniers (protecshould represent a hierarchy of conceptual, tion zones), so as to eliminate or decrease tile
structural, and procedural components
nwnber of disease-causing organisms within
directed at preventing infectious disease
the anin1al's environment. Sound epidemiotransmission within and across farms, logic principles should be used to establish
companies, facilities, regions, countries, and
zone boundaries while making use of existi.Jlf
continents. Avoidance is the most effective
physical/geographic barriers.

way to prevent disease transmission involved
with animal ownership or production. But

Global Perspective: The global nature of
given that all movement of animals within or
the animal industry results in daily shipment
across groups/borders involves risk of
of ailin1als and animal products tJu·oughout
contact, biosecurity measures are needed to
the world. This trade is regulated by tile
reduce unavoidable risk.

World Organization for Animal Health

(OIE), and such conunerce must comply

Conceptual Biosecurity: This primary
with OIE regulations, including those
level of biosecurity revolves around the
pertaining to farm-level control measures.

location of animal facilities and their
various components. The most effective

Country Perspective: To control spread
way to li..mit risk is physical isolation,
of disease, the OIE aids in the establislunent
making this a primary consideration when
of international agreement on animal
siting new confinement facilities or fam1s.

and plant sailitary (SPS) measures. Such

Facilities/farms should not be located next
an agreement within tile World Trade
to public roads, especially when the area

Organization establishes common definitioru
has a high density of animal facilities.

and describes OIE in-house procedures for

Similar isolation methods include limiting
dealing witll international trade disputes.

the use of common vehicles and facilities,

This treaty has also established guidelines
limiting access by personnel not directly
and principles governing tile transpai·ent,
involved with the operation, and controlling
objective, and defensible assessment of
the spread of disease by vermin, wild
risk. More specifically, import risk ai1alysis
anin1als, and wind.

provides in1po1ting countries with an
objective and defensible assessment of tl1e

Structural Biosecurity: This secondary
disease risks associated with importation
level of biosecurity deals with physical
of such items as animals, animal products,
factors such as farm layout, perimeter
biologic products, genetic material,
fencing, drainage, number/location of
feedstuffs, and pathologic material.

2072

BIOSECURITY

Region or State Perspective: To
region. Minin1al requirements of internaaccount for the difficulties in controlling the tional trade require that companies conform
disease status and management practices of
to international standards, thereby meeting
animal populations across the vast expanse

OIE requirements. As compartments witltin
of large countries (eg, the USA), the
the biosecurity rnbric, each trading

Terrestrial Code makes allowance for
company, region, state, or country should

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zoning and compaitmentalization. The code
classify presc1ibed OIE diseases according
defines subpopulations based on anin1al
to expected prevalence; design, docwnent,
health status, allowing member countries to
and in1plement a biosecurity plan to prevenU
limit daniaging trade effects associated with
control these diseases; and provide proof of
disease outbreaks, without exposing the
plan compliai1ce. This biosecurity plat1
importing country to risk from disease
fom1s the basis for all disease prevention,
spread. There are also "compaitments"

diagnosis, and conti·ol strategies. The plat1
based on biosecurity procedures and
should identify potential pathways for

"zones" based on geography. The requiredisease introduction/spread within the ments to estabUsh these subpopulations
company at1d describe tl1e measures being
vary based on disease specifics and the

( or that will be) taken to minintize risk as
requirements of the trading partners, and
prescribed within the OIE TeITestrial Code.

they are best decided before disease
outbreak. Factors such as disease

Primary Control Zone-Animal
epidemiology, environmental influences,

Confinement Facility: Bioexclusion
natural/artificial boundai·ies, swveillance
begins at the at1imal confinement facility,
and monitoring, and applicable biosecurity
which is the smallest epidentiologic rntit
measures ( eg, movement controls and
witltin the company. The anin1als within
husbandry) are of patticular interest. To
this facility share a common environn1ent,
establish local zones/compaitments, the
common management practices, and
veterinaty services of an exporting countiy
simi!ai· Ukelillood of pathogen exposure.

must clearly define subpopulations as

The boundaries of these facilities represent
stipulated in the Code. Relevai1t claims
well-defined batTiers to entry and an ideal
must be repmted to the vete1inaiy services
place for implementation of critical control
of an importing count1y and supported by
prof'edures. Every crossing of the facility
official, detailed documentation.

perimeter should be considered an "event"

Zone borders are based on natural,
with potential for pathogen trai1sfer or
artificial, or legal boundaries, making them
disease risk.

relatively easy to establish and officially

Reducing the risk from such events
communicate. Compaitments based on
requires an "all-in, all-out" strategy.

biosecurity procedures are more. difficult to

Thorough cleaning, decontainination, and
define. The requirements for a compartrnent chemical disinfection should be performed include defining adequate biosecurity plans,
when the facility is empty. Once aninlals
operating procedures, at1d management
arrive, the focus shifts to limiting the
practices that are well docwnented
number of events (in-house perin1eter

(including documentation of compliance).

crossings), as well as the probability of

This process involves developing a
pathogen transmission and infection during
partllership at1d clearly stipulated
unavoidable events.

responsibilities between attimal owners
and the appropriate veterinaiy authority.

Secondary Control Zone-Farm or

Requirements of biosecurity plans include Site: The next zone/compaitrnent in tile adequate and robust disease surveillance,
disease-control hierarchy is the fatm or site.

ai1i.mal identification, and traceability. This

In this case, tile epidentiologic rntit is t11e
necessitates detailed records for factors
farm rather than the containment facility.

such as animal movement and production,

There is a defined boundaiy SlllTOw1ding tile
feed sources, sources of replacement stock,
fa.tin, and the farm animals share a common
disease swveillance (including morbidity
environment with conunon management
at1d mortality), vaccination and medication
practices, thereby sharing a common
ltistory, personnel training, and visitor logs.

Ukelihood of exposure to pathogens from

Risk ntitigation also requires that the plan be
nearby containment facilities.

regularly audited, reviewed, and adjusted as

The fatm/site estabUshes real ( eg, fence)

needed.

or imaginaiy bow1daties tllat serve as access
points to tl1e secondaiy control zone, which

Company Perspective: For purposes
is a critical zone for disease control. From a
of biosecwity, compatties operate as
biosecurity standpoint, the site is considered
compartments within a com1try, state, or

"closed" if tile fanner/producer enforces full

BIOSECURl1Y

2073
biosecurity with no uncontrolled access
tJu·ough quru·anti.ne and slaughter. For
after disinfection. The site is considered
situations in which eradication is not

"open" if general biosecurity is enforced at required, collection of prevalence data
the start of transfer/depletion, with access
should be adjusted so as to differentiate
granted only to necessary vehicular traffic.

backgrom1d variation from effects of disease.

The site is "fully open" if routine control is The data collection system should be

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enforced from the point of last animal
designed so as to provide insightful and
removal. Sites involved in an outbreak
epidemiologically infonnative disease
should remain closed until the responsible
indicators. During design, it is good to keep
veterina.tian declares them clea.t1.

in mind the need for impo1ta.t1t pa.t·a.tneters

( eg, sa.tnple size) that can be used to

Tertiary Control Zone - Complex:

calculate other animal-health estimates,

Groups of animals that sha.t·e a communal
such as prevalence, incidence, morbidity,
a.t1imal handling facility (ie, a complex)

mortality, and herd/flock inunLUlity (as
constitute a tertiary control zone. The
indicated by a.titibody titers, fam1 production
complex represents its own epidemiologic
records, etc). In the absence of random

Lmit, because sites/fanns within it shru·e
sa.tnpling, such statistical estimates ca.tmot
facilities such as feed mills and processing
be taken as absolutely accurate but may
plants. Production processes within the
serve as adequate markers of the need for
complex ( eg, rea.t'ing fanns and grow-out
intervention.

fa.trns) sinlilarly constitute sepa.t·ate

For purposes of disease eradication and
epidemiologic units. All the defined ru·eas
trade, it may be necessa.ty to demonstrate
may represent tertiary control zones for
freedom from infection in the com1try, zone,
biosecurity purposes. Te1tia.ty zones are
or compartment/company. Although there
seldom fenced, so access boundaries are
may be no obvious evidence of infection in
typically imaginary.

the population, it is impossible to defini

As a cost-effectiveness measure, tertia.ty
tively prove freedom from infection Lmless a
zones are often established around
perfect ( 100% sensitive/specific) test is used
high-value sectors of the operation, such
to exan1ine eve1y member of the population.

as the valuable stock used in breeding

In this situation, the smveillance system
operations. To reduce transmission risk,
should be able to statistically estimate to a.ti
critical control points such as transit
acceptable level of confidence that infection
facilities can be established beyond the site
is below a specified prevalence level.

perimeter. At these points, procedures such

As part of health tracking, individuals
as showering, changing into protective
should be monitored for disease at regular
clothing, and transfer to site/zone-dedicated intervals. Any cl1a.t1ge in prevalence transport significa.t1tly reduce the probabilsuggests a change in incidence that may ity of disease transnlission onto the site.

require corrective action to prevent disease
spread. The frequency at which a.tlimals are

Surveillance
monitored depends on disease epidemiol

The terms monitoring and surveillance ru·e
ogy and the level of biocontainment ( eg,
both used to desc1ibe ongoing data
need for quru·antine or slaughter). Factors
collection to estimate disease prevalence
such as latent period, mode of tra.t1sn1ission
and severity in a population. However, a

( eg, vertical or horizontal), potential for
monitoring progra.tn is typically geru·ed
animal dispersion and tracking, a.t1d test
toward collecting statistically reliable
sensitivity ru·e impo1tant considerations.

prevalence data that can be used to track
trends in disease incidence and seveiity

Biocontainment
over ti.me. A surveillance progra.tn is based

Biocontainment strategies reduce the
on prevalence data from a readily available
consequence of disease challenge by
sa.tnple of the population, with the goal

Ii.nu ting the opp01tunity for challenge
being timely action to correct perceived

(bioexclusion), enhancing resistance
increases in disease incidence. The

(immunization), and preventing spread
imp01ta.t1ce of these progra.tns increases

(quarantine). When eradication is required,
when remote management-control is
quarantine is usually followed by eme1°
needed to keep up with increases in
gency slaughter. Control measures ru·e
herd/flock size and production.

routinely applied for endemic diseases but

When catastrophic outbreaks require
more sporadically for epidemic outbreaks.

eradication, the surveillance progran1 should

The tenn quarantine refers to the practice
be focused toward detecting source cases,
of enforced isolation of a.tlimals exposed to
allowing implementation of biocontainment
infectious agents, as well as the place in

2074

BIOSECURITY
which these animals are isolated and the
to hide some disease because of possible
time period of isolation. Quarantine is
public recrimination. Veterinarians and
routinely required when live animals or their caretakers can and should help dispel this products are imported. To avoid disease
apprehension by maintaining high ethical
entry into a country, region, zone, compartstandards and refraining from discussing VetBooks.ir
ment, or population, potentially infectious
one producer's problems with others.' Yet,
animals/material must be isolated until they
there comes a time when all producers must
have been shown to be disease free.

be apprised of a problem. Service workers

Enforced isolation is the first biocontainvisiting affected animals should wear protecment step when potentially infected animals tive footwear and clothing when they enter
are brought to a production setting.

the facility, and no other farm should be

Movement within or through the control
visited without adequate decontamination.

area is restricted and monitored. The size/

It is in1portant to reach a diagnosis as soon
nature of the control zone depends on
as possible. The natme of the disease will
disease risk but usually involves a containdetennine the course of action. Although it is ment facility, farm, site, or complex within a
not al ways possible to treat a disease or stop
particular company. The control zone may
its deleterious effects, identifying primary
be expanded to a 2-rnile radius for diseases
and contributing diseases is important to
of nationaVregional impmtance.

plan effectively for the futme. Vete1inaiians

Disease monitoring is used to establish
should be aware of the owner's economic
the extent of an outbreak, first within the
plight and render advice and assistance as
quarantine zone and then in a well-defined
quickly as infmmation is available or a
surrounding contact zone. The relevant
judgment can be made.

veterinary authority assun1es control in

In addition to causing serious economic
cases of foreign/notifiable disease. All vested
and emotional loss, some diseases ai·e
parties ( eg, countries, states, regions,
hazardous for people. When zoonotic
companies, owners) should prearrange an
conditions are suspected or diagnosed,
emergency response plan sufficient to
extra precautions must be taken to prevent
address relevant details of containment and
infection of attending personnel. Notifiable
eradication.

diseases require that appropriate government authorities be alerted and that all Chemoprophylaxis and Vaccination:

in-contact personnel be carefully tracked

Medication may be added to feed or water
and assessed. In some regions, certain
to reduce disease risk. Vaccination is
diseases must be reported inunediately to
commonly used to reduce the risk and/or
the state animal disease control authmities
consequence of infection an1ong exposed
so that proper investigation and action can
individuals or populations. The main
be taken to protect the affected industry.

purpose of immunization is to prevent

Every effort should be taken to ensme
clinical illness by raising the ID50 of the
appropriate nursing care, which plays a key
population. Vaccinations can be used to
role in improving the outcome of a disease
protect individuals from disease or to
outbreak. Therapeutic medication should
protect the next generation by limiting
be used only after the problem has been
direct vertical transmission and enhancing
diagnosed and recommended/prescribed by
maternal antibody transfer.

the veterinarian. Therapy is not a sustainable method of disease control and should HANDLING DISEASE OUTBREAKS
not be considered an ongoing part of any
biosecmity progran1. The flock response

Feed and water consumption and production
to medication merely provides the time
should be carefully monitored at all times, as
necessary to investigate, design, and
well as the typical sounds and behaviors of
implement further control measures to
individual anin1als. Any deviation from
ave1t additional need for therapeutic
normal indicates the possibility of infectious
medication. No drugs should be given
disease, and inrn1ediate action should be
w1til a diagnosis is made and a veterinai·ian
taken to prevent inadvertent spread of
consulted.

infection. Initial steps include setting up a

Sick animals should not be moved or
quarantine of the pen, building, farm unit
handled until they have recovered/stopped
area, or entire farm, depending on its design
shedding the disease-causing agent, unless
and progranuning; designating separate
the move is to a more favorable environcaretakers for affected animals; and ment a.s part of therapy. It is importai1t to
checking and examining sick animals last.

consider that some healthy carriers may

Owners should seek professional
remain ainong apparently recovered
diagnostic assistance, rather than trying
anin1als.

CLONING OF DOMESTIC ANIMALS

2075

CLONING OF DOMESTIC ANIMALS

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The basic concept of cloning via nuclear
mimic the activation signal of fe1tilization,
transfer is that the nucleus of a cell, taken
which stin1ulates it to develop into an
from a tissue sample of a donor individual,
emb1yo. After activation, the developing
is transferred to an enucleated oocyte, and
embryo may be trruisferred surgically to the
then the oocyte is stimulated to develop into oviduct of a recipient female or may be an emb1yo. The embryo thus produced has
cultured in vitro to a stage at which it crui be
the same genotype as the miginal donor
trruisferred to the uterus trruiscervically
individual.

(nonsurgically), as for standru·d embryo
trru1sfer.

TECHNICAL ASPECTS OF

Health and Phenotype of the Cloned

CLONING

Animal: Several factors influence the health Cells recovered from early embryos, up to
ruid phenotype of tl1e cloned individual,
the momla stage, work efficiently as donor
including epigenetic effects, mitochondrial
cells for cloning. Cloning from emb1yonic

DNA, uterine ruid postnatal environment,
cells was conducted successfully for more
mutations, ruid individual vrufation.

than a decade before the birth of the first

Epigenetic Effects: After nuclear
mammal produced via nuclear transfer
trruisfer, the ooplast must reprogrrun the
using adult somatic cells ("Dolly," a sheep DNA from the somatic cell so that it
reported by the Roslin Institute, Scotland,
functions like that of a zygote. This is
in 1997).

controlled Jru·gely by methylation ruid

The most common tissue used for cloning demethylation of bases in the DNA ruid by from adult animals is subcutaneous
modification of the histones, the proteins
connective tissue. The tissue is minced and
around which the DNA is wrnppecl.

cultured in vitro. Outgrowing fibroblasts are

Controlling the trruiscription of DNA in this
hruvested and rep lated (passaged) in new
mrumer, without altering the structure of
dishes to continue proliferation until
the DNA itself, is termed epigenetic control.

millions of cells have been produced. These

The oocyte must reprogram the DNA of the
are then typically cryopreserved for future
donor cell initially at the time of cloning,
use.

ruid then maintain the nonnal patterns of

Mature oocytes from the san1e or closely
epigenetic modification through the
related species are required for the nuclear
different stages of development. The
transfer. The genetic value of the oocytes is
amount ruid accuracy of reprogr=ing of
not importrult, although their mitochondrial
the donor DNA is probably the major reason
makeup may be, because the resulting clone for success or failure of fetal development will carry the mitochondria of the host
in cloning. Minor chruiges in epigenetic
oocyte (see below). Oocytes are typically
status may not affect tl1e general health of
recovered from slaughterhouse mate1ial
the cloned individual but may still cause it
and then matured in vitro, although in some
to vruy in phenotype from the donor ruiimal.

species, meiotically mature oocytes (from

A visible exru11ple of this is seen in the first
preovulatory follicles or from the oviduct
cloned cat, CC. CC expresses only brown
after ovulation) are collected.

coat color, whereas her genetic donor

Nuclear traI1Sfer is typically pe1fo1111ed
expresses both orange ruid brown ( eg,
using a microscope with micromanipulacalico). Because the X chromosome carries tors. The chromosomes of the oocyte are
the gene for coat color in cats, this indicates
removed, creating an enucleated oocyte, or
that in CC, X chromosome inactivation is
ooplast. The somatic cell used for cloning
not rruidom; rather, the same X chromomust be synchronized to early in the cell some is inactivated in all cells, presumably
cycle (before DNA synthesis). The somatic
because of failure to reactivate the inactive
cell is combined with the ooplast, either by

X at the time of cloning.

membrane fusion using an electric pulse or

Epigenetic effects may also influence the
by direct irtjection of the donor cell into the
phenotype of the nuclear trruisfer-clerived
ooplast via micromanipulation.

animal after bi..tth; eg, rui ruiimal with

The recombined oocyte, now containing
growth-factor genes traI1Scribed at high
the nucleus of the donor cell, is treated to
levels may grow larger thrui its cloned

2076

CLONING OF DOMESTIC ANIMALS
sibling with less active genes, even though
cation and apoptosis occur in response to
the actual nw11ber and makeup of the genes
many envirorunental and internal stimuli.

are the same. However, it has been shown in Thus, random individual variations will all species studied that major epigenetic
occur in the makeup of tissues, even in
anomalies are not passed on to the offspring individuals of the same genetic background.

of clones because of resetting of epigenetic

A visual exan1ple of this is in the markings

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status during sperm and oocyte developof cloned aninlals; individuals cloned from ment.

the same cell line tend to have white in

Mitochondrial DNA: The nuclear
similar places, but the markings can vary
transfer embryo will have the nuclear DNA
draniatically in size and shape.

of the genetic donor but have the mitochondrial DNA of the recipient oocyte. A small STATUS OF CLONING DOMESTIC
nwnber of mitochondria from the donor cell ANIMALS
may also be present, but propottionately
few. The impact of the source of mitochon

Live yow1g have been produced by nuclear
dria, or a mixture of mitochondtia, on the
transfer in aJl major domestic mammalian
traits of the progeny is currently unknown.

species: cats, dogs, horses, cattle, goats,

Because mitochondria are tl1e source of
sheep, and pigs. Cloning in cats appears to
energy for the cell, differences in mitochonbe repeatably successful; oocytes may be d1ia could potentially have an effect on
obtained using tissue recovered from
production, stamina, or other physical or
clinical ovariohysterectomies. Interspecies
behavioral traits.

cloning of closely related nondomestic cat

The heterogeneous mitochondria present
species using domestic cat oocytes has
in a female produced by nuclear transfer
produced live young.

will be passed down to the female's

Cloning in dogs is complicated by several
offspring, because they will be present in
factors. Mature canine oocytes must be
her oocytes. However, although spenn from
obtained from the oviduct after ovulation,
a male produced by nuclear transfer will
because effective methods for in vitro
carry the heterogeneous mitochondria,
maturation of canine oocytes have not been
these mitochondria will be eliminated after
developed; additionally, bitches are in
the spem1 fe1tilize an egg, so a male clone
estrus only about once eve1y 6 mo, so
can be considered to produce progeny that
oocyte availability is low and synchronizaare genetically identical to those that the tion of recipients is problematic. Cloning in
original donor animal would have produced. horses results in a low blastocyst development rate (3%-lOOA>), but viability after Environment: Uterine size and health;
transfer is an1ong the highest repo1ted;
milk production of the darn; nutritional,

-300A, of transferred embryos produce live
exercise, and training programs; and
foals, and postnatal survival is high (>85%).

handling to which the neonate is exposed

Cloning in food animal species is
may all influence t11e animal as an adult. For
facilitated by the ready availability of
example, the cloned cat, CC, is outgoing and oocytes from slaughterhouse tissue.

gregarious, whereas her genetic donor was

Cloning in sheep and cattle is inefficient
reserved. However, the genetic donor was

(5%-15% of transferred embryos result in
a research cat, raised in a cage and mmsed
live young), and 300/o-500A, of live neonates
to attention, whereas CC was raised with
die by 4 yr of age. Cloning in sheep and
an overabundance of attention and
cattle is associated with frequent placental
stimulation.

abnormalities, especially low munbers of

Mutations: Genetic mutations are
atypically large cotyledons. There is a high
potentially more likely in cloned animals,
incidence oflarge offspring syndronie in
because cultured cells are used as the DNA cloned calves and lan1bs (ie, fetal oversource. The donor cells are grown a growth with related abnormalities) and, in

11d
passaged in vitro, and this is associated
live calves, of transient metabolic abnorwith an increasing number of chromomalities such as hypoglycemia or poor renal somal abnormalities with increasing
function. Cloning in goats has similar
passages. However, cells with chromoefficiency in production of live young per somal abnormalities are unlikely to
embryo transferred, but cloned kids tend
produce viable embryos.

to have greater viability. Goat oocytes are
typically obtained by follicle aspiration

Individual Variation: Cell differentiaex vivo, and this may increase viability tion occurs in cascades, as differentiation of
of resulting clones. In pigs, lo/o-5% of
one cell type affects the status of the cells
transferred recombined oocytes produce
around it. During development, cell multipli-
live young, but cloning is made practicable

CLONING OF DOMESTIC ANIMALS

2077
by the ready availability of large numbers of
generally accepted as worthwhile, such as
oocytes and the ability to transfer hundreds
in vitro fertilization and embryo production,
of recombined oocytes to the oviducts of a
oocyte transfer, and embryo transfer. In
single recipient. Cloned piglets are generally addition, the accepted nonnal fate of many healthy; they have a higher than normal
species being cloned is to be housed for
incidence of stillbirth and of some
maxin1al production and then be slaugh

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abnonnalities but do not develop large
tered and eaten. A compelling argument for
offsp1ing syndrome.

cloning is that the potential benefits of the
procedure to the understanding of life

RATIONALE FOR CLONING
processes and animal disease, to human
health, and to food production outweigh the

Companion animals may be cloned for
cost of tl1e procedure in terms of animal
emotional reasons or as models for
welfare.

endangered species. Horses are cloned

Additional concerns rest with the effect
mainly to allow continued production of
of cloning on the entire animal population,
offspring from individuals with valuable
most commonly related to the genetic
genotypes or to retain a genetic type ( eg,
variation of the species. This is a legitimate
geldings that are exceptional perforn1ers).

concern in some species and uses, such as

Cloning of farm animals may be pe1fom1ed
in dairy cattle, in which one bull may sire
for agricultural or biomedical applications.

thousands of offspring. However, this is

Agricultural applications include producmore related to the technology of semen tion of anin1als with valuable production
freezing and distribution than to the fact
traits, such as high-producing dai1y cows,
that a bull itself was cloned. In companion
anin1als with superior carcass quality at
animals, it is improbable that the very few
slaughter, or production of additional sires
pets likely to be cloned will have an effect
of an established valuable genotype.

on the population in general. In horses,

Biomedical applications of cloning are
cloning may in fact increase genetic
largely related to the ability to perform
variation, because a major proposed use is
nuclear transfer using a cell line that is
to clone geldings that have been found to be
genetically altered (transgenic) and, thus, to
superior competitors, thus rescuing genetic
produce an animal with those characteristypes that would otl1erwise have been Jost.

tics. Biomedical applications include

Concerns about human health focus
generation of animals of specific genotypes
mainly on conswnption of food produced
as disease models, animals carrying genes
from cloned animals. After years of study,
for the production of medically important
the FDA and the European Food Safety
proteins that may be harvested from the

Authority have concluded that conswnption
milk or tissues, and animals having
of meat or milk from cloned anin1als poses
genetically altered organs ( of low inm1 unono public health risk. Therefore, remaining genicity) for transplantation to people.

concerns about consun1ption of food from
cloned anin1als is likely based more on

CONTROVERSIES
principle than on actual potential for harm.

Because cloning is used to produce

Ethical concerns about cloning may be
transgenic animals, many perceived
broadly divided into two categories:

concerns regarding cloning are actually
concern about the effect of cloning on
concerns about transgenic animals, which
animal and human welfare, and objection to
present a completely different set of
the principle of cloning, ie, to producing an
potential hazards to anin1al and hun1an
anin1al by a means other than fertilization.

health and the environment. European

Currently, cloning is associated with an
nations have relaxed their position on use
increase in animal suffering when
of cloned animals and their progeny in the
compared with production of animals by
food chain based on the Jack of evidence
standard breeding methods. This is due to
of a human health risk and the difficulty in
surgeries performed to obtain oocytes or
establishing a tracing or labeling system
transfer embryos, pregnancy losses,
to identify such meat when corning from
sickness and death of neonates, low-level
outside countries.

abnormalities in surviving young, and

A key ethical question regarding the
possible distress from disease in animals
principle of producing anin1als by cloning is
produced as disease models. These
whether this technique is violating some
concerns are somewhat mitigated by the
moral prohibition, ie, that people are
fact that most of these findings are not

"playing God" by producing emb1yos
unique to cloning; they are also associated
without using fertilization. Similar questions
with other procedures that have been
have arisen with each new reproductive

2078

CLONING OF DOMESTIC ANIMALS
technique that has been developed; however,
year. However, people currently buy
many people feel that cloning is a special
purebred dogs and cats for tl10usands of
case. This general moral aversion of the
dollars when they could get animals for no
public to the concept of cloning is enhanced
or low cost. American culture supports the
by the portrayal of cloning as a malevolent
concept that people can spend their own

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force in science fiction books and films.

money on whatever they wish. •

Counter0arguments to these moral

A related argument is that cloning turns
concerns are that cloning occurs in nature
animals into a commodity or an object,
in the form of identical twins; that people
rather than a sentient being, and that
have been producing plants and animals by
producing an animal in this way shows

"unnatural" means from the first tirne they a lack of respect for the animal as an
planted a seed in a new area or bred a cow to individual. However, animals have been a selected bull, and that this is simply a new
bought and sold since they were domestidevelopment in the same line. Embryonic cated; cun-ently semen and embryos are
cloning was being pe1fom1ed for more than
frozen, shipped across tl1e country, and

10 years before the birth of Dolly with
used to produce desired young. Cloning
essentially no public attention, and even the
does not seem to offer any unique distincbirth of two lambs cloned from cultured tion in tlus area.

cells of embryonic origin, announced a year

Commercialization of cloning brings with
before Dolly, had no public impact. Thus, it
it the possibility of fraud and of preying on
appears that the main moral issue of public
the emotions of bereaved pet owners.

concern is not the production of embryos

Cloning companies should state clearly
without fertilization, but the production of
that the technique will produce anotl1er
embryos from cells of an existing, known
individual with the same genetics as the
anin1al.

original animal; it does not "resurrect" an Arguments against cloning of companion
animal. The best simile to draw is to that of
anin1als have focused on the cost of
an identical twin born later in time; just as
producing a clone-tens to hundreds of
with naturally occuffing identical twins,
thousands of dollars-when millions of
they will be very sin1ilar but also different in
unwanted dogs and cats are killed each
many ways.

COMPLEMENTARY AND ALTERNATIVE

VETERINARY MEDICINE

Complementary and alternative veterinary
much remains unknown regarding the true
medicine (CAVM) as defined in 2001 by the
therapeutic utility of many aspects of

American Veterinary Medical Association,

CAVM. Thus, to gain a legitimate foothold
is " ... a heterogeneous group of preventive,
in modem medicine, CAVM must demondiagnostic, and therapeutic philosophies strate a rational mechanism of action and
and practices. The theoretical bases and
withstand scientific scrutiny.

techniques of CA

VM may diverge from

The diversity of approaches tl1at
veterinary medicine routinely taught in
constitute CAM range from tl1e well-studied

North American veterinary medical schools
to the bizarre and baseless. Certain
or may differ from current scientific
treatments, such as homeopathy, lack
knowledge, or both." Although some of
biologic plausibility. Others require belief
the myriad approaches have been used to
systems more consistent with faith-based
treat animals for centuries, many have not.

healing than medicine. Much of the material

Instead, they have been extrapolated from
published regarding CAM promotes
hwnan approaches without first undergoing unreliable and potentially dangerous advice.

assessment for safety and effectiveness in

CAM providers cannot always provide a
nonhunum animals.

scientific basis and critical perspective for

Despite the popularity of CA

VM among
what they practice.

some segments of the public, along with

The responsibility for protecting and
intensive promotion by certain groups,
benefiting veterinruy patients remains with

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE

2079
the scientifically educated clinician.

revised and simplified compilation of

Veterinarians who consider referring

Chinese medical theories that would help
patients for CAVM or practice modalities
address the public health needs of the ailing
have a responsibility to distinguish
masses. He also eventually found it helpful
tried-and-true from too-good-to-be-true.

to promote quintessentially Chinese

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This is accomplished by conducting
approaches as a matter of national pride.

well-designed scientific trials to investigate

Subsequently, he marketed TCM to Western
relevant clinical questions and by regularly
doctors. An Wlfo1tunate mixing of western
reviewing the medical literattu-e to reassess
metaphysics with TCM transformed
which modalities have accwnulated
acupuncture into a pseudoscientific "energy
independently confinned data. Even if a
medicine" practice that disavows science
certain clinical application has not yet
and its true underlying actions of neuroreceived research scrutiny, studies showing modulation and connective tissue effects.

a plausible and unique mechanism of action, Making matters worse, TCM practitioners as well as a safety record, can help support a cling to dubious diagnostic techniques such rational decision about whetl1er to
as tongue diagnosis and pulse diagnosis. No
recommend it.

research supports the validity or reliability

Although nw11erous modalities and
of these techniques, even for people for
treatments are associated with CAVM, the
whom these practices were developed.

ones discussed below are some of the more

FortW1ately, decades of scientific
well known or considered for vete1inary
research on its mechanisms and indicause.

tions now make it possible to practice
acupW1cture and related techniques

ACUPUNCTURE
without metaphors or belief systems.

Patients receive diagnoses based on

Acupuncttu-e refers to a method of insetting modern medical methods and informed thin, sterile, solid needles into specific sites
palpation. Needling is regarded as a means
on the body. Its myriad applications span
of afferent stimulation that engenders
analgesia to treatment of organ dysfuncmodulation of central, peripheral, and tion, neurologic abnom1alities, myofascial
autonomic nervous system function, as
restriction, immune disorders, and many
well as signal initiation and transfer among
other conditions. Although most think of
associated connective tissue structures.

needles when they hear the tem1, acupunc

Objective outcomes can be measured and
ture actually incorporates an array of
assessed through scientific research, as
interventions intended to eitller augment
results from rigorous, controlled trials lend
the needle's effects or obviate the need for
further sophistication and insights into
needling altogether. Such interventions
treatment plans and physiologic outcomes,
include electrical stimulation (ie, electrorespectively.

acupuncture); moxibustion (in which a
smoldering herb heats the acupuncttu-e

Mechanisms of Action: The belief among
point or embedded needle); low-level laser

TCM practitioners that acupW1cture works
stin1ulation (laser puncture); pressing
by moving invisible energies began witl1 a
techniques (acupressure); and injection of
mistranslation of the Chinese word "qi" into vitamins, saline, or other solutions into
energy in the 1930s. A French bankteller
sites (aquapw1cttu-e).

working in China, Georges Soulie de

Practitioners of"traditional Chinese

Morant, strongly believed that "energies"

medicine" (TCM) adhere to principles
formed tl1e basis of healing. For lack of a
developed in prescientific tin1es, replete
better word, Soulie de Morant translated
with mistaken interpretations about organ
the tenn "qi" into "energy." Thus began the functions and suffused with metaphors
misplaced notion in the West that acupW1csuch as "wind invasion" and "spleen damp tw-e moved "energy." In reality, the term "qi"

heat" instead of modem medical knowlreferred to dissolved gases and nutrients edge.

that circulated throughout the vascular

Although the roots of Chinese medicine
system. Given that acupW1cttu-e was
can be traced as far back as tl1e Han dynasty
originally a blood-letting technique, this

(206 BCE to 220 CE) or earlier, the field of
explains the correspondence between

TCM as adopted by many veterinarians is
acupW1cture charmels and blood vessels.

recent. TCM was updated and compiled

Over time, as needles became thinner and
by order of Chairman Mao Tse Tung in
more refined, acupw1ctwists ceased
the mid-twentieth century. Confronted
bleeding patients. By the 1950s, Chinese
with widespread epidemics and too few
scientists began accepting that the effects

Western-trained physicians, Mao sought a
they fow1d in patients occurred as a result

2080

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE
of the nerves being stimulated near the
evidence of serious adverse effects is
fo1111er blood vessel targets. Today, the tenn
lacking, even in late pregnancy. Coagulopa

"neuromodula.tion" has been accepted by
thies or immune compromise might
scientific acupuncturists around the world
represent contraindications if needling

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as explaining the basis for acupunctw·e's
leads to excessive bleeding or local
effects.

infection, respectively.

Research findings from physiologic

Acupuncture may be contraindicated if
studies show that acupuncture needles, or
an aninlal cannot remain still enough to
other devices, affect afferent nerve fibers
perfonn needling safely. High levels of
in the skin, subcutaneous tissue, fascia,
anxiety, fear, or aggression could counteract
muscle, tendons, vascular walls, or
health-promoting autonomic changes
periosteum, pwportedly eliciting local or
generated by acupunctw·e. ln such cases,
peripheral reflexes that have beneficial
efforts to calm the animal may be wareffects on the body.

ranted.

Several explanations exist for how

Some TCM-based acupuncture practitionacupuncture reduces pa.in. Some assert ers may clain1 that cancer is a contraindicathat acupuncture intermpts nociceptive tion for acupuncture, although no evidence
transmission at the level of the spinal cord,
exists to support their claims that unseen
producing spinal segmental analgesia, or
energies emanate from the point into the
that acupuncture alters the processing and
tumor and incite growth. The belief that
perception of pain centrally. Others have
acupuncture will encourage cancer
suggested that any pain-relieving effects
metastasis because it can augment
may be more simply attributed to placebo
circulation is similarly unfounded; however,
effects, distraction, a diffuse noxious
there is also no proof that acupw1ctw·e itself
stimulus, or psychologic alteration of the
fights cancer.

perception of pain. Various neurotransmitter and neuroendocrine responses have Adverse Effects: Acupuncture provided
been associated with acupuncture. Specific by medically educated professionals such paran1eters important for optimal effects in as vete1inarians results in few adverse acupuncture are emerging as research
effects and is generally considered safe. The
defines how treatment design impacts

1isks of invading a major organ or vessel
clinical outcomes. For example, targeting
with a needle are limited as long as the
specific de1matomes corresponding to
practitioner remains aware of the patient's
local pathology rather than remote sites
anatomy. Extreme negative reactions to a
leads to greater improvements in pain
needle may indicate that it has entered a
control, physical activity, and sleep quality.

nerve; in those cases, the needle should be

Frequency and duration of stimulus also
withdrawn. Handlers of horses have been
influence the analgesic response. Mounting
ir\jured when horses have kicked during
evidence reveals a multiplicity of
acuptmcture treatment. Needle ingestion by
mechanisms and clinical benefits from
the patient appears to constitute the most
acupuncture. Research is expanding
frequent concern in aninlals, although there
regarding the clinically relevant benefits
are no published reports of ir\jury. Adverse
that acupuncture confers on many probreactions that have been repmted in people lems, including those of inflammatory,
include fainting, skin infections, and
muscttloskeletal, neuropathic, neoplastic,
hepatitis; such reactions have not been
or visceral origin.

repo1ted in aninlals.

Indications: Acupuncture holds value

Controversies: The fundamental tenets
for treatment of acute and chronic pain,
of energy-based acupuncture remain
neurologic dysfunction, musculoskeletal
unproved. No evidence indicates that
disorders, GI motility disorders, circulatory
invisible meridians or qi energies exist. Due
problems and insufficiency, immune
to the limited nwnber of clinical studies in
dysfunction, reproductive disorders, and
acupuncture for veterinary patients and
the negative sequelae of conventional
the cmrent disavowal of the scientific basis
cancer treatment.

of acupuncture by TCM practitioners,
acupuncture has not been recognized as

Contraindications: Acupunctw·e has a
a specialty by the American Boa.rd of
strong safety profile, and few contraindica

Veterinary Specialties.

tions exist. Although pregnancy is often

Gold bead implantation, the process of
considered a contraindication, based on
intentionally i.nse1ting small bits of metal
concern that acupuncture might affect
into the body as a type of "permanent
honnone levels or uterine innervation,
acupuncture," resembles a Japanese

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE

2081
technique in which acupunctwists bmied
massage in its "manual medicine" approach, acupuncture needles into tissue and cut
ie, using the hands to help heal conditions
them off at the smface, leaving a lifelong
seen in practice.

implant.

Manual therapy frequently tai·gets the

The medical literature contains cases in
spine. When people speak about "aninlal

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which acupuncture needle fragments or
chiropractic," "veterinaiy manual therapy,"

implants have migrated to the spinal cord,
or "animal acljusting," they are usually
peritoneal cavity, heart, stomach, liver,
referring to forceful maneuvers directed to
breast, brain, bladder, kidney, and colon. In
the back or neck in an effort to alleviate pain
animals, radiographic evidence has shown
or, more generally, spinal dysfunction. Some
that in1pla.nts can migrate long distances, eg,
interventions are borrowed from the hmnan
from the hip to the thoracolun1bar region or
chiropractic field ai1d incorporate
abdominal wall. Embedding feITomagnetic
mechanical devices known as acljusting
objects in tissue may compromise the
tools or activators. When used, tllis
quality of computerized scans such as CT
hand-held device, which resembles a metal
and MRI, causing artifacts and obscming

SYTinge witl1 a rnbber knob at tl1e end,
diagnoses. So far, no studies of gold bead
delivers a rapid "thwnp" to the patient,
implantation justify the risks of migration
roughly min1icking the action of a person
and aitifact-laden imaging studies.

applying a thmnb tluust to the body. More

Additional adverse effects of implai1ts
violent and less sophisticated methods
include activation of mast cells, ai·gyTia,
applied to horses incorporate mallets and
contact dermatitis, and gold-induced
blocks of wood intended to "drive
myelotoxicity.

protruding spines into line"; all such
methods have, as yet, failed to demonstrate

MANUAL THERAPY
therapeutic utility in anilnals.

Maimal therapy is a general tem1 that refers

Mechanisms of Action: Massage
to treatment approaches involving the
focuses on soft-tissue elements-nai11ely,
hands (such as massage or chiropractic).

muscles and tl1e enveloping fascia. Benefits

Treatments done with the hands may also
such as stress and blood pressure reducbe instrument-assisted. Although manual tion, normalized gastric motility, immune
therapies are most commonly used for
regulation, and ainelioration of depression
the treatment of somatic pa.in or other
may shai·e a conu11on mechanism of action.

musculoskeletal maladies, other indica

That is, the neuromodulatory ai1d homeotions may include lymph edema, irnrntu10-static effects of massage likely pertam to
suppression, or visceral discomfort.

parasympathetic nervous system stiJ.nula

Massage teclmiques vary widely, ranging
tion.

from the traditional kneading and stroking

Evidence now supports use of massage
to deep tissue work requiiing concerted
as an aid to muscle recovery after exercise
pressme. The most commonly researched
or injury, a means to m1proved circulation,
technique is Swedish massage, also known
and a way to bolster in1mune function. It
as classic muscular massage. Swedish
also addresses GI motility dysfunction and
massage incorporates several maneuvers,
neonatal issues such as fail me to thrive.

including efflemage ( stroking and gliding),

Massage also can improve lymphatic
tapotment (percussion), petrissage
drainage in cases of lymphedema, although

(kneading), ai1d friction massage. Efflew0
the effects may be transient.

age involves tissue compression. Tapotment

In contrast to massage, the rapid tJu·usts
vibrates tissue, petrissage stretches
in chiropractic have many theoretical-but
adherent fibrous tissue, and friction
no proven-mechailism(s) of action. The
lengthens cmmectivc tissue to reduce
lack of cU1Tent knowledge tends to be
contractures. Massage techniques are
extrapolated into speculation, and
multicultural and share silnila.rities; for
clm·opractic theories may be presented as
example, Swedish massage has similarities
fact. Claims are made that chiropractic
to the Chinese manual therapy teclmique
manipulation activates muscle spmdles,

Tui Na. Other massage techniques include

Golgi tendon organs, joint capsule

German cormective tissue massage and
mechanoreceptors, and receptors in the

Rolling, a strong and sometiines painful
skin, and that silnultaneous firing of
form of"deep tissue" massage introduced
multiple types of receptors modifies CNS
in the USA. "Medical massage" addresses
activity, bltu1tmg nociception and nom1alspecific diagnoses with soft-tissue techizing muscle tone, joint mobility, and niques, with the goal of treating certain
sympathetic nervous system activity.

conditions. It differs from relaxation

However, there is inadequate basic science

2082

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE
data to substantiate any of these claims. No
fractw·es, clotting disorders, osteopenia,
chiropractic technique has been shown to
and osteoporosis.

be superior to another; little chiropractic
research has been done in veterinary

Adverse Effects: Excessive pressure
patients.

from massage and forceful thrusts from

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chiropractic both have the pot�ntial to

Indications: For massage and chiropracinjure orgailS, vessels, neural tissue, or tic in veterinary patients, indications may
bones. Deep massage of the abdomen may
include neck or back pain or stiffness,
dainage organs (rupture/bleeding) and
inability to sit straight, reduced flexibility,
nerves (from direct pressure onto ne1ves );
muscle spasms, poor perfonnance,
intense pressure could dislodge a stent or
difficulty going up or down stairs, inability
catheter or embolize thrombi. With
to walk or run in a straight line, and
chiropractic manipulation, thrusts are not
abnom1al tail caniage. However, there are
always innocuous. A heavy-handed
no data from well-designed scientific trials
individual can seriously hann or even kill
to support the utility of such interventions
ai1 animal. Even milder thrusts may injure
in dogs, cats, or horses. The evidence for
ai1imals weakened by age, joint pathology,
massage in hwnan babies and adults
osteopenia, or neoplasia.

suggests support for including this

Injuries from chiropractic usually result
approach in animals with stress, pain,
from trawna to the spinal cord or brain
aithritis, sluggish digestion, or spinal cord
arising from impacted blood vessels, discs,
iajury.

or nervous tissue. Hun1an neurologic and
neurosurgical repo1ts have revealed an

Contraindications: Because adverse
association between stroke and upper
events of complementary therapies are
ce1vical manipulation. In addition to high
underreported, the true range and incidence velocity techniques, deep massage or other of risks from massage remain w1known.

pressing techniques in the suboccipital

Patients who ai·e especially fragile or ill
region have dainaged vessels and caused
generally require briefer and gentler
neurologic inlpaitment and death. Although
treatments with less digital pressure and
rare, stroke from cervical chiropractic
compression. Soft-tissue techniques would
manipulation of hun1an patients is well
not be applied directly over areas of
recognized and likely occurs more often
infection, acute inflai11.111ation, tumor, recent
than is repo1ted. The mechanism of injury
surgical procedures, or thrombosis.

typically involves aiterial dissection or

Sin1ilarly, massage may not be ideal in areas
spasm.

of acute inflan1.111ation, skin infection, bone

A study of hwnan patients with neck pain
fracture, burn, deep vein thrombosis, or
showed that 25% of patients reported
cancer.

increased neck pain or stiffness after

Contraindications for chiropractic might
chiropractic treatment, ai1d adverse
include conditions that weaken bone or
reactions were more likely to follow higher
other structural elements such that applying force techniques. The study concluded that a thrust to a vulnerable spine or limb could
because high-force teclmiques failed to
lead to serious injury. Exainples of
demonstrate superior effectiveness to
deossifying or destabilizing conditions
low-force maneuvers, chiropractors should
include hyperadrenocorticism, neoplasia,
consider conservative manipulative
secondary renal hyperpai·athyrnidism,
procedures. Especially in geriatric or
degenerative joint disease, and disk disease.

othe1wise fragile animals, manual therapy

Some animal chiropractors have advocated
techniques from the soft-tissue therapy
chiropractic for a gainut of problems,
repertoire constitute safer approaches than
including idiopathic lan1eness, interverteforceful, high-velocity techniques.

bral disc disease, Wobbler syndrome/
cervical vertebral insufficiency, spondy

Controversies: From a mechanical
losis, cauda equina syndrome, winary
standpoint, extrapolating hwnan chiropracincontinence, neuropathies, postsurgical tic theories to animals raises questions.

rehabilitation, traw11a, and organ pathology.

Biomechanical forces on the spine of a

However, many of these may actually
quadruped differ from those in bipeds.

constitute contraindications. One research

Furthermore, the vertebrae of horses are
based hwnan CAM reference places joint
the size of a hwnan fist and are surrounded
hypermubility, arthritis, and neurologic
by muscle, tendon, and ligainent layers
problems from disc disease under the
several inches thick, leading to questions
heading of contraindications to chiropracas to whether equine vertebrae can be tic, along with cancer, infectious disease,
manipulated at all.

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE

2083

Claims that spinal joints or other
chain) absorbs a photon from laser-treated
bones move "out of place" have not been
tissue, an electron within the chromophore
substantiated. Even if such lesions exist, the becomes excited and jumps from a low- to a diagnostic measures commonly used to
higher-energy orbit. This increased electron
detect them are not reproducible or reliable.

energy provides the impetus for the system

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The overall utility of manipulative therapy
to perform cellular activities geared toward
for the treatment of a condition (including
growth and repair.

its most common indication, musculoskel

The effects of laser on mitochondria,
etal pain) has not been established.

cells, and tissue is called "photobiomodula

Finally, additional controversy arises
tion." Thls collective process encompasses
from the fact that manual therapies may
not only the effects of lasers but also those
be delivered by nonveterinarians. Manual
of light-emitting diodes (LEDs) and other
therapies pose potential risks; when they
light sources. Light therapy also causes
are practiced by overzealous therapists with vasodilation by relaxing endothelial smooth insufficient education about anatomy and
muscle, likely through ni.t1ic oxide
pathology, the risk of injury to the patient
mechanisms. Vasodilation in1proves tissue
or the practitioner increases. Lack of
oxygenation and supports the migration of
familiarity with animal behavior, zoonotic
in1mune cells into tissue, further aiding
illness, and proper restraint techniques can
recovery.

pose risks to the therapist or bystanders.

Furthem10re, nonprofessionals may not

Treatment Parameters: Many fac-
have suitable liability insurance for such
tors in1pact how light influences tissue,
incidents.

including its power, wavelength, strength,

State laws may or may not allow
pulse characteristics, tissue contact, and
nonveterinarians to treat animals. Some
the nature of its beam. As indicated above,
may allow a human chiropractor or massage photobiomodulation entails changes at the therapist to treat nonhumans but require a
subcellular, cellular, and tissular levels.

certain level of supervision by a veterinar

Within the mitochondria, activated photons
ian. Because state laws differ, veterinarians
engender increases in production of ATP,
should check into the legal framework that
modulation of reactive oxygen species, and
allows or specifically di.sallows this form of
induction of transcription factors. These
care by nonveterinarians before referring or factors encow·age cell proliferation and delegating care to them.

migration, nonnalized cytokine levels,
enhanced production of growth factors,

LASER THERAPY
modulated levels of inflammatory
mediators, and improved oxygenation

The tenn "laser" originated as an acronym
of tissue.

that describes its process, ie, light
amplification of stimulated emission of

Power and Dose: The tem1 "low level
radiation. Like acuptmcture and massage,
laser therapy" (LLLT) refers to the use of
laser therapy lessens pain, relaxes muscles,
light at much lower levels than those used
and improves circulation. It accomplishes
for tissue ablation or photocoagulation.

this by altering the physiology of cells and

Newer, high-powered therapy devices that
tissue by means of light (photons) instead of deliver power similar to surgical lasers (but an acupuncture needle or manual pressure.

with a less concentrated beam) no longer

Therefore, treatment effectiveness and the
constitute LLLT. Some even heat tissue,
types of responses seen depend heavily on
meaning that the tem1 "cold laser" is also if and how light enters living tissue.

inaccurate.

The specific dose( s) of laser required to

Mechanisms of Action: For tissue to
heal tissue and treat pain remains unclear.

absorb light and alter its physiology, a

Calculating actual joules of energy delivered
photochemical or photo biologic event must
requires calculations of considerable
occur. Ideally, this event would take place
complexity. Fo1tunately, a wide range
within the target tissue(s), whether it be
of doses shows benefit for people and
skin, muscle, fascia, nerves, vessels, bones,
experimental animals, despite the wide
and/or joints. A "photoacceptor" molecule, variety in size, color, and hair coat.

also known as a "chromophore," responds

Wavelength: Most therapy units use red
to light by initiating a series of physiologic
or near infrared light, from 600 nm to 1070
responses that engender healing and
nm. This range constitutes the "optical
improved tissue homeostasis. When a
window" wherein effective absorption into
chromophore (such as cytochrome c
tissue is maximal. That said, units with
oxidase in the mitochrondria respiratory
green, blue, and violet light (-400 nm range)

2084

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE
are becoming more popular. Visible light
immunosuppressMt medications. In
ranges from 390 to 760 run, progressing
immature patients, higher powered laser
from violet to blue, green, yellow, orange,
therapy devices may stimulate premature
and red at 600 run.

closure of epiphyses. Thus, caution is

The types and depth of tissue that
warranted over long bones in animals
respond to light therapy depend on the

<lyrold.

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wavelength delivered. Certain molecules,
such as melanin and hemoglobin, preferen

Adverse Effects: Properly used, laser
tially absorb light in the 600 run range. To
therapy appears to be ve1y safe. However,
reach deeper tissues, wavelengths (810 run,
higher powered lasers run the risk of

980 run) that absorb less in superficial tissue
inducing them1al bums when in1properly
can be used, leaving more light to reach for
used. Tattoos, when lasered, CM cause
deeper sites such as bone, the brain, and
intense pain due to the high amount of light
internal organs.

absorption by deposited pigment. Questions

Certain laser therapy units emit two or
remain about the ability of laser therapy to
more beams to target a variety of tissues.

stimulate neoplastic growth Md, if so, at

Laser bean1s differ from other types of
what wavelength(s) Md power(s ).

light therapy, including LEDs, by being

Laser light can da.JTiage the retina,
monochromatic ( existing within a na.iTow
whether reflected off shiny surfaces or
band of wavelengths), coherent (tightly
shown directly into the eye. Laser goggles
aligned), and collimated (photons travel in
protect against indirect exposure but not
parallel). The more light scatters within
against direct. One should never look into
tissue, the less intense the biologic impact,
the applicator of a laser therapy device.

which may or may not be the desired

Laser light longer thM 760 nm is invisible
outcome. However, debate continues about
to the hurnM eye. As such, unless a
the relative value Md differences between
treatment applicator produces a visible
laser light Md LEDs.

finder bea.in or audible signal, the practi

Pulsed Therapy: It remains unclea.i·
tioner will not know when the laser is
whether pulsed wave or continous wave
emitting light. This could cause inadvertent
treatment is preferable for certain coneye exposure Md retinal dM1age. It also ditions. Pulsing reduces tissue warming,
could cause confusion about where the
which is especially important to deliver light
bea.JTI is pointing. For this reason, infrared
to deeper tissue; this requires more power to laser devices that lack a clear inclicator of provide adequate energy supply to the deep
when the bea.in is on pose potential safety
tissue target(s). Furthem1ore, pulsing limits
haza.i·ds.

dM1age to nerves Md su1Tounding tissue.

Pulsing may also improve tissue

Drug Interactions: The inununostimularesponses by resonating with a funda.inental tory effects of laser therapy may counteract frequency to which cells innately respond,
immunosuppressive actions of certain
commonly exhibited by neural structures.

medications. In addition, photosensitizing
agents such as hypericin in St. Jolm's wort
may augment the dem1atologic impact of

Indications: For more thM half a century,
laser light.

scientists have recognized the potential for
photomedicine approaches to reduce

Controversies: The main controversies
infla.irnnation, pain, Md swelling, as well as
surrounding laser therapy involve questions
to speed wound healing. More recently,
and unproven claims related to pulsed
medical researchers have uncovered
therapy, the advMtage of low- or highadditional benefits pertaining to serious powered w1its, a.i1d the longterm safety
conclitions, such as myoca.i·dial infarction,
of high-powered treatment.

spinal cord injury, traun1atic brain irtjury,

Md stroke. Additional applications include
alleviation of pain, trigger point pathology,

HERBAL MEDICINE
and joint dysfunction.

Herbal (botanical) medicine involves the
practice of prescribing plMt products, or

Contraindications: Contraindications to
products derived directly from plMts, for
direct laser treatment include carcinoma,
the treatment of disease. Herbal medicine
thyroid glMd, active hemo1Thage, Md
has survived since prehistoric tin1es, in pa.it
autonomic nerve centers. Laser therapy
because, until recently, there were no
should be avoided in patients in which
effective alternatives. Some plMts do
immune stimulation is not desired,
contain biologically active ingredients, Md
including those with lymphoma or on
some pharmaceuticals in widespread use

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE

2085
today are identical to, or derivatives of,

"energetic" nature of herbs. Western herbal bioactive constituents of historic folk
prescribing practices incorporate physical
remedies. Indeed, herbal and botanical
exrunination findings akin to stru1dard
sources fom1 the origin of as much as 300Ai
medical assessments, whereas TCVM
of all modem phannaceuticals.

recommendations depend heavily on the

Evidential support concerning use of
appearru1ce of the tongue and the feel of the

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plant products in veterinary patients is
pulse. Instead of considering the pharrnacoscarce and ranges from effective and safe logic effects of plru1ts, TCVM practitioners
to ineffective and risky. However, the
rely on prescientific metaphors to describe
methodologic quality of primary studies

U1e mechrutisms of action of products
on herbal medicines for many species is
prescribed. This, by definition, leaves them
generally poor. Trials usually lack finn
unawru·e of the actual biochemical
endpoints, and periods of observation arc
processes occun-ing ru1d is inconsistent
usually short; the clinical relevance of the
with modern medical principles and ethics.

observed effects is not always clear. In
addition, data that directly compare herbal

Mechanisms of Action: As aforemenremedies with well-established pharmaceutioned, herbs are plru1t-based drugs. Howtical products are often not available.

ever, they differ from pharmaceuticals by

However, as the database on herbs
having a multiplicity of active, inactive,
continues to grow, veterinruians seeking to
ru1d unknown constituents with additive,
prescribe natmal, plru1t-based compounds
synergistic, ancVor balru1cing properties.

should inspect the latest scientific literature

The medicinal effects of herbs may vruy
for information on the compound or
from batch to batch as growing, harvesting,
product of interest.

processing, ru1d storage conditions change

Making a rational decision about an
from year to year. These factors highlight
herbal product requires knowledge of its
the challenges of not only characterizing
active ingredients, its safety and adverse
but also ru1ticipating patient responses to
effects, and whether the herb has been
plru1t-based prescriptions.

shown to be as good as or better than
pharmaceutical products available for

Indications: Herbalists recommend herbs
the same purpose. This information is
for a wide rru1ge of disorders. For some
incomplete or unavailable for most herbal
conditions, the effects of plru1t-based drugs
products. In addition, there are no standards rival those of phannaceuticals. There is or quality control testing of the products
evidence of effectiveness of botanical
regularly reconrn1ended for animals. Risk
medicine for conditions ranging rrom
versus benefit questions must be considered digestive ailments to inflrunmatory for products with unclear constituents and
conditions ru1d inlmw1e suppmt. Many
tmknown active ingredients.

herbs exhibit ru1ticancer ru1d antioxidru1t
benefits. Veterinruiru1s should consult the

Preparations: Botanical products come
latest publications in medical literature to
in a vruiety of preparations intended either
assess U1e strength of research for a
for ingestion or external application. They
condition in question, because the field ru1d
may be fresh, dried, or freeze-dried;
evidential support for a variety of condiextracted ru1d preserved in oil, alcohol, or tions is growing rapidly.

water; ru1d delivered as liquids, capsules,
pills, poultices, or powders. Other fom1s of

Contraindications: Contraindications
plru1t-derived substances include essential
to the use of herbal products ru·e mostly
oils-volatile, rapidly evaporating oils
empirical ru1d depend on the health status
obtained from the leaves, stems, flowers,
of the animal ru1d the putative actions of the
seeds, or roots of a plru1t, commonly used
herb(s) under consideration. Situations
in aromatherapy or massage.

wruTru1ting special caution include
pregnancy, presurgical states in which tl1e

Philosophical or Cultural Approaches:

ru1tiplatelet actions of plru1ts interfere witl1

The philosophical approach of the praccoagulation, ru1d cru1cer. That is, wlforeseen titioner tends to dictate U1e type(s) of
herb-drug interactions could interfere with
herbs prescribed. For exan1ple, North
conventional care ru1d cause unexpected

American botanical medicine evolved from
results.

Europeru1 and Native Arne1icru1 traditions
relie::; more on pham1acologic actions thilll

Adverse Effects: Rightly or wrongly,
on folklore and metaphysics. In compruimost herbal medicines ru·e generally son, traditional Chinese veterinruy medical
considered safe. However, because of the

(TCVM) herbology considers the supposed
lack of mru1ufacturing standards, quality

2086

COMPLEMENTARY AND ALTERNATIVE VETERINARY MEDICINE
control, and known effects in veterinary

"herbal" medicines harbor potential for
patients, herbal medicines probably
zoonotic disease transmission. ln addition
present a greater risk of adverse effects and to health concerns, animal-derived interactions than any other CA VM therapy.

products in Chinese herbs contribute

Hannful effects of herbs arise from
significantly to animal mistreatment and

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intrinsic toxicity of the plant, herb-drug
the endangerment of c�rtain species. The
or herb-herb interactions, contaminants
unknown benefits of most manunal or
introduced during processing ( eg, heavy
insect ingredients cmrently do not appear
metals, microbial contan1inants, chemical
to justify administering these agents to
toxins, or pesticides), intentionally added
veterinary patients.

adulterants (eg, pharmaceuticals), or
inappropriate prescribing. Examples

NUTRACEUTICALS AND DIETARY
of especially risky herbs with known

SUPPLEMENTS
toxicities include those containing
pyrrolizidine alkaloids ( eg, comfrey and

Nutraceuticals comprise foods, or
chaparral); natmal flea treatments made
extracts from foods, that supposedly
from pennyroyal, known to be lethal for
confer medicinal benefits. Nutraceuticals
small aninlals; and skin treatments
have become popular with the veterinary
containing tea tree (melaleuca) oil, which
community; worldwide estimates of sales
can cause severe new·ologic manifestations approach $100 billion. Such economic and hepatotoxiciLy in cats if absorbed or
success has, for the most part, not been
consumed in sufficient concentrations. For
accompanied by scientific evidence of
many herbal poisonings, no antidote exists, efficacy. As with herbs, a broad and making death from "natural" treatments
continually expanding spectrum of
such as herbs frustrating. Many Chinese
nutraceuticals exists, but the mechamixtures have toxic components; their nisms of action, indications, contraindiamount may be kept "secret" by the cations, adverse effects, and evidential
manufacturer as a proprietary ingredient.

support vary with the product and

Substances such as strychnine ( a nemospecies. It is beyond the scope of this toxin) and aconite (a cardiotoxin) are not
brief summary to discuss specific
uncommon and pose particular risks to
nutraceutical products.

veterinary patients. The w1willingness of

One type of nutraceutical in particular
manufacturers to appropriately label
warrants mention. "Glandulars," "tissue bottles with the amounts of these toxic
extracts," or other scientific-sounding
constituents raises the danger to patients
equivalent names pmportedly improve the
and public health.

healtl1 of aninlals in which the san1e glands
or tissues have become dysfunctional.

Controversies: Before the development

Although these products are not FDA
of modern pharmaceuticals, botanicalapproved for veterinary usage, veterinary based treatments for vete1inary patients
glandula.rs and related supplements are
were common, as evidenced by veterinary
heavily promoted in the lay animal health
texts of the 19th and early 2tltl1 centwies.

literature. Their usage began in the USA

However, significant differences exist
during the late 19th centmy when the
between historical and cwTent use of these
practice arose of giving fresh thyroid
products. ln the past, herbal products were
glands to patients as tre;itment for
used as treatment because underlying
hypothyroidism. Subsequently, tissues and
disease conditions had yet to be identified.

extracts from other organs ( ovary, adrenal,

Treatment "success" reflected elimination
testis, thymus, brain, etc) becan1e popular

( or spontaneous resolution) of the problem.

treatments. Once standardized medica

Because the underlying pathology was
tions and hormonal replacements became
either vague or completely unknown,
available, medical practitioners largely
diseases with sinlilar signs could not be
ceased prescribing glandular derivatives
differentiated. Veterinarians had few other
because medication offered more reliable
approaches from which to choose. These
effects without the unpredictable
factors make it exceedingly difficult to
hormonal effects of extracts and concenobjectively evaluate the true utility of trates. The use of raw bovine pancreas in
historically used herbal remedies; they also
some clogs with exocrine pancreatic
highlight the imprudence of placing undue
insufficiency is a notable exception. Of
faith in the prescribing practices of the past
specific concern with spinal cord and brain
to determine treatments today.

"glandulars" is the potential for these CNS

Animal-based ingredients such as testes,
derivatives to transmit spongiform
penis, placenta, and horn found in Chinese
encephalopathy.

MANAGEMENT OF THE NEONATE

2087

HOMEOPATHY

Contraindications: Conditions for
which regular medical treatment would

Homeopathy, a form of practice initiated
provide a more meaningful diagnosis and
in tJ1e late 18th century by the Gennan
effective treatment, and for which delay
physician Sanmel Hahnemann, refers to
of proper care could prove injurious,

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treatment of disease with sometimes
should not be treated by homeopathy.

extreme dilutions of substances that in

Adjunctive homeopathic remedies, which
w1cli]uted fonn might cause symptoms of that may be prescribed as "complementary"

same disease; these substances supposedly
treatments to more conventional
promote healing. The substances are said
therapies, have been shown to be no
to possess vital healing energies that are
different from placebo in improving the
w1changed, or even strengthened, through
quality of life of children with mild to
the dilution process. Homeopathic remedies
moderate asthma when prescribed in
usually consist of lactose pills or liquids.

addition to conventional treatment in

No !mown, or even credible, mechanism
primary care.

of action exists by which extremely dilute
homeopathic preparations might have a

Adverse Effects: Chances of homeotherapeutic effect. Controlled studies have pathic remedies causing direct toxicities
demonstrated that the homeopathic
are slight, given their extreme dilution.

"provings"-sessions in which individuals

Homeopathic literature does describe a siturecord the symptoms caused by ingestion of ation involving a transient worsening of
the remedies-cannot distinguish between
signs called a symptom aggravation or
homeopathic dilutions and placebo. Indeed,
healing "crisis." Homeopaths may regard
no study has been able to distinguish
this as a treatment breakthrough and sign
homeopathic remedies from control
of impending improvement.

solutions, by any method of analysis. As a

Some practitioners advocate giving
result, most authorities consider that any
homeopathic "vaccines" or nosodes instead
clinical effects obtained from homeopathic
of conventional vaccines to avoid perceived
remedies are actually placebo effects.

health risks of standard vaccines. However,
homeopathic vaccines have consistently

Indications: Although largely w1supfailed to provide reliable protection against ported by research, homeopaths typically
infectious agents in scientific studies of
feel that their remedies can be prescribed
both people and animals.

for most medical conditions, including
cancer. Reported veterinary uses have

Controversies: A preponderance of
included inappropriate wination in cats;
evidence indicates that effects of homeopababesiosis, atopic dermatitis, idiopathic thy cannot be distinguished from placebo.

epilepsy, and paroxysmal tachycardia in

Therefore, the question remains wh�ther it
dogs; fattening of, stillbirths, and diarrhea in is ethical or misleading to offer an pigs; postpartwn fertility, mastitis, anestrus,
ineffective treatment to patients and their
and control of ticks in cattle; diarrhea in
caregivers. The unscientific premise of
calves; salmonellosis in broiler chickens;
homeopathy calls into question its
and hel.rninth parasitism in sheep.

legitimacy as a medical treatment.

MANAGEMENT OF THE NEONATE

LARGE ANIMALS
aspect of managing the large animal darn
includes appropriate nutrition and body

Appropriate management in the peripartun1
conditioning in the pre- and postpartwn
period can substantially reduce morbidity
periods to reduce the risk of pregnancyand mortality for large animal dams and related diseases such as pregnancy toxemia,
their offspring. As much as 5% of foals,
hypocalcemia, and vaginal prolapse; as well

5o/o-109'o of calves, and 100/o-15% of the
as to optimize hygiene, colostrun1 quality,
annual lamb crops die before weaning in the and fetal and neonatal growth. Appropriate USA, with 500/o-700/o of neonatal mortality
anthelmintic therapy and vaccination of the
occurring in the frrst 3 days of life. A key
dam several weeks before parturition will

2088

MANAGEMENT OF THE NEONATE
further protect dam and offspring from
factors (prematurity, dysmatU1ity, maternal
subsequent disease.

rejection, multiple birth, or any other

Pa.iticula.r conditions affecting large
condition Ii.mi.ting neonatal mobility and
animal neonates in the immediate
strcngtl1). Manually stripping the teats of the
postpartum pe1iocl include prematw·ity,
clam to remove wax plugs and to check for
failure of passive transfer, sepsis, perinatal
the presence of colostnun may facilitate

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asphyxia, predation, mismothering,
successful nursing attempts. The neonate
meconium in1paction, a.11d various
should be exmnined for any obvious
congenital diseases. Substantial losses can
congenital problems that may inhibit the
occur in flock or herd situations, and
ability to stand or to nurse effectively,
altering problematic aspects of manageincluding signs of prematurity, musculoskelment can therefore be of great benefit.

etal abnormalities, and cleft palate (and in

Generally, equine and camelid neonates ca.11
crias, choanal atresia).

be managed more intensively than neonatal

Healthy foals begin sucking colostrU111
calves, pigs, or la.tnbs because of economic
within 1-2 hr after birth, and maternal
considerations. However, rapid assessment
m1tibodies a.re detectable in the foal's blood
and appropriate management of all large
within 6 hr. Although adequacy of passive
animal neonates in the in1mediate
transfer of immm1oglobulin is generally
postpartum period can substantially reduce
assessed at 18--48 hr, neonates at high risk
the need for intensive and expensive
of fail me of passive transfer (FPT) ancVor
measures in any species.

sepsis may be tested as early as 6--12 hr after

Growth rates of neonates a.i·e particularly
bilth. Weak or abnonnal neonates that do
rapid during the first month of life. For
not stm1d or nurse successfully within 2-4
exan1ple, the average Thoroughbred foal is
hr should be supplemented witl1 colostnun
born at -68"Ai of its matme height mid
early (commonly tube or bottle fed). A 50-kg
lOo/o-11 % of adult weight, with an average
foal requires a minimwi1 1.5---2 L (ideally
weight gain of 1 .5---1. 7 kg/day. Regular

5o/o-12% of body wt) of good.quality
monitoring of weight gain can thus be a
colostnun (-70--75 g ofigG), fed over
practical aid in detern1ining healthy growth
multiple feedings in the first 12-18 hr after
and development. Foals that lack mattu-ity
birth. Colostmm of other species has been
can display a spectrum of clinical and
used ( such as cow colostmm for foals, crias,
clinicopathologic abnonnalities that include kids, and lm11bs) but will not necessarily short silky hair coat, "floppy" ears,
provide pathogen-specific immWlity.

incomplete ossification of the tm·sal and

Commercial colostrum substitutes have
cm-pal bones, hyperextended fetlock joints,
similar lilnitations and may increase tl1e 1isk
domed forehead, abnonnal temperattu-e
of adverse immwiologic reactions if a
regulation (normal to low body temperasubsequent plasma transfusion is needed.

tme), depressed n1entation, weakness, poor

Oral administration of colostnun or
suckle reflex, and respiratory dysfunction.

colostral substitutes has only minilnal

See also NEO Al'.A.L INTENSIVE (" Allis AND
benefit in neonates> 18-24 hr after bitth

EMERGENCIES IN FOALS, p 1708, and DIARllllEA IN
because of the linlited capacity of the

NEO ATAL RUMINANTS, p 27r..

neonatal small intestine to absorb
macromolecules.

FAILURE OF PASSIVE TRANSFER

Complete FPT in foals is defmed as a
serum lgG concentra�ion of <400 mg/dL

Large animal neonates m·e born with limited
at 24 hr of age, with partial FPT being
energy rese1ves and are considered
associated with a serum IgG concentration
immwiocompetent but immunologically
of 400--800 mg/dL. Healthy, vigorous foals
naive at birth (ie, aganunaglobulinemic).

with complete FPT ( <400 mg/dL) and

Thus, ensuring tl1e provision of good.quality
high-risk foals with partial or complete FPT
colostrum by the dan1 and adequate

(IgG �800 mg/dL) should receive equine
colostnun intake by the neonate a.re c1itical
plasma (IV) that contains an IgG concentrainfluences on neonatal survival. Good.qualtion of> 1,200 mg/dL. The average IgG
ity colost11.m1 tends to be sticky, yellow, and
concentration in 1 L of equine plasma will
tl1ick with a.specific gravity of >1.060 in
typically increase the serwn IgG concentrama.res. All factors that might compromise tion of a 50-kg foal by 200-300 mg/dL;
colostnun quality, volwi1e, and delivery to
therefore, 2-4 L of plasma may be necessmy
the neonate should be recognized; these
to achieve a final serw11 IgG concentration
include maternal factors (disease dming
uf>SOO mg/dL in a foal with complete FPT
gestation, prematme lactation, maiden

(i11itial IgG <200 mg/dL).

da.tn), deli.very factors (abnonnal parturi

Frozen plasma should be thawed and
tion, placental abnormalities), and neonatal
warmed slowly to room temperattu-e using

MANAGEMENT OF THE NEONATE

2089
wam1 water, and subsequently administered especially Clostridium spp, are reported slowly tJu·ough an aseptically placed jugular
in <5% of systemic neonatal infections.

catlleter, using an appropriate blood filter

The routes of entry for tllese bacteria
set. Initially, plasma is administered at 0.5
may include tile placenta, umbilicus, and
mL/kg over 10-20 min ( -20-30 mL to an
respiratory and GI tracts.

average foal) while monitoring for

All sepsis syi1dromes ( eg, sepsis, severe
transfusion reactions. Clinical signs of
sepsis, septic shock, multiple organ

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transfusion reactions may include muscle
dysfunction) have a common patllogenesis
fasciculation, increased heart or respiratory
tllat also includes endotoxemia related to
rates, fever, respiratory distress, laryngeal
grain-negative infections. Endotoxins
swelling, abdominal pain, pale mucous
stimulate macrophages to release an array
membranes, or collapse. If no adverse
of cytokines ( eg, IL-6, IL-1, TNF-cx) and
reactions are observed dilling the initial
activate pro-inflairnnato1y enzyines ( eg,
slow infusion, tile remainder of tile
phospholipase A2). Together, tllese factors
transfusion may be administered at rates
lead to signs of inflai11mation (fever,
up to 40 mL/kg over 60-90 min ( eg, 2 L
vasodilation, myocardial depression),
tllroughout 60 min for a 50-kg foal).

impaired microcirculation, capillary leak,

Although serl1l11 IgG is measured less
and intra vascular coagulation. Sepsis
commonly in ruminants, concentrations
initially triggers a procoagulant state, which

> 1,600 mg/dL are ideal. Serum total protein
may lead to disseminated intravasculai·
may also be used as a rough estinlate of
coagulation and secondary consumptive
colostral transfer in ruminants and should
coagulopathy. A variety of otl1er pathogenexceed 5-5.5 g/dL. An IgG concentration derived molecules can set off similar host

>1,000 mg/dL is considered adequate in
responses. Thus, toxic shock syndromes
neonatal camelids. Administration of
resulting from streptococcal or Staphylo
camelid plasma ( eitller rv or IP) is an
coccus aureus infection are hyperinflai1miaacceptable treatment of FPT in llamas and tory septic syndromes that closely resemble
alpacas, altllough IP administration should
diseases characterized by endotoxemia.

be limited to vigorous neonates, to minimize

A vai·iety of immunologic and managetile risk of secondary complications.

ment factors predispose foals to sepsis.

Although foals can respond immunologi

SEPSIS IN FOALS
cally in utero to bacterial or viral infections,
their ability to do so is less than tllat of

Sepsis is a clinical syndrome defined by tile
adults. Deficits in the physiologic response
development of a systemic inflan1matory
to infectious agents in neonates relate to
response syndrome (SIRS) in response
reduced chemotaxis and killing capacity of
to proven or suspected infection. The
neonatal neutrophils, tile presence of
condition implies an extensive, whole body
antigenically naive T cells, and a qecreased
insult after invasion of bacte1ia into tissue
concentration a.Ild impaired ftmction of
or a body fluid or cavity. The presence of
monocytes. However, tile major risk factor
viable bacteria in tile bloodstream is tenned
for sepsis in foals is failure to receive ail
bacteremia. Sepsis and SIRS are two of tile
adequate quality or qua.I1tity of colostral
most common problems of equine neonates, a.I1tibodies. If colostrum intake is insufficient while bacterial infection accounts for neai·ly a.Ild IgG levels remain low, tile foal is not one-third of all foal mortality.

only deprived of specific a.I1tibody protection, but neutrophil function is also se1iously Etiology and Pathogenesis: Grai11-impaired. Otller factors that influence
negative bacteria, particularly Enterodisease incidence include tmsaiutary bacteriaceae witll a predominance of
environmental conditions, low gestational

Escherichia coli, remain the most conunon
age of the foal (prematmity or inunaturity),
isolates (60%-70%) from neonatal foals witl1
poor healtll a.Ild condition of the dam,
sepsis. However, the prevalence of
difficulty of pai1:urition, a.Ild U1e presence of
gran1-positive bacteria has increased
new patllogens in tile enviromnent against
tllroughout tin1e, and blood cultmes remain
which the mai·e has no a.Iltibodies.

important in diagnosis and treatment.

Common grain-negative pathogens include

Clinical Findings and Lesions: The

E coli, Klebsiella spp, Enterobacter spp, clinical presentation of sepsis depends on

Actinobacillus spp, Salmonella spp, and the duration of illness, the integrity of the

Pseudomonas spp. Approximately 25%-400Ai host inunune system, tile affected body of infections also involve grai11-positive
systems, and the severity a.Ild route of
bacteria, witl1 Streptococcus spp being tl1e infection. Frequently affected orga.I1
predominant isolate. Anaerobic patl1ogens,
systems include the umbilical remna.Ilts,

2090

MANAGEMENT OF THE NEONATE
and CNS, respiratory, cardiovascular,

Diagnosis: Currently, there is no ideal
musculoskeletal, renal, ophthalmic,
diagnostic tool to detect early sepsis.

hepatobiliary, and GI organs. In the early

However, a scoring system has been
stages of sepsis, clinical signs are often
developed for neonatal foals to establish the
vague and nonspecific, with affected
likelihood of neonatal infection and aid the

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neonates merely displaying some degree of
identification of sepsis at a treatable stage.

depression and lethargy. Owners report that

This "sepsis score" incorporates a combinafoals appear to lie down more than usual.

tion of historical, clinical, and laboratory

The ma.re's udder is often distended with
variables and may also se1ve as an indicator
milk, indicating that the foal is not nursing
of whole body insult, SIRS, or multiple organ
at a normal frequency.

dysfunction. However, the specific definition

Clinical signs can progress to a complete
criteria for both SIRS and sepsis a.re most
loss of suckle reflex, hyperemic mucous
rigorously validated in people and have been
membranes with a rapid ca.pilJary refill time
conceptually applied to equine neonates only
due to peripheral vasodila.tion, tachycardia.,
recently. Based on pediatric hwnan and
and potentially early petechiae related to
general veterinary guidelines, SIRS may be
capillary leak. In the advanced stage of
clinically defined by tl1e presence of at lea.st
illness, when the infection overwhelms the
two of tl1e following five clinical criteria., one
host's inmmne system and compensatory
of which must be abnormal temperature or
responses, septic shock ensues. Affected
leukocyte count: 1) core temperature below
foals are severely depressed, recwnbent,
or above the nonnal range for tl1e animal's
and hypovolemic, which manifests as cold
age; 2) tachycardia., defined as a mean heart
extremities, thready pulse, and poor
rate >2 standard deviations (SD) above
capillary refill time. Foals may be hyper- or
normal for the animal's age in the absence of
hypothermic, tachycardic, or bradycardic.

external stimulus, chronic drugs, or painful

In the face of sepsis, bacteria spread
stimuli; 3) bradyca.i·dia, defined as a mean
hema.togenously to va.iious organs,
heart rate below the nonnal range for the
manifesting as respiratory distress,
animal's age, in the absence of external vagal
pnewnonia., diarrhea, uveitis, meningitis,
stimulus, [3-blocker drugs, or congenital
osteomyelitis, or septic arthritis. Dysfuncheart disease; 4) mean respiratory rate >2 SD
tion of two or more organs is termed
above nonnal for age, or animals undergoing
multiple organ dysfunction syndrome.

mechanical ventilation for an acute process

Hypoglycemia. conunonly accompanies
not related to general anesthesia or
systemic infection and is associated with
underlying neuromuscular disease;
bacterial conswnption and reduced

5) leukocyte count increased or depressed
glycogen reserves. Severely hypoglycemic
for age (not secondary to chemotherapyfoals may be unable to rise and show induced leukopenia) or > 1()0,,(, inm1ature
depression, convulsions, and eventually
neutrophils. Infection itself may be
death. Furthermore, clinical signs
suspected or proven (by positive culture,
suggestive of relative adrenal insufficiency
tissue stain, or PCR) and ca.used by any
have been identified in animals with
pathogen, or refer to a clinical syndrome
prolonged sepsis. Primary relative adrenal
associated with a high probability of
insufficiency can occur after a direct insult
infection. Evidence of infection includes
to the adrenal glands (hemorrhage or adrenal
positive findings from clinical exanunation,
ischemia.), whereas chronic, illness-induced
imaging, or laboratory tests ( eg, WJ3Cs in a
stress may exhaust the adrenal rese1ve and
nom1ally sterile body fluid, perforated viscus,
deplete the production of cortisol. Septic
chest radiograph consistent witl1 pneumoneonatal foals are often neutropenic with a nia). Ultimately, sepsis refers to the presence
high ratio of band (inunature) to segmented
of SIRS with suspected or proven infection.

neutrophils. The neutrophils may exhibit

Depending on the specific organ systems
toxic changes, which a.re highly suggestive
involved, an un1bilical, a.bdonunal, and
of sepsis. Fibrinogen levels >600 mg,'dL in a
synovial ultra.sound exa.nunation; arterial
foal <24 hr old are indicative of an in-utero
blood gas analysis; a.i·throcentesis;
infection. Other chemistry abnonnalities
cerebrospinal centesis; and chest,
may include azotemia. due to inadequate
abdominal, and distal limb racliographs are
renal perfusion or perinatal asphyxia., and
indicated. Advanced diagnostic in1aging
increased bilirubin secondary to endotoxin
techniques ( eg, CT of the distal limbs in
dan1age to the liver. A high anion gap (>20
foals with septic arthritis) may also help
mEq/1), hyperlactatemia., hypoxemia,
with prognosis.

hypercapnia., and a mixed respiratory and

Serun1 IgG levels should be measured in
metabolic acidosis may be present with
any questionably sick neonate to eliminate
arterial blood gas analysis.

inadequate transfer of passive immwuty as

MANAGEMENT OF THE NEONATE

2091
a 1isk factor for sepsis. IgG levels <200
clinical and hemodynamic changes
mg/dL indicate complete failure of passive
associated with endotoxemia and septic
transfer of maternal antibodies, whereas
shock. Low doses of flunixin megluniine

IgG levels >800 mg/dL are considered

(0.25 mg/kg, IV, tid-qid) may help reduce
normal.

signs of endotoxemia. Additionally,

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A positive blood culture confinns the
administration of low doses of polymyxin B
presence of bacteremia in septic foals, but

(6,000 IU/kg, diluted in 300-500 mL of
a negative culture does not exclude the
saline, slowly IV) is an investigational
possibility of infection. Differential
treatment used to neutralize systemic
diagnoses include neonatal encephalopathy
endotoxin.

(seep 2094), hypoglycemia, hypothermia,

Nutlitional support is important, because
neonatal isoerythrolysis ( see p 11 ), white sepsis creates a catabolic state in foals. If
muscle disease (seep 1172), prematulity or
the foal is not nursing adequately, it should
immaturity, neonatal pneumonia, and
be fed mare's milk or a mare milk substitute
uropelitoneum (seep 1506).

at 15o/o-25% of its body weight throughout
each 24-hr period. An indwelling nasogastric tube should be placed in foals with a Treatment, Control, and Prevention:

decreased suckle reflex. Parenteral

Foals suspected of being septic should be
nutrition may also be helpful to provide
placed on broad-spectrum antibiotics active
adequate nutrients in the face of GI
against both gram-positive and gram-negadysfunction. Administration of gastric tive organisms. Penicillin (22,000 IU/kg, IV,
protectants ( eg, ranitidine, cimetidine,
qid) in combination with amikacin sulfate
omeprazole) has been proposed as an

(20-25 mg/kg/day, IV) provides good initial
adjunct therapy in sick neonates.

coverage until culture results are available.

System-specific therapy includes lavage

Metronidazole ( 10-15 mg/kg, PO or IV, tid)

of septic joints with stelile fluids, regional
may be necessary if an anaerobic infection
limb perfusion, and nasal oxygen suppmt

( eg, Clostridium) is suspected. A third

(2-10 Umin) or ventilation for foals with
generation cephalosporin ( eg, ceftiofur,
respiratory failure or central hypoventila4.4-6 mg/kg, IV, bid-qid) may also be used tion. Corneal ulceration may be treated with
as a broad-spectmm agent in foals with
low doses of topical atropine (although it
renal compromise. Cefpodoxirne proxetil
may cause ileus), NSAIDs, and broad-spec

(10 mg/kg, bid-qid) has been reconm1ended
tnun topical antimicrobials. Entropion
for treatment of bactelial infections in
generally requires mattress sutures of the
equine neonates. Cefepime ( 11 mg/kg, IV,
lower eyelid. Surgical removal of infected
tid) is a fourth-generation cephalosporin
umbilical remnants may be indicated.

with enhanced antibactelial activity.

Early goal-directed IV fluid therapy is

Prognosis: Recovery from neonatal
needed to restore tissue perfusion,
sepsis depends on the severity and
attenuate the cytokine response, and
manifestation of the infection. Currently
reverse cellular injury. Volume expansion
reported survival rates are 50o/o-81 %
should be achieved using a balanced
in referral centers, depending on the
electrolyte solution ( crystalloid) or plasma
underlying disease. Severe neonatal

( colloid). Inmrnnologic support in the fmm
pulmonary disease has been associated
of IV plasma transfusion (1-2 L) is also
with a higher mortality (35o/o-50"A,). Early
indicated to raise the IgG level to >800
recognition and intensive treatment of
mg/dL. Fluid resuscitation is aimed at
neonatal sepsis improves the outcome,
nom1alizing specific cardiovascular
although an average of 1-4 wk of intensive
variables ( central venous pressure, mean
care should be expected. If tile foal survives
artelial pressure, urine output, and central
the initial problems, it has the potential of
venous oxygen saturation), while in1proving becoming a healtl1y and useful adult. One clinical paran1eters. Severe septic shock
report documented that surviving bacteremay require initial fluid rates of 40-80
mic Thoroughbred foals were as likely to
mL/kg/hr. Because many foals are hypostart races as their siblings, although their glycemic, slower continuous infusions of
earnings were lower. The latter retrospec2.5o/o-5% dextrose-containing solution tive case series (n=423) further identified
should be administered simultaneously with that odds of survival were negatively rehydration fluids.

associated with age at admission, band

Treatment with hyperinmmne antiendoneutrophil cow1t, and serum creatinine toxin serum may be considered in foals with concentration, and positively associated endotoxemia. Antiprostaglandin drugs have
with rectal temperature, neutrophil count,
been found to counteract several of the
and arterial blood pH. Additionally, in a

2092

MANAGEMENT OF THE NEONATE
recent prospective multicenter study, septic
stages of neonatal pnewnonia Apparent
foals had increased odds of nonsurvival for
signs of lung dysfunction may also be
each 1 mmol/L increase in L-lactate
associated with nonrespiratory conditions
concentration at admission.

such as metabolic derangements ( eg, severe
acidosis), pain, abdominal crisis, fever, high

SPECIFIC CLINICAL
environmental temperatiu-es, or excitement.

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MANIFESTATIONS OF SEPSIS

Diagnosis: Thoracic radiographs are

Neonatal Pneumonia
often essential to establish ilie presence of
respiratory disease and detem1ine the type

See a(,so ENZOOTIC PNEUMONIA OF CALVES AND
and extent of lung irwolvement in neonates.

SI-IIPPING FEVER PNEUMONIA, p 1431, and ACUTE

Artelial blood gas analysis is preferentially

BRONCIIOINTEll.$TITlAL PNEUMONIA IN FOALS, p 1452.

used to assess the degree of hypoxemia ru1d

Hematogenous infection of the lung
hypercarbia. The more common arterial
occurs in association with sepsis, which
blood srunpling sites ir1 neonatal foals
may be acquired in utero from placental
include the dorsal metatru·saJ artery, the
infection or perinatally through environbrachia! artery on the medial aspect of the mental contamination ( eg, omphalitis,
elbow, tl1e carotid rute1y, and tl1e transverse
omphalophlebitis), and is more conunon in
facial artery. Thoracic ultrasonography may
neonates with failure of passive transfer
further identify tl1e presence and location

(FrP). Escherichia coli, Klebsiella spp,

(affected side) of peripheral lung consolida

Actinobacillus equuli, Salmonella spp, and tion, pleural effusion, and abscesses in foals Streptococcus spp are some of the more
witl1 pnewnonia.

common bacteria involved in neonatal
pnewnonia in foals. Descending respiratory

Treatment: Broad-spectmm ru1tibiotic
infections may be related to inhalation
treatment of septic pnewnonia should be
pneumonia (transmission of viral, bactelial,
initiated before culture results are available
or fungal airborne pathogens), aspiration of
and is targeted toward the most conunon
infected an1niotic fluid due to placental infecpathogenic bacteria ( see above). Additionally, tion, aspiration of gastric reflux, iatrogenic
intranasal oxygen tl1erapy and cardiovascular
aspiration ( oil, medication, oral supplesupport (including goal-directed fluid ments), and aspiration of milk and mecotherapy) are essential in treatrnent of niun1. Aspiration of meconiwn occurs in
compromised foals. Specific respiratory
utero in foals that experience fetal distress.

support may further include judicious

Early in life, localizing clinical signs of
suctioning, coupage, bronchodilators ( eg,
lung infection may be absent even in the
albuterol inhalants), and mucolytic agents.

presence of extensive disease. Dyspnea may Recwnbent foals should be main tamed ma be seen in severely affected foals and
sternal position to limit positional atelectasis.

manifest as an increase in respiratory rate,
effort, or thoraco-abdominal asynchrony

(paradoxical breathing). However, signs

Omphalitis, Omphalophlebitis, and
of respiratory distress and hwoxemia are

Patent Urachus
frequently vague. Even some severely

A patent urachus is the most common
hypoxemic foals may show only restless

Wllbilical abnonnality m neonatal foals.

ness or considerable resistance/struggling

Diagnosis may be based on visual appears
during handling or restraint. Auscultation
ance ( urine dripping from the un1bilicus) or
of tl1e Jw1g fields in newborn foals cru1 be
on umbilical ultrasound exrunination, which
very misleading. Fluid sounds are normal
can also exclude Lunbilical irLfections.

immediately after birth, as are crackles due

Clinical signs of infection may include
to simple atelectasis of tl1e "down" Jung
discharge, pair1, and heat and swelling of tl1e
during lateral recumbency. Conversely,
un1bilicus, altl10ugh some infections of
foals with significru1t pneumonia can have
deeper str·uctw·es may only be confinned
minimal abnonnal findings on auscultation.

via ultrasow1cl. The normal equine wnbilical

Mucous membrru1es should be exan1ined for stump is usually <18 mm in diameter at 24
color, moisture, injected vessels, and the

Ju- of age, and it decreases to <15 nu11 at 7
presence of cyanosis (which likely indicates
clays of age. The umbilical vein (as it courses
severe hypoxemia with a Pa02 <40 nunHg).

crar1ially to the liver) should be <10 mm in

Additionally, weakness, depression,
dian1eter at 24 hr after birth and is slightly
anorexia, weak or absent suckle reflex,
smaller than the arteries, which can be
dehydration, and fever may be noted in foals followed via ultrasound as they course with respiratory disease. Cough and nasal
caudally on eitl1er side of ilie bladder.

discharge are usually absent in tl1e early

Ultrasonographic abnormalities consistent

MANAGEMENT OF THE NEONATE

2093
with omphalitis or omphalophlebitis in foals times daily to the umbilical stump until the include enlargement of the vessels beyond
umbilical remnru1t is dry.

normal limits, asynunet1y of ruteries with
enlargement, abscessation of stump or
single vessel, gas shadowing indicative of an

Neonatal Uveitis
ru1aerobic infection, edema of strnctures,

Neonatal sepsis may initiate intraoculru·

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ru1d hematoma formation.

seeding or endogenous inflrunmation due
to uveal tissue injury. Secondaiy ocular

Treatment and Prognosis: A congenital
infection as well as endotoxemia, free
patent urachus and mru1y milder cases of
radical fonnation, tissue hypoxia, and
patent urachus secondary to omphalitis
alterations in pH may trigger vasculru·
may respond to local therapy ( chemical
damage at a cellular level ru1d induce
cautery with silver nitrate, topical procaine
clinical uveitis. Various chemical mediators,
penicillin G, and the1mocautery) ru1d
including histamine, serotonin, plasmin,
systemic ru1timicrobials. However, caution
kinins, complement, and ru·achidonic acid
must be used not to place caustic agents
derivatives mediate acute vasculru· chru1ges.

further than 1 cm into the stump, because

The ensuing increase in vasculru· penneabilensuing tissue necrosis may predispose to ity of the blood-oculru· bru-rier allows
fmther bacterial infection. Treatment of
cellular components, fluid, ru1d plasma
wnbilical infections may include both
proteins to escape into the surrounding
medical (Jongtem1 systemic antimicrobials)

extra vascular uveal stroma ( edema),
and surgical options (umbilical resection).

ocular fluid comprutmcnts (aqueous flare,

Foals that should be referred to smge1y
plasmoid vitreous), ru1d subretinal space
include those with substantial abscessation

(retinal detachment). Congenital and
or venous involvement that extends as fru·
acquired adnexal disease, prolonged lateral
as the liver. Mixed infections are likely, and
recumbency, dehydration, ru1d a decreased
common isolates include grrun-negative
menace response in the neonate may also
bacte1ia ( eg, E coli, Klebsiella, and
induce a reflex-mediated uveitis due to

Ent erococcus ), grru11-posi tive orgruusms
corneal trauma. Reflex-mediated uveitis is

( especially j3-hemolytic Streplococcu.s ),
generally transient ru1d leaves the uveal
ru1d ru1aerobes (includingBacleroides
tract unaltered once the corneal insult
ru1d Closlridiwn), similar to orgruusms
resolves.

identified in generalized neonatal sepsis.

Clinical signs of anterior uveitis are

Overall survival rate with appropriate
more evident and generally consist of
treatment is reported as 87%. However,
conjunctiva] hyperemia, ciliruy flush,
severe conctuTent disease such as
corneal edema, aqueous flare, hyperemia
secondary hepatic abscessation, sepsis,
ru1d swelling of the iris, miosis, and a
or multiple joint arthritis are suggestive
decrease in intraocular pressme. Signs of
of a poorer outcome. Septic peritonitis
ocular pain, blephru·ospasm, increased
or uroperitoneum are considered rru·e
lacrimation, and photophobia are variable,
complications. Umbilical infections ru·e
whereas hyphema, hypopyon, and
generally less common in neonatal crunelids intraoculru· fibrin deposition are seen in thru1 in neonatal foals.

cases of severe inflrunrnation. Intraocular
fib1in fonnation occurs due to egress of

Prevention: After ru1 tmcomplicated
essential clotting factors into the aqueous
birth, it is ideal to allow the tunbilical cord
ru1d vitreous humor during uveal inftarnmato break spontaneously when the dan1 1ises.

tion. Furthermore, the regulation of

In foals, the cord is nru-rowest at -5 cm
fibrinolysis is altered in endotoxemic
from the body wall, which is the natlli'al
lli1in1als. A prolonged increase in the activity
sepru·ation (break) point. lf the cord has to
of plasminogen activator inhibitor may
be mru1ually sepru·ated, it is best to provide
favor coagulation ru1d impede intraocular
steady traction on the cord while suppo1ting fibrinolysis.

the foal's abdomen at the umbilicus. Shru-p

Acute posterior uveitis is often
trru1section of the cord with a clan1p or
overlooked if tu1accompru1ied by appru·ent
ligature prevents retraction of the tu11bilical
changes in the anterior chrunber. Retinal
structures and may be associated with a
vascttlai· congestion, hemorrhage, edema,
greater incidence of subsequent tu11bilical
cellttlru· infiltration, or retinal detachment
complications. However, excessive
may be seen. The vitreous also tends to
hemorrhage can be addressed by trru1sient
appear hazy, with blurring of fundus details,
ligation with w11bilical tape or a clru11p.

due to cellular infiltration and proteina

After bi1th, 1 % iodine or 0.5% chlorhexidine
ceous debris. The type of inflrunmatory
solution (preferred) should be applied 2-4
cell reaction is generally classified as

2094

MANAGEMENT OF THE NEONATE
neutrophilic (suppurative ), granulomatous,

(eg, IL-I, IL-6, TNF-a) may all contribute to
or lymphocytic-plasmacytic. Neutrophilic
cell injury and/or death.

inflanunation is an acute response to

Risk factors for perinatal asphyxia may
bacterial infection and sepsis, although
include maternal ( eg, respiratory disease,
intraocular bacteria may not be present.

endotoxemia, hemoIThage/anemia, surgery/

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Neutrophils can accumulate in the anterior
cesarean delivery), placental (eg, bacterial,
chamber in the forn1 of hypopyon, which is
ftmgal- or endophyte-associated placentitis,
often sterile and thus indicative of inflammachronic or acute premature uteroplacental tion rather than local infection. Proteases
separation), and fetal causes (eg, twinning,
released from neutrophils may also induce
congenital abnormalities, dystocia,
corneal endothelial damage, thereby
meconium aspiration, sepsis, prematurity,
resulting in corneal edema. Lymphocyticdysmaturity). Fetal and maternal factors are plasmacytic inflammation is often
those that induce hypotension or reduced
suggestive of an inmmne-mediated reaction
tissue oxygenation, whereas placental
and indicates some type of chronicity.

pathology will impair uteroplacental
perfusion. Areas of chronic placental

Septic Arthritis
separations may thus lead to chronic

See
hypoxia of the fetus. However, tl1e most

SEPTIC ARTJ-JRITIS, p 1062.

acute cause of perinatal asphyxia is
complete premature placental separation

NEONATAL ENCEPHALOPATHY
at birth ("red bag" delivery).

(Neonatal maladjustment syndrome, Hypoxic
ischemic encephalopathy, Barker, Wanderer,

Clinical Findings: CNS signs are most

Dummy)

prominent in cases of perinatal asphyxia,
but renal, cardiac, GI, and pulmonary

Neonatal encephalopathy (NE) is a
systems may also be affected. A detailed,
common, noninfectious CNS disorder of
systematic examination of foals wiili NE is
neonatal foals, resulting in clinical signs
therefore warranted. Renal compromise of
such as lethargy, inappropriate behavior,
foals with NE may present as anuria or
seizures, and other neurologic deficits. The
oliguria, whereas GI effects of perinatal
condition is associated with the broader
asphyxia may include co]jc, transient ileus,
syndrome of perinatal asphyxia
meconium impaction, gastric ulcers, gastric
syndrome, which is believed to result from
reflux, bloat, diarrhea, and necrotizing
unrecognized in-utero or peripartum
enterocolitis. Cardiac arrhythmias, edema,
hypoxia, and can injure multiple organ
poor cardiac output, and systemic hyposystems. In this context, asphyxia is caused tension may result from hypoxia of ilie
by impaired oxygen d�livery to cells, most
myocardium. A decrease in pulmonary
often resulting from a combination of
perfusion may impair surfactant production
hypoxemia or anemia (leading to decreased
and lead to ventilation-perfusion mismatch
blood oxygen content), and ischemia
and secondary pulmonary atelectasis.

(decreased blood perfusion).

Hepatic and endocrine dysfunction may
also be seen. For example, perinatal

Pathogenesis and Risk Factors: Speciesasphyxia syndrome may cause lower T3 and specific information on the pathogenesis of

T

NE in foals is exceedingly scarce and mostly

4 concentrations in affected foals ilian in
age-matched healthy control subjects.

extrapolated from nonequine species.

The neurologic signs of foals with NE

Primary neuronal cell death may be related
are variable and may include weakness
to cellular hypoxia, energy failure, and

(hypotonia), mental depression (stupor,
cellular membrane depolarization, whereas
somnolence, difficult to arouse, coma),
delayed neuronal cell death is associated
seizure activity, tremors, and hypertonia.

with reperfusion injury (oxidative stress),

Seizures are relatively common and may
excitotoxicity, accumulation of intracellular
range from mildly abnonnal movement of
calciwn, activation of numerous enzymes
the face and jaw to generalized seizures
and pathways, cytotoxic actions of activated with recun1bency and paddling. Oilier microglia, inflanunation, and apoptosis. In
clinical signs include an inability to find the
this context, excessive activation of
udder, loss of suckle reflex, loss of affinity
glutamatergic neurotransmission (ie,
for the dam, loss of recognition of ilie
excitatory amino acids and neurotransmitenvironment, abnormal vocalization (11ence ters), increased production of reactive

"barker foals"), dysphagia, weak tongue
oxygen and nitrogen species, as well as fetal
tone or persistent tongue protrusion,
systemic inflammatory responses with
central blindness, opisiliotonos, irregular
production of pro-inflammatory cytokines
respiratory pattern ( apnea, abnormally slow

MANAGEMENT OF THE NEONATE

2095
respiratory rate), and proprioceptive
use of barbiturates, and mild hypercapnia
deficits. Clinical signs can be asymmetric
have been suggested to decrease cerebral
and may include a head tilt, circling, and
metabolic rate and preserve energy.

asymmetric pupillary reflexes. Foals may

Because foals have minin1al energy
appear healthy at birth but often exhibit
reserves, IV glucose administration may be

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CNS abnormalities within hours of delivery
necessary to maintain normal blood glucose
or by 1-2 days of age. Affected foals are
concentrations. lithe foal is unable to
usually afebrile unless secondary infection
nurse, nutrition can be supplied via an
or sepsis occurs.

indwelling nasogastric tube. Total
parenteral nutrition is indicated in foals

Diagnosis: Diagnosis is based on
with GI dysfunction.

compatible clinical findings and exclusion

Mannitol (0.25-1 g/kg, IV, as 2()0A, solution
of differential diagnoses. A history of
over 20 nun every 12-24 hr) has been used
dystocia, premature placental separation,
to reduce cerebral edema. Anticonvulsants
or placentitis may support a diagnosis of

(phenobarbital 2-10 mg/kg, IV, bid;

NE. The foal's CBC is usually unremarkable
diazepan1 0.1-0.4 mg/kg, IV, as needed;
unless sepsis is present. A serum chemistry
midazolain 0.04-0.1 mg/kg, IV, as needed or
may also be norn1al but often indicates organ

0.02-0.06 mg/kg/hr constant-rate infusion)

dysfunction secondaiy to hypoxic or
are implemented to treat seizures that can
cytokine-mediated injllly. For exainple, a
otherwise increase cerebral oxygen
markedly increased CK concentration may
consumption and contribute to ongoing
correlate with a recent hypoxic-ischemic
ir\illlY- Self-trauma during seizures should
muscle insult, whereas a.ii increased GGT
be limited by providing a protected or
concentration can accompai1y hepatic ir\illlYpadded environment. Trauma to the eye and Tra.J1Sient or spurious hypercreatininemia
corneal ulceration is particularly common;
may indicate adverse maternal and/or
the eyes should therefore be monitored
placental conditions, or suggest ingestion of
closely and treatment implemented if
creatinine-rich fetal fluids in neonatal foals
necessary. In recUll1bent foals, ophthalmic
experiencing periods of peripartlll11
lubricants may be used to reduce the
asphyxia. Creatinine in affected foals
incidence of corneal ir\illlY-
decreases by >500A, within 24 hr of standard

Magnesillll1 sulfate supplement.at.ion
neonatal support a.Ild generally nonnalizes
adnunistered as a constant-rate infusion
within 72 hr. However, if creatinine values

(0.05 mg/kg/hr, IV, loading dose, then 0.025
remain high, then renal dysfunction must be
mg/kg/hr maintenance) has been suggested
considered. Hypoxernia, hypercarbia ( due to
to block the release of glutan1ate, whereas
respiratory depression), acidemia, ai1d
antioxidants such as vitanuns E (5,000 JU/
hypocalcemia may also be seen in foals with
day, PO) and C (100 mg/kg/day, IV or I;'O)

NE. CSF may be normal or show an
can be adnunistered along with thiainine
increased RBC count and protein concentra

(10 mg/kg slowly IV or SC every 12-24 hr) to
tion. CNS necrosis, edema, and hemorrhage
support cellular metabolism. DMSO l()OA,
are found in some cases at necropsy;
solution (0.5 g/kg, IV) has been used as a
however, these findings are inconsistent.

free radical scavenger. Allopurinol ( 44

Differential diagnoses for NE include
mg/kg, PO, within the first 4 hr), a xanthine
bacterial meningitis, equine herpesvirus 1
oxidase inhibitor, can also be adnunistered
infection, metabolic abnormalities ( eg,
to decrease free radicals, whereas
hypoglycemia, electrolyte derangements),
pentoxifylli.ne (10 mg/kg, PO, bid) may
acid-base disturbances, kemicterus
inhibit TNF-oc production in foals with NE.

subsequent to massive hemolysis (ie,

Most foals with NE will benefit from
neonatal isoerythrolysis ), brain or spinal
intranasal adnunistration of hlllnidified
trallll1a, congenital defects ( eg, hydrocephaoxygen (3-5 Unun), whereas mechaiucal lus, hydranencephaly), and nutritional
ventilation may be required in cases of
myodegeneration (white muscle disease).

severe respiratory depression. Doxaprain

(0.02-0.05 mg/kg/hr constant-rate infusion)

Treatment and Prognosis: Treatment of
and caffeine (10 mg/kg, PO or per rectllln

NE is primarily supportive. Maintenance of
loading dose, then 2.5 mg/kg as needed)

adequate blood pressure and perfusion is
may be used as a central respiratory
vital for supporting cerebral blood flow and
stimulant. Availability of hyperbaric oxygen
avoiding further ische1nic injury. This can be therapy is limited, but it has also been used accomplished by cautiously administered,
to treat NE in foals. Foals with NE appear to
goal-directed IV fluid therapy and inotrope
be predisposed to sepsis. Whether this is
or vasopressor support, if needed, while
due to an underlying infectious process,
avoiding hypertension. Mild hypothernua,
impaired immune function, or increased

2096

MANAGEMENT OF THE NEONATE
expos me to pathogens (ie, indiscriminant
effective, because acetylcysteine is
mu-sing behavior) is unclear. In addition,
hypotl1esized to cleave disulfide bonds in
foals neurologically abnonnaJ at birth often
the mucoprotein molecules of meconiun1,
fail to nurse and conunonly have failure of
which decreases its overall tenacity. A 4%
passive transfer of immunity (seep 819).

acetylcysteine solution is made by adding 20

For these reasons, broad-spectrwn
g of baking soda ai1d 8 g ofa'Cetylcysteine to

VetBooks.ir
antimicrobials, plasma transfusion, and

200 rnL of water. A 30-french Foley catl1eter
anti-inflammatory management are
with a 30-mL balloon is inserted -2.5-5 cm
commonly indicated.

into tl1e rectwn, and the balloon is slowly

Most foals witl1 NE have a good to very
inflated to occlude tl1e rectum. Subsegood prognosis. In uncomplicated cases, quently, 100-200 mL of the 4%acetyltl1e reported swvivaJ rate is 700/o--75%, with cysteine solution is administered by gravity
complete recovery in most cases. Sepsis
flow and retained for 30-45 min. If needed,
and related complications adversely affect
treatment cat1 be repeated in 12 hr.

tl1e prognosis. Foals that remain comatose

Occasionally, repeated enemas can result in
or difficult to arouse, show no improvement
significant mucosa] irritation and persistent
in neurologic function during the first 5 days straining beyond tl1e resolution of the of life, or demonstrate severe, recurrent
meconitun impaction, thereby confounding
seizmes have a guarded to poor prognosis.

tl1e assessment of treatment success.

Surgical intervention should be

MECONIUM IMPACTION
considered if medical tl1erapy is unsuccessful, especially in the face of persistent pain Meconium is tl1e earliest feces of newborn
unresponsive to analgesics, persistent
foals. It is composed of intestinal secretachycardia, progressive abdominal tions, swalJowed anmiotic fluid, and cellular enlargement, or increased peritoneal fluid cleb1is; it has a sticky, caramelized appeai�
protein and/or nucleated cell count.

ance. Most foals pass their meconiwn within The prognosis of uncomplicated
tl1e first 9-12 hr of life. If sufficient quantities meconiwn impaction is generalJy considof meconiwn ai·e not evacuated, meconium ered good to excellent.

impaction can lead to clinical signs of
colonic obstruction, which usualJy maiufest
in the first 12-96 hr. These signs may include
abdominal pain (colic), tachypnea and

Average reported canine and feline
tachycardia, tail "swishing," restlessness, neonatal mortality rates (greatest during
straining to defecate, and abdominal (gas)

the first week of life) vary, ranging from
distention. Published reports suggest tl1at

9o/o-26%. Prudent veterinary intervention
meconiun1 impaction may l;le more likely in
in the prenatal, parturient, and postpar
foals born after >340 days of gestation and in tum periods can increase neonatal
colts. Meconiun1 can usualJy be identified
survival by controlling or eliminating
either by plain or contrast abdominal
factors that contribute to puppy
radiography or ultrasonography, or by
morbidity and mortality. Poor prepartum
cai·eful digital rectal examination ·witl1
condition of the dam, dystocia, congeniadequate restraint or sedation. On racliotal malformations, genetic defects, injury, graphs, rneconium often appears as granulai·
environmental exposure, malnutrition,
contents in tl1e ascending or descending
parasitism, and infectious disease all
colon, witl1 fluid- or gas-distended intestine
contribute to neonatal morb\dity and
proxin1aJ to tl1e obstruction.

mortality. Optimal husbandry impacts
neonatal survival favorably by managing

Treatment: Maiw cases of meconimn
labor and de! ivery to reduce stillbirths,
impaction respond to medical tl1erapy,
controlling parasitism and reducing infecinclucling judicious use of analgesics, IV
tious disease, preventing injury and
fluid therapy, oral laxatives ( 4-8 oz mineral
environmental exposure, and optimizing
oil administered via a nasogastric tube; 1-2
nutrition of the clam and neonates. Proper
oz milk of magnesia), and enemas as the
genetic screening for selection of
mainstay of therapy. Warm-water liquid
breeding animals minimizes inherited
detergent ( eg, Palmolive®) enemas (Y2
congenital defects.

teaspoon liquid detergent added to 500 mL
water) are preferred, although commercial

Immediate Postpartum Resuscitation:

phosphate (Fleet®) enemas can also be used Optimal neonatal resuscitation (if needed (repeated administration may increase risk
after birth or cesarean section) involves
of phosphate toxicity). Acetylcysteine
the same "ABC's" as any cardiopulmonary
retention enemas may also be highly
resuscitation. Prompt clearing of airways

MANAGEMENT OF THE NEONATE

2097

("A") by gentle suction with a bulb syringe, after she is fully recovered from anesthesia
and then drying and stimulation of the
and exhibiting good maternal behavior;
neonate to promote respiration (''B") and
otherwise, nursing should be directly
to avoid chilling are pe1fom1ed. Neonates
monitored and permitted every 2 hr.

should not be swung to clear airways because

Neonates lack glucose reserves and have
of the potential for cerebral hemorrhage from
minimal capacity for gluconeogenesis.

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concussion. The use of doxapran1 as a

Providing energy drni.ng or just after
respiratory stimulant is unlikely to improve
prolonged resuscitation efforts becomes
hypoxemia associated with hypoventilation
critical. Clinical hypoglycemia (blood
and is not recommended. Spontaneous
glucose levels <30-40 mg/dL) can be treated
breathing and vocalization at bitth are
with dextrose solution IV or intra.osseously,
positively associated with survival through
at a dosage ofO.� 1 g/kg (0.000�.001 gig

7 days of age. Intervention for resuscitation
body wt) using a 5%-10% solution, or a
of neonates after vagmal delivery should be
dosage of 2-4 ml/kg (0.002---0.004 mlJg body
done if the dam's actions do not stimulate
wt) of a 100/o dextrose solution. A 500-g
respiration, vocalization, and movement
neonate would get 1 -2 mL. SIDgle administrawithin 1 mm of birth.

tion of parenteral glucose is adequate if the

Cardiopulmonary resuscitation for
hypoglycemic puppy can then be fed or
neonates that do not breathe spontaneously
nurses. If a neonate is too weak to nurse or
is challengIDg yet potentially rewarding.

suckle, 0.0� 1 mL of warmed 5% dextrose

Ventilatory support should include constant
can be administered orally by stomach tube
flow 02 delivery by facemask. If this is
every 1�0 min w1til the neonate is capable
ineffective after 1 min, positive pressure
of suckling. If colostrum can be acquired
with a snugly fitting mask or endotracheal
from the dam, it can be administered ID tl1e
intubation and rebreathmg bag ( using a
same way. Dextrose solution (500/o) should

2-mrn endotracheal tube or a 12- to 16-
be applied to the mucous membranes only
gauge IV catheter) is advised. Cardiac stimubecause of the potential for phlebitis if lation ("C") should follow ventilatory
administered IV; however, circulation must
support, because myocardial hypoxemia is
be adequate for absorption from tl1e mucosa.

the most common cause of bradycardia or

Neonates administered dextrose should be
asystole. Direct transthoracic cardiac
monitored for hyperglycemia because of
compressions are advised as the first step;
itnmature metabolic regulatory mechanisms.

epinephrme is the drug of choice for cardiac

When to Stop Resuscitation: ResuscitaarresUstandstill (0.2 mg/kg, administered tion may be stopped when there has been no
best by the IV or IDtraosseous route).

response after 1�20 min of effort ( continued

Venous access ID neonates is challenging;
agonal respiration, bradycardia) or when a
the single umbilical vein is one possibility.

serious congenital defect has been detected

The proXllllal humerus, proxitnal femur, and

( cleft palate, loud murmur, gastroschisis,
proxitnomedial tibia offer IDtraosseous sites
large ornphalocele, large fontanel).

for drug administration. Atropine is not
advised ID neonatal resuscitation. The

Husbandry in the First Days of Life:

mechanism of bradycardia is hypoxemia

After resuscitation or within the first 24 hr

IDduced myocardial depression rather than
of a natural delivery, a complete physical
vagal mediation, and anticholinergicexamination should be performed. Lack induced tachycardia can actually exacerof cleft palate, a nom1al un1bilicus, and bate myocardial oxygen deficits.

functional urethral and anal openmgs

Chilled neonates may not respond to
should be established. A fontanelle, if
resuscitation. Body temperature drops
present, should be small. The oral cavity,
rapidly when a neonate is dan1p. Keeping
hair coat, limbs, umbilicus, and urogenital
the neonate wam1 is important durmg resusstructures should be visually IDspected. The citation and ID the immediate postpartum
mucous membranes should be pink and
period. During resuscitation, placing the
moist, a suckle reflex present, the coat
chilled neonate's trunk it1to a warm water
full and clean, and the urethra and anus
bath (95°-99°F) can in1prove response.

patent. A normal umbilicus is dry without

Working under a heat lamp or witl1in a Bair
surroundIDg erytl1ema. The thorax should
hugger warming device is helpful. After
be ausculted; vesicular breath sounds and a
resuscitation, neonates should be placed in
lack of mum1ur are nonnal. The abdomen
a wam1 box (a styrofoam picnic box with
should be pliant and not painful. A nonnal
ventilation holes is ideal) with warm
neonate will squim1 and vocalize when
bedding until they can be left with their
examIDed, and nurse and sleep quietly when
darn. Neonates delivered by cesarean
returned to the dam. Healthy neonates will
section should be left witl1 the dam only
attempt to right themselves and orient by

2098

MANAGEMENT OF THE NEONATE
rooting toward their dam. Neonates are
iodine in1mediately after birtl1 to reduce
highly susceptible to envirorunental stress,
contan1ination and prevent ascent of
infection, and malnutrition. Proper
bacteria into the peritoneal cavity
husbandry is critical and should include

( omphalitis-peritonitis ).

VetBooks.ir
daily exanlination of each neonate for vigor

Neonatal bacte1ial septi�emia can cause
and recording of weight.

rapid dete1ioration and result in death if not recognized and treated promptly. Predispos

Warmth: Puppies and kittens lack
ing factors include endometiitis in the dan1,
thennoregulatory mechanisms until 4 wk of
a prolonged delivery/dystocia, feeding of
age; thus, the ambient temperature must be
replacement fom1ulas, the use of ampicillin,
high enough to facilitate maintenance of a
stress, low bi1th weight ( <350 g for a
body temperature of at least 97°F (36°C).

medium-size breed dog), and chilling with

Hypothennia negatively impacts immunity,
body temperature <96°F. The organisms
nursing, and digestion. Exogenous heat
most frequently associated with septicemia
should be supplied, best in the form of an
are Escherichia coli, streptococci,
overhead heat lamp. Heating pads run the
staphylococci, and Klebsiella spp.

risk of bunling neonates incapable of

Premortem diagnosis can be challenging,
moving away from excessively hot surfaces.

because sudden death may preclude

Chilled neonates must be rewarmed
recognition of clinical signs. Commonly, a
slowly (30 min) to avoid peripheral
decrease in weight gain, failure to suckle,
vasodilation and dehydration. Tube feeding
hematulia, persistent diarrhea, unusual
should be delayed until the neonate is
vocalization, abdonlinal distention and pain,
euthennic. Hypothemtia induces ileus, and
and sloughing of the extrentities indicate
regurgitation and aspiration can result.

septicemia may be present. Prompt therapy
with broad-spectrum, bacte1icidal

Immunity: lncompletely developed
antibiotics; improved nutlition via
immune systems during the fast 10 days of
supported nursing, tube feeding, or bottle
life make neonates vulnerable to systentic
feeding; maintenance of body temperature;
infection (most commonly bacterial and
and appropriate fluid replacement are
viral). Puppies must ingest adequate
indicated. The third-generation cephalocolostrun1 promptly after birth to acquire sporin ceftiofur sodium is an appropriate
passive immunity. The intestinal absorption
choice for neonatal septicemia, because it
of IgG generally ceases by 24 hr after
alters normal intestinal flora minimally and
parturition. Colostrun1-deprived kittens
is usually effective against tl1e causative
given adult cat serun1 at a dosage of
organisms. Ceftiofur sodium should be

150 mllkg, SC or IP, developed serun1 IgG
adntinistered at a dosage of 2.5 mg/kg, SC,
levels comparable to those of suckling
bid, for no longer than 5 days. Because
littermates. However, colostrum-deprived
neonates <48 hr old have reduced thrombin
puppies given 40 mllkg of adult dog serum
levels, presumptive therapy witl1 vitamin K,
orally and parentally did not match IgG
at 0.5-2.5 mg/kg can be used (0.01-1 mg/
levels of suckling littennates. Neonates
neonate, SC) if a coagulopathy is suspected
should be encouraged to suckle promptly

(umbilical bleeding, hematuria, epistaxis).

after resuscitation is completed; this usually
necessitates close monitoring after a

Nutrition: Neonates have nlininlal body fat
cesarean section, because the dam has not
rese1ves and limited metabolic capacity to
fully recovered from anesthesia Maternal
generate glucose from precursors. Glycogen
instincts (protecting, retrieving, grooming,
stores are depleted sh01tly after birth,
nursing) usually return within 24 hr.

making adequate nowishment from nursing

The un1bilicus of neonates should be
vital. Even minimal fasting can result in
trimmed 1 cm from the abdominal wall,
hypoglycentia. Hypoglycentia can also result
ligated, and treated with 2% tincture of
from endotoxentia, septicemia, portosys-

IM;liii NORMAL RECTAL TEMPERATURE OF SMALL ANIMAL NEONATES

Period

Normal Rectal Temperature

Wk l

95°-99°F (35°-37.2°C)

Wk 2-3

97° -100°F (36.1 ° -37.8°C)

At weaning

99°-101 °F (37.2°-38.3°C)

MANAGEMENT OF THE NEONATE

2099
l&N•f I ENVIRONMENTAL WARMTH REQUIRED FOR SMALL ANIMAL NEONATES

Period

Temperature

Wkl

34o_ggop c2s_90-31_7 oc)

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Wk2-3

80 °F (26 . 7 °C)

Wk4

69° -75 °F (20.6 ° -23 .9°C)

Wk5

69°F (20 .6 °C)

temic shunts, and glycogen storage
nephrons are the last ones to become fully
abnormalities. Oral fluid and glucose
ftmctional. The ability of the neonatal
replacement may be preferable if the neonate kidney to produce a concentrated urine is has an adequate swallowing reflex and is not
less than that of the adult, and so fluid
clinically compromised. The neonatal caloric
balance is more labile in neonates. The
requirement is 133 cal/kg/day during the first
differences in neonatal respiratory ftmction
week of life, 155 cal/kg/day for the second,
mean that inhaled agents will have a more

175---198 cal/kg/day for the third, and
rapid onset and recovery. Neonates have

220 cal/kg/day for the fourth. Commercially
immature central and peripheral nervous
manufactured milk replacement fommlas
systems and immature neuromuscular
are usually superior to homemade versions,
junctions, such that less general/local
but none is equal to the dam's milk. The use
anesthetic is required to produce anestheof milk obtained from the dan1 can be sia/local block than in adults.

considered and is superior if available. An

Fluid support is indicated with neonates,
osmotic diarrhea ( usually yellow, curdled
but fluid overload is simply because of the
fecal appearance) can result from overfeedcapacity of the fluid lines used for larger ing formula, necessitating diluting the
animals. To avoid this problem, tubing with
product 500/o with water or a balanced
a much smaller internal diameter should be
crystalloid solution. Neonates should gain
used. Care must also be taken to ensure that
weight steadily from the first day after birth
the lines do not contain any air, because

( a transient mild loss from birth weight is
these very small patients may still have
acceptable on day 1 ), with puppies gaining
commwlication between the left and right

1-3 glday/lb (2 .2 kg) of anticipated adult
atrium, making it possible for IV air to result
weight and kittens 50-100 glwk. Neonatal
in coronary or cerebral emboli.

weigllts should be recorded daily for the first

Core body temperature should be

2 wk, then every 3 days until 1 mo old.

monitored, and hypothermia treated as

Healthy, well-nourished neonates are quiet
soon as possible. A supplemental source of
and sleep when not nursing. The normal
heat should be available ( circulating water
neonatal weigllt gain is an increase of
blanket or warm air blanket) to prevent

5%-100/o body wt/day.

hypothermia, because many of the
anesthetic drugs elinlinate the ability of the

Neonatal Anesthesia: Anesthesia of
neonate to thermoregulate, and neonates
the neonate may be necessitated by an
are more prone to hypothemlia than adults.

emergency or for an elective procedure.

Premedication with an anticholinergic is

The distribution and metabolism of drugs
acceptable and usually sufficient by itself.

are different in neonates than in adults.

Most neonates tolerate a simple mask

Neonates have decreased protein binding
induction with an inhalant such as
and increased permeability of the bloodisoflurane or sevoflurane. Propofol can be brain barrier. Decreased protein binding is
used as an induction drug in young animals.

due to lower albumin levels with a lower

Maintenance by mask avoids the potential
affinity for drugs. Neonates have higher
for traw11a during intubation in tiny
body water content and lower fat content
neonates, but less control of the airway
than adults. This results in a greater initial
is achieved.

volume of distribution for some drugs. In

During anesthesia of neonates, supportmost neonates, the ability to metabolize ing and monitoring cardiopulmonary
drugs (via conjugation, hydrolysis,
ftmction is especially in1portant. Cardiac
oxidation, and reduction) is reduced, as is
output in neonates depends on heart rate;
renal clearance mechanisms. Nephrogenpreventing bradycardia is more important esis in puppies is not complete until the
than in adults. Monitoring blood pressure is
third week of life; the outer cortical
also important. lf hypotension is detected or

2100

MANAGEMENT OF THE NEONATE
tissue pe1fusionjudged inadequate,
best chance of survival if kept wan11 and
treatment should be instituted. Initial
taken to local wildlife rehabilitation centers.

therapy should include reducing the a.mount Skw1ks, raccoons, foxes, and bats should of anesthetic, if possible, and increasing the
only be rehabilitated by professionals
rate of fluid administration. If these
because of potential zoonotic diseases.

treatments are ineffective, it is probably

Marine manm1als ai1d seabirds require

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better to use a positive inotrope/chronospecialized care facilities (seep 1856).

trope than a peripheral vasoconstrictor to

All neonates require physical examinatry to increase blood pressure (unless it is tion and assessment of hydration, body
very low, and a vasoconstrictor is needed to
temperature, and weight. Warmth,
raise the pressure long enough to allow
hydration, and energy are critical. Because
other therapies to work). Dopan1ine has
most orphans initially cairnot maintain or
been shown to increase blood pressure in
regulate their body temperature, supplepuppies <10 days old at 5---10 mcg/kg/min mental heat should be provided with
but has little effect on heart rate or cardiac
heating pads, hot water bottles, incandesoutput. Dobutamine appears to have little cent light bulbs, or brooders. A heat
effect at clinical doses.

gradient for ambulatory young allows
orphans to select their own comfort zone.

Thermal support of altricial species must
be closely regulated. Most placental
mammals and birds have normal body
temperatures wai·mer than that of people,

If an orphaned bird or man1mal is found,
and should feel warm to the human hand.

further infonnation should be sought before Maintaining humidity of 50%-70% in attempting wildlife rehabilitation.

housing reduces dehydration, and

Specialized books about hand-rearing wild
insulating orphans from direct heat
and domestic mammals and birds and the
prevents burns. Hypothermic orphans

National Wildlife Rehabilitators Association
should be wanned until body temperature

Web site (www.nwrawilcllife.org) are
is near normal ai1d administered warm
valuable resources. The following is a
fluids to maintain hydration or correct
general oveiview, and all species require
deficits. Once the infant is warmed and
more information for a full course of captive well hydrated, species-appropriate diets care. Correct species and age identification
can be fed to provide energy. Initial
is crucial for detennination of behavioral
feedings should be conservatively sized
considerations, weaning diets, and adult
and dilute until it has been detennined
fate. It is illegal to keep most species of
that the infant's excretory systems a.re

North American wild anin1als as pets.

functioning. Infai1ts of most species have

Pennits are required, even by veterinarians,
a stomach or crop capacity of -50 ml/kg.

to care for most wild species beyond initial

Overfeeding may result in aspiration
medical care. The USA Fish and Wildlife
pnewnonia or diarrhea. Once infants a.re

Se1vice and state natural resource agencies
stabilized, the advice of a permitted
should be contacted for applicable rules.

rehabilitator should be obtained.

Iajured limbs of wild animals should never

Hair, feathers, skin, and eyes should be
be amputated without consultation with
kept free of spilled food or excreta, and
regulatory agencies, because permanent
foods maintained hygienically. Nests/
captive placement for disabled wildlife may
housing should be cleaned regularly and
be difficult to find. Euthanasia should be
secured against vermin. Treatment for
considered when iajury resolution will
ecto- and endopai·asites or fly strike may be
result in a disabled, unreleasable anin1al.

necessary. Products deemed safe for infants

When hand-reaiing for wild release, infants
of domestic species should be used, and an
should be raised with conspecifics to avoid
exotic animal fonnulai-y consulted for
hwnan irnp1inting, using techniques that
dosing infonnation.

avoid habituation. Wild infants must be

Metabolic bone disease may develop
isolated from domestic animals.

quickly in wild orphans fed inadequate

The first step is to determine whether
diets. Co1vids, other passerines, herons,
young are truly orphaned. If chicks are
egrets, shorebirds, raptors, opossums, and
returned to nests or man1mals are left alone
canids a.re especially susceptible, including
and monitored from a.far, the pai·ent may
when transitioned off fom1ulas onto
return and resume care. Hwnan handling
inadequately supplemented anin1al protein
does not preclude most parents accepting
diets before skeletal maturity. Ground meat
returned offspring. Neonatal wildlife,
or poultry must be supplemented with
especially unidentified species, have the
calciwn cai·bonate at 5 g/ 0.5 kg of meat.

MANAGEMENT OF THE NEONATE

2101

Growing chicks require a dietary ratio of
should gain weight every day, so weight
elemental calcium:phosphorus of -2: l by
should be monitored closely.

weight.

Altricial Species: Chicks should be

Birds
warn1ed to normal body temperature,

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Nest replacements should be constructed
hydrated until droppings are produced, and
so as to provide nonambulatory chicks
then fed. Tiny, unfeathered chicks require
with a comfortable upright posture with
enVIronments as warn1 as l00°F (37.8°C);
the head elevated and legs underneath the
larger-feathered chicks do well initially in
body. Housing chicks on Hat surfaces may
temperatures of90° -95°F (32.2° -35°C).

result in splayed legs. Fractured bones are Overheated chicks may hold perpetual considered life-threatening injuries
open-mouthed postures, droop heads over
because of the requirement of functionalnest edges, and cease producing droppings ity for release. Trauma to soft tissues can
if dehydrated Not all species gape/beg

_.

be minimized by stabilizing fractures

(sWifts, rugh(Ja.rs). Some species stop
promptly. Elbow, carpus, spine, stifle, and
beggmg when full (corvids); some do not
hock fractures or luxations carry a poor
and may dangerously overeat (finches,
prognosis for release. Mid-shaft long-bone goldfinches). Crops should empty between fractures often heal well. Humerus and
feeds; not all species have crops (insectifemur fractures heal best with a simple vores, owls). Hatchlings require more water
mtramedullary pin, and pinning may be
than older chicks. Common problems that
successful even in extremely young or
cause lack of gaping include too cold, hot,
small-bodied chicks. Minimally restrictive
weak, or dehydrated; untreated illness or
splints and wraps for other fractures
injury; and misidentified species. Overfeedresult in fastest recovery and release.

ing may cause droppings that appear as

Chicks should be allowed to use stabiundigested diet.

lized, fractured limbs as normally as

Higher protein/fat, lower carbohydrate
possible during recovery. Stable callus
diets are desirable for most species.

formabon occurs in 5-7 days in nestling

Pureed, high-quality kitten or ferret kibble
passermes and m 10-21 days in largeris an acceptable temporary food for most bodied species, well before radiographic
altricial chicks, supplemented with
changes occur. Some species form joint
elemental calcium at 150 mg/kg/day, PO,
contractures easily and require physical
until on a balanced diet. Pureed, skinned
therapy after the fracture and then
prey animals (quail or adult mice
continuing intermittently for return to
including bones and organs, min�s feet
function. Chicks may heal rapidly from
and heads) form an adequate diet for
seemingly severe soft-tissue injuries.

many species. Bone fragments must be

Lacerations should have primary closure
completely pulverized to avoid GI trauma.

to minimize time in captivity and reduce

A diet of thawed-frozen prey requires
adverse effects on growing plumage.

vitamin supplementation. Vitamin E and

Antibiotic therapy against gram-negative
thian1ine supplementation is necessary for
bacteria is advisable for predator-injured
species ingesting frozen-thawed fish.

chicks; 1t should be continued until

Feeding prey frozen >6 mo should be
wounds have completely healed.

avoided. Vitamin A may be inadequate in

Meloxicam and butorphanol are commsect prey, and deficiency may occur if monly used for pain. Chicks with head
prey are fed witl1 viscera removed. Pinky
mice, _
injuries may recover well; changes in
msects, and small-bodied fish often
neurologic signs can be used as prognoscontain inadequate calcium for growing tic

_
md1cators while giving supportive
b1.rds; hence, supplementation is
care. Beak or jaw injuries must resolve
necessary.

with beak tips well aligned to ensure

Songbirds and Woodpeckers: A sin1ple
ability to forage normally al"ter release.

hand-feeding diet consists of l cup (116 g)

Nearly all North American bird species

Punna Pro-Plan® kitten kibble, 1.25-1.5 cup
feed vertebrate or inve1tebrate prey to their

(300-360 mL) water, 2 tbsp (14 g) powdered
chicks. Milk and bread, hamburger,
condensed milk, or uncooked rice should

�gg white, 750 mg calcium from CaC03, and

Y2 tsp (1.4 g) A.VI-Era® powdered avian
not be fed. Soaked dog kibble and monkey
vitamins. Do not delete or substitute
b1scmts are _inadequate for most species. All
ingredients haphazardly, soak kibble and
species require 8-12 lu· tminte1rupted sleep.

blend lll1til smooth, and feed with appropri

Self-feeding requires daylight-level lighting
ately sized syringe. For hatchlings/nestlings,
m dmrnal species. All growing chicks
feed 50 mUkg eve1y 20-45 min (by age)

2102

MANAGEMENT OF THE NEONATE

12-14 hr/day (16 hr/day for insectivores).

krill, small freshly shed mealwonns, fly

For fledglings, hand-feed 50 mUkg every
larvae, or cichlid mini-pellets) should be

1-2 hr, 12 hr/day, offe1ing appropriate
offered in shallow water at least four tin1es
self-feeding diet.

daily.

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Hummingbirds: A temporary diet

Waterfowl (Geese, E>ucks, Swans):

consists of 1 part water to 6 parts table

Natural duckweed or watercress, small
sugar or 5% dextrose, fed every 20 min. This
invettebrates, crushed hard-boiled egg,
diet does not meet hummingbird chick
small minnows, and waterfowl starter
nutrient requirements. These chicks should

(Mazuri®) should be offered. Access to
be transferred to an experienced caretaker
shallow water should be controlled; chicks
immediately. Sugar water should not be
must be able to easily exit water to wann
spilled on the bird.

under a heat source. Chicks may lose
waterproofing and become chilled if

Doves and Pigeons: Commercial diets
plumage becomes contaminated with food
for hatchlings are Roudybush™ Squab Diet
or droppings.

and Lafeber's® Emeraid® Carnivore; for
nestlings/fledglings, Kaytee® Exact® Hand

Gamebirds (Pheasants, Quail, Turkeys):

Feeding Formula. Crop capacity is 100-120

Soaked puppy kibble, small-bodied
mUkg. Birds should be fed when crop
invertebrates, small clumps of grass or
empties, 12-14 hr/day, every 1-2 hr until
weeds with soil, or commercial gamebird
eyes open and then every 3 hr until
starter can be offered.

ambulating and ingesting seed. Palpating
the crop before each feeding will assess

Mammals
self-feeding and prevent overfilling.

Hypothermia and dehydration must be

Raptors: Hatchlings can be fed small
corrected before feeding neonate man1mals.

pieces of warm, water-dipped meat every

Hairless neonates require ambient

2 hr, 12 hr/day, with blunt-tipped forceps;
temperatures of 85° -90°F (29.4 ° -32.2°C),
tiny bone pieces can be included by day 3
while haired infants may be housed at
after hatch, and casting material (skin/hair)

cooler temperatures depending on maturity
by day 5. The crop should empty between
and body condition. Once wann and
meals. Most species will pick up chopped
hydrated, milk replacer should be introprey from a dish by day 14. Feeding with a duced using this regimen: 100% oral
puppet parent can be done once the eyes
electrolyte solution, gradually increasing
open.

the strength of milk replacer in one to
several feedings to 1/.i strength, then Y2, then

Herons and Egrets: Thawed-frozen fish

%, and finally to full strength. During this

(5---20 g, sliced diagonally if larger), live
process, if the neonate develops digestive
insects, or thawed-frozen chopped mice,
upset (vomiting, diarrhea, bloating), feeding
should be offered hourly until self-feeding,
should return to the last well-tolerated ratio.

then several times daily. Hatchlings may

Overfeeding or sudden diet changes may
require force feeding; older chicks may eat
cause bloating or diarrhea. Neonates need
from a dish. Using a feeding puppet reduces
to be stimulated to elinlinate by gently
habituation.

stroking the perinea! area with wam1 moist
gauze or tissue. Dorsal sic;le up is normal
nursing posture; infants should not be put

Precocial Species: Once warm and
secure, many species drink and eat indepenon their backs to feed. The environment dently. Solitude stresses chicks; a mirror,
should be quiet.

small stuffed animals, clean feather duster,
or chicks of closely related species can be

Fawns: Fawns should be raised in groups
companions. Uncommon species and
with minimal human contact and kept away
debilit.ated hatchlings require professional
from dogs. Newborn to 2-day-old fawns
rehabilitative care for a positive outcome.

should be fed colostrum, such as Colostrx®,

Placing pebbles in water dishes may
for the first 24-48 hr. After reconstitution,
prevent quail/ducklings from drowning.

one 454--g package can be administered via

Hatchling quail/killdeer require habitat
bottle or stomach tube over 8-10 hr (5
brooders kept at 95° -100°F (35° -37.8°C).

meals/day, 30--40 mUkg). Acceptable milk
replacers include Fox Valley® Milk

Shorebirds (Killdeer, Sandpipers,

Replacer, lan1b's milk replacer, or goat's

Avocets): Live, fresh-frozen, and freezemilk. Fawns 2-7 days old should be fed four dried small invertebrate prey (tubifex
times daily, gradually increasing volume to
wom1s, brine shrimp, mosquito larvae, tiny

50 mUkg. From 8 to 14 days of age, up to 300

MANAGEMENT OF THE NEONATE

2103
mL should be fed, reaching a goal of 300 mL,

3.5 French red rubber catheter measured
tid. From 2 to 4 wk, the amount should be
to the caudal rib may be used. If syringe
increased to 460 mL, tid, adding solid food
feeding, a cut smoothed tomcat catheter

( eg, goat chow, calf manna, and alfalfa hay).

can be attached to the syringe and the

Indigenous natural browse should always
infant fed drop-wise. When eyes open

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be available. By 7 wk, fawns should be

( -45 g), infants can be taught to lap
eating solid food and fed one 480 mL bottle
fonnula from a shallow dish. When infants
daily. By 8--10 wk, fawns should eat solid
weigh -60 g and are walking, kitten
food exclusively.

kibble soaked in Esbilac® can be offered.

Once the infant is eating soaked kibble

Squirrels: For squirrels, syringe-feeding

(-80-100 g), lOOA, other natural food items
is preferred; Catac® nipples work well.

(c1ickets, worms, chopped mice, local

Eastern gray and fox squirrel neonates
fruits, high-calcium vegetables) can be
should be fed every 2 hr until 2 wk old.

introduced. Most opossums self-feed by

From 2 to 3 wk, feeding should be every 3
the time they weigh 100-120 g. Adequate
hr, eight times/day. At 4 wk, the late-night
calcium intake must be ensured to prevent
feed is eliminated. At 5-6 wk, feedings are
metabolic bone disease.

reduced to five and then to four times/day,
at 7-8 wk to three times/day, and at 10 wk

Raccoons: Gloves should always be worn
to once a day. Weight should be monitored
when handling raccoons. Raccoons are the
daily, and the squirrel fed 50 mL/kg initially, definitive hosts for Baylisascaris gradually increasing to 70 mL/kg by 3 wk.

procyonis, a roundwonn parasite that may

Acceptable milk replacers (ratios by
be transmitted to people or oilier animals,
volume) include 2:3 Fox Valley®
primaiily via feces, and result in sometimes

32/40:water, or l:Y2:2 Esbilac®, MultiMilk®,
fatal infection. Raccoons also may CaJ'ry
and water. When eyes are open and
rabies.

squirrels are ambulatory, natural foods and

Newborns weigh 60-75 g with eyes and
rodent block can be offered; fruit should
ears sealed. Incubators are necessary until
be strictly limited. Ground squirrels wean
weight is >500 g. The preferred milk
at 6 wk old, and Western gray squirrels at
replacer is KMR® or Zoo logic® 42/25

12 wk.

(1:2.25 parts powder:water). Infants
should be fed via 8 French gavage tube, or

Rabbits and Hares: Neonatal rabbit
drop by drop into the mouth (using a cut
stomachs hold 100-125 mL/kg. Healthy
smoothed tomcat catheter attached to a
neonates should be fed twice a day,
syringe) until they are stronger and/or
although feedings up to four times a day
eyes are open. Over-feeding should be
may be needed. Use of a slip-tip syringe is
avoided. The stomach should be plump
preferred. If suckling response is poor,
but not taut. Four Paws TM large squirrel
meals should be tube fed, with the volume
nipple on a 6-mL syringe may be used.

reduced by 30% and an extra feeding to

Infants should be stimulated to urinate/
ensure adequate intake. Acceptable milk
defecate after each feed until they
replacers (ratios by volume) include 2:1
eliminate without stimulation. Infants
parts KMR® powder:water (with pinch
should be weighed daily, and fed 50 mL/
of acidophilus) or 1: 1 parts Esbilac®
kg, six times a day, until they weigh 200 g.

powder:water. When the eyes open, a

They can then be fed using a preemie
variety of chopped leafy greens and grass
nipple on a bottle or from a dish at the rate

(orchard, timothy, or oat) hay should be
of 42.5 mL/kg, five times/day, until they
provided. Because hares are precocial
weigh 500 g. At a weight of 400 g, if infants

(born furred with eyes open), forage
are strong enough and their eyes are open,
should be offered immediately in addition
in addition to the milk replacer, "mush"

to milk replacer. Fruits and high-sugar
made of soaked puppy chow, high-protein
vegetables (eg, carrots) should be
baby cereal, and KMR® powder (with
avoided.

water added to create oatmeal consistency) can be offered. At 500 g, one of four Opossums: Infant opossums weighing
feeds should be mush in a dish. At 850 g,

<20 g have a poor prognosis. Infants
small bits of cut fruit and soaked puppy
weighing 20-35 g should be fed 50 mL/kg,
chow should be added, decreasing milk
six times a day; those weighing 40-100 g,
replacer to three times a day. As the

50-60 mL/kg, five tin1es a day. An acceptinfants mature, hard puppy chow, prey able milk replacer (ratio by volume) is
items (mice, fish), egg, and 10% fruits and
l :Y2:2 parts Esbilac®, MultiMilk®, and
vegetables can be offered and formula
water. Tube-feeding is preferred, and a size
feeds reduced.

2104

PAIN ASSESSMENT AND MANAGEMENT

PAIN ASSESSMENT AND MANAGEMENT

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Pain delays recovery, impacts negatively on
injury), vascular injury (eg, thromboempatient well-being, and can affect the bolic disease), endocrinopathy ( eg, diabetes
client-veterinarian relationship. Behaviors
mellitus), or infection (eg, post-herpetic
suggestive of pain are routinely used to
new-algia), possibly associated with motor,
diagnose injmies and diseases, guide
sensory, or autonomic deficits.

therapy, and provide prognostic informa

For an animal to experience pain,
tion. Obvious signs of pain alert owners and
nociceptive information must be sent to
veterinarians of a problem with the animal.

higher centers in the CNS to be integrated,

Certainly, there is nothing novel about
modulated, 3l1d interpreted into the
considering pain clinically relevant in the
conscious perception of pain. Noxious
overall evaluation of an animal. What is
stimuli 01eat, cold, mechanical, chemical)

relatively new is our understanding of the
activate free sensory ne1ve endings known
complexity of pain 311d the emphasis on
as nociceptors. A-o and C-fibers tr311smit
ethical and medical obligations to treat pain
sensory infom1ation from nociceptors to
in animals. Although limited survey data
the dorsal horn of the spinal cord, which
and anecdotal evidence suggest that the
directs and modulates input from the
management of pain is receiving more
petiphery 311d higher centers. Nociceptive
attention in veterinary medicine than
information 311iving in the dorsal horn of
before, the assessment, prevention, and
the spinal cord may activate motor new·ons
treatment of pain has yet to become 311
responsible for the reflex responses to
integral part of every physical exan1ination
noxious stimuli (such as withdrawing a
and treatment pl311.

limb). Irnport311tly, nociceptive sensory
input may be 3111plified or inhibited by

PAIN PERCEPTION
spinal intemeurons 3l1d glial cells.

Sensory infom1ation is relayed to higher

Pain serves a protective role that alerts 311
centers in the CNS along a variety of pathways
individual to injury from the environment or
that differ according to species. In general,
from within. Based on current knowledge,
nociceptive information ascends the spinal
all vertebrates, and some invertebrates,
cord along superficial 3l1d deep pathways
experience pain in response to actual or
to the brain stem with connections to the
potential tissue d3111age. Many types of pain
tl1al3111us, reticular fom1ation (responsible
are encountered, with the most co nun on
for level of arousal), =d limbic system
being acute, clu·onic, cancer, and neuro

(responsible for emotions). From these
pathic. Acute pain is sudden in onset 311d

31·eas of the brain, nociceptive informa-

C311 be severe. However, it sisappears when
tion is relayed to the cortex, where it is
the stinrnlus is removed or in a short petiod
perceived as pain. Activity in spinal nociof time, 3l1d it tends to be self-limiting.

ceptive pathways is strongly influenced by

Acute pain has a biologic function, because
descending 3l1tinociceptive systems that
it serves as a warning that something is
originate in the brain st�m. Endogenous
wrong while leading to protective behavioaJ1tinociceptive neurotraJ1smitters ( eg, ral ch311ges. Acute pain is a symptom of
endorphin, enkephalin, dynorphin,
disease, whereas chronic pain in 3l1d of itself, serotonin, 3l1d norepinephrine) inhibit the is a disease of altered neuroprocessing.

traJ1smission of nociceptive information in

Chronic pain lasts for several weeks to
the spinal cord 311d brain.

months and persists beyond the expected

The neuro3l1atomic components of the
healing time. Clu·onic pain does not setve
nociceptive/pain pathways 3l1d paina biologic function and imposes severe suppressing systems can change in response
detJimental stresses. C3l1cer pain is the
to sustained sensory input. Peripheral
result of ptimary tumor growth, metastatic
sensitization of nociceptors 3l1d central
disease, or the toxic effects of chemotherapy
sensitization of nociceptive pathways in
and radiation. C3l1cer pain can be acute,
the dorsal horn, spinal cord, and brain
chronic, or intermittent and is related to the
c311 develop as a result of extensive tissue
disease itself or the treatment. Neuropathic
trauma or nerve injury. The process of
pain originates from irtjuiy or after injury of
peripheral and central sensitization has
the peripheral or centJ·al nervous systems,
been termed "wind-up" and refers to the
such as traw11a ( eg, an1putation and crushing neuroaJ1atomic changes (plasticity) that

PAIN ASSESSMENT AND MANAGEMENT

2105
result in heightened or exaggerated pain
rely on the recognition and/or interpretation
states. Additionally, these exaggerated pain of some behavior and a.t·e subject to some states often do not respond to convendegree of va.iia.bility among observers. Pain tional analgesic therapy. The use of opioids scales based on the presence or absence is especially limited, likely because of a
of species-specific behaviors, and that

VetBooks.ir
down regulation of opioid receptors, a
minintize the interpretation of those
phenomenon that has been reported in the
behaviors, are likely to be more accurate
dorsal root ganglion and the dorsal horn.

than generic scales that rely heavily on

Thus, changes in the CNS in response to
subjective assessment and interpretation.

repeated and sustained nociceptive input

All current methods used to measure pain in

(ie, pain) complicate the clinical manageanimals are prone to errors of w1der- or ment of pain.

overestimation. Even if the a.mmmt of pa.in
is correctly estimated, detennining how

RECOGNITION AND ASSESSMENT well the individual animal is coping with OF PAIN IN ANIMALS
pain may be difficult. This is pa.tticularly
true if the animal is removed from its

Pain is a complex, multidimensional
normal environment. Assessment systems
experience with sensory and affective
must also consider the different types a.i1d
elements. All mammals process the
sources of pain, such as a.cute versus
neuroanatomic and neuropharmacologic
chron.ic or neuropa.thic pain and visceral
components involved in transduction,
pain versus soma.tic pain. Finally, all current
transmission, and perception of noxious
methods assess the effects of physical pain;
stimuli; therefore, it is expected that
none has been designed to evaluate mental
animals experience pain even if they cannot
or psychological dimensions of pain in
exactly perceive or communicate it in the
animals.

same way people do. Recognizing pain in

Physiologic parameters (eg, cha.nges in
animals is not intuitive, particularly for
heart rate, respiratory rate, arterial blood
those unfantiliar with nom1al speciespressure, pupil dilation) may be used to specific or individual behaviors. In recent
assess responses to an a.cute noxious
years, there has been an increased focus on

(painful) stimulus, pa.ii;icularly dwing
determining and measuring such specific
anesthesia., and to assess pa.in in some
pain behaviors. These efforts should
clin.ical situations ( eg, horses with acute
improve recognition and treatment of pain
colic pain). However, physiologic measurein an.i.rnals as vaJ.idated pain assessment ments often do not differentiate between
tools are developed. Nevertheless, the
animals that have undergone surgery and
accurate assessment of pain in animals
a.t·e expetiencing pain and those that did
remains a subjective and challenging
not undergo surgery. Likewise, aninfals
undertaking. Numerous factors complicate
experiencing chronic pa.in may have normal
evaluation of pain in animals. Vete1inary
physiologic para.ineters. Lack of change in
pain scales should consider the following
physiologic responses should not be
characteristics: species, breed, environment construed to mea.n there is no pain if other and rea.ting conditions, age, gender, migin
clin.ical signs suggest otl1erwise. Physiologic
of pain (eg, trauma, surgery, pathology),
pa.i·an1eters are not specific enough to
body region affected ( eg, abdominal pain,
differentiate pain from other stressors such
musculoskeletal pa.in), type of pain (eg,
as anxiety, fea.i·, or physiologic responses to
a.cute, chronic), and pain intensity. Any
metabolic conditions ( eg, a.i1emia.).

pain sea.le or methodology used for pain

Lack of fa.milia.i·ity with normal behaviors
assessment must be able to distinguish
typical of a pa.iticula.i· species or breed makes
individual sensitivities. Differences in
recogn.ition of pain-induced behaviors
pain tolerance have been demonstrated
diificult or impossible. Behavioral changes
experimentally in people and animals and
indicative of pain may be too subtle or take
play an important role in the clinical
too long to recogn.ize under routine clin.ical
management of pain. For example, the
situations in botl1 la.i·ge and small animals.

existe:1ce of a lower threshold for pain in an

Sporadic observation of a.i1imal behavior
individual does not obviate the necessity of
may not reveal signs of pain. Except in the
treatment, nor does a particula.t·ly stoic
most severe circumstances, signs of pain
nature.

may be "masked" by behavior that is

There is no "gold standard" to assess pain stereotypical of the species being observed.

in animals. Many scoring methods that

For instance, dogs may wag their tails and
include physiologic and behavioral
greet obse,vers despite being in pain. Flock
variables have been published, but few have
animals, such as sheep, may be sta.itled
been validated. Most veterinary pain scales
when an observer approaches and attempt

2106

PAIN ASSESSMENT AND MANAGEMENT
to conceal signs of pain by staying bunched
evaluation. Evaluating the degree of
up with the rest of the flock. Behavioral
lameness and sensitivity to mailipulation
changes indicating pain may not be what we
ai·e also critically important when assessing
expect. A cat sitting quietly in the back of
chronic orthopedic pain and pain of

VetBooks.ir
the cage after smgery may be in pain;
spinal origin. A compreheQSive nemologic
however, pain would not be recognized if
exanlination must be included for complete
the caregiver expects to see more active
assessment and accmate diagnosis of any
signs of pain such as pacing, agitation, or
chronic pain syndrome. Lastly, response
vocalization. Because it is difficult to detect
to therapy, such as increased activity after
sudden behavior changes, recent research
administering an NSAID, may provide
has focused more on sudden changes in
important diagnostic information regai·ding
facial expressions. The mouse and rodent
the role of pain in behavioral changes.

grimace scale appears to offer a means to

Cancer pain may have components of
assess postoperative pain in mice and rats
acute pain ( eg, expansion of a tun1or or
as effectively as manual behavioral-based
secondaiy responses to smgical, radiation,
scoring, without the limitation of such
or chemotherapy treatment), chronic pain,
schemes in tl1e latter.

and nemopathic pain ( eg, nerve entrapln general, responses to acute surgical ment). Thus, assessment of cancer pain
and traumatic pain are likely to be more
requires methods capable of detecting
marked and readily recognizable than
behavioral changes associated with both
clinical signs associated with chronic pain.

acute and chronic pain.

Often, clinical criteria used to assess clu·onic
pain ( eg, lack of activity, lack of grooming,

PAIN ALLEVIATION
decreased appetite, weight loss) are not
specific signs of pain and point only to an

Acute perioperative, trawnatic, and
underlying problem in need of further
disease-related ( eg, cancer, pancreatitis,
diagnosis. A significant time conmlitment is
plemitis, otitis extema) pain is generally
required in the diagnosis and formulation of
treated phai·macologically with one or
a treatment plan for animals in chronic pain.

more analgesics. The optimal drug or drug

Observations by owners are essential to
combinations are dete1mined principally
detect more subtle signs of chronic pain in
by the anticipated severity of pain, health
animals, such as changes in attitude or
status, and available drugs for the given
interaction with family members or
species. The more extensive the tissue
members of the herd or flock. The Helsinki
traW11a or disease-induced tissue dainage is,

Chronic Pain Index and the Canine Brief
the greater tl1e need to use ai1algesics from

Pain Inventory are owner-completed
more tl1an one drug class (multin10dal or
questionnaires designed to quantify the
balanced analgesia). Multimodal analgesia
seve1ity and impact of chronic pain in
maxinlizes the beneficial analgesic effects
companion dogs. They have been validated
of multiple drugs through additive or
for canine osteoarthritis. The Canine Brief
synergistic interactions while nlinimizing

Pain Inventory, which is based op the human adverse drug effects by lowering the dose Brief Pain Inventory, also has been validated of any individual drug.

for canine bone cancer. A thorough history

A perioperative approach to mai1aging
and physical examination are integral to the
surgically induced pain should be used,

•ffl:i!f• SELECTED ANALGESICS FOR USE IN DOGS AND CATS

Dosage {mg/kg)

Class

Drug

Pain Category

Dogs

Cats

Opioids

Agonists

Morphine

Moderate to severe

0.1-2

0.1-0.5

Hydromorphone

Moderate to evere O.Ofr0.2

0.025-0.2

Oxymorphone

Moderate to severe

0.05-0.2

0.025-0.1

Methadone

Moderate to severe

0.1-1

0.1-0.5

PAIN ASSESSMENT AND MANAGEMENT

2107
beginning with the administration of an
injuring a surgical site) is inappropriate;
analgesic before surgery (preemptive
many efficacious chemical and physical
analgesia) and continuing with appropriate
restraint modalities are available.

analgesia throughout the intraoperative

Managing painful and distressed animals
period. Three days is a useful guideline for
requires a combination of good nursing

VetBooks.ir
the duration of analgesic therapy after acute care, nonphaimacologic methods ( eg, surgical pain. Depending on multiple factors bandaging, ice packs or heat, physical ( eg, procedure performed, rehabilitation
therapy), and phaimacologic methods.

plan, species, breed), some animals require

Phai"Inacologic methods available for the
a shorter duration of therapy, whereas
treatment of acute pain may include opioids,
other animals require analgesia for longer

NSAJDs, corticosteroids, local anesthetics,
periods. Aggressive analgesic therapy of
a2-agonists, and N-methyl-D-aspaii:ate
several days' duration should be tapered

(NMDA) receptor antagonists such as
rather than stopped abruptly. As-needed
ketamine. Mai.1y animals benefit from tl1e
dosing schedules are less effective tl1an
management of anxiety. Acepromazine is
scheduled analgesic dosing to treat pain.

an effective anxiolytic in small animals

As-needed protocols require the animal to
but should be used only after appropriate
demonstrate overt pain behaviors to the
analgesics have been administered.

extent they are recognized by the veterinar

Acepromazine does not have analgesic
ian and/or owner. Aggressive prevention
properties and is not reversible.

and management of acute pain often
prevents wind-up of the noeiceptive

ANALGESIC PHARMACOLOGY
pathways, hastens return to normal
function, and decreases the risk of

Opioids: Opioids continue to be the
development of chronic pain syndromes.

cornerstone of effective pain treatment in

Minimizing stress and ensuring that
veterinai)' medicine. The opioids are a
overall care and husbandry are in accorddiverse group of naturally occwTing a11d ance with the needs of the animal improve
synthetic drugs used primarily for their
pain management. Proper housing
analgesic activity. Despite some wellconditions, nutritional support, and known adverse effects a11d disadva11tages,
interaction with other animals and/or
opioids are the most effective analgesics
people should be optimal for the given
available for the systemic treatment of
species and breed. For example, separating
acute pain in ma11y species, particularly
a sheep from the flock for pain management
dogs and cats. Opioid receptors are part of
may be quite stressful, whereas separating a
a large superfami.ly of membra11e-bound
companion animal from other animals may
receptors that are coupled to G proteins.

not be stressful, provided tl1ere is sufficient

Each opioid receptor has a unique
interaction with human caregivers.

distribution in the brain, spinal card, a11cl

Appropriate analgesia after surgery or
periphery. Opioids combine reversibly with
trawna allows animals to rest. For exan1ple, these receptors and alter the tra11smission dogs and cats often sleep but should be
and perception of pain. In addition to
arousable after surgery if their pain is
analgesia, opioids can induce other CNS
controlled. The use of pain as a means of
effects that include sedation, euphoria,
restraint (ie, to prevent the animal from
dysph01ia, a11d excitement. The clinical

SELECTED ANALGESICS FOR USE IN DOGS AND CATS (continued) Dose Interval

Constant-rate Infusion

Route

(hr)

Epidurala (mg/kg) (mg/kg/hr)

IV,SC, IM

4--6

0.1-0.2

0.05-0.2

IV,SC,IM

2-4

0.01-0.03

IV, SC, IM

2-4

0.05

IV, SC, IM

4-6

(continued)

2108

PAIN ASSESSMENT AND MANAGEMENT

SELECTED ANALGESICS FOR USE IN DOGS AND CATS (continued) Dosage (mg/kg)

VetBooks.ir

Class

Drug

Pain Category

Dogs

, Cats

Fentanyl

Moderate to severe

0.005-0.01 0.0025--0.005

Meperidine

Mild to moderate

3-10

3-5

Codeine

Mild to moderate

0.5-2

0.5-2

Codeine 60 mg/

Mild to moderate

1-2

Contraincli-
acetaminophen

(codeine) ca Led

300mg

I-lyclrococlone

Moderate

0.5

Reliable
dosages not
established

Agonist-

Butorphanol

Mild (good visceral

0.1-0.5

0.1-0.5
antagonist
analgesia)

Partial

Buprenorphine

Mild to moderate

0.005-0.02 0.01-0.03
agonist

Opioid-like

Tram ado!

Mild to moderate

5-10

1-4
a2-Adrenergic Xylazine

Sedative/analgesic,

0.05-1

0.1-1
agonists
emetic effects in
cats

Medetomicline

Sedation longer

0.001-0.02 0.001-0.01
than anesthesia

Dexmedetomidine

0.001-

0.0025-0.02

0.015

NMDA

Ketamine

Adjunctive pain

0.1-1

0.1-1
receptor
control
antagonists

Amantadine

Adjunct drug for

3-5

3-5
chronic/neuropathic
pain

Calcium

Gabapentin

Adjunct drug for

5-15

2.5-20
channel
chronic/cancer/
blocker
neuropathic pain

NKl receptor Maropitant

Visceral pain

2
l·
antagonist

Muscle

Methocarbamol
lnte1ve1tebral disc

15-20
relaxant
disease

"Prese1valive-free formulations recommended.

effects of opioicls vary between the mu
different species . For exai11ple, a 30-kg dog
opioid receptor agonists (eg, morphine,
may receive a preoperative close of
hydromorphone), pattial mu agonists (ie,
morphine (15-30 mg) that is similar to that
buprenorphine), and agonist -antagonists
for a 500-kg horse. Likewise, although

( eg, butorphanol) . Species at1d individual
butorphanol is widely used as an effective
differences in the response to opioicls are
analgesic in horses, its use as an analgesic
marked, necessitating the careful selection
in small animals is falling out of favor
of opioid and adjustment of close for
because of its expense, relatively poor

PAIN ASSESSMENT AND MANAGEMENT

2109

SELECTED ANALGESICS FOR USE IN DOGS AND CATS (cor1tin,,ed) Dose Interval

Constant-rate Infusion

VetBooks.ir

Route

(hr)

Epidurala (mg/kg) (mg/kg/hr)

IV

15-2 0min

0.004

0.002 -0.05

SC,IM

1-2

PO

6-8

PO

6-8

PO

6-12

IV, SC, IM

1-2 ( sedation

0.2 5

0.14-0.4
up to 4)

IV, SC, IM, buccal 6-12

0.005-0.03

0.001-0.005

(cats)

PO

6-8

IV, SC, IM

0.02 -0.02 5

IV, SC, IM

0.001 (loading dose),

0.001-0.003

IV, SC, IM

0.001-0.003

SC,IM,PO

4 -6

0.5 (loading dose),
intraoperative 0.01-0.02,
postoperative 0.002-0.01

PO

Once daily

PO

6-8

PO

Once daily

PO

6-8
somatic analgesic effect, and short

Recent information regarding the
duration of action. The clinical effect of an
peripheral endogenous opioid system
opioid depends on additional patient

(PEOS) has presented a unique opportunity
factors, including tl1e presence or absence
to use tile powerful analgesic effect of
of pain, health status of tl1e animal,
opiates while mininlizing w1toward
concurrent drugs administered ( eg,
systemic effects. The PEOS includes
tranquilizers), and individual sensitivity
peripheral opioid receptors (POR) and
to opioids .

peripheral leukocyte-derived opioids

2110

PAIN ASSESSMENT AND MANAGEMENT

(PLDO): endomorphins, endorphins,
immune function and because of other
enkephalins, and dynorphins. To activate
well-known adverse effects ( eg, polyphagia,
the PEOS, tissue must have sufficient
polydipsia, polyuria) after repeated dosing.

numbers of leukocytes able to secrete

However, they are used occasionally in

PLDO as well as functional POR in sufficient chronic pain syndromes, including PO for VetBooks.ir
numbers. Inflammation due to tissue
degenerative disc disease'in dogs and
damage results in accumulation of
intra-articularly for unresponsive osteoar

PLD O -secreting leukocytes at the site of
thritis. Corticosteroids and NSAIDs should
injury. Inflammation also increases the
not be administered concurrently.

number and efficiency of POR. These

For phannacology of NSAIDs and
receptors, inactive under normal conditions
corticosteroids, seep 2707.

and expressed on primary sensory neurons,
are synthesized in the dorsal root ganglion
a
and transported distally to peripheral

2-Agonists: Xylazine, medetomidine,
dex.medetomidine, detomidine, and
sensory nerve endings due to tissue injury
romifidine are potent analgesics. 0<z-Agonists
and inflan1mation. Experimental trials and
are used in large animals for standing
clinical studies show that peripheral opiates restraint and proyide both analgesia and are effective, particularly in the presence of
sedation, although there is evidence to
inflammation. For example, preservativesuggest that sedation lasts longer than free morphine has been instilled into canine
analgesia. Combination therapy with
and equine joints after arthroscopy or

0<
arthrotomy.

2-agonists and opioids induces profound
analgesia and sedation that is additive or
synergistic as compared with the effects of

Nonsteroidal Anti-inflammatory
either drng alone in both large and small

Drugs and Corticosteroids: NSAIDs
animals. The mechanism of action is through
are useful adjuncts in the treatment of

G protein---<:oupled receptors. Alpha 2A and
postsurgical pain in a variety of species,
alpha 2c receptors mediate analgesia.

because they block prostaglandin synthesis

0<2-Agonists are used as pa.it of multimodal
mediated by inhibition of cyclooxygenase
analgesia in the perioperative period in many

(COX). Decreasing inflammation after
species. a2-Receptors play an inlportant role
surgery or traun1a can greatly improve
in the modulation of pain by the CNS.

analgesia. Inflan1mation is a key component

0<z-Agonists may be used to induce analgesia
in both peripheral and central sensitization
when administered as anesthetic premedicaleading to wind-up. Early and aggressive tions (preemptive analgesia), as a constatltcontrol of wind-up is critical in the rate infusion intraoperatively, and to
prevention of chronic pain syndromes.

supplement postoperative analgesia. In

NSAIDs appear to confer synergism when
general, postoperative doses of a2-agonists
used in combination with opioids and may
are considerably lower than would be
demonstrate an opioid-sparing effect.

required preoperatively.

Significant advantages of NSAIDs include

Caution is advised to prevent excessive
availability, a relatively long duration of
sedation and concomitant ataxia, particuaction, low cost, and relative ease of larly in large animals. Furthermore, even at
administration. Lack of CNS alteration
relatively low doses, tl1ese agents cause

( sedation or dysphoria) make NSAIDs ideal
profound reductions in cardiac output and
for treating acute and chronic pain in
may cause significant atThythrnia in all
animals. Careful patient selection is critical.

species. Runlinants in particular require

Although a number of NSAIDs have been
lower doses, and arterial hypoxemia and
approved for use in dogs and horses, only
pulmonary edema have been described in
meloxicam and robenacox:ib are FDA
sheep. Careful patient selection is watTanted.

approved for use in cats in the USA.

Xylazine, medetomidine, and dexmedeto

Meloxican1 is approved for a single dose and midine (the pure s-enantiomer of the robenacoxib for up to 3 days. As with all
racemic medetomidine) may be reversed
analgesic agents, special attention to drug
in small anin1als after surgery to hasten
withdrawal times is necessary when using
recovery and minimize cardiopulmonary

NSAIDs in production animals.

depression. Once reversed, however, these

Corticosteroids also reduce inflammation
drngs provide no analgesia.

and provide analgesia. Depending on the
product, they are administered PO, IV, IM,

Ketamine: Ketanline has long been

SC, and intra-articularly. Corticosteroids are known to provide excellent somatic used less frequently in the postoperative
analgesia but ratller poor visceral analgesia.

period because of the potential to decrease

Interest in ketanline has increased because

PAIN ASSESSMENT AND MANAGEMENT

2111
of its role in preventing sensitization of

NMDA receptors. Adverse effects are
central nociceptive pathways. Ketamine is
usually mild and self-limiting ( drowsiness,
an antagonist at the NMDA receptors in the
fatigue, and weight gain with chronic
spinal cord and brain. Inhibition of the
administration).

NMDA receptors prevents or decreases

Amantadine, an antiviral agent

VetBooks.ir
central sensitization (wind-up) in
developed to inhibit the replication of
laboratory animals and people. Ketarnine
influenza A in human patients, has efficacy
may be incorporated into the anesthetic
in the treatment of drug-induced extrapyprotocol either as a bolus or a constant-rate ramidal effects and in treatment of
infusion to prevent development of

Parkinson disease. It exerts its analgesic
exaggerated or chronic pain states.

effects through antagonism of NMDA
receptors. Amantadine seems most

Other Analgesic Agents: Tramadol, a
efficacious in the management of chronic
synthetic codeine analogue, is a weak mu
neuropathic pain with signs of hyperalgesia
opioid receptor agonist. ln addition to
and allodynia. Aninlals suffering from
opioid activity, it inhibits neuronal reuptake
opioid tolerance may also benefit. A 2008
of norepinephrine and 5-hydroxytryptanline study demonstrated improved activity in (serotonin) and may facilitate serotonin
dogs witl1 NSAID-refractory osteoarthritis
release. It is recommended for acute and
when amantadine was added to meloxicam.

chronic pain of moderate to severe

Acetaminophen is not approved for use
intensity. Because of its inhibitory effects
in animals but has been used effectively for
on serot011in uptake, tramadol should not
the treatment of breaktlu·ough pain in dogs
be used in animals that may have received
at a dosage of 10-15 mg/kg, bid, for as long
monoanline oxidase inhibitors such as
as 5 consecutive days. The exact mechaselegiline, in animals on selective serotonin nism of action is unclear, although recent
reuptake inhibitors, or in animals with a
evidence suggests indirect activation of the
recent history of seizure activity. In people,
crumabinoid CB(l ) receptor. The so-called
the principal active metabolite (0-desme

COX-3, splice variant of COX-1, has been
thyl tramadol, Ml) is more active at mu
suggested as an additional mechanism for
receptors than the parent drug. Cats
acetaminophen in dogs. Acetaminophen is
produce significant an10unts of Ml, whereas not considered a classic NSAlD partly dogs produce nlinimal amounts. Oral
because of its low anti-inflrunmatory action;
bioavailability is 93% in cats but only 65% in
as such, the risk of thrombocytopenia,
dogs. Dogs elinlinate and clear tramadol
bleeding, and GI adverse effects is n1inin1al.

more rapidly than cats. The dosing interval

Hepatopathy is of concern, and routine
must be adjusted in cats. Adverse effects
sernm chenlistry evaluation is warrru1ted.

include decreased seizure thresholds,

Acetanlinophen should not be used in cats
nausea/vomiting, and in some anin1als,
because of inadequate cytochrome P 450-
altered behavior.

dependent hydroxylation (glucuronidation)

There are few clinical studies exanlining
and subsequent fatal methemoglobinemia.

the use of tra.madol in animals. However,

Maropitant is a potent selective
it has been shown to reduce nlinimu.m
neurokinin (NKl) receptor antagonist that
alveolar concentration of sevoflurane in
acts in the CNS by inhibiting substance P,
cats and is reported to have ru1 analgesic
the key neurotransnlitter involved in
effect after ovariohysterectomy similar to
vomiting. It provides visceral analgesia for
that of morphine in dogs. Trrunadol may be
conditions such as pancreatitis, cholangitis,
used alone to treat mild pain and adjuncand painful GI disorders.

tively in a multi.modal plan to treat moderate
to severe pain.

LOCAL AND REGIONAL

Gabapentin was originally developed
and licensed as a human anticonvulsant

ANALGESIC TECHNIQUES
agent and has been approved by the FDA

Local and regional anesthetic techniques are
since 1993. Reports of its antihyperalgesic
used extensively in large anin1als for a variety
effects in rodent experimental pain models
of minor and major surgical procedures.

and case reports involving hmnan patients

Local anesthetics are used in small aninlals
suffering from neuropatllic pain suggest
much less frequently and prin1arily to
increasing evidence for its use in neuropatllic facilitate suturing of nlinor lacerations.

pain. The mechrulism of action appears to he

Because of the relative ease and safety of
voltage-dependent Ca2+ chrumel blocker, and inducing general anesthesia in small aninlals, it may increase central inhibition or reduce
local and regional anesthetic techniques are
the synthesis of glutamate, even though it
often overlooked. Nevertheless, fuese
does not appear to interact directly with
tecluliques provide an excellent alternative

2112

PAIN ASSESSMENT AND MANAGEMENT
to general anesthesia for select cases and are
place for 60-90 min beneath an occlusive
being used increasingly in conjunction with
dressing. Nonclinical methemoglobinemia,
general anesthesia to in1prove postoperative
lasting as long as 24 hr, has been repo1ted in
analgesia. Local anesthetics used before
children. Repeated dosing of neonatal or
surgery may decrease the requirement for
small aninials should be done cautiously.

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potent irtjectable and/or inhalant general

Bupivacaine is the preferred drug for
anesthetics.

postoperative analgesia because of its

Conduction blockade of nerve fibers by
relatively long duration of action ( -3--8 hr).

local anesthetics is related to the size of the

Bupivacaine (0.25---0. 75%), with or without
nerve, amount of myelination, and
epinephrine, is administered in a dosage not
frequency of activity. Small sensory and
to exceed 3 mg/kg (dogs) for line or ring
autonomic fibers tend to be anesthetized
blocks of an incision, ring blocks before
before larger motor and proprioceptive
declaw in cats ( epinephrine-containing solufibers. Nerves that are repetitively tions should not be used for distal extremity
stimulated are more sensitive to local
ring blocks), intercostal nerve blocks and
anesthetics than resting nerves. The most
intraplew·al local anesthesia ( diluted to
commonly used agents are lidocaine, mepivtwice the volume) after a thoracotomy or acaine, bupivacaine, and ropivacaine.

the management of pa.in associated with

Lidocaine, the prototype aniinoamide
pancreatitis, proximal nerve infiltration
local anesthetic, decreases minimun1
during limb amputations, regional
alveolar concentration of isoflurane in a
anesthesia in which a nerve proximal to the
variety of species. It also has the potential
surgical site is targeted, tissue infiltration
to decrease ileus in horses after general
for lateral ear resections, and local blocks
anesthesia and is used commonly as an
of facial nerves (maxillary, infraorbital,
adjunct in colic surgery. This has become
mental, and mandibular). Bupivacaine is
the theoretical basis for its systemic use as -
frequently administered into the epidural
an analgesic agent. Constant-rate infusion
space at the lun1bosacral space for pelvic
of lidocaine has been advocated for pain
limb and perianal procedures. Bupivacaine
management in a number of species;
is cardiotoxic if administered IV.

notably, a number of combination a11algesic

Ropivacaine is a long-lasting amide-type
protocols ( eg, morphine, lidocaine,
local anesthetic. Its duration is similar to
ketamine [known as MLK]) have been
that of bupivacaine, but it has lower
developed for dogs. The use of constantpotential to induce cardiovascular and CNS
rate infusion lidocaine during anesthesia is
toxicity.

not recommended for cats because of their

Topical capsa.icin, the active component
increased sensitivity and its negative
in chili peppers, has been used extensively
cardiovascular effects.·
to treat pa.in associated with diabetic

Lidocaine transdermal patches have been
neuropathy, post-herpetic neuralgia, and
developed for the treatment of neuropathic
osteoarth1itis in people. Capsaicin binds
pain in people. Systemic absorption of
to the TRPVl receptor on nonmyelinated
lidocaine in dogs and cats has been reported primruy afferent pain fibers, causing to be mininlal, while local tissue concentraincreased firing through the release of tion is reported to be as much as 100 times
substance P. With repeat application,
greater than plasma concentration. The low
desensitization occurs due to degeneration
systemic absorption rate coupled with high
of these pain fibers with resultant hypoalgelocal lidocaine concentrations on the skin sia. Reinnervation occurs when use is
support the safe use of lidocaine patches in
discontinued. No controlled studies have
dogs and cats. These patches appear to
been published in veterinruy species;
result in a differential blockade, preserving
however, one study using intrathecal
sensory function of the skin and motor
resinferatoxin, a potent analogue of
function of regional muscles while inducing
capsaicin, reported encouragi11g results for
analgesia at the site for as long as 72 hr.

palliative treatment of pain in a canine

However, further clinical efficacy studies
osteosarcoma model. The benefits of these
are wananted. Patches must be applied

TRPVl ligands include specific loss of pain
close to the site of pa.in, and toxicity is of
sensation without concomitant loss of
concern if the patch is orally ingested.

motor and nonpain sensation.

EMLA cream, a eutectic mixture of 2.5%
lidocaine and 2.5% priloca.ine, has been used CHRONIC PAIN
to decrease verupuncture pain in children
and has been evaluated for use in dogs, cats,

The treatment of chronic pain relies on
rabbits, horses, and pigs. Significant results
pharmacologic and nonpharmacologic
are not achieved until the cream has been in
methods. Commonly treated chronic pain

STRAY VOLTAGE IN ANIMAL HOUSING

2113
syndromes include osteoarthritis, nonsurgianin1als when surgical intervention is not cal intervertebral disc disease, and laminitis.

approp1iate. A munber of studies using

Some chronic pain responds to drugs used
chonclroprotective agents such as polysulto treat acute pain, such as opioids and fated glycosaminoglycans, chondroitin

NSAIDs; however, other types of chronic
sulfate, glucosamine, and hyaluronic acid
pain require the addition of novel drugs such
suggest a benefit tlu·ough stimulation of

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as gabapentin, tramaclol, acetaminophen,
caitilage matJ.ix synthesis and inhibition of
and an1antadine. Regarclless of the cause or
enzymatic degradation of caitilage. However,
the species, chronic pain is itself a dynamic
the efficacy of tl1ese agents may vary with
disease process requiring careful assessspecific product used, route of administrament and frequent reassessment. Therapy tion, and underlying confonnational,
is rarely rnonornoclal, and acljustments in
pathologic, and neurologic issues. Recent
therapy are necessary over time.

work in regenerative medicine, including the

The nonpharrnacologic treatment of
use of autologous adult stem cells, may prove
chronic pain depends on the underlying
highly effective as well. Finally, acupuncture
cause and the species. Among these
and rehabilitation therapy have been used to
therapies are acupuncture, rehabilitation,
tJ.·eat chronic osteoaitluitis pain in a munber
nutraceutical supplements, low-level laser,
of vete1inaiy species with promising results.

massage, transcutaneous electric ne1ve
stimulation, and herbal supplements. The

Cancer Pain: Cancer pain presents a
body of Literature critically examining these
unique clinical challenge. Components of
is relatively small. (See also COMPLEMENTARY
cancer pain are tumorigenic (tw110Helated

AND ALTERNATIVE VETERINARY MEDICINE, p 2078).

products), in:flan1mato1y, and new·opathic.

Similai· to other forms of clu·onic pain, it does

Osteoarthritis Pain: Osteoartluitis
not always respond adequately to conunon
is the most common reason for persistent
therapies. Opioids remain a cornerstone of
pain in people, clogs, cats, and horses.

treatment and ai·e usually one pa.it of a

The nonpharmacologic goals to manage
multi.modal pla11. Other analgesics include
osteoartluitis pain include increasing

NSAIDs, tramadol, acetaininophen (in dogs),
mobility, Limiting disease progression, and
a11d an1antadine for its ability to decrease
possibly facilitating tissue repair within Lhe
wind-up. An opioid and an NSAID ai·e
joint. Weight control or reduction and mild
routinely used in combination because of
to moderate daily exercise are beneficial.

their synergistic analgesic effect. Recently,

Excessive and strenuous exercise should be
bisphosphonates have been used to treat
avoided, because it may frnther strain the
osteolytic pain associated with bony
joints and exacerbate pain, thus limiting
metastasis. Pantidronate is the synthetic
the ability to exercise routinely. Providing
analogue of inorgaitic pyrophosphate. It pas
warmth dming cold and damp weather and
proved useful in pain palliation because of
extra bedding or padding may also in1prove
its ability to adsorb to bone ntineral matrix,
comfort. Surgical removal of bone fragments inhibit pathologic lysis induced by osteoand osteochondritic lesions and the clasts, and delay progression of bony
restoration of joint stability is often
metastatic lesions.

necessary to slow the progression of disease

Sintilar to all chronic pain syndromes,
and reduce pain. Joint replacement or
cancer pain management requires frequent
arthrodesis may be indicated in severe cases.

assessment and reassessment combined

Orthotic bracing may be beneficial in small
witl1 appropriate adjustments in therapy.

STRAY VOLTAGE IN ANIMAL HOUSING

The tem1 stray voltage describes a special

(anin1al contact voltage). The grounding
case of voltage developed on the groundeclai1cl neutral systems on a fam1 or in a home neutral system of a fai111 and is defined as
wiring system should be properly bonded to

<10 volts (measured as the root-meanensure elect1ical safety. As a result, some square value of 50 or 60 Hz alternating
level of voltage between the groundedvoltage, Vnns) between two points that can neutJ.·al system and the earth (neutral-tobe contacted simultaneously by an anin1al earth voltage) is always present as a nom1al

2114

STRAY VOLTAGE IN ANIMAL HOUSING
consequence of the operation of properly
hand-foot contact. The contact voltage to
installed electrical equipment. The tenn
produce sensation can therefore be higher
stray voltage is often applied incorrectly to
for people than for cows, depending on the
otl1er electrical phenomena such as electric
conditions of the contact points. The stanfields, magnetic fields, electric cwrent dard measurement circuit used for field

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flowing in tl1e eatth (eatth cwTents), or
investigations uses a 500-ohm "shunt"

electric current flowing on a grounding
resistor to simulate the combined resistance
conductor (ground cw-rents). Electric
of a cow's body plus a conservative (lowest
currents flowing in the earth or on grounded or worst case) estin1ate of the resistance of metal objects will affect animals only if
the two contact points ( cow + contact
sufficient animal contact voltage is
resistance).

developed.

A great deal of research on the effects

If stray voltage reaches sufficient levels,
of stray voltage on dairy cows has been
animals coming into contact with grow1ded
conducted throughout the past 50 yr. The
devices may receive a mild electJic shock
most sensitive cows ( <1 %) begin to react to
that can cause a behavioral response. At

60 Hz electrical cwrent of 2 mA ( measured
voltage levels that are just perceptible to the
as the root-mean-squai·e average, or m1s)

animal, behaviors indicative of perception
applied from muzzle to hooves or from hoof

(eg, flinches) may result, with little change
to hoof. This corresponds to a contact
in no1mal ro11tines. At higher exposme
voltage level of -1 Vnns in wet locations or
levels, avoidance behaviors may result.

>2 Vnns in dry locations. N wnerous studies

Contact voltages< IO Vnns are not lethal to
have docwnented that avoidance behaviors
fatm animals or people. If neutral-to-eatth
occur at exposure levels well above tllis first
voltages >10 Vrms are measured on a fai·m,
behavioral reaction threshold. As tl1e current
tl1e safety of the farm wiring system should
dose increases above 2 mA, an increasing
be carefully evaluated by a competent
percentage of cows show mild behavioral
electriciat1.

responses, and some cows start to show

Animals respond to the current flowing
avoidance behaviors. The median avoidance
through their bodies. Ohms Jaw describes
tl1reshold for 60 Hz cun·ent flowing tJu·ough a
tl1e relationship between voltage exposure
cow is -8 mA ( or 4 Vm1S contact voltage in
and current conducted through an animal:

wet locations and >8 Vnns in dry locations).

cturent = voltage I resistance or amps=

Even when the tJu·eshold is exceeded, all
volts / ohms
cows do not respond behaviorally all the

This simple relationship has been a
time, nor do they exhibit the saine signs; howsource of much confusion and resulting ever, as the voltage increases, signs in the
contJ·oversy. Ohm's law indicates that if the
herd become more widespread and wlifmm.

voltage across animal contact points is

Cows have reswned normal behaviors within
increased, the cmrent flowing through the

1 day of removal of aversive voltage and
animal will increase. If the resistance of the
cun·ent levels.

circuit is increased, the current flowing

The only studies tl1at have docun1ented
through the atlimal will decrease. The
reduced water or feed intake in cows had
current measurement used in most studies
botl1 sufficient current applied to cause
is the milliamp (mA) or l/l,OOOtl1 of an amp.

aversion ai1d forced exposures (ie, cows

Applying Olun's law to a circuit witl1 contact could not eat or drink witl10ut being exposed voltage of 1 Vrms across a resistance of 500
to aversive voltage and current). It is typical
ohms results in current flow of 2 mA.

for voltage levels to vaiy considerably
ln most situations, cows are less sensitive
tJu·ough the normal daily operation of
to cwrent and more sensitive to voltage
electJical equipment on a farm. Decreased
than are people. While the resistat1ce of
feed and/or water intake will result only if
bovine and hwnan tissues is sirniJai·, the
cwrent exposure levels at wate1ing and
contact resistance is often lower for cows
feeding locations are sufficient to produce
than for people, particularly in wet
aversion at these locations and they occm
environments. The resistance of a cow's
often enough to interfere with drinking
body plus tile contact resistai1ce with the
and eating behaviors. If an aversive cun·ent
floor is estimated as 500 olm1s for a cow
occurs only a few tin1es per day, it is not likely
standing on a wet floor. Cows standing on a
to have an adverse effect on cow behavior.

dry surface typically have body plus contact

The more often aversive cwrent exposmes
resistance of �1,000 ohms. Cows standing or occur in areas c1itical to drinking or feeding, lying on dry bedding have a resistance mat1y
the more likely it is to affect the cows.

times lligher than tllis. The resistance of a

Studies investigating the effects of
person can be as low as 1,000 ohms for wet

!ugh-frequency or short-duration tJ·ansient
hand-foot contact to> 10,000 ohms for dry
voltages on cows clearly indicate that as the

STRAY VOLTAGE IN ANIMAL HOUSING

2115
duration of a current pulse gets shorter ( or
and many other factors related to the daily
the frequency increases), more voltage and
activities of animals. All of the docU111ented
current is required to cause behavioral
effects of excessive voltage exposure have
responses. The main cause of short-dur a been behaviorally mediated.

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tion electric pulses on farms is improperly

Results of studies to investigate direct
installed electric fences and electrified
physiologic effects that may be produced at
crowd gates. These devices are designed
levels both above and below those required
to produce a powerful electric impulse
to produce behavioral responses have
that is used to control animal behavior.

shown that blood cortisol concentrations

Improper installation of these devices can
and other stress hormones do not increase
cause these pulses to appear in unintended
at levels below behavioral response levels.

areas on the farm. The other common

Increases in stress-related hormones have
source of high-frequency events is a
been docun1ented in some, but not all, cows
switching transient that occurs when
at voltage/cUITent exposures substantially
electric equipment is turned on or off. These
higher than the threshold required for
high-frequency pulses decay quickly and do
behavioral modification. A large body of
not travel far from their source, and it is
research clearly indicates that at levels of
extremely rare for them to reach problemvoltage exposure typically used as atic exposure levels.

regulatory limits ( 1 volt at cow contact

Research suggests that swine respond to
locations, or 2 rnA of CUITent flow through a
voltage/crnTent exposure in a way similar
cow) will not result in increased somatic
to that of cows. Behavioral modification in
cell counts or incidence of mastitis.

swine has been seen above 60 Hz exposures
of -5 Vrms, with avoidance behaviors at

Diagnosis: Several common situations
exposures >8 Vrms. The body plus contact
are of concern in animal enviromnents,
resistance for swine appears to be someincluding 1) changes in drinking behavior, what higher than for cows, and 1,000 ohms
such as decreased number of drinks of
appears to be a conservative value for
water per day and increased length of time
measurement purposes. Ewes have been
per drink; 2) avoidance of locations that
shown to avoid electrified feed bowls when
may result in reduced feed or water intake;

60 Hz exposure levels exceed 5.5 Vims,
and 3) difficulty of moving or handling
whereas lambs showed this same preferanimals in some areas. If these behaviors ential behavior when exposure levels
are seen, electric testing indicating cow
exceeded 5 Vrms. Exposures to voltages
contact exposure in excess of 4 rnA (2 Vims
as high as 18 Vm1s had no effect on hens'

in wet locations witl1 a 500 ohm cow +
production and behavior. This is likely
contact resistor, or 4 Vrms in dry locations
because of the very high electrical
with a 1,000 ohm cow+ contact resistor) is
resistance of poultry, which has been
necessary to confirm a stray voltage
docU111ented to be between 350,000 and
diagnosis. Signs in pigs, ewes, and poultry

544,000 ohms.

are similar, although threshold response
levels are higher than for cows.

Clinical Findings: A wide variety of

It is critically important to use a realistic
behavioral signs have been reported in cows value of animal resistance to relate voltage exposed to voltage and cUITent. No one sign
exposures to the level of cUITent conducted
is pathognornonic, however, because these
through an animal and the resulting effects
behaviors can also be caused by other
on nerve stimulation, sensation, and
factors in the animal environment. The only
behavioral reaction. A competent field
way to determine whether stray voltage is a
investigation will include voltage measurepotential cause of abnormal behaviors is to ments at cow contact locations both with an
perfom1 electric testing.

appropriate "shunt" resistor ( cow contact The direct effects of stray voltage can
voltage) and without a shunt resistor ( open
range from mild behavioral reactions indicacircuit voltage). The shunt resistor is meant tive of sensation to intense behavioral
to represent the resistance of the body
responses indicative of pain. The severity of
resistance of a cow plus the contact
response depends on the amount of electric
resistance representative of the exposure

CUITent flowing through the animal's body,
location. Both animal-contact and open
the pathway it takes through the body, and
circuit voltage measurements are required
the sensitivity of the individual animal. The
to determine the "source resistance" of the indirect effects of these behaviors can vary
electric parts of the circuit. Note that source
considerably depending on the specifics of
resistance is different from the cow contact
the contact location, level of current flow,
resistance and can be used as a diagnostic
body pathway, frequency of occurrence,
to detennine the voltage source.

2116

STRAY VOLTAGE IN ANIMAL HOUSING

Animal-contact voltage levels should be

Prevention and Control: Off-fam1
monitored at different times of the day and
sources of stray voltage are most often
on different days to represent the nom1al
related to improper ftmction of the
operating conditions of the farm electrical
grow1ded-neutral system of the electric
system. Point-to-reference ground
utility. On-farm sources of stray voltage are
measurements can be useful for diagnostic
most often due to wiring systems that do not

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purposes. A reference ground can be
meet wi1ing codes and struldards. Deficienestablished with a copper-clad rod dtiven cies may include loose or c01Toded
into the ground at least 25 ft (8.5 m) from
connections; ground faults (shorts);
any part of the gr0tmding network on the
undersized wiling; or wiring damaged by
farm. The other contact point is typically the animals, accidents, rnoistw·e, or corrosion.

ground-neutral interconnection in the barn

The first step in a competent stray voltage
service entrance panel or some other prut of investigation is to detem1ine the source of the grounded-neutral system. Cow contact
neutral-to-eruth voltage. Faults or electric
measurements are typically Y2 to 1/, of
code violations that could pose an
point-to-reference voltage levels.

electrocution hazard should be corrected

Long, insulated meter leads (6--10 ft
immediately to protect both animals and

[2--3 rn]) facilitate measurements on the
people. If stray voltage levels are excessive,
farm and give a reasonable estimate of
a competent electrician should assess the
power frequency (60 Hz and 50 Hz) events
situation to detennine the most practical,
but introduce considerable noise to higher
safe, and efficient way to reduce neutralfrequency measurements. The measurPto-eaith voltage. Equipotential pla11es are ment of high frequency events requires
required at critical anilnal contact locations
proper equipment and careful measurement
in animal confinement facilities a11d
technique. Details on measurement
effectively eliminate contact voltage even if
techniques are available through elect1ic
substa11tial levels of neutral-to-eaith voltage
power suppliers and extension publications.

are present.

VENTILATION

Ventilation is often associated with
moisture content of the air, measured by
respirato1y health of anilnals; the quality
relative humidity.

of the air that animals breathe directly
influences a11irnal health and disease.

AIR QUALITY

Ventilation, directly and il1directly, impacts
many other aspects of anilnal health as well.

Air quality is not easily defined. It is related

Good ventilation in the lying area of
to ventilation a11d the absence ( or presence)

lactating animals helps beddil1g stay dry, a
of contanlina11ts in the air. For anim<Lls,
factor in favor of good rna111maiy health.

good air quality generally in1plies that the

Good ventilation along alleys helps to keep
ainbient aiJ· causes no harmful effects on the
walking surfaces dry, which contributes to
a11irnals iii the space. Ambient air contains
healthy feet. Good ventilation may lead to
varying ainotmts of water vapor. Moisture in
greater productivity, eg, maintaining aiJ·
the air becomes a problem when it exceeds
movement in the eating area makes animals
the relative humidity ra11ge of 60%--75%
more comfortable, especially ilnportai1t
preferred for ailimals; above this level, it is
during hot weather as an aid to maintaining
considered to be an air containinant. Other
dry matter intake. A comfo1table, wellcontamina11ts may include pathogens, ventilated lying area encourages a11imals to
haimful gases, dust, and undesirable odors.

lie down, an importrult contribution to many Concern arises from the concentration of a aspects of anilnal healtl1.

contamina11t above some predetem1ined

During ventilation, outside aiJ· is brought
level ratl1er tJian the mere presence of the
into a barn where it collects moisture, heat,
contaminant itself.

and other contarninai1ts. Air is then

Numerous viral pathogens known to
exhausted to the outside. To determine
survive in aerosols are appru·ently spread by
ventilation rates, the focus is on the
the airborne route. Two factors can be

VENTILATION

2117
significant in the relationship between
a ventilation effectiveness of 1.0, one air
microbial aerosols and disease incidence:

change would achieve a complete change of

1) the survival time of the aerosolized pathoair in the space, yielding a 100% reduction in gen, and 2) tl1e total number of pathogens
contaminant levels (if the condition of the
per volume of air (ie, concentration).

outside air is considered to be the reference

Survival is influenced by conditions of the
standard). But if ventilation effectiveness

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ambient air; conditions of tl1e ambient air
is only 0.65, one air change will reduce
and concentration are related to ventilating
contanunant levels by only 65%. As ventiair.

lation effectiveness diminishes, the

Relative hwnidity is the most important
ventilation rate required to achieve a certain
factor influencing pathogen survival and
air change rate increases.

concentration, but its effects vary greatly

When ventilation is reduced below
between pathogens-some survive best in
recommended levels-usually in a
humid conditions, others survive best in dry
nusguided effo1t in cold climates to wann
air. Maintaining a relative hwnidity in the
the barn using animal heat-less moisture is
range of 60%- 75% apparently results in the
removed. Sometimes the consequences of
shortest survival time for the greatest
the resulting moisture buildup and lack of
number of potential pathogens. Ventilation
proper ventilation ( eg, condensation) are
is used to remove moistme from an aninlal
masked by insulating the barn, using a
space with the intention of maintaining
greenhouse effect, providing supplemental
relative hwnidity in this range. Inside air is
heat, or dehwnidifying tl1e inside air. For
diluted with outside air, reducing moisture
example, adding heat to the air reduces
levels. Continuous replacement of
relative humidity, without the need for air
contaminated air with fresh, outside air is
exchange. It is quite possible to maintain
also the most effective way to reduce the
substantial quantities of moistme in the air
concentration of aerosol pathogens.

and, if accompanied by heating, keep the

Most likely, reducing the concentration of
relative hw11idity within an acceptable
any air contaminant, including gases and
range. If relative hmnidity is the only
dust, is important to reducing its detrimenmeasure of air quality, it may be deemed to tal effect. For example, ammonia is
be satisfactory. However, even though
produced by the decay of feces and mine
excess moisture may not be apparent, the
and is probably the most significant air
reduced dilution does result in increased
pollutant in cattle barns. Allowed to
concentrations of airborne disease
accumulate, ammonia's irritating effects on
organisms, harn1ful gases and dust, and
the respiratory epithelium appear to directly
undesirable odors. If these increases are
reduce the number of ciliated cells and tl1us
ignored, animal health problems are
decrease the efficiency of mucociliary
inevitable. In addition, heating of barns is
transport.

rarely economical in cold climates.

THE DILUTION EFFECT OF

COLD WEATHER VENTILATION

VENTILATION

A minimal ventilation rate is required in

Dilution reduces heat and concentrations
aninlal housing in cold weather, regardless
of moisture, as well as concentrations of
of outside temperature. This minimal rate is
airborne disease organisms, harmful gases
necessary whether tl1e barn is designed to
and dust, and undesirable odors. The
be a warm barn or a cold barn in winter. In
dilution rate of ventilation is often
addition, the minimal ventilation should be
expressed in air changes per unit time. For
continuous to maintain concentrations of
example, a ventilation rate of 4 air changes/
contanunants in the air at 1ninimal levels.

hr implies that the entire volwne of the

The minimal rate depends on outside
ventilated space is replaced 4 times every
weather, design conditions, animal factors
hour. In fact, some of the air may bypass tile

(number, type, age, and size), and whether
occupied zone in the barn, depending on
the barn is intended to be cold or warm.

geometry of the space, design of diffusers
controlling inlet air, etc. Therefore, the
effectiveness of ventilation is not lO()OA, but

Barn Categories and Winter
perhaps approaches 65%. Ventilation

Temperatures
effectiveness becomes important to the

Barn environments can be categorized
actual dilution achieved by a particular rate
according to temperatures maintained in
of ventilation (ie, to the ability of ventilating
the barn in winter. The particular
air to reduce tile concentrations of
environment, based on desired indoor
contaminants in the animal space). For
temperatme, must be established before

2118

VENTILATION
ventilation system design can begin. In
ventilation rate is always necessary,
cold barns, indoor temperatures are
ventilation openings may be closed or
allowed to fluctuate with outdoor
blocked during extreme weather to keep
temperatures. Ventilation is sufficient
manure from freezing and for other
to maintain indoor temperatures within
reasons. This practice can result in inside

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3° -6°C of outdoor temperatures. Ventilatemperatures rising 10°-20°C above the tion is largely unregulated, except to
outside temperature, significantly higher
ad.just for seasonal changes. In general,
than the 3° -6°C temperature difference
a cold barn with natural ventilation has
limit considered acceptable for cold barns.

no insulation, an open ridge and eaves,

This alone can create problems because
and sidewalls and endwalls that open.

of excess moisture buildup and a high

Providing an open ridge along with open
relative humidity. Even more seriously,
eaves has long been recognized as a way to
openings remain closed or blocked after
use a stack effect to cause air exchange,
severe weather conditions have passed.

especially to control moisture in winter.

As a consequence, blocked ventilation

Indoor temperatures are expected to be
openings restrict airflow during less
a few degrees warn1er than outdoor air
severe conditions, resulting in underventitemperature because of the heat given lation and poor environmental conditions.

off by the animals being housed. Current

A properly designed and managed
recommendations call for providing a ridge in-between barn is more like a wann barn, opening of 5 cm per 3 m of barn width and
in terms of both design and operation,
equivalent open area divided between the
than a cold barn. Thus, to avoid problems,
two eaves. Raised ridge caps are to be
the design and management of in-between
avoided. Their performance is unpredictbarns should follow the guidelines for a able because of local wind patterns, which
warm barn.

often channel winds into the structure and
increase the entry of snow and rain. The
combination of the open ridge and eaves

Consequences of Mismanaged
should be viewed as the sole source of

Ventilation in Winter
ventilation only during the most severe

Underventilation in winter is one of the
winter weather, ie, during periods when
most serious threats to the environment
temperatures reach the lowest levels or
of animals. Both improper design and
times when conditions are especially
improper management of the ventilation
windy or storn1y. During all other tin1es
may compromise animal health. In colder
in winter, additional ventilation should
climates, problems are most likely dilling
be provided.

winter, spring, and fall, especially dilling

Warm barns are well insulated and, by
rainy weather and warmer days coupled
necessity, have well-controlled ventilation
with cold nights.

systems. These barns are designed to
provide a relatively unifonn envirorunent

Reduced Dilution of Ambient Air:

throughout the winter. Tie stall barns for

AcJ.iusting ventilation for severe winter
dairy cows (indoor temperatures at least
weather and not reacJ.iusting to allow
above freezing) and farrowing and nursery
increased ventilation for milder winter
barns for swine (indoor temperatures
weather appears to be a major reason for air

25°-30°C) are exan1ples of this type of
quality problems in barns in winter. This is
housing. Keys to success include ventilating
especially true for cold barns.with manually
fans and controls chosen to match the
controlled natural ventilation. For example,
needs of the animals being housed, a
ventilation openings are closed in anticipawell-insulated building, supplemental tion of a windy, cold, blustery night, but are
heating (if required), and a ventilation
not opened the next day when, although the
system that is well managed and regulated
temperature may still be cold, the wind
to compensate for changing outside climatic subsides and the sun shines. The lack of conditions.

wind reduces ventilation and thus air

Some barns do not fit into either the
exchange and the positive effects of
warm or cold category. In-between or
dilution.

modified environment barns usually

Sometin1es, good ventilation system
have indoor temperatures in winter above
management does call for openings to be
freezing. These buildings have some
reduced. For example, a slot inlet in a
insulation, perhaps only under the roof,
mechanically ventilated tie stall barn may
and are naturally ventilated (usually with
be acl.iusted, or fabric may be placed over an
an open ridge, eaves, and sidewalls).

open sidewall to match the lower ventila

Unfortunately, even though a minimal
tion rate in winter. All openings should

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE

2119
never be covered, however, because this
when temperatures reach the lowest levels
leaves no means of air exchange for
or times when conditions are especially
moisture control.

windy or stormy. During all other times in
winter, however, additional ventilation must

VetBooks.ir

Building Components Affected
be provided. Typically, doorways are left
by Poor Ventilation: In addition to
open, pmtions of the end wall sections of
adversely affecting the animal environment,
the gable roof may be left uncovered, or
the design and operation of naturally
sidewalls away from prevailing winter
ventilated barns also influence moisturewinds may be left open for this purpose.

related deterioration in wood members and

Then, as temperatures rise into spring and
metal fasteners. In naturally ventilated dairy
summer, sidewalls and end walls are fully
free-stall barns in Michigan, where air
opened. As a general rnle, too much
exchange in winter was defeated by
ventilation is prefen-ed over too little.

blocking ventilation openings, average

Hot, muggy sun1me1 weather is one of the
wood moisture contents >30"Ai dry basis
most critical times for animal health,

( capable of supporting wood decay and
comfort, and productivity. For barns with
con-osion in metal fasteners) were found
natural ventilation, completely open
after 2-3 mo of cold weather operation.

sidewalls and end walls allow wind to blow

Moreover, restricted air movement in these
tlu·ough the animal zone for heat stress
barns inhibited drying and allowed wood
reduction. However, when winds are calm,
moisture content to remain high even
providing adequate air movement to avoid
during warm weather. Warn1, moist
heat stress is difficult. Supplemental cooling
conditions favor growth of mold, bacte1ia,
can be provided in several ways. Fans are
and decay fungi and accelerate metal
conunonly used to increase air movement.

con-osion. The presence of insulation under

The increased air velocity over the skin
the roofing in these barns fostered the
increases t11e rate at which animals are able
situation. In barns in which design details
to dissipate excess body heat. Two other
and management efforts allowed optimal air methods rely on evaporative cooling to exchange rates, increases in moisture were
either cool the air around the animals or wet
nlininlal. Even if free water from precipitathe anin1al's skin and allow body heat to tion and condensation caused slightly
evaporate the water. However, water should
increased moisture contents, adequate air
be added to the animals' environment only if
exchange, especially dwing warm weather,
ample air movement is present.

promoted drying of wood trnss components

Barns with mechanical ventilation require
so that deterioration was not a problem.

staged fans to provide ventilation ranging
from t11e minimal continuous rate, through

WARM WEATHER VENTILATION
an intermediate rate for spring and fall, to a
high rate for swnmer. An air exchange rate

In barns with natural ventilation, the
of 60 air changes/hr is considered the
combination of tl1e open ridge and eaves is
absolute minimun1 for sununer. Often,
the source of ventilation during tl1e most
ventilation rates of 90-120 air changes/hr
severe winter weather, ie, dwing periods
are provided for hot weather.

HEALTH-MANAGEMENT INTERACTION:

BEEF CATTLE

BEEF CATILE
in cow-calf operations. They include a

BREEDING HERDS
restiicted breeding season, identification of
the optimal calving season, a good heifer

Several manageiial practices increase
replacement progran1, heifer reproductive
productivity within cow-calf herds when
tract sc01ing, proper nutiition, good herd
they can be implemented economically and
health, bull breeding soundness examinapractically. These practices are mostly tions, crossbreeding, and maintaining good
associated with reproduction, because
records. Ot11er management practices
improvements in herd fe1tility generally
associated with increased beef herd
offer potential for increased profitability
profitability include decreasing unit cost

2120

HEALTH-MANAGEMENT INTERACTION BEEF CADLE
of production, use of growth promotants in
many factors, including sire fertility, herd
calves, internal and external parasite control, health aspects, and opportunities to mate.

unproved calf management, management

Breeding soundness evaluation is a
intensive grazing, preconditioning of calves,
technique to assess the reproductive
and having a marketing plan.

perfonnance of the cow herd. It includes
obtaining relevant information, analysis

VetBooks.ir

REPRODUCTION
and interpretation, and recommendations
for improvement. One measure of

In most regions of the world, there is an
reproductive perfom1ance is ilie number of
optimal period for females to calve, suckle,
bred females that actually raise a live calf.

and rebreed. This pe1iod is mostly related to Other valuable info1mation may be nutritional opportunity, although other
obtained from an analysis of the distribuenvironmental factors such as cold or heat tion of pregnancies (and calvings) that
stress and parasite populations may play a
resulted from a pa.iticular breeding sea.son.

role. Producers have traditionally aimed for

This distribution may be studied on the
females to calve during this optimal period
basis of timing (eg, 21-day estrus periods),
because they tend to breed back faster, and
breeding groups, female age or parity,
their calves are more likely to thrive, than
nut1itional opportunity (eg, BCS), etc. Such
females that calve at less opportune times.

analyses provide the basis for evaluation of

Benefits of restricted breeding seasons
either the breeding or calving season. For

(65-80 days) include enhanced production
evaluation of ilie breeding season, good
potential, favorable environmental factors,
records must be obtained at the time of
a concentrated calving season and more
pregnancy testing for the subsequent
homogeneous calf crop to sell, increased
analysis to be valid.

opportunities to perforn1 prebreeding

Because reproductive perfom1ance is an
management procedures and monitor
important economic trait in ilie cow herd,
nutrition, improved female replacement and
the reproductive capabilities of breeding
culling procedures, and the ability to detect
bulls asswne great importance. The best
problems early, using herd pregnancy diagnoassw·ance that a bull is likely to be fertile is sis and breeding season evaluation. (See af,So
a successful breeding soundness evaluation

MANAGEMEN'rOI' REPROOIJCTJON: CATTLE, p 2171.)

(see BREEDING SOUNDNESS EXAMINATION 01' THE

MALE, p 2230). A rule of thun1b for bulls is

Pregnancy Testing: The longterm goal is
ilia.t they can breed -1 cow/mo of age in
to develop a beef herd of uniform, lowa breeding season of 65-80 days. For maintenance cows U1at tluive in their given
exa.iuple, a 38-mo-old bull that passes his
environment. This goal is strengthened by
breeding soundness exan1ina.tion should be
having a restricted breeding season in
able to breed 38 cows in 65-80 days. This
which open cows are culled from the herd.

rule can be applied to bulls approximately

Often, these cows are too big, produce

14--50 mo old, wiili 50 cows per bull being
too much milk, or lack inherent fertility
the ma.ximwu.

compared wiili cows that are pregnant year
after year. In herds that are yea.rs a.way from
iliis goal, instead of simply calling cows

CULL COW SELECTION AND
pregnant or open, cows should be sorted by

MANAGEMENT
projected calving date and body condition
score (BCS). The herd pregnancy diagnosis

Culling of cattle in a beef operation usually
represents an important starting point for
implies removing iliose that ca.JU1ot meet
beef herd diagnostics and advice and is a
or maintain perforn1ance and economic
pivotal component for informed decision
criteria. for the herd. Other reasons may
include physical or tempera.Jllent problems
ma.king. It allows analysis of group patterns
for problem solving (breeding soundness
in ariin1als, as well as judicious culling
dw·ing periods of environmental hardship
evaluation, see below), as well as sorting of animals into groups for specific purposes
or economic necessity. The judicious
such as strategic feeding, calving superviremoval of nonperfonning females is also important to maintain or in1prove herd
sion, culling, or rebreeding. Herd pregnancy
diagnosis facilitates the selection of
fertility. However, the asswnption that cull
replacement females and culling for
cows are necessarily infertile may not
infertility.

always be con-ect; recent surveys indicate
iliat -43% of cull cows in the USA are
pregnant at the time of culling. All "open"

Breeding Soundness Evaluation:

females are not necessarily infertile.

Reproductive performance is influenced by

Identification of a.pprop1ia.te candidates for

HEALTH-MANAGEMENT INTERACTION: BEEF CATILE

2121
culling is critical and should be an important nutritional status in breeding females. The component of pregnancy testing.

BCS represents a subjective assessment of
body fat ( or energy reserves) that is strongly
related to female reproductive pe1formance.

NUTRITIONAL MANAGEMENT

BCS, and changes in BCS, appeai· to be more
reliable indicators of nutritional status than

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NutTition is the most important limiting
is body weight or changes in body weight,
factor of beef herd reproductive pe1fo1�
which can Va.I'}' with gut fill a.J1d pregna.J1cy
mance. An tmderstanding of the principles
status. In addition, BCS can often be
underlying the nutritional management of
assessed more conveniently than body
breeding females is necessary, including a
weight ca.J1 be measured. BCS is both
working knowledge of the different energy
repeatable and accurate in experienced
measuring systems commonly used and
hands. It is best done through visual
their applications for different classes of
appraisal, reinforced by palpation of body
animals, activities, and feedstuffs. (See
regions most likely to demonstrate fat depos

NUTRITION: CATTLE, p 2248.) Increasing
its. Group observations of BCS made from a
stocking rate tends to cause increased
distance when ailimals are in the pasture or
gain per w1it land area but can result in
paddock are less accurate than those made
decreased gain per ai1in1al. The key is to
when animals ai·e nearby in the pen or chute.

have these two factors in balance so that

BCS vaiies throughout the year and
pasture land is optin1ally grazed and gain
should be monitored regularly. In the 1-9
per animal is adequate. Overgrazed pasture

BCS system widely used in North America,
is detrimental to the environment and can
the reference standard for beef females is a
severely reduce gain per animal.

BCS of 5, which represents an average,

Nut1itional requirements Va.I'}' throughmoderately fleshed cow that is neither fat out the yeai·. The most critical pe1iods for
nor thin. However, the BCS for optimal
reproduction are inunediately precalving,
female efficiency varies with breed and
when fetal growth is maximal along with
operation and may be higher or lower. In
lactation preparation, and early postcalving, general, cows should calve when they are when maximal lactation is combined with
between condition scores 5-6 (heifers 6-7)

the need for rebreeding. (See also MANAGE
and then regain the weight lost at calving

MENT OF REPRODUCTION: CATfLE, p 2171.)

and gain slightly until breeding. It generally

Environmental conditions can strongly
takes -2 mo to gain 1 score (75-100 lb
influence the nut1itional requirements and

[34.1-45.5 kg]) for nonlactating cows under
intake of cattle. For exan1ple, cold weather
pasture conditions. Care should be taken
increases energy needs, whereas hot or
not to rely on averages, because these can
inclement weather can reduce foraging
mask vaiiations that might adversely affect
opportunity. The quality and quantity of
herd fertility.

range forage varies greatly throughout the

Whereas BCS at calving has been long
yeai· and between years, influenced by
proved to impact reproductive success,
moisture, soil fertility, plant species, and
recent studies have demonstrated that an
grazing pressure. Seasonal changes in the
increasing BCS from after calving to
nutrient density of rai1geland forages are
breeding is just as important or can be more
mainly associated with the degree of plant
important than precalving BCS in terms of
mattuity. In general, the greatest nutritional
herd fe1tility. The concept of increasing BCS
value of plants develops before maturity.

just before breeding is especially trne of

Good nutritional management involves
yearling heifers. These heifers ai·e often
matching, as far as possible, the nutrient
developed on more of a feedlot type ration
requirements of cows and nutrient density
during the winter and then turned out to
of the pasture by careful consideration of
pasture at breeding time. This causes a
factors such as the types of anin1als
decrease in available energy, which can
involved, stocking rates, plant species
significantly decrease first-service
available, season of grazing, fertilization,
conception rate. Solutions to this are to feed
and grazing methods used.

a lower energy ration during the development stage and to add additional energy to Body Condition Score: Accurate and
the diet after pasture twn-out.

tin1ely determination of the nutritional

The BCS of females at calving can provide
status of grazing animals represents a
much information about their rebreeding
challenge for beef producers, because many
prospects. However, assessment of BCS at
vai·iables can influence a cow's response to
this time provides a relatively short length
a given level of nutrition. The use of a BCS is
of time in which to meet targets if cows are
an effective indirect method to determine
too thin. Assessment of BCS in females at

2122

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE
breeding should provide the most accurate

VACCINATIONS
prediction of herd fertility, because it is
done just before U1e predictive event. The

Prebreeding vaccinations should be
disadvantage is that there is no opportunity
completed -4 wk before the start of
to correct significant shortfalls in time to
breeding and should be based on local

VetBooks.ir
affect the current breeding season.

patterns of disease and stqte and national

Assessment of BCS at the time of pregnancy
requ.irements. Replacement females should
checking has the advantage of not requiring
be vaccinated with the same vaccines given
a separate animal handling. Jt also allows
to matme females before breeding.

considerable time to remedy obvious

Precalving vaccinations are intended to
deficiencies before calving and subsequent
protect the newborn calf through colostral
rebreeding. The disadvantage is that,
transfer. The most common in1mun.izations
although it can provide clues to explain
are those that offer protection against some
current pregnancy patterns, it is again too
of the infectious causes of diarrhea in
late to remedy them. The ideal time to
neonatal calves. Others are based on local
assign BCS to cows is -2-3 mo precalving.

patterns of disease. Many of these vaccines

This gives ample time to move cows to an
have vaiiable results when used in field
optimal precalving BCS, because BCS at
conditions at1d should not be used in
calving is highly correlated to herd fertility.

substitution of excellent management

It is best if someone other than the owner
practices.

(eg, veterinarian, extension specialist, etc)

Preweaning is an important intervention
does the BCS evaluation of the herd,
that can help prepare calves for the stress of
because the owner sees the cows every day
weaning and reduce the possibility that
and is less likely to see changes.

such stress will comprom.ise the efficacy of
biologicals. Common vaccinations include
those against the clostridials and bovine

HEALTH AND PRODUCTION
respirato1y disease complex (BRD). A

MANAGEMENT PROGRAM
broad-spectrwn ai1thelmintic should also be
given at this time, because calves that have

A cost-effective herd health and producbeen on pastme have almost certainly been tion management progran1 is essential
exposed to internal pai·asites. At wean.ing,
for the economic viability of cow-calf
a second vaccination should be given
operations. Such programs vaiy by region,
for those products recommending two
relative economics, perceptions, and
ir\jections. Modified-live virus (MLV)

opportunity. A good herd health progran1
products should be given at this stage.

manages risk of disease and lowered

Another clostridial vaccination is not
productivity at a nun1ber of levels,
indicated if calves were previously
including considerations of biosecurity,
vaccinated at working and prewean.ing. For
nutrition, and the judicious use of biologics ai·eas where brucellosis is under regulato1y and parasiticides.

control, heifers should be vaccinated

One starting point for such a program
appropriately within the age ranges
is to identify cmrent production losses
stipulated.

by comparing the perforn1ance of the

Bulls should receive the same vaccines
particular herd with relevant standai·ds, eg,
as the cow-calf herd, with some exceptions.

from regional or national swveys, which

Bulls should not be vaccinated for brucan also provide an economic estin1ate of cellosis. Also, the trichomortiasis vaccine
losses.

currently approved for use in the USA is

The major disease risks for a given
not approved for bulls. Caution is advised
herd, along with appropriate preventive
with MLV infectious bovine rhinotracheitis
measmes, should be established in consultavaccines, because this virus may recrudesce tion with herd owners. The best times for
in bulls and be shed in semen; tl1e manufacherd intervention must be identified. These turer's technical services veterinarian
often coincide with other managerial tasks
should always be asked if this is a concern.

and can be synchronized to minim.ize herd

Also, if MLV infectious bovine rhinotracheidisruption and labor costs. One approach is tis vaccine is used, semen shipment to other
to devise a herd-health "calendar" in which countries may be jeopardized.

the health events are coordinated with
major operational events. Interventions for

CALF MANAGEMENT
a particular herd vaiy based on factors such
as available labor, norn1al herd working

Management of the calving season is critical
dates, calf wean.ing dates, calf management
to optimize the weaned calf crop. Research
practices, and previous disease problems.

indicates that 57% of mortal.ity is seen in the

HEALTH-MANAGEMENT INTERACTION: BEEF CATILE

2123
first 24 hr and 75% within 7 days of birth. In
decreases in morbidity. Vaccination may be a
addition, there a.re significant risk factors
useful adjunct to proper management in
for increased calf morbidity at the time of
controlling neonatal diarrhea., but U1e key is
calving that can lead to increased mortality
environmental control.

and decreased calf performance. Factors to

An excellent environmental control

VetBooks.ir
consider in calving management include
program is the "Sa.ndhills calving system"

dystocia management ( of primary concern
developed at the University of Nebraska..

in fust-calf heifers), calving environment

In this system, pregnant cows are

(including ambient temperature), passive
wintered in an area separate from the
transfer, and cow-calf pair management.

calving area. When the first cow ca.Ives or

(See MANAGEM!sNT OF llEPRODUCTION: CA'l'J'LE, is a.bout to calve, the entire herd is moved
p 2171.) A visit to the farm or ranch -4 wk
to the first calving pasture. Cows stay
before the onset of the calving season
here for 2 wk; after this time, all cows
provides the opportunity to evaluate the
with calves stay on pasture 1 while a.II
preparations made by the producer and to
cows yet to calve move to pasture 2. After
recommend any changes.

l wk on pasture 2, all cows with calves

Keeping records on calving ease and
stay and all pregnant cows move to
morbidity and mortality incidence allows
pasture 3. This continues for the next
for analysis of risks and risk groups and

6 wk. Cow-calf pairs can be combined
detection of any increased incidence of
when the youngest calf in the group is 4
disease. At least one additional visit should
wk old and at low risk of diarrhea.. This
be made to the fa.rm 2-3 wk after calving has system assures that each ca.If is born begun to assess the management and
into a clean environment, so disease
environment. Morbidity and mortality
transmission is minimal to nonexistent.

incidence levels may be established; if these

Herds that ha.cl severe morbidity and
a.re exceeded, the herd health veterinarian
mortality from scours before using the
should be called and an investigation begun.

system may have almost no health

The most conunon cause of calf
concerns after its adoption.

morbidity in the neonatal period is dianhea

In this and in all calving systems, heifers

(seep 275). It is sometimes not possible and should be wintered and calved separately
many times not in1portant to differentiate
from adult cows, because heifers have
dianheas associated with different etiologic lower immunity to pathogens than cows.

agents, especially when diarrhea occurs in
the 7- to 14-day range. Control for pathogenic a.gents of neonatal diarrhea. involves Castration and Dehorning: Castration
segregation of sick animals from the healthy of male calves in early life (before 3 mo nursery to decrease environmental contan1iof age) is less stressful to calves than na.tion and transmission. In addition,
castration pe1fonned later, when testicular

Escherichia col'i and Salmonella control size is dramatically increased. A number of
involves biosecurity rules to prevent the
methods may be used, including the open
purchase and introduction of new calves or
surgical technique, the use of rnbber rings,
cows during the calving season. Sick calves
and the Burdizzo method. Ca.Ives castrated
should be isolated quickly to prevent fruther
surgically initially exhibit more agitation
enviromnental contanlination. Once the
than calves castrated with rnbber rings, but
environment is contaminated, moist, cool
both groups resun1e nom1al behavior soon
conditions allow survival of infectious
after the operation. Dehoming early in life
agents for an extended pe1iod. C1yptois also less stressful than when pe1fonned sporidia. a.re especially suited to survival
later, when horns have increased in size.

in the enviromnent, and prevention of

Homs a.re mostly a problem for the feeding
contamination in U1e healthy nursery is
period (ie, homed calves require more bunk
critical. Conunercial vaccines for rota.virus,
space), and U1ey may ca.use bruising in
corona.virus, E coli, and Clost1idiu-m
perm1ates. Such problems a.re best managed
pe1jhngens types B and C may be given to
by polled breeding or early dehorning.

cows and heifers before calving to increase
levels of specific inununoglobulins in

Identification: Individual identification of colostrunl. An initial vaccination and booster cows and calves allows for selection based followed by a yearly booster is generally
on performance as well as for tracing the
required. If a booster vaccination is needed,
animal to its herd of origin to track or
it should be given at least 2 wk and not more
contain disease. Plastic ear ta.gs are the
than 6 wk before calving. Clinical trial data
most conunonly used method of individual
a.re not consistent; some trials report no
identification. Branding as a method of herd
effect, whereas others report significant
identification is coming under increasing

2124

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE
scrutiny for product quality and anin1al

Parasite Control: Egg burdens of calves
welfare reasons. Commercial products
are typically low at sp1ing branding but
are currently on the market that allow
may 1ise significantly by midsummer.

individual electronic identification. Such

Deworming of cows in late spring may lead
initiatives may eventually replace current
to increased weaning weights in calves.

VetBooks.ir
identification systems.

Studies exan1ining the effects of deworrning calves only at branding have been few, Vaccinations: Vaccines are available
and results were inconsistent-some
for viral and bacterial respiratory
showed positive effects, whereas others
pathogens. Residual passive immunity
fowid no effect. Dewonning of calves in
in young calves may limit the detectable
addition to cows in late spring appears to
antibody response to vaccination at an
confer minimal additional benefit. External
early age, but use of M LY infectious
parasites or cattle are estinlated to be an
bovine rhinotracheitis and bovine viral
important cause of economic loss as well.

diarrhea vaccines stimulates a significant

Studies have generally shown a weight
cell-mediated immune response in calves
gain of 10-20 lb in suckling calves when fly
with residual passive immunity to these
control is provided. The most common
diseases. Specific age recommendations
method of fly control is the use of
for initial vaccination are made by
insecticide-impregnated ear tags. With the
vaccine manufacturers. Calves vaccinated widespread use of pyrethroid insecticides at branding time or pasture turn-out may
in ear tags, emerging resistance has
be sensitized to the antigens and respond
become a problem, so rotating to organowith an anamnestic response when given phosphate or endosulfan tags can be
another vaccine at arrival in the feedlot.

helpful. Insecticide sprays and back

Recommended vaccination programs
rubbers can also be effective (and less
include clostridial and viral respiratory
expensive), but cattle must be forced to
vaccination at the time of branding. A
use them.

number of "value-added" calf programs
have been initiated, some of which

Nutrition: Suckling beef calves are
require a vaccination program at branding generally not supplemented during the time. Pneumonia incidence is typically
summer grazing period, when milk and an
low during the summer grazing periods,
increasing intake of forage provide their
making clinical effectiveness of a
diet. Deficiency of trace minerals may be
vaccination program against respiratory
a concern in some areas. Proper nutrition
disease difficult to demonstrate. Primary
of the herd before calving should provide
sensitization to increase subsequent
the calf with adequate reserves at birth.

vaccination response before.weaning may Subsequent supplementation is difficult, be the major benefit of such a vaccination
however, because trace mineral mix
program. A repeat vaccination against
intake in calves is sporadic at best. Creep
viral respiratory agents is often adminisfeeding may increase the reliability of tered to calves before weaning. Vaccina-

•
intake, but it is an expensive substitute for
tion for Mannheimia has been
available forage, and the response is
recommended for inclusion in some
highly variable. Creep feeding for 3--4 wk
preweaning or weaning vaccination
before weaning may be an effective way to
programs as well.

reduce stress and disease at weaning. (See

Infectious keratocof\iw1ctivitis (see
also NllTlllTIONAL HEQUIREMf:NTS OF 01.lEEI'

p 512) can be a significant problem in

CA"l'I"LE, p 2248.)

suckling calves, and control can be difficult.

Vaccination has shown variable results.

Weaning· Weaning is stressful because

Challenge witll a homologous strain after
tile calf is removed from its darn and has to
vaccination may provide some level of
acljust to a different diet and environment;
contTol, but chalJenge with a heterologous
population density is increased, leading to
strain creates little protection.

potential for increased disease exposure
and transmission. Management procedures

Implant Strategies: Use of hom1onal
should aim to minimize stress to calves
in1plant as a management practice for
while ensming they are in sound condition
suckling calves may increase weaning
nutritionally and in1mw1ologically.

weights by 3"/..-5%. Optimal response is seen

Castration and dehorning should be
in healtlly calves with adequate nutrition.

performed well before weaning. Comple

Heifers kept for breeding should not be
tion of vaccination, deworrning, and implant
implanted if <45 days old, and bulls should
procedures before weaning allows calves to
never be implanted. (Seep 2758.)

be weaned without handling.

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE

2125

Early weaning of beef calves at 90-150
replacement prospect. Age-adjusted fra.i11e
days of age may create more efficient use of
scores can be used to estimate the mature
feed resources by directly supplementing
size of prospects. These scores provide an
calves to maintain weight gain rather than
objective method of selecting replacements
supplementing cows to produce milk. Weanto maintain a consistent cow size suitable VetBooks.ir
ing tin1es as early as 30-60 days can increase for the environment and feed resources.

reproductive pedormance of cows and

Once potential replacement heifers are
heifers. Cows and heifers cycle and rebreed
selected, a nut1ition and vaccination
earlier in the calving season, and pregnancy
program should be instituted in preparation
rates are higher in a lin1ited breeding season
for breeding. If heifers a.i-e to calve at 22-23
after early weaning. Nutritional needs of tl1e
mo of age, they must be bred at 13-14 mo of
weaned calves must be met carefully to
age. For optinlal fertility, heifers should
ensure acceptable health and perf01111ance.

weigh -53%-65% of their mature body

Weaning this early should be done only
weight by this time. The ration must be
in an emergency situation to salvage tile
balanced to provide tile required rate of
reproductive future of cows in extremely
gain to meet the target goal of 53%-65% of
tllin (BCS <4) condition at calving. The
mature body weight in the time available.

goal is to prevent tllis situation through

Specific requirements vary witl1 the weight
strategies that improve precalving BCS
and breed of tile heifers and the amount of

(seep 2120). Weaning at 150-170 days of age time available before breeding. (See also decreases lactational stress on cows when

NUTRITION: CATTLE, p 2248.)

forage resources are limited and in1proves

Considerable resea.i"C11 on the most
cow condition. Reproductive pedormance
cost-effective ta.i·get weight for breeding
in the breeding season is not affected by
heifers has shown that it is almost always
weaning at tllis ti.me. When forage resources below the previous recommendation of 65%
are lin1ited, weaning calves to decrease tile
of mature body weight. Instead of a goal of
nutritional requirements of the cows allows
the ma.xi.Jnw11 number of heifers conceiving,
them to regain condition before winter witll
a better goal may be to have a slightly lower
less or no supplementation. It is more
percentage of heifers bred at a cost tllat is
efficient to wean tile calves and feed tllem
significantly lower than developing heifers
directly tllan to feed tile cows more to
to breed at 65% of mature body weight.

increase milk production la.Le in lactation.

Vaccination. The vaccination progra.i11

REPLACEMENT HEIFERS
for replacement heifers should provide
optimal protection from reproductive

Replacement heifer development programs
diseases and should include vaccination
generally begin at weaning as tl1e heifers
for infectious bovine rhinotracheitis (IBR)

begin preparation for their initial breeding
and bovine viral diarrhea (BYD) types I
season. However, decisions relating to use
and 2. Depending on tile local disease risk,
of honnonal growth-promoting in1plant
vaccinations for Brucella, Leplospira,
programs (seep 2758) for replacements

1hchomonas, and Campylobacter may
must be made begirming at tile working
also be indicated. Brucella vaccination is
of calves at 2-3 mo of age. Reim planting
performed according to state or regional
heifers inlencled for breeding at weaning,
regulations. Modified-live vaccines for IBR
or after 6 mo of age, is not recommended.

and BYD give tl1e broadest immunity to

Heifers that calve at 22-24 mo of age have
strain differences and should be given twice
increased lifetime production compared
to ensure a high level of immunity. Some
with heifers that calve first at 30-36 mo
evidence suggests that modified-live BYD
of age.

and IBR vaccines may transiently infect the
ova.i)' and cause decreased fertility. For tllis

Heifer Selection: Selection of replacereason, vaccination should be done ;,J mo ment heifer prospects begins at weaning,
before breeding. Vaccination of heifers with
when heifers are typically 6-8 mo old, and is

1'richomona.s vaccine increases calving rate based on birth elate, genetics, frame score,
and decreases duration of infection in
disposition, weaning weight and ratio, and
infected herds but does not prevent
clam production records. Selection of
infection. A vaccine for trichomoniasis may
heifers born early in lhe calving season
be useful in infected herds or in herds at
leads Lo replacement heifers tllat are older
high risk of infecLion, but it may not be
and heavier al Lhe sla.it of tile breeding
economic in low-risk herds.

season. Heifers should be evaluated for
strnctural soundness, and unacceptable

Management: Heifers should be
conformation should disqualify a heifer as a
adequately developed at the time of first

2126

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE
breeding, and their management during
herd for a reasonable observation period ( eg,
gestation must ensure their continued

4 wk); these animals should m1dergo the
growth. Pregnant heifers should be
same health procedures as the home herd. It
separated from the main cow herd at the
is prudent to obtain anin1als from herds in
time of pregnancy testing and maintained
which the herd health history is known and to

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separately until reentry into the breeding
have a record of vaccinations and treatments.

herd as animals move to pasture. Undernu

Before purchasing animals, buyers should be
trition during pregnancy in first-calf heifers
sure that herds have tested negative for
can lead to an increased incidence of
pa.ratuberculosis and are free of persistently
dystocia because of lack of weight and
infected BVD, tubercuiosis, and brucellosis.

size, weakness at the time of parturition,

If the herd is free of diseases such as bovine
insufficient colostrum, weak calves at
leukosis and anaplasmosis, purchasing only
birth, and a high incidence of prolonged
animals from oilier herds negative for tl1ese
postpartum anestrus, which leads to a high
diseases is vitally important. Pubertal bulls
percentage of nonpregnant animals that
should be tested for t.richomoniasis and
will need to be culled. Thus, pregnant
vibriosis when indicated. For artificial
heifers should be fed and managed
insemination (Al) programs, semen should
separately from cows and should be on a
be used only if it was processed by an
higher plane of nutrition than cows. Such
approved Al center witl1 a comprehensive
management may slightly increase calf
health progran1 for minimizing tl1e risk of
birth weight but will not increase dystocia
transmission of venereal ( and other) diseases
scores if heifers calve in BCS 6-7. Heifers
through frozen semen.

are ideally bred 2-3 wk before cows, and
they should always be bred for a shorter
period of time ( -42 days) to ensure that

BEEF FEEDLOTS
those with the highest inherent fertility are

In beef feedlots, yom1g growing cattle are
retained in the herd. This also ensures that
fed a high-energy diet to produce marketany increase in the postpartwn anestrus able beef at a low cost of gain. Depending
period after their first, perhaps difficult,
on the starting body weight and age of the
calving does not compromise their chances cattle, the period of feeding varies from 60
for cycling and rebreeding with the main
days to 12 mo. The success of a modern
cow herd.

feedlot depends on excellent management,
a favorable economic clin1ate, and relative

GENERAL HEALTH MANAGEMENT
freedom from unfortunate events such as

CONSIDERATIONS
disease epidemics or m1expected increases
in costs ( eg, feed) or decreases in tl1e price

The greatest risk for initial introduction of
received for the final product. The conmany infectious diseases into a herd is the cept of disease should include all of the
addition of subclinically infected animals,
identifiable factors that cause suboptimal
although some risk is also attributable to
perfonnance: inadequacies in feeds and
wildlife carriers. Potential sources of
feeding systems, the purchase of undesirinfection may be seen with herd additions, able types of cattle, and clinical and
or through intentional or inadvertent
subclinical disease.

movements and contacts. Herds may be

The feedlot veterinarian is responsible
classified as "closed" or "open," based on for maintaining optin1al animal l1ealth
their potential for pathogen exposure. (See
through the following activities: l ) Making
also BIOSECURITY, p 2068.) Closed herds
regular·ly scheduled visits to the feedlot. The
restrict the introduction of animals and
frequency of visits depends on the size of
vehicles from livestock sources as well as
the feedlot, the tin1e of year·, the expertise of
contact with other herds and animals. Open
the feedlot personnel, whether animals have
herds have a higher risk of introducing
recently arrived, and the degree to which
pathogens through such practices as
the veterinarian is contractually responsible
introduction of purchased replacements
for the total anin1al health progran1. 2) Being

( especially from commingled sale groups),
available for emergency visits to the feedlot
purchase of bulls, direct introduction of
when disease epidemics are seen. 3) Perforhigh-risk stocker calves ( especially into ming necropsies during visits and training
high population densities), and mingling of
feedlot personnel to do necropsies at other
anin1als of different backgrotmds, through
times. 4) Examining sick anin1als to ensure
either cooperative breeding programs or
that reasonably aceurate diagnoses are
poor herd biosecurity.

being made and rational therapy is being

In general, all purchased or introduced
given according to established treatment
animals should be separated from the home
protocol. 5) Regular·ly examining, analyzing,

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE

2127
a11d interpreting artimal health a11d

IMPLEMENTING A FEEDLOT
production data a11d making recommenda

MEDICINE PROGRAM
tions in a writte11 report. The effectiveness
of detection of sick animals, based on
response a11d relapse rates a11d case fatality

Regular Inspection: Regular inspection

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rates, should be detemtined, and the
of all areas of the feedlot should be included
effectiveness of the processing program for
in a feedlot health service. Credit for keen
new arrivals, which includes the vaccines
observation a11d a job well done along with
used a11d the medications given, should
recommendations for improvement in
be examined a11d a11alyzed regularly.

ai1in1al husba11dry should be noted a11d

6) Selecting a11d prescribing all drugs used
recorded for discussion with personnel.

in the feedlot, giving specific advice about

Attention should be given paiticularly to the
the use of drugs, and establishil1g a drug
delivery of feed a11d water, the general
residue-avoida11ce program. 7) Discussing
well-being of cattle, a11d a11y unusual characoverall a11imal health a11d production te1istics of each feeding pen. Ma11y feedlot
perfonna11ce with the feedlot ma11ager a11d
health problems ca11 be prevented witl1
other consulta11ts, setting a11imal health a11d
excellent ma11agement.

production goals, a11d monitoring achievement. 8) Comparing the feedlot with other Disease Surveillance: Continued
operations. The veterinaria11 should
disease surveilla11ce through regular
produce a monthly rep01t that compares
necropsy exai11ination of all dead cattle
processing costs, treatment costs, and death and regular observations of sick cattle are loss by arrival weight a11d days on feed.

necessaiy In colder climates, cai·casses

When the consulting veteril1aria11 is not
may freeze solid before the veterinai·ia11 is
readily available, a local practitioner ca11
available. Conversely, in wairner cliniates,
serve as a valuable resource for the feedlot.

carcasses may decompose beyond

Serving as part of the feedlot's health care
usefulness. When distance prevents the
team, the local veterinaria11 can make
consulting veteril1aria11 from perfonning a
significa11t cont1ibutions to the animal
necropsy on every a11imal that dies, a more
health program.

accessible veterinaria11 may be employed. In
ma11y cases, feedlot personnel ca11 be

ECONOMIC IMPACT OF DISEASE
trained to recognize common postmortem
lesions, take digital photographs of such

Disease may cause economic loss in
lesions a11d send them to the consulting
feedlots through mortality, treatment cost,
veterinaria11, a11d collect tissues for
or effects on productivity. The impact of
potential a11alysis.

clinical a11d subclinical disease on

A key to ma11agement of disease in
production efficiency a11d economic returns
feedlots is a fast a11d accurate diagnosis.

may be greater tha11 the losses associated

Th is requires a good swveilla11ce system, a
with mortality. A thorough understanding
systematic pla11 to search for sick al1in1als,
of the impact of disease on animal perfo1°
appropriate facilities for exa11lination ai1d
ma11ce a11d economic loss is essential to
treatment, accurate identification of
make cost-effective recommendations to
a11irnals, a11d appropriate laboratory
feedlot ma11agers. The costs associated with facilities, especially a necropsy service.

death loss, chronically ill cattle marketed

Emphasis is placed on training a11d
prematurely at a discount, a11d treatment
supervising feedlot employees in the
are obvious and easy to calculate. Hidden
detection a11d early treatment of sick cattle.

costs, such as reduced performa11ce a11d

Employees, particularly ai1y personnel
lower carcass quality, are often overlooked.

responsible for checking tile cattle pens

Treatment costs are a11other source of
for sick cattle, should be given reguJai·
economic loss. Factors influencing the
instruction in the clinical signs of common
average cost include the morbidity rate,
diseases. These include a11orexia, depresretreatment rate, cost of the drug(s), sion, lameness or abnormal gait, stiff
combination versus single a11timicrobial
movement, coughing, nasal a11d ocular
therapy, whether adjunct therapy is used,
discharge, increased breatlling rate, crusted
labor, a11d feedlot markup on the products
muzzle, sunken eyes, rough hair coat, loose
used. The morbidity rate has the strongest
or very finn feces, abnom1al abdominal fill,
influence on the average treatment cost for
a11d straining. Cattle with these or oilier
all cattle in the pen. When metaphylaxis is
signs of illl1ess are examined more closely
used to ma11age bovil1e respiratory tract
in the hospital area a11d, if necessaiy,
disease, it must be added to the total
treated. In some feedlots, treated cattle are
medical cost for the pen.

immediately returned to their original pens,

2128

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE
whereas in others cattle are kept in hospital
information, anin1al identification, and
pens until they recover. Most animals that
feed and animal health product purchases.

do not recover or that relapse after the first

The necessary output records include the
treatment are re-treated, although this
numbers of animals pulled from each pen
decision depends on the nature of the
daily, from which an epidemic curve
disease and the economics involved. If an
can be drawn; the treatment response

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animal becomes chronically ill and chances
report according to pen or drug used; the
of recovery are slim, it should be sold for
percentage of pulled animals that had a
slaughter if this is a viable option (after the
fever, which is an indication of how many
appropriate withdrawal time) or, in the case
are probably affected with an acute respiraof a calf, euthanized.

tory disease rather than a noninfectious

Pens from which sick animals are taken
disease such as grain overload; tl1e daily
should be closely observed. A pol·pntial
mortality report, which should include the
epidemic must be identified early so that
list of animals that died, along with their
pen-level intervention can be considered.

arrival elates, the dates of treatment, and

Despite its importance, pen surveillance
the causes of death; a case abstract of the
is not highly reliable for the detection of
treatment history of ea.ch individual
sick feedlot animals, particularly calves in
animal; and a close-out summary, which
the first week after arrival. l t is difficult to
includes all production costs, the health
distinguish ti.reel, gaunt calves that may have and production performance of the lot or been weaned a few clays earlier from calves
pen of cattle (including morbidity,
in the early stage of acute, undifferentiated
mortality, ratio of feed conversion to body
respiratory disease. As many as 5()0A, of
weight gain, average daily gain), the costs
animals pulled from a pen of recently
of gain per unit of gain, the number of clays
arrived calves will not show clinical signs of
on feed, and the profit or loss.

respiratory disease based on measurement
of body temperature and a ctusory clinical

Individual Treatment Record: Each
examination.

animal treated should be individually
identified, if this was not done on ent1y, and

Treatment Protocols: The vete1ina.rian
the information recorded on the treatment
must specify procedures for tl1e clinical
report. Treatment personnel should record
management of sick cattle and provide a
the feeding pen, lot number, body temperastandard protocol that outlines specific ture, body weight, disease suspected,
treatments for disease syndromes, including treatment given, and location of the animal drug dosages, treatmeut intervals, routes of
after treatment ( eg, which hospital pen).

administration, and withdrawal ti.mes. The

The severity of the illness should be
protocol should be followed strictly by all
assessed to properly evaluate response to
personnel so that the success or failure of
treatment. Late treatment in advanced
therapy can be evaluated accurately and
stages of disease, particularly respiratory
that chances of creating food safety hazards
disease, is a.major ca.use of failure to
are zero. The effectiveness of tl1e treatment
respond, even when the treatment of choice
protocol shottlcl be evaluated regularly
is instituted.

by determination of the response rates for

A report is filled out for each anin1al
tl1e various treatment regi.rnens. Failure
treated, and all subsequent treatments a.r·e
to develop and implement appropriate
recorded. The updated reports are retrieved
treatment protocols often leads to the use of
for anin1als that relapse or die. The
many different drugs indiscriminately, which cwnuJative information on the report can be then leads to excessive treatment costs and
used to decide whether an animal should be
often an increase in the case fatality rate.

culled for chronic or recurring illnesses that
a.r·e refractory to treatment, to decide on

FEEDLOT RECORDS
alternative treatments, to explain reasons
for death, and to evaluate the effectiveness

Records are essential to monitor the
of tl1e treatments recommended. Some
incidence of disease, response to treatfeedlots record animals that are removed ment, and production performance, and
from the pen but sent back untreated
they should be analyzed regularly by the
because they did not meet the temperature
veterinarian, nutritionist, and feedlot
criterion in the case definition for a given
manager. They can be maintained by
disease. This information ca.r1 be of value if
hand or by using conm1ercially available
the animal is removed again ur d.ies.

computer software. The necessary input
records include the lot description,

Daily Morbidity and Mortality
processing record, lot update, sale

Record: This record contains the number

HEALTH-MANAGEMENT INTERACTION BEEF CATTLE

2129
of treated cattle by pen and lot number, the
depending on the prevalence of disease
disease diagnosed, and the date. It provides
both in the feedlot area and in the area from
both the manager and the veterinarian with
which the cattle originated. The vaccines
a rapid assessment of the location of disease used and the vaccination schedule should problems in the feedlot. It contains
be based on the expected incidence of the
information on the number of animals
disease, the cost of the disease when it is

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removed and the number not treated and
seen, the cost of the preventive procedure
then classifies those treated according to

(vaccine plus labor), the field efficacy of the
diagnosis and whether they are a relapse or
vaccine, and other available control
new case. By using this report in conjuncprocedures.

tion with an inventory report showing filling
dates and numbers added to the pen on

NUTRITIONAL ADVICE
those dates, it is possible to generate
epidemic cwves.

Feedlots frequently consult a qualified
nutritionist to assist in the fom1ulation of

Morbidity and Treatment Analysis
cost-effective diets. The veterinarian should

Record: This aggregation of data
communicate with the nutritionist regsummarizes the morbidity rate, the relapse arding the composition of the diets and
rate, and the death rate for a lot or pen of
any changes being planned. Most of the
cattle. It is especially important as a tool to
emphasis in feedlot nutrition has been on
evaluate the overall effectiveness of the
the development of cost-effective diets that
treatment program for various diseases; the
support an optin1al growth rate without any
relapse rates and death rates are compared
deleterious effects. Considerable infonnawith goals set for the feedlot and with tion is available on the nutrient requirestandards published in the literature. The ments for feedlot cattle and on the feeds and
disposition summary alerts the feedlot
feeding systems used. (See also NUTRITION:

manager and consulting veterinarian when

BEEF" CA'l"f'LE, p 2248.)

the results are highly positive, so this

Nutritional deficiency diseases are
feedback can be relayed to all employees to
uncommon in feedlot cattle, because cattle
acknowledge their hard work, and when the
usually receive a diet that contains the
chronic or culling rates are abnormally high, nutrients required for maintenance and so that appropriate changes can be made.

promotion of rapid growth. Diets prepared
according to published standards should

Mortality Analysis: The causes of death
meet all the requirements under most
as detennined by necropsy should be
conditions. Specific nutrient deficiencies
summarized on a regular basis. A mortality
are extremely rare; however, such a
analysis includes the number of days the
situation may be seen in a small farm feedlot
anin1al was in the feedlot, any observed
that prepares its own diet with little or no
premonitory signs, and treatment ( diagnoattention to the necessity for supplementasis, drug used, and when treated). The pen tion of homegrown feeds. Altl10ugh only a
location of the animal in the feedlot at the
few nutritional diseases may affect a
time of death should also be considered.

well-managed feedlot, these diseases may
cause large economic losses when they

Feedlot Performance Summary: Most
develop. They include carbohydrate
feedlots complete a close-out sun1mary for
engorgement (grain overload or o-lactic
each group of cattle that have been finished
acidosis), feedlot bloat or ruminal tympany,
and marketed. The performance record and
and feeding errors (ie, accidental incorporafeeding summary sections include average tion of an excessive amount of a feed
daily gain, total feed consumption, feed
additive, such as monensin or urea, or
conversion ratios and cost per wlit of body
sudden unintended changes in the
weight gain, mortality rates, culling rate, and
ingredient composition of the diet).

medical costs. The financial summary
provides the profit or loss on an individual

DISEASE EPIDEMICS
and lot basis. If cattle are marketed on a grid
basis with rewards for certain carcass charac

In spite of good management, unexpected
teristics, tllis information is also included.

disease epidemics are seen in feedlot cattle.

When feeding accidents occur, many

VACCINATION PROTOCOLS
anin1als can be affected suddenly, ie, within

1-2 days. ln outbreaks of acute infectious

An important component of feedlot health
diseases, such as infectious bovine
progran1s is the planning of vaccination
rhinotracheitis, pneumonic pasteurellosis,
progran1s. Vaccination schedules vary
or Histophilus meningoencephalitis, the

2130

HEALTH-MANAGEMENT INTERACTION: BEEF CATILE
first few cases are followed by a steady
drainage. The pens and alleyways should
increase in the morbidity rate for several
be well drained a.Ild easily accessible for
days and then a decline as the outbreak
scraping the ground surface as necessa.I)'.

subsides 10-14 days after the index case.

Good drainage requires a 6% slope. To avoid

In some cases, the diagnosis may be
overstocking, each animal should be

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obvious ( eg, carbohydrate engorgement
provided with 18 m2 of space in well-drained
caused by a feeding e1Tor). In other cases
la.i1d and with 9 m2 in a paved lot.

( eg, infectious diseases of the respiratory

Cattle need protection from wind, rain,
tract), the diagnosis may not be readily
snow, excessive heat, and excessive
obvious, and a detailed epidemiotogic,
sunshine. Trees are planted as windbreaks,
clinical, and laboratory investigation may
a.I1d buildings and fences are placed so the
be required. A complete investigation may
wind is not deflected into feeding a.i·eas or
require specialists from several disciplines.

sheds. An open-front shed provides

Every effort should be made to detem1ine
protection from winter stonns and hot
the specific source of the disease. The
sununer sun. Each a.i1imal needs -1-1.5 m2
investigation should include a general
of cover. The shed should be open to the
description of the problem, a complete
south or southeast, a.Ild the front should be
history of the disease outbreak (including
high enough so the sw1 strikes the ground at
details and date of index case, total number
the back on the shortest day of the winter.

of sick anin1als, treatments, case fatality

The back of the shed should be �2.5 m high.

rate, population mortality rate, and

A covered feed bunk protects feed from
vaccination history), and clinical examinaweather dan1age and affords cattle added tion of several affected a.ilinlals (with
comfort when eating. Feed remains dry and
appropriate samples) as well as necropsies.

palatable, a.i1d waste is reduced. Shades to

After the diagnosis is detem1ined, the
provide relief from extreme stmuner heat
rationale for treatment is outlined. When
a.i·e useful in feedlots where this is a major
outbreaks of infectious disease a.i·e
concern dtuing the year.

encow1tered, the intensity of surveillance

Environmental concerns about feedlot
must be .increased to detect new cases in
operations have greatly increased in recent
the early stages of disease when response
years. Stricter envirorunental laws require
to treatment is usually good.

that all feedlot waste Md run-off be

All of the details of Ll1e outbreak should
contained in approved lagoon systems.

be listed in chronologic order and then

Pollution prevention pla.I1S must be on file
analyzed. Correlations can be made
with the approp1iate govenunent agency.

between exposure factors and the

Monitoring, testing, a.Ild record-keeping
development of new cases during the
requirements Va.I)' from country to country
course of the outbreak. Often, epidemioas well as regionally. In addition, foodbome logic determinants that explain disease
illnesses, particularly those caused by
occurrence can be identified and the

Escherichia coli 0157:H7 and Salmonella, information used to control futW'e episodes. have forced the meat-packing industly A detailed report of the outbreak, outlining
to cha.I1ge the way beef ca.i·casses are
the conclusion and recommendations,
processed. The packing industly has placed
should be prepared by the vete1ina.iian and
pressure on feedlots to provide animals that
nutritionist and submitted to the owner.

are as clean as possible.

CONTROL AND PREVENTION OF

Transportation of Cattle

DISEASE IN FEEDLOT CATTLE

Tra.I1sp01tation or shipping of cattle has long

Control and prevention of disease in
been associated with increased bovine
feedlot cattle depends on purchasing
respiratory disease (BRD) in the feedlot,
healthy animals; providing a tra.I1sportation hence the tem1 "shipping fever." With system that minimizes stress, a comfortcurrent in1provements in tra.I1Sp01tation, able feedlot pen environment, and an
however, tl1ere is no correlation between
adequate feeding system; establishing a
the distance cattle are shipped and the risk
good surveilla.I1ce system; and judiciously
of fatal fibrinous pneumonia in the feedlot.

using vaccines and, when necessa.iy,

Factors such as weaning, level of inununity,
antimicrobial agents.

commingling, and other stressors appear
more important in the risk of BRD tha.I1
distance shipped.

Feedlot Facilities

Cattle can lose considerable weight

One of the most important considerations
within the first 24-48 hr after weaning,
in the constmction of a feedlot is good
dilling shipment, a.i1d after dep1ivation of

HEALTH-MANAGEMENT INTERACTION BEEF CATILE

2131
feed and water. This loss in body weight
feedlot environment; it may include

(known as shrink) varies from a minimum
vaccinations, castration, and training
of 4% in cattle deprived of feed and water
calves to eat and drink in pens. The concept
for 24 hr to up to 9"/o in animals transported of preconditioning is based in part on
long distances over a period of 2-4 days or
inununologic and nutritional principles.

in unweaned, high-risk, lightweight calves.

Preimmunization, or vaccination of calves

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Most of the fluid and electrolyte loss can be

2---3 wk before shipment from the ranch to
restored within a few days if the animals
the feedlot, was the basis of preconditioning.

begin to eat and drink nonnally, but some

In addition to vaccination, more recent
studies show as few as 35% of high-risk
efforts have been directed toward increasing
calves conswne an appreciable amount of
the number of days weaned before
feed the fast 24 hr in the lot. Shrink > 7% has
movement and improving management
been associated with increased health
procedures on the ranch, such as genetic
problems. The total loss in body weight may
selection and nutrition, that assist calves in
not be restored for as long as 3 wk in some
making an easier transition to the feedlot.

highly stressed calves.

In the USA, preconditioning has been

Transportation equipment and facilities
defined by the following elements:

should meet local standards and be able to

1) weaning at least 30 days before sale,
transport cattle comfortably regardless of

2) training to eat from a feed bunk and to
the season of the year. Some countries
drink from a tank, 3) parasite treatment,
prohibit the transport of cattle over a

4 ) vaccination for blackleg, malignant
certain length of time without unloading for
edema, parainfluenza3, infectious bovine
rest, feed, and water. On arrival at their
rhinotracheitis, bovine viral diarrhea ( some
destination, cattle should be examined
programs also call for vaccination against
carefully for evidence of clinical disease

Mannheimia haemolytica, Pasteurella
or injwy. Provision of fresh hay, a small
multocida., and/or Histophilus somni),
amount of starter feed, and water can help

5 ) castration and dehorning with wounds
detect those that are anorectic and require
healed, 6) identification with an ear tag, and
closer examination. This is particularly

7 ) sale through special auctions. When
important if unexpected delays in transporpreconditioned calves are placed in a tation have occurred that increase the level
feedlot, they usually begin to eat and drink
of stress in the animals.

on arrival; if they have not been subjected to
unusual stressors, the incidence of disease

Cattle Purchase and Introduction to
is minimal. However, daily surveillance is
a Feedlot
still necessary to identify cases of illness.

Because these cattle generally go onto feed

Infectious diseases of the respiratory tract
more easily than calves that have not been
are major causes of morbidity and mortality
preconditioned, care must be taken not to'

during the first 30-45 days after arrival in
increase intake too quickly and cause
the feedlot. Digestive diseases, especially
digestive concerns.

carbohydrate engorgement, in cattle placed

When preconditioning is examined on a
on a high-energy diet within 30 days after
partial budget basis, the cost effectiveness
arrival in the feedlot are a major potential
for the cow-calf producer is generally quite
threat but can be controlled. The acute
favorable. Calves can gain 2---3 lb/day at a
respiratory disease complex ( see p 1431) is very low cost of gain while not getting fat.

more difficult to control in feedlot cattle,

The health program "bonus" can add
even under good management conditions.

$3-$8/100 lb to the price when calves are

The major objective on arrival at the
sold at large, special preconditioned sales,
feedlot is to get the cattle onto a high-energy
but the primary financial reward to the
diet-which will result in rapid growth-as
cow-calf producer is in the forn1 of added
soon as possible, usually within 21 days,
weight sold at a low cost of gain.

while minimizing the morbidity and

Backgrounding is a variation of
mortality associated with acute respiratory
preconditioning in which recently weaned
disease, other common infections, and
calves are grown to heavier weights, usually
digestive diseases associated with
in a smaller feedlot. The principal objective
adjustments to high-energy diets.

is to prepare these cattle to adjust to a
high-energy finishing ration in a feedlot with

Preimmunization and
minimal problems. This is achieved by
feeding the calves a growth diet that yields

Preconditioning
rapid, efficient body weight gains without

Preconditioning is the preparation of feeder
fattening. The spectrun1 of diseases seen in
calves for marketing, shipment, and the
backgrounding operations during the fast

2132

HEALTH-MANAGEMENT INTERACTION BEEF CATILE

45 days after arrival of the calves depends

Depending on the condition of the cattle, it
on whether the calves were preimmunized,
may be difficult dw·ing the first few days
preconditioned, or obtained from several
after arrival to easily distinguish sick cattle
different somces with no preconditioning.

from healthy cattle, and careful clinical

Infectious diseases of the respiratory tract

SW"Veillance every few hams may be

(eg, BRD) and of the digestive tract
necessaiy. Observations at the time of

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(coccidiosis) account for most of the losses.

feeding often reveal anorectic ai1irnals that

Recently arrived cattle of unknown
should be pulled from the pen and
backgrounds (eg, those from auction
examined.

markets) require extra SW"Veillance and
care. After a 24-hr rest, these cattle should
be vaccinated and some need to be

Processing Procedures
castrated, dehomed, and treated for internal Identification: Each animal must be and external parasites. Nonpreconditio.ned,
identified immediately, preferably with a
stressed cattle of unlmown backgrounds
color-coded and .nw11bered plastic ear tag
should be watched closely for signs ofBRD
tl1at is easily visible from a distance. In
for �3 wk after arrival. On their staiter
many feedlots, each animal is not identified
ration, the cattle are limi t -fed good-{!uality
individually but instead receives a tag with a
roughage along with a quantity of a highly
lot number (group) or pen number. Systems
palatable, .nutrient-dense concentrate
are now ir1 place that individually identify
ration. They are checked cai·efully at least
a.ni.n1als with tags tl1at can be read
twice daily for evidence of illness, and sick
electronically from a distance of 8-J O in.

cattle are identified and treated. Once the

1.nformation maintained on individual
animals ai·e determined to be healthy and
animals through this technology may
the common infectious diseases are not a
include performance, vaccination, ai1d
problem, they cai1 be moved up to finishing
treatment lustory. These tags remain on the
diets.

aiumal until slaughter, at which tin1e the

Vaccination against certain respiratory
identification from the ear tag can be
diseases at 24 hr after ai·rival is standard
transferred to tl1e overhead trolley system.

practice for most feedlot and backgrotmding operations. Vaccination should be Measurement of Body Tempera-limited to those products that actually
ture: On arrival, some anin1als may be
reduce losses resulting from respiratory
affected with a.cute disease but show no
disease. The use of metaphylactic ai1timiobvious clinical signs. Others may appeai·
crobials against respiratory disease may be
fatigued and gam1t but a.re not affected with
necessary in high-risk, non preconditioned
clinical disease. Identifying animals with
calves. Numerous studies show a financial
acute infectious disease that should be
benefit to using metaphyfactic ai1tibiotics
treated eai·Iy to n1inimize mortality can be
on high-risk calves, because BRD morbidity
difficult. The body temperature of high-risk
ai1d mortality can be greatly reduced.

cattle (eg, unweaned calves, calves from

Regardless of the system used, soon
auctions, or calves transp01ted long
after anival the cattle should be-weighed,
distances over several days) is often
examined for evidence of illness, and treated measured at processing. Animals with a if necessary. Some feedlots administer
body temperature >104°F (40°C) may be
antimicrobials to all calves considered to be
treated with an antimicrobial. Treated
at high risk of a.cute respiratory disease. If
anirnals may be tagged and n"oted in the
the illness appears different fi"om the usual
individual a.ni.n1al database, or the total
case of respiratory disease, diagnosis by a
nw11ber of animals treated (total a.mmmt
veterinarian should be sought at t11e earliest
of drug administered) in a group or pen
possible tin1e. Close exai11ination and
may be recorded.

smveillance are desirable for groups of
cattle with a.history of unusual stress. The

Vaccination: The value of vaccinating
youngest and smallest cattle often need
feedlot cattle for common infectious
special attention, ai1d it may be necessary to
diseases, particularly those of the respiraseparate them from older cattle. A reliable tory tract, has been controversial since the
history of vaccination, vitanun injections,
vaccines were introduced. Nevertheless, a
implants, and anthelmintic administration
wide vai·iety of vaccines ai·e used in feedlot
would be useful but is usually not available.

health programs.

The major objective dming the first few

Vaccines are available for the following
days is to avoid mmecessary stress and get
diseases or infections of feedlot cattle:

most cattle consun1ing the staiter ration.

infectious bovine rhinotracheitis, pneu-

HEALTH-MANAGEMENT INTERACTION BEEF CADLE

2133
monic pasteurellosis, parainfluenza 3 virus
alter metabolism so the ar1in1al increases
infection, bovine respiratory syncytial virus
body tissues and grows more rapidly. They
infection, Hislophilus somni disease
include antibacterials, antinucrobials,
complex, bovine viral diarrhea types 1 and
steroids (eg, estrogens, androgens), and

2, and clostridial disease. The vaccines
ionophores. They promote changes in
available for clostridial diseases are highly
composition, confonnation, mature weight,

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effective. The nwnber of clostridial antigens or efficiency of growth, along with changes to be used (2- to 8-way) depends on local
in the rate of live weight gain.

prevalence of clostridial diseases, including
blackleg (Closliidium chauvoei),

BEEF QUALITY ASSURANCE AND
malignant edema (C septicum ), bacillary

BEEF SAFETY PROGRAMS
hemoglobinuria (C novyi, type D [haeinolyticum ]), infectious hepatitis (C novyi, The purpose of a beef quality assurance
type B), tetanus (C lelani), and enterotox

(BQA) program is to identify ar1d avoid
emia (C perfringens types B, C, and D).

areas in the feedlot where quality or safety

Leptospirosis (Leplospira serovars Hardjo,
defects car1 be seen. The goal of the BQA

Pomona, Grippotyphosa, Canicola, and
prograrn is to assure the consw11er that all

Icterohaemorrhagiae) bacterins are also
cattle shipped from a feedlot ar·e healthy,
used in some situations.

wholesome, and safe and that their

A basic vaccination schedule for
mar1agement has met all govenunent
receiving calves should include a viral
ar1d industry staildar·ds.

respiratory vaccine plus a clostridial

The feedlot must be able to document all
vaccine. Additional vaccines should be
steps of production. Critical points in
included only if two criteria can be met: the
production must be monitored to ensure no
disease is enough of a risk that prevention is
residue violations or carcass defects. These
necessary ( eg, leptospirosis in some ar·eas ),
critical points include, but are not limited to,
and data are available to support the use of
incoming cattle, product and conunodities,
vaccines to prevent disease.

cattle handling, ar1d evaluation of outgoing
cattle. There is a built-in margin of safety for

Castration and Dehorning: These
withdrawal tin1es in the feedlot industry,
surgical procedures are best perfo1med well because most withdrawal tin1es for animal al1ead of entry to the feedlot, but invarfably
health products are shorter than the feeding
there will be bulls and homed cattle offered
periods. Feedlot personnel must be aware
for sale. When to castrate and dehom these
of situations that create high risk of
mismanaged cattle is quite controversial,
residues. Nonperfom1ing cattle could have
with studies showing that performing
orgar1 dan1age, which could prevent normal
surgery at initial processing 24 hr after
clearance of a drug product, causing
arTival was superior to delaying these
violative residues even after the preslaugttprocedures.

ter withdrawal time has elapsed.

The BQA program is based on the

Anthelmintics and Insecticides: Anthelprinciples of the Hazard Analysis of Critical mintics ar1d insecticides are administered

Control Points (HACCP) system. Each
according to local conditions. Most
production step should be evaluated for
incoming cattle will have been exposed
potential quality or safety defects, including
to internal parasites, and appropriate
bacterial contamination, which car1 cause
dewonning methods should be impleinfectious disease in cattle or employees; mented. Young cattle raised on small farms
chemical usage/contan1ination, which car1
in which tl1e stocking rate on pasture is high
lead to violative residues; and physical
may harbor helminths. Yatmg cattle may
darnage, such as injection site dar11age,
also be affected by chronic vem1inous
bruising, or broken needles in animal
pneumonia caused by D'ictyocaulus vivipa
tissues. The ar1alysis should include
nis. Most young cattle will be infected with
sanitation staildard operating procedures
coccidia, and having an appropriate

( eg, finding ways to prevent or minin1ize
anticoccidial agent in the feed is necessary.

fecal-oral contarnination).

All relevar1t govenunent regulations on

Growth-promoting Agents: Growthfeedstuffs, feed additives, and medications promoting agents (s eep 2758) increase

(including route of administration ar1d
growth rate of animals without being used
withdrawal times) must be closely followed.

themselves to provide nut1ients for growth.

Extra-label drug use must be prescribed only

They are generally administered in small
by the herd health vete1inarian. All owners
an.10unts-often via implants or in feed-to
of cattle treated witl1 medications adrninis-

2134

HEALTH-MANAGEMENT INTERACTION: BEEF CADLE
tered extra-label must comply with

Treatment Protocol Book: The herd
prescribed, extended withdrawal times that
health vete1inarian should provide a
have been set by the herd health veterinarian treatment protocol book specific to the under the guidelines of a valid veterinarianfeedlot operation. It should be reviewed client-patient relationship. The Food Animal
regularly and updated at least every 90 days.

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Residue Avoidance Databank is the primary

One copy should be kept at the treatment
resource to detennine the preslaughter
facility and another copy should be
withdrawal time when an animal has been
maintained in the feedlot office. A wi·itten
treated in an extra-label manner.

treatment protocol and cwTent prescriptions are important docun1ents the feedlot Record Keeping: All records should be
must have if there is a govenunent
kept for �2 yr after cattle have been shipped
inspection of the feedlot facilities, drug
from the feedlot. If a violative residue is
usage procedures, and residue avoidance
found in any cattle shipped for slaughter,
plans. It also provides written guidelines for
the feedlot must make applicable records
animal health progra.tns, thus minimizing
available to the appropriate govenunent
chances of mistakes or misunderstandings.

agencies. The source and cause of violative
residue should be detennined and

Culling of Feedlot Cattle
corrective action taken to prevent
reoccurrence.

Culling may be done at any point between
exa.tnination of the cattle on at-rival and a

Individual Records: Treatment records
few weeks later, before the cattle a.i·e placed
should be maintained for all cattle treated
on a high-energy diet. Diseases that justify
individually. This can be done using handwiit culling include clu·onic untluiftiness and ten records or a compute1ized record system. inappetence of undetennined etiology, Essential information includes the individual
chronic la.tninitis, chronic la.tneness caused
animal identification, treatment date( s ),
by footrot, clu·onic bloat, chronic pnewnodiagnosis, drug administered, serial/lot nia, acute and chronic pulmonary abscess,
nwnber, dosage used, approximate weight of
and bovine viral dian·hea. Each of these
animal, route and location of administration,
diseases leads to untluiftiness, and a clinical
and earliest date the animal could clear tl1e
exan1ination is necessary for diagnosis.

preslaughter witl1drawal period. The
treatment history of cattle with clu·onic
medical problems, or of tl1ose tl1at have a

Animal Welfare in Feedlots
poor, unexplained growtl1 rate, should be

Good feedlot design is in1portant to ensure
scrutinized carefully. In many cases, residue
animal comfort. Handling facilities must be
screening, such as tl1e live a.t1in1al swab test,
modem and efficient and must not induce
is advisable. Residue screening should be
animal attendants to be cruel to a.ttlmals
perfom1ed under tl1e supervision of tl1e herd
when they are being moved from one
healtl1 veterina.iian. The results of such
location to anotl1er; excessive force should
testing detennine whether a.11 animal ca.11 be
not be used to get the a.ttlmals to move. The
released for shipment.

feedlot personnel must be educated in the

Group Records: All anin1als treated as
teclutlques of low-stress cattle ha.t1dling and
part of a group (processing or mass
recognition of signs of pain and discomfort
medication) should be identified by group or
associated with certain illnesses.

lot, and tl1e treatment infommtion should be

The vete1inarian should emphasize good
recorded. Records should include the animal feedlot design and equipment that will lot or group identification, product used,
ensure comfort for the animals and minimize
serial/lot nwnber of the product, date
pain and stress associated witl1 handling
treated, dosage used, route and location of
procedures. The veterinarian must also be a
administration, and withdrawal information.

vigila.t1t guardian, denouncing inhwnane

A preslaughter withdrawal time is assigned
practices and encouraging sound animal
to the entire pen. Recording treatments
welfare management. (See also ANIMAL
under this system asswnes that every anin1al

WELFARE, p 1579.)

in tl1e lot or group received the treatment.

The health records of cattle shipped to

DEVELOPMENT OF
slaughter should be checked by feedlot

ANTIMICROBIAL-RESISTANT
personnel to ensure tl1at treated a.t1in1als

BACTERIA IN FEEDLOT CATILE
have cleared tl1e appropriate witl1drawal
times. All pesticides should be used in

The use of antin1icrobials in feedlot cattle,
accordance with label directions, and their
as in all food anin1al species, has come
use and withdrawal time should be recorded. under increased scrutiny because of

HEALTH-MANAGEMENT INTERACTION DAIRY CADLE

2135
concerns about the potential transfer of
a valid zoonotic disease concern, is not
resistant zoonotic pathogens to people and
related to an issue of resistance. The
also transfer of resistant genetic determi

American Association of Bovine Practinants to human pathogens. A pathogen of tioners publishes Pr1tdent Drug Usage

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concern related to resistance in cattle is

Guidelines, which provides guidelines

Salmonella spp. Transfer of Escherichia for antimicrobial usage in cattle feedlot
coli O 157:H7 through the food chain, while operations.

HEALTH-MANAGEMENT INTERACTION:

DAIRY CATTLE

The dairy industry is in a period of
now milked in parlors, reflecting the
economic volatility of historic proportions.

fact that most large herds are housed in

An era of modest fluctuation in milk and
free-stall or open facilities (and milked
feed pricing in the late 1990s to the early
in parlors). Most parlors are highly

2000s was followed by increases in milk
mechanized and designed to minimize
prices not seen before. The period of high
the amount of labor required, and
dairy profitability in early 2008 was soon
economics dictate that milking proceed
dampened because of substantial increases
nearly around the clock to maximize the
in production costs as a result of high fuel
return on investment.

and feed costs as the USA government

Milk quality is traditionally defined by
encouraged crop farmers to produce corn
the somatic cell count (SCC) and bacterial
for ethanol distillation. Since then, milk
count in prepasteurized bulk tank milk. In
prices have rebounded and dropped several
all developed nations, regulatory officials
times, although not to the san1e extent. USA
set allowable maximums for SCC. Since
dairy product exports have also fluctuated

1986, limits for sec and bacteria have been
widely, contributing significantly to milk
gradually lowered. The current upper lin1it
price volatility and overall profitability. As
for the bulk tank SCC is 750,000 in the USA
of early 2014, some 15% of USA dairy
and 500,000 cells/mL in Canada. The SCC
products are exported, milk prices are at an
maximwn in the EU is 400,000 cells/mL
all-time high, and feed prices are somewhat
using geometric means as the basis for
lower.

calculation.

Artificial insemination (through the

THE MODERN DAIRY INDUSTRY
commercial distribution of frozen
semen) is the preferred method of

The structure of the dairy industry in
reproductive management in most
developed countries has continued to
dairy operations. In fact, 45% of USA
evolve as production efficiency has risen.

dairy operators in 1996 reported that

Industry consolidation is the norn1, with
no breeding bulls were present on their
reduced herd nun1bers, increased herd
farms. The use of genetically elite sires
sizes, and adoption of specialized managehas contributed to increases of> 150 kg/
ment practices that encourage higher
yr in genetic merit for milk production.

productivity.

Declining fertility has accompanied

In the past, most dairy cows were
advancements in genetic merit. Dairy
housed in stall-barn facilities designed to
farms commonly record herd conception
maximize operator comfort. Today,
rates of <40%. Technologies such as
free-stall facilities are built to maximize
embryo transfer, rapid hormonal assays,
natural ventilation and cow comfort.

controlled breeding programs that use

Historically, barns were often placed in
reproductive hormones, and ultrasonogsheltered locations, whereas today they raphy are used increasingly on modern
are usually located in open fields or on
dairy farms.

hilltops to ensure adequate airflow. The

Nutritional research also has advanced
type of milking facility is also evolving;
rapidly, especially in areas such as rumen
whereas in 2007, 49.2% of operations
physiology and lipid metabolism (see NUTRIreported using tie-stall or stanchion TION: DAJRY CATTLE, p 2265). Lactating dairy
milking facilities, almost 75% of cows are
cows are generally fed either a component-

2136

HEALTH-MANAGEMENT INTERACTION: DAIRY CATILE
based ration (forages and grain are fed

ANIMAL AND HERD
separately) or a total mixed ration (TMR,

PRODUCTIVITY
forages and grain are mixed and fed
together). The basis of a successful

The productivity of an individual cow is the
nutritional program is the determination of swn of the value of the milk she produces, VetBooks.ir
nutrient content of the ration ingredients
the value of her offspring, and her individual
through laboratory testing, formulation of
market value when she leaves the herd.

nutritionally sound diets, and assurance of

Many factors influence individual cow
adequate intake of required nutrients
productivity, which is also based on
through feed bunk management. Maintainlongevity and the proportion of the cow's ing a stable, healthy rumen environment is
lifetime spent producing milk. Nonproducdifficult with component-based feeding tive periods include the period from birtl1
systems. TMR diets are generally based on
until first paiturition and dry periods before
mixing stored forages (in No1th America,
subsequent calvings. Heifers must be
usually alfalfa hay or haylage and corn
managed to reach appropriate breeding size
silage) with grains (such as high-moisture
by 13--15 mo of age to maximize lifetime
corn or soybeans) and byproducts such as
production.

cottonseed or locally available commodi

Milk yield is related to stage of lactation.

ties such as citrus pulp, brewers grains, or

Milk yield increases rapidly after calving,
bakery waste. On larger farms, cows are
reaches a plateau 40--60 days after calving,
often grouped and fed diets specifically
and then declines at a rate of 5o/<r-100/cv'mo.

formulated to meet their production and

The rate of decline is lower in first-parity
metabolic needs. Many farms use proanin1als than in older cows. Good reproducfessional nutritionists to formulate tive management ensmes that the largest
rations.

propmtion of a cow's total lifetime

Most producers raise their own replaceproduction is spent dming early highment animals, but an increasing munber of producing stages of lactation rather than
large dairy farms contract with specialized
late, lowe1°producing periods. Milk yield
heifer growing operations. In the USA, >600A,
increases with age and parity W1til about the
of newborn heifer calves are hand-fed
sixth lactation; these cows may produce up
colostrwn within the first 24 hr of life to
to 25% more milk volwne than first lactation
ensme adequate intake of immunoglobucows. Health disorders or other managelins. The feeding of waste milk from cows ment problems that reduce longevity have
undergoing antibiotic treatment or with
a negative impact on productivity.

mas ti tis is economical but may transmit
infectious diseases to the calf. To decrease
the potential for disease transmission, some

Nutritional Management
producers pastemize waste milk (15% of all

In most dairy herds, nutritional managecalves in 2007) or feed milk replacer(> 70%
ment is the most important determinant of
of calves in 2007). The an1ount of milk fed
herd productivity. The relationship between
to heifers (typically 8%--10% of body wt at
nutrition and productivity begins at bi1th.

birth) has typically been restricted to

The feeding system must deliver the
encomage conswnption of high-protein
necessaiy nutrients to each cow at the
calf sta1ters, with a goal of early rumen
correct stage of lactation to maintain
development and weaning by 8--10 wk of
optimal productivity.

age. However, calf health was found to

Research has docwnented I.fie i.mpo1tai1ce
improve when calves were fed more milk
of the ration fed to cows in the transition
than this, and current practice recomdming the 2---3 wk before calving. Dry cows mends that calves be fed an increasing
ai·e fed a diet relatively low in cai·bohydrates
amoW1t of milk-up to 12%--15% of bo<ly
and protein and high in fiber, reflecting tl1e
wt after the first week of age (10--11 ll
low nutrient demands of the non.lactating
day). Holstein heifers are now heavier
cow. The transition period ration must allow
and taller at the withers than in published
the rumen to adapt to the lower-forage, more
standards recommended from years past.

nutrient-dense lactating ration. Further, the

The goal of efficient Holstein heifer-raising
stresses associated with moving animals to
programs in North America is for heifers
the trai1sition pen and of calving itself tend
to calve at a weight of 550 kg at 22.5--25
to reduce feed consW11ption at tltis critical
mo of age. Various health management
time. Reduced feed intake in tl1e trai1sition
programs are used to reach this goal,
period is associated with excessive weight
including deworming and the use of oral
loss, reduced peak milk production, and an
coccidiostats, supplemental selenium,
increased incidence of postpaitwn diseases
and ionophores.

such as metritis, retained placenta, ketosis,

HEALTH-MANAGEMENT INTERACTION: DAIRY CADLE

2137
displaced abomasum, and fatty liver.

Component-fed herds receive grain ai1d

Research has documented the benefits of
forage separately. Advocates of component
monitoring postpartum cattle for excessive
feeding emphasize the ability to meet the
energy mobilization by measuring blood
production and metabolic needs of

13-hydroxybutyric acid, one of the ketone
individual cows throughout their produc

VetBooks.ir
bodies.

tion cycle. The prin1ai)' disadvantage of

Rations for lactating cows must strike a
component feeding systems is that the cow
balance between providing high levels of
receives concentrates separate from
energy and protein to support high milk
forages, enabling ingestion of these
production and maintaining optimal rumen
concentrates in a single feeding, leading
health and motility. Subacute rumen
to rumen acidosis and indigestion.

acidosis (SARA) is a common condition

Management-intensive grazing systems
resulting from excessive fe1mentable
can be used to meet the needs of modern
carbohydrates, inadequate fiber of adequate
dairy cows. In some regions of tl1e world
length, or a combination of the two. Health

(eg, New Zealand and Australia), pastureeffects of SARA include digestive upsets and based systems ai·e the predominant method
diaiThea, reduced feed consumption and
of feeding dairy cattle. In these truly
milk production, reduced butterfat content
pastoral systems, nutrition frequently limits
of milk, ulceration of rumen epithelium, liver productivity because of significant annual abscessation, and a se1ies of foot problems
variation in growing conditions. However,
related to subclinical larninitis.

the economic model in such a system

The choice of a feeding system is
emphasizes low costs of production rather
associated with herd size and production
than maximal productivity. In other areas
level. Three general types of feeding
such as Britain and the northeastern USA,
systems are used currently by dai1y fairners:

rotational grazing is used to provide for the
total mixed ration (TMR), component
forage requirements of lactating cattle
feeding, and mai1agement-intensive grazing.

during tl1e sp1ing and summer montl1s, and

Each of these systems, when implemented
supplemental concentrates ai1d com silage
correctly, can deliver adequate nutrients for
ai·e fed to achieve high milk production.

a highly productive dairy herd. Each system

In both situations, seasonal calving is
has its own inherent challenges in achieving
practiced to match rainy or spring season
optin1al productivity.

pasture conditions with the energy needs of

The use of TMR feeding systems has
eai·ly lactation cows. Attention to reproducincreased as more herds have adopted tive management is therefore critical for
free-stall or dry-lot housing. TMR diets have
herds that attempt to breed all cows witl1i.n
several advantages: cows consw11e the
a defined pe1iod. Production management
desired propo1tion of forages, 1isk of
progran1s for herds using mai1agementdigestive upset is reduced, feed efficiency is intensive grazing systems must include
increased, byproduct feeds may be used,
prograins to control bloat, hypomagneaccuracy of diet fom1ulation is higher, and semia, and copper and selenium deficiency.

labor needs are reduced. The performance

Pastured cattle may walk considerable
of herds using TMR diets can be lowered by
distances to hai-vest forages. Therefore, a
errors in ration formulation and feed
system to monitor and minimize laineness
delivery. An oft-quoted statement illustrates
must be included in the health delivery
the challenges of TMR feeding. There are
system.

three rations for a dairy herd: the ration on
paper as fonnulated by the nutritionist, the
ration fed to the cows, and the ration the

Reproductive Management
cows actually consume. Some common

Artificial insemination (AI) using semen
errors include inadequate or nonexistent
from genetically superior sires is the most
forage testing, variation in forage dry
in1portant factor leading to increased
matter, variation in dry-matter intakes,
productivity in the dairy industry,
ovem1ixing of diets that reduces effective
accounting for at least 150 kg increased
fiber length, errors or imprecision in the
annual production since its inception. Even
mixing of the ration, and overfeeding or
today, the genetic potential for milk
underfeeding energy to late-lactation cattle.

production greatly exceeds the actual milk

When TMR are fed, feeding mistakes are
yield achieved on most faims. Reproducoften spread across the entire group or tive disorders ai·e the most common and
herd. Health management prograi11s of
costly reasons for premature culling of
herds that receive TMR diets should include
dait)' cows (see MANAGEMENT 01' REPRODUCTION: systems to monitor the adequacy of the

CA'l"l'LE, p 2171). In conventional dairy
ration formulation and delivery.

herds in which calving occurs throughout

2138

HEALTH-MANAGEMENT INTERACTION DAIRY CATTLE
the year, suboptimal reproductive
program. The cost of raising heifers is a
management leads to the failure of cows to
significant proportion of the overall cost of
conceive in a timely fashion, or at all. Cows
production; a replacement animal does not
remaining open longer reduce productivity
begin to earn a profit until midway through

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in the following ways: 1) Open cows spend
her second lactation. A wide range of
more time in late lactation, with lower milk
mortality rates (5%-25%) is reported for
production. 2) Cows taking longer to
replacement anin1als. The highest morbidity
conceive may dry off sooner, leading to
and mortality rates on dairy farms generally
longer dry periods. 3) Risk of culling
are seen before weaning. The most
increases greatly in cows remaining open
significant causes of preweaning death are

>300 days after calving. 4) Fewer replaceinfectious diseases of the digestive and ment heifers are available. 5) Higher labor
respiratory systems. These disorders can
and treatment costs are associated with
be controlled by well-designed health
prolonged efforts to synchronize and breed
management procedures that define the
open cows.

care and housing of the dan1 during the

Successful AI requires that cows be
periparturient period, the calving process,
inseminated during estrus in a narrow range feeding adequate quantities of high-quality of optimal fertility, and that the semen be
colostrum, and the application of proper
thawed properly, transported quickly to the
preventive measures (including sound
cow, and deposited in the appropriate area
nutritional programs) for newborn calves.

of the reproductive tract. The most

Delayed age at first calving reduces dairy
important factor affecting the success of an
productivity by increasing the need for

AI program is the detection of estrus: recent
replacement animals and increasing the
data from the USA indicate that fewer than
costs of raising the replacements because of

4()0A, of estrus periods were detected in
longer feeding periods. Heifers should be
lactating dairy cattle. Efforts to improve

23-25 mo old at first calving, which means
heat detection using estrus synchronization
they should conceive when 14--16 mo old.

and artificial detection aids have been

Adequate nutrition is important to ensure
largely unsuccessful and are hampered by
that heifers are fertile and cycling at this
the reduced duration and intensity of estrus
stage and that continued growth occurs so
exhibited by modem USA Holsteins, and by
that heifers are large enough at calving to
the increasing size of farms making estrus
limit dystocia and maximize mammary
observation more difficult. Because heat
development and lactation.

detection rates are so low, some dairy
managers have returned to extensive use

Herd Size, Composition, and Culling
of natural service sires to ensure that cows
conceive promptly. In these herds, breeding

There is a well-demonstrated relationship
soundness examinations and bull managebetween productivity and herd size. One ment programs should be included to
reason for this is the greater willingness
ensure continued herd productivity. (See
for larger operations to adopt production
also
enhancing technologies. Government

BREEDING SOUNDNESS EXAMINA'l10N OF' BULI.S,
p 2231.) However, the problems associated
policies can also substantially influence
with natural service include reduced genetic herd size ( eg, countries with supply managein1provement of offspring; costs associated ment systems effectively limit the annual
with purchase, raising, and feeding bulls;
income a farm can achieve from the sale
dan1age to facilities; and danger to people.

of milk). The an10unt and productivity of

Researchers in Wisconsin and Florida
pasture can influence tl1e size of herds that
have developed hormonal synchronization
use grazing. ln these herds, productivity is
protocols that allow timed insemination to
detennined by balancing the ability of the
be performed with acceptable conception
pasture to produce nutJ.ients against the
rates. These programs have been widely
ability of the cows to produce milk. The
adopted and have enabled herds to
size of both grazing and confinement herds
dramatically increase the nun1ber of
are increasingly affected by competing
pregnant cows throughout defined time
demands for land.

periods. Many of the injections and t11e

The proportion of the herd producing
inseminations can be scheduled on a weekly milk versus the nonproductive stock ( dry basis, leading to more efficient use of labor.

cows, calves, heifers, and bulls) has an
effect on total herd productivity. Herd
composition is the result of a nwnber of

Replacement Management
interrelated management decisions, such as

Herd productivity can be profoundly
culling policy, rate of reproductive success,
affected by the success of the replacement
rate of disease, replacement management,

HEALTH-MANAGEMENT INTERACTION: DAIRY CATTLE

2139
and longtenn goals regarding herd size. The
becoming evident after calving. Diseases
ability of a herd manager to cull animals can
such as hypocalcemia (milk fever),
have a significant impact on herd composihypomagnesemia, udder edema, ketosis, tion. When numerous replacement heifers
displaced abomasum, and mastitis often

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are available, culling may intensify, leading
begin during the dry period. Dairy health
to a younger herd with improved genetic
management prograins focus on many
potential for future milk production. In
preventive practices such as vaccination,
countries such as the USA, where herd
hoof care, and nutritional monitoring during
production is not limited, longterm plans
this period.

regarding expansion often influence herd

The length of the dry period influences
composition. In some growing or start-up
milk yield in the subsequent lactation. The
herds, only nonlactating cattle are pUI0
recommended dry period is 6-8 wk. D1y
chased to reduce the risk of purchasing
periods of <40 days reduce milk yield in the
animals with infectious diseases such as
following lactation. Dry periods that are too
contagious mastitis or bovine viral diarrhea.

long may lead to excessive weight gain and

These herds often consist of a high
reduced production efficiency. Both short
proportion of first-lactation animals.

and long dry periods are most common

Decisions regarding cow removal can
when breeding dates ai·e U11certain because
significantly impact productivity of the daily of either bull breeding or inaccurate ( or herd. Culling rates vaiy between herds and
missing) reproductive records.

may be related to disease rates or disease
control programs. Fertility, mastitis, and
lameness ai·e common reasons for cow

INTERACTIONS BETWEEN
removal. Culling is an important aspect of

HEALTH AND PRODUCTION
controlling other diseases such as bovine
tuberculosis, brucellosis, paratuberculosis,

An important factor that influences dairy
and chronic mastitis caused by some
herd productivity is the an1ount and type of
contagious mastitis pathogens.

disease in the herd. The basis of disease
control prograins includes knowledge of the
frequency of disease, information about the

Environmental Conditions
biologic effect of disease, and information

Even with optimal housing situations, herd
on the effectiveness of control procedures.

productivity ca.11 be affected by environmen

Most studies repmt incidence rates of
tal conditions. High-producing cows have
only common, easily diagnosed clinical
higher dry-matter intake, generate more
diseases such as mastitis, laineness, milk
internal heat, and are less tolerant of high
fever, retained placenta, or displaced
ainbient temperature. Weather conditions
abomasum. The frequency of subclinical
that combine high atnbient temperature and
disease is much more difficult to discern.

high humidity without periods of cooling

The cost to obtain subclinical disease
generaJJy depress dry-matter intake and
infonnation is inflated by the need to use
reduce milk yield. The increased concentrascreening tests ( eg, culture or somatic cell tion of dairy farming in regions that
coU11ts [SCC] for mastitis, fecal culture or
experience considerable periods of high

ELISA for paratuberculosis) for diagnosis.

temperatures (eg, southwestern USA) has

The lack of repeated testing leads to the
resulted in more seasonal variation in milk
reporting of prevalence rather than
output.

incidence for many subclinical diseases.

Farmers have adopted a variety of

Estimates of the frequency of sporadic or
systems to combat heat stress. New
endemic infectious diseases (such as
facilities are constructed with lai·ge, open
listeriosis, infectious bovine rhinotracheitis,
sides and ends ( often >4.3 m high) and use
or leptospirosis) are also spai-se. There is
fans and sprinkler systems to keep cows
zero tolerance for some diseases that have
comfortable. Older, enclosed facilities
serious consequences for public health.

can be retrofitted with tunnel ventilation

The diagnosis of even one case of bovine
systems to provide adequate air movement.

spongifonn encephalopathy, brucellosis,

(See also VENTILATION, p 2116.)

rabies, or tuberculosis in areas thought to
be free of those conditions is cause for

Drying Off and Dry Cow
immediate action.

Management

Risk factors for most postpartum diseases

Influence of Disease on Productivity
of dairy cows are present during the dry

Increased culling, reduced milk or protein
period, with clinical signs of disease
yield, increased adult cow mortality, and

2140

HEALTH-MANAGEMENT INTERACTION: DAIRYCATILE
reduced reproductive efficiency are all
best documented direct effect is the effect of
potential results of disease in adult cows.

mastitis on milk yield. A single case of clinical

Milk production is often profoundly
mastitis can result i11 a nlilk yield loss of
reduced in cows with clinical disease. The

300-400 kg/la.elation, with vai.iations rai1ging
duration of acute clinical syndromes is
from negligible to 1,050 kg. Mastitis dwing

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often sho1t, but the effects of the disease
eai.·ty lactation is associated with higher
may persist throughout the entire lactation.

losses ( 450-550 kg) than cases seen later in

Early lactation is the highest 1isk period for
lactation. (See also MMTITIS IN CAnLE, p 1358.) many diseases. Disease dwing early

Losses resulting from subclinical disease
lactation may reduce peak milk yields
are often considerable. The best described
and therefore contribute to lower total
relationship between subclinical disease
lactational yields. Through advances in
and productivity is the effect of subclinical
a11imal husbandry and health management
mastitis on milk yield. Each 2-fold increase
programs, many farms have minimized cliniin SCC >50,000 cells/mL caused a toss of 0.4
cal syndromes associated with infectious
kg milk/day in prilnipai.·ous cows ai.1d 0.6 kg
and metabolic disease.

milk/day in multiparous cows. Total

Although epidemics of clinical syndromes lactational milk yields were estilnated to be still are seen, the nature of disease has
reduced by 80 kg for prinliparous cows and
changed on many dairy farms. The trend

120 kg for multiparous cows for each 2-fold
toward larger wlits and slu'inkirtg profit
increase in the geometric mea.11 SCC >50,000
margins has encow·aged a shift toward
cells/rnL. Other subclinical diseases ( eg,
optimizing herd or group productivity
paratuberculosis) have also been related
tJu·ough reduction of subclinical diseases,
to reduced productivity.

such as ketosis, mastitis, acidosis, and

Diseases that delay or prohibit conlamillitis, which can have a major in1pact ception have a negative effect on herd
on productivity.

productivity by prolonging the tiI11e cows

Infectious disease still represents a major
spend in lower-producing stages of
source ofloss to dairy indusbies worldwide.

lactation, by reducing the nwnber of

1n Britain, outbreaks of foot and mouth
offspring for replacements or for sale, and
disease ( as well as boville spongifo1m
by increasing the likelihood the animal will
encephalopathy) are dran1atic examples of
b(' C'ulled prematurely. Several diseases
the disastrous effects of infectious diseases
have been associated with decreased
on productivity. Other se1ious infectious
conception rates. 1l1e likelihood of
diseases such as tuberculosis, brncellosis,
conception was reduced by 14%, 1 5%, and
bluetongue, and vesicular stomatitis

21 % for cows that experienced retained
continue to affect livestock a.round the world. placenta, metritis, or ovarian cysts, 1n orth America, more conunqn infectious
respectively. Mastitis, metritis, and ovaria.11
diseases that must be actively controlled
cysts reduced the likelihood of cattle being
include the contagious mastitis pathogens
bred for the first tin1e. Postpai.'turn diseases

Mycoplasma bovis, Staphylococcus a.ureus,
that prolong negative energy balai1ce in
and StreptococC'!ls agalactiae; boville viral early lactation also have a negative effect
diai.Thea; salrnonellosis; paratuberculosis;
on reproductive performance through
and pnewnonia. Excellent control progran1s
alterations in ho1rnonal activities.

have been developed for most of these

The effect of disease on longevity has
diseases, but their adoption is quite vaiiable.

been investigated. A large proportion of

The effects of disease on productivity
cow culling is considered involuntai.y
can be direct (such as mastitis causing a

( driven by disease, mjwy, or death) rather
profound reduction in milk yield) or indirect
than for reasons of low production. The

(laineness leaclillg to reduced feed intake,
prematme removal of a cow from the herd

Urns causing reduced milk yield). Diseases
reduces lifetime milk yield. Reproductive
occwTiI1g in early lactation ca.11 also <'a.use
failure and mastitis are consistently
cascading effects that ultimately reduce
recorded as the top two reasons for culling.

productivity. For exainple, pe1ipart1.11ient
disorders often are seen as a complex, and
cows diagnosed with paiturient paresis

THE HEALTH MANAGEMENT
ai.·e at increased 1isk of retained placenta,

PROGRAM
complicated ketosis, and mastitis. Cows
with dystocia and retained placenta ai·e

The goal of health management p.rograins is
at increased 1isk of met1itis. Subclinical
to ensure the optimal cai.·e and well-being
ketosis leads to increased risk of displaced
of daily cattle and to reduce losses in
abomasun1 and reduced milk production. 1l1e productivity caused by disease ai1d

HEALTH-MANAGEMENT INTERACTION: DAIRY CADLE

2141
management errors. The health managefarms have adopted a system that ir1cludes ment program is generally developed
routine daily monitoring of body temperacooperatively by the herd veterinarian and tme and rwnen activity of cows during the
the dairy producer based on comparisons
first 7 days after calving. A.nirnals that fall
of herd perfonnance with predetermined
outside no1mal lin1its are treated according

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performance goals. The structure of health
to predefined criteria or detained for
management programs is unique to each
examination by the herd veterinarian. All
farm but is typically keyed to the scheduled
treatments administered to dairy cows
veterinary herd visits that combine routine
should be recorded in treatment logs ( either
reproductive examinations, review of
computerized or handwritten) to ensure
selected herd performance records, and
adherence to proper meat and milk
decisions and actions related to specific
withholding periods. The frequency of
herd management issues.

unscheduled visits for emergency medical
services usually diminishes in herds that
have adopted a health and production

Scheduled Farm Visits
management program.

The frequency of scheduled veterinarian
visits is somewhat dependent on herd size.

Scheduled, Traditional, and Technical

In herds of <100 cows, one or two cows

Activities: Routine reproductive exan1inacalve every week and a. single, scheduled tions account for much of the veterinarian's
monthly visit is probably appropriate. These tin1e during scheduled herd visits. Attaining herds may have more unscheduled visits for
reproductive success is an essential
examination of sick cows than herds visited
detem1inant of herd productivity. For a
more regularly. Larger herds in which cows
description of reproductive programs, seep
are calving daily warrant more frequent

2171. The end point of reproductive
visits, and weekly scheduled visits are not
examinations should be to identify
unconunon for herds of >200 cows. A trend
nonpregnant cows that can be returned to
on extremely large dairy fan11s (>2,000
the breeding program and to generate data
cows) is employment of a full-time staff
that can be used to detennine the success or
veterinarian to oversee and direct
failure of breeding programs. The impleday-to-day issues regarding health and mentation, success, and cost-effectiveness
performance. The frequency of scheduled
of scheduled breeding progran1s should be
herd visits for grass-based seasonal dairy
reviewed frequently.

operations varies depending on the herd's

On smaller fa.ims, it is often customary
stage of lactation. More frequent visits are
for the veterina.iian to perfom1 routine

.necessary in early lactation and during the
ir1dividual anin1al treatments (such as IV
breeding period.

injections), prophylactic activities (such as

Activities at herd visits fall into four
vaccinations), and some technical tasks
general categories: provision of individual

(such as dehoming calves) during
animal health care and emergency services,
scheduled herd visits. It is appropriate for
scheduled technical activities, scheduled
the veterina.i·ian, or a technician under the
analytic and training activities, and
veterinarian's supe1vision, to perfom1 these
provision of quality control programs. The
tasks, because the farm staff may not
frequency of individual activities varies.

perfom1 them often enough to become
technically proficient. On larger farms,

Individual Health Care and Emer
tl1ese tasks must often be performed on a
gency Services: The examination and
daily basis; in this case, farm employees
treatment of individual animals is an
should be trained to accomplish these tasks.

important activity during scheduled dairy
visits. Frequent herd visits allow practition

Scheduled Analytic and Training
ers to examine cows early in the course of

Activities: Conducting scheduled or
disease when the likelihood of successful
unscheduled technical activities will not be
treatment is higher. Routine visits also allow effective unless a system exists to captme veterinarians to monitor the outcome of
the results of the activities and allow for
treatments and modify treatment protocols
analysis and ongoing revision. The structure
as needed. Ideally, monitoring programs
of the health and production management
include a system to detect cows not
program must include time for the fa.imer
performing as expected. Special attention
and the herd veterinarian to analyze and
should be pa.id to the highest-risk cows,
discuss herd management issues. In herds
including frequent observation of anirnals
that depend on hired personnel to
during the peripartwient period. Some
implement designated tasks, time must be

2142

HEALTH-MANAGEMENT INTERACTION: DAIRY CATILE
scheduled to observe and effectively train
over-the-counter sales of antin1icrobials
personnel ultimately responsible for
for use in feed or water will no longer be
perfonning the activities. Development
allowed. See also TIIE VETElllNARY FEED
of standard operating procedures is one

UIHJ::GIWJ::, p 2634.

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method to ensure that agreed-on practices

Some dairy practitioners function as the
are implemented.

nutritional specialists for the 'dairy farms

Treatment protocols are used to define
they serve. TI1ey may collect feed samples
standard treatments for common diseases
for nutrient analysis, forn1ulate rations, and
on dairy farms and should be used when
advise the farmer regarding crop and
multiple people have responsibility for
haivesting conditions. These veterinarians
administering antibiotic treatments to dairy
often devote a considerable ainolUlt of their
cattle or when extra-label drng use is preprofessional time to nutritional managescribed. They also provide a mechanism for ment. Other fam1s employ a professional
increased communication about treatment
nutritionist or use a nutritionist employed
plans between the veterinarian and
by a feed company or local cooperative to
producer.

formulate the rations and submit feed

The avoidance of residues in food
samples for nutrient analysis. Regardless of
products is a major responsibility of dairy
the source of the dairy's nutrition progran1,
practitioners. Increased scrntiny regarding
the veterinariai1 can perform an essential
antinticrobial use in food-producing anin1als oversight function simply by observing body has arisen because of concern about the
condition and general health in cows in
development of antimicrobial resistance in
certain high-risk areas (peripaituricnt and
food borne pathogens. Although the level of
high milk production), monitoring the
detected ai1tibiotic residues in meat and
incidence of nutrition-related diseases such
milk products is extremely low, antibiotic
as parturient hypocalcemia and displaced
residues in bulk ntilk and carcasses are seen
abomasun1, and ensuring that the diet
occasionally. In the USA, contan1ination of
described on paper is adequately formulated
bulk milk is rare because of an effective
and delivered to the cows. Assessing
sUIVeillance system based on rapid testing
pasture conditions by periodic inspection
for selected antinticrobial agents of every
of pasture is an inlportant component of
load of raw milk Milk contantinated with
managing the nutritional progran1 of herds
antibiotics is discarded, and the producer
that use management-intensive grazing.

is fined.

These quality control activities should be

The requirements for extra-label drng use
conducted routinely as pa.it of the health
in the USA have been defined by regulatory
and production management prograin.

officials under the Aninlal Medicinal Drug

Use Clarification Act and shm).id be closely
followed. The An1erican Association of

Quality Control Programs

Bovine Practitioners has responded to

Quality control refers to activities that
societal and regulatory concerns about the
ensure consistency in perforn1ing key
use of antimicrobial agents by adopting
management processes. Vital management
recommendations for the prudent arid
areas for most herds include nutritional
judicious use of antin1icrobial agents in
management, ntilking management, and
dairy cattle. In response to concerns about
ymmg-stock progran1s. Some fan11s may
the development of antimicrobial resistance also develop quality control processes in human medicine, the FDA is requesting
for environment and housing and farn1-
that drng manufacturers begin the process
specific mai1agement of breeding bulls.

of elintinating the labeling and use of certain

Milking management should be a
antimicrobials for production pm-poses (to
standard element of quality control
increase feed efficiency or weight gain).

prograins. Tasks such as observing the

Specifically, antimicrobials of importance to milking routine and scoring tl1e condition of hun1an medicine will no longer be pennitted teats should be performed at least quarterly.

to be provided in feed or water solely for

A scheduled system of routine screening for
production pm-poses, and no new antimimastitis pathogens can be inlplemented as crobials will be approved for production
part of the milking management prograin.

pm-poses, although they can be approved

The veterinarian can teach farn1 personnel
for use in feed or water for treatment or
how to perform the Califontia Mastitis Test
prevention of disease. For producers to
as part of a SUIVei!lance prograin. Animals
use an antimicrobial in feed or water, they
routinely screened may include cows at dry
must receive a feed directive from their
off, fresh cows and heifers, and newly
veterinarian ( essentially a prescription);
purchased cows. Milk sainples can be

HEALTH-MANAGEMENT INTERACTION: DAIRY CATILE

2143
collected and submitted for culture from
comparable herd indices. In many instances,
quarters that show positive reactions.

pe1fom1ance targets have been calculated

Newborn calves and replacement heifers
as arithmetic averages, which are useful
are often housed separately from lactating
indicators of herd pertonnance when the

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cows and may not be observed routinely by
contributing data (such as milk, fat, and
the herd veterinarian. However, routine
protein yields) are nonnally distributed
surveillance of critical management issues
and have a reasonable degree of vaiiation.

such as adequate delivery of colostrum to

However, many reproductive indices and
calves and growth rates of replacement
values such as SCCs ai·e not distributed
heifers can be done as pait of scheduled
normally, and eIToneous conclusions about
herd visits. The environment of dairy cattle
herd perfom1ance may be made if averages
cai1 have considerable influence on health
alone are used to make management
and productivity. Some veterinai·ians
decisions. Appropriate frequency distliburoutinely schedule "walkabouts" through tions are more useful for these types of data.

the housing ai·eas to assess factors related

Key indicators for perfom1ance targets
to anin1al comfort and hygiene. Udder
should be defined. The monitoring system
cleanliness, hoof and hock lesions, and
should specify the indices used, the anin1als
respiratory disease are often determined
included, ai1d the time interval to reassess
by housing conditions. Herd walkabouts
progress made toward reaching each target.

should include ai·eas often ignored, such

Typical performance indicators include
as dry-cow and heifer housing.

milk production, reproductive performance, milk quality, replacement manage

Performance Targets
ment, cow removal, animal health, ai1d
special reports (see TABLE 4). Perfo1mai1ce Performance tai·gets reflect herd standards
targets should be reviewed at appropriate
of performai1ce that are perceived as
intervals with realistic expectations
indicators of successful herd management.

regai·ding the an10unt of time it takes to

They are useful as comparison values for
effect change in an index. For exai11ple,
herd perfonnance ai1d as a starting point
management actions taken to reduce days
to initiate discussions about potential ai·eas
to first calving would require �9-10 mo to
for improvement. To use a perfom1ance
become appai·ent. A more tin1ely value such
tai·get, it is necessary for a herd to have a
as age at conception would more rapidly
record system that allows for generation of
reflect current management changes.

IM;i!ii EXAMPLES OF ACTIVITIES FOR ROUTINE MONITORING·

Environment

Cow Monitoring

Monitoring

Records Monitoring

Body condition

Stalls and bedding

Milk production

Rw11en fill

Barn climate

Milk quality features

Feces consistency

Milking method

Roughage analysis

Undigested fraction in feces Milking parlor condition Drinking water quality Teat end callosity

Pasture management

Sire evaluations

Lesions of udder/teat/skin

Grass haivesting (silage) Soil analysis

Clinical disease cases

Maize haivesting (silage) Artificial insemination
records

Reproductive exaininations Floor design and

Disease and drug records
maintenance

Ectopai·asites

Ration formulation

Fan11 economics report

Locomotion and claw score Feeding management

Slaughter findings

Young stock growth

Hygiene practices

Laboratory findings

"From Noordhuizen JP, Dairy herd health and production management practice in Europe: state of the art. Proc 23rd World BuiaLrics Congress, Quebec, Canada, 2004.

2144

HEALTH-MANAGEMENT INTERACTION: DAIRY CADLE

Record Keeping
and can be overlooked easily. Most systems

A system of unique individual cow identificaalso provide for a minimal level of herd tion is a prerequisite for a successful health
analysis, such as the generation of timely
management program. The most common
perfom1ance reports for production,

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methods of animal identification are ear tags, reproduction, and disease. Some prograins collars, and branding. Increasingly, farms are
can also generate statistics. The recordusing electronic identification via transpondkeeping system should allow the producer ers on ankle bands or neck straps. At a
and veterinarian to understand and modify
mi.J1imw11, data must be recorded on birth,
the fonnulas used to generate herd perbreeding, and calving dates and periodic fom1ai1ce indices. For paraineters and
milk yield. Under ideal circwnstances,
values used to monitor herd healtl1 and
swnmarized data should be available for the
production, see TABLE 5.

nutritional progran1, disease occwTence, and

The vetetinarian should ensure tl1at
financial performance.

collected data are used in a timely manner.

Record analysis is a necessary compo

Accurate data collection is most likely when
nent of the health management cycle. Most
the producer is using the data frequently
or all dairy herd i.Jnprovement (DHI)

and understands its value. The validity of
systems allow for electronic access to
data generated from both manual and
performance data, and various computerautomated data collection systems should ized systems for herd management are used
be reviewed and critically assessed.

throughout tl1e industry. Most monitoring

Unusual results and deviations from normal
systems can be charactetized broadly as
perfonnance tai·gets should be challenged.

one of the following: 1) manual (handwrit

The producer and the vetetinai·ian should
ten) card systems, 2) on-farm computer
agree on defined actions based on the herd
progran1s, 3) DHI, or4) DHI and on-faim
status and goals. Actions are generally
computer. Regardless of the type of system
diagnostic, preventive, or treatment
used, it should be easy to use and relevant to oriented. 'fypical activities might include the day-to-day operations of the dairy.

listing animals for routine herd fertility or

One in1portant function of record systems illness exan1inations, or selecting cows is tl1e generation of"action" lists (due to to obtain milk sainples for culture, to
calve, due to dry, etc). This function is
vaccinate, to consider culli.J1g, to breed,
critical in large herds in which cattle ai·e not
to receive body condition scori.J1g, or to
individually known by the animal handlers
receive treatments.

PARAMETERS USEFUL TO MONITOR HEALTH AND PRODUCTION OF

DAIRY HERDS

Parameter

Goal

Adult Cow Disease

Average percent of herd Jaine

<25%

Metritis/endometritis incidence

<5o/o-25%

Subclinical ketosis (>1.2 mmol/1)

<10%

Clinical ketosis

<2%

Left displaced abomasum

<3o/o-5%

Milk fever

<3% of adult cows calving per month

Retained fetal membranes

<3% of cows calving per month

Cut point for ruminal acidosis
pH<5.5

Clinical mastitis monthly incidence

<3% of lactating herd

Culling and Death Loss

Annual average overall cull rate

35%

Annual average selective cull rate

>15%

(continued)

HEALTH-MANAGEMENT INTERACTION: DAIRY CATTLE

2145

PARAMETERS USEFUL TO MONITOR HEALTH AND PRODUCTION OF

DAIRY HERDS (contfriuecl)

Parameter

Goal

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Annual death loss

<10%

Annual disease and injury culling

<5%

Annual reproductive cull rate

5%-10%

% Removed <60 days in milk (lactation = 1) <4%

% Removed <60 days in milk (lactation >l) <6%

Udder Health and Milk Quality
sec legal limit

750,000 cells/mL
sec farm goal

<150,000 cells/mL ( or adjust for a dairy)

Standard plate count legal limit

100,000 CFU/mL

Standard plate count farm goal

2,000-4,000 CFU/mL

Preliminary incubation count

2,000-6,000 CFU/mL

Bulk Tank Cultures - Bacterium

Streptococcus agalactiae

OCFU/mL

Staphylococcus aureus

<50CFU/mL

Staphylococcus spp

<1,000 CFU/mL

Mycoplasma spp

OCFU/mL

Environmental streptococci

<1,000 CFU/mL

Coliforms

<500CFU/mL

General Reproductive

Standard

Average days open

100-110 (ideally low l OO's to achieve

12-mo calving)

Average gestation

283 days

Calving interval

13.5mo

Average days in milk

200

Percentage of cows <90 days in milk

25%

Percentage of cows 90-180 days in milk

25%

Voluntary waiting period (VWP)

50-60 days for cows; 80-90 days for heifers

Days in milk at first breeding

Goal: VWP + 11 days

First service conception rate

40%

Heat detection

Goal overall >500A, (national average <400A,)

Intervals between breedings

18-24 days for 65% of cows

Length of estrous cycle

18-24days

Overall conception rate

>35%

Services per conception

2

Definition of pregnancy rate

Heat detection rate x conception rate

( 21-day interval)

(continued)

2146

HEALTH-MANAGEMENT INTERACTION: DAIRYCATILE

PARAMETERS USEFUL TO MONITOR HEALTH AND PRODUCTION OF

DAIRY HERDS (continued)

Parameter

Goal

First cycle pregnancy rate

>30%

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Percent pregnant by three cycles

>50%

Overall pregnancy rate

>200;(,

Percent of herd pregnant

50%

Pregnancy Diagnosis

When to do pregnancy checks

>40 days after being bred

Ability to locate an1nion

42-65days

"Membrane slip"

Day 30 to term

Ability to locate fetus

65-95days

Placentomes present

After 3 mo of gestation

Ability to sex fetus

After 60-70 days of gestation

"Placentomes"

Day 70 to term

By anmion size (days)

35

7 mm (\,\,finger)

42

15 mm (1 finger)

48

35 mm ( 2 fingers)

53

55 mm (3 fingers)

58

75 mm ( 4 fingers)

62

90mm (palm)

65

105 mm (hand)

By fetal crown-nose length (days)

70

1.5 cm (1 finger)

80

3.5 cm ( 2 fingers)

90

5.5 cm (3 fingers)

100

7.5 cm ( 4 fingers)

110

9 cm (palm)

120

10.5 cm (hand)

Postpartnm Involution

Lochia (normal)

Day 1-2

Bright red blood, thick mucus, little smell

Day 3-7

Dark red, thin, odor not foul but objectionable

Day 7 -14

Progressively less red to white to
translucent, thicker, smell improves

Entire uterus palpable

2wk

Full reduction in size

40-45days

Epithelialization complete

40-45days

(continued)

HEALTH-MANAGEMENT INTERACTION GOATS

2147

PARAMETERS USEFUL TO MONITOR HEALTH AND PRODUCTION OF

DAIRY HERDS (continued)

Parameter

Goal

OccwTence of endometritis

>26 days after calving

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Full uterine involution

40--45 days postpartwn

Abortion

Normal embryonic loss ( <50 days)

<10%

Average rate of early embryonic loss

15%

Normal rate of abortion

3%

Major infectious abortion agents

Bovine viral diarrhea, mycotic, leptospirosis, Neospora Noninfectious causes

Heat stress

>90 °C, SOOA, relative humidity

Toxins

Nitrates: methemoglobinemia

Plants

Locoweed, snake weed, pine needles,
lupine

Urea

Excess rumen degradable protein or
nonprotein nitrogen; milk urea nitrogen

10-14mg/dL

Investigations of Health and
programs should detect problems early,

Production Problems
before considerable fmancial damage has
occWTed. Systems to investigate herd

Even on the best managed farms, unexoutbreaks have been described. Epiderniopected health and production problems logic concepts of disease investigation are
arise. Surveillance programs incorporated
useful to identify risk factors and to
in health and production management
stimulate con-ective action.

H EALTH-MANAG EM ENT

INTERACTION: GOATS

Management of goats depends on the
pregnant Angora doe without adequate
type (eg, dairy, pygmy, meat, mohair, or
energy and protein continues to grow
cashmere) and the reasons for which they
mohair, even if stressed until she aborts.

are kept ( eg, companionship or commercial

Of all fann animals, goats have the
enterprise). However, all are rwninants, and
strongest social hierarchy; thus, adequate
the basic principles of livestock husbandry
feeder space or pastme should be provided
are applicable. Dairy goats and pygmies are
so the dominant animals carmot guard feed
often raised intensively, with most of the
and prevent others from eating. The amount
feed being brought to the animals. Meat
of floor space available per doe affects the
goats and fiber goats are usually raised
amount of aggressive behavior. A goat can
extensively, with most of the diet corning
become so subordinated to its penmates
from browse and occasionally from
that it does not eat and loses condition. This
high-quality pasture at times of highest
behavioral component must be considered
nutritional need, such as the last 6 wk of
in cases of wasting goats. To maximize
gestation and the first 18 mo of life. A
longevity and to avoid fighting injuries, adult

2148

HEALTH-MANAGEMENT INTERACTION GOATS
males should be fed and housed individuwinter, perhaps more for the owners'

ally, especially during the breeding season
comfo1t than for optimal health of the goats.

when fighting increases. If group penned,

Combinations of manure packs, overhead
bucks should be kept together and given
hay-mows, or noninsulated ceilings lead to
time to get to know each other before breeddampness and ammonia buildup, especially VetBooks.ir
ing season begins. Introducing a new buck
if the barn is closed tightly. Warm, wet,
to a pen of existing bucks during breeding
poorly ventilated barns are conducive to
season may result in injury or death.

development of neonatal navel infections,

Goats are adventurous and are natural
mastitis, enteritis, pneumonia, and
climbers, and efforts to control them are
coccidiosis. Caseous lymphadenitis (the
necessary. The ultimate control would be
disease known as "abscesses"), caused by
high-tensile, electric fences; goats stand and

Corynebacterium pseudo tuberculosis
push on other fences and can be very

(ov'is), spreads rapidly in closely confined destructive. Hazards that might contribute
goats (seep 63). The slow-growing,
to broken legs and strangulations should
nonpainful lymph node abscesses
be removed. Tethering goats is potentially
eventually rupture and contaminate the
dangerous, because they are vulnerable to
feeders, walls, and other animals. Keyholedog attacks; also, if two goats are chained style feeders and head catches on milking
too close to each other, one might strangle.

stands are prime sources of transmission,

Chafing of ropes too tight on the neck can
because they promote rupture of abscesses
lead to deep abrasions and tetanus. Because
on the head and neck. The infection is
goats chew on painted smfaces, lead
spread by contact with the pus, and the
poisoning is a potential hazard in old barns.

organism can penetrate intact skin.

An efficient layout of pens, easy access to

Isolating affected goats, preferably culling
well-designed feeders, and effective control
them, and preventing environmental
of movement minimize management-related contan1ination is important. A commercial problems.

vaccine approved for goats is available, and

It is extremely difficult to keep goats' feet, autogenous bacterins have been used to urine, and feces out of many types of grain
decrease the incidence of these abscesses.

feeders, hay racks, and waterers. Goats

Intensive management of adult goats may
often refuse to eat soiled feed or water,
promote horizontal transmission of the
hay that has fallen on the floor, and grain
virus that causes cap tine arthritis and
contan1inated with urine or feces. Design
encephalitis (CAE, seep 747).

of hay feeders is critical to reduce feed

Mature bucks develop a powe1iul,
wastage. Many dairy and pygmy goats are
characteristic odor that is most intense in
bedded on wasted hay, but this practice
the breeding season, and personnel are
may lead to an increase in parasitism. Wet
reluctant to handle them. This often leads to
bedding contributes to development of
neglect of feet, failure to recognize heavy
coccidiosis in kids and staphylococcal
parasite loads, or loss of body condition.

impetigo on the udder, commonly but

The sebaceous glands on top of the head
erroneously known as "goatpox." Under
can be removed sw·gically at any age or can
similar conditions,joint-ill (seep 10114) and be cauterized at the ti.me of disbudding;
navel infections of the newborn are likely.

however, this does not render the buck

Separate, dry, well-bedded pens should be
totally odorless. Does are attracted by this
maintained for kidding. In certain areas,
smell and may refuse to be bred by a
kids are susceptible to white muscle disease descented buck if there is an odoriferous (seep 1095), which can be controlled by
one nearby; therefore, the glands should not
dietary selenium supplementation or by
be removed inadve1tently at the tin1e of
injection of vitan1in E/selenium to the
disbudding if male kids are to be kept for
pregnant doe and/or newborn. Concerns
breeding. The habit of urinating on the face,
about abortions associated with vitamin E/
beard, and forelegs also contributes to buck
selenium injection in ewes have prompted
odor and often leads to ulcerating sores in
caution about parenteral injection in
cold weather. During the breeding season,
pregnant does, and oral supplementation
most bucks lose weight, although this is not
may be preferred.

necessarily due to breeding too many does.

Housing of goats affects disease patterns.

Many bucks lose weight when housed close

Angoras in the southern and western USA
to does in heat, even when breeding is not
are usually given access to shelter only
allowed. One management strategy is to
during severe storms or for a few weeks
ensure that bucks are in prin1e physical
after the twice-yearly shearing, without
condition before the breeding season.

which they may die of cold weather stress.

In the European dairy breeds, the

Goats in the northern USA are housed in the
genetically homozygous polled doe usually

HEALTH-MANAGEMENT INTERACTION: GOATS

2149
is anatomically an intersex and, therefore,
disbuclcled 2 clays earlier to maximally
infettile. Aberrations vary from a slightly
inhibit horn growth or subsequent
enlarged clitoris visible only after puberty,
development of abnormal regrowth
to a buck-like conformation witl1 a scrotum,

(scurs). Homs may develop more slowly
penis ( often shortened), and ovotestes.

in Nubian, Nigerian Dwarf, and Pygmy

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Some phenotypically male pseudoherrnaphdoes, but disbudding before 2 wk of age rodites show male libido with breeding
is preferred to decrease pain during the
activity. Because these animals are infertile,
procedure and to prevent scur developearly recognition and culling is advisable.

ment. Hot-iron disbudding is the method

Some homozygous polled males may be
of choice, using either a restraint box and
able to sire kids, but these bucks are likely
nerve block, or general anesthesia.

to develop spern1 granulomas as they

Excessive applications of the hot iron can
mature and should be culled rather than
lead to brain damage or subsequent death.

used for breeding. Most owners reduce the

Disbudcling kids with caustic paste is not
incidence of homozygous polled animals by
recommended.

never mating two polled animals. While

Angora goats in range operations are not
most intersex goats are polled, similar
disbudded because the horns are thought to

,rnatomic aberrations are seen occasionally
be helpful against predators, and because
in horned goats. These would most
owners handle the goats by their horns.

probably be chimeras (freemartins), the

When goats are housed in winter, clisbudresult of anastomoses developing in utero ding is advantageous, because it reduces
between males and females. Such chimeras
tratu11a and prevents accidents in which
in goats are rare ( conside1ing the high
goats are trapped by their horns in feeders
frequency of twins) when compared with
and fence lines. Pygmies can be disbuclded
cattle.

according to tl1e owner's preference; it is

For foot care, seep 1092.

not a cause for disqualification or discrimination in the show ring in the USA. Dairy PERINATAL MANAGEMENT
goats generally are disbudded, and homed
anin1als usually are barred from the show

Common problems in does are extra teats,
ring in the USA. Tetanus can be seen after
double teats, and fish-tail teats witl1 double
clisbuclding or castration and, as a precauorifices. ln cattle, extra teats can be tion, antitoxin can be administered at
removed with impunity, but in dairy goats
disbudding.

tl1ere is often a functional milk gland behind

Dairy goats and pygmy bucks are
tl1e spare teat, and removal of abnonnal
castrated in the first few weeks; Angoras
teats is discouraged.

are castrated later, after they have attained

Newborn goats must be fed colostrum,
good horn growth. In males to be kept as
and if caprine ariliritis and encephalitis
pets, castration should be delayed to allow

(CAE) is a problem, heat treatment is
maximal urethral development, which
essential for control. Later, kids can be fed
reduces the likelilioocl of urolithiasis (see

(in decreasing order of desirability) goat's
p 1502). To improve their desirability as
milk, goat-milk replacer, lamb-milk replacer, pets, wetl1ers should have the scent glands, or cow's milk Any fresh milk fed should be
located caudomeclially to the horn base,
pastetuizecl or from stock known to be free
removed druing disbudding.

of CAE virus, mycoplasmas, and paratuberculosis. Newborn goats should be feel at NUTRITION

10%-12% of their body wt per day. Kids
should be provided sufficient milk or

Dai1y goats should be fed similarly to dairy
replacer at regular intervals to achieve
cattle (seep 2308 and seep 2265). A goodnormal growth.

quality hay, preferably alfalfa, should be tl1e

Kids should have access to hay and a
basis of the ration, and a 14%-160/oprotein
grain-based creep feed as early as 1 wk of
concentrate should be fed as a supplement
age. They can be weaned when they are
during lactation. Silage is not commonly fed
readily eating solid feed as most of the diet;
to goats because of the lack of mechanical
this varies from early weaning at 6 wk of
equipment. Overfeeding grain to pregnant
age Lmtil weaning as late as 12 wk of age.

does in late lactation is a conrn1on problem

Weaning may be delayed in some goat
tl1at may lead to increased levels of internal
operations because there is no conrn1ercial
fat deposition in ilie abdomen and result
outlet for doe's milk, so it is fed to kids.

in pregnancy toxemia and clystocia.

Dairy goat doe kids of European breeds

To increase salt consrunption, loose trace
should be disbudcled at 5-7 clays of age.

mineral salt (TMS) should be fed rather than

Bucks of the European breeds should be
block salt. The choice of salt should be

2150

HEALTH-MANAGEMENT INTERACTION: GOATS
based on the mineral content of available
goats kept extensively, the problem is seen
feeds in that specific area. Goats are highly
at weaning, when the kids are kept in
susceptible to copper deficiency and, unlike
smaller lots and fed supplement on the
sheep, fairly resistant to copper toxicity.

ground.

Therefore, cattle TMS, rather than sheep

In pastured and free-rariging goats,
salt with no copper, should be offered
helminthiasis can assunif great clinical

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unless the soils or water source are known
significarice. GI nematodiasis, liver fluke
to have high levels of copper. Goats raised
infestation, and lungworm infections all
for fiber may require supplementation of
may be seen. Age-related resistarice to
sulfur for proper fiber production.

parasitism in goats is weak relative to that in

Pet wethers fed substantial amounts of
other rwninants. Although most common in
grain are prone to develop urinary calculi.

yearlings during their first season on

Management practices that decrease the
pasture, clinical parasitism may be seen in
incidence of w·oiithiasis include reducing
adults as well. Poor growth, weight loss,
grain consumption, adding ammoniwn
diarrhea, a scruffy hair coat, signs of
chloride to the diet, keeping the
anemia, and intermandibular edema (bottle
calciwii:phosphorus ratio -2: 1, and keeping jaw) may be seen with GI parasitism or liver the magnesiwii level low. Perinea!

fluke disease. Haemonchus contortus
urethrostomy can be used as a salvage
infection has emerged as a major constraint
operation for commercial goats with
in the expanding meat goat indust1y in the
w·oiithiasis but is not recommended for pet
southeastern USA Persistent coughing in
goats, because recurrences of obstruction
late swimier arid autumn is the usual
and urethral scan"ing necessitate euthanasia presentation of lungworms; secondary for many. The surgical interventions of
bacterial pnewiionia with fever is a
choice for pet goats are surgical tube
conunon sequela. Parasitism is insidious on
cystotomy or bladder marsupialization. To
hobby far-ms, where the problem may not
encourage water consumption, clean, loose
exist for several years and then suddenly

TMS should be fed, and clean, fresh water
explodes as goat nwnbers continue to
available ad lib. To increase water
increase arid facilities become overstocked.

consuniption, especially for high-yielding

Tapewonn proglottids ar·e often noted in
does, water should be fresh and warm in
goat feces by owners. Although tapeworms
winter, and fresh and cool in swnmer.

are not generally considered to be of clinical
importance, their discovery can be used to
review the subject of helminthiasis with

COMMON DISEASES
owners and develop an overall par·asite
control prograni (seep 312).

Goats harbor several species of coccid.ia

Clost1idium perf1ingens type D can be
but not all exhibit clinical coccidiosis (see
fatal, and it is not always associated with the
p 207). Adult goats shed coccidia in feces,
classic "change in quality ar1d quar1tity of
contaminate the environment, and infect
feed." In problem herds, vaccination eve1y
the newborn. As infection pressure builds

4-6 mo may be necessary, because goats
up in the pens, morbidity in kids born later
may not maintain protective inununity as
increases. Signs include diarrhea or pasty
long as sheep or cattle when given the sariie
feces, loss of condition, general frailness,
commercial vaccines. Vaccination prevents
and failure to grow. In peracute cases, kids
the acute death syndrome, but occasionally
may die without clinical signs. Rotating all
even vaccinated goats may develop acute
the kids through one or two pens is
ente1itis. Affected goats develop severe
dangerous. To help prevent coccidiosis in
diarrhea arid profound depression; milk
artificially reared dai1y goats, the kids
yield drops abruptly. Death may result in
should be put in small, age-matched groups

24 hr. Treatment involves administration
in outside, portable pens that ar·e moved to
of ar1titoxin, analgesics, fluid therapy,
clean ground periodically. Eradication is not correction of acidosis, and antibiotics.

feasible, but infection can be controlled

Vaccination for contagious ecthyma
through good management practices.

( sore mouth, see p 866) is not indicated

Coccidiostats added to the water or feed are unless the disease exists on the premises.

adjuncts to a management control prograni

The main problems with infected kids are
arid not substitutes. Chronic coccidiosis is
difficulty in nursing, spreading lesions to the
one of the main causes of poor growth in
does' udders or the assistants' hands, and
kids and is responsible for the uneconomiattendance at goat shows being disallowed.

cal practice of delaying breeding for a year

Live virus vaccine is used by scarifying the
until the goat has reached adequate size
skin ( eg, inside the thighs or under the tail)

(70 lb [32 kg] for dai1y breeds). In Angora
arid painting on the vaccine. Both natural

HEALTH-MANAGEMENT INTERACTION HORSES

2151
lesions and those resulting from vaccination caprine paratuberculosis includes agar gel may last as long as 4 wk, but after the scabs
immunodiffusion, pooled liquid fecal
have dropped off, the goats can go to shows.

culture, direct fecal PCR, and ELISA. The

Chronic wasting is seen quite frecontrol program for paratuberculosis in quently; it is not a single disease but a
goats is similar to that in cattle.

syndrome. Generally, if a goat is well fed,

Caprine arthritis and encephalitis

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kept in a stress-free enviromnent, and has

(CAE, seep 747) vims has emerged as an
good teeth and a low parasite load, it should
in1portant infectious agent of intensively
thrive and produce. If it does not, and begins raised dairy goats, but all breeds of goats are

"wasting," it should be culled inunediately.

susceptible to tllis retrovims. CAE infection

The major causes of clu-onic wasting
in goats can manifest in nwnerous ways:

include poor nutrition, parasitism, dental
subclinical, persistent infection; a progresproblems, paratuberculosis, internal sive paresis of yow1g goats 2-12 mo old;
visceral abscesses due to Corynebacterium
agalactia with a finn, noninflarned udder at
pseiidotuberculosis (ovis) or 1)ueperella parturition in bred females; or an arthritic
pyogenes, locomotor problems (particularly condition with pain and swollen joints in arthritis due to retrovims infection [CAE
adults. A chronic, progressive interstitial
vims]), and clu-orlic llidden infections such
pnewnonia or a wasting syndrome may also
as metritis, peritonitis, or pneumonia.

be seen in adults. CAE infection has been

Tumors are occasionally diagnosed in older
considered p1imarily to be spread from darn
goats. These diseases are rarely treatable,
to offspring through vims-laden colostrwn
and many are contagious; tllis is the basis
and milk, and control programs have been
for the strict culling policy, wllich is vital to
aimed at separating the newborns from the
the overall productivity of a herd.

adult population and feeding heat-treated

Paratuberculosis in goats differs from
colostrwn and pastewized milk. Infection
that in cattle (seep 762); gross postmortem may persist in herds in wllich tllis is
lesions are Jess pronow1ced, and profuse
practiced due to ho1izontal transmission
diarrhea occurs less commonly in goats
between adults. Regular testing and
w1til right before death. Consequently,
rigorous culling of all seropositive goats,
many cases may go w1diagnosed until
or strict segregation of seropositive and
necropsy. The ileocecal node is the most
seronegative goats, must be practiced if
rewarding tissue for bacteriologic culture
disease eradication is the goal.

and histopathology. Diagnostic testing for

For mastitis in goats, seep 1367.

H EALTH-MANAG EM ENT

INTERACTION: HORSES

Proper management can reduce the
vaccination programs reduce morbidity
incidence of many disease conditions in
and mortality due to parasitism and
horses. Informed management of the
infectious disease. Owners should be
envirorunent and diet, routine foot and
aware of the normal vital signs and proper
dental care, and adherence to an approprimovement of a healthy horse, so that they ate deworming and vaccination program
will be better able to recognize when a
form the basis of a preventive health
health problem such as pneumonia, colic,
program. Client education is important for
or lameness develops. New modalities for
compliance; owners are more likely to
prevention and treatment are always
follow recommended changes in husevolving. In addition, the use of complebandry progran1s once they appreciate the mentary or alternative medicine such as
advantages. Diet manipulation reduces the
acupuncture, acupressure, chiropractic
incidence of certain types of colic and
procedures, photomodulation, and
exercise-induced myopathies, good dental
massage has grown in equine care (see
care improves feed utilization, minimizing

COMPLEMENTARY AND AJ:l'ERNATIVE VETERINARY
exposure to barn dusts and molds reduces

�ffiDICINE, p 2078). Knowledgeable owners
the risk of recurrent airway obstruction
working with a veterinarian and a farrier

( chronic obstructive pulmonary disease),
can result in a productive and pleasant life
and individually designed dewonning and
for every horse.

2152

HEALTH-MANAGEMENT INTERACTION: HORSES

HOUSING
botulism. Opossun1 feces can transmit
infective sporocysts of Sarcocystis

Stabled horses are exposed to numerous
neurona, the causative agent of equine
respiratory and GI pathogens, including
protozoa] myeloencephalitis (seep 1309).

viruses, bacteria, mold spores, dust mites,

Contamination of feeds by deer urine has

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and parasites. Stable environments affect
been incriminated il1 the spread of certain
disease transmission in terms of air quality
strains of Leptospira (seep 652).

and ventilation, population density, and

Regular disinfection of stables and feed
general cleanliness. Barns should be
and water buckets helps reduce persistence
constructed to optimize ventilation and
of infectious agents in the environment.

light, minimize exposw·e to dust and molds,

Organic debris inactivates most chemical
provide temperature regulation, facilitate
disinfectants; therefore, disinfection should
cleaning and disinfection, and provide
begin with physical cleaning (ie, hosing,
an1ple space for each horse. Windows and
scrubbing) of all surfaces followed by
skylights provide swilight and natural
chemical disinfection. Phenols, quaternary
ventilation. Swilight is a potent killer of
ammonium compounds, and chlorine are
many bacteria and viruses; it also promotes
the most con1111only used disinfectants. (See
coat shedding and regular estrous cycles.

also ANTISEPTICS AND DISINFECTANTS, p 2738.) Eight air changes per hour is considered

To fwther reduce spread of infectious
adequate ventilation for temperate clin1ates
disease, stalls should have walls or
and average hwnidity. (See also VENTILATION, paititions to prevent direct contact between
p 2116.) Ceiling or wall-mounted fans can
horses in acljacent stalls. Pregnai1t mares,
be used to increase air circulation on hot,
mai·es with foals, and weanlings should be
humid clays. Stall doors open at the top or
kept separate from yearlings and adult
made of heavy mesh screening provide
horses. Ideally, new arrivals should be
better ventilation. Stalls should have
isolated from the resident horse population
nonslip flooring and walls or partitions that
for 30 clays to reduce introduction of
prevent direct contact between horses in
contagious respiratory diseases, including
acljacent stalls. Suggested stall dimensions
respiI·atory viruses ( eg, equine influenza
for adult horses and for mares with foals
virus and equine herpesviruses 1 and 4) and
are 3.6 x 3.6 m and 5 x 5 m, respectively.

bacterial infections ( eg, Streptococcus

Doorways should be at least 2.4 m high x 1.2
equi). Alcohol-based hand sai1itizer gels are m wide.

very effective against most infectious respir

Recurrent airway obstruction ( chronic atory viruses and bacteria. Wall-mounted obstructive pulmonary disease [see
hand gel dispensers can be placed
p 1455]), and noninfectious inilan1111atory
strategically throughout barns ai1d tack
airway disease are associated with airway
rooms to in1prove hand hygiene and to
hypersensitivity to environmental allergens
reduce transfer of infectious diseases.

and irritants and exposure to organic dust.

The most commonly incriminated allergens
are fungal spores and pollens, but barn dust

PASTURE
is also rich in dust from shaving� sawdust,
manure, hay, animal hair and dander, silica

Horses should have an1ple tilne on good
from dirt in indoor arenas, and endotoxin.

quality pasture. The oppmtunity to graze

The amount of air contaminants increases
and exercise improves condition, prevents
with the dustiness of the barn, bedding, and
boredom-related behaviors (eg, cribbing
forage. Management techniques that help
and weaving), and reduces the risk of
prevent this condition include substituting
lai·ge-intestinal ilnpactions. Grazing on
wood chips, peat moss, or shreclclecl paper
grass also helps reduce the incidence of
for dusty straw bedding; avoiding dusty
gastric ulcers. Reducing the tin1e spent in
concentrates; using shallow rather than
poorly ventilated barns reduces exposure to
deep feed containers; and soaking hay
mai1y inhalant allergens incriminated in
before feeding at ground level. Air quality
development of recurrent airway obstruccan be unproved fwther if bedding and feed tion. Access to good forage provides a
are not stored above the stalls. Riding areas
natural source of vitan1ins and fiber. If
and the dust they generate should be
horses are feel in groups, sufficient space
situated away from stalls to reduce
should be allowed to minimize competition
exposure to dust.

and to ensw-e that even the most submissive

Feeds should be stored in dty containers
horse has access to an adequate diet.

to reduce contamination with molds and

Feeding hay and grain in elevated feeders
animal excreta. Moldy hay and silage feeding off the ground reduces ingestion of sand, have been associated with cases of equine
infective parasite eggs, and animal excreta.

HEALTH-MANAGEMENT INTERACTION: HORSES

2153

Safe, durable fencing should be used for

Horses grazing on pastures near water
pastures and paddocks to reduce the risk of
may be at increased risk of contracting
self-trauma. Double fencing between
certain diseases such as Potomac horse
paddocks minimizes transmission of
fever, caused by Neorickettsia risticii and contagious disease between horses.

disseminated by aquatic insects and snails

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Overcrowding should be avoided.

(seep 283). Pastures and paddocks should

Overgrazed pastures, which result from
be kept free of standing or stagnant water to
overstocking, lead to extremes in ground
reduce the breeding grounds for mosquitoes
conditions ( eg, dust or mud), conttibute to
carrying infectious equine viral pathogens,
increased parasite burdens, and favor
including West Nile virus and Eastern and
overgrowth of potentially toxic plants.

Western equine encephalomyelitis viruses

Excessive dust increases the risk of

(seep 1291).

respiratory infections among young horses
by inhalation of soil saprophytes, such as

NUTRITION

Rhodococcus equi (seep 1451). The 1isk of
this potentially fatal bacterial pneumonia on

During the last 20-30 yr, there has been an
fanns where the disease is enzootic can be
increased awareness of equine nutrition and
reduced by minimizing exposme of young
its irnporta.i1ce to the health of the horse.

( <4 mo old), susceptible foals to aerosolized

(See also NUTRl'l10N: HORSES, p 2312). In every R equi using environmental control
stage of life, nutrition is the foundation for
strategies such as decreasing dust formation
equine health and longevity. The dietary
on pastures and paddocks, housing foals in
needs of a horse change as it goes through
well-ventilated areas, rotating pastures,
each life stage. The great varieties of
reducing the size of mare-foal bands,
commercial feeds on the market attest
inigating and planting dirt areas with grass,
to t11e recognition of different diets for
and removing feces frequently from stalls,
different life stages. Horses must be
paddocks, indoor arenas, and pastures.

provided with an adequate supply of energy,

Breeding mares earlier in the season to
protein, vita.inins, and minerals and have
ensure foaling during colder weat11er may
access to fresh, clea.i1 water.

reduce tl1e number of susceptible foals

Adequate fresh water intake is essential
exposed to dry, dusty sun1111er conditions.

for every horse. Storage tanks, troughs, or

On fanns where R equi is endemic and foal
pails should be placed so the horse can
morbidity and mortality rates are high
reach in comfortably. Because most horses
despite attempts at pasture management, the are reluctant to put their head in a trough or incidence of disease can be reduced with
pail below eye level, the water level should
preventive administration of 1 L of
be kept high. If water levels get too low,
hyperinunune plasma containing high
many horses will refuse to drink. The
concentrations of antibodies againstR equi
optimal temperature for drinking water is'

to newborn foals within the first week of life,

68° -78°F (20° -26°C). Horses will reduce
followed by a second dose 25 days later.

water intake if the water temperature is too

Overstocking in barns and pastures favors cold or too wann. When daytime temperaoutbreaks of other contagious respiratory tures exceed 100°F (38°C), water in
infections caused by viral and bacterial
exposed pipes or hoses will be dangerously
pathogens spread between horses via
hot and should not be used for drinking or
aerosolization of respiratory tract secrebathing.

tions. Enteric infections with Clostridium

The nut1ient energy requirement of the
dijficile and C pei_fringens can become horse depends on its level of activity, the
endemic on some farms. An increased
energy content of tl1e diet, and the capacity
incidence of Clostridium dianhea in
of the animal's digestive system. The size
newborn foals has been associated with
and weight of the newborn foal is influenced
foaling on dirt, gravel, or sand surfaces, and
by the nutrition of the pregnant mare.

with stall confinement or limited turnout on

Horses fed for rapid body and skeletal
dry lots dming the first 3 days of life.

growth may develop bone abnormalities

Whenever possible, horses should not be
or be more prone to la.i11eness conditions.

pastured on sandy soils, because sand

A balanced diet should be fed according to
ingestion during grazing predisposes to
the desired rate of gain within the sound
colonic and rectal sand in1paction, chronic
para.ineters of good health. The best
dia.iThea, and weight loss. If sandy pastures
measure of growtl1 in a young horse is
are unavoidable, the risk of sand colic can
weight, and the best description of size of a
be reduced by feeding psylliun1 at regular
horse is a combination of height and weight.

intervals and by providing trace mineralized

A high conelation between the measure of
salt with equal parts of bone meal.

the heart girth and body weight in t11e horse

2154

HEALTH-MANAGEMENT INTERACTION HORSES
has been reported. In young, growing
requirement for any horse is energy. A
horses, monthly measurements are helpful
certain an1ount of energy is required for
to monitor growth changes.

maintenance and daily activity. Metabolic

There are several reasons to know the
demands are increased for such activities as
weight of horses. Many feeding requiregrowing, pelfom1ance activity, or lactation.

ments are based on percentages of the

In some activities, such as racing, jun1ping,

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horse's weight. Most feed recommendations or polo, the energy requirement may be are stated in the amount of feed (in pounds
increased by as much as I OO"A
or kilograms) the horse should receive

Diet manipulation can help treat, control,
based on body weight. In young horses,
and prevent other disease conditions.

"developmental orthopedic disease,"

Horses with recurrent airway obstruction
although a multifacto1ial condition, can be
should be fed as dust-free a feed as possible.

related to rapid growth or imbalances in

Adding water or oil to grains decreases dust.

energy, protein, and minerals (seep 1148).

Hay should be thoroughly soaked and feel

The proper balance of protein, calciw11,
close to the ground. If complete pelleted
phosphorus, zinc, and copper is important
feeds are feel, hay can be removed
in supporting healthy endochondral
completely from the diet. On sanely soils,
ossification and in stabilizing bone collagen
hay should be feel off the ground to reduce
and elastin synthesis. The amount of
sand ingestion. Dietary management can be
nutrients required in the diet for normal
used to reduce the risk of gastric ulcers.

bone development are dictated by rate of

Alfalfa hay, with its high calcium and protein
growth. Excessive energy intake contribconcentration, acts as a buffering antacid utes to osteochondrosis by decreasing bone
and has a protective effect on the nonglandensity and cortical thickness.

clular squamous mucosa. Small hay meals

Deficiency of protein must be severe to
feel frequently or access to pasture also
inte1-fere with enclochonclral ossification.

reduces the risk of gastric ulceration.

Rapidly increasing protein intake may

Nutritional management for Quaiter
produce faster bone growth; however, if the
horses with hyperkalemic periodic paralysis
diet lacks adequate minerals to support this

( see p l 04 7) is focused on decreasing increased growth, altered enclochondral
dietary intake of potassium and increasing
ossification can be seen. Calciwn and
renal potassi urn losses. Dietary manipulaphosphorus balance affect bone density, tion includes avoiding high-potassium feeds
rate of growth, and cartilage thickness.

such as alfalfa hay, brome grass, canola oil,

Inadequate amounts of copper and zinc
soybean meal or oil, and sugar or beet
have been associated with an increased
molasses ai1cl replacing them with timothy
incidence of osteochonclrosis and
or bem1ucla grass, beet pulp, and grains
osteoclysgenesis.

such as oats, com, wheat, or barley.

Some of the most common mistakes

Affected horses should be exercised
made when feeding young horses include
regularly and have access to pasture.

feeding excessive grain and leafy legun1es

Heavily muscled breeds of horses,

(eg, alfalfa, which results in too high an
including Quaiter horses, draft horses, and
energy intake), feeding a diet with too little

Waimbloocls, are prone to myopathies
zinc or copper to support rate of growth,
associated witl1 increased muscle
and feeding a diet with an improper
glycogen stores and polysaccharicle storage
calciun1:phosphorus ratio. Cereal grains and inclusions in type II muscle fibers. Successgrass forages are low in calciwn, phosphoful management of this c011dition, known as rus, protein, and lysine. Excess energy from
polysaccharicle storage myopathy, focuses
cereal grains may be more detrimental than
on increasing the fat content of tl1e diet and
excess energy from grass forages; one
eliminating or reducing grain intake. (See
reason may be that energy from grain is
also MYOPATHIES IN HOllSES, p 1176.)

derived from starch, whereas energy

Management practices to reduce the risk
from grass forage comes from microbial
of impaction include a.cl lib access to fresh
production of volatile fatty acids. Starch,
water, adequate exercise, good quality feed,
but not volatile fatty acids, stin1ulates
and good dental care. If impaction has been
insulin secretion, which has been implia problem, poorly digestible feeds ( eg, cated in stimulating hom1one changes that
mature forages) should be replaced with
contribute to osteochonclrosis.

low-fiber, highly digestible forages ( eg,

Older horses often have dental problems
growing grass or legume hays). A complete
that compromise feed intake and masticapelleted or extruded feed helps maintain tion. Extruded or soft pelleted feeds are
soft feces.

ideal. Hay should be good quality, leafy, and

Grazing lush pastures or consuming large
easy to chew. The most variable dietary
ainow1ts of legwne hay and the develop-

HEALTH-MANAGEMENT INTERACTION: HORSES

2155
ment of laminitis have long been associated. balanced diet with adequate minerals. In Anecdotal observations indicate that
horses prone to hyperadrenoc01ticism, the
pasture-associated laminitis occurs at times
use of fat-supplemented feeds with highly
of rapid grass growth ( eg, spring and early
digestible fiber and reduced starch and
summer and in the fall after rainfall) that
sugar intake is important. Horses with liver
favor accumulation of certain carbohyor kidney conditions should not be fed VetBooks.ir
drates such as fructans, starches, and
legume hays and fat-supplemented feeds.

sugars. Some horses and ponies may be

Horses confined to stalls most of the time
more susceptible to pasture-associated
are more prone to intestinal problems and
laminitis because of genetic predisposition
development of undesirable behaviors.

and other metabolic factors, including
obesity, pe1ipheral insulin resistance, and

FOOT CARE
hype1insulinemia. Strategies to reduce the
risk of laminitis focus on limiting the intake

Hoof care is essential for good mobility and
of nonstructural carbohydrates such as
comfort of the horse. "No hoof, no horse" is fructans from pasture and other feedstuffs.

a common expression as true today as it

Horses and ponies with a history of
was 200 yr ago. Proper trimming at regular
recurrent laminitis should have limited
intervals will result in good hoof and leg
pasture access during periods of rapid grass
balance. Conditions such as hoof cracks,
growth, such as sp1ing and early summer.

thrush, and white line disease can be

Nonstructural carbohydrate content also
recognized early and treated properly. All
tends to increase during the morning,
horse owners should learn to recognize the
rPaches maximal values in the afternoon,
initial signs of laminitis so that treatment
and then declines overnight. Therefore,
can be started as soon as possible. In young
a popular recommendation is to turn
foals, weanlings, and yearlings, frequent

"susceptible" individuals out on pastw·e
hoof trimming will assure proper weight
overnight or during the early morning and to bearing and bone alignment. A balanced remove them from pasture by mid-morning.

foot early in a horse's life will also help to

Stemmy, mature pastures should be
avoid potential lan1eness and alleviate
avoided, because mature grasses may
iqjuries later in life. For a horse to perform
contain more fructans. Turning susceptible
to the best of its ability, it must be sound
individuals onto pasture that has been

(free from pain). Soundness is an aspect of
exposed to low temperatures in coajunction health and is more than the absence of lamewith bright sunlight ( eg, as in the fall after a ness. A sound horse can better meet the
flush of growth followed by cool sunny
demands of physical and mental activity.

clays) should be avoided, because colder

(See also LAMENESS IN HORSES, p 1096.) temperatures reduce grass growth and
result in concentration of the fructan.

DENTAL CARE

U feeding forage, lush legume hays should
be avoided, because they tend to have

Regular dental care is essential for the
higher nonstructural carbohydrate content.

comfort and longevity of the horse. The

Soaking hay before feeding may help reduce upper jaw of the horse is wider than the the amount of fructans being fed. Grain and
lower jaw, which results in very efficient
sweet feeds should be avoided.

crushing of food particles. The chewing

The terms mature, senior, and ge1iatric
surface of the teeth are at an angle of 10-15
refer to horses that have completed their
degrees to each other. The grinding action of
growth cycle. However, because aging is a
the molar teeth tend to produce sharp points
continuous process, there is no discrete age
on the outside of the upper molars and on
range for each category. Improved methods
the lingual aspect of the lower molars.

of overall care, management, and diet have

Floating to balance the arcade is rPquired for
enabled horses to live into their 20s or 30s.

general maintenance of the horse's teeth.

This increased longevity means they are

Irregularities are most common in the
used in a variety of leisure or competitive
incisor and molar teeth of mature and
activities well into their teens or 20s. Good
geriatiic horses. The mouth of the horse
management of still-active older horses
changes throughout life, but the greatest
means recognition and evaluation of
changes occur from ages 2-5; therefore,
conditions that occur with age ( eg, arthritis,
semiannual or annual treatment is imporhyperadrenocorticism, gastric ulcers, tant. Sharp points and w1even wear can
laminitis, navicular disease, kidney or liver
cause problems not initially considered to be
dysfunction), followed by therapeutic
tooth related; eg, the horse may be prone to
management and special dietary consideramouth ulcers, choke, gastlic ulcers, back tions. Horses with arthritis require a
pain, or erratic head carriage when the bit is

2156

HEALTH-MANAGEMENT INTERACTION: HORSES
in the mouth. Behavior problems may be a
ble for diarrhea, intestinal in1pactions or
result of long, sharp teeth, an w1even arcade,
irritation (colic), and poor performance. The
or abscesses in the teeth or gwns. Complete
result can be slow growth in yow1g horses,
oral exanlination, including visualization of
poor perforn1ance, acute bouts of colic, and
the premolars and molars, requires sedation,
death in severe instances. The migrating

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a speculwn, and good lighting. Motorized
asca.rids (Parascaris equmwn) are the
dental instnunents and carbide float blades
p1irnary cause of pulmonary inflammation
have made equine dental care more precise
and intestinal rupture in foals and weanlings.

as well as more comfortable for the horse.

The control oflarge strongyles with inlproved

Age determination of horses has traditionanthelmintics has allowed the small ally been done by examining the incisor
strongyles ( cyathostomes) to become a
arcade. Although not an exact science, it is a
greater problem. Reports of tapewonns
useful tool for those with experience. (See
have also increased.

also DENTISTRY IN I.ARGE ANIMALS, p 175.) The three methods of diagnosis of
parasites are direct examination of feces,

PARASITE CONTROL
concentrations of wonn eggs by flotation,
and culture of feces for infective larva. The

Control of internal parasites is a cornerdirect exanlina.tion metl10d is quick but not stone of equine management and a
always accurate. The flotation metl10d for
continual endeavor. Control progran1s
parasite egg concentration is more accurate
should be tailored to each farm situation
to deternline tl1e type and nwnber of
and require a cooperative program between
parasites. The culture method is more
the horse owner and the veterinarian. The
suitable for laboratory use and research
principal internal parasites of horses are
pwposes. The effectiveness of any parasite
nematodes. Unfortwlately, many species
control program can be evaluated by fecal
of adult cyathostomes have developed
examination. The fecal examination should
resistance to standard doses of the
be done before administration of a particular
benzinlidazoles and the tetrallydropy:iimidewormer and tl1en again 14 days later. The dines. Among intensively managed horse
an10unt of decreases in egg population
populations, treatment with macrocyclic
will determine tl1e effectiveness of the
lactones (eg, ivermectin, moxidectin) does
deworn1er. Parasite egg cmmts that remain
not suppress strongyle egg counts for as
high after use of a particular dewormer
long as previously expected. Among foals,
indicate the presence of resistance and a
weanlings, and even yearlings, there are
need to change the control program.

increasing reports of ascarids becoming

The three major classes of anthelmintics
resistant to ivern1ectin and moxidectin.

available for parasite control in horses are

(See also GASTROINTESTINAL PARASITES OF HORSES, the avermectins, benzinlidazoles, and p 315, and ANTHELMINTICS, p 2637.)

py:i·antels. The avem1ectins have a broad

A program of anthelmintic resistance
range of activity, are safe and effective at
involves multiple parasites and multiple
low doses, and control adult and migrating
drug classes, and must consider horses of
larval nematodes. Dewornling of mares
all ages. No single parasite control progran1
inm1ediately after foaling lessens the foal's
is ideal for all horses. Age of the horse,
exposw·e to parasites in the mare's manure.

population density, region of the country,

Avermectins are not effective against
climate, method of confinement ( eg, stall
tapeworms; however, the combination of
or pasture), and pasture size and quality
ivermectin with praziquantel is effective
can affect the choice of parasite control
against tapewonns as well as large and
programs. As horses age, they develop
small strongyles, a.sea.rids, pin worms, ar1d
resistance to reinfection with certain
bots. The benzinlidazoles ( oxibendazole,
parasites, such as Strongyloides westeti
fenbendazole, and ox.fendazole) are
and Pa.rascaiis equ01um. Resistance to
effective against most nematodes but not
most strongyles is incomplete. Although
against encysted small strongyles or
anthelmintics a.re the primary method of
tapewonns. The pyrantels ar·e effective
parasite control, other factors such as
against large and small strongyles, ascarids,
pasture management and stable environand pinwonns. Pyrantels kill nematode ment are also important.

parasites slowly. Pyrantel is available as a

The parasites of greatest concern in
paste (single dose), ar1d as a tartrate salt
horses are large strongyles, small stronthat can be used as a daily dewormer mixed gyles, roundworms, pinwonns, stomach
in the feed; it is effective against tapewo1ms
bots, and tapeworn1s. GI parasites can
but not bots. The avermectins ar·e effective
cause acute medical problems as well as
against bot larva and are recommended in
chronic debilitation. They may be responsi-
the fall after tl1e botfly season.

HEALTH-MANAGEMENT INTERACTION: HORSES

2157

A fourth class of anthelmintics, the

9) Clean water sources regularly to prevent
isoquinolines, contains praziquantel, a
fecal contanlination. 10) Quru·antine new
narrow-spectrum drug approved for horses
arrivals ru1d peiform fecal exruilinations.

as a cestocide. Praziquantel is available in

Use a larvicidal treatment before turning
combination with either ivern1ectin or
out new anivals on pastures. 11) Use fecal

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moxiclectin.

egg cotmts, pe1formecl at the proper times,

To slow the development of drug-resistant to identify ru1cl m011itor !ugh, mediun1, ru1d parasites, the focus of most parasite control
low strongyle egg shedders, to monitor tl1e
programs is to reduce selection pressure for
efficacy of ru1thelmintics being used, and to
resistance by customizing deworming
evaluate new arrivals. 12) Compost mru1 ure.

protocols for the farm and individual

Properly composted mrurnre will kill
horses. This strategy includes identifying
strongyle lruvae and many ascaiid eggs.

horses most susceptible to parasites (ie, the
high egg shredders) and maximizing refugia

VACCINATION PROGRAM

(those parasites not exposed to drug
selection pressure) by reducing the overall

The goal of vaccination is to develop and
number of anthelmintic treatments
maintain both individual and herd immw1ity
administered and by monitoring the efficacy against infectious diseases. Commercial of different classes of deworn1ers using the
vaccines are available for rabies, encephalofecal egg count reduction test. An effective myelitis (Eastern, Western, and Venezueclewomiing protocol for horses should lan), tetanus, influenza, equine
incorporate a cestocide ( eg, a praziquantelherpesviruses 1 and 4, bottilism, equine containing product or a double close of
ehrlichiosis (Potomac horse fever), equine
pyrantel pamoate) and a boticide ( eg,
viral arteritis, rotavirus, West Nile virus, and
ivermectin or moxiclectin) once or twice

Streptococcus equi (strruigles). Vaccination a year to control tapeworms and bots,
programs are fonnulated based on the
respectively, and a larviciclal dose of
animal's age, use, and level of exposure.

ru1thelmintic effective against encysted

Broodmru·e vaccination is in1portant to
cyanthostomes (eg, fenbenclazole 10 mg/kg/
provide active in1mW1ity for the mare and
clay, PO, for 5 days, or a single dose of
passive immunity for the foal via transfer of
moxiclectin) during early winter months in
colostral antibodies. Vaccination guidelines
northern clin1ates or during early surnrner
for foals have been modified because of the
in warmer clin1ates. Foals should be
interference of maternal antibodies with the
maintained on a regular dewornling
initial vaccination response. Sources such
schedule every 60 clays that includes
as the An1erican Association of Equine Pracru1thelmintics safe and effective against titioners cai1 provide the most cwTent
ascarids. Treatments effective against
equine vaccination reconunendations for
other nematodes (including encysted
horses in the USA.

cyathostomes) ruicl cestodes should be

The following vaccination reconu11enincluded in the dewornling protocols for clations asswne that foals are born to
foals during the fiJst year of life.

vaccinated mares and have absorbed

Effective deworn1ing progrrui1s should
adequate colostral antibodies with IgG
also include one or more of the following
levels >800 mg/cIL.

nonchemical methods of parasite control:

Foals with failure of passive antibody

1) Avoid overstocking and overgrazing
transfer (ie, IgG levels <200 mg/dL) ru1d/or
pastures. 2) Keep pasture roughs mowed to
foals born to unvaccinated mares can
a height of 3-8 in. 3) During hot, dry weather,
receive their initial vaccination for equine
hruTow or rake pastures to disperse manure
herpesvirus 1 and 4, tetanus, and Eastern
piles ru1d e}q:>ose lruvae to sun. Rest the
and Western equine encephalomyelitis
pasture at least 3-4 wk after hruTowing.

beginning at 3-4 mo of age, followed by a

4) Cross-graze pastures with other species.

second dose 4-6 wk later ru1d a third dose

Cattle, sheep, and goats se1ve as biological
at l 0-12 mo of age. These foals can receive
vacuums for equine parasites. 5) Make at
tl1eir fiJst dose of rabies vaccine at 3-4 mo
least one cutting of hay off some pastures to
of age, followed by a booster at 12 mo.

help reduce the pru-asite burden. 6) Plant an

Influenza vaccination can be started at 6 mo
annual crop such as winter wheat. 7) Feed
of age. Foals born to mares that have never
hay and grain in raised containers ru1d not
been exposed to or vaccinated against West
directly on the ground. 8) Remove manure

Nile virus cru1 receive their fast vaccination
from stalls, paclclocks, and pastures eve1y
at 3-5 mo of age.

24-72 hr before strongyle eggs have a
chance to hatch and develop into infective

Tetanus: Clostridium tetani is present in lruvae (5-7 days during optin1al conditions).

all pruts of tl1e world. Tetanus occurs most

2158

HEALTH-MANAGEMENT INTERACTION: HORSES
commonly when wounds become

Venezuelan equine encephalitis (VEE)

contaminated with the organism from the
virus causes outbreaks of disease in horses
soil. Vaccination is recommended for all
in Mexico, Central and South America, and
horses and ponies on an annual basis. A
occasionally the southern USA. The VEE
horse with an unknown vaccination status
vaccine is a single vaccine or in combina

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that sustains an injury should receive a dose
tion with EEE and WEE. Its need is limited
of tetanus antitoxin along with a dose of
to those horses traveling to or located in
tetanus toxoid. A second dose of toxoid
endemic areas.

should be given 4 wk later. Foals from

West Nile virus (WNV) disease is
vaccinated mares should be given a
considered a zoonotic disease similar to the
three-dose series at 6, 7, and 9 mo of age.

encephalitis viruses. The bird population

Foals from unvaccinated mares should
allows for maintenance of the virus, which
receive tetanus toxoid at 3, 4, and 6 mo
is then transmitted by mosquitoes to both
of age. Whenever a vaccinated horse
people and horses. There is very little risk of
experiences a serious wound, a tetanus
disease from any infected horses. Vaccinabooster may be indicated.

tion protocols for broodmares, foals, and
adult horses are the same as those for

Equine Herpesvirus 1 and 4 (Rhino

Eastern and Western encephalitis.

pneumonitis): Two types of equine

Combination vaccines that include EEE,
herpesviruses vaccine are available, EHV-1

WEE, and WNV are available.

and EHV-4. The EHV-1 virus is the primary
cause of abortion and neurologic disease

Influenza: lniluenza is one of the most
in horses. The EHV-4 virus is the primary
frequent causes of viral respiratory disease
cause of respiratory infections, especially in
in horses and is highly contagious among
young horses. The control of rhinopneun10-
susceptible horses. Therefore, vaccination
nitis is by a combination of vaccination and
is reconunended for all foals, broodmares,
good management practices. To prevent
and horses at risk of exposure, usually as a
abortion, a killed EHV-1 vaccine should be
result of showing, racing, or shipping. Young
administered to pregnant mares at 3, 5, 7,
foals from vaccinated mares, because of
and 9 mo of gestation. Respiratory disease is maternal antibodies, should be vaccinated best prevented using a combination vaccine
at 9, 10, and 12 mo of age. Foals from
of EHV-1 and EHV-4. There is no evidence
tmvaccinated mares should be vaccinated
that vaccination protects against the
earlier. The intranasal vaccine can be used
nemologic form of the disease. Vaccine
every 6 mo in young, susceptible petiorreconunendations for foals are three doses rnance horses 2--4 yr old. A vaccination is
every 4 wk sta.Iting at 6 mo of age, and a
reconunended every 6 mo for horses
booster at 1 yr of age. Pleasme and
exposed to other horses at equine events.

perfonnance horses should be vaccinated
every 3-6 mo, depending on the risk of

Rabies: Signs of rabies include the
exposme. Broodmares should have an
inability to eat or drink, disorientation, and

EHV-4 vaccination 2--4 wk before foaling
incoordination. Rabies is fatal, and also
to ensme the availability of colostral
poses a health risk to those who handle
immunity.

infected horses. Prevention in horses is
primarily via vaccination. Broodmares

Encephalitis: Eastern equine encephalitis should be vaccinated 4-6 wk before foaling.

(EEE) virus has a wide distribution. This

Foals from vaccinated mares should be
includes the eastern USA, Central and South vaccinated at 6 and 7 mo of age and again America, and eastern Canada. In the USA,
at 12 mo of age. Foals from tmvaccinated

EEE is seen primarily in the southeastern
mares should be vaccinated at 3, 4, and 12
states but has been reported in all states
mo of age. All adult horses should be
east of the Mississippi River. EEE in horses
vaccinated armually.

is nearly always fatal regardless of
treatment. Infected horses usually become

Potomac Horse Fever: Potomac horse
comatose, seizure, and die in 36--48 lu·.

fever ( equine monocytic ehrlichiosis, equine

The virus of Western equine encephalitis
ehrlichial colitis) is caused by Ne01ickeUsia

(WEE) is primarily located in the western
ristiC'ii. Vaccination is reconunended in

USA. In recent years, reports of WEE have
endemic areas, such as near freshwater
not been conunon, probably as a result of
strean1s, rivers, ponds, and heavily irrigated
adequate vaccination programs. The virus
pastures. Annual boosters in the spring are
is not as pathogenic as EEE, and animals
recommended. Pregnant mares should
infected with WEE have a greater chance
receive a booster before foaling. Although
of survival. Mortality is usually 500/o.

the vaccine may lessen the in1pact of the

HEALTH-MANAGEMENT INTERACTION: HORSES

2159
disease, it appears not to prevent abortion
anemia. Once infected, a horse can become
in pregnant mares.

a canier for life and is a threat to other
horses. The virus is transmitted by

Botulism: Equine botulism is mostly seen
bloodsucking insects. Cun-ently, the disease
in the Mid-Atlantic area of the United States,
is w1comrnon, and most horse owners are

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but the disease has also been reported
aware of its dire consequences. A simple
worldwide. In the USA, the most common
blood test, the Coggins test, is available to
types are Band C botulism, although type A
detect infected horses. A horse that tests
has been reported in the western USA. The
positive cannot cross state lines and is
spores of Colostridium botulinum are
required to be maintained in st1ict isolation
found in the soil and are resistant to light,
for life. For horses participating in equine
drying, and heat. The Type B vaccine gives
activities or being transported across state
good protection in adult horses. Adult
lines, proof of a negative Coggins test is
horses and broodmares in areas where
required. Annual testing of every horse is
botulism is a potential hazard should
recommended. No vaccine is available.

receive initially three doses at 30-day
intervals and then annual boosters. Foals
from vaccinated mares in endemic areas

PERINATAL MARE AND FOAL
should be vaccinated at 2, 3, and 4 mo of

CARE
age, because colostral immunity does not
always occur. Foals from unvaccinated

Pregnant mares need adequate daily
mares should be vaccinated at 2, 4, and 8 wk
exercise in a paddock or pasture, and any
of age. The use of Type B vaccine in areas
horses kept together should be compatible,
where Type C occurs has uncertain results.

which helps to reduce stress. Vaccinations
and deworniing should be done before the

Streptococcus equi Infection: Strepto
mare is bred, with no vaccinations given
coccus equi infection ( equine strangles,
during the first 90 days of gestation. In
equine distemper) can be highly contagious.

general, except for rhinopneumonitis and

Use of the IM or intranasal vaccine is
possibly botulism, all vaccinations should
recommended only in those situations or
be avoided unW 30 days before foaling.

on premises where the disease has been a

Thirty days before foaling, the mare should
problem. The IM vaccine involves three
receive vaccinalions for Eastern, Western,
injections administered 2-4 wk apart,
and West Nile encephalitis, as well as for
starting at 4 mo of age in foals, with a
tetanus.

booster at 12 mo of age. If the intranasal

For the first 7 or 8 mo of gestation, the
vaccine is used, vaccination can begin at 6-9 routine diet of pasture or hay and concenmo of age, with a second dose given 3-4 wk trate to maintain good body condition is all
later and a third dose administered at 12 mo
that is necessary. Mares too thin at foaling
of age. Adult horses, if in potential disease
will not milk well, and mares too fat are
situations, should receive an annual
subject to developing larninitis or have
vaccination. Broodmares on endemic farms
foaling difficulties. During tl1e last 3 mo of
should receive an annual booster using the
gestation, the mare should be on a gradual,

IM vaccine 4-6 wk before foaling. Because
increasing plane of nutrition. The size of the
of the increased risk of inducing immunefetus increases significantly during the last mediated pul])ura hemon-hagica, horses
trimester, and the mare's weight can be
with titers to the SeM surface protein of
expected to increase. During this time, the

S equi in excess of 1: 1,600 may not need
mare should be on good-quality legume or
to be vaccinated.

grass hay and a concentrate ration of

12%--14% protein. A mare weighing

Rotavirus: Foal dian-hea as a result of
l,OOO-l,200 pounds (454-544 kg) can be
rotavirus infection can be a severe problem
expected to gain 150-200 pounds during the
on some breeding farms. Single cases or a
last trimester with the proper diet. A body
farm outbreak can occur. Therefore,
condition score of 6.5-7.5 is ideal for most
pregnant mares should be vaccinated IM
pregnant mares at foaling.

at 8, 9, and 10 mo of gestation. This will

The mare should be checked for the
increase the amount of colostral immunopresence of a Caslick's operation of the globulins. It is a vaccine for use in particular
vulva, which should be opened if present.

situations or areas of high endemicity.

The foaling process is continuous, with
labor divided into three stages. Stage 1 may

Equine Infectious Anemia: In the acute
be 1-4 hr as uterine contractions increase in
state, equine infectious anemia (swamp
strength and frequency. Stage 2 is the actual
fever) causes severe RBC destruction and
delivery of the foal, which takes 5-15 min

2160

HEALTH-MANAGEMENT INTERACTION: HORSES
unless there are complications. Stage 3 is
water, or a commercial sodium-phosphate
the passage of the fetal membranes, which
enema can be used once). Many foals will
should occur within a 3-hr period. If the
not nurse satisfactorily or with vigor unill
membranes are retained for >3 hr, then

U1e meconium has passed.

vete1inary treatment is necessary because

Foals have no immunity at birth and
severe sepsis or laminitis can result. Some
acquire it Ulrough ingestion of colostrum.

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mares may exhibit abdominal pain after

Absorption of colostral antibodies occurs
foaling, and low-dose analgesics may be
wiUlin tile first 24 hr of life. Ideally, when
helpful. The normal placenta will weigh

-12 hr old, tile foal should have a complete

-10-12 pounds (4.5-5.4 kg) or -10% of the
veterinary physical exanlination, including
foal's birU1 weight.

temperature, heart and lung auscultation,

The mare should be dewormed within
and exanlination for cleft palate, fractured

48 hr after foaling to reduce exposure of the
ribs, or entropion. Evaluation of the foal's
foal to parasites. In 90% of foalings, U1e

IgG level is most important. If U1e foal's
newborn foal is usually sternal within l hr,
serum level is <800 mg/dL, an IV transfusion
stands wiLllin 2 hr, and nurses within 3 hr.

of plasma is necessary.

The foaling stall should be at least 14 x 14

Foals should be monitored closely during
feet ( 4.3 x 4. 3 m); a double stall 12 x 20 feet
the first 7 days of life. A healtily foal can

(3. 7 x 6.1 m) is more satisfactory. The stall
become critically ill in a matter of hours.

should be bedded with traw or short stem

The mare and foal should remain in the box
hay. Wood shavings are less desirable
stall for 24---48 hr unill U1e foal is strong
because ofU1e possibility of the shavings
enough to follow tile mare at a trot or gallop.

ente1ing the foal's nostrils or mouU1 and also Then tile pair can be turned out in a small contaminating tile mare's birth canal. The
area for exercise, which is essential.

newborn foal's umbilicus should be dipped

Haltering and handling tile foal during U1e
in a dilute solution of chlorhexicline (0.5%)

fast week of life will set the stage for the
or povidone-iodine (1%) several times a day
animal's behavior in the future. Mares that
for 2-3 days.

reject U1ei.r foals usually do so right after

The passage of meconium can be
birth. This is more common in primipa.rous
facilitated by use of an enema (wan11 soapy
mares and requires intense supe1vision.

H EALTH-MANAG EM ENT

INTERACTION: PIGS

Disease in pork production is generally
management. Pigs are omnivores extremely
caused by multiple factors. Microbial
well suited to convert low-cost feedstuffs
patilogens are rarely tile sole cause-of a

(often including waste products) into meat.

healU1 problem on a pig farm. Clinical

Pigs efficiently convert feed to muscle while
disease is usually tile interaction of a
growing at a rapid rate. In addition, tileir
pathogen with en-ors in management and
fecunclity is remarkable. Female pigs reach

.

a variety of contributing influences such
sexual matuiity, breed, and produce a litter
as envirorunent and host factors. Many
of�lO piglets at -1 year of age and U1en
paU10gens are endemic in tile swine
continue to produce litters 2. 5 tin1es per year.

population and yet some farms suffer heavy

I lealth management plays a key role in
losses from disease, whereas tile impact on
profitable fam1ing enterprises. Profit is
other fanns is much less because of
based on maxin1izing income and minimizmanagement differences.

ing costs. Income is a function of tile price
received per kg of pork produced ti.mes the

Management and Economic Consid
total amount of pork produced. Therefore,
erations: Economic considerations
aspects of healtil management that ensure
influence all decisions regarding healU1 care
good reproductive perfonnance and
on pig farms. HealU1 management and
consistent pig numbers at all stages of
clisease prevention programs tend to be
production and rapid growth cont1ibute
ptioritized based on financial return,
to a steady, high income. Production
altilough 0U1er important considerations
parameters, such as pigs produced per
include animal welfare, food safety, and 1isk
sow per year and measures of tllroughput,

HEALTH-MANAGEMENT INTERACTION: PIGS

2161
should be carefully monitored to ensure the

(sows bred but failing to faiTow; generally
farm is achieving a high level of productiv80%--85% is achievable) or it may be because ity. At the same time, production costs
of prebreeding problems such as a long
must be evaluated to assess the health or
weaning-to-breeding interval ( <7 days is
profitability of a swine operation. Because
typical). A low number of litters per sow per

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feed costs are well over half the cost of
year will probably lead the herd veterinarian
production, health management initiatives
to investigate the breeding management; in
to reduce feed costs or improve feed
contrast, if litters per sow per yeai- is close
efficiency tend to be areas of high priority.

to 2.5 but pigs weaned per sow per year is

Some of the most economically important
low, the veterinariai1 can begin to investiswine diseases may present with little in the gate the farrowing room to detemline why
way of clinical signs. For example, porcine
litter size at weaning is low (10 pigs per litter
proliferative enteropathy (Lawsonia
is commonly achieved, but this nwnber is
intracellularis infection, see p 299) might increasing because of lai·ger litter sizes
cause thickening of the bowel and reduced
being born). The cause of low nwnbers
feed efficiency without signs of diarrhea or
weaned may be because of small litters
obvious illness, but the cost of the resulting
being born or a high preweaning mo1tality.

increase in feed consumption likely makes

Record analysis can be used to focus
this disease a high p1iority with regard to a
attention so that resources can be
healtl1 management program. Cost-benefit
concentrated on solving a specific problem.

of progran1s should be evaluated to avoid

In the post-weailing until market period, the
spending so much to reduce the tisk of
main production records include mortality,
tl1e disease that it outweighs the benefits
growth rate, and feed efficiency. Because
in improved perforn1ance. Therefore,
feed cost contributes substantially to the
a producer might choose to ignore a
cost of producing a market hog, measuring
management protocol directed at disease
feed conswnption and monitoring feed
control to save money longterm; however,
costs are extremely important. During the
this decision may change with time and
early growing period, pigs are extremely
circumstances, so medication and vaccine
efficient in using feed to produce muscle.

programs, for exan1ple, should be con

Feed:gain ratios of 1.5: 1 or better are
stantly assessed.

expected during the nursery phase (3-10
wk of age). As the pig approaches market

Production Records: The use of
age, metabolism changes and the pig begins
production records is an essential part of a
to produce more fat, which shifts the
herd healtl1 program. Records are used to
feed:gain ratio so tlrnt >3 kg of feed is
assess perfonnance and identify areas of
needed to produce 1 kg of gain. Overall
concern. When a general issue is identified,
through the grower-finisher phase, most
records also can be used to help pinpoint
herds achieve a feed:gain ratio of better
the problem as well as assess whether tl1e
than 3: 1. Mortality records throughout the
intervention strategy was successful.

production stage are possibly the most

Records can be used to set targets and
useful parameter to identify a health
motivate staff to achieve these targets as
problem. In general, preweaning mortality
well as help tl1e veterinarian develop paitial
of<! 10% can be achieved on most fai1ns,
budget scenarios to justify health care
with nursery mortality of SoAi--4% and
expenses.

grower-finisher mortality of 2%--3%

In breeding herds, the pai·aineter most
achievable.

commonly used to assess overall herd
petformance is average munber of pigs

Herd Size and Disease Challenge: As
weaned per sow per year. On many Notth
in most agticultural businesses, pig farming

American farms, this number is <!25; some
has an economy of scale; hence, pig fanns
producers achieve a number >30. When this
have grown larger and larger over the past
number is lower than the target, it is useful
few decades, with a trend toward vertical
to exainine tl1e specific components of the
integration in the industry. The management
paran1eter to determine the source of the
of health issues in large populations requires
problem. Pigs weaned per sow per year is a
a major focus on biosecurity ( see p 2068).

product of "pigs weaned per sow per litter"

Great efforts are warranted to keep new
and "number of litters per sow per year."

diseases from entering an inm1unologically

With a 3-wk lactation, it is possible to
naive population, in addition to prograins
achieve --2.5 litters per sow per year. If tlle
to restrict the spread of endemic diseases
number of litters per sow per year is low, it
within the herd and especially between one
may be because of a poor farrowing rate
production stage and another. The general

2162

HEALTH-MANAGEMENT INTERACTION: PIGS
strategy to prevent outbreaks of clinical
animals is likely to act as a reservoir for
disease is to minimize the level of pathogen
endemic diseases. This is particularly true
challenge while maximizing herd and
for viral diseases for which vaccination is
individual immunity. Poor management
not very effective. For example, it is a

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might result in a population of pigs with
common practice to purposely infect all
naive inunune systems encounte1ing
sows in a herd with porcihe reproductive
novel pathogens, or in stress leading to a
and respiratory syndrome (PRRS) virus (see
weakened immune system in vulnerable
p 729) using a live field strain of the virus
pigs. Alternatively, management errors
and at the same time closing the herd to new
might result in an ove1whelming pathogen
introduction if the herd is experiencing an
challenge in the case of an endemic disease
outbreak of PRRS. The goal of such a
or the entry of a new pathogen into a
program is to expose all the sows to the
population of pigs without specific

PRRS vims so that the entire herd develops
imnumity.

inunmtity. When all the sows are immune,

One of the most effective management
they will pass antibodies and not the vims in
techniques to minimize the challenge from
colostrum to the piglets. In this way, PRRS
endemic diseases and possibly to eliminate
can be eliminated from the herd.

a disease from a swine operation is the use
of all-in/all-out pig flow through the various

Health Strategies: Health strategies can
production stages. Commonly a group of
be divided into three categories. First, there
sows are moved together into a clean and
are strategies designed to live with endemic
disinfected farrowing room, and later their
diseases. Generally, these are caused by
piglets are weaned and the sows moved out
pathogens that sm'Vive in the environment
as a group; all the weanling pigs enter a
and are too difficult to elintinate, or they are
clean, empty nursery possibly on a separate
ubiquitous orgarusms that generally cause
site from the sow herd. Similarly, the pigs
little problem. The fom1er are handled by
leave the nursery as a group and enter a
maxintizing inunuruty and minintizing the
clean, empty grower-finisher barn, possibly
challenge, as outlined above. In the latter,
at a different site. This type of flow reduces
disease flare-ups are often triggered by
the chance of endemic disease continuing to environmental-management deficiencies, cycle in the population.

which if corrected will restore the healthy

In summary, many pig diseases are
state in the herd. Second, some pathogens
controlled by this combined strategy of
can be eliminated. For example, Sarcoptes
minimizing disease challenge and maximiz
scabiei var suis can be eliminated from a ing individual and herd inunuruty. For
herd using the strategic adntirustration of
example, the conunon methods used to
agents such as iverrnectin and doran1ectin.

prevent neonatal diarrhea caused by

Alternatively, diseases such as transmissible
enterotoxigenic Escherichia coli (ETEC)

gastroenteritis and PRRS can be eliminated
include all-in/all-out farrowing room
from a herd by closing the herd to new
management, the use of slatted flooring
introductions and purposely exposing all
constructed of nonporous material that is
animals to the disease to create herd
easily cleaned, and washing and disinfecimmunity. It is usually desirable in the tion protocols to ensure minimal bacte,ia
longtenn to eliminate the diseases, if
will be present in the environment to
possible and if it results in savings from
challenge the newborn piglets. At the same
reduced routine medication or vaccination.

time, it is common practice to vaccinate the

Third, there ru·e strategies to prevent
sows against ETEC before farrowing so
pathogens from entering the herd. As
they have high levels of specific immunoherd size has increased, the emphasis in globulins present in colostrum and milk to
maintaining the population of animals
provide passive immuruty to the piglets. In
free of ce1tain diseases has increased in
addition, it is necessary to ensure the piglets
importance. Some key components of a
receive these immunoglobulins, so steps
biosecmity progran1 include careful
such as cross-fostering are important.

management of replacement stock with

Disease can occur if either the challenge
quru·antine and monitoring; preventing
becomes too great or the inunune protecentry of rodents, birds, and other animals; tion waivers, so both approaches are
precautions to prevent disease transfer
important and complementary.

from trucks and fontites; and the rest1icted

Because herd size is often very large,
entry of people (See also BIOSECURJTY, 2068).

ensuring that the population as a whole has
immunity and that pockets of naive animals

Vaccination and Disease Status:

are not present within the herd can be a

Vaccination is a key health management
challenge. A subpopulation of susceptible
tool to enhance individual and herd

HEALTH-MANAGEMENT INTERACTION: PIGS

2163
immunity. Commercial vaccines are

The presence of coughing and sneezing
available for most of the important swine
might prompt fwther investigation of
diseases, and when commercial vaccines
respiratory diseases. It is common practice
are not available, autogenous vaccine may
to euthanize and conduct postmortem

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be a possibility. Generally, only a small
exantinations on untllrifty pigs to screen for
number of vaccines are used in most herds.

the presence of diseases such as enzootic

The decision to use a vaccine depends on a
pneumonia or ileitis. Analysis of blood or
nw11ber of factors and needs to be assessed
oral fluid from a representative sample of
and frequently reassessed on an individual
animals to monitor for disease is an imporherd basis. To use all of the available tant part of herd health evaluations. In
vaccines would be cost prohibitive. Criteria
addition, production records and drug use
used to decide which vaccines to incorporecords can help to assess health status.

rate into a herd vaccination program

Another information source may be abattoir
include cost (including labor) and efficacy
reports, or if possible following pigs through
of the vaccine, cost of the disease or
the slaughterhouse floor and assessing
possibly the risk of the disease occurring
lesions such as milk spots on liver that
in the herd, and availability of alternative
indicate roundworm migration.

measures that might be more useful than
vaccination. On many fam1s, gilts and

Herd Visit and Facility Inspection:

sows are vaccinated before breeding to

The herd visit is also important to deterprotect from reproductive failure caused mine possible housing-environmentalby Leptospira sp, E1ysipelothrix 1·husi
managemcnt shortcomings. Aninlal
opathiae, and parvovirus infection. It is
inspection may reveal signs of stress or
also common practice on many fam1s to
mismanagement affecting animal welfare
vaccinate sows during gestation with an
and productivity. Behavioral vices such as
enterotoxigenic E coli vaccine to boost
tail biting may indicate underlying
antibodies in the colostnm1 and milk to
environmental problems such as crowding,
protect piglets from diarrhea via passive
or insufficient resources such as waterers
in1m unity. Co nun on vaccines given to
or feeding space. A facility inspection
weaned pigs include porcine circovirns and
should spot damaged penning and flooring

Mycoplasma hyopneumoniae. Several
that could lead to injury. Air quality, room
other vaccines warrant in1portant consideratemperature, and presence of drafts can all tion for most farms, including L in tracellu
be assessed. Stocking density is possibly
laris, swine influenza virus, and PRRS vims.

the most obvious potential stressor that

The decision to vaccinate for a particular
should be investigated during a herd visit.

pathogen or develop specific control

Published guidelines for space requirestrategies sometimes depends on whether ments are being used more and more in
the disease is present on the fam1. Knowing
animal welfare audits. Space requirements
the disease status of a herd is an important

(see TABLE 6) vary according to age and consideration for a number of reasons. For
weight of pigs as well as for flooring type
example, it is critical if two sources of pigs
and other considerations such as season,
need to be mixed or sources of replacement
ventilation or cooling systems, and group
stock need to be chosen. To know what
size. Investigation of disease outbreaks
diseases are present in a herd, monitoring
may require a team approach, with a
needs to be regularly performed and
veterinarian interacting with experts in
multiple sources of infom1ation incorponutrition, building design or engineering, rated into the assessment. On herd visits,
and other fields to determine the triggering
animal inspection can identify clinical signs
factors. The longtem1 solution to a disease
of disease. Pigs that are scratching may cast
problem often depends on a change in
suspicion that mange is present in the herd.

management.

itM•il SPACE RECOMMENDATIONS FOR GROWING PIGS

Production Stage

Body Weight

Space Allowance

Nursery

Weaning to 27 kg (30 lb)

0.16-0.23 m2 (l.7-2.5 ft2)

Grower

27-68 kg (30-100 lb)

0.28---0.56 m2 (3-6 ft2)

Finisher

68 kg (150 lb) to market wt 0.74-0.84 m2 (8---9 ft2) Adapted from Zinunerman JJ, et al (eds), Diseases of Swine, 10th ed. 2012.

2164

HEALTH-MANAGEMENT INTERACTION: SHEEP

HEALTH-MANAGEMENT

INTERACTION: SHEEP

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Sheep and goats were first domesticated
predation from coyotes, wild ca.ts, bears,
around 8,000 BC, making them the first of
wild pigs, wolves, dingos, etc ( depending on
the domesticated food animals. Sheep are
the country), usually accounts for the major
extremely adaptable and found all over the
losses dming the rest of the year, private
world, particularly in arid areas that do not
practitioners are generally not a pa.it of
support other types of livestock. Because
flock health and management programs
sheep a.re raised in various environments,
in these systems. However, extensive
specific breeds have been developed to
management systems often use governmeet the needs of the environment and ment or university veterinary extension
people. More than 100 breeds have been
education and services where provided.

recorded. Different production systems

Vete1inaria.ns can use a request to solve a
are used in various areas of the world.

cmTent problem from such a producer to

Extensive year-round grazing, with large
also educate and advise on flock health.

flocks(> 1,000 sheep) and minimal sheep

This is more common in extensive grazing
handling, is the typical system of sheep
units in which sheep are confined during the
management where the climate and area to
winter months and so a.re available for
graze allow. Systems in New Zealand, South
handling and exa.inina.tion. Abortion, still

Aftica., and Australia., where forage is
births, weak la.n1bs, and open ewes require
available throughout the year, are prime
accurate diagnosis, and management of
examples of this type of management.

these problems can evolve into develop

Confinement and intensive feeding during
ment of a vaccination progra.n1, breeding
the winter months, with access to range
soundness exa.inina.tions for rains, looking
land pasture for the rest of the year, is a
at mineral and protein supplementation
common system of large sheep flocks in
programs, and other preventive programs.

parts of Europe, the UK, the western USA,

Ba.by la.inb deaths require formal
and other countries that have snow and
diagnostic aid, which can be used to
inclement weather seasonally.

develop preventive progra.n1s for Escheri

Intensively managed smaller flocks can
chia col'i, coccidia., Mannheirnia, white be found around the world, with sheep kept
muscle disease, and navel ill. Starvation
for milking, natural colored wool, purebred
deaths should lead to examining ewe body
breeding stock, sale of lambs for home
condition, preparturient supplementation,
freezer trade, and hobby flocks on small
mastitis control, and lambing management
acreages. Small flocks of breeding stock or
in general.

hobby and pet flocks a.re conm1on in the

Some knowledge of range land nuttimore developed areas of the world, tion, including toxicities a.i1d deficiencies
particularly the USA and Canada.

common to the area, feed costs, labor

Shepherding small flocks of sheep and
problems, and markets, in addition to
goats along roadsides and conunon grazing
knowledge of sheep diseases, is very helpful
areas is a typical management system in the
when giving advice and providing preven

Middle East, Asia, and Mexico.

tive progra.ins and management changes to
extensive grazing producers. The aim is to

EXTENSIVE GRAZING SYSTEMS
increase net fa.m1 income rather than just
control disease. Although the diagnosis,

Veterinary se1vices for sheep are typically
treatment, and control of disease a.i·e
not readily available in the poorer areas of
important, an overall management change
the world unless provided by governments
that will conttibute to longterm profitability
to satisfy exports to other countries. Where
may be far more important. Net income per
veterinary services are available, private
hecta.t·e/a.cre should be the major considerapractitioners a.re mostly called upon by tion of any recommended change.

extensive grazers that confine their sheep

A flock health plan, tailored to the specific
dwing the colder periods of the year for
needs of a. la.i·ge producer, should include: 1)

feeding. Veterina.iia.ns a.i·e often needed to
a good 1nineral/nutritional supplementation
manage lambing problems such as scours/
program ( after detennining any deficiencies);
diarrhea. outbreaks, baby la.nib mortalities,

2) control of external parasites (internal para.and other major disease outbreaks. Because sites may not be a problem on arid ground

HEALTH-MANAGEMENT INTERACTION: SHEEP

2165
but that should be detennined); 3) prevention to perfonn procedures such as vaccinating, of diseases for which cost-effective vaccines
docking/tailing, castrating, and hoof
are available; 4) methods to prevent
trimming as well as to treat sick animals.

introduction of contagious diseases, such as

However, larger producers in many
sore mouth/scab, caseous lymphadenitis,
countries often perform these routine

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footrot, epididymitis/bmcellosis, and Johne
procedures themselves, using veterinarians
disease; and 5) improvement of the number
for such things as cesarean sections and
of lambs weaned per ewe bred, with
help with disease conti-ol.

enhanced ewe and ram fertility and reduced

Wool production is usually a minor
lan1b mortalities (may be related to
concern on the smaller pToduction w1its;
nutritional program).

the nwnber/porn1ds/l<llos of lambs

In most sheep operations, wool is not the
marketed per ewe joinecVbrecl is the major
major source of income, so the economic
determinant of economic retwn. The
outcome from an outbreak of disease or a
greatest potential loss is ca.used by neonatal
serious nut1itional problem is usually
lamb m01tality, resulting from abo1tion,
obvious. However, in operations in which
mismothering, starvation, and hypothernua.

wool is the predominant source of income,

Second to that may be la.ck of growth weight
a moderate parasite burden or nutritional
clue to internal and external parasites,
deficiencies can cause ill-thrift, reduced
protein deficiency, and lack of lughly
kilogran1s of wool shorn per head, and
cligestible and palatable feed for ymmg
reduced fiber dian1eter. The latter outcome
lambs. Intensive management and good
may result in a more valuable fleece and
saiutation at lan1bing will reduce this loss.

thus, no reduction of income. In this

Labor-intensive lan1bing systems; intensive
situation, reduced health of the ewes may
care of yow1g lambs; and diagnosis,
not be obvious. A ewe that does not
treatinent, and occasional surgery of
conceive or aborts in the first 3 mo of
individual sheep may be justified by the
pregnancy will produce more wool than
value of the anin1als. However, preventive
a ewe that rears a lamb, because a ewe
medicine programs are greatly needed in
rearing a lamb has a higher nutiitional
these management situations to prevent the
requirement and produces less wool than a
nwnerous husbandry-related diseases
dry ewe. However, in most places, the p1ice
associated wiili lugher stocking rates.

of lamb, somewhat influenced by pelt price,

Attention to pastoral-related disease is
is worth far more than that of the wool.

importai1t in the summer (ie, internal

In some areas of the world, veterinarians
parasite control) and in ilie winter for
may be able to go beyond a flock health
problems related to closer confinement,
program by developing a comprehensive
winter nutlition, and lan1bing problems.

flock management advisory service. This

In tl1ese types of production situations,
service would adopt a whole fam1 approach
record keeping becomes critically importhat considers the physical and financial tant for improvement. Animals must be
resources of the farm/ranch and the
individually identified so iliat ilie producinteraction of livestock production with tion of each can be monitored. Some
other activities such as cropping and
corn1tries/regions, such as ilie UK, tl1e
pasture production. The stocking rate, type

Europeai1 Union, Austi·alia, Canada, and
of stock nm, timing of husbandry procethe USA mandate individual anin1al dures, marketing strategies, and risk
identification for disease tracking.

management should be reviewed as part of

Lambs should be identified at birili,
the progran1. A financial analysis of the farm usually with a wuque ear tag. The identificaas a business and preparation of fam1
tion number, date of birili, dain, type of birth
budgets and gross margin analyses is a key

(single, twin, etc), sex, and remarks such as
part of most programs. However, this type

"weak," "required help birtlung," etc, are of service has not been readily adopted by
recorded. Recording birth weight is also
producers in most places, and most
desirable. Thus, scales, one approp1iate for
veterinarians do not have the expertise.

baby lambs and anoilier to weigh marketsize lambs, are an important tool to detennine productivity.

SUMMER GRAZING WITH WINTER

Lambs should be weighed again at 50-60

CONFINEMENT (INTENSIVE
days and 100-120 days, which ir1dicates

MANAGEMENT)

some measure of ilie milking ability of ilie
ewe (60-day weight) and genetics of ilie

These types of sheep enterprises tend to use lainb (120-day weight). Comparisons of ilie vete1inary services the most. Smaller
lambs' rate of gain and twinning ai-e two
backyard producers may use veterinarians
measures iliat cai1 ilien be used to cull ilie

2166

HEALTH-MANAGEMENT INTERACTION SHEEP
ewe flock. It often is the thinnest ewe that
with other grazing animals or grazing
turns out to be the best producer, and the
around the fringes of a more productive
fattest ewe the poorest. This is a relatively
cropping or plantation enterprise. This may
basic record keeping system in which other
also be true in the Middle East, or sheep and
criteria can be assessed if desired.

goats may graze poorly productive arid

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In Australia, computer-based programs
areas that will support little else. In either
are used to compare animals within a flock
case, opportunities for major changes to the
as well as to compare flocks with other
management system are linlited.

flocks on the plan. The USA sheep industry
offers a similar plan (the National Sheep

ORGANIC SHEEP PRODUCTION

Improvement Plan), to which any producer
can subscribe.

Public demand is moving animal-based

Feed and labor are always the largest
production toward organic systems. The
annual expense for livestock producers,
standards required to allow an organic label
particularly for winter-fed or intensively
for sheep products, although allegedly
fed sheep and lan1bs. Producers and their
making the product safer for the consumer,
fanlilies usually provide the labor for
do not tend to promote animal health. They
smaller flocks, making feed the largest
prohibit the use of antibiotics, chemotheraout-of-pocket cost. Therefore, nutritional peutics, and parasiticides ("chenlicals"); management is of major importance.

therefore, organic producers cannot use

Veterinarians with knowledge of nutrition
preventive or therapeutic medications
and mineral management can be extremely
and rather must rely on "natural" or home
helpful, because feed imbalances can be
remedies with questionable effects but
costly.

no withdrawal times. This forces them to

Feedlot lamb feeding and management is
manage for disease prevention rather
also an area in which veterinary services
than use labeled medicines with known
can be very useful, providing least-cost
withdrawal times. These standards are
rations and preventing major nutritional
often aspirational rather than practical
diseases such as acidosis, urolitlliasis (see
and can lead to healtll issues and welfare
p 1502), rectal prolapse, type D enterotoxconcerns in organic flocks, even those enlia (pulpy kidney disease, seep 610), and that have excellent management systems
polioencephalomalacia (seep 1281) and
dedicated to this approach. Veterinarians
stress-related diseases such as pneumonia
can be extremely helpful in this type of

(seep 1472).

production system.

Organic flocks should be established

SHEPHERDING
from known health-status flocks that are
free of testable and eradicable diseases

Veterinary services to the small, shepherded such as or£'sore mouth, Corynebaclerium sheep and goat flocks in the Middle East and pseudo tuberculosis ( cheesy gland, caseous Asia are primarily concerned with
lymphadenitis), Brucella ovis (ram
controlling clinical diseases and improving
epididymitis), footrot, maedi/ovine
the survival rate of y0tmg lambs and kids.

progressive pneumonia, scrapie, Johne

The restricted availability and low
disease, and chlamydia! and Campylobac
nutritional value of feed limit productivity.

ler abortion. Flocks should be maintained

Sheep and goats are kept primarily as a
as closed flocks as much as practical, and
source of meat and nillk for the owner's
new genetic stock should be sourced from
fanilly and for sale as a source of cash
known health-status flocks. New stock must
income. Veterinary care is often provided
be quarantined and thoroughly exanlined
by government programs and is directed
and tested before introduction to the flock
toward control of specific contagious and
and its pastures. Preventing entry of disease
zoonotic diseases. Even though the value of
is critical, necessitating a high degree of
animals in the flock is often high relative to
biosecurity (seep 2068).

the income of the owner, the funds available

Parasitic gastroenteritis can be of
to invest in veterinary services are limited.

particular concern in organic sheep

Thus, private veterinary care is seldom
production. In addition, although the
used, even if available, despite the fact that
regulations of some countries allow
the death or severe ill health of a few
judicious use of anthelmintics and
animals can have a major in1pact on both
antiparasiticides, others do not. Managethe productivity of the flock and the ment plans must include methods to avoid
well-being of the owner.

or reduce parasitic larval intake. Grazing

In Asia, the system of land use is often
crop aftermaths, using mixed-species
complex, with sheep and goats integrated
rotational grazing, attention to stocking

HEALTH-MANAGEMENT INTERACTION: SHEEP

2167
rates, drylotting, and using pastures for
leading to shearing cuts, particularly
hay and grazing only after a good freeze for in areas that still use dipping vats for a season, can all be used to limit internal
ectoparasite control (this practice has
parasites. Other strategies that have been
largely disappeared since the advent of the
suggested include grazing plants that may
avermectin pa.rasiticides). Sheep in long

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reduce GI parasitism such as chicory,
wool at times of high rainfall tend to be at
sanfoin, birdsfoot trefoil, and the use
higher risk of infection, and some sheep are
of copper oxide needles. Breeding and
also genetically predisposed.

selecting for genetic resistance is

Caseous lymphadenitis (seep 63) may
definitely a viable option and not too
be associated with shearing by not
difficult using the help of individual fecal
separating infected or discharging sheep
egg counts.

before shearing, not shearing affected sheep
last, not changing blades and disinfecting
shears after cutting into an abscess, dipping

DISORDERS ASSOCIATED WITH
in contaminated dip, and by close confine

MANAGEMENT PRACTICES
ment of infected sheep with noninfected
sheep after shearing and at 0U1er tin1es.

Management practices, particularly feeding

Other means of spreading this very
practices, can be the primary determinant
contagious disease is the use of feed bunks
of cases or outbreaks of infectious or
or working chutes where the organism
metabolic disease in all flocks of sheep.

( Coryneba,clerium pseudo tuberculosis)

Pregnancy toxemia ( see p 1021) may be
has been smeared on slats or railings by
seen in late-pregnant ewes bearing multiple
sheep with draining abscesses. The
fetuses subjected to a falling plane of
organism can survive for up to a year in
nutrition, specifically energy. It is associated the environment. It can be controlled by with simple starvation, ewes too fat in early
vaccination.

pregnancy, ewes too fat in late pregnancy

This disease is responsible for huge
and that voluntarily reduce feed intake,
economic losses in No1th America due to
poor quality feed, and ewes subjected to
the rejection or trimming of large parts of
stress in late-pregnancy ( eg, trailing or
carcasses of affected animals when
transport, or severe environmental
slaughtered.

changes). Ewes rarely survive after showing

Enterotoxemia (Closlridium
signs of pregnancy toxemia, even with
pe1fringens type D infection, seep 610) is excellent veterinary care, and it is difficult
seen in weaned, unvaccinated lambs on a
to stop losses even after interceding with
rising plane of nutrition high in carbohyadequate feed.

drates, as when moved to better pasture

Hypocalcemia (seep 991) is seen in
or following a "flush" in pasture gro.wth, pregnant ewes or ewes in early lactation
particularly cereal grains and in feeder
subjected to a period of temporary
lambs fed grain. It generally causes a
starvation or to feeds particularly low in

"sudden deaU1" syndrome and can be
calcium, especially ewes with multiple
confused with acidosis. These animals are
fetuses, as a result of decreased food intake found dead and even if found alive can in late pregnancy. It is also seen in feeder
rarely be saved. There is an enterotoxemia
lambs on a grain-based ration without
antiserum, which if administered early, can
adequate mineral supplementation, and
be used for treatment. The vaccine is very
during drought conditions. Calcium
effective.

deficiency can be confused with pregnancy

Acidosis is seen in adults and lambs
toxemia and is often a part of the pregexposed suddenly to a higher carbohydrate nancy toxemia syndrome. Fortunately,
diet than normal and is often confused with
pure calcium deficiency can be easily
enterotoxemia. It is seen conrn1only when
treated and rectified, saving the ewe and
late-pregnancy ewes are started on grain,
her pregnancy.

when feedlot self-feeders run out of feed for

Hypomagnesemia (seep 995) may
more than a few homs, and when children
be seen during a period of temporary
not properly instructed in correct feeding
starvation in late pregnancy or early
of anin1als perfonn feeding chores.

lactation, and also after movement of

C perfringens type C infection is
lactating ewes to lush spring growth pasture generally a suckling lamb disease seen in (especially green cereal crops). As with
very young single lan1bs suckling ewes that
hypocalcemia, this condition is easily
produce an overabundance of milk or in a
treated and rectified if properly diagnosed.

lamb after its twin dies. It is also seen in

Dermatophilosis (seep 858) is
artificially reared orphan "bummer" lambs
associated with poor shearing practices
that have not had sufficient colostnun. The

2168

HEALTH-MANAGEMENT INTERACTION: SHEEP
disease can be prevented by vaccinating
overwhelming cocci.dial infection at 3 wk of
ewes close to parturition with enterotoxage. Lambs that get little or no colostrum for emia C and D vaccine to provide antibodies
whatever reason are at significant risk of
in their colostrum; saving frozen colostrum
succumbing to disease because of the lack

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from vaccinated ewes, does, or cows for
of passive in1111m1ity even after weaning.

administration to lambs that received no

Diseases particularly co'nunon to lan1bs
colostrum; or giving those lambs injections
lacking passive inunurtity are E coli scours, of enterotoxemia antiserum.

septicemias, navel ill, coccidia, pneun10nia,

Malignant edema (seep 604) and
tetanus, enterotoxemia, sore mouth, and
blackleg (seep 602) may follow wounds arthritis.

( eg, improper sheaiing, vaccination).

Coccidiosis can cause a sudden death

However, these are clostridial diseases not
syndrome at 21 days of age if the infecting
commonly seen in sheep.

dose was large enough. Otherwise, U1e

Tetanus (seep 611) may also be seen
disease is chai·acterized by the area around
in unvaccinated sheep and lambs after a
a yow1g lan1b's tail smeared with diarrhea.

wound associated with procedures such as

If not treated, the diaiThea can tum bloody
castration, docking (tailing), shearing, or
after a time and the lamb can dehydrate and
vaccination pe1fo1med in contan1inated
die. The lambs' environment or the dam's
yards/corrals. Te tan us has been specifically
containinated teats is the source of the
associated with the use of elastrator
infections; most adults carry small to

( castrating) bands to remove tails and
moderate amounts with no signs. Lambs,
testicles of young lambs. Vaccinating ewes
too, can carry moderate infections and
with a C /etani-containing vaccine shortly
show only lack of vigor and weight gain.

before lambing will prevent the disease for

Coccidia is the most common cause of
up to 60 days of age if the lambs receive
poor-doing lambs and significant loss to
their dams' colostrtm1.

the producer.

Black disease (seep 603) is caused by C

Coccidiosis can be controlled by keeping
novyi type D. Sudden death is a hallmark of the lambs' ai·ea clean and dry and by
this disease seen among unvaccinated
treating ewes before lambing with a
grazing sheep on pastures with wet areas
coccicl.ostat. Feeding coccidiostats in feed
that support the snail that is the intermediaccessible only to the lambs such as ate host of Fasciola hepatica. The
cl.ecoquinolate, amproliun1, lasalocicl., or
organism, which produces a potent toxin,
monesin furtl1er controls the disease. It is
colonizes the necrotic areas of the liver
treated with sulfonamides.

caused by the migrating flukes on their way

Ovine posthitis (pizzle rot) is seen in
to the gallbladder.

me1ino wethers on high-protein pasture

C novyi is also the cause of "big head"

and in breeding ran1s kept in corrals or
in rams, in which necrotic and anaerobic
paddocks, particularly with moist areas
tissue on the head caused by the head
where the anin1als prefer to lie during hot
butting of mwaccinated fighting rams
pe1iods of the clay. Amrnonimn salts in the
becomes infected with the anaerobic
urine are broken down by soil organisms
clostridial organisms. Black disease and big
contai11inating the wool ai·ound the
head can be prevented by vaccinating.

prepuce, and the resultant NH, causes

Navel ill (E coli and E1ysipelas erosions and scabbing of the preputial
arthritis) ( see p 625) are associated with orifice. It can interfere with breeding
navel infections of lambs born in muddy or
because of pain and discomfort. Clipping
dirty areas and that have not had their
wool around the preputial opening, keeping
navels dipped in 7% iodine at birth. These
animals in dry paddocks, and reducing
two infections are often confused with one
protein in the diet will help eliminate the
another and are usually seen around 3 wk
problem.

of age, although sin11ne1ing infections can

Actinobacillosis (seep 589) is seen in exacerbate later. Other causes may be
sheep grazing on abrasive, thorny pasture.

contaminated dip or poor hygiene at

For disease risks associated with
docking/tailing or castration.

pasture or with specific plants ( eg, bloat,

Poor lambing management and
polioencephalomalacia, hemolytic anemia,
sanitation of the lan1bing ai·ea can result in
esophageal obstruction, enterotoxemia in
significant economic loss due to varied
sheep, and goiter in the lambs born to ewes
problems ranging from baby lan1bs dying
grazing Brassica spp ), see POISONOUS PLANTS, of hypothermia-related hypoglycemia,
p 3103. For the risk of nutritional deficiency
starvation due to mismothe1ing or ewes
or toxic disease associated with formulated
with mastitis, and sudden death due to
feeds, see NUTRITION: SHEEP, p 2345.

HEALTH-MANAGEMENT INTERACTION: SMALL ANIMALS

2169

HEALTH-MANAGEMENT INTERACTION:

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SMALL ANIMALS

Proper management to prevent and control

In the past, there has been some question
disease has histo1ically been a higher
concerning the overvaccination or
p1iority in production animal medicine
hype1imrnw1ization of both dogs ai1d cats.

than in small animal medicine. However,

Vaccine-associated sarcomas, specifically
appropriate management is just as
fibrosa.rcoma, have been an increasing probimportant for small animals, whether their lem in cats (seep 955). The etiology of this environment is that of a single or multipletun1or is not completely understood, but it pet household or a more intensive housing
appears at vaccination sites of rabies ai1cl
situation such as a kennel or cattery.

FeLV vaccines. In dogs, there has been some

Responsible pet ownership must be
correlation between vaccination and
emphasized to all those owning and
immune-mediated disorders such as
considering owning pets. Areas of client
inunune-mecliated hemolytic anemia.

education that should be emphasized

Cw-rent canine vaccination guidelines,
include the following: 1) routine ca.re and
published in 2011 by the Ame1ican Animal
grooming, 2) preventive health ca.re, 3)

Hospital Association, identify core and
parasite control, 4) nutrition, 5) household
noncore vaccines. Core vaccines include
hazards, and 6) housing requirements and
distemper, pai-vovirus, and adenovirus-2.

environmental factors.

A killed rabies vaccine is also core and is

Routine care and grooming not only
available as a 1-yr and 3-yr product. The
help maintain pet health but also allow
specific vaccine schedule is 8 wk, 12 wk,
identification of health problems early in the
and 16 wk of age. The first booster should
course of disease. Compared with disease
be given no later thai1 1 YT after the final
in people, disease in animals is generally
vaccine dose of the initial series. Subseidentified at a later stage. Close observation quent boosters should be administered
of pets allows for evaluation of changes
every 3 yr. Current feline vaccination
in appetite, thirst, urination, defecation,
guidelines, published in 2013 by the
ambulation, and general behavior. Any

American Association of Feline Practitionchanges may suggest the need for a more ers, suggest vaccination for panleukopenia,
thorough examination and possible
herpesvirus 1, calicivirus, and feline
intervention. Special attention should be
leukemia virus (FeLV). Additional vaccines
given to hair coat, skin, ears, eyes, and teeth.

may be suggested depending on risk of

Anal sac in1paction and overgrowth of nails
exposure, eg, indoor versus outdoor or
a.re common problems.

cattery situations. Current recommenda

Preventive health care in small animals
tions for vaccination sites also follow the
primaiily involves vaccination ai1d pai·asite
guidelines of the Arnericai1 Association for
prevention. Vaccines ai·e available for a

Feline Practitioners. This protocol can also
variety of infectious diseases in dogs,
be used for dogs. The guidelines suggest
including distemper, pa.rvovirns, hepatitis,
that cats be vaccinated in ai1 area ai11enable
leptospirosis, tracheobronchitis, rabies,
to surgical resection, ie, distal limbs rather

Lyme disease, and corona.virus. Vaccines
than torso. Vaccines for feline panleukopeavailable against infectious diseases in cats nia virus, feline herpesvirus 1, and feline
include those for panleukopenia, rhinotracalicivirus ai·e administered below the right cheitis, calicivirns, rabies, feline .irtfectious
elbow. FeLV vaccines are given below the
peritonitis (FIP), and feline leukemia virus
left stifle, and rabies vaccines below the

(FeLV).

1ight stifle. Vaccinating clogs and cats less

Vaccination schedules vaiy but gene.rally
frequently has also been suggested. A
require an initial vaccination at 6-8 wk of
triatU1ual vaccination protocol for vaccines
age, followed by additional vaccinations at
other than rabies has been adopted at many

3-wk intervals until the animal is 4--5 mo old.

institutions. It is also recommended to

After this, most vaccines a.re given annually.

rese1-ve vaccines for certain diseases such

Rabies vaccination is dictated by state law
as FeLV, Lyme disease, leptospirosis, feline
or localjwisdiction. First-time vaccination
immunodeficiency vims, and FIP for at-risk
for diseases other than rabies in adult
ai1irnals.

animals should include an initial vaccina

Other preventive health ca.re measw-es
tion followed by at least one booster.

may include castration or ovaiiohysterec-

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HEALTH-MANAGEMENT INTERACTION: SMALL ANIMALS
tomy, and annual veterinary examinations.

shating an owner's home, concerns are

The current trend in preventive health care
generally limited. However, outdoor
is to emphasize an annual examination
housing must provide cover from direct
separate from visits for vaccination. The
sunlight, shelter from excessive wind and
preventive health visits allow the veterinarextreme temperatures, adequate ventila

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ian to see the animal frequently and detect
tion, and an adequate supply of fresh water.

disease at an earlier stage.

These factors are critical in kennels and

Parasite control continues to be
catte1ies. Drainage must be appropriate for
important. The primary encloparasites
proper satlitation, and surfaces must be
include GI parasites such as roundworms,
suitable for cleaning and disinfection.

whipworn1s, and tapeworms (seep 412, et

Hazardous environmental conditions can
seq). Heartworn1 disease (seep 127), an
result in hyperthennia, sunburn, dehydraimportant clinical entity in both clogs and tion, hypothermia, or frostbite. Housing
cats, is preventable with prophylactic
must also be sale and keep pets away from
therapy. Although a treatment is currently
dangers such as other atlimals, motor
available for heartwonn disease in dogs, no
vehicles, and malicious mischief. If animals
sale or acceptable treatment is available for
are restrained by a leash or a chain, care
cats. The American Heaitwonn Association
should be taken that self-trauma cannot
provides treatment guidelines for canine
be inflicted. Some municipalities have
and feline heartworn1 disease. The primary
introduced chain laws to prevent this type
ectoparasites include fleas, ticks, and mites.

of injury.

Botl1 oral and topical products are available

Miscellaneous considerations include
for flea control in dogs and cats. Another
obedience training, which may help reduce
important aspect of parasite control
aggressive interactions with other animals
includes prevention of zoonotic diseases
and people.

such as visceral larva migrans and

Traveling with pets is another
toxoplasmosis. Bartonella may also be an
important consideration. If crossing state
important vector-borne disease affecting
lines, a healtll certificate should be issued.

people.

When international travel is planned,

Nutrition is an important and often
owners should be advised to become
overlooked aspect of pet ownership. Most
familiar with the appropriate health,
pet foods on the market have been
quarantine, agriculture, and customs
formulated based on significant research
requirements. Transport of animals by
and development. Specialty diets are
airlines is under the jurisdiction of tile
available (both over-the-counter and from
specific airline company, but a veterinarian
veterinarians, including presc1iption diets)

should be consulted and a health certificate
for young, growing, and geriatric pets, as
issued. Aninlals should not be allowed to
well as for specific disease processes.

tide unrestrained in motor vehicles and

Overfeeding and oversupplementation may
should never be allowed to ride in tile back
lead to numerous problems, and feeding of
of open vehicles such as pick-up trucks.

table scraps should be kept to a minimum.

Motion sickness (seep 1267) and anxiety

(See also NUTRITION: SMALL ANIMALS, p 2354.) are common problems in dogs and cats

Water quality should not be overlooked,
when traveling. The phenothiazine
especially in rural areas and in kennels and
tranquilizer acepromazine may be beneficial
catteries. Fresh water should be available
in this situation, and antillistamiite therapy
ad lib.

such as diphenhydraniine may be useful.

Household hazards provide a variety of

Maropitai1t citrate is also approved for
dangers to dogs and cats. Potential hazards
treatment of motion sickness.

include electrical cords, lead-based paint,

The potential disease-management
cleaning supplies, antifreeze (seep 3046),
interaction between pets and owners is
houseplants (seep 3103), insecticides (see important in prevention of zoonotic
p 3058), prescription drugs (seep 3032), illicit diseases, especially when pets are owned
and abused d!ugs (seep 3038), alcoholic
by immunocompromised people. Pet
beverages, chocolate (seep 2966), artificial owners with human immunodeficiency
sweeteners (xylitol, seep 2698), sewing
virus or tl10se being treated with chemoneedles, fish hooks, and many others. (See also therapy or other immunosuppressive agents HOUSEHOLD HAZARDS, p 3000.) Elements of house
can salely own animals but should consult
design, such as steep stairs, slippery floors,
both their veterinarian and physician.

open windows, etc, may also be hazardous.

Most atlimal-associated infections,

Housing requirements and environ
including tllose due to Toxoplasma gondii,
mental factors are an in1portant consid

Cryptosporidium, Salmonella, and
eration for pets. For compatlion animals

Campylobacter, appear to be acquired by

MANAGEMENT OF REPRODUCTION: CADLE

2171
immunosuppressed individuals from
of litter boxes or using gloves when doing
sources other than exposure to animals.

so, avoiding dog feces, avoiding young or

The possible exception may be Bartonella,
unhealthy pets in favor of healthy or adult
or cat scratch disease. Because the risk of
pets, having sick animals evaluated by a
zoonotic transmission is low, animals pose
veterinarian, not allowing cats to hunt, not

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minimal risk to irnrnunocomprornised
feeding pets undercooked meat, and
people if basic precautions are followed.

preventing coprophagy or access to

Precautions include avoiding the cleaning
garbage.

MANAGEMENT OF

REPRODUCTION: CATTLE

Dairy and beef producers should strive to
herd, bulls, and calves; 7) evaluating
increase reproductive efficiency as a key
reproductive failure and abortions; 8)

driver of economic efficiency in the sector.

providing adequate facilities; and 9)

Reproductive efficiency, or "pregnancy
ensuring that the calf is well cared for at
rate," is defined as the proportion of cows
birth and receives adequate colostrun1.

eligible to be bred that become pregnant
during an estrous cycle ( or approximately

NUTRITION

21 days), and which determines the calving
to conception interval at the end of the

Nutrition is one of the most important
voluntary waiting period. As pregnancy rate
management factors in reaching calf crop
increases in dairy herds, the calving to
goals and in attaining a short calving season
conception interval decreases, and the herd
every year in beef breeding herds. The
status becomes, on average, less "days in
limiting nutrient related to reproduction in
milk" (DIM). This has the effect of
beef and dairy cattle is usually energy;
increasing the potential amount of milk
although dairy cattle are usually fed rations
produced per day of herd lifetin1e, because
that supply adequate energy during
yield classically declines at 0.3% per day
lactation, genetic drivers for milk producafter peak lactation production. A major tion inevitably lead to a period of some
and realistic goal of every beef cow/calf
negative energy balance postpartuni. The
operator should be to raise or market 85
level of energy and body condition before
calves per 100 cows every year. Greater
calving primarily influences when a beef
reproductive efficiency also reduces the
cow returns to estrus, whereas level of
nun1ber of cows culled for reproductive
energy after calving primarily influences
failure; collectively, these changes increase
subsequent conception. Feed requireherd income.

ments vary during the reproductive cycle

Reproductive pe1formance in both beef

( see p 2248).

cow/calf and dairy operations can be

There are four periods of beef cow
improved by the following: 1) properly
nutrient requirements, and generally three
identifying and managing animals to carry
for dairy cows. Period 1 is the interval from out reproductive programs; 2) keeping
calving to breeding; it is -70--90 days and is
records that enable determination of
the period of greatest nutritional demand.

in1portant herd indices, such as percent calf

The dairy cow is at maximal milk produccrop, pregnancy rate, length of calving tion and recovering from the stress of
season, culling rates, calf morbidity and
parturition. During this period, she is
mortality, breeding efficiency of bulls, and
expected to be ready to breed.

performance and production information;

Period 2 is the interval from rebreeding

3) meeting the nutritional requirements of
to weaning the beef calf; it is -120-150 days
various classes of livestock in the herd,
in beef cows. Periods 2 and 3 overlap in
emphasizing nutritional needs and cost
daily cows and are not as easily separated
efficiencies; 4) establishing a breeding
as in beef cattle. The beef cow should gain
progran1 for heifer replacements and cows;
weight while still milking. Although some

5) practicing sire selection and reproductive
dairy cows maintain body weight, many
management; 6) adopting a vaccination/
high producers continue to lose weight
irnrnunization program for the cow/calf
during this period.

2172

MANAGEMENT OF REPRODUCTION: CATTLE

Period 3 is from weaning to 50 days
beef calf or milk for sale represents
before calving; it lasts -100 days and is the
signillcant investment and risk.

pe1iod of least nutritional demand. The beef

To provide the essential nutrient
cow has only to maintain her condition and
requirements during various stages of the

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continue fetal development. The dairy cow
reproductive cycle, major forages and
should be managed to gain or lose body
homegrown cer als should be analyzed to
weight during the last months of lactation to monitor nut1ient content and actual value.

achieve target body condition ready to enter Variation in amounts of trace minerals is the stable dry pe1iod.

common between and within different

Period 4 is a critical stage and is the 50
geographic areas. Globally, different
days before calving; it is dming this tin1e
systems are used to determine energy levels
that 75% of fetal growth occurs. Cows are
of the ration, such as the metabolizable
usually not lactating during this "dry
protein (MP) or "Feed into Milk" (FiM)

period." Cow condition at calving is critical
models or the Total Digestible Nutrient
to rebreeding; the onset of estrus after

System and the California Net Energy
calving is delayed in cows that lose weight

System. All are commonly used, and
or are thin and not gaining during late
application should be tailored to fit the
pregnancy.

individual operation.

Dai1y cows are usually fed ( see p 2265)

Even within nutritional need categories,
for optimal milk production throughout
cattle benefit from feeding and handling in
their 305-day lactation. It is assumed they
subgroups: lightweight heifers at weaning
will lose weight during heavy lactation (the
need to gain more than heavier heifers to
early months) and regain the loss during the
reach puberty by breeding season; first-calf
remainder of lactation. Dairy cows should
heifers require special attention from both
not be overfed during the dry period
an energy and competition standpoint if
because of a genetic predisposition to
they are expected to breed and conceive
sacrifice body condition to maximize milk
at the proper time. These heifers are still
production through insulin resistance.

growing, as well as lactating, and they may

This leads to the increased probability of
not have the rumen capacity to meet
metabolic diseases, eg, type II ketosis and
postcalving energy needs on forage alone.

fatty liver disease (seep 1024 and see

Monitoring of growth rates is important
p 1018), during early lactation as insulin
to achieve successful rearing targets.

resistance leads to excessive fat mobiliza

Supplemental feeding of both high-energy
tion from adipose tissue storage and
and high-protein feeds to first-calf heifers
overwhelms the capacity of lipoprotein
may be required for optin1al reproductive
transport mechanisms in the bovine liver to
potential. Calves from first-calf beef heifers
transport and metabolize lipid. In addition,
may be weaned 30--40 days earlier than
dairy cows should be fed to mininuze the
calves from cows in the main herd to allow
incidence of calving-related disorders ( eg,
the heifer more time to grow and recover
dystocia, hypocalcemia, and retained fetal
from demands associated with lactation.

membranes), including c.;ontrol of dietary

Thin, old, and small cows may not
cation-anion balance (DCAB), which have
compete favorably with heavier cows
a negative effect on fertility and health
within the same herd and olten benefit
postpartum.

from being fed as a.separate subgroup.

The amount of cow feed required per

Lactating daily cattle are usually fed
pound or kg of calf weaned is fairly
according to milk production. They may be
constant, although larger cows require more fed concentrate on an individual basis or feed for maintenance than smaller cows.

divided into groups according to milk

Cows that give more milk require more feed, production and fed an appropriate total generally with a higher level of protein.

mixed ration.

Increased milk is produced at the expense
of reproduction when feed is not adequate

BREEDING PROGRAM FOR
to meet all needs.

HEIFER REPLACEMENTS AND

The protein requirement of young
cows
growing stock and heavy-milking cows is
often a limiting factor, while mature dry

If a cow is to ca.Ive consistently, she must
cows are often overfed protein. Heifers
deliver her first calf early. Puberty is a
must be fed adequately from weaning to
function of breed, age, and weight. Beef
breeding if they are to calve at 2 yr of age;
heifers that are bred at 13-15 mo and ca.Ive
this target is critical for herd economics,
at 22-24 mo have two advantages: they get
because before this point the absence of
closer attention from herdspeople by

MANAGEMENT OF REPRODUCTION: CADLE

2173
calving before the main herd starts to

Although genuine anestrus is generally
calve, and subsequently they have the
not common in dairy cows, "subestrus" with extra time needed to rebreed with the
poor estrous expression or irregular estrous
mature cow herd. For heifers to breed at
cycles in cows may result from a munber of

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14 mo, they should have attained at least
factors, including poor management or

65%-75%of their projected mature weight;
nutrition, disease, injury, or disturbances in
therefore, adequate nutrition is of major
endocrine ftmctions. In many dairy herds,
importance. The breeding season for virgin
detection of estrus for AI is inefficient,
beef heifers should stait 3 wk before that
because not all cows are identified in estrus
of the main cow herd. The above considbecause of human en-or, attenuated erations do not apply to dairy cattle, which
expression of estrus in high-producing
calve throughout the year; however,
cows, and adverse responses to heat stress.

scheduling heifer calvings at the stai;; of a

Systematic breeding progran1s for AI at a
seasonal calving dairy herd such as in New
predetennined time (ie, timed AI [TAI]),

Zealand or Ireland represents an opp01'tuwithout the need for estrus detection, nity to "reset" the calving pattern. Lifetime coupled with early rebreeding of nonpregprofit of dairy replacement heil"ers is na.nt cows are successful options for
maximized when heifers calve at 23--25 mo
reproductive management of lactating dairy
of age. Thus, to maintain genetic progress
cows. These systems optimize pregnancy
and maximize profitability, heifer breeding
rate by synchronizing follicle development,
strategies on dairy operations should
regression of the c01pus luteum (CL), and
include artificial insemination (AI) that
precise induction of ovulation to provide a
results in attainment of pregnancy to allow
fixed TAI. Incorporation of TAI in dairy herd
calving at --24 mo of age.

reproductive management programs

To compensate for the greater att1ition
reduces labor requirements for detection of
rate usually seen with virgin heifers, a
estrus while improving overall reproductive
greater munber should be bred than is
performance and maximizing profit.

needed to maintain or increase herd

Silent heat refers to nom1al follicular
numbers, eg, 1500Ai.

development and ovulation without evident
signs of estrus. Its frequency decreases as
lactation progresses, so that incidence is

Irregularities of Estrus and Anestrus
low by 4 mo postpartLll11. Cows with true

Breeding will not occur if the cow is
silent heats may be detected only tlu·ough
anestrous, or if estrus is undetected.

rectal palpation or ultrasound of the

Genuine anestrus is not common in dairy
ovaries, via accelerometers/activity meters,
cows but is more common in postpartun1
or the use of progesterone assay in milk or
beef cows in below target body condition.

plasma.

Anestrus, subestrus, or irregular estrous

Cyclic changes occur in the ovary over
cycles in cows may result from a nwnber

18--24 days. These changes generally can
of factors, including poor management or
be recognized and the time of the cycle
nutrition, disease, injury, or disturbances
estimated, particularly in the 3-4 days
in endocrine functions. One of the most
before ovulation, at the ti.me of ovulation, or
impo1'tant management factors in aii;i.ficially 3-4 days after ovulation. The CL regresses bred herds is failure to detect or observe

3-4 days before the onset of estrus; it
estrus. The average duration of estrus is 18
becomes smaller in size and changes from a
hr, but in many cows it is appreciably
diestrous, liver-like consistency to one more
shorter. A systematic program for detection
fibrous. Estrus is evidenced by the presence
of estrus is important if cows are to be bred
of a palpable follicle, an absent or regressed
at the right time. A producer must be

CL, and fum uterine tone. The vaginal
familiar with signs of estrus. Aids in estrus
mucosa is edematous, the cervix is relaxed
detection that are valuable adjuncts to the
and hyperemic, and a variable amount of
heat-detection program include chalk
clear serous mucus is frequently seen at the
marks on the tailhead, chemically or
vulva, which is puffy and swollen. The
electronically activated devices attached to
immediate postovulatory period is
the tailhead of the cow that reveal when
characterized by blood in the mucous
other cows have mounted, and a vaginal
discharge and an ovary with a corpus
probe that measures the electrical
hemorrhagicwn, which on palpation is
conductivity of the vaginal mucus.

recognized as a soft area (5--15 mm in

Accidental access of bulls to cows and
diameter) in the ovaiy The CL is detectable
failure to keep proper breeding records
by day 4--5 as a small and somewhat softer
often result in apparent anestrus because
structure than the mature CL, which
of pregnancy without a service history.

reaches maximal size by day 7.

2174

MANAGEMENT OF REPRODUCTION: CADLE

The examiner can sometimes predict the
not respond to gonadotropin or steroid
next estrus from previous observations
hormone treatment.

around estrus, and the cow can be watched
closely at the next anticipated estrus. The

BULL REPRODUCTIVE
primary behavioral sign of estrus-standing

MANAGEMENT

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to be mounted-is the accurate predictor of
ovulation. In cows that are approaching

A desirable goal for beef producers is a
ovulation, the appropriate time can be

95% calf crop delivered within 45-65 days,
estimated, and the cow bred on secondary
with an optimal weaning weight obtained
signs such as mounting other cows;
at the most efficient cost. Bull selection,
however, breeding on secondary signs may
management, and evaluation of perforbe associated with wide variation in time to mance are integral aspects of beef
ovulation. Aged gametes ( either semen or
improvement. The bull can affect calving
oocytes) are associated with reduced
percentage as well as quality of calves. The
embryo viability.

use of perfom1ance-tested bulls (beef and

Regimens have therefore been developed
dairy) is reconunended for both natural
for administration ofprostaglandins (PGs)

breeding and artificial insemination.

and their analogues alongside other products

A disease control program for bulls
to synchronize estrus and to reduce
should include the following procedures:

dependence on estrus detection. Prosta1) Before use, bulls should be checked for glandins are effective only if a cow has a
brucellosis, tuberculosis, trichomoniasis,
functional CL. A range of synchronization
and paratuberculosis (ie, from a herd free of
options are in conunon use, including
paratuberculosis). Bulls previously used in
double prostaglandin regin1ens, GnRH and
other herds, particularly herds in which
prostaglandin protocols, and regimens that
disease status is not known, may spread
use combinations of GnRH and prostaglandin diseases, particularly can1pylobacteriosis alongside intravaginal progesterone-releasand trichomoniasis. Prophylactic sheathing devices. For estrus synchronization, the washing witl1 antibiotics may reduce the
prostaglandin or its analogue is administered
risk of Campylobacter transmission.

to all cows. In those in days 6---18 of the cycle, 2) Depending on prevailing health status the CL will regress and estrus will occur in
and market requirements, bulls should

2-7 days. The others may either have been
be vaccinated against infectious bovine
in estrus recently or will be in a few days.

rhinotracheitis, bovine viral diarrhea,

Eleven days later, all cows will be between
clostridia, Haemophilus, can1pylobacteridays 6 and 18 of their cycle, and prostaglanosis, and leptospirosis if available. Vaccines din is administered a second time. Most
should be administered around puberty, at 6
cows will be in estrus tn 3---4 days and will
mo and 1 yr of age, and then arumally, 1 mo
ovulate in 4-5 days. Breeding is done either
before the breeding season. 3) Breeding
on signs of estrus or fixed time. Cystic ovary
soundness exanlinations should be
disease (seep 1354) may be responsible for
performed annually at the most economiirregularities of the estrous cycle, eg, follicucally advantageous time for the producer lar cysts ( an estrus, nymphomania, and

(usually 1 mo before the breeding season).

shortened cycles) and luteal cysts

All bulls should be on the premises 2 mo

( an estrus).

before the breeding season to allow them to

Under certain circumstances, ovaries
adapt to the environment. Isolation of all
are nonfunctional. They can be recognew additions to the herd (bulls or cows) nized as smooth, small, bean-shaped
is recommended for proper adaptation
structures on a single examination, or
and preparation. A breeding soundness
reveal no activity or change after several
exanlination consisting of a thorough
examinations over a period of 3 wk. The
physical exanlination, including internal
most common causes are low total energy and external genitalia, measurement of intake during late winter or droughty
scrotal circunlference, and microscopic
summer pastures, and excessive loss of
exanlination of semen for sperm motility
body weight in lactating dairy cows
and morphology, should be conducted -1
postpartum.

mo before the breeding season. Opportuni

The stress of chronic or severe disease,
ties are emerging for more objective
irtjury, or ovarian tumors may intenupt
methods of semen evaluation to be used
ovarian activity and result in anestrus.

alongside standard microscopy, such as

Congenital defects, such as freemartinism
computer-assisted semen analysis (CASA)

and ovarian hypoplasia, result in estrual
for motility and flow cytometry to assess
failure. Inactive ovaries are treated by
morphologic defects. (See also BREEDING
correcting the basic cause; they usually do

SOUNDNESS EXAMINATION OF BUU.S, p 2231.)

MANAGEMENT OF REPRODUCTION CATILE

2175

During the breeding season, the bull
high health replacement strategies. The
should be watched closely for mating
worldwide adoption of AI for genetic
behav10r. The standard recommendation
improvement in dairy cattle was made
is 25 cows per bull. There are significant
possible by development of a progeny test
variations in this ratio, depending on the
system and subsequent use of milk

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breeding soundness and libido of individual
production records as an objective measure
bulls, differences in terrain, and length of
of performance on which to select superior
breeding season.

bulls, techniques for freezing semen, and

The weight loss that develops in bulls
hqmd mtrogen storage refrigerators.

during the breeding season should be

The development of objective systems
restored during the off-period, but
such as EBVs to measure econonl.ic traits
overconditioning should be avoided.

in beef cattle ( eg, growtll rate, carcass
conformation and composition, efficiency

BREEDING
of feed conversion) and thus the more
accurate selection of sires, as well as

The breeding program may use either
control of the estrous cycle, is leading to
artificial insemination (AI) or natural
an mcrease m use of Al in beef cattle.

service. AI has been commercially available

Pr?cessing of frozen semen is a highly
for >60 yr; it is widely used in dairy cattle
specialized technique. Attention to detail at
but is used much less in beef cattle because
each step is important to maintain semen
of handling and labor costs. AI offers a
quality. The freezability of semen varies
selection of bulls with known genetic
among bulls. However, semen of high
potential, such as measured by estin1ated
motility and morphology quality generally
breeding values (EBVs) for traits such as
freezes well. Best results are obtained when
ease of calving or growth rates. When
semen is processed in a properly equipped
nutrition and heat detection are properly
laboratory by experienced staff at an Al
managed, satisfactory results are obtained.

center.

Failure to detect estrus is the major reason
for w1successful AI. When cows are

Collection and Handling of the Semen
properly inseminated with good-quality

Sample: (See also BREEDING SOUNDNESS
semen at the proper time, 50%-60"A, may

EXAMINATION OF'THE MALE, p 2230.) Semen is
conceive on first service, the san1e
collected using an artificial vagina or by
percentage on second service.

electroejaculation ( electrical stimulation of

Embryo transfer (seep 2239) is frequently the seminal vesicles and ampullae ). As long used to increase the nwnber of progeny
as the sample is of 11.igh quality, freezability
from the most valuable beef and dairy cows.

and fertility should be normal. These

Sexmg of semen has been adapted to
techniques should not be used if the tull
conunercial field usage and is increasingly
is unable to naturally service a cow for
used. Sexmg of embryos is becoming more
reasons that could be genetic.

readily available and practical for field

Most Al in cattle today is performed
usage, and some cloning teclmiques are
with frozen semen. Frozen semen may be
emerging in availability.

maintained for years; extenders pernl.it

Heifers should be bred according to size
more insemination doses to be processed
and age at puberty; at first breeding they
from one collection of semen maintain the
should be 65%-70"A, of their projected mature fertility of the semen longer, irotect the body weight, with dairy heifers achieving
spermatozoa from sudden temperature or

> 125 cm withers height at tll.is stage.

pH change, and prolong viability. Semen is

Selection of bulls to be used for natural
usually extended with citrate-buffered egg
service should be based on likely size of tl1e
yolk or heat-treated skim nl.ilk plus glycerol,
calf at birth;
sugars, enzymes, and antibiotics. Final

_the bull's own birth weight ( not
his ad
extension is designed to package 0.25 rnL or

_ult weight) is a useful guide, but
genetic proofs such as EBVs are vital.

0.5 mL of semen containing 20-30 million

Heat synchronization of heifers and cows
spermatozoa at time of freezing.

is possible, but such progran1s depend on

Extenders are often divided into fraction
adequate management and cooperation.

A and fraction B. The initial extension of

Also, sufficient skilled labor to breed and
semen is done with fraction A at the same
assist during calving is essential.

temperature, eg, 86°F (30°C). The extended
semen is then cooled to 41 °F (5°C) over

Artificial Insemination (Al)

40-50 nun, or more slowly. Holding the
extended semen at this temperature for 3-4

In cattle, AI is used primarily for genetic
hr enables the antibiotics in fraction A to
rmprovement of livestock and to facilitate
complete their action before being inhlbited

2176

MANAGEMENT OF REPRODUCTION: CADLE
by the cryoprotectant glycerol. Fraction B
although many factors other than semen are
contains a c1yoprotectant such as ethylene
involved in attaining high fertility. Motility
glycol or glycerol (eg, 14%) and is added at
after thawing is an important ctite1ion. An

5°C in equal quantity to the extended semen. adequate number of motile spermatozoa at VetBooks.ir

Each AI center has its own standard
the time of insemination is critical. Morphoextenders and processing procedures.

logic exan1ination also l elps assess the role

Glycerol ( 11 o/o-13%) may be used with
of semen in infertility cases. Comparisons
milk-based diluents. Before freezing, semen
within herds of diagnosable pregnancies
should be stored for 4-18 hr at 5°C.

resulting from the suspect semen and from

For freezing, bull semen is usually
semen from other bulls may be useful.

packaged in appropriately identified plastic

Estrus detection continues to be the most
straws (0.25 or 0.5 mL). Optimal freezing
important factor that influences AI
rates are known for many cell types, and
efficiency. This factor should be investispermatozoa can withstand a wide range of gated first, and inseminator proficiency
rates. In practice, extended semen is frozen
second. The latter includes an evaluation of
in liquid nitrogen vapor before being
thawing temperature, time of thawing in
plunged into liquid nitrogen at -320°F
relation to actual insemination, temperature

(-196°C). Storage in liquid nitrogen tanks is
changes from thawing to insemination, site
safe for �20 yr, and semen is transported in
and speed of semen deposition, and sanitary
such tanks. The level of liquid nitrogen in
procedures. If semen is purchased from a
tanks must be monitored to avoid semen
reputable supplier, it is unusual for the
losses, which is seen when the tanks
cause of the infertility to be poor-quality
become defective or when liquid nitrogen
semen, although transport and storage
gradually evaporates.

factors should be considered.

Because spermatozoa do not survive for
long after thawing, the semen should be
used immediately. Thawing is best done as

PREGNANCY DETERMINATION
quickly as possible without damaging the
semen by overheating. In practice, straws

Pregnancy detem1ination is recommended
may be thawed in warm water (95° -98°F
to maximize breeding efficiency. In beef

[35° -36.5°C]) for �30 sec and immediately
herds, the breeding season ( natural service
placed in the cow's reproductive tract.

or AI) is ideally fixed at a length of 60-70

Recommendations by the AI center that
days. This gives the average cow two or
processed the semen should be followed.

three se1vices to conceive. Cows that are
not pregnant or were bred late should be

Insemination Technique: The rectovagiidentified; if kept in the herd, they will calve nal method is used almost exclusively. After
later in the season. Maintenance costs are
thoroughly cleaning the external genitalia
significant, although they vary widely by
with disposable toweling, one gloved hand
fam1 and by year.

is introduced into the rectum and grasps

Pregnancy deteflllination of beef cows
the cervix. The insemination pipette is
should be done shortly after the breeding
introduced through the vulva and vagina to
season is over(eg, 45-60 days); if the
the external cervical os. By manipulating
breeding season struts June 1 and ends
the cervix, along with light cranial pressure
eai·ly in August, it can be done dUting late
on the pipette, the pipette is advanced

September while the cows still have plenty
through the annular rings of the ce1vix to
of flesh from summer pasture. It is then
the junction of the internal ce1vical os and
possible to profitably market nonpregnant
the body of the uterus. The semen should be
cows before expensive winter feeding
expelled slowly (5 sec) to avoid sperm loss.

struts. When excessive returns are noted

If insemination records and consistency
or bull perfo1manee issues are suspected,
of the cervical mucus suggest possible
early pregnancy detemlination by
pregnancy, the pipette should be advanced
ultrasound 50 days after the start of the
less than one-half of the way through the
breeding season can be invaluable. A target
cervix, and the semen expelled. The optimal of 65% of cows should be pregnant to the time to inseminate is between the last half
first cycle in beef herds, and so by 50 days
of standing estrus and 6 hr thereafter, which
this can be measured as pregnai1cy
is desctibed as the "AMIPM rule," in that cows detemlination success 30 days after
observed beginning standing heat in the
breeding. Supplementary AI or new bull
morning should be inseminated that
power can be implemented with poor
afternoon, etc.

success, alongside further investigation.

If fertility problems atise when AI is being

Dairy cows should be exanlined to
used, the semen should be investigated,
detem1ine their pregnancy status and if

MANAGEMENT OF REPRODUCTION: CATILE

2177
found open can be synchronized into estrus
ureaplasmas, mycoplasmas, alld others not
with prostaglandin F2a, or timed Al. In cows yet identified.

that are open or that have not been detected

Mycotic abortion usually is caused by
in heat, the decision on which horn1ones to

Aspergillus or Mucorspp, which reach the VetBooks.ir
use to induce estrus is based on evaluating
uterus hematogenously and cause abortion
the ovruies for CL, follicles, ru1d ovatiru1
in late gestation. In many of these fetuses,
cysts. The most common method to
the skin is not affected; in otl1ers, 1ingwonndetermine pregnancy and evaluate ovaties like lesions are seen. The placenta
is transrectal palpation and, increasingly,
frequently is severely affected witl1 necrosis
the use of ultrasonography. Ultrasonograof the cotyledons and tllickening of tl1e phy may have the following advantages:

intercotyledonruy ru·eas. Diagnosis is based

1) Non pregnant cows can be found eru·Jier
on identification of tl1e fungus tlu·ough

(28---32 days after breeding), and diagnostic
culture of tl1e fetal or placental tissues,
information on the status of the ovaties ru1d
histologic examination of these tissues,
utems Call be obtained. 2) The viability of
or direct exanlination of cotyledons after
the embryo or fetus can be assessed, eg, by
clearing with potassium hydroxide
visualization of a fetal herut beat. 3) Twins
solution. These abortions ru·e almost
are more readily detected. 4) Sex of the
always sporadic, alld the only means of
fetus can be determined. 5) Age of the
control is to reduce exposure to the fungi.

conceptus Call be estimated more accu

Sporadic losses may result from Listeria
rately. 6) The producer can be shown the
sp (a bacterium occasionally present in
conceptus, which could be reassuring in
silage when pH is> 7); nliscellaneous
herd cases of embryonic losses.

bacte1ia such asHaemophilus sp,

Other herd health exaniinations should

'!'1 ·u eperella pyogenes, Staphylococcus
be considered while the cows ru·e being
aureus, Bacillus cereus, Pasl,eurella
checked for pregnancy. These include an
mullocida, Pseudomonas aeruginosa,
accurate evaluation of body condition, the

Streptococcus bovis, Chlamydia sp, ru1d
reproductive tract, teats and udder, feet and
others; or viruses ( eg, bluetongue ).

legs, teeth, and early neoplastic eye lesions.

Noninfectious causes of abortion are

Vaccinations, internal and external parasite
numerous; the most common include 1)

control, and processing of beef calves also
recessive or lethal genes ( or both) such as
can be done at this time.

cervical vertebral malforn1ation, hydrocephalus, osteopetrosis ("mru·ble bone"

disease), arthrog1yposis ("crooked calf'

EMBRYONIC DEATH, ABORTION,
syndrome), and several others, some not

AND ABNORMAL FETAL
fully identified; 2) toxins ( eg, excessive

DEVELOPMENT
nitrates from feed or water), certain pine
needles, poisonous plants (eg, lupine,

Pregnancy may be terminated prematurely,
locoweed), or mycotoxins (moldy feeds);
resulting in abortion due to death of the

3) hom1onal imbalances in the pregnant
conceptus or failure of the uterine
dam; 4) injuries affecting the pregnant cow;
environment to support the fetus. Abnormal
and 5) nutritional deficiencies, particularly
fetal development may result in abortion or
of vitamin A, vitan1in E or selenium (or
in a calf that. dies soon after birth. Many
both), iodine, and manganese.

cases of bovine abortion are not diagnosed.

Heat stress in cattle can cause early

(See also ABORTION IN LARGE ANIMALS, p 1333.) embryonic death and lower the herd
pregnancy rate. The mechatlism by wllich

Etiology: Vimses, bacte1ia (including
heat stress affects embryonic smvival is
rickettsia and chlamydiae), molds,
complex. Heat stress can disrupt eru·ly
protozoa, or other infectious agents may
embryonic development. Effects of heat
attack the placenta or the fetus, or both.

stress on embryonic survival decrease as

Some of these microorgatlisms reach the
emb1yos advance in development. Heat
utems hematogenously; others (such as
stress at day 1 or days 1-3 after breeding
venereal infections) are contracted during
reduces embryonic survival. In contrast,
mating.

heat stress of superovulated cows at day 3,

Infectious abortion may be sporadic or a

5, or 7 after estrus did not affect embryonic
herd problem. Herd problems usually ru·e
development in one study.

associated with significru1t losses and may
be caused by infectious bovine rhinotra

Diagnosis: Accurate diagnoses of
cheitis, bovine viral diarrhea, brucellosis,
reproductive loss contribute to the
leptospirosis (vatious serotypes), campylocumulative herd history and provide criteria bacteriosis, trichomoniasis, anaplasmosis,
to evaluate the impact on herd perfonnance

2178

MANAGEMENT OF REPRODUCTION: CADLE
and the need for implementation of
bloodlines that prove to be carriers of
preventive measmes. Laboratory assistance recessive or lethal genes. Appropriate is needed in most cases. Carefully selected,
housing and handling facilities decrease
properly preserved, quality specimens
the incidence of accidents and provide an
should be submitted to a diagnostic
environment conducive to health. The cattle
laboratory for analysis. Even with these,
producer and veterinarian,should work

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the exact cause of an abortion may not be
together to assess the herd's reproductive
detected, especially if it is noninfectious.

perfom1ance, tailor a vaccination program

Laboratory diagnosis of abortion may
to the herd's specific needs, and diagnose
include serology and examination of the
and control potential herd problems.

fetus and placenta. However, a definitive

For successful abatement of heat stress,
diagnosis of bovine abortion remains
the environment of the cow must be
challenging because, in many cases, the
modified to maintain the cow within a
causative agent may have challenged a cow
normal temperature range of 10l.3°-l02.8°F
months previously and may no longer be

(38.5°-39.3°C). Common approaches
present when abortion occms.

include providing shade (to intercept solar

Defective newborn calves can be
radiation) and fans or sprinklers to promote
recognized only by a thorough examination
evaporative cooling. Tactically avoiding
and sometimes only after some time has
breeding at hottest times of the year may be
passed.

advisable.

Infectious diseases in a herd can disrupt

Prevention and Control: Several
and reduce reproductive efficiency by
factors are critical to prevent and control
causing embryonic or fetal death, abortion,
abortion and development of defective
or illness and death of neonates. A complete
calves. Measmement and management of
vaccination progran1 will not eliminate
herd health status and planning to control
reproductive problems but may prevent or
infectious disease risk with appropriate
reduce losses associated with specific
boundary and purchased stock biosecurity
infections ( see TABLES 7 and 8).

alongside vaccination programs are
essential. A balanced nutritional progran1

CALVING MANAGEMENT
helps control losses associated with mineral
or vitamin deficiencies and poor-quality

Dystocia is expected to occur in -10%-15%
feeds, including moldy grains and forages.

of first-calf heifers and in 3%-5% of mature

Genetic selection and accurate recordcattle. Although dystocia cannot be keeping help to detect and elinlinate
eliminated from a herd, the incidence can be

VACCINATION/IMMUNIZATION PROGRAM TO PROTECT AGAINST

PREPARTUM DISEASES OF THE BREEDING HERD

Disease

When to Vaccinate/Immunize

Heifers

Brucellosis

Calfhood

IBRa, BVDb

Before weaning and before
breeding

Campylobacteriosis, leptospiro

Before breeding
sis, trichomoniasis

Cows

IBR,BVD

May booster early before
breeding

Campylobacteriosis, leptospiro

Each year, before breeding
sis, trichomoniasis

Bulls

IBR,BVD

Calfhood and booster before first
breeding

Ca.mpylobacteriosis, leptospirosis Each yeax, before breeding

"Infectious bovine rhinotracheitis
b Bovine viral diarrhea

MANAGEMENT OF REPRODUCTION CATTLE

2179

VACCINATION/IMMUNIZATION PROGRAM TO PROTECT AGAINST

DISEASES OF THE NEONATAL CALF

When to

Vaccinate/

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Disease

Immunize

Heifers and cows Rota viruses and corona viruses, Escherichia As on label
coli bacterins, clostridial bacterins

Calves

Rotaviruses and corona viruses (if indicated) As on label greatly reduced by management decisions

Stage 2 is characterized by abdominal
made before the breeding season and during contractions due to the fetus in the vaginal gestation.

canal and ends witl1 expulsion of the fetus
through the vulva. Birth should be expected

Nutrition: Heifers and cows should
within 1-4 lu· for heifers. A mature cow
maintain body condition before calving,
should calve in <3 hr if the presentation of
but overconditioning causes excess fat
the calf is normal; if no progress is seen
deposition in the udder and results in lower
within l hr, assistance may be required.

milk production. Excessive fat deposition in

Disruption of labor may occur witil
tl1e pelvis also may result in dystocia. Good
inapprop1iate intervention or social group
body condition aids in calving ease, early
stresses. "Just in time" calving strategies are return to cyclicity in beef cows, and also
based around tile need to minimize social
milk production. There is a balance to
group changes at the point of calving,
achieve between avoiding excessive
because tilese social changes are associated
condition, which leads to dystocia, and
with challenges to dry-matter feed intake.

insufficient condition, which leads to

Stage 3 is expulsion of the fetal membranes
postcalving subestrus/anestrus.

and initiation of uterine involution.

Expulsion of the fetal membranes normally

Calving Facilities: Dedicated calving
occurs within 12 hr after parturition.

facilities may be needed in many herds.

Feeding preparturient cows in the late

They should be in good repair and
morning ( 11 AM -noon) and again at night
functional before the calving season starts.

(9:30-10 PM) encourages cows to calve

Weather conditions, geographic differdtuing tile day (7 AM-7 PM), when a problem ences, and local experience usually dictate
is more likely to be identified and assistanc�
how much attention and individual care
more likely to be available.

calves will need immediately after birth.

Paiturition is often difficult for botil fetus

The calving environment ( eg, calving sheds, and dam. Many factors influence the degree small pastures) must be clean, dry, and
of difficulty, including breed, age, nutrition,
protected from the weather. A clean area to
and pelvic area of the dam; breed and
handle dystocia problems is also needed.

genotype of the sire; gestation length; and

Calving in a clean area, separated from the
sex, size, position, and presentation of the
rest of the herd, helps to reduce calfhood
fetus. Some, though not all, of these factors
diseases, particularly diarrhea (scours) and
are directly influenced by management.

Johne's disease. In large herds, several

When dystocia (see below) develops,
small calving pastures that allow regular
survival of both dam and calf depends on
rotation may help to reduce buildup of
proper assistance. This requires identificadisease-causing organisms. When calving tion of the problem, proper facilities, and
stalls are used during inclement weather,
adequate help. A delay in assisting may
they should be cleaned and disinfected
mean the loss of the calf or injury and even
between calvings.

death of the cow. However, it is important to
allow sufficient time for the dan1 to dilate

Calving: Close observation of labor is
before applying traction. Before assisting
necessary to detennine when or whetiler a
the delivery, tile position of the fetus must
delivery should be assisted. Labor is divided
be detemlined accurately, and any
into three stages. Stage 1 begins with
abnonnal presentation corrected. If the calf
uterine contractions and dilation of the
is simply too large to pass through the birth
cervix and ends with passage of the anmion
canal without danger to the cow or calf, a
and part of the fetus into the vagina. Stage
cesarean section or other surgical

1 may last 1-24 hr, with 1-4 hr being nom1al.

assistance may be necessary.

2180

MANAGEMENT OF REPRODUCTION: CADLE

Management After Calving: Muddy
disproportion is a major contributing cause
lots, crowding, filth, chilling, and inclement
of dystocia. Calf birth weight, tl1e size of tl1e
weather make the calf more vulnerable to
pelvic area of the dan1, and the inte1wlationdisease organisms and may result in ships of tl1ese two factors are major
siclmess and possibly death for botl1 dam
detenninants of dystocia. The weight of the

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and calf. Provision of adequate trough space,
calf is a function Oi genetic and environmenie, 1 m per fresh cow, and lying space in tal factors. Genetic factors include sex,
bedded yards, ie, 1.25 m2/l,OOO kg milk yield,
length of gestation, breed, heterosis,
are key factors for freshly calved dairy cows
inbreedil1g, and genotype. Nongenetic
to maximize feed intake and minimize risk of
factors include age and parity of the dam,
poor hygiene on udder health. (See also
nutrition of tile dam dming various phases

I IE:AJ;rJ I-MANAGEMENT INTERACTION: CA'ITLE,
of gestation, and environmental temperap 2119, and MANAGEMl!l{l"OFTIIE N80NA'm, p 2087.) ture. Efforts to manage the dystocia rate and moderate its effects should focus on

Passive Transfer: Calves receive
replacement heifer development, sire
inlrnunity passively from tile dam through
selection using EBVs for calving ease,
ingestion of colostrnm. The calJ's imnume
and early dystocia intervention.

system is in1mature at birtll and depends on
acquisition of passive immunity for disease

Replacement Heifer Development:

protection in early life. Immunoglobulins

Dystocia rates in beef heifers may not be

(IgG and IgM) and lymphocytes are
controlled by nutritional restriction dming
absorbed directly across tile gut into the
late pregnancy. On tile contrary, tl1e loss
ca!J's circulation to provide in1mm1ity.

of 0.5 kg/day dtui.ng the last trimester of

The ability of tile gut to absorb these large
pregnancy in beef heifers is associated
molecules and cells is a transient phenomwitll weak labor, increased dystocia rate, enon; gut closure is complete by 24 hr, and
reduced calf growth rate, prolonged
absorption has decreased significantly
postpartwn anestrns, reduced pregnancy
by 6-8 hr of age. Ingestion of adequate
rate, and increased morbidity and mortality.

an1ounts of quality colostrmn as early as

It is reconrn1ended that heifers be fed to
possible after bi.Ith is important for calf
allow modest rates of gail1 (0.5 kg/day)

survival and growtll. Calves with failure of
during late pregnancy. Protein malnutrition
passive transfer (FPT) are 3-9 times more
in late pregnancy has been associated with
likely to become sick before weanillg, and
weak calf syndrome and may be a factor

5 times more likely to die before weanmg
contiibuting to neonatal mortality.

than calves witil adequate passive transfer.

Measurement of the pelvic area of tl1e dam

Minilnizing tile incidence of FPT should
to predict dystocia is sometimes used as a
emphasize dystociarnanagement, proper
c1iterion for selection of replacement heifers,
nutrition, and intervention for calves at high
even though pelvic area alone explaillS only
risk of FPT. Cows tilat have dystocia should
a small proportion of the variability in
be milked out inunediately, and tl1e calf
dystocia. Pelvic area measmements before
actively fed colostrmn to ensw'e ingestion.

tl1e breeding season or at the ti.me of

Calves should consume 3-4 Las soon as
pregnancy exanlination have been used to
possible after calving by nasogastric tube as
estimate the pelvic area before calving.

necessary. Cows witil poor udder confonna

Those heifers witl1 a small pelvic area before
tion or mastitis should be milked, and the
the breeding season may then be culled or
colostrnm fed to tile calf to ensure timely
selectively mated to easy calving buJ!s, and
intake. Colostrum supplements may not
tl1ose witl1 a small pelvic area at tl1e ti.me of
prove adequate, as shown in controlled
pregnancy examination may be aborted,
clinical trials, to increase serm11 IgG levels.

cuJ!ed, or identified for careful observation at

Vaccination of tile cow witil pathogens
calvil1g. Some evidence suggests that culling
causing enteric disease in calves before
heife1s witll the narrowest pelvic width may
calving may be a useful acljunct to good
be more effective tilan cuJ!illg based on
overall management in reducing morbidity.

pelvic area; however, such "pelvin1etry"

Hygienic management of colostrum is vital
measmements may only detect the outlier
to effective absorption, and eitiler careful
anilllals in tl"tis multifacto1ial condition.

pasteurization or cooling of lidded
contail1ers should be considered.

Sire Selection: A combillation of cuJlillg
heifers with small pelvic areas and using

DYSTOCIA MANAGEMENT
bulls tilat siI·e calves witll small birtll weights
may reduce dystocia significantly. Using only

Dystocia management must begin witil
tile sires' birtll weight to control calf birtl1
proper heifer development. Fetopelvic
weight and dystocia is not effective. A large

MANAGEMENT OF REPRODUCTION: CADLE

2181
number of nongenetic influences affect birth

Appropriately Early Intervention:

weight, such as age of the dam, environment, Despite tl1e best efforts to avoid dystocia, and birth type. The ability to identify sires
some cases will be seen. Early intervention
approp1iatc for use on replacement heifers
minimizes tl1e effects of clystocia on calves;
has advanced signilicantly.

however, heifers especially may require

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The use of estitnated breeding values
significant time to dilate to pomt of delivery.

(EBVs) or expected progeny differences

Heifers should be monitored regularly and

(EPDs) for bir'th weight is more effective
provided witl1 assistance promptly if stage II
than using only sire birth weight in selecting
labor is prolonged ( eg, 1 hr). Producers need
for acceptable birth weights. EPDs are
to identify the level of dystocia and growth
reported in the units of the trait they reflect
that is economically acceptable and select a

( eg, pounds for birth weight). Along with
bull to match. They must be weU trnined to
each EPD is rep01'ted an accuracy ranging
mte1vene appropriately it1 dystocia and
from Oto 1. Higher accuracies ir1cticate a
recognize when to call the vete1imuian. A
higher level of confidence tl1at the stated
general rule is that if a heifer has not made

EPD truly reflects the bull's effect. EPDs
significant progress in clelivermg her calf
most effectively help compare bulls rather
witl1in 30 min, it is tirne to get help.

than identify tl1e specific effect a bull will
have on a herd. For exan1ple, a bull with a

COW-CALF PAIR MANAGEMENT
birth weight EPD of 4.0 would be expected
to sire calves 6 lb heavier on average than a

Cows and heifers should be moved from
bull with a birth weight EPD of-2.0 when
winter grounds to calving grounds 2 -3 wk
bred to the same group of heifers. An
before calving season begms. They should
attempt should be made to identify bulls
be sorted into groups based on estimated
with good calvit1g ease EBV figures and low
calving date. This elate can be detennined at
birth-weight EPD for use on heifers while
the tit11e of pregnancy exanlination, when
maintaining at least moderate weaning and
cows and heifers a.re grouped based on
yearling weight EPD. Th.is is best achieved
estimated duration of gestation. Separation
by the use of AI sires with high accuracy
of the herd into groups allows more

EPD. EPD can be calculated on yearling
concentrated obse1vation of a smaller
bulls with no progeny, but tl1e accuracy is
nun1ber of cows or heifers that are more
low. Until recently, EPDs were useful only
likely to calve and potentially need help.

in comparisons wiiliin breeds; however,

Cows and heifers should be observed to
methods for across-breed EPDs have now
ensure tl1ey accept and mother tl1eir· calves.

been developed. This is of particular use

Heifers especially are at risk of calf
in selecting bulls to control dystocia ir1
rejection, which increases the risk of calf
crossbreeding programs. Two recent
disease. If heifers do not accept tl1eir calves
innovations in the use ofEBVs/EPDs for
and allow nursing witl1in a short tinie, they
management of dystocia are the calving
should be brought into the calving barn and
ease EPD and tl1e maternal calving ease
restrained to allow the calf to suck. Heifers

EPD. Calving ease EPD is related to birtl1
that experience dystocia. and human
weight EPD but may predict calving ease
assistance are at increased risk of rejecting
more effectively. Maternal calving ease is
tl1eir calves. Cows or heifers that expe1ia measure of tl1e effect of the maternal ence ctifficulty in calving or mothering
grandsire and the ease with which a bull's
should be moved to the calving barn for
daughters will calve.

assistance and monitormg. Pairs ente1ing

As the birth weight of tl1e calf increases,
the calving barn are at increased risk of
the incidence of dystocia often also
disease because of dystocia, mismothering,
increases. Calving difficulty is higher for
hypothermia, and exposure to a higher
male than female calves. Abn01rnal
population density. Once a pair enters tl1e
presentations of tl1e calf accounted for 22%
calving barn, they should not go to the
of dystocias and 4% of all bi1ths it1 one study. general nursery pasture but to a separate Most dystocias are seen in primiparous
high-risk nursery. Calves in the high-risk

2-yr-old heifers, and the frequency
nursery can be monitored more closely for
decreases witl1 increasing age and weight of
morbictity and treated promptly. Segregathe cow. Some studies have suggested that tion of these high-risk calves also avoids
cows t11at previously experienced dystocia
exposure of the rest of the herd. Considera are more likely to do so again. Environmention should be given to management of tal effects may also have an effect on calf
infectious diseases such as Johnes ctisease
birth weight and dystocia. Culd weatl1er
by segregating higher-risk cows from
may ir1crease birth weights and subselower-risk cows tllroughout this calving quently increase tl1e incidence of clystocia.

management period.

2182

MANAGEMENT OF REPRODUCTION CADLE

Once cows or heifers have calved, the
multiply in clinically ill calves and cause
pair should be moved out of the calving
high levels of environmental contaminaarea to a nursery pasture within 24 hr.

tion. The morbidity nursery may be

When the pair has bonded and passive
combined with the high-risk nursery, but
transfer has occurred, movement to a
this increases exposure of the high-risk

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nursery with decreased population density
calves to pathogens. Ill calves should not
minimizes infection rates. Sick calves in
be returned to the general nursery area.

the healthy nursery pasture should be

Treatment equipment should be disinremoved and brought to the barn for fected thoroughly between calves to avoid
treatment if necessary and placed in a
transfer of infectious agents from calf to
morbidity nursery. Infectious agents can
calf.

MANAGEMENT OF

REPRODUCTION: GOATS

PUBERTY AND ESTRUS
pregnant, and although natural service will
not interfere with pregnancy, these does

Goats are spontaneously ovulating,
should not be artificially inseminated.

seasonally polyestrous animals with peak

Ovulation can occur anytin1e from 9 -72 hr
sexual activity occurring in the fall when
after the onset of estrus, typically toward
day length is decreasing. Factors that affect
the end of standing estrus. The ovulation
onset and lengtl1 of the breeding season
rate varies based on breed, season, and
include geographic location (latitude and
nut1ition. Angora goats typically have a
climate, specifically), breed, social
single ovulation but may have two if
structure, and photoperiod. In temperate
sufficient nutrition is available. The average
regions, the natural breeding season is
ovulation rate has been reported to be 1. 7
mostly restricted to the fall and winter to
eggs per doe in Boer goats and 1.5 in Maure
allow for kidding in the spring and summer,
goats. "Focused feeding," in which a
when nutritional conditions are adequate.

nutritional boost is supplied in a short

Under tropical and subtropical conditions,
period of time, has enhanced reproductive
where temperature and photoperiod are
efficiency in nuninants without affecting
less variable, certain breeds can have an
body condition. Also known as both "acute"

extended breeding period if appropriate
or "immediate nutrient" effect, this practice resources are available to allow for kidding
leads to a positive energy balance, which
year-round. The average duration of the
increases leptin and insulin concentrations,
goat estrous cycle is 21 days but can vary
enhances glucose uptake, and is positively
with different breeds or environment.·A
associated with increased folliculogenesis
relatively high frequency of short cycles is
and increased ovulation rate. Supplementacharacteristic of goats and tend to occur in tion with 13-carotene, a vitan1in A and
young does, at the onset of the breeding
retinoid precursor, at 50 mg/goatlday has
season, and with prostaglandin induction of
been shown to produce this effect in does.

ovulation. Longer cycles may be seen later

The onset of puberty typically occurs at
in the season.

6--8 mo of age but varies depending on the

The average duration of standing estrus is season of birth, breed, nutritional status, 36 hr but can range from 24--48 hr dependand presence of a male. Pygmy goats and ing on age, breed, season, and presence of
does of larger breeds may reach puberty as
a male. Breed-specific estrus duration has
early as 3 mo old; however, breeding should
been reported for Mossi (20 hr), Angora (22
be delayed until the animal has reached at
hr), Creole (27 hr), French Alpine (31 hr),
least 6()0;6 of its mature body weight to allow

Boer (37 hr), and Matou (58 hr) breeds.

for higher conception rates and safer

Estrus detection is based on behavioral
partruition. Larger goat breeds (eg, Nubian,
signs, bleating, flagging of the tail, reddened

La.Mancha, Boer, and Saanen) can be safely
vulva, vaginal discharge (which causes the
bred at -70 lb (32 kg). Angora kids should
tail hairs to stick together), and occasional
weigh a mininuun of 27 kg and are

"riding" by other does, although this last frequently not bred until they are 1 V2-2 Y2 yr
sign is far less common than in cattle. Goats
old. Puberty in well-grown bucks can be
can show overt signs of estrus while
seen as early as 4 mo.

MANAGEMENT OF REPRODUCTION: GOATS

2183

BREEDING SOUNDNESS
reproductive exan1ination in a young

EXAMINATION
breeding buck should include confirmation
that both testicles have descended. The

The external genitalia of does should be
scrotum should be evaluated for size,
examined for abnonnalities such as an
lesions, or other signs of injury. Testicular

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enlarged clitoris, hypotrophic vulva, or
hypoplasia occurs in only -20,,6 of intact
increased urogenital dist.ance that suggest
bucks and is mostly associated witl1
intersex, a condition common in homozyintersex condition, but it may also be a gous polled females, especially in Alpine,
manifestation of malnutrition. As in otl1er

Saanen, and Toggenburg breeds. Intersex
species, scrotal circmnference is positively
goats are sterile and should be culled.

correlated with semen production capacity

Occasionally, a doe has a shortened vagina
and should be >25 cm in mature bucks(> 14
and no cervix, and segmental aplasia of
mo old). Scrotal circumference can vary by
va.iious parts of the tract can occur. A specuseason and decrease by as many as 3 cm lum can be used to exa.inine the walls of the
outside the breeding season. Because
vagina, vestibules, and cervix to sea.i·ch for
scrotal circumference and body weight are
lesions in does with fertility issues.

positively correlated in bucks, scrotal

Transabdominal and/or transrectal
circmnference measurements are of
ultrasonography can be used to exa.inine the minimal value before 14 mo of age.

uterus and ova.i·ies for cysts, pseudopreg

The testicles and epididymis should be
nancy, or other abnom1alities. In cases of
synrn1etJ.ical and finn on palpation. Any
valuable breeding does, surgical laparosasyn1metry or changes in tone may indicate copy or laparotomy may be used to check
infection or injury and will likely adversely
for causes of infertility such as oviductal
affect fertility. Orchitis a.i1d epididymitis are
blockage, tumors, adhesions, or segmental
both ra.i·e, occuning in -1 % of breeding
aplasia that may not be visible on speculum
bucks, and affected bucks should be tested
exa.i11ination or ultrasonography.

for Brncella melitensis, because bred does

A thorough physical exan1ination of
are at risk of stillbirths and abmtions. Other
the buck before the breeding season is
causes of orchitis and epididyn1itis are of
important to determine the ability of the
minin1al concerns for transmission;
buck to safely mount and breed a doe.

however, treatJ.nents a.i·e generally

Bucks should have a body condition score
unrewa.i·ding. Gaseous lyn1phadenitis (see
of 3-3.5 ( out of 5) and be structurally sound
p 63), spermatic granuloma, and calcificawith no visible foot or leg abnonnalities.

tion of the testicles ( which also may be due

The buck should be in overall good health,
to Corynebacterium pseudo tuberculosis
because a.i1emia due to heavy pa.i·asite
infection) all reduce or eliminate the buck's
infections and chronic debilitating diseases,
fertility, and infected bucks should be
such as pneumonia, can lead to loss of
culled. In extreme cases, ultrasound may be
libido. Any degree of foot abnonnalities,
used to detennine whether one or both
from overgrown hooves to severe lanlinitis,
testicles are affected and if herni-castration
may cause the bucks to be reluct.ant to
is an option.

mmmt and should be treated appropriately.

Evaluation of semen quality is another

Bucks with caprine arth1itis-encephalitis
important part of the breeding sotmdness
virus infection ( see p 7 4 7) may have painful, exanlination. Semen can be collected either
enlarged stifles, and if they are even able to
by use of an artificial vagina or with an
mount, are usually reluct.ant to ejaculate
electroejaculator. The former yields a
because of pain.

higher quality sa.inple but requires the

A complete assessment of the reproducpresence of a doe in heat to perfom1.

tive orga.i1s should be performed and

Electroejaculation is more convenient and,
include an evaluation of the penis and
thus, used more commonly. Once semen is
prepuce. The buck is set on his rwnp, and
obtained, it should be maintained at 37°C
the shoulders pushed down to cwve the

(98.6°F) and evaluated as quickly as
spine convexly; this makes it easier to
possible. Grossly, the semen should be
protrude the penis. Shearing wounds
cloudy, white, and free of urine, blood, pus,

(especially in Angoras), prior bala.i1oposthior dirt. Occasionally, semen will be an tis, and old fly-strike wounds a.i1d scarring
off-yellow color and may be normal but
arom1d the prepuce may make protrusion of
should be examined more closely for wine
the penis impossible. Prior amputation of
cont.an1ination. The semen should be
the urethral process to prevent obstruction
evaluated microscopically for motility,
by a calculus has no apparent deleterious
morphology, and presence ofWBCs. Gross
effect on breeding ability. Although
motility can be measured by placing a drop
cryptorchidism is ra.i·e, a thorough
of undiluted semen on a wam1ed slide and

2184

MANAGEMENT OF REPRODUCTION: GOATS
evaluating on low-magnification. A
have had estrus induced outside the nom1al
satisfactory sample should exhibit
breeding season; therefore, collections are
anywhere from general oscillation to
more successful when young bucks are
vigorous swirling. Sporadic oscillation to no
used. The optimal sperm concentrations
motility at all indicates poor semen viability.

depend on the individual buck and

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Individual and progressive motility should
production settings but should be -200-400
also be measured by diluting the semen with million/mL to account for an approxin1ate an isotonic diluent ( eg, 0.9% saline) and

500/o death and damage rate during semen
evaluating microscopically. Sperm cells
processing and thawing. There is no
should be counted to determine a percentlegislation or industry-wide standard in age of progressively motile spem1, with a

North America that governs the collection,
minimum of 30% being acceptable. Spem1
processing, and sale of frozen semen, but
morphology should also be assessed
country-specific legislations should be
microscopically, with a minimwn of 700/o
reviewed and followed before exporting
normal being acceptable. (See ai,so BREEDING
semen.

SOUNDNESS EXAMINATION OF THE MALE, p 2234.)

Embryo transfer allows for dissemination
of valuable female genetics. Its application

BREEDING
in goats is somewhat limited because of tl1e
variable response of does to superovulation

Natural service is the easiest and most
techniques. Control of tl1e estrous cycle is
common breeding system. Most hobby
crucial to ensure adequate timing for
operations have a low doe: buck ratio (5: l )

induction of superovulation, which is
because of multiple breeds and different
achieved by treating witl1 conunercially
bloodlines. Bucks have a strong libido and
available follicle-stimulating honnone
can breed far more does than this, although

(FSH) products. Lapa.roscopic insemination
as they get older, and especially during the
of semen is reconunended to confirm that
off-season, they are less efficient.

superovulation occuned (via visualization

Aitificial insemination (Al) is increasingly
of multiple corpora lutea) and to allow for
being used by goat producers, because it
the greatest conception rate. Embryo
allows for both dissemination of valuable
retrieval can be achieved surgically,
genetics and control of sexually transmitted
laparoscopically, or transcervically, with
diseases. Proper heat detection ancVor
surgical techniques providing tl1e highest
hormonal synchronization of the estrous
recovery rates. Embryos can then either be
cycle is essential and may lead to increased
transferred inunediately via laparoscopic or
labor and costs. Ovulation in does occurs
surgical techniques into synchronized does
toward the end of standing estrus; thereor frozen in liquid nitrogen.

fore, insemination must occur around this
tin1e to be effective. The M1:PM rule is

INDUCTION OF ESTRUS
generally used: if the doe is first noticed
to be in standing heat in the morning, Al

Estrus can be induced in several ways,
should be pcrfonned in the evening ( or vice
depending on the tin1e of year and the
versa). However, breed-specific.estrns
relationship to tl1e doe's natural breeding
durations should be considered when
season. Out-of-season breeding is of interest
deciding the best time to inseminate.

to dairy goat owners, because it reduces

Vaginal (pericervical deposition) or cervical
seasonal fluctuation in tl1e herd's milk

(intracervical deposition) insemination
production. In meat production systems,
techniques are inexpensive and easy to
increasing conception rates and litter sizes
perform and can result in acceptable
are important and can be manipulated using
pregnancy rates if fresh semen is used.

hom10ne therapy.

However, if frozen semen is used, transcer

The sudden introduction of an odorifervical or laparoscopic intrauterine inseminaous buck often advances the onset of tion techniques must be used, which are
cycling by a few weeks, and tl1e does also
more expensive and require more skilled
may show some synchronization. The buck
personnel. Frozen semen in 0.25--0.5 mL
should be housed well away from tl1e does
straws may be purchased directly from

( out of their sight and smell) for 2:3 wk
buck owners or custom collectors.

before introduction. Even if tl1e whole

Semen can be collected for Al in an
group does not cycle, this method can
artificial vagina or with an electroejaculator.

get a few to conceive in the theoretically

Most bucks will mount a doe in P.strus and
out-of-season period.

ejaculate; with training tl1ey can ejaculate

Providing 20 hr of light per day in January
year round and even mount wethers. Older
and February (northern USA), witl1 a
bucks are often reluctant to breed does that
sudden return to available daylight on

MANAGEMENT OF REPRODUCTION: GOATS

2185

March 1, will bring goats into estrus several
clay 27. Transrectal ultrasound is more
weeks later. In this system, it is more
difficult and time consmning but can
difficult for the owner to pick out the does
diagnose pregnancy as early as 20 days.

that are in estrus; consequently, running a

The accuracy of transabdominal ultrasound
young, vigorous buck with the does gives
to differentiate the presence of a single

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tl1e highest conception rate. If a po1tion of
fetus from multiples varies from 45o/o-55%
the herd is artiiicially synclU'onized, some

(possibly higher with skilled operators).

of the remaining does also may come into

It is extremely difficult to accurately
estrus.

differentiate between twins, triplets, and

The Animal Medicinal Drug Use
quadruplets using ultrasound at any time

Clarification Act of 1994 (AMDUCA)

during gestation. Fetal sexing may be
places limits on extra-label drug usage in
perfom1ed by skilled ultrasonographers
food-producing anin1als in the USA and
between clays 55 and 70 of gestation and is
restricts extra-label use to animals that
more accurate in singles versus multiples.

are suffering or in danger of death. U ncler

Routine radiography can be used to detect

AMDUCA, pharmaceuticals cannot be
pregnancy witl1 lO()OA, accuracy after day
used to alter reproduction for production

70 and can detect the mm1 ber of kids after
purposes, and the following comments
day 75.

about manipulating reproduction are

Progesterone concentrations can be
provided for use in cotmtries outside the
measured in milk or serum, but samples

USA.

must be collected precisely one cycle after

If the corpus lutemn is fm1ctional, a
the doe was bred. Whereas low progestersynthetic PGF2a analogue will induce one levels can confim1 a nonpregnant
estrus; however, this is not effective clming
status, high progesterone is not a positive
anestrus. Additionally, it may provoke short
pregnancy test, because it cannot differenticycles that tend to be seen normally at the ate between mid cycle, true pregnancy, or
beginning of the season. Melatonin in1planls false pregnancy. Plasma progesterone levels may also be used to produce sho1t-day
in pregnant does have been reported to be
effects and induce sexual activity in both
higher in triplets versus twins versus single
does and bucks.

fetuses at 84--21 days before kidding. The

Progestagen treatment, followed by
estrone sulfate test, perfom1ed on plasma,
administration of FSH or pregnant mare
milk, or urine, is another way to determine
sermn gonadotropin (PMSG), will cause
pregnancy. Between 15 and 20 days after
out-of-season estrous activity. Good
conception, the level of estrone sulfate,
conception rates can be achieved with
a conjugated estrogen produced by the
this system, and fixed-time insemination
conceptus, increases substantially and stays
is feasible, but these products (FSH and
increased throughout pregnancy. Higher

PMSG) are not approved for use in goats.

concentrations of estrone sulfate have aeen

Progestagen treatment can be in the form of
repo1ted in does carrying twins or triplets
injections with an oily base every 3 clays,
than those bearing a single fetus. Abortion,
impregnated vaginal sponges ( eg, flurogefetal death, or resorption ca.uses tl1e estrone stone acetate or methyl acetoxyprogestersulfate level to drop; therefore, the test also one ), norgestomet implants, oral
is a useful measure of fetal viability.

administration of melengestrol acetate,

Pregnancy-speciiic protein B (PSP-B), also
or a controlled intravaginal drug-releasing
known as pregnancy-associated glycoprodevice, or CIDR (which is a fonn of tein, is produced by the placenta and can be
progestagen-impregnatecl silastic for
detected in serum or plasma of pregnant
vaginal use). A commercial product
does by ELISA at least 30 days after
marketed for use in swine containing both
breeding.

PMSG and hmnan chorionic gonadotropin

Precocious milking is conrn1on in
will also cause does to cycle outside the
heavy-milking strains of goats. It can be
nonnal breeding season when administered
seen in a virgin doe or during the first
at the end of progestagen treatment.

pregnancy. Therefore, udder development
is no guarantee of pregnancy.

PREGNANCY DETERMINATION

Hydrometra, or pseudopregnancy, is well
documented in goats, although its ca.use is

Pregnancy detemtination can be performed largely m1known. Aseptic fluid a.ccunrnla.tes using real-time ultrasonography and is very
within the uterus and is accompanied by
accurate with a skilled operator. Transabhigh peripheral concentrations of progesterdominal ultrasound is quick and reliable one due to a failure of luteolysis. It can be
and can detect pregnancy as early as 25
both shorter or longer than a true pregnancy
days, witl1 the fetal heart beat detectable by
and occurs in 3o/o-3()0A, of dairy herds.

2186

MANAGEMENT OF REPRODUCTION GOATS

Approximately 500/o of pseudopregnancies
whereas dexan1ethasone (20 mg) requires
occur as a result of early embryonic death

-48 hr to induce kidding. Viability of
at �40 days of gestation. An additional
multiple fetuses may be compromised if
mechanism involves spontaneous persisparturition is induced before day 144.

tence of the corpus lutewn, which occurs

Pregnancy toxemia in goats is simiJai· to
more commonly in older goats, does bred
that in sheep (seep 1021). It occurs during VetBooks.ir
out of the natural breeding season, or after
the final 6 wk of pregnancy and is more
induced ovulation. In some cases, ovaiian
common in overconditioned does and in
cysts may also be present; therefore, it is
does pregnant with multiple kids. It is
recommended to always treat for both.

caused by reduced feed intake coupled with

Usually, the udder enlarges, but tme
high energy demand, leading to ketosis.

filling does not occur. The doe may show

Treatment depends on severity of the
behavioral signs of impending parturition,
condition and can range from dietary
possibly even calling or searching for the
modification with oral administration of
nonexistent kid. The diagnosis can be made
propylene glycol to intensive supportive
by excluding pregnancy coupled with the
cai·e with administration of IV fluids with
presence of clinical signs. This condition
dextrose, insulin, and pregnancy induction.

can be treated with prostaglandin to lyse the

Vitamin B,2 may also be administered as an
corpus luteum, and does may be able to
appetite stimulant. Lactational ketosis is
conceive again if diagnosed and treated
similar and occw·s within the first 3 wk of
early. However, if the condition persists or
lactation in high-producing dairy goat
recurs, the chances of future conception
breeds; clinical signs include irritability,
decline. For commercial dairy herds,
anorexia, reduced milk production, and
this can produce moderate to severe
weight loss. Treatments include IV glucose,
economic losses.

oral glucose, and/or oral propylene glycol,

Goats tend to have a high incidence of abordepending on severity. Hypocalcemia or tion, with chlamydiosis ( Chlamydia psiltaci) milk fever (seep 991) is seen in high-producand toxoplasmosis (Toxoplasma gondii) ing, older (>3 Y1) dairy goats, but not neai·ly
being commonly identified causes in the USA
so frequently, nor as severely, as in cattle.

( see ABORrION IN GOATS, p 1340). In cases of Treatment includes IV administration of
abo1tion, the fetus and placenta should be
calcium gluconate or calciw11 boroglucosubmitted to a diagnostic laboratory to nate solution.

exclude infectious causes. Paired serum

Vaginal prolapse is fairly common (see
sainples should be obtained from the doe
p 1390) in does and is believed to have a
and saved in case serology is indicated. A
hereditary component. It may intermittently
thorough history, including nutrition and any
occur dming late pregnancy due to
recent changes in husbandry, should be taken. increased intra-abdominal pressure.

If complete vaginal prolapse occurs,

PREGNANCY
intervention is required to prevent injmy,
infection, or dystocia. Owners should be

Gestation length is 145-155 days ( average
advised that vaginal prolapses will recur

150 days) and can be affected by breed,
with each pregnancy, so they can decide
litter weight, environment, and parity.

whether to cull the anin1al.

Generally, first-kidding does have one or
two kids, and in subsequent kiddings,

PARTURITION
triplets and quadmplets are not w1common,
especially in large, well-fed, heavy milkers.

Partm·ition tends to be W1eventful in goats,

Quintuplets and sextuplets are rare.

with the incidence of dystocia <5%. If the

Progesterone production for maintenance
doe has been in active labor for 30 min with
of pregnancy is entirely dependent on the
no progress, assistance is likely required.

corpus luteum, with a drastic decline in

Most kids present cranially, in dorsosacral
progesterone occurring 12-24 hr before
position, witl1 limbs extended. If kids
kidding. Induction of paitmition is a useful
present caudally, which is more conunon in
technique to increase survival in dairy goat
twins, triplets, and quaclmplets than
kids and to catch and separate kids from
singletons, assistance for delivery is more

<la.ins before they suckle in herds with
likely to be required. The most common
control progran1s for caprine arthritis
cause of dystocia is when two or more kids
encephalitis vims and mycoplasma.

present at the san1e time; other causes

Induction with synthetic PGF,o. analogues
include malposition, fetomatemal
such as cloprostenol (125 mg) or dinoprost
mismatch, failure of cervical dilation
tromethainine ( 10 mg) usually results in

(ringwomb ), vaginal prolapse, uterine
delivery of kids -30-35 hr after ir\jection,
torsion, and uterine inertia. Most dystocias

MANAGEMENT OF REPRODUCTION HORSES

2187
can be corrected by repositioning kids and
antibiotics are warranted. Clostriclial
providing lubrication and traction.

organisms (Clostridium tetani and C

However, in more severe cases, fetotomy or
pe'lfringens) may colonize the uterus,
cesarean section may be indicated. Extreme reswting in a frequently fatal toxemia that care must be exerted when assisting with
requires aggressive suppmtive care,
kidding to prevent ute1ine tears, which can
antibiotics, and antitoxin therapy. Less

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be diagnosed on palpation of the uterus
severe causes of metritis may lead to a
after the dystocia. Small tears can be treated cluonic endometritis and cause infertility by hastening involution of the uterus with
if not treated.

oxytocin administration. Larger tears may

Uterine prolapse is uncommon in goats
require surgical intervention to minimize
but may occur after dystocia. Treatment
excessive bleeding and peritonitis. Systemic is similar to that in other species, and antibiotics, anti-inflanunatory drugs, and a
prognosis is good if recognized and treated
clost1idial vaccine booster shottld be
early.

provided after a prolonged dystocia.

In extremely cold weatl1er, newborn kids

Retained placenta (not passed 12 lu after
shottld be dried ( especially the ears) to
parturition) is unconunon in goats and is
prevent frostbite. Heat lamps are not
usually associated with selenium deficiency,
necessary if tl1e kids are dry, well fed, and
the birth of a mununi.fied or rotten fetus, or a out of a draft. Kids born in intensive systems difficwt delivery. It can be treated by gentle
should have their navels dipped in tincture
traction or horn10ne therapy to facilitate
of iodine to prevent infection. Angora,
expwsion, but diagnosis and treatment of
pygmy, and meat kids are typically raised on
the tmclerlying cause will usually solve the
the dan1. Dairy goat kids often are removed
problem. Metritis is almost always a sequela
at birth and, after receiving colostrtun, fed
of retained placenta, and systemic
from a bottle or nipple-pail.

MANAGEMENT OF

REPRODUCTION: HORSES

REPRODUCTIVE CYCLE
follicles or corpora lutea. The cervix may
be closed but not fu111 and tight,.or it may

Nearly all mares are seasonally polyestrous
be thin, shmt, and dilated. As the length of
and cycle when the length of daylight is
daylight increases, mares undergo a vernal
long. Anestrus is seen during the winter
transition and the ovaries become active,
when daylight length is sho1t. During
with nun1erous large (>25 nun) follicles.

anestrus, the uterus is flaccid, and the

The cervix and uterus have minimal tone.

ovaries are inactive with no significant

Mares have tluee or four prolonged
intervals of estrus (periods of sexual
receptivity to the stallion) during the vernal transition, but ovttlation does not occur. The
end of vernal transition is marked by a surge
of luteinizing honnone and subsequent
ovttlation. After this ovttlation, tl1e first

21-day interovttlatory period of that
breeding season occurs and a regular
estrous cycle is established.

Although tl1e mare continues to ovulate
regwarly every 21 days throughout the
breeding season, the length of estrus varies,
ranging from 2-8 clays, and the length of
diestrus varies accordingly to maintain a

During the vernal transition, the mare's

21-day interval. Early in the breeding
ovaries will enlarge and contain numerous
season, estrus tends to be longer, whereas
large (>25 mm) follicles but no luteal
around the sununer solstice tl1e mare may
structures. Courtesy of Dr. Patricia Sertich.

be sexually receptive for only 2-3 days.

2188

MANAGEMENT OF REPRODUCTION: HORSES

Mares have two follicular waves each
incliviclually in a stall or as a group in a
cycle. The first wave of follicular developlighted paddock.

ment occurs dming diestrus, and these
follicles become atretic. The second wave

Manipulation of Ovarian Activity:

occurs after luteolysis and is associated

Ovai.·ian activity is frequently mat1ipulated

VetBooks.ir
with estrus. Early in estrus, the endometiial
by administration of hom10nes to facilitate
folds of the uterus are edematous, but the
scheduling of breeding appointI11ents and to
edema wanes as ovulation approaches.

limit the nwnber of breedings per estrus.

Usually, one follicle becomes dominant and

Breedings should be spaced for stallions
ovulates when it is <!30 mm in diameter. The
with large books of mares so that semen
dominant follicle enlarges and then softens
use is optin1izecl. Geographic locations
just before ovulation. The oocyte is released
and transportation constraints may also
through the ovulation fossa. A corpus
necessitate scheclulecl breedings. Many
hemorrhagicum and subsequent co1pus
situations can benefit from an ovulation
luteum fonn and produce progesterone,
control prograi.n. (See also HOllMONAL CONTllOL
which stimulates closure of the cervix and

OF ESTRUS, p 2244.)

an increase in uterine tone. This corpus

Administration of prostaglanclin (PGF,a),
lutewn will be mature and become

IM, to a mare in cliestrus causes luteolysis
responsive to prostaglanclin in -5 clays. If
ai.1d allows a follicle to matw-e and ovulate.

pregnancy is not established, luteolysis

The corpus lutem11 must be 5-14 days old to
occurs at 14 days, and the mare returns to
respond to PGF2a. The mai.·e will come into
estrus and continues to cycle.

estrus 2-5 days after administration of

PGF2a. Tin1e to ovulation is variable (3-10

Artificial Manipulation of Photoperiod: clays) and depends on the stage of the After winter anestrus and the vernal transimai.·e's cw-rent folliculai.· wave and on the tion, cyclicity naturally starts sometime
size and character of follicles at the tin1e of
in the spring, when breeding can begin.

PGF.,a administration. It is recommended

Because changes in the mare's genital tract
that the mai.·e's ovaries be exai.nined by
are seen in response to the length of
palpation and ultrasonography at the tin1e
daylight, the onset of ovulation and
of PGF2a administration to optimize the
subsequent regular estrous cycles-and
prediction of ovulation.

thus, the onset of the breeding season--can

Dinoprost, a natw-ally occw-ring PGF2a
be hastened by exposing the mare to 16 hr

(1 mg/45.5 kg, IM), may cause transient
of light per day; 8-10 wk are required for
adverse effects such as lowered body
mares to respond. If the breeding season is
temperatw-e, increased heai.t at1d respirascheduled to begin February 15, mares t01y rates, sweating, muscle crai.11ping,
should be exposed to daily supplemental
colic, ataxia, and weakness. Signs are seen
ai.tificial lighting starting on December 1.

within 15 min and usually subside within 1

Mares need to experience a natural
hr. Synthetic preparations, eg, cloprostenol
photoperiocl of decreasing length of daylight soclitm1 (0.55 mcg/kg, IM), have fewer in the fall. Mai.·es cai.1 then be abruptly
adven;e effec.:L8.

exposed to 16 hr of light each day, or the

Hmnai.1 ch01ionic gonaclotropin (HCG)

supplemental light can be gradually

2,500-5,000 lU, IV or IM, has been adminisincreased to a 16-lu- day throughout 60 days.

tered ( off-label use) to hasten ovulation of a

In an abrupt lighting prograi.n, mai.·es living
dominant follicle dw-ing estrus. If the mare
in natw-al daylight are exposed to supplehas a preovulatory follicle <!35 mm diai.neter, mental light from -4:30 pm until 11:00 pm
ovulation occurs within 36-48 lu- after
daily. In a less expensive, energy conservadministration. An FDA-approved ing, stepwise progran1, mares can be
preparation of deslorelin acetate is available
exposed to 3 hr of supplemental light in the
ai.1d eliminates the need to use HCG
evening the first week of December, and
off-label. This sustained-release GnRH
then the supplemental light is increased by
analogue will cause ovulation within 48 hr

30 min each week until rnai.·es are exposed
of administration to an estrous mare with a
to 16 hr of light each clay. An automatic

30-40 mm follicle.

timer aids compliance and saves on labor.

Ovulation can be timed accurately using

The supplemental light must be aclclecl at
the following protocol (not FDA approved):

dusk; light added in the morning before

On days 1-10, 10 mg of estradiol 17-13 and
dawn is not effective. A minimum of 10

150 mg of progesterone are administered
foot-candles (107 lux) of incai.1clescent or

IM. On day 10, clinoprost (1 rng/45.5 kg, IM)

fluorescent light is necessary. 111e ai.nount
is also administered. On day 16, mares come
of light should allow one to comfortably
into estrus, and insemination should be
read newsprint. Mai.·es cai.1 be stimulated
performed on clay 19 or 20. Most (85%)

MANAGEMENT OF REPRODUCTION: HORSES

2189
mares ovulate on day 20, 21, or 22. This
stimulus for semen collection from a
regimen is effective at any time in cycling
stallion.

mares except when a large, dominant

Mai·es nonnally have three or four
follicle <48 hr from ovulation is present.

prolonged periods (7-14 days) of sexual

If a mature follicle is present, the protocol
receptivity during the vernal transition

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should not begin until after ovulation.

before tl1e first ovulation of tl1e breeding

Altrenogest is a synthetic progestin that
season occurs. Sin1ilar long periods of
suppresses the receptive sexual behavior of
sexual receptivity occur eluting the
estrus. Altrenogest is administered at 0.44
auttunnal transition between the breeding
mg/kg, PO by dose syringe or top-dressed on season a11d winter ai1estrus.

feed for 12-15 days. Estrus occurs 4-5 days
after treatment ends, with variable tinting of
ovulation (8--15 clays). Although altrenogest

BREEDING SOUNDNESS
effectively suppresses estrus (sexual

EXAMINATION OF THE MARE
receptive behavior), it does not consistently
control the time interval to ovulation.

A comprehensive reproductive evaluation
is recommended for the mare that has

Estrus Detection: Frequent palpation
unknown or questionable fe1tility.

and ultrasonography of t11e genital tract,

Abnom1alities can be diagnosed a11d
excellent record keeping, and administraapprop1iate therapy instituted to con-ect tion of hom10nes allow vete1inaiia.ns to
any problem before breeding is scheduled.

intensively monitor ai1d manipulate a mai·e's

A coordinated plan of management should
estrous cycle. But breeding mai1agement
be developed based on the mai·e's history
can be optimized if a good estms detection
of reproductive performance, previous
prograin is in place. A mare detected in estrus treatments, exainination findings, will prompt the breeding fai,n ma11ager to
laboratory test results, and intended use.

exainine and prepai·e the mare for breeding.

Theriogenologists typically exanline

Estrus may be tl1e first indication tl1at a
mai·es for breeding sotmdness before
pregnai1t mai·e has experienced early
purchase or breeding or when a mai·e is
embryonic death or an abortion.

barren. A complete breeding soundness

The mare should be presented to a
exainination incl ucles exai11ination of the
stallion (teaser) daily or every other day
external genitalia and mammary glaitd,
during the breeding season, a11d tl1e mare's
palpation and ultrasonography per rectum
behavioral response accurately inte1preted
of the internal genitalia, ma11ual a11d visual
and recorded. Mares in estrus raise their
vaginal exanlination (vaginoscopy), aerobic
tail, squat, minate, eve1t t11e vulvar lips to
culture of an endometrial swab/sainple,
expose the clitoris, and ultin1ately tolerate
cytologic evaluation of an endometrial
copulation. Mai·es in diestms usually squeal, swab/san1ple, and hist·oJogic evaluation kick, bite, and reject the stallion's advances.

of ai1 endometrial biopsy sainple.

Adequate exposure to ai1d contact with the
ln tl1e case of a yoW1g, healthy, maiden
teaser may be needed to elicit the mai·e's
mai·e, palpation ai1cl ultrasonography per
response; a mai·e with a domina11t follicle
rectutn to detennine the presence of a
may initially not appear receptive because
utems of normal size and consistency,
of ne1vousness or inexperience. Some
normal active ovaiies, and functional cervix
mai·es witl1 foals by tl1eir side may not
may suffice. Perinea\ confom1ation should
exhibit estms to the teaser because of their
be evaluated. A ma11ual vaginal exainination
protective nature. The mai·e's behavior
should be performed to confim1 the hymen
when teased should be consistent with the
is patent. If there is evidence of pneW110vafindings on exan1ination of the genital tract.

gina or vaginitis, conunonly present in slin1,

Response to teasing can determine whether
fit, racing fillies, a11 endometrial swab and
estrus has begw1 and indicate when a mai·e
biopsy are indicated.

should be palpated ai1d bred. Failure to

In postpaitun1 mares, palpation a11d
return to estrus 2---3 wk after breeding may
ultrasonography per rectum are required
suggest that tl1e mare is pregna11t.

to evaluate uterine involution. A manual

Mai·es in seasonal anestrus may remain
vaginal exainination should be pe1fom1ed to
passive in the presence of a stallion.

ascertain whether tl1e reproductive tract

Some ai1estms mai·es will be receptive
was trawnatized during foaling. Thorough
when confronted by a stallion ai1d will
evaluation of tl1e cervix requires direct
tolerate a stallion's sexual advances. This
manual palpation per vagina of the r.ervix
tolerance seems to be due to a lack of
after foal heat ovulation when the mare is in
progesterone, similar to the tolera11ce seen
di estrus and under progesterone stimulain an ovariectomized mare when used as a tion. Mai·es that had foaling problems ( eg,

2190

MANAGEMENT OF REPRODUCTION: HORSES
dystocia, retained placenta) require a more
incontinence. The size and shape of the
extensive evaluation. All postpartum mares
clitoris should be assessed. A mare with an
have a transient endometritis during uterine
excessively large clitoris may have been
involution; therefore, uterine swab and
androgenized either by excessive exogbiopsy typically provide more useful enous ho1mone administration dwi.ng

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inforn1ation if delayed for �3 wk after
pregnancy or by endog nous hormones in
partLu-ition.

an intersex condition (male pseudoher

Barren mares require a complete
maphrodite). om1al vulvar lips have good
breeding sow1dness examination. Occasiontone and apposition and form the first ally, hysteroscopy, endocrine assay, or a
barrier of the uterus against environmental
karyotype may provide additional
contaminants. The vulvar lips should be
infom1ation.

parted to detern1ine the competency of the
vestibulovaginal fold. lf air readily aspirates

Signalment and History: A standard
into the vagina, the mare may be prone to
breeding soundness examination fotm to
pneumovagina and may require a vulvorecord examination fmdings can be helpful plasty (Caslick operation).

in ensuring all areas are covered during

For per rechm1 procedures, the exan1iner,
the examination. The horse should be
weruing a clean exrunination sleeve with
accurately identified.

water-soluble lubricant, must first empty the

Detern1ination of stage of reproductive
rectw11 of feces. Palpation and ultrasonogcycle and estrous cycle is essential for raphy per rectwn pem1it assessment of the
proper evaluation and interpretation of
internal genital tract. Each part of the
laboratory test results. The history should
ge11ital tract should be systematically
include previous length and character of
palpated. Typically, a real-time 5-10 MHz
estrus, breedings and their results, therapy,
lineru· ultrasoUI1d probe, which produces a
and specific reproductive problems. In
rectangular, cross-sectional in1age of the
particular, histologic findings of an
structLll'e scarmed, is used for ultrasonoendometrial biopsy sample reflect the stage graphic exruninations of the reproductive
of the mare's reproductive cycle and any
ti·act. Ovarian size and character as well as
recent intrauterine activities (breeding,
the presence of ru1 ovulation fossa should
treatment, foaling). Regardless of the
be noted. Anechoic follicles should be
history, the mare's nonpregnant status
measured and cow1ted, and the presence
should be confi.Imed before performing
of a hyperechoic corpus luteLU11 recorded.

any procedures ( eg, endometlial swab,

Normal oviducts are not routinely examined
endometlial biopsy, direct manual cervical
because their small size prevents palpation
palpation) that would compromise an
and imaging.

existing pregnancy (seep 2194).

The size, shape, ru1d contents of the
uterus should be recorded. The mare's

Restraint: The mare can be restrained in
uterus is T -shaped with the horns perpenhand, in stocks, or placed against a stall dicular to the body of the utems. It is
wall with the hindquarters positioned in a
suspended in the pelvic cruiaJ by the broad
doorway. For fractious mares, a twitch
ligament, which is attached dorsally to the
may provide short-tem1 restraint to allow
sublwnbru· region. Ultrasonography pern1its
completion of the examination. For the
accurate assessment and measurement of
occasional situation in which the temperathe uterine horns. The size and character of ment of the mare poses risk of injury to the
any anechoic endometrial cysts should be
mare or examiner, chemical restraint may
recorded for reference so their presence
be used. A combination of acepromazine
will not be confused with a conceptus (0.02 mg/kg) and xylazine (0.3-0.5 mg/kg)

dwi.ng subsequent early pregnancy
administered JV works well for short
examinations.

procedures. lf possible, the external

The uterus has several endometliaJ fold
genitalia should be evaluated before
that increase the surface area of the uterine
tranquilizers are administered, because the

ILunen. The endometrial folds should be
drug's use will alter the tone and compecarefully assessed dU1i.ng palpation per tency of the perineum.

rectwn by "slipping" the folds through the examiner's fingers along the entire length

Physical Examination: The mare's tail
of each horn. The character of the uterus
should be wrapped and tied to one side. The
changes during the estrous cycle. During
tail and inner thighs should be examined for estrns, the endometi·ial folds become edemathe presence of dried exudate indicative of tous, causing the uterine horns to have
genital infection or urine staining that may
alternating ru·eas of hypo-and hyperechobe associated with urine pooling or genicity when a cross-section is viewed

MANAGEMENT OF REPRODUCTION: HORSES

2191
ultrasonographically. As estrus progresses,
swab by microorganisms in the structures
the edema in the endometrial folds wanes so
caudal to the uterus that would hinder
that it is minimal by the time of ovulation.

accurate interpretation of the culture

After ovulation and development of U1e
results.

corpus luteum, the uterus is stimulated by

A double-guarded occluded uterine
progesterone, uterine tone increases, and
swab is gently guided through the cranial

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the endometrial folds are no longer
end of the cervix. Once inside the uterine
edematous. After 14-18 days of gestation,
body, the inner guard is advanced from the
the endometrial folds are not readily
outer guard, and the swab is exposed to the
palpable because of the gradual but marked
uterine lmnen for 30-60 sec. The swab tip
increase in uterine wall thickness.

is withdrawn into the inner guard, which

The length, width, and tone of the cervix
is then witl1drawn into the outer guard
are palpable per rectum; however, complete
before the entire swabbing instrument is
evaluation of the cervix requires direct
removed from the uterine body. The swab
palpation per vagina (seep 2193). A ce1vical tip is carefully placed into a transport
evaluation also seives as a bioassay,
system, which is vital to maintain viability
because the cervix changes in response
of tl1e organisms from the time of sample
to the steroid honnone status of the mare.

collection m1til aerobic culture in the

During anestrus, ovarian steroid serum
laboratory. Stuart's carrier medimn may
concentrations are low, and the cervix is
maintain microorganisms for as long as
either short, thin, and open or closed but

72 hr if stored at ambient temperature. A
readily opened. After the first ovulation of
second endometrial sample may be taken
the season and during subsequent periods
in1mediately after the first or simultaneously
of di estrus, serum progesterone concentrawith a uterine swab or cytology brush. This tions are increased and the cervix is closed,
sample is then evaluated cytologically by
with a long cylindrical shape. During estrus,
rolling it onto a glass microscope slide,
senun progesterone concentrations are low,
fixing and staining with a Romanowsky-type
and estrogen concentrations are high; the
stain, and viewing it microscopically for
cervix is relaxed and edematous. Visual
evidence of neutrophils, debris, and

(speculum) vaginal examination will allow
microorganisms.

fmther assessment of the character of the

A low-volun1e uterine lavage can be
ce1vix.

performed in mares with negative culture

Urine in the vagina (urovagina) may
results despite obvious clinical signs of
be seen sporadically or be a chronic
endometritis. Sterile saline (60-150 mL) is
problem. Mares with urovagina may have
infused into the uterus using a closed
an abnonnal voiding pattern, and the
system with a small uterine catheter.

endometrium may show histologic evidence Oxytocin (20 lU, lV) is administered to of chronic irritation. The neck of the
enhance uterine evacuation. The effluent is
bladder can be used to indicate the caudal
collected by gravity flow into a sterile centriboundary of the vagina during ultrasonografuge tube and then centrifuged. The pellet is phy. The vagina can be imaged dorsal to U1e
then swabbed, placed into transport media,
bladder and examined for any acctm1ulation
and submitted for aerobic culture. A second
of echogenic fluid caudal to the cervix. A
swab can be made of the pellet for cytologic
definitive diagnosis of urovagina requires
examination after staining.

direct obseivation of urine in the vagina via

Most laboratories streak the swabs on 5%
vaginoscopy.

sheep blood agar for general growth and on

MacConkey's agar for growth of gram-nega

Endometrial Swab: Before an endometive organisms, after which cultures are trial swab is taken, the non pregnant status
aerobically incubated at 37°C (98.6°F).

of the mare must be confinned because the

Organisms conm10.nly isolated that are
swabbing could lead to termination of a
associated with endometritis include
pregnancy (seep 2194). The perinemn is

[3-hemolytic streptococci (9(J'loStreptococ
cleansed with povidone-iodine scrub,
cus zooepidemicus, lOOA,S equisimilis), rinsed, and dried. The operator dons a

Escherichia coli, Pseudomonas (65%
ste1ile sleeve or clean exan1ination sleeve

P aeruginosa ), and Klebsiella pneumoniae.

with the hand encased in a sterile glove. A

Organisms isolated that are commonly
water-soluble lubricant free of bacteriosuspected to be contaminants include static chemicals is placed on the back of the
a-hemolytic streptococci, Actinobacillus
hand and lower arm. When obtaining an
equuli, Salmonella enteritidis, Pasteurella
endometrial swab san1ple, the vestibule,
like species, and Staphylococcus, Entero
vagina, and cervix must be passed. Care
bacter, Acinetobacter, Proteus, Citrobacter,
must be taken to avoid contamination of the Alcaligenes, and Aeromonas spp.

2192

MANAGEMENT OF REPRODUCTION: HORSES

In most cases, the mixed growth of a
infusion by diluting with sterile saline to an
few miscellaneous microorganisms is
infusion volume of60-100 mL. Systemic
not significant. A heavy growth of any
administration of antibiotics may be
microorganism should be considered
considered if the microorganism, managesignificant unless obvious contamination ment situation, and ease of treatment

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has occurred. Clinical signs must be
indicate. Two doses of)ong-acting ceftiofur
correlated with culture results to
crystalline free acid (6.6 mg/kg, IM) can be
determine clinical significance and to
administered 96 tu· apart for adequate serwn
develop a therapeutic plan. Isolation of
concentration for 10 days, which may be an
an organism transmitted venereally, such
efficacious treatment for endometritis due
as Taylorella equigenilalis (requires a
to S zooepidemicus.

special culture system) and certain strains
of Pseudomonas and Klebsiella spp, is Endometrial Biopsy: An enclornetrial
considered a significant finding. Occasionbiopsy sample is usually obtained immedially, microorganisms causing a pyometra ately after the endometrial samples have
may not be detected on aerobic culture,
been procured. It should be kept in mind
because products of the inflammatory
that manipulation of the endornetiiwn can
reaction prohibit their growth.

quickly cause a neuti·ophilic response in the

Aerobic culture results of the endomeendornetriun1. Preparation for biopsy is the trial swab should be used as a diagnostic
same as for taking a swab (see above). The
adjtmct and not as the sole detenninant in
basket of the biopsy instrument should be
diagnosing a uterine infection. A positive
kept closed during positioning to prevent
culture result must be accompanied by
accidental procurement of vagina, cervix,
evidence of inflammation for the diagnosis
or examination glove. The instrument is
of endometritis to be made. Mares exhimanually guided with the gloved hand biting clinical signs of infection ( uterine
tJu·ough the caudal genital ti·act into the
fluid as seen on ultrasonographic examinauterine lumen. While keeping the instrution per rectwn, tail matting or uterine ment in place within the uterus with the
discharge, and the presence of inflammanongloved ( external) hand, the gloved hand tory cells seen on a stained smear from a
is carefully witl1drawn from the genital tract
uterine sample) with a positive endomeand inserted into the rectum to allow trial swab are likely to have endometritis.

positioning of the basket of the biopsy

Inflammation seen on histologic evaluation
instrwnent at the ventral lun1inal surface of
of the endometrium confirms the diagnosis
the base of a uterine horn. The instrument
of endometritis. In these cases, the culture
jaws are then opened, the uterine wall is
results are useful in determining the
pressed into the side of the basket, and the
sensitivity of the causative microorganism
jaws are closed. The jaws should be kept
and developing an antimicrobial treatment
closed while the instrwnent is withdrawn
plan.

from the genital tract. The tissue should be

The following antibiotics (see TABLE 9 ) gently teased from the basket and placed
have been used for daily (3-7 clays) uterine
into Bouin's fixative. If the sample will not

•&h•fl INTRAUTERINE ANTIBIOTICS FOR USE IN MARES

Antibiotic

Intrauterine Dose

Penicillin (sodiun1 or potassiLm1 salt)

5million U

An1picillin
l-3g

Ticarcillin

3-6g

Tica.rcillin with clavulanic acid

3-6g

Carbenicillin

2-5g

Gentarnicin sulfate diluted with 20 mL sodiLun bicarbonate l g
and 20 mL saline

Arnikacin sulfate
l-2g

Ceftiofur sodium
lg

Clotrimazole

400-700mg

MANAGEMENT OF REPRODUCTION: HORSES

2193
be processed within a few days, it should be

I. Category II is a broad category that
transferred into 700Ai ethanol or 1 OOAi
includes most mares. It has been divided
formalin.

into Category IIA, for mares with less

It is not unusual for a small amount of
severe changes, and Category IIB, for
uterine bleeding to occur after biopsy. The
mares with more severe changes. The

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biopsy procedure is not detrimental to
estimated foaling rate is 500/o-80% in mares
fe1tility, and a mare can conceive from a
with Category IIA endometria and 100/o-500Ai
breeding that occurred during an estrus
in mares with Category IIB endometria.

when biopsy was pe1formed.

Often, therapy may improve the state of the

Histologic evaluation of the endomeendometrium by reducing inflanunation, trium provides prognostic information
cystic glandular distention, and lymphatic
about the mare's ability to carry a foal to
lacunae. Improvement in the endometrium
term. The luminal contents may indicate
may allow for better classification at a later
the presence of uterine fluid or exudate.

date. There is no effective treatment to

Epithelial cell height is related to
decrease the severity of periglandular
hormone status; cells are cuboidal during
fibrosis. Category III is the poorest
anestrus and low to tall columnar during
classification, and these endometria have
the breeding season. Transepithelial
widespread, severe changes that include
cells may indicate active inflammation.

periglandular fibrosis or inflan1mation.

The pattern, character, and location of

A widespread pattern of distribution of
inflammation indicate the chronicity of
slight to moderate changes may be more
response-neutrophils indicate an acute
deleterious than more severe changes that
reaction, and lymphocytes and plasma
are infrequent and only involve individual
cells indicate a chronic reaction. Focal
glands. The estimated foaling rate of a
or diffuse cellular distribution pattern,

Category III endometrium is <10%.

frequency of inflammatory cells, and

During interpretation of the findings on
degree of infiltration (slight to severe)

histologic evaluation of an endomet1ial
relate to severity of inflammation.

biopsy san1ple, the extent of normal,

Histologic evidence of significant
unaffected endometrium is more significant
inflammation, combined with a report of
than the presence of any particular lesion.

growth of microorganisms from aerobic

In barren mares with a Category I or TIA
culture of endometrial swab and the
endometriun1, other reproductive abnorpresence of clinical signs of infection malities or poor breeding management

(uterine fluid, uterine discharge), support
should be investigated as the cause of
the decision that an endometrium would
infertility.

benefit from therapy to decrease
inflammation.

Vaginal Examination: The perineum.

Knowledge of the pattern of distribution
is cleansed, rinsed, and dried before the
and severity of periglandular fibrosis is
visual vaginal examination via specul un1.

prognostically useful. Fibrosis surrounding

The vulvar lips are separated, and the
groups of glands ("fibrotic nest") is thought speculwn is advanced cranially at a dorsal
to be more clinically significant than fibrosis angle so as to pass over and through the of individual glands. Periglandular fibrosis
transverse (vestibulovagina.l) fold of the
may interfere with endometrial gland
vagina. Resistance against the specultm1 by
function and may be a factor causing early
this fold of tissue indicates good tone and
embryonic death. Glandular distention
function. A bright light is necessary to
nonnally develops during pregnancy, but
adequately view the cervix and vaginal
widespread cystic glandular distention in
wall. The character of the cervix reflects
the nonpregnant mare is undesirable. Cystic
the hormonal status of the ma.re. As the
glandular distention is often associated
speculw11 is being withdrawn, it should be
with periglandular fibrosis and may result
noted whether the vestibulovaginal fold
from an accumulation of gland secretions
occludes the vagina. The competency of the
proximal to the occlusion of the endomevestibulova.ginal fold is important, because trial gland by periglandular fibrosis.

it forms the second barrier for the uterus

Endometria are classified in four
against external contaminants.

categories that attempt to predict ability to

Thorough evaluation of the completecarry a foal to term. Category I indicates ness and competency of the cervix can be
no significant changes are present in the
accomplished only by direct palpation per
endometrium, and no treatment is required.

vagina while the mare is under progesterone

The estin1ated foaling rate is 800/o-900Ai. An
stimulation (ie, cervix closed). The cervix
endometriun1 with any notable periglanduforms the third barrier for the uterus against lar fibrosis cannot be classified as Category
external contaminants.

2194

MANAGEMENT OF REPRODUCTION HORSES

PREGNANCY DETERMINATION
uterus enlarges, its dorsal surface comes
back into reach in late gestation. One should

The schedule for detem1ination of
always confirm that two uterine horns with
pregnancy varies among breeding fanns.

palpable endometrial folds caimot be

One schedule is as follows: 1) days 14-18--identified in the pelvic canal before making VetBooks.ir
check for pregnancy and twins; if open,
a midterm pregnaiiey diagnosis.

mare can be rebred on days 19-20; 2) days

25-30-valuate nonnal embryo develop

Ultrasonography: The spherical shape
ment (heaitbeat present at 24-25 days),
of the equine emb1yo and the chai·acteristic
recheck for twins; 3) days 40-60-evaluate
pattern of development of the fetal
normal fetal development; 4) fall checkmembranes pemlit accw·ate estin1ation of confum mai·e is still pregnant.

stage of gestation by ultrasonography until

45 days after ovulation. The embryo may

Palpation Per Rectum: The pregnant
first be imaged in the uterus witl1 a 5-10
cervix should be tightly closed and

MHz linear transducer at 9-10 clays as a
elongated witll a prominent portio vaginalis
round anechoic yolk sac 4 mm in cliaineter.

14-21 days after ovulation. Uterine tone

The spherical conceptus moves tlu·oughout
increases and tl1e utetine wall tllickens so
the ltunen of tile ute1ine horns and uterine
tllat by 14-18 days, tl1e endometrial folds can
body from day 6--16. The early conceptus is
no longer be readily palpated per rectum.

seen to have a bright white (echogenic) line

The conceptus develops in a recognizable
on tl1e dorsal and sometimes the ventral
pattern of size and shape, allowing estimaaspect of its in1age tllat is called a specular tion of age based on palpable charactetistics.

reflector, which is a.ii aitifact seen when tile

In maiden and bairen mares, at 25-28 days of
ultrasow1d bean1 strikes the wide, smooth
gestation, a cai·eful, ex"])etienced exaininer
surface of the conceptus at a 90° angle. This
may be able to feel tile embryonic vesicle
specular reflector, emb1y01lic motility, and
ventrally at tile base of one ute1ine horn, as
linear growth rate may help differentiate an
a bulge 3.5 cm in diaineter. At 30 days, the
eai·ly ( <16 day), motile embryo from some
uterine horns ai·e small witll pronounced
ute1ine cysts.

tone, and tile conceptus ca.ii be felt as a
ventral bulge 4 cm in diaineter and positioned at the base of the gravid uterine horn.

The uterine wall is tllin over tl1e expanding
conceptus. At 42-45 days, tl1e conceptus
occupies about half of tile gravid utetine
horn and is 5-7 cm in dian1eter. By 48--50
days, tile enlargement of tile conceptus
begins to involve tl1e ute1ine body and is

6--8 cm in diai11eter and 8--10 cm long.

At 60 days, nearly the entire gravid horn
and half of tl1e uterine body is occupied by
conceptus, but tile nongravid horn remains
small witll considerable tone. The 60-day
conceptus is 8--10 cm in diaineter and 12-15
cm long. After 85 days, tile turgidity of tile
conceptus decreases so that the fetus
becomes palpable. At 90 days, tile conceptus fills tile entire uterus, and tile era.ilia!

portion of tile uterus may extend over tile
brin1 of tile pelvis into tile abdominal cavity.

After 100-120 days of gestation, the
gravid uterus is positioned era.ilia! to the
pelvic brim in the abdominal cavity. The
ovaries are positioned crailially and
ventrally and closer togetller because of the
doW11ward traction exe1ted by the enlai·ging
uterus on the broad ligan1ent. After 150 days
of gestation, tile ovaries are not routinely
felt per rectum. Dilling midgestation, tl1c
gravid uterus may be difficult to reach,

Sonogram of 29-day conceptus in a mare.

because it is positioned ventrally in the

The dorsal anechoic yolk sac is nearly equal
abdomen. But as tile conceptus/gravid
in size to developing ventral allantoic cavity.

Courtesy of Dr. Patricia Sertich.

MANAGEMENT OF REPRODUCTION: HORSES

2195

At day 17-18, the conceptus has a

Strongyloides westeri, which can cause
characteristic "guitar-pick" shape. At day diarrhea in young foals.

21, the embryo proper can be seen in the
ventral aspect of the yolk sac, and by 24

VACCINATIONS
days the allantoic cavity is visible as an

VetBooks.ir
anechoic compartment ventral to the

Vaccination programs should follow a
embryo proper. At day 25, a heart beat
continuous, year-round schedule based on
should be present in the embryo proper. As
local health problems. Vaccination against
the allantoic cavity enlarges, the yolk sac
rhinopneun1onitis should be performed at
comprises a decreasing proportion of the

5, 7, and 9 mo of gestation. Vaccines that
concept.us. The position of the allantois and
require annual boosters should be
relative sizes of the developing allantoic
administered 4-6 wk before the mare's due
cavity and the regressing yolk sac can
date to stimulate the dam to produce
indicate the stage of gestation between days antibodies that will be transferred to the 24 and 45. At 30 days, the allantoic cavity
foal via the colostrnm (see TABLE 10).

occupies approximately one-half of the

Detailed information regarding ctm·ent
concept.us, so that the size of the yolk sac is
vaccination recommendations is available
equal to that of the allantoic cavity. At 45
on the AAEP website (www.aaep.org).

days, the only visible fluid cavity is the

Colostrnm should be ingested in the first
allantoic cavity, and the fetus appears to

24 hr of life to effectively provide passive
be suspended from the dorsal wall of the
transfer of immunoglobulins.

uterns by its umbilical cord and is positioned in dorsal recumbency.

ABORTION

Endocrine Tests: Cells from the

See also ABORTION IN HORSES, p 1343. 1win
chmionic girdle of the conceptus invade
pregnancy is the most conunon noninfectious
the endometrium to form endometrial cups
cause of abmtion in mares. ln most cases,
that produce equine chorionic gonadotropin uterine capacity and subsequent placentation (eCG). lncreased sernm concentrations of
are inadequate to support two fetuses to
eCG 40-120 days after ovulation indicate
term. Although twins may spontaneously
the presence of endometrial cups.

reduce to a viable singleton early in gestation

Concentrations of eCG may remain

( <60 days), visible abortions tend to be seen
increased until 120 days, even if fetal death
after 7 -9 mo. Premonitory clinical signs of
occurs (false-positive). A false-negative
impending abortion may be only premature
result will be obtained if eCG assay is used
manunary gland development. Fetal memas a pregnancy test in a pregnant mare branes should always be examined for large
before 40 or after 120 days of gestation.

avillous areas typically located betweeq the

Estrone sulfate is produced by the fetus
twin concept.uses.

and is a good indicator of fetal viability.

Because of the risk of abortion and

Plasma and urine concentrations of estrone
dystocia in a mare carrying twins, if twins
sulfate are increased after 60 days and 150
are detected by ultrasonography per rectum
days, respectively, of pregnancy. Either
at <30 days, reduction to one embryo by
endocrine assay can be used properly as a
manual crnshing per rectum is recompregnancy test only if the breeding and mended. Between 30-60 days of gestation,
ovulation dates are known.

transvaginal aspiration of one conceptus
may result in a viable singleton. At

PARASITE CONTROL DURING
approximately 60 days of gestation, one

P REGNANCY
fetus may be eliminated by cervical
dislocation. After 110 days of gestation,

Most anthelmintics are safe for use
one twin may be reduced by intracardiac
throughout pregnancy, but precautions and
injection of potassium chloride guided by
contraindications on package inserts should transabdominal ultrasonography. Success be heeded. ln general, anthelmintics should
rates vary depending on the procedure
not be administered to mares during the
performed, the experience of the veterinarfirst 60 days of gestation ( organogenesis).

ian, and the character of the pregnancy.

Parasite control programs should be

Pregnancy should be monitored repeatedly
tailored to meet the particular farm needs.

by ultrasonography after twin reduction.

See also GASTROINTESTINAL PARASITES m- HORSES, The most common cause of viral abortion
p 315, and ANTHELMINTICS, p 2637. Pregnant
in mares is equine rhinopnewnonitis, which
mares should be administered ivermectin
is caused by equine herpesvirus 1 (EHV-1 ).

or a benzimidazole 1-3 days before foaling

These abortions occur predominantly in the
to prevent lactogenic transmission of
last trin1ester and usually are not associated

2196

MANAGEMENT OF REPRODUCTION: HORSES
lh=iii•·I EXAMPLE OF VACCINATION SCHEDULE FOR BROODMARES

Vaccine

Schedule

Equine rhinopneumonitis

EHV-1 at 5, 7, and 9 mo of gestation; EHV-1/EHV-4

VetBooks.ir

(inactivated)

4-6 wk before due date

Tetanus (toxoid)

4-6 wk before due date

Equine influenza

4-6 wk before due date; if unvaccinated, initially
administer two doses at 4-6 wk intervals and then a
third dose 4-6 wk before due date

Eastern and Western equine

Usually administered to mares in late spring or
encephalomyelitis
early summer before onset of insect season; initially administer two doses at a 4-6 wk interval; 4-6 wk
before due date

Rabies

4-6 wk before due date

Botulism (toxoid)

Initially three doses at 4-6 wk intervals, then annual booster 4-6 wk before due date

West Nile virus

Initially two closes at a 4-6 wk inte1val; 4-6 wk
before due date

Rotaviral diarrhea

8, 9, and 10 mo of gestation

Equine viral arteritis

A negative titer should be documented by a

(modified-live virus)

USDA-approved laboratory before vaccination;
pregnant mares should not be vaccinated; open
mares should be vaccinated before breeding to a
positive stallion that is shedding the virus;
vaccinated horses must be isolated for 3 wk after vaccination; annual boosters recommended;
positive titers may cause problems if mare is to be
expmted or bred on ce,tain farms. (Stallions should
also be vaccinated 3 mo before breeding.)

Equine monocytic ehrlichiosis

Initially administer two doses at a 3-4 mo interval; (Potomac horse fever)

4-6 wk before due date
with a respiratory infection. All pregnant
a.J1d Aspergillus spp. Effo1ts to reduce the mares should be vaccinated against EHV-1
incidence of these abortions should include
at 5, 7, and 9 mo of gestation.

good breeding hygiene, treatment of genital

The equine aiteritis virus can cause
disease before breeding, maintaining good
equine viral aiteritis (EVA) abo1tion. An
body condition throughout pregnancy, and

EVA-seronegative mare scheduled to be
vuJvoplasty (Caslick operatjon) to prevent
bred to an EVA-positive stallion that is
pnetu11ovagina. Mai·es at risk of placentitis
shedding the aiteritis virus in the semen
should be exai11ined by ultrasonography per
should be vaccinated before breeding.

rectw11 periodically during late gestation for

Horses must be isolated for 3 wk after EVA
evidence of genital infection and placental
vaccination. Mares should not be vacciabnormalities as evidenced by uterine nated against EVA during pregnai1cy.

discharge and increased uteroplacental

Sporadic abortions due to placentitis
tluckness.

can be caused by bacterial and mycotic

Any aborted fetus a.J1d fetal membranes
infections of the placenta. These ai·e
should promptly be submitted fresh or
predominantly ascending infections acquired cooled (never frozen) to a diagnostic ilirough fue caudal genital tract but may also
laboratory to determine the cause of the
be focal or diffuse. Bacte1ia involved include
abortion.

St1'eplococc:us zooepidemicus, Escherichia
coli, f(lebsiella pnewnoniae, Pse'!ldomonw;

PARTURITION
ae1uginosa, SlaphylococC'lts aure'!lS,

RhodococC'lts eqiii, andActinobacillus

The pregnant rnai·e should be taken to tl1e
equuli. Mycotic orgarti.sms include Mucor foaling location 3-4 wk before the expected

MANAGEMENT OF REPRODUCTION: HORSES

2197
foaling date to enhance immunity against
microvilli and is refen-ed to as the cervical
pathogens present in the environment.

star. The chorioallantois usually ruptures at

Antibodies will be sequestered in colostrum
the cervical star, and the release of the
for passive inununity in the newborn.

tea-colored allantoic fluid marks the end

Quality of colostrum will be improved by
of the fast stage of parturition. In Jay

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administe1ing booster vaccinations 4---6 wk
terminology, this event is referred to as the
before the mare's due date (see also
mai·e "breaking her water."

VACCI ATIONS, p 2195).

Stage II starts with the rupture of the

Foaling box stalls should be large (at least chorioallantois and ends when the fetus is 3.5 x 3 x 3.5 m). The foaling area should
expelled. Second stage labor usually lasts
have good ventilation and be well bedded

15-30 min. When the fetus engages the
with clean, dry straw. The walls should be
ce1vix, the Ferguson reflex occurs and
solidly constructed and free of sharp edges.

stimulates the mai·e to have abdominal

Mares may benefit from foaling outdoors
contractions. The allantoic fluid lubricates
on turf, weather permitting. Regardless of
the cai1al, facilitating expulsion of the
location, the mare should be observed
anmion and fetus. Vaginal distention causes
without disturbance.

release of oxytocin and further myometrial

Evaluation of the premonitory signs of
and abdominal contractions. The ai1rnion
parturition is useful but does not permit
appeai-s at the vulvai· lips as a whitish,
precise prediction of the tin1e of delivery.

fluid-filled membrane. The straining effo1ts

The manm1ary gland starts developing 3-6
of the mare consist of three to four strong
wk before foaling and distends with
contractions, followed by a sho1t period of
colostrum in most mares 2-3 clays before
rest. During the actual expulsion of the foal,
parturition. Colostrum may drip from the
the mare usually assumes lateral recumteats and dry to form a waxy material at bency with all fow· Jin1bs extended.

each teat orifice. This "waxing" develops in The foal is nonnally delivered in an

-95% of mares 6-48 hr before foaling, but in
ante1ior, longitudinal presentation and
some cases, it is not seen at all or it may
clorsosacral position with the head, neck,
precede parturition by many clays. Before
and forelimbs extended. One front hoof of
the mare foals, the calciun1 and potassium
the foal usually precedes the other hoof by
content of udder secretions increase, and

-15 cm, facilitating passage of the elbows
the sodium content decreases. Water
and shoulders tlu·ough t11e pelvic cai1al. The
hardness chemical tests have been used to
foal is usually born with tl1e un1bilical cord
measure these in mammary gland secreintact and covered by the ainnion, which is tions to predict paiturition.

ruptured by movements of the mare or foal.

If a mare has had a vulvoplasty (Caslick

If ainnion remains over the foal's nose, an
operation) dming pregnancy, it is necessary
attendai1t should remove it to prevent
that a.ii episiotomy be pe1fonned -2 wk
suffocation. If left undisturbed, the mai·e 1hay
before pa1turition.

lie for some time with the foal's hindlimbs in
the vagina If the foal has not been delivered

Stages of Parturition: It is critical to
within 30 min of the rupture of t11e chmioalunderstand the norn1al progression of lantois and release of tl1e allantoic fluid,
events during paiturition. Abnormal events
obstetric inte1vention is indicated.

can then be identified and intervention

Stage III involves expulsion of the fetal
provided as needed. Paiturition is divided
membranes. Normally, fetal membrane
into three stages.

passage occtll'S rapidly (within 3 hr) after

Stage I is chai·acterized by signs of
delivery of the foal. The weight of tl1e
abdominal discomfort ai1d restlessness clue
ainnion and cord may help the chorion
to uterine contractions. Patches of sweat on
separate from the endometrium. Progresthe flank ai1d behind the elbows usually sive traction by the amnion and moderate
appear a few hours before foaling. The
ute1ine contractions originating at the tip of
uterine contractions increase in frequency
the horn cause complete separation of the
and intensity, causing the fetus to engage
chorioallantois, which may become
into the cervix and pelvic canal. The fetus
inverted dming the process. The mare may
rotates from a dorsopubic to a dorsosacral
stand with the anmion hanging from the
position before expulsion. Mai·es may roll
vulva at the level of the hocks or below. If
during the first stage, which is thought to
the mai·e kicks at the hanging membranes,
facilitate rotation of the fetus.

endangering the foal, the exposed

Increasing pressure in the uterm; causes
membranes should be tied in knots to
the chorioallantois to protrude through the
sho1ten the length to above the hocks.

internal os of the cervix. The chorion over

If t11e fetal membranes have not been
the cervix is smooth-it does not have
passed by 3 hr after parturition, oxytocin

2198

MANAGEMENT OF REPRODUCTION: HORSES

(20 IU, IV or IM) should be administered at

Sedation can be provided by administra15- to 30-min intervals until membranes tion of xylazine (0.5-1 mg/kg, IV) and
pass. If fetal membranes are still retained at
butorphanol (0.01-0.02 mg/kg, IV). If

8 hr after foaling, therapy for retained
abdominal straining prevents adequate
placenta should be instituted (seep 1381).

vaginal exan1ination and fetal mutation,

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epidural anesthesia may be administered

Premature Separation of the Pla
using xylazine (0.17 mg/kg) and lidocaine
centa: Norn1ally, the translucent white

(0.22 mg/kg) diluted to a total voltune
amnion appears first at the vulvar lips
of 8mL.

during the expulsion stage of labor.

The front legs of the fetus should be

Premature separation of the placenta is
identified and extended out the vulva.

characterized by the appearance of the

Obstetrical chains should be applied with
bright red, velvety, intact chorioallantois
one loop of the chain at the distal metacarbetween the vulvar lips before the foal is pus and a second loop around the pastern to
delivered. The presence of the chorion at
decrease trauma to the fetlock joint. The
the vulvar lips indicates that it has separated chains will aid manipulation and assist the from the endometrium before the foal is
application of traction. Once the head is
able to breathe spontaneously. The
exposed and the neck extended, it may be
chorioallantois must in1mediately be
possible to intubate the fetus and adminisruptured and the foal manually delivered, or ter low-flow oxygen using a portable oxygen
the foal will asphyxiate. The severity and
tank or ventilate with a resuscitator (bagduration of hypoxia that results detern1ines valve mask). Proper rotation of the fetus
the severity of neurologic abnormalities
may be facilitated by the mare getting up
displayed by the foal (periparturn asphyxia
and down. After confirming that the fetus is
or hypoxic ischemic encephalopathy [see
in the proper 01ientation, manual traction
p 20941).

can be applied, initially dorsally and then
caudally. Once the foal's chest is exposed,

DYSTOCIA
traction should be applied in a ventral
caudal direction. Traction should be applied

Most causes of dystocia in the mare are
intennittently in rhythm with the mare's
due to abnormal presentation, position, or
abdominal contractions.

posture. A dead or compromised fetus

After the foal is delivered, an internal
often is not properly positioned in the
examination of the genital tract per vagina
pelvic canal. Dystocia due to fetal-maternal
should be perfo1med to identify any
disproportion or primary uterine inertia is
lacerations in the mare's genital tract or
rare in mares. A vaginal exanlination should
the presence of a twin. A few low doses
be perfonned if the foal is not delivered
of oxytocin (5-10 IU, IV or IM) can be
within 30 min after rupture of the chorioaladministered every 15-20 min to stimulate lantois or if second-stage labor does not
passage of the fetal membranes and uterine
begin after >4 hr of obvious first-stage labor. evacuation. Repair of prinlary perinea!

The initial exan1ination may be perlacerations usually can be delayed until forn1ed in the standing mare. The perineum
after foal heat, but the dorsal aspect of the
should be cleansed with povidone-iodine
vulvar lips should be temporarily sutured
scrub and rinsed well with water. Efforts
if pneumovagina/pneumometra develops.

should be made to maintain hygiene at all
times. A diagnosis of the presentation,

Controlled Vaginal Delivery: If
position, and posture must be made, and a
resolution of the dystocia seems challengplan formulated to mutate the fetus into an ing or not possible in the standing ma.re
ante1ior longitudinal, dorsosacral position
because of the mare's straining or the
with head, neck, and front limbs extended.

orientation of the fetus, a controlled vaginal

Copious amounts of clean lubricant will
delivery should be considered. This is
ease mutations and fetal expulsion.

perfo1med in an anesthetized mare. Field

Excessive mechanical or manual traction
anestl1esia can be accomplished by first
should be avoided. Length of tin1e spent on
heavily sedating with xylazine (1 mg/kg, IV)

manipulations and any progress should be
followed by diazepan1 (0.05-0.1 mg/kg, IV)

noted. Once the fetus is properly presented
and ketamine (2.2-2.5 mg/kg, IV). If gas
and positioned in the pelvic canal, if it
anesthesia is available, routine induction
cannot be delivered using traction exerted
and maintenance by inhalation will provide
by two strong adults, the diagnosis should
longer working time and greater relaxation.

be reconsidered and plan of action altered.

If general anesthesia and a cont.rolled

Compassion for the foaling mare must be
vaginal delivery are likely, epidural
considered in case management decisions.

anesthesia should not be done. The mare's

MANAGEMENT OF REPRODUCTION: HORSES

2199
hindquarters are hoisted to allow the GI
body weight. Placentitis or placental edema
tract to move cranially in the abdomen,
may increase the weight of the membra.I1es.

providing space to more readily perfonn

Integrity of thejllllction between the fetal
fetal manipulations. It is prudent for
and maternal components of the placenta is
managers of large breeding farms to have a
essential for normal fetal development. The

VetBooks.ir
designated location on the farm where a
mare has a diffuse microcotyledonary,
mare could be anesthetized and its
epitheliochorial, nondeciduate type of
hindquaiters elevated (hobbles, winch,
placentation, which directly reflects the presfront end loader readily available) to hasten ence of abnorn1alities in the endometrilll11.

resolution of a dystocia.

Retained Fetal Membranes: Fetal

Cesarean Section: If vaginal delivery
membra.I1es that are not expelled within
attempts fail, the mare's value justifies it,

3 hr of pai·tm·ition ai·e considered to be
and surgical facilities are available, a
retained. Fetal membrane retention may be
decision should rapidly be made to deliver
complete, but commonly only the nongravid
the foal by cesareru.1 section to spai·e the
horn is retained. If the typically puckered
mai·e's caudal genital tract from further
nongravid tip is not observed, it is asslll11ed
trauma. Treatment for retained placenta
to be retained. If any membranes are
should be initiated immediately after
hanging from the vulva of a postpartum
surgery. Barring complications, mares can
mare, tl1e anlnion and cord should not be
usually be rebred 60 days after cesareru.1
cut and removed, because their weight
section.

provides tension thought to enl1ancc
placental sepai·ation and expulsion. Fetal

Fetotomy: If surgical facilities are not
membranes not passed within 3-10 hr are
available or the economic situation prevents considered to be pathologic and can lead to referral to a surgical facility, a fetotomy may
metritis, endotoxemia, and subsequently
allow delivery of the fetus. In the mare,
lan1initis with fatal results. Accordingly, it is
fetotomy is usually reconm1ended only if
prudent to treat the condition as potentially
fetal expulsion can be accomplished after
one or two cuts. Care should be taken to
avoid dainage to the mare's cervix and
pelvic canal. Treatment for retained
placenta should be initiated immediately
after fetal delivery.

EXAMINATION OF THE FETAL

MEMBRANES

Normally, the membranes ai·e ruptured by
the foal over the avillous cervical star region
of the chorioallantois. The chorion (red
velvety surface) and allantois (shiny surface
containing many blood vessels) should be
examined. Normally, the chorionic surface
color ranges from red to brownish red.

Patches of discolored, thick, exudate-covered chorioallantois at the cervical stai· or between the two horns may indicate an
ascending or focal placentitis, respectively.

The fetal membranes should be examined
for completeness, paying particular attention
to the presence of the edematous gravid horn
tip and puckered nongravid horn tip.

The ainnion has a white translucent
appearance a.Ild may contain many blood
vessels neai· the umbilical cord. Small, pale
ainniotic plaques Ca.J.1 n01mally be seen
along the mnbilical cord.

Fetal and neonatal foal deaths may be
associated with pathologic changes present

If membranes are seen hanging from the
vulva in a mare that foaled>3 hr prior, the
in the fetal membranes. Typically, the fetal
mare is considered to have retained fetal
membra.I1es weigh-l()OA,....11%of the foal's
membranes. Courtesy of Dr. Patricia Sertich.

2200

MANAGEMENT OF REPRODUCTION: HORSES
serious. If dystocia or trawnatic uterine
should be evaluated for size, shape, ar1d
manipulation has occun-ed, aggressive
consistency. The testes should be freely
treatment for retained membranes should
movable within the scrotun1 and have a total
be instituted immediately after parturition.

scrotal width >8 cm. The length (L), width

For early (3--8 hr) retention, 10-20 JU

(W), and height (H) of the testicles can be

VetBooks.ir
oxytoci.n can be repeatedly administered
detennined using calipers or ultrasonogra

IV or IM eve1y 30 min w1til the fetal
phy to calculate the volwne of each testicle
membranes have passed. The dose of
using the equation: 0.523 (L x W x H) =
oxytocin should be decreased if the mare
testicular volun1e. The stallion's daily sperm
shows severe signs of colic or discomfo,t.

output (DSO) car1 then be predicted by the

Milking or sucking also stimulates endogequation: total testicular volwne x 0.024 -
enous release of oxytocin. Mares that retain

0. 76 = DSO. The internal genitalia, inguinal
fetal membranes >8 lu· should be adminisrings, ar1d a01ta and iliac vessels are tered broad-spectrum antibiotics, such as
evaluated by palpation and ultrasonography
potassiwn penicillin (22,000-44,000 JU/kg,
per rectw11. For semen collection and

IV, qid), gentamicin (2.2 mg/kg, IV, qicl), or
evaluation techniques and c1iteria
flunixin meglwnine (0.25-0.5 mg/kg, IV, tic!).

considered for determination of breeding
soundness classifications, seep 2230.

THE EARLY POSTPARTUM PERIOD

Swabs of the external genital tract

(penile fossa and the urethra before and

Ute1ine involution is characterized by
after ejaculation) can be obtained and
expulsion of the fetal membranes and
submitted for aerobic culture to detect
contraction of the uterus, cervix, and broad
the presence of possible pathogens. If
ligaments to nom1al nongravid dimensions.

consistent heavy growth of potential

To achieve max:inlal reproductive efficiency,
pathogens such asPseudomonas
a broodmare must produce a foal every year. aeruginosa, Klebsiella pneumoniae, or Horses have an average gestation length of

Streptococcus zooepidemicus is seen on

-340 days. Therefore, to maintain a 12-mo
aerobic culture of swabs of the penile
foaling interval, the mare must be bred again
fossa or urethra and there is a history of
within 25 clays of foaling. Mares can be bred
repeated infection in mar·es bred, it may be
on "foal heat," which is the fu-st postpartwn necessary to breed by artificial inseminaestrus that occurs G-11 days after foaling in tion using semen extender containing an
most mar·es. However, mares that experiappropriate antibiotic to which the enced dystocia or retained membranes and
isolated organism is sensitive. If natural
metritis should not be bred on foal heat.

service is required, semen extender

Foal heat pregnancy rates are higher for
containing that antibiotic may be infused
mares bred after 10 days postpartum.

into the mare's uterus before servicing.

The fertility of the fu-st breeding may be

Stallions fow1d to have an overgrowth
increased if breeding is delayed and PGF2a
of P aeruginosa on the external genitalia

( dinoprost, l mg/45.5 kg, IM, or clopros

(penis, prepuce) may benefit from a
tenol, 0.55 mcg/kg, IM) administered -5 days once-daily rinse of the penis ar1d prepuce after the foal heat (fu"St) ovulation. The mare using a dilute acid solution prepared by
can then be bred at the ensuing estms just
mixing 10 mL 38%HCl (concentrated) with
before the second postpartwn ovulation.

4 L of water. Rinsing should be repeated
daily until P aeruginosa is no longer

BREEDING SOUNDNESS
isolated. Stagnant water should be removed

EXAMINATION OF THE STALLION from the stallion's environment.

If a heavy growth of K pnewnoniae

See also BREEDING SOUNDNESS EXAMINATION OF'

is isolated from the stallion's penis and

THE MALE, p 2230. The breeding soundness
prepuce, a daily rinse of the penis and
exanlination should begin with a thorough
prepuce may be considered using a dilute
history, including information regarding
bleach solution prepared by mixing 45 mL
libido, mating ability, nwnber of mares bred,

5.25% sodiwn hypochlorite (bleach) with 4 L
pregnancy rates, prior illness or injwy, and
of water. This rinsing should be pe1formed
any medications administered. A general
daily for 1-2 wk and then discontinued for
physical exanlination should be performed,

4 days, after which swabs should be taken
noting lameness (particularly of the back
from the penile fossa ar1cl preputial fold for
and hindlimbs) and heritable conditions that aerobic culture. 'I):eatment car1 be repeated may affect breeding ability or desirability as
if needed. Stagnant water and sawdu:st
a sire. The penis and prepuce should be free
bedding should be eliminated from the
of lesions. The testes ar1d epididymides
stallion's envirorunent.

MANAGEMENT OF REPRODUCTION: PIGS

2201

If Taylorella eqiiigenilalis is present, the warm water to reduce contamination from
stallion should not be used for breeding (see
the mare's genital tract.

p 1371). The isolation of 'T equigenitalis
requires special culture conditions; the

Artificial Insemination: Semen is obt.ained

VetBooks.ir
organism will not grow in routine aerobic
using an artificial vagina; motility, morpholcultures. Stallions with lesions of coital ogy, and concentration of spem1 are
exanthema (seep 1357) should not be used
detenninecl; and the number of morphologifor breeding until skin ulcers are completely cally normal, progressively motile spenn is
healed.

calculated. Semen extender containing an
antibiotic is then slowly added to semen to
improve spem1 swvival. The temperature of

BREEDING
the semen extender should be similar to the
temperatlue of tl1e semen at the time of

Natural Service: Mares are conunonly
dilution. A commonly used semen extender is
bred by natural se1vice. The proper time to
glucose skim milk extender (made with 4.9 g
breed is determined by teasing, palpation,
glucose, 2.4 g instant nonfat d1y milk, and
and ultrasonography per rectun1, which

100 mL sterile distilled water). One oftl1e
permits detection of estrns and the presence
following antibiotics can be added: piperacilof a dominant follicle. Estrous mares should lin 100 mg (1 mg/mL); ticarcillin 100 mg
be bred when a follicle >30--35 mm is present

(1 mg/mL); reagent grade gentamicin, which
or begirming on day 2--3 of estrns and every
must be buffered with 2 mL 8.4% NaHC03,
other clay until ovulation occurs or the mare

100 mg (1 mg/mL); or arnikacin sulfate 100 mg
goes out of heat. Mares ovulate 0-48 lu·

(1 mg/rnL). Effective proptietmy semen
before the end of estrus. Breeding should
extenders are also available conunercially.

take place before ovulation. Ovulation can

The mm·e is prepm·ed for insemination by
be induced by administration of cleslorelin if
application of a tail wrap and cleansing of the
the mare has a dominant follicle. (See also
perinew11. If soap is used, it should be rinsed

MANIPULATION OF OVARIAN ACTIVITY, p 2188.)

thoroughly to remove a11y residue. Mares

A tail wrap should be applied on the
should be inseminated with at least 250-500
mare, and the perineum cleansed. The
x 106 progressively motile, morphologically
stallion's penis should be rinsed with water
nonnal spem1atozoa before ovulation.

before breeding to remove smegma and to
lnsemination is accomplished by depositing
minimize contan1ination of the mare's
the semen into the body of the uterus
reproductive tract. The mare should be
using a sterile, plastic insemination pipette.

slowly introduced to the stallion and teased Disposable sterile equipment is recomuntil obvious signs of receptivity (tail raise, mended to prevent contamination. Nom1al
abduction ofhindlegs, eversion of vulvar
spetm can be expected to remain viable in
lips, urination) are displayed. A nose twitch the mare's reproductive tract for at least'48
may be used for additional restraint but
hr. Mares should be examined by palpation
may intetfere with the mare's expression
a11d ultrasonography per rectum to confum
of sexual receptivity. For breeding, the
tl1at ovulation occurs. Stallion semen ca11 be
stallion should be fitted with a wellextended, cooled to 4 °C, and packaged for adjustecl halter with large rings that allow
transpmt in a conunercial tra11sport device.

the chain shank to freely slide. During

If semen from fertile stallions is properly
breeding, the stallion should be controlled
handled, good pregnancy rates can be
adequately to prevent injury to the mare.

achieved when tl1e semen is used up to

After breeding, the penis can be rinsed with 48 hr later.

MANAGEMENT OF REPRODUCTION: PIGS

Management of conunercial swine breeding
along with herd protection, minimizes the
herds involves a thorough tmderstanding of
risk of disease loss when combined with
reproductive physiology, genetics, nutrition, intensive management, sound nutrition, and immunology, disease control, environment,
genetic selection. The breeding program
and other factors. (See also ABORTION IN PIGS, should be evaluated at specified intervals
p 1341.) The closed-herd concept, which
to ensure that progress in both efficiency
emphasizes preventive medicine strategies
and productivity is being made. Several

2202

MANAGEMENT OF REPRODUCTION PIGS
efficiency/production parameters to

SOW AND GILT MANAGEMENT
review when analyzing herd reproductive
pe1fom1ance are shown in TABLE 11. The

Selection: Gilt selection for genetic
postweaning perlormance of a breeding
improvement should be indexed based on
herd's offspring can be measured through
such categories as growth rate, disease

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assessment of such parameters as feed
status, sexual development, reproductive
conversion ratio, average daily gain, total
history (including dam's perlonnance as
days to market, and postweaning death loss. to wean-to-service and wean-to-estrus Problems on a swine farm can have a
intervals, litter size, milking ability, and pigs
single cause or be caused by a combination
weaned), structure/confonnation, and
of genetic, nutritional, environmental,
underline (including teat number [7 pair]

health, and management factors. When
and placement). Of potential replacements,
investigating a herd problem, the practiup to 30%-400/o may be culled, with most tioner can best benefit from remaining
eliminated because of problems with
focused on the herd and not individual
structure/conformation, teat issues, and
animals. Accurate, up-to-date records
genital defects. Prepubertal gilts are usually
are essential when investigating a herd
fed a sex-specific ration ad lib until they
problem. When analyzing a herd and its
reach market weight (250-275 lb [ 113-125
records, a certain percentage of "abnormal"

kg]) or are 5-6 mo old. At that time, selected
aninlals and/or reproductive problems are
animals are then moved into gilt developto be expected.

ment, where they are fed a diet formulated

REPRODUCTIVE BENCHMARKING INDICES USED IN COMMERCIAL

SWINE HERDS

Intervention

Reproductive Index

Target

Level

Wean-to-estrus interval (95% in estrus by

<7 days

>9 days

10 days postweaning)

Wean-to-service interval

�5 days

>7 days

Repeat services at 21 ( ± 2) days

<8.5%

>11%

Abnormal returns to-service (25-37 days)

<3%

>5%

Multiple matings (if not using fixed timed

>89%

<86%
insemination)

Abortions

<1.5%

>2.5%

Not-in-pig

1%

2%

Farrowing rate

>86%

<82%

Total piglets born/litter

>12.5

<12

Live piglets born/litter

>11.5

<11

Stillbirths

<6%

>8%

M=ies

<1.5%

>3%

Litter scatter ( �8 pigs/litter)

<12%

>15%

Pigs weaned/litter

>10.4

<9.5

Preweaning mortality

<13%

>18%

Litters/mated female/year

>2.3

<2.2

Pigs weaned/mated female/year

>24

<22

Nonproductive sow days (without gilt pool)

<40

>50

Culling rate

300/o-50%

<300/o and >50%

MANAGEMENT OF REPRODUCTION: PIGS

2203
specifically for introduction into the

Strict culling criteria should be estabbreeding herd and are exposed to boars to lished for ilie gill pool. Gilts in which first
stimulate estrus cyclicity.

visible estrus does not occur by 136 kg body
wt and 210 days of age should be culled.

Disease Precautions: Porcine reproduc

Initial estrus in gilts may be weak, so a

VetBooks.ir
tive and respiratory syndrome (PRRS),
robust estrus detection program with
parvovirus, porcine circovirus type 2,
experienced perso1mel is essential. Some
porcine epidemic diarrhea virus, pseuproducers may elect to use exogenous dorabies (Altjeszky disease), Japanese
hormones to bring these reproductively
encephalitis, influenza, brucellosis,
inefficient gilts into estrus; if this is the case,
chlamydiosis, leptospirosis, and other
tl1e progeny should not be kept for breeding
infectious diseases can directly or indirectly
herd replacements. Gilts iliat have been
affect reproductive pe1iom1ance depending
serviced for two or three consecutive
on animal age at infection and stage of
estrous cycles and do not conceive should
gestation. The reproductive herd (gilts,
also be culled.

sows, and boars) should be vaccinated, at a

Timing of estrus can be controlled by
minirnwn, against leptospirosis, parvovirus,
adding a progestagen to the feed ( eg,
and erysipelas. Brought-in gilts should be
altrenogest at 15-20 mg/day for 14-18 days).

isolated for a minimwn of 45---60 days,

Estrus will be seen in gilts 4-9 days after ilie
during which visual observation and
last feeding and wiili appropriate boar exposerial testing (ie, serology, oral fluids) for sure. This allows estrus in gilts to be
exposure to undesirable infectious diseases
synchronized with that of a batch of weaned
should be done. To minimize ilie nun1ber
sows or fom1ation of a group of gilts iliat
of days for introduction of iliese gilts into
will fan·ow together. Prostaglandins can
ilie breeding herd, the latter po1tion of ilie
also be used as an abo1tifacient to
isolation period can be used for acclimatisynchronize estrus when administered after zation to ilie herd's resident pathogens
day 12 and before day 55 of gestation;
ilirough ilie introduction of cull sows,
females generally come into heat 4-7 days
internal grow-finish hogs, and manure
later. The cost-benefit of these programs
exchange and/or feedback. This natural
should be assessed before in1plementation.

exposure to endemic herd pathogens
can provide essential protection against

BOAR MANAGEMENT
diseases such as PRRS, parvovirus, and
influenza.

Male fertility in ilie breeding program more
often ilian not receives too little attention in

Puberty: Early puberty is desirable to
herd healili programs. As wiili other food
decrease production costs and is considanin1al species, boars should be exan1ined ered a good indicator of reproductive
for breeding soundness before use in a
capability. Onset of puberty depends on a
breeding program, whenever iliey show
variety of factors, including genotype,
lack of libido or inability to copulate, or if an
liveweight, nutritional status, season, and
increased nwnber of females bred by ilie
management (including exposure to the
boar retwn to estrus -3 wk later. At a
boar). Exposure to asexually mature boar,
minirnun1, a breeding soundness evaluation
also known as the "boar effect," is ilie most should include a history, general physical
influential of all management factors. The
examination (including genital examinaboar effect is strongest when females are tion), a semen evaluation, and a behavior
exposed to the sight, sound, touch, and
evaluation (seep 2237).

smell of a mature boar, and it decreases as
the nwnber of senses stin1ulated by the

Selection: When selecting a boar for
boar decrease. Consequently, ilie boar
a breeding program, factors such as
effect is greatest wiili direct contact using a
origination from a specific disease-free
mature, sterile boar. Exposure of pe1ipuherd, perfonnance, soundness and bertal gilts (5--6 mo old) to a mature boar
conformation, age of puberty, and other
for 10-15 min/day appears to provide an
pertinent parameters related to reproducadequate stimulus. Along with the boar tion should be considered. All boars that are
effect, other management tools to
to be used in a breeding program should, at
manipulate the onset of puberty include
a minimwn, be seronegative for brucellosis,
select crossbreeding, housing changes
porcine reproductive and respiratory

( eg, confinement to outside pens and vice
syndrome, and pseudorabies (Altjeszky
versa), and forming new groups by mixing
disease). Additionally, all boars should be
gilts from different pens of similar health
isolated and acclimatized for at least 45--60
status.

days and be tested/retested for diseases

2204

MANAGEMENT OF REPRODUCTION: PIGS
naive to the herd before introduction into
genotype, age, and weight of boa.rs between
the herd. If involved in the selection

142-282 days of a.ge a.i1d 185-375 lb (84-171
process, boars from large litters (>10
kg) body wt. Testicula.i· size increases until
piglets) that reach puberty early (5Y2--6 mo)

-18 mo of age; testicula.i· growth and sperm

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tend to produce highly productive daughters nw11bers increase at tl1e greatest rate who also reach puberty at an early age.

between 5 a.i1d 12 mo of age. Because age

Perfom1ance para.meters such as feed
a.t1d testicula.i· weight a.i·e imp01ta.I1t
efficiency, backfat, and average daily gain
identifiers of early sexual development,
a.re also highly heritable.

boa.rs should be 2'.8 mo old before use in a

Skeletal confo1mation and examinabreeding progra.i11.

tion for current or potential locomotor

The testicles ca.i1 be affected by diseases
dysfunction should be assessed. Any

( eg, brucellosis, a.ctinoba.cillosis) a.i1d a.i·e
unsoundness that may interfere with the
vulnerable Lo trauma by ha.i1dlers or other
boa.r's ability to approach, mount, and
a.I1in1als or as a result of improperly
successfully breed/ejaculate should be
designed or maintained facilities. They
determined. Acute or chronic musculoshould contain no nodules or soft masses.

skeletal conditions may elicit pa.in that

The initial reaction of testicles to ti·a.w11a
ca.uses the boar to appear uninterested in
or infection is swelling; if untreated, the
mounting. Boa.rs a.re usually selected as
longterm result is testicular atrophy,
breeding prospects at 3-6 mo. The genetic
identified by increased furnness a.t1d loss
background of the boar should be
of resiliency. Asynunetry, as a result of
consistent with the intended use. Selection
unilateral atrophy, is potentially dclcte1ious
of boa.rs with heritable defects such as
to fertility, a.i1d semen evaluation may reveal
wnbilical or inguinal hernias, cryptorchida.zoospermia, oligospermia, asthenoism, rectal prolapse, and poor tmderlines spermia, or morphologic cha.i1ges indicative
can be a.voided by careful analysis of the
of testicular da.inage.

source herd production records.

Behavioral Evaluation and Semen

History: A complete history should

Collection: Collection allows evaluation
include the age and origin of the boar,
of libido a.t1d ability to mate a.i1d ejaculate;
source herd health, i.mmwuza.tions,
in addition, it provides a sample ejaculate.

previous disease problems and treatments,

Precopulatory behavior involves visual a.t1d
exposure to other animals and premises,
olfacto1y stimulation. The boar grunts or
as welt as the ti.me spent in isolation and
barks rhythmically, chomps jaws, salivates,
exposure to the present premises and its
a.t1d typically engages in head-to-head
breeding a.nin1als. It should also include,
contact with the sow or dtumny, followed
if available, a description of the boa.r's
by nuzzling her fla.t1ks to test for voluntaiy
previous libido, ma.ting behavior, concepinunobiliza.tion. These activities should be tion rates, litter size, and pe1iorma.nce of
observed, because a.berra.i1t sexual behavior
relatives and other boa.rs in the herd. For
may result in infertility. Consta.I1t head
young boa.rs, observations of sexuaj
mounting is a common problem with
behavior may be useful.

i.nexperienced boars.

Poor libido is likely ca.used by behavio

Physical and Genital Examinations:

ral rather than endocrinologic problems.

A general physical exanuna.tion should be

Fighting a.t1d domination by older boa.rs
pa.rt of every fertility evaluation. Attention
and sows ca.t1 inhibit libido in young boa.rs.

should be given to body condition and

Breed a.i1d strain differences a.i·e also seen;
conformation, including the back and legs,
the tendency to be timid, nervous, a.t1d
and locomotor function. Osteomala.cia,
nonaggressive ca.i1 be influenced by
osteoa.ithrosi.s, and a.it.hritis, which may
selection in a breed over several generaresult in la.ineness and reluctance to mount tions a.t1d ca.i1 result in boa.rs with poor
or bear weight on the rea.i· legs, a.re serious
libido. Pain from genital lesions or
problems.

musculoskeletal problems ca.i1 have a

The testicles, epididynudes, a.i1d scrottu11
strong negative effect. Libido ca.i1 also be
should be exan1ined and palpated for size,
impaired by a.i1 unfa.inilia.r environment, tl1e
synunetiy ( d cm difference in dia.i11eter),
presence of a feared person, or distractions
consistency, and pathologic changes. An
such as available feed.

appreciation of normal testicular consist

Once the boar has mounted, erection a.t1d
ency is necessa.iy to detect subtle changes.

protrusion of the penis occur as the boa.i·

The penis and prepuce should be exa.i11ined
searches for the vulva. Close observation is
for a.bnonnalities during semen collection.

necessa.iy to notice injuries a.i1d lesions of

Testicular size is directly correlated with
the penis as welt as improper erection.

MANAGEMENT OF REPRODUCTION: PIGS

2205

Congenital and genetic problems include
receptacle), because it coagulates into a
incomplete erection, penile hypoplasia,
semisolid mass that can interfere with
masturbation into the diverticulum (ie,
subsequent evaluation of semen quality.

"balling up"), and persistent frenulum.

The boar then ejaculates the milky to

There are basically two methods of
cream-colored, sperm-rich fraction. The
semen collection in the boar-the
final, sperm-poor fraction contains the

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gloved-hand method and electroejaculation.

largest volume of fluid and gel. Care should

A third method using a water-jacketed
be taken to let the boar complete the ejacuartificial vagina is no longer in common use.

lation, voluntarily withdraw the penis from

Although satisfactory ejaculates can be
the hand, and dismount. Some boars will
obtained using either the gloved-hand or
go through two or more complete ejacuelectroejaculation methods, the glovedlations before voluntarily dismounting.

hand method is preferable because it is

Semen collection by electroejaculation
simpler and reproductive behavior can be
is done only on an anesthetized boar. An
simultaneously assessed. The boar is
iitjectable anesthetic that will allow
allowed to mount an estrous female or
for 15-30 min of general anesthesia is
collection dummy and attempt to copulate.

recommended. The rectum is cleaned out

Boars used for artificial insemination are
using a lubricated hand, and a lubricated
usually trained from the onset to mount a
rectal probe is inserted. The penis is then
collection dummy. The boar should then be
exteriorized with the aid of Bozeman
approached quietly from the rear without
sponge forceps and grasped with a surgical
being touched or frightened. Preputial fluids
sponge wrapped around the penis 5--10 cm
are first evacuated by massaging the
distal to the glans penis. Electrostimulation
prepuce to prevent contamination of the
of the boar is performed as in the bull or
ejaculate. The back of the gloved hand is
ram, with the ejaculate collected in a clear,
then placed against the ventral abdomen of
plastic bag that envelops the glans penis.

the boar just cranial to the preputial orifice,
and the penis is allowed to thrust into the

Semen Evaluation: Standard tests used
gloved hand. Digital pressure is applied to
to evaluate boar semen include sperm motilthe distal 3-6 cm of the penis. If properly ity, morphology, concentration, total
stimulated, the boar will fully extend the
numbers, and ejaculate volume. The
penis and become very quiet. This is
ejaculate should be protected from changes
followed immediately by ejaculation. Once
in temperature, osmotic pressure, and pH
the tip of the penis is firmly in the hand and
during handling and analysis. All equipment
ejaculation has begun, it continues for ;:,,3--7
and materials that come into contact with
min. If the boar dismounts when the attempt
semen should be warmed to 35° -39°C.

is made to grasp the penis, he should be

Sperm motility should be evaluated as
allowed to make several false mounts until
soon as possible after collection. Estimating
he is aggressively attempting intromission
sperm motility in an ejaculate by examining
again. Most experienced boar trainers
the mass activity or swirl motion of a drop
achieve a >96% success rate in training
of semen on a slide is of limited value and is
boars to mount a dummy and to ejaculate.

not recommended. Gross sperm motility

A nervous boar may not allow the penis to
is best estimated on prepared samples in
be locked into the hand, even after several
which a monolayer of individual sperm
attempts. Semen can be collected from
can be visualized using light microscopy.

many such boars by allowing them to

To do this, a 5--10 µL drop of semen is placed
achieve natural intromission and lock the
on a prewarmed slide and overlaid with
penis into the sow's cervix to begin the
a coverglass. Sample motility is then
ejaculation, then quickly retrieving the
subjectively estimated to the nearest 5% by
penis and locking it into the hand. The boar
viewing several random fields under 20x
will continue to ejaculate, and the major
magnification.

portion of the ejaculate can be collected.

Sperm morphology can be a valuable

A prewarmed (37°C) thermos or
indicator of fertility potential, especially
styrofoam cup is a convenient and
in those ejaculates with a high percentage
economical collection vessel. The
of abnormal sperm. When using brightpre-sperm fraction, consisting of 5--15 mL of light microscopy, stained slides are
fluid, is usually ejaculated first and allowed
necessary to provide adequate contrast to.

to fall on the ground (ie, it is not collected).

evaluate sperm morphology. When using

The boar then usually ejaculates a small
higher resolution microscopy (ie, phaseamount of gel, which is filtered out of the contrast, differential interference contrast),
ejaculate by a double layer of coarse gauze
glutaraldehyde or buffered formalin

(placed over the mouth of the collection
preserved samples can be used. A minimum

2206

MANAGEMENT OF REPRODUCTION: PIGS
of 100 (preferably 200) spem1 should be
frequently, compute1°automated semen
assessed for morphology of the head,
analysis systems are being used to
midpiece, and principal piece (ie, the tail
objectively determine spenn motility, sperm
distal to the midpiece ). Sperm can be
morphology, and spem1 concentration.

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categorized into three groups: normal,
spem1 with abnom1al heads, and spem1

Interpretation of Findings: Semen
with abnormal tails (midpiece, principal
values can be affected by frequency of boar
piece, including cytoplasmic droplets).

use, age, environment, disease, level of

Samples with a high number of sperm
nutrition, genotype, and method ofspem1
defects can be examined further, and
cell fixation. Therefore, boars that do not
abnormalities classified as major and minor
have acceptable semen values are not
defects. Acrosome morphology should also
necessarily subfertile or infertile. Spemtiobe assessed if possible.

grams can change dramatically over a short

Several techniques are available to
period of time, and boars shottld not be
determine spem1 concentration in a filtered
culled on the evaluation of a single
boar ejaculate. A crude, subjective,
ejaculate. Breed differences in onset of
qualitative estimation of spenn concentrapuberty, libido, mating ability, and tion can be done by assessing visual opacity
conception rate have been seen.

of a raw ejaculate, either by direct

Environment can affect fe1tility over a
examination or with the aid of a Karras spershort period of time, primarily because of miodensimeter. Analytical detennination of
disturbances in the them10regulation of tl1e
sperm concentration can be performed by
testes. Boars exposed to cold or hot
measuring opacity via a calibrated ( spectro)

environmental temperatures may have
photometer on a diluted semen san1ple. It is
abnormal spenniograms for ?.7 wk after the
essential that the photometer be calibrated
insult. Severe exposure may result in
for boar semen. Even with a calibrated
abnormal spem1iograms for a longer time or
photometer, estimates of spem1 numbers
may even lead to permanent spermatogenic
may be ±300A, from that of the actual
disruption. Any disease that increases body
concentration; this can be attributed, in
temperature, and tlrns disrupts thennoregupart, to in1proper technique, human error, lation of the testes, also has the potential to
and/or the inherent opacity of the secretions cause temporary sub- or infertility.

of the accessory sex glands present in the
boar ejaculate. Photometric readings can

Guidelines for Boar Evaluation:

also be inaccurate if the reading is outside

Ideally, libido, mating ability, semen quality
the calibration curve or optimal operating

(see TABLE 12), and breeding results
range. A second, more direct method to

( conception rate and litter size) should be
measure sperm concentration is with a
considered. The duration of spem1atogenhemocytometer or counting chamber. In esis and spermatozoa! maturation is -51
this method, concentration can be
days in the boar. If a boar produces an ejacudetem1ined by diluting a portion of the late of low or marginal quality when
filtered ejaculate to a 1:200 ratio-most
examined in vitro, additional ejaculates
easily done using a Unopette® system. The
should be assessed at 1- to 2-wk intervals to
hemocytometer should be charged, and the
ascertain whether quality has improved
charged unit allowed to set for 5 min, so that over tin1e. Boars with spenniograms that do the spem1 settle into one visual field. Using
not improve over 2-3 mo are wuikely to
microscopy, a sperm count is pe1fom1ed
ever improve. Boars with azoospem1ia on
and calculated as nom1ally done for RBC
two complete ejaculates or that are unable
determination. Determining spenn
to achieve complete erection should be
concentration using a counting chamber is
culled immediately. Those that have penile
tedious and ti.me consuming, making its use
lesions or blood in the semen should be
on a routine basis impractical in most
sexually rested for ?.2-3 wk and reevaluated.

commercial operations.

For boars with persistent frenulwn or that

After calculating spem1 concentration/
habitually masturbate in the diverticulwn,
mL, total spem1 nun1bers in an ejaculate can surgical correction is recommended; be calculated by multiplying spem1
however, the progeny should not be kept for
concentration with the total volume (in mL)

breeding, because these conditions are
of the gel-free ejaculate. Ejaculate volume
most likely heritable. All results of the
can be measured by using a wam1ed
fertility examination must be considered in
measwing apparatus ( eg, graduated
relation to age, disease history, envirorunencylinder, disposable plastic measuring cups) tal stress, prior breeding usage, mating or by measuring the weight of the ejaculate
system, and the techniques of semen

(with 1 g equivalent to 1 mL). More
collection and handling.

MANAGEMENT OF REPRODUCTION: PIGS

2207

SUGGESTED MINIMUM SPERMIOGRAM VALUES FOR BREEDING

BOARS

Parameter

Natural Service

Artificial Insemination

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Color

Opaque to white

Opaque to white

( vulvar discharge)

Total sperm numbers

>35 x 109 spenn/ejaculate >35 x 109 spenn/ejaculate Gross motility (raw)

>600h

>70%

Abnormal morphology

<25%

<20%---25%

(including cytoplasmic
droplets)

Cytoplasmic droplets

<15%

<15%-200h

(both proximal and distal)

BREEDING MANAGEMENT
averting the adverse affects of undernow-ishment on early reproductive performance.

Estrus: Sows and gilts are nonseasonal

In countries in which gilts arc not routinely
and polyestrous, with the estrous cycle
provided full feed, increasing energy intake
lasting 18---24 (average 21) days. Sows are
for 10 days before estrus (ie, "flushing") is behaviorally anestrous during pregnancy.

perfonned. This has optin1ized ovulation

Ovulatory estrus usually is not seen dw-ing
rate under these circwnstances. To prevent
lactation except under conditions of group
undernow-islm1ent in recently weaned
rearing, high feed levels, or boar contact.

sows, an energy-dense diet should be fed

Partial weaning or gonadotropin treatment
until after estrus and breeding.

can induce estrus dw-ing lactation, but the

Behavioral changes are most pronounced
results are inconsistent and not economical.

when the sow or gilt is exposed directly to

Nmmal uterine physiology is reestablished
the sight, sound, odor, and attention
by 20---25 days postpartun1. Most sows

(nuzzling and grunting) of a matill'e boar.

exhibit estrus 3-7 days after weaning.

A sow or gilt in standing heat nom1ally

Estrus in gilts and postweaning anestrous
assumes a rigid, in1rnobile, receptive stance
sows can be initiated with exogenous
when exposed to a boar. Physical changes
hormones. However, these hormones
such as vulvar swelling and discha.ge are
circumvent natill'al selection for reproducoften Wlfeliable; they do, however, appear tive efficiency, and this should be kept in
to be more marked in gilts than sows and
mind when they are used in breeding
commonly develop 2---3 days before estrus.

management progran1s. Exogenous

The ultimate criterion of estrus is either
horn10nes should not be used as a longstanding to the boar or a positive response tern1 solution to address reproductive
to the "riding test" ( an attendant applies inefficiency in a herd.

pressw-e with the hands in the loin area,

Estrus lasts ---36---48 hr in gilts and �48---72
then gently sits on the pig's back to elicit
hr in sows. Time to estrus after weaning and
the standing reaction); this test is best
dw-ation of estrus in sows can be influenced
conducted in the presence of a boar ( eg, in
by length of lactation, nutrition, body
an adjacent pen) or, as an alternative, after
condition, genetics, and other management
exposing the sow to a synthetic boar-odor
practices (see TABLE 13). Estrus is characteraerosol or taint rag.

ized by behavioral ( eg, mounting, fence

Anestrus is a common problem. Failw-e to
walking, vocalizing, tilted ears, kyphosis)

detect estrus must be distinguished from
and sometimes physical ( eg, vulvar
true cases of ovarian inactivity. First-litter
swelling, vaginal discharge) changes.

and early-weaned sows are particularly

Ovulation generally occurs in mid to late
vulnerable to postweaning anestrus. The
estrus. DW'ing ovulation, ---15---24 ova are
pri.miparous sow must support her own
released over a 1- to 4-hr period. Ovulation
growth as well as maintenance and lactation
rate increases over the first fow- parities, so
demands, while her feed intake capacity is
that the fourth to sixth litters tend to be the
not yet fully developed. This problem can be
largest in number. Ovulation rate can
avoided by breeding only gilts in good
decrease when gilts or sows are undernourcondition; not overfeeding during the first ished. Most gilts are on full feed, thereby
gestation; and encouraging energy intake

2208

MANAGEMENT OF REPRODUCTION PIGS
iM:iiifi FACTORS AFFECTING OVARIAN ACTIVITY OF PIGS

Stage of Breeding Affected

Proven or Suspected Factors

Puberty

After Weaning After Service

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Insufficient male stimulation

+"

+

Housing and social environment

+

+

High ambient temperature

+

+

+

Season of year (summer/fall)

+

+

+

Photoperiod

+

7c

Genotype

+

+

Nut1ition

+

+

+

Short lactation

+

Large litter reared

+

Adapted, with permission, from Meredith MJ, Pig News and Information 5, 1984, published by CAB

International, Wa!Hngford, Oxon, UK

" Effect has been demonstrated
b No evidence for effect

< Effect unce1tain
during the first lactation by frequent feeding

Fixed-time insemination protocols
of high-density diets, wet feeding, and
continue to gain interest in the swine
avoiding high temperatures in the farrowing industry. Cun-ent reconm1endations call for rooms. Management practices such as
the use of progestins to prime the gilt before
segregated early weaning, modified
administration of a GnRH analogue. With
medicated early weaning, and medicated
sows, a GnRH analogue is administered
early weaning recommend weaning as early

83--96 hr after weaning. Breeding of both
as 10 days postpartum; postweaning
gilts and sows is then pe1forrned 20-33 hr
anestrus is not an uncommon sequela of
after GnRH administration ( depending on
these management techniques. General
product and route of administration).

guidelines to minin1ize the negative effect

Exogenous prostaglandin induces
of early weaning on sow reproduction
luteolysis of the corpus luteum only after
recommend weaning at no Jes" than 14-16
day 12 of the estrous cycle and, therefore,
days into lactation for prirniparous sows, at
is not a practical agent for estrous cycle
no less than 12-14 days into lactation for
control; however, estrus may be synchrosows on their second litter, and at no less nized by induction of abortion in sows
than 9-11 days into lactation for sows on
pregnant> 15 days by administration of
their third or subsequent litters.

PGF2a (15 mg, IM, then 10 mg, IM, 12 hr
later) or an equivalent analogue. Estrus may

Hormonal Control of the Estrous
also be synchronized by feeding altrenogest

Cycle: Estrous synchronization may be

(15--20 mg, PO, daily for 14-18 days), with
achieved by synchronized weaning of
estrus being observed 4-9 days after the last
lactating sows; estrus occurs 4-10 days
dose with appropriate boar exposure.

later. Administration of a commercially

Combination eCG and hCG may be given on
available combination of 400 TIJ of equine
the day of progestagen withdrawal to better
chorionic gonadotropin ( eCG) and 200 TIJ
synchronize estrus.

of human chorionic gonadotropin (hCG)

per 5 mL dose given as a single IM injection

Breeding: The three methods of breeding
within 12 hr after weaning tightens the
are pen mating (boar run with females),
synchronization, and estrus occurs 4-5 days hand mating (supervised natural mating), after weaning. This eCG and hCG combinaand artificial insemination (Al). Pen mating tion also induces estrus in gilts with delayed
is generally found on smaller operations and
puberty and in sows with postweaning
works best in a pen of pigs in various stages
an estrus.

of the estrous cycle. Pen mating with a

MANAGEMENT OF REPRODUCTION: PIGS

2209
group of recently weaned sows is less
market hog offspring. Minimum suggested
desirable, because their estrous cycles may
values for extended semen used within
occm close together and lead to overuse of

72 hr after collection are provided in
the boar. In hand mating, the female is

TABLE 14. Total sperm numbers in a close of
usually mated two or three times dming
semen depend on quality and storage time

VetBooks.ir
estrus, with the first service on the first day
of the semen .

of standing estrns, and subsequent matings

. Boars should not be overused (see
at 24-hr intervals; confinned matings should

TABLE 15). If sows are weaned in groups, a
be recorded. Many conm1ercial producers
boar-to-sow ratio of I :4 for matme boars
breed the sow or gilt once daily as long as
and 1:2 for young boars is recommended. In
she will accept the boar. The use of two
hand mating, a matme boar should be used
different boars may increase the nwnber of
for �2 breedings/day. When using natural
pigs per litter but may mask infertility in one
service, a boai�to-sow ratio of J: 15-1:25
of tl1e boars.

(average 1:17 or 18) is usually needed. When

In Al programs, heat detection is
using Al, tl1e boai·-to-sow ratio cai1 be
performed either twice or once per day. If
increased to 1:15 0 -1:400.

heat detection is performed twice per day,
gilts should be inseminated twice, 8--12 hr

Pregnancy: Sperm cells reach the oviducts
after the onset of standing heat and again
within 30 min of mating, and fertilization

12-16 hr later. Sows should be inseminated
can occur within 2-6 hr. Fertilization rates

24 hr after onset of standing heat and again
approach lOOOA, in sows, but embryo

18--24 lu· later. If heat detection is pe1formed
mmtali.ty up to 300/o-4()0A, accounts for the
once per day, gilts should be inseminated
usual litter size of 10-16 pigs. Embryos
within 4 hr and SOWS within 12-16 lu· from
enter the uterus -48--60 Ju· after ovulation.

when they were first seen in standing heat.

Embryos hatch from tl1e zona pellucida and

A second insemination should be perfom1ecl fonn blastocysts 144 hr after ovulation.

as described above for those animals that

Maternal recognition of pregna11cy
remain in standing heat.

( embryos secreting estradiol) occurs by

Timing of Al may need to be modified
day 10-14 of gestation, witl1 intrauterine
based on a particular farm's availability of
migration and distribution of embryos.

labor, building design, or herd genetics.

Embryo attaclm1ent begins by day 13-14,

Some experienced users of Al obtain
with in1plantation complete by day 40; a
satisfactory results in gilts with a timed,
mininuun of four embryos must be present
single insemination; however, performing
at tltis tin1e for pregnancy to continue.

two inseminations is more common.

Skeletal mineralization develops by day 35,

Inseminations can be performed using
witll fetuses irnmunocompetent by day
either single-sire (sourced from one boar)

70-75. Fetal deaths that occur after clay .35
or pooled (sourced from multi.pie [three
can result in expulsion or retention of recogto six] boar ejaculates) extended semen.

nizable piglets. Retained dead fetuses in this

In general, single-sire matings are
sterile environment become mummified
performed when particular genetic (ie,
and are usually expelled at tl1e time of
breeding or show animals) offspring are
faiTowing. The average gestation length is
desired, whereas matings with pooled

114 ± 2 days and is somewhat shortened in
semen are used as a means to produce
sows with large litters.

MINIMUM SUGGESTED VALUES OF EXTENDED PORCINE SEMEN

FOR USE IN AN ARTIFICIAL INSEMINATION PROGRAM

Semen Variable

Value

Gross sperm motility

<!70%

Normal sperm morphology

<!75%

Sperm concentration

25 to 65 x JOG sperm/mL

Dose volume ( cervical deposition)

<!70mL

Microbial content

No significant aerobic growth

Arrival temperature

15°-19°C

2210

MANAGEMENT OF REPRODUCTION: PIGS

SUGGESTED GUIDELINES FOR BOAR USAGE BASED ON BREEDING

PROGRAM

Artificial Insemination

Natural Mating

VetBooks.ir

Boar Age Semen Collection

, Pen-breeding

(mo)

Frequencya

Matings/day Matings/wk

(females/mo)

6 -8

1 time/wk

4

<8

8-12

1-2 times/wk

5-7

8-10

>13

<!4 times/2 wk

2 (spaced)

8-10

10-12

Adapted from Althouse GC. Animal Health and Production Compendium, 2002, by CAB International, Wallingford, Oxon, UK.

" Depends on boar libido

Embryos are at greatest risk of dying
include blood flow in middle uterine or
during the first 30 days, and efforts should
umbilical arteries, fetal heartbeat, and fetal
be directed toward avoiding stresses to the
movements. Real-tin1e ultrasonography
sow (eg, overfeeding, heat, handling or
involves visualization of a 2-dimensional
moving, immunization) during this critical
image of scanned tissues directly under the
period. Pregnancies of <16 days are
transducer. Ultrasonographic techniques
especially sensitive to heat stress. Avoidare generally used at 22-75 days to ing exposure to outside animals reduces
determine pregnancy, with real-tin1e
disease risk. Feed intake should be
ultrasonography being used as early as 18
reduced to the limit feeding level of 4-5 lb
days after breeding. Although uncommonly

( -2 kg) immediately after breeding to
used for this pw-pose, rectal palpation can
avoid embryo loss due to high energy
be performed to confirm pregnancy at >30
intake. Farrowing less than five piglets is
days gestation. The exan1iner palpates for
indicative of embryo death after the time
fremitus, size, and position of the middle
of attachment.

(medial) uterine artery in relation to the

To increase colostral antibodies, the gilt
external iliac artery. The tone and tension
or sow should be i.J.mnunized during the
of the cervix and weight and contents of
last 6 wk of gestation. An i.J.nmunization
the uterus can also be used to help confirm
program may include vac�ination against
pregnancy. Other techniques such as

Escherichia coli, atrophic rhinitis, and
hormonal assays (eg, estrone glucuronide,
erysipelas, and provision of any other
progesterone, prostaglandin) and vaginal
vaccines appropriate for the disease
biopsy can be used but are not economisituation on the i.J.1dividual farm.

cally feasible.

Pregnancy Determination: Several

Parturition: The prepartmient period
techniques are available for pregnancy
involves restlessness and nest building the
determination (see TABLE 16). Pregnancy is
last 24 hr. Man1ll1ary glands l:)ecorne turgid,
most commonly diagnosed by noting that
and the secretion changes from serous to
the female does not return to estrus in
milk as parturition approaches. Pruturition

18-25 days; this is 75%-85% accmate.

is initiated by increased cortisol levels,

Ultrasonography is another popular
which also stinmlate release of prostaglantechnique, and three types can be used: din (PG) F2cv. from the uterus. PGF2cv. causes
pulse echo (A-mode), Doppler, and
luteolysis of the corpora lutea and release of
real-ti.J.ne. Pulse echo or amplitude depth
relaxin, which causes relaxation of the birth
involves emitting ultrasonic waves from a
canal and cervix. Oxytocin is released from
hand-held transducer placed on the skin in
ilie pituitary gland, which causes uterine
the flank area. Reflected waves from a
contractions and onset of labor. Piglets are
fluid-filled area (ie, developing conceptus
usually delivered at frequent intervals
or fetus) are picked up by the transducer

(10-15 min; 5-45 min range). Uterine horn
and converted into either an audible or
evacuation is random.

visual signal. Doppler ultrasonography

The stillbirth rate usually is 5%-10%;
detects changes in sound frequency (fluid
intra-uterine deaths are due to infection,
movement) using an audible signal;
incorrect position in the uterine horn
movements mdicative of pregnancy
during delivery, or anoxia. Anoxia is seen

MANAGEMENT OF REPRODUCTION: PIGS

2211

•d=i!lti COMMON TESTS FOR DETECTION OF PREGNANCY IN PIGS

Application of Test After Breeding

Technique

Test'.lype

(Accuracy)

Estrus detection

Indirect

Daily testing 18-25 days (75%-85%)

VetBooks.ir
and through gestation (98%)

External physical signs

Indirect

>55 days (gilts); >84 days (sows)

Rectal palpation (sows)

Indirect

30 days (94%), >60 days (100%)

Ultrasonography

A-mode

Indirect

30-75 days (95%)

Doppler

Direct/Indirect

�35 days (>85%)

Real-time CB-mode)

Direct

�22 days (>95%)

when the umbilical cord ruptures or
period by injecting 20 IU of oxytocin IM
becomes constricted because of the

15-24 hr after the PGF2ct injection. This
extreme length of the uterine horn, or
shortens the interval to parturition but can
when there is a delay in transit along the
be accompanied by ar1 increase in dystocia.

birth canal. Stillborn and weak piglets also

Successful farrowing can also be induced
may be due to low temperatures in the
by giving a single vulvomucosal injection
farrowing house or low Hgb levels ( <9 g/dL)

of 5-10 IU of oxytocin.

in the sow. Any increase in the time

Incidence of dystocia is low (1%-2%) in
interval between pigs born (eg, due to
sows. As with all polytocous species,
exhaustion, atony of the uterus, or
uterine inertia accounts for most dystocia in
dystocia) increases the chance of injury
swine. Other causes include fetal malposior death to the piglets still in the uterus.

tion, obstruction of the bilth canal,

Piglets are born in both cranial (60%) and
deviation of the uterus, fetopelvic disprocaudal ( 40%) presentation. Assistance pmtion, and maternal excitement. A
can be provided in the form of oxytocin
tl10rough digital exaniination of the bilth
injections (10-30 IU) and manual removal
canal is prerequisite to therapeutic
of piglets. Walking the sow for a few
illtervention. Medical therapy for unobmoments also can be helpful. The number structive dystocia may include use of an
of pigs born alive can be increased by
ecbolic agent ( oxytocin at 20-30 IU evers 30
approximately one per sow if an attendant
mil1, up to three tilnes). Administration of
is present to assist delivery (see below).

injectable calcium may be warranted if

Passage of the fetal membranes should
uterine illertia is suspected.

occur within 4 hr of delivering the last

Lactation peaks at 3-4 wk postpartum.

piglet.

Sows tl1at have been on an 8-wk lactation

Farrowing can be induced by IM
produce 400-700 lb of milk. Poor lactation is
injection of 10-15 mg of natural PGF2ct or
a significant cause of Ltnpail·ed productivity
equivalent dose of synthetic analogues.

in pigs (see POSTPARTUM DYSGALACTIA SYNDllOME, Farrowing generally occurs 18-36 hr later
p 1373).

(most within 22-32 hr) in 80%-90% of sows
when PGF2ct is given at or after 112-113
days gestation. Induction can be used so

Preweaning Mortality: Supervised
that most farrowings occur during normal
farrowi11g alone can help to reduce piglet
working hours, avoiding evenings,
mortality, because it minimizes stillbirtlls,
weekends, and holidays. Good records are
facilitates access of piglets to needed
essential, and average days of gestation for
warmtl1, allows for observation of nursing
the sow herd and individual breeding dates
activity, and prevents crushing and
for each sow must be known. PGF.,ct must
cannibalism. Other management techbe used within 72 hr of the expected niques available to reduce piglet mmtality
farrowing date to prevent an increase in
include cross-fostering, split-suckling,
stillbirths. The slightly premature piglets
well-designed farrowing crates and pens,
require good environmental conditions,
prepartum vaccil1ation of sows, appropriate
particularly in cold weather. Farrnwings
feedillg programs for lactating sows, and
may be concentrated into an even shorter
cleanliness.

2212

MANAGEMENT OF REPRODUCTION: SHEEP

MANAGEMENT OF

REPRODUCTION: SHEEP

VetBooks.ir

When establishing a flock health manage

Well-grown ewe lall1bs with a body
ment program for reproduction, it is
condition score of3-3.5, paiticulai-Jy of the
important to remember these points:

meat breeds, cai1 be mated at 7-8 mo of age

1) Sheep are short-day polyestrous
all cl 70% of mature body wt. Two exceptions
breeders, ie, estrus occurs in response to
exist: lainbs born in the autwnn to a spring
shortening clay length. 2) The ovulatory
breeding will reach puberty in the spring
season tends to be in the auttunn and early
allci be less fe1tile to a.ii induced estrus, alld
winter months; the an ovulatory season in
some breeds of sheep are slow maturing
the late winter, sp1ing, and early sw11mer

( eg, rallge breeds) allci may not be fertile
months; and the transition season in the late
at 7-8 mo of age. However, breeding ewe
summer months. 3) There is tremendous
lainbs early is encouraged; ewes that breed
breed-to-breed vaiiation in prolificacy and
as lai11bs are able to produce more la.nib
length of the ovulato1y season.

crops in their lifetime thall those bred as

2-yr-olcls.

REPRODUCTIVE PHYSIOLOGY

Ewe la.i11bs should be separated from rain
lainbs by 5 mo of age to avoid unwanted

Ewes are seasonally polyestrous, cycling
pregnallcies, alld from all mai·ket la.inbs to
eve1y 16-17 clays during the breeding
avoid overconclitioning from a diet too high
season. The major environmental factor
in energy. Overconditioned ewe la.inbs are
controlling the estrous cycle is the
less fertile ai1cl produce less milk thall those
photoperiocl. Decreasing photoperiod after
feel to achieve a body condition score of3.

the summer solstice causes secretion of

Follicle development allci ovulation rates
melatonin, which triggers the hypothalai1rns
are major clete1111inants of fertility.

to produce gonaclotropin-releasing

Ovulation rate is a polygenic trait showing
horn1one. Geographic location and
marked breed difference; hetitability
enviromnental temperahtres also modify
estimates ai·e moderate (0.3%--0.5%).

the length of anestrus, as does the breed of

Although by selecting replacement alli.Inals
sheep. Fine-wool breeds ( eg, Rainbouillet,
born as twins or t1iplets will slowly increase

Merino), tropical breeds, and Dorsets have a prolificacy withi.I1 a flock, using more sh01ter anestrous period thai1 other breeds
maternal breeds is recommended because
such as the Suffolk, Hainpshire, Border
their offspring will also have desirable traits

Leicester, and Columbia. Regardless of this
of better mothering allci milk production.

breed-related variation in the length of the

Nutritional supplementation sta1ting a
breeding season, all breeds are most fertile
few weeks before mating ("flushing") may
in the autumn, ai1cl anestrus is ai1 nnlikely
result in higher ovulation rates if the ewes
problem associated with regulai· armual
ai·e not in good body condition (score <3).

mating.

Ewes already in good fit will have a si.Inilai·

The duration of estrus ( -30 tu") is
ovulation rate allci will not respond further
influenced by the breed alld age of the ewe,
to flushing. The diet should be balanced for
the onset of pube1ty, the presence of the
protein (not >14% crude protein) allci have a
male, and the season. Estrous periods that
good availability of energy. High levels of
occur in the auttmm ai·e longer and more
soluble protein cai1 cause early embryonic
intense, all cl maiden ewes have a shorter
death tlu·ough increased urea nitrogen
all cl less intense estrus thall matw-e ewes.

levels in the blood. Overfeeding of energy

The optimal time to mate ewes (naturally or
to ewes in good body condition Call cause
a.itificially) is in the first half of the estrous
decreased fertility.

period, or 12-18 hr after the onset of estrus.

Ewes show no overt signs of estrus, a.i1cl

Estrus Induction in Acyclic Ewes:

heat detection requires the presence of a

Estrus alld ovulation Call be induced i.I1
rain, a teaser rain (made infertile by either
allestrous ewes by tl1e introduction of rains
vasectomy or epidiclymectomy), or a

(ra.i11 effect) or by treatment with exogenous
testosterone- or estrogen-treated wether.

progestagen or equine chmionic gonaclotro

The age of puberty of ewe lai11bs varies
pin ( eCG), or tlu·ough the effects of melatonin
greatly a.i1d is influenced by breed, nutrition,
either by mailipulating the photope1iocl in
presence of the ra.i11, allci season of birth.

housed sheep or through the use of

MANAGEMENT OF REPRODUCTION: SHEEP

2213
exogenous melatonin in the feed or as an

Estrus Induction/Synchronization:

implant. (See also J IORMONAL CONTllOL OF' ESTRUS, Estrus induction in acyclic ewes requires
p 2244.) Factors affecting fertility after estrus exposure to exogenous progestagen for a induction include breed, season, lactation,
minitmm1 of 5 days; most progran1s use 7

VetBooks.ir
nutritional status, and postpartum pe1iod, as
days. The progestagen used may be either
well as the ewe's dry/suckling status, ran1 to
natural progesterone delivered intra.vagiewe ratio, tin1e of ram introduction, mating nally in a controlled intra.vaginal drngby natural or aitificial insemination, and releasing device (CIDR), or melengestrol
number of inseminations ( one or two).

acetate (MGA) fed at 12-hr intervals at a

The sudden introduction of novel rams
dose of 0.125 mg/head. Ovulation and
or teasers ("ram effect") to anestrous
subsequent fertility is usually poor unless
ewes can induce the onset of ovarian
eCG is given at removal of the progestagen;
cyclicity during the transition season,
usually 500 IU is administered. If ewes ai·e
most often 4-6 wk before the onset of the
cycling, then either the progestagen
ovulatory season in seasonal breeds;
exposure needs to be sufficiently long
however, it works poorly to synchronize
to outlast any CLs present on tile ovaiies.

estrus once the ewes have started to

This is usually l l -14 days. Use of eCG at
cycle. Responding ewes commonly
progestagen removal tinle is optional
ovulate within 48 hr of rain introduction

(200-400 IU) and is generally not necessary
but usually are not receptive, ie, the estrus dlll'ing the ovulatory season if aitificial is silent. In ewes with a silent estrus,
insemination is not being used. Shorter
ovulation is followed by the formation of
exposures in cycling ewes can be used if
either a normal or a short-lived (5-6 days)

prostaglandin (PG) F2a or its analogues is
corpus luteum (CL). After regression of
administered either at, or 12-24 hr before,
a normal CL, most ewes display estrus
pessary or CIDR removal. Estrous cyclic

( -19 days after ram introduction). After
ewes can also be synchronized by two
regression of a short-lived CL, ewes
injections of PGF,a or its analogues 8--11
ovulate without di.splaying estrus and
days apait, although fertility is poorer
commonly form a normal CL. Regression
than with progestagen progran1s. Estrus
of this CL results in estrus ( -25 days after
commonly is seen 1-3 days after progestaram introduction). This gives two peaks of gen removal, with a shorter interval dming
breeding activity and very good synchrothe autlmm or with the use of CID Rs, or nization of estrus without the use of
within 3 days of the second PGF,a injection.

exogenous hormones.

Acyclic, seasonally anestrous ewes cai1

Ram Management: Before a progrllill
be induced into estrus and ovulation with
is set up, the veterinai·ian should be sure
exogenous melatonin. Ewes are given
sufficient nlUllbers of ran1s ai·e available for
melatonin 6 wk before joining and are
the progran1 and that the rllills ai·e fe1tile.

isolated from rai11s dming that period. The

During tile normal ovulatory season and
joining pe1iod should cover two complete
without synchronization, a raill to ewe ratio
estrous cycles (35 days). Exogenous
of 1:40 is usually sufficient, although if tl1e
melatonin is more successful towai·d the
ran1s are young, or the environment is
end of the seasonal anestrous period, ie,
rough, then the nun1ber of ewes per rain
transition period. This product is not
should be lowered. This is also true if estrus
commercially available in many countries.

is synchronized, in which case the ran1 to

A simiJai· effect can be obtained by manipuewe ratio should be -1:10 to 15. When lating the photoperiod under management
breeding out of season, rllill fertility is
progrllills in which the ewes and rains are in
usually lower, and if estrus is synchronized
confinement housing. Usually starting in
the ran1 to ewe ratio should be -1:5 to 7.

late autumn up to the winter solstice, ewes
are exposed to aitificial light, usually 16 hr/
day for 8--12 wk At the end of this period

MEASURING REPRODUCTIVE

(eg, mid-winter), the length of light

PERFORMANCE
exposlll'e is reduced to 8 hr/day. This may
require darkening windows to reduce

Reproductive performance is measured by
exogenous light sources and completing
several paraI11eters. The most conm1only
bain chores dming only those 8 hr to avoid
used ones ai·e the proportion of ewes
using lights during the dark period. After
exposed or mated to the rai11 that lainb (the

6--8 wk, ewes will start to cycle. lf the rllills
measure of fertility), the proportion of lan1bs
are housed under sinlilar conditions, scrotal
born (alive and dead) per ewe lllillbing (also
circumference and breeding capacity will
called drop rate and a measure of prolifiincrease.

cacy ), and age at first \an1bing. Also often

2214

MANAGEMENT OF REPRODUCTION: SHEEP
measured are lambs tail-docked per ewe

Breed: Breed selection can greatly
lambing (lambs marked); lambing percentinfluence reproductive performance, age (number of lambs born per ewe exposed
particularly prolificacy and age at first
to the ram); and weaning percentage
lambing. Sheep breeds around the world

(percentage of lambs weaned per ewe
are very diverse in perforn1ance, and it is

VetBooks.ir
exposed to the ram), although the latter is
advisable to be fan1iliar with the traits of
more of an economic measure. To measure
some of the more popular ones. Tern1inal
lamb losses, it is preferable to calculate
sire breeds such as Suffolk, Hampshire, and
stillbirth rates and preweaning mortality

Texel are often used to obtain rapid growth
rates as a proportion of lambs born and
and muscling. Traditionally, these breeds
lan1bs born alive, respectively.

are only moderately to lowly prolific and so

Goals for reproductive performance vary
are not prefetTed in the ewe flock except to
tremendously between different sheepproduce replacement terminal sire ran1s.

raising systems and must be matched with

Maternal breeds should possess the
the management system and constraints.

following characteristics: fertile, prolific,

Extensive range flocks that produce
easy lan1bing with good maternal instincts
primarily wool ( eg, the Australian Merino)

( eg, bonding), high milk production,
may seek only flock replacement so that
longevity, suitable for the envirorunent ( eg,
lambing rates of <900/o, l lamb born/ewe
grassland, confinement, hilly country), and
lambing, and <0.8 la.mbs weanecVewe
for some management systems, long
lambing are considered acceptable. Ewes
ovulatory seasons. Within each geographic
a.re traditionally not expected to lamb until
region and production system, specific

2 yr of age. Conversely, flocks that produce
breeds tend to be more commonly used.

primarily meat w1der conditions that

Some of the more popular maternal breeds
require the feeding of stored feeds ( eg,
in northeastern North America are the
where growing seasons are short) ancVor

Fit111ish Landrace, Romanov, and Polled
housing for a significant proportion of the

Dorset. ln western USA, range breeds are
year must have much better fecundity and
more popular.

lan1b weaning percentages to be economi

Some regions conunonly use a crossbred
cally viable. Age at first lambing should be
sheep that includes traits from several

12-14 mo, and a ewe should raise at least
breeds. In a crossbreeding system, maternal

1.8 or more likely 2 lan1bs/yr. Fertility rates
heterosis is used to improve perfmmance,
during the ovulatory season should be
ie, the offspring (the Fl generation) possess

95%-1000/o in ewes and 90% in ewe lan1bs.

traits that are better than the average of

Producers seeking to further increase
their parents, also known as hybrid vigor. A
ewe production and to reach the more
well-known example is the British "mule"

lucrative lamb meat markets.also practice
sheep in which ewes of a hill breed ( eg,
accelerated lambing in which ewes lamb

Scottish Bla.ckfa.ce) that possess the traits
every 8 mo (ie, three lambings in 2 years) or
of hardiness and good mothering but are not
every 7.2 mo (the Cornell Star system, see
prolific are crossed with a ran1 of a lowland
p 2216). Both of these systems require that
prolific heavy-milking breed ( eg, Bluefaced
ewes breed during the anovulatory and

Leicester). The resultant Fl ewe is a prolific,
transition season, as well as the ovulatory
heavy-milking mother with longevity and
season. However, in most of the world,
hardiness. No ram lambs are retained for
autun111 breeding with spring lambing is the
breeding. These ewes are then bred to a
predominant reproduction management
tern1inal sire ( eg, Suffolk or Texel). The
system, which coincides with optimal grass
offspring of this mating-a terminal
production for the lambs and lactating
cross-gain well and have good carcass
ewes, regardless of the desired prolifica.cy
characteristics.

of the management system.

Composite breeds are the result of a
plarmed crossbreeding program coupled
with stringent selection based on prese

FACTORS AFFECTING
lected production traits. The more

REPRODUCTIVE PERFORMANCE
successful are phenotypically stable and
are considered new breeds. In the USA,

Reasons for reproductive failure in the ewe
the Polypay, a composite of the Fitlllish
and ram are nun1erous. Performance must

Landrace, Targhee, Dorset, and Rambouilbe considered in light of the management let, is very prolific and hardy and has
system and genetics of the breed. If targets
excellent wool production. The Rideau
are not being met, the following can be used
sheep, developed in Canada, is a composite
as a guideline to investigate contributing
ofFitlllish Landrace, Dorset, Suffolk, and
factors.

East Friesian. These ewes are very prolific,

MANAGEMENT OF REPRODUCTION: SHEEP

2215
heavy milkers, and excellent mothers and

Reproductive Failure of the Ewe: As
are frequently used in accelerated lambing
with tile ram, ewes may fail to be mated, or
programs. Other exan1ples of popular
be mated but do not become pregnant. In
composites include the Katahdin (Nortll
addition, tile ewe may not maintain the

American haired sheep), Dorper (South
pregnancy or have decreased prolificacy.

Africa and North America), Coopwo1th

Again, the possible reasons are numerous.

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(New Zealand and Australia), C0tTiedale

Ewes may not be mated because of tile

(New Zealand), and British Milk Sheep (UK
following: 1) The ewe may already be
and Canada).

pregnant. 2) It may be anovulatory season,
which is longer in ewe lan1bs. 3) The ewe

Reproductive Failure of the Ram:

lamb may be prepubertal, influenced by

Rams may fail to mate the ewes, even when
growtll (nutrition) and breed. 4) If a
the ewes are in estrus, or mating may occur
synchronization/estrus induction program
but pregnancy does not ensue. Possible
is used, there could be a fatal error in the
reasons are nw11erous. For failure to mate,
progran1, eg, loss of CIDR, too low dose of
these include: 1) The ewes are being mated
eCG, or improper MGA feeding program.

but the marking harness or crayon is not

5) Phytoestrogens or specific mycotoxins
functioning properly. 2) The ran1 lacks
may temporarily or permanently suppress
libido because it is ill witl1 another disease,
estrus. 6) Ewes may be too tllin, lactating,
is too thin, is too old, it is during the
or recently weaned. 7) Ewe lambs tllat are
anovulatory period, or the weather is too
overfed postpubertally may not cycle.

hot. 3) The ram is reluctant to breed,

8) Ewes may display behavior such as
perhaps because of the pain of infectious
dominating tile ram or being shy, particubalanopostllitis (pizzle rot), contagious larly maiden ewes. 9) There may be a
ecthyma of the penis or prepuce, or
freemartin/pseudohe1maphrodite
because it is lame and cannot mount
condition.

comfortably. 4) The ram may be inexperi

Ewes may not conceive or maintain
enced and has not been "taught" how to
pregnancy because of the following: 1) The
breed by observing a more experienced
synchronization program is not correct, eg,
ran1. 5) The ran1 may not be able to cope
rams a.rejoined too early witil tile ewes
properly with tile environment, eg, a
before tlley are in estrus or too low a dose of
barn-raised ram turned out to mountainous
eCG is given and ovulation does not occur.

pasture. 6) Too few ran1s are available to

2) There is pathology of tile reproductive
breed the ewes ( ran1 to ewe ratio) for the
tract. 3) Early embryonic death occurs,
type of ram (age, experience), conditions
which can be due to a number of issues,

(paddock vs range), time of year (ovulatory
eg, seleniw11 deficiency, specific abortion
vs anovulatory), or synchronization
disease ( eg, border disease, toxoplasmosis,
programs. 7) Rams may have behavioral
chlamydiosis), stress, heat shock in early
issues such as inter-ran1 aggression, shy
pregnancy, or high levels of soluble protein
rams, or rams "falling in love" with or
in the feed leading to high urea nitrogen
disliking specific ewes.

levels in the blood. 4) Abortion (mid to late

Mating not followed by pregnancy may
term), if not observed, may also present as
present as ewes being marked repeatedly,
failure to conceive or maintain pregnancy.

a spread-out lambing period, and/or poor

Reasons for poor prolificacy in ewes that
prolificacy in the ewes. Many of the reasons
become pregnant include insufficient
for failure to mate can also influence failure
energy at breeding when in poor body
to achieve pregnancy. Additional reasons
condition Oow body condition score), very
for lack of pregnancy after mating include
young or very old age, anovulatory or
impaired fertility due to disease such as
transition season, insufficient dose of eCG,

B1ucella ovis infection, chorioptic mange of early embryonic death ( see above), and the scrotwn, infertility after a fever, or otller
genetics.

causes of orchitis and/or epididyrnitis;
impaired fertility due to mechanical reasons

BREEDING PROGRAMS
such as excessive heat or cold, inguinal
hernia, or injury from fighting; in1paired

The most conunon breeding program is
fertility due to environmental honnone
annual lan1bing in which autumn-mated
disrupters ( eg, phytoestrogenic plants);
ewes lan1b in the spring. However, to
inadequate testicular circumference
produce lambs for more lucrative markets,
because of age, season, genetics, or disease;
ewes are bred in early autwnn or late
abnormalities of tile penis due to a
swnmer to Jamb in winter ( eg, January for
congenital defect or trawna; and sperm
the Easter lan1b market in March or April)

abno1malities.

or bred in late spring to lamb in autumn ( eg,

2216

MANAGEMENT OF REPRODUCTION: SHEEP

September for the Cluistmas lamb market).

weaning and before breeding. Breeds that

This requires the use of programs that
are naturally fertile out of season ( eg,
advance the ovulatory season into the late

Dorset, Merino) have an advantage in these
summer (ram effect, melatonin) or induce
systems.

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estrus during the anovula.tory period in the

Accelerated lambing systems are
spring (progesta.gens in the form of CIDR
commonly used in northeastern USA and
devices or MGA; photoperiod manipula

Canada. and a.re becoming more common in
tion). However, producers whose flocks

South Africa and New Zealand. However,
lan1b out of season rarely adhere to an
tl1e increased revenue from extra market
annual breeding program, because overall
lambs sold into higher value markets must
production is generally too low to account
be carefully weighed against the increased
for the increased costs associated with
input costs such as feed availability, labor,
lambs born in the winter or autumn; instead, and housing (for winter lambing).

these producers adopt an accelerated
program to take advantage of the ewe's
ability to lan1b more than once per year.

PREGNANCY DETERMINATION

The two most popular accelerated
lambing programs are the "3 lambings in 2

Accurate detern1ina.tion of pregnancy
years" (3 in 2) and the Cornell Star system.

facilitates differential ewe management by

The former requires the producer to manage allowing the separation of multiple pregnant two flocks that lamb every 8 mo (January,
ewes for supplementary feed and lan1bing

May, and September), alternating the first
supervision and the culling of nonpregna.nt
and second flocks. For exan1ple, in the
ewes. Procedw·es for diagnosis of
northern hemisphere, over 24 mo, a ewe
pregnancy can involve detection of ewes
would be bred in the ovulatory season to
that do not return to estrus (nonmarking
lamb in the spring (December to lan1b in
by ram or teaser fitted with harness and

May), then the transition season to lan1b in
crayon); tra.nsa.bclomina.l, real-tin1e
the winter (August to lamb in January, and
ultrasonographic scanning; rectoabdominal
then the anovula.tory season to lan1b in the
palpation (from 70 clays); abdominal
autumn (April to lan1b in September). If the
palpation (from 100 days); measurement of
ewe was found to be open at pregnancy
plasma progesterone concentrations 18
scarming -50 days after breeding, it could
days after ma.ting ( detectable progesterone
be "slipped" to the other flock and
levels indicate an active CL); and laparosreexposed to the ram. To be successful, copy (from 30 days). Rea.I-time ultrasonogbreeding exposmes would need to be short raphy is a rapid, highly sensitive and very
to shmten the lambing interval, and lambs
specific test for pregnancy diagnosis of
would need to be weaned by 2 mo of age to
ewes ( and does). For detection of early
allow breeding back
pregnancy (eg, 2�0 clays), it is done most

The Cornell Star system is similar but
accurately trans rectally. When imaging is
more tightly controlled. Ewes lan1b every
clone later in pregnancy, the ultrasono7.2 mo instead of eve1y 8 mo. This means a graphic transducer is placed i.n the woolless
ewe can lan1b five tinles in 3 yT. L<'.!ngth of
area of both flanks and the bean1 directed
exposure to the ram, time for ewes to wean
forward and upward toward the last rib on
lan1bs and be rebrecl, lan1bing, and lactation
the opposite side. It is possible to exan1ine,
are all very short.

at low cost, 100-150 ewes/hr and to

Although the benefits of these progran1s
accma.tely diagnose single and multiple
a.re considerable in tenns of increased
fetuses.

productivity and access to lucrative lamb
markets, tl1ey require a high level of

PRENATAL LOSSES
management to work well. Poor flock
fertility tends to create a system heavily

In healthy sheep, fetal losses after
weighted to spring lan1bing, because ewes
pregnancy diagnosis is performed a.re
bred in the late sp1ing that do not conceive
normally low, ie, <2%. However, embryo
a.re re bred in the a.utwnn when more
loss can be surprisingly high without an
naturally fertile. Disease control programs
apparent problem at lan1bing (up to 30% of
must be very well managed; there is little
conceptions). Embryo death before day 12

"down tin1e" in the barns or pastures for
does not disturb the normal cycle length,
cleanup of conta.n1ina.ted environments. In
whereas embryo death after tl1is time
addition, ewe nut1ition must IJe such that
increases cycle length and may appear as
body condition scores do not get too low
repeat marking and a stretched-out lambing
during lactation, because there is no
period. Pathologic levels of embryo loss a.re
opportunity for ewes to regain weight after
due to issues mentioned previously, but

MANAGEMENT OF REPRODUCTION: SHEEP

2217
some losses occur in healthy ewes, with
changing the crayon color every 14-17
higher levels in more prolific breeds.

days. When fewer than expected ewes ai·e

Fetal loss in the second and third
marked, poor ran1 libido, insufficient
trimester is generally low in healthy flocks.

number of rains to breed the ewe flock, or

However, when it is abn01mally high and
anestrus is suspected. When ewes are

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due to a pathologic process, it may appear as serially marked with different colors, an observed abortion, abnonnal discharge
conception failure or eai·ly embryonic death
during pregnancy, open ewes at lan1bing,
is suspected.

stillbirth, early neonatal mortality, or all of

The ram to ewe ratio varies with breed,
the above. Causes are most often infectious
maturity of ran1, and whether synchronizabut may also be nutritional deficiencies or tion or induction of estrus is being
toxins. The most commonly diagnosed
practiced. Ratios of 1:40 ai·e common in
causes of abortion are Chlamydia abortus,
fann flocks, but excellent fe1tility can be

Campylobacter jejuni, Campylobacter
achieved with a lower ratio if ran1s from
fetusfetus, Toxoplasmagondii, border
prolific breeds ai·e used ( eg, Finnish
disease virus, Coxiella burnetii, Cache

Landrace ). For rain effect, the ratio should

Valley virus, Salmonella Abortusovis and
be 1:20; for estrus synchronization, 1: 10 to
other salmonellae, iodine deficiency,

15 (in season); and for estrus induction (out
seleniw11 deficiency, and some plant toxins
of season), 1:5 to 1:7.

( eg, locoweed). Abortion rates of 25%-300/o

Length of ram exposure dw'ing the
are not wmsual in these outbreaks, but in
ovulatory season should be limited to two
general an abortion rate >5% is considered
or three cycles so as to tighten the lambing
abnormal and should be investigated.

period to optimize lan1bing management
and lamb survival. Excellent fertility can be

RAM MANAGEMENT
achieved with a breeding exposure of 35-42
days (2-2 Y2 cycles). Poor fertility indicates

To achieve maximal fe1tility, rams should
ai1 issue with the breeding management.

be physically examined for reproductive

Flock dispersion should be avoided at
fitness to detect any abnormalities that may
mating, but n01mal hanclling should not
limit mating. (See also BREEDING SOUNDNESS
affect mating. Because younger ewes have a

EXAMINATION OF RAMS, p 2233.) The scrotum
shorter, less intense estrous period, they ai·e
and its contents and the penis and prepuce
better mated separately from older ewes
must be carefully examined. The size and
with expe1ienced, although not necessarily
symmetry of both testes and epididymides
older, rains.

should be assessed, and both testes should
be firmly palpated for consistency and

Collection of Semen: The artificial
resilience. Any palpable lesions, particularly vagina is used most commonly for collection of the epididymis, should be considered
of ran1 semen. It is prepared for collection by
potentially contagious ( eg, Brucella ovis
the introduction of warm water (100°-l30°F
and Histophilus somni!Actinobac'illus

( 40° -55°C]) and air between the outer casing
seminis ). Appropriate tests should be
and soft inner sleeve, lubrication with
performed to establish a flock diagnosis to
petrolatwn in the end where intromission
initiate a test and eradicate program for
of the penis occurs, and attachment of a
infected rams. Semen can be collected
graduated collecting glass at the opposite
and evaluated to screen potential sires,
end. Ranis quickly learn to m0tmt a
paiticularly in single-sire mating systems.

restrained ewe, and intromission and

All screening procedures should be done
ejaculation ai·e extremely rapid.

6-8 wk before mating to allow mai1agement

The second method of semen collection
changes of the ran1 tean1 or purchase of
is by electroejaculation, for which the ran1
replacements for defective ran1s.

may be restrained on its side. The lubricated

Supplementai-y feeding of the ran1s can
bipolar electrode is inserted into the
be staited 6 wk before joining. High-protein
rectw11. The withdrawn penis is held with a
grains, paiticulai·ly lupines, increase both
piece of gauze to facilitate inse1tion of the
testicular size and the number of cells in the
glans into a 10- to 15-mm diaineter
gern1inal layers of the testicle, resulting in
graduated collecting tube. Ejaculation
increased sperm production. However,
usually occurs after a few short electrical
dietai-y protein levels> 14% have been
stimulations; "stripping" of the w·ethra may associated with infectious balanoposthitis
be helpful when expulsion of semen seems
due to Co1ynebacterium renale (seep 1372, incomplete. ElectToejaculation is less also called pizzle rot).

reliable than the artificial vagina; specimens

Mating activity can be monitored by using vary in quality and can be contaminated a breeding harness on the ran1s and
with wine.

2218

MANAGEMENT OF REPRODUCTION: SHEEP

The volume of semen collected with the
mL, single-dose synthetic straws at liquid
artificial vagina is 0.5---1.8 mL, and the
nitrogen temperature (196°C) is successful
concentration of the spemmtozoa is 2.5-6 x
in maintaining sperm viability, but there

109/mL. Semen obtained by electroejaculamay be a range in motility after thawing and tion generally is of larger volume but lower
in fertility between rams or processing

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concentration.

batches. Use of frozen-thawed SE)men may
result in lambing rates of 500A, with cervical

Evaluation of Semen: Immediately
insemination and 500/o-SOOA, with intrauterine
after collection, the semen is assessed for
insemination.

contamination, volume, concentration of

Freeze-thawing reduces the numbers of
spem1atozoa, and sperm motility (wave
motile sperm. Chilling results in membrane
motion and sperm progression).

changes that reduce the longevity of sperm.

The membrane changes are sinlilar to

Extension of Semen: Semen can be
capacitation and acrosome reactions, and
processed by extending or diluting,
affected spem1 are thus ready to fertilize
packaging, and storing. Semen may be
oocytes. Fresh seminal plasma mitigates the
extended 5-fold, depending on the initial
effects of some of the capacitation changes.

concentration, the processing and storage
method, and whether the semen will be

ARTIFICIAL INSEMINATION
used fresh, chilled, or frozen-thawed. Most
semen extenders or diluents are based on

The optimal time for insemination with

Tris, egg yolk, and additional cryoprotecnonfrozen semen is 12-18 hr after the onset tants such as glycerol. Commercial extender
of estrns. When estrns has been synchroconcentrates contain cryoprotectants and nized or induced using progestagens and
require the addition of egg yolk and
gonadotropins and/or ram effect, most ewes
double-distilled water. These extenders can
are in estrns within 36-48 hr and ovulate at
be used for either fresh or frozen semen.

-60 hr. Insemination should be done 48--58

Extenders for fresh and chilled semen
hr after pessary removal for cervical
include whole, skin1med, or reconstituted
insemination, or 48--60 hr for intrauterine
cow's milk that has been heated to 92° -95°C
insemination with frozen-thawed semen,
for 8--10 min in a water bath to inactivate
with highest conception at -53-54 hr.

toxic factors, egg yolk/glucose/citrate (15%

Extended fresh or chilled semen can
egg yolk, 0.8%glucose [anhydrous], 2.8%
be placed into the vagina or cervix, and
sodium citrate dihydrate in glass-distilled
extended fresh, chilled, or frozen-thawed
water). The addition of Tris or glycerol
semen can be placed into the uterns.

improves the sperm survival of frozen

Frozen-thawed semen reconstituted with
thawed semen. The reconstitution of
fresh seminal plasma can be placed into
frozen-thawed semen with fresh seminal
the cervix with conception rates >500A..

plasma improves its fertilizing ability when
used for intracervical insemination but not

Vaginal Insemination: An artificial
for intrauterine insemination. The number
insemination pipette with a 1 -2 mL syringe
of motile spem1atozoa and the volume ofan
attached is placed deep into the vagina.

insemination dose for the ewe depends on

This method is quick and involves minin1al
the site of insemination and the method of
restraint of the ewe. For cervical inseminaprocessing. For vaginal insemination, tion, the ewe is restrained to linlit move0.3-0.5 mL with 300 million motile ment and to present the hindquarters at a
spermatozoa is used; for cervical inseminaconvenient height for easy access to the tion, 0.05---0.2 mL is used with 100, 150, and
vagina. After cleaning the vulvar region, the

180 million spermatozoa of fresh, liquidcervix is located with the aid of a speculum stored, and frozen-thawed semen,
and suitable illumination, and the inseminarespectively. Intrauterine insemination by tion made as deeply as possible into the
laparoscopy requires 0.08--0.25 mL (with a
cervical canal. A long, thin inseminating
total of 20 million motile spennatozoa) into
tube with attached syringe or a semiautoeach uterine horn.

matic insenlinating device can be used. The
relatively long, tortuous, and fum-walled

Storage of Semen: Ram semen may
cervical canal of the ewe usually precludes
be stored for up to 24 hr by cooling the
penetration by the tube for > 1 cm. In old,
extended semen to 2°-5°C over 90-120 min
multiparous ewes with cervical tissue
and by holding at this temperature. Fertility
distortion, the difficulty increases, and the
decreases rapidly and is low by 48 hr.

semen is deposited into the posterior folds

Freezing and storage of ram semen in
of the cervix. In periparturient ewes, the

0.25---0.3 mL, three-dose pellets or in 0.25
cervix may be fully penetrated. In maiden

MANAGEMENT OF REPRODUCTION: SMALL ANIMALS

2219
ewes, in which inse1tion of the speculwn
is then raised at the posterior end so that
and dilation of the vagina can cause injury,
the ewe is tilted at -45° with the lateral
the semen should be deposited in the
abdomen presented to the operator. The
anterior vagina.

anesthetized sites allow for entrance of two
trocars and cannulae; carbon dioxide is

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Intrauterine Laparoscopic Insemina
insufflated through the first cannula to
tion: Food and water should be withheld
distend the abdomen. The laparoscope is
from the ewe for -12 hr. Ewes should be
inserted through the near cannula, the
sedated with 1.5---2 mg xylazine, IM, and
uterine horns are visualized, and a glass or
placed in cradles that restrain and inve1t
plastic inseminating pipette or sheathed
them, first in dorsal recwnbency for
inseminating gun is inserted through the
preparation of the abdomen. Local
second cannula. Semen is deposited into the
anesthetic may be injected SC at two sites
lwnen of the uterus. Conception rates are

( -4 cm on each side of the ventral midline
sinu.lar if semen is deposited into one or
and -6 cm anterior to the udder). The cradle
both horns of the uterus.

MANAGEMENT OF REPRODUCTION:

SMALL ANIMALS

BREEDING SOUNDNESS
junction, cranial to the urethral papilla. The

EXAMINATION
heritability of such defects is unlrnown.

Strictures of the vagina or vestibule are not

Female: The breeding soundness
uncommon in the bitch and usually prevent
exanlination should begin with a thorough
normal copulation, but if pregnancy ensues
reproductive and medical history, including
from mating without a tie or from artificial
inforn1ation on previous cycles ( onset and
insemination, dystocia can result. Septate
regularity), breeding management (past and
strands can be easily resected surgically, but
intended), outcome of any breeding( s ), and
circumferential strictures are difficult to
relevant fanu.ly history, as well as routine
resolve without episiotomy and major
medical infonnation ( diet, medications,
revision, and tend to reform. Elective
enviromnent, health status). A thorough
artificial insemination and cesarean section
physical exanli.nation, with particular
may be preferable if the bitch has outstandattention given to the genitalia and ing breeding potential.

manlffiary glands, should be perforn1ed.

Routine vaginal cultures are not advised

Vestibulovaginal defects (strictures) should
because the vagina normally harbors a wide
be excluded by digital exanli.nation.

variety of bacte1ia, including j3-hemolytic

Evaluation of the mammary glands should
streptococci and Mycoplasma spp. Bitches
include inspection of the nipples for nom1al
should be screened for brucellosis before
anatomy. Screening for hereditary defects
each estrus when breeding is planned. A
common to the breed should be advised,
negative Brucella canis screening test is
which may require techniques such as
reliable; positive results warrant further
radiography ( eg, elbow dysplasia),
specific ( eg, agar gel inmumodiffusion
ultrasonography (eg, renal dysplasia),

[AGID]) serologic evaluation, culture, or
ophthalmoscopy ( eg, cataract), specific

PCR, because false-positives are conm1on.

DNA testing ( eg, progressive rod-cone

Clinicians should contact their commercial
degeneration), as well as the physical
laboratory or veterinary school for updated
exanli.nation (eg, patellar luxation).

screening protocols. Queens should be

Digital vaginal exanli.nation and
screened for feline leukemia virus and feline
vaginoscopy of the bitch may detect
in1munodeficiency virus as medically
strictures or other defects of the vulva or
indicated. Bitches and queens >5 yr old
vagina that may !under copulation or
should also have their general health
whelping. Vaginal strictures are more
assessed by performing a CBC, serwn
commonly congenital than acquired and
chemistries, and a urinalysis.

may be in the fonn of either a septate strand

Before an anticipated breeding, females
or a circumferential band. They most
should be in optimal body condition to
conunonly forn1 at the vestibulovaginal
improve conception rate and whelping

2220

MANAGEMENT OF REPRODUCTION: SMALL ANIMALS
outcome. Breeders commonly skip cycles
mallagement, outcome of ally breedings
between breedings; this is not optimal
ab'eady perfom1ed, relevai1t faI11ily history,
husbandry because the inevitable exposure
as well as routine general history ( diet,
to estrogen (queen) and progesterone
medication, environment, ai1d healtll

(bitch, sometimes queen) dming the estrous
status). Screening for relevallt heritable

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cycle promotes cystic endometrial
defects of concern for the breed should be

'

hyperplasia and may result in pyometra.

advised.

Bitches and queens kept in optimal health

A thorough physical exainination should
can be bred sequentially and should be
be performed, with particulai· attention
ovariohysterectornized or ovariectomized
given to the genitalia. The penis should be
when no further breedings are planned.

fully extruded from the prepuce alld

Proper nutrition and exercise strategies for
exainined. This may require sedation in
pregnancy and lactation should be outlined.

toms. lf hair accmnulates around the base of

Bitches should be currently vaccinated
tile feline penis, it Call prevent copulation
for core infectious cliseases ( canine
and should be removed. Prostate size ai1d
distemper, paivovirus, adenovirus 2, ai1d
symmetry should be assessed in dogs by
rabies). Other noncore vaccinations should
sinmltai1eous abdo1ninal and rectal
be administered only according to good
palpatjon or with ultrasonography; this is
medical practice (appropriate for the dog's
not generally necessary in cats because
age, health status, home and travel
prostate disease is rare. Palpable abnorenvironment, and lifestyle). Queens should malities (pain or asymmetly) or semen
similarly be vaccinated approp1iately
abnom1alities always warrallt ultrasono

(based on duration of immUllity recommengraphic evaluation of tile prostate alld dations) for feline distemper, rhinotracheifurther clinical testing as indicated ( eg, tis, ai1d calicivirus. Vaccination against
urinalysis, cytology, culture). The testes alld
rabies virus, feline leukemia virus, ai1d other epididyrni should be palpated carefully for noncore diseases should be done when
symmetJy alld nonnalcy-abnonnalities
indicated by good medical practice, based
again warrallt ultrasonographic evaluation.

on risk factors associated with the cat's age

The scrotun1 should be evaluated for
alld husballdry. Unnecessary revaccination
evidence of dermatitis or ITauma, which Call
of bitches alld queens before breeding is not
impact fertility. A small ainow1t of mucoid
advised, because little improvement in
discharge at the preputial opening is normal
immunity Call be expected ai1d adverse
in dogs. (See also REPRODUCTTVE DISEASES OF
effects may be seen. Vaccination during

THE MALE SMALL ANIMAL, p 1400.)

pregnaI1cy is advised only when prior

C1yptorchidism, a common genital defect
vaccination status is lacking or unknown,
in males, is diagnosed if either or both testes
alld risk of exposure is high ( eg, a shelter).

ai·e not present in the scrotum at puberty;

In that case, the use of recombinant core
testicles nom1ally descend into the scrotwn
vaccines is optimal.

by 6-16 wk of age. Descent as late as 10 mo

The use of preventive medication for
has been documented in dogs. Unilateral
heartwonn disease ai1d internal and
cryptorchidism does not result in infertility.

external parasite control (according to •

In dogs, cryptorchidism is hereditary, alld
ma.Ilufacttll'ers' recommendations) during
affected aninlals should not be bred. Both
pregnancy alld lactation is advised.

late descent and failure of descent are

Appropriate isolation of the pregnallt
heritable. Botll parents of affected
female during the last half of pregnallcy for
individuals should be implicated as carriers.

infectious disease prevention is important

Because retained testes have a higher

( eg, avoiding exposure to canine herpesincidence of neoplasia ai1d torsion, bilateral virus in the bitch alld upper respiratory
orchiectomy is reconunended. Attempts at
infections in the queen). Client education
inducing descent with medical therapy with
concerning normal whelping a.Ild queening
gonadotropins or testosterone have been
events alld about the timely identification
tmsuccessful a.Ild ai·e not ethical. Orchioof dystocias is essential. Fetal alld uterine pexy is also considered unethical. Failure of monitoring systems developed for routine
one testis to develop (true monorchidism)

use in tile bitch and queen improve neonatal
may be seen in dogs but is rare. Serwn
survival witll reduced morbidity alld
luteinizing hom1one (LH) levels ai·e high
mortality for the dam.

(>l ng/mL) if a dog or cat is completely
neutered.

Male: The breeding soundness exainina

A persistent penile frenulwn prevents
tion for males should begin witll a tllorough
protrusion of the penis from the prepuce
reproductive alld general health history,
alld thus copulation. Treatment is surgical.

including past alld intended breeding

Deviation of the penis is uncommon; these

MANAGEMENT OF REPRODUCTION SMALL ANIMALS

2221
animals require assistance in breeding or
phosphatase can be measured in the
may be bred via artificial insemination.

ejaculate to assess whether the ejaculate

Hypospadias prevents n01mal sperm
was complete, because it is an epididy.mal
transport from the testes to the glans penis
marker. Levels >5,000 mcg/dL indicate the
and is easily detected by physical examinaejaculate included the second, nom1ally VetBooks.ir
tion. Small defects may close spontanesperm-rich fraction. Levels <5,000 mcg/dL
ously, but some type of reconstmctive
indicate either bilateral obstmctive disease
surgery involving urethrostomy and penile
or libido problems preventing the release of
amputation is usually necessary. Phirnosis
the second fraction. Sperm function is not
can be caused by stenosis of the preputial
assessed with routine semen evaluation.

opening, which may be congenital or result

Acrosomal evaluation requires special
from chronic inflammation (trauma or
techniques that are not usually commerbacterial dem1atitis). Any underlying cause cially available.

should be treated and then, if necessary, the

Collection of semen for evaluation is
opening enlarged surgically.

difficult in toms, unless the cat has been

Semen Evaluation: Ideally, a complete
trained to ejaculate into an artificial vagina
semen evaluation should be pe1ionned in
or electroejaculation equipment is available.

male dogs intended for breeding and

Cats can be trained to ejaculate with manual
repeated at least annually in active stud
stimulation in some instances, but training
dogs. Semen is readily collected from most
can take weeks to months. Chemical
dogs by manual stimulation; the presence
ejaculation using urethral catl1eterization
of a teaser ( estmal) bitch is advised to
under dexrnedetomidine sedation or by fine
optimize results by improving libido. All
needle aspiration of the testes for spenn
equipment (artificial vagina, collecting
cytology has been described. Nonspecific
tubes, pipettes, slides, and coverslips)

methods of evaluating a tom for spennatoshould be room to body temperature, dry, genesis include evaluation of urine for
and free of water and contaminants such as
spenn and collecting a vaginal wash from
chemical disinfectants. The canine ejaculate the queen in1mediately after copulation.

consists of three fractions-the first and

Spe1m disappear from the vagina within
third are of prostatic 01igin, while the

1 -2 hr of copulation. Warm saline (0.05-1
second is sperm-1ich. Spenn production
mL) is flushed into the vagina of the queen
is related to testicular size, so large dogs
and aspirated, the sample is centrifuged,
should produce higher spem1 counts than
and the sediment exan1ined (new methylene
small dogs.

blue or routine hematologic stains are

Semen evaluation should include an
adequate). Breeding a questionable tom to
assessment of libido, total spe1m count per
a proven queen may be the most practical
ejaculate (nom1al in dogs is 200-400+
way to assess his fertility. Adequate coital
million), spe1m motility (normal >90%
contact to induce ovulation should be
progressively motile, with moderate to fast
confirmed by measuring progesterone
speed), and morphology (>900Ai nonnal).

levels in the queen 1-2 wk after breeding.

The sperm count (sperm/mL) is usually
determined with a hemocytometer or by

BREEDING MANAGEMENT
spectrophotometry. Spem1 per ejaculate is
calculated by multiplying the spenn count

Dogs
by the volume of semen collected. Motility

Bitches may be bred naturally or also
is evaluated in an unstained sample as soon
artificially inseminated using fresh, chilled,
as the sample is collected, ideally using
or frozen-thawed semen. The practice of
clean slides prewannecl on a slide warmer.

ovulation tinung has become increasingly

Several commercially available stains are
desirable to breeders. Owners of popular
suitable for morphology exan1ination; eosinstud clogs commonly pernut a limited nigrosin and Giemsa stains are used most
number of breedings ( usually two) and may
commonly.

need to prioritize bitches based on their

An adequate amount of the third fraction
timing. Owners of bitches wish to minimize
should be collected to ensure that the entire
travel time to the stud dog facility. Boarding
sperm-rich fraction has been acquired and
of bitches in season can be reduced with
to permit evaluation of the prostatic
recognition of their fe1tile period. The use
component, which should be clear (free
of extended and chilled semen and frozen
of urine and cellular contan1ination ).

semen, or subfe1tile stud dogs, necessitates

Subfertility or infertility should never be
ovulation timing for optin1al conception.

diagnosed based on one collection. If the

Proper ovulation timing pemuts accurate
sample is azoospennic, semen alkaline
evaluation of gestational length and is

2222

MANAGEMENT OF REPRODUCTION SMALL ANIMALS
essential in the evaluation of apparent
serosanguineous to hemorrhagic vulvar
infertility in bitches. In addition, litter size
discharge of uterine origin is present, and
is optimal with properly timed breedings.

the vulva is mildly enlarged. Vaginal

Sound knowledge of the canine reproduccytology shows a progressive shift from tive cycle is essential. (See ai,so REPRODUCTIVE
small parabasal cells to small and large

VetBooks.ir

DISEASES OF'TI-IE F'EMALE SMALL ANIMAL, p 1393.)

intern1ediate cells, superficial-qitermediate

Individual bitches may vary from normal,
cells, and finally superficial ( comified)

be presented at variable times during their
epithelial cells, reflecting the degree of
estrous cycle for evaluation, and sometimes
estrogen influence. RBCs are usually, but
exhibit pathologic variations in cycles. Each
not invariably, present. The vaginal mucosa!

of these scenarios requires veterinary
folds appear edematous, pink, and round.

interpretation. The normal canine reproduc

FSH and LH levels ru·e low during most of
tive cycle can be divided into four phases,
proestrus, rising during the preovulatory
each having characteristic behavioral,
surge. Estrogen rises from basal anestrous
physical, and endocrinologic patterns,
levels (2-10 pg/rnL) to peak levels (50-100
although considerable variation exists.

pg/rnL) at late proestrus, while progester

Bitches with normal estrous cycles but
one remains at basal levels ( <l ng/mL) until
unexpected patterns must be differentiated
rising at the LH surge (2-4 ng/mL).

from those with true abnonnalities.

Proestrus lasts from 2 or 3 days to 3 wk,

Detection of individual vruiation within the
with 9 days average. The follicular phase of
normal range of events in a fertile bitch can
the ovarian cycle coincides with proestrus
be crucial to breeding management.

and very early estrus.

Evaluation of the estrous cycle for true

During estrus, the healthy bitch displays
abn01malities is an important part of the
receptive or passive behavior, enabling
evaluation of an apparently infertile bitch.

breeding. This behavior correlates with

The interestrous interval is nonnally
decreasing estrogen levels and increasing

4-13 mo, with 7 mo the average. The
progesterone levels. Serosanguineous to
anestrus phase of the estrous cycle is
hemorrhagic vulvar discharge may din1inish
marked by ovarian inactivity, uterine
to variable degrees. Vulvar edema tends to
involution, and endometrial repair. An
be maximal. Vaginal cytology remains
anestrous bitch neither attracts nor is
predominated by superficial cells; RBCs
receptive to male dogs. No overt vulvar
tend to decrease but may persist throughdischarge is present, and the vulva is small.

out. Vaginal mucosa! folds become

Vaginal cytology is predominated by small
progressively wrinkled ( crenulated) in
parabasal cells, with occasional neutrophils
conjunction with ovulation and oocyte
and small numbers of mixed bacteria. The
maturation. Estrogen levels decrease
endoscopic appearance of vaginal mucosa!

markedly after the LH peak to variable
folds is flat, thin, and red.

levels, while progesterone levels steadily

The physiologic controls tenninating
increase ( usually 4-10 ng/mL at ovulation),
anestrus are not well understood, but the
marking the luteal phase of the ovarian
deterioration of luteal ftmction and the
cycle. Estrus lasts 3 days to 3 wk, with an
decline of prolactin secretion seem to be
average of 9 days. Estrous behavior may
prerequisites. The tern1ination of anestrus is precede or follow the LH peak-its duration marked by an increase in the pulsatile
is variable and may not coincide precisely
secretion of pituitruy gonadotropins, follicle with the fertile period. Prin1ary oocytes stinmlating honnone (FSH), and luteinizing
ovulate 2 -3 days after the LH peak, and
hormone (LH), induced by gonadotropinoocyte maturation is seen 2--3 days later; the releasing hormone (GnRH). Hypothalrunic
life span of secondary oocytes is 2 -3 days.

GnRH secretion is itself pulsatile, its

During di.estrus, tl1e healthy bitch
intermittent secretion is a physiologic
becomes refractory to breeding, with
requirement of gonadotropin release. Mean
diminishing attraction of male dogs. Vulvru·
levels of FSH are moderately increased, and
discharge din1inishes, and edema slowly
those of LI-I slightly increased, during
resolves. Vaginal cytology is abruptly
anestrus. At late anestrus, the pulsatile
altered by the reappearance of pru·abasal
release of LH increases, causing the
epithelial cells and frequently neutrophils.

proestrous folliculogenesis. Estrogen levels

The appearance of vaginal mucosa! folds
are basal (2-10 pg/mL) and progesterone
becomes flattened and flaccid. Estrogen
levels at nadir ( < 1 ng/mL) in late anestrus.

levels are variably low, and progesterone

Anestrus norn1ally lasts 1-6 mo.

levels steadily rise to a peak of 15--80 ng/rn L

During proestrus, the bitch attracts male
before progressively declining in late
dogs but is still not receptive to breeding,
diestrus. Progesterone secretion depends
although she may become more playful. A
on both pituitary LH and prolactin

MANAGEMENT OF REPRODUCTION SMALL ANIMALS

2223
secretion. Proliferation of the endometrium

If vaginal cytology is performed until the
and quiescence of the myometrium develop
diestral shift is seen, the LH sw·ge,
under the influence of increased progeste1�
ovulation, and the fertile period can be
one levels.

analyzed retrospectively.

Diestrus usually lasts 2-3 mo in the
absence of pregnancy. Paiturition te1�

VetBooks.ir
minates pregnancy 64--66 days after the

Luteinizing Hormone: At the end of the

LI-I peak. Prolactin levels increase in a
follicular phase of the estrous cycle, a
reciprocal fashion to falling progesterone
marked increase in LI-I over usual baseline
levels at the tennination of diestrus or gestavalues develops over 24--48 hr, followed by tion, reaching much higher levels in the
a return to baseline values. This surge is
pregnant state. Mainrnary ductal and
thought to occur in response to the decline
glandular tissues increase in response to
in estrogen levels and increase in progesterprolactin levels.

one levels. The LI-I surge triggers ovulation,

Estrogen, LH, and progesterone are imp01� making it the central endocrinologic event tant in ovulation timing. All may be assessed
in the reproductive cycle of the bitch.

as pait of a reproductive evaluation.

Daily serial measurement of LH to
identify tl1e exact date of the LI-I surge is an

Estrogen: Increased estrogen causes an
accurate diagnostic tool to time breedings.

increased turnover rate of vaginal epithelial

Affordable semiquantitative in-house kits
cells, resulting in the progressive cornificaai·e available to measure senun LI-I levels in tion seen on vaginal cytology. Progressive
dogs and to identify the preovulatory LI-I
edema of the vaginal mucosa also develops
surge and thus the ti.me of ovulation and the
and can be visualized with endoscopic
true fertile pe1iocl. Blood san1ples must be
examination. Estrogen assays are perforn1ed drawn daily (at approximately the saine by mai1y commercial laboratories; however,
ti.me) for LI-I testing, because the LI-I surge
the i.nforn1ation is of little value for ovulation may last only 24 lu· in many bitches. The kits tin1ing because peak estrogen levels vary
can be subject to vaiiable interpretation, so
from bitch to bitch, and even relative
tl1e san1e person should run the tests if
changes do not correlate to ovulation or the
possible. Progesterone testing should
fertile period. Estrogen is best assessed by
always be performed concurrently in case
serial vaginal cytologies and vaginoscopy.

the LI-I surge is missed.

Estrogen levels do not indicate the fertile
period, because ovulation is triggered by the

Progesterone: Progesterone levels begin

LH surge and not an estrogen peak.

to rise at approxinmtely tl1e time of tl1e LI-I

Examination of the cells on the surface
surge (before ovulation). Rising progesterof the vaginal epithelium can provide one acts synergistically with declining estroinformation about the stage of the estrous gen to reduce edema of the vulva and
cycle. Proper technique is important so that
vagina, which can be seen on vaginoscopic
the cells obtained are representative of the
exainination. Other observable clinical
hormonal changes occurring. The sai11ple
signs are minimal. Serial blood san1ples
should be collected from the cranial vagina;
performed every 2 clays may identify the
cells from the clitoral fossa, vestibule, or
initial rise in progesterone ( usually >2 ng/
caudal vagina are not as indicative of the
mL), which indicates that the LI-I surge has
stage of the cycle. Under the influence of
occurred. Progesterone can be assayed by

1ising estrogen levels, the number of layers
radioi.rnmunoassay at most vete1inary
composing the vaginal epithelium increases
commercial laboratories. Several in-house
drainatically, presumably to provide
semiquantitative kits are also available.

protection to the mucosa during copulation.

No single absolute value of progesterone

As estrogen rises during proestrus, the
correlates to any particular stage of the
maturation rate of the epithelial cells
cycle. Progesterone varies from 0.8-3 ng/mL
increases, as does the nw11ber of keratiat the point of the LI-I surge, from 1--8 ng/mL
nized, cornified epithelial cells seen on a
at ovulation, ai1d from 4--20+ ng/mL during
vaginal smear. Full cornification continues
the fe1tile period. However, if accurate
throughout estrns until the "diestral shift"

serial quantitative progesterone assays are
occurs 7--10 days after the LI-I surge,
obtained, the LI-I surge may be estin1ated as
signifying the first day of diestrus. The
the day a distinct increase in progesterone
vaginal smear then changes abruptly, with
level is seen. Although this is not as accurate
appearance of neutrophils ai1d epitl1elial
as actual identification of the LI-I surge by
cells changing from full cornification
assay, estimation by progesterone levels is
to 40%--600Ai inunature (parabasal and
still very useful and is often more widely
intermediate) cells over the next 24--36 hr.

available and convenient.

2224

MANAGEMENT OF REPRODUCTION: SMALL ANIMALS

When timing breeding using semiquantiidentified, which gives a retrospective tative in-clinic progesterone assays, only a
evaluation of the breeding just completed.

range of progesterone is obtained, which

In addition, at least one progesterone assay
makes it difficult to accurately identify the
should be performed after clay O is identified

VetBooks.ir
day of the initial rise in progesterone or the
to document that levels continue to rise.

trne fertile period. Teclmical problems with

This illustrates sustained corpti:, luteum
these kits have also been seen. Therefore,
function and strongly suggests tl1at an
tl1ese assays should be used only for routine
ovulatory cycle has occurred.

breedings in which a wider margin of error

Insemination with extended, chilled
is acceptable. A gemeral guideline is that
semen should be done on days 4 and 6, or
when progesterone is >2 ng/mL, breeding

3 and 5, after day 0. The days chosen can
should begin. Optimal ovulation timing
depend on overnight shipping possibilities
should use quantitative progesterone assays and the schedules of all involved paities.

from commercial laboratories (the cost

Frozen semen breedings should be done
difference is minimal). Regardless of which
on day5 or6.

assay is used, an additional test should

Vaginoscopy may be perfo1med
always be performed 2-4 days after the first
throughout tl1e cycle as an adjunct to
rise is detected to indicate that the cycle has
vaginal cytology ai1d hormonal assays,
progressed as expected, a functional corpus
especially when evaluating an unusual
luteum has been formed, and ovulation has
cycle. Behavior ai1d other observations
occurred.

should also be made. Ovulation timing is
most accurate when information from

Use of Hormonal Evaluation to Time
several tests is pooled (vaginal cytologies,

Breeding: Owners of breeding animals
vaginoscopy, and progesterone or LH tests).

should be advised to notify their veterinarian when tl1ey first notice U1at a bitch for Artificial Insemination: Artificial
which timing is planned is in season, based
insemination is becoming more common in
on vaginal discharge or vulvar swelling/
cai1ine reproduction, permitting the use of
attraction to males. Even the most astute
shipped semen, assistance for ge1iatric or
owner may not notice the true onset of
subfe1tile males, coverage of dominant
proestrus for a few days. Early proestrns
females, and advanced reproductive
should be documented with vaginal
technology such as intrauterine deposition
cytology ( <500/o comification/superficial
of semen. Insemination may be performed
cells). A baseline progesterone level
with fresh, chilled, or frozen semen. All

(usually 0-1 ng/mL) might be informative
instruments should be clean and free of any
if the true onset of tl1e cycle is unknown.

chemical contan1ination. After semen has

Vaginal cytology should be performed
been collected and evaluated (seep 2221), it every 2 days until comification progresses
can be deposited in the cranial vagina of the
significantly, usually > 70% superficial cells.

bitch using a rigid insemination pipette of

At that point, serial honnonal assays should
appropriate length, or into tl1e uterus via
begin. For routine breedings, progesterone
transcervical catheterization. Access to tl1e
testing may be clone every other day until a
uterus via laparoscopy or lapai·otomy is less
rise in progesterone >2 ng/mL is identified.

desirable because of invasiveness.

The day of the initial rise in progesterone

Semen (the second fraction) may be

>2 ng/mL is identified as "day O." Breedings diluted with extenders and chilled for later or
are advised on clays 2, 4, and 6.

distant use (witllin 48 hr), or extended and

When increased accuracy of ovulation
frozen in liquid nitrogen (in straws or pellets)

ti.ming is necessaiy ( eg, frozen or chilled
for longtenn storage. Phosphate-buffered egg
semen breedings, infe1ti.lity cases,
yolk diluent or Tris-buffered diluent is used
breedings with subfertile stud dogs), daily
most often; several commercial extenders

LH testing is recommended. Once tl1e LH
ai·e available. A drop of chilled semen should
surge is identified, breeding days may be
be warmed for evaluation before use. Frozen
planned. The clay of the LH surge is also
semen should be tl1awed as directed by the

"clay 0." It is useful to perform vaginal
c1yopreservation center, evaluated, and
cytology every 2 -3 days until comification
immediately insenlinated. Dogs should be
is complete (generally >800/o-900/o superficial screened for B1ucella canis when semen is cells). This maximal cornification usually
collected for c1yoprese1vation.

develops before the fertile period and
continues until the onset of di estrus, which
is usually a few clays after the end of the

Cats
fertile period. Vaginal cytology may be

The queen should be taken to the tom when
continued until the diestral shift is
showing signs of estrus. The breeding ai·ea

MANAGEMENT OF REPRODUCTION SMALL ANIMALS

2225
should be familiar to the tom, quiet, and
females because of the increased risk
have good footing and a minimum of
of cystic endometrial hyperplasia and
interference, while permitting observation.

pyometra, as well as other adverse effects

The courtship should not be inte1Tupted

( eg, mammary hyperplasia and neoplasia,

VetBooks.ir
unless there is concern for the safety of
hyperglycemia secondary to insulin
either cat. Toms have been known to mate
resistance, and rebound hyperprolactinto the point of physical exhaustion, but emia and lactation).

queens n01mally go through a period of

Suppression (and induction) of estrous
rolling and grooming after a breeding and
cycles by the use of synthetic GnRH
may not let the tom remount for some time.

in1plants has been described in the bitch; it

Because ovulation is induced by
can be successful, but the products are not
vaginal-cervical stimulation, multiple
universally available. Estrus induction in
breedings over 2 -3 days are advised.

the bitch can be accomplished with oral

Periods of separation between matings
prolactin inhibitors ( cabergoline 2.5-5 mcg/
prevent exhaustion and diminish the
kg/day); anestrus of at least 2 mo duration
chances of fighting. The stress of transpormust precede induction.

tation may affect reproductive functions in

Ovulation can be induced in estrual
nervous queens. Evaluation for pregnancy
queens physically or, more reliably,
can be perfonned 21-30 days after breeding
honnonally to produce a luteal phase
by abdominal palpation and ultrasonogra

( di.estrus or metestrus) of -45 days.

phy.

Physical methods include mating with a
vasectomized tom ( very effective) or

MANIPULATION OF THE
inserting a sterile swab or glass rod into

ESTROUS CYCLE
the vagina. The latter should be performed
repeatedly for best results. Hormonal

The estrous cycles of dogs and cats are not
methods include administration of human
as easily manipulated as in other species.

chorionic gonadotropin at 500 ill/cat or

Most protocols are not based on controlled

GnRH at 25 mcg/cat. Both are given JM,
studies, so manipulation of the estrous cycle once daily for 2 days.

in valuable breeding individuals is not
advised. Although onset of a particular cycle PREGNANCY DETERMINATION
may be delayed, return to n01mal cycling is
highly variable. Induction of estrus is

Fertilization occurs in the oviducts in both
possible in late anestrus bitches by using
the bitch and queen. Implantation of zygotes
prolactin inhibitors ( eg, bromocriptine,
in the uterus occurs at -18 days in the bitch
cabergoline ).

and 14 days in the queen. This is accompa

Ovariohysterectomy or ovariectomy is
nied by the fonnation of small swellings
the best method to prevent estrus in the
along the uterine horns (deciduomata) by
bitch and queen. Longtern1 suppression of

-21 days. These a.re palpable, assuming the
estrus by using androgens is not advised,
anin1al is cooperative, at this time. Fetal
because it is not documented to be safe in
growth is rapid during early pregnancy, and
breeding bitches. Common adverse effects
these swellings double in di.a.meter every 7
are breaktl1rough proestrus, clitoral
days. After day 35-38, they become
hypertrophy, vaginitis ( especially in
indistinct, and palpation becomes difficult
prepubertal bitches), increased activity of
until late pregnancy when fetal heads and
skin sebaceous glands, mild epiphora, and
rumps are palpable as firm, nodular
alterations in hepatic function studies. After
structures in the ventral posterior abdomen.

treatment is discontinued, return to estrus is A commercial relaxin assay, specific and

-70-90 days but variable. Conception rates
sensitive for pregnancy diagnosis in the
are reportedly normal by the second cycle
bitch after 30 days gestation, is available.

after treatment. If given to pregnant bitches,

Although the fetal skeleton begins to
synthetic androgens induce severe
calcify as early as day 28, it is not detectable
developmental anomalies in the urogenital
by routine radiography until approxinlately
system of female puppies. The safety and
day 42-45 and is quite prominent by day
efficacy of injectable testosterone, as is

4 7-48. Radiography at this time is not
practiced commonly in racing Greyhounds,
teratogenic. Late gestational radiography
has not been supported by controlled

(>55 days) is the best method to determine
studies and is not advised. Androgens
litter size. Fetal dentition becomes visible
should not be given to cats.

at term, and its appearance can be used to

The use of megestrol acetate, a synthetic
confirm fetal develpment adequate for an
progestagen, is not advised in breeding
elective cesarean section when ovulation

2226

MANAGEMENT OF REPRODUCTION: SMALL ANIMALS
ltM!ii GESTATIONAL AGE IN DOGS AND CATS

Dogs: Gestational Age ± 3 days

Cats: Gestational Age ± 2 days

<40 days

>40 days

>40days

VetBooks.ir

(6 x GSD") + 20

(15 x BPb) + 20

25'>< BP+ 3

(3 x CRU) + 27

(7 x BDci) + 29

11 x BD + 21

(6 x HD) + (3 x BD) + 30

Days before parturition = 64--6 6 minus

Days before parturition= 61 minus
gestational age
gestational age

"Gestational sac diameter (cm)

bBiparietal diameter (cm)

ccrown rump length (cm)

d Body diameter at the liver (cm)

timing is not available and breeding dates
increase the risk of pyometra, are unreliable
are vague or spread over many days.

in ten11inating pregnancy, and are not

Ultrasonography is also useful in
advised.

pregnancy determination and permits

Safe and effective tem1ination of
evaluation of fetal viability. Ultrasonography
pregnancy is possible in both the bitch and
is best perfom1ed at 25----35 days gestation.

queen by administration of prostaglandin

Before 21 days, "false-negative" results are F,a (natural hormone) at0.1 mg/kg, SC, tid
seen. Doppler-type instruments allow one to
for 48 hr followed by 0.2 mg/kg, SC, tid to

"hear" the fetal heart, which beats 2----3 times effect ( until all fetuses are evacuated as
faster than that of the dam. Placental sounds
confirmed by ultrasonography). Treatment
may also be heard. Ultrasonography is
times can reach 14 days. In the bitch,
especially helpful in differentiating pregnancy treatment time can be reduced ( usually by from other causes of uterine distention ( eg,

48 hr) by the concurrent administration of
hydrometra, pyometra, mucometra).

prostaglandin E (misoprostol) intravagi

Ultrasonographic measurements can be used
nally at 1 -3 mcg/kg/day. The adverse
to calculate gestational age ( see TABLE 1 7).

effects of prostaglandins at this dosage

Gestational age in cats can also be

(panting, trembling, nausea, and diarrhea)

detemiined by the following formula:

are mild and transient. The therapeutic
window for prostaglandins is narrow, and
mean litter crown run1p length (in cm) =
doses should be calculated carefully.

0.242 3 x gestational age -4.21 65

Synthetic prostaglandins ( cloprostenol

1 -3 mcg/kg every 1 2 -24 hr to effect) more

PREVENTION OR TERMfNATION
specifically target the myometrium,

OF PREGNANCY
causing fewer systemic adverse effects,
and are currently preferred.

Unplanned and unwanted mating of cats

Pregnancy can also be reliably temiinated
and dogs is a common concern. Pregnancy
in the bitch by administration of dexamethacan be completely prevented or temiinated sone at0.2 mg/kg, PO, bid to effect. The
by ovariohysterectomy. Sixty percent of
owner should be informed of the adverse
misbred bitches do not conceive, so
effects of corticosteroid administration ( eg,
confirmation of an undesired pregnancy
panting, polyuria, polydipsia).

is advised before proceeding. Postcoital

Combination drug protocols ( cabergoline
douches are of no value in preventing

5 mcg/kg, PO, divided every 24 hr for as long
unwanted pregnancy. Although injectable
as 10 days, cloprostenol l mcg/kg given SC
estrogens, when administered appropritwice at -2 8 and 3 2 days after the LH surge) ately, can prevent pregnancy, their use
have been reported to terminate pregnancy
involves great risk of serious adverse
reliably with minimal adverse effects,
effects, including pyometra and potentially
shortest treatment times, and greatest
fatal bone marrow suppression, and they
sucess rates; their cost and need for
are not advised. 1f used, they must be
compounding are disadvantages.

administered soon after copulation, before

Antiprogestins (aglepristone) are safe
potentially fertilized ova reach the uterus.

and effective abortifacients; availability

Oral estrogens given during diestrus greatly
remains problematic.

MANAGEMENT OF REPRODUCTION SMALL ANIMALS

2227

WHELPING AND QUEENING
minimally by determining the onset of
cytologic diestrns, to evaluate length of

Normal gestation in the bitch is 56---58 days
gestation at tem1.

from the first day of diestrus, or 64-66 days

A predictable and safe way to induce
from the initial rise in progesterone from
successful parturition in the bitch and

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baseline (generally >2 ng/rnL), or 58-72
queen has not been developed.

days from the first instance that the bitch
pem1itted breeding. Parturition in the queen
occurs 64-66 days from the LH surge

LABOR AND DELIVERY
triggered by copulation.

Normal Labor: Stage I labor in the bitch

Predicting length of gestation without
and queen normally lasts 12-24 hr, during
prior ovulation timing is difficult because of
which time the myometrial contractions
the disparity between estrual behavior and
of the uterus increase in frequency and
the actual time of conception in the bitch,
strength and the cervix dilates. No
and the length of time semen can remain
abdominal efforts (visible contractions) are
viable in the reproductive tract ( often ?:.7
evident during stage I labor. Bitches and
days). Breeding dates and conception dates
queens may exhibit changes in disposition
do not con-elate closely enough to permit
and behavior during stage I labor, becoming
accurate prediction of whelping dates.

reclusive, restless, and nesting intemtit

Additionally, clinical signs of tenn
tently, often refusing to eat and sometimes
pregnancy are not specific-radiographic
vomiting. Panting and trembling may be
appearance of fetal skeletal mineralization
seen. Vaginal discharge is clear and watery.

varies at tenn, and fetal size varies with

Nonna! stage II labor is marked by visible
breed and litter size. A drop in rectal
abdontinal efforts, which are accompanied
temperature to a mean of 98.8°F (range
by myometrial contractions that culminate

98.1 °-100.0°F) (37.1 °C [range 36. 7°-37.8°C])

in the delivery of a neonate. 'Iypically, these
is seen in most bitches 8-24 hr before
efforts should not last > 1-2 hr between
whelping. Breed, parity, and litter size can
puppies or kittens, although great vaiiation
also influence gestational length. Subtle
exists. The entire delivery can take 1 to >24
signs of impending delivery include
hr; however, nom1al labor is associated with
relaxation of the perineum, man1111ary
shorter total delivery time and intervals
engorgement, and a change in the appearbetween neonates. Vaginal discharge can ance of the gravid abdomen, but these
be clear, serous to hemon-hagic, or green
changes are not sensitive or specific.

(uteroverdin). 'Iypically, bitches and queens

Because there is no means to effectively
continue to nest between deliveries and
manage prematurely bom puppies,
may nurse and groom neonates intemtitpremature intervention in the whelping tently. Anorexia, panting, and trembling !lfe
process is undesirable. Likewise, an
conm1on.

excessively conservative approach resulting

Stage III labor is defined as the delivery of
in intrauterine fetal death is undesirable as
the placenta. Bitches and queens typically
well.

vacillate between stages II and III of labor

Bitches typically enter stage I labor
until tl1e delivery is complete. During
within 24 hr of a decline in serun1 progesnom1al labor, all fetuses and placentae are terone to <2-5 ng/mL, which develops in
delivered vaginally, although they may not
cor\junction with increased circulating
be delivered together in every instance.

prostaglandins and is commonly associated
with a transient drop in body temperature

Dystocia: Dystocia results from mater

( <99°F [37.2°C]). Monitming serial
nal factors ( uterine inertia, pelvic canal
progesterone levels for impending labor is
ai10malies), fetal factors (oversize,
problematic because in-house kits enabling
malposition, malposture, anomalies), or
rapid results are inherently inaccurate
a combination of both. Clinically, uterine
between 2 and 5 ng/rnL. Commercial
inertia developing after the delivery of one
laborato1ies offering quantitative progesteror more neonates (secondary inertia) is the one by radioimmunoassay or hemi!UTI1inesmost con1111on cause of dystocia.

cence typically have a 12-24 hr turnaround

Dystocia can be objectively diagnosed
time, which is not rapid enough to make
if uterine contractility is inappropriate
decisions about in1111ediate obstetric

(generally infrequent, weak myometrial
intervention. Progesterone levels can drop
contractions) for the stage of labor, or if
rapidly in a matter of hours. If progesterone
excessive fetal stress results from labor.

is <2 ng/mL, gestation is likely at tem1 and

Subjectively, dystocia is diagnosed if stage I
labor pending. Clearly, it is beneficial to
labor is not initiated at tem1, if stage I labor
obtain information about ovulation timing,
is >24 hr without progression to stage II, if

2228

MANAGEMENT OF REPRODUCTION: SMALL ANIMALS
stage II labor does not produce a vaginal

The neonate should be weighed
delivery within 1-4 hr, if fetal or maternal
accurately as soon as it is dry and then twice
stress is excessive, if moribund or stillborn
daily for the first week. Any weight loss
neonates are seen, or if stage II labor does
beyond the first 24 hr indicates a potential

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not result in the completion of deliveries in
problem and should be given immediate
a timely manner (within 12-24 hr).

attention (eg, supplemental feeding,

Uterine and fetal monitors can be used
assisted nursing, evaluation for sepsis).

to detect and monitor labor and to manage

Neonates should gain 1()% of their body
dystocia. Unresponsive uterine inertia,
weight daily.

obstructive dystocia, aberrant ute1ine
contractions, or progressive fetal distress

PERIPARTURIENT PROBLEMS
without response to medical management
are indications for cesarean section.

Bitches and queens should deliver in a

Medical management includes adminisfainiliar area where they will not be tration of calcium gluconate and oxytocin
disturbed. Unfainiliar surroundings or stranbased on the results of monitoring. Drugs gers may impede delive1y, interfere with
are given only after 8-12 hr of an estabmilk letdown, or adversely affect maternal lished contraction pattern (stage I labor)

instincts. This is especially true in young or
as detected by the uterine monitor and
primiparous animals. The dan1's apprehenonly if inertia is detected when stage II sion or nervousness may subside in a few
labor is anticipated. Premature adminishours, but in the meantime the neonates tration of drugs results in suboptimal
must receive colostrun1 and be kept warm;
response.

nursing should be closely supervised. The

Generally, the administration of calcium
use of acepromazine at low dosages (0.01
increases the strength of myometrial
mg/kg, PO, bid-tid) can effectively relax
contractions, while oxytocin increases the
nervous dains and does not sedate neonates
frequency. Calcium gluconate (Hl0Ai solution, detectably nor interfere with milk 1 ml/22 kg body wt bid-qid) is given when
production.

uterine contractions are ineffective or

A nervous dain may ignore the neonates
weak. It can be given SC, avoiding the
or give them excess attention. She may lick
potential for cardiac irritability associated
and bite at the umbilical stump, causing
with IV administration. Oxytocin (0.5-2 U in hemo1Thage or dan1age to the abdominal bitches; 0.25-1 U in queens) is given when
wall that may lead to evisceration. Excess
uterine contractions are less frequent than
grooming of the neonate may prevent it
expected for the stage of labor. The most
from nursing. If the dain's maternal instincts effective time for treatment is when ute1ine
fail, she may assume sternal recumbency
inertia begins to develop, before the
and not allow nursing, or leave the neonates
contractions stop completely. High doses
w1attended. It is not unusual for the dan1 to
of oxytocin saturate the receptor sites and
pick up the pups and to reaITange them in
make it ineffective as a uterotonic. If fetal the box, especially after delive1y of each
stress is evident (persistent bradycardia)

pup; however, she should then asswne the
and response to medications is poor,
no1mal nursing position.

cesarean section is indicated.

The principal metabolic disease
associated with pregnancy is puerperal

POSTPARTUM CARE
hypocalcemia (seep 992). It is rare in cats and most common in dogs weighing <20 kg,

Palpation and, if necessaiy, radiography
exacerbated by improper perinatal nutrition
should be used to detennine that all puppies ( excessive calciunlfphosphorus supplemenor kittens have been delivered. The routine tation or an imbalanced prenatal diet).

postpartum administration of oxytoxin or

Common inflanm1atory diseases in the
antibiotics is unnecessary in healthy dains
postpartum period include metritis and
with nursing neonates, unless the placenta
mastitis. Retention of a placenta or its
has been retained. The dain's body
remnants could lead to metritis. Signs
temperature and the character of the
include continued straining as if in labor, the
postpartum discharge or lochia and milk
presence of a fusiform mass associated with
should be monitored. Nmmally, the lochia
the uterus (best identified by ultrasonois dark red to black and is heavy for the graphic evaluation), abnormal vulvar
first few days after parturition. It is not
discharge, fever, and lethargy as the
necessary that the dain consume the
infection develops. If given within 24 hr
placentas. Disinfection of the neonatal
of labor, oxytocin may cause passage of
umbilicus with tincture of iodine helps
the placenta; if oxytocin is ineffective,
prevent bacte1ial containination.

prostaglandin F2a (0.1 mg/kg, SC, every

MANAGEMENT OF REPRODUCTION SMALL ANIMALS

2229

12-24 hr) or cloprostenol ( 1-3 mcgtkg, SC,
tomy should not have a negative effect on
eve1y 12-24 hr to effect) can usually induce
bitches a.11d queens with adequate lactopassage of the placenta.

genesis at term. If this is seen, a genetic

Mastitis (seep 1396) is more common in
component may be involved.

bitches than in queens. The bacte1ia

Lactation can be stimulated if treatment

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associated with mastitis tend to be coliforms
is prompt. Mini-dose oxytocin (0.5--2 U/
or Slaphylococcus spp. Galactostasis can
dose, SC, eve1y 2 hr) should be adminispredispose bitches to mastitis, as can tered. The neonates should be removed
excessive human manipulation of the
from the dan1 before each injection and
manunary glands. Ma.nunaiy glands should be returned 10 min later. The neonates should observed to ensure that all ai·e being nursed.

be supplemented adequately to ensure

Significant postpartum uterine hemorsurvival, but not excessively, so that they rhage is rai·e. Oxytocin ( <24 hr postpa.rtwn)

will suckle vigorously. Mainmaiy glands
and prostaglandins ca.11 be administered if
should be gently ha.11d st1ipped if suckling is
the uterus is healthy; ovaiiohysterectomy
not vigorous. ConcuJTent administration of
must be perfom1ed if hemorrhage is
metoclopra.111ide (0.1-0.2 mg/kg, SC, tid-qid)

unabated and significant (ie, ca.using blood
promotes prola.ctin release. Acepromazine
loss anemia). Screening for an tmderlying
at mild tranquilization dosages may also
coagulopa.thy and appropriate therapy
facilitate milk letdown. Therapy should
should be undertaken.

continue until lactation is adequate, usually

Uterine subinvolution results in

12-24 hr later.

hemorrhagic spotting for> 12-16 wk (the
nmmal period of involution in the bitch).

INFERTILITY

Treatment is urmecessary unless blood loss
is significant, because the condition resolves

The most common cause of infertility in
spontai1eously. Future fertility is unaffected.

dogs and cats is related to husbandry

Agalactia ( other than that ca.used by
problems. Breeding with a proven fertile
severe illness) is tmconunon in dogs and
male must occur at the optimal time for the
ca.ts. Determination that lactation is
female. Infectious, a.11atomic, metabolic,
adequate should be performed before
and functional problems associated with
elective cesarean section. If an emergency
infe1tility a.re seen less frequently. (See also cesai·ean section is required, regardless of

JNF'ERTJLITY, p 1328.)

the status of lactation, inte1vention is

The only confirmed infectious cause of
indicated (see below). Bitches and queens
infertility in the bitch is brucellosis (see
with inadequate lactation at tenn should
p 1402). This highly contagious disease
be thoroughly evaluated for metabolic or
caused by Bnicella canis results in abortion inflanunato1y disorders (metritis, eclan1pa.11d infertility in bitches and infertility in sia, mastitis), nutritional and hydration
males. A rapid slide agglutination test
status, or peripa.rturient pa.in, and treated

(RSAT) kit to detect serwn antibodies is
appropriately. Evaluation of a hemogran1,
conunercially available. If the RSAT is
serum chemistries, vaginal discharge, and
negative, the bitch is presmned to be
ultrasonographic evaluation of the uterus

Bnicella-free; if positive, further confmnamay be required. The nom1al presence of tory laboratory testing is indicated ( eg,
colostrum (typically not copious) should

AGID, PCR, 2-mercapto-etha.110! RSAT).

not be confused with a.galactia. The level of

In cats, infectious causes of infertility
neonatal contentment and daily weight gain
include toxoplasmosis, feline leukemia

(after the first 24 hr) indicates adequate
virus infection, feline infectious pe1itonitis,
lactation. Milk letdown is promoted by
and feline viral rhinotracheitis. These may
oxytocin release, a reflex niggered by
cause abortion, neonatal death, fetal
nursing; therefore, neonates must spend
resorption, and apparent infertility.

adequate time suckling. Disruption of the

Anatomic causes of infertility include
pitJ.ritary-ovaiian-manunary gland a.xis can
acquired a.11d congenital problems. Fibrosis
result in idiopathic a.galactia. Agalactia ca.11
of the oviducts or uterine horns, probably
be associated with premature delivery of
a result of inflainmation after infection or
neonates. IatJ.·ogenic agala.ctia can result
trauma, leads to infertility. Diagnosis is via
from progesterone supplementation dming
laparotomy with dye studies. There is no
gestation and should be avoided unless
reliable treatment, although microsurgery
essential.

may be attempted. Sin1ilai·Jy, bilateral

Because estrogen promotes lactogenesis,
obstrnction of tl1e spenn ducts can cause
the adequacy of manm1aiy development
azoospennia a.11d infertility. High environshould be assessed before removal of the mental temperature and excessive
ova.lies at cesarean section. Ova.riohysterec-
conditioning resulting in increased body

2230

MANAGEMENT OF REPRODUCTION: SMALL ANIMALS
temperatme can induce either temporary or
estrus appear ( not administered for >5
permanent azoospermia. Kennel or cattery
days).

management should allow for breeding

Acquired anestrus may result from
males to remain cool during the summer.

previous oophorectomy, exogenous

Scrotal dermatitis can have the same result.

hom10nal treatment (including glucocm�

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Disorders of sexual differentiation result in
ticoids), profound hypothyroidism, or
infertility ( eg, hennaphroditism, pseudohe1� ovarian disease ( cysts or neoplasia).

maphroditism).

Diagnosis is based on history, physical

Metabolic causes of infertility, other
exan1ination, biochemical evaluation,
than in severely ill individuals, are rare.

ultrasonography, and laparotomy.

Hypothyroidism has no effect on male libido

Prolonged estrus may be caused by
or semen quality. Hypothyroid bitches might ovarian cysts that produce estrogen, not cycle or have increased abortion rates,
functional ovarian tun10rs, or exogenous
or neonatal smvival may be poor.

estrogens (including hwnan transdermal

Estrous cycle abnom1alities can cause
honnone replacement therapy). Exogenous
infertility. Prolonged anestrus may be
honnones should be discontinued.

congenital or acquired. Some large breeds of

Laparotomy with histopathology is usually
dogs may not have their first estrus until they
indicated, because medical attempts at
are �2 yr old, and some individuals and some
inducing ovulation (hwnan cho1ionic
breeds typically have only one estrous cycle
gonadotropin, FSH, GnRH) are usually
each year. Congenital fonns of anestrus may

W1rewarding. Prolonged diestms can result
be clue to lack of function of the hypothafrom luteal cysts in the ovary. Medical lamic-pituitary axis or ovarian dysgenesis.

manipulation with prostaglandins is usually

The diagnosis of congenital anestrus

W1rewarding, and ovariectomy with
is based on the age of the animal and
histopathology is indicated.

exclusion of all other possible causes

Prostatitis can be subclinical or

(including ctu·omosomal defects, endocrine
contribute to subfe1tility and infertility in
disorders, and previous oophorectomy).

dogs. Benign prostatic hyperplasia does

Because cyclicity in queens is detem1ined
not affect fertility.

by photoperiocl, lighting conditions should

Testicular neoplasia, commonly
be approp1iate for several months before
producing estrogen, usually causes
congenital anestrus is diagnosed and
infertility. Castration of the affected testis
exogenous hom10nes are administered. One may allow the other testis to regain its reported method to induce estrus in cats is
ability to produce sperm, but the prognosis

FSH at 2 mg/cat, IM, once daily until signs of
is guarded.

BREEDING SOUNDNESS EXAMINATION

OF. THE MALE

The breeding soundness examination
or manual stin1ulation in the presence of a

(BSE) involves a complete and systematic
female in estrus. Therefore, mating ability
evaluation of the reproductive potential of
is seldom evaluated in bulls and rams for
a given male, including mating ability and
routine BSE in which semen is typically
libido, general physical examination and
collected via electroejaculation.

inspection of the genital organs, and

The components of semen quality
assessment of sperm production and
evaluation are: 1) semen volume and
quality. The BSE is not a direct evaluation
sperm concentration, which allow for the
of fertility: this can be confirmed only by
calculation of the total nwnber of sperm in
successful production of offspring after
the ejaculate; 2) spem1 motility, including
breeding a fertile female. The specific male
gross motility (runlinants only) and percent
animal must be properly identified, and a
individual spem1 motility (total and
detailed history is important because subprogressive) of a diluted sample; and 3) the or infertile males might require more
percent morphologically nmmal spenn. A
exhaustive evaluation. The evaluation of

Rornanowsky-stained cytology sample also
mating ability and libido is possible only
allows for evaluation of red (hemospermia)

when collecting semen via artificial vagina
or white (pyospennia) blood cells in the

BREEDING SOUNDNESS EXAMINATION OF THE MALE

2231
ejaculate. When collecting semen from
sotmdness examination (BSE). However,
ruminants via electroejaculation, the sperm
if possible, the bull should be observed
production potential is estimated by
serving cows to allow assessment of his
measuring scrotal circwnference. Scrotal
desire to breed, ease of mounting, ability to
circwnference is correlated with daily
achieve erection and extend the penis, and

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sperm output and therefore the serving
presence of penile deviation or other
capacity of a bull or ram (ie, number of
abnonnalities that may prevent successful
females he can settle in a linlited time).

service. Libido and serving capacity tests

After the BSE is complete, the male is

( scoring the nun1ber of services achieved
classified as a satisfactory, questionable,
during a set time that a bull is in a pen with a
or unsatisfactory prospective breeder. An
restrained cow) have been devised but are
anin1al with physical defects that may be
time conswning and difficult to standardize
inherited (including cryptorchidism) should
under field conditions. In addition, the
be declared unsatisfactory. Guidelines for the results are difficult to interpret in light of BSE in each domestic species are included in
the vaiiety of stocking conditions used, eg,
the following species-specific discussions.

single versus multiple bulls or small
paddocks versus large ranges.

BSE forms have been developed and

Spermatogonial Stem Cells and
should be used to ensure the systematic

Prospects for Preservation of Male
completion of the exanlination and accurate

Fertility: Spennatogonial stern cells
reporting of results. The bull should be

(SSCs) are stem cells located against the
restrained in a chute for the exanlination.

basement membrane of the serniniferous

Body condition should be scored, and a
tubules. As such, they can regenerate themgeneral physical exanlination conducted selves but also give rise to daughter cells
with special attention paid to the feet, legs,
that follow the replication and differentiaeyes, and sheath. The inguinal tings and tion path toward the generation of mature
internal ge11italia should be palpated per
sperm. Of particular interest is that SSCs
rectum to detect any abnom1alities, eg,
are present throughout the life of a given
senlinal vesiculitis. The scrotum should be
male and hence may provide an avenue to
palpated to evaluate the testes, epididypreserve or even restore male fertility.

nlides, spermatic cords, and scrotal skin.

Although much work is still needed for

The testes should be symmetrical in size,

SSCs to become a reality in the management
smooth, resilient, and freely movable within
of male infertility, these cells have been
the scrotum. Cryptorchidism is considered
isolated and partially characterized in boars,
an undesirable heritable trait and renders a
bulls, tom cats, and stallions. Most
bull unsatisfactory for breeding even though
knowledge derives from studies in the
his semen quality nlight be acceptable. In
mouse, in which SSCs can be cultured indefiruminants, the epididynlides nm caudomenitely, cryopreserved, genetically modified, dially along the testes in a dorsoventral
and transplanted into the testes of sterile
orientation, with the tail most ventrad. The
recipient mice for generation of mature
epididynlis should have no palpable masses.

sperm cells. Studies are underway to pursue

The measurement of scrotal circwnference
these goals in domestic species. In the

(SC) is considered a reliable predictor of
future, SSCs may be used to preserve
paired testis weight, which in tum provides
fertility in valuable domestic species as well
an accurate estimate of daily sperm
as in tl1eir endangered wild counterparts ( eg, production and quality. The SC should be felids). Moreover, SSCs could also become
measured at its maximal diameter, and size
an integral tool in the assessment of male
depends greatly on bull age and breed. As a
fertility or ability to restore fertility in a given general rule, SC should be �30 cm for bulls male. In addition, and given some of tile

< 15 mo old, 31 cm for bulls 16---18 mo, 32 cm
advances in assisted reproductive technolofor bulls 19-21 mo, 33 cm for bulls 22-23
gies in domestic species, it is feasible that
mo, and 34 cm for bulls �2 yr old. However,

SSCs could be differentiated into haploid
readers should consult the latest published
genn cells in vitro for intracytoplasnlic
breed-specific average SC measures.

sperm ir\jection and the generation of

Although not used routinely in practice,
offsp1ing from valuable azoospennic males.

additional techniques to evaluate the scrotal
contents include thern1ography and
ultrasonography. Bull testes must be 2° ---6°C

BULLS

(35.6° -42.8°F) cooler than core body
temperature for optimal spern1 production,

In bulls, assessment of libido is often not
and increases in scrotal temperature
possible during a routine breeding
negatively affect semen quality. Infrared

2232

BREEDING SOUNDNESS EXAMINATION OF THE MALE
the1mography can be used to evaluate
usually require a higher voltage for ejacuscrotal temperature, which should yield a lation. ln some la.i·ge bulls, tl1e probe may
left to right symmetry with a 6° to 4 °C ( 42.8°
not reach the correct a.i·eas for stunulation;
to 39.2°F) temperature gradient from top to
having two or more probe sizes is recom

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bottom. Abnormal thermogra.ms are almost
mended if BSEs are to be clone on a va.i·iety
always associated with poor sperm quality
of sizes of bulls. The semen collected via
and have been correlated with decreased
electroejaculation is not representative
pregnancy rates. Conversely, evaluation of
of a full ejaculate in regard to volume
the testes by ultrasonography does not
and concentration, and thus the sperm
appear to improve the predictive value of
production potential of the bull is based on
standard evaluation techniques (physical
tl1e evaluation of SC. Conversely, sperm
examination, palpation, SC measurement,
quality (motility and morphology) does not
sperm evaluation). Therefore, it appears
differ from that in an ejaculate collected
that the value of ultrasonography as a tool
with an AV.

in BSE in bulls rests on assessment and

If an AV is to be used, bulls a.i·e induced to
characterization of grossly detectable
mount a teaser a.tm11al ( eg, restrained steer,
lesions of the testes.

cow, or phantom), and tl1e erect penis is

For the purpose of a routine BSE, semen
directed into the AV by the collector as the
is most often collected via electroejaculabull mounts. In preparing the AV, the tion; semen can be collected with an
temperature, which is a critical factor in
artilicial vagina (AV) in bulls trained to use
stimulating ejaculation, is maintained at
one (eg, those in bull studs). The penis

105° -107°F ( 40.5° -42°C). Temperatures up
usually extends during electroejaculation
to l 18°F ( 48°C) may assist collections in
and should be exan1inecl at tl1at time for any
untrained bulls. The AV should be lubricated
abnormalities. If it is not extended during
with nonspermiciclal jelly. The typical
electroeja.cula.tion, it should be gently
volume of an ejaculate is 4-8 mL, and the
exteriorizecl for examination by grasping
concentration 1-1.5 billion sperm/mL. A
the glans with a cotton gauze and, if
semen sample can be collected from some
necessary, by putting pressure on the
bulls by transrectal massage of the
sigmoid flexure iJ1m1ediately caudal to tl1e
accesso1y sex glands. With this technique,
scrotum. Preputial wash samples may be
erection seldom occurs. After the rectum is
ta.ken for isolation and culture of Campylo
completely emptied, the vesicular glands
bacterj"etus venereal-is (using Clark's are massaged with a backward motion tmtil
medium) or Tritrichomonasfoetus (using
a few mL of fluid drop from the sheath. The

Dian10ncl's medium or a commercially
a.tnpullae are tl1en massaged, and an
available diagnostic medium kit), in
assistant collects the semen as for
particular when investigatu1g subfe1tility
electroejaculation. This metl1od is not
in bulls �4 yr old.

always successful, and the quality of the

The electroejaculator consists of a rectal
semen emission is usually lower tl1a.t1 the
probe that has a series of linear banded
ejaculate collected by the other two
electrodes connected to a va.tia.ble current
methods.

and voltage source. The bull is restrained

Sperm concentration, ejaculate volume,
in a chute, the rectum is emptied, and the
and the total number of sperm in the
entire lubricated probe is inserted rectally
ejaculate are evaluated only if the sa.tnple
with the electrodes oriented ventrally. A
has been collected with an AV. The semen
hand-operated rheostat pennits intermittent san1ple should be evaluated unmediately for pulses of current to be given as the voltage
spem1 motility. The mate1ials that contact
is gradually increased. The response varies
the sperm should be at the same temperaconsiderably, but it is conm1on to use 2- to ture as the sperm (to a.void temperature

4-sec pulses repeated at 5- to 7-sec intervals.

shock), clean, cl.ty, and nontoxic. Motility

After a va.tiable mm1ber of such stimulaevaluation is best when the temperature of tions, erection and protmsion of the penis
the semen is either maintained at -37°C
may be seen, followed by a.flow of semiJ1al

( -98.6°F) during the sho1t time before it is
fluid, or the bull may ejaculate into tl1e
evaluated, or when the semen is gently
sheath without protmcling the penis. The
wam1ed to 37°C before evaluation. Both
semen may be collected by any convenient
gross motility ("swirl pattern") in the semen metl1ocl; typically a mbber AV cone iJ1sertecl
and motility of individual spermatozoa.

within a plastic cylinder attached to an
should be assessed; individual motility is the
l8-iJ1. handle, with a test tube attached to
more accurate measure and should be used
the cone, is used. ln some bulls, ejaculation
for classilication of the bull.

is seen only after a final series of momenta.ty

Gross motility is a function of spem1
pulses at 1- to 2-sec intervals. Older bulls
concentration and individual sperm motility

BREEDING SOUNDNESS EXAMINATION OF THE MALE

2233
and is evaluated in an undiluted drop of
alternatively, testicular degeneration. For
semen placed on a slide without a coverslip
a better assessment of the types of cells
and exan1ined at low power ( -lOOx). The
present in semen, staining an air-d1ied smear
intensity of wave motion may be classified
of fresh semen with Romanowski stain is

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into fom categories: very good-intense
recommended. This simple technique can
swirling, rapid dark and light waves;
provide critical infom1ation, in particular
good-slower swirling, waves not as
when cells other than mature sperm are
intense; fair-slow movement with fewer
present in the sample.

waves; or poor-very little or no swirl

A san1ple of the semen should be fixed in
activity. Individual motility is assessed in
a buffered fonnaldehyde saline solution to
a sample diluted with warmed saline or
evaluate spenn morphology. This is best
semen extender. A drop of diluted sperm is
done with the fixed, w1stained sperm
placed on a slide, covered with a coverslip,
examined under high power ( l,OOOx) using
and examined at 200--400x. The proportion
a phase-contrast microscope. At least 100
of sperm that are moving progressively
sperm should be counted, and the
across the field of view is estimated by
proportion of sperm showing different
finding multiple groups of -10 sperm and
types of abnormaljties noted. However, the
estimating how many sperm are progressive only munber used in the evaluation of the versus how many are not.

bull is the proportion of nonnal spenn,

The environments in which BSE are done
which should be >700/o. Spem1 plasma
are variable, and there is a high chance of
integrity, which is required for sperm
temperatW"c shock to sperm before they
fw1ction, can be assessed with the use of a
may be evaluated. Therefore, >300/o
vital stain such as eosin. Eosin penetrates
individual progressive motility, or fair gross
cells with a disrupted sperm membrane,
motility, is considered acceptable. If the
which appear pink on evaluation under light
examination is performed tmder optimal
microscopy, in contrast to live cells, which
conditions, some associations ( eg, the
do not stain. Eosin is often combined with

Canadian Bovine Practitioners Association)

lligrosin, which provides a dark background
recommend a minimum of 600/o motility for
that allows better observation of live/dead
a bull to be classified as a satisfactory
sperm cells. An eosin-lligrosin-stained
potential breeder.

smear can also be used to assess spe1111

Visual estimates of spenn motility are
morphology, although it is considered less
considered appropriate for bull classificareliable than using phase-contrast tion in field BSEs. However, in commercial
mjcroscopy of an unstained wet preparaartificial insemination centers, sperm tion. Other, more sophisticated measures
motion evaluation is performed using
of spenn function are not used routinely in
computer-assisted spem1 analysis (CASA),
cattle BSEs, although they may become
which provides more objective values as
more common in referral and artificial
well as specific measures not only of
insen1ination centers. Such tests may
percent motile spem1 but also of velocities
include combinations of fluorescent probes
and the track followed by each spem1. For
and flow cytometry to assess membrane
instance, the combination of measmes such
integrity, mitochondrial function, or spem1
as beat cross frequency, lineaTity, average
chromatin integrity, and functional assays
path velocity, straightness, and curvilinear
such as ability of spem1 to undergo in vitro
velocity have been correlated with bull
capacitation, zona binding, and/or
fertility. Moreover, some of the motion
homologous in vitro fertilization.

measures evaluated by CASA such as

Bulls are classified as "satisfactory
cmvilinearvelocity, straightness, and
potential breeders" if they have no physical
linearity correlate with sperm function such
abnormalities that would prevent breeding
as the acquisition of hyperactivated motility.

and if they meet the mininlal qualifications

The presence of cells other than spennatofor SC, spenn motility, and sperm morpholzoa in the sample should be investigated ogy. Bulls that do not meet these criteria are
while estimating motility. RBCs, WBCs, and
classified as "unsatisfactory potential
excess numbers of round epithelial cells and
breeders" or, if the results are marginal
developing forms of spermatozoa may
or questionable, they are considered
indicate a genital tract abnom1ality. Careful

"classification deferred" and a retest
evaluation of the tract, especially the internal should be recommended.

genitalia, may indicate the source ofWBCs.

The most common cause is seminal

RAMS
vesiculitis. Round, immatW"e germ cells and
spermatozoa with proximal cytoplasmic

In rams, the breeding sow1dness examinadroplets may indicate immaturity or, tion (BSE) is perfonned much as for bulls,

2234

BREEDING SOUNDNESS EXAMINATION OF THE MALE
using an electroejaculator with a smaller

Because the ejaculate is typically collected

(ram) probe. Body score is classified as 1-2,
with an AV, spenn production may be
questionable (underconditioned); 3-4,
measured rather thai1 estimated from
satisfactory; and 5, questionable ( overconscrotal circumference. Semen volume ditioned). Any major abnormalities of the
should be 0.5-2 mL, and concentration

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external genitalia or lumps or irregulaiities

1.5-4 billion spemt!mL.

of the testes or epididymides render the ram
unsatisfactory. Epididymal masses are

STALLIONS
commonly found to be spern1 granulomas
caused by infection withBrucella ovis,

Given the high economic value of some
which is a major cause of reproductive loss
stallions ai1d the willingness to breed horses
in sheep. B ovis may also be associated with based more on tl1eir competitive potential testiculai· atrophy. Scrotal circtunference
tl1ai1 on their breeding soundness, many
should be 2:28 cm for rains 8-14 mo old (>36
resources and expensive tests are
cm is exceptional) ai1d 2:32 cm for ran1s >14
sometimes used to evaluate breeding
mo old (>40 cm is exceptional). Scrotal
soundness, and especially to assess spenn
circumference lower than satisfactory is
function in those stallions proven subfe1tile
questionable. Motility of individual
after their first breeding season or
spermatozoa is evaluated as for bulls, with
displaying potential defects after a routine

> 700A, progressive motility being excepbreeding sotmdness exanlination (BSE).

tional, >300A, satisfactory, 1 OO/er-3()0A,

Classically, a complete BSE of the stallion
questionable, and 00/o unsatisfactory. The
has comprised a history, general physical
percentage of morphologically nmmal
exan1ination, exainination of the external
spenn should be >500Ai; between 3()0A, and
and internal genitalia, culture of urethral

5()0A, is questionable, and <300A, unsatisfacand possibly penile swabs, ai1d collection tory; >800A, norn1al sperm is exceptional.

and evaluation of at least two ejaculates

Presence of >5 WBCs per high power field
collected 1 hr apart for total spern1 number,
is questionable (WBCs ai·e correlated with
spenn motility, and spern1 morphology.

B ovis infection). An ELISA test for B ovis The history should include the stallion's
should be done on range rains and rams
p1ior fertility ai1d type of management used

>9 mo old. A positive test renders the ram
for breeding. If <10 mares were bred,
unsatisfactory. Suspect tests should be
individual mare fertility should be considrepeated. (See also RAM MANAGEMENT, p 2217.) ered if pregnai1cy rates were low. If the

Any rain with one unsatisfactory rating in
stallion has been racing or training recently,
ai1y paraineter is classified "unsatisfactory"; he may have been receiving anabolic steroids
a ram with a questionable rating in any
or other drugs. Stallions recently retired
paran1eter is "questionable.': For a ram to
from a pe1fonnance career may be evaluated
be classified exceptional, he must have
again in 3----6 mo if they fail the initial BSE.

exceptional ratings in scrotal circunlference,

During the physical exan1ination, the
sperm motility, and spern1 morphology. All
stallion should be evaluated for general body
other rams are considered "satisfas;tory."

condition and the presence of any conditions
that might interfere with breeding. Geneti

BUCKS
cally inherited defects, including parrot
mouth and catai-acts, render the stallion unfit

Breeding soundness exanlination in bucks
for breecling. Blindness, lan1eness or ataxia,
has not been detailed to the extent that it
penile paralysis, or other defects that prevent
has in rams. The testes should be palpated
the stallion from breeding also render him
carefully. Brucella ovis infection is rare, but unsatisfactory as a breeding prospect.

sperm granulomas are frequently related to

Recent evidence supports cryptorchidism as
the polled condition; these are most often
a potentially inherited defect in horses, thus
found in the head of the epididymis.

rendering the stallion an unsatisfactory

Cryptorchidism is also common and
prospective breeder.

heritable; as in other species, cryptorchid

Scrotal palpation should be perfonned
bucks should not be used for breeding.

and may be done after the first ejaculation

Testiculai· degeneration is a common cause
when tl1e stallion may be more relaxed.

of fertility loss in older bucks. Semen is

Total scrotal width should measure >8 cm
collected using an artificial vagina (AV);

(preferably >9 cm), as assessed with a blunt
bucks are easily trained for this method and
caliper across both testes together. The
do not tolerate an electroejaculator. An
testes should be finn, resilient, and
electroejaculator might be used only if the
homogeneous on palpation. The epididybuck is sedated. Paran1eters for semen mides nm dorsally along tl1e testes, in a
evaluation are similar to those for rams.

craniocaudal orientation, with tl1e tail most

BREEDING SOUNDNESS EXAMINATION OF THE MALE

2235
caudad. The tail of the epididyrnis is easily
of any abnormalities. They are felt as flaps
palpable, whereas the body and head of the
of peritoneum that form pockets in the
epididyrnis tend to blend with the dorsal
abdominal lining at the 3 o'clock and 9
surface of the testis. Rotation of one testis
o'clock locations at the entrance of the pelvis.

180° (the tail of the epididyrnis being

Semen is collected from the stallion using

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palpated on the cranial aspect of the testis;
an artificial vagina(AV) filled with water at
also called torsion of the spermatic cord) is

-50°C ( -122°F), which typically cools to
common and has no clinical significance in

42° -45°C (107.6° -l 13°F) by the time of
healthy stallions.

collection; some stallions might be

Ultrasonography is also commonly used
accustomed to higher AV temperatures
to evaluate scrotal contents and to take

(50° -55°C [ 122° -131 °F]) for adequate
individual measurements of each testis. A
stimulation, but the internal temperature of
portable console fitted with a linear 5 MHz
the AV should not exceed 55°C (131 °F) at the
transducer typically used for reproductive
time of semen collection. The stallion is
evaluation of mares can be used. The testes
teased to an estrous ( or ovariectomized)

should have a homogeneous echoic
mare; once an erection is achieved, the penis
appearance; a cross or longitudinal sec-
is washed with wann water and blotted dry
tion of a central vein that mns along the
with a paper towel. lithe penile skin is
longitudinal aspect of the testis st:a.Iting at
suspected to harbor potentially transmissible
the cranial pole is a hallmark of the norn1al
bacteria ( eg, Klebsiella pneumoniae or
equine testis and should not be confused

Pseudomonas aeruginosa ), a culture swab
with pathology. The tail of the epididyrnis
of the sheath and fossa glandis should be
and spermatic cord display a homogeneous
obtained before the penile area is washed

"cheesecloth-like" appearance; asymmetric
and rinsed for semen collection. Smegma can
dilations of the vessels of the spern1atic cord
fill the dorsal urethral diverticulwn, located
may be consistent with varicose veins and
dorsal to the urethral process, and harden to
may or may not affect blood flow and testis
forn1 a "bean." This can cause initation and function. Measurements of the width (Y{),
swelling and should be removed. After the
height (H), and length (L) of each testis can
penis is washed and dried, a swab sample of
be used to calculate testis volume and to
the distal urethra is obtained. The stallion is
estimate expected daily sperm output by
then allowed to mount the mare or phantom
applying the following fonnulas: testis

(breeding dwnrny ), and the semen is
volume= (Yv x H x L) x 0.5233 for each testis;
collected by diverting the penis into the AV.

daily sperm output= (0.024 x testis volume)

A second swab sample is taken from the

- 0. 76, in which testis volume is the total
distal uretlu-a inlrnediately after ejaculation.

volume, or the sum of volume for both testes.

The stallion should be given 1 hr of rest

The penis is usually examined while it is
before the second ejaculate is collected.

washed before the first semen collection.

The culture results of the uretlu-al swab

The penis can vary in size with no effect on
san1ples can be difficult to interpret.

fertility. It should be freely distensible from

Prewash penile cultures usually show
the sheath without lesions. Of the internal
moderate to heavy growth of mixed bacteria
genitalia of the stallion, the ampullae,

Preejaculate urethral swabs also may reveal
vesicular glands, and lobes of the prostate
growth of a mixed bacterial population.

gland are palpable per rectum. The vesicular

Growth of Pseudomonas or Klebsiella may glands are difficult to palpate unless the
indicate that the penis has been colonized by
stallion is first teased to a mare in estrus to
these organisms; in the USA these are the
stimulate filling of the glandular lumina with
only bacteria (besides Taylorella equigeni
fluid. The bulbouretlu·al glands are covered
talis, the cause of contagious equine
by muscle, making it impossible to palpate
metritis, see p 1371) that, in some cases, may their structure. Transrectal ultrasonography
be passed to mares and cause endometritis.

can be used to more thoroughly evaluate

The postejaculate uretlu-al swab should yield
each of the accessory sex glands and pelvic
less bacterial growth, because the urethra
urethra. Because of the danger inherent in
has been "washed" by the ejaculate. High
adequately restraining a stallion, some
nwnbers of bacteria, especially of a single
veterinarians perform a transrectal
species, on the postejaculate swab may
examination only if dee.med necessary
indicate infection of the internal genitalia,
because of an abnormal finding on the
most commonly tl1e urethra and/or seminal
remainder of the exanunation, such as blood
vesicles.

or pus in the ejaculate. When perfonn.ing

The ejaculate should be evaluated for
palpation per rectwn on a stallion, the
gross appearance, volume, spenn conceninternal inguinal rings should also be tration, spern1 motility, percentage of
palpated to detemline their size and presence morphologically normal sperm, and

2236

BREEDING SOUNDNESS EXAMINATION OF THE MALE
percentages of specific spe1matozoal
or JC-1 in conjunction with flow cytometry
morphologic abnom1alities. The ejaculate
have also been used to evaluate mitochonshould be free of pus, urine, or blood. The dlial potential and hence integrity. In
n01mal ejaculate may contain gel, a viscous,
addition, the combination of these with other

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clear to cloudy material, that 01iginates from
fluorescent stains offers the advantage of
the seminal vesicles and forms the third and
concomitantly evaluating viability and
last fraction of the ejaculate. Because it is
clu·omatin integrity in a large nw11ber of
ejected last, the gel fraction can be removed
sperm. In this regard, the spenn structure
by having an in-line filter at the mouth of the
chromatin assay, which assesses sperm
collection bottle in the AV (preferred), or
chromatin stability, has been tl10roughly
alternatively, by pouring the ejaculate
reseai·checl in stallions and moderately
through a milk filter once in the laboratory.

c01Telated with fe1tility. It is a good

The analysis of the semen is clone on the
a.cljunctive test for stallions in which routine
gel-free (sperm-rich) fraction. Concentralaboratory test results do not correlate with tion may be determined using a hemocysubfe1tility or infe1tility. Finally, true tests of tometer or a properly calibrated
spenn function (ie, ability to fertilize an
photometric instmment. Several instmoocyte) have been restricted because of the ments specially designed for this purpose
inability to capacitate stallion spem1 in vitro
are commercially available. Sperm motility
or to perform in vitro fertilization in this
and morphology evaluations are perfo1mecl
species. Recent advances in tlus area may
as described for the bull (seep 2231);
pemut tl1e application oftl1ese assays for
however, the sperm concentration is much
more meaningful evaluation of stallion
lower in stallions (typically 100-400 million/
spem1.

mL), so only individual sperm motility is

In addition to assessing sperm quality,
evaluated. Assessment of motility should be
once two ejaculates have been collected, the
performed with both raw semen and semen
total number of spem1atozoa. in each is calcudiluted with a good quality extender. Semen lated as volume (gel-free) x concentration.

should be warmed to 35°-37°C (95°-98.6°F)

The total nwnber of sperm in the second
before assessing spenna.tozoal motility.

ejaculate of two collected 1 hr apai"t is

Notably, conventional measures of spem1
considered a rough estimate of the daily
quality correlate only moderately with
sperm output for that stallion (ie, ejaculates
fertility, and vaiiations in the percentages of
ai·e considered to be representative if the
motile/progressively motile and morphologisecond ejaculate contains about half the cally n01mal spenn account for only 200/o of
number of spenn as tl1e first). The second
the total variation in fertility. Given the
ejaculate should have a.bout the same, or a
limitations of standard spem1 tests in predictslightly higher, percentage of morphologiing fertility or identifying s.ubfertile stallions, cally nom1al spem1, as well as the saine or
other sperm tests have been evaluated ai1cl
better motility than the first. If spenn
may be applied for stallion BSEs perfmrned
numbers or quality differ from this guideline,
in referral centers. While not necessaiily
then either prolonged spern1 storage in the
providing a better correlation with fertility,
excwi:ent ducts has occwi:ed ( see below),

CASA offers a more objective and complete
or one of the ejaculates was not complete,
assessment of spem1 motion characteristics.

and a third ejaculate should be obtained. The

As in bulls, certain changes in different
third ejaculate should have a.bout half as
motion pai·an1eters, nan1ely increases in
many spe1m as the second ejaculate, and the
curvilinear velocity and decreases in linearity
saine or better morphology and motility. A
and straightness, correlate with the
tlurcl ejaculate may also be collected if the
acquisition of hyperactiva.tecl motility, which
sperm evaluation does not appeai· to agree
has been recently chai·acte1izecl in stallions.

with the total scrotal widtl1 ( eg, high sperm

In addition, computer-assisted sperm head
nun1bers from a stallion with small testes) or
morphometry (shape) assessment has been
the calculated daily sperm output. Prosuggested as a useful a.cljunctive test to longed storage of spern1 in the excurrent
predict stallion fertility. Membrane integ1ity
ducts results in high numbers in the initial
can be easily evaluated via eosin-nigrosin
ejaculate, but these spe1m may have poor
staining (as in bulls), and tl1e hypoosmotic
motility and morphology.

swelling test or ability of spem1 to swell to

Some stallions with extreme spern1
establish an osmotic equilibritm1 with a
storage require daily collection for 7-10 days
hypoosmotic surr0tmding mediwn may also
before representative ejaculates ai·e obtained
hold some value for spenn membrane

( spenn evaluation results ai·e consistent on
evaluation; however, a direct correlation
successive collections). In extreme cases,
with fertility has not been established.

sperm may a.ccwnulate in the ainpulla.e and

Fluorescent probes such as rhoclainine 123
inspissate, causing blockage of the ductuli

BREEDING SOUNDNESS EXAMINATION OF THE MALE

2237
deferentiae. This may result in no sperm or
ported semen. Under these circumstances,
few sperm, typically with detached heads,
longevity of spermatozoal motility should
present in the ejaculate. Multiple attempt.s at
be tested using commercial semen
collection may be necessary before the
containers before a decision is rendered
blockage is cleared. Relief of the blockage is
regarding fertility potential.

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typically evident by the ejaculation of very
large numbers of dead sperm with detached

BOARS
heads.

In cases of severe ampullary blockage

In postpubertal boars, testes should be
or in stallions with ejaculatory problems,
synui1etric ( <l cm difference), with each
attempts at semen collection might initially
testis having a minin1um length and width of
yield only clear seminal fluid. In such

8 and 5 cm, respectively. Semen is collected
instances, it might be warranted to
with the boar mounted on a phantom or an
differentiate between these problems and
estrous sow. As the penis is extruded, the tip
azoospermia (ie, lack of sperm production)

(incorporating the coiled part) is grasped
before successive semen collection
with a gloved hand and compressed; this
attempts. For this purpose, collected
stimulates full erection and ejaculation. The
seminal fluid can be submitted for
opening of the urethra is -1 cm proxinlal to
determination of alkaline phosphatase
the tip of the glans, and care must be taken
levels. Because alkaline phosphatase
not to block it while applying digital
concentrations are high in epididymal fluid,
pressure. The volume of semen is high, and
a value <100 U/L is consistent with blockage
ejaculation occurs over a long period, so
or ejaculation failure, whereas a value
semen is usually collected into an insulated

> 1,000 U/L is consistent with collection of
container to maintain a relatively constant
epididymal fluid and thus true azoospem1ia.

temperature. A filter or opened gauze

In a satisfactory potential breeding
sponge is fastened across the opening of the
stallion, sperm numbers after >5 days of
container to filter out gel and debris. Nom1al
sexual rest should be ;;:8---10 billion in the
semen values for the boar are volume,
first ejaculate and ;;:4 billion in the second

50-500 mL; sperm concentration,
ejaculate. Total spem1atozoal motility

>50 x 106/mL; progressive motility,
should be ;;:65%, and progressive motility

> 700Ai; total sperm per ejaculate, >60 x lOq;

;;:5()0A,. At least 50% of the spem1 should be
and percentage of morphologically n0tmal
morphologically nom1al. A stallion is
spenn, >800A,.

considered satisfactory if it produces at
least 1 billion progressively motile and

DOGS
morphologically normal spem1 in the
second ( or third) ejaculate of two ( or three)

A complete breeding soundness examinacollected 1 hr apart.

tion (BSE) in dogs consists of a history,

Stallions are classified as "satisfactory,"

physical examination, semen evaluation,

"questionable," or "unsatisfactory" potential and testing for Brucella can is. If infe1tility breeders based on the results of the above
is suggested from the history, it should
detailed examination. However, classificabe established that adequate breeding tion can be somewhat subjective, and an
management was practiced and that bitches
excellent finding in one category can
had normal fertility when bred to other
balance a marginal finding in another.

dogs. The time sequence of litters sired and

Satisfactory potential breeders should
bitches that did not conceive should be
achieve a seasonal pregnancy rate of >800A,
recorded, as should any recent illness during
when bred to 50 mares by natural breeding
or before the time the bitches were bred.

or to 120 mares by artificial insemination

These should be assessed to determine
under no1mal management conditions.

whether the infe1tility may be transient ( eg,

Questionable potential breeders may
fever can adversely affect semen production
experience difficulty in doing the above.

for >60 days after the initial insult).

Typically, stallions are placed in this

A general physical examination should be
category if a problem is detected that might
performed. Dogs with abnonnalities such as
resolve over time with or without treatment; severe joint disease or spinal problems may thus, a recheck is reconunended within
not be able to mom1t. Endocrinopathies

6-12 mo. Unsatisfactory breeders have
such as hyperadrenocmticism or hypothyproblems that may profoundly reduce their roidism may reduce fertility; these may be
fertility or have undesirable heritable traits
associated with abnonnalities in weight or
that may be transmissible to their offspring.

hair coat. The penis and prepuce should be

Some stallions may be used to inseminate a
exaniined; problems such as persistent
percentage of mares with cooled-trans-
frenulum, growths, or swelling due to

2238

BREEDING SOUNDNESS EXAMINATION OF THE MALE
balanoposthitis may prevent nonnal
veterinarians freeze swabs of estrous bitch
intromission. Abrasions or lacerations on
wine or vaginal secretions for this purpose,
the penis may bleed during breeding, and
but the reaction of male dogs is variable.

blood may be seen in the semen.

A collecting cone such as tl1e liner of a bull

The prostate should be digitally palpated
artificial vagina, lubricated with sterile

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per rectum. The most common prostatic
nonspennicidal lubricant or petroleumjelly
problem in mature (>5 yr old) intact dogs is
and attached to a test tube, can be used. The
benign prostatic hyperplasia (BPH); the
penile sheatll is gently pulled back, and the
prostate appears uniformly enlarged and is
cone is slipped over the penis. As soon as the
not painful on palpation per rectum. Dogs
bulbus glandis is exterio1ized from the sheatl1
with BPH might be asymptomatic or have a
and is within the cone, tile penis is grasped
history of hematuria and/or hemospennia
through the cone, inl.rnediately caudal to tile
or rectal tenesmus. In dogs with clinical
bulbus. Constant pressure is maintained
signs, the treatment of choice is castration,
caudal to the bulbus, and erection and
although breeding dogs can be treated medieventually ejaculation should be achieved.

cally with 5a-reductase inhibitors, which

Contact of the penis with tile lubricated cone
prevent the conversion of testosterone
typically stin1ulates tl1e dog to thrust into the
to dihydrotestosterone. Treatment is
cone, and the penis is compressed through
important, because affected dogs are
tile cone caudal to tile bulbus as described
predisposed to developing prostatitis.

above. Semen may also be collected witll the

Ultrasonography has become a common
gloved hand technique, by stin1ulating tile
adjunctive tool for prostate evaluation in
dog's penis within the prepuce until a partial
dogs, allowing for accurate measurements
erection is achieved; tile prepuce is then slid
and assessment of the gland's echotexture
caudally, behind the bulbus glandis, and
for identification of potential pathologies, in steady pressure is applied as witll the cone which case a fine needle or biopsy
technique U11til the dog ejaculates. A cup or
instrun1ent can be guided to sample a lesion. tube fitted witll a funnel is held over tile tip The scrotum, testes, and epididymides
of tile penis to collect tile ejaculate. Some
should be palpated. Small, soft testes are
breeders simply use a plastic bag held over
usually associated with poor semen quality;
tl1e penis to collect semen.

greatly enlarged testes suggest orchitis or

The first (prostatic, clear) fraction and
epididymitis. Lumps suggesting neoplasia
the second (sperm-rich, cloudy) fraction
may also be palpable. Scrotal abnormalities
should be collected. After these fractions
such as dermatitis may adversely affect
are ejaculated, close inspection of the
semen quality by decreasing scrotal
collection tube should demonstrate that
them1oregulation. Length, width, and height clear (prostatic) fluid is starting to layer on of testes should be measured with blunt
the cloudy second fraction; at this point, tile
calipers; these ri1easurements are often of
collection may be stopped. The dog may
value for future comparison in cases of
continue to ejaculate prostatic fluid for up
suspected testicular degeneration.

to 10 min before the erection subsides. The

Additionally, total scrotal width is highly
sheatll should be exanlined after tile penis is
correlated with body wt and an estimate
retracted to ensure tllat the penis is situated
of the dog's spenn production potential.

nonnally witllin tile sheatll and that no hair

Ultrasonographic examination of the
is caught within tile sheatll. Residual
scrotal contents is valuable not only to
protrusion may occur if the sheath rolls
obtain more accurate measurements
inward as tile penis retracts.

but also to evaluate for the presence of

Semen evaluation consists of detemlinatesticular or epididymal masses, which may tion of appearance, volume, concentration,
not always be readily palpable in the early
motility, and percent morphologically
stages of a pathologic process.

normal sperm. Yellow, brown, or red samples

Semen collection is performed witll the
may indicate tile presence of blood or urine
dog on good footing ( eg, a rug) rather than
in the ejaculate. The volume is variable,
on a slippery surface or table. Care should
depending on how much prostatic fluid was
be taken not to intinlidate the dog; thus, any
collected and tile size of tile dog; it ranges
general exanlination procedures are best
from <2 to >20 mL but is typically -5 mL.

perfonned after semen collection. Semen

Spem1 motility should be evaluated
may be collected in tile absence of a bitch
immediately using wanned equipment; this

(altllough sperm munbers may be lower),
should yield> 700/o progressively motile
but the presence of a bitch is preferable,
spermatozoa. Sperm morphology is
especially for inexperienced dogs. The
detemlined as for bulls (seep 2231). At least pheromone methyl paraben may be helpful

800/o of the spem1 should be morphologically
for collection in tile absence of a bitch; some normal. The concentration is detemlined

EMBRYO TRANSFER IN FARM ANIMALS

2239
using a hemocytometer. To do this, the
the feedback mechanism to the pituitary.

sperm is diluted at 1: 100, and the number of

Because abnonnal spem1 quality may be
sperm in the large central square (made up of induced by a recent transient disease or 25 smaller squares) on the hemocytometer is
exposure to toxins, and spem1atogenesis
counted. The nun1ber of sperm counted x 106
might resume, collections should be repeated

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is the concentration of spermatozoa/mL. The
about every 3 mo for -1 yr before a definitive
total number of spenn in the ejaculate is
prognosis for breeding can be given.

calculated as volume x concentration. Total

Azoospemlia is relatively common in dogs.

sperm nun1ber in the ejaculate ranges from

It may be due to failure of the clog's testes to

400 x 106 to> 1,000 x 106 and is correlated
produce sperm, or to failure of the sperm to
with body wt; as a general rule, a dog should
exit the testes because of epidiclyrnal
produce -10 x l 06 spem1/J.b body wt.

blockage or incomplete ejaculation. As in

Every dog investigated for infertility
stallions, the ejaculate may be tested for the
should be screened for Brucella canis.

presence of alkaline phosphatase, which is

(See also BRUCELLOSIS TN DOGS, p 1402.)

secreted by the epididymis. A high value

Spenn quality may be nonnal or

(5,000----40,000 ll!L) indicates fluid from the
abnormal, or no sperm may be seen in the
epidiclynlis was collected and thus is
ejaculate. lnfertility is rare in dogs with a
consistent with true azoospennia Low
normal sperm evaluation and, if seen, the
values ( <5,000 ill!L) suggest epidiclyrnal
history should be reviewed for mismanageblockage or ejaculation failure; semen ment or bitch infertility. The presence of
collections should be repeated, using a

WBCs or RBCs in the ejaculate suggests
strong stimulus such as a bitch in estrus.

inflanunation of the tract, most commonly

A cystocentesis should be performed after
prostatitis; culture of prostatic fluid and
semen collection to cletemline whether
appropriate treatment may help fertility.

retrograde ejaculation is occurring; swab

If sperm quality is abnormal, the history
san1ples of the vagina of a bitch after natural
should again be reviewed to detennine
mating may also be performed to detemline
whether the dog has been sick recently or
whether the dog is not ejaculating because
has received any drugs, especially anabolic
of aversion to manual collection. Careful
steroids. Other recognized causes of
palpation and ultrasonographic exanlination
abnormal sperm quality include inflanunashould be perfmmed to detect any abnormaltion of the scrotum or other factors that may ity of the epididymides or spermatic cords, be causing a high scrotal temperature,
such as absence ( epididyrnal aplasia) or
testicular neoplasia ( ultrasonography of
blockage of the epididynlis.

the testes is recommended because many

A dog is considered "satisfactory" if all
neoplasms of the testes are not palpable),
the above findings are within nom1al linlit'l
trauma to the area of the scrotum, or
and the dog is seronegative for B canis.

brucellosis. However, most cases of low

Breeding dogs should be retested annually
sperm quality in dogs are idiopathic.

for B canis. As in other species, "question

The dog's pituitary status can be investiable" dogs are those with a condition that gated but is usually unrevealing. Luteinizing
nlight resolve over time ( eg, recent febrile
hormone and follicle-stimulating hom1one
episode with temporary testicular degeneraare typically nonnal to high in dogs with tion, BPH), whereas a dog with an untreatabnormal semen quality, because the able condition or an inllerited disorder is
degenerating testes are not able to provide
classified as "unsatisfactory" for breeding.

EMBRYO TRANSFER IN FARM ANIMALS

Embryo transfer has proved to be a
strategic use of elite females through
powerful technology in genetic improvemultiple ovulation embryo transfer ment of farm aninlals, primarily to

(MOET) programs. In addition to
propagate the genes of females of superior
conventional methods to produce embryos
pedigree. In cattle, particularly in the dairy
available for transfer, new technologies
industry, breeding programs have been
that produce embryos after cloning by
developed to promote genetic progress by
somatic cell transfer or transgenesis are

2240

EMBRYO TRANSFER IN FARM ANIMALS
available but not widely used commeris typically administered (IM) over 4-5
cially.

consecutive days, twice daily in decreasing

Embryo transfer protocols have also been doses. Both conunercial FSH preparations extensively used in research c1itical to
can be diluted into 20 mL of saline solution

VetBooks.ir
understand several areas of biology and
and given over 4-5 days. A typical 4-day FSH
medicine, such as fetal-maternal interactreatment protocol is as follows: day 1, 4 mL
tions, models of human and animal
bid; day 2, 3 mL bid; day 3, 2 mL bid; day 4,
diseases, production of transgenic animals
l mL bid (total volume= 20 mL). FSH
to produce therapeutic proteins for people,
treatments typicalJy begin on day 10 after
etc. However, this discussion is restricted to
estrus. On the Utird or fourth day of FSH
the principles and methods currently used
treatment, a. luteolytic iajection of PGF2o is
in commercial embryo transfer offaim
given and repeated 12 hr later. Estrus can be
animals. Except in horses, embryo transfer
expected 36-48 hr later, and the artificial
programs in most manm1als include
insemination can be scheduled based on the
administration of drugs that superovulate
observed heat (12 and 24 hr after onset of
females to allow the probability that
estrus) or by appointment (72, 84, and 96 hr
multiple embryos are collected per
after the administration of PG F 20<) that is
procedure. Globally, it was reported in 2012
accompanied by administration of an a.gent
that 699,586 bovine embryos were collected
to induce ovulation, human chorionic
from superovulated cows, and 443,533
gona.dotropin or gonadotropin releasing
bovine embryos were produced via in vitro
hormone (GnRH). Many variations of
fe1tilization procedures.

methods to increase tl1e efficiency of
superovulation prograins in cattle exist.

CATI LE

For example, the induction of a new follicle
wave before gonadotropin treatments is

Although collection of a single embryo is
desirable to increase the ova.iy response to
occasionally done in cattle, the vast
superovulatory treatments. lr\jections
majority of embryo transfers in cattle are
of estradiol or GnRH, or transva.ginal
progranm1ed after a hormonal treatment to
aspiration (follicle ablation) of the
superovulate donor cows and to maximize
dominant follicle (known as dominant
recovery of embryos during tl1e collection
follicle removal [DFR]) a.t'e examples of
procedure. In cattle, there are two generally
approaches to induce a new follicle wave. A
accepted methods of superovulation. One
new follicle wave emerges 4, 2, or 1-2 days
method consists of administering a single
after treatments with estradiol, GnRH, or

IM irtjection (2,000-2,500 IU) of equine

DFR, respectively. Responses to gona.dotrochorionic gonadotropin ( eCG), typically on pin treatments to induce superovulation are
day 10 of tl1e estrous cycle (in which.day O
best when treatments are statted when the
is defined as the day cows are observed in
follicle wave emerges. These treatments
estrus), followed 2--3 days later by two
aim to promote a more uniform follicle
iajections of prostaglandin F2o ( dinoprost
recruitment and growth that ultimately may
or cloprostenol) 12-24 hr apart. The other.

result in more viable embryos per procecommonly used method is to administer dure. In the USA and many other countries,
follicle-stimulating hormone (FSH). The
the use of estrogen prepa.t'ations is not
superovulatory response induced by eCG
approved for use in reproduction.

treatment is often greater than that induced

Management of recipients can be done
by FSH; however, more embryos of
after observation of natural estrus or based
transferable (good) quality are produced
on synchronization protocols. In either
on average after FSH treatment. For this
scena.iio, a luteolytic dose of PGF2o is given
reason, FSH has become the method of

-12 hr before the first treatment of PGF2o of
choice of superovulating cows for
donor cows. Recipient cows ovulating on
commercial use. The two most conm1only
the satlle day as donor cows are preferred
used commercial FSH preparations are
for emb1yo transfer, but asynchrony of
made from porcine pituitary extracts and

± 1 day has produced pregnancy rates
contain some contatnination witl1
comparable to tl1ose of perfectly synchroluteinizing horn1one (LH). Whereas high nized recipients. It is expected that 75%-90"A, amounts of LH in FSH preparations may
will respond to the superovulation
interfere with optimal superovulato1y
treatment, but 20"/o--30% of flushed cows
response, it is believed that a low level of LH do not produce embryos of transferable contanlination does not interfere and may
quality. Among tl1ose cows tl1a.t successfully
even be needed for superovulation.

respond to the FSH treatment, the variability

Although some good results have been
in producing good quality embryos is very
reported with a single administration, FSH
good (from Oto >20 per flush). On average,

EMBRYO TRANSFER IN FARM ANIMALS

2241
a production of 5-7 embryos of good quality

All embryos are transferred to a clean
per embryo collection is considered a good
dish (with wells) containing holding media
conunercial outcome.

similar in composition to the flush media

Embryo collection is done on day 7 of
except for a higher concentration of bovine

VetBooks.ir
the cycle when uterine stage embryos
fetal/calf serum (10%--200Ai) or bovine serum

(morula and blastocysts) are expected to
albumin (0.4%). As with flush media,
be recovered. Before the embryo colleccomplete holding media are also available tion, the donor cow is palpated and the
conu11ercially. Embryos are then visualized
ovarian response to the superovulation
at a higher magnification ( 40--60x) and
treatment assessed manually by deten11inclassified according to theiI morphology, ing the number of palpable corpora lutea in stage of development ( unfertilized oocytes, the ovaries. The procedure to collect the
early morula, tight morula, blastocyst,
embryos from the uterus (flush) involves
expanded blastocyst, hatched blastocyst,
the following steps: 1) An epidural with
etc), and quality (excellent, good, fair, poor,

5--7 mL of lidocaine is given. 2) The
degenerate). The quality score is based on
perineum is carefully washed with hand
morphologic assessment of the physical
soap or an antiseptic scrub ( chlorhexidine
integrity of embryos and morphologic
or iodine); depending on the animal and
characteristics according to the stage of
cervical size, a 12--24 French Foley-type
emb1yonic development, compaction
catheter placed over a metal rod (stylet) is
status, color of cytoplasm, areas of cellular
introduced in the vagina as the palpating
degeneration, number of extruded
arm is placed in the rectum to manipulate
blastomeres, size of perivitelline space, and
it through the cervix. 3) Once inside the
the size and sphericity of the embryo.

uterus, the catheter is advanced beyond

Only emb1yos classified as fair, good, or
the uterine body until it is located at the
excellent should be transferred. Embryos are
first third of one of the uterine horns; the
kept in holding media after being "washed"

rod inside the catheter is then withdrawn
at least tlu·ee times. Embryo washing is
and the cuff is inflated with 15--20 mL of air, pe1fom1ed by transferring emb1yos into depending on the size of the uterine horn,
different, clean wells containing holding
which varies with breed, age, parity, etc.

media This procedure, reconrn1ended by the

4) Each uterine horn is then flushed with

International Embryo Transfer Society, aids
commercially available, complete, and
in removing cellular debris and potential
ready-to-use flushing media; these embryo
pathogens adhered to tl1e zona pellucida.

flushing solutions also contain antibiotics

Embryos are kept in holding media at room
and bovine serum albumin as a source of
temperature until tl1ey are transferred to
protein. Some commercial preparations
recipients or prepared for freezing, bisection
of complete flush media also contain

("splitting"), or detennination of gender by surfactants to minimize the formation of
emb1yo sexing. Alternatively, embryos can
foam and bubbles in the embryo search
be refrigerated in transfer mediun1 for up to
dish. In the past, the flush media had to be

24 hr witl1 no appreciable loss of viability.

prepared for each collection and consisted

Splitting embryos into identical halves by
primarily of Dulbecco's phosphate
microsurgery is practiced by a few cmmnerbuffered saline with added antibiotics and cial embryo transfer tea.ms. The number of

1 % fetal/calf bovine serum ( or alternatively,
embryos to be transferred can be doubled

0.1 % bovine serum albumin); around the
with only a minor reduction in pregnancy
world, many flushes are still prepared in
rates. However, techniques to freeze
this manner. 5) The uterine horn may
manipulated embryos requi!e improvement.

be lavaged by repeated small volume

Si.nee 1978, tl1e CUITent preferred and most

(25-50 mL) infusions of flush media that
c01mnon method to transfer cattle embryos
are allowed to drain into an embryo filter.

into synchronized recipients is via nonsurgi

Alternatively, the uterine horn may be
cal techniques. The embryo is loaded into a
flushed continuously; 1--2 L of flush media
small plastic straw (0.25 mL) fitted into a
is used to flush a cow uterus. 6) After the
specialized (Cassou-type) insemination
flush is completed, the cuff is deflated and

"gU11." The emb1yo transfer gU11 is tl1en
the contents of the catheter are carefully
placed into tl1e vagina protected by a
allowed to flow into the emb1yo filter
disposable sterile cover sheath to prevent
located at the end of the outflow tubing.

contamination of the tip of the gun with

7) The embryo filter is then taken to the
potential perinea] and vaginal contaminants.

laboratory, and its contents are dispensed

The gun is passed through tl1e cervix, aided
into a search dish with grid and visualized
by palpation per rectum, and advanced into
using a stereoscope ( dissecting microthe ute1ine horn ipsilateral to the corpus scope) at lOx magnification.

luteum. The contents of the straw are then

2242

EMBRYO TRANSFER IN FARM ANIMALS
deposited as cranial as possible into the
given. Estrus is typically detected by
uterine horn with care to avoid prolonged
vasectomized bucks/rams; artificial
and unnecessary manipulation. After direct
insemination should take place 12---24 hr after
transfer of single fresh embryos, 60%---700,1, of
estrus is detected or 45---50 hr after progestarecipients are expected to become pregnant; gen removal. Intracervical or transcervical

VetBooks.ir
transfer of two embryos may result in
aitificial insemination is difficult and requires
pregnancy rates as high as 900Ai. A significant
advanced training and practice. Increased
proportion of bovine embryo transfers are
pregnancy rates are obtained by laparoscopic
made with frozen-thawed embryos ( ---46%)

artificial insemination, because it allows the
and, with good management, pregnancy
semen to be deposited in the cranial aspect
rates routinely are >500Ai. Under the same
of the utetine horns.

management conditions and well-trained

Surgical embryo collection is still very
staff, the pregnancy rate of frozen-thawed
common, but lapai·oscopic and nonsurgical
embryos is expected to be lOOAi lower than
transcervical catheterization procedures
that de lived from transfers of fresh bovine
are consistently improving and yielding
embryos. Although increased pregnancy
good results, albeit still lower than those
rates may be obtained with transfer of
obtained with surgical methods. Embryos
multiple embryos, the tisk of dystocia and
are collected 7---8 days after estrus.

retention of fetal membranes associated
with twin pregnancies and the increased

PIGS
probability of producing freemartin calves
preclude widespread use of this approacl1.

Embryo collection and transfer in pigs is

The use of sexed semen in embryo transfer
not yet done commercially or as intensively
programs is considered economically viable,
as in ruminants. Until recently, embryo
especially if attention is given to inseminate
transfer in pigs was primarily perfonned
donor cows with spe1m numbers comparafor research purposes. In 2012, Canada, ble to those used in artificial inseminations

France, and Ireland were the only countries
with conventional nonso,ted semen.

to report the commercial collection and
transfer of 2,4 78 swine embryos. Owing to

SHEEP AND GOATS
the high ovulatory rate in sows, superovulation treatment may or may not be used in The amotmt of embryo transfers done in
embryo transfer procedures. Embryo
small ruminants are a fraction of those
collection can be done soon after a genetirecorded for cattle. Globally, almost 900,000
cally valuable sow is slaughtered and the
embryo transfers were repmted for cattle in
reproductive tract is collected for embryo

2012, while only 12,458 were reported for
retrieval. Surgical collection of embryos
sheep and 1,013 for goats. In addition to
is also performed using ventral laparotcommercial and market fac.tors limiting the omy of the caudal abdomen. Most embryo
production of emb1yos in small ruminants,
transfers are performed using surgical
current embryo transfer techniques in
techniques (abdominal ventral laparotsheep and goats almost exclusively consist omy under general anesthesia). Recently,
of surgical and/or laparoscopic methods for
nonsurgical techniques to collect and
embryo collection and transfer.

transfer porcine embryos have been

Donor and recipients are synchronized
developed ai1d proved successful, but they
using progestagens with an i.Itjection of
require specialized equipment and highly

PGF2a given on the day the intravaginal
skilled individuals. Embryos are typically
progestagen device is inserted. Because of
collected 4-7 days after ovulation. Current
the additional superovulation honnonal
pregnancy rates with nonsurgical techtreatment donor females receive, recipients niques remain lower than those obtained
come into estrus earlier than donor ewes
after surgical embryo transfers. Embryos
and does; therefore, the progestagen source
should not be transferred to the uterine

(typically an intravaginal device) in
body, because this results in low pregnancy
recipients is removed 12 hr before it is
rates. The transfer of 16---22 embryos per
removed in donors.

recipient is recommended to achieve

FSH is commonly used to superovulate
optimal pregnancy rates.

small ruminants. As in cattle, FSH is
commonly administered twice daily in a

HORSES
seties of decreasing doses administered over

3 days (eg, day 1 = 5 and 5mg; day 2 = 3and 3

Embryo transfer in the equine industry has
mg; day 3 = 2 and 2 mg). On the last day of
been prin1arily used to obtain offsp1ing from

FSH treatment, the progestagen source is
mai·es with rest1icted reproductive potential
removed and a luteolytic iltjection of PGF2a

(mares with undiagnosed subfe1tility,

EMBRYO TRANSFER IN FARM ANIMALS

2243
uterine pathologies, or simply older mares)

recipients. Daily ultrasonography of the
or from pe1fonnance mares that must
uterus and ovaries of donor and potential
remain nonpregnant to continue to compete.

recipient mares during estrus provide critical

Most breed associations allow the registrainforn1ation about the time of ovulation, tion of foals born by embryo transfer, and an
which is essential for detern1i.ning the day of
increasing number now allow the registraovulation and day of embryo collection and VetBooks.ir
tion of multiple foals born in the same year.

to assist in the selection of qualified recipient

Because of this recent increased acceptance
candidates for embryo transfer.

by breed registries, many horse breeders

Nonsurgical techniques are currently
have obtained several foals in one breeding
used to collect and transfer horse embryos.

season from a single donor mare.

Embryo collection is usually perforn1ed on

Superovulating mares with a purified
day 7 or 8 ( day O = ovulation). The use of
form of equine follicle-stimulating horn1one
good standard techniques generally yields
extract preparation ( eFSH) to increase
a recove1y rate of -75%; this rate can be as
ovulation and embryo recovery rates is no
high as 900;6 for young maiden or fe1tile
longer commonly done commercially.

mares or as low as 100/o--200;6 in subfertile

Difficulties with manufacturing suitable
mares. Before embryo collection, palpation
gonadotropins and the variable response
per rectum and ultrasonography are
of mares to FSH stimulation have preperforn1ed mainly to docwnent the presence cluded widespread commercial use of this
of the corpus luteun1, the degree of cervical
approach to produce equine embryos. It
tone, and absence of any fluid in the uterus.

was thought that the low embryo recovery

Mild soap or povidone-iodine scrnb can be
rate in mares ovulating >4 follicles/ovary
used to wash the perinea! region, followed
could be attJibuted to an inability of the
by a thorough rinsing with clean water.

ovarian fossa to accommodate multiple

Sedation is not used in most cases, but
ovulations in that area, or alternatively,
it may be needed when working witl1
excessive response to the FSH stimulation
uncooperative mares. Acepromazine should
could result in dysmatured oocytes.

be avoided, because it may cause relaxation

A recent advance in embryo transfer
of the uterus and potentially impair fluid
technologies in commercial settings has
recovery or manipulation of the reproductive
been the possibility of producing in vitro
tract during flushing of tl1e uterus; sedation
equine embryos using intracytoplasmic
with an etragoni.st ( eg, xylazine, detomidine)

sperm injection (ICSI). Frozen semen from
is preferred. Embryo collection is perfom1ed
deceased stallions can be efficiently used to
using a routine transcervical uterine lavage
produce in vitro embryos by using only a
procedure, using a silicone catheter with an
portion of a frozen semen straw to provide
inflatable cuff. Using sterile technique, the
spern1 for the ICSI procedure. The number
silicone catheter (2� in. long, French
of ICSI-derived equine embryos is expected
size 28--37, depending on the size of the
to continue to increase sharply during the
reproductive tract of tl1e mare) is introduced
next few years.

through the cervix into the uterns, and then

The horse embryo is notoriously
tl1e balloon is inflated (typically 60--80 mL)

challenging to cryopreserve, probably owing witl1 air or collection mediun1; the catheter is to its relatively large diameter and the
then gently pulled back so tl1e cuff seals the
presence of an embryonic capsule that limits
internal cervical os. Complete flush media
interaction between cryoprotectant agents
with antibiotics, surfactant, and bovine
and the embryo. Embryos of mornla or early
serum albun1in is available commercially and
blastocyst stage ( <6.5 days after ovulation)

ready to use. Alternatively, as with cattle,
are preferable for cryopreserving, because
flush media can be prepared with Dulbecco's
after thawing, older embryos have invariably phosphate-buffered saline and 1 o/o--5% fetal low morphologic quality that results in poor
bovine sernm; 1-2 Lare infused into tl1e
pregnancy rates. A vitrification media for
uterus and then allowed to flow back into
horse embryos is commercially available,
a graduated cylinder or plastic bucket to
and acceptable pregnancy rates varying
measure the recovered volun1e. Once the
from 40%--6()0;6 have been reported.

uterns is filled, it can be gently manipulated

Successful cryopreservation of expanded
per rectw11 to aid the recovery of fluid. An
equine blastocysts also has been reported
embryo filter equipped with a 75-micron
for embryos tl1at had their blastoceles
mesh is usually connected to tl1e end of the
collapsed after embryo biopsy procedures.

outflow tubing to yield -40--60 mL of fluid. In

Because one of two embryos are typically
some cases, an ir\jection of oxytocin (10 IU)

recovered from the donor mare, it is
may be given to minimize the retention of a
in1portant that breeding soundness
large amount of flush media in the uterns.

evaluations are done for both donor and

The recovered fluid should be clear and free

2244

EMBRYO TRANSFER IN FARM ANIMALS
of significant amow1t of deb1is and blood.

the estrous cycle and daily transrectal

Nearly lOOOAiof the fluid used to lavage the
ultrasonography. Good pregnancy rates
utems should be recovered. A total of 4-8 L
result from using recipients that have
offlush media is used to complete the
ovulated from l day before the donor to 3

VetBooks.ir
embryo collection procedure (flush). If
clays after the donor. In addition, progestaretention of fluid is suspected or if the gens such as altrenogest may pe used until
outflow of media is intenupted, trans rectal
the day of pregnfil1cy exanlination 4-5 days
ultrasonography may be used to assess the
after the transfer ( -12-13 days of gestation).

presence of intralurninal fluid. A conunon

The nonsurgical embryo transfer is
cause of intermpted outflow drainage of
performed using transce1vical catl1eterizaflush media results from placing the tip of the tion. Plastic straws, 0.25 or 0.5 mL, are used
catheter intrace1vically and not in the body
to load the embryo; tile colW1U1 of medium
of the uterus: the media easily flow into the
containing the embryo should be suruterus but not outward.

rounded by two small columns of air, which

Once the flush is completed, the
fil·e in twn surrounded by two columns of
remaining fluid in the filter is searched in a
medium. The straw loaded with the emb1yo
sterile dish with g1id ru1der a magnification
is fitted into fill emb1yo transfer "gru1."

of 15x using a stereomicroscope. Once the

Emb,yo trm1sfer sheaths with side delivery
embryo is foru1cl, it is transferred to a well
cm1 nlinimize emb1yo damage during the
in a sterile tissue culture dish containing
transfer procedure.

holding media ( commercial, ready-to-use
with 0.4% albru11in or made with Dulbecco's

Preparation for Short Storage and
phosphate-buffered saline plus 100Ai-2()0A,

Transport: Horse breeders without
fetal bovine serwn). The emb1yo should be
m1 adequate nwnber of recipients filld
washed at least 3 times by transfening into
veterinarim1S with modest investment in
two other wells previously filled with
equipment cm1 collect emb1yos filld prepfil·e
holding media. Embryo manipulation is
tl1em for sho1t storage m1d trm1Sport to a
done witl1 a 0.25-mL straw connected to a
centralized embryo trm1sfer facility.

tuberculin syringe with a 16-gauge needle,

Pregnancy rates do not appear to differ
a 0.5-mL straw directly connected to a
from those obtained witl1 fresh embryos,
tuberculin syringe, or a capillfily pipette (20
especially if embryos are shipped cotmte1°to11L) attached to a tuberculin syiinge. After cotmter on the sm11e day they are collected.

being washed, tl1e embryo should be

Embryos fil·e routinely shipped in con1111ertransferred to a recipient mfil·e ( witllin 1 hr) cially available holding media that fil·e
or prepared for short storage and transporready-to-use prepfil·ations containing 0.4%
tation. The stage of the emb1yo (momla,
bovine serwn albru11in m1d m1tibiotics. The
efil·ly, or expanded blastocyst) and quality
embryo is placed into a 2-mL polypropylene

(1, best; 5, dead) should be recorded.

cryotube vial or a 5-mL snap-cap tube tl1at

Although surgical transfer of equine
contains the holding media. The tube witll
embryos was once thought to yield higher
the emb1yo is tl1en placed into a semen
pregnfil1cy rates than nonsurgical transfer
shipping container designed to cool m1d
techniques, the latter fil·e now the preferred
trm1sport horse semen. The container is
method to trfil1sfer horse emb1yos.

preferably shipped to m1 em b1yo trm1Sfer

Recipient mares should be reproductively
facility on the san1e day the collection is
sound and in good body condition and
performed using fill airline carrier ( c0tmterhealth. Synchronization of ovulation should to-coru1ter) or processed for overnight
be maximized by hom1onal mfil1ipulation of
delivery using a commercial carrier.

HORMONAL CONTROL OF ESTRUS

Hom10nes are con1111only used to manipulate animals, and superovulate cyclic aninlals.

the estrous cycle. The major inclications for

Effective treatments for these manipulations
hom10nal control of estrus are to induce lutevaiy ainong species. A nwnber of treatments olysis, induce ovulation of a mature follicle,
currently lack regulato1y approval; label
suppress estrus, induce cyclicity in anestrous instmctions should be followed.

HORMONAL CONTROL OF ESTRUS

2245

HORSES

Treatment with estracliol cypionate is
longlasling, but repeated or high doses may

Estrous behavior may be undesirable in
cause aggressive or defensive behavior
perfom1ance horses and can be suppressed
when the mare is approached by a sLallion.

in mares by administration of progestagens,

Treatment with estrogen in the presence

VetBooks.ir
either progesterone in oil (150-300 mg/day,
of progesterone ( eg, in a cyclic mare in

IM) or altrenogest (0.44 mg/kg/day, PO). In
diestrus) will not induce estrous behavior.

the past, oral progestagen was preferable

Ovulation may be induced in mares with
because of muscle in-itation from the
mature preovulatory follicles (>33 mm
injectable preparation. However, progesdiameter) by administration ofhrn11an terone in a biorelease vehicle is available
chorionic gonadotropin (hCG), 2,500 IU, IV;
by prescription from a comporn1cling
by administration of a deslorelin implant,
pham1acy. This preparalion (1.5 g, IM)

2.2 mg, SC; or by administration of
is administered once eve1y 7-10 days.

deslorelin, 1-2 mg, IM, in a biorelease

Treatment with progestagens for 15 clays
vehicle. Ovulation is seen in 85% of ma.res
cltffing the late transition season can
witllin 48 lu, typically 36-42 hr after hCG or
advance the fu-sl ovulation of the year by
injectable deslorelin treatment or 40--44 lu·

-10 days. Although these preparations
after treatment with a deslorelin implant.

suppress estrous behavior, they may not

Repeated use of hCG over a long period is
effectively suppress follicle growth and
associated with antibody formation and
ovulation in cyclic ma.res.

may decrease response to treatment; this

Ovulation may be syncluonizecl in mares
has not been seen with deslorelin. Use of
by administration of progesterone in oil
deslorelin in implant form has been

(150 mg) and estradiol 1713 in oil (10 mg/clay,
associated with periods of anestrus in

IM, for 10 clays) wiLl1 prosta.glandin F2a
treated mares, especially if the corpus

(PGF2a; 10 mg, IM) administered on the
luteum of ovulation is lysecl with prostaglantenth clay. Progesterone plus estradiol in din. For this reason, many veterinarians
a biorelease vehicle is also available by
remove the implant after ovulation is seen;
prescription from a compounding
tlus is easily perfom1ed if tl1e in1plant is
pharmacy. Mares should come into estrus
placed in Llle vulvar mucosa.

-3 days after the end of treatment, and 85%

Mares do not superovulate in response to
of mares ovulate 9-13 days after Ll1e encl of
equine chmionic gona.clotropin (eCG), and
treatment.

they do not respond well to follicle-stimulat

Estrus may be induced in diestrous mares ing hormone (FSH) derived from other (having a corpus luternn that is 5 or more
species, but Ll1ey may be superovulatecl
days postovulation) by treatment with

(average of tluee to fow· follicles ovulated)

PGF�a (10 mg, IM) or cloprostenol (250
by treatment with equine FSI-1 (no longer
mcg, IM) to lyse the corpus luteum. Mares
commercially available in tlle USA). GnRI-1
should return to estrus in -3 clays and
given al 2-20 mcg/hr (by infusion ptm1p)

ovulate an average of 9-10 days after
throughout -10 days induced nonnal
prostaglandin treatment. The time to
follicular growlll and ovulation in anestrous
ovulation is variable, however, depending
mares; the larger close induces superovula.on the size of the largest follicle on the ovary tion (average of three follicles). Cyclicity at the time of prostaglandin administration.

has also been induced in anestrous mares

PGF.,a ca.uses nwnerous transient adverse
by Lreat:ment with 200 mcg GnRH every 6 hr,
effects in h01-ses, including sweating, colic,

500 mcg GnRH every 12 hr, or by admillistraand trembling. Greatly reduced doses of tion of a GnRH agonist, buserelin (10 mcg,
cloprostenol (25 mcg) also effectively

SC), every 12 hr plus hCG (2,500 IU, IV)

induce luteolysis in mares while virtually
once a follicle has reached 35 nun in
eliminating the unwanted adve1-se effects of
diameter. The clopan1ine receptor antago

PGF2a. However, although widely used in
nist dompe1idone (1.1 mg/kg/day, PO) alone
mares, cloprostenol is labeled only for use
or in combination witl1 GnRH (250 mcg, SC,
in cattle. Prostaglandin causes luteolysis
qid) has also been used to stimulate
of a mature corpus luternn and so does
follicular development in mares witl1
not induce estrus in anestrous ma.res.

quiescent ovaries.

Behavioral estrus may be induced in
anestrous or ovariectomized mares by

CATI LE
administration of estradiol 1713 in oil ( 1-10
mg, TM) or estradiol cypionate (0.5 mg, IM).

In cows, ovulation may be syncluonized

Mares should show estrus 12-24 hr after
with a progestagen and estrogen combinair\jection. This estrus is not associated will1
tion treatment, a two-dose prostaglandin
follicular growth and is not fertile.

regil11en, or a GnRH and prostaglandin

2246

HORMONAL CONTROL OF ESTRUS
combination. Administration of PGF2ac (25
head/day for 14 days for estJus synchroniza mg, IM) or prostaglandin analogue ( cloprostion. Fertility after this treatment is low, and tenol at 500 mcg, IM) to cows with a corpus
females should not be bred. This protocol
luteum from 5 days after ovulation results
could be i:Jnproved by adrniniste,ing PGF2ac
in estrus in -2-5 days. Two prostaglandin

17 days after the last feed containing MGA.

VetBooks.ir
ir\jections given 12-14 days apart synchro

The fertility of this estrns is reestablished.

nize estrus and ovulation in most cows.

Ovulation may be induced in cows with

Time to estrns is more variable than with
matme follicles (10-15 mm dian1eter) by
progesterone suppression, so insemination
treatment with GnRH at 100-250 mcg, IM;
should be based on detection of estrus.

luteinizing hormone (LH) at 25 mg, IM; or

Ovulation may also be synchronized by
hCG at 5,000-10,000 IU, IM. Because the
administration of GnRH, 100 mcg, IM ( day
endogenous LH peak develops at the onset

0), followed by prost.aglandin treatment on
of estrns, this administration wiU not speed
day 7 and a second GnRH treatment on day
the time of ovulation in estrous cows but

9. Cows should be inseminated 0-20 hr after
may be used to ensme luteinization in cows
the second GnRH treatment. This GnRH and
with histories of cystic ovarian disease or to

PGF2ac protocol is termed "ovsynch." There i:J1duce ovulation in anestrous postpartum
are many variations on this protocol, using
cows.

additional steroids, prostaglandin, or GnRH

Superovulation may be achieved in cows
treatments, that may increase the degree of
by treatJnent with eCG (not currently
synchrony or pregnancy rates after rutificial
commercially available in the USA) in
insemination.

mid-di.estrus followed by prostaglandin

A progesterone-releasing intravaginal
induced luteolysis 2-3 days later, or by
device (PRID) consists of micronized
treatJ11ent with FSH (potencies differ, refer
progesterone distJibuted homogeneously
to label instructions), typically IM, bid for
in an inert silicone rubber coated onto a

4-5 days, at a decreasing or constant dose
cylindrical stainless spiral coil. The PRID is
with administration of prostaglandin (25-35
maintained in the vagina for 7 days, and a
mg, IM) usually on day 3 or 4 of treatment.

luteolytic dose of PGF2ac is administered 1

FSH treat111ent is discontinued at t11e onset
day before or at "pull-out" day. There are no of estrns.

milk or meat withdrawal requirements. In
noncycling animals, an ir\jection of equine

GOATS AND SHEEP
chorionic gonadotropin ( eCG) is administered when the PRID is removed.

In cycling goats, luteolysis may be induced

A controlled intravaginal drug-release
by administration of PGF2ac (2.5-5 mg, IM)

(CIDR) device may also be used for estrus
or cloprostenol (62.5-125 mcg, IM) as early
synchronization. A CIDR is an intravaginal
as day 3. In sheep, PGF2ac (�15 mg) or
device constrncted of a pi:ogesteronecloprostenol ( 125 mcg) is effective after day impregnated medical silicone elastomere

5 of the cycle ( estrns is day 0). Estrus may
molded into a T-shape. It is labeled for
be synchronized by two doses of prostaglanestrns synchronization in beef and dairy din, 11-13 days apart in does or 7-9 days
cattle. Cows are administered GnRH, and
apart in ewes. Estrns may also be synchroconcomitantly a CIDR is inserted and nized in cyclic or anestrous does and ewes
maintained for 7 days. At the time of
by administration of progestagens;
removal, cows receive an injection of
impregnated intravaginal sponges

PGF2ac. Cows can be inseminated, with or

(medroxyprogesterone or fluorgestone)

without another GnRH injection, 48-72 hr
have been the most widely used agents for
after PGF2ac injection. The most effective
control of ovulation but are not currently
synchronization treatment, an IM i:Jtjection
available for clinical use ill the USA. In small
of a combination of 5 mg estradiol valerate
ruminants, a controlled internal drug
and 3 mg norgestomet, with an ear i:Jnplant
release (CIDR) intravaginal plastic device
of 3 mg norgestomet left in for 9 days, is no
i:J11pregnated with progesterone (300 mg)

longer commercially available in the USA
can also be used. The CIDR is maintained in
because of the ban on the use of estrogens
the vagina for 7 days, and a luteolytic dose
in food anin1als. Note that all estrns
of PGF2ac administered 1 day before or at
synchronization protocols are less effective
device removal. The estrns response is high
in Bos indicus cattle and B indicus
within 72-84 hr. A portion of a bovine
crossbreds than in Bos taurus cattle.

norgestomet ear i:Jnplant (1.5--mg/goat) or

Melengestrol acetate (MGA) is a steroidal
ir\jection of progesterone in oil (10 mg/day,
progestagen used as a feed additive to

IM) has also been effective. In sheep and
promote growth and suppress estrus in
goats, the ear in1plant is placed subcutaneheifers. MGA is used at a dosage of 0.5 mg/
ously near the base of the ear or the base of

HORMONAL CONTROL OF ESTRUS

2247
the tail and then removed 7-9 days later.

after day 12 of tl1e estrous cycle and,

Progestagen treatment is administered for
therefore, is not a practical agent for estrous

10-14 days in sheep and for 14--21 days in
cycle control; however, estrus may be
goats. Ewes should be joined with rams the
synchronized by induction of abortion in
day after cessation of treatment; does return
sows pregnant> 15 days by administration

VetBooks.ir
to heat on the second or third day after
of PGF,a (15 mg, IM, then 10 mg, IM, 12 hr
treatment ends. Injection of equine
later) or cloprostenol ( 1 mg, followed 24 hr
chorionic gonadotropin ( eCG; 100-500 IU)

later by 0.5 mg); sows return to estrus 4--10
at the end of treatment increases synchronidays after treatment. Oral altrenogest zation of ovulation or ovulation rate.

(15---20 mg/day, PO, for 14--18 days) may be

Alternatively, in does, progestagens may be
used for estrus synchronization and for
given for 11 days with eCG and prostaglanimprovement of farrowing rate and litter din administered on day 9, and fixed-time
size in mature sows. In lactating sows, one
insemination perfom1ed on days 12 and 13.

daily dose of altrenogest from the day of

In regimens involving treatments other than
weaning until 5 days before the planned
prostaglandin alone, fertility may be
breeding day is also effective and results
reduced on the first estrus after treatment in in estrus 4--9 days after completion of ewes but not in does. During the non breedtreatment. Estrus may also be synchronized ing season, melatonin implants (18 mg)

by using bovine norgestomet implants ( one
induce fertile estrus 50-70 days after
implant followed by addition of a second
implant insertion. Better results are
implant 9 days later) removed 19 days after
obtained when melatonin implants are
initiation of treatment; neither treatment is
inserted early or during the transitional
currently approved in the USA for swine.

period. The implant is biodegradable and

Combination eCG and hCG may be given on
does not need to be removed. Estrus
the day of progestagen withdrawal to hetter
synchronization may be improved by using
synchronize estrus.

an estrus synchronization protocol at the
end of implant action. During the nonbreed

DOGS
ing season, a source of gonadotropin is also
required. The most common gonadotropin

In bitches, estrus suppression, for no more
used is eCG, administered at the end of a
than 24 mo, can be accomplished by
progestagen treatment ( or 24 hr before
administration ofmibolerone (an androdevice removal). The dose of eCG depends gen, 30-180 mcg/day, PO, depending on
on the season, breed, age, and postpartum
the weight of the bitch). To be effective,
interval, an10ng other factors. A high eCG
treatment must be started at least 30 days
dose is characterized by superovulation,
before estrus. Estrus is variable but typically
low fertility, shortened estrous cycles,
develops soon after cessation of treatment;
pregnancy loss, and problems with multiple
fertility should be normal by the second
lan1bs or kids. The repetitive use of eCG has
estrus after treatment. If the bitch has
produced antibodies against eCG in certain
already entered proestrus, the progestagen
sheep and goats, resulting in modification
rnegestrol acetate (2.2 mg/kg/day, PO, for
in the time of ovulation and consequent

8 days) may be used to stop the cycle.

reduction of fertility when artificial

Administration must start in the first 3 days
insemination at a fixed time is done.

of proestrus (vulvar bleeding). The next
estrus usually develops 4--6 wk earlier than

PIGS
expected. To delay estrus, treatment with
megestrol acetate (0.55 mg/kg/day, PO, for

In pigs, estrus synchronization may be

32 days) is begun in late an estrus ( up to a
easily achieved by synchronized weaning
few weeks before estrus is expected). After
of lactating sows; estrus is seen 4--10 days
treatment, estrus is seen in 2 -9 mo (typically
later. Administration IM of a commercially

5---6 mo), and fertility is not affected.

available combination of equine chorionic

Neither mibolerone nor megestrol acetate
gonadotropin ( eCG; 400 IU) and human
is recommended for use in bitches on their
chorionic gonadotropin (hCG; 200 IU), per
first estrus or in bitches pri.Jnarily used for

5 mL dose, given as a single injection within
breeding. Adverse effects of progestins such

12 hr after weaning, tightens the synchronias megestrol acetate include cystic zation, and estrus is seen 4--5 days after
endometrial hyperplasia and pyometra;
weaning. This eCG and hCG combination
longtem1 treatment may result in obesity,
also induces estrus in gilts with delayed
diabetes mellitus, and neoplasia of the
puberty and in sows with postweaning
uterus and mammary glands. Mibolerone
anestrus. Exogenous prostaglandin induces
may cause skin, vaginal, and clitoral
luteolysis of the porcine corpus luteurn only
changes.

2248

HORMONAL CONTROL OF ESTRUS

Clinical use of deslorelin for estrus
release formulation of deslorelin marketed
suppression is under investigation.

for use in mares.

Extended-release implants of deslorelin can

The most widely studied gonadotropin
suppress estrus for> 1 yr in bitches without
for estrus induction in canids is equine

VetBooks.ir
apparent adverse effects and with full
chorionic gonadotropin ( eCG), which is
return to fertility.

available in tile USA only i11 a porcine

Estrus induction in bitches remains
product that contains a combination of 80
problematic, and none of the drugs

IU eCG and 40 IU hCG/mL. A single 5-mL
presented below are approved for this use
injection of tllis product was highly
in the USA. Many methods have been
effective for inducing proestrus in 89.5% of
proposed, but repeatability is low and
treated bitches, but ovulation rate was poor.

fertility of the induced estrus is variable.

However, whelping rates of 50%-84% have

Estrus induction in the bitch before
also been reported when eCG and hCG were
endometrial involution is complete (135
used to induce estrus in bitches.

days after the most recent estrus) can result
in reduced fertility. The dopamine agonists

CATS
cabergoline (5 mcg/kg/day, PO, until 2 days
after onset of proestrus), metergoli.ne

Megestrol acetate may be used to suppress

(0.56-1.2 mg/kg, IM, every third day until
estrus in queens by treating with 5 mg/cat
proestrus ), and bromocryptine (0.3 mg/
daily for 3 days, tilen 2.5-5 mg once weekly
bitch for 3 days followed by 0.6-2.5 mg per
for a maximwn of 10 wk. Administration
bitch for 3-6 days after onset of proestrus)

of megestrol acetate to queens is an extraare reported to induce fertile estrus in most label use of tl1e drug, and informed consent
bitches. Average length of treatment was
should be obtained from tile owners. The

16-19 days. Two notable adverse effects of
queen should be allowed an estrus before
dopanti.ne agonist treatment in the bitch are
resuming tl1erapy. Mibolerone is also not
vomiting and coat color changes.

approved for use in queens (because

Use of deslorelin in1plants may also be
of hepato-toxicity) but is effective at
effective for induction of estrus but has

50 mcg/cat/day, PO. Longtem1 deslorelin
been associated witl1 low progesterone
implants have also suppressed estrus in
values during diestrus and, subsequently,
cats, but the lengtll of suppression is
prolonged estrus suppression. Removal of
variable. Estrus may be induced in queens
the implant 10 days after inse1tion may
witl1 follicle-stimulating hormone (FSH), 2
overcome this problem. Induction of estrus
mg, IM, tile ftrst day, then 0.5-1 mg, IM, daily
with GnRH analogues continues to be
for 4 additional days. Recommended doses
investigated. SyncJu·onous estrus using
of hwnan chorionic gonadotropin (hCG)

whole (2.1 mg) or half(l.05 mg) deslorelin
range from 25 to 500 IU. The higher doses
implants after termination of diestrus with
are more effective at inducing ovulation

PGF2a has been reported. The PGF2a protobut may also result in oocyte degeneracol started witil a low dosage (50 mcg/kg, tion. For queens with anovulation or for

SC, bid) on tl1e first day, followed by a
queens undergoing artificial insenti.nation,
moderate dosage (100 mcg/kg, SC;bid) on
ovulation of mature follicles (present on day
tile second day, and then a full dosage (250

2 of estrus) may be induced by treatment
mcg/kg, SC, bid) for 5 days. Encouraging
with hCG at 250 IU, IM, or GnRH at 25 mcg,
results have also been repo1ted using a

IM. Ovulation is reported to occur 25-27 hr
single 1.5-mg IM injection of a sustained-
after hCG administration to queens.

NUTRITION: BEEF CATTLE

NUTRITIONAL REQUIREMENTS
ample nutrients, such that matw·e and
young growing cattle can consun1e

Beef cattle production, whetl1er on range,
sufficient good-quality mixed pasture
improved pasture, or in ilie feedlot, is most

(grasses and legwnes) for nonnal growth
economic when feedstuffs are used
and maintenance. However, mature pasture,
effectively. Young growing grass or otl1er
crop residues, or forage crops harvested in a
high-quality pasture crops usually supply
manner iliat results in shattering, leaching,

NUTRITION: BEEFCATILE

2249
or spoilage may be so reduced in nutritive
lactating cow at the 4.4 °C temperatme will
value (particularly energy, protein,
consume 11.4 gal. (43.1 L) per day.

phosphorus, and provitamin A or

!3-carotene) that they are suitable only in a

Energy: Productive animals need
maintenance ration for adult cattle. Such
essentially two types of energy. Energy of

VetBooks.ir
feedstuffs should be supplemented if used
maintenance is that needed to maintain
for any other purposes.

respiration, circulation, digestion, etc.

The mineral content of forages is

Therefore, in calculating total energy needs,
influenced by the corresponding mineral
the net energy for maintenance, or NE,,.,
levels in the soil and by excess levels of
must be considered. The energy required for
some minerals that reduce the availability of growth and reproduction is called the net others. Mature forages also may be lower in
energy for production, or NE,. It is the
mineral content, especially phosphorus.

amount of energy intake deposited as

Normally, supplemental minerals are
muscle and/or fat in animals gaining weight.

supplied in a free-choice mineral mix or

(See TABLES 18---22.)

force-fed in the total mixed ration.

Except for preruminant calves, beef

Certain nutrients are required by beef
cattle can meet their maintenance energy
cattle in the daily ration, whereas others can requirements from roughages of reasonably be stored in the body. When body stores of a
good quality (green, leafy, fine-stemmed,
nutrient are high, eg, vitamin A, dietary
free of mold and weeds). A shortage of
supplementation is unnecessary until such
energy may exist on overstocked pastures,
stores are depleted. However, it may be
with inadequate feed allowance or
difficult to determine when body stores
poor-quality forages, or during a drought.

have been depleted until advanced signs

For production, additional energy from
of deficiency start to appear.

concentrates or co-product feeds may be

The following are dietary requirements
necessary, especially when forages of fair
for maintenance, growth, finishing,
to poor quality are consumed.

reproduction, and lactation in beef cattle.

Especially in cold weather, roughages of
vaiying quality may have similar mainte

Water: Water, although not considered a
nance energy values. Heat released during
nutrient per se, is required for regulation of
digestion and assin1ilation-called "heat
body temperature, as well as for growth,
incrernent"-contributes to the maintereproduction, lactation, digestion, nance of body temperature for wintering
metabolism, excretion, hydrolysis of
stock
nutrients, transportation of nutrients and
waste in the body,joint lubrication, plus

Protein: Protein requirements currently
many more functions. Restricting water
are evaluated as metabolizable protein,
intake results in impaired performance.

which is interchangeable with absorbed

An animal will expire more quickly from a
protein. Metabolizable protein defines
water deficiency than from a deficiency of
the protein more neai·ly as that which is
any nutrient.

available to the animal for maintenance and

Because feeds themselves contain water,
production. It is defined as the combination
and the metabolism of ingested feeds
of the true protein absorbed by the
releases water ( called metabolic water), not
intestine, supplied by microbial synthesized
all of the anin1al's water needs have to be
protein plus undegraded intake protein
met by drinking water. Thirst is the result of

(UIP). The latter often has been called
need, and anin1als drink to meet this need.

"bypass" protein.

The need for water results from an increase

Energy deficiency due to low feed intake
in the electrolyte concentration in the body
or intake of poor quality feed is the most
fluids, which activates the thirst mechacommon deficiency that limits growth, nism.

development in heifers and bulls, milk

Many factors, including temperature and
production, and reproduction, with protein
body weight, affect water consumption in
deficiency being the next most common.

cattle. An 800-lb (364-kg) heifer at an

Protein deficiency of long duration
environmental temperature of 4.4°C (40°F)

eventually depresses appetite, with eventual
can be expected to conswne 6.3 gal. (23 L)

weight loss and unthri.ftiness, even when
per day; at 21 °C (70°F), this will increase to
ample energy is available.

9.2 gal. (34.8 L). At the same 4.4°C tempera

Feedstuffs vary greatly in protein
ture, a 400-lb (182-kg) heifer will cunswne
digestibility. Fur example, the protein of

-4 gal. (15.1 L). Note that water consumpcommon grains and most protein suppletion and body weight are not correlated by a ments is -75o/o--85% digestible, that of alfalfa
straight-line relationship. A 900-lb ( 409-kg)

hay -70%, and that of grass hays usually

2250

NUTRITION: BEEF CADLE

MEAN NUTRIENT CONTENT OF FEEDS COMMONLY USED

IN BEEF CATILE DIETS•

DE

ME

NEm

NEg

TDNs

VetBooks.ir

Feedstuff

(Meal/kg) (Meal/kg) (Meal/kg) (Meal/kg)

(%)

Alfalfa (Medicago saliva)

Fresh

2.73

2.24

1.38

0.80

62

Fresh, late vegetative

2.91

2.39

1.51

0.92

66

Fresh, full bloom

2.22

1.81

0.97

0.42

50

Hay

2.65

2.17

1.31

0.74

60

Hay, sun-cured, early

2.65

2.17

1.31

0.74

60
bloom

Hay, sun-cured, mid

2.56

2.10

1.24

0.68

58
bloom

Hay, sun-cured, full

2.43

1.99

1.14

0.58

55
bloom

Silage

2.78

2.28

1.41

0.83

63

Barley (Hordeum vulgare)

Grain

3.84

3.03

2.06

1.40

88

Silage

2.65

2.17

1.31

0.74

60

Beet pulp, dried

3.26

2.68

1.76

1.14

74

Bermuda grass (Cynodon dactylon)

Fresh

2.82

2.31

1.44

0.86

64

Hay, sun-cured

2.16

1.77

0.93

0.39

49

Brewer's grains, dried

2.39

2.39

1.51

0.91

66

Citrus pulp, dried

3.62

2.96

2.00

1.35

82

Com (Zea mays indentata)

Distiller's grains,

3.88

3.18

2.18

1.50

90
dried

Gluten feed

3.53

2.89

1.94

1.30

80

Grain, cracked

3.92

3.25

2.24

1.55

90

Silage, well-eared

3.17

2.60

1.69

1.08

72

Cotton (Gossypium spp)

Seed

3.97

3.25

2.24

1.55

90

Meal

3.31

2.71

1.79

1.16

75

Molasses, cane

3.17

2.60

1.70

1.08

72

Oats

3.40

2.78

1.85

1.22

77

Sorghum (Sorghum

3.62

2.96

2.00

1.35

82
bicolor), grain

NUTRITION BEEF CADLE

2251

MEAN NUTRIENT CONTENT OF FEEDS COMMONLY USED

IN BEEF CATTLE DIETS• (continued)

Crude

Crude

Dry

Protein

Fiber

Ash

NDF

ADF

Ca
p

Matter

VetBooks.ir

(%)

(%)

(%)

(%)

(%)

(%)

(%)

(%)

Alfalfa (Med'icago saliva)

18.9

26.5

10.5

47.1

36.8

1.29

0.26

23.4

22.2

24.2

10.2

30.9

24.0

1.71

0.30

23.2

19.3

30.4

10.9

4.79

3.7
l.19

0.26

23.8

18.6

26.1

8.6

43.9

33.8

1.40

0.28

90.6

19.9

28.5

9.2

39.3

31.9

1.63

0.21

90.5

18.7

28.0

8.5

47.1

36.7

1.37

0.22

91.0

17.0

30.l

7.8

48.8

38.7

1.19

0.24

90.9

19.5

25.4

9.5

47.5

37.5

1.32

0.31

44.2

Barley (Hordeum vulgare)

13.2

3.37

2.4

18.1

5.8

0.05

0.35

88.1

11.9

2.92

8.3

56.8

33.9

0.52

0.29

37.1

9.8

20.0

5.3

44.6

27.5

0.68

0.10

91.0

Bermuda grass (Cynodon dactylon)

12.6

28.4

8.1

73.3

36.8

0.49

0.27

30.3

7.8

2.7

76.6

38.3

8.0

93.0

29.2

7.8

4.18

48.7

31.2

0.29

0.70

90.2

6.7

12.8

6.6

23.0

23.0

1.88

0.18

91.l

Corn (Zea mays indentata)

30.4

6.9

4.6

46.0

21.3

0.26

0.83

90.3

23.8

7.5

6.9

36.2

12.7

0.07

0.95

90.0

9.8

2.3

1.5

10.8

3.3

0.03

0.32

90.0

8.7

19.5

3.6

46.0

26.6

0.25

0.22

34.6

Cotton (Gossypium spp)

24.4

25.6

4.2

51.6

41.8

0.17

0.52

89.4

46.1

13.2

7.0

28.9

17.9

0.20

1.16

90.2

5.8

0.5

13.3

0.4

1.00

0.10

74.3

13.6

12.0

3.3

29.3

14.0

0.01

0.41

89.2

12.6

2.76

1.9

16.1

6.4

0.04

0.34

90.0

( continued)

2252

NUTRITION: BEEF CATTLE

MEAN NUTRIENT CONTENT OF FEEDS COMMONLY USED

IN BEEF CATILE DIETS• (continued)

VetBooks.ir

DE

ME

NE,..

N�"

TDNs

Feedstuff

(Meal/kg) (Meal/kg) (Meal/kg) (Meal/kg)

(%)

Soybeans (Glycine

3.70

3.04

2.06

1.40

84
max), meal

Wheat (1hticum aestivum)

Wheat bran

3.09

2.53

1.63

1.03

70

Fresh, early

3.22

2.64

1.73

1.11

73
vegetative

" Dry-matter basis; DE, digestible energy; ME, metabolizable energy; NE,,,, net energy for maintenance; NE,, net energy for gain; TDNs, total digestible nuu·ients; NDF, neu!Tal detergent fiber; AD�� acid detergent fiber.

Adapted, with permission, from Nutrient Requ'ire,neuls qf'Be�f'Callle, 2000, National Academy of Sciences, National Academy Press, Washington, DC.

35%-500/ci. The protein of low-quality feeds,

Minerals: Qualitatively, beef cattle require such as weathered grass hay, range grass, or
the same mineral elements as do dairy
cottonseed hulls, is digested poorly. Thus,
cattle; however, the relative quantities of the
even though total protein intake may appear several minerals are different (see TABLE 23, to be adequate, metabolizable protein might
p 2262). The minerals most apt to be
be deficient.

deficient in beef cattle diets are sodium (as

A lack of protein in the diet adversely
salt), calcium, phosphorus, magnesiwn,
affects the microbial protein production
zinc, copper, and seleniwn. In some areas,
in the rumen, which in turn reduces the
including the interior of the USA, iodine
utilization of low-protein feeds. Thus, much
may be deficient in diets for pregnant cows;
of the potential nutritive value of roughages
likewise, there are regional deficiencies

( especially energy) may be lost if protein

(probably reflecting soil deficiencies) of
levels are inadequate.

several trace minerals, including copper,

Urea and other sources of nonprotein
cobalt, and selenium. However, there are
nitrogen (NPN) are used commonly in
areas where some mineral elements ( eg,
commercial protei11 supplements to supply
selenium, molybdenwn) are present at toxic
one-third or more of the total nitrogen
levels. Attempts have been made to correct
requirement. Such products are broken
natural soil deficiencies for trace minerals
down readily by the ruminal microbial
by soil fertilization practices. Thus, it is
protein to anunonia and then synthesized
ilnplied that a beef producer needs to know
to high-quality microbial protein. The use
the mineral and trace milleral coµtent of the
of NPN needs available sources of ample
feedstuffs used in cattle rations. A general
phosphorus, trace minerals, sulfur, and
approach to prevent such deficiencies is
soluble carbohydrates for the microbial
to feed a conunercial salt mineral mix
synthesis of utilizable protei11. The amow1t
developed for the geographic location
of crude protein (% N x 6.25) supplied by
of the herd.

NPN must be stated on the feed tag

The salt (NaCl) requirement for beef
accompanyil1g conunercial supplements.

cattle is quite low (0.2% of the dry matter);

Toxicity is not a se1ious problem when w·ea
however, there appears to be a satiety
is fed at recommended levels and mixed
factor involved-almost all animals
thoroughly with the other ingredients of the
appear to seek out salt if it is not readily
ration. However, rapid ingestion of urea at
available. Range cattle may consume 2-2.5
levels >20 g/100 lb (45 kg) body wt may lead
lb (1 kg) salt/head/mo when forage is
to toxicity (seep 3043). Several urea-molassucculent but about half that amount ses liquid supplements, containing as much
when forage is mature and drier. When salt
as 100/c, urea, currently are self-fed to beef
is added to a free-choice protein feed to
cattle. Caution should be exercised when
limit intake, beef cows might consume> 1
cattle are started on such supplements.

lb salt/day over long periods of time

NUTRITION: BEEF CATILE

2253

MEAN NUTRIENT CONTENT OF FEEDS COMMONLY USED

IN BEEF CATTLE DIETS• (co11tin11ecl)

Crude

Crude

Dry

VetBooks.ir

Protein

Fiber

Ash

NDF

ADF

Ca
p

Matter

(%)

(%)

(%)

(%)

(%)

(%)

(%)

(%)

51.8

5.4

6.9

10.3

7.0

0.46

0.73

90.9

Wheat (T'liticum aestivum)

17.4

11.3

6.6

42.8

14.0

0.14

1.27

89

27.4

17.4

13.3

46.2

28.4

0.42

0.40

22.2
without adverse effects if they have plenty

The total ration should provide a calcium:

of drinking water. Signs of a salt deficiency phosphorus ratio of 1.2 to 2: 1, with cows are rather nonspecific and include pica
at minin1w11 of 1.2: 1 and feedlot steers at
and reduced feed intake, growth, and milk
minimum of 2: 1. Wider ratios appear to be
production.

tolerated if the minimum requirements

Calcium is the most abundant mineral
for each mineral element are met and if
element in the body; --98% functions as a
adequate vitamin D (exposure to sunlight)

structural component of bones and teeth.

is available. Range cattle should be

The remaining 2% is distributed in extracelprovided a mineral supplement that has as lular fluids and soft tissues and is involved
much or more phosphorus I han calcium,
in such vital fw1ctions as blood clotting,
because green forage is many times higher
membrane permeability, muscle contracin calcium. Research has shown that tion, transmission of nerve impulses,
intake among cattle receiving free-choice
cardiac regulation, secretion of certain
mineral mix is highly variable. One study
hormones, and activation and stabilization
showed that 14%--15% of cows with
of certain enzymes. Most roughages are
free-choice access to mineral in block or
relatively good sources of calciwn. Cereal
loose fonn conswned zero mineral. The
hays and silages and such crop residues
only time cattle should be offered mineral
are relatively low in calciwn. Although
free choice is when they are grazing and
leguminous roughages are excellent
no other feed is being fed. If cows are
sources of calcium, even nonlegwne
consuming any other feed, the salt and
roughages may supply adequate calciw11
mineral should be mixed with the ration so
for maintenance of beef cattle. When cattle all cattle will ingest the prescribed an10unt are fed such roughages produced on
of mineral.

low-calcium soils, or when finishing cattle

Approximately 800Ai of the phosphorus
are fed high-grain diets with limited
in the body is found in the bones and teeU1,
nonlegume roughage, a calcium deficiency
with the remainder dist1ibuted among the
may develop. Because lactating beef cows
soft tissues. Phosphorus may be deficient in
do not produce nearly the amount of milk
some beef cattle rations, because roughages
that dairy cattle do, their calcium
often are low in phosphorus. F\uthermore,
requirement is much less. Nevertheless,
as forage plants mature, their phosphorus
it is sound management to provide a
content declines, making mature and
free-choice salt mineral mixture tailored to weathered forages a poor sow·ce. Phosphothe environment and production class of rus has been described as the most prevalent
the grazing cattle. Salt should always be
mineral deficiency for grazing cattle
mixed with mineral, because salt drives
worldwide. Most natural protein suppleintake. Cows have almost zero "nutritional ments are fairly good sources of phosphowisdom," ie, they do not seek out rus. Because adequate phosphorus is critical
feedstuffs or minerals when they are
for optinlal pe1fom1ance of beef cattle,
deficient, with the exception being sodium, including growth, reproduction, and o adding mineral to the salt generally
lactation, a phosph01us supplementation
improves intake among cattle with
program is reconunendecl using eiilier a
free-choice access to the mineral mix.

free-choice mineral mixture or direct

2254

NUTRITION: BEEF CADLE

NUTRIENT REQUIREMENTS OF PREGNANT REPLACEMENT

BEEF cows•

Months Since Conception

VetBooks.ir

1

2

3

4

5

6

7

8•

9

NE,,, required (Meal/day)

Maintenance 5.98

6.14

6.30

6.46

6.61

6.77

6.92

7.07

7.23

Growth

2.29

2.36

2.42

2.48

2.54

2.59

2.65

2.71

2.77

Pregnancy

0.03

0.07

0.16

0.32

0.64

1.18

2.08

3.44

5.37

Total

8.31

8.57

8.87

9.26

9.79

10.55 11.65 13.23 15.37

MP required (g/day)

Maintenance 295

303

311

319

326

334

342

349

357

Growth

118

119

119

119

119

117

115

113

110

Pregnancy

2

4

7

18

27

50

88

151

251

Total

415

425

437

457

472

501

545

613

718

Calciwn required (g/day)

Maintenance 10

11

11

11

12

12

12

13

13

Growth

9

9

9

8

8

8

8

8

8

Pregnancy

0

0

0

0

0

0

12

12

12

Total

19

19

20

20

20

20

33

33

33

Phosphorus required (g/day)

Maintenance 8

8

8

9

9

9

10

10

10

Growth

4

4

3

3

3

3

3

3

3

Pregnancy

0

0

0

0

0

0

7

7

7

Total

12

12

12

12

12

13

20

20

20

Average daily gain (kg/day)

Growth

0.39

0.39

0.39

0.39

0.39

0.39

0.39

0.39

0.39

Pregnancy

0.03

0.05

0.08

0.12

0.19

0.28

0.40

0.57

0.77

Total

0.42

0.44

0.47

0.51

0.58

0.67

0.79

0.96

1.16

Body wt(kg)

Shrunk body 332

343

355

367

379

391

403

415

426

Gravid

3

4

7

12

19

29

44

64
uterus mass

Total (kg)

333

346

359

374

391

410

432

459

490

Total (lb)

733

761

790

823

860

902

950

1,010 1,078
a Mature weight, 533 kg (1,173 lb); calf birth weight, 40 kg (88 lb); age at breeding, 15 mo; breed code Angus; see TABLE 18 for abbreviations. The concentration of vitamin A in all diets should be 2,200
lU/kg (1,000 lU/lb) of dry matter.

Adapted, with permission, from Nutrient Requirements of Beef Cattle, 2000, National Academy of Sciences, National Academy Press, Washington, DC.

NUTRITION BEEF CADLE

2255
supplementation in the diet. In a phosphorus (seep 996). A potassiwn deficiency might be deficiency, reduced growth and efficiency of
anticipated when diets extremely high in
feed conversion, decreased appetite,
grain are fed ( eg, in finishing cattle), because
impaired reproduction, reduced milk
grains may contain <0.5% potassim11. A
production, and weak, fragile bones can be
marginal to deficient level of potassim11 in

VetBooks.ir
expected. There does not appear to be any
growing and finishing cattle results in
advantage to feeding more phosphorus than
decreased feed intake and rate of gain.

is recommended. Furthern1ore, feeding

However, this effect is subtle and probably
excess phosphorus contributes to increased
would not be noticed other tl1an by the very
environmental pollution. Good somces of
experienced cattle feeder. Body stores of
supplemental phosphorus include steamed
potassiwn are small, and a deficiency may
bone meal, mono- and dicalcium phosphate,
develop rapidly. It is good practice to
deftuorinated rock phosphate, and phossupplement rations for growing and finishing phoric acid. Corn co-products like corn
cattle such that they will contain >0.6%
gluten and distillers grains with solubles
potassium on a dry-matter basis.

are also high in phosphorus. Because most

Copper and cobalt deficiencies are likely
grains are relatively good somces of phosmore widespread than previously thought.

phorus, feedlot cattle rarely suffer a phos

Cobalt functions as a component of vitamin
phorus deficiency, although phytic acid

B,2. Cattle do not depend on dietary vitamin
chelation of phosphorus in grains may

B12, because rwninal microorganisms can
render up to one-half of it unavailablesynthesize it from dietary cobalt. In cattle, especially for monogastric animals such
therefore, a cobalt deficiency is a relative
as swine and poultry.

vitan1in B12 deficiency, and such cattle show

Magnesium maintains elect1ical
weight loss, poor i.t11111m1e function, unthriftipotentials across nerve endings. In a ness, fatty degeneration of the liver, and pale
deficiency, the lack of control of muscles is
skin and mucosa. Copper functions as an
obvious. However, nonnally deficiencies are essential component of many enzyme not anticipated. A magnesium deficiency in
systems, including tl1ose that involve the
calves results in excitability, anorexia,
production of blood components. Recomhyperemia, convulsions, frothing at the mended levels of cobalt and copper should
mouth, and salivation, but such a condition
be provided in the diet, either by supplemenis uncommon. Usually, a magnesiw11
tation of tl1e total mixed ration or as part of deficiency is seen in the spring in more
the free-choice mineral mix or supplemental
mature grazing cattle under field conditions
mix.

(ie, grass tetany, seep 996). The initial signs Iodine is an integral part of thyroxine
are nervousness, reduced feed intake, and
and, as such, is largely responsible for
muscular twitching about the face and ears.

control of many metabolic functions.

Animals are uncoordinated and walk with a

Typically, coastal regions subjected to
stiff gait. In advanced stages, affected cows
iocline-can)'ing winds off the ocean have
fall to the ground, convulse, and die sho1tly
abundant supplies of iodine; however, in
after. A blood sample from affected cows
inland soils (in the USA, especially between
would show a serum magnesium level of <2
the Allegheny and Rocky mountains), the
mg/dL, with a corresponding calciun1
soil generally does not have sufficient iocline
deficiency. This condition is sufficiently
to meet most livestock needs. Iodine
prevalent that many beef cow herd
requirements in cattle can be met ademanagers supplement in the spring with quately by feeding stabilized iodized salt.

magnesium oxide at 28-56 g/head/day. Beef

Selenium is part of the enzyme
cows generally do not like magnesiwn
glutathione peroxidase, which catalyzes the
oxide; dilution by mixing it with ground
reduction of hydrogen peroxide and lipid
corn or incorporating it into a free-choice
hydroperoxides, thus preventing oxidative
liquid supplement improves acceptability.

damage to the body tissues. White muscle

Potassium is the major cation in
disease in calves (seep 1172), characterized intracellular fluid and is in1portant in
by degeneration and necrosis of skeletal
acid-base balance; it is involved in regulation
and heart muscles, is the result of a
of osmotic pressure, water balance, muscle
seleniun1 deficiency. Vitamin E plays a role
contractions, nerve impulse transmission,
in preventing such conditions. Other signs
and several enzymatic reactions. Potassiwn
of a seleniwn deficiency include unthriftideficiencies nom1ally are not anticipated in ness, weight loss, reduced immune
cattle diets because most forages are good
response, and decreased reproductive
sources, containing 1 %-4%. In fact, the high
performance. Seleniun1 can be included in
potassiwn content of spring pasture grass is
mineral mixes at a level up to 120 ppm so
one of the highest risk factors for grass tetany that cattle intake is 3 mg/head/day.

2256

NUTRITION: BEEF CADLE
llllll1·I NUTRIENT REQUIREMENTS OF BEEF cows•

Months Since Calving

VetBooks.ir

1

2

3

4

5

NE,,,required (Meal/day)

Maintenance

10.25

10.25

10.25

10.25

10.25

Lactation

4.78

5.74

5.17

4.13

3.10

Pregnancy

0

0

O.Ql

0.03

0.07

Total

15.03

15.99

15.43

14.41

13.42

MP required (g/day)b

Maintenance

422

422

422

422

422

Lactation

349

418

376

301

226

Pregnancy

0

0

2

4

Total (g)

771

840

799

725

652

Total (lb)

l. 7

1.9

1.8

1.6

1.4

Calcium required (g/day)0

Maintenance

16

16

16

16

16

Lactation

16

20

18

14

11

Pregnancy

0

0

0

0

0

Total

32

36

34

30

27

Phosphorus required (g/day)b

Maintenance

13

13

13

13

13

Lactation

9

11

10

8

6

Pregnancy

0

0

0

0

0

Total

22

24

23

21

19

Gain in weight from pregnancy/dayb

Grams

0

0

20

30

50

Pow1ds

0

0

0.04

0.07

0.11

Milk production/day

Kilograms

6.7

8.0

7.2

5.8

4.3

PoW1ds

14.7

17.6

15.8

12.8

9.5

Weight of conceptus

Kilogran1s

0

0

1

3

PoW1ds

0

0

2

2

7

"Mature weight, 533 kg (1, 172 lb); calf birth weight, 40 kg (88 lb); age at calving, 60 mo; peak milk, 8 kg (17.6 lb); age of calf at weaning, 30 wk; breed code Angus; milk protein, 3.4%; calving interval, 12 mo; see TAULE 18 for abbreviations. Crystalline vitamin A should be added at a level of 2,200 [U/kg (1,000 IU/lb) dry matter feed.

b No allowance made for gain because these are mature cows.

Adapted, with permission, from Nutrient Requirenumls of Beef Callie, 2000, National Academy of Sciences, National Academy Press, Washington, DC.

NUTRITION: BEEF CATILE

2257
lhNll1·1 NUTRIENT REQUIREMENTS OF BEEF cows• ( continued) Months Since Calving

VetBooks.ir

6

7

8

9

10

11

12

10.25

8.54

8.54

8.54

8.54

8.54

8.54

2.23

0

0

0

0

0

0

0.16

0.32

0.64

1.18

2.08

3.44

5.37

12.64

8.87

9.18

9.72

10.62

11.98

13.91

422

422

422

422

422

422

422

163

0

0

0

0

0

0

7

14

27

50

88

151

251

592

436

449

472

510

573

673

1.3

1.0

1.0

1.0

1.1

1.3

1.5

16

16

16

16

16

16

16

8

0

0

0

0

0

0

0

0

0

0

12

12

12

24

16

16

16

28

28

28

13

13

13

13

13

13

13

4

0

0

0

0

0

0

0

0

0

0

5

5

5

17

13

13

13

18

18

18

80

120

190

280

400

570

770

0.18

0.26

0.42

0.62

0.88

1.25

1.70

3.1

0

0

0

0

0

0

6.8

0

0

0

0

0

0

4

7

12

19

29

44

64

9

15

26

42

64

97

141

Vitamins: Although cattle probably have
ruminal microflora, and vitamin C is
a metabolic requirement for all the known
synthesized in the tissues of all cattle.

vitamins, dietary sources of vitan1ins C

However, if rumen function is impaired,
and Kand the B-vitamin complex are not
as by starvation, nutrient deficiencies,
necessary in all but the very young.

or excessive levels of antimicrobials,

Vitamin Kand the B vitamins are
synthesis of these vitamins may be
synthesized in sufficient amounts by the
impaired.

2258

NUTRITION: BEEF CADLE

NUTRIENT REQUIREMENTS OF GROWING AND FINISHING BEEF

CATTLE"

Body Weight in kg (lb)

200 (440)

250 (550)

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MAINTENANCE REQUIREMENT

NE"' (Meal/day)

4.1

4.84

MP(g/day)

202

239

Calcium (g/day)

6

8

Phosphorus (g/day)

5

6

GROWTH REQUIREMENT (AVERAGE DAILY GAIN IN KG [LB)) NE required for gain (Meal/day)

g

0.5 (1.1)

1.27

1.50

1.0 (2.2)

2.72

3.21

1.5 (3.3)

4.24

5.01

2.0 (4.4)

5.81

6.87

2.5 (5.5)

7.42

8.78

MP required for gain (g/day)

0.5 (1.1)

154

155

1.0 (2.2)

299

300

1.5 (3.3)

441

440

2.0 (4.4)

580

577

2.5 (fi.5)

718

721

Calcium required for gain (g/day)

0.5 (1.1)

14

13

1.0 (2.2)

27

25

1.5 (3.3)

39

36

2.0 (4.4)

52

47

2.5 (5.5)

64

59

Phosphorus required for gain (g/day)

0.5 (1.1)

6

5

1.0 (2.2)

11

10

1.5 (3.3)

16

15

2.0 (4.4)

21

19

2.5 (5.5)

26

24

"Weight at small marbling, 533 kg (l,173); weight range, breed code Ang•.1s; see TABLE 18 for abbreviations. The concentration of vitamin A in all diets for finishing steers and heifers is 2,200 JU/kg (1,000 IU/lb) dsy diet.

Adapted, with permission, from Nulrienl Requirements of Beef Callle, 2000, National Academy of Sciences, National Academy Press, Washington, DC.

NUTRITION: BEEF CADLE

2259

NUTRIENT REQUIREMENTS OF GROWING AND FINISHING BEEF

CATTLE" (continued)

300 (660)

350 (770)

400 (880)

450 (990)

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MAINTENANCE REQUIREMENT

5.55

6.23

6.89

7.52

274

307

340

371

9

11

12

14

7

8

10

11

GROWTH REQUIREMENT (AVERAGE DAILY GAIN IN KG [LB]) 1.72

1.93

2.14

2.33

3.68

4.13

4.57

4.99

5.74

6.45

7.13

7.79

7.88

8.84

9.77

10.68

10.06

11.29

12.48

13.64

158

157

145

133

303

298

272

246

442

432

391

352

577

561

505

451

710

687

616

547

12

11

10

9

23

21

19

17

33

30

27

25

43

39

35

32

53

48

43

38

5

4

4

4

9

8

8

7

13

12

11

10

18

16

14

13

22

19

17

15

Vitamin A can be synthesized from
of the beef breeds are much less efficient.

13-carotene contained in feedstuffs such as

Therefore, providing supplemental vitamin
green forages and yellow com. However,

A to beef cattle should be considered.

this ability varies among breeds; Holstein

Vitamin A is one of the few vitamins that
cattle perhaps are the most efficient
cattle store in their livers-as much as a
converters of carotenes, whereas some

6-mo supply. Cattle on a diet deficient in

2260

NUTRITION BEEF CADLE
iM:iif %1 NUTRIENT REQUIREMENTS OF GROWING BEEF BULLS·

BodyWeightinkg(lb)

300(660)

400(880)

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MAINTENANCE REQUIREMENT

NE,.. (Meal/day)

6.38

7.92

MP(g/day)

274

340

Calcium (g/day)

9

12

Phosphorus (g/day)

7

10

GROWTH REQUIREMENT (AVERAGE DAILY GAIN IN KG [LB)) NEg required for gain (Meal/day)

0.5 (1.1)

1.72

2.13

1.0 (2.2)

3.68

4.56

1.5 (3.3)

5.74

7.12

2.0 (4.4)

7.87

9.76

2.5 (5.5)

10.05

12.47

MP required for gain (g/day)

0.5 (1.1)

158

145

1.0 (2.2)

303

272

1.5 (3.3)

442

392

2.0 (4.4)

577

506

2.5 (5.5)

710

617

Calcium required for gain (g/day)

0.5 (1.1)

12

10

1.0 (2.2)

23

19

1.5 (3.3)

33

27

2.0 (4.4)

43

35

2.5 (5.5)

53

43

Phosphorus required for gain (g/day)

0.5 (1.1)

5

4

1.0 (2.2)

9

8

1.5 (3.3)

13

11

2.0 (4.4)

18

14

2.5 (5.5)

22

17
a Weight at maturity, 890 kg (1,958 lb); breed code Angus; see TABLE 18 for abbreviations. Vitamin A should be added at a level of2,200 IU/kg (1,000 IU/Ib) feed dry matter.

Adapted, with permission, from Nii t,ien l Requirnmen t.s of Beqf Cattle, 2000, National Academy of Sciences, National Academy Press, Washington, DC.

NUTRITION: BEEF CATILE

2261

NUTRIENT REQUIREMENTS OF GROWING BEEF BULLS• (continued) 500 (1,100)

600 (1,320)

700 (1,540)

800 (1,760)

MAINTENANCE REQUIREMENT

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9.36

10.73

12.05

13.32

402

461

517

572

15

19

22

25

12

14

17
l9

GROWTH REQUIREMENT (AVERAGE DAILY GAIN IN KG [LB]) 2.52

2.89

3.25

3.59

5.39

6.18

6.94

7.67

8.42

9.65

10.83

11.97

11.54

13.23

14.85

16.41

14.74

16.90

18.97

20.97

122

100

78

58

222

175

130

86

314

241

170

102

400

299

202

109

481

352

228

109

9

7

6

4

16

12

9

6

22

17

12

7

28

21

14

8

34

25

16

8

3

3

2

2

6

5

4

2

9

7

5

3

11

8

6

3

14

10

6

3
vitamin A may not begin to show signs for
apparent in the y0tmg suckling calf within
several weeks. Newborn calves, which

2-4 wk of birth, while the dam may appear
have small stores of vitamin A, depend on
healthy.

colostrnm and milk to meet their needs. If

It is sound practice to provide 2-5 lb
the dam is fed a ration low in carotene or

( 1-2 kg) of early-cut, good-quality legwne
vitamin A during gestation ( eg, in winter),
or grass hay in the daily ration of stocker
severe deficiency signs may become
cattle and pregnant cows to prevent

2262

NUTRITION BEEF CATILE

REQUIREMENTS AND MAXIMUM TOLERABLE LEVELS OF

MINERALS FOR BEEF CATILE•

Requirement

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Growing and

Early

Maximum

Mineral

Finishing

Gestation Lactation

Tolerable Level

Chlorine (%)

Chromium (mg/kg)

1,000

Cobalt (mg/kg)

0.10

0.10

0.10

10

Copper (mg/kg)

10

10

10

100

Iodine ( mg/kg)

0.50

0.50

0.50

50

Iron (mg/kg)

50

50

50

1,000

Magnesium (%)

0.10

0.12

0.20

0.40

Manganese (mg/kg)

20

40

40

1,000

Molybdenum (mg/kg)

5

Nickel (mg/kg)

50

Potassium (%)

0.60

0.60

0.70

3

Selenium (mg/kg)

0.10

0.10

0.10

2

Sodium(%)

0.06-0.08

0.06-0.08

0.10

Sulfur(%)

0.15

0.15

0.15

0.40

Zinc (mg/kg)

30

30

30

500

• Requirements for calcium and phosphorus are listed in the preceding nutrient requirement tables.

Adapted, with permission, from N"trient Reqi,irements ofBeqf" Catt.le, 2000, National Academy of Sciences, National Academy Press, Washington, DC.

vitamin A deficiency. Most commercial
that an extremely high dose (6 million U)

protein and mineral supplements are
would be needed to supply adequate
fortified with dry, stabilized vitamin A. The
vitamin A for 7 mo. As with all vitan1ins and
daily requirements for beef cattle appear to minerals, a steady supply in the di.et is the be -5 mg of carotene or 2,000 JU of vitamin
ideal method for supplementation.

A/100 lb ( 45 kg) body wt; lactating cows

Vitamin D deficiency is comparatively
may require twice this amount to maintain
rare in beef cattle, because they are usually
high vitamin levels in the milk.

outside in direct sunlight or fed sun-cmed

Vitamin A deficiency under feedlot
roughage. In northern latitudes during long
conditions can cause considerable loss to
winters, or in show calves kept in the barn
cattle feeders, especially if high-concentrate or turned out only at night, a deficiency is and com silage rations low in carotene have
possible. The ultraviolet rays of sunlight
been fed. Destruction of carotene during
convert provitamin D found in the skin of
hay storage or in the GI tract, or the failme
animals (7-dehydrocholesterol) or in
of beef cattle to convert carotene to vitamin
harvested plants ( ergosterol) to active

A efficiently, may increase the need for
vitan1in D. Direct exposme to sunlight,
supplemental vitamin A. Growing and
consumption of sun-cured feed, or
finishing steers and heifers fed low-carotene supplementary vitamin D (300 IU/45 kg diets for several months require 2,200 IU of
body wt) prevent a deficiency.

vitamin A/kg of air-dry ration. Commercial

For tl1e interrelationships of vitamin E and
vitamin A supplements are not expensive
selenium in reproduction and in the etiology
and should be used when such rations are
of various myopathies and the predisposition
fed and any danger of a deficiency exists. An of a relative thianline (vitamin 81) deficiency, alternative way to supply supplemental
see NUTRITIONAL MYOPATHIES, p 1172. (See af,so vitamin A is by IM injection: studies show

POLIOENCEPHAWMALAClA, p 1281.)

NUTRITION: BEEF CADLE

2263

FEEDING AND NUTRITIONAL

Under profitable systems of management,

MANAGEMENT
a mature beef cow should maintain her
weight from fall to fall. Lactation requires

Feeds for beef cattle vary widely in quality,
more nutrients than gestation. However,
palatability, and essential nutrient content
feeding beef cows more than is necessary

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( see TABLE 18). To be most effective, any
for satisfactory production, such as is
supplement must be patterned to fit the kind
frequently done in purebred herds and show
and quality of roughage available. Chemical
herds, is also undesirable. Large accunmlaanalyses of roughages are very useful to tions of body fat may lead to lowered
detennine their nutrient deficiencies and
conception rates, difficult calving, a lower
adequacies. Under certain systems of
calf crop, and a shorter life span for the cow.

management, beef cattle are wintered on low

A system of "creep feeding" can be
quality roughages and thus may not receive
practiced in which suckling calves are
the reconm1ended nutrients for optimal
allowed access to a grain mixture in a
perfonnance. lf heifers are fed low.quality
self-feeder in an enclosure or to high-quality
roughages during winter, they will produce
forage in an adjacent pasture where only
inadequate quality and quantity of colostrum,
calves have access. A creep-feed mixture of
take longer to deliver their calves, and have
high-fiber co-product feeds such as com
poor rebreeding rates. Titls can be prevented
gluten, dry distiller's grains, and soyhulls
by ensuring that heifers are fed a balanced
can be combined with a salt-vitamin-mineral
ration that will allow them to calve in body
mix to provide a palatable ration for the
condition score 6.5--7 (0-9 scale). Cattle
calves. The mixture should be rather large
should always be fed an adequate ration that
particles to prevent dustiness. A commerallows them to thrive in their given environcial 14%--16% protein creep feed may be ment. (See TABLES 19-22.)

used as an alternative.

Feeding and nutritional management

Growing bull calves should also receive a
for three systems of beef production are
balanced ration. Young bulls should not be
discussed separately. (See BEEP CATTLE
fed large amounts of starch, with gains of

BREEDING HERDS, p 2119.)

2.&--3.5 lb (l.l-1.6 kg) per day being very
adequate. Yearling bulls grown on extremely

The Breeding Herd
high energy diets are more likely to have
ln many areas, producers follow a late winter/ disease issues and reduced longevity in the early spring calving progran1 (February to
breeding herd. Mature bulls commonly are

May in the USA), depending on the available
wintered in the same manner as the cow herd,
feed, growth of early pasture, and prevailing
with a greater feed allowance during the late
climate. Fall calving has become more
winter. ln highly fitted show bulls, a gradual
prevalent, particularly in the south. Wintering
reduction in the ration and much exercise are
the lactating cow presents a much greater
needed before they will be in suitable shape
nutritional problem than does wintering the
and condition for pasture breeding. Breeding
pregnant, nonlactating cow. Spring-born
stock should have adequate nutrients in their
calves commonly are weaned at 6--7 mo, and
ration and be gaining weight before and
their darns bred back while on pasture.

during the breeding season. Deficiency of

Heifers may be bred to calve first as 2-yr-olds
several nutrients, especially carotene,

(22-25 mo) if good winter feeding is
phosphorus, energy, and protein, reduces
practiced to ensure adequate development.

fertility. These nutiients should be present in

Heifers should weigh 55o/er-600/o of mature
adequate amounts in the ration at least 6--8
body wt at breeding time and should be fed
wk before breeding.

well thereafter to allow for continued growth,
good milk production, and prompt rebreed

Stocker Cattle
ing.

It is conm10n practice to feed calves and

Mature cows have greater body reserves
yearlings to make moderate gains in winter,
and lower nutrient requirements than
with faster and less expensive gains on
heifers; therefore, they can be wintered on
sunm1er pasture. Such cattle may be sold as
rations of poorer quality. Their ration should feeders in the spring or finished out in dry provide a mininmm of 8% total or crude
lot the following fall. The cost of winter gain
protein in the dry matter; if it does not, then
on harvested feeds invariably is higher than

1 -2 lb (0.&--1 kg) of a 20%--30% protein
sunm1er gain on pasture; hence, it is
supplement or its equivalent should be fed
advisable to winter cattle so as to make the
daily. A mineral mix and salt should be
greatest possible gains on pasture. To
provided. Cows should calve in body
maintain good health, weanling calves
condition score 5.5--6 (0-9 scale).

should gain> l lb (0.5 kg)/day. Two pounds

2264

NUTRITION: BEEF CADLE

(1 kg) of grain plus 1-2 lb (0.5---1 kg) of
effective implants is ---0.23 kg (0.5 lb )/day,
protein supplement are recommended in
and the improvement in the feed to gain
addition to nonlegume roughage. If legw11e
ratio is 0.56 kg feed/kg gain.

roughage is fed, no protein supplement is

Ionophores are antibiotics that alter tile

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needed. Older cattle, particularly if they
chemistry of tile rumen by altering the
enter the winter in fleshy condition, may just rrn11en microflora to produce increased maintain their weight. A free-choice mineral
proportions of propioni.c acid and decreased
mixture with trace mineralized salt should
proportions of acetic and butyric acids.

be supplied. Limited am0tmts of grain fed to

These three acids, called volatile fatty acids
yearling cattle on pasture during the late

(VFAs), are the products of nU11inal
swnmer may increase their market value.

fermentation and can be absorbed from the
digestive tr·act of tile cow and used as energy

Finishing Cattle
sources. Because prop ionic acid releases

This phase of beef production consists of full
more energy per rnlit weight to the host cow
feeding of grain with limited am0tmts of
upon oxidation than do tile oilier two VFAs,
roughage until market weight and finish are
it is important in beef cattle production.

reached. Older cattle may reach finish weight

In modern feedlot diets, ionophores
on pasture alone ( or with only a few potmds
improve feed efficiency by 2.5%---3.5%,
of grain/day) or after 60--90 days in the feedlot decrease dry matter intake 3%, and increase on high-grain rations to inlprove market
average daily gain (ADG) 2.5%. A more
grade and to remove any yellow tinges from
dran1atic in1provement in ADG is seen in
their body fat ( due to stored carotene from
cattle fed ionophores on high-roughage diets
pasture forage). Weanli.ng calves can be
than in cattle fed high-energy diets. This is
shipped directly to the feedlot and fed
explained by energy availability between tl1e
finishing rations for 150--250 days, whereas
two systems. On high-energy diets, cattle eat
yearlings require ---150 days. Grain constmipw1til they meet energy requirements; tllus, tion of cattle on full-feed is ---2---2.5 lb/100 lb
ionophores help them derive more energy

(l kg/45 kg) body wt. Roughage consW11ption
per unit of ingested feed, and tlley eat less.

usually is limited to approximately one

On high-roughage diets, which have less
fornth to one-third of tl1e total concentrate
energy per unit weight, cattle constUlle feed
constunption after cattle are on full-feed.

tmtil the rumen will hold no more. In grazing

Cattle consWTie ---3"A, of their body wt/day
or high forage feeding systems, if ionophores
when self-fed mixed rations. For calves,
are fed, tllese cattle derive more energy per

---1.5---2 lb ( d kg) of a 33% protein supplement tmit of feed consWTied, and tl1us gain more.

is required daily for best gains and market

Additional benefits of feeding ionophores
grades when nonlegtUlle roughage is fed.

include improving tl1e consistency of feed

The grain (concentrate) atlowance
intake in cattle fed high-grain diets, thus
for finishing cattle should be increased
reducing the incidence of nuninal acidosis
gradually over 2-3 wk from the time they
along with control of coccidiosis.

are started on a finishing program to get

13-Agoni.sts are the newest of tile perfm0
them on full feed. Feeding too much grain to mance moclifiers used in feedlot operations.

finishing cattle too rapidly can lead to lactic

These feed additives are absorbed in tile
acidosis or fow1der (seep 225).

blood and distributed to muscle tissue, where
tlley bind to specific 13 receptors. Their action
results in increased protein syntbesis, which

PERFORMANCE MODIFIERS
results in increased muscle fiber size. The 13-agoni.st ractopan1i.ne is fed for the final

See also GROIVTII PHO�IOTANTS AND PllODUCTION

28--42 days before slaughter, whereas

ENHANCERS, p 2758.

zilpaterol is fed for the final 20-40 days before

There are tllree groups of performance
slaughter. Pe1iormance improvements of
modifiers used in beef cattle production:

13-agonists include live slaughter wt 18---22 lbs,
hormone-like growth enhancers; rw11inal
hot carcass wt 20--30 lbs, ADG ( during
chemistry modifiers, which alter volatile

13-agonist feeding period of 20-42 days)

fatty acid production in the rnmen; and

8.5%---30%, feed efficiency ( during 13-agoni.st

13-agonists, which increase muscle.

feeding pe1iod of 20-42 days) 12.5%--31 %,

Ho1111one-like growth enl1ancers for
and dressing percentage 0--1.5 rnlits.

finishing beef cattle have been used for

13-agonists can increase muscle shear
almost 70 yr. There are many inlplant
force and reduce the percentage of cattle
choices, and the specific implant protocol
that grade prin1e and high choice, so use
needs to be tailored to the cattle genetics,
in cattle with low genetic potential for
nutrition, and marketing plan. The average
tenderness and/or marbling may be less
increase in daily gain due to the use of
advantageous.

NUTRITION: DAIRY CATTLE

2265

NUTRITION: DAIRY CATTLE

VetBooks.ir

NUTRITIONAL REQUIREMENTS

DMI through the period of late gestation and
early lactation.

During lactation, dairy cows have very high

Feed factors also affect DMI. Total ration
nut1itional requirements relative to most
moisture concentrations >500Ai generally
other species (see TABLE 24). Meeting these decrease DMI, although this may be related
requirements, especially for energy and
more to fermentation characteristics than
protein, is challenging. Diets must have
to moisture per se, because high-moisture
sufficient nutrient concentrations to
feeds for dairy cattle are typically from
support production and metabolic health,
fermented ( ensiled) sources. Rations high
while also supporting rumen health and the

(>30%) in neutral detergent fiber (NDF) may
efficiency of fermentative digestion.

also limit feed intake, although the degree to
which this occurs is related to the source of

Feed Intake

NDF. Environment also affects feed intake

Under nearly all practical management
with temperatures above the them1al
conditions, dairy cows and growing dairy
neutral zone (>20°C [68°Fl), resulting in
heifers are fed ad lib. Thus, voluntary feed
reduced DMI. Monito1i.ng DMI, when
intake is the major limitation to nutrient
possible, is a useful tool in diagnosing
supply in dairy cattle. Feed intake is usually
nutritional problems in diets of dai1y cows.

characterized as dry matter intake (DMI)

to compare diets of variable moistme
concentrations. DMl is affected by both

Carbohydrates
animal and feed factors. Body size, milk

Energy .requirements for lactating daily
production, and stage of lactation or
cows are met primarily by carbohydrate
gestation are the major animal factors. At
fractions of the diet. These consist of
peak DMI, daily DMI of high-producing
fibrous and nonfibrous carbohydrates.

cows may be 5% of body wt, and even higher Fibrous cai·bohydrate proportions are in extremely high-producing cows. More
generally measured as ND F and expressed
typical peak DMI values are in the range of
as a percentage of dry matter. Nonfiber

3.5%-4% of body wt. In mature cows, DMI
carbohydrate (NFC) propo1tions are
as a percentage of body weight is lowest
calculated by subtracting the proportions
dming the nonlactating, or dry, period. In

(as dry matter) of NDF, crude protein, fat,
most cows, DMI declines to its lowest rate
and ash from lOOOAi. Nonfiber carbohydrates
in the last 2-3 wk of gestation. Typical DMI
priinarily consist of sugars and fructans,
during this period is <2% of body wt/day,
starch, organic acids, and pectin. In
with intake rates depressed more in fat
fennented feeds, fe1rnentation acids also
cows than in thin ones. Feed intake dming
contribute to the NFC fraction. The sum of
this period has an important relationship to
sugars and stai·ch is referred to as nonstrucpostpartum health, with low DMI and tural carbohydrate (NSC), which should not
associated prepartum negative energy
be confused with NFC. Balancing fiber and
balance increasing the risk of postpaitmn

NFC fractions to optimize energy intake and
disease. After calving, DMI increases as
run1en health is a challenging aspect of
milk production increases; however, the
dairy nutrition.

rate of increase in feed consumption is such

In general, fiber in the diet supports
that energy intake lags behind energy
run1en health. Fiber in the rumen, especially
requirements for the first several weeks of
fiber from forage sources that have not been
lactation. Milk production and associated
finely chopped or ground, maintains rumen
energy requirements generally peak arow1d
distention, which stimulates motility, cud

6--10 wk into lactation, whereas DMI usually
chewing, and salivaiy flow. These actions
does not peak until 12-14 wk into lactation.

affect the rumen environment favorably by

This lag in DMI relative to energy requirestimulating the endogenous production of ments creates a period of negative energy
salivaiy buffers and a high rate of fluid
balai1ce in early lactation. Cows are at
movement through the rumen. Salivary
greater risk of metabolic disease dw·ing this
buffers mai.r1tain run1en pH in a desirable
period than at other times during their
range, while high fluid flow rates increase
lactation cycle. Management and nutritional
the efficiency of microbial energy and
strategies should be designed to maximize
protein yield. Fiber, however, delivers less

2266

NUTRITION: DAIRY CATILE
lh=l!i{I FEEDING GUIDELINES FOR LARGE-BREED DAIRY CATTLE·

Dry

Close

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(Far off)

(Close up)

Body wt, lb (kg)

l,500 (675)

l,500 (675)

DMI, lb (kg/day)

32 (14)

22 (lO)

Milk, lbb (kg/day)

CP(%)C

9.9

12.4

RDP(%)

7.7

9.6

RUP(%)

2.2

2.8

MP(%)

6.0

8.0

NEL, Meal/lb (Meal/kg)

0.60 (l.32)

0.65 (l.43)

ME, Meal/lb (Meal/kg)

NDF(%)

40

35

ADF(%)

30

25

NFC(%)

30

34

Calcium (%)

0.44

0.48

Phosphorus(%)

0.22

0.26

Magnesium (%)

O.ll

0.40

Chlorine (%)

0.13

0.20

Sodium(%)

0.10

0.14

Potassium (%)

0.51

0.62

Sulfur(%)

0.20

0.20

Vitamin A (IU/day)

80,300

83,270

Vitamin D (IU/day)

21,900

22,700

Vitamin E (IU/day)

1,168

1,200

Adapted, with permission, from Nu.trient Reqitirements of Da'i1y Cattle, 2001, National Academy of Sciences, National Academy Press, Washington, DC.

a DMI, dry matter intake; CP, crude protein; RDP, rumen degradable protein; RUP, rumen undegraded protein; MP, metabolizable protein; NE,,, net energy lactation; ME, metabolizable energy; NDF, neutral detergent fiber; ADF, acid detergent fiber; NFC, non-fiber carbohydrate. '!race mineral added to ration (expressed as ppm): cobalt: 0.11; copper 10-18; iodine: 0.3-0.4; iron: 13-130; manganese: 14-24; selenium: 0.30; zinc: 22-70.

b Milk components: 3.5% fat, 3.0% true protein, and 4.8% lactose.

c All concentration values are on a dry-matter basis.

"These cows will lose body weight (values >0.82 not feasible).

dietary energy than NFC. Fiber is generally
concentrations promote rumen health but
less fennentable in the rumen than NFC,
provide relatively less energy than diets
and rumen fermentation is the major
high in NFC.

mechanism by which energy is provided,

To increase the energy supply, dietary
both for the animal and the rumen

NDF concentrations are usually reduced by
microbes. Therefore, diets with high NDF
adding starch and other sources of NFC.

NUTRITION DAIRY CADLE

2267

•tfl!fJ• FEEDING GUIDELINES FOR LARGE-BREED DAIRY CATILP (continued) Cows

Heifers ( age in mo)

24

VetBooks.ir

Fresh Early

Mid

Late

6

12

18

(Close up)

1,500

1,500

1,500

1,500

440

660

1,000

1,375

(675)

(675)

(675)

(675)

(200)

(300)

(450)

(625)

34 (15) 66 (30)

52 (24)

45 (20)

11 (5)

16 (7)

25 (11)

23 (10)

77 (35) 120 (55) 77 (35)

55 (25)

19.5

16.7

15.2

14.1

12.3

11.4

8.8

15.0

I0.5

9.8

9.7

9.5

9.4

9.5

8.8

10.1

9.0

6.9

5.5

4.6

2.9

1.9

0.004

4.9

13.8

11.6

10.2

9.2

7.2

7.0

5.3

9.7
l.Olct

0.73

0.67

0.62

0.72

(2.22)

(1.61)

(1.47)

(1.36)

(1.58)

0.93

1.03

0.82

(2.05)

(2.27)

(1.80)

30

28

30

32

30

32

33

35

21

19

21

24

20

22

24

25

35

38

35

32

35

30

25

34

0.79

0.60

0.61

0.62

0.41

0.41

0.37

0.40

0.42

0.38

0.35

0.32

0.28

0.23

0.18

0.23

0.29

0.21

0.19

0.18

0.11

0.11

0.08

0.40

0.20

0.29

0.26

0.24

0.11

0.12

O.IO

0.20

0.34

0.22

0.23

0.22

0.08

0.08

0.07

0.14

1.24

1.07

1.04

1.00

0.47

0.48

0.46

0.55

0.20

0.20

0.20

0.20

0.20

0.20

0.20

0.20

75,000 75,000

75,000

75,000

24,000

24,000

36,000

75,000

21,000 21,000

21,000

21,000

6,000

9,000

13,500

20,000

545

545

545

545

240

240

360

1,200

This increases the rate and extent of rumen

Reconunended minimum NDF concentrafem1entation, which leads to greater energy tions depend on the source and physical
availability. Increased ruminal fermentation
effectiveness of the NDF and the dietary
also leads to the increased production of
concentration of NFC. Fiber from forage
volatile fatty acids, which tends to lower
sources is, in general, more effective at
rumen pH. At rumen pH values <6.2, fiber
stimulating salivation and cud chewing than
digestion is reduced; at values s5.5, fiber
is fiber from nonforage sources. Thus, one
digestion is severely diminished, feed intake
va.iiable in the assessment of dietary NDF
may be reduced, and rumen health is
adequacy is the proportion ofNDF coming
generally compromised. There is a
from forages. Minirmun NDF concentrations
reciprocal relationship between NFC and
in the diets for high-producing cows are

NDF proportions, so the adverse effects of

25o/o-300,.1,, When fiber sources from forage
high dietary NFC may be especially evident
make up <!75%of the NDF, then total NDF
as cud chewing and salivary flow may be
concentrations in the lower end of this range
simultaneously diminished because of
may be acceptable ( see TABLE 25). When a
reductions in dietary NDF
smaller portion of total NDF is derived from

2268

NUTRITION: DAIRY CADLE

RECOMMENDED MINIMUM NDF CONCENTRATIONS BASED ON

PROPORTION OF NDF COMING FROM FORAGE SOURCES•

NDF from Forage(% of

NDF from Forage Minimum Total NDF (% of

VetBooks.ir

Dietary Dry Matter)

(% ofNDF)

Dietary Dry Matter)

19

75

25

18

66

27

17

58

29

• Reprinted with permission from the National Academies Press, copyright 2001, National Academy of Sciences. As the propmtion of neutral detergent fiber (NDF) from forage sources decreases, tl1e minimum requirement for total NDF increases. These represent minimum requirements; diets with higher NDF concentrations present no problem and are generally appropriate for animals with relatively low energy requirements.

forage somces, then total NDF concentraproportions ofNDF coming from forage tions should be in the upper end of this range.

sources. These reconunendations must be

Maxirrnun reconunended NFC concentraviewed as broad guidelines rather than strict tions are 38%--44%. Diets with higher NFC
rules. F actors including the total fem1entabilconcenl.raLions will benefit from higher ity of the diet as well as the ferrnentability of

DRY MATIER, ENERGY, CRUDE PROTEIN, FIBER, AND NON-FIBER

CARBOHYDRATE CONCENTRATIONS OF SOME FEEDSTUFFS

COMMONLY FED TO DAIRY CATILE•

Metabolizable Net Energy

Dry Matter Energy
for Lactation

(%)

(Meal/kg)

(Meal/kg)

Ground shell corn

88

3.12

2.01

Corn silage

35

2.33

1.45

Pasture

20

2.46

1.54

Hay ( cool-season grasses)

84

2.02

1.23

Hay crop silage ( cool-season gr�ses)

42

1.92

1.16

Grass-legume mix hay

85

2.07

1.25

Grass-legume mix hay crop silage

44

1.96

1.23

Legume hay

84

2.09

1.28

Legume hay crop silage

43

2.01

1.22

Oats ( rolled)

90

2.78

1.77

Sorghum silage

29

1.85
l.ll

Soybean meal (solvent extracted,

89

3.31

2.13

44%CP)

Cotton seeds

90

2.91

1.94

Dried distillers grains with solubles

90

3.03

1.97

Corn and cob meal

89.2

2.91

1.86
a Reprinted with permission from the National Academies Press, copyright 2001, National Academy of Sciences. Energy values are estimated based on a consumption rate 3 times the rate of consumption at maintenance. These are representative values intended primarily for relative comparison among feeds. Analyzed values of actual feed samples will vruy substru1tially, especially runong forages.

NUTRITION: DAIRY CADLE

2269
the NDF influence the NDF requirement.

nance, growth, and lactation. The net

Diets with highly fermentable NDF sources
energy (NE) system takes into account the
require higher total concentrations ofNDF
differences in efficiency of ME utilization
but provide more energy per mass unit of
for each of these processes and assigns a

VetBooks.ir

NDF than diets with less fennentable NDF.

separate NE value to individual feedstuffs

Feeding management schemes such as
based on each of these energy-requiring
totally mixed rations result in lower
processes, ie, body maintenance, growth,
minimum NDF concentrations than feeding
and lactation. Thus, in the USA, in which
dietary components individually (seep 2265).

the NE system is typically used, energy
values of feedstuffs for ruminants are
expressed as NE for maintenance (NE,i),

Energy

NE for gain (NEc;), and NE for lactation

Dietary energy is usually measured in

(NEL). This system is cumbersome and
megacalories (Meal) or megajoules (MJ).

nonintuitive and has many computational

When the energy in a given feedstuff is
disadvantages compared with alternative
expressed in terms of the Meal or MJ
systems based directly on ME. However,
actually available for metabolism, heat
the NE system has the major advantage of
production, or storage in the animal, the
more equitably comparing the energy
term metabolizable energy (ME) is used.

values of forages to concentrates when

The efficiency of utilization of ME varies
used in ruminant diets. TABLE 26 has typical
based on the physiologic functions
values for ME, NE,., NEM, and NEc, for
supported, which include body mainte-
some feedstuffs conunonly fed to dairy

DRY MATTER, ENERGY, CRUDE PROTEIN, FIBER, AND NON-FIBER

CARBOHYDRATE CONCENTRATIONS OF SOME FEEDSTUFFS

COMMONLY FED TO DAIRY CATTLE" (continued) Net Energy for Net Energy

Neutral

Non-fiber

Maintenance
for Gain

Detergent

Carbohydrate Crude

(Meal/kg)

(Meal/kg)

Fiber(%)

(%)

Protein(%)

2.16

1.48

9.5

75.47

9.4

1.57

0.97

45

40

8.8

1.67

1.06

45.8

19.6

26

1.33

0.75

58

21.6

13

1.25

0.68

58

18.2

17

1.35

0.77

50.8

23.8

18.4

1.32

0.74

50.4

21.5

19

1.38

0.8

43

27.3

20.8

1.32

0.74

43

25.1

22

1.9

1.26

30

50.2

13.2

1.18

0.62

61

21.9

9.1

2.29

1.59

15

27.6

49.9

1.96

1.31

50.3

5.1

23.5

2.07

1.41

39

24.4

30

2

1.35

21.5

65.2

8.6

2270

NUTRITION: DAIRY CATILE
cows. The values in these and other

Energy requirements per kg of milk
published tables are estimates of the
produced at various milk fat concentrations
energy delivered to lactating cows
are given in TABLE 28.

consuming feed at three tin1es the

The required dietary energy concentramaintenance consumption rate, ie, three tion is a function of the energy requirement

VetBooks.ir
times more feed than they would consume
and the feed intake rate. Calculated
were they not in production. The listed
requirements for dietary energy concentravalues are typical averages for the feeds; tion typically are ve1y high in early lactation
the actual values for individual feeds may
because the rate of milk production is high
vary considerably, especially for forages.

relative to the feed intake rate. However,

Laboratory analyses of feeds and forages
the ration energy density concentrations
are always advisable for both comparative
required to meet the energy requirement
evaluation and ration balancing. Values for
of cows in very early lactation may be too

ME and NE cannot be measured directly by high to be compatible with adequate typical laboratory analyses. These and any
dietary fiber concentrations (seep 2265). In other energy values on a laboratory report
general, cliets with energy concentrations
are estimates, usually based on formulas

> 1. 71-1. 76 Meal/kg do not contain adequate
with acid detergent fiber concentration as
fiber to support good fllTilen health and
the primary independent variable. Many
function. Thus, dairy cows in early lactation
contemporary computer programs for
typically cannot meet their energy
ration evaluation or balancing in dairy
requirements and are expected to lose
cows do not rely on laboratory estimates of weight. During the first 3 wk of lactation, feed energy concentrations. Rather, they
daily cows conunonly have rates of
estimate the contributions of individual
negative energy balance in the range of
feeds to the energy supply based on feed

-5 to -10 Meal/day. The risk of metabolic
characteristics, intake rates, and estimated
disease increases with the degree of
rates of passage through the rumen. Such
negative energy balance, altllough tllere is
programs are frequently referred to as
great variability among individual cows in

"models." When using programs of this
the capacity to adapt to negative energy
type, the estin1ated energy values of
balance without incurring metabolic
individual feeds will diminish with
disease. Feed intake, rather than milk
increasing rates of feed intake.

production, is generally the most limiting

In tile USA, energy requirements of adult
factor influencing energy balance in early
dairy cows are typically expressed in tenns
lactation dai1y cows. Thus, nutritional
of NE,. This applies to pregnant dry cows as
management strategies that result in rapid
well as lactating animals. Maintenance
increases in feed intake rates after calving
requirements for mature cows of various
are the most beneficial in terms of both cow
mature body weights are given in TABLE 27.

health and productivity.

MAINTENANCE ENERGY REQUIREMENTS FOR COWS OF VARIOUS

BODY WEIGHTS

Body Weight (kg)

Daily Energy Requirement (Meal NEJday)

400

7.16

450

7.82

500

8.46

550

9.09

600

9.70

650

10.30

700

10.89

750

11.47

800

12.03

NUTRITION DAIRY CATTLE

2271

•tliifl:• DIETARY NET ENERGY REQUIREMENT FOR MILK PRODUCTION

Dietary Energy Requirement/day/kg

Milk Fat Concentration(%)

Milk Produced (Meal NEL)

VetBooks.ir

3.5

0.70

4

0.75

4.5

0.80

5

0.84

5.5

0.89

6

0.94

6.5

0.99

Fats
daiiy diets, up to 400 g ( -2% of diet dry

Supplemental fats can be added to increase
matter) may be added as vegetable fa.ts,
energy concentration. Fat concentrations
particularly if the fats a.re added as oil seeds,
in typical dairy diets without supplemental
which tend to be less detrin1ental than free
fat are usually low, -2.5% of dry matter.

oils. An additional 200-400 g may be added

Supplemental fats may be added to attain a
from highly saturated or preferably
total ration fat concentration of -6% of dry
rumen-inert sources, generally not to
matter. Fats in rwninant diets can induce
exceed a total of 6.5% fat in the total dietary
undesirable metabolic effects, both within
dry matter.

the rumen microbial population and within
the animal. Ramifications of these effects

Protein
include reduced fiber digestion, indigestion

The protein requirements of lactating dairy
and poor rumen health, and suppression of
cows a.re high because of the demand for
milk fat concentration. The major benefit of
amino acids for milk protein synthesis. Two
supplemental fat in ruminant diets is that
systems of describing the dietary protein
dietary energy concentration can be
supply and requirements for dai1y cows are
increased without increasing the NFC
in general use: the crude protein system and
concentration.

the metabolizable protein system. The

Fats may be supplemented from
crude protein system considers only the
vegetable sources such as oil seeds, animal
total a.mount of dietary protein, or protein
sources such as tallow, and specialty fat
equivalent from nonprotein nitrogen
sources that a.re manufactured to be nunen
sources. Crude protein values a.re based on
inert, ie, not interact with the metabolism of
the measurement of total dietary nitrogen
rumen microbes. Supplemental fats from
and the assun1ption that protein is 16%
vegetable sources generally have a
nitrogen. The crude protein system is
relatively high proportion of unsaturated
relatively simple to use and has provided a
fatty acids. Unsaturated fats adversely
traditional means of fommlating dairy cow
affect rumen microbial activity. In addition,
rations. TABLE 29 provides general guidelines these fatty acids a.re extensively converted
for the required crude protein concentrato saturated fatty acids in the rumen. When tion of diets for large- and small-breed dairy
fed in excessive dietary concentration,
cattle at various levels of production. It can
intermediate products from the saturation
be used for general evaluations of the
process may escape the rumen and be
protein adequacy of dairy diets. The
absorbed by intestinal digestion. Some of
metabolizable protein (MP) system is more
these products a.re trans-fatty acids, some of complex than the crude protein system, and which directly suppress mammary butterfat
it was developed in recognition of the fact
synthesis. Supplemental fats from animal
that not all crude protein provided to cows
sources a.re more saturated and thus less
may be available for absorption as amino
detrimental to microbial activity and less
acids.

apt to result in suppression of butterfat

MP refers to amino acids absorbed from
synthesis. Rumen-inert fats a.re designed to
the small intestine and available for
have little or no effect on rumen microbial
metabolism. MP in rwninants is derived
activity and mammary butterfat synthesis.

from two sources: microbial protein

In general, when supplementing fats to
synthesized in the rwnen and dietary

2272

NUTRITION: DAIRY CATILE

RECOMMENDED MINIMUM DIETARY PROTEIN CONCENTRATIONS

FOR DAIRY COWS AT VARIOUS LEVELS OF PRODUCTION"

Dietary Protein Requirements(% of Dry Matter)

VetBooks.ir

Large-breed Cows

Smitll-breed Cows

Milk Production

Crude

Metabolizable Crude

Metabolizable

(kg/day)

Proteinb

Proteinc

Protein

Protein

18

15.0

12.9

23

16.4

13.1

27

14.5

11.0

17.5

13.3

32

15.0

11.2

18.4

13.3

36

15.8

11.5

19.0

13.3

40

16.5

11.7

45

17.3

11.9

50

17.8

12.0

55

18.3

12.1

3 This table is intended to provide a general reference for initial evaluations of dairy diets, not a standard against which rations are balanced. Calculation of dieta.iy metabolizable protein concentrations generally requires specialized software.

b Crude protein requirements were generated by Spart.an Dairy 3.0 (Michigan State University), assuming a mature cow in mid lactation.

c Metabolizable protein requirements were generated by the Nut1ient Requirements of Daily Cattle Computer Program that accompanies Nu.t,·ient Reqnirnnum.t� of Dai,y Cattle, 2001, National Academy of Sciences, National Academy Press, Washington, DC.

proteins that escape rumen degradation.

In general, specialized software, commer

Protein escaping rumen degradation is
cially available, is necessary to fom1ulate
referred to as rumen undegraded protein
dairy diets using the MP system. Even with

(RUP), while protein that is broken down in
such software, many variables must be
the rumen is referred to as rumen degraded
estimated with unce1tainty. Therefore,
protein (RDP). Both sources are in1portant
calculations of MP supply must be
and must be considered in diet �valuation
recognized to be approximations.

and formulation.

Dietary ingredients vary in their proportion

RUP passes unaltered through the rumen
of RUP and RDP In general, feeds with high
and forms a direct source of protein for
moisture and high protein concentrations,
intestinal digestion and amino acid
eg, legunie silages, will have a high proporabsorption. Nitrogen from RDP, in contrast, tion ofRDP. ln contrast, feeds that have been
must be incorporated into newly syntheprocessed and especially those that have sized microbial protein before it will
tmdergone drying will have relatively high
provide amino acids available for intestinal
proportions of RUP. The proportions of RUP
absorption. The efficiency with which RDP
and RDP in diets and individual ingrediis recovered as microbial protein depends ents are not fixed but can vary somewhat
on the growth rate of the rumen microbes,
depending on intake rate. At high rates of
which in turn depends on the supply of
feed intake, the rate of feed passage tlu-ough
fermentable energy sources in the rwnen.

the runien is high; thus, t11ere is less

Thus, diets with sufficient RDP and
opportunity for rumen protein degradation
relatively high energy concentrations will
than with tl1e same feeds at lower intake
result in high yields of microbial protein,
rates. Therefore, on tl1e same diet, RUP
which will become available for intestinal
proportions are higher in animals witl1 high
digestion and absorption as MP. Calcularates offeed intake tl1an in t11ose wit11 low tions that balance dairy diets for MP must
rates of feed intake. Ani.Jnals most likely to
consider the complex interrelations among
benefit from supplements selected for high
fermentable energy sources, RUP, and RDP.

RUP proportions are tl1ose witl1 relatively

NUTRITION: DAIRYCATILE

2273

Crude protein

Along with overall protein requirements,
intake
dairy cows, as all other animals, have
specific an1ino acid requirements. However,
evaluating dairy cow diets relative to an1ino
acid requirements is more difficult than

VetBooks.ir
making similar evaluations of diets for

RDP

+ Recycling monogastric animals. This is because the amino acid supply for dairy cows and other
ruminants is a combination of the amino
acids provided by the microbial protein and

N-.. +

Rumen

N
urea
the RUP Microbial protein has an excellent

Ene(gy0

I

+ amino acid profile, and diets with a large
supply of microbial protein typically meet

Excretion
amino acid requirements if MP require

MCP
ments are met. In some cases, however,
high-producing dairy cows may benefit from
the selection of RUP sources with specific
amino acid profiles, or from adding

Abomasum
rumen-protected forms of specific amino
and Small

Protein
acids. Software is available that estimates

Intestine
available for
the amino acid supply for dairy cows on
digestion and

MP
different diets. The first limiting amino acids
absorption
in typical dairy cow diets are lysine and
methionine. With typical feedstuffs, if the

MP requirement is met and the dietary
lysine:methionine ratio is -3: 1, then the
an1ino acid requirements for milk produc

Undigested
tion are probably being optimized.

protein

The relationship of dietary protein intake to
metabolizable protein supply. The two

Water
branch points (indicated by 1 and 2)

The availability of high-quality water for ad
constitute the major variables relating the
dietary crude protein supply to the
lib consumption is critical. Insufficient
metabolizable protein supply. The first
water intake leads in1mediately to reduced
branch point represents the proportion of
feed intake and milk production. Water
protein that is degraded in the rumen. This
requirements of dairy cows are related to
branch point is influenced by inherent
milk production, DMI, ration dry matter
properties of the protein and the rate of
concentration, salt or sodiun1 intake, and
ingesta passage through the rumen. The
ambient temperature. Valious fonnulas
second branch point represents the
proportion of nitrogen from degraded
have been devised to predict water
protein that is recaptured as microbial
requirements. Two formulas to estimate
protein. This is influenced by the microbial
water consumption of lactating dairy cows
growth rate, which depends on the supply of
are as follows:

rumen available energy. Nitrogen that is not
recaptured as microbial protein is absorbed

FWI = 12.3 + 2.15 x DMI + 0. 73 x milk
from the rumen as ammonia and converted
to urea by the liver. Some urea is recycled

FWI = 15.99 + 1.58 x DMI + 0.9 x milk+
back to the rumen, but a large portion is

0.05 x Na+ 1.2 x minin1un1 temperature
excreted in urine. RUP, rumen undegraded
protein; RDP, rumen degraded protein; N,

Note: FWI is free water intake (water
nitrogen; MCP, metabolizable crude protein;
consumed by drinking rather than in feed),

MP, metabolizable protein.

DMI is in kg/day, milk is in kg/day, Na is in
g/day, and temperature is in °C. Water
high protein requirements and relatively low
conswned as part of the diet contributes to
rates of feed intake. Cows in very early
the total water requirements; thus, diets
lactation and young, rapidly growing heifers
with higher moisture concentrations result
are the prin1ary exan1ples. Supplements
in lower FWI.

formulated for high RUP proportions are

Providing adequate access to water is
commonly known as rumen bypass protein
clitical to encourage maximal water intake.

supplements; however, even with these types

Water should be placed near feed sources
of supplements, some portion of the protein
and in milking parlor return alleys, because
is degraded in the rumen.

most water is consumed in association with

2274

NUTRITION DAIRY CATILE
feeding or after milking. For water troughs,

Water with nitrate concentrations >40 mg/L
a minimum of 5 cm of length per cow at a
should be avoided. General recommendaheight of 90 cm is recommended. One water tions for sulfate concentrations in drinking
cup per 10 cows is recommended when
water are <500 mg/L for calves and < 1,000
cows are housed in groups and given water
mg/L for adult cattle. The specific sulfate

VetBooks.ir
via drinking cups or fountains. Individual
salts present in water may affect the
cow water intake rates are 4-15 Umin.

response of cattle; iron sulfate is the most

Many cows may drink simultaneously,
potent depressor of water intake. TABLE 31
especially right after milking, so trough
lists potential elemental contan1inants of
volun1es and drinking cup flow rates should
drinking water with upper-limit guidelines.

be great enough that water availability is not
limited during times of peak demand. Water
troughs and drinking cups should be
cleaned frequently and positioned to avoid

Minerals
fecal contanlination.

Calcium and Phosphorus: Calciwn

Poor water quality may result in reduced
requirements of lactating dairy cows are
water consumption, with resultant
high relative to other species or to
decreases in feed consumption and milk
nonlactating cows because of the high
production. Several factors detem1ine water calcium concentration in milk. Thus, quality. Total dissolved solids (TDSs ), also
inorganic sources of calciun1, such as
referred to as total soluble salts, is a major
calciwn carbonate or di.calcium phosphate,
factor that refers to the total amount of
must be added to the rations of lactating
inorganic solute in the water. TDS is
dairy cows. For the first 6----8 wk of lactation,
generally expressed in units of mg/Lor parts most dairy cows are in negative calcium per million (ppm) which are nun1erically
balance, ie, calcium is mobilized from bone
equivalent values (see TABLE 30). TDS is not to meet the demand for milk production.

equivalent to water hardness, which is a

This period of negative calciwn balance
measure of the amount of calcium and
does not appear to be detrimental so long as
magnesiun1 in water. Water hardness has
there is sufficient dietary calciw11 such that
not been shown to affect dairy cow
bone reserves can be replenished in later
performance.

lactation. The availability of dietary calcimn

Other inorganic contanlinants that affect
for absorption varies with dietary source.

water quality include nitrates, sulfates, and

Dietary calcium from inorganic somces is
trace minerals. Concentrations of nitrate
generally absorbed with greater efficiency

( expressed as nitrate nitrogen) <l O mg/Lare than that from organic sources. Fmthersafe for run1inants. At concentrations >20
more, cows in negative calcium balance
mg/L, cattle may be at risk, especially if
absorb calciw11 more efficiently than cows
nitrate concentrations in the feed are high.

in positive calciwn balance.

GUIDELINES FOR-TOTAL SOLUBLE SALTS (TOTAL DISSOLVED

SOLIDS) IN DRINKING WATER FOR CAITLE

Total Soluble Salts

(mg/L)

Comments

<1,000

Safe and should pose no health problems.

1,000-2,999

Generally safe but may cause a mild temporary diarrhea in aninlaJs not accustomed to the water.

3,000-4,999

Water may be refused when first offered to aninrnls or cause temporary diarrhea. Animal performance may be less than optimwn because water intake is not maximized.

5,000-6,999

Pregnant or lactating animals should not drink such water.

May be offered with reasonable safety to aninlals when maxinmm performance is not required.

�7,000

These waters should not be offered to cattle. Health problems and/or poor production will result.

Reprinted with permission from the National Academies Press, copyright 2001, National Academy of Sciences.

NUTRITION: DAIRY CATILE

2275

CONCENTRATIONS OF POTENTIALLY TOXIC NUTRIENTS AND

CONTAMINANTS IN DRINKING WATER GENERALLY CONSIDERED

SAFE FOR CATTLE

Element

Upper-limit Guideline (mg/Lor ppm)

VetBooks.ir

Aluminum

0.5

Arsenic

0.05

Boron

5.0

Cadmium

0.005

Chromium

0.1

Cobalt

1.0

Copper

1.0

Fluorine

2.0

Lead

0.015

Manganese

0.05

Mercury

0.01

Nickel

0.25

Selenium

0.05

Vanadium

0.1

Zinc

5.0

Reprinted with permission from the National Academies Press, copyright 2001, National A�ademy of Sciences.

When calculating calcium requirements,
responsive at the ti.me of paiturition,
newer nutritional models take into account
allowing cows to maintain serw11 calciwn
the variability in calcium availability from
concentrations during lactation. This
different sources. This availability generally
approach requires diets with calciwn
ranges from 75%-85% for inorganic calcium
concentrations near 0.3% of dry matter.

supplements to a low of 3()0A, for forage

Such diets are difficult to formulate with
sources of calciw11. This approach makes it
available feedstuffs while still meeting other
difficult to generate general recommendanutritional requirements. Another approach tions for total dietary calcium concentrais to feed an acidifying diet, usually referred tions across various diets. Generally, diets
to as a diet with a low or negative dietary
with large portions of forage from legume
cation-anion difference (DCAD). The
sources will have minit11w11 calcium
low-calcium diet approach is not additive
concentration requirements in the range of
with the DCAD approach to milk fever

0. 71 o/<Hl. 75%, while diets with forages from
prevention. When low-DCAD diets are fed,
primarily grass (including com silage)

total dietary calciun1 concentrations should
sources will have minimum calcium
be near 0.9%, which is substantially greater
concentration requirements in the range
than the requirement for a dry cow on a
of 0.42%-0.47%.

conventional diet.

'l\vo approaches are taken with respect to

Phosphorus nutrition for lactating dairy
the calcium supply for dry cows, each with
cows has dynamics similar to those of
the objective of preventing milk fever, or
calcium. The efficiency of phosphorus
parturient paresis (seep 988). One approach absorption is affected by physiologic state is to place cows in a calciw11-deficient state
and dietary source. As is the case with
during the last 2-3 wk of gestation; the
calcium, most dairy cows in early lactation
rationale is to stimulate parathyroid
are in negative phosphorus balance.

hormone secretion and skeletal calciun1

Phosphorus mobilized from bone eai·ly in
mobilization before calving. This makes
lactation is replaced during later lactation
calcitllll homeostatic mechanisms more
when feed intakes are higher. Yow1g animals

2276

NUTRITION: DAIRY CADLE
and animals in negative phosphorus balance estimated at an additional 1.4 g/day after absorb phosphorus more efficiently than do

190 days of gestation. For large-breed dairy
older animals or animals in positive
cows, this results in a sodium requir·ement
phosphorus balance. Phosphorus from
of --9-10 g/day. Unsupplemented dry cow

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inorganic somces is more available than
diets seldom provide sodiw11 at >3 g/day.

that from organic feed sources.

Therefore, daily supplementation of dry

Judiciously balancing diets to meet, but
cow diets with a minimum of 6--7 g of
not exceed, phosphorus requirements is
sodiw11 per day (--15-16 g of salt) is
important for dairy cow petformance and
important. Additional salt is necessaiy
enviI"Oiunental stewardship. Excess
during heat stress. Although salt should
phosphorus excreted iI1 feces is one of
be supplemented to d1-y cows in required
tl1e major pollutant risks associated with
atnoW1ts, excessive salt supplementation is
livestock production. Newer nutritional

Wlllecessaiy and may contribute to udder
models account for vaiiation in phosphorus
edema at calving.

availability from different somces, but there

Supplemental magnesium may need to
is less vai"iation iI1 availability ainong
be fed with diets containing high proporphosphorus sources than an1ong calcium tions of grass forages, especially those
sources. In general, concentrates when fed
consisting of rapidly growing pasture
to 1uminat1ts have a phosphorus availability
grasses. Such forages typically have low
of 7096, and forages close to 64%. Inorgailic
magnesiwn concentrations as well as high
mineral supplements ai·e usually rated at
concentrations of potassiwn and organic

75o/<r-80% availability, but rock phosphate is
acids, which interfere with the availability
ve1y low, --300Ai. Total dietaiy phosphorus
of dietat-y magnesiW11. Magnesiwn oxide
concentration requiI"ements for most dairy
is the typical magnesiwn supplement in
diets will be in tl1e range of 0.35%-0.4%, and
nm1inant diets.

for dry cows, 0.3%--0.35%. Phosphorus

Dairy cattle, like other animals, have no
supplementation for dry cows is seldom
dietaiy requir·ement for inorganic sulfur.

necessaiy.

The dietary requirement for sulfur reflects

The dietaiy calcium:phosphorus ratio is
only the dietat-y requirement for sulfu1°
not of particular importat1ce in rumrnants.

containing atnino acids. In rnminants,

Ratios from 7: 1 to 1: 1 are acceptable, so long nm1en microbes can synthesize sulfuras tl1e total ai11ount of each element meets containing atnino acids from non protein
the dietary requirements.

sources of nitrogen at1d sulfur. DaiI-y cow

Serum concentrations of calciwn at1d
diets most likely to require supplemental
inorganic phosphorus ai·e of value in
sulfur ai·e those with low protein concenassessing the sho1t-term homeostasis of trations and tl1ose with supplemental
these minerals but of little value in assessing nonprotein nitrogen. In general, a longterm nutritional status. Bone ash
nitrogen:sulfur ratio of 15: 1 is recomconcentrations ai·e the best way to assess mended in rwninat1t diets.

longtenn calciw11 and phosphorns

Recommended dietary concentrations for
nutritional status.

typical daiI-y cow diets are: soditUll (0.23%),
chloride (0.29%), potassitun (1.1 %),

Other Macrominerals: Other macrominmagnesium (0.21%), at1d sulfur (0.21%).

erals requiI"ed in daiI-y cow diets include
sodiwn, potassium, chloride, magnesiwn,

Trace Minerals: The trace minerals
and sulfur. Of tl1ese, sodium generally
typically supplemented or measured in
needs to be supplemented, typically as
dai1y cow diets include cobalt, copper, iron,
sodiw11 chloride or co nun on salt. Insuffimanganese, seleniwn, iodine, and zinc. or cient dietary sodium results in reduced feed
these, selenimn and copper are the trace
iI1take with subsequent reductions in atlimal minerals most likely to be deficient. Several performance. Signs of severe salt deficiency
ai·eas of Notth America, Europe, and other
include lickiI1g and chewing on fences and
continents are characterized by growing
otl1er environmental objects, w"ine drinking, conditions that result iI1 feeds witl1 low and general ill tlu'ift. Milk production is
selenium concentrations. In these areas,
reduced within 1-2 wk of removing
livestock feeds need to be supplemented
supplemental salt from the diets of lactating
with seleniwn. Sources of supplemental
cows. Completely withholding salt from dry
seleniw11 include sodiwn selenite, sodium
cow diets in atl effo1t to prevent udder
selenate, and selenomethionine. The latter
edema at calving is not a good practice.

source is typically referred to as organic

Maintenat1ce requiI·ements for sodiwn in
seleniwn.

nonlactatiI1g cows are estimated at 1.5 g/100

Selenium deficiency is known to cause
kg body wt/day, with gestation requirements myopathies in calves, which may affect

NUTRITION: DAIRY CADLE

2277
cardiac or skeletal muscle (ie, white muscle
nostrils and lower legs, ai1d weakening of
disease, seep 1172). In adult cattle,
the hoof horn are signs of prolonged zinc
selenium deficiency appears to suppress
deficiency. N 01mal concentrations of serum
immune function and especially neutrophil
zinc are 0. 7-1.3 mcg/mL. Concentrations

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function. It also increases the 1isk of

<0.4 mcg/mL are considered deficient.

retained placenta, although feeding

Iron deficiency is extremely rare in adult
selenium in excess of requirements does not cattle, because iron is ubiquitous in tile prevent this condition. Dietary seleniwn
environment and the endogenous concenrequirements in dairy cattle are estimated at trations of iron in most feedstuffs will more

0.1-0.3 mg/kg diet dry matter. In the USA,
than meet requirements. Signs of iron

0.3 mg/kg dry matter is the maximum legal
deficiency are primarily anemia and low
concentration of supplemental selenium in
senun iron concentrations. Adequate serum
dairy cattle diets.

iron concentrations ai·e 110-150 mcg/dL.

The selenium status of cattle can be

However, tllese concentrations drop quickly
accurately assessed from blood or serum
in the presence of inflainmatory disease,
concentrations. Whole blood concentraand such changes in serum iron concentrations of 120-250 ng/mL or senun concentrations should not be interpreted as being due tions of 70-100 ng/mL in adult cattle
to a dietary deficiency. Suckling calves ai·e
indicate adequate selenium status.

tile only group of cattle generally at risk of

Recommended dietary copper conceniron deficiency and to which supplemental trations in cattle diets are 10-15 mg/kg diet
iron need be provided.

dry matter; however, the dietary copper

Iodine deficiency occurs with some
requirement depends greatly on the
frequency in cattle and is primarily mailifest
concentration of interfe1ing substances.

by goiters in newborn calves. The required

These include primaiily sulfur and
dietary iodine concentration is generally
molybdenwn, but iron, zinc, and calcium

-0.2 mg/kg of dietary dry matter. However,
may also interfere with copper availability.

dietary iodine concentrations of 0.6 mg/kg

The adsorption efficiency for dietary copper
are reconunended as a safety factor because
in rwninants is nom1ally quite low, 4%-5%.

of tl1e potential presence of goitrogenic

However, with increasing concentrations
substances in common protein suppleof dietary sulfur and/or molybdenum, ments.

absorption efficiency may be reduced to
sl%.

Copper deficiency is characterized by

Vitamins
loss of hair pigmentation, Joss of hair

Vitamin A: Preformed vitamin A, or
ai·ow1d the eyes, anemia, and general ill
retinal, does not exist in any plant material,
tl1rift and suppressed immunity. In severe
so tllere is no vitan1i.n A in natural diets for
cases, persistent diarrhea may also occur.

dairy cattle. Vitainin A activity from natural

The copper status of cattle can be
sources comes primarily from 13-carotene,
assessed from liver or serum copper
which is found in plants and is particularly
concentrations. Liver concentrations <20
abundant in fresh forages. 13-carotene is
mg/kg dry tissue or semm concentrations
labile; its concentrations in forages are not

<0.5 mcg/mL indicate copper deficiency.

constant but diminish with time in storage.

Because the liver is a physiologic storage

Therefore, measurement of !3-carotene
site for copper, copper concentrations in
concentrations in feeds is not practical and
the liver will be reduced before serum
seldom done. Reconunended vitamin A
concentrations.

consumption rates for various classes of

Dietary manganese deficiencies in dairy
cattle are based on providing supplemental
cattle are less common tllan deficiencies of
vitan1in A, which is de1ived from commercopper or selenium. Signs include poor cial sources: for adult cows (lactating and
growth ai1d skeletal defom1ities in newborn
dry)-110 IU/kg body wt, which is -4,400
calves and reproductive abnormalities,

IU/kg dry diet; for growing heifers-SO IU/kg
including anestrus, in adult cows. Recently
body wt, which is -2,500 IU/kg dry diet.

recommended dietary manganese

Conditions tllat can increase dietary vita.in in
concentrations for cattle are l&-25 mg/kg;

A requirements in adult cows include low
previous recommendations have been as
forage diets, high com silage diets, poor
high as 40 mg/kg dry matter.

quality forages, and infection.

Recommended zinc concentrations in

The vitainin A status of cattle may be
the diets of dairy cattle and calves are 23-63
assessed via serum or hepatic vitan1in A
mg/kg dry matter. Signs of zinc deficiency
concentrations. The liver stores vitamin A
include reduced feed intake and general ill
for release dwing periods of insufficient
tllrift. Parakeratosis, particularly arow1d tile dietary intake, tlrns making liver tile ideal

2278

NUTRITION: DAIRY CATTLE
tissue for nutritional assessment. For adult
manifestations of deficiency include
cattle receiving diets with recommended
nutritional myopathy (white muscle
supplemental vitamin A concentrations,
disease, see p 1172) in young calves and
hepatic vitamin A concentrations are
diseases in older cattle including retained

300-1, 100 mg/kg dry tissue ( expressed as
placenta and increased susceptibility to

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retinol). Clinical signs of vitamin A
environmental mastitis'.

deficiency do not occur until these rese1Ves

Recommended rates of vitainin E intake
have been substantially depleted. Adequate
vaiy based on gestation stage: ternlinal dry
serum vitamin A concentrations in adult
period-LS fU/kg body wt, which is -90 fU/kg
cattle are 225-500 ng/mL, with values
dry matter; lactation-0.8 fU/kg body wt,
usually dropping to -150 ng/mL within l wk
which is -30 fU/kg dry matter. Much higher
of calving.

concentrations are occasionally supple

Calves a.re born with low body stores
mented when environmental mastitis is a
of vitamin A and depend on colostrnm
paiticuJai· problem. Vitanlin E is essentially
consumption to supply hepatic vitamin A
nontoxic, and there is little risk of oversupstores. The NRC recommends dietary plementation.

vitamin A concentrations for young calves

Vitamin E supplements may be natural or
at -9,000 ill/kg diet dry matter. Most milk
synthetic. Natural sources of vitamin E are
replacer diets have substantially higher
derived from plant oils a11d ai·e designated
concentrations of vitanlin A, possibly

RRR-a-tocopherol or D-a-tocopherol, based
because vitamin A requirements may be
on stereoisomer characte1istics of their
increased by infectious diseases, especially
chemical strncture. Syntl1etic supplements
those affecting the respiratory or enteric
ai·e designated all rac-a-tocopherol, or
epithelitm1.

DL-a-tocopherol. The natural-source

Vitamin A deficiency is associated initially supplements appear to have much greater with night blindness followed by poor
biologic activity.

growth, poor hair coats, and suppressed

Blood sernm vi.ta.min E concentrations
imn1tmity. In adult cattle, vitamin A
may be used to assess vi.tan1in E status in
deficiency is associated with retained
dairy cattle. Senm1 concentrations of
placentas and impaired fertility.

2-4 mcg/mL are generally adequate.

However, in addition to vitainin E nut1i

Vitamin D: Vitamin Dis necessaiy for the
tional status, these concentrations are
absorption and metabolism of calcium and
influenced by the total concentration of
phosphorus. Recent reseai·ch suggests that
serum lipid, with higher serum lipid
vitamin D may also be necessaiy for immune
concentrations resulting in higher vitainin
cell function. Vitanlin D3 ( cholecalciferol)

E concentrations. Senm1 lipids are generally
can be formed by the solar irradiation of skin
low in late gestation and high in the period
or vi.tanlin D, by the solar in-a.diation of
of peak feed intake. To compensate for tl1is
forages. However, relia11ce on natural vitanlin fluctuation, senm1 vitainin E concentrations D formation is considered unreliable, and
are sometimes expressed as a ratio, with
vitamin D requirements are basei:f on
some serum lipid component, such as
recommendations for supplement addition
cholesterol or triglyceride, used as tl1e
to diets. The recommended rate of vitainin D
denominator.

supplementation for adult dairy cows is 30
ill/kg body wt, which would be supplied by

Other Vitamins: Most ruminant diets
diets with -1,000 ill/kg dry matter.

provide adequate ainounts of vitan1in K

Vitai1lin D status can be assessed via
and the B vitai1lins, either through natural
blood serum concentrations of 25-hydroxyfeedstuffs or synthesis by microbial activity cholecalciferol. Adequate values ai·e 20-50
in the nm1en. Thus, there ai·e no recomng/mL, with concentrations <5 ng/mL
mended dietary concentrations of these
indicating deficiency.

vitamins for nuninants.

Vitamin E: Vitainin Eis present in
relatively high concentrations in fresh

FEEDING AND NUTRITIONAL
forages. Thus, cattle receiving pasture or

MANAGEMENT
fresh-cut forages may require little vitai11in

E supplement. In contrast, vitai11in E

Three general types of nutritional ma11agedegrades in stored forages, so dairy cattle ment systems are typically used in dairy
on typical confinement-reared diets require
production: confinement systems with totally
supplemental vitanlin E.

mixed rations (TMRs ), confinement systems

Vitainin E functions to protect cellulai·
in which concentrates and forages are fed
membranes from oxidative dan1age. Clinical separately, and pasture-based systems.

NUTRITION: DAIRY CATILE 2279

Totally Mixed Rations
or fiber, is useful in assuring that the

TMRs have all dietary components included
ingredient nutrient profiles and proporin a single uniform mixture. TMRs have the tions are consistent with the intended diet
nutritional advantage over other types of
fonnulation and are stable over time.

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feedmg systems, in that fiber and nonfiber

Management of feed delivery and
ration components are delivered in unifom1
availability is another important aspect in
proportions throughout the feeding period.

the use ofTMR mixes. Cattle should have

This minin1izes fluctuations in rumen pH
continuous or nearly continuous access to
and promotes healthy rumen conditions
feed. Adequate bunk space is impo1tant,
even at relatively high rates of energy intake. W1th reconunendations for optimal linear Adequate management ofTMR systems
space usually 45-60 cm/anin1al. Bunks
requrres a means of accurately weighing
should be cleaned daily, and the orts
each component of the mixture and a mixer
weighed so that daily feed intake for the
capable of incorporating forages and
group may be calculated. 1b assure optimal
concentrates into a uniform product. Several
feed availability, orts should be 2%-4% of the
types of suitable mixers with self-contained
total ainount fed. Paiticle length of the orts
weighing devices are available commercially. should be measured to assure that sorting of Many mIXers are lin1ited in their capacity to
the feed, which usually results in large
mIX long-stemmed forage into the diet thus
particles bei?g left behind, is not occurring.

limiting the use of dry hay in TMR die�. This

For effective use ofTMR diets, cows must
means that maintaining particle size
be separated into feeding groups: minin1ally,
adequate to deliver sufficient effective fiber
a lactatmg and a nonlactating group, and
can be a challenge with TMR diets. Limiting
opttmally, two or more lactating cow groups
the durat10n of the mixing process helps
and two dry cow groups. One dry cow group
maintain sufficient effective fiber if silages
should comprise those cows in the first 4--6
have adequate particle length initially and
wk of the dry period, and the other those in
the paiticles are not further comminuted
the 2-4 wk before calving. Diets for lactating
during the mixing process. Sieves to monitor
cow groups should be fommlated with a lead
paiticle size in TMR mixes are available
factor, meaning the diet should be balanced
commercially. See
for more milk production than the average of

TABLE 32 for reconm1ended
paiticle size distribution in TMR mixes
the group. This is to ensure that the nutrient
based on a popular sieving system.

requirements of the higher-producing cows

Frequent monitoring of dry-matter
m the group ai·e met. Optimal lead factors
concentrations of moist feeds is paiticularly
depend on the nun1ber of feeding groups and
in1portant in the management ofTMR diets.

thetr stage of lactation. When two groups of

This is because diets are formulated based
lactatmg cows ai·e used, feeding for >200A, of
on the nutrient concentrations of the feeds
the average production is frequently
on a dry-matter basis, but the ingredients
reconunended.

are mixed based on their moist weight.

Therefore, accurate dry-matter concentra

Unmixed or Component-fed Rations
tion values are critical to ensure the nutrient Confmement feeding systems in which profile of the final diet is as intended.

concentrates are fed separately from forages

Routine analysis of the TMR mixture for
are traditional in many areas of the world.

major nutrient fractions, such as moisture

Advantages of this system relative to the

PA RTICLE SIZE RECOM MENDATIONS FOR TOTALLY

MIXED R ATIONS•

Percentage by

Pore Sizeb (cm)

Particle Size (cm) Weight

Upper sieve

1.9

>1.9

2-8

Middle sieve

0.79

0.77-1.9

30-50

Lower sieve

0.13

0.18-0.77

30-50

Bottom pan

<0.18

<20
a B ased on the use of the Penn State Particle Separator. Data from J. Heiru-ichs and p Kononoff pennsylvarua State Uruvers1ty.

b Pores are square, so the largest opening is the diagonal.

2280

NUTRITION DAIRY CATILE

TMR system include the lack of need for spehave low NDF concentrations. Thus, rwnen cialized mixing and feed delivery equipment
fennentation conditions, particularly pH,
and the ability to adjust concentrate feedi.ng
may be a problem. Supplementing the
an1ounts to the needs of individual animals.

pasture witl1 dry forages to maintain

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A major disadvantage is that starch and
adequate effective fiber concentrations
other noniiber carbohydrates are generally
is frequently necessary. '

provided in a small nwnber of meals per day,

Dry matter consW11ption in pasture
typically at milking ti.me. Thus, there is the
systems may lin1it nutrient intake because
possibility for large fluctuations in rwnen
maximal consumption rates are lower than
pH, which may impair fiber digestion and
in confinement systems. This will limit
contribute to poor rwnen health. Systems
energy intake, thus requiring supplemental
have been developed to avoid large
energy sources to be fed to achieve high
concentrate meals. These include compulermilk production. Milk production rates in delivered diets in which cows are electroniunsupplemented pasture feeding situations cally identified and a compute1ized feeding
a.re seldom >25 kg/day. Energy supplements
apparatus delivers small, individually
may include starches such as cereal grains
progran1med meals throughout the day.

or highly fern1entable fiber sources such as

In addition to the potential for fluctuagrain byproducts. Protein, and paiticularly tions in rwnen pH, another disadvantage of
sources of RUP, may also need to be
component feeding systems is the inability
supplemented. Protein concentrations
to monitor forage intake. This is because
in pastw·e grasses may be high but are
there is no direct need to weigh the amount
generally highly nunen degradable.

of forage offered if it is not being mixed with
other diet components. Thus, there is no
means to accurately adjust concentrate

FEEDING YOUNG CALVES
intake to match fluctuations in forage
consW11ption. This becomes a particular

To assure adequate passive transfer of
problem in hot weather during which forage
antibodies, all calves should receive at least
consW11ption may be reduced substantially

2 L of high-quality colostrW11 within 6 hr of
while concentrate consW11ption is less
birth. Colostrwn feeding should continue
affected. This leads to alterations in the

W1til calves are 3 days old, but the initial
intended proportions of fiber and nonfiber
feeding of colostrilll1 is critical for passive
carbohydrates in the diets.

transfer of inunwuty.

Pasture-based Feeding Systems

Traditional System of Replacement

Modern means of pasture management

Dairy Calf Feeding
have evolved to optimize use of forage

After the period of colostrilll1 feeding, the

.resources in pasture systems. Such systems
traditional nutritional strategy for raising
require intensive management of pasture
dai1y replacement calves has been to
for optimal dry-matter and nutrient yields
minimize liquid feed consun1ption,
and for optimal feeding and nutrition of
maxinuze solid feed consumption, stinmlate
high-producing modern dairy cows. To
early rumen development, and weai.1 calves
achieve these objectives, paddocks must be
at a relatively young age ( usually 4--S wk).

rotated frequently, so forages are conswned

Although growt11 rates are less than
at an optimal stage of growth and overgrazmaxin1al, feed costs ai·e minimal. In addition, ing does not occur. Pastures are typically
the risk of enteric disease after weaning is
divided into paddocks via the use of easily
less than during the liquid feeding period,
moved electric fences. Cattle are rotated
making early weaning beneficial in the
th.rough paddocks as forages reach stages of maimgement of enteric disease.

growth optimal for both dry-matter yields

Under this system, targeted rates of gain
and nutrient composition.

for calves of the large dairy breeds are

From a nutritional standpoint, the three

-400-600 g/day for the first 3-4 wk of life.

major challenges of pasture-based dairy

This requires a d.Iy-matter intake of 600-750
systems are maintaining favorable rW11en
g/day; -450 g of this is supplied from liquid
fern1entation conditions, maintaining
feed, which equates to -4 L of milk or
adequate dry matter intake, and meeting
reconstituted milk replacer/day for calves
energy and protein requirements. Managing
weighing 40-50 kg at birth. This ainount

!'Wl1en health and dietary fiber adequacy can should be divided between at least two be as challenging with pasture-based
feedings/day. The remaining dry matter
systems as with other dairy feeding systems. should come from a high-quality calf starter, Lush, rapidly growing pasture grasses with
which is a concentrate mixture specially
high energy and protein density typically
prepared for young calves. As calves grow,

NUTRITION DAIRY CADLE

2281
the amount of liquid feed/day remains
are born with small, nonfunctional rwnens,
constant, and increases in growth rate are
and rapid rumen development is critical for
accounted for by increases in calf starter
early weaning. Rwnen maturation is
consumption.

stimulated by the presence of fermentation

Liquid feeds for young calves include
products, particularly buty:Iic acid. Thus,

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milk, waste milk, excess colostnun, and
introduction of highly fermentable substrate
milk replacers. Milk and excess colostrum
into the diet is important to rumen developcan be high-quality feeds for suckling ment. High-quality calf staJ.ters are composed
calves, but adequate biosecwity precauof highly fermentable carbohydrates in a tions, such as pasteurization and screening
mixture that is coarse in texture, contains
of cows for chronic infectious diseases such few fine or powdery particles, and has a as bovine leukosis and Johne's disease,
relatively high fiber concentration ( -12"/o-
need to be in place.

15% NDF). The crude protein concentration

Milk replacers are designed to mimic
should be -18o/o-24% on a dry-matter basis.

bovine milk and thus contain a source of

Calves should not be fed hay before weaning.

protein, fat, and carbohydrate. Protein

Hay consw11ption may actually impede
concentrations in milk replacers vary from
nunen development, because hay is less

18% to as much as 30% on a dry-matter basis
fermentable than concentrate.

but typically are 20%-25%. Protein sources

A critical factor in stimulating starter
in milk replacers vary and may substantially
consun1ption is the availability of fresh
affect the quality of the replacer. Proteins
water. Calves should have readily available
de1ived from milk sources, such as whey
fresh water. Water conswnption will vary
protein isolate, delactosed whey, dried skim
greatly by calf but may be >4 llday in
milk, and casein, are generally excellent
addition to milk or milk replacer.

sources of protein, but the quality of even
these protein sources may be affected by

Feeding Calves in Cold Weather
processing methods. Other animal proteins
such as plasma proteins also may be of good The lower limit of the thermoneutral zone quality. Plant protein sources vary in their
for calves between birth and 3 wk of age is
acceptability, particularly for calves <3 wk

20° C and for calves >3 wk old, 10° C.

old. Appropriately processed plant proteins

Maintenance energy requirements increase
may be acceptable but are generally less
as temperatures fall below these values. To
desirable than animal proteins for calves
compensate for these increased energy

<3 wk old. Plant proteins acceptable for use
requirements, milk replacers with fat
in milk replacers include soy protein isolate
concentrations <Cl5% should be fed in cold
and soy protein concentrate; these proteins
weather. Furthermore, the an1ount of dry
may be processed to reduce antigenicity
powder should be increased by 50 g/day for
and to remove antinutritional factors such
each incremental decline of 5° C below the
as trypsin inhibitor. The degree of processthermoneutral zone. For example, if calves ing varies by manufacturer, and not all milk

<3 wk old are receiving milk replacer
replacers containing these protein sources
powder at 450 g/day at <C20° C, the amount
are of equal quality. Unprocessed soy flour
should be increased to 650 g/day at 0° C and
is an unacceptable protein source for milk
to 900 g/day at -25° C. The dry powder
replacers.

should be reconstituted with proportionate

Fat concentrations in milk replacers vary
increases in the amount of water. Feeding
from lO"Ai to as high as 30"Ai, with most in the this an10unt of liquid frequently requires
range of 15o/o-20"Ai. Fat sources usually
more than two feedings per day. In addition
contain some coconut oil and major
to milk or milk replacer, fresh water should
contributions from tallow, choice white
be made available at least twice per day.

grease, or lard. Lecithin and/or monoglycerides are usually added as emulsifying agents.

Feeding Calves with Enteric Disease

Fat concentration substantially influences

Diarrhea is a common condition in young
the energy concentration of milk replacer.

calves and frequently results in life-threat

In cold climates in which high energy
ening dehydration. Electrolyte solutions
conswnption is critical for young calves, fat
administered orally can be beneficial in
concentration should be <Cl5%. The drawback supp01ting hydration and successfully of higher fat concentrations is that the rate of
treating calves with diarrhea. To help
starter consun1ption is reduced as replacer
control and correct dehydration, it may be
fat concentrations increase.

necessary to reduce milk or milk replacer

Early introduction of solid feed is
feeding for a brief period after the onset
in1portant for replacement calf rearing. Solid
of diarrhea. Nutritionally, however, the
feed stimulates rumen development. Calves
objective is for calves being treated for

2282

NUTRITION: DAIRY CADLE
diarrhea to be back receiving milk or milk

However, such RUP concentrations would
replacer as soon as possible. With appropribe difficult to achieve without inclusion of ate use of oral electrolytes, milk or milk
anin1al-protein products or specially
replacer feeding should be reinstituted
processed protein supplements. Diets such
within 12-24 hr after the onset of diarrhea.

as those in these exainples would best be

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Electrolyte solutions can be fed along with
delivered as TMR.

,
milk or milk replacer. Supporting the calf

Heifers of appropriate body weight
with adequate nutrition speeds restoration
become sexually mature at -15 mo old and
of the gut epithelium and generally
should be bred at that time. After breeding,
improves calf health and immunity.

requirements for protein and energy during
gestation may be met with good quality

FEEDING CALVES FROM
forages. In general, the feeding of com

WEANING THROUGH
silage during this period should be limited

MATURATION
to no more than one-half of the diet dry
matter, preferably less. This it to prevent

After weaning, calves should receive
fattening, which increases disease risk at
free-choice calf staiter until 3 mo old. If hay
calving.

is fed during this period, it should be of

Optimal growth rates of dairy heifers
excellent quality and fed in limited amounts. between 2 mo of age and conception are Energy requirements for adequate growtl1 in important for dairy herd profitability.

calves 3-15 mo old may be derived lai·gely

Insufficient growth rates result in either an
from good quality forage. Meeting protein
older age at first calving, which increases
requirements during this period is
the cost of heifer rearing, or smaller dams
challenging, because protein requirements
at first calving, which limits milk producare high relative to energy requirements.

tion and conception rates during the first

This is because in replacement heifers, lean
lactation. Conversely, excessive growth
body weight gain is preferred over fattening. rates, especially those associated For sainple diets for large-breed dairy
primarily with fattening, can adversely
heifers 3-15 mo old, see TABLE 33. The crude affect subsequent milk production and
protein concentrations of these exainple
also increase the risk of metabolic
diets are high, because there is excess RDP.

problems at calving. Target growth rates
lf rumen bypass (high RUP) ingredients
between weaning and conception should
were included, the crude protein concentrabe 700-900 g/day. As growth rates increase tions could be lower and still meet the
within this rai1ge, the proportion of crude
metabolizable protein requirements.

protein and RUP in the diet needs to be

EXAMPLE DIETARY CHARACTERISTICS FOR GROWING

REPLACEMENT HEIFERS

BodyWt(kg)

100

150

200

250

DMI (kg/day)

3.1

4.2

5.2

6.1

Concentrates (% of dry matter)

40

20

5

0

Forage (% of dry matter)

60

80

95

100

Crude protein (% of dry matter)

21

20

18.5

18.4

Metabolizable protein(% of dry matter)

11.7

9.6

8.5

7.7

RUP(%ofCP)

32%

28%

22%

21%

RDP(%ofCP)

68%

72%

78%

79%

ME (Meal/kg)

2.5

2.4

2.2

2.2

Based on requirements generated by the computer program that accompanies Nutrient Requirements of Dairy Callie, 2001, Nalional Aca<.lerny of Sciences, National Academy Press, Washington, DC. The crude protein requirements of animals <150 kg are relalively high and could be reduced by tl1e use of protein sources witll higher RUP proportions. DMI, dry matter intake; RUP, rumen w1degradable protein; RDP, rumen degradable protein; ME, metabolizable energy.

NUTRITION: DAIRYCATILE

2283
increased to support greater lean body
and size. Calves between weaning and 5
gain and prevent fattening. Weight and
mo old should be kept in groups of six or
height should be measured periodically
less. Older calves may be kept in larger
to check that growth rates and frame
groups, but animal size should be fairly
development are as intended. The growth
uniform.

response of heifers to apparently similar

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diets varies greatly among farms, making
the monitoring of growth rates particu

ACCELERATED CALF-REARING
larly important. For target body weight

PROGRAMS
values at a range of age increments for
heifers of various mature body sizes, see

In accelerated calf rearing progran1s, larger

TABLE 34.

quantities of liquid feeds are fed during the

The different dietary requirements of
preweaning period, and larger proportions
calves at various ages dictate that they be
of concentrates are fed during the growing
kept in separate pens based on their age
period. Weaning is later, and solid feed

IU:11111 RECOMMENDED BODY WEIGHTS FOR HEIFERS OF DIFFERENT AGES

Approximate Target Body Wt (kg)

% of Mature Small

Medium

Large

Heifer Age (mo)

Body Weight Breeds

Breeds

Breeds

Birth

6.2

28

34

47

1

9.1

41

50

68

2

12.3

55

68

92

3

16.2

73

89

122

4

20.0

90

110

150

5

23.7

107

130

178

6

27.5

124

151

206

7

31.2

140

172

234

8

35.0

158

193

263

9

38.9

175

214

291

10

42.5

191

234

319

11

46.3

208

255

347

12

49.9

224

274

374

13

53.7

242

295

403

14

57.4

258

316

430

15

61.1

275

336

458

16

64.7

291

356

485

17

68.5

308

377

513

18

72.2

325

397

541

19

76.0

342

418

570

20

79.6

358

438

597

21

83.3

375

458

625

22

87.1

392

479

653

23

90.8

409

499

681

2284

NUTRITION: DAIRY CADLE
consumption is delayed (relative to

FEED ADDITIVES
traditional programs). After weaning, forage
is not offered until heifers are >3 mo old.

Many non-nutrient feed additives are

Dietary protein concentrations during the
marketed and approved for use in dairy
pre- and postweaning periods a.re increased
ca.UJe (see TAIJLE; 35).

(relative to traditional progran1s) to a.sslU'e

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adequate lean gain and to a.void excessive

NUTRITION AND DISEASE
fattening. Rates of gain can be as high as

1 kg/day, with heifers entering the mi.I king

Nutrition has a large effect on the occlll'herd at 22-23 mo old. Close monitoring is rence and severity of many diseases of dairy
necessary to a.sslU'e that heifers have
cattle. See TABLE; 36 for brief descriptions of adequate fran1e development and do not
nutritiona!Iy associated diseases, disease
become excessively fat.

signs, etc.

•hi:i•§j FEED ADDITIVES INCLUDED FOR NON-NUTRIENT BENEFITS

Additive

Effect

Feeding Rate

HIGH PROBABILITY OF POSITIVE ECONOMIC RETURN IN

GENERAL FEEDING SITUATIONS

Rumensin

Increased feed efficiency, improved 200-400 mg/clay energy metabolism

Sodium bicarbonate Improved feed consumption,

0. 75% of dry matter
and other buffers
stabilization of rumen pH, increased
butterfat production

Yea.st cu.lture

Improved feed consumption,

Variable, consu.lt
improved fiber digestion
manufacturer directions

HIGH PROBABILITY OF POSITIVE ECONOMIC RETURN IN

SPECIFIC PROBLEM SITUATIONS

Strong anion

Improved calcium homeostasis, milk Variable, calculate DCADa, additives for
fever prevention
monitor urine pH and dryprepa.rtum diets
ma.tter intake, late
gestation only

Propylene glycol

Improved energy metabolism,

300-500 mUday, late
ketosis prevention
gestation and early
lactation only

Niacin

Improved lipid metabolism,

6 glda.y, include protected
improved run1en fermentation,
and unprotected solU'ces
increased feed efficiency and milk
component concentrations

Mycotoxin

Many products available; effective

Variable, consu.lt
neutralizers
ness best demonstrated against
manufacturer instructions
a.fla.toxin; effectiveness against
trichothecene toxins including

DO Nb or vomitoxin needs further
evaluation.

Protected choline

Improved lipid metabolism, fa.tty

15 glda.y, late gestation and
liver and ketosis prevention
early lactation only
a DCAD ( dietary cation-anion difference)

b DON (deoxynivalenol)

NUTRITION DAIRY CADLE

2285

DISEASES OR CLINICAL SIGNS IN DAIRY CATTLE THAT MAY BE

RELATED TO DIETARY CHARACTERISTICS OR NUTRITIONAL

DEFICIENCIES

Sign

Possible Nutrient or Dietary Involvement

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Abortion (seep 1333) Deficiencies of trace minerals or vitamins, especially selenium, vitamin A, or vitamin E

Anemia (seep 7)

Possible copper or cobalt deficiency in adult cattle; iron deficiency in young calves ( unlikely in adult cattle) Blindness and night

May be an initial isolated sign of polioencephalomalacia; may be blindness
associated with vitamin A deficiency, with or without signs of corneal opacity

Bloat ( see p 227)

Consumption of legume pastures or finely ground, high-starch diets (such as are frequently fed to feedlot cattle) are predisposing; cattle not acclimated to these diets are particularly susceptible

CNS signs

Incoordination, blindness, nystagmus, thrashing, and opisthotonos may be associated with polioencephalomalacia; high-starch diets with microbial inactivation of thian1ine and high-sulfur diets such as those associated with heavy feeding of distiller's grains and solubles

Congenital defects

Deficiencies of vitamin A, manganese, or copper

Convulsions

Sign of vitamin A deficiency, particularly if they occur intermittently interspersed wiili periods of normal activity in growing calves; should be differentiated from nervous coccidiosis Cystic ovaries

Energy insufficiency and associated subclinical ketosis in early (seep 1354)

lactation are predisposing; vitamin E and selenium deficiency speculated to contribute

Diarrhea

Nun1erous dietary factors, including abrupt changes in diet, especially those associated with increases in dietary nonfiber carbohydrates and dietary rumen fermentability; lush rapidly growing pasture and increased dietary protein or salt concentrations Displaced abomasum Both metabolic and nutritional causes; feeding should be to (seep 238)

prevent ketosis and stimulate high dry-matter intakes; both pre- and postpartum diets are important in management Dyspnea

Atypical interstitial pneumonia associated with movement of cattle from poor pasture to lush pasture; associated with ruminal conversion of tryptophan to 3-methyl in dole Fatty liver (see

Overfattening in late lactation or during the dry period p 1018)

accompanied by poor feed intake in late gestation and early lactation

Hypomagnesemic

Functional and absolute magnesium deficiency; risk increases tetany ( see p 996)

with consumption of lush pasture grasses, especially with high potassium concentrations

Inappetence

Many nutritional deficiencies (protein, mineral, vitamin) (off feed)

eventually result in reduced feed intake

In coordination

Blind staggers associated with chronic selenium intoxication; demyelinization associated with copper deficiency

Infertility

Energy is the most clearly associated nutrient; insufficiencies of carotene or manganese may affect ovarian function

( continued)

2286

NUTRITION DAIRY CADLE

DISEASES OR CLINICAL SIGNS IN DAIRY CATTLE THAT MAY BE

RELATED TO DIETARY CHARACTERISTICS OR NUTRITIONAL

DEFICIENCIES (continued)

Sign

Possible Nutrient or Dietary Involvement

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Ketosis (seep 1024)

Excessive lipid mobilization and insufficient gluconeogenesis; overfattening in late gestation and insufficient feed intake in early lactation are the primary nutritional influences Laminitis (seep 1082) Chronic or acute laminitis and their sequelae are thought to result from diets with high concentrations of nonfiber carboh y drates Milk fever (parturient Caused by failure of calcium homeostasis rather than dietary paresis, seep 988)

calcium deficiency; control by feeding low-calcium diets or acidifying diets prepartum

Pica and dirt eating

Common causes are not well determined; sodium deficiency, potentially phosphorus deficiency, low-fiber diets implicated Polioencephalomala Associated with either ruminal destrnction of thiamine or with cia (seep 1281)

ruminal production of hydrogen sulfide associated with high-sulfur diets; more common in feedlot than dairy cattle Retained fetal

Deficiencies of selenium, vitamin A, or vitamin E, but adding membranes
these nutrients to adequate diets will not reduce incidence; (seep 1381)

metabolic problems associated with prepartum negative energy balance may also be predisposing

Rickets and osteoma Insufficient calcium, phosphorus, or vitamin D consumption lacia (seep 1051)

Rumen acidosis,

Usually associated with major errors or inconsistencies in feed acute clinical
delivery in which high starch intake occurs in cattle unaccustomed to such diets; associated with formation of lactic acid in the rumen with severe drops in rumen pH

Rumen acidosis,

Associated with lactation diets with high nonfiber carbohydrate chronic subclinical
concentrations and low fiber concentrations; also associated (seep 225)

with high rumen concentrations of volatile fatty acids and rumen pH values s;5.2

Skin problems

Problems such as dull, brittle hair coats, hypotrichia, easily depilated hair, hyperkeratosis, thin skin, and poor healing may be associated with nutritional problems; deficiencies of vitamin A and zinc, generalized protein-calorie malnutrition Sudden death

Deficiencies of vitanlins A or E, selenium, or copper Suppressed immunity Generalized immunosuppression, including both cellular and humoral immunity, may occur due to malnutrition; specific nutrient deficiencies include vitamin A, vitamin E, zinc, copper, and selenium; also generalized protein-calorie malnutrition Toxicities

Many toxicities associated with feed borne toxicants; including nitrates, cyanide, many mycotoxins, toxic plants

Urolithiasis

Diets with high phosphorus and low fiber concentrations (seep 1502)

Wasting and failure

Signs of many nutritional deficiencies, as well as of chronic to thrive
diseases such as internal parasitism; cobalt deficiency is a well-documented cause of ill thrift in cattle; protein-calorie malnutrition should always be evaluated

White muscle disease Dietary deficiency of selenium or vitamin E

(seep 1172)

NUTRITION: EXOTIC ANO ZOO ANIMALS

2287

NUTRITION: EXOTIC AND ZOO ANIMALS

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The field of zoo and exotic animal nutrition
may be needed sometimes, depending on
continues to make advances that result in
the animal and circumstances.

better diets. Exotic animal nutritionists in

Although the NRC requirements are less
zoos and in the feed industry are studying
directly applicable to other species, they
problems and generating information on
can still serve as a useful general reference
proper nutritional management for many
to evaluate the nutritional adequacy for
species.

most birds and mammals. The formulation

All animals require nutrients and energy
and evaluation of diets for reptiles and
in a metabolizable form. The nutrients and
amphibians is even more difficult, because
energy must be properly balanced and in the there are no domestic animal models and correct fom1 to acconrn1odate particular
because metabolic rates of poikilothermic
tastes, digestive systems, and feeding
animals fluctuate with changes in ambient
methods. For example, large psittacines
temperature. Once the nutrient concentratypically use their feet to hold food, whereas tions for the diet have been established, the other species obtain or position food using
types and an10unts of foodstuffs, methods
other appendages ( or they do not manipuof presentation, and feeding frequencies late food). If a commercial extruded food is
should be selected based on the physical
fed, the pieces must be large enough for the
and behavioral attributes of the species.

bird to grasp easily. Diets for exotic and zoo

All food should be of good quality. Spoiled
animals have been developed by consideror moldy foods, or foods stored for long ing food habits in the wild, oral and GI tract
periods ( eg, > 1 yr for most bagged feeds and
morphology, nutrient requirements

6---12 mo for most frozen foods) should not
established for domestic and laboratory
be fed. The practice of "topping off' the feed
animals and people, nutritional research on
bowl daily or every other day should be
exotic species, and practical experience.

discouraged, because uneaten food on the

The ultimate criteria to evaluate the
bottom can spoil. Food and water dishes
suitability of a diet for a given species are
should be thoroughly cleaned before adding
growth, reproductive success, and
food or water. Clean, fresh water should
longevity.

always be available to nonmarine species.

The mininlum nutrient requirements

Trace mineral salt blocks, bricks, or
established by the National Research Council "spools" are conunonly offered to ungu

(NRC) for domestic and laboratory animals
lates, psittacine birds, and some roaents.

can be useful starting points in setting target

Cafeteria-style feeding is strongly
nutrient levels for an exotic species. For
discouraged, because captive animals
exan1ple, the Nutrient Requirements of Small
rarely select a balanced diet if given a wide

RUlllinants, published by the NRC in 2007,
selection of foods. Usually, a nutritionally
contains nub.itional infom1ation on cervids
complete commercial product or in-house

( white-tailed deer, red deer, wapiti, and
mixture that cannot be sorted should
caribou) and camelids (llamas and alpacas).

comprise the bulk of the diet, with com

For many exotic species that have
ponents such as meat, fmit, and seeds
closely related domestic counterparts, diets comprising only a small percentage.

can be formulated to contain nutrients that

Pelleted diets are especially important
would meet the requirements established
with psittacines, to avoid self-selection
for ungulates, mustelids, canids, felids,
of calcium-deficient seeds.

rodents, primates, lagomorphs, gallina

To improve consumption of pelleted
ceous and anseriform birds, and fish.

diets, feeding should be done in the

However, nutrient requirements estabmorning, with the other food items offered lished by the NRC should be used only as
during the day. All diet items to be fed
guidelines, because the goals of livestock
should be weighed, and the actual intake
producers in feeding their animals include
recorded.

rapid and efficient gain and high milk yield

Muscle and organ meat, fruit, most grains
or egg production-goals that differ from
and seeds, and most insects are poor
the goals in zoo animal management. In
sow·ces of calcium, and excess consumpzoos and other exotic animal collections, a tion can result in calci un1 deficiency.

maintenance diet should be fed in general,

Calcium gut-loading diets containing at least
although a breeding or other specific diet

12%---15% calcium should be fed to insects.

2288

NUTRITION EXOTIC AND ZOO ANIMALS

Dusting with a balanced calcium-phosphoconditions of high temperature or low rus powder is also a possibility; however, it
hw1lidity in which evaporative losses Ca.Jl be
is doubtful this can add enough calcium to
expected. The salt content of water should
the diet. Other sources of calcium include
be known, because some species are less

VetBooks.ir
oyster shell, cuttle bone, and ground
tolerai1t tha.Jl otl1ers. Animals feel dry feeds
calciwn carbonate tablets.

(pellets, extrusions, hay, etc) require more

Obesity is more common than inadequate
water tha.J1 those fed succulent feeds.

nutrient intake. Ungulates, primates, and

Potable water should be available ad lib.

carnivores can rapidly become overweight

Ma.J1y a.Jlin1als in the wild conswne much
when excess amounts of a high-quality diet
of their water in the foods tl1ey eat. When
are offered, paiticularly when activity is
low-moisture foods ai·e conswnecl (pellets,
limited. In some birds ( eg, ratites, waterextrusions, etc), some animals, depending fowl), rapid growth rates increase the
on how water is presented, may not
incidence of leg and wing problems. Both
maintain adequate hydration. Ma.J1y
adult and growing animals should be
free-ra.J1gi ng small ai1d tropical lizards
routinely weighed to monitor chai1ges. If
receive water from foods ai1cl from licking
weighing four times a yeai· is not possible,
drops that accumulate after rainfall. When
a body score index should be performed.

in captivity, they frequently do not drink

If a dietary change is contemplated
readily from containers. In nature, birds of
because of suspected nutrient imbala.J1ces,
prey do not drink; however, in captivity,
deficiencies, or toxicities, the diet currently
they do drink sometimes, depending on the
fed should first be computer-ai1alyzecl to
circwnstai1ces, so clea.J1 &inking water
assess nutrient concentrations. Ingredient
must be available at all times.

or nutrient cha.J1ges Ca.Jl then be made based

Hunlidity may be especially importa.Jlt
on correcting a suspected or confim1ed
to maintain hydration of many reptiles,
health problem. For captive, exotic ailimals,
especially tropical species. Daily misting
establishing a.Jld maintaining clietai-y
with wann water is aJl irnp01ta.Jlt source of
histories ca.ii be particulai·ly helpful in
hydration for some lizards that may not be
health assessment. Activity patterns of
observed drinking sta.Jlding water. Eye
individuals are also important ( eg,
lesions in senliaquatic twtles ( eg, box
atherosclerosis is relatively common in
tmtles) a.Jlcl some tortoises may be the
obese birds).

result of low environmental hmltidity ( or
possibly upper respiratory tract disease)

Nutritional Supplements: The use of
ai1cl not vita.Jllin A deficiency. Conjunctivitis
nutritional supplements is populai· among
may respond better to supportive a.J1tibiotic
ailimal caretakers. Although many keepers
therapy a.Jld higher hunlidity tha.Jl to
ai1d pet owners use nutritionally complete
supplemental vita.Jllin A Dietary histories
feeds that require no· supplementation,
may be especially important in such cases,
supplements are still often provided.

because ma.J1y captive twtles are feel

The nutrient content of tl1e current diet
commercial food, which is mostly cat food
should be established or estimated first
high in vitainin A
to detemtine whether a.Jly �upplement is

For a discussion of nutrition for orpha.J1ed
needed or whether a supplement should be
ailimals, seep 2100.

discontinued. Unfortunately, diets ai·e rai·ely
evaluated first to cletem1ine which nutrients

(if a.J1Y) are unbala.J1cecl.

If a nutrient is deficient in a cliet, a specific The exact nutritional requirements for most supplement in a specific ainount should be
species of birds ai·e still unknown. The
recommended. Excessive supplementation
exceptions are birds raised for food or other
of some nutrients ( eg, some fat-soluble
products, such as poultry, ducks, ostriches,
vita.J11ins, seleni w11, copper) Ca.Jl be just as
and pheasa.Jlts. Avia.Jl diets for ma.J1y species
harmful as not enough because of toxicity
are extrapolated from the Nutrient
a.Jlcl nutrient imbala.J1ce. Diets consisting

Requirements of Poultry published by
primarily of grain products a.Jlcl cultivated
theNRC.

fruits a.J1cl vegetables may need nlicronut1ient supplementation; however, supple

PSITTACINES
ments vai-y widely in tl1eir composition.

The pet bird population consists largely of

Water: Water intake should be assessed
psittacine species, primarily passerine� arnl
routinely but especially in ailimals with
other genera such as those that include
compromised renal function, in lizards or
toucailS. Psittacines eat mainly a pla.J1tbirds prone to gout, a.J1d in a.Jlimals under based cliet a.Jld Ca.Jl be classified overall as

NUTRITION EXOTIC AND ZOO ANIMALS

2289
florivores. The content of the diet-fruit,
acid cysteine, because feathers average 25%
nectar, seeds, or a combination-varies by
of the total body protein content of birds.

species. Some species ingest a percentage of

Excessively high dietary protein has the
insects or carrion. Although requirements
potential to cause renal insufficiency and

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and dietary sensitivities vary among
gout in birds with preexisting renal
psittacine species, the pelleted and extruded
impairment or a genetic predisposition to
diets that have been produced for parrots
gout. Cockatiels with no preexisting renal
have tremendously improved the nutritional
disease have been shown to tolerate
intake and subsequent health and quality of
extremely high dietary protein levels ( up to
life of these birds. However, pelleted diets

709t>) with no renal impaim1ent. A genetic
differ in content and quality and must be
predisposition to renal disease/gout has
evaluated individually. Extruded pellets in
been documented in some strains of poultry
different shapes and sizes are available for
and may be seen in other avian species.

maintenance and breeding purposes. Many

Sudden, dran1atic increases in dietary
pellets contain omega-3 fatty acids as well as
protein may overload the kidneys, producing
probiotics.

hyperuricenua and visceral gout. When

Psittacine nutrition has been the focus
increased dietary protein is indicated, it
of research throughout the past several
should be increased gradually to avoid renal
decades. Several myths of psittacine
dan1age.

nutrition have been debunked during this
period. Grit, while probably necessary for

Fat: Dietary fat provides essential fatty
some passerines and Columbifom1es to aid
acids, energy, and hormone precursors. It
in mechanical digestion, is not needed by
also contributes to egg yolk formation and
psittacines. If seeds are consumed by
aids in absorption of fat-soluble vitamins.

psittacines, they are hulled before ingestion.

Diets should contain 5%-12% fat, depending

Monkey chow biscuits are nutritionally
on the species, the general condition of the
incomplete, and some brands tend to harbor psittacines, and the physiologic stage and bacteria or promote excessive gram-negabrood condition. At least 1 % of the dry diet tive bacterial growth when included in bird
should consist of PUFA ( eg, linoleic acid).

diets. Strictly seed diets, regardless of

Excessive dietary fat leads to obesity,
supplementation, are suboptimal for
metabolic diseases, cardiac disease, and
psittacine species. Deficiencies of vitamin
atherosclerosis (see also PET BIRDS, p 1885).

A, protein (the amino acids lysine and

The fat requirements of psittacines for
methionine, in particular), calcium, and
reproduction are generally lower than those
other nutrients are seen in most psittacine
of poultry, because the psittacines' altricial
species on seed-based diets. Conversely,
young do not require the same quantity of
excessive vitamins, such as vitamin A, are
fatty acids as do the precocial young_ of
added to some pelleted diets, which can
chickens. However, diets that are borderline
have equally detrimental effects.

deficient often manifest as problems in
either the psittacine hen or the chicks

Protein: Protein (amino acid) requireduring reproduction.

ments of psittacines have not been well
established. The amino acid deficiencies

Vitamins: Vitamin A is necessary for
most consistently noted in psittacine birds
vision, reproduction, immunologic
on seed-based and table-food diets are
integrity, and growth, and for the maintelysine and metluonine. Fiber content must nance of epithelial cells in respiratory, GI,
always be considered when determining
and renal tissues. Vitamin A deficiency has
dietary protein requirements, because
historically been noted in psittacines on
increased fiber causes increased fecal
all-seed diets, so supplementation is
protein "loss." Birds with low-fiber, more commonly recommended. However,
readily digestible diets (such as nectarindiscriminate supplementation leads to feeding lories and lorikeets) may do well on
vitamin A toxicosis, as well as to decreased
diets with easily digestible protein levels as
absorption of other fat-soluble vitamins
low as 3%-5%. Adult maintenance levels of
and carotenoids. In nature, psittacines do
protein for budgerigars and cockatiels
not consume vitamin A but obtain vitanun

(7%-12%) are lower than those for African

A precursors such as carotenoids from vari

Grey parrots (10%-15%). Protein requireous plants. Pelleted diets should contain ments for growth and for egg-laying hens
vitamin A at levels of 5,000-8,000 IU/kg of
are higher than maintenance levels in all
feed. Higher an10unts should be avoided.

birds. Periods of heavy molt also greatly

The source of vitanun A added to bird feed
increase protein requirements, particularly
is not regulated, and significant quality
tl1e need for the sulfur-containing anuno
control issues have been documented.

2290

NUTRITION: EXOTIC AND ZOO ANIMALS

Ideally, a quality pelleted diet for psittacspecies. Most passerines maintained as pets ines will contain multiple carotenoids

(finches and canaries) have hlstorically
and other vitan1in A precursors, with a
been fed primarily seed and are considered
minimum level of vitanlin A.

florivorous to granivorous. Commercial

Some carotenoids in birds are precurseed mixtures for canaries often contain VetBooks.ir
sors for the body's fom1ation of vitanlin A.

a mixture of canary, rape, niger, hemp,

Carotenoids also act as antioxidants and are linseed, and oats. Most of these comn,er necessary in some species ( such as canaries cially available seed mixtures are dei1 • ient
and flamingos) for feather pigmentation.

in nun1erous vitanlins and amino acids. The

The primary function of vitamin Dis
fat-soluble vitanlins A, 03, E, and Kare
to increase absorption of calcium and
generally low, the calcium:phosphorus ratio
phosphorus. Vitanlin D can be obtained
is poor, and the amino acids lysine and
either directly from the diet or from UVB
methionine are insufficient. High amounts

(285--315 nm) light exposure. Vitanlin D
of fat in seed-based diets can lead to obesity
deficiency is probably rare in nature because and to nutritional disorders in the offered of exposure to sunlight. Birds living in polar
food ( eg, calcium and vitanlin deficiency,
conditions get theirvitanlin D during the
as well as an anlino acid disorder).

winter by consUilling diets with hlgh

Egg food (hard-boiled egg-based soft
amounts ofvitanlin D (eg, fish, plankton).

food with added vitamins and minerals)

In the absence of natural sunlight, the
has traditionally been fed by canary
minimun1 oral vitamin D requirement for
breeders during the reproductive season,

Afiican Greys is likely to be 500-1,000 TIJ/kg.

with soaked seed added to increase accept

Vitamin D deficiency may be caused by
ance. Extruded pellets, such as organic
dietary deficiency or lack of exposure to
pellets or pellet-based mash, which

UVB radiation. Limited studies have shown
contains balanced nutrients, are offered by
that species variation in psittacines for UVB
many breeders as a nutritionally consistent
light requirements exist. Unfortunately,
alternative. Pellets are fed for maintenance
many birds are housed totally indoors, and
or breeding purposes. Extruded pellets
owners often mistakenly assume either that
fed for breeding contain 18o/<r-22% crude
the birds do not need direct sunlight or that
protein as well as a limited amount of fat
the sunlight the birds receive through glass

(5o/<r-8%), compared with the high amounts
will supply UVB radiation. Owners of pet
of fat in seeds.

birds should be encouraged to expose their

Soluble grit (ie, oyster shell, cuttlebone)

bird to direct sunlight ( with appropriate
should be provided to canaries and finches.

cautions regarding excessive heat) or to

Sprouts, fruits, and vegetables may be
purchase and properly use UVB bulbs.

psychologically stin1ulating and enhance

However, pet bird owners must consider
breeding in these passerines.

that the further away from the equator, the

Plun1age colors in canaries partially
less UVB is generated, especially in late
depend on the pigments in the diet. For
autunm, winter, and early spring. Some
example, red-colored canaries are fed
research indicates that UVA and/or UVB can canthaxanthins before breeding season.

affect vitamin D synthesis in sori1e bird

Carotenoids vary in their bioavailability, and
species, the finding of food, well-being, and
there are species differences in the types of
feather colors. However, more research is
carotenoids absorbed and metabolized.

needed to determine how much UVA and/or

UVB is needed for each bird species.

Vitamin D toxicity is caused by excessive

COLUMBIFORMES
supplementation. Some psittacine species,
notably macaws, are sensitive to excessive

(Pigeons and doves)

dietary vitanlin D and may develop

Most pigeons are either primarily granivosoft-tissue calcification and renal failure.

rous or fiugivorous, with some inverte

Toxic levels for psittacines have not been
brates also consumed. Seed-eating pigeons
established, but levels that may be toxic for
and doves can be fed commercial pigeon
poultry begin at 2,800 TIJ/kg of feed.

pellets (2 mm). These pellets should be

For discussion of vitamin E, seep 2291.

comparable in composition to that listed in
the NRC requirement of growing chickens

6--12 wk old. Alternatively, psittacine small

PASSE RINES
pellets and mash are accepted by most

Columbiformes but, depending on the

The order Passeriformes contains >5,000
composition, may have to be supplemented.

species of birds and includes frugivorous,

Columbiforn1e parents feed their young
carnivorous, insectivorous, and granivorous with crop milk, whlch is produced from

NUTRITION EXOTIC AND ZOO ANIMALS

2291
desquamated epithelial cells and glandular
an organ meat-based diet is fed, vitamins
secretions of the crop. Crop milk is 1ich in
and minerals should be supplemented;
fat and protein, devoid of carbohydrates,
calcium supplementation should be 10 g
has a low pH, and contains several
of calciwn carbonate/kg of fresh meat.

Lactobacillus species. Seed-eating pigeons

VetBooks.ir
switch in 3-5 days from crop milk produc

PISCIVOROUS BIRDS
tion to feeding their young mostly regurgitated seed. Frugivorous pigeon squabs ( eg, Penguins, pelicans, and other fish-eating
crowned pigeons) rely on crop milk for at
species in the wild feed primarily on fish,
least 30 days.

crustaceans, and squid. These food sources
vary in their fatty acid, vitamin, and

RAPT ORS
carbohydrate contents. In captivity, squid,
smelt, herring, mackerel, and whiting fish

Raptors include birds of prey from many
are commonly available. One of the most
genera. Most medium to large raptors
important aspects of feeding piscivorous
consume whole vertebrate prey. Commonly
birds is fish quality (seep 2297). It is advised fed items include mice, rats, day-old chicks,
to feed several fish species, although in
quail, and pigeons. Kestrels generally
some cases one species of fish has been fed
consume insects. Fish are the natural diet of
for a lifetin1e. Captive seabirds develop
piscivorous raptors such as ospreys and sea
strong preferences for a particular fish if it
eagles. If fish is fed, thiamine supplementais fed exclusively for prolonged periods, tion (30-35 mg/kg feed) as well as vitamin E
which can lead to botil nutritional

(100 mg/kg) is advised.

deficiencies and inanition if the feeder

Commercial diets for birds of prey are
fish becomes unavailable.

available and consist mostly of a mash of

Supplements commonly given to captive
several different prey items with a specific
penguins include vitamins A, D, 81, and E.

amount of vitan1ins and minerals.

The need for these and the quantity that

Small raptors (100-200 g) eat as much
must be supplemented depends on the
as 20%-25% of their body wt/day; rap tors
quality and content of the primary diet.

weighing 200-800 g eat 15%, raptors

Supplements can be added to the fish as
weighing 800-7,000 g eat 6%-10%, and
tablets, as a gel, or as a liquid to be injected
raptors > 7,000 g eat 3.5% of their body wt/
in the fish.

day. Captive raptors should be weighed

Dietary salt (NaCl; 0.5-1 g salt/bird/day)

regularly, and food volume adjusted as
is often provided to birds in freshwater
needed to prevent emaciation as well as
exhibits to help maintain proper functioning
obesity. If weighing is not possible, the
of the salt glands.

breast-comb can be checked: if sharp, the
animal is emaciated; if fat, it is obese.

Thiamine: The process of thawing fish in

The best food for birds of prey is mice and running water depletes them of water-solurats; however, day-old chicks and other ble vitanlins. Additionally, several fish
whole birds or mammal species also are an
species contain thiaminase, leading to
adequate feed. The egg yolk of day-old
thiamine (81) deficiency during the
chicks should not be removed when fed,
defrosting process.

because it contains a considerable amount

Supplementation of thiamine is
of vitamins and minerals. It is advised not
recommended at 30-35 mg/kg fish, daily.

to feed animals from the wild ( eg, rats,
pigeons, rabbits) because of potential

Vitamin E: Most fish are deficient in
diseases, toxins, and poisonings.

vitanlin E. Clinical signs of vitamin E

Although whole prey, including their
deficiency in piscivorous birds include
organs, should be a complete nutrient
weakness and inability to stand or hold the
sufficient feed, it is advised to add a small
wings in normal posture. Severe generalized
amount of a balanced vitamin and mineral
myopathy with muscle atrophy, degenerasupplement, especially when the birds are tion and necrosis, and replacement with
under stress. Prey with relatively large
fibrous connective tissue can occur witil
bones must be avoided because of
chrome pronounced vitanlin E deficiency.

obstructions in the gizzard, which prevent

Supplementation with 100 ru vitamin E/kg
casting. Birds <12 days old should not be fed
fish has been proposed. However, oversuptoo many bones, because they cannot digest plementation (vitamin E at 500-10,500 nJ/kg
them, and metabolic bone diseases can
food) may result in decreased growt11 and
result. Metabolic bone diseases can also
coagulation disorders, possibly from
result when a chick is growing too fast. Birds creating vitamin K deficiency ratiler tilan of prey should not be fed before travelling. If
directly from vitamin E toxicity.

2292

NUTRITION: EXOTIC AND ZOO ANIMALS

Hand feeding of species and individuals of
spp) consume invertebrates, mollusks,
concern will ensure that each bird receives
beetle larvae, and in the case of the Indian
the proper amount of food and supplement.

blue peafowl, even the venomous cobra.

Some piscivorous species will accept

Other gallinaceous birds consume almost

VetBooks.ir
commercial bird-of-prey diets, trout pellets,
exclusively vegetable material. The
and/or mice in the diet, as well as fish.

tragopans (Tragopan spp ), some pheasants

(Syrmaticus spp ), and several species of

WATERFOWL
grouse are largely vegetarian. Tragopans
consume sprouts, grasses, mosses, berries,

The order Anserifo1mes includes ducks,
and a few insects. In captivity, tragopans
geese, and swans. These waterfowl vary
can be fed luceme, grasses, cucwnbers,
from strictly herbivorous (swans, most
apples, and different kinds of berries.

geese, most ducks) to highly piscivorous

Grouse are noted for their ability to feed on

(marine ducks, mergansers). Commercial
plants containing quinones, which are not
duck or game-bird pellets should contain
consumed by other anin1als. Captive grouse

14o/er-l 7% protein and 3o/o-6%fat with an
should receive natmal foods or at least large
adequate vitamin mineral supplement.

amounts of leaves, grass, and berries

During breeding season, the amount of
supplemented with a limited quantity of
protein can be increased to 16o/er-18%. In
pellets and grain. Feeding these largely
winter in colder areas, more fat can be
herbivorous species with gan1e bird or
added by adding 200/o of com to the diet.

domestic fowl commercial diets will result

Piscivorous waterfowl consume mostly a
in suboptimal fertility and health.

fish-based pellet containing 25o/er-400/o

Coccidiostats are added to some poultry
protein and 5o/er-100/o fat. Some breeders
feeds. Monensi.n is commonly used and is
prefer to feed a "sinking" or "floating" watertoxic for guinea fowl. All gallinaceous birds fowl pellet in the water. However, pellets
should have access to grit. Poultry pellets
fed in water should not be allowed to
generally contain adequate calciun1 and
dissolve before consumption.

vitamins, and additional supplementation

Swans and geese are fed the same diet as
should be done only when a deficiency exists.

herbivorous ducks. Although waterfowl can
live on only nutrient adequate pellets,

RATITES
usually some lettuce is also fed.

Diets of only lettuce and com, which

See also RATITES, p 1960.

are unfortunately often provided, lead to

Ratites are flightless birds and do not
protein and multiple vitamin deficiencies.

require the high-energy diets of flighted

These often manifest as poor plumage,
birds. Ostriches, rheas, and emus consume
swollen joints, and podod�m1atitis.

low-q_uality roughage in natme, which is

As is true for most bird species, young
fem1ented in their intestinal tract. The
waterfowl should be fed starter pellets with
nutritional requirements of juveniles are
higher fat (5o/er-8%) and protein (16o/er-200/o)

much higher in protein and calcium than
content. However, excessively rapid growth
those of adults. Breeders have even higher
of large waterfowl must be avoicfed to
calcium requirements (see TABLE 37).

prevent bone and joint deformities, such

In most parts of the world, the comme r as angel wing and perosis.

cial breeding market for ratites is declining;
however, in some areas signiiicant nun1bers

GALLINACEOUS BIRDS
of ostriches and nandus are being kept.

Ratite production for meat and leather has

Many gallinaceous birds are omnivorous.

necessitated the development of diets to

Commercial diets for domestic fowl, domesmaximize growth and minimize cost.

tic turkeys, and Japanese quail are available. Bringing an anin1al to market in minimal During nonbreeding periods, a maintenance
time is financially advantageous, but
diet can be offered two or three times daily
excessively rapid growth can lead to
and generally should contain <200/o crude
angular deformities of the legs.

protein. During the breeding season, food

Cassowaries are rainforesc ratites and are
should be offered free choice and contain
primarily frugivorous. They are not raised
a higher protein content (200/er-25% crude
commercially, and their nutritional
protein).

requirements are not docwnented. Adult

Most quail are primarily seed-eaters and
birds often consume 3--5 kg of food/day. Diets
are easy to feed. Some Old World quail
fed in zoos include fruits and vegetables such
species are insectivorous and must be
as bananas, apples, tomatoes, papaya,
provided a diet with specific protein
watermelon, grapes, mangoes, plwns,
requirements. Peafowl in general (Pavo
nectarines, cherries, kiwi fruit, figs, sweet

NUTRITION: EXOTIC AND ZOO ANIMALS

2293
potatoes, and carrots. These are corrunonly
team approach is critical to improve
supplemented with animal protein ( eg,
nutrition for multiple species. The keepers'

day-old chicks, mice, dry dog food).

experience regarding the birds' habits and
preferences, combined with input from the

VetBooks.ir

MYNAHS
curator, veterinarian, and outside nutritional consultants are all necessary. Input Mynah birds of the fan1ily Sturnidae are
from other institutions where a given
omnivorous. Preferred food items in the
species has a history of longevity and
wild include fruits, a variety of insects, and
successful reproduction can be invaluable.

small reptiles and amphibians. In captivity,

In large collections, decreasing waste,
a low-iron pelleted diet to prevent iron
spoilage, overfeeding, and excessively
storage disease (<;100 ppm iron) and fruit
time-consuming diet preparation must be
are generally fed. Fruits high in vitamin C
considered along with improvement of the
should be avoided, because these facilitate
birds' nutritional intake.

iron absorption.

During breeding, insects such as meal

MAMMALS
worms are preferred by the parents for
feeding their young. Calcium gut-loading or
dusting of insects with calcium powder will

HANDREARING ZOO MAMMALS
help prevent hypocalcemia in the chicks.

Successful nutrition of handreared

TOUCANS
mammals requires 1) selecting a formula
that will support adequate growth and not

In nature, toucans (Ra.mphastos spp) eat
cause GI upset; 2) offering it at proper
mostly fruit but also consume insects,
intervals, in proper amounts, and in the
rodents, and invertebrates. Like mynahs,
proper way to ensure acceptance and
toucans are susceptible to iron storage
prevent overfeeding, underfeeding, or
disease. Their basic diet should be a
aspiration into the lungs; and 3) keeping all
low-iron pellet with a variety of fruits
feeding utensils clean and disinfected. If

(apples, banana, grapes) offered daily. If the
success is judged in terms of survival and
bird picks the frnit preferentially over the
not in comparison with maternal-raised
large toucan pellets, the pellets can either
growth and health, most precocial species
be crnshed, or very small low-iron pellets
maintained in captive collections have been
can be mixed with the fruit, so the pellets
handreared successfully. Handrearing more
adhere to the fruit and are ingested. These
altricial species ( eg, marsupials, rodents,
long-beaked birds may have difficulty
rabbits) is generally less successful unless
drinking water and may become dehydrated
the young have been dam-raised to a more
if not provided a large enough drinking pan.

advanced stage.

Whenever possible, data on milk com

MANAGING AVIAN ZOOLOGICAL
position and hand rearing case histories

COLLECTIONS
should be consulted before attempting to
bottle-raise a species for the fast tin1e.

When working with large zoological

Extensive books with general infom1ation
collections containing disparate species, a
on handrearing birds and hanclrearing wild
l�·H!III SELECTED NUTRITIONAL REQUIREMENTS FOR RATITE PRODUCTION"

Age

Estimated

Crude

Calcium

Diet

(mo) BodyWt(kg) Protein(%) (%)

Fiber(%)

Pre-starter

0-2

0.8-10.5

25

1.2-1.5

Starter

2-4

11-28

21.5

1.2-1.5

>4

Grower

4-6

29-52

17

1.2-1.5

>4

Finisher

6-10

53-90

13.5

0.9-1.0

Post-finisher

10-20

91-110

8.5

0.9-1.0

Maintenance

Mature

8.0

0.9-1.0

6

Breeder

Laying

14

2.0-2.5

8
a Portions reprinted with pem1ission of Spix Publishing, Donnelly R., Clinical Avian Medicine, 2006.

2294

NUTRITION EXOTIC AND ZOO ANIMALS
and domestic manm1als are available.

provide additional local gut protection.

However, most milk composition data are

Colostrun1 from domestic cows has proved
not available for most species, and some of
satisfactory for many exotic rwninants and
the published data are of dubious value.

can be stored frozen. When colostrun1 is fed,

Lactose content of milk varies widely
the best way to do so is to offer it from the

VetBooks.ir
between different species.

dam or from a similar species from the same

Animals ( eg, pinnipeds, rabbits) that
stable. Studies suggest that conspecific
nonnally consume milk low in lactose gene1° serum, collected aseptically, can be given ally produce little lactase and often develop

PO or SC as a substitute for colostrum.

severe GI problems and diarrhea when fed a

Frequency of feeding and the amount fed
high-lactose milk, eg, bovine. Similarly,
depends on natural nursing behavior,
adding sucrose to milk formulas is often
fom1ula composition, and the desired rate
contraindicated, because many neonates
of gain as well as practical labor restricproduce little sucrase. Many species have tions. The stomach capacity of most species
been raised using diluted evaporated milk or
can be estimated at 50 mUkg. Overfilling the
commercial calf, lamb, foal, or doe milk
stomach leads to GI upset, decreased transit
replacers ( eg, most ungulates), commercial
time, and diarrhea. Daily intake, as a rule,
dog milk replacer ( eg, canids, procyonids,
should not exceed 20"A, body wt/day and
bears, bats, edentates, mustelids, rabbits,
should be divided into frequent feedings
rodents), commercial cat milk replacer ( eg,
that do not exceed 35-40 mUkg. In general,
felids), hun1an infant fomiulas in general
most newborns should be fed every 2-4 hr,

( eg, most prinmtes ), and soy-based hun1an
and daily metabolizable energy intake (kcal)

infant fonnulas in particular ( eg, rabbits,
should be -210 x body wt (kg}°-75_ Appetite,
some marsupials). In some cases, these
condition of feces, and general health
basic fonnulas can be modified to better suit
should be monitored closely. Pulmonary
the needs of a particular species by adding
aspiration is the main problem during bottle
ingredients such as egg yolk, butterfat,
feeding. Body weights should be recorded
cream, and casein. Supplementation with
at frequent intervals. Smaller, more altricial
vitamin and mineral products may be
species often must be fed by stomach tube.

warranted. Some companies offer a range of

See also CARE OF' ORPHANED NATIVE BIRDS AND
products with different amounts of protein

MAMMAIB, p 2100.

and fat, so the desired amount of protein or
fat can be provided in the fo1mula See

BATS

TABLE 38.

It is preferred that some species ( eg,

Captive insectivorous bats frequently are
ungulates, marsupials, mink) receive
fed diets consisting primarily of mealcolostrum within 12-48 hr of birth to acquire worms. Crickets, fruit flies, blowfly larvae, inmlunoglobulins necessary for survival.

and other insects also are commonly

Including some colostrum in the diet of
offered. Because insects typically are low
ungulates for up to 2---3 wk after birth may
in calcium, they should be maintained on a

NUTRIENT REQUIREMENTS FOR HANDREARING SELECTED ZOO

MAMMALS

% of Dry Matter

Dry

Carbohydrates/

Animal

Matter

Protein Fat

Lactose

Horses, rhinos

8--12

15-20

2-15

59-75

Primates

2-14

7-15

25-35

50-60

Elephants, ruminants, pigs

12-23

21-27

30-45

20-37

Rodents, carnivores, deer

18--34

28-42

32-55

5-25

Rabbits, bears

30-40

25-45

40-50

5-10

Seals

41-61

10-20

74---82

0-2

Marsupials

23--28

NUTRITION EXOTIC AND ZOO ANIMALS

2295
calciw11-enriched diet so that the bat will
accept insects from a food dish by being
conswne the insect's high-calciwn gut
placed directly on the live food.

contents. A suitable mealwom1 diet can be

Many insectivorous bats can be mainformulated using 35% wheat middlings, 35%
tained successfully in captivity using
ground dry dog or cat food, and 3096 ground
artificial liquid or solid diets ( see TABLE: 39).

VetBooks.ir
calciwn carbonate, which should be fed at

Liquid diet can be placed in shallow plastic
least 3 days. Gels containing water and a
trays positioned near wire or branches for
calciun1 solution can also be fed. Frugivothe bats to land on and hang from while rous bats should be fed a diet that contains a feeding. Leftover liquid diet should be low amount of iron to prevent iron storage
replaced daily. Solid diets usually include
disease. The diet could contain a low-iron
bananas as the major ingredient. Additional
pellet for birds mixed with apples, bananas,
ingredients frequently offered include
and oranges.

papaya, apple, pear, melon, grape, and

Often, captive insectivorous bats must be
cooked caiTot and sweet potato. C3lllled cat
fed by hand when flying insects are not
or dog food, chopped eggs, and mealworms
available. Some bats can be trained to
also have been fed witl1 the fruit.

itM•itl DIETS OF SELECTED MAMMALS

Freshwater Otter Diet

Percent(%)

Ground horse or cow meat

38

Ground beef heart

20

Ground dry cat food

13

Beet pulp

2.9

Mirra-Coat®

1.9

Calcium carbonate

0.8

Poultry fat

4.9

Water

16.9

Lactose

0.04

Yogurt

0.72

Mineral-vitamin mix

0.84

All ingredients should be combined in a large mixer, divided into daily po1tions, and frozen. Lactose for lactobacilli can be added in yogwt to help maintain freshness.

Lactose and yogurt are optional.

Liquid Diet for Bats

Percent(%)

Dry mix:

Mixed baby cereal

20.7

Wheat germ

4

Nonfat dried milk powder

9

Calcium caseinate

15.8

Sugar

45.5

Protein supplement ( casein-based)

3

Mineral-vitamin mix

2

The dry mix (100 g) should be mixed with canned peach nectar (540 mL), water (260
mL), and com oil (6 mL), and fed witll peeled bananas.

( continued)

2296

NUTRITION: EXOTIC AND ZOO ANIMALS

•M=iiifl DIETS OF SELECTED MAMMALS (continued) Large Herbivore Pellet for Grazers

Percent(%)

Wheat middlings

30

VetBooks.ir

Alfalfa hay, sun-cured, ground (16% crude protein)

22

Com grain, ground

19.1

Soybean meal without hulls ( 48% crude protein)

11.4

Alfalfa meal, dehydrated (17% crude protein)

10

Sugarcane molasses

5

Soybean oil

1

Phosphorus supplement

0.8

Sodium chloride

0.5

Mineral premix"

0.1

Vitan1in premixb

0.1

Calculated composition ( dry-matter basis): 89% dry matter, 19% crude protein, 4.3% fat, 16% acid detergent fiber, 12% crude fiber, 0. 75% calcium, 0. 7% phosphorus

"Mineral premix (mg/kg of premix): 75,000 Zn, 50,000 Fe, 30,000 Mn, 10,000 Cu, 800 l, 200 Se, and 100 Co
b Vitamin premix (per kg of premix): 5,000,000 IU ,�tamin A, 400,000 IU vitamin D,, 200,000 mg vitamin E, 500,000 mg choline, 40,000 mg niacin, 20,000 mg pantothenic acid, 4,000 mg riboflavin, 20 mg vitamin B,,

CARNIVORES
diet ( dry-matter basis). Apparently, exotic
cats, like domestic cats, are unable to

Most zoos in the USA use nutritionally
convert carotene to vita.min A, tryptophan
complete commercial diets to feed exotic
to niacin, and linoleic acid to a.ra.chidonic
felids, canids, mustelids, and viverrids
acid. They also probably cannot syntl1esize
rather than attempt to prepare diets
adequate tauiine (a taurine deficiency has
in-house. In other parts of the world, a
been reported in leopards) and would be
whole or partial carcass ( eg, of cows or
susceptible to ammonia toxicity if fed an
horses) may regularly be fed. Other prey
arginine-deficient diet. Therefore, these
animals, such as rabbit and chicken, are
nutrients should be considered dietary
also regularly offered. A supplement
essentials for all felids.

containing at a minimun1 calciun1, vitanlin

Frozen and canned cat foods usually are

A, iodine, tamine, and some B vitamins
more palatable than dry m;ies to exotic ca.ts.

should be added to the meat diet. Feeding

Many zoos prefer to use frozen diets over
a complete mixed diet greatly reduces
canned products, because generally they
incidence of nub.itional problems in captive
are less expensive and large quantities a.re
exotic carnivores; however, such a diet
easier to feed. The soft, han1bmge1°like
regularly causes fecal problems. Most
consistency of commercial diets can result
commercial diets are based on horsemeat
in excess calculus deposits and periodontal
and its byproducts, but diets based on beef
disease if hard or ui1processed items are not
and poultry are also available. Typical lesser
also provided. All ca.ts fed a soft diet should
ingredients include fish meal, soybean meal, receive bones with some meat intact twice beet pulp, and ground com, as well as
weekly. Horse or beef shank bones are
mineral and vitanlin supplements.

suitable for large cat species; oxtails, rib

Exotic feline diets are usually higher than
bones, or whole rodents can be used for
canine diets in fat, protein, and vita.nlin A.

smaller ca.ts. Mice, rats, and chicks are

A diet suitable for most cat species contains
frequently included in tile diets of smaller

45%-500/o protein, 300/o-35% fat, 3o/o-4% crude
ca.ts. Rodents, poultry, fish, and organ and
fiber, l.2o/o-l.5% calcium, 1 o/o-1.2% phosphochunk muscle meats can be offered as rus, and 20,000-40,000 IU of vitanlin A/kg
occasional treat items to administer medica.-

NUTRITION: EXOTIC AND ZOO ANIMALS

2297
tion or to stimulate appetite, but generally

(0.5-1 L) to polar bears before their
they are not required as dietary staples for
hibernation starts.

large cats fed commercial diets.

Canids can be fed frozen, canned, or dry

INSECT IVORES, EDENTATES, AND

VetBooks.ir
canine diets. Although most canids are less

AARDVARKS
particular than cats, frozen and canned
foods are generally preferred over dry ones.

Most sJu·ews, hedgehogs, tenrecs, and

Bones should be included in the diet when
moles can be fed frozen cat food supplesoft foods are fed. Canids can also be fed mented with mealworms, earthwonns,
meat, with the right an1ount of vitamins and
crickets, and mouse pups. Ground meat
minerals added, varied with small prey
fortified with minerals and vitamins, canned
animals like rats, mice, rabbits, and chicken.

dog food, cooked egg, and small an10unts of

Small amounts of fruits and vegetables can
fruits and vegetables also are readily
be included in the diets of foxes and coyotes.

accepted by many species. Bacterial

Most mustelids and viverrids do well on
hazards have been associated with the
frozen feline diets or canned cat foods; a
feeding of raw, meat-based diets to some
meat-based diet supplemented with the
species. Carnivorous and insectivorous
tight amount ofvitan1ins and minerals is
small manunals appear patticularly
also appropriate. Many species readily
susceptible, and septicemia and deaths
accept small amounts of fruits, vegetables,
have been reported. Cairned, meat-based
and cooked egg. Mice, fish, and chicks can
products are a safer alternative.

be offered as occasional treat items and to

Armadillos will eat frozen feline diet,
stimulate appetite and activity. Rib bones
moistened dry cat food, catrned dog food, or
can be given twice weekly to promote
ground meat f01tified with nunerals and
dental health. Canned foods may be more
vitanuns. Milk, chopped egg, cooked sweet
palatable but are not recommended as a
potato, diced banat1a, and other fruits also
base diet, because ferrets may not be able to
are consumed. Vitat11in K supplementation
eat enough to meet their needs for calories
of ai·madillos has been recommended to help
and protein. See TABI,E 39 for a diet used
prevent hemorrhages: 5 mg of menadione
successfully for freshwater otter species.

sodiun1 bisulfite/kg dry diet should be

Procyonids can be fed diets similar
adequate. Sloths can digest fiber, but if they
to those offered to small canids, or an
are kept in an envirotunent that is too cold,
adequate meat diet can be fed. Feeding a
their digestion rate will be very slow. Their
good-quality dry dog food along with apple,
diet should consist of a mixture of primate
banana, and carrot is satisfactory for
at1d high-fiber primate diets and some green,
raccoons and helps minimize obesity
diced vegetables and preferred leaves. Food
problems that commonly result when
pat1s should be placed in such a way that the
frozen or canned diets are fed. The red
animal can hang from a perch while feeding.

or lesser panda has been maintained

In captivity, aai·dvarks, lesser anteaters,
successfully on commercial high-fiber
and giant anteaters readily accept semiliquid
primate biscuits and bamboo. The
diets instead of tel111ites, ants, and other
herbivorous food habits of the giant panda
natural foods. Artificial diets typically consist
require large amounts of ban1boo suppleof milk, water, ground meat, and/or mented with high-fiber primate biscuits.

meat-based product such as frozen feline

Bears can be fed meat supplemented with diet, mink chow or dry dog food, hard-boiled vitanuns and minerals, frozen canine diet,
egg, protein powder, baby cereal, and a
dry clog food, fish, and commercial
nuneral-vitat11in supplement. All ingredients
omnivore biscuits. Polar and Kodiak bears
ai·e nuxecl in a blender to the consistency of
do well on a diet of25%frozen canine diet,
a tluck gruel. For adult giant anteaters, a

25%fish (eg, smelt), 15%dry dog food, 15%
commercial diet is available. Loose feces may
omnivore biscuits, l()OA, bread, and 1()%
develop when a senuliquid diet is fed. If tlus
apples. Conunercial diets fonnulated
occurs, nulk and water can be withdrawn
especially for polar bears are available.

gradually from tl1e fonnula. As a precaution,

Other bear species can be fed less fish
vitatnin K often is added to all eclentate diets.

and more omnivore biscuits, bread, and
produce. Bananas and green vegetables
can be included in the diet of sun, sloth,

MARINE MAMMALS
spectacled, and black bears. Food intake of
captive bears varies widely with the season.

See also MARINE MAMMALS, p 1856.

Intakes generally are maximal during

Fish are the primary food of captive
summer and early fall and minimal during
marine mat11111als except for the herbivowinter. It is advisable to feed extra cod oil rous sirenians. The purchase and subse-

2298

NUTRITION: EXOTIC AND ZOO ANIMALS
quent proper storage and handling of

Thianune should be added ( at 30-35 mg/
high-quality fish are the most important
kg fish, as fed daily) to any marine mammal
aspects of feeding cetaceans and pinnipeds.

feeding program because of the possibility of

On receipt, fish should always be
thianune destruction by thiaminases found
inspected for quality. The following are
in several fish species. Supplemental vitamin

VetBooks.ir
useful for evaluation: l) The boxes should

E helps compensate for oxidative destrucbe checked to see whetl1er catch dates are tion of natural vitamin E in fish dwing
indicated. 2) Overall appearance of the fish
storage and helps protect against the
should be good. 3) Gills should be red (light
deleterious effects of peroxides formed in
pink gills indicate considerable time may
stored fish. Oily fish such as mackerel, which
have elapsed before tl1e fish were frozen
are high in unsaturated fatty acids, are
after being caught). 4) Eyes should not be
particularly susceptible to vitamin E destrucsw1ken, indicating dehydration. 5) Flesh of tion and peroxidative dan1age. Vitamin E at
tl1awed fish should be firm, skin should be

100 IU/kg fish, as fed per day, is generally
intact and not discolored, and tl1ere should
recommended whenever fish are fed.

not be a bad odor. 6) There should not be

Although subject to some debate, salt
excess water and blood pooled on the

(NaCl) supplementation of pinnipeds
bottom of frozen cases, which indicates the'

maintained in freshwater is sometimes
fish have thawed and been refrozen. 7)

reconunended to prevent hyponatrenua; 3 g

Ideally, the lenses of frozen fish should be
salt/kg fish should be adequate. Although
cloudy, which indicates tl1e fish have been
supplemental vitamin C is frequently given
properly stored at or below -30°C before
to captive cetaceans, there is no conclusive
pw·chase (higher temperatures often result
evidence it is beneficial. Evidence indicates
in clear lenses).

hepatic vitanun A levels in captive dolpluns

To mininuze peroxidative damage and
are often much lower than in their wild
nutrient destruction, fish should be stored
counterparts. Although specific recommenat or below -25°C. Most fish species should dations cannot be made, vitan1in A
not be stored >6 mo if at all possible. A
supplementation of some captive cetacean
maximum of3-4 mo is recommended for
diets may be desirable.

fatty fish such as mackerel; lean fish such as

Food intake in ma.tine manunals varies
smelt may remain in good condition for up
considerably, depending on fat content of
to 9 mo. Ideally, fish should be thawed
fish, water temperature, and activity.

overnight under refrigeration. If this is not

Performing Atlantic bottlenose dolphins
possible, thawing at room temperature is
generally eat 7-10 kg fish/day. Adult seals
preferable to thawing in water, which can
and sea lions consume -5%----8% of tl1eir body
cause significant nutlient leaching. Thawing wt in fish/day. Captive sirenians can be temperature should not be > l 0°C.

maintained on a diet of lettuce, cabbage,

Individually quick frozen fish are preferred
alfalfa, and aquatic plants ( eg, water
by many zoos, because proper quantities
hyacinth).

can be thawed without waste.

As a general rule, marine matnmals

MARSUPIALS
should be given marine fish. Composition
of marine fishes can vary greatly between

Most didelphid marsupials can be fed dry or
species and even within species dependcanned dog or cat food. Smaller species can ing on age, season, and catch location.

be fed caimed prin1ate diet. Hard-boiled egg,

Fish that have been used successfully
green vegetables, caiTot, sweet potato,
include Atlantic and Pacific herring;
apple, and banana cai1 also be offered.

Atlantic, Pacific, and Spanish mackerel;

Dasyurids (eg, marsupial "nuce," native
bluerunner; capelin; and anadromous
cats, Tasmaiuan devils) and bandicoots
smelt. Squid are readily consumed by
can be fed catmed or frozen feline diet. In
many pinnipeds, and clams can be
addition, crickets, mealworrns, and mouse
included in walrus diets. No commercial
pups can be given to smaller species; larger
substitute for fish has been developed that
species can be given mice ai1d shank or rib
will be accepted by cetaceans, but such
bones. Wombats and the lai·ger macropod
products have been used with some
marsupials can be fed a combination of
success for pinnipeds. The regular diet of
large herbivore pellets, rabbit pellets, or
any marine mammal should consist of two
special kangaroo pellets. Rat kangaroos will
or more fish species to help ensure a
eat a combination of mouse pellets and
balanced di.et. It is not recommended to
rabbit pellets. To prevent Jumpy jaw, the diet
feed fish that are threatened in the wild.

of marsupials should contain at least 200 mg

For example, Marine Stewardship Council
of vitai11in E and 0.2 mg of seleniwn/kg dry

(MSC) fish can be fed.

matter.

NUTRITION: EXOTIC AND ZOO ANIMALS

2299

Green vegetables, carrot, sweet potato,
regularly or to perform body condition
apple, and banana can be offered to all
scoring.

herbivorous and omnivorous marsupials.

Monkey biscuits containing high-quality

For herbivores, greens and vegetables
protein (18%-22.5% cmde protein) should
should be added in limited amounts; these
be fed to New World primates to ensure that

VetBooks.ir
marsupials should be fed a good-quality hay
their higher protein requirements are met.

that has not too long stems. Currently,

Regular monkey biscuits can be fed to
captive koalas can be fed successfully only

Old World species depending on other
on leaves of certain species of eucalyptus.

components in the diet, although many

Special pellets for koalas are being tested
larger Old World species such as gibbons,
and may be available in the future.

orangutans, chimpanzees, and gorillas
also need high-fiber products. Laboratory

PRIMATES
p1imate biscuits are typically fom1ulated
with very low fiber levels ( eg, 5%). Because

In general, prin1ates can be fed a diet based
many of the natural foods consun1ed by
on commercial monkey biscuits or canned
these species appear to contain very high
primate diet. Marmosets should be fed
fiber levels ( eg, >200/o), increasing the
a marmoset diet. Moderate amounts
dietary fiber intakes of larger primate
of assorted carrot, sweet potato, apple,
species is widely practiced. High-fiber
banana, and orange also can be offered;
biscuits should comprise at least 50% of the
however, it is advised to feed greens and
dietary dry matter, and browse should be at
green vegetables, which are more comparaleast 400/o of the diet fed. Most of the time, ble to tl1e natural diet. Monkey biscuits
however, these an1ounts are not available,
and the canned products should comprise
and greens and vegetables can be a

20% of the dry-matter intake of gorilla and
replacement for the browse.

orangutan diets; fruits and treat items

Cultivated fruits should be used sparingly
should comprise �200/o. Green vegetables
for great apes and leaf-eating species
and browse should be at least 40% of the
because, compared with cultivated green
diet, depending on the species.

vegetables, they are typically high in sugars

Feeding only greens and vegetables, with
and simple carbohydrates and low in
vitamin and mineral supplements, is being
protein and calcium. Monkey biscuits can
tested in several species of primates. Diets
be made more palatable for some species
should be developed and offered in such a
by soaking them in water or fruit juice. To
way that enrichment is supported.

prevent leaching of nutrients, the biscuits

Dietary crude protein ranges for
should be placed in a thin film of liquid so

Pongidae such as gorillas are 14%--16%
that the liquid is drawn up into the biscuit.

and for New World primates such as

Other items commonly included in
pinches 18%--22%. The unsaturated fatty
primate diets include hard-boiled egg (if
acid composition should be at least 2.5%
cholesterol is not a concern), yogurt, and

(2h n-6 fatty acids). Neutral detergent fiber
bread. Grapes, raisins, peanuts, crickets,
in the dry matter ranges from at least 10%
and mealwonns are treat items well liked by
in macaques, to 10% in marmosets, 30% in
most species. However, these items should

Howlers and langurs, and 20% in lemurs,
be fed two or three times a week at the
chimpanzees, and gorillas. Acid detergent
most, not every day. The energy amount of
fiber ranges from 5% in macaques, to 5% in
these enrichment items should not exceed
marmoset and tamarins, 10%in lemurs

5%--100/o of the energy consumed by the
and Pongidae, and 15% in Howler and
animal.

langur diets. For all primates, the diet

Mouse pups are favored items for many
should contain 0.8% calcium and 0.6%
smaller primates. However, callitrichid
phosphorus. Primate diets should contain
hepatitis in tamarins and marmosets has

5,000--8,000 IU vitamin A and 800--1,500 IU
been associated with the feeding of
vitamin D, except diets for squirrel
newborn mice infected with lymphocytic
monkeys and marmoset/tamarin should
choriomeningitis vims. Most zoos have
contain 2,400 IU vitamin D. The vitamin C
discontinued the feeding of mouse pups
level should be at least 200 mg/kg dry
to these New World primates. Sunflower
matter. The maintenance metabolic rate
seeds, instant rice, cracked com, and

(kcal/day) is for Pongidae (gorillas,
stu·edded coconut can be scattered around
orangutans), 3,621; baboons, 1,099--1,324;
the exhibit or holding areas to promote
langurs, 632--637; Rhesus macaques,
foraging activity. The an1ount of energy used

567--1146; marmoset, 31--76; and tamarin,
for these enrichment feeds should not

57--105. Obesity should be prevented;
exceed 5%--100/o of planned dietary energy.

therefore, it is important to weigh animals

Hay should be provided for nesting

2300

NUTRITION: EXOTIC AND ZOO ANIMALS
materials and diversion, and it can act as a
of milling. Supplementation is done,
foraging substrate.

because tl1e amount of vitamin C consun1ed

Many zoos offer meat to their great apes;
via green vegetables, oranges, multiple
although meat is often relished by the
vitan1ins, chocolate, fruit juice, or fruit-juice
animals, there is no evidence it is necessary
powders may not be sufficient.

VetBooks.ir
if tl1e diet is properly balanced. Because

Members of the subfamily Colobinae are
hypercholesterolemia is seen in many
perhaps the greatest challenge in proper
captive gorillas, the feeding of meat may be
feeding of captive primates. Pregastric
contraindicated. For most primates, meals
fermentation, similar to that in ruminants,
should be offered at least twice daily.

occurs in tl1e complex stomach of these

Smaller species may benefit from even more species. In the wild, leaves and high-fiber frequent feedings.

fruits and nuts form a major part of tl1e diet

New World primates use vitan1in 02
of most colobines. Therefore, natural diets
poorly. It is particularly important that
are high in fiber, and animals spend much
these species receive an adequate source
tin1e foraging. Offering a rich, rapidly
of stabilized vitan1in 0,1 ( cholecalciferol) in
consumable diet of monkey biscuits and
their diet if they are not exposed daily to
fruit (easily digestible sugars and starches)

direct sunlight. Marmosets require up to
in captivity presents a situation quite
four tin1es the an10unt of vitamin 03
different from tl1at typically found in the
required by other New World primates.

wild, and it may frequently cause GI

Because of potential vitan1in O toxicity,
problems. In addition, some evidence
commercial marmoset diets shoulcl be fed
suggests that a high percentage of colobus
only to marmosets. In noncommercial
monkeys may be sensitive to starch and
mixtures for smaller primates ( mixtures of
gluten.

cut apples, bananas, and cereal products

Commercial, preferably gluten-free,
with vitan1ins and minerals added), vitanun
high-fiber monkey biscuits (25%-50%

03 should be included; however, care should neutral detergent fiber and up to 15%-35%
be taken to prevent vitamin O toxicity.

acid detergent fiber) have been developed

Several cases of rickets in some Old
to feed captive colobines. A diet consisting

World species at weaning have been
of 309n of a palatable high-fiber biscuit and
reported. This may be because barred,

�7()0A, green vegetables and fresh browse is
outdoor primate exhibits have been
recommended for most colobines. Only a
replaced with indoor, albeit more naturalishigh-fiber primate biscuit and browse is the tic, exhibits. Although most free-ranging
preferable food for colobines. If the biscuit
primate species probably satisfy their
is not readily accepted, adding a limited
requirement for vitanun O by exposure to
amount of applesauce or banana flavor can
ultraviolet B (UVB) from sunlight, captive
increase palatability. Also, alfalfa pellets
animals may rely entirely on a dietary
and a good-quality alfalfa hay can be
source. Wants at weaning appear to be
provided in limited quantities. If a glutenparticularly at risk because milk levels of sensitive enteropathy is suspected, any
vitamin Dare probably quite low, and many
product that contains wheat, barley, rye, or
foods the young begin to eat are not fortified oats should be removed from the diet. In with this vitan1in. Exposing the infant or
colobines, dietary changes always should
juvenile to natural sunlight may be the best
be made gradually to allow tl1eir gastric
solution, because assuring that a dietary
microflora time to adapt.

supplement is consumed by a young
primate may not be possible.

RODENTS AND LAGOMORPHS

The an1ount ofUVB from sunlight is the
highest in and around the equator; in

Most rodent and lagomorph species do well
regions at latitudes farther away from the
on diets based on commercial laboratory
sun the amount of radiated UVB, particurodent pellets or rabbit pellets. Rabbits, larly in autumn, winter, and spring, is not
hares, pikas, mannots, and prairie dogs can
enough. Lights that emit energy in the UVB
be maintained on rabbit pellets, alfalfa or
range can be practical for use with primates, grass hay, and a limited amount of assorted provided precautions are taken to prevent
vegetables. Most other sciurids can be
the primates from being able to touch the
fed rat pellets and a limited mixture of

UVB lan1P-
sunflower seeds, millet, corn, and rolled

All primates require a source of vitamin
oats. Ground squirrels can also be offered a

C, which is added to commercial monkey
limited amount of green leafy vegetables,
biscuits. Most of the time, stable vitan1in C
carrot, and apple. Most mmids, cricetids,
is added to the pellet, meaning it will not
gophers, domlice, and jerboas do well on
undergo significant destruction within 6 mo
rat pellets; for smaller species, mouse

NUTRITION: EXOTIC AND ZOO ANIMALS

2301
pellets, a seed and grain mix, green leafy
contain fungi or bacteria ( eg, Clostrid'ium
vegetables, carrot, and apple can be fed.

botulinum) that can produce lethal toxiJ.1s.

Hay should be made available to voles

In addition to hay, a pelleted diet that
and lemmings. Captive voles may be
contains proteiJ.1, minerals, and vitamins in
difficult to manage unless a high-fiber rabbit
concentrations adequate to meet the needs

VetBooks.ir
pellet is used. Muskrats, agoutis, and
of domestic species and those wild species
capybaras will eat a combination of rat and
for which data are available ( eg, white-tailed
rabbit pellets along with alfalfa hay, carrot,
deer) should be offered. See TABLE 39 for and apple. Porcupines can be fed rat pellets,
composition of a san1ple pellet for large
rabbit pellets, and dry dog food in equal
herbivores. In the frequent situation in
pmtions along with some apple, carrot, and
which aniJ.11als are fed as a group rather than
bread; evergreen (willow) branches should
as individuals, it is preferable to use a
be made available whenever possible. It is
pelleted diet that is not excessively high in
also advised to provide bones for gnawing.

digestible energy ( -3 kcal DE/g dry matter

Beavers will eat a combination of rabbit
is suggested) and that contains sufficient
pellets, large herbivore pellets, and dry dog
fiber to support proper rumen or colon
food, regularly augmented with willow,
function. This precaution reduces the
poplar, aspen, or alder branches.

possibility of w1toward effects (eg, rumen

Guinea pigs can be offered conunercia.l
acidosis, colic, obesity) caused by
guinea-pig pellets, which are rabbit pellets
overconsmnption of concentrates.

with vitamin C added, along with greens and Depending on the nutritional status of the carrot. Although guinea pigs and cavies are
aninlal, -0.5-1.5 kg should be fed per
the only rodents known to require a dietary
aniJ.nal. Overfeeding can result iJ.1 obesity.

source of vitamin C, lagomorphs and

Animals should be weighed regularly, or
rodents may benefit from it.

body condition scoring performed.

A specialized pellet with high an1ounts of
neutral detergent fiber (NDF) and acid

SUBUNGULATES AND
detergent fiber (ADF) is recommended for

UNGULATES
browsers ( eg, giraffe, kudu, okapi, reindeer),
and a pellet with moderate an1ounts of NDF

Hay comprises the bulk of the diet for
and ADF is reconm1ended for grazers ( eg,
most ungulates in captivity and should be
elephant, bison, banteng, adda.x antelope).

available for most of the day rather than fed

The intermediate feeding anin1als should
at intervals as meals. In general, a leafy
get an equal mix of the browser and grazer
legume hay, eg, alfalfa, should be used for
pellets. Preferably, the diet of browsers
species that are primarily browsers ( eg,
should consist of equal parts of browser

Gira.ffidae, Cervidae, sitatunga, bongo,
pellets, good palatable alfalfa, and browse.

duiker, tapir), whereas a good-quality grass

Diets for grazers and browsers should
hay is satisfactory for most grazers or bulk
contain high an1ounts of vitamin E and
feeders (eg, zebra, elephant, bison, buffalo,
biotin to prevent muscle dystrophy and hoof
wildebeest, camel). Legwne hays are higher
problems.

in nitrogen and calcitun and, if of good

A pellet size of :V16 iJ.1. is satisfactory for
quality, are more digestible than grass hays.

most aitiodactyls, whereas a pellet or cube

Hay should be leafy and green, free of mold,
size of Y.! iJ.1. ( -13 mm) helps mininlize waste
dirt, excess weeds, and other foreign matter, when fed to larger perissodactyls and and should not be overmature. Several zoos
subungulates. Commercial cattle products
are test-feeding hay and alfalfa silage. In
should not be fed to zoo herbivores because
general, palatability is good.

of palatability problems and low vitanlin E

Hay analysis can be very useful to
levels, and some products may contain
evaluate quality and design proper feeding
non protein nitrogen sources such as urea
programs. "Poor" hay will have a good fiber that ai·e not tolerated by llindgut-fem1entiJ.1g
percentage, but the protein quality can be
species ( eg, equids ). Also, the ainount of
low and poor, and the mineral status,
easily digestible energy may be high, leading
especially of calciwn, can be too low. Low
to obesity. Tapirs should get a mixture of
levels of calciwn can cause poor bone
grazer and browser pellets combined with
calcification and also affect the calcium
some greens, alfalfa, and browse.

level in the blood, which can cause bu.th

In general, most large ungulates (>250
problems.

kg) conswne 1.5%--2% of their weight in dry

Precautions should be taken if feed..iJ.ig
matter daily. Smaller species ( <250 kg)

silage products. If the silage was not
generally consun1e 2%--4%. Offering a
processed or stored properly or contamipelleted diet at lO'Y(}--15% of the dry-matter nated by animal or meat products, it may
intake is adequate for most grazers if

2302

NUTRITION: EXOTIC AND ZOO ANIMALS
good-<i.uality hay is fed. The amount of

REPTILES
minerals and vitamins should be balanced
in the pellets in such a way that the total

See also REPTILES, p 1967.

diet (including greens, browse, and hay)

Appropriate husbandry of reptiles is as
should be adequate. When hay quality
in1po1tant as providing adequate nutrients.

declines, or for more delicate species, the

Photoperiod, temperature, humidity,

VetBooks.ir
percentage of high-fiber pellets should be
substrate, and cage "furniture" can affect increased. Ungulates and subungulates
feeding behavior and, thus, nutrient
should always have salt blocks available,
intake. Temperature and humidity
preferably with a balanced vitan1.in and
gradients within a reptile enclosure allow
mineral supplement. However, excessive
the animal to select warm, dry spots or
licking can become a neurotic behavior and
cooler, moist areas. Competition for
should be prevented.

preferred sites and for food pans in an

Elephants should receive extra calciun1,
enclosure with multiple animals should
because mostly poor hay with a low level of
also be assessed. Sufficient numbers of
calcium is fed. Because of the sensitivity to
warm spots, UVB exposure spots, and food
hemosiderosis, black rhinos should be fed a
pans should be available for all animals
diet with a low level of iron ( <100 mg/kg dry
within an enclosure. Visual barriers may
matter). Browse can contain significant
be useful to reduce competition for
an1ounts of iron; however, rose leaves
preferred sites or food dishes.

contain low an1ounts. It is speculated

Prey such as rabbits, rats, or mice should
that other tmgulate species may also
come from conunercial breeding centers
get hemosiderosis. It is advised that all
and be offered dead to prevent irtjury to the
ungulates be exposed to UVB from sunlight,
reptile and for welfare reasons of the
because it has been suggested that oral
offered prey. Although it is not conm1on,
supplementation of vitamin Din some cases prey have been known to attack predators is not sufficient ( elephant, kudu ).

and can inflict serious bites. Offering dead

Hay should be fed from a rack rather
prey can also reduce tile chance of irtjury to
than off the ground for most species
the predator caused by striking the walls of

(elephants are an exception). Hay racks
tile enclosure. However, some reptiles may
should be located at eye level for tall
initially need tile stimulation of live prey,
browsers such as giraffes and gerenuks.

particularly if tiley are not adapted to

Pellets can be offered from a covered
captivity. The possibility of disease or
trough or (rubber) feed pans. Regularly
parasite transmission from prey to predator
feeding the pelleted diet in an animal's
should be considered.

holding area can facilitate close observa

Vertebrate prey should be fed nutritiontion and easy capture. If possible, anin1als ally complete diets appropriate for the
should be fed separately to ensure that
species ( eg, mouse diet, rabbit diet, rat diet,
each individual receives a similar amount
etc). The nutrient content of the prey
of food. If feeding separately is not
depends on what it is fed ( eg, mice raised
possible, at least two widely separated
on a diet deficient in vitamin A have
feeding stations may be neoessary to
decreased liver storage of this essential
reduce conflict and to ensure that
nutrient). Additionally, if frozen mice or
subordinate anin1als obtain their share
rats are routinely used to feed carnivorous
of food.

reptiles, freezer storage conditions should

In addition to hay and pelleted diet,
be optimal ( eg, s6 mo and in thick, plastic
assorted fruits and vegetables often are fed
bags to retard dete1ioration). Methods of
to exotic ungulates. For most species, these
thawing that minimize water loss are also
items usually are not necessary except as
important. Because many carnivorous
an occasional treat; the amount should
reptiles rely on tileir prey not only as
be limited to <l ()OA, of the total diet. The
sources of nutrients but also as sources of
exception might be for tilose species tl1at
water, the state of hydration of the prey can
regularly feed on fruits and succulents in
be very important.

the wild. It may be advisable to include

Familiarity witil a species' food habits in
some greens and vegetables ( -0.5 kg/100 kg
the wild is essential if approp1iate foods and body wt) in the diet of species such as
nutrient levels are to be offered. Common
okapi, duikers, dik diks, bongo, and tapirs.

practice has been to offer two or more

Fresh, frozen, or dried browse is consw11ed
different prey species, because differences
avidly by most captive ungulates and
in nutrient content exist among vertebrate
subungulates and should be offered to
and invertebrate prey. Reduced dependence
browsers if possible ad lib, because it
on a single food or prey species is also
in1proves rumen function.

desirable, because some prey items may be

NUTRITION: EXOTIC AND ZOO ANIMALS

2303
periodically difficult to obtain. Dependence
product formulation and specific nutrient
on a single prey item is frequently seen in
concentrations. Unfortunately, little
snakes and may be unavoidable.

controlled research has been conducted

Many commercial diets for reptiles are
on nutrient requirements of reptiles, and
marketed. Products for carnivorous,
claims of product superiority may not
herbivorous, and omnivorous reptiles are
have a scientific justification.

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now available in frozen, freeze-dried,

Herbivorous reptile pellets should make
canned, extruded, pelleted, or sausage
up 25o/er-500A, of the diet of herbivorous
forms. Acceptability may be better when
reptiles. Animals should be fed 1 %-4% of
the commercial diets are offered to
their body weight on a dry-matter basis.

reptiles when they are young. Appropri

Vegetables with a low amount of oxalate
ately formulated, manufactured diets for
should be fed to prevent kidney stones.

reptiles are a potentially simpler and

A good quality grass hay or a so-called
more economical alternative to feeding
herbs-hay should be fed. No more than 50%
fresh produce or live prey. However,
of the diet should consist of fresh greens,
some of these diets may not be formuftuits, and vegetables. The an1ount of fruit lated rationally, and frequently little
should be no more tl1an 5%. In Europe, often
information concerning micronutrient
herbs and dandelions are fed to herbivorous
concentrations is provided by the
reptiles. Fresh, clean water must be
manufacturers. When selecting a
available at all times.

commercial product, the buyer should

See TABLE 40 for recommended nutrient obtain accurate information about
concentrations for reptiles.

RECOMMENDED NUTRIENT CONCENTRATIONS FOR

REPTILES

Concentration•

Carnivorous

Omnivorous

Herbivorous

Nutrientb

Reptiles

Reptiles

Reptiles

Crude proteinc

300/er-50%

200/er-25%

18o/er-22%

Fat

3o/er-6%

Crude fiber

200/er-35%

Arginine

1.0%

1.8%

Isoleucine

0.5%

1.3%

Lysine

0.8%

1.5%

Methionine

0.4%

0.4%

Methionine + cysteine

0.75%

0.75%

Threonine

0.7%

1.()0A,

Tryptophan

0.15%

0.3%

Linoleic acid"

1.00A,

1.00A,

Calcium

0.8o/er-l.1%

1.00/er-l.5%
l.4o/er-2.0%

Phosphorus

0.5o/er-0.9%

0. 6o/er-O. 9%

0. 8o/er-l. ()OA,

Potassium

0.4o/er-0.6%

0.4o/er-0.6%

Sodium

0.2%

0.2%

Magnesimn

0.04%

0.2%

Manganese

5 ppm

150 ppm

Zinc

50 ppm

130 ppm

Iron

60-80 ppm

200 ppm

( continued)

2304

NUTRITION: EXOTIC AND ZOO ANIMALS

RECOMMENDED NUTRIENT CONCENTRATIONS FOR

REPTILES (cont-inued)

Concentration a

VetBooks.ir

Carnivorous

Omnivorous

Herbivorous

Nutrientb

Reptiles

Reptiles

Reptiles

Copper

5-Sppm

15ppm

Iodine

0.3-0.6ppm

0.4ppm

Selenium

0.3ppm

0.3ppm

Riboflavin

2-4ppm

Sppm

Pantothenic acid
lOppm

60ppm

Niacin

1 0-40ppm
lOOppm

VitaminB12

0.020ppm

0.025ppm

Choline

1,250-2,400 ppm

3,500ppm

Biotin

70-lOOppb

400ppb

Folacin

200-SOOppb

6,000ppb

Thian1inec
l-5ppm

5ppm

Pyridoxi}'le
l-4ppm
lOppm

VitaminN

5,000--10,000 IU/kg 1 5,000 IU/kg

Cholecalciferol (vitan1i.J1

500-1,000 IU/kg

500--1,000 IU/kg

D3)g

Vitamin Eh

200IU/kg

200IU/kg

" Nutrient concentrations are recommended minimums for carnivorous reptiles and averages for omnivorous reptiles.

b Nutrient levels expressed on a dry-matter basis.

c Tawine requirements have not been determined for reptiles (the requirement for cats is 400-500 mg of taurine/kg dry diet).

"A dietary source of a.rachiclonic acid at 200 mg/kg dry diet may be necessary.

• Thiamine concentrations should be increased to 10-20 mg/kg if frozen, thawed fish constitute >25%
of the diet offered.

r A source of preformed vitamin A may be required because it is not !mown if reptiles can convert carotenes to retinol (vitamin A), although it is likely that herbivorous reptiles can.

8 Requirements for vitamin D may be partially or totally satisfied by exposure to sunlight or appropriate sources of artificial ultraviolet light. These suggested concentrations are not sufficient to prevent signs of vitamin D deficiency in green iguanas.

"300 Wlkg dry matter is advisable if the diet is high in fat, especially unsaturated fat.

Ulcerative Stomatitis: Vitamill C syn

Gout: Although most reptiles excrete
thesis has been reported in many reptile
nitrogen primarily as uric acid, aquatic
species. It has been suggested that
reptiles typically excrete excess nitrogen as
ulcerative stomatitis seen in snakes and
urea or an1monia . The relative proportions
lizards may be associated with a vitamin C
of varfous nitrogenous wastes may depend
deficiency, although there is no supportive
on the amount and composition of feed,
evidence. In controlled studies with gaiter
frequency of feeding, and state of hydration.

snakes (Thamnophis sp) fed supplemental

The excessive precipitation of urate crystals
vitainin C, tissue levels and body stores
in joints, kidneys, or other organs (gout) can
remained stable , although synthesis by the
be a common condition in some species of
snakes was reduced.

captive reptiles. The etiology is not clear, but

NUTRITION: EXOTIC AND ZOO ANIMALS

2305
it is conunonly thought that diets high in
with as much as 3,000 IU vitan1in D/kg did
protein may predispose reptiles to gout.

not prevent bone fractures and cortical

Impaired renal function and dehydration
thinning in green iguanas. Bulbs emitting
have also been suggested as possible causes.

UVB placed over the lizards al -12-18 in. for

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If poo1°quality protein is fed (unbalanced

12 hr/day appeared to reverse the signs in
amino acids) or when tissue is catabolized
the least severely affected lizards.

for energy, uric acid excretion increases.

Because some lizards seek a warm spot

Although gout in some reptiles is associated
to increase body temperature, placement
with increased circulating levels, postpranof a warming bulb, usually incandescent, dial transient increases in circulating mic
acljacent to a UVB bulb helps ensure
acid may be seen in some species and
adequate exposure to UVB light. Exposure
confound the diagnosis. Assming an
to unfiltered natural sunlight, depending on
adequate state of hydration in a susceptible
latitude, during wanner months and use
animal may help prevent uric acid
ofUVB bulbs during the rest of the year
precipitation in joints and organs. Feeding
usually eliminate the risk of bone disease
diets low in protein to carnivorous reptiles
caused by insufficient absorption of calcium
is unwise, because they are adapted to

(due to a vita.min D deficiency).

feeding on high-protein prey.

Some lizard species may be unable
to absorb sufficient dietaiy vitainin D3,

Vitamin D and Ultraviolet Light: Most
although the reason is poorly understood.

vertebrates can either absorb vitamin D

New World primates are believed to have
from the diet or synthesize it in the skin
exceptionally high dietary requirements for
from 7-dehydrocholesterol using energy
vitamin D, which may be related to lower
from ultraviolet (UVB) light of certain
nwnbers of vitainin D cellular receptors
wavelengths (290-315 nm) in a temperaturethan are present in Old World p1imates.

dependent reaction. Thus, vitan1in D is

Similar metabolic differences may exist in
required in the diet only when endogenous
some basking lizard species, although this
synthesis is inadequate, as develops when
has not been established. UVB bulbs are
anin1als are not exposed to UV light of
sold in pet stores, but label claims may not
appropriate wavelengths.

be reliable.

Many captive basking species appear

UVB Lighting: Three types of'UVB
susceptible to rickets or osteomalacia. Bone lighting are on the market: fluorescent fractures, soft-tissue mineralization, renal
tubes, compact fluorescent lamps, and
complications, and tetany can develop.

mercmy lamps. Fluorescent tubes supply

Reptiles frequently show few premonitory
a diffuse light with a low an1otmt of visible
signs, although lethargy, inappetence, and
light. Heat racliation is low, and the UVB
reluctance to move are commonly reported.

gradient is fairly unifonn. The light from

Serum calcium concentrations may not be
fluorescent tubes resembles more or less
diagnostically useful. Although blood levels
the natural UVB in the shade of a sunny day
of vita.min D can be measured, normal
spread over a relatively large area. Compact
values for most species are not known.

fluorescent lan1ps provide a more intensive

Supplementation with iqjectable calcium

UVB gradient focused on a small area.

and vitamin D may provide some sho1t-term

These lan1ps are characte1ized by fairly
relief. However, exposure to UV light, or
low intensity visible light and little heat.

lack of it, may be an in1portant, yet often

Mercmy lamps (vapor spot and narrow
overlooked, factor in the differential
spots) produce an intensive UVB gradient
diagnosis. Complicating the diagnosis
on a smaller area, producing heat and an
may be soft-tissue mineralization, seen
intense light.

radiographically or at necropsy.

Mercury lamps can become very hot. Rep

In green iguanas, metastatic calcification
tiles must be prevented from getting burned
may not result from vita.min D toxicity.

dming UVB basking. It is important to

Iguanas with both fractured bones and
recognize that when a UVB lan1p is added to
extremely low or tmdetectable levels of
a terrariwn, the emission of UVB drops with
circulating 25-hydroxycholecalciferol also
the square of the distance; this explains the
had calcified soft tissues. The etiology of the
low exposure level ofUVB at the level of the
metastatic calcification is not understood
reptile when the lan1p has been hung too
and is contrary to conventional understandhigh.

ing of the signs of vitamin D deficiency and

The radiation ofUVB declines during the
toxicity in domestic species. Dietary
lighting time. In general, UVB lamps should
sources of vitamin D may not be sufficient
be replaced once a.year. However, it is best
to prevent rickets and osteomalacia. Diets
to regularly measure the a.mount ofUVB

2306

NUTRITION: EXOTIC AND ZOO ANIMALS
with meters used in the artificial sunbath
and mineral mixture, and, if needed, to
industry. A "D3 Yield Index" that compares add antibiotics or coccidiostats. Mostly a
the vitamin Drproducing ability of the lamp complete diet is fed in a sausage; however, with the sun is under development.

tests are also being clone with gel feeding to

How long and how much exposure to
reptiles.

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UVB is needed in reptiles is not exactly

The scent of preferred foods can be
known. In general, reptiles that need UVB
rnbbed on the new item. Alternatively, the
must be exposed to 30 min to 2 Ju· of UVB
prefen-ed foods can be inserted into, or
each day. However, there can be exceptions.

attached to, the new food. Anoles, yellow

For example, bearded dragons do not
rat snakes, frogs, and smelt, depending on
develop metabolic bone diseases if they are
natural feeding habits, can be fed when
exposed only a few times a week to UVB for
homeotherms are not accepted. Prey size
a limited time.

is usually proportional to snake size and

Enlisting the assistance of a specialist is
should not be much larger in dia.ineter than
advised, because tl1ere is no ideal UV bulb
the snake's head. Snakes tl1at are routinely

(seep 1969).

handled can be fed in a separate tank to
reduce biting. To reduce the chance of

CROCODILIANS
regurgitation, snakes should not be handled
for 3 days after feeding.

Captive alligators and crocodiles are usually

Most species should be fed every 1-2 wk.

fed a combination of rodents, poultry, fish,

Some large, less active snakes may typically
and meat-based diets. A varied diet is
go 6 wk between feedings. Force-feeding
recommended. Diets consisting primarily of
should be used only if necessary. Animals
fish should include tlu·ee or more different
can be force-fed whole prey lubricated with
species of fish and should be supplemented
egg white by gently inserting the food a few
with 30-35 mg of thiamine and 100 IU
inches clown the throat using forceps. Tube
vitamin E/kg of fish, as fed. Signs of vitamin
feeding is also possible using ground

E deficiency (eg, steatitis) have been

(homogenized) prey.

reported in crocodilians fed fish inadequately supplemented with vitamin E.

TURTLES

Although previously reported otherwise,
alligators can digest some carbohydrate;

Many freshwater turtles in the wild eat
however, the total carbohydrate in the diet
primarily animal matter but also consume
should not exceed 20%. Commercial, dry
some plant material. Some species may
alligator diets are being marketed, largely
be carnivorous when young and shift to
to reduce the cost and to improve nutrient
omnivorous or herbivorous feeding
intakes of farmed alligators; their use is
patterns as adults. Most aquatic turtles
still uncommon irt zoos.

cannot be considered strict carnivores,
because they consume at least some plant

SNAKES
material. Commercially available turtle
feeds are available from ma.i1y manufactur

Snakes feed almost exclusively on
ers, although nutrient content can vary
vertebrate or invertebrate prey. A few
widely. These products are usually
species are specialized egg feeders. Most
manufactured as extruded or pelleted
boids, pythons, vipers, colubrids, crotalids,
diets and are typically 30o/o-50% protein.

and elapids are fed mouse pups, mice,

Such diets may be appropriate for
chicks, hamsters, rats, guinea pigs,
carnivorous and omnivorous turtles,
chickens, ducks, or rabbits. Frozen, thawed
although the more omnivorous species
prey are usually used in zoos; thawing under would benefit from the addition of some refrigeration is recommended. After
fruits or vegetables.

thawing, prey should not be fed cold but at

A sa.inple diet for ca.inivorous and
room temperature, or preferably wa.imer.

onmivorous turtles consists of the following

Some species ( eg, king cobra, hognose
feed items: water (272 g), gelatin (unsweetsnake, gaiter snake) feed primarily on other ened or dry, 34 g), com oil (11 g), spinach
poikilothern1s in the wild. Some of these

(23 g), cooked sweet potato (23 g), Vionate®
species can be switched, at least in pa.it, to

(a vita.inin/mineral supplement, 5 g), trout
homeothermic prey, which is often more
pellets (50 g), a.i1d vita.J11in E at 50 IU/g (1 g).

available a.i1d less expensive.

This diet contains on a dr-y-matter basis 4 7%

Minced prey is sometimes fed in agar, gel,
protein, 14%fat, l.5%calciurn, 0.55%
or sausage forn1. Adva.11tages include the
phosphorus, vita.irun A at 10,000 IU/kg,
ability to forn1ulate and feed a nutritionally
vitamin D3 at 1,000 IU/kg, vitamin E at 279
complete diet, to add a balanced vitamin

IU/kg, and vita.inin C at 280 mg/kg.

NUTRITION: EXOTIC AND ZOO ANIMALS

2307

TORTOISES
in tl1ese, and in most insects, are extremely
low (0.03%----0.3"Ai calcium with 0.8%-0.9%

Tortoises are herbivorous and, like
phosphorus), the inverse calcium:

herbivorous lizards (see below), must
phosphorus ratio must be co1Tected before
consmne plant material to maintain healthy
the insects are fed to lizards. A diet with
gut physiology. Microbial fennentation of
a balanced vitamin and mineral mixture

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plant fiber can be a significant source of
and containing 12% calcimn as calcimn
nutrients for tortoises. Diets of tortoises
carbonate can be fed to crickets or
in the wild often contain> 15% protein
mealwonn larvae 3 days before tl1e insect is

( dry-matter basis) in plant materials
fed to the lizard. However, this diet should
consumed, because natural vegetative
not be used to maintain a cricket colony.

materials are usually high in protein in the

Within 2 days of feeding the high-calcium
pre-seed stage, although a part of that
diet, the gut of tl1e insect is filled with
protein is indigestible. Although small
calcium, raising the calciun1 concentration
tortoises consmning pelleted diets can use
of the insect to -0.8%----0.9% and resulting in a
plant fiber effectively, they should be fed
calcium:phosphorus ratio of -1.2: l. A
more frequently tl1an larger aninlals. Small
satisfactory high-calcium diet for crickets
and large tortoises can be maintained on
can be inexpensively made by using 29%
appropriately formulated, extruded,
wheat middlings, 10% corn meal, 40%
pelleted, or coarsely grotmd tortoise diets.

grom1d dry cat or dog food, and 21%ground

Larger to1toises, such as Aldabra or
oyster shell or calcium carbonate (see a.lso

Galapagos tmtoises, can consmne grass or

BATS, p 2294, for meal worm diet). Larger
alfalfa hay along with a complete pelleted
insectivorous lizards may also consmne
food fonnulated for tortoises or exotic
mouse pups and earthworms.

herbivores. Hay should be cut short,

Carnivorous lizards may be offered
because the mouth shape of these tortoises
mouse or rat pups, adult mice and rats,
makes it impossible for them to chew long
chickens, and eggs. The size of prey should
hay. A vegetable mix consisting of broccoli,
be appropriate for the lizard species.

green bearLS, leafy greens ( eg, romaine,

Omnivorous lizards are usually fed a
green leaf lettuce, endive), kale, and
combination of foods, including insects,
shredded carrots may be fed as a supplevertebrate prey, and a chopped vegetable ment to a fonnulated tortoise diet. Such
mixture ( see rn1rro1sEs, p 2307, for vegetable mixes contain adequate protein, calcium,
mix). Most lizards should be fed daily
and micronutrients; only limited vitamin and

U uveniles and small species) or at least
mineral supplements should be added.

every other day. Large carnivorous species

Cultivated fruits are typically poorer sources should be fed once or twice a week.

of protein, calcium, and micronutrients and,

Herbivorous lizards are adapted to
if fed in significant a.mounts, vitamins and
ferment plant fiber in enlarged hindguts. The
minerals should be added. Some herpetolomicrobes in the cecum and colon digest plant gists offer oyster shell and pea gravel to
fiber that tl1e lizard could not otherwise use.

tortoises, because "mining" activity has been As with tortoises, herbivorous lizards should seen in free-ranging animals.

be fed plant-based diets to assure healthy gut

Shell deforn1ities in tortoises have been
ftmction. The use of insects, vertebrate prey,
thought to result from rapid growth
or diets high in fruits is not advised, because
associated with consmnption of high--pro-these feeds are low in fiber and are tein diets. Humidity and temperature also
inappropriate for herbivores. Diets for
may influence shell deformation.

lizards may be commercial preparations
formulated for herbivorous reptiles, or

LIZARDS
vegetable mixes (seep 2307).

The feeding patterns of lizards are

FISH
extremely diverse. Lizards may be
insectivorous ( eg, day and leopard gecko,

Knowledge of fish nutrition is increasing,
whiptail lizard, anole, chameleon),
but it has been mostly focused on commercarnivorous ( eg, varanids such as monitor cial fish and not on specific fish held in cold
lizard, Gila monster, Mexican beaded
or warm freshwater or seawater tanks.

lizard), omnivorous ( eg, many igua.nid and

Pellets and flakes are available; some claim
agarnid species), or herbivorous (eg, igua.nid to be especially developed for specific species, prehensile-tailed skink ).

species, but detailed nutritional information

Insectivorous lizards in captivity are
is not always available. Pellets fed in water
usually fed diets of meal worm larvae or
should not be allowed to dissolve before
crickets. Because calcium concentrations
eating to prevent pollution of the water.

2308

NUTRITION EXOTIC AND ZOO ANIMALS

Marine fish can be herbivorous,
heavy metals or organic components such
carnivorous, or omnivorous. Gra,;ing or
as PCB and DDT.

herbivorous fish eat plant materials from

Vitamins should be added to fish diet5,
the rocks of the sea and need more fiber
including vitamins E and B, and stabilized
than carnivorous fish. This can be
vita.min C. Iodine should be added to

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accomplished by feeding plant material in
prevent struma in sharks and rays. Some
a basket in the water or by feeding an
zoos also add glucans. Vitamins and
herbivorous fish pellet. Carnivorous fish
minerals can be injected into the fed fish.

should be fed a diet with high amounts of

Alternatively, tablets can be added just
protein and fat, which can be a pellet or
behind the gills of the fed fish.

different fish species. Nonpelleted food

Fish products or pellets should contain
for fishes can consist of artemia, algae,
the right amount and type of feed. Regularly
squid, herring, mackerel, whiting, sprat,
checking whether the fish are too fat or too
bream, and shrimp. It is important to
thin is an impmta.nt factor in proper feeding.

know the origin of the food, because

In a mixed exhibit, the feeder should ensure
threatened fish or fish harvested in areas
that all fish get tl1e right an1ount and type of
or ways that negatively affect the
food. If possible, sharks should be fed
environment should not be fed. Moreover,
individually.

the fish should not be contaminated with

See also NUTRITIONAL DISEASES OF FISH, p 1798.

NUTRITION: GOATS

Although goats and sheep have several
intake in goats include lactation, environsimilarities, their nutrient requirements mental temperature, water content of
differ in several ways. Goats exhibit sigforage consumed, amount of exercise, nificant differences from sheep in grazing
stage of production (growth, maintenance,
habits, physical activities, feed selection,
lactation, etc), and salt and mineral content
milk composition, carcass composition,
of tl1e diet. Goa.ts grazing lush pastures may
and metabolic disorders. Goats browse
conswne much lower quantities of water
more than sheep, whereas sheep tend to
than those feeding on dry hay. Still, it is
be true grazers. Still, many of the principles
imperative to allow free access to water for
useful for sheep feeding and nutrition are
all goats regardless of age, breed, purpose,
applicable for goats. The basic assessment
stage of life cycle, or environment.

for nutritional well-being should be body
condition or body fat covering. Goats in

Energy: Energy limitations may result
good flesh, or with normal fat sfores, are
from inadequate feed intake or from poor
usually being fed a diet witl1 adequate
diet quality; excessive water content of the
energy and to a lesser extent, protein.

feedstuffs also may become a. limiting

(See also NUTRITION: SHEEP, p 2345.)

factor. Energy requirements.are affected by
age, body size, body condition, stage of

NUTRITIONAL REQUIREMENTS
production (growth, maintenance,
pregnancy, and lactation), and concurrent

Water: Goa.ts should be provided unlimited medical conditions ( eg, parasitism, dental access to fresh, clean, nonsta.gnant sources
disease, arthritis). Energy requirements also
of freely accessible water. Goa.ts are among
may be affected by the environment, hair
the most efficient of domestic animals in
growth, activity, and relationship with other
their use of water; however, only -1 ()DA, of
nutrients in the diet. Increased temperature,
body water loss may prove fa.ta.I. They
humidity, sunshine, and wind velocity may
appear to be less subject to high temperadecrease energy requirements. Shearing ture stress than other species of domestic
mohair from Angora goats and pashmina.

livestock. In addition to a lesser need for
from Cashmere goats decreases insulation
body water evaporation to maintain
and results in increased energy needs (at
comfort in hot climates, goats can conserve
least in colder environments).

body losses of water by decreasing losses in

Goa.ts exhibit a wide range of grazing
urine and feces. Factors affecting water
activity, ranging from light activity for goats

NUTRITION: GOATS

2309
under intensive management, through
mineral requirements for goats are similar
moderate activity on sem.iarid land, to high
to those for sheep. (For detailed nutrient
activity for goats grazing on sparsely
requirements for goats, refer to the most
vegetated grassland and on mountainous
current Nutrient Requirements of Srnall
pastures that necessitate long-distance

Rum.inanls, published by tl1e National

VetBooks.ir
travel daily.

Research Council [www.nap.edu].) Feed.ing

The best assessment of energy intake
to meet the goat's needs will maximize its
adequacy in goats is proper body condition
production, reproduction, and immune
or fat covering the loin, brisket, inner thigh,
system. The addition of specific nlinerals
and ribs. Using herd/individual medical

(phosphorus for dry winter forages,
record systems, a standardized body
selenium in deficient areas, etc) to salt
condition score (1-5, with 1 being extremely (NaCl), preferably in granular form and tllin, to 5 being extremely obese) should be
offered free choice, helps prevent most
used to monitor body fat changes and make
nlineral deficiencies and improves
less subjective decisions with respect to
perfonnance.

longtenn dietary energy adequacy. If

Calcium requirements are generally met
animals are parasite- and disease-free, yet
under grazing cond.itions witll either Angora
underconditioned, then tl1ey are usually
or meat-type goats, but levels should be
being fed an energy-deficient diet; the
checked in high-producing dairy goats
reverse is true for obese animals. The
because a deficiency can lead to reduced
energy values required for growth and
milk production. Adequate levels of calciwn
lactation are very comparable to the
for lactating goats are necessary to prevent
nun1bers used for sheep and cattle,
parturient paresis (milk fever). In browsing
respectively. Therefore, sheep nutrition
or grain-fed goats, the addition of a calciun1
principles from an energy standpoint will
supplement ( dicalcium phosphate,
probably suffice when dealing witll all
limestone, etc) to the feed or to a salt or
classes of goats, except for lactating dairy
trace mineral-salt mixture usually meets
goats.

calciwn requirements. Legumes ( eg, clover,
alfalfa, kudzu) are also good sources of

Protein: Protein is required for most
calciun1.

normal fimctions of tlle body, including

Phosphorus deficiency results in slowed
maintenance, growth, reproduction,
growll1, unthrifty appearance, and
lactation, and hair production. Protein
occasionally a depraved appetite. Goats can
deficiencies in the diet deplete stores in the
maintain milk production on phosphorusblood, liver, and muscles and pred.ispose deficient diets for several weeks by using
animals to a variety of se1ious and even fatal phosphorus from body reserves, but dming ailments. Feed intake and dietary digestibillong periods of phosphorus deficiency, milk ity are reduced if dietary crude protein is
production was shown to decline by 600/o:

<6%, further compound.ing an energy-pro

The calciwn:phosphorus ratio should be
tein deficiency; tllus, for maintenance of
maintained between 1:1 and 2:1, preferably
mature, healthy animals, the d.iet should

1.2-1.5:1 in goats because of their predispohave a minimum of 7% crude protein.

sition for urinary calculi. Phosphorus

Dietary crude protein requirements are
deficiency in grazing goats is more likely
higher for growth, gestation, and lactation.

than a calciun1 deficiency. In cases of

Most forages contain adequate amounts
struvite calculi, the ratio should be
of d.ietary protein for maintenance, but
maintained at 2: 1.

lactating, growing, sick, or debilitated

Magnesium deficiency is associated with
animals may require diets fortified with
hypomagnesemic tetany (grass tetany), but
legumes or protein supplements ( eg,
ordinarily this condition is less conunon in
soybean meal, cottonseed meal, etc).

grazing goats than it is in cattle. Goats do

Feed.ing adequate to slightly greater
have marginal ability to compensate for low
an10unts of protein than required appears to
magnesium by decreasing tl1e amount of
aid in the control (both resistance and
magnesiun1 they excrete. Both urinary
resilience) of internal nematode parasites.

excretion and milk production are reduced
in a magnesimn deficiency.

Minerals: Requirements for minerals have

Salt (NaCl) is usually recognized as a
not been established definitively for goats at
necessary dietary component but is often
either maintenance or production levels.

forgotten. Goats may consmne more salt

Research has been conducted with goats in
than is required when it is offered ad lib; this
nlineral metabolism stud.ies, especially with
does not present a nutritional problem but
calciun1 and phosphorus. ln general, these
may depress feed and water intakes in some
data support assumptions that several
arid areas where salt content of the drinking

2310

NUTRITION: GOATS
water is quite high. Salt formulations are
appear to be much more resistant to copper
used as carriers for trace minerals, because
toxicity than sheep.

goats have a clear drive for sodium intake.

Selenium deficiency in the diet is usually

Potassium has an important role in
associated with nut1itional musculai·
metabolism. However, forages generally are dystrophy, retained placentas and metritis, quite rich in potassium, so a deficiency in
poor growth, weak or prematme kids, and

VetBooks.ir
grazing goats is extremely rare. Marginal
mastitis.

potassium intake is seen only in heavily
lactating does fed diets composed

Vitamins: Recommendations for vitamin
predominately of cereal grains. Excessive
requirements of goats are even more sparse
potassium intake (particularly in late
than for mineral requirements. At best,
gestation) may be associated with
almost all vitanlin reconunendations for
hypocalcemia in dairy goats. If hypocalce-
goats must be based on those for sheep (see

1nia is a herd problem, attention should be
p2345).

paid to reducing or monito1ing potassiumrich feedstuffs ( eg, alfalfa).

HERBAGE A.ND BROWSE

Iron deficiency is seldom seen in mature
grazing goats. Such deficiency might be

UTILIZATION
seen in yow1g kids because of their minimal

In contrast to other fam1 aninlals, except
stores at birth, plus the low iron content of
llamas, goats prefer shrubs and tree leaves,
the danl's milk. This is more co nun only seen whether deciduous or evergreen. Because in kids fed in complete confinement and
of this preference, goats have been used to
heavily pa.rasitized animals. Iron deficiency
control encroaching shrub-type growth in
can be prevented by access to pasture or a
pastmes. Goats consume approximately the
good quality trace mineral salt containing
same weight of forage as do sheep of similai·
iron. In severe cases, and for kids reared in
size. Goats tend to select highly digestible
confinement, i.ron dextran iajections at 2- to
portions of most forages and show a

3-wk intervals (150 mg, IM) for the first few
preference to browse along fence lines and
months may be curative. In the cases of
rough areas. Goats usually perforn1 on
mixed iron/selenium deficiencies, caution
improved pastmes and prefer browse to
should be used when iajecting iron dextrans grass ( a diet of >80% browse).

unW the selenium deficiency is also

Browse (leaves and twigs of trees and
corrected.

slm1bs) generally contain higher levels of

Iodine deficiency in the soil, and in the
crude protein and phosphorus dming their
crops produced thereon, is seen in some
growing season than do grasses. However,
areas of the USA. Therefore, iodine should
some palatable browse species are limited
be provided in stabilized salt. Conditional
in value because of one or more inhibitors
iodine deficiency may develop with normal
that may bind or otl1erwise prevent use of
to marginal iodine intake in goats consumnutrients contained in tl1e plants. One such ing goitrogenous plants. Marked deficiency
inhibitor is lignification of woody twigs and
of iodine results in an enlarged thyroid; poor tree leaves, which physically binds ( or growth; small, weak kids at birth; and poor
encapsulates) the desirable nutrients.

reproductive ability.

Certain oils (terpene-based comp0tmds) are

Zinc deficiency results in parakeratosis,
present in relatively high concentrations in
stiffness of joints, smaller testicles, and
some range shrubs and apparently inhibit
lowered libido. A minimal level of 10 ppm
growth of run1en bacte1fa. High concentraof zinc in the diet, or a trace mineral salt tions of tannins are present in certain
mixture of 0.5%--2% zinc, prevents
browse plants and depress digestion of
deficiencies. Excessive dietary calcium
feedstuffs by binding enzymes or by

( alfalfa) may increase the likelihood of zinc
inhibiting enzymatic activity. Excessive
deficiency in goats.

tannins may also increase sulfur require

Copper deficiency may result in
ments, which may be more critical for
microcytic anemia, poor production, lighter
hair-producing goats. However, in spite of
or faded hair color, poor fiber quality,
tl1ese potential problems, when given the
inferWity, poor health and slowed growth,
opportunity to choose, goats appear to be
some forms of metabolic bone disease,
able to select more digestible and beneficial
diatThea, and possibly a greater susceptibilbrowse. Grazing or browsing tannin-conity to internal parasites. Copper deficiency taining plants may help control many
in a diet may be caused by inadequate
species of internal nematode parasites.

copper intake, a lowered copper-molybde

For sample rations for kids and goats,
nun1 ratio, or excessive dietary sulfur. Goats see TABLE 41.

NUTRITION GOATS

2311

•M:iiil• SAMPLE RATIONS FOR GOATS•

For a 30-kg (66-lb) goat in a nonproductive state, minimal activity, maintenance only: Chickpea straw 630 g (1.4 lb)

Alfalfa, fresh 95 g (0.20 lb)

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For a 50-kg (110-lb) goat in a nonproductive state, minimal activity, maintenance only: Wheat straw 716 g (1.6 lb)

Alexandrian clover, fresh 333 g (0. 73 lb)

For a 20-kg ( 44-lb) kid gaining 50 g/day, minimal activity: Alfalfa hay, full bloom 80 g (0.18 lb)

Com grain 360 g (0. 79 lb)

For a 30-kg (66-lb) kid gaining 150 g/day (0.33 lb): Chickpea straw 500 g (1.1 lb)

Com grain 400 g (0.88 lb)

Linseed meal 65 g

For a 40-kg (88-lb) doe in late gestation with minimal activity: Johnsongrass hay 960 g(2.l l lb)

Sorghum grain 350 g (0. 77 lb)

For a 70-kg (154-lb) doe producing 5 kg (11 lb) of milk testing 3.5% butterfat: Com silage (dough stage) 1,000 g (2.2 lb)

Alfalfa hay, full bloom 500 g ( 1.1 lb)

Com grain 1,365 g (3.00 lb)

Soybean meal 280 g (0.62 lb)

• Dry-matter basis

NUTRITIONAL DISEASES
which can lead to the secondary complication of enterotoxemia.

Enterotoxemia: This feed-related malady
causes almost sudden death due to a toxin

Polioencephalomalacia: Clinical signs
produced by Clostridium per:fringens type D include disorientation, dullness, aimless and sometimes type C. The organism appears wandering, loss of appetite, circling, to be widespread in nature. Under conditions
progressive cortical blindness, extensor
of high carbohydrate consumption or high
spasms, and occasionally head pressing.

intake of immature succulent forage, the

Some anin1als become recumbent and may
causative bacte1ia multiply rapidly and
eventually die without treatment. Diets that
produce an e toxin that increases intestinal
produce a low rumen pH or that are high in
pem1eability. (See also ENTEROTOXEMIAS, p 609.) grain and low in forages predispose

Some cases of enterotoxemia are seen in
nuninants to polioencephalomalacia. Such
goats, usually those fed diets with high
dietary conditions can result in depressed
concentrations of carbohydrates. DiaIThea,
production of thianune, the production of
depression, lack of coordination, digestive
thiamine antimetabolites, or the production
upsets, coma, and death may be seen after
of thiaminases in the rumen.

excessive carbohydrate feeding of both baby

Affected anin1als can usually be treated
kids and mature goats. The best method to
successfully with thiamine (200-500 mg, IV,
prevent enterotoxemia in stable-fed goats is

IM, or SC). Although response is dramatic
frequent, small-volume feeding of milk, grain,
and almost in1mediate, if significant brain
and forage. Large meals fed once a day
damage has occurred, anin1als rarely return
should be avoided. Acute indigestion and a
to a satisfactory level of production.

nunen pH of <4.8 indicates lactic acidosis,

Therefore, prompt treatment is critical.

2312

NUTRITION: GOATS

The diet should be modified to reduce grain

Difficult and painful urination is evidenced
and increase forage intake. During times of
by straining, slow urination, stomping of the
stress, or when predisposing diets are
feet, and kicking at the area of the penis.

unavoidable, the inclusion of thiamine

Blockage of the flow of urine generally is
mononitrate in the diet may aid in prevenseen only in intact or castrated males. The VetBooks.ir
tion. (See also POLIOENCEPHAI..OMALACIA , p 1281.) blockage may rupture the urinary bladder, resulting in a condition known as water

Pregnancy Toxemia: Seen in late
belly, and cause death. It is common when
pregnancy, pregnancy toxemia is much more
diets with high concentrations of cereal
common in dams can}'ing multiple fetuses.

grains are fed (feedlot lambs, pet goats, etc).

Clinical features include ab.normally

Affected animals excrete an alkaline urine
increased blood levels of ketone bodies with
that has a high phosphorus content.

concurrent hypoglycemia Affected animals

The incidence of urinary struvite calculi
exhibit many of the signs desc1ibed for
can be reduced by lowering phosphorus
enterotoxemia ( see above). During late
consumption to n1inin1al levels and
gestation, the developing fetuses have high
maintaining a calciwn:phosphorus ratio
demands for glucose; in an attempt to meet

>2: 1 (with the phosphorus content <0.45%
the glucose needs, the darn begins to metaboof the diet). The use of anionic salts such as lize adipose tissue (fat). The ability of the
ammoniwn chloride (0.5% of the complete
liver to metabolize this extra fat load is
diet), dietary tetracycline, adequate vita.min
compromised, with a subsequent increase

A ( or [3-carotene) intake, increased dietary
in the release of ketone bodies into the
intake of NaCl, reducing grain intake,
bloodstrean1. Signs include depression,
minimizing use of pelleted cereal grains,
dullness, opisthotonos, and eventually death.

and ensuring an adequate source of fresh,

In early stages of the disease, when signs
clean, palatable water free choice have
fast appear, a drench of 200-300 mL of
proved beneficial. Affected animals
propylene glycol or glycerol can be used as
drenched with an1mo11iwn chloride
an energy source for the dam to prevent so

(7-14 g,'day for 3-5 days) may show a good
much body fat from being metabolized.

response. In range sheep and goats, the

However, the administration of glucose
disease is associated with conswnption of

(5% dextrose or 50-120 mL of 23% calciwn
forages having a high silica content. (See
borogluconatc solution into a liter of
also NONINFECTIOUS DISEASES OF' Tl I E URINARY

5% dextrose IV) is the treatment of choice.

SYSTEM IN LARGE ANIMALS, p 1502.)

Prevention should be aimed at maintaining
a proper body condition score, identifying

White Muscle Disease: White muscle
females with twins and triplets and feeding
disease is caused by low levels of seleniwn
accordingly, reducing the incidence of
and possibly vita.nun E. It seems to develop
chronic disease, shearing long-fibered does in less frequently in goats than in sheep. Signs late gestation, and possibly including niacin
include stiffness ( especially in the hindquar

(1 g,'day in the diet during late gestation) in
ters), tucked-up rear flanks, arched backs,
the diet. Ensuring adequate winter feedstuffs
pnewnonia, and acute death. On necropsy,
while monitoring body conditiQn changes
white striations are found in cardiac, diathroughout gestation will help reduce the phragmatic, and skeletal muscles. Levels of
incidence of this condition. (See also

AST and lactic dehydrogenase are increased,

PR EGNANCY TOXEMIA IN EIVESA,\ID 001':S, p 1021.) indicating muscle damage. Blood levels of
the selenium-containing glntathione

Urinary Calculi: Calculi result from
peroxidase are reduced. (See also NUTRITIONAL
mineral deposits in the urinary tract.

MYODEGEN ERATION, p 1172.)

NUTRITION: HORSES

Horses are maintained for a much longer
tions given below are based on both practime tl1an most farm anin1als and have more tical expe1ience and scientific research.

varied uses as athletes and service and

Detailed recommendations can be fow1d in
companion anin1als. Feeding progran1S,

Nutrient Requirements of Horses, 6th Ed,
therefore, must sustain a long, productive,
published in 2007 by the National Research
and athletic life. The feeding recommenda-

Council (NRC).

NUTRITION: HORSES

2313

NUTRITIONAL REQUIREMENTS
during the watering sessions are not linlited.

Inadequate water access will reduce feed

Horses can use hay and other roughages as
intake and increase the incidence of
nutrient sources much more efficiently than
impaction colic, anhidrosis, and other

VetBooks.ir
other nonruminants such as poultry or pigs,
metabolic disorders.

although utilization is less efficient than in
mminants. Traditionally, it was stated that a
good source of roughage should comprise

Energy: Energy requirements may be
at least 50"A, of the total equine ration by
classified into those needed for mainteweight. Current recommendations are that nance, growth, pregnancy, lactation, and
horses receive at least 1.5%--2% of their body work Equations to estimate energy weight in forage or forage substitutes such
requirements at any state of perfom1ance
as hay cubes or other high-fiber source
or production have been derived primarily
daily. The average maximum daily dry
from studies of light horse breeds (see
matter intake is 2.5%-3% body wt ( although

TABLES 42 and 43). However, the need
some breeds and age groups, notably ponies for energy differs considerably among and weanlings, can exceed those maxiindividuals; some horses require much mums if on good pastures); therefore,
greater amounts of feed than others ("hard
forage or forage substitutes should be the
keepers"), and others are much more
major components of an equine ration. The
efficient at feed digestion/utilization ("easy
main sites of fennentation in horses are in
keepers"). Digestibility of feedstuffs also
the cecum and large colons, where products
often differs significantly from published
of microbial fem1entation, such as volatile
values. Therefore, the caloric recommendafatty acids, amino acids, and vitamins, are tions provided herein should be considered
also absorbed. Microbial fem1entation also
only a starting point to detennine the actual
occurs in the stomach and small intestine
energy needs of a given horse.

to lesser degrees, depending on the type of

Amounts fed should be adjusted to
feed. Enzymatic digestion of carbohydrates,
maintain a body condition score between
protein, and fats occurs only in the

4 and 6 (see TABLE 44). Emaciated and very duodenum and jejunum. Any of these
thin horses have decreased stress and cold
nutrient sources that escape small-intestinal tolerance and increased susceptibility to digestion/absorption are passed on for
infections. Obese horses have decreased
microbial degradation in the large intestine,
tolerance of exercise and heat, increased
where their fermentation will alter pH and
risk of laminitis and lipoma strangulation
microbial activity, both acutely and
colic, and if fasted, hyperlipidemia and
longterm.

hypertriglyceridemia. Obesity is also
associated with insulin resistance and

Water: Water requirements depend largely glucose intolerance.

on environmental conditions, amount of

Maintenance: For maintenance of body
work or physical activity being performed,
weight and to support nom1al activity, the
type and amount of feed, and physiologic
daily digestible energy (DE) requirement
status of the horse. The minimal mainte

(in Meal) of the nonworking adult horse in
nance daily water requirement of a
good body condition is estimated to be
sedentary adult horse in a thennoneutral
on average 33.3 kcal/kg body wt, with a
environment is 5 UlOO kg body wt/day,
minimum requirement of 30.3 kcal/kg for
assuming the horse is consmning at least
easy keepers or draft/warmblood types of

1.5% of its body wt in feed dry matter.

horses and 36.3 kcal/kg for hard keeper

However, a 500-kg horse will usually drink
adult horses. For obese or emaciated

21--29 L of water per day when fed a mixed
horses, the estiniated ideal body weight in
hay/grain ration or pasture. If fed only dry
kg should be used in the equation rather
hay, water intake will almost double.

than current body weight. For weight gain,

Lactation or sweat losses also increase
it is estimated tllat 1 unit of change in body
the needs by 50"/o--200"Ai. A 500-kg horse condition score takes 16-20 kg body wt gain
exercising for 1 hr in a hot environment will
and that each kg of gain requires 20 Meal DE
need to drink 72--92 L of water to replace
above maintenance requirements. Caloric
sweat and evaporative losses. Lactating
intake in obese horses should not be
mares need 12--14 L per 100 kg body wt to
restricted severely for prolonged periods of
sustain good health and milk production.

time because of the risk of hyperlipidemia,

Unlin1ited free access to clean water is
especially in ponies and donkeys.

usually recommended, although horses

Cold weather increases the energy
can easily adapt to only periodic access
requirement by 0.00082 Meal DE/kg body wt
throughout the day if the amounts offered
for each degree Celsius drop below the

2314

NUTRITION HORSES

ESTIMATED DAILY NUTRIENT REQUIREMENTS OF GROWING

HORSES AND PONIES

Daily Nutrients Per Animal a

VetBooks.ir

Body

Daily

Digestible Crude

Age

Weight Gain

Energy

Protein

Vitamin

(mo)

(kg)

(kg)

(Meal)

(g)

Ca(g) P(g)

Ab(JU)

ADULT WEIGHT 200 KG (PONIES)

4

67

0.34

5.3

268

15.6

8.7

3,000

6

86

0.29

6.2

270

15.5

8.6

3,900

12

128

0.18

7.5

338

15.1

8.4

5,800

18

155

0.11

7.7

320

14.8

8.2

7,000

24

172

0.07

7.5

308

14.7

8.1

7,700

ADULT WEIGHT 500 KG (AVERAGE HORSES)

4

168

0.84

13.3

669

39.1

21.7

7,600

6

216

0.72

15.5

676

38.6

21.5

9,700

12

321

0.45

18.8

846

37.7

20.9

14,500

18

387

0.29

19.2

799

37.0

20.6

17,400

24

365

0.18

18.7

770

36.7

20.4

19,300

ADULT WEIGHT 900 KG (DRAFT HORSES)

4

303

1.52

23.9

1,204

70.3

39.l

13,600

6

389

1.30

28.0

1,217

69.5

38.7

17,500

12

578

0.82

33.8

1,522

67.8

37.7

26,000

18

697

0.51

34.6

1,438

66.7

37.1

31,400

24

773

0.324

39.2

1,492

66.0

36.7

34,800
a Assumes good-quality forage with or without additional concentrates. Maximal daily intake is estimated to be 2.5%-3% body wt in dry matter.

b One mg of 13-carntene equals 4(Jt) IU of vitamin A for the horse.

Adapted from Nutrient Requirements of Horses, 2007, National Academy of Sciences, National Academy Press, Washington, DC.

lower critical temperature (LCT) of the

(56.5X-0·145)/l,OOO times body wt in kg plus
animal. However, the LCT of cold-adapted
the calo1ic requirements for growth= (1.99
adult horses in Canada was estimated to be

+ l.21X- (0.021X2) x ADG, using the above

-15°C, whereas donkeys acclimatized to
equation(s) for the maintenance DE, and X
summer temperatures in Nevada had an
as the age in months and ADG as the desired

LCT of26°C. Wind, precipitation, and body
average daily gain in kg. This equation will
condition also affect LCT. Therefore, LCT
give an estimate of caloric requirements;
must be estimated based on regional
intakes should be adjusted to maintain body
average temperatures and conditions and
condition scores of 5 or 6 in growing horses.

perhaps type of horse. For example, draft

Warmblood, draft, and draft-cross breeds
breeds with thick hair coats would tolerate
may require 10%-200;(, less than calculated
lower temperatures than a thin-haired,
by the equations above to sustain rapid
thin-skinned Thoroughbred.

growth and avoid obesity.

Growth: For grow1h, the daily DE

Pregnancy and Lactation: During
requirement of light horse breeds is
pregnancy, if the mare is not exercised or
estimated to be maintenance DE Meal/day=
exposed to extreme weather conditions,

NUTRITION: HORSES

2315

ESTIMATED AVERAGE DAILY NUTRIENT REQUIREMENTS OF

MATURE HORSES AND PONIES

Daily Nutrients Per Animala

VetBooks.ir

Body

Digestible Crude

Daily Milk

Weight

Energy

Protein

Vitamin

Production

(kg)

(Meal)

(g)

Ca(g)

p (g)

Ab(IU)

(kg)

MAINTENANCE

200

6.7

252

8

6

6,000

500

16.7

630

20

14

15,000

900

30.0

1,134

36

25.2

27,000

LAST 90 DAYS OF GESTATION

214-226

7.7-8.6

319-357

14.4

10.5

12,000

500

19.2-21.4

797-893

36

26.3

30,000

600

34.6-38.5

1,434-

64.8

47.3

54,000

1,607

LACTATING MARES, FIRST 3 MO

200

12.2-12.7

587-614 22.4-23.6 14.4-15.3 12,000

6.0-6.5

500

30.6-31.7

1,468---

55.9-59.0 36.0-38.3 30,000

15.0-16.3

1,535

900

52.4-54.4

2,642-

100.6-

64.9-68.9 54,000

26.91-29.3

2,763

106.4

LACTATING MARES, 3 MO TO WEANING

200

10.9-12.2

506-587 15.0-22.4

9.3-10.5 12,000

4.4-6.0

500

27.2-30.6

1,265-

37.4-55.9 23.2-36.0 30,000

10.9-14.9

1,468

900

46.3-52.5

2,277-

67.4-

41.8---64.9 54,000

19.6-26.9

2,642

100.6

"Assumes good-quality forage with or without additional concentrates. Maximal daily intake is estimated to be 2.5%-3.0% body wt in dry matter. Ranges are given for requirements that change witJ1
time of pregnancy/lactation.

b One mg of 13-carotene equals 400 1U of vitanun A for the horse.

Adapted from Nut1·ienl Reqiiinnnenls of Horses, 2007, National Academy of Sciences, National Academy Press, Washington, DC
maintenance DE intakes are usually

To support lactation, the NRC has
adequate until the last 90 days of gestation.

estimated that 792 kcal of DE/kg of milk

Energy requirements during months 9, 10,
produced per day (see TABLE 43) should be
and 11 of gestation are estimated by
added to the increased (36.3 kcal/kg body
multiplying estimated maintenance
wt) maintenance needs. Lactating light
requirements by 1.11, 1.13, and 1.20,
horses (eg, Thoroughbred, Quarter horses)

respectively. Voluntary intake of roughage
maintained body weight when fed 28---31
decreases as the fetus gets larger, and it may

Meal DE/day. Draft mares may require as
be necessary to increase the energy density
much as 43 Meal/day. However, this
of the ration by using supplemental
recommended level of energy intake has
concentrates in late pregnancy.

increased body weight gain in lactating

2316

NUTRITION: HORSES

•h=iiil• BODY CONDITION SCORES FOR HORSES

Score

Description

VetBooks.ir

Emaciated

Spinous processes, ribs, tailhead, tuber coxae, and ischii prominent. Bone structure of neck, withers, and shoulders easily visible. No fat palpable over lwnbar vertebral transverse processes.

2 Very thin

Slight fat covering spinous processes and tailhead. Transverse processes slightly rounded. Ribs, tailhead, and tuber coxae and ischii prominent. Bone structure of neck, withers, and shoulders faintly discernible.

3 Thin

Fat buildup halfway on spinous process and tailhead; both prominent, but individual ve1tebrae in tailhead not visible.

Transverse processes cannot be felt. Slight fat buildup over ribs and tuber coxae but easily visible. Tuber ischii not discernible.

Withers, neck, and shoulder accentuated, but bone structure not visible.

4 Lean

Slight ridge visible over loin, faint outline of ribs visible.

Tailhead prominence depends on confonnation, but fat palpable around it. Tuber coxae not visible. Withers, shoulder, and neck not obviously thin.

5 Moderate

Loin is flat (no crease or ridge). Ribs not visible but easily felt.

Fat around tailhead is spongy, withers rounded over spinous process, and shoulders and neck blend smoothly into body.

6 Moderately

May have slight crease down loin, ribs barely palpable with light fleshy
pressure, and fat around tailhead soft. Some fat palpable on side of withers, neck, and behind shoulder.

7 Fleshy

May have crease down loin, and ribs difficult to feel. Fat deposited along withers, behind shoulder, and along neck.

8 Fat

Crease down loin. Ribs very difficult to feel; fat around tailhead very soft. Fat filling area over withers and behind shoulder with noticeable thickening of neck

9 Obese

Obvious crease down loin. Patchy fat deposits over ribs. Fat bulging around tailhead, along withers, behind shoulders, and along neck. Flank filled with fat (no abdominal tuck).

pony mares, indicating that it may exceed

For these reasons, DE recommendations
the needs of some breeds or individuals.

for various activities of light horses (see

The mare's body condition should be

TABLE 45) should be adjusted to meet
evaluated on a regular basis and maintained
individual needs and to maintain body
in the range of 5 to 7 using the body
condition scores between 4 and 6 for
condition scores of l to 9 ( described above)

optimal athletic performance.

throughout pregnancy and lactation. Ma.res
should be maintaining or gaining in
condition to optimize reproductive success

Protein and Amino Acids: Although
dwing the breeding season, even if lactating
some amino acid synthesis and absorption
at the same time.

occurs in the cecun1 and large intestine, it is
not sufficient to meet the an1ino acid needs

Work: The energy requirements of work
of growing, working, or lactating horses;
are influenced by many factors, including
therefore, the protein quality of the feed
type of work, condition and training of the
provided to these classes of horses is
horse, fatigue, environmental temperature,
in1portant. Weanlings require 2.1 g, and
and skill of the rider or driver. As the
yearlings 1.9 g, of lysine/Mcal DE/day.

dma.tion of exercise increases and level of

Requirements for other dietary amino acids
activity is maintained, the DE requirement
have not been well established; however,
per unit of time worked actually decreases.

the crude protein recommendations given

NUTRITION: HORSES

2317

ENERGY REQUIREMENTS OF WORK FOR LIGHT HORSES• AND

DESIRABLE BODY CONDITION SCORES

Body Condition

VetBooks.ir

Activity

DE (Meal/day)

Score

Idle (maintenance)

0.033 x body wt

4-6

(kg)

Halter competition, pleasure trail riding

1.20 x DE for

5-6
maintenance

Performance/show (park, English, and

1.4 x DE for

5-6

Western pleasure, youth activity), equest1ian
maintenance
instruction

Ranch work, frequent strenuous show

1.60 x DE for

4-5

( cutting and roping, barrel racing), endurance maintenance trail ride, lower level 3-day event (hunt course,
stadium jumping, dressage), polo

Race training, elite 3-day event

1.9 x DE for

4-5
maintenance

" 200-600 kg body wt
in TABLES 42 and 43 should be adequate if
deficiencies; therefore, mineral supplegood quality forages and concentrates ments should complement the composition
are used in the ration. The amino acid
of the basic ration. For exan1ple, if the horse
balance in alfalfa and other legumes such
is consuming mostly roughage with little or
as soybeans appears to be better than that
no grain, phosphorus is more likely to be in
found in cereal grains or some grass hays.

short supply, especially for growth, than

This should be considered when fonnulatcalcium. However, if more grain than ing rations, especially for rapidly growing
roughage is being fed, a deficit of calcium is
young horses.

much more conunon. The total mineral

Growing horses have a higher need for
contribution and availability from all parts
protein (14%-16% of total ration) than
of the ration (forages and roughages,
mature horses (So/e>-10% of total ration).

concentrates, and all supplements) should

Aged horses (>20 yr old) may require
be considered when evaluating the mineral
protein intakes equivalent to those for
intake. However, aside from actual feeding
young, growing horses to maintain body
trials, no suitable test for availability of
condition; however, hepatic and renal
dietary minerals exists. Blood concentrafunction should be assessed before tions do not reflect dietary intake adeincreasing the protein intake of old quately for any of the macrominerals,
horses. Fetal growth during the last third
especially calci_Lm1.

of pregnancy increases protein requirements somewhat (10%-11% of total Calcium and Phosphorus: Requirements
ration), and lactation increases requirefor calcium and phosphorus are much ments still further ( 12o/<>-14% of total
greater during growth than for maintenance
ration). Work apparently does not
of mature animals. The last third of
significantly increase the protein
pregnancy and lactation also appreciably
requirement, provided that the ratio of
increase the requirement. Aged horses (>20
crude protein to DE in the diet remains
yr old) may require more phosphorus than
constant and the increased energy
is required for adult maintenance (0.3%-
requirements are met.

0.4% of total ration). Excess calcium intake

(>1% of total ration) should be avoided in

Minerals: Because the skeleton is of such
aged horses, especially if renal fw1ction is
fundamental importance to performance
reduced.

of the horse, calcium and phosphorus

For all horses, the calciwn:phosphorus
requirements deserve careful attention
ratio should be maintained at > 1: 1. A

(TABLES 42 and 43). Excessive intakes of
desirable ratio is -1.5: 1, although if adequate
certain minerals may be as hannful as
phosphorus is fed, foals can apparently

2318

NUTRITION: HORSES
tolerate a ratio of up to 3: 1 and young adult
for growth have not been well established
horses a ratio even higher. Work does not
but have been estimated to be 0.07% of the
appreciably increase calcium or phosphorus total ration. Most feeds used for horses requirements as a portion of diet.

contain 0.1 % --0.3% magnesiwn. Although

Salt: Salt (NaCl) requirements are
deficiencies are unlikely, hypomagnesernic

VetBooks.ir
markedly influenced by sweat losses. It is
tetany has been reported in lactating mares
reconunended that horse rations contain
and stressed horses. The upper lin1it of

1.6---1.8 g salUkg feed dry matter, although
reconm1ended intake is estin1ated to be 0.3%
there are lin1ited data on the precise
of ration dry matter based on data from
requirements. Sweat losses may cause NaCl
other species, but adult horses have been
losses >30 g (1 oz) in only 1-2 hr of hard
fed rations with higher magnesiun1 content
work, and feed concentrations of salt for
without apparent adverse effects. Anecworking horses are recommended to be at dotally, high magnesiwn intake has a
least 3.6 g NaCl/kg feed dry matter. The
pharrnacologic calming effect on horses, but
upper limit for salt inclusion in the ration of
large doses of magnesiwn sulfate (ie, Epsom
even hard-working horses is reconunended
salts) are also laxative.

at 6% of the total ration. However, NaCl is

Potassium: The reconunended potasthe only mineral for which horses are situn intake for maintenance in adult horses
known to have true "nutritional wisdom."

is 0.05 g/kg body wt. Most roughages

Horses voluntarily seek out and consw11e
contain > 1 % potassiwn, and a ration
salt in amounts to meet their daily needs if
containing 2:500A, roughage provides more
given the opportunity. Salt or salt blocks
than sufficient potassium for maintenance
should be available free choice. Supplemenanin1als. Working horses, lactating mares, tal salt may be provided by oral dosing or
and horses receiving diuretics need higher
added to feed or water in addition to
potassiw11 intakes because of sweat, milk,
free-choice salt to replace acute losses
and urinary losses. Hard work may increase
during hard work, but prolonged, excessive,
intake needs by a factor of 1.8. It has been
forced supplementation will enhance
proposed that rations fed to hard working
excretion, which will reduce the ability to
horses should provide 4.5 g potassiwn/Mcal
adjust to acute losses in the future. Forced

DE. Potassiwn chloride is the most
oral administration of concentrated salt
common salt used to supplement rations.

pastes (electrolytes) to dehydrated horses

However, upper safe limits have not been
can cause abdominal malaise. Some horses,
established, and although excesses are
usually those confined to stalls, will ingest
usually efficiently excreted by the kidneys
excessive amounts of salt, possibly due to
in healthy horses, acute hyperkalemia
restricted feed intake and/or boredom. This
caused by the rapid absorption of concenwill not cause health ptoblems as long as trated salt mixtw-es can induce potentially
adequate water is available, although it will
fatal cardiac arrhythmias. Forced oral
increase water intake and urination. Salt
supplementation with large doses of
poisoning is unlikely unless a deprived
potassiwn salts should be avoided, even
horse is suddenly allowed free access to
in hard working horses.

salt, or if water is not available to horses
force-fed salt ( eg, electrolyte mixtures given

Iodine: Iodized salts used in salt blocks

PO during competitions). Excessive salt
or commercial feeds easily fulfill the dietary
content of feed or water will limit voluntary
iodine requirement ( estimated to be 0.35
intakes, precluding toxicity but putting the
mg/kg feed dry matter), as do forages grown
horse at risk of energy deficits.

in iodine replete soils. Late pregnant mares

The most satisfactory method to provide
may require slightly higher intakes (0.4 mg/kg
supplemental calciun1, phosphorus, and salt
feed dry matter), but iodine toxicity has
is to furnish a mixture of one-third trace
been noted in pregnant mares conswning
mineral or plain salt and two-thirds
as little as 40 mg of iodine/day. Goiter clue
dicalciwn phosphate free choice. Trace minto excess iodine intake has been well eral salt blocks do not contain additional
docun1entecl in both mares and their foals,
calciwn or phosphorus.

and several cases were associated with

Magnesium: The daily magnesiun1
large amounts of dried seaweed (kelp) in
requirement for maintenance has been
the diet. Except in regions where the soils
estimated at 0.015 g/kg body wt based
are known to be severely iodine deficient,
on limited studies. Working horses are
iodine supplementation should not be
estimated to require 0.019 to 0.03 g/kg body
necessary for horses.

wt for light to strenuous exercise, respec

Copper: The dietary copper requirement
tively, due to sweat losses. The requirements for horses is probably 8--10 ppm, although

NUTRITION: HORSES

2319
many commercial concentrates fonnulated
which is sufficient to produce clinical signs
for horses contain >20 ppm. The presence
of toxicity (seep 3085). Exercise increases of 1-3 ppm of molybdenum in forages,
glutathione peroxidase (selenium-containwhich interferes with copper utilization in ing enzyme) activity and may increase need
ruminants, does not cause problems in
for supplementation in heavily exercised

VetBooks.ir
horses. However, excessive iron supplehorses. No more than 0.002 mg/kg body wt mentation (fairly conunon, especially in
should be supplemented on a daily basis;
perfonnance horses [see below]) may
toxicity has been seen with as little as 5 mg
inhibit adequate absorption. Copper
seleniwn/kg feed d1y matter.

deficiency may cause osteochondritis
dissecans in young, growing horses and is

Other Minerals: The requirement for
associated with a higher risk of aortic or
sulfur in horses is not established.

uterine artery rupture in adults. Copper

However, sulfur-containir1g amino acids
deficits may also cause hypochromic

(methionine) and vitamins (biotir1) are
microcytic anemia and pigmentation loss.

essential for healtl1y hoof growth. If the

Horses are extremely tolerant of copper
protein requirement is met, the sulfur intake
intakes that would be fatal to sheep.

of horses is usually -0.15% dry-matter

However, excessively high copper intakes
intake-a concentration apparently
potentially reduce the absorption and
adequate for most individuals. Sulfur
utilization of selenium and iron, and should
deficits may contribute to poor hoof quality.

be avoided.

The dietary requirement for cobalt is
apparently <0.05 ppm. It is ir1corporatecl

Iron: The dietary maintenance requireir1to vitamm 812 by microorganisms ir1 the ment for iron is estimated to be 40 mg/kg
cecum and colon and, therefore, is an
feed dry matter. For rapidly growing foals
essential nutrient per se only if exogenous
and pregnant and lactating mares, the
sources of B,2 are not incorporated ir1to the
requirement is estimated to be 50 mg/kg
ration. The upper limit of intake is estimated
feed dry matter. Virtually all commercial
to be 25 mg/kg feed dry matter based on
concentrates fom1ulated for horses and
data from other species.

most forages contain iron well in excess of

Manganese requirements for horses
the recommended concentrations. Only
have not been well established; an10unts
horses with chronic blood loss ( eg, parasitfound in the usual forages ( 40-140 mg/kg ism) should be considered to be at risk of
city matter) are considered sufficient.

iron deficiency. Excess iron intake poten

Rock phosphates, when used as mir1eral
tially interferes with copper utilization. The
supplements for horses, should contain
presence of anemia (low PCV or red cell

<0.1%fluorine. Fluorine intake should not
volume) alone is not sufficient indication
exceed 40 mg/kg feed city matter. Excessive
for ir·on supplementation in horses.

ingestion can result in fluorosis, although

Zinc: The zinc requirement is estimated
horses are more resistant to fluorir1e
to be 40 mg/kg feed dry matter, although
excesses than are rw11ir1ants.

there is evidence that this recommendation

Although molybdenum is an essential
may be as much as twice the actual
cofactor for xanthme oxiclase activity, no
requirement to prevent signs of deficiency
quantitative requirement for horses has
in most horses. This mineral is relatively
been demonstrated. Excessive levels (>15
innocuous, and intakes several tirnes the
mg/kg feed dry matter) may interfere with
requirement are considered safe, although
copper utilization.

ir1takes >1,000 ppm have induced copper

Vitamins:

deficiency and developmental orthopedic
disease in young horses.

Vitamin A: The vitamm A requirement of
horses can be met by 13-carotene, a natw·ally

Selenium: The dietary requirement for
occurring precursor, or by active forms
selenium is estin1ated to be 0.1 mg/kg feed
of the vitamin ( eg, retinol). Fresh green
dry matter in most regions. However, there
forages and good-quality hays are excellent
are regions of the world (including the
sources of carotene, as are corn and carrots.

lower Great Lakes, the Pacific northwest,

It is estimated that 1 mg of 13-carotene is
the Atlantic coast, and Florida ir1 the USA,
equivalent to -400 lU of active vitamin
as well as parts of New Zealand) where soils A. However, because of oxidation, the are profoundly deficient in this important
carotene content of forages decreases with
but potentially very toxic trace mir1eral. In
storage, and hays stored > 1 yr may not
other areas (incluclmg parts of Colorado,
furnish sufficient vitamin A activity. Horses

Wyoming, and North and South Dakota),
consuming fresh green forage for 3-4 mo of
forages may contain 5-40 ppm of seleniw11,
the year usually have sufficient stores of

2320

NUTRITION: HORSES
active forms of vitamin A in the liver to

Vitamin K: Vitanlin K is synthesized by
maintain adequate plasma concentrations
the microorganisms of the cecum and colon
for an additional 3-6 mo. Rations for all
in sufficient quantities to meet the normal
classes of horses should provide a minimw11 requirements of horses. However, VetBooks.ir
of30 IU active vitamin Nkg body wt
consumption of moldy sweet clover hay

(whether as [3-carotene or an active
may induce vitanlin K -dependent coagulasynthetic fo1m such as reti.nyl acetate).

tion deficits (seep 3156). The synthetic form

Prolonged feeding of excess retinyl or
of vitan1i11 K (menadione) is nephrotoxic if
retinol compounds(> 10 times recomadministered parenterally to dehydrated mended a.mounts) may cause bone fragility,
horses.

bone exostoses, skin lesions, and bilth
defects such as cleft palate and microoph

Ascorbic Acid: Mature horses synthesize
thalmia (based on data from both horses
adequate amounts of ascorbic acid for mainand other species). The proposed upper tenance from glucose in the liver. Some
safe concentration for clu·onic administrahorses may need supplemental ascorbic tion is 16,000 IU of the active form of the
acid (0.01 g/kg body wt/day) during periods
vitan1in per kg feed dry matter. There is no
of severe physical or psycho logic stress, eg,
known toxicity associated with [3-carotene
prolonged transportation or weaning. Oral
in horses.

availability is variable. Ascorbyl palrnitate
is reportedly more readily absorbed than

Vitamin D: Horses exposed to �4 hr of
ascorbic acid or ascorbyl stearate.

sw1light per day or that consume sun-cured

Prolonged supplementation to nonstressed
hay do not have dietary requirements for
horses may reduce endogenous synthesis
vitamin D. For horses deprived of sunlight,
and/or enhance excretion, resultil1g i11
suggested dietary vitamin D,1 concentradeficiencies if supplementation is abruptly tions are 800-1,000 IU/kg feed dry matter
discontinued.

for early growth and 500 IU/kg feed dry
matter for later growth and other life

Thiamine: Although thiamine is
stages. Vitamin D toxicity is characterized
synthesized in the cecum and colon by
by general weakness; loss of body weight;
bacte1ia and -25% of this may be absorbed,
calcification of the blood vessels, heart,
thiamine deficiency has been reported in
and other soft tissues; and bone abnormalihorses fed poor-quality hay and grain.

ties. Dietary excesses as small as 10 tilnes

Although not necessarily a minimum value,
the recommended amounts may be toxic

3 mg thiamine/kg ration dry matter has
and a.re aggravated by excessive calcium
mai11tained peak food conswnption, nonnal
intake.

gail1s, and nonnal blood thiamil1e concentrations in skeletal muscle in young horses.

Vitamin E: No minimal requirement for

As much as 5 mg/kg feed d1y matter may be
vitamin E has been established. However,
necessary for horses exercising strenuously,
it has been established that selenium and
although verifiable deficits have not been
vita.min E work together to prevent
recorded. Occasionally, horses are poisoned
nutritional muscular dystrophy (white
by conswnmg plants that contam thia.mimuscle disease, seep 1095), equine nases, which results in acute deficits
degenerative myeloencephalopathy, and

(seep 3089).

equine motor neuron disease. Evidence of
vitan1in E deficiency is most likely to appear

Riboflavin: Riboflavil1 deficits have not
in foals nursing mares on dry winter pastw-e
been docwnented i11 horses. Previous
or horses fed only low-quality hay unsupplecorrelations with low riboflavin intake and mented with conm1ercial concentrates.

recurrent uveitis in horses have not been

Horses forced to exert great physical effmt
substantiated. However, there is no
and/or fed high-fat (>5%) rations may have
evidence of toxic effects as a result of
increased needs for vitamin E. However, if
supplementing this water-soluble vitami11,
selenium intakes are adequate, it is likely
and daily intakes of 0.04 mg riboflavin/kg
that 50 IU vitamin E/kg feed dry matter is
body wt are reco1m11ended.

adequate for most stages of the life cycle

Vitamin B 12: Intestinal synthesis of
and moderate activity. Supplementation
vitamin 812 is probably adequate to meet
with 500-1,000 IU vitan1in E may be
ordil1a.ry needs, provided there is sufficient
necessary for horses working ha.rd and/or
cobalt in the diet. Deficiencies of cobalt in
fed high-fat(> 7%) rations. Excessive
horses have not been repo1ted. Vitan1in 812
supplementation (>5,000 IU/day for an
is absorbed from the cecwn, and feeding a
average adult horse) results in decreased
ration essentially devoid of vitamm 812 for
vitamin A absorption and should be

11 mo had no effect on the nom1al
avoided.

hematology or apparent health of adult

NUTRITION: HORSES

2321
horses. Vitamin B injected parenterally
before feeding can help alleviate this

12
into racehorses and foals is rapidly and
problem.

nearly completely excreted via bile into the
feces.

VetBooks.ir

Feeds

Niacin: Niacin is synthesized by the
bacterial flora of the cecum and colon and

Pasture: Good pasture provides both
is synthesized in the liver from tryptophan.

an excellent source of nutrients and the

There is no known dietary requirement for
oppo1tunity to exercise. The pasture should
niacin in healthy horses.

be kept as free of weeds as possible by
regular mowing or clipping. A legwne-grass

Other Vitamins: Folacin, biotin,
mixture offers the advantages of good
pantothenic acid, and vitamin 86
nutrient supply, persistence, and durability.

probably are synthesized in adequate

Ideal mixes vary with region, and local
quantities in the no1mal equine intestine.

recommendations from specialists should

However, biotin supplementation (15-25
be followed. However, some forages should
mg/day) has been documented to improve
not be used for horse pastures. Alsike clover
hoof quality in adult horses with soft, shelly

(Trifolium hybridum) and kleingrass
hoofwalls.

(Panicum coloratum) are potentially
hepatotoxic to horses, and Johnson grass

FEEDING PRACTICES

(Sorghum halepense) and Sudan grass (S
sudanense) contain cyanogenic glycosides.

Ideally, horses should be given free access

Buffel (Cenchrus spp), panic (Panicum
to hay and/or pasture forages with salt and
spp ), pangola (Digitaria decumbens ),
water ad Jib. Horses should not be offered
kikuyu (Pennisetum spp ), and Seta1ia spp

>0.5% of their body weight in high starch/
grasses all contain potentially harmful
sugar grain-based concentrates ( eg,
concentrations of oxalates. None of these
textured grain, pellets, or extruded feed) in
forage species should be used for horse
a single feeding. More than this in a single
pastures.

meal reduces digestive efficiency and

In sandy areas, horses should be provided
predisposes to problems such as gastric
with supplemental hay when pasture is
ulcers, insulin resistance, lan1initis, and
short (ie, overgrazed) to prevent sand
colic. If large an1ounts of grain-based
ingestion and subsequent colic. The hay
concentrates are being fed (>0.4% body wt/
should be offered in feeders or on a
day), the total amount offered daily should
platfonn to reduce sand ingestion. The
be divided into two or more feedings. Most
use of psylliwn products to enhance the
horses fed good-{!uality forages require little
elimination of sand from the equine GI tract
to no concentrate supplementation.

can be expensive, and efficacy has not been

Exceptions are hard-working horses or
well documented. Supplemental hay is also
those with limited access to good-{juality
recommended in any situation when the
forage ( <2% body wt in feed dry matter).

pasture is limited in quality (lots of weeds,

It has been well documented that feeding
undesirable weeds) or quantity to avoid

>506A, of the total ration in the form of
weed ingestion and preserve the pasture
grain-based concentrates increases the risk
cover.

of colic and laminitis in adult horses. High
starch/sugar intake also has been correlated

Hay: Common types of hay used to feed
to increased incidence of insulin resistance
horses include both grass hays, such as
in both adult and young growing horses.

timothy, brome, coastal Bermuda, or

Large (>0.25% body wt) meals of grainorchard, and legumes such as alfalfa or based concentrates should not be offered
clover. Legume-grass mixtures are generally

< 1 hr before strenuous exercise, transport,
high-yielding and contain considerably
or other stress, or to exhausted horses with
more protein, minerals, and vitamins than
poor gut motility.

do grasses alone. However, they may be

Because horses are particularly sensitive
more difficult to cure in a wann, hun1id
to toxins found in spoiled feeds, all grains
clinlate and more prone to mold. Coastal
and roughages offered should be of good

Bennuda grass has been associated with an
quality and free of mold. Grains should be
increased risk of impaction colic, especially
stored at a moisture content of <13%. In
when harvested late. Alfalfa may be
warm, humid areas, mold inhibitors may
contaminated with blister beetles and also
help reduce feed spoilage. In contrast,
tends to be more allergenic than grass hays
excessively dry, dusty feeds tend to initiate
or clover. Oat hay has been used in some
or aggravate respiratory problems.

regions and, if properly harvested and

Dampening or soaking such feeds in water
baled, is roughly equivalent to good-{juality

2322

NUTRITION HORSES
grass hays. Teff grasses are used in some

Sorghum grain (milo) and wheat should
regions of the world but may be deficient in
be fed with care. These grains must be
calciwn and should be used with caution ( or cracked or rolled if fed to horses. They are only if an accurate nutrient analysis is
not commonly used in horse rations.

done), especially for growing, pregnant, or

Other concentrate sources of energy/

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lactating horses.

protein used in various regions of the world

The form in which harvested forages are
include dried peas (Great Britain), sugar
provided to horses is of concern. Highcane pulp (Brazil), fava beans (Middle moisture haylages and silages made from

East), and bread (note that additives such as
whole com plants should be used with
sesame or chocolate might cause positive
caution as forage sources for horses
drug-test reactions).

because of the risk of molds. Moldy com
silage especially can cause fatal leukoen

Other Supplements: Wheat bran and
cephalomalacia. Feeding large round bales
rice bran are byproduct supplements
of hay in pastures can be economically
conunonly fed to horses. However, both are
advantageous if feeders that reduce waste
very high in phosphorus(> 1.2%), and the
are used, but it has been docun1ented to
proper calciwn:phosphorus ratio should be
increase the risk of botulism. Cubed or
maintained when any fom1 of bran is added
chopped forages are often recommended as
to the diet. Wheat bran is not laxative,
substitutes for long-stem hay or pasture and
contrary to popular belief, but is extremely
for horses that have trouble chewing.

palatable to horses and often used as a wet

Forage-based cubes may need to be soaked

"mash" to increase water intake or mask the in water to decrease the risk of choke, at
flavor of other supplements. Because of its
least initially.

high phosphorus content, wheat bran is not
recommended as a major or daily compo

Concentrates and Other Supple
nent of the ration unless the calciwn intake
ments: Concentrates include all grains
is carefully balanced. Rice bran is a high-fat
and byproduct feeds high in energy and/or
product added to rations of horses that need
protein ( eg, wheat bran, soybean meal, rice
extra calories. Many rice bran products
bran). Processing grains before feeding is
have added calciwn to offset the high
often desirable to in1prove nutrient
phosphorus content but still are designed to
availability. However, cracked or rolled
be fed in only limited ( <l kg/day) amounts.

grains are more susceptible to mold.

Beet pulp, a byproduct of the sugar beet

Because of differences in density, grains
industry, is added to horse rations as both a
should be measured by weight, not volume.

source of calories and fiber. It contains

Oats, one of the most traditional grains
moderate amounts of calciwn and protein
for horses, may be fed whole, rolled, or
and can be safely fed on a daily basis in
crimped. Processing increases the bulk
larger an10unts than the bran products.

20%-30% and improves digestibility by

Shredded beet pulp usually should be

-10%. "Hulled" or "naked" oats are more soaked in water before feeding to horses.

energy dense than regular oats and should

Beet pulp pellets do not require presoaking
be introduced slowly to reduce the risk of
and are often included in concentrate
founder or colic.

mixes.

Barley is a good grain for horses. It is

Edible oils and fats may be added to
higher in energy than regular oats but lower
rations to increase the energy density.

than com. It may be fed as the only grain to

Normal horse rations contain only 3%-4%
horses that have a high energy need. Barley
fat, but horses can easily tolerate up to l()OA,
should be rolled or crimped to improve
fat if it is introduced slowly and they are
digestibility. Palatability, however, is not as
given 3-4 wk to fully adapt to the change.

high as that of oats or com.

Corn and vegetable oils are commonly used.

Corn (maize) is a high-energy feed,

Edible oils should be introduced slowly to
useful for horses that are working hard or
the ration to avoid diarrhea. Although highly
in need of extra weight gain. However, the
digestible, animal fat is not commonly used
starch in corn is less digestible than that of
in horse rations.

oats and can more easily bypass small-intes

Soybean meal is a palatable protein
tinal digestion, resulting in colic and/or
supplement with good anlino acid balance
lan1initis if suddenly fed in large amow1ts.

for use in concentrate mixes. It may be fed

To maximize digestibility, shelled com may
when pastures or hay are low in protein
be cracked or rolled, but the moisture level
and are of poor quality or when protein
should be low enough to avoid spoilage
requirements are greatest, such as during
during storage. Moldy com can cause fatal
early growth or lactation. Linseed meal or
leukoencephalomalacia.

cottonseed meal should not be used as a

NUTRITION: HORSES

2323
protein supplement for young, growing

46 and 47 can be used as guidelines, but
horses because of their low lysine content,
body condition should be monitored and
but they are adequate for adult horses.

amounts adjusted accordingly. The maximal

Cane molasses is frequently added to
d1y matter intake in 24 hr is only 3%--3.5%
grain mixtures (sweet feeds). It is highly
of a horse's body wt, and many horses

VetBooks.ir
palatable, minimizes separation of "fines,"

voluntarily conswne <2.5% of their body wt
and reduces dustiness of concentrate
in dry matter in 24 hr. Feed intake should
mixtures. It is also high in potassiwn. The
therefore be monitored.

readily fem1entable carbohydrates and

The need for concentrate supplementamoisture that cane molasses contains may tion while on pasture depends on pasture
increase mold growth in hot weather and
quality but is more important for young
freeze solid in cold winter weather. High
horses and lact.ating mares. If the pasture is
sugar/starch (>30%nonstructural carbohyof good to excellent quality, no supplemendrate) rations have been docwnented to tation other than water and salt are needed
induce relative insulin resistance in horses
by most adult horses at maintenance or in
and are associated with increased incidence
light work It is desirable to creep-feed
of vices such as wind sucking and wood
nursing foals at the rate of 0.5%--1 % body wt
chewing.

with concentrates formulated specifically

Limestone of a high grade (3Soh calciwn)

for growth. Good-quality hay may be needed
may be used as a supplemental source of
even when on pasture, especially in winter.

calciun1. When both supplemental calciwn

Forage-based total mixed rations
and phosphoms are needed, dicalciw11
and "complete" feeds, which may have
phosphate, steamed bone meal, or
concentrates added, have been developed
defluorinated rock phosphate is recomfor horses. These can be textul'ed, pelleted, mended. Dicalciwn phosphate is particucubed, or extruded products. They have the larly good because the cost per unit of
advantage of unifonn quality, complete
phosphorus is low, the elements are quite
control over nutrient intake, suitability for
available, and it is fairly palatable.

horses with bad teeth, less dustiness (which

Salt (NaCl) should be provided in a block
reduces respiratory problems), and reduced
or in granular form free choice to all horses.

bulk for storage and transport. Disadvan

Salt content of forages in some regions
tages include an increased risk of choke and

(notably the southwestern USA) and many
increased wood chewing, especially with
commercial feeds may reduce the need for
the pelleted and extruded feeds fed as the
supplemental salt but, because of variable
sole source of nutrition. Most, however, are
losses in sweat, exact needs are hard to
sufficiently high calorie that they need to be
estimate. Horses, if given the opportunity,
limit fed ( <2.5% body wt/day). Wood
will voluntarily conswne sufficient salt to
chewing and boredom can be minimized oy
meet their longterm needs for maintenance,
feeding long-stern hay with these products
even in hot climates. For maintenance, in
or by dividing the total daily allotment into
horses that do not have high mineral needs,
multiple small feedings. Damage to stables
trace mineralized salt that contains added
and fences can be reduced by treating wood
iodine, iron, copper, cobalt, manganese,
with foul-tasting substances or by covering
zinc, and seleniwn is often used. The need
or replacing wood with metal in vulnerable
for these additional minerals varies with the
areas.

locality.

Exercise- and/or heat-induced sweat

NUTRITIONAL DISEASES
losses can cause acute sodiwn/chloride/
potassiun1 deficits that must be replaced

Reports of uncomplicated nutrient
more rapidly than voluntary homeostatic
deficiencies in horses are rare. The
mechanisms can accommodate. It is
nutrients most likely to be deficient are
conunon in these circwnstances ( eg,
caloric sources, protein, calciwn, phosphope1fom1ance horses) to give oral electrolyte rus, copper, sodiwn chlmide, and seleniun1,
drenches before, dw'ing, and/or after strenudepending on age and type of horse and ous activities.

geographic area. Signs of deficiency are
frequently nonspecific, and diagnosis may
be complicated by deficiencies of several

Feeding Rates
nutrients simultaneously. The consequences

Individual differences in the need for energy of increased susceptibility to parasitism and and nutrients and gross variations in
bacterial infections may be superimposed
nutrient contents of feedstuffs make it
over still other clinical signs. Sin1ple
difficult to generalize about the amount of
excesses are more common. Nutrients most
feed to provide. The amounts given in TABLES
commonly given in excess of needs, leading

2324

NUTRITION: HORSES

RECOMMENDED NUTRIENT CONCENTRATIONS IN RATIONS• FOR

HORSES AND PONIES

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Digestible Crude

Energy

Protein Ca
p

Vitamin A

(Meal/kg) (%)

(%)

(%)

(IU/kg)d

Mature horses and ponies,

I.SO

7.2

0.21

0.15

1,650
maintenance

Mares, last 90 days of

2.15

9.5

0.41

0.31

3,280
gestation

Lactating mares, first 3 mo

2.35

12.0

0.47

0.30

2,480

Lactating mares, 3 mo to

2.20

10.0

0.33

0.20

2,720
weaning

Stallions, breeding season

2.15

8.6

0.26

0.19

2,370

Creep fed

2.80

16.0

0.65

0.35

1,800

Foal (3 mo old)

2.70

14.0

0.65

0.35

1,500

Weanling (6 mo old)

2.60

13.1

0.55

0.30

1,680

Yearling (12 mo old)

2.50

11.3

0.40

0.22

1,950

Long yearling ( 18 mo old)

2.35

10.4

0.32

0.18

2,050

2-yr-old (light training)

2.40

10.1

0.31

0.17

2,380

Mature working horses

Light workr

2.20

8.8

0.27

0.19

2,420

Moderate workg

2.40

9.4

0.28

0.22

2,140

Intense workh

2.55

10.3

0.31

0.23

1,760
a 90% dry matter

O Good quality legume-grass hay; DE = digestible energy c Grass hay
d One mg of 13-carotene equals 400 IU of vitamin A for the horse.

• Concentrate containing 3.2 Meal DE/kg; A or B refers to suitable concentrates (see TABLE 47).

r Western pleasure, bridle path hack, equitation
g Ranch work, roping, cutting, barrel racing, jumping

" Race training, polo

Adapted, with permission, from Nutiient Requiremenls of Horses, 1989, National Academy of Sciences, National Academy Press, Washington, DC.

to toxicity or induced deficits of other

The brain is least affected, but the size of the
nutrients, are energy, phosphorus, iron,
gonads may be strikingly decreased, and
copper, selenium, and vitamin A.

estrus may be delayed. The itru11une system
is adversely affected, resultit1g in increased

Energy Deficiency: Many nonspecific
risk of vit·al diseases. The young skeleton is
changes found in horses with caloric
extremely sensitive, and growth slows or
deficiency can result from inadequate intake, may completely stop. A decrease in adipose maldigestion, or malabsorption. Weight loss
tissue is an early and conspicuous sign and is
is the cardinal sign of inadequate energy
seen not only in the subcutis but also in the
intake. In partial or complete starvation,
mesentery; around the kidneys, uterus, and
most internal organs exhibit some atrophy.

testes; and in the retrope1itoneurn. Low-fat

NUTRITION: HORSES

2325

RECOMMENDED NUTRIENT CONCENTRATIONS IN RATIONS• FOR

HORSES AND PONIES (continued)

Example Diet Proportions

VetBooks.ir

Hay Containing 2.0 Meal DEfkgb

Hay Containing 1.8 Meal DE/kg<

Concentrate (% Y Roughage(%)

Concentrate (% Y Roughage (%)

0

100

0

100

20B

80

25A

75

40A

60

50A

50

30B

70

40A

60

25A

75

30A

70

70A

30

50A

50

70A

30

50A

50

60A

40

40B

60

50A

50

30B

70

40B

60

40B

60

50B

50

0-25B

75

25B

75

40B

60

50B

50

50B

50

60B

40
content of long bone manow is a good

Jack of a specific essential an1ino acid. The
indicator of prolonged inanition. The ability
effects of deficiency are generally nonspeto pe1fom1 work is impaired, and endogcific, and many of the signs do not differ enous nitrogen losses increase as muscle
from the effects of partial or total caloric
proteins are metabolized for energy, causing
restriction. In general, the horse will have
muscle wasting.

poor-quality hair and hoof growth, weight
loss, and inappetence. In addition, there

Energy Excess: Overfeeding high-calorie
may be decreased formation of Hgb, RB Cs,
feeds results in obesity in horses and may
and plasma proteins. Milk production is
contribute to developmental orthopedic
decreased in lactating mares. The following
clisease in growing horses. However, some
liver enzymes have shown decreased
horses, especially those that are sedentary,
activity: pyruvic oxidase, succinoxidase,
can become obese on only good-quality hay
succinic acid dehydrogenase, D-an1ino acid
or pasture. Obesity increases the risk of
oxidase, DPN-cytochrome C reductase, and
laminitis (presumably associated with
uricase. Corneal vascularization and lens
relative insulin resistance) and colic, clue
degeneration have been noted. Antibody
to strangulation of the small intestine by
fomiation is also impaired.

pedunculatecl mesenteric lipomas. Obese
horses and ponies have reduced heat and
exercise tolerance.

Mineral Deficiencies and Excesses:

Nutritional Secondary Hyperparathy

Protein Deficiency: A deficiency of
roidism (Bighead, Bran disease): Horses
dietary protein maybe caused by either
of all ages fed grass hay or pastme and
inadequate intake of high-quality protein or
supplemented with large amow1ts of

2326

NUTRITION: HORSES

CONCENTRATES SATISFACTORY FOR USE WITH HAYS AS

INDICATED IN TABLE 46

Ingredienta

Formula A

FormulaB

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Cornb or sorghum grain, rolled or cracked

45

55

Oatsb, rolled or crimped

24

24

Soybean meal ( 44% crude protein)

20

10

Cane molassesc

8

8

Limestone (34% Ca)

0.5

0.5

Calcium phosphate, mono basic (16% Ca, 22% P)

1.5

1.5

Trace mineral saltcl
lOO"A,
lOO"A,

Analysis

Digestible energy (McaVkg)

3.2

3.2

Crude protein (%)

16

12

Digestible protein (%)

12

8.5

Calcium(%)

0.60

0.58

Phosphorus (%)

0.67

0.62

" Except for the cane molasses, all figures are on a 90% dry-matter basis.

b Barley may be used to replace the com or sorghum and the oats, by using weights of barley equal to the combined weights of the grains replaced.

c Cane molasses is not an essential pa.it of a concentrate mixture, but it may help to minimize separation of "fines" ru1d reduce dustiness.

"Providing NaCl, Fe, Cu, Mn, Co, I, Zn, ru1d Se (from sodium selenite) to provide 0.2 mg selenium/kg concentrate.

grai n -based concentrates or wheat bran are
levels may be increased. An insidious
most likely to develop relative or absolute
shifting lan1eness may be seen. Bone
calcium deficiencies leading to nub:itional
changes resemble those described for
secondary hyperparathyroidism. ]::xcess
calcium deficiency. Affected horses may
phosphorus intake (Ca:P ratio <l) causes the
start to consume large quantities of soil or
same clinical signs. Blood concentrations of
exhibit other manifestations of pica before
calcium do not reflect intake because of
other clinical signs are apparent.

homeostatic mechanisms, although blood
inorganic phosphorus may be increased

Salt Deficiency: Horses are· most likely to
because of mobilization of bone mineral
develop signs of salt (NaCl) deficiency when
content. Serum alkaline phosphatase activity
worked hard in hot weather. Sweat and
is usually increased, and clotting time may be urinary losses are appreciable. Horses prolonged slightly. Young, growing bone is
deprived of salt ti.re easily, stop sweating,
frequently rachitic and brittle. Fractures may
and exhibit muscle spasms if exercised
be common and heal poorly. Swelling and
strenuously. Hemoconcentration and
softening of the facial bones and alternating
acidosis may be expected. Anorexia and
limb lan1eness are frequently reported. (See
pica may be evident in chronic deprivation,
ai,so
although these are not specific signs of salt

OS'TEOMALACIA, p 1052.)

deficiency. In lactating mares, milk

Phosphorus Deficiency: Phosphorus
production seriously declines. Polyuria and
deficiency is most likely in horses being fed
polydipsia secondary to renal medullary
poor-quality grass hay or pasture witl10ut
washout may l>e seen in prolonged deficits.

grain. Senun inorganic phosphorus
concentrations may be decreased, and

Potassium: Chronic dietary deficiency
serum alkaline phosphatase activity
of potassium results in a decreased rate of
increased. Occasionally, senun calcium
growtll, anorexia, and perhaps hypokalemia.

NUTRITION HORSES

2327

However, most forages contain more than

Seleniwn excesses of as little as 5 ppm in
sufficient potassium for the average horse.

the ration cause loss of mane and tail hairs

Acute deficits due to sweat losses are more
and sloughing of the distal po1tion of the
likely and may cause muscle tremors,
hoof.

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cardiac arrhytlunias, and weakness. Excess
potassium intake, especially if given as a
bolus PO or IV, also will induce cardiac

Vitamins: A vitamin A deficiency may
arrhytlunias such as atrial fibrillation.

develop if dried, poor-quality roughage is
fed for a prolonged period. If body stores of

Magnesium: Foals fed a purified diet
containing magnesium at 8 mgtkg (3.6 mg/J.b)

vitamin A are high, signs may not appear for
exhibited hypomagnesemia, nervousness,
several months. The deficiency is cha.racte1�
muscular tremors, and ataxia followed by
ized by nyctalopia, lacrirnation, keratiniza.tion of the cornea, susceptibility to collapse, with increased respiratory rates,
sweating, convulsive paddling, and death
pnewnonia, abscesses of the sublingual
after a few weeks. However, most
gland, incoordination, impaired reproduccorrm1only used feeds contain magnesium tion, capricious appetite, and progressive
weakness. Hooves are frequently defonned,
well in excess of the 70-100 mgtkg dry
ration currently recommended. Oversupplewith the horny layer m1evenly laid down and mentation of this mineral is more likely.

unusually brittle. Metaplasia of the
intestinal mucosa and achlorhydria have

Although the effects of excessive magnesitun intake in horses have not been been reported. Genitourinary mucosa]

metaplasia may be expected. Bone
detem1ined, based on data from other
species, it may cause clinical signs of
remodeling is defective. The foran1ina do
not enlarge properly dming early growth,
calciw11 deficiency.

and skeletal defonnities are evident. The

Iron: Iron deficiency may be secondary to
latter may be seen in foals of vita.min Aparasitism or chronic blood loss and results deficient mares.

in microcytic, hypochromic anemia.

Vitamin Eis very labile and quickly lost

However, it is highly unlikely that even
with storage in both hays and commercial
anemic horses are iron deficient. Iron
feeds. It is an important antioxidant, and
excess interferes with copper metabolism
deficiency has been reported to be
and also causes microcytic, hypochromic
associated with an increased incidence
anemia. Blood transferrin concentrations
of rhabdomyolysis, impaired immune
are the most reliable method to detennine
flmction, reproductive failme, and ocular
the iron status of a horse.

lesions. Some prolonged, aggressive

Zinc: Zinc deficiency in foals causes
antibiotic treatments, such as recomreduced growth rate, anorexia, cutaneous mended for equine protozoa! myelitis, have
lesions on the lower extremities, alopecia,
also been reported to induce vitan1in E
decreased blood levels of zinc, and
deficits. Fresh forages, however, are
decreased serwn alkaline phosphatase
excellent somces of vitamin E, and horses
activity. Excesses (>1,000 ppm) were
with free access to good pasture rarely need
associated with developmental orthopedic
supplementation.

disease in young horses. The effects of

If sun-cmed hay is consun1ed or the
excesses or deficits of zinc have not been
horse is exposed to sunlight, it is doubtful
documented in adult horses.

a vitamin D deficiency will develop.

Prolonged confinement of young horses

Copper: An apparent relationship
offered only limited amounts of sun-cmed
between low blood copper concentrations
hay may result in reduced bone calcificaand uterine artery rupture in aged parturient tion, stiff and swollen joints, stiffness of mares suggests reduced copper absorption
gait, irritability, and reduced serum calciun1
with age or reduced ability to mobilize
and phosphorus. Clinical signs are easily
copper stores. Dietary deficiency may cause
reversible with supplementation or
aortic aneurysm, contracted tendons, and
exposme to swilight.

improper cartilage fonnation in growing

Signs of experimental thiamine
foals. Excessive copper intake may
deficiency include anorexia, weight loss,
interfere with seleniun1 and/or iron
incoordination, decreased blood thiamine,
metabolism.

and increased blood pyrnvate. At necropsy,

Selenium: Seleniun1 deficiency results in
the heart is dilated. Similar signs have been
reduced serwn selenium, increased AST
seen in bracken fem poisoning (see
activity, white muscle disease, and perhaps
p 3089). Under normal circLU11stances, the
rhabdomyolysis in working horses. (See
natmal diet plus synthesis by microorgan
also NUTRITIONAL MYOPATl·IIES, p 1185.)

isms in the gut probably meet the need for

2328

NUTRITION HORSES
thiamine. However, needs may be
of grains. Bran mashes are usually
increased by stress.

palatable, but tl1e addition of molasses,

Although natural feeds plus synthesis
applesauce, and salt may increase t11eir
within the gut nom1ally provide adequate
acceptance in anorectic horses.

VetBooks.ir
riboflavin, limited evidence indicates an

When horses expe1ience pain or fever,
occasional deficiency when the diet is
analgesics can improve food intake; NSAIDs,
of poor quality. The first sign of acute
such as dipyrone, flwlixin meglW11ine,
deficiency is catarrhal conjw1ctivitis in one
meclofenamic acid, and phenylbutazone,
or both eyes, accompanied by photophobia
can be used. Prolonged use of phenylbutaand lacrimation. The retina, lens, and ocular zone should be avoided because of tl1e
fluids may deteriorate gradually and result
adverse effects of gastric and small -intestinal
in impaired vision or blindness. Equine
ulceration and renal papillary necrosis.

recwi-ent uveitis (seep 508) has been linked Tube feeding is a second way to provide
to riboflavin deficiency but may be a sequela
nuttition to horses that will not (or carmot)

of leptospirosis or onchocerciasis.

eat voluntarily. A normal stomach tube may

The nom1al feedstuffs of horses generally
be passed several times a day or may be
contain very little vitamin B,2. However,
sutured to the nosttil and left as an indwelling
horses can synthesize this vitan1in in the
feeding tube. This is an effective method to
gut, from which it is absorbed.

provide nutrients to sick neonates. It is also
an inexpensive metl1od to replace fluid and

FEEDING THE SICK HORSE
electrolyte losses. Enteral nuttitional
supplements used in hwnan medicine are

Nutritfon is an important part of the
particularly useful to provide sufficient
management and treatment of sick horses.

caloric intake to adult h01ses. These products

Stresses (eg, sw·ge1y, severe 01thopedic
have a known caloric content, which
problems, or infection) can significantly
facilitates calculation oftl1e animal's needs.

increase caloric needs clue to an increase

Soaking a complete pelleted feed in water
in catabolism. In addition, anorexia or
can make a s!Ltrry for tube feeding; however,
dysphagia can lead to inadequate intake of
when feeding a slwzy in tllis marmer, the
tl1e proper nutrients. The consequences
stomach tube may clog with feeclstuff.

of not providing proper nutrition include

The third metl1od to provide energy and
impainnent of tl1e immune system, delayed
protein to sick horses is through use of total
wound and fracture healing, hypoproteineor partial parenteral nuttition (TPN or PPN).

mia, muscle wasting, and weakness.

Fluid administration (IV) can maintain

Generally, supportive nutritional t11erapy
hydration in horses unable either to drink
should be considered if an adult horse has
or absorb fluids. Conm1on replacement
been hypophagic for. �3 clays. Neonatal foals
solutions include socliwn chloride, lactated
require some energy source within 24 hr of

Ringer's, and 5% dextrose. The nutritional
decreased intake.

value of these fluids is insignificant. Fat and

The order of nutrient priorities is water,
amino acid solutions are also available. The
energy, electrolytes, and pr.otein. Some
components of parenteral nutrition are
wate1�soluble vitamins are poorly stored in
glucose, an1ino acids, lipid, trace minerals,
the body and should be supplemented. The
and multivitamins. The resultant solution is
basal energy requirement (BER) in kcal/day
hype1tonic and is delivered by constant
can be calculated by tl1e following formula:

infusion tiu·ough a.jugular catheter. Delivery

BER= 70 (body wt in kg)0·75. For example,
is optimized tllrough use of a fluid pun1p.

BER is -6,8 00 kcal/day for a 450-kg horse

Blood and mine glucose should be
and l,300kcal/day fora. 50-kg foal. Severe
monitored twice daily to regulate the rate
illness or trawna (eg, barn fire bwns)

of infusion. TPN is costly and requires
significantly increase these needs.

intensive care and monitoring, which limits

There are several methods to provide
its usefulness in adult horses.

nutritional supp01t to a.sick horse. The
simplest method is to encourage the horse

Nutrition for Specific Diseases/
to eat on its own. Unusual feed preferences

Problems: Horses with recurrent airway
may be seen. Offering a variety of feeds and
obstruction (seep 1455) are frequently
letting the horse choose can best determine
sensitive to the dust and molds foWld in
what is most palatable to the animal. Many
n01mal hay. They often inlprove when hay is
horses will eat fresh, green grass even
removed from their diet and they are placed
though they refuse other feeds. Alfalfa hay
on a complete ration tl1at is pelleted or
is more palatable than grass hays. Whole
contains a roughage source such as beet
oats and sweet -feed mixtures of rolled
pulp. They do best on pasture. Anotl1er
grains and molasses are the most appetizing
source of dust-free roughage is haylage.

NUTRITION: PIGS

2329

Diarrhea in horses is primarily a colonic
birth-preferably within the first 3-12 hr.

disease. Traditionally, affected horses are fed

Antibody-rich plasma-replacement products
less grain and more hay. This increase in
for IV administration are available but are
dietary fiber can bind water and may result
expensive and provide protection of

VetBooks.ir
in better fom1ed feces. If weight loss is a
questionable dw·ation.

concunent problem, it may be better to main

A nurse mare, preferably with a good
tain grain intake. Grain is digested mainly in
disposition, is best for the overall care of an
the small intestine, and hay in the large
orphan foal. TI1e amnion and/or placenta of a
intestine. Unless the small intestine is also
mare who has lost a newborn foal can be
affected, feeding grain helps maintain body
placed over the orphan foal to increase the
mass. (See also COLIC IN HOllSES, p 248, and ma.re's acceptance of the foal. The mare and

INTESJ'lNAL DISEASES IN HORSES AND F'OALS, p 281.)

foal should not be left unattended until the

The role of nutrition in horses with
ma.re has accepted the orphan; physical or
hepatic disease (seep 329) is to provide
chemical restraint of the mare may be
adequate energy, thus easing the liver's role
required initially and repeated on several
in energy production and decreasing the
occasions before she will accept the new foal.

a.mount of metabolic waste to which the

If a nurse ma.re is not available, a. lactating
liver is exposed. Parenteral or enteral
dai1y goat (positioned on a stand or bale of
glucose administration may be imp01tant as
hay or straw) may serve as an alternative.

an energy source in anorectic horses. In

Constant monit01ing is necessary, because
horses that are eating, cereal grains should
the foal should be fed every 4 hr.

provide adequate carbohydrates. Com is the

Artificial mare's milk diets ru1d goat's
grain of choice because of its low-protein,
milk have also been used successfully to
high-carbohydrate content. High-protein
feed orphan foals. Foals should be fed
feeds, such as alfalfa hay, should be avoided. every 1-2 Ju· for the first 1-2 days of life, Horses excrete significant an1ounts of
then every 2-4 hr for the next 2 wk at the
calciun1 in their urine. In cases of renal
rate of 250-500 mL per feeding, using a
disease, low-protein, low-calcium diets
wanned milk container ru1d an rutificial
should be fed. Com and grass hay are the
nipple. Of the various artificial nipples
feeds of choice.

available, those designed for use by lan1bs
are best suited for foals. The feeding

FEEDING THE AGED HORSE AND
intervals may be lengthened gradually after

THE ORPHAN FOAL

2 wk; however, the amount per feeding
also should be increased so that the foal

Aged horses often lose weight because of
consumes lOo/o--15% of its body wt/day.

dental wear. Their teeth lose the grinding

A foal should be encouraged to drink
surface, which results in poor mastication
freshly prepared milk out of a bucker, ad lib,
of food. Aged horses also may have reduced
early in life. After 1 mo, the foal can be
protein, fiber, and phosphorus digestion.

encouraged to eat grain mixes (with �18%

Feeding a moistened, complete pelleted
crnde protein designed for growing foals)

ration designed for aged horses may
and good-quality hay in addition to the milk
improve the horse's well-being.

or milk replacer. The foal can be weaned off

If an orphan foal has not received
the milk replacer at 3 mo of age. Fresh water
colostrun1 from its dam, it must receive
should be available to the foal at all tin1es
either colostrnm from another mare or
from birth. (See also PERINATAL MARE AND l'OAL
frozen-stored colostrum within 24 hr of

CARE, p 2159.)

NUTRITION: PIGS

NUTRITIONAL REQUIREMENTS
provides estin1ates of the an10unts of these
nutrients for various classes of swine under

Pigs require a nwnber of essential nutrients
average conditions. However, factors such
to meet their needs for maintenance,
as genetic variation, environment,
growth, reproduction, lactation, and other
availability of nutrients in feedstuffs,
functions. The National Research Council
disease levels, and other stressors may

(NRC), in its publication, Nutrient
increase the needed level of some nutlients

Requirements of Swine (updated in 2012),
for optimal pe1fonnance and reproduction.

2330

NUTRITION: PIGS

The NRC uses a modeling approach to take
primaiily derived from the oxidation of
some of these factors into consideration in
carbohydrates and fats. In addition, ainino
its estimates of requirements for energy,
acids (from protein) that exceed the animal's
amino acids, calcium, and phosphorus,
requirements for maintenance and tissue
but requirements for other minerals and
protein synthesis provide energy when their

VetBooks.ir
vitamins are estimated strictly from
carbon skeletons are oxidized. Antibiotics,
empirical data.

chemotherapeutic agents, microbial

Although the NRC addresses factors such
supplements (prebiotics and probiotics),
as lean growth rate, gender, energy density
enzymes, ai1d other feed additives are often
of the diet, environmental temperatme,
added to swine diets to increase the rate and
crowding, parity, stage of gestation, and
efficiency of gain, to improve digestibility,
various measures of sow productivity when
and for other purposes, but they are not
estimating nutrient requirements, nutritionconsidered nutrients.

ists, feed manufacturers, veterinarians, or

The NRC estimates of nutrient requireswine producers may wish to include higher ments for various body weight groups of levels of certain nutrients than those listed
pigs from 5-135 kg body wt, expressed as
by the NRC to ensure adequate intake of
dietat)' concentrations, are shown in TABLE
nutrients and for insmance purposes. Any

48. Requirements for gestating and lactating
negative effects from oversupplementing
sows, expressed as dietary concentrations,
diets are generally minimal except in cases
are shown in TABLE 49. The dietary concenof extreme imbalance.

trations listed in the NRC tables are based

Swine require six general classes of
on a given ainount of feed intake; if intake
nutrients: water, carbohydrates, fats, protein is less than the amOLmt listed, the dietary (amino acids), minerals, and vitan1ins.

concentration may need to be increased

Energy, although not a specific nutrient, is
to ensure an adequate daily intake of the
an important nutritional component and is
nutrients.

DIETARY NUTRIENT REQUIREMENTS OF GROWING PIGS ALLOWED

AD LIB FEED (90% DRY MATIER)•,b,c

Body Weight (kg)

75-

100-

5-7

7-11 11-25 25-50 50-75 100

135

NE content of diet

2,448

2,448

2,412 2,475 2,475 2,475 2,475

(kcal/kg)<l

DE content of diet

3,542

3,542

3,490 3,402 3,402 3,402

3,402

(kcal/kg)<l

ME content of diet

3,400

3,400

3,350 3,300 3,300 3,300 3,300

(kcal/kg)<l

Estimated ME intake

904

1,592

3,033 4,959

6,989 8,265 9,196

(kcal/day)

Estimated feed intake +

280

493

953 1,582

2,229 2,636

2,933
wastage (g/day)•

Body wt gain (g/day)

210

335

585

758

900

917

867

Body protein deposition

128

147

141

122

(g/day)

AMINO ACIDS, TOTAL (%)1

Arginine

0.75

0.68

0.62

0.50

0.44

0.38

0.32

Histidine

0.58

0.53

0.48

0.39

0.34

0.30

0.25

Isoleucine

0.88

0.79

0.73

0.59

0.52

0.45

0.39

Leu cine
l.71
l.54
l.41

1.13

0.98

0.85

0.71

NUTRITION: PIGS

2331

DIETARY NUTRIENT REQUIREMENTS OF GROWING PIGS ALLOWED

AD LIB FEED (90% DRY MATIER)•,b,c (continued) Body Weight (kg)

VetBooks.ir

75-

100-

5-7

7-11 11-25 25-50 50-75 100

135

Lysine

1.70

1.53

1.40

1.12

0.97

0.84

0.71

Methionine

0.49

0.44

0.40

0.32

0.28

0.25

0.21

Methionine + cystine

0.96

0.87

0.79

0.65

0.57

0.50

0.43

Phenylalanine

1.01

0.91

0.83

0.68

0.59

0.51

0.43

Phenylalanine + tyrosine

1.60

1.44

1.32

1.08

0.94

0.82

0.70

Threonine

1.05

0.95

0.87

0.72

0.64

0.56

0.49

Tryptophan

0.28

0.25

0.23

0.19

0.17

0.15

0.13

Valine

1.10

1.00

0.91

0.75

0.65

0.57

0.49

Approximate crude

24-26

22-24

21-23

19.3

17.l

15.2

13.4
proteing

MINERALS

Calcium(%)

0.85

0.80

0.70

0.66

0.59

0.52

0.46

Phosphorus, total (%)h

0.70

0.65

0.60

0.56

0.52

0.47

0.43

S'ITD phosphorus (%)h

0.45

0.40

0.33

0.31

0.27

0.24

0.21

ATID phosphorus (%)h

0.41

0.36

0.29

0.26

0.23

0.21

0.18

Sodium(%)

0.40

0.35

0.28

0.10

0.10

0.10

0.10

Chlorine(%)

0.50

0.45

0.32

0.08

0.08

0.08

0.08

Magnesium(%)

0.04

0.04

0.04

0.04

0.04

0.04

0.04

Potassium (%)

0.30

0.28

0.26

0.23

0.19

0.17

0.17.

Copper (ppm)

6.00

6.00

5.00

4.00

3.50

3.00

3.00

Iodine (ppm)

0.14

0.14

0.14

0.14

0.14

0.14

0.14
lron(ppm)

100

100

100

60

50

40

40

Manganese (ppm)

4.00

4.00

3.00

2.00

2.00

2.00

2.00

Selenium (ppm)

0.30

0.30

0.25

0.20

0.15

0.15

0.15

Zinc(ppm)

100

100

80

60

50

50

50

VITAMINS AND FATIY ACIDS

Vitamin A (IU/kg)i

2,200

2,200

1,750

1,300

1,300

1,300

1,300

Vitamin D (IU/kg)i

220

220

200

150

150

150

150

Vitamin E (IU/kg)i

16

16

11

11

11

11

11

Vitamin K (menadione,

0.50

0.50

0.50

0.50

0.50

0.50

0.50
mg/kg)

Biotin (mg/kg)

0.08

0.05

0.05

0.05

0.05

0.05

0.05

Choline (g/kg)

0.60

0.50

0.40

0.30

0.30

0.30

0.30

Folacin (mg/kg)

0.30

0.30

0.30

0.30

0.30

0.30

0.30

2332 NUTRITION PIGS

DIETARY NUTRIENT REQUIREMENTS OF GROWING PIGS ALLOWED

AD LIB FEED (90% DRY MATIER)•,b,c (continued) Body Weight (kg)

VetBooks.ir

75-

100-

5-7

7-11 11-25 25-50 50-75 100

135

Niacin, available (mg/kg)i

30.00

30.00

30.00

30.00

30.00

30.00

30.00

Pantothenic acid (mg/kg)

12.00

10.00

9.00

8.00

7.00

7.00

7.00

Riboflavin ( mg/kg)

4.00

3.50

3.00

2.50

2.00

2.00

2.00

Thiamine (mg/kg)

1.50

1.00

1.00

1.00

1.00

1.00

1.00

Vitamin 86 (mg/kg)

7.00

7.00

3.00

1.00

1.00

1.00

1.00

Vitamin B,2 (mcg/kg)

20.00

17.50

15.00

10.00

5.00

5.00

5.00

Linoleic acid (%)

0.10

0.10

0.10

0.10

0.10

0.10

0.10
a Adapted, with permission, from Nut1"ient Requirements of Swine (2012), National Research Council, National Academies Press, Washington, DC.

O Estimates of nutrient requirements are for the midpoint of the weight range as determined by the NRC growth model for pigs of mixed gender (1:1 ratio of barrows and gills) with high-medium lean growth rate (mean whole body-protein deposition of 135 g/day) from 25-125 kg body wt.

c Estimates of amino acid, calcium, and phosphorus requirements differ for barrows, gilts, and intact boars, for pigs with differing lean growth rates, for pigs fed ractopamine, and for boars immunized against gonadotropin-releasing hormone. For additional info1mation, see Nut rienl Requirements of Swine (2012), National Reseru·ch Council, National Academies Press, Washington, DC.

"NE= net energy, DE= digestible energy, ME= metabolizable energy. Dieta,y energy contents relate to corn and soybean meal-based diets. DE and ME are calculated from NE.

e Assumes 5% feed wastage.

r Total runino acid requirements apply to corn-soybean meal-based diets. For 5- to 25-kg pigs, lysine percentages a,·e estimated from empi.tical data, and the other runino acids are based on the ratios of anlino acids to lysine based on a,11ino acid requirements for maintenru1ce and growth. The requirements for 25- to 135-kg pigs ru·e estimated from the NRC growth model.

s The calculated crude protein levels are based on corn-soybean meal cLiets containing 0.1% supplemental lysine ru1d 3% minerals ru1d vitami.t1s. In addition, specialty ingredients (lactose, dried whey, dried blood plasma, dried blood cells, etc) a,·e included in diets for 5-11 kg pigs.

"STTD = standardized total lrnct digestible, ATI D = apparent total tract digestible, ATTD phosphorus ru1d total phosphorus requiren;ents apply to com and soybeaJ1 meal-based diets.

; Conversions: I IU vitaJnin A = 0.30 mcg reti..nol or 0.344 mcg retinyl acetate; l lU vitamin D, or D,,

= 0.025 mcg cholecalci..ferol; l JU vitanlin E = 0.67 mg of o-u-tocopherol or 1 mg of DL-a-tocopherol acetate.

i The niacin in corn, grain sorghum, wheat, and bru·ley is unavailable. Similru·ly, the niacin in byproducts made from these cereal grains is poorly available w1less the by-products have undergone fermentation or wet-milling process.

Water: Pigs should have free and
reduces perfonnance and milk production
convenient access to water, beginning
and may result in death if the restriction is
before weaning. The an1ount required
severe.

varies with age, type of feed, environmental

Water quality is important Water should
temperatme, status of lactation, fever, high
be relatively free of microbial contaminaminary output (as from high salt or protein tion; if not, chlorination may be necessary.

intake), or diarrhea. Normally, growing pigs

Excessive minerals in water may create
consume -2-3 kg of water for every kg of
problems. Water should have <1,000 ppm of
dry feed. Lactating sows consume more
total dissolved solids (TDS). Higher levels of
water because of the high water content of

TDS (2,000-5,000 ppm) can cause diarrhea
the milk they produce. Water restriction
or temporary water refusal, TDS levels of

NUTRITION: PIGS

2333

5,000-7,000 should be avoided for breeding

Energy: Energy requirements are
animals, and TDS levels> 7,000 ppm are
expressed as kilocalories (kcal) of
unfit for pigs. Pigs tolerate moderate levels
digestible energy (DE), metabolizable
of sulfates in water, but high levels (>3,000
energy (ME), or net energy (NE). DE and

VetBooks.ir
ppm) of sulfates should be avoided.

ME values are used most commonly, but

REPRODUCTIVE MEASURES AND DIETARY NUTRIENT

REQUIREMENTS OF GESTATING AND LACTATING SOWS•,b

Gestation

Lactation (21-day)

Reproductive Measures

Parity

3

2+

Body weight at

140

185
breeding (kg)

Anticipated gestation

65.0

52.2
weight gain (kg)

Anticipated litter size

12.5

13.5

Day of gestation

0-90 90-115 0-90

90-115 -

Body weight

175

210
postfarrowing (kg)

Litter size

11

11.5

Daily weight gain of nursing

230

230
pigs (g)

Nutrient Requirements

NE content of diet

2,518 2,518

2,518 2,518

2,518

2,518

(kcal/kg)c

DE content of diet

3,388 3,388

3,388 3,388

3,388

3,388

(kcal/kg)<

ME content of diet

3,300 3,300

3,300 3,300

3,300

3,300

(kcal/kg)<

Estimated ME intake

6,678 7,932

6,928 8,182

18,700

20,700

(kcal/day)

Estimated feed intake

2,130 2,530

2,210

2,610

5,950

6,610

(g/day) + wastagect

Body wt gain (g/day)

578

543

472

408

Body wt loss (21-day

7.7

5.8
lactation, kg)

AMINO ACIDS, TOTAL(%)•

Arginine

0.32

0.42

0.23

0.32

0.50

0.48

Histidine

0.22

0.27

0.16

0.20

0.37

0.36

Isoleucine

0.36

0.43

0.27

0.33

0.52

0.50

Leu cine

0.55

0.75

0.41

0.59

1.05

1.01

Lysine

0.61

0.80

0.45

0.62

0.93

0.90

(continued)

2334

NUTRITION: PIGS

REPRODUCTIVE MEASURES AND DIETARY NUTRIENT REQUIREMENTS

OF GESTATING AND LACTATING SOWS•,b (continued) Gestation

Lactation (21-day)

VetBooks.ir

Day of gestation

0-90 90-115 0-90

90-115

Methionine

0.18

0.23

0.13

0.18

0.25

0.24

Methionine + cystine

0.41

0.54

0.32

0.44

0.51

0.49

Phenylalanine

0.34

0.44

0.25

0.35

0.51

0. 49

Phenylalanine + tyrosine

0.61

0.79

0.46

0.62

L07

L03

Threonine

0.46

0.58

0.37

0.48

0.62

0.60

Tryptophan

0.11

0.15

0.09

0.13

0.18

0.17

Valine

0.45

0.58

0.34

0.46

0.81

0.78

Approximate crude proteinr 1L9

14.7

9.6

12.0

16.6

16.1

MINERALS

Calcium(%)

0.61

0.83

0.49

0.72

0.71

0. 68

Phosphorus, total (%)g

0.49

0.62

0.41

0.55

0.62

0. 60

STID phosphorus (%)g

0.27

0.36

0.21

0.31

0.36

0. 34

ATID phosphorus (%)g

0.23

0.31

0.18

0.27

0.31

0. 29

Sodium(%)

0.15

0.15

0.15

0.15

0.20

0. 20

Chlorine (%)

0.12

0.12

0.12

0.12

0.16

0. 16

Magnesiw11 (%)

0.06

0.06

0.06

0.06

0.06

0. 06

PotassiWTI (%)

0.20

0.20

0.20

0.20

0.20

0. 20

Copper (ppm)

10.00 10

10

10

20

20

Iodine (ppm)

0.14

0.14

0.14

0.14

0.14

0. 14

Iron (ppm)

80

80

80

80

80

80

Manganese (ppm)

25

25

25

25

25

25

Selenium (ppm)

-0.15

0.15

0.15

0.15

0.15

0. 15

Zinc (ppm)

100

100

100

100

100

100

VITAMINS AND FATT Y ACIDS

Vitamin A (IU/kg)"

4,000 4,000

4,000

4,000

2,000

2, 000

Vitamin D (IU/kg)"

800

800

800

800

800

800

Vitamin E (IU/kg)1'

44

44

44

44

44

44

Vitan1in K (menadione,

0.50

0.50

0.50

0.50

0.50

0.50
mg/kg)

Biotin (mg/kg)

0.20

0.20

0.20

0.20

0.20

0.20

Choline (g/kg)

L25

L25

L25

L25

LOO

LOO

Folacin (mg/kg)

L30

L30

L30

L30

L30

L30

Niacin, available (mg/kg)i

10

10

10

10

10

10

Pantothenic acid (mg/kg)

12

12

12

12

12

12

Riboflavin (mg/kg)

3.75

3.75

3.75

3.75

3.75

3.75

(continued)

NUTRITION: PIGS

2335

REPRODUCTIVE MEASURES AND DIETARY NUTRIENT REQUIREMENTS

OF GESTATING AND LACTATING SOWS•,b (continued) Gestation

Lactation (21-day)

VetBooks.ir

Day of gestation

0-90 90-115 0-90

90-115

Thiamine (mg/kg)

1.00

1.00

1.00

1.00

1.00

1.00

Vitamin 86 (mg/kg)

1.00

1.00

1.00

1.00

1.00

LOO

Vitamin 812 (mcg/kg)

15

15

15

15

15

15

Linoleic acid (%)

0.10

0.10

0.10

0.10

0.10

0.10
a Adapted, with permission, from Nul'1ient Requirements of Swine (2012), National Research Council, National Academies Press, Washington, DC.

b Estimates of amino acid, calcium, and phosphorus requirements during gestation differ for parity 1, 2, 3, and 4+ sows, stage of gestation, body weight at breeding, anticipated litter size, and other factors. Requirements for these nutrients during lactation differ for paiity I and 2+ sows, body weight after fai-rowing, litter size, and other factors. For additional information, see Nutrient Requirements of Swine (2012), National Research Council, National Academies Press, Washington, DC.

c NE= net energy, DE= digestible energy, ME= metabolizable energy. Dietary energy contents related to corn ai1d soybeai1 meal-based diets. DE ai1d ME ai·e calculated fru111 NE.

d Assumes 5% feed wastage.

c Total amino acid requirements apply to com-soybean meal-based diets.

'The calculated crude protein levels ai·e based on com-soybean meal diets containing O.!%supplementaJ lysine ai1d 3% minerals and vitamins.

g SITD = standai·dized total tract digestible, AITD = apparent total tract digestible, AITD phosphorus ai1d total phosphorus requirements apply to com ai1d soybeai1 meal-based diets.

h Conversions: l JU vitamin A= 0.30 mcg retinol or 0.344 mcg retinyl acetate; l JU vitamin D, or D,, =

0.025 mcg cholecalciferol; I JU vitan1in E = 0.67 mg of D-a-tocopherol or l mg of Dl.ra-tocopherol acetate.

'The niacin in corn, grain sorghum, wheat, and barley is unavailable. Similarly, the niacin in byproducts made from these cereal grains is poorly available unless the by-products have undergone fermentation or wet-milling process.

tl1ere is a trend in tile industry to fommlate
required for maintenance, muscle growtll;
diets on tile basis of NE. The NRC deterdevelopment of fetuses and suppo1ting mines energy requirements on the basis of
tissues in gestating sows, and milk produc

NE, and tilen DE and ME are estin1ated from tion in lactating sows. Of tl1e 22 amino acids, NE. Energy requirements of pigs are

12 are syntilesized by tile aninlal; tile otiler influenced by tileir weight ( which influ10 must be provided in tile diet for nom1al ences the maintenance requirement), tileir
growtll. The 10 dietary essential amino acids
genetic capacity for lean tissue growtll or
for swine are arginine, histidine, isoleucine,
milk production, and tile environmental
leucine, lysine, metllionine, phenylalanine,
temperature at which they are housed. The
threonine, tryptophan, and valine. Cystine
an10unt of feed consumed by growing pigs
and tyrosine can meet a portion of tile
allowed to consume feed ad lib is controlled
requirement for rnetllionine and phenylalaprincipally by tile energy content of the diet.

nine, respectively. The percentages of crude

If tl1e energy density of the diet is increased
protein listed in TABLES 48 and 49 provide tile by including supplemental fat, voluntary
required levels of lysine (tile first limiting
feed consumption decreases. Pigs fed such
amino acid) and sufficient amounts of tile
a diet generally will gain faster, and
other essential anlino acids in diets
efficiency of gain will improve, but carcass
consisting of com and soybean meal. The
fat may increase. If tile diet contains
dietary lysine requirement dwing tl1e early
excessive amounts of fiber (>5o/<r-7%)

starter phase is quite high (1. 7(J'lo) but
without commensurate increases in fat, tile
decreases to 1.53"/o and 1.40% during tl1e
rate-and especially the efficiency-of gain
middle and final starter phases, respectively.

a.re decreased.

The requirement continues to decrease
tilroughout tile growing-finishing stage from

Protein and Amino Acids: Amino acids,

1.12% during the early growing phase to
normally supplied by dietary protein, are

0. 71 % during late finishing.

2336

NUTRITION: PIGS

The amino acids of greatest practical
requirements as a percent of the lysine
importance in diet formulation (ie, those
requirement. Additionally, it is becornrng
most likely to be at deficient levels) are
more popular to fom1ulate swine diets on
lysine, tryptophan, threonine, and
the basis of standardized ( or true) or

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methionine. Com, the basic grain in most
apparent digestible amino acids. This
swine diets, is markedly deficient in lysine
method is particularly advantageous when
and tryptophan. The other principal grains
substantial an10unts of byproduct feeds are
for pigs (grain sorghum, barley, and wheat)

included in the diet.

are low in lysine and threonine. The first
limiting amino acid in soybean meal is
methionine, but sufficient amounts are

Minerals: These nutritional elements have
provided when soybean meal is combined
many important functions in the body. The
with cereal grains into a complete diet that
dietary requirements for the essential
meets the lysine requirement. An exception
macro- and trace minerals are listed in
might be in young pigs that consume diets

TABLES 48 and 49.

with high levels of soybean meal or diets

Calcium and Phosphorus: Although
containing dried blood products low in the
used primarily in skeletal growth, calcium
sulfur-amino acids.

and phosphorus play important metabolic

Milk protein is well balanced in essential
roles in the body and are essential for all
amino acids but usually is too expensive
stages of growth, gestation, and lactation.

to be used in swine diets, except for very

The NRC estimates requirements of 0.66%
young pigs. Dried whey, commonly used
calcium and 0.56% total phosphorus for
in starter diets, contains protein with an
growiI1g pigs of 25-50 kg body wt. The
excellent profile of an1iI10 acids, but the
requirements are higher for younger pigs
total protein content of whey is low. Diets
and lower for finishing pigs, but the ratios of
based on com and animal-protein byprodcalcium:phosphorus are approximately the ucts ( eg, meat meal, meat and bone meal)

same for all weight groups. These levels are
are mferior to com-soybean meal diets,
adequate for maxiinal growth ( rate and
but they can be unproved significantly by
efficiency of gain), but they do not allow for
adding tryptophan or supplements that
maxiinal bone mineralization. Generally,
are good sources of tryptophan. Animal
maxiinal bone ash and strength can be
proteins are also good sow-ces of minerals
achieved by including 0.1 % ---0.15% additional
and B-complex vitamins.

calcium and phosphorus in the diet.

Diets fonnulated for early weaned pigs

For gestating and lactating sows, calthat contain high levels of dried anin1al cium and phosphorus requirements are
plasma or dried blood cells may be deficient
influenced by stage of gestation (the first 90
in methionine. Howevet, high levels of
days versus the final 25 days of gestation),
methionine can depress growth, so
parity, milk production, and other factors
methionine should not be added indiscrimi

(see TABLE: 49). The higher requirements
nately to diets. Supplemental valine may be
during late gestation are attributed to rapid
of value in com-soybean meal <lie ts fed to
development of the fetuses. Swine
lactating sows, but it is still too expensive
producers may choose to feed slightly
to be considered as a dietary supplement.

higher levels to sows to ensure adequacy

Lysine is generally the first limiting amino
of these rnrnerals and to prevent posterior
acid in almost all practical diets, so if diets
paralysis in heavy milkmg sows. The
are fom1ulated on a lysine basis, the other
calcium and phosphorus requirements
amino acid requirements should be met.

listed are based on daily feed intakes of

However, caution must be exercised when a

4.7---5.7 lb (2.1---2.6 kg) during gestation and
crystalline lysine supplement is included in

13.1---14.6 lb (5.9---6.6 kg) during lactation
the diet to meet a portion of the pig's lysine

(these amounts include 5% wastage). If less
requirement. A general rule of thumb is that
feed is consumed per day, the percentages
crude protein content can be reduced by 2
of calcium and phosphorus may need to be
percentage points and the diet suppleacljusted upward.

mented with 0.15% lysine (0.19%

The ratio of total calcium:total phospholysine• HCJ). However, greater reductions rus should be kept between 1.25:1 and 1:1
in dietary protein coupled with additional
for maxiinal utilization of both minerals. A
lysine may result in deficiencies of
wide calciurn:phosphorus ratio reduces
tryptophan, threonine, and/or methionine
phosphorus absorption, especially if the
unless they are also supplemented.

diet is marginal in phosphorus. The ratio

It is quite common today to formulate
is less critical if the diet contains excess
swine diets based on the concept of "ideal"

phosphorus. When based on digestible
protein; ie, to express essential amino acid
phosphorus, the ideal ratio of calcium to

NUTRITION: PIGS

2337
digestible phosphoms is between 2: 1 and
has been used to prevent cannibalism, but

2.5:1.

controlled studies do not support this

Most of the phosphoms in cereal grains
practice.

and oilseed meals is in the fom1 of phytic

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acid (organically bound phosphoms) and

Iron and Copper: These minerals are
is poorly available to pigs, whereas the
involved in many enzyme systems. Both
phosphorus in protein sources of anin1al
are necessary for fo1mation ofHgb and,
origin, such as meat meal, meat and bone
therefore, for prevention of nub.itional
meal, and fish meal, is in inorganic form and
anemia. Because the amowit of iron in milk
is highly available to pigs. Even in cereal
is very low, suckling pigs should recei".e .

drains, availability of phosphorus vanes.

supplemental iron, preferably by IM ll\]ect10n

For exan1ple, the phosphoms in com is only
of 100--200 mg in the fonn of iron dextran,

10%-2()0A, available, whereas the phosphorus iron dexb.in, or gleptoferron during the first in wheat is 5()0A, available. Therefore, swine

3 days of life (see also IRON TOXIC'ITY IN NEWBORN
diets should be fom1ulated on an "available
r1cs, p 3077). Giving oral or il"(jectable iron phosphorus" basis to ensure that the
and copper to sows will not increase piglet
phosphorus requirement is met. The NRC
stores at bi.Ith nor will it increase the i.I·on in
publication expresses the digestible
colostrw11 and milk sufficiently to prevent
phosphorus requirements as apparent total
anemia i11 neonatal pigs. High levels of i.I·on in
tract digestible (A'ITD) and standardized
lactation feed results in i.I·on-rich sow feces
total tract digestible (S'ITD) phosphorus.

that pigs can obtain from the pen. Iron can

ATTD phosphorus represents the phosphoalso be supplied by mixing fernc arrunornwn ms digested, and S'ITD phosphorus is the
citrate with water in a piglet waterer or by
digestible phosphorus corrected for
frequently placing a mixture of iron sulfate
endogenous phosphorus excret10ns.

and a canier, such as ground com, on the

Phosphorus supplements such as
floor of the farrowing stall.

monocalcium or dicalcium phosphate,

The copper requi.I·ement for growing pigs
defluorinated phosphate, and steamed
is low (3--6 ppm) but higher for sows. The
bone meal are excellent sources of highly
estimated copper requirement of 5 ppm for
available phosphoms. These supplements
sows in the previous NRC publication was
also are good sources of calciwn. Ground
increased to 10 ppm for gestation and 20
limestone also is an excellent source of
ppm for lactation in the 2012 edition.

calciwn.

Copper at phannaceutical levels in the

Phosphorus is considered a potential
diet (100--250 mg/kg) is an effective growth
environmental pollutant, so many swine
stin1ulant for weanling and growing pigs.

producers feed diets with less excess

The action of copper at high levels appears
phosphorus than in the past to reduce
to be independent of, and additive to, the
phosphorus excretion. Supplemental
growth-stilnulating effect of antibiotics.·
phytase, an enzyme that degrades some of

Copper sulfate at high levels in the diet
the phytic acid in feedstuffs, is commonly
results in very dark-colored feces. Also, high added to diets to further reduce phosphorus
copper diets result i.11 marked increases in
excretion. The general recommendation is
the copper content of excreted manure.

that dietary calciwn and phosphorus can

Iodine: The thyroid gland uses iodine
both be reduced by 0.05%--0.10/owhen �500
to produce thyroxine, which affects cell
tmits of phytase per kg of diet are included.

activity and metabolic rate. The iodine
requi.I·ement of all classes of pigs is 0.14

Sodium and Chloride: These minerals
are provided by common salt, which
mg/kg of diet. Stabilized iodized salt concontains 4()0A, sodium and 60% chloride.

tains 0.007% iodine; when fed at sufficient

The recommended level of salt is 0.25% in
levels to meet tl1e salt requi.I·ement, it will
growing and finishing diets, 0.5--0. 75% in
also meet the iodine needs of pigs.

starter diets, and 0.5% in sow diets. These

Manganese: A1tl10ugh essential for
levels should provide ample sodium and
normal reproduction and growth, the
chloride to meet the animal's requirements.

quantitative requirement for manganese is

Animal fish and milk byproducts can
not well defined. Manganese at 2--4 mg/kg in
contrib�te s�me of the sodiwi1 and chloride
the diet is adequate for growth, but a higher
requirement.

level (25 mg/kg) is needed by sows during
gestation and lactation.

Potassium, Magnesium, and Sulfur:

Practical diets contain an1ple amowits of

Zinc: Zinc is an important trace mineral
these minerals from the grain and protein
with many biologic functions. Grain-soysources and supplemental sources a.re not bean meal diets must contain supplemental
needed.' Magnesium oxide supplementation
zinc to prevent parakeratosis (seep 975).

2338

NUTRITION: PIGS

Higher levels of zinc may be needed when
pigs, 1 mg of chemically determined
dietary calcium is excessive, especially in
carotene in com or a com-soybean mixture
diets typically high in phytic acid such as
is equal to 267 JU of vitamin A
com-soybean meal diets. Phannacologic

The use of stabilized vitamin A is
levels of zinc (1,500-3,000 mg/kg) as zinc
common in manufactured feeds and

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oxide have consistently been found to
in vitamin supplements or premixes.

increase pig performance dwi.ng the

Concentrates containing natural vitamin A
postweaning period. In some instances,

(fish oils most often) may be used to fortify
high levels of zinc oxide have been reported
diets. Green forage, dehydrated alfalfa meal,
to reduce the incidence and severity of
and high-quality legwne hays are also good
postweaning diarrhea. Responses to zinc
sources of (3-carotene. Both natw·al vitamin
oxide and antibiotics seem to be additive in

A and (3-carotene are easily destroyed by air,
nature, much like the responses to high
light, high temperatw-es, rancid fats, organic
copper and antibiotics; however, there is no
acids, and certain mineral elements. For
advantage to including high copper and high these reasons, natural feedstuffs probably zinc in the same diet. Similar to copper, high
should not be entirely relied on as sources
levels of dietary zinc cause increased zinc
of vitamin A, especially because synthetic
content in the excreted manure. For sows,
vitamin A is very inexpensive. An internathe estimated zinc requirement was tional unit of vitan1in A is equivalent to 0.30
increased from 50 ppm in the previous NRC
mcg of retinol or 0.344 mcg of retinyl
publication to 100 ppm in the 2012 edition.

acetate.

Selenium: The seleniwn content of soils

Vitamin D: This antirachitic, fat-soluble
and, ultimately, crops is quite variable. In
vitamin is necessary for proper bone growtl1
the USA, areas west of the Mississippi River
and ossification. Vitan1in D occurs as the
generally contain higher amounts of
precursor sterols, ergocalciferol (vitamin
seleniwn, whereas areas east of the river

D2) and cholecalciferol (vitamin D3), which
tend to yield crops deficient in selenium.

are conve1ted to active vitamin D by UV

Under most practical conditions, 0.2-0.3 mg
radiation. Although pigs can use vitamin D2
of added seleniwn/kg of diet should meet

(irradiated plant sterol) or vitamin D3
the requirements. This trace mineral is

(irradiated animal sterol), they seem to
regulated by the FDA, and the maximal
preferentially use D3. Some of the vitanlin D
amount of seleniwn that can be added to
requirement can be met by exposing pigs to
swine diets is 0.3 mg/kg.

direct sunlight for a short period each day.

Chromium: This trace mineral, which is a

Sources of vitanlin D include in-adiated
cofactor with insulin, is required by pigs, but yeast, sun-cured hays, activated plant or the quantitative requirement has not been
animal sterols, fish oils, and vitanlin
established. In some studies, chromiwn at
premixes. For this vitan1in, 1 JU is equivaa supplemental level of 200 mcg/kg (ppb) lent to 0.025 mg of cholecalciferol. The
improved carcass leanness in finishing pigs
estimated vitan1in D requirement of 200
and improved reproductive performance in

JU/kg for gestating and lactating sows was
gestating sows, but these effects have been
increased to 800 JU/kg in the 2012 NRC
somewhat inconsistent.

publication.

Cobalt: Cobalt is present in the vitamin

Vitamin E: This fat-soluble vitanlin serves

B,
as a natural antioxidant in feedstuffs. There

2 molecule and has no benefit when added
to swine diets in the elemental form.

are eight naturally occw-ring forms of
vitamin E, but o-cx-tocopherol has the

Vitamins: These micro.nutrients serve
greatest biologic activity. Vitamin Eis
many important roles in the body. The
required by pigs of all ages and is closely
estin1ated requirements for tl1e essential
in ten-elated with seleniwn. The vitan1i..n E
vitamins are given in
requirement is 11-16 JU/kg of diet for

TABLES 48 and 49.

growing pigs and 44 JU/kg for sows. Some

Vitamin A: This fat-soluble vitamin is
nutritionists recorrunend higher dietary
essential for vision, reproduction, growth
levels for sows in the eastern com belt of
and maintenance of epithelial tissue, and
the USA, where seleniwn levels in feeds are
mucous secretions. Vitamin A is found as
likely to be low. Vitamin E supplementation
carotenoid precursors in green plant
can only partially obviate a seleniwn
mate1ial and yellow com. (3-Carotene is the
deficiency.

most active form of the various carotenes.

Green forage, legwne hays and meals,

Unfortunately, only about one-fourth of the
cereal grains, and especially the germ of
total carotene in yellow com is in the fonn
cereal grains contain appreciable amounts
of (3-carotene. The NRC suggests that for
of vitamin E. Activity of vitamin Eis

NUTRITION: PIGS

2339
reduced in feedstuffs when exposed to
vitamin, but animal products are good
heat, high-moisture conditions, rancid fat,
sources. Although some intestinal synthesis
organic acids, and high levels of certain
of tl1is vitamin occurs, vitamin B,2 is
trace elements. One IU of vitamin E activity
generally included in vitamin premixes for
is equivalent to 0.67 mg of o-cx-tocopherol or
swine.

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1 mg of DL-cx-tocopherol acetate.

Thiamine: This vitamin has important

Vitamin K: This fat-soluble vitamin is
roles in the body, but it is of little practical
necessary to maintain normal blood
significance for swine because grains and
clotting. The requirement for vitamin K is
other feed ingredients supply ample
low, 0.5 mg/kg of diet. Bacterial synthesis
amounts to meet the requirement in pigs.

of the vitamin and subsequent absorption,
directly or by coprophagy, generally will

Vitamin 86: A group of compow1ds called
meet the requirement for pigs. Although
the pyridoxines have vitamin B6 activity and
rare, hemorrhages have been reported
are impmtant in an1ino acid metabolism.

in newborn as well as growing pigs, so

They are present in plentiful quantities in
supplemental vitamin K is recommended
the natural feed ingredients usually fed to
at 2 mg/kg of diet as a preventive measure.

pigs. The requirement for vitamin B0 in

Generally, hemonhaging problems can be
young pigs (5-25 kg) was increased by 3-4
traced back to the feeding of diets with
fold in the 2012 NRC publication compared
moldy grain or other ingredients that
witl1 the previous edition.

contain molds.

Choline: Choline is essential for the

Riboflavin: This water-soluble vitamin
nom1al functioning of all tissues. Pigs can
is a constituent of two important enzyme
synthesize some choline from methionine
systems involved with carbohydrate,
in the diet. Sufficient choline is found in the
protein, and fat metabolism. Swine diets are
natural dietary ingredients to meet the
normally deficient in this vitamin, and the
requirements of growing pigs. However,
crystalline fom1 is included in premixes.

in some studies, choline supplemented at

Natural sources include green forage, milk

440-800 mg/kg of diet increased litter size in
byproducts, brewer's yeast, legwne meals,
gilts and sows. Natmal sources of choline
and some fermentation and distillery
include fish solubles, fish meal, soybean
by-products.

meal, liver meal, brewer's yeast, and meat
meal. Choline chloride, which is 75%

Niacin (Nicotinic acid): Niacin is a
choline, is the common fonn of supplemencomponent of coenzyn1es involved with tal choline used in feeds. If choline is added
metabolism of carbohydrates, fats, and
as a supplement to sow diets, it should not
protein. Pigs can conve1t excess tryptophan
be combined with other vitamins in a
to niacin, but tl1e conversion is inefficient.

premix, especially if trace minerals are

The niacin in most cereal grains is
present, because choline chloride is
completely unavailable to pigs. Swine diets
hygroscopic and destroys some of the
are normally deficient in tl1is vitamin, and
activity of vitamin A and other less stable
the crystalline fonn is included in premixes.

vitamins.

Natural sources of niacin include fish and
anin1al byproducts, brewer's yeast, and

Biotin: This vitamin is present in a highly
distiller's solubles. Based on recent
available form in com and soybean meal,
research, the NRC increased the niacin
but the biotin in grain sorghwn, oats, barley,
requirement to 30 ppm during all phases
and wheat is less available to pigs. There
of growth.

is evidence that when these latter cereal

Pantothenic Acid: This vitamin is a
grains are fed to swine, especially breeding
component or coenzyme A, an important
animals, biotin may be marginal or deficient.

enzyme in energy metabolism. Swine

Reproductive perfom1ance in sows has
diets are deficient in this vitamin, and the
been found to improve with biotin
crystalline salt, D-calciwn pantothenate,
additions. Although not as clear, there is
is included in vitamin premixes. Natural
evidence that reproductive perfonnance
sources of pantothenic acid include green
also is improved with addition of biotin to
forage, legun1e meals, milk products,
com-soybean meal diets. ln some instances,
brewer's yeast, fish solubles, and certain
biotin supplementation decreased footpad
other byproducts.

lesions in adult pigs. For insurance, biotin
supplementation is recommended,

Vitamin 812: This vitamin, also called
especially for sow diets. Raw eggs should
cyanocobalamin, contains cobalt and has
not be fed to pigs because egg white
nwnerous important metabolic functions.

contains avidin, a protein that complexes

Feedstuffs of plant origin are devoid of this
with biotin and renders it unavailable.

2340

NUTRITION PIGS

Folacin: This group of compounds has
intake. These intake levels can be used as a
folic acid activity. Sufficient folacin is
guide to project total feed requirements or
present in natural feedstuffs to meet the
presc1ibe in-feed medication.

requirement for growth, but some studies

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have shown a benefit in litter size when

Gestating Gilts and Sows: For
folic acid was added to sow diets.

gestating gilts and sows, the NRC estin1ates
that a feeding level of approximately 4. 7--4.9

Ascorbic Acid (Vitamin C): Pigs are
thought to synthesize this vitamin at a rapid
lb/day (2.1-2.2 kg/day) during the first 90
enough rate to meet their needs under
days of gestation and 5.6---5. 7 lb/day (2.5-2.6
nonnal conditions. However, a few studies
kg/day) for the final 25 days to farrowing of
have shown benefits in perfom1ance of
a corn-soybean meal diet (3,300 kcal ME/kg)

early-weaned pigs under stressful condiprovides sufficient energy for maintenance; tions when this vitamin was added to the
some lean and fat tissue accretion
diet.

(particularly in gilts); and the energy needs
of the developing fetuses, placenta, and

Fatty Acids: Linoleic acid, arachidonic
other supporting tissues (see TABLE 49).

acid, and probably other long-chain,

Mature sows do not need more energy than
polyunsaturated fatty acids are required by
that required for maintenance and some
pigs. However, the longer chain fatty acids
increase in body weight. If gestation diets
can be synthesized in vivo from linoleic
contain oats, alfalfa meal, or other energy
acid, so linoleic acid is considered the
diluents, higher feeding levels will be
dietary essential fatty acid. The NRC
needed to meet the saw's daily energy
estimates the linoleic acid requirement at
requirement. Attempts to limit voluntary

0.1 % for growing and breeding swine. The
feed intake during gestation by allowing ad
requirement is generally met by the fat
lib access to extremely high-fiber diets has
present in natural dietary ingredients. The
not been successful; invariably, excess
oil in com is a rich source of linoleic acid.

weight gain occurs.

Producers should adjust the feeding level
of pregnant gilts and sows to keep them in

FEEDING LEVELS AND
good condition. Excess body condition at

PRACTICES
the end of gestation is often associated with
reduced feed intake du.ring lactation and

Performance of weanling, growing, and
sometimes results in reduced litter size,
finishing pigs; gestating sows; and lactating
greater incidence of dystocia, more pig
sows and their nursing pigs is related to
overlay, and a greater incidence of
both the quality of the diet and the amount
postpartmn dysgalactia syndrome (see
consumed on a daily basis. Knowing the
p 1373). Poor body condition results in a
an1ow1t of feed anin1als consume is
greater incidence of shoulder sores in sows,
important in the overall feeding managelower birth weights, and thin sows at ment process. Weanling, growing, and
weaning wiili delayed return to postweanfinishing pigs are ordinarily allawed to ing estrus ( or even anestrus ). Litter size at
consmne feed ad lib, and the an10unt
the subsequent farrowing can also be
consumed is affected by the energy density
negatively affected if sows are in poor
of the diet, environmental temperattffe,
condition at breeding.

gender, and feed quality ( eg, absence of

The amino acid requirements of first-litter
molds), as well as a host of other managegilts are higher than those for sows. Both ment factors such as feeder design,
gilts and sows require higher levels of
crowding, etc.

dietary amino acids du.ring the latter stage
of gestation ilian in the initial 90 days of

Growing-Finishing Pigs: Daily feed
gestation. (See TABLE 49.)

intakes of va.rious weight classes of
growing-finishing pigs fed a diet containing

Lactating Gilts and Sows: The NRC

3,300 kcal of ME/kg (typical of a corn-soyestimates that lactating gilts and sows bean meal diet) as estimated by the NRC
nursing 11-11.5 pigs that gain 240 g/day
growth model are shown in TABLE 48. These
during a 21-day lactation require 13.1-14.6
intake levels represent an average for
lb (6.0-6.6 kg) of feed (3,300 kcal of ME/kg)

barrows and gilts. Feed intakes will be
daily to meet their energy requirements (see
slightly higher for barrows and slightly less

TABLE 49). The amow1t of energy and feed
for gilts weighing 50-135 kg. Preventing
depends on nmnber of pigs nursed, weight
overcrowding and cooling pigs with
gain of the pigs (both of these factors
automatic water sprayers during hot
influence milk production), and weight loss
weather help to alleviate reduced feed
of the sow. High-energy diets should be fed

NUTRITION: PIGS

2341
ad lib to sows during lactation, or sows
will result in a lysine deficiency. Wheat can
should be hand-fed all they will consume
constitute all of the grain in a swine diet.

three times daily. Proper temperature

The two main types of wheat grown in the
regulation in the farrowing room and the

USA, hard red winter and soft red winter,

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use of drip-coolers during hot weather help
have equivalent nutritional value.

to alleviate low feed intake.

Barley has -85o/<>-90% of the feeding

If feed intake is too low, sows will lose
value of corn, even though it usually
excessive weight during lactation (see
contains 2o/<>-3% more protein. Scabby
p 2340). If this is a problem, including 3o/<>-6% barley should not be fed to pigs.

fat in the lactation diet or top-dressing the

Oats have a relatively low energy content
lactation feed with additional fat should be
and, therefore, should not account for
considered. If problems persist, more

>2001<>-25% of the cereal grain in the diet.

energy during the final 3-6 wk of pregnancy

Generally, when oats are included in the
may be helpful.

diet, the rate and efficiency of gain should

Diets high in protein and an1ino acids
be expected to decline. Rolled oats groats
should be fed to prolific sows nursing large
are sometimes used in starter diets because
litters to maximize milk production and to
of their excellent palatability.

prevent excessive weight loss of the sow.

Cereal grains should be ground or rolled

Such sows may require diets containing
to maximize their feeding value. Com and
l 6o/<>-18% or more crnde protein ( minimtm1
grain sorghum should be reduced to a
of 0.9% lysine). If energy intake is sufficient, mediwn-fine particle size (550-600
high-protein lactation diets will minimize or
microns). Wheat should be ground more
even eliminate weight loss in sows during
coarsely (650-700 microns) to prevent
lactation.

pasting. Fine grinding improves feed
conversion, but excessive reduction in

Major Feed In
paiticle size may lead to an increased
gredients
incidence of gastric ulcers. Pelleting of diets

A fundamental principle of the economics
may result in a small improvement in gain
of pork production is to feed the most
and especially feed efficiency. In general,
economical cereal grains and to correct the
the benefit is greatest with pelleted diets
deficiencies by supplementation with
that contain high levels of fiber, such as
good-quality protein sources, minerals, and
barley-based diets. Cereal grains should
vitamins. Dependable mineral and vitan1in
be as free as possible from mycotoxins.

premixes or complete manufactured

Aflatoxins, vomitoxin, zearalenone,
supplements are commercially available.

fun10nisins, and other mycotoxins can

Fortified com-soybean meal diets are very
reduce animal perfonnance, depending on
popular in pig operations, but other cereals
level in the feed, and can especially cause
and protein sources can be used.

reproductive problems in breeding animals.

Corn (maize) is by far the most widely

Soybean meal accounts for >900A, of the
used grain for feeding pigs in the USA. It is
supplemental protein fed to pigs in the USA.

very palatable and high in energy but

It is very palatable and has an excellent
relatively low in crnde protein. In addition,
amino acid profile that complements the
com is deficient in lysine, tryptophan,
amino acid pattern in cereal grains. Ground,
threonine, and several other essential amino full-fat soybeans can also be fed to swine acids, as well as vitamins and minerals.

but only after they are heated (by extrusion

Grain sorghum is a major energy source
or roasting) to inactivate the trypsin
for pigs in western and southwestern USA.

inhibitors and other heat-labile antinutri

The protein content is variable depending
tional factors.

on factors such as variety, whether the crop

Canola meal also is an excellent protein
was grown on irrigated or dry land, amount
source. Low-gossypol cottonseed meal
of fertilizer used, and other environmental

( <100 ppm free gossypol), peanut meal,
factors. In general, grain sorghum can be
sunflower meal, and other oilseed-based
substituted for com on an equal-weight
meals can be used in swine feed but
basis, but because the ME value is slightly
generally not as the sole source of
lower than that of corn, a poorer feed
supplemental protein because of the lower
conversion should be expected.

lysine content of their protein. Animal

Wheat has about the same energy
protein sources such as meat meal, meat
content as corn and contains 2o/<>-3% more
and bone meal, or fish meal can supply a
protein and 0.05o/<>-0. l % more lysine than
portion of the supplemental protein in
corn. Wheat can be substituted for corn on
swine diets.

either an equal-weight basis or on a lysine

Distillers dried grains with solubles
basis, but not on a crnde protein basis or it

(D DGS) is a byproduct that has received a

2342

NUTRITION PIGS
lot of attention in recent years because of
management and sanitation. Nutritional
the increased number of ethanol plants that
anemia should be prevented by giving an
use com to produce ethanol for fuel. This
iron i.ajection before 3 days of age or by
byproduct is an excellent and generally
other means discussed previously. Pigs from
economical feed ingredient for swine.

large litters may be transferred to sows with

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Although DDGS has essentially no starch
smaller litters after they receive colostrunl;
and considerably more fiber than com, it is
however, the transfer should be done within
considerably higher in fat ( com oil); hence,
the first 24 hr after birth. A palatable pig
the ME content of DDGS containing 9%---12% starter diet should be provided beginning at fat is sin1ilar to that of com. Recently, some

2---3 wk if pigs are weaned later than 3 wk of
ethanol plants extract a portion of the oil
age. (See also 1-IEAJ:rH-MANAGEMENT INTERACTION: from the solubles before adding the solubles PIGS, p 2160, and MANAGEMENT OF REPRODUCTION: back to the dried grains. This results in a

PIGS, p 2201.)

"low-fat" DDGS, generally 5o/o-9% fat, which has slightly less ME than conventional

Feeding Management of Weanling

DDGS. Further removal of fat, called

"de-oiled DDGS" ( <5%fat) has substantially Pigs
less ME than either of the other types of

Pigs weaned at an early age (3---4 wk)

D DGS, so it has a lower feeding value.

perfom1 best if fed a complex starter diet for

DDGS is also higher in protein than com,

1---2 wk after weaning. Typically, the starter
but the quality of protein (ie, balance of
diet contains dried whey and/or lactose,
amino acids), like com protein, is poor.

dried blood products, and a high level of

A considerable an10unt of research has
lysine. Some producers use a medicated
been done with DDGS in recent years. Diets
early weaning program or segregated early
containing 200/o-25% DDGS are well utilized
weaning progran1 to produce healthier pigs.

by pigs, but when high levels ( >300Ai) of

This entails weaning at 10---16 days of age

DDGS are fed in finishing diets, body fat
and requires excellent nutritional manageof pigs becomes more unsaturated, as ment. Such diets should contain even higher
evidenced by higher iodine values. This
levels of lysine as well as high levels of
results in softer, more flexible bellies that
lactose (as the sugar or from dried whey)

are more difficult to process into bacon
and 3o/o-7%dried animal plasma. A gradual
slices. To overcome this problem, producers transition should eventually be made to should consider either removing DDGS
less expensive starter diets and then to
from the late finishing diet or reducing the
com-soybean meal diets.

level of DDGS to l()OA, during the final 3---4 wk

The nutritional needs of growing-finishing
of the finishing pe1iod.

pigs are best met by a full-feeding progran1.

Limit-feeding reduces the rate and
efficiency of gain but may improve carcass

Feeding Management of Sows and
quality of finishing pigs. Proper design and

Litters
adjustment of self-feeders is necessary to

Gestation diets adequate in all nutrien�
prevent feed wastage or restricted growth.

should be fed to sows to produce healthy,
vigorous pigs. Sows should be fed so that

Growth Stimulants
they are in good body condition at farrow

For many years, antibiotics and other
ing-not too fat or too thin. Thin sows tend
chemotherapeutic agents have commonly
to farrow smaller pigs that have a poorer
been added to swine diets to promote
chance of survival than larger, more vigorous growth and feed efficiency, reduce mortality pigs. After farrowing, the sow should be
and morbidity, and improve health. The
returned to full feed as soon as possible.

greatest response to these growth enhancing

Constipation in sows is generally not a
agents is in young pigs, with lesser responses
problem if the sow is eating well. Wheat bran
as pigs progress in age and weight. The
or dried beet pulp can be included in the
levels of antibiotics fed and drug withdrawal
farrowing diet at 5o/o-100A, if constipation is
requirements should be in accordance with
a problem, or chemical laxatives such as
manufacturers' recommendations and legal
potassium chloride or magnesium sulfate
restrictions. (See also GROWTH PROMOTANTS AND
can be included in tl1e diet at 0.75o/o-1%.

PRODUCTION ENHANCERS, p 2758.)

Newly farrowed pigs should be checked

The antibiotics approved as feed additives
to ensure that each has nursed. lf necessary,
for swine include bacitracin methylene
milk flow may be stimulated by giving
disalicylate, bacitracin zinc, bamberrnycins,
oxytocin. lf the sow is slow in coming into
chlortetracycline, lincomycin, neomycin,
milk, weak pigs may benefit from receiving
oxytetracycline, penicillin, tiamulin, tylosin,
artificial milk, but success depends on good
and virginiamycin. Chemotherapeutic

NUTRITION: PIGS

2343
agents include carbadox, roxarsone,
approved for use in pigs in the USA. These
sulfamethazine, and sulfathiazole. Several
agents affect nutrient requirements, in
of these are approved only in combination
particular by increasing the dietary
with certain other additives. Apramycin also
requirements for amino acids.

is approved for use as a water medication.

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Also, pharmaceutical levels of zinc

(1,500--3,000 ppm) as zinc oxide, or copper

NUTRITIONAL DISEASES

(100-250 ppm) as copper sulfate or tribasic
copper chloride are effective growth

Diagnosis of nutritional deficiencies by
stin1ulants in young pigs.

observation is difficult. Quite often, the

However, FDA action has changed how
clinical signs are the result of a complex of
antibiotics can be used. According to Final
mismanagement and infectious diseases,

Guidance 213 and the Veterinary Feed
including parasitism, as well as malnutri

Directive (VFD) rule, antimicrobials
tion. For most nutritional deficiencies, the
medically impo1tant in human medicine
signs are not specific, eg, poor appetite,

(this includes all of the antimicrobials
reduced growth, and unthriftiness.

approved for swine except carbadox,

Deficiency of a single nutrient may bring
bacitracin, and barnbem1ycins) previously
about inanition, and the subsequent
used at subtherapeutic levels for production
starvation may cause multiple deficiencies.

purposes (improved growth and efficiency)

Then, too, a nutritional deficiency may exist
are no longer allowed for that purpose.

without the appearance of definite signs. In

Instead, they are allowed only for disease
the field, the deficiency may be only slight
prevention and only under veterinary
or borderline, which makes diagnosis
supe1vision and oversight. This regulation
difficult.

applies to antibiotics used in feed or water.

Diagnosis of a deficiency by observing

Companies that produce those antimicrothe response to nutritional therapy is not bials are asked to voluntatily remove the
always clear, paiticularly for longtenn
production improvement clain1 on their
deficiencies, the lesions of which may be
product labels. These products will no
irreversible. A nutritional deficiency should
longer be available to producers on an
be diagnosed positively only after obser0

"over-the-counter" basis; they will only
vance of several of the expected clinical
be available on a VFD basis.

signs and a careful review of the dietary,

Microbials that are directly fed ( once
disease, and management history of the
referred to as probiotics), such as live
aninlals.

cultures of Lactobacillus acidophilus,

Stre'J)lococcusfaecium, and Saccharo

Protein Deficiency: Protein deficiency,
myces cerevi.siae, have been evaluated as
which may result from suboptimal feed
possible substitutes for antibiotics, but
intake or a deficiency of one or more of the
controlled studies have not shown
essential anlino acids, causes reduced gains,
consistent, beneficial responses from their
poor feed conversion, and fatter carcasses
inclusion. In some instances, inclusion of
in growing and finishing pigs. In lactating
specific sugars ( marmanoligosaccharides,
sows, milk production is reduced, excess
fructooligosaccharides [ also called
weight loss occurs, and sows may fail to
prebioticsl) have shown promise as
exhibit postweaning estrus or have delayed
possible alternatives to antibiotics for
return to estrus. For optimal use of protein,
young pigs, but growth responses are less
all essential ainino acids must be liberated
consistent and of lower magnitude than
during digestion at rates conunensurate
from the inclusion of antibiotics. The
with needs. Therefore, protein supplements
direct-fed microbials and oligosaccharides
should not be handfed at infrequent
are thought to encourage growth of
intervals but should be mixed with the grain
desirable microorganisms in the GI tract,
or be available at all times with grain on a
such as lactobacilli species and bifidobactefree-choice basis.

ria that partially displace some of the less

No evidence has been presented to
desirable microorganisms, including some
support the theo1y of"protein poisoning" in pathogenic microbes.

pigs. Diets containing as much as 35o/<>-500A, Certain "repartitioning agents" have been
protein were found to be laxative and less
tested with finishing swine and found to be
efficiently used, but no toxic effects were
very effective in improving growth rate,
noted.

feed <.:onversion, and carcass learmess.

Examples are 13-agonists, such as ractopa

Fat Deficiency: Certain long-chain
mine and porcine somatotropin. As of 2015,
polyunsaturated fatty acids are essential for
ractopanline is the only such agent
swine. Linoleic acid is essential in the diet

2344

NUTRITION: PIGS
and is used to produce longer-chain fatty
than the recommended an1ount of calcium.

acids that are probably also essential. A

The exact mode of action of zinc in the
linoleic acid deficiency induces hair loss,
prevention of parakeratosis is not known.

scaly dennatitis, skin necrosis on the neck

Deficiencies of selenium and/or vitamin

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and shoulders, and an unthrifty appearance

E can cause sudden death of young, rapidly
in growing pigs. Conventional swine diets
growing pigs (seep 1174). In addition,
generally contain adequate fat from the
selenium/vitamin E deficiency in nursing
natural ingredients to furnish ample
pigs makes them more susceptible to iron
amounts of essential fatty acids.

toxicosis from iron injections (seep 3077.) Mineral Deficiency: Deficiencies of

Vitamin Deficiency: Most commercial
calcium or phosphorus result in rickets
diets are fortified with vitamins, and vitamin

( see p 1051) in growing pigs and osteomalapremixes are readily available for fa.m1-cia (seep 1052) in mature pigs. Signs include mi.xed feeds, so deficiencies are less defmmity and bending 0f long bones and
common than they were years ago.

lameness in young pigs, and fractures and

Deficiency of vita.min A results in
posterior paralysis ( a result of fractures in
disturbances of the eyes and the epithelial
the lwnbar region) in older pigs. Sows that
tissues of the respiratory, reproductive,
produce high levels of milk and nurse large
nervous, winary, and digestive systems.

litters are particularly susceptible to

Reproduction is impaired in sows, and
posterior paralysis toward the end of
they may fa.tTow blind, eyeless, weak, or
lactation or after weaning if dietary calciun1
malformed pigs. Herniation of the spinal
or phosphorus is deficient. These signs can
cord in fetal pigs is reported as a unique sign
also result from a deficiency of vita.min D,
of vita.tnin A deficiency in pregnant sows.

but phosphorus deficiency is the most

Growing pigs deficient in vitamin A show
common cause.

incoordination and develop night blindness

Pigs fed diets low in salt (NaCl) grow
ru1d respiratory disorders. Vita.tnin A
poorly and inefficiently, largely because of a
deficiency is rru·e because of the ability of
marked reduction in feed intake. Although
the liver to store this vitamin.

not specific for salt deficiency, poor hair and

Signs of vita.min D deficiency include
skin condition may also develop. There
rickets, stiffness, weak a.t1d bent bones,
have been reports of salt-deficient pigs
and posterior pru·alysis. These signs are
attempting to consume urine of other pigs.

indistinguishable from those of a calciwn

Sows fed diets deficient in iodine produce or phosphorus deficiency (see above).

hairless pigs that are weak or stillborn. With

Vita.min E deficiency can result in poor
a borderline deficiency, the newborn pigs
reproduction and impaired immune system.

may be weak only at birth,-but their thyroids

Many of the signs of vitan1in E deficiency
are enlarged and have histologic abnormaliare similar to those of seleniwn deficiency ties. (See also NON-NEOPLASTIC P,NLARGEMENT OF

(see above).

THE THYROID GLAND, p 558.) Some feedstuffs

Pigs deficient in vitamin K have

(including soybeans and soybeao meal)

prolonged blood clotting time and may die
contain goitrogens that may cause marginal
from hemorrhages. Certain components in
goiter if iodine is not included in the diet.

moldy feed can interfere with vita.tnin K

Iodized salt at recommended levels prevents
synthesis. Also, excessive levels of dieta.t-y
this deficiency.

calcium interfere with vitan1in K activity,

Deficiencies of iron and copper reduce causing these signs.

the rate of Hgb forn1ation and produce

In pigs deficient in riboflavin, reproductypical nutritional anemia. Signs of tion is impaired; postpubertal gilts fail to
nutritional anemia in suckling pigs include
cycle but show no other clinical signs.

low Hgb and RBC count, pale mucous

Deficient sows are ru10rectic and fat-row
membranes, enlarged heart, skin edema
dead pigs 4-16 days prematurely. The
about the neck and shoulders, listlessness,
stillborn pigs have very little hair, often are
and spastic breathing (thwnps). Iron
partially resorbed, and may have enlarged
deficiency is more common than copper
forelegs. Growing pigs fed diets low in
deficiency and is most conunon in nursing
riboflavin gain weight slowly and have a
pigs that do not receive an iron ir\jection or
poor appetite, a rough coat, an exudate on
oral iron early in life.

the skin, and possibly cataracts.

A deficiency of zinc results in parakerato

Pigs deficient in niacin have inflammasis (seep 975) in growing pigs, particularly tory lesions of the digestive tract and exhibit
when fed diets high in phytic acid ( or
diarrhea, weight loss, rough skin and coat,
phyta.te, the primary form of phosphorus in
ru1d dermatitis on the ears. Intestinal
cereal grains and oilseed meals) and more
conditions can be due to niacin deficiency

NUTRITION: SHEEP

2345
or bacterial infection. Deficient pigs
damage. Sows deficient in choline have
respond readily to niacin therapy and,
reduced litter size and may give birth to
although not a cme for infectious enteritis,
spradclle-legged pigs.

adequate dietary niacin probably allows the

Biotin deficiency includes excessive
pig to maintain its resistance to bacte1ial
hair loss, skin ulcerations and dermatitis,

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invasion.

exudates around the eyes, inflan1mation

Growing pigs and pregnant sows develop
of the mucous membranes of the mouth,
a typical "goose-stepping" gait, ataxia, and a transverse cracking of the hooves, and
noninfectious bloody diarrhea when maincracking or bleeding of the footpads.

tained on diets deficient in pantothenic

Neonatal pigs fed synthetic diets low in
acid. When the deficiency becomes severe,
vitamin B show hyperinitability, voice
anorexia develops.

12
failtu-e, and pain and incoorclination in the

Pigs with a choline deficiency exhibit
hindquaiters. Histologic examination of the
incoordination and an abnom1al shoulder
bone mai-row reveals ai1 impaired hematoconfonnation. At necropsy, they may have poietic system. Fatty livers ai·e also noted
fatty livers and usually show kidney
at necropsy.

NUTRITION: SHEEP

The economical and efficient production of
recommendations are -1 gal. (3.8 L) of
sheep for meat, wool, show ancl/or pets is
water/day for ewes on dry feed in winter, 1 \,1,
contingent on proper feeding, husbandry
gal.I day for ewes nursing lainbs, and \,1, gal./
practices, and health care. All of these are
day for finishing lainbs. In many range
influenced by dietary intake. Maintenance
areas, water is the limiting nutrient; even
of breeding animals, a high percentage of
when present, it may be w1potable because
the lainb crop weaned, growth of lan1bs,
of filth or high mineral content. For best
optimal weaning weights, and a heavy
production, all sheep should have their
fleece weight and fleece quality are
water availability monitored daily during all
in1pmtant to efficiency. The nutritional
weather conditions. However, the cost of
requirements for maintenance, reproducsupplying water often makes it economical tion, growth, finishing, and wool production
to water range sheep every other day. When
are complex because sheep are maintained
soft snow is available, range sheep do not·
under a wide variety of environmental
need additional water except when dry
conditions; however, attempts should be
feeds such as alfalfa hay and pellets are fed.

made to ensure each production unit or

If the snow is crusted with ice, the crust
individual sheep has adequate nutrient
should be broken to allow access. Still,
intake to be healthy and productive.

when possible, sheep should have wtlirnited
access to fresh, clean water.

NUTRITIONAL REQUIREMENTS

Energy: Because so much of the diet can

An adequate diet for optin1al growth and
depend on grass and forage that is either
production must include water, energy
sparse or of poor quality, the provision of

(cai·bohydrates and fats), proteins, minerals, adequate energy is important. Poor-quality and vitanuns. Under field conditions of
forage, even in abundance, may not provide
particulai· stress, additional nutrients may
sufficient available energy for maintenance
be needed. (For detailed nutrient requireand production. The energy requirement of ments for sheep, refer to the most current
ewes is greatest during the first 8-10 wk of

Nutrient Requirements of Small Rumi
lactation. Because milk production declines
nants, published by the National Reseai·ch
after this pe1iod and the lainbs have begun

Council [www.nap.edu].)

foraging, the requirement of the ewe is then
reduced to prelainbing levels. The easiest

Water: A cleai1, fresh, easily accessible
way to assess energy adequacy in sheep is to
source of water should be available at all
perfom1 and record body condition using an
times. As a minimwn requirement in
objective 1-5 scoring system, with 1 being
temperate environments, the usual
extremely thin and 5 being extremely obese.

2346

NUTRITION: SHEEP

The body condition score is determined

Seleniwn should be included in rations,
by palpating the amount of fat covering
nuneral mixtures, or other supplements in
on the spinous processes and transverse
deficient areas. Sheep diets usually contain
processes in the lumbar region. Most
sufficient potassium, iron, magnesiw11,
healthy productive ewes will have a score of sulfur, and manganese. Of the trace VetBooks.ir

2-3.5 . Sheep with a score of 1-2 should be
nunerals, iodine, cobalt, and copper status
exanuned and fed to attain a lugher score,
in ewes are best assessed via analysis of
whereas those with a score >3.5 should be
liver biopsy tissue. Zinc adequacy can be
feel less. Dietary changes should be done
assessed from the careful collection of
slowly, and abrupt reduction in total energy nonhemolyzed blood placed in trace
intake should always be avoided, particuelement-free collection tubes. Selenitun larly in middle to late gestation.

status is easily assessed by collection of
whole, preferably heparinized, blood.

Protein: Good-quality forage and pasture
generally provide adequate protein for

Salt: In the USA, except on certain
mature sheep. However, sheep do not digest
alkaline areas of tl1e western range and
poor-quality protein as efficiently as do
along tl1e seacoast, sheep should be
cattle, and there are instances when a
provided with ad lib salt (soditm1 chloride).

protein supplement should be fed with

Sheep need salt to remain tluifty, make
mature grass and hay, or when on winter
economical gains, lactate, and reproduce.

range. Therefore, a minimum of7%dietary

Mature sheep will conswne -0.02 lb (9 g) of
crude protein is needed for maintenance in
salt daily, and lambs half tlus amount. Range
most sheep. Protein requirements depend
operators commonly provide 0.5-0. 75 lb
on the stage of production (growth,

(2 2 5-350 g) of salt/ewe/mo. Salt as
gestation, lactation, etc) and the presence

0. 2%-0.5% of the dietary dry matter is
of certain diseases (internal nematode
usually adequate.

parasites, dental disease, etc). If available

Calcium and Phosphorus: In plants,
forages are unable to supply adequate
generally the leafy parts are relatively high
dietary crude protein, protein supplements,
in calciun1 and low in phosphorus, whereas
such as oilseed meals ( cottonseed meal,
the reverse is true of the seeds. Legun1es, in
soybean meal) or conunercially blended
general, have a higher calciwn content than
supplements should be feel to meet nutrient
grasses. As grasses matme, phosphorus is
requirements. Protein should be fed to
transferred to the seed (grain). Furthermeet, but not exceed, requirements. Excess more, the phosphorus content of the plant
protein feeding can be beneficial in cases of
is influenced markedly by the availability
excessive internal parasite burdens but
of phosphorus in the soil. Therefore,
result in increased production costs and
low-quality pastw·e devoid of legumes and
may result in higher incidences·of diseases
range plants tends to be naturally low in

( eg, heat stress, pizzle rot).

phosphorus, particularly as the forage

Sheep can convert nonprotein nitrogen
matures and the seeds fall.

(such as mea, a.nunoniwn phosphate, and

Sheep subsisting on mature, brown,
biuret) into protein in the rwnen but -
stmui1er forage and winter range sometimes
possibly less efficiently than beef cattle.

develop a phosphorus deficiency. Sheep

This source of nitrogen can provide at least
kept on such forages or fed low-quality
a part of the necessary supplemental
hay with no grain should be provided a
nitrogen in high-energy diets with a
phosphorus supplement (ie, defluorinated
nitrogen:sulfur ratio of 10:1. ln lamb-finishrock phosphate) added to a salt-trace ing diets, the inclusion of alfalfa, approved
mineral nuxture. Because most forages have
growth stinrnlants, and a source of
a relatively high calciwn content, particufermentable carbohydrates (eg, ground larly if tllere is a mixture of legwnes, diets
com, ground milo) enhance nitrogen
usually meet maintenance requirements for
utilization.

tlus element. However, when com silage or
other feeds from the cereal grains are fed

Minerals: Sheep require the major
exclusively, ground lin1estone should be fed
nunerals sodiwn, chlorine, calciwn,
daily at the rate of0.02-0.03 lb (9-14 g).

phosphorus, magnesium, sulfw·, potassium,

Sheep seem to be able to tolerate wide
and trace minerals, including cobalt,
calcium:phosphorus ratios as long as their
copper, iodine, iron, manganese, molybdediets contain more calcium than phosphonum, zinc, and seleniun1. Trace nuneralized rus. However, an excess of phosphorus
salt provides an economical way to prevent
may be conducive to development of
deficiencies of sodium, chlorine, iodine,
urinary calculi or osteodystrophy. A
manganese, cobalt, copper, iron, and zinc.

calcium: phosphorus ratio of 1 .5 : l is

NUTRITION: SHEEP

2347
appropriate for feedlot lambs. For pregnant free access. Levels of 7-10 ppm or higher ewes, the diet should contain �0.18% and,
may be toxic.

for lactating ewes, �0.27%. A content of

0.2%--0.4% calcium is considered adequate,

Zinc: Growing lambs require -30 ppm of
as long as the ratio is maintained between
zinc in the diet on a dry-matter basis. The

1:1 and2:l.

requirement for norn1al testicular develop

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ment is somewhat higher. Classic zinc

Iodine: Occasionally, the iodine
deficiency (parakeratosis) is more common
requirements of sheep are not met in the
in other small rwninants (goats), but is
natural diet and thus iodine supplements
occasionally encountered in sheep,
must be fed. Goitrogenic substances are
particularly if fed excessive quantities
found in many types of plants ( eg, Brassica
of dietary calcium Oegumes).

spp) and inte1fere with the use of iodine by
the thyroid. Regions naturally deficient are
fow1d throughout the western USA, in tl1e

Vitamins: Sheep diets usually contain an

Great Lakes area, and in other parts of the
ample supply of vitamins A (provitarnin A),
world. A deficiency of iodine ( manifested as

D, and E. Under certain circumstances,
goiter in tl1e adult and as lack of wool and/or however, supplements may be needed. The goiter in lan1bs) can be prevented by feeding B vitamins and vitamin K are synthesized by stabilized iodized salt to pregnant ewes.

the nunen microorganisms and, tmder

The young of iodine-deficient ewes may
practical conditions, supplements are
be aborted, stillborn, or born with goiters.

wmecessary. However, polioencephaloma

Diets containing iodine at 0.2%----0.8% ppm
lacia can be seen and is due to aberrations
are usually sufficient, depending on the
in rwninal thianiine metabolism, secondary
animals' level of production (maintenance/
to altered ruminal pH and/or microflora
growth, lactation, etc).

content. Vitan,in C is synthesized in the
tissues of sheep. On diets rich in carotene,

Cobalt: Sheep require -0. 1 ppm of cobalt
such as high-quality pasture or green hays,
in their diet. Cobalt-deficient soils are found
sheep can store large quantities of vitan"lin A in North America but are relatively rare
in the liver, often sufficient to meet their compared with other parts of the world.

requirements for as long as 6 mo.

N orn1ally, legwnes have a higher content

Vitamin D2 is derived from sun-cured
than grasses. Because cobalt levels of the
forage, and vitamin D3 from exposure of the
feedstuffs are seldom known, a good
skin to ultraviolet light. When exposure of
practice is to feed trace mineralized salt
the skin to sunshine is reduced by
that contains cobalt.

prolonged cloudy weather or confinement
rearing, and when the vitamin D

Copper: Pregnant ewes require -5 mg

2 content of
of copper (Cu) daily, which is the an1ount
the diet is low, tl1e amount supplied may be
provided when the forage contains �5 ppm.

inadequate. The requirement for vitan"lin D

However, the amount of copper in the diet
is increased when the amounts of either
necessary to prevent copper deficiency is
calcium or phosphorus in tl1e diet are low or
influenced by the intake of other dietary
when the ratio between them is wide. But
constituents, notably molybdenwn (Mo),
such dietary modification should be done
inorganic sulfate, and iron. High intake of
cautiously, because vitamin D toxicity is a
molybden w11 in the presence of adequate
severe syndrome. Fast-growing lambs kept
sulfate increases copper requirements.

in sheds away from direct swuight or

Because sheep are more susceptible than
maintained on green feeds (high carotene)

cattle to copper toxicity, care must be taken
during the winter months (low in-adiation)

to avoid excessive copper intake (see
may have impaired bone fom1ation and
p 3073). Toxicity may be produced in lan1bs
show other signs of vitamin D deficiency.

being fed diets with 10-20 ppm of copper,

Norn1ally, sheep on pasture seldom need
particularly if the Cu:Mo ratio is> 10: 1. The
vitamin D supplements.

Cu:Mo ratio should be maintained between

The major sources of vitan"lin E in the

5:1 and 10:1.

natural diet of sheep are green feeds and the
germ of seeds. Because vitan"lin E is poorly

Selenium: Seleniwn is effective in at least
stored in the body, a daily intake is needed.

partially controlling nutritional muscular

When ewes are being fed pomcquality hay or
dystrophy. Areas east of the Mississippi
forage, supplemental vitamin E may result

River and in the northwestern USA appear
in improved production, lamb weaning
to be low in seleniun1. The dietary requireweights, and colostnm1 quality. Vitamin E
ment is -0.3 ppm. Providing selenium-deficiency in you.ng lambs may contribute to containing mineral mixture may prevent
nutritional muscular dystrophy if seleniw11
seleniwn deficiency if animals are allowed
intake is low.

2348

NUTRITION: SHEEP

FEEDING PRACTICES
of projected ma.tw-e weight at lambing. If
pasture production is inadequate, ewes may

Feeding Farm Sheep
be confmed and fed high-quality hay and a

Sheep make excellent use of high-quality
small an1otmt of grain if necessary. Breeding

VetBooks.ir
roughage stored either as hay or low-moiswhile grazing legume pastures ( eg, sage, tw-e, grass-legume silage or occasionally
white clovers) may tend to depress the size
chopped green feed. Good-quality hay or
of the lamb crop, lowering the intake of
stored forage is a highly productive feed;
certain feedstuffs. After ma.ting, ewes can
poor0quality forage, no matter how much is
be maintained on pasture, thus allowing
available, is suitable only for maintenance.

feed to be conserved for other times of the

Hay quality is detennined primarily by the
year. Good pasture for this period allows the
following: 1) its composition, eg, a mixture
ewes to enter the winter feeding period in
of grasses and legumes such as brome/
good condition. When pasture is unavailalfalfa or bluegrass/clover; 2) the stage of able, an appropriate ration should be
maturity when cut, eg, the grass before
formulated (see TABLE 50).

heading and alfalfa before one-tenth bloom·

During the last� wk of pregnancy,

3) method and speed of harvesting because'

growth of the fetus is rapid. This is a. critical
they affect loss of leaf, bleaching by sun,
period nutritionally, particularly for ewes
and leaching by rain; and 4) spoilage and
carrying more than one fetus. Beginning�
loss dw-ing storage and feeding. In general,
wk before lambing, the plane of nut1ition
the same factors influence the quality of
should be increased gradually and continued
silage. Complete analysis of cut-stored
without interruption unW after lambing. The
forages enhances the utilization of these
amount offered depends on the condition or
feedstuffs and allows for the most efficient
fat coveting of the ewes and quality of the
use of supplemental grains and minerals.

forage. lf ewes a.re in fair to good condition,

0.5-0. 75 lb (225-350 g) daily is usually

Feeding Ewes
sufficient. The roughage content of the
ration should provide all the protein required

The period from weaning to breeding of
for all nonla.cta.ti.ng ewes. lf necessary, the
ewes is critical if a high twinning rate is
ewes may be classified according to age,
desired. Ewes should not be allowed to
condition, and nwnber of fetuses and
become excessively fat but should make
divided into groups for different treatment.

daily gains from weaning to breeding. The
rate of gain depends on the desired weight

Lactating Ewes: Succulent pasture
but should be -60%-70% of projected
furnishes adequate energy, protein,
ma.tw-e weight at breeding and 8001<>-90%
vitamins, and minerals for ewes and lambs;
l&H•ii·I RATIONS FOR PREGNANT EWES UP TO 6 WK BEFORE LAMBING

Ration No.

Feed

1

2

3

4
lb (kg)

lb (kg)

lb (kg)

lb_(kg)

Legume hay, such as

3--4.5

1.5-2
alfalfa, clover, or

(1.36-2.04)

(0.68-0.91)

lespedeza

Com or sorghun1 silage

4-5

(1.81-2.27)

Legwne grass,

6-8
low-moisture silage

(2. 72-3. 63)

(50%)

Cottonseed, soybean,

0.25 (0.112)

linseed, or peanut meal

(90%); limestone (10%)

Minerals8
ad lib
ad lib
ad lib
ad lib
a Mineral mix: 2 parts dicalcium phosphate to 1 pait trace mineralized salt

NUTRITION SHEEP

2349
itM•iii GRAIN MIXTURE FOR PREGNANT EWES Mixture No.

Feed

1

2

3

4

VetBooks.ir

%

%

%

%

Whole barley, corn, or wheat

60

75

75

50

Whole oats

30

25

50

Beet pulp, dried

25

Wheat bran

JO
no added grain is necessary. When pasture

Rearing Lambs on Milk Replacer:

is not being used ( confinement rearing),

Orphaned lambs, extras, triplets, or those
ewes should be fed one of the rations
from poor0mil king ewes can be raised on
outlined for pregnant ewes in TABLE 50, and
milk replacers to in1prove productivity. Such

1-1.5 lb ( 450-675 g) of one of the grain
lan1bs should receive 10"/o--20"Ai of t11eir body mixtures in TABLE 51. Ewes should have
wt in colostnm1 divided into multiple
access to a mixture of trace mineralized salt
feedings within 18--24 hr of birth. If ewe
and dicalcium phosphate. Ewes with twin
colostrwn is unavailable, a frozen, pooled
or triplet lambs should be separated from
supply from several cows can be used. Milk
those with single lambs and fed more
repla.cers designed specifically for lambs a.re
concentrates (grain) ancl/or better-quality
available and contain -300Ai fat, 25% protein,
forages. Ewes nursing twin lambs produce
and a high level of antibiotic. Under certain

2096-400,(, more milk than those witl1 singles.

conditions, it may be advisable to inject

Under confinement rearing or accelerated
orphaned Jambs with vitamins A, D, and E
lambing, lan1bs are commonly weaned at
and seleniwn. In hanclrearing systems, ewe

2 mo of age. The ewe's milk production
milk replacers a.re preferable; however,
declines rapidly after this period, and creep
good quality repla.cers designed for calves
feed is more efficiently conve1tecl into
may be fed to lan1bs. When mixing milk
weight gains when fed to lan1bs t11an to
replacers, care should be ta.ken to ensure
the ewe.

tl1a.t the powder and water are properly
mixed into a suspension. Feecling small

Feeding Lambs
quantities throughout nwnerous feedings

From -2 wk of age, lan1bs should have free
helps reduce the incidence of bloat ancl/or
access to creep feed. Where pasture is
diarrhea.. Milk repla.cers should be feel at
limited, they should be creep-fed for 1-2 mo

10"/o--200A, oftl1e lan1b's body wt, divided into until adequate forages are available. If

4-6 feedings/clay clming the first week of life.

pastme will not be available until the lan1bs

The nwnber of feedings can be reduced over
are 3-4 mo old, they can be fmishecl in a dry
time to twice a clay by 3-4 wk of age.

lot. The grain used should be ground coarse

Multiple-nipple pails or containers can
or rolled, but as the feeding period
be used. Cold milk replacer can be used by
progresses, whole grains may be used.

older lan1bs who nurse more often. By 9 -10

Small an1otmts of fresh, clean grain should
days of age, lambs should be given water in
be slowly introduced to the lambs' cliet. The
addition to the milk if a creep ration is
amount of grain is increased gradually until
offered. They can be weaned abruptly at 4-5
tl1e lambs are on full feed.

wk of age if consun1ption of creep feed and

Feeding lan1bs from birtl1 Lo market in a
water intake is at a reasonable level.

dry lot, togetl1er with early weaning at 2-3
mo of age, has become more popular

Finishing Feeder Lambs: Lambs should
throughout tl1e USA. A complete diet of hay,
be preconditioned before they leave tl1e prograin, and vitamin-mineral supplement is ducer's property. This includes sta.Iting on
ground, mixed, and eitl1er feel as is or
feed, vaccinating, worming, and under some
pressed into pellets 3/,u- or %-in. (5-10 mm)

conditions, sheaiing. lf this is not clone, the
long. Such lambs usually reach market
lambs should be rested for several days and
weight in 3 !&-4 mo. See also TABLE 52 for fed dry, average-quality hay after arrival at
exan1ples of creep rations used in dry lot
the feedlot. See also TABLE 53 for some
feeding.

recommended formulas for finishing lambs.

2350

NUTRITION: SHEEP

IM;liiti CREEP RATIONS FOR SUCKLING AND EARLY-WEANED LAMBS

Mixture No.

Feed

1

2

3

4

VetBooks.ir

%

%

%

%

Alfalfa hay, leafy ground

25

30

40

Dehydrated alfalfa leaf meal

53.5

20

48

Com, shelled

35

Com or wheat

55

Oats or barley

20

Soybean, linseed, or cottonseed meal

19

10

10

10

Molasses

3.5

8.5

5.5

Bone meal or dicalcium phosphate

Limestone

1

Trace mineralized salt

0.5

0.5

0.5

0.5

Antibiotic

0.002 0.002

There is no best method or diet for
may be started on pasture or crop residue
finishing lan1bs. They may be finished on
and moved to grain feeding systems as the
good to excellent quality forage (alfalfa,
forage is used up. When fed in a dry lot, they
wheat) with no supplemental grain. They
are usually allowed free access to feed-
itM•iii RECOMMENDED FORMULAS FOR FINISHING LAMBS·

Starter 10-day

Period

High Roughage

High

Corn

Feed

Loose Pelleted Loose Pelleted Concentrate Silage Grain (com,

500

200

780

400

1,500

540
barley, or milo )b

Alfalfa hay

1,280

1,700

1,000

1,400

200

Molasses

100

100

100

Oilseed meal

100

100

100

Urea

45

Beet pulp

200

200

Silage

1,350

Limestone

10

35

10

Trace mineral-

10

20

20

35
ized salt

Antibiotic (g)

50

20

20

10

20

10

Vitan1inA

1,000,000

(TU/ton)

• Lb/ton or kg/mettic ton; feeder lambs should have -14% crude protein in rations ( dry basis).

b Wheat can be subsUtuted for other grains, but a period of time should be allowed for adaptation.

NUTRITION: SHEEP

2351
stuffs. These diets may be completely
consist of high-protein pellets or cottonseed
pelleted, ground and mixed, a mixture of
meal and salt, mediwn-protein pellets,
ground forage (alfalfa) pellets and grain,
low-protein pellets or com, alfalfa hay, and
and/or high-concentrate type. Self-feeding
minerals. When the diets of sheep on the
usually results in maximal feed intake and
western winter range are supplemented
gain, and labor costs may be reduced.

properly, the lamb crop can be increased

VetBooks.ir

Hand-feeding can be mechanized with an

100/o-15% and wool production increased
auger system or self-unloading wagon. It
by -1 lb ( 400-500 g) per ewe.

involves feeding at regular intervals so that

One recommended practice is to feed
the lambs conswne all the feed before more

-0.25 lb (115 g) of high-protein (36%)

feed is offered. Feed consumption and gain
supplement or 0.33-0.5 lb (150-225 g) of
can be controlled. When used, com silage
mediun1-protein (24%) pellets -3 wk before
should be hand-fed to mininuze spoilage.

and dming the breeding season, during

Producers who feed lambs year-round,
extremely cold weather, and for -1 mo
or feed heavy lambs, usually prefer to place
before green feed starts in the spring. In
the lambs on full feed as soon as possible
addition, small lan1bs, small yearling ewes,

(10-14 days). Lambs can be started safely
old ewes witl1 poor teeth, and thin ewes
on self-fed, ground, or pelleted diets
should be separated from the main flock
containing 60%-700,'o hay. Within 2 wk, the
and fed one of the above supplements from
hay can be reduced to 3()0A,...4()0A, when the
approximately December 1 (northern
ration is not pelleted. Other roughages such
henusphere) tmtil shearing time. In many
as cottonseed hulls or silage can be used in
instances, the old ewes, lambs, and
a sinular manner.

yearlings from more than one band can be

Com, sorghw11, or alfalfa silage can
maintained in a flock for special dietary
replace about half the hay with hand-feedsupplementation.

ing, but finish and yield will be decreased to

When sheep a.re unable to obtain a full
some extent. See ai,so TABLE 52 for rations ration of forage because of deep snow or
that can be used in self-feeding. Com,
other weather conditions, 1-3 lb ( 450-1,350
barley, milo, wheat, or a mixture of these
g) of alfalfa hay and 0.2-0.3 lb (90-150 g) of
are used; 0.5% salt and 0.5% bone meal or
a low-protein pellet mixtme or com should
equivalent should be added to the grain.

be fed (see TABLE 54). If alfalfa hay is not Pelleting of ra.tions for fuushing lambs is
available, 0.5-1 lb (225-450 g) per head of a
beneficial when low-grade roughages or
low-protein pellet mixtme should be fed
high-roughage rations are used. Caution
daily for emergency feeding periods.

should be used when feeding large amounts
of wheat; lambs not adapted to it are more

Deficiencies of Range Forages: Defiapt to develop a.cute indigestion than if fed ciencies most apt to be seen among range
grains such as com, sorghum, or barley.

forages a.re protein, energy, salt, and

Mineral supplements, including salt,
phosphorus. These are most prevalent as
should be offered separately whether or not
the forages approach ma.tmity or are
they are included in the grain nuxture.

dormant, and they may appear singly or in

Approved growth stimulants usually increase combination. Range sheep often travel long growth rate 100/o-15% and feed efficiency
distances and are exposed to cold weather,

So/o-lOOA, but may decrease carcass quality.

resulting in higher energy requirements.

Protein supplements (soybean or

Feeding Mature Breeding Rams
cottonseed meal, alfalfa pellets, etc)

Ma.tme breeding rams should be grazed on
increase digestibility and use of poor-qualpastme when available, or fed rations 1, 2, ity forages. When possible, the inclusion of
or 3 according to
a phosphorus supplement ( eg, dicalcium

TABLE 50. If ran1s are in a
thrifty condition at breeding time and the
phosphate, monocalcium phosphate,
ewes are on a good flushing pastme, it
defluorinated rock phosphate) to a salt
should not be necessary to grain-feed the
or trace nuneral salt mixture may greatly
ran1s while with the ewes. Rams should be
improve productivity.

maintained at a good body condition (3-3.5

Most ranges used for winter grazing are
on a 1-5 scale) before the breeding season.

considered adequate in carotene, because
many species of browse furnish as much
carotene as sun-cured alfalfa hay. However,

Feeding Range Sheep
when sheep are required to graze dry grass

The conditfon of the sheep, the amount and
ranges for >6 mo without intermittent
kind of forage on the range, and the clin1atic
periods of green feed, vita.nun A suppleconditions detemune the kind and a.mount ments are recommended. The addition of
of supplement to feed. Supplements usually

45-50 IU of vitamin Nkg/day improves

2352 NUTRITION SHEEP

IH=lllll PATTERN FOR RANGE SUPPLEMENTS FOR SHEEP

Proportions oflndividual

Feeds(%)

VetBooks.ir

Recommended

Supplement

Amount of Protein

Suggested

Group

Subgroup

Feedstuff

Maximum High Medium Low

Energy feeds Grains

Barley

75

33

57.5

Com

60

5

10

15

Wheat

60

Milo

60

Oats

15

Screenings No.

10

Mill feeds

Wheat mixed feed

10

Shorts

10

Molasses

15

5

5

10

Beet pulp

10

10

Protein

30%-40%

Cottonseed meal

75

62.5

32.5

5
supplements Protein feeds Linseed meal

25

Soybean meal

75

10

10

Peanut meal

25

20%--30%

Corn gluten feed

15

Protein feeds Corn distiller's

10
dried grains

Wheat distiller's

10
grains

Brewer's dried

5
grains

Safflower meal

25

Cull beans

15

Mineral

Bone meal or

4

3

2
supplements
defluorinated

• phosphate

Di calcium

0.5

0.5
phosphate

Disodiurn
phosphate

Monocalciurn
phosphate

Monosodium
phosphate

Salt or trace
mineralized salt

Vitamin

Dehydrated alfalfa

20

12.5

6
supplements
meal

Sun-cured alfalfa

20
meal

Vitamin A and
carotene
concentrates

Total

100 100

100

( continued)

NUTRITION: SHEEP

2353

•th•ii• PATTERN FOR RANGE SUPPLEMENTS FOR SHEEP (continued) Proportions of Individual

Feeds(%)

VetBooks.ir

Recommended

Supplement

Amount of Protein

Suggested

Group

Subgroup

Feedstuff

Maximum High Medium Low

Suggested composition

Total crude protein (%)

36

24

12

Phosphorus (%)

1.5

0.5

Carotene (mg/kg)

35

17

Rate of feeding (g/day)115

150-225 90-
ewes

450
productivity in cases of extended

Enterotoxemia: This feed-related
consumption (>2 mo) of dry or weathered
malady causes almost sudden death in
forages.

sheep due to a toxin produced by

Clostridium perfringens type D and

Mineral Mixtures: On the range, portable sometimes type C. The organism appears mineral boxes are convenient for sheep.

to be widespread in nature. Under

One of these mineral mixtures should be fed conditions of high carbohydrate consumpfree choice. A salt and dicalcium phosphate tion or high intake of in1mature succulent
or phosphorus supplement ( defluorinated
forage, the causative bacteria multiply
rock phosphate) can be used if there are no
rapidly and produce an e toxin that
iodine or trace-mineral deficiencies. Iodized
increases intestinal permeability.

salt is substituted for regular salt when an

Protection of lambs is possible by vaccinatiodine deficiency exists, and trace ing twice at least 10 days apart with C
mineralized salt is substituted if deficiencies peifringens type D toxoid or by adminisof trace minerals are present.

tering antitoxin at birth. (See also

Under winter range conditions, the

ENTEROTOXEMJAS, p 609.)

an1ount of phosphorus supplement that
should be added to range pellets varies with

White Muscle Disease: White muscle
the type of range forage available, the rate
disease is caused by low levels of selenium
of feeding, and the ingredients used in the
and possibly vitamin E. Signs include
pellets. It is suggested that 36%, 24%, and
stiffness (especially in the hindquarters),

12% protein pellets contain 1.5%, 1 %, and
tucked-up rear flanks, arched backs,

0.5% phosphorus, respectively. When
pneumonia, and acute death. On necropsy,
feeding supplemental protein, 36% protein
white st.J.iations are found in cardiac,
pellets should be fed at the rate of 0.25 lb
diaphragmatic, and skeletal muscles. Levels

( 115 g) per head daily, the 24% protein
of AST and lactic dehyclrogenase are
pellets at 0.33-0.5 lb (150-225 g), and the
increased, indicating muscle damage. Blood

12% protein pellets at 0.2---0.5 lb (90-225 g),
levels of the selenium-containing glutatogether with alfalfa or clover hay. Care thione peroxidase are reduced. Although
should be taken when adding supplemental
several feedstuffs are fairly 1ich in selenium
phosphorus and magnesium to the diet of
and vitamin E, it may be a good managerams or whethers, because this is associment practice in deficient areas to il\ject ated with urolithiasis.

lambs shortly after bilth with a preparation
of vitamin E and selenium designed for
parenteral use. The use of a selenium and/or

NUTRITIONAL DISEASES
vitamiI1 E supplemented trace mineral
mixture (up to 90 ppm) as the only source

Nutritional diseases in sheep are for the
of salt fed may be useful as a preventive
most part the san1e as those seen in goats
measure. (See also NUTRITIONAL MYOPATHIES IN

(see NlITRITION: GOATS, p 2308).

RUMINANTS AND PIGS, p 1172.)

2354

NUTRITION: SMALL ANIMALS

NUTRITION: SMALL ANIMALS

VetBooks.ir

Domestic dogs and cats are both members

Body weight in combination with body
of the order Camivora. Observations of feral condition score (BCS) is used in many canids indicate that their feeding habits are
species to provide an estimate of nutritional
broad and include vaiious pa.its of plants
adequacy and can help detemline ideal body
as well as both small and large prey. By
weight. BCS is a semiquantitative assesscomparison, cats do not show omnivorous ment of body composition that ranges from
feeding behaviors and have a requirement
cachectic to severely obese. Physical
for specific animal-derived sources of
exanlination, visual observation, and
nutiients, such as preformed vitamin A,
palpation are used to assign a BCS.

ai·achidonic acid, and taurine. As a result,

Two BCS systems exist for dogs and cats,
dogs are classified nutritionally as omnia 5 -point system and a 9-point system (see vores, while cats are classified as true

TABLE 55). In a 9-point system, each unit
carnivores.

increase in BCS above ideal represents body

Using appropriate feeding practices is
weight -10%--15% greater than ideal body
one of the most in1portant components of
weight. For exan1ple, a dog or cat with a
maintaining companion animal health.

BCS of7 is approximately 20%--30% heavier

Nutritional management is also inlportant
than its ideal weight.

as an integral part of both preventive health

Pai·aineters used to assess BCS include
care and treatment protocols for medical
evaluation of fat cover over the ribs, down
and surgical patients, and ignoring
the top line ( waist), around the tail base, and nutiitional needs can often be more
ventrally along the abdomen (abdominal
detlimental to a dog or cat than the illness
tuck in front of hind legs). It is in1portant to
or ir\jury for which it is being treated.

use both a visual assessment and palpation

Feeding an appropriately fonnulated and
to assign a BCS ( see TABLE 56).

tested complete and balanced commercial
diet is the sinlplest way to meet the
nutritional requirements of dogs or cats.

NUTRITIONAL REQUIREMENTS

Ntunerous products are available, and many

AND RELATED DISEASES
ai·e fonnulated for specific life stages.

However, dogs and cats can thrive eating

Dogs are a biologically diverse species, with
a variety of commercial or appropriately
normal body weight of 4-80 kg (2-175 lb).

formulated home-prepared foo"ds.

Nonnal birth weight of pups depends on

Despite the wide availability of commerbreed type (120-550 g). The first2 wk of a cially complete and balanced diets for dogs
puppy's life is spent eating, seeking warmth,
and cats, malnutrition still occurs.

and sleeping. External food sources beyond

Malnutrition is defined as an in1balance
bitch's milk are rarely needed, unless the
of nutlients and includes both nutlient
bitch cannot produce enough nlilk or the
deficiencies and nutiient excesses. In recent puppy is orphaned. In these cases, the years, obesity has become the most
puppy must be handreared. Growth rates of
common nutritional disorder encountered
puppies ai·e rapid for the first 5 mci; in this
in small animal medicine. Obesity is a
period, pups gain an average of2-4 g/day/kg
serious medical condition that can lead to a
of their anticipated adult weight. The
variety of related health problems as well as
growth rate begins to plateau after 6 mo,
shortened life span.

ai1d growth may be completed by 8-12 mo

•th•ifi BODY CONDITION SCORE SCALES• FOR DOGS AND CATS

Body Condition

5-Point Scale

9-Point Scale

Very thin

1

Ideal weight

3

4-5 (dogs); 5 (cats)

Obese

5

9
a The scale used should be noted in the record ( eg, BCS = 4/5 or BCS = 4/9).

NUTRITION: SMALL ANIMALS

2355

14H•!1) PARAMETERS USED TO ASSESS BODY CONDITION SCORE

Body

Overhead

Condition

Ribs

View

Side View

Tail Base

Very thin

Ribs easily felt with Accentuated Severe

Bones are raised

VetBooks.ir
no fat cover;
hourglass
abdominal
with no tissue
prominent visibility shape
tuck
between the skin
of individual ribs in
and bone
dogs with short hair
coats

Ideal

Ribs easily felt with Lumbar waist Abdominal Smooth contour slight fat cover;
well-propor-
tuck
but bones can be
individual ribs not
tioned
present
felt under a thin
visible
layer of fat

Obese

Ribs difficult to feel Lumbar waist No

Thickened and
under thick fat cover not visible
abdominal
difficult to feel
tuck; fat
under prominent
hangs from layer of fat; dimple
abdomen
may be visible at
tail base
of age in small and medium breeds and by
hamburger and rice diet to dogs or cats

10---16 mo in large and giant breeds.

can induce calcium deficiency and

By comparison, the average mature body
secondary hyperparathyroidism. Raw,
weight of domestic cats is 3.2 kg (7 lb) for
freshwater fish contain thiamine
toms and 2.8 kg (6 lb) for queens. Normal
antagonists and can induce thiamine
birth weight of kittens is 90---100 g. The
deficiency when fed to cats. Feeding liver
growth rate is exceptionally rapid for the
can induce vitamin A toxicity in both dogs
first 3-4 mo, and kittens gain 50-100 g/wk.

and cats.

The growth rate begins to plateau at

Cats have some dietary requirements that

150---160 days of age, and growth is usually
are different from those of dogs and can
completed within 200---220 days.

develop nutritional deficiencies when fed

Dogs and cats require specific dietary
diets fommlated to meet the nutritional
nutrient concentrations based on their life
needs of dogs. For example, unlike dogs,
stage. The Association of Ame1ican Feed
cats require dietary sources of vitamin A,

Control Officials (AAFCO) publishes dog
arachidonic acid, and taurine. Cats also
and cat nutrient profiles for adult mainterequire higher quantities of fat and protein nance and reproduction (see TABLES 57 and than dogs, as well as of the anlino acid

58). The National Research Council (NRC)

arginine and the vitamins niacin and
also publishes nutrient profiles for dogs
pyridoxine ( vitanlin B6). Cats lack the
and cats for various life stages, most
enzyme glucokinase, which unfortunately
recently in 2006 (see TABLES 59 and 60). Both has Jed some to believe that cats cannot AAFCO and NRC list minimum nutrient
digest dietary carbohydrates. Cats produce
requirements and maximum nutrient
the enzyme hexakinase, which allows them
requirements for nutrients with potential
to digest and use properly processed dietary
toxicity.

carbohydrates.

In developed countries, nutritional

Well-intentioned owners occasionally
diseases are rarely seen in dogs and cats,
cause problems by feeding dogs and cats
especially when they are fed good quality,
certain hun1an foods. For example, raisins
commercial, complete and balanced
and grapes contain an unknown substance
diets. Nutritional problems occur most
that is toxic to dogs and can cause kidney
commonly when dogs and cats are fed
damage. Chocolate contains theobronline
imbalanced homemade diets, when cats
and much smaller amounts of caffeine, both
are fed diets formulated for dogs, or when
of which are metl1ylxanthines. Dogs and
dogs or cats are fed certain human foods.

cats metabolize theobronline much more

Dog or cat foods or homemade diets
slowly than people. Initial signs of toxicity
derived from a single food item are
include GI signs, such as vomiting and
inadequate. For example, feeding
diarrhea. This can progress to polyuria,
predominantly meat or even an exclusive
muscle tremors, cardiac arrhythmias,

2356

NUTRITION: SMALL ANIMALS
lffl;lllil AAFCO NUTRIENT REQUIREMENTS FOR DOGS•

Growth and

Adult Maintenance

Reproduction

VetBooks.ir

Nutrient

Minimum

Minimum

Maximum

Protein(%)

22.0

18.0

Arginine (%)

0.62

0.51

Histidine (%)

0.22

0.18

Isoleucine (%)

0.45

0.37

Leucine (%)

0.72

0.59

Lysine(%)

0.77

0.63

Methionine + cystine (%)

0.53

0.43

Phenylalanine + tyrosine (%)

0.89

0.73

Threonine (%)

0.58

0.48

Tryptophan (%)

0.20

0.16

Valine(%)

0.48

0.39

Fat(%)

8.0

5.0

Linoleic acid (%)

1.0

1.0

Minerals

Calcium(%)

1.0

0.6

2.5

Phosphorus (%)

0.8

0.5

1.6

Ca:Pratio

1:1

1:1

2:1

Potassium (%)

0.6

0.6

Sodium(%)

0.3

0.06

Chloride (%)

0.45

0.09

Magnesium(%)

0.04

0.04

0.3

Iron (mg/kg)

80

80

3,000

Copper (mg/kg)

7.3

7.3

250

Manganese (mg/kg)

5.0

5.0

Zinc (mg/kg)

120

120

1,000

Iodine (mg/kg)

1.5

1.5

50

Selenium (mg/kg)

0.11

0.11

2

Vitamins

Vitamin A (IU/kg)

5,000

5,000

250,000

Vitan1in D (IU/kg)

500

500

5,000

Vitamin E (IU/kg)

50

50

1,000

Thiamine (mg/kg)

1.0

1.0

Riboflavin (mg/kg)

2.2

2.2

Pantothenic acid (mg/kg)

10

10

Niacin (mg/kg)

11.4

11.4

( continued)

NUTRITION: SMALL ANIMALS

2357

AAFCO NUTRIENT REQUIREMENTS FOR DOGS• (continued) Growth and

Adult Maintenance

Reproduction

Nutrient

Minimum

Minimum

Maximum

VetBooks.ir

Pyridoxine (mg/kg)

1.0

1.0

Folic acid (mg/kg)

0.18

0.18

Vitamin B,2 (mg/kg)

0.022

0.022

Choline (mg/kg)

1,200

1,200

"Nutrient requirements are indicated on a dry-matter basis. These AAFCO nutrient profiles for dog foods presume an energy density of 3.5 kcal ME/g dry matter. Rations >4 kcal/g should be corrected for energy density.

lrtNlli:I AAFCO NUTRIENT REQUIREMENTS FOR CATS•

Growth and

Adult Maintenance

Reproduction

Nutrient

Minimum

Minimum

Maximum

Protein(%)

30.0

26.0

Arginine (%)

1.25

1.04

Histidine(%)

0.31

0.31

Isoleucine (%)

0.52

0.52

Leucine (%)

1.25

1.25

Lysine(%)

1.20

0.83

Methionine + cystine (%)

1.10

1.10

Methionine (%)

0.62

0.62

1.5

Phenylalanine + tyrosine (%)

0.88

0.88

Phenylalanine (%)

0.42

0.42

Taurine (extruded,%)

0.10

0.10

Taurine(canned,%)

0.20

0.20

Threonine (%)

0.73

0.73

Tryptophan (%)

0.25

0.16

Valine(%)

0.62

0.62

Fat(%)

9.0

9.0

Linolcic acid (%)

0.5

0.5

Arachidonic acid (%)

0.02

0.02

Minerals

Calcium(%)

1.0

0.6

Phosphorus (%)

0.8

0.5

Potassium(%)

0.6

0.6

Sodium(%)

0.2

0.2

Chloride(%)

0.3

0.3

( continued)

2358

NUTRITION: SMALL ANIMALS
itti=i•ii:i AAFCO NUTRIENT REQUIREMENTS FOR CATS• (conti,nued) Growth and

Adult Maintenance

Reproduction

Nutrient

Minimum

Minimum

Maximum

VetBooks.ir

Magnesium(%)

0.08

0.04

Iron (mg/kg)

80

80

Copper (mg/kg)

5

5

Iodine (mg/kg)

0.35

0.35

Zinc (mg/kg)

75

75

2,000

Manganese (mg/kg)

7.5

7.5

Selenium (mg/kg)

0.1

0.1

Vitamins

Vitan1in A (IU/kg)

9,000

5,000

750,000

Vitanlin D (IU/kg)

750

500

10,000

Vitainin E (IU/kg)

30

30

Vitainin K (mg/kg)

0.1

0.1

Thiamine (mg/kg)

5.0

5.0

Riboflavin (mg/kg)

4.0

4.0

Pyridoxine (mg/kg)

4.0

4.0

Niacin (mg/kg)

60

60

Pantothenic acid (mg/kg)

5.0

5.0

Folic acid (mg/kg)

0.8

0.8

Biotin (mg/kg)

0.07

0.07

Vitanlin B12 (mg/kg)

0.02

0.02

Choline (mg/kg)

2,400

2,400

"Nutrient requirements are indicated on a dry-matter basis. These AAFCO nutrient profiles for cat foods presume an energy density of 4 kcal ME/g dry matter. Rations >4.5 kcaVg should be corrected for energy density.

2006 NRC NUTRIENT REQUIREMENTS FOR ADULT DOGS

(MAINTENANCE)•

Nutrient

Recommended

(Amount/1,000 kcal ME)h

Minimum

Maximum Allowance

Protein (g)

20

25

Arginine (g)

0.70

0.88

Histidine (g)

0.37

0.48

Isoleucine (g)

0.75

0.95

Leucine (g)

1.35

1.70

Lysine (g)

0.70

0.88

Methionine (g)

0.65

0.83

Methionine + cystine (g)

1.30

1.63

Phenylalanine (g)

0.90

1.13

( cont-inued)

NUTRITION: SMALL ANIMALS

2359

2006 NRC NUTRIENT REQUIREMENTS FOR ADULT DOGS

(MAINTENANCE)• ( continued)

Nutrient

Recommended

(Amount/1,000 kcal ME)b

Minimum

Maximum Allowance

VetBooks.ir

Phenylalanine + tyrosine (g)

1.48

1.85

Threonine (g)

0.85

1.08

Tryptophan (g)

0.28

0.35

Valine (g)

0.98

1.23

Fat(g)

82.5

13.8

Linoleic acid (g)

16.3

2.8
o:-Linolenic acid (g)

0.11

Eicosapentaenoic +

2.8

0.11
docosahexaenoic acid (g)

Minerals

Calcium (g)

0.50

1.0

Phosphorus (g)

0.5

0.75

Potassium (g)

1.0

Sodium (g)

75

200

Chloride (mg)

300

Magnesium (mg)

45

150
lron(mg)

7.5

Copper(mg)

1.5

Manganese (mg)

1.2

Zinc (mg)

15

Iodine (mcg)

175

220

Selenium (mcg)

87.5

Vitamins

Vitamin A (retinol equivalents)

16,000

379

Cholecalciferol (mcg)

20

3.4

Vitamin E (o:-tocopherol, mg)

7.5

Vitamin K (menadione, mg)

0.41

Thiamine (mg)

0.56

Riboflavin (mg)

1.05

1.3

Pantothenic acid (mg)

3.75

Niacin(mg)

4.25

Pyridoxine (mg)

0.375

Folic acid (mcg)

67.5

Vitamin B,2 (mcg)

8.75

Choline (mg)

425

• Reprinted with permission from the National Academies Press, copyright 2006, National Academy of Sciences.

" ME ; metabolizable energy

2360

NUTRITION SMALL ANIMALS

2006 NRC NUTRIENT REQUIREMENTS FOR PUPPIES AFTER

WEANING•

Nutrient

Recommended

VetBooks.ir

(Amount/1,000 kcal ME)h

Minimum

Maximum Allowance

PROTEIN, GROWING PUPPIES 4-14 WK OLD

Protein (g)

45

56.3

Arginine (g)

1.58

1.98

Histidine (g)

0.78

0.98

Isoleucine (g)

1.30

1.63

Leucine (g)

2.58

3.22

Lysine (g)

1.75

>20

2.20

Methionine (g)

0.70

0.88

Methionine + cystine (g)

1.40

1.75

Phenylalanine (g)

1.30

1.63

Phenylalanine + tyrosine (g)

2.60

3.25

Threonine (g)

1.63

2.03

Tryptophan (g)

0.45

0.58

Valine (g)

1.35

1.70

PROTEIN, GROWING PUPPIES 2:14 WK OLD

Protein (g)

35

43.8

Arginine (g)

1.33

1.65

Histidine (g)

0.50

0.63

Isoleucine (g)

1.00

1.25

Leucine (g)

1.63

2.05

Lysine (g)

1.40

1.75

Methionine (g)

0.53

0.65

Methionine + cystine (g)

1.05

1.33

Phenylalanine (g)

1.00

1.25

Phenylalanine+ tyrosine (g)

2.00

2.50

Threonine (g)

1.25

1.58

Tryptophan (g)

0.35

0.45

Valine (g)

1.13

1.40

FAT, MINERALS, AND VITAMINS, ALL PUPPIES

Fat(g)

330

21.3

Linoleic acid (g)

65

3.3
cx-Linolenic acid (g)

0.2

Arachidonic acid (g)

0.08

Eicosapentaenoic +

11

0.13
docosahexaenoic acid (g)

( continued)

NUTRITION: SMALL ANIMALS

2361

2006 NRC NUTRIENT REQUIREMENTS FOR PUPPIES AFTER

WEANING• (continued)

Nutrient

Recommended

VetBooks.ir

(Amount/1,000 kcal ME)b

Minimum

Maximum Allowance

Minerals

Calcium (g)

2.0

18

3.0

Phosphorus (g)

2.5

Potassium (g)

1.1

Sodium (mg)

550

Chloride (mg)

720

Magnesium (mg)

45

100

Iron (mg)

18

22

Copper ( mg)

2.7

Manganese (mg)

1.4

Zinc (mg)

10

25

Iodine (mcg)

220

Selenium (mcg)

52.5

87.5

Vitamins

Vitamin A (retinol equivalents)

3,750

379

Cholecalciferol (mcg)

20

3.4

Vitamin E (cx-tocopherol, mg)

7.5

Vitamin K (menadione, mg)

0.41

Thiamine (mg)

0.34

Riboflavin (mg)

l.05
l.32

Pantothenic acid (mg)

3.75

Niacin (mg)

4.25

Pyridoxine (mg)

0.375

Folic acid (mcg)

68

Vitamin B12 (mcg)

8.75

Choline (mg)

425

" Reprinted with pennission from the National Academies Press, copyright 2006, National Academy of Sciences.

b ME = metabolizable energy
seizures, and death. Macadan1ia nuts are
called persin, which can cause dyspnea,
also potentially toxic to dogs and cats and
pulmonaiy edema, and pleural ai1d
can cause weakness, depression, vomiting,
pericardia] effusion in goats and possibly
ataxia, muscle tremors, hyperthermia, and
dogs. Food high in fat, such as chicken
tachycardia. As few as six macadarnia nuts
skin, can result in some dogs developing
can be toxic to dogs. Onions and garlic
pancreatitis. Broccoli toxicity has been
contain thiosulfate, which can cause
reported to occur in dairy cattle, but it is a
oxidative damage to RBCs and result in
poorly documented problem in dogs and
anemia. Onions are more toxic than garlic.

cats. Sugar-free foods containing xylitol can

Guatemalan avocados contain a substance
cause liver dainage in dogs. Raw food diets

2362

NUTRITION: SMALL ANIMALS

2006 NRC NUTRIENT REQUIREMENTS FOR ADULT CATS

(MAINTENANCE)•

Nutrient

Recommended

(Amount/1,000 kcal ME)b

Minimum

Maximum

Allowance

VetBooks.ir

Protein (g)

40

50

Arginine (g)

1.93

Histidine (g)

0.65

Isoleucine (g)

1.08

Leucine (g)

2.55

Lysine (g)

0.68

0.85

Methionine (g)

0.34

0.43

Methionine + cystine (g)

0.68

0.85

Phenylalanine (g)

1.00

Phenylalanine+ tyrosine (g)

3.83

Threonine (g)

1.30

Tryptophan (g)

0.33

Valine (g)

1.28

Taurine (g)

0.080

0.10

Fat(g)

82.5

22.5

Linoleic acid (g)

13.8

1.4

Arachidonic acid (g)

0.5

0.015

Eicosapentaenoic +

0.025
docosahexaenoic acid (g)

Minerals

Calcium (g)

0.40

0.72

Phosphorus (g)

0.35

0.64

Potassium (g)

1.3

Sodium(mg)

160

170

Chloride (mg)

240

Magnesium (mg)

50

100

Iron (mg)

20

Copper(mg)

1.2

Manganese (mg)

1.2

Zinc(mg)

18.5

Iodine (mcg)

320

350

Selenium (mcg)

75

Vitamins

Vitamin A (retinal

25,000

250
equivalents)

Cholecalciferol (mcg)

188

1.75

( continued)

NUTRITION: SMALL ANIMALS

2363

2006 NRC NUTRIENT REQUIREMENTS FOR ADULT CATS

(MAINTENANCE)• (continued)

Nutrient

Recommended

(Amount/1,000 kcal ME)b

Minimum

Maximum

Allowance

VetBooks.ir

Vitamin E (a-tocopherol, mg)

10

Vitamin K (menadione, mg)

0.25

Thiamine (mg)

1.40

Riboflavin (mg)

1.0

Pantothenic acid (mg)

1.15

1.44

Niacin(mg)

10.0

Pyridoxine (mg)

0.5

0.625

Folic acid (mcg)

150

188

Vitamin B,2 (mcg)

5.6

Choline (mg)

510

637
a Reprinted with permission from the National Academies Press, copyright 2006, National Academy of Sciences.

" ME = metabolizable energy

2006 NRC NUTRIENT REQUIREMENTS FOR KITTENS AFTER

WEANING•

Nutrient

Recommended

(Amount/1,000 kcal ME)b

Minimum

Maximum

Allowance

Protein (g)

45

56.3

Arginine (g)

1.93

8.75

2.4

Histidine (g)

0.65

>5.5

0.83

Isoleucine (g)

1.08

>21.7

1.4

Leucine (g)

2.55

>21.7

3.2

Lysine (g)

1.70

>14.5

2.1

Methionine (g)

0.88

3.25

1.1

Methionine + cystine (g)

1.75

2.2

Phenylalanine (g)

1.00

>7.25

1.3

Phenylalanine + tyrosine (g)

3.83

17

4.8

Threonine (g)

1.30

>12.7

1.6

Tryptophan (g)

0.33

4.25

0.40

Valine (g)

1.28

>21.7

1.6

Glutamic acid (g)

18.8

Taurin e (g)

0.080

>2.22

0.10

Fat(g)

82.5

22.5

Linoleic acid (g)

13.8

1.4

( continued)

2364

NUTRITION: SMALL ANIMALS

2006 NRC NUTRIENT REQUIREMENTS FOR KITTENS AFTER

WEANING• (conUnued)

Nutrient

Recommended

VetBooks.ir

(Amount/1,000 kcal ME)h

Minimum

Maximum

Allowance
a-Linolenic acid (g)

0.05

Arachidonic acid (g)

0.05

Eicosapentaenoic +

0.025
docosahexaenoic acid (g)

Minerals

Calciwn (g)

1.3

2.0

Phosphorns (g)

1.2

1.8

Potassium (g)

0.67

1.0

Sodium (mg)

310

350

Chloride (mg)

190

225

Magnesium (mg)

40

100

Iron (mg)

17

20

Copper(mg)

l.l

2.1

Manganese (mg)

1.2

Zinc (mg)

12.5

18.5

Iodine (mcg)

450

Selenium (mcg)

30

75

Vitamins

Vitamin A

20,000

250

( retinol equivalents)

Cholecalciferol (mcg).

0.70

188

1.4

Vitamin E ( a-tocopherol, mg)

9.4

Vitamin K (menadione, mg)

0.25

Thiamine (mg)

1.1

1.40

Riboflavin (mg)

1.0

Pantothenic acid (mg)

1.15

1.43

Niacin(mg)

10

Pyridoxine (mg)

0.5

0.625

Folic acid (mcg)

150

188

Vitamin B12 (mcg)

5.6

Choline (mg)

510

637

" Reprinted with permission from the National Academies Press, copyright 2006, National Academy of Sciences.

b ME � metabolizable energy

NUTRITION: SMALL ANIMALS

2365

DAILY MAINTENANCE ENERGY REQUIREMENTS FOR DOGS

AND CATS

Animal

MERa (kcal/day)

VetBooks.ir

Healthy adult dogs

Intact

1.8 x RERb

Neutered

1.6 x RER

Obese prone

1.4 x RER

Healthy puppies

<4mo old

3xRER

>4mo old

2xRER

Healthy adult cats

Intact

1.4 x RER

Neutered

1.2 x RER

Obese prone

1.0 x RER

Healthy kittens

2.5xREW

• MER = maintenance energy requirement
b RER = resting energy requirement
c Kittens can alternatively be fed free choice

( see p 2375) are also not recommended for
allow for optimal use of proteins and to
dogs and cats. Raw meat products may
maintain optimal body weight and condition
contain pathogens. (See ai,so FOOD HAZARDS, through growth, maintenance, activity,
p 2964.)

pregnancy, and lactation.

Nutrient deficiencies have also been seen

Energy requirements for dogs and cats
in dogs and cats fed "natural," "organic," or are not a linear function of body weight.

"vegetarian" diets produced by owners with Recent evidence indicates that dogs
good intentions. Many published recipes
maintained in households require fewer
have been only crudely balanced by
calories per day than dogs kept in kennels,
computer, if at all, using nutrient averages.

but considerable variability exists. Breed

In addition, most homemade diets do not
differences also affect caloric needs
undergo the scrutiny and rigorous testing
independent of body size, eg, Newfoundapplied to conunercial complete and lands appear to require fewer calories/day
balanced diets. If pet owners wish to feed
than Great Danes. Other factors that
their pets homemade diets, the diets should
determine daily energy needs include
be prepared and cooked using recipes
activity level, life stage, percent lean body
fommlated by a veterinary nutritionist.

mass, age, and environment. Even when

Some nutritional diseases are seen
specific fom1ulas are used, any given anin1al
secondary to other pathologic conditions or
may require as much as 300A, more or less of
anorexia, or both. Owner neglect is also a
the calculated amount. Consequently,
frequent contributing factor in malnutrition.

general recommendations may need to be
modified within this 300A, range, and body

Energy: The most useful measure of
condition scoring should be regularly
energy for nutritional purposes is metabolizperfom1ed.

able energy (ME), which is defined as that

The precise ME values for many dog food
portion of the total energy of a diet that is
ingredients have not been experimentally
retained within the body. It is typically
determined and are often estimated using
measured in calories or joules. The caloric
those for other rnonogast1ic species ( such
content of pets foods is usually expressed in
as pigs) or calculated using Atwater
kilocalo1ies (kcal), which is 1,000 calories.

physiologic fuel values modified for use

Dogs and cats require sufficient energy to
with typical dog food ingredients. Likewise,

2366

NUTRITION SMALL ANIMALS
the precise ME values for many cats are

Nutrient Classifications
not !mown, although it is believed that
the factors used for dogs may apply. The

The six classes of nutrients are water,
modified Atwater ME values for dogs are
protein, fat, carbohydrates, vita.Jllins, and

3.5 kcal/g for carbohydrate and protein and
minerals. Only protein, fat, a.J1d carbohy

VetBooks.ir

8.5 kcal/g of fat. The impact of vaiious
drate provide energy; vita.J11ins, minerals,
envirorunental temperatures is described in
a.J1d water do not.

the recent NRC publication on nutrient
requirements of dogs and cats and has been

Water: Water is the most importa.Jlt
documented under certain conditions. For
nutrient; a lack of water Ca.Jl lead to death in
exainple, energy requirements increased
a matter of days. Clea.J1, fresh water should
from 120 to 205 kcaJ/kgO· 75 in Huskies as
be available at all times. Multiple water
ainbient temperatures decreased from 14°C
sources encourage consmnption. This is
in summer to ---20°C in winter. Effects of
paiticularly important in cats, which often
environmental temperature are not well
do not dtink a lot of water.

characterized in cats, because most of the

Several approaches have been used to
reseai·ch was done under thermoneutral
estimate daily water needs. There are

(68°---72°F (20°---22°C]) conditions. However,
general guidelines for daily fluid requireunacclimatized adult cats increased their ments in dogs ai1d cats, but individual
daily caloric intakes nearly 2-fold when
variations exist. The qua.J1tity of water
environmental temperatures of 23°C and
required depends on a nm11ber of different

0°C were studied.

factors, including the a.J1imal's diet,
environment, activity level, a.Ild health

Caloric Requirements: Energy requirestatus. The moisture content of caimed pet ments are quite variable ainong dogs and
foods varies from 600/o to >87%. Dry pet
cats. Animals with the saine body weight can foods contain 3%---11 % water, a.Ild semin10ist have 3-fold variation in daily kcal requirefoods contain 25%---35% water. As a result, ments, which ai·e affected by age, neute1ing
dogs and cats consunling predon1ina.J1tly
status, physiologic status (growth, gestation, caiu1ed food generally drink less water tl1an lactation, etc), physical activity, environthose consunling predominantly dty diets.

mental temperature, and any underlying

In a thermoneutral environment, most
abnom1alities. Any reconunendations for
mammalian species need -44---66 mllkg
kcal requirements are only starting points
body wt. Another approach considers that
and may need to be modified based on the
water needs appear to be highly associated
response of the individual dog or cat.

with the a.J110unt of food consumed. In this

Many formulas are available to calculate
case, daily maintenance fluid requirements
caloric requirements for dogs and cats. A
in mL should equal the a.Jlin1al's MER in kcal
simple method for healthy dogs and cats
of ME. A third technique sets daily water
struts with calculating the resting energy
intake as 2---3 tin1es the dietary dty matter
requirement (RER). The RER is the energy
intake. When provided ainple ainounts of
requirement for a healthy but fed aiumal, at
water, healthy a.Jlin1als can effectively
rest in a thermoneutral envirot1ment. It
self-regulate their intake. Water deficiency
includes energy expended for recovery

CaJ1 be seen as a result of poor husbandly or
from physical activity and feeding. There
disease. Dehydration is a se1ious problem in
is an exponential a.Ild a linear fom1ula for
ma.J1y different disorders, including those of
calculating RER. The exponential formula
the GI, respiratory, a.Ild urirraiy systems.

(RER = 70 [body wt in kg0 751) ca.Jl be used
for anin1als of a.J1y body weight, whereas the

Protein: Protein is required to increase a.J1d linear fom1ula (RER = 30 x [body wt in kg] +
renew the nitrogenous components of the

70) is restricted for use in anin1als that
body. A primaiy function of dietary protein
weigh >2 kg and <45 kg.

is as a source of essential a.J11ino acids ai1d

The maintena.J1ce energy requirement
nitrogen for the synthesis of nonessential

(MER) is the energy requirement of a
a.J1lino acids. Anlino acids supply both
moderately active ai1imal in a therrnoneunitrogen for the synthesis of all other tral environment. It includes energy needed
nitrogenous compounds a.Ild energy when
to obtain, digest, and absorb food in
catabolized. Ten ainino acids are essential in
ainounts to maintain body weight, as well
the diet of dogs: arginine, histidine,
as energy for sponta.Jleous activity. The
isoleucine, leucine, lysine, methionine,
fom1Ulas to calculate MER t.ake into
phenylalanine, threonine, tryptopha.Il, a.J1d
account age a.J1d neuter status.

valine. Cats have a dietary requirement for

Fom1ulas for daily maintena.J1ce energy
aJ1 additional a.J11ino acid, taurine. Other
requirements (kcal/day) are listed in TABLE 63.

nonessential a.J11ino acids may become

NUTRITION: SMALL ANIMALS

2367
conditionally essential when an animal has
protein as dry matter (AAFCO guidelines)

an underlying disorder that either interferes
or -20 g protein/1,000 kcal of ME required
with synthesis of the amino acid or results

(NRC guidelines).

in its excessive consumption or loss.

Optimal diets for growing kittens should

Protein requirements of dogs and cats
contain at least 24%-28% ME as protein or
vary with age, activity level, temperament,

30% protein as dry matter ( AAFCO

VetBooks.ir
life stage, health status, and protein quality
guidelines) or 45 g protein/1,000 kcal ME
of the diet. Most commercial dog foods

(NRC guidelines). Optimal diets for adult
contain a combination of plant- and
cats should contain -200A, ME as protein
animal-based proteins, with protein
or 26% protein as dry matter (AAFCO
digestibilities of 75%-900Ai. Digestibility is
guidelines or 40 g protein/1,000 kcal ME
less for plant protein ingredients, protein

(NRC guidelines). Growing kittens are more
of poor biologic value, and for poor-quality
sensitive to the quality of dietary protein
diets. If excessive heat is used in processing, and anlino acid balance than are adult cats.

proteins can become chemically unavail

Protein suitable for cats must supply >500
able for digestion and absorption; however,
mg of taurine/kg diet dry matter. Unless
these are not the types of temperatures
synthetic essential anlino acids are added,
typically used to produce commercial pet
some animal protein is necessaiy in the diet
foods.

to prevent taurine depletion and develop

Healthy adult dogs need a minimun1 of
ment of feline central retinal degeneration

2.62 g of protein of high biologic value per
or dilated cardiomyopatl1y.

kg metabolic body wt (ie, BW ,go 75)/day

Without sufficient energy from dietai-y fat

(NRC guidelines). Healthy puppies 4-14 wk
or carbohydrate, dietary protein ordinarily
old and >14 wk old need a minimum of9.7 g
used for growth or maintenance of body
and 12.5 g of protein of high biologic value
functions is less efficiently converted to
per kg metabolic body wt/day, respectively.

energy. Too little high biologic protein in

The cat has a higher protein requirement
the diet, relative to the energy density, can
than most species, and healthy adult cats
cause an apparent protein deficiency.

need a .mininlwn of 3.97 g of protein of high

Signs produced by protein deficiency
biologic value per kg metabolic body wt/day. or an in1proper protein:calorie ratio may Healthy kittens need a minimun1 of 9.4 g
include any or all of the following: reduced
of protein of high biologic value per kg
growth rates in puppies and kittens, anemia,
metabolic body wt/day. The biologic value
weight loss, skeletal muscle atrophy, dull
of a protein is related to the nwnber and
unkempt hair coat, anorexia, reproductive
types of essential amino acids it contains
problems, persistent Wlfesponsive
and to its digestibility and metabolizability.

parasitism or low-grade microbial infection,

The higher the biologic value of a protein,
impaired protection via vaccination, rapid
the less protein is needed in the diet to
weight loss after injury or during diseas�,
supply the essential amino acid requireand failure to respond properly to treatment ments. Egg has been given the highest
of injw-y or disease. High protein intakes per
biologic value, and organ and skeletal meats
se do not cause skeletal abnormalities in
have a higher biologic value than plantdogs (including osteochondrosis in large based proteins.

breeds) or renal insufficiency later in life

General guidelines for dietary protein
in dogs or cats.

requirements in dogs and cats exist, but
requirements vary depending on the

Fats: Dietary fat consists mainly of
digestibility of the protein in the diet. If an
triglyceride witl1 varying amounts of free
animal is consuming a diet containing
fatty acids and glycerol. Lipids can either
predominantly plant protein sources,
be simple (triglycerides, wax) or complex
protein requirements may be higher than if

( containing many other elements).

the animal is consunling a diet containing

Triglycerides are divided into sh01t,
predominantly animal protein sources. The
medimn, and long chain based on the
dietary requirement for protein in healthy
number of carbon atoms in the fatty acid
adult dogs is satisfied when the dog's
chain. Essential fatty acids are long-chain
metabolic need for amino acids and
fatty acids that cannot be synthesized in the
nitrogen is satisfied. Optimal diets for
body; most fatty acids consumed in the diet
growing puppies should contain a minimum
are long-chain fatty acids. Most nutrients
of 22% protein as dry matter (AAFCO
conswned are digested and absorbed in the
guidelines) or 45 g protein/1,000 kcal ME for
small intestines, where they then enter the
puppies 4-14 wk old and 35 g protein/1,000
blood supply via the portal vein and are
kcal ME for puppies >14 wk old (NRC guidedelivered to the liver. When long-chain fatty lines). Adult clogs require a nlinimwn of 18%
acids are conswned, tl1ey are digested and

2368

NUTRITION: SMALL ANIMALS
absorbed into the small-intestinal epithelial
guidelines) or 21.3 g fat/1,000 kcal ME (NRC
cells; however, they are not transp01ted
guidelines). Optimal diets for adult dogs
directly into the blood supply but rather
should contain a minimum 5% fat as dry
enter the lymphatics first. There are conflic t matter (AAFCO guidelines) or 1.3 g of fat ing studies regarding the fate of dietary
per kg metabolic body wt/day (NRC

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medium-chain fatty acids. Most studies
guidelines) or 10 gfat/1,000 kcal ME (NRC
suggest that medium-chain fatty acids do
guidelines). Optimal diets for growing
not require initial transport in the lymphatkittens 3lld adult cats should contain a ics and instead can be absorbed from the
mininlum go1o fat as dry matter (AAFCO
intestines directly into the blood supply via
guidelines), 4. 7 g of fat per kg metabolic
the portal vein.

body wt/day for kittens, 4. 7 g of fat per kg

Fatty acids are either saturated,
metabolic body wt/day for kittens, 2.2 g of
indicating there are no double bonds, or
fat per kg metabolic body wt/day for adult
unsaturated, indicating there are one or
cats (NRC guidelines), or 22.5 g fat/1,000
more double bonds. Fatty acids that contain
kcal ME for growing kittens 3lld adult cats
more than one double bond are called

(NRC guidelines).

polyunsaturated fatty acids (PUFA). PUFA

Dogs 3lld cats have a dietm,1 requirement
are designated as either omega-3, omega-6,
for specific EFA, including linoleic acid, fill
or omega-9 fatty acids, depending on the
unsaturated EFA found in appreciable
location of tl1e first double bond. The more

3ll1ounts in com and soy oil. Cats also have
double bonds a fatfy acid contains, the more a dietary requirement for fillother unsatuprone it is to rancidity if not properly rated EFA, m·achidonic acid. Unlike dogs,
preserved. Saturated fatty acids m·e used
cats Cfilillot readily convert linoleic to
primarily for energy in the body, whereas
arachidonic acid, which must be obtained
unsaturated fatty acids m·e found in cell
from anin1al sources. Recommendations
membranes 3lld blood lipoproteins.

for dietary intake of both linoleic acid 3lld

Dietary fatty acid profiles are reflected in
arachidonic acid are -5 g 3lld 0.2 g/kg diet,
the fatty acid composition of tissues 3lld cell respectively, for kittens 3lld adult cats. Both membrfilles. In general, as the fat content of
linoleic acid 3lld m·achidonic acid are
a diet increases, so does the caloric density
omega-6 fatty acids.

3lld palatability, which promotes excess

Recent studies suggest that o:-linolenic
cal01ie consumption 3lld obesity. Fat is a
acid (fill omeg a -3 fatty acid) is also essential
concentrated source of energy, yielding
in dogs filld possibly in cats. This omega-3

-2.25 times the ME (as fill equal dry-weight
fatty acid is found primarily in flaxseed oils.

portion) of soluble carbohydrate or protein.

The 3ll1ount of dietary a-linolenic acid

The addition of too much dietm,1 fat relative
needed likely depends on the linoleic acid
to other nutrients may result in excessive
content. Although the required 3ll10unts
energy intake and subsequent suboptin1al
of this omega-3 fatty acid are presently
intakes of protein, minerals, 3lld vitmnins.

unknown, current minimal recommend a

Dietary fats also facilitate the absorption,
tions include 0.8 g/kg diet of o:-linoleic acid
storage, and trfillsport of the fat-soluble vitawhen linoleic acid is 13 g/kg diet ( dry-matter mins (A, D, E, 3lld K). They m·e also 1'I. source basis) for puppies 3lld 0.44 g/kg diet of
of essential fatty acids (EFA), which
o:-linoleic acid when linoleic acid is 11 g/kg
maintain functional integrity of cell
diet ( d1,1-matter basis) for adults. In
membra11es 3lld m·e precursors of
addition, the longer chain omega-3 fatty
prostaglfilldins and leukotrienes.

acid, docosaliexaenoic acid (Olli\), may

Dietary fats, especially the unsaturated
be conditionally essential for normal
variety, require a protective (natural or
neurologic growtl1 3lld development of
synthetic prese1vatives) filltioxidation
puppies 3lld kittens. Puppies fed diets
system. If 3lltioxid3llt protection from a
containing DHA perform better in learning
natural preservative system ( eg, vitmnin C
experiments filld are easier to train thfill
or mixed tocopherols) or from synthetic
puppies fed diets without DHA. Eicosapenpreservatives (eg, BHA, BH1� ethoxyquin) taenoic acid (EPA) is fillother longer chain
in the diet is insufficient, dietm,1 3lld body
omega-3 fatty acid that has been shown to
polyunsaturated fats become oxidized 3lld
be beneficial in tl1e diet for treatment of
lead to steatitis. Rfillcid fats in the diet can
certain skin, renal, and GI conditions, as
also result in fat-soluble vitmnin deficiency.

well as cancer, arthritis, and hyperlipidemia.

Dietary fat requirements vm,1 with age

These longer chain omega-3 fatty acids are
filld species. Optimal diets for growing
found primarily in marine sources of lipids.

puppies should contain a minimum 8% fat as Very little o:-linolenic acid gets converted to dry matter (AAFCO guidelines) or 5.9 g of

DHA/EPA in dogs 3lld cats. Therefore, when
fat per kg metabolic body wt/day (NRC
choosing omega-3 fatty acids to treat certain

NUTRITION: SMALL ANIMALS

2369
medical conditions, it is best to choose
from dietary cai·bohyd.rates. The use of
marine somces. NRC recommends a level
dietaty protein to synthesize energy in dogs
of 0.025 g/1,000 kcal ME of a combination
diverts ainino acids away from ftmctions
of DHA and EPA for both kittens and adult
such as SY11thesis of nonessential amino

VetBooks.ir
cats. NRC recommends levels of DHA and
acids and building muscle. Carbohydrates

EPA in the diet of 0.13 g/1,000 kcal ME for
cai1 become conditionally essential when
puppies and 0.11 g/1,000 kcal ME for adult
energy needs are high, such as during
dogs.

growth, gestation, and lactation. Different

Most commercial adult dog foods
cai·bohydrate somces have vaiying
typically contain 5o/o-15% fat ( dry-matter
physiologic effects. In cats, cai·bohydrates
basis). Puppy diets usually contain 8o/o-20"A,
apparently are not essential in the diet when
fat ( dry-matter basis). One reason for this
an1ple protein and fats supply glucogenic
wide range of fat content is the pmpose of
atnino acids and glycerol. However,
the diet; work, stress, growth, and lactation
properly cooked nonfibrous carbohydrates
require higher levels than maintenance. As
are utilized well by botl1 cats and dogs. In
much as 60% of the calories in a cat's diet
both dogs and cats, if starches ai·e not
may come from fat, although diets that
cooked, they ai·e poorly digested ai1d may
contain 8%-40% fat ( d1y-matter basis) have
result in flatulence or diarrhea. Except for
also been fed successfully. Because fat can
t11e occasional case of lactose or sucrose
add considerably more calories to a finished
intolerance, most cooked cai·bohydrates ai·e
diet, the an10w1t of protein relative to
well tolerated in botl1 dogs and cats.

energy must be balanced appropriately to
the life stage and typical intakes expected

Fiber: Fiber is defined as the edible parts
for an animal's size and needs.

of plants or analogous cai·bohydrates tl1at

EFA deficiencies are extremely rare in
are resistant to digestion and absorption in
dogs and cats fed properly preserved
the small intestine and have complete or
complete and balanced diets formulated
paitial fermentation in the Jai·ge intestine.

according to AAFCO profiles. Deficiencies

AJtl10ugh tl1ere is no dietaiy requirement for
of EFA induce one or several signs, such as
fiber in clogs and cats, there ai·e heal th
a dry, scaly, lusterless coat; inactivity; or
benefits of having certain fiber somces in
reproductive disorders such as anestrus,
the diet. Fiber is resistant to hydrolysis by
testicular underdevelopment, or lack of
mainmalian digestive secretions but is not
libido. Fatty acid supplements are often
an inert traveler through t11e GI tract.

recommended for dogs with dry, flaky skin

Increased levels of fiber in diets increase
and dull coats, but underlying metabolic
fecal output, normalize transit time, alter
conditions should always be evaluated first.

colonic microflora and fermentation
patterns, alter glucose absorption and

Carbohydrates and Crude Fiber:

insulin kinetics, and, at high levels, can

Carbohydrates in pet foods include low- and depress diet digestibility.

high-molecular-weight sugars, starches, and

The diverse natme of fiber has led to
various cell wall and storage nonstarch
nwnerous classification methods. One way
polysacchaiides or dietary fibers. The four
fiber is classified is based on its solubility.

carbohydrate groups functionally are

Soluble fibers have greater water-holding
absorbable ( eg, monosaccharides such as
capacity than insoluble fibers. Fiber somces
glucose, galactose, ai1d fructose), digestible
such as beet pulp, cellulose, and rice bran

(eg, disacchatides, some oligosaccharides),
have low solubilities, while gum arabic,
fem1entable (eg, lactose, some oligosacchamethylcellulose, and inulin have high rides), and poorly fem1entable (eg, fibers
solubility. Psyllium contains both low-solusuch as cellulose, which is an insoluble ble and high-soluble fiber. Although tl1e
fiber).

classification of fiber based on its solubility

Although there is no minimum dietaiy
is sWI used, fiber is better classified based
requirement for simple carbohydrates or
on its rate of ferment.ability. Fermentation is
starches for dogs and cats, certain tissues,
defined as the capacity of fiber breakdown
such as the brain and RBCs, require glucose
by intestinal bacteria, and this definition
for energy. If inadequate ai11otmts of dietaty
more accmately assesses the potential
carbohydrates are available, the body will
benefits of fiber in the GI tract. Fem1entasynthesize glucose from glucogenic ainino tion of fiber produces the short-chain fatty
acids and glycerol. Cats n01mally use
acids acetate, propionate, and butY)·ate.

glucogenic an1ino acids and glycerol to

Short-chain fatty acids have nwnerous
synthesize glucose, which is one reason
benefits, including supplying energy to the
why cats are classified as true carnivores.

large-intestinal epithelial cells, stimulating

However, dogs usually synthesize glucose
intestinal sodiwn and water absorption, and

2370

NUTRITION: SMALL ANIMALS
lowe1ing the pH in the large intestines-an
fiber, which is what is listed on pet food
environment that favors survival of benefilabels, quantifies insoluble dietary fiber, cial bacte1ia in the GI tract.

which is primarily cellulose, some ligni.n,

Conversely, fermentation also produces
and a small amount of hemicellulose.

less desirable substances such as gases

However, it does not measure a large

VetBooks.ir
anunonia, and phenols. Highly fem1en�ble
portion of insoluble dietary fiber, nor any of
fibers are rapidly metabolized by intestinal
the soluble dietary fiber. Therefore, crude
bacteria and produce large amounts of gas
fiber is not an accurate measure of total
that can result in cramping and diarrhea.

dietary fiber. The physiologic effects of fiber

Production of less desirable fermentation
are not wli.form across all fiber types, and
products can be minimized by using a
relymg solely on fiber content listed on pet
moderately fem1entable fiber source·
food labels does not accurately reflect
examples include beet pulp, inulin, ru\d
either fiber content and fiber types in
psyllium. Beet pulp provides good fecal
commercial pet foods, or the physiologic
quality in dogs without affecting other
effects from a diet.

nutrient digestibility when included at
s7.5% ( dry-matter basis).

Dietary ferrnentable fiber also functions

Vitamins: Most commercial dog and cat
as a prebiotic in dogs and cats. Prebiotics
foods are fortified with vitamins to levels
are defined as nondigestible food ingredithat exceed minin1al requirements. There is ents that selectively stimulate the growth
no AAFCO dietary requirement for vitamin
or activity of beneficial bacteria in the

C for dogs and cats, because they are able to
intestines, such as Bijidobacterium and
synthesize it in the liver. Although dogs and

Lactobacillus. They also inhibit the survival cats can synthesize vitan1in C in levels
and colonization of pathogenic bacteria.

sufficient to prevent signs of deficiency,

The beneficial bacteria produce short-chain
supplementation may provide additional
fatty acids and some nutrients ( eg, some B
health benefits because vitanli.n C functions
vitamins and vitanli.n K). Beneficial bacteria
as a free radical scavenger and an antioxialso function as inlrnw10modulators and dant in the body.

reduce liver toxins ( eg, blood anline and

There is also no AAFCO dietaly
ammonia).

requirement for vita111i.n K for dogs and cats,

Dietary fructooligosaccharides (FOS)

because intestinal bacteria are able to
and marmanoligosaccharides (MOS) also
synthesize it. However, any condition that
promote the survival and growth of
alters the intestinal nli.croflora, such as
beneficial bacteria in the GI tract. FOS are
antibiotic therapy, may result in vitanli.n K
nondigestible oligosaccharides consisting
deficiency. As a result, NRC rec0111.111ends of chams of fructose molecules. Dietary
vitaimn Kat 0.33 mg/1,000 kcal ME in
sources of FOS include beet pulp, psyllium,
puppies, at 0.45 mg/1,000 kcal ME in adult
and chicory. Beneficial bacteria are able to
dogs, and at 0.25 mg/1,000 kcal ME in
use FOS as a metabolic fuel, whereas
kittens and adult cats.

pathogenic bacteria cannot. FOS also

Deficiencies of fat-soluble vitamins (A, D,
enhance the effectiveness of the GI inlrnune
and E m dogs; A, D, E, and Kin cats) and
system. MOS are sinli.Iar to FOS, except the
some of the 11 water-soluble B-complex
predominant sugar molecule in MOS is
vitanli.ns have been produced experimenmannose instead of fructose. Dietary tally. Water-soluble vitamins are usually
sources of MOS include natural fibers found
readily excreted if excess amounts are
in yeast cells. MOS use a different mechaconsumed and are thought to be far less nism than FOS to inhibit the growth of
likely to cause toxicity or adverse effects
harmful bacteria. Pathogenic bacteria
when ingested in mega.doses. Vitanli.n B12 is
attach to the intestinal wall using finger-like
the only water-soluble vitainin stored in the
projections called fin1briae. Fimbriae bind
liver, and dogs may have a 2- to 5 -yr depot.

to specific mannose residues on intestinal

Fat-soluble vitanli.ns ( except for vitamin K
cells. Fimb1iated mannose-specific
in cats) are stored to an appreciable extent
pathogens can also bind to MOS instead of
in the body, and when vitanli.ns A and D are
adl1ering to the intestinal epithelium, and
ingested in large amounts (10-100 times
harmful bacte1ia are then excreted in the
daily requirement) throughout a period of
feces.

months, toxic reactions may be seen. Only

Several chemical methods are used to
clinically relevant vitan1in-related in1baldetermine the fiber level of a food· all ances are descrihecl below.

extract the components of fiber t� different

Vitamin A: Excessive consun1ption of
degrees, which results in different estimates liver can lead to hypervitanli.nosis A and of fiber level for the same feedstuff. Crude
may produce skeletal lesions, including

NUTRITION: SMALL ANIMALS

2371
deforming cervical spondylosis, ankylosis
been reported in kittens fed diets deficient
of vertebrae and large joints, osseocartilain vitamin D, even though dietary amounts genous hyperplasia, osteoporosis, inhibited
of calciwn and phosphorus were normal. In
collagen synthesis, decreased chrondrogenrickets, serum calcium and phosphorus are esis in growth plates of growing dogs, and
decreased or low nom1al with a correspondnarrowed intervertebral foramina.

ing high parathyroid hormone level; bone

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Unlike most other mammals, cats cannot
mineralization is decreased, and tl1e
convert 13-carotene to vitamin A, because
metaphyseal areas are enlarged. Osteomalathey lack the intestinal dioxygenase enzyme cia rarely causes clinical signs in dogs or
necessary for 13-carotene cleavage.

cats. Hypervitaminosis D causes hypercal

Therefore, cats require a preformed source
cemia and hyperphosphatemia with
in their diet, such as that supplied by liver,
irreversible soft-tissue calcification of the
fish liver oils, or synthetic vitamin A.

kidney tubules, heart valves, and large

Signs of a vitamin A deficiency in cats are
vessel walls. Death in dogs is either related
similar to those in other species, except that
to chronic renal failure or acutely due to a
classic xerophthalrnia, follicular hyperkeramassive aortic rupture. Death in cats is tosis, and retinal degeneration are rarely
related to chronic renal failure.

seen and usually are associated with
concomitant protein deficiency. Nonethe

Vitamin E: In cats, steatitis results from a
less, cats fed diets deficient in vitamin A
diet high in PUFA, particularly from marine
exhibited cortjunctivitis, xerosis with
fish oils when these are not protected with
keratitis and corneal vascularization, retinal
added antioxidants. Kittens or adult cats
degeneration, photophobia, and slowed
develop anorexia and muscular degenerapupillary response to light. Certain of these tion; depot fat becomes discolored by brown
alterations also result from the retinal
or orange ceroid pigments. Lesions are seen
degeneration that is seen in taurine
in cardiac and skeletal muscles and are
deprivation.

sinlilar to tl1ose described in otl1er species.

Hypovitaminosis A in cats may exhaust

Thiamine: Thiamine deficiency generally
vitamin A reserves of the kidneys and liver;
does not develop in cats fed properly
affect reproduction to cause stillbirths,
prepared, conunercial, complete, and
congenital anomalies (hydrocephaly,
balanced diets. Thian1inase, which tends to
blindness, hairlessness, deafness, ataxia,
be high in uncooked freshwater fish, can
cerebellar dysplasia, intestinal hernia), and
produce a deficiency by rapid destruction
resorption of fetuses; and cause the same
of dietary thian1ine. Although canned
changes in epithelial cells noted in other
conu11ercial cat foods may contain fish, the
anin1als. Squamous metaplasia of tl1e
heat associated with canning is sufficient to
respiratory tract, cortjunctiva, endomedestroy thiaminase. Destruction of thiamine trium, and salivary glands has been noted.

has also resulted from treatment of food

Changes such as subpleural cysts lined by
with sulfur di.oxide or overheating during
keratinizing squamous epithelium and
drying or canning, but deficiencies are now
extensive infectious sequelae are frequent
rare.

in tl1e lungs and are occasionally noted in

Thiamine-deficient cats develop anorexia,
the cortjunctiva and salivary glands. Focal
an unkempt coat, a hunched position, and
dysplasia of pancreatic acinar tissue and
with time, convulsions that become more
marked hypoplasia of seminiferous tubules,
severe, leading later to prostration and
depletion of adrenal lipid, and focal atrophy
death. At necropsy, small petechiae may
of the skin have been reported. Borderline
be found in the cerebrum and rnidbrain.

deficiency is more common, especially in

Diagnosis can be confirmed in the early
chronic ill health.

stages by giving 100----250 mg thian1ine, PO

Rctinol at 9,000 IU/kg of diet should meet
or IM, bid for several days. Recovery occurs
dietary needs for vitamin A dwing gestation
in minutes to hours but, if the diet is not
and lactation and exceed the needs of
supplemented after this treatment, relapse
growing kittens. See TABLES 58, 61, and 62 for can be expected. Thiamine deficiency may
dietary levels of vitamin A and otl1er nutrients cause a n wnber of other neurologic reconunended by AAFCO and NRC.

disorders, including impairment of
labyrinthine 1ighting reactions, seen as head

Vitamin D: Vitan1in D deficiency results
ventroflexion and loss of tl1e ability to
in rickets in young anin1als and osteomalamaintain equilibrium when moving or cia in adult anin1als. Classic signs of rickets
jumping; in1pairment of the pupillary light
are rare in puppies and kittens and most
reflex; and dysfunction of the cerebellum,
often are seen when homemade diets are
suggested by asynergia, ataxia, and
fed without supplementation. Rickets has
dysmetria.

2372

NUTRITION: SMALL ANIMALS

Minerals: Minerals can be classified into

Excess intakes of calcium are more
three major categories: macrominerals
problematic for growing ( weaning to 1 yr)

(sodium, potassium, calcium, phosphorns,
lai·ge- and giant-breed dogs. Excessive
magnesium) required in gram amounts/day,
supplementation (>3% calciun1 [ dry-matter

VetBooks.ir
trace minerals of known importance (iron,
basis]) causes more severe signs of
zinc, copper, iodine, fluorine, selenium,
osteochondrosis and decreased skeletal
chromium) required in mg or mcg amounts/
remodeling in young, rapidly growing
day, and other trace ntinerals important in
large-breed dogs thai1 in dogs fed diets with
laboratory animals but that have an unclear
lower dietaiy calciwn (1 o/o--3"A, [ dry-matter role in companion anin1al nut1ition ( cobalt,
basis]). The clinical signs of lai11eness, pain,
molybdemun, cadmiun1, arsenic, silicon,
and decreased mobility have not been
vanadium, nickel, lead, tin). A balanced
reported in small-breed dogs or more slowly
amount of the necessary dietary minerals in
growing breeds fen the higher calciwn
relation to the energy density of the diet is
an1ow1ts.

in1portant. As intake of a mineral exceeds

Magnesium is ai1 essential cofactor of
the requirement, an excessive amount may
mai1y intercellular metabolic enzyme
be absorbed, or a large amount of the
pathways ai1d is rarely deficient in complete
unabsorbed mineral may prevent intestinal
ai1d balanced diets. However, when calciun1
absorption of other minerals in adequate
or phosphorns supplementation is
amounts. Indiscriminate mineral suppleexcessive, insoluble and indigestible mentation should be avoided because of the
mineral complexes form within the intestine
likelihood of causing a mineral imbalance.

and may decrease magnesium absorption.

Mineral deficiency is rare in well-bal

Clinical signs of magnesi1-m1 deficiency in
a.nced diets. Manipulation of dietary intake
puppies are depression, lethargy, ai1d
of calcium, phosphorns, sodiun1, magnemuscle weakness. Excessive magnesiwn sium (dogs and cats), and copper (dogs)

is excreted in the wine. In cats, there is
for therapeutic effect is common. Limited
evidence that magnesium concentrations
evidence exists for the recommendations

>0.3% (dry-matter basis) may be detrimental
of dietary mineral requirements for cats in
if the diet is too alkaline.

TABLES 61 and 62; many are based on the
mineral content of successfully fed diets.

Trace Minerals: Iodine deficiency is rai·e
when complete and balanced diets are fed

Macrominerals: Calcium and phosphobut may be seen when high-meat diets ai·e rns deficiencies are uncommon in wellused (dogs and cats) or when diets contain balanced growth diets. Exceptions may
saltwater fish (cats). Kittens with iodine
include high-meat diets high in phosphorns
deficiency show signs of hyperthyroidism in
and low in calciwn and diets high in
the ,"rly stages, with increased excitability,
phytates, which inhibit absorption of trace
followed later by hypoth r
y oidism and
minerals. In dogs and cats, the requirements
lethai·gy. Abnormal calcium metabolism,
for dietary calciun1 and phosphorus are
alopecia, and fetal resorption have been
increased over maintenance during growth,
reported. The condition can be confirmed
pregnancy, and lactation. In dogs, the
by thyroid size (>12 mg/100 g body wt) ai1d
optimal calcium:phosphorus ratio should
histopathology at necropsy. The cause of
be -1.2-1.4: l; however, minimun1 and
hyperthyroidism that develops in older
maximum ratios by AAFCO are 1:1 to 2.1:1.

cats with increased blood thyroxine and

Less phosphorns is absorbed at the higher
triiodothyronine is unknown.

ratios, so an approp1iate balance of these

Iron and copper found in most meats are
two minerals is necessary. Also, insufficient
used efficiently, ai1d nutritional deficiencies
supplies of calciwn or excess phosphorus
ai·e rare except in anin1als fed a diet
decrease calciun1 absorption and result in
composed almost entirely of milk or
initability, hyperesthesia, and loss of muscle vegetables. Deficiency of iron or copper is tone, with temporary or permanent
mai·ked by a microcytic, hypochromic
paralysis associated with nutritional
anemia and, often, by a reddish tinge to
secondaiy hyperpai·athyroidism. Skeletal
the hair in a white-haired animal.

demineralization, paiuculai·ly of the pelvis

Deficiency of zinc results in emesis,
and vertebral bodies, develops with calciun1
keratitis, achromotrichia, retarded growth,
deficiency. By the time there is a pathologic
and emaciation. Decreased zinc availability
fracture and the condition can be confirmed
has been noted in canine diets containing
radiographically, hone demineralization is
excessive levels of phytate, which
severe. Often, there is a history of feeding a
emphasizes the value of feeding trial tests
diet composed almost entirely of meat, liver, over laborat01y nutrient analyses of pet fish, or poultry.

foods.

NUTRITION SMALL ANIMALS

2373

Manganese toxicity has been reported to
very different proxinlate analyses. A
produce albinism in some Siamese cats; a
guaranteed analysis for protein may list a
deficiency of manganese in other species
minimal level of25%, while the product may
results in bone dyscrasia.

(and usually does) contain >25%. A certain
vaiiance above or below a minimum or

VetBooks.ir

DOG AND CAT FOODS
maxinuun should be expected. Consequently, whenever possible, the mai1ufac

Pet Food Labels
turer's average nutrient profile should be

Current regulations require that all labels of
used to evaluate a food.

pet foods manufactured and sold in the USA

Direct product comparisons made
must contain the following items: 1) product between like ( similai· water content) nan1e, 2) net weight of the product, 3) name
products (ie, dry vs dry, or cairned vs
and address of the manufacturer, 4) guarcarmecl) ai·e generally valid. However, anteed analysis, 5) list of ingredients,
comparisons across different food types

6) the words "dog or cat food" (intended
should be made on a cl1y-matter or caloric
animal species), 7) statement of nutritional
basis. As a general rule, dry-food analyses
adequacy, and 8) feeding guidelines. The
can be conve1ted to a dry-matter basis by

AAFCO has also adopted an amendment
simply adding 10% to the as-is value,
that will require all pet food labels to
because most diy foods contain -10016 water
contain information on the calorie content

( eg, a dry-food protein content of 25% on ai1
of the diet, expressed both in kcal ME/kg
as-fed basis is equal to 27.5% d1y-matter
and per fanli.liar household unit ( eg, cups,
basis). Cairned food analyses can be
cans).

conve1ted to a d1y-matter basis by simply

The product name is the primary means
multiplying by 4, because most carmed
by which a specific pet food is identified.

foods contain -75% water (ie, a canned-food

The way ingredients are listed in the
protein content of 6% on an as-feel basis is
product name may also indicate the
equal to 24% dry-matter basis). Alternapercentage of that ingredient present in the tively, the approximate percent d1y matter
product, eg, using the tem1 "beef' in the
of a nutrient in a product can be calculated
product nan1e requires that beef ingreclients
from tl1e infonnation in the guai·anteed
must be at least 700;6 of the total product or
analysis. First, dry matter in t11e diet is

�95% of the total weight of all ingredients,
calculated by subtracting the moisture level
excluding water. Using the tem1 "beef
from 100%. Next, the percent of the nutrient
dinner," "beef en tree," or "beef platter," etc, of interest on a dry-matter basis is
implies that beef must be at least 10016 of the
calculated using the following equation:

total product, and at least 25% but not more

(% nutrient [as fed],% dry matter in diet) x
than 95% of the total weight of all ingredi100 = -% of nutrient ( dry matter) ents, excluding water. Using the term "with
beef' means at least 3% of the total product

Ingredient List: 1n the USA, all pet foods
must be beef, and using the tenn "beef
sold must be registered witl1 state feed
flavor" in1plies that there is only enough
control officials and must contain approved
beef in the product to be detected by taste
ingredients generally regai·ded as safe,

(<3%).

unless they are for specialized purposes

The product weight must be listed on the
such as the amelioration or prevention of
front of the pet food label within the bottom
disease. Such foods are considered to be
third of the principal display panel.

drugs and must be approved by the FDA.

Ingredients ai·e listed in descending order

Guaranteed Analysis: This part of the
of weight, on an as-fed basis, in the food.

label lists the minin1al amounts of crude

Although a food ingredient (eg, chicken)

protein and crude fat and the maximal
may be listed first, if that ingredient is 75%
amounts of water and crude fiber on an
moisture, it will contribute a much smaller
as-fed (not dry-matter) basis. This analysis
percentage of total nutrients to the food dry
does not specify the actual an1ount of
matter. 1n addition, an ingredient such as
protein, fat, water, and fiber in the product.

corn may be listed by individual types, eg,
lnstead, it indicates the legal minimums of
flaked com, ground com, screened com,
protein and fat and the legal maximums of
kibbled com, etc. In this case, the total corn
water and crude fiber content contained in
amount may be a significant an10unt of the
the product. A laborato1y proximate
total food dry matter, but when presented as
analysis lists the actual nutrient concentraindividual types, each type appeai-s lower tions in the food, and two foods that have
on the ingredient list. This is referred to as
identical guaranteed analyses may have
ingredient splitting.

2374

NUTRITION: SMALL ANIMALS

No reference to quality or grade of an
the direction of a veterinarian) a.re
ingredient is allowed to be listed; therefore, exempted from AAFCO testing.

it is difficult to evaluate a product solely on
the basis of the ingredient list. The value

Feeding Guidelines: These must be
of this list is limited to determining the
expressed in common tem1s, such as "feed

VetBooks.ir
sources of the proteins and carbohydrates

(weight/unit of product) per body wt of dog
for dogs or cats. This kind of information is
or cat." They a.re general recommendations
useful when evaluating animals experiencat best, and body weight and body condition ing an adverse reaction to a food, possibly
must be monitored to prevent over- or
due to an allergy or intolerance to one or
underfeeding.

more ingredient sources such as beef,
wheat, etc.

Product formulations can be either fixed

Pet Food Product Types
or open. In a fixed formula, combinations

Conunercial dog and cat foods a.re available
of ingredients and nutrient profiles do not
in three principal fonns: canned, dry, and
change regardless of fluctuating market
semin1oist. The classifications used depend
prices of the ingredients. In an open
on the processing method and water
formula, ingredients, and possibly actual
content more than on the ingredient content
nutrient profiles, change depending on
or nutrient profile. Complete and balanced
availability and market prices. Most
commercial dog and cat diets a.re fomlllcommercial complete and balanced lated to provide adequate quantities of ea.ch
diets have a fixed fom1ula.tion.

required nutrient without an intolerable
excess of any nutrient. Supplementation

Statement of Nutritional Adequacy:

of particular nutrients to conunercially

This statement indicates how the food was
produced complete and balanced dog and
tested (feeding versus laboratory analysis
cat foods should be done carefully and only
or fonnula.tion) and for which life stage the
with a.pprop1iatejustifica.tion. Dog foods
food is intended. AAFCO recognizes only
a.re not satisfactory for ca.ts because most
fow- life stages: growth, maintenance,
dog foods a.re lower in protein, often do not
gestation, and lactation. The tem1 "all life
contain assw-ed concentrations of tallline,
stages" is frequently used on a label and
and a.re not designed to produce a. mina.ry
indicates that the product has been either
pH of <6.5 (which helps prevent the
formulated or tested for growth. By default,
crystallization of struvite or ma.gnesiumit is anticipated that such a food would also a.11unonilllll-phospha.te in the feline urina.i-y
pass a maintenance protocol, because
tract. (See also FELINE WWER URINARY TRACT
testing a food for growth generally includes

DISEASE, p 2383.)

gestation and lactation. There a.re no

AAFCO-a.pproved nutrient profiles for

Dry Food: This is the most popular
ge1ia.t1ic, senior, or weight loss stages.

category of pet food in the USA and some

The statement "complete and balanced"

other countries. Dry foods generally contain
indicates the product contains all nutrients

-900Ai dry matter and 1 O"Ai water. Approxipresently known to be required by dogs or mately 95% of dry dog and cat foods a.re
ca.ts and that these nutrients a.re properly
extruded, ie, they a.re ma.de by combining
balanced to the energy density of the diet.

a.11d cooking ingredients (grains, meat and

The "complete and balanced" clainl must be meat byproducts, fa.ts, minerals, and
substantiated by successfully completing
vita.inins), then forcing the mixture through

AAFCO feeding trials, or the food must
a die. During cooking and extrusion, a
contain at least the minimal a.mount of ea.ch
temperatw-e of -150°C ( -302°F) converts
nutrient recommended by AAFCO. There
the starches into a fonn more easily
a.re cautions "against the use of these
digested, destroys toxins and inhibitory
requirements Oevels) without demonstrasubstances, and flash ste1ilizes the product.

tion of nutrient availability" because some

The food is then enrobed with fat and/or
of the requirements a.re based on studies
digest (material derived from controlled
in which the nutrients were supplied as
degradation of a.Ilimal tissues, eg, chicken
plllified ingredients and, therefore, a.re
digest) during d!-ying to increase
not representative of ingredients used in
palatability.

commercial pet foods. Laboratory analysis

Advantages of dry food include a lower
does not address the issue of bioa.vaila.bility.

cost than canned or soft-moist food, and

Supplements, snacks, treat products (ie,
refrigeration of unused portions is not
those intended for intennittent or suppleneeded. Certain types of dry food may also mental feeding), and therapeutic or dietary
provide beneficial massage of the teeth and
products (ie, those intended for use under
gums to help decrease pe1iodontal disease

NUTRITION: SMALL ANIMALS

2375

(although unless specifically fonnulated to
consistency, higher cost, and the difficulty
deter it, remain mainly ineffective in dogs
in fom1ulating ru1d preprui.ng a nutritionally
for this purpose).

complete and balanced diet. It is most
difficult to fornrnlate a nutritionally

Canned Food: Canned dog and cat foods
complete and balanced diet with sufficient
contain 68%--- 78% water and 22o/<r-32% dry
nuttient density in a small volume of food

VetBooks.ir
matter. Many of the same ingredients are
that is palatable for cats. Many homeused in canned pet foods as in dry-extruded cooked diets result in foods that are high in
types but usually not at the san1e levels of
protein and caloric density and have
inclusion. Given their high moisture
inappropriate calciurn:phosphorus ratios
content, canned foods typically contain
and inadequate levels of calciw11, copper,
higher amounts of fresh or frozen meat,
iodine, fat-soluble vitrunins, and several of
poultry, or fish products and animal
the B vitan1ins. Many published recipes for
byproducts. Many cairned pet foods contain
feline diets have very high ash or mineral
textmed proteins derived from grains, such
levels because of the extent of synthetic
as wheat or soy. These materials function as
nutrient supplementation required. If
meat a11alogues, having a physical structme
owners choose to feed a home-cooked diet,
similar to that of meat and high nuttitional
they should use a recipe fonn u lated by a
quality. The use of meat in combination with veterinary nutritionist (vs found on the some of the textmed proteins not only

Internet). It is also important to realize iliat
controls costs but can in1prove the overall
no home-cooked diets have undergone the
nutritional profile of the final product.

testing and research used to formulate

Canned pet food processing begins with
complete a11d balanced commercial pet
blending meat or meat analogues and fat
foods.

ingredients with water and dry ingredients,
such as vitan1ins and n1inerals, for proper

Raw Meat-based Diets: Raw meat-nutt·ient content. The mixture is blended based diets have received a lot of attention
and sometimes ground to produce a fine
in recent years. The controversy, lack of
slurry, depending on product profile. After
good data, and paucity of high-quality
cans are filled, they are sealed and retorted
research make it difficult for vete1i.nruians

(a heat and pressure-cooking process that
to make infonned recommendations to pet
also sterilizes the contents), assuring
owners regarding this feeding practice.

destruction of foodborne pathogens.

However, the America11 Animal Hospital

Advantages of canned food include a long

Association, the American Veterinary
shelf life in a durable container and high

Medical Association, ru1d the Canadian
palatability. However, canned food is more

Veterinruy Medicial Association have all
expensive than dry food.

developed statements discouraging the
feeding of raw or undercooked animal

Soft-moist Food: Soft-moist dog and cat
source protein to dogs and cats. In addition,
foods contain 25%-409(, water and 600/o-75%
in 2010, the Delta Society's Pet Partners
dry matter. They do not require refrigeration

Progrrun initiated a policy precluding
and are preserved using hurnectants-subanimals eating raw meat-based diets from stances that bind water so tlrnt it is
participating in the Therapy Animal
unavailable for bacteria and mold growtl1

Progran1.

and assure shelf life. They include simple

There are two main types of raw meat-sugars (usually sucrose), sorbitol, based diets: home-prepared and commercial.

propylene glycol, and salts. Many soft-moist

In addition, a variety of raw dried or
foods ru·e acidifled using phosphoric, malic,
freeze-dried pet treats fall under this
or hydrochloric acid to fwther retard
category. Home-prepared diets include a
spoilage. Advantages of soft-moist foods
variety of feeding regimens, including BARF
include convenience, high energy digestibil

(Bone and Raw Food or Biologically
ity, and palatability. However, soft-moist

Appropriate Raw Food), the Ultimate Diet,
food is more expensive tl1an dry food.

and ilie Volhard Diet. Conm1ercial raw meat-based diets most conm1only are fresh, frozen, Home-cooked Diets: Dogs can be
pastewized, or freeze-dried. Some of these
successfully maintained on properly
commercial diets are fom1ulated to meet
fonnulated home-cooked diets; this is

AAFCO nutrient profiles, but many are not.

much more difficult in cats. Advantages of

One of the biggest areas of controversy
home-cooked diets include the use of fresh,
surrounding these types of diets are the
high-quality ingredients chosen by the
safety of iliese diets to not only ilie pets
owner. Disadvantages include preparation
consuming iliem, but to the pet owners and
time, variable quality control and diet
oiliers who are exposed to the animals

2376

NUTRITION: SMALL ANIMALS
consuming them. Even if owners purchase
and bones to dogs and cats is tile 1isk
meat meant for hmnan consumption to
associated witl1 esophageal and intestinal
produce home-prepared diets, there is no
foreign bodies and pe1foration. Feeding raw
assurance these ingredients are free of
bones has also been associated with slab
pathogens and safe to consume tmcooked.

fractures and other dental problems in dogs.

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Raw chicken is a conunon source of

Proponents of raw diets often cite that

Salmonella, and it is estimated that 21 o/o--44% raw meat-based diets are the evolutionary of chicken purchased from retail locations
diet of dogs and cats and that domestic dogs
meant for human consumption throughout
and cats have never evolved into being able

North Ame,ica is contanunated with
to digest and absorb commercial pet foods.

Salmonella. Even if a pet owner takes

However, a recent report shows that clogs
precautions while handling and preparing
have 36 regions of the genome that differ
these diets, it has been shown that after
from that of wolves, and 10 of these regions
consumption of a single meal contaminated
play a c1itical role in starch digestion and fat
with Salmonella, 44% of dogs shed
metabolism. Therefore, the genetic makeup

Salmonella in their feces for as long as 7
of domestic dogs and cats is not the san1e as
days, and none of these clogs was symptothat of wolves. Proponents of raw diets also matic for Salmonella infection. Salmonella cite that cooking destroys essential enzymes
contanunation rates for beef and pork
needed for digestion. While a small amount
intended for hwnan consumption are
of protein is destroyed during cooking, and
estimated to range from 3.5%--4%; however,
enzymes are proteins, there is no evidence
beef and pork are a source of other potential
that aninlals or people require tl1ese
pathogens, including the pathogenic strain
exogenous sources of enzymes. In addition,
ofE coli 0157:H7. Campylobacle'l'Spp is many of these enzymes are destroyed in the
estimated to be present in 29"/o-7 4% of
highly acidic environment in tile stomach
chicken, and Listeria. spp is estimated to be and never reach tl1e small intestines, where
present in 15o/o-34% of chicken and 25o/o-52"Ai most nutJients are absorbed.

of beef and pork. In two separate studies,

Finally, veterinarians must also consider
conswnption of raw meat was shown to
the potential legal implications of recomsignificantly increase the seroprevalence mending raw meat-based diets. While
rate of To.xoplasma gondii in cats.

zoonotic risks can be associated with

Some commercial raw meat-based diets
feeding both commercial and home-preare frozen or freeze-dried; however, neitl1er pared diets, if a pet owner, for example,
freezing nor freeze-drying destroys all the
develops a Salmonella infection from
potential patl10gens in tl1ese products. Some feeding a contaminated commercial diet, conm1ercial raw meat-based diet manufacthe pet food manufacturer is generally at turers now use high-pressure pasteurization
risk of legal action. However, veterinarians
in an attempt to reduce tl1e 1isk of pathowho recommend home-prepared raw gens. Although tllis process can reduce the
meat-based diets are potentially liable if an
numbers of many patl10gens, it usually does
owner becomes sick from preparing these
not completely elinunate tl1em, and bacteria
diets or as a result of pets shedding
and viruses vary in tl1ei.r susceptibility to
pathogens in their feces.

tl1is process. Conrn1ercial pet foods have
also been recalled in recent years because

FEEDING PRACTICES
of contanunation from Salmonella;
however, considering the number of

Domestication and use of.dogs and cats as
commercially available pet food products,
companions may have modified eating
the percentage of products affected is
patterns of these animals to varying extents.

relatively small compared with the munber

Easier access to food and consistency of
of raw meat-based diets affected.

food quality has led to increased food

Another concern, particularly of
consw11ption and the possibility of
home-prepared raw meat-based diets, is
decreased energy expenditw·e overall.

nutrient imbalances. In a European study

Hence, there is greater 1isk of obesity. At the
that evaluated 95 homemade raw meatsan1e time, longevity of companion animals based diets being fed to dogs, 60% had major
has also increased and, along with it, the
nutritional imbalances. There have been a
emergence of other chro11ic progressive
number of case reports pertaining to the
diseases such as osteoarthritis, cancer, and
development of vitanun D--dependent 1ickets inunune and cognitive disorders. Healthy type I and nutritional secondary hyperparadogs and cats eat a variety of foods. During thyroidism associated with dogs being fed
a 24-hr period, most clogs will eat 1-3 meals,
raw meat-based diets. Other concerns
whereas most cats will eat frequent small
regarding the practice of feeding raw meat
meals, as many as 18 a day.

NUTRITION: SMALL ANIMALS

2377

Although odor, consistency, taste, and
warm water, and the food can be wai-rned to
learned dietary habits detemune which
release odors and fiavors that encourage
foods a dog will eat, most dogs are
consumption. Dry-matter digestibilities are
indiscriminate eaters. Finicky, begging dogs

600/er-900A, for dog food and 75o/er-900Ai for cat

VetBooks.ir
have learned such behaviors. Likewise,
food because of ingredient quality,
odor, consistency, taste, and learned dietary
crude-fiber content, processing, and level of
habits detennine which foods a cat prefers,
intake. Small, formed, brown feces suggest
but how much a cat will eat is affected by
high nutrient digestion and absorption,
factors such as noises, lights, food
while large volumes of pale feces indicate
containers, the presence or absence of
less dietary utilization.

people or other animals (including other
cats), physiologic state, and disease. Cats

Maintenance: After a dog has reached
can and will refuse to eat to the point of

-900Ai of its expected adult weight, a diet
starving themselves under stressful
less nutrient dense than the growth diet
conditions. These cats are at risk of
is recommended. The dietary goal is to
developing hepatic lipidosis, which can be
maintain optimal body weight and conclition
fatal if not treated early and aggressively.

for that particular dog. Some adult dogs can

Some dogs and cats have adequate
be fed free choice, but most catmot without
appetite controls and maintain an optimal
becoming obese. The best feeding regin1en
body condition, even with dietary changes.

to use in most adult dogs to prevent obesity

By contrast, other dogs and cats overeat,
is po1tion-controlled feeding, eg, feeding
consume excessive calo1ies, and become
two premeasured meals at regulai· times
obese. The thickness of the fat layer over
each day. Most dogs will eat all their food
the rib cage and pelvic bones is a good
immediately, but some dogs will graze
indicator of obesity, as is regular body
throughout the day.

condition scoring over time (see TABLES 55

Many owners feed treats and snacks,
and 56).

which are often ai1 important aspect of

Dietary modifications are required by
the hun1an-animal bond. Complete and
changes in life stage, environment, body
balanced treat products that use low-fat,
weight and condition, and disease. Energy
high-fiber ingredients are available.

density varies from 2,500 to >5,000 kcaVkg

However, most treats are not complete ai1d
dry matter for dog foods and from 3,000 to
balanced; therefore, to prevent nutrient

>5,000 kcaVkg dry matter for cat foods.

deficiencies, the total daily ainount of treats

Therefore, general feeding recommendashould be < 1 ()OA, of tl1e total caloric intake.

tions cannot be given for all dogs and cats

Nutritional supplements ai·e not required
on any particular food. Instead, feeding
and, in fact, may be hai-n1ful. In an animal
recommendations should be individualized.

prone to obesity, the caloric content of all

The best feeding method is one that
treats fed should be considered in an effort
maintains optimal body weight and
to match energy intake to expenditure.

condition, bearing in mind that disease

Regular assessment of the anin1al's body
conditions may require dietary changes.

condition helps ensure minimal weight gain

When a dietary change is necessary, it
beyond optimal adult values tiu·oughout life.

should not be done abruptly. New food

Most inactive, neutered adult cats can be
should be introduced gradually tJu·oughout
fed a reduced fat diet (9% dry-matter basis)

5-7 days. Also, it is better to offer slightly
ad lib, but increasing the insoluble fiber
less than the calculated new food amount.

content may be necessary in some animals

Overindulgence and abrupt changes are
to satisfy hunger. Cats exposed to vai"iations
frequently the inciting cause of GI disorders
in temperature ( eg, cats that remain
that may ultimately lead to diet refusal. In
outdoors yeai�round or at night) may eat
dogs, the new food should be introduced
more during the winter. The need for a
slowly by replacing 25% more of the old
different nutritional profile in older cats
food every day or two until the new diet
versus middle-aged cats may be necessary.

makes up the entire amount fed. Cats can

Middle-aged cats are at increased risk of
easily become habituated to a paiticular
developing obesity, whereas older cats
food and may resist any dietary change. In
often have a difficult time keeping weight
cats, new food should also be introduced
on. The ability of older cats to digest protein
slowly. Some cats have definitive preferat1d fat is often less than that of younger and ences for dry food, whereas others prefer
middle-aged cats. Therefore, it is important
the san1e food moistened or catmed.

to feed a diet witl1 highly digestible protein

If the dog or cat is to be switched from
and fat sources. The quantity of these
a catmed to a dry diet, it may be useful to
nutrients in the diet may also have to be
moisten the product by adding sufficient
modified ( usually increased) to compensate

2378

NUTRITION SMALL ANIMALS
for impaired protein and fat digestion.

of gestation, the total amount of food

However, depending on activity level
offered should be increased at least
feeding a food with a different fat and fiber

200/o-300/o over the amount for maintenance.

content (increased or decreased as needed)

Growth diets are often used during
may be reqmred to maintain optimal body
gestation because of their higher energy
weight and condition.

VetBooks.ir
density and smooth transition after
parturition to support lactation.

Growth and Reproduction in Dogs:

Growth, pregnancy, and lactation greatly

Lactation: Depending on litter size
increase nutrient demands over those of
lacta_ting bitches often require energy'levels
maintenance. Growth diets have increased

2-4 tl.l11es those of maintenance to avoid
nutrient density, digestibility, and bioavailexcessive loss of body condition. Ad lib ability to provide nutrients necessary in a
feeding using a complete and balanced
smaller volm11e of food. Supplementation of
growth diet containing 100/o--200/o fat
calcium, phosphorus, and vitamin D beyond

( dry-matter basis) that has passed an
amounts present in complete and balanced
approved AAFCO feeding trial is recomdiets designed for growth and reproduction is mended to maintain lactation and to permit rarely necessary and may be contraindicated.

optimal body weight and condition to be
required by weaning. If a bitch loses

. Growth: Overfeeding during growth
s
mcreases growth rate. This is not desirable

_ignificant body condition during lactat10n, the fat content of the diet should be because it is incompatible with proper
increased to 200/o--300/o fat ( dry-matter
skeletal development and also contributes
basis), and she should be fed ad lib.

to obesity later in life. Feeding methods for
growing puppies should be individualized
for the puppy and owner. General recom

Growth and Reproduction in Cats:

mendations are that puppies between

One of the most imp01tant differences
weaning and 6 mo of age should be fed three
between queens and bitches is that pregnant
times a day; puppies 6--12 mo old should be
queens exhibit a linear increase in weight
fed twice daily. Large- and giant-breed

(fetal growth) tl1roughout pregnancy. As a
puppies should be fed complete and
result, pregnant queens need to consume
balanced growth diets that have been tested
more calories almost immediately after
in feeding trials and that contain calcium
becoming pregnant. In contrast, fetal
fat, and protein at levels closer to the
growth is minimal during the first two
rninin1ums stated by AAFCO. Small-breed
trimesters of pregnancy in the bitch and
puppies may have to be fed more than three
caloric intake does not generally ha�e to be
times a day using a tested diet that contains
increased until sometime between the end
calcium, fat, and protein at levels greater
of the second trimester and the beginning
than the mininlums stated by AAFCO.

of the third trin1ester.

Only limited data have been published

Because queens tend to lose weight
with respect to breed growth curves.

during lactation regardless of diet fed, it

Nonetheless, a slow growth rate is
has been assun1ed that net tissue reserves
preferable to a fast growth rate. Weight
should increase somewhat in preparation
gams should be closely monitored (weekly), for lactation. A growth diet for kittens that and feeding recommendations adjusted
contains l OO/o-35% fat, 300/o-400/o protein, and
such that the puppy gains a small amount of
low ( <5%) fiber ( dry-matter basis) should
weight each week. When growing largebe fed. Growing kittens and pregnant and breed puppies were fed 50%-- 700/o of their
lactating queens can be fed ad lib or several
littermate's ad lib intake, adult height,
tin1es a day to meet tl1eir daily needs. During
length, and bone or muscle mass were not
the latter third of gestation, the ai11om1t of
stunted; only total body fat was affected. It
food and level of nutrient intake normally
is difficult to stunt the growth of a puppy
increases an average of25%, although
bemg fed a complete and balanced growth
energy intakes for cats during pregnancy
diet that has passed an approved AAFCO
have been estimated to be as much as 400/o
feeding trial using meal feeding of an
greater than for maintenance. Some queens
appropriate amount for 2--3 tin1es/day.

may eat less early in gestation and
immediately before parturition; such

Gestation: Feeding recommendations
changes are of concern only if prolonged.

for pregnant bitches through the first

Queens require 2--3 tin1es the normal food
two-thirds of gestation are the same as
intake during lactation, depending on litter
those for maintenance. A common mistake
size. Supplementing an already balanced
is to overfeed during early gestation and to
diet is not necessary and should be
underfeed during lactation. In the last third
discouraged.

NUTRITION: SMALL ANIMALS

2379

Geriatric Dogs and Cats: Older dogs
nutritional requirements of many sick dogs
and cats may not be as efficient in metaboand cats are qualitatively the same as those lizing dietary protein than younger animals.

of healthy ones; however, they differ in the

They may actually require more dietary
an10unts required-certain nutrients may
protein than their younger counterparts to
be needed in greater amounts or may need

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maintain protein reserves and maximize
to be restricted.

protein turnover rates. In addition,
decreased fat digestion occurs with age in

Adverse Reaction to Foods: Food
cats, so geriatric cats may actually require a
reactions are classified using specific
higher-fat diet than their younger counterterminology. An adverse reaction to a food parts. In contrast, some dogs and cats begin
is a clinically abnonnal response to any type
old age considerably overweight, whereas
of food ingested. Food intolerance is a type
others may show some loss of condition.

of adverse reaction that does not involve the

Feeding an appropriate food with a different irrun une system, eg, food poisoning. A food nutrient profile with respect to energy, fat,
allergy is a type of adverse reaction that
or fiber content (increased or decreased)

does involve the immune system, eg, colitis
may be needed to maintain optimal body
or atopic dennatitis. (See also FOOD ALLERGY, weight and condition. Geriatric dogs and
p 855, and LOCALIZED ANAPIIYLACTIC REAC.TIONS,
cats should be monitored in a preventive
p 824.)

health program that includes pe1iodic

Dogs and cats with food allergy usually
assessments of body weight and condition.

have GI signs ( eg, vomiting or diarrhea, or

The incidence of chronic degenerative
both) or a prwitic skin condition, especially
organ disease increases with age, and early
in the regions of the ea.rs, rear, and feet. The
diagnosis fosters earlier treatment and more prevalence of true food allergies is very effective nutritional management.

small. Some dogs and cats with nonseasonal
pruritus a.re having an adverse reaction to

Work or Stress: The caloric needs of
food. Unfortunately, food allergy cannot be
working or stressed dogs may exceed the
differentiated from food intolerance, and
levels of a maintenance diet, depending on
skin testing for food allergies is unreliable.

the animal and extent of work performed.

Blood tests a.re also an uru·eliable way to

Most diets designed for work or stress have
diagnose food allergies in dogs and cats.

increased levels of animal fats, with the

Hence, given all the possible etiologies and
other nutrients appropriately balanced to the limited diagnostics available, any animal increased energy density. At extreme levels
suspected of having an adverse reaction to
of stress ( eg, an Alaskan sled dog requiring
food should undergo a food trial. The length

10,000 kcaVday), many recommend not only
of time needed for a food trial depends on
increasing the percent ME from fat but also
the condition being managed. Food trials
from protein, while minimizing the
for adverse reactions to food associated
contiibution of carbohydrate.

with clinical signs involving the GI tract

Any dally feeding recommendation
should continue for ;,,2 wk, whereas food
should be considered an estimate or starting trials for clinical signs involving dermatopoint and should be modified based on logic conditions should continue for ?'cl0-12
continual evaluation of the dog's weight and
wk
condition, skin and coat, pe1iorrnance, and

Dw'ing a food trial, the only item fed
general attitude. Feeding a smaller a.mow1t
should be a diet containing a single novel
of the dally ration ( eg, 1/, of the dally
protein source or a hydrolyzed.protein diet.

an1ount) before beginning a work shift is

A careful dietary history must be obtained
recommended with the remainder being fed
from the pet owner before selecting the
thereafter. Plenty of fresh water should be
type of diet. If the owner elects to feed a
available, and opportunities to stop work
commercially prepared food, several
for a water break should be scheduled in
products a.re available for dogs that use
any dally work routine for these dogs.

single novel protein sources ( eg, kangaroo,
venison, rabbit, duck, or fish). Commercially available diets available for cats use NUTRITION IN DISEASE
protein sources consisting of rabbit, duck,

MANAGEMENT
venison, and lan1b. Fish is not a novel option
for most cats, and there is a possible, but yet

Nutrition is an inlporta.nt part of disease
unclear, relationship between adverse food
management, even though few disorders
reactions in cats fed fool.ls containing
can be cured solely with diet. The interacscombroid fish and histamine content. Most tion between illness, health, and nutritional
in1portantly, the fo1mulation of whatever
status is multifactorial and complex. The
product or diet ls fed must be fixed to

2380

NUTRITION: SMALL ANIMALS
ensure that the ingredient composition is
ingredients as pet foods and treats. Other
consistent from batch to batch. These
therapies such as hyposensitiza.tion and
products are more expensive not only
flea control are necessary in animals with
because of their unique and lin1ited sources
concurrent disease. Testing various suspect

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of protein but also because of the quality
ingredients by reintroducing them to the
control procedures required to enstu·e fixed
diet one at a tin1e followed by recurrence of
fom1Ulations and to eliminate cross-conclinical signs is affinnation of an adverse tamination with previous production
reaction to that ingredient. Dietary
batches of different foods.

ingredients reintroduced may reproduce

A newer alternative diet commercially
clinical signs as early as 12 lu· after ingestion
available for use in clogs and cats with
but can take as long as 10 clays. Lifelong
suspected adverse reactions to food is a
treatment is dietary avoidance, which may
hydrolyzed proLein diet. Protein is the most
be difficult if the offending ingredients are
common nutrient associated with adverse
not positively identified.

reactions to food, because it is needed to
btidge two IgE molecules together to cause
the release of histamine. The protein in

Anemia: Iron or copper deficiency ( or
hydrolyzed diets is broken down into
both) is the major ca.use of hypochromic,
smaller peptide fragments that are too sho1t
microcytic anemia. A folic acid and 812
to btidge two IgE molecules. Although these ( cobala.min) deficiency also produces diets are helpful in many dogs and cats with
anemia. Most commercial diets have more
adverse reactions to food, they a.re
than required an10unts of iron, copper, and
expensive, and some animals with allergies
vitan1ins; therefore, secondary ca.uses such

Lo the protein sources in these diets will still
as inadequate food intake, malabsorption,
react to the typical hydrolyzed protein diet.

hemorrhage, or heavy parasite infection

Therefore, a novel protein diet is often tried
should be investigated. Feeding an
first; if clinical signs do not resolve, then a
unbalanced homemade diet may also result
hydrolyzed protein diet can be used.

in anemia..

Simplified homemade diets are also

Rarely can severe iron deficiency be
possible using the same protein sources
corrected with diet alone, and feeding large
suggested above ( or other ingredient
quantities of liver in an attempt to correct
sources the owner wants to test). Homeiron deficiency is usually ineffective and can made diets actually allow for a wider
result in vitamin A toxicosis. Most animals
selection of source ingredients. Beef, wheat, require a supplemental source of iron adminand dairy products should be discouraged istered either PO or IM to correct severe iron
for use as a protein source in dogs, and
deficiency and, depending on the underlying
beef, fish, and da.i1y products should be
cause, may need to continue receiving a
discouraged for use in ca.ts, because a.nin1als supplemental source of iron indefinitely.

have likely been exposed to these sources

If the underlying cause of iron deficiency
if previously fed foods with an open
is related to hemorrhage, parasitism,
formulation. The basic recipe shopld closely constuning an unbalanced diet, or c011Sun1-resemble "complete and balanced," but
ing too little of a complete and balanced diet,
single somces of protein can be sequentially once the tmderlying ca.use is eliminated and tested and replaced. The owner is responsithe iron deficiency is corrected, longterm ble for quality control and consistency and
supplemental iron may not be necessary.

must be willing to make such a diet for �2

Folic acid and vita.min B12 are necessary
wk for GI conditions and �10-12 wk for
to support nmmal cell division, and
dermatologic conditions. On average, there
treatment for vitan1in B12 deficiency usually
is no price advantage in ma.king a homerequires parenteral administration of made diet over using commercially
vitamin B12• Vitan1in B12 deficiency develops
prepared foods. Formulating a homemade
most commonly from intestinal malabsorpdiet containing hydrolyzed protein is both tion; however, it can also result from
very difficult and expensive.

shmt-gut synclrome. Vila.min B12 absorption

The trial diet should be exclusively fed for in the GI tract is limited to the ilew11, and the recommended length of tin1e, and all
surgical removal of large portions of the
treats, snacks, and table foods eliminated
ileun1 may result in the need for lifelong
unless they are made of the exact same
parenteral B
ingredients as the trial diet or contain a

12 supplementation.

hydrolyzed protein source. All chewable

Anorexia: Partial anorexia is seen when
medications and supplements must be
the anin1al is eating some food but not
elin1inated from the trial diet, because most
enough to provide at least 30 kcal/kg body
contain the same protein and additive
wt in dogs and 40 kcal/kg body wt in cats.

NUTRITION: SMALL ANIMALS

2381

Complete anorexia occms when the animal
reasonably manage and the animal can
does not consume any food for -3 days.

tolerate.

Anorexia (partial or complete) accompa

It is advisable to take a stepwise approach
nies many underlying disorders, including
to reintroduction of calories, and multiple

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drug reactions or reactions to environmensmall meals are often tolerated better than tal changes. Pain may also be a significant
large meals. Vomiting, diarrhea, or refeeding
contributor to anorexia, and in most cases
syndrome can be a consequence of being
when the pain is adequately cont.rolled, the
too aggressive with reintroduction of
anorexia resolves. Learned food aversions
calories. The size of the tube determines
may also contribute to anorexia. This
what dietary options can be used. Sizes 5 or
occurs most commonly when animals are

8 French tubes usually limit feeding to liquid
started on a therapeutic diet while they are
enteral diets. Larger esophagostomy or
ill, eg, offering a therapeutic diet to manage
gastrostomy tubes can also accommodate
renal failure while the animal is still in a
critical care diets and blenderized
uremic crisis. Food aversions can also occur therapeutic diets. If use of a feeding tube is as a result of force-feeding. Obviously,
contraindicated or a tube caimot be placed,
therapeutic diets do not help if they are not
dogs and cats can be maintained by IV
consumed. Eating some of a diet that is less
solutions that provide adequate calories,
than optimal is better than none of the
protein, electrolytes, B vitainins, ai1d

"right" one. Asstm1ing that an animal will selected trace minerals until access to the
eat a therapeutic diet when it gets hungry
small intestine is possible. Unfo1tunately,
enough is inappropriate, and allowing an
the parenteral route is more expensive and
animal to starve in an attempt to stimulate
is associated with a higher incidence of
its appetite is never recommended. If a
complications, including catheter problems,
particular diet is refused, an altemative(s)

infection, and electrolyte abnormalities.

should be tried until one that the animal will
eat is identified. Anorectic dogs and cats can Cachexia: Cachexia is most commonly sometimes be persuaded to eat by adding
associated with cases of neoplasia or
highly flavored substances to the diet ( eg,
chronic renal or cardiac disease. Cachexia
animal fat, meat dtippings, fish [fish juices
appears to be a response to increased
or oils for cats]) or by hand-feeding. If these
catabolism with either normal or decreased
are not successful, nutritional support
appetite. The deterioration of the animal's
intervention may be necessary.

condition clearly indicates that nutritional

Nutritional support can be provided by
requirements are not being met, and the
either enteral or parenteral routes. Unless
dietary goal is to increase the caloric density
there is a contraindication to using the gut,
ai1d palatability of the food while meeting
enteral support is usually preferred over
the animal's requirements for protein and
parenteral support. Enteral support is more
other nutrients. The usual management of
physiologic, cheaper, and safer than
cachexia is to feed smaller an1ounts of a
parenteral support. In addition, more
more calorically dense (ie, higher fat
dietary options are available for enteral
content), complete and balanced diet more
support than for parenteral support.

frequently (3-6 meals/day). The form of

Many options for feeding tubes are
food ( dry or carmed) that the dog or cat
available, including esophagostomy tubes,
prefers should be feel. Tube feeding and
nasogastric or nasoesophageal tubes,
partial or complete parenteral nutritional
gastrnstomy tubes, and jejunostomy tubes.

support ( see above) should also be

Both esophagostomy tubes and nasogastric
considered if the dog or cat continues
or nasoesophageal tubes can be placed
to lose weight and condition.

without the need for any specialized
equipment. Nasogastric tubes are used

Diarrhea: Diarrhea can result from
more commonly for short durations (1-7
numerous GI diseases and can also occur
days) or when sedation or anesthesia are
secondary to disease outside the GI tract.

contraindicated. Esophagostomy tubes and

Primary causes of GI disease are numerous
gastric tubes are more commonly used
ai1d include adverse reaction to food,
when nutritional support is required for
infections (bacterial, parasitic, fungal,
longer dmations (weeks or months). Dogs
and viral), inflainmatory bowel disease,
and cats can be maintained at home with
neoplasia, and toxin- or drug-induced.

tube feedings ( except in the case of

Certain breeds of dogs are predisposed
jejunostomy tubes) after the procedure
to GI disease. German Shepherds are at
has been accepted by the animal and fully
increased risk of developing antibioticexplained to the owner and if the frequency responsive diarrhea (fonnerly known as
of feeding is something the owner can
small-intestinal bacterial overgrowth),

2382

NUTRITION SMALL ANIMALS

CHARACTERISTICS OF SMALL-BOWEL AND LARGE-BOWEL

DIARRHEA

Characteristics

Small Bowel

Large Bowel

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Blood in feces

Melena

Hematochezia

Fecal quality

Loose, watery "cow-pie"

Loose to semifonned

Fecal volume

Large quantities

Small quantities

Frequency of

Normal to increased

Increased
defecation

Mucus in feces

Absent

Usually present

Tenesmus

Absent

Usually present

Urgency

Absent

Usually present

Weight loss

May be present

Rare

Doberman Pinschers and Rottweilers are at
digestible balanced diet containing
increased risk of pa.ivoviral enteritis, and
prebiotics in cats. Constipated ca.ts tend to

Yorkshire Terriers a.i·e at increased risk of
do poorly on diets supplemented with
lymphangiectasia.

insoluble fiber. Animals should be fed 2-4

Clinical signs associated with diarrhea
ti.mes/day. In dogs, adding ca.imed pwnpkin
a.i·e different in small-bowel versus
or psylliwn to the diet is also sometimes
la.i·ge-bowel diarrhea (see TABLE 64). Dietary effective in mild cases of constipation.

recommendations may vary depending on
where the diarrhea is localized and the

Congestive Heart Failure (CHF): One
underlying cause.

objective in managing CHF is to reduce water

Animals with small-bowel diarrhea
retention; restricting sodiwn intake and
usually benefit from a highly digestible diet,
lowering sodiwn levels encow·age diw-esis.

whereas those with large-bowel diarrhea

Typical commercial dog wd cat foods have a
often benefit from prebiotics (seep 2369).

sodiwn content of 0.45%--0.9"A, ( 450-900 mg

Small, frequent meals (3-6/day) should be
sodiwn/100 g diet dry matter). Dieta.iy
offered. Probiotics are an additional tool
sodiwn restriction is classified as mild ( 400
available for management of small- or
mg sodium/100 g diet dry matter) to severe
la.i·ge-bowel diarrhea. Probiotics are defined

(240 mg sodimn/100 g diet city matter). In
as nutritional supplements containing live,
view of these values, commercial dog and
viable, beneficial bacteria in. sufficient
cat diets ca.J111ot even be classified as mild
nwnbers to provide a health benefit. Not all
sodiwn restriction. Therefore, commercially
probiotics a.i·e created equal-a probiotic
prepa.i·ed low-sodiwn diets or recipes that
effective in one species may be ineffective
use low-sodiwn foods must be substituted.

in another. Probiotic bacteria provide many

Sodium restriction often requires a special
of the san1e benefits to the host as prebiotdiet, although some manufactw-ers provide ics. Synbiotics are a mixtw·e of prebiotics
veterina.iy therapeutic diets for hea.it
and probiotics in which the prebiotic
disorders. When using a home-prepared diet,
increases the swvival of and now-ishes the
all processed meats, cheeses, bread, heart,
probiotic bacteria. Although clinical studies
kidney, liver, salted fats, whole eggs, and
of probiotics in dogs and cats are limited,
snack foods should be avoided. Foods
probiotics have been helpful in nwnerous
reasonably low in sodiwn include beef,
causes of diarrhea. -
rabbit, chicken, horsemeat, lamb, freshwater fish, oatmeal, corn, and rice.

Constipation: Constipation results from

Failed cardiac contractility may
impaired peristalsis or increased water
contribute to CHF, and taurine supplemenabsorption from the large intestine. The tation should be used to exclude a possible
objective of dietary management is to
depletion of this a.inino acid in ca.i·diac
provide a balanced diet with increased
muscle. Both dogs wd cats can develop
a.mounts of insoluble fiber (10%-25%
dilated cardiomyopathy secondary to
dry-matter basis to effect) or moderately
taw-ine deficiency. Some breeds of dogs
fennentable fiber in dogs or a highly
with dilated cardiomyopathy may respond

NUTRITION: SMALL ANIMALS

2383
favorably to carnitine supplementation,

Cats most commonly develop type 2 DM,
which has also been beneficial in some
although some cats may develop type 1,
breeds of dogs with CHF (including Boxers
often secondary to chronic pancreatitis.

and Cocker Spaniels), in dogs with cystine

The most common risk factors for DM in
or urate urolithiasis, and in dogs consuming
cats are obesity and increasing age. Most

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a protein-restricted diet. Because obesity
of these cats develop an1yloid-mediated
can be a contributing factor in CHF, a weight destruction of pancreatic islets. Although management program is needed in obese
residual insulin capacity remains in most
animals in addition to sodium restriction.

type 2 diabetic cats, insulin resistance is a

In some instances, edema may give the
characteristic of this form ofDM.

appearance of obesity and mask emacia

Feline DM is similar to type 2 DM in
tion. The edema should first be resolved,
people, and the main goals of therapy for
so that body weight and condition can be
diabetic cats are to control excess body
evaluated. If the animal is underweight,
weight and maintain optimal body
the food intake should be increased or the
condition, to reduce postprandial hyperglycaloric content of the diet increased. If cemia and glucose toxicity, and to stimulate
renal failure is also present, protein and
endogenous insulin secretion. Transient
phosphorus intake must be restricted.

OM occurs in -200,i, of diabetic cats, and
these cats go into spontaneous remission

Diabetes Mellitus {DM): Most DM in
usually within 1-4 mo after starting therapy
dogs is type I (insulin dependent) due to
for DM. The most likely reason for this is
immune-mediated destruction of pancreatic
that untreated diabetic cats may develop
islet cells (seep 579). Although insulin
glucose toxicity, and hyperglycemia
sensitivity remains high in most diabetic
decreases pancreatic 13-cell function. When
dogs, no residual insulin production is left
the cat is treated for DM and hyperglycemia
in the pancreas, and exogenous insulin
is contro!Jed, the glucose toxicity interfe1°
therapy is required. Some dogs develop DM
ing with pancreatic islet cell function is
as a result of chronic pancreatitis causing
removed.

widespread destruction of both endocrine

Traditionally, diabetic cats have been fed
and exocrine pancreatic tissue. Obesity
fiber-supplemented diets similar to those
does not appear to be a risk factor for
recommended for diabetic dogs, and some
developing DM in dogs, although obese
cats have clone we!J. H owever, more
dogs can have insulin resistance. Type 2 DM
recently it has been shown tl1at feeding
has not been reported in dogs, although
diabetic cats a diet high in protein (>45% of
some dogs may develop diestrus-associated
calories) and low in carbohydrates ( <200,i, of
diabetes that results in insulin resistance
calories) improves glucose regulation and
secondary to progesterone production.

increases incidence of spontaneous

Remission of diabetes is possible when
remission. Nonetheless, some diabetic cats
dogs are spayed or diestrus ends.

may have concurrent diseases for which the

Some diabetic dogs have concurrent
dietruy management takes precedent.

diseases, such as hyperadrenocorticism,
and they may be very difficult to regulate

Feline Lower Urinary Tract Disease
if the hyperadrenocorticism remains

{FLUTD): FLUTD (seep 1531) has many
untreated. Underlying urinary tract
possible underlying causes, including
infection can also result in poor regulation urolithiasis, urethral plugs, urinary tract
and insulin resistance until the infection is
infection, neoplasia, neurologic abnormalicured. For diabetic dogs receiving insulin ties, feline idiopathic cystitis (FIG), and
therapy, the nutritional requirements of any
anatomic defects, The underlying cause
concurrent disease may take precedence
ofFLUTD must be determined, because
over the dietary therapy for diabetes.

treatment for one cause may be contraindi

Dietary recommendations for diabetic dogs
cated for other causes. The most common
without concurrent disease include feeding
cause of FLUTD is FIG, fo!Jowecl by
a diet that contains a moderate amount of a
urolitlliasis. Urethral plugs are most
blend of soluble and insoluble fiber (3.5
commonly composed of either mucus or
g/100 kcal), such as a mixture of beet pulp
mucus and struvite crystals. Urinary tract
and ce!Julose. Independent of the type of
infections in cats without renal failure or
diet chosen, dietary intake should be
diabetes mellitus is uncommon.

consistent from day to day. Diabetic dogs

Urine dilution appears to be helpful in the
usually require insulin twice a day, and it is
treatment ofFIC, because it decreases the
recommended that dogs be fed first to
concentration of substances in the urine
ensure they eat before administering
that may be irritating to the bladder mucosa.

insulin.

Nwnerous ways to dilute urine have been

2384

NUTRITION: SMALL ANIMALS
investigated in cats, but one of the safest
certain specific nutrients in the diet, such
and most effective is to feed a canned-food
as soy protein, lead to tl1e development of
diet. Other dietary modifications have been
gastric dilatation in susceptible dogs (see
used to dilute urine, including sodium
p 384). The most common risk factors for

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supplementation. Although sodium-suppledeveloping gastric dilatation and volvulus mented diets are helpful in cats with FIC,

(GOV) include breed risks (ie, large breeds
they are contraindicated in cats with
with a deep chest), eating only one meal/
underlying renal disease. Highly acidic diets
day, elevated feeding bowls, and vigorous
are not recommended, because highly
exercise 1 hr before or 2 hr after eating.

acidic urine may increase sensory nerve

Prophylactic gastropexy has been shown to
fiber transmission in the bladder and
prevent GDV if pe1fonnecl at the time of
increase pain perception. Regardless of
elective sw-gical neutering, arid owners of
treatment, clinical signs of FIC usually sponhigh-risk breeds should be so advised. Otl1er taneously resolve in 2-7 days. Unfo1turecommendations to prevent GOV include nately, FIC recurs within 12 mo in
feeding multiple small meals/day and
approximately half of the cats that
avoiding vigorous exercise before arid
experience spontaneous remission, and
after eating.

multiple recurrences are possible.

The two most common uroliths in the

Head Trauma, Burns, and Respiratory
lower urinary tract of cats are magnesium

Diseases: It is tmknown whetl1er the
ar11monium phosphate (struvite) and
metabolic effects and energy expenditure
calcium oxalate, although other mineral
in dogs at1cl cats with severe head trawna,
types are possible. Dietary management
burns with �5()0A, loss of skin, or prolonged
varies depending on the specific mineral
clyspnea are the sarne as those in people
composition of the urolith; however,
with sin1ilar conditions. However, it is a
regardless of composition, diluting the urine
reasonable supposition. The brain is one of
is inlportant. Medical dissolution is an option tl1e most metabolically active tissues; thus, for struvite w-oliths but not for calcium
providing aggressive nutritional support
oxalate w-oliths. Producing a dilute urine
ear·ly is essential. Head trauma significantly
reduces the concentration of minerals and
alters neurologic control of metabolic rate,
crystals that fo1111 w-oliths. Feeding a caruieclwhich is usually increased. Burns and otl1er foocl diet and encow-aging water intake, eg,
causes of significant areas of skin loss
with water fow1tains, ar·e safe and sin1ple
increase heat and water loss to the
ways to dilute mine. Three major pet food
environment, thereby increasing energy
comparlies have fommlated cliets for cats to
needs. Increased respiratory rate and
manage both strnvite arid calcium oxalate.

clyspnea are deceptively intense work that

Two of these diets have high levels of sodium also result in increased energy needs. If a and, therefore, are contraindicated in cats
clog or cat is in an oxygen cage for > 1 clay,
with underlying renal disease. Diets reduce
nut1itional support (feeding IV or via
risk factors for developing w-oliths but
feeding tube) should be instituted.

unfo1twiately do not prevent recwi:ence,

Brain traw11a, burns, and sepsis are all
which is common for calciw11 oxalate.

conditions with high metabolic demar1ds,
and the amount of energy needed var·ies

Fever: Fever increases energy requireamong animals. In all cases, energy is ments because of increased metabolic
provided minimally at 30 kcal/kg body wt
activity-a 1 °F (0.5°C) rise causes ar1

(dogs) or 40 kcal/kg body wt (cats) and
increase in caloric need of -7 kcal/kg body
increased in increments of 5 kcal/kg as the
wt/clay. A highly palatable diet should be feel
condition progresses and if weight Joss is
in quantities that can be consumed easily,
appar·ent. The energy sow·ce should be
and the caloric content should be increased
predominantly fat (600h-900A, calories from
by feeding a higher fat diet, if such a diet is
fat, 100/o-4()0A,from glucose), because the
not contraindicated. Because ar1in1als with
body metabolism is predominantly lipolytic
fever generally have a decreased appetite,
tmder these conditions, with the liver
offering smaller meals more frequently witl1
utilizing fat better than glucose during
personal attention and encouragement may
response to bwns or traw1ia. Protein intake
help stimulate intake. Feeding a feline
rn ust also be matched with the energy
growth diet or a calorically dense recoveryintake to avoid net protein arid muscle type diet also increases protein and energy
catabolism. Food that is 300/o-45% protein
intake in smaller feedings.

and 25o/,,...30%fat (dry-matter basis) and that
is complete arid balanced for all other

Gastric Dilatation (Bloat): Cw-rently,
nutrients should be fed using tube feeding.

tl1ere is little evidence to suggest that

Hw11an baby foods are not suitable for this

NUTRITION: SMALL ANIMALS

2385
purpose. These nutritional goals can also be
and parenteral fluid support may be needed
met by parenteral (IV) nutrition, rememberin many cats, at least initially. In encephaloing that enteral and parenteral suppo1t are pathic cats with hepatic lipidosis, dietary
not mutually exclusive.

protein may need to be restricted but should

VetBooks.ir
not be severely so. These cats usually have

Hepatic Disease: Dietary recommenprotein malnutrition secondary to anorexia, dations for dogs vary depending on the
and providing too little dietary protein can
underlying cause and seve1ity of liver
intetfere with hepatic repair and regeneradysfunction, and care must be taken to tion.

avoid overwhelming the metabolic capacity

See also HEPATIC DISEASE IN S�L<\LL ANIMAI.S, of the liver. In contrast, it is equally
p429.

important not to unnecessarily restrict
protein intake, because protein require

Hyperlipidemia in Dogs: Hyperlipiments are as high or higher in dogs with liver demia in dogs can be primary or secondary disease than in dogs without liver disease.

to hypothyroidism, pancreatitis, hepatic

Therefore, in dogs without encephalopathy,
disease, diabetes mellitus, nephrotic
providing adequate intake of energy and a
syndrome, hyperadrenocorticism, or
hlgh-{!uality protein is essential to ensure a
high-fat diets. Hyperlipidemia is present
positive protein and energy balance and
when blood lipids are increased with or
enable hepatic regeneration. Dietary
without gross lipemia and probably results
antioxidants, such as vitamins C and E, as
from abnormalities in the synthesis or use
well as taurine, may also help minimize
of plasma lipoproteins. In primary
oxidative damage. Dietary copper restrichyperlipidemia, the abnormalities can be tion is recommended in dogs with docufamilial and might be genetic, as has been mented increased copper levels in the liver.

suggested in Miniature Schnauzers. Some

In dogs with hepatic encephalopathy,
dogs with hyperlipidemia are asymptoreduced levels of high-{!uality protein may matic. Clinically affected dogs may have
be necessary to reduce the accumulation of
recurrent seizures, depression, recurrent
an11110nia and other hepatic toxins. Soluble
pancreatitis, vomiting, acute blindness,
fiber or moderately fennentable fiber is
corneal opacity, and xanthogranulomas.

helpful; colonic fermentation of these fibers

The goal of dietary management is to
produces short-chain fatty acids, which
decrease the digestion and absorption of fat
reduce both the intralwninal pH of the
by feeding a diet restricted in fat ( <10%
colon and the absorption of ammonia.

dry-matter basis). The use of fish oil capsule

Short-chain fatty acids also increase the
supplements at a dosage of 1 g/4.5 kg body
blood supply to the colon and the amount of
wt either once a day or in divided doses,
anm10nia transported into the colon.

depending on the number of capsules

Frequent feeding of small meals (4-6/day) needed, helps reduce senun triglyce1ide lowers the amount of nutrients or metaboconcentrations. Although fish oil supplelites that require hepatic processing at a ments generally do not return serum
single time, thereby imposing Jess metabolic triglycerides to normal values, partial demand on the liver. Animals with liver
reduction is believed to mitigate the risk
disorders are frequently anorectic. Thus,
of pancreatitis or other problems related
food consun1ption and body weight and
to marked increases of this lipid.

condition should be monitored.

Feline hepatic lipidosis is the most

Malabsorption and Maldigestion in
common liver disease in cats. It usually

Dogs: Diseases of the small intestine and
occurs in obese cats that are anorectic.

pancreas often lead to a vague clinical

This life-tlrreatening condition requires
syndrome characterized by weight Joss,
aggressive nutritional support to reverse
vomiting, diarrhea (with or without
the changes in the liver. Most cats require a
steatorrhea), and changes in appetite. In
feeding tube. Energy-dense, high-protein
such cases, a highly digestible diet low in
diets, such as critical care diets, are usually
fiber (0-5%), moderate in fat (10%-15%)

selected for cats without encephalopathy.

and protein (20%-25%), and containing

A step-wise reintroduction to calories is
carbohydrate from noncereal byproduct
necessary to prevent complications, such
sources is recommended. Supplemental
as vomiting or electrolyte abnom1alities.

water-soluble vitamins should also be used.

Hypokalernia is the most frequent

Malabsorption and maldigestion are often
electrolyte abnormality, and it can be
secondary to other underlying GI disease,
exacerbated by too aggressive reintroducsuch as irLflarnmatory bowel disease.

tion to calories. Cami tine supplementation

Appropriate management of the underlying
is also beneficial. Fluid needs must be met,
disease may reverse rnalabso11Jtion and

2386

NUTRITION: SMALL ANIMALS
maldigestion. Exocrine pancreatic
many adipokines are increased in obesity,
insufficiency (EPI) is one of the most
which results in persistent, low-grade
common causes of malabsorption/
inflammation and increased oxidative stress
maldigestion in dogs. Certain breeds of
that plays a role in many chronic diseases,
dogs, eg, Gem1an Shepherds, are at
such as osteoarthritis and diabetes mellitus.

VetBooks.ir
increased risk of developing EPI. EPI can

Treatment for obesity should include
also result from severe or chronic pancreboth short- and longte1m goals. Short-term atitis. In EPI, supplementation with a
goals are to lose weight and reach an ideal
powdered enzyme supplement, mixed with
body condition score. Longtem1 goals are to
the food a few minutes before feeding,
maintain ideal body condition score. Botl1
should be considered. Parenteral adminisof these goals require modification of tration of vitamin B12 (cobalamin) is also
behaviors that resulted in the dog or cat
required in some aninlals with EPI,
becoming overweight. Recommendations
especially cats. (See also MALABSORP'l'ION
for lifestyle changes should be done in the

SYNDROMES IN SMALL ANIMALS, p 400.)

context of maintaining the owner-animal
bond. If this is ignored, owner compliru1ce

Obesity: Obesity is the most common
is unlikely.

nutritional health problem in dogs and

The most successful weight loss
cats, and obesity-associated health risks
programs include a combination of caloric
continue to increase. Obesity is the
restriction and exercise. The first step is to
excessive accumulation of adipose
obtain a thorough diet history, followed by
tissue-for dug:; and cats, >200/o above ideal
calculating the calo1ic intake appropriate
body weight. Dogs and cats 100/o-200/o above
to induce weight loss. Determining 600/o of
ideal body weight are considered over

MER for dogs and 700/o of MER for cats is
weight. It is estimated that 24o/o-44% of dogs
one way to calculate starting caloric intake
and 25o/er300/o of cats seen by veterinarians
for a weight management progrrun.

are overweight or obese, and -500/o of dogs

Regardless of the formula used, the

5-10 yr old are overweight or obese.

calculated caloric intake is only a starting

Obesity occms when energy intake
point and may require modification based
exceeds energy expenditme. Risk factors
on response.

for developing obesity include 1) lack of

The next step is to decide on a diet for the
exercise, 2) breed predisposition (breeds
weight loss program. Maintenance diets are
with an increased risk include Labrador
generally not recommended for weight loss

Retrievers, Miniatme Schnauzers,
progrruns, because tl1ey are formulated to

Dachshunds, Shetland Sheepdogs, Cocker
meet the nutritional needs of moderately

Spaniels, Beagles, Basset Hom1ds, and Cairn active adults. Restricting caloric intake using Terriers), 3) increasing age (metabolic rate
maintenance diets may result in inadequate
decreases with age as lean muscle mass
intake of some nutrients. Therapeutic weight
decreases and fat mass increases, 4) neuterloss diets are fonnulated to be restricted in ing, 5) certain endocrine disorders, and
calories while providing other nutrients in

6) certain drugs, such as corticosteroids and
approp1iate amounts. Adequate protein
phenobarbital.

levels ru·e important in any weight loss diet

Health problems associated with obesity
chosen. Most diets formulated for weight
include decreased life expectancy, impaired
loss also have increased levels of dietary
quality of life, chronic inflammation,
fiber. It is better to divide total daily caloric
pulmonary and cardiovascular problems,
intake into multiple meals rather than one
exercise and heat intolerance, joint and
large meal. If giving treats is a.ii important
musculoskeletal problems ( eg, arthritis),
owner-pet interaction, providing the owner
compromised immune function, pancreatiwith low-calorie treat options is important.

tis (dogs), diabetes mellitus and hepatic

Most treats are not complete and balanced,
lipidosis (cats), and increased morbidity
so they should be restricted to <100/o of the
and mortality dming and after anesthesia.

total caloric intake to avoid causing nutrient

Adipose tissue was long considered
imbalances.

metabolically inert, and its primary role in

The next step is to decide on a rate of
disease was attributed to stress on the joints weight loss: a reasonable goal is loss of -1 %
caused by increased weight bearing and
of body wUwk. lf the anin1al is losing weight increased workload on the heart. However,
at a slower rate tl1an that chosen but is
it is now known that adipose tissue is not
doing well otherwise ancl the owner is
inert, but rather a major endoc1ine organ
satisfied, tl1en it may be best to allow
that produces honnones and protein facweight loss to continue at the slower rate. The tors and signals called adipokines. The
anin1al's weight should be monitored every
expression, production, and release of

2 wk and the program modified if needed

NUTRITION: SMALL ANIMALS

2387
based on response. Any weight loss is good
are important. F1uid rates must be sufficient
weight loss, and celebrating successes with
to account for maintenance needs as well as
the owner helps maintain motivation.

ongoing losses. Crystalloid therapy or

Obese cats undergoing weight loss are
plasma transfusions may be necessary in
at increased risk of developing hepatic
hypoalbwninemic dogs. Food and water are

VetBooks.ir
lipidosis. Cats must continue to consume
usually withheld until vomiting ceases.

adequate calories and nutrients. If a cat

Severe cases may require total parenteral
does not like the weight loss diet chosen,
nutiition. Once vomiting has ceased, small
then an alternative should be found.

amounts of water are offered first. If there is

Starvation is never a safe or humane way
no vomiting, then small amounts of an easily
to cause weight loss.

digestible diet should be fed until the dog
recovers. (See also CANINE PARVOVJRUS, p 373.) Pancreatitis in Dogs: The goal in
treating pancreatitis is to minimize

Chronic Kidney Disease (CKD): Nwnerstimulation of the exocrine function of the ous metabolic abnormalities that may alter
pancreas until inflammation has decreased.

an aninlal's nutritional status develop in

Often, the dog has multiple episodes of vomprogressive renal failure. These include iting. A standard treatment is nothing per os
impaired clearance of nitrogenous products

(NPO) until vomiting ceases, which can last
of protein metabolism; inlpaired regulation

3-15 days. Antibiotic, fluid, and electrolyte
of sodiun1, potassium, and phosphorus;
therapy during NPO treatment is essential,
acidosis; impaired vitamin D metabolism;
and IV nutritional support (total parenteral
and often anorexia. The objective of dietary
nutrition) should be instituted if NPO
management in renal failure is to lessen the
therapy continues for �3 days. Adult and
metabolic demands on the kidneys and to
young dogs can be nutritionally maintained
diminish metabolic end-products that
by IV parenteral solutions that provide
cannot be readily excreted. The first
adequate calories, protein, electrolytes, B
consideration is to ensure normal water
vitamins, and selected trace minerals until
homeostasis. Regardless of whether the
oral feeding is possible. If the dog appears
aninlal is polyuric, oliguric, or anuric, water
painful or w1comfortable, medications to
should always be readily available. In
manage pain as well as plasma transfusions
addition, dietary management remains the
should be administered.

mainstay of therapy for anin1als with CKD.

Unfortunately, total parenteral nutrition

Therapeutic renal diets are fonnulated to
does not provide any nutrients to the enteroaddress many of the metabolic abnormalicytes, and atrophy of the gut occurs as in ties associated with CKD. Any therapeutic
starvation. The aTilino acid glutamine
renal diet should be phosphorus restlicted,
provides --400A, of the energy needs to the
supplemented with omega-3 fatty acids·
small-intestinal epithelial cells; it can be

(EPA/DHA) that come from fish oil,
provided orally in very small quantities
alkalinizing, supplemented with B vitamins,
every 8 hr to provide some nutrition for
and in cats supplemented with potassiun1.

the enterocytes.

In addition, feeding moderately fern1entable

When oral feeding can be resumed, a
fiber can facilitate enteric dialysis and
commercially prepared, easily digestible
provide a nonrenal route of urea excretion.

diet that has moderate fiber ( 10%--15%

Newer research has also shown the benefits
dJy-matter basis) and is low in fat (5o/erl00A,)

of antioxidants in the management of CKD
can be fed in small, frequent meals (3-6
in dogs. The rate of decline of glomerular
times/day). Because recurrent episodes
filtration rate by use of both dietary omega-3
of pancreatitis are common, feeding a
fatty acids and antioxidants were additive.

complete and balanced low-fat diet is

In addition, research in dogs is also showing
recommended for longterm management.

that higher protein levels than what are

Obesity and hyperlipidemia are common
typically used in most therapeutic renal
concunent problems and should be
diets is beneficial as long as the diets are
investigated and resolved.

phosphorus rest1icted. Energy should be
supplied prin1arily via feeding relatively

Parvovirus Enteritis in Dogs: Parvomore digestible fat and carbohydrates.

virus enteritis is most common in puppies

The criteria used ( eg, serw11 creatinine

6-24 wk old. It is extremely infrequent in
concentration, BUN) to define when dietary
adult dogs. It is characterized by vomiting,
modifications should be made are under
diarrhea ( often bloody), and weight loss.

debate. However, it is easier to change the

Severe cases can result in sepsis and
diet when the aninlal is feeling reasonably
disseminated intravascular coagulation. IV
well than when it is anorectic. There is good
fluids, anti emetics, and antibiotic therapy
evidence that aninlals with International

2388

NUTRITION SMALL ANIMALS

Renal Interest Society (IRIS) Stage 3 and 4

Dalmatians and English Bulldogs, a.re

CKD benefit from dietary management, and
predisposed to developing urate uroliths
there is likely to be benefit in changing the
without overt liver dysfunction. Medical
diet early in the course of renal disease, such dissolution is an option and consists of VetBooks.ir
as that associated with IRIS Stage 2 CKD.

using a protein-restricted diet low in purines

Additional symptomatic and supportive
and alkali.nizing the urine in combination
care, such as H2-blockers, antiemetics,
with treatment with allopurinol, a xanthine
medications to treat hypertension, intestinal
oxidase inhibitor. The use of low-dose
phosphate binders, calcit1iol, erythropoiallopurinol as a strategy to prevent etin, and potassiw11 gluconate (in cats) may
recwi:ences is discouraged. Instead, water
be necessary as the disease advances.

should be added to the diet in the maximal
amount the dog can tolerate without

Urolithiasis in Dogs: The most common
needing to urinate overnight. Recurrence
mineral composition for uroliths in dogs a.re
rates are high, especially in dogs 1-6 yr old;
primarily struvite (magnesium-an1moniwnhowever, this stone type becomes much phosphate) and calciwn oxalate, followed
easier to manage once the dogs reach
by urate and cysteine. Regardless of the
middle age.

type of stone, diluting the w'i.ne ( eg, by

Cysti.ne urolithiasis is due to a renal
encouraging water consumption) is
tJ.tbular defect. It is most conm1on in
warranted.

Dachshunds, English Bulldogs, French

Struvite stones are more common in

Bulldogs, and Newfoundlands. Medical
females than males. Most struvite stones
dissolution is an option using dietary
in dogs a.re induced by infection with
management and thiola. However,
urease-producing bacteria. Although diet
protein-restricted diets should be used with
can be used to try to dissolve these stones,
caution, because some of these dogs also
the most inlportant therapy is to treat the
have aminoaciduria and carnitinuri.a. (See
winary tract infection. Struvite stones can
also UROLITHIASIS IN SMALL ANIMALS, p 1525.) be medically dissolved, after which
calculolytic therapeutic diets a.re usually

Steatitis in Cats: Steatitis (pansteatitis,
unnecessary. Preventing a recurrence of
yellow fat disease) is seen most often in
the urinary tract infection and prompt
kittens fed exclusively large an1ounts of
treatment of a recurrence a.re inlpo1ta.nt.

unsaturated fatty acids, oily fish such as

Calcium oxalate stones are not amenable
tuna or mackerel (packed in oil not water),
to medical dissolution and must be removed
diets that do not have an appropriate
through voiding, urohydropropulsion,
balance of antioxidants relative to
surgery, or laser lithotripsy in symptomatic
polyunsaturated fats, or diets that have gone
dogs. Two approaches a.r-e used for dietary
rancid. Clinical signs are anorexia, fever,
management: 1) feeding an alkalinizing,
pain over the thorax and abdomen,
protein-restJ.icted diet low in oxalate, or
neutrophilia, and subcutaneous nodules of

2) feeding a diet supplemented with sodiun1
necrotic fat. Cats with steatitis should be
to encourage water consumption and
fed diets restricted in polyw1saturated fatty
production of dilute urine. Despite dietary
acids (monounsatu rated and saturated fats
management, the recwrence rate is high (33"A, are permitted) and given vitanli.n E
in the first year and 50% by the third year).

supplementation at 10-20 mg, bid for 5---7

Urate uroliths can occur in cases of liver
days. The diet of choice is a: commercial
disease, most commonly po1tosystemic
food to which vitanli.n E ( a-tocopherol) or
shunts. However, two breeds of dogs,
other antioxidants have been added.

PUBLIC HEALTH

VetBooks.ir
pl,JBLIC HEALTH PRIMER 2390

Public Health Agencies 2390

Role of the Veterinarian in Public Health/One Health 2391

Significant National Public Health Achievements 2393

National Public Health Indicators 2395

Essential Public Health Functions 2396

Public Health Foci of Prevention 2396

Basic Principles of Epidemiology 2397

Epidemiologic Terms and Concepts 2397

Descriptive Epidemiology 2399

Analytical Epidemiology 2399

Observational Studies 2400

Interventional Studies 2402

Bias 2402

Error 2403

Variable Associations and Causality 2403

Sensitivity and Specificity 2403

Disease Outbreak Investigation 2404

Basics of Food Safety 2406

Foodbome Pathogen Requirements 2406

Food Processing and Preservation 2406

Incidence and Impact of Foodbome Diseases 2408

Factors in Emerging Foodbome Illness Trends 2408

Role of Food Animal Veterinarians in Control of Food borne Pathogens 2409

Food Safety Regulation 2410

Public Health Law 2411

Primary Sources of State Public Health Authority 2411

Selected General Federal Emergency Legal Authorities 2411

Zooeyia 2413
zOONOSES 2414

Pathogens and Host Species 2414

Transmission Between Animals and People 2414

Role oflmmunosuppression 2415

Emergence and Reemergence 2416

Treatment 2417

Prevention 2417

Zoonotic Diseases (Table) 2418

Bacterial Diseases 2418

Rickettsial Diseases 2432

Fungal Diseases 2438

Parasitic Diseases 2440

Arthropod Diseases 2462

Viral Diseases 2466

Prion Disease 2483

2390

PUBLIC HEALTH PRIMER

PUBLIC HEALTH PRIMER

VetBooks.ir

Although only a minority of veterinarians
cian assistants, psychologists, pharmacists,
report primary public health employment,
entomologists, etc, also contribute according
virtually all veterinarians contribute to the
to the scope of their respective practices.

overall public health effort. According to the

No medical profession exists in a vacuum.

World Health Organization, "health is a state

Many public health practitioners possess
of complete physical, mental and social
specific training, and various board-certifying
well-being and not merely the absence of
bodies, accrediting entities, and professional
disease or infinnity." Public health can be
societies bolster this training by requiling
defined as the totality of all evidence-based
experience and fostering collaboration. These
public and p1ivate efforts that preserve
include the American College of Preventive
and promote health and prevent disease,

Medicine, the American College of Veterinary
disability, and death. The concept of One

Preventive Medicine, the An1erican Public

Health is the collaborative effort of multiple Health Association, tl1e American Society of health science professions, together with

Public Health, and the Association of State
their related disciplines and institutionsand Tenitorial Health Officials.

working locally, nationally, and globally-to

Several overarching public health organizaattain optimal health for people, domestic tions have jointly developed a set of core
animals, wildlife, plants, and our environcompetencies that reflect skills appropriate ment.

to the effective delivery of public health

One Health can be thought of as having
services. Core competencies are divided into
three major subcomponents: basic sciences,
the following eight domains: 1) analytid
clinical medicine, and public health. Major
assessment skills, 2) policy development/
components of public health include
program planning skills, 3) communication
population health, community health, mental skills, 4) cultural competency skills, 5) health, environmental/ecological health,
community dimensions of practice skills,
and occupational/recreational health. The

6) public healtl1 sciences skills, 7) financial
differentiating variables among these compoplanning and management skills, and 8) nents are the dynan'lics of the population(s),
leadership and systems thinking skills.

changing social/health behaviors, and,
perhaps most importantly, the selection of

PUBLIC HEALTH AGENCIES
the population to study/surveil. A relevant,
frequently debated question is the definition

In the USA, responsibilities and authorities
of the "environment." Typically, it is equated for health services are spread across
with the "physical" environment and implies federal, state, and local levels of governall influences other than social, econon'lic, ment. In addition, certain nongovernmental
cultural, and genetic. An additional underorganizations pe1fom1 critical functions lying theme in One Health is the econon'lic
regarding the provision and influence of
environment in which it ( and all professions
public health policies.

that contribute to it) is pursued. Therefore,
an understanding of basic economics is key

Federal level: The Constitution contains
to understanding the most practical applicano legal basis for the provision of health care tion of ( and opportunity for) One Health in a
to the general population. Therefore, as per
particular community, country, or region.

the Tenth Amendment, this responsibility
automatically falls to tl1e states. When the

Public Health Practitioners: A generally
federal government directly influences
accepted definition of a public health pracnational health care issues, it generally does titioner does not exist. However, for practical so under the auspices of the Constitution's purposes, any healtl1 professional who

Interstate Commerce Clause, which gives
sees and acts beyond the single patient is

Congress the power "to regulate commerce
functioning in a public health capacity.

with foreign nations, and among the several

Most typically, this includes physicians,
states, and with the Indian tribes." The
veterinarians, dentists, nurses, epiden'liolofederal government also significantly gists, laboratorians, industrial hygienists,
influences health care issues in an indirect
public health inspectors, and regulatory
fashion through the provision of federal
agency administrators. Allied health profunds. Commonly, funds allocated to state fessionals, including optometrists, physi-and local governments for healtl1 issues are

PUBLIC HEALTH PRIMER

2391
contingent on that entity participating in

6) environmental health programs ( eg, safe
national programs such as disease reporting
drinking water, waste treatment), 7) state
and adhering to national health goals and

Medicaid program, and 8) regulation and
standards.

licensing of medical professionals ( eg,

The Department of Health and Human
veterinarians, physicians, dentists, etc).

VetBooks.ir

Services (DHHS) is the primary public
health agency at the federal level and serves

Local Level: Local public health agencies
to assess the general health of the nation,
are structured and empowered to provide
establish national goals and policies, and
services where they are most effective-at
direct federal efforts in suppo1t of the states. the community level. These services may Major public health-oriented components
be primary or delegated from the state level
of DHHS include the Agency for Healthcare
and commonly include the following:

Research and Quality (AHRQ), the Agency

1) immunizations not covered under private
for Toxic Substances and Disease Registry
insurance systems, 2) disease surveillance

(ATSDR), the Centers for Disease Control
and investigation, 3) communicable disease
and Prevention (CDC), the Food and Drug
control, 4) inspection and licensing of food

Administration (FDA), the Health Resources establishments, 5) public health screening and Services Administration (HRSA), the
programs, 6) tobacco control programs,

Indian Health Service (II-IS), the National

7) disaster preparedness and response, and

Institutes of Health (NIH), and the

8) care for the underserved, indigent, and

Substance Abuse and Mental Health
disabled.

Services Administration (SAMHSA).

Other federal departments with significant

Nongovernmental Organizations
equities in national health care and public

(NGOs): An NGO is any nonprofit,
health responsibilities include 1) Department
voluntary citizens group organized on a local,
of Agriculture (USDA), which is responsible
national, or international level. Task-oriented
for meat inspection and disease prevention
and staffed by individuals sharing common
and control; 2) Department of Defense
interests, NGOs perforn1 a variety of service

(DoD), which is responsible for health care
and hun1anitarian functions. F\mctions of
policies and provision of health care for
health-oriented NGOs may include raising
active duty members, fanilly members, and
citizen concerns to governments, advocating
retirees; 3) Department of Homeland Security and monitoring health policies, and (DHS), which is responsible for disaster
encouraging political participation through
planning and response; 4) Department of the
public information dissemination. NGOs that

Interior (Dol), which operates the National
exist and act domestically ( and overseas in

Park Service (public health and disease
some cases) in the public health sector
outbreak investigations on National Park
include the American Red Cross, the
lands), the Bureau of Indian Affairs (treaty

American Cancer Association, the An1erican
obligations to tribes, including provision

Lung Association, the CDC Foundation,
of health care and environmental health

Heifer International, the March of Dimes, and
infrastructure projects), and the Bureau of
the Bill and Melinda Gates Foundation.

Reclamation (provides potable drinking
water and agricultural irrigation water to

ROLE OF THE VETERINARIAN IN
much of the western USA); 5) Department of

Veteran Affairs (VA), which is responsible for

PUBLIC HEALTH/ONE HEALTH
health care policies and provision of health

Most veterinarians contribute, directly
care for qualified veterans, and administers
or indirectly, to public health goals and
significant civilian medical education
outcomes. Veterinary public health
systems; and 6) Environmental Protection
contributions can be categorized into

Agency (EPA), which sets and enforces
six core domains, described below.

national environmental health standards.

Diagnosis, Surveillance, Epidemiology,

State Level: The state is the primary public Control, Prevention, and Elimination health legal authority. Although specific
of Zoonotic Diseases: Most private
activities and delegations may vary from
veterinary practitioners contribute to public
state to state, state public health responsibilihealth during routine practice. Both large ties generally include the following: 1) collecand small animal practitioners become tion and maintenance of vital health data,
skilled diagnosticians for acute and chronic

2) maternal and child health, 3) diagnostic
diseases of animals that may affect the
and public health laboratories, 4) state-
owners and their fanillies and the surroundwide nutrition progran1S, 5) regulation of ing communities. Specific examples of public
health facilities (including nursing homes),
health activities include perfomling routine

2392

PUBLIC HEALTH PRIMER
healtl1 examinations, maintaining immuniza

Management of Health Aspects of
tion regin1ens, in1plementing parasite control

Laboratory Animal Facilities and
programs, advising on ilie risks of anin1al

Diagnostic Laboratories: The
contact for inmrnnocompromised individucha.Uenges of recog1'lizing resurgent VetBooks.ir
als, facilitating tl1e use of guide and service
infectious diseases ru1d developing novel
dogs for people wiili disabilities, and
therapeutics have placed W1precedented
promoting tl1e benefits of ilie human-animal
emphasis on managing and maintaining
bond for tl1e disabled and elderly, as well
laboratory anin1al colonies for research ru1d
as war veterans and oiliers suffering from
diagnostic efforts. Providing these se1vices
post-traumatic stress disorder. Conu11w'lities
both successfully ru1d humanely fa.Us to ilie
are best se1ved when veterinarians approach
veterinruiru1s in tl1ese institutions. Because
collective healili issues witl1 a "herd healtl1"

few nations have ilie inclividual capacity to
perspective, applying relevant epiden'liologic
provide iliese se1vices interna.Uy, increasing
principles. ln addition to iliese direct
emphasis is being placed on international
services, veterinary practitioners report
collaboration ru1d reference centers, mru1y
disease events and trends to state public
of which focus on zoonotic diseases and
healili and regulatory agencies, collaborate
compru·ative medicine. Because most
wiili human medical coW1terpruts on
outbreaks of zoonotic disease occur in
zoonotic diseases, and advise local healtl1
tropical regions devoid of local swveillance
boards and conm'lissions. These relationru1d diagnostic and response capacity, ilie ships would not exist if not for ilie inextricarole of these international collaboration and ble link between ru'lirnal and hW11an health.

reference centers likely will expand,

In addition to managing direct zoonotic
requiring lru·ger nwnbers of trained,
diseases in animals, vete1inruians also
experienced veterinru-y personnel.

diagnose, investigate, and control indirect
zoonoses ru1d non-zoonotic conm1unicable

Biomedical Research: Building on ilie
diseases iliat affect human health. Exrunples information from public healtl1 smveillru1ce, include West Nile disease ru1d cocciclioidoreseru·ch institutions must follow wiili a mycosis an1ong pet animals, and bovine
greater tmderstlli1ding of ilie interactions
leukosis, foot and mouth disease, fowl pox,
between hosts, pru·asites, vectors, pailioru1d many otl1er diseases iliat affect ilie food gens, ru1d the environment. Establishing a
supply, the national economy, and the
causal link between humru1 ru1d anin1al
livelihood of ilie nation's frun1ers.

disease relies on such research efforts, often

Many factors contribute to the increasing
through some combination of molecular
vulnerability of livestock to infectious
studies, mailiematical theory, ru1d experidisease. These include increasing intensity mental epidemiology, using eiilier field or
and concentration of produc;tion agricullaboratory research. As highlighted by ilie tme, genetic convergence of many food

World Healili Orgru'lization, reserud1 of
producing species, accessibility of liveendenlic ru1d resmgent zoonoses is o�en stock to external contact ( despite rigorous
handicapped by a lack of basic knowledge
biosecurity measmes), scale and frequency
of host-parasite interactions. For many
of rulimal trru1sport ( domestic ru1d •
zoonotic species, even ilie route of
international), increasing size of feedlots,
transnlission to people remains W1ce1ta.in.

lack of immunity to foreign ru1i.mal diseases,

In some cases, the molecular biology of
the relatively porous natme of national
tl1e agents in humru1 ru1d ru1imal·hosts may
borders, ru1d the significant shortage of
be very different. For exru11ple, there ru·e
trained foreign ru1i.mal disease diagnostimajor research efforts ain1ed towru·d the ciru1s ru1d epidemiologists. Although
identification of virulence factors for E coli
many significru1t cliseases trru1smitted by

0157:H7 and the reasons for ilieir differenfood-producing ru'limals ( eg, brucellosis, tial expressions in people ru1d cattle.

tuberculosis, coxiellosis/Q fever, etc) have
been eradicated or controlled in Nortl1

Health Education and Extension: Al

America ru1d Emope by pastewization and
though training new veterinary practitioninspections at slaughter, still many others ers ru1d disseminating new capabilities to
are seemingly ubiquitous ( eg, listeriosis,
those already in practice falls lru·gely on the
sal.monellosis, staphylococcosis, etc) ru1d
nation's academic ( especia.Uy lru1d-grant)

cause a significant fraction of ilie national
institutions, virtually all veterinru·iru1s
burden of food borne morbiclity and
help educate ilie public on ilie threat of
mortality. Each year in ilie USA, iliere ru·e
infectious ru1d noninfectious diseases. At
reported approxin1ately 20,000 foodbome
the collegiate level, tl'lis will increasingly
illnesses, 4,200 hospitalizations, and 80
involve multidisciplinary relationships
deailis, most of which are caused by
between schools of medicine, veterinary
pathogens of anin1al 01igin.

medicine, sociology, ru1d basic scienct>s.

PUBLIC HEALTH PRIMER

2393

Enabling appropriate lrnowledge and
being a mi.nor fraction. Exa.inples include
awareness among the public requires a
oversight of food safety inspection
skillful blend of risk perception and risk
progra.ins, disease surveilla.i1ce and
awareness, especially because community
outbreak mvestigation, laboratory ani.n1al
stakeholders play significant roles in 1isk
care, biomedical research, and public health

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resolution. Most epidemiologists are
progran1 management a.i1d leadership.

employed by govenunental or i.ndusttial

At the state level, each depa.iiment of
stakeholders that have not historically been
agriculture typically has a State Veterina.i·ian
viewed as valid proxies for the public. This
who is responsible for protecting the
represents an impo1tant oppo1tu.nity,
livestock, poultry, a.i1d aquaculture
perhaps responsibility, for veterinary
industries directly, and tl1e public indirectly,
practitioners to remain lrnowledgeable
tiu·ough the prevention, early detection,
about disease tlu·eats and credible sources
contairu11ent, and eradication of economiof that knowledge for their commtmities.

cally unportant livestock, poultry, and fish
diseases that, in many cases, are transmis

Production and Control of Biologic
sible to people. The State Veteri.na.iia.i1

Products and Medical Devices: Enstu' regulates the unportation, tra.i1sportation, i.ng that animal drngs, vaccines, and devices
and processing of animals a.i1d is responsia.re safe and efficacious is a shared ble for the control and eradication of
responsibility between the FDA, the USDA,
poultty and livestock diseases, regulation
and the EPA. ln general, the FDA, specifiof fish fa.imi.ng, and emergency response cally the Center for Veterinary Medicine,
progra.ins. Welfa.i·e of fann anm1als is
regulates animal drugs, animal feeds, and
monitored, a.i1d when necessary, the
veterina.iy devices, whereas the USDA

Office of the State Veterinarian conducts
regulates animal vaccines and biologics.

investigations and prosecutions relatmg

Specific to pesticides, FDA regulates certain to cases of cruelty to animals.

flea and tick products for a.i1i1nals, whereas

Currently, 41 states and territories
the EPA regulates others. Within each of
employ veterinarians i11 their state health
these govenu11ental agencies, veteri.na.iians
departments as State Public Health
serve to encourage the development of

Veteri.na.i·ians (SPHVs). SPHVs generally
novel products a.i1d, at the sa.ine time,
work in zoonotic disease control a.i1d
protect the conswners of those products
prevention, directly focusmg on protecti11g
from false or misleading clai111s.

public health. They typically a.i·e located in

Another unportant fU11ction regarding
health department divisions of epidemiolbiologic agents is the regulation of their ogy, toxicology, or envirorunental health.

storage, use, and tra.I1Sfer. Because of

A final category of governmental
inherent virulence and transmissibility,
activity is legislative; a relatively small
access to many disease pathogens, tem1ed
number of veterina.i·ians se1ve at various
select agents, has increasingly been
levels to promulgate laws, rules, and
limited to legitimate facilities for legitunate
regulations that serve to protect public
uses. The Federal Select Agent Progra.in is
health, domestic preparedness, a.i1d
jointly administered by the CDC and the
national defense. Veterinarians se1ve i11

USDA's Anunal a.i1d Plant Health lnspection
the United States House of Representa

Se1vice (APHIS). This effort oversees the
tives, in senior leadership positions of
possession, use, and tra.I1Sfer of certain
several United States Cabinet-level
biologic agents and toxins that have the
departt11ents (including USDA, DHHS,
potential to pose a severe threat to the

DoD, and DHS), and as legislative liaisons
public, to animal or plant health, or to
for professional associations such as the
animal or plant products.

AVMA. They are assisted in their legislative efforts by the communicative action Government/Legislative Activity:

of practicing veterinarians across the

Significant nwnbers of veterinarians are
nation. It is through this pathway that
employed at va.iious levels of state and
ideas and issues a.i·e effectively transmitfederal government. More tha.i13,000
ted to legislators and translated into
veterina.i·ia.i1s are employed at the federal
improved legal and policy outcomes.

level, nearly two-thirds of which a.i·e with
the USDA. Other federal agencies employ

SIGNIFICANT NAT IONAL PUBLIC
ing la.i·ge numbers of veterinarians include

HEALTH ACHIEVEMENTS
the DoD (Anny and Air Force) and DHHS

(CDC, FDA, and NIH). Public health

Dwing the 20th century, the healtll and
progra.ins comprise the vast majority of
life expectancy of Ame1ica.I1S unproved
these oppo1tunities, with direct a.i1i111al ca.i·e
dranrntically. Since 1900, tile average

2394

PUBLIC HEALTH PRIMER
life span of people in the USA has increased
first discove1y of a viral cause of a cancer,
by 30 yr, largely attributable to advances in
fowl leukosis (1908). On a broader scale,
public health. To commemorate these
the first cancer-preventing vaccines, which
advances, the CDC named the following as
are to protect against Marek disease and
the Ten Great Public Health Achievements,
feline leukemia vims, were developed by

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1900-1999: vaccination, motor vehicle safety, veterinarians and are contributing to safer workplaces, control of infectious
development of human applications.

diseases, mortality decline from coronary

4) Livestock herd health and production
heart disease and stroke, safer and healthier
optimization: Dr. C.L. Cole, who was at the
foods, healthier mothers and babies, family

No1th Central Experiment Station at Grand
planning, fluoridation of drinking water, and

Rapids, Minnesota, was the first to
recognition of tobacco as a health hazard.

demonstrate that large nw11bers of cows

To further conunemorate national
could be bred successfully by artificial
advances in public health and to specifically
insemination (1937-1938). The first calf sired
highlight the veterinary public health
by artificial insemination of frozen semen
contribution to the overall effort, the
was born in 1953. A 10-yea.r dairy production
following were named as the Ten Great
study published in the late 1940s noted that

Veterinary Public Health Achievementsan1ong the many benefits of annual physical United States, 1901-2000.

examinations for dairy cattle was an average

1) Eradication of animal disease: Largely
increase in milk production of 40%. More
attributable to national programmatic
recently, widespread application of
effotts involving local, state, and federal
preventive medicine and environmental
vete1inarians, the following diseases were
health best practices serve to maximize
declared eliminated from animal populadairy cow healtl1 and comfott, all but tions within the USA: contagious pleuroeliminating milk as a source of food borne pneumonia (1892), fowl plague (1929),
illness. Moreover, annual milk production
foot-and-mouth disease (1929), glanders
increased from 5,000 to 21,000 lb per cow.

(1934), dourine (1942), cattle tick fever

5) Food safety (human): Although the 1904

(1943), vesicular exanthema of swine (1959), publication of Upton Sinclair's provocative screwwom1 myiasis (1959), sheep scabies
book The Jungle led to the dismissal of Dr.

(1973), exotic Newcastle disease (1974), and Daniel E. Salmon from the fledging Bureau classical swine fever (hog cholera, 1978).

of Animal Industry, the resultant public

2) Laboratory anin1al science: The first
furor successfully reinvigorated his mission
professor of laboratory animal science in the and facilitated the promulgation of the USA was Dr. Carl Schlotthauer, appointed

Meat Inspection Act of 1906. Dr. Salmon's
in 1945 at the University of Minnesota. Dr.

contribution to foodbome disease control

Charles Griffin oversaw the development of
was considered so valuable that the
pathogen-free animal colonies at tl1e New

Salmonella spp were named for him. In 1900, York State Board of Health Laboratories
the first local conunwlity instituted routine
from 1919 to 1954. Otl1er veterinary pioneers
microbiologic examination of milk. In 1908,
in laboratory animal medicine included Dr.

Chicago required pasteUiization of dairy

William Thorp at the National Institutes of
products and, in 1948, Michigan was the first

Health, Dr. Jan1es Steele at the CDC, and Dr.

state to require milk pasteUiization. In the

Karl Meyer at the University of California at

1920s, veterinarians also accomplished the

San Francisco.

basic work in developing the USPHS (FDA)

3) Infectious disease control: In 1900,

Pasteurized Milk Ordinance and Code.

tuberculosis was the leading cause of

Although slow to achieve industry acceptdeath in people in the USA and commonly ance, inadiation of food has substantial
resulted in malfom1ations in the bones of
beneficial effects on the safety and quality of
children. Of this disease burden, 400A,-500/o
many foodstuffs. Previously approved for
was reported to be bovine in origin, as the
items such as spices, fruits, vegetables, and
result of drinking unpasteurized milk.

poultry, ionizing radiation was approved

Constant public health (Pasteurized Milk
for use in 1999 to reduce bacterial loads on

Ordinance; FDA) and veterinary disease
frozen raw meat and meat by-products.

control (USDA eradication program)

6) Recognition and enhancement of the
measures have eliminated this route of
hUinan-animal bond: Throughout recorded
transmission in the USA. The early 1900s
history, mankind has prutnered and benefited
also saw the discovery of the etiologic
from association with domesticated animals.

agents for many prevalent animal diseases.

The dairy cow is recognized as the "foster

Among these were African horse sickness
mother of the human race," and the horse, ox,

(1900), rinderpest (1902), sheeppox (1902),
donkey, camel, water buffalo, reindeer, and
rabies (1903), hog cholera (1903), and the
yak have provided mankind with our primary

PUBLIC HEALTH PRIMER

2395
transport and tractor power for thousands
compact containers. Dr. Robert A. Whitney,
of years. Indeed, the histo1ies of all animals,

Jr. (USPHS) served as Deputy Surgeon
including people, cannot be dissociated.

General and later as the Acting Surgeon

That symbiotic partnership, perhaps the

General in 1993. Today, veterinarians in tl1e
cornerstone of veterinary medicine, became

U.S. Am1y, Air Force, and Public Health
the life work of Dr. Leo Bustad, who once

Se1vice contribute substantially to militaiy

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stated, "One cannot have a healthy commuand civilian public health missions, such as nity without a strong human-animal
hurnan and animal disease control,
bond." An enhanced understanding of that
occupational healtl1, food safety, medical
inextricable bond has led to relationships
research, deployment health surveillance,
between people and animals, including guide
and biologic waifai·e/terrmism defense.

dogs for the vision and hearing impaired and

10) Integration with public health
militaiy working dogs and dolphins. Fw.ther,
practitioners: Under tile leadership of
the positive physical and psychological

Dr. Karl Meyer, an early architect of
benefits of hun1an-animal relationships, such
veterinary public health, the Hooper
as the lowering of blood pressure and as

Foundation of Medical Research became
companions for older, ill, and traun1atized
a leading institute for the study of
people, have been described.

comparative medicine and zoonotic

7) Border inspection/surveillance: The
diseases. Additionally, he developed the

USDA has primary responsibility for preoriginal curriculum for the University of venting the introduction or reintroduction

California School of Public Health. One
of foreign animal diseases into the USA
of the many important achievements by

The Herculean proportions of tllis task are

Dr. James H. Steele was the status
exemplified by the fact that before free trade,
elevation of veterinarians in the USPHS
the USA imported 1.9 million cattle, 700,000
from sanitarians to veterinary medical
swine, and about 28 million birds annually.

officers. Dr. Calvin Schwabe's seminal

Inspecting representative samples of these
work, Veterinmy Medicine and Human
animals and their by-products is the direct or

Health (1964), provides one of the most
indirect task of USDA veterinaiians. This
concrete examples of this integration.

effort has been greatly aided since 1954 by
the USDA Foreign Animal Disease Diagnostic

NATIONAL PUBLIC HEALTH

Laboratory on Plum lsland, New York, which
provides valuable research toward the

INDICATORS
prevention and control of these biologically

Unfortunately, there are no direct measureand economically devastating diseases.

ments of public health in a population.

Sinli.l.arly, veterinarians employed by DHHS/

Therefore, it is difficult to compare

CDC's Division of Global Migration and
overarching changes over tin1e or against

Quarantine and the U.S. Fish and Wildlife
other populations, except with sruTogates

Service (Depai1ment of the Interior) oversee
such as surveillance for specific diseases/
progranis to control importation of
events and specific population attributes.

nonhuman p1irnates, vector species, and

Accepted among many public health
potentially dangerous or iitjutious wildlife
officials is some combination of tile
species.

following national healtl1 indicators: 1) life

8) Surgery and medicine: Regional
expectancy at birth (years)-tile average
anesthesia via the spinal route was first
nurnber of years tilat a newborn could
introduced in the USA at the 1926 AVMA
expect to live, if he or she were to pass
meeting. Dr. Otto Stader developed the first
tllrough life exposed to the sex- and
steel pin metilod for external fracture
age-specific death rates prevailing at tl1e
fixation. In tile 1950s, Dr. H. A Gorman
time of his or her birth; 2) infant mortality
developed the first prosthetic hip joint, and
rate (per 1,000 live births )-the probability

Dr. F. L. Earl discovered tile tranquilizing
of a child born in a specific year dying
effects of reserpine.

before reaching the age of 1 yr; 3) age9) Uniformed services veterinary medicine: standardized mortality rate (nurnber/unit In 1916, with the establislm1ent of the United
population)-a weighted average of the

States Anny Veterinaiy Corps, the USA was
age-specific ( ages 30-70) mortality rates per
the last of tl1e industrialized countries to

100,000 persons, in which the weights are
commission a corps of military veterinarians.

the proportions of persons in the corre

During World War II, aimy veterinarians
sponding age groups of the WHO standard
were credited with providing higher quality
population; 4) childhood inllllunization rate
rations for troops, as well as more space for

(%)-the percentage of children (19-35 mo
armaments on cargo ships by tilorough.ly
old) who have received the recommended
trimming meat products and freezing tl1em in
combined vaccine series; 5) annual

2396

PUBLIC HEALTH PRIMER
population growth rate (%)-average

5) Develop policies and plans that support
exponential rate of annual growth of the
individual and community health efforts.

population over a given time period;

Policies and laws can effectively modify

6) density of physicians (mm1ber/w1it
human behavior and reduce negative health

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population)-nwnber of medical doctors
outcomes. Examples include limiting access

(physicians), including generalist and
to high-calorie beverages in school-age
specialist practitioners, per 10,000 pet"

children and "dram shop liability" to
sons; 7) gross national income per capita
discourage overconsumption of alcoholic

($USD)-total annual pw·chasing power,
beverages in public establishments.

standardized to the US dollar; 8) govern6) Enforce laws and regulations that ment expenditme on health as a percentage
protect health and ensure safety. The
of total government expenditure(%); 9) per
existence of policies and laws is not
capita total expendjture on health ($USD);
enough; compliance must be enforced to

10) population median age (years);
ensure the overall safety and health of the

11) obesity (%)-adults (>20 yr old) who
community. Ongoing assessment and
have a body mass index (BMI) �30 kg/m2.

education efforts are undertaken to ensure
that these policies and laws remain

ESSENTIAL PUBLIC HEALTH
relevant and known to the public.

FUNCTIONS

7) Link people to needed personal health
services and assure the provision of health

Under the auspices of DHHS, the USPHS
care when otherwise unavailable. Having
developed (and adopted in 1994) the followaccess to care when it is needed is important ing ten essential public health functions
in helping individuals prevent and avoid
to assist state and local health agencies
unfavorable health outcomes and medical
achjeve their mission of promoting physical costs. Components of these efforts are and mental health and preventing disease,
ut1dertaken at the local, state, and federal
injury, and disability.

levels to provide a coordinated system of

1) Monitor health status to identify
health care.

community health problems. A generally

8) Assure a competent public health and
accepted defmition of public health
personal health care workforce. Competent
smveillance is "the ongoing systematic
health care workers provide care more
collection, analysis, interpretation, and
effectively and efficiently than those less
djssemination of outcome-specific data
competent. This is facilitated by licensing
essential to the planning, implementation,
and credentialing processes, incorporating
and evaluation of public health practice."

core public health competencies into

Without Ws type of activity over tin1e, basepersonnel systems, and adopting continual line data cannot be analyzed for adverse
quality improvement opportunities for
events and trends.

public health workforce members.

2) Diagnose and investigate health

9) Evaluate effectiveness, accessibility,
problems and health hazards in the
and quality of personal and populationcommunity. As an adjunct tp surveillance, based health se1vices. Given scarce
public health agencies conduct targeted
resources, it is imperative to assess whether
screening programs ancl/or surveys to
programs and policies achieve intended
detect problems and hazards in the
outcomes. Cost-effectiveness analyses have
community. When detected, they are invesbeen proposed as one strategy to infom1
tigated to determine their magnitude, and
policymakers on how best to allocate health
results are used to inform public educacare resources.

tion and prevention efforts.

10) Support/sponsor research for new

3) Inform, educate, and empower people
insights and innovative solutions to healtll
about health issues. Once priorities have
problems. From the evidence-based results
been established through swveillance,
of coordinated research programs, healtl1
detection, and investigation, educational
and health care problems can be better
activities that promote improved health
understood and in1proved over time.

should be disseminated.

4) Mobilize conm1unity partnerships to

PUBLIC HEALTH FOCI OF
identify and solve health problems. Public

PREVENTION
health agencies at all levels can mobilize
conununity partnerships to solve health

When considering opportunities and methods
problems. Of particular importance is identito address healtl1 problems, til!'ee stages of fication of potential stakeholders who can
prevention are generally recognized:

contribute to or benefit from public health

1) Ptirnary prevention-focuses on avoidinterventions.

ing development of a disease by preventing

PUBLIC HEALTH PRIMER

2397
it before exposure. Examples of primary

Epidemiologic Terms and Concepts
prevention strategies include immunization
programs, health education, and smoking

The natural history of a disease in a
cessation interventions. Because disease is
population, sometimes termed the disease's

VetBooks.ir
largely avoided by these strategies, prin1ary
ecology, refers to tile cow"Se of the disease
prevention is generally regarded as the most from its beginning to its final clinical cost-effective forn1 of prevention.

endpoints. The natural history begins before ,

2) Secondary prevention-focuses on
infection (prepathogenesis period) when
early disease detection and intervention,
the agent sinlply exists in the environment,
ideally before the onset of clinical signs.

includes tl1e factors that affect its incidence

Examples include screening programs
and distribution, and concludes with either
against various forn1s of cancer ( eg, breast,
its disappearance or persistence ( endemcolon, prostate, etc), postexposure rabies nicity) in that environment. Although
prophylaxis, tuberculosis skin tests, and
knowledge of the complete natural history is
infectious disease contact investigations.

not absolutely necessary for treatment and

3) Tertiary prevention-focuses on the
control of disease in a population, it does
treatment and rehabilitation of individuals
facilitate the most effective interventions.

with disease(s). Examples include antimi

An in1portant epidemiologic concept is
crobial therapies, hypertension drugs, and
that neither health nor disease occlli'S
heart attack and stroke rehabilitation.

randomly iliroughout populations.

Because this stage focuses its effmts after a

Innumerable factors influence the temporal
disease is established, tertiary prevention
waxing and waning of disease. A disease is
has proved the most expensive form of
considered endemic when it is constantly
prevention.

present wiili.in a given geographic ai·ea. For
instance, ani.n1al rabies is endemic in tl1e

BASIC PRINCIPLES OF

USA An epidemic occw'S when a disease

EPIDEMIOLOGY
occlli'S in larger nwnbers tl1an expected in
a given population and geographic area.

The definition of epidemiology is "the study

Raccoon rabies was epidemic throughout tile
of disease in populations and of factors that
eastern USA for much of ilie 1980s and 1990s.

determine its occurrence over time." The

A subset of an epidemic is an outbreak,
purpose is to describe and identify opportuniwhen tile higher disease occurrence occurs ties for intervention. Epidemiology is conin a smaller geographic area and shorter cerned with the distribution and detern1iperiod of tinle. Finally, a pandemic occW'S
nants of health and disease, morbidity, ir\jury,
when an epidemic becomes global in scope
disability, and mortality in populations. For

(eg, influenza, IIlV/AIDS).

veterinary epidemiology, this intervention

The population at risk is an extremely
is to enhance not only healtl1 but also
important concept in epidemiology anti
productivity. Distribution implies tl1at
includes members of the overall population
diseases and other health outcomes do not
who are capable of developing tile disease
occur randomly in populations; determi
or condition being studied. This concept
nants are any factors tl1at cause a change in a seems sinlple at first, but misinterpretations health condition or other defined characteriscan lead to erroneous study results and tic; morbidity is illness due to a specific
conclusions. As a sinlple exainple, a study
disease or health condition; mortality is
of testicular cancer among residents in a
deatl1 due to a specific disease or healili
population should not include women in tl1e
condition; and tile population at risk can
population at risk (frequently expressed as
be people, animals, or plants.

tile "denominator" in an epidemiologic ratio).

Epidemiology is applied in many areas of

A ratio is the value obtained from dividing
public healili practice. Among tl1e most
one quantity by another (X/Y). The nwnerasalient are to observe historical health tor and denominator may be independent of
trends to make useful projections into the
each oilier. In fact, in epidemiology, the term
future, discover (diagnose) current health
ratio is applied when the nwnerator is not a
and disease burden in a population, identify
subset of the denominator. For example, in a
specific causes and risk factors of disease,
class of veterinary students in which 88 are
differentiate between natural and intenfemale and 14 are male, the sex ratio of tional events ( eg, bioterrorism ), describe
female students to male students is 88/14,
the natural history of a paiticular disease,
or6.3 to 1.

compare vaiious treatment and prevention

A proportion is a type of ratio in which
products/techniques, assess the impact/
the nwnerator is part of the denominator
efficiency/cost/outcome of interventions,

(N[A + Bl). Therefore, they are not
p1ioritize intervention strategies, and
independent. For example, suppose that,
provide fow1dation for public policy.

among domestic dogs testing positive for

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PUBLIC HEALTH PRIMER
internal parasites in Glendale, Arizona, 889
fatality rate, which is the number of deaths
were male and 643 were female. The propo1� due to a particular disease occurring among tion of female dogs among those found
individuals afflicted with that disease in a
to have parasite infections would be
given time period. In another example,

643/(889 + 643), or 0.42.

consider a large veterinary practice in the

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A rate is another type of ratio in which
southwest USA that frequently sees dogs
the denominator involves the passage of
with coccidioidomycosis. The practice
time. This is in1portant in epidemiology,
diagnosed 542 clinical cases in a particular
because rates can be used to measure
year, 83 of which died from the disease in the
the speed of a disease event or to make
course of that year. The month in which the
epidemiologic comparisons between
most cases were diagnosed was September,
populations over tin1e. Rates are typically
in which 97 cases were diagnosed. Further,
expressed as a measure of the frequency
at a single point in time (perhaps based on
with which an event occurs in a defined
the results of a serosurvey of dogs in the
population in a defined time ( eg, the number practice area), 237 dogs of 6,821 dogs with of foodbome Salmonella infections per
active records in the practice had the

100,000 people annually in the USA).

disease. In this scenario, the prevalence

Incidence is a measure of the new
of coccidioidomycosis at the time of the
occurrence of a disease event ( eg, illness
serosurvey would be 237/6,821 or 0.035
or death) within a defined time period in

(3.5%); the incidence in September would be
a specified population. 1\vo essential

97 cases, and the incidence rate would be
components are the number of new cases

97/6,821 or 0.014 ( l.4%). Finally, tl1e annual
and the period of time in which those new
mortality rate due to coccidioidomycosis
cases appear. In an exan1ple regarding the
would be 83/6,821 or 0.013 (l.3%), and the
class of veterinary students, if 13 of them
case fatality rate would be 83/542 or 0.153
developed influenza over the course of 3

(or 15.3%).

mo (one quarter), the incidence would be

Public health surveillance is defined as

13 cases per quarter.

the ongoing systematic collection, analysis,

An incidence rate takes the population
interpretation, and dissemination of
at risk into account. In the previous examoutcome-specific data essential to the ple, the incidence rate would be 13 cases
planning, implementation, and evaluation
per quarter/102 students, or 0.127 cases
of public health practice. In epidemiology,
per quarter per student. Incidence rates
health surveillance is accomplished in either
are usually expressed by a m ultiplier that
passive or active systems. Passive surveilmakes the nun1ber easier to conceptualize lance occurs when individual healtl1 care
and compare. In this example, the multiplier providers or diagnostic laboratories send would be 100, and the incidence rate would
pe1iodic reports to the public health agency.

be 12. 7 cases per quarter per 100 students

Because this reporting is voluntary ( some

( or 12. 7"/o). An attack rate is an incidence
times referred to as being "pushed" to health rate; however, the period of susceptibility is
agencies), passive surveillance tends to
very short (usually confined to a single
underreport disease, especially in diseases
outbreak).

•
witl1 low morbidity and mortality. Passive

A similar concept to incidence is prevasurveillance is useful for longtenn trend lence. Prevalence (synonymous with "point
analysis (if reporting criteria remain
prevalence") is the total nun1ber of cases
consistent) and is much less expensive than
that exist at a particular point in time in a
active surveillance. An example of passive
particular population at risk. Again using the
surveillance is the system of officially
influenza example from above, if 7 students
notifiable diseases routinely reported to CDC
had influenza at the same time during the
by select health departments across the USA.

academic quarter, the prevalence would be

Active surveillance, in contrast, occurs

7/102 or 0.069 cases per class ( or 6.9%).

when an epidemiologist or public health

Measures of disease burden typically
agency seeks specific data from individual
describe illness and death outcomes as
health care providers or laboratories. In tl1is
morbidity and mortality, respectively.

case, the data are "pulled" by the requestor, Morbidity is the measure of illness in a
usually during emerging diseases or
population, and numbers and rates are
significant changes in disease incidence.

calculated in a sinillar fashion as with

Active surveillance is usually much more
incidence and prevalence. Mortality is
expensive and labor intensive; it typically is
the corresponding measure of death in a
lin1ited to sh01t-tem1 analyses of high-in1pact
population and can be applied to death from
events. An example is tl1e 1 -yr surveillance
general (nonspecific) causes or from a
conducted by CDC of the rapid increase in
specific disease. In the latter case, cause-incidence of coccidioidomycosis among specific mortality is expressed as the case
people in Arizona in 2007-2008.

PUBLIC HEALTH PRIMER

2399

Descriptive Epidemiology

Case reports are accounts of single or

Given that neither health nor disease is
a few noteworthy health-related incidents
equally distributed throughout a population,

( eg, an epidemiologic description of a case
epidemiologists use various methods to study of hun1an rabies).

and desclibe their occurrence. In descnptive

Case series are listings of a la.i·ger number

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epidemiology, diseases are classified
of cases usually presented consecutively
according to the valiables of person, place,

( eg, a characteiization of dog bite incidents
and time.

in a population of veterinarians and/or

Person: Who is affected by this disease?

technicians over time). Case series articles

This is relevant, because certain variables
are useful for comparing variables of person,
may highlight changes in disease status and
place, or tin1e as they appear to affect tl1e
can be used to focus additional studies and
ocCUITence of a pa.iticulat' disease.

interventions. Common person variables

Cross-sectional studies are one-time
include age, sex, race, socioeconomic
assessments of the incidence or prevalence
status marital status, religion, smoker/
of a disease in a defined population, which
nons1�oker etc. In the case of animals,
is usually selected at random from a larger
equivalent �ariables may include species,
population at risk ( eg, a serosurvey of .

breed, reproductive status ( eg, intact vs
veterinariatlS for the presence of antibodies
neutered, pregnant vs nonpregnant),
to Bartonella henselae organisms to
function ( eg, meaUmilk/fiber production,
detem1ine risk factors and for cat scratch
race horse vs working horse vs pleasure
disease). Cross-sectional studies are
horse, companion dog vs mili
especially useful in forming hypotheses

�y working

_to
dog), and wild/feral vs domesticated (cats).

be addressed by follow-on analytic studies.

Place: Where does this disease occur?

Two main types of bias in desc1iptive

Place valiables commonly illustrate geoepidemiology at'e selection bias and obsergraphic differences in the occurr vation bias. Selection bias results from the

_ence of a
particular disease. Focused studies can help
identification of subjects/cases from a
epidemiologists to detennine why those
subset that is not representative of the entire
differences have occurred and to identify
population at risk A nonmedical exa.i11ple of
specific lisk factors. Common place valiables selection bias would occur in a voter survey, include comparisons across national, state,
intended to predict tl1e outcome of a
and municipal boundalies and between
political election, but drawn from _a sa.inple
urban and rural conununities. For animal
of voters from either high-or low-income
populations, "place" may refer to housing
status neither of which would be represent

( eg, indoors vs outdoors, pen nun1ber or
ative �f the overall voting population.

stall) or type of herd management ( eg,

Observation bias arises from systematic

.

intensive feedlot confinement vs extensive
differences in the method of obtaining
grazing). Place may also relate to lisk of
infonnation from subjects/cases. Consider
exposure to infectious a.ilinlals at sale barns
a study comparing library usage between
or during shipment or to external factors
students at two universities. Sigrii.ficant
such as severe weather and natural disasters.

differences might result if students from

Time: When and over what time period
one university were queried over the phone

(hours, days, weeks, day vs night) does this
regarding libra.iy visits, whereas students at
disease occur? Tinle valiables are in1portant
the other university were directly observed
to describe when disease occurs in relation
for actual usage. In general, bias in
to va.iious factors of potential exposure and
descriptive studies is not as prevalent or
vulnerability. In aninlals, time may refer to
sigrii.ficant as bias in analytical studies.

milking shift, breeding season, la.inbing/

In sununa.iy, descriptive epidemiolo_gy
calving season, at weaning, during shipment,
serves to describe the occurrence of disease
on anival at the feedlot, dry vs wet season,
in a population. Descriptive methods are
etc. Common time valiables include seculat'

conunonly applied to little-known diseases;
trends ( changes over long periods of time),
they use preexisting data, address the .

seasonal/cyclic periods, and specific pomts in questions of who/where/when, �d identify time ( eg, outbreaks, epidemics, clusters, etc).

potential associations for more in-depth

When a particular disease is observed
analytical studies.

relative to the variables of person, place,
and time, it is often systematically described Analytical Epidemiology to facilitate more in-depth study. These

Analytical studies at'e applied to study the
systematic descriptions commonly take
etiology of disease, to identify a causal
the form of case reports, case series, or
relationship between exposures and health
cross-sectional studies.

outcomes. They are typically used when

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PUBLIC HEALTH PRIMER
insights of a particular health issue are
variables such as demographics, geography,
available, commonly from previous
and the social enviromnent.

descriptive studies. In evaluating the

Ecologic studies also have several
causality of disease associations, analytical
disadvantages. First, tl1e measw-ement of

VetBooks.ir
studies address the question of "why" as
many exposw-es is in1precise, especially of
opposed to the "person/place/time" of
large groups in which the influence( s) of
descriptive studies.

tl10se exposw-es is difficult to define or not

Once potential associations have been
equally exe1ted. This phenomenon of unequal
observed between those who have a
variable exertion results in another potential
particular disease and those who do not,
drawback to ecologic studies. Known as
further investigations are undertaken to
ecologic fallacy, it is described by "associadetermine causality and identify effective tions observed at the group level do not
interventions. The first step in an analytic
necessarily hold true at the individual level."

study is to fom1 some conjecture regarding

As an example, one could determine that the
observed exposures and health outcomes. In
average IQ of a class of veterinary students is
analytical studies, this conjecture is tem1ed
above average (which, by definition, would
the null hypothesis, meaning that the default be 100). lf a particular· student was randomly assumption is that there is no association
selected from that class, could it be infen-ed
between the exposure in question and the
tl1at that student's IQ was above 100? The
disease outcome. Note that this asswnption
answer is no, because of the difference
of no association is made even though the
between average and median. If the class had
epidemiologist often thinks that some
only a few people above average, but these
association actually exists. Once the null
students were significantly above average,
hypothesis is generated, studies are designed
and the rest of the students were only slightly
to test it and either reject it (by finding that
below average, tl1e distribution would be
some association actually does exist between
skewed towar·d a higher IQ when, in actuality,
exposure and disease outcome) or accept it
many members of tl1e class would be below

(by finding that no association exists).

average.

Analytical epidemiology is accomplished
tl1rough either observational studies or

Cohort Studies: In tl1is type of study, a
inte1ventional studies. In the former, the
group of individuals (tem1ed a cohort) is
investigator does not control the exposw-e
obse1ved over time for changes in health
between the groups under study and typically outcomes.

cannot randomly assign subjects to study

When the period of the study is from
groups.

the present into the future, the study is a
prospective cohort study. In tlus case,
the cohort is assw11ed to share a particular
exposure and is followed over time to

Observational Studies:

docun1ent the occurrence of new instances

Ecologic Studies: The unit under study
of a particular disease or outcome. Obviously,
is a group of people or animals versus an
each member of the cohort must not have the
individual. The group has no size limitation
disease or outcome at tl1e beginning of the
but must be able to be defined. For instance,
study. One of the most famous medical
the group could be a kennel of dogs, a class
prospective coho1t studies is the Franungof veterimuy students, or the citizens of an hain Heart Study. Researchers began the
entire country. Once defined, the group is
study in 1948 by recruiting 5,209 men and
analyzed against some exposure to see what
women, 30-62 yr old, from the town of
outcome(s) ensue. Examples of ecologic

Franungharn, Massachusetts. Since that tin1e,
studies include Dr. John Snow's analysis of
they have accomplished extensive serial
the association between the incidence of
physical exar11inations and swveys relating to
cholera in London and where people
the development of cardiovascular disease.

obtained their drinking water, an analysis of

The major advantage of the prospective
how tobacco taxes affect tobacco usage, and cohort study is that many different an analysis of certain occupations for
exposures can be considered and ar1alyzed
resultant hearing loss.

for influencing tl1e outcome under study.

Ecologic studies have several advantages

Disadvantages include the high cost in
over other types of observational studies.

terms of money and time dwing the period

They are relatively quick, easy, and inexof the study and the inability to study very pensive. Individual data are not necessary,
rare diseases or health outcomes unless the
only aggregate data for the group( s) under
cohort is extremely large.

study. Finally, tl1ey are useful in generating

When the period of the study is from the
information about the overall context of
past to the present, the study is a retrospec
health, especially how it is affected by
tive cohort study. The methodology is very

PUBLIC HEALTH PRIMER

2401
similar to that of the prospective cohort
and the incidence in intact male dogs was
study, except that all the events ( exposures

0.36%. ln this case, the relative risk would
and outcomes) have already occurred; the
be 1.37/0.36 or 3.8. This could be stated as
investigator is merely looking back rather

"Neutered male dogs would be nearly four
than forward. Retrospective studies are
times as likely as intact male dogs to

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conceived after some individuals have
develop prostate cancer."

already developed the outcomes of interest.

The investigators jwnp back in time to

Case-Control Studies: ln this type of
identify a cohort of individuals at a point in
study, subjects are selected as either having
time before they developed the outcomes of
a particular outcome (cases) or not having
interest, and try to establish their exposure
the outcome (controls). They are then
status at that point in time. They then
compared in a retrospective way to identify
determine whether the subject subsequently differences in their exposures that might developed the outcomes of interest. If so,
explain the differences in outcomes. Ideally,
they can analyze the exposure( s) that may
cases and controls should be as similar as
have contributed to those outcomes.

possible in all characteristics except the

Retrospective cohort studies have several outcome in order to make the compaiisons advantages over prospective cohort studies.

simpler and more meaningful. That is why

They typically take less time and are less
some investigators "match" cases and
expensive. Additionally, they can address
controls. ln one notable example, a very
rare outcomes, because the cases are
large case-control study in 1950 studied
selected after having already developed the
people with lung cancer and demonstrated
disease or outcome. Disadvantages include
a very positive association between
a potentially high possibility of selection
smoking and lung cancer. Although it did
bias, the fact that individuals may have
not prove causality alone, it "'-as instrun1endifficulty recalling certain exposures tal in the U.S. Surgeon General's now-stand

(termed recall bias), and the requirement
ai-d warnings.

for the existence of medical and/or

Case-control studies have several
exposure records.

advantages. They are inherently retro

Regardless of being retrospective or
spective, so they are relatively quick and
prospective, the measure of association of
inexpensive. Because the cases have
all cohort studies is the relative risk (RR).

already been identified, they are appropriate

Relative risk is calculated by dividing the
for studying rare diseases and exan1ining
incidence rate of the disease or outcome in
multiple exposures. Disadvantages include
the exposed individuals by the incidence
the fact that, like cohort studies, they are
rate in the unexposed individuals. An RR
prone to selection, recall, and observer bias.

of 1 means there is no difference in risk

Additionally, their application is limited to
between the two groups. An RR <l means
the study of one outcome.

that the outcome is less likely to occur in

The most conunon measurement of
the exposed group than in the unexposed
association in case-control studies is the
group. Conversely, an RR> 1 means the
odds ratio. The odds ratio (OR) represents
outcome is more likely to occur in the
the odds that an outcome will occm from a
exposed group than in the unexposed
particular exposure, compared with the odds
group. Consider an example in which
of the outcome occurring in tl1e absence of
the incidence of prostate cancer among
that exposure. ORs are calculated using a
neutered male dogs was found to be 1.37%,

2 x 2 frequency table (TABLE 1).

•M:iii• CALCULATING AN ODDS RATIO

Outcome Status

+

Exposure Status

+
a
b
c
d
a = Number of exposed cases
b = Number of exposed non-cases
c = Number of unexposed cases
d = Number of unexposed non-cases

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PUBLIC HEALTH PRIMER

OR= ale= ad
ing disease etiologies; observational studies
b/d be
are much better suited for this purpose.

An OR of 1 means the exposme did not

Nonrandomized (Community) Trials:

affect the odds of the outcome. An OR > 1
ln this type of study, the units are groups
means the exposure is associated with a

( or comm unities) of paiticipants assigned

VetBooks.ir
higher odds of the outcome, and an OR <l
to treatment or control conditions.

means the exposure is associated with a

Although the communities may be selected
lower odds of the outcome. Although a
at random, tile individuals within tl1em
higher OR indicates a stronger association
obviously are not. These studies ai·e
between exposure and outcome, it does not
conunonly undertaken to assess the quality
necessarily in1ply statistical significance and, and effectiveness of educational prograins, by itself, is not enough to prove causality.

behavioral changes, or mass interventions
such as water fluoridation.

lnterventional Studies: The other
category of studies that comprise analytical

Bias
epidemiology are interventional studies.

Bias is defined as tile systematic deviation
ln contrast to observational studies, the
of results or inferences from truth. Bias is
investigator using an interventional
extremely difficult to completely avoid
approach can intentionally change some
when undertaking scientific study.

form of exposure between several groups

Therefore, studies ai·e designed in ways that
to detemline differences in outcome(s). ln
minimize the sources and effects of bias.

medical research, these exposures typically

Exainples of bias are described below.

include interventions such as vaccines,

The Hawthorne effect: Participants
therapeutic drugs, sw·gical techniques, or
in a study may act or behave differently
medical devices. The results of inte1venbecause tlley know tl1ey are being studied.

tional studies can be very powerful in

In 1924-1932, workers at the Hawtl10me
proving causality or identifying efficacy

Works ( an electric company near Chicago)

of various inte1ventions. lnterventional
were studied to see whether productivity
studies typically take one of two fonns,
was greater depending on how much light
either a randomized controlled ( clinical)

was provided at work Results showed that
trial or a nonrandomized ( co nun unity) trial.

productivity increased during the comse of

Randomized Controlled (Clinical) Trials:

the study regardless of tile changes in light;
ln this type of study, participants are
the workers just performed better because
selected from a population and randomly
of the attention. When the study ended,
assigned to one of two groups, one being the productivity went back to prestudy levels.

study group and the other being the control

Recall bias: Cases and controls may
group. Study groups receive the intervenremember an exposure differently (and tion, and the controls do not.

non-randomly). Usually, cases remember

Bias can be introduced in such a trial
exposures more cleai·ly than controls.

when either the participants or the investiga

Selection bias: This occms when
tor know which participants are in which
selected controls are not representative
group. This bias can be alleviated in one of
of the population from which the cases
two ways. First, in a single-blinded design,
were selected. ln oilier words, there is an
the participants are unaware whether they
importai1t chai·acteristic of tile controls
are in the study group or the control group.

tllat make them different from tile general

Additionally, in a double-blinded design,
population. An exan1ple is tile healtliy
neither the investigator nor the participants
worker effect, which refers to the phenomare aware of the group assignments.

enon that employed groups have lower

A major advantage of randomized
mortality than the general population.

controlled clinical trials is an inherently

Therefore, if tl1e study groups are comhigh validity for identifying differences in prised of differing fractions of employed
therapeutic efficacy of various inte1venand unemployed people, the results may tions. Perhaps tile major disadvantage is the
very well be skewed.

high potential for ethical implications if an

Observer bias: The investigator, having
intervention with great potential benefit is
knowledge of the outcome(s), might record
intentionally withheld from the control
exposures differently between cases ai1d
group ( eg, tile historic Tuskegee Syphilis
controls.

Study). For this reason, it can be very

Confounding: ln epidemiologic
difficult to legally use hun1an paiticipants in
studies, a confatmder is a variable tllat is
many such trials. Additionally, this type of
not considered in the study design but is
study is not usually applicable for discover-
associated witll the exposure and exerts

PUBLIC HEALTH PRIMER

2403
an effect on the outcome. Confounders can
causally associated. However, in most
either produce a false association between
epidemiologic studies, the relationship
variables or mask a trne association between between variables (such as exposure variables. An example of the former was a
and outcome) is much more difficult to
spurious conclusion drawn from a study of
ascertain and requires more extensive
the relationship between alcohol consumpanalysis. Several sets of systematic criteria VetBooks.ir
tion and heart disease. In the study, it was
for determining causality have been
concluded that alcohol conswnption was
proposed: 1) Strength-Although a small
significantly associated with heart disease.

association does not mean tl1at there is not

Smoking was later identified as a confounda causal effect, the larger the association, er, because smoking was correlated both
the more likely that it is causal. 2) Consistwith alcohol conswnption and also with ency-Repeatedly sinlila.r findings observed
heart disease. When corrected for the effects
by different persons in different places with
of this confounder, no association was found
different samples strengthen the likelihood
between alcohol consumption and heart
of a causal effect. 3) Specificity-Causation
disease.

is more likely in a very specific population
at a specific site and disease with no other

Error
likely explanation. The more specific the

When analyzing results of an epidemiologic
association between an exposure and an
study, there are two catego1ical types of
outcome, the higher the probability of
error when either accepting or rejecting the
causation. 4) Temporality-The outcome
null hypothesis.

must occur after tile exposure. 5) Biological

'lype I error, also known as a false gradient-Greater exposure generally
positive, is when the null hypothesis is
results in greater incidence of the outcome.

rejected when it actually should have been

However, in some cases, the mere presence
accepted. In otl1er words, this is the eITor of
of the exposure, without regard to its
accepting an alternative hypothesis (the real magnitude, can trigger the effect. In yet hypothesis of interest) when the results can
other cases, an inverse relationship is
actually be att1ibuted to chance. 'Iype I
observed when greater exposure of a
error ( which can never be zero) is generally
protective factor leads to lower incidence
reported as the P value. In scientific
of outcomes. 6) Plausibility-A rational,
studies, the most commonP value is .05,
explainable mechanism between cause and
which means an e1Tor of <5% of detecting
effect is helpful (but may be limited by curan association between a variable and an rent knowledge). 7) Coherence-Agreement
outcome is acceptable.

between epidemiologic and laboratory

'lype II error, also known as a false
findings increases the likelillood of a causal
negative, is when the null hypothesis is
effect. 8) Analogy-The effect of sin1ilar
accepted when it actually should have been
associations between other variables of
rejected. In other words, the study did not
exposure and outcome may be considered.

have adequate power to detect an association between a variable and an.outcome Sensitivity and Specificity
when the association actually existed.

Veterinary practitioners use many

Variable Associations and Causality
diagnostic tests to determine what may be
wrnng with an animal and how it may be

In epidemiology, variables are either
treated. The diagnostician 111Ust realize
associated or they are not. If the variables
tl1at these tests are fallible and tl1at results
are not associated, there is no relationship;
are usually only close approximations of
they are independent. If the variables are

"truth." We can assume that an animal
associated, that relationship can be either
either has a medical condition or does not;
positive or negative. If two variables are
however, no tests are 1 OOOA, sensitive and
positively associated, the values of both
specific. That is, no test can eliminate
variables increase or decrease together.

the potential for false-positive and false

If they are negatively associated, the value
negative results. However, there are
of one variable increases when the other
methods to interpret test results to reduce
decreases. Finally, if an association exists
their inherent fallibility. Those tests or

(positive or negative), it is either causal or
diagnostic procedures known to produce
non causal related to the outcome.

the absolute best results are termed "gold

When two variables are associated, it
standard" tests. It is against these gold
is sometimes obvious as to whether it is
standards tllat newer, usually faster and
causal. Consider the relationship between
more convenient, tests a.re measured in
animal bites and rabies; we know they are
tem1s of sensitivity and specificity.

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PUBLIC HEALTH PRIMER

Sensitivity is the probability of a
positive. PPV is calculated as true positives
positive test result when the disease is
divided by the sw11 of the tme positives and
actually present. A sensitive test is "positive the false positives: a/(a + b). False-negative
in disease" and minimizes false-negative
test results do not affect the PPV. Therefore,
results, thus minimizing type II error.

if the PPV of a test is 1000/o, the validity of a

VetBooks.ir

Specificity, in contrast, is the probability
negative test result is still unknown.

of a negative test result in the absence of

The negative predictive value (NPV) is
disease, thereby correctly classifying an
the probability of a patient not having the
individual as disease-free (regarding that
disease condition when the test is negative.

particular condition). A specific test is

NPV is calculated as tme negatives divided

"negative in health" and minimizes
by the sum of the true negatives and the
false-positive results, thus minimizing type
false negatives: di( c + cl). False-positive test l error. To calculate the sensitivity and
results do not affect tl1e NPV. Therefore, if a
specificity of a test, consider the following
test was reported to have an NPV of 100%,

2 x 2 table (see TABLE 2).

the validity of a positive test result is still

Sensitivity and specificity a.re inversely

Wlknown.

propmtiona.l, ie, when one increases, the

PPV and NPV a.re clinically relevant,
other decreases. Therefore, the accuracy of
because they a.re directly related to the
a test is a trade-off between each of these
prevalence of disease. For diseases of high
parameters. Screening tests tend to have
prevalence, the PPV of a test will be high
higher sensitivity and lower specificity,
and the NPV will be low. For rarer diseases,
because the purpose of such a test is to
the opposite will be true, ie, the PPV will be
detect the maximum nw11ber of individuals
low and the NPV will be high. For these
with the pa.rticula.r disease condition. A
reasons, the assumed prevalence of a
negative test result, therefore, strongly
disease must be taken into accotmt when
implies that disease is absent, whereas a
interpreting diagnostic test results.

positive result may require additional,
confirmatory testing. For that reason,
positive tests are oft-en followed up with

Disease Outbreak Investigation
a confirmatory test that displays higher

Public healtl1 officials investigate disease
specificity to identify which positive results
outbreaks to control them, to prevent
are tme and which a.re false. Given the high
additional illnesses, and to learn how to
specificity of confirmatory tests, a positive
prevent similar outbreaks from happening
result strongly implies that disease is
in the futw·e. Whether an outbreak is
present.

foodborne in migin or from another

In clinical medicine, two additional
infectious somce, the methodology is
diagnostic test para.meters a.re relevant. The
sin1ila.r. The following steps in investigating
positive predictive value (PPV) of a test
disease outbreaks a.re used by the CDC:

is the probability of a patient actually having prepare for field work, con.film the the disease condition when t11e test is
existence of an outbreak, verify the
itM•il CALCULATING TEST SENSITIVITY AND SPECIFICITY

Gold Standard

Disease Present

Disease Absent Total

Positive
a
b
a+b

Test Result

Negative
c
d
c+d

Total
a+c
b+d
a = True positives; Lhc Lest has correctly diagnosed the disease b = False positives; tl1e test is positive but disease is absent c = False negatives; the test is negative but disease is present d = True negatives; the test correctly diagnosed the absence of disease Sensitivily is the true positives divided by the sum of the true positives and the false negatives: a/(a +c)

Specificity is the true negatives divided by the sum of the true negatives and the false positives: cl/(b + d)

PUBLIC HEALTH PRIMER

2405
diagnosis, establish a working case
r
definition, engage in systematic case
finding, apply descriptive epidemiology,

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f----
develop and test hypotheses ( analytical
epidemiology), implement control
measures, and communicate findings.

Although these steps are accomplished
in a systematic fashion, they frequently

I __
overlap or occur concurrently. For example,
establishing a working case definition
typically begins while tl1e diagnosis is in tl1e

Epidemic curve common point source.

process of being verified and continues

Courtesy of Dr. Donald L. Noah.

tl1rough the injtial process of systematic
case finding.

Establishing a working case definition
is the method by which public health
officials define what individuals are
included as official cases in the outbreak
and illustrate the boundaries of the
outbreak. An effective case definition is
critical because it may be confusing,
especially in the absence of definitive
diagnostics, to differentiate between
actual disease cases and those ill from
other causes. The case definition defines a

Epidemic curve common continuous source.

case in terms of person, place, and time.

Courtesy of Dr. Donald L. Noah.

Person criteria typically include vulnerability factors such as age, sex, signs/
symptoms, or attendance at certain meals
or public functions. Place criteria usually
include a geographic boundary such as a
state or local area, a school class, or a
particular restaurant. Time parameters
may be after an implicated meal (if
food borne) or oilier types of exposures.

Case definitions are usually based on
either clinical signs or diagnostic test
results. The former is more subjective
than the latter but can be just as effective,

Epidemic curve common intermittent source.

especially in field epidemiologic condi

Courtesy of Dr. Donald L Noah.

tions. As the investigation ensues and
more information becomes available,
it may be necessary to revise the case
definition. However, this is done judiciously, because changes to the case definition result in changes to the
epidemic curve.

The epidemic ( epi) curve shows
progression of an outbreak over time. The
horizontal axis represents the date when an

.....

Ep

,�
idemic curve propagated source.

•
individual became ill, also called the date of
onset. The vertical axis is tl1e number of
individuals who became ill on each date.

Courtesy
of Dr. Donald L. Noah.

These are updated as new data come in and
thus are subject to change. The epi curve is
complex and may be limited by infornrntion
deficiencies and inaccurate case definjtions.

Despite these potential lin1itations, detailed
curve can show useful infonnation
infonnation regarding tl1e dates and
regarding the nature of the outbreak.

numbers of reported cases is visually useful.

The overall shape of the epi curve can give

Moreover, in addition to the magrutude and
clues to the type of exposure that resulted in
duration of the outbreak, the shape of tl1e
tl1e outbreak. 'Iypical epi curves from

2406

PUBLIC HEALTH PRIMER
common sources include 1) a common
nlicrobial access to nub·ient som·ces. early
specific point source in which all cases
all foods are washed, rinsed, sifted, s01ted,
were exposed at the same time and place
or trimmed dming processing, which se1ves

(eg, a foodbome illness outbreak);
to limit the i.Jlitial level of contaniination.

2) a common sow·ce with continuous

Additionally, simple packaging increases
expos me in which although the source is
the shelf life of many foods and prevents

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common, cases gradually rise before either
contanlination from the envi.J·onment and
peaking or plateauing and declining; and
otl1er food items.

3) a common source with intem1ittent

Acidity (measmed by pH): The optimal
exposw-e in which the peaks occm· at irregupH range for microbial growtl1 is 4.6-7.5.

lar times corresponding to the earlier

Therefore, for items such as bottled sauces/
exposw-es. ln addition to outbreaks having
condi.J11ents and pickled foods, a common
common sow-ces, they can have propaand effective preservation technique is to gated sources, in which cases can directly
lower the pH (acidify) of the item below 4.6.

infect other cases separate from the initial

Conversely, some food products ( eg, fish,
sow-ce. ln a propagated source outbreak,
olives, eggs) can be processed with sodim11
person-to-person transmission occurs,
hydroxide Qye) to raise the pH above this
often through several cycles before
range.

declining.

Temperatme: The optima.I temperatme

Another attribute of an outbreak that can
range for many food borne pathogens is
be illustrated by the epi curve is tl1e period

40°F-140°F. For tllis reason, prepared foods
of incubation. For example, in a common
are held in tllis range for as little time as
point sow-ce outbreak, the investigation
possible. As a general rule, 4 hr is considfrequently identifies the event ( eg, meal, ered the maxi.J11a.l tin1e in this danger zone
social gathering, etc) when the expos me
to limit microbial growtll.

occmred. ln this case, the peak of cases

Ti.J11e: Bacteria reqt1ire time to propagate
occm· one incubation period after the
to the point of being infective and virulent.

exposw-e event. ln a propagated source

In genera.I, 4 hr is considered the maximal
outbreak, the peaks of cases occur one
time period in tl1e temperature danger zone
incubation period apait.

in retail food establishments.

Oxygen: Most food borne pathogens are
aerobic in natlU'e, ie, they require oxygen for

BASICS OF FOOD SAFETY
multiplication. Oxygen also facilitates the
spoilage process. Techniques that limit

The USA has the safest and most plentiful
available oxygen include drying, carming,
food supply in the world. These attJibutes are bottling, vacum11 packaging, adding frequently and mistakenly taken for granted.

antioxidants, and modifying the storage
ln truth, however, they are maintained by
ab11osphere by replacing oxygen with an
motivations such as increases in production
il1e1t gas such as nitrogen or cai·bon dioxide.

efficiency, reductions in market uncertainty,

An added benefit to a modified/controlled
and tl1e goal of higher profits.

atmosphere is that it slows the ripe1ling
process and can extend the shelf life of

Foodborne Pathogen Requirements
many fruits and vegetables by months.

Moisture: Foods lower in water activity

Nearly all foods contain pathogens, which
are more resistant to U1e growth of many
originate from either tl1e product itself or
food borne patl1ogens. By definition, the
containination dming processing. As an
water activity (aw) of water is l. Foods with
example, CDC reports that 24% of' san1pled
an aw <0.85 are considered generally safer
raw chicken paits were contaminated with
than foods with a higher aw. Tecluliques

Salmonella organisms. Regardless of their

U1at lower the water activity of foods
som·ce, pathogens have common environinclude drying, dehydratil1g, freezing, salt/
mental/nut1itional requirements, each of
sugar CW'ing, and pickling.

which presents various control opportLUlities. The acronym FAT TOM can aid in leai11ing these common requirements.

Food Processing and Preservation

Food (some somce of energy): Controlling Vi.Jtually all foods are processed to some this requirement is perhaps the most difficult
degree. Exillllples of minin1al processing
because, as the nutrient content of tl1e food
tecluliques include washing, peeling,
is reduced, tl1e quality and usefulness is
slicing, juicing, freezing, dryi.J1g, fem1enting,
sinlilarly reduced. However, certain methods and pastelU'izing. More extensive processof processing and prese1ving serve to limit ing techniques include baking, frying,

PUBLIC HEALTH PRIMER

2407
smoking, toasting, puffing, shredding,
dmes; each plant must maintain records of
flavoring, coloring, and fortifying.

the entire process, as well as records to ve1ify

Regardless of the degree, foods are
the plan.

processed for the purposes of preservation,

The primary purposes of food presPrvasafety, variety, convenience, nutiitional tion are to inhibit the growth of pathogenic

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enhancement, and increased marketability.

microorgarlisms and to retar·d organic

Although these processing techniques have
degradation such as oxidative rar1cidity.

resulted in a safer and more plentiful supply,

Ma11y processes involve the use of multiple
health concerns about food processing have
techniques. In aclclition to extending the
been raised because of certain atti·ibutes
shelf life of food products, the quality a11d
of processed foods, such as added sugar,
acceptability of ma11y food products, such
soditun, saturated/trans fats, refined grains,
as cheese, yogwt, a11d pickled onions, are
low fiber content, and their conducive natme actually enhanced by the prese1vation toward W"Lhealthy behaviors. Moreover,
process. These purposes are attained
processing techniques such as grinding
through one or more actions of the preset'increase the surface area of foods, as in the vation process. They include reducing U1e
case of han1bw·ger, which renders them
existing pathogen load, alte1ing the pH and
more capable of supporting the growth of
temperatme, lowering the oxygen content,
pathogenic microorgarlisms.

reducing the water available for microbial

In the 1960s, the National Aeronautics
growtl1, and providing a physical barTier to
and Space Administration (NASA) asked
contarnination.

the U.S. Army and the Pillsbury Company

Traditional food preservation teclmiques,
to develop safe foods for marITTed space
aimed toward one or more of the above
flights. In a novel approach, Pillsbury
purposes, include the following: d1ying
required contractors to identify "critical

(reduces water necessary for microbial
failme areas" and eliminate them from
growtl1), refrigeration (slows microbial
the production system. This systematic
growth and enzymatic activity), freezing
approach became known as the Hazard

(prese1ves food for longer periods), salt or

Analysis Critical Control Point (HACCP)

sugar curing (reduces water [especially in
process. The underlying principle of
meats ar1d fruit]), smoking (coats foods

HACCP, which focuses on health safety
with natmal antimicrobials), pickling and
issues rather than quality bsues, is to
brining (reduces both aw and pH), canning
prevent the hazards dw-ing processing
a11d bottling (reduces oxygen and provides
rather than merely inspecting the end
physical barrier to contamination), jellying
product. Since that time, HACCP has been

( cooking in a mediLU11 that cools to fonn a
mandated by FDA and USDA for many
gel [ eg, aspic]; reduces aw), jugging (meats
food production sectors and also has
stewed in earthenware jugs or casseroles),
been implemented in the cosmetics and
burying (reduces aw, oxygen, light, tem-
pharmaceutical industries.

perature, a11cl pH), a11cl fermenting (acids

The HACCP process consists of the followbeneficial microbes that successfully ing seven principles: l) Conduct a hazard
compete witl1 pathogens; also lowers pH
analysis, ie, detem1ine the hazards ar1d
a11cl acids alcohol).

preventive measures that could be applied

More modem food preservation
to prevent them. 2) Identify c1itical control
techniques are listed below.

points, ie, any point, step, or procedw·e in

1) Pasteurization is used mainly for dairy
a food manufactLUing process at which
products and otl1er liquid foods, and it can
controls can be applied. 3) Establish critical
reduce microorganisms by 99.999%. In a
limits for each critical control point, ie, the

"high temperature, short time" process, the maximLU11 or rnini111LU11 value to which a
product is held at 161 °F for 15 sec. In a11
physical, biologic, or chemical hazard must

"ultra-high temperature" process, pasteuribe controlled at a critical control point.

zation is achieved after reaching 275°F for

4) Establish critical control point monitming

2 sec. In a less conventional technique,
requirements, which are necessary to ensme
home pasteurization involves holding the
that the process is under control at that
product at 145°F for 30 min. Finally, a11
point. 5) Establish corrective actions, or

"extended shelf life" process combines
actions that must be taken when monitoring
heating with filtration.

indicates a deviation from an established

2) VacuLU11 packaging is usually in air-tight
critical limit. 6) Establish procedures to
bags or bottles.

ensure the HACCP system is working as

3) Additives typically involve the adclition
intended, ie, validate the specific HACCP
of antimicrobials to limit the growth of
plan. 7) Establish record keeping proce-
microorganisms or antioxidants to inhibit

2408

PUBLIC HEALTH PRIMER
estimation has yet been perfom1ed. The

World Health Organization has initiated this
process but reports that efforts are lin1ited
by regional lack offllilcling, public health

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infrastructure, and political will. However,
despite specific data, the burden seems
obvious; diarrheal diseases, many of which

Food irradiation radura. Since 1986, all food
are foodbome in origin, kill approximately
treated with irradiation must display this radura.

1.9 million children worldwide.

In the USA, the foodborne diseases are
not generally reportable, so their burden
spoilage. Common antimicrobials include

Likely is significantly underestimated.

calcium propionate, sodium nitrate, sodium

Contributing to this underestimation is that
nitrite, disodiwn EDTA, and various sulfites.

many foodborne illnesses lack the severity,

Conm10n antioxidants include butylated
duration, and specific diagnosis required
hydroxyanisole (BHA), butylated hydroxyfor definitive identification and interventoluene (BHT), ascorbic acid (vitamin A), tion. Recent estimates by the CDC indicate
and tocopherol (vitan1in E).

that foodborne pathogens cause approxi4) Irradiation, which is commonly termed mately 9.6 million illnesses, 57,500

"cold pasteurization," involves exposing the hospitalizations, and 1,500 deaths each
product to low-dose ionizing gamma rays
year in the USA.

from a radioactive source such as cesium

In an effort to maintain awareness of

(Cs-137) or cobalt (Co-60). The process
food borne disease events and trends, CDC
does not render the food radioactive but
conducts the Foodborne Diseases Active
results in the killing of nearly all smface

Surveillance Network (FoodNet), which
pathogens. Commonly used for products
monitors the incidence of nine foodborne
such as spices and fruits, food irradiation is
pathogens in ten USA cities, covering
endorsed by the World Health Organization
approximately 15% of the American
and approved by the FDA. Since 1986, all
population ( see TABLE 3).

food treated with irradiation must display

CDC reports that this epidemiologic
the radura.

situation has not changed appreciably since

5) Pulsed electric field electroporation

2006, suggesting that there are gaps in the
consists of brief pulses of a strong electric
current food safety system and a need for
field that enlarges cell membrane pores,
better, more effective interventions.

which kills microorganisms. It is commonly
used for fruitjuices.

6) Modified atmosphere replaces oxygen

Factors in Emerging Foodborne
with an inert gas such as nitrogen or carbon

Illness Trends
dioxide. It is commonly used for salads,

Pathogenic organisms that contaminate
grains, apples, bananas, and fish.

food and result in food borne illness are

7) Nonthermal plasma treats food
dynamic in tl1at they adapt to new foods,
surfaces with "flame" ofhelitun or nitrogen.

processes, and human behaviors. The

8) High pressurization reduces microorfollowing categorical factors contribute ganisms while retaining freshness. It is
to foodbome illness trends.

commonly used for deli meats and
guacamole.

Human Demographics and Behavior:

9) Biopreservation is the addition of

The proportion of the USA population that
beneficial microbes such asLactobacillus
is inununocompromised is increasing
to compete with pathogens.

because of factors such as advancing age,

10) "Hurdle" technology combines
w1derlying disease, and therapeutic drug
multiple techniques to produce additive
regimens. Additionally, people consume
benefits. An example of placing multiple
more fresh fruits and vegetables, which may
hurdles in such a combination might involve be more contaminated than processed or high temperature and salt curing during
prepared foods, and consume an increasing
processing, addition of antioxidants before
nun1ber of meals outside the home. Finally,
packaging, and low temperature during

"organic" foods have not been shown to be
storage and transportation.

microbiologically safer and in some cases
may even increase the risk from certain

INCIDENCE AND IMPACT OF
foodbome pathogens.

FOODBORNE DISEASES

Technologies Within the Food

The global burden of food borne diseases is

Industry: Increasing concentration and
difficult to assess, because no overarching
vertical integration of many food produc-

PUBLIC HEALTH PRIMER

2409
hhh•D FOODBORNE PATHOGENS IN TEN USA CITIES

Pathogen

Incidence of Illness per 100,000 Population

Salmonella

15.19

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Campylobacler

13.82

Shigella

4.82

Cryptosporidium

2.48

Shigatoxin-producing E coli

2.32

Vibrio

0.51

Yersinia

0.36

Listeria

0.26

Cyclospora,

0.03
tion sectors have resulted in foods of higher change constantly, requiring correspondquality and greater consistency but with ingly dynan1ic interventions.

certain inherent vulnerabilities. Foods

( and constituent ingredients) are transported
in larger batch sizes, over longer distances,

Economic Development and Land
and are processed into an increasing

Use: USDA reports a continuing decrease
nwnber of end products. This means that
in the number of farms in the USA, with the
refrigeration breakdowns and cross-conaverage nwnber of livestock animals on tamination incidents can result in more
remaining farms increasing. This concenwidespread effects of food recalls and trates the number of animals that may be
illness outbreaks.

affected, both by contagious pathogens and
by interventions such as quarantines and
depopulation efforts. Increases in ocean

International Travel and Com
water temperature have been associated
merce: The concept of "traveler's
with increases in the nun1ber and scope of
diarrhea" is expanding because, increasfood borne illnesses from certain seafood ingly, bulk food shipments cross internaproducts such as oysters.

tional borders at least as often as people.

Therefore, foodborne illnesses acquired
from foreign foods can be contracted

Lack of Food Safety Education: Health
without leaving home. Additionally, when
classes at the intermediate and high school
people travel, they frequently take cultural levels rarely, if ever, cover food safety in foods with them to share with extended
favor of topics such as sexually transmitted
family. Despite prohibitions against such
diseases, drug abuse, and teen pregnancy.

importation practices, -4,000 pounds

With the increasing fraction of two-worker
of meat products are confiscated from
and single-parent homes, time demands
travelers each month from Haiti to the
may also preclude education of children in

USA. Undoubtedly, this represents only a
food safety principles and further contribfraction of the amount actually crossing ute to the lack of awareness.

the border.

ROLE OF FOOD ANIMAL

Microbial Adaptation: Foodborne

VETERINARIANS IN CONTROL OF
pathogens have inexorably adapted to

FOODBORNE PATHOGENS
traditional preservation techniques. Others
may even be selected by various techniques. Veterinarians in food animal practice Finally, antimicrobial resistance patterns
and government service contribute

2410

PUBLIC HEALTH PRIMER
significantly to tl1e safety of the food
statutes, regulations, and enforcement
supply. These roles can be categorized
actions.

by stage of production ( eg, antemortem,
postmmtem, and general).

Department of Agriculture: The

Antemortem activities include assurance Department of Agriculture consists of the of aninlal welfare, zoonotic disease

Food Safety and Inspection Service (FSIS)

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recognition and prevention, inspection of
and the Animal and Plant Health Inspecpreslaughter animals, and antibiotic residue tion Service (APHIS). The FSIS is the
testing.

primary food regulatory agency within

Postmortem activities include carcass

USDA, domestic ar1d imported (and
inspection and tissue residue detennination. employs most of the veterinarians in General activities begin witll herd
federal service). FSIS responsibilities
healtll programs, including disease
include inspecting food animals for
treatment and prevention, husbandry/
disease before and after slaughter;
handling/environmental advice, reproducinspecting meat and poultry slaughter and tive efficiency, vaccination regimens, nutriprocessing plants; in pecting domestic tion, stress reduction, commodity group
and impo1ted meat and poultry products
protocols ( eg, Beef Quality Assurance),

(raw and processed); inspecting proand biosecurity and biocontainment plans.

cessed egg products (liquid, dried, ar1d
ln addition to herd healtl1, other impo1tant
frozen but not eggs in shells); analyzing
activities include appropriate/judicious
food products for microbial, chemical,
use of antimicrobials, disease surveillance, and toxicologic agents; seeking voluntary illness/outbreak/epidemic investigation
recalls of unsafe meat and poultry
and mitigation, vaccination against
products; conducting and sponsoring
specific high-consequence or high-prevaresearch on meat and poultry safety, ar1d lence pathogens (eg, E coli 0157:I-17 and
educating industry and consumers on

Salmonella), collaboration with other
safe food handling practices.

healtll professionals (One Health), food

APHIS is responsible for livestock
facility inspection (eg, production, retail,
production ar1d transpmt (preslaughter);
storage), import/export examinations,
inspection and quarantine at U.S. Po1is of
health department leadershlp, public

Entry; and vete1inar-y services, including
health (risk) communication, food supply
surveillar1ce ar1d disease control/eradication
after disasters, and research into safer
prograrns, as well as representing USA
food production processes.

animal agriculture internationally.

FOOD SAFETY REGULATION

Department of Health and Human

Services (DHHS}: The Food and Dmg

In the USA, food safety is a shared

Administration (FDA) and tile Centers for
responsibility at various governmental

Disease Control and Prevention (CDC) ar·e
and private levels. Federal departments
witllin DHHS.

and agencies have regulatory authority

The FDA is the primary food regulatory
over virtually all food prol'lucts. State and
agency within DHHS. It is responsible
local governments typically are responsifor domestic and imported food sold in ble for sanitary inspections of restaurants
interstate commerce, including shell eggs
and food preparation sites. Food industry

(but not meat and poul
sectors have internal quality control

.try), bottled water,
wine beverages <7% alcohol, livestock
procedures to ensure both safe products
feeds, veterinary drugs, infant formulas,
and adherence to regulatory requireand dietary supplements; adulteration ments. Finally, informed consumers are
and misbranding of foods, drugs, and
charged with the safe storage, preparacosmetics; inspection of food production tion, and service of privately obtained
establishments and warehouses for
foods.

contamination by microbial, chemical,

At the federal level, responsibilities
and toxicologic agents; and HACCP
are shared between Congress, various
programs for seafood products and fruit/
regulato1y agencies, and the court system.

vegetable juices. The FDA also works

Congress enacts statutes tllat give agencies
with industry to recall unsafe food
autl10rity to regulate food safety and
products, as well as conducts research
enforce those regulations. Typically, tllese
and educates industry and consumers.

statutes are specific in identifying individual

The CDC investigates food borne illness
agencies but broad in allowing discretion in
outbreaks (in conjunction with states),
how tllose agencies exercise their authority.

maintains nationwide disease surveillance

Finally, the cowts review challenges to

(FoodNet), develops and advocates for

PUBLIC HEALTH PRIMER

2411
public health policies, conducts research
example is the federally enacted Airline
and educational programs in foodbome

Smoking Ban.

illness, and trains state and local food safety
persmmel.

The CDC also operates the Division of

Primary Sources of State Public

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Global Migration and Quarantine, which

Health Authority
is the enforcement authority for Interna

Police Power: Authority of "police power"

tional Health Regulations. This Division
usually is invoked to protect the common
investigates deaths and disease outbreaks
good. Not synonymous with criminal
on all international vessels (commercial
enforcement, this authority establishes
and cruise ships and aircraft) and is resmeans by which a community promulgates ponsible for quarantine stations at major
and enforces self-protective measures.

international ports of entry to intercept)

Examples include regulation of health care
destroy smuggled bushmeat, vector
professionals and facilities; establishment
species, and other contraband of public
of health and safety standards; quarantine,
health concern.

health, and inspection laws to limit the

In addition, the CDC operates the Cruise
spread of infectious diseases; mandatory

Ship Inspection Service, which is an
vaccination programs; age restrictions for
enforcement authority responsible for
drinking alcohol and pw·chasing tobacco
sanitary inspection of cruise ships.

products; and requirements for speed limits,
seatbelts, and helmets.

Department of Defense: The DoD is

Parens Patriae Power: This is the power responsible for emergency food supplies,
of the state to serve as guardian of persons
research activities on military food rations
under legal disability. Exan1ples include

(many civilian applications), and approves
juveniles and the insane.

food and water sources for all military bases. State Constitutional Power: These autl10rities are granted tmder each individual

Department of Homeland Security:

state constitution ( varies by state).

The OHS prevents terrorist attacks on USA

After the terrmist attacks of September
soil (to include foodbome, crop, livestock)

11, 2001, tl1e "Ame1ithra.x" attacks, natural and ostensibly has primary authority during
disasters such as Hurricane Katrina, the
attack and response phases.

severe a.cute respiratory syndrome (SARS)

outbreak, and pandemic influenza., the

Department of Commerce: The DoC
federal government strengthened its legal
is responsible for management of living
preparedness for all types of public health
ma.tine resources, including fisheries.

emergencies. These activities addressed a
variety of concerns related to emergency
declarations, quarantine and isolation,

Environmental Protection Agency:

licensure and liability of health care

The EPA has authority over pesticides,
workers, and mutual aid.

herbicides, and fungicides. The EPA
determines the safety of pesticides and sets
tolerance levels in foods, regulates toxic

Selected General Federal
substances to prevent entry into food and

Emergency Legal Authorities
the environment, and establishes and

Homeland Security Act of 2002:

enforces safe drinking water standards.

This Act merged 22 disparate agencies and
organizations into the new Department of

PUBLIC HEALTH LAW

Homeland Secw·ity (OHS), including the

U.S. Coast Guai·d and the Federal Emer

The U.S. Constitution makes no specific
gency Management Agency (FEMA). The
provision for health or public health.

Act charged OHS with securing the nation

Therefore, in accordance with the Tenth
against terrorist attacks and carrying out

Amendment, these powers are reserved by
tile functions of all transferred entities,
the states. However, a salient exemption
including acting as a focal point regarding
from this federal exclusion is represented
natural and manma.de crises and emergency
by the concept of legal preemption. Rooted
planning.

in the "Supremacy Clause" of the Constitution (Article VI), preemption occurs when Robert T. Stafford Disaster Relief
a state law is invalidated after being
and Emergency Assistance Act of
determined to conflict with a federal law.

1988: The Stafford Act authorizes the

In the absence of a federal declaration of

President to declare a "major disaster" or emergency, federal preemption is rare; one

"emergency" in response to an event (or

2412

PUBLIC HEALTH PRIMER
threat) that overwhelms state or local
communicable diseases and to help state
government resources. Declaration under
and local authorities enforce quarantine
the Act triggers access to federal technical, regulations.

financial, logistical, and other assistance
to state and local governments. The gover

Strategic National Stockpile: The

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nor of an affected state must first respond

Stockpile (including drugs, vaccines,
to the disaster and execute the state's
biologic products, medical devices, and
emergency plan before requesting that
other supplies) is maintained by the
the President declare a major disaster or

Secretary ofDHHS, in collaboration with
emergency, and the governor must certify

Director of the CDC , and in coordination
that the magnitude of the emergency
with the Secretary of DHS, to provide for the
exceeds the state's capability. As of 2013,
emergency health security of the USA. The
tribal leaders can also request a Stafford

Secretary may deploy stockpile assets in

Act declaration from the President. The
response to an actual or potential public

President may declare an emergency
health emergency to protect public health
without the request of a governor or tribal
or safety, or as required by the Secretary
leader if the emergency involves "federal
ofDHS.

primary responsibility" (such as an event

Bioterrorism Preparedness and
occurring on federal property, eg, the

Response Act of 2002: This Act amends
bombing of the Murrah Federal Building
the Public Healtl1 Se1vice Act to "improve
in 1995).

the ability of the United States to prevent,
prepare for, and respond to bioterrorism and

National Emergencies Act: This Act
other public health emergencies." The Act
authorizes the President to declare a
requires the Secretary of DHHS to "develop

"national emergency." The declaration of
and implement" a coordinated strategy in
emergency must specify the powers or
tl1e fom1 of a national preparedness plan.

authorities made available by virtue of the

Regulations to Control Communicable
declaration.

Diseases: Regulations to control conununicable diseases authorize the Secreta.Iy of Emergency Management Assistance

DHHS to make and enforce regulations "to

Compact (EMAC} of 1996: Enacted
prevent the introduction, transmission, or
by every state, this agreement facilitates
spread of conununicable diseases" into the
resource sharing among member states

USA from foreign cow1t1ies or from one
during an emergency. A governor's
state into anotl1er. These regulations also
declaration of emergency and request
authorize the apprehension, detention,
for assistance triggers EMAC for the
exaniination, and conditional release of
requesting state. An assisting state then
individuals with certain conununicable
responds to the request by providing
diseases that are specified in an executive
the needed resources. Further, EMAC
order of the President.

establishes that the requesting state
is responsible for compensating tne

Executive Order 13295 (Amended}:

assisting state for any expenses incurred.

Revised List of Quarantinable

Communicable Diseases: This Exe

Public Health Service Act: Originally
cutive Order identifies the nine commuenacted in 1944, this Act has been an1ended nicable diseases ( cholera, diphtheria,
several times to facilitate various types of
infectious tuberculosis, plague, smallpox,
responses, listed below.

yellow fever, viral hemorrhagic fevers,
severe acute respirato1y syndrome [SARSJ,

Public Health Emergencies: Authorizes
and pandemic influenza), for which an
the Secretary of DHHS to detennine that
individual can be apprehended, detained,
a public health emergency exists if" 1) a
examined, or conditionally released by
disease or disorder presents a public health
federal public healtl1 authorities.

emergency; or 2) a public health emergency,
including significant outbreaks of infectious
diseases or bioterrorist attacks, otherwise

Interstate Quarantine (42 CFR, Part
exists."

70): This allows the CDC Director to take
measures to prevent the spread of communi

General Grant of Authority for
cable diseases from one state into anotl1er,

Cooperation: This grant states that the
including in tl1e event the Director dete1°

Secretary of DHHS shall assist states and
mines that the measures taken by the health
local authorities to prevent and suppress
authmities of a state are insufficient to

PUBLIC HEALTH PRIMER

2413
prevent such spread of communicable
some protections from liability for
disease.

economic damages for activities relating
to the work of tile organizations. Under

Pandemic and All-Hazards Prepared
the Act, to be fotmd not liable for tl1e injury
ness Act of 2006: This Act identifies
caused by a negligent act or omission of

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the Secretary of DHHS as the lead federal
the volunteer, the volunteer must have
official for public health emergency
been acting witl1in the scope of his or
preparedness and response. It also provides
her responsibilities in tJ1e nonprofit or
new authorities to develop countermeasgovernment agency. The volunteer must ures, establishes mechanisms and grants
have appropriate licensure or certification
to continue strengthening state and local
if required for the volunteer's duties; he
public health security infrastructure, and
or she must not have acted with gross
addresses surge capacity by placing the
negligence, reckless disregard, willful or

National Disaster Medical System under
criminal misconduct, or flagrant indifferthe purview of DHHS.

ence; and the injury cannot have occurred
while tile volunteer was intoxicated.

Social Security Act: Authority to

Waive Requirements During National

Posse Comitatus Act of 1878: This

Emergencies: This autholizes the

Act generally prohibits the use of federal

Secreta.Jy of DHHS to waive or modify
milita.Jy personnel in a law enforcement
certain requirements of Medicare, Medicaid, capacity within tile USA unless authorized and the State Children's Health Insurance
by the U.S. Constitution or an act of

Program during ce1tain emergencies.

Congress. Certain exceptions exist, such as
when the Deprutment of Defense aids the

Public Readiness and Emergency

Deprutment of Justice in respondiJ1g to an

Preparedness Act of 2005: This Act
emergency situation involving a weapon of
authorizes tl1e Secretary of DHHS to issue
mass destruction.

a declaration that provides inununity from
tort liability for claims of loss ( except willful Insurrection Act of 1807: This Act misconduct) caused by, arising out of,
grru1ts autho1ity to the President to call tile
relating to, or resulting from administration

National Guard into federal service in tl1e
or use of countermeasures to diseases,
event of an insurrection in ru1y state or if a
threats, and conditions determined by the
state fails to uphold llie constitutional rights

Secretary to constitute a present or credible
of its citizens.

risk of a f1-1ture public health emergency.

Emergency Use Authorization: The

ZOOEYIA

Secreta.Jy of DHHS may, based on the request
of the Secretary of eitiler DHS, DoD, or DHS,

Zooeyia is defined as "the positive inverse
declare that circumstances exist to justify an
of zoonosis" and represents the innumer

Emergency Use AutJ10rization (EUA) for an
able benefits tl1at stem from lnm1an
tmapproved drug, device, or biologic
interaction willi animals. (See also THE
product, or for an unapproved use of an

IIUMAN-ANIMAL BOND, p 1575.) Too often, that
approved drug, device, or biologic product.

interaction focuses on negative issues such
as disease and injury ratl1er than on the

Pandemic and All-Hazards Prepared
positive contributions to our physical, men
ness Reauthorization Act of 2013:

tal, and social well-being. These contribu

This Act established strean1li.ned mechations are mru1i.fested at both the individual nisms to facilitate certain medical counterru1d community levels. Documented measure preparedness and response
individual benefits of interaction with
activities without having to issue an EUA
ru1imals include increased physical activity,

(which can be a time- and resource-intensmoking cessation, hypertension control, sive process). These new authorities are
reduced ru1xiety, and treatment of postfocused toward medical products against traumatic stress disorder. Interaction
chemical, biologic, radiologic, and nuclear
with domestic animals contributes at tl1e
emergencies.

comnumity level by facilitating social
interaction, promoting a sense of safety,

Volunteer Protection Act of 1997:

enhancing the "give and take" communica

This Act supports and promotes the
tion between neighbors ru1d fellow pet
activities of organizations that rely on
owners, and perhaps even lowering overall
volunteers by providing the volunteers
health care costs.

2414

ZOONOSES

ZOO NOSES

Zoonotic diseases present challenges

The occurrence of a pathogen in both

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not only to veterinarians but also to all
people and animals does not always mean
professions concerned with public health.

it is a significant zoonosis. Some diseases

Cooperation between veterinarians and
are acquired from the environment, and
public health physicians has been an
transmission between animal or hwna.n
important factor in zoonosis control
hosts is either absent, or occurs very rarely
programs. An exan1ple of this collaboration
and under unusual conditions. These a.re
is the eradication of bovine tuberculosis,
considered infections common to people
first in Denmark, Sweden, Finland, and
and animals rather tl1an true zoonoses.

Norway, and then in the USA, Canada,

Histoplasrnosis, blastomycosis, and coccidiand other countries. Unfortunately, oidomycosis, for exan1ple, are acquired by
some zoonoses that are well controlled
inhaling the microconidia. of soil ftmgi, but
in developed nations, such as bovine and
the organisms exist as yeasts in tissues.

porcine bmcellosis, bovine tuberculosis,

Some a.gents, such as Candida spp, are
and rabies, remain major problems in the
widespread commensals in healtl1y people
developing world. Diseases can also
and animals and can cause disease when
reemerge in areas where they have been
the host becomes debilitated. Although
eradicated. Newly recognized zoonotic
such organisms might be transmitted from
organisms such as Hendra and Ni pall
anin1als to people, this transfer has little
vimses are emerging, and many other
epidemiologic significance. In some
zoonoses remain a constant concern.

cases, organisms were once thought to be
zoonotic, but cw-rent knowledge, particu

PATHOGENS AND HOST SPECIES
larly the use of genetic techniques, has
changed that perception. For example,

Zoonotic diseases can be caused by

Streptococcus agalactiae was once thought
bacteria, vimses, fungi, parasites, or p1ions.

to be acquired from animals, but most

Because organisms are more readily
strains in people are now known to be
transmitted between closely related hosts,
distinct from anin1al strains. There are also
most of these agents are pathogens of
some organisms (eg, sinlian foamy viruses)

mammals. A particularly large mUTiber
that can be transmitted from aninlals to
of diseases are shared by people and
people, but witl1 no currently known
nonhw11a.n primates. Birds, repWes,
consequences.

amphibians, fish, and invertebrates can
also be sources of infection (see TABLE 4).

Many of the zoonotic agents in poikilo

TRANSMISSION BETWEEN
thcnns are parasitic, but these species can

ANIMALS AND PEOPLE
also carry zoonotic bacteria and viruses
including Salmonella, West Nile vims, and

Zoonotic pathogens can be acquired during
opportlmistic Mycobacterium spp. People
close contact with an animal, generally
are incidental hosts for many zoonoses;
tllrough inhalation, ingestion, or o\;her
however, some agents have both human
mechanisms resulting in the contamination
and anin1al reservoirs. In some cases,
of mucous membranes, damaged skin, or
aninlal reservoirs have been revealed after in some cases, intact skin. Sow-ces of
a disease was controlled in people. Yellow
organisms include body fluids, secretions
fever, for example, is known to have
and excretions, and lesions. Unprotected
a.zoonoticjungle cycle in nonhun1an
contact with tissues during necropsies often
primates, as well as an urban cycle
ca.nies a high risk of transmission. Aerosols
maintained in people. Wildlife is increasa.re occasionally involved, particularly in ingly recognized as a reservoir for zoonoses,
confined spaces. Fomites can transmit
including some that were U10ught to be
some a.gents; the likelihood of this route
stJictly livestock pat110gens. Reverse
correlates with the organism's persistence
zoonoses are ca.used by human pathogens
in the environment. Some organisms are
transmitted to animals. In some cases, these
spread by ingestion of contaminated food
a.gents can later infect people. For example,
or water and may infect large nwnl>ers of

Mycobacterium tuberculosis, the agent of
people. Sources of zoonotic pathogens in
hw11an tuberculosis, can colonize the bovine foodborne disease include undercooked udder and be shed in milk.

meat or other animal tissues (including

ZOONOSES

2415
seafood and invertebrates), unpastemized
routes of transmission. Often, the people
milk and dairy products, and contaminated
most at risk are healtl1 care workers and
vegetables. Insect vectors, serving as either
close fan1ily members. However, diseases
biologic or mechanical vectors, are
such as plague have the potential to spread
impmtant in transmitting some organisms.

widely in hunutn populations under some

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The risk of acquiring a zoonosis can be
conditions. Some zoonotic diseases are not
affected by many factors, including the
contagious during casual contact but can be
susceptibility of the host (seep 2415), the spread by transfusion or organ transplantapotential route(s) of transmission, the tion, or from motl1er to fetus in utero. A
number of organisms shed by the animal,
particularly wide variety of agents, from
and the ability of the agent to cross species
encysted parasites to latent viruses, are
barriers. Some pathogens, such as Bacillus
potentialJy transferable in organs. Agents
anthracis, readily infect people with
that were well controlled in tl1e organ donor
appropriate exposure; others are uncomcan be reactivated in the recipient, who is mon zoonoses even when exposure is
immm10suppressed by drugs taken to
frequent. Certain occupations or activities
prevent rejection. Transfusion can also
can significantly increase the probability
bypass nom1al barriers if the agent is fottnd
of exposure. Contact with soil dming
in the blood at tl1e time of the donation. The
gardening or childhood play carries a risk
bovine spongifonn encephalopathy agent,
of infection with pathogens tl1at reside
for example, is ordinarily transmitted from
temporarily or pennanently in tl1e soil, such host to host only by ingestion of tissues, but
as Toxocara spp or Sporothri.x schenckii.

it can be acquired in transfused blood.

Veterinary practice, agricultural activities,
and pet ownership are obvious hazards.

ROLE OF IMMUNOSUPPRESSION

Dogs, cats, livestock, or birds may also
bring wildlife pathogens into closer

The spectrum of zoonotic illness vaiies
proximity to people. The animal can be
from skin eruptions or mild, self-limiting
infected directly with the agent, either
infections easily misdiagnosed as htunan
clinicalJy or subclinicalJy, or it may act as
influenza to serious, life-threatening
a transport host for infected arthropods
disease. Some zoonoses can affect healtlw
such as ticks. Nontraditional pets have a
people, whereas others are prin1ari]y found
relatively high probability of being infected
in individuals with debilitating illnesses
with zoonotic agents, especialJy when
and other conditions that compromise
captured directly from the wild. During an
immunity. Zoonoses that are mild or
outbreak of monkeypox in the USA, the
asymptomatic in healthy hosts can be
virus spread from exotic African rodents,
serious illnesses or have unusual presentaimported as pets, to pet praitie dogs and tions in those who are immunocomprothen to people. Activities that bring people mised. In some cases, a suppressed inunune
into closer contact with wildlife, including
response may also slow diagnosis if
hunting, fishing, and camping, can result
conunon tests rely on serology.

in exposure to organisms carried in wild

Primary immunodeficiencies, which
anin1als ( eg, Francisella tularensis,
are congenital defects, may affect

Yersinia pestis, and Leptospira spp) or humoral or cell-mediated immunity, or
transmitted by artl1ropod vectors ( eg,
both. Some primary immunodeficiencies

Borrelia burgd01j'eri and West Nile virus).

increase susceptibility to a single category

Hunters, in particular, may contact
of pathogens, while others broadly
patl10gens in animal tissues during
suppress defenses. Some may remain
butchering. The growing popularity of
unnoticed except as an unusual susceptiecotourism has resulted in hun1an exposure bility to certain illnesses, whereas others
to some exotic wildlife diseases. The
arc obvious from infancy. Secondary
prevalence of other zoonoses may be linked
immunodeficiencies can be caused by
to cultural practices such as eating raw fish,
any acquired condition that compromises
gastropods, or mollusks. Knowledge of a
the immune system. Examples include
person's leisure and vocational activities,
splenectomy, diseases that affect metatravel, and pet ownership can sometimes bolism (eg, diabetes), illnesses such as
raise the index of suspicion for zoonoses
cancer that result in generalized debilitathat are uncommon in urban populations.

tion, and infections such as malaria or

Once a zoonotic disease has been

AIDS. Some illnesses, such as chronic
acquired by a person, it can sometimes be
lung disease, can increase susceptibility
transmitted from person to person. The risk
by affecting innate (nonspecific) defenses.

varies with the specific disease, the agent's

Injuries and burns can compromise the
ability to spread readily in people, and the
skin defenses that prevent pathogens

2416

ZOONOSES
from entering the body, as can indwelling
hwnan population also exerts pressures that
catheters and implanted medical devices.

ultimately result in increased contact with

Drugs can suppress immunity as an
wildlife. Climate change can be a factor in
intended effect ( eg, drugs used to treat
disease emergence, particularly for
autoimmune diseases or prevent rejection
a.rtlrropodbome pathogens such as

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in organ transplant patients) or as an

Rickellsia spp. A warmer climate not only
adverse effect. Some drugs used in cancer
allows vectors to survive tl1e winter but also
chemotherapy are highly immunosupprespermits a longer transmission sea.son.

sive. (See also IMMUNOLOGIC DISEASES, p 817.) Climate changes may also favor some

Physiologic states can also affect
non-aithropodborne diseases; for exan1ple,
immunity. The immw1e system is relatively
increased rainfall has been linked to
immature in newborns and yow1g children,
outbreaks of plague in some areas.

and it declines in older adults. Pregnancy

Technologic and industrial changes in
may result in risks to the mother, the fetus,
food production can contribute to disease
or both. For exan1ple, in some geographic
emergence by increasing tl1e concenlocations, the case fatality rate for hepatitis tration, movement, and mixing of anin1als.

Eis -1 % in the general population but may

Long-distance trat1Spo1t has been associreach 200A, among pregnant women. Other ated with increased shedding of enteric
pathogens, such as Toxoplasma gonclii,
pathogens, including Salmonella. Decreased
may severely damage the fetus while
genetic diversity may eliminate species,
remaining mild in the mother.

breeds, or individuals with innate resistance
to a disease. The development of large-scale

EMERGENCE AND REEMERGENCE fa.tins and food-processing facilities has led OF ZOONOTIC DISEASES
to tl1e exposure of greater nwnbers of
people to a contanlinated food source.

Emerging diseases a.re commonly defmed
lncrea.sed mobility of people, ailimals, and
as illnesses that have increased in incidence
goods allows diseases to spread quickly.

during the pa.st two decades or a.re Likely to

Viruses that fonnerly died out after affecting
increase in the near future. Many of these
small nwnbers of animals at1cl/or people ca.ii
diseases a.re zoonotic. A zoonotic disease
now find many susceptible hosts within a
can emerge as the result of increased
short petiod. The SARS corona.virus spread
human contact with the animal host(s),
to 30 countries on 6 continents within
aninlal tissues, vectors, or environmental
months of tl1e initial outbreak. Occasionally,
sources of the pathogens. It may also result
the pathogen itself may become more
from an increased prevalence of the agent in virulent or better adapted to people, or it domesticated or wild a.ninlals or in vectors.

may undergo changes that affect transmis

Many cwTently emerging and reemerging
sion patterns. More virulent strains of the
diseases have reservoirs in wildlife and/or

West Nile virus have emerged since the
a.re foodborne.

1980s, and a new variant, which can

Factors that can ca.use emergence include
replicate more rapidly in mosquitoes, has
altered hw11an demographics or behavior,
become established in North America.

ranging from societal upheavals tha.t"cause

Some diseases a.re emerging not because
people to leave urban areas to sin1ple
tl1ey ai·e more common but because they ai·e
changes in food preferences. For example,
better recognized. Increased recognition can
the popularity of prewa.shed greens can
result from improved cliagnostic techniques,
facilitate some outbreaks of E coli 0157:H7.

increased use of la.bora.tories for identifica

Breakdowns in public health measures such
tion of specific pathogens, and better
as sanitation and vaccination also increase
awareness an10ng physicians. Some spotted
the spread of disease. Changing land use
fever Rickellsia spp ai·e emerging, in pa.rt, patterns may alter the nw11ber of reservoir
because the increased use of molecular
hosts, increase the incidence of infection in
techniques facilitates tl1eir identification.

these animals, encourage genetic changes in

Ma.rburg virus, once thought to be a very rai·e
the pathogen ( eg, recombination with other
and less virulent relative of ebolaviruses,
strains), or b1ing a.nin1al hosts or disease
was recently found to have ca.used
vectors into closer contact with people.

hemmThagic disease in workers at one

Because many mosquitoes preferentially

African nline since the 1980s or earlier. Tllis
breed along tl1e edges of forests rather than
focus of bat-transnlitted infections was only
deep among the trees, deforestation can
recognized when highly fatal outbreaks
increase populations of these species.

affected hundreds of people in the Demo

Degradation of their natural habitats, as well
cratic Republic of the Congo in 1998---2000.

as the ready availability of food near hwnan
lncrea.sed hwnan susceptibility has
dwellings, can encourage wildlife to move
contributed to the emergence or recogniinto suburban areas. The growth of the tion of some opportwlistic pathogens. The

ZOONOSES

2417
number of inununocomprornised people
its anin1al reservoir(s). In some countJies,
has been increased by factors such as
livestock diseases such as bovine and
the AIDS epidemic, the success of organ
porcine brncellosis and bovine tuberculotransplantation programs, and the sis have been eradicated, ai1d the preva

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improved smvival of those with ptimary
lence of Salmonella in poultry has been
and secondary immm10deficiencies.

significantly reduced. Vaccination ( eg,

Modem medicine also allows more people,
rabies), ti·eatment of clinical cases, flea and
many of whom develop chronic conditions,
tick control, periodic testing for enteric
to survive to an advanced age.

pai·asites or other pathogens, and other
disease control measures in domestic

TREATMENT
animals can also protect people. Hmnan
vaccines are available for a few diseases,

The treatment of zoo no tic and nonzoonotic
and arthropod control measures decrease
diseases of animals is similar; however,
the risk of vectorborne infections.

treatments that prolong the shedding of

Foodbome zoonoses can often be
zoonotic organisms should be avoided
interrnpted by using good sanitation and
unless there are overriding considerations.

hygiene during food preparation, eliminating

For example, antibiotic treatment is usually
cross-containination of foods, cooking all
contraindicated in uncomplicated Salmo
foods of animal origin (including inverte
nella-associated diarrhea, because these
brates such as mollusks and snails) to safe
drugs may prolong shedding of this
temperatures, and thoroughly washing
organism. Conversely, animals t11at cany
vegetables shortly before eating. Prions
zoonotic organisms may sometimes be
caimot be destroyed by cooking; meat
treated to reduce hmnan exposure, even
inspection and elimination of the pathogen
when the infection is subclinical or expected from anin1als remain the only ways to to be sel f -limiting, such as a minor skin
reduce tl1e risks from these agents. Modem
lesion caused by dennatophytes. During
water treatJnent procedures elin1inate most
treatment of zoonotic diseases, every
waterborne zoonoses. Where such facilities
precaution should be taken to prevent
are unavailable, drinking water should be
hmnan infection. Professional judgment is
boiled, filtered, or otherwise treated to
required to detennine whether to keep the
remove pathogens. Accidental ingestion
animal in its home environment or isolate it
of lake or strean1 water should be avoided.

in a hospital ward. Factors to consider

The containination of irrigation water used
include the potential severity of the disease
for agriculture has become an increasing
in people, the susceptibility of individuals in
concern with tl1e rise of pathogens such
the household, and the ability of hmnan
as enterohemorrhagic Escherichia coli
caregiver(s) to effectively perfom1 barrier

(eg, E coli 0157:H7). Measures such as
nursing, sanitation, and hygiene protocols.

composting livestock manure before

The owner should always be infonned if
spreading it on fields may lower the risks
treatment is not certain to eliminate the
from this source. However, post-harvest
pathogen, which could then persist in a
procedures to elinlinate containination are
latent or chronic, subclinical form. Zoonotic
also critical.

concerns may dictate euthanasia of the

It is often difficult to avoid diseases
anin1al, especially when the disease is likely
acquired from the environment. However,
to be fatal.

measures to eliminate skin contact with

People who may have contracted a
soil, such as weaiing gloves when gardening zoonotic disease should be refetTed to their
and avoiding dust inhalation, are helpful.

physician for diagnosis and treatment. The

During contact with appai·ently healthy
physician should be given any information
animals, good hygiene (including hand
necessary to facilitate diagnosis, paiticularly
washing) is an in1p01tant preventive
if the disease is unusual and would not
measure. Hand washing is paiticularly
ordinarily be among the differential
importai1t before eating or any other
diagnoses. Sin1ultaneous elinlination of the
hand-to-mouth contact. In fairs, petting zoos,
pathogen from both animal and hmnan hosts
or other envirorunents where the public may
is ideal, to prevent it from cycling between
contact animals, hand-washing facilities
the hosts. Public health authorities must be
should be provided, and eating or drinking in
contacted when a rep01table zoonotic
the animal areas should be discouraged.

disease ( eg, rabies) is found in an animal.

Children <5 yr old should be supervised
closely; their inunune systems are generally

PREVENTION
more vulnerable to pathogens, they are less
likely to follow sanitary precautions, and

People can be protected from some
they are more likely to engage in risky behavzoonoses by eliminating the pathogen from iors such as tasting dirt. Detailed zoonosis

2418

ZOONOSES
control programs for various types of
isms. Owners should be counseled to avoid
facilities have been published.

any direct contact with feces, as well as to

Protective measures in veterinary
practice excellent hygiene when handling
hospitals include barrier precautions
the pet. The litter box should be cleaned

(including gloves, protective outerwear,
daily, preferably by a household member

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and other personal protective equipment
who is not imm unocompromised, to reduce
as appropriate), good hygiene, sanitation
the risk of toxoplasmosis. Similarly,
and disinfection, appropriate disposal of
cleaning aquariun1s canies the risk of
infectious material, and use of isolation
exposure to Mycobacterium marinum and
units for animals with known zoonoses.

is best done by a healthy individual. Regular
veterinary visits, with periodic screening

Prevention in lmmunocompromised
for intestinal parasites and/or other

Populations: COlmseling inummocomzoonotic pathogens as appropriate, are promised owners must stiike a balance
essential for all pets. Pets that develop
between awareness of the risks from
dian·hea or other diseases should be
zoonoses and acknowledgement of the
brought in promptly for diagnosis.

hw11an-animal bond and the psychologic

Any new pet should be exanlined by a
benefits of animal companionship. 1f the
veterinarian to ensure it is not carrying
person chooses to have a pet, the veterinarintestinal parasites, mites, dermatophytes, ian can help make that decision as safe
or other zoonotic pathogens. A healthy,
as possible. Topics to discuss include the
unstressed adult dog or cat with a known
risks from feeding raw meat or eggs, the
history and no recent exposure to environprevention of garbage eating and coprophaments with high concentrations of gia in dogs, the importance of flea and
pathogens is preferable to a puppy or kitten.

tick contJ·oJ, and the dangers of allowing
lmmunocompromised persons should avoid
cats and dogs to lnmt. Pets should not
contact with reptiles, baby chicks, or
be allowed to drink non potable water,
ducklings, all of which may shed Salmo
including water from lakes or sti·eams and
nella. Some amphibians and exotic
water from toilet bowls. Claws should be
mruru11alian pets may also have a higher
kept clipped short to reduce the risk of
likelihood of can-ying Salmonella.

scratches, and rough play that might

Avoidance of strays, wildlife, nonhuman
encourage biting or scratching should be
primates, and anin1als with diarrhea or any
avoided. Regular and thorough cleaning of
other illness is particularly important. It is
bedding and cages prevents the accumulaalso prndent to stay away from animals in tion of debris that can shelter microorgan-fairs, petting zoos, farms, schools, and

•th•i• GLOBAL ZOONOSES•

Causative

Animals

Disease

Organism-

Involved

BACTERIAL DISEASES

Actinomycosis

Actinomyces bovis and

Manrn1als

(seep 590)

other species in ru1imals
may affect people, but
most htrman infections
ru·e caused by commen-
sals of people, especially

Actinomyces israelii

Anthrax (seep 593) Bacillus anthracis

Mainly in cattle, sheep, goats, horses,
wild herbivorous animals; virtually
all rnanrn1als and some birds are
susceptible to high dose

ZOONOSES

2419
similar settings, and to take additional
most cases. An indication of the mortality
precautions if avoidance is impractical.

rate among healthy individuals has been

Veterinarians have a vital role in
provided for many infections. However,
educating immunocompromised owners on
there is almost always a chance of death
the risks from zoonotic diseases, as well as
whenever lesions can become generalized,

VetBooks.ir
the steps that can be taken to decrease risk.

vital organs may be affected, secondary

Educational materials such as signs and
infections occur, and/or the patient is
brochures may prompt owners to ask for
immunosuppressed. The mortality rate is
advice. Educational materials can also be
often influenced by the availability of
used to warn pregnant women of the risks
medical care, and it is generally lower when
from toxoplasmosis and other zoonotic
advanced medical support is available. The
pathogens, or to remind owners that their
risk of death from some bacterial diseases
veterinarian can provide help with safe
with high mo1tality rates can be nearly
pet selection and zoonosis prevention in
eliminated with prompt antibiotic
households with children. Guidelines on
treatment.

zoonosis prevention for therapy animals

If a disease is known to have unusual
used in hospitals and convalescent homes
manifestations or to be particularly conunon
have also been published.

and/or severe in in1munocompromised
people, this has been noted. In addition to
these diseases, many pathogens car1 cause

ZOONOTIC DISEASES
more severe disease and/or wmsual signs in
in1rnunocompromised patients. Wmmation

TABLE 4 lists zoonotic bacterial, viral, fungal, on the geographic rar1ge of an organism
and parasitic diseases, grouped by category.

should be taken as a rough guide. The

Many proven zoonoses, including some
precise ranges of many pathogens have not
diseases that are rare in people, organisms
been completely determined. Organisms
that are maintained p1imarily in people,
may also expar1d their range or be eradicated
some prin1a.te diseases, and diseases ca.used from ar·eas where they were once abundant.

by fish and reptile toxins have been omitted.

In this table, "worldwide" indicates those The table is intended to give a general
organisms that are widespread and found
clinical picture of ea.ch disease; current
on all major continents, although they may
medical texts or review articles should be
absent from some areas ( eg, polar regions
consulted for a more complete description.

or some islands). In some cases, organisms

Clinical signs are listed; asymptomatic
indicated as being present on a continent
infections can also be assumed to occur in
may nevertheless have a limited distJ.ibution.

•M=ili• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

BACTERIAL DISEASES

Worldwide; very rare Probably contact;

Granulomas, abscesses, skin lesions;
in people
actinomycosis usually
chronic bronchopneumonia;
disseminates from
abdominal mass that may mimic a
endogenous human flora tumor; endocarditis; sepsis

Worldwide but distri Occupational contact

Early signs vary with route of
bution is focal;
exposure (abraded skin, inoculation; pa.pule to ulcerative skin common in Africa,
mechanical transmission lesions; mild to severe gastroenteritis Asia, South An1erica, by biting flies, other

± hematemesis, bloody diarrhea,

Middle East, parts of routes); ingestion/
ascites (abdominal GI form); sore

Europe
foodborne, rarely
throat, dysphagia, fever, neck
airborne
swelling, mouth lesions ( oropharyngeal GI form); pneumonia; all may progress to sepsis, meningitis;
untreated cases fatal in 5o/<r-20%

(cutaneous) to 100% (inhalation)

(continued)

2420

ZOONOSES

•§:j•j• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Arcobacler

Arcobacler butzleri,

Poultry, cattle, pigs, sheep, horses,
infections

A cryaerophilus,
shellfish; some studies detected

A skirrowii, possibly
these orgarlisms in dogs and/or cats
others

Bordetellosis

Bordetella bronchisep

Dogs, rabbits, cats, pigs, guinea pigs,

(seep 1464 and
lica
other mammals
p 1491)

Borreliosis (seep 659)

-Lyme disease

Borrelia burgd01feri

Wild rodents, insectivores, hedgesensu Jato complex
hogs, har·es, other mammals; birds

(B burgd01feii sensu
are reservoirs for agent; deer are
stricto, B gminii,
hosts for tick vector only (blood

B afzelii, B spielmanii,
meals)

Bjaponica)

-Tickbome

B recurrentis,

Wild rodents, insectivores, possibly
relapsing fever

B crocidurae, B lwicalae, birds

B hermsii, B persica,

B hispanica, others; some
species such as B duttoni
are human pathogens and
not zoonotic

---Southern tick-

Etiology uncertain; various
associated rash illness Borrelia spp suggested Brucellosis ( see

Brucella abortus

Cattle, bison, water buffalo, African
p 1348 and p 1402)

buffalo, elk, deer, sheep, goats,
can1els, South American can1elids;
other mammalian spillover hosts

B melitensis

Goats, sheep, camels; other
mammalian spillover hosts

B suis biovars 1-4; biovar Swine and wild pigs (biovars 1, 2, 3), 5 has not been reported

European hares (biovar 2), reindeer
in people
and caribou (biovar 4); B suis also in
some other mammals

ZOONOSES

2421

•d=iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Worldwide

Ingestion of contaminated Gastroenteritis; bacteremia, mainly water, undercooked meat in patients with chronic illnesses; ( especially poultry) has
endocarditis, peritonitis; emerging
been suggested
and incompletely understood

Worldwide;

Exposure to saliva or

Sinusitis, bronchitis, pertussis-like
uncommon in people sputum, aerosols
illness; pneumonia and disseminated
disease ( eg, endocarditis, peritonitis,
meningitis), usually in immunocompromised; wound infection Agents exist
lxodes spp bites

Nonspecific febrile illness early;
worldwide where
target skin lesions in many; may
lxodes ticks are
progress to arthritis, neurologic,
found; human cases
cardiac, and/ or skin signs (acrohave been reported
dermatitis chronica atrophicans );
inNorth Ame1ica,
syndromes may vary with infecting

Europe, Australia,
agent
parts of Asia,

Amazon region of

South America

Africa, Asia, Europe, Tick bites (mainly

High fever, malaise, headache,

Americas; species

Ornithodoros spp)

myalgia, chills; neurologic signs
varies with region
or abortion possible; recurring
episodes, often milder, after a
symptom-free period; death in 2o/o-5%

USA; most cases in

Tick bite (Amblyomma

Resembles Lyme disease
southeast
americanum)

Once worldwide,

Ingestion ( especially

Extremely variable, subacute and
now eradicated from unpasteurized dairy prod undulant to sepsis; often nonspecific domestic animals in ucts or undercooked
febrile illness with drenching sweats
some countries or
meat), contact with
early; arthritis, spondylitis,
regions; reservoirs in mucous membranes and epididymo-orchitis, endocarditis, wildlife in some
broken skin; strain 19
neurologic, other syndromes if
disease-free areas
vaccine
chronic; case fatality 5% in untreated

Asia, Africa, Middle Ingestion (including

As above; this species highly

East, Mexico,
unpasteurized dairy
pathogenic for people

Central and South
products or undercooked

America, some parts meat), contact with
of Europe
mucous membranes and
broken skin; Rev 1 vaccine

Biovars 1 and 3 world Ingestion, direct contact As above wide in swine-raising with mucous membranes
regions except
and broken skin
eradicated or nearly
eradicated from
domestic pigs in some
countries; biovar 2 in
wild boar in Europe;
biovar 4 in Arctic

2422

ZOONOSES

•M:iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Brucellosis

Bcanis

Dogs; evidence of infection in wild

(continued)

canids including coyotes, foxes

B pinnipedialis and

Marine mammals

Bceti

Campylobacter

C jejuni, C coli,

Poultry, cattle, swine, dogs, cats,
enteritis (seep 191)

occasionally other
rodents, other mammals, wild birds
species; some strains of

C jejuni seem to have
broader host ranges than
others

Campylobacterfetus Cfetus subspfetus (most C fetus subsp fetus and C subsp vene
infection
cases), Cfetus subsp
real is in cattle, sheep, goats; C fetus testudinum (proposed
subsp testiidinum in reptiles
name); possibly C fetus
subsp venerealis

Capnocytopha,ga

C canimorsus,

Dogs, cats
infection

Ccynodegmi

Cat scratch disease Bartonella henselae;

Cats and other felids; other

B clarridgeiae and other Bartonella spp in canids, rodents, Bartonella �pecies also
rabbits, other animals
implicated rarely in
cat scratch disease or
other conditions ( eg,
endocarditis)

Chlamydiosis

Chlamydia

C abortus in sheep, goats, cattle,

( see also PSrr1'Acos1s, (Chlamydophila) other manm1als; C felis in cats
p 2428)

abortus, Cfelis

Clostridial diseases Clostridium difficile;

Ribotypes from some calves, pigs,

(seep 601)

some ribotypes found in dogs are identical to some ribotypes animals have been
found in people
in1plicated as potential
zoo noses

ZOONOSES 2423
l&H•il GLOBAL ZOONOSEsa (conl'inued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Worldwide; rare in

Probably via ingestion or

Probably as above
people
contact with mucous
membranes, broken skin;
close contact, especially
with animals that recently
aborted or gave birth

Atlantic, Arctic, and Laboratory exposw·e;

Few cases known: mild to severe

Pacific oceans;
somces of other infections febrile illness, sintilar to that caused by Mediterranean sea
unknown (possibly contact other En.cello spp; neurobrucellosis with animals or exposure with headache and chronic neurologic to seawater); rare or
signs; spinal osteomyelitis
underdiagnosed in people

Worldwide

Foodbome ( especially

Gastroenteritis from mild cases to
poultry and other meats, fulminating or relapsing colitis; unpasteurized dairy prod occasional sequelae such as reactive ucts); waterborne;
arthritis; occasionally, other
contact with infected
syndromes, including sepsis
animals (fecal/oral)

Worldwide

Probably direct contact

Opportunist; sepsis, meningitis,
or ingestion; often
endocarditis, abscesses, other
unknown
systemic infections in elderly,
immunocompromised, or infants;
abortions, pretenn births in pregnant
women, neonatal sepsis; gastroenteritis not prominent in most cases Probably worldwide Bites or scratches

Fever, localized infections to
bacteremia or sepsis, endocarditis,
meningitis; often in immunocompromised or elderly

Worldwide

Often associated with

Lymphadenopathy (may be absent in
scratches, bites,
elderly), fever, malaise, skin lesions at
especially from cats;
inoculation site in immunocompetent,
potential for other
usually self-linuting with complicaexposures to broken skin tions ( eg, endocarditis, neuroretinitis, via saliva; exposure of
neurologic disease) uncommon;
conjunctiva
inoculation into eye results in conjunctivitis ± ocular granuloma and local lymphadenopatl1y; risk of bacterernia,
dissenunated disease, bacillary
angiomatosis in inm1unosuppressed

Cfelis worldwide;

Contact with animals;

C abortus: abortions, septicemia;

C abortus in most

C abortus probably

C Jelis suspected agent of keratoconsheep-raising areas contact with pregnant or junctivitis, also implicated in other but not Australia or aborting ruminants
conditions ( controversial)

New Zealand

Worldwide

Possible zoonosis; from Gastroenteritis, varying in severity contact or ingestion in
from diarrhea to fulminant colitis,
contaminated meat; also usually in cortjunction with antibiotic from environment and
use
contact with infected
people

( continued)

2424

ZOONOSES

•§=i•I• GLOBAL ZOONOSES• (continuecl)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Clostriclial diseases Clostridium perfrin

Domestic and wild animals, people

(continued)

gens, type A (most
common), C, or D;
environmental or
endogenous source, with
some potential for
zoonotic transmission

Catynebacterium

C ulcerans,

C ulcerans in cattle, pigs, small
ulcerans and

C pseudotubercitl osi s
rnminants, dogs, cats, ferrets,

C pseudotubercu/o
other domestic and wild animals;
sis infections

C pseudotuberculosis in sheep,
goats, cattle, horses, camelids,
other manm1als

Dermatophilosis

Dermatophilus

Cattle, horses, deer, sheep, goats,

(seep 858)

congolensis
other mammals

Enterohemorrhagic E coli 0157:H7; also

Especially cattle, sheep; also goats,

Escherichia coli
implicated are types
bison, deer, pigs, other species of
infectionsb

0157:H, and members of mammals, birds
serogroups 026, 0103,

0104, 0111, 0145, and
others

Erysipeloid

Erysipelothrix

Swine, sheep, cattle, rodents, marine

(seep 625)

rhusiopathiae
mammals; many other domestic and
wild manm1als and marsupials, birds

(including poultry), reptiles, fish,
mollusks, crnstaceans

Glanders

Burkholderia rnallei

Equids are reservoirs; felids, many

(seep 706)

other domesticated and wild
mammals also susceptible

Helicobacter

H pullorum, H suis,

Poultry (H pullorum), rodents
infection
other species suspected

(H pw.lorum and other species), pigs
aszoonoses

(H suis), dogs (H canis), many other manm1als

ZOONOSES

2425

•th•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Worldwide

Foodbome (usually type Foodbome gastroenteritis, usually A); nonfood-associated
brief, self-limited except in debilitated;
intestinal infection;
nonfood-related intestinal infection
wound contaminant,
with prolonged dia.tThea, sometimes
usually environmental;
bloody, mainly in elderly after
may be endogenous in
antibiotics; life-threatening necrotic
debilitated from GI or
enteritis, often in debilitated; gas
urogenital tract
gangrene, sepsis; necrotic ente1itis, gas
gangrene, sepsis are fatal if not treated

Probably worldwide; Direct contact, consump Acute upper respiratory illness with uncommon in people tion of unpasteurized
sinusitis, sore throat, tonsillitis, or
but may be
milk products
more severe pharyngitis resembling
increasing
diphtheria (pseudomembranous
pharyngitis); cardiorespiratory
complications possible; peritonitis;
isolated skin infection; some cases
serious or fatal

Worldwide,

Usually direct contact with Pustular desquan1ative dem1atitis, especially in warmer lesions; mechanical
other skin lesions
regions
transmission on arthropod
vectors, fomites possible

Worldwide

Ingestion of undercooked Diarrhea or hemorrhagic colitis; up meat ( especially groW1d
to 15% of patients with hemorrhagic
beef), vegetables or water colitis progress to hemolytic uremic contaminated with feces;
syndrome (HUS); case fatality rate
direct contact with feces
for HUS is 3o/o-5%, higher in some
or contaminated soil
populations ( eg, 5o/o-l 0% in children,
up to 50% in elderly)

Worldwide

Contact with animal

Localized cellulitis, usually selfproducts; via skin, limiting, often on hands; generalized
usually after scratch or
skin lesions (uncommon); arthritis,
puncture wound;
often in finger joints near skin lesion;
contaminated soil
endocarditis ( with high mortality,

(survives for weeks to

38%); generalization with sepsis, other
months)

syndromes uncommon and often in
inununocomprornised

Middle East, Asia,

Contact with infected ani Mucous membrane or skin lesions; Africa and South
mals, tissues through
pneumonia and pulmonary abscess;

America
broken skin, mucous
sepsis; chronic abscesses, nodules,
membrane; ingestion;
ulcers in many organs, weight loss,
inhalation
lyrnphadenopathy; case fatality rate
varies with form, but >95% in
untreated septicemia

Uncertain; possibly

Gastroenteritis or diarrhea, liver
ingestion of undercooked disease; bacteremia in immunosup-meat or direct contact
pressed patients

( continued)

2426

ZOONOSES

•ih•i• GLOBAL ZOONOSESa (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Leprosy (seep 692)

Mycobacterium leprae

Armadillos; nonhuman primates

(rare)

Leptospirosis

Leptospira spp

Domestic and wild animals; reservoir

(seep 646)

hosts include rodents, dogs, cattle,
pigs, farmed red deer, others

Listeriosis

Listeria monocytogenes Numerous mammals, birds, fish, (seep 656)

(types most often
crustaceans
associated with disease
are V>a, V>b, 4b ), Listeria
ivanovii (rare)

Melioidosis

Burkholderia pseudo

Sheep, goats, swine; occasional cases

(Pseudoglanders,
mallei ( other species
in many other terrestrial and aquatic
seep 661)

of soil-associated
mammals; also reptiles, some birds

Burkholderia, such as
including parrots, tropical fish

B oklahomensis sp nov in

North America, rarely
linked to human
infections)

Methicillin-resistant S aureus that carry

Pigs ( major reservoirs for livestock-

Staphylococcus
mecA gene; some strainS
associated strain CC398, also carry
aureus (MRSA)

maintained in anin1als

ST9); cats, dogs mainly acquire
infections

( eg, livestock-associated
strains from people; MRSA also

CC398), other strains mainly reported in other mammals, in people but anin1als can
including horses, cattle; birds,
become carriers
including poultry, psittacines; turtles

Mycobacteriosis

Mycobacterium avium

Many species of mammals, some

(seep 687)

complex
birds

ZOONOSES

2427

•iM•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Armadillos in parts of Transmission of animal

Various skin lesions, sensory nerve
southern USA, Mexico, leprosy to people likely
lesions and deficits, nasal mucosa]

South America; non-
lesions; mild, self-limiting to
hwnan primates in
progressive destruction

Africa, possibly other
locations; only hwnan
reservoirs in other
areas

Worldwide

Occupational and

Asymptomatic to severe, sometimes
recreational exposure,
biphasic; nonspecific febrile illness
or exposure to rodentfollowed by aseptic meningitis or contaminated material
icteric fom1 ( especially liver, kidney,
in urban locations;

CNS involvement, hemorrhages
especially skin, mucous
possible); pulmonary hemorrhage and
membrane contact with
edema, other syndromes; uveitis can
contaminated urine,
be sequela.; case fatality rate varies
infected fetuses, or repro with syndrome (uncommon in aseptic ductive fluids; water- and meningitis, 5%-15% in icteric fonn, foodborne

3()0/o-{)Oo/o in severe pulmonary fonn)

Worldwide

Foodbome, especially

Acute, self-limited feb1ile gastroenunpasteurized dairy prod teritis or mild, flu-like illness; ocular ucts, raw meat and fish,
disease, conjunctivitis; abortion,
vegeta.bles,processed
premature or septicemic newborn if
foods contaminated after infected dtuing pregnancy; meningiprocessing; ingestion of tis, meningoencephalitis, septicemia
contaminated water, soil; in elderly, in1munosuppressed, and direct contact with
infants; pa.pular or pustular rash ±
infected animals;
fever, chills in healthy adults after
nosocomiaJ in hospitals, handling infected fetuses
institutions

Asia, Africa,

Wound infection,

Mimics many other diseases; acute

Australia, South
inhalation, and ingestion; localized infections, including skin America, Middle
organisms live in soil and lesions, cellulitis, abscesses, corneal East, Caribbean
surface water; most cases ulcers; pulmonary disease, septicea.re acquired from mia, internal organ abscesses; often
environment, but direct
occurs in in1munocompromised;
transmission from
case fatality rate varies with fonn,
animals is possible

>90% in untreated septicemia

Worldwide; can be

Usually by direct contact Opportunist; localized skin and reverse zoonosis or

(typically with asymptosoft-tissue infections, invasive zoonosis; major
matic carrier animals);
disease including septicemia, toxic
strains in animals
other routes also
shock syndrome; mortality varies
can vary with region described; can be
witl1 syndrome and success in finding
nosocomiaJ in hospitals
antibiotic

Worldwide

Environmental, ma.inly

Soft-tissue and bone infections;
from water, and/or soil;
cervical lyn1pha.denitis; pulmonary
infection common to
disease, often in in1munocompromised
people and animals
or those with preexisting lung
conditions; disseminated in in1ffiunocompromised, especially AIDS
patients with uncontrolled disease

( continued)

2428

ZOONOSES

•th•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Mycobacteriosis

M avium

Cattle, sheep, goats, camelids, deer,

(continued)

paratuberculos'is
other ruminants; rabbits and other
nonrurninants; cm:vids

Mycobacteria other than Cattle, other ruminants; swine, cats, tuberculosis (includes
dogs, koalas, other mammals,

M simiae, M kansasii,
an1phibians, reptiles (uncommon),

M xenopi, M scrofula
fish; predominant Mycobacterium
ceum, M szulgai,
spp vary with host

M chelonae, M marinum,

M ulcerans, others)

Mycoplasma

Mycoplasma spp

Livestock, nonhuman primates,
infections
marine man1mals, cats, dogs,
rodents, other manunals

Pasteurellosis

Pasteurella multocida

Many species of domestic and wild

(seep 765 and
and other species
animals, including dogs, cats,
p 1944)

livestock, rabbits, birds

Plague (seep 677)

Yersinia pestis

Rodents (eg, squirrels, prai1ie dogs,
rats) and lagomorphs (pikas in Asia)

are main reservoir; many mammals
can be incidental hosts; cats and wild
felids especially susceptible

Psittacosis and

Chlamydia

Psittacine birds ( especially
omithosis

(Ch/,amydophila)

parakeets, cockatiels), pigeons,

(seep 2808)

psillaci
turkeys, ducks, geese, and other
domestic or wild birds; man1111alian
strains of C psitlaqi also exist

(zoonotic potential still undetermined)

Rat bite fever

Streptobacillus

Rodents; might also be transmitted
moniliformis
by carnivores (eg, dogs, cats,
ferrets), which are probably infected
or transiently colonized from rodents

Spirillum minus

Rodents; might also be transmitted
by carnivores, which are probably
infected or transiently colonized
from rodents

ZOONOSES

2429

•H=i!i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Worldwide

Ingestion; accidental

Postulated involvement in Crohn's
irtjection of vaccine
disease after ingestion ( controversial); severe local reaction if vaccine accidentally irtjected

Worldwide;

Environmental, from

Same syndromes as M avium
distribution varies
water and/or soil
complex; some organisms tend to be
with the organism
associated with certain syndromes

( eg, M marinum, M ulcerans, with
ulcerative or nodular dermatitis)

Worldwide; zoonotic Direct contact; bites;

Asymptomatic carriage; cellulitis;
infections rare
wound contan1ination,
other syndromes, including
including accidental
respiratory disease, septic arthritis,
inoculation
septicemia have been reported,
especially in immunocompromised

Worldwide

Wounds, scratches, bites, Wound infections, cellulitis most close contact with mucus common; other syndromes possible, membranes
including osteomyelitis, septic
arthritis, sepsis, meningitis, respiratory
disease; systemic conditions more
common in inlmunocompromised

Foci in No1th and

Flea bites, aerosols,

Febrile flu-like syndrome with

South America, Asia, handling infected animals swollen, very painful draining lymph Middle East, and
or tissues ( contact with
node(s) (buboes); pneumonia; sepsis

Africa
broken skin or mucous
can occur in either bubonic or
membranes), bites or
pneun1onic form; case fatality rate in
scratches, eating
untreated 40o/er-70% (bubonic) t<,
uncooked infected

100% (pneumonic); < 5%mortality if
tissues
bubonic forn1 treated early

Worldwide

Inhalation of respiratory Influenza-like febrile illness with secretions or dried guano nonproductive cough that may progress to pneumonia; complications, including endocarditis, myocarditis, meningoencephalitis, hepatitis, glomerulonephritis, and other organ
dysfunction; sepsis; some cases fatal
if untreated, < 1 % with treatment

Probably worldwide Bites and scratches;

Fever, severe myalgia and joint pain,
handling or kissing a
headache, rash, sometimes GI signs;
rodent, exposure to
complications, including polyarthritis
rodent urine; can be

(usually but not always sterile),
waterborne or foodborne hepatitis, endocarditis, focal abscesses, sepsis possible if untreated; overall
case fatality rate 10%--13"A, if untreated

Organism is

Mainly bites and

As above, but indurated, often
common only in Asia scratches
ulcerated lesion at inoculation site;
can relapse; some (minority) may
have distinctive rash (large
violaceous or reddish macules);
polyarthritis is rare; overall case
fatality rate 7o/er-l 0% if untreated

2430

ZOONOSES

•§=iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Salmonellosis

Salmonella enterica and Widespread in mammals, birds, (seep 195)

S bongori (> 2,500
reptiles, amphibians, including
serovars)

domestic species; also in crustaceans; higher-risk pets for human exposure may include reptiles,
amphibians, young poultry, some
exotic mammals

Streptococcal

Streptococcus spp,

S suis in swine; S equi zooepidemi
infections
including S suis, S equi
cus in horses; S canis in dogs, cats; zooepidemicus, S canis, S iniae in fish; each species can also S iniae, possibly others
be found in other animals

Tuberculosis (see

Mycobacterium bovis

Cattle, bison, African buffalo,
a/,so MYCOBACTERIOSIS,
cervids, brushtail opossums,
p 2426, p 2869, and
badgers, kudu can be reservoirs;
p 687)

swine and many other mammals can
be spillover hosts

Mycobacterium caprae

Mainly goats, also infects other
ruminants; can occur in other
mammals, including pigs, horses,
cervids, camels, carnivores

Mycobacterium microti Rodents thought to be reservoir; can occur in domestic animals, including
cats, dogs, ferrets, livestock

Tularemia

Francisella tularensis

Rabbits, rodents, cats, sheep, other

(seep 692)

subsp tularensis more
mammals, birds, reptiles, fish; often
virulent, F tularensis
in wild animals
subsp holarctica

(F tularensis type B) less
virulent, F tularensis
subsp mediasiatica,

F tularensis subsp
novicida

Vibriosis

Vibrio parahaemolyticus Marine and estuarine shellfish, fish; also environmental in aquatic
environments

ZOONOSES

2431

•iM•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Worldwide

Foodbome infection or

Gastroenteritis to sepsis; focal
fecal-oral; some cases of infections possible; especially severe occupational and
in the elderly, young children, or
recreational exposure
immunocompromised

Worldwide

Ingestion, especially of

Skin and soft-tissue infections;
unpasteurized dairy prod pharyngitis; other conditions, ucts, pork; direct contact including pneumonia, meningitis, often through broken
artlu;tis, endocarditis, streptococcal
skin; the hun1an pathogen toxic shock syndrome, sepsis S pyogenes can also
colonize bovine udder
and be transmitted in
milk

Once worldwide,

Ingestion (unpasteurized Skin lesions, cervical lymphadenitis now eradicated or
dairy products, tmder

(scrofula), pulmonary disease;
rare in some
cooked meat including
genitourinary disease; can affect
countries
bushmeat), inhalation,
bones and joints, meninges;
contanlination of breaks gastroenteritis
in the skin

Reported mainly in

Thought to be ingestion

Extrapulmonary conditions,

Europe
or direct contact with
including skin lesions, meningitis,
livestock, similarly to
lymphadenitis, pericarditis, urinary,

Mbovis
dissemination; also pulmonary
disease

Appears to be rare

Most reported cases have been
human zoonosis
pulmonary; can also cause extrapulmonary disease

F tularensis subsp

Contact with mucous

Nonspecific febrile illness,
tillarensis almost
membranes, broken skin; lymphadenitis; ulcerative skin exclusively in North insect bites (tabanids,
lesions, exudative pharyngitis and

America; F tularen
mosquitoes, hard ticks); stomatitis, conjunctivitis, gastroen
sis subsp holarctica fomites; ingestion in food teritis, respiratory signs or pneumoin North America, or water; inhalation
nia, sepsis; case fatality rate 5%

Europe, Asia;

Oocalized disease, untreated) to

F tularensis subsp

>50% (untreated typhoidal form or
mediasiatica in
severe respiratory disease)

Central Asia;

F tularensis subsp
novicida reported in

North America,

Australia, Spain

Worldwide

Ingestion; wound

Gastroenteritis; dysentery ( espeinfections
cially in some geographic regions);
wound infections (mild to severe,
including necrotizing fasciitis);
sepsis; severe wound infections and
sepsis usually in in1munocompromised or those with liver disease ( case fatality rate for sepsis 29%)

( continued)

2432

ZOONOSES

•§=iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

BACTERIAL DISEASES (continued)

Vibriosis

V vulnijicus

Marine shellfish, crustaceans ( eg,

(continued)

shrimp), fish; also environmental in
aquatic environments

V cholerae O 1/0139

Oysters, crabs, shrimp, mussels;

( epidemic strains)

most cases acquired from people

V cholerae non-01/0139 Oysters, other seafood; also (nonepidemic strains)

environmental in aquatic environments

Yersiniosis

Yersinia pseudo tubercu Many species of mammals, including losis
swine, dogs, cats, rodents, wild
mammals, birds

Y enterocolitica; not all

Many domestic and wild mammals,
serotypes are pathogenic including rodents; some birds, reptiles, an1phibians; zoonotic
serotypes most common in pigs

(major zoonotic source), pathogenic
types also occur in dogs, cats

RICKETTSIAL DISEASES

Human ewingii

Ehrl'ichia ewingii

Dogs,deer proposed
ehrlichiosis

(fo1merly granulocytic ehrlichiosis)

Human monocytic

Ehrlichia chaffeensis

Deer are probably major reservoir
ehrlichiosis
in North America, dogs and other

(seep 803)

canids, lemurs, other mammals can
also be infected

ZOONOSES

2433

•§;iii• GLOBAL ZOONOSES• (contim,ed)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

BACTERIAL DISEASES (continued)

Worldwide; human

Ingestion ( often raw

Wound infections from mild, selfcases have been
oysters); wound infection limited lesions, bullae to cellulitis, reported in North
from water or handling
myositis; necrotizi.ng fasciitis; gastro

America, Europe,
hosts
enteritis; sepsis, usually in irnrnuno

Asia
compromised or those with liver
disease, other debilitating illnesses;
case fatality rate for sepsis >500A., and
up to 25% for wound infections

Rare/absent to

Ingestion

Mild to severe, voluminous diarrhea,
epidemic in different
vomiting, dehydration; severe cases
regions; one focus
fatal if untreated, but low mortality if
along USA Gulf
treated

Coast in shellfish

Worldwide

Ingestion; wound

Gastroente1itis, usually mild and selfinfection
limited; wound infections; septicemia,
usually in imrnunosuppressed or those
with liver disease ( case fatality rate for
sepsis 4 7%---600A. or higher)

Agent probably

Ingestion of contami

Gastroenteritis ( enterocolitis);
worldwide;
nated water, food (includ pseudoappendicitis (with mesenteric prevalence may vary ing meat [especially
lymphadeni.tis, tenninal ileitis, fever,
between regions
pork], vegetables);
abdominal pain); severe GI bleeding
fecal-oral (animal
possible in some cases of colitis;
contact); dog bite (rare)

pharyngitis; sequelae may include
erythema nodosum, reactive arthritis;
sepsis, especially in elderly or imrnunocompromised

Worldwide;

Ingestion

Gastroenteritis with watery diarrhea
prevalence of human
especially in young children, bloody
disease may vary
feces uncommon; pseudoappendicibetween regions
tis; sequelae may include erythema

( commonly reported
nodosum, reactive arthritis; sepsis,
in Europe)

other syndromes

RlCKETTSIAL DISEASES

Southeastern and

Ticks, including

Few cases described; fever,
south central USA;

Amblyomma ameri
headache, malaise, myalgia, nausea,
has been detected in canu1n
vomiting; many patients were

South America
irnrnunosuppressed

N01th America; also Ticks, including

Asyn1ptomatic to nonspecific febrile
reported in South

Amblyomma ameri
illness; rash in many pediatric cases,

America, Asia, and
caniim
some adults; may progress to

Africa
prolonged fever, renal failure,
respiratory distress, hemorrhages,
cardiomyopathy, neurologic signs,
multiorgan failure; more severe in
immunosuppressed, elderly;
estimated case fatality rate 2o/o--3%

(continued)

2434

ZOONOSES

•ttH•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

RICKETISIAL DISEASES {continued)

Human granulocytic Anaplasma, phagocy

Wild rodents, deer may be reservoirs
anaplasmosis
tophilum (formerly
in North America; livestock, wild

(formerly human

Ehrlichia phagocytophi ungulates, wild rodents may be granulocytic
lum and E equi)

reservoirs in Europe; many other
ehrlichiosis)

animals ( eg, equids, ruminants, dogs,
cats, birds) can also be infected

Infection by other

E canis, E muris-like

Dogs and other canids thought to be

Ehrlichia species
organism implicated
reservoirs for E canis, might also
rarely in human illness
occur in felids; rodents may be
reservoirs for E muris

Q fever (Query fever, Coxiella burnetii

Sheep, cattle, goats, cats, dogs,
seep 623)

rodents, other mammals, birds, ticks

Sennetsu fever

Ne01ickettsia sennetsu

Uncertain, possibly fish

Spotted fever group
of Rickettsia

-African tick bite

R afticae

Ungulates
fever

-Mediterranean

R conorii subsp conorii Dogs, rabbits implicated as spotted fever;
reservoirs; other animals can be

Boutonneuse fever;
infected

Tick bite fever;

-Israeli spotted

R conorii subsp

Reservoir hosts uncertain
fever, Astrakhan
israelensis (Israeli
spotted fever, Indian spotted fever), R conorii
tick typhus
subsp caspia (Astrakhan
spotted fever), R conoiii
subsp indica (Indian tick
typhus)

-Fleabome spotted Rfelis (synonym

Unknown; dogs have been suggested
fever; Cat flea typhus ELB agent)

as possible amplifying hosts

ZOONOSES

2435

•§:iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

RICKETTSIAL DISEASES (continued)

Worldwide

Tick bites (Jxodes spp)

Resembles human monocytic
ehrlichiosis; often asymptomatic to
mild in immunocompetent; rash
uncommon; estimated case fatality
rate <1%

E canis worldwide;

Ticks (E canis transmitted Rare cases of febrile illness, in both E muris Eastern
by Rhipicephalus sangui healthy and immunosuppressed Europe to Asia; E
neus, E muris by Haernamuris-like organism physalis.fwva and lX'Odes in North Ame,ica
persu/.catus complex)

Worldwide

Mainly airborne; exposure Febrile influenza-like illness; atypical to placenta, birth tissues, pneumonia, hepatitis, endocarditis in anin1al excreta; occasion some; possible pregnancy complicaally ingestion (including tions; overall case fatality rate 1 o/o-2%
unpasteurized milk);
if untreated
tickborne infections
probably rare or
nonexistent in people

Japan, Malaysia,

Thought to be ingestion

Relatively mild, nonspecific, febrile

Laos, possibly other of raw fish
illness, resembles infectious

Asian count1ies
mononucleosis

Sub-Saharan Africa, Bite of infected tick

Nonspecific febrile illness; painful
eastern Caribbean

(mainly Amblyomma
regional lymphadenopathy in many;
hebraeum, A variega
eschars often multiple; nuchal
tum, also A lepidum,
myalgia; sometimes sparse maCttlopossibly Rhipicephalus papular and/or vesicular rash; deaths
decoloratus, Rhipicepha do not seem to occur lus appendiculatus)

Europe, especially

Bite of infected ticks

Nonspecific febrile illness; eschar

Mediterranean;

(mainly Rhipicephalus

(typically single) may or may not be
cases reported in
sanguineus, also others), present; rash, often maculopapular, sub-Saharan Afiica
crushing tick
in most; life-threatening disseminated disease or neurologic signs possible but uncommon; case fatality
rate 1 o/o-3% if untreated

Israeli spotted fever

Bite of infected ticks

Astrakhan spotted fever and Indian
in Middle East,

(mainly Rhipicephalus
tick typhus resemble Mediterranean
reported in Europe;
spp ), crushing tick
spotted fever, but Israeli spotted

Astrakhan spotted
fever may be more severe
fever in Russia,

Kazakhstan; Indian
tick typhus in Asia

(Indian subcontinent)

North and South

Flea bites; mainly

Few clinical cases have been

America, Europe,
associated with
described but resembles other

Asia, Africa,

Ctenocephalides felis
spotted fevers; febrile illness; rash in
probably worldwide (cat flea), also infects
most; eschar may be uncommon;

C canis and other fleas
most cases seem to be mild but CNS
involvement, pneumonia possible

(continued)

2436

ZOONOSES

•M:fij• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

RICKETTSIAL DISEASES (continued)

-Queensland tick

R australis

Bandicoots, rodents
typhus

-Rickettsial pox

R akari

Mice; also rats, Korean voles

-Rickettsia parkeri R parkeii
rickettsiosis

-Rocky Mountain

R iickettsii

Rodents, rabbits, opossums, and
spotted fever
other small mammals might amplify;

(seep 806)

dogs can be infected

-Tickbome

R slovaca, R raoultii

Uncertain; wild boar may be involved
lymphadenopathy;

Dermacentor
necrosis-erythemalymphadenopathy

-Other tickbome

R sibirica., Rjaponica,

Various vertebrates
species in spotted

R helvetica, R honei, R hei-
fever group
longjiangensis, R aeschli-
mannii, R massiliae,

R monacensi, R amblymnmii, others

Typhus group of

Rickettsia

-Murine typhus;

R typhi (formerly

Rats are major reservoir; cats,

Fleabome typhus

R mooseri)

opossums, possibly dogs, other
species in peridornestic cycle

ZOONOSES

2437

•4):jjj• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

RICKETTSIAL DISEASES (continued)

Australia

Bite of infected Ixodes

Febrile illness, eschar may be
tick, especially
present, rash ( either maculopapular

I holocyclus, I tasmani
or vesicular) in most; mild in most,
but serious disseminated disease,
complications, death possible

Organism may be

Bite of infected rodent

Eschar (single) in most; febrile
cosmopolitan;
mites, Liponyssoides
illness; maculopapular rash prohuman cases seem
sanguine'itS
gresses to vesicular, pustular,
to be uncommon
resembles chickenpox; self-limiting

North America,

Bite of infected ticks,

Resembles Rocky Mountain spotted
detected in parts of Amblyomma macula
fever (RMSF) but seems to be milder

South America
tum; also found in other in most cases; differs from RMSF in Amblyomma spp
that eschars occur in most cases

(may be multiple), petechial rash
does not seem to be characteristic

Western hemisphere Bite of infected ticks,

Moderate to severe febrile illness;
especially Dermacenlor
macular to generalized petechial
variabilis, D andersoni rash; edema in some; usually no (D variabilis in USA);
eschar; neurologic, pulmonary,

Amblyomma cajennense, hemorrhagic, and kidney signs in A aureolatum in South
some; sepsis; gangrene; case fatality

America; Rhipicephalus rate 15%-3()0A, or higher (up to 85%) if sanguineus in Arizona,
untreated, -3% or less with treatment

Mexico, and South
in North America but higher in parts

America; also from
of Brazil
crushing tick

Europe to Central

Bites of infected ticks;

Eschar, local lymphadenopathy;

Asia

R slovaca especially in
localized alopecia at bite site; mild

Dermacentor margina
illness, fever and rash uncommon; no
tus, D reticulatus;
deaths repo1ted

R raoultii in Rhipicephalus pumilio, D nutlalli, other Dermacentor spp

Worldwide;

Bites of ixodid ticks;

Inoculation site eschar (most); febrile
distribution varies
specific vector varies by
illness with headache, myalgia,
by species
species
sometimes other signs; rash; local
lymphadenopathy (some species);
major signs, risk of complications,
severity vary with species of Rickellsia

Worldwide,

Infected rodent fleas,

Fever, severe headache, central rash
especially warmer
usually via flea feces; cat (not always observed); other signs, regions
fleas seem to be involved including arthralgia, cough, nausea/
in some cycles
vomiting in some; m01tality rate 4%
without treatment

(conlin11ed)

2438

ZOONOSES

•ttN•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

RICKETTSIAL DISEASES (continued)

-Scrub typhus;

Orientia tsutsugamushi Rodents, insectivores Chigger-borne
and related species
rickettsiosis

-Typhus

R prowazekii

Flying squirrels

FUNGAL DISEASES

Aspergillosis;

Aspergillus spp

Birds and mammals

Allergic bronchopulmonary aspergillosis

(seep 2901)

Blastomycosis

Blastomyces

Dogs, cats, horses, marine mammals,

(seep 634)

dermatitidis
other mammals

Coccidioidomycosis Coccfdioides immitis,

Cattle, sheep, horses, llamas, dogs,

(seep 637)

C posadasii
many other marnmals

Cryptococcosis

Cryplococcus neofor

Birds including pigeons, psittacines

(seep 637)

mans var grubii,

(mainly grows in guano; temporary

C neoformans var
colonization of intestinal tract also
neoformans, C galtii
possible); clinical cases in cats, other
mammals

ZOONOSES

2439

•&=iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

RlCKETISIAL DISEASES (continued)

VetBooks.ir

Asia, Australia,

Bite of infected larval

Eschar in some; rash, headache, fever,
islands of southwest trombiculid mites
painful lyrnphadenopathy, body aches,
ern Pacific Ocean;

(chiggers)

interstitial pneumonitis, GI signs;
cases are usually
pnewnonia, neurologic signs or
concentrated
cardiac complications in some; mild to
regionally in "typhus
severe; convalescence prolonged; case
islands"

fatality rate up to 30%-5U'/o if untreated

Eastern USA

Squirrel lice or fleas

Nonspecific febrile illness, rash; GI
suspected
signs in some; sepsis possible; appears
to be somewhat milder than nonzoonotic typhus, which has a mortality rate of 2U'/o--6U'/o if untreated

FUNGAL DISEASES

Worldwide

Environmental exposure Allergic respiratory signs, especially ( decaying vegetation or
in people with certain respiratory
grains); infection
conditions or immw10deficiencies;
common to people and
allergic sinusitis; pneumonia
animals, insignificant as
sometimes with dissemination in
zoonosis
immunocompromised (can be fatal);
chronic pulmonary disease ±
aspergilloma (fungus ball); localized
infections of other organs, tissues

Distribution in

Environmental exposure, Acute to chronic pulmonary disease; environment
organism is most
skin or bone lesions; meningitis,
uncertain; clinical
common in moist soil;
other syndromes, disseminated
cases focal; locally
infection common in
disease possible; course mild to
acquired cases report people and animals; also severe, some cases fatal ed in parts of North
reported rarely by animal

America, Africa,
exposure

Middle East, India

Especially south

Principally environmental Self-limited, febrile, flu-like illness, western USA,
exposure (inhalation of
sometimes with cough, chest pain in

Mexico, Central and arthrospores), including
healthy host; serious, possibly

South America; in
fungal cultures; infection
life-threatening pulmonary disease
arid or semiarid foci; common in people and ani or disseminated infection with some cases might be mals, one wmsual case
cutaneous/subcutaneous lesions,
acquired outside
reported after necropsy of persistent meningitis or osteomyeliusual foci horse with disseminated
tis, especially in inununocomprodisease
mised

Worldwide

Principally environmen

Respiratory signs, mild to severe,
tal exposure, especially
often self-limiting in healthy host but
pigeon nests for
more likely to be severe in immuno

C neoformans, trees for
compromised; dissemination with

C gattii; via inhalation or CNS disease, ocular signs, other through the skin;
syndromes, most often in irnrnunoinfection common in compromised; skin lesions, either
people and animals, insig localized from inoculation ( uncomnificant as zoonosis mon) or from disseminated disease

( continued)

2440

ZOONOSES

•§:iii• GLOBAL ZOONOSES• (conUnued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

FUNGAL DISEASES (continued)

Histoplasmosis

Hisloplasma ca,psula

Dogs, cats, bats, cattle, sheep,

(seep 639)

tum var capsula,tum
horses, many other domestic and
wild mammals, birds

H capsulatum var

As above
duboisii

Malassez'ia infection Mala,ssezia spp Dogs, cats, other animals

Ringworm

Microspoium and

Dogs, cats, hedgehogs, cattle, sheep,

(Dermatophytosis,

Trichophyton spp
goats, horses, rodents, other
seep 872)

mammals, birds, very raxely reptiles

Sporotrichosis

Sporothrix schencki'i

Cats, other mammals, birds

(seep644)

PARASITIC DISEASES-PROTOZOANS

Babesiosis

Babesia microli

Rodents, insectivores, lagomorphs,

(seep2l)

complex, B duncani
some other mammals; reservoirs

(formerly WA-1), and
uncertain for some species
other species

Bdivergens

Cattle; B divergens or closely related
organism in farmed reindeer, wild
cervids

B bovis; uncertain

Cattle, water buffalo, African buffalo,
zoonosis; some historical possibly other species
cases were probably

Bdivergens

ZOONOSES

2441

•tliii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

FUNGAL DISEASES (continued)

Worldwide; clinical

Principally environmental Flu-like, febrile illness, usually cases often cluster in exposure, avian or bat
self-limiting in healthy hosts; skin
regional foci
feces encourage growth
lesions; chronic pulmonary disease,
of organism; infection
usually with preexisting lung disease;
common in people and
dissemination in very young, elderly,
animals; insignificant as
immunocompromised
zoonosis

Africa

As above

Usually skin and subcutaneous
lesions, osteolytic bone lesions but
can disseminate

Worldwide

Exposure to symptomat Dennatitis; zoonotic strains might be ic animals; nom1al levels implicated in fungemia in preterm on skin not thought to be neonates, other immunocomproa significant risk mised

Worldwide

Direct skin/hair contact

Skin and hair lesions, usually
with infected animals,
pruritic; rare skin dissemination
fomites
in inlmunocompromised

Worldwide;

Prinlarily environmental

Papules, pustules, nodules, ulcerative
epizootics in cats in in vegetation, wood, soil;
skin lesions, may follow course of

South America
inoculation from
draining lymphatics; mucosa can be
environment in penetrataffected; extracutaneous involvement, ing wounds (splinters,
especially bones, joints; disseminated
bites, pecks), skin contact disease (including meningitis) can be with lesions, especially in seen in inlmunocompromised; acute cats; bites, scratches,
or chronic pulmonary disease
other close contact
resembling tuberculosis after
in1plicated during feline
inhalation, especially with underlying
epidemics; inhalation rare lung disease (rare)

PARASITIC DISEASES-PROTOZOANS

Babesia spp world

Bite of infected Ixodes

Many irnrnunocompetent patients may
wide in wild animals, ticks for B micro ti
have mild to moderate flu-like, febrile
many agents not
illness; mild to severe hemolytic
identified to species;
anemia, especially severe in in1!11unohuman illness due to compromised and elderly; respiratory,

B micro ti complex
hepatic, renal, and other organ
reported in North
dysfunction; recurrent or chronic

America (most),
infection may develop; dual infection

Europe, Asia,
with B burgdo1feri may worsen both

Australia
diseases; death possible in severe cases

Europe, possibly

Tick bites (Ixodes

Usually in splenectomized; acute,

North Africa; similar ricinus)

severe hemolysis; persistent high
organisms might be
fever, headache, myalgia, abdominal
present in North
pain, sometin1es GI signs; shock and

America; reported in
renal failure; cases progress rapidly;

Asia (China)

usually fatal if untreated; milder
flu-like cases have been rep01ted in
in1munocompetent patients

Africa, Asia, Central Tick bites (Rhipicepha
and South America, lus microplus and

Mexico, Australia,

R anniilatus)

parts of Europe
r ,......,..., �,;,.,,,,,, .,,,.,.,

2442

ZOONOSES

•th•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-PROTOZOANS (continued)

Balantidiasis

Balantidium coli and

Swine, rats, nonlmman primates,
related species
other animals

Chagas' disease

Tlypanosoma cruzi

Opossums, lagomorphs, rodents,

(American trypanoarmadillos, dogs, cats, other wild and somiasis, see p 38)

domestic man1mals

Cryptosporidiosis

Oryptosporidiiim

Cattle and other rmninants, dogs,

(seep 209)

parvum, C canis, C felis,
cats, rabbits, other domestic and

C meleagridis, C cunicu-
wild manunals, birds, reptiles, fish
lus, Cviatorum, Cmuris,
and other species

(C lwminis and likely
some genotypes of

C parvum are adapted
mainly to people)

Giardiasis

Giardia intestinalis,

Many domestic and wild mammals,

(seep 211)

also known as G duode
including dogs, cats, rmninants,
nalis (fo1merly
aquatic manm1als such as beavers

G lamblia); only some
genotypes seem to have
zoonotic potential

Leishmaniosis

Leishmanja irifantum

Wild canids and dogs are primary

-Visceral (Kalaazar;
reservoirs, also in other manunals
seep800)

-Cutaneous and

L tropica complex

Dogs (L peruviana), rodents,
mucocutaneous

(exceptL tropica, which various wild mammals act as is maintained in people), reservoir hosts; other mammals can L braziliensis complex,
be infected

L mexicana complex,
others

ZOONOSES

2443

•§=iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-PROTOZOANS (continued)

Worldwide

Ingestion, especially of

Asymptomatic to mucoid, bloody
water contaminated with feces; intestinal hemorrhage and feces
perforation possible; rare extraintestinal cases

Western hemi

Fecal material of reduviid Acute disease-erratic fever, sphere-southern
bug in family Triatomidae adenopathy, headache, myalgia, USA, Mexico,
contaminates bite
hepatosplenomegaly, swelling at

Central and South
wounds, abrasions, or
inoculation site and eyelid; myocar

America
mucous membranes;
ditis or encephalitis in some; worse
ingestion in contan1iin immunocompromised
nated food

Chronic forn1 (in WYo-300/oof patients)

---cardiomyopathy, megaesophagus,
megacolon, other forms; reported
annual mortality rate in chronic form

0.2"1<>--19% (higher rates from studies
that include only cardiac patients)

Worldwide

Fecal-oral; ingestion of

Self-limiting gastroenteritis in
contan1inated food and
healthy; can be cholera-like and
water; inhalation
persistent in in1munocompromised,
with weight loss, wasting; cholecystitis; respiratory signs, pancreatitis, other syndromes mainly in immunosuppressed

Worldwide

Ingestion of water and

Gastroenteritis, may be persistent
less often food; direct
fecal-oral (hands or
fomites)

Asia, South America, Bite of sand flies

Undulating fever, hepatosplenorne

Caribbean, Africa,

Phlebotomus and
galy; some have cough, diarrhea,
the Middle East,

Lutzomyia spp
lymphaclenopathy, weight loss,

Europe (Mediterrapetechiae or hemorrhages on mucous
nean spreading
membranes, nodular lesions or
no1th), North
darkening of skin; pancytopenia; mild

America
cases with only a few signs may
resolve on their own, but most other
cases fatal if untreated

Mediterranean, Asia, As above

Papules to ulcers or nodules on skin ±

Africa, Middle East,
mucous membranes; single or multiple

Mexico to South
lesions; localized or disseminated; may

America, Caribbean;
persist or recur; atypical forms in
localized focus in
unmunosuppressed;cutaneous form

USA (Texas and
rarely fatal, mucocutaneous form can

Oklahoma)

be disfiguring and may be fatal if
pharynx affected

( conl,inued)

2444

ZOONOSES

•M:jf j• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-PROTOZOANS (continued)

Malaria of nonhu

Nonhuman primate

Old and New World monkeys, apes
man primates
associated Plasmodiitm
spp, P knowlesi, rarely

P cynomolgi, others also
potential zoo noses

Microsporidiosis

Microsporidia of

Widespread in vertebrates, including

Enterocytozoon
primates, rabbits, rodents, dogs, cats,
bieneusi, Encephalito
cattle, pigs, goats, birds, fish; also in
zoon cuniculi, E intesti invertebrates
nalis, E hetlem, others;
both zoonotic and anthropnotic transmission
reported for some agents

Rhinosporidiosis

Rhinosporidium seeberi; Natural hosts thought to be fish and (seep 644)

some strains may be host amphibians; also found in various specific
mammals, including horses, cattle,
mules, dogs, and cats; birds

Sarcocystosis

Sarcocystis suihominis, People, nonhuman primates are (Sarcosporidiosis,
also called S meischeri
definitive hosts; swine are intermedi
seep 1058)

ana
ate host

S hominis, also called

People, nonhuman primates are

S fusiform'is
definitive hosts; cattle are intermediate host

Sarcocystis spp;
s

People are intermediate host; species
nesbitli may be one
of Sarcocystis and definitive host(s)

cause
are often unknown; definitive host
for S nesbitti thought to be snakes

Toxoplasmosis

Toxoplasma gondii

Felidae, including domestic cats, are

(seep 685)

definitive hosts; essentially all other
mammals (including livesteck) and
birds thought to be susceptible as
intermediate hosts

Trypanosomiasis

Trypanosoma brucei;

T brucei rhodesiense reservoirs may

(African sleeping

T brucei rhodesiense is
include cattle, sheep, antelope,
sickness, seep 35)

zoonotic; T b1·ucei gambi hyenas, lions, other wildlife, people; ense is primarily a human also isolated from other mammals pathogen, although some
anin1als ( eg, pigs) can be
infected and might serve
as minor reservoirs

ZOONOSES

2445

•tM•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-PROTOZOANS (continued)

P kno1vlesi in Asia;

Bite of anopheline

Febrile episodes with chills;
other t,pecies exist in mosquitoes
headache, myalgia, malaise, cough,

Centr� and South
nausea, vomiting, and other

America, Asia, Africa
symptoms in some; cases range from
mild, self-limiting to fatal (3% case
fatality rate for P knowlesi)

Worldwide

Fecal-oral; direct contact; Keratitis; acute diarrhea (traveler's ingestion of contamidiarrhea); chronic diarrhea in
nated food or water;
immunocompromised; may
aerosols; possibly
disseminate to systemic disease with
vector-transmitted
variable symptoms in immunocompromised

Worldwide,

Environmental exposure, Nasal and other mucous membrane especially in tropics; probably water
masses and polyps (mainly nose, nasoendemic in South pharynx, eye); may cause obstruction;

America, Asia, and
rare disseminated disease with

Africa
osteolytic lesions or affecting viscera;
rare skin and subcutaneous lesions

Worldwide

Ingestion of raw pork

Gastroenteritis, usually mild, or
asymptomatic

Worldwide

Ingestion of raw beef

Gastroenteritis, usually mild or
asymptomatic

Worldwide;

Assumed to be ingestion Main syndrome is myositis, acute and symptomatic cases
of oocysts shed in feces
self-limited to chronic, moderately
mainly in Asia,
of definitive host( s) or
severe; also cough, arthralgia,
proba))ly because of sporocysts
transient pruritic rashes, headache,
distribution of definimalaise, lymphadenopathy in some tive host

Worldwide

Ingestion of oocysts shed Lyrnphadenopathy or mild, febrile, in feces of infected cats
flu-like syndrome or uveitis in

(including contaminated immunocompetent, nonpregnant soil, food, water) or
host; often severe in imrnunocomingestion of tissue cysts promised, with neurologic disease,
in undercooked meat or
chorioretinitis, myocarditis, pneun10-
unpasteurized milk
nitis, or disseminated disease;
infection of fetus may result in CNS
danrnge or generalized infection;
abortions and stillbirths

Africa; common

Bite of infected tsetse fly Painful chancre at bite site in some below the Sahara

( Glossina spp)

patients; intermittent fever, headdesert
ache, adenopathy, rash, arthralgia;
neurologic signs such as somnolence,
seizures; cardiac complications possible; gamb'iense disease may last years; rhodesiense disease acute, may
last weeks to months; both usually
fatal without treatment

(continued)

2446

ZOONOSES

•@:iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-TREMATODES (FLUKES)

Clonorchiasis

Clonorchis sinensis

Dogs, cats, swine, rats, other

(Chinese liver fluke)

mammals are definitive hosts; fish

(and snails) are intermediate hosts

Dicrocoeliasis

Dicrocoelium dendi-lti

Ruminants, especially sheep, goats,
cum, possibly D hospes
cattle, occasionally other domestic

Oancet flukes)

and wild manunals are definitive
hosts; land snails (first) and ants

(second) are intermediate hosts

Echinostomiasis

Echinostoma revolutwn, Cats, dogs, rodents, pigs, other E ilocanum, E hortense,
mammals; birds, including poultry,
and other Echinostoma
are definitive hosts; fish, shellfish,
spp; Echinochasmus
tadpoles, snails are intermediate
japonicus and other mem hosts
bers of Echinostomatidae
can also be zoonotic

Fascioliasis

Fasciola hepatica

Cattle, sheep, water buffalo, horses,
rabbits, other herbivores are
definitive hosts; snails are intermediate hosts

F gigantica

Cattle, buffalo, goats, sheep, zebras,
other mammals are definitive hosts;
snails are intermediate hosts

Fasciolopsiasis

Fasciolopsis biiski

Swine, people are definitive hosts;
snails are intermediate hosts

Gastrodiscoidiasis

Gastrodiscoides

Swine, people, nonhuman primates,
hominis; uncertain
rodents, other manunals are
whether people and
definitive hosts; snails are intennediswine carry the same ate hosts
strains

Heterophyiasis

Heterophyes spp,

Cats, dogs, foxes, wolves, cattle,

Haplorchis spp, other
other mammals, fish-eating birds are
heterophids
definitive hosts (host varies with
species of parasite); fish (and snails)

are intennediate hosts

Metagonirniasis

Metagonimus yokoga

Cats, dogs, rats, other fish-eating
wai, M miyatai,
manunals, possibly birds are

M takahashii, and other definitive hosts; fish (and snails) are Metagonimus spp
intermediate hosts

ZOONOSES

2447

•@�iii• GLOBAL ZOONOSESa (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-TREMATODES (FLUKES) (continued) Asia

Ingestion of undercooked Cholecystitis symptoms, indigesinfected freshwater fish tion, diarrhea, mild fever; chronic
or shrimp containing
infections associated with
encysted larvae
cirrhosis, pancreatitis, or cholangiocarcinoma

D dendriticum on

Ingestion of infected ants Abdominal discomfort, flatulent all major continents
indigestion; occasionally GI signs

(may be focal);

(diarrhea, constipation, vomiting,

D hospes in Africa
pain); weight loss, fatigue; biliary
south of Sahara
obstruction, cholangitis, hepatodesert
megaly, or acute urticaria possible

Most human cases in Ingestion of undercooked Abdominal discomfort; diarrhea, Asia, Western Pacific; fish, shellfish, snails, or
especially in heavy infestation;
this group of
amphibians (frogs)

malnutrition, anemia, e<lema may
parasites is widely
occur, especially in children;
distributed, including
intestinal perforation has been

Europe, Americas,
reported

Middle East

Worldwide or nearly Ingestion of contami

Gastroenteritis, hepatomegaly, fever,
worldwide;
nated greens, eg,
urticaria possible acutely; biliary
previously thought
watercress, or water that colic and obstructive jaundice in to be mainly in
contains metacercariae
chronic cases; aberrant migration
temperate areas but
with extrahepatic signs ( eg,
may be more widely
pulmonary infiltrates, neurologic
distributed
signs, lymphadenopathy, skin lesions
or subcutaneous swelling) in some

Thought to occur

As above

Signs resemble fascioliasis caused by
mainly in tropical

Fhepatica
areas: Africa, Asia,

Middle East, and
western Pacific

Asian pig-raising

Ingestion of aquatic

Often asymptomatic; gastroenteritis;
regions
vegetables or contamiintestinal bleeding, obstruction, or nated drinking water
perforation possible; facial, abdomicontaining metacercariae nal, extremity edema may occur Asia (including the

Possibly ingestion of

Mild diarrhea if high parasite burden

Philippines), also
water or aquatic plants
reported in Africa,

Volga delta in Russia

Middle East

Ingestion of undercooked Diarrhea with mucus, colicky pain; (especially Nile
fish containing encysted heart or CNS involvement possible; delta), Turkey, Asia
larvae
severity of signs may vary with
species

Human illness

Ingestion of undercooked Diarrhea with mucus, anorexia, mild mainly in Asia, also
freshwater fish containepigastric pain or abdominal cramps; reported in Siberia;
ing encysted larvae
malabsorption, weight loss if high
parasites have been
parasite burden
found in Ew·ope

(contin11ed)

2448

ZOONOSES

•t}i•j• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-TREMATODES (FLUKES) (continued) Metorchiasis

Metorchis conjunctus,

Dogs, foxes and other canids, cats,

Canadian liver fluke
raccoons, muskrats, mink, other fisheating mammals are definitive hosts; fish ( and snails) are intetmediate hosts

Nanophyetiasis

Troglotrema salmincola Raccoons, foxes, dogs, cats, skunks, (also calledNanophyel'US and other fish-eating mammals and salmincola)

birds are definitive hosts; salmonid
and some non-salmonid fish (and
snails) are intermediate hosts

Opisthorchiasis

Opisthorchis felineus

Cats, dogs, foxes, swine, seals, other

( cat liver fluke)

fish-eating mammals are definitive
hosts; fish ( and snails) are intermediate hosts

O viverrini (small liver

People, dogs, cats, rats, pigs,
fluke); zoonotic
fish-eating mammals are definitive
transmission can occur,
hosts; fish and snails are intermedibut people are important ate hosts hosts

Amphimerus pseudofe

Various mammals, birds, reptiles are
lineus
definitive hosts; fish suspected as
intermediate hosts

Paragonimiasis

Paragonimus wester

Dogs, cats, swine, wild carnivores,

(Lung fluke disease) mani, P heterotremus,
opossums, and other mammals are

P africanus, P mexi
definitive hosts; snails and freshwa
canus, and other species ter crustaceans are intermediate hosts; wild boars, sheep, goats,
rabbits, birds, other animals are
paratenic hosts

Schistosomiasis,

Schistosoma japonicum Many man1mals, including cattle, intestinal and
water buffalo (important host in
hepatic

Asia), swine, dogs, cats, deer, horses,
nonhuman primates, and rodents, are
definitive hosts; snails are intermediate hosts

ZOONOSES

2449

•#H•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-TREMATODES (FLUKES) (continued) North America;

Ingestion of w1dercooked Fever, abdominal pain (mainly human infection rare freshwater fish containepigastric ), anorexia during acute ing encysted laivae
stage; effects of clu·onic infection
uncertain

North America along Ingestion of undercooked Mild gastroenteritis Pacific coast, Russia fish or roe

Europe, Kazakhstan, Ingestion of undercooked Acute febrile illness with arthralgia, Russia, Ukraine
freshwater fish containlymphadenopathy, skin rash; suppuraing encysted larvae tive cholangitis and liver abscess in
subacute, chronic stages; possible
increased 1isk of cholangiocarcinoma

Southeast Asia

Ingestion of undercooked Upper abdominal pain, diarrhea, freshwater fish containfever, jaundice possible acutely; ing encysted laivae
chronic infections with cirrhosis,
pancreatitis, high incidence of
cholangiocarcinoma

North and South

Undetermined but

America
probably ingestion of
undercooked fish

Flukes are world

Ingestion of undercooked, Chills, fever possible dwing wide ( distribution
infected freshwater
migration to lungs; pulmonary
varies with species); crustaceans ( crabs,
disease resembling tuberculosis
most human
crayfish); metacercariae
with cough, blood-tinged sputum;
infections in Asia,
on containinated hands,
abdominal fom1 with dull pain,

Africa, tropical
fornites after preparing
tenderness, possibly diarrhea; less

America
crustaceans, or underoften, neurologic signs, migratory cooked meat from
skin nodules, other organ-specific
paratenic hosts such as
symptoms; predominant signs vary
wild boars
with species of fluke

Asia

Penetration of unbroken Acute disease can include urticaria!

skin by cercariae from
rash, mild signs, isolated pulmonary
infected snails in water
signs, or Katayaina syndrome ( occurs
especially after fast infection; febrile
illness, sometimes with cough,
diarrhea, abdominal pain, hepatosplenomegaly, and/or rash/urticaifa); apparent clinical recovery may be
followed by chronic intestinal
schistosomiasis with abdominal pain/
discomfort, diarrhea ± blood; chronic
hepatic schistosorniasis with
hepatosplenomegaly followed by liver
fibrosis, ascites, portal hypertension
with hematemesis and/or melena,
portocaval shunting with pulmonary
signs; ectopic parasites can cause
seizures, paralysis, meningoencephalitis; intestinal and hepatic lesions tend to progress rapidly; death can occur

( continued)

2450

ZOONOSES

•@:iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

PARASITIC DISEASES-TREMATODES (FLUKES) (continued) VetBooks.ir

Schistosomiasis,

S mansoni

People, nonhuman primates are
intestinal and
major reservoir (definitive) hosts;
hepatic (continued)

also in rodents, insectivores, cattle,
dogs; snails are intermediate hosts

S mattheei; S bovis and

Definitive hosts are artiodactylid rumi

S margrebowiei might
nants ( cattle, sheep, goats, waterbuck,
also be zoonotic
wildebeest, antelope, buffalo), also
found in nonhuman primates; snails
are intcnncdiate hosts

S mekongi

People are rese1voir (definitive)

hosts; also found in dogs, pigs; snails
are intenuediate hosts

S intercalatum,

Primarily people, rodents may also

S guineensis
be definitive hosts; some other
mammals, including nonhuman
primates, susceptible to infection;
snails are intermediate hosts

Schistosomiasis,

S haematobium

People are main reservoir ( definitive
urinary
host); occasionally infects nonhuman primates, pigs, buffalo, sheep, rodents, or other manuuals; snails
are intem1ediate hosts

Swimmer's itch

Schistosome cercariae

Birds, mammals are definitive hosts;

(Cercarial de1matifrom Schistosoma spp
snails are intennediate hosts
tis)

(mammals); Gigantobil-
harzia, Trichobilharzia,
and Austrobilharzia spp

(birds)

PARASITIC DISEASES-CESTODES (TAPEWORMS)

Bertielliasis

Bertiella studeri,

Nonhuman primates are usual hosts;

B mucronata
otl1er mammals, including dogs,
people can be infected

Coenuriasis

Taenia multiceps

Definitive hosts are canids;

(Coenurosis)

intennediate hosts are sheep, other
herbivores

T serialis

Definitive hosts are canids;
intermediate hosts a.re la.gomorphs,
rodents, occasionally other
man1mals

ZOONOSES

2451

•M=i!i• GLOBAL ZOONOSES• (conlin1led)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-TREMATODES (FLUKES) (continued) Africa, Middle East, Penetration of unbroken Acute disease in some; intestinal South America,
skin by cercariae from

(most often) and/or hepatic

Caribbean
infected snails in water
schistosomiasis similar to

S japonicurn but not as rapidly
progressive; glomerulonephritis a
possible complication; ectopic CNS
parasites tend to cause transverse
myelitis; also causes genital
schistosomiasis with reproductive
problems; death can occur

Southern Africa;

Penetration of unbroken Suggested agent in intestinal and seems to be rare in
skin by cercariae from
hepatic schistosomiasis
people, and some
infected snails in water
infections may have
been misidentified

Southeast Asia

Penetration of unbroken Acute disease absent or very rare; skin by cercariae from
intestinal and hepatic schistosomiainfected snails in water sis; death can occur

Africa

Penetration of unbroken Intestinal schistosomiasis only, often skin by cercariae from
mild or asymptomatic; occasionally
infected snails in water
bloody feces, diarrhea

Africa (including

Penetration of unbroken Acute disease in some; chronic Madagascar,
skin by cercariae from
disease--hematuria, dysuria, kidney

Mauritius), the
infected snails in water
failure; calcification of bladder wall,

Middle East
ureter, and bladder can lead to bladder
cancer; ectopic CNS parasites tend to
cause transverse myelitis; genital
schistosorniasis; death can occur

Worldwide

Penetration of unbroken Self-limiting urticaria, pruritus, rash; skin by cercariae from
fever, local lymph node swelling
infected snails in freshpossible in some cases
and saltwater

PARASITIC DISEASES-CESTODES (TAPEWORMS)

Asia, South America, Ingestion of infected

Most cases asymptomatic; abdomi

Africa; can occw· in oribatid mites in food
nal pain, vomiting, diarrhea,
imported primates in
constipation, weight loss
other areas

Worldwide in

Ingestion of tapeworm

Painless skin swelling; possible CNS
scattered foci;
eggs in canine feces, may involvement (signs of mass lesion in mainly reported
be via water, vegetables, brain) or Jarva in eye
from Europe, Asia
soil

Africa, Europe,

As above

Painless skin swelling; also in

North America,
muscles and retroperitoneally; CNS

Australia; rare in
involvement possible
people

( contin1led)

2452

ZOONOSES

•§:iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-CESTODES (TAPEWORMS) (continued) Coenuriasis

T brauni

Definitive hosts are canids; interme

(Coenurosis)

diate hosts are gerbils, wild rodents,

(continued)

also people

Cysticercosis

Taenia solium (see also People are definitive hosts; swine, Taeniasis)

other mammals are intermediate
hosts (people can be both definitive
and intermediate hosts)

T crassiceps

Foxes, also other canids and
carnivores, including dogs, are definitive hosts; rodents, insectivores, rabbits, occasionally other mammals
are intem1ediate hosts

Diphyllobotlu·iasis

Diphyllobothrium lcitum Dogs, bears, seals, sea lions, gulls, (Fish tapeworm

(Dibothriocephalus
and other fish-eating mammals and
infection)

latus), D nihonkaiense,
birds are definitive hosts; freshwater

D pacifi,citm, D dendrit'i or marine fish (and copepods) are cum, and other Diphyl
intermediate hosts
lobothrium spp

Dipylidiasis (Dog

Dipylidium caninum

Dogs, cats, wild canids, some other
tapeworm infection)

wild carnivores are definitive hosts;
fleas are intermediate hosts

Echinococcosis

Echinococcus granulo

Dogs, other canids, hyenas are
sus sensu lato
definitive hosts; sheep, goats, cattle,
water buffalo, swine, camels, cervids,
rodents, otl1er manunals, or marsupials are intermediate or aberrant hosts; strains of parasite can be adapted to
different intem1ediate hosts

E muliilocularis

Foxes and other wild canids and felids
are usual definitive hosts, but parasite
can also mature in dogs, cats;
intermediate hosts are usually rodents,
insectivores, some other manunals

E oligarthrus

Wild felids are definitive hosts, can
mature in cats; agouti, pacas, spiny
rats are intem1ediate hosts

Evogeli

Bush dogs are usual definitive host,
can mature in other canids, including
dogs; pacas, agouti, nutria, nonhuman primates, and other mammals can be intermediate hosts

Hyrnenolepiasis

Hyrnenolepis nana ( dwarf People, nonhuman primates, rodents tapeworm); most human
are definitive hosts; insects,
infections probably
including fleas, flour beetles, cereal
transmitted from people,
beetles are intermediate hosts
but zoonoses possible

ZOONOSES

2453

•tM•I• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-CESTODES (TAPEWORMS) (continued) Africa

As above

Most often in subcutaneous tissues

(skin swelling) or eye, also CNS

Worldwide where

Ingestion of eggs

Inflammation in CNS caused by death
swine are reared;

(including autoinfection of small larva or growth to large size most cases seen in
from adult parasite in

( often years after infection); can cause

Africa, Asia, Central human intestine)

seizures, other CNS signs; less often in
and South America
eye or heart; massive numbers in
muscles can also be symptomatic

North America,

Ingestion of eggs

Tissue invasion (mainly subcutane

Europe, Asia, and
ous, muscle), ocular; one paraverteother areas where bral pseudohematoma with local
foxes are present
bleeding, one CNS larva; many but
not all cases in irnmunocompromised

Worldwide;

Ingestion of undercooked Usually asymptomatic; may cause distribution of
infected fish
mild abdominal distress, diarrhea
species varies

( chronic relapsing diarrhea possible
in some cases)

Worldwide;

Ingestion of dog or cat

Usually in children; asymptomatic or
uncommonly
fleas
mild abdominal distress, diarrhea;
reported in people
proglottids in feces resemble
cucumber seeds

Worldwide, strains

Ingestion of tapeworm

Cause space-occupying lesions of
differ in distribution eggs in food or water, to
organs, especially lung, liver, also
mouth on hands; eggs
other organs, rarely CNS; cyst grows
stick to fur and hands
slowly, can cause death if untreated;
rupture can cause allergic reactions,
dissemination of cysts

North America

Ingestion of tapewonn

Usually involves liver with mass

(mainly Canada to
eggs in food or water, to
lesions, occasionally lung or CNS;
north central USA), mouth on hands; eggs
primary lesion can metastasize to
northern and central stick to fur and hands
many organs; without treatment,

Eurasia

70%--100% cases are fatal

Central and South

Ingestion of tapeworm

Has been seen in a variety of internal

America; rare in
eggs in food or water, to
organs,eyes
people
mouth on hands; eggs
stick to fur and hands

Central and South

Ingestion of tapeworm

Usually involves liver, may invade

America
eggs in food or water, to
adjacent tissues; mortality high in
mouth on hands; eggs
advanced cases, even with treatment
stick to fur and hands

(22% in one study)

Worldwide

Accidental ingestion of

Mainly in children; mild abdominal
tapeworm eggs or
distress, decreased appetite,
infected insects;
irritability are most common; weight
autoinfection possible
loss, flatulence, diarrhea possible

(continued)

2454

ZOONOSES

•M=if ii GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-CESTODES (TAPEWORMS) (continued) Hymenolepiasis

H diminuta (mouse

Rats, mice are definitive hosts;

(continued)

tapeworm, rat tapeworm) insects, including fleas and cereal beetles are intem1ediate hosts

Inermicapsifer

Inermicapsifer spp

Rodents, people are definitive hosts
infection
in Africa; people may be exclusive
host outside Africa

Raillietina infection R celebensis, R demer

Rodents, nonhuman prin1ates are
ariensis; most Railli
definitive hosts for R celebensis,
etina spp have not been R demerariensis; other species in reported in people
birds, man1111als; arthropods,
including ants, are intermediate
hosts

Sparganosis

Spirometra spp

Dogs, cats, wild canids and felids are

(pseudophyllidean
definitive hosts; copepods are first
tapeworms, second
intem1ediate host; fish, frogs, reptiles
larval stage)

are second intermediate hosts;
primates, pigs, weasels, rodents,
insectivores, other man1mals, birds
are paratenic hosts

Taeniasis

-Asian taeniasis

Taenia asiatica (also

Domestic and wild pigs, occasionally
called T taiwanensis,
cattle, goats, monkeys are intem1edi

T saginata asiatica
ate hosts; people are definitive hosts

-Beef tapeworm

T saginata

Cattle, water buffalo, llamas,
disease
reindeer, camels, other domestic and
wild ruminants are intermediate
hosts; people are definitive host

-Pork tapeworm

T solium

People are definitive host; swine,
disease; cysticerco-
occasionally other mammals,
sis and neurocysti-
including people, are intermediate
cercosis
hosts

PARASITIC DISEASES-NEMATODES (ROUNDWORMS)

Angiostrongyliasis

Angiostrongylus

Cotton rats and other rodents are
coslmicensis, also called definitive hosts; slugs are intermedi

Parastrongylus
ate hosts
costaricensis

ZOONOSES

2455

IM=i!ii GLOBAL ZOONOSEsa (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-CES TODES (TAPEWORMS) (continued) Worldwide

Ingestion of infected

Mild abdominal symptoms of short
insects in food
duration

Africa, southeast

Probably ingestion of

Mild abdominal symptoms, if any

Asia, tropical
infected arthropods

America

R demerariensis in Probably ingestion of

Vague discomfort, many cases
tropical America
infected arthropods in
asymptomatic; gastroenteritis,

(human cases mainly food
possibly other signs; mainly in

Ecuador, Cuba,
children

Guyana, Honduras);

R celebensis in Asia,

Australia, Africa

Worldwide; human

Ingestion of infected

Nodular, itchy skin lesions that can
cases most common cyclops (in water) or
migrate; conjunctiva! and eyelid
in Asia
undercooked intermedilesions; mticaria, painful edema; ate or paratenic host;
other organ involvement, including
application of contami

CNS, eye
nated tissues to skin ( eg,
as poultice)

Asia

Ingestion of undercooked Vague abdominal complaints and animal products, usually proglottid passage; anal pruritus; visceral organs such as
possible that ingestion of eggs may
liver and lung
be followed by larval migration and
disseminated disease (uncertain/
controversial)

Worldwide

Ingestion of undercooked Mild abdominal discomfort and meat containing larvae
proglottid passage; gravid proglottids
may travel to ectopic sites and cause
symptoms; eggs do not cause
disseminated disease

Worldwide where

Ingestion of undercooked Adult stage in intestine (taeniasis) swine are reared;
pork containing larvae
mild or asymptomatic; cysticercosis
most cases seen in
causes taeniasis;
usually asymptomatic for years until

Africa, Asia, Central ingestion of eggs
cysticercus becomes large or death
and South America

(including autoinfection of small cysticerci result in inflammafrom adult wonn in tion in CNS (seizures, other CNS
intestine) causes
signs) or infrequently in eye or heart;
cysticercosis
massive numbers in muscles can also
be symptomatic

PARASITIC DISEASES-NEMATODES (ROUNDWORMS)

Mainly in Central

Accidental ingestion of

Acute abdominal angiostrongyliasis;
and South America, slugs or possibly plants
severe pain resembles appendicitis,

Caribbean parasite
contaminated by their
especially in children; rarely, more
has also been
secretions
insidious disease with liver
reported in North
involvement; complications can

America
include intestinal ischemia,
perforation; fatalities possible

(continued)

2456

ZOONOSES

•#N•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) Angiostrongyliasis

Angiostrnngylus

Rodents (rats, includingRattus and

(continued)

cantonensis, also called Bandico/,a spp) a.re defmitive hosts; Paras trongylus
snails, slugs are intermediate hosts;
canlonensis
land planarians, crustaceans ( crabs,
shrin1p, prawns), an1phibians, fish,
reptiles are para.tenic hosts

Anisakiasis

Anisakis, Pseudoter

Marine man1mals ( cetaceans and
ranova, and Contra
pinnipeds) and fish-eating birds are
caeciim spp
definitive hosts; fish, crustaceans,
and cephalopod mollusks are
intermediate or paratenic hosts

Ascariasis

Ascaris suum; poten

Pigs, also reported occasionally in
tially zoonotic ( controother mammals, including nonhuman versial)

primates, sheep, cattle

Cap illariasis

-Hepatic

Capillaria hepatica

Rodents major host, also in many
capillariasis

(also called Calodium
other wild and domestic manunals
hepaticum)

-Intestinal

C philippinensis (also

Aquatic birds, people can be
capillariasis
called Pamcapillaria
definitive hosts; freshwater fish
philippinensis)

are intermediate host

-Pulmonary

C aerophila (also called Dogs, cats, other carnivores capillariasis

Eucoleus aerophilus)

Dioctophymosis

Dioctophyma renale

Mink, dogs, and other carnivores

(Giant kidney worm
are definitive hosts; annelids are
infection)

intermediate hosts; frogs, fish are
pa.ratenic hosts

Dra.cunculiasis

Dracunculus medinen

People, nonhwnan primates are

(Guinea worm
sis; people are most
definitive hosts; infections have also
infection)

important host but
been reported in animals, but parasite
possible role for zoonotic identification sometimes W1certa.in; transmission in some
domestic animals not thought to
locations
maintain parasite but possible
exceptions ( eg, dogs in Chad);
copepods are intermediate hosts

Fila.riasis

-Dirofilariasis

Dirofuaria immilis

Dogs, cats, other mammals
especially carnivores, mustelids,
primates are definitive hosts (mainly
patent in dogs and wild canids );
mosquitoes are intermediate hosts

ZOONOSES

2457

•t}i•j• GLOBAL ZOONOSES• (conti.nued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) Originated in Asia,

Ingestion of raw/

Eosinophilic meningitis or meninspread to many other w1dercooked inte1mediate goencephalitis, spinal cord involveregions, mainly or paratenic host ( or
ment; ocular involvement with
tropics, including
accidental ingestion on
decreased vision; transient abdomi

Americas, Caribvegetables); possibly inges nal pain, prw-itus in some; most cases bean, Middle East,
tion of plants contamirelatively mild and self-limiting, but Australia
nated by secretions of
some fatal
intem1ediate host

Worldwide but many Ingestion of undercooked Gastroenteritis with upper quadrant cases in northern
marine fish, squid,
pain; parasite usually in stomach;

Asia and western
octopus
small-intestinal infections unusual

Ew-ope
but can occw-; colon, esophagus
rarely involved; oropharyngeal worm
can cause hematemesis, cough;
urticaria and other allergic signs
after ingestion of live or dead worn1s

Worldwide,

Ingestion of eggs from

Visceral larva migrans (respiratory
prevalence varies
environment (shed in
signs, fever during larval migration);
feces)

GI signs

Worldwide in

Ingestion of embryonated Acute or subacute hepatitis with scattered foci
eggs in soil
marked eosinophilia; subclinical
to fatal

Philippines, Thailand, Ingestion of undercooked Enteropathy with protein loss and also reported
infected fish
malabsorption; diarrhea, abdominal
occasionally in other
pain; weight loss can be severe; death
parts of Asia, Middle
possible

East,Cuba

Worldwide; rare in

Accidental ingestion of

Fever, cough, bronchospasm,
people
infective eggs in soil or
bronchitis, dyspnea; can mimic
contaminated food
bronchial carcinoma

Worldwide; rare in

Ingestion of infected fish, Renal colic, hematuria, pyuria, people
frog, or annelid
ureteral obstruction, various kidney
complications can be fatal; subcutaneous nodule

Asia (mainly Indian Ingestion of infected

No symptoms until just before
subcontinent) and
cyclops in water
laiviposition ( -1 Y1); papule to

Africa
vesicular skin lesion to ulcer that
opens in water to reveal wmm;
allergic reaction common at this
time, and secondary infection may
occur

Worldwide

Bite of infected mosqui

Fever, cough acutely, larvae result in
toes
infarr:t or coin lesion in the lungs;
often asY1nptomatic; rarely involves
eye or other body sites

(continued)

2458

ZOONOSES

•4N•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) Dirofilariasis

D tenuis, D repens, rarely D teniiis in raccoons; D repens (continued)

other species
mainly patent in dogs and some wild
canids ( eg, foxes); also infects cats
but not usually patent

-Malayan filariasis

Brngia malayi;

Cats, wild felids, pangolins, other
subperiodic form is
carnivores, nonhuman primates
of uncertain origin,
susceptible
thought to be zoonotic
or maintained in both
animals and people;
periodic form is
exclusive to people

Filariasis caused by Brugia spp other than Various domestic and wild manm1als,
other Brugia species B malayi, including including dogs and cats, are

B pahangi
definitive hosts

Gnathostomiasis

Gnathostoma spini

Dogs, cats, wild carnivores are
gerum, G binucleatum,
definitive hosts (G doloresi and
and some other

G hispidum in pigs and wild boars);

Gnathostoma spp
copepods, freshwater fish, eels,
frogs, snakes, chickens, snails, pigs
are intermediate or paratenic hosts

Gongylonemiasis

Gongylonema pulchrum Rwninants, domestic and wild swine, other mammals, birds are definitive
hosts; coprophagous insects ( eg,
beetles, cockroaches) are intermediate
hosts

Larva migrans,

Ancylostoma brazil

Cats, dogs, wild carnivores are
cutaneous (see also iense, A caninum,
definitive hosts

GNATl·IOSTOMIASIS,

A ceylan'iciim, Unci
above)

naria stenocephala

Bunostomum phleboto

Cattle
rnum

Strongyloides stercoralis S stercoralis in dogs, cats, primates, and other Strongyloides including people; other species in spp found in animals
swine, sheep, goats, cattle, horses,
raccoons, and otl1er domestic and
wild mammals

ZOONOSES

2459

•hi=i!i• GLOBAL ZOONOSES• (contin,,ed)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) VetBooks.ir

D tenuis in North

Bite of infected mosqui

Subcutaneous nodule or submucosal

America; D repens in toes
swelling, some migratory and/or

Asia, Europe, Africa
painful; subconjunctival (rarely
intraocular); internal location

(mainly lung but also brain, other
organs) possible

Asia; subperiodic

Bite of infected mosqui

Lymphatic filariasis: recurrent
fom1 limited to
toes, Mansonia spp
painful lyrnphadenitis, lymphangitis,
peninsular Malaysia,
mainly associated with
often preceded by prodromal illness

Thailand, and parts of subperiodic fonn
with malaise or urticaria; may

Indonesia, Vietnam,
progress to elephantiasis, usually of
and the Philippines in
legs; hypersensitivity syndrome with
swamp-forest
cough, chest pain, asthmatic attacks
environments
especially at night

Asia, Africa,

Mosquitoes

Occasional zoonotic infections ( eg,

Americas
cutaneous nodules, granuloma in
lymph nodes)

Worldwide; most

Ingestion of undercooked Fever, malaise, gastroenteritis, human cases from
fish, poultry, or other
wticaria, soon after ingestion;

Asia; emerging along intermediate or paratenic migratory skin lesions (intermittent Pacific coast of
host, drinking water
swelling, often painful or pruritic, or

Mexico, Ecuador,
contaminated with
linear erythernatous lesions) after

Peru, Argentina
copepods containing
weeks to years; may involve viscera,
larvae; handling meat
eye, or CNS; CNS involvement can be
that contains larvae
fatal or result in pennanent damage
with reported case fatality rates of

7%-25%

Worldwide; rare in

Ingestion of infected

Movement of parasite in sub mucosa
people
beetles, probably on
of mouth is sensed; local irritation;
vegetables; possible
pharyngitis, stornatitis possible
inhalation of small beetles

Worldwide;

Contact with infective

Itchy, serpiginous, migrating skin
distribution varies
larvae that penetrate
lesions; papules, nonspecific dermatiwith the species skin, usually via soil
tis, vesicles; wheezing, cough, and
urticaria may occur; myositis or
ocular lesions possible; eosinophilic
enteritis after ingestion of A
caninum; A ceylanicum can also
become patent in intestine, causing

GI signs, anemia

Temperate regions

As above

As above

Worldwide, more

Contact with infective

Larva currens (linear, serpiginous
common in tropics
larvae that penetrate
urticaria! inflammation, often rapidly
and subtropics
skin, from soil or direct
progressive); S stercoralis may also
contact with feces;
mature in intestine, causing enteritis
autoinfcction possible
and other signs (see below)

with S stercoralis

( conlin1led)

2460

ZOONOSES
ltM•il GLOBAL ZOONOSEsa (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) Larva rnigrans,

Toxocara canis, Tcati,

Dogs and wild canids (T canis ), cats
visceral ( see also
possibly others
and wild felids (T cati) are definitive

ANGJOSTRONGYL!ASIS,
hosts; many species can be paratenic
p 2454, and ANISAKIASIS,
hosts
p 2456)

Baylisascaris procyonis, Raccoons, kinkajous are definitive possibly other species of hosts; dogs can be definitive or Bayliscascaris
intermediate host; many man1mals

(including people), marsupials, and
birds are inte,mediate or paratenic
hosts

Oesophagostomia

Oesophagost,omum spp, Primates, including people sis, Ternidensiasis

Ternidens d eminutus;
zoonotic potential may
vary with parasite
species/strain and
geographic area

Onchocercosis

Onchocerca gutturosa,

Definitive hosts include cattle,

O cervicalis, 0 jakutensis, horses, cervids, wild boars, dogs and O dewitteijaponica, 0
other canids, camels, other species
reticulata, 0 lupi, others

Strongyloidiasis

Strnngyloides sterco

S stercoralis in dogs, cats, foxes,
ralis; most human
primates, including people
infections thought to be
from strains adapted to

. people; frequency of
maturation of canine

S stercoralis in people
undetennined, thought to
be rai;:e

Sfuelleborni

Primates, including people

Thelaziasis

Thelazia callipaedia,

Definitive hosts are dogs and other

(Eyeworms)

T californiensis,
canids, cats (Tcallipaedia); dogs,
possibly Trhodesii
wild manunals, occasionally cats

(T californiensis ); flies are
intermediate hosts

Trichinosis

Trichinella spiralis and Main reservoir may be wild carni

(Trichinellosis)

subspecies, Tnativa,
vores (foxes, badgers, wolves, lynx),

T britovi, T nelsoni,
omnivores (bears, boars); also in any

Tpseudospiralis,
mammal that eats ( or is fed) meat,
possibly others
including domestic swine, rodents,
cats, clogs, horses, marine mammals;
also birds (Tpseudospiralis); T
zimbabwensis ( zoonotic potential
unknown) can infect reptiles

ZOONOSES

2461

•ih•i• GLOBAL ZOONOSESa (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) Worldwide

Ingestion of embryonated Fever, wheezing cough, upper abdomieggs shed in feces of dogs nal discomfort; other symptoms, incluand cats; via soil, water, ding neurologic signs, skin rashes also
food, fomites
possible; may wax and wane for
months; eye involvement ( ocular
migrans) may resemble retinoblastoma

North America,

Accidental ingestion of

Nonspecific signs, including fever,

Europe, Japan
embryonated eggs in soil, lethargy; hepatomegaly, pneun10niwater, or fecal-contan1itis, parasitic meningoencephalitis nated material

(may be fatal in infants, young
children), ocular disease; other
syndromes, including cardiac disease

Parasites found in

Ingestion of infective

Abdominal pain and one or more

Africa, Asia, South
larvae in soil, often in
masses± mild fever; intestinal

America; human
food or water
obstruction or abscessation possible;
cases mainly
multinodular form (less common)

reported in Af1ica
with abdominal pain, persistent
diarrhea, weight loss; rarely ectopic
in omen tum, liver, or skin

Distribution varies

Probably transmitted by Ocular disease, subcutaneous with species
black flies (Diptera:

nodules

Simuliidae), possibly
other vectors

S stercoralis

Contact with infective

Frequently asymptomatic in healthy;
worldwide; more
larvae that penetrate
possible larva currens (see LARVA
common in tropical skin, in soil or direct

MIG RANS, p 2458); respiratory signs in
and subtropical
contact with feces;
some (cough to bronchopneumonia),
climates
autoinfection possible
especially in elderly, immunocom-.

promised; abdominal pain, diarrhea,
sometimes with periodic urticaria! or
maculopapular rash; disseminated
strongyloidiasis, neurologic
complications, septicemia, and death
may occur in immunocompromised

Africa, Asia, and in

As above

Associated with abdominal pain,
captive prin1ates in
occasional diarrhea, not well studied
other areas

T callipaedia in Asia, Flies release parasite Cortjunctivitis; corneal scarring,

Europe; T californ
larvae on cortjunctiva
opacity in chronic cases
iensis in North

America ( western

USA); rarely in people

Worldwide,

Ingestion of undercooked Gastroenteritis in some; followed by especially in
pork, horse meat, game,
fever, headache, severe rnyalgia,
temperate regions;
and other tissues
facial swelling ( especially eyelids);
some species are
containing viable cysts
ocular pain, rashes, or pruritus
limited in their
possible; pneumonitis, CNS, or
distribution
myocardial involvement can occur;
inapparent to fatal

(continued)

2462

ZOONOSES

IM=iiii GLOBAL ZOONOSEsa (contin'Ued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) Trichostrongyliasis

Trichostrongylus spp

Cattle, sheep, other domestic and
wild ruminants, sometimes other
mammals

Trichuriasis

Trichuris suis, possibly

T vulpis in canids; T suis in domestic (Whipworm

T mtlpis and other species; and wild swine infection)

main species in people is

T trichiura, but zoonotic
infections are unusual

PARASITIC DISEASES-ACANTHOCEPHALANS

Acanthocephaliasis, ]J,facracanthorhynchus

Hosts vary with parasite species;

Macracanthorhyn
hirudinaceus and other definitive hosts include domestic and chosis
species
wild pigs, rodents, muskrats, arctic
foxes, dogs, sea otters, other terrestrial
and marine manunals; intennediate
hosts are beetles, cockroaches,
crustaceans; fish are paratenic hosts

PARASITIC DISEASES-ANNELIDS (LEECHES)

Hirudiniasis

Limnatis nilotica and

Cattle, buffalo, other domestic and

(internal)

other aquatic leeches
wild mammals, probably frogs

ARTHROPOD DISEASES

Acariasis (Mange)

Mites of Sarcoptes,

Mammals and birds

Cheyletiella, Dermanys-
sus, and Ornitlwnyssus
spp, Notoedres cati,

Trixacarus caviae,

Liponyssoides san-
guineus; possibly others

(uncommon)

Myiasis

Cochliomyia hominivo-

Manunals; rare in birds
rax and Clnysomya
bezziana (screwworms)

Cordylobia anthro

Mammals, often found in dogs,
pophaga, rarely
rodents

C rodhaini (Tumbu flies)

ZOONOSES

2463

•§:iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

PARASITIC DISEASES-NEMATODES (ROUNDWORMS) (continued) VetBooks.ir

Worldwide

Ingestion of infective

Asymptomatic or mild
larvae on vegetables or in gastroenteritis
contaminated water, soil

Worldwide,

Ingestion of embryonated T suis can colonize people, who especially warm,
eggs on plant foods,
develop GI signs; rare larva migrans
humid climates
water, or in soil
or intestinal infections suggested
from T vulpis (controversial
identification)

PARASITIC DISEASES-ACANTHOCEPHALANS

Worldwide

Ingestion of infected

Gastroenteritis, may lead to gut
beetles, other intermediperforation or intestinal obstruction; ate hosts, or fish
some cases asymptomatic

PARASITIC DISEASES-ANNELIDS (LEECHES)

Africa, Asia,

Drinking unfiltered water Attaches to nasopharynx, pharynx, southern Ew-ope,

(leech enters nares or
esophagus, occasionally deeper in

Middle East
mouth), wading in deep
respiratory tract, or in genitoUiinaiy
water ( enters genitouritract; pressme and/or pain at naiy tract)

attachment site; bleeding ( eg,
hemoptysis, hematemesis, epistaxis,
vaginal bleeding), anemia ( can be
severe); other signs depend on location

ARTHROPOD DISEASES

Worldwide

Contact with infected

Itchy skin lesions
animals, fomites

C hominivorax in

Flies lay eggs on host,

Painful, pruritic, foul-smelling,

South America,
larvae enter wounds (as
enlarging dem1al and subdem1al

Caribbean; C bez
small as a tick bite),
woU11ds or nodules, often with serosan
ziana in Asia, Africa, mucous membranes
guineous discharge; some infestations

Middle East
in cavities, including nasal cavity; larvae
can invade living tissue, locally destructive (including bone, eye, sinuses, or cranial cavity); can be fatal if U11treated

Africa, Middle East; Larvae from environment Furuncular swelling at site of also reported in
invade unbroken skin
invasion, often feet; fever, malaise,

Mediterranean
focal lymphadenopathy possible
region ofEmope

( continued)

2464

ZOONOSES

•M=i!i• GLOBAL ZOONOSESa(conlinued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

ARTHROPOD DISEASES (continued)

Myiasis

Cuterebra spp

Rodents, lagomorphs, occasionally

(continued)

other mammals

Dermatobia hominis

Man1mals, some birds

(hwnan botfly)

Gasterophilus spp

Equids, occasionally other mammals

(equine botfly)

Hypoderma lineatum,

H bovis and H lineatum in cattle,

H bovis (warbles), and
sometimes other man1mals; other
other Hypoderma spp
species primarily parasites of deer,
caribou, or yaks

Oestrus ovis, Rhino

O ovis mainly in sheep, goats, also
estrus purpiireus
other mammals; R purpureus mainly
in equids

Wohifahrtia spp,

W vigil in rabbits, rodents, mink,

Woh/fahrtia vigil,
foxes, dogs, and other carnivores,

W magnijica
other manm1als; W magnijica in
sheep, cattle, dogs, other mammals,
some birds, especially geese

Pentastomid

Armillifer spp (tongue

Definitive hosts are snakes;
infections
worms)

intennediate hosts are rodents and
other wild animals

ZOONOSES

2465

•§:iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

ARTHROPOD DISEASES (continued)

North America

Larvae from vegetation

Subcutaneous fmunculoid nodule(s);
enter host in natural
creeping skin eruption (w1common);
cavities or invade intact
ocular lesions; rarely larvae might be
skin
found in upper respirato1y tract

South and Central

Eggs carried by other

Nonmigratory larvae in furuncles;

America, Mexico
insects (cg, mosquitoes); episodes of pain, intense pruritus, larvae hatch and
sometimes with lymphangitis or
penetrate skin of
lymphadenitis; can invade eyelids,
mammalian host when
eye sockets, mouth, especially in
insect lands
children

Worldwide

Accidental exposure to

Serpiginous, pruritic red stripes on
larvae
skin resembling cutaneous laiva
migrans; very rai·ely might reach
stomach (nausea, vomiting)

North America,

Eggs laid on host, larvae Usually subcutaneous (slowly Europe, Asia;
invade skin
moving furuncles that can appear
species distribution
and disappear) or similar to
varies
cutaneous larva migrans; endophthalmia uncommon; H lineatum may also cause an eosinophilic syndrome
with fever, muscle pain, sometimes
respiratory, cardiac, or neurologic
signs

O ovis worldwide,

Larvae are deposited in

Conjunctiva! form, with lacrimausually in warmer
nares, conjunctiva,
tion and sensation of irritating
climates; R pur
occasionally lips/mouth
foreign body in eye, ocular
pureus in Asia,
by adult fly
destruction rare; nasal form with

Africa, Emope
localized pain or pruritus,
congestion, headache; also
reported in pharynx (inflammation,
vomiting, dysphagia), rarely ear;
usually self-limiting (except inside
eye), because larvae cannot
develop beyond first stage in
people

W vigil in North

Laivae deposited on host W vigil causes subcutaneous America; W mag
or nearby, penetrate
abscesses, furuncles; W magnifica
nijica in Europe
lesions (both agents) or
has been reported from skin, eye,

(mainly Mediterraintact skin (W vigil) and vulva, ear, orotracheal region nean), north Africa, natural orifices

Asia

Africa, Asia

Ingestion, via water or

Usually asymptomatic; large
vegetables contaminated nwnbers of parasites can cause with eggs (from feces or
multifocal abscesses, masses, or
saliva of snakes);
obstruction of ducts in internal
undercooked snake
organs; symptoms vaiy with location;
meat; contan1inated
death rare
hands, fomites after
handling snake meat

( continued)

2466

ZOONOSES

•tliii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

ARTHROPOD DISEASES (continued)

Pentastomid

Linguatula serrata

Definitive hosts are dogs and other
infections
canids, felids; intermediate hosts are

(continued)

herbivores ( especially sheep, goats,
lagomorphs) and people

Tick paralysis

More than 40 species

Various animals carry ticks

(seep 1314)

of ticks are capable of
causing this disease;

Dermacentor a:nde,·soni,

D varia.bilis most
common in North

America

Tunga infections

Tung a penetra,ns ( sand

People, dogs, pigs, other mammals
fleas, jiggers)

VIRAL DISEASES

Alkhurma virus

Alkhurma virus (family

Sheep, goats, camels
infection

Flaviviirdae, genus

Flavivirns ); may be a
variant or strain of

Kyasanur Forest virus

Barmah Forest virus Barmqh Forest virus

Natural hosts unknown; horses,
infection; epidemic

(family Togaviridae,
brushtail possums may be hosts
polyarthritis
genus Alphaviros)

Buffalopox virus

Vaccinia virus, Buffalo

Water buffalo, cattle
infection
pox virus strain (family

Poxviridae, genus

Orthopoxvints)

California encephali California encephalitis

Many wild and domestic man1.111als
tis virus serogroup
virus serogroup (family

(California

Bunyaviridae, genus
serogroup)

Orthobunyaviros );
infections
includes California, La

Crosse, Tahyna, Inkoo,

Jamestown Canyon,

Morro Bay, Snowshoe
hare, Guaroa, Lun1bo,

Chatanga, and other
viruses

ZOONOSES

2467

•M=iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

ARTHROPOD DISEASES (continued)

Worldwide

Ingestion of water or

Ingestion of eggs-usually asymptovegetables contaminated matic; ocular or pulmonary signs, with eggs (from feces,
abdominal pain, icterus, and other
saliva, or nasal discharge symptoms possible from invasion of of definitive host);
internal organs
ingestion of larvae in

Ingestion of larvae-throat irritation,
undercooked liver or
pain; edema, congestion of nasopharlymph nodes from
ynx may cause dyspnea, difficulty
intermediate hosts
swallowing; most severe cases are
probably in people who have been
sensitized

Worldwide

Tick attachment

Ascending flaccid paralysis, may be
preceded by prodromal flu-like
illness (malaise, weakness); can
cause respiratory paralysis, also
paresthesia; ends when tick is
removed

Africa, Central and

Skin contact with

Penetration of skin and burrowing

South America,
contaminated soil
result in pain and itching around

Caribbean, south
discrete sores, often on feet; may be

Asia
secondarily infected

VIRAL DISEASES

Middle East, mainly Ticks (Omithodoros and Febrile illness, often with GI signs reported in Saudi

Hyalomma spp ); direct

(eg, vomiting, abdominal pain);

Arabia, also Egypt
contact with animal meat encephalitic/neurologic and via broken skin or
hemorrhagic signs in some; case
ingestion of unpasteurfatality up to 25% in early reports, ized camel milk linked to recently <l %
some cases

Australia

Mosquito bites; Culex

Resembles disease caused by Ross
annulirostris and Aedes River virus (seep 24 78) but seems to spp implicated
persist longterm in fewer patients,
rash more common

Indian subcontinent Skin contact with

Pox skin lesions mainly on hands,

(south Asia), Egypt, infected anin1als, often
face, legs, buttocks; occasionally

Indonesia
when milking
lymphadenopathy, fever, malaise

North and South

Mosquito bites

Syndromes, severity vary with the

America, Europe,
virus; flu-like illness, meningitis, or

Africa, Asia; possibly
encephalitis common with North
worldwide;

American viruses
distribution of each
virus varies

(continued)

2468

ZOONOSES
irN•il GLOBAL ZOONOSES· (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

VIRAL DISEASES (continued)

-La Crosse

La Crosse virus (Califor

Chipmunks, squirrels are major
encephalitis
nia encephalitis virus
amplifying hosts; rabbits, foxes, and
serogroup)

other mammals can be infected

-Tahyna fever

Tahyna virus (California Hares, rabbits, rodents, hedgehogs, encephalitis virus
and other mammals
serogroup)

Camel pox

Camelpox virus

Old World camelids, possibly other
species

Chikungunya virus

Chikungunya virus

Sylvatic cycle in nonhuman primates,
infection

(family Togaviridae,
possibly rodents in Africa; virus
genus Alphavirus)

thought to be maintained in people in

Asia, but sylvatic cycle may also exist

Colorado tick fever

Colorado tick fever virus Rodents; also found in porcupines, (family Reoviridae, genus lagomorphs, deer, elk, and other Coltivurus; Salmon River mammals
virus and California hare
col ti virus may be variants

Contagious ecthyrna Orf vi.J.us (family

Sheep, goats, camelids, reindeer,

(Orf, seep 866)

Poxvi.J.·idae, genus
wild ungulates; rare cases in dogs

Parapo:rvirus)

Cowpox (seep 868) Cowpox virus (family

Rodents are usual rese1voir host;

Poxviridae, genus
also in domestic and wild cats,

Orthopoxvirus)

occasionally cattle, other mammals

ZOONOSES

2469

•§:iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

VIRAL DISEASES (continued)

North America

Mosquito bites

Many cases mild and flu-like;
meningitis or encephalitis with
seizures, paralysis, and focal
neurologic signs possible; most cases
in children; estimated case fatality
rate < 1 % in cases with encephalitis

Europe, Asia, Africa Mosquito bites ( culicine Influenza-like illness, sometimes and anopheles)

including GI signs; arthritis or
respiratory signs, including bronchopneUJnonia in some; meningitis possible; most often in children; does
not appear to cause fatal disease

Middle East, Asia,

Direct contact

Skin lesions similar to cowpox,

Africa, possibly
variola virus infections
other areas;hUJnan
cases recently
described in India in
can1el handlers, rare
unconfirmed cases
suggested in other
locations

Asia, Africa

Mosquito bites ( espe

Febrile illness, may have rash and/or
cially Aedes spp)

GI signs; arthralgia, especially in
small joints, and myalgia prominent,
may persist for months; myocarditis,
neurologic signs, hemorrhages
reported in a few cases

Rocky Mountain

Tick bites (primary

Nonspecific febrile illness; pharynregion of N01th
vector is Dermacentor
gitis, rash, or GI signs possible;

America
andersoni)

biphasic or triphasic in some;
complications ( eg, neurologic signs,
hemorrhages, pericarditis, myocarditis, orchitis) uncommon but can occur in severe cases; deaths rare

Worldwide

Occupational exposure

Papule(s) that un1bilicate and ulcerate,
via contact with broken
usually on hands; dissemination rare;
skin (both live animals
large lesions refractory to treatment
and meat processing)

can be seen in inununosuppressed

Parts of Europe and Contact exposure via

Papules, vesicles that become

Asia
broken skin, bites,
pustular, to ulcerative nodules, scars;
scratches
single or multiple lesions, often on
hands; regional adenopathy and
malaise, flu-like symptoms in some;
lesions remain localized in healthy
people; more extensive or generalized disease may be seen in children, people with eczema, immunocompromised; severe cases can involve respiratory mucosa; rare fatal cases

( eg, complications of encephalitis)

( continued)

2470

ZOONOSES

•tth•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VIRAL DISEASES (continued)

VetBooks.ir

Crimean-Congo

Crimean-Congo

Cattle, rodents, sheep, goats, hares,
hemorrhagic fever
hemorrhagic fever virns
other manunals, some birds

(seep 751)

(family Bunyaviridae,
genus Nairovirus)

Eastern equine

Eastern equine encepha

Birds are principal reservoir hosts in
encephalomyelitis
lomyelitis virus (family

North An1erica, snakes might have

(seep 1291)

Togaviridae, genus
role in overwintering virus; rodents,

Alphavirus); North
marsupials might be reservoir hosts

American lineage 1
in South America; clinical cases seen
strains more virulent
in equids and occasionally other
than South American
mammals and birds; mammals are
lineages
almost always dead-end hosts

Ebola hemorrhagic

Zaire ebolavirns, Sudan

Bats are reservoir hosts for Zaire
fever
ebolavirus, Ivory Coast
ebolavirus and suspected reservoir
ebolavirns, Bundibugyo
hosts for others; primates, duikers,
ebolavirus (family Filovir possibly other mammals can be idae, genus Ebolavirus ); infected

Reston ebolavirus does
not seem to affect people

Encephalomyo

Encephalomyocarditis

Rodents may be reservoir hosts;
carditis
virns (fan1ily Picornaviri also in swine, nonhuman prin1ates, dae, genus Cardiovirus); elephants, other mammals, and wild thought to be zoonotic
birds

Foot-and-mouth

Foot-and-mouth disease Cattle, swine, sheep, goats, other disease (seep 629)

virns (family Picornaviri cloven-hoofed animals (Artiodacdae, genusAphthovirus, tyla), a few mammals in other orders types 1'., 0, C, SAT 1, SAT

2, SAT 3, and Asia 1)

Hantaviral diseases

-Hantaviral

Sin Nornbre, Black Creek Rodents; each virns tends to be pulmonary

Canal, Bayou, Andes,
associated with a single reservoir
syndrome

Bennejo, Choclo,
host

Araraquara, Juquitiba,

Laguna Negra, and Castelo
dos Sonhosviruses, others

(family Bunyavilidae,
genus Hantavirus)

-Hemorrhagic fever Hantaan virns, Dobrava

Rodents; each virus tends to be
with renal syndrome virus, Puun1ala virus,
associated with a single reservoir

Seoul virus, Saaremaa
host, but Seoul virus is carried by
virus, others (family
both Rattus norvegiC'us and R rattus

Bunyaviridae, genus

Ha,nta,virus)

ZOONOSES

2471

•M=iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VIRAL DISEASES (continued)

VetBooks.ir

Africa, Middle East, Tick bites, especially

Fever, headache, pharyngitis, abdomcentral Asia,

Hyalomma but also
inal symptoms, petechial rash,
southeastern

Rhipicephalus, Derma
hemorrhage, hepatitis, other organ

Europe;appears to
centor, other species; skin involvement in some cases; very be spreading
contact with animal or
severe in pregnant women; case
human blood or tissues or fatality rate 3o/er--50%, varies with crushed ticks; ingestion of region
unpasteurized milk

Western hemisphere Mosquito bites; Culiseta Nonspecific febrile illness may be melaniira important in
followed by severe encephalitis,
maintenance cycle in
especially with North American
birds in North America;
lineage; neurologic sequelae
various mosquito species common after encephalitis; case (Aedes, Coquillettidia,
fatality rate 30o/er--70% with North

Cule:r) can transmit to

American lineage; more severe in
people
infants and elderly

Africa

Contact with infected

Initially nonspecific febrile illness;
tissues ( especially
maculopapular rash with desquan1anonhuman primates and tion; mild to severe bleeding duikers); probable
tendency develops a few days after
transmission from bats in onset; mortality rate 36o/er--90%, varies caves
with isolate

Worldwide in

Uncertain

Nonspecific febrile illness, someanimals
times with GI signs, and/or decreased
reflexes have been reported in adults,
with recovery within several days;

CNS signs, including paralysis, have
been reported in children

Asia, Africa, Middle Contact exposure, often People may become temporary nasal East, South America in laboratories or other
carriers of virus but do not usually
high concentrations of
become ill; mild influenza-like
virus
disease with vesicular lesions occurs
very rarely

North and South

Aerosols from rodent

Prodromal stage with nonspecific

America
excretions and secrefebrile illness; followed by respirations; contact with tory failure, cardiac abnormalities;
broken skin and mucous hemorrhagic signs possible with membranes; rodent bites South American viruses; significant kidney disease uncommon; mortality
rate varies with the virus, but can
reach 400/er-60%

Europe, Asia; Seoul Aerosols from rodent

Prodromal stage with abrupt onset of
virus is worldwide
excretions and secrefever, headache, back pain, sometimes tions; contact with
petechiae, GI signs (maybe severe);
broken skin and mucous followed by hypotension, renal signs to membranes; rodent bites renal failure with oliguria; hemorrhage, other syndromes in some; mortality rate
varies with the virus, from < 1 % (Pmunala
virus) to 100/er--15%(Hantaan virus)

( continued)

2472

ZOONOSES

•M:if j• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

VIRAL DISEASES (continued)

Hendra vims

Hendra virus (family

Fruit bats are normal reservoir host;
infection

Paramyxoviridae, genus horses can be infected

(seep 707)

Henipavirus)

HepatitisE

Hepatitis E virus,

People; animals, including swine,
mammalian isolates
wild boar, deer, rabbits, ferrets, rats,

(fan1ily Hepeviridae,
mongoose, others; swine and
genusHepevi1'u.s);
probably other hosts are rese1voirs
genotypes 3 and 4 zoofor human infections
notic; genotypes 1 and

2 maintained in people

Herpes B vims

Cercopithecine

Can·ied in genusMacaca (Old World
disease
herpesvims 1 (McHV,
macaques), with lifelong latency and

Herpesvirus simiae,
potential for periodic shedding after

B virus) (family
infection; other nonhuman primates

Herpesviridae, genus
susceptible; cell cultures

Simpi,exvirus)

lnfl uenza virus
infections

-Avian influenza

Influenza A vims (family Avian influenza viruses in wild and Orthomyxoviridae, genus domestic birds, especially poultry; Influenzavirus A); avian uncommon in mammals influenza viruses; many
severe human cases
linked to Asian lineage

-H5N 1 highly pathogenic
avian influenza (HPAI)

virnses, but other viruses
also cause illness

-Swine influenza

Influe11za A virus (fan1ily Usually in pigs; also turkeys; can Orthomyxoviridae, genus infect mink, ferrets
lnjluenzavi1us A); swine
influenza viruses

Japanese encephali Japanese encephalitis

Swine, wild birds are important
tis (Japanese B
virus (fan1ily Flaviviridae, maintenance hosts; horses ill but encephalitis)

genus Flavivinis)

epidemiologically unimportant in
amplification; other mammals,
reptiles, amphibians may be infected,
usually asymptomatically

Kyasanur Forest

Kyasanur Forest virus

Rodents, shrews, other small
disease

(family Flaviviridae,
mammals might be reservoirs ( uncergenus Flavivirus) tain); affects monkeys; possible
infections in other mammals, birds

ZOONOSES

2473
itM•il GLOBAL ZOONOSEsa (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

VIRAL DISEASES (continued)

Australia

Direct contact with

Respiratory infection, encephalitis
infected animals (all

(including recunent encephalitis);
human cases have been
few cases described but several were
linked with horses) or
fatal
contaminated tissues

Worldwide; human

Fecal-oral spread;

Mild, self-limiting hepatitis to Liver
and zoonotic
consumption of raw or
failure, more severe in pregnancy
genotypes may differ undercooked meat and
and can result in abortion, death of
in prevalence
liver; waterborne,
newborn, premature birth; usually
between areas
contact with animal
acute, but can be chronic in
reservoirs
organ-transplant patients; case
fatality rate <l % to 4% in general
population, up to 200/o in pregnant

Worldwide, can be

Monkey bites and

Influenza-like symptoms; vesicular
common, especially scratches, contamination skin lesions, pain, or itching around in closed groups of
of mucous membranes
wound, followed by severe encephan1acaques;human
with infected saliva,
litis with seizures, paralysis, coma;
cases rare
secretions

85% mortality rate

Worldwide,

Usually by contact with

Avian influenza viruses can cause
distribution of
infected poultry; avian
coajunctivitis, human influenza-like
strains varies
viruses may be shed in
illness, or severe disease with
respiratory secretions
multiorgan dysftmction, death;
and feces
severity of disease varies with
influenza strain

Worldwide

Usually by contact with

Seems to resemble human influenza;
infected animals; swine
severity of disease varies; fatal cases
influenza viruses occur in have been reported uncommonly respiratory secretions

Asia, Australia,

Mosquito bites (Culex

Fever, chills, myalgia, severe

Papua New Guinea, tritaeniorhynchus
headache, GI symptoms; can

Pacific islands from important in maintenance progress to severe encephalitis; Japan to the
cycle, other Culex and
neurologic sequelae very common

Philippines

Aedes spp can transmit); in smvivors of encephalitis; case also through broken skin fatality rate 15%--300/o
or mucous membranes
after direct contact with
infected tissues

India

Tick bites ( especially

Nonspecific febrile illness; course

H aemaphysalis
may be biphasic; hemorrhagic signs
spinigera, also others)

( eg, ecchymoses, purpura, petechiae,

GI bleeding, epistaxis) and/or
neurologic signs possible in second
stage; prolonged convalescence in
many; case fatality rate -3%

(continued)

2474

ZOONOSES

•h=iii• GLOBAL ZOONOSESa (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

VIRAL DISEASES (continued)

Lassa fever

Lassa virus (family

Wild rodents, usually multiman1mate

Arenaviridae, genus
mouse

Arenavirus)

Louping ill (Ovine

Louping ill virus (family

Sheep, goats, also in llan1as, cattle,
encephalomyelitis,

Flaviviridae, genus
horses, other domestic and wild
seep 1299)

Flavivirus)

manrn1als, grouse, ptannigan

Lyrnphocytic

Lyrnphocytic choriomen Reservoir mainly house mouse; can choriomeningitis
ingitis virus (family
be maintained in some other mice,

Arenaviridae, genus
hamster populations; also infects

Arenavirus)

guinea pigs, chinchillas, rats,
nonhuman primates, some other
mammals

Marburg hemor

Marburg virus (fan1ily

Bats are reservoir hosts; primates
rhagic fever

Filoviridae, genus
can be infected

Ma,rburgvirus)

Menangle virus

Menangle virus (fanlily

Fruit bats are normal reservoir host;
infection

Paramyxoviridae)

pigs can also be reservoir

Middle East

MERS coronavirus

Unknown reservoir host, possibly
respiratory
bats; source of infection for people
syndrome (MERS)

uncertain, camels implicated

Milker's nodules

Pseudocowpox virus

Cattle

(Pseudocowpox,see (fanlily Poxviridae, genus
p868)

Parapoxvirus)

Monkeypox

Monkeypox virus (family Nonhuman primates, some wild and Poxviridae, genus
pet rodents, including Gambian rats,

Orthopo:1;virus); Congo
dormice, prairie dogs, African

Basin clade causes more squirrels, some other man1mals such severe illness than West
as opossums; full host range

African clade
uncertain

ZOONOSES 2475

•@=iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VIRAL DISEASES (continued)

VetBooks.ir

West Africa

Contact with rodent

Gradual onset of nonspecific febrile
excretions, secretions,
illness, may be followed by chest pain,
or tissues; aerosols
cough, GI signs, hepatitis; severe swelling of head and neck, hypotension/
shock can develop; pleural/pericardial
effusions; hemorrhagic syndrome less
conm1on; overall mortality rate 1 % in
endemic areas; case fatality rate 2()0A,
among hospitalized patients

UK, Nmthern

Tick bites (Jxodes

Biphasic influenza-like illness,

Ireland; also
ricinus ); aerosol exposure sometimes followed by meningitis or reported in Norway, in laboratory, contaminameningoencephalitis, paralysis, joint Spain; uncommon in tion of skin wounds,
pain in second phase; not usually
people
contact with infected
fatal
anin1als; possibly ingestion
of milk

Worldwide

Contact with host

Ranges from mild flu-like illness to
excretions and secrebiphasic with meningitis in second tions; bites; possibly
phase; complications (eg, arthritis,
ingestion
parotitis, orchitis) possible; can
cause congenital defects (CNS
defects, chorioretinitis, and other
ocular lesions) or abortion; rarely
fatal in immunocompetent ( overall
case fatality rate <1 %)

Africa

Contact with infected

Initially nonspecific febrile illness;
tissues ( especially
maculopapular rash with desquan1anonhuman primates); tion; hepatitis; mild to severe
probable transmission
bleeding tendency develops a few
from bats in caves
days after onset; mortality rate

20%-88%, varies with isolate

Australia

Close direct contact with Severe illness with fever, severe tissues, amniotic fluid or headache, myalgia, lyrnphadenopablood of pigs reported in thy, drenching sweats, macular rash human cases

Middle East

Pneumonia, more likely in people
with coexisting illness or immunosuppression but also in healthy; -500A> of known cases were fatal

Worldwide

Skin contact ( especially

Papular to nodular red skin lesions;
broken skin) with lesions self-limiting
on cow's udder or mouth
of calf; also from fomites

West and central

Contact with lesions,

Smallpox-like disease; flu-like

Africa
blood or body fluids,
symptoms followed by maculopapular
fomites; bites; aerosols
rash, which develops into vesicles,
during close contact
pustules, scabs; lyn1phadenopathy
prominent; respiratory signs, encephalitis possible; case fatality rate varies with strain, < 1 % to 100/o--l 7% or higher;
milder in those vaccinated for smallpox

( continued)

2476

ZOONOSES

•tM•i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

VIRAL DISEASES (continued)

Murray Valley

Murray Valley encephali- Wild water birds
encephalitis
tis virus (family

Flaviviridae, genus

Flavivirus)

Newcastle disease

Newcastle disease vims/ Domestic and wild birds

Avian paran1yxovirns l

(family Paran1yxoviridae,
genus Avulavirn,s)

New World

Arenavirnses in Tacaribe Rodents
hemorrhagic fever
complex (family Arenavir-

(Argentinean,
idae, genusArenavirus):

Bolivian, Venezuelan Juin virus (Argentine HF),
and Brazilian

Machupo virus (Bolivian
hemorrhagic fevers HF), Guanarito virus

[HF])

(Venezuelan HF), Sabia
virus (Brazilian HF),

Chapare virus; possibly
others

Nipah virus infection Nipah virus (family

Fruit bats are normal reservoir;

(seep 721)

Paran1yxoviridae, genus swine can be reservoir; occasionally Henipa,virus)

in other mammals (spillover hosts)

Omsk hemorrhagic

Omsk hemorrhagic fever Voles, muskrats; also found in oilier fever
vims (family Flaviviridae, animals
genus Flavivirus)

Powassan virus

Powassan virus (fan1ily

Rodents (grow1dhog, squirrels, mice)

encephalitis

Flaviviridae, genus
and oilier small mammals thought to

Flavivirus); two closely be reservoirs
related lineages in
different reservoirs

ZOONOSES

2477

•@§iii GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

VIRAL DISEASES (continued)

Australia, New

Mosquito bites (Culex

Asymptomatic or mild nonspecific

Guinea
annulirostris)

febrile illness in majority; encephalitis, often with neurologic sequelae, or poliomyelitis-like flaccid paralysis
in small number of patients; case
fatality rate 15%--30% in encephalitic
form

Mildly virulent

Occupational exposure,

Highly virulent (velogenic) strains

(lentogenic, mesogeusually after contact with can cause self-limiting conjtmctivitis, nic strains) are found large amounts of virus
possibly other syndromes
worldwide; highly
virulent ( velogenic)

strains found in Asia,
the Middle East, Africa,

Central and South

America, pa.tis of Mexico; also in com1orants
in USA

South America,

Viruses found in rodent

Gradual onset of nonspecific signs,
related viruses might excretions, secretions,
including myalgia, headache, and
exist an1ong rodents tissues; inhalation of
fever; may develop petechial or
in Mexico
aerosolized virus or
ecchymotic hemorrhages, bleeding,
direct contact with

CNS signs, hypotension/shock; case
mucous membranes
fatality rate in untreated Bolivian
or broken skin
hemorrhagic fever 5%--30%,
untreated Argentine hemorrhagic
fever 15%--30%

Malaysia, Bangla

Direct contact with

Initial signs flu-like with fe'(er,
desh, and Northern
infected pigs or
headache, myalgia, sometimes

India; virus is
contruninated tissue;
vomiting; encephalitis ar1d meningiprobably endemic in direct or indirect ( eg, tis; respiratory disease, including
southeast Asia, but
contaminated fruit juice) acute respiratory distress syndromes outbreaks seem to
bat-to-hun1ar1 transmisin some; septicemia; other complicacluster in certain geo sion tions in severely ill; case fatality rate
graphic areas

33%--75%

Siberia

Tick bites (Dermacentor Biphasic febrile illness with spp ); direct contact with headache, GI signs, ± hemorrhages body fluids or carcasses

(nose, gums, lungs, uterus); CNS
of muskrats and possibly signs in minority of patients; other animal hosts
mortality rate <3%

North America,

Ixodes spp ticks, also

Nonspecific febrile illness; may
eastern Russia
found in Dermacen/or
progress to neurologic signs, which
andersoni
may be severe; some cases fatal

( continued)

2478

ZOONOSES

•h=i!i• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VIRAL DISEASES (continued)

VetBooks.ir

Rabies and

Lyssavirnses: rabies vims Wild and domestic canids, Mustelirabies-related (family Rhabdoviridae,
dae, Viverridae, Procyonidae, and
infections
genus Lyssavirus) and
order Chiroptera (bats) are

(seep 1302)

the related lyssavirnses, important reservoir hosts; all Duvenhage vims, Mokola mammals are susceptible; bats are vims, Australian bat
reservoir hosts for Duvenhage virus,
lyssavirns, European bat Australian bat lyssavirns, and lyssavirnses 1 and 2, lrkut European bat lyssavirnses; Mo kola virus, possibly others
vims carried in rodents and shrews

Rift Valley fever (see Rift Valley fever virus Sheep, goats, cattle, buffalo, African
p 768)

(family Bunyaviridae,
buffalo, camels, nonhuman primates;
genus Flavivirus)

squirrels and other rodents; puppies
and kittens

Ross River virus

Ross River vims (family

Marsupials, including wallaby,
infection, Ross River Togaviridae,genus
brushtail possum, might be natural
fever; epidemic

Alphavirus)

hosts; dusky rat also proposed; people,
polyartluitis
horses, ruminants, pigs, rabbits, other
mammals ( minor hosts) may also be a
source of virus during epidemics

St. Louis encephali

St. Louis encephalitis

Wild birds, domestic fowl; rodents,
tis
virus (family Flaviviridae, bats, other mammals might also

.genus Flavivirus)

maintain vii.Uses in South America

Severe acute

SARS-coronavirns

Bats are thought to be reservoir
respiratory

(family Coronaviridae,
hosts; can also infect palm civets,
syndrome (SARS)

genus Coronavirus)

raccoon dogs, cats, pigs, ferrets,
rodents, nonhuman prinlates, other
mammals

Sindbis virus disease Sindbis vims (fan1ily

Birds (passerifom1s suspected as

Togaviridae, genus
main reservoirs/amplifying hosts);

Alplw.virus)

occasionally found in other
vertebrates

Tanapox

Tanapox vims (family

Nonhuman primates

Poxviridae, genus

Yatapo:xvirus ); Yaba-like
disease vims may be a
variant of tanapox vims

ZOONOSES

2479

•tM•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

VIRAL DISEASES (continued)

Rabies is worldwide

Bites of diseased animals; Paresthesias or pain at bite site; with some exceptions: aerosols in closed
nonspecific prodromal signs such
completely absent
environments
as fever, myalgia, malaise; mood
from some islands;
changes progress to paresthesias,
countries also
paresis, seizures, and many other
considered rabies-free
neurologic signs; survival in clinical
if no cases in people
cases thought to be very rare
or domestic animals
for 2 yr; rabies-related
lyssaviruses found
only in Eastern

Hemisphere

( distribution varies)

Africa, foci on

Mosquito bites (Aedes

Influenz a -like febrile illness in most;

Arabian peninsula,
spp and Culex triten
complications, including hemotThagic

Indian subcontinent iorynchus ); contact with fever, meningoencephalitis in <5%; tissues
ocular disease in 1%--100/o; other
syndromes include acute renal failure
or thrombosis; death w1common
except with hemorrhagic syndrome

Australia, South

Mosquito bites (espe

Mild fever, arthralgia ± aithritis,

Pacific Islands
cially Culex annuliros
headache, rash; small joints most
tris and Aedes spp)

affected but large joints can also
be involved; arthralgia, myalgia,
lethargy may persist for months

Western hemisphere Mosquito bites (Culex

Flu-like illness sometimes followed
tarsalis, C pipiens
by meningitis or encephalitis, focal
quinquefasciatus
neurologic signs, dysuria; more
complex, C nigripalpus, severe in elderly and those with also reported in other
debilitating diseases; case fatality
genera)

rate of 5%--200/o reported in epidemics

China, southeast

Contamination of

Fever, myalgia, headache, diarrhea,

Asia
mucous membranes with cough; viral pneumonia with rapid respiratory droplets or
deterioration; case fatality rate 15%
virus on fomites; possibly
aerosol transmission

Virus widespread in Mosquito bites; Culex

Fever, arthritis, rash, prominent

Eastern hemisphere; and Culiseta, also others myalgia; nausea, vomiting, mild human cases tend to
jaundice in some; joint pain can
occur in limited
persist for months; seems to be mild
geographic regions
or asymptomatic in most children; no
fatal cases reported

Asia, Africa, and in

Direct contact through

Nonspecific febrile illness and
monkey colonies
broken skin; mosquitoes papulovesicular or nodular lesions suspected to be vector in (lesions may be pruritic or tender), Africa
often on extremities; more than one
or two skin lesions uncommon

( continued)

2480

ZOONOSES

•@Mi• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

VIRAL DISEASES (continued)

Tickborne encepha

Tickborne encephalitis

Small mammals especially rodents;
litis (Far eastern
virus (TBEV) (family
also in goats, sheep, dogs, and other
tickborne encephali Flaviviridae, genus
man1mals; birds
tis, Russian

Flav'ivirus ); three
spring-summer
subtypes:European
encephalitis, Central (TBEV-Eu [least

European tickborne virulent]), Siberian
encephalitis)

(TBEV-Sib ), Far Eastern

(TB EV-FE)

Usutu virus

Usutu virus (fan1ily

Birds
infections

Flaviviridae, genus

Flavivirus)

Vaccinia-related

Vaccinia or vaccinia-like Reservoir uncertain; found in wild poxviruses
viruses (family Poxvirirodents, cattle, horses, nonhuman dae, genus Orthopoxvi
primates
rus) of uncertain origin

Venezuelan equine

Venezuelan equine

Enzootic subtypes maintained in
encephalomyelitis
encephalitis virus (fan1ily rodents, other small man1mals, bats; Togaviridae, genus
epizootic subtypes an1plified in

Alphavirus)

equids; occasionally in other
man1mals and birds

Vesicular stomatitis Vesicular stomatitis

Swine, cattle, horses; occasionally in

Indiana virus, vesicular

South American camelids, sheep, and
stomatitis New Jersey
goats; also rodents; serologic
virus, vesicular stomatitis evidence of infection in many wild Alagoas virus, and Cocal
man1111als, especially bats
virus (family Rhadbovilidae, gem!:' Vesiculovirus) Wesselsbron fever

Wesselsbron virus

Ruminants, especially sheep, goats;

(fa.nilly Flaviviridae,
also evidence of infection in other
genusFlavivirus)

manunals, including lemurs; can
infect birds

West Nile fever and

West Nile virus (family

Birds are primary reservoir hosts;
neuroinvasive

Flaviviridae, genus
also affects horses, other mammals,
disease (seep 1291) Flavivirus); lineage alligators, possibly other reptiles and

1 and lineage 2 viruses
amphibians
are both pathogenic

ZOONOSES

2481

•ih•i• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

VIRAL DISEASES (continued)

Eurasia; TBEV-Eu

Tick bites (mainly Ixodes Often biphasic, with flu-like febrile mainly Europe to
ricinus and I perscula
illness in initial stage; neurologic signs
former USSR;
tus; also other species);
from mild meningitis to severe

TBEV-FE mainly
may be ingested in milk
encephalitis in some; myelitis or flaccid

Asia to fonner USSR;
poliomyelitis-like paralysis ( usually

TBEV-Sib mainly in
arms, shoulders, levator muscles of

Siberia
head); possibility of clu·onic and
progressive fonns, especially with

TBEV-Sib; case fatality rate <2"Ai

(TBEV-Eu ), 2"/o-3% (TB EV-Sib); case
fatality rate 200/o-30% in TBEV-FE may
be based on severe cases

Africa, Europe

Mosquito bites ( Cui,e.x

Very few cases identified: fever with
spp)

rash, fever with jaundice, or
meningoencephalitis

Appear to be

Direct contact

Pox skin lesions (papules, pustules,
endemic in Brazil
ulcerative nodules), may be accompanied by fever, lymphadenopathy Western hemisphere; Mosquito bites (Aedes,

Most have nonspecific febrile illness,
enzootic strains

Cul£x, and Psoroplwra
can be followed by neurologic signs;

F1orida to South
spp ); exposure to

<5% children, < 1 % adults progress to

America; epizootic
aerosolized debris from
encephalitis with case fatality rate of
strains emerge in
infected laboratory rodents; 10%--35% (highest rates in children South America, spread laboratory accidents

<5 yr old)

North and South

Contact with animals or

Usually asymptomatic; may develop

America; most likely in laboratory, probably
acute, febrile, flu-like illness; vesicles
not endemic north of also from insect bites,
can be found in mouth, pharynx, or

Mexico but sporadic including mosquitoes and inoculation site (eg, hands); outbreaks
biting flies (Phlebolomus self-limiting
spp, Lutzomyia spp, and
black flies)

Southern Africa,

Mosquito bites (mainly

Nonspecific febrile illness ±
southeast Asia

Aedes spp, possibly
maculopapular rash or ocular signs
others); also by contact
in some; few cases described but
with contaminated
seems to be self-limiting
material

Eastern and Western Mosquito bites (primarily Nonspecific febrile illness, occasionhemisphere Cule.r, univittatus, Cule.r, ally with rash; some cases progress spp ); also by handling
to encephalitis, meningitis, and/or
infected birds or reptiles acute flaccid paralysis that resembles or their tissues
poliomyelitis; occasionally other
syndromes; worse in elderly and
immunocompromised; case fatality
rate -10% in all patients with
neurologic disease, but higher in
elderly

2482

ZOONOSES

•M=iii• GLOBAL ZOONOSES• (continued)

Causative

Animals

Disease

Organism

Involved

VetBooks.ir

VIRAL DISEASES (continued)

Western equine

Western equine

Birds are reservoir hosts, may also
encephalomyelitis
encephalomyelitis virus
cycle in jackrabbits, rodents; equids,

(seep 1291)

(fan1ily Togaviridae,
other mrunmals are incidental hosts;
genus Alphavirus)

virus also found in reptiles,
an1phibians

Yellow fever

Yellow fever virus (frunily Nonhuman primates

Flaviviridae, genus

Flavivirus); only jungle
cycle is zoonotic (people
are reservoir for urban
cycle)

PRION DISEASE

Vruiant Creutzfeldt

Bovine spongiform

Cattle ru·e most important host; also

Jakob disease
encephalopathy prion
infects other nm1inants, cats and
other felids, lemurs

"Many proven zoonoses, including some relatively rare artlu·opodbome viral infections and helminth infections, have been omitted, as well as those diseases caused by fish and reptile toxins.

b Enterotoxigenic, enteroinvasive, enLeropathogenic, and enteroaggressive strains are not considered zoonotic.

ZOONOSES

2483

•t+iii• GLOBAL ZOONOSES• (continued)

Known

Probable Means of

Clinical Manifestations

Distribution

Spread to People
in People

VetBooks.ir

VIRAL DISEASES (continued)

Americas

Mosquito bites (Aedes,

Nonspecific febrile illness may be

Culex, and Ochlerotatus followed by encephalitis in infants spp); Culex tarsalis
and children, uncommonly in adults;
important in maintecase fatality rate 3%-4%
nance cycle in birds

South America,

Mosquito bites (Hae-ma

Nonspecific, mild to severe febrile

Africa
gogus spp and Sabethes
illness followed by liver and renal
spp in jungle cycles in
failure in some; hemorrhages ( eg,

South America, Aedes
epistaxis, hematemesis, melena,
spp in jungle cycles in
uterine hemorrhage) and often

Af1ica)

jaundice in severe cases; cases with
hemorrhages often fatal

PRION DISEASE

Most cases in the UK Ingestion of bovine

Neurodegenerative disorder similar
but also in many
products, especially
to sporadic Creutzfeldt-Jakob
other countries
those contaminated with disease but often in younger patients CNS tissues
and progresses more rapidly; always
fatal

VetBooks.ir

PHARMACOLOGY

VetBooks.ir

INTRODUCTION 2490

Extra-label Drug Use, Compounded Drugs, and Generic Drugs 2490

Disposition and Fate of Drugs 2492

Passage of Drugs Across Cellular Membranes 2492

Drug Absorption 2493

Bioavailability 2495

Drug Distribution 2495

Drug Metabolism 2496

Drug Excretion 2498

Pharmacokinetics 2499

Apparent Volume of Distribution 2499

Drug Clearance 2500

Drug Action and Pharmacodynamics 2502

Drug Concentration and Effect 2503

Agonists and Antagonists 2503

Structure-Activity Relationships 2504

Signal Transduction and Drug Action 2504

Drug Dose and Clinical Response 2505

Pharmacodynamics of Antimicrobial Drugs 2507

Routes of Administration and Dosage Forms 2508

Oral 2508

Oral Modified-release Delivery Systems for Ruminants 2511

Parenteral 2511

Topical 2514

Inhaled 2518

Chemical Residues in Food and Fiber 2518

Foodstuffs of Animal Origin 2519

Animal Fibers 2521

Nanotechnology 2522

SYSTEMIC PHARMACOTHERAPEUTICS

CARDIOVASCULAR SYSTEM 2525

Diuretics 2525

Furosemide 2527

Thiazide Diuretics 2528

Potassium-sparing Diuretics 2529

Positive Inotropes 2529

Cardiac Glycosides 2529

Phosphodiesterase Inhibitors 2531

13-Adrenergic Agonists 2532

Angiotensin-converting Enzyme Inhibitors 2533

2486

PHARMACOLOGY

Vasoactive Drugs 2534

Arterial Dilators 2534

Arterial and Venous Dilators 2535

Phosphodiesterase 5 Inhibitor 2535

VetBooks.ir

Antiarrhythmics 2535

Drugs Acting on the Blood or Blood-forming Organs 2540

Hematinics 2540

Hemostatics 2542

Anticoagulants 2542

DIGESTIVE SYSTEM 2544

The Monogastric Digestive System 2544

Drugs Affecting Appetite 2544

Drugs to Control or Stimulate Vomiting 254 7

Therapy of Gastrointestinal IBcers 2550

Drugs Used in Treatment of Diarrhea 2552

Drugs Used in Treatment of Chronic Colitis 2555

Gastrointestinal Prokinetic Drugs 2556

Cathartic and Laxative Drugs 2559

Drugs Affecting Digestive Functions 2560

The Ruminant Digestive System 2561

Drugs for Specific Purposes 2561

Drug Disposition in the Ruminoreticulum 2564

THE EYE 2565

Routes of Administration 2565

Local Anesthetics 2566

Infectious Disease 2566

Intraocular Inflammation 2568

Miscellaneous Feline Conditions 2570

Glaucoma 2570

INTEGUMENTARY SYSTEM 2571

Antibacterials 2571

Antifungals 2573

Antiparasitics 2576

Antihistamines 2577

Essential Fatty Acids 2578

Hormonal Therapy 2578

Immunomodulators 2581

Psychotropic Agents 2584

Vitamins and Minerals 2584

MUSCULAR SYSTEM 2586

Neuromuscular Blocking Agents 2586

Skeletal Muscle Relaxants 2588

Anabolic Steroids 2590

PHARMACOLOGY

2487

NERVOUS SYSTEM 2590

Anticonvulsants or Antiepileptic Drugs 2590

Antiepileptic Drugs Used to Stop Ongoing Seizure Activity 2591

Maintenance Anticonvulsant or Antiepileptic Therapy 2596

VetBooks.ir

Tranquilizers, Sedatives, and Analgesics 2600

Psychotropic Agents 2601

REPRODUCTIVE SYSTEM 2606

Effect of Reproductive Therapy on the Fetus or Neonate 2608

RESPIRATORY SYSTEM 2608

Antitussive Drugs 2608

Species Approach to Inflammatory Airway Disease 2609

Systemic Therapy of Inflammatory Airway Disease 2610

13-Adrenergic Receptor Agonists 2610

Methylxanthines 2611

Anticholinergic Drugs 2612

Glucocorticoids 2612

Cyproheptadine 2613

Antimicrobial Therapy 2613

Inhalation Therapy of Airway Disease 2613

Spacers 2614

13rAgonists 2614

Glucocorticoids 2615

Ipratropium Bromide 2615

Cromolyn Sodium and Nedocromil 2615

Lidocaine 2615

Suggested Treatment Regimens 2615

Expectorants and Mucolytic Drugs 2616

Decongestants 2616

Respiratory Stimulants 2616

URINARY SYSTEM 2617

Bacterial Urinary Tract Infections 2617

Fungal Urinary Tract Infections 2622

Bacterial Prostatitis 2622

Diuretics 2623

Dopamine 2625

Glomerular Disease 2625

Diabetes Insipidus 2625

Controlling Urine pH 2625

Cystine-binding Agents 2625

Urinary Incontinence 2626

Urine Retention 2627

2488

PHARMACOLOGY

CHEMOTHERAPEUTICS

INTRODUCTION 2627

Antimicrobial Drug Factors 2628

VetBooks.ir

Mechanism of Action 2628

Drug Disposition 2629

Adverse Effects and Toxicity 2629

Virulence and Resistance 2630

Dosing Regimens 2634

Requirements for Successful Antimicrobial Therapy 2635

Combination Therapy 2636

ANTHELMINTICS 2637

Mechanisms of Action 2637

Pharmacokinetics 2639

Withholding Periods 2642

Safety 2642

Resistance 2644

Benzimidazoles 2645

Imidazothiazoles 2646

Tetrahydropyrimidines 264 7

Macrocyclic Lactones 264 7

Salicylanilides, Substituted Phenols, and Aromatic Amide 2650

Praziquantel and Epsiprantel 2650

An1ino-acetonitrile Derivatives 2650

Cyclic Octadepsipeptides 2650

Spiroindoles 2651

Miscellaneous Anthelmintics 2651

Combination Anthelmintics 2651

ANTIBACTERIAL AGENTS 2652

'3-Lactan1 Antibiotics 2652

Penicillins 2654

Cephalosporins and Cephamycins 2659

Aminoglycosides 2662

Miscellaneous Aminocyclitol Antibiotics 2669

Quinolones, including Fluoroquinolones 2669

Sulfonamides and Sulfonamide Combinations 2674

Tetracyclines 2679

Phenicols 2683

Macrolides 2687

Streptogramins 2690

Lincosamides 2690

Miscellaneous Antimicrobial Agents 2692

Polymyxins 2692

Bacitracins 2693

Glycopeptides 2693

Fosfomycin 2693

PHARMACOLOGY

2489

Novobiocin Sodium 2694

Tiamulin Fumarate 2694

Ionophores 2694

Rifamycins 2694

VetBooks.ir

Nitrofurans 2695

Nitroimidazoles 2696

Hydroxyquinolines 2697

ANTI FUNGAL AGENTS 2697

Polyene Macrolide Antibiotics 2698

Imidazoles 2701

Flucytosine 2703

Griseofulvin 2704

Allylamines 2705

Iodides 2706

Topical Antifungal Agents 2706

ANTI-INFLAMMATORY AGENTS 2707

Pathophysiology of Inflammation 2707

Chemical Mediators oflnflammation 2707

Antihistamines 2709

Corticosteroids 2710

Nonsteroidal Anti-inflammatory Drugs 2714

Chondroprotective Agents 2721

ANTINEOPLASTIC AGENTS 2722

Alkylating Agents 2726

Antimetabolites 2731

Mitotic Inhibitors 2732

Antineoplastic Antibiotics 2733

Hormonal Agents 2734

Miscellaneous Antineoplastic Agents 2734

Ancillary Antineoplastic Agents 2737

Treatment of Canine Lymphoma 2737

ANTISEPTICS AND DISINFECTANTS 2738

Acids and Alkalies 2739

Alcohols 2739

Biguanides 2739

Oxidizing Agents 2740

Metals 2741

Phenols and Related Compounds 2742

Reducing Agents 27 42

Surface-active Compounds 2743

Other Antibacterial Agents 27 44

Vapor-phase Disinfectants 2744

ANTIVIRAL AGENTS 2744

Vidarabine 2745

Acyclovir 2745

2490

PHARMACOLOGY

Penciclovir and Famciclovir 2745

Ribavirin 2745

Zidovudine 2747

VetBooks.ir

Amantadine 2747

Miscellaneous Antiviral Agents 27 48

ECTOPARASITICIDES 2748

LargeAnimals 2748

Small Animals 2754

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS 2758

Steroid Hormones 2758

Growth Hormone 2764

[3-Adrenergic Agonists 2764

Antimicrobial Feed Additives 2765

Probiotics 2766

VACCINES AND IMMUNOTHERAPY 2767

Active Immunization 2767

Adjuvants 2768

Types of Vaccines 2768

Administration of Vaccines 2770

Vaccine Failure 2772

Adverse Reactions 2772

Production of Vaccines 2773

Passive Immunization 2773

Nonspecific Immunotherapy 2774

PHARMACOlOGY INTRODUCTION

Once a diagnosis has been made and medical EXTRA-LABEL DRUG USE, treatment is deemed necessary, safe and

COMPOUNDED DRUGS, AND
effective pharmacologic agents that exert
the appropriate actions should be selected.

GENERIC DRUGS

A dosing regimen should be individualized

A new animal drug (NAD) is "any drug
for each patient. In addition to the route,
intended for use in animals other than
which often is based on drug availability
man ... not generally recognized as safe and
or convenience, a number of factors should
effective for the use under the conditions
be considered when designing a dosing
prescribed, recommended, or suggested in
regin1en. These include host considerations
the labeling of the drug." A drug's label
that may alter the response to or disposition
includes the label on the product itself as
of the drugs. Adjustment in route, dose, or
well as any accompany ing material in or
interval may be indicated based on host
on the package, including the package
and drug factors. For antimicrobial drugs,
insert.

microbial factors, including resistance, also

To use an NAD in a legal manner,
should be considered. Finally, particularly
veterinatians must adhere to the specificafor food anin1als, public health, environmentions noted on the label. Otherwise, the drug tal implications, and regulatory constraints
is being used in an extra-label manner.

must be considered.

Extra-label drug use, whether actual or

PHARMACOLOGY INTRODUCTION

2491
intended, occurs when the drug is used in a
compounded products is compounding
manner not in accordance with approved
intended to circrnnvent the drug approval
label directions. This includes but is not
process, resulting in mass marketing of
limited to a different dosage, interval, route,
products that have had little or no quality

VetBooks.ir
indication, or species.

control to ensure purity, potency, and

In 1994, Congress passed the Animal
stability. The FDA considers a com

Medicinal Drug Use Clarification Act
pounded product to be an adulterated,

(AMDUCA), which legalized extra-label
ie, unapproved, new anin1al drug and
drug use by vete1ina.nans as long as specific
thus a violation. Conditions under which
criteria or restrictiohs are met. Most
compounding is not subject to regulatory
rest.rictions are largely applicable to
actions include a legitimate practice
extra-label drug use in food animals. For

(pharmacy or veterinary; includes
both food and nonfood animals, a valid
licensure), operation within the conform
veterinary-client-t,atient relationship
ity of state law, for pharmacists in response
must exist. For food animals, in the absence
to a prescription, and for veterinaiians
of a drug labeled for the intended use,
operating within a valid veterinary-clientextra-label drug use might involve drugs patient relationship. Compounding of
approved for use in other food animals,
human drugs and, very occasionally, bulk
approved for use in honfood animals, or
drugs into appropriate dosage forms may
approved for use in people. Restrictions
be acceptable in certain circrnnstances. A
regarding extra-label drug use of nonfood
legitimate medical need must be identified
animal and hrnnan drugs are progressively

( eg, health or life of the animal is threatened
restrictive. Extra-label drug use in food
or suffering may occur). Additionally, there
animals is permitted only by or under the
must be no marketed, approved animal
supervision of a veterinarian, is allowed
or hrnnan drug, regardless of whether it is
only for therapeutic purposes (ie, the
used as labeled or in an extra-label fashion,
animal's health is suffering or threatened), is that may be substituted for the componot allowed when the drug is administered w1ded agent. Occasionally, other rare
in feed, is not permitted if it results in
circun1stances may be considered. In 2013,
violative food resid1.1es or any residues that

Congress passed the Drug Quality and
may present a 1isk to public health, and is

Security Act that, an1ong other things,
not allowed if specifically prohibited by the
increases regulation of compounding

FDA
in human medicine. However, this Act

Drugs specifically prohibited in food
does not cover compounding of animal
animals by the FDA as of May 2015 include
products, and Congress is examining
chloramphenicol, clenbuterol, diethylstilfurther actions to more effectively bestrol, dirnetridazole, ipronidazole, other
regulate such compounding.

nitroimadazoles, furazolidone, nitrofura

Pham1acists often can dispense an
zone, sulfonamide drugs in lactating dairy
equivalent, less expensive, nonproprietary
cattle ( except for those specifically

(generic) drug without prescriber approval.

approved), fluoroquinolones, aglycopep

An exception occurs if a state has a mandatides (eg, vancomyCln), phenylbutazone in tory substitution law or if the brand name
female dairy cattle �20 mo old, cephalospoproduct is dispensed along with a "disrins ( except cephap\.rin) in cattle, swine, pensed as written" order. Generic products
chickens, or turkeys for disease prevention,
must not only contain the same active
and amantadine or neuran"linidase inhibitor
ingredient as the proprietary drug but also
classes of drugs usea to treat influenza A
meet bioequivalence standai·ds. Generics
in poultry and ducks.

may be pharmaceutically equivalent but may

Use of a compOllll.ded preparation also
not be therapeutically equivalent. Substituconstitutes extra-label drug use. However, tions of generic drugs for proprietary drugs
a major distinction i!!; that a compounded
are recommended only for those drugs
preparation undergoes no regulatory
shown to be therapeutically equivalent.

assessment or approval. Conditions under

Those hrnnan drugs tested by the FDA and
which compounding is legal also are
found to be therapeutically equivalent are
specified in the AMDUCA. Compounding
listed in Approved Drug Products with
includes any manipl.\lation of the drug

Therapeutic Equivalence Evaluations,
beyond that stipulat�d on the label.

othe1wise known as the "Orange Book."

Guidelines regarding the compounding of

However, status of a generic drug is relevant
pham1aceuticals under the direction of a
only for the approved species and, as such,
vete1inarian are del.i..11eated in Compliance
therapeutic equivalence of a hun1an generic

Policy Guideline 7125.40. Among the
drug does not apply to extra-label use of that
greatest concerns of the FDA regarding
drug in an anin1al.

2492

PHARMACOLOGY INTRODUCTION

Although AMDUCA legalizes extra-label
cell in thickness (eg, hepatic sinusoids).

drug use in the USA, selected states or other

Multi.layered tissues each may present
countries may have additional or compledifferent types of barriers, eg, skin is mentary regulatory or legal restiictions. In all protected by the dense stratwn comeum, instances, it is important to read carefully the which is absent in mucous membranes.

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label instructions for use of specific drugs.

Not all drugs must pass through cell
membranes; pa.racellular movement

DISPOSITION AND FATE
between cells increasingly is an in1po1tant

OF DRUGS
movement for some drugs, eg, in ilie GI ti·act.

Drugs and other molecules cross cellular

The goal of drug tl1erapy is to achieve a
membranes by several processes. Methods
pharmacologic response. The magnitude of
by which drugs move include bulk flow
the pharmacodynarnic response to a dJ.ug

(eg, movement witl1 blood, glomerular
generally reflects the number of receptors
filtration), passive diffusion, carrier-mediwith which the drug interacts ( drug-receptor ated transport (ie, active or facilitated
the01y). Because tissue drug concentrations
transport), and pi.nocytosis. Of these,
generally parallel tissue concenti·ations, the
passive diffusion is most in1po1tant for
ideal dose will result in plasma drug
movement of dJ.1.1g molecules and otl1er
concentrations in a "therapeutic range." This xenobiotics (foreign chemicals), as well
population statistic is defined by a maximum
as many endogenous compounds.

drug concentration, above which the risk of

The rate at which a drug passively
adverse events ( eg, toxicity) increases, and a
diffuses ilirough membranes is influenced
minimum drug concentration, below which
by several factors, the most important of
therapeutic failure may result. Plasma drug
which is the concentration gradient of
concentrations generally fluctuate during a
diffusible ( eg, dissolved) drug across the
dosing interval, because they are impacted
membrane. However, otl1er host and drng
by four drng movements acting simultanefactors influence ilie rate and extent of ously on the drug: absorption from the site
passive diffusion. Host factors iliat increase
of noni.ntravenous adJ.ninistration into the
diffusion include penneability and surface
plasma, distribution into tissues and then
area of the membrane; tltickness of the
back into plasma, where tl1e dJ.ug can then
membrane negatively in1pacts diffusion.

be eliminated from the body either by

Drug characteristics iliat influence diffusion
metabolism or excretion of parent drug
include molecular weight, lipophilicity, and
and/or metabolites. Many factors influence
degree of ionization. Most drugs are "small
each of these four drug movements (ADME)

molecules" ( <900 daltons), but diffusibility and tlms the time course of plasma drug
is more likely to occur for drugs <500
concenti·ations after a dose is administered
daltons. Drugs must be sufficiently lipid
by any route. Understandi.ng tl1ese factors, in
soluble (lipophilic) to pass through some
turn, is important to individualizing drug
level of cell membrane lipid bilayer to reach
therapy for tl1e patient, because dosing
most drug receptors. The lipid-to-water
regimens are modified to acljust for
partition coefficient describes the
physiologic (eg, species, breed, gender, age),
distiibution (ratio) of a drug ( concentraphannacologic ( eg, drug-drug or drug-diet tion) in a lipid compared wiili water media.

interactions), and pathologic (eg, renal,

The distiibution coefficient also takes into
hepatic, or cardiac disease) influences on
acc0tmt ionization.

drug disposition. Pharmacoki.netics is ilie

Many drugs are weak organic acids or
science iliat mailiematically describes the
bases. At physiologic pH, they tend to be
tin1e course of plasma drug concentrations
partially ionized ( dissociated) and partially
after administration of a dose, ie, the result
nonionized (undissociated); the ratio of ilie
of ADME on plasma drug concenti·ations.

respective fonns depends on tl1e dissociation constant CPI<a) of the drug, ie, the pH at Passage of Drugs Across Cellular
which ilie drug is present in equal concentration in ionized and nonionized forms, and Membranes
ilie pH of tl1e solution in which tl1e drug is

Each of the drug movements generally
dissolved. Only nonionized fraction diffuses
relies on ilie drug passing ilirough cell
ilirnugh lipid membranes. Distiibution
membranes (transcellular). Membrane
across any membrane of a drug with any
barriers may be composed of several layers
given PI<a reflects the degree of ionization
of cells ( eg, skin, vagina, cornea, placenta)

and thus environmental pH on each side of
or a single layer of cells ( eg, enterocytes,
the membrane. The Henderson Hasselbach
renal tubular epithelial cells), or iliey may
equation predicts the ratio of ionized vs
consist only of a boundary less than one
non ionized drug. In general, weak acids are

PHARMACOLOGY INTRODUCTION

2493
nonionized in acidic compared with alkadistribution of one of the competing line environments, and weak bases are
molecules.

nonionized in alkaline compared with

Pinocytosis is an important transport
acidic environments. The more sin1ilar the
process in mat1U11alian cells, particulru·ly
environmental pH is to that of the pl(,. of a
intestinal epitl1elial cells at1d renal tubulru·

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weak acid or base, the more nonionized is
cells. Drugs that exist in solution as
the drug and the more likely it will diffuse.

molecular aggregates have large molecular

As long as the ratio of nonionized to ionized
masses themselves or that are botmd to
drug is ;:,Q.01, the drug is considered
macromolecules may be transferred across
diffusible.

membranes by pinocytosis.

Not all drugs must pass through cell
membranes to reach their receptor.

Drug Absorption

Aqueous pores in lipoproteinaceous
biologic membranes offer a means of

Absorption from the GI Tract: Many
xenobiotic movement through the
factors influence orally administered drugs.

membrane for predominantly aqueous

Before absorption, orally administered
soluble drugs. Lipid-insoluble (water-soludrugs must disintegrate and then dissolve; ble) compounds pass easily through tl1ese
dissolution often is the rate-linliting factor
pores and to a lesser degree directly through in oral drug absorption. Drugs may be the membrane. A hydrostatic or osmotic
formulated by manufacturers to result in
pressure difference across a membrane
extended ( occwTi.ng throughout tl1e GI
facilitates movement by promoting water
tract) or delayed absorption. Often, release
flow tl1rough the aqueous pores. Bulk
kinetics of these drugs limit extrapolation
fluid movement carries or "drags" solute
of dosing regimens from one species to
molecules through the pores as long as
another. Once an orally administered drug
the solute molecules are smaller than
has dissolved, multiple factors influence its
the aqueous charm els.

absorption. Drug chru·acteristics include

Several specialized transfer processes
molecu]ru· size, lipophilicity, ru1d drug pK,.

account for the passage of certain organic

Drug pl(,. is pruticularly important in the
ions and other large lipid-insoluble

GI tract, because environmental pH is
substances across biologic membranes.

markedly variable an1ong the different

Active transport, facilitated diffusion, and
regions or compartments. Host factors (in
exchange diffusion are three distinct types
addition to environmental pH) detemlining
of carrier-mediated systems used to move
oral absorption include epithelial permespecific substances across cellular ability, GI motility, surface ru·ea (being
membranes. The highly selective carriergreatest in the small intestine, which is the mediated systems are principally used
major site of drug absorption), transport
for transporting nutrients and natural
and metabolizing proteins, and GI blood
substrates across biologic membranes.

(which maintains the concentration

Among the mechanisms of active transport
gradient) and lymphatic flow. Epithelial
are transpo1t proteins that move compem1eability is influenced by disease.

pounds, including drugs, into or out of

Additionally, in those species in which
cells. Transpmt proteins are located at
colostrum absorption is in1po1tant,
portals of entry ( eg, enterocytes of the
epithelial pe1meability is much greater. GI

GI tract or sinusoidal hepatic cells) or
motility is irnportat1t because it influences

"sanctuary" tissues (eg, brain, CSF,
mixing of lurninal contents, which is
placenta, prostate, eyes, or testicles),
necessary for dissolved drug to come into
where they attempt to ensure that
contact with absorptive surfaces. Gastric
xenobiotics do not enter the protected
motility detem1ines gastric emptying, which
tissue. As such, transport proteins are
in turn influences tl1e rate of drug absorpable to influence each drug movement tion. Chru1ges in GI blood flow have minimal

(absorption, distribution, metabolism, and
impact on drug absorption, because
excretion). The most well known of the
although GI blood flow maintains tl1e
transport proteins is the ATP-binding
concentration gradient necessary for
cassette superfamily of efflux transportpassive diffusion, it is rarely the rate-limiters, which includes P-glycoprotein, the ing factor. Both efflux transport proteins
mu]tidrug resistance protein. Substrates

(eg, P-glycoprotein) and drug-metabolizing
for P-glycoprotein include both xenobiotenzymes located in the GI epithelium cat1
ics and dietary components. Additional
markedly decrease drug absorption,
transport proteins carry cations, anions,
contributing to a "first-pass effect." These or organic compounds. Competition for
proteins are subject to clinically relevant
transport increases oral absorption or
drug interactions and are likely to differ

2494

PHARMACOLOGY INTRODUCTION
among physiologic influences ( eg, species,
and generally are rather small molecules,
gender, age). A drug entering the portal
they diffuse practically instantaneously
circulation will be exposed to hepatocytes
into the blood in the alveolar capillaries.

before reaching systemic circulation. If a

In contrast, for drugs administered as

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large proportion of the drug (>75%) is
aerosols, particles containing drugs can be
removed or extracted as it passes through
deposited on the mucosal surface of the
the liver, the oral bioavailability of the drug
bronchi or bronchioles, or even in the
will be markedly reduced, also resulting in a
alveoli, with the site influenced by particle

"first-pass effect." For such drugs, the oral size and breathing rate and depth. Whether
dose is proportionately higher than the
or not the drug is absorbed from these sites
parenteral dose. Food can markedly alter
depends on the characteristics previously
oral absorption of drugs by either diluting it,
described.

or more importantly, binding to it so that it
is not absorbed.

Absorption from Injection Delivery

Sites: After nonintravenous injection,

Absorption from Topical
diffusible drug molecules traverse the

Administration: Drugs may be absorbed
capillary wall by a combination of diffusion
through the skin after topical application;
and filtration. Diffusion is the predominant
however, tl1e stratum comeum presents an
mode of transfer for lipid-soluble moleffective barrier to transdennal movement ecules, small lipid-insoluble molecules,
of most drugs into circulation. As such,
and ions. Because most capillaries are
many drugs are absorbed after paraceltular
fenestrated, all drugs, whether lipid-soluble
rather than transcellular movement. Intact
or not, cross the capillary wall at rates that
skin allows the passage of small lipophilic
are extremely rapid compared with their
substances but efficiently retards the
rates across other body membranes. In fact,
diffusion of water-soluble molecules in
the movement of most drug molecules in
most cases. Lipid-insoluble drugs generally
various tissues is limited only by the rate of
penetrate the skin slowly compared with
blood flow rather than by the capillary wall.

their rates of absorption through other

However, endothelial cells of sanctuaries,
body membranes. Absorption of drugs
such as the blood-brain or CSF barrier,
tlu·ough the skin may be enhanced by heat,
retina, and testicles, have tight intercellular
moisture, or disruption of the stratum
junctions, thus restricting movement of
comeum. Occlusive dressings increase
drugs.

heat and moisture; transdennal patches

Aqueous solutions of drugs are usually
also disrupt the stratum comeum. Smaller
absorbed from an IM injection site within
molecules are more conducive to transder10-30 min, provided blood flow is unin1mal drug delivery. Different transdennal
paired. Faster or slower absorption is
systems have been developed with the
possible, depending on the concentration
intent of systemic drug delivery. Certain
and lipid solubility of the drug, vascularity
solvents (eg, dimethyl sulfoxide [DMSO])

(including nwnber of vessels and state of
may facilitate the penetration of drµgs
vasoconstriction), the volw11e of irtjection,
through the skin. Damaged, inflamed,
the osmolality of the solution, and other
or hyperemic skin allows many drugs to
phannaceutical factors. Substances with
penetrate the dermal bani er much more
molecular weights >20,000 daltons are
readily. For example, drugs administered
principally taken up into the lymphatics.

transdermally as pluronic lecithin or other

Absorption of drugs from subcutaneous
gels presumably penetrate the stratum
tissues is influenced by the same factors
corneum because it is disrupted, becoming
that detennine the rate of absorption from
more permeable. The same principles that

IM sites. Some drugs are absorbed as
govern the absorption of drugs through the
rapidly from subcutaneous tissues as from
skin also apply to the application of topical
muscle, although absorption from injection
preparations on epithelial surfaces. In
sites in subcutaneous fat is always
contrast to skin, mucosal epithelium has
significantly delayed.

no stratum corneum, facilitating drug

Increasing blood supply to the injection
absorption. An advantage of the buccal
site by heating, massage, or exercise
mucosa is that a drug avoids first-pass
hastens the rate of dissemination and
metabolism.

absorption.

The rate of absorption of an iajected drug

Absorption from Tracheobronchial
may be prolonged in a nwn ber of ways,

Surfaces and Alveoli: Because volatile
including inunobilization of the site, local
and gaseous anesthetics have relatively
cooling, a tourniquet, incorporation of a
high lipid-to-water partition coefficients
vasoconstrictor, an oil base, and implant

PHARMACOLOGY INTRODUCTION

2495
pellets and insoluble "depot" preparations.

be so large (>65,000 daltons) or so highly

Among these depot preparations are drugs
bound to plasma proteins iliat it remains in
that are converted to less soluble esters,
ilie intravascular space after IV administrawhich must be released by esterases ( eg, tion. Compounds that penneate freely

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procaine and benzathine esters of penicillin
tlrrough cell membranes become disttibor acetate esters of steroids) or less soluble uted, in time, tl1roughout ilie body water
complexes (eg, protantine zinc insulin), or
to both extracellular and intracellular
that are administered as insoluble microfluids, with ilie extent depending on drug crystalline suspensions ( eg, methylprednichemistry. Substances iliat pass readily solone acetate).

tlrrough and between capillary endothelial
cells, but do not penetrate oilier cell

Bioavailability
membranes, are distributed into ilie
extracellular fluid space. Drugs may also

Bioavailability refers to the extent to which undergo redistribution in the body after a drug is absorbed into the body and thus is
initial high levels are achieved in tissues
available to act on its intended target site.

that have a rich vascular supply, eg, ilie

A drug is considered lOOW, bioavailable
brain. As tl1e plasma concentration falls,

(F=l) when given intravenously (although
the drug readily diffuses back into ilie
pulmonary metabolism may make this not
circulation to be quickly redistributed to
entirely true). Bioavailability of a particular other tissues wiili high blood-flow rates, route or fonnulation is the ratio of the area
such as the muscles; over time, the drug
under the plasma drug concentration
also becomes deposited in lipid-rich tissues
versus time curve (AUC) of the drug when
with poor blood supplies, such as the fat
the drug is given via that route or as that
depots. Most drugs are not distributed
preparation to the AUC when the drug is
equally throughout ilie body but tend to
given intravenously at the san1e dosage
accumulate in certain specific tissues or

(in mg/kg):

fluids. The general principles that govern

F = AUC
the passage and distribution of drugs
non-1vfAUC,v
across cellular membranes (seep 2492) are

The equation must be adjusted for dosage
applicable to drug distribution. Basic drugs
when appropriate:

tend to accumulate in tissues and fluids
with pH values lower than the pl(,, of ilie

F = (AUCnon-iv) x (dose,v)/(AUC,v) x
drug; conversely, acidic drugs concentrate

( dosenon-1v)

in regions of higher pH, provided the free

Two products are considered bioequivadrug is sufficiently lipid soluble to penetrate lent if they result in the san1e rate and extent ilie membranes that separate the compartof absorption. Rate of absorption is ments. Even small differences in pH across
reflected as the maxinmm plasma drug
boundary membranes, such as those iliat
concentration (C
exist between plasma (pH 7.4) and other

,,,.J and the time (T,,,.J that

C
tissues such as CSF (pH 7.3), milk (pH

,,,ax occurs. Thus, two drugs are bioequivalent if their AUC, C,,,ax, and T"'"" do not 6.5-6.8), renal tubular fluid (pH 5--8),
significantly differ. Two different preparaand inflamed tissue (pH 6-7) can lead to tions or routes of administration may be
unequal distribution of drugs, referred to
equally bioavailable but not bioequivalent.

as "ion-trapping." Only freely diffusible and Genetic drugs must be demonstrated to be
unbound drug molecules are generally able
bioequivalent.

to pass from one compartment to anoilier.

Once a drug reaches the systemic

However, some drugs are transported by
circulation, all other d.tug movements
carrier-mediated systems across certain

(distribution, metabolism, and excretion)

cellular membranes, which leads to higher
will be tl1e same regardless of the route or
concentrations on one side than ilie oilier.

preparation. However, in some instances,

Examples of such nonspecific transport
absorption may be so slow ( eg, delayed or
mechanisms are found in renal tubular
extended-release fom1ulation, absorption
epithelial cells, hepatocytes, and the
impacted by food) that it limits ilie rate at
choroid plexus. Among the transport
which ilie d.tug is elintinated ( metabolized
proteins, genetic differences in P-glycoproand/or excreted) from the body.

tein profoundly in1pact drug movement,
particularly at portals of xenobiotic entry
or sanctuaries.

Drug Distribution

Passive diffusion of drugs from capillar

After absorption into the bloodstream,
ies to tissues may be limited by binding to
drugs are disseminated to all parts of the
plasma proteins. The most important is
body. Occasionally, ilie drug molecule may
albwnin, aliliough the globulins and,

2496

PHARMACOLOGY INTRODUCTION
especially, et-1 acid glycoprotein (for bases)

Inflanm1ation, presented by for example
may also play a significant role. In general,
meningoencephalitis, can substantially alter
protein binding is considered clinically
tl1e pem1eability of the blood-brain barrier.

relevant if �80"!.,. For such drugs, factors

In general, direct injection into the CSF is
influencing binding can impact drug
undesirable because of the risk of unex

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disposition. These include plasma pH,
pected effects.

concentration of plasma proteins, con

In pregnant animals, the degree of
centration of the drug, or the presence of a
placentation may determine the extent of
competing agent with a greater affinity for
a placental barrier. Nutrients such as
the limited number of binding sites. For
glucose, an1ino acids, minerals, and even
example, a potentially toxic compound
some vitan1ins are actively transpo1ted

(such as most NSAIDs) may be 98% bound,
across the placenta. The passage of drugs
but if for any reason it becomes only 96%
across tl1e placenta is largely by lipid
bound, then the concentration of the free
diffusion, and the factors discussed above
active drug that becomes available in the
play a role. The distribution of drugs within
plasma is doubled, with potentially hamlful
the fetus follows essentially the san1e
consequences. The concentration of a drug
pattern as in the adult, with some differadministered in overdose may exceed the ences with respect to the volumes of drug
binding capacity of the plasma protein and
distribution, plasma-protein binding, blood
lead to an excess of free drug, which can
circulation, and greater permeability of
diffuse into various target tissues and
interceding membranous baniers. Drugs
produce exaggerated effects. Other reasons
that are potentially teratogenic should be
the fraction of unbound drug might increase
avoided, particularly in early gestation.

include hypoalbuminemia and competition

The manm1ary gland epitl1elium, like
with other highly protein-bound drugs. The
other biologic membranes, acts as a lipid
degree of protein binding of a drug cannot
bani er, and many drugs readily diffuse from
be extrapolated among the species, but in
the plasma into milk. The pH of nom1al milk
most species, NSAIDs, antifungal imidavaries, being 6.5-6.8 in goats and cows. As zoles, and doxycycline are examples of
such, weak bases tend to accumulate in
highly protein-bound drugs. More rapid
milk. Drugs delivered by intra.mammary
clearance of the now unbound drug may
infusion can diffuse into plasma to a greater
mitigate the impact of higher drug
or lesser degree by the same processes
concentrations.

noted earlier.

Dissociation of a drug from plasma

Once a drug is distributed into tissues,
proteins also influences elimination from
binding to macromolecules such as protein
the body in that those drugs more tightly
components of cells or fluids, dissolution in
bound tend to have much longer eliminaadipose tissue, formation of noncliffusible tion half-lives, because they are released
complexes in tissues such as bone, incorpogradually from the plasma protein reservoir ration into specific storage granules, or

( eg, cefovecin or long-acting sulfonamides).

binding to selective sites in tissues all

Most unbound drugs distribute. easily
impede movement of drugs back into
from capillaries to extracellular fluid.

plasma and account for differences in

However, only the more lipid-soluble drugs
the cellular and organ distiibution of
can distribute to all tissues because of the particular drugs.

presence of physiologic barriers presented
by "sanctuaries" (eg, blood-brain, placental, and mammary barriers). For the CNS, drugs

Drug Metabolism
may gain access through either the capillary

Drugs that are lipid soluble will be passively
circulation (blood-brain barrier) or the CSF
reabsorbed as urine concentrates in the

(also a blood barrier). Drugs penetrate into
kidney unless they are converted by
the cortex more rapidly than into white
enzymatic processes to water-soluble drugs.

matter, probably because of the greater

This is accomplished by drug metabolism.

delivery rate of drug via the bloodstream

Metabolism and subsequent excretion of
to the tissue.

drugs together comprise drug "elimination"

The pharmacologic factors and consefrom the body. Most drug metabolism quences of the diverse rates of entry of
occurs in the smooth endoplasmic
different drugs into the CNS are clinically
reticulum of the liver. Metabolism generally
relevant in that water-soluble, ionized drugs
consists of two phases: Phase I induces a
are less likely to enter the CNS, whereas
chemical change (most frequently
drugs with low ionization, low plasmaoxidation, but also reduction) that renders protein binding, and a fairly high lipid-water
the drug more conducive to phase II. Phase
partition coefficient penetrate more rapidly.

II is a conjugative or synthetic addition of a

PHARMACOLOGY INTRODUCTION

2497
large, polar molecule that renders the drug
adults. In those instances in which
water soluble and an1enable to renal
metabolic capacity has been demonstrated
excretion.

to be less, postnatal development in the

Four possible sequelae follow phase I
liver appears to be biphasic, consisting of a
metabolism: 1) inactivation (eg, most
rapid and nearly linear increase in activity

NSAIDs); 2) activation from a "pro-drng" to during the first 3-4 wk, followed by slower

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the active form of the chug ( eg, enalap1il to
development up to the tenth week
enalaprilat); 3) modification of activity, ie,
postpartum. In older animals, decreases
fonnation of active metabolites that may be
in hepatic mass, hepatic blood flow, and
characterized by activity greater than ( eg,
drng-metabolizing enzyme activity should
tran1adol), less than (eg, diazepam), or equal lead to longer closing intervals, and for to that of the parent compound; and 4)

drugs characterized by first-pass metaboformation of toxic met.abolites, which is lism, to lower oral doses.

generally due to direct cell damage ( eg,

Many disease states impair the nom1al
acetaminophen). In some instances the
activity of the hepatic clrng-metabolizing
toxic metabolite acts as an antigen, causing
enzyn1e systems, which in tum decreases
immune-mediated toxicity (eg, sulfonaclearance and thus prolongs the half-lives of nudes). Because phase II drug metabolism
many ch·ugs. Hepatotoxicity, acute hepatitis,
almost exclusively inactivates drngs (the
or other extensive liver lesions invaiiably
notable exception being some acetylated
depress enzyn1e activity. Evidence of
and methylated drngs), it often protects the
decreased plasma alb1m1in as a result of
organ of metabolism from chug-induced
hepatic disease generally indicates that
toxicity. This is particularly true with the
hepatic drug metabolism will likewise be
addition of glut,athione, which scavenges
decreased. Hypothyroidism tends to
oxygen radicals; in tl1e face of drug toxicity,
decrease, and hyperthyroidism increase

N-acetylcysteine will increase intra.cellular
drug-metabolizing enzyme activity.

glutatluone. Multiple isofom1s of phase II

Pharrnacogenon1ics refers to tl1e study of
drug-metabolizing enzymes exist. Glucuronthe genetic basis for differential response to ide (the addition of which is catalyzed by
drugs. Differences in the duration of action
glucuronide transferase) is the most
of drugs in vaiious species frequently can be
common phase II reaction; cats are deficient
attributed to differences in their rates of
in some, but not all, glucuronyl transferases.

biotransformation. Species variations in

Other important phase II enzymes include
drug metabolism are common. CYP450 3A4
sulfation ( deficient in swine), acetylation
is responsible for the broadest substrate

( deficient in clogs), and methylation. Amino
activity in people, but tlus may not be true
acid conjugations are particularly in1portant
in aiumals and certainly may vary among
in avian species.

species.

Phase I chug metabolism is largely, but

Differences in content and activity of CYP
not exclusively, accomplished by hemeenzymes among ages, genders, and species containing enzymes referred to as
are likely to play a role in differences to
cytochrome P450 (CYP450). More tl1an 20
response to drugs. Polyn1orphisms an10ng
superfanulies have been identified, with
the breeds can result in "poor" versus
some being specific for some ch·ug or chug

"efficient" metabolizers, with the fonner
classes but others characte1izecl by broad
predisposed to chug toxicity because of
substrate specificity. Among the major
decreased metabolism. Such variants for
superfan1ilies are CYP3A, which in people
certain enzyn1es have been described in
has been demonstrated to be responsible
people as being responsible for potentially
for the larger proportion of drug metabolethal differences in drug metabolism.

lism. Others imp01tant to drug metabolism

Several other factors impact the rate and
are CYP2C and CYP2D. CYP enzymes are
extent of drug metabolism. Drug interacresponsible for synthesis ( eg, adrenal tions may reflect induction ( eg, phenobarbisteroids, fatty acids) and metabolism of tal, rifa.mpin, griseofulvin) or inhibition (eg,
many endogenous compounds.

chloramphe11icol, cimetidine, imidazole

Drug metabolism has largely been
antiii.mgals) of CYP enzymes, with tl1e
considered to be negligible in early life,
impact varying an1ong isoenzymes and the
with neonates being less able to elinunate
sequelae of drug metabolism. Nutritional
lipid-soluble ch·ugs than adults; dosing
state and disease ( especially hepatic
intervals should be prolonged in such
clisease) can also impact clrng metabolism.

instances. However, evidence is emerging

The liver is not the only site of CYP450
that some pediatric animals may have
activity, with sanctuaiies and portals of
increased rather than decreased metabolic
entry being exan1ples of sites where CYP
capacity for some drugs compared with
activity can alter several aspects of ADME.

2498

PHARMACOLOGY INTRODUCTION

In addition to differences in CYP450
plasma proteins usually does not hinder
enzymes, differential handling of enantiotubular excretion of drugs. Transpo1t mers is increasingly recognized among
proteins exist for weak acids (an.ions),
species. Enantiomers are mirror images of
bases (cations), or organic compounds.

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drug molecules that result when groups of

Most (passive) reabsorption of non.ionized,
atoms rotate around a center or "chiral"

lipid-soluble drugs occurs as urine is
carbon. Generally, such compounds are
concentrated in the distal and collecting
sold as racemic mixtures (50:50 of each
tubules. Acidification or alkalinization of
isomer); however, the body frequently
the urine may alter the rate of excretion of
handles each stereoisomer differentially,
some drugs because of ion trapping in the
witl1 differences also being seen among
tubular fluid.

species. Many cardiac drugs and NSAlDs

Concurrent administration of eitl1er
exist as racemic mixtures of enantiomers.

acidic or basic drugs that are substrates

This must be remembered when either
for car1ie1°mediated secretion processes
dosages or withdrawal times are extrapoprolongs the elimination of the drug that lated from one species to another. However,
has the lesser affinity for the can·ier sites,
some drugs are sold only as one isomer or

Urns increasing its dtu-ation of action.

the other, with the name often reflecting as

Among the more in1po1tant factors
such ( eg, levetiracetam, dexrnedetornidine,
impacting renal excretion is renal or cardiac
esomeprazole). Species differences have
disease. Decreased renal blood flow will
been better documented for phase ll
result in a proportional decrease in renal
metabolism. Among the more important
excretion. However, renal disease may
phase II reactions and the species in which
also be accompanied by changes in the
the reactions are deficient are glucuronidametabolic capacity of the kidneys and tion (cats), glutathione transferase
production of toxins that will compete with

(impo1tant for scavenging potentially toxic
drug for protein-binding sites. Changes in
metabolites), sulfation (swine), and
acid-base balance may also influence urine
acetylation (dogs).

pH.

Drugs and their metabolites may also be
excreted either passively or actively by

Drug Excretion
hepatocytes into the bile canalicu.li and,

The body can clear itself of drugs either
ultimately, into the duodenwn in the bile.

by metabolism or excretion. Excretion

Generally, biliary excretion occurs for drugs
irreversibly removes drugs or metabolites
with molecular weights tl1at exceed 600
from the body. The kidneys are the p1incipal
daltons. Biliary excretion is a relatively slow
organ of excretion, but the liver, GI tract,
process. Further, many drugs excreted in
and lungs also may play impq1tant roles.

bile as glucuronide conjugates may become

Milk, saliva, and sweat are usually of less
unconjugated by intestinal microflora.

importance, although the presence of an

Released drug can be reabsorbed into the
active drug in milk may affect nursing young systemic circulation, resulting in "enteroheand contributes to milk discard times.

patic circulation." Such recirculation often

Renal excretion of foreign compounds
accounts for prolonged half-lives of drugs
is accomplished either by glomerular
that are prin1arily excreted in bile.

filtration, passive diffusion into and out

Impairment of the excretory functions of

(eg, resorption) of the tubular lun1en, and
the hepatocytes or obstruction qf bile flow
carrie1°mediated secretion ( eg, active
due to any cause interferes with the biliary
transport or facilitated diffusion).

excretion of drugs. Dose or interval should

Among the more important factors
then be adjusted accordingly.

detennining renal excretion is renal blood

The otl1er routes of excretion are of
flow, which in tum is influenced by cardiac
lesser clinical in1portance. Many drugs are
output. Glomerular filtration in particular,
excreted in tl1e feces either because of
but also carrier-mediated transport, is
limited oral absorption or diffusion directly
influenced by changes in cardiac output.

into the GI tract. The ruminoreticulwn can

Drugs that impact renal blood flow ( eg,
act as a drug reservoir because of ion
angiotensin-converting enzyme inhibitors)

trapping or can remove a drug because of
can also impact renal clearance.

microbial metabolism. The tracheobron

Only w1bound molecules <66,000 daltons
clual tree also may be a potential avenue
are readily filtered through the glomerular
of excretion, as is alveolar elimination of
membranes into the tubular lun1en. Most
inhalant anesthetics. The main factors
active tubular secretion of drugs into
governing elinlination by this route are the
tubules (renal exe1tion) occurs in the
same as those deteffilining the uptake of
proximal convoluted tubule. Binding to
inhalant anesthetics-the concentrations in

PHARMACOLOGY INTRODUCTION

2499
plasma and alveolar air and the blood/gas
decline in plasma drug concentrations
partition coefficient. The man1mary and
initially is rapid, but once distribution
salivary glands excrete drugs by nonionic
reaches a "pseudo" equilibrium such that
passive diffusion. The salivary route of
the amount of drug moving into tissues

VetBooks.ir
excretion is important in ruminants because
equals that moving back into plasma,
they secrete such voluminous an1ounts of
plasma drug concentration will decline
alkaline saliva, although such drugs are
only because of elimination from the body
likely to enter the GI tract.

(metabolism and excretion). Each drug
movement is "first order," meaning a

PHARMACOKINETICS
constant fraction or percentage (rather than
amount) moves per unit time. As such, the

Predicting how a drug behaves in the body
tin1e course of the drug in plasma must be
can bP. accomplished through mathematical
plotted sernilogarithmically (y = log plasma
modeling of the time course of the drug in
drug concentration, x = time). The result
the body, or pharmacokinetics. Simplistiwill be a decline in plasma drug concentracally, pharmacokinetics describe what the tions that can be "fitted" by two lines: the body does to the drug, whereas pharmacofirst line, representing distribution and dynamics describe what the drug does to
eli1nination, which declines very rapidly
the body. Pharmacokinetics are determined

( steep slope), followed by a second
by following changes in plasma drug

"terminal" line, with a flatter slope because concentrations after a dose of the drug is
it represents elin1ination only. If the
administered at least via the desired route
terminal line is drawn back to the y-axis,
and ideally also after IV administration
the Y intercept represents the plasma drug

(100".,(, bioavailability). The tin1e course of concentration after distribution has reached
plasma drug concentrations is mathematipseudoequilibrium ("B"). The slope of this cally "modeled" such that physiologic
tenninal line is the elin1ination "rate
events in1pacting the changes in drug
constant," k,,, and from it is derived the
concentration might be detennined. Most
elinlination half-life, t112. The line that
pharmacokinetic studies are conducted in
describes distribution also is characterized
healthy animals, yet dosing regimens should by a Y intercept (the drug concentration in be individualized to adjust for physiologic
the "central" compartment, or "A") and a (age, gender, species, and breed), pharma

"distribution" rate constant ( often referred cologic ( drug interactions), or pathologic
to as a or k,i); it is from this rate constant

( eg, renal or hepatic disease) differences
that a distribution half-life can be deteror for animals receiving multiple drugs.

mined. Once the curve is mathematically

The phannacodynainic response to a
described by slopes and Y intercepts, given
drug generally reflects the nun1ber of
any time (t) point after the drug is adminisreceptors with which the drug interacts tered, the an10unt of drug in the body or the

( drug-receptor theory). In most instances,
plasma drug concentration (C ) can then be
tissue drug concentrations parallel plasma
p
predicted (C ) = Ae·at + Be-kt in which e is
drug concentrations.

p
the natural log. From this data, clinically

After intravenous administration, the
relevant paraineters that influence the
most relevant phannacoki.netic parameters
dosing regimen are then detemlined.

that describe a drug and provide a basis for
the dosing regimen ai·e the apparent volume
of distribution and the plasma clearance,

Apparent Volume of Distribution
both of which detennine the elimination

If both the dose (mg/kg) and the drug
rate constant and elimination half-life.

concentration in plasma (the Y intercept of

Additional paraineters include the
the temlinal component of the plasma drug
distribution rate constant and half-life and,
concentration [PDC] versus time curve, or
if the drug is also given orally, the absorp

"B") are known, then an "apparent" volun1e tion rate constant and half-life.

of distribution cai1 be calculated from Vc1 =

After a drug is administered by rapid IV
dose/PDC. This theoretical volume

( eg, bolus) injection, the drug will be
describes the volun1e to which the drug
immediately distributed to the "central"

must be dist1ibuted if the concentration
vascular compaitment, which includes
in plasma represents the concentration
highly perfused organs. Also immediately,
throughout the body (ie, distribution has
plasma drug concentrations decline for two
reached equilibrium). The term "apparent"

reasons: distribution of drug from plasma
underscores the fact that where the drug is
into tissues and back, and elimination from
distributed caru10t be determined from V
the body because of irreversible removal
d;
only that it goes somewhere. The pharma

(ie, metabolism or excretion). As such, the
cokinetic measure used to indicate the

2500

PHARMACOLOGY INTRODUCTION
pattern of distribution of a drug in plasma

However, a nwnber of clinically significant
and in the different tissues, as well as the
factors can influence tl1e Vc1, including age
size of the compartment into which a drug

(larger in neonates and pediatlics, smaller
would seem to have distiibuted in relation
in geriati:ics); ftmctional status of the
to its concentration in plasma, is lrnown as
kidneys (decreased with dehydration), liver

VetBooks.ir
the apparent volume of distiibution CVc1). It

(increased with edema), and heart; fluid
is usually reported as liters per kilogram
accumulations; concentration of plasma

(Ilkg) and is detenninecl by measuring peak
proteins (influencing unbound drug only);
plasma drug concentrations after distribuacid-base status (particularly if ion ti·apping tion has reached equilibrium for a drug
causes tl1e drug to accumulate in tissues);
administered IV. That concentration is
inflammatory processes or necrosis; and
compared with the IV dose that was given:

any other causes for alteration in the degree

V" = dose/PDC. For exan1ple, if 12 mg/kg
of plasma-protein binding.

of phenobarbital is given, and the resulting PDC after distribution has occurred is 20 mg/L, then the apparent volume

Drug Clearance
to which phenobarbital is disttibuted

As soon as a drug reaches the systemic

CVc1) = (12 mg/kg/20 mg/L) or 0.6 Ilkg.

circulation, it in1mediately begins to be

The V" is useful for three reasons. First,
cleared from plasma. Clearance is the
and perhaps most importantly, it can be used
volume of blood from which a drug is
to calculate a close if tl1e target PDC is
irreversibly eliminated, or cleared. Plasma
known: dose = V rl x target PDC. For example, is most commonly sampled; however, if the V" of phenobarbital is 0.6 Ilkg, and the plasma clearance represents the sum
target concentration of phenobarbital in a
clearances by all organs. If the drug is
drug-naive anin1al is 10 mg/L, the IV dose
cleared by only a single organ, then plasma
would be 10 mg/L x 0.6 Ilkg or 6 mg/kg.

clearance is the clearance of that organ.

Second, if the PDC at any time after the dose

Clearance is a volume and, as such, its units
is known, the V" can be used to calculate how are volume/mass/time ( eg, ml/kg/min). An much drug is left in the body. Finally, tl1e V"

alternative definition of clearance is tl1e
can be used to predict the relative ability
volun1e of plasma tl1at would contain the
of the drug to distlibute to different body
amount of drug excreted per unit time; this
compartinents: if the drug is limited to the
definition demonstrates tl1e link between
extracellular compartinent (interstitial fluid,
volwne of distribution (V") and clearance: if
plasma), as is typical of water-soluble drugs,
the elimination rate constant is known, it
this represents 20%-30% of the body weight,
describes the fraction of tl1e V" cleared and,
and the V" of such a drug should be <0.3 Ilkg.

together, they can be used to calculate

Lipid-soluble drugs are generally able to
clearance (CL) from the PDC vs tin1e curve:

penetrate cell membranes.and thus are

CL= V" x k0/tin1e (min). As such, like V,,,
distlibuted to both extracellular and

CL directly influences k0,, ie, rate at which
intracellular fluid, which represents -600,i, of
drug is eliminated from tl1e body: as
the body weight. Such drugs are generally

CL increases, kc, becomes more steep.

characterized by a V" >0.6 Ilkg. Some drugs

Clearance is independent of tl1e Vc1 of a drug
are limited to the plasma compartment and
and thus the concentration of drug in the
do not distlibute well. An exan1ple would be
blood; no matter how much drug is in Lhe
a dn1g very tightly bound to plasma proteins;
blood, ilie same volume will be cleared per
for such drugs, the V" approxiniates the size
wlittime.

of the blood compartinent, or >0.1 Ukg.

The two major organs responsible for

However, as the drug is freed from ilie
clearance are the liver and kidneys. Once
protein, it will leave the plasma compartinent a drug is metabolized, it is irreversibly and distribute into tissues. Many drugs are
eliminated from ilie body. Its metabolites,
characte1ized by a V" that exceeds the body
however, must be excreted (usually by the
weight of ilie animal (ie, > l Ukg). For
kidneys). Hepatic clearance is defined as
example, the mean digoxin V" in clogs is
the volwne of plasma totally cleared per

13 Ukg. This points out tliat tl1e basis to
unit time as blood passes through the liver.

detennine V" is PDC: if the drug leaves tl1e

The rate of hepatic clearance depends on
plasma, regardless of where it goes, tl1e V"

drug delivery to the liver, ie, blood flow (Q)

will increase. For digoxin, the drug binds to
and the exti·action (E) ratio of the drug, or
cardiac tissue; however, this is known only
fraction of the drug removed as it passes
because follow-up studies demonstrated as
through the liver. Extraction, in turn, is
such.

determined by ilie intrinsic clearance (meta

The v. of a drug is usually constant over
bolic capacity) of the liver. Drugs cleared by
a wide close range for a given species.

the liver fall into two major categmies.

PHARMACOLOGY INTRODUCTION

2501

"Flow-limited" drugs are extracted so
elimination, component of the PDC vs time
rapidly that Q becomes the limiting factor
curve. A "hybrid" parameter, k01 is impacted of hepatic clearance. Binding to plasma
by both CL and V ct· CL determines the
proteins will not influence clearance of
decline in PDC; thus, the greater the volume
such drugs. In contrast, the rate-limiting
of drug cleared, the steeper the slope, or k.,.

step of"capacity-limitecl" drugs is intrinsic The impact ofVd on half-life reflects its

VetBooks.ir
clearance, ie, the metabolic capacity of the
effect on PDC: a larger V d means less drug is
liver. For such drugs, binding to serum
in the volume of blood cleared by the liver
proteins will decrease the rate of clearance.

or kidneys. As such, the rate of elimination

As such, highly protein-bound drugs are
declines as Vd increases, resulting in an
refe1Tecl to as "capacity limited, binding
inverse relationship. The elimination
sensitive" as opposed to drugs not highly
half-life of a drug is the time that lapses as
protein bound and thus "capacity limited,

PDC declines by 50%. It is calculated from
binding insensitive."

the slope of the line k.,: t"2 = 0.693/k01• The Hepatic disease differentially impacts
relationship between k., and half-life reflects
flow- and capacity-limited drugs. Hepatic
the fact that half-life becomes run of the
clearance of flow-limited drugs will
slope (t,-t1) as C, declines by 500A, (ie, C/C2 =
markedly decrease with changes in hepatic

2). The natural log of 2 = 0.693. Because tm
flow such as might occur with portosysis the inverse of k.,, then t"2 is directly temic shunting. When administered orally,
proportional to Vd Oarger Vd results in a
such drugs are normally characterized by
longer half-life) and inversely propo1tional
a high first-pass metabolism and reduced
to CL. Note that CL and Vd can be prooral bioavailability. With portosystemic fow1clly altered, yet t, 12 may not change. For shunting, oral bioavailability can markedly
example, in an animal dehydrated because
increase and, as such, oral closes must be
of renal dysfunction, CL may be decreased
decreased in proportion to the shtmtecl
by 50%, doubling t112• However, if the animal
blood. Changes in hepatic mass and
is markedly clehyclratecl, then V., will
function will impact capacity-limited drugs.

decrease because of contraction of extracel

In general, if liver disease has negatively
lular fluid voltune. Because more drug is in
impacted semm albumin and BUN, the
each mL of blood cleared by tl1e kidney, the
intrinsic metabolic capacity of the liver
san1e an10unt of drug may be elin1inatecl,
is also likely to be negatively impacted.

and as such k.1 or t"2 may not change.

However, if protein-binding decreases for

The elin1ination half-life determines the
a highly protein-bound drug such that more
time to steady-state ( see below) and the
of the drug is unbound, hepatic clearance
time for a drug to be elin1inated from tl1e
may not be as negatively impacted.

body once drug administration is discontin

Renal clearance is defined as the volume
ued. Once a drug is discontinued, 500A, of the
of plasma totally cleared of a drug per unit
drug is eliminated in one half-life, 75% in the
time (eg,l min) during passage through the
second (half of 500Ai), 87.5% in the third, and
kidneys. The renal clearance of clmgs
so on. For practical purposes, most drug is
depends primarily on renal blood flow but
eliminated by 3-5 half-lives. The t"2 along
also is in1pacted by urine pH, extent of
with tolerances determines withdrawal or
plasma-protein binding, urine concentrating milk discard times in food anin1als. The ability, and concomitant use of certain
relationsl1ip between closing interval and
drugs. Serum creatinine or serun1 creatinine
elin1ination half-life also determines
clearance can be used to assess changes in
whether a drug will fluctuate or acctm1ulate
renal clearance as renal function declines.

during a closing interval.

Either the close or interval can be proportionately modified. For drugs with a short Single-dose Concentration Curves
half-life, intervals are more appropriately

After Extravascular Administration:

prolonged ( compared with decreasing

When a drug is adn1inisterecl by an
close) as semm creatinine increases; for
extravascular route, plasma drug concendrugs that acctm1ulate because of a long trations rise until a peak or maximum drug
half-W"e, the close or interval might be
concentration (C,rnc,) is reached. Once the
propo1tionately decreased or prolonged,
drug enters circulation, it is subjected
respectively.

immediately and simultaneously to
distribution, metabolism, and excretion.

Elimination Rate Constant: Among the

The plasma drug concentration vs time
most commonly cited phannacokinetic
curve after extravascular administration
paran1eters is the elin1ination half-life. It is
has an additional Y intercept and slope, with
cle1ivecl from the elimination rate constant,
the slope reflecting the rate constant of
k.,, which is the slope of the tern1inal, or
absorption, !<,.. The absorption half-life is the

2502

PHAkMACOLOGY INTRODUCTION
time that elapses as 500A, of the drug is
of tl1e d!ug remains in tl1e body when tl1e
absorbed into the system. Absorption genernext dose is given. Such drugs will begin ally is sufficiently slow that drug distributo accumulate witl1 tl1e first dose and tion is generally "masked" by the absorption will continue to do so until a "steady state"

phase. As such, as plasma drug concentraequilibriunl is reached such tl1at tl1e an10unt VetBooks.ir
tions decline after Cmax is reached, the slope
of drug elinu.nated dming each dosing
generally reflects k01
interval is equivalent to tl1e amount of cl.rug

.

The tem1 "bioavailability" is used to
ad!ni.nistered during that same interval. The
express the rate and extent of absorption
accmnulation ratio describes tl1e magnitude
of a drug (see above).

of increase of eit11er Cmax or C"';" at steady state compared witl1 tl1e first dose. The

Steady State Plasma Concentration
longer tl1e half-life compared witl1 tl1e dosing

(Repeated Administration or Con
interval, the greater tl1e accwnulation ratio.

stant IV Infusion): In some cases, the

The time to steady state, regardless of tl1e
desired therapeutic effect of a drug is
drug or dose is 3-5 drug elinu.nation halfproduced with a single dose. However, to lives. However, ad!ninistration must occur
achieve a satisfactory response, it is
witl1 tl1e san1e preparation at tl1e same dosing
frequently necessary to maintain drug
regi.n1en. In such cases, 50% of t11e plateau
concentrations in the therapeutic range for a or steady-state concentration will be reached longer time. Ratl1er than administering large
in one t,r2, 75%at two t,,2, 87.6%at three t,r2,
doses, which could result in potentially
and 93.6% at four t,r2. As witl1 d!ug elin1i.natoxic plasma drug concentrations, multiple tion, for practical pw-poses, steady state is
dosing occurs at regular, safer intervals. For
achieved by 3-5 half-lives. Response to tl1e
drugs witl1 a very short half-life, the drug
drug, whetl1er efficacy or toxicity, cannot
may be administered through a catl1eter
be assessed until steady state is reached.

as a constant-rate infusion, which is

Because tl1e amom1t of drug in tl1e body is
essentially continuous IV delivery. The rate
large compared witl1 each dose, manipulating
of administration depends on tl1e amount of
plasma drug concentrations for such drugs
fluctuation in drug concentration that can
is difficult, because changes require dosing
occur during a dosing interval, which in tum
for 3-5 half-lives at tl1e new dose.

is determined by tl1e relationship between

If tl1e time to reach steady state, and thus
t1t2 and tl1e dosing interval, T.

time to therapeutic effect, is unacceptable,

If a drug is administered at an interval
steady-state plasma d!ug concentrations
substantively longer tl1an its half-life, most of
may be acl1ieved more rapidly by adnu.nistl1e drug will be eliminated during each tration of a loading dose or doses (dose= V"

dosing interval. As such, little drug remains
x target concentration; if the drug is given
witl1 tl1e subsequent dose, and plasma drug
orally, dose = (V jF) x target concentration.

concentrations will fluctuate CC.m, to Cm;,,)

However, tile drug is not at steady state but
during tl1e dosing interval. For exan1ple, if a
only at steady state concentrations. If tl1e
drug witl1 a 4-hr half-life is administered every maintenance dose does not maintain what 12 Ju·, 87.5% oftl1e drug will be eliminated
tl1e loading dose achieved, tl1en as steady
during each dosing interval. Willi eaclrdose,
state at the maintenance dose is reached,
tl1ere is a risk of drug concentrations
plasma drug concentrations may increase
becoming subtl1erapeutic; increasing tl1e
to toxicity or decline to a subtherapeutic
dose will result in a small increase i.n Cm;n
concentration. Drugs with very shprt
but may substantially increase Cmax, tl1us
half-lives are often administered by
increasing tl1e risk of toxicity. A more
constant-rate infusions in animals in critical
appropriate response would be to decrease
condition; in such cases, tl1e interval is
tl1e dosing interval. However, tl1is may be
infinitely short compai-ed witl1 tl1e half-life,
necessary only if drug efficacy depends on
and the drug will accumulate until steady
tl1e presence of tl1e drug. For exan1ple, tl1is
state is reached. The rate of infusion (mcg/
degree of fluctuation may be acceptable for
kg/min) is equal to the CL (mUnun/kg) x
a concentration-dependent antinucrobial.

target concentration (mcg/mL); a loading

However, if tl1e drug is an anticonvulsant,
dose should be given if the time to steady
tl1e risk of seizures increases just before tl1e
state is w1acceptably long.

next dose. If tl1e drug is tin1e--<lependent,
drug concentrations may drop below tl1e

DRUG ACTION AND
minimum inhibitory concentration oftl1e

PHARMACODYNAMICS
infecting nucrobc. In contrast to drugs with
a short half-life, drugs witl1 a long half-life

Pharmacodynarnics is the study of the
compared with tl1e dosing interval will
biochemical and physiologic effects of
accumulate witl1 each dose, because much
drugs and their mechanisms of action on tl1e

PHARMACOLOGY INTRODUCTION

2503
body or on microorganisms and other
given by the Hill equation, which can be
parasites within or on the body. It conwritten as:

siders both drug action, which refers to
the initial consequence of a drug-receptor

E =Emax X C
interaction, and drug effect, which refe

VetBooks.ir
rs

EC50 + C
to the subsequent effects. The drug action
of digoxin, for example, is inhibition of
in wllich E is the effect obse1ved at
membrane Na
concentration C, E

+fK+-ATPase; the drug effect

"'"" is the maximal
is augmentation of cardiac contractility. In
response that can be produced by the drug
this example, the clinical response might

(efficacy), EC50 is the concentration of d!ug
comprise improved exercise tolerance.

that produces 5QOA, of maximal effect

Not all drugs exert their pham1acologic

(potency), and the Hill coefficient n is the
actions via receptor-mediated mechanisms.

slope of the log10 concentration-effect

The action of some drugs-including
relationship (sensitivity).

inhalation anesthetic agents, osmotic

The above equation describes a
diuretics, purgatives, antiseptics, antacids,
rectangular hyperbola when response
chelating agents, and urinary acidifying

(y-axis) is plotted against concentration
and alkalinizing agents-is attributed to

(x-axis). However, dose- or concentrationtheir chemical action or physicochemical response data is generally plotted as drug
properties. Certain cancer and antiviral
effect (y-axis) against log10 dose or
chemotherapeutic agents, which are
concentration (x-axis). The transfo1mation
analogues of pyrimidine and purine bases,
yields a sigmoidal curve that allows the
elicit their effects when they are incorpopotency of different d!ugs to be readily rated into nucleic acids and serve as
compared. In addition, the effect of drugs
substrates for DNA or RNA synthesis. The
used at therapeutic concentrations
effect of most d!ugs, however, results from
commonly falls on the portion of the
their interactions with receptors. These
sigmoidal curve that is approximately .

interactions and the resulting conformalinear ie between 2QOA, and SQOA, of maximal tional changes in the receptor initiate
effect. This makes for easier interpretation
biochemical and physiologic changes that
of the plotted data.

characterize the drug's response.

Agonists and Antagonists

Drug Concentration and Effect

An agonist is a drug that binds to receptors

Drug therapy is intended to result in a
and thereby alters (stabilizes) the proporparticular phannacologic response of tion of receptors in the active conformation,
desired intensity and duration while
resulting in a biologic response. A full
avoiding adverse drug reactions. The
agonist results in a maximal response by
relationship between the ad!ninistered
occupying all or a fraction of receptors. A
dose and the clinical response has been
partial agonist results in less than a maximal
investigated for some d.iugs using a
response even when the d.iug occupies all of
phannacokinetidpharmacodynanlic (PK/
the receptors.

PD) modeling approach, which is generally

There are four types of drug antagonism.

based on the plasma concentration

Chemical antagonism involves chenlical
response relationship. For other drugs, a
interaction between a drug and either a
simpler relationship between the concentrachemical or another drug leading to a tion and effect in an idealized in vitro system
reduced or nil response. Physiologic
is modeled mathematically to conceptualize
antagonism occurs when two drugs acting
receptor occupancy and drug response. The
on different receptors and pathways exert
model assumes that the drug interacts
opposing actions on the san1e physiologic
reversibly with its receptor and produces
system. Pharmacokinetic antagonjsm is
an effect proportional to the number of
the result of one drng suppressing the effect
receptors occupied, up to a maxin1al effect
of a second drug by reducing its absorption,
when all receptors are occupied. The
altering its distribution, or increasing its
reaction scheme for the model is:

rate of elimination. Pharmacologic
antagonism occurs when the antagonist
inhibits the effect of a full or partial agonist
k,
by acting on the san1e pathway but not

Drug (D) + Receptor (R) ....:; DR -> Effect necessarily on the same receptor.

k,

Pharmacologic antagonists comprise
in which k, and k, are rate constants.

three subcategories. A reversible

The relationship between effect and the
competitive antagonist results in
concentration of free d.iug for the model is
inhibition that can be overcome by

2504

PHARMACOLOGY INTRODUCTION
increasing the concentration of agonist. The
profound changes in potency. For example
presence of a reversible competitive
the substitution of a proton by a methyl
antagonist causes a parallel rightward shift
group accounts for codeine being -1,000
of the log concentration-effect cmve of the
times less potent than morphine in its action

�gonist without altering Emax or EC50. An
on opioid receptors.

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rrreversible competitive antagonist also
mvolves_ competition between agonist and

Signal Transduction and Drug Action
antagorust for the same receptors, but
stronger binding forces prevent the effect of

Most receptors are proteins. The best
the antagonist being fully reversed even at
characterized of these are regulatory
high agonist concentrations. The p�esence
proteins, enzymes, transport proteins, and
of an irreversible competitive antagonist
structural protems. Nucleic acids are also
causes a rightward shift of the log concenimportant drug receptors, particularly for tration-effect cmve of the agonist that
cancer chemotherapeutic agents.

generally displays decreased slope and

The receptors for several neurotransmitr
ters modulate the opening and closing of ion

�duced maximum effect. A noncompetitive antagonist inhibits agonist activity by charmels through ligand gating or voltage
blocking one of the sequential reactions
gatmg. The nicotinic acetylcholine receptor
between receptor activation and the

1s an example of a ligand-gated receptor; it
pharmacologic response. Noncompetitive
allows Na• to flow down its concentration
antagonism is generally reversible but can
gradient into cells, resulting in depolarizabe irreversible. Noncompetitive antagonists t10n. Most clinically useful neuromuscular
and irreversible competitive antagonists
blocking drugs compete with acetylcholine
cause similar perturbations in the log
for the receptor but do not initiate
concentration-effect curve of agonists.

!on-channel opening. Other ligand-gated

Isolated tissue experiments are used to
wn charm els include the CNS receptors
distinguish the two subcategories, because
for the excitatory an1ino acids (glutamate
noncompetitive antagonists are generally
and aspartate ), the inhibitory amino acids
reversible.

('y-aminobutyric acid [GABA] and glycine),

Agonists, but not antagonists, elicit an
and certam serotonin (5-HT3) receptors.

effect even when they bind to the same site

The soditun charmel receptor is an exan1ple
on the same receptor. An explanation is
of a voltage-gated receptor; these are
provided by both structural and functional
present in the membranes of excitable
studies, which indicate that receptors exist
nerve, cardiac, and skeletal muscle cells. In
in at least two confom1ations, active and
the resting state, the Na•/K•-ATPase ptunp
inactive, and these are in equilibrium.

m these cells maintains an intracellular Na•

Because agonists have a higher affinity for
concentration much lower than that in the
the receptor's active confo1mation a"onists
extracellular environment. Membrane depodrive the equilibritun to the active �tate larization causes channel opening and a
thereby activating the receptor. Conve/sely,
transient influx of Na• ions, followed by
antagorusts have a higher affinity for the
mact1vatwn and return to the resting state.

receptor's inactive conformation antl push

The action of local anesthetics is due to
the equilibrium to the inactive state
their direct interaction with voltage-gated
producing no effect.

Na• channels.

The concept of spare receptors explains

Many transmembrane receptors are
a maximtun response being achieved when
linked to guanosine trip hosp hate binding
only a fraction of the total number of
protems, which activate second messenger
receptors is occupied. For exan1ple, an
systems. Two in1portant second messenger
action potential and maximal twitch of
systems are cyclic adenosine monophosmuscle fibers is elicited when 0.13% of the phate ( cAMP) and the phosphoinositides. In
total number of receptors at a skeletal
cAMP second messenger systems, binding
neuromuscular junction is simultaneously
of the ligand to the receptor increases or
activated. From a functional perspective,
decreases adenylyl cyclase activity, which
spare receptors are significant, because
m tum regulates the formation of cAMP
they increase both the sensitivity and speed
from adenosine ttiphosphate. The
of a tissue's responsiveness to a ligand.

activation of protein kinase A by cAMP
results in the phosphorylation of proteins
and a physiologic effect. From a therapeutic

Structure-Activity Relationships
standpoint, drug binding to 13-adrenergic,

Structure-activity relationships are
histanune H2, or dopa.mine D 1 receptors
exploited in drug design, because small
activates adenylyl cyclase, whereas binding
changes in chemical structure can produce
to rnuscarinic M2, a2-adrenergic, dopanline

PHARMACOLOGY INTRODUCTION

2505

D2, opiateµ and o, adenosine A1, or GABA
interfere with neurotransmission in
type B receptors inhibits adenylyl cyclase.

parasites. A case in point is macrocyclic

In phosphoinositide second messenger
lactones, which potentiate inhibitory
systems, membrane phosphatidylinositol
neurotransmission via GABA and gluta4,5-biphosphate is hydrolyzed to 1,4,5-trismate-gated chlorine channels (see VetBooks.ir
phosphate (IP3) and 1,2-diacylglycerol

ANTHELMINTICS, p 264 7).

(DAG) by activation of phospholipase C.

Both IP3 and DAG activate kinases, and in
the case of IP3, this involves the mobiliza

Drug Dose and Clinical Response
tion of calcium from intracellular stores.

To make rational therapeutic decisions, it is

The action of nw11erous drugs is due to
necessary to understand the fundamental
their interaction with receptors that rely
concepts linking drug doses to concentraon these second messengers, which tions to clinical responses. The concentrainclude a1-adrenergic, muscarinic M1
tion-response relationships for drugs may
or M2, serotonin 5-HT2, and thyrotropinbe graded or quanta!. A graded concentra
releasing hormone receptors.

tion-response curve can be constructed

Protein tyrosine kinase receptors are
for responses measured on a continuous
generally transrnembrane enzymes that
scale, eg, heart rate. Graded concentrationphosphorylate proteins exclusively on response curves relate the intensity of
tyrosine residues, rather than on serine or
response to the size of the close and, hence,
threonine residues. They include endocrine
are useful to characte1ize the actions of
hormone receptors for insulin and
drugs. A quanta! concentration
receptors for several growth hormones.

response curve can be constructed for

Intracellular receptors mediate the action
drugs that elicit an all-or-none response, eg,
of honnones such as glucocorticoids,
presence or absence of convulsions. For
estrogen, and thyrnid hormone and related
most drugs, the doses required to produce
drugs. The hormones, which regulate gene
a specified quanta! effect in a population
expression in the nucleus, are lipophilic
are log nonnally distributed, so that the
and freely diffuse through the cell memfrequency distribution of responses plotted brane to reach the receptor. Glucocorticoid
against log dose is a gaussian normal
receptors reside predominantly in the
distribution curve. The percentage of the
cytoplasm in an inactive fonn until they
population requiring a particular dose to
bind to the glucocorticoid steroid ligand.

exhibit the effect can be detem1ined from

This results in receptor activation and
this curve. When these data are plotted as
translocation to the nucleus, where the
a cwnulative frequency distribution, a
receptor interacts with specific DNA
sigmoidal dose-response curve is generated.

sequences. Unlike glucocorticoid receptors,

The equilibrium dissociation constant
the receptors for estrogen and thyroid
of the receptor-drug complex, K0, is the
hormone reside in the nucleus.

ratio of rate constants for the reverse (k2)

Intracellular receptors are also important
and forward (k1) reaction between the
in mediating the action of antimicrobial
drug and receptor and the drug-receptor
drugs, including the penicillins, sulfonacomplex (seep 2503). K0 is also the drug mides, trirnethoprirn, aminoglycosides,
concentration at which receptor occupancy
phenicols, macrolides, and fluoroquinois half of maxirnun1. Drugs with a high K0
lones. The mechanisms of action include

(low affinity) dissociate rapidly from
inhibition of bacterial protein synthesis,
receptors; conversely, drugs with a low K0
inhibition of cell wall synthesis, inhibition

(lligh affinity) dissociate slowly from
of enzymatic activity, alteration of cell
receptors. These effects impact the rate
membrane permeability, and blockade
at which biologic responses end.

of specific biochemical pathways.

Potency refers to tl1e concentration

Receptor-mediated mechanisms of action

(EC,,o) or close (ED50) of a drug required to
of several classes of anthelmintics are well
produce 500/o of the drug's maximal effect as
tmderstood. For example, the benzirnidadepicted by a graded dose-response curve.

zoles and pro-benzirnidazoles bind to

EC50 equals K0 when there is a linear
nematode tubulin, preventing its polymerrelationship between occupancy and ization dilling microtubular assembly and
response. Often, signal amplification occurs
thus disrupting cell division. Depletion
between receptor occupancy and response,
of ATP as the result of salicylanilides
which results in the EC50 for response being
uncoupling oxidative phosphorylation and
much less (ie, positioned to the left on the
the inhibition of enzynies in the glycolytic
x-axis of the log dose-response curve) than
pathway by benzene sulfonamides are other

K0 for receptor occupancy. Potency
examples. Several classes of anthelmintics
depends on both the affinity of a drug for its

2506

PHARMACOLOGY INTRODUCTION
receptor and the efficiency with which
drug-receptor interactions include
drug-receptor interaction is coupled to
electrostatic forces, van der Wa.al forces,
response. The dose of drug required to
and the forces associated with hydrogen
produce an effect is inversely related
bonds and hydrophobic bonds. Variation in
to potency. In general, low potency is
the strength of these forces, and therefore

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important only if it results in a need to
the thennal energy in the system, dete1°
administer the drug in large doses that are
mines the degree of association and
impractical. Quantal dose-response curves
dissociation of the drug and the receptor.

provide information on the potency of drugs Covalent binding of drug to receptor that is different from the information

( exemplified by fluoroquinolones acting on
derived from graded dose-response curves.

bacteria) leads to fonnation of an irrevers

In a quantal dose-response relationship, the
ible link.

ED50 is the dose at which 500Ai of individuals

The therapeutic index of a drug is the
exhibit the specified quanta! effect.

ratio of the dose that results in an undesired

The median inhibitory concentration,
effect to the dose that results in a desired
or IC50, is the concentration of an antagonist effect. The therapeutic index of a drug is that reduces a specified response to 500Ai of
usually defined as the ratio of LD50 to ED50
the maximal possible effect.

( median lethal and median effective doses,

Efficacy (also referred to as intrinsic
respectively, in 500Aiof individuals), which
activity) of a drug is the ability of the drug
indicates how selective the drug is in
to elicit a response when it binds to the
eliciting its desired effect. Values ofLD50
receptor. As discussed above, confom1aand ED50 for this purpose a.i·e derived from tional changes in receptors as a result of
quanta! dose-response curves generated in
drug occupancy initiate biochemical and
animal studies.

physiologic events that characterize the

The information obtained from dose- and
drug's response. In some tissues, agonists
concentration-response curves is critically
demonstrating high efficacy can result in a
important when choosing between drugs
maximal effect, even when only a small fracand when determining the dose to tion of the receptors is occupied (the
administer. A drug is chosen largely on the
concept of spare receptors is discussed
basis of its clinical effectiveness for a
above).

particular therapeutic indication. In this

Selectivity refers to a drug's ability to
context, the drug concentration at the
preferentially produce a particular effect
receptor ( determined by the pharmacokiand is related to the structural specificity netic properties of the drug) and the efficacy
of drug binding to receptors. For example,
of the drug-receptor complex are the
cyclooxygenase-2 (COX-2) preferential
primary determinants of a drug's clinical

NSAIDs demonstrate partial specificity for
effectiveness. The administered dose of a

COX-2, the inducible enzyme formed at sites drug, by comparison, depends to a greater of inflammation. By compa.iison, COX-2
extent on potency than on maximal efficacy.

selective NSAIDs are without significant

The maximal efficacy of the drug-recepeffect on COX-I, the constitutive enzyme tor complex to result in a graded effect is
that performs a range of physiologic

E,.,ax or I,.,ax on a graded dose-response
functions. For certain drugs, selectivity
curve. E,.,"" or I,.,"" is derived from a is species dependent. For exa.inple,
quantitative dose-response relationship for

S( + )-carprofen is COX-2 selective in dogs a single animal and varies a.inong individuand cats, nonselective of COX-I and COX-2
als. The extrapolation of this value of Emax
in horses, and COX-2 preferential in calves.

to a clinical case is only an estimate, but it

Specificity of drug action relates to the
facilitates a comparison of the maximal
number of different mechanisms involved.

efficacy of drugs that result in a specified

Exa.t11ples of specific drugs include atropine
effect by identical receptors. A drug's

( a muscarinic receptor antagonist),
potency (ie, EC50, ED50, or IC50) obtained
salbutarnol (a 132-adrenoceptor agonist), and from either graded or quantal dose-response cimetidine (an Hrreceptor antagonist). By
cwves is used to detem1ine the dose that
contrast, nonspecific drugs result in drug
should be administered. The slope of the
effects through several mechanisms of
graded dose-response curve (n in the Hill
action. For exa.t11ple, phenothiazine causes
equation, p 2507) provides information
blockade of D2-dopamine receptors,
concerning the dose range over which a
cx-adrenergic receptors, and muscarinic
drug elicits its effect. Other information
receptors.

concerning the selectivity of drug action

The affinity of a drug for a receptor
and the therapeutic index is also obtained
describes how avidly the drug binds to the
from the graded dose-response curve. When
receptor (ie, the KD). The chemical forces in
quantal effects are being considered,

PHARMACOLOGY INTRODUCTION

2507
information concerning pharmacologic
properties that define any drug, namely Emax
potency, selectivity of drug action, the
or Imax ( efficacy); ECw ( or ECM or EC00)

margin of safety, and the potential

(potency); and slope (n) in the Hill equation,
variability of responsiveness among
which indicates sensitivity and selectivity.

individuals is obtained from quanta!

PK/PD modeling permits breakpoint values

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dose-response ctuves.

to achieve a bacteriostatic or bactericidal
effect, or bacterial eradication to be

Pharmacodynamics of Antimicrobial
computed, which are used to optimize
efficacy and mini.Jnize resistance.

Drugs

The approach used to investigate the

Time-effect Relationships: The ability
pham1acodynamics of antimicrobial drugs
of cl.rugs to reach the receptor is detennined

( and parasiticides) differs from that of other by pharmacokinetic parameters that veterinary drugs on account of the need
characterize the absorption, distribution,
to address target pathogens that have
and clearance of a drug. There may not be
structure, biochemistry, and capacity for
a simple temporal correlation between
replication which are markedly dissin1ilar
plasma concentration of a drug and its
to those of their mammalian host. The
therapeutic effect. Plotting plasma
individual drugs within each group of
concentrations (x-axis) versus therapeutic
antimicrobial drugs differ in potency and in
effect (y-axis) in chronologic order displays
antimicrobial spectrum of activity. The minithe data as a loop for some drugs. This mum inhibitory concentration (MIC), which
phenomenon is referred to as hysteresis in
is the lowest concentration of drug that
the concentration-effect relationship. The
completely inhibits bacterial growth, is
effect of most drugs lag behind the plasma
detennined in vitro as a measure of
concentration. This results in a countersusceptibility of bacterial species and clockwise hysteresis loop. For example, the
strains to a given drug. Importantly, the

NSAID robenicoxib has prolonged local

MICw provides a measure of potency, EC,,o.

effects after blood concentrations have

Other surrogate markers of bacteriologic
decreased below effective levels. A
effect exist and include the mini.Jmm1
clockwise hysteresis loop is obse1vecl
bactericidal concentration (MBC), which is
for cocaine and pseucloephedrine when
the concentration of antimicrobial dmg that
tachyphylaxis develops (see below). The
produces a3-log-unit or 99.9"Ai reduction in
temporal correlation between plasma
bacterial count, postantibiotic effect, subconcentration and therapeutic effect also MIC postantibiotic effect, and tin1e-kill data.

varies for the different classes of antago

More recently, the application of PK/PD
nists. For instance, the extent and duration
principles to antimicrobial drug action
of action of a competitive antagonist
has led to PK/PD integration and PK/PD
depends on its concentration in plasma;
modeling. PK/PD integration brings
which depends (in part) on its rate of
together data from PK and PD studies. The
elimination. This requires that the close be
surrogate PK/PD index that best correlates
adjusted accordingly to maintain plasma
with efficacy for a given drug is selected
concentrations in the therapeutic range.

based on the drug's killing mechanism,

By contrast, the duration of action of
namely concentration dependent, time
an irreversible antagonist is relatively
dependent, or codependent (ie, both time
independent of its rate of elin1.ination and,
and concentration detennine outcome).

therefore, plasma concentration, and more

The PK/PD index selected for aminogylycodependent on the rate of turnover of sides, which act by concentration-dependreceptor molecules.

ent killing mechanisms, is Cma./MIC ratio

(Cmax is the maximwn plasma concentration

Down-regulation and Up-regulation
after administration of a drug by a
of Receptors: The density of most
nonvascular route); for [3-lactams, which
receptors is not constant with time, which
act by time-dependent killing mechanisms,
has important therapeutic implications.

it is T>MIC (T is the time for which plasma

Down-regulation of receptors may occur
concentration exceeds MIC, expressed as a
as a result of continual stin1ulation by an
percentage of the dosage interval); and for
agonist and manifests as tl1e development
fluoroquinolones, which act by concentraof tachyphylaxis, which demonstrates a tion-dependent killing mechan.isms, AUC/
clockwise hysteresis loop in the concentra

MIC ratio (AUC is the area under the plasma tion-effect relationship. Conversely, drug concentration-tin1e cwve) is selected.

additional receptors can be synthesized in

The objective of PK/PD modeling is to
response to chronic receptor antagonismdefine the three key pharmacodynamic a phenomenon known as up-regulation.

2508

PHARMACOLOGY INTRODUCTION

Because more receptors are now available,

Oral Route of Administration and
a hyperreactive response occurs when the

Dosage Forms
cell is exposed to an agonist.

The oral route of ad.ministration is fre

ROUTES OF ADMINISTRATION
quently used in botl1 companion at1cl food

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AND DOSAGE FORMS
animals. In clogs ru1cl cats, tablets, capsules,
solutions, and suspensions ru·e administered

A diverse range of dosage fonns and
orally; pastes ru·e also applied to the
delivery systems has been developed to
forelimbs of cats from which they a.re licked
provide for the care and welfare of animals.

at1cl ingested. In horses, solutions and

The development of dosage forms draws on
suspensions ru·e administered by nasogasthe discipline of biopharrnaceutics, which tric tubes, pastes ru·e applied to the tongue,
integrates an understanding of fonnulaand granules a.re added to rations for tions, dissolution, stability, and controlled
ingestion. The oral route of ad.ministration
release (pharmaceutics); absorption,
is the most widely used in cattle, pigs, and
distribution, metabolism, and excretion
poultry. Forn1ulations range from premixes

(pha.rmacokinetics, PK); concentrationru1cl drinking water additives to licks, pastes, effect relationships and drug-receptor
drenches, tablets, capsules, and boluses.

interactions (pha.rmacodynamics, PD); and

Oral dosage fonns a.re usually intended
treatment of the disease state (therapeufor systemic effects resulting from drug tics). Formulation of a dosage fonn typically absorption from the GI tract; however, some involves combining an active ingredient
oral suspensions, eg, kaolin, ru·e intended
and one or more excipients; the resultant
to produce local effects, at1d. these ru·e not
dosage form detem1ines the route of
absorbed.. Disadvantages of the oral route
administration and the clinical efficacy and
of administration include the relatively slow
safety of the drug. Optimization of drug
onset of action, the possibilities of irregular
doses is also critical to achieving clinical
absorption, the destruction of acid-labile
efficacy and safety. Increasingly, a PK/PD
drugs in the stomach, and tile wisuitability
mod.el that describes U1e drug response is
of this route for many high-moleculru·

U1e basis of dose optimization. The PK and
weight drugs. Oral dosage forms require

PD phases a.re linked by the premise that
careful phatrnaceutical forn1ulation.

free drug in the systemic circulation is in

Oral dosage fom1s comprise liquids
equilibrium with the receptors. The PD

(solutions, suspensions, emulsions, elixirs,
phase generally involves interaction of
and syrups), semisolids (pastes), and solids
the drug with a receptor, which triggers

(tablets, capsules, powders, granules,
post-receptor events and eventually leads
premixes, at1d medicated blocks). These
to a drug effect ( see p 2503).

dosage forms together with exrunples of

Drug delive1y strategies for veterinary
modified-release delivery systems for
formulations are complicated. by the
ruminants ru·e discussed below.

diversity of species and breeds treated,

A solution is a. mixture of two or more
the wide range in body sizes, different
components tllat form a single phase that is
husbandry practices, seasonal vruiations,
homogeneous down to tile molecular level.

cost constraints associated. with the value

Solutions offer several advantages over
of the anin1al being treated, the persistence
oilier dosage fonns. Compared with solid
of residues in food and fiber (seep 2518),
dosage fom1s, solutions are absorbed faster
and the level of convenience, among other
and generally cause less irritation of the GI
factors. Innovative solutions have been
mucosa. Moreover, phase sepru·ation on
developed to meet many of these challenges
storage is not a concern with solutions, as

( eg, the convenient dosing option offered
it may be for suspensions ru1d. emulsions.

by topical spot-on formulations to treat

The disaclvru1tages of solutions include
external and internal pru·asites on clogs and
susceptibility to microbial contamination
cats, the rnicroencapsulation of NSAIDs
at1d tile hydrolysis in aqueous solution of
as a way to mask taste when these agents
susceptible active ingredients. In addition,
ru·e acid.eel to the rations of horses). The
the taste of some drugs is more unpleasant
ru1atomy of the GI tract of rwninru1ts
when in solution. A range of additives is
presents unique opporl1.1nities for conused in the formulation of oral solutions, trolled-release drug clelive1y systems, and
including buffers, flavors, antioxidants, and
many such systems a.re on the mru·ket. For
preservatives. Oral solutions provide a
exrunple, controlled-release boluses have
convenient meat1s of dn1g administration
been developed. to deliver antimicrobials,
to neonates at1d young animals.

ru1thelmintics, production enhancers,

A suspension is a coarse dispersion of
nut1itional supplements, and other drugs.

insoluble drug patticles, generally with a

PHARMACOLOGY INTRODUCTION

2509
diameter> 1 µrn, in a liquid (usually
istic used to advantage to solubilize
aqueous) medium. Suspensions are usefi.Ll
medicinal agents. If the active ingredient is
to administer insoluble or poorly soluble
sensitive to moistw-e, it may be formulated
drugs or when the presence of a finely
as a flavored powder or granulation and
divided form of the material in the GI tract
reconstituted in water immediately before

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is required. An example of the latter is the
oral administration. Noru11edicated elixirs
treatment of"frothy bloat" with dimethyl
ai·e used as the vehicles for phai·maceutical
polysiloxanes, which relies on a dispersion
formulations.

of finely divided silica in the forestomach of

A syrup is a concentrated aqueous
rnminants. The taste of most drugs is less
solution of sugai· or a sugai· substitute with
noticeable in suspension than in solution,
or without flavoring agents and a waterbecause the drug is less soluble in suspensoluble drug. Sucrose is the most frequently sion. Particle size is an important detenniused sugar, and syrnps usually contain nant of the dissolution rate and bioavailabil600/o--800/c,. Syrups may also conta.in cosolity of drugs in suspension. In addition to the vents, solubilizing agents, thickeners, or
excipients described above for solutions,
stabilizers. Norunedicated syrups are used
suspensions include swfactants and thicas vehicles for water-soluble drugs.

kening agents. Surfactants wet the solid

A paste is a two-component semisolid in
paiticles, thereby enswing the pai1:icles
which drug is dispersed as a powder in an
disperse readily throughout the liquid.

aqueous or fatty base. The paii;icle size of

Thickening agents reduce the rate at
the active ingredient in pastes can be as
which particles settle to the bottom of

Jai·ge as 100 µrn. The vehicle containing tl1e
the container. Some settling is acceptable,
drug may be water; a polyhydroxy liquid
provided the sediment can be readily
such as glycerin, propylene glycol, or
dispersed when the container is shaken.

polyethylene glycol; a vegetable oil; or a

Redispersion of the suspension may not
mineral oil. Other fomrnlation excipients
be achievable if the sediment has packed
include thickening agents, cosolvents,
closely to fom1 a hard mass, a process
adsorbents, htunectants, and preservatives.

!mown as "caking."

The thickening agent may be a naturally

An emulsion is a system consisting of
occwTing material such as acacia or
two immiscible liquid phases, one of which
tragacanth, or a synthetic or chemically
is dispersed throughout the other in the
modified derivative such as xanthum gum
forn1 of fme droplets; droplet diaineter
or hydroxypropylmetl1yl cellulose. The
generally ranges from 0.1-100 µm. The two
degree of cohesiveness, plasticity, ai1d
phases of an emulsion are !mown as the
syTingeability of pastes is attributed to
dispersed phase and the continuous phase.

U1e thickening agent. It may be necessary

Emulsions ai·e inherently unstable ai1d are
to include a cosolvent to increase the
stabilized through the use of an emulsifying
solubility of the drug. Syneresis of pastes
agent, which prevents coalescence of tl1e
is a fom1 of instability in which the solid
dispersed droplets. Creaining, as occurs
ai1d liquid components of the formulation
with milk, also occw-s with phamiaceutical
separate over time; it is prevented by
emulsions. However, it is not a serious
including an adsorbent such as microcrysproblem because a unifo1m dispersion talline cellulose. A hW11ecta.nt ( eg, glycerin
returns upon shaking. Creanling is,
or propylene glycol) is used to prevent
nonetheless, w1desirable because it is
the paste that collects at the nozzle of the
associated with an increased likelihood of
dispenser from forn1ing a hard crust.

the droplets coalescing and the emulsion

Microbial growtl1 in the formulation is

"breaking." Other additives include buffers, inhibited using a preservative. It is critical
antioxidants, and prese1vatives. Emulsions
that pastes have a pleasant taste or ai·e
for oral administration are usually oil (the
tasteless and ai·e able to be used throughout
active ingredient) in water, ai1d they
a wide temperature rai1ge. Pastes are a
facilitate the administration of oily
popular dosage form to treat cats and
substances such as castor oil or liquid
horses and can be easily and safely
paraffin in a more palatable form.

administered by owners.

An elixir is a sweetened, usually

A tablet consists of one or more active
hydroalcoholic solution of a bitter or
ingredients and nun1erous excipients
nauseous drug intended for oral administraand may be a conventional tablet that is tion. The hydroalcoholic character of elixirs
swallowed whole, a chewable tablet, or a
allows, within lim.its, both water�soluble and modified-release tablet (these ai·e comalcohol-soluble medicinal substances to be monly refe1Ted to as modified-release
mainta.ined in solution. The proportion of
boluses when the unit size is large).

alcohol in elixirs vai·ies widely, a characte,�

Conventional and chewable tablets are

2510

PHARMACOLOGY INTRODUCTION
used to administer drugs to dogs and cats,
dosing. Granules and powders generally
whereas modified-release boluses are
behave sinlilarly; however, granules must
administered to cattle, sheep, and goats.

deaggregate before dissolution and

The physical and chemical stability of
absorption.

tablets is generally better than that of liquid

A premix is a solid dosage form in which

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dosage forms. The main disadvantages of
an active ingredient, such as a coccidiostat,
tablets are a relatively slow onset of action
production enhai1cer, or nutritional
because of the need to pass into the
supplement, is fonnulated with excipients.

intestine and then undergo disintegration

Premix products are mixed homogeneously
and dissolution before absorption across
with feed at rates ( when expressed on an
the gut wall, the low bioavailability of
active ingredient basis) that range from a
poorly water-soluble drugs or poorly
few milligrains to -200 g/ton of feed. They
absorbed drugs, and the local irritation of
are administered to poultry, pigs, and
the GI mucosa that some drugs may cause.

ruminants. The density, paiticle size, and

A capsule is an oral dosage form usually
geometry of the premix paiticles should
made from gelatin and filled with an active
match as closely as possible those of the
ingredient and excipients. Two conunon
feed in which the premix will be incorpocapsule types are available: hard gelatin rated to facilitate u.niforn1 mixing. Issues
capsules for solid-fill fonnulations, and soft
such as instability, electrostatic charge, and
gelatin capsules for liquid-fill or semisolidhygroscopicity must also be addressed. The fill fonnulations. Soft gelatin capsules are
excipients present in premix fonnulations
suitable to forn1ulate poorly water-soluble
include caniers, liquid binders, diluents,
drugs because they afford good drug release anticaking agents, and antidust agents.

and absorption by the GI tract. Gelatin

Caniers, such as wheat middlings, soybean
capsules are frequently more expensive
mill run, and rice hulls, bind active
than tablets but have some advantages.

ingredients to their swfaces and are

For example, paiticle size is rai·ely altered
in1po1tant in attaining uniform mixing of the
during capsule manufacture, and capsules
active ingredient. A liquid binding agent,
mask the taste ai1d odor of the active
such as a vegetable oil, should be included
ingredient and protect photolabile
in the formulation whenever a caiTier is
ingredients.

used. Diluents increase the bulk of premix

A powder is a formulation in which a
formulations, but unlike caniers, they do
d.rng powder is mixed with other powdered
not bind the active ingredients. Exan1ples
excipients to produce a final product for
of diluents include ground limestone,
oral administration. Powders have better
dicalciwn phosphate, dextrose, and kaolin.

chemical stability than liquids and dissolve

Caking in a premix fonnulation may be
faster than tablets or capsules because
caused by hygroscopic ingredients and is
disintegration is not an issue. This translates addressed by adding small an1ounts of antiinto faster absorption for those drugs caking agents such as calciwn silicate,
characterized by dissolution rate-limited
silicon dioxide, and hydrophobic starch.

absorption. Unpleasai1t tastes can be more

The dust associated with powdered premix
pronounced with powders than With other
formulations can have serious implications
dosage forms and can be a paiticular
for both operator safety and economic
concern with in-feed powders, leading to
losses and is reduced by including a
variable ingestion of the desired dose.

vegetable oil or light mineral oil in the

Moreover, sick ani.nlals often eat less and
forn1ulation. An alternative approach to
ai·e therefore not ainenable to treatment
overcoming dust is to granulate the premix
with in-feed powder formulations. Drug
fonnulation.

powders ai·e principally used prophylacti

A medicated block is a compressed feed
cally in feed or formulated as a soluble
material that contains an active ingredient,
powder for addition to drinking water or
such as a dr11g, anthelmintic, swfactant (for
milk replacer. Powders have also been
bloat prevention), or a nutritional suppleformulated with emulsifying agents to ment, and is commonly packaged in a
facilitate their administration as liquid
cardboard box to feed to livestock.

drenches.

Ruminants typically have free access to the

A granule is a dosage forn1 consisting of
medicated block over several days, ai1d
powder paiticles that have been aggregated
vai"iable conswnption may be problematic.

to form a lai·ger mass, usually 2-4 mm in

This concern is addressed by ensuring the
diaineter. Grai1ulation overcomes segregaactive ingredient is nontoxic, stable, tion of the different particle sizes during
palatable, and preferably of low solubility.

storage and/or dose administration, the

In addition, excipients in the fonnulation
latter being a potential source of inaccurate
modulate conswnption by altering the

PHARMACOLOGY INTRODUCTION

2511
palatability and/or the hardness of the
glass boluses are retained in the rumen for
medicated block. For example, molasses
up to9mo.

increases palatability, and sodium chloride

Intraruminal pellets containing seleniwn
decreases it. Additionally, the incorporation
or cobalt are available for sheep. Selenium
of a binder such as lignin sulfonate in blocks or cobalt is released throughout a period of VetBooks.ir
manufactured by compression, or

-3 yr from the pellet matrix, which consists
magnesium oxide in blocks manufactured
of compressed iron grit. When selenium or
by chemical reaction, increases hardness.

cobalt intrarwninal pellets are administered

The hygroscopic nature of molasses in a
alone, a "grinder" is usually coadministered fonnulation may also impact the hardness
to prevent the formation of calciw11
of medicated blocks and is addressed by
phosphate coatings on the surface of the
using appropriate packaging.

pellets.

Copper capsules, which contain oxidized

Oral Modified-release Delivery
copper wire particles encapsulated in

Systems for Ruminants
gelatin, are available for adult sheep and
goats. After oral administration, the gelatin

Several modified-release delivery systems
capsule dissolves in the rW11en and releases
have been developed that take advantage
the particles of copper oxide. The particles
of the unique anatomy of the ruminant
progress to the abomasrn11, where some are
forestomach. Prominent among these
trapped in the mucosa! folds and release
systems are intraruminal boluses, which
copper.

contain a range of active ingredients
including parasiticides, nutritional
supplements, antibloat agents, and

Parenteral Route of Administration
production enhancers. They a.re adminis
and Dosage Forms
tered using a balling gun. Most of the

A drug given parenterally is one given by a
commercially available intraruminal
route other than the mouth (topical dosage
boluses are continuous-release devices that
forms are considered separately). The three
rely on erosion, diffusion from a reservoir,
main parenteral routes of drug administradissolution of a dispersed matrix, or an tion are IV, IM, and SC, and in all cases
osmotic "driver" to release the active
administration is usually via a hollow
ingredient. The pay-out period for
needle. Injectable preparations are usually
intraruminal boluses is commonly> 100
sterile solutions or suspensions of drug
days. Regurgitation during rumination is
in water or other suitable physiologically
prevented by the bolus having a density
acceptable vehicles. Volwnes delivered can
of -3 g/cm3 or a variable geometry.

range from milliliter to liter quantities. The

Other types of oral modified-release
time of onset of action for IV administration
delivery systems are also available for
is seconds, and for IM and SC injections is
ruminants. For example, sustained-release
minutes. Depot injectable preparations
boluses that deliver sulfonamides throughachieve prolonged release and maintain out a period of -72 hr are available to treat
therapeutic concentrations of drug
cattle. In addition, sustained-release boluses throughout 2-5 days. The bioava.ilability of containing methoprene or diflubenzuron
a drng, particularly from prolonged-release
are approved for the control of manurefommlations, can be influenced by the breeding flies in cattle.

location of the IM injection site. SC implants

The intraruminal devices to supplement
and pellets also achieve prolonged release
ruminants with selenium, cobalt, or copper
of drug. A number of recombinant proteins
include soluble glass boluses and intraruand peptides are orally inactive and must be minal pellets. Boluses of soluble glass
given by the parenteral route. Specialized
containing selenium, cobalt, and copper
dosage fom1s, usually for parenteral
are available for cattle and sheep. Because
administration, are required for vaccines. In
glass is susceptible to sudden changes in
food animals, intramarnmary infusions and
temperature, glass boluses should be at
intravaginal devices a.re adnlinistered by the
least 15° -20°C at the time of administration
parenteral route.

to avoid fracturing, which in turn may lead

Parenteral dosage fonns and delivery
to regurgitation. Glass boluses are designed
systems include irtjectables (ie, solutions,
to dissolve in ruminal fluids, thereby
suspensions, emulsions, and dry powders
releasing the incorporated elements. The
for reconstitution), intraman1mary
composition of the glass detennines the
infusions, intravaginal delivery systems, and
solubility of the bolus, with an increase in
implants. These dosage forms and delivery
the ratio of monovalent to divalent cations
systems as well as the special consideraresulting in an increase in solubility. The tions relating to intra-articular injections,

2512

PHARMACOLOGY INTRODUCTION
recombinant proteins and peptides, and
suspending agents, and buffers. Surfactants
vaccines are discussed below.

wet the suspended powders and provide

A solution for injection is a mixture of
acceptable syringeability while suspending
two or more components that form a single
agents modify the viscosity of the formulaphase that is homogeneous down to the tion. The ease of injection and the availabil

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molecular level. "Water for injection" is the ity of the drug in depot therapy are affected
most widely used solvent for parenteral
by the viscosity of the suspension and the
formulations. However, a nonaqueous
paiticle size of the suspended drug. These
solvent or a mixed aqueous/nonaqueous
systems afford enhanced stability to active
solvent system may be necessaiy to
ingredients that are prone to hydrolysis in
stabilize drugs that are readily hydrolyzed
aqueous solutions. Injectable suspensions
by water or to improve solubility. A range of
are commonly used. Compared with that
excipients may be included in parenteral
of injectable solutions, the rate of rlrug
solutions, including antioxidai1ts, antimicroabsorption of injectable suspensions is bial agents, buffers, chelating agents, inert
prolonged, because additional time is
gases, and substances to adjust tonicity.

required for disintegration and dissolution

Antioxidants maintain product stability by
of the suspended drug particles. The slower
being preferentially oxidized over the shelf
release of drug from an oily suspension
life of the product. Anti.microbial preservacompared with that of an aqueous tives inhibit the growth of any microbes
suspension is attributed to the additional
accidentally introduced when doses are
time taken by drug paiticles suspended in
being withdrawn from multiple-dose
an oil depot to reach the oil/water boW1dai-y
bottles, and they act as adjw1cts in asep-
and become wetted before dissolving in
tic processing of products. Buffers ai·e
tissue fluids.

necessai-y to maintain both solubility of

An emulsion for injection is a heterogethe active ingredient and stability of the neous dispersion of one immiscible liquid in
product. Chelating agents are added to
another; it relies on an emulsifying agent for
complex and thereby inactivate metals,
stability. Parenteral emulsions ai·e rare,
including copper, iron, ai1d zinc, which
because it is seldom necessary to achieve an
generally catalyze oxidative degradation
emulsion for drug administration. Untowai·d
of drugs. Inert gases are used to displace
physiologic effects after IV administration
the air in solutions and enhance product
may occur, including emboli in blood
integrity of oxygen-sensitive drugs.

vessels if the droplets are > 1 µm in dian1eter.

Isotonicity of the formulation is achieved

Formulation options for injectable
by including a tonicity -adjusting agent.

emulsions ai·e also severely restricted,

Failing to adjust the tonicity of the solution
because suitable stabilizers and emulsifiers
can result in the hemolysis or crenation of
are very limited. Exan1ples of parenteral
erythrocytes when hypotonic or hypertonic
emulsions include oil-in-water, sustainedsolutions, respectively, ai·e given IV in release depot preparations (given IM), and
quantities> 100 mL. Injectable formulations
water-in-oil emulsions of allergenic extracts
must be sterile and free of pyrogens.

(given SC).

Pyrogenic substances are prin1artly lipid

A dry powder for parenteral administrapolysaccharides derived from microorgantion is reconstituted as a solution or as a isms, with those produced by gran1-negative
suspension inunediately before injection.

bacilli generally being most potent.

The principal advantage of this dosage

Injectable solutions are very commonly
form is that it overcomes the problem of
used, and aqueous solutions given IM result
instability in solution. Proteins and other
in immediate drug absorption, provided
materials that are extremely heat sensitive
precipitation at the injection site does not
caimot be dried in phai,naceutical driers.

occur.

Rather, freeze-drying, or lyophilization, is

A suspension for injection consists of
used to produce a porous powder that
insoluble solid paiticles dispersed in a liquid reconstitutes readily.

medium, with the solid particles accoW1ti.ng

Intramammary infusion products to
for 0. 5o/o-30% of the suspension. The vehicle
treat mastitis are available for lactating and
may be aqueous, oil, or both. Caking of
nonlactating (dry) cows. Lactating cow
injectable suspensions is minimized
intrainainma1-y infusions should demonthrough the production of flocculated strate fast and even distribution of the drug
systems, comprising clusters of paiticles
and a low degree of binding to udder tissue.

(floes) held together in a loose, open

These properties result in lower concentrastrncture. Excipients in injectable tions of drug residues in the milk In
suspensions include antimicrobial
contrast, it is desirable for nonlactating cow
preservatives, surfactants, dispersing or
fonnulations to demonstrate prolonged

PHARMACOLOGY INTRODUCTION

2513
drug release and a high degree of binding
containing norgestomet dispersed in
to mammary secretions and udder tissues.

polyethylene methacrylate or silicone, a

Particle size is particularly important,
biocompatible tablet implant containing
because it affects both the rate of release
deslorelin (a GnRH agonist) for use in
of the active ingredient and irritancy to the
mai·es that does not require removal, and a

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udder tissue. Drug paiticle size in nonlactatsustained-release pellet of melatonin, which ing intrainammary fom1Ulations is usually
is implanted in the ear of ewes to enhance
smaller than in those for lactating cows,
breeding performance. Testosterone pellets
which is critical to reduce iITitancy during
are available to implant il1 the ears of
prolonged retention in the udder. Thickenwethers at doses of 70-100 mg eve1-y 3 mo ing agents are added to modify the rate of
for the prevention of ulcerative posthitis.

release of the suspended particles from
oil fonnulations, and antioxidants ai·e

Special Dosage Form Considerations
commonly incorporated to prevent
with Intra-articular Injections: The
rancidity. Mastitis infusion products are
dosage forms used in intra-articular
often tenninally ste1ilized by irradiation.

administration are sterile aqueous

Intra vaginal delivery systems include
solutions. In horses, the two most common
controlled il1temal drug-release (CIDR)

reasons for intra-articulai· injections ai·e
devices, progesterone-releasing intravaginal to anesthetize or "block" a joint during devices (PRIDs ), and vaginal sponges.

a lameness examination and to treat

These systems ai·e used for estrus synchrononinfectious inflan1matory joint diseases nization in sheep, goats, and cattle. Silicone
such as synovitis and capsulitis. Drugs,
is used in the manufacture of the T-shaped
including glucocorticoids, pentosan

CIDR device and the coil-shaped PRID,
polysulfate sodium, and hyaluronic acid, are
whereas intra vaginal sponges are made
administered intra-articularly in inflanm1afrom polyurethane. The active ingredients tory joint disease. The intra-aiticular
in these systems are synthetic or natural
administration of glucocorticoids avoids
hormones such as progesterone, metl1ylacethe adverse effects associated with large toxy progesterone, fluorogestone acetate,
systemic doses. In dogs, hyaluronate
or estradiol benzoate. An applicator
sodium is administered by intra-articular
consisting of a speculum and a separate
injection for adjunctive treatment of
plunger is used to insert sponges into the
synovitis.

vaginal cavities of sheep and goats, and

PRIDs into the vaginal cavities of cattle. A

Special Dosage Form Considerations
different type of applicator is used to insert
with Recombinant Proteins and

CIDR devices into the vaginal cavities of

Peptides: Recombinant proteins and
sheep, goats, and cattle. Retention in the
peptides are used in some countries to
vagina depends on either tl1e wings (CIDR
increase feed conversion efficiency and
device) or the entire device ( sponges and
milk production in cattle (bovine growth

PRIDs) expanding. With all three devices,
hormone), increase feed conversion
gentle pressure is exerted on the vaginal
efficiency and produce leaner carcasses in
wall. Retention of the device is >95%.

pigs (porcine growth hormone), for the

Most implants used in veterinaiy
chemical shearing of sheep ( epidennal
medicine are compressed tablets or
growth factor), to reduce the incidence of
dispersed matrix systems in which the drug
skeletal weaknesses leading to leg injruies
is uniformly dispersed within a nondegradain horses (equine growth hormone), and ble polymer. Drug release from dispersed
for other uses. Recombinant proteins and
matrix systems involves dissolution of the
peptides have been fom1Ulated as solutions,
drug il1to tl1e polymer, followed by diffusion
lyophilized powders, implants, and
of t11e drug tl1rough the polyn1er and
microparticles. The chemical and physical
partitioning from the surface of the polymer
instability of recombinant proteins and
into tl1e surrounding aqueous environment.

peptides is a special consideration during

Implants are available to il1crease weight
formulation development. The major causes
gain ai1d feed conversion efficiency in food
of chemical il1stability are proteolysis,
anilnals. These implants are typically
deamidation, oxidation, and racemization.

prepared in a maimer similai· to tablets. One

Causes of physical instability are aggregacontrolled-release ilnplant consists of a tion, precipitation, denaturation, and
cylindrical core of silicone, surrounded by
adsorption to surfaces. A range of strategies
an outer layer of estradiol-loaded silicone.

has been reported to stabilize formulations

A range of implants is available to enhance
containing recombinant proteins and
reproductive performance in breeding
peptides, including the choice of carrier
attimals. These include ear implants
vehicle ( eg, oleaginous vehicles), the use

2514

PHARMACOLOGY INTRODUCTION
of lyophilization excipients, the use of
extensive range of topical formulations is
stabilizers such as sugars and detergents,
used in the control of fleas, lice, mites, and
chemical modification of the proteins and
ticks. These include insecticidal and
peptides, and the use of site-directed
acaracidal soaps, foams, shampoos, sprays,
mutagenesis to synthesize more stable

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and rinses. Also available are topical
proteins.

delivery systems such as spot-on formulations and flea and tick collars and medal

Special Dosage Form Considerations
lions. In food anin1als, a diverse range of
with Live Vaccines, Inactivated and
topical dosage forn1s and delivery systems

Subunit Vaccines, and DNA Vaccines:

are used to control external parasites. For

The organisms in live vaccines are subjected
example, most pow"on formulations,
to freeze drying and, less commonly, to deep
plunge and shower dip concentrates, and
freezing at or below -70°C. To maintain the
jetting fluids are suspension concentrates
viability of organisms under these conditions,
or emulsifiable concentrates. In addition,
formulations include complex mixtures of
many pour-on formulations display endectoproteins, peptides or amino acids, sugars, and cidal activity in cattle. The efficacious mineral salts. The viability of organisms is
systemic concentrations attained with these
additionally protected using stabilizers such
preparations result from the animal's licking
as lactose or other saccharides, skim milk,
behavior and, to a lesser extent, percutaneand senun.

ous absorption of the active ingredient.

Formulations used for inactivated and

Nun1erous methods are used to apply
subunit vaccines consist of antigen(s),
parasiticides to farm animals (see below). A adjuvants, stabilizers, and preservatives
special consideration relating to the use of

(in the case of multiple-dose products).

topical dosage fo1ms is the potential for

Inactivating agents such as phenol,
residues in wool and mohair to occur. The
thiomersal, and formaldehyde are used to
topical route of administration is also used
kill the virus or bacteria without destroyto deliver therapeutic agents systemically.

ing the critical integrity of the antigens

Transdennal patches, for instance, are used
necessary to induce a protective immune
to deliver analgesics to the systemic
response. Adjuvants enhance the
circulation.

immunogenicity of antigens by stimulat

The topical dosage forms available to
ing the immune system and prolonging
treat animals include solids ( dusting
antigen release. In this respect, aluminum
powders), semisolids (creams, ointments,
hydroxide, aluminum phosphate, and oil
pastes, and gels), and liquids (solutions,
emulsions are generally preferred to
suspension concentrates, suspoemulsions,
confer antibody-mediated immunity,
emulsifiable concentrates, paints, and
whereas saponin, qui! A, and immunitytinctures). These dosage forms as well as stimulating complexes are preferred to
the specialized topical dosage fo1ms and
confer cell-mediated immunity.

delivery systems for transdern1al drug

Plasmid DNA vectors have been used
delivery and parasite control are discussed
to express antigens in vivo to generate
below.

inunune responses. Two delivery S:','Stems

A dusting powder is a finely divided
for DNA vaccines have been reported. In
insoluble powder containing ingredients
one system, the segment of DNA is coated
such as talc, zinc oxide, or starch. Coarse
with gold and administered to the patient
powders often have a gritty feel, whereas
using a "gene gun." The other delivery
powders containing paiticles that are <20
system uses a viral vector or plasmid to
µmin all din1ensions have a smooth feel.

carry the DNA segment into the patient.

Some dusting powders absorb moisture,
which discourages bacterial growth. Others

Topical Route of Administration and
are used for their lubricant prope1ties. The
use of dusting powders is indicated on skin

Dosage Forms
folds and contraindicated on wet surfaces,

The topical route of administration is
because caking is likely to result.

used for local treatment of skin, control

A cream is a semisolid emulsion
of external and internal parasites, and
formulated for application to the skin or
transdern1al delivery of therapeutic agents.

mucous membranes. Droplet diaineter in

Drugs applied to the skin for local effect
topical emulsions generally ranges from
include antiseptics, antifungals, anti-inflan1-

0.1-100 µm. Cream emulsions are most
matory agents, and skin emollients. The
commonly oil-in-water but may be
rate of d1ug release from ointments, creams, water-in-oil. The former readily rub into the and pastes is principally detennined by the
skin (hence the term "vanishing" crean1)

semisolid base used. In dogs and cats, an
and are removed by licking and washing.

PHARMACOLOGY INTRODUCTION

2515

By comparison, water-in-oil emulsions
mixtures. They are applied to the external
are emollient and cleansing. Water-in-oil
auditory canal.

emulsions are also less greasy and spread

A lotion is usually an aqueous solution
more readily than ointments, and they

( or suspension) for application to inflamed,
soothe inflamed skin as a consequence of
ulcerated skin. Lotions cool the skin by

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the water in the fomrnlation evaporating.

evaporation of solvents, leaving a filrn of

An ointment is a greasy, semisolid
d1y powder. Lotions are suitable for use
preparation that contains dissolved or
on hairy areas and for lesions with minor
dispersed dmg. A range of ointment bases
exudation and ulceration.

is used, including hydrocarbons, vegetable

A suspension concentrate for topical
oils, silicones, absorption bases consisting
use is a mixture of insoluble, solid active
of a mixture of hydrocarbons and lanolin,
ingredients, which are typically at high
emulsifying bases consisting of a mixture
concentratfons, in water or oil. Suspension
of hydrocarbons and an emulsifying agent,
concentrate formulations are generally
and water-soluble bases. Ointment bases
water-based; the water-insoluble active
influence topical dmg bioavailability via
ingredients and inert ingredients are of
two mechanisms. First, their occlusive
very small particle size (0.1-5 µrn). Other
prope1ties are responsible for hydrating the
formulation additives include suspending
stratum comeum, which enhances the flux
agents, surfactants, and other excipients
of dmg across the skin. Second, they affect
to ensure the production of a shelf-stable,
drug dissolution within the ointment and
pourable product. Surfactants wet,
drug partitioning from the ointment into the
disperse, and stabilize the solid particles in
skin. Ointments are effective emollients
the continuous phase, prevent flocculation,
because of their occlusive nature. They are
and prevent changes in particle size.

indicated for chronic, dry lesions and

Thickening agents are included to increase
contraindicated in exudative lesions.

the viscosity of the formulation, thereby

A paste for topical use is a stiff preparaovercoming sedin1entation of the sustion containing a high proportion of finely pended particles and affording good
powdered solids such as starch, zinc oxide,
longterm stability. Suspension concentrates
calcium carbonate, and talc. Pastes are less
are used topically as pour-ons, plunge and
greasy than ointments, because much of the
shower dip concentrates, and jetting fluids.

fluid hydrocarbon fraction is absorbed onto

A suspoemulsion combines the
the solid particles; they are also less
elements of an emulsion and a suspension,
occlusive than ointments. Pastes are
allowing active ingredients with widely
indicated for ulcerated lesions.

varying physical properties to be fom1ulated

A gel is a nongreasy, semisolid, aqueous
in a single product. 'fypically, a suspoemulsolution. The semisolid properties are due sion contains one or more solvent-soluble
to a polymer imparting a continuous
active ingredients in an emulsion phase,
structure to the hydrophilic liquid. The
combined with one or more low solubility
polymers used include natural gums such as active ingredients in a continuous aqueous tragacanth, pectin, and agar; semisynthetic
suspension phase.

materials such as methylcellulose,

After dilution, an emulsifiable concenhydroxymethylcellulose, and carboxytrate for topical use produces a two-phase methylcellulose; and synthetic polymers
system involving two in1J11iscible liquids,
such as carbopol. Medicaments are
a dispersed phase, consisting of fine oil
generally well released from gels, which are
droplets ranging in size from 0.5 µm to
easily washed off on account of their water
several hundred microns, and a continumiscibility.

ous phase. Addition of an emulsifiable

A solution for topical use is a mixture of
concentrate formulation to water results in
two or more components that form a single
the fom1ation of an emulsion, which relies
phase down to the molecular level. Topical
on surface-active agents concentrating at
solutions include eye drops, ear drops, and
the oil/water interface. Active ingredients
lotions. Eye drops are sterile liquids that
that are soluble in water-immiscible organic
contain a range of dmgs, including local
solvents are frequently fonnulated as
anesthetics, antibiotics, anti-inflammatory
emulsifiable concentrates. The flocculation
agents, and dmgs acting on the autonomic
of oil droplets in emulsifiable concentrate
nervous system of the eye. They are instilled fomrnlations leads to a layer of cream that onto the eyeball or within the cor\junctival
can be readily dispersed by mild agitation,
sac. Ear drops are solutions of dmgs such as whereas the coalescence of droplets leads antibiotics, insecticides, or anti-inflan1mato tl1e inversion or "breaking" of the tory agents. The vehicle may be water,
emulsion. Water with a high content of Ca2+
glycerol, propylene glycol, or alcohol/water
and/or Mg2+ reacts with anionic surfactants

2516

PHARMACOLOGY INTRODUCTION
in the emulsifiable concentrate formulation;
rate-limiting release membra.J1e, a.J1d a.J1
this affects both spontaneity of emulsificaadhesive layer to secure the patch to the tion and stability. Zinc sulfate, used as a dip
skin. The physicochernical properties of
additive to minimize the spread of
a drug suitable for tra.J1Sdermal delivery
dermatophilosis in sheep, also adversely
ideally include low molecula.i· weight ( <500

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affects emulsions.

daltons), high potency, water solubility (to

A flank paint comprises an antifoan1ing
facilitate movement of the drug out of tl1e
agent such as a detergent or mineral oil and
reservoir a.J1d to allow passage through tl1e
is used to prevent pasture bloating in cattle.

epidermal and dermal layers of the skin),

A flank paint is applied to the flanks of
and lipid solubility (to permit penetration
animals, from where it is licked off and
of tl1e stratum comeum of the skin).

ingested. Bloat, or rwninal tyrnpany, refers

Fenta.J1yl, a synthetic opioid agonist, is
to excessive accumulation of gas in the
delivered by tra.J1sdermal patch in dogs,
rumen. Frothy bloat commonly develops in
cats, a.J1d horses.

cattle on pasture, pa.iticularly those grazing
lush, leguminous pastures. Frothing of

Specialized Topical Dosage Forms,
rwnen ingesta occurs when the viscosity

Delivery Systems, and Application
of the fluid is increased. Froth obstructs

Methods for Parasite Control: The
the ca.i·dia of the stomach, preventing the
control of internal a.J1d external parasites of
eructation of excessive gas produced in
companion a.J1d food-producing a.J1in1als has
the rumen. Antifoan1ing agents reduce
led to development of specialized dosage
the stability of the froth by lowering the
fonns, delive1-y systems, a.J1d application
viscosity of the fluid ingesta.

methods unique to veterina.i-y medicine.

A tincture for topical application uses

A spot-on formulation is a solution of
a vehicle containing 15%-SOOA, alcohol, requi1°
active ingredient( s) that typically contains a
i11g the preparation to be tightly stoppered
cosolvent a.J1d a spreading agent. The active
and not exposed to high temperatures. In
ingredients in spot-on products for flea, GI
addition to alcohol, tiI1ctures may contain
parasite, or hea.itworn1 control in dogs
cosolvents, stabilizers, and solubilizers.

a.J1d cats include fipronil, imidacloprid,

Iodine ti.nctw·e is a topical anti-infective that
sela.inectin, pyriproxyfen, ivermectin, a.J1d
contai11S 44o/1>-500A, alcohol. The reddish
moxidectin. Spot-on f'onnulations are also
brown color of iodine tinctw·e produces skin
available to control lice in cattle. The
staining that delineates treated ski11. Friar's
physicochemical properties of the active
balSa.Jn is compoW1d benzoin tincture and is
ingredient(s) are imp01ta.J1t detern1i.na.J1ts of
used to protect and toughen ulcerated or
topical or tra.J1sdem1al behavior. Topical
fissured skin.

activity against ectopa.i·asites depends to
some extent on the active ingredient

Specialized Topical Dosage Forms
spreading, mixing with the sebwn coating
and Delivery Systems for Transdermal the skin a.i1d hair, a.J1d fom1ing depots in the Drug Delivery: A transdermal delivery
pilosebaceous units. The mecha.itism of
gel consists of a vehicle, most commonly
percutaneous drug absorption varies
pluronic lecithm organogel (PLO gel),
between species a.J1d is not completely
which delivers drug via the transdem1al
understood. However, low molecular
route to the bloodstrea.in. The micellar
weight a.J1d a high lipid/water partition
composition of PLO gel enhances skin
coefficient tend to favor passage of the drug
penetration of the pha.i111aceutical agent
through the skin.

present in the formulation. PLO gel is

Backliner products for sheep consist of
generally well tolerated a.i1d is nontoxic if
pow0on a.J1d spray-on formulations for tl1e
ingested. However, not all drugs are suitable control of lice and sheep blowflies. Sheep for transdem1al application, and there a.i·e
lousicides include synthetic pyrethroids,
relatively few studies of the bioavailability
orga.I1ophosphates, a.i1d insect growth
of drugs from compoW1ded transdem1al
regulators. These products a.i·e fonnulated
gels. Transdennal gels a.i·e used to deliver
for pou1°on application within 24 hr after
drugs to treat several diseases in dogs and
shearing (ie, off-shears) or spray-on
cats, including undesil"able behavior,
application (in sho1t-wool sheep with wool
ca.i·diac disease, a.i1d hyperthyroidism. The
growth <6 wk, a.J1d in long-wool sheep with
dose is applied to the inner surface of the
wool growth >6 wk). Theil" efficacy against
pinnae, thereby offering ease of administralice depends on topical activity a.J1d not on tion, especially in cats.

percutaneous absorption of tl1e active

A transdermal delivery patch typically
ingredient into the bloodstream. Tra.I1Slocaconsists of a drug incorporated into a tion of the pesticide from the application
reservoir, a protective backing layer, a
site to remote sites at concentrations lethal

PHARMACOLOGY INTRODUCTION

2517
to lice is critical to the efficacy of these
direct sunlight by roofing. A draining pen
products and, in the case of pour-on
located at the exit of the vat allows dip wash
applications, is facilitated by the increased
that drains off treated animals to return to
secretion of wool grease that occurs at
the vat. Dip chemicals ai·e usually formushearing.

lated as aqueous solutions, emulsifiable

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The active ingredients in sheep blowfly
concentrates, or suspension concentrates,
products include insect growth regulators,
all of which ai·e diluted with water before
synthetic pyrethroicls, and organophosuse. The high costs associated with plunge phates. After their topical application, sheep clipping relate principally to the costs of blowfly larvicicles fom1 follicular depots and chemicals for chai·ging large vats, labor, subsequently translocate as a coating on
and the disposal of the hazardous wastes.

new wool growing out of the follicles.

Plunge dips must be managed properly and

Hand-jetting of long-wool sheep ( wool
the pesticide maintained at the concentragrowth >6 wk) is done to control lice, keels, tion recommended by the manufacturer.

mites, and sheep blowflies. The pesticides

Dipping of sheep and cattle is associated
used include rotenone, synthetic pyrewith "stripping" of tl1e active ingredient throids, organophosphates, insect growth
from the dip wash ( eg, pesticide loss from
regulators, and macrocyclic lactones.

the dip wash occw·iing at a greater rate tl1an

Hand-jetting involves the use of a hanclpiece
water loss) and is categorized as mechatli

( or wand) to "rake" a pesticide solution into cal or chemical. In the case of sheep,
the wool along the dorsal midline and
mechatlical stripping results from tl1e
sometimes into tl1c breech, crutch, and poll.

fleece acting as a sieve toward the active

The solution is applied under pressure and
ingredient, with the degree of filtration
penetrates to the skin.

being primai·ily cletem1ined by paiticle

Some pour-on products on the market
size. Chemical stripping is clue to the
are formulated to deliver an active
preferential absorption of pesticide by the
ingredient percutaneously. The macrocyclic
fleece. To counteract stripping, a complex
lactones ivem1ectin, moxiclectin, cloramecclip management regimen that involves ti.n, and eprinomectin are formulated as
reinforcement and "topping-up" is used.

pow0on preparations for application to

Reinforcement refers to the addition of
cattle. These formulations are usually
undiluted chemical product to the dip
solutions or emulsi.fiable concentrates
without the addition of water, whereas
for dilution with water before use. The
topping-up refers to the addition of water
principal route of percutaneous absorption
and undiluted chemical product to the dip
for most drugs in people is the intercellular
vat to return the volilllle to the slatting level.

pathway, making the intercellular lipid

Proper clip management also minimizes
matrix the primaiy banier to absorption.

contanlination of the dip with orgatlic

However, this may not be the case in species matter. This requires that the race leading to in which the emulsifying properties of skin
the vat is constructed of concrete or slats to
secrPtions and the lai·ge nw11bers of follicles remove ditt from the a.tlitnals' feet and that and glands per unit surface area must be
anitnals be held in a yard overnight before
considered (eg, cattle and sheep). Ionized
dipping, during which time they are offered
solutes, for example, are reported to cross
water but no feed.

the skin of animals via shunt pathways

Hand spraying generally results in

(sweat ducts, follicles). Pour-on products

Wleven coverage of a.tlitnals and is
ai·e fom1ulated to spread without run-off
considered an inefficient method of
when applied to the skin and to be resistant
application. By compai·ison, recirculating
to rain. The formulation also facilitates the
and nonrecit·culating spray races facilitate
partitioning of the drug out of the vehicle
whole body spraying and wet cattle to the
and into the skin and transpo1t of the drug
skin. The situation with sheep is differentacross tl1e skin. The control of tl1ese the very short contact titne in a spray race
processes is ctitical, because some drug is
litnits tl1e uptake of insecticide, which
required to remain at the skin i.fthe drug is
means the fleece seldom becomes
to be active against external parasites that
saturated. Because of this, spray races
are not blood sucking. In addition, too rapid
should be used as an adjunct to shower
passage of drug tl1rough tl1e skin may result
or plunge dippit1g of sheep.

in w1acceptable chemical residues in tissues

Shower dips ai·e less labor intensive than
or milk.

plunge dips and are cheaper to operate. A

The plunge dipping of sheep and cattle
typical shower dip consists of a swnp
for external parasites requires a clipping vat,
containing the dip wash, a pun1p, and a
which may be a pottable unit or a permashoweting pen constructed with a concrete nent in-ground structure shielded from
floor a.t1d fitted with rotating and fixed

2518

PHARMACOLOGY INTRODUCTION
nozzles. There are two types of shower dips:

where cattle congregate. Back rubber'S
a conventional shower dip in which the
are charged by soaking thoroughly in
swnp volwne is periodically maintained
oil-containing pesticide, typically a
by adding fresh dip wash, and a constant
synthetic pyTeth.roid, ar1 organophosphate,

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replenislm1ent shower dip i:n which a
or a combination of the two. The oil retards
smalJ-volwne sump is continually filled
evaporation of the insecticide and enhances
from a large-volume supply tank to maintain adherence to the animal's coat.

dip levels. Proper dip management requires

Dust bags facilitate the self-treatinent
attention to the factors described above for
of cattle to contI·ol flies and lice. They
pltmge clipping. In addition, all equipment
are consb'Ucted of an inner porous bag
must be functioning properly for the fleece
containing the active ingredient, which is
to become satmated. Sheep should not be
commonly a synthetic pyreth.roid or an
dipped (by either the plunge or shower
orgar1ophm;µhate, and an outer weatl1e1°
method) until shearing wounds have healed
proof ski.rt. Dust bags ar·e hung in lanes
to avoid closbidial infections or caseous
or gateways so that passing cattle brush
lymphaclenitis caused by Co1ynebacterium
against them and receive a topical
pseudotuberculosis. Moreover, the correct
application of pesticide.

use of bacte1iostats is recommended to
prevent post-dipping lan1eness caused by

Inhaled Dosage Forms and Delivery

Erysipelothri.x insidiosa.

Systems

Insecticidal collars are plasticized
polymer resins in1pregnated with an active
lnhalational anesthetics ar·e critical in
ingredient. CoUars for the contI·ol of ticks
management of ar1estl1esia CwTently,
and fleas on clogs and cats release the active
enfiw·ar1e, halot11ane, isoflw·ane, methoxyingredient as a vapor, a dust, or a liquid, tlurane, and nio·ous oxide are tl1e most
depending on the physicochernical
commonly used inhaled anesthetic agents.

properties of the chemical. Volatile liquid

These agents are usually delivered to
insecticides such as dichlorvos or naled ar·e
anin1als in a car'!ier gas that includes
used in vapor-release coUar'S. The insectioxygen, using an anestl1etic machine fitted cide disbibutes through the collar· matrix as
with one or more vaporizers and a patient
a vapor before being released. Powdered
breathing circuit.

insecticides such as phosmet, sti..rofos,
lnllalational therapy of airway disease
carbaryl, ar1d propoxur are used in
is used to deliver !ugh concentrations of
dust-release coUars. Translocation of the
drugs to the I ungs while avoiding or
active ingredient within the collar matrix
minimizing systentic adverse effects. 1b be
leads to deposits fom1ing at the swiace;
delivered into the ai1ways, a drng must be
distribution of the insecticide to the animal
presented as an aerosol, either as solid
depends on the animal's physical activity.

particles or liquid droplets in air. Particle or

Nonvolatile liquid insecticides such as
droplet size Jar·gely detennines the extent
chlorfenvinphos or diazinon are used in
to which t11e drng penetrates t11e alveoli.

liquid-release collars. The active ingredient

Particles too small or too large for optin1al
disbibutes as a liquid in the collar matrix
delivery into alveolar· sacs ar·e either
and to the swiace, where it is released. The
exhaled or deposited on larger bronchial
animal's activity plus the dissolution of
airways. Compared witl1 delivery by tl1e oral
lipophilic insecticides in skin secretions are
or par·enteral routes, tl1e on�et of pham1acoin1portantfactors in translocation of the logic action of inhaled agents is faster and
insecticide from the collar· to the artimal.

the doses adntinistered smaller, tl1ereby

Two types of insecticide-releasing ear
reducing the potential incidence of adve1'Se
tags to control flies on cattle are available.

systemic effects. The delivery systems used

One is constructed from a polymer that
for inhalational tl1erapy of airway disease in
provides structmal support and acts as a
artimals are nebulizers ar1d metered-dose
release rate-controUing matrix. The other is
inhalel'S. In the poultiy industiy, inhalation
a membrane-based ear tag that consists of
of aerosolized vaccines is a common way to
an insecticidal reservoir with a relatively
in1mwtize flocks of birds.

in1perrneable backing on one side ar1d a
rate-cono·olling membrane on the other.

CHEMICAL RESIDUES IN FOOD

Both types rely on the animal's ear and head

AND FIBER
movements and groonting to transfer
insecticide from the swface of the ear tag

Veterinary drugs and pesticides are used
to the anin1al's skin or to other anin1als.

routinely in animal production to marrnge

Back rubbers typically consist of bmlap
diseases ar1cl control par·asites, ar1d crop
supported across lanes, gateways, or areas
protection chemicals are used in production

PHARMACOLOGY INTRODUCTION

2519
of animal feeds. It is possible, therefore, for
contains residues above the MRL. Surveilfoodstuffs of animal origin to be adullance programs, by comparison, take terated with residues of veterinary drugs
san1ples from animals suspected of having
and pesticides, and for animal fibers to be
violative residues on the basis of clinical
contaminated with residues of ectoparasigns or herd history. Food from animals VetBooks.ir
siticides. Veterinarians must consider the
identified with violative residues of
in1plications of both possibilities when
veterinary drugs or pesticides do not enter
providing for the health and welfare of
the food chain.

animals. First, animals and animal products

Residue monitoring is also a trade
destined for human consumption must not
requirement, either mandatory or as
contain residues of drugs or pesticides that
an expectation, of impo1ting countries
exceed legally permitted concentrations.

allowing market access to food products

Second, pesticide residues in fiber have
derived from animals. Compliance with the
potential implications for public health,
national standards of impo1ting countries
occupational health and safety, and
becomes more difficult when the health
environmental safety.

standards, regulatory policies, and

MRL-setting approaches of the exporting

Chemical Residues in Foodstuffs of
country and importing country differ. The

Animal Origin
situation is further exacerbated when
patterns of use differ across countries or

Chemical residues can be found in anin1al
when the minor status of a disease or pest
tissues, milk, honey, or eggs after ad.minisin a country does not warrant product tration of veterinary drugs and medicated
registration, in which case MRLs are
premixes, application of pesticides to
unlikely to be established.

animals, or consumption of stockfeeds

Regulat01y autho1ities w1de1take
previously treated with agricultural
premarket approval assessments of
chemicals.

applications in suppo1t of new veterinary
drugs and medicated feeds. These

Residues Resulting from Veterinary
assessments consider scientific data

Drugs, Medicated Feeds, or Applica
submitted by the sponsor. In the case of
tion of Pesticides: Extensive regulatory
veterinary medicines proposed for use in
and monitoring systems have been estafood-producing animals, the data must blished to ensure that chemical residues
demonstrate the safety of any residues
in food do not constitute an unacceptable
remaining in the edible tissues or products
health risk. The premarket approval process from treated animals. These data describe undertaken by regulatory authorities for
the compound's toxicology, metabolism,
new veterinary drugs and medicated feeds
pharmacokinetics, residue depletion, and
evaluates the quality, safety, and efficacy of
dietary exposure. The key paran1eters
these products. For veterinary medicines
de1ived in the safety and residue evaluaintended for administration to food-productions are defined below.

ing animals, an additional consideration is

The acceptable daily intake (ADI) is
the safety of edible tissues and products
the amount of a vete1inary drug, expressed

(milk, honey, eggs) derived from treated
on a body weight basis, that can be ingested
animals. Regulatory authorities establish
daily over a lifetime without an appreciable
maximum residue lin1its (MRLs) or
risk to human health. The ADI is established
tolerances and set withdrawal times that
based on a review of animal studies on
ensure residues of the active constituent
toxicologic, pharrnacologic, or micro biowill not exceed the MRL when the label logic effects as appropriate. Conservative
instrnctions for the product are followed.

safety factors are built into the ADI.

Residue programs consist of two

The safe concentration is the maximal
principal activities: monitoring and
allowable concentration of total residues of
surveillance. Residue-monitoring progran1s
toxicologic concern in edible tissue. The
randomly sample food commodities from
safe concentration is calculated from the
anin1als. San1ples are assayed for residues

ADI and considers the weight of an average
of specific veterinary drugs, pesticides, and
person and the amount of meat, milk, honey,
environmental contaminants, and the
or eggs consumed daily by a high-consun1-
residues are assessed for compliance with
ing individual.

the applicable MRL or environmental

An MRL, or tolerance, is the maximal
standard. The number of samples taken for
concentration of residue resulting from the
monitoring purposes typically provides a
use of a vete1inary drug ( expressed in mg/kg

95% probability of detecting at least one
or mcg/kg on a fresh-weight basis) that is
violation when 1 % of the animal population
legally permitted as acceptable in or on a

2520

PHARMACOLOGY INTRODUCTION
food. It is based on the type and an1ow1t
the animal and invalidates the stated withof residue considered to be without any drawal titne. In addition, a rai1ge of physiotoxicologic hazard for hwnan health as logic and pathologic factors may modify the
expressed by the ADI. Other relevant public
drug's disposition in the ai1i.mal and prolong
health risks and aspects relating to food
drug elimit1ation.

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technology, good practice in the use of

In the USA, some veterinaiy or hwnan
veterinaiy drugs, and ai1alytical methodolodrugs can be used extra-label ( off-label) gies are also considered when establishing
in food-producing anitnals under the Animal
theMRL.

Medicmal Drug Use Clarification Act,

The marker residue is the parent drug,
provided ce1tain conditions are met (more
its metabolites, or any combination of these, information can be obtained on the FDA with a known relationship to the concentrawebsite, www.fda.gov). Veterinarians must tion of the total residue in the last tissue to
be mindful, however, that the extra-label
deplete to the safe concentration. When the
use of a small number of veterinaiy drugs
marker residue in the target tissue has
is prohibited by the FDA Extra-label use
depleted to the MRL, the total residue will
refers to use in a species not included m the
have depleted to the safe concentration in
product labeling or at a dosage rate higher
alJ edible tissues.

thai1 that stated m the product labeling.

The target tissue is the edible tissue

For drugs used m this ma.I111er, data are
with residues that deplete to a concentrainadequate to demonstrate the safety of tion below the MRL at a slower rate than
food products derived from the treated
that in other edible tissues. It is considered
anm1al. An understanding of phannacokisuitable for monitoring compliance with the netic principles a.lJows extended with

MRL of each edible tissue from a treated
drawal times to be estimated both when
ai1itnal. The tai·get tissue is frequently liver
vete1inai-y drugs are used ill ai1 extra-label
or kidney for the purpose of domestic
mai1ner and in situations that may lead to
monitoring, and muscle or fat for monitorchanges ill the kinetic behavior of a drug m ing meat or cai·casses in international trade.

an mdiviclual animal. The pharmacokinetic

The withdrawal time is the period of
principles involved as well as two relevant
time between the last administration of a
practical examples that demonstrate such
drug and the detection of residues of that
occw-rences ai·e discussed below.

drug to levels below the MRL in food from

The elitnination half-life is the time
a treated a.Illinal. Compliance with the
requit·ecl for the concentration of a drug to
preslaughter withdrawal titne ensures the
be reduced by 50%. Therefore, 99.9"A, of an
total residues deplete to below the safe
administered dose is eliminated over 10
concentration, ai1cl the mai·ker residue
half-lives. In food-producing a.Illinals, the
depletes to below the M�L. Failure to
residues of drugs with longer tem1inal
observe the correct withdrawal titne is the
elitnination half-lives take longer to deplete
most common cause of violative residues
to below the MRL. The pharrnacokinetic
of veterinaiy cl.rugs it1 food.

behavior of the drug dete1mmes whether the

Regulatory authorities determine
elm1iI1ation half-life m tissues will exceed
withdrawal titnes based on resiaue
the elimination half�life m plasma. In
depletion data that has been generated
food-proclucmg a.Illinals, the tenninal
using healthy aiilinals representative of
elitnination half-life for the slow elimination
those typically treated with the specific
phase, or "I phase, of the residue concentraproduct. The drug formulation used in these tion versus titne profile determmes the
trials is identical to the market formulation,
withdrawal time. Half-life is cletenninecl by
which is administered at the maximal label
both cleai·ance (Cl) and volwne of distriburate. The withdrawal titne is usually tion (Ve!) as shown by the relationship:

cletennmed statistica.lJy, taking into account
variability ai11ong ai1it11als in drug disposit
tion.

112 = 0.693 x Vd

Cl

Unlike an MRL, which applies to a
veterinary drug regai·dless of the dosage

Clearance is the blood volun1e cleai·ecl
fo1m, route of administration, or dosage
of drug per unit titne and refers to the
regitnen, the withdrawal tit11e stated in
irreversible elitnination of a drug from the
the product labeling applies only to that
body. The principal organs of elimination
paiticulai· formulation when administered
are the liver and kidneys; orgai1 clearance is
by the recommended route and in
related to blood flow ai1d the efficiency of
accordance with the dosage regitnen.

drug removal. To clete1mit1e hepatic

Altering ai1y of these factors modifies the
cleai·ai1ce, for exan1ple:

pharmacokinetic behavior of the drug in

ClH = QI! X E11

PHARMACOLOGY INTRODUCTION

2521
in which Q = blood flow and E = the
tissues, milk, honey, or eggs derived from
extraction ratio. Factors that affect hepatic
these animals.

clearance include hepatic function, hepatic

For approved uses of crop protection
microsomal enzyme activity, and hepatic
chemicals that ar·e likely to result in dietary
blood flow.

exposure of food-producing arumals,

Volume of distribution relates the
regulatory authorities establish animal

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amount of drug in the body to the concenconrn1odity MRLs. The approach adopted tration of drug in plasma. For a drug
for establishing these MRLs is fundamenadministered IV, the relationship is: tally different from the one that applies to
veterinary drugs. Animal transfer studies,

Vd = an1ount of drug in body (dose)

which allow detem1ination of the relationconcentration (C
ship between the level of chemical in the
ma.J
ai1in1al diet and the concentration of residue

V d is a characteristic property of the drug
found in edible tissues, milk, honey, and
rather than the biologic system. A drug
eggs, ar·e pivotal in determining MRLs.

confined to the vascular compartment has a

MRLs for animal tissues, milk, honey, and
minimal value of Vd equal to plasma
eggs are established at concentrations that
volume. Factors influencing Vd include the
cover the highest residues expected to be
size of the drug molecule, lipid solubility,
found from the estimated livestock dietary
drug pKa, and tissue blood flow. Certain
exposure. Human dietary exposure
disease states effect changes in the V d of a
assessments are also performed to verify
drug, particularly changes in drug binding.

that food complying with MRLs is safe

If it is necessary to administer a drug to a
for consumption. In animal production
healthy animal at twice the reconunended
systems, compliance with aiumal conrn10drate, the elimination half-life of the drug is ity MRLs relies on adherence to a stipulated
unchanged. Assuming the pharmacokinetic
period to allow residues in the crop to
behavior of the drug demonstrates
deplete before it is fed to animals, a
first-order kinetics, which is generally the
stipulated period to allow residues in the
case, doubling the administered dose will
arumal to deplete before slaughter, or a
increase the depletion tin1e by one half-life.

combination of both.

Thus, the withdrawal time should be
extended by one hall�life to arrive at the
same concentration as observed for the

Chemical Residues in Animal Fibers
reconunended rate. However, if a drug is

From an economic standpoint, the major
administered to an unhealthy animal with
animal fibers are wool and mohair. Although
impaired drug excretion in which clearance
this discussion primarily focuses on
is reduced by 50%, it can be seen from the
pesticide residues in wool, many of the
relationship for half-life shown above that
concepts apply equally to mohair.

reducing clearance by 50% will double the

Flies, lice, keds, and mites adversely
half-life. Accordingly, the withdrawal time
affect wool production and have animal
should be doubled to arrive at the same
welfar·e implications for the sheep industry.

concentration as seen in an arumal with a

Ectoparasiticides have been the mainstay
fully functional excretory system.

to manage infestations of these parasites in

The predicted result should always be
sheep flocks for mar1y year·s. Two i.mportai1t
verified using a rapid-screening test. The
manifestations of chenucal application to
detection of residues is likely to signal that
sheep ar·e the emergence of resistant strains
the withdrawal time should be extended
of par·asites and the contamination of wool
and the rapid-screening test repeated.

with pesticide residues. These two factors
are linked, because the application of

Residues Resulting from Consump
pesticides to resistant strains of flies or lice
tion of Stockfeeds Treated with
increases the likelil10od of treatment failure

Agricultural Chemicals: The use of
and the need to re-treat later in the
agricultural chemicals can result in residues
wool-growing season. Higher residues in
in crops and pastures that are subsequently
both the wool on treated sheep and in
consumed by animals. During drought
harvested fleeces are possible conseconditions, the feeding of potentially quences. Nonetheless, late-season
contaminated crop byproducts, such as
applications are justified in some situations
stubbles and fodder, and processed
on aiumal health and welfare or economic
fractions, including grape mare, citrus pulp,
grotmds. In view of community health and
fruit pomace, and cannery wastes, is likely
safety expectations and changing environto become more prevalent. In all cases, mental standards, wool producers are
chemical residues may result in the edible
seeking ways to manage external parasites

2522

PHARMACOLOGY INTRODUCTION
on sheep that rely less on chemicals.

pesticides, respectively. In addition,

Integrated pest management (IPM)

long-wool backline applications of synthetic
approaches may involve various husbandry
pyrethroid pesticides can result in residue
options, such as shearing and crutching to
concentrations at the tips ofbackline

VetBooks.ir
combat flystrike; genetic improvements,
staples high enough to cause dem1al
such as selecting against animals susceptierythema in shearers and wool handlers. In ble to fleece rot and flystrike; biologic and

Australia, such occupational health risks
environmental controls, such as the use of
are managed by prescribing a sheep
fly traps; and the selective use of chemicals.

rehandling period in the product labeling.

Pesticide residues in wool are influenced

The sheep rehandling period is the time that
by many factors, including the chemical
must elapse between the application of the
and formulation used, the method of
ectoparasiticide a.i1d safely handling the
application, the rate and timing of the
treated a.ilimal. If sheep must be handled
chemical application, and the length of wool
during the rehandling period, personal
at the time of application. (See a.Isa ROUTES
protective equipment should be used.

OP ADMINISTRATION AND DOSAGE FORMS, p 2508 .)

Chemical residues on treated wool

The product types and chemical groups
may pose a risk to the environment when
commonly used in the management of flies
effluent is discharged during processing
and lice on sheep include off-shears backline ( eg, into rivers). This concern has led to or spray-on products containing insect
the enactment of legislation to protect
growth regulators (IGRs), organophosphate
the environment. For some pesticides,
pesticides (OPs), and synthetic pyrethroid
environmental quality standards at
pesticides; short-wool plunge or shower dips concentrations that will not harm the most that use IGRs, magnesium fluorosilicate,
sensitive organisms in aquatic ecosystems

OPs, and spinosad; long-wool backline or
have been established. In the EU, textile
spray-on products containing IGRs; and
products are subject to eco-label requirelong-wool jetting products containing IGRs, ments. In Australia, environmental risks
macrocyclic lactones, OPs, or spinosad.

posed by residues of ectoparasiticides on

Wool producers must ensure that pesticides
treated wool are mitigated by assigning a
are applied in accordance with the label
wool-harvesting interval (also referred to
directions. With some chemicals, application as a wool withholding period). The woolto sheep with >6 wk wool growth results in ha.ivesting interval is the ti.me that must
unacceptably high residues remaining in
elapse before treated sheep may be shorn,
wool to the next shea.iing. Repeat applicaensUiing that harvested wool meets the tions of pesticides may also result in higher
prescribed environmental residue limits.

wool residues at the next shearing, and

The depletion of pesticide residues in
backline products conunonly leave higher
wool has been mathematically modeled
residues at the site of application.

to predict the likely consequences of

Although the use of sheep ectoparasititreatments at different ti.mes during the cides can result in significant chemical
wool-growing season and to detennine how
residues on treated wool, any risk to public
late a pesticide may be applied to sheep
health is successfully mitigatetl by the
without resulting in excessive residues
following steps. First, scouring removes
at shea.iing. Modeling is a useful tool to
residual pesticide from processed wool
determine wool-harvesting intervals and to
destined for the manufacture of woolen
help wool producers choose a pesticide and
garments. Second, in the case of lanolin
method of application. Test kits to quantify
used in pharmaceuticals and cosmetics and
pesticide residues in wool are also available.

as nipple emollients by nursing mothers,
any residual pesticide associated with the

NANOTECHNOLOGY
wax component is removed during refining
of the lanolin. Additional assurance

Nanotechnology is a new enabling techregarding the quality of low-pesticide grades nology with the potential to revolutionize of lanolin is provided by compliance with
animal health. A nanomaterial has been
the applicable regulatory standards.

defined as a material engineered to be < 100

With respect to occupational health
ru11 in one or more dimensions. A nanometer
and safety, residual pesticide in wool wax
is one one-billionth of a meter; to put the
poses a hazard to shearers and other wool
nanoscale into perspective, a hUinan hair is
handlers during wool harvesting. For

-80,000 nm in dia.ineter. Chemicals at the
instance, nervous disorders and dermal
nanoscale display physical and chemical
irritation have allegedly occurred in
behaviors that can differ markedly from
shearers after shearing sheep treated with
those of the bulk chemical (eg, in optical
certain OPs and synthetic pyrethroid
properties, conductivity, or electromagne-

PHARMACOLOGY INTRODUCTION

2523
tism). These behaviors are attributed to a
tissues or cell types. Similarly, magnetic
combination of the small size, chemical
nanoparticles under the inf! uence of an
composition, physicochemical properties,
alternating magnetic field transport drugs
and swface structw·es of nanomaterials. Of
to their sites of action. Individualized and

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major importance to the development of
targeted drug therapy across animal species
nanotechnologies for anin1al health will
is an extension of the "smart" drug delivery be a thoughtful, thorough, and balanced
concept. With this approach, miniature
assessment of the benefits and risks
sensing and delivery devices, some with
involved. Risks can originate from any novel
embedded PK/PD algoritluns or using
hazards of nanomaterials, the distribution
nanodelivery platforms that provide local
profiles of nanomaterials in animals, the
feedback on delivery mechanisms, are
exposure of people to nanomaterials, and
envisioned. Also envisioned are nanoscale
tl1e toxicity and fate of nanomatelials in the
devices with tl1e capability to detect and
environment. Additional challenges relate to
treat an infection, nutrient deficiency, or
the detection and analysis of nanomatelials.

other health problem before symptoms are

This discussion focuses on the applic a evident. In the case of antibiotics, the tion of nanotechnology in the delivery of
envisioned system would use less drug,
veterinary drugs and vaccines, a field
thereby relieving concerns surrounding
predicted to expand. Many of the benefits
the potential development of antibioticof nanotechnology in drug delivery are the resistant strains of bacteria and thus increasresult of improved apparent solubility or ing food safety for consumers. Exciting
stability or both; an increased concentration advancements in the field of vaccine of drug at the site of action (increased
delivery are also being made ( see vaccine
efficacy); a decreased concentration of drug
delivery and vaccine adjuvants, below).

at locations in the body remote from the site

The ratio of swface area to volwne of a
of action (reduced systemic toxicity); and
drug nanocrystal is orders of magnitude
modified pharrnacokinetics, including
greater than that of its microscale or
controlled release.

macroscale dl-ug cow1terpart. Poorly water

There are nwnerous "drivers" of
soluble drugs with a bioavailability that is
nanotechnology-based drug delivery.

dissolution-rate limited demonstrate

Pharmaceutical considerations are one
markedly improved bioavailability when
such dliver (see drug nanocrystals, below); administered in a nanoform. Another
another is the need for vete1inary nanornedadvantage is that drug nanocrystals icines that overcome problems refractory to
demonstrate reduced valiability in
conventional therapy. One objective of
bioavailability for the fed and fasted states.

"smart" drug delivery is to target specific Nanosized drug crystals are produced either
sites. This strategy allows the use of smaller
by top-down technology, in which
quantities of drug than would otherwise be
micronized particles are subjected to
possible. The passive targeting of intravemilling or grinding, or by bottom-up technously administered drug, for example, nology involving nanoprecipitation.

depends on the enhanced permeability and

Drugs and proteins conjugated to
retention (EPR) effect, a phenomenon
polymers such as polyethylene glycol
whereby nanoparticles extravasate at sites
degrade more slowly than do drugs or
of increased vascular pern1eability, such as
proteins alone. As a consequence,
twnors, infections, and areas of inflanm1aconjugates remain in the circulation longer tion, and then accwnulate at these sites.

than the parent drug or protein. A prolonged

Swface modification of nanoparticles is
circulation tin1e allows for less frequent
used to prolong the circulation time and
administration and results in increased
enhance the EPR effect. For example,
extravasation of drug due to the EPR effect
coating nanoparticles with the hydrophilic
and, consequently, a higher drug concentrasubstance polyethylene glycol lessens tion at the site of action.

opsonization through a steric effect, thereby

Dendrimers are highly branched
reducing the subsequent uptake of
polymers consisting of an initiator core;
nanoparticles by the reticuloendothelial
interior layers composed of repeating
system. Conversely, uncoated nanoparticles
units; and tern1inal moieties that can
are rapidly phagocytosed, a process used to
be functionalized to modify solubility,
advantage to treat intracellular parasites
miscibility, and reactivity of the resulting
and infections located in phagocytic cells.

macromolecule. From a drug-carrying

In a separate process known as active drug
perspective, dendrimers are relatively new.

targeting, nanoparticles with targeting

High loadings of dl-ug can be incorporated
moieties (eg, antibodies, ligands) attached
into the dendrin1er core or attached to the
to their swfaces are able to bind to specific
tenninal moieties on the dendrin1er surface.

2524

PHARMACOLOGY INTRODUCTION

Dend1irners are particularly attractive for

Magnetic nanoparticles have two
ocular, pulmonary, and oral drug delivery.

therapeutic applications: drug delivery and

Polyplexes are complexes of polymers
therapeutic hyperthermia. The former
and DNA with promising benefits for gene
application involves drug-coated magnetic
therapy.

nanopaiticles that are general.ly >50 nm in

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Polymeric micelles comprise an
size. After IV administration, these nanointernal zone known as the "core" and an paiticles are directed to the site of drug
external zone known as the "sheU" formed
action using a magnetic field. Subsequent
by amphiphilic block copolymers such as
retention of the nanopaiticles at the site of
poly(propylene oxide), poly(L-an1ino acids), action is also achieved using a magnetic and poly( esters). Tl1e advantages of
field, and this facilitates localized drug
polymeric micelles for dmg delivery include release. By comparison, magnetic nansolubilization of poorly soluble molecules opaiticles for therapeutic hype1thermia are
and sustained drug release due to drug
smaller in size (-5 run). I-lyperthermia via
encapsulation protecting the drug from
hysteresis energy loss results when an
degradation and metabolism. Polymeric
external alternating magnetic field is
micelles can also enhance the delivery of
applied to the magnetic nanoparticles.

drugs to desired biologic sites, thereby

A typical outcome oft.11erapeutic hyperimproving therapeutic ef'ficacy and t.11e1mia is tUlllor cell necrosis.

attentuating unwanted adverse effects.

An example of a nanoteclmology-based

Liposomes are self-assembled vesicles
device for vaccine delivery is the
that possess a central aqueous cavity

Nanopatch®, used in people to deliver
smTounded by a lipid membrane fmmed by
vaccines detmally. The Nanopatch®
a concentric bilayer(s) (also known as a
is a silicon wafer the size of a postage
lamella[ e ]). When liposomes come in
stamp with thousands of projections
contact with biologic cells, they tend to

(>20,000/cm3), each of whlch is -100 µrn
unravel and merge with the membrane of
long and with a tip diameter of -1 µm. The
the cell, releasing their payload of drugs or
tips of the projections are dry coated with
other agents. Liposomes can be designed to
vaccine at t.11e nanoscale; hence, there is no
achieve various functions, including the
requirement for refrigeration of the vaccine
protection of the active ingredient from
during storage and transport. When t.11e
degradation in the GI tract, the transport of
device is applied to a patient's skin, the
drugs to sites of action, and prolongation of
projections protrude into the wet cellulai·
the residence time of the active ingredient
envirorunent below the skin smiace; on
in vivo.

wetting, t.l1e vaccine is delivered in <2 min.

Solid lipid nanoparticles are synthe

Only one one-hundredt.11 of the dose
sized from solid lipids. The�e nanoparticles
delivered conventional.ly by a needle ai1d
demonstrate excellent physical stability
syringe is administered to acrueve a
and protect the incorporated dmg from
comparable inllllunologic response, which
chemical degradation; however, low drug
is consistent with skin having more immune
loading capacity is a disadvantage. Studies
cells than muscle.

suggest it will be possible to develop a range

Nanotechnology-based vaccines may
of dosage forms, allowing solid lipid
decrease unwanted inflaim11atory response.

nanoparticles to be delivered by most

For example, studies have shown that the
routes of administration.

delivery of 50 nm ovalbumin a<;ljuvant

Polymeric nanoparticles consist of two
coupled to polystyTene nanobeads to sheep
main fo1ms: polymeric nanocapsu.les and
do not cause inflanm1atory reactions at t.11e
polymeric nanospheres. Polymeric
injection site. Thls outcome is thought to be
nanocapsules can be prepared from natural
attributed to the fact that adjuvants at the
and synthetic materials such as chitosan
nanoscale mimic the size of viruses, which
and poly(lactide-co-glycolide ), respectively.

ai·e well tolerated by cells.

From a drug delivery perspective, polyn1eric

Nanoclays have nmnerous applications,
nanocapsu.les demonstrate a hlgh dmg
including the delivery of agrochemicals ai1d
loading capacity and facilitate increased
t.l1e control of blue-green algae in waterdrug bioavailability and controlled dmg ways, and mai1y potential applications in
release. Other applications of polymeric
hlllllan and veterinary medicine. For
nanocapsules include the detection,
example, nanobiohybrids ai·e nanoclay
diagnosis, and treatment of disease, and
hosts with vai·ious biologic materials such
imaging. Polymeric nanospheres differ from
as DNA intercalated between the layers
polyn1eric nanocapsules, because drug is
that have potential applications in gene
physical.ly and unifonruy dispersed in a
t.11erapy. The nanobiohybrid host system
dense polyn1eric matrix with the fotmer.

is comprised of magnesium-alun1inum

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2525
layered double hydroxides wherein the
optical properties, including high-level
positive charge of the sheets of magnesium
fluorescence, long-tenn stability,
and aluminum hydroxides is balanced by
simultaneous detection of multiple signals,
the negative charge of hydrated anions.

and tunable emission spectra. In the

Through ion exchange, the interlayer anions
future, they may be used as a multifunc

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can be replaced with negatively charged
tional therapeutic for lymph node
biomolecules such as DNA. After delivery
mapping, identification of molecular
to a biologic system, nanobiohybrids are
targets, photodynamic therapy, drug
phagocytosed, and the biologic material
delivery, and surgical oncology. Quantum
released from the inorganic host either by
dots with cadmium selenium/zinc sulfide
dissolution of the inorganic host in the
cores with sizes ranging from 13-24 nm
acidic envirorunent of lysosomes or through emit different narrow wavelengths of reverse ion-exchange within the cellular
detectable light. This capability would
fluids.

allow detection of heterogenous tumors

Gold nanomaterial is biocompatible,
by coating quantum dots of different core
and when formulated as gold nanoparticles
sizes, and therefore emitting different
it is used in the diagnosis and treatment of
wavelengths of light, with different
diseases such as cancer. For therapeutic
cancer-specific antibodies to help
purposes, gold nanoparticles are coated
understand optimal tumor therapy. The in
with disease-specific swiace moieties and a
vitro toxicity associated with the core of
hydrophilic substance such as polyethylene
quantum dots (eg, cadmium selenium) can
glycol to prolong circulation tin1e. Near
generally be overcome by coating the core
infrared irradiation is used to visualize and
with other metals such as zinc sulfide or
destroy gold-targeted cancer cells by optical adding a protective hydrophilic coating hype1the1mia.

(eg, polyethylene glycol). Further research

Carbon nanotubes are being invesis necessary to evaluate the longterm tigated as nanovector systems. These
stability of quantum dots in vivo, which
nanomaterials have a high optical absorbis a major barrier to clinical translation.

ance at infra1:ed frequencies and may in the

Increased bioavailability as well as
future be used in a similar manner to gold
in1provements in targeted and controlled
nanoshells. The possible longterm toxicity
delivery of existing drugs and their
of carbon nanotubes due to bioaccumulaapplication through nanotechnology should tion is currently under investigation.

improve ease of administration and safety

Quantum dots are luminescent
and efficacy profiles for both anin1als and
semiconductor crystals with unique
people.

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE CARDIOVASCULAR SYSTEM

See also PRINCIPLES OF THERAPY 01' CARDIOVASCUdiuretics. They differ in their relative potency LAR DISEASE, p 74, MANAGEMENT OF HEART PAJLUllE,
and mechanisms of action. The loop
p 103, and FLUID THERAPY, p 1675.

diuretics are the most potent and have a

See table I for a listing of commonly used
high ceiling, enabling tl1em to be used in a
cardiovascular drugs and dosages. See also
dose-dependent way to treat mild to
p2625.

life-threatening CHF. Additionally, they can
be administered orally or parenterally.

DIURETICS

Thiazide diuretics are mild to moderate in
potency. They are typically used in conjunc

Diuretics are the cornerstone of therapy in
tion with a loop diuretic ( eg, furosemide) in
management of animals witl1 congestive
animals with severe refractory CHF.

heart failure (CHF) characterized by

Historically, the use of potassium-sparing
cardiogenic pulmonary edema, pleural
diuretics ( eg, spi.ronolactone) has been
effusion, ascites, or a combination of these
reserved for those animals that have right
signs. Three classes of diuretics are used to
heart failure or have become hypokalemic
treat CHF in dogs and cats: loop diuretics,
secondary to the use of other diuretics, or for
thiazide diuretics, and potassiW11-sparing
those animals refractory to other agents.

2526

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

COMMONLY USED CARDIOVASCULAR DRUGS AND

DOSAGES

Drug

Dosage

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Amiodarone

Dog: 8-10 mg/kg, PO, every 12-24 hr for 7-10 days, then reduce to 4-6 mg/kg/day for longtenn treatment

Amlodipine

Dog: 0.1-0.2 mg/kg, PO, bid; or 0.2-0.4 mg/kg/day, PO

Cat: 0.625-1.25 mg/cat, PO, once to twice daily

Aspirin (antiplatelet

Dog: 5-10 mg/kg, PO, every 1-2 days
dosage)

Cat: 1-2 mg/kg/day, PO; or \/,i of an 81-mg tablet/cat, PO, every 3 days (or twice per week)

Atenolol

Dog: 0.2-1 mg/kg, PO, bid

Cat: 1-2.5 mg/kg, PO, bid; or 6.25-12.5 mg/cat, bid

Benazepril

Dog: 0.25-0.5 mg/kg, PO, once to twice daily

Cat: 0.25-0.5 mg/kg, PO, bid; or 0.5 mg/kg/day, PO

Clopidogrel

Dog: loading dose for rapid onset of action (90 min) 10 mg/kg, PO (once); 1-2 mg/kg/day, PO, longLem1

Cat: 1/.i of a 75-mg tablet (18.75 mg)/day/cat, PO

Diltiazem

Dog: 0.5-2 mg/kg, PO, tid (standard formulation);

1-4 mg/kg, PO, bid (sustained release)

Cat: 7.5 mg/cat, PO, tid (standard formulation);

3-6 mg/cat, PO, once to twice daily (sustained release) Dobutamine

Dog: 2.5-15 mcg/kg/min, CRI3

Enalapril

Dog: 0.25-0.5 mg/kg, PO, bid

Cat: 0.25-0.5 mg/kg, PO, bid; or 0.5 mg/kg/day, PO

Furosemide

Dog: 2-4 mg/kg, IV, IM, SC, every 1-6 hr; 0.25-1 mg/kg/hr, CRI; or 1-5 mg/kg, PO, bid-tid

Cat: 0.5-2 mg/kg, IV, IM, SC, every 1-8 hr; 0.25-0.6 mg/kg/hr, CRI; or 1-2 mg/kg, PO, once to twice daily

Heparin

Dog: 100-200 U/kg, SC, tid-qid (unfractionated)

Dog and cat: 100-200 IU/kg, SC, once to twice daily (low molecular weight)

Hydralazine

Dog: 0.5-3 mg/kg, PO, bid

Lidocaine

Dog: 2-4 mg/kg, IV; 25-75 mcg/kg/min, CRI

Mexiletine

Dog: 4-6 mg/kg, PO, tid

Nitroglycerin ointment

Dog: 4-12 mg, topically, bid (maximum 15 mg/dog/dose) 2% (1 in. = 15 mg)

Cat: 2-4 mg/cat, topically, tid-qid for 1-2 days

Pirnobendan

Dog, cat: 0.25-0.3 mg/kg, PO, bid

Procainamide

Dog: 4-6 mg/kg, PO, every 2-4 hr (regular fonnulation); 10-20 mg/kg, PO, tid (sustained release); 2-25 mg/kg, slow IV bolus to effect, or CRI at 25-40 mcg/kg/min

Qttinidine sulfate

Dog: 5-10 mg/kg, IV, qid; or 6-20 mg/kg, PO, tid-qid Quirudine gluconate

Dog: 6-20 mg/kg, IM, qid; or 6-20 mg/kg, PO, tid-qid

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2527

COMMONLY USED CARDIOVASCULAR DRUGS AND

DOSAGES (continued)

Drug

Dosage

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Sildenafil

Dog: 1-3 mg/kg, PO, bid-tid

Sotalol

Dog, cat: 1-2.5 mg/kg, PO, bid

Spironolactone

Dog: 1-2 mg/kg, PO, bid; or 2 mg/kg/day, PO

Cat: 1-2 mg/kg, PO, once to twice daily

Torsemide

Dog: 0.25-0.4 mg/kg, PO, once to twice daily
a CRI = constant-rate infusion

All diuretics share a similar adverse effect
dogs and cats. Torsemide is anotl1er loop
profile, including electrolyte and acid-base
diuretic tl1at is -10 times as potent and has a
disturbances, dehydration, and prerenal and
longer duration of action than furosemide
renal azotemia. The relative 1isk of azotemia
with a similar adverse effect profile.

is increased when a diuretic is used con

However, current clinical experience with
currently with an angiotensin-converting
torsemide is far less than that of furoseenzyme (ACE) inhibitor and/or an NSAID
mide; thus, furosemide remains the diuretic
or otl1er potential renal toxin. Diuretics may
of choice in dogs and cats with CHF.

also increase the risk of digoxin toxicity. In
addition, diuretic resistance can develop

Preparations and Disposition:

with longtem1 treatment. The most common

Furosemide is available in oral (tablets,
electrolyte and acid-base abnom1alities
suspensions) and parenteral fom1ulations.

include hypokalemia, hyponatremia,

Compounded liquids (from tablets) may be
hypomagnesemia, and metabolic alkalosis.

better tolerated in cats than the commer

These effects are potentiated by the use of
cially available, alcohol-based, 1% syrup.

more tl1an one diuretic (sequential nephron

All loop diuretics inhibit sodiwn,
blockade), concurrent hyporexia/anorexia,
potassiwn, and chloride reabso1ption in
and tl1e use of higher doses. Typically,
the tl1ick po1tion of the ascending loop of
potential adverse effects are more severe

Henle, leading to inhibition of sodiwn and
in cats than in dogs.

conunensurate water reabsorption in the

Numerous factors detemline tl1e response
nephron. Furosemide diuresis results in
to diuretic therapy. These include tl1e
enl1anced excretion of sodium, chloride,
potency of the drug, the dosage administered, potassiwn, hydrogen, calcium, magnesium, the duration of action of the drug, the route of and possibly phosphate. Chloride excretion administration, renal blood flow, glomerular
is equal to or exceeds sodiwn excretion.

filtration rate, and neplu·on function. The

Enhanced hydrogen ion excretion without
plasma concentration depends on the route
a concomitant increase in bicarbonate
of administration (IV administration will
excretion can result in metabolic alkalosis.

produce a higher concentration than PO

Despite the increase in net acid excretion,
administration) and the dose. The duration of rninary pH falls slightly after furosemide effect will also detennine the total diuretic
administration, while urine specific gravity
effect produced in a certain time period.

is generally reduced to approximately

Animals witl1 CHF may become refractory 1. 006-1. 020.

to furosemide because of decreased delivery

In addition to its diuretic effects, furoseof the drug to the nephron as a result of mide acts as a mild systemic venodilator,
reduced renal blood flow or hormonal
decreasing systemic venous pressure
stimulus for sodiwn and water retention.

before diuresis occurs, especially after IV

Therefore, strategies to increase renal blood
administration. Furosemide df'creases
flow and/or plasma concentration may
renal vascular resistance. Thus, it acutely
an1eliorate diuretic resistance.

increases renal blood flow ( -50%) without
changing glomerular filtration rate.

Furosemide is highly protein bound

Furosemide

(86o/c,-9 l %). The ratio of kidney to plasma

Fw·osemide is a loop diuretic and the most
concentration is 5: 1. A small an1ount of
conm1only used diuretic to treat CHF in
furosemide (lo/c,-14%) is metabolized to a

2528

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
glucuronide derivative in dogs, but this

Clinical Use: For treatment of life-tlrrea.tmetabolism does not occur in the liver. In ening cai·diogenic pulrnonai-y edema in
dogs, --45% of furosemide is excreted in the
dogs, parenteral dosages of 2-4 mg/kg,
bile and 55% in the urine. After IV adminisevery 1-B hr, IV, IM, or SC in dogs and tration, furosemide has an elin1ination

0.5-2 mg/kg, every 1-8 hr, IV, IM, or SC in

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half-life of --1 hr, and its onset of action is
cats are typically used. Dosing intervals
within 5 min; peak effects occur within 30
depend on the response to therapy; initially,
min, and duration of effect is 2--3 hr.

boluses c,m be given eve1y 1 -2 hr ai1d

Approximately 50% of the drug is cleared
decreased to eve1-y 4-8 hr in dogs, and given
from the body within the first 30 min, 90%
every 2 hr and decreased to eve1-y 6-8 hr in
within the first 2 hr, and almost all is
cats. Alternatively, a constai1t-rate infusion
eliminated within 3 hr.

(CRI) of 0.25-1 mg/kg/hr in dogs or

Fw·osemide is rapidly but incompletely

0.25-0.6 mg/kg/hr in cats could be used.

absorbed after PO administration with a

Bolus administration and CRI for treatment
bioavailability of 40%--500/o. The tenninal
of life-tlrreatening pulmonary edema is
half-life after administration PO is
tapered over 12-24 hr as clinical signs
biexponential. The initial phase has a
resolve. Typical starting dosages for
half-life of --30 min, with the second phase
longterm management of CHF in dogs ai·e
half-life of --7 hr. The initial disposition

2 mg/kg, PO, bid, with a range of 1-5 mg/kg,
phase has the most effect on plasma

PO, bid-tic!, and in cats are 1 mg/kg/day, PO,
concentration, witl1 concentration
with a.range of 1 -2 mg/kg, PO, once to twice
decreasing from therapeutic to subtl1eradaily to a maxim wn total daily dose of peutic within 4--6 hr of PO administration.

4--6 mg/kg.

After PO administration, onset of action

Furosemide should be stored at 15°-30°C
occurs within 60 min, peak effects occur
and protected from light. Parenteral
within 1 -2 lu·, and duration of effect is --6 hr.

fo1mulations having a yellow color have

In healthy dogs, a dose of furosemide given
degraded and should not be used. Furoseat 2.5 mg/kg, IM, results in maximal mide tablets tl1at have been exposed to light
nat1iuresis (beyond tl1at dose there is no
may be discolored and should not be used.

further increase in sodium excretion).

Furosemide injection can be mixed with

This occurs at a plasma concentration of

0.9% saline or Ringer's solution. A precipi

--0.8 mcg/mL. Because the diuretic effect of
tate may form if the injection is mixed with
furosemide depends on its hematogenous
strongly acidic solutions such as those
delivery to the kidneys, aninlals with
containing ascorbic acid, tetracycline,
decreased renal blood flow ( eg, those
adrenaline (epinephrine), or noradrenaline
with heart failure) need a higher plasma

(norepineph1ine). Furosemide injection
concentration (higher dose) to produce the
should not be mixed with lidocaine,
san1e effect observed in healthy dogs. This
alkaloids, antihistainines, or morphine.

is achieved by adn1inistering higher oral
doses or by administering the drng IV.

Thiazide Diuretics

Cats are more sensitive to furosemide
than dogs. Clinically, cats commonly require The thiazides act primarily by reducing no more than 1-2 mg/kg, PO, once to twice
membrane pem1eability to sodiwn and
daily for longterm treatment of pulmonary
chloride in the distal convoluted tubule.

edema. However, higher dosages may be

They promote pota.ssiwn loss at this site
needed in cats with severe heart failure
and produce large increases In urine sodiwn
because of reduced renal blood flow.

concentration but only mild to moderate
increases in urine volmne. The thiazides are
ineffective when renal blood flow is low,

Drug Interactions and Toxicity: Drug
which may explain their la.ck of efficacy as a
interactions and adverse effects/toxicities
sole agent in aninlals with severe heait failure.

are typically those described for diuretics as
a class. However, some special considera

Preparations and Disposition: Hydrotions for furosemide bear mentioning.

chlorothiazide is available in tablet form. In

Furosemide has the potential for ototoxicdogs, tltiazides are well absorbed after oral ity. When adn1inistered as the sole agent,
a.dntinistration. Hydrochlorothiazide has an
furosemide in dosages >20 mg/kg, IV, can
onset of action within 2 hr, peaks at 4 hr, and
result in loss of hearing in dogs. Dosages
lasts 12 hr.

of 50-100 mg/kg result in profound loss of
heaiing. Furosemide can also potentiate the

Drug Interactions and Toxicity: Drng
ototoxic and nephrotoxic effects of other
interactions include a decrease in efficacy
drugs such as the a.minoglycosides.

of anticoagulants and insulin and ai1

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2529
increase in efficacy of digoxin, loop
kidneys. Peak diuresis occws as late as
diuretics, vitamin D, and some anesthetics.

2-3 days after adnunistration.

Thiazide diuretics are also reported to
prolong the half-life of quinidine.

Drug Interactions and Toxicity: Poten

The most common adverse effects of
tial toxicities include hyperkalemia, wluch
thiazide diuretics a.re electrolyte disturmay be exacerbated by concmTent therapy VetBooks.ir
bances. Thiazide diuretics are potassium
with an ACE inhibitor, especially if fw·osewasting, and when combined with loop rnide is not also ad.nunistered. Facial excoriadiuretics, the likelihood of adverse effects tion has been reported in cats, but initial
such as azotemia and hypokalemia are
reports may overestimate the frequency.

increased. They may also increase calcium
reabso.rption and thus lead to hypercalce

Clinical Use: In dogs with CHF, particumia. Adverse effects, including renal failure, lai·ly those with ascites secondaiy to right
can be minimized when hydrochlorothiheart failw·e, an increased plasma aldosterazide is added to chronic CHF treatment one concentration may be present, and the
protocols that include high-dose furosernide effect of these diuretics may be enllanced.

by reducing the total daily dose of

However, potassiun1-sparing diuretics are
furosemide by approximately 25'Xr50% and
weak dim·etics when used alone and thus
staiting at the lower end of the monother should never be used as sole agents in apy dosage range for hyd.rochlorothiazide
animals with heait failure. When potassiwn

(2 mg/kg, PO, bid).

spaiing diuretics are administered with other
cliuretics such as fw·osemide, potassiwn

Clinical Use: Compared with that of
loss is decreased, which may be beneficial.

furosernide, the relative potency of thiazide

Recent studies suggest that adding spironodiuretics is low in dogs and cats when used lactone to chronic CHF treatment in dogs
as monotherapy; thus, they ai·e rarely used
may inlprove survival. The increasing use of
as first-line diuretics in these species.

spironolactone in veteri.naiy medicine is

Thiazides are primaiily used in dogs that
related to these potential cardioprotective/
have developed furosemide resistance
anti.fibrotic effects and not its diuretic effect
and ai·e commonly referred to as rescue
per se. The dosage of spironolactone for
diuretics in dogs. The typical monotherapy
diuretic use is 2-4 mg/kg/day. Lower dosages
dosage for hydrochlorothiazide in dogs is

(0.5-1 mg/kg, bid) may be considered for

2-4 mg/kg, PO, bid. When hyd.rochlorothiinhibition of the RAAS. Typical dosages for azide is added to furosemide, the initial
adjunctive treatment of CHF in dogs are
dosage should be 2 mg/kg, PO, bid. The

1-2 mg/kg, PO, bid, or 2 mg/kg/day, PO;
typical monotherapy dosage for hyd.rochlosinliiar dosages are used for a cardioprotecrothiazide in cats is 0.5-2 mg/kg, PO, once to tive indication in dogs. Typical dosages for twice daily.

adjunctive treatment of CHF in cats are

1-2 mg/kg, PO, once to twice daily.

Potassium-sparing Diuretics

This class of diuretics acts by inhibiting the

POSITIVE INOTROPES
action of aldosterone on distal tubular cells
or by blocking sodiwn reabso.rption in the

Positive inotropes increase the strength of
latter regions of the distal tubule and
cardiac muscle contraction by increasing
collecting tubules, exerting a mild diuretic
the quai1tity of intracellular calciw11
effect compai·ed with that of fw·osemide.

available for binding by muscle proteins,

Spironolactone is structurally similar to
by increasing the sensitivity of contractile
aldosterone and binds competitively to
proteins to calcimn, or a combination of
aldosterone-bind.ing sites in the distal
both (eg, pimobendai1). This, in tum,
tubule. Because of its aldosterone
augments contractile protein interaction in
antagonism, spironolactone is also
the myocai·dial cell. lntracellulai· calciun1
considered an inlubitor of the renin-angiocan be increased by altering the Na•/Ca2•
tensin aldosterone system (RAAS) ai1d thus
exchai1ge pwnp, by increasing production
a neuroendocrine modulator. Spironolacof cyclic adenosine monophosphate tone is the most commonly used potassiwn

( cAMP) via stimulation of adenylate
spai·ing diuretic in veterinary medicine.

cyclase, or by decreasing degradation of
cAMP via inhibition of phosphodiesterases.

Preparations and Disposition:

Spironolactone is available as a tablet for oral Cardiac Glycosides ad.rninistration. It is highly protein-bound,

The probable mechanism of action for
metabolized by the liver, ai1d excreted by the
the modest inotropic effect of digoxin is

2530

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
inhibition of the membrane-bound Na+fK+

Absorption of oral cligoxin is variable;

ATPase pump; when this occurs, Na+ inc

-600A, of the tablet formulation is absorbed.

reases in the cell, the exchange of Na+ for

With little hepatic metabolism, almost all

Ca2+ via the Na+/Ca2+ exchange pump is
tl1e absorbed drug reaches the vasculatu.re.

augmented, and there is a small increase in

Absorption is slowed by food. Digoxin is

VetBooks.ir
calcium influx. The increased intracellular
distributed slowly and concentrated in
calciwn in turn leads to increased release of
cardiac tissues, and -25%is botmd to

Ca2+ from the sarcoplasmic reticulum and
plasma proteins. It is primaiily eliminated
increased contractility of the cardiac
unchanged via the kidneys (15% is
muscle. However, because these changes
metabolized and excreted via tl1e liver); its
are modest, digoxin does not result in
half-life ( -2�9 hr in dogs, and extremely
significant inotropy, and the availability of
variable in cats) is sti·ongly influenced by
more potent oral positive inotropes has
renal function. Steady state is reached after
superseded its use for this indication.

-5 half-lives, and maintenance doses should

Digoxin also has a combination of both
theoretically achieve a therapeutic serum
proa.rrhythmic and antia.rrhythmic
concentration within 2-4 clays.

properties. TI1e alterations in the ratio of
intracellular and extracellular electrolytes

Drug Interactions and Toxicity:

caused by digoxin can result in increased

A mm1ber of medications can increase
automaticity and cardiac arrhythmias.

plasma cligox.i.n concenti·ations, including

Negative chronotropic effects are due to
aspirin, quinidine, chlorainphenicol,
decreased conduction velocity in the
aininoglycosides ( eg, neomyci.J1), ainiodaratrioventricular (AV) node via increased one, anticholinergics, Lliltiazem, esmolol,
parasympathetic tone, as well as direct
flecainicle, tetracycline, and spironolaceffects that help slow AV nodal conduction tone. Furosemide, hyclrochlorotl1iazide,
and prolong the AV nodal cell refractory
amphotericin B, and glucocorticoids
period. Digoxin also has parasympathomideplete body potassiwn and tlms potentiate metic effects on the sinoatrial node and atlia.

digitalis intoxication and proaiThythmic

In addition, it potentiates vagal ( cholinergic)

effects. Admi.Jtistration of 13-adrenergic
activity in the heait. The changes in
agonists (eg, clobutamine) also increases
conduction can lead to AV nodal blockade
tl1e risk of proarrhythmia. Longterm
and reductions in heait rate (ventlicular
administration of phenobarbital may
response rate) when digoxin is used to treat
decrease digox.i.n concentrations by
supraventricular anhytlunias, including
increasing clearance. Calciun1 charm el
atrial fibrillation. However, digoxin is
blockers and 13-blockers will potentiate
rarely efficacious as a single agent for this
action on the AV node conduction,
indication. Digoxin has a narrow therapeutic
increasing 1isk of AV block.

window, and at toxic levels it can directly

Toxic effects witl1 digitalis glycosides are
slow sinus nodal activity due to increased
common a.11d can be lethal. Cats ai·e more
sensitivity to acetylcholine. Because the
sensitive to digox.i.n than dogs. Probably the
atlia are sensitive to acetylcholine, atlial
most frequent cause of toxicity is inadverconduction is also enhanced in the diseased tent overdosing. The potential for toxicity is
heart, which can then lead to atrial
increased with hypokale1nia and azotemia.

aiThythmias. Digoxin is believed to improve

The likelihood and severity of toxicity are
vascular baroreceptor responsiveness,
related to the severity of cardiac disease.

thereby mi.J1in1izing sympathetic activation

Other factors that would require dosage
in heart failure states. TI1is is accomplished
adjustment to prevent toxicity include renal
via decreasing plasma catecholamine
failure (azotemia), hypothyroidism,
concentrations, which affect both sympadecreased muscle mass (a significant thetic ne1ve activity and plasma renin
ainotmt of digox.i.n is bound to skeletal
activity, tl1ereby mini.Jnizing sympatl1etic
muscle), ascites, hypercalcemia, a.11d
activation. In this way, digoxin may be
myocardial failu.re leading to reduced renal
considered to be a neuromodulator. Lastly,
blood flow. Signs of toxicity relate to the GI
digoxin also has been reported to have a mild system ( most common adverse effects) or cliw·etic effect via tl1e Na+/1(+ ATPase pw11ps

CNS, or marlifest as arrhythmias, with
present in tl1e renal tubular epitl1elial cells.

digitalis capable of inducing a.11y type of
cardiac a.IThythmia. GI signs of toxicity

Preparations and Disposition: The
include diarrhea, anorexia, and nausea and
oral form of digoxin is the most widely
vomiting due to direct stin1ulation of the
used preparation. Otl1er preparations
chemoreceptor trigger zone. Frequently,
are available but not used routinely
these are the earliest indications of toxicity.

in veterinaiy medicine.

Neu.rologic effects include malaise and

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2531
drowsiness. Digmdn toxicity can be
methylxanthines, theophylline is the most
diagnosed (and avoided) by monitoring
cardiopotent. In addition to their cardiac
plasma drug concentrations. Treatment of
effects, methylxanthines have significant
intoxication includes discontinuing therapy

CNS, renal, and smooth muscle effects,
with digitalis and potassium-depleting
including on bronchial smooth muscle. The

VetBooks.ir
diuretics and administering phenytoin
use of methylxanthines in cardiac disease is

(blocks AV nodal effects of digitalis),
lin1ited to conditions that would benefit
lidocaine (for ventricular arrhythmias), and
from bronchodilation.

if indicated, potassiwn (preferably PO).

Pimobendan is a benzimidazole

Atropine may be useful to treat both
pyridazinone derivative and is a positive
clinically significant sinus bradycardia and
inotrope and balanced systemic arterial and
second- or third-degree heart block induced
venous dilator. In failing hearts, it exerts
by cholinergic augmentation. Arrhythmias,
positive inotropic effects primarily through
clinical signs, and electrolyte abnormalities
sensitization of the cardiac contractile appashould be treated as clinically indicated on a ratus to intracellular calciun1. As a PDE 3
case-by-case basis.

inhibitor, pimobendan can potentially
increase intracellular calcium concentra

Clinical Use: In general, the availability
tion and myocardial oxygen conswnption.

of other medications with similar activities

However, the cardiac PDE effects of
and more favorable risk-benefit ratios
pimobendan are reportedly minimal at
with respect to toxicity have dran1atically
pharmacologic doses in dogs with heait
reduced the clinical use of digoxin in dogs.

disease, which is a major advantage relative

Digoxin is rarely if ever used in cats for
to other inotropic PDE inhibitors such as
any indication. Current typical clinical
milrinone. PDE 3 inhibitors such as
indications in dogs are for adjunctive (in
pimobendan result in balanced vasodilation
combination with another antiarrhythmic)

( combination of venous and arterial
treatment of supraventricular arrhytlunias
dilation) leading to a reduction of both
such as atrial fibrillation or flutter, as part
cai·diac preload and afterload. In addition,
of management of chronic, advanced, or
pimobendan may have some direct
refractory CHF, or to treat vasovagal
endothelial-derived vasodilatory effects.

syncope.

The significance of alterations in proinflain

Maintenance dosages are 0.003-0.011 mg/
matory cytokine concentrations such as
kg, PO, bid, for dogs, and 0.005-0.01 mg/kg,
tun10r necrosis factor-13 and interleukins 113

PO, every 24--48 hr for cats. In general,
and 6 on the progression of heart failure has
initial dosages should be at the lower end
been docun1ented in many forms of heart
of the range and rounded down, and then
disease. Maladaptive alterations in these
titrated up, if needed, based on measurecytokine concentrations are associated with ment of serum digoxin levels (target serwn
increased morbidity ai1d mo1tality, and
concentrations 0.8-1.2 ng/mL 8-12 hr after
pin10bendan has demonstrated beneficial
administration). Toxicity can occur even in
modulation of several such cytokines in
animals that have levels in the therapeutic
various models of heart failure.

range. Levels should be monitored 3-5 days

Pimobendan reportedly may have some
after initial treatment (8-12 hours after
platelet inhibitory effect in dogs and cats,
administration) and every 6 mo thereafter
but the clinical significance of this is not yet
or sooner if signs of toxicity develop.

clear. Lastly, PDE 3 inhibition in cardiomyo

Digoxin dosages should be calculated based cytes leads to more rapid relaxation; thus, on lean body weight and reduced in obese
pimobendan can also be considered to be a
or cachectic animals and in the presence of
positive lusiotrope.

ascites. Known electrolyte disorders should
ln dogs, pin10bendan is extensively
be corrected before digitalis glycosides are
metabolized, and both the parent drug and
administered.

active metabolite are >900A, bound to plasma
protein. The steady state volun1e of

Phosphodiesterase Inhibitors
dist1ibution of pimobendan is 2.6 Ukg, and
the tem1inal elin1ination half-lives of

Phosphodiesterase (PDE) inhibitors, also
pimobendan and its active metabolite are
known as inodilators, block the breakdown

0.5 and 2 hr, respectively. Oral bioavailabilof cAMP and therefore increase intracelluity is reduced by food rn1til steady state is lar cAMP concentrations. The result is an
reached in a few days. Consequently,
increase in myocardial contractility and
pimobendan should be administered on an
peripheral vasodilation. Methylxanthine
empty stomach at least 1 hr before feeding
derivatives have been classified as PDE
for maximal effects when starting therapy.

inhibitors, but this is controversial. Of the

Hemodynamic effects after PO administra-

2532

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
tion on an empty stomach peak in l hr and
than either drug alone. Botl1 medications
last 8-12 hr; therefore, pimobendan can
should be titrated up slowly while
provide rapid short-term support to dogs
monitoring for atThythmias, blood pressure,
with acute or decompensated heart failure.

and clinical response to treatment.

IV preparations are available in some

Dopan1ine is contraindicated in the face
countries.

of ventricular atThythmias and when a pheo

VetBooks.ir

Pimobendan is approved for treatment of
chromocytoma is suspected. Care should be

CHF due to dilated carcliomyopathy (DCM)

used in tl1e setting of ao1tic stenosis. lf tl1e
and chronic degenerative mitral valvular
animal has recently taken a monoainine
disease (DMVD) in clogs. It has also been
oxiclase inhibitor, the rate of clopan1ine
shown to prolong symptom-free survival in
metabolism by the tissue will fall ai1cl the

Doberman Pinschers with occult DCM.

dosage should be reduced to one-tenth of

Pimobenclan has an excellent safety profile,
usual.

and clinical data suggest that it is safe when

Dobutamine is a synthetic drug similai·
administered concomitantly with other
to clopainine, but it does not cause release
medications commonly used in treatment of of norepinephrine and therefore has canine CHF. Rep01tecl adverse effects are
minimal effects other than l31 activity.

minimal, but the main one is GI intolerance

Dobutamine is a more effective positive
of tl1e chewable tablet formulation.

inotrope thai1 dopamine with less chrono

Pimobendan is contraindicated in clogs
tropic effects, although it does not dilate
with known outflow tract obstruction ( eg,
the renal vascular bed. Its plasma half-life
subaortic stenosis ). Pimobenclan is not
is-2 min. Dobutainine is prepai·ecl as a
approved for use in cats. A nwnber of
solution to be diluted witl15%dextrose
retrospective studies in cats, using dosages
or normal saline. When compared with
similar to those used in dogs, suggest it is
dopamine, dobutainine is the preferred
well tolerated, but there is no definitive

13-adrenergic agonist for short-term therapy
proof of efficacy.

of refractory CHF when pin10benclan alone

The mechanism of action of the
is not successful or insufficient. Dobutainine
bi pyridine derivatives amrinone and
causes an immediate increase in blood
milrinone is probably in11ibition of PDE
pressure clue to increased cardiac output. It
and increased levels of intracellular cAMP.

is given as a CRI at 2-15 mcg/kg/min; heait

Both anrrinone and milrinone are available
rate, blood pressure, and cai·cliac output
for IV administration and are suitable only
should be monitored. In cats, clobutainine
for sho1t-term management of CHF.

has a longer half-life and causes CNS

However, with the wide availability and
stimulation, so lower infusion rates
known efficacy of pin10bendan, these

(0.5--10 mcg/kg/min) should be used. It is
medications have fallen out of favor for
rai·ely indicated in cats.

treatment of CHF.

Compared with other inotropic drugs,
epinephrine, with its 131 and 132 effects,
jl-Adrenergic Agonists
causes tl1e greatest increase in the rate
of energy usage and myocardial oxygen

These drugs cause a positive inot;ropic
demand. This increase in oxygen need
effect by activating 13-receptors with
may be detrimental to tl1e failing heait.

subsequent stimulation of aclenylate

Epinephrine also causes vasoconstriction
cyclase and increased cAMP.

ai1d bronchodilation. Epinephrine is rapidly

Dopamine is an endogenous catecholametabolized in the GI tract and is not mine precursor with selective 131 activity.

effective after administration PO. Absorp

However, it also stimulates release of
tion is more rapid after IM versus SC
norepinephrine. At low closes, it stimulates
administration. Epinephrine is available in
renal cloparninergic receptors, which causes several preparations and is effective after increased renal blood flow and diuresis. It

IV, pulmonary, and nasal administration.

is rapidly metabolized by the body and

However, because of the decreased
has a half-life of <2 min. Dopamine is
efficiency of cai·cliac work, epineplu"ine is
available as a solution, which is further
not used as a positive inotropic agent but
diluted with saline or dextrose. It is
rather for emergency therapy of cardiac
administered IV, usually by CRT (1-15 mcg/
arrest and ai1aphylactic shock. Ventriculai·
kg/min). Cardiac arrhytlunias may develop
atThythmias should be expected and ai·e a
clue to 13-aclrenergic activity. Indications
contraindication to using epinephrine
include carcliogenic or enclotoxic shock and
except in ljfe-threatening situations.

oliguria. In carcliogenic shock, infusion of

Isoproterenol is a nonspecific 13-agonist
equal concentrations of clopan1ine and
that, like epinephrine, increases myocardial
dobutarnine may afford more advantages
oxygen demand. Tachycai·clia and tl1e

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2533
potential for other arrhythmias excludes
bioavailability is -600/o. Serum concentraits use in a cardiac patient except for tion of enalaprilat peaks in 3-4 hr. The
short-tem1 therapy of bradyarrhythmias
half-life is -11 hr, and effects last 12-14 hr,

(eg, AV block). It is typically used as a CRI
indicating the need for dosing intervals of
to effect based on the heart rate desired.

every 12 hr if 24-hr suppression of ACE
is desired. Excretion of enalapril and

VetBooks.ir
enalaprilat is primarily renal; therefore, the

ANGIOTENSIN-CONVERTING
half-life of enalap1il/enalaprilat is increased

ENZYME INHIBITORS
in animals with severe CHF (reduced renal
perfusion) or renal failure, and dose

Angiotensin-converting enzyme (ACE)

reduction may be warranted.

inhibitors are widely used to treat chronic

Like enalapril, benazepril is a prodrug

CHF in dogs and cats. In the pathogenesis
converted to its main active metabolite
of CHF, the proteolytic enzyme renin is
benazeprilat in the liver. Benazepril is well
released by the kidneys and acts on
absorbed in dogs, and oral bioavailability
angiotensinogen, which is produced by
increases by -35% with repeated dosing.

the liver and distributed in the blood, to

After administration of oral benazepril,
produce angiotensin I. The fonnation of
benazeprilat concentration peaks in plasma
angiotensin II from angiotensin I occurs
within 1 -3 hr and is rapidly distributed.

through the action of ACE. Angiotensin II

Benazeprilat is excreted approximately
causes retention of Na+ and water, in pa.it
equally in the bile and urine in dogs. The
through stimulation of the synthesis and
terminal half-life is -3.5 hr. This combined
release of aldosterone by the adrenal
excretion may allow better dosing control in
cortex. Angiotensin II also causes vasoconanimals with preexisting renal insufficiency; striction, thus increasing systemic vascular
however, benazepril is no more renal
resistance. ACE also results in degradation
protective than any other ACE inhibitor
of bradykinin and, thus, ACE inhibitors lead
at equipotent doses. When benazepril is
to increased levels of bradykinin that
administered longterm, dosages from
contribute to their vasodilatory effects. By

0.25-1 mg/kg produce indistinguishable
inhibiting the formation of angiotensin II,
effects at the tin1e of peak effect (2 hr after

ACE inhibitors prevent vasoconstriction

PO administration) and at trough effect
and reduce retention of Na+ and water in

(24 hr after PO administration); thus, dosing
animals with CHF. ACE inhibitors are
intervals may be as long as 24 hr, but
balanced vasodilators, reducing both
benazepril is often dosed every 12 hr to
preload and afterload. The effects during
ensure continuous ACE throughout the day.

CHF include decreased vascular resistance
and cai·diac filling pressures and increased

Drug Interactions and Toxicity:

cardiac output and exercise tolerance. How

Hypotension may develop with concurrent
ever, ACE inhibitors have only a mild effect
use of ACE inhibitors and other vasodilators
on afterload reduction and should not be

( eg, amlodipine) or diuretics. Concurrent
used as monotherapy in animals with severe use of potassium-sparing diuretics ( eg, systemic hypertension(> 160 mmHg).

spironolactone) may cause hyperkalemia.

Enalapril and benazepril appeai· safe when
used concomitantly with fu.rosemide,

Preparations and Disposition: Enalpimobendan, digoxin, antiarrhythmics, april and benazepril ai·e widely used ACE

13-blockers, bronchodilators, and cough
inhibitors and are available in a vaiiety
suppressants. However, it has been
of tablet sizes for oral administration.

suggested that concurrent use of NSAIDs

Compai·ed with enalapril and benazepril,
may increase risk of adverse effects.

captopril has a greater propensity for GI

ACE inhibitors have a good safety profile
adverse effects and a sh01ter half�life in
and have been used safely in combination
dogs, necessitating more frequent dosing;
with other cai·diovascular drugs (including
thus, its use has fallen out of favor. A
diuretics and pimobendan). However,
wide variety of other ACE inhibitors ( eg,
azotemia may develop, and monitoring of
lisonop1il, rainipril) ai·e sometimes used

BUN and creatinine (with possible dosage
in veterinary medicine. Choice in pa.it is
adjustments) is wai-rai1ted. This possible
often related to drug availability, cost, and
complication is the result of the partial
availability of canine and feline pharmacoloss of renal autoregulation of blood flow kinetic and pharmacodynainic data.

mediated by angiotensin II. Other possible,

After absorption from the GI tract,
albeit rai·e, adverse effects include GI
enalapril is converted in the liver to the
disturbances (anorexia, vomiting, diarrhea),
active metabolite enalaprilat. Oral
syncope due to hypotension, weakness, and

2534

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
ataxia. Preexisting renal disease and

Arterial Dilators
dehydration increase the risk of adverse
effects; thus, anin1als witl1 these predispos

Hydralazine is an arteriolar vasodilator,
ing conditions should be monitored closely.

tile mechai1ism of action of which is not

Cough is a common adverse effect of this
clearly elucidated. It directly rela,'<'.cs the

VetBooks.ir
class of drugs in people but is not a
vascular smooth muscle in systemic
recognized problem in dogs or cats.

arterioles by inhibiting calciwn fluxes into
the cell or by increasing local prostacycli.n

Clinical Use: ACE inhibitors are
concentrations. Hydralazine has no effect
indicated in treatment of CHF in dogs and
on systemic venous tone. It is bound to
cats stemming from a wide variety of
smooth muscle, which results in a biologic
diseases. However, there is no proof that
half-life longer fuan plasma half-life.

ACE inhibitors may delay the onset of CHF

Hydralazine is well absorbed after
in asymptomatic animal:, with cardiac
administration PO but (in people) is subject
disease. ACE inhibitors are also frequently
to first-pass metabolism. The incidence of
used (typically in combination witl1 other
toxicity caused by hydralazine may be
aiterial dilators) to manage systemic
significant ai1d related to its potency as an
h
aiterial dilator leading to h
ypertension in dogs and cats. Somewhat
ypotension. The
paradoxically, ACE inhibitors such as
potency of hydralazine can be both
benazepril have been shown to be beneficial
beneficial and detrin1ental: it results in good
in treatment of some fom1s of renal disease.

to profound i.mprovement in most animals

Enalapril is approved in the USA to treat
in which it is indicated, but it can also result

CHF secondaiy to DCM and MMVD in dogs.

in systemic hypotension. The effective

Benazepril is approved in several countries
dosage range in dogs is 0.&-3 mg/kg, PO, bid.

other thai1 tl1e USA to treat CHF in dogs.

This dose must be titrated, starting with a

The recommended dosage of enalapril and
low dose and titrating up to an effective
benazepril for treatment of CHF in dogs is
clinical endpoint while monitoring for

0.25--0.5 mg/kg, PO, once to twice daily.

hypotension. Doses may need to be even

However, based on tl1e half-life, if continuous
lower when hydralazine is combined with

ACE inhibition is desired and well tolerated,
oilier chugs that have arte1ial dilat01y
then a 12-lu- dosing interval is reconm1ended.

effects.

The reconm1ended dosage for adjunctive

Calcium channel blockers as a class
treatment of CHF in cats is 0.25--0.5 mg/kg,
are considered vasodilators, but individual

PO, bid, or 0.5 mg/kg/day, PO. Similar doses
agents have different relative potencies
ai·e used when enalapril or benazep1il is used
and additional effects. Calcium chaimel
to treat systemic h
blockers are also class lV antiarrhyfurnics,
ypertension. However,
enalapril and benazepril have only modest
negative inotropes (an adverse property),
arte1ial vasodilatory effects and should not
and positive lusitropes ( drugs fuat improve
be used as monotherapy in anin1als with
relaxation of cardiomyocytes ).

severe systemic h

Amlodipine primarily affects tile
ypertension ( systolic blood
pres.sure >160--180 mmHg). In general,
calciwn chaimels in tile small arterioles,
rega.rdles.s of clinical indication, stattipg at
leading to arterial dilation. Atnlodipine is
tile lower dose range and increasing to
the only calciwn chaimel blocker used in
maximal dose witl1 monitoring of renal
veterinaiy medicine fuat has potent arterial
fw1ction, serun1 potassiw11, and systemic
dilatory effects with negligible effects on
blood pres.sure is reconunended. Higher
inotropy and conduction. The effects of
doses of benazepril, if tolerated, may be
ainlodipine are similar to those ofhydralaindicated to treat some fonns of renal zine, and it is used for similar indications in
disease ( eg, protein-losing glomerulopafuy ).

dogs and cats. Atnlodipine appears to be
better tolerated by the GI tract. The effec

VASOACTIVE DRUGS
tive dosage range in dogs is 0.1-0.2 mg/kg,

PO, bid, or 0.2-0.4 mg/kg/day, PO. The

Vasodilator drugs can be categorized as
effective dosage range in cats is 0.62&-1.25
afterload reducers or preload reducers.

mg/cat, PO, once to twice daily. This dose

Afterload is reduced by dilation of arterioles
must be titrated, starting with a low dose

(ie, resistance vessels), whereas preload is
and titrating up to an effective clinical
reduced by dilation of veins (ie, capacitance
endpoint while monitoring for hypo tension.

vessels). Atterial dilators ai·e used in

Doses may need to be even lower when
treatment of systemic hypertension in dogs
amlodipine is combined with other drugs
and cats and as adjw1ctive treatment for CHF fuat have arterial dilatory effects. In in dogs, particularly when CHF is secondaiy
resistant systemic hypertension, doses at
to degenerative mitral valve disease.

tile higher end of the range ai·e needed. In

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2535

CHF in dogs, initial dosages should be at the
undergoes significant first-pass metabolism.

lower end of the range and titrated to effect

Prazosin is rarely used clinically in small
with appropriate monitoring. Gingival
anin1als to treat primary cardiac disease.

hyperplasia has been reported as an adverse The dosage in dogs and cats is 0.5-2 mg/kg effect of amlodipine in dogs and cats.

per animal, PO, bid-tid, or 0.07 mg/kg, PO,

VetBooks.ir
bid-tid.

Arterial and Venous Dilators

(Mixed dilators)

Phosphodiesterase 5 Inhibitor

Organic nitrates and nitrites relax both

Sildenafil is an orally active phosphodiesarterial and venous vascular smooth muscle terase 5 inhibitor. Phosphodiesterase 5
through a complex series of events. At low

(PDE 5) is found in a relatively high
concentrations, which are generally used
concentration in the lungs and the corpus
clinically, venous dilation predominates, and cavemosum otthe penis. In dogs, pulmonet systemic vascular resistance is usually nary hypertension is a clinically important
not affected. Pharmacologic effects occur
disease with high morbidity and mortality
rapidly. First-pass metabolism limits the use
rates; it is typically a sequela of another
of these drugs to IV, sublingual, and topical
disease process and thus requires a

(ointment) administration. Tolerance is a
balanced therapeutic approach that targets
problem with sustained administration.

the underlying etiology as well as palliation

Nitroglycerin, an organic nitrate,
of clinical signs. An in1portant goal of
relaxes vascular smooth muscle. However,
therapy is to reduce pulmonary artery
the dosage of nitroglycerin used clinically
resistance. Conventional systemic arteriolar
results in predominantly venous dilation
dilators have no preferential effect on
and preload reduction. Nitroglycerin is
pulmonary vasculature and thus have no
indicated for acute (emergency) adjunctive
benefit and may worsen clinical signs
treatment of CHF in dogs and cats; however,
attributable to puln10nary hypertension.

efficacy for this indication in these species

Inhibition of PDE 5 in the small arterioles
is anecdotal. It is available for IV and sub linof the lung leads to dilation that is more gual use and as an ointment. The 2%
significant than dilation of the systemic
ointment preparation (1 in. = 15 mg) is the
aiterioles. In people with pulmonaiy
most commonly used; it is applied to the
hypertension, PDE 5 inhibitors improve
hairless portion of the animal's skin
both exercise tolerance and quality of life.

(abdomen or ear). The dosage in dogs is

Sildenafil has been used in dogs for

4-12 mg, topically, bid ( maxinmm of 15 mg/
adjunctive treatment of clinical signs
dog per dose) for 1-2 days, and in cats, 2-4
related to pulmonary hypertension
mg/cat, topically, every 6---8 hr for 1-2 days.

secondary to a variety of etiologies; proof of

The most prevalent adverse effect involves
efficacy remains predominantly ai1ecdotal,
accidental exposure of veterinary personalthough it does appeai· to be safe and well nel, which can be avoided by careful
tolerated for this indication.

application and labeling of application sites.

The typical starting dosage in dogs is

Nitroprusside is one of the most potent

1 mg/kg PO, tid, or 1-2 mg/kg, PO, bid.

vasodilators available. It is an organic nitrate

The reported dosage range is 1-3 mg/kg,
and reduces preload ( venous dilation) and

PO, bid-tid. Efficacy may be potentiated
afterload ( arterial dilation) in a dose-dependwith coadministration of L-arginine at ent marmer. Advantages of nitroprusside

250-500 mg/dog, PO, bid. Adverse effects
include potency, rapid onset of action, and
of sildenafil appear to be rai·e in dogs, but
short half-life. The main disadvantage is that
anecdotally systemic hypotension is
it must be administered by CRI (1-10 mcg/
possible. There are no reported drug
kg/min, IV), with appropriate, typically
interactions, and published reports have
invasive, blood pressure monitoring.

docun1ented use of sildenafil in dogs in

Nitroprusside is indicated in dogs for
combination with many other medications,
emergency reduction of blood pressure in
including conventional heart failure
a hypertensive crisis and for ilmnediate
medications ( eg, diuretics, ACE inhibitors,
afterload reduction ( severe, life-threatening
piI11obendan), with no recognized adverse

CHF). Nitroprusside should only be used for
effects.

48---72 hr because of buildup of its toxic
metabolite, cyanide.

Prazosin is an a

ANTIARRHYTHMICS

1-adrenergic receptor
blocker and thus considered to be a mixed

AntiaiThytlunics are typically classified
vasodilator. It is effective when given PO,
according to their predominant electrobut tolerance develops rapidly. It also physiologic effect on myocardial cells.

2536

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

However, the electrophysiologic effects of
gluconate are in dogs, 6-20 mg/kg, IM, qid,
some agents span more than one class, and
or 6-20 mg/kg, PO, tid-<1.id; and in horses,
some have ancillary properties unrelated to

1-1.5 mg/kg, IV, every 5-10 min. Individualtheir antiarrhythmk effects. However, this ized therapy is necessary because of
classification scheme typically does not aid
significant phannacodynarnic variation

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in selection of an antiarrhythmic for a
arnong anin1als and the potential for toxicity.

specific clinical indication ( eg, ventricular

Car·diotoxicity can marlifest in the fmm of
vs supraventricular arrhythmias). Many
vent.ticular· arThythmias. The atropine-like
antiarrhytlunics have never been used with
effects of quinidine may result in increased
any frequency in veterinary medicine (and
in1pulse conduction through the AV node to
are not covered here). In ad di lion, many
the vent.tides and paradoxical acceleration
of these agents (in particular the class I
in vent.ticular response in aninlals with atrial
medications) have fallen out of favor for
fibrillation. Quinidine, particularly in the
treatment of arThytlunias in people, and as a
sulfate fonn, can cause vasodilation and GI
consequence their availability and costs are
adverse effects (25% of dogs). In horses,
becoming problematic.

swelli.ng of the nasal mucosa, urticarial
wheals, ar1d larninitis are other potential

Class I Drugs
adverse effects. The most important clinical
problem lintiting use of quinidine is

Class I agents comprise the group of agents
exacerbation of hear-t failure after adminisgenerally known as "membrane-stabilizing tration, likely as a consequence of its
drugs" such as quinidine, procainarnide, ar1d
negative inotropic effects. In general,
lidocaine. These agents work by selectively
quinidine use should be avoided in dogs with
blocking a proportion of the fast sodiw11
severe myocar·dial failure or in dogs that
charm els in cardiomyocytes, leading to
have, or have had, hear-t fa.ilme. Quinidine
depression of phase O of the action potential should not be used in cats. Monitoring the and subsequent reductions in conduction

ECG and serwn quinidine concentration car1
velocity. These agents are often subdivided
reduce the likelihood of adverse effects.

into three subclasses (A, B, and C) based on

Procainamide effects are similar to
their concurrent effects on repolarization;
those of quinidine. However, its effects
however, this has little clinical relevance.

on the autonomic nervous system are
significar1tly weaker (less antivagal effect).

Class IA Drugs: Class IA drugs used in

Procainarnide has efficacy against
veterinary medicine include quinidine and
ventricular and supraventricular· arrhythprocainarnide.

mias and has been used for both indications

Quinidine is related to the ar1ti.rnalarial
in dogs. It is often used par·enterally in
drug quinine. In addition to its membranecombination with lidocaine to treat stabilizing propetties inherent to Class I
life-threatening ventricular· arrhytl1.rnias.

agents, it also has indirect, antivagal

The par·enteral formulation has also been

("atropine-like") effects in the atria. It has used to treat supraventricular arrhytlunias,
efficacy against supraventricular and
including conversion of recent onset at.tial
ventricular arrhytl1.rnias. Its main mdication
fibrillation. The oral fmmulation is useful to
in veterinary medicine is to treat atrial
treat vent1icular arrhythmias and supravenfibrillation. It has the potential to conve1t tricular arrhythmias secondary to accessory
atrial fibrillation to sinus rhytlun and is used
path ways. It has little efficacy in longterm
for this indication in horses. In dogs, it is
management of atrial fibrillation. Procainaused to facilitate synchronized cardiove1�
mide is rapidly and almost completely
sion of attial fibrillation. It is not typically
absorbed after administration PO. Only
used for rate control of chronic atrial

-200Ai is protein bound. Procainan1ide is
fibrillation in dogs or horses, or to treat
extensively biotrar1sformecl by the liver to
ventricular arrhytlunias. The sulfate
metabolites that ar·e generally inactive in
preparation of quinidine is absorbed rapidly
dogs. Both oral ("regular" and sustainedafter administration PO. The gluconate fonn release) and parenteral fonnulations (IV
is absorbed more slowly. It can be given IM
ar1d IM administration) are available. The
but is painful. Although 900A, of quinidine is

"regular" fonnulation necessitates dosing
protein-boW1d, dist.tibution is rapid to most
every 4 hr for maintenance in clogs, severely
tissues. The half-life varies ar110ng species
limiting its use for longterm treatment. The
and is -6 hr in dogs and -8 hr in horses.

sustained-release product has fallen out of

Dosages of quinidine sulfate are as
favor in people, limiting its availability; it is
follows: in dogs, 5-10 mg/kg, IV, qid, or 6-20
not currently available in the USA.

mg/kg, PO, tid-<1.id; and in horses, 22 mg/kg,

Procainarnide is dosed in dogs at 2 mg/kg,

PO, every 2 hr. Dosages of quinidine
slow IV bolus, to a maximum cumulative

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2537
dose of 25 mg/kg over 10-15 min, continuing It is most often an adjunctive treatment in if needed as a CRI at 25-40 mcglkg/nun or at
severe, chronic ventricular arrhythnuas not

10-20 mg/kg, tid-qid, IM or SC. The oral
well controlled by sotalol alone or in dogs

(regular) fo1mulation is dosed at 4-6 mg/kg,
that do not tolerate sotalol. It has fallen out

PO, every 2-4 hr (maintenance dose every
of favor for treatment of people; thus, its

VetBooks.ir

4 hr), and the sustained-release formulation
availability is linutecl and cost is increasing.

at 10-20 mg/kg, PO, tid.

It should be administered at its lowest

Toxicities include hypotension and AV
effective dose with food to limit toxicity.

block (IV administration only), proarrhyth

Common adverse effects include anorexia,
nua (longtenn administration), alteration in
vomiting, tremors, and hepatic toxicity.

coat color (longterm administration), and

Hepatic enzymes should be evaluated

GI disturbances with the oral formulations.

before treatment and periodically (approximately every 6 mo) during chronic Class 18 Drugs: Class IB drugs used in
treatment as well as any time GI disturveterinary medicine include lidocaine, bances develop during treatment. The
mex:iletine, tocainide, and phenytoin.

dosage in dogs is 4-6 mg/kg, PO, tid.

Lidocaine is used predominantly for

Tocainide is an analogue of lidocaine
acute treatment of ventricular arrhythmias.

used to treat ventricular arrhythnuas in

It has no efficacy against supraventricular
dogs. Sinular to mexiletine, it is rarely used
arrhythmias and minimal effects on the
as monotherapy for ventricular arrhythautonomic nervous system. It is ideal for mias. It is most often an add-on treatment
acute treatment because it has a rapid onset
of choice for severe chronic ventiicular
of action and short half-life ( -1 hr in a dog)

arrhytlunias not well controlled by sotalol
and is effective and safe. The short half-life
alone, in dogs that do not tolerate sotalol,
facilitates rapid changes in serum concenor if mexiletine is not available or cost trations and, therefore, titration to effect.

prohibitive. It has fallen out of favor for

Liclocaine is extensively metabolized by the
treatment of people; thus, its availability
liver; thus, hepatic disease and reduced
is linutecl and cost is increasing. Potential
hepatic blood flow can prolong the half-life.

adverse effects include CNS and GI

Hypokalemia seriously impairs the efficacy
disturbances (35% of dogs), hypotension,
of lidocaine. Lidocaine is available only as a
bradycardia, tachycardia, other arrhythparenteral fomrnlation for IV administramias, and progressive corneal edema.

tion. It should not be infused through the

Because of these adverse effects, use of
same catheter or line as other medications.

tocailude is limited if other efficacious

The typical clinical approach in dogs is to
agents are available. Tocainide has been
administer 2 mg/kg, IV boluses over -1 min
used in clogs at 15--20 mg/kg, PO, tid.

to effect (slowing the ventricular arrhyth

Phenytoin has a linuted spectrum of
mia or conversion to sinus rhytlun) or to a
antian·hytlmuc activity. Its primary use is in
cumulative close of 8 mg/kg over -30 nun.

management of cligitalis-inducecl arrhyth

Given the ve1y short half-life, repeat boluses nuas, because it abolishes digitalis-inclucecl or a CRI (25--75 mcg/kg/min) is needed to
abnom1al automaticity. The recommended
maintain rhythm control. Liclocaine is rarely dosage in dogs is 30 mg/kg, PO, ticl, or 10
indicated in cats, because clinically
mg/kg, IV, over 5 1nin.

significant or life-tlu-eatening ventricular
arrhythmias are rare in th.is species. The

Class IC Drugs: Exan1ples of drugs in
dosage in cats is O.l--0.4 mg/kg, IV bolus
this class include encainide, flecainide, and
over -1 min, then increase to a total dose of
propafenone. These drugs are not typically

0.25--1 mg/kg, IV slowly, if no response. This
used in veterirnuy medicine.

can be followed by a CRI ( 10-20 mcglkg/
min). Lidocaine has few undesirable effects.

Toxicity is manifest in dogs primarily as GI

Class II Drugs
and CNS signs. Drowsiness or agitation may

Class II antianhythm.ic drugs are the
progress to muscle twitching and convul[3-adrenergic receptor blocking agents.

sions at lugher plasma concentrations.

[3-Blockers are classified as nonselective

Hypotension may develop if the IV bolus is

(block both [3, and [3
given too rapidly. In cats, which are more

2 receptors) or selective

(block predominantly [3
susceptible to toxicity, cardiac suppression

1 receptors). As a
class, all [3-blockers are dose-dependent
and CNS excitation may be seen.

negative inotropes and chronotropes.

Mexiletine is an oral analogue

Although characterized as class II
of lidocaine used to treat ventricular
antiarrhythnuc agents, [3-adrenergic
arrhythmias in dogs. It is rarely used as
blockers are used for a variety of indications
monotherapy for ventricular arrhythnuas.

in veterinary medicine, including control of

2538

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
inappropriate or undesirable sinus

CHF is life-threatening, abrnpt cessation
tachycardia, treatment of ventricular and
should still be a.voided. Potential adverse
supraventricular arrhythmias, manageeffects are dose related and more likely if ment of chronic hypertension in dogs and
underlying systolic function is present.

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cats, and palliation of adverse effects of

Adverse effects include myocardial
uncontrolled hyperthyroidism in cats and
depression, bradycardia (sinus and AV
pheochromocytoma in dogs. They are well
block), and hypotension.

recognized for their cardioprotective effects

Carvedilol is a third-generation
in people with heart failure, leading to

13-blocker that has a more complete
improved survival. Data and experience
adrenergic blocking spectrum. Carvedilol
supporting this indication in veterinary
blocks 13,, 132, and a, receptors and has
medicine is lacking in dogs and cats, and
some ancillary antioxidant effects. It is
the relative risks of initiation of a 13-blocker
routinely used in treatment of heart failure
in the face of heart failure should not be
in people. Its oral bioavailability is highly
ignored. The earliest generation of this class variable in dogs. Carvedilol has been was nonselective, blocking both 13, and 132
mainly evaluated in veterinary medicine
receptors ( eg, propranolol). Subsequent
for its potential survival benefits in canine
generations became selective 13,-receptor

DCM and cardiovascular disease with and
blockers in an attempt to limit the adverse
without CHF, but experience to date is
effects associated with 13rreceptor
limited and thus it is not routinely used for
blockade (eg, atenolol). Third-generation
this indication. If 13-blockers are used for

13-blockers ( eg, carvedilol) were developed
this indication, the general rule of thumb
to be more complete adrenergic blockers
is to never initiate in the face of active
and are 13,, 132, and o.1-receptor blockers.

heart failure (pulmonary edema), start

Carvedilol may also have some important
low (initial dose), go slow (and titrate up),
antioxidant effects that have contributed to
and aim high (target dose tolerated). The
its proven efficacy for treatment of heart
initial dosage in dogs is 0.15-0.25 mg/kg,
failure in people.

PO, bid, titrated up by increasing the dose

Propra.nolol, the prototype, is competi

-25% every 2 wk while monitoring for
tive and nonselective, blocking both 13, and
clinical signs suggestive of decompensa132 receptors. The dosage in dogs is 0.2-1
tion. The target dosage is 1 mg/kg, PO,
mg/kg, PO, tid (titrate dose to effect) and in
every 2 hr (if tolerated). Higher target
ca.ts is 0.4-1.2 mg/kg (2.5-5 mg/cat), PO, tid.

doses may be tolerated in dogs concur

Use of propra.nolol should be a.voided in
rently receiving pimobendan and in dogs
dogs and ca.ts with evidence of primary
with cardiovascular disease (vs those
respiratory disease ( eg, asthma).

with DCM).

Atenolol is a 13,-selective blocking a.gent
and is the most commonly used 13-blocker
in veterinary medicine. Because it is

Class Ill Drugs

13,-selective, it has less potential to ca.use or

The predominant electrophysiologic effect
contJibute to bronchospasm.in predisposed
of class III drugs is potassimn channel
dogs and ca.ts, although the 13,-selectivity is
blockade leading to prolongation of the
likely limited or absent at high doses. The
cardiac action potential and its refrac-
dosage in dogs is 0.2-1 mg/kg, PO, bid, and
tory period. The two drugs in this class
in ca.ts 1 -2.5 mg/kg, PO, bid, or 6.25-12.5
commonly used in veterinary medicine
mg/cat, PO, bid. Some references suggest
are sotalol and a.miodarone.

cats can be dosed every 24 hr, but most

Sota.Joi is an oral class Ill drug with
cardiologists believe that continuous
nonselective 13-blocking activity. Sota.Joi

13-blockadc (the clinical target) is not
is the most commonly used longtem1
possible with daily dosing. In both dogs and
treatment for hemodynamically significant
cats, titrating up gradually is required,
ventricular arrhythmias in dogs and ca.ts.

especially if atenolol is initiated in the face

It is often used as monothera.py for this
of active or stable CHF or in DCM. In
indication but can be combined with
general, dogs and ca.ts without CHF and
mexiletine if rhythm control is suboptimal
nonnal systolic function can tolerate higher
with sotalol alone. It has some efficacy in
initial and target dosages. Abrnpt discontreatment of atrial fibrillation (rate control), tinuation should be a.voided; if cessation
but it is not as efficacious as other agents
is indicated, titrating down gradually is
and is not commonly used for this
recommended. If CHF develops in an
indication. Sota.Joi is safe and well tolerated
animal receiving a.tenolol, the dosage
and is often used in combination with other
may need to be reduced and the drug
drugs commonly used to treat heart disease
eventually discontinued, but unless the
and heart failure, including ACE inhibitors,

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2539
furosemide, spironolactone, and
nun1ber of known conm10n adverse effects
pimobendan. Because it has f3-blocking
that limit its longterm (>6 mo) use clinically.

effects, it should not be combined with

Adverse effects seem to be related to dose
other f3-blockers ( eg, atenolol) or other
and duration of treatment and include

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negative inotropes ( eg, diltiazem ). In
significant increases in liver enzymes, GI
addition, it should not be combined with
signs, thyroid dysf1mction, blood dyscrasias
another class III agent (eg, amiodarone).

(neutropenia), and proarrhythmia. The

The dosage in dogs and cats is 1-2.5 mg/kg,
liver effects seem to be the most common

PO, bid. It should be used with caution and
adverse effect encountered clinically and
at the lower end of the dosage range in
are typically reversible after cessation of
patients with CHF or DCM or when
therapy. The oral dosage in dogs is 8-10
combined with mexiletine. In this situation,
mg/kg, PO, once to twice daily for 7 -10
titrating up ( dosage increases every 10-14
days, and then decreased to 4-6 mg/kg/clay
days) to a higher target dose may be
for longtem1 treatment; the parenteral
attempted if lower doses are not efficacious. dosage in dogs is 2-5 mg/kg, IV, infused Dogs and cats with no1mal systolic function
over 30-60 min. Formulations preserved
can tolerate higher initial and target doses.

with polysorbate 80 should not be used IV

Possible adverse effects include negative
because of risk of anaphylactoid reaction
inotropy, bradyarrhythmia (sinus and AV
and angioeclema.

block), and proanhythmia.

Amiodarone is a class III drug with a
variety of other properties. Its predominant

Class IV Drugs
electrophysiologic effect is to prolong the

The predominant electrophysiologic effect
refractory period of atrial and ventricular
of class IV antiarrhythmic drugs is blockade
myocardiwn and the AV junction. In
of the slow calcium channels in cardiac cells
addition, it has class I effects (sodium
and vascular smooth muscle. The two drugs
channel-blocking properties), some class II
in this class commonly used in veterinary
effects (f3- and a-receptor blockade), and
medicine are diltiazem and an'\lodipine. The
some class IV effects ( calciwn channel
relative affinity of a drug in this class for
blockade). Amiodarone is used to treat
cardiac versus vascular tissue detennines
life-threatening ventricular anhythmias
its predominant effect. Amlodipine (see

( rhythm control) and atrial fibrillation ( rate
p 2534) is most active in vascular smooth
control) in dogs refractory to other, more
muscle, where it causes vasodilation and is
common treatments. In some cases, it is
thus considered to be a vasodilator.

used because of its effectiveness in

Diltiazem is most active in cardiac cells.

treatment of both ventricular and supra

Diltiazem blocks entry of calciwn into
ventricular arrhythmias. It is rarely used
cardiomyocytes during the action potential,
as a first-line drug.

leading to a close-dependent reduction in

Amiodarone has unusual pharmacokinetcalciun1 release from the sarcoplasmic ics. After repeated administration in dogs,
reticulwn, limiting the availability of
it has a long half-life of 3.2 days, with
calciwn to the contractile apparatus, and
myocardial concentrations reaching 15
resulting in negative inotropy and positive
times that of plasma The long half-life
lusitropy. It also blocks calcium channels
suggests a long time is needed to produce a
in the specialized conduction tissue in the
significant effect once treatment is initiated
heart, on which automaticity of intrinsic
as well as for effects to end if treatment is
pacemaker cells and AV conduction depend
discontinued. However, some clinical effect
for normal fw1ction. Blockade of these
appears to occur within hours of PO
calciwn channels can therefore slow heart
administration, especially if a higher loading rate and AV conduction. Diltiazem is dose is used, which is likely a consequence
therefore typically indicated for treatment
of the large and variable nwnber of
of atria.I fibrillation ( rate control) and other
metabolites.

supraventricular arrhythmias in dogs and

Amiodarone is often used in combination
cats. Another historical indication is for
with other drugs commonly used to treat
treatment of feline hypertrophic cardiomyheart disease and heart failure, including opathy. However, limited practicality in

ACE inhibitors, furosemide, spironolactone, combination with its unconfirmed efficacy and pin1obencla.n. Because it has f3-blocking
for feline hype1trophic cardiomyopathy has
effects it should not be combined with other caused diltiazem to fall into disfavor for this f3-blockers ( eg, atenolol) or other negative
indication. Diltiazem has no effect on
inotropes ( eg, diltiazem ). In addition, it
ventricular arrhythmias.

should not be combined with another class

The dosage in dogs is 0.05--0.2 mg/kg, IV,

III agent ( eg, sotalol). Amiodarone has a
over 5 min, which can be repeated to a

2540

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
cumulative dose of 0.3 mg/kg, after
is not readily absorbed. Dietary deficiency
which the dog should be reassessed or
of B 12 is rare; deficiency usually results
an oral fo1mulation initiated. In dogs, the
from poor absorption from the GI tract.

dosage of the standard oral formulation is

Vitamin B,2 absorption is complex and

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0.5-2 mg/kg, PO, tid, and of the sustaineddepends on gastric acid, pepsin, and intrinrelease fonnulation 1-4 mg/kg, PO, bid.

sic factor secreted from gastric parietal

In cats, the dosage of the standard oral
cells or pancreatic duct cells. Intrinsic
formulation is 7.5 mg/cat, PO, tid, and of the
factor binds to and protects vitamin B12
sustained-release formulation 30-60 mg/cat,
from digestion. In this form, B,2 binds

PO, once to twice daily. Initial doses should
to highly specific receptor sites in the
be at the lower end of the dose range and
brush border of the ileum, where it enters
titrated up to a clinically effective dose.

enterocytes by pinocytosis. Interference

Blood pressure and heait rate and rhythm
with its absorption in the ileum results
should be monitored during IV administrain continuous depletion, although maiw tion. Dogs and cats without CHF and with
months of defective absorption are
normal systolic function can tolerate higher
necessary before deficiency develops.

initial and target dosages. The sustained

Vitamin B12 is bound in the plasma to
release fonnulation cannot be made into
transcobalan1in. It is stored in large
suspensions but can be refom1ulated into
quantities in the liver and slowly released
lower-dose capsules.

as needed. It is excreted into the bile but

Possible adverse effects include systemic
undergoes enterohepatic cycling.

hypotension, negative inou·opy and

Vitainin B12 (clogs: 100-200 mcg/day, PO
bradycardia ( sinus or AV block), and
or SC; cats: 50-100 mcg/day, PO or SC) is
exacerbation of CHF GI signs are the
available in oral and parenteral preparations
common noncardiac adverse effect and are
of cyanocobalainin. There are no significant
more common in cats, especially with
toxicities associated with therapy.

sustained-release preparations. Diltiazem is

Indications for therapy are limited to cases
often used in combination with other drugs
of vitan1in B,2 malabsorption, such as
commonly used to u·eat heait disease and
ileectomy, gastrectomy, or deficiency
heait failure, including ACE inhibitors,
malabsorption syndromes ( eg, exocrine
furoselnide, spironolactone, and
pancreatic insufficiency). Chronic
pin10bendai1. Because diltiazem is a negative administration of Hrreceptor blockers inotrope and chronotrope, it should not be

( cin1etidine, raiutidine, fan1otidine) can also
administered concun·ently with a [3-blocker.

lead to vitan1in B,2 deficiency, because ai1

Amlodi pine is selective for calciumacid environment is necessary for its channel blockade in vascular smooth
absorption.

muscle, with minimal effects on cardiac

Folic acid is needed for DNA and RNA
calcium trai1sport. Amlodipine is recomsynthesis. Anelnia associated with folic acid mended for hypertension in cats and dogs.

deficiency is characterized as megaloblastic. Sources of folic acid in the diet include DRUGS ACTING ON TAE BLOOD
yeast, liver, kidney, ai1d green vegetables,
although it can also be fonned by microbes.

OR BLOOD-FORMING ORGANS

Folic acid is stored in the liver but not as
avidly as vitai11in B,

Hematinics

2• Because folic acid is
destroyed by catabolic processes every

Anelnia can be treated pharmacologically
day, serum levels decrease rapidly in the
by providing components needed for RBC
presence of deficient diets. Absorption
production, including hemoglobin
of folic acid is not as sensitive as that of
synthesis, ai1d by stimulating bone marrow
vitan1in B,2, although jejunal pathology
fom1ation of RBCs.

can result in folate deficiency.

Vitamin B12 is essential for DNA

Folic acid ( dogs: 5 mg/clay, PO; cats: 2.5
synthesis. Deficiency causes inhibited
mg/day, PO) is available in both oral and
nuclear maturation ai1d division. RBC
parenteral formulations. Significant toxicity
maturation arrest in the bone marrow
is not associated with therapy. Indications
leads to megaloblastic or pernicious
for therapy include inadequate intake due
anemia. Vitan1in B12, a porphyrin-like
to administration of selected drugs ( eg,
compound consisting of a ring structure
methotrexate, potentiated sulfa drugs,
that contains centrally located cobalt, is
some anticonvulsants [ eg, primidone and
derived from the diet and microbial synthephenytoin]), liver disease, malabsorption, sis in the GI tract. However, except for
or other chronic debilitating diseases.

ruminants, microbial production occurs in

Iron is necessary for hemoglobin
the large intestine, from which vitan1in B12
forn1ation. It is available in the diet either

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2541
as a heme form, which is a small percenis 100 U/kg, SC, 3 times/wk for4 mo, while tage of the total but readily absorbed, or a monitoring PCV, followed by a maintenance
nonheme fom1. Absorption of the nonheme
dosage of 75-100 U/kg, SC, 2-3 tin1es/w k.

form is profoundly affected by diet. Iron is

The most significant adverse effects in dogs
absorbed from the proximal jejunum, where and cats are development of antibodies to VetBooks.ir
it immediately combines in the enterocyte

ERP, resistance to treatment, and worsening
to the globulin tra.nsferrin. It is transported
of anemia. Other potential adverse effects
in the plasma in this form, but the binding
include iron deficiency, hypertension, fever,
is loose and iron can be easily transferred
local cellulitis, arthralgia, mucocutaneous
to tissues. Iron enters cells via specific
ulcers, polycythemia, and CNS disturbances
receptors that interact with tra.nsferrin.

(seizures).

In the cell, iron combines with the protein

Anabolic steroids are compounds
apofenitin to become feITitin, the soluble
structurally related to testosterone that
form of iron storage. Smaller quantities are
have similar protein-anabolic activity but
also stored as the insoluble hemosiderin;
minimal androgenic effects, such as
the amount of this storage fonn increases
masculinization. As part of their anabolic
when the total amotmt of iron in the body is activity, these compounds increase the
much more than apoferritin can accommocirculating RBC mass and possibly date. There is no mechanism for the
granulocytic mass. Clinical indications for
excretion of iron other than via the GI tract.

use of anabolic steroids include chronic,

GI elimination occurs by exfoliation of
nonregenerative anemias. Response to
enterocytes containing iron, biliary
therapy is vaiiable, and the time to clinical
elimination, and elimination of dietary iron
improvement is long, frequently �3 mo. The
that has not been absorbed.

proposed mechanisms of action include

Indications for iron therapy are limited to
increased ERP production via ERP-stimutreatment or prevention of iron deficiency lating factor, differentiation of stem cells

(eg, blood loss, pregnancy). Iron is available
into ERP-stimulating factor-sensitive cells
in both oral and parenteral preparations.

(eg, hemocytoblasts), and direct stimulation

Oral preparations should be ferrous salts,
of erythroid-progenitor cells. The effect of
such as sulfate ( dogs: 100-300 mg/day; cats:

anabolic steroids requires adequate ERP

50-100 mg/day), gluconate, and fumarate.

levels and sufficient cells in the bone

Therapy can be continued for several
maiTow. Thus, the effectiveness of anabolic
months to replenish body iron stores.

steroids in treating anemia may be limited,

Response to iron therapy can be assessed
depending on the cause.

by monitoring circulating hemoglobin

Anabolic steroids can be divided into two
concentrations. Adverse effects are
categories depending on the presence or
dose-related. Parenteral preparations are
absence of an alkyl group at tl1e 17-car.bon
indicated for initial treatment of iron
position. They ai·e available as oral ai1d
deficiency or if oral preparations cannot be
parenteral preparations, including oil-based
tolerated or are not feasible ( eg, in neonatal
products intended for slow release. The
pigs). Iron dextrans can be given as a single
absorption 3.lld disposition of anabolic

IM injection (100 mg) at 2-4 days of age in
steroids depend on the type of prepai·ation
newborn piglets. Toxicity may be seen and
and the animal species. Most are eliminated
is manifest as pale skin, bloody diarrhea,
after hepatic metabolism. The alkylated
and shock (seep 3077). When efficacy of
products are more effectively absorbed
parenteral preparations is compared,
when given PO and are more effective
deA'tran complexes and hydrogenated
stiniulants of bone marrow. Alkylated
dextrans are more effective than dextrins.

3.llabolic steroids include oxyn1etholone

Hemoglobin formation requires pylidoxine

(dogs 3.llci cats: 1-5 mg/kg, PO, eve1y
and the trace elements copper and cobalt

18-24 hr). Nonalkylated 3.llabolic steroids

(necessary for B12 synthesis by nm1inal
include nandrolone decanoate ( dogs:

microftora). "Shotgtm" preparations contain 1-1.5 mg/kg/wk, IM; cats: 1 mg/kg/wk, IM; a combination of hematinic agents; the
horse: 1 mg/kg, IM, once every 4 wk).

efficacy of such products is questionable. As

Boldenone undecylenate is approved for
with any hematinic preparation, provision
horses at 1.1 mg/kg, IM, every 3 wk. Adverse
of these compounds will be ineffective if the
effects of anabolic steroids include sodium
nutritional status of the animal is poor.

and water retention, virilization, and

Epoetin alfa is the synthetic fonn of the
hepatotox:icity. The alkylated products are
human glycoprotein erythropoietin (ERP).

more hepatotox:ic than the nonalkylated

Epoetin alfa is indicated in treatment of
products, particularly in cats. Cholestatic
anemia associated with chronic renal
liver d3.111age develops eai·Jy and can be
failure in dogs and cats. The initial dosage
significant but frequently is reversible.

2542

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

Hemostatics
during therapy. The lag period after adminis4'0philized concentrates of one or more tration of phytonadione and synthesis of
clotting facLors are available as topical or
new clotting factors is 6---12 hr.

local hemostatics. Most act to provide an

Desmopressin is a synthetic analogue

VetBooks.ir
aitificial factor or structural matrix that
of vasopressin and is used to tJ.·eat diabetes
facilitates control of capillary bleeding. An
insipid us. ln animals with von Willebrand
intact hemostatic mechai1ism is necessary.

clisease, desmopressin transiently increases

These absorbable products are indicated for von Willebrand factor and shortens bleeding capillary oozing from small, superficial
time. It may be useful in dogs with von Willevessels. Concentrated factors include brand disease (0.4 mcg/kg, SC; 1 mcg/kg, IV,
thromboplastin, thrombin (available as a
diluted in 20 mL of saline and given over 10
powder, solution, or sponge), collagen, and
min), to permit surgical procedures or
fibrinogen. Artificial matrices include fibrin
control capillary bleeding.

foan1, absorbable gelatin sponge, and
oxidized cellulose.

Anticoagulants

Astringents act locally by precipitating

Anticoagulants interfere eitl1er directly
proteins. These agents do not penetrate
or indirectly with the clotting cascade.

tissues and, thus, ai·e restJ.icted to surface

Heparin is a heterogeneous mixture of
cells. They can be dan1aging to surrounding
sulfated (anionic) mucopolysaccharides
tissues. Exainples include feJTic sulfate,
named because of its initial discovery
silver nitrate, and taimic acid.

in high concentrations in the liver. It is

Epinephrine and norepinephrine are
prepared from porcine intestinal mucosa
hemostatics by vi1tue of their vasoconstricand bovine Jung. It acts indirectly to tive effects. They may be included in topical
facilitate endogenous anticoagulai1ts,
medications to decrease blood flow to the
specifically antithrombin III and hepaiin
tissues, or applied intrai1asally in tai11pons
cofactor II. These molecules fonn stable
to decrease epistaxis.

complexes with (and tl1Us inactivate)

Systemic hemostatics include fresh
clotting factors, especially thrombin.

blood or blood components administered to

Heparin is released in its active fonn after
animals that. have a coagulation factor
inactivation of the clotting factor and tl1Us
deficiency. Exainples include fresh plasma,
cai1 interact with other molecules. The
fresh frozen plasma, cryoprecipitate, and
effect is greater with low concentrations of
platelet-rich plasma.

hepaiin. Hepaiin is also antitlrrombotic due

Vitamin K is a hemostatic only in
to binding to endothelial cell walls, thus
instances of vitainin K deficiency. It is necesimpailing platelet aggregation and sary for hepatic synthesis o( coagulation
adhesion.

factors II, VII, IX, and X. The principal

Clinical indications for heparin therapy
indication is treatJ.nent of rodenticide
include the prevention or treatment of
toxicity, moldy sweet clover poisoning
venous or pulmonary embolism and

( dicurnarol), and sulfaquinoxaline toxicity.

embolization associated witl1 atrial

Vitan1in K1 (phytonadione) is a plant form
fibrillation. It is also used as an anticoaguof vitainin K that is safer and more effective lant for diagnostic use and blood transfuwith more rapid restoration of coagulation sions. Heparin is used in conjw1ction with
factors than other analogues such as
blood and/or plasma to treat dil,seminated
vitai11in K3 (menadione). The prefeJTed
intravascular coagulation (DIC) and otl1er
routes to administer phytonadione are
hypercoagulable conditions. It has also

SC and PO, although it can be given by
been used to clear hyperlipidemia.

slow IV (anaphylactic reactions have been

Heparin is available as a sodium or
reported) or IM injections. After IM adminiscalciW11 salt. Absorption and clistribution tration, bleeding may occur at the injection
of hepaiin are limited by the large size and
site. The dosage regimen selected depends
polaiity of tl1e molecule. Oral absorption is
on the nature of the anticoagulant toxicity.

poor; hence, it is a parenteral anticoagulant.

Vitainin K1 must be given as long as the

Although anticoagulant activity is first order,
anticoagulai1t is present in the body at toxic
half-life of the drug is close-dependent,
levels; this duration varies depending on the
steady-state concentrations are difficult to
rodenticide. Second-generation coumaiin
achieve, and pharmacokinetics vary ainong
derivatives or indai1ediones are potent and
individuals. Heparin is metabolized by
have long half-lives. Several weeks of
hepaiinase in tl1e liver and by reticuloenvitanlin K1 therapy may be necessai-y after dothelial cells. Metabolites of hepaiinase
ingestion of these long-acting rodenticides.

activity are excreted in the urine. The half

Coagulation status should be monitored
life is prolonged in renal or hepatic failure.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM

2543

Heparin can be given IV ( either intermitof vitanlin K. Their anticoagulant activity tently or as a constant infusion) or SC. Deep

(and therefore therapeutic or toxic effect)

SC or intrafat in,jection prolongs persistence is delayed for 8-12 hr after administration of therapeutic concentrations. Large
or accidental ingestion because of the

VetBooks.ir
hematomas can develop after deep IM
persistence of factors synthesized before
irtjection. High-dose heparin therapy ( dogs:

administration. Factor VII has the shortest

150-250 U/kg, SC, tid; cats: 250-375 U/kg,
half-life and is the first factor to become

SC, bid) has been reconunended for
deficient.

established thromboembolism. Lower

The vitamin K antagonists are rapidly and
dosages (dogs and cats: 75 U/kg, SC, tid;
completely absorbed after administration
horses: 25-100 U/kg, SC, tid) are indicated

PO. Levels peak in 1 hr. They are almost
in management of DIC. Blood coagulation
totally protein bouncl in plasma, and their
times ( eg, activated partial throm boplastin
volume of distribution is limited to the
time) should be monitored during therapy.

plasma volume. They are metabolized by

Adverse effects and toxicities of heparin
the liver to primary metabolites and then
are limited to potential hemorrhage and,
coajugated to glucuronides. They undergo
because heparin is a foreign protein,
an enterohepatic cycle. A variety of factors
possible allergic reactions. Heparin is
can increase the activity of these drugs,
contraindicated in bleeding animals and in
including hypoproteinemia, antimicrobial

DIC unless replacement blood or plasma
therapy, hepatic disease, hypermetabolic
therapy is also given.

states, pregnancy, and the nephrotic

Low-molecular-weight heparins
syndrome. The potential for drug interac

(LMWHs, eg, dalteparin and enoxaparin)

tions is significant. Because they are highly
are alternatives to "unfractionated heparin"

protein bound, they can be displaced by
and are used extensively in people as
other drugs that are protein bound ( eg,
anticoagulants for various thromboembolic
acetylsalicylic acid and phenylbutazone ),
conditions. LMWHs differ from heparin in
and their anticoagulant effects can be
that the molecular weights are approxiincreased to the point of toxicity. Drug mately one-tenth that of heparin, dosing can interactions also are seen with other be once to twice daily in people, there is no
antihemostatics.

need to monitor activated partial thrombo

Warfarin sodium is the most commonly
plastin time, the risk of bleeding and
used therapeutic preparation. The dosage is
thrombocytopenia is smaller, and the effect

0.1-0.2 mg/kg/day, PO, for dogs and cats,
on thrombin is less than that of heparin.

and 0.067-0.167 mg/kg/day, PO, for horses.

LMWHs target antifactor Xa activity.

Toxicity, manifest as hemoIThage, is a major

Limited efficacy, safety, and dosing data
concern with vitamin K antagonists.

are available to guide use in veterinary

Coagulation times (particularly prothrom-
medicine. However, a suggested dosage
bin time), CBCs, and clinical evidence of
regimen for dalteparin in dogs and cats is
bleeding ( eg, occult blood in feces and

100-200 ill/kg, SC, once to twice daily, and a
urine) must be monitored carefully dwing
suggested dosage regin1en for enoxaparin in
warfarin therapy.

dogs and cats is 1-2 mg/kg, SC, bid, while

Fibrinolytic agents increase the activity
monitoring prothrombin time. Individual
of plasmin (fibrinolysin), the endogenous
responses to LMWHs appear to be quite
compound responsible for dissolving clots.

variable in cats.

The inactive precursor of pl as min is

Vitamin K antagonists ( oral anticoaguplasminogen, which exists in two forms: lants) differ from heparin primarily in their
plasma soluble forn1 and fibrin ( clot) bound
duration of activity and magnitude of effect.

fonn. Streptokinase and streptodornase are

Their primary importance has been because

:synthesized by streptococci and activate
of their toxic rather than therapeutic
both forms of plasminogen. They are used
effects. Therapeutic indications include oral locally as a powder, infusion, or irrigation in longterm treatment and prevention of
treatment of selected chronic wotmds ( eg,
recurrence of thrombotic conditions (eg,
bums, ulcers, chronic eczemas, ear
aortic or pulmonary thromboembolism and
hematomas, otitis externa, osteornyelitis,
venous thrombosis) in cats, dogs, and
chronic sinusitis, or other chronic lesions)

horses.

that have not responded to other therapy.

There are several groups of vitamin K

Tissue-type plasminogen activator (tPA)

antagonists. They interfere with the hepatic
preferentially activates the fibrin-bound
synthesis of vitamin K-<lependent clotting
form of plasminogen. Unlike parenterally
factors by blocking the reduction of vitamin
administered streptokinase, tPA does not

K epoxide after clotting factor synthesis,
induce a systemic proteolytic state.

thus effectively reducing the concentration

Selective clot lysis occurs without

2544

SYSTEMIC PHARMACOTHERAPEUTICS OF THE CARDIOVASCULAR SYSTEM
increasing circulating plasmin; thus, tPA has of thromboxane, a potent platelet a lower risk of bleeding than does parenaggregator and vasoconstrictor. In addition teral streptokinase. Although tPA has been
to its inhibitory effects on cyclooxygenase,
used to treat aortic thromboembollsm in
aspirin irreversibly acetylates thrombox

VetBooks.ir
cats (0.25-1 mg/kg/hr, IV, for a total dosage
ane synthetase, the specific enzyme
of 1-10 mg/kg), both the 1isk of death clue to
responsible for synthesis of thromboxane.

reperfusion (and release of toxic metabo

Aspirin is a potent inhibitor of platelet
lites) and the e>,.l)ense of this genetically
activity; new platelets must be generated
engineered product may limit its use.

before the effects of aspirin on platelet

Anti thrombotic drugs affect platelet
activity disappear. At higher dosages,
activity, which is normally controlled by
aspirin inhibits prostacyclin, a prostaglansubstances (such as prostaglandins) din product that com1teracts the thrombogenerated both outside and within the genic effects of thromboxane. Thus, aspirin
platelet. Platelet activity can be modulated
must be used cautiously for antiplatelet
by interacting with these substances.

effects. The anti.platelet dosage for dogs is

NSAJDs inhibit the forn1ation of cyclo5-10 mg/kg, PO, every 24-48 hr, and for oxygenase, the enzyme responsible for
cats 80 mg, PO, every 48-72 hr. Clopidogrel
synthesis of prostaglandin products from
is an anti thrombotic agent used in small
arachiclonic acid that has been released
animals in treatment of autoimmune
into cells and platelets. The forniation of all
hemolytic anemia and in cats with aortic/
prostaglanclins is inhibiterl, including that
pulmonary thromboembolism.

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE DIGESTIVE SYSTEM

See also PRINCIPLES OF THERAPY OF' GI DISEASE, chylomicrons in the intestinal mucosa and
p 161.

very low-density lipoproteins in the liver.

After oral ad.ministration, d.irlotapicle has
in vivo selectivity for intestinal MTP. The
mechanism of weight loss action is not
completely understood., but clirlotapide
appears to reduce fat absorption and send a

DRUGS AFFECTING APPEJITE
satiety signal from lipid-filled enterocytes.

Dirlotapide also decreases appetite in a

Disorders of appetite are very common in
close-dependent manner, probably via
vete1inary patients. Obesity from overfeeding increased release of peptide YY into the is common in companion animals and is best
circulation. The decrease in food intake is
managed by educating the owner and regulatresponsible for most of the weight ing the anin1al's diet. Anorexia is a common
reduction effect.

clinical problem seen with many systemic

Dirlotapide is available systemically,
diseases, which exacerbates disease-induced
but absoqJtion in clogs is highly vruiable.

catabollsm. ln the anorexic animal that does

Absorbed dirlotapide is metabolized in
not respond to coaxing with small quantities
the liver; parent drug and metabolites are
of highly palatable foods, drug therapy may
secreted in the bile, with potential for
be used to stimulate appetite. The effect of
enterohepatic circulation. Although blood
specific drugs on food intake can involve
concenu·ations do not directly correlate
hunger, satiety, or enhancement of the
with effectiveness ( effectiveness has been
positive evaluation of taste.

linked to drug concentrations in the gut),
they seem to correlate witl1 systemic

Appetite Suppression: Dirlotapide is
toxicity.

a microsomal Uiglyceride u·ansfer protein

Dirlotapide is available as a 5 mg/mL

(MTP) inhibitor developed specifically for
solution for oral ad.ministration. The dosage
weight loss in dogs. MTP catalyzes the
is adjusted according to the weight loss of
assembly of triglyceride-rich apollpoeach individual dog. The initial dosage of protein B-containing llpoproteins to form

0.5 mg/kg is doubled. after 14 days and then

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2545
adjusted monthly; the maximum permitted
treatment of the tmderlying disease.

daily dosage is 1 mg/kg, although dosages as

Anabolic steroids stimulate hematopoiesis,
high as 10 mg/kg have been administered
appetite, and weight gain. Adverse effects of
to dogs without severe adverse effects in
anabolic steroid therapy include hepatotox

VetBooks.ir
safety studies. Dirlotapide can be used
icity, masculinization, and early closure of
without changing the dog's current feeding
bony epiphyses in yotmg animals. Anabolic
or exercise regimens, but food intake
steroids are contraindicated in animals with
should be monitored during weight
congestive heaitfailure because of sodium
stabilization to establish feeding and
and water retention. Because of human
exercise routines that will minimize weight
abuse potential, anabolic steroids are
gain after treatment. Anorexia, emesis, and
controlled substances. Although once
loose feces occur in some dogs. The

(in)famous for abuse in people and horses,
incidence of emesis generally increases
stanozolol and boldenone undecylenate are
with dose and decreases with treatment
no longer marketed by veterinary pharmatime. Increases in hepatic transanlinase ceutical companies in North America.

activity were seen in dogs treated with > 1.5

Currently, any anabolic product for
mg/kg/day but were not associated with
vete1inary use can only be obtained from a
clinical signs or histopathologic evidence
compounding pharmacy. Use of anabolic
of hepatic degeneration or necrosis.

steroids in perfonnance horses is prohibited

Dirlotapide should not be used in cats. It
by most equine sport organizations, and
increases the risk of hepatic lipidosis during
detection tin1es can be >2 mo.

weight loss in obese cats. Dirlotapicle is not

Glucocorticoids increase gluconeogenrecommended for use in dogs currently esis and antagonize insulin for an overall
receiving longterm glucocorticoid therapy
hyperglycemic effect. Appetite is stun ulated
or in dogs with liver disease. In people,
by the steroid-induced euphoria. Continued
adverse reactions associated with ingesting
use of glucocorticoids has catabolic effects
dirlotapide include abdonlinal distention,
because skeletal muscle and collagen
abdominal pain, diarrhea, flatulence,
proteiI1s are broken down to provide the
headache, increased serum transaminases,
precursors for gluconeogenesis.

nausea, and vomiting.

When used as anxiolytics, the benzodiazepines (BZD) becan1e well known for Appetite Stimulation: Anabolic
their appetite stimulation effects indepensteroids are synthetic de1ivatives of dent of their anxiolytic activity. Stereospetestosterone that have enhanced anabolic cific bindmg of a BZD to GABA A receptors
effects with reduced androgenic effects.

in the parabrachial nucleus produces a

Anabolic steroids do not directly affect
strong close-dependent (ie, voracious)

hunger, satiety, or sensory perception of
increase in food conswnption. Hunger level
food. Instead, they antagonize the catabolic
and degree of satiety has no effect on
effect of glucocorticoids and the negative

BZD-iI1duced food intake. So, it appears that
nitrogen balance associated with surgery,
the BZDs do not modulate hunger or satiety
illness, trauma, and aging. In all cases,
directly but act specifically to enhance taste
improved nitrogen balance depends on
and other sensory characteristics of food.

adequate protein/calorie intake and

By manipulating the stereospecificity of the
itM•ii DRUGS USED TO STIMULATE APPETITE

Drug

Dosage

Diazepam

Cats: 0.005-0.4 mg/kg, IV

Oxazepan1

Cats: 2 mg, PO, bid

Cyproheptadine

Cats: 1-4 mg, PO, bid

Mirtazapine

Cats: 3. 75 mg/cat(\!,\ of a 15-mg tablet), PO, every 3 days Dogs: 1/.1 of a 15-mg tablet for dogs <7 kg, Y2 of a 15-mg tablet for dogs 8--15 kg, 15 mg for dogs 16--30 kg, 30 mg for dogs

>30 kg; no higher than 30 mg per dog

Megestrol acetate

Dogs: 5 mg/kg/day, PO

Prednisone/prednisolone 1 mg/kg, PO, every other day

2546

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

BZD clrngs, appetite-selective partial agonist aclrenergic adverse effects ( orthostatic compounds have been developed that have
hypotension and sexual dysfunction).

actions disassociated from the other major

Antihistarninic drowsiness is a common
effects of full agonists ( eg, anmesia,
effect. Mi.rtazapine is used for disease condi

VetBooks.ir
sedation, incoorclination, anxiolysis).

tions in which inappetance and nausea go

Likewise, inverse agonists of the BZD
together, such as in the treatment of GI
receptors reduce food consumption. BZD
disease or liver or kidney disease. Mirtazareceptor antagonists block the appetitepine can also be used to alleviate the nausea simulating effects of the full or partial
and appetite loss that accompanies
agonists, as well as the appetite-suppressive
chemotherapy. o.-Aclrenergic receptors
effects of the inverse agonists. So, there is
in the chemoreceptor trigger zone are
a bidirectional control of food intake
important in inducing emesis in cats.

mediated by a conm1on subset of BZD

Clinically, mi.rtazapine is an effective
receptors. Levels of f ood intake, ranging
appetite stimulant and antiemetic for cats
from voracious consumption at one
with chronic kidney disease and appears to
extreme to complete anorexia at the other,
be a useful acljunct in nutritional managewith every level in between, can be achieved ment of these cats. There is little pharmaby the relative concentration of agonists cokinetic infommtion on mi.rtazapine in
and inverse agonists binding to those BZD
clogs and cats, but miltazapine shows sexual
receptors specifically involved in the
effects in hepatic metabolism in people, so
control of appetite. Diazeparn is an appetite it is likely there is similar variation in stimulant when administered IV to cats. lf
metabolism in dogs and cats and the
responsive, cats begin eating within a few
potential for variation in efficacy.

seconds of IV administration, so palatable

Mirtazapine is typically given once a day
food should be available before injection.

to clogs and twice a week to cats. It should

Oxazepam, a metabolite of cliazeparn, can
be used with caution in clogs and cats with
be given orally to cats. Diazeparn is the
severe liver or kidney disease, because
more effective appetite stimulant but also
miltazapine clearance will be reduced. In
causes a greater sedative effect than
cats and small clogs, it is difficult to reduce
oxazepam.

the dose, because the smallest tablet

Cyproheptadine is an antihistamine
manufactured carmot be accurately cut
with serotonin-antagonist action used
much smaller than the regular closing
clinically in cats as an appetite stimulant.

schedule allows. In this situation, a

It acts as a 5-HT2 receptor antagonist. The
compounding pharmacy could be employed
lateral hypothalanms n01mally excretes
to create a lower close, or the closing
endogenous opiates, which stimulate
schedule can be extended. This is especially
eating. The release of these endogenous
irnpo.rtant for cats with liver disease.

opiates is inhibited by serotonin and

Megestrol acetate is a synthetic
cholecystokinin release, thus inhibiting
progestin. It has significant antiestrogen
eating. Cats are very sensitive to changes
and glucocorticoicl activity, with resulting
in serotonin concentrations,..so serotonin
adrenal suppression. It is used to stimulate
antagonists are very potent in cats. CNS
appetite and promote weight gain in people
excitement and aggressive behavior may
with cancer and cachexia (related to
occur in some cats.

acquired inununocleficiency syndrome) and

Mirtazapine is an antidepressant used
may have a sintilar effect in anorectic cats
to treat moderate to severe depression in
and clogs. Megestrol acetate is contraindipeople. Mirtazapine is not a serotonin or cated in pregnant anilnals and in anin1als
norepinephrine reuptake inhibitor (SSRis
with uterine disease, diabetes mellitus, or
such as fluoxetine are noted to decrease
manunary neoplasia. In cats, megestrol
appetite). It is an antagonist ofpresynaptic
acetate can induce a profow1cl adrenocortio.2-aclrenergic auto receptors and heterocal suppression, adrenal atrophy, and receptors on both norepinephrine and
diabetes mellitus, which may or may not be
serotonin (5-HT) presynaptic axons, plus is
reversible. Toxicity is less of a problem in
a potent antagonist ofpostsynaptic 5-HT2
clogs.

and 5-HT3 receptors. This mechanism of

Other drugs used as appetite stirnulants
action maintains equivalent antidepressant
include B vitamins and glucocorticoids.

efficacy but rninin1izes many of the adverse

B vitanlin preparations are administered
effects conm10n to both t1icyclic antidepresorally and parenterally to debilitated sants and SSRis. Because of its unique
animals, especially horses, to promote
pharrnacologic profile, mirtazapine usually
appetite. Glucocorticoicls increase
does not cause anticholinergic effects,
gluconeogenesis and antagonize insulm f or
serotonin-related adverse effects, or
an overall hyperglycemic effect. Appetite is

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2547
stimulated by the steroid-induced euphoria.

underlying thyroid, liver, or kidney

Continued use of glucocorticoids results in
dysfunction and should be investigated.

catabolic effects, as skeletal muscle and

Dogs also vomit often (frequently after
collage proteins are broken down to provide eating grass) and often eat their own vomit.

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the precmsors for gluconeogenesis.

Neurotransmitters of Emesis:

DRUGS TO CONTROL OR

Acetylcholine (muscarinic receptors) and

STIMULATE VOMITING
substance P (NK-1 receptors) act on the
emetic center. The CRTZ is stimulated by

Animals possess an arsenal of special
dopan1ine (D2 receptors), aradrenergic
abilities for survival, many of which are
drugs (NE receptors), serotonin (5-HT3
used for food consumption. Ingesting food
receptors), acet-ylcholine (Ml receptors),
can lead to exposme of internal organs to
enkephalins, and histamine (Hl and H2
possible food-related disorders, including
receptors).

viral and bacterial infection, toxins, and
a -Adrenergic receptors in the CRTZ
allergens. Smell and taste are not always
are important in inducing emesis in cats.

effective in detemlining the quality of food,
az-Adrenergic agonists (eg, xylazine) are
so nausea, vomiting, and diarrhea are
more potent emetics in cats than in dogs.

additional mechanisms of defense of the

5-HT l A antagonists ( eg, buspirone) and

GI system.

aradrenergic antagonists ( eg, aceproma

Humorally mediated emesis results from
zine, yohimbine, mirtazapine) suppress
emetogenic substances in the systemic
vomiting in cats.

circulation that activate the chemoreceptor

CRTZ D2 dopamine receptors are not as
t1igger zone (CRTZ) in the area postrema.

important in mediating humoral emesis in

The CRTZ lies outside the blood-brain
cats as they are in clogs. Apomorphine, a
barrier. Nemally mediated emesis results

D2 dopamine receptor agonist is a more
from activation of an afferent nemal
reliable emetic in dogs than cats, and
pathway typically coming from the

D2 dopan1ine receptor antagonists ( eg,
abdommal viscera and synapsing at one
metocloprarnicle) are not very effective
or more nuclei in the emetic center. Most
antiemetic drngs in cats.

pharmacologic interventions focus on the

Histamine Hl and H2 receptors are found
humoral pathway of emesis, based on
in the CRTZ of dogs but not cats. Histamine
nemotransmitter interactions at the CRTZ.

is a potent emetic in dogs but not cats, and

The neural pathway has received less

H 1 antagonists ( eg, diphenhydranline) are
emphasis, even though it is a much more
ineffective for motion sickness in cats.

important pathway.

Muscaiinic M 1 receptors are found in the

Nausea is an aversive experience that
vestibular apparatus of cats. Mixed Ml/M2
often accompanies emesis; it is a distinct
antagonists ( eg, atropine) inhibit motion
perception, different from pain or stress.

sickness in cats.

Nausea is more difficult to treat than emesis

Substance P binds to NK-1 receptors,
using antiemetic drugs. This became
which are found in the gut and the emetic
apparent with the excellent control of
center of the CNS. Substance P induces
drug-induced emesis from cancer chemoemesis, and selective substance P antagotherapy, but human patients still experience nists ( eg, maropitant) are potent antiemetnausea. This suggests that nausea and ics in both dogs and cats with a broad
vomiting are separate physiologic
spectrum of activity against a variety of
processes.

emetic stimuli.

Motion-induced emesis appears to have a
very early evolutionary origin, because it is

Emetic Drugs: Emetic drugs are usually
present in most anin1al models of emesis.

administered in emergency situations after

Motion sickness is thought to result from
ingestion of a toxin ( see TABLE 3). They
sensory conflict regarding the body's
generally remove <800/o of the stomach
position in space, yet there is no satisfactory contents. The most reliable emetic clrngs act theory as to why people and animals have
centrally to stimulate the vomiting center,
this mechanism in the first place.

either directly or via the CRTZ.

Nausea and vomiting, as defense systems

Apomorphine is an opioid drug that acts
of the GI tract, by necessity must have a low
as a potent central dopanline agonist to
threshold for activation. Cats are well
directly stimulate the CRTZ. Therefore, it is
known for their tendency to vomit,
less effective in cats than in dogs. It can be
particularly when attempting to dislodge
administered PO, IV, or SC; the IM route is
hairballs from the throat or upper GI tract.

not as effective. It can also be applied

Chronic vomiting in cats may indicate
directly to cor\junctival and gingival

2548

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

IH=iiii EMETIC DRUGS

Drug

Dosage

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Apomorphine

Dogs: 4 mg/kg, PO; 0.02 mg/kg, IV; 0.3 mg/kg, SC; 0.25 mg in the conjunctiva! sac

Xylazine

Cats: 0.4-0.5 mg/kg, IV or IM

Hydrogen peroxide Dogs: 5-10 mL, PO
membranes, using the tablet formulation,

Antiemetic Drugs: Protracted vomiting
which can easily be removed once emesis
is physically exhausting and can cause
is initiated. Vomiting usually occurs in
dehydration, acid-base and electrolyte

5-10 min. Although apomorphine directly
disturbances, and aspiration pneumonia
stimulates the CRTZ, it has a depressant

Antiemetic drugs are used to control
effect on the emetic center. Therefore, if
excessive vomiting once a.i1 etiologic
the first dose does not induce emesis, addidiagnosis has been made, to prevent motion tional doses are not helpful. Because the
sickness and psychogenic vomiting, and
vestibular apparatus may also be involved in to control emesis from radiation and a.pomorphine-induced vomiting, sedate and
chemotherapy (see TABLE 4). Antiemetics
motionless animals will not vomit as readily
may act peripherally to reduce afferent
as active animals. Excitement that results
input from receptors or to inhibit efferent
from a.pomorphine in ca.ts can be treated
components of the vomiting reflex
with the opioid antagonist naJoxone.

response. They may also act centrally to

Xyla.zine is an etra.drenergic a.gonist
block stimulation of the CRTZ and emetic
used primarily for its sedative and analgesic
center.

action. It is a reliable emetic, pa.tticularly in

The phenothiazine tranquilizers are
cats, in which it stimulates the CRTZ.

c,2-adrenergic antagonists and antagonize

Because xylazine can produce profound
the CNS stimulatory effects of dopa.mine
sedation and hypotension, animals should
and decrease vomiting from a variety of
be closely monitored after administration.

causes, including motion sickness in cats.

Hydrogen peroxide (3%) applied to the These drugs also have antihistaminic and back of the pharynx stimulates vomiting
weak anticholinergic action. Phenothiazine
via the ninth cranial nerve. Small doses
tranquilizers used as antiemetics include

(5-10 mL) of hydrogen peroxide can be
acepromazine, chlorpromazine, and
administered via oral syringe until emesis
prochlorperazine. Potential adverse effects
occurs. It should be administered
include hypotension due to c,-adrenergic
cautiously, especially in ca.ts, because
blockade, excessive sedation, extrapyramiaspiration of hydrogen peroxide foa.tn dal signs, and a. lowering of the seizme
ca.uses severe aspiration pneumonia..

threshold in anin1als with epilepsy.

When small a.mounts a.i·e administered, 3%

Extra.pyra.tnidal signs can be counteracted
hydrogen peroxide is relatively nontoxic.

with an antihista.tnine ( eg, diphenhy-

Stronger concentrations ( eg, hair dye
dranune).

peroxide) a.re more toxic.

The a.nticholinergic drugs block

Other products have been used but are
cholinergic afferent pathways from tl1e
not recommended to induce emesis in dogs

GI tract and the vestibular system to the
and ca.ts. Syrup of ipecac is no longer
vomiting center. Alone, they are less
recommended for "home use" in people or
effective than the other emetics. Aminopenanimals. The active ingredient is emetine, a tan1ide is approved for use in dogs and cats
toxic alkaloid, which produces vomiting by
in the USA as an irtjectable formulation and
acting as a stomach irritant. If repeated use
oral tablets. It should be more efficacious
fails to induce emesis, then gastric lavage is
in the treatment of motion sickness in
necessa.iy to remove the emetine to prevent
ca.ts than in dogs, because musca.rinic
additional toxicosis. Although sometimes

M l receptors a.re found in the vestibular
suggested, sodium chloride (salt) and
apparatus of cats. Aminopentamide has
powdered mustard should not be used.

low efficacy for other causes of vomiting.

Mustard is rarely effective and can be

The antihistamines can block both
inhaled and ca.use lung damage, whereas
cholinergic a.i1d histanunic nerve transmissalt toxicity can easily occur if overdosed sion responsible for transmission of the
and can result in fatal cerebral edema
vestibular stimulus to the vonuting center of

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2549
f M:i!JI ANTIEMETIC DRUGS

Drug

Dosage

Acepromazine

0.025--0.2 mg/kg, IV, IM, SC, maximum 3 mg; 1-3 mg/kg, PO

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Chlorpromazine

0.5 mg/kg, IV, IM, SC, tid-qid

Prochlorperazine

0.1 mg/kg, IM, tid-qid; 1 mg/kg, PO, bid

Aminopentamide

0.022 mg/kg, PO, SC, or IM, bid-tid

Dimenhydrinate

4-8 mg/kg, PO, tid

Diphenhydramine 2-4 mg/kg, PO, tid

Butorphanol

0.2-0.4 mg/kg, IM, once to twice daily

Metoclopramide

0.1-0.5 mg/kg, IM, SC, or PO, tid; 0.01-0.02 mg/kg/hr, IV infusion Ondansetron

0.1-0.2 mg/kg, PO, once to twice daily; 0.1-0.15 mg/kg, IV, bid-tid Granisetron

0.5--1 mg/kg, PO, bid; 0.1-0.15 mg/kg, IV, bid-tid

Dolasetron

0.6-1 mg/kg/day, IV

Maropitant

2 mg/kg, PO or 1 mg/kg/day, SC, for up to 5 days (acute vomiting); 8 mg/kg/day, PO, for up to 2 days (motion sickness)

dogs. The conunonly used histantlne (Hl)

The serotonin antagonists onclanseblocking drugs are diphenhyclram.ine and tron, granisetron, and dolasetron a.i·e
dimenl1ydrinate ( diphenhydramine plus
specific in.11.ibitors of serotonin subtype

8-ch.lorotheophylline ). They may cause mild

3 receptors in the CRTZ. These receptors
sedation, especially diphenlwclrantlne, but
a.i·e located peripherally on va.gal nerve
paradoxical CNS stimulation may also
tem1inals and centrally in the area postrema
occur, presumably from anticholinergic
of the bra.in. Cytotoxic drugs and radiation
effects.

damage the GI mucosa, causing release

Metoclopramide exerts its antiemetic
of serotonin. These are the most effective
effects via three mechanisms. At low closes,
antiemetics used in people undergoing
it inhibits clopantlnergic transmission in the
radiation and chemotherapy, and they

CNS, whereas at high closes, it inhibits
have been used in ca.ts and dogs receiving
serotonin receptors in the CRTZ. Peripherchemotherapy. Although very effective ally, metoclopra..mide increases gastric and
at controlling vomiting associated with
upper duodenal emptying. Metoclopram.icle
chemotherapy and drug-induced vomiting,
is a useful a.ntiemetic for clogs. Because
these drugs do not prevent or relieve

CRTZ 02 dopa.mine receptors are not very
nausea, wll.ich may be more debilitating
important in mediating humoral emesis in
than vonl.iting. They are not effective for
cats, metoclopran1ide is less effective in
emesis caused by motion sickness. All
ca.ts than in clogs. It is used to control
serotonin subtype 3 antagonists have been
emesis induced by chemotherapy, nausea
associated with prolongation of the QT
and vomiting associated with delayed
interval in people. Adverse effects of
gastiic emptying, reflux gastritis, and viral
dolasetron include ECG changes (PR and
ente1itis. There is tremendous individual

QT prolongation, QRS widening) caused by
va.iiability in metoclopranl.ide pha.i1na.cokidolasetron metabolites that block sodiun1
netics, and oral bioa.vai.lability is only -500'6
cha.imels.

because of a sign.iiicant first-pass effect. At

Butorphanol is an effective antiemetic
high doses or with rapid IV administration,
for dogs receiving cisplatin chemotherapy.

metoclopra.mide ca.uses CNS excitement by

It ca.uses only mild sedation. It is believed to
dopantlne antagonism (si.mila.i· to the
exert its antiemetic effect directly on the
phenothiazine ti·anquilizers). Extrapyra.i11.ivomiting center.

clal signs can be counteracted with an

Maropitant is a ncuroki.nin 1 (NK-1)

antiltistan1ine such as diphenlwdrantlne.

receptor antagonist approved to treat and

Metoclopramicle should not be adminisprevent emesis in clogs and cats. Substance tered if a GI obsti1.1ction or pe1foration is

P is a regulatory peptide that binds to the
suspected.

NK-1 receptors and induces emesis. NK-1

2550

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM
receptor antagonists are believed to provide
drooling, lethargy, lack of appetite, and
antiemetic activity by suppressing activity
diarrhea. Maropitant injections may also
at the nucleus of the solitary tract, where
cause a stinging sensation; this can be
vagal afferents from the GI tract converge
minimized by keeping the injectable

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with inputs from the CRTZ and other
solution refrigerated and, once the drug
regions of the brain involved in the control
is drawn up, injecting right away at the
and initiation of emesis. Despite its
refrigerated temperature. A few dogs may
selectivity for the NK-1 receptor, maropitant
vomit after treatment. Giving maropitant
blocks apomorphine, cisplatin, and syrup of
with a small amount of food will help avoid
ipecac-induced vomiting in dogs, which
tlus.

suggests that activation of the nucleus of the
solitary tract is a final common step in the

THERAPY OF GASTROINTESTINAL
initiation of emesis. Despite being very

ULCERS
effective antiemetics in people, NK-1
receptor antagonists have little effect on

GI ulceration is a conunon problem in small
chemotherapy-associated nausea in people
and large anin1als, in association with
or hydromorphone-induced nausea in dogs.

physiologic stress ( endogenous c01tisol),

Maropitant injectable is approved for
dietary management, or as a sequela of
vomiting in cats �16 wk old and acute
adnunistration of ulcerogenic drugs ( see
vomiting in dogs �8 wk old at 1 mg/kg/day.

p 393 and seep 218). Helicobacter

Maropitant tablets are approved for acute
organisms, the most frequent cause of
vomiting in dogs �8 wk old (2 mg/kg), and to
ulcers in people, appear to be involved in
prevent vomiting due to motion sickness in
some cases of gastritis in anin1als ( see
dogs �16 wk older (8 mg/kg). Dogs should
p 394). Anti ulcerative drugs include
not be fed for l lu· before giving maropitant.

antagonists that interact with stin1ulatory

The best tin1e to give maropitant is 2 hr
receptors Oustanune H2-receptor antagobefore travelling, with a small an10unt of nists, muscarinic receptor antagonists, and
food. The tablets should not be wrapped
gastri.n receptor antagonists), agonists that
tightly in fatty food such as cheese or meat,
interact with inhibitory receptors (somatobecause this may keep the tablets from statin and prostaglandin E analogues), and
dissolving and delay the effect of maropitant. irreversible inhibitors ofH+fK+-ATPase Adverse effects are rare with maropitant,

(proton pump inhibitors). Antiulcerative
but the most conu11on ones are excessive
drugs are listed in TABLE 5.

lffl:HJI ANTIULCERATIVE DRUGS

Drug

Dosage

Antacids

2-10 mL, PO, every 2-4 hr

Sucralfate

Cats: 250 mg, bid-tid

Dogs: 500 mg to 1 g, tid-qid

Foals: 1-2 g, qid

Ci.metidine

Dogs: 5-10 mg/kg, PO, qid

Horses: 4 mg/kg, IV, bid; 18 mg/kg, PO, bid

Ranitidine

Dogs: 0.5 mg/kg, PO, SC, or IV, bid

Horses: 1.3 mg/kg, IV, bid; 11 mg/kg, PO, bid

Famoti.dine Dogs: 0.5-1 mg/kg/day, PO or IV

Horses: 0.4 mg/kg, IV, bid; 3 mg/kg, PO, bid

Omeprazole Dogs: 0.5-1 mg/kg/day, PO

Horses: 4 mg/kg/day, PO, for treatment; 2 mg/kg/day, PO, to prevent recurrence

Misoprostol Dogs: 2-5 mcg/kg, PO, tid-qid

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2551

Antacids: The common antacids are bases cimetidine, has minimal effect on ranitiof aluminum, magnesium, or calcium dine, and slightly enhances absorption of

(aluminum hydroxide, magnesiwn oxide or
fan10tidine. Some evidence suggests tl1at
hydroxide, and calcium carbonate). These
cinletidine strengthens the gastric mucosa]

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drugs neutralize stomach acid to fom1 water defenses against ulceration and enhances and a neutral salt. They are usually not
cytoprotection. Cin1etidine reduces the
absorbed systemically. In addition to their
metabolism of other drugs (warfarin, phenyacid-neutralizing ability, antacids decrease toin, lidocaine, metronidazole, theophylpepsin activity, binding to bile acids in the line) by inhibiting hepatic microsomal
stomach and stimulating local prostaglanenzyme systems. Ranitidine interacts din (PGE,) production. Over-the-coW1ter
differently than cinletidine and only
antacid preparations are combinations
minimally (100/o) inllibits hepatic metaboof magnesium hydroxide and aJuminW11
lism of some drugs. Fan10tidine seems to
hydroxide; such combinations optintize the
have no effect on metabolism of other
buffering capabilities of each compoW1d
drugs. Antacids should be given 1 hr before
and balance the constipating effect (from
or after cimetidine to avoid interactions.

altm1inw11 hydroxide) and the laxative

Famotidine may be given with antacids;
effect (from magnesium hydroxide). Up to
ranitidine may be given with low doses of

200/o of the magnesium can be absorbed after antacids. Sucralfate may alter absorption administration PO and can cause hypennagof cin1etidine and ranitidine.

nesemia in animals with renal insufficiency.

Cimetidine suppresses gastiic acid

Antacids frequently interfere with the GI
secretion in dogs for 3 -5 hr. Because
absorption of concurrently administered
ranitidine has a longer elimination half-life,
drugs ( eg, digoxin, tetracyclines, fluoroquiit suppresses acid for up to 8 hr and it may nolones ). AlW11inum-containing antacids
be administered less frequently. Fan1otidine
inlpair absorption of phosphate. Because
can be administered once a day. Oral
they are difficult to administer and require
bioavailability in horses for these drugs is
frequent dosing, they are not as popular as
only 100/o--300/o, so large oral doses must be
newer therapies.

adnlinistered.

Sucralfate: Sucralfate is an anti ulcera

Proton Pump Inhibitors: Proton pwnp
tive drug that has a cytoprotective effect
inhibitors (PPis) irreversibly block the
on GI mucosa It disassociates in the acid

H•/K•-ATPase proton pW11p of the gastric
environment of the stomach to sucrose
parietal cell. They are given in an inactive
octasulfate and aJW11inW11 hydroxide.

fom1, which is neutrally charged (lipophilic)

Sucrose octasulfate polymerizes to a
and readily crosses cell membranes into
viscous, sticky substance that creates a
intracellular compartments (like the
protective effect by binding to ulcerated
parietal cell canaliculus) that have acidic
mucosa. This prevents "back diffusion"

environments. The inactive drug is
of hydrogen ions, inactivates pepsin, and
protonated, rean·anges into its active fonn,
adsorbs bile acid. In addition, sucralfate
and irreversibly binds to and deactivates the
increases the mucosaJ synthesis of prosproton pW11p. The most widely used PPI is taglandins, which have a cytoprotective
omeprazole. In dogs and horses, a single
role. Because sucralfate is not absorbed, it
dose of omeprazole inllibits acid secretion
causes virtually no adverse effects. Dosage
for 3-4 days, despite a relatively short
reginlens are extrapolated from human
plasma half-life. This is because of
dosages. Although sucralfate is frequently
accumulation of the drug in paiietal cell
administered to horses and small aninlaJs as
canaliculi and the in-eversible natme of
an ulcer preventive, there is little evidence
proton pump inllibition. A specific equine
of efficacy in animals, and it may prevent
product has been developed, because oral
the absorption of truly useful drugs.

bioavailability of the hW11an omeprazole

Animals in renal fail me may have increased
formulation or compounded fom1ulations is
aJW11inum absorption.

poor in horses. Although ulcers in horses
will heal while on omeprazole therapy, they

H2-Receptor Antagonists: Cimetidine,
tend to recm once therapy is discontinued.

ranitidine, and famotidine are the

Human fom1ulations are used in dogs and
commonly used H2-receptor antagonists.

cats. In people, adverse effects from

Ranitidine is 3-13 times as potent on a
suppression of gastric acid secretion
molar basis as cinletidine in inhibiting
include hypergastrinemia, which causes
gastric acid secretion. Famotidine is 20-150
mucosaJ cell hyperplasia, hypertrophy of
times as potent as cinletidine. In people,
the gastric rugae, and eventually developfood tends to delay the absorption of ment of carcinoids. It has also been

2552

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM
associated with acute renal failure and
additional mechanism for increased acid
disorders of calciwn homeostasis, including
secretion that occurs after discontinuation
fractw·es associated with longterm use.

of therapy.

Studies in rodents show that PP!s can

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exacerbate NSAID-induced intestinal

Misoprostol: Misoprostol is a synthetic
damage from significant shifts in ente1ic
prostaglandin E1 analogue used in dogs to
microbial populations. Prevention or
reduce the risk of GI ulcers induced by
reversal of this dysbiosis may be an
ch.ronic NSAID therapy. Misoprostol
important clinical consideration for
suppresses gastric acid secretion by
reducing the incidence and severity of
inhibiting the activation of histamine-sensi

NSAID enteropathy. Therefore, omeprazole
tive adenylate cyclase. It has a cytoprotecis contraindicated for chronic therapy.

tive effect from stimulation of bicar·bonate

Omeprazole is also a microsomal enzyme
and mucus secretion, increased mucosa!

inhibitor (to a sinlila.r extent as cimetidine).

blood flow, decreased vascular permeabil

For animals that cannot receive oral
ity, and increased cellular· proliferation and
medications, rv i.ajectable fom1ulations
migration. Misoprostol is clinicaUy effective
approved for people (pantoprazole and
in preventing GI bleeding ar1d ulceration
esomeprazole) can be considered for use.

from NSAID therapy but not from methylprednisolone sodium succinate, and it is Acid Rebound: Acid rebound is an
less efficacious than H,-receptor antagoincrease in gastric acid secretion above nists or PP!s for treatment of ulcers.

pretreatment levels after discontinuation of

Adverse effects of misoprostol are mainly
antiulcer therapy. Rebound is reported after
limited to diatThea and flatulence.

the use of histanline H2-receptor antagonists Magnesiwn-contai.11.ing antacids may and PP!s and is thought to be due to
aggravate the diarrhea. Misoprostol is
increased serum gastrin and/or upregulacontraindicated in pregnant clogs, because tion of the H2-receptors. An increased
it can induce abortion.

gastrin level, or hypergastlinemia, is a
secondary effect that occurs during ch.ronic

DRUGS USED IN TREATMENT OF
inhibition of gastric acid secretion, such as
with longterm anti ulcer therapy. Gastrin is

DIARRHEA
the primary regulator of gastric acid

Therapy for diarrhea includes fluids, electrosecretion, which is mediated by histar11ine lyte replacement, maintenance of acid/
released by the enterochromaffin-like (EGL) base balance, and control of discomfort.

ceU. Increased plasma gastiin stin1ulates

Antiparasitic drugs or dietary therapy can
and up regulates EGL ceUs to produce and
also play an in1portant role in treat111ent of
release more histamine to stimulate parietal
some types of diarrhea. Additional therapy
cells. In addition, an increase in parietal ceU
may include intestinal protectar1ts, motility
mass may occur with the chronic use of
modifiers, antimicrobials, anti-inflammatory

H2-blockers or PP!s, and this may b� an
drugs, and antitoxins (see TABLE 6).

IM:i!ii ANTIDIARRHEAL DRUGS

Drug

Dosage

Kaolin-pectin

1-2 ml/kg, PO, qid

Activated charcoal

2-Sg/kg, PO

Bismuth subsalicylate

1-3 ml/kg/day in divided doses, PO

Anlinopentarnide

0.1-0.4 mg, IM, SC, or PO, bid

Isoproparnicle

0.2-1 mg/kg, PO, bid

Propantheline

0.25-0.5 mg/kg, PO, bid-tid

Paregoric

0.06 mg/kg, PO, tic!

Diphenoxylate

0.05-0.l mg/kg, PO, qid

Loperan1ide

0.08 mg/kg, PO, tid-qid

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2553

Mucosal Protectants and Adsorbents:

significantly decrease intestinal motility and

Kaolin-pectin fonnulations are popular
secretions. Their pru·asyrnpatholytic effects
for symptomatic therapy of diarrhea. Kaolin
decrease segmental ru1d propulsive

VetBooks.ir
is a form of aluminum silicate, and pectin
intestinal smooth muscle contractions and
is a carbohydrate extracted from the 1ind
relax spasms of srnooili muscle. Aliliough
of citrus fruits. The manufactmers claim

U1ey do not alter ilie cow·se of the disease,
that kaolin-pectin acts as a demulcent and
anticholinergic drugs decrease the mgency
adsorbent in the treatment of diruThea
associated wiU1 some fom1s of diarrhea in

This action is claimed to be related to the
small animals, tl1e 3111otmt of fluid secreted
binding of bacte1ial toxins ( endotoxins and
into ilie intestine, and abdominal cr3lllping
enterotoxins) in the GI tract. However,
associated with hypermotility. Because few
clinical studies have not demonstrated any
of ilie types of diarrhea seen in animals can
benefit from administration of kaolin-pectin.

be classified as "hypermotile," use of

It may change the consistency of the feces

311ticholinergic drugs is limited in vete1inary
but neither decreases the fluid or electrolyte
medicine. Intestinal motility is already
loss nor shortens the duration of illness.

impaired in many 311in1als with diarrhea,

Nevertheless, it is often administered to

311d these drugs may actually worsen the
small animals, foals, calves, lambs, and kids.

diarrhea The anticholinergic drngs also

Kaolin-pectin products may adsorb or bind
have profound systemic pharmacologic
other drugs administered PO and reduce
effects. If iliey ru·e ad.ministered in sufficient
bioavailability.

doses to affect intestinal motility, possible

Activated charcoal is detived from
adverse effects include severe ileus,
wood, peat, coconut, or pecan shells. The
xerostomia, urine retention, cycloplegia,
material is heated ru1d treated in such a way
tachycardia, 311d CNS excitement. Chronic
that many large pores are formed, which
administration may lead to serious
dr3lllatically increases the internal sU1face
intestinal atony.

ru·ea. Activated charcoal is available in a

Atropine is the best known 311ticholinervaJiety of pore sizes. The formulations sold gic drng, but because it has m311y oilier
for cl.rug and toxic311t adsorption typically
systemic effects, it is not ordinaiily used
have pore sizes of 10-20 A. Activated
for 311 anticliruTheal effect. To avoid CNS
charcoal is very effective for adsorbing
excitement, quaternary 3lllines such as
bacterial enterotoxins and endotoxins that

3lllinopentamide, isoproprunide, 311d
cause some types of diaJThea. It also
propanilieline are preferred, because they
adsorbs many drngs and toxins 311d
do not cross U1e blood-brain barrier readily.

prevents GI absorption, so it is a common

Hyoscine butyl bromide is an 311tispasnonspecific treatment for intoxications.

moclic and ai1ticholinergic drng that relaxes

Activated charcoal is not absorbed, so
the smooth muscle of the GI tract. It is
overdose is not a problem.

approved for treatment of uncomplicated,

AIU10ugh other "mucosal protectants"

spasmodic colic in horses. Initial relief of
have questionable efficacy, bismuth
colic pain is seen within 5-10 minutes, with
subsalicylate is considered by many human a duration of action of 3-4 hr. Because of its gastroenterologists to be the symptomatic
parasympailiolytic effects, it causes
treatment of choice for acute diaJThea.

transient tachycru·dia; therefore, heait rate

Its efficacy has been proved in controlled
monitming is not 311 effective indicator of
clinical tiials in people with acute diarrhea
response to treatment for up to 30 min after

( enterotoxigenic Escherichia coli or
treatment. It will also decrease gut sounds

"traveller's diaJThea"). Bismuth adsorbs
for 30 min after administi·ation. Rectal
bacte1ial enterotoxins and endotoxins and
relaxation will also make rectal palpation
has a GI protective effect. The salicylale
easier. It may also be beneficial in cases of
component has antiprostaglandin activity.

choke, 311d it will relieve acute bronchocon

Practically all of the salicylate is absorbed
striction in horses with recun·ent airway
systemically when administered to dogs ru1d
obstruction. Hyoscine butylbromide cai1 be
cats. Some animals may dislike ilie taste of
administered concurrently with NSAIDs
bismuU1 subsalicylate, and owners should be 311d sedatives.

waJ11ed U1at it will turn U1e feces black. This Opiates have both ru1tisecretory and
may interfere wiili evaluating U1e feces for
antimotility effects by action on the �1 (mu)

hemorrhage. Salicylate toxicosis is possible,
and 6 (delta) receptors of the GI tract. They
especially in cats.

decrease propulsive intestinal contractions
and increase segmentation for 311 overall

Motility-modifying Drugs: Anticholin
constipating effect. They also increase GI
ergic drugs are common ingredients in
sphincter tone. There is some evidence that
antidiaJTheal preparations, because iliey
opiates inhibit colonic motor activity in

2554

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM
horses. In addition to affecting motility,
by producing "carrier" animals ( eg,
opiates stimulate absorption of fluid,
salmonellosis). Nonabsorbed antimicrobielectrolytes, and glucose. Their effects on als are frequently combined with motility
secretory diarrhea are probably related to
modifiers, adsorbents, and intestinal

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inhibition of calcium influx and decreased
protectants in some preparations. Many
calmodulin activity. They are frequently
of these combinations are irrational.

used for treatment of diarrhea in dogs, but

Antimicrobials frequently are a treatment
their use in cats is controversial because
for diarrhea in animals, but there are few
they may cause excitement. The constipatconditions that have a lrnown etiology for ing effects of morphine and codeine have
which antimicrobial therapy is indicated.

been lrnown for many years, but they are

Campylobacter enteritis, from infection
not used clinically as antidiarrheal drugs.

with Campylobacter jejuni, is seen in cats

Paregoric is a tincture of opium product and
and dogs and can be zoonotic. Treatment
a controlled substance (5 mL of paregoric
alleviates clinical signs, but animals usually
corresponds to -2 mg of morphine).

remain carriers. Suggested antimicrobial

Diphenoxylate and loperamide are two
therapy includes erythromycin, enrofloxasynthetic opiates that have specific action cin, clindan1ycin, tylosin, tetracycline, or
on the GI tract without causing other
chloran1phenicol. Intestinal bacterial
systemic effects. They have been used in
overgrowth is usually due to Escherichia,
small animals and large animal neonates.

coli or Clostridium spp, so therapy is Diphenoxylate is a controlled substance
initiated with an oral drug effective in the
in a formulation that contains atropine to

GI lumen with anaerobic activity ( eg,
discourage abuse; at therapeutic doses,
metronidazole, amoxicillin, ampicillin,
there is no effect from the atropine. Opiates
tylosin, or clindamycin). Equine monocytic
can have potent effects on the GI tract and
ehrlichiosis (seep 283) is caused by the
should be used cautiously. Loperamide is
rickettsial organism Neorickeltsia
available over-the-counter.

(Ehrlichia) risticii but clinically

Loperamide should not be used in dog
resembles salmonellosis. Treatment of
breeds lrnown to be sensitive to ivem1ectin
choice is IV oxytetracycline. Oral doxycy

(Collies, Australian Shepherds, Old English
cline can be used in mildly affected horses.

Sheepdogs) without genetic testing. These

Enteritis from a variety of pathogens is
dogs may have a gene mutation (ABCB-1
common in young animals. When integrity
gene deletion) that causes a functional
of the intestinal mucosa is lost, septicemia
defect in P-glycoprotein, which controls
or endotoxemia is likely. Signs of sepsis
drug movement in many tissues. In people
include severe bloody diarrhea, fever,
and genetically nom1al dogs, large doses of
scleral injection, dehydration, and
loperamide do not cause the typical CNS
alteration in the leukogram ( early leukoeffects of opioids, because loperamide does penia in endotoxic shock, followed by
not achieve high concentrations within the
leukocytosis ). If septicemia or endotoxemia

CNS because of P-glycoprotein-mediated
is suspected, systemic antimicrobials are
efflux of loperamide. Dogs with the ABCB-1
wan·anted along with NSAIDs. Neonates
gene deletion show signs of ptyalism,
with diarrhea deteriorate rapidly before
panting, ataxia, and recurnbency at doses of
culture and sensitivity results are available.

loperamide that do not affect healthy dogs.

Therefore, broad-spectrum antimicrobial

These drugs are contraindicated in
therapy should be initiated. Suggested
infectious diarrhea, because slowing GI
antimicrobials ( depending on species)

transit time may increase the absorption of
include fluoroquinolones, a penicillin or
bacterial toxins. In dogs, constipation and
cephalosporin plus an aminoglycoside
bloat are the most common adverse effects.

(gentamicin, an1ikacin), ampicillin or

Potentially, paralytic ileus, toxic megacolon, amoxicillin, tetracyclines, potentiated pancreatitis, and CNS effects can develop,
sulfonamides, chloran1phenicol, or
especially in cats.

florfenicol. In septic animals, GI absorption
is likely to be altered, so parenteral

Antimicrobial Therapy: The efficacy of
adn1inistration is preferred.

antimicrobials in the therapy of diarrhea is
unlrnown or unproved in most clinical

Nonsteroidal Anti-inflammatory
situations. In most cases of diarrhea in small Drugs (NSAIDs}: The antiprostaglandin animals, a bacterial etiology is not
acLiviLy of NSAIDs may be beneficial wiLh
identified. In large animals, antimicrobial
some types of diarrhea and may be
therapy has not been shown to alter the
important in treatment of septicemia or
course of bacterial enteritis, and in some
endotoxen1ia. Prostaglandins are important
cases, is thought to perpetuate the disease
intracellular messengers for stimulating

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2555
hypersecretion by the intestinal mucosa,

Because ilie salicylate component is
possibly by stimulating an increase in cAMP
only minimally absorbed, its systemic

Antiprostaglandin drugs may directly inhibit effects are minimal. The sulfonamide fluid and electrolyte hypersecretion by tl1e
component may cause keratocoajun

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intestinal cells. NSAIDs should be
ctivitis sicca in dogs, and the salicylate
administered cautiously, because tl1ey have
component may cause toxicity in cats.

adverse GI, hepatic, and renal effects.

Dosage recommendations for sulfasalazine
vary widely, and ilie dosage is gradually

DRUGS USED IN TREATMENT OF
reduced after an initial response. New

CHRONIC COLITIS
products have been developed to overcome ilie difficulty of ilie 5-aminosalicylic The specific cause of chronic colitis in
acid reaching tl1e colon and ilie systemic
animals is frequently unknown; ilierefore, it
adverse effects. Mesalarnine is a pH-sensiis difficult to prescribe a specific treatment tive, coated 5-aminosalicylic acid. The
for the underlying disorder (see TABLE 7).

polymer coating prevents release of ilie

Colitis is often classified as plasmacytid
active drug until it reaches ilie colon.

lymphocytic, eosinophilic, histiocytic, or

Olsalazine consists of two molecules of
granulomatous. The goal of colitis ilierapy 5-aminosalicylic acid joined togeilier by
is to restore normal intestinal motility and
an azo bond. Mesalan1ine is also available
to relieve inflan1mation, spasm, or ulceras an enema. Rectal administration allows ation. In small animals, dietary ilierapy is a
delivery of active drug to ilie colon. It
major component of ilierapy for chronic
appears useful in dogs witl1 chemoilierapycolitis (seep 377).

induced hemon-hagic colitis or wiili

Sulfasalazine is composed of sulfapyriidiopathic distal proctitis. It may also be dine and 5-aminosalicylic acid (mesalauseful in dogs wiili perianal fistulas.

mine) joined by an azo bond. The bond is

Tylosin is a macrolide antimicrobial
broken by bacteria in ilie colon to release
used successfully in some animals wiili
ilie two drugs. The sulfonamide component
colitis. It is commonly administered on a
is absorbed into ilie circulation, whereas
chronic basis as an alternative to sulfasalathe salicylic acid component is active zine therapy. The mechanism of action is
locally in ilie GI tract. Less than half of ilie
unknown, but it is suspected that its activity
salicylate component is absorbed systemiagainst mycoplasmas, spirochetes, and cally. Clinical efficacy appears to be
chlamydiae is important. Best results are
primarily due to ilie anti-inflan1matory
attained when ilie powdered form, labeled
effect of ilie salicylate component. There
for use in swine, is mixed witi1 food or
is evidence for antilipoxygenase activity,
added to water. Some anin1als may find ilie
decreased interleukin-I, decreased
bitter taste unpalatable.

prostaglandin synthesis, and oxygen radical

Metronidazole has fair efficacy against
scavenging activity. Sulfasalazine is

Giardia,, and it is also efficacious in some con1monly used in small animals in the
cases of diarrhea in which giardiasis was
ilierapy of ulcerative or idiopathic colitis or
not definitively diagnosed. It is suspected
of plasmacytic-lymphocytic colitis once
iliat this efficacy is related to ilie activity
dietary causes have been excluded.

of metronidazole against anaerobic

IM=i!D DRUGS USED FOR CHRONIC COLITIS

Drug

Dosage

Sulfasalazine

I0-30 mg/kg, PO, bid-tid

Tylosin

40-80 mg/kg/day

Metronidazole

I0-30 mg/kg, PO, once to tl1ree times daily

Prednisone

2-4 mg/kg, PO, every oilier day

Budesonide

3 mg/m2/day, PO

Raw linseed oil

I oz/day in the feed

Azathioprine

50 mg/m2, PO, daily for 2 wk, ilien every other day

Chlorambucil

2 mg/m2, PO, every other day

2556

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM
bacteria. Metronidazole also has an

GASTROINTESTINAL PROKINETIC
immunosuppressive effect on the GI

DRUGS
mucosa by decreasing the cell-mediated
response. Adverse neurologic effects have

Pro kinetic dtugs increase the movement of

VetBooks.ir
been reported in dogs and cats treated with
ingested material tl1rough tl1e GI tract (see
metronidazole. Diazepam appears effective

TABLE 8). They are useful in tl1e treatment
for treatment of neurotoxicity.

of motility disorders, because they induce

The efficacy of glucocorticoids for
coordinated motility patterns. Unfortutreating colitis is probably related to their nately, some prokinetic drugs may produce
anti-inflan1matory and i.J.mnunosuppressive
a mm1ber of serious adverse effects that
capabilities. Some cases of colitis may be
complicate tl1eir use.

clue to autoantibodies and T lymphocytes

The enteric nervous system of the GI tract
directed against colonic epithelial cells.

can function independently of the CNS to

Glucocorticoicls suppress the i.J.mnune
control bowel function. Because tl1ere are
reaction and are used when biopsy results
no nerve fibers that actually penetrate tl1e
suggest eosinophilic or plasmacytic-lymintestinal epitheliwn, the enteric nervous phocytic colitis. They are used in clogs, cats,
system uses enteroenclocrine cells such as
and horses, often when all other forms of
tl1e enterochromaffin cells as sensory
therapy have failed. Immunosuppressive
transducers. More tl1an 95% of the body's
doses of oral prednisone or dexamethasone
serotonin is located in tl1e GI tract, and
are usually administered and slowly tapered

>900/o of that store is in the enterochromaffin
to every-other-day therapy with the lowest
cells scattered in the enteric epithelium
effective dose.

from the stomach to the colon. The

Budesonide is a glucocorticoid used
remaining serotonin is located in tl1e enteric
in people to treat asthma, rhinitis, and
nervous system, where 5-HT acts as a neuroinflammatory bowel disease. Budesonide transnutter. From the enterochromaffin
has a high affinity for glucocorticoid
cells, serotonin is secreted into tl1e lamina
receptors, high hepatic clearance, and high
prop1ia in high concentrations, which
local and low systemic activity compared
overflow into the portal ci.J.·culation and
with prednisone or dexamethasone. The
intestinal lumen. The effect of serotonin on
human formulation of budesonide consists
intestinal activity is coordinated by 5-HT
of coated granules with a matrix of ethyl
receptor subtypes. The 5-HTlP receptor
cellulose to target release into the lumen
i11itiates peristaltic and secretory reflexes,
of the ilewn or ascending colon. It is not
and so far no drugs have been developed to
known whether the hun1an budesonide
target this specific receptor. The 5-HT3
formulation provides release in the same
receptor activates extrinsic sensory nerves
anatomic site in dogs, but it appears
and is responsible for the sensation of
clinically effective in some dogs.

nausea and induction of vomiting from

N-3 fatty acids have been suggested for
visceral hypersensitivity. Therefore, specific
therapy in people with ulcerative colitis or

5-HT3 antagonists such as ondansetron and

Crohn disease. The addition of n-3 fatty
granisetron are very effective for treatment
acids to the diet makes fewer n-6 fatty acids
of vonuting seen with chemotl1erapy.

available for the arachiclonic acid cascade.

Stimulation of the 5-HT4 receptor increases

Several fommlations are available for small
the presynaptic release of acetylcholine and
ani.J.nals, and raw linseed oil may be added
calcitoni.J.1 gene-related peptide, thereby
to horses' grain for this effect.

enhancing neurotransmission. This enhan

Potent mm1unosuppressive dtugs such
cement promotes propulsive peristaltic and
as azathioprine are used to manage some
secretory reflexes. Specific 5-HT4 agonists
fonns of colitis. Azathioprine is metabolized
such as cisapricle enhance neurotransmisto 6-mercaptopuiine, which is i.J.mnunosupsion and depend on natural stimuli to evoke pressive by i.J.1terfering with nucleic acid
peristaltic and secretory reflexes. This
syntl1esis and by impai.J.ing lymphocyte
makes tl1ese drugs very well tolerated,
proliferation. It may take several weeks
because they do not induce perpetual or
or montl1S of therapy for azatluoprine to
excessive motility. It is also the reason for
become maxin1ally effective. Cats particuthe lm1itations of these cln1gs, because they larly should be monitored for adverse effects,
are not effective if enteric nerves have
mcluding myelosuppression, hepatic disease,
degenerated or become nonfunctional
and acute pancreatic necrosis. Chloran1bucil

(as in cats with end-stage megacolon).

has been used in place of azathioprine m

Metoclopramide is a central clopan1isome difficult or refractory cases of feline nergic antagonist and peripheral 5-HT3
inflanm1atory bowel disease. It is too
receptor antagonist and 5-HT4 receptor
expensive to use in all but very small dogs.

agonist with GI and CNS effects. In tl1e

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2557

IH=i!j:• PROKINETIC DRUGS

Drug

Dosage

Metoclopra

Dogs and cats: 0.2-0.5 mg/kg, PO or SC, tid; 0.01-0.02 mg/kg/hr, IV

VetBooks.ir
mide
infusion

Horses: 0.125-0.25 mg/kg, diluted in 500 mL of polyionic solution and administered IV over 60 min

Domperidone

0.1-0.5 mg/kg, IM; 0.5-1 mg/kg, PO

Cisap1ide

Dogs: 0.1 mg/kg, PO, tid

Cats: 2.5 mg/cat, tid for cats <5 kg, and 5 mg/cat for cats >5 kg Erythromycin

0.5-1 mg/kg, PO, bid-tid

Ranitidine

1-2 mg/kg, PO, bid

Nitazidine

2.5-5 mg/kg, PO, bid

Lidocaine

Horses: 1.3 mg/kg, IV, as a bolus followed by a constant-rate in.fusion of 0.05 mg/kg/min
upper GI tract, metoclopramide increases

Metoclopramide readily crosses the
both acetylcholine release from neurons
blood-brain barrier, where dopamine
and cholinergic receptor sensitivity to
antagonism at the CRTZ produces an
acetylcholine. Metocloprarnide stimulates
antiemetic effect. However, dopamine
and coordinates esophageal, gastric,
antagonism in the striatum causes adverse
pyloric, and duodenal motor activity. It
effects known collectively as extrapyramiincreases lower esophageal sphincter dal signs, which include involuntary
tone and stimulates gastric contractions,
muscle spasms, motor restlessness, and
while relaxing the pylorus and duodenum.

inappropriate aggression. Concurrent use

Inadequate cholinergic activity is incrimiof phenothiazine and butyrophenone nated in many GI motility disorders;
tranquilizers should be avoided, because
therefore, metoclopramide should be most
they also have central antidopaminergic
effective in diseases in which nonnal motility activity, which increases the potential for is diminished or in1paired. Metoclopramide
extrapyramidal reactions. If recognized in
speeds gast1ic emptying of liquids but may
time, the extrapyramidal signs can be
slow the emptying of solids. It is effective in
reversed by restoring an appropriate
treating postoperative ileus in dogs, which
dopamine: acetylcholine balance with the
is characterized by decreased GI myoelecanticholinergic action of an antihistamine, tric activity and motility. Metocloprarnide
such as diphenhydramine hydrochloride
has little or no effect on colonic motility.

given IV at a dosage of 1 mg/kg.

Metocloprarnide is primarily indicated for

Cisapride is chemically related to
relief of vomiting associated with chemometoclopramide, but unlike metoclopratherapy in dogs, as an antiemetic for dogs mide, it does not cross the blood-brain
with parvoviral enteritis, and for treatment
barrier or have antidopaminergic effects.

of gastroesophageal reflux and postopera

Therefore, it does not have antiemetic
tive ileus. GI obstruction, such as intussusaction or cause extrapyrarnidal effects ception in puppies with parvoviral enteritis,

( extreme CNS stimulation). Cisapride is a
must be excluded before initiating
serotonin 5-HT4 agonist with some 5 -HT3
metoclopramide therapy. Its pro kinetic
antagonist activity, so it enhances the
action is negated by narcotic analgesics and
release of acetylcholine from postganglianticholinergic drugs, such as atropine.

onic nerve endings of the myenteric plexus

Drugs that dissolve or are absorbed in the
and antagonizes the inhibitory action of
stomach, such as digoxin, may have
serotonin (5-HT3) on the myenteric plexus,
reduced absorption. Bioavailability may be
resulting in increased GI motility and
increased for drugs absorbed in the small
increased heart rate. Cisapride is more
intestine. Because of accelerated food
potent and has broader pro kinetic activity
absorption, metocloprarnide therapy may
than metoclopramide, increasing the
increase the insulin dose required in
motility of the colon, as well as that of the
animals with diabetes.

esophagus, stomach, and small intestine.

2558

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

Cisap1ide is especially useful in animals

Macrolide antibiotics, including
that experience neurologic effects from
erythromycin and clarithromycin, are
metoclopramide. Cisapride is very useful
motilin receptor agonists. They also appear
in managing gast1ic stasis, idiopathic
to stimulate cholinergic and noncholiner

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constipation, and postoperative ileus in
gic neuronal pathways to stimulate
dogs and cats. Cisapride may be especially
motility. At microbially ineffective doses,
useful in managing chronic constipation in
some macrolide antibiotics stimulate
cats with megacolon; in many cases, it
migrating motility complexes and
alleviates or delays the need for subtotal
antegrade peristalsis in the proximal GI
colectomy. Cisapride is also useful in
tract. Erythromycin has been effective in
managing cats with hairball problems and in
the treatment of gastroparesis in human
dogs with idiopathic megaesophagus that
patients in whom metoclopran1ide or
continue to regurgitate frequently despite
domperidone was ineffective. Erythromya carefully managed, elevated feeding cin increases the gastric emptying rate in
program. In comparative studies of GI
healthy dogs, but large food chunks may
motility in people and animals, cisapride
enter the small intestine and be inadis clearly superior to other treatments.

equately digested. Erythromycin induces

Initially, the only adverse effects reported
contractions from the stomach to the
in people were increased defecation,
tem1inal ileum and proximal colon, but
headache, abdominal pain, and cramping
the colon contractions do not appear to
and flatulence; cisapride appeared to be
result in propulsive motility. Therefore,
well tolerated in animals. As cisapride
erythromycin is unlikely to benefit patients
becan1e widely used in management of
with colonic motility disorders.

gastroesophageal reflux in people, cases of

Human pham1acokinetic studies indicate
heart rhythm disorders and deaths were
that erythromycin suspension is the ideal
reported to the FDA These cardiac
dosage form for administration of erythproblems in people were highly associated romycin as a prokinetic agent. Other
with concurrent drug therapy or specific
macrolide antibiotics have pro kinetic
underlying conditions. In veterinary
activity with fewer adverse effects than
medicine, adverse reactions to clinical use
erythromycin and may be suitable for use
of cisapride have not been reported.

in small animals. Both erythromycin and

Cisap1ide for animals can only be obtained
clarithromycin are metabolized by the
through compounding veterinary pharmahepatic cytochrome P450 enzyme system cies.

and inhibit the hepatic metabolism of other

Domperidone is a peripheral dopanline
drugs, including theophylline, cyclosporine,
receptor antagonist that has been marketed
and cisapride. Nonantibiotic derivatives of
outside tl1e USA since 1978. It is available in
erythromycin are being developed as

Canada as a 10-mg tablet. Currently, it is
prokinetic agents.

available in the USA only as an investiga

Ranitidine and nizatidine are
tional new drug (1%oral domperidone gel)

histamine H,-receptor antagonists that are
to treat agalactia in mares due to f@scue
pro kinetics in addition to inhibiting gastric
toxicosis. Domperidone regulates the
acid secretion in dogs and rats. Their
motility of gastric and small-intestinal
pro kinetic activity is due to acetylchosmooth muscle and has some effect on linesterase inhibition, with the greatest
esophageal motility. It appears to have very
activity in the proximal GI tract. Cimetidine
little physiologic effect in the colon. It has
and fan10tidine are not acetylcholinesterantiemetic activity from dopanlinergic ase inhibitors and do not have pro kinetic
blockade in the CRTZ. But because very
effects. Ranitidine and nizatidine stimulate
little domperidone crosses the blood-brain

GI motility by increasing the amount of
barrier, reports of extrapyramidal reactions
acetylcholinesterase available to bind
are rare; however, if a reaction occurs, the
smooth muscle muscarinic cholinergic
treatment is the san1e as for reactions to
receptors. They also stimulate colonic
metocloprarnide. Domperidone failed to
smooth muscle contraction in cats through
enhance gastric emptying in healthy dogs
a cholinergic mechanism.

in one study. In other studies, however,

Ranitidine causes Jess interference with
domperidone was superior to metoclopracytochrome P450 metabolism of other mide in stimulating antral contractions in
drugs than does cimetidine, and nizatidine
dogs but not cats, and it improved
does not affect hepatic microsomal enzyme
antroduodenal coordination in dogs.

activity, so both drugs have a wide margin of

Because of its favorable safety profile,
safety.

domperidone appears to be an attractive

IV lidocaine is used in the treatment of
alternative to metoclopranlide.

postoperative ileus in people and has been

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2559
shown to be useful in treating ileus and
nerve plexi. They also activate secretory
proximal duodenitis-jejunitis in horses.

mechanisms, provoking fluid accumulation

It is thought to suppress firing of p1imary
in the GI lumen. These drugs can have
afferent neurons, as well as to have
potent effects, and excessive fluid and

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anti-in.flan1TI1atory properties and direct
electrolyte loss can result. They act directly
stimulatory effects on smooth muscle. It
or indirectly (if a metabolic conversion is
is also thought to suppress the prin1ruy
necessary before the compound is active).

afferent neurons from firing, as well as have

Emodin is an irritant glycoside that is an
anti-inflrunmatory properties and direct
active ingredient in several products. Its
stimulatory effects on smooth muscle. Most
action is limited to the Jru·ge intestine, and
horses respond within 12 hr of starting an
it may take 4--6 hr for an effect to be seen.

infusion.

Repeat doses should be avoided in horses
because of the long latent period and risk

CATHARTIC AND LAXATIVE
of severe superpurgation. The naturally

DRUGS
occurring emodins ( eg, sem1a) ru·e found
in hun1an formulations.

Cathartics and laxatives increase the

Vegetable oils are indirect-acting
motility of the intestine or increase the bulk
catl1artics. They are hydrolyzed by pancreof feces. The dosages for all of these drugs atic lipase in the small intestine to irritating
are highly empirical and usually extracted
fatty acids. Castor oil is a potent catl1artic.

from human dosages (see TABLE 9). Clinically, It is hydrolyzed to release ricinoleic acid, these drugs are administered to increase
which causes increased water secretion in
passage of gut contents associated with
tl1e small intestine. Raw linseed oil ( cooked
intestinal impaction, to cleanse the bowel
linseed oil is toxic) is hydrolyzed to release
before radiography or endoscopy, to
linoleates, which are less irritating tl1an
eliminate toxins from the GI tract, and to
ricinoleic acid. In smaller daily doses, linseed
soften feces after intestinal or anal surge,y.

oil is a mild lubricant laxative and a source of
fatty acids for horses.

Stimulant Cathartics: Stimulant

Senna and bisacodyl are stimulant

(initant) cathartics appear to stin1ulate
cathartics that affect the large intestine and
intestinal motility via an irritant effect on
a.re found in many over-tl1e-counter hun1an
the mucosa or stimulation of intranmral
laxative formulations.

•th•ii CATHARTIC AND LAXATIVE DRUGS

Drug

Dosage

Castor oil

Dogs: 5-25 mL, PO

Foals: 25-50 mL, PO

Bisacodyl

Dogs: 5-20 mg, PO, once to twice daily

Cats: 2.5-5 mg, PO, once to twice daily

Magnesium sulfate (Epsom salts)

Dogs: 5-25 g, PO

Cats: 2-5 g, PO

Horses: 30-100 g, PO

Magnesium hydroxide (milk of magnesia) Dogs: 5-10 rnL, PO

Cats: 2-6 mL, PO

Horses: 1-4 L, PO

Lactulose

Dogs: 5-15 mL, PO, tid

Cats: 2 -3 mL, PO, ti.ct

Docusate sodiun1, docusate calcium,

Dogs and cats: 2 mg/kg/day, PO
docusate potassium

Horses: 10-20 mg/kg in 2 L water

2560

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

Hyperosmotic Cathartics: These drugs
carbohydrates. The term "fiber" is used to are poorly absorbed from the GI tract and
desc1ibe the "insoluble carbohydrates" that draw fluid into the intestine by osmosis. The
resist enzymatic digestion in the small
fluid content of the feces increases, which
intestine. Found in the cell walls of plants

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causes intestinal distention and promotes
and grains, the most common fibers are
peristalsis. Although hyperosmotic
cellulose, hemicellulose, pectin, gun1s, and
cathartics are relatively safe, overdoses can
resistant starches. Almost all carbohydrate
cause excessive fluid loss and dehydration,
sources contain some fiber. Some of the
so adequate water intake must be assured.

most common sources of fiber in pet foods

Examples of hyperosmotic cathartics
include rice hulls, com and com byprodinclude magnesium salts, sodium salts, ucts, soybean hulls, beet pulp, bran, peanut
and sugar alcohols.

hulls, and pectin. Adding fiber to a diet

Magnesium salts are frequently used PO improves colon health, helps with weight as saline purgatives. No1mally, only 200/o of
management, and helps with diarrhea,
the magnesitm1 is systemically absorbed
constipation, and diabetes mellitus. Many
and eliminated by the kidneys. If absorption
commercial brands of pet food are available
is excessive or renal elimination is impaired, in a high-fiber formula. Bulk laxatives may then severe hypem1agnesemia and
cause bloating and flatulence. Contrary to
metabolic alkalosis may develop.

popular belief, bran mashes do not cause

Sodium salts can be given PO as saline
a laxative effect in horses. In cats with megacathartics but are more commonly colon, high-fiber diets are used initially to
administered as sodiwn biphosphate or
help manage constipation when there it; still
sodium phosphate enemas. These should
some normal colonic motility. But once the
not be used in cats because fatal hyperphoscolonic inne1vation has deteriorated, the diet phatemia, hypocalcemia, and hypemamay need to be switched to a low-residue tremia may result.

diet with aggressive laxative treatment.

Sugar alcohols, such as mannitol and
sorbitol, are poorly absorbed and fe1mented

Lubricant Laxatives: These act by
in the temlinal ileum and large intestine.

coating the surface of the feces with a

Lactulose is a synthetic disaccharide
wate1�immiscible film and by increasing the
fermented in the large intestine to produce
water content of the feces to provide a
acetic, lactic, and other organic acids that
lubricant action. Lubricant laxatives usually
have an osmotic effect. Lactulose is used
contain mineral oil or white petroleum.

to treat chronic constipation in cats with

Chronic use may reduce intestinal
megacolon. It is also used in the manageabsorption of fat-soluble vitan1ins and cause ment of hepatic encephalopathy, in which
a granulomatous enteritis. Mineral oil is
acidification of the large intestine promotes
very commonly used in horses and cattle,
fonnation of nonabsorbable animonium ions and commercial products are available to and quaternary anlines, thereby reducing the
promote passage of hairballs in cats.

need for detoxification by the liver.

Polyethylene glycol (PEG3350) IB a

Fecal Softeners (Surfactants):

large molecular weight, water-soluble

Docusate sodium, docusate calcium, and
polymer used widely in people as a bulking
docusate potassiw11 are salts that decrease
and softening agent for treatment of constipaswface tension and allow water to tion. It is not metabolized by the intestinal
accumulate in the feces. Docusat!l also
bacte1ial flora and is minimally absorbed by
increases cAMP in colonic mucosa! cells,
the intestines. It fonns hydrogen bonds with
which increases ion secretion and fluid

100 molecules of water per molecule,
penneability. Usually considered very safe,
creating high osmotic pressures within the
concentrations of dioctyl sodiun1 sulfosucbowel lumen. The osmotic pressure prevents cinate (DSS) ranging from 3---5 times the
absorption of water out of the lwnen. It is
recommended dosage produced severe
relatively free of adverse effects. PEG3350 is
diarrhea, rapid dehydration, and death in
readily available in a powder fom1, which can
horses. DSS should not be administered
be added to a dog or cat's regular food. It can
concurrently with mineral oil; soaps are
also be adnlinistered as a solution via
formed and oil absorption is increased.

nasogastric tube. Unlike fiber laxatives, it
does not cause bloating or gas.

DRUGS AFFECTING DIGESTIVE

FUNCTIONS

Hydrophilic Colloids ("Bulk Laxatives"): The bulk laxatives use fiber to draw water in Pancrealipase contains the pancreatic to the bowel. Fiber is made up of several
enzymes lipase, amylase, and protease. It
different compounds, all of which are
is de1ived from the pancreatic tissues of

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2561
swine. These enzymes help digest and
absorb fats, proteins, and carbohydrates.

Pancrealipase is used to treat dogs and cats
with exocrine pancreatic insufficiency.

Other than the forestomachs (rumen,

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Several formulations are available,
reticulum, omasum), the components of
including oral capsules, tablets, and
the ruminant GI tract ar·e similar to those
delayed-release capsules and tablets. The
of monogastric mar1m1als, and the use of
powdered forms can be added to food, and
pham1acologic agents to treat diseases of
the dosage adjusted to maintain nom1al
the glar1dular stomach (abomasum) and
feces. Antacids may diminish the efficacy
intestine follows p1inciples conm1on to
of pancrealipase, whereas H2-receptor
both monogastric and ruminant species.

antagonists may increase the amount of

Ruminants differ significantly from otl1er
pancrealipase that reaches the duodenuni.

mammals in that much of their feed

Ursodiol, also !mown as ursodeoxyundergoes microbial predigestion in the cholic acid, is a naturally occurring bile
forestomachs, chiefly in the rumen and
acid. It suppresses hepatic synthesis and
reticulwn. There is also postgastric
secretion of cholesterol and decreases
fermentation in the cecum and colon, but
intestinal absorption of cholesterol.

tl1is is much less in1portant than in some

Reducing cholesterol saturation allows
other herbivores, eg, horses.

solubilization of cholesterol-containing

Ruminoreticular motility or fennentation
gallstones. Ursodiol also increases bile flow
is depressed in many conditions, including
and reduces the hepatotoxic effect of bile
improper feeding ( overload or deficiency of
salts by decreasing their detergent action.

specific nut1ients), lack of water, infectious

In small animals, ursodiol may be useful
cliseases, intoxications, lesions of any part
in treatment of cholesterol-containing
of the upper GI tract, metabolic states ( eg,
gallstones, idiopathic hepatic lipidosis,
hypocalcemia), or reduced flow of alkaline
and chronic active hepatitis. The dosage
saliva that allows pH to fall and the
in dogs and cats is 15 mg/kg/day, PO.

microbial population to be altered to an

S-Adenosylrnethionine (SAMe) is an
extent that is har111ful to the ar1imal. (See
endogenous molecule synthesized by cells
also DISEASES or THE RUMINANT FORESTOMACII, throughout the body. Formed from the
p 221 et seq.)

aniino acid methionine and ATP, SAMe is an

The p1imary objectives of pharmacothe,,
essential part of three major biochemical
apy are to remove the cause and to promote
pathways: transmethylation, transsulfurathe return of normal digestive function by tion, and aminopropylation. Deficiency of
meeting or reestablishing the requirements

SAMe is associated with cellular derangefor optimal ruminoreticular function as ments in hepatocytes, and there is evidence
quickly as possible. This may include any of
that a SAMe deficiency may contribute to
tl1e following: 1) ens wing an appropriate
abnonnalities of cellular structure and
substrate for microbial fem1entation; 2) profw1ction in many body tissues, including the viding any cofactors ( eg, phosphorus,
liver. Exogenous administration of SAMe
sulfur) necessary for microbial fem1entaappears to improve hepatocellular function tive processes; 3) removing any soluble
in in vivo and in vitro studies without
end-products, 1mdigested solid residues, and
cytotoxicity or significant adverse effects.

gas; 4) maintaining continual flow culture

SAMe increases hepatic glutathione levels
of nllllinal microorganisms; 5) ensuring tliat
in cats and dogs. Glutathione is a potent
the contents of tl1e r1.mlinoreticulum are
antioxidant that protects hepatic cells
fluid; 6) maintaining optimal intraruniinal
from toxins and death. The daily dosage is
pH (generally between 6 and 7); and

18 mg/kg, rounded to the nearest size of

7) promoting active nmlinoreticular activity.

enteric-coated tablet, and given on an
empty stomach.

Milk thistle is used as a natural remedy

DRUGS FOR SPECIFIC PURPOSES
for diseases of the liver and biliary tract.

Silymarin is the active ei-.'tract and contains

Esophageal Obstruction: Esophageal
flavonignar1s that reportedly act as
obstruction due to a foreign body (see
antioxidants, scavenging free radicals arid
p 215) leads to severe discomfort and acute
inhibiting lipid peroxidation. Several
free-gas bloat. Physical removal of the
controlled clinical trials have demonstrated
object may be harnpered by marked spasm
the benefits of milk thistle in hunian patients of tl1e surrounding muscle. Specific with acute or chronic liver disease. A
spasmolytic drugs such as acepromazine
veterinary fonnulation has been approved
may be used (0.05-0.1 mg/kg, IV, IM, or SC in
in the USA for dogs and cats.

cattle). Alternatively, the moderate sedative

2562

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM
and muscle relaxant effects of a low dose
nli.croflora will then be more appropriately
of xylazine (0.05 mg/kg, IM in cattle) or
adapted. Provided the illi.tiating condition
detomidine (0.02-0.05 mg/kg, IM in cattle)

or lesion is responding favorably, improvemay aid removal of obstructions. None of ment almost invariably follows the

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these compounds has been approved by the
reestablishment of normal nmlinal

FDA for use in cattle.

nlicroflora, with consequent nom1alization
of the fermentation process and nm1inore

Ruminotorics: Agents and mixtures that
ticular motility. When the runlinoreticular
promote forestomach function (fermentacontents are putrified, ingesta must first be tion and motility) are known as ruminotoremoved before transfer of fresh rwninal rics. Formulations that contain glucogenic
fluid. This can be accomplished using a
substrates, minerals, cofactors, and bitters
large-bore stomach tube or by perfomling a

( eg, nux vomica) have limited application
nm1enotomy. Acetic acid ( vinegar, 4--10 L,
in current therapy ofruminoreticular

PO) can be aclnli.nistered to cattle with
indigestion. Generally, restoration of the
putrefaction of the rumen associated with
nom1al ruminoreticular environment using
high rumen pH.

a physiologic approach is much more
satisfacto1y.

Antifoaming Agents: Therapeutic

Oral administration of specific alkalinizapproaches to the control of acute frothy ing or acidifying agents should not be
bloat involve administration of antifoarning
routinely undertaken in cases of indigesagents to reduce foan1 stability and to tion. Magnesitm1 oxide or magnesiun1
promote release of free gas, which is then
hydroxide are strongly alkali.nizing agents
promptly ernctated. (See also BLOAT IN
able to substantially increase rumen pH and
llUMINANTS, p 227.)

thus create a hostile environment for rumen

Acute frothy bloat in cattle should be
protozoa. These compounds, when given at
treated with poloxalene, which may be
label dose to daily cattle, result in signifiadnli.nistered as a drench or by stomach tube cant decrease in rumen fermentation and

(25-50 g). Frothy bloat can be prevented by
a decrease in number of rumen protozoa.

adnli.nistering poloxalene as a top dressing

Therefore, these compounds should only
to feed (1 g/45 kg body wt/day) or in a
be administered to cattle with a confirmed
molasses block (1.5 g/45 kg body wt/day).

diagnosis of graiI1 overload.

Polymerized methyl silicone (3.3% emulsion

Mineral oil (1-2 L) or dioctyl sodiwn

[cattle: 30-60mL; sheep: 7 -15 mL]) may be
sulfosuccinate (DSS, 90-120 rnL in 1 -2 L of
used in a sinlilar manner as poloxalene,
water) administered PO or via nasogastric
altl10ugh direct intraruminal iltjection via a
tube followed by gentle ruminal massage
needle or cannula may be more satisfactory
can help promote the dissolution and
in this case. Aclmilli.stration of docusate
passage of impacted fibrous ruminal omasal
sodium in emulsified soybean oil (6-12 fl oz
or abomasal contents. DSS can markedly
contailli.ng 240 mg/mL) or ad.Ininistration of
depress rumen protozoa; thus, rwninal
vegetable oils alone, such as peanut oil,
transfaunation should follow use of this
sunflower oil, or soybean oil ( cattle: 60 mL;
agent ifrwninal hypomotility continues.

sheep: 10--15 mL), also relieves acute frothy
bloat when given PO. The incidence of frothy

Ruminal Fluid Transfer: Fresh rwninal
bloat in feedlot cattle may be reduced by
fluid is considered to be the best available
including ionophores (such as monensin)

"rnminoto1ic," because it contaiI1s viable either in the ration or adnli.nistering as
rwninal bacteria(! x 108-1011/mL) and
controlled-release capsules.

protozoa(! x 105-106/mL) as well as many
useful fermentation factors (volatile fatty

Ruminoreticular Antacids: Rumi11al
acids, microbial protein, minerals, vitanli.ns,
alkalinizing agents are principally used to
buffers). Strained fresh rwninal juice (at
treat rumillal lactic acidosis (pH <5.5) clue
least 3 L, but 8-16 L is ideal in cattle; sheep
to grain engorgement or soluble carbohyrequire -1 L) given PO or by tube is drate overload. (See also GRAIN OVERLOAD IN
indicated in cases of rnminoreticular stasis.

RUMINANTS, p 222.) The resultant systemic

Rw11inal fluid can be aspirated through a
dehydration and acidosis necessitate
stomach tube from the nmli.noreticulum of
immediate correction of fluid and electrolyte
healthy animals using an extractor pun1p
balance and restoration of a viable nli.crobial
or by siphoning, or it can be collected at
population. Often, the latter involves
slaughterhouses. A rumen-cannulated
removal of rwninoreticular contents and
donor animal is particularly convenient. It is
replacement with fresh nmli.noreticular
best for the donor to be on a ration sinlilar
fluid. Antacids that may be given PO, bid-tid,
to that of the recipient, because the rwninal
include magnesiun1 hydroxide ( cattle:

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

2563

100--300 g; sheep: 10-30 g) and magnesium

Motility modifiers are ca.tego1ized based
carbonate (cattle: 10--80 g; sheep: 1---8 g).

on their mechanism of action. These can

Antacids should be mixed in -10 L of warm
be cholinergics (parasympa.thomimetics),
water to ensure adequate dispersion through a.drenergics, antidopanti:nergics, serotoner

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the ruminoreticular contents. Administragics, motilin a.gonists, opioid receptor tion PO of activated charcoal (2 g/kg) is
blockers, or sodium channel blockers
believed to protect the rurninoreticular

(lidoca.ine ).

mucosa from further injury by inactivating

The use of parasympathomimetic agents
toxins. Oral administration of sodium

( eg, neostigmine, physostigmi:ne, bethanebicarbonate (baking soda), either as powder chol) is seldom appropriate. These drugs
dissolved in water or commerciaIJy available have choli:nergic effects, which are solutions prepared for IV infusion, rapidly
potentially hazardous. N eostigmine ( cattle:

neutralize the rnrnen pH but are accompa0.02 mg/kg, SC; sheep: 0.01-0.02 mg/kg, SC) nied by rapid release of large amounts of
generalJy produces tl1e fewest adverse

C02• Because of decreased rnrnen motility in effects but tends to increase frequency, ruminants with acute rnrnen acidosis, these
rather than strengtl1, of rwni:noreticular
animals are at increased risk of developing
contractions. Neostigmine given as a
potentialJy life-threatening free gas bloat.

constant-rate IV infusion (87.5 mg in 10 L
of sodiun1-gl ucose infusion at 2 drops/sec)

Ruminoreticular Acidifying Agents:

has been used to treat cecal dilatation/

Rwninal acidifying agents are used to treat
dislocation. However, the stin1ulatory effect
rwninal stasis or simple indigestion as well
of neostig1ni:ne is not always reliable, and
as acute ammonia poisoning. In rwni:nal
some inhibition of motility can be seen. This
stasis, the intrarumi:nal pH often increases
may be due to the adrenergic component
to >7.5 because of the constant inflow of
associated with ganglion stimulation by
bicarbonate-rich saliva in the absence of
cholinergic agents.

active rwninal fermentation and formation

Bethanechol (0.07 mg/kg, SC, tid for 2
of volatile fatty acids. In acute ammonia
days) has been used to treat spontaneous
intoxication, the increased intraruminal
cecal dilatation without torsion. Potential
pH increases tl1e activity of urease and
adverse effects include salivation and
facilitates the absorption of free anunonia
diarrhea. Reconunenda.tions involving

(pl<,. of a.mmoniwn is 9.1 ). Administration of neostignti:ne and betl1anechol have not weak acids in cold water returns the pH of
been confumed in randomized, controlled
ruminoreticular content toward physiologic
expe1iments. Neither compound has been
levels, promotes the uptake of volatile fatty
approved by the FDA for use in cattle.

acids, depresses the absorption of

Parasympa.thomimetics are sometimes
ammonia, and inhibits excessive urease
used in practice to conservatively treat
activity. Acetic acid ( 4%-5%) or vinegar
left displaced a.bomaswn in cows, although

( cattle: 4---8 L; sheep: 250-500 mL) is the
tl1e literature indicates tl1at use of tl1ese
most common acidifying agent used.

compounds is of no value for this purpose.

N-butylscopolammonium bromide

Modulators of Ruminoreticular

(nonlactating adult cattle: 0.2 mg/kg, IM

Motility: The use of motility modifiers in
or IV; calves: 0.4 mg/kg, IM or IV) is a
cattle is controversial, because evidenceparasympatl1olytic agent approved for based data demonstrating clinical efficacy
the control of dia.tThea. in cattle in some
are scarce. Several diseases, including

European countlies. The commercial
paralytic ileus, cecal dilatation, and
formulation is combined with an NSAID,
a.bomasal displacement, are accompanied
metarnizole (nonlactating adult cattle: 25
by GI tract motility disorders. Pharmacomg/kg, IM or IV; calves: 50 mg/kg, IM or IV).

logic motility modification may hasten

Administration of N-butylscopolammoniwn
recovery in some cases. However, in most
bromide (80 mg/cow) in combination witl1
instances, the most effective strategy to
dipyrone has been proposed as a conservareestablish motility is correction of the tive trea.t111ent of spontaneously occurring
underlying disorder (hypocalcemia.,
right-side displacement of the abomasum in
endotoxemia., alkalemia, obstruction, or
cattle. However, this has not been demonorgan displacement) followed by restorastrated in randomized, controlled studies.

tion of the nom1al rwninoreticular

N-butylscopolanm10nium bromide is not
enviromnent through transfaunation.

approved by tl1e FDA, and tl1e use of

Fwthem1ore, conditioned responses to the
dipyrone in food animals in the USA is
presence of feed and feeding itself a.re physiprohibited.

ologic means by which runti:noreticular

Ati·opine (0.04 mg/kg, IV) has been fow1d
motility can be notably enhanced.

to mitigate a.bomasal contractions for 1-3 hr.

2564

SYSTEMIC PHARMACOTHERAPEUTICS OF THE DIGESTIVE SYSTEM

Atrnpine sulfate (0.5 mg/kg, IV) adminissupport the use of opioids or lidocaine in tered 5 min before placement of a reticular
rw11inallts have not been published.

magnet is suggested to prevent magnet loss
into the cranial sac of the rnrnen. Atropine

DRUG DISPOSITION IN THE

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(40 mg/cow as a 1%solution, SC) is also used RUMINORETICULUM
to detem1ine disrnption offorestomach
motility in cattle suspected to have vagal

Morphologic and functional charactetistics
indigestion. An increase of> 16% in heart
of the nuninoreticulwn that make it suitable
rate 15 min after atropine administration is
for fem1entative digestion of plant material
considered indicative of severe dismption
also affect the activity, distJibution, ar1d
of forestomach motility.

absorption of many &ugs, particularly when

Xylazine hydrochloride (0.2 mg/kg, IV)

given PO. The anaerobic and reductive
administered 5 min before placement of a
environment of the 11.munoreticulwn and ilie
reticular· magnet may prevent loss into the
presence of mally n1icrobial enzymes result
cranial sac of the rumen but will also result
in inactivation of dn1gs such as trimethoprim
in deep sedation of the arrin1al ar1d thus is
and cardiac glycosides. Slow and inefficient
unlikely to be of ar1y practical use. Xylazinemixing of dn1gs in the lar·ge volume of the induced atony of the reticulornmen may be

11.munoreticular fluid delays attainment of
reversed by pretreatment with tolazoline
w1ifonn concentrations throughout tl1e

(0.5 mg/kg, IV), atiparnezole hydrochloride
multiphasic ingesta alld retards absorption

(0.08 mg/kg), or yohin1bine (0.2 mg/kg, IV).

from the mn1inoreticulwn. Absorption is also

Adverse effects ofxylazine in cat-Ue include
affected by the polarity alld ionization status
bradycardia, hypothemua, salivation, diuresis, of the &ug, which is detem1ined by the pl{,, of rnminal bloat, ar1d aspiration pneumonia
the &ug alld the pH of Ll1e nm1inoreticular

Neither xylazine nor its antidotes have been
fluid. 111e latter depends on tl1e diet ar1d the
approved by the FDA for use in cattle.

relative contJibutions of alkaline saliva and

Metocloprar11ide ( cattle: 0.15 mg/kg, IM;
aciclic rwninoreticula.r fluid. Aside from the
sheep: 0.023-0.045 mg/kg) has cholinergic
many effects that the ruminoreticular
and alltidopan1inergic effects but does not
environment Call have on the activity alld
appear· to increase the myoelectJic activity
disposition of &ugs, tl1e &ugs Ll1emselves
of the pyloric alltrum in either species.

may have w1intended effects on rw11inore

However, metocloprall1ide at 0.5 mg/kg
ticuJar· function. In particular·, broad-specgiven IM or IV to goats has been shown to trum alltibacterial agents alld antiprotozoal
i11crease myoelectlic activity of the pyloric
agents can dismpt tl1e notmal balance of
alltJ1.un but not the body of the abomasum.

n1icroflora in the rwninoreticulW11.

Because metocloprall1ide Call cross the

These factors affecting ilie activity and
blood-bra.in barrier, restlessness alld
disposition of drngs in the rnminoreticulum,
excitement ar·e potential adverse effects.

together with the possible effects of drugs

Metocloprall1ide has not been approved
on rw11inoreticular· fW1ction, complicate
by the FDA for use in cattle.

oral adn1inistration of drugs to rnn1inar1ts.

Erythromycin lactobionate is a macrolide

In young allimals, Ll1ese undesirable effects
alltin1icrobial that increases gut myoelectJic
can be avoided by making use of the esophaactivity by binding to motilin recepto1s in geal groove reflex. Tl1is reflex, which is
intestinal smooth muscle cells. In cows,
elicited by receptors in the moutl1 and
e1ythromycin (0.1 mg/kg, IV, or 1 mg/kg, IM)

pharynx, is well developed in suckling
was found to increase myoelectJical activity
neonates but becomes less reliable in older
in the abomasurn alld duodenwn for >2 hr.

animals. After -24 mo in cattle and -18 mo

This effect was increased to 6-8 hr when
in sheep, provoked reticular groove closure
e1ythromycin was administered in polyethylis often irregular, incomplete, or absent.

ene glycol at 10 mg/kg, IM. Erythromycin is

Run1inoreticu1ar morphology and
approved by Ll1e FDA only for tream1ent of
function has less influence on drng
shipping fever, pnewnonia, footi·ot, ar1d
disposition in neonatal ruminants thall in
metJitis at 2.2 mg/kg, IM. Deep IM irtjection
adults. At birth, tl1e forestomachs are
in muscles of tl1e neck is recommended
underdeveloped, alld the newborn nuninallt
because of tl1e 1isk of pain, swelling, ar1d
is essentially monogastric. Drugs that ar·e
tissue blemishes at the irtjection site.

usually destroyed in the nuninoreticuhun

The pro kinetic seroto11inergic dmg
of adults ( eg, tlimethoprim) may be well
cisap1ide ( cattle: 0.08 mg/kg) is widely used
absorbed during the first 2--3 wk of life. This
in equine medicine, yet significant pro kinetic developmental pattern depends on the effects have not been conclusively
period between bilth alld iJ1itiation or a
demonstrated in rw11inar1ts. Furthennore,
roughage diet alld exposw·e to microbes in
definitive clinical alld experimental data to
the environment.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE EYE

2565

SYSTEM IC PHARMACOTH ERAPEUTICS

OF THE EYE

VetBooks.ir

See also OPIITIIALMOLOGY, p 488.

ROUTES OF ADMINISTRATION

The anatomy of the eye presents unique
opportunities for topical and/or systemic

The three primary methods of delive1y of
medical treatment of neural tissue. Like
ocula.i· medications to the eye a.i·e topical,
the brain, the eye has protective barriers
local ocular (ie, subconjunctival, intra.vitfrom the vascular system. The bloodreal, retrobulhar, intracameral), and ocular barriers (ie, the blood-aqueous
systemic. The most appropriate method
and blood-retinal baniers) allow the eye
of administration depends on the area of
to control entry of inflammatory cells,
the eye to be medicated. The conjunctiva,
protein, and low-molecular-weight
cornea, a.11terior chamber, and iris usually
compotu1ds from the systemic circulation.

respond well to topical therapy. The eyelids

The blood-aqueous barrier is a
ca.11 be treated with topical therapy but
fLU1ction of the iris and ciliary body
more frequently require systemic therapy.

epithelium. In the iris, the capillary

The posterior segment always requires
endothelium is not fenestrated, but there
systemic therapy, because most topical
are tight junctions. In the ciliary body,
medications do not penetrate to the
there are tight connections between the
posterior segment. Retrobulbar and
apical ends of the nonpigmented epithelial
orbital tissues are treated systemically.

cells. Breakdown of this barrier results in

SubconjLU1ctival or sub-Tenon's therapy,
entry of protein and cells into the anterior
although not a true form of systemic medichan1ber and is seen as aqueous flare or cation administration, has the potential to
plasmoid aqueous. The blood-retinal
increase both drug absorption and contact
barrier is composed of two layers: an
time. Medications both leak onto the cornea
endothelial and epithelial portion. The
from the entry hole of iitjection a.Ild cliffuse
endothelial part is composed of the
through the sclera into the globe. Drugs
endothelium of the retinal capillaries,
with low solubility such as corticosteroids
which are also nonfenestrated. The
may provide a repository of drug lasting
epithelial portion is the retinal pigment
days to weeks. Appropriate amounts of
epithelium. When treating the eye via the
medication must be used. Large amounts,
systemic circulation, these barriers can
especially of long-acting salts, can cause a
limit the entry and amount of medicasignificant inflammatory reaction. For tions into the eye, especially highly watersub-Tenon's injections, 0.5 mL per site is soluble compounds. They are less effective usually safe a.Ild effective in small a.Ilimals, in the face of inflammation, and many
a.Ild <; I mL Ca.Il be used in large a.Ilirnals such drugs gain increased access to the
as horses a.Ild cows.

intraocular structures when the eye is

Retrobulbar medications are used
inflamed. The time required for drugs to
infrequently for therapeutics. In cattle, the
reach their peak concentrations in the eye
retrobulbar tissues can be anesthetized
depends highly on the physicochemical
with local a.I1esthetic (lidocaine/bupiviproperties of the particular drug.

caine) for enucleation using either a

The presence of baniers such as the ilis,

Peterson block (15-20 mL) or a4-point
ciliary body, and Jens, as well as nom1al
block of the orbit (5-10 rnllsite). Whenever
movement of aqueous hLU11or through the
a.Ily medication is placed into the orbit,
pupil and out the trabecular and uveoscleral extreme care must be taken to ensure tl1at mesh work can further limit the distribution
the medication is not inadvertently iitjected
of drugs. Several enzymes are present in
into a blood vessel, the optic ne1ve, or one
the cornea and ciliary body. These can
of the orbital fora.men. Retrobulbar
metabolize drugs to inactive metabolites
injection has a high 1isk of adverse effects
before and after the compound reaches the
and should not be used unless t11e clinician
ante1ior chamber. Drugs predominantly
is expelienced and the animal is approp1ileave the anterior chamber with the ately restrained.

aqueous hLU11or via the corneal trabecular

Systemic medication is required for
and/or uveoscleral mesh work, although
posterior segment therapy and to complesmall a.inoLUlts may move posteriorly into ment topical therapy for the anterior
the vitreous.

segment. The blood-ocular ba.i·riers can

2566

SYSTEMIC PHARMACOTHERAPEUTICS OF THE EYE
limit absorption of less lipophilic drugs,

TREATMENT OF INFECTIOUS
but inflammation will initially allow greater

DISEASE
drug concentrations to reach the site. A5
the eye starts to heal, these barriers will

Feline Herpesvirus Keratitis and

VetBooks.ir
again become more effective and can limit

Conjunctivitis: Systemic antiviral drugs
further drug penetration. This should be
to treat feline ocul.ar herpesvirus are needed
considered when treating posterior
only in circumstances when topical antiviral
segment disease, eg, blastomycosis in
therapy is not effective. Famciclovir (the
small anin1als with hydrophilic drugs such
prodrug of penciclovir) at 15-30 mg/kg, PO,
as itraconazole.

bid-tid for 10-14 clays (or empirically at

After topical administration, up to 8091, of

31.25 mg/kitten or small cat, or 62.5 mg/cat,
the applied drug(s) is absorbed systemically
bid for 2 wk) is the drug of choice for
across the highly vascularized nasopharynti·eatinent and longterm management.

geal mucosa. Because absorption via this

Acyclovir has also been used at 200 mg, PO,
route bypasses the liver, there is not the
bicl-tid, although repeated closing can cause
large first-pass metabolism seen after oral
systemic toxicity and is not reconm1ended
administration. Depending on the drugs
as first-line treatinent. Previously, lifelong
used, this can result in systemic adverse
oral L-lysine (250-500 mg/day) was
effects. Topically applied [3-blockers used in
recommended to help prevent or reduce the
the treatment of glaucoma can cause heart
severity of recurrent feline herpesvirus
block, atiial tachycardia, congestive heart
infections. However, recent work has
failure, bronchospasm, dyspnea, and
shown that oral L -lysine can actually
decreased exercise tolerance. These drugs
exacerbate feline herpesvirus infections.

should be used very carefully in older

Recombinant hw11an a-interferon
aninlals or in aninlals with cardiac or

(5-25 U/day, PO and topically) has also been
respiratory disease. Cushing syndrome can
recommended and may work by inhibiting
be easily induced in small or medium-sized
replication of herpesvirus and enhancing
clogs with chronic use of potent topical
macrophage activation and lyn1phocytesteroids.

mediatecl cytotoxicity.

LOCAL ANESTHETICS

Feline Chlamydia! Conjunctivitis:

Feline co11iW1ctivitis caused by Chlamydia

Parenterally, local nerve blocks are an
felis ( see p 506) that is nonresponsive to excellent aid for routine ocular evaluation
topical tetracycline therapy can be treated
and diagnostic procedures in horses. The
with oral doxycycline (10 mg/kg/day, or
auriculopalpebral block is the most helpful

5 mg/kg, bid). To avoid esophageal stiictures,
block to limit blepha.rospasm-during
aninlals should be ti·eated with 3--5 mL of
examination. This procedure blocks some
oral fluid after dosing to ensure the tablets
of the motor nerves of the upper eyelid and
pass into the stomach. All cats in the
enables the examiner to control the horse's
household should be treated for at least
upper eyelid. The amiculopalpebralnerve

4 wk, or for 2 wk after clinical signs have
is a branch of the facial nerve and can be
resolved. To avoid issues associated with
palpated as it runs across the superior
tetracycline use in pregnant queens or yoWlg
margin of the zygomatic arch. To block
cats, systemic macrolides such as erythrosensory input, a supraorbital nerve block mycin (15-25 mg/kg, PO, bid, or lD-15 mg/
or a ring block is used. The supraorbital
kg, PO, tid for 3--4 wk) or azith.romycin
nerve is a branch of the frontal ne1ve that

(10-15 mg/kg/day, PO, for 3--5 days then
traverses the supraorbital foran1en of the
twice weekly for 3 wk) are also effective.

upper orbit. If placed correctly, a dose of

Alternatively, potentiated an1oxicillin

1-2 mL of lidocaine is usually sufficient

(12.5-25 mg/kg, bid for 3 wk) can be used. If
to block either the auriculopalpebral or
signs recur after tJ·eatI11ent ceases, therapy
supraorbital nerve. The block is usually
should be continued for an additional 4--5 wk.

effective within 3-5 min and can last up
to 2 -3 hr.

Feline Toxoplasmosis: Many cases

The same principles are used in food
of feline anterior uveitis with increasing
anin1als, such as cattle, in which both a

Toxoplasma gondii titers, as shown by
retrobulbar and ring block may be used.

serology and anterior chamber centesis,

A correctly placed retrobulbar block will
remain undiagnosed. Chorioretinitis is often
block cranial nerves II, ill, IV, the ophthal-
the most common presentation. Treatinent

1nic branch ofV, and VI. The ring block is
is clindan1ycin at 8-17 mg/kg, PO, tid, or
needed to inhibit sensory input from the

10-12.5 mg/kg, PO, bid for 3-4 wk, in
skin around the eye.

association with topical corticosteroids

SYSTEMIC PHARMACOTHERAPEUTICS OF THE EYE

2567

(0.5%---1% prednisolone acetate or 0.01%
or 1 mo after all signs of the clisease have
dexamethasone alcohol tid-qid) and topical
resolved. Adverse effects include anorexia,
atropine for mydriasis. Adverse effects of
which is associated with liver toxicity. Cats
clindamycin include anorexia, vomiting,
can be treated with 10 mg/kg/day or 5 mg/kg,
and dian-hea, mainly at the higher doses.

bid; however, there are few published cases

VetBooks.ir

Other systemic antibiotics less frequently
of successful treatment in cats. Ketoconaused include the synergistic combination of zole may also be used to treat blastomycosulfonan1ides (sulfadiazine, sulfamethazine, sis, but because the onset of effect is so
sulfan1erazine, 100 mg/kg/day, PO) and
slow, other triazoles should be used initially.

PY1imethamine (2 mg/kg/day, PO) for 1---2

Arnphotericin B deoxycholate is also
wk. Adverse effects include gastric upsets
effective but is nephrotoxic. The dosage
and bone marrow suppression. Frequent

(dogs: 0.5 mg/kg, IV; cats: 0.25 mg/kg, IV) is
hematologic monitoring is recommended
given three times weekly until the anin1al
if therapy is to last >2 wk.

becomes azotemic or a cumulative dose
of 4-6 mg/kg in dogs or 4 mg/kg in cats is

Feline and Canine Rickettsial
reached. An1photericin B lipid complex

Infection: Anterior and posterior uveitis
used at the san1e or a slightly higher dosage
and chmioretinitis secondary to infection
is less nephrotoxic.

with Ehrlichia or Rickettsia spp ( see p 803) The predominant lesion of histoplasmois common. Tetracyclines ( doxycycline at sis (seep 639) is granulomatous choroiclitis, 5---10 mg/kg, once to twice daily for dogs,
but anterior uveitis, retinal detachment, and
and 10 mg/kg, bid, for cats, for 14-21 days)

optic neuritis can be present. Treatment
are tl1e drugs of choice and have excellent
options are itraconazole (10 mg/kg, PO)

intraocular penetration. ln a dog from an
or fluconazole (2.5---5 mg/kg, PO) once to
area associated with rickettsial disease, it
twice daily for 4-6 mo, or amphotericin B
is rational to empirically treat uveitis with
deoxycholate (0.25---0.5 mg/kg, IV, every 48 hr)

doxycycline pending serology. Enrofloxacin
until a cun1ulative dose of 5---10 mg/kg

(3 mg/kg, PO, bid for 7 days) can also be

(dogs) or 4-8 mg/kg (cats) is reached.

used, although care should be taken not to

Because of its lipophilic nature and ability
exceed the dosage associated with retinal
to cross the blood-ocular ba.niers,
toxicity in cats (>5 mg/kg/day). Chloran1-
fluconazole is recommended for use in
phenicol is not recommended, because it
ocular disease, although anin1als have also
directly interferes with heme and bone
had complete resolution when treated with
marrow synthesis. Appropriate topical and
the more hydrophilic triazole itraconazole.

systemic NSAID therapy is also recom

Ocular signs are present in 15% of
mended to control ocular inflan1mation.

cryptococcosis (seep 637) cases and are

When the intraocular inflammation is severe
more common in cats than in dogs.

or tl1ere is a serous retinal detachment,

Treatment can be with an1photericin B
short-term (2-7 days) corticosteroids
deoxycholate (0.1-0.5 mg/kg, JV, three

(0.25---0.5 mg/kg, PO, once to twice daily) may times per wk) alone or in combination be used concun·ently 24-48 hr after the start
with flucytosine (30---75 mg/kg, bid-qicl for
of oral antibiotic therapy. Animals can regain
up to 9 mo). Ketoconazole, itraconazole,
some vision after reattaclunent of the retina;
and fluconazole are also effective. In cats,
the an10unt depends on the duration of the
ketoconazole is administered PO at either
detachment and degree of inflanunation.

5---10 mg/kg, bid, or 10---20 mg/kg/day for

6-10 mo. lf toxicity occurs, the dosage can

Canine and Feline Ocular Mycoses:

be changed to 50 mg/kg/cat, PO, every other

Dogs and cats diagnosed witl1 ocular
clay. 1n clogs, dosages are either &---15 mg/kg, mycoses require systemic treatment. Along

PO, bid, or 30 mg/kg/day, PO, for 6-10 mo.

with systemic antifungals, topical and

Systemic absorption from the GI tract is
systemic anti-inflan1rnatories and topical
significantly enhanced by food. Adverse
mydriatics/cycloplegics are needed to
effects of ketoconazole include anorexia,
control the secondary and potentially
cliarrhea, vomiting, and increased liver
blinding intraocular inflan1mation.

enzY1nes. Because of poor CNS penetration,

Blastomycosis (seep 634) is more
ketoconazole is not reconunenclecl for use
conunon in dogs than cats. Up to 40% have
as the sole agent in ocular cryptococcosis.

ocular signs, usually anterior uveitis.

Itraconazole (cats: 5---10 mg/kg, PO, bid, or

Treatment options include parenteral

20 mg/kg/day, PO) is less likely to cause
an1phote1icin B deoxycholate or PO or IV
adverse effects than ketoconazole, and its
triazoles. ln clogs, itraconazole is used at 5

GI tract bioavailability is enhanced by fatty
mg/kg, PO, bid for 5 days, then continued at
food. Like ketoconazole, its hydrophilic

5 mg/kg/day, PO, for a minimun1 of 60 days
nature leads to poor clistribution into the

2568

SYSTEMIC PHARMACOTHERAPEUTICS OF THE EYE

CNS, but it has been successful in treating

Florfenicol, at a single dose of 40 mg/kg, SC,

CNS and ocular cryptococcosis. Adverse
or two doses of 20 mg/kg, IM, 48 hr apa.it, is
effects are mainly associated with the GI
also effective. The organism is also sensitive
tract (anorexia and vomiting), buL liver
to tI"i.metlloprim-sulfona.I1l.icle (15-30 mg/kg, disease can also develop. Liver enzymes

IM or IV, once to twice daily) or a single SC

VetBooks.ir

(ALT) should be monitored every 2 wk for
close of tilmicosin (5-10 mg/kg), ceftiofur
the first mo.nth of treatment and monthly

(6.6 mg/kg), or tulatliromycin (2.5 mg/kg).

thereafter. Fluconazole is more lipophilic

M bovis is resistant to systemic macrolides, and has better bioavailability than
li.ncosa.inides, and often penicillins.

itraconazole. It also penetrates the CNS

Chla.inydial keratocor\junctivitis in sheep
better (60"1<,-800/oof senmi levels) and causes and goats and nonchla.I11ydial keratoconfewer adverse effects than itraconazole. The junctivitis caused by Mycoplasma spp in dosage for cats and dogs is 5-15 mg/kg, PO,
goats can be treated witll systemic antionce to twice daily for 6--10 mo.

biotics in addition to topical tllerapy. These

Ocular coccidioidomycosis ( see p 637) is
include oxytetracycline (6--11 mg/kg, IV
more conu11on in dogs than in cats. Ocular
or IM), florfenicol (20 mg/kg, IM or SC),
involvement requires systemic treatment
tylosin (10 mg/kg, IM), erythromycin base
with ketoconazole ( dogs: 15-20 mg/kg,

(2.2-15 mg/kg, IM, once to twice daily), or

PO, bid; cats: 15-20 mg/kg, PO, once to twice
tilmicosin (10 mg/kg, IM). Mostani.nlals are
daily), although there is poor CNS and ocular treated with a single close because of penetration. Ketoconazole can be toxic in
management issues involved in treating
cats, so itraconazole (5-10 mg/kg/day, PO)

flock outbreaks.

would be a safer choice. Treatment is for 3--6
mo or longer, and relapses are common.

Penetrating Trauma: All penetrating

Arnphoterici.n B deoxycholate can also be
wounds of the eye should be considered
used (0.4-0.5 mg/kg, IV, every 4S-72 hr) until
infected, and animals should be ti·eatecl
a cm11ulative dose of S-11 mg/kg is reached.

promptly with systenl.ic broad-spectrmn

Over the past 10 yr, a nmnber of newer
bactericidal antibiotics. For dogs and cats,
t1iazoles (voriconazole, ravuconazole [both
oral a.inoxicilli.n-clavula.ilic acid (10-20
fluconazole derivatives], and posaconazole
mg/kg, bid) is appropriate. When feasible,

[an itraconazole de1ivativel) with broader
culture and sensitivity a.Ild cytology
spectnun of activity against systemic
perfonned on anterior cha.I11ber centesis
mycoses (including those resistant to other
sa.i11ples best guide appropriate a.i1tibiotic
azoles) have become available. Infomiation
selection. Treatment should continue for a
on their clinical usage is limited and mostly
mi.nimmn of 14-21 days. In horses, the
published as pha.imacokinetic studies or
combination of systenl.ic penicillin G
individual case reports. I)oses have been
procaine (22,000-44,000 U/kg, IM, bid) Md
extrapolated from their use and preclinical
gentamicin (6.6 mg/kg/day, IM or IV) is a.ii
toxicology tiials in people, and using these
approp1iate choice.

doses must be done carefully. Because posa

In all cases, intensive systemic NSAIDs
conazole is primarily metabolized in most

(flunixin 0.5-1 mg/kg, IV or PO, once to twice
species by glucuronidation, ca.i'e needs to be daily; ketoprofen 1.1-2.2 mg/kg/day, PO or taken with the dose and duration, especially

IV) a.i·e wa.iTa.i1tecl to control the severe
in cats. Voriconazole is predominantly
infla.imnation usually associated with tllese
hepatically metabolized, and in toxicology
injuries. Because treatI11ent duration in tllese
trials, chronic usage at 12 mg/kg for 6--12
cases extends beyond label recommendamonths caused hepatotoxicosis. Ve1y tions of 5 days, an appropriate H2-blocker
limited information is available on tile

( ra.Ilitidine, fa.inotidine) or proton pmnp
use of ravuconazole in dogs and cats.

inhibitor ( omeprazole) should be used

The cun-ent literature should be reviewed
prophylactically to prevent gastiic ulcerabefore using any of these compounds.

tion. When infla.inmation is also associated
witl1 leakage of lens mate1ial into tile a.nte1ior

Infectious Keratoconjunctivitis: 1)-eatcha.inber, the only treatinent to conLrol tl1e ment of infectious keratocor\jm1ctivitis (see
i.nfla.I1u11ation is removal of tile lens.

p 512) associated witll Moraxella bovis in
cattle is improved witll use of systemic

TREATMENT OF INTRAOCULAR
antibiotics. Oxytetracycline and florfenicol

INFLAMMATION
are the two most commonly used. Two closes
of parenteral long-acting oxyteti·acycline (20

Ma.Ily infectious a.Ild noninfectious diseases
mg/kg, IM or SC) 4S-72 hr apa.it is effective,
cause intraocular infla.inmation. Unless
altl1ough ca.i·e should be taken using
infla.imnation is controlled early, in-eversteti·acycli.nes in endemic a.iiaplasmosis areas. ible dan1age and blindness may result.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE EYE

2569

Topical and systemic corticosteroids and
every day or every other day; or cyclo

NSAIDs are used to control inflammation,
sporine 5 mg/kg daily, every other day, or
depending on the cause. Care should be
once weekly with or without concurrent
taken when using longtern1 treatment.

low-dose prednisone or prednisolone.

Adrenocortical suppression can develop,

Adverse effects of azathioprine include

VetBooks.ir
and anin1als must be weaned off treatment
pancreatitis, liver disease, and bone marrow
slowly after the inflammation has resolved.

suppression. Frequent hematology and

In all species, control of noninfectious
serwn biochemistry monitoring is
intra.ocular inflanllllation involves use of
reconunended. There are fewer adverse
high initial doses of systemic corticosteeffects with mycophenolate and cycloroids (prednisone 1-2 mg/kg) in combinasporine. These are mainly related to the GI tion with topical corticosteroids (0.5% or
tract and include anorexia, vomitiI1g, and

1 % prednisolone acetate or 0.1% dexadiarrhea. In uveodern1atologic syndrome, methasone alcohol, tid-<iid). Some cases of
recwTence is common and prognosis for
infectious disease ( eg, rickettsial infections) longtern1 control is only fair. Many animals can be treated with low doses of systemic
become blind from secondaty glaucoma
corticosteroids but only after antibiotic
associated with the chronic uveitis and/or
therapy has been started for 24---48 hr.

retinal detaclm1ent and degeneration.

Topical steroids can be started at the san1e
time as systemic antibiotic therapy. If the

Canine Optic Neuritis: Inflatnmation
cause of intra ocular inflanllllation is
of the optic nerve is more conm1on in dogs
unknown, a combination of topical corticothan in other species. It can be caused steroids and systemic NSAIDs is also
by infection ( eg, distemper, systemic
appropriate. Use ofH2-blockers or proton
mycoses ), neoplasia, contiguous inflan1-
pump inl1ibitors should be considered
mation, or granulomatous infiltration
when starting therapy; GI, liver, and renal

(reticulosis/granulomatous encephalomyparameters should be routinely monitored.

elitis). Systemic corticosteroids (prednisone, 1-2 mg/kg, PO) for extended periods Canine Immune-mediated Disease:

( often weeks) are used in an attempt to

Inrnmne-mediated ocular disease is not
retain vision. Granulomatous encephalomyuncommon in dogs. This can include elitis is responsive to early treat1nent with
episcleritis, nodular granulomatous
systemic cotticosteroids.

episclerokeratitis ( often seen in Collies as a

Damage to the optic nerve as a result of
raised granulomatous lesion involving the
traun1a is treated with systemic corticosteepisclera and third eyelid and infiltrating roids at silnilar dose rates as above. Prointo the cornea), and extra.ocular muscle gnosis depends on the degree of damage.

myositis. In addition to infectious anterior
and posterior uveitis, immune-mediated

Equine Uveitis: The principles of
uveitis ( uveodermatologic syndrome)

anti-inflatnmatory treatment for equine
associated with an inllll tme reaction to
uveitis (seep 508) are very similar regardless melanin is seen in a number of breeds,
of the illitiating cause. In acute uveitis,
more commonly those of Arctic origin.

systenlic NSA.IDs (flunixin meglumine,

These diseases can be treated with either

0.25---1 mg/kg, IV or PO, bid) are used in
combined topical and oral corticosteroids
cof\itmction with topical and/or subcoajunc

(prednisone, 0.5---1 mg/kg, bid) or a lower
tival corticosteroids to control the intra.ocucorticosteroid dose in combination with lar inflanllllation. Phenylbutazone does not
another immw10suppressive drug. This
seem to be as effective in the illitial treatment
could be oral azathioprine ( l.5-2 mg/kg/day,
of equine uveitis. Horses are often treated
reducing the dose after 3--5 days), mycowith high doses of NSA.IDs for longer than phenolate mofetil (7-20 mg/kg, bid for
label recommendations ( often 7-10 days);

3-4 wk, then reducing the dose to 10 mg/kg/
once the uveitis is controlled, the dose is
day), or cyclospotine (5 mg/kg, bid for 2 wk,
slowly tapered over 2-3 wk ConcwTent
decreasing to daily if clinical improvement).

gastric protection with either an H,-blocker

An alternative treatment for episcleritis in

(ranitidine, 6.6 mg/kg, PO, tid, or 1 mg/kg,
dogs >10 kg is niacinanlide (500 mg, PO)

IV, tid; or famotidine, 0.23--0.35 mg/kg, IV,
and tetracycline (500 mg, PO), tid,
bid-tic!, or 1.88---2.8 mg/kg, PO, bid-tic!) or a
decreasing to once to twice daily once
proton pun1p inhibitor ( omeprazole, 4 mg/kg/
improvement occurs.

day, PO) is reconunended. Renal function

Many cases of iI11lllune-mediated ocular
should be monitored, and extreme care
disease can be kept in remission with either
taken if the horse is also being treated with
azathioprine, 1-2 mg/kg, PO, eve1y 3-7 days
gentat1liciI1. Oral aspirin (25 mg/kg/day)

for 1-8 mo; mycophenolate mofetil, 10 mg/kg has been used longtenn to help prevent

2570

SYSTEMIC PHARMACOTHERAPEUTICS OF THE EYE
recurrence in horses diagnosed with equine
should be rechecked 1 wk after starting
recurrent uveitis. Suprachoroidal cyclotherapy, and blood pressure regularly sporine implants are now more commonly
monitored. Adverse effects of ainlodipine
used for longtem1 management ( up to 3 YlJ
ai·e unconunon but include azotemia,
lethargy, hypokalern.ia, and tachycardia

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Equine Optic Neuritis: Trauma to the
poll in horses associated with rearing and

TREATMENT OF GLAUCOMA
hitting objects or falling over backward can
result in sudden blindness. This is associated

Topical medications, such as prostaglanwith overextension or sheaiing of the optic dins, miotics, [3-blocking adrenergics, and
ne1ve within the optic canal secondaiy to
topical cai·bonic anhydrase inhibitors, are
movement of the brain in the skull. Treatthe prin1aiy drugs for treatment of ment is systemic anti-inflan1mato1y agents,
glaucoma (seep 497), but these are often
usually NSAIDs at higher dosages (flunixin
supplemented with systemic drugs.

meglumine, 0.5-1. 1 mg/kg, IV or PO) and
for longer than label recommendations.

Osmotic Diuretics: In the emergency

Prophylactic use of H,-blockers or a proton
treatment of acute glaucoma, intraoculai·
pump inhibitor is recommended. In addition,
pressure must be reduced urgently. This
dimethyl sulfoxide (DMSO; 1 glkg, IV as a 2001<, is done pharmacologically using osmotic solution in saline or 5%dextrose in water
diuretics such as maimitol or glycerol in
given daily for 3 days, then eve1y other day
combination witl1 other topical and systemic
for6 days) can be used. When given IV, DMSO drugs. Osmotic diuretics are lai·ge-molecucan cause hemolysis at1d hemoglobinuria.

lai·-weight molecules that increase the

Prognosis is poor for any return of vision if
osmotic pressure of plasma relative to the
there has been no in1provement after 72 lu·.

aqueous and vitreous. Most of the water in
the eye is in the vitreous. Dehydration of the

TREATMENT OF MISCELLANEOUS vitreous allows the lens and iris to move FELINE CONDITIONS
posteriorly, opening tl1e iridocomeal angle.

The otl1er effect is to decrease formation of
aqueous hwnor. Mannitol is given ( 1-1.5 g/kg,

Feline Eosinophilic Keratitis: Eosino

IV over 20-30 min), witl1 tl1e effect peaking
philic keratitis is associated with infiltration
in 2-3 hr and lasting up to 5 hr. Mannitol is
of eosinophils into the feline cornea It may
not metabolized and thus can be used in
be an unusual inunune response to latent
diabetic aninlals. Glycerol (1-2 g/kg, PO) can
feline herpesvirus. Treatment with topical
be used but is unpalatable, and most dogs
steroids usually is sufficient, but some cases vomit. With both drugs, water should be do not respond. Oral megestrol acetate
witllheld for 3--5 hr, and the animal should

(0.5 mg/kg/day until a response is noted, then be given regular opportunities to urinate.

1.25 mg, PO, 2-3 tin1es weekly as required)

Kidney and cardiac function should be
helps to improve or resolve the corneal
checked before treatment, and cardiac
inflan1mation via an unknown mechatlism.

function monitored during treatment.

However, its use is associated with adverse

Mannitol can be used again within 8-12 lu· if
effects such as diabetes mellitus, adrenoc01°
initial control of intraocular pressure is not
tical suppression, and uterine hyperplasia,
maintained; longtenn control is unlikely if
and this drug should be used with extreme
intraocular pressures do not stay within the
caution. Megestrol acetate cat1 also be
normal rat1ge after two treatments.

dangerous to women handling the pills.

Carbonic Anhydrase Inhibitors: Oral

Feline Hypertensive Retinopathy:

cai·bo.nic anhydrase inhibitors are also used

Older cats can present with sudden blindto treat and manage acute glaucoma. These ness due to serous retinal detacl1ments
inhibit the enzJ111e cai·bonic anhydrase in
secondaiy to systemic hypertension, or less
the nonpigmented ciliaiy epitheliW11
conunonJy hyperthyroidism. Treatment is
responsible for catalyzing the following
with the calcium chaimel blocker ainlodireaction: C0
pine (0.625 mg/cat once to twice daily; some

2 + HP <-- carbonic anhydrase

--. H
cats may require 1.25 mg/cat, bid) ai1d

2C03 ..... H+ + HC03-

The bicarbonate and sodiun1 ions are
systemic c01ticosteroids (prednisone,
actively transported into the anterior

0.5-1 mg/kg, PO) to help control the
chan1ber, leading to passive movement of
posterior inflai11mation. Retinas can
water. This mecha.Il.ism produces 400/o--6001<,
reattach once blood pressure returns to the
of aqueous hW11or. Drugs used include
normal range. At least 5001<, of cats will regain methazolainide (2-4 mg/kg, PO, bid-ti cl), some clinical vision if treated eai·ly. Cats
acetazolanlide (5-8 mg/kg, PO, bid-tid), ai1d

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2571
dichlorphenamide (2-4 mg/kg, PO, bid-tid).

Potassium supplementation can be given

Methazolamide is the drug of choice.

with potassium bicarbonate or citrate (1-2

Maximal effect occurs 3-6 hr after
g/day) added to the food. Cats are more
administration. The most common adverse
sensitive than dogs to the adverse effects
effect is a metabolic acidosis that causes
of these drugs and need careful monitoring.

VetBooks.ir
panting. Other effects can include

In general, systemic carbonic anhydrase
vomiting, diarrhea, and hypokalemia.

inhibitors are not recommended for use in

Acetazolamide commonly causes anorexia. cats.

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE INTEGUMENTARY SYSTEM

See also Pll!NCIPLES OP TOPICAL THERAPY, p 844.

ar·e the most common bacteria isolated from

Drugs that may be used in tl1e integw11en

U1e epidem1is of cats. Actinomycetes and
tary system fall into several therapeutic
mycobacte1ia are rare opportwlistic
categories: antimicrobials ( antibacterials,
invaders in dogs and cats. Bactericidal
antifungals), antiparasitics, NSAIDs,
drugs expected to be effective against these
inmmnomodulators, hormones, psychotropic
bacteria should be used when treating the
agents, and vitamin and mineral supplements.

first occurrence of pyoderma in an animal.

Several factors may contribute to tl1e

Bacterial skin disease in lar·ge ar1in1als
development of tile particular clinical
may be caused by Derrnalophilus
presentation. Each factor should be identified
congolensis, staphylococci, Corynebacte
ar1d treated for tl1erapy to succeed. For
rium spp, Actinomyces, and rar·ely Bacillus exarnple, recurrent otitis may have a primary
spp or Pseudomonas spp. Draining tracts or

W1derlying skin disease but be complicated
abscesses in the skin of sheep or goats may
by both predisposing and perpetuating
be caused by Co1ynebacterium pseuclotu
factors. F\uther, successful treatment of skin
berculosis. Fusobacterium spp and
disease may require longterm or lifelong

Bacteroides spp ar·e the primary invaders in therapy and is frequently a matter of
i.nterdigital necrobacillosis (footrot). The
successful control ratl1er than "cme."

spirochete Borrelia suilla is a secondary
invader of skin lesions caused by sar·coptic

ANTIBACTERIALS
mange or ear biting in swine. Clostridial •
diseases in cattle and erysipelas in swine are

Most canine skin infections are caused
disorders tl1at involve tl1e integwnentary
by coagulase-positive Staphylococcus
system and cause serious economic losses.

pseudintermedius (fo1merly S interme

Metllicillin resistance ( a mar·ker for resis
dius ), which commonly produce
tance to all 13-lactam antibiotics, including

13-lactarnase. Other staphylococcal species
penicillins, cephalosporins, and car·bapenhave been described, including S aureus, ems) is the most in1portant mecharlism of

S schleiferi, and S hyicus. There does not resistance in staphylococci; tl1e rep01ted
appear to be any difference in the disease
incidence of antimicrobial-resistant bacteria
patterns or clinical signs produced by the
has increased mar·kedly over the past 5-10 yr,
different species, although species-specific
although tllis varies depending on the
differences in antimicrobial resistance
geographic location. For example, a 2010
profiles have been seen in North America,

Japanese study reported the incidence of
with S pseudinterrnedius and S aureus
metllicillin-resistar1t S pseudintennedius
showing more resistance than S schleiferi

(MRSP) at 66. 7%. Many metllicillin-resistant
coagulans. Species identification requires
isolates are also multidmg resistant
molecular techniques such as PCR detection

( resistant to more tl1an three classes of
of species-specific them10nuclease genes
antibiotics), which makes clinical manage

(nuc) or 168 rDNA sequencing, because
ment, particular·ly empirical therapy, more
phenotypic differentiation is unreliable.

difficult. Before the increase in incidence of

Occasionally, Proteus spp, Pseudomonas
resistant strains, if the exudative cytology
spp, and Esclunichia coli are secondary
showed the presence of an active infection
invaders of the dermis. Pasteurella
with coccoid organisms, empirical antibiotic
mullocida and 13-hemolytic streptococci
treatment could begin. The rise of anti.micro-

2572

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM
bial resistance has led to the development of

Empi.J.ic therapy may still be appropriate in
guidelines by several organizations (British
the case of first-ti.J.ne or previously untreated

Veterinary Association [www.bva.co.uk],
superficial infections in which positive

Federation of European Companion Animal
exudative cytology (witl1 coccoid bacteria)

Veterinary Associations [www.fecava.org],
has been established. The following may be

VetBooks.ir

International Society for Companion Anin1al
used as first-line antimicrobials: cephalexin,

Infectious Disease [www.iscaid.org]) on the
cephadroxil, amoxicillin-clavulanate,
appropriate use of antibiotics for case
trin1ethop1im-sulfas, li.ncosan1ides, and
management. (See TABLE 10.)

cefovecin (if owner compliance is consid-
it-h•ii·I DOSAGES OF ANTISTAPHYLOCOCCAL ANTIBIOTICS

Drug

Dosage

CEPHALOSPORINS

Cephalexin

20-30 mg/kg, bid, PO

Cephadrox.il

Dogs: 20 mg/kg, bid, PO

Cats: 20 mg/kg/day, PO

Cefaclor

10-25 mg/kg, bid, PO

Cefovecin

8 mg/kg, SC, every 14 days

Cefpodoxime

5-10 mg/kg/day, PO

PENICILLINS

Amoxicillin-clavulanate

13.75 mg/kg, bid, PO

Oxacilli.J.1

22 mg/kg, tid, PO

FLUOROQUINOLONES

Enrofloxacin

5 mg/kg/day, PO

Marbofloxacin

2 mg/kg/day, PO

Orbifloxacin

2.5 mg/kg/day, PO

Difloxac.in

5 mg/kg/day, PO

Pradofloxacin

3 mg/kg/day, PO

SULFONAMIDES

Trimethoprim-sulfadiazine

15-30 mg/kg, bid, PO

Tri.J.nethopri.J.n-sulfamethoxazole 15-30 mg/kg, bid, PO

MACRO LI DES

Erytlu·omycin

15-30 mg/kg, tid, PO

Clindamycin

Dogs: 10-20 mg/kg, bid, PO

Cats: 12.5-25 mg/kg, bid, PO

Azithromycin

10 mg/kg/day, PO

OTHERS

Lincomycin

10-20 mg/kg, bid, PO

Chlora.mphenicol

50 mg/kg, tid, PO

Rifa.mpin

5-10 mg/kg, once or twice daily, PO

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2573
erect an issue). Culture and sensitivity testing

Rifampin may cause hepatic enzyme
should be performed in any of the following
induction and increase in hepatic enzyme
circwnstances: infections that have not
activity, particularly alkaline phosphatase.

responded to appropriate empiric therapy,

Some dogs may develop a fatal hepatotoxpresence of deep infections (nodules, ici.ty. Other adverse effects include GI

VetBooks.ir
hemorrhagic bullae, draining tracts),
upset, hemolytic anemia, thrombocytoperod-shaped or unusual organisms on nia, and orange discoloration of body
cytology, recurrent or relapsing infection,
f1uids. Liver enzymes should be monitored
history of previous courses (particularly
at least every 2 wk for the duration of
multiple) of antibiotic therapy, nonhealing
therapy.

wounds, recent potential exposme of owner
or affected animal to methicillin-resistant

ANTIFUNGALS
staphylococci in health care environments,
or history of prior MRSP infections. Second

The antifungal drugs used most commonly
line antimicrobials should be used only if
to treat integun1entary diseases are listed in
there is no sensitivity to first-line antimicrobi

TABLE 11.

als on cultme and sensitivity testing. These
antibiotics are not appropriate for empiric

Griseofulvin: Griseofulvin has a ve1y low
therapy and include cefovecin ( except when
solubility in water; GI absorption is variable
owner compliance is an issue), cefpodoxin1e,
and incomplete with tl1e n1icronized fom1.

and fluoroquinolones ( difloxaci.n, enrofloxa

Absorption may be enhanced by administracin, marbofloxacin, orbifloxacin, pradofloxation with a fat-containing meal or by formucin). Third-line antimicrobials should be used lations using polyethylene glycol or very only in cases in which there is evidence of
small particles (micronization). The ultrarnisensitivity, no sensitivity to first or secondcronized fonn is nearly lOOOA, absorbed.

line antin1icrobials, and topical antiseptics

Griseofulvin is concentrated in skin (the
are not feasible or effective. Tl1ird-line
highest concentration is in the stratw11
antin1icrobials include an1inoglycosides,
comew11), hair, nails, fat, skeletal muscle, at1d
azitlu·omycin, chloramphenicol, claritlu·omyliver at1d can be found in the stratwn comewn cin, imipenem, rifarnpin, and ticarcillin. Witl1
within 4 lu· of dosing. It is also secreted in
the increase in metl1icillin- ar1d multidrugsweat and is deposited in keratinocytes and resistar1t strains of staphylococci., the use of
remains lightly bound dwing differentiation,
topical antiseptics has increased. They can
so new skin growth is the first to be clear
be used as sole tl1erapy for nilld to moderate
of infection. It is effective only against
superficial infections ar1d can reduce the
dennatophytes, eg, Microspoium, 1'richo
treatment dmation in more severe infections. phyton, and Epidennophyton.

111ere is little evidence that even multidrug

In dogs, adverse effects ( eg, vomiting,
resistant staphylococci. are not susceptible to
diarrhea) and increased liver enzymes
topical ar1tiseptics.

predominate. In cats, ar1emia, leukopenia,

Dmation of therapy varies with the type
vomiting, diarrhea, depression, pruritus,
of infection present but should continue
fever, at1d ataxia have been described. Bone
until the clinical lesions have resolved and
marrow suppression ( usually manifest as
cytology is normal. In general, superficial
neutropenia) may occur idiosyncratically,
infections should be treated for 7 days
especially in feline inununodeficiency virus
beyond smface healing (commonly 3-4 wk);

(FIV)-positive cats and in kittens. FTV status
deep infections should be treated 7-21 days
should be determined before use, and
beyond resolution, which may require
griseofulvin avoided in kittens <8 wk old.

treatment dmations of 8---12 wk if continued

The reactions may be more conm1on ar1d
improvement is seen. Clinical resolution of
severe in Persian, Himalayan, Siamese, and

MRSP infections may take longer thar1

Abyssinian cats. Teratogenicity is a major
metl1icillin-susceptible S pseudinterme
problem in all species.

dius infections, but this is most likely due to Hemograrns should be collected every
infection chronicity and secondary char1ges

2 wk and close observation maintained.

of the skin rather than to any inherent

Leukopenia is more common in FTV-positive
virulence of the bacterial strain.

cats, so screening should be done before

The potential for serious adverse effects
initiating treatment.

when using either chloramphenicol or
rifampin should be understood. Chloram

Ketoconazole: Ketoconazole is a
phenicol can cause a dose-dependent bone
synthetic, broad-spectnm1 antifungal drug
marrow suppression ( cats more sensitive),
belonging to tl1e imidazole fan1ily. It is a
although GI irritation, inappetence, and
potent inhibitor of ergosterol (a main
weight loss are the most common.

membrane lipid of flmgi) synthesis. Fungal

2574

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM
itMIIII DOSAGES OF ANTIFUNGAL MEDICATIONS

Drug

Dosage

Griseofulvin

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Microsize

25---60 mg/kg, PO, bid

Ultramicrosize 2.5---15 mg/kg, PO, bid

Ketoconazole

10 mg/kg/day, PO; 20 mg/kg, PO, every 48 hr

Itraconazole

5---10 mg/kg/day, PO

Fluconazole

10-20 mg/kg, PO, bid

Amphotericin B

Dogs: 0.25---0. 75 mg/kg, IV, 3 times/wk to total cumulative dose of 4--8 mg/kg or until azotemia develops

Cats: 0.1-0.25 mg/kg, IV, 3 times/wk to cumulative dose of 4--6 mg/kg Flucytosine

25---50 mg/kg, PO, tid-qid

Terbinafine

10-30 mg/kg/day, PO

Potassium iodine Dogs: 40 mg/kg, PO, once or twice daily with food Cats: 20 mg/kg, PO, once or twice daily with food
cells are thus unable to maintain the
after 10 days, the dosage may be increased
integrity of plasma membranes, which leads
to 15 mg/kg/day.

to cell wall ruptw-e. Because the therapeutic

Ketoconazole requires an acidic environeffect of ketoconazole is delayed, amphoment for optimal absorption, so H2-blockers tericin B is often used in combination for
or antacids should not be administered
cases of serious systemic disease.

concUITently.

For dermatophytosis, ketoconazole

In dogs, the most common adverse
is active against Triclwphyton ve,rucosum,
effects are inappetence, vomiting, pruritus,

Tequinum, Tmenlagrophytes,Micro
alopecia, and reversible lightening of the
spornm canis, and M nanum. lt is also hair coat. Anorexia may be reduced by
active against the yeast Malassezia
administe1ing the dose with food. Cats
pachydermatis and Cryplococcus neof01°
appear to be more sensitive to ketocona
mans and is normally used at 10 mg/kg/day,
zole. Clinical signs of toxicity include

PO. For candidiasis, the dosage is 10 mg/kg/
anorexia, fever, depression, dian·hea, and
day, PO, for 6-8 wk. In some chronic cases, a
increased liver enzymes. Dosages> 10
maintenance dosage of 2.5---5 mg/kg can be
mg/kg/day are rarely given. Hepatotoxicity
used. Coccidioidomycosis responds better

( cholangiohepatitis and increased liver
to ketoconazole than to a.mphotericin B in
enzyn1es) has also been repmted.

many instances, with a minin1al treatment
period of 12 mo in animals with disseminated ltraconazole: The primary antifungal disease. Blastomycosis, histoplasmosis,
mechanism of action of itraconazole seems to
and cryptococcosis may be treated with a
be the same as that of ketoconazole; however,
combination of ketoconazole and an1phoit has a greater potency, decreased toxicity, te1icin B (the combination is not more
and a wider spectrum of activity. Even at high
effective than the latter alone, but there are
dosages, it does not alter hormone levels in
fewer nephrotoxic signs). For blastomycorats, dogs, or people. Itraconazole should be sis, a 4--6 mg/kg total dose of amphotericin B
administered witll food; the concurrent
is combined with ketoconazole (20 mg/kg/day administration of antacicls, H2-blockers, and in dogs, and 10 mg/kg/day in cats). For
cholinergics is contrainclicated.

histoplasmosis, amphotericin B (2-4 mg/kg
ltraconazole is effective against
total dose) is combined with ketoconazole
dermatophytes, Candida, Cryptococcus,

(20 mg/kg/day in dogs, and 10 mg/kg/day in

HistoJ)lasma, Blastomyces, and SJ)oro
cats).

thrix spp, and the protozoans Leishman·ia Ketoconazole inhibits cortisol synthesis
and 1'1-ypanosoma. For dermatophytosis
and has been used to treat canine hype1c
in dogs, the dosage is 5 mg/kg/day.

adrenocorticism at 10 mg/kg/day. lf the

For systemic mycoses, the dosage is
cortisol level is still above resting levels

5-10 mg/kg/day, but the addition of

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2575
arnphotericin should be considered in
by electrolytes or urinalysis at least weekly
rapidly progressing infections. For

( urinalysis detects toxicity earlier tha.11
treatment of dem1atophytosis and
biochemistry); BUN, creati.June, PCV, a.i1d
systemic mycoses in cats, the dosage
total plasma proteins should be checked
is 10 mg/kg/day.

before the administration of each dose.

A severe, dose-related ulcerative

Monthly maintena.11ce therapy is recom

VetBooks.ir
dem1atitis ( due to vasculitis) has been seen
mended to avoid relapses.

in 5%-lOOA, of dogs given itraconazole in doses

The major adverse effect seen with a.inphoof 10 mg/kg. lf the condition is identified tericin B is nephrotoxicity-most dogs incur
early, drug withdrawal leads to resolution;
some kidney da.i11age. The damage is not
if not recognized early, severe, extensive
correlated with either total dose or dm-ation
necrosis and sloughing can develop.

of therapy. The causes of toxicity include
vasoconstiiction, in1paired acid excretion,

Fluconazole: F1uconazole is a fungistatic
a.11d direct tubular irtjury. Cats are more
triazole compmmd with a mode of action
sensitive, so lower doses are recommended.

similar to that of ketoconazole. However,

Adverse effects such as fever, nausea, a.11d
it does not affect man1malian honnone
vomiting a.i·e less severe if diphenhydra.I11lne
synthesis. Because of its small molecular size (0.5 mg/kg, IV), aspirin (10 mg/kg, PO), or and low lipophilicity, it may be more useful in hydrocortisone sodium succinate (0.5 mg/kg, treating CNS mycoses.

IV) is given before adnunisti-ation of

Fluconazole is effective against
a.111photericin B.

superficial dermatophytes and Candida,

C1yptococcus, His toplasma, and Blasto

Flucytosine: Tlus fluorinated pyrin1idine
myces spp. The dosage is 2.5--10 mg/kg/day
was developed as a.11 antineoplastic agent.

in dogs. Cats with cryptococcosis can be

It interferes with RNA metabolism a.11d
given 2.5--10 mg/kg, bid.

protein synthesis in fungal cells. It is well

F1uconazole has had limited use in small
absorbed a.i1d enters the CNS in high conanimals. In people, it can cause occasional centrations. Most of the drug is excreted

GI adverse effects ( eg, vomiting, dia.iThea,
uncha.11ged in the wine.

anorexia, nausea).

Flucytosine is effective against Clyplococcus neoformans, Candida, a.11d other Amphotericin B: Arnphotericin is a
yeasts but has little or no effect on other
lipophilic polyene from Streptomyces
fungi. Resista.11ce develops frequently; thus,
nodosus that binds to sterols ( especially
it is given in combination witl1 arnphotericin
ergosterol), causing increased pem1eability

B. It is used almost exclusively for
a.11d leakage of nutrients a.11d electrolytes. It is treatment of cryptococcosis. The dosage poorly absorbed from the GI tract a.11d must
in dogs a.11d cats is 25--50 mg/kg, tid-qid.

be given parenterally. IV administration gives

GI tract disturba.11ces (vomiting, dia.iTbea,
good penetration, except into muscle, bone,
a.11orexia), bone marrow suppression
eye, or synovial fluid.

(anemia, leukopenia, thrombocytopenia),

Arnphotericin B is used in progressive
a.11d cuta.I1eous eruption ( depigmentation,
or disseminated deep mycosis. It may be
ulceration, exudation, a.11d crust formation)

combined with flucytosine or minocycline
are the most common adverse effects.

for treatment of Candida a.11d C1yptococcus. Rifa.inpin potentiates the effect of Terbinafine: Terbinafi:ne is a.11 allyla.111ine a.111photericin onAspergill·us (which is
compound that inte1feres with fungal sterol
usually resista.I1t against a.inphotericin
biosynthesis at a.11 early stage, causing
alone), Candida, a.11d Histoplasma.

deficiency of ergosterol, intracellular

Amphotericin B is insoluble in water a.11d is
acetmmlation of squalene, a.11d fungal cell
prepared as a.11 IV solution by fomung a colloideath. It achieves high concentrations in dal dispersion with sodium deoxycholate.

hair follicles, hair, sebwn-rich skin, nail

Because it is inactivated by sunlight, it should
plates, a.11d nails. In people, levels exceeding
be stored in the dark Dilution with la.i·ge
the minimwn inhibitory concentration may
volumes of 5% glucose (10 mg a.inphote1icin
be found for up to 3 wk after treatment has

B/100 rnLfluid) is recommended to reduce
ended. There are a.11ecdotal reports of its
nephrotoxicity. The dilution should be given
use against Trichophyton, Microsporum,
over 2-6 hr. lf a bolus is given in 10-60 mL of
a.11d Epidermophyton, as well as Malasse
dextrose (via a butterfly catheter), supple
zia dermatitis. The dosage in cats is 10-30
mental fluid diuresis is helpful. Amphotericin
mg/kg/day. In people, rare cases of hepatic

B is given at 0.15--0.5 mg/kg every 48 hr until a
toxicity are seen, along with GI tract signs
total cumulative dose of 4-12 mg/kg is

( eg, nausea, vomiting, dian·hea) a.i1d skin
reached. Renal toxic effects a.i·e monitored
signs (eg, mticaria, itch, erythema).

2576

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

Systemic Iodine: The mechanism of

8 mg/kg, SC, leads to listlessness and
action of systemic iodine is unknown; no
ataxia; 30 mg/kg induces ataxia in swine.

fungicidal effects are seen in vitro. It is used

Some dog breeds (Collies, Shetland
in small animals for sporotrichosis; in cattle

Sheepdogs, Old English Sheepdogs,
for actinomycosis and actinobacillosis; and

Australiai1 Collies, and their crosses) have
in horses for mycetomas, zygomycosis, and
an abnmmality in the blood-brain baiTier

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Sporothrix schenckii. Dogs are treated with associated with a mutation of the multiple potassiwn iodide 40 mg/kg, PO, bid; cats
drng resistance gene MDRl, which allows
with potassiwn iodide 20 mg/kg, PO, once
increased ivermectin into the CNS and
to twice daily; cattle with sodiw11 iodide
results in toxicity. Dogs that are homozy60 mg/kg, IV, weekly; and horses (sporotrigous for the mutation produce a severely chosis) with sodiw11 iodide, 40 mg/kg/day,
truncated P-glycoprotein ( < 10% of the

IV, for 2-5 days, followed by potassiwn
normal ru11ino acid sequence) and will
iodide, 2 mg/kg/day, PO, for 60 days.

develop ivem1ectin toxicity at a11y of the

In small animals, vomiting, dianhea,
dosages used to treat demodicosis. The
depression, and inappetence (especially
critical point seems to be 120-150 mcglkg,
in cats) may develop. Ocular and nasal
at which trru1sient, nonfatal clinical signs
discharge, scaling, and a dry hair coat also

(myd1iasis, ataxia, tremors) are seen. At
may be seen in dogs. In large animals,
higher dosages, collapse, coma, and
seromucoid discharge, lacrimation, cough,
respiratory collapse may develop. Similar
variable appetite, joint pain, and sebon-hea
idiosyncratic reactions may develop in a11y
sicca with partial alopecia may develop.

breed, so a gradually increasing dose ( daily

Systemic iodine may also cause abortion
progression of 50, 100, 150, 200, tl1en 300
and should not be used in pregnant or lactatmcglkg) should be given to identify ing aninials.

susceptible individuals. Administration
should be stopped if any adverse effects are
seen. One cat treated with 4 mg of the oral
paste ( -70 mcglkg) showed ataxia,

ANTI PARASITICS
blindness, tremors, ru1d mydriasis, with
retinal atrophy in one eye 10 lu· later.

lvermectin: Ivennectin is an avem1ectin
and a fe1mentation product of Streplomyces

Milbemycin: Milbemycin is derived from
aveimitilis (see also MACllOCYCLlC LACI-ONES, fe1111entation products of Streptomyces
p 264 7). It acts as a GABA agonist, causing
hygroscopicus illld, like ive1mectin, acts as paralysis in susceptible aithropocls a11d
a GABA agonist but witl1 a wider spectrunl
nematodes. It is used in small animals for
of activity against intestinal pru·asites. lt has
treatment of Sai-coptes scabiei, Otodecles
been used extra-label in dogs to treat nasal

ClJiwtis, Cheyletiella blakei, C yasguri,
mites, scabies, and generalized demodicoa11d Demodex ca1iis; in cattle for psoroptic sis. No adverse effects have been seen in
ma11ge, lice, a11d Hypodei·ma laivae; in horses ivermectin-sensitive breeds. The dosage in for equine filruial dem1atitis from Onchocei"ca dogs is 1-2 mg/kg every 7 days for 3-5
cernicalis; a11d in swine for Sai·coples scabiei. treatments for nasal mites a11d scabies a11d In small rulimals, all use for Skin condi1-2 mg/kg/day for Demodex.

tions is extra-label in the USA For De,nodex,
the dosage is 0.3-0.6 mg/kg/day, PO, until

Moxidectin: Moxidectin belongs to
two negative skin scrapings 1 mo apait. For
the milbemycin class of compow1ds. It is

Sarcoptes, Otodecles, ru1d Cheyletie/J,a, the registered for heruuvonn control (Dirofi
dosage is 0.3 mg/kg, PO, repeated in 2 wk.

/ai"ia imm'ilis) but has also been used In cattle, 0.2 mg/kg is given as a single SC
extra-label for treatment of Otodectes and
ir\jection for Psoroples a11d lice. In horses, demodicosis in dogs. In cattle, it is used to

0.2 mg/kg, PO, kills microfiJrufae but not
treat lice (Linognalhus viluli, Solenopoles
adult Onchoce,-ca cernicalis, so relapse may capilla tus, Bovicola bovis ), mites
be noted within 2 mo of treatment. In swine,

(Psoroptes, Chorioptes bovis), ticks
the dosage is 0.3 mg/kg, SC, repeated in 2 wk,

(Boophilus microplus ), illld fly warbles
or 0.1--0.2 mg/kg in feed for7 days.

fill cl grubs (Hypodei·ma bovis, Hypoderma.

In mru11mals, GABA is fow1d only in
lineatuin ). In sheep, it is used for Psorobia the CNS a11d does not readily cross the
ovis infestation. The dosage is 0.2-0.4
blood-brain bruTier. At least 10 times the
mg/kg/day, PO, in dogs a!ld 0.2 mg/kg in
nom1al dose of ivermectin is needed for
cattle a11d sheep.

toxic reactions. Ataxia, depression, and
visual impaim1ent develop in horses given

Selamectin: This semisynthetic macro2 mg/kg, PO. In cattle, 4 mg/kg by drench or cyclic lactone is applied topically but acts

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2577
systemically. It is effective against

Sodium Stibogluonate: Sodium

Ctenocephalides spp (both adults and
stiboglucoante is used for treatment of
larvae), Sarcoptes scabiei, Otodectes
cutaneous leishmaniasis, either as a sole
cynotis, and Dermacenlorvariabilis.

therapy or in combination with allopuri

The dosage in dogs and cats is 6 mg/kg,
nol, pai·omomycin, or pentamidine. The
applied topically.

exact mode of action is unknown, but it is

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believed to interfere with energy metabo

Lufenuron: Lufenuron is an insect growth
lism in Leishmania an1astigotes. Dosage in
regulator that inhibits the synthesis of chitin, dogs is 30-50 mg/kg/clay, IV or SC, for 3-4
a c1itical component of insect exoskeletons.

wk. If adverse effects occur (musculoskel

It is taken up by adult fleas while feeding.

etal pain, increase in liver transai11inases,

While it has no effect on adult fleas, it
pancreatitis, myocai·dial i.ttjury, hemolytic
prevents development of the intem1ediate
anemia, leukopenia, renal dysfunction), the
stages of the flea life cycle (ie, eggs, larvae,
dose may be administered every other day
pupae). It is effective against Ctenocephal
for longer periods. Note that IV adminis
ides spp in dogs and cats at a dosage of 10
tration should be over 5 min to minimize
mg/kg, PO, once a month. Chit.in is also a
carcliotoxicity.

component in the fungal cell wall of
clennatophytes. An initial study showed
efficacy of lufenuron in treating small aninlal

ANTIHISTAMINES
dern1atophytosis; however, additional
studies have failed to show efficacy.

Antihistainines block either H, or H2
receptors. H, receptors ai·e responsible for

Nitenpyram: Nitenpyran1 inhibits the
pllllitus, increased vasculai· pem1eabi.lity,
nicotinic acetylcholine receptor. It is used to release of i.nflanirnatory mediators, ai1d treat Ctenocephalicles spp in dogs and cats attraction of i.nflaim11atory ceUs. H, blockers
at a dosage of l mg/kg, PO. Nitenpyram has
act by competing witJ1 histamine for 1 -I,-recepa short half-life and kills fleas on the animal tor sites on effector cells (they do not block
within 30 min of administration. It is toxic to release of histainine but can antagonize its fleas for only 24-48 hr and is normally used
effects). 111ey also have anticholinergic,
in combination with an insect growth
sedative, ai1d local anesthetic effects and vary
regulator to provide continuous flea control. greatly in their potency, dosage, incidence of adverse effects, and cost.

Spinosad: Spinosad stimulates the nico

Second-generation H, blockers ( eg,
tinic acetycholine receptor, which causes
te1fenadine, ceti.razine, loratadine,
activation of motor neurons and results
astemazole) are less likely to cross the
in involuntary muscle contractions and
blood-brain barrier, or they have a low
tremors, leading to paralysis and death of
affinity for brain compared with peripheral
the insect. It is used to treat Ctenophalides

I -I, receptors. They have not proved useful
spp in dogs at a dosage of 31-70 mg/kg
to date in controlling pllllitus in small monthly and in cats at a dosage of 50-90
animals. Responses to antihistamines vary
mg/kg monthly. It may trigger severe signs
considerably, and several trials may be
of ivermectin toxicity if administered
necessary to find one effective for an aninlal
concurrently with extra-label, high-dose

( see TABLE 12). Anti.his ta.in in es may act ivermectin.

synergistically with NSAIDs, glucocorticoids, or fatty acid supplements and may allow dosages of these agents to be reduced
lndoxacarb: Indoxaca.rb blocks sodium
in some cases.

channels in the insect to cause paralysis First-generation antihistainines may
and death. It is effective against Ctenophal
cause drowsiness or GI signs ( eg, vomiting,
icles spp, both adults and laivae, and is apdiarrhea). Overdoses may cause CNS
plied as a spot-on topically, once a month.

hyperexcitability and may be fatal.

Anticholinergic properties lead to

Cythioate: Cythioate is an organophoshypertension (and thus contraindicated in
phate that kills via anticholinesterase
cardiac patients), dry mouth, blun·ecl vision
activity. It is indicated for Ctenocephalides

( contraindicated in glaucoma), and urinary
spp infestations at a dosage of 3 mg/kg, PO,
retention. Hydroxyzine is teratogenic. They
twice weekly (dogs) or 1.5 mg/kg, PO, twice
may also stimulate appetite (paiticularly
weekly (cats). Although effective blood
cyproheptadine).

levels are maintained for <12 hr, senun

Second-generation antiJ1istainines are
cholinesterase activity may be decreased
cardiotoxic at high doses. High closes of
for > 1 mo after closing.

terfenadine and astemizole lead to

2578

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

14N•iti ANTIHISTAMINE DOSAGES

Drug

Dosage

Diphenhydramine

2-4 mg/kg, bid-tid

Hydroxyzine

0.5-2 mg/kg, tid-qid

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Clorpheniramine

Cats: 2-4 mg, bid

Dogs <20 kg: 4 mg, tid

Dogs >20 kg: 8 mg, tid; 0.25-0.5 mg/kg, tid

Cyproheptadine

0.25-0.5 mg/kg, tid; 1.1 mg/kg, bid

Terfenadine

5 mg/kg, bid

Clemastine

Cats: 0.05 mg/kg, bid

Dogs: 0.1 mg/kg, bid

Trimeprazine

1 mg/kg, bid

Cetilizine

Dogs: 1 mg/kg or 10-20 mg per dog, once or twice daily Cats: 1 mg/kg or 5 mg per cat, once or twice daily

Fexofenadine

Dogs: 2-5 mg/kg, once or twice daily

Cats: 10-15 mg per cat, once or twice daily
prolonged QT intervals and arrhythmias ( eg, another, and increasing the close to several ventricular tachycardia, cardiac arrest).

times the label recommendation can help

Cardiotoxicity has been repo1ted only as a
in some cases. Approximately 20% of dogs
result of overdose in animals with impaired
and 50% of cats with allergic pruritus will
hepatic metabolism.

show some improvement. There are few
adverse effects; however, pancreatitis has

ESSENTIAL FATTY ACIDS
rarely been reported. Large closes may also
cause weight gain or diarrhea.

Fatty acids are essential components
of cell membranes ani:I are an integral

HORMONAL THERAPY
component of the intercellular barrier in
the stratum corneum. Essential fatty acids

Glucocorticoids: Glucoco1ticoids have
cannot be synthesized and therefore must
profound effects on nearly all cell types and
be supplied in the diet. The essential fatty
organ systems, particularly inlmunologic
acids most important for homeostasis of
and inflanunatory activity. They may be
the skin in dogs and cats are linoleic acid
used il1 either an anti-inflanunatory or
and linolenic acid. The anti-inflammatory
irnmunosuppressive capacity, depending on
properties of fatty acids are thought to be
the dosage selected. Glucocorticoids are
due to competitive inhibition of arachiused for hypersensitivity clerniatoses, donic acid metabolism, leading to a
contact derniatitis, inunune-mediated
reduction in inflan1matory leukotriene and diseases (eg, pemphigus, pemphigoid, lupus prostaglandin synthesis and activity, and
erythematosus), and neoplasia (eg, mast
to the formation of metabolic byproducts
cell tumor, lymphoma). Glucocorticoids
of normal fatty acid metabolism that have
may be classified according to their·
direct anti-in£Jan1matory properties.

dmation of effect and relative potency (see

Essential fatty acids are indicated for

TABLE 13). They may be administered PO, IV,
pruritic inflammatory diseases ( eg,

IM, or SC.

allergies, feline eosinophilic granuloma),

The a.nti-inflanunatory dosage of
crusting diseases (eg, discoicl lupus
prednisolone is 0.5-1 mg/kg/day in dogs
erythematosus), and onychodystrophy.

(severe cases may require 2 mg/kg/day) and

Many commercial products are available

1-2 mg/kg/day in cats. This dosage is given
and may be used at the manufacturers'

for an induction period of 5-7 clays and then
recommended close. Lack of response to
reduced to the lowest possible mai.ntenance
one product does not preclude response to dosage (ideally 0.25 mg/kg, every 48--72 lu·

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2579
itM•iFI GLUCOCORTICOIDS

Drug

Relative Potency

Duration of Effect

Hydrocortisone (cortisol)

<12hr

Prednisolone

4

12-36hr

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Prednisone

4

12-36hr

Methylprednisolone

5

12-36hr

Triamcinolone

5

12-36 hr

Flumethasone

15-30

36--48 hr

Betamethasone

25

>48hr

Dexarnethasone

30

>48hr
or lower in dogs). Maintenance doses must
winary tract infections, pyodem1a, and
be given �48 hr apart to minimize adrenal
pulmonary infections. Urinary tract
suppression and chronic adverse effects.

infections may develop in many animals on

The immunosuppressive dosage of predlongtem1 glucocorticoid therapy (68"/o in nisolone is 2.2 mg/kg/day in dogs (up to
one study), and these atllllals may show no

6.6 mg/kg/day may be required in severe
clinical signs of the infection. Urine should
disease) and 4.4 mg/kg/day in cats.

be cultured for bacterial growth every 3-6

The induction period is generally longer
mo in all animals on longtenn therapy.

(10-20 days) than with anti-inflammatory

Progressive hepatocellular swelling due
dosing but is then gradually tapered in a
to glycogen accwnulation may develop
stepwise fashion to an alternate-day dosing
during glucoco1ticoid therapy. Alkaline
regimen once there is evidence of disease
phosphatase (ALP), ALT, at1d )'-glutat11yl
remission. Treatment should never be
transferase all show progressive increases.

stopped abruptly, because of the risk of
ln dogs, the initial ALP increase is due to
inducing signs of hypoadrenocorticisrn. lf
hepatic ALP but later is due to a cortisone
relapse occurs druing the tapering process,
isoenzyme.

the dose is increased to at least one step

Most injectable fonns are labeled for IM
above the point at which the relapse
use; however, they are commonly given SC.

occurred and tapered again if possible. ln

Local areas of alopecia, pigmentation, and
many cases, therapy may be withdrawn
epidermal and dern1al atrophy may be seen
entirely without relapse, whereas others
with SC ir\jection.

require lifelong treatment.

Administration PO is preferred, because

Thyroid Hormone: Thyroid hormones
dosing can be more closely regulated and
ai·e indicated as replacement therapy for
physiologic processes are disrupted less
primaiy, secondary, and tertiary hypothythan with repositol forms. ln some cases, roidism. Most cases of canine hypothyroiddifficulties with animal handling or owner ism are primary in nature and are due to
adherence may require injectable therapy.

autoirrunune destruction of the thyroid

This is nom1ally satisfactory for acute,
gland. Drug-induced low hormone levels
short-tem1 disease that does not require
or "euthyroid sick syndrome" are not
repeated administration ( eg, a single
indications for supplementation with
injection of methylprednisolone acetate
thyroid hormones.

alters adrenocortical function in dogs for

Synthetic levothyroxine (T4) is the drug
up to lOwk).

of choice for canine hypothyroidism. Most

Adverse effects include polyuria,
dogs respond clinically to a dosage of
polydipsia, polyphagia, weight gain,

0.02 mg/kg, bid. Insufficient serum levels
increased susceptibility to infection, GI
after 4-6 wk of treatment or lack of a
ulceration, pancreatitis, osteoporosis,
clinical response after 12 wk are indications
hyperglycemia, steroid myopathy, and
to increase the dose. Synthetic liothyrnnine
calcinosis cutis. The extent and severity of

(T3) may be used for those rare ailin1als that
adverse effects are related to the dose,
cat1.11ot convert T 4 to T 3• It should not be
duration, and type of glucocorticoid used,
used for routine treatment of hypothyroidalong with individual animal sensitivity. The ism, because it bypasses the nonnal cellular
most commonly encountered infections are
regulatory pathways at1d has a short

2580

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM
half-life. Dosage is 4-6 mcg/kg, PO, bid-tid.

reticula.ris and paitial or complete necrosis

Crude preparations from thyroid tissue and
of the zona glomerulosa. It is used to treat
synthetic thyroid hom10ne combinations
pituitary-dependent hyperadrenocortithat min1ic the T,:T,1 ratio in people should cism. Before starting therapy, food intake
not be used in animals.

(ainount), ti.me taken to eat, and the 24-hr

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Signs of thyrotoxicosis in cats and dogs
water intake should be recorded to
are rare. They include polymia, polydipsia,
detennine a baseline. Once this has been
nervousness, aggressiveness, p,mting,
established, a loading close is administered
diarrhea, tachycardia, pyrexia, and pnuitus.

daily (25 mg/kg, bid) until the animal

Complications in dogs are usually related to
becomes lethai·gic, water intake drops,
concmrent cardiac or adrenal insufficiencies. appetite is reduced, or the animal has other In anin1als with a marginal cardiac reserve, T, GI adverse effects (vomiting, diarrhea) or meclication should be initiated at one-fourth
after 5 clays of administration. An ACTH
the recommended dosage and gradually
stimulation test should be performed to
increased to full dosage over a 1-mo period.

confinn whether adequate suppression
of the adrenals has been achieved.

Trilostane: Trilostane is a hormonally

Most clogs respond to o,p'DDD therapy at
inactive, steroid competitive inhibitor of
the initial loading dose within 5-10 days, and
the adrenal enzyn1e 3[3-hyclroxysteroicl
the decision to change to maintenance
dehydrogenase. It is used in treatment of
therapy should be based on clinical signs
pituitary-dependent hyperadrenoco1ticism.

(reduced appetite and water intake) and

It inhibits the production of progesterone

ACTH stimulation test results. Dogs with a
and 17-hydruxyprogestrone and their end
post-ACTH plasma cortisol concentration
products, including adrenal, gonadal, and

<25 nmoVL should receive no medication
placental hom10nes. However, the inhibition for 2 wk ai1d should then be treated with of adrenal steroiclogenesis occms at lower

25 mg/kg/wk divided into 2 or 3 doses. Dogs
doses than those required to inhibit steroid
with a post-ACTH plasma cortisol concenhom1one synthesis in other organs. The tration of 25-125 nmoVL should receive
recommended starting dosage for clogs

25 mg/kg/wk in 2 or 3 doses, and dogs with
is 2-10 mg/kg/clay, PO, but this may be
a post-ACTH cortisol concentration> 125
increased or decreased, based on periodic
nmoVL should receive 50 mg/kg/wk.

adrenoco1ticotropic honnone (ACTH) stin1u

Dming maintenance therapy, an ACTH
lation test results (perfonnecl 3--8 hr after
stimulation test should be pe1fonned after
trilostane administration). If the post-ACTH

1 mo and then every 3-4 mo. If the post-ACTH
plasma cortisol concentration is <20 nmoVL,
plasma cortisol concentration is <25 nmoVL,
trilostane administration should be stopped
the dose of o,p'DDD should be reduced; if
for 48--72 hr and the ACTH stimulation test
the concentration exceeds 125 nmoVL, the
repeated. If the post-ACTH plasma cmtisol
dose should be increased, usually by about
concentration is 20-200 nmoVL, the dosage

20%-25% weekly. Although most dogs are
should not be altered. If the post-ACTH
stable on maintenance therapy, their adrenal
plasma co1tisol concentration is >200
reserve may not be adequate to handle
mnoVL, the dosage should be increased.

major stress (physiologic or psychologic). In

Adverse effects include depression,
these cases, o,p'DDD administration should
ataxia, hypersalivation, vomiting, muscle
be discontinued and replaced with glucocortremors, and skin changes. Sudden death ticoids (0.2 mg/kg/day, PO, tapered) clming
has been reported in a small number of
this period.

cases. Iatrogenic hypoadrenocorticism can

Adverse effects are relatively corrunon,
occm but is generally reversible. Because
paiticularly in cases of o,p'DDD overdose.

of its inhibition of placental hormones,

'111ese include signs of hypoadrenocorticism,
trilostane is contraindicated in pregnant and eg, weakness, ataxia, depression, vomiting, nursing animals and in any animals intended diarrhea, and inappetence. Biochemical and for breeding. Serial biochemical, electrohematologic ai1alysis may be umemai·kable lyte, and hematologic analyses and ACTH
despite systemic illness. Treatment includes
stin1ulation tests should be performed to
lowering the dose or ceasing administration
monitor hepatic and renal function before
of o,p'DDD and supplementing with
treatment and at 10 clays, 4 wk, 12 wk, and
glucocorticoi.ds. Clinical i.mprovement is
every 3-6 mo thereafter.

usually seen within 1--{i hr. Iatrogenic hypoadrenocorticism is the most setious adverse Mitotane (o,p' DDD): o,p'DDD is a
effect and may develop at ally ti.me during
chlorinated hydrocarbon with potent
maintenance treatment. Administration of
aclrenocorticolytic effects causing selective
o,p' DDD should be stopped and approptiate
necrosis of the zona fasciculata and zona
supplementation with glucocorticoids a!ld

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2581
m.ineralocorticoids started. Other rare CNS
empirical. Hypoestrogenism in spayed
adverse effects include ataxia, apparent
female dogs may be treated with diethylstilblindness, circling, and head pressing.

bestrol (0.02 mg/kg/day for 3 wk of every
month until hair regrows or for a maximum

Progesterones: The two most commonly
total dose of 1 mg/dog). After hair regrows,

VetBooks.ir
used forn1s of progesterone are megestrol
the maintenance dosage should be given 1-2
acetate and medroxyprogesterone acetate.

times/wk. An alternative protocol is to treat

Megestrol acetate has a quick onset of action
every other day or twice weekly until a
and potent glucocorticoid and slight rninerresponse is seen. Hair regrowth should be alocorticoid activity, and it may be given PO.

evident in 3-4 wk, with a complete response

Medroxyprogesterone acetate is antiestrowithin 4 mo. Exogenous estrogen can cause genic and has significant glucocorticoid
bone marrow hypoplasia, so a CBC and
activity. Neutered male and female cats with
platelet count should be performed weekly
bilateral alopecia suspected to be caused by
during therapy. Other potential adverse
sex honnone in1balances may respond to
effects include induction of estrus,
treatment. TI1e dosage of megestrol acetate is
hepatotoxicity, nymphomania, abortion,

2.5---5 mg/cat, PO, every 48 lu-, decreasing to
pyometra, or prostatic hyperplasia. Cats are
every 1-2 wk for maintenance. Medroxyprohighly sensitive to estrogens, and a total gesterone acetate is given at a dosage of
dose of 10 mg of diethylstilbestrol can be

50---100 mg/cat, IM, and may be repeated in
lethal.

3---6 mo.

Hypoandrogenism of male dogs may

Progestagens should be avoided
be treated with methyl testosterone, 0.5---1
whenever possible because of adverse
mg/kg, PO, up to a total maximal dose of
effects; severe, prolonged adrenocortical

30 mg every 48 hr. Alternatively, testostersuppression is seen even with low doses.

one proprionate can be given IM once

Diabetes mellitus has been reported in cats
weekly at dosages of 0.5-1 mg/kg, or eve1y
treated with megestrol acetate. Decreased

4-16 wk at 2 mg/kg. Complications include
spermatogenesis, pyometra, increased
aggressive behavior, greasy hair coat,
levels of growth horn10ne with acromegaly,
prostatic hypertrophy, and hepatotoxicity.

mammary gland hyperplasia and tumors,

Liver ftmction should be evaluated before
and behavioral changes may be seen.

treatment and monthly during therapy.

Repositol testosterone, 12 mg/cat, IM,

Growth Hormone: Growth hormone
may be given once for treatment of feline

(somatotropin) is a polypeptide produced
acquired symmetric alopecia or may be
by the anterior pituitary that acts either
combined with a low dose of diethylstilbesdirectly on target tissues or indirectly trol, 0.625 mg/cat, IM, or with a low dose of
tlu-ough insulin-like growth factors
estradiol, 0.5 mg/cat, IM. Hepatobiliary

(somatomedins) produced by the liver
disease has been reported in cats given

(see also TIIE PITUITARY GLAND, p 542). It is testosterone.

necessary for hair growth and for development of elastin fibers in the sk.in. lt is used to Melatonin: Melatonin is produced in the
treat growth hormone-responsive alopecia
pineal gland and is involved in the control
in dogs. Either bovine, porcine, or human
of photoperiod-dependent molting of some
growth honnone (0.1 IU/kg, 3 times/wk for
manunals. Secretion is inversely related to

4-6 wk) is effective. Hair usually regrows in
daylight length and is highest during the

2 -3 mo, and remission may last from 6 mo
winter. Various canine hair-growth
to 3 yr. Growth horn10ne is diabetogenic,
disorders including recurrent flank
and dogs can develop transient or permaalopecia, pattern baldness, and excessive nent diabetes mellitus during therapy.

tricholemmal keratinization have in1proved

Weekly monitoring of blood glucose before
with melatonin supplementation. Recun-ent
and during therapy is recommended.

flank alopecia may be treated with 36-mg SC
implants. Oral melatonin is also available;

Sex Hormones: Several syndromes
an empirical dosage of 3-6 mg/dog, tid-qid,
in dogs and cats have been attributed to
has been used successfully.

imbalances of sex horn10nes; however,
the etiopathogenesis of these disorders is

IMMUNOMODULATORS
generally poorly documented. Hypoestrogenism in spayed female dogs, hypoandrogenism in male dogs, and feline acquired lmmunostimulants
symmetric alopecia may respond to
lmmunostimulation is used to enhance a
sex-horn10ne therapy. Dosages for
deficient immunologic response; however,
sex-horn10ne replacement therapy are
an.in1als that appear to benefit from these

2582

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM
agents are not severely immunosuppressed.

Azathioprine: Azathioprine is converted

The most common use of irnmunostimuto 6--mercaptopu1ine in the liver. It competes lants in dogs is for chronic, recmrent
with pwines in the synthesis of nucleic
staphylococcal pyodem1a. For primary
acids and prevents prolil'eration of rapidly
therapy, irnrnunomodulatory bacterins
dividing cells. It is used for treatment of

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should not be substituted for antibiotics;
pemphigus disorders, bullous pemphigoid
they should be used concurrently with an
and SLE in dogs, ocular inflammation in
appropriate antibiotic until the infection has the uveodem1atologic syndrome, and been resolved. The in1rnunomodulator is
histiocytomas. There is a3- to5-wk lag
then continued and success judged on the
period before its effects are evident, so it
time to and severity of any infection relapse. is often initially combined witl1 glucocorti

They are clearly helpful as adjunct agents or
coids. The dosage is 2.2 mg/kg (50 mg/m2),
for maintenance tl1erapy for some dogs with daily for 2 wk, and then reduced to every 48
recuITent pyodenna but have no benefit in
hr. In dogs, it may be used in combination
other cases.

with metronidazole (10 mg/kg/day) for

Staphage lysate is a preparation of
perianal furunculosis, although smgery may

Staphylococcus aureus and polyvalent
be necessaiy to remove residual scaiTing.

staphylococcus bacteriophage. When given

GI adverse effects (vomiting, diarrhea)

concuITently witl1 antibiotics, staphage
may be avoided by administering witl1 food
lysate (0.5 mL, SC, twice weekly, or 1 mL,
or lowering the dose. Bone matTOW

SC, weekly) has improved the response
suppression may also develop. All tl1ree
of dogs with superficial staphylococcal
cell lines can be affected, but leukopenia
pyodenna compared with antibiotics alone.

is the most common. The CBC should be

The mechanism of action is believed to be
monitored every 2 wk during induction and
stimulation ofT lymphocytes and activation
at least every 4 mo during maintenance
of phagocytic cells. Deficient IgM levelstherapy. Acute pancreatitis and hepatotoxbut not IgA or IgG levels-may be nom1alicity has been reported in dogs. Azathioized with treatment.

prine is contraindicated in cats because of

S aitreus bacterin-toxoid, used for
rapid, lethal bone maJTow suppression.

prevention of staphylococcal mastitis in
cattle, has been used with some success in

Cyclophosphamide: Cyclophosphamide
cases of canine bacterial hypersensitivity.

is an alkylating agent used to treat a wide

Various treatment protocols have been
variety of cancers, especially lymphoreticuadvocated. One schedule consists of 0.1 mL, lar neoplasms, and is usually given in
intradermally, daily for 5 days, then weekly
combination witl1 other drugs. It may also
for 1 mo, tl1en at monthly intervals. At
be used short-tenn in severe cases of SLE,
co!l'esponcling times, doses given SC
rhetmiatoid artllritis, pemphigus complex,
increase from 0.15 niL to 1.9 mL. Local swelland vasculitis. The dosage for immunosuping at the ir\jection site, fever, and malaise pression is 1.5-2.5 mg/kg, every 48 hr. The
are common adverse effects in dogs.

dose should be given in the morning so that

Propionibacterium acnes bacterin is
it does not remain in the bladder overnight.

labeled for use in dogs (0.25-2 mL, IV,

Because most ailimals treated with cyclo1-2 times/wk) and appears to have some phosphainide also receive corticosteroids,
benefit as adjunct treatment for recurrent
polyuria induced by the steroids may be
pyoderma.

somewhat protective. rhe potential for

Many other in1111unostinrnlants have been
hemorrhagic cystitis and bladder fibrosis
described for use; however, responses in
limits the use of cyclophospha111ide to no
dermatologic disorders have been
more than 3--4 mo. GI tract toxicity, bone
equivocal.

marrow suppression, alopecia, infe,tility,
and teratogenic effects may also be seen.

lmmunosuppressants

Chlorambucil: Chloran1bucil is an

Glucocorticoids: Glucocorticoids are the alkylating agent sinlilar to cyclophosphaimmunosuppressive agents most commonly mide. However, it is slower acting and the used to treat immune-mediated skin disease
least toxic of the group. It may be used for

(seep 827). A range of other immunosuptreatment of inlmune complex diseases in pressants may be used either concwTently
which azathioprine or cyclophosphainide
with glucocorticoids or alone for the
ai·e not tolerated, and it may be given to
treatment of various immune-mediated
cats. The dosage is 0.1-0.2 mg/kg/clay,
dennatoses, inclucling systemic lupus
reduced to every other day once a response
erythematosus (SLE), pemphigus complex,
is seen. It is mostly used in combination
bullous pemphigoid, and vasculitis.

with glucocorticoids but can be used with

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2583
azathioprine in dogs only in particularly
clear cells, antigen presentation, histamine
refractory cases. It may also be used to
release from mast cells, neutrophil
replace cyclophosphamide if hemorrhagic
adherence, natural killer cell activity, and
cystitis develops. Adverse effects are rare

B-cell growth and differentiation.

and include bone marrow suppression

Cyclosporine is used for treatment of

( which generally develops within 7-14 days

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atopic dennatitis and anal furunculosis.

of starting treatment and resolves in 7-14

Extra-label use for the treatment of
days), GI irritation, and seizures. Delayed
irnmune-mediated disorders (pemphigus,
hair regrowth has been repo1ted in shaved

SLE) and epitheliotropic lymphoma has
dogs.

been less successful. Response has been
good when used for sebaceous adenitis.

Crysotherapy: Gold salts have anti

The dosage for atopic dermatitis in dogs is
inflammatory, antirheurnatic, immunomod5 mg/kg/day for 30 days, after which the ulating, and antimicrobial (in vitro) effects.

dose may be reduced to alternate-day or

Parenteral and oral fonns are available.

even third-day dosing in some anin1als. The Aurothiomalate is given parenterally. It is
dosage for anal funmculosis is 7.5 mg/kg/day.

absorbed rapidly and reaches peak levels in

The dosage for feline atopic dennatitis is

4--6 hr. Rising sernm values are noted for

7 mg/kg/day for 30 days and then reduced

5-10 wk. Beneficial effects are seen 6---12 wk
to 7 mg/kg alternate-day dosing.

after the start of treatment. The oral fonn is

Adverse effects include GI signs (nausea,
auranofin. Only 25% is absorbed, and lower
vomiting, soft feces, diarrhea), gingival
and more predictable plasma concentrahypertrophy, hirsutism, and papillomatosis tions are fow1d. The half-life is -21 days, but

(which generally decreases when the dose is
the retention and tissue accwnulation are
decreased). Drugs that inhibit cytochrome
only 1 % (parenteral gold 30%). Results with

P450 ( eg, ketoconazole) potentiate cyclothis compound are equivocal in dogs. Gold sporine toxicity significantly. If ketoconasalts are indicated for canine and feline zole (10 mg/kg, bid) is also administered to
pemphigus unresponsive to glucocorticoids
anin1als witl1 anal funmculosis, the dosage of
and feline plasma cell pododernmtitis.

cyclosporine can be reduced to 1 mg/kg, bid.

Routine protocols start with a test dose

This induction close is maintained for 4 wk

IM (1 mg if <10 kg body wt, 5 mg if >10 kg
and tl1en reduced if tl1e response is adequate
body wt). The next week a second test dose
or adverse effects (vomiting, letlmrgy)

is given IM (2 or 10 mg), and if no adverse
develop.

reactions are seen, treatment continues at

1 mg/kg, IM, weekly until remission. Once in
remission, the dose is given every 2 wk and

Oclacitinib: Oclacitinib is a Janus
may later be reduced to monthly injections.

kinase (JAK) inhibitor and exerts its ac

Occasionally, a higher dosage (1.5-2 mg/kg)

tion tl1rough tl1e inhibition of a variety of
may be required to induce remission.

pn.uitogenic cytokines (eg, IL-31) ancfpro

Treatment effects are not seen for 6---12 wk,
inflammatory cytokines dependent on JAK
so other medications ( commonly glucoco1

1 or JAK 3 enzyme activity. However, it may

°
ticoids) must be given at therapeutic doses
also exe1t effects on other cytokines ( eg,
during this time. Gold salts should not be
involved in host defense or hematopoiesis)

administered with other cytotoxic drngs
with t11e potential for adverse effects.

because of the increased risk of toxic

It is rapidly absorbed and reaches peak
reactions. Adverse effects include allergic
plasma concentrations witl1in 1 hr, leading
reactions (skin ernption, oral reactions),
to rapid onset of clinical effect. It is
nephrotoxicity, and bone marrow
indicated for the treatment of prwitus
suppression. Toxic epidern1al necrolysis
associated with allergic clennatitis in dogs
has been reported in dogs starting gold
at a dosage of 0.4--0.6 mg/kg, bid, for 2 wk
therapy in1mediately after azathioprine, so
and then reduced to once daily administraa 4-wk washout period is recommended in tion for maintenance tl1erapy. In a doublethese cases.

blind, placebo-controlled study for
treatment of atopic de1matitis, tl1e

Cyclosporine: Cyclosporine in1pairs the
treatment success was 66% in reducing
proliferation of activated T cells by inhibiting prnritus and 49";6 for Canine Atopic transcription ofinterleukin-2, gene

Dermatitis Extent and Severity Index
activation, and RNA transcription. This early

(CADESI) scores.

inhibition ofT cells also leads to reduced
production of other cytokines, mast cells,

Sulfones: Dapsone is an anti-inflammaand eosinophils, and inhibition of mononu-tory, antibacterial sulfone that inhibits

2584

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM
neutrophil chemotaxis and adhesion to
been used in limited numbers of a.ilimals for
basement membrane zone antibodies,
a variety of conditions, including vasculitis,
degranulation of mast cells, action of
canine fa.inilial clermatomyositis, ulcerative
lysosomal enzymes, and activation of
dermatitis of Shetla.i1d Sheepdogs and
the alternative complement pathway.

Collies, rabies vaccine--inclucecl ischemic

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Dapsone also inhibits synthesis of IgG,
alopecia, ear margin clemrntosis, contact

IgA, and prostaglandins, as well as T -cel1
allergy, and atopic dennatitis. The dosage is
responses. Although it is used for a variety 10 mg/kg, bid-tid. Once a response is seen, of diseases characterized by accumulathe dosage may be tapered to once or twice tion of neutrophils in people, the results
daily. GI-related adverse effects have been
are more equivocal in dogs. However, it
reported (eg, nausea, vomiting).

has been used for pemphigus foliaceus
and erythematosus, subcorneal pustular

PSYCHOTROPIC AGENTS
dermatosis, 1eukocytoclastic vasculitis,
and IgA dermatosis. The dosage is l mg/kg, Psychotropic drugs have been used tid ( dogs only) for 2-4 wk or until a
extra-label for treatment of feline psychoresponse is seen, then every 24-48 hr.

genic alopecia and canine acral lick

Longterm therapy is not recommended.

de,rnatitis, syndromes characterized by

Mild anemia or severe leukopenia, blood
excessive self-licking ( see also ABNORMAL
dyscrasias, hepatotoxicity, or skin

REPETITIVE BEHAVIORS IN DOGS, p 1561, and FELINE
reactions may develop. Animals should be

COMPULSIVE DISORDEHS, p 1574). Classes of drugs
monitored by CBC, urinalysis, BUN, and
used include a.i1tidepressants, antipsychotics,

ALT every 2 wk during induction. Cats are
opiate antagonists, a.nxiolytics, and mood
particularly sensitive to toxicity, and a
stabilizers (see table 14).

dosage of l mg/kg/day is recommended.

Sedation is the most conunon adverse

Concurrent use may allow the dosage of
effect of diazepa.i11. It is also an appetite
glucocorticoids to be reduced.

stimulant in cats. Idiosyncratic fatal hepatic
necrosis has been reported in several cats

Tetracycline and Niacinamide:

treated for as little as 8---14 days. T!icyclic

Although the precise mechanism of action
antidepressants a.i·e potent H, blockers in
is unknown, tetracyclines may inhibit in
addition to inhibiting uptake of serotonin
vitro lymphocyte blastogenic transformaand norepinephrine. These drugs can tion and antibody production, activation of
induce ca.i·diac arrhythmias and lower the
complement ( component C3), prostaglanseizme threshold. Other adverse effects din synthesis, lipases and collagenases, and include dry mouth, hypersalivation, sup iress leukocyte chemotaxis in vitro and vomiting, constipation, urina.iy retention, in vivo. Niacinan1ide blocks IgE-induced
ataxia, disorientation, depression, and
histamine release, inhibits phosphodiesteranorexia. Tricyclic antidepressants should ases, and decreases protease release by
not be used concurrently with monoa.inine
leukocytes. The combination is indicated
oxidase inhibitors, including an1itraz dips
for disco id lupus crythematosus and
for demodicosis. Dosages should be tapered
pemphigus erythematosus. These diseases
slowly when discontinued.

are characterized by leukocyte chemotaxis
seconcla.iy to complement activation by

VITAMINS AND MINERALS
antigen-antibody complexes and by release
of proteases. Dogs weighing > l O kg a.i·e

Retinoids: Natmally occmring and
given 500 mg of each drug tic!. If a clinical
synthetic compounds witl1 vita.inin A
response is seen, the frequency may be
activity include retinal, retinoic acid, a.i1d
decreased to once or twice daily. Vomiting,
retinol derivatives or analogues. At tl1e
diarrhea, and anorexia a.i·e the most
molecula.i· level, retinoids are in1po1tant
common adverse effects.

in regulation of proliferation, growth,
differentiation, and maintenance of

Pentoxifylline: Pentoxifylline results in a
epithelial tissues. Retinoids also affect
range of immunologic and rheologic effects,
proteases, biosynthesis of mucopolysacchaincluding increases in RBC and WBC
rides, prostagla.i1dins, cellular adhesion,
defmmability; decreases in RBC and
cellula.i· communication, and inununity.

platelet aggregation, leukocyte endothelial

They prevent tumor promotion by inhibition
adherence, natmal killer cell activity,
of omithine decarboxylase, a key enzyme
neutrophil clegranulation, and production of for cell proliferation and differentiation.

monocyte TNF-a, IL-1, IL-4, and IL-12; and

Vita.inin A (1,000 IU/kg) has been used for
inhibition ofT- ancl B-cell activation. It has
follicula.i· keratosis in cats. However, tl1e

SYSTEMIC PHARMACOTHERAPEUTICS OF THE INTEGUMENTARY SYSTEM

2585

•ffl:iif i• PSYCHOTROPIC DRUGS USED FOR SKIN DISORDERS

Drug

Dosage

ANTIDEPRESSANTS

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Clomipramine

Dogs: 1-3 mg/kg, bid

Cats: 0.5-1.5 mg/kg/day

Amitriptyline

1-3 mg/kg, bid

Doxepin

0.5-2 mg/kg, bid

Fluoxetine

1 mg/kg/day

ANXIOLYTICS

Diazepam

1-2 mg/kg, bid

Phenobarbital

0.5-2.2 mg/kg, bid; 15 mg/cat, twice weekly

Hydroxyzine

2.2 mg/kg, tid

OPIATE ANTAGONISTS

Naltrexone

2.2 mg/kg/day
retinoids used most commonly are

Zinc: Zinc is an important factor of many
isotretinoin ( 13-cis-retinoic acid) and
enzyn1e systems and is necessaiy for
etretinate (no longer available but replaced
maintenance of growth, metabolism, nom1al
with acitretin, a metabolically active
reproduction, and hormonal regulation. It is
metabolite of etretinate).

essential for keratinization and inrnmne

Isotretinoin is indicated for Schnauzer
function. Zinc supplementation is given in
comedone syndrome, ichthyosis, feline
cases of insufficient intestinal absorption,
acne, sebaceous adenitis, epitheliotropic
including deficiency syndrome I (Sibe1ian
lymphoma, keratoacanthoma, and

Huskies, Alaskan Malamutes) and syndrome
sebaceous gland hyperplasias and

II (rapidly growing dogs on zinc-deficient
adenomas. The dosage is 1-3 mg/kg/day.

diets). Dietaiy deficiency may be either

Adverse effects include conjunctivitis,
absolute or relative-diets high in phytates
mucocutaneous drying, alopecia, pruritus,
or minerals may inhibit zinc absorption. For
hyperactivity, vomiting, and diarrhea. In
syndrome I, zinc supplementation is given
dogs, blood chemistry increases not
as elemental zinc 1 mg/kg/day, PO (zinc
normally associated with clinical disease
sulfate 10 mg/kg, zinc gluconate 5 mg/kg, or
include plasma cholesterol, triglycerides,
zinc methionine l. 7 mg/kg). Supplementa

AL 1� AST, and alkaline phosphatase.

tion is typically lifelong. If the response is

Rarely, keratoconjunctivitis sicca may
insufficient after 4 wk, the dose should be
develop in dogs. Conjunctivitis, anorexia,
increased by 500Ai. Low-dose corticosteroids
diarrhea, and vomiting are the major
may also enhance zinc absorption through
adverse effects in cats. All retinoids are
induction of metallothionein in some
potent teratogens, and teratogenicity may
nonresponsive cases. Animals with
persist for up to 2 yr after treatment with
syndrome II normally respond to correction
etretinate because the half-life is -100
of the diet with resolution within 2-6 wk,
days. Skeletal abnormalities that may be
although supplementation speeds this
seen with longterm therapy, including
process.

premature closure of the epiphyses in

Hereditaiy zinc deficiency associated
growing animals, cortical hyperostosis,
with deficient intestinal absorption has also
periosteal calcification, and long-bone
been reported in Friesian, Danish Black
demineralization, are less common with

Pied, and Shorthorn cattle. There is a rapid
etretinate than with isotretinoin. Monitorresponse to zinc oxide given at 0.5 g/day, ing during longterm therapy should

PO, or zinc sulfate at 2 g, PO, given weekly.

include complete physical examinations

Response to zinc supplementation is usually
and serum chemistry profiles at monthly
rapid ( a few clays) except for cases of
intervals for the first 3-4 mo and then
achromotrichia, which requires several
every 4-6 mo.

weeks for resolution.

2586

SYSTEMIC PHARMACOTHERAPEUTICS OF THE MUSCULAR SYSTEM

SYSTEMIC PHARMACOTHERAPEUTICS

VetBooks.ir

OF THE MUSCULAR SYSTEM

Drugs that affect skeletal muscle function
and consequently paralysis. Exan1ples of
fall into several therapeutic categories.

prejunctional blocking agents include

Some are used during surgical procedures
biotoxins, electrolytes, local anesthetics or
to produce paralysis (neuromuscular
other drngs, and antibiotics. Biotoxins
blocking agents); others reduce spasticity
include black widow spider venom, which

(skeletal muscle relaxants) associated with
depletes acetylcholine stores; botulinum
various neurologic and musculoskeletal
toxin, which decreases acetylcholine release;
conditions. In addition, several therapeutic
tetradotoxin from the puffer fish and
agents influence metabolic and other
saxitoxin from shellfish, which block
processes in skeletal muscle, including the

Na+-conducting channels; and grayanotoxin
nutrients required for normal muscle
found in rhododendrons, which facilitates
function used to prevent or mitigate
excessive Na+ entry tlu·ough the sarcolenuna,
degenerative muscular conditions. For
leading to constant depolarization of tl1e
example, selenium and vitamin E are used
membrane. Electrolytes include excess
to prevent or treat muscular dystrophies

Mg2+, which inhibits release of acetylcholine
such as white muscle disease (seep 1172).

from the axon and w1couples the excitation

The steroidal, nonsteroidal, and various
contraction process by competing with Ca2+;
other anti-inflammatory agents ( eg,
and depleted Ca2+ levels, which decrease
dimethyl sulfoxide) are also commonly
release of acetylcholine and impainnent of
used to treat acute and chronic inila.mmaexcitation-contraction coupling. Local tory conditions involving skeletal muscle.

anesthetics in higll concentration can

Anabolic steroids promote muscle growth
stabilize membranes by blocking both Na+
and development and are ad.ministered in
and K+ channels; hernicholinium can inhibit
selected cases in which serious muscle
synthesis of acetylcholine by blocking
deterioration has developed as a complicacholine uptake into tl1e nerve. Antibiotics, tion of a primary disease syndrome.

such as the aminoglycosides, polymyxins,

The clinical pharmacology of the
tetracyclines, and lincosarnides, appear to
neuromuscular blocking agents, skeletal
act by decreasing tl1e availability of Ca2+ at
muscle relaxants, and anabolic steroids are
membrane-binding sites on the axonal
discussed below. (For anti-inflammatory
terminal and perhaps by reducing the
agents, seep 2707.)

sensitivity of the nicotinic receptors to
acetylcholine.

NEUROMUSCULAR BLOCKING

Postjunctional blocking agents are used

AGENTS
clinically and act either by blocking the nicotinic receptors in a competitive fashion The peripherally acting skeletal muscle

(nondepolarizing agents) or by interacting
relaxants characteristically interfere with the with these receptors in a manner that does trans.mission of impulses from motor nerves
not allow the membrane to repolarize so
to skeletal muscle fibers at the neuromuscu that paralysis results ( depolarizing agents).

lar junction, thus reducing or abolishing

The mechanisms involved in the latter case
motor activity. The skeletal muscle paralysis
are not fully understood. All of the neurothat ensues is not associated with depression muscular blocking agents are structurally
of the CNS. Animals are fully conscious
similar to acetylcholine (actually two
throughout the period of inunobilization
molecules linked end-to-end). The
unless an anesthetic or hypnotic agent is
depolarizing agents are usually simple linear
ad.ministered concurrently.

structures, and the nondepola.rizing agents

Neuromuscular transmission can be
are more complex bulky molecules. With a
modified either at the axonal membrane
single exception (vecuroniun1), all have a

(prejunctional blockade) or at the
quaternary nitrogen in their structure, which
cholinergic receptors in the sarcolenuna
makes these drugs poorly lipid soluble.

(postjunctional blockade).

There are no clinically useful d.tugs that act Competitive Nondepolarizing prejunctionally, but a number of important

Agents: The members of this group
substances can impair the synthesis, storage,
of peripherally acting skeletal muscle
and release of acetylcholine, thus resulting in
relaxants are often referred to as curarizing
prejunctional blockade at the motor endplate
agents because of their relationships with

SYSTEMIC PHARMACOTHERAPEUTICS OF THE MUSCULAR SYSTEM

2587
the curare alkaloids that were first used

( aillinoglycosides, polymyxins, tetracyclines,
clinically. The currently available drngs,
and lincosatnides ), and various other drugs
which interact with nicotinic cholinergic

( quinidine, procaine, lidocaine, diazepai11,
receptors on skeletal muscle cells and
and barbitw·ates ). Several states, such as
render them inaccessible to the transmitter
hyper- and hypomagnesemia, hypokalemia,

VetBooks.ir
function of acetylcholine (and thus produce
acidosis, and hypothemlia, also prolong the
a flaccid paralysis) include tubocura.rine,
action of tllis group of dn1gs. Animals with
metocurine ( din1ethyltubocurarine),
myasthenia gravis ai·e much more susceptigallamine, pancuronium, alcuroniw11, ble to the action of muscle relaxants.

atracuriWll, vecuroniW11, and fazadiniWll.

Indications for the use of nondepolarizing

In general, nondepolarizing muscle
neuromusculai· blocking agents include
relaxants are not absorbed from the GI tract
muscle relaxation of the operative field,
and must be administered parenterally,
hypoxemic atlimals resisting mechailical
usually IV. Plasma-protein binding is
ventilation, tracheal intubation, ailimals
insignificant, and there is rapid equilibration
with unstable cardiovascular function that
but only within the extracellular fluid. The
require anesthesia but catmot tolerate
blood-brain and blood-placental barriers are cardiac depression, cesarean section in rarely crossed. Tubocuraiine, metocurine,
toxic or high-risk aninlals, epileptifom1
and gallatlline are not biotrat1Sfom1ed to
convulsions not controllable with usual
any extent and are excreted unchanged,
ai1ticonvulsant agents, tetaims, strychnine
principally in the urine but sometimes in
poisoning, shivering animals in which the
bile. The other members of tl1e group
metabolic demand for oxygen should be

W1dergo metabolic 1;rat1Sformation to some
reduced, and capture of ce1tain exotic
degree, and the metabolites ai·e excreted
species ( eg, gallai1line used for inllllobilizaby both renal and biliary routes in most tion of crocodiles). Anin1als should always
instances. The elimination half-lives at
be carefully monitored when tmder the
standard dosages are 60-100 min, and the
influence of neuromuscular blocking drugs,
duration of paralysis is 30-60 min, except in
and support of ventilation is essential.

the case of atracuriWll and vecuroniWll,

The action of the competitive relaxants
which have shorter actions of -20--30 min.

can be reversed by anticholinesterase

After IV administration of these agents,
drugs, especially neostigmine, after the
the skeletal muscles become totally flaccid
administration of atropine, which elimiand nonresponsive to neuronal stimulation.

nates excessive muscarinic responses. This

Muscles capable of rapid movement, such as
attribute is a great advantage for this group
those of the eye, are pai·alyzed before the
of peripherally acting muscle relaxai1ts.

lai·ger muscles of the head and neck, which

The selection of dose rates ( see TABLE 15) are followed by those of the lin1bs and body.

serves only as general guidelines for t:he use

Lastly, the diaphragm becomes paralyzed,
of competitive blocking agents.

and respi.ration ceases. If ventilation is
controlled (tracheal intubation ai1d

Depolarizing Agents: Succinylcholine
positive-pressure ventilation), there are no

(suxamethonium) is the only conllllonly
adverse effects, and full recovery ensues in
used, peripherally acting muscle relaxant
reverse order, with the diaphragm regaining
that is a depolarizing agent. Decamethofunction first. All of tl1e currently used niWll, tl1e other member of the group, is
nondepolarizing muscle relaxants have
rarely used clinically.

cardiovascular effects, many of which are

Depolarizing blocking drugs occupy
mediated by autonomic and histanline
the postjunctional cholinergic receptors
receptors. Tubocuraiine and, to a much
and, by mechatlisms that remain obscure,
lesser extent, metocurine result in hypotenelicit prolonged depolarization of tl1e sion, which probably results from the
endplate region. This prevents the synaptic
liberation of histanline and, in larger doses,
membrane from completely repolarizing,
from ganglionic blockade. Premedication
thus rende1ing the motor endplate w1rewith an antihistanline reduces tubocurarinesponsive to the nom1al action of acetylchoinduced hypotension. PancuroniWll causes line. Characteristically, succinylcholine
a moderate increase in heart rate and, to a
elicits transient muscle fasciculations
lesser degree, cardiac output. Gallatlline
before causing neuromusculai· paralysis.

increases heart rate by both a vagolytic

The onset of action of succinylcholine is
action and sympathetic stinlulation.

rapid after IV injection (20-50 sec), and the

A nw11ber of agents can potentiate the
duration of the effect is usually 5---10 min in
activity of neuromusculai· blockers. These
most species. Succinylcholine is rapidly
include other peripherally acting skeletal
hydrolyzed by pseudocholinesterases in
muscle relaxants, inhalant anesthetics
the plasma and liver in most species, but

01alothane, methoxyflurane), antibiotics
substantial genetic differences exist.

2588

SYSTEMIC PHARMACOTHERAPEUTICS OF THE MUSCULAR SYSTEM
ittN•ifi COMPETITIVE NONDEPOLARIZING AGENTS AND ANTAGONISTS

Drug

Dosage

NONDEPOLARIZING AGENTS

VetBooks.ir

1\1bocurarine chloride

Horses: !>0.22-0.25 mg/kg , IV

Dogs, cats: !>0.4 mg/kg, IV

Gallamine triethiodide

All species ( except pigs): 0.8-1 mg/kg, IV

Pancuronium bromide

Dogs, cats: 0.6 mg/kg, IV

Alcuronium chloride

Dogs, cats: 0.1 mg/kg, IV

Atracurium besylate

Dogs, cats: 0.5 mg/kg, IV

ANTAGONISTS

Neostigmine

0.04 mg/kg, with atropine at 0.04 mg/kg, IV

Pyridostigmine

0.2-0.25 mg/kg, with atropine at 0.04 mg/kg, IV

Edrophonium

0.125 mg/kg, IV

Other phannacologic effects are associfor immobilization for castration without ated with the depolarizing muscle relaxants.

local or general analgesia. The use of

After IV administration of succinylcholine,
succinylcholine for game-cropping
transient muscle fasciculations are usually
procedures is also highly undesirable.

evident, although general anesthesia tends to

No antagonists are available to reverse
attenuate them. Succinylcholine-induced
the action of the depolarizing muscle
cardiac a.1Thythmias are many and varied.

relaxants. Continued positive-pressure

Succinylcholine stimulates all autonomic
ventilation until recovery occurs is the
cholinergic receptors-both nicotinic and
only therapy in cases of overdosage.

muscarinic. Sudden hyperkalemia may be

The IV dose rates for succinylcholine by
precipitated by succinylcholine, and muscle
species are as follows: horses: 0.125----0.20 mg/
pain is seen with the use of succinylcholine
kg ( -8 min recun1bency); cattle: 0.012--0.02
in the absence of anesthesia After recovery
mg/kg ( -15 min recumbency); dogs: 0.22-1.1
from succinylcholine-induced muscle
mg/kg ( -15---20 min paralysis); and cats:

paralysis, muscle damage and even

0.22-1.1 mg/kg ( -3---5 min paralysis).

myoglobinuria can develop. Malignant
hyperthermia (seep 1027) or clinical signs

SKELETAL MUSCLE RELAXANTS
related to this syndrome may also follow the
use of succinylcholine in susceptible animals.

Muscle spasticity is a characteristic of

Factors that can alter the activity of
many clinical conditions, including trauma,
competitive blocking agents (seep 2586)

myositis, muscular and ligamentous sprains
can also affect the action of succinylcholine. and strains, intervertebral disc disease, In addition, previous (within 1 mo) or
tetanus, strychnine poisoning, neurologic
concmTent use of organophosphate
disorders, and exertional rhabdomyolysis.

anthelmintics or external parasiticides can

An increase in tonjc stretch reflexes
have a significant impact on the recovery
originates from the CNS with involvement
time from succinylcholine immobilization
of descending path ways and results in
because of prolonged inhibition of the
hyperexcitability of motor neurons in the
pseudocholinesterase enzyme systems.

spinal cord. Drug therapy (see TABLE 16)

A genetically mediated deficiency of
alleviates muscle spasms by modifying the
pseudocholinesterases also has been
stretch reflex arc or by interfering with the
identified in certain strains of sheep. Cattle
excitation-coupling process in the muscle
are much more susceptible to the effects
itself. Centrally acting muscle relaxants
of succinylcholine than other species.

block interneuronal pathways in the spinal

The indications for the clinical use of
cord and in the midbrain reticular activating
succinylcholine are similar to those for the
system. Some drugs also have sedative
nondepolarizing agents. However, it must
effects, which are beneficial to animals
be emphasized that succinylcholine should
that are anxious or in pain. The hydantoin
never be used as an agent for euthanasia or derivatives have a direct action on muscle.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE MUSCULAR SYSTEM

2589

Methocarbarnol is a centrally acting
act as a spinal cord depressant at the intemeumuscle relaxant chemically related to ronal level, and inhibit presynaptic acetylchoguaifenesin. Its exact mechanism of action line release. Clinically, diazepam is used as an
is unknown, and it has no direct relaxant
adjunct to anesthesia, in management of
effect on striated muscle, neive fibers, or the
clinical signs of tetanus, and in treatment of

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motor endplate. It also has a sedative effect.

functional urethral obstruction and uretlu·al

In dogs, cats, and horses, methocarbarnol
sphincter hypertonus in cats.

is indicated as adjunct therapy of acute

Dantrolene, a hydantoin derivative, is
inflanm1atory and traun1atic conditions
structurally and pham1acologically different
of skeletal muscle and to reduce muscle
from oilier skeletal muscle relaxants.

spasms. Because methocarbarnol is a CNS

Dantrolene has a direct action on muscle,
depressant, it should not be given with other
probably by interfering with the release of
drugs that depress the CNS. Overdosage is
calcium from the sarcoplasmic reticulum.

generally characterized by CNS depression,

It has no discernible effects on respirntory
but emesis (small anin1als ), salivation, wea k and cardiac function but can cause ness, and ataxia may be seen.

dizziness and sedation. In vete1inary

Guaifenesin (glyceryl guaiacolate) is
medicine, dantrolene is used to treat
a centrally acting muscle relaxant believed
malignant hypertl1ermia in various species,
to depress or block neive impulse transmisporcine stress syndrome, equine postanession at the intern uncial neuron level of the thetic myositis, and equine exertional
subcortical areas of the brain, brain stem, and rhabdomyolysis (seep 1027 and p 1202).

spinal cord. It also has mild analgesic and

Phenytoin is a hydantoin derivative,
sedative actions. Guaifenesin is given IV to
primarily used as an anticonvulsant in
induce muscle relaxation as an adjunct to
people. Phenytoin has shown efficacy
anesthesia for short procedures. It relaxes
in some horses susceptible to exe1tional
both laryngeal and pharyngeal muscles,
rhabdomyolysis. Phenytoin may alter the
allowing easier intubation, but has little effect function of neurotransmitters at the on diaphragm and respiratory function. It
neuromuscular junction, ilie release of
may cause transient increases in cardiac rate
calcium from the sarcoplasmic reticulum,
and decreases in blood pressure. It is also
and sodium flux at the sarcolemma.

used in treatment of horses with exertional

Dosages are adjusted in horses to maintain
rhabdomyolysis and in dogs with strychnine
semm concentrations of 5--10 mcg/mL.

intoxication. Overdose results in apneustic

Baclofen is a centrally acting skeletal
breathing, nystagmus, hypotension, and
muscle relaxant used to control spasticity
contradictory muscle 1igidity. Treatment of
and pain in people with multiple sclerosis
overdose is supportive until the drug is
and spinal disorders. Baclofen is structurally
cleared to nontoxic levels.

similar to the inhibitory neurotransmitter

Benzodiazepines, such as diazepam, affect
ganuna-anlinobutyric acid (GABA). It acts as
polysynaptic reflexes at the supraspinal level,
a GABA receptor B agonist to reduce calcium

•fu:iiit·i SKELETAL MUSCLE RELAXANTS

Drug

Dosage

Methocarban10l

Dogs, cats: 44 mg/kg, IV, up to 330 mg/kg/day for tetanus or strychnine poisoning; 132 mg/kg/day, PO, divided bid-tid Horses: 4.4-5.5 mg/kg, IV

Guaifenesin

Dogs: 44-88 mg/kg, IV

Horses, run1inants: 66--132 mg/kg, IV

Diazepam

Cats: 2-5 mg, PO, tid, for urethral obstmction

Dantrolene

Horses: 15-25 mg/kg, slow IV, qid; 2 mg/kg/day, PO, for prevention of exertional rhabdomyolysis

Swine: 3.5 mg/kg, IV

Phenytoin

Horses: 6--8 mg/kg/day, PO, increase by 1 mg/kg every 3 days until rhabdomyolysis is prevented or the horse appears sedated

Baclofen

Dogs: 12 mg/kg, PO, tid

2590

SYSTEMIC PHARMACOTHERAPEUTICS OF THE MUSCULAR SYSTEM
influx into presynaptic neive terminals,
to nuclear chroma.tin, stimulating the
thereby decreasing the amount of excitatory
production of specific messenger RNA.

neurotransmitters released by primary

The messenger RNA then regulates the
afferent neurons in the spinal cord and bra.in.

enzyme synthesis responsible for the

Th.is results in reduced muscle tone as well
physiologic activity of the anabolic steroid.

as pa.in associated with spasticity. Because of

Anabolic steroids stimulate and maintain

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a very narrow safety margin, ba.clofen has
a positive nitrogen balance by reducing
limited use in veterinary medicine. It has
renal elinlina.tion of nitrogen, sodium, potasbeen used to treat dogs with tetanus and to siwn, chloride, and calciw11. Production of
reduce urethral resistance in treatment of
myosin, sa.rcoplasm, and myofibrilla.r
urinary retention. Ba.clofen transiently
protein is enhanced. Anabolic steroids
inhibits lower esophageal sphincter
promote appetite, weight gain, and
relaxation in dogs and theoretically is of
in1proved mental attitude, so they a.re used
benefit in the treatment of gastroesopha.geal
to reverse debilitation associated with
reflux disease. Ba.clofen is not recommended
surgery, traun1a, illness, glucocorticoidfor use in ca.ts. Even at therapeutic doses, induced catabolism, and aging. In all cases,
dogs may show clinical signs of vomiting,
improved well-being depends on adequate
depression, and vocalization. With overdose,
intake of protein and calories and on
the severity of CNS signs can be substantial
treatment of the underlying disease.

and may include dysphoria., lateral recum

Anabolic steroids have a variety of
bency, or coma Treatment of ba.clofen
undesirable effects. They induce androtoxicity should include rapid and aggressive genic effects, such as increased libido in
decontanlina.tion, along with intensive
males and abnormal sexual behavior in
supportive treatment. Management of
females, along with adverse reproductive
affected dogs may require positive-pressure
effects, including a.zoospermia., anestrus,
ventilation as a result of severe obtundation,
testicular a.trophy, and clitoral hypertrophy.

respiratory depression, and respiratory

They promote edema formation due to
arrest or hypoventila.tion. Cyproheptadine, a
sodium and water retention. lcterus can
serotonin antagonist, may be given orally or
develop due to intrahepa.tic cholestasis.

rectally as needed to reduce vocalization or

Anabolic steroids can induce epiphysea.l
disorientation. IV lipid emulsion has been
plate closure, thereby retarding growth.

useful to treat some dogs with ba.clofen

Anabolic steroids a.re used in treatment of
toxicity.

debilitated animals; however, they a.re often
misused to gain a competitive advantage in

ANABOLIC STEROIDS
performance a.nin1als. Approved veterinary
formulations a.re no longer marketed in

Anabolic steroids a.re synthetic derivatives

North America. Currently, any anabolic
of testosterone with enhanced anabolic
product for veterinary use (aside from
activity and reduced androgenic activity.

bovine ear in1plants) can be obtained only

Testosterone or its derivatives diffuse
from a compounding pha.rma.cy. Use of
through cell membranes of target organs
anabolic steroids in performance horses is
and combine with specific receptor proteins prohibited by most equine sport organizain the cytoplasm. The receptor-hormone tions, and drug detection tin1es can be
migrates into the cell nucleus and binds

>2 mo.

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE NERVOUS SYSTEM

Drugs used to modify or treat disorders

NATURAL TREATMENT FOR BEILAVIORAL PROBLEMS,
of the neivous system fall into several
p 1543.

categories: anticonvulsants or antiepileptic
drugs (AEDs), tranquilizers, sedatives,

ANTICONVULSANTS OR
analgesics, and psychotropic agents. See
also

ANTIEPILEPTIC DRUGS

PRINCIPLES OF THEIW'Y OF NEUROLOGJC

DISEASE, p 1220, ANALGESIC PHARMACOLOGY,

Anticonvulsants or antiepileptic drugs
p 2107, and PRINCIPLES OF Pl-LAllMACOLOGIC AND

(AEDs) a.re used to stop an ongoing seizure

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2591
or to dE:crease the frequency or severity of

Foals and Horses
anticipated future seizures. During a seizure
episode or status epilepticus, the route of

Diazeparn in horses has a long elimination
administration for AEDs is IV ( see
half-life (7-22 hr). In foals, the dosage is

TABLE 17).

For longterm maintenance, the oral route

0.05--0.4 mg/kg, slowly IV ( or about 5--20 mg/
close); higher doses can be fatal to neonates.

is preferred, although absorption may be

For seizures in adult horses, diazeparn can
limited or variable depending on the drug

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be given at 25-50 mg/horse, IV. To prevent
used (see TABLE 18). SC or IM iajections are further seizures after initial diazepam
seldom used because of the variability in
iajection, IV phenobarbital may be staited
drug abso1ption.

as a follow up at 12-20 mg/kg, IV over 20
min, and then maintained at a dosage of

ANTIEPILEPTIC DRUGS USED TO

6.65--9 mg/kg over 20 min, bid or tid. If
sedation occurs, the dose should be

STOP ONGOING SEIZURE ACTIVITY reduced. Alternatively, treatment of seizures ln status epilepticus, treatment is essential
in foals can be initiated with phenytoin at
to prevent death from hyperthern1ia,

5--10 mg/kg, IV or PO, with subsequent
acidosis, hypoperfusion, and hypoxia.

treatments of 1-5 mg/kg, IV, IM, or PO, every

Because diazeparn has a rapid onset of

2--4 hr for 12 hr and later maintained with
action that prevents the spread of the
oral phenytoin at 2.83--16.43 mg/kg, tid,
seizure, it is usually the drug of choice to
although erratic plasma concentrations may
control status epilepticus and stop seizures
limit usefulness. The dose may need to be
in small and large animals.

reduced if sedation occurs.

•h=iiifl DRUGS USED FOR TREATMENT OF STATUS EPILEPTICUS

Drug

Species and Dosage

Diazepan1

Dogs, cats: 0.5--2 mg/kg, IV bolus; can be repeated 2-3 times at intervals of 5--10 min; CR!" 0.5--2 mg/kgthr

Foals: 0.05--0.4 mg/kg, IV slowly

Adult horses: 25-50 mg/horse, IV

Ruminants: 0.5-1.5 mg/kg, IV or IM

Midazolarn

Dogs, cats: 0.2 mg/kg, IV bolus; can be repeated 2 -3 times at intervals of 5--10 min; CRI 0.05-0.5 mg/kgthr

Phenobarbital

Dogs, cats: For those not already on maintenance phenobarbital, loading dose of 15 mg/kg, slowly IV. Alternatively, 3-6 mg/kg, IV or IM, every 15--30 min until a total dosage of 20 mg/kg is reached. ln an animal already receiving maintenance phenobarbital, a single 3 mg/kg bolus, IV or IM, CRI 3-10 mgthr to effect.

Foals, adult horses: loading dose of 12-20 mg/kg, IV over 20 min, then 6. 65--9 mg/kg, IV over 20 min every 8--12 hr

Sodiwn pentobarbital Dogs, cats: 2-15 mg/kg, IV, to effect to stop motor activity Foals, adult horses: 2--4 mg/kg, IV to effect

Levetiracetam

Dogs: 20-60 mg/kg, IV; can be repeated at 8-hr intervals Propofol

Dogs, cats: 2.5--4 mg/kg, IV, to effect to stop motor activity; CRI 0.1-0.3 mg/kg/min to effect

Phenytoin

Dogs: 2-5 mg/kg as slow IV infusion

Foals, adult horses: 5--10 mg/kg, IV followed by 1-5 mg/kg, IV, IM, or PO, every 2--4 hr until seizures stop and maintenance dose started
a CR! = constant-rate infusion

2592

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

IM=iiif:i ANTIEPILEPTIC DRUGS

Drug

Dosage and Frequency

Half-life

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FIRST-LINE MAINTENANCE ANTIEPILEPTIC DRUGS

Phenobarbital

Dogs: 2-4 mg/kg, PO, bid (starting

40-90 hr
dose); up to 10 mg/kg, bid

(Beagles 25-38 hr)

Cats: 2-4 mg/kg, PO, bid (starting

34-43hr
dose)

Horses: 3-5 mg/kg/day, PO, as a starting 18hr
dose; up to 11 mg/kg/day, PO

Foals: as above

13 hr

Ruminants: 11 mg/kg/day, PO

Bromide

Dogs, cats: 20-40 mg/kg, PO, once

Dogs: 20-46 days

(potassium salt)

daily or divided bid if GI upset.

Cats: 10 days

Caution using bromide in cats

Horses: 5 days

(see comments) .

Dogs: loading dose 400-600 mg/kg, PO
divided into 4 doses, given over 1-4 days

Horses: 90 mg/kg/day, PO

Bromide

17-30 mg/kg, PO, once daily or divided

(sodium salt)

bid if GI upset . The dose of sodium
bromide is less than that of potassium
bromide to account for the higher
bromide content.

Diazepam

Cats: 0.25-0.5 mg/kg, PO, bid-tid

Cats: 15-20 hr

SECOND-LINE (ADD-ON) ANTIEPILEPTIC DRUGS FOR DOGS

Clonazepam

Dogs: 0.1-0.5 mg/kg, PO, bid-tid

1.5-3 hr

Clorazepate

Dogs: 0.5-1 mg/kg, PO, tid

5-6hr

Felbamate

Dogs: 15 mg/kg, PO, tid; increase by

5-6hr

15 mg/kg biweekly until seizures
controlled; maximal (toxic) dosage

300 mg/kg

SYSTEM IC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2593

•th•j1:• ANTIEPILEPTIC DRUGS (continued)

Time to

Steady State

Therapeutic Level

Adverse Effects/Comments

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FIRST-LINE MAINTENANCE ANTIEPILEPTIC DRUGS

Adjust dosage in all species by monitoling
serum levels and seizure dia1y.

l0-24days

15--45 mcg/mL

Sedation, polydipsia, induces P450

(66-200 iimol/1),
system, increase in alkaline phosphatase
preferably keep values
common; liver failure is possible but
within 20-35 mcg/mL
uncommon.

(85-150 innol/1)

l0-30 mcg/mL

Liver enzymes do not typically increase in
cats.

10--40 rncg/rnL

(43-175 µmol/1)

Dogs: 100-200

Bromide alone:

Sedation, weakness, polydipsia, vomiting,
days

1--3 mg/mL
polyphagia, skin rash. Reduce dose with

Cats: 6wk

(15-20 µmol/1)

renal insufficiency. High chloride intake
increases bromide elimination. Chloride

Bromide/phenobarbital
content of diet should be stable. Use with
combined: 1-2 mg/mL
extreme caution in cats and monitor with
thoracic radiographs because bronchial/
asthmatic signs may be fatal in cats.

See potassium bromide comments.

While oral diazepam is not effective 'as
maintenance AED in dogs, it can be used
in cats as a maintenance AED. Sedation
and liver failure are potential problems in
cats.

SECOND-LINE (ADD-ON) ANTIEPlLEPTIC DRUGS FOR DOGS

22-77ng/mL

Extremely potent benzodiazepine;
sedation; withdrawal signs if drug stopped
abruptly.

1-2 days

20-75mcg/L

15 times less potent than clonazepam;
sedation; withdrawal seizures. Can
increase phenobarbital concentration.

1 day

125-250 iu1101JLa

Nervousness, keratoconjunctivitis sicca,
mild thrornbocytopenia, leukopenia;
induces P450 system; liver disease. Use
with care with other potentially hepatotoxic drugs.

(continued)

2594

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

•t4:iii1:• ANTIEPILEPTIC DRUGS (continued) Drug

Dosage and Frequency

Half-life

Gabapentin

Dogs: 10 mg/kg, PO, tid; up to 30-60

3-4 hr

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mg/kg, tid

Levetiracetam

Dogs: 20 mg/kg, PO, tid

4-10 hr

Topiramate

Dogs: 5-10 mg/kg/day, PO, bid

2-4 hr

Valproic acid

Dogs: 10-60 mg/kg, PO, tid

90-120 min

Zonisamide

Dogs: 5 mg/kg/day, PO, bid, if

15-20 hr
phenobarbital is not concurrently given;

10 mg/kg, PO, bid if phenobarbital is
concurrently administered.

"Therapeutic range established for people

Other ways to control ongoing seizure
be repeated up to three times at intervals of
activity include sodiwn pentobarbital (2-4

5-10 min. However if seizures occur after
mg/kg, lV to effect), a mixture of 12% chloral the second or third bolus, a constant-rate hydrate and 6% magnesium sulfate at a rate
infusion (CRI) of cliazepam at 0.5-2 mg/kg/hr
not exceeding 30 mUmin to avoid excessive
may be more effective ( especially if titrated
depression, or a mixture of 44-88 mg/kg of
based on seizure control and sedation

5% guaifenesin and 2.2-6.6 mg/kg thiamyal,
level), and lV phenobarbital should be
given lV to effect. Horses with seizures
strutecl as a preventive (seep 2595). When
induced by toxins or adverse drug effect
diazepatn is used as a CR!, it should be

(eg, xylazine) can be treated with diazepan1
mixed with 5% dextrose or 0.9% saline. It

(0.1-0.15 mg/kg, lV). If cerebral edema is
should not be mixed with lactated Ringer's
suspected, see PlllNCIPLES OF TIIERAPY OF Tl-IE
solution, because the calciwn may ca.use

NEHVOUS SYSTEM, p 1220.

precipitation of the diazepatn. Because
plastic will absorb diazepam, it should not

Ruminants
be left in plastic syringes ol' lV sets for

Diazepam has been used at 0.5-1.5 mg/kg,
prolonged intervals. When cliazepat11 is

IM or lV. In sheep and goats, pentobarbital
administered as a CRI, it is thought that the
at 20-30 mg/kg can be used lV to effect to
initial pass-tlu·ough in the lV set saturates
induce anesthesia. The duration of effect is
the surface of the tubing such tl1at there is

5-30 min.

no further absorption. IflV access is not
possible in dogs, diazepam can be administered rectally at 0.5-2 mg/kg (2 mg/kg if Dogs and Cats
the clog is receiving phenobarbital) or

A variety of drugs can be used to stop
intranasally at 0.5 mg/kg. Rectal cliazepru11
seizures in clogs and cats.

has been reconunendecl as at1 at-home
emergency treatment for some dogs that

Benzodiazepines: Diazepam is the most
have clusters of seizures; it can be
common benzodiazepine used in dogs and
administered up to three times in a 24-hr
ca.ts to reduce motor activity and permit
period by owners.

placement of an lV catheter. When used

Other benzodiazepines that can be
as an lV bolus (0.5-2 mg/kg), the dose may
used in clogs to stop seizure activity are

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2595

•h=i!j1:• ANTIEPILEPTIC DRUGS (continued) Time to

Steady State

Therapeutic Level

Adverse Effects/Comments

<24hr

4---16 mg/La

Sedation, dizziness, ataxia, fatigue,

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(7 0 -120 µmol/1)

diarrhea; reduce dose with renal
dysfunction.

2-3days

35-120 �m101/L"

Restlessness, vomiting, ataxia at dosages

>40 0 mg/kg/day

3-5days

2-25mg/L

GI upset, irritability

(15-60 µmol/L)a

<24 hr

Probably ineffective due to very short
half-life; liver, alopecia, and pancreatitis;
vomiting usually avoided by giving drug
with food.

3--4 days

10--40 mg.IL

Sedation, ataxia, loss of appetite.

(45-180 µmol/1)

Potential adverse effects ( eg, keratoconjunctivitis sicca, bone marrow dyscrasia, hepatopatlly, vasculitis, and metabolic
acidosis) could occur because of
sulfonamide base.

clonazepa.111 (0.05-0.2 mg/kg, IV; the IV form
ter sites. After IV administration, propofol
of tile drug may not be available in tile USA), rapidly crosses the blood-brain barrier a.11d lorazepa.Jll (0.2 mg/kg, every 4---6 hr), and
usually has an onset of action of d min.

midazolain (0.2 mg/kg, IV or IM; CRI dose

However, the duration of action after a

0.0 5-0.5 mg/kg/hr).

single bolus is only -2-5 min. When used
as a single dose (2.5--4 mg/kg, IV) in dogs

Barbiturates: Phenobarbital is often
and cats, -25% of the calculated dose is
used in status epilepticus cases to prevent
administered every 30 sec until the desired
further seizure activity. For animals not
effect is reached. If seizures recm after 1-2
already on maintenance phenobarbital, a
injections, a propofol CRI (0.05-0.2 up to 0.4
loading dose of 15 mg/kg, slow IV or IM,
mg/kg/min) can be used if definitive airway
can be used. Alternatively, 3-6 mg/kg, IV
control and hemodynan1ic support are
or IM, can be administered every 15-30
available and if the a.Jlirnal ca.11 be closely
min to attain the desired serum concentramonitored. During IV injection, seizme-like tion; serum level increases by -5 mcg/mL
signs of excitement, paddling, nystagmus,
for every 3 mg/kg dose of phenobarbital. It muscle twitching, and opistllotonos may is usually not necessary to exceed a total
sometin1es be seen.

dose of 20 mg/kg. If injectable phenobarbi

Sodium pentobarbital is generally
tal is effective in preventing or controlling
reserved for treatment of uncontrollable
seizures, an oral maintenance dose may
status epilepticus in dogs and cats,
be initiated, with the pla.11 to decrease or
especially when diazepain and phenoba.t"

stop injectable anticonvulsa.11t infusions
bital have failed (see TABLE 17). In tllese with.in the following 24 hr. Caution is necesspecies, it is administered at 2-15 mg/kg to sary when administering both diazepain
effect for anestllesia. Pentobai·bital is a
and phenobarbital, because a potentiation
respiratory depressant, so respiratory
of their effects increases tile risk of
assistance must be readily available. The
respiratory a.11d cardiovascular collapse.

drug is irritating if administered perivas

Propofol is a short-acting IV hypnotic
culai·ly or subcutaneously. As the animal
anesthetic agent that may have anticonvulrecovers from the drug's effects, excitesant activity because it is GABA-mimetic, ment may occur, which can be mistaken
stabilizing GABA-inhibitory new·otransmit-
for seizme activity.

2596

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

Inhalation Anesthesia: ln some cases,
be tapered gradually over a few weeks to
inhalation anesthesia is necessary to control
avoid precipitating a seizure. Tape1ing
or stop seizure activity. This requires constant phenobarbital is crucial, because it is monitoring and mechanical ventilation.

addictive and can result in withdrawal
seizures if stopped abruptly.

VetBooks.ir

Alternative Methods to Stop a

Seizure: Phenytoin at 2-5 mg/kg has been
used as a slow IV infusion in dogs to stop a

Maintenance Antiepileptic Drugs
seizure. Ocular compression (application of

(Anticonvulsants)

digital pressure to one or both eyes) may be

In dogs, phenobarbital and bromide are
beneficial via stimulation of the vagus nerve. considered first-line maintenance AEDs, An implantable pacemaker device that
but levetiracetam and zonisamide are often
delivers repetitive stimulation to the left
used as well. ln cats, phenobarbital is the
ce1vical vagus nerve has been investigated
usual first choice, but levetiracetam and
in dogs and may be of benefit in some
zonisarnide a.re becoming more acceptable;
epileptic animals. Acupuncture points KID 1
dia.zepam is an alternative choice. In
and/or GV 26 might also be of benefit.

ruminants, phenobarbital is the first choice;
in horses, both bromide and phenobarbital
have been used.

MAINTENANCE

ANTICONVULSANT OR

Phenobarbital: Phenobarbital has a long

ANTIEPILEPTIC THERAPY
record of safety, efficacy, low cost, and
convenience in regard to monitoring sernm

The decision to start maintenance
concentrations. For longterm maintenance
anticonvulsant or antiepileptic therapy
in ca.ts and dogs, phenobarbital may be
should be based on the frequency and
given at 2-4 mg/kg/day, PO, bid. In all
severity of the seizures, the age of onset,
species, it takes -2 wk to approach a
the likely cause(s) of the seizures, and the steady-state plasma concentration, because results of diagnostic testing. In general, a
oral absorption is extremely variable and
maintenance antiepileptic drug (AED)

the half-life is long. Drug levels a.re
should be considered in animals that have monitored 2 wk after initiation of therapy, had more than one or two seizures within

2 wk after any dosage change, and usually
a 6-mo period (assuming these seizures
every 6--12 mo once seizure control is
were not caused by repeated toxin
achieved. Serum therapeutic concentraexposure) or in animals that have had tions are 15-45 mcgtmL. The dosage should
more than one seizure of unknown cause
be adjusted on the basis of serum level and
on any particular day. A maintenance
the history of seizure control. Tolerance to

AED should also be considered if the first
phenobarbital therapy may develop in dogs
seizure episode is protracted or severe,
treated continually for months to years and
or during an episode of status epilepticus
may result in decreased seizure control;

(as a followup to emergency treatment,
however, an increase (25%) in the dose
seep 2591).

usually will result in improved seizure

Treatment should begin with a single
control.

drug at the minimal required level for

Phenobarbital causes physical depeneffect. Owners should keep a calendar to dence, and thus abrupt withdrawal may
document the frequency and pattern of
ca.use "barbiturate withdrawal" seizures.

seizures as a guide for treatment strategy.

Hepa.totoxicity and liver failure in dogs

This calendar, in conjunction with serum
have been associated with high serum

AED levels, can be used as a guide for
concentrations (>35 mcgtmL), necessitatdosage and drug treatment changes. lf ing the serum level checks every 6--12 mo.

seizure control is unsatisfactory, the drug

Adverse effects such as sedation, polydiplevel should be checked. If the level is not sia, polyuria, and polypha.gia are common
within the middle of the therapeutic range,
but may decrease within tl1e first few
the dose should be increased before adding
weeks. Other, less common adverse
or switching to a new drug. Doses may be
effects a.re idiosyncratic hyperexcitability,
doubled in early stages and increased by
dermatitis, anemia, neutropenia, tl1rombo25%-500/c, in later stages. Monotherapy is cytopenia, gingival hyperplasia, and
prefe1Ted, but if the drug level is well into
osteomala.cia.. Phenobarbital has also
the middle or high therapeutic range, it may
been used to treat episodic dyscontrol
be necessary to consider the addition of
syndrome (rage) in dogs when seizure
another AED. To discontinue any AED,
activity is demonstrable via electroenexcept bromide, the dose of the drug should cephalogram recordings.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2597

Oral phenobarbital has been used in
loading dosage of 400-600 mg/kg of bromide
rwninants at 11 mg/kg/day and in horses at
is divided into four doses and given with

3---11 mg/kg/day. Senun concentrations
food over a 1- to 4-day period. Smaller
should be checked periodically.

doses, such as 50 mg/kg, bid for 4-6 days,
may reduce adverse effects ( eg, nausea and

VetBooks.ir

Bromide: Bromide appears to stabilize
vomiting) caused by rapid increase in serum
neuronal cell membranes by interfe1ing
bromide concentrations. The regular
with chloride transport across cell
maintenance dose can be started at the
membranes and by potentiating the effect
same tin1e as the loading dose or immediof GABA via hyperpolarizing membranes.

ately afterward. The loading dose regimen

Bromide (potassiwn or sodium salt) can
can be discontinued if the dog becomes too
be used as a first-choice AED in dogs with
sedated, or smaller divided daily doses can
epilepsy, as an adjunctive AED in dogs with
be tried. A serwn sample can be submitted
refractory seizure disorders, or for dogs
within 2 wk after loading to detem1ine
that have unacceptable adverse effects
whether a therapeutic level has been
related to phenobarbital or other AEDs. In
reached. (lf cost is an issue, however, a
countries where bromide is not available as
sample is best checked in 4 mo when
a pharmaceutical formulation (USA), ar1
steady-state concentrations have been
ar1alytical grade may be obtained from a
reached.) The therapeutic range for
chemical supply compar1y, although caution
bromide is 1-2 mg/mL (10-20 mmol/L) with
is recommended in handling and packaging.

concuffent phenobarbital treatment, or 1-3

Bromide can be formulated into a solution
mg/mL (10-30 mmol/L) for bromide as a
of various concentrations (100 mg/mL, 200
monotherapy. However, the dosing regimen
mg/mL, 250 mg/mL are convenient ones) or
needs to be tailored for each animal; the
into tablets or capsules.

upper end of the therapeutic range is only

The elimination half-life is extremely long
limited by adverse effects of bromide.

(24 days) in dogs; therefore, it takes -4 mo

Bromide is generally well tolerated by
to achieve steady state kinetics. Bromide
dogs, but potential adverse effects include
is renally eliminated and thus should not be
bitter taste, gastric irritation, nausea
used in dogs with renal dysfunction without

(particularly with the potassiwn form),
careful monitoring. lf azotemia is present, a
polywia, polydipsia, polyphagia, sedation,
different AED can be used, or the initial
ataxia, and pancreatitis. It should be
bromide dose can be reduced by half and
administered with food; the amount and
serwn concentrations monitored. Because
type of food given should be kept constant,
it does not undergo hepatic metabolism,
because variable dietary salt content will
bromide is useful in dogs with liver disease.

affect the elin1ination of bromide via the

As adjunct therapy with phenobarbital,
kidneys. Bromide tl1erapy must be titrated
potassium bromide can be administered at
to the individual anin1al based on careful

20-40 mg/kg/day, PO, either as one dose or
therapeutic drug monitoring and careful
divided into two or more doses; the sodiwn
monitoring by the owner for early signs
bromide dosage is slightly lower at 17-30
of toxicity. Reports of hindlirnb weakness
mg/kg/day, PO. When bromide is used as the
should be investigated as potential bromide
sole treatment for epilepsy in dogs, higher
toxicosis by measuring serum bromide
dosages (50-80 mg/kg/day) may be
concentration and discontinuing bromide
necessary. Dogs on a high salt diet may
for several days to see whether the
require dosages of 50-80 mg/kg/day to
weakness improves. Severe bromide
maintain adequate senun concentrations,
toxicosis (bromism) is characterized by
because high chloride intake increases
lethar·gy, disorientation, delliiwn, and
bromide loss in the urine and lowers senun
ataxia progressing to quadriplegia and
bromide concentrations. Many laboratory
coma. Bromide toxicity can be seen at any
assays carmot distinguish between sernm
concentration in an unusually sensitive dog,
bromide and chloride ions, so serum
but it is rar·e when bromide is used alone and
chloride values may be rep01ted as falsely
when serum concentrations are <1.5 mg/mL
high.

(15 mmol/L). When used in combination

Because a daily maintenance dose may
with phenobarbital, bromide toxicity car1 be
take 4 mo to reach steady state serum
seen at concentrations of 2-3 mg/mL (20-30
concentration, there are situations ( eg,
nunol/L). Severe signs of toxicity are easily
severe seizures, seizures that occur on a
treated by IV adn1inistration of 0.99(, sodiun1
monthly basis, the need to rapidly switch
chloride, which promotes renal excretion of
from phenobarbital to bromide because of
the bromide ion.

phenobarbital toxicity) when a loading dose

Bromide is an effective maintenance AED
of bromide should be administered. An oral
in cats, but the incidence of adverse effects

2598

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM
does not warrant its routine use unless there Acute hepatic failure has been repo1ted is no other choice. Approximately 25%--500,-6
in cats given diazepam for behavioral
of cats administered bromide developed
problems; thus, a pretreatment chemistry
signs of bronchial disease characterized by
profile should be evaluated before using
a cough and marked pulmonary infiltrates
diazepam, and cats should be watched

VetBooks.ir
seen on radiographs. In some cases, the
closely during the first 2 wk of use.

asthmatic changes were fatal, but in most
cases the signs resolved after discontinua

Newer or Adjunctive
tion of bromide.

Bromide has been used in horses as

Anticonvulsants
a maintenance AED, but there are no

Levetiracetam: This pyrrolidine-based
published studies on its clinical efficacy.

anticonvulsant has an unknown mechanism

Pharmacokinetic studies have suggested
of action. It has been used as an a(\junct
that a loading dose of potassiun1 bromide of

AED for dogs and cats and is occasionally

120 mg/kg/day over 5 days and maintenance
used as monotherapy. In clogs, it has
dosages of --90--100 mg/kg/day will likely
excellent oral bioavailability, does not
result in effective sernm bromide concenappear to undergo hepatic metabolism, is trations.

prin1arily excreted unchanged in the urine,
and has a half-life of --4 lu-. It appears very

Primidone: Prirnidone is a barbiturate that
safe with no to few adverse effects (ataxia,
has tlu-ee metabolites: phenobarbital,
sedation, vomiting) repo1ted at the routine
primidone, and phenylethyh11alonamide. TI1e
dosage ranges. Levetiracetam is initially
phenobarbital metabolite is likely the major
administered at 20 mg/kg, PO, tid, in dogs;
functional one, and there may not be an

10--20 mg/kg, PO, tid, in cats. 1f adverse
advantage to using p1irnidone over
effects occur, the dosage should be reduced
phenobarbital. Nevertheless, one report
to 20 mg/kg, bid, and increased to 20 mg/kg,
indicated that dogs with seizures that are not
tid, gradually. Studies suggest that 600,-6 of
well controlled witl1 phenobarbital may
clogs respond initially; however, after 4-8
respond better to printidone ( eg, psychomomo, tl1ere is a loss of effect in ll, of previous tor seizures). TI1e initial dosage ( dogs only) is
responders because of development of

5--15 mg/kg/day in tlu-ee divided doses,
tolerance. In dogs, the dosage can be
increased over time to a maximw11 of 35
increased every 2 wk in increments of 20
mg/kg/day. Effective se1U111 levels are
mg/kg if therapeutic benefit has not been
determined by the serw11 level of phenobarbinoted. Adverse effects of salivation, tal (15-45 mcg/rnL). lf printidone is switched
restlessness, vontiting, and ataxia at
to phenobarbital, one grain of phenobarbital
dosages >400 mg/kg/day have been seen
can be substituted for 250 mg printidone.

experimentally in dogs but resolved within

Prin1idone may be more likely to cause

24 hr of discontinuing the drug. Therapeutic
hepatotoxicity than phenobarbital, and it
monitoring is generally not necessary when
has been associated with hepatic necrosis
using this drng, and there does not appear
and lipidosis and bile canaliculi obstrnction. to be a correlation between serum drug ALT, sernm alkaline phosphatase, and/or
concentration and therapeutic efficacy.

bile acids should be monitored. Other

An IV formulation can be used in status
adverse effects and signs of overdosage
epilepticus.

are sinlilar to those of phenobarbital.

Printidone is not recommended for use in

Zonisamide: Titis sulfotian1ide-based
cats because of toxicity concerns. However,
anticonvulsant restiicts the propagation
preliminary studies suggest printidone at 40
and spread of seizures and suppresses
mg/kg/day for 90 days may be acceptable in
epileptogenic focus activity. It has been
cats.

used as first-line AED as well as an adjunct

AED in dogs not adequately controlled by

Diazepam: Diazepam is not suitable for
phenobarbital and bromide. Although some
oral maintenance therapy in dogs, because
of it is metabolized by tl1e P450 enzyme
it is absorbed poorly, has a short half-life of
system, much is excreted W1Changed in the

2.5--3.2 hr, and tolerance to its anticonvulurine. Dogs receiving concurrent drug sant effects develops rapidly. However, cats
therapy known to induce hepatic microsonot only have a longer half-life (15--20 hr) mal enzymes (ie, phenobarbital) require
than dogs but also do not develop a
nearly twice the dosage of zonisan1ide to
tolerance to the anticonvulsant effects.

acltieve and maintain serW11 concentrations

Thus, diazepam can be used as a maintethan dogs receiving zonisamide alone. Thus, nance treatment in cats, with dosages
the dose of zonisamide in clogs receiving
ranging from 0.25--0.5 mg/kg, PO, bid-tid.

phenobarbital is 10 mg/kg, PO, bid. In dogs

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2599
not on drugs that induce hepatic microsoanemia and liver toxicity. There is no mal enzymes, the dosage is 5 mg/kg, PO,
clinical information on use of felban1ate in
bid. The dosage in cats has varied from 5
cats.

mg/kg, PO, bid, to 5-10 mg/kg/day, PO. The
recommended therapeutic range is 10-40

Valproic Acid: Valproic acid (10-60 mg/

VetBooks.ir
mg/mL; trough concentrations can be
kg, tic!) has been used as an adjunct to
measured -7-10 days after initiating
phenobru·bital and prin1idone in dogs with
treatment or altering the dosage. The
refractory seizures. It has also been used to
adverse effects are usually mild, such as
treat aggressive behavior problems ( see
transient ataxia, loss of appetite, lethargy,
p 2601). Common adverse effects include
and vomiting. Although the drug appears
transient GI distress, alopecia, sedation,
safe, owners should be warned that because and vomiting. Hepatic failure is rare. Use of the sulfonamide base, potential adverse
of valproic acid in dogs is lin1ited because
effects ( eg, keratoconjw1ctivitis sicca, bone
of rapid metabolism.

mruTow dyscrasia, hepatopathy, vasculitis,
and metabolic acidosis) could occur. A

Clonazepam: Clonazepan1, unlike
nonfatal hepatopathy in a clog was
diazeprun, can be used in dogs for oral
attributed to zonisru11ide.

maintenru1ce therapy, because anticonvulsant tolerru1ce develops less rapidly, the Gabapentin: This synthetic analogue of
saturability of its metabolism reduces the
the inhibitmy neurotransmitter 1-aminoelimination rate at therapeutic concenbutyric acid (GABA) inhibits seizure activity trations, and because it is more highly via multiple mechanisms, including
absorbed orally (pruticularly in micronized
inhibition of neuronal sodiwn channels and
fonnulations). For maintenance therapy
potentiation of the release and action of
in dogs, it may be used alone at 0.5 mg/kg,

GABA. It is well absorbed in dogs after oral
tid, but it is best used as an adjunct to
administration and undergoes both hepatic
phenobru·bital at dosages of 0.1-0.5
and renal metabolism. In dogs, the initial
mg/kg/day. Diarrhea sometin1es develops
dosage is 10-15 mg/kg, PO, tid. Higher
with clonazeprun, but this may be avoided
dosages (30-60 mg/kg, PO, tid-qid) may be
by starting with once daily dosing and
necessruy but can produce sedation and
increasing the frequency to tJu·ee times
ataxia. If excessive sedation occw-s, a lower
daily over a period of several days.

dose should be used initially and gradually
increased. Therapeutic monitoring is not

Carbamazepine: Carbamazepine is not
usually necessruy with this drug. No drug
recommended for use in dogs because of
interactions have been reported. Gabapena rapid induction of hepatic enzymes that tin has been used in cats at 5-10 mg/kg,
elin1inate the drug quickly. Although plasma
bid-tic!.

concentrations declined rapidly in dogs on
a 1-wk regirnen of 30 mg/kg, tid, one case

Felbamate: Felba.mate is a dicru·ban1ate
report described adequate seizure control

AED that exerts its ru1ticonvulsant effects
despite undetectable drug concentrations
through multiple mechanisms, including
in plasma, possibly due either to an active
potentiating GABA-mediated neuronal
metabolite or to a highly sensitive drug
inhibition, inhibiting voltage-sensitive
reaction. Cai·ban1azepine has been used to
neuronal calciun1 and sodium channels, and
treat aggressive behavior problems in cats
blocking N-methyl-o-aspartate-mediated

(seep 2601).

neuronal excitation. It is primarily (70%)

renally excreted in dogs, with the remainder

Clorazepate Dipotassium: Clorazepate
of the drug undergoing hepatic metabolism.

dipotassimn (0.5-1 g/kg, tic!) has been

The reconunended initial dosage is 15 mg/
proposed as an adjm1ct to phenobarbital
kg, PO, tid, but the dose can be increased
treatment in dogs. Severe withdrawal
every 14--21 days in increments of 15 mg/kg
symptoms, even lethal seizures, may apperu·
if therapeutic benefit has not been noted.

after abrnpt discontinuation of chronic

The principle advantage of felbrunate is a
clorazepate treatment, in spite of the
lack of sedation, and adverse effects are
relatively low tolerance liability of clorazereportedly rare. Potential adverse effects pate. Administration of phenobarbital alters
are hepatotoxicity, reversible myelosupthe deposition of clorazepate such that the pression, generalized tremors, and possibly
an1ount of nordiazeprun in circulation during
keratoconjunctivitis sicca; regular
each dose interval is significantly reduced.

monitoring for anemia and liver dysfunction Adequate control of seizures in epileptic in dogs is reconunended. ln people,
dogs, therefore, may require higher dosages
felbrunate has been associated with aplastic
of clorazepate when coadministered witl1

2600

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM
phenobarbital. However, clorazepate may

Topiramate: Topiramate is a newer
increase phenobarbital concentrations,

AED that is well tolerated by people and
resulting in adverse effects.

increasingly used for neuropathic pain. In
one report, it was listed as an adjunct AED

Phenytoin: Phenytoin (ctiphenylhydanfor dogs, but its effectiveness is not yet VetBooks.ir
toin) is no longer recommended for mainteknown. Because the elimination half-life is nance use in dogs, cats, or foals because of
short in dogs (2-4 hr), it is probably not an
undesirable pharmacokinetic properties.

effective anticonvulsant, but a dosage of

Its metabolism is too rapid in dogs, which

5-10 mg/kg, bid, has been suggested. There
reduces its effectiveness, and too slow in
have been no clinical studies to date, and
cats, which increases the risk of toxicity
only limited infom1ation is currently

( salivation, vomiting, weight loss). In foals,
available.

phenytoin has erratic plasma concentrations.

It may still be used in status epilepticus in

TRANQUILIZERS, SEDATIVES,
dogs as a slow IV irtjection of 2-5 mg/kg.

AND ANALGESICS

Mephenytoin: Mephenytoin, although

Tranquilization reduces anxiety and induces
related to phenytoin, has been effective in
a sense of tranquility without drowsiness.

dogs (10 mg/kg, tid) because of a slower

Drug-induced sedation has a more profow1d
rate of elimination. It may be combined
effect and produces drowsiness and
with phenobarbital or bromide. Adverse
hypnosis. Analgesia is the reduction of pain,
effects consist of sedation only, but perioctic
which according to a drug's effect, may be
hematologic monitoring is advised, because
more pronounced in either the viscera or
blood dyscrasia and hepatotoxicity are
the musculoskeletal system (seep 2104).

reported in people.

Many drugs cannot be categorized by only

TRANQUILIZERS AND SEDATIVES WITHOUT ANALGESIC

EFFECTS

Dosage

Drug

Dogs

Cats

Ferrets

BENZODIAZEPINES

Diazepam

1-mg/kg, IV or PO
l mg/kg,IV

2 mg/kg,IM

Midazolan1

0.2-0.4 mg/kg, IV or IM

0.2-0.4 mg/kg, IV
or IM

BUTYROPHENONE

Azaperone

PHENOTHIAZINES

Acepromazine

0.05-0.1 mg/kg, IV, IM, or

0.11-0.22 mg/kg, IV, 0.1-0.25 mg/kg,
maleate

SC; 0.55-2.2 mg/kg, PO,

IM, or SC; 1.1-2.2

IM or SC
tid-qid
mg/kg, PO, bid-tid

Chlorpromazine

0.55-4.4 mg/kg, IV; 1.1-6.6 1-2 mg/kg, IV or IM,
hydrochloride
mg/kg, IM; 3.2 mg/kg, PO, bid
tid-qid as needed

Promazine

2-6 mg/kg, IV, IM, or PO,

2-4.4 mg/kg, IV, IM,
hydrochloride
tid-qid
or PO, tid-qid

Triflupromazine

1.1-2.2 mg/kg, IV;

4.4-8.8 mg/kg, IM
hydrochloride

2.2-4.4 mg/kg, IM

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2601
one phannacologic effect, ie, as tranquilizextra-label use, or precautions in the use ers, sedatives, or analgesics. For exan1ple,
of these drugs; the product label and
many psychotropic drugs can either
referenced texts should be consulted for
tranquilize or sedate according to the dose
infom1ation on the pham1acology and
administered, and many sedatives are also
alternative applications of each drug.

VetBooks.ir
analgesics. Also, drugs classified as
tranquilizers, sedatives, and/or analgesics
may have additional effects ( eg, behavioral

PSYCHOTROPIC AGENTS
modification, antiemesis).

For drugs commonly used in various

Anxiolytics, antipsychotics, antidepresspecies for tranquilization, sedation, or sants, and mood stabilizers used to treat
analgesia, see TABLES 19 and 20. Drugs that human behavioral disorders are being used
have some of these effects but are
more corrunonly in veterinary medicine as
used mainly for other properties ( eg, as
acljuncts to behavioral modification therapy
antispasmodics, antiemetics, or preanes

(see ai,so PRINCIPLES OF PHARMACOLOGIC AND
thetics) are not listed. Single-use doses

NATURAL TREATMENT FOR BEHAVIORAL PROBLEMS,
are emphasized because many situations
p 1543). Few veterinary clinical studies have
require only a brief dll!'ation of effect, but
been reported, and guidelines for veterinary
frequency of administration is also provided
use are grounded on therapeutic applicafor drugs likely to be used for multiple-dose tions in human medicine.

therapy. The dosages listed serve only as
a general guideline and apply to the use
of each drug alone, not to a combination

Anxiolytics
for anesthesia or neuroleptanalgesia. No

Anxiolytics, including the benzodiazepines
reference is made to schedule restrictions,
and an azapirone (buspirone), have been

TRANQUILIZERS AND SEDATIVES WITHOUT ANALGESIC

EFFECTS (continued)

Dosage

Rabbits

Horses

Cattle

Pigs

BENZODlAZEPINES

1-5 mg/kg, IV, IM;

0.05-0.4 mg/kg, IV

0.5-1.5 mg/kg, IV 0.5-10 mg/kg, IM;

2-10 mg/kg, IM or IP

0.5-1.5 mg/kg, IV

2 mg/kg, IM or IV

BUTYROPHENONE

0.4-0.8 mg/kg, IM

2.2 mg/kg, IM

PHENOTHIAZINES

1-5 mg/kg, IM

0.04-0.l mg/kg/day,

0.05--0.1 mg/kg,

0.1--0.2 mg/kg, IV,

IV, IM, SC, or PO

IV, IM, or SC

IM, or SC

3 mg/kg, IV or IM (may

0.5-4 mg/kg, IM
produce myositis)

0.4-1 mg/kg, IV or IM; 0.4-1 mg/kg, IV or 0.4-1 mg/kg, IV or 1-2 mg/kg, PO

IM; 1.6--2.8 mg/kg, IM

PO

0.22-0.33 mg/kg, IV or

IM (maximum 100 mg/
horse/day)

2602

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM
itM•f 1·• ANALGESICS

Dosage

Drug

Dogs

Cats

Ferrets

VetBooks.ir

OPIOID ANALGESICS•

Buprenorphine

0.01-0.02 mg/kg, SC, bid

0.005-0.01 mg/kg,

0.01-0.03 mg/kg,

SC or IM, bid

TV, IM, or SC,
bid-tid

Butorphanol

0.2---0.4 mg/kg, IM or SC;

0.1---0.2 mg/kg, TV;

0.05---0.4 mg/kg,
tartrate

0.55 mg/kg, PO, every

0.2---0.4 mg/kg, IM or IM, every 4-6 hr

6---12 hr

SC, every 4 hr

Medetomidine

0.002-0.03 mg/kg, IM, TV, 0.002-0.03 mg/kg,
or SC

IM, TV, or SC

Meperidine

2-10 mg/kg, IM or SC,

2-5 mg/kg, IM or

2-5 mg/kg, IM or
hydrochloride
every 2 hr

SC, every 2 hr

SC, every 2-4 hr

Morphine sulfate

0.22-0.88 mg/kg, IM, TV

0.1 mg/kg, IM or SC, 0.5-5 mg/kg, IM
slowly, or SC, every 4-6
as needed
orSC,qid
hr as needed

N albuphine

0.5-2 mg/kg, SC, every

1.5-3 mg/kg, TV,

4-Shr
every 3hr

0>.s'Ymorphone

0.05-0.1 mg/kg, TV, IM, or 0.025-0.05 mg/kg,

0.05-0.2 mg/kg,
hydrochloride

SC, every 1-3 hr

TV, IM, or SC

TV or IM, bid-qid

Pentazocine lactate 2 -3 mg/kg, IM, every 4 hr;

5-10 mg/kg, SC

15 mg/kg, PO, tid
or IM, every 4 hr

NONOPIOID SEDATIVE ANALGESICS

Xylazine hydro0.5-1 mg/kg, TV; 1-2 mg/

0.5-1 mg/kg, TV; 1-2 1 mg/kg, IM or
chloride
kg, IM or SC
mg/kg, IM or SC

SC

Detomidine

NON PSYCHOTROPIC ANALGESICS

Acetan1inophen

15 mg/kg, PO, qid as

Contraindicated
needed

Aspirin

10-25 mg/kg, PO, bid

10 mg/kg, PO, every 0.5-20 mg/kg,

48 hr

PO, once to
three tin1es daily

Carprofen

4 mg/kg/day, TV or SC

4 mg/kg/day, TV or

SC

Dipyrone

28 mg/kg, TV, IM, SC, or

28 mg/kg, TV, IM,

PO, tid

SC, or PO, tid

Flunixin meglu-

1-2 mg/kg/day, PO, TV, or Use of flunixin

0.5-2 mg/kg, SC,
mine

IM, up to 3 days; use of
meglumine in cats
once to twice
flunixin meglUllline in
has decreased since daily
dogs has decreased since the introduction of
the introduction of other other NSAIDs with

NSAIDs with higher
higher therapeutic
therapeutic indexes.

indexes.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2603

•tth•f1•• ANALGESICS (continued) Dosage Rabbits

Horses

Cattle

Pigs

VetBooks.ir

OPIOID ANALGESICS•

0.02-0.05 mg/kg,

0.005-0.02 mg/kg,

SC, IM, or IV, bid

IM or IV, bid-qid

0.1-0.5 mg/kg, IV, 0.05-0.1 mg/kg, IV, IM, Adult: 20-30 mg, IV, 0.1-0.3 mg/kg, IM
every 4 hr
or SC
jugular

5-10 mg/kg, IM or 0.2-0.4 mg/kg, IV; 1-3 500 mg/cow, IV

1-2 mg/kg, IM or IV

SC, every 2-3 hr
mg/kg, IM or SC
slowly, IM or SC

2-5 mg/kg, SC or 0.2 mg/kg, IV; 0.2-0.4

0.2-1 mg/kg, IM,

IM, every 2-4 hr
mg/kg, IM
every4 hr

1-2 mg/kg, IV,
every4 hr

0.1-0.2 mg/kg, IM, 0.02-0.03 mg/kg, IV or

0.075 mg/kg, IM
every 2-4 hr

IM

10-20 mg/kg, SC

0.33 mg/kg, IV

2-5 mg/kg, IM,
or IM, every 4 hr;
every4hr

5 mg/kg, IV, every

2-4hr

NONOPIOID SEDATIVE ANALGESICS

0.1-1 mg/kg, IV; 0.5-1 0.05-0.l mg/kg, IV;

2 mg/kg, IM
mg/kg, IM or SC

0.1-0.2 mg/kg, IM

0.02-0.04 mg/kg, IV or

IM

NON PSYCHOTROPIC ANALGESICS

5-20 mg/kg/day,

30-47.5 mg/kg, PO,

26 mg/kg, IV; 100-124 10-20 mg/kg, PO,

PO
bid-qid
mg/kg, PO, bid
every4hr as
needed

1.5 mg/kg, PO, bid 0. 7 mg/kg/day, IV, IM, 0. 7 mg/kg/day, IV, IM, or SC
or SC

5-10 glhorse, IV or IM, 50 mg/kg, IV, IM, or

50 mg/kg, IV, IM, or
tid as needed

SC

SC

1.1 mg/kg, SC or

1-2.2 mg/kg, IV; 2.2

1.1-2.2 mg/kg, IM or 1-2 mg/kg/day, IV

IM, bid
mg/kg/day, IM or PO

PO, once to three
or IM
times daily

2604

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

•iM•f 1'• ANALGESICS (continued) Dosage Drug

Dogs

Cats

Ferrets

VetBooks.ir

Ketoprofen

2 mg/kg/day, SC, IM, or IV, 1 mg/kg/day, SC up
up to 3 days; 1 mg/kg/day, to 3 days, or PO up

PO, up to 5 clays
to 5 days

Meclofenamic acid 2.2 mg/kg/day, PO

2.2 mg/kg/day, PO

Phenylbutazone

15-22 mg/kg, PO; 15 mg/ 15 mg/kg, IV, tid;
kg, IV, bicl-tid (maximum 10-14 mg/kg, PO,

0.8 g/dog/day or 44 mg/
bid; use of
kg/day); use of phenylphenylbutazone in
butazone in dogs has
cats has decreased
decreased since the
since the introducintroduction of other
tion of other

NSAIDs with better

NSAIDs with better
safety margins.

safety margins.

a Recommended dosages of opiates may produce excitement in cats and horses.

used to treat generalized anxiety and panic

Buspi.rone differs from the benzodiazdisorder in dogs and cats, as well as urine epines in phannacologic properties (ie, it
spraying in cats. Benzodiazepines, such as
blocks serotonin pre- and postsynaptically
diazepan1, alprazolam, oxazepam, and
and acts as a dopamine agonist), onset of
clorazepate, act by binding to -y-anlino
action (delayed onset of7-30 days), and
butyTic acid (GABA) receptors and
lack of sedative effect. Buspi.rone appears
enhancing GABA-mediated chloride influx.

to offer no greater control for anxiety

They may cause sedation and muscle
related behaviors than the benzocliazepines,
relaxation; dependence and withdrawal
but it helps treat urine spraying in cats at
signs also can occur.

2.5-7.5 mg/cat.

Diazepam has been recommended to
alleviate fear-related behaviors in clogs and
social anxiety and urine spraying in cats.

Anti psychotics

However, benzocliazepines may not

Antipsychotics are classified as lowalleviate fear-related aggression in certain potency agents (acepromazine, chloranimals but instead may cause a paradoxipromazine, and thioridazine hydrochloride) cal increase in such behaviors. Although
and high-potency agents (haloperidol,
diazepam has been reported to diminish
fluphenazine, trifluoperazine hydrochlourine spraying in cats, most cats resume ride, prochlorperazine, thiothixene,
spraying when the drug is withdrawn.

risperidone). Low-potency agents require

There have been rare reports of hepatic
larger doses and produce more sedation,
failure within 3-5 days of starting diazepan1
more anticholinergi.c adverse effects, and
in cats.

cardiovascular effects, but they have a

Oxazepam ( dogs 0.2-0.5 mg/kg, PO, once
lower incidence of extrapyramidal adverse
to twice daily; cats 1-2.5 mg/cat, PO, bid)

effects (parkinsonism, dystonia, dyskineand alprazolarn have been used to treat sia, and akathisia) than the high-potency
fears and phobias in both dogs and cats. In
agents. All the antipsychotics are used for
addition, alprazolam has been used to treat
nonselective tranquilization and diminishnight-time anxiety in clogs (0.01-0.1 mg/kg, ing behavioral arousal. Acepromazine is

PO) and refractory housesoi.ling in cats (0.1
commonly used for infrequent anxietal
mg/kg or 0.125-0.25 mg [total close] per cat,
episodes, but it may induce a para

PO, bicl-tid). Clorazepate has been used to
doxical hyperactivity in some dogs and
treat anxiety in cats ( 1. 75-3. 75 mg/cat, PO,
cats. In one report, a clog with aberrant
once to twice daily). Diazepam, clonazbehavior (tail chewing, growling, epam, and clorazepate dipotassium also
snapping, barking) was controlled
have anticonvulsant properties.

with thioridazine at 1.1 mg/kg.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM

2605

•tM•f 1'• ANALGESICS (continued) Dosage Rabbits

Horses

Cattle

Pigs

VetBooks.ir

3mg/kg, IM

2.2 mg/kg/day, IV

2.2 mg/kg, IV;

3 mg/kg/day, IM

2.2 mg/kg/day, PO

4.4 mg/kg, PO, bid on 2-5 mg/kg, IV; 4-8

2-5 mg/kg, IV; 4-8
day l; 2.2 mg/kg, PO,
mg/kg,PO
mg/kg,PO
bid for 4 days; 2.2 mg/
kg, PO, daily or every
other day

Mood-stabilizing Drugs

The tricyclic antidepressants include

Mood-stabilizing drugs Oithiurn, carbamazamitriptyline, imipramine, clomipramine, epine, and valproic acid) are tmrelated
and doxepin. Case reports indicate that
chemical compow1ds used in hwnan
treatment success for behavioral disorders
medicine to treat bipolar disorder,
is highly variable an1ong drugs within the
impulsivity, emotional reactivity, and
same chemical class. The antil1istru.11inic
aggression. Carbamazepine and valproic
effect of these agents may be a useful
acid are also antiepileptic drugs. Ca.rban1azadjunct in controlling pruritus due to atopy epine has been used in cats (25 mg/cat, PO,
and food allergies. Adverse effects include
bid) to decrease fear-related aggression
vomiting, diru.Thea, hyperexcitability,
against people, but it may paradoxically
sedation, ru.Thythmias including tachycarincrease aggression against conspecifics.

dia, orthostatic hypot.ension, mydriasis,

Lithiwn is excreted unmetabolized via the
reduced laclimation and salivation, urine
urine. Serum concentration monitoring is
retention, constipation, and weight gain.

necessru.y because of its nru.Tow therapeutic

Widening of the QRS complex on an ECG
index (recommended range: 0.8-1.2 mEq/L). has been used as an early indication of Adverse effects include polyu.ria, polydiptoxicity. It may take 7-30 days for drugs to sia, memory problems, weight gain, ru.1d
be effective. Arnitriptyline hydrochlolide
diarrhea. In one report, lithium (75 mg total
has been used in dogs at 1-2 mg/kg for
dose, bid) was used to treat owner-directed
separation anxiety, anxiety-related
aggression and psychotic behavior (random
aggression, urination due to submission or
air-snapping, pawing) in a Cocker Spaniel.

excitement, and allergy-related pru.ritus,
and in cats at 0.5-1 mg/kg for uline marking
and hypervocalization. Imipraniine

Antidepressants
hydrochloride has been used in dogs at

Antidepressants are classified as tricyclic

2.2-4.4 mg/kg, bid-tid, for wination due to
compounds (tertiru.y ru.nines, secondru.y
submission or excitement. Clomiprru.nine
ru.nines), selective serotonin reuptake
hydrochl01ide has been used in dogs at
inhibitors, and atypical antidepressants.

1-3 mg/kg to reduce lick behavior for cru.iine

They can be used to treat behavioral
lick grru.iuloma ru.id for stereotypies such as
disorders, including obsessive-compulsive
circling ru.id tail chasing, and in cats at
behaviors, stereotypies, aggression, and

0.5 mg/kg. In some countries, it is approved
inappropliate elimination. The mode of
for treatment of separation anxiety in dogs.

action is to block reuptake of serotonin and/

Doxepine has been used in dogs at 3-5 mg/kg.

or norepineph.rine or to reduce neurotrans

Selective serotonin reuptake
mitter turnover. All have a lag time until a
inhibitors, including fluoxetine, sertraline,
behavioral effect is seen.

ru.id paroxetine, have been used to treat

2606

SYSTEMIC PHARMACOTHERAPEUTICS OF THE NERVOUS SYSTEM
psychogenic alopecia, allergy-related
honnones to treat behavioral problems is
pmritus, owner-directed aggression, feaiful
currently considered a "last resort" therapy behaviors, obsessive-compulsive behaviors,
because of the risk of adverse effects. In
and urine marking. It may take 7-30 days for
castrated and intact male dogs, megestrol
these dmgs to be effective. The most
acetate has been used to treat aggression,

VetBooks.ir
common adverse effects ai·e changes in
wine marking, ai1d roan1ing. Likewise, in
appetite and GI signs, although seizures
neutered male cats, megestrol acetate can
have been reported. These drugs inhibit
reduce spraying, but potential adverse
liver P450 enzymes, so drug interactions are
effects of inducing diabetes mellitus,
possible. Dosages for fluoxetine are 1 mg/
manunary gland hyperplasia and adenocarkg/day, PO, for dogs, and 0.5-1 mg/kg/day, cinoma, and bone maiTow suppression

PO, for cats.

make it risky to use. Medroxyprogesterone
acetate, an injectable, long-acting progestin,
has been used to treat aggression, urine

Other Agents and Hormones
marking, and roanting; however, it is rai·ely

Monoantine oxidase inhibitors, such as
used because of the risk of adverse effects
selegi.line, are used for cognitive impairai1d availability of other, safer behavioral ment in aging dogs. The use of progestin
drugs.

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE REPRODUCTIVE SYSTEM

See also PlllNCIPLES OF THERAPY OF THE
like effects in domestic anin1als, is used for

REPRODUCTIVE SYSTEM, p 1328.

stin1ulation of gonads ( as a test for cryptor

Dmgs used to regulate or control tl1e
chidism and also for treatment of ovarian
reproductive system are often naturally
cysts in cattle or clogs). It is also used to cause
occurring honnones or chemical modificaovulation of mature ovarian follicles in cows tions of hom10nes. Gonadotropin-releasor mares in controlled-breeding progran1S.

ing hormone (GnRH) and its analogues are
hCG is given parenterally; plasma levels peak
used for treatment of ovarian cysts and for
in -6 hr. It is primarily distributed to fue
control of ovarian follicular .dynantics in
ovaries in females and tl1e testes in males,
cattle, for estrus induction (by pulsatile
altl1ough some is also distributed to the renal
administration) in mares and bitches, and
proxin1al tubules.

for stimulation of testicular function ( eg, in

Equine chorionic gonadotropin (eCG)

testing for cryptorchidism ). Implants of
has FSH activity in most species and is used

GnRH analogues ( eg, deslorelin) are effective to induce ovarian folliculai· growth, both for for induction of estrus and ovulation in mares superovulation and for estms induction.

and bitches and, in higher doses over a

(See also HORMONAL CONTROL OF ESTRUS, p 2244, prolonged pe1iod, ai·e useful for contracepat1d MANAGEMENT OF REP!lODUCTIO)'I: CATTLE, tion in male and female anin1als ( such as
p 2171 et seq.)

dogs) by mediating longterm (�12 mo)

Estradiol esters ( eg, valerate, cypionreversible infertility caused by downregulaate, or propionate) have a longer duration of tion of GnRH receptors.

action than the pai·ent compound. These

Follicle-stimulating hormone (FSH),
compounds are used in bitches, mares, and
usually extracted from animal pituitary
cows for induction or enhancement of
glands, stimulates follicular growth and
fertile estms or for induction of estrous
estrogen production in females and
behavior; treatment of urinary incontinence
spermatogenesis in males. It is used for
in bitches; and for antitun10r activity in
superovulation of several domestic species.

prostatic and perianal tumors. Availability

It has also found application in induction
of these compounds and restrictions on
of fertile estms in bitches and queens.

fueir use vary by country. Estrogenic

Prolonged FSH use or higher doses can
therapy may cause bone maITow supprescause adverse effects such as cystic sion and potentially fatal aplastic anemia
endometrial hyperplasia and follicular cysts. in dogs and cats; its use is also associated Human chorionic gonadotropin (hCG),
with development of cystic endometrial
which exerts mainly luteinizing hormone--
hyperplasia in these species, and it may

SYSTEMIC PHARMACOTHERAPEUTICS OF THE REPRODUCTIVE SYSTEM

2607
have teratogenic effects in pregnant
induce predictable onset of estrus ( or
animals. Because of these potential
synchronization of estrus) in a variety of
complications, estrogens are no longer
species. They may also be used for
recommended for termination of pregnancy
termination of pregnancy either alone or in
in cases of mismating.

combination with corticosteroids ( cattle,

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The nonsteroidal synthetic compound
sheep) or dopaminergic agents (dogs).

diethylstilbestrol also has estrogenic

These compounds also ca.use marked
activity; its use is prohibited in food animals
uterine contractions, which may be useful
in the USA. Estrogen antagonists, such as
for expulsion of uterine contents in
tamoxifen, have been proposed for
pathologic conditions ( eg, pyometra.).

treatment of metastatic mammary

Oxytocin is used to promote milk
carcinoma in dogs.

letdown, to treat agala.ctia, as an adjunc

Progesterone and synthetic progestive treatment of mastitis, and to cause tins are used for suppression or postponecontraction of the uterus either to induce ment of estrus in bitches and queens. They

( or supplement) labor or to enhance
have also been used in behavior modificapostpartum uterine contraction and tion and to treat dem1atologic disorders.

expulsion of uterine fluid or fetal mem

Progesterone supplementation is used to
branes. It is administered parenterally
support pregnancies regarded as at risk

(IV, IM, or SC). Oxytocin may be given

( eg, in pregnant mares with potentially
intranasa.lly, but absorption can be en-atic.

endotoxemic conditions) and in horses or

Uterine relaxation is ca.used by f32-min1etic
clogs with demonstrated hypoluteoidism.

agents, such as clenbuterol. Such agents

Adverse effects of progestin administration
have been used to postpone parturition (to
in small animals include induction of cystic
reduce obstetrical complications in heifers)

endometrial hype1plasia, adrenocortical
and to facilitate obstetric manipulations in
suppression, induction or exacerbation of
large domestic animals. Clenbuterol use in
diabetes mellitus, and mammary gland
food-producing anin1als is illegal in the
development. Mifepristone (a progester

USA.

one-receptor antagonist) has been used

Dopa.minergic agents, such as
experimentally as a canine abortifa.cient;
bromocryptine or ca.bergoline, cause
epostane, a progesterone-synthesis
decreased serum prolactin concentrations.

inhibitor, also terminates canine pregnancy.

They are useful in treatment of pseudopreg

Testosterone is used for estrus
nancy in dogs (brornocryptine at 10 mcg/kg,
suppression (particularly in racing

PO, for 10 days, or at 30 mcg/kg for 16 days)

Greyhounds). Mibolerone, a weak
and as an adjunct to PGF2cx in terminating
androgenic steroid, is used to prevent estrus pregnancy, although not approved in the in bitches. It should not be used in

USA for this use. Prola.ctin is luteotrophic.

Bedlington Terriers or ca.ts, and it may
in some species, including dogs.

exacerbate perianal tumors. After PO

Dopa.mine antagonists, such as
administration, mibolerone is absorbed
sulpiride, have shown promise in the
from the intestine, metabolized in the liver,
manipulation of seasonal breeding
and excreted in the urine and feces. Chronic
species-their use hastens the onset of
administration of testosterone may ca.use
estrous cycles in mares in the spring.

testicular degeneration in male anin1als.

In the UK and New Zealand, melatonin is

Finastetide, a 5cx-reductase inhibitor,
labeled for use in sheep (and goats in New
prevents the conversion of testosterone

Zealand) to improve early breeding and
to 5cx-dihyclrotestosterone, the active
ovulation rates. It is available as an 18-mg
androgen in male accessory sex glands. It is

SC implant; combined with exposure to
useful in the treatment of benign prostatic
rams, its use is associated with hastened
hyperplasia of dogs (0.1-0.5 mg/kg/day, PO).

onset of the breeding season and increased

Flutan1ide blocks dihydrotestosterone
prolifica.cy.

receptors and is used for the same purpose.

Glucocorticoids, especially the C-16

Chemical modifications of testosterone
substituted steroids dexa.methasone,
potentia.te its anabolic actions while
beta.methasone, and flumethasone, are used
minimizing virilizing effects. These
for induction of parturition in rwninants
compounds (eg, boldenone undecylena.te,

( eg, dexamethasone 20-30 mg, IM, given
stanozolol, nandrolone decanoa.te) are used
within 2 wk of normal tenn). Their
for their anabolic effects in convalescing or
therapeutic administration may inadverathletic animals. Protracted use may cause tently lead to abortion. Xyla.zine and other
at least temporary infertility in both sexes.

cx2-a.drenergic agents ca.use myometrial

Prosta.gla.ndin F 2 a and its analogues are contraction that may harm the fetus or used ma.inly for their luteolytic effects to
impede obstetrical manipulations.

2608

SYSTEMIC PHARMACOTHERAPEUTICS OF THE REPRODUCTIVE SYSTEM

EFFECT OF REPRODUCTIVE

Jones may affect developing cartilage,

THERAPY ON THE FETUS OR
and tetracyclines affect bone and tooth

NEONATE
development. Teratogenicity has been
associated with use of the antifungal agents

VetBooks.ir

An important component of reproductive
g1iseofulvin and ketoconazole in pregnant
pharmacology encompasses the effect
ai1in1als. All cai1cer chemotherapeutic
of treatment on the fetus or neonate of
agents are potentially harmful to developing
medication administered to pregnant or
fetuses. Glucocorticoids may induce
lactating dan1s that are nursing. Many
palatoschisis or other defects in puppies.

factors influence the ability of a drug to

Any administration of medication to
cross the placenta, including placental
lactating animals requires consideration of
architecture of the particular species, but in
the excretion of the drug or its metabolites
general, drugs that are lipid-soluble,
in milk ai1d of the effects on suckling
nonionized, and of low molecular weight
neonates. Milk produced for human
can be expected to cross the placenta
consumption must be free of potentially
readily. An1ong antimicrobials, aminoglycoharmful residues, and all relevant Jaws and sides are associated with nephrotoxicity
regulations regarding usage and appropriate
and ototoxicity in the fetus, fluoroquino-
withdrawal tin1es should be followed.

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE RESPIRATORY SYSTEM

See also PRINCIPLES OP THERAPY OP RESPIRATORY
infection. ln dogs and cats, coughing occurs

DISEASE, p 1416.

because of a prin1ary disease process, such

Drugs used to treat respiratory tract
as Bordetella bronchiseptica infection
diseases fall into several categories:

("kennel cough") or chronic bronchitis in
antitussives, bronchodilators, anti-inflanunadogs, or feline asthma or heartwom1-associtories, expectorants, decongestants, and ated respiratory disease in cats. ln most
respiratory stirnulai1ts. ln addition, antinticrocases, addressing the prin1ary disease will bials and antifungals are in1p01:tant in tl1e
resolve the cough. Antitussive therapy is
therapy of many respiratory diseases.

symptomatic and is primarily for the
comfort of the animal and the owner. Most
antitussive drugs are opiates or opioids

ANTITUSSIVE DRUGS
that directly suppress the cough center in
the medulla oblongata (see TABLE 21). The

A cough is a sudden, explosive exhalation
antitussive effect does not appeai· to be
of air tl1at functions to cleai· mate1ial from
related to the binding of traditional opiate
the airways. Coughing is one way in which
receptors (mu and kappa). For exan1ple,
tl1e lungs and airways are protected from
dextromethorphan is an opioid derivative
inhaled particles. Coughing sometimes
with good antitussive activity, but it does
brings up sputum (also called phlegm), a
not have activity at opiate receptors and is
mixture of mucus, debris, and cells expelled
not analgesic or addictive.

from the lungs. The cough reflex has both

Morphine is an effective antitussive
sensory (afferent) and motor (efferent)

at doses lower than those that produce
pathways. The internal laryngeal nerve
analgesia and sedation. It is not commonly
carries the sensory inforrnation away from
used for antitussive activity because of
the area above the glottis in the trachea to
adverse effects and tl1e potential for abuse
the cough center located in the medulla
ai1d addiction. Morphine has poor oral
oblongata via the vagus ne1ve. Stimulation
bioavailability due to a significai1t first-pass
of tlus area by dust or foreign particles
effect by the liver.

produces a cough to remove the foreign

Codeine is methylmorphine; methylamaterial from the respiratory tract before it tion of morphine significantly improves
reaches the lungs. Mucus production in the
the oral bioavailability by reducing the
bronchi is an airway defense mechaiusm,
first-pass effect. Codeine phosphate and
and it increases with inflanm1ation and
codeine sulfate are found in mai1y

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM

2609
itM•ili ANTITUSSIVE DRUGS

Drug

Dosage

Codeine

Dogs: 1-2 mg/kg, PO, bid-qid

VetBooks.ir

Hydrocodone

Dogs: 0.25 mg/kg, PO, bid-qid

Butorphanol

Dogs: 0.055-0.11 mg/kg, SC, bid-qid, or 0.55-1.1 mg/kg, PO, bid-qid Cats: 0.1-0.4 mg/kg, SC, bid-qid
preparations, including tablets, liquids,

SPECIES APPROACH TO
and syrups. Codeine has analgesic effects

INFLAMMATORY AIRWAY
that are about one-tenth that of morphine,
but its antitussive potency is about equal

DISEASE
to that of morphine. The adverse effects of Dogs, cats, horses, and people develop codeine are significantly less than those
spontaneous bronchoconstriction
seen with morphine at antitussive doses.

associated with airway inflammation and

Toxicity ( especially in cats) is exhibited as
characterized by chronic cough and wheeze.

excitement, muscular spasms, convul

Attacks of airway obstruction are induced
sions, respiratory depression, sedation,
by exposure of susceptible animals to
and constipation. Codeine should not be
antigens (typically hay dust, molds, and
used after GI tract surgery because of its
pollens). Effective therapy of allergic airway
effects on intestinal motility. The potential
disease is species dependent because of
for addiction and abuse of codeine is
the inflammatory mediators involved in
considerably lower than that for morbronchoconstriction. The pathogenesis of phine.

feline asthma differs from allergic airway

Hydrocodone is chemically and pharmadisease in other species in that cats are cologically similar to codeine but more
exceptionally responsive to serotonin
potent. It is combined with an anticholiner

(5-hydroxytryptamine). Serotonin, which
gic drug (homatropine) to discourage abuse is released from degranulating mast cells, by people. It can be prescribed for small
appears to be the major mediator of
animals but should be used with caution in
allergen-induced bronchoconstriction in
cats.

cats. Cats also appear to suffer from chronic

Dextromethorphan is technically not
bronchitis, similar in clinical presentation to
considered an opiate, because it does not
feline asthma; the main feature that differen-.

bind to traditional opiate receptors and is
tiates these two conditions is the lack of
not addictive or analgesic. It is the o-isomer
bronchoconstriction in chronic bronchitis.

of levorphanol. The L-isomer of levorphanol

In dogs, chronic bronchitis is an inflammahas addictive and analgesic properties.

tory, chronic pulmonary disease that results

Although it is recommended anecdotally to
in cough and can lead to exercise intolertreat cough, a pharmacokinetic study in ance and respiratory distress but is typically
dogs demonstrated a short elimination
not characterized by severe bronchoconhalf-life, rapid clearance, and poor oral striction. In horses, there are two clinical
bioavailability, making its use as an orally
syndromes of airway inflammation.

administered cough suppressant in dogs

Recurrent airway obstruction, or "heaves,"

questionable.

is an inflanunatory, obstructive airway

Butorphanol, an opioid agonist-antagodisease clinically evident in middle-aged nist, is used as an analgesic and antitussive
horses. Inflammatory airway disease is a
in dogs. As an antitussive in dogs, butorphalow-grade inflammation of the small nol is 4 times more potent than morphine
airways that is a common cause of poor
and 100 times more potent than codeine.

performance in young to middle-aged,

At antitussive dosages, it may produce
athletic horses. Inflanunatory airway
considerable sedation in dogs. Because
disease is typically not treated in ruminants
butorphanol has poor bioavailability, the
or swine.

oral dose in dogs is 10 times the SC dose.

The goals of therapy for inflammatory

In cats, butorphanol is primarily used as
airway disease are to prevent recurrent
an injectable analgesic. In some cats, it may
exacerbations of airway obstruction and
cause pain on injection, as well as myd1iareduce emergency visits and expenses, to sis, disorientation, swallowing/licking, and
provide optimal chronic anti-inflammatory
sedation.

therapy with minimal or no adverse effects,

2610

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM
to maintain (near) "nom1al" pulmonary
nonspecific stimulation of other receptors
function, and to meet the owner's expectaand its short dmation of action make it tions of quality of life for their animal.

unsuitable for longterm use. Epinephrine is
available as a 1 mg/mL solution. Its onset of

VetBooks.ir

SYSTEMIC THERAPY OF
action is immediate, and the duration of

INFLAMMATORY AIRWAY
effect is 1--3 hr.

DISEASE

Isoproterenol is a potent 13-receptot'

agonist. It is selective for 13 receptors, but
cardiac (13,) effects make it unsuitable

13-Adrenergic Receptor Agonists:

for longtenn use. It is administered by

The 13-adrenergic receptor agonists have
inhalation or injection and has a sho1t
beneficial effects in treatment of bronduration of action ( <l hr). For emergency choconstrictive respiratory tract diseases
relief of bronchoconstriction in horses, it is

(see TABLE 22). Bronchial smooth muscle given by slow IV solution at a dilution of
is inne1vated by l3,-adrenergic receptors.

0.2 mg/50 mL of saline. Administration i.S

Stimulation of these receptors leads to
discontinued when the heart rate doubles.

increased activity of the enzyme adenylate

Terbutaline is a 13
cyclase, increased cAMP, and relaxation of

2-receptor agonist
similar to isoproterenol but longer acting
bronchial smooth muscle. Stin1ulation of

(6----8 hr). It may be available in some

13 receptors on mast cells decreases the recountries as an injectable solution, powder lease of inflan1111atory mediators from mast
inhaler, or oral syrup and tablets. For ca.ts
cells, but other inflammatory cells are not
with feline asthma that experience frequent,
suppressed. There is some evidence that
severe bronchoconstrictive episodes

13-adrenergic receptor agonists increase
despite chronic glucocorticoid therapy,
mucociliary clearance in the respiratory
injectable terbutaline can be dispensed to
tract. The 13-adrenergic receptor agonists
owners with instructions to administer 0.01
should be used with caution in animals
mg/kg, SC, to treat episodes of bronchoconwith preexisting cardiac disease, diabetes striction at home. An increase in the cat's
mellitus, hyperthyroidism, hype1tension, or
heart rate to 240 bpm and a 50"A, decrease in
seizme disorders, or that are being treated
respiratory rate indicates a positive effect.

with digoxin, tricyclic antidepressants, or

Terbutaline also can be given as chronic oral
monoamine oxidase inhibitors.

therapy at 0.625 mg/cat, bid(\!,\ of a 2.5-mg

Epinephrine (adrenaline) stimulates a
tablet). It should not be used in cats with
and 13 receptors, resulting in pronounced
hypertrophic cardiomyopathy or glaucoma,
vasopressive and cardiac effects in addition
in which 132-receptor stimulation would be
to bronchodilation. Epinephrine is rese1ved
detrimental.

for emergency treatment of .life-tJu·eatening

Albuterol (salbutamol) is sintilar to
bronchoconstriction (eg, anaphylaxis). The
terbutaline and may be used systemically in

•th•ffj 13-ADRENERGIC RECEPTOR AGONIST DRUGS

Drug

Dosage

Epinephrine

Dogs: 0.05-0.5 mg, intratracheally or IV

Cats: 0.1 mg, IV or IM

Large animals: 0.1 mg/kg, IV, SC, or IM

Isoproterenol

Dogs: 0.1-0.2 mg, IM or SC, qid

Cats: 4-6 mcg, IM, every 30 min as needed

Horses: 0.4 mcglkg, IV (diluted)

Terbutaline

Dogs, cats: 0.1 mg/kg, SC, every 4 hr, or 0.03 mg/kg, PO, tid Horses: 0.0033 mg/kg, IV, or 0.2-0.6 mg/kg, PO, bid

Albuterol

Dogs: 0.05 mg/kg, PO, tid

Horses: 8 mcglkg, PO, bid

Clenbuterol

Horses: 0.8--3.2 mcglkg, PO, bid

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM

2611
dogs and horses. Oral syrup, oral tablets,
animals in most countries and should not be
and oral extended-release tablets are
used in horses that will be sent to slaughter.

available, but albuterol is more commonly
used as inhalation therapy.

Methylxanthines: The methylxanthines,

Clenbuterol is used in the treatment

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particularly theophylline, are bronchodi.laof recUITent airway obstruction in horses; it tors (see TABLE 23). Once the mainstay of is not used in dogs and cats. It is available as
human asthma therapy, theophylline has a
an oral syrup and may be available as an
high incidence of adverse effects, and its
injectable solution for IV injection in some
use has diminished with the development
countries. Results of efficacy studies for
of metered-dose or disk inhalers for local
bronchoconstriction have been conflicting,
drng delivery. The methylxanthines have a
but clenbuterol appears to significantly
variety of pharmacologic effects on various
increase mucociliary transport in horses
organ systems, including bronchial smootl1
with the disorder. The dosage is increased
muscle relaxation, CNS stimulation, mild
gradually until a satisfactory clinical
diuresis, and mild cardiac stimulation.

response is seen. If there is no response at

The respiratory effects of methylxanthe highest recommended dose, the horse thines are the result of several cellular
is considered to have irreversible bronchomechanisms. Antagonism of adenosine is spasm. It should not be administered

CUITently thought to be the most inlportant
chronically to horses with recUITent airway
action. Adenosine induces bronchoconstlicobstrnction without concUITent anti-inflamtion in asthmatic animals and antagonizes matory therapy. The most common adverse
adenylate cyclase. Adenylate cyclase is
effects of clenbuterol are tachycardia and
responsible for the synthesis of cAMP,
muscle tremors. Clenbuterol inhibits
which controls bronchial smooth muscle
uterine contractions, so it should be used
relaxation and inhibits the release of
dUiing late pregnancy only if this effect
inflammatory mediators from mast cells.

is desired for obstetric manipulations.

Metl1ylxanthines also inhibit phosphodies

Clenbuterol is also a repartitioning agent; it
terase, which further increases inti·acellular
directs nutrients away from adipose tissue
cAMP. They also inhibit calcium mobilizaand toward muscle. The result is increased tion in smooth muscle, inhibit prostaglancarcass weight, increased ratio of muscle to din production, augment the release of
fat, and increased feed efficiency. Because
catecholamines from storage granules,
there is a significant hUinan health risk from
and increase the availability of calcium
clenbuterol residues, it is banned in food
to contractile proteins of the heart and

•th•if• METHYLXANTHINE BRONCHODILATORS

Drug

Dosage

Theophylline (parenteral)

Dogs: IO mg/kg, IV (slow) or IM

Horses: 15 mg/kg, IV (slow)

Theophylline ( oral)

Dogs: 5-7 mg/kg, PO, tid

Cats: 3 mg/kg, PO, bid

Horses: I0-15mg/kg, PO, bid

Theophylline ( extended-release tablets)

Dogs: 20 mg/kg/day, PO

Cats: 25 mg/kg/day, PO

Horses: 15 mg/kg/day, PO

An1inophylline (parenteral)

Dogs: IO mg/kg, IV (slow)

Cats: 5 mg/kg, IV (slow)

Horses: 5 mg/kg, IV (slow)

An1inophylline ( oral)

Dogs: IO mg/kg, PO, tid

Cats: 5 mg/kg, PO, bid

Horses: 15 mg/kg, PO, bid

2612

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM
diaphragm. In addition to promoting
effective bronchodilators that reduce the
bronchial smooth muscle relaxation,
sensitivity of irritant receptors and inhibit
methylxanthines decrease the release of
vagally mediated cholinergic smooth
inflanunatory mediators from mast cells
muscle tone in the respiratory tract.

VetBooks.ir
and increase mucociliary transport.

Cholinergic stin1ulation causes broncho

Theophylline is available in several
constriction; asthmatic individuals appear
formulations, including ir\jectable, aqueous
to have excessive stimulation of cholinergic
solutions, elixirs, tablets, and capsules.

receptors.

Theophylline base is poorly soluble in water

Atropine is primarily used as a
and often results in GI irritation when
preanesthetic to prevent bradycardia and
administered PO. Aminophylline is a
reduce ail'way secretions, and as emergency
theophylline salt that is 78o/o--86% theophyltherapy of dyspneic aninlals with organoline. It is more water soluble and results in phosphate intoxication. Atropine is also
less GI irritation. Other theophylline salts,
used for bronchodilation in horses; a low IV
such as oxtriphylline (a choline salt), aye
dose (0.014 mg/kg) is more effective and
available, and their theophylline content
less toxic than IV theophylline. A test dose
must be considered when developing a drug
of 0.022 mg/kg may also be used to
dosage regimen.

determine prognosis in horses with

Several sustained-release formulations
recurrent ail'way obstruction; if pulmonary
of theophylline are suitable for use in dogs
function does not improve with a test dose
and cats and may be administered less
of atropine, successful management with
frequently than the regular formulations.

bronchodilators is unlikely. Atropine should

After oral administration, theophylline is
be used with caution, because even low
rapidly and completely absorbed. Therapeudoses may cause tachycardia, ileus, tic plasma concentrations, extrapolated
neurologic derangement, and blurred vision
from people, are 5---20 mcg/mL. Animals are
in horses.

sensitive to high concentrations of

Glycopyrrolate is twice as potent as
theophylline, especially after rapid IV
atropine in people and does not cross the
administration, and toxicity may be seen
blood-brain barrier. Its onset of action is
with concentrations <20 mcg/mL. Theophylslower than atropine, but its duration of line tablets may become trapped in bezoars
effect is longer. Information about use in

( such as hairballs in cats), and continued
horses is sparse, but doses of 2-3 mg can
absorption can result in toxicity. Cardiac
be given IM, bid-tid.

arrhytlunias, CNS excitement, tremors,

N-butylscopolammonium bromide is
convulsions, and GI irritation may be seen.

an anticholinergic drug approved to relieve

Theophylline undergoes enterohepatic
spasmodic colic in horses. Unlike atropine,
recirculation, so activated charcoal is

N-butylscopolan1moniurn bromide does not
recommended if clinical signs are present,
cross the blood-brain barrier. Adverse
no matter how long after the drug was
effects are mininlal and include transient
administered. Theophylline metabolism
tachycardia, decreased borborygmi, and
is inhibited by erythromycin, ci.rnetidine,
transient pupillary dilatation. In horses with
propranolol, enrofloxacin, and marbofloxarecmTent ail'way obstruction challenged cin; concomitant therapy can result in
with moldy hay, N-butylscopolanunonimn
theophylline toxicity. Theophylline
bromide was a potent bronchodilator, with
metabolism is induced by rifampin and
maximum relief occurring 10 min after IV
phenobarbital, which may necessitate
adnlinistration. The bronchoclilatory effect
increasing the dose of theophylline.

is short lived, dissipating within 1 hr of drug

Theophylline is used to treat both cardiac
administration.

and respiratory diseases in dogs and cats.

Theophylline is also used in management of
intrathoracic collapsing trachea and various Glucocorticoids: The glucocorticoids forms of canine bronchitis, but it is less
inhibit the release of inflammatory mediators
effective than glucocorticoids such as
from macrophages and eosinophils but do
prednisone. Theophylline or arninophylline
not inhibit tl1e release of granules from mast
was used in horses in the management of
cells. Glucocorticoids decrease synthesis of
recurrent ail'way obstruction, but efficacy
prostaglandins, leukotrienes, and plateletwas often poor and use of these drugs has activating factor, which play important roles
been replaced by [3-agonist bronchodilators
in the pathophysiology of respiratory tract
delivered by metered-dose inhalers.

inflammation. Studies suggest glucocorticoids enhance the action of aclrenergic Anticholinergic Drugs: The antichoagonists on a2-receptors in the bronchial linergic (parasympatholytic) drugs are
smooth muscle. Because ofirnmunosuppres-

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM

2613
sive effects, glucocorticoids a.re generally
co kinetic studies of cyproheptadine suggest
avoided in infectious respiratory diseases.

that some cats may require doses as high as

For severe attacks of canine bronchitis,

8 mg to reach therapeutic concentrations.

feline asthma, or recurrent airway obstruc

Because of its long elimination hall�life (12
tion, parenteral injection of glucocortihr), cyproheptacline requires several days to VetBooks.ir
coids usually provides rapid relief. For
reach steady-state concentrations, and 4-7
chronic therapy in dogs, oral prednisone is
days may be needed to see clinical effects.

usually the drug of choice. Prednisone is a

Serotonin antagonism in the appetite center
prod rug; it is metabolized by the liver to the
stimulates appetite, so weight gain may be a
active drug prednisolone. Pha.rmacokinetic
problem. Lethargy, depression, and
studies have shown poor oral bioava.ilabilincreased appetite may occur within 24 hr ity of prednisone in cats and horses.

of initiating therapy.

Therefore, it is preferable to administer
prednisolone to these species. In dogs,

Antimicrobial Therapy: Antinlicrobial
a typical anti-inflan1matory dosage is
therapy may or may not be necessary in

0.5-1 mg/kg, with chronic therapy on an
treatment of airway inflammatory diseases.

every-other-day basis. A similar dose

Antimicrobial therapy should be started
of prednisolone can be used in cats; if
for cats with tracheobronchial cultures
prednisone is used, higher doses may
suggestive of a true bacterial infection or
be necessary. Cats a.re somewhat resistant
those positive for Mycoplasma. Myco
to the effects of glucocorticoids, and
plasma spp can be isolated from healthy
dosages of prednisone of l mg/kg/clay may
clogs but a.re not found in healthy cats.

be necessary for chronic therapy of feline

Doxycycline, a.zitllromycin, and fluoroquinasthma. Alternatively, 20 mg of methylpredolones treatMycoplasma infections nisolone acetate can be administered IM to
effectively. Secondary bacterial infection
asthmatic cats every 3 wk. For emergency
from Streptococcus zooe-pidemic'lls may
treatment of clyspneic cats, a shock dose of
exacerbate inflanll11atory airway disease
an TV glucocorticoid (prednisone sodium
in horses and can easily be treated witll
succinate, 5-10 mg/kg; or dexamethasone
penicillin, ceftiofur, or a trimetl10prirn/
sodium phosphate, 1-2 mg/kg) should be
sulfonan1ide.

used. It is common for clinical signs to
resolve in cats with feline asthma or

INHALATION THERAPY OF
chronic bronchitis that a.re treated with

AIRWAY DISEASE
oral glucocorticoids despite persistent
lower airway inflan1mation, so therapy

The current approach to management of
should be tapered very carefully. Although
in11anll11atory airway disease is through
prednisolone can be administered to
inhalation tl1erapy with nebulizers or
horses, the small tablet sizes available
metered-dose inhalers (MDis ). With
make it inconvenient, so equine fonnulainhalation therapy, high drug concentrations of oral clexan1ethasone (10 mg/450
tions a.re delivered directly to tile lungs via
kg) a.re recommended. The injectable
nebulizers or MDis, and systemic adverse
formulation of dexa.methasone can be
effects a.re avoided or nlinirnized. The onset
given TV to horses with acute bronchoconof action for inhaled bronchodilators and striction and dyspnea. Flumethasone or
anti-inflanm1atory drugs is substantially
isoflupredone may also be used in horses.

shorter than tllat of oral or parenteral

Isoflupredone is as effective as clexa.methafommlations. Nebulizers have long been sone in the treatment of recurrent airway
used in animals, but the overall efficiency of
obstruction in horses, but as in cattle, it is
drug delivery is low, and the equipment is
associated with hypokalemia.

cumbersome and inconvenient for owners.

Administration of medications via MDis

Cyproheptadine: Because of the role of
is conll11onplace in treatment of human
serotonin in allergen-induced bronchoconasthma and seems to benefit management striction in cats, the serotonin antagonistJ
of animals as well. Human MD Is a.re
antihistamine cyproheptadine (2 mg, PO,
designed to provide optimal lung delivery
once to twice daily) may be used as an
after act11ation during a slow, deep
adjunct to glucocorticoids and bronchoclilainhalation. However, this is in1possible to tors to block bronchoconstriction in
control in animals. The addition of spacers
chronically asthmatic cats. In experimental
enables MD Ts to be used in anirnals. Spacers
models of feline asthma, cyproheptacline
decrease tl1e a.mount of drug deposited in
decreased airway hyperreactivity but did
the oropha.rynx ( up to 8096 of the actuated
not significantly decrease eosinophilic
close with the MDI alone), thereby reducing
airway inflammation. However, pha.rrna-
systenlic drug absorption. Drugs available

2614

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM
in MDI fommlations include �ragonists,
plugging. In general, �2-agonists are
glucocorticoids, ipratropiwn bromide,
extremely safe for use in animals when
cromolyn sodiwn, and nedocromil. Each
used as needed for bronchoconstriction.

product delivers a set an1ount of drug per

Toxicity typically requires a large overdose,

VetBooks.ir
actuation (puff). In the USA, MDis are
such as when dogs chew on and puncture
labeled according to the an1ount of drug
the inhaler, receiving a very large dose at
delivered at the mouthpiece, whereas in
one tinle (there are 200 doses in an

Canada and the EU they are labeled
albuterol/salbutamol inhaler). Massive
according to the amount of drug delivered
overdose may induce severe tachycardia
from the valve. MDis are color-coded to aid
and hypokalemia, which, in turn, lead to
identification. Even in human medicine, the
extreme weakness, incoordination, and
relative potencies, risks of adverse effects,
potentially cardiac standstill. Other less
and optimal dose of the different inhaled
serious signs include dilated pupils, severe
asthma medications remain unclear.

agitation and hyperactivity, hypertension,

Unfortunately, some drugs that would
and vomiting.

be useful in veterinary patients are not

Albuterol (salbutamol) is the medication
available in MDis; dry powder inhalers are
of choice in all species for inhalation
not suitable for use in anin1als. Clinical use
therapy of acute airway obstruction. It
of MDI medications in asthmatic cats, dogs
relaxes smooth muscle and increases
with chronic bronchitis, and horses with
airflow within minutes of administration;
recurrent airway obstruction is promising
effects last 3-6 hr. Although effective for
but mostly anecdotal, and clinical trials are
symptomatic relief, the �2-agonists do not
needed to detennine the most efficacious
control inflammation, and monotl1erapy
therapies.

may exacerbate asthma and increase
morbidity and mortality. Racemic albuterol

Spacers: MDis (eg, OptiChamber.,.M,

(R, S albuterol) is the most commonly

AeroChamber®) used in hwnan patients
prescribed short-acting �2-agonist and is
may be modified for use in dogs and cats,
composed of al: 1 mixture of (R)-albuterol
and small aninlal-specific spacers are

(the R enantiomer) and (S)-albuterol (the
available (eg, AeroKafrM, AeroDawgTM,

S enantiomer). The R-enantiomer has

Feline Breathe EasyTM, Nebu]aifTM). The
bronchodilatory and anti-inflan1matory

OptiChamberTM must be modified with a
effects, and the S-enantiomer paradoxically
suitable face mask, such as the type used to
is associated with increased airway

"mask" cats for anesthesia. The AeroChamhyperreactivity and pro-inflammatory ber is available with a variety of face masks
effects. The paradoxical exacerbation of
intended for infants, children, and adults
asthma with regular use of inhaled racemic
that will conform to-a variety of veterinary
albuterol in people is thought to be linked
patients. The N ebulair and Feline Breathe
to preferential accwnulation of S-albuterol

Easy spacers are valveless, so the actuation
in the lung, which has a much slower
must occur with the mask applied to the
metabolism than R-albuterol. Neutrophilic
face of the anin1al. The AecoKat and
airway inflan1mation in healthy cats was

AeroDawg are equipped with "flapper"

induced when receiving treatment with
valves so the dog or cat can be visualized
albuterol containing the S-enantiomer.

breathing in the medication. MDis were

These data suggest that the fonn of
originally used in horses via the Aeroalbuterol commonly prescribed to mask TM, but the mask is bulky and rather
asthmatic cats can actually cause inflamexpensive. The Aerohippus""' is sinlilar to mation in "healthy" cats without preexistthe AeroKat and AeroDawg, with a large, ing airway disease. The S-enantiomer also
bell-shaped cone that fits over a horse's
exacerbates eosinophilic airway inflammanostril. It also has a valve indicator.

tion in experin1entally asthmatic cats. This
increase in airway inflammation associated

132-Agonists: Short-acting �,-agonists with use of albuterol can be attenuated by
such as albuterol (salbutamol) in MDis
concurrent use of glucocorticoids. Proper
are the medications of choice to treat acute
control of the underlying inflan1mation
exacerbations of bronchoconstriction,
should reduce albuterol use to an as-needed
because they relax smooth muscle and
only basis. One actuation (100 mcg Canada;
promptly increase airflow. Although

90 mcg USA) of albuterol can be adminiseffective for symptomatic relief, �2-agonists tered for relief of bronchoconstriction as do not control inflan1mation. Airway
needed until clinical signs resolve.

obstruction may persist despite approptiate

Salmeterol is a long-acting �2-agonist; its
use of inhalant bronchodilators because of
onset of action is slow (15-30 min), but its
bronchial wall edema and airway mucus
duration of action is> 12 hr. The long

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM

2615
duration of action is due to diffusion into
augmented muscarinic receptor response
the plasma membrane of the pulmonary
to acetylcholine. Modulation of muscaiinic
cells followed by slow release from the
receptors with anticholinergic drugs may
cells to interact with l?,2 receptors. It is not
be usefol to treat asthmatic cats. Ipratro

VetBooks.ir
recommended for use in acute bronchoconpiun1 has shown efficacy for recUffent striction, but daily use with glucocorticoids
airway obstruction in horses. It is not well
provides better control of symptoms than
absorbed after inhalation, so it does not
simply increasing the glucocorticoid dose.

cause systemic ai1ticholinergic effects.

It is not available in an MDI in all countries,
and the dry powder inhaler is not suitable

Cromolyn Sodium and Nedocromil:

for animal use.

Cromolyn sodium and nedocromil sodium

Other l?,2-agonists that may be available
are chloride-charmel blockers that
in MDis include isoproterenol, fenoterol,
modulate mast cell-mediator release and
formoterol, and terbutaline. Isoproterenol
eosinophil recruitment. They are both
was conunonly used to treat asthma before
available in MDis. Cromolyn sodium and
the more widespread use of albuterol,
nedocromil sodium have strong hwnan
which has more selective effects on the
safety profiles, but nedocromil sodium has
airways. In Europe, an epidemic of deaths
been reported to have a broader spectrwn
due to cardiotoxicity from overuse of
of efficacy. In people, the clinical response
isoproterenol inhalers led to withdrawal of
to these drugs is less predictable than the
the products. North American products
response to glucocorticoids. There are no
have clear warning labels regarding the
published reports of the use of cromolyn or
potential toxicity.

nedocromil in asthmatic cats or dogs with
bronchitis; however, pretreatment with

Glucocorticoids: Inhaled glucocorticoids
nedocromil sodium aerosols attenuated
are the most potent inhaled anti-inflanunaviral-induced airway inflan1111ation in tory drugs available. In people, early

Beagle puppies. Further investigation of
intervention with inhaled glucocorticoids
these drugs in asthmatic cats seems
improves asthma control, nom1alizes lung
wai-ranted given the sensitivity of this
ftmction, and may prevent iffeversible
species to serotonin released from
airway dan1age. The potential risk of
degranulating mast cells.

adverse effects is well balanced by their
efficacy in management of chronic

Lidocaine: Lidocaine, conunonly used as
inflanunation. Oral candidiasis ( thrush),
a local ai1esthetic and antiarrhythmic agent,
dysphonia, and reflex cough and bronchois used as a steroid-sparing treatment in spasm are the most common adverse effects human astluna Initially used topically to in people; all of these effects are reduced
prevent cough during bronchoscopic
by use of a spacer. The risk of systemic
procedures, lidocaine, administered via
adverse effects, such as suppression of the
nebulization, is effective for intractable
hypothalamic-pituitary axis, is less than
cough and asthma by inhibition of
with oral prednisone therapy. Inhaled
eosinophil-active cytokines. Nebulization
glucocorticoid fonnulations include
provides direct drug delivery to the lung,
fluticasone, beclomethasone, flunisolide,
with minimal systemic drug absorption and
and triamcinolone. Cuffently, fluticasone is
few adverse effects. Nebulized lidocaine
considered the most potent fom1ulation
reduced airway hyperresponsiveness in
with the longest duration of action and is
experimentally asthmatic cats but did not
the most commonly used inl1aled glucocoraffect airway eosinophilia, so it probably ticoid in veterinary patients.

should be combined with glucocorticoids
in management of feline asthma.

lpratropium Bromide: Ipratropium
bromide is a quaternary derivative of

Suggested Treatment Regimens: For
atropine that lacks its adverse effects and
emergency management of dyspnea in cats
is available in an MDI (500 mcg/actuation),
and dogs, 2-4 puffs of albuterol should be
alone or in combination with albuterol. In
given every 5 min until clinical signs resolve.

people with asthma, ipratropiun1 bromide

Additional therapy may include oxygen ai1d
is used as an additional reliever medication
an IV dose of a rapid-acting glucocorticoid.

to reverse bronchoconstriction when

C=ent recommendations for therapy of
inhaled short-acting l?,2-agonists do not
feline asthma and cailine bronchitis are to
provide enough relief. Its anticholinergic
use albuterol only as needed for bronchodiaction also decreases mucous secretions.

lation and fluticasone bid. For initial therapy

In an experin1ental model of feline asthma,
of moderately affected anin1als, a5-day
longtem1 antigen sensitization caused an
course of oral prednisone ( or prednisolone)

2616

SYSTEMIC PHARMACOTHERAPEUTICS OF THE RESPIRATORY SYSTEM
at 1 mg/kg may be helpful. Severely
tl1ione, which is a scavenger of oxygen-free
affected animals may require 1 mg/kg of
radicals. Aerosolization of acetylcysteine
prednisone ( or prednisolone) every other
can cause reflex bronchoconst1iction due
clay. Adjw1ctive therapy with other inhaled
to irritant receptor stimulation, so its use

VetBooks.ir
or orally administered anti-inflammatories
should be preceded by bronchodilator
and bronchoclilators may be useful in some
therapy.

aninlals. Therapy must be individualized for

Dembrexine is a phenolic benzylamine
each animal.

available in some countries for respiratory

For horses with recurrent airway
disease in horses. The proposed effect is
obstruction, environmental management
through an alteration of the constituents
and a combination of bronchodilator and
and viscosity of abnormal respirat01y
anti-inflan1111atory therapy is reconunended. mucus and an improved efficiency of Cun·ent recommendations are to use 500
respiratory clearance mechanisms. It also
mcg of albuterol every 2 hr as needed and
has an antitussive action and enhances
fluticasone at 2--4 mcg/kg bid. Beclomethaconcentrations of antibiotics in lung sone has also been used at 1-3 mcg/kg, bid,
secretions. It is supplied as a powder that
but it causes more adrenal suppression in
is sprinkled on the feed at a dosage of 0.33
horses than fluticasone at these doses.

mg/kg, bid.

EXPECTORANTS AND

DECONGESTANTS

MUCOLYTIC DRUGS

Decongestants are conunonly used in

Expectorants and mucolytic drugs are
people to treat allergic rhinitis, but they
used to increase the output of bronchial
are rarely used for this purpose in aninlals.

secretions, enhance the clearance of

The oc-adrenergic agonist drugs cause local
bronchial exudate, and promote a
vasoconstriction in mucous membranes,
productive cough. Saline expectorants are
which reduces swelling and edema. They
promoted to stinmlate bronchial mucous
are used topically as nasal decongestants
secretions via a vagally mediated reflex
in allergic and viral rhinitis, or systemically
action on the gastric mucosa. However,
in combination witl1 antiltistanlines as
there are no well-designed studies that
respiratory tract decongestants. Antihistasupport these claims. Exan1ples of these mines are effective for treatment of allergic
drugs include ammonium chl01icle,
rhinitis in people when combined with
ammonium carbonate, potassium iodide,
the oc-adrenergic agonist drugs, but their
calciwn iodide, and ethylenediamine
effectiveness in animals has not been
dihydroiodide. Iodine-containing products
demonstrated. The topical oc-adrenergic
should not be administered to pregnant,
agonist drugs act within minutes with few
hyperthyroid, or milk-producing animals.

adverse effects, but extended use may cause

Direct stimulants of respiratory
rebound hyperemia and mucosa! damage.

secretions include the volatile oils, such as

Systemic administration can result in
eucalyptus oil and oil of lenwn. They are
hypertension, cardiac stimulation, urinary
believed to directly increase respiratory
retention, CNS stinmlation, and mydriasis.

tract secretions. Their efficacy in animals

Systemic administration of antihistamines
is unknown.

often causes sedation.

Guaifenesin (glyceryl guaiacolate) is a
centrally acting muscle relaxant that may

RESPIRATORY STIMULANTS
also have an expectorant effect. It may
stinmlate bronchial secretions via vagal

Doxapram stimulates the medullary
pathways. The volume and viscosity of
respiratory center and the chemoreceptors
bronchial secretions does not change, but
of the carotid artery and aorta to increase
particle clearance from the airways may
tidal volume. Other portions of the CNS
accelerate. It is a common component of
are stimulated only when high doses are
hwnan cold remedies in combination with
administered. Doxapram is used primarily
clextromethorphan.

in emergency situations during anesthesia

N-acetylcysteine is available as a 100/o
or to decrease the respirat01y depressant
solution that can be nebulized. Its mucolytic effects of opiates and barbiturates.

effect is the result of the exposed sulfuydryl

Recommended dosages are 1-5 mg/kg,
groups on the compound, which interact

IV, in dogs and cats, or 1-2 drops under
with disulfide bonds on mucoprotein.

the tongue of apneic neonates. In adult

Acetylcysteine helps to break down
horses, the dosage is 0.5-1 mg/kg, IV,
respiratory mucus and enhance clearance.

while foals are dosed carefully at

It may also increase the levels of gluta-

0.02-0.05 mg/kg/min, IV.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM

2617

SYSTEMIC PHARMACOTHERAPEUTICS

OF THE URINARY SYSTEM

VetBooks.ir

See also PRINCIPLES OF THERAPY OF UlllNARY

Pseudomonas spp. In UTis in horses, E coli, DISEASE, p 1496.

Streptococcus, and Enlerococcus spp predominate, whereas Co1ynebacte1ium

BACTERIAL URINARY TRACT
re,iale and E coli are the most common INFECTIONS
pathogens in ruminants. In immunocompromised animals, funguria from Candida spp Bacterial urinary tract infections (UTis)

may occur.

typically result from nom1al skin and GI

Antimicrobials are tl1e cornerstone ofUTI
tract flora ascending the urinary tract
therapy, and many animals with recurring
and overcoming the nonnal urinary tract

UTis are managed empirically with repeated
defenses that prevent colonization.

courses (see TABLE 24). This approach fails if Bacterial UTI is the most common
the underlying patl10physiology preclisposinfectious disease of dogs, affecting 14% of ing the animal to the UT! is not addressed;
all dogs during their lifetime. Although UTis
as well, it encourages emergence of
arc uncommon in young cats, the incidence
resistant bacteria. With chronic UTI from
ofUTI is much higher in older cats, which
highly resistant bacteria, tl1erapeutic
may be more susceptible to infection
options are extremely limited.

because of diminished host defenses
secondary to aging or concomitant disease

Antimicrobial Therapy: Urine culture

(such as cliabetes mellitus, renal failure,
is the "gold standard" for cliagnosis of UTI.

or hyperthyroid.ism). Approximately

Indications to perform urine culture include
two-thirds of those cats also have some
visualization of bacte1ia during mine
degree of renal failure. Bacterial UTis in
sediment exaniination, evidence of pyuria,
run1inants are associated with catheterizadilute urine ( <l.013 SG), inununosupprestion or parturition in females and as both a sion, and cliabetes mellitus or hyperadrenocause and consequence of urolithiasis in corticism. Antimicrobial susceptibility
males. In horses, UTis are uncommon and
testing should be done with complicated
typically associated with bladder paralysis,
or recurrent cases ofUTis, immunosupurolithiasis, or urethral damage.

pressed animals, animals recently

Unlike hun1an patients, veterinary
catheterized, or animals treated with
patients are often asymptomatic, and the
antimicrobials within the preceding 3 wk

UTI may be an incidental finding. The

(because of selection for antimicrobial
consequences of untreated UTI include
resistance). In addition, culture and
lower urinary tract dysfunction, urolith.iasis,
susceptibility testing should be performed
prostatitis, infertility, septicemia, and
in cases that do not respond within 7 clays of
pyelonephritis with scarring and eventual
therapy for UT! or in cases associated with
kidney failure. Coagulase-positive staphylomultiple pathogens.

cocci are involved in the formation of

High urine concentrations of antimistruvite (MgNH,PO,) calculi in dogs. In crobials a.re correlated with efficacy in
intact male dogs, UTI frequently extends to
treatment of uncomplicated cystitis. But
the prostate gland. Because of the bloodin complicated cases and in pyeloneph.ritis, prostate ban·ier, it is clifficult to eradicate
tissue concentrations may be equally
bacteria from the prostate, and the minary
important. Most antimicrobials undergo
tract may be reinfected after appropriate
renal elimination to a great extent, so
treatment, causing a systemic bacteremia,
mine concentrations may be up to 100
infecting the rest of the reproductive tract,
times peak plasma concentrations. Drug
or causing an abscess within the prostate.

excretion through tl1e kidney involves

Large, retrospective stuclies have
various processes such as secretion
documented the most common species
and/or reabsorption in different parts of
of uropathogens in dogs and cats, with
the nephron, depending on tlie molecular

Esche,ichia coli being the single most
structure of the drug, its pl(,., the pH in the
common pathogen in both acute and
tubular fluid, and degree of protein binding.

recurrent UTis. The other common

The flow of wine tl1rough the urinary tract
pathogens include Staphylococcus,
is pa.it of the defense against invading patl10-

Proteus, Streptococcus, Klebsiella, and
gens, because the flow offluid rinses the

2618

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM

DRUGS COMMONLY USED TO TREAT URINARY TRACT INFECTIONS

IN SMALL ANIMALS

Drug

Suggested Dosage

Typical Antimicrobial Activity

VetBooks.ir

Amoxicillin

11 mg/kg, PO, bid-tid

Staphylococci, streptococci,
enterococci, Pmteus, some E coli

Ampicillin

25 mg/kg, PO, tid

Staphylococci, streptococci,
enterococci, Proteus, some E coli

Amoxicillin-clavu25 mg/kg, PO, tid

Staphylococci, streptococci,
lanic acid
enterococci, Proteus, some E coli

Cephalexin/

20-30 mg/kg, PO, bid-tid

Staphylococci, streptococci, Proteus,
cefadroxil

E coli, Klebsiella

Cefovecin

8 mg/kg, SC, every 14 days Proteus, E coli

Cefpodoxime

5---10 mg/kg/day, PO

Proteus, E coli

Ceftiofur

2 mg/kg/day, SC

Proteus, E coli

Choramphenicol

Dogs: 25-50 mg/kg, PO,

Staphylococci, streptococci,
bid-tid
enterococci, E coli

Cats: 50 mg/kg, PO, bid

Doxycycline

5 mg/kg, PO, bid

Streptococci, some activity against

E coli, staphylococci, and enterococci
at high urine concentrations

Enrofloxacin,

2.5---10 mg/kg/day, PO

Staphylococci, E coli, Proteus,
orbifloxacin,

Klebsiella, Pseudomonas, Entero
marbofloxacin,
bacter
pradofloxacin ( cats
only)

Gentamicin

4-6 mg/kg/day, SC

Staphylococci, some streptococci,
some enterococci, E coli, Proteus,

Klebsiella, Pseudomonas, Enterobacter

Nitrofurantoin

5 mg/kg, PO, tid

Staphylococci, some streptococci,
enterococci, E coli, Klebsiella,

Enterobacter

Tetracycline

18 mg/kg; PO, tid

Streptococci, some activity against

E coli, staphylococci, and enterococci
at high urine concentrations

Trimethoprim-sulfa 15 mg/kg, PO, bid

Streptococci, staphylococci, E coli,

Proteus, some activity against

Klebsiella
epithelial linings. High mine antimicrobial
selected antimicrobial should be easy for
concentrations are important for eraclicaowners to administer, have few adverse tion of bacteria in the urine, but for infection effects, and be relatively inexpensive. Once of the bladder wall or renal tissue it is
mine culture and sensitivity results are
necessary to use antimicrobials that have
known, the bacterial minimum inhibitory
active concentrations in the tissues. Sernm
concentration (MIC) can be compared with
or plasma concentrations are useful
the mean urinary concentration of the drug
surrogate markers for antimicrobial concenand an appropriate antimicrobial chosen.

trations in the renal or bladder tissues.

Amoxicillin and ampicillin are

In addition to having the appropriate
bactericidal and relatively nontoxic, with a
antimicrobial activity and achieving
spectrum of antibacterial activity greater
effective concentrations in urine, the
than that of penicillin G. They have

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM

2619
excellent activity against staphylococci,

Cefpodoxime is an oral, third-generation
streptococci, enterococci, and Proteus, and cephalosporin approved for use in dogs for
may achieve urinary concentrations high
skin infections (wounds and abscesses), but
enough to be effective against£ coli and
it is used extra-label for treatment of canine

Klebsiella. Pseudomonas and Enterobacter UTI. Cefpodoxin1e has a relatively long

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are resistant. Amoxicillin is more bioavailhalf-life in dogs, so it is dosed once daily.

able in dogs and cats (better absorbed from

Ceftiofur is an ir\jectable cephalosporin
the GI tract) than ampicillin, hence the
approved for respiratory disease in horses,
lower dosage. Absorption of ampicillin is
swine, and cattle and for treatment of
also affected by feeding, so therapeutic
canine UTI caused by E coli and Proteus.

success may be easier to achieve with

Ceftiofm has pharmacokinetic properties
amoxicillin. As penicillins, they are weak
very different from those of other cephaloacids with a low volume of distribution, so sporins. After il\iection, ceftiofur is
they do not achieve therapeutic concentrainm1ediately metabolized to desfmoylceftitions in prostatic fluid.

ofur, which has different antimicrobial

Amoxicillin-clavulanic acid has an
activity than the parent compound. Desfmincreased spectrum of activity against oylceftiofm has equivalent activity to
gram-negative bacte1ia because of the
ceftiofm against E coli (MIC 4 mcg,'mL) but
presence of clavulanic acid. Clavulanic acid
is much less active against Staphylococcus
irreversibly binds to i3-lactan1ases, allowing
spp and has variable activity against
the an10xicillin fraction to interact with the

Proteus (MIC 0.5-16 mcg,'mL). Because
bacterial pathogen. This combination
of the instability of desfw·oylccftiofm,
usually has excellent bactericidal activity
microbiology services use a ceftiofw· disk
against i3-lactan1ase-producing staphylowhen perfom1ing susceptibility testing, so cocci, E coli, and Klebsiella. Pseudomonas a false expectation of therapeutic efficacy
and Enterobacter remain resistant.

may result for some pathogens. Pseu

However, clavulanic acid tmdergoes some
domonas, enterococci, and Enterobacter
hepatic metabolism and excretion, so much
spp are resistant to ceftiofm and desfuroylof the antimicrobial activity in the bladder ceftiofm. Ceftiofw· is associated with a
may be due to the high concentrations of
duration- and dose-related thrombocytopeamoxicillin achieved in urine. Thus, despite nia and anemia in dogs, which would not be
an unfavorable susceptibility report for
expected with the recommended dosage
amoxicillin, clinically amoxicillin alone may
regimen.

be as effective as an10xicillin-clavulanic

Chloramphenicol has a high voltm1e of
acid to treat UTis.

distribution, and high tissue concentrations

Cefadroxil and cephalexin are
can be achieved, including in the prostate of
first-generation cephalosporins. Cefadroxil
male dogs and cats. It is active against a
is a veterinary-labeled suspension product,
wide range of gran1-positive and many gran1-
whereas cephalexin is available in both
negative bacteria, against which it is usually
hwnan and veterinary formulations as
bacteriostatic. Chloramphenicol is typically
tablets, paste, or suspension products. Like
active against enterococci, staphylococci,
the penicillins, they are bactericidal, acidic
streptococci, E coli, Klebsiella, and
drugs with a low volwne of distribution and

Proteus. Pseudomonas are resistant. North
are relatively nontoxic. Vomiting and other

American isolates of methicillin-resistant

GI signs may occm in dogs and cats treated

Staphylococcus aureus and Staphylococ
with cephalosporins. Cephalosporins
cus pseudintermedius are typically
have greater stability to 13-lactamases than
susceptible. Well known for causing
penicillins, so they have greater activity
idiosyncratic (non-dose-dependent) anemia
against staphylococci and gram-negative
in people and dose-dependent bone marrow
bacteria They have excellent activity against suppression in anin1als, its use in both StaphylococC'us spp, Streptococcus spp, E
human and veterinary medicine is
coli, Proteus, and Klebsiella. Pseudomonas, increasing because of resistance to other
enterococci, and Enterobacter are resistant.

antinlicrobial drugs.

Cefovecin is an iJ'\iectable, third-genera

Enrofloxacin, orbifloxacin, and
tion cephalospo1in approved for treatment
marbofloxacin are all fluoroquinolones
of dogs with a UTI due toE coli or Proteus.

approved to treat UTis in dogs; although all

In cats, it is only approved for skin infections are used in cats, only some are approved for but may be used in an extra-label manner
this use. Pradofloxacin is only approved
for UTls. With SC dosing, therapeutic
for skin infections in cats in North America,
concentrations are achieved for 14 days,
but it is approved for treatment of UT! in
making this an attractive treatment choice
dogs in Emope and is used to treat feline
for fractious animals.

UT!. The fluoroquinolones are bactericidal,

2620

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM
amphoteric drugs. They possess acidic and
because it has a very low volume of
basic properties but are very lipid soluble at
distribution, and therapeutic concentraphysiologic pH (pH 6-8) and thus have a tions are attained only in urine. It is
high volume of distribution. All fluoroquinconsidered a carcinogen, so it is banned for VetBooks.ir
olones usually have excellent activity
use in food-producing animals, but its use in
against staphylococci and gram-negative
small animals is increasing with the rising
bacteria, but they may have variable activity
rates of antimicrobial resistance to
against streptococci and enterococci. The
veterinary antimicrobials. Nitrofurantoin is
therapeutic advantages of these drugs are
used for infections caused by E coli,
their gram-negative antimicrobial activity
enterococci, staphylococci, Klebsiella spp, and high degree of lipid solubility. They are
and Enterobacler spp. It is increasingly
the only orally administered antimicrobials
indicated for treatment of UTis caused by
effective againstPseudomonas. Therefore,
multidrug-resistant bacteria, which are
fluoroquinolones should be reserved for
otherwise difficult to treat using conven

UTis that involve gram-negative bacteria,
tional veterinary antimicrobial agents. The
especially Pseudomonas, and for UTis in
pharmacokinetics and adverse effect profile
intact male dogs and cats because of their
of nitrofurantoin have not been investigated
excellent penetration into the prostate
in dogs, cats, or horses, and the need for
gland and activity in abscesses. They are
multiple daily dosing makes it inconvenient
concentration-dependent killers with a long
for owners.

postadministration effect, so once daily,

Tetracyclines are bacteriostatic,
high-dose therapy for a relatively short
an1photeric drugs with a high volume of
duration of treatment is effective.

dist1ibution. Tetracyclines are broad

F1uoroquinolones should be avoided for
spectrurn antimicrobials, but because of
chronic, low-dose therapy, because this
plasmid-mediated resistance, susceptibility
encourages emergence of resistant bacteria
is variable in staphylococci, enterococci,
that are cross-resistant to other antimicro

Enterobacler, E coli, Klebsiella, and
bial drugs as well. Cases that involve

Proteus. In most tissues, Pseudomonas spp Pseiidomonas should be carefully
are resistant. However, the tetracyclines
investigated for underlying pathology,
are excreted unchanged in urine, so high
which must corrected if at all possible. Once urinary concentrations may result in Pseudomonas spp become resistant to the
therapeutic efficacy. Doxycycline is a very
fluoroquinolones, there are no other
lipid-soluble tetracycline better tolerated in
convenient therapeutic options.

cats and reaches therapeutic concentra

Gentamicin and the other aminoglycotions in the prostate, so it may be useful for sides are very large, polar (water-soluble)

some UTis. Doxycycline may also be
molecules, so they have a low volume of
effective to treat methicillin-resistant stapdistribution and do not penetrate the hylococcal UTis. If capsules are adminisblood-prostate barrier. They are not tered, it is critical to have the animal drink
absorbed orally and must be given by SC,
afterward to ensure passage into the

IM, or IV injection. The aminoglyco.sides
stomach. If capsules remain in the
have a similar spectrum of activity to that
esophagus, severe local necrosis with
of the fluoroquinolones, but their use for
subsequent esophageal stricture can occur.

UTI is limited because of the necessity of

Trimethoprim-sulfonamides (TMPparenteral irtjections and the 1isk of toxicity sulfas) are combinations of tw0-very
with anything but short-term use. Like the
different drugs that act synergistically on
fluoroquinolones, the aminoglycosides are
different steps in the bacte1ial folic acid
concentration dependent, bactericidal
pathway. Trimethoprim is a bacteriostatic,
killers with a long postadministration effect, basic drug with a high volume of distribuso once-daily therapy of sho1t duration is tion and a short elimination half-life,
effective and minimizes the risk of
whereas the sulfonamides are bacterionephrotoxicity. They can be considered for static, acidic drugs with a medium volume
in-hospital or outpatient treatment of UTI
of distribution and long half-lives (ranging
due to fluoroquinolone-resistant pathogens;
from 6 to >24 hr). These drugs are fornmhowever, the importance of identifying and lated in a 1:5 ratio of TMP to sulfa, although
correcting underlying pathology must be
the optimal bactericidal concentration is
emphasized.

a ratio of 1:20 TMP:sulfa. Microbiology

Nitrofurantoin is a human product
services use the 1:20 ratio in susceptibility
available as tablets, capsules, and a
testing; however, the widely varying
pediatric suspension. It is not commonly
pharmacokinetic properties of this drug
used in veterinary medicine. It is typically
combination make it difficult to determine a
used only for treatment of UTI in people,
therapeutic regimen that achieves the 1:20

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM

2621
ratio at the infection site. Although the
or species of bacteria -SO"A, of tl1e time;
combination does penetrate the bloodtherefore, antimicrobial culture and prostate barrier, sulfa drugs are ineffective
susceptibility is still indicated. Antimicrobial
in pwulent material because of freely
therapy should be stalted as previously
available para-aminobenzoic acid from
described and when urine cultme is

VetBooks.ir
dead neutrophils. The combination of
negative, continued daily at Y, the total daily

TMP-sulfa is synergistic and bactericidal
dose. The antimicrobial should be adminisagainst staphylococci, streptococci, E coli, tered last thing at night to ensme that the
and Proteus. Activity against enterococci
bladder contains urine with a high antinliand Klebsiella is variable, and Pseudomo
crobial concentration for as long as possible.

nas is resistant. TMP-sulfas are associated Approp1iate antimicrobials for chronic,
with a number of adverse effects, and
low-dose therapy include arnoxicillin,
chronic low-dose therapy may result in bone ampicillin, amoxicillin-clavulanic acid, man·ow suppression and keratoconjunctividoXYcycline, cephalexin, cefadroxil, and tis sicca in dogs.

nitrofurantoin. A trimethop1im-sulfonan1ide
can be used, but folate supplementation

Dosage Regimens for UTI: Cmrently,
should be provided ( 15 mg/kg, bid) to
the dw·ation of therapy for UTI is controverprevent bone marrow suppression; there is sial. Although animals are routinely treated
also the tisk of keratoconjw1ctivitis sicca
with antimicrobial drugs for 10-14 days,
developing with longterm use. Although
shorter dmation antimicrobial regimens
attractive for owner convenience, tllirdare routinely prescribed in human patients, generation cephalosporins such as
including single-dose fluoroquinolone
cefpodoxin1e and cefovecin and fluoroquintherapy. A clinical comparison of3 days olones should not be used for longterm
of therapy with a once-daily high dose of
therapy. During longtem1 therapy, urine
eru-ofloxacin with 2 wk of twice daily
cultme should be repeated every 4-6 wk. As
arnoxicillin-clavulanic acid showed
long as the culture is negative, therapy is
equivalence in the treatment of simple UTI
continued for 6 mo. If bacterimia occurs, the
in dogs. However, fmther studies are needed
infection is treated as an acute episode witl1
to detennine the optimal dosage regimens
an appropriate antimicrobial. After 6 mo of
for different classes of antimicrobials, and it
bacteria-free wine, the longtenn, low-dose
is inappropriate to use fluoroquinolones as
antimicrobial therapy may be discontinued,
first-line therapy for sin1ple UTls. Animals
and many anin1als will not have additional
with complicated UTI may require longer
recmrences. In some cases, longterm therapy
courses of therapy, and underlying
may be continued for years in animals that
pathology must be addressed. Chronic
continue to have recmrent UTis.

complicated cases of UTI, pyelonephritis,
and prostatitis may require antimicrobial

Therapeutic Failures: Treatment failures
treatment for 4-6 wk, with the risk of
may be due to poor owner compliance,
selecting for antimicrobial resistance. A
inappropriate choice of antinlicrobials,
follow-up urine culture should be perfonned
inappropriate dose or duration of treatment,
after 4-7 days of therapy to detemline
antinlicrobial resistance, superi.nfection,
efficacy. If tl1e same or a different pathogen
or an underlying predisposing cause ( eg,
is seen, then an alternative therapy should be urolitl1iasis, neoplasia, machal diverticula).

chosen and the culture repeated again after

If treatment for a simple or complicated

4-7 days. Urine should also be cultmed 7-10

UTI fails, a thorough evaluation should be
days after completing antimicrobial therapy
performed to determine and, when possible,
to detennine whetl1er the UTI has resolved
address the cause of failure. When faced with
or recmred.

a tl1erapeutic failure, the practitioner must
consider whether the UTI is due to a relapse

Managing Multiple Episodes of UTI:

or a reinfection. Relapses due to infection

In dogs and cats, ifUTI occurs only once or
by mopathogens witl1 enl1anced intrinsic
twice yearly, each episode may be treated as
virulence occur witl1 what should be effective
an acute, uncomplicated UTI. If episodes
antimicrobial tl1erapy. Strains of uropathooccm more often, and predisposing causes genic E coli have a number of vintlence
ofUTI carmot be identified or corrected,
mechanisms that enable them to invade,
chronic low-dose therapy may be necessary.

survive, and 1mtltiply witllin the uroepithe

Low antimicrobial concentrations in the
liUlll. The sequestration of uropathogenic
urine may inte1fere with fimbriae production E coli within the bladder uroepitheliun1
by some pathogens and prevent tl1eir
presents a great therapeutic challenge in both
adhesion to the uroepitheliun1. In dogs,
hw11an and vete1i.nary patients. There is no
recmrent UTis are due to a different strain
clear consensus in the human medical

2622

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM
literature about how to approach these
identification. Treatment includes
recruTent and persistent UTis.

eliminating potential predisposing factors

( eg, excessive endogenous or exogenous

Antimicrobial Resistance in Uropatho
corticosteroids, urinary catheters)

VetBooks.ir
gens: Acquired resistance to antimicrobiand administering anti fungal drugs als by uropathogens is of great concern in
with or without urinary alkalinization.

both human and veterinary medicine. The

Fluconazole is the antifungal drug of
prevalence of multidrug resistance in
choice for treatment of candidal cystitis.

uropathogens is increasing, particularly in

The dosage in cats is 50 mg/cat, PO, once
infections in dogs and cats. Extended-specto twice daily, and in dogs is 2.5-5 mg/kg/
trum 13-lactamase genes are increasingly
day, PO, divided bid. The duration of treatidentified in E coli isolates from companion ment needed to eliminate infection is
animals. Increases in the occU1Tence of
unknown but may be as short as 7 days.

fluoroquionolone-resistantE coli in dogs
have been widely reported. Because the
mechanism ofresistance to fluoroquinolones

BACTERIAL PROSTATITIS
frequently involves efflux pumps, it also
conveys multidrug resistance. Fluoroquin

Bacterial prostatitis is a common prostate
olone resistance is also increasing in other
disease in sexually intact male dogs and
uropathogens, including enterococci,
may be seen in intact male cats. It can

Proteus mirabilis, and Staphylococcus
develop as an acutely fulminating systemic
pseudintennedius isolates. Meth.icillindisorder or, most commonly, as a chronic resistant staphylococci have been identified
problem associated with recurrent UTis.

in cases of canine UTI. There is increasing

Care should be taken when rectally
evidence that animals are an in1portant
palpating an acutely infected prostate,
reservoir of antimicrobial-resistant bacteria
because septicemia/endotoxemia can
causing infections in people. Enterococci
occur. Most, if not all, sexually intact
isolated from canine UTis have been
male dogs with UTI also have infectious
associated witl1 several different resistant
prostatitis. The prostate gland is uniquely
phenotypes, with most exhibiting resistance
different from the rest of the urinary tract
to three or more antimicrobials. One
because of the acidity of the prostate

Enterococcusfaecium isolate displayed
glands, leading to a decreasing pH
high-level resistance to vancomycin and
gradient from the blood through the tissue
gentamicin. Sequence analysis suggested
to the acinar glands. The distribution of
that resistance was due to gene exchange
antin1icrobials in the prostatic tissue as
between hrunan and canine enterococci. The well as in the prostatic secretions depends use of "last resort" human antinticrobials in completely on the local pH (6.4) and the
veterinary patients with resistant infections
pK" of the drugs. For alkaline drugs, a high
is controversial. Vancomycin, intipenemdegree of ionic trapping leads to high cilastatin, meropenem, fosfomycin,
antimicrobial concentrations in the tissue
quinupristin-dalfopristin, aod tigecycline
and secretions, whereas the acidic drugs
should not be used routinely in treatment of
such as the 13-lactam antimicrobials do not

UTI in animals. N onantinticrobial control of
reach concentrations equivalent to plasma
infection should be considered whenever
concentrations. The choice of antimicrofeasible. Custom-made vaccines, cranberry bial for treatment should be based on
juice/extract, probiotics and adherence/
culture and susceptibility results, and on
colonization inhibitors, and establishment of the ability of the drug to penetrate the asymptomatic bacteriuria may help preserve blood-prostate barrier. Ideal antimicrobithe efficacy of antimicrobials.

als should be very lipid-soluble, basic, and
not highly protein-bound. Fluoroquinolones are the best empirical choice for E

FUNGAL URINARY TRACT
coli infections, whereas chloramphenicol,

INFECTIONS
doxycycline, or trimethoprim-sulfas can
otherwise be considered with favorable

Although uncommon, most fungal UTls in
culture and susceptibility results.

dogs and cats are caused by Candida spp.

Antimicrobial therapy may need to be

Finding Candida organisms in the urine
continued for up to 2 mo, which may
may indicate sample contamination;
promote emergence of antimicrobial
however, finding Candida organisms in
resistance. Chronic bacterial prostatitis
two serial urine samples collected by
may be difficult to cure. Neutering the dog
cystocentesis is consistent with infection
may increase the likelihood of successful
and warrants culture and definitive
therapy and prevent recurrence.

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM

2623

DIURETICS
of diuretic action is 2 and 6 hr after IV and

PO administration, respectively. Furose

Diuretics are used to remove inappropriate
nlide is llighly protein bound (91%-97%),
water volume in animals with edema or
almost totally to albw1lin. It is cleared
volume overload, coITect specific ion
through the kiclneys by renal tubular

VetBooks.ir
in1balances, and reduce blood pressure
secretion. Bioavailability of oral furoseand pubnonary capillary wedge pressw·e nlicle is low ( only 500A, is absorbed).

(see TABLE 25). They are classified by their Furosemicle is usually closed to effect. For
mechanism of action as loop diuretics,
acute, short-term therapy, single IV, IM, or
carbonic anhydrase inhibitors, thiazides,

SC closes of 4-6 mg/kg are given. The major
osmotic diuretics, and potassium-sparing
adverse effect from acute aclnlinistration of
diuretics. The efficacy and use of each class
large closes is acute intravascular volume
of diuretic depends on the mechanism and
reduction, which worsens cardiac output
site of action. Patterns of electrolyte
and hypotension and may precipitate acute
excretion vary between classes, whereas
renal failure. Chronic therapy in cats and
maximal response is the same within a
some dogs can be accomplished by therapy
class. Therefore, if one drug within a class is
every second or third clay. Higher than
ineffective, a different drug from the same
normal doses of furosemicle may be
class will likely be ineffective as well.

required in animals with renal disease due

Combining diuretics from different classes
to fimctional abnormalities of the renal
can lead to additive and potentially
tubule and binding of furosenlicle to protein
synergistic effects. See also p 2525.

in the urine. if escalating doses of furosemicle are required to control fluid retention, Furosemide: Furosemicle is a sulfonaadding other types of volume-modifying mide derivative and the most commonly
medications, such as a potassimn-sparing
administered diuretic in veterinary medicine. diuretic or an angiontensin-converting Furosemicle is a loop diuretic; it inhibits the
enzyme (ACE) inhibitor, may help avoid
reabsorption of sodimn and chlmicle in the
adverse effects.

thick, ascencling loop of Henle, resulting in

Furosemide therapy is associated with a

Joss of sodium, chloride, and water into the
number of adverse effects. By nature of its
wine. Furosemide induces beneficial
mechanism of action, it causes dehydration,
hemoclynamic effects before the onset of
volume depletion, hypokalemia, and
diuresis. Vasodilation increases renal blood
hyponatremia, which may be excessive and
flow, thereby increasing renal perfusion and
cletrin1ental. Furosemicle's most important
lessening fluid retention. It appears that renal drug interaction is with the digitalis vasodilation depends on the local synthesis
glycosicles digoxin and digitoxin. The
of prostaglandins.

hypokalemia induced by furosemicle.

The elimination half-life of furosemicle is
diuresis potentiates digitalis toxicity. As
short in most animals ( -15 min). The effect
long as animals continue to eat, hypokapeaks 30 min after IV administration and lemia does not usually develop. Hypoka1-2 hr after PO administration. The duration Jemia also predisposes animals to itM•ffj DOSAGES OF DIURETICS

Drug

Dosage

Furosemicle

4-6 mg/kg IV, IM, or SC, as needed for acute therapy Dogs: 2-4 mg/kg, PO, once to three times daily

Cats: 1-2 mg/kg, PO, once or twice daily

Large anin1als: 0.5-1 mg/kg/day, IV or IM

Hyclrochlorothiazide

Dogs and cats: 2-4 mg/kg, PO, once or twice daily

Chlorothiazide

Dogs and cats: 20-40 mg/kg, PO, once or twice daily

Spironolactonc

Dogs: 2-4 mg/kg, PO, bid

Mannitol

0.25-0.5 g/kg, IV

Dimethyl sulfoxide

Large animals: 1 g/kg, IV or via nasogastric tube

2624

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM
hyponatremia by enhancing antidiuretic
refractory heart failure. Because of the
honnone secretion and the exchange of
potential for hyperkalemia, spironolactone
sodium ions for lost intracellular potassium
should not be adnunistered concurrently
ions. Concurrent administration of NSAIDs
with potassium supplements. It has been

VetBooks.ir
may interfere with furosemide's prostaglanshown to be safe when used at low doses din-controlled renal vasodilation and
with concwTent ACE inhibitor tl1erapy.

reduce U1e diuretic effect. Furosemideinduced dehydration of airway secretions Carbonic Anhydrase Inhibitors:

may exacerbate respiratory disease.

Carbonic anhydrase inhibitors act in the
proxin1al tubule to noncompetitively and

Thiazide Diuretics: The U1iazide
reversibly inhibit carbonic anhydrase,
diuretics, hydrochlorothiazide and
which decreases the formation of carbonic
chlorothiazide, are not as potent as
acid from carbon dioxide and water.

furosemide and thus are infrequently used

Reduced formation of carbonic acid results
in veterinary medicine. The thiazides act on
in fewer hydrogen ions within proxin1al
the proximal portion of the distal convotubule cells. Because hydrogen ions a.re luted tubule to inhibit sodium resorption
normally exchanged with sodium ions from
and promote potassium excretion. They
the tubule lumen, more sodiun1 is available
may be administered to animals that cannot to combine with urinary bicarbonate.

tolerate a potent loop diuretic such as

Diuresis occurs when water is excreted
furosemide. They should not be adminiswith sodiun1 bicarbonate. As bicarbonate tered to azotemic animals, because tl1ey
is eliminated, systemic acidosis results.

decrease renal blood flow. Because the

Because intracellular potassium cru1
thiazides act on a different site of the renal
substitute for hydrogen ions in the sodium
tubule than other diuretics, they may be
resorption step, carb011ic anhydrase
combined with a loop diuretic or potasinhibitors also enhance potassium sium-sparing diuretic for treatment of
excretion.

refractory fluid retention. Adverse effects
are electrolyte and fluid balance distur

Osmotic Diuretics: Osmotic diuretics
bances, similar to furosemide. Thiazides
include mannitol, dimethyl sulfoxide
decrease renal excretion of calcium, so

(DMSO), urea, glycerol, and isosorb
they should not be used in hypercalcemic
ide. Mrumitol is commonly used in small
animals.

animals but is expensive for use in adult
large animals, so DMSO is often used in

Potassium-sparing Diuretics: Potasits place. Mannitol acts as a protectant sium-sparing diuretics include spirono
against further renal tubular damage and
lactone, amiloride,.and triamterene.

initiates an osmotic diuresis. The initial

Spironolactone is the one most frequently
dosage is 0.25-0.5 g/kg, given IV over 3-5
used in veterinary medicine and is a
min. A response should be noted within
competitive antagonist of aldosterone.

20-30 min. If a response is seen, the

Aldosterone is increased iI\_animals with
dose can be repeated every 6-8 hr, or a
congestive heart failure when the reninconstant-rate infusion of 2-5 ml/min of a angiotensin system is activated in response

5o/o-10% solution can be given. The total
to hyponatremia, hyperkalemia, and
daily dosage should not exceed 2 g/kg. If
reductions in blood pressure or cardiac
diuresis is not seen, the initial dose can be
output. Aldosterone is responsible for
repeated up to a total dosage of 1.5-2 g/kg.

increasing sodium and chloride reabsorp

However, repeated doses usually are not
tion and potassium and calcium excretion
more effective and increase the likelihood
from renal tubules. Spi..ronolactone
of complications (eg, edema).

competes with aldosterone at its receptor

DMSO is an oxygen-derived free radical
site, causing a mild diuresis and potassium
scavenger and an osmotic diuretic. lt is
retention. Spi..ronolactone is well absorbed
used in large anin1als to treat inflammatory
after administration PO, especially if given
and edematous conditions. It is a very
with food. It is highly protein bound (>90%)

potent solvent that can penetrate intact
and extensively metabolized by the liver to
skin and carry other chemicals along with
the active metabolite, canrenone. It is
it. It penetrates all body tissues and
primarily eliminated by tl1e kidneys. The
produces an odor that many people crumot
onset of action for spironolactone is slow,
tolerate. The dosage is 1 g/kg, IV or via
and effects do not peak for 2-3 days.

nasogast1ic tube, as a 10% solution diluted

Spironolactone is not recommended as
in 5% dextrose or lactated Ringer's solution
monotherapy but can be added to furose

(higher concentrations can cause
mide or tluazide therapy to treat cases of
intravascular hemolysis).

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM

2625

DOPAMINE
should be managed as the need arises.

Thromboembolism may be prevented by

Dopamine, an adrenergic neurotransmitter
giving aspirin at 0.5-5 mg/kg bid, to high-risk
with specific receptors in the renal
animals such as those with serum albumin
vasculature, is frequently used to combat

<2 g/clL, plasma fibrinogen >400 mg/c!L, or

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reductions in renal blood flow that may
plasma antithrombin Ill activity <700/o.

contribute to acute renal failure. It also
increases glomerula.r filtration and sodium

DIABETES INSIPIDUS
excretion. Dopamine has a very short
half-life and is administered as a constant

Nephrogenic diabetes insipid us is a
rate infusion of 2-5 mcglkg/min. Higher
physiologic condition in which the kidneys
dosages cause tachycardia, cardiac
fail to concentrate urine despite adequate
arrhythmias, and peripheral vasoconstricamounts of antidiw·etic honnone (ADH).

tion. Animals that do not produce urine

Central, or pituitary-dependent, diabetes
with dopamine alone may respond to a
insipid us develops when there is a lack of
combination of dopamine and furosemicle.

ADH production. Animals with central

Dopan1ine is given as above, and furosediabetes insipidus can be given desmopresmide is given at 1 mg/kg/hr, by IV bolus. If sin acetate. The nasal spray formulation
no improvement occurs within 6 lu·, concan be used, with 1-4 drops administered version is unlikely, and infusion should be
into the conjW1ctival sac once or twice daily.

discontinued. Dialysis (hemodialysis or

Alternatively, the parenteral fo1m can be
peritoneal dialysis) may be required to
given at 0.5-2 mcg, SC, once or twice daily.

maintain these anin1als.

Thiazide diuretics may reduce polyuria by

300/o-500/o in anin1als with nephrogenic or

GLOMERULAR DISEASE
central diabetes insipid us. Inhibition of
sodium resorption in the ascending loop of

Angiotensin-converting enzyme (ACE)

Henle leads to decreased total body sodium
inhibitors may be beneficial in management
and contraction of the extracellular fluid
of clogs and cats with chronic renal failure
volume. The net effect is to increase sodium

(CRF). Renal disease progresses to CRF as
and water resorption in the proximal renal
a consequence of functional adaptations
tubule. Chlorothiazide is given at 20-40 mg/
of the remaining nephrons, including
kg,PO, bid.

glomerular hyperperfusion and hypertension controlled by angiotensin II. These CONTROLLING URINE pH
responses initially enhance nephron
filtration capacity and compensate for the

The ideal urine pH should be 7.0-7.5 in dogs
decrease of glomerular filtration rate but
and 6.3-6.6 in cats. If the urine pH remains
are detrimental in the longtem1 and cause
below these values after diet modification,
further nephron loss. Administration of
potassium citrate at 80-150 mg/kg/clay,

ACE inhibitors lowers glomerular pressure

PO, divided bicl-tid, can be given to increase
by decreasing systemic blood pressure and
the pH. Ammonium chloride (200 mg/kg/
locally inhibiting angiotensin IL In anin1als
day, PO, divided tic!) and DL-methionine
with CRF, ACE inhibitors may decrease

(1,000-1,500 mg/cat/day, PO) are the urinary
proteinuria caused by changes in glomeruacidifiers of choice. Chronic urine lar membrane penneability and selectivity
acidification, and ensuing acidosis, can be
from mechanical injury induced by
harmful and should not be instituted
glomerular hypertension, potentially
without complete evaluation of the animal.

slowing disease progression. ACE inhibitors
also tend to increase appetite and body

CYSTINE-BINDING AGENTS
weight in animals with renal failure.

Enalapril is used in clogs at a dosage

Cystinmia, with subsequent cystine urolith
of 0.5 mg/kg, PO, once or twice daily;
fo1mation, results from an inherited
benazepril is used in cats at a dosage
disorder of renal tubular transp01t. Cystine
of 0.5-1 mg/kg/clay, PO.

stones are dissolved by dietary modifica

Dimethyl sulfoxide (DMSO) has been
tion, urinary alkalinization or neutralization,
used in clogs with amyloiclosis with variable
and the use of cystine-binding agents.

results. It is given at a dosage of 80 mg/kg/

Uiinary alkalinization or neutralization is
day, divided tic!, and given as a 100/o solution
accomplished as described above.

either PO or SC. Thromboembolism and

Tiopronin at 15 mg/kg, PO, bid, or
systemic hypertension are frequent
o -penicillamine at 15 mg/kg, PO, bid, given
complications of glomerular diseases in
with food, are both cystine-binding agents.

clogs, and to a lesser extent in cats, and

Tiopronin has fewer adverse effects and is

2626

SYSTEMIC PHARMACOTHERAPEUTICS OF THE URINARY SYSTEM
the recommended choice. Both agents can
enterohepatic recirculation. Estrogens
cause Coombs'-positive anemia, tlu·ombosensitize the urethral sphincter to cytopenia, increased liver enzyme activity,
cx-adrenergic stimulation; tl1erefore, DES
glomerulonephritis, lymphadenopathy,
therapy is synergistic with cx-adrenergic

VetBooks.ir
cutaneous hypersensitivity, and delayed
drugs. DES is given as a daily loading dose
wound healing. Penicillamine also causes
for 7---10 clays and then reduced to once
vomiting. Once stones are dissolved, a
weekly dosing, if possible, to avoid toxicity.

prevention protocol can be instituted.

Treated dogs are susceptible to bone

Dietary modification witl1 or without
marrow suppression from estrogen,
urinary alkalinization may be all that is
typified by early thrombocytopenia and
needed to prevent stone formation;
potentially fatal aplastic anemia. Hemahowever, tiopronin may also be needed topoietic toxicity is rarely seen in cats.

if uroliths recur.

Other adverse effects seen in dogs include
alopecia, cystic ovaries, cystic endomet1ial

URINARY INCONTINENCE
hyperplasia, pyometra, prolonged estrus,
and infertility. When used once weekly in

Urinary incontinence is most commonly
spayed female dogs, adverse effects from
caused by uretlu·al sphincter incompetence.

DES are rare.

It is most conunon in large breed, spayed
cx-Adrenergic agonists such as phenylfemale dogs (11 % ---20% incidence) but may propanolamine (PPA), ephedrine,
be seen in intact females, male dogs, and
pseudoephedrine, and phenylepluine act
cats. Estracliol-17[3 concentrations decrease
directly on smootll muscle receptors to
after ovariohysterectomy in bitches,
increase urethral tone and maximal urethral
resulting in deterioration of uretllral closure
closure pressure. Although often more
within 3---6 mo. Currently, tllere are no
clinically effective tllan DES, their action
approved drugs to treat incontinence in
is short lived, usually requiring dosing bidanimals, and most of the human products tid. Of this class of drugs, PPA is tl1e most
traditionally used have been removed from
effective and results in fewer cardiovascular
the market because of toxicity concerns.

adverse effects. Previously available in

Some estrogen compotmds and
over-the-counter cold medications and
cx-adrcncrgic drugs may still be available
appetite suppressants, it was witllclrawn
to vete1inarians tl1rough compounding
from the human market because of toxicity
pharmacies (see TABLE 26).

associated with overuse as a diet aid.

Diethylstilbestrol (DES) is a nonsteroiclal Ephedrine, pseudoephedrine, or phenylestrogen dei-ivative tllat closely resembles eph1ine may be med but are less efficacious
the natural estrogen, estracliol. Because it is than PPA. Adverse effects of cx-adrenergic inexpensive and infrequently administered,
drugs include excitability, restlessness,
it is the first choice to treat urinary
hypertension, and anorexia.

incontinence in female dogs. It is orally

In male dogs, testosterone injections are
bioavailable and reaches peak plasma
used to treat urinary incontinence but are
concentrations in 1 hr in dogs; it has an
generally less effective than estrogen
elimination half-life of 24 hr because of
therapy in female dogs.

IM=iiffj DRUGS USED TO TREAT URINARY INCONTINENCE

Drug

Dosage

Diethylstilbestrol

Dogs: 0.1---0.3 mg/kg/clay, PO, for 7---10 days, followed by 1 mg/dog/wk

Phenylpropanolan1ine

Dogs: 1.5---2 mg/kg, PO, once to three times daily

Ephedrine

Dogs: 1.2 mg/kg, PO, bid-tid

Cats: 2-4 mg/kg, PO, bid-tid

Pseudoephedrine

Dogs >25 kg: 30 mg/dog, PO, tid

Dogs <25 kg: 15 mg/dog, PO, tid

Testosterone propionate Dogs: 2.2 mg/kg, IM, every 2---3 days Testosterone cypionate Dogs: 2.2 mg/kg, IM, every 30---60 days

CHEMOTHERAPEUTICS INTRODUCTION

2627

URINE RETENTION
irreversible antagonist, has been used
with some success. The dosage for dogs or

Disorders of micturition characte1ized
cats is 0.25 mg/kg, PO, bid.

by urine retention and a distended bladder

Diazepam is a benzodiazepine arudolytic
are usually caused by hypocontractility
that is also a central muscle relaxant. Dosages

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of the bladder or by urethral obstruction.

sufficient to allow for urethral relaxation may

Prolonged bladder distention leads to
also cause sedation. The dosage in dogs is 0.2
breakdown of the tight junctions between
mg/kg, PO, tid, and in cats is 0.5 mg/kg, IV.

detrusor muscle cells of the bladder, which

Diazepam given PO may cause idiosyncratic
prevents normal depolaiization and
acute hepatic necrosis in cats.

contraction of the detrusor muscles.

In animals with detrusor hyporeflexia

An adrenergic antagonist may be
or bladder atony, bethanechol chloride
indicated when manual expression or
may be of some benefit. This cholinergic
voluntary voiding is nonproductive because
agonist stinmlates the initiation of detrusor
urethral sphincter tone is excessive, as
muscle contraction. The dosage for dogs is
is often the case in cats after relief of

5---25 mg/dog, PO, tic!, and for cats is 2.5---7.5
obstruction. Phenoxybenzamine, an
mg/cat, PO, tid.

CH EMO THERAPEUTICS INTRODUCTION

Treatment with any chemotherapeutic
maintaining high standards of proof of
agent involves an understanding of the
efficacy and safety as well as clinician
complex interrelationships among the host
flexibility in the design of dosing regimens is
animal, the infecting pathogen, and the
a testament to the complex host, drug, and
drug, the interactions of which comprise the microbial interactions associated with chemotherapeutic triangle. The advent of
infections.

resistance places ftuther emphasis on

Chemotherapy is the use of chemical
consideration of these factors when
agents in treatment or control of disease.

selecting a dosing regin1en. That the FDA

However, the term is most often used in the
struggles to identify the most reasonable
context of controlling harmful pathogens
way to approve antimicrobials while
through their chemical destruction. As such,

ANIM AL

CHEMOTHERAPEUTIC -- Impairment or Destruction___.. PATHOGEN

AGENT

._

Resistance------

Chemotherapeutic triangle

2628

CHEMOTHERAPEUTICS INTRODUCTION
the chemotherapeutic aimamentarium

ANTIMICROBIAL DRUG FACTORS
includes antibacterial, antiviral, ai1tifungal,
antipai·asitic, and antineoplastic compounds.

Mechanism of Action

Chemotherapeutic agents may be

Understanding tl1e mechanism of action

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selectively toxic to invade micro- or

(MOA) of ai1tibacterial agents is important
macroorganisrns, but in many cases, they
for several reasons. The MOA clete1111ines
can also result in adverse effects in the host.

whether the antibacterial action is likely to

This is paiticulai·ly trne when the infecting
be bactericidal or bacteriostatic, and
pathogen is eukaiyotic ( eg, fungal organwhether tl1e relationship between plasma isms, cancer cells) versus prokaiyotic ( eg,
drug concentration (PDC) and organism
bacterial). To avoid toxic manifestations,
minimum inhibitory concentration (MlC) is
paiticulai·ly for drugs targeting eukaiyotes,
concentration dependent or tin1e depenthe dose rate often becomes c1itical; dent. Fwther, MOA often is related to the
additionally, the clinical condition of the
mechanism(s) by which resistance emerges.

aiurnal and concurrently administered drugs For some antimicrobials, the MOA also can be responsible for adverse events.

relates to the mechanism(s) of toxicity.

This discussion of chemotl1erapeutic

Finally, if combination therapy is to be
agents focuses on infecting bacterial
considered, drugs with MOAs that
pathogens; fungal ai1d viral pathogens are
complement one another should be chosen.

discussed in their respective chapters. A11y

The major MOA of antimicrobial agents,
time a drug is used with the intent to kill the
witl1 exan1ples of each type, are as follows
target, multiple factors impact therapeutic

(see a/,so ANTIBA rERIALAGENTS, p 2652):

success. The most obvious is that the target

1) inhibition of cell wall synthesis: f\-lactams
organism will implement mechanisms

(penicillins, cephalosporins, and cephan1ywhereby it can avoid haim, the most notable cins), glycopepticles (vancomycin), being resistance mechanisms. However,
bacitracin, fosfomycin; 2) irnpainnent of cell
microbes in paiticulai· ai·e associated with
membrane function: polymyxin B, colistin;
nw11erous virulence factors and other

3) inhibition of protein synthesis through
mechanisms for self-protection, often also
binding eitl1er to a single (tetracyclines,
making the host sick at the sanie time.

chlorainphenicol, macroli.des, li.ncosainides)

Likewise, host factors, which seemingly
or botl1 ( aniinoglycosicles) ribosomal
should help the host fend off infection, can
subunits; 4) inhibition of DNA syntl1esis
become detrimental to therapeutic success.

and replication: novobiocin, quinolones,

For most infections, a functional inlrnwle
metroniclazole; 5) inhibition of DNA-dependsystem is pai·ai11ount to therapeutic success. ent RNA polymerase: rifan1ycins; and Drug factors also influence therapeutic

6) inhibition of folic acid and consequently
success, most notably because drugs must

DNA synthesis: sulfonanlides, tJirnethoprin1.

be able to penetrate any body tissue to

Most mechanisms will result in killing
successfully kill the microbe. These include

(rather than s1a.t:ic) efficacy, with notable
tl1e interactions between th� three points
exceptions being drugs that inhibit a single
of the chemotl1erapeutic triangle: host,

1ibosomal unit, or tl1e use of a sulfonanlide
microbe, and drug. If tl1e goal of antinlicrowithout a diaininopy:ridine potentiator such bial tl1erapy is to simply resolve clinical
as tJimetl1op1irn or ormetoprim. Knowing
signs of infection, then attention may not be
whether a drug is conceutration or tin1e
given to the critically important aspects of
dependent is impo1tant for design of a
therapy. In general, the use of ai1 antimicrodosing regimen. Concentration-dependent bial to which an isolate is susceptible will
cl.rugs include tl1e fluoroquinolones and
reduce the size of the infecting innocu!Wll
aininoglycosides. They are more effective
but is likely to leave behind a residual, yet
when peak cl.mg concentJ·ations at the site
resistant, inoculun1. I.n1munocompetent
of irtfection exceed the MIC of the infecting
animals are more likely to eradicate this
microbe by 10 or more. Such drugs also
residual population, but at-risk animals may
exhibit a long postantibiotic effect,
not. As such, the population may regrow to
paiticu.lai·ly towai·d grain-negative
a size capable of once again causing clinical
organisms. Tllis effect results in continued
signs ( eg, 103-105 CFU in the urinaiy tract).

inhibition of microbial growth after brief

Much of the following discussion is
exposure to the drug. Thus, for such cl.rugs,
intended to suppo1t the design of closing
the dose rather than the interval, is
regimens ( approp1iate choice of drug, close,
important. For time-dependent drugs,
and interval) that maximize antimicrobial
dosing regimens should be designed such
efficacy while mininlizing the risk of
that drug concentrations remain above the
emergent ai1tin1icrobial resistance.

MlC for most of the dosing interval. For

CHEMOTHERAPEUTICS INTRODUCTION

2629
such drugs, the dose may need to be
susceptible isolates witll MI Cs approaching
increased to surpass the MIC of the
the breakpoint. Lipid-soluble drugs, in
organisms, but the interval should be
contrast, distribute to total body water and,
designed to maintain the concentrations.

therefore, are better able to reach intracel

Exan1ples of time-dependent drugs include
lular organisms or infections in sanctuaiies.

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the 13-lactams, "bacteriostatic" drugs, and Some drugs are characterized by volwnes of
the sulfonamides. Designing a convenient
distJ.ibution tl1at exceed 11/kg, indicating
dose for time-dependent drugs with very
tl1e drug accumulates or becomes trapped
short-half lives is difficult. For example,
at some sites. Few antinl.icrobials appeai· to
most penicillins have an elimination half-life be tightly bollJld to plasma proteins.

of -1-2 lu·, and as such, the majority ( -90"A,) Exceptions include doxycycline, minocywill be eliminated in 3--6 hr (for amoxicillin, cline, and cefovecin. For cefovecin, its tight

-4 hr). As such, dosing regimens should be
binding to circulating albumin accounts for
at least every 8, if not every 6, hr. Choosing a
its very long hal f -life. Several antinlicrobials
drug with a longer half-life, if the isolate is
undergo hepatic metabolism, with some
sufficiently susceptible, is more prudent.

drugs (eg, ceftiofur, enrofloxacin)

Some drugs are both concentration and
metabolized to an active metabolite tl1at cai1
time dependent; eg, efficacy of the
contJ.ibute substantively to antinl.icrobial
fluoroquinolones can be enhanced by
activity. Some drugs Wldergo substantive to
adding a second dose in the face of
exclusive excretion in tile bile, including the
treatment of an organism with a high,
macrolides, minocycline (and some of doxyyet susceptible, MIC.

cycline), and clindarnyci.n. For such drugs,
cai·e must be taken in tl1ose species that

Drug Disposition
have a GI microflora subject to antinl.icrobial disruption; use for urinary tract Drug disposition (absorption, distribution,
infections should be avoided. Many drugs
metabolism, and excretion) of antimicrobiai·e excreted renally and subsequently als can impact therapeutic efficacy and
concentrated in tl1e urine, including
should influence the design of tile dosing
l3-lactai11s, aminoglycosides, most fluororegimen. Most antimicrobials are adminisquinolones, and several tetracyclines.

tered orally. Exceptions include those
destroyed by GI acidity (eg, some 13-lactams,
and particularly penicillins) or microbes (ie,

Adverse Effects and Toxicity
rwninants) and those insufficiently UJlstable Toxicity is associated with harm in the for oral preparation. Food can impact
animal ai1d thus is discriminated from
absorption of some drugs, most notably
adverse effects, although such effects are
tetracyclines ( except doxycycline) and tile
rarely life threatening. Because bactet"ia are
fluoroquinolones (rate but not extent
prokaryotic, most antimicrobials do not
in1pacted). A drug tl1at has a very high oral
interact with eukaiyotic host targets. As
bioavailability in one species carmot be
such, mechanisms of ai1tiJ.nicrobial toxicity
assumed to have a sin1ilarly high oral
ai·e generally not related to mechanisms of
bioavailability in another. For example, tl1e
antibacterial action. An exception is drugs
oral bioavailability of ciprofloxacin is good
tl1at tai·get nl.icrobial cell membrai1es
in people but fair or negligible in dogs and

(polymi.xins), tl1e use of which is generally
horses. Most antimicrobials must potenlin1ited to topical administration. Additiontially reach any body tissues. Antimicrobials ally, mainrnalian nl.itochondrial topoisomertllat have a distribution limited to extracelases ai·e subject to damage by fluo1inated lular fluid, ie, "water-soluble" drugs, include quinolones, resulting in a diversity of
the 13-lactams, fosfomycin, aminoglycoadverse effects. Drugs that disrupt sides, and some members of the sulfonamicrobial flora may be letllal to some mides and tetracyclines. Lipid-soluble drugs species, particularly hindgut fennenters dist1ibute to total body water and include

(horses, rabbits). The release of endotoxin
the fluoroquinolones, macrolides,
when treating a large, grai11-negative
clindamycin, many sulfonanl.ides, and
inoculwn may be problematic for some
doxycycline or nl.inocycline. In general,
drugs ( especially penicillins), paiticularly in
drugs tllat are water soluble distJ.ibute well
horses. Several classes of a.ntiJ.nicrobials
to extJ.·acellular fluid of most organs, but
exhibit toxicity =elated to their (known)

there are exceptions. For example, only
mechanism of action. For exai11ple, the

-300/o of an1oxicillin reaches tracheobronaniinoglycosides are nephrotoxic because chial secretions, and distJ.ibution into
tl1ey are actively accumulated in and
sanctuaries is limited. Doses of such drugs
eventually disrupt renal tubular cells, and
should be increased, particularly for
selected fluoroquinolones cause retinal

2630

CHEMOTHERAPEUTICS INTRODUCTION
degeneration in cats due to phototoxicity in
succumb to the drug, resultillg ill a residual
the retina. Chloramphenicol is associated
population that expresses resistance to the
with ilTeversible bone marrow suppression
drug even though exposure has been
in people, because it is conve1ted to a toxic
discontinued. However, with time, mutated
metabolite. Drug interactions might
bacteria, which are often physiologically

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contiibute to some adverse effects as well.

impaired, also will disappear. Generally,

For example, chlora.mphenicol is a marked
mutations confer resistance only to the drug
inhibitor of drug-metabolizing enzymes, and
or drug class, ai1d mutated cells may be less
its use with potentially toxic drugs
virulent. There are exceptions, with
metabolized by the liver should be avoided.

fluorinated quinolones beillg an example of

Selected fluoroquil10lones inhibit selected
a mutation that emerges in the presence of
clrng-metabolizing enzymes. Macrolides as a
the drug and targets multiple clrngs. This
class may compete for both P-glycoprotein
reflects their MOA, which results ill
and thus impact all aspects of clrng movedamaged. DNA Subsequent mutations ment, as well as inhibit some
illclude those that alter regulators of efflux
drug-metabolizing enzymes.

pW11ps. A marked increase in efflux activity
results in MDR.

Acquired resistance also can be shared

Virulence and Resistance
horizontally by trai1sfer from one organism

Antilnicrobial resistance is a common
to another. Such resistance emerges in
reason for therapeutic failure. Resistance is
response to the presence of the drug.

a natural response to exposw·e to toxins,

Shared resistance occurs rapidly, often
incluclil1g antilnicrobials. However,
during the course of therapy and often
although resistance is not desirable in an
resulting in the transmission of multiple
infecting pathogen, resistance by itself,
genes tai·geting multiple cl.rugs. Transfer
including multiclrng resistance (MDR), is
via plasmids is the most recognized mechanot the problem. Rather, it is the virulent nism of shared resistance. Plasmids are
organism that causes harm to the animal.

composed of extrachromosomal DNA, ie,

Acquisition of virulence factors or genes

DNA not vital to cell function. Plasmids are
necessary for survival in a hostile environreplicons, meaning they are capable of ment is responsible for illness. A virulent,
replicating autonomously in the host.

MDR organism is paiticularly problematic.

Multiple mechanisms exist whereby

Bacterial resistance to clrngs can be either plasmids can enter a bacterial cell.

inherent or acquired. Genes coding inherent

Transformation, which occurs in only
resistance are present in all strains of an
a limited number of bacteria, is accomorganism, with expression independent of plished. by passage of naked DNA from
antimicrobial exposure. The "spectrwn" of
donor to recipient. Trai1sduction illvolves
ai1timicrobial drugs reflects inherent
transfer via a bacteriophage that inserts
resistance. For exainple, bacterial wallitself into recipient bacteria. Phageclefective vaiiants (such as L-fonns, mediated transduction occurs in some
spheroblasts, and protoplasts) are resistai1t
gram-positive ( especially Staphylococcus
to cell-wall inhibitors. Conversely,' cell-wall
aitreus) as well as grain-negative species.

access to some drugs is prevented because

The most common method is conjugation
of ilnpermeability reflecting very small
in which DNA passes from the donor cell
po1ins in selected gran1-negative bacteria
to the recipient via a bridge formed during

( eg, Pseudomona.s ae,uginosa ).

direct cell-to-cell contact. This is the

In contrast to mherent resistai1ce,
most sophisticated. form of transmission,
acquired resistance occurs only in selected
because the donor must have the necstrains of an organism, usually emerging in essary surface appendage (sex pilus) to
response to exposure to an antimicrobial.

form the bridge that is coded for by a

Genes for resistai1ce cai1 be acquired either
resistance transfer factor on the plasmid. A
spontaneously due to mutations or through
sillgle CFU may contain multiple plasmids,
sharil1g of genetic material via plasmids or
each of which in turn may carry multiple
transposons. Mutations most conunonly
genes conferring resistance to multiple
occur by chai1ce, with the likeli110od that at
drugs. An10ng the disadvantages of
least one CFU in any given population being
plasmid-mediated resistance is the ease of
resistant to any chosen cl.rug increasillg as
sharing between gram-negative organisms
the population reaches 107 CFU. Because
and less commonly between gram-positive
the mutation is transmitted to daughter
organisms; transfer can also occur between
cells, it will remain in the population
gram-positive and gram-negative organgenome ("vertical" resistai1ce). Selection isms. Although plasmid-mediated resipressure causes less susceptible isolates to stance can occur rapidly, plasmids are

CHEMOTHERAPEUTICS INTRODUCTION

2631
generally shed by the bacterium once the
resistance to fluoroquinolones, or mutations
drug is no longer present.

in ribosomal submtits that confer resistance

Among the mechanisms whereby
to various ribosomal inhibitors. Mutations
genetic sequences can be transferred
also generally cause single-drug resistance.

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between extrachromosomal (plasmid)

Other less conm1on methods include the
and chromosomal DNA is the transposon,
presence of alternative metabolic patl1ways
which is a DNA sequence that can change
that circlll11vent the effect of the drug ( eg,
position in a genome. Transposons can
sulfonamides) or increased syntllesis of a
carry chromosomal DNA from one
key metabolic intermediate tllat would thus
bacterial cell to a plasmid and back. These
require higher concentrations of the drug
transpositional sequences may be carried

( eg, para-aminobenzoic acid in sulfonantide
on gene cassettes. Integrons are generesistance).

capturing systems found in plasmids,

Acquired resistance will be clinically
chromosomes, and transposons. Integrons
manifested as an increase in the MIC of the
can carry genes imparting antimicrobial
isolate to the drug in question. Notably,
resistance; generally, such resistance
resistance can emerge in an isolate that yet
in1pacts multiple drugs. Once incorporated
remains susceptible if the increase in MIC
into chromosomal or plasmid DNA, the
has not exceeded the MIC breakpoints
genes are subsequently expressed or
detennined for that drug. For recurrent
disseminated even further. Problematiinfections, identifying the underlying cause cally, in addition to resistance genes,
is likely to be paramount to avoiding
these cassettes may also include virulence
antin1icrobial resistance, including MOR.

factors. This is exemplified in certain

Among the clinically relevant gram-negative
strains of methicillin-resistant Staphylo
isolates developing MOR are E coli and
coccus aureus (MRSA), which reflects

Klebsiella. Gran1-positive organisms
acquisition of the mec gene, encoding for a developing MOR include MRSA and its
mutated penicillin-binding protein-2, which canine and feline com1terpart, methicillinprevents binding by any 13-lactam drug.

resistant S pseudinl ennediu s (MRSI).

Infection by MRSA has transitioned from

Enterococcus is another gram-positive
hospital acquired, occurring only in the
isolate for which MOR is both natural and
immunocompromised, to community
emerging. Clostridillm difficile is an
acquired because of acquisition of a
example of an obligate anaerobic organism
virulence gene that facilitates infectivity.

for which MOR is clinically important.

Acquired resistance primarily reflects three
major cellular mechanisms: 1) Intracellular
drug concentrations can be reduced.

Antimicrobial Resistance and the

Multiple mechanisms can accomplish this.

Veterinarian: Two major aspects of

Drug movement into the microbial cell can
antinticrobial use are of particular concern
be prevented by decreasing p01in munber or
to veterinaiians: the likelihood of causing a
size or, more commonly, by transporting the
patl10genic organism to become resistant
drug out of tl1e cell ttu·ough efflux transpo1t
to current antinticrobial therapy and tlle
pumps located in the cell membrane. These
likelihood of commensal organisms,
mechanisms result in resistance to multiple
regardless of location in the body, becoming
drug classes. 2) Microbes can produce
resistant to future antimicrobial therapy.

enzymes that destroy certain drugs or drug

Although designing the dosing regimen such
classes. This mechartism generally targets
that all infecting organisms are killed will
only a single drug class. Exan1ples include
minimize the risk of acquired resistance in

13-lactamases and enzymes that target
the patient, any and all antinticrobial use
fosfomycin, arninoglycosides, or phenicols.

contributes to global concerns regarding

These enzymes can be expressed constituantinticrobial resistance. Historically, vete1itively, or on exposure to the drug, induced naiy use of antin1icrobials has focused on
such that expression is increased. In general, agricultural (eg, food-animal) applications.

the addition of larger R groups on the drug

Yet, the concern is shifting to also include
molecule sterically hinders the ability of
use in companion animals, particularly with
destructive enzymes from reaching the
greater awareness of the risk of transfer of
vulnerable site of the drug molecule.

resistant commensal organisms between

3) Microbes can acquire mutations that
pets and people.

change the target such that it no longer

The role of antin1icrobial tllerapy in the
binds to the drug. Exan1ples include mutated advent of antimicrobial resistance is well penicillin-binding proteins that confer
recognized. Minimizing the risk of emerging
methicillin resistance to staphylococci,
resistance might be approached based on
mutations in DNA gyrases that confer
following the "3 Ds": decontantination,

2632

CHEMOTHERAPEUTICS INTRODUCTION
de-escalation, and designing a dosing
infections associated with an W1derlying
regimen.

cause is patticularly problematic. Resis

Decontamination decreases the spread
tance is more likely in these anin1als,
of potentially resistant microbes and
particularly if dosing regin1ens are
includes attentiveness to hygiene not only

(inadvertently) designed for promotion

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in the hospital but also in the home
rather than for avoidai1ce of resistance.

environment.

Data are just beginning to emerge in

De-escalation includes avoiding
veterinary medicine indicating that shorter
inappropriate or unnecessary systemic
duration of appropriately designed dosing
antimicrobial use. For exan1ple, the use of
regimens cat1 be just as effective as
low levels of antibiotics (as in animal feeds)

longer-tem1 tllerapy.

or improper dosing regin1ens may lead to a

De-escalation also might be accomhigh incidence of acquired resistance in a plished by initiating tl1erapy witl1 a
given population; as such, this practice
higher-tier drug ai1d switching to a
increasingly is coming w1der critical
lower-tier drug as soon as possible. Reasons
scrutiny. Identifying the need to treat with
that an antimicrobial might be considered a
systemic antimicrobials is among the most
higher-tier dmg, witll use supported by
important questions to be addressed.

culture and susceptibility data, versus a

Clinical signs consistent with infection
lower-tier drug, which might be used

(fever, inflammation, pain, neutrophilia) are
empirically, include the following:

not diagnostic of infection. The presence of
spectrum, with more narrow-spectrwn
bacte1ia does not necessarily indicate that
drugs being reserved for problematic
systemic antimicrobial therapy is indicated.

infection ( eg, anunoglycosides and

Bacte1ia may reflect normal flora, which
gram-negative infections, vancomycin and
must be distinguished from pathogenic

MRSA), safety, mechanisms of resistance
microbes. If in a culture, this may reflect a
that will emerge should tllerapy fail ( eg,
poorly collected sample. Single rather than
chugs causing emergence of extendedmultiple (three or more) organisms is more spectnun 13-lactamases or MDR), and
indicative of a pathogen. The extent of
importance to human health ( eg, vat1comygrowth may be used to support infection; cin, linezolids, fosfomycin, etc).

for example, the presence of bacteria in

Designing the dosing regimen should
urine collected by cystocentesis is not
be approached such that tile entire infecting
considered an infection wlless > 1,000-
inoculum is killed by tl1e chosen anti.micro100,000 CFUs are present. Presence of bial. It may be among tile most difficult "D"

infection alone does not justify systemic
to implement, because it requires not only
treatment with antimicrobials. For example, W1derstanding the relationship between despite approval of antimicrobials to treat
plasma or tissue drug concentrations and
feline abscesses, most might be better
tile MIC of tile infecting microbe but also
managed by local treatment. Asymptomatic
being willing to modify routine recombacteriwia might be more wisely not mended dosing regimens as needed for
treated with systemic antimicrobials W1Lil
individual patients. This requires delineaclinical signs become evident; nonvirulent tion of host, microbial, and drug factors tllat
organisms may be acting as commensals,
might impact antimicrobial tllerapy, either
preventing infection with more virulent
negatively or positively. Even if a microbe is
pathogens. The use of topical therapy
historically considered "susceptible," tile should be considered when possible; not
amoW1t of drug required to effectively
only can much higher concentrations be
inhibit its growth is likely to be greater now
achieved at the site of infection, the
than it was when tl1e drug was originally
systemic impact of antimicrobials on
approved. Successful treatment of infection
microbiota can be minimized.

(ie, resolution of clinical signs) does not

De-escalation might also reflect shorter
avoid the advent of resistance. In healtlly,
duration of therapy. Identifying the most
imn1W1ocompetent animals, adequate
appropriate duration can be problematic.

reduction of pathogen inoculum might be

Sho1t-tenn therapy at high doses and sho1t
sufficient for the host to overcome residual
intervals should be sufficient to kill the
microbial growth, whereas in atl ai1imal at
infecting microbe, negating the need for
risk, tltis residual growth may emerge as
longer duration therapy at lower concentraa resistant population after an initial tions or shorter intervals that might
response. The more "at risk" tl1e atl.imal is facilitate resistance. However, for slower
in being wrnble to overcome a residual
growing organisms or nonhealing tissues,
resistant inoculW11, the more important that
longer durations might be prudent. The
dosing regimens be designed to kill tile
longterm use of antimicrobials for
microbes. "Dead bugs don't mutate" should

CHEMOTHERAPEUTICS INTRODUCTION

2633
be the guiding impetus for antimicrobial
promise as a result of disease, malnutrition,
use.

or concurrent drug therapy, or local

Designing appropriate dosing regimens
immunocompromise caused by invasive
requires the following: 1) The pathogen( s)

procedures may contribute to failure. The
should be identified and characterized,
more "at risk" the animal is in being unable VetBooks.ir
including antimicrobial susceptibility, so
to overcome a residual resistant inoculum,
that the drug matches the organism as
the more important that dosing regimens be
closely as possible, nanowing the spectrum
designed to kill the microbes (ie, "dead bugs
of drug used. The role of culture and
don't mutate"). Because dosing regimens
susceptibility testing in selecting the drug
should be designed to kill, bactericidal
and designing the dosing regin1en is
drugs should be chosen whenever possible.

becoming increasingly important. With

Bactericidal drugs include f3-lactams
notable exceptions, the ability to predict

(penicillins and cephalosporins ), fluoroinfecting pathogens is limited. Exceptions quinolones, aminoglycosides, and poteninclude respiratory tract infections in food tiated (not single) sulfonamides. Tetracyanin1als, pyoderma in dogs and, with clines, chlorarnphenicol, macrolides (eg,
lin1itations, urirnuy tract infections in dogs
azithromycin), and lincosamides (eg,
and cats. However, for urinary tract
clindamycin) are bacteriostatic. However,
infections, E coli is a cause in only 500/o of the distinction between "cidal" and "static"

cases. The more complicated the infection,
is based on in vitro conditions and may not
the less likely it is that the infecting
reflect what occurs in the animal. In general,
pathogen can be predicted. Likewise, even if however, it is easier to achieve killing the correct pathogen is identified, predictconcentrations of a bactericidal than of a ing susceptibility in all but the most
bacteriostatic drug.

uncomplicated infections is likely to be
limited. This is true both historically and in

Special Considerations for Food
the individual patient. Even historically

Animal Veterinarians: The use of

"susceptible" organisms are characterized
antibiotics in food animals, including use
by higher MIC. For example, only 500/o of
as growth promotants, contributes to the
clinical E coli collected from dogs or cats transfer of resistance genes an10ng bacteria
are susceptible to amoxicillin. If the anin1al
and ultimately from food animals to people.

has previously received antimicrobials,

Additionally, contamination of food with
patterns of assumed susceptibility may no
resistant pathogenic bacteria during the
longer be relevant for that animal. 2) Once
processing of food is a concern. Carcasses
drugs to which the isolates are susceptible
may be contaminated at slaughter and
are identified, one that is more likely to
processing, and subsequent improper
penetrate the infected tissue should be
handling or cooking of the product may
chosen. This includes taking into consideralead to infection in people. The develoption host and microbial responses to ment of resistant pathogenic bacteria in
infection. Often, this requires that the drug
poultry treated with fluoroquinolones has
be lipid soluble. A variety of host and
been documented. Wection of the human
microbial factors contribute to antimicropopulation is of particular concern, because bial failure by presenting barriers to drug
the bacterial resistance created in the
penetration. Debris (eg, inflammatory
animal after veterinary use of a drug or
materials, necrotic tissue, foreign bodies)

drug class may result in resistance to
and biofilm or reduced blood flow and
hwnan drugs of the same class. Whereas
hypoxia contribute to failure. The organism
the organism developing resistance might
is intracellular in location and able to avoid
be nonpathogenic, transfer of the resistance
detrimental effects by phagocytic cells.

gene to other bacteria in the human GI tract

Even urinary tract infections may present
may result in a pathogenic organism
several barriers. Simply choosing a drug
becoming resistant and ultimately in
that is renally excreted may not be
therapeutic failure in people. When
adequate. Renal function may not be
selecting drug therapies for food animals,
nonnal, such that urine (and drug) is not
vete1ina.rians must be aware of the potential
concentrated. Bacteria are in the urine and
for resistance. Use of antibacterial drugs
also inside uroepithelial cells. Particularly
should be in the context of a valid veterinarwith chronic infections, the microbes may ian-client-patient relationship. Selection
be protected by biofilm and in a state of
should be based on all information available
quiescence such that they are less

( clinical findings, experience, laboratory
susceptible to many antimicrobial drugs.

data, physical examination findings, culture

Other factors must be considered when
and sensitivity data). Pathogens should be
designing the dosing regin1en. Irnmunocom-
identified, and drugs with the narrowest

2634

CHEMOTHERAPEUTICS INTRODUCTION
spectrum of activity with known effectiveexceed the MIC by 10- to 12-fold (for ness against the pathogen should be used.

concentration [sometimes referred to as

Client education is important to prevent
dose-dependent ru1tin1icrobials], such as the
unnecessary use of antibacterial agents
aI11inoglycosides ru1d the fluorinated

(such as using "leftover" antibacterial drugs quinolones) or be above the MIC (T>MIC)

VetBooks.ir
to treat a new occurrence of disease), to
for most (500/er 75%) of the dosi11g interval
advise on proper withdrawal guidelines of

(time-dependent ru1tibiotics, such as
any prescribed drugs, and to ensure that
cell-wall inhibitors [13-lactruns, fosfomycin,
drugs of the proper classes are administered vru1comycin], sulfonrunides, and most at proper closes and through appropriate

"bacteriostatic" drugs). To compensate for routes.

drug disposition to tissue sites and the

The Veterinary Feed Directive (VFD):

effect of host factors on ru1tibiotics, dosages

In June 2015, the FDA released the final
for most drugs should result in plasma drug
version of the VFD rule. The VFD an1ends
concentrations several times higher than
the Animal Drug Availability Act of 1996 (21
the calculated concentration-dependent or

CFR Prut 558), ru1d it delineates the FD A's
time-dependent MIC in the infected tissues
strategy to promote the judicious use of
or fluids. For dose-dependent drugs,
antimicrobials in food animals. A VFD drug
efficacy is enhru1ced by increasing the dose;

(which includes prescription drugs ru1d
for ti.me-dependent drugs, therapeutic
ove1°the-cow1ter drugs as a third potential
efficacy is enhru1ced by increasing the dose
category) is defined as "a drug intended for
and shmtening the dosing interval or by
use in or on aI1in1al feed." The drug may be
choosing a drug with a long half-liJe.

ru1 approved new ru1imal drug. A veterinruy

In today's infectious disease environfeed directive, or order, is the wTitten ment, appropriate design of a dosi11g
statement issued by a licensed veterinariru1,
regilnen should depend not on labeled
in the cow-se of practice, that orders the use
doses, but rather on access to infomiation
of the VFD drug, or combination VFD drug,
regarding the current pharrnacodynrunics
in or on ru1ilnal feed. A VFD order cru1 only
of the infecting microbe (ie, MIC from the
be issued w1der the supervision of a
pathogen cultured from the patient, or the
licensed veterinariru1, ru1d issuing veterinru�

MIC90 of a sample population of the
iru1s cru1 only do so within the framework of
pathogen collected from the target arwnal)

a valid veterinary-client-patient relationship
ru1d the pharrnacokinetics of that drug in the
as defined by the state in which the issuing
tru·get species. Appropriate pharmacokiveterinariru1 is licensed ru1d practicing ( or netic parruneters on which the dosing
federal definition in the absence of a state
regimen should be designed include
definition of a veteri11ary-client-patient
maxilnwn plasma concentration, or Cmax,
relationship). The rule describes the federal
for concentration-dependent dr1.1gs, ru1d
process to authorize VFD drugs, which must Cmax Md drug elinunation half-life for be subject to a new animal drug approval,
time-dependent drugs. Supportive
ru1d to establish ru1 ru1tin1icrobial considered infom1ation for design of dosil1g regi111ens medically necessruy as a VFD drug. The rule
often CM be fotmd in the literature. For
further defines two categories ofVFD drugs: exrunple, iJ the MIC of aPseudomonas category I, which is not associated with a
aeruginosa isolate for ru11ikacin ( a
withdrawal tune, and categmy 11, which
concentration-dependent drug) is 4 mcg/
requires some withdrawal time in at least
mL, the dose should be selected so that
one species in which the product is
peak plasma drug concentrations achieve
approved. Mixing of categmy II medicated

40-48 mcg/mL. Ideally, tissue concentrafeeds requiJ·es a medicated feed mill license.

tions should be that high as well. As such,

Guidelines by the FDA delineate the specific the dose should be adjusted fmther if the information that should be included on the
drug does not penetrate the tissue well i11

VFD. These guidelil1es il1clicate that
the presence of mru·ked inflrumnatory
extra-label use of a medicated feed is not
debris. Cephalexin is a time-dependent
permitted.

drug. If Staphylococcus pseuclintmmedius
cultured from a skin biopsy in a dog has an

DOSING REGIMENS

MIC of 2 mcg/mL, then the dosing regimen
should be selected to assure that drug

The design of a dosing regimen begins with
concentrations are >2 mcg/mL for at least
ru1 assessment of the mini111al inhibitory

500/er75% (Md ideally lOOOA,) of the dosing
concentration (MIC) of the ru1tibacterial
interval. The half-life of cephalexin is -3 hr
agent for a particular pathogen. Depending
in dogs. Using data reported in the literature
on the ru1timicrobial, plasma or tissue drug
for dogs, M oral dosage of cephalexin at
concentrations should either mru·kedly

22 mg/kg will achieve a C,,,ax of 25 mcg/mL.

CHEMOTHERAPEUTICS INTRODUCTION

2635

In one half-life, concentrations (mcg/mL)

data did not discriminate between
will decline to 12.5; in the second, to 6.25,
cornmensal and pathogen. The use of
in the third to 3.125, with concentrations
cytology should not be overlooked.

below target by the fourth half-life, or 6 hr.

Examination of a direct smear stained with

Thus, three elimination half-lives, or 9 lu-,

Wright's or Gram's stain may help to

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can elapse before the target MIC is reached,
establish the types of pathogens involved
and the next dose should occur by 9 lu-.

(gram-positive or gran1-negative rods or

Shortening the interval is generally more
cocci) and direct initial antibacterial
cost-effective than increasing the dose of
therapy. However, even if the pathogen is
time-dependent drugs, particularly for drugs correctly identified, the ability to predict with a short half-life-for each half-life to
the susceptibility pattern of the infecting
be added to the T>MIC, the dose must be
pathogen has markedly decreased in recent
doubled. Amoxicillin (with or without
years. If the anin1al has not been previously
clavulanic acid) has been an extremely
exposed to antimicrobials, it is safer to
popular lower-tier drng used for urinary
assw11e that standard expected susceptibiltract and soft-tissue infections. For the ity patterns for first-tier drugs ( eg,
latter, at 10 mg/kg, the drug achieves a
an1oxicillin with or without clavulanic acid
concentration of -5 mcg/mL in plasma. At
for E col'i or cephalexin for Staphylococcus an MIC of 2 mcg/mL, only one half�life can
pseudintermedius) may be relevant.

lapse. The half-life of an1oxicillin is only

However, if exposure to antimicrobials has

1-1.5 hr, indicating that dosing should occm
previously occurred, eg, because of
every 3 hr. As such, amoxicillin may not be
recm:rence of the cwTent infection,
an appropriate choice for soft-tissue
treatment of a different infection, or even
infections, and if used, it should be dosed at
exposure to antimicrobials through another
least every 8 hr, if not more often. However,
household member, culture and susceptibilbecause it is excreted in the urine, it is a ity testing might be prudent. Under field
good first choice to treat w1complicated
conditions, culture and susceptibility
minary tract infections, as long as urine is
testing may be difficult to accomplish. Use
retained in the bladder.

of an antibiogram, either generated locally

The integration of pharrnacokinetics and
for tl1e practice or based on national data,
pharmacodynamics can also be accommight help identify current susceptibility plished based on package insert infonnapatterns. Antibiograms reflect cmrent tion of more recently approved drugs. For
population susceptibility patterns. Package
example, for concentration-dependent
insert data or recent literature may also help
drugs, the C,,,a., should be at least 10 x the
select a drug based on population MIC

MIC00 of the target microorganism for that
statistics; such data can also be useful for
drug. For ti.me-dependent drugs, plasma
design of dosing regimens. Even in the event
drug concentrations should be above the
of culture submission, empirical ant.imicro

MIC90 of the infecting microbe for �5()0A,
bial therapy may need to be initiated before
of the dosing interval.

susceptibility data are received. If
susceptibility data indicate tl1e isolate is

REQUIREMENTS FOR
resistant, therapy should not change if tl1e

SUCCESSFUL ANTIMICROBIAL
anin1al has responded to the chosen drug.

THERAPY

Reculture might be important after therapy
has been completed. If the anin1al has not
responded, the data collected before

Clinical Diagnosis: Successful chemotreatment may no longer accmately predict tl1erapy usually requires a specific
the infecting population because the drug
diagnosis, even though a reasonable
may have changed susceptibility patterns.

preliminary diagnosis is often all that is
possible, at least initially. The presence of

Culture and Susceptibility Testing:

bacteria requiring systemic therapy should

Isolation and characterization of the
be confinned as much as possible; fever,
causative pathogen, susceptibility testing,
inflammation, and leukocytosis are
and determination of the MIC provide a
supportive of but not diagnostic for
sound foundation from which to select tl1e
bacterial infection.

antimicrobial drng and the dosage regimen.

However, culture and susceptibility data

Microbiologic Diagnosis: Treatment
are only as good as how the sample was
should be aimed at a specific pathogen
collected, handled, and tested. San1ples
whenever feasible. Care must be taken
must be collected without contamination.

when predicting the infecting pathogen

Free catch urines, swabs from endotracheal
based on histo1ic data, because often such
tubes, culture of drain tubes, and swabs

2636

CHEMOTHERAPEUTICS INTRODUCTION
from the surface of a contaminated wound

0.25 mcg/mL for enrofloxacill should not be
are all examples of unacceptable culture
illterpreted as beillg better than an MIC of2
samples. Swabs are less than ideal; not only
mcg/mL for ainikacin. The drug to which the
is the temptation to collect a contaminated
isolate is most susceptible to, based on
sample greater, but the swab itself can be
susceptibility data, is the drug with the MIC

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inhibitory to growth. Whenever possible,
most below the C,,.a, achieved in the animal
a tissue or fluid sample is preferred, with
at the recommended dose. However, this
handling of the sample left to the laborat01y. may not necessarily be the best drug to Equally important is proper refrigeration.

treat the mfection, based on other host,

For exan1ple, with a reproduction rate as
microbial, and dmg factors. Fmally, just
short as 20 min, E coli in an unrefrigerated because an isolate has been indicated as
mine sample can rapidly grow from lOl to

"S" on a culture report does not mean the

> 1 05 CFUs, thus transitioning from no
isolate has not developed some level of
infection to infection while overgrowing the
resistance. Rather, particularly for
true pathogens. The laboratory must also
commonly used dmgs, MIC for a specific
be selected carefully; it should follow
isolate may be approaching the CLSI
guidelines promulgated by the Clinical
breakpoint. Therefore, it is still considered

Laboratory Standards Institute (CLSI), use

"S," despite it having developed some level veterinary rather than hwnan materials,
of resistance. Therefore, doses for anti.Jnicroand be directed by a veterinary clinical bials ideally should err on the side of higher
microbiologist.

doses (concentration- or ti.Jne-dependent

Of the culture and susceptibility
dmgs) or shorter illtervals (time-dependent
procedures routinely used by laboratories,
dmgs ); the more at risk the a.ni.Jnal is for
tube ( or micro) dilution procedures are
therapy to fail, with development of a
preferred to agar gel procedures, because
recurrent, resistat1t mfection, the more
they can provide a mini.J11un1 inhibito1y
ill1po1tant the design of the dosing regi.Jnen.

concentration (MIC) of the drug toward an

In addition, data from even appropriately
isolate of the mfecting organism that has
collected sainples tested under ideal
been cultured from the aninlal. The MIC can
conditions remain subject to limitations.

be used to not only select the drug but also

Testing caimot take into a.ccotmt the impact
to design the dosing regi.Jnen. Some key
of distribution to the site of i.Jtfection, host
points regardillg susceptibility testillg may
factors such as inflammation, or microbial
facilitate illterpretation. The S (susceptible), factors, illcluding the size of the inoculum.

I (illtermediate), or R (resistant) illdicator

These and other factors may indicate a need
accompanymg each MIC is detennined by
to modify the dosillg regi.Jnen to assure
comparillg the MIC of the isolate to MIC
adequate concentrations at the site of

"breakpoillts" detem1illed by CLSI. An
illfection. Lipid-soluble dmgs may become
isolate with an MIC below the breakpoint
increasingly i.Jnportant as mfection
established for each drug is considered "S,"

becomes more complex. Most antimicroversus an isolate with an MIC at or above bials are lipid soluble, with the 13-lactams
the breakpoint, which is considered "R."

(penicillins, cephalosporins) beillg common

Although the actual concentratiotls tested
exceptions.

for all drugs are generally the same, the
range tested varies for each drug, as do the

COMBINATION THERAPY
breakpoillts. For example, for enrofloxacin,
tested concentrations generally range from

Treatment with antill1icrobial combillations

0.5 to 2 mcg/mL; for amikacin, from 4 to 32
may be necessary ill certain cases. The
mcg/mL; and for ticarcilli.J1, from 16 to 128
administration of two or more agents may be
mcg/mL. The current susceptible and
beneficial ill the following situations: 1) to
resistant CLSI breakpoints (mcg/mL),
treat mixed bacterial infections ill which the
respectively, established for each drug are
orgat1isms are not susceptible to a common

<0. 5 and > 4 for enrofloxacill, and <4 and a.gent, 2) to ac\tieve synergistic antimicrobial

>64 for amikacill. These breakpoillts are
activity against particularly resistant strains
followed by any laboratory in the USA that

( eg, Pseudomonas aeruginosa,), or 3 ) to
follows CLSI protocols or guidelines. That
reduce the risk of or overcome bacterial
the concentrations differ for each drug,
resistance. In general, combillation therapy
reflects, ill part, the different drug concenis most appropriate with a mixed i.Jtfection trations achieved ill plasma (and thus
or when an empi.Jical selection must be
tissues) for each dmg when adrni.Jtistered at
made in a life-threaterting situation.

recommended dosillg regill1ens. Because

Additive or synergistic effects are seen
the concentrations tested and achieved m
when antibacterial agents are used ill
the ani.J11al vaiy for each drug, an MIC of
combination. Prime exan1ples are the

ANTHELMINTICS

2637
combination of clavulanic acid with

!ins, cephalosporins, aminoglycosides,
amoxicillin or ticarcillin ( or sulbactam with
trimethoprim/sulfonamides ("potentiated"), ampicillin), in wltich the first agent prevents
metronidazole, quinolones, rifampin, and

13-lactamase destruction of the second
glycopeptides. The following antimicrobials
agent, or the combination of a diaminopyat usual concentrations are generally VetBooks.ir
rin1idine such as trimethoprim or ormebacteriostatic: tetracyclines, the phenicols toprim with a sulfonamide. Antibactelial

( eg, chloramphenicol, florfenicol),
antagonism may also emerge, sometimes
macrolides, lincosamides, spectinomycin,
with serious consequences. Generally,
and the sulfonamides (nonpotentiated).

bacteriostatic agents act in an additive

Ideally, antimicrobial selection should be
fashion with one another, whereas
based on different mechanisms of action
bactericidal agents are often synergistic
and on complementary spectra of activity.

when combined. However, the effects of

13-Lactams are often selected, because their
several bactericidal antibiotics are
action may facilitate movement of other
substantially impaired by simultaneous use
drugs through the damaged cell wall into
of drugs that impair microbial growth or
the microbe. Examples of combination

"bacteriostatic" drugs ( eg, most 1ibosomal therapy for mixed infections include the
inhibitors). Tltis is a general guideline only;
use of clindan1ycin, metronidazole, or the
many exceptions are known, and confoundsemi.synthetic penicillins for their anaerobic ing factors also play a role. Classification of
coverage in combination with an1inoglycoantimicrobials as bactericidal or bacteriosides for their gran1-negative efficacy.

static can also be misleading, because

Synergism against certain bacterial

"bactericidal" drugs can be rendered
pathogens frequently can be acltieved with
bacteriostatic if sufficient drug concentracombinations of penicillins or cephalospotions are not achieved at the site of rins and arni.noglycosides. The combined use
infection. However, in general, the following
of trimethoprirn with selected sulfonamides
common antimicrobials at MIC concentraor clavulanic acid with other 13-lactams are tions are likely to be bacte1icidal: penicil-other examples of synergistic effects.

ANTHELMINTICS

Many highly effective and selective
operation of the esophageal groove reflex),
anthelmintics are available, but such
and characteristics of the parasite ( eg, its
compounds must be used correctly,
location in the body, its degree of hypobiojudiciously, and with consideration of sis, susceptibility of the life stage, or
the parasite/host interaction to obtain a
susceptibility to the anthelrnintic ).

favorable clinical response, accomplish

There are several classes of anthelnlingood control, and mininlize selection for tics: benzimidazoles and probenzimidaanthelmintic resistance. Any decrease or zoles, salicylanilides and substituted
increase of the reconunended dose rate
phenols, in1idazotltiazoles, tetralwdropyrimust always be discomaged. Underdosing midines, organophosphates, macrocyclic
is likely to result in lowered efficacy and
lactones and, more recently introduced, the
possibly increased pressure for developan1ino-acetonitrile derivatives, the cyclic ment of resistance. Overdosing may result
octadepsipeptides, and the spiroindoles.

in toxicity without necessarily increasing

Although it may be thought that chemoproduct efficacy.

therapeutic control of helminth infections is

Most anthelmintics generally have a wide
curTently satisfactory, selection for parasite
margin of safety, considerable activity
resistance is an increasing concern.

against immature (larval) and mature stages
of helminths, and a broad spectrum of

MECHANISMS OF ACTION
activity. Nonetheless, the usefulness of any
anthelmintic is limited by the intrinsic

Antl1elmintics must be selectively toxic to
efficacy of the drug itself, its mechanism
the parasite. This is usually achieved either
of action, its pharmacokinetic properties,
by inhibiting metabolic processes that are
characteristics of the host animal ( eg,
vital to the parasite but not vital to or absent

2638

ANTHELMINTICS
in the host, or by inherent pharmacokinetic
mitochondrial membrane. Although
properties of the compound that cause the
isolated nematode mitochondria are
parasite to be exposed to higher concentrasusceptible, many fasciolicides are tions of the anthelmintic than are the host
ineffective against nematodes in vivo,
cells. While the precise mode of action of
apparently due to a lack of drug uptake.

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many anthelmintics is not fully understood,

Exceptions are the hematophagous
the sites of action and biochemical mechanematodes, eg, Haemonchus and nisms of many of them are generally known.

Bunostomum.

Parasitic helminths must maintain an

Clorsulon is rapidly absorbed into the
appropriate feeding site, and nematodes
bloodstream. When Fasciola. hepalica
and trematodes must actively ingest and
ingest it (in plasma and bound to RBCs),
move food through their digestive tracts to
they are killed because glycolysis is
maintain an appropriate energy state; this
inhibited and cellular energy production
and reproductive processes require proper
is disrupted.

neuromuscular coordination. Parasites
must also maintain homeostasis despite

Neuromuscular Coordination:

host immune reactions. The pharmacologic

Interference with tllis process may occur by
basis of the treatment for helminths
inhibiting the breakdown or by mimicking
generally involves interference with the
or enhancing the action of neurotransmitintegrity of parasite cells, neuromuscular ters. The result is paralysis of the parasite.

coordination, or protective mechanisms

Either spastic or flaccid paralysis of an
against host immwtity, which lead to
intestinal helnlinth allows it to be expelled
starvation, paralysis, and expulsion or
by the normal peristaltic action of the host.

digestion oJthe parasite.

Specific categories include drugs that act
via a presynaptic latrophilin receptor

Cellular Integrity: Several classes

( emodepside ), various nicotinic acetylchoof anthelmintics impair cell structure, line receptors (agonists: imidazothiazoles,
integrity, or metabolism: 1) inhibitors of
tetraliydropyrinlidines; allosteric modulatubulin polymerization-benzin1idazoles tor: monepantel; antag01list: spiroindoles),
and probenzirnidazoles (which are
glutamate-gated chloride charmels
metabolized in vivo to active benzimida

(avennectins, milbemycins), GABA-gated
zoles and thus act in the same marmer); 2)

chloride channels (piperazine ), or via
uncouplers of oxidative phosphorylationinhibition of acetylcholinesterases salicylanilides and substituted phenols; and

( cownaphos, naphtl1alophos).

3) inhibitors of enzymes in the glycolytic

Organophosphates inhibit many enzymes,
pathway----clorsulon.

especially acetylcholinesterase, by

The benzirnidazoles inhibit tubulin
phosphorylating esterification sites. This
polymerization; it is believed that the other
phosphmylation blocks cholinergic nerve
observed effects, including inhibition of
transmission in the parasite, resulting in
cellular transport and energy metabolism,
spastic paralysis. The susceptibility of
are consequences of the depolyrnerization
cholinesterases by host and parasite varies,
of microtubules. Inhibition of these
as does the susceptibility of these different
secondary events appears to play an
species to organophosphates.

essential role in the lethal effect on worms.

The imidazotlliazoles are nicotinic

Benzimidazoles progressively deplete
anthelnlintics that act as agonists at
energy reserves and inhibit excretion of
nicotinic acetylcholine receptors of
waste products and protective factors from
nematodes. Their anthelmintic activity is
parasite cells; therefore, an important factor
mainly attributed to their ganglion-stim uin their efficacy is prolongation of contact lant (cholinomimetic) activity, whereby
time between drug and parasite. Crossthey stimulate ganglion-like structures in resistance can exist among all members of
somatic muscle cells of nematodes. This
this group, because they act on the same
stimulation first results in sustained muscle
receptor protein, [3-tubulin, which is altered
contractions, followed by a neuromuscular
in resistant organisms such that none of the
depolaiizing blockade resulting in paralysis.

benzinlidazoles can bind to the receptor

Hexamethoniun1, a ganglionic blocker,
with high affinity.

inhibits the action of levamisole.

Uncoupling of oxidative phosphorylation

Monepantel, the only commercially
processes has been demonstrated for the
available anlino-acetonitrile derivative, is a
salicylanilides and substituterl phenols,
direct agonist of the mptl-1 charmel, which
which are mainly fasciolicides. These
is a homomeric charmel belonging to the
compounds act as protonophores, allowing

DEG-3 family of nicotinic acetylcholine
hydrogen ions to leak through the inner
receptors. Binding of monepantel to the

ANTHELMINTICS

2639
receptor results in a constant, uncontrolled
stimulate a postsynaptic receptor. Recent
flux of ions and finally in a depolarization
findings indicate that a second emodepside
of muscle cells, leading to irreversible
target is the calcimn-activated potassium
paralysis of the nematodes. These receptors
channel slo-1. Binding to the latrophilin
are tmique in that they are found only in
receptor and the slo-1 ion channel leads to

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nematodes.

inhibition of pharyngeal pumping, paralysis,

Derquantel, a semisynthetic member of
and death.

the spiroindole class of anthelmintics, is an

The mode of action of praziquantel is not
antagonist of B-subtype nicotinic acetylchocertain, but it rapidly causes tegun1ental line receptors located at the nematode
damage and paralytic muscular contraction
neuromuscular junction; it inhibits 45-pS
of cestodes, followed by their death and
channels, leading to a flaccid paralysis of
expulsion.

nematodes.

Piperazine acts to block neuromuscular

PHARMACOKINETICS
transmission in the parasite by hyperpolarizing the nerve membrane, which leads to After administration, anthelrnintics are
flaccid paralysis. It also blocks succinate
usually absorbed into the bloodstream and
production by the worm. The parasites,
transported to different parts of the body,
paralyzed and depleted of energy, are
including the liver, where they may be
expelled by peristalsis.

metabolized and eventually excreted in

The macrocyclic lactones act by binding
the feces and urine. The disposition of
to glutamate-gated chloride channel
anthelrnintics throughout the body is
receptors in nematode and arthropod nerve
considerably more complex than can be
cells. This causes the channel to open,
described by a set of pharrnacokinetic
allowing an influx of chloride ions. Different parameters in the peripheral circulation.

chloride channel subunits may show

Improved drug performance requires
variable sensitivity to macrocyclic lactones
knowledge of drug behavior in the
and different sites of expression, which
multicompartmental system, including the
could account for the paralytic effects of
complex interaction between formulation
macrocyclic lactones on different neuroand route of administration, physicochemimuscular systems at different concentracal properties of the compound, and tions. The macrocyclic lactones paralyze
physiology of the compartment into which
the pharynx, the body wall, and the uterine
the drug is distributed.

muscles of nematodes. Paralysis (flaccid) of

Although many helminth parasites reside
body wall muscle may be critical for rapid
in the lumen or close to the mucosa, others
expulsion, even though paralysis of
live at sites such as the liver and lungs; for
pharyngeal muscle is more sensitive. AE
action against these, absorption of drug
the macrocyclic lactone concentration
from the GI tract, injection site, or skin is
decreases, motility may be regained, but
essential. Intestinal parasites come in
paralysis of the pharynx and resultant
contact not only with the unabsorbed drug
inhibition of feeding may last longer than
passing through the GI tract but also with
body muscle paralysis and contribute to
the absorbed fraction in the blood as they
worm deaths. None of the macrocyclic
feed on the intestinal mucosa, and with any
lactones are active against cestodes or
that is recycled into the gut. This is an
trematodes, presumably because these
important aspect of efficacy of many of the
parasites do not have a receptor at a
benzimidazoles.

glutamate-gated chloride channel.

The pharrnacokinetics of an anthelmintic,

Emodepside acts presynaptically at the
its rate of metabolism and excretion, and its
neuromuscular junction, where it attaches
safety profile detennine the length of the
to a latrophilin-like receptor. This receptor
withdrawal time; this period can vary
belongs to the group of so-called G-protein
an1ong species and can also be affected by
coupled receptors. Stimulation of the
route of administration and dose. The usual
latrophilin-like receptor by emodepside
site of metabolism of anthelmintics is the
activates a signal transduction cascade via
liver, where oxidation and cleavage

Gq-protein and phospholipase C, causing an
reactions commonly occur.

increase in intracellular calciun1 and
diacylglycerol levels. At the end of the signal

Benzimidazoles and Probenzimida
transduction cascade, vesicles containing
zoles: With a few exceptions, eg,
inhibitory neuropeptide fuse with presynapalbendazole, oxfendazole, and triclabendatic membranes. After fusion of these zole, only limited an1ounts of any of the
membranes, inhibitory neuropeptides may
benzimidazoles are absorbed from the GI
be released into the synaptic cleft to then
tract of the host. The lin1ited absorption is

2640

ANTHELMINTICS
probably related to the poor water solubility Tetrahydropyrimidines: Pyrantel of these drugs. The little absorption that
tartrate (or citrate) is well absorbed by pigs
occurs is generally rapid, 2-7 hr after dosing
and dogs, less well by nuninants. The
wi.th flubendazole and 6-30 hr after dosing
pamoate salt (synonym embonate) of
wi.th albendazole, fenbendazole, and
pyrantel is poorly soluble in water; this

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oxfendazole, depending on the species.

offers the advantage of reduced absorption

Many of the benzimidazoles and their
from the gut and allows the drug to reach
metabolites re-enter the GI tract by passive
and be effective against parasites in the
diffusion, but the biliary route is the most
large intestine, which makes it useful in
important pathway for secretion and
horses and dogs. Metabolism of pyrantel is
recycling of benzimidazoles in the GI tract.

rapid, and the metabolites are excreted

A nwnber of benzi.midazoles ( eg,
rapidly in the urine (400/oof the dose in
febantel, thiophanate, netobimin) exist in
dogs); some llllchanged drug is excreted in
the form of prodrugs that must be metabotl1e feces (principally in rwninants). Blood lized in the body to the biologically active
concentrations usually peak 4-6 hr after PO
benzirnidazole carbamate nucleus. Febantel
administration.

is hydrolyzed to the active metabolite

Moran tel is the methyl ester analogue of
fenbendazole, and netobirnin undergoes
pyrantel and, in rw11inants, it tends to be
processes of reduction, cyclization, and
safer and more effective than pyrantel. It
oxidation to yield albendazole sulfoxide.

is absorbed rapidly from the upper small

Benzirnidazole sulfoxides such as oxfendaintestine of sheep and metabolized rapidly zole and albendazole sulfoxide bind poorly
in the liver; -17% of the initial dose is
to parasite 13-tubuli.n and probably act as
excreted in the urine as metabolites within
prodrugs for fenbendazole and albendazole,

96 hr after dosing.

respectively. The thiometabolites have high
affinity for helm in th tub ulin.

Macrocyclic Lactones: Macrocyclic

Metabolism of the benzimidazoles is
lactones are hydrophobic, an in1portant
variable and may alter their activity; eg,
characteristic of this class of anthelmintics.

albendazole is rapidly and reversibly

Regardless of their route of administration,
oxidized to its sulfoxide form. The sulfoxide macrocyclic lactones are distributed may be irreversibly oxidized to its sulfone,
tlu·oughout the body and some concentrate
which is signilicantly less active than the
in adipose tissue. Liver tissue contains the
sulfoxide. Similarly, fenbendazole and
highest residue for the longest, reflecting the
oxfendazole (fenbendazole sulfoxide) are
route of elimination. Although the magniinterchangeable, but the oxidation product tude of lipophilicity differs an1ong chemical
fenbendazole sulfone is less active and is
types, the linlited vascularization and slow
not reduced back to the sulfoxide or thio
turnover rate of body fat and tl1e slow rate of
metabolites.

release or exchange of dmg from these lipid
ln rwninants, the benzimidazoles are
reserves can prolong the residence of drug
most effective if deposited into the rumen.

in the peripheral plasma Ive1mectin is

Ad.ministration directly into tl1e abomaswn,
arguably the least lipophilic macrocyclic
via the esophageal groove, may shorten the
lactone, with tl1e possible exception of
duration for drug absorption and increase tl1e ep1inomectin. Moxidectin is -100 times rate of excretion in the feces, which may
more lipophilic than ivermectin. Doramectin
reduce efficacy. For example, inunedi.ate
is less lipophilic than moxidectin but more
arrival of oxfendazole in the abomaswn after
than ivennectin or eprinomectin.

dosing reduces its efficacy from 91% to 45%

Ivermectin was the first commercially
against thiabendazole-resistant strains of
available macrocyclic lactone and has been

Haemonchus contortus. The mrnen acts as a the most extensively studied. When given drug rese1voir from which plasma concentrarv, ivermectin has an elin1ination half-life of tions can be sustained, slowing tl1e passage

32-178 hr, depending on species. Despite
of wiabsorbed drug tlu·ough the GI tract.

the higher dose rate of the injectable
formulation in pigs (300 mcg/kg) compared
lmidazothiazoles: The absorption and
with that of cattle (200 mcg/kg), the
excretion of levami.sole is rapid and not
maxirnwi1 concentration (C,,,aJ and area
affected by the route of administration or
under the Cluve (AUC) in peripheral plasma
ruminal bypass, because it is highly soluble.

in pigs are about one-tllird those in cattle.

ln cattle, blood concentrations of levami.

Although the elimination half-life after SC
sole peak < 1 hr after SC administration.

and IV ad.ministration of ivem1ectin is of

These concentrations decline rapidly; 900/o
similar duration, slow absorption from the
of the total dose is excreted in 24 hr, largely
iajection site may broaden the concentrain the urine.

tion-time profile, with cmax in peripheral

ANTHELMINTICS

2641
plasma of cattle occurring as late as 96 hr.

to plasma protein. When they reach the

The C"'"" and AUC in pigs and goats are bile ducts, they are in the main excretory
considerably lower than those in cattle,
channels for the active metabolites of the
horses, and sheep. Pigs, and possibly goats,
fasciolicides and are exposed to toxic
may metabolize ivermectin faster than other concentrations. This may explain why VetBooks.ir
species.

mature flukes are more vulnerable to most

In rnminants, the macrocyclic lactones
fasciolicides than inlmature ones. The
are, like benzi.rnidazoles, most effective if
higher concentrations of fasciolicides and
deposited directly into the rnmen. A 3- to
their metabolites in feces than in urine

4-fold decrease in C.,.ax and AUC of iversuggest that the bile ducts are their main mectin after intra-abomasal compared
excretory pathways.

with intrarnminal ad.ministration has been

It is important to understand the
reported. Significantly, time to maximal conpham1acokinetics of prescribed anthelmincentration of ivermectin was reduced from tics. For example, nitroxynil has good

23 hr to 4 hr with the fonner route of
efficacy againstF hepatica in cattle and
delivery.

sheep and against H contortus, but because

Concentrations of ivermectin are high in
rnmen bacteria metabolize and destroy the
digesta sampled from the distal intestine,
activity of nitroxynil, it must be ir\jected.

indicating that biliary secretion is an
important pathway for clearance of

Amino-acetonitrile Derivatives: After
macrocyclic lactones. This pathway also

PO administration, monepantel is quickly
has been conclusively demonstrated for
absorbed into the bloodstrean1 and
clearance of benzinlidazole compounds.

metabolized to a major extent within 4 hr

The extended high concentration in bile is
into monepantel sulfone. The sulfone
influenced by prolonged exchange of drug
expresses in vitro anthelmintic activity
from lipid reserves and the enterohepatic
similar to tl1at of the parent molecule and is
recycling of biliary compounds through the
responsible for the anthelnlintic effect in
portal and biliary pools. The macrocyclic
animals, because 95 % of the administered
lactones are primarily excreted in tl1e feces,
dose is metabolized into the sulfone. The
the remainder ( <l OOA,) in the urine. The more cmax of monepantel sulfone was 4 foldlipophilic macrocyclic lactones are also higher compared with that measured for tl1e
excreted in milk.

parent compound. After PO ad.ministration
in sheep of the recommended dosage of

Salicylanilides and Substituted

2.5 mg/kg, the elinlination half-life of the

Phenols: Secretion via the liver and bile is sulfone metabolite in plasma was 48. 7 hr,
especially important for drngs active against with a mean residence time of 79.3 hr.

adultFasciola spp. The fasciolicidal effects Approximately 27% of the ad.rninisterep
of salicylanilides (such as rafoxanide) in
dose is excreted through the feces in the
sheep depend on persistence of the drug in
fom1 of the sulfone derivative. The
plasma, which influences their transport
remaining an10unt is further metabolized
throughout the body and rate of elimination. and partly excreted through urine ( up to Closantel, rafoxanide, and oxyclozanide

30% of the ad.ministered dose). In addition
have long temlinal half-lives in sheep (14.5,
to the sulfone, the parent monepantel

16.6, and 6.4 days, respectively), which are
contributes to the anthelmintic activity
related to the high plasma-protein binding
against abomasal nematodes, because the

(>99%) of these three drngs. Residues in
concentration of the parent monepantel is
liver are detectable for weeks after
considerably higher in the abomasum than
administration. Associated with persisin plasma.

tence, however, is the need for longer
withholding periods. Oxyclozanide also

Cyclic Octadepsipeptides: Studies in
is bound to plasma protein and then
rats have been done to assess the general
metabolized in the liver to the anthelmintidistribution, metabolism, and excretion cally active glucuronide and excreted in
patterns of emodepside after PO and IV
high concentration in the bile duct, where it
ad.ministration. Bioavailability after PO
encounters the mature flukes.

administration is -500Ai. Emodepside is
lnlrnature flukes in the liver parenchyma
distributed throughout the whole organism,
ingest mainly liver cells, which contain little
but highest concentrations are found in fat
anthelmintic; plasma-protein binding limits
tissues, where it forms a deposit that is
entry of the drng into the tissue cells. As the
slowly released. Emodepside is excreted
flukes grow and nligrate through the liver,
predominantly via the bile and then
they cause extensive hemorrhaging and
eliminated in the feces. Approxin1ately half
come into contact witl1 anthelmintic bound
of the administered dose is excreted within

2642

ANTHELMINTICS
the first 24 hr. The elimination half-life after
is also longer: 21-77 days for closantel,
both PO and IV administration is 39-51 hr.

rafoxanide, and nitroxynil, compared with

Approximately 45%-56% of the adminis3-14 days for oxyclozanide. The low tered dose is excreted unchanged, the rest
plasma-protein binding of diamfenetide,
in the form of inactive metabolites. After
coupled with the rapid excretion of its

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topical administration in cats, emodepside
active metabolite, necessitates only a short
is absorbed slowly into the bloodstrean1.

withdrawal time. Similarly, withholding

Maximwn plasma levels are reached 2-3
periods for milk vary widely. Closantel and
days after treatment. Absorption after PO
nitroxy.nil carmot be used in lactating
administration in dogs is higher if adminisanimals when milk is intended for hmnan tered to fed animals.

conswnption, whereas oxyclozanide has a
withdrawal ti.me of only 60 hr.

Spiroindoles: Pharmacokinetics

Levamisole and morantel are rapidly
demonstrate that after a single oral
excreted; thus, withholding periods for
administration, maximwn concentrations
meat are short, and frequently there is no, or
of derquantel were reached at 4.2 hr. The
only a short, withholding period for milk.

terminal half-life of derquantel was 9.3 hr,

However, in some countries, levamisole
and the absolute bioavailability was 56.3%.

cannot be used in lactating animals when

Metabolism of derquantel is extensive and
milk is intended for hw11an consun1ption.

complex. Derquantel undergoes biotrans

Ivennecti.n and doramectin are excreted
fom1ation to a large nwnber of metabolites
in milk and are not recommended when
over a short time and, as a result, extensive
milk is intended for hwnan consumption.

variation in metabolites has been found in

Commensurate with the long period of
tissues and over tin1e periods.

activity of macrocyclic lactones, ivem1ectin,
aban1ectin, doran1ectin, and moxidectin

Praziquantel: Praziquantel is rapidly and
have significant withholding periods before
almost completely absorbed from the GI
slaughter ( eg, 35 days), which vary with the
tract. After absorption, praziquantel is
formulations and local regulations. Residual
distributed to all organs; it is believed to
concentrations of moxidectin in milk after
re-enter the intestinal lwnen via the mucosa
topical administration are below threshold
and bile in dogs. Praziquantel is rapidly
limits, resulting in no milk withholding
hydroxy lated into inactive forms in the liver
period in many countries. The chemical
and secreted in bile. It has a wide safety
structure of the macrocyclic lactone
margin.

molecule has been manipulated to change
the milk partitioning coefficients in lactating

WITHHOLD NG PERIODS
dairy animals. For example, only 0.1 % of the
total dose of eprinun1ectin is eliminated in

Most anthelmintics have withholding
the milk, resulting in no withholding period
periods if milk or meat from treated animals
for milk worldwide.

is intended for hwnan conswnption; the

Monepantel has a withdrawal period of
specific requirements for each must be

7 -14 days for meat and is not approved for
observed. Of the benzimidazoles, thiabendause in lactating animals producing milk for zole is absorbed and excreted most quickly;
hwnan consmnption.

fenbendazole, oxfendazole, and albenda

In combination with aban1ectin,
zole are absorbed and excreted over a
derquantel has a withholding period of 14
longer period, which necessitates withholddays for meat and is not approved for use in ing periods of 8-14 days before slaughtering
lactating animals producing milk for hwnan
for meat and 3-5 days before milking for
consumption.

hwnan conswnption. Other members of the
group have withholding periods between
these extremes, but withholding periods are

SAFElY
longer for bolus fonnulations.

A similar relationship between the rate of

Most anthelmintics have wide safety
metabolism and activity against immature
margins, ie, the dosage that can be given
parasites also exists with certain fasciolito an animal before adverse effects are cides. Closantel, rafoxanide, and nitroxynil
induced is much higher than the dosage
bind more strongly to blood proteins than
reconunended for use. The wide safety
does oxyclozanide, and therefore remain in
margin of benzimidazoles is because of their
the blood for longer periods. While this
greater selective affinity for parasitic
greater persistence is associated with

[3-tubulin than for mammalian tissues.

greater activity against in1.lllature liver

Nonetheless, this selective toxicity is not
flukes, the withholding period for slaughter
absolute; some toxic effects based on

ANTHELMINTICS

2643
antimitotic activity (teratogenicity or
barrier. A P-glycoprotein deficiency in
embryotoxicity) can occur in some target
certain anin1als decreases the ability to
species, and some benzimidazoles,
pump avermectins, milbemycins, and other
depending on the dose rate, are contraindidrugs across cell membranes. The net effect VetBooks.ir
cated in early pregnancy.

is an increase in systemic bioavailability,

The safety index (SI) is not as wide for
because animals deficient in P-glycoprotein
levamisole (SI= 4-6), nor for most of the
are not able to actively pun1p the macrocychemicals active against liver flukes (SI =
clic lactones out of the CNS or efficiently

3--6). Manunalian toxicity with levan1isole is
process these drugs. This decreases the
seen more often than with benzimidazoles,
ability to redistribute, metabolize, and
although toxic signs are unusual unless the
excrete macrocyclic lactones, as well as
normal therapeutic dosage is exceeded.

antineoplastic drugs, opioids, aceproma

Levamisole toxicity in the host animal is
zine, digoxin, and ondansetron, resulting in
largely an extension of its antiparasitic
toxicity with what would be considered
effect, ie, cholinergic-type signs of
normal doses in most animals. There have
salivation, muscle tremors, ataxia,
been cases of CNS depression in cattle
urination, defecation, and collapse. In fatal
breeds (Murray Grey) and in individual dogs
levamisole poisoning, the inunediate cause
of multiple breeds, but these were first
of death is asphyxia due to respiratory
recognized in purebred and crossbred
failure. Atropine sulfate can alleviate such

Collies. Nervous signs (idiosyncratic
signs. Levamisole may cause some
reactions), including depression, muscle
inflanunation at the site of SC injection, but
weakness, blindness, coma, and death, were
usually this is transient. Toxicity increases
seen when high doses were administered.

if other anticholinergic drugs ( eg, organo

Because salicylanilides, substituted
phosphates) are given at the same time.

phenols, and aromatic amides are general

Because of their low absorption from the
uncouplers of oxidative phosphorylation,
gut, tetrahydropyrin1idines have a high
their Sis are lower than those of many other
safety margin. Adverse effects (vomiting in
anthelnlintics. Nonetheless, they are safe if
dogs and cats) are rare. Toxicity increases
used as directed. Adverse effects are most
when other cholinergic drugs ( eg, levamicommonly seen in anin1als that are severely sole, organophosphates) are used
stressed, in poor condition nutritionally or
simultaneously.

metabolically, or have severe parasitic infec

The margin of safety for organophostions. Mild anorexia and unfom1ed feces phates is generally less than that of the
may be seen after treatment at recombenzinlidazoles, and strict attention to mended dosages. High dosages may cause
dosage is necessary. Generally, their toxicity blindness, hype1thermia, convulsions, and is additive; thus, concurrent use of other
death-classic signs of uncoupled
cholinesterase-inhibiting drugs should be
phosphorylation.

avoided. Atropine and 2-PA.i\'l are used as

The an1ino-acetonitrile derivatives target
antidotes to organophosphate toxicity (see
a nematode-specific receptor that is absent
also p 3064). Organophosphates also can be
in mammals and other organisms. Because
hazardous to people. Being lipid soluble,
of this specific mode of action, monepantel
they are readily absorbed through unbroken has a very favorable safety profile.

skin. Sprays, collars, and washes of

Monepantel has been administered to lambs
organophosphates used for small animals
in doses up to 30 times higher than the
can present significant hazards to young
recommended dose without any adverse
infants after ingestion, inhalation, or
effects. In addition, repeated oral administranscutaneous absorption.

tration of monepantel at three times the

Manunals are generally not adversely
recommended dose every 5 days over an
affected by macrocyclic lactones. The SI for
entire reproductive cycle was not associthe macrocyclic lactones is typically wide, ated with any treatment-related adverse
but both aban1ectin and moxidectin are
effects on the reproductive performance of
contraindicated in calves and foals <4 mo
rams or ewes or on the viability of their
old, respectively, because of narrow safety
offspring, and it was systemically very well
margins in these classes of stock. Othertolerated.

wise, single administration at -10 times and

Emodepside appears to be of low acute
multiple administration at 3 times the
toxicity in a variety of laboratory animal
recommended therapeutic dose levels do
species and by a variety of routes. Although
not have any secondary effects on healthy
overt signs of toxicity include depressed
host animals.

neurologic and respiratory function, they

Manm1alian safety appears to depend on
occur only at dose rates far in excess of the

P-glycoprotein activity in the blood-brain
recommended therapeutic dose in cats.

2644

ANTHELMINTICS

Repeated treatment at three times the

There are limited repo1ts of resistance
therapeutic dose was tolerated in pregnant
against levanusole, pyrantel, and benzimidaand lactating dams/queens, so adverse zoles in Oesophogoslomum denlalum in
effects on reproductive function of the
pigs.

dams and/or kitten health are not antici

Multidrug (benzimidazoles and macrocy

VetBooks.ir
pated when the product is administered at
clic lactones) resistance in cattle nematodes
the recommended treatment dose. Safety in
has been documented on farms in New
dogs was established only for puppies

Zealand, the Americas, and Europe, and tl1is

�12wk old.

will probably become more widespread. In

The combination of derquantel and
most cases of resistance against macrocyabamectin did not result in any adverse clic lactones, Coope,ia spp were identified clinical effects in ewes and lambs under
as the resistant worm species, but
field conditions, other than a conunonly
macrocyclic lactone resistance is also
reported, mi.Id, transient coughing.

emerging in Osterlagia oslertagi. The full
extent of anthelmintic resistance in cattle

RESISTANCE
nematodes is unlrnown.

The development of sigi1ificant levels

The development of nematode and
of resistance seems to require successive
trematode resistance to various groups of
generations of helmintl1s exposed to tl1e
anthelmintics is a major problem. Compared
same class of anthel.n1intic. However,
with development of antibiotic resistance
evidence suggests tl1at genes for resistance
in bacteria, resistance to anthelm.intics in
are invariably present, at a low frequency,
nematodes has been slower to develop
for any given antheh11intic. Selection for
under field conditions. However, resistance
resistance sin1ply requires the preferential
is becoming widespread, because relatively
killing of the susceptible parasites and
few chemically dissin1ilar groups of
survival of the parasites with the resistance
anthelmintics have been introduced over the
genes. Side-resistance is frequently seen
past several decades. Most of the conm10nly
between members of the be.nzin1idazole
used anthelmintics belong to one of three
group because of their sin1ilar mechanisms
chemical classes, be.nzin1iclazoles, in1iclazoof action; control of benzin1idazole-resistant thiazoles, and macrocyclic lactones, within
para'lites by levamisole can be expected
which all individual compounds act in a
because of its different mode of action.

similar fashion. Thus, resistance to one

Altl10ugh there is no evidence for crossparticular compound may be accompanied resistance between Jevan1isole and
by resistance to other members of the group
benzin1idazoles, this does not mean that

(ie, side-resistance).

worms resistant to both kinds of drugs will

In nematodes of small iuminants, and
not evolve if both types of anthelmintics are
especially inHaemonchus conlorlus,
used frequently. Nematodes resistant to
resistance to all classes of broad-spectrum
levanusole are cross-resistant to morantel
anthelrnintics has reached serious levels
because of the sin1ilarities of their mecha-
in many parts of the world. Resistance also

11.isms of action. When resistance to the
has been found in Trichoslrongylus spp,
reconunendecl dose rate of an avermectin

Cooperia spp, and Teladorsagia spp appears in some species of nematodes, a
in sheep and goats. Reports of multiple
milbemycin, at its recommended dose rate,
resistance to most major classes of
may still be effective. However, there is
anthelmintics are increasing. Recently,
side-resistance among the avermectins and
resistance to monepantel has occurred in the the milbemycins, which are within the same field (New Zealand) in at least two nematode
class of anthel.n1intics, and continued use of
species (Teladorsagia circwncincla and
either subgroup will select for macrocyclic

Trichoslrongylus colubriformis) after
lactone resistance.

being administered on 17 separate occasions

Recently, it was demonstrated in
to different stock classes and in <2 yr of the

Haemonchus contortus and Onchocerca
product first being used on the farm.

volvulus that macrocyclic lactone

Resistance to benzimidazoles is
anthelmintics can affect 13-tubulin, although
widespread in cyathostome nematodes of
no mechanistic explanation for tl1is has
horses. Parascaris equonim resistance to
been published. However, it suggests that
macrocyclic lactones (ivermectin and
macrocyclic lactone use may select for
moxidectin) has been rep01tecl in many
benzimidazole resistance, because benzicountries. Macrocyclic lactone resistance midazole resistance appears to be largely
in cyathostomes is only occasionally
clue to a single polymorphism being
suspected, however, and the problem is
selected. However, benzimidazole
still not considered to be serious.

resistance was widely reported before the

ANTHELMINTICS

2645
commercial use of macrocyclic lactones.

all the other benzimidazoles, triclabenda

Ivermectin resistance has usually been
zole has no activity against roundworms.

repotted in areas of the world where

Because most benzin1idazoles are sparingly
benzimidazole resistance is already
soluble in water, they are generally given
widespread. In using anthelmintic combina

PO as a suspension, paste, or bolus,

VetBooks.ir
tions or rotations, consideration should be
although topical fom1ulations have also
given to the genetic interactions in the
been developed. Differences in the rate
parasite between benzi.midazole and
and extent of absorption from the GI tract
macrocyclic lactone anthelmintics in terms
depend on such factors as species, dosage,
of selection for the alleles that confer
fonnulation, solubility, and operation of the
benzi.midazole resistance.

esophageal groove reflex. Flubendazole

Every exposure of a target parasite to an
and fenbendazole are also available as an
anthelmintic exerts some selection pressure oral suspension or emulsion for application for development of resistance. Therefore,
through drinking water, for administration
management practices designed to reduce
to pigs and chickens.

exposure to parasites and to min.i.mize the

The most effective of the group are those
frequency of anthelmintic use should be
with the longest half-life, such as oxfendareconunended. The development of an zole, fenbendazole, albendazole, and their
anthelmintic resistance problem may
prodrugs, because they are not rapidly
theoretically be delayed by rotating
metabolized to inactive products. Effective
chemicals with different modes of action
concentrations are maintained for an
annually between dosing seasons. Drug
extended period in the plasma and gut,
combinations may be another appropriate
which increases efficacy against in1mature
choice, provided the anthelmintics used in
and arrested larvae and adult nematodes,
the combination are both effective and
including lw1gwonns.

select for different resistance mechanisms.

They are more effective in ruminants and

In parasite control, economic benefit is
horses, in which their rate of passage is
best obtained by careful management
slowed by the rumen or cecwn. Because the
practices. Planned ( or targeted) treatment
nature of their anti.parasitic action depends
of a whole flock or herd should be based on
on prolongation of contact tin1e, repeated
the biology, ecology, and epidemiology of

(2-3 times) PO administration of a full close
the parasite(s), with particular reference to
at 12-hr intervals increases their efficacy,
climatic conditions. There is a trend among
even against benzi.midazole-resistant
parasitologists to recommend replacing
worms. In addition, a reduced feed intake,
current practice for wonn control involving
which reduces the flow rate of digesta,
repeated dosing of whole groups of animals
increases the availability of benzin1idazoles.

with "targeted selective treatments" in

In the case of oxfendazole, and probably
which only individual animals showing cliniother benzimidazoles, the major route of cal signs or reduced productivity are given
exposure is biliary metabolites, followed by
drugs.

enterohepatic recycling of the drug after
absorption from the small and large

BENZIMIDAZOLES
intestine. Wonns in the mucosa of the small
intestine may be exposed to more recycled

The benzimidazoles are a large chemical
anthelmintic than to drug contained in the
family used to treat nematode and
passing ingesta in the GI tract.

trematode infections in domestic animals.

They also have limited activity against

Ruminants: In ruminants, PO treatment
cestodes. However, with the widespread
with the benzirnidazoles removes most of
development ofresistance and the availabilthe major adult GI parasites and many of ity of more efficient and easier to administhe larval stages. The relative rates of ter compounds, their use has decreased in
oxidation in the liver and reduction in the
ruminants. They are characterized by

GI tract vary between cattle and sheep, with
a broad spectrum of activity against
the metabolism and excretion of benzi.midaroundworms (nematodes), an ovicidal zole compow1ds being more extensive in
effect, and a wide safety margin. Those of
cattle than in sheep. Consequently, the
interest are mebendazole, flubendazole,
systemic antl1elmintic activity of most
fenbendazole, oxfendazole, oxibendazole,
benzin1idazoles is greater in sheep than in
albendazole, albendazole sulfoxide,
cattle, and dose rates in cattle are often
thiabendazole, thioµhanate, febantel,
higher than those in sheep. Albendazole,
netobi.min, and triclabendazole. Netobin1in,
fenbendazole, oxfendazole, and febantel are
albendazole, and triclabendazole are also
active against inhibited fowth-stage larvae
active against liver flukes; however, unlike
of Oslertagia spp; however, inconsistent

2646

ANTHELMINTICS
efficacy has been reported. Efficacy against
various members of the benzimidazole

Dictyocaulus viviparus has also been
group. Activity againstStrongyloides
noted for these insoluble benzimidazoles.

wesle'li vai·ies also, but Oxywis equi is Oxfendazole, albendazole, and febantel are
usually removed by any of the benzimidaminimally teratogenic in sheep, whereas zoles at the reconunended dose.

VetBooks.ir
fenbendazole, mebendazole, and oxibendazole are not. An oxfendazole pulse-release Swine: Benzi.J.nidazoles (eg, fenbendazole,
bolus for intrarnminal use has been
flubendazole) show high efficacy against
developed for cattle in Europe; five or six
both adult and immature stages of Ascaris
therapeutic doses of oxfendazole (750 or
sicum. Benzimidazoles are also highly

1,250 mg/tablet) are released approximately
effective against most other swine
every 3 wk in the rumen. A sustainednematodes.

release fenbendazole bolus is also available
for cattle in some European countries; it

Dogs and Cats: In dogs and cats,
contains 12 g fenbendazole and has a
mebendazole, fenbendazole, febantel,
continual release profile of>l40 days. An
oxfendazole, oxibendazole, and flubendaalbendazole slow-release capsule has been zole ai·e used for treatment of roundwonns,
marketed in Europe and Australasia for
hookworms, and tapeworms. However,
small lUlllinants. This device contains 3.85 g
treatment must be given for 3 days.

of albendazole and delivers a daily dose of

36. 7 mg for 105 days. It is an efficient device

Birds: Mebendazole, flubendazole, and
to control benzimidazole-susceptible
fenbendazole can be used effectively
nematodes. It may also prevent infection
against nematodes of the GI and respiratory
with benzimidazole-resistant larvae but
tracts of birds.

does not reduce existing infections.

In cattle and sheep, triclabendazole at

IMIDAZOTHIAZOLES

10 mg/kg, PO, is highly effective against
immature Fasciola hepatica in the liver

The anthelmintic activity of tetrainisole, a
parenchyma and against the matw·e stage in
racemic mixture, resides in the L-isomer,
the bile ducts. Albendazole and netobimin
levainisole. It is corrm1only used in cattle,
at 20 mg/kg are active against mature F
sheep, pigs, goats, and poultry to treat
hepatica; the other benzimidazoles and
nematode infections; it has no activity
probenzimidazoles used for nematode
against flukes and tapewom1s. It is normally
control have only a marginal efficacy
administered PO or SC, and efficacy is
against liver flukes. Because of the lack of
generally considered equivalent with either
efficacy against the in1111ature stages, only
route. Topical preparations for cattle have
triclabendazole is indicated for treatment of
been developed.

acute fascioliosis. However, triclabendazole

Levainisole acts on the roundworm
resistance has been reported in several
nervous system and is not ovicidal. Its
countries. Triclabendazole is not approved
broad spectrum of activity, ease of use
for use in lUlllinants in the USA.

(being water soluble), reasonable safety

Benzimidazoles also have "some
margin, ai1d lack of teratogenic effects
anthelmintic activity againstMoniezia spp
have allowed it to be used successfully.

in sheep and cattle.

Because of its mechanism of action, the
peak blood concentration is more relevant

Horses: In horses, the benzimidazoles
to its antiparasitic activity than the
are characterized by effective removal
duration of concentration. Levan1isole

(90%--lOQOA,) of almost all mature strongyles,
resistance appears to be associated with a
but third- and fourth-stage larvae are more
loss of cholinergic receptors. Levan1isole
difficult to eliminate. High levels and
has immunostirnulant effects at dosage
repeated administration may be necessaiy
rates higher than those used for anthelminfor extra-intestinal migrating stages of large tic activity, and it has been used in people
strongyles and for small-strongyle larvae
and to a limited extent in other animals in
embedded or encysted in the wall of the
several diseases.

intestine. However, widespread resistance
to benzimidazoles in cyathostome

Ruminants: In rnminants, levainisole
nematodes of horses limits their usage.

(pour-on, injectable, and oral fom1ulations)

Repeated doses are thought to be advantais highly effective against the common adult geous, because the lethal effect of benzimi

GI nematodes and lungwonns and many
dazoles is a slow process-hence, their
laival stages. It lacks efficacy against
recent incorporation into feed supplements.

arrested larvae, such as those of Ostertagia

Ascarid removal in horses varies with
ostertagi. Levan1isole slow-release boluses

ANTHELMINTICS

2647
are available in some countries and contain
combined with pyrantel in some anthelmin22.05 mg levamisole. They release 2.5 mg tic preparations for dogs (and people) to
dming the first 24 hr and the remainder over
increase activity against whip worms.

a 60-day pe1iod.

VetBooks.ir

Swine: Levamisole (injectable and oral

MACROCYCLIC LACTONES
fom1Ulations) is highly effective against
both adult and immatmes stages of Ascaris

The macrocyclic lactones (avermectins
suum. Levamisole is also highly effective
and milbemycins) are products or
against other adult swine nematodes,
chemical derivatives of soil microorganexcept for 1hchwis suis.

isms belonging to the genus Streptomyces. The avermectins in commercial use Dogs: In some countries, levamisole
are iverrnectin, abarnectin, doramectin,
is available as an oral fotmulation for
eprinomectin, and selamectin. Commertreatment of Toxocara canis infections.

cially available milbemycins are milbemycin oxime and moxidectin. The macro

Birds: In poultry, levarnisole is mainly used cyclic lactones have a potent, broad
to remove ascarid infections. Because it is
antiparasitic spectrum at low dose levels.

water soluble, it is available as an oral

They are active against many immature
formulation for administration through
nematodes (including hypobiotic larvae)

drinking water.

and arthropods. The published literature
contains reports of use to treat infections

TETRAHYDROPYRIMIDINES
of >300 species of endo- and ectoparasites
in a wide range of hosts. Moreover, a

Pyrantel was first introduced as a broadsingle therapeutic dose can persist in spectrun1 anthelmintic against GI nemaconcentrations sufficient to be effective todes of sheep and has also been used in
against new nematode infections for
cattle, horses, dogs, cats, and pigs. It is
prolonged periods after treatment.

available as a citrate, tartrate, embonate,

The macrocyclic lactones are well
or pan10ate salt.

absorbed when administered PO or

Aqueous solutions arc subject to
parenterally; the pour-on formulations
isomerization on exposure to light, with
exhibit greater variability. Regardless of
a resultant loss in potency; therefore,
the route of administration, macrocyclic
suspensions should be kept out of direct
lactones are extensively distributed
sunlight. It is not recorru11ended for use in
throughout the body and concentrate
severely debilitated animals because of its
particularly in adipose tissue. However, the
levamisole-type pharmacologic action.

route of administration and formulatiop

Pyrantel is used PO as a suspension,
may affect the drug pham1acokinetics. The
paste, drench, or tablets. Both pyrantel and
residence time of macrocyclic lactones
morantel are effective against adult gut
administered SC may also be influenced
wom1s and larval stages that dwell in the
by the body condition of the animal.

lumen or on the mucosa! surface.

Effective levels are reached in the GI
system, lungs, and skin regardless of the

Ruminants: Pyrantel tattrate is effective
route of administration. There is, however,
as a broad-spectrum anthelmintic in
a very complex interaction between
ruminants; however, its activity is mainly
phannacokinetic compartments and the
limited to the adult GI nematodes.

quantitative and qualitative availability of
drug/metabolite in one compartment. For

Horses: Pyrantel is effective against adult
example, the association of macrocyclic
ascarids, large and small strongyles, and
lactones with digesta affects absorption;
pinwonns. At double the recommended
systemic availability and elimination of
dose, it has limited activity against the
ivennectin given PO may differ significantly
ileocecal tapewom1 Anoplocephala
with feed quantity or composition in sheep.

pe1joliata.

Also, the practice of feed withdrawal before

PO treatment broadens the pharrnacoki

Swine: Pyl'antel tartrate is used in swine
netic profile, significantly increasing
to treat Ascaris and Oesophagostomum.

anthelmintic efficacy.

Dogs and Cats: Pyrantel pamoate or
embonate is effective against the common

Environmental Effects

GI nematodes, except for whip worms.

Although there has long been concern over

Oxantel, a phenol analogue of pyrantel, is
the use of chemical additives in livestock

2648

ANTHELMINTICS
feed ( eg, potential consequences of

Persistent Efficacy
insect-free manure), the effects on
nontarget dlUlg insects and dung dispersal

A single therapeutic dose of an avem1ectin
primarily becan1e a concern with the
can persist in concentrations sufficient to

VetBooks.ir
macrocyclic lactones. The commercially
be effective against susceptible nematode
available macrocyclic lactones are primarily infections for prolonged pe1iods. The excreted in the feces, and a broad range of
clinical significance of prolonged efficacy is
insecticidal activities has been observed
in1portant. Sustained availability protects
against dlUlg-inhabiting insect species.

artin1als from reinfection by some nematode

Extensive fate and effects studies have

( and arthropod) species for several weeks,
been conducted with the macrocyclic
which helps control pests that intermitlactones, with most data reported for tently or constantly challenge livestock.

ivern1ectin. Ivern1ectin in feces or soil

Large variations in the persistent efficacy
degrades at a slow but significant rate. In a
of a particular macrocyclic lactone against
no1thern hemisphere winter environment,
a particular· worm species have been
decomposition is slow (half-life of91-217
reported. Potential reasons for these
days); when exposed to an outdoor SlUlUner
variable results include study design and
environment, ivem1ectin in soil has a
host- and parasite-related factors. Persistent
half-life of 7-14 days.

efficacy has been investigated mainly

Although macrocyclic lactones are highly
against the three major cattle nematodes
toxic to some species of aquatic organisms,

Oslertagia osterlagi, Cooperia oncophora,
their tight soil-binding mitigates against
and Dictyocaulus viviparus, and the sheep
aquatic exposure via rlUl-off or leaching.

nematodesHaernonchus conlort·us and

Macrocyclic lactones have little adverse

Teladorsagia circurncincla. The duration
effect on freshwater algae and virtually
of persistent efficacy varies according to the
none on germination or growth of plants;
macrocyclic lactone and formulation used
however, residues in animal feces have the
and may be ( excluding specific long-acting
potential to affect arthropod development
formulations) 14--45 days for Ostertagia,
in a variety of ways. The larvae of cyclor0-35 days for Cooperia, and 21-42 days for rhaphous Diptera ar·e generally more

Dictyocaiilus. The persistent efficacy of
sensitive to ivermectin and other macrocyoral moxidectin (2-5 wk) gives it a special clic lactones than are Coleopteran larvae.

role in control of haemonchosis and T

Mature adult Coleoptera ar·e usually
circimicincta in sheep and in resistance
w1aifected by macrocyclic lactone residues
development.

fotmd in dw1g, probably because they are
exposed to less macrocyclic lactone residue Cattle: Ivermectin, eprinomectin, abarnecthan their bulk-feeding larvae. Overall, the tin, dorarnectin, and moxiclectin ar·e
commercially available milbemycins appear variously available as PO, SC, and pour-on to be less hannful to fly and beetle lar'Vae
fo1mulations for use in cattle. The SC and
tested than the avennectins. There is no

PO fom1ulations are given at 0.2 mg/kg,
evidence that ivermectin residues exert any
whereas the pom0on fonnulation is used
direct effect on the development or survival
at 0.5 mg/kg. Topical administration (ie,
of earthworms; however, effects on other
pom0on formulations) is more convenient
dlUlg-feeding organisms, in particular fly
but results ar·e more variable between
and beetle larvae, may disturb tl1e processes animals than when administration is SC or of succession.

PO. Grooming behavior of cattle has a major

Although macrocyclic lactones have the
influence on the plasma disposition of
potential to disrupt the ecology of dlUlg
topical macrocyclic lactones. Undesirable
fauna if given in persistent fo1mulations
subtherapeutic concentrations in both
or sustained-release devices, there is no
treated ar1d lUltreated cattle may contribute
evidence for longte1m adverse effects of
to development of drug resistance.

macrocyclic lactone residues on the

An oil-based, long-acting formulation
degradation of dlUlg pats or on tl1e accwnof ivermectin (3.15% w Iv ivermectin) is ulation of dung on pasture. In most
available in Brazil and most Latin American
husbandry systems, a large propo1tion
ar1d African colUltries. One low-volume SC
of the feces will not contain residues of
dose (1 mL/50 kg, equivalent to ivennectin
macrocyclic lactones, thus providing a
at 630 mcg/kg) effectively treats and
large reset'Voir of safe habitat for clung
prophylactically controls many internal and
insects. Therefore, it is lUllikely that use of
external parasites of cattle for up to 77
macrocyclic lactones will have a significant
clays. A long-acting parenteral fornmlation
ecotoxicologic in1pact on a global or
for moxidectin has also been developed.

regional scale.

The injectable solution (1 mg/kg, SC,

ANTHELMINTICS

2649
behind the ear) is an oil-based formulation
avennectins and the milbemycins, so this
containing lOOA, moxidecti.n; it is registered
efficacy is temporary. Oral moxidectin has
in Latin America, Australasia, and some
a persistent efficacy of up to 5 wk for

European countries. In controlled studies,

Haemonchus conlortus and Teladorsagia
the periods of protection against some
circumcincla. Ivermectin controlled

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nematode infections using this long-acting
release capsules have been used by sheep
moxi.dectin formulation were 90-150 days
producers. The delivery rate, maintained for
according to the species. Recently, a

100 clays, is 0.8 mg ivermectin/day for sheep
long-acting injectable formulation of

20-40 kg in weight and 1.6 mg/day for sheep
eprinomectin (1 mg/kg, SC, in front of the
weighing 41-80 kg.

shoulder) was registered for use in cattle.

Treatment provides persistent parasite
control for 100-150 days, depending on

Swine: In pigs, ivern1ectin and doramectin
parasite species.

are given at 0.3 mg/kg body wt, SC, or

The macrocyclic lactones have a ve1y
ivermectin is given in feed for 7 days at 0.1
high (>98%) efficacy against all stages
mg/kg body wt/day for the treatment of all

(including inhibited forms) of the common
adult and larval stages of the common swine
cattle nematodes. The least susceptible
parasites, including tl1e kidney worm
nematodes are Cooperia and Nemalodirus

Slephanurus. The exception is 'I'richuris spp. Because of their high potency and
suis, in which efficacy is -800A,.

elimination tJu·ough milk, the macrocyclic
lactones are not recommended for use in

Horses: Ivennectin and moxidectin are
animals that produce milk for human
the two most common macrocyclic lactones
consumption. Eprinomectin and moxidecavailable for use in horses. In certain ti.n pour-ons are exceptions and have no
regions, abamectin is also available.

milk withdrawal ti.me in many countries.

lvem1ectin and aban1ectin are used in

A wide range of effective chemoprophyhorses at a dosage of 200 mcg/kg, whereas lactic systems has been developed to
moxidectin is used at 400 mcg/kg. Ivennecprevent outbreaks of parasitic gastroenteritin, aban1ectin, and moxidectin are effective tis and control infections in first-season
against a broad range of adult and migrating
grazing calves. Strategic anthelmintic medilarval stages of nematode (including large cation during the first half of the grazing
and small strongyles) and arthropod
season, using carefully timed administra

(Gaslerophilus spp) parasites. The only
tion of macrocyclic lactones, has proved
repo1ted difference in efficacy of the two
to be highly effective in western Europe
products is that at therapeutic dosages,
for the control of GI nematodes of grazing
ivern1ectin has not shown significant
calves during their first year. Because of
efficacy against the arTested stages and
differences in management, pasture
intramucosal developing stages of the
infectivity, and climate, it is difficult to
cyathostomes, arid moxidectin appears less
identify which progran1 is most effective.

potent against stomach bots (Gaslerophi

Any chemoprophylactic program should
lus spp ). The persistence of moxidectin in be beneficial, as long as it is adapted to
circulation can provide horses with 2-3 wk
the epidemiologic situation and farm
of protection from infective cyathostome
management.

larvae. Moxidectin and ive1mectin may not
be tl1e drugs of choice to treat infections

Small Ruminants: Ivermectin, doran1ecwith Parascaris equorum because of tin, and moxidectin are variously available
emerging resistance.

as PO, SC, and IM forn1ulations for use in
small runtlnants. As for cattle, the macrocy

Dogs and Cats: Ivermectin, selamectin,
clic lactones have a very high (>98%)

moxidectin, and milbemycin oxime may be
efficacy against all stages, including inactive
used in dogs for tl1e prevention of heartforn1s, of the c01mnon sheep and goat wonn disease arid control of GI roundnematodes. However, because of manageworms. Many canine parasites ar·e ment practices leading to selection for
susceptible to ivermectin at tl1e dosages
resistance to macrocyclic lactones among
used in other anin1als; however, because
nematodes of small ruminants, mainly in
some clogs ar·e adversely affected at tl1ese
the southern hemisphere, their use is
levels, ive1mectin is used in dogs at 6 mcg/
more problematic (seep 2644). Although
kg body wt, PO, given at 1-mo intervals, to
moxidectin, at its recommended dose rate,
prevent development of DirojUaria
can initially be effective against some
immitis, the cause of heartwom1 disease.

parasite strains resistant to ivermecti.n,

At higher dosages(> 100 mcg/kg), some
tl1ere is side-resistance between the

Collies and individual dogs of otl1er breeds

2650

ANTHELMINTICS
are adversely affected by ivennectin. At
time of administration or, more likely, by
a dosage of0.5 mg/kg, PO, milbemycin
persisting in blood until the flukes start to
oxime is used for prevention of heartwo1111
ingest blood and become exposed to
infection and for treatment of hookhigher drug concentrations. They are all VetBooks.ir
wonns, ascarids, and whip worms in dogs.

given PO, except nitroxynil, which is

Moxidectin is also effective for prevention
typically given SC.

of heartworm infection at a dose rate of

N iclosarnide is used PO to treat cestode

3 mcg/kg, PO. The safety of milbemycin
infections (Dipylidium caninum and
and moxidectin in dogs, including those

Taenia spp) in dogs.

sensitive to macrocyclic lactones, appears
to be similar to that of ive1111ectin.

Selan1ectin, an avermectin monosaccha

PRAZIQUANTEL AND
ride, and moxidectin are available in topical

EPSIPRANTEL
formulations. Selamectin and moxidectin
are also true endectocides at their reco

Praziquantel and epsiprantel are closely
mmended dosages, because their activity
related analogues that have high efficacy
encompasses common intestinal nemaagainst cestode parasites at relatively low todes (eg, Toxocara), heartworms, and
dose rates but no effect on nematodes.

external parasites (fleas, biting lice, and

Praziquantel PO is highly effective against
mites).

cestodes of ruminants ( eg, Moniezia spp,

Stilesia), horses (Anoploceplw.la pe,fo

Other Species: Ivermectin and other
liata), dogs, cats, and poultiy. The PO
avermectin/milbemycin compounds have

(5 mg/kg), SC (5.8 mg/kg), or spot-on (cats,
been used extensively as antiparasitic

12 mg/kg) administration of praziquantel in
agents in a wide variety of exotic pets,
dogs and cats is lOOOA, effective against
including ferrets, rabbits, rodents, birds,

Dipylidium caninum, Taenia spp, and
and reptiles. Although the activity of these

Echinococcus spp (both adult and
compounds was first established in
immature fonns ). Praziquantel at a dosage
laboratory animal parasite systems, their
of 40 mg/kg is also effective against
use in rodents and other exotic pets is

Schistosoma infections in cattle (and
extra-label, and treatment protocols are
people).

often established through empirical clinical

Epsiprantel at 5 mg/kg is used specifically
experience rather than controlled studies.

to treat the conunon tapeworms of dogs and
cats, including adultE granulosus.

SALICYLANILIDES, SUBSTITUTED

PHENOLS, AND AROMATIC

AMINO-ACETONITRILE

AMIDE

DERIVATIVES

The members of this chemical grouping

Amino-acetoniti·ile derivatives are a class
include salicylanilides (brotianide,
of synthetic compounds with high activity
clioxanide, closantel, niclosamide,
against GI nematodes, including isolates
oxyclozanide, rafoxanide), substituted
resistant to all other commercially available
phenols (bithionol, disophenol, hexachlobroad-spectrwn anthelmintic classes, rophene, niclofolan, menichlopholan,
because of their novel mode of action.

nitroxynil), and the ar·omatic an1ide

Efficacy studies have shown that monepandiarnfenetide (dian1phenethide). All tel (2.5 mg/kg, PO) effectively controls
members of these groups ar·e active mainly adult and IA stages of rwninant nematodes, against adult stages of liver flukes. They
including strains that are resistant or
are used extensively against fasciolusis
multidrug resistant to the other currently
and haemonchosis in sheep and cattle.

available broad-spectrunl anthelmintic

Dian1fenetide is unique in that it has excepclasses.

tionally high activity against the youngest
immature stages of the liver fluke in sheep, CYCLIC OCTADEPSIPEPTIDES
with a diminution of activity as the flukes
mature. The lowered efficacy of a number

Emodepside has demonsti·ated anthelminof the salicylanilides ar1d substituted tic activity in studies conducted in sheep,
phenols against immature flukes may be
cattle, horses, and dogs directed against
due to the high protein binding of these
tiichostrongyles, rounclwonns, hookdrugs in the blood. A munber of these wonns, whipwonns, lar·ge and small
compounds, however, appear to have
strongyles, and lungworms. Emodepside
activity against 6-wk-old flukes in cattle
has been shown to possess resistanceand sheep, by affecting them either at the breaking properties against certain

ANTHELMINTICS

2651
ivermectin-, benzimidazole-, and levamiclays, although it is reported that one sole-resistant nematode strains in sheep
irtjection at 44 mg/kg provides better relief
and an ivermectin-resistant nematode
of clinical signs.

isolate in cattle. Emodepside is currently

Clorsulon is a sulfonamide given PO as a
available in some countries in combination
suspension for infections with (mainly)

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with praziquantel (for treatment of cestode
adult liver flukes in sheep and cattle and as a
infections) as a topical fommlation (3 mg/kg) SC injection for cattle, in combination with for the treatment of ascarids and hookivem1ectin. In plasma, clorsulon is bound to wom1s in cats (including larval stages) and
protein and, when ingested by liver flukes,
as an oral fommlation (1 mg/kg) for the
inhibits enzymes of the glycolytic pathway.

treatment of ascaricls, hookwom1s, and

Clorsulon has a wide safety margin and

Trichuris in clogs (including larval stages).

is licensed for use in some countries ( eg,

For dogs, emoclepside is also available in

Australia, Europe) in lacLaling dairy cows
combination with toltrazuril as an oral
producing milk for human consumption. It
suspension for coccidia and GI nematode
is not licensed in the USA
control.

Bunamidine is an anticestoclal compound. It is used in small animals and is most effective if given after fasting. It is

SPIROINDOLES
absorbed and metabolized in the liver and

Derquantel has been approved as a
leads to digestion of tapewom1s in the gut of
combination anthelrnintic product with
the host. Vomiting and mild diarrhea may be
abamectin. By adding abamectin to
seen, and exercise or excitement should be
derquantel, the spectrum of parasite species avoided in clogs soon after administration.

against which this combination exhibits

Nitroscanate, like the substituted

�95% efficacy is significantly increased. At
phenols, probably acts by uncoupling
the dose rate selected for tl1e combination
oxidative phosphorylation. It is used in
product, derquantel has excellent anthelsmall anin1als against To.xocara, 1bxas
mintic activity against the adult and IA
cmis, Taenia, Dipylidium, Ancylostoma,
stages of Trichostrongylus spp and

Uncinaria, and Echinococcus spp.

Nematodirus spp and the adult stage of

Vomiting occasionally occurs after

Haemonchus spp, and has demonstrated
treatment.

variable efficacy against Teladorsagia

A nun1ber of organophosphates have
circumcincta and the IA stages of H
been used as anthelmintics; however,
contortus.

because of their relative toxicity, limited
efficacy against immature stages, narrow
margin of safety, and contamination of tl1e

MISCELLANEOUS ANTHELMINTICS environment through fecal excretion, their use has declined. Dichlorvos is used as

Piperazine is rapiclly absorbed from the GI
an anthelrnintic in horses, pigs, clogs, and
tract, and piperazine base can be detected in cats; trichlorfon in horses against bots, the urine as early as 30 min after administraascarids, and oxyuricls; and cow11aphos, tion. The excretion rate is maxinlal at 1--8 hr, crufomate, haloxon, and naphthalophos and excretion is practically complete within
in runlinants. Because of its high volatility,

24 hr. The spectrum of activity of piperazine
dichlorvos is a pruticularly versatile
is largely against ascarid parasites in all
organophosphate that cru1 be incorporated
animal species (including people). The
as a plasticizer in vinyl resin pellets; it is
safety margin is wide.

released slowly from the inert pellets as

Diethylcarbamazine (DEC), a derivative
they pass through the GI tract, providing a
of piperazine, also acts to paralyze
therapeutic concentration along the tract.

nematodes by interfering with nerve

Dichlorvos is particularly useful in pigs
function. Historically, DEC was widely used
against all major adult nematodes and was
for heartworm prevention in clogs. It was
one of the first broad-spectrun1 anthelrningiven daily PO throughout the mosquito tics to be used in this species. There is little
season to prevent patent infections. Before
or no activity against lru'Val migrating

DEC use, dogs must first be cleared of adult
nematodes.

heartworms and rnicrofilariae to avoid an
often fatal reaction. DEC has also been used

COMBINATION ANTHELMINTICS
to treat prepatent Dictyocaulus viviparus
infections (see LUNGWORM INFECTION, p 1421) The principle that combinations of
in cattle, although it is relatively ineffective
chemotherapeutic agents benefit a.J.limals
against the adult worms. It is routinely given by maintaining drug efficacy in the IM at 22 mg/kg body wt for 3 consecutive
presence of resistance has been repeateclly

2652

ANTHELMINTICS
demonstrated for diverse pathogens and
resistance-allele frequencies are low, and
builds on knowledge gained from insectithat the likelihood of resistance occurring cide, pesticide, and herbicide use. Also,
to a combination anthelmintic product will
combinations of anthelmintics are being
increase with increasing resistance-allele
used more and more. According to the
frequency to its individual constituent
recent guidelines of the World Association
actives.

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for the Advancement of Veterinary

3) To overcome existing species-

Parasitology, there are three main reasons
specific resistance profiles. The wide use of
to use fixed-dose combinations of
anthelmi.ntic combinations, often necessia.nthelmintics: tated by ilie very hlgh frequency of resistance

1) To cover the desired breadtl1 of
to one or more available constituent actives
spectrum. For example, derquantel
when used alone, has revealed no issues of

( spi.roindole class) has been approved for
special concern with the routine use of such
use in some countries as a combination
products.

anthelmi.ntic product with aban1ecti.n (macro

Three primary areas of concern are
cyclic lactone class). The combination
apparent with fixed-dose commercial
exhibits �95% efficacy against a significantly
anthelmintic combination products, viz,
increased spectrum of parasite species.

drug-drug interactions (safety and efficacy

2) To mininuze (delay) the development
implications of phannacokinetics and
and spread of resistance to new and existing pharrnacodynan1ics), common mechanisms anthelmintic classes. Mathematical
of resistance, and best-practice managesimulation studies have demonstrated that ment to ensure appropriate use for
the full benefit of combination anthelmi.ntic
sustainability of parasite control with the
product therapy is realized when initial
products.

ANTIBACTERIAL AGENTS

[:',-LACTAM ANTIBIOTICS
different PBPs, accounting for differences
in spectrw11 and resistance. During bacterial

[3-Lactam antibiotics, named after the active
cell growth, while the peptidoglycan
chemical component of the drug (the
structure is being fonned, autolysins

4-membered [3-lactam ring), include the
continually cleave cell wall lattices, in

6-membered ring-structured penicilli.ns,
anticipation of providing acceptor sites for
monobactams, and ca.rbapenems; and the
new strands of bacte1ial cell synthesis.

7-membered ring-structured cephalospo

N01n1al bacterial growth depends on a
rins and cephamycins. In addition to their
balance between cell wall autolysis and
chemical structure, the major difference
synthesis. The [3-lactam drug mimics the
between tl1ese two subclasses of [3-lactams

PBP substrate, thus inhibiting.the PBP and
is their susceptibility to [3-lactamase
ilius cell wall synthesis. In the face of
destruction, with the cephalospo1i.ns, in
continued autolysin activity, the cell wall
general, being more resistant.

becomes deformed. The cell, whlch is
generally hypertonic compared with its

Antimicrobial Activity
environment, is no longer impern1eable to
the flow of small molecules and is suscepti

Mode of Action: [3-Lactams impair
ble to osmotic lysis. The effect of the
the development of bacterial cell walls by

[3-lactams when present in sufficient
interfering with transpeptidase enzymes
concentrations is generally bactericidal
responsible for the fonnation of the
toward most bacteria ( an exception is in
cross-links between peptidoglycan strands.

listeriosis for whlch penicillins a.re

These enzymes are associated with a group
bacteriostatic and cephalosporins are
of proteins in both gram-positive and
ineffective). However, at subinhlbitory
gran1-negative bacteria called the penicillinconcentrations, [3-lacta.rn antibiotics do binding proteins (PBPs ). At least nine
exert residual effects on bacterial structure
different PBPs comprise the cell wall;
and function that, in turn, promote
different l3-lactan1 antibiotics may target
host-mediated cell death.

ANTIBACTERIAL AGENTS

2653

Some bactetial isolates, when treated

·injluenzae is readily crossed by f3-lactam with inhibitors of cell-wall synthesis,
antibiotics, Escherichia coli presents a
undergo inhibition of growth but not lysis
greater obstacle to these agents, and the
at usual concentrations. These "tolerant"

outer membranes of Pseudomonas
organisms are defective in their production
aeruginosa are penetrated with great
or use of autolytic enzymes and can survive
difficulty by most (3-lactan1 compound:;.

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exposure to (3-lactam antibiotics. Clinically,

Penicillins, aminopenicillins, first- and
relapses and failures in serious infections
second-generation cephalosporins, and
due to tolerant organisms may be prevented
selected other f3-lactams cannot penetrate
by the frequently synergistic effect of the
the outer membrane of P aeruginosa. In
aminoglycosides with (3-lactan1 antibiotics.

addition, porins are frequently associated

As with other bacteticidal drugs, f3-lactams
with efflux proteins that effectively remove
are most effective during the log phase
drug that has successfully penetrated the
of growth. In any bacterial population, a
lipopolysaccharide covering of gramfew organisms will always be quiescent.

negative organisms.

Because the (3-lactan1s are active against

The chemical nature of (3-lactams
only growing bacte1ia, the static organisms

(penicillins, cephalosporins, and the
are unaffected and may persist. These

(3-lactamase inhibitors), as well as their

"persisters" may then develop nom1ally
concentration gradients, also greatly
after the antibiotic is removed.

influence their penetration of bacteria to

(3-Lactam antibiotics have little influence
tl1eir targets at the surface of the cytoplason fom1ed bactetial cell walls, and even mic membrane, giving tise to the differences
susceptible organisms must be actively
between antibacterial spectra of the vatious
multiplying or growing. (3-Lactams are most
classes of penicillin. (3-Lactams are often
active during the logarithmic phase of
used in combination with other antibiotics
bacterial growth. They also tend to be
that disrupt the integrity of tl1e membranes
somewhat more active in a slightly acidic
and thereby facilitate access by f3-lactatns.

environment (pH 5.5-6.5), perhaps because

The genetic loci controlling pem1eability
of enhanced membrane penetration. They
generally have been considered to be
also are likely to be less effective in the preschromosomally located, but they also may ence of hypertonic tissues.

be plasmid-specified genes.

Efficacy of the (3-lactams is related to the
time that plasma or tissue drng concentra

(3-lactamase Resistance: The most
tions exceed the minimun1 inhibitory
in1portant mechanism of bacterial
concentration (MIC) of the infecting
resistance to f3-lactarn antibiotics is
organism (T >MIC). Generally, concentraenzymatic inactivation by f3-lactan1ases by tions should remain above the MIC for
cleavage of the 4-member (3-lactan1 ring.

approxin1ately 25% ( carbapenems) tolOOOAi

Cleavage results in the inability of the drugs

(amoxicillin) of the dosing interval.

to bind to the target PBPs. There currently
are >800 different (3-lactarnases, representing six major classes, witl1 the enzyn1e Bacterial Resistance: Only microorganvarying wit.h the organism and drugs isms that have cell walls are susceptible to
tat·geted varying with the enzyn1e. The
the action of f3-lactan1 antibiotics. Within
increase in the nwnber of enzymes reflects,
this range of bacteria, resistance to
in part, pressure brought with the increas

(3-lactams is well recognized and takes a
ingly widespread use of (3-lactarns and the
nwnber of forms.

continued manipulation of the drugs in an

Permeability Barrier: In gram-positive
attempt to circwnvent bacterial (3-lactarnase
organisms, capsular materials may hinder
production. For exatnple, the addition of
access to the cytoplasmic membrane,
larger R groups on the f3-lactatn structure
but this rarely limits the diffusion of the
rendered cephalosporins to be resistant to
cell-wall inhibitors. Gran1-negative bacteria
penicillinases. However, cephalosporinases
have a restricting sieving mechanism
emerged with continued use offirst

(porins) in their outer membranes ( external
generation cephalosporins. Second- and
cell wall), which reduces the penetration
third-generation cephalosporins reflect
of several types of antibiotics. Different
modifications, including larger R groups that
species of gram-negative bacteria exhibit
hindered f3-lactarnase access to the (3-lactan1
varying pem1eability barriers to f3-lactam
ting. Inhibitors of (3-lactarnases ( clavulanic
antibiotics, and these impair access of the
acid, sulbactarn) were added to minimize
antibiotics to the membrane-associated
penicillin destruction. As a result, newer
binding proteins. For example, the
f3-lactan1ases emerged. Approval and use of
pem1eability barrier of H aemophilus
tl1ird-generation cephalosporins have been

2654

ANTIBACTERIAL AGENTS
associated with emergence of extendedreflect the lack of affinity of a PBP to this spectrum [3-lactamases (ESBLs), paiticusubclass of drugs. Changes in PBP-2 of larly by E coli, Klebsiella, and Proteus, that Staphylococcus spp render the organism
target third-generation cephalosporins (but
resistant to all l3-lactan1s. Methicillin

VetBooks.ir
not cephainycins such as cefoxitin). In
resistance in StaphylocOCC'US spp reflects
contrast, carbapenems (inlipenem and
acquisition of the mec gene, which results in meropenem) ai·e not subject to ESBLs that
a mutation in PBP-2. As such, no l3-lactat11
tat·get third-generation cephalosporins, but
can bind to this protein, resulting in
they are subjected to carbapenemases.

resistance to all [3-lactam drugs. Problem[3-Lactamases do not discrinlinate ainong atically, genes conferring methicillin
the drugs within class, meatling both hw11an
resistance may be accompatlied by genes
and veterinary drugs will be targeted.

conferring multidrug resistance.

Interestingly, clavulanic acid is not
susceptible to ESBLs; susceptibility data

Cell Wall-deficient Microbes:

indicating resistance to cephalosporins but

Orgai1isms that have no cell wall, such as
susceptibility to ainoxicillin-clavulatlic acid

Mycoplasma, are intrinsically resistant to
indicates ESBL fonnation.

[3-lactams. A phenotypic form of resist[3-Lactamases are produced by both ance can occur when spheroplasts
gran1-positive (Staphylococcus aureus,

(incomplete cell wall) or protoplasts

S epidermidis, S pseudinlermedius but

(absence of cell wall) are present. These
generally not enterococci) and grain-negative so-called "L-forms" must be present in a orgatlisms. Some of these enzymes are active
hyperosmotic environment (eg, the renal
exclusively against penicillins, others ai·e
medulla) to survive; otherwise, they will
principally active against cephalosporins,
lyse. The clinical significance of this form
and several types hyclrolyze both equally. The of resistance is unclear.

type and concentration of [3-lactamases are
also specific to bacterial species. Grai11-

PENICILLINS
positive l3-lactat11ases generally are excreted
into the external environment as exoen

The penicillins are ainong the earliest
zymes, produced in large quantity, plasmid
classes of antibacterial clrugs. Penicillins are
mediated (single determinant), usually
divided into subclasses based on chenlical
inducible (rarely constitutive), unable to
structure ( eg, penicillins, monobactams,
initiate self-transmission (rely principally
and carbapenems), spectrum (narrow,
on trai1sduction ), and are active primarily
broad, or extended), source (natural,
against penicillins. Staphylococcal strains
semisynthetic, or synthetic), and susceptiare the main gran1-positive bacteria in which bility to l3 -lactat11ase destruction. Matlipula[3-lactamase resistance develops, often very tion of some clrugs has improved the
quickly. Gran1-negative [3-lactatnases
spectrum, resistance to l3-lactan1ase
generally are heterogeneous (wide range),
destruction, or clinical pharmacologic
retained within the periplasmic space,
chai·acteristics that enhance efficacy.

produced in small quantity, often co.nstitu-.

tive (less often inducible), able to initiate

Classes by Spectrum
self-transnlission ( cortjugation mechatlisms ),
and active against both penicillins and

All penicillins are ineffective toward cell
cephalospori.ns. The impact of [3-lactatnase
wall-deficient microorgatlisms such as
protectors such as clavulatlic acid may not

Mycoplasma or Chlamydia spp.

be as positive for treatment of grain-negative
versus grain-positive orgatlisms. Grain

Narrow-spectrum 13-Lactamase
negative bacteria capable of resistance as a
sensitive Penicillins: This group includes
result of [3-lactamase production include
naturally occurring penicillin G (benzylpeni

Escherichia, Haemophilus, K/,ebsiella,
cillin) in its various pharmaceutical fonns

Pasteurella, Proteus, Pseudomonas, and
and a few biosynthetic acid-stable

Salmonella spp; resistance may take longer
penicillins intended for oral use (penicillin V
to develop in some of these strains.

[phenoxymethyl-penicillin] ai1d phenethicillin). Penicillins in this class are active Specific Bacterial-binding Proteins:

against many gran1-positive but only a

Resistance to [3-lactam antimicrobial
lin1ited nwnber of gran1-negative bacteria.

agents can be acquired by alterations in

These drugs ai·e also effective against
the PBP targets of these drugs. A loss or
anaerobic organisms. They are, however,
decrease in affinity of crucial PBP can lead
susceptible to [3-lactamase (penicillinase)

to a significant increase in resistance to
hyclrolysis.

[3-lactatns. For exainple, resistance of

Penicillin G and its oral congeners ( eg,
enterococci to cephalosporins appears to
penicillin V) are active against both aerobic

ANTIBACTERIAL AGENTS

2655
and anaerobic gram-positive bacteria and,

Examples of this class include carboxypeniwith a few exceptions (Haemophilus and cillins ( carbenicillin, its acid-stable indanyl

Neisseiia spp and strains of Bacteroides ester, and ticarcillin), ureido-penicillins
other thanBfragilis), are inactive against

(azlocillin and mezlocillin), and piperazine
gram-negative organisms at usual concenpenicillins (piperacillin).

VetBooks.ir
trations. Organisms usually sensitive in

The anti-Pseudomonas and other
vitro to penicillin G include streptococci,
extended-spectrum penicillins are active
penicillin-sensitive staphylococci,
against most of the usual penicillin-sensi

Trueperella (Arcanobacterium) pyogenes,
tive bacteria. They often have a degree of

Clostridium spp, E1ysipeloth1ix rhusi

�-lactarnase resistance and are usually
opathiae, Actinomyces bovis, Leptospira
active against one or more characteristic

Canicola, Bacillus anthracis, Fusifoimis
penicillin-resistant organisms. Yet, as a
nodosus, and Nocardia spp.

class, they remain susceptible to destruction by �-lactamases. Exan1ples include Broad-spectrum 13-Lactamase
the use of carbenicillin, ticarcillin, and
sensitive Penicillins: Penicillins in this
piperacillin against? aeruginosa and
class are derived semisynthetically and are
several Proteus strains, and the use of
active against many gram-positive and
piperacillin against P aeru.ginosa, several gram-negative bacteria. However, they are

Shigella and Proteus strains, and some readily destroyed by the �-lactamases

Citrobacter and Enterobacter spp.

(produced by many bacteria). Many

Streptococcusfaecalis is often resistant to members of the group are acid stable and
these new extended-spectrum penicillins.

are administered either PO or parenterally.

Imipenem and meropenem are relatively

Of those used in veterinary medicine,
resistant to �-lactan1ase destruction. Their
aminopenicillins, eg, ampicillin and
spectrum includes a wide variety of aerobic
amoxicillin (which may also be produced
and anaerobic microorganisms, including
naturally), are the best !mown. Several
most strains of Pseudomonas, streptoampicillin precursors more completely cocci, enterococci, staphylococci, and
absorbed from the GI tract also belong to

Listeria. Anaerobes, including Bacte
this class ( eg, hetacillin, pivampicillin,
roidesfragilis, are highly susceptible.

talampicillin).

A large munber of gram-positive and

13-Lactamase-protected Penicillins:

gram-negative bacteria (but not

Several naturally occurring and semisyn

�-lactamase-producing strains) are
thetic compounds can inhibit many of
sensitive to the semisynthetic broadthe �-lacta.mase enzymes produced by spectrum penicillins ( ampicillin and
penicillin-resistant bacteria. When used
amoxicillin). Susceptible genera include
in combination with broad- or extended

Staphylococcus, Streptococcus, True
spectrum penicillins, there is a notable
perella, Clostiidium, Escherichia,
synergistic effect because the active

Klebsiella, Shigella, Salmonella, Proteus,
penicillin is protected from enzymatic
andPasteurella. Although bacterial
hydrolysis-and thus is fully active against
resistance is widespread, the combination
a wide variety of previously resistant
of � -lactamase inhibitors and broad-specbacteria. Examples of this chemotherapeutrum penicillins markedly enhances the tic approach include clavulanate-potentispectrum and efficacy against both ated amoxicillin and ticarcillin as well as
gram-positive and gram-negative pathogens. sulbactan1-potentiated ampicillin and Clavulanate-potentiated amoxicillin is an
tazobactam-potentiated piperacillin.

excellent example of such a synergistic
association.

Narrow-spectrum 13-Lactamase

Mecillinam is less active than ampicillin
resistant Penicillins: This group,
against gran1-positive bacteria but is highly
through substitution on the penicillin
active against many intestinal organisms
nucleus (6-aminopenicillanic acid), is

( except Proteus spp) that do not produce
refractory to a greater or lesser degree

�-lactamases.

to the effects of various �-lactamase
enzymes produced by resistant gram

Broad-spectrum �-Lactamase
positive organisms, particularly Staphylosensitive Penicillins with Extended coccus aureus. However, penicillins in

Spectra: Several sernisynthetic broadthis class are not as active against many spectrum penicillins are also active against
gram-positive bacteria as penicillin G and

Pseudomonas aeruginosa, certain Proteus are inactive against almost all gram-negaspp, and even strains of Klebsiella, Shigella, tive bacteria. Acid-stable members of this and Enterobacter spp in certain cases.

group may be given orally and include

2656

ANTIBACTERIAL AGENTS
isoxazolyl penicillins, such as oxacillin,
and susceptibility to microbial enzymatic
cloxacillin, dicloxacillin, and flucloxacildegradation.

lin. Methicillin and nafcillin are available
as parenteral preparations. Temocillin
is a semisynthetic penicillin that is

Pharmacokinetic Features

VetBooks.ir
i3-lactan1ase stable but also active against

The pharmacokinetics of the many
nearly alJ isolates of gram-negative
penicillins differ substar1tially. The general
bacteria except Pseiidomonas spp.

guidelines below emphasize singular·ly

The semisynthetic i3-lactan1ase-resistant
significant aspects.

penicillins, such as oxacillin, cloxacillin,
floxacillin, and nafcillin, have spectra
similar to those noted above (although often Absorption: Most penicillins in aqueous at
solution are rapiclJy absorbed from parenhigher MIC) but also include many of the teral sites. Absorption is delayed when the

13-lactamase-producing strains of staphyloinorganic penicillin salts are suspended in cocci ( especially S aureiis and S epidermidis vegetable oil vehicles or when the sparingly

).

soluble repository organic salts ( eg, procaine
penicillin G and benzathine penicillin G)

Carbapenems: lmipenem and meropeare ad.ministered parenteralJy. Although nem are among the most active drugs
prolonged absorption results in longer
against a wide variety of bacte1ia. Imipenem
persistence of plasma and tissue drug
is de1ived from a compound produced by

Streptomyces cattleya.

concentrations, peak concentrations may

Aztreonam is a
not be sufficiently high to be effective
related (monobactar11) compound but
against organisms unless MI Cs are low. The
differs from other 13-lactams in that it has a
penicillin G repositol salts should never be
second 1ing that is not fused to the i3-lactan1
injected IV. Only selected penicillins are
ring.

acid stable and can be administered PO at
standard closes. Absorption from the upper

General Properties

GI tract differs markedly in amount and rate

Structure-activity Relationships:

among the various penicillins. Penicillin

The penicillins, particularly the 13-lactam

V must be given at high oral doses. The
ring, ar·e somewhat unstable, being sensitive an1inopenicillins ar·e orally bioavailable, to heat, light, extremes in pH, heavy metals,
although food in1pairs the absorption of
and oxidizing and reducing agents. Also,
ampicillin. Paracellular (as opposed to
they often deteriorate in aqueous solution
traI1Scellular) transport may play a major
and require reconstitution with a diluent
role in oral absorption. The indanyl form
just before injection. Penicillins are poorly
of car·benicillin is orally bioavailable, but
soluble, weak organic acids administered
effective concentrations are likely to be
parenterally either as suspensions in water
achieved only in the wine. Serun1 concenor oil or as water-soluble salts. For exar11ple, trations of penicillins generally peak within
sodium or potassium salts of penicillin G

2 hr of PO administration. Penicillins may
are highly water soluble and are absorbed
also be absorbed after intrauterine infusion.

rapidly from injection sites, whereas

There is no infmmation regarding bioavailorganic esters in microsuspension such ability of hun1an gene1ic products when
as procaine penicillin G or benzathine
used off-label in veterinary patients.

penicillin G ar·e gradually absorbed over

1-3 (or even more) days, respectively. The

Distribution: After absorption, penicillins
trillyd..rate fonns of the semisynthetic
ar·e widely distributed in body fluids and
penicillins have greater aqueous solubility
tissues. The volume of clistiibution tends to
than the parent compounds and ar·e usually
reflect extracellular compartmentalization,
preferred for both parenteral and oral use.

although some penicillins (including

The i3-lactan1 nucleus that characterizes
carbapenems) penetrate tissues quite well.

penicillins, when cleaved by a i3-lactan1ase

Potentially therapeutic concentrations of
enzyme (penicillinase), produces penicilloic the various penicillins ar·e generally found acid derivatives that are inactive but may
in tl1e liver, bile, kidneys, intestines, muscle,
act as the antigenic cletemlinants for
and I wigs, but only very low concentrations
penicillin hypersensitivity. Modification of
are found in poorly perfused ar·eas such as
the 6-an1inopenicillanic acid nucleus, either
the cornea, bronchial secretions, cartilage,
by biosynthetic or semisynthetic means, has and bone. The diethylarnino salt of produced the array of penicillins used
penicillin G produces particularly high
clinically. These differ in their antibacterial
concentrations in pulmonary tissue. The
spectra, pharmacokinetic characteristics,
penicillins usually do not readily cross the

ANTIBACTERIAL AGENTS

2657
nonnal blood-brain, placental, mammary, or to 90 hr. Penicillin residues in milk also prostatic barriers unless massive doses are
have been fow1d after intrauterine infusion.

given or inflammation is present. Penicillins
may be substrates for P-glycoprotein efflux

Pharmacokinetic Values: Selected
from the CNS. Selected penicillins are able
pharmacokinetic values for some penicillins

VetBooks.ir
to penetrate nonchronic abscesses and
in a few species are listed in TABLE 27.

pleural, peritoneal, or synovial fluids.

Penicillins, in general, have veiy shmt

Penicillins are reversibly and loosely bow1d
elimination half-lives, which is problematic
to plasma proteins. The extent of this
for time-dependent cl.rugs. For exan1ple,
binding varies with particular penicillins

--900/o of an1oxicillin will be eliminated
and their concentration, eg, an1picillin is
within 4 hr in dogs, suggesting that ar1 8-hr
usually --20% bound, and cloxacillin may
dosing interval is appropriate. Fom1Ulations
be --800/o bound. Pregnar1cy increases the
that prolong absoqJtion after IM administravolume of distribution, which has the effect tion ar·e appropriate for time-dependent
of lowering the concentration of drug
cl.rugs, assw11ing peak concentrations
produced by a given dose.

sw-pass the MIC of the infecting microbes.

Dosage modifications may be necessary

Biotransformation: Penicillins ar·e
because of age or disease. However, the
generally excreted unchanged, but fractions general safety of 13-lactarns may negate the of a given dose may undergo metabolic
need for dose adjustment in all but profound
trar1sformations by w1known mechanisms
renal disease.

( usually <200/o metabolized). Penicilloic acid
derivatives that are formed tend to be
allergenic.

Therapeutic Indications and Dose

Rates

Excretion: Most (60%--900/o) of a

The penicillins are commonly used to treat
parenterally administered penicillin is
or prevent local arid systemic infections
eliminated in the urine within a short time
caused by susceptible bacteria. Several

(eg, up to 900/o of penicillin G within 6 hr),
acute infectious disease syndromes are
which results in high concentrations in
specifically responsive. Because of their
urine. Approximately 200/o of renal excretion synergistic interaction with other antimioccurs by glomerular· filtration and --800/o by crobials, they are often used as part of
active tubular secretion-a process that
combination therapy. Penicillins also are
may be deliberately inhibited (to prolong
used topically in the eye and ear· as well as
effective concentrations in the body) by
on the skin; intrarnarnmary administration
probenecid and other weak organic acids.

is common for treatment or prevention of

Anuria may increase the half-life of
bovine mastitis. Amoxicillin with or without
penicillin G (normally --30 min) to 10 hr.

clavulanic acid is among the first-choice

The biliary route also may be a major
antin1icrobials for treatment of canine or
excretory pathway for the broad-spectrum
feline urinary tract infections.

semisynthetic penicillins. Clearance is

A selection of general dosages for some
considerably lower in neonates than in
penicillins is listed in TABLE 28. The dose
adults. Penicillins ar·e also eliminated in
rate and frequency should be adjusted as
milk, although often only in trace arnounts
indicated by changes in MI Cs in tar·get
in the normal udder, and may persist for up
antimicrobial populations, ar1d as necessary

IO=iiii ELIMINATION, DISTRIBUTION, AND CLEARANCE OF PENICILLINS

Elimination

Volume of

Half-life

Distribution

Clearance

Penicillin

Species

(min)

(mIJkg)

(mIJkg/min)

Penicillin G

Dogs

30

156

3.6

Horses

38

301

5.5

Ampicillin

Dogs

48

270

3.9

An1oxicillin

Cattle

84

493

4.0

Ticarcillin

Dogs

48

347

4.9

2658

ANTIBACTERIAL AGENTS

•ffl:ilf .J:• DOSAGES OF PENICILLINS

Penicillin

Dosage, Route, and Frequency

Sodium penicillin G

10,000-20,000 IU/kg, IV or IM, qid

VetBooks.ir

Potassium penicillin G

25,000 IU/kg, PO, qid

Procaine penicillin G

10,000-30,000 IU/kg, IM or SC, once to twice
daily

Benzathine penicillin G

10,000-40,000 IU/kg, IM (horses) or SC (cattle),
every 48-72 hr

Penicillin V

15,000 IU/kg or 8-10 mg/kg, PO, tid-qid

Cloxacillin

10---25 mg/kg, lM or PO, qid

Ampicillin

5-10 mg/kg, IV, IM, or SC, bid-tid; 10-25 mg/kg,

PO, bid-qid

Amoxicillin

4--10 mg/kg, IM, once to twice daily; 10-20
mg/kg, PO, bid-qid (dogs)

Sodium carbenicillin

10---20 mg/kg, IV or IM, bid-qid

Potassium clavulanate:amoxicillin

10-20 mg/kg (amoxicillin) and 2.5-5 mg/kg

(1:4)

(clavulanate), PO, bid-qid

Probenecid (prolongs blood concen1-2 rng/1,000 IU penicillin G (dogs), PO, qid trations of penicillins that have short
plasma half-lives or that are costly)

Amoxicillin-clavulanic acid

10-20 mg/kg, PO, bid-qid

Imepenem

1-7 mg/kg, IV or IM, bid-tid

Meropenem

12-24 mg/kg, IV or SC, bid-tid

Ticarcillin (with or without clavulanic 40-110 mg/kg, IM or IV, tid-qid acid)

to achieve and maintain an appropriate
contribute to the sodium load in congestive

T>MIC for circumstances presented in the
heait failure.

individual animal.

Interactions: Active renal tubulai·

Special Clinical Concerns
secretion is delayed in the presence of

Adverse Effects and Toxicity: Organ
selected organic ions, including salicylates,
toxicity is rare. Hypersensitivity reactions
phenylbutazone, sulfona.I11ides, a.Ild other
to penicillin as a hapten reflects, in part,
weak acids. Gut-active penicillins potentiate
fomiation of penicillinoic acid. Hypersensithe action of a.I1ticoagula.I1ts by depressing tivity (paiticularly in cattle) includes skin
vitai11in K production by gut flora. Absorpreactions, angioedema, drug fever, serw11
tion of ainpicillin is impaired by the
siclrness, vasculitis, eosinophilia, ai1d
presence of food. l3-lactan1s in general
anaphylaxis. Cross-sensitivity an1ong
interact chemically with the a.I11inoglycopenicillins is well recognized. Intrathecal sides Md should not be mixed in vitro.

administration may result in convulsions.

Ampicillin a.Ild penicillin G are incompatible

Guinea pigs, chinchillas, birds, snakes, and
with mMy other drugs and solutions a.Ild
turtles ai·e sensitive to procaine penicillin.

should not be mixed.

The use of broad-spectrum penicillins may
lead to superinfection, a.Ild GI disturba.I1ces

Effects on Laboratory Tests: Laboramay occur after PO administration of tory detemiinations may be altered,
a.I11picillin. Potassium penicillin G should
depending on the penicillin used. Alkaline
be administered IV with some caution,
phosphatase, AS1� ALT, Md eosinophil
especially if hyperkalemia is present.

count may be increased. A false-positive

The sodium salt of penicillin G may also

Coombs' test may also result after penicillin

ANTIBACTERIALAGENTS

2659
therapy. A positive test for urine glucose

First-generation Cephalosporins:

and protein is also possible. Procaine is

This group includes cephalothin (no
detectable in the urine of horses for several
longer marketed in the USA), cephaloridays after administration of procaine dine, cephapirin, cefazolin, cephalexin,
penicillin; withdrawal tin1e before
cephradine, and cefadroxil. Cephalosporins

VetBooks.ir
competition may be up to 6 days.

in this group are usually quite active against
many gran1-positive bacteria but ar·e only

Drug Withdrawal and Milk Discard
moderately active against gran1-negative

Times: Regulatory requirements for
orgarusms. They are ineffective against
withdrawal times for food animals and milk
enterococci. Susceptible gram-negative
discard times vary among countries. These
bacteria include Escherichia coli and
must be followed carefully to prevent food

Proteus, Klebsiella, Salmonella, Shigella,
residues and consequent public health
and Enterobacter spp. Cefazolin is more
implications. The tin1es listed in TABLE 29
effective against£ coli than cephalexin, the serve only as general guidelines.

latter of which is minin1ally susceptible.

Although generally less susceptible to

13-lactamase destruction than penicillins,

CEPHALOSPORINS AND
they are susceptible to cephalosporinases.

CEPHAMYCINS

They are not as effective against anaerobes

The cephalosporins, and the closely related
as are the penicillins.

cephamycins, are similar to penicillins in
several respects, sharing pharmacologic

Second-generation Cephalosporins:

group features.

This group includes cefan1andole, cefoxitin

(a cephamycin), cefotiam, cefachlor, cefuroxime, and ceforarude. These agents are Classes and Antibacterial Spectra
generally active against both grar11-positive

Cephalosporins include cephan1ycins, the
and gram-negative bacteria. Moreover, they
latter of which differ from other cephaloare relatively resistant to J3-lactan1ases sporins in that they contain a 7-alpha-methcompared with first-generation drugs.

oxy group, which imparts resistance to

They are ineffective against enterococci,
extended-spectrun1 13-lactamases .. The early Pseudomonas aeruginosa ( with the cephalosporins differed mainly with respect frequent exception of cefoxitin), Actino
to pharmacokinetic characteristics.

bacter spp, and many obligate anaerobes

Whereas penicillins were classified based

(again, cefoxitin is an exception).

on source ( natural versus semisynthetic)

and spectra, cephalosporins are classified

Third- and Fourth-generation
by generations (1-4). Later generations are

Cephalosporins: The third-generatiqn
more resistant to 13-lactam destruction and
cephalosporins include ceftiofur, ceftriaxare often characterized by extended but one, cefsulodin, cefotaxirne, cefoperazone,
variable spectra.

moxalactam (not a true cephalosporin), and
ittN•fJI DRUG WITHDRAWAL AND MILK DISCARD TIMES OF PENICILLINS

Withdrawal

Milk Discard

Penicillina

Species

'lime (days)

Time (days)

Procaine penicillin G

Cattle

IO (at label dosage)

3

30 (at 20,000 IU/kg, bid)

Sheep

9

Pigs

7

Benzathine penicillin G

Cattle

30

Ampicillin

Cattle

6

Prerun1inant

15
calves

Amoxicillin

Cattle

30

2
a All administered IM

2660

ANTIBACTERIAL AGENTS
several others, including cefpodoxirne and
tions of the 7-aminocephalosporanic
cefovecin, approved for use in dogs and for
acid nucleus and substitutions on the
use in dogs and cats, respectively. Cefepime
sidechains by semisynthetic means have
is a fourth-generation cephalosporin. The
produced differences among cephalosporspectnun of third- and fmuth-generation ins in antibacterial spectra, 13-lactamase

VetBooks.ir
cephalospo1ins varies and should be
sensitivities, and pharmacokinetics.

confinned based on culture and susceptibility testing before use. The spectrum of Antimicrobial Activity
veterinary third-generation cephalosp01ins
should not be considered extended in that
efficacy often does not include Pseudo

Bacterial Resistance: Resistance to
monas or other problematic coliforms.

the cephalosporins includes mechanisms

Ceftiofur has been specifically approved
described in general for 13-lacta.ms (see
for use in cattle with bronchopneumonia,
p 2652). Cephalosporins generally are stable
especially if caused by Mannheimia
against the plasmid-mediated l3-lactan1ases
haemolytica or Pasteurella mullocida.

produced by gran 1 -positive bacteria such

Although it is approved for use in dogs to
as Staphylococcus aure-us. Several types
treat minary tract infections (injectable),
of inducible 13-lactamases produced by
other more convenient drugs are generally
gram-negative organisms may be mediated
used. Cefpodoxirne and cefovecin are
by either plasmids or chromosomally and
particularly effective agamstStaphylococ
may hydrolyze either or both penicillins
cus pseudintermedius, while retaining fair
and cephalosporins (cross-resistance).

efficacy toward gram-negative organisms

Second- and particularly third-generation
such as E coli, Klebsiella, and Proteus.

cephalosporins have greater stability

Some drngs approved for use in people have against gram-negative 13-lactamases.

only moderate activity against gram-posi

However, third- and fourth-generation
tive bacteria ( again, enterococci are
drugs a.re susceptible to extended-spectrum
resistant) but have extensive activity

13-lactamases, the presence of which on
against a wide variety of gram-negative
susceptibility testing is indicated based on
bacteria, includingPseudomonas spp,
resistance to these drugs but susceptibility

Protei,s vnlgaris, Enternbacte1· spp, and
to clavulanic acid.

Citrobacter spp ( eg, cefota.xin1e, ceftazidirne). Third- and fourth-generation Pharmacokinetic Features
cephalosporins were designed to be increas

Limited information regarding the
ingly resistant to 13-lactamases. However,
pharmacokinetics of cephalosporins in
differences in chemical structme have been
ailin1als is available.

overcome by the formation of exl;endedspectrum l3-lactan1ases that target third-Absorption: Only a few cephalosporins
and fourth-generation drugs (but not, as a
ai·e acid stable and thus effective when
general rule, cepha.mycins ). Ceftiofm is a
administered PO ( eg, cephalexin, cephrathird-generation cephalosporin with a dine, cefadroxil, cefpodoxi.rne, and
gram-negative spectrum that is more sirnilar cefachlor). They a.re usually well absorbed, to that of first-generation cephalosporins.

ai1d bioavailability values a.re 75%--900/o.

There is no information regai·ding bioava.il

General Properties
ability of human generic products wµen
used off-label in veterinary patients. The

The physical and chemical properties of
others a.re administered either IV or IM, with
the cephalosporins are similar to those of
plasma concentrations peaking --30 min
the penicillins, although the cephalosporafter injection. Ceftiofur is available in ins are somewhat more stable to pH and
a sustained-release form; its duration of
temperature changes. Cephalosporins are
action is extended by administration at
weak acids derived from 7-aminocephalothe base of the ear in food animals.

sporanic acid. They are used either as the
free base form for PO administration (if

Distribution: Cephalosporins are
acid stable) or as sodium salts in aqueous
distributed into most body fluids and
solution for parenteral delivery (sodium
tissues, including kidneys, lungs,joints,
salt of cephalothin contains 2.4 mEq
bone, soft tissues, and the biliary tract, but
sodium/g). Cephalosporins also contain
in general, the volume of distribution is
a 13-lactam nucleus susceptible to

<0.3 I/kg. However, poor penetration into

13-lactamase ( cephalosporinase)

the CSF, even in inflammation, is a notable
hydrolysis. These 13-lactamases may or
feature of the standard cephalosporins.

may not also target penicillins. Modifica-

Cephalosporins m·e substrates for

ANTIBACTERIALAGENTS

2661

P-glycoprotein efflux from the CNS. The
elimination of the newer cephalosporins
third-generation cephalosporins (eg,

( eg, cefoperazone) may be significant.

moxalactam) may achieve good penetra

Generally, these 13-lactam antibiotics
tion into the CSF. The degree of plasmamaintain effective blood concentrations for protein binding is variable ( eg, 20% for
only 6-8 hr. Exceptions include ceftiofur,

VetBooks.ir
cefadroxil and 80% for cefazolin). The high
cefpodoxime, and cefovecin.

degree of protein binding of cefovecin

(90% dogs, 99% cats) contributes to its long

Pharmacokinetic Values: Plasma
elimination half-life (5.5 days in dogs, 6.9
half-lives of cephalosporins are quite
days in cats). However, drug concentravariable, being as short as 30-120 min, but tions in transudate remain above the
generally are longer than those of penicil

MIC00 of both Staphylococcus interme
lins. For example, the half-life of the
dius and E coli for up to 14 days. Third-approved cephalexin product in dogs is 7.3
or fourth-generation cephalosporins are
hr (9 hr if given with food). Third-generation
often able to penetrate the blood-brain
cephalosporins tend to have longer plasma
barrier and are frequently indicated in
half-lives in people, but this is not always
bacterial meningitis caused by susceptible
the case in other animals-substantial
pathogens.

species differences exist. A selection of
phannacokinetic values for cephalosporins

Biotransformation: Several cephalois listed in TABLE 30 to serve as a guide.

sporins (such as cephalothi.n, cephapi.rin,

Dosage modifications are often required in
ceftiofur, cephacetJile, and cefota.x.ime) are
hepatic and renal disease.

actively cleacetylated, primarily in the liver
but also in other tissues. The deacetylatecl

Therapeutic Indications and Dose
derivatives are much less active, with the

Rates
exception of ceftiofur. Ceftiofur is
metabolized to several active metabolites,

First-generation cephalosporins have
including an acetylated metabolite, that can
proved useful, particularly for infections
contribute significantly to efficacy. Few of
involving Staphylococcus spp (eg, oral
the other cephalosporins are metabolized
cephalexin for clem1atitis) and for surgical
to any appreciable extent.

prophylaxis (eg, cefazolin). However, their
efficacy appears to be declining because of
emerging resistance, including methicillin

Excretion: Most cephalosporins,
resistant organisms. Ceftiofur is approved
including cefpodoxirne and cefovecin,
for use in a variety of food animals. It is
are renally excreted. Tubular secretion
approved for bovine respiratory disease
predominates, although glomerular
principally caused by Pasteurella spp and
filtration is important in some cases
in urinary tract infections in clogs. Use of

(cephalexin and cefazolin). In renal failure,
ceftiofur for treatment of soft-tissue
dosages might be reduced, although the
infections in dogs is not recommended,
need for doing so is not clear. Biliary
because proper dosages and safety have not

ELIMINATION, DISTRIBUTION, AND CLEARANCE OF

CEPHALOSPORINS

Elimination

Volume of

Half-life

Distribution

Clearance

Cephalosporin Species

(min)

(mUkg)

(ml/kg/min)

Cefazolin

Horses

45

188

5.5

Cefotaxin1e

Sheep

25

134

9.0

Cefpodoxirne

Dog

300

150

Cefovecin

Dog

5.5 days

90

Cephalexin

Dogs

7.3-9 hr

Cefadroxil

Dogs

120

Cats

150-180

Ceftiofur

Cattle

-360

2662

ANTIBACTERIAL AGENTS
been documented. Cefpodoxime (PO) and

Interactions: In vitro incompatibilities
cefovecin (SC) also have been approved for
are quite common for cephalosporin and
use in dogs and in dogs and cats, respeccephamycin preparations; an exception tively. Cephalosporins are particularly
exists when mixing with weak bases such as
useful to treat infections of soft tissue and

VetBooks.ir
aminoglycosides. Potential pham1acokibone due to bacteria that are resistant to netic interactions are similar to those of the
other commonly used antibiotics. Cefazolin
penicillin group.

(IV) has been used prophylactically 1 hr
before surge1y. More than most penicillins,

Effects on Laboratory Tests: Several
cephalospmins may penetrate tissues and
laboratory detem1inations may be altered
fluids sufficiently (CSF being an exception
by the cephalosporins. Alkaline phosfor most) to be effective in management phatase, AST, ALT, lactate dehydrogenase,
of osteomyelitis, prostatitis, and arthritis.

and BUN may be increased. A false-positive

Oral cephalosporins can be effective in

Coombs' test and a false-positive urine
management of urinary tract infections,
glucose may occur. Hypematremia may be
except those due to Pseudomonas
caused by the sodium salts of various cepha
aen1ginosa. Cephalexin should be
losporins.

anticipated to be ineffective against E coli.

Cephapirin benzathine is used for dry-

Drug Withdrawal and Milk Discard
cow therapy, and cephapirin sodium is

Times: Although prolonged tissue residues
used to treat mastitis. Except for cephapi-
for most cephalosporins are not anticipated,

1in, extra-label use of cephalosporins is
withdrawal tin1es are not available for most
banned in major food animal species.

of the cephalosporins because they are not

A selection of general dosages for some
approved for use in food animals in most
cephalosporins is listed in TABLE 31. The
countries (see TABLE 32). An exception exists dose rate and frequency should be adjusted
for ceftiofur, the witl1drawal time of which
as needed for the individual animal.

varies witl1 the product.

Special Clinical Concerns

AMINOGLYCOSIDES

Adverse Effects and Toxicity: The

(Aminocyclitols)

approved cephalosporins are relatively
nontoxic. IM injections can be painful, and

Aminoglycosides are mostly bactericidal
repeated IV administration may lead to local drngs that share chemical, anti.microbial, phlebitis. Nausea, vomiting, and diarrhea
phaimacologic, and toxic characteristics.

may occasionally be seen. Hypersensitivity
reactions of several fom1s h:we been seen,

Classes
with cross-reactivity to penicillin allergies

Narrow-spectrum Aminoglycosides:

possible. Superinfection may arise with the

Included in tltis group ai·e streptomycin and
use of cephalosporins, and Pseudomonas
di..hydrostreptomycin, which are mainly
or Candida spp are likely opportunistic
active against aerobic, gran1-negative
pathogens.

•
bacteria.

•th•ili DOSAGES OF CEPHALOSPORINS

Cephalosporina

Dosage, Route, and Frequency

Cephalexin

20-60 mg/kg, PO, bid-tid

Cephapirin

30 mg/kg, IM or IV, every 4-6 hr

Cefazolin

20-25 mg/kg, IM or IV, tid-qid

Cefpodoxin1e

8 mg/kg, SC, every 14 days

Cefovecin

5-10 mg/kg, PO, once to twice daily

Cephalexin

10-30 mg/kg, PO, tid-qid

Cefadroxil

22 mg/kg, PO, bid

Ceftiofur

1.1-2.2 mg/kg/day, IM
a All for use in small animals, except ceftiofur, which is for use in cattle.

ANTIBACTERIAL AGENTS

2663

DRUG WITHDRAWAL AND MILK DISCARD TIMES OF

CEPHALOSPORINS

Cephalosporin

Withdrawal Time

Milk Discard Time

VetBooks.ir

Ceftiofur

2-16 days, depending on
formulation

Sodium cephapirin

4 days before slaughter

4days

(i.ntramammary)

Benzathine cephapirin

42 days after latest infusion

3 days after calving

( dry-cow treatment)

rnilk not used for food

Expanded-spectrum Aminoglyco
toxicities. Aminoglycosides are typically
sides: Neomycin, framycetin (neomycin
quite stable. When the water solubility of an

B), paromomycin (aminosidine), and
aminoglycoside is marginal, it is usually the
kanamycin have broader spectra than
sulfate salt that is used for PO or parenteral
streptomycin that includes many gramadministration. The p]{,.s of these drugs are negative aerobic bacteria, as well as
generally between 8 and 10, and as a result,
synergistic activity toward selected
they tend to be ionized at physiologic pH,
gra m -positive organisms. Gentan1icin,
which may limit drug movement, paiticutobran1ycin, an1ikacin (synthesized from lai·ly in acidic environments.

kanamycin), sisomicin, and netilrnicin are
arninoglycosides with extended spectra that Antimicrobial Activity include Pseudomonas aeruginosa.

Mode of Action: Aminoglycosides are

Miscellaneous Aminoglycoside
more effective against rapidly multiplying

Antibiotics: The chemical structure of
organisms, and they affect and ultimately
apramycin differs somewhat from that of
destroy bacteria by several mechanisms.

the typical an1inoglycosides but is similar

They need only a short contact with
enough to be included in this class. The
bacteria to kill them and, as such, are
structure of spectinomycin is unusual, but it
concentration dependent in their actions.

is fairly comparable to other aminocyclitols

Their main site of action is the membranewith regard to its mechanism of action and associated bacterial ribosome through
antibacterial spectrum.

which they interfere with protein synthesis.

To reach the 1ibosome, they must first cross

General Properties
the lipopolysaccharide (LPS) covering

(grain-negative organisms), the bacterial

Chemically, the aminoglycoside antibiotics
cell wall, and finally the cell membrane.

are characterized by an aminocyclitol

Because of the polarity of these compounds,
group, with arninosuga.rs attached to the
a specialized active transport process is
an1inocyclitol ring in glycosidic linkage.

required.

Because of minor differences in the

The first concentration-dependent step
position of substitutions on the molecules,
requires binding of the cationic aminoglythere may be several forms of a single coside to anionic components in the cell
aminoglycoside. For exan1ple, gentan1icin
membrane. The subsequent steps are energy
is a complex of gentamicins C, and C2, and
dependent and involve the transpo1t of the
neomycin is a mixture of neomycins B and
polar, highly chai·ged cationic ai11inoglyco

C and fradiomycin. The an1ino groups
side across the cytoplasmic membrai1e,
contribute to the basic nature of this class
followed by interaction with the 1ibosomes.

of antibiotics, and the hydroxyl groups

The driving force for this transfer is
on the sugar moieties contribute to high
probably the membrane potential. These
aqueous solubility and poor lipid solubility.

processes are much more efficient if the

If these hydroxyl groups are removed (eg,
energy used is aerobically generated. The
tobramycin), antibiotic activity is markedly
efficacy of the an1inoglycosides is markedly
increased. Differences in the substitutions
cmtai.led in ai1 anaerobic environment.

on the basic ring structures witl1in the

An1inoglycosides are associated with a
various ami.noglycosides account for the
postantibiotic effect in a number of bacteria,
relatively minor differences in anti.microprincipally gram-negative ( eg, E coli, bial spectra, patterns of resistance, and

Klebsiella pneumoniae, P aeruginosa ).

2664

ANTIBACTERIALAGENTS

The effect generally lasts 2-8 hr after

Bacterial Resistance: Several mechaexposure and allows for dosing intervals nisms of resistance to the an1inoglycoside
longer than the half-lives of the drugs.

antibiotics have been described. These may

Several features of these mechanisms are
be plasmid or clu·omosomally mediated.

of clinical significance: 1) The antibacterial

Impaired transport across the cell

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activity of the an1inoglycosides depends on
membrane is an inherent mechanism of
an effective concentration of antibiotic
nonplasmid-mediated resistance that occurs
outside the cell. 2) Anaerobic bacteria and
in anaerobic bactelia ( eg, Bacteroides
induced mutants are generally resistant,
fragilis and Clostridiitm pe1:f1ingens ), because they lack appropriate transpo1t
because the transpo1t process is active and
systems. 3) With low oxygen tension, as in
oxygen-dependent. Facultative anaerobes
hypoxic tissues, transfer into bacteria is

( eg, enterobacte1ia and Staphylococcus
diminished. 4) Divalent cations ( eg, calciwn
aiireiis) are more resistant to the anlinoglyand magnesiw11) located in the LPS, cell cosides when in an anaerobic environment.

wall, or membrane can interfere with

Impaired transport can be induced by
transport into bacteria because they can
exposure to sublethal concentrations of these
combine with the specific anionic sites and
antibiotics. Exan1ples include streptomycin
exclude the cationic aminoglycosides.

resistance among strains of P aernginosa,

5) Passive movement of aminoglycosides
low-level an1inoglycoside resistance among
across bacterial cell membranes is
enterococci, and gentamicin resistance in
facilitated by an alkaline pH; a low pH may

Streptococcus faecal is.

increase membrane resistance more than

Impaired ribosomal binding may not

100-fold. 6) Changes in osmolality also can
be a clinically important fom1 of single-
alter the uptake of aminoglycosides.

step resistance, because generally the dmgs

7) Some aminoglycosides are transp01ted
bind to multiple sites on the ribosomes.

more efficiently than others and thus tend

Exceptions include E coli strains in which
to have greater antibacterial activity.

a single-step mutation prevents the binding

8) Synergism is conunon when aminoglycoof streptomycin to the ribosome. The sides and 13-lactam antibiotics (penicillins
san1e mechanism has been described in
and cephalosporins) are used in combina

P ae1·uginosa.

tion. The cell-wall injury induced by the

Enzymatic modification of aminogly

13-lactam compounds allows increased
cosides may be either plasmid-encoded or
uptake of the a.minoglycoside by the
chrornosomally mediated. Enzynies occur
bacteria because of easier accessibility
in both gram-negative and gram-positive
to the bacterial cell membrane.

bacteria.. More tl1an 50 enzymes have been

The intra.cellular site of action of the
identified, with three major types, each
aminoglycosides is th� ribosome, which
including several subclasses: acetylating
is irreversibly bound by aminoglycosides,
enzymes (acetyltransferases), a.denyla.ting
particularly at the 30 S but also the 50 S
enzymes (nucleotidyltransferases), and
subunits (which comprise the 70 S subunit).

phosphorylating enzyn1es (phosphotrans

Variability occurs between aminoglycosides ferases ). The susceptibility of each with respect to tl1eir affinity and degree of
anlinoglycoside to specific enzymatic attack
binding. The nwnber of steps in protein
varies among each subclass. Although
synthesis that are affected also varies.

cross-resistance is common, there are

Spectinomycin cannot induce misreading of differences in susceptibility patterns.

the mRNA and often is not bacte1icidal, in

Chemical modification stabilizes the drug,
contrast to the other bactericidal members.

which decreases susceptibility to enzyn1atic

However, at low concentrations, all
destruction. For exan1ple, chemically
aminoglycosides may be only ba.cteriostatic. modified kanamycin yields an1ikacin, which A cell-membrane effect also occurs
is more resistant to enzyniatic hydrolysis.

with aminoglycosides. The functional

Other mechanisms of resistance
integrity of the bacterial cell membrane
include 1) increased concentration of
is lost during the late phase of the transport
divalent cations (especially Ca2+ and Mg2+),
process, and high concentrations of
which act to repel ionized dmg from the
aminoglycosides may cause nonspecific
microbe, and 2) increased production by
membrane toxicity, even to tl1e point of

P ae1uginosa mutants of the outer cell
bacterial cell lysis.

membrane protein, Hl, resulting in

Efficacy of anlinoglycosides is enhanced
resistance to gentarnicin. Note that efficacy
if peak plasma or tissue drug concentrations will be reduced in the presence of decreased exceed MIC by 10-12 tin1es. Once-daily
pH (eg, acidic urine or abscesses), which
dosing has been used to enhance both
increases resistance to relatively high
efficacy and safety.

concentrations of aminoglycosides.

ANTIBACTERIAL AGENTS

2665

Antibacterial Spectra: Streptomycin
after IP administration can be rapid and
and dihydrostreptomycin (no longer
substantial. Short dosing intervals,
available in the USA) are characte1ized by
including continuous infusions, are
naiTow spectra, and efficacy is limited by
contraindicated for all an1inoglycosides.

VetBooks.ir
bacterial resistance. Gran1-negative bacilli

Once-daily therapy is indicated for safety
are still susceptible, including strains of
considerations. Serum concentrations of

Actinomyces bovis, Pasleurella spp, E coli, aininoglycosides may reach bactericidal Salmonella spp, Campylobacter Jetiis,
levels after repeated intrauterine infusion,

Ll3'J)tospira spp, and Brucella spp.

particularly in endometiitis.

Mycobacterium tuberculosis is also
sensitive to streptomycin.

Distribution: Aminoglycosides are polar

The spectra of neomycin, frainycetin,
at physiologic pH, limiting distribution to
ai1d kai1ainycin are broader, with clinical
extracellular fluids, with minimal penetrause targeting grain-negative organisms, tion into most tissues. Exceptions include
including E coli and Salmonella, Kleb
the renal cortex of the kidneys and the
siella, Enternbacter, Proteus, and
endolymph of the inner ear, sites at which

Acinetobacter spp. Aminoglycosides
aininoglycosides increasingly accwnulate
with spectra that include Pseudomonas
as ionization increases. The extracellular
aeruginosa (gentan1icin, tobrainycin,
fluid compart111ent normally approximates
an1ikacin, sisomicin, and netilmicin) are

25% of body weight, but this volume ca.ii
also often highly effective against a wide
change substantially, which leads to
vaiiety of aerobic bacteria. Because of their
indirectly propo1tional chat1gcs in the
efficacy against P aeruginosa, aminoglycoconcentration of an an1inoglycoside. For sides might be considered higher-tier drugs. exan1ple, extracellular fluid space contracts Selected staphylococci ai·e susceptible,
with dehydration and during gran1-negative
but treatment should be based on
sepsis, causing concentrations to increase,
synergistic effects, ie, combination with
whereas the distJ·ibution volume of aininoother at1tirnicrobials (eg, 13-lactams).

glycosides increases with congestive hea1t

With such combination therapy, generally
failure or ascites, causing concentrations to
low doses of aininoglycosides are used.

decrease. Concentrations tend to be lower

Because oxygen is necessary for active
in neonates, which have a large extracellutransport of drug into the microbe, caution lar fluid compaitment relative to body
is recommended when treating facultative
weight. Aminoglycosides are not apprecianaerobes in a low-oxygen environment.

ably bound to plasma proteins (usually

Obligate anaerobic bacteria and fungi are

<200/o). Therapeutic concentrations ( -10
not appreciably affected; streptococci are
times the MIC of the infecting microbe)

usually only moderately sensitive or quite
can be achieved in the synovial, pleui;al,
resistant.

and even peritoneal fluids, especially if
inflat1rn1ation is present. However, effective
concentrations ai·e not reached in CSF,

Pharmacokinetic Features
oculai· fluids, milk, intestinal fluids, or

The phannacokinetic features of the
prostatic secretions. Fetal tissue and
aininoglycosides are sinillar in most
anlniotic fluid concentrations ai·e very
species.

low in most species.

Absorption: Aminoglycosides are

Biotransformation, Excretion, and
poorly absorbed (usually <10%) from the

Pharmacokinetic Values: The aininoglyhealthy GI tract. However, pem1eability cosides ai·e excreted W1Changed in the urine
may be increased in the neonate and in the
by glomerular filtration, with 800/o-900/o of
presence of enteritis and other pathologic
adtninistered drug recoverable from tl1e
changes, allowing absorption to be signi:fiurine witl1in 24 hr of IM administration. A cai1tly greater. In the presence of renal
variable fraction of filtered aininoglycoside
failure, toxic (trough) concentrations may
is absorbed onto the brush border of the
accumulate. Aminoglycosides can be
proximal tubule ai1d loop of Henle cells.

administered slowly by bolus IV injection

Binding is facilitated by ionization. After
or SC or IM routes. Absorption from IM
binding, the drug is transported into the
injection sites is rapid and nearly complete
cell, sequestered in lysosomes. Rupture of

(>90% availability), except in severely
lysozymes results in release into the cytosol.

hypotensive at1inlals. Blood concentrations

Excessive accumulation ( mainly in the
usually peak within 30-90 min after IM
renal cortex) leads to a characteristic
administration. Absorption after SC
tubular cell necrosis. Glomerular filtration
injection may be protracted. Absorption
rates differ between species at1d are often

2666

ANTIBACTERIAL AGENTS
less in neonates, which may explain the
limited selection of pharmacokinetic values
greater sensitivity to aminoglycosicles in
for two typical aminoglycosides (see
newborn foals and puppies.

TABLE 33) serves as a basis for any required

Elimination varies with glomeruJar
dosage modifications that may be necessary
filtration changes associated with cardiobecause of age or renal insufficiency. The VetBooks.ir
vascular and renal function, age, fever, and
best way to alter a dosage regimen of arninoseveral other factors. Half-life also will vary glycosides is to monitor plasma concentradirectly and proportionately with the tions to assure that 10 tin1es the MIC is
volume of the extracellular fluid compartachieved at peak concentrations, and ment. The an1inoglycosides have relatively
concentrations less than target (generally
short plasma half-lives ( -1 hr in carnivores

<2 mcg/mL) are achieved before the next
and 2-3 hr in herbivores). The elimination
dose (''trough" concentrations).

kinetics often follow a tlrree-compartment
model, indicating a "deep" compartment
that reflects binding of drug in the renal

Therapeutic Indications and Dose
tubular cell. Approximately 900/o of the

Rates
injected drug, including that within

Despite their potential to cause nephrotoxtherapeutic concentrations, is excreted icity, the anlinoglycosides are commonly
unchanged tlrrough the kidneys during the
used to control local and systemic

13 phase of elimination. The remaining deep
infections caused by susceptible aerobic
or --y phase is excreted over a protracted
bacteria (generally gram-negative). Several
period, probably due to the gradual release
arninoglycosides are used topically in the
of the antibiotic from renal intracellular
ears and eyes and via intrauterine infusion
binding sites (tenninal elimination half-life
to treat endometritis. Aminoglycosides
often 20-200 hr). Concentrations in plasma
occasionally may be infused into the udder
during this phase are generally below what
to treat mas ti tis. In general, because of their
would be considered therapeutic. The
concentration dependency and potential for

ELIMINATION, DISTRIBUTION, AND CLEARANCE OF

AMINOGLYCOSIDES

Volume of

Elimination

Distribution

Clearance

Aminoglycoside Species Half-life (min)

(mIJkg)

( mIJkg/min)

Gentamicin

Dogs

75

335

3.10

Horses

110

190

1.23

Foals

200

300

1.04

Amikacin

Dogs

60

300

3.50

Horses

45

207

0.75

Sheep

115

200

0:70
itM•ili DOSAGES OF AMINOGLYCOSIDES

Aminoglycoside

Dosage, Route, and Frequency

Gentan1icin

6-12 mg/kg/day, IM or SC

Kanamycin

25-30 mg/kg/clay, IM or SC

Streptomycin/clihydrostreptomycin

15-25 mg/kg/day, IM or SC

Amikacin

15-22 mg/kg/day, IM or SC

Netilmicin

6-12 mg/kg/day, IM or SC

Neomycin

15 mg/kg, PO, once to twice daily

0.5-1 g/day/quarter (intramamrnary)

ANTIBACTERIALAGENTS

2667
nephrotoxicity, aminoglycosides are
hydrothorax, or ascites, provided their renal
administered once daily (same total daily
function is unin1paired.

dose; "high" dose), thus minimizing the risk of nephrotoxicity. If used at lower doses for

Special Clinical Concerns
synergistic activity against gram-positive

VetBooks.ir
organisms, such as staphylococci, lower

Adverse Effects and Toxicity:

doses (300/o-500/o of the higher dose) might

Ototoxicity, neuromuscular blockade,
be given at more frequent intervals.

and nephrotoxicity are repo1ted most

A selection of general dosages for some
frequently; these effects may vary with the
aminoglycosides is listed in TABLE 34. The
an1inoglycoside and dose or interval used,
dose rate and frequency should be adjusted
but all members of the group are potentially
as needed for the individual animal.

toxic. Nephrotoxicity is of major concern

If monitoring, two time points ( a peak
and may result in renal failure due to acute
and a second san1ple 4 hr later) is ideal such
tubular necrosis with secondary interstitial
that an extrapolated peak concentration
damage. Aminoglycosides accumulate in
can be detem1ined, along with an eliminaproximal tubular epithelial cells, where they tion half-life. The peak should be collected
are sequestered in lysosomes and interact
after distribution into tissues is complete, or with ribosomes, mitochondria, and other

-1 hr. The "trough" in this scenario should intracellular constituents to cause cell
be collected 2-3 half-lives later ( eg, 4-6 hr
injury. The greater the ionization ( eg, the
after dosing) such that concentrations will
more the an1ine groups and the lower the
still be detectable. If a single sample is
pH), the greater the active uptake. Kidneys
collected to detemune safety, a trough
must have a drug-free period to eliminate
concentration Oust before the next dose) is
accumulated drugs. As such, persistence of
indicated. Trough concentrations generally
an1inoglycosides in plasma and thus urine
should be <2 mcg/mL. For efficacy, a 1.5-2
is likely to predispose the tubular cells to
hr peak concentration might be collected;
toxicity, and the risk may by reduced by
peak concentrations should be 10-12 times
allowing plasma drug concentrations to
the MIC of the infecting organism. For renal
drop below recommended concentrations
function, both a peak and detectable trough

(generally 1-2 mcg/mL) before the next

(taken well before the next dose, because
dose. N onoliguric renal failure is the usual
concentrations may not otherwise be
observation; it is generally reversible if
detectable) are indicated so that a half-life,
damage is not sufficiently extensive to harm
and, if IV administration is used, clearance
the basement membrane, although recovery
might be calculated. As a precaution, the
may be prolonged.

following general guidelines may be

Renal function should be monitored
followed in cases of renal failure in which
during therapy; however, no indicator of
plasma creatinine values are increased ( see
renal disease is sufficiently sensitive to

TABLE 35).

prevent continued damage once nephrotox

The treatment interval should be
icity is detected. Polyuria, decreased urine
increased in neonates ( especially puppies
osmolality, enzymuria, proteinuria,
and foals), in renal failure, and in obese
cylindruria, and increased fractional sodium
animals. Doses may be increased in
excretion are indicative of arninoglycoside
neonates or pediatric anin1als, in which the
nephrotoxicity. Later, BUN and creatinine
volume of distribution is greater than in
concentrations may be increased. Early
adults, and in anin1als with edema,
changes or evidence of nephrotoxicity can

DOSAGE MODIFICATIONS OF AMINOGLYCOSIDES IN RENAL

FAILURE

Increase in Normal Serum or

Plasma Creatinine (mg/dL)

Dose and Dosage Interval
d

Full dose at usual dosage interval

2-fold increase

Full dose at usual dosage interval or increased to

50%plus usual dosing interval (eg, 36 hr)

3- to 4-fold increase

Full dose, doubling usual dosage interval

>4-fold increase

Aminoglycosides contraindicated

2668

ANTIBACTERIAL AGENTS
be detected in 3-5 days, with more overt

All an1inoglycosides, when adlninis-
signs in 7-10 days. Several factors
tered in doses that result in high plasma
predispose to aminoglycoside nephrotoxiconcentrations, have been associated with cosis, incl ucling age ( with young [ especially
muscle weakness and respiratory arrest
the newborn foal] and old animals being
attiibutable to neuromuscular blockade.

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sensitive), compromised renal function,

The effect is more pronounced when
total dose, duration of treatment, dehydraa.ininoglycosides a.i·e used with other drugs tion and hypovolemia, acidmia, acidosis,
that cause neuromuscular blockade and
hypomagnesemia, severe sepsis or
with gas anesthetics. Neomycin, kananiyendotoxemia, concurrent administration cin, an1ikacin, genta.i11icin, and tobramycin
of furosemide, and exposme to other
are listed in order of most to least potent for
potential neplu·otoxins ( eg, methoxyfluthese neuromuscular effects. The effect is rane, amphotericin B, cisplatinurn, and
due to the chelation of calciun1 and competiperhaps some cephalosporins ). In renal tive inhibition of the prejunctional release
insufficiency, generally the interval between
of acetylcholine in most instances (there are
doses is prolonged (rather than reducing the some differences among aniinoglycosides).

dose) to minimize toxicity, while avoiding a

The blockade is antagonized by calcium
negative impact on efficacy. Dosing in the
gluconate and somewhat less consistently
morning may decrease toxicity in diurnal
by neostigmine.

animals. The 1isk of toxicity is less in

CNS disturbances rarely include
alkaline mine. Nephroactive drugs,
convulsions or collapse after rapid IV
including those that alter renal vascular
administration. Other adverse effects
response (eg, autoregulation) should be
include superinfection when used topically
avoided or used cautiously ( eg, NSA!Ds,
or PO, a malabsorption syndrome clue to
diuretics). Treatment with N -acetylcysteine
attenuation of intestinal villous function
should be considered (see ototoxicity,
when used PO in neonates, occasional
below).

hypersensitivity reactions, contact

Aminoglycosides can cause ototoxicity,
dem1atitis, cardiovascular depression, and
which may manifest as either auditory or
inhibition of some WBC functions ( eg,
vestibular dysfunction. Binding or damage
neutrophil migration a.i1d chemotaxis and
to mitochondria plays a prominent role in
even bactericidal activity at high concentraototoxicity. Vestibular iajmy leads to tions).

nystagmus, incoordination, and loss of the

1ighting reflex. The lesion is often irrevers

Interactions: Enhanced nephrotoxicity
ible, although physiologic adaptation can
may become evident witl1 concurrent adminoccur. Ototoxicity is not unusual in people, istration of anlinoglycosides and otl1er
but relevance to veterinary patients is not
potentially nephroactive (such as dimetics)

clear. Cats are particularly sensitive to the
or nephrotoxic ( such as NSA!Ds) agents.

toxic vestibular effects, although occur

Nemomuscular blockade is more likely
rence at therapeutic concentrations after
when a.i1linoglycosides are administered at
systemic administration is unlikely.

the same tin1e as skeletal muscle relaxants

However, anunoglycosides shouid not be
and gas anesthetics. Arninoglycoside
administered topically into the ear unless
ototoxicity is enhanced by the loop-acting
the tyrnpanic membrane is intact. Hearing
diuretics, especially furosemide. Cardiovasimpairment reflects pe1manent damage and cular depression may be aggr�vatecl by
loss of the hair cells in the organ of Corti.

ami.noglycosides when administered to

Loss of high-frequency hearing is followed
animals under halothane a.i1esthesia. High
by deafness, which may not be complete if
concentrations of carbeni.cillin, ticarcillin,
sufficiently low doses or dmations were
and piperacilli.n inactivate an1inoglycosides
used. Aminoglycosides should be avoided in because of direct interactions both in vitro working clogs that depend on hea.iing ( eg,
and in vivo in tl1e presence of renal fail me.

guide dogs). Factors increasing the risk of

Synergistic interactions that enhance
vestibular and cochlea.i· damage a.i·e the
antibacterial efficacy have been docun1ented
san1e as for nephrotoxicity but also include
when aniinoglycosides a.i·e adtninistered
preexisting acoustic or vestibular in1pairwitl1 other antimicrobials, pa.iticularly ment and concmrent treatment with

13-lactams.

potentially ototoxic drugs. The ototoxic
potential is greatest for genta.inicin,

Effects on Laboratory Tests: BUN,
sisomicin, and neomycin, and least for
senm1 creatini.ne, serum tra.i1san1i.nases,
netilmicin. In people, treatment witl1
and alkaline phosphatase values may be

N-acetylcysteine has deceased the risk of
increased. Proteinuria is a significant
a.ininoglycoside ototoxicity.

laboratory finding.

ANTIBACTERIAL AGENTS

2669

Drug Withdrawal and Milk Discard
active against several strains of strepto

Times: Note that withdrawal times do not
cocci, a wide range of gran1-negative
exist for drngs not approved for used in
bacteria, and Mycoplasma spp; most
food animals. Regulatory requirements for

Chlamydia spp are resistant. It is poorly
withdrawal times for food animals and milk
absorbed from the GI tract but is rapidly

VetBooks.ir
discard times vary among countries. These
absorbed after IM administration, with
must be followed carefully to prevent food
blood concentrations peaking within l lu·.

residues and consequent public health

Like arninoglycosides, spectinomycin
implications. The times listed serve only as
penetrates tissues rather poorly and
general guidelines (see TABL8 36).

distributes principally into extracellular
fluid. Metabolic transformation of

Miscellaneous Aminocyclitol
spectinornycin is limited, and 80% can be

Antibiotics
recovered unchanged in the mine over

24-48 hr; -75% is eliminated by glomerular

Apramycin (administered orally) is used to
filtration in -4 hr. At usual doses, no major
control enteric gran1-negative infections,
toxic reactions have been repo1ted. It is
particularly E coli and salmonellae in calves administered boU1 PO at 20 mg/kg, bid, and
and piglets. It also is active against Proteus, IM at 5-10 mg/kg, bid. Withdrawal time for

Klebsiella, Bmchyspira, and Mycoplasma
pigs is usually -3 wk.

spp. There is little cross-resistance within
the aniinoglycosides, and plasmid-mediated
resistance is yet to be confirmed. Apramy

QUINOLONES, INCLUDING
cin is poorly absorbed after administration

FLUOROQUINOLONES

PO (<I O"Ai). It is rapidly absorbed from
parenteral injection sites. Plasma concen

Quinolone carboxylic acid derivatives are
trations peak within 1 -2 hr ofIM adminissynthetic antimicrobial agents. Naliclixic tration. Apramycin distributes only into
acid and its congener oxolinic acid have
the extracellular fluid and is excreted
been used for treatment of urinary tract
unchanged in the urine (95% within 4 clays).

infections for years, whereas flumequine

The elimination half-life in calves is -4-5 hr.

has been used successfully in several

Apramycin is toxic in cats but considered
cotmtries to control intestinal infections in
safe in most other species (3----6 times the
livestock. Many broad-spectrun1 antinlicrorecommended oral dose rarely produces bial agents have been produced by
toxicity). The oral dose rate is 20-40 mg/kg!

modification of the various 4-{juinolone ring
day, for 5 days. The parenteral dose rate is
structures.

20 mg/kg, bid. The withdrawal time in pigs
and calves (in Europe) is 28 days after oral

Classes
use.

Known generically as quinolones or

The structure of spectinomycin differs

4-quinolones, these drugs are derived from
from Uiat of the aminoglycosides, but it also
several closely related ring structures Uiat
binds to bacterial ribosomes and interferes
have certain conu11on features. Exan1ples of
with protein synthesis. However, the effect
the quinolone carboxylic acids and species
is bacteriostatic raU1er than bactericidal.

in which they are approved are presented

Spectinomycin can be inactivated by an
in TABL8 37. Naliclixic acid, considered a
enzyme coded for by an R factor, but mutant first-generation drug, is the earliest of resistance due to diminished ribosomal
the quinolones. In general, subsequent
binding is perhaps more common. It is
generations are based on spectrum, but this

••• DRUG WITHDRAWAL AND MILK DISCARD TIMES OF

AMINOGLYCOSIDES

Route

Approximate Withdrawal Time (days)

Oral

20-30 (3 for neonatal pigs)

Parenteral

100-200 ( 40 for neonatal pigs [ often not approved for food animals])

Udder infusion

2-3" (often not approved for food animals)

"Milk discard time

2670

ANTIBACTERIAL AGENTS
often reflects similar changes in chemical
anaerobic activity ( eg, sparfloxacin,
structure. Subsequent drugs contain a
pradofloxacin, moxilloxacin). If the
fluorine group and, as such, are referred
substitution is with a rnethoxy group (rather
to as fluoroquinolones. Most veterinary
than a halogen), the risk of phototoxicity is
drugs and many human drugs, including
reduced.

VetBooks.ir
ciprofloxacin, are considered second

The qui..nolones are an1phote1ic and, with
generation. Pradofloxacin is an example of
a few exceptions, generally exhibit poor
a later-generation drug approved for use in
water solubility at pH 6-8. Although the
cats (USA) or dogs and cats (European
impact on therapeutic efficacy is not clear,

Union).

they appear to act as weak bases in that they
are much less effective in acidic thar1 in

General Properties
nonacidic urine pH. ln concentrated acidic

Within the diversity of their various ring
urine, some quinolones fom1 needle-shaped
structures, the qui..nolones have a number
crystals, although this apparently has not
of common functional groups essential for
been reported with clinical use. Liquid
their antimicrobial activity. For example,
fom1ulations of various qui..nolones for PO
the qui..nolone nucleus contains a carboxylic
or parenteral administration usually contain
acid group at position 3 and an exocyclic
freely soluble salts in stable aqueous
oxygen at position 4 (hence the tem1
solutions. Solid formulations (eg, tablets,

4-quinolones), which are believed to be the
capsules, or boluses) contain the active
active DNA-gyrase binding sites. Various
ingredient either in its betaine fmm or,
modifications have produced compounds
occasionally, as the hydrochloride salt.

with differing physical, chemical, phar,nacokinetic, and ar1timicrobial properties. For Antimicrobial Activity
exan1ple, the side chain attached to the
nitrogen at position 1 affects potency.

Mode of Action: The qui..nolones inhibit

Replacement of the ethyl group at this
bacterial enzyme topoisomerases, including
position with a bulkier group ( eg, the
topoisornerase II (otherwise known as DNA
cyclopropyl group of ciprofloxacin and
gyrase) and topoisornerase IV. Bacterial
similar drugs) enhances grain-negative

DNA supercoils and then uncoils during
and positive spectra. Addition of a fluorine
replication. Supercoiling requires trarIBient
atom at position 6 profoundly enhances
nicks that are subsequently sealed after
the gram-positive spectrun1, whereas the

DNA polymerase passes. Topoisomerase
addition of a (heterocyclic nitrogen-contain

II allows for single strand nicks in the
ing) piperazyl ring at position 7 enhances

DNA that support coiling ar1d uncoiling.

bacterial penetration ar1d potency, includ

Topoisomerase IV supports disentangleing toward Psendomonas aeruginosa.

ment of DNA as chromosomes separate.

Substitutions on the piperazyl ( eg, ofloxacin

Inhibition of topoisomerases reduces
and its L isomer, levofloxacin; sparfloxacin)

supercoiling, resulting in disruption of the
enhance gram-positive penetration,
spatial arrangement of DNA, and reduces
whereas substitutions at position 8 enhance

DNA repair. Man1malian topoisomerase
iiM•ifi QUINOLONES AND SPECIES APPROVALS IN THE USA Quinolone

Species

Ciprofloxacin

Dogs, cats

Danofloxacin

Dogs, cattle

Difloxacin

Dogs

Enrofloxacin

Dogs, cats, cattle, swine

Marbofloxacin

Dogs, cats

Norfloxacin

Dogs, cats

Orbifloxacin

Dogs, cats

Pradofloxacin

Cats

Sarafloxicin

Voluntarily withdrawn

ANTIBACTERIAL AGENTS

2671
enzymes fundamentally differ from
targets. However, even with tllis second
bacte1ial gyrase and are not susceptible to
step of resistance, MIC are often below the
quinolone inhibition. The quinolones are
resistant breakpoint range on which
usually bacte1icidal; susceptible organisms
susceptibility testing is based. With tl1e
lose viability within 20 min of exposure
second increase in MIC, mutations in efflux

VetBooks.ir
to optimal concentrations of the newer
pump regulators also emerge, causing
fluoroquinolones. Typically, cleating of
marked increase in expression. As a result,
cytoplasm at the periphery of the affected
high-level, multidrug resistance emerges.

bacterium is followed by lysis, rendering

Another mechanism of resistance is the
bacteria recognizable only as "ghosts."

combined effect of increased efflux pumps

Quinolones are associated with a
and decreased porins that act in concert
postantibiotic effect in a number of
to reduce intracellular concentrations.

bacteria, principally grain-negative ( eg,

Virulence of refractory mutants may not

E coli, Klebsi.ella pneumoniae, P aerugi
dinlinish.

nosa ). The effect generally lasts 4-8 hr after Note that if resistance does emerge to one
exposure.

fluoroquinolone, it is likely to impact all

Efficacy of the fluorinated quinolones
fluoroquinolones. However, resistance
depends on concentrations in plasma that
may be slower to emerge to newer drugs,
exceed the MIC of the infecting organism
incl ucling gemifloxacin, trovafloxacin,
by 10- to 12- fold. As such, the drugs ai·e
gatifloxacin, or pradofloxacin, because of
concentration dependent. However,
larger side chains that facilitate binding to
efficacy also is correlated to the magnitude
either DNA gyrase or topoisomerase IV.

of the area under the inllibitory curve

(AUC:MIC); as such, efficacy also takes

Antimicrobial Spectra: The fluorointo account elimination half-life.

quinolones are active against a wide range

The fluoroquinolones can have significant
of gran1-negative organisms and several
antibacterial activity at extraordinarily low
grain-positive aerobes. Th.is includes E coli,
concentrations, although efficacy towai·d

Salmonella, Klebsiella, Enterobacter,
some organisms ( eg, E coli) is bimodal:

Pi-ate-us, and generally Pse-udomonas
some isolates are very susceptible (MIC
aeruginosa .. The fluoroquinolones are

<0.01-0.5 mcg/mL), whereas the MIC for a
active against intracellular pathogens,
significant number of other isolates is very
including, eg, B1ucella spp. Quinolones

!ugh (>64 mcg/mL). In general, MIC for most
also have significant activity against
susceptible microbes, including E coli,

Mycoplasma and Chlamydia spp. Obligate Klebsiella, Proteus, P aeruginosa, and
anaerobes tend to be resistant to most

Staphylococcus have increased since the
quinolones, as are most enterococci
approval of the quinolones in the eai·ly

(previously group D Streptococcus spp

1990s.

(Enterococcusfaecalis and Enterococcus
faecium ). Nocardia and atypical mycobac

Bacterial Resistance: Chromosomal
teria may also be susceptible.

mutational resistance to the original

The newer third- and fourth-generation
fluoroquinolones was considered to be
fluorinated quinolones, such as pradofloxalow in frequency, and plasnlid-mediated cin, are often characterized by an effective
resistance nonexistent. However, resistance anaerobic spectrum.

is increasingly being recognized, indicating

A synergistic effect has been demon- .

that therapy based on cultme and susceptistrated in vitro between quinolones and bility is prudent. In general, cross-resistance

13-lactarns, an1inoglycosides, clindamycin,
should be anticipated among the more
and metr011idazole.

closely related members of this class.

Grain-negative bacteria more commonly
target DNA gyrase; emerging resistance is

Pharmacokinetic Features
more often associated with changes in the

An1ong the few quinolones that have been

GyrA compared to the GyrB subunit. In
studied to any degree in domestic animals,
contrast, the primary tai·get of gram-positive pharmacokinetic differences can markedly organisms tends to be topoisomerase IV,
differ. Because of the physicochemical
with resistai1ce mechanisms targeting it,
nattu-e of the group, this is to be expected.

followed by changes in DNA gyrase. Use of

A general overview follows, but some
the drug selects for resistance. High-level
diversity should be anticipated.

resistance (3-4 times the breakpoint MIC)

generally reflects a second-step mutation

Absorption: Quinolones are commonly
that leads to changes in the ainino acid
adnlinistered PO, although fom1s of enrosequence of subsequent topoisomerase floxacin ai1d ciprofloxacin are available

2672

ANTIBACTERIALAGENTS
for IV, IM, and SC ( enrofloxacin) administraglucuronic acid then ensues, followed by tion. Absorption into the blood after IM or
excretion. In contrast, only -100/o of

SC delivery is rapid; after administration
ma.rbofloxacin is metabolized.

PO, blood concentrations usually peak
within 1-3 hr. Bioavailability is often >80%

VetBooks.ir

Excretion: Renal excretion is the major
for most quinolones, except for ciprofloxaroute of elimination for most quinolones.

cin and in ruminants with functional

Both glomerula.r filtration and tubular
forestomachs, in which bioavailability may
secretion a.re involved. Urine concentrabe as low as 0 -20%. The presence of food tions a.re often high for 24 hr after adminismay delay absorption in monogastric tration, and crystals may form in
animals, which may impact efficacy. The
concentrated acidic urine. The clinical
bioavailability of ciprofloxacin after
significance of this finding is tmclea.r. In
adminislTation PO in dogs is variable and
renal failure, clearance is impaired, and
can be as little as 40%; it is 0-200/o in cats and
reductions in dose rates are essential.

horses. Marbofloxacin oral bioavailability is

Bilia.Iy excretion of pa.rent drug, as well
almost 1000/o.

as conjugates, is an in1portant route of
elimination in some cases ( eg, ciproftoxa

Distribution: With few exceptions, the
cin, ma.rbof1oxacin, di.floxacin, pef1oxacin,
quinolones penetrate all tissues well and
nalidbdc acid). Quinolones appear in the
quickly. Particularly high concentrations
milk of lactating animals, often at high
are fow1d in organs of elimination (kidneys,
concentrations that persist for some tin1e.

liver, and bile), but concentrations fow1d
in prostatic f1ui.d, bone, endometriwn, and

Pharmacokinetic Values: The clearance

CSF a.re also quite notable. Most quinolones
and volwne of dist1ibutions of the drugs
also cross the placental ba.ITier. The

Va.IY a.Inong species, resulting in differences
apparent volmne of distribution of most
in plasma half-lives. Plasma concentrations
quinolones is large. The degree of plasmaattained a.re usually directly proportional to protein binding is extremely va.Ifable, from
the dose administered but also Va.IY with

-10% for norfloxacin to 300/o for enrofloxacin volume of distribution and oral bioavailabilin clogs and >90% for nalidi.xi.c acid.

ity. Package inserts should be consulted for

Fluorinated quinolones as a group

C,,,.Lx for those drugs approved for use in the
accumulate in phagocytic WBCs.

target species.

Biotransformation: Some qui.nolones

Therapeutic Indications and Dose
a.re eliminated unchanged (eg, ofloxacin),

Rates
some 31·e pa.ItiaJly metal:>olizecl ( eg,

Quinolones a.re indicated for the treatment
ciprof1oxacin, enrof1oxacin), and a few 31·e
of local and systemic infections caused by
completely degraded. Metabolites 31·e
susceptible microorganisms, particularly
sometimes active; enrof1oxacin is de-ethylagainst deep-seated infections and atecl to form ciprof1oxacin. Ch31·acteristiintracellular pathogens. Therapeutic ca1ly, phase I reactions result in a nwnber of
success has been obtained in respi.rato1y,
prin1a.Iy metabolites (up to six have been
intestinal, mi.na.Iy, and skin infections, as
described for some quinolones) that retain
well as in bacterial prostatitis, meningoensome antibacte1ial action. Conjugation with cephalitis, osteomyelitis, 3.I}d arthritis.

l&HifH PHARMACOKINETICS OF SELECTED FLUOROQUINOLONES

Elimination

Volume of

Clearance

Drug

Species

Half-life (hr) Distribution (Ilkg) (mUmin/kg)

Enrof1oxacin

Cats

7

4.3

Dogs

4.4

3.7

11

Mares

4-7

2

0.5-4

Ma.rbof1oxacin Dogs

12

2

1.5

Orbif1oxacin

Cats

4.5

1.3

Dogs

5.4

1.2

ANTIBACTERIALAGENTS

2673

Because of their lipid solubility and ability
probably should not be used in cats. The
to accumulate in phagocytic WJ3Cs,
presence of renal disease may increase
quinolones should be considered for use in
tllis risk. Pradofloxacin may be tl1e least
infections located in tough to penetrate
retinotoxic, followed by marbofloxacin and

VetBooks.ir
tissues. Therapeutic failure is iil<ely to result orbifloxacin, but each of these appears to be with multidrug-resistant organisms; this
safe in cats at doses that would be necessary
coupled with their emerging adverse events
to achieve targeted C,,,,L/MIC ratios for
should cause these drugs to be considered
susceptible organisms. The mechrulism is
second tier for dogs and cats.

not known. Quinolones tend to be neuro

A selection of general dosages for some
toxic, and convulsions can occur at high
quinolones is listed in TABLE 39. 'The dose
doses. Vomiting and iliarrhea rarely develop
rate and frequency should be adjusted as
witl1 fluoroquinolones. Dermal reactions
needed for the inilividual anim;J.l and the
and photosensitization have been described

MIC of the infecting organisms. Plasma drug in people, but the occurrence seems low.

concentrations should approximate 10

Hemolytic anemia has also been seen.

times the MIC of the infecting rrucrobe.

AdmiI1iste1ing large doses of quinolones for

Higher doses are encouraged tl!lless
ru1y length of time dllling pregnancy has
mitigating circumstances precl1.1de the
resulted in embryonic loss ru1d maternal
increase; in such instances, unless the MIC
toxicity. Because 11.igh prolonged dosages in
is very low, alternative antinlicrobials might
growing dogs have produced cartilaginous
be considered. In dogs and cats, use ideally
erosions leadmg to pern1anent lan1eness,
is based on culture and susceptjbility testing excessive use of quinolones should be when possible. Extra-label use of fluoroavoided in i.Jmnature animals. Quinolone quinolones is prohibited in food animals.

admiilistration in horses has not yet been
extensively stuilied, but t11ere is some

Special Clinical Concerns
inilication that dan1age to the cartilage in
weightbeari..ngjoints may be seen.

Adverse Effects and Toxicity:

In 2008, tl1e FDA added a "black-box"

Although adverse effects with t11e older
warning for seven fluoroquinolones that
quinolones (nalidixic and oxoJi(l.ic acids)

increased tl1e risk of tenili.nitis and a tendon
were relatively common, the newer ones
rupture.

seem to be well tolerated. However, several

An emerging toxicity associated with
adverse effects can limit use in selected
fluoroquinolones is mitotoxicity, ie, dan1age
species. Retinal degeneration may occur
to n1itochond1ial topoisomerase or other
acutely in cats, with the risk greatest for
mitochondrial structures. Mitochondrial
enrofloxacin; because these drugs are
effects may not emerge lllltil some time
concentration dependent, enrotloxacin
after fluoroquinolone therapy is instituted.

l&N•itl DOSAGES OF QUINOLONES

Quinolonea

Species

Dosage, Route, and Frequency

Nalidixic acid

Cats, dogs

3 mg/kg, PO, qid

Enrofloxacm

Dogs

5-20 mg/kg, PO, once to twice daily

2.5 mg/kg, SC, once, then PO

Beef cattle (not veal or dairy)

7.5-12.5 mg/kg, SC, once

2.5-5 mg/kg/day, SC

Pigs

2.5-5 mg/kg/day, PO or IM

Prerumma.nt calves

2.5-5 mg/kg/day, PO or SC

Marbofloxacin

Cats, dogs

2. 75-5.5 mg/kg/day, PO

Difloxacin

Dogs

5-10 mg/kg/day, PO

Orbifloxacin

Cats, dogs

2.5-7.5 mg/kg/day, PO

Pradofloxacin

Cats

7.5 mg/kg/day, PO

"Extra-label use of fluorinated qui11olones in food-producing animals is prohibited in the USA.

2674

ANTIBACTERIAL AGENTS

Although the entirety of the clinical imadnunistered 1-4 times/day, depending pact of this toxicity is not known, nor its
on the drug, to control systenuc infections
relevance to vete1inary medicine, adcaused by susceptible bacteria. In some verse events ranging from neurologic to
instances, adntinistration of the sulfona

VetBooks.ir
musculoskeletal to cardiovascular may
nude can be less frequent if tl1e drug is
ultimately be attributed to this effect.

elintinated slowly in tl1e species being
treated. Sulfonamides included in this class,

Interactions: The fluorinated quinolones
depending on the species, are sulfathiazole,
may be involved in a number of drug
sulfamethazine (sulfadinudine), sulfan1erainteractions. Antacids or other drugs zine, sulfadiazine, sulfapyridine, sulfabrocontaining multivalent cations and momethazine, sulfaethoxypyiidazine,
sucralfate appear to interfere with the GI
sulfamethoxypyridazine, sulfadimetl10xine,
absorption of the quinolones. Nitrofuranand sulfachlorpyiidazine.

toin impairs the efficacy of quinolones
if used concun-ently for Ulinary tract

Highly Soluble Sulfonamides Used for
infections. Quinolones inhibit tl1e biotrans

Urinary Tract Infections: A few very
formation of methylxanthines, with
water-soluble sulfonamides, eg, sulfisoxatheophylline being the most clinically zole (sulfafurazole) and sulfasonudine, are
relevant, but also including caffeine and
rapidly excreted via the urinary tract (>900Ai
theobromine. This is a class effect, with the
in 24 hr) mostly in an unchanged fom1;
risk varying an10ng the fluoroquinolones in
because of this, they are prinmrily used to
people. A similar ranking of risk is not
treat Ul·inary tract infections.

available for veterinary medicine. In people,
cyclosporine concentrations may also be

Poorly Soluble Sulfonamides Used for
increased by concun-ent administration

Intestinal Infections: Some sulfonanude
with fluoroquinolones, leading to prolonged
derivatives, such as sulfaguanidine, are so
and potentially toxic plasma concentrainsoluble that they are not absorbed from tions.

the GI tract ( <5%). Phthalylsulfatluazole and
succinylsulfathiazole undergo bacte1ial

Effects on Laboratory Tests: AST, ALT,
hydrolysis in the lower GI tract with the
alkaline phosphatase, and BUN may be
consequent release of active sulfathiazole.

increased. Urine glucose may be altered,

Salicylazosulfapyiidine (sulfasalazine) is
and urinalysis may reveal needle-shaped
also hydrolyzed in the large intestine to
crystals.

sulfapyridine and 5-antinosalicylic acid, an
anti-inflammatory agent tl1at might be used
for management of ulcerative colitis in dogs.

SULFONAMIDES AND

SULFONAMIDE COMBINATIONS

Potentiated Sulfonamides: A group

Sulfonamides are the oldest and remain
of diarninopyrimidines (trimethoprirn,
among the most widely used antibacterial
methoprim, ormetoprin1, aditop1in1,
agents in veterinary medicine, chiefly
pyiinlethanune) inhibit dil1ydrofolate
because of low cost and their relative
reductase in bacteria and protozoa far more
efficacy in some conunon bacterial
efficiently than in man1111alian cells. Used
diseases. The synergistic action of
alone, these agents are not particularly
sulfonamides with specific diantinopyrimieffective against bacteria, and resistance·
dines renders these drugs much more
develops rapidly. However, when combined
effective than sulfonamides alone.

with sulfonamides, a sequential blockade
of nucrobial enzyn1e systems occurs with
bactericidal consequences. Exan1ples of

Classes
such potentiated sulfonamide preparations

The many available sulfonanudes and
include trimethoprim/sulfadiazine ( co-trin m sulfonamide derivatives can be categorized zine ), trimetl10prim/sulfamethoxazole
into several types, based mainly on their

( co-trimoxazole ), trimethoprim/sulfadoxine
indications and duration of action in the

( co-trimoxine ), and ormetoprim/sulfabody. Probably the most conunon classificadirnethoxine. Sulfonamides are used in tion is based on water versus lipid solubility
combination with pyiinlethantine to treat
or duration of effect. Although there are
protozoal diseases such as leishmaniasis and
many sulfonamide antinucrobials, only a
toxoplasmosis. (See a/,so TABLE 41, p 2679.) few are used clinically in animals.

Topical Sulfonamides: Several

Standard Use Sulfonamides: In most
sulfonamides are used topically for specific
species, members of this large group are
purposes. Sulfacetanude is not highly

ANTIBACTERIAL AGENTS

2675
efficacious but is occasionally used to treat
of several enzymes needed for the
ophthalmic infections. Mafenide and silver
biogenesis of pmine bases and other
sulfadiazine are used on bum wounds to
metabolic reactions necessary for
prevent invasion by many gram-negative
fonnation of RNA Protein synthesis,

VetBooks.ir
and gram-positive organisms. Sulfathiazole
metabolic processes, and inhibition of
is commonly included in wound powders
growth and replication occm in orgaiusms
for the same purpose.

that cannot use preformed ( eg, dietary)

folate. The effect is bacteriostatic, although

General Properties
a bactericidal action is evident at the high

The sulfonan1ides are derivatives of
concentrations that may be found in urine.

sulfanilamide, which is the nucleus

Dian1inopyritnidines such as trimethoprim
common to all. The addition or substitution
inhibit dihydrofolate reductase, which is
of vaiious functional groups to the ainido
further into the folic acid synthesis pathway.

group or in which various substitutions on

The combination of a sulfonai11ide ai1d a
other ainino groups result in compounds
diaminopyrimidine results in synergistic,
with varying physical, chemical, phain1acobactericidal actions on susceptible logic, and antibacterial properties. Although organisms; as such, the combination is amphoteric, sulfonrunides generally behave
referred to as a "potentiated" sulfonan1ide.

as weak organic acids and are much more

The optin1al ratio in vitro for the
soluble in alkaline aqueous solutions than
combination of trimethoprim or om1ein acidic solutions. Those of therapeutic toprim ai1d a sulfonamide depends on
interest have pl<,, values of 4.8-8.6.

the type of microorganism but is usually

Water-soluble sodimn or disodimn salts are

-1:20. However, the commercially available
used for pai·enteral administration. Such
preparations use a ratio of 1:5 because
solutions ai·e highly alkaline, somewhat
of phaimacokinetic considerations that
unstable, and readily precipitate with the
presmnably result in the optimal ratio at
addition of polyionic electrolytes. In a
the site of infection.

mixture of sulfonamides ( eg, the sulfapy

Sulfonanudes are most effective in the
ri1nidine group), each component drug has
early stages of acute infections when
its own solubility; therefore, a combination
organisms are rapidly multiplying. They
of sulfonamides is more water soluble than
ai·e not active against quiescent bacteria.

a single drug at the san1e total concentra

Typically, there is a latent period before
tion. This is the basis of triple sulfonamide
the effects of sulfonainide therapy become
mixtmes used clinically. The N-4 acetylated
evident. This lag period occurs because the
sulfonamides, except for the sulfapyrimibacteria use existing stores of folic acid, dine group (sulfamethazine, sulfamerazine,
folinic acid, purines, thymidine, and ainino
sulfadiazine), are less water soluble than
acids. Once these stores are depleted,
their nonacetylated forms. This has bearing
bacteriostasis occurs. Bacterial growth can
in the development of sulfonanude
resmne when the concentration of PABA
crystalluria. The highly insoluble sulfonaincreases or when the level of sulfonamide mides (phthalylsulfathiazole and succinylfalls below an enzyn1e-inhibitory concentrasulfathiazole) are retained in the lmnen of tion. Because of the bacteriostatic natme
the GI tract for prolonged periods and are
of sulfonamides, adequate cellulai· ai1d
known as "gut-active" sulfonamides.

humoral defense mechanisms are critical

Trimethoprim and om1etoprim are basic
for successful sulfonamide therapy when
drugs.

used as sole agents. Even potentiated
sulfonan1ides, which are bactericidal, are
tin1e dependent in their antibacterial

Antimicrobial Activity
efficacy.

Alt.hough all of the sulfonrunides have

Mode of Action: The sulfonamides are
the san1e mechaiusm of action, differences
structural analogues of pai·a-aminobenzoic
are evident with respect to activity, phaimaacid (PABA) and competitively inhibit cokinetic fate, and even antimicrobial
dihydropterate synthetase, an enzyme that
spectrun1 at usual concentrations. The
facilitates PABA as a substrate for the
differences are due to the variety of physiosynthesis of dihydrofolic acid (folic acid).

chemical characteristics seen an10ng the

Dihydrofolate is a precursor for fo1ma-
sulfonai11ides.

tion of tetral1ydrofolate (folinic acid), an

The efficacy of sulfonamides can be
essential component of the coenzyn1es
reduced radically by excess PABA, folic
responsible for single carbon metabolism in
acid, thynune, pLUine, methionine, plasma,
cells. Sulfonamides are antimetabolites that
blood, albmnin, tissue autolysates, and
substitute for PABA, resulting in blockade
endogenous protein-degradation products.

2676

ANTIBACTERIAL AGENTS

Bacterial Resistance: Resistance to
monogastric animals. Absorption from the
sulfonamides is both chromosomally and
runlinoreticulum is delayed, especially if
plasmid mediated. Altered proteins such
ruminal stasis is present. Therapeutic doses
that affinity is reduced appears to be the
of sulfonamides are usually administered

VetBooks.ir
most common mechanism of resistance.

PO except in acute life-threatening

For example, in staphylococci, chromosominfections when IV infusions are used to ally mediated resistance reflects mutations
establish adequate blood concentrations
in genes encoding for dihydropterate
as rapidly as possible. Sulfonamides are
synthetase and plasmid-mediated resisfrequently added to drinking water or feed tance reflects mutations in dihydrofolate
either for therapeutic purposes or to
reductases, with the latter causing
improve feed efficiency. A few highly
high-level resistance to tri.methop1im.

wate1"soluble preparations may be irtjected

Staphylococci may have acquired some

IM ( eg, sodium sulfadirnethoxine) or IP
mechanisms of sulfonanlide resistance from ( some irritation of the peritoneum can be enterococci. Because sulfonamides act in a
seen). Absorption is rapid from tl1ese
competitive fashion, overproduction of
parenteral sites. Generally, sulfonamide

PABA can also preclude inhibition of
solutions are too alkaline for routine
dihydropterate synthetase. Alternate
parenteral use.

pathways of folic acid synthesis may

Trimethoprim is rapidly absorbed after
also contribute to low-level resistance.

administration PO (plasma concentrations

Cross-resistance between sulfonamides is
peak in -2-4 hr) except in nmlinants, in
common. Resistance emerges gradually and which it tends to be trapped in tl1e is widespread in many animal populations.

runlinoreticulw11 and appears to under-

Plasmid-mediated sulfonamide resistance
go a degree of nlicrobial degradation.

in intestinal gram-negative bacteria is often

Absorption occurs readily from
linked with ampicillin and tetracycline
parenteral injection sites; effective
resistance.

antibacterial concentrations are reached in

< 1 hr, and peak concentrations in -4 hr.

Antimicrobial Spectra: The spectrum
of all sulfonamides is generally the same.

Distribution: Sulfonamides are distrib

Sulfonamides inhibit both gram-positive
uted throughout all body tissues. The
and gran1-negative bacteria, Nocardia,
distribution pattern depends on the

Actinomyces spp, and some protozoa such
ionization state of the sulfonamide, the
as coccidia and Toxoplasma spp. More
vascularity of specific tissues, the presence
active sulfonamides may include several
of specific barriers to sulfonamide diffusion,
species of Streptococcus, Staphylococcus,
and the fraction of the administered dose

Salmonella, Pasteurella, and even
bound to plasma proteins. The unbound

Escherichia coli in their spectra. Strains of drug fraction is freely diffusible. Sulfona

Pseudomonas, Klebsiella, Proteus,
nlides are bound to plasma proteins to a

Clostridium, and Leptospira spp are most greater or lesser extent, and concentrations
often highly resistant, as Me 1ickettsiae,
in pleural, pe1itoneal, synovial, and ocular
mycoplasmas, and most Chlamydia.

fluids may be 500h-900A, of that in blood.

Sulfadiazine is ;,,g()OA, bound to plasma
proteins. Concentrations in the kidneys

Pharmacokinetic Features
exceed plasma concentrations, and those in

There are notable differences among the
the skin, liver, and lungs are only slightly
many sulfonanlides with respect to their
less than the con-esponding plasma
phannacokinetic fate in the various species.

concentrations. Concentrations in muscle

The standard classification of short-,
and bone are -500A,of those in the plasma,
medium-, and long-acting sulfonamides
and those in the CSF may be 200/o--8()0A, of
used in hwnan therapeutics is usually
blood concentrations, depending on the
inappropriate in veterinary medicine
pmticular sulfon8.11lide. Low concentrations
because of species differences in disposiare found in adipose tissue. After parenteral tion and elimination.

administration, sulfamethazine is found in
jejuna! and colonic contents at about the

Absorption: Sulfonamides may be
smne concentration as in blood. Passive
administered PO, IV, IP, IM, intrauterine,
diffusion into milk also occurs; altl1ough
or topically, depending on the specific
the concentrations achieved are usually
preparation. Except for the poorly absorbed inadequate to control infections, sulfonasulfonamides intended for local treatment mide residues may be detected in milk.

of intestinal infections, most are rapidly and

Trimethoprim and ormetoprim are basic
completely absorbed from the GI tract of
drugs that tend to accumulate in more

ANTIBACTERIAL AGENTS

2677
acidic environments such as acidic mine,
and 2.9 hr in pigs. The recommended dose
milk, and ruminal fluid.

rates and frequencies reflect this disparity in

Trimethoprim diffuses extensively into
elimination kinetics.

tissues and body fluids. Tissue concentra

The plasma half-life of trimethop1im is

VetBooks.ir
tions are often higher than the correspondquite prolonged in most species; effective ing plasma concentrations, especially in
concentrations may be maintained for> 12
lungs, liver, and kidneys. Approximately
hr, with the result that the frequency of

300/er-600A, of trimethoprim is bound to
adnunistration is usually 12-24 hr. The
plasma proteins. The extent of metabolic
elinunation rates of trimethoprim in sheep
transformation of trimethoprim has not
seem to be much shorter than in monogasyet been established, although there is a tric species.

suggestion that hepatic biotransformation
can be extensive, at least in ruminants. This

Therapeutic Indications and Dose
may not be the case in all species; >500A,
of a dose is excreted unchanged in many

Rates
instances. Trimethop1im is largely excreted

The sulfonamides a.i·e commonly used
in the urine by glomerular filtration and
to treat or prevent acute systenuc or local
tubular secretion. A substantial amount may infections. Disease syndromes treated with also be fom1d in the feces. Concentrations
sulfonanudes include actinobacillosis,
in milk are often 1 -3.5 times higher than
coccidiosis, mastitis, met1itis, colibacillosis,
those in plasma.

pododermatitis, polya.iilrritis, respiratory
infections, a.i1d toxoplasmosis.

Biotransformation: Sulfonamides are

Sulfonan1ides are more effective when
usually extensively metabolized, mainly by
administered ea.i·ly in the course of a
several oxidative pathways, acetylation, and disease. Chronic infections, particularly conjugation with sulfate or glucuronic acid.

with large a.inounts of exudate or tissue

Species differences are marked in this
debris present, often are not responsive.

regard. The acetylated, hydroxylated, and

In severe infections, the initial dose should
conjugated fonns have little antibacterial
be adnunistered IV to reduce the lag time
activity. Acetylation (poorly developed in
between dose and effect. For drugs with a
dogs) reduces the solubility of most
long elinunation half-life, the initial dose
sulfonanudes except for the sulfapyrinudine should be double the maintenance dose.

group. The hydroxylated and conjugated

Adequate drinking water should be
forms are less likely to precipitate in mine.

available at aJI times, a.i1d mine output
monitored. A course of treatment should

Excretion: Most sulfonamides are
not exceed 7 days under usual circlllllexcreted primarily in the mine. Bile, feces, stances. If a favorable response is·seen
milk, and sweat are excretory routes of
witlun 72 hr, treatment should be continued
lesser significance. Glomerular filtration,
for 48 lu- after remission to prevent relapse
active tubular secretion, and tubular
a.i1d the emergence of resistance. The ability
reabsorption are the main processes
to mount an in1mune response must be
involved. The proportion reabsorbed is
intact for successful sulfona.i11ide therapy.

influenced by the inherent lipid solubility of

A selection of general dosages for some
individual sulfonanudes and their metabosulfonan1ides is listed in TABLE 40. The dose lites and by urinary pH. U1inary pH, renal
rate and frequency should be adjusted as
clearance, and the concentration and
needed for the individual anin1al.

solubility of the respective sulfonanudes
and their metabolites deternune whether

Special Clinical Concerns
solubilities are exceeded and crystals
precipitate. This can be prevented by

Adverse Effects and Toxicity: Adverse
alkalinizing the urine, increasing fluid
reactions to sulfona.inides may be due to
intake, reducing dose rates in renal
hypersensitivity or direct toxic effects.

insufficiency, and using triple-sulfonanude

Possible hypersensitivity reactions include
or sulfonanude-diaminopyrimidine
urtica.iia, angioedema, waphyla.xis, skin
combinations.

rashes, drug fever, polyarth!itis, hemolytic
wemia, and agrwulocytosi.s. Keratitis sicca

Pharmacokinetic Values: There are
is a recognized ad.verse effect. The aJiergic
great differences between the pha.imacokiresponse ta.i·gets, in prut, metabolites of the netic values of various sulfona.i11ides in
aryl anune of sulfona.inides. Because dogs
animals, and extrapolation of these values is are deficient in acetylation, they may be at rarely appropriate; for example, the plasma
risk of increased fom1ation of phase I
half-life of sulfadiazine is 10.1 hr in cattle
metabolites associated. with adverse effects.

2678

ANTIBACTERIAL AGENTS
itM•IH DOSAGES OF SULFONAMIDES

Dosage, Route, and

Sulfonamide

Species

Frequency

VetBooks.ir

Sulfathiazole

Horses

66 mg/kg, PO, tid

Cattle, sheep, pigs

66 mg/kg, PO, every 4 hr

Sulfamethazine

Cattle

220 mg/kg/day, PO or IV (initial
dose; half for subsequent
doses)

Sulfadiazine

All

50 mg/kg, PO, bid

Sulfadimethoxine

All

55 mg/kg/day, PO (initial dose;
half for subsequent doses)

Sulfaethoxypyridazine

Cattle

55 mg/kg/day, PO

Pigs

110 mg/kg/day, PO (initial dose,
half for subsequent doses)

Sulfapyridine

Cattle

132 mg/kg, PO, bid (initial dose,
half for subsequent doses)

Succinylsulfathiazole

All

160 mg/kg, PO, bid (initial dose;
half for subsequent doses)

Crystalluria with hematuria, and even
tions leads to maturation defects in
tubular obstruction, is not common in
hematopoiesis due to impaired folinic acid
veterinary medicine. Acute toxic manifessynthesis. This effect is readily reversible by tations may be seen after too rapid IV
supplementation with folinic acid.

administration or if an excessive dose is
injected. Clinical signs include muscle

Interactions: Sulfonanlide solutions
weakness, ataxia, blindness, and collapse.

are incompatible with calciun1- or other

GI disturbances, in addition to nausea and
polyionic-containing fluids as well as many
vomiting, may occur when sulfonanlide
other preparations. Sulfonanlides may be
concentrations are sufficiently high in the
displaced from their plasma-protein-binding
tract to disturb normal microfloral balance
sites by other acidic drugs with higher
and vitamin B synthesis. Sulfonanlides
binding affinities. Antacids tend to inhibit
depress the cellulolytic function of ruminal
the GI absorption of sulfonamides.

nlicroflora, but the effect is usually transient

Alkafulization of the urine promotes

(unless excessively high concentrat:ions are
sulfonanlide excretion, and urinary
reached). Several adverse effects have been
acidification increases the risk of crystallureported after prolonged treatment, ria. Some sulfonamides act as microsomal
including bone marrow depression ( aplastic
enzyme inhibitors, which may lead to toxic
anemia, granulocytopenia, thrombocytopemanifestations of concurrently adnlinisnia), hepatitis and icterus, peripheral neuritis tered drugs such as phenytoin.

and myelin degeneration in the spinal cord
and pe1ipheral nerves, photosensitization,

Effects on Laboratory Tests: Bilirubin,
stomatitis, conjunctivitis, and keratitis sicca.

BUN, bromsulphthalein (BSP®), eosino

Mild follicular thyroid hyperplasia may be
phils, methemoglobin, AST, and ALT may be
associated with prolonged adnlinistration of
increased. Platelet, RBC, and WBC counts
sulfonanlides in sensitive species such as
are often decreased. Urinalysis may show a
dogs, and reversible hypothyroidism can be
change in color, glucose, porphyrins, and
induced after treatment with high doses in
urobilinogen. Sulfonamide crystals may
dogs. Several sulfonamides can lead to
also be found.

decreased egg production and growth.

Topically, the sulfonamides retard healing

Regulatory Considerations and Drug
of uncontanlinated wounds.

Withdrawal and Milk Discard Times:

Up to 10 times the reconunended dose

Sulfonamides are among the drugs for
of trirnethoprim has been given with no
which extra-label use restrictions exist in
adverse effects. Prolonged administration of
lactating dairy cattle. Currently allowable
trirnethoprin1 at reasonably high concentra-
drugs are sulfadimethoxine, sulfabro-

ANTIBACTERIAL AGENTS

2679

•th•ili DOSAGES OF POTENTIATED SULFONAMIDES

Combination Sulfonamide

Dosage, Route, and Frequency

Trimethoprim/sulfadiazine

15-60 mg/kg/day, PO, IV, or IM

VetBooks.ir

Ormetoprim/sulfadimethoxine

55 mg/kg/day, PO (initial dose; half for subsequent
doses)

FH=iiiti DRUG WITHDRAWAL AND MILK DISCARD TIMES OF SULFONAMIDES

Withdrawal

Milk Discard

Sulfonamide

Species

Time (days)

Time (hr)

Sulfamethazine

Cattle

10"

96

Pigs

14

Sulfabromethazine

Cattle

10

96

Triple sulfonamide solutionb

Cattle

10

96

Sulfadimethoxidine

Cattle

7

60
a 28 days for slow-release bolus
b 8% sodium sulfamethazine, 8% sodium sulfapyridine, 8% sodium sulfathiazole methazine, and sulfathoxypyiidazine. In

(tetracycline, oxytetracycline, chlortetracyaddition, sulfonamide residues, particularly cline ), intermediate-acting ( demethylchlorin swine and poultry, continue to be a focus tetracycline and methacycline), and
of detection. Because of adverse effects in
long-acting (doxycycline and minocycline).

people, including allergic reactions,

The newest class of tetracycline-related
attention must be made to withdrawal
antimicrobials are the glycylcyclines,
times. Regulatory requirements for
represented by tigecycline, which contains
withdrawal times for food animals and milk
a bulky side chain compared with
discard times vary among countries and
minocycline.

may change. These must be followed
carefully to prevent food residues and
consequent public health implications.

General Properties

There are some prohibitions on use of
sulfonamides in the USA, including use in

All of the tetracycline de1ivatives are
dairy cattle. The times listed in
crystalline, yellowish, an1photeric sub

TABLE 42
serve only as general guidelines.

stances that, in aqueous solution, form salts
with both acids and bases. They characteris

TETRACYCLINES
tically fluoresce when exposed to ultraviolet
light. The most common salt fonn is the

The tetracyclines are broad-spectrum
hydrochloride, except for doxycycline,
antibiotics with similar antimicrobial
which is available as doxycycline hyclate or
features, but they differ somewhat from
monohydrate. The tetracyclines are stable
one another in tem1s of their spectra and
as dry powders but not in aqueous solution,
pham1acokinetic disposition.

particularly at higher pH ranges (7-S.5).

Preparations for parenteral administration
rn ust be carefully fom1ulated, often in

Classes
propylene glycol or polyvinyl pyrrolidone

There are three naturally occurring
with additional dispersing agents, to provide
tetracyclines ( oxytetracycline, chlortetrastable solutions. Tetracyclines fonn poorly cycline, and demethylchlortetracycline)

soluble chelates with bivalent and trivalent
and several that are derived semisynthetications, particularly calcium, magnesium, cally (tetracycline, rolitetracycline,
alun1inwn, and iron. Doxycycline and
methacycline, minocycline, doxycycline,
minocycline exhibit the greatest liposolubillymecycline, etc). Elin1ination tin1es permit ity and better penetration of bacteria such as
a further classification into short-acting

Staphylococcus aureus than does the group

2680

ANTIBACTERIAL AGENTS

DRUG WITHDRAWAL A ND MILK DISCARD TIMES OF POTENTIATED

SULFONAMIDES

Combination

Milk Discard

VetBooks.ir

Sulfonamide

Withdrawal Time (days)

Time (days)

Trimethoprim/

3

7
sulfadiazine

Trimethoprim/

5 (PO), 28 (parenteral)

sulfadoxine
as a whole. This may contribute to their
or by cortjugation (as in many enterobacteefficacy in treatment of gingival diseases ria). A second mechanism of resistance is
that may be associated with bacterial
the production of a "protective" protein tllat glycocalyx. Tigecycline is a glycylcycline
acts by eitller preventing binding, dislodging
derivative of minocycline; its large side
tlle bom1d drng, or altering tl1e negative
chain decreases the risk of resistance.

impact of binding on ribosomal fimction.

Among the tetracyclines, tigecycline is

Antimicrobial Activity
characterized by less resistance due to

Mode of Action: The antimicrobial
efflux or 1ibosomal protection. Rarely,
activity of tetr·acyclines reflects reversible
tetracyclines can be destroyed by acetylabincling to the bacterial 308 ribosomal tion. Resistance develops slowly in a
subunit, and specifically at the aminoacylmultistep fashion but is widespread because tRNA acceptor ("A") site on the mRNA
of the extensive use of low concentrations
ribosomal complex, thus preventing
of tetracyclines.

ribosomal translation. This effect also is
evident in mammalian cells, although micro

Antimicrobial Spectra: All tetracyclines
bial cells are selectively more susceptible
ar.·e about equally active and typically have
because of the greater concentrations seen.

about the same broad spectrum, which

Tetracyclines enter microorganisms in par.t
comprises botll aerobic and anaerobic
by diffusion and in part by an energygram-positive and gram-negative bacteria, dependent, car.·rier-mediated system
mycoplasmas, rickettsiae, chlamydiae, and
responsible for the high concentrations
even some protozoa (ar.11ebae). Tetracyachieved in susceptible bacteria. "'!'he clines generally are tlle dntg of choice to
tetracyclines ar.·e generally bacteriostatic,
treat rickettsiae and mycoplasma. Among
and a responsive host-defense system is
the susceptible organisms is Wolbachia, a
essential for their successful use. At high

1ickettsial-like intracellular endosymbiont
concentrations, as may be attained in urine,
of nematodes, includi.ngDirqfilmia
they become bactericidal because tl1e
immitis. Str·ains of Pseudomonas
organisms seem to Jose the functional
aern,ginosa, Proteus, Sen·atia, Klebsiella,
integrity of the cytoplasmic membrane.

and Trueperella spp frequently are

Tetracyclines are more effective against
resistant, as are many patllogenic Escheri
multiplying microorganisms and tend to be
chia coli isolates. Even though tllere is
more active at a pH of 6-6.5. Antibacterial
general cross-resistance among tetracyefficacy is described as time dependent.

clines, doxycycline and minocycline usually
are more effective against staphylococci.

Bacterial Resistance: The most common
mechar.lism by which microbes become

Pharmacokinetic Features
resistant to tetracyclines is decreased

Absorption: After usual oral dosage,
accmnulation of drug into previously
tetracyclines are absorbed primar.ily in the
susceptible organisms. Two mechanisms
upper small intestine, ar.1d effective blood
include 1) impaired uptake into bacteria,
concentrations are reached in 2-4 hr. GI
which occurs in mutar.1t strains that do not
absorption can be impaired by sodimn
have the necessary transport system, and
bicar.·bonate, aluminum hydroxide,

2) the much more common plasmid- or
magnesimn hydroxide, iron, calcium salts,
transposon-mediated acquisition of active
and ( except for the lipid-soluble tetracyefflux pun1ps. The genomes for these clines doxycycline and minocycline) milk
capabilities may be transferred eitl1er by
and milk products. Oral bioavailability,
transduction (as in Staphylococcus aureus)

however, can vary markedly among drngs,

ANTIBACTERIAL AGENTS

2681
with chlortetracycline being the least and
filtration rate, renal disease, and the
doxycycline the most orally bioavailable.

particular tetracycline used. Biliru·y

Tetracyclines at therapeutic concentrations
elimination is always significant, comshould not be administered PO to rumimonly being --10%--20%, even with VetBooks.ir
nants: they are poorly absorbed and can
parenteral administration. Doxycycline
substantially depress rurninal microfloral
appears to be eliminated through feces
activity. Specially buffered tetracycline
predominantly through intestinal cells,
solutions can be administered IM and IV.

rather thru1 bile. Only --16% of an IV dose

Through chemical manipulation (especially
of doxycycline is eliminated unchanged
choice of carrier and high magnesiwn
in the mine of dogs. A portion of doxycycontent), the absorption of oxytetracycline cline is also renally excreted in active form
from TM sites may be delayed, which
in some species. For minocycline, bile
produces a long-acting effect. Tetracyclines
appears to be the major route of excretion.

can also be absorbed from the uterus and

Tetracyclines ru·e also eliminated in milk;
udder, although plasma concentrations
concentrations peak 6 hr after a parenteral
remain low.

dose, and traces ru·e still present up to 48 hr
later. Concentrations in milk usually attain

Distribution: Tetracyclines distribute

--50%--60% of the plasma concentration and
rapidly and extensively in the body,
are often higher in mastitic milk. Tetracyparticularly after parenteral administraclines also are excreted in saliva and tears.

tion. They enter almost all tissues and body
fluids; high concentrations are found in the
kidneys, liver, bile, lungs, spleen, and bone.

Pharmacokinetic Values: The plasma

Lower concentrations are found in serosal
half�lives of tetracyclines are 6-12 hr and
fluids, synovia, CSF, ascitic fluid, prostatic
can be longer depending on age (slower
fluid, and vitreous humor. The more
elimination in animals < 1 mo old), disease,
lipid-soluble tetracyclines ( doxycycline
and the tetracycline itself (see TABLE 44).

and minocycline) readily penetrate tissues

In large anin1als, daily injections of standru·d
such as the blood-brain barrier, and CSF
dosages usually are sufficient to maintain
concentrations reach --300/o of the plasma
effective inhibitory concentrations.

concentrations. Doxycycline is the most

Long-acting fonnulations of oxytetracyextensively dist1ibuted. Because tetracycline, when injected IM, generally produce clines tend to chelate calcium ions (less
plasma concentrations >0.5 mcg/mL for --72
so for doxycycline ), they are deposited
hr. Tetracyclines usually are administered
irreversibly in the growing bones and in

PO bid-tid ( every 12--24 hr for doxycycline
dentin and enamel of unerupted teeth
ru1d minocycline).

of young animals, or even the fetus if
transplacental passage occurs (seep 2658).

Drug bound in this fashion is pharmaco

Therapeutic Indications and Dose
logically inactive. Tetracyclines are bound

Rates
to plasma proteins to vru)'ing degrees ( eg,

The tetracyclines ru·e used to treat both
oxytetracycline, 30%; tetracycline, 60%;
systemic ru1d local infections. However,
doxycycline, 90%).

resistance ru1d their bacteriostatic nature
suggest caution with empirical use for

Biotransformation: Biotransformation
bactetial infections, particulru·ly in dogs ru1d
of the tetracyclines seems to be limited
cats. Specific conditions include infectious
in most domestic animals, and generally
keratoconjunctivitis in cattle, chlru11ydiosis,
about one-third of a given dose is excreted
heruuvater, ru1aplasmosis, actinomycosis,
unchru1ged. Rolitetracycline is metabolized
acti.nobacillosis, nocardiosis ( especially
to tetracycline. Doxycycline and minocyminocycline ), ehrlichiosis ( especially cline may be more extensively biotransdoxycycline), Wolbachia, eperythrozoonofom1ed thru1 other tetracyclines ( up to 400/o sis, ru1d haemobartonellosis. Minocycline
of a given dose).

ru1d doxycycline are often effective to a
somewhat lesser degree against resistru1t

Excretion: Tetracyclines are excreted
strains of StaphylococC'us aureus.

via the kidneys (glomerular filtration)

In addition to ru1timicrobial chemotherand the GI tract (biliary elimination and apy, tl1e tetracyclines are used for other
directly). Generally 50%--80% of a given
purposes. As additives in ru1in1al feeds, U1ey
dose is recoverable from the urine,
serve as growth promoters. Because of the
although several factors may influence
affinity of tetracyclines for bones, teeth,
renal elimination, including age, route
and necrotic tissue, they cru1 be used to
of administration, urine pH, glomerular
delineate tumors by fluorescence.

2682

ANTIBACTERIALAGENTS

•th•ii• ELIMINATION, DISTRIBUTION, AND CLEARANCE OF TETRACYCLINES

Volume of

Elimination

Distribution

Clearance

VetBooks.ir

Tetracycline

Species

Half-life (hr) (mIJkg)

(mIJkg/min)

Oxytetracycline Dogs

6

3,000

4.23

Calves

10-13

1,500-2,400

3.45

(<3 mo old)

Cattle

7-10

800-1,000

3.33

Horses

8 -10

1,100

2.89

Minocycline

Dogs

7

2,000

3.21

Doxycycline

Dogs

7-10

930
l. 7

Cats

5

340

1.0

Horses

9

Demethylchlortetracycline has been used

Tetracyclines chelate calciW11 in teeth and
to inhibit the action of antidiuretic
bones; they become incorporated into these
hormone in cases of excessive water
structures, inhibit calcification ( eg,
retention. Because of either their metallohypoplastic dental enamel), and cause proteinase-inhibiting effects or their
yellowish then brownish discoloration. At
binding of calcium, they are used to
extremely high concentrations, the healing

"stretch" flexor digital tendons in neonatal processes in fractured bones is impaired.

foals. Finally, they are being used to reduce

Rapid IV injection of a tetracycline can
the risk of adverse events and to enhance
result in hypotension and sudden collapse.

killing of adult heartworms ancVor

This appears to be related to the ability of
microfilaria before adulticide therapy.

the tetracyclines to chelate ionized calcium,

A selection of general dosages for some
although a depressant effect by the
tetracyclines is listed in TABLE 45. The dose
propylene glycol carrier itself may also be
rate and frequency should be adjusted as
involved. This effect can be avoided by slow
needed for the individual animal.

infusion of the drug (>5 min) or by
pretreatment with IV calciwn gluconate.

The IV administration of undiluted

Special Clinical Concerns
propylene glycol-based preparations leads

Adverse Effects and Toxicit : Because
to intravascular hemolysis, which results
several diverse effects may result from
in hemoglobinmia and possibly other
administration of tetracyclines, caution
reactions such as hypotension, ataxia,
should be exercised. Superinfection by
and CNS depression.

nonsusceptible pathogens such as fungi,

Because tetracyclines interfere with
yeasts, and resistant bacte1ia is always a
protein synthesis even in host cells and
possibility when broad-spectrum antibiotics therefore tend to be catabolic, an increase are used. This may lead to GI disturbances
in BUN can be expected. The combined use
after either PO or parenteral administration
of glucocorticoids and tetracyclines often
or to "persistent infection" when they are leads to a significant weight loss, particuapplied topically (eg, in the ear). Severe and larly in anorectic anin1als.

even fatal diarrhea can occur in horses

Hepatotoxic effects due to large doses
receiving tetracyclines, especially if the
of tetracyclines have been reported in
anin1als are severely stressed or critically ill. pregnant women and in other animals.

High doses administered PO to ruminants

The mortality rate is high.

seriously disrupt microfloral activity in the

The tetracyclines are also potentially
ruminoreticulwn, eventually producing stasis. nephrotoxic and are contraindicated Elimination of the gut flora in monogastric

( except for doxycycline) in renal insuffianimals reduces the synthesis and availability ciency. Fatal renal failure has been repm'Led
of the B vitamins and vitamin K from the large
in septicemic and endotoxemic cattle given
intestine. With prolonged therapy, vitamin
high doses of oxytetracycline. The
supplementation is a useful precaution.

administration of expired tetracycline

ANTIBACTERIAL AGENTS

2683
itM•iH DOSAGES OF TETRACYCLINES

Dosage, Route, and

Tetracycline

Species

Frequency

VetBooks.ir

Tetracycline

Cats, dogs

7 mg/kg, IM or IV, bid

20 mg/kg, PO, tid

Oxytetracycline

Cats, dogs

7 mg/kg, IM or IV, bid

20 mg/kg, PO, tid

Cattle, sheep, pigs

5--10 mg/kg/day, IM or IV

Calves, foals, lambs, piglets

10-20 mg/kg, PO, bid-tid

Horses

5 mg/kg, IV, once to twice daily

Doxycycline

Dogs

5-10 mg/kg/day, PO

5 mg/kg/day, IV

Before heartworn1 adulticide

10 mg/kg, PO, bid, for 30 days
therapy
products may lead to acute tubular

Tetracyclines also bind to the calcium ions
nephrosis.

in Ringer's solution.

Swelling, necrosis, and yellow discolora

Methoxyflurane anesthesia combined
tion at the ir\jection site almost inevitably
with tetracycline therapy may be nephroare seen. Phototox.ic de1matitis may occur tox.ic. Microsomal enzyme inducers such as
in people treated with demethylchlortetraphenobarbital and phenytoin may sho1ten cycline and other analogues, but this
the plasma half-lives of minocycline and
reaction is rare in other animals. Hypersendoxycycline. Except for minocycline and sitivity reactions occur; for example, cats
doxycycline, the presence of food can
may develop a "drug fever" reaction, often substantially delay absorption of tetracyaccompanied by vomiting, diarrhea, clines from the GI tract. The tetracyclines
depression, inappetence, fever, and
are less active in alkaline urine, and urine
eosinophilia.

acidification can increase their antimicro

The tetracyclines can inhibit WBC
bial efficacy.

chemotaxis and phagocytosis when present
in high concentrations at sites of infection.

Effects on Laboratory Tests: Tetracy

This clearly hinders normal host defense
clines may increase amylase, BUN,
mechanisms and compounds the bacteriobromsulphthalein (BSp@), eosinophil static activity of tetracyclines. The use of
count, AST, and ALT. Tetracyclines used in
immunosuppressive drugs such as
combination with diuretics are often
glucocorticoids impairs immunocompeassociated with a marked rise in BUN.

tence even further.

Cholesterol, glucose, potassiun1, and

Doxycycline administered in tablets has
prothrombin time may be decreased. A falsebeen associated with esophageal erosion in positive urine glucose test is also possible.

cats. The incidence is reduced if administration is followed by a 5-mL volume of fluid.

Doxycycline may be associated with GI

Drug Withdrawal and Milk Discard
upset; this might be reduced by administer

Times: Regulatory requirements for
ing the drug with food.

withdrawal times for food a.ninlals and milk
discard times vary among countries. These
must be followed carefully to prevent food

Interactions: Absorption of tetracyclines
residues and consequent public health
from the GI tract is decreased by milk and
in1plications. The withdrawal tin1es listed in
milk products ( except for doxycycline and

TABLE 46 se1ve only as general guidelines.

minocycline), antacids, kaolin, and iron
preparations. Tetracyclines gradually lose

PHENICOLS
activity when diluted in infusion fluids and
exposed to ultraviolet light. Vitamins of the

Chlora.mphenicol is a highly effective and

B-complex group, especially riboflavin,
well-tolerated broad-spectrum antibiotic.

hasten this loss of activity in infusion fluids.

However, because it ca.uses blood

2684

ANTIBACTERIAL AGENTS
hth•it·I DRUG WITHDRAWAL AND MILK DISCARD TIMES OF TETRACYCLINES

Tetracycline

Species

Withdrawal Time (days)

Ox:ytetracycline•

Cattle

15-22

VetBooks.ir

Pigs

22

Poultry

5

Ox:ytetracycline (lon g -acting)•

Cattle

28

Chlortetracycline

Cattle

10

Pigs

1-7

"Not for use in lactating dairy cows
dyscrasias, it is prohibited for use in
bacterial isolates, high-level plasmidfood-producing anin1als in several mediated resistance reflects the produccountries, including the USA and Canada.

tion of chloramphenicol acetyltransferase

Thiamphenicol is less effective but safer

( encoded for by the cal gene) and results
than chloran1phenicol; flotienicol,
in acetylation of the molecule, which can
a thiamphenicol derivative, is significantly
no longer bind to the ribosome. Other
more active in vitro than chloran1phenicol
inactivating enzymes also may be involved.

against many pathogenic strains of bacteria.

In resistant gran1-negative bacteria,

Florfenicol is approved for use in cattle.

chloran1phenicol acetyltransferase is a
constitutive enzyme; in gram-positive

General Properties
organisms, the enzyme is inducible. The

Chloramphenicol is a relatively simple
fluorine atom of florfenicol prevents
neutral nitrobenzene detivative with a bitter
acetylation, thus enhancing the efficacy
taste. It is highly lipid soluble and is used
of this drug. InPseudomonas aeiuginosa
either as the free base or in ester fom1s ( eg,
and m strains of Proteus and Klebsiella the neutral-tasting pa.Imitate for administraspp, resistance is also nonenzymatic and is tion PO and the water-soluble sodium
based on an inducible pem1eability block
succinate for parenteral illiection ).

that is both chromosomal and plasmid

Chloramphenicol is a relatively stable
mediated. Reduced permeability contribcompound and is unaffected utes to low level resistance. Very rarely,

. by boiling,
provided that a pH of 9 is not exceeded. The
resistance may reflect altered ribosomal
nitrophenol group of chloramphenicol is
subunit structure and bindmg. Resistance
replaced by a methyl sulfonyl group for
to chloramphenicol often develops
thiamphenicol and florfenicol; florfenicol
togeU1er with resistance to tetracycline,
also contains a fluorine molecule. These
erythromycm, streptomycin, ampicillin,
structural changes m1prove efficacy, reduce
and other antibiotics because of multiple
toxicity, and for tlorfenicol, the fluorme
genes beiI1g carried on the same plasmid.

molecule reduces bacterial resistance.

Antimicrobial Spectra: Many genera of
gram-positive and gran1-negative bactetia

Antimicrobial Activity
and several anaerobes such as Bacteroides

Mode of Action: The phenicols inhibit
fragilis, as well as Rickellsia and Chla
microbial protem synthesis by binding to
mydia spp are susceptible. Chloramphenithe 508 subunit of the 708 tibosome and col is notable for its anaerobic spectnun. Of
m1pairing peptidyl transferase activity.

special note is the efficacy against many

Because peptide-bond formation is

Salmonella spp but the resistance of most
inhibited, peptides cannot elongate. The
strains of P aeruginosa.

effect is usually bacteriostatic but, at high
concentrations, chloramphenicol may be

Pharmacokinetic Features
bactericidal for some species. Protem
synthesis is inhibited m both prokaryotic

Absorption: Absorption occurs
and eukaryotic (mitochondrial) ribosomes.

promptly and rapidly from the upper

GI tract when chloramphenicol base is

Bacterial Resistance: Resistance
administered PO to nonruminant animals.

against chloramphenicol develops slowly

Blood concentrations usually are maximal
and in a stepwise fashion. In clinical
in 1-3 hr. Because ruminal microflora

ANTIBACTERIAL AGENTS

2685
readily reduce the nitro group, chloram

Biotransformation: Unlike many other
phenicol is inactivated in the ruminoreticuantibacterial agents, chloramphenicol lum and is not available for absorption. The undergoes extensive hepatic metabolism.

larger ester forms of chloramphenicol

Although some nitroreduction and other

VetBooks.ir
require hydrolysis by lipases to release the
phase I reactions occur, free chloramantibiotic for absorption from the GI tract; phenicol is biotransformed primarily
thus, the systemic availability of chloran1-
by glucuronide conjugation. Urinary
phenicol is delayed when the palmitate and
products after administration of chlorother ester preparations are used. Generic amphenicol sodium succinate include
inequivalence has been seen with oral
inactive forms, mainly the unhydrolyzed
dosage forms. The presence of food and
sodium succinate and the glucuronide;
intestinal protectants does not interfere
only 5%-15% appears as biologically active
with absorption of chloramphenicol,
chloramphenicol.

although drugs that depress GI motility do.

There are several clinical concerns

Florfenicol is rapidly absorbed after adminwith respect to the biotransformation of istration PO, although milk interferes with
chloramphenicol. In cats, a characteristic
absorption.

genetic deficiency in glucuronyl trans

Chloran1phenicol sodium succinate may
ferase activity leads to plasma half-lives
be injected both IV and IM. However,
that are often considerably longer than
hydrolysis is required in the body because
those in other species (eg, cats, 5.1 hr;
only free chloran1phenicol base is active.

ponies, 54 min), and dosages need to be

The kinetics of this hydrolysis reaction may
adjusted accordingly. Phase I metabolism
be slow and incomplete, with considerable
may also be deficient in cats. Very young
individual and species variability. The
animals frequently do not have full
absorption of chloramphenicol base itself
microsomal enzyme capabilities, and the
from IM injection sites is notably restricted.

plasma half-lives of chloramphenicol in

For example, in horses, the therapeutic
the young ( <4 wk old) of many species
blood concentration of 5 mg/mL is achieved
are often much longer than those of
at a dosage of 50 mg/kg body wt, IM, after
adults. Foals appear to be a notable
only 6-8 hr. Chloran1phenicol base is
exception to this generalization. Liver
absorbed after IP injection. Florfenicol is
disease also prevents chloramphenicol
available as an injectable solution intended
from undergoing normal metabolic
for IM use.

degradation, and active antibiotic
accumulates in the body.

Distribution: Approxinlately 40%--60% of
chloramphenicol in plasma is reversibly

Excretion: The principal route of
bound to albumin, and the free fraction
excretion of parent drug (minor) and
readily diffuses into almost all tissues
glucuronide is renal. Free chloramphenicol

(including the brain); highest concentraand the chloran1phenicol sodium succinate tions are reached in the kidneys, liver, and
dosage form undergo glomcrular filtration
bile. Substantial concentrations ( --500!., of

(5%--10%), whereas the glucuronide
plasma values) are also reached in many
metabolite is eliminated by tubular
body fluids such as the CSF and aqueous
secretion (900/o--95%). Only 5o/o--15% of
humor. Milk concentrations are --500,,(, those
chloran1phenicol is present in the urine in
of plasma but may be higher in mastitis.

the active, unchanged form. The biliary

Transplacental diffusion is seen in all
route also plays a part in excretion, but
species, with concentrations of --75% being
enterohepatic cycling is often pronounced,
reached in the fetus as compared with the
and usually only a small an10unt of
dam. Chloramphenicol does not attain
chloran1phenicol is recoverable in feces.

effective concentrations in normal synovial

Enterohepatic cycling prolongs blood
fluid but does so in septic arthritis. The
concentrations to some degree in herbiblood-prostate barrier is an exception to the vores.

extensive intracorporeal distribution of
chloran1phenicol, and concentrations in the

Pharmacokinetic Values: The plasma
inflan1ed prostate are low to nil. Approxihalf-life of chloramphenicol varies an1ong mately 15%--200!., of peak serum concentraspecies and depends on age in some tions are seen within abscesses. Florfenicol
species. The specific volumes of distlibualso penetrates most boc1y tissues, although tion usually reflect the extensive diffusion
penetration of CSF and aqueous humor is
into tissues (see TABLE 47). Dose rates and less than that of chloramphenicol.

frequencies are typically adjusted for the

Florfenicol does penetrate the milk of
species and age of the anin1al. Florfenicol
lactating cows.

is eliminated by the kidneys.

2686

ANTIBACTERIAL AGENTS

ELIMINATION AND DISTRIBUTION OF CHLORAMPHENICOL AND

FLORFENICOL

Elimination

Volume of

VetBooks.ir

Drug

Species

Half-life (hr) Distribution (mUkg)

Chloramphenicol

Cats

5.1

2,360

Dogs

4.2

1,700

Calves

5.0

1,080

(<I wk old)

Cattle

3.0

1,580

Horses

0.9

950

Florfenicol

Cattle

18.3

700

Therapeutic Indications and Dose
duration and may appear after the drug has

Rates
been discontinued. Peripheral blood
showing pancytopenia. may be associated

Chloramphenicol is used to treat both
with hypoplastic or a.plastic bone marrow.

systemic and local infections. Salmonellosis The incidence is -1:25,000-40,000. The and Bacleroides sepsis have been specific
a.plastic anemia appears to reflect la.ck of
indications, but use of chloramphenicol has
the nitro group and, as such, does not ca.use
decreased in the absence of an easily
a.plastic anemia. Because tissue residues in
accessible, commercially available,
food animals might induce a.plastic anemia
approved preparation. Florfenicol is
in people, use of chloramphenicol in food
approved for use in treatment of bovine
animals is prohibited in the USA and several
respiratory disease.

other countries. A fonn of a.plastic anemia,

General dosages for chloramphenicol and apparently a type of hypersensitivity florfenicol are listed in TABLE 48. The dose
reaction to chloramphenicol, has been
rate and frequency should be acljusted as
recognized in dogs and ca.ts.

needed for the individual animal.

GI disturbances can develop in all
nonruminant animals treated with oral

Special Clinical Concerns
chloramphenicol. Use in neonatal calves
leads to a malabsorption syndrome

Adverse Effects and Toxicity: In
associated with ultrastructural and
people, chloramphenicol (but not florfenifunctional changes of the small-intestinal col) can produce two distinctive syndromes
enterocytes. Anorexia and depression have
of bone marrow suppression. One form is
been seen in cats treated for> l wk.

characterized by nonregeneratlve anemia

Because chloramphenicol can suppress

(with or without thrombocytopenia or
ana.mnestic in1.111une responses, animals
leukopenia), increased serum iron, bone
should not be vaccinated while being
marrow hypocellularity, cytoplasmic
treated with this antibiotic. Because of the
vacuolization of blast cells and lyn1phoability of chloramphenicol to inhibit protein cytes, and maturation arrest of erythroid
synthesis, excessive topical application on
and myeloid precursors. This suppression is
wounds may delay healing.

dose-dependent and reversible. Daily doses

In both male and female rats, chloramof 50 mg/kg for 3 wk can produce similar phenicol has adversely affected the
effects in cats. Milder hematologic effects
structure and functions of the gonads. In
are evident in dogs at much higher daily doslarge animals, adverse signs a.re most often ages (225 mg/kg). Such blood dyscrasias
associated with propylene glycol-based
may also be seen in susceptible neonatal
preparations that, when infused rapidly IV,
animals given standard adult doses of
may result in collapse, hemolysis, and
chloramphenicol. This toxic effect is
death.

postulated to be due to interference with

N otwithsta.nding the severity of the
mRNA and protein synthesis in rapidly
chloran1phenicol-associated adverse effects
multiplying cells.

noted above, chlora.mphenicol is relatively

The second fom1 of bone marrow
safe, provided overdosage is a.voided,
suppression is an irreversible aplastic
courses of therapy are limited to 1 wk, the
anemia that is not related to dose or
dose is reduced for newborn anin1als and

ANTIBACTERIALAGENTS

2687
l&H•IH DOSAGES OF CHLORAMPHENICOL AND FLORFENICOL

Drug

Species

Dosage, Route, and Frequency

Chloramphenicol

Cats

45-60 mg/kg, PO, IV, or IM, bid

VetBooks.ir

Dogs

45-60 mg/kg, PO, IV, or IM, tid-qid

Horses

50 mg/kg, PO, tid-qid, or IV, every 2-4 hr

Florfenicol

Cattle

20 mg/kg, IM, repeated in 48 hr
for animals with impaired liver function,

MACROLIDES
and there is no evidence of a preexisting
bone marrow depression.

The macrolide antibiotics typically have a
large lactone ring in their structure and are

Interactions: Chloramphenicol is a
much more effective against gram-positive
potent noncompetitive microsomal enzyme
than gran1-negative bacteria. They are also
inhibitor that can substantially prolong the
active against mycoplasmas and some
duration of action of several drugs
rickettsiae. (See also POLYENE MACROLIDE
administered concurrently. Frank toxic

ANTIBIOTICS, p 2698.)

effects are likely if administration is
repeated. Examples of such drugs include

Classes
pentobarbital, codeine, phenobarbital,
phenytoin, NSAIDs, and coumarins.

Macrolides fall into three classes, depend

In combination with sulfan1ethoxypyriing on the size of the macrocyclic lactone dazine, chloramphenicol can cause hepatic
ring. None of the 12-membered 1i.ng group is
dan1age. Chloramphenicol also delays the
used clinically. Erythromycin and the
response of anemia to iron, folic acid, and
closely related oleandomycin and troleanvitanlin B
domycin belong to the 1 4-membered 1i.ng

12• It interferes witl1 the actions
of many bactericidal drngs, such as the
group. Azithromycin (synthesized from
penicillins, cephalosporins, and anlinoglycoerytllfomycin) and garnithromycin are sides, and such combinations should not be

15-ring members, a subclass referred to as
used under most circumstances. Aqueous
azalides. Of tl1e 16-membered ring group,
solutions of chloran1phenicol sodiun1
spiran1ycin,josamycin, tylosin, and
succinate should not be mixed with other
tilmicosin (synthesized from tylosin), are
preparations before administration because
used clinically. Tulathromycin contains
of a high incidence of incompatibility.

three anline rings and is classified as a

Chloramphenicol should not be
trianlilide. Ketolides, which include tylosin
administered concurrently with other
and spiramycin, are closely related
antibacterial agents that bind to the 508
macrolides.

ribosomal subunit ( eg, the macrolides and
lincosarnides).

General Properties

A macrolide is actually a complex mixture of

Effects on Laboratory Tests: Chloramclosely related antibiotics that differ from one phenicol may cause increased alkaline
another with respect to the chemical substituphosphatase concentrations and prothromtions on the various carbon atoms in the bin times. WBC and tlu·ombocyte counts
structure and in the anlinosugars and neutral
may be decreased. Anemia becomes evident sugars. For example, erytilfomycin is mostly in extreme cases. A false glucosuria test is
e1ytilfomycin A, but B, C, D, and E forms may
possible.

also be included in the preparation.

The macrolide antibiotics are colorless,

Drug Withdrawal and Milk Discard
crystalline substances. They contain a

Times: The use of chloramphenicol in
dimethylanlino group, which makes tl1em
food aninlals is prohibited in several
basic. Although they are poorly water soluble,
countJ.ies including the USA; in others,
they do dissolve in more polar organic
withdrawal times vary considerably and
solvents. Macrolides are often inactivated
may be as long as 2 wk. Withdrawal time for
in basic (pH > 10) as well as acidic environflorfenicol is 28 days. Florfenicol should not ments (pH <4 for erytilfomycin). The multiple
be used in daily cattle �20 mo old, veal
functional groups make it possible for them
calves, calves <l mo old, or calves on an
to undergo a large number of chemical
all-milk diet.

reactions. More stable ester forms, eg,

2688

ANTIBACTERIALAGENTS
acetylates, estolates, lactobionate, succinates, spectra are charactetized as broader and propionates, and stearates, are commonly
include Mannheimia haemolytica and
used in pharmaceutical preparations.

Pasteurella multocida, as well as the
above-mentioned gram-negative bacteria.

Antimicrobial Activity

Helicobacter also is generally included in VetBooks.ir

Mode of Action: The antimicrobial
the spectrun1. Azitluomycin, derived from
mechanism seems to be the same for all of
erytluomycin, includes Bordetella in its
the macrolides. They interfere with protein
spectnun. Bacteroidesfragilis strains are
synthesis by reversibly binding to the 50S
moderately susceptible to macrolides.

subunit of the ribosome. They appear to

Macrolides are active against atypical
bind at the donor site, thus preventing the
mycobacteria, Mycobacterium, Myco
translocation necessary to keep the peptide
plasma, Chlamydia, andRickettsia spp
chain growing. The effect is essentially
but not against protozoa or fungi. In vitro
confined to rapidly dividing bacteria and
sy.nergism is seen witl1 cefamandole
mycoplasmas. Macrolides are regarded

(againstBJragilis), ampicillin (against
as being bacteriostatic but demonstrate

Nocardia asteroides), and tifampin
bactericidal activity at high concentrations.

(againstRhodococcus equi).

Macrolides are significantly more active at
higher pH ranges (7.8-8). Macrolides are

Pharmacokinetic Features
considered to be time dependent in terms

Absorption: Macrolides are readily
of antimicrobial efficacy.

absorbed from tl1e GI tract if not inactivated

The macrolides appear to have immuby gastric acid. Oral preparations are often nomodulatory effects useful to treat
enteric-coated, or stable salts or esters
respiratory infections, in particular, those

(such as stearate, lactobionate, glucohepassociated withPseudomonas aeruginosa, tate, propionate, and ethylsuccinate) are
based on efficacy at doses (concentrations)

used. Plasma concentrations peak within
considered ineffective against susceptible

1-2 hr in most cases, although absorption
bacteria.

patterns may be erratic because of tl1e
presence of food and may depend on the

Bacterial Resistance: Lack of cell wall
salt or ester used. Absorption from the
pem1eability renders most gram-negative
ruminoreticulum is usually delayed and is
organisms inherently resistant to macrounreliable. Erythromycin and tylosin may lides. There are a few exceptions, and
also be administered IV or IM. Tilmicosin,
gram-negative forms without cell walls
ganlithromycin, and tulathromycin are
a.re usually susceptible. Resistance to
administered SC, except in swine, for wllich
macrolides in gram-positive organisms
an oral tilmicosin preparation is available.

results from alterations in ribosomal

Absorption after il\iection is rapid, but pa.in
structure (target site methylation or
and swelling can develop at the injection
mutation) and loss of macrolide affinity.

sites.

Post-translational methylation results in
cross-resistance to lincosamides and

Distribution: Macrolides become widely
streptogramins. Macrolide resistance may
distributed in tissues, and concentrations are
be intrinsic or plasmid-mediated and
about the san1e as in plasma, or even higher
constitutive or inducible; it may develop
in some instances. They actually accumulate
rapidly ( erytluomycin) or slowly (tylosin)

witllin many cells, including macrophages, in
and generally results in cross-resistance
which they may be �20 times tl1e plasma
between macrolides. Efflux from cells is a
concentration. WBCs will then facilitate
second in1portant mechanism of resistance
distribution to the site of inflan1ma.tion. This
for some members of this class, as is, less
accumulation accounts in pa.it for the long
frequently, drug inactivation.

dosing interval that cha.i·a.ctetizes some
ma.crolides (eg, tilmicosin). With spiramycin,

Antimicrobial Spectra: Macrolides are
the tissue concentrations remain especially
active against most aerobic and anaerobic
high, even though plasma concentrations are
gran1-positive bacteria, although there is
rather low. Ma.crolides tend to concentrate in
considerable variation as to potency and
the spleen, liver, kidneys, and pa.iticula.rly the
activity. In general, macrolides are not
lungs. They enter pleural and ascitic fluids
active against gram-negative bacteria, but
and concentrate in the eye but do not
some strains of Pasteurella, Haemophihis,
distribute to the eye or the CSF (only 2%-13"Ai and Neisseria spp may be sensitive.

of plasma concentration unless tl1e meninges

Exceptions include tilmicosin, ganlithroare inflan1ed). They concentrate in the bile mycin, and tulathromycin, for which the
and milk Up to 75% of the dose is bound to

ANTIBACTERIALAGENTS

2689
plasma proteins, and they bind to Cl'.1-acid
often regai·ded as alternatives to penicillins
glycoproteins rather than to albumin.

for treatment of streptococcal ai1d
staphylococcal infections. General

Biotransformation: Metabolic inactivaindications include upper respiratory tract tion of the macrolides is usually extensive,
infections, bronchopneumonia, bacterial

VetBooks.ir
but the relative proportion depends on the
enteritis, metritis, pyodennatitis, urinary
route of administration and the particular
tract infections, arthritis, ai,cl others.

antibiotic. After administration PO, 800;6 of

Macro lid es ai·e inclica.tecl for treatment of
an e1ytlu·omycin dose undergoes metabolic

Rlwdococcus respiratory tract infections in inactivation, whereas tylosin appears to be
foals. Fo1mulations to treat mastitis are also
eliminated in an active form.

available ai1d often have the aclvai1tage of a
short withholding time for milk. Tilmicosin,

Excretion: Macrolide antibiotics and their
ga.mithromycin, ai,d tula.thromycin ai·e
metabolites are excreted mainly in bile
approved for use in treatment of bovine

(>60%) and often UJ1dergo enterohepatic
respiratory diseases associated with
cycling. Urinary clearance may be slow and

Mannheirnia haernolylica, Pasteurella
variable (often <10%) but may represent a
rnullocida, a.i,d Histophilus sornni. In more significant route of elimination after
swine, tilmicosin phosphate is added to feed
parenteral administration. For example, in
or water for control of swine respiratory
people, 14% of azithromycin and 200/o-4()0;6
disease.

of clarithromycin is excreted unchanged in

A selection of general dosages for some
urine. The concentration of macrolides in
macrolides is listed in TABLE 49. The dose
milk often is several times greater than in
rate and frequency should be adjusted as
plasma, especially in mastitis.

needed for the individual ai,imal.

Pharmacokinetic Values: Macrolides

Special Clinical Concerns
tend to be characterized by high oral
bioavailabiJity, but this is vaiiable ai11ong

Adverse Effects and Toxicity: Toxicity
species, drugs, ai,d salts. For exaniple, oral
ai,cl adverse effects are UJ1common for most
bioavailability for tylosin is 0.35 for the
macro I ides ( except tilmicosin ), although
tartrate salt versus 0.14 for the phosphate.

pa.in ai,cl swelling may develop at injection

For azithromycin, oral bioavailability is 39%
sites. Hypersensitivity reactions have
in foals 6-10 wk old, 59% in cats, ai,d 97% in
occasionally been seen. E1ytlu·omycin
dogs. The accwnulation of macrolides
estola.te may be hepa.totoxic ai,d ca.use
among different tissues contributes to the
cholestasis; it may also induce vomiting ai,d
large volwne of distribution (for azithromydiarrhea, particularly when high doses are cin 12 Ukg in dogs, 23 Ukg in cats, 22 Ukg in
administered. Horses are sensitive to
foals 6-10 wk old) ai,d long elimination
ma.crolide-incluced GI disturbai,ces that cai,
half-life (for azithromycin, 29 hr in clogs, 35
be serious ai,cl even fatal. In pigs, tylosin
hr m cats, ai,d 20 hr in foals). For tulathromay cause edema of the rectal mucosa mild mycin, the elimination half-life is 65 hr in _
ai,al protrusion with diarrhea, ai,d anal
calves and 69 hr in pigs 2-3 mo old. Because
e1ythema. and pruritus. After 5 mg/kg/day,
of these long half-lives, tin1e to steady state
dogs had a greater tendency to develop
may be prolonged, and a loading close may
ventricular tachycardia ai,cl fibrillation
be indicated for multiple closing. 'Jylosin,
during a.cute myocardial ischemia.

however, is ai, exception, with a volume of

Tilmicosin is characterized by cardiac
distribution approximating 1 Ukg ai,d a
toxicity (tachycai·clia ai,cl decreased
half-life of 1-2 hr. Another exception is
contractility). Pai·enteral (but not oral)

azithromycin, which has a half-life in cats
administration should be a.voided in swine
that varies ai,1ong tissues, reaching > 72 hr
ai1d extra-label use should be a.voided.

for some. Effective plasma inhibitory

Cattle have died after rv injection of
concentrations ai·e maintained for -8 hr
tilrnicosin, ai,cl hUJ11a.I1 iajwy is possible
after administration PO ai,d for -12-24 hr
after accidental exposure.

after IM injection. Dosage frequencies are
commonly 2-3 times/day, PO, or 1-2 times/

Interactions: Macrolide antibiotics
clay, pai·enteraJJy.

probably should not be used with chloran1-
phenicol or the lincosainides, because they

Therapeutic Indications and Dose
may compete for the saine 508 ribosomal
binding site, alt.hough the in vivo signifi

Rates
cance of this potential interaction is UJ1clear.

The ma.crolides ai·e used to treat both

Activity of macrolides is depressed in acidic
systemic ai,d local infections. They are
environments. Ma.crolide preparations for

2690

ANTIBACTERIAL AGENTS
itM•ikl DOSAGES OF MACROLIDES

Macrolide

Species

Dosage, Route, and Frequency

Erythromycin

Cattle

8---15 mg/kg, IM, once to twice daily

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Cats

15 mg/kg, PO, tid

Foals

25 mg/kg, IM, tid

Tylosin

Cattle

10-20 mg/kg, IM, once to twice daily

Pigs

10 mg/kg, IM, once to twice daily

7-lOmglkg, PO, tid

Cats

10 mg/kg, IM, bid

Tilmicosin

Cattle

10 mg/kg, SC, once

Tulathromycin

Cattle

2.5 mg/kg, SC, once

Swine

2.5 mg/kg, IM, once

Gamithromycin

Cattle

6 mg/kg, SC, once

Azithromycin

Dogs

5-10 mg/kg, PO, once to twice daily
parenteral administration are incompatible
macrolide-lincosantide-streptogra.ntin
with many other phannaceutical prepara

(MLS) group. However, whereas the
tions. Erythromycin and troleandomycin
individual A and B components act in a
and other ma.crolides are microsomal
bacteriostatic fashion when used as sole
enzyme inhibitors that depress CYP3A4
agents, together the affmity for the

(in people) and thus the metabolism of
ribosome is enhanced, ca.using them to be
many drugs. Macrolides also are substrates
bactericidal. Streptogra.ntins include
for and potentially potent inhibitors of
virginiamyci.n. Streptogra.ntins are used to

P-glycoprotein efflux pwnps.

treat vancomycin-resistant staphylococci
and Enterococcus faecium.

Effects on Laboratory Tests: Alkaline
phosphatase, bilirubin, bromsulphthalein

LINCOSAMIDES

(BSP®), total WBC count, eosinophil count,

AST, and ALT may increase. Cholesterol

General Properties
concentrations may decrease.

Lincosamides a.re derivatives of an an1ino

Drug Withdrawal and Milk Discard
acid and a sulfur-containing octose. They

Times: Regulatory requirements for
a.re monobasic and more stable in salt forms
withdrawal times and milk discard times

(11ydrochlorides and phosphates).

vary among countries. These should be
followed carefully to prevent food residues

Antimicrobial Activity
and consequent public health implications.

The withdrawal times listed in

Mode of Action: Lincomycin and

TABLE 50
serve only as general guidelines. Ti!rnicosin
clindamycin bind exclusively to the 508
is characterized by a 28-day withdrawal
subunit of bacterial ribosomes and suppress
time and should not be used in any species
protein synthesis. Lincosan1ides, macroother than adult cattle (but not in dairy lides, and chloran1phenicol, although not
cows >20 mo old).

structurally related, seem to act at this same
site. The lincosa.mides are bacteriostatic or
bactericidal depending on the concentra

STREPTOGRAMINS
tion. Activity is enl1anced at an alkaline pH.

Efficacy is considered time dependent.

The streptograrnin antibiotics include
two distinct groups. Group A contain a

Bacterial Resistance: Lincosarnides are

23-membered unsaturated ring with lacgenerally ineffective against facultative tone and peptide bonds, and group B are
anaerobic (but not anaerobic) gran1-negadepsipeptides (lactone-cyclized peptides).

tive bacteria. Resistance to lincosantides

These antibiotics are included in the
appears slowly, perhaps as a result of

ANTIBACTERIAL AGENTS

2691

IM=iiii·I DRUG WITHDRAWAL AND MILK DISCARD TIMES OF MACROLIDES

Withdrawal

Mille Discard

Macro Ii de

Species

Time (days)

Time (hr)

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Erythromycin

Cattle

14

36-72

Pigs

7

Tylosin

Cattle

21

96

Pigs

14

Tilmicosin

Cattle

28

0

Tulathromycin

Cattle

18

Swine

5

Gamithromycin

Cattle

63"

a EU withdrawal; withdrawal period for USA (35 days) pending; withdrawal period for Canada is 49 days.

chromosomal mutation. Plasmid-mediated
clindamycin phosphate IM; the latter
resistance has been found in strains of
reaches peak plasma concentration m

Bacleroidesfragilis. Resistance appears

1-3 hr.

to be due to plasmid or chromosomally
mediated post-transcriptional methylation

Distribution: Lincosanlicles are widely
of the 508 ribosomal subunit. Cross-resistdistributed in many fluids and tissues, ance occurs with macrolides and streptoincluding bone, but significant concentragramins. Other mechanisms include tions are not attained m the CSF even when
increased activation of an efflux pump and
the meninges are inflamed. They diffuse
destruction of the drug.

across the placenta in many species.

Approxin1ately 900A, of clindamycin is bound

Antimicrobial Spectra: Lincomycil1
to plasma protems. It also accumulates in
has a limited spectrnm against aerobic
polymorphonuclear WBCs and alveolar
pathogens but a fairly broad spectrum
macrophages such that concentrations
against anaerobes. Clindamycin is a more
exceed those of plasma 50-fold. Clindamyactive analogue with somewhat different cin is able to penetrate glycocalyx, such as
pharmacokinetic patterns. Many gran1-
that associated with dental tartar.

positive cocci, except for enterococci, and

Mycoplasma are inhibited by lincosanlides,

Biotransformation: After admmistrabut most gram-negative organisms are tion PO, -500Ai of a dose of lincomycin and
resistant. Clindamycin is less effective

800/o-900A, of a close of clindamycin are metatoward ureaplasmas. Bacteroides spp and bolically altered in the liver. Metabolites
other anaerobes are usually susceptible.

often retain activity. Liver disease impairs

Closliidium difficile strains appear to be
the biotransformation of lincosamides.

regularly resistant.

Excretion: Unchanged antibiotic and

Pharmacokinetic Features
several metabolites may be excreted in
bile and urine. In people, as little as l()OA,

Absorption: Lincomycin is incompletely
of clindan1ycin is excreted in the urine.

absorbed from the GI tract, especially if

The proportions depend on the route of
admillistered soon after feeding; plasma
administration. Concentrations remain
concentrations peak within 2-4 hr.

high in the feces for some days, and

Absorption from IM injection sites is good;
growth of sensitive microorganisms in
plasma concentrations peak in 1-2 hr.

the large intestine may be suppressed for

Approxinlately 9()0A, of an oral dose of
up to 2 wk. Milk is also an ilnportant
clindamycin is absorbed, and effective
excretory route.

plasma concent.raLions are acllieved more
rapidly than with lincomycin. Absorption is

Pharmacokinetic Values: The elilninanot significantly affected by the ingestion of tion half-life of lincosarnides is frequently
food. Clindamycin palnlitate is used PO, and >3 hr, and the apparent volume of distribu-

2692

ANTIBACTERIAL AGENTS
tion is> 1 J.lkg. They are usually adminisagents and skeletal muscle relaxants.

tered bid. In dogs, clindamycin has an

Kaolin-pectin prevents their absorption
elimination half-life of 3.9 hr and a volume
from the GI tract. They should not be
of distribution of 1.4 J.lkg.

combined with bactericidal agents or with
the macrolides.

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T herapeutic Indications and Dose

Rates

Effects on Laboratory Tests: Alkaline
phosphatase, AST, and ALT may be

The lincosamides are indicated for infections
increased.

caused by susceptible gram-positive
organisms, particularly streptococci and

Drug Withdrawal Times: In several
staphylococci, and for those caused by
countries, there is a 2-clay withdrawal time
anaerobic pathogens. Clindamycin is
for pigs.

approved for use in cats and clogs for
treatment of infected wounds, abscesses, and
dental infections. Clindan1ycin has also been
used to treat selected protozoa] diseases,
including toxoplasmosis, but usually in
combination with other antimicrobials.

A number of antinlicrobiaJ agents are used

A selection of general dosages for some
periodically for several diverse purposes.

lincosarnides is listed in TABLE 51. The close Several of these are discussed below.

rate and frequency should be adjusted as
needed for the individual animal.

POLYMYXINS

Special Clinical Concerns

This group of polypeptide antibiotics
includes polymyxin B and polymyxin E, or

Adverse Effects and Toxicity: No
colistin. Because of toxicity, these drugs are
serious organ toxicity has been repottecl,
most commonly used topically, or PO for
but GI distw·bances do occw·. Clinclamycintreatment of intestinal infections. Colistiinducecl pseudomembranous enterocolitis methate is a form of colistin intended for

( caused by toxigenic Clostridium dif[u;ile)

parenteral admi.Ilistration. Polymyxins are
or disruption of GI flora is a se1ious adverse
bactericidal; they interact strongly with
reaction in a nwnber of species and can be
phospholipids in bacterial cell membranes
lethal; thus, clindan1ycin is contraindicated
and radically dismpt their pem1eability and
for use in some in horses, guinea pigs,
function. The polymyxins are more effective
han1sters, rabbits, chinchillas, and
against gram-negative than gram-positive
mrninants. Lincosamicles are contraindibacteria. Their rather narrow spectt·w11
cated in horses, because severe and even
includes Enterobacter, Klebsiella,
fatal colitis may develop. Skeletal muscle

Salmonella, Pa.steurnlla, Bo'!'detella,
paralysis may be seen at high concentra

Shigella, Pseudomonas spp, and Esche1i
tions. Hypersensitivity reactions occasion
chia coli. Most Proteus or Neisserla spp ally are seen. Lincosanlides shouldJ'lot be
are not susceptible. Although intrinsic
used in neonates because of their limited
bacterial resistance to polymyxins is
ability to metabolize clmgs.

recognized, resistance is w1comrnon and is
chromosome-dependent only. Polymyxins

Interactions: Lincosanlicles have additive
act synergistically when combined with
new·omuscular effects with anesthetic
potentiated sulfonamides, tetracyclines,

IM=i!iii DOSAGES OF LINCOSAMIDES

Lincosamide

Species

Dosage, Route, and Frequency

Lincomycin

Cattle

10 mg/kg, IM, bid

Pigs

10 mg/kg, IM, bid

7 mg/kg, in-feed

Dogs

20 mg/kg/day, PO

Cats

10 mg/kg, IM, bid

25 mg/kg, PO, bid

Clindamycin

Dogs, cats

5--10 mg/kg, PO, bid

ANTIBACTERIALAGENTS

2693
and some other antibacterials; they also
cally because of their pronounced
reduce the activity of endotoxins in body
nephrotoxicity. However, they are used
fluids and may be beneficial in endotoxlocally in wound powders and ointments, cmia. Their action is inhibited by divalent
dermatologic preparations, eye and ear
cations, unsaturated fatty acids, and
ointments, and as feed additives in swine

VetBooks.ir
quaternary ammonium compounds.

and poultry rations for growtl1 promotion.

Polymyxins are not absorbed after PO or

In antibiotic-associated pseudomembratopical administration; plasma concentranous colitis caused by Clostridium difficile tions peak -2 hr after parenteral administracytotoxin, bacitracin (given PO) is tion. Blood concentrations usually are low,
considered an alternative to vancomycin.

because polymyxins bind to cell mem

Hypersensitivity reactions to bacitracins are
branes as well as tissue debris and purulent
seen occasionally.

exudates. The polymixins undergo renal
elimination mostly as degradation products, GLYCOPEPTIDES
and their plasma half-lives are 3-6 hr. They
are notably nephrotoxic and neurotoxic

Vancomycin is a complex glycopeptide that
and, as such, systemic tl1erapy at antimicrobinds to precursors of the peptidoglycan bial doses should be avoided. Neuromusculayer in bacterial cell walls. This effect lar blockade can be seen at higher
prevents cell wall synthesis and produces a
concentrations. Intense pain at sites of
rapid bactericidal effect in dividing bacteria.

irtjection and hypersensitivity reactions also Its efficacy is time dependent. Vancomycin can be expected. Polymyxin B is a potent
is active against most gram-positive bacte1ia
histan1ine releaser. The main indication for
but is not effective against gram-negative
parenteral use of polymyxins is life-threatcells because of their large size and poor ening infection due to gram-negative bacilli
penetrability. Resistance to vancomycin
or Pseudomonas spp that are resistant to
does not readily develop. The drug is widely
other drugs. Polymyxins are also used PO
clistributecl in the body. Excretion (in active
against susceptible intestinal infections.

form) is via the kidneys; in renal insuffi

Anti-endotoxin binding activity is an
ciency, striking accumulations may develop.

additional therapy via slow IV bolus. Topical The plasma half-life in dogs is 2-3 hr. The application is common, eg, for otitis
only indication for use of parenteral
extern a.

vancomycin is serious infection clue to

Recommended dose rates for polymyxins
methicilli.n-resistantStaphylococcus
vary considerably. A general guideline is
aure1£S. Although poorly absorbed, oral

20,000 U/kg, PO, bid; 5,000 U/kg, IM, bid;
vancomycin is used to treat antibiotic-asso50,000-100,000 U by intramanm1ary ciated enterocolitis, especially if caused by
infusion; 100,000 U intrauterine in cattle. IV

Clostridium difficile. Febrile reactions and administration of polymyxins is potentially
thrombophlebitis (because of tissue
dangerous.

irritation) at injection sites may be seen.

Hypersensitivity reactions are seen

BACITRACINS
infrequently. Ototoxicity and nephrotoxicity
were fairly common in the past but are rare

Bacitracins are branched, cyclic, decapeptoday because of fewer impurities in the tide antibiotics. Bacitracin A is the most
final form.

active of the group and the main component of the commercial bacitracin FOSFOMYCIN
preparations used either topically or PO.

These antibiotics are bactericidal. They

Fosfomycin, a phosphonic acid iliat
interfere with cell membrane function,
contains a carbon-phosphorus bond, is a
suppress cell wall formation by preventing
natural antibiotic produced by Streptomy
the fom1ation of peptidoglycan strands, and
cesfmdiae. It is a phosphoenolpyruvate
inhibit protein synthesis. Bactericidal
analogue that irreversibly inhibits
activity requires the presence of divalent
phosphoenolpyruvate transferase, an
cations, such as zinc.

enzyme that catalyzes the first step of

The spectrum of bacitracins is described
pepticloglycan synthesis of microbial cell
as broad, but it is used primarily to treat
walls. Its in vitro spectrum is broad, with
gram-positive infections. Resistance is rare.

potential efficacy toward isolates express

Bacitracins are often used in combination
ing multidrug resistance, including
with neomycin and polyn1yxins to enhance

E1;cherichia coli and methicillin-resista.nt the antibacterial spectrun1.

staphylococci. As a cell wall inhibitor,

Bacitracins are not appreciably absorbed
fosfomycin is bacte1icidal when present at
from the GI tract and are not used systemi-
the site of infection at therapeutic

2694

ANTll:lACTERIALAGENTS
concentrations. Cell wall inhibition is time

The subsequent disruption of cell memdependent, but fosfomycin also exhibits a brane permeability results in antibacterial
concentration-dependent effect. Resistance
effects. Monensin is an ionophore antibiotic
to fosfomycin is unconm10n and reflects the
derived from Streptornyces that forms

FosX or FosA enzyme, which hydrolyzes the complexes with monovalent cations, VetBooks.ir
drug. The gene for this protein is chromoincluding sodiwn and potassiwn. The somally mediated. When resistance occurs,
complexes are transported in a nonpolar
it generally is not associated with multimanner across the bacterial cell membrane.

drug resistance. Studies in people have

As such, it acts as an Na+fH+ antiporter.

demonstrated that fosfomycin distributes

Monensin blocks intracellular protein
well to soft tissues, reaching tl1erapeutic
transpo1t, resulting in antibacterial and
breakpoints. Adverse effects of fosfomycin
antin1alarial effects. Monensin is used
appear to be limited to diarrhea. Approved
extensively in the beef and dairy industries
for human use in the USA as the tromethin feed to prevent coccidiosis and improve an1ine salt, its indication is as a one time ( or
feed efficiency. Monensin also increases the
up to 3 days) treatment of uncomplicated
production of propionic acid and thus
urinary tract infections in people. Fosfomyprevents bloat.

cin has been added to the World Health

Organization's list of critically important

RIFAMYCINS
drugs. Accordingly, its use should be
reserved, along with other critically

Several semisynthetic derivatives ( rifan1yimportant drugs, to situations in which cin SV, 1ifampin [1ifampicin], tifamide) of
lower-tier drugs are no longer appropriate.

natural rifamycins have been used as
extended-spectr1m1 antibiotics. Rifamycins

NOVOBIOCIN SODIUM
interfere with the synthesis of RNA in
microorganisms by binding to subw1its of

Novobiocin is a narrow-spectrwn antibiotic
sensitive DNA-dependent RNA polymerase.

that may be bacteriostatic or bactericidal at

They are active against gram-positive
higher concentrations. It is active mostly
organisms, some mycobacteria, a few
against gran1-positive bacteria but also
strains of gran1-negative bacteria ( mostly
against a few gram-negative bacteria. There
cocci; bacilli are more resistant), some
is a synergistic effect with tetracyclines.

anaerobes, and chlamydiae. At high

Many species of bacteria can develop
concentrations, they are also active against
resistance to novobiocin. Adverse reactions
several viruses. Ftmgal and yeast infections
are quite frequent after administration. Its
resistant to rifampin alone often respond
main use is in combination with other
when a rifamycin is added to an antifungal
agents for treatment of bovine.mastitis.

agent ( eg, amphotericin B). Resistance to
rifan1ycins may develop rapidly as a 1-step

TIAMULIN FUMARATE
process. For this reason, they should be
administered in combination with other

Tiamulin hydrogen fumarate is a sernisynantimicrobials, such as penicillins, thetic derivative of pleuromutilin. Tiamulin
erythromycin, miconazole, and an1phois active against gram-positive bacteria, tericin B.

mycoplasmas, and anaerobes, including

The primary use of the rifamycins in

Brachyspira hyodysentmiae. It is also
people has been to treat tubercul9sis.

clinically effective in treatment of swine

Rifan1pin has been used in foals to control
dysentery and mycoplasmal arthritis.

Rhodococcus equi pneun1onia. Because

Tiamulin is well absorbed when adminis1ifamycins penetrate tissues and cells to a tered PO. The dosage is 8.8 mg/kg/day
substantial degree, they are particularly
for 3-5 days, in either food or water. The
effective against intracellular organisms.

parenteral dosage for mycoplasmal

Rifampin is readily but incompletely ( -40%)

pneumonia in pigs is 15 mg/kg. 1n poultry,
absorbed from the GI tract, and plasma
tiamulin interferes with monensin and
concentrations peak within 2-4 hr.

salinomycin metabolism, and if the drugs

Concun-ent feeding may reduce or delay
are fed together, they become toxic.

absorption. Rifan1pin may also be adminis

Generally, however, tianutlin has few
tered IM or IV. Approximately 75'Yer-80% of
adverse effects.

rifampin is bound to plasma proteins. It is
widely distributed in body tissues and fluids

IONOPHORES
because of its high lipid solubility. Rifampin
is biotransformed to several metabolites,

Ionophores are lipid-soluble molecules that
some of which are active, and is primarily
transport ions across lipid cell membranes.

excreted in bile ( used for cholangitis in

ANTIBACTERIAL AGENTS

2695
people) and to a lesser degree in urine.

signs seen with excessive doses of

Enterohepatic cycling of the parent drug
nitrofuran derivatives include CNS involveand its mam metabolite (desacetylrifampin) ment (excitement, tremors convulsions
conunonly occurs. The elimination half-life
peripheral neuritis), GI disturbances, po�r
of rifa.mpin is dose dependent: in horses it
weight gam, and depression of spennato

VetBooks.ir
is -6 hr; in dogs, -8 hr. The plasma half-life
genesis. Various hypersensitivity reactions
progressively sho1tens by -400A, during the
can also be seen. Some nitrofurans are
first 2 wk of treatment because of the
carcinogenic, and their future use is in
induction of hepatic microsomal enzymes;
doubt.

conversely, it is increased with hepatic

Nitrofurans are among the drugs for
dysfunction.

which extra-label use is prohibited in food

Rifan1pin is usually well tolerated and
animals in the USA.

produces few adverse effects. GI disturbances and abnormalities in liver function Nitrofurantoin

(icterus) have been reported in people.

Hypersensitivity reactions can also result

The mechanism of action of nitrofur-
from 1ifampin administration, and renal
antoin is unique. It is reduced by bacte1ial
failure is a possible consequence when
flavoproteirlS to reactive intennediates
intennittent dosage schedules are followed.

that inhibit bacterial ribosomes and other

Partial, reversible imrnunosuppression of
macromolecules. Protein synthesis
lymphocytes develops. Urine, feces, saliva,
aerobic energy metabolism, DNA �d
sputum, sweat, and tears are often colored

RNA synthesis, and cell wall synthesis are
red-orange by rifampin and its metabolites.

inhibited. Nitrofurantoin is bactericidal in

CNS depression after IV administration and
urine at therapeutic doses. Resistance is
temporary inappetence are seen in horses.

rare. Nitrofurantoin is used to treat urinary

The dose range for rifampin in horses is
tract infections caused by susceptible bacte10-25 mg/kg/day, PO or parenterally.

ria, such as Esche'lichia coli, Staphylococcus aureus, Streptococcus pyogenes, and Aerobacter aerogenes. Pro/,eus spp,

NITROFURANS

Pseudomonas aeruginosa, and Streptococ

Nitrofurans are synthetic chemotherapeutic cus faecalis are usually resistant. After agents with a broad antimicrobial spectrun1· administration PO, nitrofurantoin is rapidly they are active against both gram-positive
and completely absorbed (the macrocrystal
and gran1-negative bacteria, including
fonn takes longer) and is swiftly elinlinated

Salmonella and Giardia spp, trichomoby the kidneys, mainly by tubular secretion nads, amebae, and some coccidial species.

( -400A, in the unchanged form). Sen1111

However, when compared with other
concentrations are low, and little unbow1d
antimicrobial chemotherapeutic agents,
drug is available for diffusion into the tissues.

their potency is not of particular note. The

The plasma half-life is only -2 0 min. Nitronitrofurans appear to inhibit a number of furantoin is concentrated in acid urine.

microbial enzyn1e systems, including those

When the pH reaches -5, the drug becomes
uwolved m carbohydrate metabolism, and
supersaturated without precipitation,
they also block the initiation of translation.

and its antibacterial action is maximal.

However, their basic mechanism of action

Nitrofurantoin can be administered PO or
has no� yet been clarified. Their primary
parenterally. The dosage for dogs and cats
action IS bacteriostatic, but at high doses

1s4.4 mg/kg, PO, tid for4-10 days. Adverse
they are also bactericidal. They are much
effects are not common at usual dosages,
more
but nausea, vomiting, and diairhea can

_active in acidic environments (pH 5.5

1s optimal for nitrofurantoin activity).

develop. CNS disorders have been seen

Resistant mutants are rare, and clinical
and polyneuropathy is a serious effect
resistance emerges slowly. Among
seen in people. Animals with decreased
themselves, nitrofurans show complete
renal function have a predisposition for
cross-resistance, but there is no crosspolyneuritis. Various manifestations of resistance with any other antibacterial
hypersensitivity reactions can be seen.

agents.

Yellow discoloration of teeth occasionally

Because of very slight water solubility,
has been reported in very young aninlals.

the rutrofurans are used either PO or
topically. No nitrofuran is effective

Nitrofurazone
systemically. They are either not absorbed

Nitrofurazone is only slightly soluble in
at_all from the GI tract or are so rapidly
water but, in general, corresponds to nitroelimmated that they reach inhibitory furantoin in tem1s of its mechanism of
concentrations only in the urine. Toxic
action, antimicrobial spectrun1, potency,

2696

ANTIBACTERIALAGENTS
and physicochemical characteristics. Its
active against obligate anaerobic bacteria. It
main indications include the treatment
is not active against facultative anaerobes,
of bovine mastitis, bovine metritis, and
obligate aerobes, or microaerophilic
wounds. However, pus, blood, and milk
bacteria other than Campylobacter fetus.

reduce the antibacterial activity. Nitrofura

At concentrations readily attained in serun1

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zone is also used as a feed additive (0.05%)

after PO or parenteral administration,
to control intestinal bacterial and coccidial
metronidazole is active againstBacteroides
infections. The withdrawal time for
fragilis, B melaninogenicus, F'usobacte
nitrofurazone in pigs is 5 days.

iium spp, and Clostridium pei.fringens
and other Clostridium spp. It is generally

Furazolidone
less active against nonsporefomling,

This is a nitrofuran with a wide range
gram-positive bacilli such as Actinomyces,
of antimicrobial activity that includes

Propioniba.cterium, Bifidobacterium, and

Clostri.dimn, Salmonella, Shigella, Staphy

Eubacterium spp. Metronidazole is also
lococcus and Streptococcus spp, and E coli.

somewhat less active against gram-positive

It is also active against Eimeria and
cocci such asPeptostreptococcus and

Histomonas spp. It is usually administered

Peptococcus spp, but the less sensitive

PO to treat intestinal infections but may also strains are usually not obligate anaerobes.

be applied topically. The usual oral dose of

Metronidazole is bactericidal at
furazolidone in calves is 10-12 mg/kg, bid
concentrations equal to or slightly higher
for 5--7 days. Caution should be exercised
than the minimal inhibitory concentration.

when treating small calves ( eg, Jersey

The precise mode of action is unclear, but
breed) to avoid excessive dose rates, lest
reduction in an anaerobic environment
neurotoxicity result; signs include head
yields a compound that then binds to DNA,
tremors, ataxia, visual impairment, and
causing loss of the helical structure, strand
convulsions.

breakage, and impairment of DNA function.

Only susceptible organisms (bacte1ia and
protozoa) appear to be capable of metabo

Miscellaneous Nitrofurans
lizing tl1e drug.

Nifuraldezone, like furazolidone, is used

The pharrnacokinetic pattern of
to control bacterial enteritis in calves.

metronidazole generally follows that

Nifurprazine is used only topically as an
expected of a highly lipid-soluble basic
antibacterial agent. Furaltadone is used
drug. It is readily but vaiiably absorbed
both PO to prevent intestinal infections
from the GI tract (bioavailability 60%-100%),
and directly into the teat to treat mastitis.

with seflil1l concentrations peaking within

1-2 hr, and becomes widely distributed in all

NITROIMIDAZOLES
tissues. Metronidazole penetrates the bloodbrain barrier and also attains therapeutic The 5-nitroirnidazoles are a group of drugs
concentrations in abscesses and in
that have both antiprotozoal and antibacteempyema fluid. It is only slightly bound to rial activity. Nitroimidazoles with activity
plasma proteins. Biotransfom1ation is quite
against trichomonads and arriebae include
extensive, and parent drug and metabolites
metronidazole, tinidazole, nin1orazole,
are excreted by both the renal and biliary
flunidazole, and ronidazole. Metronidazole
routes. The elimination half-life in dogs is
and nimorazole are effective in treatment

-4.5 hr, and in horses, 1.5-;3.3 hr.

of giardiasis, whereas din1etridazole,

The principal clinical indications for
ipronidazole, and ronidazole control
metronidazole include the treatment of
histomoniasis in poultry. Several nitroimidaspecific protozoa] infections ( amebiasis, zoles have activity against trypanosomes.

trichomoniasis, giardiasis, and balantidia

Metronidazole, ronidazole, and other
sis) and anaerobic bacterial infections such
nitroin1idazoles are active against anaerobic as those that may be seen in abdominal bacteria. Metronidazole is the compound
abscesses, peritonitis, empyema, genital
that has been the most studied and is
tract infections, periodontitis, otitis media,
discussed as the prototype of the group.

osteitis, arthritis, and meningitis, and in

Extra-label use of nitroimidazoles is
necrotic tissue. Metronidazole has been
prohibited in food anin1als in the USA.

successfully used to prevent infection after
colonic surgery. Nitroimidazoles also act as

Metronidazole
radiosensitizers, and metronidazole has
been used as an acljunct to the radiotherapy

Metronidazole has been used for many
of solid tun1ors.

years in therapeutic management of tricho

Adverse effects are not commonly
moniasis, giardiasis, and amebiasis. It is
associated with metronidazole. High doses

ANTIFUNGALAGENTS

2697
may induce signs of neurotoxicity in dogs,

HYDROXYQUINOLINES
such as tremors, muscle spasms, ataxia, and
even convulsions. Reversible bone marrow

The 8-hydroxyquinolines are a group
depression has been repo1ted. The drug
of synthetic compounds with antibacterial,
should not be used in pregnant animals,
antifungal, and antiprotozoal activity.

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particularly during the first trimester,

The best-known compounds of this class
although the evidence for carcinogenicity
are iodochlorhydroxyquin ( clioquinol),
and mutagenicity is still tenuous. Metronidiiodohydroxyquin (iodoqu.i.nol), broxyquinodazole may produce a reddish brown line, and hydroxyquinoline. Because they are
discoloration of the urine due to unidentinot absorbed from the GI tract to any degree, fied pigments.

their main use has been to treat intestinal

Recommended dose rates for metroniinfections caused by bacteria or protozoa dazole in dogs are 44 mg/kg, PO, followed

(such as Giardia). Hydroxyquinolines are
by 22 mg/kg, qid, for anaerobic infections;
also used topically for skin infections caused

25 mg/kg, PO, bid, for giardiasis; and
by bacteria and fungi. Hydroxyquinolines are

66 mg/kg/day, PO, for trichomoniasis.

potentially neurotoxic when used for

Courses of therapy are generally 5-7 days. prolonged periods. The dose for a 455-kg Both PO and IV preparations are
horse is 10 g/day, PO, using a decreasing
available.

dosage regimen to discontinue medication.

ANTIFUNGAL AGENTS

Pathogenic fungi affecting animals are
and potential resistance to some drugs.

eukaryotes, generally existing as either

Cryptococcus and occasionally Sporothrix filamentous molds (hyphal forms) or
schenckii produce an external coating or
intracellular yeasts. Fungal organisms
slime layer that encapsulates the cells and
are characterized by a low invasiveness and
causes them to adhere and clump together.

virulence. Factors that contribute to fungal

Finally, regarding drug access, most
infection include necrotic tissue, a moist
infections are located inside host cells, the
environment, and irnmunosuppression.

lipid membrane of which can present a

Fungal infections can be primarily
final barrier.

superficial and irritating ( eg, dermatophyto

Discontinuing therapy after clinical
sis) or systemic and life threatening ( eg,
signs have resolved but before infection is
blastomycosis, cryptococcosis, histoplasmoeradicated also leads to therapeutic failure.

sis, coccidioidomycosis ). See also DERMATO

Therapy should extend well beyond clinical

PHYTos,s, p 872, and FUNGAL INPECTIONS, p 632.

cure. Once drugs reach the site of action,

Clinically relevant dimorphic fungi grow as
therapeutic success is impeded by the
yeast-like forms in a host but as molds in
nature of fungal infections. Fungal growth is
vitro at room temperature; they include
slow, yet most anti.fungal drugs work better

Candida spp, Blastomyces dermatitidis,
in rapidly growing organisms. Likewise,

Coccidioides immitis, Histoplasma
most anti.fungal agents are fimgistatic in
capsulatum, Sporothrix schenckii, and
action, with clearance of infection largely

Rhinosp01idium.

dependent on host response. As such, the

Several factors can lead to therapeutic
duration of therapy is long, and the "get in
failure or relapse after antifungal therapy.

quick, hit hard, and get out quick" recom

Drug access to fungal targets is often commendation for antibacterial therapy is not promised. Host inflan1matory response
appropriate for anti.fungal therapy; care
may be the first barrier, followed by
must be taken to not discontinue therapy
location in sanctuaries (brain, eye, etc) as a too early. However, longer duration of second barrier for some infections, and the
therapy contributes to another conunon
organisms themselves as a third barrier.

cause of therapeutic failure: host toxicity.

The fungal cell wall is rigid and contains

Because both the anti.fungal target organism
chitin, which along with polysaccharides,
and the host cells are eukaryotic, the
acts as a barrier to drug penetration. The
cellular targets of fungal organisms are
cell membrane contains sterols such as
often similar to the host structures. Therefore,
ergosterol, which inffuences the efficacy
as a class, antifungal drugs tend to be more

2698

ANTI FUNGAL AGENTS
toxic than antibacterial drugs, and the

Antifungal Activity
number of antifungal drugs approved for
use are markedly fewer than the number of

Mode of Action: The polyenes bind to
antibacterial drugs. Drugs that can be used
sterol components in the phospholipidlocally (including topically) or charactersterol membranes of fungal cells to form VetBooks.ir
ized by distribution to sites of infection (eg,
complexes that induce physical changes in
liposomal products) may decrease this risk.

the membrane. The number of conjugated

The slow growth that characterizes fungal
bonds and the molecular size of a particular
infections means that acquired resistance
polyene macrolide influence its affinity for
occurs less commonly than in bacterial
different sterols in fungal cell membranes.

infections. Therapeutic failure may also

Amphotericin B has a greater affinity for
reflect the inability of the immunocomprofungal ergosterol, the major sterol in fungal mised host to overcome residual fungal
membranes, than for eukaryotic (host) cell
populations inhibited by the drug; those
membrane cholesterol. The long polyene
antifungals that are also (positive)

structure causes the formation of channels
immunomodulators may be more effective.

in the fungal cell membrane. The resultant

A nwnber of serious systemic fungal
loss of membrane permeability results in
diseases are well recognized in several parts
the loss of critically important molecules.

of the world (seep 632). Antifungal agents

Potassiw11 ion efflux from the fungal cell
have greatly reduced previously recorded
and hydrogen ion influx cause internal acidihuman mortality rates due to systemic fication and a halt in enzymatic functions.

mycoses. A relatively na1Tow selection of

Sugars and amino acids also eventually leak
dtugs is used in these cases.

from an arrested cell. Fungistatic effects are
most often evident at usual polyene

POLYENE MACROLIDE
concentrations. High drug concentrations

ANTIBIOTICS
and pH values between 6.0 and 7.3 in the
surrounding medium may lead to ftmgicidal

Arnphotericin B is the model polyene
rather than fungistatic action.

macrolide antibiotic and is the sole member

In addition to these direct effects on
of this class used systemically. Polyene
susceptible yeasts and fungi, evidence
anti.fungal antibiotics are large molecules,
suggests that amphotericin B may also act
consisting of a long polyene, lipid-soluble
as an i.m.mtmopotentiator (both humoral
component and a markedly hydrophilic
and cell mediated), thus enhancing the
component. Amphotericin B acts as both a
host's ability to overcome mycotic
weak base and a weak acid, and as such is
infections.

amphoteric. The polyene macrolides have
been isolated from various strain� of

Fungal Resistance: Polyene macrolides
bacteria; amphotericin B is an antibiotic
are inherently resistant to dermatophytes.

product of Stre'J)tomyces nodosus.

Acquired resistance to the polyene

Amphotericin B, nystatin, and pimaricin
antifungal macrolides is rare both clinically

(natan1ycin) are the only polyene macrolide
and in vitro. Pythium, a pseudofungus, is
antibiotics used in veterinary medicine."The
less susceptible, because it contains limited
polyenes are poorly soluble in water and
ergosterol in its cell membranes. Resistance
the common organic solvents. They are
has been documented for Candida spp,
reasonably soluble in highly polar solvents
which are among the more rapidly growing
such as dimethylformamide and dimethyl
fungal organisms. In general, resistance
sulfoxide. In combination with bile salts,
develops slowly and does not reach high
such as sodium deoxycholate, amphotericin
levels, even after prolonged treatment.

B is readily soluble (micellar suspension) in

5% glucose. This colloidal preparation has

Antifungal Spectra: The polyene antibiotbeen used for IV in.fusion. The polyenes ics have broad antifungal activity against
are unstable in aqueous, acidic, or alkaline
organisms ranging from yeasts to filamenmedia but in the dry state, in the absence tous fungi and from saprophytic to
of heat and light, they remain stable for
pathogenic fungi, but tl1ere are great
indefinite periods. They should be adminisdifferences between the susceptibilities of tered parenterally ( diluted in 5% dextrose) as ilie various species and strains of fungi. They freshly prepared aqueous suspensions. Lack
are ineffective against dern1atophytes. In
of stability indicates that labeled expiration
vitro susceptibilities (both resistant and
dates should be adhered to once the product
highly susceptible) do not always correlate
is diluted. Amphotericin B is also prepared
well with the clinical response, which
as liposomal and lipid-based preparations,
suggests that host factors may also play a
enhancing its safety without loss of efficacy.

role. Many algae and some protozoa

ANTIFUNGALAGENTS

2699

(Leishmania, 1'1ypanosoma, Trichomonas,

Approximately 5% of a total daily dose of
and Ent,amoeba spp) are sensitive to the
an1photericin B is excreted unchanged in
polyenes, but these compounds have no
the urine. Over a 2-wk period, -200,1, of the
significant activity against bacteria,
drug may be recovered in the urine. The
actinomycetes, virnses, or animal cells.

hepatobiliary system accounts for 200/o-300,1,

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Amphotericin Bis effective against yeasts
of excretion. The fate of the remainder of

( eg, Candid.a spp, Rhodotorula spp, an1photericin B is unknown.

C?yptococcus neojormans ), dimorphic fungi

( eg, Histoplasma capsulatum, Blastomyces

Pharmacokinetics: Amphotericin B has
dermatil'idis, Coccidioides immitis ),
a biphasic elimination pattern. The initial
de1matophytes ( eg, 'l'richophyton,
phase lasts 24 hr, during which levels fall

Microsporum, and Epidermophyton spp ), rapidly (700,1, for plasma and 500,1, for urine).

and molds. It also has been used successfully The second elimination phase has a 15-day to treat disseminated sporotiichosis,
half-life, during which plasma concentrapythiosis, and zygomycosis, although it may tions decline very slowly. Arnphotericin Bis
not always be effective. Nystatin is mainly
usually infused IV, every 48-72 hr, w1til the
used to treat mucocutaneous candidiasis,
total cunrnlative dosage has been reached.

but it is effective against other yeasts and

The disposition of the various lipid-comfungi. The antimicrobial activity of pimaiicin plexed ainphotericin B products is vaiiable.

is similar to that of nystatin, although it is

Because of its small size, AmBisome® is
mainly used for local treatinent of candidichai·acterized by the slowest uptake by a5is, trichomoniasis, and mycotic keratitis.

reticuloendothelial cells and thus the
highest plasma drng concentrations of

Preparations: Amphotericin Bis available ai11photericin B. However, the ainount of as an IV solution complexed to bile acids
free versus complexed ainphotericin Bis
but also as several different preparations
not cleai·. AmBisome also was able to
complexed to lipid mixtures. Because
achieve CNS concenti·ations and was
reticuloendothelial cells phagocytize the
associated with the least nephrotoxicity in
lipid component, directed delivery to the site hwnan studies. ArnBisome has been studied of fungal infection is facilitated, reducing
in Beagles. Achievable amphotericin
renal exposure. Prolonged antifungal
concentrations were much higher at
activity ( compared with nonliposomal
equivalent doses of AmBisome compared
prepai·ations) has been documented.

with other products; further, dogs were able
to well tolerate 4 mg/kg for 30 days.

Pharmacokinetic Features

Amphotericin concentrations accumulate
with multiple dosing when administered as

Absorption: The polyene macrolide

ArnBisome.

antibiotics are poorly absorbed from
the GI tract. Amphotericin Bis usually
administered IV or topically and occasion

Therapeutic Indications and Dose
ally locally, intrathecally, or intraocularly.

Rates

Nystatin and piran1ycin are mostly applied

Arnphotericin B is used principally to treat
topically. Nystatin is given PO to treat
systemic mycotic infections. Despite its
intestinal candidiasis. Absorption is
ability to cause nephrotoxicity (seep 2702),
minimal from sites of local application.

ainphotericin B remains a commonly used
antifungal agent because of its effective

Distribution: Amphotericin Bis widely
ness. Multiple approaches to delivery have
distributed in the body after IV infusion.

been described in an attempt to minin1ize

It associates with cholesterol in host cell
nephrotoxicity. In addition, dosing
membranes throughout the body and is
continues until a maximal cumulative dose
subsequently released slowly into the
is reached, with the ainount varying with
circulation. Penetration into the CSF,
the fungal organism. Nystatin is primarily
saliva, aqueous humor, vitreous humor, and indicated for treatl11ent of mucocutaneous hemodialysis solutions is generally poor.

(skin, oropharynx, vagina) or intestinal

Amphotericin B becomes highly bound to
candidiasis; pimaricin is mainly used in
plasma lipoproteins ( -95%). Complexing
therapeutic management of mycotic
ainphotericin B with various lipid-based
keratitis.

products alters the distribution.

General dosages for some polyene
macrolide antibiotics are listed in TABLE 52.

Biotransformation and Excretion:

The dose rate and frequency should be

The disposition of ainphote1icin Bis not
adjusted as needed for the individual
well described in companion ariin1als.

animal.

2700

ANTIFUNGALAGENTS
l&N•iti DOSAGES OF POLYENE MACROLIDE ANTIBIOTICS

Polyene Macrolide

Dosage, Route, and Frequency

Amphotericin B (0.1 mg/mL in 5%

0.1-1 mg/kg, given IV slowly, 3 times/wk

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dextrose)

Total dose: 4--11 mg/kg

Amphotericin B lipid complex injection 1-3 mg/kg, IV, every other day or 3 times/wk (Abelcet®)

Total dose: 12-24 mg/kg

Amphotericin B liposome

3- 4 mg/kg, IV, every other clay or 3 times/wk

(AmBisome®)

Total dose: 12-30 mg/kg

Nystatin

50,000-150,000 U, PO, tid (dogs)

Pimaricin (5% ophthalmic solution)

l drop, instilled into the eye, every 1-2 hr

Special Clinical Concerns

B. Pretreatment with antiemetic and
antihista.minic agents prevents the nausea,

Adverse Effects and Toxicity: Oral
vomiting, and hypersensitivity reactions.

administration of nystatin can lead to

Giving corticosteroids IV also limits severe
anorexia and GI disturbances. The IV
hypersensitivity reactions. Mannitol (1 g/kg,
infusion of amphotericin B can cause an

IV) with each dose of amphotericin B, and
anaphylactoid reaction due to direct mast
sodium bicai·bonate (2 mEqlkg, IV or PO,
cell degranulation. A pre-test dose is
daily) may help prevent acidification
recommended to detect this reaction, and
defects, metabolic acidosis, and azotemia;
pretreatment with H1 antihistamines and
however, clinical evidence of efficacy has
short-acting glucocorticoids may be
not been proved. Saralasin (6-12 mcg/kg/
appropriate. Th.rombophlebitis may occur
min, IV) and dopamine (7 mcg/kg/min, IV)

with perivascular leakage. The primary
infusions have prevented oliguria and
toxicity associated with amphotericin B
azotemia induced by ainphote1icin B in
is nephrotoxicity. Within 15 min of IV
dogs. Administering IV fluids or fu.rosemide
administration of amphotericin B, renal
before ainphotericin B prevents proaiterial vasoconstriction occms and lasts now1ced decreases in renal blood flow and
for 4--6 hr. This leads to diminished renal
glomerular filtration rate. Newer preparablood flow and glomerular filtration.

tions in which an1photericin B is mixed with

Because ainphotericin B binds to the
lipid or liposomal vehicles (particularly
cholesterol component in the membranes
liposomes) ai·e safer ai1d have maintained
of the distal renal tubules, a change in
efficacy.

penneability occurs in these cells, leading to
polymia, polydipsia, concentration defects,

Interactions: A.mphotericin B may be
ai1d acidification abnormalities. The net
combined with otl1er antin1icrobial agents
result is a distal renal tubulai· acidosis
with synergistic results. This often allows
syndrome. The metabolic acidosis leads to
both the total dose of ainphotericin B ai1cl
bone buffering, U1e excessive release of
the length of therapy to be decreased.

calcium into the circulation, and ultin1ately

Exainples include combinations of
neph.rocalcinosis due to calciw11 precipita5 -flucytosine and ainphotericin B for tion in the acidic environment of U1e distal
treatment of cryptococcal meningitis,
tubules. Almost eve,y animal treated with
minocycline and ainphotericin B for
an1photericin B develops some degree of
coccidioidomycosis, and irnidazole ai1cl
renal impairment, which may become
an1photericin B for several systemic
permanent depending on the total
mycotic infections. Rifainpin may also
cumulative dose.

potentiate the antifungal activity of

The ad.ministration of ainphotericin B
ainphotericin B.

can lead to a nw11ber of other adverse

Drugs that should be avoided clming
effects, including anorexia, nausea,
ai11photericin B therapy include aininoglyvomiting, hypersensitivity reactions, drug cosides (nephrotoxicity), digitalis drugs
fever, nom10cytic normochromic anemia,

(increased toxicity), curai"izing agents
cardiac arrhythmias (and even aITest),

(neuromuscular blockade), mineralocortihepatic dysfunction, CNS signs, ai1d coids (hypokalemia), thiazide diuretics
thrombophlebitis at U1e injection site.

(hypokalemia, hyponatremia), anti.neoplas

A number of acljuvant Ll1erapies ai·e used
tic drugs (cytotoxicity), and cyclosporine
to minimize adverse events of ai11photericin

(nephrotoxicity).

ANTIFUNGALAGENTS

2701

Effects on Laboratory Tests: Treatstrains of yeasts and fungi, but neither ment with polyene macrolide antibiotics
natural nor acquired resistance appears
increases plasma bilirubin, CK, AST, ALT,
to be prevalent.

BUN, eosinophil count, and urine protein,
and decreases plasma potassium and

Antimicrobial Spectra: The antifungal

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platelet count.

imidazoles also have some antibacterial
action but are rarely used for this purpose.

IMIDAZOLES

Miconazole has a wide antifungal spectrun1
against most fungi and yeasts of veterinary

Imidazoles may have antibacterial,
interest. Sensitive organisms include
antifungal, antiprotozoal, and anthehnintic

Blastomyces clerma titiclis, Paracoccicli
activity. Several distinct phenylimidazoles
oicles brasiliensis, Histoplasma capsula
are therapeutically useful antifungal agents
tum, Canclicla spp, Coccidioides immitis, with wide spectra against yeasts and

C1yptococcus neoforrnans, andAspergillus
filamentous fungi responsible for either

Jwnigatus. SomeAspergillus and
superficial or systemic infections. The

Madurella spp are only marginally
anthehnintic thiabendazole is also an
sensitive.

imidazole with antifungal properties.

Ketoconazole has an anti.fungal spectrwn

Clotrin1azole, miconazole, econazole,
similar to that of miconazole, but it is more
ketoconazole, itraconazole, and fluconazole
effective against C immitis and some otl1er are the most clinically important members
yeasts and fungi. ltraconazole and
of this group. Posaconazole and voriconafluconazole are the most active of the zole are among the newer drugs; v01iconaantifungal i.rnidazoles. Their spectrum zole is approved for use in people to treat
includes din1orphic fungal organisms and
aspergillosis.

dennatophytes. They are also effective
lrnidazoles generally are poorly soluble
against some cases of aspergillosis
in water but can be dissolved in organic

(60%-700A,) and cutaneous sporotiichosis.

solvents such as chlorofonn, propylene

Clot1·in1azole and econazole are used for
glycol, and polyet110xylated castor oil (prepasuperficial mycoses ( de1matophytosis and ration for IV use but dangerous in dogs). An
candidiasis); econazole also has been used
exception is fluconazole. lmidazoles are
for oculomycosis. Thiabendazole is effective
weak di basic agents. Alterations in
againstAspmgillus and Penicillium spp, side-chain structure determine antifungal
but its use has largely been replaced by the
activity as well as the degree of toxicity.

more effective intidazoles. Voriconazole is
approved for hmnan use in treatment of

Antifungal Activity

Aspei·gillus but is effective against many

Mode of Action: Imidazoles alter the cell
other fungal organisms.Posaconazole may
membrane permeability of susceptible
be more effective than itraconazole or
yeasts and fungi by blocking the synthesis
fluconazole but may be associated with
of ergosterol ( demethylation of Janosterol is
more adverse effects.

inhibited), the primary cell sterol of fungi.

The enzyme targeted is a fungal cytochrome

Pharmacokinetic Features

(CYP450). Other enzyn1e systems are also

Absorption and Distribution:

impaired, such as those required for fatty

The imidazoles are rapidly but sometimes
acid synthesis. Because of the drug-induced
erratically absorbed from the GI tract;
changes of oxidative and peroxidative
plasma levels peak witllin 2 hr after adminisenzyn1e activities, toxic concentrations of tration PO. Fluconazole is an exception,
hydrogen peroxide develop intracellularly.

being close to 100% bioavailable after

The overall effect is cell membrane and
administration PO. Except for fluconazole,
internal organelle disruption and cell death.

an acidic environment is required for

The cholesterol in host cells is not affected
dissolution of the in1idazoles, and a
by the in1idazoles, although some drugs
decrease in gastric acidity can reduce
impair synthesis of selected steroids and
bioavailability after administration PO. The
drug-metabolizing enzymes in the host.

rate of absorption appears to be increased

Because in1idazoles impair synthesis, a lag
when the drug is given with meals, but
tin1e to efficacy occurs. This lag ti.me may be
reports are conflicting. Because oral bioavprolonged because of the long half-life of ailability can be very poor with noncomt11ese drugs.

mercial inlidazole products, caution is
recommended with compounded products,

Fungal Resistance: Sensitivity to the
and monitoring is recommended if a
imidazoles varies greatly between various
compounded preparation is used.

2702

ANTIFUNGALAGENTS

Imidazoles appear to be widely distributed that have not responded to griseofulvin or in the body, with detectable concentrations
topical therapy, Malassezia infection in
in saliva, milk, and cerumen. CSF penetradogs, aspergillosis, and sporotrichosis in tion is poor except for fluconazole, which
animals that cannot tolerate or do not
reaches 500/1r-900A, of plasma concentrations.

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respond to sodium iodide. For serious

Most imidazoles ( except fluconazole) are
infections, combination with amphotericin
highly protein bound in the circulation

B is strongly recommended. Among the

(>95%), most to albumin. The highest
irnidazoles, tluconazole may be more likely
concentrations of i.rnidazoles are found in
to distribute into tissues that are tough to
tl1e liver, adrenal glands, lungs, and kidneys.

penetrate. Both itraconazole and tluconazole are generally preferred to other Biotransformation and Excretion:

in1idazoles for treatment of systemic fungal

Hepatic metabolism is the primary route of
infections, including aspergillosis and
elimination. Metabolism of ketoconazole
sporotrichosis. Topically applied in1idazoles
and most other in1idazoles by oxidative

(clotrirnazole, miconazole, econazole) are
pathways is extensive. Only -2%-4% of a
used for local dennatophytosis. Thiabendadose adnunistered PO appears w1changed zole is included in some otic preparations
in the urine. Itraconazole is metabolized to
for treatment of yeast infections.

an active metabolite that may contribute

Enilconazole is an in1idazole that can be
significantly to antimicrobial activity. The
applied topically for treatment of dermatobiliary route is the major excretory pathway phytosis and aspergillosis. It has been used

(>800A,); -200A, of the metabolites are
safely in cats, dogs, cattle, horses, and
eliminated in the urine. Fluconazole (in
chickens and is prepared as a 0.2% solution
people) is eliminated (;,c9()0A,) unchanged in
for treatment of fungal skin infections.

the urine. The kinetics of voriconazole have

When infused into the nasal turbinates of
not yet been evaluated in anin1als.

dogs with aspergillosis, enilconazole treated
and prevented the recurrence of fungal

Pharmacokinetics: The rate of eliminadisease. When applied topically to dog and tion of ketoconazole appears to be dose
cat hairs, enilconazole inhibits fungal
dependent-the greater the dose, the longer
growth in 2 rather than 4--8 treatments, as is the elimination half-life. There is also a
necessary with other topically administered
biphasic elimination pattern, with rapid
antifungal agents.

elimination in the first 1 -2 hr, then a slower

General dosages for the antifungal
decline over the next 6-9 hr. Ketoconazole
in1idazoles are listed in TABLE 53. The dose
is usually administered bid. The half-life of
rate and frequency should be adjusted as
itraconazole is longer (up to 48 hr in cats),
needed for the individual animal.

thus allowing treatment once to twice daily.

Because of the long half-life and mechanism

Special Clinical Concerns
of action (impaired synthesis of the fungal
cell membrane), time to efficacy may take

Adverse Effects and Toxicity: The
longer than drugs that have more rapid
imidazoles given PO result in few adverse
actions (such as an1phofericin B).

effects, but nausea, vomiting, and hepatic
dysfunction can develop. Ketoconazole in
particular is associated with hepatotoxicity,

Therapeutic Indications and Dose
especially in cats. Because irnidazoles also

Rates
inhibit CYP450 associated with steroid

The irnidazoles are used to treat systemic
synthesis, as a result, sex steroids, including
fungal diseases, dem1atophyte infections
testosterone and adrenal steroid ( cortisol),

IM=iiiii DOSAGES OF IMIDAZOLES

Imidazole

Dosage, Route, and Frequency

Enilconazole

10 mg/kg in 5-10 mL, bid for 7-14 days

Fluconazole

5-10 mg/kg, PO, once to twice daily

Itraconazole

5-10 mg/kg, PO, once to twice daily

Ketoconazole

5-20 mg/kg, PO, bid (dogs)

Thiabendazole

44 mg/kg/day, PO, or 22 mg/kg, PO, bid

ANTI FUNGAL AGENTS

2703
metabolism is inhibited. Adrenal responcells do not convert large amounts of siveness to adrenoco1ticotropic hom1one
flucytosine to fluoromacil ru1d, thus, are

(ACTH) will be decreased, pruticularly with
not affected at usual dosage levels.

ketoconazole. Reproductive disorders
related to ketoconazole administration may

Fungal Resistance: Resistru1ce to
be seen in dogs. Vmiconazole is associated
flucytosine cru1 develop rapidly even during

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with a number of adverse effects in people,
the course of treatment; this precludes its
including vision disturbru1ces.

use as the sole treatment for mycotic
infections. The mechru1isms of resistance

Interactions: Imidazoles, in general,
ru·e not completely tmderstood.

inhibit the metabolism of many drugs.

Although ketoconazole has the broadest

Antifungal Spectra: The following are
inhibitory effects, fluconazole followed by the main orgru1isms usually sensitive to itraconazole also inhibit metabolism.

flucytosine: Cryptococcus neof<nmans,

Concurrent administration of these drugs

Candida albicans, other Candida spp, with other drugs metabolized by the liver

To-iulopsis glabrata, Sporothrix schenckii,
ru1d potentially toxic should be done only

Aspergillus spp, ru1d agents of chromoblaswith extreme caution. lmidazoles also ru·e tomycosis (Phialophorn, Cladosp01ium).

substrates for P-glycoprotein trru1sport

The other fungi responsible for systemic
protein ru1d may compete with other
mycoses ru1d dennatophytes are resistant to
substrates, causing higher concentrations. flucytosine.

Many of the substrates for P-glycoprotein
ru·e also substrates for CYP450. Rifru11pin,

Pharmacokinetic Features
which is a P-glycoprotein substrate,
decreases serum ketoconazole because

Absorption and Distribution: Flucytoof microsomal enzyme induction. The sine is rapidly ru1d well absorbed from the
absorption of the imidazoles, except

GI tract, with plasma levels peaking in 1-2
for that of fluconazole, is inhibited by
hr in ru1irnals that have received the drug for
concurrent administration of cimetidine,
several days. The drug is widely distributed
ranitidine, ru1ticholinergic agents, or
in the body, with a volume of distribution
gastric ru1tacids. The risk of hepatotoxicapproximating the total body water.

ity is increased if ketoconazole ru1d

Flucytosine is minimally bound to plasma
griseofulvin are administered together.

proteins. There is excellent penetration into

Imidazoles might be used concurrently
body fluids such as the CSF, synovial fluids,
with other ru1tifu.ngals to facilitate
ru1d aqueous humor.

synergistic efficacy.

Biotransformation and Excretion:

Effects on Laboratory Tests: Treat

Nearly all (85%-95%) of ru1 oral dose is
ment with imidazoles increases AST, ALT,
excreted unchru1ged. Flucytosine is
plasma bilirubin, ru1d plasma cholesterol.

principally excreted by glomerular filtration

Adrenal responsiveness is altered.

(>80%). The clearru1ce of flucytosine is
approximately equivalent to that of
creatini.ne. In renal fail me, elimination

FLUCYTOSINE
of flucytosine is mru·kedly impaired.

Flucytosine (5-fluorocytosine) is a
fluorinated pyrin1idine related to fluoro

Pharmacokinetics: With noimal renal
macil that was initially developed as ru1
function, the plasma half-life of flucytosine
ru1ti.neoplastic agent. It should be stored in
is usually 2-4 hr but may be up to 200 hr
airtight containers protected from light.

with oliguria. Serum levels of 50-100 mcg/

Solutions for infusion ru·e unstable ru1d
mL are usually in the therapeutic rru1ge.

should be stored at 15° -20°C. Usually, it
is given PO in capsules.

Therapeutic Indications and Dose

Antifungal Activity

Rates

The more common indications for

Mode of Action: Flucytosine is
flucytosine include c1yptococcal meningitis,
converted by cytosine derullinase in fungal
used together with runphotericin B ( -300/o
cells to fluoromacil, which then inte1-feres
of isolates develop resistru1ce during the
with RNA ru1d protein synthesis. Fluoromacom-se of treatment); cru1didiasis (-900/o of cil is metabolized to 5-fluorodeoxyuridylic
isolates ru·e usually sensitive); aspergillosis
acid, ru1 inhibitor of thymldylate synthetase.

(some strains are sensitive at <5 mcg/mL);

DNA synthesis is then halted. Mrunmaliru1
ctu·omomycosis (some strains ru·e very

2704

ANTIFUNGALAGENTS
sensitive); and sporotiichosis (some cases
cells. The inhibition of nucleic acid
may respond).

synthesis and the formation of hyphal cell

General dosages for flucytosine are 25--50
wall material also may be involved. The
mg/kg and 30-40 mg/kg, PO, ticl-qicl in clogs
result is distmtion, irregular swelling, and
and cats, respectively. The close rate and
spiral curling of the hypha.e. Griseofulvin is

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frequency should be adjusted as needed for
ftmgista.tic rather than fungicidal, except in
the incliviclual anin1al. Dosage modification
young active cells.

is essential in renal failure. Flucytosine
semm levels should be monitored if

Fungal Resistance: Demiatophytes can
possible.

be ma.de resistant to griseofulvin in vitro.

Special Clinical Concerns

Antifungal Spectra: Griseofulvin is
active againstMicrosporum, Epidei·mo

Adverse Effects and Toxicity: F1ucyto
phylon, and Trichophylon spp. It has no sine is often well tolerated over long periods, effect on bacteria. (incluclingAclinomyces but toxic effects may be seen when serum
a.i1d Nocardia spp ), other fungi, or yeasts.

levels are high (>100 mcg/mL). These
include GI signs (nausea, vomiting, diarrhea) Pharmacokinetic Features and reversible hepatic and hematologic
effects (increased liver enzymes, anemia,
neuti·openia, thrombocytopenia). In dogs,

Absorption: Plasma levels peak -4 hr
erythernic and alopecic demiatitis may
after administration PO, but absorption
be seen but subsides when the drug is
from the GI tract continues over a prolonged
discontinued.

period. Absorption is highly va.ifable and
influenced by a number of factors. The rates
of disaggregation and dissolution in the GI

Interactions: There is synergistic
antiftmgal activity between an1photericin B
tract limit the bioavailability of griseofulvin;
and ketoconazole, and the combination may thus, microsizecl and ultra.i11icrosizecl retard the emergence of strains resistant to
pa.iticles are usually used. High-fat meals,
flucytosine. The renal effects of amphoma.i·ga.i·ine, or propylene glycol significa.i1tly tericin B prolong elimination of flu cytosine.

enhance GI a.bso1vtion of griseofulvin a.i1d

If flucytosine is used together with
a.re indicated if the microsized particles are
immunosuppressive drugs, severe
used.

depression of bone marrow ftmction
is possible.

Distribution: Griseofulvin is deposited
in keratin precursor cells within 4-S hr of

Effects on Laboratory 1ests: Treatadministration PO. Sweat a.i1cl transde1mal ment with flucytosine increases alkaline
fluid loss appear to play an i.mpo1ta.i1t role
phosphatase, AST, ALT, and other liver
in griseofulvin transfer in the stratum
leakage enzymes, and decreases RBC, WBC, comeun1. When tl1ese cells differentiate, and platelet counts.

griseofulvin remains bound and persists
in keratin, ma.king it resistant to fungal

GRISEOFULVIN
invasion. For this reason, new growth of
hair, nails, or horn is the first to become free

Griseofulvin is a systemic antiftmgal agent
of fungal infection. As the ftmgus-conta.ining
effective against the conunon denna.tokeratin is shed, it is replaced by nom1al skin phytes. It is practically insoluble in water
and hair. Only a small fraction of a dose of
and only slightly soluble in most organic
griseofulvin remains in the body fluids or
solvents. Pa.iticle sizes of g1iseofulvin vary
tissues.

from 2. 7 im1 ( ultra.i11icrosizecl) to 10 pm

(microsized).

Biotransformation and Pharmacokinetics: Depending on the species, 100/<r-500/o Antifungal Activity
of a griseofulvin dose is excreted al.most
exclusively as metabolites in the urine, and

Mode of Action: Dermatophytes
tl1e remainder in the feces for -4-5 clays
concenti·ate griseofulvin through an
after ad.ministration. The elimination
energy-dependent process. Griseofulvin
half-life of griseofulvin is -24 hr in several
then disrupts the mitotic spindle by
species. The drug can be detected in 48-72
interacting with the polyn1erized microtuhr at the base level of tl1e skin, in 6-12 days bules in susceptible demiatophytes. This
in the lower qua.tier, and in 2-19 days in the
leads to production of multinuclea.te ftmgal
middle section of the horny layer.

ANTIFUNGALAGENTS

2705

Therapeutic Indications and Dose
mate tolnaftate. Their mechanism is

Rates
competitive inhibition of squalene
epoxidase, blocking conversion of

Griseofulvin is used for dermatophyte
squalene to lanosterol, leading to squaline
infections in dogs, cats, calves, horses, and
accumulation and ergosterol depletion

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other domestic and exotic animal species.

in the cell membrane. Terbinafine has a

Most derrnatophytes are sensitive, but
much higher affinity for fungal than for
certain species present greater therapeutic
mammalian squaline epoxidase. Avid
challenges than others. Several may
uptake of terbinafine into body fat and
require higher dose rates for satisfactory
epidermis presumably enhances treatment
control.

for dermatophytes of superficial yeast

General dosages for griseofulvin are
pathogens of the skin. However, data are
listed in TABLE 54. The dose rate and
emerging to potentially support its use for
frequency should be adjusted as needed
systemic fungal infections. Terbinafine is
for the individual animal.

also active against yeasts ( eg, Blastomyces
dermatitidis, C1·yptococcus neofo1mans,

Special Clinical Concerns

Sporothm schenckii, Histoplasma

Adverse Effects and Toxicity: Adverse
capsulatum, Candida, and Pityrosporum
effects induced by griseofulvin are rare.

spp). Terbinafine increasingly is used in

Nausea, vomiting, and diarrhea have been
combination with other antifungal drugs
seen. Hepatotoxicity has also been reported. to enhance efficacy. Effects are fungicidal.

Animals with impaired liver function should

The allylamines appear to be more efficanot be given griseofulvin, because its biocious than griseofulvin for treatment of transforrnation will be reduced and toxic
dermatophyte infections. Efficacy has also
levels may be reached. Idiosyncratic (Type
been demonstrated against S schenckii

B or Type II adverse reaction) toxicity in
and Aspergillus. Terbinafine may enhance
cats has been reported. Clinical signs are
efficacy of other antifungal drugs for a
neurologic, GI, and hematologic. Griseofulvariety of fungal disorders and pythiosis.

vin is contraindicated in pregnant anin1als

In contrast to terbinafine, tolnaftate is

( especially mares and queens) because it is
limited to treatment of dermatophytes.

teratogenic.

Resistance to the allylamines is rare, but
the drugs potentially can be affected by

Interactions: Lipids increase GI
multidrug resistance efflux mechanisms.

absorption of griseofulvin. Barbiturates

Terbinafine, available in oral and topical
decrease its absorption and antifungal
preparations, is well absorbed (80% in
activity. Griseofulvin is a microsomal
people) after PO administration. Fat
enzyme inducer and promotes the
facilitates absorption. High concentrabiotransfonnation of many concurrently tions occur in the stratum corneum,
administered drugs. The combined use of
sebum, and hair. Terbinafine is metaboketoconazole and griseofulvin may lead to lized by the liver in people; the elimination
hepatotoxicity.

half-life is sufficiently long to allow oncedaily administration, with steady state Effects on Laboratory Tests: Treatnot occurring for 10-14 days in people.

ment with griseofulvin increases alkaline

Adverse effects of terbinafine after PO
phosphatase, AST, and ALT. Proteinuria
administration are limited to GI and skin
may be detected.

signs; hepatobiliary dysfunction is a rare
adverse event. Because inhibition of

ALLYLAMINES
ergosterol synthesis occurs at a step
before cytochrome P450 involvement, the

The allylamines include terbinafine,
allylamines do not affect steroid synthesis
naftifine, and the much older thiocarba-
as do the irnidazoles.

ltM•iii DOSAGES OF GRISEOFULVIN

Species

Dosage, Route, and Frequency

Dogs, cats

Microsized: 10-30 (up to 130) mg/kg/day, PO, or divided bid-tid Ultranlicrosized: 5-10 (up to 50) mg/kg/day, PO

Horses, cattle

5-10 mg/kg/day, PO, for 3-6 wk, or longer if required

2706

ANTI FUNGAL AGENTS

IODIDES
is wise, especially when dealing with
zoonotic fungi.

Sodium and potassium iodide have both

Preparations may be used in the form
been used to treat selected bacterial,
of solutions, lotions, sprays, powders,

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actinomycete, and fungal infections,
creams, or ointments for dem1al applicaalthough sodiun1 iodide is preferred. The in tion, or in the form of i.rrigant solutions,
vivo effects of iodides against fungal cells
ointments, tablets, or suppositories for
are not well understood. Iodide is readily
intravaginal use. The concentration of
absorbed from the GI tract and distributes
active principle in these preparations
freely into the extracellular fluid and
varies and depends on the activity of the
glandular secretions. Iodide concentrates
specific agent.

in the thyroid gland (50 times correspond

The clinical response to local antifungal
ing plasma level) and to a much lesser
agents is unpredictable. Resistance to
degree in salivary, lacrimal, and tracheomany of the available drugs is common.

bronchial glands. Longterm use at high

Spread of infection and reinfection add to
levels leads to accumulation in the body
the difficulty of controlling superficial
and to iodinism.

infections. Perseverance is often an

Clinical signs of iodinism include
essential element of therapy.

lacrimation, salivation, increased respira

Some topical antifungal agents that
tory secretions, coughing, inappetence, dry
have been used with success in various
scaly skin, and tachycardia. Cardiomyopaconditions and species include iodine thy has been reported in cats. Host defense
preparations (tincture of iodine, potassiun1
systems, such as decreased irnmunoglobuiodide, iodophors ), copper preparations lin production and reduced phagocytic

( copper sulfate, copper naphthenate,
ability of leukocytes, are also impaired.

cuprimyxin), sulfur preparations (mono

Iodinism may also lead to abortion and
sulfiram, benzoyl disulfide), phenols
infertility.

(phenol, thymol), fatty acids and salts

Sodium iodide has been used success

(propionates, undecylenates), organic
fully to treat cutaneous and cutaneous/
acids (benzoic acid, salicylic acids), dyes
lymphadenitis forms of sporotrichosis;

(crystal [gentian] violet, carbolfuchsin),
attempts to control various other mycotic
hydroxyquinolines (iodochlorhydroxyinfections with iodides yield equivocal quin), nitrofurans (nitrofuroxine,
results.

nitrofurfurylmethyl ether), imidazoles

The dosage for sodiun1 iodide (2091<,

(miconazole, tioconazole, clotrimazole,
solution) is 44 mg/kg/day, PO, for dogs, and
econazole, thiabendazole), polyene

22 mg/kg/day, PO, for cats. The dosage for
antibiotics (amphotericin B, nystatin,
horses is 125 mL of 200Aisodium iodide
pimaricin, candicidin, hachimycin),
solution, IV, daily for 3 days, then 30 g, PO,
allylan1ines (naftifine, terbinafine),
daily for 30 days after clinical remission.

thiocarban1ates (tolnaftate), and miscel

The dosage rate for treating actinornycosis
laneous agents (acrisorcin, haloprogin,
and actinobacillosis in cattle is 66 mg/kg, by
ciclopirox, olamine, dichlorophen,
slow IV, repeated weekly. Potassium iodide
hexetidine, chlorphenesin, triacetin,
should never be injected IV.

polynoxylin, amorolfine).

Amorolfine is a topical antifungal
agent used to treat onychomycosis and

TOPICAL ANTI FUNGAL AGENTS
dermatophytosis. It is prepared as a cream
or nail lacquer. Arnorolfine is a morpho

A number of agents that have antifungal
line derivative that appears to interfere
activity are applied topically, either on
with the synthesis of sterols essential for
the skin, in the ear or eye, or on mucous
the functioning of fungal cell membranes.

membranes (buccal, nasal, vaginal) to

In vitro, activity has been shown against
control superficial mycotic infections.

some yeasts and dimorphic, dematia

Concurrent systemic therapy with griseoceous, and filamentous fungi (Blastomy
fulvin is often helpful for therapeutic
ces dermatitidis, Candida spp, Histo
management of dermatophyte infections.

plasma capsulatum, Sporothrix schenckii,

The hair should be clipped from affected
and Aspergillus spp ). Despite its in vitro areas and the nails trimmed to fully
activity, amorolfine is inactive when given
expose the lesions before antifungal
systemically and thus is limited to topical
preparations are applied. Bathing the
use in treatment of superficial infections.

animal may also be helpful. Isolation or

Its role in treatment of fungal infection in
restricted movement of infected animals
animals is not clear.

ANTI-INFLAMMATORY AGENTS

2707

ANTI-INFLAMMATORY AGENTS

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Inflanm1ation is the complex pathophysiir\jury. In response to adhesion, molecules ologic response of vascularized tissue to
released from activated endothelial cells,
ir\jury. The ir\jury may result from various
leukocytes, platelets, and erythrocytes in
stimuli, including thermal, chemical, or
ir\jured vessels become sticky and adhere to
physical damage; ischemia; infectious
the endothelial cell surfaces. Polymorphoagents; antigen-antibody interactions; and nucleai· leukocytes such as neutrophils are
other biologic processes. After tissue ir\jury,
the first cells to infiltrate the site of i11jury.

the process of tissue healing includes three

Basophils and eosinophils are more
distinct phases: an inflanm1atmy phase, a
prevalent in allergic reactions or parasitic
repair phase, and a remodeling phase. The
infections. As inflai1miation continues,
desired outcome of the inflammatory
macrophages predominate, actively
response is isolation and elin1ination of the
removing dainaged cells or tissue. If the
i.r\jurious agent to prepare for the repair of
cause of ir\jmy is eliminated, the subacute
tissue damage at the site of iajmy and
phase of inflammation may be followed by
restoration of function. Finally, new tissue
a period of tissue repair. Blood clots are
formed during the repair phase ( eg, scar
removed by fibrinolysis, and daniaged
tissue) may be remodeled over several
tissues ai·e regenerated or replaced with
months.

fibroblasts, collagen, or endothelial cells.

During the remodeling phase, the new

PATHOPHYSIOLOGY
collagen laid down dming the repair phase

OF INFLAMMATION

(mainly type III) is progressively replaced
by type l collagen to adapt to the original

The initial in.flanU11ation phase consists
tissue. However, if i.nflaim11ation becomes
of three subphases: acute, subacute, and
chronic, fmther tissue destruction and/or
chronic ( or proliferative). The acute phase
fibrosis occurs.

typically lasts 1 -3 days and is characterized
by the five classic clinical signs: heat,

CHEMICAL MEDIATORS
redness, swelling, pain, and loss of function.

OF INFLAMMATION

The subacute phase may last from 3-4 days
to -1 mo and corresponds to a cleaning

Biochemical mediators released during
phase required before the repair phase. If
in.flan1mation intensify ai1d propagate the
the subacute phase is not resolved within
inflailllllatory response ( see TABLE 55). These

-1 mo, then infla.nm1ation is said to become
mediators are soluble, diffusible molecules
clu-onic and can last for several months.

that can act locally and systemically.

Tissue can degenerate and, in the locomotor

Mediators derived from plasma include
system, chronic inflanunation may lead to
complement and complement-derived
teaiing ai1d rupture. Alternatively, after the
peptides and kinins. Released via the classic
subacute inflanU11atory phase, tissue can
or alternative pathways of the complement
repair and be strengthened during the
cascade, complement-derived peptides
remodeling phase.

(C3a, C3b, and C5a) increase vascular

From a mechanistic point of view, the
pern1eability, cause smooth muscle conacute response to tissue ir\jury occurs in traction, activate leukocytes, and induce
the microcirculation at the site of injury.

mast-cell degranulation. C5a is a potent

Initially, there is a transient constriction of
chemotactic factor for neutrophils and
arterioles; however, within several minutes,
mononuclear phagocytes. The kinins ai·e
chemical mediators released at the site
also important inflaimnato1y mediators.

relax arteriolar smooth muscle, leading to

The most important kinin is bradykinin,
vasodilation and increased capillaiy
which increases vascular permeability and
permeability. Protein-rich fluid then exudes
vasodilation and, importantly, activates
from capillaiies into the interstitial space.

phospholipase A2 (PLA2) to liberate

This fluid contains many of the components
arachidonic acid (AA). Bradykinin is also
of plasma including albumin, fibrinogen,
a major mediator involved in the pain
kinins, complement, and inmmnoglobulins
response.

that mediate the inflammatory response.

Other mediators are derived from ir\jured

The subacute phase is characterized by
tissue cells or leukocytes recruited to the
movement of phagocytic cells to the site of
site of inflan1mation. Mast cells, platelets,

2708

ANTI-INFLAMMATORY AGENTS
ltM•ifi ACTIONS OF INFLAMMATORY MEDIATORS

Action

Mediatorsa

Vasodilation, increased vascular

Histan1ine, serotonin, bradykinin, C3a, C5a, LTC,,

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pem1eability

LTD.,, PGl2, PGE,, PGD,, PGF2, activated Hageman
factor, kinonogen fragments, fibrinopeptides

Vasoconstriction

TXA2, LTB,, LTC4, LTD4, C5a

Smooth muscle contraction

C3a, C5a, histamine, LTB.,, LTC,, LTD4, TXA2,
serotonin, PAF, bradykinin

Mast cell degranulation

C5a,C3a

Stern cell proliferation

IL-3, G-CSF, GM-CSF, M-CSF

Chernotaxis

C5a, LTB4, IL-8, PAF, 5 -HETE, histamine, others

Lysosomal granule release

C5a, IL-8, PAF

Phagocytosis

C3b,iC3b

Platelet aggregation

TXA2,PAF

Endothelial cell stickiness

IL-1, TNF-a, LTB4

Granuloma formation

IL-1, TNF-a

Pain

PGE2, bra.dykinin, histan1ine, serotonin

Fever

IL-1, IL-6, TNF-a, PGE2

"C = complement, LT= leukot,iene, PG = prostaglandin, TX= U1romboxane, PAF = platelet activating factor, IL= interleukin, CSF = colony stimulating factor, HETE = hydroxycicosatetranoate, TNF =
tumor necrosis factor
and basophils produce the vasoa.ctive
tract and CNS. Serotonin also increases
a.mines serotonin and histamine. Histavascular permeability, dilates capillaries, mine ca.uses a.iteriolar dilation, increased
and causes contraction of nonvascular
capillary pem1ea.bility, contraction of
smooth muscle. In some species, including
nonvascular smooth muscle, and eosinophil rodents and domestic ruminants, serotonin chernota.xis and can stimulate nociceptors
may be the predominant vasoactive a.llline.

responsible for the pain respon�e. Its

Cytokines, including interleukins 1-10,
release is stimulated by the complement
tun1or necrosis factor a (TNF-a ), and
components C3a. and C5a and by lysosointerferon 'I (INF-'{) are produced predomimal proteins released from neutrophils.

nantly by macrophages and lymphocytes

Histamine activity is mediated through the
but can be synthesized by other cell types as
activation of one of four specific histamine
well. Their role in inflanuna.tion is complex.

receptors, designated H,, H2, H3, or H,,

These polypeptides modulate the activity
in ta.i·get cells. Most histamine-induced
and ftmction of other cells to coordinate and
vascula.i· effects are mediated by H1
control the infla.inmatory response. Two of
receptors. H, receptors mediate some
the more irnpmtant cytokines, interleukin-1
vascular effects but a.i·e more inlportant

(IL-1) and TNF-a, mobilize and activate
for their role in hista.i11ine-induced gasttic
leukocytes, enha.11ce proliferation of B and
secretion. Less is understood about the role

T cells and natural kiJler cell cytotoxicity,
of H,1 receptors, which may be localized to
and a.i·e involved in the biologic response to
the CNS. I -I. receptors are located on cells
endotoxins. IL-1, IL-6, and TNF-a mediate

1
of hema.topoietic origin, and I -11 antagonists
the acute phase response and pyrexia. that
a.i·e promising drug candidates to treat
may accompany infection and can induce
infla.inrnatory conditions involving mast
systemic clinical signs, including sleep and
cells and eosinophils (allergic conditions).

anorexia In the acute phase response,

Serotonin (5-hydroxytrypta.mine) is a
interleukins stimulate the liver to synthesize
vasoa.ctive media.tor similar to histan1ine
acute-phase proteins, including complement
fow1d in mast cells and platelets in the GI
components, coagulation factors, protease

ANTI-INFLAMMATORY AGENTS

2709
inhibitors, and metal-binding proteins. By
platelet-aggregating agent involved in
increasing intracellular Ca2+ concentrations
thrombus fo1mation.

in leukocytes, cytokines are also important

Fotmd predominately in platelets,
in the induction of PLA2• Colony-stimulating
leukocytes, and the lungs, 5-LOX catalyzes
factors (GM-CSF, G-CSF, and M-CSF) are
the formation of unstable hydroxyperoxides

VetBooks.ir
cytokines that promote expansion of neutrofrom AA. These hydroxyperoxides are phil, eosinophil, and macrophage colonies
subsequently conve1ted to peptide
in bone marrow. In chronic inflammation,
leukotrienes. Leukotriene B4 (LTB4) and
cytokines IL-1, IL-6, and TNF-cx contribute to 5-hydroxyeicosatetranoate (5-HETE) are the activation of fibroblasts and osteoblasts
strong chemoattractants stimulating
and to the release of enzymes such as
polymorphonuclear leukocyte movement.

collagenase and stromelysin that can cause

LTB. also stimulates the production of
cartilage and bone resorption. Experimental

1
cytokines in neutrophils, monocytes, and
evidence also suggests that cytokines
eosinophils and enhances the expression of
stimulate synovial cells and chondrocytes

C3b receptors. Other leukotrienes facilitate
to release pain-inducing mediators.

the release of histamine and other autacoids

Lipid-derived autacoids play i.mporta.nt
from mast cells and stimulate bronchiolar
roles in the inflan1matory response and are
constriction and mucous secretion. In some
a major focus of research into new antispecies, leukotrienes C4 and D, are more inflammatory drugs. These compounds
potent than histamine in contracting
include the eicosanoids such as prostaglanbronchial smooth muscle.

dins, prostacyclin, leukotliencs, and

Platelet activating factor (PAF) is also
thromboxane A and the modified phosphoderived from cell membrane phospholipids lipids such as platelet activating factor
by the action of PLA2. PAF, syntl1esized by

(PAF). Eicosanoids are synthesized from
mast cells, platelets, neutrophils, and

20-carbon polyunsaturated fatty acids by
eosinophils, induces platelet aggregation
many cells, including activated leukocytes,
and stimulates platelets to release
mast cells, and platelets and are therefore
vasoactive amines and synthesize tJu·omwidely distributed. Hom10nes and other boxanes. PAF also increases vascular
inflammatory mediators (TNF-cx, bradypermeability and causes neutrophils to kinin) stinntlate eicosanoid production
aggregate and degranulate.

either by direct activation of PLA,, or

The role of the free radical gas nitric
indirectly by increasing intracellular Ca2+
oxide (NO) in inflammation is well
concentrations, which in tum activate the
established. NO is an important cell-signalenzyme. Cell membrane damage can also ing messenger in a wide range of physiocause an increase in intracellular Ca2+.

logic and pathophysiologic processes. Small

Activated PLA2 directly hydrolyzes AA,
amOLmts of NO play a role in maintaining
which is rapidly metabolized via one of two
resting vascular tone, vasodilation, and
enzyme pathways-the cyclooxygenase
antiaggregation of platelets. In response to

(COX) pathway leacling to the fonnation of
certain cytokines (TNF-cx, IL-1) and otl1er
prostaglandin and thromboxanes, or the
inflammatory mediators, the production of

5-lipoxygenase (5-LOX) patl1way that
relatively large quantities of NO is stinmproduces the leukotrienes.

lated. In larger quantities, NO is a potent

Cyclooxygenase catalyzes the oxygenavasodilator, facilitates macrophage-induced tion of AA to fonn the cyclic endoperoxide
cytotoxicity, and may contribute to joint

PGG2, which is converted to the closely
destruction in some types of aithritis.

related PGH,. Both PGG, and PGH, are
inherently unstable and rapidly converted

ANTIHISTAMINES
to various prostaglandins, tluomboxane A,

(TXA,), and prostacyclin (PGI1). In the

Antagonists that selectively block specific
vascular beds of most anin1als, PGE1, PGE2,
histamine receptors have been developed.

and PGI1 are potent arteliolar dilators and

H1 antagonists block the actions of histaenhance the effects of otl1er mediators by mine responsible for increased capillai-y
increasing small-vein pe1meability. Other
permeability and wheal and edema
prostaglandins, including PG F 2u and
formation. However, because histamine
tlliomboxane, cause smooth muscle
is only one component of an incredibly
contraction and vasoconstriction.

complex inflarnmatory cascade, antihista

Prostaglandins sensitize nociceptors
mines have ve1-y weak anti-inflai1rn1atory
to pain-provoking mediators such as
activity. H1 antihistan1ines may be useful to
bradykinin and histamine and, in high
treat inllllediate hypersensitivity reactions
concentrations, can directly stimulate
such as anaphylaxis by blocking bronchosensory nerve endings. TXA2 is a potent constliction ai1d vasodilation. H1 antagonists

2710

ANTI-INFLAMMATORY AGENTS
may be less effective to treat allergic inflacorticoids is potentially detrimental to mmatory diseases, such as atopy, primarily
several metabolic, honnonal, and immunobecause mediators other than histamine logic ftmctions.

play in1p01tant roles in such conditions. H2

All therapeutic corticosteroids have a

VetBooks.ir

(now classified as inverse agonists of the H2

21-carbon steroid skeleton, sin1ilar· to
receptor, such as cin1etidine and ranitidine)

hydrocortisone (c01tisol). Modifications
antagonists are routinely used to block the
to this skeleton selectively alter the degree
gastric secretory effects of histanline and
of anti-inflammatory activity and the
have limited anti-inflammatory effects.

metabolic consequences and vary the
duration of activity and protein-binding
affinity of the resultant compotmd. The

CORTICOSTEROIDS
introduction of an additional double bond
between C-1 and C-2 of cortisol in all

Two classes of steroid hom1ones, mineralosynthetic corticosteroids selectivity corticoids and glucocorticoids, are naturally increases glucocorticoid and anti-inflammasynthesized in the adrenal cortex from tory activity. However, this single modificacholesterol. (See ai,so THE ADRENAL GLANDS, tion does not affect mineralocorticoid
p 573.)

activity, resulting in an enllanced glucoco1ti

Mineralocorticoids ( aldosterone) are
coid/mineralocorticoid potency ratio, eg,
so nar11ed because they a.re in1portant in
prednisolone is -4- to 5-fold more selective
maintaining electrolyte homeostasis.

than cortisol. Additional fluorination at the

However, mineralocorticoids also trigger a

C-9 position enllances both glucocorticoid
broader range of functions in nonclassic
and mineralocorticoid activity, as in
target cellular sites, including some effects

9a-fluorocortisol (fludrocortisone) and
on wound healing after irtjury. In addition,
isoflupredone. Fludrocortisone (ad.minisa chronic and inappropliate (relative to tered as fluclrocortisone acetate) is 125-intravascular volun1e and dietary sodiun1
fold more potent than cortisol for mineralointake) increase in aldosterone secretion corticoid effect and only 10-fold more for
evokes a wound healing response in the
glucocorticoid effect. Thus, it is used in
absence of tissue irtjury. This can lead to
small animal medicine for its mineralocorantialdosterone (eg, spironolactone) drug ticoid selectivity in the treatment of
treatment being reconrn1ended to prevent
ad.renoco1tical insufficiency.

tmdesired heart remodeling and fibrosis.

Isoflupred.one is used as an anti-inflam

Glucocorticoids suppress virtually
matory drug in cattle but lacks selectivity
every component of the inflammatory
for mineralocortoid. effects and increases
process; they inhibit PLA2, decrease
the risk of severe hypokalemia. When a
synthesis of interleukins and munerous
fluorinated. d.elivative is substituted. at the
other proinfla.mmatory cytokines, suppress

C-16 by an OH radical or a CH3 group, the
cell-mediated immunity, reduce complenew C-16 substituted compound. ( eg, ment synthesis, and decrease production
triamcinolone, dexametha.sone, betamethaand activity of leukocytes. Unsurprisingly sone) has virtually no mineralocorticoid
then, glucocorticoids are by far the most
effect but remains a potent anti-inflanrn1aefficacious anti-inflammat01y drugs. They t01y glucocorticoid.. This la.st substitution
are also the most commonly used antion C-16 yields a new property to these inflammatory drugs. However, because their fluorocorticosteroid.s, enabling them to phar-macologic and physiologic effects are
trigger pa.rtulition in various species, includso broad, the potential for adverse effects is ing cattle. Dexametha.sone and flun1ethaconsiderable.

sone (shott-acting fommlations) can induce

Glucocorticoids play significant roles in
parturition when ad.ministered. after 255
carbohydrate, protein, and lipid metabodays of gestation in cattle, but induced.

lism; the in1mune response; and the
calving is usually associated. with a high
response to stress. Natural glucocorticoids
incidence of ad.verse effects, including
also have some mineralocorticoid activity
retained. placenta.

and therefore affect fluid and electrolyte

Many corticoid.s are ad.ministered. as
balance. While corticosteroids can be highly esters. Esterification of the alcohol at C-21
effective in suppressing or preventing
d.etem1ines the extent of water/lipid.

inflanrniation, their physiologic and
solubility and controls the in vivo disposipharmacologic mechanisms of action are tion of the compound.. Estelification with a
mediated by the san1e receptor. This
monoacid, such as acetic acid, yields
explains why their pharmacologic and
water-insoluble drugs (eg, methylpred.nisophysiologic effects are inllerently linked, lone acetate) that can be used as long-acting
and why supraphysiologic exposure to
formulations when administered. by the IM,

ANTI-INFLAMMATORY AGENTS

2711

SC, or intra-aiticular route. Other waterformulation. Esterification at C-17
insoluble esters are diacetate, terbutate, ai1d ( valerate) produces a lipophilic compOLmd pivalate. By contrast, esterification of the
with an enhanced topical:systemic potency
saine corticoid by a diacid such as succinic
ratio. Other approaches to achieve local
acid can yield a hydrosoluble ester, due to
glucocorticoid activity while minimizing

VetBooks.ir
the second acid function (as for methylpredsystemic effects involve the formation of nisolone sodium succinate) allowing a salt
analogues that are rapidly inactivated after
to be fom1ed. Phosphate esters are also
their systemic absorption. Fluticasone
hydrosoluble. Solutions of free steroids or
propionate, which is not a prodrug, is
of hydrosoluble esters can be administered
directly used to treat IW1g conditions.

by the IV or IM route and are often used to

Similarly, beclomethasone dipropionate (a
treat life-threatening conditions such as
prodrug) locally yields an active metabolite
heaves or hypersensitivity reaction. Esters

(bcclomethasone 17-monopropionate) that
may also be used PO, but hydrolysis occurs
in tum yields beclomethasone, which has
in the lwnen of the digestive tract (pancrevery weak anti-inflainmatory activity.

atic esterase) and the free active moiety is

Therapeutic corticosteroids are typically
absorbed; thus, a formulation may be
classified based on their relative glucocortilong-acting when administered parenterally coid and mineraloc01ticoid potency (ie, the
but short-acting when given orally ( eg,
relative intensity of drug activity related to
prednisolone acetate).

its concentration, a property that should

Nearly all esters are inactive prodrugs
not be confused with efficacy) as well as
and require hydrolization to release their
duration of effect (see TABLE 56). CompoW1ds active moiety. Hydrolysis by esterases or
with the most potent glucocorticoid activity
pseudoesterases may occur either in body
are also the most potent suppressors of the
fluids such as blood or synovial fluid
hypothalainic-pituitary-adrenal axis

(acetate) or mainly in liver (succinate).

(HPAA).

Thus, for a local administration the choice
of an appropriate ester is importaJ1t.

Mode of Action: Glucocorticoids are

Hydrolysis may be only partial; for exainple,
capable of suppressing the inflanrnrntory
the bioavailability of methylprednisolone
process through nw11erous pathways. They

(the active moiety) from its hydrosoluble
interact with specific intracellular receptor
ester, methylprednisolone sodiwn
proteins in target tissues to alter the
succinate, is only 500Ai in dogs after IV
expression of cotticosteroid-responsive
administration, which must be considered
genes. Glucocorticoid-specific receptors in
when detem1ining a dosage regimen.

the cell cytoplasm bind with steroid liga11ds

Substai1ces having a ketone radical in
to form honnone-receptor complexes that

C-11, in lieu of an OH radical required for
eventually translocate to the cell nucleus.

binding of the corticoid to its cellular

There, these complexes bind to specific
receptors, are also prodrugs. Cortisone,

DNA sequences a11d alter their expression.

prednisone, and methylprednisone are

The complexes may induce the trai1scripprodrugs of cortisol. These prodrugs are tion of mRNA, leading to synthesis of new
back transfom1ed to their alcohol form in
proteins. Such proteins include lipocortin, a
the liver by an l l-!3-hydroxylase. There is no
protein known to inhibit PLA:c, and thereby
reason to administer them locally, because
block the synthesis of prostaglai1dins,
the activity of these prodrugs relies on
leukotrienes, a11d PAF Glucocorticoids also
hepatic metabolic activity. They are not
inhibit the production of other mediators,
reconunended for use in aJ1imals with
including AA metabolites such as tl10se
hepatic insufficiency. Prednisone is
produced via COX activation (both COX-1
reported to have poor efficacy for treatment
a11d COX-2), cytokines, the interleukins,
of heaves in horses because it is poorly
adhesion molecules, and enzymes such as
absorbed, ai1d its active metabolite,
collagenase.

prednisolone, is rarely produced. By
contrast, prednisolone has good bioavail

Physiologic and Pharmacologic
ability and is reconunended in horses.

Effects: Peripherally and in the liver,

Other structural modifications allow
glucocorticoids have importaJ1t effects on
more lipophilic substai1ces to be obtained,
carbohydrate, protein, and lipid metabosuch as the introduction of an acetonide lism. In the periphery, glucocorttcoids
between C-16 and C-17 ( eg, triaincinolone
stimulate lipolysis and protein breakdown,
acetonide). Trian1cinolone acetonide, which releasing glycerol a11d aininu acids that act is not a prodrug of triaincinolone, can be
as substrates for gluconeogenesis. As a
used for intra-articular adn1inistration in
result, chronic exposure to excessive
horses to treat osteoarthritis or as a topical
glucoc01ticoids may lead to muscle wasting

2712

ANTI-INFLAMMATORY AGENTS
itM•iii RELATIVE POTENCIES OF COMMONLY USED CORTICOSTEROIDS

Relative

Relative

Duration of

Glucocorticoid Mineralocorticoid

Effecta (Alcohol

Compound

Activity

Activity

Form)

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Cortisol
l
s

Prednisone

5

0.8

Prednisolone

5

0.8

Methylprednisolone

5

0.5

Fludrocortisone

10

125

I

Isoflupredone

25

25

L

Triamcinolone

5

0

Triamcinolone

30

0
acetonide

Dexamethasone

25

0

L

Betamethasone

25

0

L

Flumethasone

120

0

L
a S = short (-12 hr), l = intermediate (-24 hr), L = long (-48--72 hr) and redistribution of body fat typical in

(ADH) secretion and decreased renal
animals with hyperadrenocorticism. In the
sensitivity to ADH. Glucocorticoids can
liver, glucocorticoids stimulate hepatic
increase renal excretion and decrease the
gluconeogenesis and increase the hepatic
intestinal absorption of calciW11, causing
synthesis and storage of glycogen. It is
depletion of calcitm1 stores. Glucocmtibelieved that gluconeogenesis is stimulated coids also inhibit osteoblasts, stimulate
through the transcription of enzymes such
osteoclasts, and increase parathyrnid
as glucose-6-phosphatase and phosphosecretion, which could affect bone healing.

enolpyrnvate carboxykinase. Glucocorti

A nwnber of mechanisms are responsible
coids also decrease glucose uptake in
for the anti-inflammatory and immunosupperipheral tissues, including adipose tissue pressive actions of glucocorticoids. In
and mammaiy glands, further contributing
homeostasis, glucocorticoids help maintain
to an increase in blood glucose. In daily
normal vascular permeability and microcil�
cattle, the reduction of milk yield is a major
culation ai1d stabilize cellular and lysosomal
mechanism of the glucose-sparing effect of
membranes. However, in acute inflan1macorticoids. In response to increased blood tion, glucocorticoids decrease vasculai·
glucose, there is a compensatory increase in
permeability and inhibit the migration and
insulin. However, glucocorticoids inhibit
egress of polyrnorphonuclear lymphocytes
the suppression of gluconeogenesis by
into tissues. Glucocorticoids suppress
insulin and cause insulin resistance in
cell-mediated inmmnity by mducing
peripheral tissues, further contributing to
apoptosis in nonnal lymphoid cells;
hyperglycemia.

inhibiting the clonal expansion ofT and

Although not as potent as the rnineralo

B lymphocytes; and reducing the number
corticoid aldosterone, nonfluorinated
of circulating eosinophils, basophils, and
glucocorticoids (prednisolone ai1d
monocytes. In contrast, glucocorticoids
methylprednisolone) do have some effects
inhibit margination of neutrophils and
on water and electrolyte balance, enhancincrease the release of matw-e neutrophils ing potassiwn excretion and sodiw11
from the bone marrow. Inflamed tissue,
retention primarily due to their activity in
phagocytosis, and toxic oxygen-free radical
the kidneys. Fluorinated corticoids,
production ai·e inhibited in macrophages
provided that they are substituted at C-16
ai1d monocytes. In the later stages of
as in dexamethasone and triamcinolone,
inflammation, glucocmticoids inhibit the
have no mineralocorticoid activity but
activity of fibroblasts, reducing fibrosis
rather exe1t a polyuric/polydipsic effect
and the fom1ation of scar tissue. However,
due to an inhibition of antidiw-etic hormone they may also slow wound healmg.

ANTI-INFLAMMATORY AGENTS

2713

Glucocorticoids modulate the synthesis
albwnin. Only the unbound p01tion is
and release of a nwnber of chemical
available to exert physiologic and pharmamediators of inflammation, including cologic effects and to cross physiologic
prostaglandins, leukotrienes, histamine,
barriers such as the blood-brain barrier or

VetBooks.ir
cytokines, complement, and PAF; they also
the udder. Generally, glucocorticoids are
suppress the production of inducible NO
metabolized in the liver, where they are
synthase and chondrodestructive enzymes
reduced and conjugated, forming inactive
such as collagenase.

water-soluble derivatives excreted by the

Glucoc01ticoids have effects on other
kidney.

hormone systems. All anti-inflammatory
glucocorticoid drugs in use today inhibit the Adverse Effects: Adverse effects of HPAA, which can result in clinically
glucoco1ticoids conunonly result from the
significant adverse effects when stopping
longterm use of supraphysiologic doses to
a prolonged corticoid treatment.

control inflanunatory or immunologic
disorders. Longte1m administration may
lead to iatrogenic Cushing syndrome,

Administration and Pharmacokinetics:

characterized by polyuria, polydipsia,

Steroid formulations are available for oral,
bilaterally symmetric alopecia, increased
parenteral, and topical use. Many, including
susceptibility to infection, muscle atrophy,
preclnisone, prednisolone, methylprednisoand redistribution of body fat. The lone, and dexarnethasone are well absorbed
gluconeogenic and insulin antagonistic
when administered PO and are particularly
effects of glucoc01ticoids may precipitate
useful when anti-inflanunatory treatment is
the onset of diabetes mellitus or exacerbate
required for a period of one to several
diabetes in animals with existing disease.

weeks. Other preparations are available for

Longterm suppression of the HPAA may
parenteral use. The sodiwn phosphate and
cause adrenal gland atrophy and resultant
succinate salts are highly water soluble,
iatrogenic secondary hypoadrenocorticism.

providing a rapid onset of action when given In affected anin1als, abrupt discontinuation IV Other i.r\jectable fonnulations include
of glucocorticoid therapy may lead to an
insoluble esters such as methylpredniso

Addisonian-like crisis characterized by
lone acetate and triamcinolone acetate,
lethargy, weakness, vomiting, and diarrhea.

which have limited water solubility. The

In severe cases, circulatory shock and deatl1
systemic absorption from these preparamay result.

tions is very slow and may result in

Glucocorticoids induce glycogen
anti-inflan1matory effects and associated
accun1ulation in hepatocytes, resulting

HPAA suppression for several weeks.

in hepatopathy and hepatomegaly, and

Corticosteroid preparations available for
stimulate production of the steroid-specific
topical or intralesional administration can
isoenzyme of alkaline phosphatase. Slow
be effective in treating inflammation of the
turnover of enterocytes and inllibition
skin, eyes, or ears. Although controversial,
of protective prostaglandins in the gut
intra-articular administration of glucocortidue to glucocorticoids may contribute to coids has been used in people and animals,
development of GI ulceration. Furtherparticularly horses, to manage inflammamore, glucoc01ticoids potentiate tl1e tory joint disease. In horses, for intra-articuulcerogenic effects of NSAIDs. Glucocortilar administration, triamcinolone acetonide coids reduce collagen synthesis and may
is preferred over rnethylprednisolone
lead to thinning and increased fragility of
acetate. Glucocorticoids are absorbed
the skin. Alterations in fluid and electrolyte
systemically from sites of local administrabalance may result in sodium and fluid tion in amounts that may be sufficient to
retention and hypokalemic alkalosis. In
suppress the HPAA.

horses, high doses of glucocorticoids may

Following absorption, -900A, of cortisol
induce or exacerbate lan1initis. Significant
is reversibly bound to plasma proteins,
mood and behavioral changes have been
primarily corticosteroid-binding globulin
described in people receiving co1ticosteroid

(CBG) and albumin. Among synthetic
therapy and may be seen in animals as well.

c01ticoids, only prednisolone binds

Although inununosuppression may be a
specifically and with high affinity to CBG.

desired effect of glucoc01ticoid therapy in

Prednisolone can displace cortisol from its
autoimmune disease, susceptibility to

CBG binding site, explaining the immediate
infection may increase, or latent infections
decrease of plasma cortisol after prednisomay be reactivated. Urinary tract infections lone is administred IV, a decrease not
are common in animals receiving glucocorassociated with HPAA inhibition. Other ticoids for longterm therapy of inflarnmasynthetic corticoids are mainly bound to tory or immunologic disease. In joints,

2714

ANTI-INFLAMMATORY AGENTS
glucocorticoids may reduce the fonnation

NSAIDs in companion animals being
of chondrocyte collagen and synovial fluid
routine. NSAIDs have the potential to
and contribute to the development of septic
relieve pain and inflammation without the
arthritis. Strict aseptic technique must be
myriad potential metabolic, hemodynamic,

VetBooks.ir
observed when administering intra-articular and inlmunosuppressive adverse effects injections of steroids.

associated with corticosteroids. However,

The adverse effects oflongtenn (>2 wk)

all NSAIDs have the potential f or other
glucocorticoid therapy can be diminished
adverse effects that should be considered in
using an alternate-day treatment regimen.

overall management of the inflan1matory

Once inflan1mation has been controlled
process.

using daily therapy with a drng that has
intern1ediate duration of activity ( eg, oral

Mode of Action: Generally, the
prednisolone or prednisone ), a gradual
classification NSAID is applied to drngs that
change to alternate-day therapy can be
inhibit one or more steps in the metabolism
made.

of arachidonic acid (AA). Unlike corticosteroids, which inhibit nun1erous pathways, Therapeutic Uses: Short-acting soluble

NSAIDs act primarily to reduce the
steroids such as the succinate esters have
biosynthesis ofprostaglandins by inhibiting
been routinely used in the treatment of
cyclooxygenase (COX). ln general, NSAIDs
septic shock, but this indication is
do not inhibit the formation of 5-lipoxygecontroversial. The action of corticoids on nase (5-LOX) and hence leukotriene, or the
hemorrhagic and cardiogenic shock is not
fonnation of other inflanunatory mediators.

established, even though product labeling

The novel NSAID tepoxalin is an exception
includes this use as an adjunct to fluid
in that it inhibits both COX and 5-LOX.

therapy. Glucocorticoids are also routinely

The discovery of the two isoforms of COX
used in the treatment of cerebral edema,

(COX-1 and COX-2) has led to greater
although controlled clinical trials supportunderstanding of the mechanism of action ing their effectiveness are lacking.

and potential adverse effects of NSAIDs.

Glucocorticoids are used commonly to

COX-1, expressed in virtually all tissues of
treat allergy and inflammation such as
the body (eg, gut and kidney), catalyzes the
prruitic dennatoses and allergic lung and GI
formation of constitutive prostaglandins,
diseases. ln acute cases of atopic or flea
which mediate a variety of nonnal
allergy dern1atitis, anti-inflan1matory
physiologic effects, including hemostasis,
dosages (prednisolone, 0.5-1 mg/kg/day)

GI mucosa! protection, and protection of
alleviate p.ru.ritus and limit self-trauma from
the kidney from hypotensive insult. In
scratching until the underlying cause can be
contrast, COX-2 is activated in damaged
addressed. Similar dosages are used in the
and inflamed tissues and catalyzes the
management of ctu·onic allergic bronchitis
fonnation of inducible prostaglandin,
and feline asthn1a. Short-acting corticosteincluding PGE
roids have also been used in treatment of

2, associated with intensifying
the inflammatory response. COX-2 is also
acute respiratory distress syndrome in
involved in thennoregulation and the pain
cattle and chronic obstrnctive pulmonary
response to injury. Therefore, COX-2
disease in horses. Historically, corticosteinhibition by NSAIDs is thought to be roids have been used to treat several
responsible for the antipyretic, analgesic,
musculoskeletal disorders, including
and anti-inflammatory actions of NSAIDs.

osteoarthritis, myositis, and in1mune

However, concurrent inhibition of COX-1
mediated arthritis. More recently, the
may result in many of the unwanted effects

NSAIDs have become first-line therapy for
of NSAIDs, including gastric ulceration and
musculoskeletal disorders, particularly in
renal toxicity. Because NSAIDs vary in their
the treatment of osteoarthritis in companability to inhibit each COX isoforn1, a dntg ion animal species. ln most inflan1matory
that inhibits COX-2 at a lower concentration
conditions, glucocorticoids should be used
than that necessary to inhibit COX-1 would
in cortjunction with therapies that target the
be considered safer. This concept has
underlying cause.

propelled the development of the "COX-2
selective" NSAIDs. Although ratios of

COX-1:COX-2 inhibition by various NSAIDs

NONSTEROIDAL ANTI
in people and animals have been reported,

INFLAMMATORY DRUGS
caution is advised when interpreting such
ratios, because they vary greatly depending

The in1po1tance of pain management and
on the selectivity assay used. The COX
the use ofNSAIDs in animals has increased
selectivity of NSAIDs also varies by species;
dramatically in recent decades, with use of

COX selectivity ratios reported for people

ANTI-INFLAMMATORY AGENTS

2715
cannot be directly extrapolated to other
damage. As analgesics, they are generally
species.

less effective than opioids and are therefore

In general, drugs with ratios suggesting
generally indicated only against mild to
preferential activity against COX-2 may
moderate pain in people. However, in

VetBooks.ir
have fewer adverse effects due to COX-1
veterinary medicine, NSAlDs also find use
inhibition. ln dogs, favorable ratios have
in management of severe pain, optin1ally in
been reported for carprofen, meloxicam,
combination with an opioid.

deracoxib, firocoxib, and robenacoxib,

As antipyretics, NSAlDs reduce body
whereas unfavorable ratios have been
temperature in febrile states. Although the
repo1ted for aspirin, phenylbutazone, and
beneficial effects of the febrile response
vedaprofen. COX-I-sparing drugs are
usually outweigh the negative effects,
associated with less GI ulceration and less

NSAlD inllibition of PGE2 activity in the
platelet inhibition; however, it may be an
hypothalanms may provide symptomatic
oversimplification to assume that complete
relief and improve appetite. In Europe,

COX-2 inhibition is without potential risk.

NSAlDs have been used in conjw1ction with

R ecent research has suggested that COX-2
antibiotics for treatment of acute respiracan be induced constitutively in valious tory diseases in cattle. They may reduce
organs, including the brain, spinal cord,
morbidity through their antipyretic and
ovary, and kidneys. In dogs, COX-2 mRNA
anti-infla.111matory effects and prevent
is present in the loop of Henle and the
development of irreversible !W1g lesions.

maculae densa and may play an important

The effects of some NSAIDs on chondrorole in the protective response to hypotencyte metabolism have been investigated.

sion. However, a study that failed to

Some, including aspirin, naproxen, and
demonstrate COX-2 expression in canine
ibuprofen, are considered chondrotoxic,
kidneys raised questions regarding its role.

because tl1ey inhibit the synthesis of

COX-2 also appears to be important in the
cartilage proteoglycans. Others, including
healing of GI ulcers in people, and certain
carprofen and meloxicain, may be

COX-2-specific inhibitors delay ulcer
considered chondroneutral, or depending
healing experimentally. Although COX-1
on dose, actually stimulate the production
plays a primary role in regulating homeostaof cartilage matrix. The potential beneficial sis, it may play a more significant role in
or deleterious effects of NSAlDs on
inflammation than originally proposed.

chondrocyte metabolism remain to be

NSAlDs enter the pocket of the COX
clarified.

enzyme, whereupon steric hindrance

A therapeutic area in which NSAID use
prevents entry of AA. Aspirin is unusual in
may become impo1tant is in the treatment
that it irreversibly acetylates a.serine
a.11d prevention of cancer. Epidemiologic
residue of COX, resulting in a complete loss
studies in people show that aspirin ttse is
of COX activity. Thus, the duration of the
associated with a significant reduction in
aspilin effect depends on the turnover rate
the incidence of colon cancer. Newer
of COX; activity is lost for the life of the
evidence suggests that the therapeutic
platelet (7-10 days) after aspilin administraeffect of NSAIDs on colon cancer is tion, explaining the duration of aspirin's
mediated by inllibition of COX-2, which may
effect on hemostasis. Unlike aspirin, most
be upregulated in many premalignant and
other NSAlDs (including salicylic acid, an
malignant neoplasms. In veterinary
active metabolite of aspirin) are reversible
medicine, piroxicam has been shown to
competitive COX inhibitors; their duration
reduce the size of tumors such as transiof inhibition is primarily detem1ined by the tional cell carcinoma in dogs. Specific
elimination pharmacokinetics of the drug.

COX-2 inhibitors may prove useful as a
primaiy or adjunctive therapy in the

Pharmacologic Effects: All NSAlDs,
management of cancer.

except for acetaminophen ( also nan1ed
paracetamol), are antipyretic, analgesic,

Administration and Pharmacokinetics:

and anti-inflammatory. They are routinely

Most NSAlDs are weak orgailic acids that
used for the relief of pain and inflan1mation
are well absorbed after PO administration.

associated with osteoarthlitis in dogs and

However, food can impair the oral
horses and for colic, navicular disease, and
absorption of some NSAlDs ( eg, phenyllaminitis in horses. The use ofNSAlDs for butazone, meclofenamate, flunixin, and
the relief of perioperative pain in companrobenacoxib ). Several NSAlDs arc available ion animals is standard practice. ln general,
as parenteral formulations for IV, IM, or SC

NSAlDs provide only symptomatic relief
administration. Some parenteral formulafrom pain and inflanm1ation and do not tions are highly alkaline ( eg, phenylbutasignificantly alter tl1e course of pathologic zone) and may cause tissue necrosis if

2716

ANTI-INFLAMMATORY AGENTS
injected perivascularly. Once absorbed,
and melena. Horses may develop oral,
most NSAIDs are extensively ( up to 9go1o)

lingual, or colonic ulceration v.>ith
bound to plasma proteins, with only a small
accompanyi.J.1g signs of colic, weight loss,
proportion of unbound drug available to
and diarrhea.

VetBooks.ir
be active in the tissues. NSAIDs may also

GI blood loss may be fUither complicated
compete for binding sites with other highly
by impaired platelet function; NSAIDs, by
protein-bound compounds, leading to some
mhibiting COX-1, prevent platelets from
drug displacement; however, this displacefom1ing TXA2, a potent aggregatillg agent.

ment has little therapeutic consequence

Because TXA2 inhibition causes prolonged
because it does not affect the concentration
bleeding, evaluation of buccal mucosa!

of the free drug. Because NSAIDs are highly
bleeding ti.J.ne is advised in ani.J.nals for
protein bound and extravasation of protein
which surgery is anticipated. Blood
occurs in inflanunation, NSAIDs tend to
dyscrasias after longtenn NSAID therapy
concentrate in areas of inflammation.

have been repmted i.J.1 cats, dogs, and

Consequently, their duration of action
horses. Acetaminophen (paracetamol)

typically exceeds that predicted by
admmistration in cats is associated with
elimination half-life.

Heinz body anemia, metl1emoglobillemia,

Most NSAIDs are biotransformed in
hepatic failure, and death. Bone marrow
the liver to inactive metabolites that are
dyscrasias associated with phenylbutazone
excreted either by the kidney via glomeruadministration have also been reported.

lar filtration and tubular secretion or by the

Nephropathies associated with chronic
bile. Mavacoxib is an exception, mostly

NSAID use are common in people. Animals
being excreted unchanged in the bile.

with underlymg renal compromise receiving

Biotransfonnation and eli.J.nination half

NSAIDs could experience exacerbation or
lives vary significantly by species ( and in
decompensation of their disease. It is imporsome cases by breed or strain, as is the case tant to maintain hydration and renal
for some COX-2 inl1ibitors in Beagles), so it
perfusion ill ani.J.nals receiving NSAIDs,
is not possible to safely extrapolate dosages
especially tl10se undergoing anesthesia or
from one species or ani.J.nal to another.

surgery and in horses with colic.

Some NSAIDs, including naproxen,

Hepatopathies are relatively cmru11on in
etodolac, and rneclofenan1ic acid, undergo
people and ani.J.nals receivi.J.1g NSAIDs.

extensive enterohepatic recirculation in

NSAID administration routillely induces
some species, resulting in prolonged
mild hepatic changes characterized
elimillation half-lives.

primarily by increases ill liver enzymes
without clinical signs or hepatic dysfunc

Adverse Effects: All NSAIDs have the
tion. Rare reports of idiosyncratic reactions
potential to induce adverse reactions, some
resultmg in hepatic dysfunction or failure
of which can be life threatenillg. Many
have been reported in people ( acetfilllllloreactions to NSAIDs are dose-related and phen and others), dogs (acetanlmophen,
are typically reversible with discontinuation carprofen, etodolac), and horses (phenylof therapy and supportive care.

butazone). Cytopathic (hepatocellular

Vomiting is the most common adverse
injury, necrosis), cholestatic, and mixed
effect. GI ulceration is the most conunon
histopathologic patterns of injwy have been
life-th.reatenmg adverse effect. Loss of GI
documented. NSAIDs should be used with
protective mechanisms results from
caution in animals with preexisting hepatic
inl1ibition of constitutive prostaglandins
disease.

that regulate blood flow to the gastric
mucosa and stillrnlate bicarbonate and
mucus production. This disrupts the

Specific Nonsteroidal Anti
al kalille protective barrier of t11e gut,
inflammatory Drugs
allowing diffusion of gastric acid back illto

Based on structure, most NSAIDs can be
the mucosa, illjurillg cells and blood vessels
divided mto two broad groups: carboxylic
and causing gastritis and ulceration. As
acid and enolic acid derivatives. The main
organic acids, NSAIDs, especially aspirin,
subgroups of enolic acids are the pyrazomay also cause direct chemical irritation lones (phenylbutazone) and the oxicams
of the GI mucosa. The enterohepatic

(meloxicam, piroxicam). Carboxylic acid
recirculation of certain NSAIDs may result
subgroups include the salicylates (aspirin),
in high biliary concentrations that increase
propionic acids (ibuprofen, naproxen,
ulcerogenic potential in the gut. NSAIDcarprofen, ketoprofen, and vedaprofen), illduced GI bleeding may be occult, leading
fenemates (tolfenamic and meclofenamic
to iron-deficiency anemia, or be more
acids), phenylacetic acids (acetan1inophen),
severe, resulting in vomiting, hematemesis,
and aminonicotmic acids (fluni.xin). The

ANTI-INFLAMMATORY AGENTS

2717
newer coxib class of selective COX-2
salicylates slowly. In addition, salicylate
inhibitors includes a diaryl-substituted
metabolism is saturable and, if overexpopyrazole ( celecoxib) and a diaryl-substisure clue to an aspirin overdose occurs, tuted isoxazole (valdecoxib), both available
plasma salicylate elimination may follow a
for human use. Four NSAIDs of the coxib
zero order and slower elimination kmetics.

VetBooks.ir
class, deracoxib, firocoxib, robenacoxib,

The elimination half-life of salicylic acid in
and mavacoxib have been introduced in
cats approaches 40 hr, whereas it is -7.5 hr
veterinary medicine.

in clogs.

Because aspirin is not approved for

Aspirin: By far the most widely used
veterinary use, definitive efficacy studies

NSAID in people, aspirin is primarily used
have not been performed to establish
in veterinary medicine for relief of mild to
effective dosages. Recon1111endecl dosages
moderate pain associated with musculoin dogs are l�O mg/kg, PO, bid-tid. Aspirin skeletal inflammation or osteoaithritis.

has been used for its anti clotting effect i..!1

The salicylic ester of acetic acid, aspirin
the treatment of laminitis in horses at a

(acetylsalicylic acid) is available in several
dosage of 10 mg/kg/day, PO. In cats, aspirin
different dosage forms, including bolus (for
may be used for its antiplatelet effects in
cattle), oral paste (for horses), oral solution
thromboembolic disease at a dosage of 10

(for poultry), and tablets (for dogs).

mg/kg, PO, every 48 hr, to allow for

Enteric-coated products used in human
prolonged metabolism. Adverse effects are
medicine are not reconunended in dogs,
conunon after aspirin administration and
because gastric retention may lead
appear to be dosage dependent. Even at
to erratic plasma exposure. After PO
therapeutic dosages of 25 mg/kg, plain
administration, aspirin is rapidly absorbed
aspirin may induce mucosa! erosion and
from the stomach and upper small intestine.

ulceration in clogs. Vomiting and melena

Aspirin is subjected to a large, first-pass
may be seen at higher closes. The PGE,
effect in the liver to yield salicylic acid,
analogue misoprostol may decrease GI
its main active metabolite. In addition, the
ulceration associated wiU1 aspirin and other
aspirin fraction that gains access to the

NSAIDs. Aspirin overdose in any species
systemic circulation is also rapidly
can result in salicylate poisoning, characterhydrolyzed to salicylic acid with a half-life ized by severe acid-base abnonnalities,
of -15 min. After oral aspirin administrahemorrhage, seizures, coma, and death.

tion, salicylic acid is considered the main
active substance in the systemic circulation.

Acetaminophen: Acetaminophen

Aspirin prin1arily inhibits COX-1, whereas

(paracetan10l) is a para-aminophenol
salicylic acid has more balanced COX-1/
derivative with analgesic and antipyretic

COX-2 activity. In addition, aspirin may
effects sin1ilar to those of aspirin, but it has
irreversibly bind to COX-1 through
weaker anti-inflan1111atory effects than does
acetylation of a serine residue near the
aspirin and other NSAIDs. The reason for
enzyme active site. Because of this
this anomaly is that acetanlmophen 's
irreversible binding, the anticoagulant
selective COX-2 inhibition is via enzyme
activity of aspirin lasts far longer than its
reduction; the high levels of peroxides in
anti-inflan1111atory effect; a single aspirin
areas of inflan1111ation are thought to
dose of 20 mg/kg in a horse may prolong
interfere with COX-2 reduction peripherally,
bleeding for 48 hr. Depending on its route of
whereas the low peroxide levels in the brain
administration, aspirin may have different
and spinal cord account for any centrally
pharmacologic effects. For ineversible
mediated analgesia. Acetaminophen does
platelet COX-1 inhibition (to treat a thromnot inhibit neutrophil activation, has little boembolic condition), aspirin given IV is
ulcerogenic potential, and has no effect on
more efficient than aspirin given PO
platelets or bleeding time. The recombecause, for the same dose, aspirin mended dosage of acetaminophen in dogs
exposure is greater for the IV route of
is 10-15 mg/kg, PO, tid. Dose-dependent
administration.

adverse effects include depression,

After absorption, both aspirin and
vomiting, and methemoglobinemia. Use in
salicylate are widely distributed through
cats is contraindicated because of their
most tissues and fluids and readily cross the
deficiency of glucuronyl transferase, which
placental barrier. Approximately 80"1<>-90"A, makes them susceptible to methemoof salicylate is bound to plasma proteins.

globinemia and centrilobular hepatic

Metabolism and eli..rnination is via hepatic
necrosis.

conjugation with glucuronic acid, foJJowed
by renal excretion. Cats, which lack

Phenylbutazone: One of the earliest
glucuronyl transferase, metabolize

NSAIDs approved for use in horses and

2718

ANTI-INFLAMMATORY AGENTS

5-7 days in horses and 1.1 mg/kg/day for 5-7
days in dogs. In cattle, administration of
meclofenamic acid results in a biphasic
pattern of absorption, with an initial peak

VetBooks.ir
plasma concentration reached at -30 min
and a secondary peak 4 hr after dosing.

In horses, meclofenamic acid is rapidly
absorbed, but feeding before dosing may
delay absorption. The onset of action is
slow, requiring 2-4 days of dosing for a
clinical effect. Although it is effective in the
treatment of chronic laminitis, meclofenamic
acid has a therapeutic index that may be
lower than that of other NSAIDs.

Phenylbutazone toxicity, right dorsal colitis
in a horse (ultrasound). Courtesy of Dr. Sameeh

M. Abutarbush.

Tolfenamic Acid: Tolfenamic acid is an
anthranilic (fenemate) NSAID class
approved for use in Europe and other
count1ies. It is used for fever, postoperative
dogs, phenylbutazone (PBZ) is a pyrazolone
pain, and acute and chronic inflanmiatory
derivative available in tablet, paste, gel, and
conditions in cats, dogs, cattle, and pigs.

parenteral fo1rnulations. The plasma
halt�life of PBZ is 5-6 hr in horses and dogs

Flunixin: In the USA, the nicotinic acid
and >30 hr in cattle (a reason that PBZ is not
derivative flunixin (as the meglumine salt) is
approved for use in cattle). When given PO,
approved for use in horses as PO and

PBZ adsorbs to hay in the diet, to then be
parenteral fonnulations. The recommended
released during fermentation in the hindgut.

dosage is 1.1 mg/kg/day for 5 days, IV or PO.

Although this potentially may reduce GI

Flunixin is rapidly absorbed after PO or IM
absorption and bioavailability, the clinically
administration, and tl1e elimination hal f -life
relevant effect is a delay in absorption. Once is short (-2--3 hr). Elinlination is primarily absorbed, binding to plasma proteins is high
by renal excretion. Flunixin is effective for

(99%in horses). PBZ is metabolized by the
the treatment of visceral pain associated
liver to several active (oxyphenbutazone)

with colic in horses. It is also used to reduce
and inactive metabolites, which are
the inflammatory-mediated hemodyna.mic
excreted in urine. One of the major
response to endotoxin, although it is
therapeutic uses of PBZ is to treat acute
w11ikely to reduce mortality associated witl1
laminitis in horses. Laminitis is treated
endotoxemic shock. The dosage recominitially with iajectable PBZ at dosages up to mended in horses is 1.1 mg/kg, bid, or 0.25

8.8 mg/kg, followed by therapy PO at 2.2-4.4
mg/kg, tid. Toxicity in horses is rela-
mg/kg, bid. Because the therapeutic index
tively uncommon, but GI ulceration and
for PBZ is relatively narrow (PBZ exhibits
erosion may develop. Flunixin has been
zero order metabolism), the dosage should
used to treat mastitis and acute puhnonary
be adjusted to the minimum possible to
emphysema in cattle, although it is not
maintain comfort and avoid toxicity. GI
approved for these indications. Chronic
effects ( eg, anorexia) and depression are
adnlinistration of flunixin to dogs may result
the most frequent adverse effects associin severe GI ulceration and renal dan1age.

ated with PBZ. Ulcers may develop in the

Flunixin is not marketed in the USA for
mouth, stomach, cecum, and right dorsal
dogs, but it is approved in Europe and other
colon. The ulcerogenic potential of PBZ in
countries.

horses is greater than that of flunixi.n and
ketoprofen. PBZ dosages of3-7 mg/kg, PO,

Carprofen: Carprofen is an NSAID of
tid, are recommended in dogs. In dogs, PBZ
tl1e arylpropionic acid class available in
has been associated with bleeding
the USA in caplet and chewable tablet
dyscrasias, hepatopathies, nephropathies,
formulations. An injectable fom1ulation
and rare cases of irreversible bone marrow
is also available in the USA and Europe.

suppression.

Carprofen is approved by the FDA to
manage pain and i.nflan1mation associated

Meclofenamic Acid: Mcclofenanlic acid
with osteoarthritis and acute pain
is a fenemate (anthranilic acid) NSAID
associated with soft-tissue and orthopedic
available for horses as a granular preparasurgery in dogs. The reconunended dosage tion and for dogs as an oral tablet. The
is 4.4 mg/kg/day or divided bid, PO. In
recommended dosage is 2.2 mg/kg/day for

Europe and other cow1tries, carprofen is

ANTI-INFLAMMATORY AGENTS

2719
also registered for use in horses and cattle
potent inhibitor of COX and bra.dykinin and
and for short-term therapy in cats. In dogs,
may also inhibit some lipoxygenases. Its
oral bioavailability is high (9QOA,), and plasma efficacy is comparable to that of opioids in concentrations peak -2-3 hr after dosing.

the management of pain after orthopedic

VetBooks.ir

The elin1ination half-life is -8 hr. As with
and soft-tissue surgery in dogs. After
other NSAIDs, carprofen is highly (99%)

administration PO, ketoprofen is rapidly
protein bound. Elintlnation is via hepatic
absorbed and has a tenninal half-life in ca.ts
biotransfom1ation, with excretion of the
and dogs of 2--3 hr. As with other NSAIDs,
resulting metabolites in feces and urine.

ketoprofen is metabolized in the liver to

Some enterohepatic recycling occurs. The
inactive metabolites that are eliminated by
exact mechanism of action of carprofen
renal excretion. Adverse effects, including
is unclear. Although it has greater selectivity GI upset, a.re sim ila.r to those of other for COX-2 over COX-1, carprofen is

NSAIDs. Other adverse effects, including
considered a weak COX inhibitor. In vitro
hepatopa.thies and renal disease, have been
assays with canine cell lines indicate that
repo1ted in a.ninlals. Because of potential
it is 129-fold more selective for COX-2,
antipla.telet effects, ca.re should be
whereas in vitro assays with canine whole
exercised when using ketoprofen periblood indicate that it is 7-to 17-fold more opera.tively.

selective for COX-2. Equine whole blood
assays indicate that it is 1.6-folcl more

Etodolac: The pyranoca.rboxylic acid
selective for COX-2, and feline whole blood
etoclola.c is approved for use in dogs in the
assays indicate it is >5.5-folcl more selective

USA. The elintlna.tion half-life is -8-12 h.r,
for COX-2. Other mechanisms of action,
allowing closing at 10-15 mg/kg/day, PO.

including inhibition of PA,, may be

Extensive enterohepa.tic recirculation
responsible for its anti-inflammatory
has been reported in clogs, followed by
effects. Ca.rprofen has been used extenelimination of etodola.c and its metabolites sively in clogs since its introduction, and
in the liver and feces. In in vitro studies,
adverse events have been comparable to
etodolac was more selective in inhibiting
those of other NSAIDs (ie, -2 events/1,000

COX-2 than COX-1, although in vitro canine
clogs treated). Approxinlately one-fourth
whole blood assays have also shown it to be
of the adverse reactions reported were GI
nonselective. Etodola.c has been shown to
signs, including vomiting, diarrhea, and
inhibit macrophage chemota.xis and has

GI ulceration. Renal and hepatic adverse
demonstrated efficacy for the treatment
effects a.re rare, as with other NSAIDs.

of la.meness associated with hip dysplasia..

Potentially se1ious idiosyncratic hepatopa

Although the risk of GI ulceration is low
thies, characterized by a.cute hepatic
at therapeutic doses, ad.ministration of
necrosis, have been reported in some
three ti.mes the label dosage resulte-d in
clogs. Approxin1a.tely one-third of the clogs

GI ulceration, vomiting, and weight loss
developing hepa.topa.thies while receiving
in toxicity studies. GI, hepatic, and renal
ca.rprofen were La.bra.clor Retrievers,
adverse reactions have been reported after
although a true breed predisposition has
administration of etodola.c, similar to those
not been established. As with any NSAID
of other NSAIDs.

therapy, clinical laboratory monitoring for
hepatic claniage is advised, especially in

Vedaprofen: The a.rylpropionic acid
geriatric a.ninlals that may be predisposed
de1iva.tive veda.profen is available in Europe
to more serious complications.

in a gel fo1mula.tion for horses and dogs and
in an iltjectable fomrnlation for horses.

Ketoprofen: Ketoprofen is another

Vedaprofen is indicated for the treatment
propionic acid derivative available in the
of pain and inflammation associated with

USA and other countries as a l()OA, iltjectable
rnusculoskeletal disorders in dogs (0.5 mg/
solution for horses, and in Europe and
kg/day) and horses (1 mg/kg, bid) and for

Canada as tablets and a. l % iltjectable
the treatment of pain associated with colic
solution for dogs and cats. Ketoprofen is
in horses (2 mg/kg, IV, as a single injection).

recommended for acute pain (up to 5 clays)

After administration PO, vedaprofen is
in both clogs and ca.ts. In horses, it is used
rapidly absorbed. Bioa.vaila.bility is
for pain and inflammation associated with
generally high but may be reduced if the
osteoarthritis and for visceral pain
drug is administered with food. The
associated with colic. The recommended
terminal half-life is 10-13 hr in dogs and
dosage is l mg/kg/day for up to 5 days, IV

6--8 hr in horses. Vedaprofen undergoes
or PO, in clogs and ca.ts; 2.2 mg/kg/day for up extensive biotransfonna.tion to hydroxyto 5 days, IV, in horses; and 3 mg/kg/day for la.ted metabolites, which a.re excreted in

1--3 days, IV or IM, in cattle. Ketoprofen is a
urine and feces.

2720

ANTI-INFLAMMATORY AGENTS

Meloxicam: Meloxicam is an oxicam
a!Jowing dosing at 5 mg/kg/day, PO.

NSAlD available as an oral syrup and

COX-1:COX-2 ratios from in vitro canine
injectable solution. It is approved for human whole blood assays indicate it is 384-fold use in the USA and Canada and for use in
more selective for COX-2. As with other

VetBooks.ir
dogs in the USA. In Europe and other

NSAlDs, protein binding is high, at -96%.

cow1tries, it is approved for use in dogs,

GI safety appeai-s to be greater than that
cats, cattle, and horses. A potent inhibitor
of nonspecific NSAlDs.

of prostaglandin synthesis, meloxicarn is
used for the treatment of acute and chronic

Robenacoxib: Robenacoxib is a
inflammation associated with musculoskelcoxib-class highly selective COX-2 inhibitor, etal disease and for the management of
structura!Jy related to the human NSAlDs
postoperative pain. In dogs, a one-time
cliclofenac and !W1tiracoxib. Robenacoxib is
loading dose of 0.2 mg/kg, PO, is recomused for the control of pain and inflammamended, followed byO.l mg/kg/day, PO.

tion associated with osteoarthritis,

Once a therapeutic effect is seen, the dosage mthopedic and soft-tissue surge1y in clogs can be titrated to the lowest possible dose.

(approved in Europe), and for musculoskel

COX-I :COX-2 ratios reported for meloxietal disorders and soft-tissue surgeries in can1 suggest the drug is COX-2 selective,
cats (approved in the USA and Europe).

with in vitro canine whole blood assays

Dosage is 2 mg/kg, PO, initially and then
indicating it is 2. 7- to 10-fold more selective

1-2 mg/kg/day thereafter (for up to 6 days
for COX-2. Once absorbed, meloxicam is
in cats). COX-l :COX-2 ratios from in vitro
highly protein bound (97%) and has a
canine whole blood assays indicate it is
relatively Jong elin"lination half-life (>12 hr).

128-folcl more selective for COX-2. As with

GI safety appears to be greater for
other NSAlDs, protein binding is high, at
rneloxican1 than for nonselective NSAlDs,

-98%. GI safety appeai-s to be greater than
and meloxica.m has been shown to be
that of nonselective NSAIDs. The eliminachondroneutral in rodent studies.

tion half-life is l hr after oral administration.

Adn"linistration with food decreases

Deracoxib: Deracoxib, the first NSAID of
bioavailability of robenacoxib.

the coxib class approved for use in dogs, is
available in a beef-flavored chewable tablet

Mavacoxib: Mavacoxib is a coxib-class
fommlation in the USA. Deracoxib has been

COX-2 inhibitor approved in Europe and
shown to inhibit COX-2-rnediated PGE,

Australia for the control of pa.in and
production. COX-1:COX-2 ratios repmted
inflan1mation associated with degenerative
for deracoxib in in vitro cloned canine ceU
joint disease in dogs. Mavacoxib is
assays indicate it is 1,275-fold more selective structura!Jy related to the human NSAlD
for COX-2, whereas ln vitro canine whole
celecoxib; however, substitution of a meiliyl
blood assays indicate it is 12- to 37-fold
group with a single fluorine a.torn has
selective for COX-2. Deracoxib is indicated
conferred great resistance to metabolism,
for the control of postoperative pain and
resulting in an elimination half-life of 17
inflammation associated with orthopedic
days in yoW1g Beagle dogs. Unlike the major
surgery at a dosage of 3-4 mg/kg/day for up
route of elimination of other NSAlDs, that of
to 7 days, PO, and for the control of pain and
mavacoxib is biliaiy excretion ofilie parent
i.nflanm1ation associated with osteoa.1thritis
molecule. In field t1ials conducted in aged
a.t a dosage of 1-2 mg/kg/day, PO. Once
dogs wiili osteoarthritis, ilie half-life was
absorbed, protein binding is >90%, and the
foW1d to be even longer at 44 days, and in
elimination half-life is 3 hr.

these older dogs, approxin1ately l in 20
exhibited a half-life of >80 days. These

Firocoxib: Firocoxib is a coxib-class
population phannacokinetic studies in

NSAID approved in the USA and Europe
target patients were used to optimize ilie
for the control of pain and inflammation
close regin1en. The long half-life means
associated with osteoaithritis and for the
mavacoxib has a tmique dose regimen: ilie
control of postoperative pain and inflanunainitial close is 2 mg/kg, PO, repeated 14 clays tion associated with soft-tissue and orthopelater; iliereafter, ilie closing interval is l mo, dic surgery in dogs. In Canada, Australia,
with the total coW"Se not exceeding seven and New Zealand it is approved for use in
closes (6.5 mo). Food significantly increases
osteoarthritis and soft-tissue and orthopebioavailability. COX-1:COX-2 ratios from in dic surgery. It is available in a chewable
vitro canine whole blood assays indicate
tablet formulation. After administration
mavacoxib is 128-fold more selective for

PO, firocoxib is rapidly absorbed and then

COX-2. As with oilier NSAIDs, protein
elin1inated by hepatic metabolism and fecal
binding is high, at -98%. GI safety appears to
excretion. The elimination half-life is -8 hr,
be greater ilian that of nonselective NSAIDs.

ANTI-INFLAMMATORY AGENTS

2721

The elimination half-life is 1 hr after oral
naproxen, dogs are extremely sensitive to
administration.

its adverse effects.

Coxib class drugs, including celecoxib

Tepoxalin: Tepoxalin is a dual inhibitor of
and valclecoxib, developed for use in hwnan
both cyclooxygenases (COX-1 and COX-2)

medicine are COX-2 selective. In clinical

VetBooks.ir
and 5-lipoxygenase (5-LOX). From a
studies, the incidence of GI ulceration in
mechanistic perspective, its LOX activity
patients receiving valclecoxib or celecoxib

(reduction of leukotriene production) may
was significantly less than that of those
reduce components of inflammation not
receiving naproxen. The use of these drugs
controlled by COX isoenzyme inhibition. It
in animals has yet to be fully investigated.

is available for dogs as an oral tablet. The

One pharmacokinetic study with celecoxib
initial dosage is 20 mg/kg, followed by a
in Beagles demonstrated variability in drug
maintenance dosage of' 10 mg/kg/day.

elinlination between clogs. In that study, one

Tepoxalin is rapidly absorbed and reaches
subgroup of Beagles metabolized celecoxib
peak plasma concentration 2-3 hr after
much more rapidly tl1an the other, wiU1
administration. Its plasma half-life is short
elimination hall�lives of -2 and 18 hr,

(2 hr), but it is metabolized to a carboxylic
respectively. Until fwther data are available
active metabolite (tepoxalin pyrazol acid)

regarding tl1e pharmacokinetics and safety
that has a long half-life (12-15 hr). The
of these drugs in animals, tl1eir use in
metabolite, tepoxalin pyrazol acid, lacks the veterinary medicine is not recommended.

LOX activity of the parent molecule. BoU1
tepoxalin and its actiVP metabolite are

CHONDROPROTECTIVE AGENTS
highly bound to plasma protein (98o/o-9goA,).

The most commonly reported adverse
effects are GI related (eg, dia.rrhea and

Polysulfated Glycosaminoglycan:

vomiting in -20% of dogs treated for 4 wk).

Polysulfatecl glycosaminoglycan (PSGAG)

is a semisynthetic glycosan1inoglycan

Other NSAIDs: A large number of
prepared from bovine tracheal cartilage and
prescription and nonprescription NSAIDs
composed of a polymeric chain of repeating
are available for human use. However,
clisaccha.ricle units. The primary glycosamibecause of species dilierences in metabonoglycan in PSGAG is chonclroitin sulfate.

lism, efficacy, and toxicity, many are not

PSGAG is approved for IM use in dogs and
recommended for use in animals. For
intra-articular and IM use in horses for the
example, in dogs, indomethacin is highly
control of signs associated wilh noninfectoxic to the GI tract and may result in severe tious degenerative or traumatic arthritis. In ulceration, hematemesis, and melena at
horses, tl1e recommended dosage is 500 mg,

U1erapeutic doses. Piroxicam undergoes

IM, every 4 days for 28 clays, or 250 nig by
extensive enterohepatic recycling in dogs,
intra-articular injection once weekly for 5
resulting in a prolonged plasma half-life. GI
wk. In clogs, the recommended dosage is
ulceration and bleeding and renal papillary

2 mg/lb, IM, twice weekly for up to 4 wk.

necrosis have been seen in dogs receiving

After IM ir\jection, PSGAG is absorbed into
piroxican1 at dosages of 0.3-1 mg/kg/day.

tile systemic circulation and eventually

Ibuprofen is an arylpropionic acid
incorporated into both healtlly and
derivative used in dogs as an anti-inflammadamaged cartilage. The exact mechanism of tory agent. However, dogs are much more
action is unknown, but in vitro studies show
sensitive to the development of GI adverse
that PSGAG inhibits PGE2 and catabolic
effects from ibuprofen administration than
enzymes such as stromelysin, elastase, the
are people. At therapeutic doses, adverse
metalloproteases, and otl1ers. PSGAG also
effects seen in dogs include vomiting,
increases the synthesis of hyalw·onic acid,
diarrhea, GI bleeding, and renal in.t'ection.

proteoglycan, and collagen in vitro. Toxicity

Ibuprofen is not recommended for use in
associated witll administration of PSGAG
dogs or cats.

has been minimal. Because PSGAG is

N aproxen has been used in horses at a
chemically similar to heparin, overdosage
dosage of 5-10 mg/kg, once to twice daily.

may inhibit coagulation, and conctUTent use

Bioavailability is lower ( -50%) for naproxen
of aspirin may prolong bleeding times. The
than for other NSAIDs, and the elimination
use of PSGAG is contraindicated in septic
half-life is -5 hr in horses. In dogs, the
joints.

elimination half-life of naproxen is 35---7 4 hr,
preswnably because of extensive enterohe

Pentosan Polysulfate Sodium:

patic recirculation. The pharmacokinetics

Pentosan polysulfate sodium (PPS) is
in dogs also appear to be breed dependent.

a polysulfate ester of xylan, a polymer

Because of the prolonged half-life of
prepared semisyntlletically from beech-

2722

ANTI-INFLAMMATORY AGENTS
wood plant material. PPS is chemically
lubricating function in joint movement. As
and structurally similar to heparin and
with other chondroprotective agents, the
glycosarninoglycan. The compound is
mode of action is m1cleai·. However,
approved by the FDA for use as an oral
because synovial fluid viscoelasticity is
capsule for the treatment of interstitial
decreased in osteoarthritis, the intra-articu

VetBooks.ir
cystitis in people. An injectable product is
lar administration of hyaluronan may
available for use in people, dogs, and horses
improve joint lubrication. Hyaluronan
in Australia and other countries. The mechainhibits PGE2 synthesis in vitro and in vivo nism of action is unknown. PPS stimulates
and may inhibit i.nflan1matory enzymes and
hyaluronic acid and GAG synthesis in
reduce pain. Most clinical use has been in
damaged joints, inhibits proteolytic
horses, in which it appears to have minimal
enzymes including metalloproteinases,
adverse effects.

and scavenges free radicals. PPS may also
decrease cytokine activity. In canine models

Orgotein: Orgotein is a wate1"soluble
of osteoarthritis, IM administration of PPS
metalloprotein containing copper and zinc.

significantly decreased overall ca.ttilage

Found in low concentrations throughout
damage. Because PPS has a hepa.t'in-like
the body, orgotein has superoxide
structure, coagulopathies may be seen. PPS
dismutase activity scavenging free oxygen
is given once a week for 4 consecutive
radicals. Orgotein, available as an injectable
weeks, then once every 6 or 12 mo.

fonnulation, has been used for treatment of
soft-tissue inflan1mation in horses and of

Hyaluronan: Hyaluronan (formerly
arthritis in dogs. Although it has been used
hyaluronic acid), a polydisaccharide of
as an IM or SC injection, orgotein is typically
glucuronic acid and glucosa.mine, is a
administered as an intra-articular injection,
component of synovial fluid and articular
because its large molecular size may limit
cartilage. In the USA, a purified fraction of
absorption via other routes. Intra-articular
the sodimn salt of hyaluronic acid extracted
administration is effective in cases of acute
from rooster combs is available for
lameness in horses, altl10ugh the onset of
treatment of horses with osteoartluitis.

therapeutic response may be slow (2-6 wk).

Hyaluronan is responsible for the viscosity

Reports indicate that orgotein apparently
of the synovial fluid and contributes to its
has a wide safety margin.

ANTINEOPLASTIC AGENTS

Anti.neoplastic chemotherapy is an
be traditional chemotherapy. Clinically
impo1tant component of small animal
useful cllugs achieve a degree of selectivity
practice and is routinely used for selected
on the basis of certain characteristics of
tumors of horses and cattle. Effective use of
cancer cells that can be used as pharrnacoantineoplastic chemotherapy depends on logic targets. These characteristics include
an understanding of basic principles of
rapid rate of division and growth, va.t-iations
cancer biology, drug actions, toxicities, and
in the rate of drug uptake or in the
drug ha.t1dling safety.

sensitivity of different types of cells to
pa.tticular drugs, and retention in tl1e

Tumor Growth and Response to
malignant cells of hormonal responses

Chemotherapy: The fundamental
characteristic of the cells from which the
biochemical and genetic differences
cancer is derived, eg, estrogen responsivebetween cancer cells and healthy cells are ness of certain breast carcinomas.

areas of intense investigation, because

Aspects of normal cell growth and the cell
these divergences are not fully understood.

cycle provide the rationale for and are of

None of the empirically developed
major importance in successful application
conventional anti.neoplastic drugs appea.t-s
of antineoplastic chemotherapy. In the S
to act on a process entirely LU1ique to cai1cer
phase, DNA synthesis occm-s; the M phase
cells. Newer therapies that specifically
begins with mitosis and ends with
target markers or pathways unique to
cytokinesis; and the G0 phase is a dormant
particular cancers are evolving. However,
or nonproliferative phase of the cell cycle.

the mainstay of cancer therapy continues to

Tumor doubling time is related to the length

ANTI NEOPLASTIC AGENTS

2723
of the cell cycle and the growth fraction
by PO, IV, SC, IM, topical, intracavitary,

(the proportion of a population of cells
intralesional, intravesicular, intrathecal, or
undergoing cell division). Antineoplastic
intra-arterial routes. The route chosen
agents can be classified according to a
depends on the individual agent and is
number of schemes relative to effects at
detennined by drug toxicity; location, size,

VetBooks.ir
different stages of the cell cycle. In the
and type of twnor; and physical constraints.

simplest sense, cycle-nonspecific agents are

Antineoplastic agents are commonly
considered to be lethal to cells in all phases
administered in various combinations of
of the cell cycle. Cells are killed exponendosages and timing; the specific regimen is tially with increasing drug levels, and the
referred to as a protocol. A protocol may
dose-response curves follow first-order
use one or as many as five or six different
kinetics. Phase-specific agents exert their
antineoplastic agents. Selection of an
lethal effects exclusively or primarily during
appropriate protocol should be based on
one phase of the cell cycle, usually S or M;
type of twnor, grade or degree of maligthe greater the rate of cell division, the more nancy, stage of the disease, condition of the effective the drug. The G0 phase of the cell
animal, and financial considerations.

cycle is in1portant, not as a target for chemo

Preferences of individual clinicians for
therapeutic agents, but as a time during
treatment of specific neoplastic conditions
which dormant tumor cells can escape or
may also vary. Regardless of the protocol
repair the effects of drug therapy.

chosen, a thorough knowledge of the
mechanism of action and toxicities of each

Principles of Antineoplastic Chemo
therapeutic agent is essential.

therapy: The decision to use antineoplas

Combination antineoplastic chemotic chemotherapy depends on the type of therapy offers many advantages. Drugs
tumor to be treated, the stage of malignancy, with different target sites or mechanisms the condition of the animal, and financial
of action are used together to enhance
considerations. Chemotherapy can be used
destruction of tumor cells. If the adverse
as an adjuvant to surgery and irradiation
effects of the component agents are
and can be administered immediately after
different, the combination may be no more
or before the primary treatment. Neoadjutoxic than the individual agents given vant therapy is administered before surgery
separately. Combinations that include a
or irradiation and is intended to improve the cycle-nonspecific drug administered first, effectiveness of the primary therapy by
followed by a phase-specific drug, may
possibly decreasing tumor size, stage of
offer the advantage that cells surviving
malignancy, or presence of micrometastatic
treatment with the first drug are provoked
lesions. Responses to cancer chemotherapy
into mitosis and, therefore, are more
can range from palliation (remission of
susceptible to the second drug. Another
secondary signs, generally without increase
advantage of combination therapy is the
in survival time) to complete remission (in
decreased possibility of development of
which clinically detectable tumor cells and
drug resistance.

all signs of malignancy are absent). The

Special considerations associated with
percentage and duration of complete
administration of antineoplastic drugs
remissions are criteria for the success of
include evaluation of the animal's quality of
a particular chemotherapeutic protocol.

life, medical and nutritional support, control

Effective clinical use of antineoplastic
of pain, and psychologic comfort for the
drugs depends on the ability to balance the
owner. Many owners who choose to treat
killing of tumor cells against the inherent
neoplasia in their pets have experienced
toxicity of many of these drugs to host cells.

cancer themselves or have been involved

Because of the narrow therapeutic indices
with individuals or family members who
of antineoplastic agents, dosages are
have had cancer. Discussion of neoplasia in
frequently calculated based on body surface pets should be handled tactfully and should area (BSA) rather than body mass.

provide the owners with appropriate

However, evidence suggests that small dogs
infonnation for decision-making.

and cats may best be treated based on body
weight to avoid overdosage. This is

Resistance to Antineoplastic Agents:

especially true if the primary toxicity is

Failure to respond, or resistance, to
bone marrow suppression. Evidently, BSA
antineoplastic agents can be seen for
does not correlate well with either stem cell
several reasons. Pharmacokinetic
nwnber in the bone marrow or resulting
resistance is seen when the concentration
hematopoietic toxicity. Correlation is better
of a drug in the target cell is below tl1at
between body weight and these toxicities.

required to kill the cell. This may be due to

Antineoplastic agents can be administered
altered rates of drug absorption, distribu-

2724

ANTI NEOPLASTIC AGENTS
tion, biotransformation, or excretion. In
antagonists a.re used in human oncology to
addition, marginal blood flow to a tumor
treat delayed emesis, and there is evidence
may not provide sufficient drug, resulting in
they may work synergistically or at least in
inadequate therapeutic drug concentrations
an additive fashion with 5HT3 inhibitors. ln
and the potential for creation of a populaaddition to the NK-1 inhibitor maropitant, VetBooks.ir
tion of quiescent, less susceptible cells.

conu11on antiemetic therapy in veterinary

Cytokinetic resistance is seen when the
oncology includes metoclopra.mide, which
tumor cell population is not completely
ftmctions through direct antagonism of
eradicated; this may be a result of donnant
central and peripheral dopamine receptors.

twnor cells, dose-limiting host toxicity

This drug has the added benefit of
associated with drug therapy, or the
stin1ulating motility of the upper GI tract
inability to achieve a 100% kill rate even at
without stimulating gastric, biliary, or
therapeutic drug dosages. Resistance can
pancreatic secretions. This effect cru1 be
also develop via biochemical mechanisms
useful in dogs that develop ileus secondary
within the twnor cell itself that block
to vincristine administration.

transport mechanisms for drug uptake, alter

Allergic reactions and anaphylaxis may
target receptors or enzymes c1itical to drug
also be of inunedia.te concern with selected
action, increase concentrations of healthy
drugs ru1d can be treated with antiliistametabolites antagonized by the antineoplasmines or corticosteroids as needed. In more tic drug, or cause genetic changes that
severe cases, epinephrine and IV fluids may
result in protective gene amplification or
be indicated.

altered patterns of DNA repair. Acquired

Other delayed toxicities may develop
muJtidrug resistance can result from
days to weeks after antineoplastic therapy.

amplification and overexpression of a

Myelosuppression, a common delayed
multiclrug resistance gene. This gene
toxicity, cru1 be life-threatening because of
encodes a cell transmembrane protein that
the increased risk of infection associated
effectively pwnps a variety of structurally
with neutropenia Less commonly,
unrelated antineoplastic agents out of the
increased risk of hemorrhage associated
cell. As intra.cellular drug concentrations
with throm bocytopenia and anemia may be
decline, twnor cell swvi val and resistance
seen.

to therapy increase.

Other in1portant delayed toxicities
include tissue dan1a.ge associated with

Patterns of Toxicity: Conventional
extra.vasation of selected drugs, and
antineoplastic a.gents that a.ct primarily on
alopecia. ca.used by hair follicle damage,
rapidly dividing and growing cells produce
particularly in nonshedding breeds with
multiple adverse effects or toxicities,
continuous hair growth. Adverse effects on
including bone marrow or myelosuppresspenna.togenesis and tera.togenesis may be sion, GI complications, and imnumosupof concern in breeding animals. Unlike in pression. Patterns of toxicity may be either
people, chemotherapy-induced stoma.titis
a.cute or delayed. Acute vomiting may
or ulcerative enteritis are rru·e events in
develop during administration of an
dogs and cats.

emetogenic drug or within 24 hf after

Prevention and management of toxicities
administration of chemotherapy, probably
are crucial to successful antineoplastic
from direct stimulation of the chemoreceptherapy. Collection of an adequate database tor trigger zone. Several drugs are available
before treatment can identif-y potential
aimed at preventing these toxicities,
problems so that contra.indicated drugs can
including dolasetron, ondansetron, and
be a.voided. Several antineoplastic agents
maropitant citrate. Dolasetron and
should not be used in the presence of
ondansetron a.ct as serotonin receptor
specific organ impainnent. For example,

(5HT3) antagonists that work centrally on
doxorubicin should not be used in dogs with
the brain to prevent emesis. Ma.ropitant
certain cardiac abnormalities that impair
citrate is an oral or subcutaneous FDAleft ventricular ftmction, mid cisplatin is approved meclication for acute nausea/
contraindicated in animals with impaired
vomiting in veterinary medicine. It works by renal ftmction.

inhibiting both central and peripheral vomit

When a drug is chosen, supportive or
ing pathways by blocking new-okinin-1
preventive therapy aimed at ameliorating
receptors to prevent activation of the
toxic adverse effects may be required.

emetic center.

Potential cardiotoxicity of doxorubicin may

Administration of oral antiemetics may
ue abrogated wiLh coadrnini!;LraLion of
be indicated for delayed GI toxicities, which dexra.zoxane, an iron chelator that inhibits can occur 3-5 days after chemotherapy
fonna.tion of free ra.clica.ls implicated in
administration. New-okinin-1 receptor
myocarclial injury. Active diw-esis should

ANTI NEOPLASTIC AGENTS

2725
accompany admillistration of nephrotoxic
use of closed system transfer devices that
agents (eg, cisplatin). Administration or
limit escape of air from drug vials into the
availability of appropriate antihistamines
environment. Administration of chemomay be indicated with L-asparaginase and therapy should occm in dedicated areas,
doxorubicin therapy.

and meticulous attention to technique

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The availability of recombinant products
should be maintained. Intravenous lines
is an additional resource to manage
used to administer chemotherapy should be
myelosuppression and inu11w10suppression
prin1ed with nontoxic solution whenever
induced by antineoplastic chemotherapy.

possible. Disposal of contaminated vials,

Recombinant hwnan (rhG-CSF) and canine
syringes, needles, and gloves in this area

(rcG-CSF) granulocyte colony-stimulating
should be anticipated, and the proper
factors have been used effectively to manage puncture-proof chemotherapy waste cytopenias induced by chemotherapy and
containers provided.

radiation therapy. Administration of rcG

Personal protection equipment should

CSF results in a rapid, significant increase
be used for chemotherapy preparation,
in neutrophil nwnbers that is sustainable
administration, cleanup, and disposal. This
as long as the factor is administered.

should include powde1°free chemotherapy

Neutrophil counts drop quickly when
gloves, nonpermeable gowns, respiratory
therapy is discontinued. Neutrophi.l
protection, plastic-backed underpads for
phagocytosis, superoxicle generation, and
the working swface, eye and/or splash
antibody-dependent cellular cytotoxicity
protection, shoe covers, and a spill kit.

all increase with G-CSF treatment. Until

Another potential route of exposure to
rcG-CSF is commercially available,
antineoplastic agents is by absorption of
longtem1 (>2---3 wk) or repeated use of
drug through the skil1. This could occur
recombinant hwnan products should be
during preparation or administration of
avoided in clogs and cats, because it can
drug, cleaning of 01e drug preparation area,
result in anti-factor antibody formation
or handling of excreta from animals that
and a subsequent decline in targeted cell
have received selected cytotoxic drugs.

nwnbers.

Conscientious wearing of disposable,

Prophylactic antibiotics have been shown powde1°free gloves and careful handling of to reduce hospitalization rates and death in
drug-contaminated needles or catheters
hwnan cancer patients receiving chemomay avoid most exposures of this type.

therapy. These are occasionally used in

Re-capping of needles containing drug
veterinary medicine to reduce the
residues is discouraged to avoid accidental
occurrence or severity of hematologic and
self-inoculation. In addition, use of sprayers
nonhematologic complications that can
and pressw·e washers to clean cages,
result from administration of particular
kennels, or stalls of treated animals should
chemotherapy agents.

be avoided to minimize aerosolization of'

hazardous wastes.

Safe Handling of Antineoplastic

Antineoplastic agents can be inadve1°

Chemotherapeutic Agents: Most
tently ingested if food, drink, or tobacco
antineoplastic chemotherapeutic agents are
products are allowed in the vicinity of drug
potentially toxic as mutagens, teratogens, or preparation areas, treatment areas, or carcinogens. Handling of these agents can
kennels housing treated animals. Any
result in hazardous personal or environmeningestible materials should be restricted tal exposure in several ways.

to a separate area that is far enough away

A conunon route of exposure is
to avoid any possible contanlination with
inhalation due to aerosolization during
these agents.

mixing or administration of cytotoxic drugs.

All personnel should handle antineoplas

This may occur when a needle is withdrawn
tic agents with care. Women of child-bearing
from a pressurized drug container or on
age should be particularly cautious, and
expulsion of air from a drug-filled syringe.

women who are pregnant or breastfeeding

Transferring drugs between containers,
should not handle antineoplastic drugs.

opening drug-filled glass ampules, or

A somce of exposure to cytotoxic drugs
crushing or splitting oral medications
that is conunonly overlooked is the handling
may also aerosolize drug residues.

of body fluids and excreta of treated

The best way to prepare cytotoxic drugs
patients. Unifom1 guidelines to handle these
to avoid aerosolization is in a biologic safety potentially dangerous substances have not cabinet or hood; a Class II, type A vertical
been published. Nevertheless, sin1ple
laminar air flow hood exhausted outside
measures can be taken to help minimize
the building is recommended. Aerosol
exposure of veterinary personnel and pet
exposures can be fw-ther decreased through owners. Collection of biologic samples,

2726

ANTI NEOPLASTIC AGENTS
such as blood, urine, or tissue, should be
of DNA repair systems are also common
performed before chemotherapy adminismechanisms of resistance.

tration. The duration and type of precau

Individual alkylating agents are generally
tionary measures that should be taken after
cell-cycle nonspecific alld can be sub

VetBooks.ir
treatment depend on the half-life and routes
grouped according to chemical structure
of elimination of the drug administered. Pet
into nitrogen mustards, ethylenearnines,
owners and veterinary hospital personnel
alkyl sulfonates, nitrosoureas, alld triazene
should be advised to allow dogs to urinate
derivatives.

and defecate in a confined area outdoors,
away from spaces where people may

Nitrogen Mustards: The most common
congregate or children play. A mask should
subgroup of alkylating agents used is the
be worn when cleaning litterboxes, and the
nitrogen mustard group. Mechlorethanli.ne
contents placed in a sealed plastic bag. The
hydrochloride is the prototype of the
use of low-dust kitty litter should be
nitrogen mustards alld is conunonly used in
encouraged. Powder-free, disposable gloves veterinary medicine to treat lymphoma in should be used when cleaning up urine,
conjunction with other chemotherapeutics.

feces, or vomitus. Veterinarians ar·e

Because of the highly unstable nature alld
encouraged to contact their local boar·d of
extremely short duration of action of
health and other federal, state, and local
mechlorethanli.ne, its use is somewhat
regulato1y agencies for regulations
linlited in veterinary medicine. Derivatives
regarding disposal of hazar·dous waste.

of meclllorethar11ine conunonly used for
various neoplasias include cyclophosphamide, chlorarnbucil, alld melphalall.

Classification of Antineoplastic

Cyclophosphamide is a cyclic phospha

Chemotherapeutic Agents: Convenmide derivative of mechloretharnine that tional cytotoxic anti.neoplastic agents can
requires metabolic activation by the
be grouped by biochemical mechanism of
cytochrome P450 oxidation system in the
action into the following general categories:

liver. Cyclophosphalllide is given PO or IV,
alkylating agents, antimetabolites, mitotic
alld dose-lin1iting leukopenia associated
inhibitors, anti.neoplastic antibiotics,
with bone marTow suppression is the
hormonal agents, and miscellaneous. The
clinically relevant drugs used in veterinary
p1irnary toxicity. However, among the
alkylating chemotherapy agents, the
medicine are discussed below, and the
myelosuppressive effect of cyclophosphaindications, mechanism of action, and mide is considered relatively sparing of
toxicities of selected agents ar·e summarized platelets alld progenitor cells. Sterile in TABLE: 57.

hemorrhagic cystitis may result from
aseptic chemical in.flan1mation of the

ALKYLATING AGENTS
bladder urothelium caused by acrolein, a
metabolite of cyclophospharnicle. Preven

Alkylating agents form highly reactive
tion of this toxicity is key to its manageintern1ediate compounds that ar·e able to ment. Specifically, concurrent
transfer alkyl groups to DNA Alkylation
administration of a diuretic, such as
can result in miscoding of DNA st.rands,
furosemicle, may be used when cyclophosincomplete repair of alkylated segments phanlide is given as a single dose to provide

( which leads to strand breakage or
a dilutional effect. In addition, cyclophosdepurination), excessive cross-linking of pharnide may be given in the morning so

DNA, and inhibition of st.rand separation at
that patients Call be provided several
mitosis. Monofunctional alkylating agents
opportunities to urinate throughout the clay
transfer a single alkyl group and usually
to minimize contact time of acrolein with
result in miscoding of DNA, strand
the bladder lining. In patients with evidence
breakage, or depurination. These reactions
of sterile hemorrhagic cystitis, cyclophoscan result in cell death, mutagenesis, or pharnide use should be discontinued.

carcinogenesis. Polyfunctional alkylating

Although the signs may be self-limiting,
agents typically cause st.rand cross-linking
treatment with fluids, NSAIDs, methylsulfoand inhibition of mitosis with consequent nylmethane (MSM), alld int.ravesicular
cell death. Resistance to one alkylating

DMSO may be considered. Mesna is a drug
agent often implies resistance to other
that binds and inactivates the urotoxic
drugs in the same class and can be caused
metabolites of cyclophospharnide within the
by increased production of nucleophilic
bladder. Mesna coadnlinistered with fluid
substances that compete with the target
diuresis is recommended when ifosfarnide

DNA for alkylation. Decreased pern1eation

(all analogue of cyclophosphar11ide) or
of alkylating agents alld increased activity
high-close cyclophospharnide is used.

ANTINEOPLASTIC AGENTS

2727

MECHANISMS OF ACTION, INDICATIONS, AND TOXICITIES OF

SELECTED ANTINEOPLASTIC AGENTS

Major

Drug

Mechanism of Action

Indications

Toxicities

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ALKYLATING AGENTS

Cyclophospha - Undergoes hepatic

Lymphoma,

Nausea, vomiting
mide
biotransformation to
mammary

(infrequent),
active metabolites that
adenocarciQPma,
moderate to severe
alkylate DNA; alkylation sarcomas,
myelosuppression,
leads to miscoding of
lyrnphocytic
sterile hemorrhagic

DNA and cross-linking
leukemia
cystitis
of DNA strands

Melphalan

Alkylates DNA causing

Multiple myeloma Nausea, vomiting,
miscoding and
anorexia, moderate
cross-linking of DNA
myelosuppression
strands

(may be more
myelosuppressive in
cats)

Chlorambucil

Alkylates DNA causing

Chronic lympho-

Nausea, vomiting,
miscoding and
cytic leukemia,
mild to moderate
cross-linking of DNA
small-cell
myelosuppression
strands; slowest-acting
lymphoma
alkylating agent

Lomustine

Alkylates DNA causing

Lymphoma, mast

Nausea, vomiting,

(CCNU)

miscoding and
cell tumor,
moderate to severe
cross-linking of DNA
histiocytic
myelosuppression
strands; inhibits both
sarcoma, CNS

(may be delayed for

DNA and RNA synthesis; neoplasias,

4-6 wk), hepatotoxic-
not cross-resistant with multiple myeloma ity, nephrotoxicity, other alkylating agents
pulmonary toxicity

Streptozotocin Inhibits DNA synthesis; lnsulinoma

Severe, potentially
high affinity for
fatal nephrotoxicit)'.

pancreatic 13 cells

(if given without
diuresis) and
hepatotoxicity,
nausea (inunediate
and delayed),
vomiting, mild
myelosuppression

Dacarbazine

Undergoes hepatic

Lyn1phoma,

Severe acute nausea,

(DTIC)

biotransformation to
sarcomas
vomiting, phlebitis,
active metabolites that
moderate myelosup-
alkylate DNA; inhibits
pression, hepatotox-

RNA synthesis
icity, anecdotal
reports of pleural
effusion in cats
lfosfamide

Analogue of cyclophos-

Various sarcomas Nausea, vomiting,
phamide; w1dergoes
myelosuppression,
hepatic biotransfo1rnation
sterile hemorrhagic
to active metabolites that
cystitis, possible
alkylate DNA; alkylation
nephrotoxicity
leads to miscoding of

DNA and cross-linking of

DNA strands

(continued)

2728

ANTINEOPLASTICAGENTS

MECHANISMS OF ACTION, INDICATIONS, AND TOXICITIES OF

SELECTED ANTINEOPLASTIC AGENTS (continued) Major

Drug

Mechanism of Action

Indications

Toxicities

VetBooks.ir

ANTI METABOLITES

Methotrexate

Inhibition of dihydro-

Lymphoma

Nausea, vomiting,
folate reductase that is
moderate myelosuprequired for formation
pression, GI
of tetrahydrofolate, a
ulceration, hepatonecessary cofactor in
toxicity, pulmonary
thymidylate synthesis;
toxicity
thyn1idylate essential for

DNA synthesis and
repair

5-Fluorouracil

Pyrinlidine analogue;

Carcinomas

Systemic: nausea,
interferes with DNA

(systemic); cutane vomiting, moderate
synthesis and may be
ous carcinomas
myelosuppression,
incorporated into RNA

(topical)

neurotoxicity, GI
to cause toxic effects
ulceration, neurotoxicity, hepatotoxicity

Topical: local
irritation, pain,
hyperpigmentation

Cannot be given to
cats (fatal neurotoxicity)

Cytarabine

Pyrimidine analogue;

Lymphoma

Nausea, vomiting,
incorporates into DNA

(including CNS),
moderate myelosupcausing steric hindrance leukemias; no pression, nephrotoxand inhibition of DNA
activity in solid
icity, hepatotoxicity
synthesis
tumors

Gemcitabine

Pyrimidine analogue;

Limited efficacy

Mild nausea, vomiting,
incorporates into DNA,
seen in lyn1phoma mild to moderate
causing steric hindrance and various
myelosuppression,
and inhibition of DNA
carcinomas
pulmonary toxicity,
synthesis
nephrotoxicity

ANTIBIOTIC ANTINEOPLASTICS

Doxorubicin

Intercalates and binds to Lymphoma,

Nausea, vomiting,

DNA, disrupting helical leukemias,
moderate rnyelosupstructure and DNA
multiple myeloma, pression, hemmThagic
template; inhibits RNA
osteosarcoma,
colitis, severe
and DNA polymerases;
hemangiosarcoma, cutaneous reactions if
causes DNA topoisomer and various other
extravasated; red
ase II-mediated chain
sarcomas and
urine (not hematuria),
scission; generates free carcinomas
transient ECG changes
radicals that cause DNA
and arrhythmias,
scission and cell
nephrotoxicity,
membrane damage
anaphylactoid
reactions

Cumulative doserelated congestive
heart failure in dogs;
cw11ulative neplu-otoxicity in cats

( cont,i ,wed)

ANTINEOPLASTICAGENTS

2729

MECHANISMS OF ACTION, INDICATIONS, AND TOXICITIES OF

SELECTED ANTINEOPLASTIC AGENTS (continued) Major

Drug

VetBooks.ir

Mechanism of Action

Indications

Toxicities

Mitoxantrone

Topoisomerase

Lymphoma,

Nausea, vomiting,

II-mediated chain
various carcinomoderate to severe
scission; DNA aggregamas
myelosuppression,
tion, oxidation, and
diarrhea, bluish
strand breakage
discoloration to
sclera; less severe
adverse effects than
others in this group

Bleomycin

Mixture of glycopep

Carcinomas

Nausea, vomiting,
tides; generates oxygen
myelosuppression,
radicals that cause chain
fever, allergic
scission and fragmentareactions including
tion of DNA
anaphylaxis,
hyperpigmentation,
skin ulceration,
pneumonitis,
pulmonary fibrosis

Dactinomycin

Intercalates and binds to Lymphoma,

Nausea, vomiting,

(Actinomycin D) DNA, disrupting helical various sarcomas moderate to severe structure and DNA
myelosuppression,
template; inhibits RNA
phlebitis; severe
and DNA polymerases;
tissue reaction if
causes DNA topoisomerextravasated
ase II-mediated chain
scission; generates free
radicals that cause DNA
scission and cell
membrane damage

MITOTIC INHIBITORS

Vinblastine

Binds to tubulin, leading Lymphoma and

Mild nausea,
to disruption of mitotic
leukemias, mast
vomiting, severe
spindle apparatus and
cell tumors
myelosuppression,
arrest of cell cycle
neurotoxicity with
high doses, inappropriate secretion of
antidiuretic hormone

Vincristine

Binds to tubulin, leading Lymphoma and

Mild to moderate
to disruption of mitotic
leukemias,
nausea, vomiting,
spindle apparatus and
transmissible
mild to moderate
arrest of cell cycle
venereal cell
myelosuppression,
tumors, various
severe tissue reaction
sarcomas
if extravasated,
cumulative peripheral neuropathy,
constipation,
paralytic ileus,
inappropriate
secretion of
antidiuretic hormone

(continued)

2730

ANTI NEOPLASTIC AGENTS

MECHANISMS OF ACTION, INDICATIONS, AND TOXICITIES OF

SELECTED ANTINEOPLASTIC AGENTS (continued) Major

Drug

Mechanism of Action Indications

Toxicities

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Vinorelbine

Binds to tubulin, leading Primary lung

Mild nausea,
to disruption of mitotic
tumors, limited
vomiting, myelosupspindle apparatus and
efficacy in mast
pression
a1Test of cell cycle
cell tumors

Paclitaxel

Binds to tubulin,

Mammary

Myelosuppression,
stabilizing microtubule
carcinoma,
nausea, vomiting,
polymer and a.ITesting
squamous cell
hypersensitivity
mitosis
carcinoma

(when Cremor EL is
used as vehicle)

MISCELLANEOUS

Cisplatin

Reacts with proteins and Osteosarcoma,

Intense nausea,
nucleic acids; fom1s
cai·cinomas, and
vomiting, mild to
cross-links between
mesothelioma
moderate myelosup

DNA strands and
pression, potentially
between DNA and
fatal neplu·otoxicity if
protein; disrupts DNA
not given with
synthesis
diuresis, anaphylaxis,
ototoxicity,
peripheral neuropathy, hyperuricemia,
hyperrnagnesemia

Ca.I111ot be given to
cats (fulminant
pulmonaiy edema)

Carboplatin

Reacts with proteins and Osteosarcoma,

Mild nausea,
nucleic acids; forms
carcinomas
vomiting, dia.IThea,
cross-links between
moderate to severe

DNA strands and
myelosuppression
between DNA and
protein; disrupts DNA
synthesis

L-Asparaginase

Inhibits protein

Acute lymphoid

Hypersensitivity
synthesis by hydrolyzing leukemias and
reactions, anaphytumor cell supply of
lymphoma
laxis especially after
asparagine
repeated .doses,
alteration in
coagulation
paran1eters,
hepatotoxicity,
pancreatitis (people),
potential inhibition of
immune responsiveness (B and T cells)

Mitotane

Destroys adrenal zona

Pituitary

Nausea, vomiting,

(o,p'DDD)

fasciculata and zona
hyperadrenocorti anorexia, dia.IThea,
reticulaiis
cism, palliation of adrenal insufficiency,
adrenal cortical

CNS depression,
tumors
dermatitis

( continued)

ANTINEOPLASTIC AGENTS

2731

MECHANISMS OF ACTION, INDICATIONS, AND TOXICITIES OF

SELECTED ANTINEOPLASTIC AGENTS (continued) Major

Drug

Mechanism of Action Indications

Toxicities

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Hydroxymea

Inhibits conversion of

Polycythemia vera, Nausea, vomiting,
ribonucleotides to
granulocytic and
mild myelosuppresdeoxyribonucleotides by basophilic sion, alopecia,
destroying ribonucleoleukemia,
sloughing of claws,
side diphosphate
thrombocythemia, dysuria
reductase
investigational for
meningiomas

Procarbazine

Mechanism is unclear;

Lymphoma, as part Nausea, vomiting,
inhibits DNA, RNA, and ofMOPP
myelosuppression,
protein synthesis,
chemotherapy
diarrhea
perhaps through
protocol; brain
alkylation
tumors

HORMONES

Prednisone

Lympholytic; inhibits

Lymphoma, mast

Sodium retention, GI
mitosis in lyn1phocytes
cell tumors,
ulceration, protein
multiple myeloma, catabolism, muscle
palliative
wasting, delayed
treatment of brain wound healing,
tumors
suppression of hypothalamic-pituitaryadrenal axis,
inununosuppression

Chlorambucil, the slowest-acting
nitrosourea, is used for palliation of
nitrogen mustard, achieves effects gradually malignant pancreatic islet-cell tumors or and often can be used in aninlals with
insulinomas. Other nitrosomeas, such as
compromised bone marrpw. It can cause
carmustine and lomustine, readily cross
bone marrow suppression, which is usually
the blood-brain barlier and have been useful
mild; however, periodic monitoring is
in management of lymphoma. (including
recommended with longtem1 administraepitheliotropic cutaneous lyn1phoma.), mast tion. This drug is given PO and is most
cell tmnors, histiocytic sarcomas, and CNS
commonly used in treatment oi chronic,
neoplasias. Dacarbazine (DTIC), a triazene
well-differentiated cancers; it is considered
derivative, has been used either in
ineffective in rapidly proliferating tumors.

combination with doxorubicin or as a

Melphalan, an !.,-phenylalanine
single-agent treatment for rnia.psed canine
delivative of mechlorethamine, is given PO
lymphoma. and soft-tissue sarcomas.

or IV and is plima.lily used in vete1ina.ry

Temozolomide is an oral inliclazotetramedicine to treat multiple myeloma..

zine de1iva.tive of da.carbazine and belongs
to a class of chemotherapeutic a.gents that
enter the CSF and do not require hepatic

Other Alkylating Agents: Of the other
metabolism for activation. In people, it is
subgroups of alkyla.ting agents, several have
used for refractory malignant gliomas and
lin1ited but specific uses. Triethylenethio
malignant melanomas. There have been
phosphora.mide (thiotepa.), an ethylenreports in the veterina.iy litera.tw·e of its use imine, has been reported as an intra.vesias a substitute for dacarbazine (DTIC).

cular treatment for transitional cell
carcinoma. of the bladder or as an intra.ca.vitary treatment for pletffal and peritoneal effusions. Busulfa.n, an alkyl sulfona.te, is ANTI METABOLITES
used specifically in treatment of chronic

Antimetabolites resemble normal cellular
myelocytic leukemia. and polycythemia
substances and so can subvert nom1al
vera.. Streptozotocin, a natmally occmring metabolic pathways in a toxic ma.rmer.

2732

ANTI NEOPLASTIC AGENTS

Three subgroups of antirnetabolites are
injections are usually required. Inhibition
used: folic acid, pyrimidine, and purine
of conversion to AraCTP or increased
analogues.

degradation of AraCTP can account for
development of resistance.

Folic Acid Analogues: The prototype

Gemcitabine is anotl1er nucleoside

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folic acid analogue is methotrexate, an
analogue of cytidine which, unlike
inhibitor of dihydrofolate reductase, the
cyta.rabine, has activity against solid
enzyme that catalyzes conversion of folic
tumors. The drug requires active carrier
acid to tetrahydrofolate. Tetrahydrofolate
transport into the cytoplasm where it is
deficiency blocks reactions requiring folate
ternlinally activated via phosphorylation;
coenzymes, disrupting both DNA and RNA
consequently, serum levels may not predict
synthesis. Methotrexate is an S phase-speintracellul:u concentrations. By acting as a cific drug that must be actively transported
counterfeit nucleotide, coupled with the
across cell membranes. It can be given PO,
ability to inhibit multiple enzymes needed

IV, IM, or intrathecally. Methotrexate is
for pyridine biosynthesis and DNA repair,
excreted in the urine, and at high doses may
gemcitabine is capable of self-potentiation
precipitate in renal tubules. Folinic acid can
and synergism with other agents, particube used to bypass the metabolic blockade larly alkylators. Gemcitabine has also been
produced by folic acid analogues and thus
used as a radiation sensitizer.

result in rescue of treated cells. Because
tumor cells appear less efficient at transport

Purine Analogues: Two purine
of folinic acid, some degree of selectivity is
analogues, 6-mercaptopurine (6-MP) and
achieved in the rescue. Resistance to metho

6-thioguanine (6-TG), are rarely used in
trexate may develop due to impaired
veterinary medicine. In people, these drugs
transport of the drug into cells, production
are occasionally used for acute leukemias
of altered fom1S, or increased concentraor other autoimmune disorders.

tions of dihydrofolate reductase.

MITOTIC INHIBITORS

Pyrimidine Analogues: Two pyrimidine
analogues, 5-fluorouracil and cytarabine,

Vinca Alkaloids: The vi.nca alkaloids
are commonly used.

are large, complex molecules derived from

5-Fluorouracil must be converted to an
the periwinkle plant. Binding to tubulin,
active 5-fluoro-2 '-deoxyuridine-5' -
the major component of cellular microtuphosphate form to bind the enzyn1e bules, accounts for the antineoplastic
thymidylate synthetase and block or inhibit
effects of these drugs. Vinca alkaloids

DNA and RNA synthesis. This drug is considinhibit microtubule polymerization and ered S phase-specific. It is used IV but is also increase microtubule disassembly. The available for topical use. Metabolism is via
mitotic spindle apparatus is disrupted, and
the liver, and the drug readily enters CSF.

segregation of chromosomes in metaphase

Occasional CNS reactions have been
is arrested. These effects account for the
reported in dogs. Severe irreversible
primary M-phase action of vinca alkaloids,
neurotoxicity and sudden death have been
although other antitubulin effects related
described in cats. In people, neurotoxicity
to cytoskeletal maintenance and protein
is related to deficiency in the enzyme
trafficking may be seen. The two drugs of
dihydropyrinlidine dehydrogenase, but this
importance in this class are vincristine
has not been investigated in veterinary
and vinblastine. Both are given IV, and
species. Resistance may develop by
both cause severe local vesication if
decreased activation of the drug or
iajected perivascularly. Drug extravasaacquisition of altered thyn1idylate syntion may cause severe tissue reactions and thetase that is not inhibited.

promote exacerbation of self-trauma. The

Cytarabine ( cytosine arabinoside) is an
vinca alkaloids are metabolized primarily
analogue of 2 '-deoxycytidi.ne and must be
in the liver but may be partially excreted in
activated by conversion to a 5' -monophosan unchanged form in the urine. Although phate nucleotide. The nucleotide analogue,
vinca alkaloids are related structurally,

AraCTP, inhibits DNA synthesis by substiresistance to one does not imply resisttution of arabinose for deoxyribose in the ance to all drugs in this category. Vincrissugar moiety of DNA; cytarabine may also tine use is limited by neurologic toxicity
inhibit DNA repair enzymes. This drug is
that may include a slowly reversible

S phase-specific, and its effectiveness in
sensorimotor peripheral neuropathy and
hematopoietic neoplasms is directly
muscle weakness. In comparison, the
proportional to exposure of cells to the
dose-limiting toxicity associated with
drug; continuous infusion or repeated
vinblastine is related to rnyelosuppression

ANTI NEOPLASTIC AGENTS

2733
and leukopenia; neurologic toxicity

DNA helix to uncoil, which destroys the
develops only at high doses.

DNA template and inhibits RNA and DNA

Vinorelbine is a second-generation
polymerases. Scission of DNA is thought
sernisynthetic vinca alkaloid that is
to be mediated by either the enzyme
derived from vinblastine but with broader
topoisomerase II or by generation of free

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anti tumor efficacy. According to studies
radicals. Intracellular interactions of
in the veterinary literature, this drug may
anthracycline antibiotics result in the
have efficacy in canine primary lung and
formation of semiquinone radical intem1ecutaneous mast cell tumors.

diates capable of generating hydrogen
peroxide and hydroxyl radicals. Considered

Taxanes: Paclitaxel and docetaxel are
cell-cycle nonspecific because of the
antimicrotubule agents extracted from the
damage associated with radical formation,

Pacific and European yew trees, respecthese drugs probably have their maximal tively. Taxanes bind to tubulin subunits,
effect during the S phase of the cell cycle.

enhance microtubule polyme1ization, and

The anthracycline antibiotics are given IV;
inhibit microtubule depolymerization.

they are severe vesicants if administered

Formation of stable microtubule bundles
perivascula.rly and may cause a severe,
disrupts tubulin equilibtium and blocks
delayed phlebitis. Administration of a free
normal progression through metaphase,
radical scavenger, dexrazoxane, may limit
and mitosis is arrested. These agents are
the extent of tissue damage seen with
actively used in human medicine, but
extravasation of this clrng. The anthracyhypersensitivity reactions related to the cline antibiotics are metabolized in the liver
vehicle Cremophor EL have limited the
to a variety of less active and inactive
drug's utility in veterinary medicine. A new
products.

water-soluble, micellar formulation of

Doxorubicin toxicity can be manifested
paclitaxel has received conditional approval in a variety of acute and delayed reactions.

by the FDA for treatment of canine

Acute effects include hypersensitivity
mammary carcinoma and squamous cell
reactions (from nonspecific histamine
carcinoma. Myelosuppression and GI
release), extravasation injury, or transient
effects ( diarrhea, mucosa] ulceration, and
cardiac arrhythmias. Delayed toxicities can
emesis) have been repo1ted in dogs treated
be severe, with the major problem in clogs
with paclitaxel.

being cumulative, dose-related cardiac
toxicity associated with binding of the drug

ANTINEOPLASTIC ANTIBIOTICS
to cardiac DNA and free radical clan1age to
myocardial membranes. A nonspecific

The antineoplastic antibiotics are products
decrease in cardiac fibrils occurs, which
of Streptomyces. The important drugs in
leads to congestive heatt failure illll"esponthis group include actinomycin D ( dactinosive to digitalis. Because the cai·diotoxic mycin ), doxorubicin, mitoxantrone, and
effects of cloxorubicin are related to the
bleomycin. Drugs less conunonly used
peak plasma concentrations (rather than
include daunorubicin, mithramycin, and
area under the curve), slow IV administramitomycin.

tion over 15--30 min is recommended to help

Actinomycin A was the firstStreptomy
lessen cardiac injury. Myocai·clial damage
ces antibiotic isolated and was followed by from cloxorubicin also can be prevented by
related antibiotics, including actinomycin
coadministration of clexrazoxane, at lO

D. Actinomycin D binds with doubletimes the close of cloxorubicin. In cats, strancled DNA and blocks the action of RNA
cumulative closes of doxorubicin can result
polymerase, which prevents DNA transcripin neph.rotox:icity at1cl should be avoided or tion. Actinomycin D is considered cell-cycle
used judiciously in cats with preexisting
nonspecific and is given IV but does not
renal insufficiency.

cross the blood-brain barrier. Resistance

Dose-limiting toxicities of cloxorubici.t1
may develop because of decreased cellular
include severe myelosuppression and GI
uptake of the drug. Occasionally, it is used
upset. Also, if cloxorubicin is used in
as a substitute for doxorubicin in dogs with
conjunction with radiation therapy, damage
questionable cardiac function or for those
by radiation may be augmented. This
dogs that have exceeded the cumulative
radiation sensitization effect may necessicardiotoxic close of doxorubicin.

tate reduction i.t1 radiation or drug dosages,

The anthracycli.ne antibiotics, particuor both. Because of the significant toxicity larly doxorubicin, have become in1portant
associated with use of cloxorubicin,
antineoplastic antibiotics. These drugs
newer-generation drugs specifically aimed
intercalate and bind to DNA between base
at reduction of cardiac toxicity have been
pairs on adjacent strands. This causes the
developed aticl are available in hwnat1

2734

ANTI NEOPLASTIC AGENTS
medicine. Two of these, idarubicin and
another agent. U.nfo1tunately, resistance to
epirubicin, have been stuclied, but neither is
a given glucocorticoid may develop rapidly
in conunon use in veterinary meclicine.

and typically extends to other glucocorti

A pegylated liposomal encapsulated forrn
coids. Toxic effects of glucocorticoid
of doxorubicin, called doxorubicin HCL
therapy can include peptic ulceration,
liposome iI\iection, has been used
glucose intolerai1ce, polydipsia and

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effectively in both human and veterinary
polywia, immunosuppression, pancreatimeclicine. The liposomal formulation results tis, osteopenia, hypokalemia, cataracts, in a longer drug circulation time and
and muscle wasting. Prednisone and
reduced myelosuppression and carcliotoxicprednisolone are commonly used to treat ity. ln dogs, the dose-linliting toxicity of
lymphoreticular neoplasms in combination
liposomal doxorubicin is a cutaneous
with other drugs. Because they readily
reaction called palmar-plantar erythroenter the CSF, dexamethasone, prednisone, dysesthesia. ln cats, a delayed nephrotoxicand prednisolone are especially useful in ity is the dose-linliting toxicity of both
treatment of leukemias and lymphomas
conventional and liposomal doxorubicin.

of the CNS.

Mitoxantrone, an antlu·aceneclione
lndirect benefits of glucocorticoid
related to the anthracycline antibiotics, has
therapy in cancer include symptomatic
shown promise in veterinary medicine for
improvements in appetite and attitude,
treatment of lymphoma and vaiious
suppression of norunfectious fevers,
carcinomas. The mechanism of action
management of hypercalcemia of maligof mitoxantrone is similar to that of the nancy (after a definitive diagnosis has been
anthracyclines, but most adverse effects are
made), and relief of edema associated with
less severe than those of doxorubicin. An
spinal cord and brain tumors. However,
exception is myelosuppression, which is
evidence from several sources suggests that
more profound with nlitoxantrone than
treatment of certain lymphomas with
doxorubicin.

predrusone may increase resistance of

Bleomycin is actually a mixture of
neoplastic cells to subsequent cycles of
bleomycin glycopeptides that differ only in
antineoplastic chemotherapy through
their ternlinal antine moiety. The cytotoxic
induction ofMDR-1-related P-glycoprotein
action of these glycopeptides depends on
expression.

their ability to cause chain scission and
fragmentation of DNA molecules. Cells

MISCELLANEOUS
accw11ulate in the G2 phase of the cell cycle,
which accounts for the classification of

ANTINEOPLASTIC AGENTS
bleomycin as a G2 and M phase-specific

Several drugs used as antineoplastics do not
agent. Bleomycin may also affect DNA
fall into any of the categories mentioned
repair enzymes. Given IV or SC, bleomycin
thus fai·. These include L-asparaginase,
does not cross the blood-brain barrier; a
cisplatin, nlitotane (o,p'DDD), hydroxylarge portion is excreted via the kidneys.

urea, etoposide, ai1d procarbazine.

Bleomycin has ntinin1al myelosuppressive

L-Asparaginase is an enzyn1e derived
and inm1unosuppressive activities but does
from Escherichia coli that catalyzes
have an unusual delayed pulmonary
hydrolysis of asparagine. Because some
toxicity. Pulmonary toxicity, which is
tW11or cells have poor expression of
cumulative, may begin as a nonspecific
asparagine synthe.tase and ai·e tu1able to
pnetu11onitis that progresses to pulmonary
produce the anlino acid asparagine,
fibrosis. Dangers from pulmonaiy
treatment with this drug deprives these cells
complications are especially in1portant in
of exogenously supplied asparagine ai1d
older animals with preexisting pulmonary
ultin1ately linlits protein synthesis. Because
disease.

protein synthesis is active in the G1 phase of
the cell cycle, L -asparaginase is considered

HORMONAL AGENTS
to be a G1 phase-specific drug. Preferred
routes of adntinistration for L-asparaginase

Hon11onal therapy for neoplasia commonly
include IM and SC. Anaphylaxis on repeated
involves use of glucocorticoids. Direct
adnlirustration of L-aspai·aginase may occur
ai1titumor effects are related to their
as a result of host anti-asparaginase
lympholytic properties; glucoco1ticoids
antibody production; pretreatment of
can inhibit mitosis, RNA synthesis, and
atlilllals with ai1tihistai11ine helps to prevent
protein synthesis in sensitive lyn1phocytes.

this acute toxic reaction. Anti-asparaginase

Glucocorticoids are considered cell-cycle
antibody production may also account for
nonspecific and are often used in chemodevelopment of tumor resistance, as can a therapeutic protocols after induction by
decreased tun1or cell requirement for

ANTI NEOPLASTIC AGENTS

2735
asparagine. A related drug, pegaspargase, is
conversion of ribonucleotides to deoxyribomodified from L-asparaginase by covalent nucleotides, and blocks DNA synthesis.

modification with monomethoxypolyethyl

Cells are arrested in the G,-S interface.

ene glycol. The conjugated drug produces

Mechanisms of resistance include amplificafewer hypersensitivity reactions than does tion of the RNDR gene or development of

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L-asparaginase.

RNDR with reduced sensitivity to hydroxy

Cisplatin ( cis-diamine-dichloroplatimea. Loss of claws has been associated num) functions primarily as a bifunctional
with hyd.roxymea use in anin1als.

alkylator but is included in the miscellane

Epipodophyllotoxins are semisynthetic
ous category because of its unusual
glycosides of podophyllotoxin derived from
structure. It is a platinum ion complexed
the mandrake plant. Although these toxins
to two chloride ions and two ammoniwn
bind tubulin, their mechanism of action is
molecules. Cisplatin causes inter- and
mu-elated to disruption of mic.rotubules.

intrastrand DNA cross-linking that disrupts

Instead, they are thought to stinrnlate DNA

DNA helices and prevents DNA synthesis.

cleavage mediated by topoisomerase IL Of

Cisplatin is cell-cycle nonspecific and has
the two drugs in this class, etoposide and
been used both for its direct antitumoral
teniposide, the former has been used
and radiation-sensitizing effects. It is
primarily in treatment of testicular
administered by IV drip in combination with
carcinoma.

aggressive saline diuresis. Excretion is

Procarbazine is considered to function
prolonged, with up to 500A, of a dose still
as an alkylating agent but is included in the
present in the body 5 days al'ter administramiscellaneous category because tl1e exact tion. Extreme, dose-limiting, proximal
mechanism of action is not known. It is
tubular renal necrosis typifies the delayed
typically used as part of the MOPP protocol
adverse effects of cisplatin along with other
that includes mechlorethamine, vincristine
responses that may include ototoxicity,

(tradename Oncovin®), procarbazine, and
moderate bone marrow suppression,
prednisone for dogs with lyn1phoma. This
peripheral nemopathy, and renal potassimn
diug is metabolized and activated in the
and magnesiwn wasting. Cisplatin causes
liver. GI toxicity and myelosuppression are
fatal pulmonary edema in cats and must not
the p1imary concerns associated with tl1e
be used in this species.

MOPP protocol.

Because of the extreme toxic adverse
effects of cisplatin, newer generation

Biologic Response Modifiers in Cancer
derivatives such as carboplatin and others

Therapy: In recent years, a nmnber of
have been developed. Carboplatin is
alternative modes of cancer therapy have
effective as an acljunct to smgery for
become increasingly available in vete1inary
treatment of osteosa.rcoma. Nausea and
medicine. These novel fonns of therapy
vomiting are less severe than with cisplatin,
work in myriad ways, including enhanced
and carboplatin is not considered neph.roinunune recognition, altered blood vessel toxic. It is, however, myelosuppressive, with fonnation, or by exploitation of specific neutropenia being the dose-limiting toxicity. pathways that are aberrant or overexpressed Carboplatin is excreted th.rough the
in neoplastic cells. The widespread use of
kidneys; consequently, dogs or cats with
these newer therapies alone or in combinaevidence of compromised renal function tion with conventional chemotl1erapy has
require dose acljustments to avoid excessive transformed the approach to treatment of toxicity. Ca.rboplatin is considered safe for
many cancer patients.

administration to cats.

NSAIDs represent one class of biologic

Mitotane ( o,p'DDD ), a derivative of the
response modifiers tl1at work by inhibiting
insecticides DDT and DDD, causes selective frequently overexpressed COX-2 enzyn1e destruction of norn1al and neoplastic
activity present in many twnor types.

adrenal cortical cells. Mitotane may act by

Several studies have proposed that tllese
inhibiting production of steroids induced by
drugs may work by reducing cell proliferaad.renocorticotropic hormone, which tion, increasing apoptosis, inhibiting
causes atrophy of the inner zones of the
angiogenesis, and modulating immune
adrenal cortex. Mitotane is administered
function. Piroxican1 has been the drug most

PO, and plasma concentrations can be
researched in dogs, but any of the newer
detected for several weeks.

NSAIDs with more COX-2 selective

Hydroxyurea, a simple hyd.roxylated
inhibition (such as deracoxib or meloxiderivative of mea, is most commonly used can1) theoretically may yield equal or
in treatment of polycythemia vera.

improved effects. (See also NONSTEllOJDAL

Hyd.roxyu.rea inhibits ribonucleoside

ANTI-INFLAMMATORY DRUGS, p 2714.) The
diphosphate reductase (RNDR), limits the
clinical usefulness of COX-2 inhibitors has

2736

ANTINEOPLASTIC AGENTS
been demonstrated in canine transitional
the label dosage of 3.25 mg/kg, PO, every 48
cell carcinoma, squamous cell carcinoma,
hr) result in sufficient target inhibition with
and other tumor types in dogs and cats.

substa.J1tially reduced toxicity.

NSAIDs are often combined in antiangio

Development of a therapeutic vaccine to
genic protocols.

stimulate active inmmnity against cancer

Metronomic or antiangiogenic dosing of
has long been a goal in botl1 human ai1d

VetBooks.ir
chemotherapy is a novel or nontraditional
veterinaiy oncology. This becai11e a reality
way to administer chemotl1erapy that
with introduction of a caiune melanoma
consists of the administration of low doses
vaccine. The vaccine exploits the ilm11w1e
of oral chemotherapy agents at very short
response induced by hun1an tyrosinase,
intervals, often daily. This treatment
ai1 enzyme in the pathway of melanin
approach targets the tumor neovasculature
formation. The vaccine contains a human
by leveraging the exquisite sensitivity of
tyrosinase gene inse,ted into a bacterial
endotl1elial progenitor cells and ilmnature
plasnud, which is adnunistered trai1sderendothelium to modest doses of alkylating mally. The antibodies ai1d T -cell responses
agents. Studies indicate that antiangiogenic
produced by xenogeneic tyrosinase
factors, such as tlu·ombospondin-1, increase cross-react with the tyrosinase overexduring metronomic chemotherapy. In pressed on cai1ine melai1oma cells. Initial
addition, anti tumor immunosuppression
studies reported prolonged survival in dogs
mediated tlu·ough T regulatmy cells may be
with advai1ced stage oral malignai1t
mediated by metronomic protocols. Disease melai10ma treated with radiation tl1erapy or stabilization is considered a successful
surgery of the primaiy trnnor, followed by
outcome of low-dose chemotherapy,
vaccine administration.

because direct cytotoxicity to neoplastic

Passive inummotl1erapy using monoclocells is not tl1e intent of metronomic nal antibodies has grown substantially in
chemotl1erapy. Prelirninaiy studies in the
human oncology in recent years. Monocloveterinaiy literature suggest this is a nal antibodies may attach to specific
promising alternative to maxin1ally
antigens on cai1cer cells, tl1ereby either
tolerated doses of conventional chemomarking tl1e cai1cer cells for destruction by tl1erapy, paiticularly in a microscopic
tl1e immw1e system or in1pairing functional
disease setting, and has the added benefit
pathways witlun the neoplastic cells.

of linuted adverse effects.

Furthermore, monoclonal ai1tibodies may

Targeting of specific pathways tl1at are
be cor\jugated to oilier ai1tineoplastic agents
aberrant or dysregulated in cancers has

(such as chemotl1erapy agents, radionuyielded novel therapies in a variety of clides, or other toxins) to allow for more
human cancers. An exainple of such a tai·get
targeted delive1y of cytotoxic therapy to
is tl1e receptor tyrosine kinases (RTKs),
cancer cells while spaiing normal tissues.

wluch mediate processes involved in tun10r

The introduction of anti-CD20 monoclonal
growth, progression, and metastasis. These
antibodies in humai1 oncology has
drugs are competitive inhibitors of ATP, ai1d
revolutionized the treatment of B-cell
so prevent receptor phosphorylation ai1d
lymphoma with sigruficai1tly in1proved
subsequent downstream signal transducoutcomes versus chemotl1erapy alone.

tion. Mutations in c-kit, an RTK gene

In veterinaiy medicine, ai1ti-CD20 ai1d
involved in mast cell differentiation ai1d
anti-CD52 monoclonal ai1tibodies have
proliferation, has been reported in
received either USDA or conditional
approxin1ately a quarter of caiune mast cell
approval to treat canine B-cell and T-cell
tumors. Toceranib has been approved by
lymphoma, respectively. The mechanisms
the FDA, ai1d biologic response rates of
by which these antibodies work is not fully

70%---9091> have been reported in dogs that
understood, but several potential mechahave mast cell tumors with recognized c-kit nisms include antibody-dependent
mutations. Moreover, toceraiub has activity
cell-mediated cytotoxicity, cornplementagainst other members of the split-kinase dependent cytotoxicity, and direct signaling
fairuly of RTKs, such as vasculai· endothelial
leading to inhibition of proliferation or to
growth factor receptor, platelet-de,ived
apoptosis. Field studies of each of these
growth factor, and ot11ers. Prelin1inaiy
antibodies are tmderway.

evidence indicates that toceranib has

Biologic response modifiers aimed at
activity against a vaiiety of carcinomas ai1d
enhancing innate ai1titumor defense
metastatic osteosarcoma, leading to tumor
mechanisms of the host has been an area
regression or more often to prolonged
of active investigation. Nonspecific ilnrnudisease stabilization. Recent reports nornodulators, including intact bacteria or
indicate that dosages of toceranib rai1ging
bacterial cell components, acernaiman, II,.2,
from 2.4---2.9 mg/kg, PO, every 48 hr (below
ll,.12, inte1feron alpha, levan1isole, ai1d

ANTINEOPLASTICAGENTS

2737
cimetidine, have been reported with
induction of apoptosis, inhibition of new
variable efficacy to enhance immune
blood vessel formation, and reduction of
responsiveness and improve outcomes after tun1or cell adhesion to bone matrix.

surgery or antineoplastic chemotherapy.

Retinoids are a class of compounds

Liposome-encapsulated muran1yl tripeptide
structurally related to vitan1iJ1 A. In

VetBooks.ir
phosphatidylethanolamine (L-MTP-PE) is
preclinical studies, all-trans retinoic acid
perhaps tl1e best studied nonspecific

(tretinoin), 13-cis retiJ10ic acid (isotretiimmunomodulator in veterinary medicine.

noin), and the aromatic retinoids etretinate

This synthetic bacterial wall component has
and acitretin have preventive and tilerapeubeen used effectively with chemotilerapy to tic effects on carcinogen-induced premaligconfer a survival advantage in dogs with nant and malignant lesions in both human
splenic hemangiosarcoma and osteosarand veterinary medicine. Isotretinoin and coma.

etretinate have been used with limited

Development of immunomodulators such therapeutic success in superficial squamous as lymphokines and cytokines ( eg, intercell carcinoma and cutaneous lyn1phoma. In leukins, interferon, and tumor necrosis
people, dran1atic therapeutic effects have
factor) for clinical use in cancer patients has been obse1ved in treatment of acute not been fully realized, largely because of
promyelocytic leukemia witil tretinoin. The
toxicity. Consequently, these agents are not
mechanism of action of retinoids is thought
commonly used in veterinary medicine.

to occur through modulation of cell

Blocking angiogenesis is an attractive
proliferation and differentiation. Retinoids
forn1 of anticancer therapy, because tumors
vary in tileir capacity to induce clifferentiamust develop their own vascular supply if tion and to inltlbit proliferation in a variety
they are to grow beyond a few millimeters in of hwnan and veterinary cell lines.

diameter. Various drugs, such as angiostatin, tlrrombospondin-1, and matrix TREATMENT OF CANINE
metalloproteinase in11ibitors, have been
investigated with varying results. Specific

LYMPHOMA
angiogenesis inhibitors for veterinary

Lymphoma is tile canine tumor most
patients are not yet conunercially available.

frequently treated witil chemotherapy. It is

At present, metronomic chemotherapy
the most common hematopoietic neoplasia
combinations are the most practical
of dogs
approach to antiangiogenic therapy in

(seep 40) and cats and is also among the most responsive to chemotl1erapy. Four
clinical cases.

antineoplastic agents, vincristine, cyclophosphamicle, doxorubicin, and prednisone, ANCILLARY ANTINEOPLASTIC
form tl1e basis for many lymphoma

AGENTS
treatment protocols. Treatments based on
these four drugs are often abbreviated as

Supplementary agents are occasionally

CHOP (cyclophosphantlcle, hydroxydaunoused in veterinary oncology to citiler rubicin [cloxorubicin], Oncovin® [a trade
enhance the effect of certain chemotherapy
nan1e of vinclistine], and prednisone)

treatments or support the well-being of the
protocols. One commonly used CHOP
patient. Drugs in this category include
protocol in veterinary medicine is shown in
antiemetic therapy, prophylactic antibiotics, TABLE 58; nearly 40 protocols for manage

COX-2 inhibitors (NSAIDs), and various
ment of lymphoma in dogs have been
pain medications.

published.

Bisphosphonates are frequently used in

The most common recommendation in
veterinary oncology for a variety of reasons,
veterinary oncology is to use a discontinuincluding to treat bone pain from plimary ous chemotherapy protocol, as opposed to
bone tumors or bone metastasis, and to
maintenance or continual chemotherapy.

effectively treat hypercalcemia of malig

Discontinuous chemotherapy in dogs
nancy. Bisphosphonates belong to a class of
appears to have the same or similar
drugs tilat directly inhibit osteoclast activity remission and survival duration as a and the subsequent resorption of bone. In
traditional maintenance protocol. For this
people, these drugs are used for various
treatment approach, all chemotherapy is
conditions that are charactelized by bone
discontinued for patients in a complete
resorption and bone fragility, such as
remission at the encl of the treatment
osteoporosis. In addition to their inhibitory
protocol. At the first signs of recurrence of
effects on osteoclasts, bisphosphonates are
lymphoma, reinduction using tile miginal
believed to exert direct cytotoxic effects on
chemotherapy protocol should be used.

some cancer cells. These effects include

Studies have suggested that dogs receiving a

2738

ANTI NEOPLASTIC AGENTS

CHOP MULTIDRUG CHEMOTHERAPY FOR TREATMENT OF CANINE

LYMPHOMA

Drug

Dosage

Schedule

VetBooks.ir

L-Asparaginase

10,000 IU/m2, SC

Wk l

Vincristine

O.fHJ.7 mg/m2, IV

Wk 1, 3, 6, 8, 11, 13, 16, and 18

Cyclophosphamide

250 mg/m2, IV or PO

Wk 2, 7, 12, and 17

Doxorubicin

30 mg!m2, IV, for dogs

Wk 4, 9, 14, and 19

> 10 kg; 1 mg/kg for dogs

<lO kg

Prednisone

2 mg/kg/day, PO

For first week, then 1.5 mg/kg/
day, PO, for 7 days, then 1 mg/kg/
day, PO, for 7 days, then 0.5 mg/
kg/day, PO, for 7 days, then
discontinue.

discontinuous protocol were more likely
well tolerated, less expensive, and easy to
to achieve a second remission when they
administer but are considered to be less
relapsed than dogs that received longterm
effective than a CHOP-based protocol.

or maintenance chemotherapy. If reinduc

CHOP-based chemotherapy protocols
tion fails, then use of rescue protocols
provide the basis for most lymphoma
should be considered.

chemotherapy protocols in cats, although

Other lymphoma protocols include a
there is currently no consensus treatment
non-doxorubicin-based combination
protocol reconunended for this species. In
protocol (COP) or a protocol consisting of
general, fewer studies document the clinical
single-agent doxorubicin administered
effectiveness of various CHOP combinaevery 3 wk. These protocols are generally tions in cats than in dogs.

ANTISEPTICS AND DISINFECTANTS

Antiseptics and disinfectants are..nonselec

Topical anti-infective agents are
tive, anti-infective agents that are applied
extensively used in surgery for antisepsis of
topically. Their activity ranges from sin1ply
the sut·gical site and surgeon's hands and to
reducing the number of microorganisms
disinfect surgical instruments, apparel, and
to within safe limits of public health
hospital premises. Other common uses
interpretations (sanitization), to destroying
are as disinfectants for home and fam1
all microorganisms (sterilization) on the
premises, food processing facilities, in
applied surface. In general, antiseptics are
water treatment, in public health sanitation,
applied on tissues to suppress or prevent
and as antiseptics in soaps, teat dips, dairy
microbial infection. Disinfectants are
sanitizers, etc. Antiseptics also have been
gemlicidal compounds usually applied to
used to treat local infections. However, in
inanin1ate sutfaces. Sometimes the san1e
most cases, systenlic chemotherapeutic
compound may act as an antiseptic and a
agents are prefeffed, because they often
disinfectant, depending on the drug
penetrate better into the foci of infection
concentration, conditions of exposure,
and a.re less likely than the topical antinumber of organisms, etc. To achieve infectives to Jose their potency when in
maximal efficiency, it is essential to use the
contact with body fluids and debris in the
proper concentration of the drug for the
infected area.

purpose intended. The logic that "if a little is Ideally, antiseptics and disinfectants
good, twice as much is better" is not only
should have a broad spectrun1 and potent
uneconomical but often has toxicologic
gernlicidal activity, with rapid onset and
implications.

long-lasting effect. They should not be

ANTISEPTICS AND DISINFECTANTS

2739
prone to development of resistance in target

A 2"A, solution of soda lye ( contains 94%
microorganisms. They should withstand a
sodiwn hydroxide [Na.OH]) in hot water
range of environmental factors ( eg, pH,
is used as a disinfectant against many
temperature, hw1lidity) and must retain
common pathogens, such as those causing
activity even in the presence of pus,
fowl cholera and pullorum disease. It is a

VetBooks.ir
necrotic tissue, soil, and other organic
potent caustic and must be handled with
material. High lipid solubility and good
care.

dispersibility increase their effectiveness.

CalciW11 oxide (CaO), ie, lime (hydrated

Antiseptic preparations should not be toxic
or air-slaked lime), soaked in water
to the host tissues and should not impair
produces Ca(OH)2. Aqueous suspensions of
healing. Disinfectants should be nondeslaked lime are used to disinfect premises.

structive to applied surfaces. They should
be readily biodegradable, not accw11ulate

ALCOHOLS
in the environment, or react with other
chenticals to produce toxic residues.

P1imary aliphatic alcohols are gemlicidal.

Offensive odor, color, and staining

Their potency increases but water solubility
properties should be absent or nlinimal.

decreases with chain length Wltil amyl

Most of these compoW1ds exert their
alcohol (6 carbons) is reached. Antimicroantimicrobial effect by denaturation of bial effect is related to their lipid solubility
intracellular protein, alteration of cellular

(daniages bactelial membranes) and their
membranes ( often through extraction of
ability to coagulate cytoplasmic proteins.

membrane lipids), or enzyme inhibition.

However, they do not destroy bactetial

Although most classes of antiseptics and
spores. Ethyl alcohol (ethanol) and
disinfectants have been in use for decades,
isopropyl alcohol (isopropanol) are the
the emergence of nlicrobial resistance to
most widely used alcohols. They can be
some agents, especially in the hospital
used in concentrations of 300/o--90% in
environment, has led to continued research
aqueous solutions; best results are usually
into the development of new compounds.

obtained with 700A, ethanol or 500A, isopropanol. Higher concentrations tend to be less ACIDS AND ALKALIES
effective. Isopropanol is slightly more
potent than ethanol because of its greater
depression of stu-face tension. "Rubbing

Acids: Hydrogen ion is bacteriostatic at
alcohol" is a mixture of alcohols, with
pH -3-6 and bactericidal at pH <3 . Strong
isopropanol as its plincipal ingredient. It is
nlineral acids (HCl, H2S04, etc) in concentraused as a skin disinfectant and rubefacient.

tions of0.1-1 N have been used as disinfect

Alcohol-based hand tinses have rapid-acting
ants; however, their corrosive action linlits
antiseptic effects. This makes them useful
their usefulness. Un-ionized weak organic
in mininlizing the transntission of transient
acids can readily penetrate and disrupt
flora acquired from infected patients and
bacterial cell membranes. Acids are used
reducing nosoconlial diseases.

as food preservatives ( eg, benzoic acid),
antiseptics ( eg, boric acid, acetic acid),

BIGUANIDES
filllgicides ( eg, salicylic acid, benzoic acid),
spermatocides ( eg, acetic acid, lactic acid),

Chlorhexidine is the most popular
and cauterizing agents ( strong nlineral
antiseptic of tllis group. It has potent
acids).

antimicrobial activity against most

Acetic acid, 1 %, can be used in surgical
gram-positive and some gram-negative
dressings. At 5%, it is bactericidal to many
bacteria but not against spores. A 0.1 %
bacte1ia and has been used to treat otitis
aqueous solution is bacteticidal against
extema produced by Pseudomonas,

Staphylococcus aureus, Escherichia coli,

Candida, Malassezia, or Aspergillus spp.

and Pseudomonas aeruginosa in 15 sec.

Skin and hides that have been contanlinated However, it is relatively ineffective against by anthrax spores can be disinfected with
other gram-negative orgartisms, spores,

2.5% HCI.

filllgi, and most viruses. N osocontial
infections by Pseudomonas spp have

Alkalies: Hydroxyl ion also exerts
developed from the use of contanlinated
antimicrobial activity. At a pH >9 , it inhibits
chlorhexidine solutions in which the
most bacteria and many viruses. Hydroxbacteria persisted. In susceptible organides of sodiwn and calciW11 are used as isms, chlorhexidine disrupts the cytoplasdisinfectants. Their irritant or caustic mic membrane. Its activity is W1affected
property usually precludes their applicaor enhanced by alcohols, quaternary tion on tissues.

ammoniwn compoW1ds, and alkaline

2740

ANTISEPTICS AND DISINFECTANTS
pH, and is somewhat depressed by hlgh
usefulness as an antiseptic is limited,
concentrations of organic matter (pus,
hydrogen peroxide is finding increased
blood, etc), hard water, and contact with
application as a disinfectant in water

VetBooks.ir
cork. It is incompatible with anionic
treatment and food processing facilities and
compounds, including soap.

for sterilization of dental and surgical instru

Chlorhex:idine is one of the most
ments.

commonly used stU"gical and dental

Accelerated hydrogen peroxide
antiseptics. A 4% emulsion of chlorhexidine
fom1ulations are synergistic blends of
gluconate is used as a skin cleanser, a 0.5%

0.5%--2% hydrogen peroxide with anionic

(w/v) solution in 70% isopropanol as a
and nonionic surfactants and stabilizers that
general antiseptic, and a 0.5% solution in
possess broad-spectrun1 antimicrobial

70% isopropanol with emollients as a hand
activity. They are effective against bacteria,
rinse. Chlorhexidine soaps have good
spores, mycobacteria, viruses, and fungi,
residual activity, which may be advantawith short contact times. Accelerated geous when applied as a presurgical scrub
hydrogen peroxide formulations are
for prolonged stU"gical procedures.

noniITitating to eyes and skin and are

Chlorhex:icline-alcohol mixtures are
biodegradable, decomposing to water and
particularly effective in that they combine
oxygen with no active chemical residues.

the antiseptic rapidity of alcohol with the

They have become leading disinfectants
persistence of chlorhexidine. Because of its
in human hospitals and dental clinics. A
antiseptic prope1ties and low potential for
disadvantage is the potential to damage
systemic or dermal toxicity, chlorhexidine
soft metals, such as brass, copper, and
has been incorporated into shan1poos,
alun1inwn, and carbon-tipped instruments.

ointments, skin and wound cleansers, teat

Peracetic acid and the combination of
dips, and surgical scrubs. A 1% chlorhexperacetic acid (0.23%) and hydrogen idine acetate ointment is used as a topical
peroxide (7.35%) have been recognized as
antiseptic in treatment of external wounds
useful sterilants and antiseptics, combining
in dogs, cats, and horses. Contact dermatitis the broad antimicrobial spectrum and lack has been reported in up to 8% of hwnan
of harmful decomposition products of
patients after repeated topical exposure.

hydrogen peroxide with greater lipid

Little data are available on hypersensitivity
solubility and freedom from inactivation by
reactions in anin1als.

tissue catalase and peroxidase. They can be
used over wide temperature (0°-40°C) and

OXIDIZING AGENTS
pH (3--7.5) ranges and are not affected by
organic matter. They are effective against
bacteria, yeasts, fungi, and vi.ruses at

Peroxides: These compounds generally
concentrations of 0.001 o/o--0.003"A, and are
exert a short-acting germicidal effect on
sporicidal at 0.25o/o--0.5%. Consequently,
most organisms through release of nascent
peracetic acid products have been accepted
oxygen, which in-eversibly alters microbial
worldwide in the food industry, including
proteins. Most have Little or no action on
meat and poultry processing plants and
bacte1ial spores. Nascent oxygen is rendairies, and are replacing traditional dered inactive when it combines with
disinfectants for some medical devices.

organic matter.

Solutions of 0.2% peracetic acid applied to

Hydrogen peroxide solution (3%)

compresses effectively reduce microbial
liberates oxygen when in contact with
populations in severely contaminated
catalase present on wound surfaces and
wounds.

mucous membranes. One mL of 3%

Sodium perborate, used in antiseptic
hydrogen peroxide liberates 10 mL of
solutions and in mouthwashes, acts by
oxygen at standard temperature and
decomposing into sodiwn metaborate and
pressure. The effervescent action mechanihydrogen peroxide, which then gradually cally helps remove pus and cellular deb1is
liberates oxygen.

from wounds and is useful to clean and

Benzoyl peroxide slowly releases
deodo1ize infected tissue. The antimicrobial oxygen to act as an antiseptic. However, action is of short duration and is limited to
it can cause skin initation. It also has
the superficial layer of the applied smface
keratolytic and antiseborrheic activity,
because there is no penetration of the
whlch makes it useful in treating pyoderma
tissue. However, the use of hydrogen
in dogs.

peroxide in partially closed spaces, such as

Potassium peroxymonosulfate is a
operative wounds, may result in oxygen
broad-spectrnm disinfectant with increasembolization due to dissection of gas under ing use in barns and kennels. A 1% solution
pressure into tissues. Although its
in water is highly effective against bacte1ia,

ANTISEPTICS AND DISINFECTANTS

2741
viruses, and fungi, maintaining good activity

Chlorine: Chlorine exerts a potent
in the presence of organic matter.

germicidal effect against most bacte1ia,

Potassium permanganate has broad
viruses, protozoa, and fungi through
antimicrobial properties, but its intense
fom1ation of undissociated hypochlorous
purple color in solution, which stains
acid (HOC!) in water at acid to neutral pH.

tissues and clothing brown, is a disadvan

It is effective against most organisms at a
tage. It is an effective algicide (0.01%) and
concentration ofO.l ppm, but much higher

VetBooks.ir
virucide (1 %) for disinfection, but concenconcentrations are required in the presence trations> 1: 10,000 tend to initate tissues.

of organic matter. Alkaline pH ionizes

Old solutions twn chocolate brown and lose chlorine and decreases its activity by their activity.

reducing its penetrability. Chlorine has a
strong acid smell. It is irritating to the skin

Halogens and Halogen-containing
and mucous membranes, including the

Compounds: Iodine and chlorine are
respiratory tract, and Call cause severe
among the oldest topical antimicrobial
bronchospasms ru1d acute lung injmy. It is
agents. They owe their activity to high
widely used to disinfect water supplies ru1d
affinity for protoplasm, where they are
ina.nin1ate objects ( eg, utensils, bottles,
believed to oxidize proteins and interfere
pipelines) in dairies, crerune1ies, ru1d milk
with vital metabolic reactions.

houses. Chlorine dioxide has recently

Iodine: Elemental iodine is a potent
replaced chlorine as a disinfectant for
gernticide with a wide spectrum of activity
d1inking water in some jmisdictions,
and low toxicity to tissues. A solution
because it fom1s fewer by-products.

containing 50 ppm iodine kills bacte1ia in 1

Inorganic chlorides include sodium
min and spores in 15 min. It is poorly soluble hypochlorite solutions (bleach). A 2o/ir-5%
in water but readily dissolves in ethanol,

NaOCI solution is a conunonly used ru1d
which enhances its antibacte1ial activity.

effective disinfectant. Calcium hypochlorite

Iodine tincture contains 2% iodine and
is used as a disinfectant.

2.4% sodium iodide (Na!) dissolved in 50%

Organic chlo1ides contain chlorine
ethanol; it is used as a skin disinfectant.

weakly bonded to nitrogen, which is slowly

Strong iodine tincture contains 7% iodine
released for gennicidal activity. They are
and 5% potassium iodide (JG) dissolved in
generally less initant, more stable, and

95% ethanol; it is more potent but also more
more convenient to use than hypochlo1ite
initating than tincture of iodine. Iodine
solutions.

solution contains 2"A, iodine and 2.4% Na!

dissolved in aqueous solution; it is used as a

METALS
nonirritant antiseptic on wounds and
abrasions. Strong iodine solution (Lugol's

Inorganic mercuric bichlo1ide, one of the
solution) contains 5% iodine and 10% JG in
eru·ly antiseptics, was later replaced by the
aqueous solution.

less irritant ru1d less toxic organic merctuilodophores ( eg, povidone-iodine and als, eg, merbromin, thimerosal (49%
poloxame1�iodine) are combinations of
mercury), nitromersol, ru1d phenylmercmic
iodine with a solubilizing agent or carrier;
nitrate. At moderate concentJ·ations, tl1e
they are more stable and water soluble than
organic mercmials ru·e bacte1iostatic and
older formulations. They slowly release
act by inhibiting bacterial enzymes tJu·ough
iodine as an antimicrobial agent and are
their affinity for sulfhydryl groups. This
widely used as skin disinfectants, particueffect can be reversed by sulfu1�containing larly before surgery. They do not sting or
compounds, eg, cysteine or glutathione.

stain. Iodophores are nontoxic to tissues

Mercurials are not effective against spores.

(although contact dem1atitis can result from Use of mercurial antiseptics or disinfectants repeated exposure) but may be corrosive to
has decreased, partly because of their
metals. They are effective against bacteria,
environmental persistence and contanlinant
vi.ruses, and fungi but less so against spores.

potential. Repeated application of topical

Jodophor solutions retain good antibacterial mercurials cru1 result in significru1t activity at pH <4, even in the presence of
absorption ru1d systemic toxicity.

organic matter, and often change color

Silver compounds can have caustic,
when the activity is lost. Phospho1ic acid is
astringent, ru1d antibacterial effects. Silver
often mixed with iodophores to maintain an
ions combine with sulfhydryl, runino,
acidic medium. They have been used in teat
phosphate, ru1d cru·boxyl groups, and tlrns
dips to control rnastitis, as dairy sanitizers,
precipitate proteins, in addition to
and as a general antiseptic or disinfectant
interfe1illg witl1 essential metabolic
for vruious dem1al ru1d mucosa! infecti,ms.

activities of microbial cells.

2742

ANTISEPTICS AND DISINFECTANTS

A 0.1 % aqueous silver solution is

Hexachlorophene (a trichlorinated
bactericidal and somewhat irritating,
bis-phenol) has a strong bacteriostatic
whereas a 0.01% solution is bacteriostatic.

action against many gram-positive

A 0.5% solution is sometimes applied as a
organisms (including staphylococci) but
dressing on bums to reduce infection and
only a few gram-negative ones. It is used
induce rapid eschar formation. Colloidal
widely in medicated soaps. Frequent

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silver compounds, which release silver ions
washings every day with hexachlorophene
slowly, are bacte1iostatic and have a more
soaps lead to sufficient retention of residue
sustained effect. They do not irritate the
on the skin to provide prolonged bacteriotissues and have little astringent or caustic static action. Washing with otl1er soaps
effect. They are generally used as mild
promptly removes these residues. Repeated
antiseptics and in ophthalmic preparations.

exposure of skin to high concentrations of
hexachlorophene may lead to sufficient
absorption of the antiseptic to cause

PHENOLS AND RELATED
spongifom1 degeneration of the white

COMPOUNDS
matter in the brain, cerebral edema, and
neivous disorders. To prevent such

Phenolic compounds used as antiseptics
neurotoxicity, products containing >0.75%
or disinfectants include pure phenol and
hexachlorophene are available only by
substitution products with halogens and
prescription. Accidental oral ingestion
alkyl groups. They act to denature and
of hexachlorophene results in acute
coagulate proteins and are general
poisoning.

protoplasmic poisons.

Pine tar is a viscid blackish brown liquid,

Phenol ( carbolic acid) is one of the
used primarily for antiseptic bandaging of
oldest antiseptic agents. It is bacterioswounds of the hoof and horn. Pine tar tatic at concentrations of O.lo/o-1% and is
contains phenol derivatives that provide
bactericidal/fungicidal at 1 o/o-2%. A 5%
antinucrobial properties.

solution kills anthrax spores in 48 hr. The

Chloroxylenols are broad-spectrum
bactericidal activity is enhanced by EDTA
bactericides wiili more activity against
and warm temperatures; it is decreased
gram-positive than gran1-negative bacteria.

by alkaline medium (through ionization),

They are active in alkaline pH; however,
lipids, soaps, and cold temperatures.

contact with organic matter dinunishes

Concentrations >0.5% exert a local
their activity. Streptococci are more
anesthetic effect, whereas a 5% solution is
susceptible than staphylococci. Parachlostrongly irritating and con-osive to tissues.

rometaxylenol (PCMX) and d.ichloro

Oral ingestion or extensive application to
metaxylenol (DCMX) are the two most
skin can cause systemic toxicity, manicommonly used members of this group.

fested primarily by CNS and cardiovascular

DCMX is more active than PCMX. Strong
effects; death may result.

solutions of these compounds can cause

Phenol has good penetrating power
irritation and have a disagreeable odor.

into organic matter and is mainly used

A 5% chloroxylenol ( eg, PCMX) solution
for disinfection of equipmen·t or organic

(in a-terpineol, soap, alcohol, and water) is
materials that are to be destroyed ( eg,
diluted with water (1:4) for skin sterilization
infected food and excreta). Because of
and (1:25 to 1:50) for wound cleansing and
its irritant and con-osive properties and
inigation of the uterus and vagina. PCMX is
potential systemic toxicity, it is not used
also combined with hexachlorophene to
much as an antiseptic currently, except to
enhance its antibacterial spectrum and to
cauterize infected areas, eg, the infected
prevent contamination by gran1-negative
umbilicus of neonates. It is also incorpoorganisms.

rated into cutaneous applications for
pruritus, stings, bites, bums, etc, because

REDUCING AGENTS
of its local anesthetic and antibacterial
properties to relieve itching and control

Formaldehyde is a gas, whereas glutaralinfections.

dehyde is an oil at room temperature.

Cresol ( cresylic acid) is a mixture of

However, botl1 are readily soluble in water.

ortho-, meta-, and paracresols and their

Their solutions are irritating or caustic to
isomers. It is a colorless liquid; however,
tissues, causing coagulation necrosis and
after exposure to light and air, it turns pink,
protein precipitation, but have potent
then yellowish, and finally dark brown. A 2%
germicidal properties against all organisms,
solution of either pure or saponated cresol
including spores. Their solutions do not lose

"lysol" in hot water is commonly used as a appreciable antinucrobial properties in the
disinfectant for inanimate objects.

presence of organic matter and are

ANTISEPTICS AND DISINFECTANTS

2743
noncorrosive to metals, paints, and fabric.

skin and mucous membranes. Soaps

Both are used as disinfectants. Formalin
emulsify lipoidal secretions of the skin and
contains 37% formaldehyde gas in aqueous
remove, along with most of the accompanysolution with variable an10unts of methyl ing dirt, desquaniated epithelium and
alcohol to prevent polymerization. A
bacteria, which are then 1i.nsed away with

1 o/er-100/o solution of formaldehyde is
the lather. The antibacterial potency of

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commonly used as a disinfectant. Glutaral
soaps is often enhanced by inclusion of

(glutaraldehyde ), a 1 o/er-2% alkaline solution
certain antiseptics, eg, hexachlorophene,

(pH 7.5--8.5) in 700/o isopropanol, is a more
phenols, carbanilides, or potassium iodide.

potent germicide than 4% formaldehyde,

They are 'incompatible with cationic
effective against all microorganisms,
surfactants.

including viruses and spores. It is often
used to sterilize surgical and endoscopic

Cationic Surfactants: Cationic deteri.nstrun1ents and plastic and rubber gents are a group of alkyl- or aryl-substiapparatus. It is a known sensitizer, causing tuted quaternary a.i1unoniw11 compounds
occupational contact dermatitis, as well as

(eg, benzalkoniun1 chloride, benzathoniun1
bronchial and laryngeal mucous membrane
chloride, cetylpylidinium chloride) with an
irritation.

ionizable halogen, such as bromide, iodide,

Orthophthaldehyde (OPA) is an
or chloride. The major site of action of these
aromatic aldehyde sinli.lar to glutaraldecompounds appears to be the cell memhyde but with several potential advantages.

brane, where they become adsorbed and

Typical 0.55% solutions have excellent
cause changes in permeability. The activity
stability over a wide pH range (3-9), are
of older quaternary animoniw11 compounds
less toxic and irritating to eyes and nasal
is reduced by hard water and by porous or
passages, and have a barely perceptible
fibrous materials (eg, fabrics, cellulose
odor. They are compatible with most
sponges) that adsorb them. They are also
materials, including flexible endoscopes.

inactivated by anionic substances (eg,

OPA solutions are faster acting than
soaps, proteins, fatty acids, phosphates).

glutaraldehyde against mycobacteria but

Therefore, they are of limited value in the
have somewhat less sporicidal activity. A
presence of blood and tissue debris.

potential disadvantage of OPA is that it

However, newer dialkyl quaternary
stains proteins (including unprotected skin)

animonium compounds (fourth generation,
gray, so it must be handled with caution.

including dodecyl dimethyl a.inmonium

Sulfur dioxide, as a gaseous fumigant,
bromide, dioctyl dimethyl anunoniun1
is produced by burning sulfur in closed
bromide, etc) purportedly remain active
spaces. For maxinlal effect, the surface
in hard water and are tolerant of anionic
should be moist, because the gas dissolves
residues. Fifth-generation quaternaries are
in water to fom1 sulfurous acid, which is
mixtures of the fourth generation with the
bactericidal. However, this reducing effect
second generation and demonstrate greater
of the acid can also corrode metals, rot
biocidal activity under conditions of high
fablics, and bleach dyes.

soil load, making them useful disinfectants in barns and footbaths. Quaternary SURFACE-ACTIVE COMPOUNDS
an1monium compounds are effective
against most bacteria, enveloped viruses,

Surfactants lower the surface tension of an
some fungi (including yeasts), and protozoa
aqueous solution and are used as wetting
but not against nonenveloped viruses,
agents, detergents, emulsifiers, antiseptics,
mycobacteria, and spores. Aqueous
and disinfectants. As antimicrobials, they
solutions of 1: 1,000 to 1:5,000 have good
alter the energy relationship at interfaces.

antimicrobial activity, especially at slightly

Based on the position of the hydrophobic
alkaline pH, and are commonly used for
moiety in the molecule, surfactants are
disinfection of noncritical instruments and
classified as anionic or cationic.

hard surface cleaning. When applied to skin,
they may form a film under which microor

Anionic Surfactants: Soaps are dipolar
ganisms can survive, which linlits their
anionic detergents with the general fom1ula
reliability as antiseptics. Concentrations

RCOONa/K, which dissociate in water into

> 1 % are i.njulious to mucous membranes.

hydrophilic K+ or Na+ ions and lipophilic

Octenidine dihydrochloride is a
fatty acid ions. Because NaOH and KOH are
cationic surfactant used increasingly in
strong bases ( whereas most fatty acids are

Europe as an alternative to quaternaries,
weak acids), most soap solutions are
chlorhexidine, and iodophores for skin,
alkaline (pH 8-10) and may irritate sensitive mucous membrane, and wound antisepsis.

2744

ANTISEPTICS AND DISINFECTANTS

OTHER ANTIBACTERIAL AGENTS

VAPOR-PHASE DISINFECTANTS

The antibacterial activity of dyes was first

Alkylating agents such as formaldehyde,
reported in 1913. Interestingly, the
ethylene oxide, and propylene oxide are

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discovery of sulfonamides as chemotherabroad-spectrum biocides active against peutic agents ensued from the antibacte1ial
bacteria, viruses, and fungi, including spores.

activity observed in the dye prontosil.

Ethylene and propylene ox.ides are

Azo dyes ( eg, scarlet red and phenazohighly reactive gaseous fwnigants used to pyridine HCI) are most active in an acidic
sterilize animal feed, human food, surgical
medium and are effective against gramequipment that carmot be autoclaved ( eg, negative organisms. Scarlet red is often
endoscopes, gloves, syringes, catheters,
used as a 5% ointment on sores, ulcers, and
tubing, implantable devices), laboratory
wounds. Pyridium is often incorporated as
equipment, etc. Both are noncorrosive.

an analgesic with sulfonamides to treat

However, ethylene oxide has better
winary tract infections.

penetrability than propylene oxide and,

Acridine dyes ( eg, acriflavine, proflavine,
therefore, is more conrn1only used. For
aminacrine) are more active against
this application, ethylene oxide is mixed
gram-positive bacteria. Their activity is
with chlorofluorocarbons or carbon
enhanced in alkaline meditun and antagodioxide and sold in gas cylinders.

nized by hypochlorites. lmpregnated

Other gaseous disinfectants ( eg,
bandages and gauze and acriflavine jelly
fom1aldehyde, sulfur dioxide, methylbrohave been used extensively for treatment nlide) have been used infrequently because
of burns.

of their toxic or corrosive properties.

ANTIVIRAL AGENTS

The conventional approach to control
nom1al pathways of tl1e host. For these
of viral diseases is to develop effective
reasons, particularly compared with
vaccines, but this is not always possible.

antibacterial drugs, antiviral drugs are

The objective of antiviral activity is to
characterized by a narrow therapeutic
eraclicate the vims while. minimally
margin. Nephrotoxicity is emerging as an
impacting the host and to prevent further
adverse reaction to antiviral drugs in human
viral invasion. However, because of their
medicine. Therapy is fwther complicated by
method of replication, viruses present a
viral latency, ie, the ability of the virus to
greater tl1erapeutic challenge than do
incorporate its genome in tl1e host genome,
bacteria.

•
with cli..tlical infection becoming evident

Viruses comp1ise a core genome of
without reexposure to the organism. In vitro
nucleic acid surrounded by a protein
susceptibility testing must depend on cell
shell or capsid. Some viruses are fwther
cultures, which are expensiye. More
surrounded by a lipoprotein membrane
importantly, in vitro inhibitory tests do not
or envelope. Viruses carmot replicate
necessaiily correlate witl1 tllerapeutic
independently and, as such, are obligate
efficacy of antiviral drugs. Pa.rt of tile
intracellular parasites. The host's pathways
discrepancy between in vitro and in vivo
of energy generation, protein synthesis, and
testing occurs because some drugs requi..t·e

DNA or RNA replication provide the means
activation (metabolism) to be effective.

of viral replication. Viral replication occurs

Only a few antivi..t·al drugs ai·e reasonably
in five sequential steps: host cell penetrasafe ai1d effective against a lin1ited number tion, disassembly, control of host protein
of viral diseases, and most of tllese have
and nucleic acid synthesis such that viral
been developed i..t1 people. Few have been
components are made, assembly of viral
studied in aI1i..t11als, and widespread clinical
proteins, and release of the virus.

use of antiviral drugs is not common in

Drugs that target viral processes must
veteri..t1ary medicine. The advent of human
penetrate host cells; further, because
in1munodeficiency vi..t11s (HIV) and the
viruses often asswne direction of cell
development of tile cat as a model of HIV
division, drugs that negatively impact a
infection has somewhat increased tile
virus are also likely to negatively impact
ani..tnal knowledge base. Only a selection

ANTIVIRALAGENTS

2745
of the more promising agents and their

ACYCLOVIR
pmpo1ted attributes are b1iefiy discussed.

Most antiviral drugs interfere with viral

Acyclovir (acycloguanosine) ai1d its L-valyl
nucleic acid synthesis or regulation. Such
ester prodrug valacyclovir, represent a new

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drugs generally are nucleic acid analogues
generation of antiviral agents, mainly
that interfere with RNA and DNA producbecause of the unique mechanism of action.

tion. Other mechanisms of action include

This purine nucleoside is phosphorylated
interference with viral cell binding or
more efficiently by virus-induced thyn"licline
interruption of virus U11coating. Some vi.ruses
kinase tl1ai1 host thyinidine kinase. Once
contain unique metabolic pathways that serve activated to the t1iphosphate form, it is a as a target of drug therapy. Drugs that simply
better substrate and inhibitor of viral,
inhibit single steps in the viral replication
versus host, DNA polyinerase. Bincling to
cycle are virustatic and only temporaiily halt

DNA polyinerase is irreversible. Once
viral replication. Thus, optimal activity of
acyclovir is incorporated into viral DNA,
some drugs depends on an adequate host
the DNA chain is tern"linatecl.

immune response. Some antiviral drugs may

Acyclovir is relatively safe (probenecid
enhance the inrn1U11e system of the host.

renders the drug safer) and is useful against

TABLE 59 lists the dosage rates for some
a vai"iety of infections caused by DNA
commonly used ai1tiviral drugs.

viruses, especially the herpesvirus family.

However, resistance is increasing. Acyclovir

Pyrimidine Nucleosides: A vaiiety of
is U11able to eli..n1inate latent infections. It is
pyiimidine nucleosides (both halogenated
available as an ophthalmic ointment, a
and nonl1alogenated) effectively inhibit the
topical ointment and creai11, an IV
replication of herpes simplex viruses with
preparation, ai1d vaiious oral formulations.

limited host-cell toxicity. The exact

The proclrug deoxyacyclovir is more readily
mechanism of action of these compoU11ds
absorbed from the GI tract than acyclovir.

appeai-s to reflect substitution of pyiimidine

Anotl1er similar antiviral pwine nucleoside
for thyinicli..ne, causing defective DNA
analogue is ganciclovir, a synthetic guai1ine
molecules. Idoxwicli..ne is effective for
effective against hwnan cytomegalovirus.

treatment of herpesvirus infection of the

Its mechanism of action is similar to that of
superficial layers of the cornea (h.erpesvirus
acyclovir.

keratitis) and of the skin but is toxic when
administered systemically.

PENCICLOVIR AND FAMCICLOVIR

Triflwidine, also an analogue of
deoxythymidine, is currently the agent of

Fainciclovir is tl1e prodrug fo1111 of
choice for treatment of herpesvirus keratitis penciclovir. Penciclovir is very similar to in people. The other antiviral pyrimicli..ne
acyclovir in terms of mechanism of actitm
nucleosides have not been used clinically to
ai1d spectrwn. Although it is much. less
any notable extent.

potent than acyclovir, penciclovir accwnulates to much 11.igher concentrations inside Purine Nucleosides: Ce1tain pwine
the cell. Penciclovir has been studied in cats
nucleosides have proved to be effective
receiving fan1ciclovir at 62.5 mg for 3 clays; it
antivirals ai1d ai·e used as systemic agents.

appeared to be well tolerated.

VIDARABINE

RIBAVIRIN

Vidai·abine, or araA, is used topically for

Ribavirin is a synthetic tria.zole nucleoside
ocular herpesvirus and systemically for

( an analogue of guanosine) with a broad
h.erpetic encephalitis and neonatal
speclrwn of activity against many RNA
herpesviral infections. This drug is an
and DNA vi.ruses, both in vitro ai1d in vivo.

adenosine derivative tl1at is phosphorylatecl

Susceptible virnses include adenoviruses,
by cellular enzyines to a triphosphate
herpesviruses, orthomyxoviruses,
compoU11d that inhibits many viral and
pai·amyxovi..ruses, poxviruses, picornavihwnan DNA polyinerases and thus DNA ruses, rhabcloviruses, rotavin1ses, a11d
synthesis. Herpesviral enzyines are -20-fold
retroviruses. Viral resistance to ribavirin
more susceptible to t11e drug tl1an host DNA.

is rare. The action ofribavirin involves

Vidarabine is administered IV in large
specific inhibition of viral-associated
volwnes of fluid and is rap icily inactivated. It enzyi.11es, inhibition of the capping of viral may produce bone marrow suppression and
mRNA, and inl"libition of viral polypeptide

CNS adverse effects when high blood levels
syi.1thesis. It is well absorbed, widely
are reached. An ophtl1almic solution also is
clistributed in the body, eliminated by renal
available.

and biliaiy routes as botl1 parent drug and

2746

ANTIVIRAL AGENTS
ll·Hllfl DOSAGES OF ANTIVIRAL DRUGS

Drug

Preparation

Dose, Route, and Frequency

Indication

Idoxuridine

0.1% ophthalmic

1 drop, topical, every 5-6 hr
solution

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0.5% ophthalmic

1 drop, topical, every 1-2 hr
solution

Trifluridine

1 % ophthalmic

1 drop, topical, every 2 hr initially Ocular
solution

( 2 days), then 3---8 times daily
herpesvirus
infection

Vidarabine

3% ophthalmic

0.4--1 cm ointment, topical, every Ocular
solution

5-6 hr; 3-6 times daily
herpesvirus
infection

200mg/mL

10-30 mg/kg/day, TV, as CRI for
suspension for

12-24hr
injection

Acyclovir

200-mg capsules or 200 mg, PO, qid, every 4 hr, or Feline
tablets

5 times daily
herpesvirus

5% cutaneous

Cover lesion, topical, every 3 hr,
ointment

6 times daily

200mg/ 5mL

80 mg/kg/day (mixed with peanut Pacheco's
suspension
butter), PO, for 7 -14 days
disease in
birds

500 mg/vial

250-500 mg/m2, TV, tid, infused
powder
over at least 1 hr

Ganciclovir

500 mg/vial

2-5 mg/kg, IV, bid -tid
powder

Ribavirin

11 mg/kg/day, IV, for 7 days

Susceptible
viral
infections

6 g/ 100 mL vial

Using SPAC- 2 nebulizer only,
powder
inhalation, 8-18 hr period daily

Zidovudine

10 mg/mL syrup;

5-20 mg/kg (cats), PO or SC,

FIV,FeLV

10 mg/mL injection bid-tid

Amantadine

100- and 500-mg

100 mg total (human), PO, once to
capsules
twice daily

Syrup 10 mg/mL

100 mg/day total Quveniles ), PO

Rimantadine

200-300 mg/day total (human), PO

Interferon a-2 3 x 106 IU/vial

3 x 106 IU/person/day, SC, IM;

FeLV-associ-

0.5-5 U/kg/day, PO; 100,000 U/kg/ ated disease
day,SC

1 U/day, PO

FeLV appetite
stimulant

15-30 U, PO, IM, SC, once daily on FIP,FIV
alternate weeks

CR! = constant-rate infusion; FeLV = feline leukemia virus; FIP = feline infectious peritonitis; FFV =
feline in11nunocleficiency virus

ANTIVIRALAGENTS

2747
metabolites, and has a plasma half-life of 24
elimination half-life is -1.5 hr, and volume
hr in people. It does not have a wide margin
of distribution is 0.82 IJkg. Drug concentraof safety in domestic anin1als. Toxicity is tions remain above the effective concentramanifest by anorexia, weight loss, bone tion 50 (EC50) of 0.19 mcgtmL for feline
marrow depression and anemia, and GI
immw10deficiency virus for at least 24 hr
disturbances. It has been successfully
after either IV or PO administration.

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administered by topical, parenteral, oral,

Although this concentration is higher than
and aerosol routes. Efficacy depends on the
that associated with myeloid suppression
site of infection, method of treatment, age
of human cells, adverse effects in ca.ts are
of the animal, and infecting dose of virus.

limited to transient restlessness, mild

Results of human influenza studies with
anxiety, and hemolysis.

ribavirin have been equivocal.

Studies in ca.ts regarding the efficacy of

AZT ( 10--20 mg/kg, bid for 42 days) for feline

ZIDOVUDINE
leukemia. virus infection indicated that AZT
prevents retroviral infection if administered

Zidovudine (azidothymidine, AZT) is a
immediately after viral exposure and may
thyrnidine analogue. Within the virusreduce replication if administered to infected cell, the 3' -azido group is used
previously infected animals. Serum-neutralby retroviral reverse transcriptase and izing antibodies developed in some of the
incorporated into DNA transcription,
infected cats, and the ca.ts became resistant
preventing viral replication. The shared
to subsequent viral challenge. There was no
mechanism of action is inhibition of
altered progression of disease in ca.ts when

RNA-dependent DNA polymerase (reverse
treatment was withheld until 28 days after
transcriptase). This enzyme is responsible
infection, although the level of viremia. was
for conversion of the viral RNA genome into
much lower than in untreated ca.ts. AZT
double-stranded DNA before it is integrated
appeared to be nontoxic in uninfected cats,
into the cell genome. Because these actions
although 3 of 12 infected kittens becan1e
occur early in replication, the drugs tend to
anorectic and icteric and were vomiting
be effective for acute infections but are
after 40 days of treatment. AZT may ca.use
relatively ineffective for chronically

Heinz body anemia. CBCs should be
infected cells. Cellular a-DNA polymerases
performed on ca.ts receiving AZT.

are inhibited only at concentrations 100-fold
greater than those necessary to inhibit

AMANTADINE
reverse transcriptase, thus rendering this
drug relatively safe to host cells. Cellular

Amantadine, and its derivative rimanta

-y-DNA polymerase, however, is inhibited
dine, a.re synthetic antiviral agents that
at lower concentrations.

appear to a.ct on an early step of viral

AZT is effective against a variety of
replication after a.tta.clunent of virus to
retroviruses at low concentrations.

cell receptors. The effect seems to lead

Resistance to AZT is associated with point
to inhibition or delay of the uncoa.ting
mutations resulting in amino acid substituprocess that precedes primary transcriptions in the reverse transcriptase. Prolonged tion. Amanta.dine may also interfere with use of AZT can facilitate viral resistance.

the early stages of viral mRNA transcrip

The risk of resistance also appears to
tion. Ama.nta.dine at usual concentrations
correlate with CD4 cell count and the state
inhibits replication of different strains of
of infection. Viral susceptibility to AZT may
influenza. A virus, influenza. C virus, Sendai
return after the drug has been discontinued
virus, and pseudora.bies virus. It is almost
for a period of time.

completely absorbed from the GI tract,

Granulocytopenia and anemia are the
and -90% of a dose administered PO is
major adverse effects of AZT in human
excreted unchanged in the urine over
patients. The risk of toxicity increases in
several days (hwnan data). The main
human patients with low (CD4) lymphocyte
clinical use has been to prevent infection
counts, high doses, and prolonged therapy.

with various strains of influenza. A viruses.

Granulocyte colony-stimulating factor is

However, in people, it also has been found
indicated for management of granulocytoto produce some therapeutic benefit if penia. CNS adverse effects a.re more likely
taken within 48 hr after the onset of illness.

as therapy is begun. The risk of myelosup

Amanta.dine and its derivatives may be
pression is increased by drugs that inhibit
given by the PO, intranasal, SC, IP, or
glucuronida.tion or renal excretion and may
aerosol routes. It produces few adverse
be increased in ca.ts.

effects, most of which are related to the

After a single dose of AZT at 25 mg/kg in

CNS; stimulation of the CNS is evident at
ca.ts, bioa.va.ila.bility is -75%-100%. The
very high doses.

2748

ANTIVIRALAGENTS

MISCELLANEOUS ANTIVIRAL
metabolite that inhibits viral neuramini

AGENTS
dases of human influenza viruses. Mature
influenza viruses bud off from the cell in a

Several drug classes continue to be
sphere of host phospholipid membrane.

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investigated mainly because of their in vitro

The virus will adhere to the cell until
antiviral activities. Their potential clinical
neuraminidase has been cleaved from
usefulness remains obscure in most
the sialic acid residues of the host cell
instances. Included among these agents are
membrane. Neuran1idases allow separation
thiosemicarbazones, guanidine, benzinudaand subsequent release of viral progeny.

zoles, arildone, phosphonoacetic acid,

Hydrolysis, or activation, occurs in the
rifan1ycins and other antibiotics, and

GI tract and liver. The use of oseltanuvir
several natural products.

for treatment of viral diseases in dogs

Oseltamivir is a prodrug that, when

(paivovirus and parainfluenza) is Urns fai·
hydrolyzed, yields the carboxylated
anecdotal.

ECTOPARASITICIDES

ECTOPARASITICIDES USED

Ectoparasites with stages that live off

IN LARGE ANIMALS
the host (ticks, flies, etc) are less easily
controlled. Only a small proportion of the

Arthropod parasites (ectoparasites) are
ectoparasite population can be treated on
major causes of livestock production losses
the host at any one time, ai1d other hosts
throughout the world. In addition, mai1y
may maintain them. Some tick species stay
arthropod species can act as vectors
on the host only long enough to feed, wluch
of disease agents for both aninlals and
may be as short as 30 nun or as long as
people. Treatment with various parasiti21 days. Biting flies, such as the horn fly, can cides to reduce or elinunate ectoparasites
be found continually on the backs and
is often required to maintain health and to
undersides of cattle, where they suck blood
prevent economic loss in food aninlals.

up to 20 times a day; other biting lies ( such

Some ectopai·asiticides were derived from
as stable flies and horse lies) and mosquipesticides used to protect crops. The choice toes feed to repletion, then leave the ruumal
and use of ectoparasiticides depend to a
to lay eggs. Nonbiting flies, such as the face
large extent on husbandry and managefly or house fly, may visit infrequently but ment practices, as well as on the type of
can be very armoying and may transmit
ectoparasite causing the infestati.OJl.

disease agents. Larvae of certain blowflies

Endectocides are capable of killing both
live on the skin or in tissues of sheep ru1d
internal and external parasites. Accurate
other animals and cause cutaneous myiasis.

identification of the parasite or correct

Larvae of other flies spend several months
diagnosis based on clinical signs is
inside anin1als ( eg, nasal bots in .. tl1e nasal
necessary for selection of the appropriate
passages of sheep and goats, bots in the
parasiticide. The selected agent can be
stomach of horses, and cattle grubs or
administered or applied directly LO the
warbles in the back or esophageal tissues).

anin1al, or introduced into the environment

(See a/,so ,LIES, p 885.)

to reduce the aithropod population to a

Many ectoparasite infestations are
level that is no longer of economic or health
seasonal and predictable and can be
consequence.

countered by prophylactic use of ecto

Parasites that live pern1anently on the
parasiticides. For exrunple, in temperate
skin, such as lice, keds, and nutes, can be
cotmtries, lies are seen predominantly
controlled by directly treating the host.

from late spring to early autw1m, tick

Some mange nutes burrow into the skin and
populations often increase in the spring
are therefore more difficult to control with
ru1d auttmrn, and lice and mite infestations
sprays than are lice and keds, which are
can be more common during the autwnn
found on the surface of the skin. However,
and winter months. Treatments can be
once these obligate parasites are eraditargeted at anticipated times of peak cated, reinfection occurs only from contact
activity as a way to limit parasite populawith other infected animals.

tions and disease.

ECTOPARASITICIDES

2749

Products are available for parenteral

This state renders the ne1ve vulnerable to
administration or for topical application by
repetitive discharge from small stimuli that
various methods, including dips, sprays,
would nonnally cause an action potential in
pour-ons, spot-ons, dusting powders, and
a fully repolarized neuron.

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ear tags. The method used depends on the

The cyclodienes appear to have at least
target parasite and host. (See ROUTES OF
two component modes of action: inhibition

ADMINISTRATION AND DOSAGE FORMS, p 2508.)

of -y-aminobutyric acid (GABA)-stimulated

Importantly, most topical ectoparasiticides

CJ- flux and interference with Ca2+ flux. The
used in the USA are pesticides regulated by
resultant inhibitory postsynaptic potential
the U.S. Environmental Protection Agency
leads to a state bf partial depolarization of

(EPA). This is an important distinction from
the postsynaptic membrane and vulnerabilproducts regulated by the U.S. Food and ity to repeated discharge. A sinlilar mode of

Drng Administration (FDA), because it is
action has been reported for lindane, which
illegal to use an EPA-regulated pesticide
binds to the picrotoxin side of GABA
product inconsistent with its label
receptors, resulting in an inhibition of
directions (www.epa.gov). The regulating

GABA-dependent CJ- ion flux into the
agency should be identifiable on the product neuron.

label. The National Pesticide Information

DDT and BHC were used extensively for

Retrieval System (NPIRS) is a searchable
flystrike control but subsequently replaced
database of EPA-registered products
in many countries by more effective

(http://ppis.ceris.purdue.edu/).

cyclodiene compounds, such as dieldrin and
aldrin. Both the development of resistance

Chemotherapeutic Agents
and environmental concerns led to their
withdrawal. DDT and lindane were widely

Most ectoparasiticides are neurotoxins,
used in dip formulations to control sheep
exerting their effect on the nervous system
scab, but they have mostly been replaced by
of the target parasite. Those used in large
the organophosphates and subsequently the
animals can be grouped according to
synthetic pyrethroids.

strncture and mode of action into the
organochlorines, organophosphates and

Organophosphates and Carbamates:

carbarnates, pyrethrins and pyrethroids,

The organophosphates comprise a large
macrocyclic lactones (avermectins and
group of chemicals, many of which are
rnilbemycins), formarnidines, insect growth
available for topical application and in ear
regulators, and a number of miscellaneous
tags as well as for premise control of
compatmds, including synergists ( eg,
parasites. There have been many products
piperonyl butoxide ). There are also a
available worldwide for use in domestic
number of useful compounds with repellent
animals, although only a few of the available
rather than insecticidal activity, including
compounds continue to be used for
butoxypolypropylene-glycol and
on-animal treatment.

N,N-diethyl-3-methylbenzanlide (DEET,

Organophosphates are neutral esters
previously called N,N-diethyl-metatoluaof phosphoric acid or its thio analogue that mide).

inhibit the action of acetylcholinesterase

(AChE) at cholinergic synapses and at

Organochlorines: Organochlorine
muscle end plates. The compound minlics
compounds have been withdrawn in many
the strncture of acetylcholine (ACh); when
parts of the world because of concerns
it binds to AChE, it causes transphosphory regarding environmental persistence.

lation of the enzyn1e. The transphorylated

Organochlorines fall into three main

AChE is unable to break down accumulatgroups: 1) chlorinated ethane derivatives, ing ACh at the postsyl'aptic membrane,
such as DDT ( dichlorodiphenyltrichloroethleading to neuromuscular paralysis. The ane ), DDE (dichlorodiphenyldichloroethdegree oftransphorylation of the enzyn1e ane), and DDD (dicofol, methoxychlor);
helps to detern1ine the activity of the

2) cyclodienes, including chlordane, aldrin,
organophosphate. Eventually, the AChE is
dieldrin, hepatochlor, endrin, and toxametabolized by oxidative and hydrolytic phene; and 3) hexachlorocyclohexanes
enzyme systems.

such as benzene hexachloride (BHC), which

Organophosphates can be extremely
includes the -y-isomer, lindane.

toxic in animals and people, inhibiting

Chlorinated ethanes cause inhibition of

AChE and other cholinesterases (see
sodium conductance along sensory and
p 3064). Chr011ic toxicity results from
motor nerve fibers by holding sodium
inhibition of an enzyn1e known as neuropachannels open, resulting in delayed thy target esterase (NTE) or neurotoxic
repolarization of the axonal membrane.

esterase and is associated with particular

2750

ECTOPARASITICIDES
compounds. NTE hydrolyzes the fatty acids
excellent knockdown (rapid kill) but have
from the membrane lipid, phosphotidylchopoor residual activity because of instability.

line, and inhibition ofNTE appears to cause

Pyrethrin I is tile most active ingredient for
structural changes in neuronal membranes
kill, and pyrethrin II for rapid insect
and a reduction in conduction velocity,
knockdown.

which may be manifest as posterior

Pyrethroids are syntllesized chemicals

VetBooks.ir
paralysis in some animals. Cases of
modeled on the natural pyrethrin molecule.

organophosphate toxicity are treated with

They are more stable, thus have longer
oximes or atropine.

residual activity, and have a higher potency

Organophosphates used topically include
than natural pyretllrins.

coumaphos, diazinon, dichlorvos, malathion,

The mode of action of pyrethrins and
tetrachlorvinphos, trichlorfon, phosmet, and
synthetic pyrethroids appears to be
pirimiphos. Ear tags containing chlorpyrifos,
interference witll sodium channels of the
coumaphos, diazinon, or pirimiphos are
parasite nerve axons, resulting in delayed
available. These compounds are generally
repolarization and eventual paralysis.

active against fly larvae, flies, lice, ticks,

Synthetic pyrethroids can be divided into
and mites on domestic livestock, although
two groups (types I and II, depending on the
activity varies between compounds and
presence or absence of an o:-cyano moiety).

differing fonnulations. Chlorpyrifos can be

Type I compounds have a mode of action
used in microencapsulated form for residual
similar to that of DDT, involving interferactivity and improved safety. Diazinon and ence with tile axonal Na+ gate leading to
propetamphos have been available in dip
delayed repolarization and repetitive
fonnulations to control psoroptic mange in
discharge of the nerve. Type II compounds
sheep. Both eliminate mites and protect in a
also act on the Na+ gate but do so without
single application when correctly applied.

causing repetitive discharge. The letllal

Diazinon provides longer residual protection activity of pyrethroids seems to involve than propetamphos. In cattle, a number of
action on botll peripheral and central
compounds have been used for systemic
neurons, while peripheral neuronal effects
control of warble fly grubs and lice as
alone probably produce tile knockdown
pour-on applications or in hand sprays,
effect. Some preparations contain a
spray races, or dips for tick control.

synergist ( eg, piperonyl butoxide ), which

Carbamate insecticides are closely
inhibits breakdown of pesticides by
related to organophosphates and are
microsomal mixed-function oxidase
anticholinesterases. Unlike organophos

( cytochrome P450) systems in insects.

phates, they appear to cause a spontane

Pyrethroids are generally safe in
ously reversible block on AChE without
mammals and birds but are highly toxic to
changing it. The main carban1ate compound
fish and aquatic invertebrates. Concerns
used in veterinary medicine is propoxur.

have been expressed over tlleir environ

Carbary I, anotller carban1ate previously
mental effects, particularly in relation to
used in veterinary medicine, has been
the aquatic environment, leading to tlleir
withdrawn from the veterinary market.

witlldrawal as sheep dips in some countries.

Some of the more common pyrethroids
used include 13-cyfluthrin, bioallethrin,

Pyrethrins and Synthetic Pyrethroids:

cyfluthrin, cypermethrin, deltamethrin,

A number of pyrethroids are available in
fenvalerate, flumethrin, lambda cyhalothrin,
many countries as pour-on, spot-on, spray,
phenothrin, permethrin, prallethrin, and
and dip formulations with activity against
tetramethrin. The content of some syntlletic
biting and nuisance flies, lice, and ticks on
pyrethroids is also expressed in terms of tile
domestic livestock. Flun1ethrin and high
drug isomers, eg, cypermethrin prepar a cis-cypennetlui.n are also active against tions may contain varying proportions of
mites and have been used to treat psoroptic
their cis and trans isomers. Thus, cypermemange of sheep.

thrin ( cis:trans 60:40) 2.5% is equivalent to

Natural pyrethrins are derived from
cypermethrin ( cis:trans 80:20) 1.25%. In
pyretllrum, a mixture of alkaloids from tile
general, cis isomers are more active than

Chrysanthemum plant. Pyrethrum extract,
tile corresponding trans isomers.

prepared from the pyrethrum flower head,
contains several molecules collectively

Macrocyclic Lactones (Avermectins
known as pyretlui.ns (pyretlui.n I and II,
and Milbemycins): Avermectins and the
cinerin I and II, and jasmolin I and II).

structurally related rnilbemycins, collec

Pyrethrins are lipophilic molecules tllat
tively referred to as macrocyclic lactones,
generally undergo rapid absorption,
are fermentation products of Streptomyces
distJ.i.bution, and excretion. They provide
avermitilis and S cyanogriseus, respec-

ECTOPARASITICIDES

2751
tively. Avem1ectins differ from each other
half-life of these compounds also deterchemically in side chain substitutions on the nlines residue levels in meat and milk and lactone ring, whereas milbemycins differ
the subsequent compulsory withdrawal
from the avem1ectins through the absence
periods after treatment in food-producing
of a sugar moiety from the lactone skeleton.

animals.

A number of macrocyclic lactone com

Macrocyclic lactones bind to glutamate

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pounds are available for use in anin1als
receptors of glutamate-gated chloride
and include the avern1ectins abamectin,
channels, triggering CJ- ion influx and
doramectin, eprinomectin, ivennectin, and
hyperpolariza.tion of parasite neurons,
selamectin, and the milbemycins moxideclea.ding to flaccid paralysis. These moltin and milbemycin oxime. These comecules have low affinity for mammalian pounds are active against a wide range of
ligand-gated chloride charmels and do not
nematodes and arthropods and are often
readily cross the blood-brain barrier.

refen-ed to as endectocides.

Endectocidal activity, particularly against

Formamidines: Amitra.z is the only
ectoparasites, is variable and depends on
fonnarnidine used as an ectoparasiticide. It
the active molecule, the product formulaappears to a.ct by inllibition of the enzyme tion, and the method of application.

monoanline oxidase and as an agonist at

Macrocyclic lactones can be given PO,
octopamine receptors. Monoanline oxidase
parenterally, or topically ( as pour-ons and
metabolizes an1ine neurotransmitters in
spot-ons). The method of application
ticks and mites, and octopa.mine is thought
depends on the host and, to some degree, on
to modify tonic contractions in parasite
the target parasites. In cattle, for example,
muscles. Amitra.z has a relatively wide
available endectocide products can be given safety margin in mammals; the most PO, by injection, or topically using pour-on
frequently associated adverse effect is
fomrnlations. The latter are generally more
sedation, which may be associated with an
effective against lice (Linognathus,
agonist activity of an1itra.z on otrreceptors in

Haematopinus, and to some extent
manunalian species.

Bovicola) and headfly (Haematobial

Amitra.z is available as a spray or dip for

Lyperosia) infestations than equivalent
use against mites, lice, and ticks in domestic
compounds administered parenterally.

livestock. It controls lice and mange in pigs

In sheep, PO administration of some
and psoroptic mange in sheep. In cattle, it
endectocides has little effect against
has been used in dips, sprays, or pour-ons
psoroptic mite infestations (Psoroptes
for control of single-host and multihost tick
ovis ), but parenteral administration
species. In dipping baths, a.rnitra.z can be
increases activity, providing both protection stabilized by the addition of calcium and control depending on the product used.

hydroxide and maintained by standard

The route of administration and product
replenishment methods for routine tick
formulation influence the rates of absorpcontrol. An alternative method involves the tion, metabolism, excretion, and subsequent use of total replenishment formulations in bioavailability and pharmacokinetics of
which the dip bath is replenished with full
individual compounds. Avennectins and
concentration of a.rnitra.z at weekly intervals
milbemycins are highly lipophilic, a
before use. Amitra.z is contraindicated in
property that varies with only minor
horses.

modifications in molecular structure or
configuration. After administration, these

Chloronicotinyls and Spinosyns:

compounds are stored in fat, from which
lmida.clop1id is a chloronicotinyl insectithey are slowly released, metabolized, and cide, a synthesized chlorinated derivative
excreted. Ivermectin is absorbed systemiof nicotine. Spinosad is a fermentation cally after PO, SC, or dermal administration;
product of the soil a.ctinomycete Saccha
it is absorbed to a greater degree and has a
ropolyspora spinosa. Both compounds
longer hal f -life when given SC or dermally.

bind to nicotinic acetylcholine receptors

Excretion of the unaltered molecule is

(but at different sites) in the insect's CNS,
mainly via the feces, with <2% excreted in
lea.ding to inhibition of cholinergic transmisurine of runlinants. In cattle, the reduced sion, paralysis, and death. Spinosa.ct has
absorption and bioavailability of ivermectin
been developed in some countries for use
given PO may be due to its metabolism in
on sheep to control blowfly strike and lice.

the rumen. The affinity of these compounds
for fat explains their persistence in the body

Insect Growth Regulators: Insect
and the extended periods of protection
growth regulators (IGRs) a.re used
afforded against some species of internal
throughout the world and represent a
and external parasites. The prolonged
relatively new category of insect control

2752

ECTOPARASITICIDES
agents. They constitute a group of chemical
use in cattle as a tick development inhibitor.

compounds that do not directly kill the

When applied as a pour-on, it provides
adult parasite but interfere with growth and
longterm protection against tl1e 1-host tick,
development. Because they act mainly on

Rhipicephalus (Boophilus) microplus.

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immature parasite stages, IGRs are not

Triazine and pyrinlidine derivatives are
usually suitable for rapid control of
closely related compounds that are also
established adult parasite populations.

chitin inhibitors. They differ from the ben

Where parasites show a clear seasonal
zoylphenyl ureas both in chemical structure
pattern, IGRs can be applied before any
and mode of action, ie, they appear to alter
anticipated challenge as a preventive
the deposition of chitin into the cuticle
measure. They are widely used for blowfly
rather than its synthesis.

control in sheep but have limited use in

Cyromazine, a triazine derivative, is
other livestock.

effective against blowfly larvae on sheep

Based on their mode of action, JGRs can
and lan1 bs and also against otl1er Diplera
be divided into chitin synthesis inhibitors
such as houseflies and mosquitoes. At

(benzoylphenyl ureas), chitin inhibitors
reconunended dose rates, cyromazine

(triazine/pyrinlidi.ne derivatives), and
shows only limited activity against
juvenile hormone analogues (S-methoprene, established strikes and must therefore be pyriproxyfen). Several benzoylphenyl ureas
used preventively. Blowflies usually lay eggs
have been introduced to control ectoparaon damp fleece of treated sheep. Although sites. Chitin is a complex aminopolysaccha-larvae are able to hatch, the yotmg larvae

1ide and a major component of the insect's
immediately come into contact with
cuticle. During each molt, it has to be newly
cyromazine, which prevents the molt to
formed by polymerization of individual
second instars. The efficacy of a pour-on
sugar molecules. The exact mode of action
preparation of cyromazine does not depend
of the benzoylphenyl ureas is not fully
on factors such as weather, fleece length,
w1derstood. They inhibit chitin synthesis
and whether tl1e fleece is wet or dry. Control
but have no effect on the enzyme chitin
can be maintained for up to 13 wk after a
synthetase. It has been suggested that they
single pour-on application, or longer if
interfere with the assembly of the chitin
cyromazine is applied by dip or shower.

chains into nlicrofibrils. When immature

Dicyclanil, a pyrimidine derivative, is
insect stages are exposed to these
highly active against dipteran larvae. A pourcompounds, they are not able to complete on fonnulation, available in some countlies
ecdysis and die dwing molting. Benzoylphefor blowfly conti·ol in sheep, provides up to nyl ureas also appear to have a transovarial

20 wk of protection.

effect. Exposed adult female insects

The juvenile hormone analogues mimic
produce eggs in wllich the compound is
the activity of naturally occw-ringjuvenile
incorporated into the egg nutrient. Egg
hormones and prevent metamorphosis to
development proceeds normally, but tl1e
the adult stage. Once the larva is fully
newly developed larvae are incapable of
developed, enzymes within the insect's
hatching. Benzoylphenyl ureas spow a
circulatory system desti·oy endogenous
broad spectrun1 of activity against insects
juvenile honnones, prompting development
but have relatively low efficacy against ticks
to the adult stage. The juvenile hormone
and mites. The exception is fluazuron,
analogues bind to juvenile honnone
which has greater activity against ticks and
receptor sites, but because they are
some mite species.

structurally different, are not destroyed by

Benzoylphenyl ureas are highly lipopllilic
insect esterases. Metamorphosis and
molecules. When administered to the host
further development to the adult stage does
they build up in body fat, from which tl1ey
not proceed. S-Methoprene is a terpenoid
are slowly released into tl1e bloodstream
compound with very low manunalian
and excreted largely unchanged. Diflubentoxicity that mimics a juvenile insect zw-on and flufenoxuron are used to prevent
hormone and is used as a feed-through
blowfly strike in sheep. Diflubenzuron is
larvicide for homfly (Haematobia) control
available in some countries as an emulsifion cattle.

able concentrate for use as a dip or shower.

It is more efficient against first-stage larvae

Miscellaneous Compounds: Piperonyl
than second and third instars and is
butoxide and MGK 264 (N-octyl bicycloheptherefore recommended as a preventive, tene dicarboximide) are used as synergistic
providing protection for 12-14 wk. It may
additives in the control of arthropod pests.

also have potential to control a nwnber of

They are commonly formulated together
major insect pests such as tsetse flies.

with insecticides such as natural pyrethrins.

Fluazuron is available in some countries for

The degree of potentiation of insecticidal

ECTOPARASITICIDES

2753
activity is related to the ratio of compofor control of the horn fly, Haematobia nents in the mixture; as the proportion of
irrilans. Given the large numbers of adult
piperonyl butoxide or MGK 264 increases,
females that must be attracted and killed to
the amount of natural pyrethrins required to
achieve effective population management,

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evoke the same level of kill decreases. The
this is often not possible with the visual and
insecticidal activity of other pyretlu·oids,
olfactory baits available. One notable
particularly of knockdown agents, can also
exception is in the control of the tsetse fly
be enhanced by the addition of piperonyl

(Glossina spp ), for which high levels of conbutoxide or MGK 264. Piperonyl butoxide trol can be a<;:hieved due to their very low
inhibits the microsomal enzyme system of
rate of reproi:luction and the availability of
some arthropods and is effective against
highly effective baits and traps. In Australia,
some mites. In addition to having low
a nonretw11 insecticide-free trap to catch
man1malian toxicity and a long record of

Lucilia cup1ina is commercially available.

safety, it rapidly degrades in the environ

The ability of this trap and bait system to
ment.

suppress fly populations and to reduce

Various products from natural sources,
strike incidence has been investigated in the
as well as synthetic compounds, have been
southern hemisphere witl1 variable results,
used as insect repellents. Such compounds
although reductions in strike incidence of
include cinerins, pyrethrins andjasmolins
up to 46% have been reported.

(seep 2750), citronella oil, di-N-propyl
isocinchomeronate, butoxypolypropylene
glycol, picaridin, DEET, and DMP ( dimeth

Safety Restrictions
ylphthalate). The use of repellents is
advantageous as legislative and regulatory

It is important to be aware of and follow
authorities become more restrictive toward
safety restrictions to prevent poisoning or
the use of conventional pesticides. They are
injury to treated animals. All organophosused mainly to protect horses against phates available for use on animals ar·e
blood-sucking arthropods, particular·ly
cholinesterase inhibitors. They should not
midges (Cu/icoides).

be used sinmltar1eously or within a few days

Insecticides may be used to provide
before or after treatment or exposw·e to
environmental control of some insects
other cholinesterase-inhibiting drugs,
by application to premises. The insect
pesticides, or chemicals. They should not
pheromone (Z)-9-tricosene is incorporated
be applied to young, sick, convalescent, or
into some products to attract insects to the
stressed animals.

site of application.

Pyrethroid insecticides available for use
on lar·ge anin1als are considered safe but

Other Control Methods
have general precautionary statements on
their labels, particularly in relation to

Biologic Control: The use of natmally
disposal and their potential ecotoxicologic
occurring biologic pathogens, such as
effects.

nematodes, bacteria, fungi, and viruses,

Some parasiticides may be used only by
offer an interesting approach to ectoparaor tmder the supervision of a veterinarian; site management. Bacillus thuringiensis
others are available via agricultural
has been used on sheep to prevent blowfly
suppliers and pharmacists directly to tl1e
strike and body lice. The use of fungal
public. Approvals vary from country to
pathogens such asMetarhizium aniso
count1y. Labels for pesticides contain
pliae has also been investigated for control explicit it1forn1ation on hazards to animals,
of ticks on livestock and mites on cattle and
people, and tl1e environment; storage of
sheep.

tm used insecticide; and disposal of the
container. For each insecticide, the label is

Off-host Control: The control of
the primary source of ituomiation on uses
populations of arthropod pest species using
and safety instructions, which should be
nonreturn traps and tar·gets (screens),
car·efully followed.

usually accompanied by semiochemical

Restrictions ar·e applied to many of the
baits, has been considered widely for
ectopar·asiticides it1dicated for use in
parasites such as ticks or flies. The aim is to
food-producing ar1inlals to ensure that
attract ar1d kill tar·geted pests in appropriate
unacceptable residues ar·e not present in
nun1bers during the stages in which tl1ey ar·e
products intended for hun1an consun1ption.

off the host. This approach has been used as These restrictions may require that artitnals a component of the eradication of the
are not slaughtered for prescribed periods
primary screwwonn fly, Cochliomyia
after administration of the product or that
hominivorax, from North America and
the product is not used in artitnals produc-

2754

ECTOPARASITICIDES
ing milk for human consumption. Labels
influx of Cl- into the nerve cell. This inltibits
and data sheets on all products contain
nerve activity and causes paralysis of the
specific instructions on restrictions,
parasite. Selan1ectin is presented as a single
including withdrawal periods, and must be
active ingredient; moxidectin is combined
followed.

with inudacloprid (see NEONICOTINOIDS,
below); and eprinomectin has been

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ECTOPARASITICIDES USED
combined with fipronil (see PHENYLPYRAZOLES, IN SMALL ANIMALS
p 2756), S-methoprene (see INSECT GROWf!-1

REGULATORS, p 2756), and praziquantel. These

Flea and tick infestation is a major health
macrocyclic lactones are applied topically,
problem in dogs and cats, and control
rapidly absorbed through the skin, and
presents an economic burden to owners.

distributed via the blood. They have activity

Traditionally, a wide array of ectoparasitiagainst a variety of internal and external cides has been available, and switching
parasites.

an1ong brands was frequent, leading to
problems in achieving acceptable external

Cholinesterase Inhibitors: Two groups
parasite control. Veterinarians are uniquely
of compounds, organophosphates and
qualified to explain the host/parasite
carbamates, share the same mechanism of
interrelationships and advise owners on
action-inhibition of acetylcholinesterase.

selection of the most suitable control

This enzyme nom1ally is responsible for
program. However, many pet owners
acetylcholine (neurotransmitter) destrucstill purchase flea and tick products in tion. Applications of organophosphates or
supermarkets or pet supply shops where
carbamates to insects produce spontaneprofessional advice is not available. Recent ous muscular contractions followed by
advances in product technology have
paralysis. The binding of organophosgreatly expanded the available options for phates to acetylcholinesterase is more
veterinarians and pet owners. However, this
persistent, if not permanent, whereas the
wide array of available parasiticides can
interaction with carbamates is reversible.

lead to confusion. Veterinarians should

These compounds were once very popular
become fanilliar with these technologic
for their prolonged action and potency.

improvements in both insecticidal

However, the use of organophosphates has
chemistry and delivery systems and
declined because their low margin of safety
encourage client education by their staff.

and slight variance from approved use or
continued use may lead to toxicity. When

Active Chemical Ingredients
these compounds are used for flea or tick
control, it should be determined before

Nomenclature can be confusing if the
treatment whether any other cholinestershorter approved name is not used and the ase inhibitor has been used on the animal
full chemical nan1e is written ( eg, chlorpyrior in its environment. Organophosphates fos versus 0,0-diethyl 0-[3,5,6 trichloro 2]

for small animal therapy include chlorpyriphosphorothioate). The use of trade names fos, dichlorvos, malathion, diazinon,
can cause added confusion. Altnough most
phosmet, fenthion, chlorfenvinphos, and
commercial products contain only one
cythioate. Carbamates include carbaryl
active ingredient, it is not uncommon for
and propoxur.

two or more to be combined to provide
enhanced efficacy or broader spectrun1

Chlorinated Hydrocarbons: These
of activity. All labels should be read
compounds are beconting less popular
carefully for ingredients, age and species
because of their persistence in the
restrictions, and directions for use.

envirornnent, although tlus factor brought
the benefit of prolonged action. Lindane and

Macrocyclic Lactones: Currently, tlu-ee
methoxychlor are still occasionally used.

macrocyclic lactones are used for control of

(See also CI-ILORINATED HYDROCARBON
internal and external parasites in dogs and

COMPOUNDS, p 3060.)

cats: selamectin and aprinomectin, which
are semisynthetic avermectins, and

Neonicotinoids: The neonicotinoids
moxidectin, a semisynthetic milbemycin.

are a class of insecticides referred to as

Although the exact mode of action of
nitroquanidines, neonicotinyls, chloronicomacrocyclic lactones is not fully elucidated, tines, and recently as chloronicotinyls. The
it is believed that they bind to glutamateneonicotinoids are modeled after natural gated chloride charmels in the parasites'

nicotine. Three compounds in this category
nervous system, increasing their penneabilare currently available for veterinary use: ity and allowing for the rapid and continued
dinotefuran, intidacloprid, and nitenpyram.

ECTOPARASITICIDES

2755

All neonicotinoids act as agonists on the
were originally developed for use against a
postsynaptic acetylcholine receptors in
variety of insects infesting vegetables, fruit,
insects. This inhibits cholinergic transmisand row crops. Indoxacarb is the only sion, resulting in paralysis and death.

member of this group currently being used

Imidacloprid is applied as a spot-on topical
in veterinary medicine. It is considered a
product and is used primarily to control
pro-insecticide that is metabolized within

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fleas on both dogs and cats. It also has
the insect to a more active fonn, which is an
excellent activity against lice. Although it

N-decarbomethoxylated metabolite that is
has potent residual activity, it is readily
at least 40 times more potent than parent
soluble in water, so swimming and repeated
indoxacarh This metabolic conversion of
bathing may compromise its duration of
indoxacarb, known as bioactivation, is
activity. Nitenpyram is administered PO in
attributed to actions of esterase and
pill fonn to kill fleas in both dogs and cats.

an1idase enzymes within the insect. The

It is absorbed rapidly, with maximal blood
active metabolite exerts its effect by
concentrations reached within 1.2 hr in
blocking the voltage-gated sodium ion
dogs and 0.6 hr in cats. Fleas begin to die
channels in insects. Indoxacarb is
within 20-30 min of administration, with
administered topically in a spot-on
lOO"A, flea mortality within 3-4 hr. The
formulation for control of fleas on dogs
compound is rapidly elinlinated, with >90%
and cats. Indoxacarb has also been
excreted in the urine within 24-48 hr,
combined with permethrin for control
primarily as unchanged nitenpyran1. Even
of ticks on dogs.

though irnidacloprid and nitenpyram are
classified sin1ilarly, their mechanisms of
lsoxazolines: Isoxazolines are a new
action appear to be different. Although
class of compounds that have both potent
imidacloprid is described as a paralytic,
insecticidal and acaricidal activities.

nitenpyran1 produces hyperexcitability in

Isoxazolines have a novel mode of action
fleas before death.

and specifically block arthropod ligand

The newest addition to the neonicogated chloride channels. Afoxolaner and tinoids is dinotefuran, considered a
fluralaner are currently the only two
third-generation neonicotinoid. The
compounds approved for use in veterinary
structure of dinotefuran is unique in that it
medicine. Both are unique in iliat they were
was derived from that of the acetylcholine
the first oral flea and tick products. The
molecule rather than nicotine. It has been
compounds are readily absorbed after oral
proposed that dinotefuran does not bind to
administration and provide 4-12 wk of
the same sites as imidacloprid and other
insecticide and acaricide activity.

neonicotinoids but at a different site in the
nerve synapse. Dinotefuran is applied as a

Insect Growth Regulators: These .

topical spot-on with different formulations
compounds inhibit the development of
for dogs and cats. The cat formulation is
immature stages of insects. They are
combined with the insect growth regulator
generally classified as either juvenile
pyriproxyfen and is used primarily to
hormone mimics (insect growth regulacontrol fleas. The dog formulation contains tors) or as chitin synthesis inhibitors pyriproxyfen and permethrin and is

(insect development inhibitors). Metholabeled for control of fleas, ticks, and prene, fenoxycarb, and pyriproxyfen are
mosquitoes.

similar in structure to insect juvenile
hormone and are classified as juvenile

Formamidines: This small group of
hormone mimics. When these compounds
acaricidal compounds has the proposed
are applied to flea larvae or into their
mode of action of binding to octopamine
environment, they are absorbed by the
receptors, a specific group of receptors
larvae and act like natural insect juvenile
found in Acari. In veterinary medicine, the
hormone. Juvenile hormone analogues
only approved formarnidine is arnitraz. It is
bind to juvenile hormone receptor sites;
used primarily as an acaricide to control
larvae are prevented from completing
ticks and mites. It is available as a dip for
metamorphosis and subsequently die.

control of canine demodicosis, and it will

These compounds also have ovicidal and
also control scabies. An arnitraz-impregembryocidal activity against flea eggs when nated collar is also marketed for control
applied topically to dogs at1d cats. Female
of ticks on dogs. Amitraz is not approved
fleas in the hair coat absorb the juvenile
for use on cats.

hormone analogue, which affects viability
of developing eggs. These compounds are

Oxadiazines: Oxadiazine insecticides can
active against a wide range of insects,
control a broad spectrum of insects and
including mosquito larvae; methoprene is

2756

ECTOPARASITICIDES
used as a larvicide in the strategic control causing paralysis. Although the activity is
of mosquito-borne diseases. For flea
rapid, without sufficient exposure paralyzed
control, their outdoor use should be limited insects can also recover rapidly. The to specific flea habitats to avoid adverse
synergists piperonyl butoxide and N-octyl
effects on beneficial insect species.

bicycloheptene dicarboxymide i.nteliere

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Lufenuron, a benzoylphenyl urea,
with the insect detoxification mechanism
inhibits the formation of chitin (a polymer
and can potentiate the activity of pyreof N -acetyl glucosamine), which is a major throids. Natural pyrethrum is extracted
component of insect exoskeletons. During
from chrysanthenuun flowers and is notable
each larval molt, chitin is reformed by
for its rapid but brief action and relative
polymerization. Lufenuron intelieres with
lack of toxicity in dogs and cats.

polymerization and deposition of chitin,

Synthetic pyrethroids are pyretlmm1-like
killing developing larvae either within
compounds t11at generally have greater
the egg or after hatching. Lufenuron is
potency and residual effects but are less
administered PO to dogs or cats or by
well tolerated in cats. Some pyrethroids,
injection to cats. Female fleas feeding
such as pem1ethri.n, can be highly toxic to
on treated animals are prevented from
cats. Pyrethroids are generally classified by
producing viable eggs or larvae. Other
developmental generation. First-generation
insect development inhibitors, such as
pyretl1roids are generally unstable in heat
diflubenzuron (another chiton inhibitor)

and sunlight (eg, allethtin); second-generaand cyromazine (a moulting disruptor), tion are more photostable, isomeric
also have considerable activity against
mixtures (eg, cype1methrin, pe1methrin);
developing fleas. Insect growth regulators
third-generation are photostable and more
and insect development inhibitors affect
neurologically active isomers obtained by
many insect species that undergo
isomeric enrichment ( eg, X.-cyhalothri.n,
complete metamorphosis, but they have

[3-cyfluthrin); and fourth-generation are
little or no activity against ticks or other
nonester pyretht·oids ( eg, MTI 800,

Acari, which undergo incomplete
flufenprox, etofenprox).

metamorphosis.

Spinosyns: Spinosyns are a novel family

Phenylpyrazoles: This group of
of insecticides derived from the fermentacompounds has broad-spectrum activity tion of the actinomycete, Saccharopoly
that is both insecticidal and acaricidal. The
spora spinosa. The two most abundant
members of this group currently available
products derived from the fermentation
for use in veterinary medicine worldwide
process are spinosyns A and D, which are
include fipronil and pyriprole. These
the major active components of spinosad.

compounds bind to -y-am.inobutyric acid

Spinosad is used to control a wide variety
and glutamate-gated receptor sites of
of insects, i.ncluding flies and fleas.

insect nervous systems, inhibiting the flux

Spinosyns have a novel mode of action,
of CJ- into nerve cells, which results in
primarily targeting binding sites on
hyperexcitability. These compounds have
nicotinic acetylcholine receptors distinct
broad-spectrum activity againsl; fleas, ticks, from other insecticides such as neonicotimites, and lice. Numerous fipronil-containnoids. Spinosyns also affect -y-a.minobutyric ing fo1mulations are available worldwide,
acid receptor function, which may
including an alcohol-based fipronil-only
contribute fu1ther to their insecticidal
spray, several si,ot-on formulations that
activity. These actions cause excitation
contain only fipronil, a spot-on combinaof the insect nervous system, leading to tion with the insect growth regulator
involuntary muscle contractions, prostramethoprene, and nun1erous combination tion with tremors, and finally paralysis.

formulations that contain fipronil and

Spinosad has activity against fleas and is
various pyrethroids. Fipronil is very
formulated as a chewable tablet for dogs

Iipophilic; it accumulates in the sebaceous
and cats. A topical spot-on spinosyn
glands, has very low solubility in water, and formulation called spinetora.m has been has prolonged residual activity on both
developed for cats.

dogs and cats.

Repellents: N,N-dietl1yl-3-methylbenza

Pyrethrins and Pyrethroids: These
mide (DEET, previously called N,N-diecompounds rapidly disrupt sodium and thyl-met a -toluamide) remains the most
potassiun1 ion transport in nerve memeffective among cwTently available insect branes, resulting in spontaneous depolarizarepellents for people. It is a broad-spectrw11
tions, augmented neurotransmitter
repellent effective against mosquitoes,
secretion, and neuromuscular blockade,
biting flies, chiggers, fleas, and ticks.

ECTOPARASITICIDES

2757

However, the effectiveness of DEET
parasites, along witl1 the mode of action of
formulations for dogs and cats has not been
the particular molecules, is also important.

proved, and safety is a concern because

Often, perceived product failures are a
concentrated forn1ulations containing
result of massive reinfestation from the

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DEET have caused weakness, paralysis,
environment, incorrect product use, or
liver disease, and seizures in pets. DEET
tmrealistic expectations.

should not be administered to dogs or cats.

The synthetic pyrethroid permetluin is

Safety
a rapidly acting neurotoxicant that can
produce what is tern1ed a "hot-foot" effect Although LD50 data concerning the safety or
and is often described as a repellency.

toxicity of an insecticidal product is often

Various permethrin formttlations are
helpful, LD50 values are not always the best
labeled as repellents for ticks, mosquitoes,
indicator of the safety of specific insecticide
and fleas.

formulations applied to pets or premises.

Consideration must be given to the

Synergists: Synergists are generally not
concentration of product (mg/mL),
considered toxic or insecticidal but are used application rate (mg or g/m2 for environwith insecticides to enhance their activity.

mental products, and mcg or mg/kg for

They are used p1imarily to potentiate the
topicals), route of exposure ( dermal or
activity of pyrethrum or pyretlu·oids.

oral), total dose, and the species exposed.

Synergists inhibit cytochrome P450-

The actual risk of exposure during
dependent monooxygenases or glutath.ione
treatment, after treatment, or after

S-transferases, enzyn1es produced by
accidental ingestion can be assessed only
microsomes in insect tissues. They bind the
after evaluation of these c1iteria.

oxidative enzymes that would norn1aUy

Because animal toxicity can be modified
break down the insecticide and prevent
by formulation technology, active ingredithem from degrading the toxicant.

ents are not the sole guide to saJety

Piperonyl butoxide and N-octyl bicyclohepassessment of a product. Most commertene dicarboxarnide are common synercially available products have undergone gists.

adequate safety evaluation for regulatory
approval; the label noting such approval

Target Parasite Efficacy
remains the best source of infmrnation.

Cats are sensitive to many insecticides, and

Because of specific f01mulation and drug
use of tl1ese insecticides on or near cats
delivery technology, certain insecticides
must be done with caution. Human and
are used in a wide variety of ectoparasite
environmental safety also should be
control products. Efficacy of specific
considered, especially when treating
compoU11ds can vary against target species,
premises ( eg, some compounds may bn!ak
and resistance to insecticides may develop
down into more toxic components; older
in specific locations, especially with
products on the shelf might have been
incorrect, prolonged, or repeated use. It
withdrawn because of safety concerns).

cannot be assumed that ticks and fleas are

Generalizations should not be made,
controlled by the same active compoU11ds;
because formulations generally safe for
product labels should be carefully read.

grass application may induce skin reac

Products that contain compounds
tions, or even fatal reactions, in sensitive
specifically active against the target parasite individuals and certain breeds of dogs should be chosen, whether tl1e concern is
and cats.

fleas, ticks, mites, or a combination of these
parasites.

Duration of activity (ie, "knockdown"

Delivery Systems
or sustained effects) can be the prinlary

Consumer convenience is an in1portant
concern in product choices. Products
factor in product choice, especially for flea
should be evaluated based on both their
and tick control. An array of delivery
immediate and residual speed of kill. A
systems has historically been available:

rapid residual speed of kill is critically
powders, aerosols, sprays, shampoos,
important when attempting to manage flea
rinses, dips, spot-ons, mousses, injectables,
allergy dermatitis and to reduce the chances oral tablets or liquids, and impregnated colof a tick transmitting a pathogen.

lars. However, the safety, efficacy, and ease

Modem parasiticides available for flea
of use of the newer spot-on and oral
and tick control in companion animals
application systems have rendered many
provide superior parasite control, but an
of the older application technologies

U11derstanding of the life cycle of the
essentially obsolete.

2758

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS

GROWTH PROMOTANTS AND

PRODUCTION ENHANCERS

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Achieving increased efficiency of converplaced a total ban on beef and pork from sion of feed into human food products of
nations that allow the use of l3AAs, whereas
high quality, without posing any significant
other countries have adopted the maximwn
risk to the conswner, is an important goal
residue limits (MRLs) for tl1e compounds as
of livestock producers worldwide. The
established by the Codex Alin1entarius
physiologic mechanisms involved in

Commission. The FDA applies a greater
converting feed into muscle, fat, and bone

MRL in the USA than the Codex standard.

by animals are increasingly being eluci

The use of antimicrobial compounds
dated. Recently, consumer concerns about
specifically for growth-promotion purposes,
additives for food production have focused
as opposed to their use for control or
on animal safety, organoleptic quality, and
treatment of bacterial infection, has also
the potential hwnan health hazards of the
come under increased attention internationfood we eat.

ally because of rising concerns over

A number of approaches may be taken
antinucrobial resistance by pathogenic
to improve conversion of animal feed into
bacteria of concern in hwnan medicine.

meat; two of the more practical approaches

Direct cause-effect evidence of anti.microare hormonal treatments and anti.microbial bial use in livestock leading to bacterial
feed additives. The honnonal approach
resistance in human medicine is virtually
includes administration of anabolic steroid
nonexistent, requiring more complicated
honnones, use of growth horn1one (GH)

epidemiologic study. However, numerous
or insulin-like growth factor (IGF-1) to
studies have linked use of specific drugs in
augment endogenous GH levels, and use of
livestock, eitl1er for disease therapy or for

13-adrenergic agonists (13AAs) to preferengrowth-promotion purposes, to increased tially increase nutrient partitioning to
prevalence of drug resistance in target
muscle (see TABLE 60). The antimicrobial bacterial species. Results of tl1ese
feed additives approach includes feeding
investigations are equivocal and have been
of antibiotics to decrease populations of
the focal point of intense scrutiny and
pathologic bacteria in host GI tracts, use
debate. In the absence of resoundingly
of compow1ds to manipulate ruminal
clear cause-and-effect data, and because
fennentation by changing the ruminal
preservation of the continued efficacy
microflora population in healthy animals,
of existing antin1icrobial compounds is
and use of probiotics to promote beneficial
paramount, the cautionary principle has
microflora in the GI tract.

prevailed and will likely lead to greater

The use of hormonal treatments and
restrictions on the use of antimicrobials
anti.microbial feed additives in J'.)roduction
for growth promotion in livestock and
animals is currently under debate in many
for therapeutic purposes as well.

areas and is banned in some because of
concerns surrounding their possible effects

STEROID HORMONES
on people.

The EU has banned beef produced using

In general, the principle that dictates which
growth-promotant implants since 1981.

type of hormone to be used is the need to

Despite subsequent findings by the
supplement or replace the particular

European Economic Community's own
horn10ne type that is deficient in the animals
panel of scientific experts, referred to as tl1e
to be treated. Females produce estrogens

"Lamming Committee," by the World Trade
nonnally, so better results are obtained

Organization, and by the international Codex from the adnunistration of androgens, eg, Alimentarius Corrunission indicating tl1at
trenbolone acetate (TBA). Estrogens should
appropriate use of approved growth-promotnot be used in animals to be retained for ing horn10nes poses no hwnan health risk to
breeding purposes.

conswners, the EU has continued its ban.

Manufacturers' instructions must be

More recently, use of l3AAs for growth
followed to ensure proper implant
promotion in swine and beef production has placement and dose admil1istration.

come under scrutiny in the international

Anabolic hormones should not be
meat trade community. Some countries,
administered by IM il\jection for growthincluding the EU, Russia, and China, have promotmg purposes. Additionally, steroid

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS

2759
hom10nes must not be used for anabolic or

8o/er-12% faster than steers, have better feed
other purposes unless the indication is
efficiencies, and produce leaner carcasses.

specifically approved by the appropriate

Superior perfom1ance of bulls is due to the
regulatory body. The EU has banned the use
steroids produced in the testes (mainly
of honnonal growth promoters in meat
testosterone but also estradiol, which in
production. Appropriate swveillance

1uminants is also anabolic and is produced

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programs have been established to ensure
in relatively large quantities). Testosterone,
compliance by producers.

or one of its physiologically active
metabolites, binds to receptors in muscle
and stimulates increased incorporation of

Endogenous Steroids
anlino acids into protein, thereby increasing

The steroidal compounds used for anabolic
muscle mass without a concomitant
purposes in food animals are estradiol,
increase in adipose tissue. Estradiol, on the
progesterone, and testosterone. Gender and
other hand, may act by stimulation of the
maturity of an anin1al influence its growth
somatotropic axis to increase growth
rate and body composition. Bulls grow
hom1one and thus IGF-1 production and

NATURAL STEROID HORMONES FOR CONSIDERATION AS

GROWTH PROMOTERS

Duration

Potential
of Effect Growth

Adverse

Hormone

Dosage

(days)

Response Effects

Estradiol

1-Pellet

20mgEBb+

100-120
lOo/er-15% Transient

200mgP4c
increase in

(steers)

sexual
behavior

2-Pellet

20mgEB +200 100-120

5o/er-15%

Udder
mg testosterdevelopment
one propionate

(heifers, cull
cows)

3-Pellet
lOmgEB+lOO 100-120

0-8%
mgP4(veal
calves)

4-Silastic

45 mg estradiol

365
lOo/er-15% Transient
rubber

(steers)

increase in
sexual
behavior

5-Silastic

24 mg estradiol

200
lOo/er-15% Transient
rubber

(steers)

increase in
sexual
behavior

6-Poly lactic 28 mg estradiol

365
lOo/er-15% Transient
acid

(steers)

increase in
sexual
behavior

Progester-

See 1 and3
one
above

Testoster-

See2above
one

• Implants must be placed SC between the ear cartilage and skin to comply with label instructions so that consumption of residues may be avoided.

b Estradiol benzoate
c Progesterone

2760

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS
availability by modulation of the IGF
the compressed pellet may be to slow down
binding proteins. Naturally produced
the release rate of estradiol. In high
endogenous steroids are not orally active,
concentrations in blood, testosterone
require picogram concentrations of
induces male sexual behavior ( eg,
estradiol and nanogram concentrations of
aggression and mounting), but this is not

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testosterone in blood for physiologic
seen with the concentrations delivered by
effects, and can transiently affect the
compressed pellets in the ear (1 ng/mL).

behavior of treated animals (see TABLE 60).

Behavior resulting from use of 20 mg EB
and 200 mg progesterone is not different

Estradiol: A potent anabolic agent in
from that seen after the use of 20 mg EB

1uminants at blood concentrations of 5-100
and 200 mg testosterone propionate.

pg/mL, estradiol is administered as an ear
implant, either as compressed tablets or

Progesterone: Unambiguous data
silastic rubber implants. When estradiol
suggesting progesterone is anabolic in farm
is formulated as compressed tablets, a
animals does not exist. Its major use is to
second steroid ( usually testosterone, TBA,
slow the release of estrad.iol from comor progesterone) is typically present when pressed pellet implants.

administered to feedlot cattle fed a
high-energy diet, in a ratio of -1 part

Synthetic Steroids
estradiol to either 5 or 10 parts of the other,
androgenic, steroid. The release of

Synthetic steroids are commercially
hormones from compressed pellets is
available in some countries because of their
biphasic, with a relatively rapid rate lasting
efficacy, their relatively mild androgenicity,

2-7 days after insertion (50-100 times
and because they cause few behavioral
greater than baseline), followed by a slower
anomalies (see TABLE 61). Commercial
rate of release for the next 30-100 days
synthetic steroids are androgenic (TBA) or

(5-10 times greater than baseline).

progestogenic (melengestrol acetate [MGA]).

Hormone concentrations gradually decline

Synthetic steroidal androgens are not
up to day 80-100, when concentrations are
commonly used as anabolic agents except
no different from those in control animals.

for TBA. TBA is currently the only synthetic

Estrad.iol fonnulated in silastic rubber
androgen approved for use for growth
enhances the effective life span of the
promotion in cattle; it is used to a lesser
implant relative to pelleted fom1ulations.

extent in sheep and not in pigs or horses.

The pattern of release includes a short-lived

It has weak androgenic activity but has
spike in plasma estrogen concentration for
greater anabolic activity tl1an testosterone.

2-5 days after insertion, followed by a stable When administered repeatedly dUiing the but modest increase (5-10 times greater
feedlot phase when cattle are fed a
than baseline). Toward the end of the
high-energy diet, TBA can alter the physical
effective life span of tl1e implant, there is a
appearance and behavior of steers, causing
gradual decline to estradial concentrations
them to look and act like bulls. TBA has
found in control anin1als.

significant anabolic effects on its own in

Estrad.iol, on its own, increases nitrogen
female cattle and sheep, but in castrated
retention, growth rate by 10"/<>-20% in steers, males it gives maximal response when used
lean meat content by 1 o/o--3"/o, and feed
in conjunction with estrogens. It is
efficiency by 5o/<>-8%. It can be used in steers administered as a pellet-type i_mplant
to best advantage, but it also has anabolic
contairJ.ng 140-200 mg TBA for heifers and
effects in heifers and veal calves. It works
cull cows, and it can be used with estradiol
best in lambs in cmtjunction with androgens.

in doses ranging from 140-200 mg TBA as

It is not effective as an anabolic agent in pigs. either combined or separate implants.

MGA is an orally active synthetic
progestagen. It is fed at dosages of 0.25-0.5

Testosterone: A potent anabolic agent at
mg/day per heifer in the feed. It suppresses
the relatively high concentrations of 1-5 ng/
recurrent estrus in feedlot heifers and
mL in peripheral circulation, testosterone is
increases growth rate and feed efficiency
not used on its own as an anabolic agent in

(see TABLE 61). It is not effective in pregnant farm animals, because it is very difficult to
or spayed heifers or in steers. Its mode of
achieve the effective physiologic concentraaction is to suppress ovulation, presumably tions for long periods (up to 100 days) with
by suppressing luteinizing honnone (LH)

current delivery systems. It is generally used pulse frequency; however, large follicles as a propionate fonnulation in conjunction
develop, which can increase concentrations
with 20 mg estrad.iol benzoate (EB) in a
of estradiol and growth hormone, and hence
compressed tablet implant; its major role in
growth. MGA is permitted for use in the

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS

2761

SYNTHETIC STEROID HORMONES FOR CONSIDERATION AS

GROWTH PROMOTERS

Duration

Potential
of Effect

Growth

Adverse

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Hormonea

Dosage

(days)

Response

Effects

TBA

200 mg (heifers, cull

60-90

5%--12%
cows)

TBA+EB

200 mg TBA+ 28 mg EB 90-120

10%-20011>

Transient

( steers, heifers)

increase in
sexual
behavior

100 mg TBA+ 14 mg EB 90-120

10%-2()0A,

Transient

(steers)

increase in
sexual
behavior

TBA+E

200 mg TBA + 20 mg

90-120

E ( steers, heifers)

120 mg TBA+ 24 mg

90-120

E (steers)

140mgTBA+

14mg

90-120

E (heifers)

80 mg TBA+ 16mg

90-120

E (steers)

80mgTBA+8mg

90-120

E (heifers)

40mgTBA+ 8mg

90-120

E (steers and heifers
grazing pasture)

TBA+E

200 mg TBA + 40 mg

200

E (steers)

Zeranol

36 mg zeranol

90-120

10%--15%

12 mg zeranol

90-120

100/o-15%

MGA

0.25---0.5 mg/day, PO

As long as 3%--10%

Increased
it is given
mammary
development
after longterm
administra-
tion
a TBA = trenbolone acetate; EB = estradiol benzoate; E = estradiol 1713; MGA = melengestrol acetate Note: All administered as pellet implants except MGA, which is administered in feed.

USA but not in the EU. When used in the

Synthetic Nonsteroidal Estrogens
absence of a growth-promoting implant,

Two major classes of synthetic nonsteroidal

MGA increases growth rate through the
estrogens have been used as production
increased estradiol released by the follicles;
enhancers in food aninials. Stilbene
however, when used in conjunction with
estrogens ( either diethylstilbestrol [DES]

either estradiol or combination estradiol/
or hexestrol) have been batU1ed in most

TBA implants in the feedlot, the growthcountries as anabolic agents because of promoting benefits of MGA are prin1atily
residue and food safety concerns.

derived from suppression of the excess,

The discovery of a naturally occurring
unproductive, and potentially hannful
estrogen, zearalenone (produced by the
activities associated with recurrent estrus.

fungi Fusarium spp ), led to the develop-

2762

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS
ment of the synthetic analogue zeranol.

In steers and heifers in the feedlot and

Zeranol is estrogenic and has a weak affinity provided a high-energy diet, use of an for the uterine estradiol receptor. It is used in
androgen plus an estrogen horn1one combinaanimal production as a SC ear implant at a tion is common. Pellet-type implants are
dose of 36 mg for cattle and 12 mg for sheep,
effective for as long as 150 days; rein1planting
with a dmation of activity of90-120 days. In
cattle after 70-100 days should be considered

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steers, zeranol increases nitrogen retention,
because of decreasing response from the
growth rate by 12"/o-15%, and feed converpellet-type implants over time.

sion by 6o/o-100Ai. However, lower responses

Results from large-pen studies (>25
are seen in heifers. Its effects are additive to
animals/pen) show that heifers benefit from
those of androgens (generally TBA).

a combination of estracliol, TBA, and MGA.

In small-pen research, however, when fed in
combination with growth-promoting

Use in Cattle
implants, MGA use results in reduced gain,

Calves have a high conversion of feed into
feed efficiency, and ribeye area, as well as
animal tissue compared with yow1g growing
increased fatness. These contrary findings
swine or poultry. Therefore, their responses
suggest that although progesterone may
to anabolic agents are variable. Responses of
have an "anti-growth promoting" effect, the 0-l()OA, have been obtained when zeranol was
growth-promotion benefit realized from
given to 3-mo-old castrated male calves. Bull
suppression of estrus overcomes the minor
calves in an intensive bull beef system can be
negative physiologic impact of progestergiven an estrogen implant at 1 -2 mo of age to one in conventional large feedlot pens.

suppress testicular development, which may

In some studies in which bulls were
lead to subsequent reduction in moW1ting and treated with estrogens, growth rate aggression. A growth response of -5%-8% is
increased by 2"/o-lOOA,, and testicular growth
also obtained from this implant. Reimplantawas suppressed with a subsequent reduction tion every 80-100 days is necessary if
in moW1ting and aggression. This should
compressed pellet in1plants are used.

make the bulls easier to manage on the fa.n11

A major limitation to the use of anabolic
and less subject to "dark cutting" after
agents in lightweight weaned calves is the
slaughter. The mechanism involved appears
low liveweight gain they may achieve
to be the reduction of the gonadotropic
because of poor nutritional status. Hence,
hormones LH and follicle-stin1ulating
anabolic agents should be considered only
hormone (FSH) from the pituitary gland
if the weanlings are expected to gain >0.25
by estrogen, which has a strong negative
kg/day. Zeranol, estradiol, and TBA can
feedback effect on LH and FSH secretion.

be used in male castrates. Dairy heifer

This reduction in LH and FSH results in
replacements carmot be given steroid
decreased testicular size and lower testosterimplants as weanlings.

one levels, with a consequent reduction in

Greater and more consistent responses are
aggressive behavior. However, there appears
obtained in yearling and older cattle than in
to be suffident testosterone secreted to
calves or weanlings, due pruparily to greater
maintain an anabolic effect. Therefore, the
intake and to the higher plane of nutrition.

repeated use of estrogens in bulls beginning

In the case of pellet-type implants with
at 1-3 mo of age may lead to a honnonal
effectiveness of90-120 days, consideration
castration effect with increased growth rate.

can be given to rein1planting cattle midway
through the grazing season, provided gains

Use in Horses

>0.5 kg/clay are maintained. Silastic implants

The use of anabolic agents in horses is not
of estradiol are effective for 200-400 clays,
recommended because of adverse effects
depending on dose used. Daily gains in feedlot on the reproductive system. Administration cattle fed a high-energy diet may be increased
of a steroid ho1111onal androgen analogue

200/o-3()0A, after implantation with an estrogen
decreases testicular size in stallions.

and an androgen; daily gain in pasture cattle is

Decreased hormonal concentrations,
typically improved by l OO/o-15%.

especially LH, testosterone, and inhibin,

Responses to growth promotion are good
adversely affect testicular histology and
when animals are on a high plane of nutrition. spem1atogenesis and transiently decrease Feed conversion efficiency is improved, and
spem1 output and quality. One of the most
lean meat content of the carcass is generally
commonly used compoW1ds is 19-nortestosincreased. Although less clear, conformaterone for therapy in debilitated and anemic tion of implanted cattle tends to improve.

horses. However, use of these compoW1ds is

Negative impacts of implants on marbling
contraindicated, and longterm treatment or
content of the loin muscle can be minimized
large closes have serious adverse effects on
by finishing cattle to a fat-constant endpoint.

reproductive tract flli1ction.

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS

2763

Use in Other Species

Buller syndrome generally affects 2"/o--3"/o of In pigs, the growth responses from the use
the feedyard steer population, but this rate
of estradiol, progesterone, and zeranol are
can double or triple during the late swnmer
variable but generally low. TBA seems to
and early fall months. An increase in yearling
increase lean meat content of pig carcasses.

steers off native grass pastme (which are

In sheep, the responses to anabolic
usually given a high-dose implant immedi

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agents parallel those obtailled in cattle.

ately on arrival), ditunal temperatw-e fluctua

The most consistent responses have been
tions Q1ot days and cool nights that shift
obtained in lambs finished on high-concensocial activity to early evening hours), dusty trate diets; a 1()%--15% increase in daily gaill
pen conditions ( exacerbated by evening
can be expected. Anabolic steroids should
social activity), feeding com or hay that may
not be used in lambs to be retained for
be moldy, and incomplete fem1entation on
breeding. Also, in1plantation with zeranol
freshly harvested silage can also contribute
reduces testicular development in ran1
to increases in buller syndrome. Feedlot
lambs and delays the onset of puberty and
pens with a greater nw11ber of animals
reduces the ovulation rate in female sheep.

experience a greater incidence of bull er

Moreover, the short finishing period and the
activity, and the incidence of hullers increases
extensive nature of some production
linearly with increasing mtmber of animals
systems militate agaillst widespread
within a pen above 80--100 animals per pen.

practical use of growth promotants in

Til.is suggests the agonistic behavior is a
sheep on economic grow1ds.

population phenomenon, requiting a ctitical

In poultry, responses to estrogens
mass of both the dontinant, mounting
include increased fat deposition. Androanimals and the animals they are attempting gens, however, have given conflicting
to mount. Bullers have been shown to have
responses. Hence, their use is of no
greater circulating concentrations of
practical significance at this tin1e.

monoanl.ine oxidase and reduced circulating

In fish, methyl testosterone can induce
concentrations of progesterone than
sex reversal in raillbow trout, thereby
non-buller pen mates. These effects
promoting growth and improved feed
generally last for 1--10 days after inlplantaconversion efficiency.

tion and then subside. However, there have
been a few reports of undesirable behavior in
steers that lasted for 4--1() wk. The cause of

Possible Complications
this unpredictable adverse behavior is not

Any hormonal implant has a negative
clear; it may be a function of rearing and
feedback effect on pituitary gonadotropins,
socialization climate. It is generally more
thereby reducing LH and FSH secretion.

severe in dairy cattle used for beef produc

TI1erefore, they can affect the onset of
tion. If the problem is severe, the buller
puberty and the regularity of estrous cycles,
steers should be identified and removed;
as well as reduce conception rate in females
if very severe, removal of the in1plants or
and testicular development ( and thus spenn
administration of 50--100 mg of progesterone
output) in males. Hormonal growth promoin oil for a nun1ber of days to suppress behavtants should never be used in animals that are ior should be considered.

or may be used for breeding purposes, nor

In addition to buller syndrome, estrogenic
should they be used before puberty to
implants may increase the size of rudimenincrease growth in yearling thoroughbreds or tary teats.

young pedigree bulls for show purposes. lf
given to pregnant heifers, TBA results in
increased incidence of severe dystocia,

Factors Affecting Response
masculin.ization of female genitalia of the

A nun1ber of factors affect the response
fetus, increased calf mortality, and reduced
to growth-promoting in1plants, including
milk yield in the subsequent lactation.

genetic makeup, plane of nutrition, and

The major problem thought to be
the sex and age of the animal.

associated with estrogenic implant use in the

Animals should be gaining a minimum of
feedyard has been a transient increase in

0.25 kg/day before an economic response
mounting behavior and aggression,
is obtailled. Implants are best used in
commonly referred to as buller syndrome
animals on a high plane of nutrition and

(seep 1552). However, it is also believed that under good husbandry conditions. They are
the estrogen in the implant alone is not
an aid to, but not a substitute for, good
sufficient to cause bulle1-s. TI1e "buller" is the husbandry. Consequently, there is little
animal being pursued by one or more pen
economic incentive in implanting cattle
mates that repeatedly attempt to mount the
destined for a 3- to 4-mo "store period,"

buller throughout the day and several days.

during which time animals are fed to gaill

2764

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS
little or no weight. Responses are reduced in substitution. The f3AAs bind to [3-a.drenergic calves (based on health condition and diet),
receptors, which have been classified into
and responses are good in yearlings.

[31, [32, and [33 subtypes based on the

Prior implantation does not affect the
physiologic response obtained. [31 receptors
response to the next implantation. Also,
are located prin1arily in cardiac muscle but

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once the implant effect has ceased, the rate
also can be found in skeletal muscle,
of gain reverts to the rate that would be

[32 receptors in tracheal and skeletal
expected in nonimplanted animals,
muscle, and [33 receptors in brown adipose
assuming the level of feeding is the same.

tissue. In general, f3AAs have specificity

Also, extra weight induced by implants in
for receptor subtypes, thereby providing
early life is transferred through to extra
specificity regarding their physiologic
carcass weight at slaughter.

actions. However, there are multiple
receptor subclasses in most tissues, and

GROWTH HORMONE
the relative concentJ·a.tions of [31 and [32
receptors in a tissue detennine the

The peptide most commonly used to enhance
physiologic response. Muscle and adipose
growth and production is growth hom1one
cells have predominantly [32 receptors. f3AA

(GH). Its chemical structure is species-speuse leads to an increase in muscle mass cific, and it has a short half-life (20-30 min). It caused by upregulation of mRNA transcripis not orally active and is rapidly digested and tion, resulting in increased protein cleared by the gut, liver, and kidney; thus, it
synthesis, and a decrease in carcass fat due
must be administered via a parenteral route.

to decreased rates of lipid accretion. The

Sustained-release (14-28 days) fom1ulations
exact proportion of receptor subtypes
have been developed for use in cattle to
varies between tissues and also across
obviate the need for daily injections. When
species, resulting in species-specific
administered to cattle, GH increases growth
responses to select f3AAs. For example,
rate (5%--lOOAi), feed conversion efficiency,
swine a.re believed to have more [31 than
and the carcass lean:fat ratio. Gender has

[32 receptors in their skeletal muscle;
little effect on response in cattle. Response to
ruminants are believed to have more [32

GH is lower in older cattle with greater fat
than [31 receptors. The physiologic activity
deposition. There is an interaction between
of f3AAs depends on the close, receptor bindmagnitude of response and nutritional level; ing specificity, mode of administration, rate
protein content and specific amino acid
of absorption, and metabolic clearance rate
composition may be important to achieve
in treated animals. Also, because tissue
maximal responses. The effects of GH are
becomes refractory to exogenous f3AA
largely additive to those obtained from
administration, f3AAs are fed only during
steroid implants. GH improves growth and
the final days of the finishing phase;
feed efficiency in sheep but not in poultJy.

extended feeding ultimately results in a

Recombinant GH in pigs has dramatic
complete loss of tissue response to f3AAs.

effects, resulting in an increase in daily gain

The major use of f3AAs in food animal

(200Ai), decrease in feed intake (5%), and a
production is to increase carcass leanness
decrease in the feed:gain ratio (20%). A lOOAi
and lean tissue produced per animal. ln
increase in Jean content and a 35% decrease
cattle and sheep, weight gain, gain:feecl ratio,
in adipose tissue may be realized in swine.

and meat content are increased by 1 ()0,.(,...2()0A, AdministJ·a.tion of bovine GH at 25 mg/day to
and lipid content is decreased by 7%-200Ai. ln
lactating cattle increases milk yields of dairy
swine and chickens, respons"es are much
cows by as much as 200A,. GH has been
lower, with pigs responding better than
approved for commercial use in some
chickens. Weight gain is increased by ZOAi-4%,
countries to increase milk production.

and gain:feed ratio is slightly improved in
chickens but not in pigs. Meat content is

13-ADRENERGIC AGONISTS
increased by ZO/o-4% and lipid content
decreased by 7o/o--8% in chickens and pigs.

As of 2015, there are two [3-adrenergic

Adverse effects depend on compound
agonists (f3AAs) approved for use as growth
administered, close used, and species
promotants in feedlot cattle in the USA:

treated, but those selected for commercial
ractopamine and zilpaterol. Phenetha.nola.use have minimal adverse effects. They are mine f3AAs are chemically sinlilar in
orally active. Dosage level of tl1e compound
structure to epinephrine and norepinephused affects the response obtained; tl1e rine and have paracrine, neurotransmitter,
optimal dose often varies for different
and endocrine (ho1111onal) effects. There is
production variables measured. The most
a range of f3AA compounds resulting from
consistent effects are increased proportion
structural modifications and aromatic ring
of lean meat, but tl1e effects on meat quality

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS

2765
vaiy with compound used, dosage given,
simplistic. Antimicrobial compounds ai·e
duration of treatment, and species treated.

administered in tl1e feed at low dose rates

Cettain compounds have been reported to
relative to high doses required for therapeudecrease tenderness of meat in cattle. The tic effects. Feed additives can be given once
use of 13-agonists as growth promoters is
the n.m1en is fw1ctioning, although some

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banned in the EU. Illegal use of clenbuterol
antibiotic compounds can be fed to calves
in cattle and certain l3AAs in poultry is a
before this point.

threat in some countries, requiring vigilance

Antimicrobial growth promotants
by regulato1y authorities. The longtenn
commonly used in livestock are detailed in
accumulation of these compounds in hair

TABLE 62. Anliimicrobials ai·e used in male
and ocular tissue has been used to screen
and female animals without adverse effects
for their presence in some countries.

on ovarian and testiculai· development or
function because they are poorly absorbed.

ANTIMICROBIAL FEED ADDITIVES Unlike at1abolic steroids, they do not affect carcass composition. Antimicrobials are

Maintenance of healthy animals requires
conunonly used in conjunction with
prevention of infection by pathogenic
estradiol, zeranol, or TBA, and generally
organisms. In addition, specific alteration
their combined effects are additive.

of a host's microflora may have beneficial
effects on aimnal production by alteration
of n.m1inal flora, resulting in changes in the
lonophore Antibiotics
proportions of volatile fatty acids produced

Ionophores ( eg, monensin and lasalocid)

during n.m1inal digestion. Thus, antimicromodify the movement of monovalent bial compounds may improve production

(sodium and potassium) and divalent
efficiency of healthy animals fed optimal

(calcium) ions a.cross biologic membranes,
nutritional regimens. Production-enhancing
modify the n.unen micro flora, decrease
antimicrobial compounds cat1 be classified
acetate and methane production, increase
as ionophore or nonionophore antibiotics.

propionate, may improve nitrogen

This distinction is in1portant, because
utilization, at1d cat1 increase dry matter
ionophores have no use in hwnan medicine
digestibility in n.m1inants. Their main effect
and do not have any link or possible effect
is to increase feed efficiency, but they may
on antimicrobial resistance to therapeutic
also in1prove growth rates of run1inants on
antibiotics in either people or food animals;
high-roughage diets. Administration of
to group all antin1icrobials together for
monensin to cattle results in 2%-1 (JOA,
debate about the risk to tl1erapeutic
improvement in liveweight gain (in animals
antibiotics is ill advised and overly
on a high-roughage diet), 3o/<r-7% increase in

ANTIBACTERIAL GROWTH PROMOTERS FOR POTENTIAL USE IN

LIVESTOCK PRODUCTION

Compound

Class

Absorption

Effects

Batnbennycins

Phosphogly

Not absorbed

Increase FCE•, growth
colipid
promotion in poultry,
cattle

Lasalocid sodiwn

Ionophore

Increase FCE in cattle

Monensin sodium

Ionophore

Poorly

Increase FCE, increase
absorbed

DLWGb in cattle at1d
latnbs

Salinomycin

Ionophore

Increase DLWG and FCE

Virginiatnycin

Peptide

Not absorbed

Growth promotion in
poultry

Zinc bacitracin

Peptide

Not absorbed

Growth promotion in
poultry

" Feed conversion efficiency
b Daily Hveweight gain

2766

GROWTH PROMOTANTS AND PRODUCTION ENHANCERS
feed conversion efficiency, and up to a 6%
by 2%-10'% at1d feed conversion efficiency
decrease in food conswnption. Initially,
by 3%-9"A,. Their effects are greater in yormg
monensin was used only as a feed additive
animals, at1d production responses are
for rwninants fed in confinement, but its use reduced when production conditions are has been extended to grazing animals. Other optin1ized (good housing, optin1al health, ionophores generally have similar effects.

and hygiene). They have minimal effects

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Doses range from 6-40 ppm in the diet.

on carcass composition other than that

Jonophores are absorbed from the gut,
because of in1proved growth rate.

rapidly metabolized by the liver, and reenter

The development of microbial resistance
the gut from bile. Some ionophores also
to antibiotics in treated animals, which can
have a therapeutic use ( eg, for prevention
then be spread to people, is an important
of coccidiosis in rwninants and poultry).

concern regarding the widespread use

Although ionophore antibiotics are used
of antimicrobial feed additives in food
for prevention of coccidiosis in rwninants
production. There is circumstantial evidence
and poultry, ionophores are not used in
that use of subtherapeutic doses of antinlicrohtm1an medicine, and there are no medically bials creates selective pressw-e for the
important analogues of the ionophores used
emergence of antimicrobial resistance, which
in hmnan medicine. Therefore, there is no
may be transmitted to the conswner from
obvious relationship between ionophore
food or through contact with treated anin1als
use in livestock production and the concern
or animal manw-e. A ban on the use of
regarding resistance of bacterial pathogens
antibiotics as feed additives decreased
to antimicrobial compormds important in
drug-resistant bacteria in a Danish study.

hmnan medicine.

Although overall mortality rates of chickens
were not affected, more feed was conswned

Nonionophore Antibiotics
per kg of weight. Therapeutic use of

These compormds are used to selectively
antibiotics was increased, but the total
modify microbial populations within animals
volwne of at1tibiotic use was significantly
to in1prove production efficiency and to
decreased. The EU has banned bacitracin,
maintain health by combating low-level
car·bodox, olaquindox, tylosin, virginian1ycin,
infections, particularly in intensive systems.

avilarnycin, flavophospholipol, lasalocid

Phosphog]ycolipid antibiotics ( eg, flavophossodiwn, monensin sodiw11, and salinomycin pholipol) alter rumi.nal flora by inhibiting the
as of 2009. There has been no reported
action of some gram-positive gut microorevidence of any reduction in antinlicrobial ganisms and peptoglycan fonnation, yielding
resistance in hwnan bacteiial pathogens as a
sinlilar production responses to those proresult of the EU ban. This is rmderstandable duced by ionophores. l.n addition, flavophosgiven that the most important and concerning pholipol has been shown to Influence the
cases of antinlicrobial resistance in hwnan
hindgut microflora populations, resulting in
medicine, namely methicilli.n-resistant
competitive exclusion of some harmful

St.aphywcocciis aureus (MRSA), vancomypathogens such as Escherichia col'i and cin-resistant enterococcus (VRE), Strepto
various species of Salmonella. A less w1der
coccitS pneumoniae, at1d others, are not
stood effect of flavophospholipol is the
food-borne patl1ogens, are not formd in food
reduction in plasmid transfer of antimicrobial or compartion anin1als, at1d the drugs of resistar1ce. Given the seemingly contradicinterest are not used at1d were not used tory and highly charged interests of desire for
before the bar1 in livestock. The. issue of
a generalized reduction in the use of antibioat1tinlicrobial resistance is critical for the tics for livestock production arid the potential
in1mediate and long-tenn futw-e of hurnat1
use of a specific antibiotic for reducing antimedicine; however, tl1e complexity of the microbial resistance, this potentially volatile
issue at1d the difficulty with which it must be
topic has not been comprehensively assessed. assessed ensw-e that clear artSwers are not The means by which specific compormds
inuilinent and the debate over the most
exert their antin1icrobial effect differ.

appropriate path forward in the USA at1d

Antibiotics may have a nitrogen-sparing
abroad will continue.

effect, thereby increasing the availability
of amino acids to the animal.

PROBIOTICS

Most feeds for broiler and pig production

Probiotics promote tl1e establishment and
in some cormtries contain antimicrobial
development of a desirable intestinal
growth promoters. These compounds can
nlicrobial balat1ce. There is a delicate
also be administered to calves, yearlings,
balance between nonnal and pathoge1lic
and finishing cattle either in milk replacer or
nlicroorgarlisms. Tllis balance can be upset
in supplementary concentrates. Antibiotic
by poor husbat1dry conditions, disease, or
compormds, in general, increase growth rate stressors (eg, trat1sport). Bacteria that

VACCINES AND IMMUNOTHERAPY

2767
produce lactic acid can, in general, be benefiproduction benefits are variable, and cial to the animal; certain yeasts may also be
positive responses are more likely when a
beneficial. Their ability to increase growth
stressful management change may result in a
and promote health are claimed to be due
change in balance of gut microflora. Thus,
to one or more of the following factors:

they are useful in some cases to mininlize GI
preventing colonization of the gut by
upsets or to help overcome stress due to

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pathogenic coliforms, altering GI absorption
weaning or transport. The unicellular yeast
rate, and inhibiting bacterial growth and
fungus may also have beneficial effects on
influencing the balance of bacteria in the gut. nun en fem1entation, thereby improving The probiotic feed additives consist of
digestion and feed efficiency. The effect of
selected strains of lactobacilli and streptoprobiotics in older anin1als may be reduced cocci that alter the microbial species present
because of the well-established, balanced
in the GI system to the benefit of the treated
population of microflora that is less sensitive
animal. Unicellular yeasts are also used. The
to nlinor detrimental husband1y challenges.

VACCINES AND IMMUNOTHERAPY

The adaptive immune system responds to

An ideal vaccine for active immunization
nlicrobial invasion by producing protective
should confer prolonged, strong inu11unity
antibodies or cell-mediated inmmnity, or
in vaccinated anin1als, as well as rapid onset
both. Appropriate administration of specific
of immunity. It should not cause adverse
microbial antigens, as in a vaccine, can
effects and should be inexpensive, thermoprovoke effective, longterm resistance to and genetically stable, and, for production
infection. Conserved microbial molecules
anin1als, adaptable to mass administration.

can also stimulate the development of

It should preferably stimulate inunune
innate inm1une responses. This too
responses distinguishable from those due to
enhances resistance to infection and may
natural infection, so that vaccination and
be clinically useful.

eradication may proceed simultaneously.

Vaccination is not always an innocuous

ACTIVE IMMUNIZATION
procedure; adverse effects can and do
occur. Therefore, all vaccination must be

Active in1munization involves ad.ministragoverned by the principle of informed tion of vaccines containing antigenic
consent. The risks of vaccination must not
molecules ( or genes for these molecules)

exceed those caused by the disease itself.

derived from infectious agents. As a result,

Vaccines may contain either living or
vaccinated anin1als mount acquired inmmne killed organisms or purified antigens from responses and develop prolonged, strong
these organisms. Vaccines containing living
inununity to those agents. When properly
organisms tend to trigger the best protective
used, vaccines are highly effective in
responses. Killed organisms or purified
controlling infectious diseases. Several
antigens may be less immunogenic than
criteria determine whether a vaccine can or
living ones. Because they are unable to grow
should be used. First, the actual cause of the and spread in the host, they are less likely to disease must be deternlined. Although this
optin1ally stimulate the inunune system.

appears self-evident, it has not always been

Living viruses from vaccines, for example,
followed in practice. For example,
infect host cells and grow. The infected cells

Mannheimia haemolytica can be isolated
then process the viral antigens, triggering a
consistently from the lungs of cattle with
response dominated by cytotoxic T cells, a
respiratory disease; however, these bacteria

Thl response (seep 814). Killed organisms
are not the sole cause of this syndrome, and
and purified antigens, in contrast, comvaccines against the primary viral pathomonly stimulate responses dominated by gens are required for full protection. In
antibodies, a Th2 response. This antibody
some important viral diseases ( eg, equine
response may not generate optimal
infectious anemia, feline infectious
protection against some organisms. As a
pe1itonitis, and Aleutian disease in mink),
result, vaccines that contain killed
antibodies may contribute to the disease
organisms or purified antigens usually
process, and vaccination can therefore
require the use of adjuvants to maximize
increase disease severity.

their effectiveness. Adjuvants may,

2768

VACCINES AND IMMUNOTHERAPY
however, cause local inflammation, and

!ants include lipopolysaccharicles ( or their
multiple doses or high doses of antigen
derivatives); killed anaerobic c01ynebacte-
increase the risks of producing hypersensi1ia, especially Propionibacteiium acnes tivity reactions.

and Bordetella pei·tussis; and saponins

Killed vaccines should resemble the living (triterpene glycosicles) cle1ivecl from the VetBooks.ir
organisms as closely as possible. Chemical
bark of the soapbark tree (Quillaja
inactivation should cause minin1al change
saponaria). Saponin-basecl acljuvants
to their antigens. Compounds used in this
may selectively stimulate Th 1 activity.

way include formaldehyde, ethylene oxide,

Acljuvants can be combined. For
ethyleneimine, acetylethyleneimine, and
example, very effective acljuvants can be

(3-propiolactone.

constructed by combining patticulate or
depot acljuvants with an immunostimula

Adjuvants
tory agent.

To maximize the effectiveness of vaccines,
especially those containing poorly antigenic

Types of Vaccines
components or highly purified antigens,

Subunit Vaccines: Although vaccines
adjuvants are usually aclclecl. Acljuvants
containing whole killed orgat1isms are
enhance response to vaccines and/or balance/ economical to produce, they contain many shift the Thl/I'h2 immune response. They can
antigens that do not contribute to protective
reduce the amount of antigen to be injected or immWlity. They may also contain toxic the nwnbers of closes administered, and they
components. Thus, it may be advantageous
may promote prolonged inunw10logic
to identify, isolate, ai1d purify the critical
memory. It is believed that adjuvants work
protective antigens. These can then be used
ttu·ough three major mechanisms.

in a vaccine by themselves. Thus, purified

Depot acljuvants prot ct antigens from
tetanus toxin, inactivated by treatment with
degradation and prolong inm1une responses
fom1alin (tetanus toxoicl), is used for active
as a result of the sustained release of
immunization against tetanus. Likewise,
antigen. Examples of depot-forming
the attachment pi.Ii of enteropathogenic
adjuvants include aluminwn salts, such as

Escherichia coli can be pmifiecl and
alwninun1 hydroxide, alun1inun1 phosphate,
incorporated into vaccines. The antipilus
and alwninWTI potassiWTI sulfate (alun1), as
antibodies protect anin1als by preventing
well as calcium phosphate. These alwnbacterial attachment to the intestinal wall.

basecl adjuvants also serve as very potent
stimulators of toll-like receptors.

Antigens Generated by Gene

A second class of adjuvants consists of

Cloning: The cost of physically purifying a
patticles that effectively deliver antigen to
specific antigen may be prohibitive. In such
antigen-presenting cells and so enhance
cases, it may be approp1iate to clone the
antigen presentation. The inlmune system
genes coding for protective antigens. The
traps and processes particles such as

DNA encoding the desired antigens may be
bacte1ia or other microorganisms much
inserted into a bacterium or yeast, which
more efficiently than solubl� antigens. As a
then expresses the protective antigen. The
result, particulate antigens are much more
recombinant organism is propagated, and
effective than soluble ones. Exan1ples of
the antigens encoded by the inserted genes
such adjuvants include emulsions,
are hat-vested, purified, and administered as
microparticles, inm1une-stin1ulating
a vaccine. An example of-such a vaccine is
complexes (ISCOMs), and liposomes.

one directed against the cloned subunit of

Immunostimulatory adjuvants consist of

E coli enterotoxin. The cloned subtmits are molecules that enhance cytokine production antigenic and function as effective toxoicls.

and so selectivity stin1ulate helper cell

A pmified subWlit protein vaccine, called
responses. Many contain microbial products

OspA, encoded by a gene from B01Telia
that often .represent pathogen-associated
bitrgd01feri effectively protects clogs
molecular patterns. As a result, they activate
against Lyme disease.

clencl1itic cells and macrophages th.rough

It is possible to clone viral antigen genes
toll-like receptors and stin1ulate the
in plai1ts. This has been successfully
secretion of critical cytokines such as IL-1
achieved for viruses such as transmissible
and IL-12. These cytokines in turn promote
gastroenteritis and Newcastle disease. The
helper T-cell responses and drive and focus
plants used include tobacco, potato, and
the adaptive in1.rnw1e responses. Depencling
corn. These plants contain very high
on the specific microbial product used, they
concentrations of antigen, at1d successful
may enhance either Thl or Th2 responses.

vaccination may result from feeding the

Commonly used microbial in1munostimu-
plants to anin1als.

VACCINES AND IMMUNOTHERAPY

2769

Some recombinant vaccines contain viral

Under rare circumstances, virulent
structural proteins assembled into virus-like organisms may be used for vaccination, eg, particles (VLPs ). One or more viral proteins
vaccination against contagious ecthyma
may be present in the VLP, and the particles

( orf) of sheep. Lambs are vaccinated by

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may be either nonenveloped or enveloped.

rubbing dried, infected scab material into

VLPs present viral antigen in a particulate
scratches made on the inner thigh, which
form, and these antigens more closely
produces local infection with only linlited
resemble those of the infectious virus. VLPs
effects on the lambs; they become solidly
are potent irnmunogens and may not require immune. Because vaccinated ani.n1als may adjuvants. Because VLPs contain no viral
spread the disease, however, they must be
genetic material, they cannot replicate in
separated from unvaccinated stock for a
the vaccinee. The effectiveness ofVLPs for
few weeks.

animal vaccination has been shown in many

Considerable care must also be exercised
experimental systems, but no veterinary
in the preparation, storage, and handling of

VLP-based vaccines are commercially
modified-live vaccines to avoid temperature
available at this time.

extremes that can reduce viability of the
organisms.

Attenuated Vaccines: The use of live
organisms in vaccines presents many

Gene-deleted Vaccines: Attenuation of
advantages. Most especially, they are
viruses by prolonged tissue culture can be
usually more effective than inactivated
considered a prinlitive form of genetic
vaccines in triggering cell-mediated immune engineering. Ideally, this resulted in the responses. Their use, however, also
development of a strain of virus that was
presents certain hazards. Thus, the
unable to cause disease. This was often
virulence of a live organism used for
difficult to achieve, and reversion to
vaccination must be attenuated, so that it is
virulence was a constant hazard. Molecular
able to replicate but is no longer pathogenic.

genetic techniques now make it possible to

The level of attenuation is critical to vaccine
modify the genes of an organism so that it
success. Underattenuation will result in
becomes irreversibly attenuated. Deliberate
residual virulence and disease ( reversion to
deletion of the genes that code for proteins
virulence); overattenuation will result in an
associated with virulence is an increasingly
ineffective vaccine. Rigorous reversion to
attractive procedure. For example,
virnlence studies must be performed to
gene-deleted vaccines were first used
demonstrate stability of the attenuation.

against the pseudorabies herpesvirus in

Attenuated vaccines should not be used
swine. In this case, the thym.idine kinase
to vaccinate species for which they have
gene was removed from the virus.

neither been tested nor approved.

Herpesvirus requires thymidine kinas<;! to

Pathogens attenuated for one ani.n1al may
return from latency. Viruses from which this
be over- or under-attenuated in other
gene has been removed can infect neurons
anin1als. Thus, they may either cause
but cannot replicate and cause disease.

disease or fail to provide adequate

Sin1.ilar genetic manipulation can be used
protection.

to restrict the ability of bacteria to grow in

Attenuation has historically involved
vivo. For example, a modified-live vaccine
adapting organisms to growth in unusual
is available that contains streptomycinconditions. Bacteria were attenuated by dependentMannheimia haemolytica and
culture under abnom1al conditions, and

Pasteurella multocida. These mutants
viruses were attenuated by growth in
depend on the presence of streptomycin for
species to which they are not naturally
growth. When used in a vaccine, the
adapted. Vaccine viruses may also be
absence of streptomycin will eventually
attenuated by growth in alternative media,
result in the death of the bacteria, but not
such as tissue culture or eggs. This has been
before a protective inuuune response has
done for canine distemper, bluetongue, and
been stimulated.

rabies vaccines. Prolonged tissue culture

Additionally, it is possible to alter the
was, for many years, the most usual method
expression of other antigens so that a
of attentuation.

vaccine will induce an antibody response

For some diseases, related organisms
distinguishable from that caused by wiJd
nonually adapted to another species may
strains. This allows for a way to distinguish
impart limited immunity. Examples include
infected from vaccinated ani.nlals ( referred
measles virus, which can protect dogs
to as DIVA).

against distemper, and bovine viral diaiThea
virus, which can protect pigs against

Virus-vectored Vaccines: Another
classical swine fever.

method to produce a highly effective living

2770

VACCINES AND IMMUNOTHERAPY
vaccine is to insert the genes that code for

Polynucleotide (DNA) Vaccines:

protection antigens into an avirulent "vector"

Animals may also be inlmunized by
organism. These vaccines are created by
injection of DNA encoding viral antigens.

deleting genes from the vector and replacing

This DNA can be inserted into a bacterial
them with genes coding for antigens from the plasmid, a piece of circular DNA that acts as pathogen. The recombinant vector is then
a vector. When the genetically engineered

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administered as the vaccine, and the inseited plasmid is injected, it can be taken up by genes express the antigens when body cells
host cells. The DNA is then transcribed, and
are infected by the vector virus. The vector
mRNAs are translated to produce vaccine
may be attenuated so that it will not be shed
protein. Transfected host cells thus express
from the vaccinate, or it may be hostthe vaccine protein in association with restricted so that it will not replicate itself
major histocompatibility complex class I
within the tissues of the vaccinate.

molecules. This can lead to the develop

Virus-vectored vaccines are well suited for
ment of not only neutralizing antibodies
use against organisms that are difficult or
but also cytotoxic T cells.

dangerous to grow in the laboratory.

This type of DNA vaccine is used

The most widely used vaccine viral
successfully to protect horses against West
vectors are poxviruses such as fowlpox,

Nile virus infection. This approach has been
canarypox, vaccinia, and herpesvirus. These applied experimentally to produce vaccines viruses have a large genome that facilitates
against the viruses that cause avian
insertion of new genes. They also express
influenza, lymphocytic choriomeningitis,
relatively high levels of the recombinant
canine and feline rabies, canine parvovirus,
antigen. In at least some cases, vectored
bovine viral diarrhea, feline immunodefivaccines appear able to induce immunity ciency virus-related disorders, feline
even when high levels of maternal antibody
leukemia, pseudorabies, foot-and-mouth
are present. Canarypox-vectored vaccines
disease, bovine herpesvirus-1 related
that incorporate genes obtained from
disease, and Newcastle disease, among
canine distemper virus are now used to
others. Because they can produce a
immunize dogs, and a similar vector
response sinlilar to that induced by
containing the gene encoding rabies
attenuated live vaccines, these poly.nucleoglycoprotein effectively protects dogs tide vaccines are ideally suited for use
and cats against rabies.

against organisms that are difficult or

An innovative exan1ple of a vectored
dangerous to grow in the laboratory. Some
vaccine involves the use of a yellow fever

DNA vaccines appear to be able to induce
viral chimera to protect against West Nile
in1munity even in the presence of very high
virus. This technology uses the capsid and
titers of maternal antibody. Immunization
nonstructural genes o(the attenuated
with pwi.fied DNA in this way allows
yellow fever vaccine strain l 7D to deliver
presentation of viral antigens in their native
the envelope genes of other flaviviruses
form, because they are synthesized in the
such as West Nile virus. The resulting virus
san1e way as antigens du1ing a viral
is a yellow fever/West Nile virus chimera
infection.

that is much safer than either of the parent
viruses. The margin of safety can be further

Administration of Vaccines
increased by introducing targeted point
mutations into the envelope genes.

Route of Administration: The most

Another example is a vaccine directed
common method of vaccine administration
against Newcastle disease. The vector is
is by SC or IM injection. This approach is
fowlpox virus, into which Newcastle
excellent for relatively small nwnbers of
disease HA and F genes are incorporated.

animals and for diseases in which systemic

It has the benefit of conferring in1munity
in1111unity is important. ln addition, the
against fowlpox as well.

veterinarian can be sure that an ani.nlal has

Vectored vaccines are also commercially
received the appropriate dose of vaccine.

available for avian influenza, West Nile virus

However, local inlmunity is sometimes
and influenza infection in horses, feline
more important than systemic immunity,
leukemia, and for vaccinating wildlife
and in these cases, it is more appropriate
against rabies. These vaccines are stable
to administer the vaccine at the site of
and can work in the absence of an adjuvant,
microbial invasion. For exan1ple, intranasal
and like the gene-deleted vaccines, allow
vaccines are effective in protecting cattle
for DIVA. Some are adaptable to mass
against infectious bovine rhinotracheitis,
vaccination. Field data collected on tl1ese
cats against feline rhinotracheitis and
vaccines indicate strong immunity and
calicivirus infections, and poult1y against
limited adverse effects.

infectious bronchitis and Newcastle

VACCINES AND IMMUNOTHERAPY

2771
disease. Unfortunately, these techniques
against disease caused by tl1at specific
require handling each individual animal.

patl1ogen while maternal antibodies are

Aerosolization of vaccines enables them
present. However, passive antibody titers
to be inhaled by all the animals in a herd,
decrease exponentially. These maternal
group, or flock-an obvious advantage
antibodies may drop below protective levels

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when the unit is large. This method is
while, at tl1e same time, preventing
commonly used in the poultry industry.

successful in111ltmization. Inactivated

Alternatively, a vaccine may be adminisvaccines are not very effective in conferring tered in feed or drinking water, eg,
protective in111lunity in the face of maternal
vaccination of poultry for Newcastle
antibodies. Modified-live vaccines, however,
disease and avian encephalomyelitis. Fish
may induce a protective primary iJ11111w1e
and sluimp may be vaccinated by inrn1erresponse and some immunologic memory.

sion in a solution of antigen, which is

Because tl1e precise tune of loss of maternal
absorbed tl1rough their gills.

in1munity cannot be predicted, young
animals must usually be vaccinated multiple

Combination Vaccines: Because of tl1e
times to ensure successful iJ11mt111ization.

complexity of many disease syndromes or

The interval between vaccine doses
to avoid giving animals multiple injections,
depends on an anin1al's in111lunologic
it is common to use mixtures of organisms
memory. The duration of tl1is memory
in single vaccines. For example, for bovine
depends on multiple factors, such as the
respiratory disease complex, combined
natme of tl1e antigen, the use of live or dead
vaccines are available for bovine respiratory organisms, acljuvants used, and tl1e route of syncytial virus, infectious bovine rhinotraadministration. Some vaccines may induce cheitis virus, bovine viral dia.IThea virus,
inummity tl1at persists for an animal's
parainfluenza 3 virus, and Mannheimia
lifetime. Other vaccines may require
haemolytica. Combination vaccines are
boosting only once every 2-3 yr. Even killed
also commonly used in dogs and cats.

viral vaccines may protect some aniJ11als

When a mixture of different antigens
against disease for many years. Unfo1tuis inoculated simultaneously, they may nately, the miJ1imal dmation of in111lunity
compete with one another. However,
has rarely been reliably measured. Annual
manufacturers have recognized this and
revaccination has been tl1e traditional rule,
modified vaccines accordingly. Vaccines
because tl1is approach is administratively
should never be mixed indiscriminately,
siJnple and has the advantage of ensu1ing
because one component may dominate
tl1at an anin1al is regularly seen by a
and interfere witl1 responses to tl1e oilier
veterinarian. It is likely that this is more
components.

tl1an sufficient for most viral vaccines.

Some veterinarians and owners have

Individual anin1al and vaccine variability
expressed concern tl1at tl1e use of vaccine
make it difficult to estimate tl1e dmation
mixtures in tl1is way may somehow
of protective in111lunity. Within a group of

"overwhelm" tl1e in1111t111e system. This
animals, tl1ere may be a great difference
concern is unf0t111ded. The immune system
between tl1e shortest and longest duration
has evolved to respond to complex
of protection. Vaccines may differ
organisms and multiple sinrnltaneous
significantly in their composition, and
challenges. The sin1ultaneous administraaltl1ough all may induce inununity in the tion of multiple vaccines to an animal does
short term, it cannot be asswned that they
not present difficulties to the in1111une
confer equal longtem1 immunity. A
system of nonnal, healthy animals.

significant difference likely exists between
tl1e miniJnal level of iJrnnunity requiJ·ed to

Vaccination Schedules: Altl1ough it is
protect most aniJnals and tl1e level of
not possible to devise precise schedules
in1munity required to ensure protection of
for each vaccine, certain principles are
all animals.

common to all metl1ods of active in1111uni

A veterinaiian should al ways assess tl1e
zation. Newborn animals are passively
relative 1isks and benefits to an animal
protected by maternal antibodies and, in
when determining tl1e frequency of
general, cannot be vaccinated until
revaccination. Owners should be made
maternal immunity has waned. If stimulaawai·e iliat protection can be maintaiJ1ed tion of inununity is deemed necessary at
reliably only when vaccines are used in
tl1is stage, tl1e mother may be vaccinated
accordance with the protocol approved by
during late pregnancy, timing tl1e doses so
vaccine licensing authorities. The duration
tl1at peak antibody levels are reached at the
of it11111unity claimed by a vaccine manufactime of colostrum forn1ation. Neonatal tmer is tl1e minin1al duration supported by
animals with antibodies are protected
the data available at tl1e tin1e of approval.

2772

VACCINES AND IMMUNOTHERAPY

It is common practice to rate vaccines
not be protective; vaccination against an
according to their in1portance. Essential
already contracted disease is usually

( or core) vaccines should be given to all
impossible.

animals of a species, and veterinarians

The immune response, being a biologic

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should ensure that immunity is maintained
process, never confers absolute protection
throughout an animal's life by appropriate
nor is equal in all individuals of a vaccinated
revaccination. Optional ( or noncore)

population. Because the response is
vaccines protect animals against sporadic,
influenced by many factors, the range in a
mild, or uncommon diseases and should be
random population tends to follow a n01mal
used only when circun1stances warrant and
distribution: the response will be average in
when the benefits clearly outweigh the risks
most animals, excellent in a few, and poor in
involved. For example, essential vaccines in
a few. An effective vaccine may not protect
dogs in the USA would normally include
those with a poor response; it is difficult to
canine distemper, paivovirus, adenovirns,
protect lOQOA, of a random population by
and rabies. Optional vaccines may include
vaccination. The size of this unresponsive
canine coronavirus, pai·ainfluenza, Borde
population varies ai11ong vaccines, and its
tella, leptospirosis, and Lyme disease.

significance depends on the nature of tl1e
disease. For highly infectious diseases in

Prime-boost Strategies: It has long
which herd in1rnunity is poor and infection
been normal practice to use exactly the
is rapidly and efficiently trai1smittecl ( eg,
same vaccine for boosting an inunune
foot-and-mouth disease), the presence of
response as was used when first priming an
unprotected animals can permit the spread
animal. However, there is no reason why
of disease and disrupt control progran1s.

different forms of a vaccine should not be

Problems also can aiise if the unprotected
used for priming and for boosting. This
animals are individually important, as in the
approach is known as a prin1e-boost
case of companion anin1als or breeding
strntegy. Under some circumstances, this
stock In contrast, for diseases that are
may result in significantly improved vaccine
inefficiently spread ( eg, rabies), 600/o--7QOA,
effectiveness. Prime-boosting has been
protection in a population may be sufficient
most widely investigated in attempts to
to effectively block disease transmission
improve the effectiveness of DNA vaccines.

within that population and tl1erefore may be

Combinations usually involve p1iming with
satisfactory from a public healtl1 perspeca DNA vaccine and boosting with either a tive.

recombinant vaccine or with recombinant

The most important cause of vaccination
protein antigens.

failure in young animals is the inability of a
vaccine to inunwuze in the presence of

Vaccine Failure
maternal antibodies. Vaccines may also fail

There are many reasons why vaccination
when the immune response is severely
may fail. In some cases, the vaccine may not
suppressed, eg, in heavily parasitized or
be effective because it contains strains of
malnowishecl anin1als. (Such anin1als
organisms or antigens that are different
should not be vaccinated.) Stress, including
from the disease-producing agent. In other
pregnancy, extremes of cold and heat, and
cases, the method of manufacture may have
fatigue or malnowishment, may reduce a
destroyed the protective epitopes, or there
nom1al immune response, probably clue to
may simply be insufficient antigen. Such
increased glucocorticoid production.

problems are uncommon and can be
avoided by using vaccines from reputable

Adverse Reactions
manufacturers. More commonly, ai1

Modem, commercially produced, licensed
effective vaccine may fail because of
vaccines are very safe. Nevertheless, they
unsatisfactory administration or storage.

are not always innocuous. The more

For exai11ple, a live bactelial vaccine may
conunon Iisks associated with vaccines
lose potency as a result of use of ai1tibiotics.

include residual virulence and toxicity,

Route of administration may also affect
which may cause injection-site reactions,
efficacy. When vaccine is administered to
depression, allergic responses, disease in
poultry or mink by aerosol or in drinking
in1munodeficient hosts (modified-live
water, the aerosol may not be evenly
vaccines), neurologic complications, and
distributed throughout a building, or some
rarely, contamination with other live agents.

animals may not drink adequate amounts.

For exan1ple, lesions of mucosal disease

Also, chlorinated water may inactivate
may be seen in calves vaccinated against
vaccines. If an animal is incubating the
bovine viral diaiThea. Vaccines that contain
disease before vaccination, the vaccine may
killed grai11-negative orgai1isms may also

VACCINES AND IMMUNOTHERAPY

2773
contain bacterial cell-wall components that
tests il1clude confirmation of the identity of
stimulate release of interleukin-1 and can
the organism used, freedom of the vaccme
cause fever and leukopenia and occasionfrom contamination with extraneous ally abortion. In general, it is prudent to
organisms, and host and non-host safety

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avoid vaccinating pregnant animals unless
toxicity tests. Because the living organisms
the 1isks of not vaccinating are greater.

fotmd in vaccmes norn1ally die over tilne, it

Recent studies have indicated that vaccines
is necessary to ensure that they will be
are more likely to cause adverse effects in
effective even after storage (stability).

small dogs than in large. This is because

Although properly stored vaccines may still
both receive the same quantity of vaccine,
be efficacious after the expiration of their
and the smaller anin1als receive a relatively
designated shelf life, this should never be
larger "dose." Certain modified-live virus asslUlled; expired vaccines should not be
bluetongue vaccines have been repo1ted to
used.

cause congenital anomalies when given to
pregnant ewes. The stress from a vaccina

PASSIVE IMMUNIZATION
tion reaction may be sufficient to activate
latent infections. For example, activation of

Passive ilnmunization involves the
equine herpesvirus has been demonstrated
production of antibodies m one anin1al by
after vaccination against African horse
active m1n1unization. These antibodies can
sickness. Another adverse reaction is the
be stored (as immlllloglobulins) and then

"sting" that occurs when some vaccines are administered to susceptible anm1als to
administered. This can cause problems for
confer ilnmediate but short-lived protecthe vaccinator if the vaccinated animal tion. The transfer of maternal antibody to
objects strenuously. Some vaccines and
offspring via the placenta or colostrum is
vaccine mixtures may cause mild, transient
the natural (and ve1y il11portant) form of
il1m1unosuppression.

passive m1n1llllization. Irnmunoglobulms

In addition to potential toxicity, vaccines,
may be produced in cattle against anthrax,
like any antigen, may provoke hypersensiill dogs agaillst distemper, and in cats tivity. For example, rapid allergic reactions
against panleukopenia. Their most

(type I hypersensitivity) may occur
ilnportant role is m protection against
in response to any of the antigens fom1d in
toxigenic organisms, eg, C/ost1idiimi
vaccines, including those from eggs or
tetani or C pe1J1ingens. These ll11nllll10-tissue-culture cells. All forms of hypersensiglobulins are generally produced in yom1g tivity are more commonly associated with
horses by a series of inm1ll1Uzing inoculamultiple injections of antigen; therefore, tions.

they tend to be associated with use of

To check the potency of preparations of
inactivated products. Inm1une complex
inununoglobulill, comparison is made with

(type III) reactions are also potential
an international biological standard and
hazards of vaccination. These may cause an
expressed il1 mternational lU1its (!Us).

il1tense local inflan1matory reaction or a

Tetanus ll11nlunoglobulin is given to animals
generalized vascular disturbance such as
to confer immediate protection against
purpura. An example of a type III reaction is
tetanus. At least 1,500-3,000 !Us of immunoclouding of the cornea in dogs vaccinated globulin should be given to horses and
against canine aclenovirus 1. Delayed (type
cattle; at least 500 !Us to calves, sheep,

IV) hypersensitivity reactions, expressed as
goats, and pigs; and at least 250 !Us to dogs.

granuloma formation, may develop at the

The exact amount varies with the amount of
site of inoculation in response to the use
tissue dan1age, degree of wolllld contammaof depot adjuvants. Some chronic inflammation, and time elapsed smce injmy. Tetanus tory reactions to long-acting feline vaccines
ilnmm10globulm is of little use once clinical
may eventually lead to development of a
signs appear, although massive closes of up
fibrosarcoma at the injection site in cats.

to 300,000 !Us may help.

Monoclonal Antibodies: In a normal

Production of Vaccines
ilnmune response, antibodies are produced

In most countries, government autho1ities
by many different plasma cell populations
regulate the production of biologics.

and are thus said to be polyclonal. Although

In general, regulatory authorities license
these antibodies all cornbil1e with a specific
establishments that produce vaccines and
antigen, they are a heterogeneous mixture
inspect those premises to ensure that the
of protems. Homogeneous antibodies can
facilities and the methods used are
be generated through the use of cloned cell
satisfactory. All vaccines are checked for
lines called hybridomas; these monoclonal
safety, purity, potency, and efficacy. Safety
antibodies represent an alternative source

2774

VACCINES AND IMMUNOTHERAPY
of passive immunization. Currently,

NONSPECIFIC IMMUNOTHERAPY
however, these are mainly made by mouse
hybridomas (and thus consist of mouse anti

Under some circumstances, it may be
bodies) and may sensitize other animal
desirable to enhance the activity of an
species.

animal's inunune system. This may include

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Monoclonal antibodies are commonly
stimulation of the nom1al in1mune response
used in diagnostic tests. Because they are
to enhance protection and treatment of
homogeneous and specific, these antibodies immunosuppressive conditions. Several can differentiate between closely related
types of inununostirnulators have been used
infectious agents in a manner impossible
in veterinary medicine. They commonly
with conventional antibodies. For example,
contain microbial components, and many
they can differentiate between the rabies
act by stimulating one or more toll-like
vi.ruses obtained from skunks, bats, or dogs.

receptors or related receptor systems.

POULTRY

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CIRCULATORY SYSTEM

BLOODBORNE ORGANISMS 2780

Aegyptianellosis 2780

Isosporiasis 2781

Filariasis 2782

Haemoproteus Wection 2782

Leucocytozoonosis 2783

Plasmodium Wection 2784

Other Bloodbome Organisms 2785

CHICKEN ANEMIA VIRUS INFECTION 2785

DISSECTING ANEURYSM IN TURKEYS 2787

INCLUSION BODY HEPATITIS/HYDROPERICARDIUM SYNDROME 2788

PERI RENAL HEMORRHAGE SYNDROME OF TURKEYS 2789

SPONTANEOUS CARDIOMYOPATHY OF TURKEYS 2790

DIGESTIVE SYSTEM

CANDIDIASIS 2791

COCCIDIOSIS 2791

CORONAVIRAL ENTERITIS OF TURKEYS 2797

CRYPTOSPORIDIOSIS 2798

DUCK VIRAL ENTERITIS 2799

HEXAMITIASIS 2801

NECROTIC ENTERITIS 2802

ROTAVIRAL INFECTIONS IN CHICKENS, TURKEYS, AND

PHEASANTS 2803

TRICHOMONOSIS 2804

ULCERATIVE ENTERITIS 2805

GENERALIZED CONDITIONS

AVIAN CAMPYLOBACTER INFECTION 2806

AVIAN CHLAMYDIOSIS 2808

AVIAN NEPHRITIS VIRAL INFECTIONS 2812

AVIAN SPIROCHETOSIS 2813

COLIBACILLOSIS 2814

2776

POULTRY

DUCK VIRAL HEPATITIS 2815

ENTEROCOCCOSIS 2816

ERYSIPELAS 2817

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FATTY LIVER HEMORRHAGIC SYNDROME 2820

SUDDEN DEATH SYNDROME OF BROILER CHICKENS 2821

FOWL CHOLERA 2822

FOWLPOX 2824

Fowlpox in Chickens and Turkeys 2824

Pox in Other Avian Species 2826

GOOSE PARVOVIRUS INFECTION 2826

HELMINTHIASIS 2828

HEMORRHAGIC ENTERITIS/MARBLE SPLEEN DISEASE 2833

HISTOMONIASIS 2835

INFECTIOUS BURSAL DISEASE 2837

LISTERIOSIS 2839

MALABSORPTION SYNDROME 2840

MYCOPLASMOSIS 2841

Mycoplasma gallise'J)ticum Infection 2841

Mycoplasma synoviae Infection 2843

Mycoplasma meleagridis Infection 2844

Mycoplasma iowae Infection 2845

MYCOTOXICOSES 2846

NEOPLASMS .2848

Marek's Disease

2849

Lymphoid Leukosis 2851

Reticuloendothelio�is 2854

Neoplasms of Unknown Etiology 2855

NEWCASTLE DISEASE AND OTHER PARAMYXOVIRUS

INFECTIONS 2856

Newcastle Disease

2856

Other Avian Paramyxovirus Infections 2858

OMPHALITIS 2859

POISONINGS 2859

RIEMERELLA ANATIPESTIFER INFECTION 2864

SALMONELLOSES 2865

Pullorum Disease 2865

Fowl Typhoid 2866

Paratyphoid Infections

2866

STAPHYLOCOCCOSIS 2867

POULTRY

2777

STREPTOCOCCOSIS 2868

TUBERCULOSIS 2869

TURKEY VIRAL HEPATITIS 2871

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MISCELLANEOUS CONDITIONS OF POULTRY 2871

Ascites Syndrome 2871

Breast Blisters 2873

Breast Buttons 2873

Cannibalism 2873

Fluke Infections 2874

Pendulous Crop 2874

Urate Deposition (Gout) 2874

INTEGUMENTARY SYSTEM

ECTOPARASITES 2875

Bedbugs 2875

Fleas 2875

Flies and Gnats 2875

Biting Midge 2875

Black Fly 2875

Pigeon Fly 2876

Fowl Ticks 2876

Lice 2876

Mites 2877

Chicken Mite 2877

Common Chigger 2877

Depluming Mite 2877

Feather Mite 2878

Northern Fowl Mite 2878

Scaly Leg Mite 2878

Cyst Mite 2878

Tropical Fowl Mite 2878

Turkey Chigger 2878

Mosquitoes 2879

GANGRENOUS DERMATITIS 2879

MUSCULOSKELETAL SYSTEM

DISORDERS OF THE SKELETAL SYSTEM 2880

Noninfectious Skeletal Disorders in Broilers 2881

Noninfectious Skeletal Disorders in Breeders 2882

Infectious Skeletal Disorders 2882

MYOPATHIES 2883

Exertional Myopathy 2883

Deep Pectoral Myopathy 2883

Capture Myopathy 2884

2778

POULTRY

Transport Myopathy of Turkeys 2884

Mechanically Induced Myopathy 2884

Rupture of the Gastrocnemius Tendon 2885

Rupture of the Peroneus (Fibularis) Longus Muscle 2885

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Nutritional Myopathy 2885

Toxic Myopathy 2885

Injection Site Injury 2886

Minimal Myopathy 2886

Genetic Myopathy 2886

VIRAL ARTHRITIS 2886

NERVOUS SYSTEM

AVIAN ENCEPHALOMYELITIS 2888

BOTULISM 2889

VIRAL ENCEPHALITIDES 2891

WEST NILE VIRUS INFECTION IN POULTRY 2893

REPRODUCTIVE SYSTEM

ARTIFICIAL INSEMINATION 2895

DISORDERS OF THE REPRODUCTIVE SYSTEM 2896

Cystic Right Oviduct 2896

Defective or Abnormal Eggs 2896

Egg-bound or Impacted Oviducts 2896

Egg Peritonitis 2896

False Layer 2897

Hypocalcemia, Sudden Death, Osteoporosis, or Cage Layer Fatigue 2897

Internal Layer 2897

Infertility 2898

Neoplasia 2898

Oophoritis and Ovary Regression 2898

Prolapse of the Oviduct 2898

Salpingitis 2898

Sex Reversal 2899

EGG DROP SYNDROME '76 2899

RESPIRATORY SYSTEM

AIR SAC MITE 2901

ASPERGILLOSIS 2901

AVIAN INFLUENZA 2902

AVIAN METAPNEUMOVIRUS 2904

BORDETELLOSIS 2907

INFECTIOUS BRONCHITIS 2909

POULTRY

2779

INFECTIOUS CORYZA 2911

INFECTIOUS LARYNGOTRACHEITIS 2912

QUAIL BRONCHITIS 2913

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NUTRITION AND MANAGEMENT

NUTRITIONAL REQUIREMENTS 2914

FEEDING AND MANAGEMENT PRACTICES 2919

Feeding Methods 2920

Vaccination Programs 2920

Management of Growing Chickens 2920

Management of Laying Chickens 2922

Organic Production Practices 2925

NUTRITIONAL DEFICIENCIES 2929

Protein, Amino Acid, and Energy Deficiencies 2930

Mineral Deficiencies 2930

Calcium and Phosphorus Imbalances 2930

Manganese Deficiency 2933

Iron and Copper Deficiencies 2933

Iodine Deficiency 2934

Magnesium Deficiency 2934

Potassium, Sodium, and Chloride Deficiencies 2934

Selenium Deficiency 2936

Zinc Deficiency 2936

Vitamin Deficiencies 2936

Vitamin A 2936

Vitamin D3 2937

Vitamin E 2938

Vitamin K 2939

Vitamin B12 2939

Choline 2940

Niacin (Nicotinic Acid) 2940

Pantothenic Acid 2940

Riboflavin 2941

Folic Acid (Folacin) 2942

Biotin 2942

Pyridoxine (Vitamin B6) 2943

Thiamine 2943

2780

BLOODBORNE ORGANISMS

BLOODBORNE ORGANISMS

VetBooks.ir

Avian blood may contain various disease
buffy coat should be expressed from the cut
agents, including viruses, bacteria,
end with a small ainount of plasma to make
rickettsiae, protozoa, microfilariae, and
a suspension, and a thin smeai· prepared.

rarely fungi. These organisms can be

Stained buffy coat smears are recomidentified by microscopic examination of mended to detect bacteria, spirochetes, and
wet mounts, buffy coat, or blood smears
chronicLeucocytozoon, Tlypanosoma, or
or by appropriate culturing and molecular

Isospora (Atoxoplasma) infections. An
techniques. Microscopically, some are
excellent technique to identify low nwnbers
within blood cells (Plasmodium, Haemo
of motile organisms such as spirochetes and
proteus, Leucocytozoon, I sospora
microfilariae is direct exainination of the
f Atoxoplasma/, Hepatozoon, Babesia,
buffy coat by darkfield or phase contrast

Aegyptianella), while others are free in
microscopy. The buffy coat and all of the
the plasma (Tlypanosoma, microfilariae,
plasma should be expressed onto a glass
bacteria, spirochetes). None Jive exclusively slide and covered with a coverglass, wllich in the blood; most are found in tissues but
is depressed slightly to spread the buffy
are present in blood during part of their life
coat. The buffy coallplasma interface
cycle. Some, such as microfilariae and
should be exainined with dai·kfield or

Plasmodium, may have a periodicity when
reduced light microscopy to detect motile
nw11bers or stages of parasites vary with
organisms.

tin1e. In such cases, examining multiple

To make a diagnosis of infection with
smears at intervals will increase the
an intracellular blood protozoan on a tl1in
likelil10od of obtaining a diagnosis.

blood film, it first should be detem1ined

Seasonal variations in infection rates relate
that the "parasites" in question are neither to the activity of artlu·opod vectors. When
normal structure nor artifact. The following
possible, tissue cytology is also a useful
should then be detemlined: the host cell and
acljunct to exan1ination of blood. Most
whether it is normal or defo1med beyond
blood borne organisms are either uncomidentification, whether pigment granules monly or not associated with clinical

(hemozoin) ai·e present or absent, and
disease. However, weakened or injured
whether merogony is occuning (see
birds infected with hemoprotozoa may

TABLE 1). Identification of an organism
have higher mortality and slower recovery
beyond genus is difficult and usually
than uninfected birds. Exainination for
wmecessary for clillical pw-poses.

blood borne organisms should be included

Serologic ai1d molecular diagnostic
in the clinical and diagnostic procedures
methods have been developed for avian
for ai1y ill bi.rd.

hernoparasites but are usually not available

Thin blood smears should be rrfade with
commercially. Molecular methods are very
blood directly from the bird, if possible.

sensitive and can detect infection when

Anticoagulants, storage, and cooling of the
parasite numbers are too low to be detected
blood can distort protozoa! morphology and in blood or tissue smears or bY. histology.

introduce artifacts. A small drop of blood

Hemoparasites can also be studied by subincan be collected using a SY1inge and needle.

oculation of infectious blood in birds of the

The drop should be spread on a clean glass
saine or a known susceptible avian species.

slide to make a thin smear. A Romanowsky

Bacteria can usually be identified by blood
type stain that gives good polychromatic
culture ai1d molecular metllods.

coloration (eg, Giemsa stai.n) should be
used. At least 200 oil-i.nunersion fields

AEGYPTIANELLOSIS

( -20,000 RBC) for single smears or 100 for
multiple smears from the saine bird should

Aegyptianellosis is an acute, tickbome,
be exainined. Leucocytozoon and microfebrile disease caused by Aegyptianella filai'iae are found ai·ound the periphery of
spp, a rickettsia in the fan1ily Anaplasmatasmears and can be easily seen on low-power ceae. Wection of avian species, including
magnification.

cllickens, tw·keys, guineafowl, quail,

Blood borne orgailisms in plasma or
pigeons, crows, waterfowl, ratites, fal

WBCs are concentrated in the buffy coat.

cons, passerines, and psittacines has been

The microhematocrit tube is cut just below
described. A pullorum is pathogenic in
the buffy coat above the packed RBCs. The
chickens. Ticks, especially Argas spp,

BLOODBORNE ORGANISMS

2781
itM•il CHARACTERISTICS OF PROTOZOA ENCOUNTERED IN AVIAN BLOOD

Pigment

Merogony

Protozoan

Host Cell

Present
in Blood

Plasmodium

RBC

Yes

Yes

VetBooks.ir

H aemoproteus

RBC

Yes

No

Leucocytozoon

RBC or WBC; distorted

No

No
and enlarged often
beyond recognition

Isospora

WBC; in nuclear

No

No•

(Aloxoplasma)

indentation

Hepatozoonb

WBC, large, elongated

No

No
oval shape

Babesiab

RBC

No

Noc

• Multiple intracellular parasites may be seen in acute infections.

"Unconunon to rare.

c Babesia are pyriform and may be in a V, X, or fan pattern.

transmit the organism; infection can also be
synonymous with lsosopora and unified
reproduced by blood inoculation. Organin a single group of coccidia with intraisms stain purple with Romanosky stain and extra-intestinal forms.

and appear as single or multiple, round,

Isosporiasis is a disease of passerine

"signet-ring" (0.3-4 µm) or irregular oval birds. Canaries, finches, sparrows, and
bodies in RBCs often lateral to the nucleus.

species of the Stwnidae family ( starlings,

They must be differentiated from trophozomynalls) are most often affected. Very rare ites of Plasmodium and gan1etocytes of
cases of infection have also been reported

Haemoproteus. Infections are most
in raptors. Poultry are not known to be
common in tropical and subtropical areas
affected.

of Africa, Asia, and Europe; infection of

Isospora has a direct life cycle that
wild turkeys in Texas has been reported.

includes an intestinal and an extra-intestinal,

In endemic areas, infection is mild or
systemic phase. Schizogony occurs in the
asymptomatic. Ruffled feathers, anorexia,
intestinal epithelial cells as well as the
droopiness, diarrhea, fever, and high
circulating mononuclear cells. Garnetogony
mortality in younger birds can occur in
and oocyst formation occur in the intestinal
introduced or otherwise susceptible birds.

epithelial cells, and oocysts are passed in

Anemia, which can lead to right-side heart
the feces. Transmission is fecal-oral.

failure and ascites, enlargement of the liver

Infection is most often not pathogenic,
and spleen, enlarged discolored kidneys,
and high parasitemia may be seen in young
and pinpoint serosal hemorrhages, can be
birds. In susceptible species or weakened
seen. Infestation with larval argasid ticks
birds, mortality can be high (as much as
andB01relia infection (seep 2813) may 80%) and rapid, especially in fledglings.

accompany the disease.

Isospora infection complicates manage

Tetracyclines, especiaJ!y doxycycline,
ment and is a threat to successful captive
effectively control the disease and possibly
breeding of some species such as tl1e
elinlinate the organism from chronically
endangered Bali mynalls. Clinical signs
infected birds. Tick control is an in1portant
include listlessness, diarrhea, anorexia, and
adjunct to treatment.

weight loss. In acutely affected birds, there
is marked hepatomegaly and splenornegaly,
often with multi.focal necrosis. The enlarged

ISOSPORIASIS
liver and gaJ!bladder can be seen through

(Atoxoplasmosis, Lankesterellosis)

the abdominal waJI, especially if it is
moistened with alcohol, which provides the

The taxonomic position of the Ei.meriidae
basis for the common name of black spot
coccidia generaAtoxoplasma and lsospora disease in passerine birds. Parasite-infected
has been subject to debate. It is currently
mononuclear cells a.re present in blood and
suggested thatAto.xoplasma be considered
organ impression smears or aspirates,

2782

BLOODBORNE ORGANISMS
especially in the liver and spleen. Oocysts
with bloodsucking insects ( eg, lice,
are present in droppings. Isospora are
mosquitoes, midges) serving as intermedipale-staining, nonpigmented, oval, ate hosts. Adults mature in body cavities,
intracytoplasmic bodies within monoincluding the eye and ventricles of the brain, nuclear cells thought to be lymphocytes.

respiratory system, cardiovascular system,

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Usually, cells contain a single parasite, but
or connective tissues; some produce
multiple organisms can be seen in severe,
characteristic subcutaneous nodules.

acute infections. Presence of the protozoan

Microfilariae may be numerous in circulacauses the nucleus to curve around it, giving tion, especially in the skin vasculature.

the appearance that the organism is located

Microfilariae can be seen in blood smears.

within an indentation of the nucleus.

However, a buffy coat smear obtained from

Diagnosis is difficult in chronically
a microhematoc1it tube is a more sensitive
infected older birds. Very few parasites are
method of diagnosis. Increased numbers of
present in blood and tissues, and oocysts
microfilariae have been seen in stressed
are shed intermittently, sometimes in high
individuals, but they rarely cause clinical
numbers. A PCR test is available and can
disease or mortality. A possible exception
be pe1formed on blood, tissues, or feces,
is infection of emus with Chandlerella
although its sensitivity is poor in fecal
quiscali, a common filarid of the brain of
samples. PCR is useful to detennine tl1e
free-living grackles. Affected emus show
incidence and prevalence in a collection,
signs of CNS disease ( eg. torticollis, ataxia).

confu111ing the diagnosis, and possibly

C quiscali apparently does not produce
evaluating the efficacy of treatment. PCR
microfilariae in emus. Treatment witl1
cannot be used to ascertain that a bird is free
ivem1ectin, fenbendazole, or levamisole,
of Isospora, however. Buffy coat and organ
and surgical removal of adult parasites,
smears are other but less sensitive diagnostic have been used.

metl1ods. Negative findings should not be
interpreted to mean that infection is not
present. In some chronically infected birds,

HAEMOPROTEUS INFECTION
hepatic and splenic enlargement persists
because of infiltrations with high numbers

Haemoproteus spp is the most common
of large lymphoid cells that serve as host
blood parasite in birds, especially nondocells for the parasite. Histopathologically, mestic birds. More than 120 species have
organisms are difficult to find and identify,
been repo1ted. Haemoproteus spp are
and lesions may be mistaken for those of
found in free-living ducks, quail, and turkeys
lymphoma.

but are rare to absent in conunercial flocks,

Toltrazuril, sulfachlorpyridazine, and
probably because of lin1ited vector
sulfachlorpyrazine have successfully
exposure or very specific feeding habits of
reduced mortality and oocyst shedding. It is

Culicoides spp and hippoboscid flies, the
unlikely that these drugs clear the organism
invertebrate vectors. Haemoproteus is
from tl1e bird. Good management proceconsidered nonpathogenic in most avian dures, including isolation of age groups and
species. Birds are usually asymptomatic;
scrupulous cleanliness (particularly daily
however, Haemoproteus infection may
cleaning before oocysts sporulate) help
be more often significant than previously
control the disease. Disinfectants have little
thought, based on increasing reports
effect on oocysts.

docun1enting decreased host fitness,
nestling mortalities, fledging success, and

FILARIASIS
delayed recovery in infected birds versus
uninfected birds. Anemia, anorexia, weight

Microfilariae are commonly found in the
loss, and depression have been reported.

blood of some wild bird species but are rare

Rarely fatal disease occurs. Clinical disease
to absent in poultry except in southeast Asia is usually attributed to anemia, presence of where infections in chickens and waterfowl
megaloschizonts in the musculature, or
occur. Prevalence of microfilariae in wild
host-cell destruction.

birds varies from 3% to 6% but can be as high

In poultry, infection with H lophortyx in
as 200A, in some species such as ptarmigan,
bobwhite quail caused clinical disease and
swans, and geese. When psittaciformes
increased mortality with as much as 20%
were commonly imported, it was not
flock loss. Quail 5---10 wk old were usually
unusual to observe microfilariae in tl1eir
affected, and clinical signs included
peripheral blood, especially in imported
reluctance to move, prostration, and death.

cockatoos.

Gross lesions included congested spleen

At least 16 genera of filarids are found in
and liver and hemorrhagic streaks in tl1e
avian species. All have an indirect life cycle,
muscles. Histology revealed myositis with

BLOODBORNE ORGANISMS

2783
megaloschizonts in the musculature,
antierythrocytic factors produced by
especially of the legs and back, and
the parasite, high nW11bers of the large
hemosiderin accwnulation in the splenic
gametocytes blocking pulmonary capillarmacrophages. Experimental infection in ies, or pai·asites invading the endotheliW11 of
turkeys with H meleagridis resulted in
vessels in tissues (brain, heait, etc) where

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lan1eness, diarrhea, anorexia, and depresthey form megaloschizonts that occlude sion. Histologic lesions were associated
vessels and result in multifocal necrosis.

mainly with megaloschizont development in

Pai·asitemia often increases dramatically
the musculature. Infection in racing pigeons
in late April and early May ( called spring

( called pigeon malaria) is commonly
rise),just before arthropod vectors, black
asymptomatic but often blamed for poor
flies (Simulium spp ), or bi.ting midges
perfom1ances that are due to other diseases

( Culicoides spp) increase. Ducks that have or inadequate housing and management.

recovered from infection with L simondi

Clinical disease in Colw11bifonnes is rare.

may relapse when light cycles are manipu

Diagnosis is made by examination of
lated to increase egg production. Increased
stained blood smears and observation of
levels of prolactin have been suggested as a
large, pigmented gametocytes in mature
possible cause.

RBCs that paitially or occasionally

Acute disease is seen more often in the
completely encircle the nucleus without
young with high pai·asitemia and when black
displacing it. Merozoites are not seen in the
flies or biting midges ai·e most abundant.

pe1ipheral blood. Schizogony within the

Subacute or chronic disease is seen in the
endothelial cells of the ltmg, liver, and
yotmg outside fly season and in older birds
spleen may be seen histologically. PCR tests
at a.J1Y season; parasitemia is usually low.

for Haemoproteus have been developed.

Recovered birds remain cai-riers a.J1d serve

Little is known about effective treatment.

as a rese1voir for young, susceptible birds.

Antimalarial drugs reduce the parasitemia
but do not eliminate the parasite. Chloro

Clinical Findings, Lesions, and
quine, prirnaquine, quinacrine, and

Diagnosis: Ducklings or turkey poults ai·e
buparvaquone have been used in pigeons.

listless and show various combinations of

Combinations of chloroquine and primathe following signs: anemia, leukocytosis, quine or chloroquine and mefloquine have
tachypnea, anorexia, diarrhea with green
been used to treat owls. Treatment is not
droppings, a.J1d CNS signs. Mortality in
recommended in asymptomatic birds.

ducklings can reach 700A,. Mortality is low in

Measures to control invertebrate vectors,
adult ducks or turkeys. Egg production and
such as screening of aviaries, help prevent
hatchability is decreased. Signs are evident
transmission and heavy infections.

-1 wk after infection and coincide with the
onset of parasitemia. Visibly affected birds
die after 7 -20 days or may recover with

LEUCOCYTOZOONOSIS
sequelae of poor growth and egg production. Hemorrhages, splenomegaly, and Infections withLeucocytozoon spp are
hepatomegaly are seen. Grossly visible white
most often subclinical but can occasionally
dots in affected orga.J1s are megaloschizonts.

cause clinical and even fatal disease. Mortal

Histologic lesions are associated with
ity varies greatly with the strain of parasite,
megaloschizont development in the spleen,
species, degree of exposure, age, immune
liver, heart, and other organs. Infection with
status, and other factors. Outbreaks of

L caulleryi in chickens has a tropism for the leucocytozoonosis have been reported in
chickens (Asia, Africa), turkeys (North

Anlerica), waterfowl (North Anlerica,

Europe, Asia), and a nW11ber of free-living
and captive avian species throughout the
world. Species in domestic birds include

L simondi in waterfowl; L smilhi in turkeys; and L caulleryi, L sabrazesi,

L andrewsi, and L schoutedeni in chickens. L caulleryi can be highly pathogenic, causing a lethal hemorrhagic disease of
chickens in southeast Asia. L simondi
causes mortality in ducks a.J1d geese.

N wnerous Leucocytozoon spp infect
nondomesti.c birds. Clinical disease and

Leucocytozoon parasite in the peripheral
mortality result from anemia caused by
blood of a turkey. Courtesy of Dr. Jean Sander.

2784

BLOODBORNE ORGANISMS
reproductive tract and is associated with
resident ( eg, Hawaiian avifauna) birds,
oviduct inflanmrntion and edema and
respectively. Passerine birds con1rnonly
decreased egg production. Peritoneal,
carry the organism asymptomatically.

perirenal, and subdural hemorrhages are

Cold-climate species held ouside their
repmted with severe disease.

natural range are particularly susceptible to

In blood smears, gan1etocytes may be
develop clinical disease ( eg, penguins, snowy

VetBooks.ir
seen, especially along the edges and tail of
owls, and gyrfalcons in captivity). Invertethe smear. Leucocytozoon is identified by brate hosts are ornithophilic mosquitoes,
large gametocytes that lack pigment and
usually Culex, Culisela, or Aedes spp.

distort the host cell (RBC or WBC), making
it no longer identifiable. The shape of

Clinical Findings, Lesions, and
gametocytes varies: some are elongated

Diagnosis: Infection withPlasmodium
with long tapering extremities, whereas
spp may be nonclinical or cause illness
others are round. Serology may detect prior
characterized by weakness, lassitude,
infection. PCR tests have been developed
dyspnea, anemia, abdominal distention,
for diagnosis of leukocytozoonosis.

increased right heart weight, ocular
hemorrhage, biliverdinuria, and death.

Treatment and Control: Treatment

Death results from severe anemia or
usually is not effective. Preventive medblockage of capillaries in the brain, lung, ication using pyrimethamine (1 ppm)

or other vital organs by exoerythrocytic
and sulfadimethoxine (10 ppm) combined
meronts in endothelial cells. The liver and
in the feed controls L caulleryi. Clopidol
spleen are markedly enlarged and often

(0.0125%---0.025%) controls L smilhi.

discolored (dark brown to black). Pig

Measures to control invertebrate vectors
mented parasites including meronts are
are helpful. Hurnoral in1rnunity resulting
found in both i.J.11rnature and mature RBCs.

from vaccination will protect against

Infrequently, parasites are found in

L caulleryi infection. Treatments with
thrombocytes and WBCs. In birds that die
quinacrine hydrochloride or trimethoprim/
acutely, organisms may be sparse or absent
sulfan1ethoxazole solution have been used
in blood, but numerous meronts can be found
in raptors; parasitemia is reduced, but the
in capillaries by histology or exanlination of
infection is not cleared.

squash or impression smears of brain, lung,
liver, and spleen. Serologic and molecular

PLASMODIUM INFECTION
diagnostic methods exist but are not
available commercially. Serology and PCR

P/.asrnodium spp infect a wide variety of
can detect infection when parasites are too
domestic and wild birds in most areas of the
few to be identified in blood smears.

world. Infection is often· not species specific.

Thirty-five species of P/.asmodium are

Treatment and Control: Therapy is
considered valid species. P gallinaceum,
variably effective in treating infected birds

P juxlanucleare, and P durae are the most or flocks. Persistent parasitemia or relapse
pathogenic species found in poultry.

may occur during and after treatment.

P gallinaceum infects chickens in Asia and

Birds that survive initial infections may be

Africa and causes low mortality in indigrefractory to subsequent infections.

enous chickens; however, rates may be

Prevention of exposure to mosquitoes
as high as 80%-900Ai in commercial birds.

by appropriate housing is essential.

P juxtanucleare infects chickens and

No antimalarial drug is commercially
turkeys in Asia, Afiica, and South America;
available or approved to treat poultry
most infections are mild or asymptomatic.

flocks. However, a mixture of trimethoprin1

P durae infects turkeys and gallinaceous
and sulfaquinoxaline in the feed for a 5-day
birds other than chickens in Africa; mortality
period has been shown to be efficacious
in turkeys can approach 1 OOOAi. P hermani
against experimentally induced P gallina
infects turkeys and bobwhite quail. Clinical
ceum malaria in chickens. An experimenmalaria has not been reported from poultry tal study on the pathogenicity and
in North America, but indigenous wild
chemotherapy of P durae suggested that a
turkeys can become infected with at least
combination of sulfamonomethoxine and
four differentPlasmodium species. The
sulfachloropyrazine could be an effective
most common species affecting wild birds
therapy; halofuginone was suggested for
is P relic tum, which has been found in at
chemoprophylaxis in endemic areas.

least 360 species of birds. Asymptomatic

Chloroqui.J.1e administered by gavage at
infections in endemic or introduced birds

50 mg/kg in Leghorn chickens experimencan be spread via mosquitoes and cause fatal tally infected with P juxtanucleare may
disease in introduced ( eg, zoo birds) or
have reduced parasitemia.

CHICKEN ANEMIA VIRUS INFECTION

2785

In caged birds and penguins, chloroquine
to be any of several bloodsucking insects.

( 10 mg/kg) and primaquine (0.3---1 mg/kg) is

Tr·eatment is not Wa.J.Tanted.

given orally and followed by administration

Borreliae are tickborne (Argas spp)

of chloroquine (5 mg/kg) 6, 24, and 48 hr
spirochetes that can cause fatal systemic
later. Chloroquine in drinking water (250
disease. Penicillins, te1tracyclines, tylosin,
mg/120 mL) has also been used in songbirds. and tick control are used for prevention VetBooks.ir

Grape or orange juice can disguise
a.J.ld treatment. (See also AVIAN SPIROCHETOSIS, chloroquine's bitterness. Treatment
p 2813.)

including both primaquine and chloroquine

Babesia spp a.,.·e uncommon, non pigis recommended over chloroquine alone, mented, pyrifom1-shaped, erytluocytic
because only prirnaquine is active against
protozoa.,.1 parasites of birds. Natural
the tissue schizonts. Chloroquine has
infections of penguins, falcons, cranes, and
activity against erythrocytic schizonts and
several other avian species occm. Ticks a.,.·e
garnetocytes. Prirnaquine also has activity
considered to be the invertebrate hosts. V, X,
against erythrocytic gan1etocytes. When
or fan shapes characterize dividing fonns.

aliquoting the medications, note that a

Knowledge regarding their significance,

500-mg tablet of chloroquine contains 300
treatment, or control in birds is limited. Only
mg of active base, and a 26--mg primaquine

B shortti, which rarely occurs in falconitablet contains 15 mg of active base.

formes, has been reported to be pathogenic.

In raptors, control of the disease has

Repo1ted treatment in infected falcons was
been achieved by oral administration of

IM administration of2 or 3 doses of i.midomefloquine (30 mg/kg) repeated 12, 24, and ca.,.·b dipropionate (5-13 mg/kg) 1 wk apa.,.t.

48 hr after the initial dose. Alternatively, a

Hepalozoon is a protozoan parasite
combination of chloroquine (25 mg/kg) and
infrequently identified in birds. Prevalence
primaquine (1.3 mg/kg) can be given orally
in wild birds is 2o/<r-5%. It produces relatively and is followed by the administration of
large, nonpigmented, elongated ga.,.netochloroquine (15 mg/kg) 12, 24, and 48 hr cytes with rounded ends that can be found
later. In endemic areas, mefloquine once a
in WBCs. Gan1etocytes a.,.·e usually not
week (30 mg/kg) has been used successfully
located within an indentation of the
for chemoprophylaxis in large falcons.

nucleus, whereas lsospora is oval and

In a DNA vaccine trial in captive African
pa.,.tially encircled by the nucleus. The life
black-footed penguins, parasitemia and
cycle in birds is unce1tain, but argasid ticks
clinical disease were successfully reduced.

and fleas have been identified as probable
vectors for Hepalozoon infecting swallows.

lxodes ticks, mites, and other artluopods

OTHER BLOODBORNE
may also be involved. Hepatozoon spp a.,.·e ORGANISMS
not known to be pathogenic.

Zoites of other sporozoa ( eg, Toxoplasrna,

Trypanosomes have been described in

Sarcocyslis) and organisms nonnally in the
several avian species but rarely if ever cause digestive tract ( eg, trichomonads, coccidia, clinical disease. They are more commonly
histomonads) may be transiently found in
identified in organ smears, especially bone
blood. The latter often also produces liver
marrow, than in peripheral blood, and can
lesions. (See also TRICHOMONOSIS, p 2804, and be cultured. Invertebrate hosts are thought
lllSTOMONIASIS, p 2835.)

CHICKEN ANEMIA VIRUS INFECTION

(Chicken infectious anemia, Blue wing disease,

Anemia dermatitis syndrome, Hemorrhagic aplastic anemia syndrome) Etiology, Epidemiology, and Patho
capsid protein, but VP2 may be needed as a
genesis: Chicken anemia virus (CA V), a 25 scaJfold protein to allow proper folding of nm, nonenveloped, icosalledral virus with a

VPl. VP2 has also a dual-specificity protein
single-stranded, circular DNA genome, is
phosphatase (DSP) activity, and mutations
the only member of the Gyrovirus genus of
affecting the DSP activity resulted in
the Circoviridae fa.J.11ily. The genome codes
attenuation of virus replication in vivo. VP3,
for three viral proteins (VP). VPl is the
or apoptin, is a nonstructmal protein that

2786

CHICKEN ANEMIA VIRUS INFECTION
induces apoptosis in infected cells. CAV
against other pathogens. In addition to
infects only chickens, although antibodies

T-cell defects, macrophage functions such
have been detected in Japanese quail. The
as Fe-receptor expression, phagocytosis,
virus is present worldwide based on
and antin1icrobial activity may be impaired.

serology and virus isolation. The disease,

Subclinical, horizontally acquired infection

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chicken infectious anemia, has been
with CAV in broiler progeny of seropositive
described in most countries where chickens parent flocks may be associated with are raised commercially.

impaired economic perfom1ance.

Horizontal transmission of CAV is by the
fecal-oral route, perhaps by the respiratory

Clinical Findings: Signs of illness or
route, and through infected feather follicle
adverse effects on egg production do not
epithelium. Vertical transmission occurs
occur when seronegative adult chickens
when seronegative hens become infected
become infected. However, vertical
and continues until neutralizing antibodies
transmission or infection of maternal
develop. Chicks hatched from these eggs
antibody-negative chicks before l wk of age
are viremic, and CAV can rapidly spread
can cause clinical disease 12-17 days after
horizontally from these chicks to susceptihatching or infection. Chicks are anorectic, ble, maternal antibody-negative hatchlethargic, depressed, and pale. PCV is low mates. Roosters shedding CAV in semen are

(in chicks, anemia is defined as a PCV 527),
another source of vertical transmission.

and blood smears often reveal anemia,

Vaccination of seronegative flocks before
leukopenia, or pancytopenia depending
the onset of egg production is recommended on the state of the disease. Blood may be to prevent vertical transmission.

watery and clot slowly. Mmtality rates are

Maternal antibody-negative chicks are
variable but may be high with secondary
susceptible to infection and disease until
complicating infections.

1-2 wk old. In contrast, maternal antibodypositive chicks are protected from disease Lesions: Organs are pale; the thymus
and probably from infection. Age resistance
is generally atrophied, and the bursa of
to clinical disease, but not infection, begins

Fabricius may be small. Bone marrow is
at -1 wk of age. The age resistance can be
pale or yellow. HemoIThages may be present
overcome by coinfection with viruses
in or under the skin, muscle, and other
causing inununosuppression such as bursal
organs. Histologically, lymphoid cell populadisease virus (seep 2837), Marek's disease tions are depleted in pri.rnaiy and secondary
virus (seep 2849), and reticuloendotheliosis lymphoid organs. Granulocytic and
virus (seep 2854).

e1ythrocytic compartments in the bone

Many SPF flocks develop antibodies
maITow are atrophic or hypoplastic.

to CAV during or after onsft of sexual
development. Spread of infection by

Diagnosis: A tentative diagnosis is based

CAY-contaminated embryo- or cell-cultureon history, signs, and gross and histopathoderived vaccines is possible.

logic lesions. Confirmation requires

When day-old susceptible chicks are
detection of virus or viral DNA in the
inoculated IM with CAV, viremia·occurs
thymus or bone marrow. PCR and
within 24 hr. Virus can be recovered from
quantitative PCR techniques are commonly
most organs and rectal contents as long as
used to demonstrate the presence of CAV.

35 days after inoculation. The principal sites Viral isolation can be used but is slow and of CAV replication are hemocytoblasts in
expensive. To isolate CAV, chloroformthe bone marrow, precursor T cells in the treated extracts of tissues are inoculated in
cortex of the thymus, and dividing CD4 and

MDCC-MSBl or MDCC-147 cultures (both

CDS cells in the spleen. Replication in the
are lymphoblastoid cell lines derived from
hemocytoblasts leads to anemia, while

Marek's disease tumors) or into susceptible,
replication in the T cells causes inununoinununocompromisecl and maternal suppression. Neutralizing antibodies are
antibody-negative day-old chicks.

detectable 21 days after infection, and

Commercial ELISA kits ai·e available to
clinical, hematologic, and pathologic
detect serun1 antibodies to CAV and can
parameters return to nom1al -35 days after
be used to identify breeder flocks that are
infection. CAV infection has adverse effects
seronegative before egg production and
on proliferative responses of spleen
to monitor the efficacy of vaccination.

lymphocytes and on the production of
interleukin-2 and interferons by spleno

Treatment and Prevention: There is
cytes. Wection can cause a marked
no specific treatment. Secondaiy bacterial
decrease in generation of antigen-specific
infections may be treated with antibiotics.

cytotoxic T cells and T-helper cells directed

Live vaccines are available for vaccination

DISSECTING ANEURYSM IN TURKEYS

2787
of antibody-negative breeder flocks before
homogenates of tissues from affected
the start of egg production. Administration
chickens to the drinking water have been
is by injection or by addition to the drinking
used to ensure infection and seroconverwater depending on the type of vaccine sion of parent flocks before they begin to lay
available in individual countries. A vaccine

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eggs, thereby diminishing the risk of egg
has been approved in the USA for use in
transmission. However, these procedures
broilers as young as 7 days old; administraare extremely risky and not acceptable.

tion is by addition to the d1inking water. In

Because of the synergism between CAV and
some areas, transfer of litter to noncontan1iother immunosuppressive viruses, control nated premises and the addition of crude
of the latter is also in1portant.

DISSECTING ANEURYSM IN TURKEYS

(Aortic rupture, Internal hemorrhage)

Dissecting aneurysm is a fatal disease

Clinical Findings: Affected turkeys that
of turkeys. It is characterized by sudden
had shown no premonitory signs are found
death of rapidly growing birds with massive
dead with marked pallor of the head and
internal hemorrhage. The hemorrhage
neck. Occasionally, a caretaker observes an
results from rupture of aneurysms formed
apparently healthy turkey die within a few
in various parts of the vascular system. The
minutes. The incidence is usually <1% but
frequency with which the posterior aorta is
may be as high as 1 ()OA,. In the past, when
affected has given rise to the term "aortic
male turkeys were in1planted with stilrupture." The disease has been reported in bestrol, the incidence was as high as 2()0A,.

North America, Europe, and Israel. Most
breeds of turkeys are susceptible, and the

Lesions: The carcass is markedly anemic,
largest and most rapidly growing males,
with large quantities of clotted blood in the

8--24 wk old, are affected most often;
pe1itoneal cavity and over the kidneys or in
females are also affected but at a lower
the pericardia! sac. The rupture in the ventral
incidence.

wall of the posterior aorta at about the
position of the testes, or in the cardiac atrium,

Etiology: The cause is unknown. Likely,
can be located readily by carefully washing
several factors contribute to the developaway the blood clot. The aortic lwnen may ment of fatal cases. For the disease to occur, contain an organized, adherent thrombus at turkeys must be fed and managed in such a
the site of rupture. Ruptures in smaller blood
way that they grow rapidly, and they must
vessels are more difficult to locate. Almost
have a genetic susceptibility. A prolonged
always, an intimal thickening or a large,
lipemia generally develops during the
fibrous plaque is present in the region of the
period of rapid growth, and the period of
rupture. The tunicas intin1a and media are
greatest mortality typically corresponds to a thrown into deep folds and separated from sharp rise in blood pressure, with dissecting
the twtica adventitia. Marked accwnulation
aneurysms developing at the site of
of lipids in the thickened intin1a and in the
arteriosclerotic plaques. The lipernia may
fibrous plaques can be identified by stains.

result from a high dietary intake of fat or

Fibers of the twtica media may show
from the effects of hormonal factors, such
degenerative changes and infiltration with
as high dietary concentrations of estrogens.

heterophils and macrophages.

Although [3-anlinopropionitrile, the toxic
agent in Lathyrus odoratus, is capable of

Diagnosis: The diagnosis is made by
producing the disease, there is no evidence
finding large clots of blood in the coelomic
that this or other nitriles are responsible for
cavity ( aortic rupture) or within the peridissecting aneurysms in turkeys under cardia! sac ( auricular rupture) of rapidly
natural conditions. The enzyme lysyloxigrowing male turkeys. Dissecting aneurysm dase, isolated from turkey aortas and active
should be differentiated from hypertensive
on tropelaston and collagen cross-linking,
angiopathy (seep 2789), which is also seen
was found to be much lower in males than
in rapidly growing turkeys. In hypertensive
in females; this may be a factor in the
angiopathy, the major lesions include
development of spontaneous aortic
pulmonary edema and supcapsular
aneurysms in male turkeys.

perirenal hemorrhage.

2788

DISSECTING ANEURYSM IN TURKEYS

Treatment, Control, and Preven
or slowing growth rate by reducing the
tion: There is no known treatment.

energy level of the diet. High-fat diets

Coagulants and vitamin Kare useless,
should not be fed during this period. Some
because there is no defect in the clotting
studies have indicated that the incidence of
mechanism. Losses sometimes may be
aortic ruptme can be reduced by adding
reduced during the critical period between
copper at 125-250 ppm to the diet from at

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16 and 23 wk of age by limiting feed intake
least 4 wk of age w1til market.

INCLUSION BODY HEPATITIS/

HYDROPERICARDIUM SYNDROME

(Hepatitis hydropericardium)

Adenoviruses are widespread throughout
transmission has been described in progeny
all avian species. Studies have demonfrom breeder flocks infected with AAV
strated the presence of antibodies in
serotypes 4 and 8. Horizontal transmission
healthy poultry, and viruses have been
has also been demonstrated; young chicks
isolated from normal birds. Despite their
in contact with infected chicks can die of
widespread distribution, most aclenoperacute IBH/HP. Wection with some viruses cause no or only mild disease;
strains of AAVs may result in minimal
however, some are associated with
hepatic disease; however, if birds have been
specific clinical conditions. Avian
infected with immunosuppressive viruses
aclenoviruses (AAVs) in chickens are the

(IBDV, CAV, Marek's disease), the clinical
etiologic agents of two important diseases
disease becomes evident.

known as inclusion body hepatitis (IBH)

and hydropericarclium syndrome (HP).

Clinical Findings, Lesions, and

Although in some cases each disease is

Diagnosis: Sudden mortality usually is
observed separately, the two conditions
seen in chickens <6 wk old and as young
have been frequently observed as a single
as 4 clays of age. Mortality n01mally ranges
entity; therefore, the name hepatitis
from 2%--400/o, especially when birds are
hyclropericarclium has been widely used

<3 wk old. However, in some outbreaks,
to describe the pathologic condition. The
mortality has reached 80%. M01tality rates
syndrome is an acute disease of young
also vary depending on the pathogenicity
chickens associated with anemia,
of the virus and infection with other viral
hemorrhagic disorders, and hyclropericaror bacterial agents. Signs associated with dium. It is a common disease in several
diseases caused by otl1er pathogens ( eg,
countries, where broilers are severely
bacteria, fungi, or viruses) conm10nly occm
affected, resulting in high mortality rates.

if birds are immunosuppressed.

Etiology, Transmission, and Pathogenesis: The AAVs classified in the genus Avia.denovirus (formerly group I) are the
etiologic agents of this condition. Although
there are 12 different serotypes of AA V, the
most conunon viruses isolated in cases of

IBH/HP belong to serotypes 4 and 8. These

AAVs are capable of producing the disease
without the inununosuppressive effects of
associated viruses such as infectious bursal
disease (IBDV, seep 2837) or other inununosuppressive agents. However, the association with inunw10suppressive viruses such as

IBDV and chicken anemia virus (CAV, see
p 2785) will result in a more severe disease.

Horizontal and vertical transmission

Hepatitis hydropericardium (right), normal
play an important role in IBH/HP. Vertical
liver on left. Courtesy of Dr. Pedro Villegas.

PERI RENAL HEMORRHAGE SYNDROME OF TURKEYS

2789

Flocks of3- to 5-wk-old broilers with HP

Vaccines against IBH/HP are not
may not show specific clinical signs, but
commercially available in the USA;
abrnpt onset of mortality, lethargy, huddling
however, in other countries both live and
with ruffled feathers, and yellow, mucoid
inactivated vaccines are used to control
droppings may be seen. The duration of the
the syndrome. The AAV serotypes most
infection usually ranges from 9-14 days with
frequently used to prepare commercial

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morbidity of 10%-300,{, and a daily mortality of vaccines are serotypes 4 and 8. Prin1ary 3"1<>-5%. Gross lesions include as much as 10
breeders with stringent bioseclllity
mL of a straw-colored transudate in the
practices sometimes use autogenous
pericardia! sac, generalized congestion, and
inactivated vaccines to ensure the transfer
an enlarged, pale, friable liver. Histopathoof maternal immunity from breeding flocks logic lesions include myocardial edema in
to their progeny. In Australia, a live vaccine
the heart with degeneration, necrosis, and
given via drinking water was developed for
mild mononuclear cell infiltration. Basophilic breeders between 10-14 wk of age. In other intranuclear inclusion bodies may be present
countries, including Mexico, Pakistan,
in the liver. A tentative diagnosis is based on
and many countries in South America,
typical microscopic findings and confumed
inactivated vaccines are routinely used to
by isolating adenovirnses from the liver.

vaccinate breeders and broilers. When

Serology, restriction enzyme analysis, and
breeders are properly vaccinated,

PCR are used to classify adenovirnses
antibodies generated by the vaccine are
isolated from clinical cases. This infonnatransmitted to the progeny, providing tion is used for epidemiologic studies.

protection against field infections and
clinical disease. Broilers are vaccinated at

Treatment and Prevention: As with

<10 days of age when their parents either
many other viral diseases, there is no
do not have serotype-specific adenovirns
treatment. Antibiotics may help prevent
antibodies or maternal antibody transmissecondary bacterial infections. Sulfonamides sion is erratic because of in1proper are contraindicated if evidence of hematovaccination procedures that result in a logic disease or inununosuppression is seen.

substantial nun1ber of unvaccinated birds.

PERIRENAL HEMORRHAGE SYNDROME

OF TURKEYS

(Hypertensive angiopathy, Sudden death syndrome of turkeys) Perirenal hemorrhage syndrome (PHS) is

Gross lesions include food in crop and
a noninfectious cardiovascular disorder
stoma.ch, enlarged dark red to purple
usually affecting rapidly growing male
spleen, variable retroperitoneal hemorrhage
turkeys 8-15 wk old. It is characterized by
around one or both kidneys, generalized
sudden death, perirenal hemorrhage, and
congestion, and pulmonruy edema
hypertrophic cardiomyopathy. Mortality is
occasionally accomprulied by hemorrhage.

usually 0.5%-2% but can be higher; there is

Body condition is usually good to excellent.

no morbidity. Healthy, rapidly growing

Cardiac hypertrophy involving the left
flocks are more likely to be affected.

ventricle and intraventricular septlll11 may

The pathogenesis is unknown, but PHS is
also be seen. Microscopic changes are
apparently Ullrelated to pulmonary function
consistent with gross findings and include
or hypertension. Inadequate or inappropriate
pulmonary congestion and edema with
cardiac response to exercise, resulting in
renal perivenous hemorrhage. Intimal
systemic hypotension and vasodilation,
vacuolation and medial hyperplasia of
ventricular arrhythmia, and sudden death,
arteries and arterioles have been described
appears most likely. Acute congestive heart
in multiple organs, pruticularly the kidney,
failure secondary to cardiac hype1trophy is
spleen, and lung of turkeys with PHS; howalso a potential cause. Renal hemorrhage ever, sinlilar lesions can be seen to a lesser
may occur due to severe passive congestion;
extent in tissue of nonnal turkeys.

acute blood loss is likely not the primary

Diagnosis is based on history, typical
cause of death because the extent of perirenal gross lesions, and absence of infectious hemorrhage is variable and often mild.

agents. PHS has several characteristics in

2790

PERIRENAL HEMORRHAGE SYNDROME OF TURKEYS
common with aortic rupture (seep 2787)

Increased room temperature and step up/
and sudden death syndrome of broilers (see
step down lighting programs have also
p 2821). Extensive PHS lesions can resemble reduced PHS. Activities that increase aortic rupture, and these two disorders can
cardiovascular stress ( eg, moving birds,
occur simultaneously in the same flock
tilling litter, noise) should be minin1ized,

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There is no specific treatment. Factors
especially between 7 and 15 wk of age.

that decrease growth rate and activity also

Lower ambient temperatures (55°F [l3°C]),
tend to decrease PHS. Reserpine (0.5 ppm
intermittent lighting, and leaving toes
feed) decreases PHS, but aspirin (0.005%) or
unclipped increase mortality from PHS. PHS
increased calcium has no effect. Reserpine
may occur in conunercial flocks of healthy
is not listed in the Feed Additive Compenmale turkeys, regardless of management dium as approved for use in feed for turkeys. practices used to prevent its occurrence.

SPONTANEOUS CARDIOMYOPATHY

OF TURKEYS

(Round heart disease)

Spontaneous cardiomyopathy of young

4 wk of life, with mortality peaking at 2-3
turkeys is characterized by sudden death
wk Many poults die suddenly, but some
due to cardiac arrest and is not related to
may have ruffled feathers, drooping
other ca.rdiomyopathies of poultry.

wings, and a general unthrifty appearance.

The exact etiology of spontaneous

They may show labored, gasping
cardiomyopathy in turkeys is unknown.

breathing before death. After 3 wk of age,

However, studies using furazolidone to
mortality is sporadic. Characteristically,
produce dilated cardiomyopathy in
the affected poult in the first 4 wk of life
turkeys have indicated altered membrane
has a greatly enlarged heart due to
transport resulting in myocardial failure.

dilatation of both ventricles, congested

CK, glycolysis, glycogen, myofibril, Krebs
lungs, and a swollen liver. Ascites,
cycle enzymes, fatty acid oxidation, and
anasarca, pulmonary edema, and
soluble proteins are all reduced. The
hydropericardium may be present. In
calcium-transport ATPase activity of the
older poults, enlarged hearts are due to
sarcoplasmic reticulum is increased.

marked hypertrophy of the ventricles in

This pattern of biochemical changes is
addition to dilatation. Histologically,
consistent with ischemia playing a role in
lesions of abnormal hearts are nonspecific
the pathogenesis of spontaneous cardioand include congestion, damage of the myopathy in turkeys.

myofibrils of the cardiocytes, and focal

Although most deaths occur during the
infiltration by lymphocytes.

brooding period, the ratio of heart weight to

Generally, diagnosis is based on history
body weight of affected birds is increased
and gross findings at necropsy; although an
throughout the growing period. The chronic

ECG can be used, it is of little practical use.

cardiac insufficiency causes reduced

Sodiun1 and polychlorinated biphenyls or
growth rate, resulting in attacks on affected
related compounds may produce similar
birds by their healthy cohorts. In affected
syndromes.

turkeys surviving to market age, body

No treatment is available. Hypoxia
weights are reduced an average of3 lb
during incubation, transportation, or

(1.4 kg). Some outbreaks of the condition
brooding has been associated with
have been associated with hypoxia during
increased incidence, and enhanced
incubation of the eggs or during transportaventilation during these periods appears to tion of poults from the hatchery to the
be critical. Practitioners have occasionally
brood farm. It is possible that stratification
noted association of high levels of dietary
of air in poorly ventilated facilities without

( or drinking water) copper and increased
circulation fans may similarly contribute to
incidence of spontaneous cardiomyopathy.

heart damage, with subsequent expression

Good brooding practices may reduce
of this disease later in life.

mortality, because overheating has also

Most deaths from spontaneous
been postulated to increase the incidence
cardiomyopathy occur during the first
of this disease.

COCCIDIOSIS

2791

CANDIDIASIS

(Thrush, Crop mycosis, Sour crop)

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Candidiasis is a mycotic disease of the
ing tissue invasion histologically and by
digestive tract of various avian species,
culture of the organism. However, culture
including chickens, turkeys, and quail
alone is no't diagnostic of disease, because
caused by Candida albicans. It commonly
the yeast-like fungus is commonly isolated
develops after use of therapeutic levels of
from clinically normal birds. Young chicks
various antibiotics or when using unsanitary and poults are most susceptible.

drinking facilities. Lesions are most

Improving sanitation and minimizing
frequently found in the crop and consist
antibiotic use in poultry help reduce the
of thickened mucosa and whitish, raised
incidence of ca.ndidiasis. Ca.ndidiasis can be
pseudomembranes. The same lesions may
treated or prevented with copper sulfate at
be seen in the mouth and esophagus.

1:2,000 dilution in the drinking water, but its

Occasionally, shallow ulcers and sloughing
effectiveness is controversial. Nysta.tin, an
of necrotic epitheliun1 may be present.

a.ntifungal medication, in the feed (220 mg/

Listlessness and inappetence may be tl1e
kg of diet) or drinking water (62.5--250 mg/L
only signs. A presumptive diagnosis may
with sodiun1 la.uryl sulfate, a surfactant, at
be made on obse1vation of gross lesions.

7.8--25 mg/L) for 5 days may be effective for

Diagnosis can be confrrrned by demonstrat-
tile treatment of affected turkeys.

COCCIDIOSIS

Coccidiosis is ca.used by protozoa. of the
adequate moisture and oxygen), tllis
phylum Apicomplexa, fa.nilly Ein1eriida.e. In
requires 1-2 days. The prepatent period is
poultry, most species belong to the genus

4-7 days. Sporulated oocysts may survive

Eimeria and infect vaiious sites in tile
for long pe1iods, depending on environmenintestine. The infectious process is rapid tal factors. Oocysts ai·e resistant to some

( 4-7 days) and is characterized by parasite
disinfectants commonly used around
replication in host cells witl1 extensive
livestock but are killed by freezing or high
da.n1a.ge to the intestinal mucosa. Poultry
environmental temperatures. (See also
coccidia. are generally host-specific, and the

COCCIDIOSIS, p 203.)

different species parasitize specific pai'ts

Pa.thogenicity is influenced by host
of tile intestine. However, in gaine birds,
genetics, nutritional factors, concurrent
including quail, the coccidia. may parasitize
diseases, age of the host, and species of tile
tl1e entire intestinal tract. Coccidia. ai·e
coccidiun1. Eimeria necatrix and Eimeria distributed worldwide in poultry, gaine birds
tenella are the most pathogenic in chickens, reared in captivity, and wild birds. (See also
because schizogony occurs in tile lainina

CRYPTOSPORIDJOSIS, p 209.)

propria and crypts of Lieberkiihn of tile
small intestine and ceca, respectively, and

Etiology: Coccidia. ai·e almost universally
causes extensive hemon-hage. E kofoidi and
present in poultry-raising operations, but

E legionensis are the most pathogenic in
clinical disease occurs only after ingestion
chuka.rs, and E lettyae is most pathogenic in of relatively large numbers of sporula.ted
bobwhite quail. Several Eimeria species
oocysts by susceptible birds. Both clinically
are patl10genic in pheasants, particularly
infected and recovered birds shed oocysts

E pfwsiani and E colchici. Most species in their droppings, which contaminate feed,
develop in epithelial cells lining the villi.

dust, water, litter, and soil. Oocysts may

Protective immunity usually develops in
be transmitted by mechanical carriers ( eg,
response to moderate ai1cl continuing
equipment, clothing, insects, fann workers,
infection. True age-inu11unity does not occur,
and oilier animals). Fresh oocysts are not
but older birds are usually more resistant
infective until they sporulate; under optimal
tl1a.n young birds because of earlier exposure
conditions (70°-90°F [21 °-32°C] with
to infection.

2792

COCCIDIOSIS

Clinical Findings: Signs of coccidiosis
range from decreased growth rate to a high
percentage of visibly sick birds severe
diarrhea, and high mortality. F�ed and
water consumption are depressed. Weight
loss, development of culls, decreased egg

VetBooks.ir
production, and increased mortality may
accompany outbreaks. Mild infections of
intestinal species, which would otherwise

Gross lesions of Eimeria tenella with frank be classed as subclinical, may cause depighemorrhaging into cecal pouches in a broiler chicken. Courtesy of Dr. Jean Sander.

mentation and potentially lead to secondary infection, particularly Clostridium spp infection. Survivors of severe infections remay be thickened. In severe infections cover in 10-14 days but may never recover
coagulative necrosis and sloughing of the
lost performance.

mucosa occw·s tlrroughout most of the

The lesions are almost entirely in the
small intestine.

intestinal tract and often have a distinctive

E maxima develops in the small
location and appearance that is useful in
intestine, where it causes dilatation and
diagnosis.

thickening of the wall; petechial hemor

Chickens: E tenella infections are found rhage; and a reddish, orange, or pink
only in the ceca and can be recognized by

Viscous mucous exudate and fluid. The
accunmlation of blood in the ceca and by
exte1ior of the midgut often has numerous
bloody droppings. Cecal cores, which are
whitish pinpoint foci, and the area may
accunmlations of clotted blood, tissue
appear engorged. The oocysts and
debns, and oocysts, may be fow1d in birds
gametocytes (particularly macrogarnetoswviving the acute stage.

cytes ), which are present in the lesions are

E necatri.x produces major lesions in the distinctly large.

ante1ior and middle portions of the small

E mitis is recognized as pathogenic in the intestine. Small white spots, usually
lower small intestine. Lesions are indistinct
intermingled with row1ded, bright- or
but may resemble moderate infections of
dull-red spots of various sizes, can be seen

E brunetl'i. E mitis can be distinguished on the serosal surface. This appearance is
from E brunetti by finding small, round sometin1es described as "salt and pepper."

oocysts associated with the lesion.

The white spots are diagnostic for

. E praecox, which infects the upper small

E necatrix if clun1ps of large schizonts can mtestme, does not cause distinct lesions
be demonstrated microscopically. In severe
but may decrease rate of growth. The
cases, the intestinal wall is thickened and
oocysts are larger than those of E acei,
the infected area dilated to 2 -2.5 tim�s the
mtlina and are nun1erous in affected
nonnal diameter. The lumen may be filled
areas. The intestinal contents may be
with blood, mucus, and fluid. Fluid loss may
wate1y. E prnecox is considered to be of
result m marked dehydration. Although the
less economic importance than the other
damage is in the small intestine, the sexual
species.

phase of the life cycle is completed in the

E hagani and E mivati develop in the ceca. Oocysts of E necatiix are found
anterior part of the small intestine. The
only in the ceca. Because of concurrent
lesions of E hagani are indistinct and
infections, oocysts of other species may
difficult to characterize. However,
be found in the area of major lesions

E mivati may cause severe lesions similar
misleading the diagnostician.

to those of E acervulina. In severe

E acervulina is the most common cause
infections, E mivati may cause reddening
of infection. Lesions include numerous
of the duodenum because of denuding of
whitish, oval or transverse patches in the
the villi. Some consider these species to
upper half of the small intestine, which may
be of dubious provenance, but work with
be easily distinguished on gross examinamolecular diagnostics seems to support tion. The clinical course in a flock is usually
their validity.

protracted and results in poor growth an

Turkeys: Only four of the seven species
increase in culls, and slightly increased
of coccidia in turkeys are considered
mmtality.

pathogenic: E adenoides, E dispersa,

E b1·unetti is found in the lower small

E gallopavonis, and E meleagrimit·is.

intestine, rectunl, ceca, and cloaca. In

E innocua, E meleagridis, and E sub
moderate infections, the mucosa is pale and
rotunda are considered nonpathogenic.

disrupted but lacking in discrete foci, and

Oocysts sporulate within 1-2 days after

COCCIDIOSIS

2793
expulsion from the host; the prepatent
of coccidiosis occur in ducklings 2-4 wk
period is 4-6 days.

old; morbidity and mortality may be high.

E adenoeides and E gallopavonis infect the lower ileum, ceca, and rectum. These

Geese: The best known coccidial
species often cause mortality. The
infection of geese is that produced by
developmental stages are found in the

E truncata, in which the kidneys are

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epithelial cells of the villi and crypts. The
enlarged and studded with poorly circmnaffected portion of the intestine may be scribed, yellowish white streaks and spots.

dilated and have a thickened wall. Thick,

The tubules are dilated with masses of
creamy material or caseous casts in the gut
oocysts and urates. Mortality may be high.

or excreta may contain enormous nun1bers

At least five i>ther Eimeria spp have been of oocysts. E meleagrimitis chiefly infects reported to parasitize the intestine of geese,
the upper and mid small intestine. The
but these are of lesser importance.

lan1ina propria or deeper tissues may be
parasitized, which may result in necrotic

Diagnosis: The location in the host,
enteritis (seep 2802). E dispersa infects the appearance of lesions, and the size of
upper small intestine and causes a creamy,
oocysts are used in detennining the species
mucoid enteritis that involves the entire
present. Coccidial infections are readily
intestine, including the ceca Large numbers
confirmed by demonstration of oocysts
of gametocytes and oocysts are associated
in feces or intestinal scrapings; however,
with the lesions.

the number of oocysts present has little

Common signs in infected flocks include
relationship to the extent of clinical disease.

reduced feed consun1ption, rapid weight

Severity of lesions as well as knowledge of
loss, droopiness, ruffled feathers, and
flock appearance, morbidity, daily mortality,
severe diarrhea. Wet droppings with mucus
feed intake, growth rate, and rate of lay are
are common. Clinical infections are seldom
important for diagnosis. Necropsy of
seen in poults >8 wk old. Morbidity and
several fresh specimens is advisable.

mortality may be high.

Classic lesions of E tenella and E necatrix are pathognomonic, but infections of other

Game Birds: The Chinese ringneck
species are more difficult to diagnose.

pheasant, the chukar partridge, and the

Comparison of lesions and other signs with
bobwhite quail, extremely popular as game
diagnostic charts allows a reasonably
birds, are reared in large numbers under
accurate differentiation of the cocci dial
conditions sinillar to those of chickens.

species. Mixed coccidial infections are

Losses in these birds from coccidiosis
conunon.

often exceed 500/o of a flock. In pheasants,

A diagnosis of clinical coccidiosis is
the conunon species are E phasiani,
warranted if oocysts, merozoites, or

E colchici, E duodenalis, E tetartooimia,
schizonts are seen microscopically and if·
and E pacif1,Ca. Chukars are infected by two lesions are severe. Subclinical coccidial
species: E kofoidi and E legionensis.

infections may be unimportant, and poor

Bobwhite quail are infected mainly by
performance may be caused by other flock

E lettyae, E dispersa, and E coloni. Treatdisorders.

ment and control of these coccidia are
sinillar to that in poultry; however,

Control: Practical methods of manageamprolium appears to be of little use.

ment cannot prevent coccidial infection.

Monensin and salinomycin are the approved Poultry that are maintained at all times on drugs for quail, and lasalocid and sulfawire floors to separate birds from droppings din1ethoxine/ormetop1im are the approved
have fewer infections; clinical coccidiosis is
drngs for chukars.

seen only rarely w1der such circw11stances.

Ducks: A large number of specific

Other methods of control are vaccination or
coccidia have been reported in both wild
prevention with anticoccidial drugs.

and domestic ducks, but validity of some of

Vaccination: A species-specific immunity
the descriptions is questionable. Presence
develops after natural infection, the degree
of Eimeria, Wenyonella, and 1'yzzeria spp of which largely depends on the extent of
has been con.finned. T perniciosa is a
infection and the number of reinfections.

known pathogen that balloons the entire

Protective inununity is primaiily a T-cell
small intestine with mucohemorrhagic or
response.

caseous material. Eimeria spp also have

Conunercial vaccines consist of live,
been described as pathogenic. Some species sporulated oocysts of the various cocci dial of coccidia of domestic ducks are considspecies administered at low doses. Modem ered relatively non pathogenic. In wild
anticoccidial vaccines should be given to
ducks, infrequent but dramatic outbreaks
day-old chicks, either at the hatchery or on

2794

COCCIDIOSIS
become apparent and because dmgs
cannot completely stop an outbreak.

Therapeutic treatments are usually given
by water because of the logistical restraints
of feed administration. Antibiotics and

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increased levels of vitamins A and Kare
sometimes used in the ration to improve
rate of recovery and prevent secondary
infections.

Continuous use of anticoccidial drngs
promotes the emergence of drng-resistant
strains of coccidia. Various programs are

Release of merozoite from mature schizont
used in attempts to slow or stop selection of
new methylene blue, 100x. CourtesyofDr.Jea�
resistance. For instance, producers may use

Sander.

one anticoccidial continuously through
succeeding flocks, change to alternative
anticoccidials every 4-6 mo, or change
the farm. Because the vaccine serves only to anticoccidials dming a single growout introduce infection, chickens are reinfected

(ie, a shuttle program). While there is little
by progeny of the vaccine strain on the
cross-resistance to anticoccidials with
farm. Most commercial vaccines contain
different modes of action, there is
live oocysts of cocciclia that are not
widespread resist.ance to most drngs.

attenuated. The self-limiting nature of

Coccidia can be tested in the laboratory
coccidiosis is used as a form of attenuation
to detennine which products are most
for some vaccines, rather than biologic
effective. "Shuttle progran1s," in which one attenuation. Some vaccines sold in Europe
group of chickens is treated sequentially
and South America include attenuated lines
with different drngs ( usually a change
of cocciclia. Research has shown promise
between the starter and grower rations), are
for vaccination in game birds.

conm1on practice and offer some benefit in

Layers and breeders maintained on floor
slowing the emergence of resistance. In the
litter must have protective immunity.

USA, the FDA considers shuttle progran1s

Historically, these birds were given a
as extra-label usage, but producers may use
suboptimal dosage of an anticoccidial drng
such programs on the recommendation of a
during early growth, with the expectation
veterinarian.

that immunity would continue to develop

The effects of anticocciclial drngs may
from repeated exposure to wild types of
be coccidiostatic, in which growth of
coccidia. This method has never been
intracellular coccidia is arrested but
completely successful because of the
development may continue after drng
difficulty in controlling all the factors
withdrawal, or coccidiocidal, in which
affecting reproduction of cocciclia under
coccidia are killed during their developpractical conditions. Although anticoccidial ment. Some anticoccidial drngs may be
drugs have been preferred for protection
coccidiostatic when given short-term but
of these birds, vaccination progran1s are
coccidiocidaJ when given longtenn. Most
gaining popularity. Better administration
anticoccidials currently used in poultry
techniques and choice of coccidia strains in
production are coccidiocidal.

the product are improving the feasibility of

The natm·al development of �mnunity to
vaccination in broilers.

coccidiosis may proceed during the use of
anticoccidials in the feed. However, in the

Anticoccidial Drugs: Many products are
production of broilers during a short
available for prevention or treatment of
growout of37-44 days, this may be of little
coccidiosis in chickens and turkeys ( see
consequence. Natural in1111unity is

TABLES 1 and 2). Detailed instmctions for use important in replacement layer pullets,
are provided by all manufacturers to help
because tl1ey are likely to be exposed to
users with management considerations
cocci dial infections for extended periods
and to ensure compliance with regulatory
after termination of anticoccidial drngs.

approvals.

AnticoccicliaJ programs for layer and

Anticoccidials are given in the feed to
breeder flocks are intended to allow
prevent disease and the economic loss
immunizing infection while guarding
often associated with subacute infection.

against acute outbreaks.

Prophylactic use is preferred, because

Anticoccidials are commonly withdrawn
most of the damage occurs before signs
from broilers 3-7 days before slaughter to

COCCIDIOSIS

2795
meet regulatory requirements and to reduce

The modes of action of anticoccidial
production costs. Because broilers have
drugs are poorly understood. Some that
varying susceptibility to infection at this
are better known are described below.

point, the risk of coccidiosis outbreaks is

Knowledge of mode of action is in1portant in

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increased with longer withdrawal.

understanding toxicity and adverse effects.

Turkeys are given a preventive anticoc

Amprolium is an antagonist of thiamine
cidial for confinement-reared birds up to

(vitanun B1). Rapidly dividing coccidia have

8---10 wk of age. Older birds are considered
a high requirement for thiamine. Amprolium
less susceptible to outbreaks.

has a safety margin of -8: 1 when used at
lffl:1111 DRUGS FOR PREVENTION OF COCCIDIOSIS IN POULTRY

Use Level(% in feed)

Withdrawal

Drug•

Chickens

Turkeys

Time (days)

Amproliun1

0.0125-0.025

0.0125-0.250

0

Amprolium+

0.0125-0.025 +

0
ethopabate

0.0004-0.004

Clopidol or

0.0125-0.025

0
meticlorpindol

Decoquinate

0.003

0

Diclazuril

0.0001

0.0001

0

Dinitolmide

0.004-0.0125

0.0125-0.01875

0

(zoalene)

Halofuginone

0.0003

0.00015-0.0003

4-7
hydrobromide

Lasalocid sodium

0.0075-0.0125

0.0075-0.0125

3

Maduran1icin

0. 0005-0. 0006

5
an1monium

Monensin sodium

0.01--0.0121

0.006---0.01 b

0

Narasin

0.006---0.008

0

Narasin + nicarbazin 0.003-0.005 (of

5
the combination)

Nicarbazin

0.0125

4

Robenidine

0.0033

5
hydrochloride

Salinomycin sodium 0.0044-0.0066

0

Semduramicin

0.0025

0

Sulfadimethoxine +

0.0125 + 0.0075

0.00625 + 0.00375

5
om1etoprin1

"Approved in the USA; compiled from various sow-ces, including, with pennission, the Feed Additive Compendium, The Miller Publishing Co., 2008. Anticocciclials not approved in the USA but available in various other countries include clazuril, a combination of clopidol plus methylbenzoquate, and vruious combinations of ionophores with nicru·bazin.

b Up to 10 wk of age.

2796

COCCIDIOSIS

•t4;i!i• DRUGS FOR TREATMENT OF COCCIDIOSIS IN CHICKENS

Feed or

Use Level, Treatment

Withdrawal

Drug a

Water

Duration

Time (days)

Amprolium

Water

0.012%---0.024%, 3---5 days;

0

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0.006%, 1---2 wk

Chlortetracycline

Feed

0.022% + 0.8% calcium,

0
not more than 3 wk

Oxytetracycline

Feed

0.022% + O. lSo/<r-0.55% calcium,

3
not more than 5 days

Sodium sulfachloro-

Water

0.03%, 3 days

4
pyrazine monohydrate

Sulfadimethoxine

Water

0.05%, 6 days

5

Sulfan1ethazine

Water

0.1%, 2 days; 0.05%, 4 days

10

(sulfadimidine)

Toltrazuril

Water

25 ppm, 2 days

NAb
a Approved in the USA, except for toltrazuril

"Not applicable
the highest recommended level in feed
sulfonanudes and often are used in nuxtures

(125---250 ppm). Because an1prolium has
with these compounds.

poor activity against some Eimeria spp, its Halofuginone hydro bromide is related
spectrum has been extended by using it in
to the antimalarial drug feb1ifuginone and is
mixtures with the folic acid antagonists
effective against asexual stages of most
ethopabate and sulfaquinoxaline. The
species of Eimeria. It has both coccidiprimary use of amprolium today is for ostatic and coccidiocidal effects, but
water treatment during clinical outbreaks.

coccidia may become resistant after

Clopidol and quinolines (eg, decoquinextended exposure.

ate, methylbenzoquate) are coccidiostatic

The ionophores (monensin,
against early development of Eime,ia.

salinomycin, lasalocid, narasin,
spp by inhibiting mitochondrial energy
maduramicin, and semduramicin) form
production. Clopidol and quinolin�s have
complexes with various ions, principally
a broad species spectrum and are somesodium, potassium, and calcium, and times mixed together for synergism. Howtransport these into and through biologic ever, resistance may develop rapidly during
membranes. The ionophores affect both
extended use.

extra- and intracellular stages of the para

Folic acid antagonists include the
site, especially during the early, asexual
sulfonamides, 2,4-dianunopyrinudines,
stages of parasite development. Drug
and ethopabate. These compounds are
tolerance was slow to emerge in chicken
structural antagonists of folic acid or of
coccidia, probably because of the
para-anunobenzoic acid (PABA), wluch is a
biochemically nonspecific way these
precursor of folic acid. (The host does not
fermentation products act on the
synthesize folic acid and has no requirement
parasite. Recent surveys suggest that
for PABA.) Coccidia rapidly synthesize
drug tolerance is now widespread, but
nucleic acids, accounting for activity of
these products remain the most impor

PABA antagonists. Although resistance to
tant class of anticoccidials.

antifolate compounds is widespread, they are

Some ionophores may depress feed
conm1only used for water treatment when
consumption when the dosage is above
clinical signs are already evident. Diaveridine, recommended levels. Primarily, this is the onnetoprim, and pyrimetharnine are active
result of reduced feed consumption, but the
against the protozoan enzyme diliydrofolate
reduced growth may be offset by improved
reductase. They have synergistic activity with
feed conversion.

CORONAVIRAL ENTERITIS OF TURKEYS

2797

Nicarbazin was the first product to

Robenidine, a guanidine compound,
have truly broad-spectrum activity and
allows initial intracellular development of
has been in common use since 1955.

coccidia but prevents formation of mature

Although not completely understood,
schizonts. It is coccidiostatic when given
the mode of action is thought to be via
short term and coccidiocidal long term.

inhibition of succinate-linked nicotina

Drug resistance may develop during use.

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mide adenine dinucleotide reduction and

A 5-day withdrawal period is needed to
the energy-dependent transhydrogenase,
eliminate untoward flavor caused by
and the accumulation of calcium in the
residues in poultry meat.

presence of ATP. Nicarbazin is toxic for

Roxarsone is an organic a.rsenical
layers, causing mottling of egg yolks,
compound. It has significant activity
decreased egg production, and blanching
against E tenella and is used in combinaof brown egg shells. A 4-day withdrawal tion with ionophores to improve control
period is required in broilers. Medicated
of that species. A withdrawal period is
birds are at increased risk of heat stress in
required.

hot weather.

Diclazuril and toltrazuril are highly

Nitrobenzamides (eg, dinitolrnide)

effective against a broad spectrum of
exe1t their greatest coccidiostatic activity
coccidia. Diclazuril is used mostly for
against the asexual stages. Efficacy is
prevention at 1 ppm in the feed, whereas
limited to E tenella and E necatrix unless toltrazuril is used primai·ily for treatment
combined with other products.

in the water.

CORONAVIRAL ENTERITIS OF TURKEYS

(Bluecomb, Mud fever, Transmissible enteritis)

Coronaviral enteritis is an acute, highly
through a flock and from flock to flock on
contagious disease of tw·keys characte1ized
the sanle or neighboring farms. Mechanical
by depression, anorexia, dianhea, and
movement of the virus may occur by people,
decreased weight gain. Mortality may be
equipment, vehicles, and insects. Dai·kiing
high, paiticularly in young poults, but failure
beetle laivae and domestic house flies ai·e
to gain body weight in adult birds may be
potential mechanical vectors. Wild birds,
more important economically. The causative rodents, and dogs also may serve as agent is turkey coronavi.Jus (TCV), but
mechanical vectors. There is no evidence
clinical disease usually is complicated by
that TCV is egg transmitted; however, poults
otl1er ente1ic viral, bacterial, and protozoal
may become infected in the hatchery via
infections.

contaminated personnel and fomites such
as egg boxes from infected fai'llls.

Epidemiology: Coronaviral enteritis
has been identified in turkeys in the USA,

Clinical Findings: Clinical signs occur

Canada, Brazil, Italy, UK, and Australia.

suddenly, usually with high morbidity. Birds

The clisease has been reported in most
exhibit depression, anorexia, decreased
turkey-producing regions of the USA.

water consumption, watery diaii:hea,

Turkey coronavirus affects turkeys of
dehydration, hypothermia, and weight loss.

all ages; however, clinical disease most

Droppings typically are green to brown,
conm10nly is seen in young turkeys during
watery, and frothy, and may contain mucus
the first few weeks of life. Turkeys are
and urates. Affected flocks have increased
believed to be the only natw-al host
mortality, growth depression, ai1d poor feed
for TCV.

conversion. Morbidity generally approaches

TCV is shed in feces of infected birds and

1000/o, but mortality is vai·iable; mo1tality
spread horizontally through ingestion of
may be high depending on the age of tl1e
feces and feces-contaminated materials.

birds, concUITent infection, management

Virus is shed in droppings of turkeys for
practices, and weatl1er conditions.

several weeks after recovery from clinical

In breeder hens, egg production drops
disease. Infection generally spreads rapidly
rapidly. Egg quality also is affected; hens

2798

CORONAVIRAL ENTERITIS OF TURKEYS
produce white, chalky eggs lacking nonnal
must be distinguished from other enteric
pigmentation.

viral, bacterial, and parasitic infections,

Lesions: Gross lesions are seen primarily
including those caused by astrovirus,
in the intestines. The duodenum and
rotavirus, reovirus, Salmonella spp, and

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jejunum generally are pale, thin-walled, and
crytosporidia.

flaccid; ceca are distended with gas and
watery contents. Emaciation, dehydration,

Prevention and Treatment: Prevention
and atrophy of the bursa ofFabricius also
is the preferred method to control TCV. No
may be seen.

commercial vaccine is available. Infected

In the intestines, microscopic lesions
turkeys shed virus in feces for prolonged
consist of a decrease in villous length and
periods after recovery; these turkeys, their
increase in crypt depth; the columnar
feces, and the materials their feces contact
epithelium changes to a cuboidal epitheare potential sources of infection for other liwn, and these cells exhibit a loss of
susceptible turkeys. Feces from infected
microvilli. There is a decrease in the number turkeys can be carried on a variety of of goblet cells, separation of enterocytes
fomites, including clothing, boots,
from the lamina propria, and infiltration of
equipment, feathers, and trucks. Other
the lamina prop1ia with heterophils and
potential vectors, such as wild birds,
lymphocytes.

rodents, dogs, and flies, also may be

In the bursa of Fabricius, the nom1al
involved in transmission. Biosecurity
pseudostrati.fied colwnnar epithelitun is
measures must be instituted to prevent
replaced by a stratified squamous epitheintroduction ofTCV via potentially lium, and intense heterophilic inflammation
contaminated personnel, fomites, anin1al
is seen within and w1demeath the epitheand insect vectors, and infected turkeys.

lium.

TCV may be eliminated from contaminated premises by depopulation followed by thorough cleaning and disinfection of houses

Diagnosis: Diagnosis generally requires
and equipment. After cleaning and disinfeclaboratory assistance, because other enteric tion procedures, premises should remain pathogens of turkeys may cause similar
free of birds for a mininlum of3-4 wk.

clinical signs and lesions. Laboratory

There is no specific treatment for TCV
diagnosis is based on virus isolation,
enteritis. Antibiotic treatment reduces
electron microscopy, serology, or detection
mortality but not growth depression, most
of viral antigens or viral RNA in intestinal
likely by controlling secondary bacterial
tissues, the bursa of Fabricius, or intestinal
infections. No beneficial effect was seen
contents. Preferred clinical samples for
when glucose, electrolytes, or calf milk
diagnostic analyses include serum,
replacer was added to drinking water.

intestinal contents, and fresh tissues

Effective management procedures to

(intestines and bursa of Fabricius); these
reduce mortality include raising brooder
samples should be kept cold (on ice at4°C
house temperatures and avoiding crowded
or frozen) at all times. Coronaviral en!eritis
conditions.

CRYPTOSPORIDIOSIS

Cryptospo1idiosis is caused by protozoa
found in the bursa and in the respiratory

(phylum Apicomplexa) that are members
tract. Cryptosporidiosis is more severe in
of the fan1ily Cryptosporidiidae and are
turkeys than in chickens and is frequently
related, but distinct, to coccidia of the
fatal in quail.

generaEimeria, Isospora, Sarcocystis,

The life cycle of CnJptosporidium
and Toxoplasma. Until recently, it was
involves asexual and sexual phases and
thought that there were 19 species in the
culminates in oocyst production. In the
genus Cryptosporidium, but research has
host, the oocyst forms four sporozoites
shown that most are merely species that
without sporocysts. The life cycle is not
lack host specificity. Cryptosporidia are
self-limiting, because some oocysts are
parasitic in the intestine of ma.nm1als (see
thin-walled and release sporozoites (after
p 209), but in birds they are commonly
trypsin/bile stimulation) that reinfect

DUCK VIRAL ENTERITIS

2799
most common clinical signs include
diarrhea and dehydration. In addition to
diarrhea, the parasites can infect the
respiratory tract and lead to coughing,
gasping, airsacculitis, and sometimes

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death. Lungs become gray and wet. Signs
may last several weeks.

Diagnosis is by microscopic examination of tissue scrapings or histologic examination of tis'sues from the bursa,
cloaca, and trachea. The small (5 µm)

oocysts can be diagnostic but are difficult
to see. Concentration of intestinal

Cryptosporidium on tracheal mucosa of a
turkey, H&E, 40x.

scrapings using saturated sugar solution

Courtesy of Dr. Jean Sander.

and examination by phase-contrast or
interference-contrast microscopy may
improve visualization. Positive identification should be petformed by trained adjacent tissues. The endogenous cycle is
researchers or diagnosticians.

short (4-7 days), the endogenous stages

There are no satisfactory control
are small ( 4-7 µm), and the parasites are
measures except isolation and good
just beneath the epithelial cell memsanitation. None of the known anticoccidial branes.

dmgs is effective against Cryplosporidium

In turkeys and chickens, Cr1.Jplospo
spp. Unlike C1yplosporidium spp of other
ridium have been found in the sinuses,
mammals, the avian species are not
trachea, bronchi, cloaca, and bursa. The
infectious to people.

DUCK VIRAL ENTERITIS

(Duck plague, Anatid herpes, Eendenpest, Entenpest, Peste du canard) Duck viral enteritis (DVE) is an acute,
mammals, or people ai1d does not pose a
highly contagious disease of ducks, geese,
zoonotic risk.

and swans of all ages, characterized by
sudden death, high mortality (particularly

Etiology and Pathogenesis: The
among older ducks), and hemorrhages and
causative agent ofDVE (species Anatid
necrosis in internal organs. It has been
herpesvims 1) is a member of the fainily
reported in domestic and wild waterfowl in

Herpesviridae, subfamily Alphallerpesviri

Europe, Asia, North America, and Africa,
nae, and genus Mardivirus. Field strains of resulting in limited to serious economic
this virus display differences in virulence,
losses on domestic duck fam1s and
but all seem to be immunologically
sporadic, limited to massive die-offs in wild identical. The vims is sensitive to lipid waterfowl. In the USA, considerable losses
solvents and heat (10 min at 56°C [132.8°FJ).

due to DVE have been reported in the

Significant titer reduction is observed at
concentrated duck-producing areas located pH 5, 6, and 10; rapid inactivation occurs in Long Island, New York
at pH3and 11.

Members of the family Anatidae ( ducks,

The virus induces vascular dan1age,
geese, and swans) are the natural hosts for
especially in smaller blood vessels,
the vims. There are differences in susceptivenules, and capillaries. This results in the bility to the vims, with Muscovy ducks being development of generalized hemorrhages the most susceptible. However, naturally
and progressive degenerative changes of
occurring infections have been reported in
pai·enchymatous organs. Recently, it has
a vaiiety of domestic ducks such as Pekin,
been proposed that apoptosis and necrosis

Khaki Can1pbell, Indian mnners, and mixed
of lymphocytes induced by this virus may
breeds. The age at infection ranges from
result in lymphoid depletion and possibly

7 days to maturity. The infection has not
immunosuppression. An irnrnunosuppresbeen reported in other avian species, sive state induced by DVE may also explain

2800

DUCK VIRAL ENTERITIS
the presence of secondary infections
initially develop into elevated, yellowish,
by Pasleurella multocida, Riemerella
crusted plaques and organize into green,
analipestifer, and Escherichia coli, which superficial scabs, which may coalesce into
are frequently seen in natural outbreaks of
large, patchy, diphthe1itic membranes. The

DVE in ducklings.

mucosa! lesions align pai·allel with tl1e
longitudinal folds in the esophagus.

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Epidemiology and Transmission:

Hemorrhagic aimular bands can be seen in

The virus is mainly transmitted by direct
different portions of the intestines, which
contact from infected to susceptible ducks
correspond to necrosis and hemorrhage
or by indirect contact with a contan1inated
of the gut-associated lymphoid tissue. In
environment. Water seems to be a natural
geese, intestinal lymphoid disks ai·e
route of viral transmission. Outbreaks are
analogous to the aimular bands in ducks,
frequent in duck flocks with access to
and "button-like" ulcers may be seen.

bodies of water cohabited with free-living

Diphthe1itic esophagitis may be commonly
waterfowl. Parenteral, intranasal, or oral
seen in swans. Lurni.na of the intestines ai1d
administration of infected tissues can
gizzai·cl are often filled with blood. The liver
establish experimental infection. A carrier
is enlai·ged, pale copper in color, and may
condition is suspected in wild birds.

have pinpoint surface hemorrhages mixed

Recovered birds become latently infected
with white necrotic foci. The pancreas may
carriers and may shed the virus pe1iodihave petechiation and multifocal necrosis.

cally. DVE virus may undergo latency like

The lymphoid organs are severely
other herpesviruses, and the trigeminal
affected; the spleen may be normal or
ganglion seems to be a latency site for the
smaller in size and darkened clue to
virus. Recovered birds may carry the virus
congestion. The thymic lobes may be
in its latent form, and viral reactivation
petechiated, and thymic atrophy has been
may be the cause of outbreaks in susceptirepo1ted with some strains. The bursa of ble wild and domestic ducks.

Fabricius may be severely congested or
hemorrhagic. In ducklings, tl1e lesions of

Clinical Findings: The incubation period
the lymphoid tissues ai·e more evident than
is 3-7 days. Sudden high and persistent
tl1e lesions in other visceral organs. A lesion
mortality is often the first sign of the
that can be easily detected on necropsy is
disease. Mortality vaiies and can be
a clear, yellow fluid that infiltrates and

5%-lOO"Ai, depending on virulence of the
discolors the subcutaneous tissues from the
infecting viral strain. Adult ducks usually
thoracic inlet to the upper third of the neck.

die in higher propo1tions than young ones,

In mature hens, hemorrhages may be seen
increasing the economic significance of the
in deformed and discolored ovai'ian
disease. Sick birds are unabJe to stand and
follicles, and ruptured yolk and free blood
show indication of weakness and depresmay be found in the abdominal cavity.

sion. Photophobia, inappetence, extreme

Microscopically, eosinophilic intranuclea.r
thirst, droopiness, ataxia, nasal discharge,
inclusions may be seen in the epithelial cells
soiled vents, and watery or bloody diarrhea
of the GI tract and in the thymus, bursa,
may be seen. Adult ducks may die 1n good
spleen, esophagus, cloaca, liver, coajunctiva,
flesh. In contrast, ducklings frequently show and Harderian gland. Occasional intracytodehydration and weight loss, as well as blue plasrnic inclusions are also scattered in the
beaks and blood-stained vents. Dead males
epitl1elial cells of the coajunctiva, esophamay have prolapse of the penis. In laying gus, bursa ofFab1icius, and cloaca.

flocks, egg production may drop sharply.

Lesions: The lesions are indicative of
disseminated intra.vascular coagulopathy
and necrosis of the mucosa and submucosa
of the GI tract and lymphoid tissues.

Damage of blood vessels iliroughout tl1e
body induces hemorrhages in vaifous
tissues or the presence of free blood in
body cavities. Petechial and ecchymotic
hemorrhages on the heait ("paint-brush"

appearance), liver, pancreas, mesentery,
ai1d other organs ai·e chai·acteristic. Specific
mucosa! eruptions, found in the oral cavity,
esophagus, ceca, rectum, and cloaca,

Duck viral enteritis, mottled thymus with
undergo progressive alterations during the
multiple petechiae and necrotic focal areas.

course of the disease. Macular hemorrhages

Courtesy of Dr. Alejandro Banda.

HEXAMITIASIS

2801

Diagnosis: Presumptive diagnosis is
hem01Thagic enteritis, trawna, drake damage,
based on disease history and lesions.

and various toxicoses. Newcastle disease,

Definitive diagnosis may require viral
avian influenza, and fowlpox may cause
isolation or identification of DVE. Different
similar lesions but are rarely reported in
diagnostic protocols based on PCR are
ducks. Established cases should be reported
available, either by conventional or
to the appropriate regulatory agency.

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quantitative real-time PCR. These molecular
techniques provide much more rapid and

Prevention, Treatment, and Control:

efficient diagnosis of this disease than other

There is no treatment. Contact with wild,
methods. The tjssues to collect are liver,
free-flying waterfowl and direct or indirect
spleen, esophagus, and portions of small
contact with contaminated birds or
intestine that show suggestive lesions.

material (free-flowing water) should be

Isolation of the virus from liver, spleen, or
avoided. Control is effected by depopulakidney tissues may be attempted in various tion, removal of birds from the infected
cell cultures (preferably prin1ary Muscovy
environment, sanitation, and disinfection.

duck embryo fibroblasts or Muscovy duck

Prevention is based on mruntenance of
embryo liver cultures), duck embryos, or
susceptible birds in a disease-free
ducklings. Inoculating the cho1ioallantoic
environment or immunization. A chickenmembrane of9- to 14-day-old embryonated embryo-adapted, modified-live virus

Muscovy duck eggs may result in isolation of vaccine has been approved in the USA to the virus, but this method is not as sensitive
immunize domestic ducks in zoological
as IM inoculation of day-old ducklings.

aviaries and by private aviculturists. A

Muscovy ducklings are more susceptible

0.5-mL dose is administered SC or IM to
than White Pekin ducklings. Neutralization
domestic ducklings >2 wk old. Breeding
with specific antiserum in these systems
flocks should be revaccinated annually.

confirms the identity of the virus. F1uores

The vaccine can be used in an outbreak,
cent antibody testing can demonstrate DVE
because it elicits rapid protection after
viral proteins. Serologic tests have little
vaccination. It is not approved for use in
value in the diagnosis of acute infections.

wild ducks. An inactivated vaccine, which

Serum neutralization tests have been used to appears to be as efficacious as the monitor exposure to the virus in wildfowl.

modified-live vaccine, has not been tested

Differential diagnoses include duck viral
on a large scale and is not currently
hepatitis, pasteurellosis, necrotic and
licensed.

HEXAMITIASIS

Hexarnitiasis is an acute, infectious,
environmental conditions outside tl1e bird
catarThal ente1itis of turkeys, pheasants,
and, therefore, may be more in1portant in
quail, chukar· partridges, ar1d peafowl. The
the transmission of tl1e disease. Up to \/3 of
highest mortality occurs in birds 1-9 wk old.

the recove1ing birds become car·1iers and

Natural infection has not been observed in
shed parasites in their droppings.

chickens. Pigeons are susceptible to another
species of Sp'ironucleus (S columbae).

Hexarnitiasis is rare in North America.

Clinical Findings and Lesions:

Signs of hexarnitiasis are nonspecific
and include watery diarrhea that may

Etiology: The causative protozoan
be yellowish later in the disease, dry
parasite in turkeys, S meleagridis (fom1erly unkempt feathers, listlessness, and rapid

H e.xamita meleagridis) is spindle-shaped;
weight loss despite the fact the birds
averages 8 x 3 µm; and has four anterior, two continue to eat. Birds may die in coma or anterolateral, and two posterior flagella. It
convulsions. Bulbous dilatations of the
has not yet been cultured in experimental
small intestine (especially duodenum
media, although it has been grown in the
and upper jejunum) filled with watery
allantoic cavity of developing chicken and
contents are characteristic. The crypts of
turkey embryos. It is transmitted directly by

Lieberkiihn contrun myriad S meleagridis,
ingestion of contaminated feces and water.

which attach to the epithelial cells by their

Encysted hexarnitids are resistant to
posterior flagella.

2802

HEXAMITIASIS

Diagnosis: Diagnosis of hexamitiasis

Prevention and Treatment: Because
depends on finding the flagellates by
many birds remain carriers of Sp'ironiicleus,
microscopic examination of scrapings
breeder turkeys and young poults should
of the duodenal and jejuna! mucosa.

be raised on separate premises if possible,

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Spirnnucleus spp move with a rapid,
preferably with separate attendants. Wire
darting motion (in contrast to the jerky
platforms should be used under feeders and
motion of trichomonads). To avoid
waterers. Pheasants and quail may also be
contamination of instruments with other
carriers and should not be raised in the
cecal protozoa, the duodenum should be
same location as poults. Indirect transmisopened first. Spironucleus spp may be sion can occur if affected fecal material is
demonstrated in poults that have been
transferred to another location by
dead for several hours if the scrapings are
contanlinated equipment or clothing.

placed in a drop of warm (104°F [40°C]),

There is no effective treatment or vaccine
isotonic saline solution on the slide.

for hexamitiasis, although oxytetracycline

Presence of a few Spironucleus in birds

(0.22% in the feed for 2 wk) or chlortetracy

>10 wk old may be unimportant in terms
cline (0.022%--0.044% in the feed for 2 wk)

of the disease but still act as a reservoir
may be of some benefit to control secondary
of infection.

infections.

NECROTIC ENTERITIS

Necrotic enteritis is an acute enterotoxemia fishmeal), wheat, barley, oats, or rye The clinical illness is usually very short, and
predispose birds to the disease. Anything
often the only signs are a severe depression
that promotes excessive bacterial growth
followed quickly by a sudden increase in
and toxin production or slows feed passage
flock mortality. The disease primarily affects rate in the small intestine could promote the broiler chickens (2--5 wk old) and turkeys
occU1Tence of necrotic enteritis. In many

(7--12 wk old) raised on litter but ca.n also
cases, concurrent coccidiosis ( especially
affect conunercial layer pullets raised in

Eimmia maxima, and E acervulina to a cages. Early mortality is often related to
lesser extent) is associated with outbreaks
coccidiosis vaccination programs, with
in conunercial broilers, although recent

Eimeria cycling in these flocks.

investigations with NetB-positive isolates
have reportedly caused disease without

Etiology and Pathogenesis: The
predisposition from Eimm·ia infections.

causative agent is the gram-pqsitive, obligate,
anaerobic bacteria Closl1'idium pmjhngens. Clinical Findings and Lesions: Most It is usually isolated on blood agar, incubated
often the only sign of necrotic enteritis in
anaerobically at 37°C (98.6°F), on which it
a flock is a sudden increase in mortality.

produces a double zone of hemolysis. There

However, birds with depression, ruffled
are two primary C pmfringens types, A and
feathers, and diarrhea may also be seen.

C, associated with necrotic enteritis in

The gross lesions are primarily found in
poultry. Toxins produced by the bacteria
the small intestine Qejumun/ileum), which
cause damage to the small intestine, liver
may be ballooned, friable, and contain a
lesions, and mortality.

foul-smelling, brown fluid. The mucosa

C pe1:fringens is a nearly ubiquitous
is usually covered with a tan to yellow
bacteria readily found in soil, dust, feces,
pseudomembrane often referred to as a
feed, and used poultry litter. It is also a

"Turkish towel" in appearance. This pseunormal inhabitant of the intestines of domembrane may extend throughout the
healthy chickens and turkeys. The
small intestine or be localized. The disease
enterotoxemia that results in clinical
usually persists in a flock for 5--10 days,
disease most often occurs either after a
and mortality is 2%--500,1,.

change in the intestinal microflora or from a
condition that results in damage to the intes

Diagnosis: A presumptive diagnosis is
tinal mucosa ( eg, coccidiosis, mycotoxicobased on gross lesions and a gran1-stained sis, salrnonellosis, ascarid larvae). High
smear of a mucosa! scraping that exhibits
dietary levels of animal byproducts ( eg,
large, gram-positive rods. Histologic

ROTAVIRAL INFECTIONS IN CHICKENS, TURKEYS, AND PHEASANTS

2803

Prevention, Control, and Treatment:

Because C peifringens is nearly
ubiquitous, it is important to prevent
coccidiosis, especially E acervulina and

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E maxima infections, as well as changes
in the intestinal microflora that would
promote its growth. This has traditionally
been accomplished by adding antibiotics
in the feed such as virginiamycin (20 g/ton
feed), bacitracin (50 g/ton feed), and
lincomycin (2 g/ton feed), as well as
ionophore-class anticoccidial treatments.

The move to antibiotic-free feeds has also

Mucosa I surface of small intestine of a
been associated with markedly increased
broiler chicken infected with Clostridium
use of coccidiosis vaccines, resulting in
perfringens (necrotic enteritis). Courtesy of
early circulation of mixed Eimeria

Dr. Billy Hargis.

infections that are associated with the
resurgence in incidence of necrotic
findings consist of coagulative necrosis of
enteritis. Avoiding drastic changes in
one-third to one-half the thiclmess of the
feed and minimizing the level of fishmeal,
intestinal mucosa and masses of short, thick wheat, barley, or rye in the diet can also bacte1ial rods in the fibrinonecrotic debris.

help prevent necrotic enteritis. When

Isolation of large numbers of C per:fringens, higher amounts of wheat, barley, or from intestinal contents that produce the
rye are necessary, use of enzymes for
double zone of hemolysis as described
nonstarch polysaccharides in the feed has
above, can confirm the diagnosis. Double
reduced the level of necrotic enteritis in
zone hemolysis should not be used as the
flocks fed these cereals. Administration
sole criterion for identification of C pe1frin
of selected probiotics or competitive
gens, because some strains do not produce
exclusion cultures has been used
both toxins responsible for the hemolysis
successfully to both prevent and
characteristics. Differential media
treat clinical necrotic enteritis (prespecifically designed for isolation of sumably by preventing proliferation of

C pe1:fringens is available and may be

C perfringens).

useful for diagnosis.

Treatment for necrotic enteritis is most

Necrotic enteritis must be differentiated
commonly administered in the drinking
from lesions produced by Eime1ia brunetti
water, with bacitracin (200-400 mg/gal for
and also from ulcerative enteritis. Uncom5-7 days), penicillin ( 1,500,000 u/gal. for plicated coccidiosis rarely produces lesions

5 days), and lincomycin (64 mg/gal. for
as acute or severe as those seen with

7 days) most often used. In each case, the
necrotic enteritis. Ulcerative enteritis
medicated drinking water should be the
caused by C colinum usually produces focal sole source of water. Moribund birds lesions from the distal portion of the small
should be removed promptly, because
intestine (ileum) to the ceca and is almost
they can serve as a source of toxicosis
always accompanied by hepatic necrosis.

or infection due to cannibalism.

ROTAVIRAL INFECTIONS IN CHICKENS,

TURKEYS, AND PHEASANTS

Rotaviral infections are characterized by
share a common group antigen with
enteritis and diarrhea in young birds, but
mammalian rotaviruses. Group D rotachickens have been infected without viruses have been identified only in avian
showing clinical signs.

species. The relationships of the other two

Avian rotaviruses consist of four distinct
avian serotypes to mammalian serotypes
serotypes (A-D). Group A rotaviruses
have not been established. Transmission

2804

ROTAVIRAL INFECTIONS IN CHICKENS, TURKEYS, AND PHEASANTS
is horizontally by the oral route. Egg
directly or after ultracentrifugation.

transmission has not been reported.

Numerous rota.viral particles -70 nm in

Early signs of diarrhea (wet litter),
diameter, with double-shelled capsids,
depression, and poor or abnormal appecan be seen and are distinguishable from tite can be seen 2-5 days after infection.

reovirus by their more sharply defined

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Dehydration occurs rapidly, and mortality
outer edges. For viral isolation in
can be as high as 30%-50% in pheasants but
chicken-embryo liver cells or chick
is lower in turkeys and chickens. The
kidney cells, fecal material must be
survivors appear healthy but smaller
treated with trypsin. Isolated rota.viruses
than nonnal. Lesions consist of dilated
belong mostly to serotype A and, in
intestines filled with yellowish, frothy,
general, do not cause cytopathic effects
watery contents. Often, the carcass is
on primary isolation. The presence of
dehydrated. Mortality is variable and is
virus can be demonstrated 2-3 days after
usually due to dehydration and emaciation
inoculation by immunofluorescent
or secondary bacterial infections.

staining. Reverse transcriptase PCR is

Early diarrhea and inappetence that
currently used to detect the virus in gut
sometimes end with death are indicative
contents.

but not pathognomonic of rota.viral

No commercial vaccines are available.

infection. Fecal samples or intestinal

Thorough cleaning and disinfection of
contents can be examined by electron
infected houses is advisable to limit
microscopy with negative staining, either
infection. There is no specific treatment.

TRICHOMONOSIS

Ttichomonosis in domestic fowl, pigeons,
appear as small, yellowish areas on the oral
doves, songbirds, and hawks is charactermucosa. They grow rapidly and coalesce to ized, in most cases, by caseous accumulafonn masses that frequently completely tions in the throat and usually by weight
block the esophagus and may prevent the
loss. It has been te1med "canker," "roup,"

bird from closing its mouth. Much fluid may
and, in hawks, "frounce."

a.ccun1ulate in the mouth. There is a watery
ocular discharge and, in more advanced

Etiology: Both Trichomonas gallinae
stages, exudate about the eyes that may
and a newly recognized species, T stablei'i,
result in blindness. Birds lose weight rapidly,
are the causative organisms of tJichomonobecome weak and listless, and sometimes sis. These flagellated protozoa live in the
die within 8---10 days. In chronic infections,
sinuses, mouth, throat, esophagus, liver,
birds appear healthy, although trichomona.ds
and other organs. Ttichomonosis is more
can usually be demonstrated in scrapings
prevalent among domestic pigeons and wild
from the mucous membranes of the throat.

doves than among domestic fowl, although
severe outbreaks have been reported in

Lesions: The bird may be riddled with
chickens and turkeys. Some trichomonad
caseous, necrotic foci. The mouth and esophstrains ca.use high mortality in pigeons and agus contain a mass of necrotic material that
doves. Hawks may become diseased after
may extend into the skull and sometimes
ea.ting infected birds and conunonly show
through the surrounding tissues of the neck
liver lesions, with or without throat
to involve the skin. In the esophagus and
involvement. Pigeons and doves transmit
crop, the lesions may be yellow, rounded,
the infection to their offspring in contamiraised areas, with a central conical caseous nated pigeon milk. Contaminated water
spur, often referred to as "yellow buttons."

is probably the most important source

The crop may be covered by a yellowish,
of infection for chickens, turkeys, and
diphthelitic membrane that may extend to
songbirds, and the parasite has been shown
the proventriculus. The gizzard and intestine
to survive at least 20 min in distilled water.

a.re not involved. Lesions of internal organs
a.re most frequent in the liver; they vary
from a few small, yellow areas of necrosis

Clinical Findings: The disease course
to almost complete replacement of liver
of trichomonosis is rapid. The first lesions
tissue by caseous necrotic deb1is. Adhesions

ULCERATIVE ENTERITIS

2805
and involvement of other internal organs

Control: Because trichomonads in
appear to be contact extensions of the liver
pigeons are so readily transmitted from
lesions.

parent to offspring in the nmmal feeding
process, chronically infected birds should

Diagnosis: Lesions of trichomonosis
be separated from breeding birds. In

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are characteristic but not pathognomonic;
pigeons, recovery from infection with a
those of pox, fungal disease, Salmonella.,
less vimlent trichornonacl str·ain appears to
and other infections can be similar.

provide some protection against subsequent

'Ihchomonosis has sometimes been confused attack by a more virulent strain. Successful with histomoniasis (seep 2835) because of
treatments include carnidazole (10 mg/kg
the similarity in liver lesions. Diagnosis
body wt), metronidazole (60 mg/kg body
should be confirmed by microscopic
wt), and dirnetridazole (50 mg/kg body wt,
examination of a smear of mucus or fluid

PO; or in the drinking water at 0.05% for 5-6
from the throat to demonstrate the
clays). None of these drngs is approved for
presence of trichomonads. Trichomonads
use in birds in the USA, but they could be
can be cultured easily in various artificial
used in non-food-producing birds by
media such as Dian1ond's media, 0.2%
veterinary prescription. Bi.rd feeders and

Loeffler's dried blood serum in Ringer's
waterers should be cleaned regularly and if
solution, or a 2% solution of pigeon serum
an outbreak of trichornonosis is docuin isotonic salt solution. Good growth is mented or suspected, feeders and waterers
obtained at 98.6°F (37°C). Antibiotics may
should be removed for -2 wk and cleaned
be used to reduce bacterial contamination.

with a 10% bleach solution.

ULCERATIVE ENTERITIS

(Quail disease)

Ulcerative enteritis was first diagnosed in
introduced by flies feeding on contan1inated
bobwhite quail (Colinus virginianus). It
fecal material or by recovered carrier birds.

also affects chickens, turkeys, pheasants,

Wected birds shed the bacterium in their
grouse, and other galli.naceous birds. The
droppings. Bobwhite quail are the most
disease has also been reported in pigeons
susceptible to this highly contagious
and psittacine birds. In Japanese quail
disease. Most cases are reported in captive

(Cotuinix coturnixjaponica), only
populations of bobwhite quail, suggesting
experimentally induced cases have been
that management plays a role in t11e
reported in highly inbred populations. An
incidence. C colinum spores can survive in
ulcerative enteritis-like disease is caused by ilie premises for monilis. Clostridium spp Clostridium peifringens in Co turn ix quail.

have been isolated from water samples

Ulcerative enteritis occurs worldwide and
obtained from &inker pipes in which
may be acute or chronic.

biofilm and mineral deposits were present.

After oral infection, tl1e bacte1i urn

Etiology, Epidemiology, and Patho
adheres to the intestinal villi, producing
genesis: Clostridium colinum is the enteritis and ulcers in portions ofilie small
etiologic agent. It is an anaerobic, fastidious
intestine and upper large intestine. Bacilli
to culture, gram-positive, spore-fom1ing,
migrate to ilie liver via portal circulation,
slightly curved rod, -1 x 3-4 µrn wide, witl1
producing necrotic foci tl1at later coalesce
subtem1inal, oval spores. In chickens, the
into extensive hepatic necrosis. Infarcts of
disease is a complex that is linked to stress,
ilie spleen are common. Stained smears of
coccidiosis, infectious bursal disease, and
the lesions reveal the rod-shaped C colinum
other predisposing factors. To induce
microorganism. Aliliough toxigeni.city tests
experimental disease in bobwhite quail,
in mice have been negative, the role of an in

> 106 viable bacterial cells rn ust be
situ-produced toxin in the pathogenesis has
administered PO; chickens inoculated
been suggested but not demonstrated.

at tl1e san1e levels are not affected.

Birds that develop chronic ulcerative

Clinical Findings: In susceptible
enteritis or that have recovered from ilie
bobwhite quail, sudden death occurs
disease remain can-iers. Infection can be
without signs or weight loss and with up

2806

ULCERATIVE ENTERITIS
to 100% mortality in just 2--3 days. Acute
enteritis from coccidiosis (seep 2791) may
lesions include hemorrhagic enteritis of the
be difficult, because both diseases may be
duodenum. In chickens and other game
present simultaneously. Necrotic enteritis
birds, the course of the disease is less severe ( see p 2802) and histomoniasis (seep 2835) VetBooks.ir
and is accompanied by anorexia. Signs are
may also present a diagnostic problem, but
sinillar to those seen in coccidiosis:

the hepatic lesions of ulcerative enteritis
depressed, listless birds with humped
help differentiate it from tl1ese diseases.

backs, ruffled feathers, diarrhea, and

C colinum can be isolated from liver
sometimes bloody or watery white
samples cultured in strict anaerobic
droppings, especially in quail in the
conditions in prereduced blood glucoseprolonged course. Chickens recover within yeast horse plasma medium. A fluorescent

2--3 wk, and mortality rarely exceeds 100/o.

antibody test has been used to accurately

Lesions: In early disease stages, tl1e most
diagnose ulcerative enteritis. PCR assay
common lesions include small, round ulcers has also been reported as an effective surrounded by hemoIThages in the small
diagnostic test.

intestine, ceca, and upper large intestine.

Small ulcers later coalesce to form larger,

Prevention, Treatment, and Control:

sometimes perforating ulcers, producing

Bacitra.cin in the feed at 200 g/ton is used for
local or diffuse peritonitis. The presence
prevention in quail. Streptomycin (0.006%)

of blood in the gut resembles coccidiosis.

and furazolidone (0.02%) in ilie feed are

Characteristic yellow to gray necrotic foci
effective to treat ilie disease. Prevention
are the predominant lesions in the hepatic
must start wiili good management practices
parenchyrna. Splenomegaly with hemor

( eg, a.voiding the introduction of new birds
rhages and necrotic areas may be present.

into existing flocks). High population
density is a predisposing factor. The use of

Diagnosis: Gross postmortem lesions,
cages is recommended in quail breeding.

including intestinal ulcerations and yellow

Sick and dead birds should be removed
to gray necrotizing lesions in the liver, assist
promptly. Total cleanup between flocks,
in diagnosis. C colinum can be seen in grarnpest control in and around the premises, stained smears of the liver and intestinal
and periodic treatment of watering systems
lesions. In bacteremic birds, the microorwith irmocuous chemicals that dissolve ganism can also be found in blood and spleen mineral and or biofilm build-up a.re good smears. In chickens, differentiating ulcerative preventive measures.

AVIAN CAMPYLOBACTER INFECTION

Can1pylobacteriosis is a significant
vibrionic hepatitis" by administering
enterocolitis of people frequently acquired
isolates of C jejuni to chickens.

tlrrough consumption of undercooked

Commercial poultry and free-living birds
poultry meat contan1ina.ted with Campylo
are natural reservoirs of the them1ophilic
bacter jejuni. It is the lea.ding bacterial ca.rnpyloba.cters ( C jejuni, C coli, and
cause of sporadic enteritis in developed

Clari) and other poorly defined species.

countries. It can also be acquired from

It is estimated that more than ha.If of all
handling backyard poultry as well as
commercial broiler and turkey flocks
diarrheic companion anin1als and from
harbor C jejuni, although the prevalence
contan1inated water. The organism
can vary from 0% tol00% depending on
colonizes the intestine of chickens, turkeys,
season (lowest in fall and winter and
and waterfowl but is generally nonpa.thohighest in swnmer). The organism has been genic in birds. Some strains of C jejuni have isolated from numerous birds, including been reported to ca.use enteritis and death

Columbae and domestic and free-living
in newly hatched chicks and poults;

Gallifonnes and Anserifom1es.

however, it has not been possible to satis-

C jejuni has been found in all areas of
fy Koch's postulates and reproduce ilie
commercial poultry production. Isolation of
syndrome previously tenned "avian
the organism is a function of swveillance

AVIAN CAMPYLOBACTER INFECTION

2807
and ability of laboratory personnel to

Diagnosis: Fecal specin1ens should be
culture and identify Campylobacter spp.

collected using swabs, tllen placed in

Cary-Blair transport medium. Alternatively,

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Etiology and Epidemiology: C jejuni
cecal droppings can be collected into sterile
is the predominant species associated with
laboratory san1pling bags and packed on
foodborne infection derived from poultry.

ice. Eruiclu11ent culture of specimens in

C coli and C lari can also be recovered from semisolid motility medium facilitates the intestinal tract of poultry and have also
isolation when small numbers of C jejuni
been implicated in foodborne infection.

are present. Campylobacter can be cultured

Environn1ental contanlination is probably
on many different selective media, but
the most conu11on source of infection for
commonly available formulations contain
poults, chicks, and ducklings. Litter can

Brucella, agar base and bovine blood with
remain infective for long periods, subject to
as many as seven antibiotics that inhibit
at least a l()OA, moisture level and neutral pH.

overgrowtll of Enterobacteriaceae. They

Exposed chicks and poults become
also can be cultured on blood agar by
colonized and can continue to excrete
selective filtration; bacteria in a 1/10 diluted

C jejuni for their lifetimes. Contanlinated fecal sample are allowed to penetrate a filter
water may introduce infection into poultry

(0.45 µm pores) placed on the surface of a
flocks, and nonchlorinated water derived
blood agar plate. After the liquid is absorbed
from a dan1, river, or shallow well should be
into the plate, the filter is removed.

regarded as a possible source. Rats, mice,

Thermophilic Campylobacter spp shoulcl.

wild birds, darkling beetles, and houseflies be cultured at 42°C under humid, microcan infect flocks; equipment and footwear aerophilic conditions (85% nitrogen, l()OA,
contanlinated with feces from an infected
carbon dioxide, and 5% oxygen) for 48 Ju·.

source may also serve as a vehicle of

Some strains require a hydrogen-enriched
transmission. Once C jejuni has been
atmosphere (5%). Campylobacler spp of
introduced into the environment, rapid
significance in poultry are oxidase- and
transmission within the flock occurs, with
catalase-positive, indole-negative, and
subsequent colonization of a high proportion
reduce selenite. The thern1ophilic species
of exposed breeders, commercial-meat, or
may be characte1ized on the basis of
laying-strain poultry. Some strains of
hippurate hydrolysis; nalidixic acid

Campylobacter can be transmitted vertically, sensitivity is no longer reliable because of either on tlle surface of eggs or by transovarthe increasing prevalence of fluoroquinoial transmission. It has been isolated from the lone-resistant C jejuni. The Penner or Lior reproductive tracts of hens and roosters.

serotyping schemes can be used to classify

C jejmii 1ibotyp.i.ng, or pulsed-field gel
analysis can distinguish among various

Clinical Findings and Lesions: Many

C jejuni isolates.

chicks are colonized with Campylobacter
spp early in life with no associated clinical

Control and Prevention: Because
signs or pathology.

C jejuni is not found as a specific pathogen Most chicks display no lesions associated
under commercial conditions, treatment
with Campylobacterinfection. Some
of poultry flocks is not a consideration. If
studies have reported that challenged

C jejuni is considered a problem in companchicks may exhibit distention of the ion bird aviaries or in exotic species,
jejunum, disseminated hemorrhagic
antibiotics such as erythromycin can be
enteritis, and in some cases, focal hepatic
administered in drinking water. Galliforn1es
necrosis. Microscopic lesions of infected
should receive a dosage of 10-30 mg/kg for
chicks include edema of the mucosa of the

4 consecutive days, and Psittaciformes ancl.

ileum and cecum with C jejuni in tlle brnsh exotics should be medicatecl. at 3�0 mg/kg.

border of enterocytes. Mononuclear

Because of the zoonotic risk associated with
infiltration of the sub mucosa and villous

C jejuni and its ability to rapidly develop atrophy occur, with intraluminal accumulaantibiotic resistance, antibiotics should be tion of mucus, erythrocytes, and mononuused with caution in companion birds.

clear and polymorphonuclear cells.

Fluoroquinolones and erythromycins are

However, infected flocks seldom exhibit
tlle classes of antimicrobials used to treat
increased mortality rates or decreased feed
people for campylobacteriosis.

conversion. It is unclear whetller tllese

Preharvest prevention of Campylobacter
findings represent a true clinical syncl.rome
infection in conm1ercial species is based on
in chicks, because challenge studies
strict biosecurity, decontanlination of
frequently result in no lesions.

housing between successive flocks,

2808

AVIAN CAMPYLOBACTER INFECTION
exclusion of rodents and wild birds, and
immersion chillers, and reduction in
insect eradication. Chlorination of drinking
manual handling by installation of
water to 2 ppm and operation of farms on a
advanced automated equipment can
stlict "all-in/all-out" basis occasionally reduce C jejuni contamination on poultry
reduces the prevalence of infection. In the
meat. Chemical disinfectants, such as

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context of commercial production in the
chlorine, peracetic acid with hydrogen

USA where earth-floored housing is used
peroxide, and trisodiw11 phosphate,
and litter is recycled, preharvest control of
glutaraldehyde and succinic acid, and

C jejuni is impractical. Innovative methods organic compounds, such as lactic and
of prevention, such as competitive
acetic acids, may effectively reduce
exclusion, bacteriophage therapy, bacterio

C jejuni on poultry carcasses in the cins, and the use of vaccines, are under
processing plant. Some research indicates
intensive investigation. Withholding feed
that bacteriophages and bacteriocins may
from broilers and turkeys for at least 12 hr
also be useful. However, the regulations
before slaughter and thorough decontaminaregarding chemical or biological sanitizers tion of transport coops and modules reduce
that can be used in processing plants and
fecal contanunation and lower U1e level of
the performance standards for Campylo

C jejuni introduced into processing plants.

ba.cter in the plant are currently in flux.

Gan1ma irradiation at levels of 1-3 kGy

Zoonotic Risk: C jejuni is a major source effectively elin1inates C jejuni from of food borne enteritis in people; contan1ipoultry carcasses and prorlucts. Irradianated, undercooked poultry is responsible tion has been endorsed by a number of
for >50% of cases investigated. The
international health agencies, but
condition was recognized in the mid-1970s,
irradiated foods are not widely available in
and the signiiicance of the organism has
the USA because of consumer concerns.

become apparent with in1proved methods

The risk of foodborne C jejuni infection
of isolation and identification. Nonchlorincan be reduced through cooking of poultry ated grotmd water, unpasteurized milk,
to achieve a core temperature of74°C
young diarrheic pets, and contanunated
for l min. Concurrent hygienic storage,
beef and pork products are also responsible
handling, and preparation are necessary to
for infection of people.

prevent contamination of prepared foods,

Improved washing of carcasses, use
work surfaces, and utensils by raw poultry
of counter-flow scalding, elin1ination of
and other meats.

AVIAN CHLAMYDIOSIS

(Psittacosis, Ornithosis, Parrot fever)

Avian chlamydiosis can be an inapparent
chlan1ydia share an identical genus-specific
subclinical infection or acute, subacute, or
antigen in their lipopolysaccharide but
chronic disease of wild and domestic birds
often differ in the composition of other
characterized by respiratory, digestive, or
cell-wall antigens, thus providing a basis
systemic infection. Infections occw·
for serotypic identification. Eight serotypes
worldwide and have been identified in at
are recognized; of these, six (A-F) infect
least 460 avian species, particularly caged
avian species and are distinct from
birds (primarily psittacines ), colonial
mammalian Chlamydia serotypes. More
nesting birds (eg, egrets, herons), ratites,
recently, strains of C psittaci have been
raptors, and poultry. Among poultry,
classified using genetic differences in the
turkeys, ducks, and pigeons are most often
ompl gene into nine genotypes. Seven of
affected. The disease is a significant cause
these (A, B, C, D, E, F, and E/B) are found in
of economic loss and hun1an exposure in
avian species and usually correspond to the
many parts of the world.

equivalent serotype. Each avian serotype/
genotype tends to be associated with

Etiology and Epidemiology:

certain types of birds (see TABLE 4). The Chlamydia psittaci, fonnerly renamed
same serotype/genotype may cause mild

Chlamydophila psittaci, is an obligate
disease or asymptomatic infection in one
intracellular bacteriwn. All strains of
species but severe or fatal disease in

AVIAN CHLAMYDIOSIS

2809
another species. Serotype A and Dare
those causing in1munosuppression, can
highly virulent for turkeys and can cause
initiate shedding in latently infected birds
mortality of �30%. Serotypes Band E are
and cause recurrence of clinical disease.

most frequently recovered from wild birds.

Carders often shed the organism intennit

Avian serotypes are capable of infecting
tently for extended peliocls. Persistence of

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people and other manunals.

C psillaci in the nasal glands of chronically Transmission is by the fecal-oral route or
infected birds may be an importat1t source
by inhalation. Respirato1y discharge or feces
of organisms.

from infected birds contain elementary

Longtenh inapparent infections lasting
bodies that are resistant to drying and can
for months to years are common and are
remain infective for several months when
considered the normal Ch/.a.mydia-host
protected by organic deb1is ( eg, litter and
relationship. The prevalence of infection
feces). Airborne particles and dust spread
vai·ies considerably between species and by
the organism. After inhalation or ingestion,
geographic location. Infection is endemic in
elementary bodies attach to mucosa!

commercial turkey flocks; no clinical signs
epithelial cells and are internalized by
or mild respiratory signs and low mortality
endocytosis. Elementary bodies within
ai·e the corru11on presentations. Outbreaks
endosomes in the cell cytoplasm inhibit
are rare. Although chickens are relatively
phagolysosome formation and differentiate
resistant to clinical disease, asymptomatic
into metabolically active, noninfectious
infection is frequent. Epidemiologic studies
reticulate bodies that divide and multiply by
report prevalence varying from l()OA, to >900A,
binaiy fission, eventually fo1ming nwnerous
using serology, culture, or PCR detection;
infectious, metabolically inactive elementaty 3o/cr-500A, of surveyed wild avian populations bodies. Newly formed elementary bodies are
may be seropositive.

released from the host cell by lysis. The
incubation pe1iod is typically 3-10 clays but

Clinical Findings and Lesions: Severity
may be up to several months in older birds
of clinical signs and lesions depends on the
or after low exposure. Host and microbial
virulence of tl1e orgai1ism, infectious close,
factors, route at1cl intensity of exposure,
stress factors, and susceptibility of the bird
and treatment detemune clinical course.

species; asymptomatic infections are

Possible sources of C psillaci include
common. Nasal and ocular clischai·ge,
infected birds, asymptomatic caiTiers,
conjW1ctivitis, sinusitis, green to yellowvertical transmission from infected hens, green droppings, fever, inactivity, ruffled
infected mammals, and contat11inated
feathers, weakness, inappetence, and
environments. Stressors ( eg, trai1sp01t,
weight loss can be seen in clinically affected
crowding, breeding, cold or wet weather,
birds. Clinical pathology test results vaiy
dietary changes, or reduced food availabilwith the organs most affected and severity ity) and concwTent infections, especially
of the disease. Hematologic changes most

ASSOCIATIONS BE TWEEN AVIAN GENOTYPES OF CHLAMYDIA

PSITTACI AND TYPES OF BIRDS

A

B
c

D

E

E/B

F

Psittacines

++

+

+

+

Pigeons, doves

+

++

++

+

Wateifowl

+

+

++

+

++

Turkeys

+

+

+

++

+

+

+

Chicken

++

+

++

+

+

Passe1ines

+

++

Ratites

++

Wild birds

++

++

++ ; Genotype most commonly associated with this bird species or group.

+ ; Genotype less commonly associated with this bird species or group.

2810

AVIAN CHLAMYDIOSIS
often present are anemia and Jeukocytosis
radiology or typical gross lesions are
with heterophilia and monocytosis. Plasma
adequate for a tentative diagnosis.

bile acids, AST, LDH, and uric acid may be

The combination of a serologic and an
increased. A radiograph or a laparoscopy
antigen detection test, especially PCR, or

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may reveal an enlarged liver and spleen and
culture, is a practical diagnostic scheme
thickened airsacs. Necropsy findings in
to confiml chlamydiosis. In live birds, the
acute infections include serofibrinous
preferred sample for bacterial culture or
polyserositis (airsacculitis, pericarditis,

PCR is a single conjunctiva!, choanal, or
perihepatitis, peritonitis), pneumonia,
cloaca! swab. Multiple samples collected
hepatomegaly, and splenomegaly. Multiple
throughout 3-5 days are recommended
tan to white to yellow foci and/or petechial
for detection of intermittent shedding by
hemorrhages can be seen in the liver and
asymptomatic birds.

spleen. Similar lesions are seen in other

Antibodies may or may not be detectable
systemic bacterial infections and are not
depending on the test used and on the level
specific for avian chlamydiosis. Multifocal
and stage of infection. Interpretation of
necrosis in the liver and spleen is associated
titers from single serum san1ples is difficult.

with small granular, basophilic intracyto

A 4-fold increase in titers between paired
plasmic bacterial inclusions in multiple cell
acute and convalescent san1ples is
types; occasional heterophils; and increased diagnostic, and high titers in a majority of mononuclear cells (macrophages,
samples from several birds in a population
lymphocytes, plasma cells) in hepatic
are sufficient for a presumptive diagnosis.

sinusoids and splenic sinuses. Necrosis

Serologic methods include direct and
results from direct cell lysis or vascular
modified direct complement fixation,
damage. The latter is also the source of the
elementary body agglutination, antibody
generalized serofib1inous exudate. In

ELISA, and indirect immunofluorescence.

chronic infections, enlargement and

The elementary body agglutination test
discoloration of the spleen or liver may be
detects IgM and is useful to dete1mine
noted. Necrosis and bacte1ial inclusions are
recent infection. The complement fixation
not seen, but the mononuclear cell response metl10ds are more sensitive than agglutinais present in these birds. Lesions are usually tion methods. High antibody titers may
absent in latently infected birds, even
persist after treatment and complicate
though C psillaci is often being shed.

evaluation of subsequent tests.

Antigen detection methods include

Diagnosis: Because of the variety
in1rnunohistochemistry ( eg, inununofluoresof clinical presentations and common cence, inununoperoxidase), ELISA, and
occurrence of latently infected carriers, no

PCR. ELISA kits developed for detection
single diagnostic test can reliably detemline
of Chlamydia trachomatis in people are
infection. Procedures to detect the
available commercially and are relatively
organism or antibodies are used. In general,
inexpensive. Their exact specificity and
tl1e more acute the disease, the greater the
sensitivity for detection of C psillaci is
nwnber of infective organisms .md the
most often unknown; they appear to
easier it is to make a diagnosis. When birds
have good specificity but somewhat low
are acutely ill, clinical findings, including
sensitivity. These kits are most useful when
hematology, clinical chemistries, and
birds are clinically ill. PCR is the most
sensitive and specific test, btit results may
differ between laboratories because of the

Jack of standardized PCR prin1ers and
laboratory method variations. False-positive
results are a.concern witl1 PCR, because
cross-contanlination can occur relatively
easily. The organism can also be identified
in inlpression smears of affected tissues ( eg,
liver, spleen, and Jung). Chlamydiae stain
purple with Giemsa and red witl1 Macchiavello and Gimenez stains.

Immunohistochemistry is usually more
sensitive than the histochemical stains
mentioned above for detecting bacteria in
tissue.

Marked hepatomegaly in an ornate lorikeet

Confimlation requires isolation and

(Trichoglossus ornatus) with chlamydiosis.

identification of C psittaci in chick embryo

Courtesy of Dr. A J. Van Wettere.

or cell cultures (BGM, L929, Vero) at a

AVIAN CHLAMYDIOSIS

2811
qualified laboratory. Cloaca!, choanal,
oxytetracycline residues in eggs of laying
oropharyngeal, conjunctiva!, or fecal swabs
hens is 9 days, and persistance of doxycy

(in a special Chlamydia transport media)

cline residues is 26 days after administrafrom live birds, or tissues (liver and spleen tion at 0.5 g/L for 7 days.

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preferred) from dead birds should be

In pigeons and companion birds, use of
refrigerated and submitted promptly to
chlortetracycline-medicated feeds for 45
the laboratory. Freezing, drying, improper
days was historically a standard recomhandling, and improper transport media can mendation for imported birds (seep 1897).

affect viability. The laboratory should be

Difficulties in palatability of the feed itself
contacted for directions to submit samples.

or the high level of antibiotic necessary for

Concurrent infections with other, more
adequate blood levels have limited its use.

easily diagnosed diseases ( eg, colibacillosis, Doxycycline is the current drug of choice, pasteurellosis, herpesvirus infections,
because it is better absorbed, has less
my co tic diseases) may mask chlan1ydial
affinity for calcium, better tissue distribuinfection. Laboratory and clinical findings tion, and a longer half-life than other
should be correlated. Chlamydiosis must be
tetracyclines. Doxycycline added to feed
distinguished from other respiratory and
or water can also result in adequate blood
systemic diseases of birds.

levels and has less effect on normal
intestinal flora than does chlortetracycline.

Prevention and Treatment: Human and

The dosage and duration of the treatment
avian chlamydiosis is a reportable disease;
varies between species. Protocols derived
state and local governmental regulations
from controlled studies performed in the
should be followed wherever applicable.

particular species treated should be used

No effective vaccine for use in birds is
when available (seep 1897). See also
available. Treatment prevents mortality
information in the Compendium of
and shedding but cannot be relied on to

Measures To Control Chlamydophila
eliminate latent infection; shedding may
psillaci lnfection Among Humans
recur. Tetracyclines ( chlortetracycline,

(Psittacosis) and Pet Birds (Avian
oxytetracycline, doxycycline) are the

Chlamydiosis), 2010, National Association
antibiotics of choice. Drug resistance to
of State Public Health Veterinarians
tetracyclines is rare, but reduced sensitivity

(NASPHV). When specific information
requiring higher dosages is becoming more
is lacking, an empiric starting dosage of
common. Tetracyclines are bacteriostatic

400 mg/L of water, or 25-50 mg/kg/day, PO,
and effective only against actively
has been suggested.

multiplying organisms, making extended

Appropriate biosecurity practices are
treatment times (from 2-S wk, during which
necessary to control the introduction and
minin1un1-inhibitory concentrations in
spread of chlamydiae in an avian populablood must be consistently maintained) tion. Minimal standards include quarantine
necessary. When tetracyclines are
and examination of all new birds,
administered orally, additional sources
prevention of exposure to wild birds, traffic
of dietary calciun1 ( eg, mineral block,
control to minimize cross-contan1ination,
supplement, cuttle bone) should be reduced
isolation and treatment of affected and
to mininlize inte1ference with drug
contact birds, thorough cleaning and
absorption.

disinfection of premises and equipment

Outbreaks of clinical disease in poultry

(preferably with small units managed on
flocks are not common. Treating infected
an all-in/all-out basis), provision of
flocks with chlortetracycline at 400-750
uncontaminated feed, maintenance of
g/ton of feed for a minimum of2 wk has
records on all bird movements, and
effectively decreased potential risk of
continual monitoring for presence of
infection for plant employees. The
chlamydia! infection.

medicated feed must be replaced by

The organism is susceptible to heat (it
nonmedicated feed for 2 days before
may be destroyed in <5 min at 56°C) and
slaughter and processing. Calcium
most disinfectants ( eg, 1: 1,000 quaternary
supplementation must be withheld during
ammonium chloride, 1: 100 bleach solution,
treatment with chlortetracycline, with

700/cialcohol, etc) but is resistant to acid and
calcium concentration in the feed reduced
alkali. It may persist for montlls in organic
to s0.7%. Medicated feed should be
matter such as litter and nest material, but
provided for 45 days if elimination of
tllorough cleaning before disinfection is
the organism is attempted. Use of some
necessary.

tetracycline antibiotics and doxycycline in
poultry is prohibited, and state regulations

Zoonotic Risk: Avian chlan1ydiosis is a
should be followed. Persistence of
zoonotic disease that can affect people after

2812

AVIAN CHLAMYDIOSIS
exposure to aerosolized organisms shed

C psittaci in poultry industry workers is from the digestive or respiratory tracts of
likely underestimated. Precautions should be
infected live or dead birds or by direct
taken when examining live or dead infected
contact with infected birds or tissues.

birds to avoid exposure ( eg, dust mask and

Human disease most often results from
plastic face shield or goggles, gloves,

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exposure to pet psittacines and can occur
detergent disinfectant to wet feathers,
even if there is only brief contact with a
and fan-exhausted examining hood).

single infected bird. Other persons in close

Some individuals, especially pregnant
contact with birds such as pigeon fanciers,
women and those with impaired immtmity,
veterina.J.ians, farmers, wildlife rehabilitaare more susceptible than others. The tors, zoo keepers, and employees in
illness in people is usually respiratory and
slaughtering and processing plants or
varies from flu-like symptoms to systemic
hatcheries are also at risk. Recent studies
disease with pneumonia and possibly
showed that zoonotic transmission of
endocarditis and encephalitis.

AVIAN NEPHRITIS VIRAL INFECTIONS

Avian nephritis viral infections are contavisceral urate deposits (baby chick gious infections of chickens characterized by nephropathy).

renal dan1age and visceral urate deposits,
growth retardation, and limited mortality

Lesions: Nephritis is a common

(0-lOOAi). They are seen mainly in chickens
necropsy finding. Gross and microscopic

<7 days old, but interstitial nephritis can be
lesions are often seen in the kidneys.

seen in chicks as old as 4 wk. These

Swelling, paleness, or yellowish discolorainJ'ections have been reported worldwide.

tion with excessive urate deposition is

Subclinical infections are common and have
frequent. Histologic lesions consist of a
been detected by serologic surveys in some
degeneration of the epithelial cells with

SPF flocks and in turkeys.

infiltration of granulocytes, interstitial
lymphocyte infiltration, and moderate
fibrosis. In the latter stages, lymphoid

Etiology and Transmission: The causal
follicles develop.

viruses are avian nephritis viruses (ANVs,

Some ANVs, formerly known as ELVs,
which are astroviruses), some of which were
induce only intestinal lesions varying from
previously recognized as enterovirus-like
decreased length of the microvillus border
viruses (ELVs). There is some evidence that
to total desquamation of the intestinal
a taxonomically distinct astrovirus, chicken
epithelium.

astrovirus (CAstV), also causes kidney
disease and growth retardation. The

Diagnosis: Nephropathogenic strains of
descriptions below relate to ANV only.

infectious bronchitis virus (seep 2909) and Strains of ANV vary in virulence and in

CAstV isolates also cause interstitial
antigenicity. Transmission occurs by direct
nephritis. Therefore, when nephritis is
or indirect contact. Indirect evidence
diagnosed, it is necessary to isolate the
suggests that egg transmission may occur.

causative agent.

Infection can be transmitted by oral

ANV and related viruses may be isolated
administration of virus to day-old birds. Vilus by inoculation of suspected material is consistently isolated from the kidneys or

(kidney or rectal contents) in the yolk sac
feces during the first 10 days after infection.

of SPF chick embryos and in chick kidney
cells. However, many ANVs are difficult to

Clinical Findings: Clinical signs vary
isolate. The best way to detect ANV is by
from none to mortality resulting from
reverse transcriptase (RT)-PCR or realkidney disease or severe growtl1 retardatin1e, quantitative RT-PCR of kidney or gut tion. Diarrhea and growth retardation are
content samples. These tests are designed
common in broilers. Outbreaks with
to detect multiple strains and allow quick
mortality of 0-lOOA, can occur in chicks
differentiation from other viruses.

newly hatched to as old as 7 days; ca.J.·dinal

Sero logic diagnosis can be made using
necropsy findings are renal damage and
direct or indirect imrnunofluorescence,

AVIAN SPIROCHETOSIS

2813
seroneutralization, or ELISA tests, but

Treatment and Prevention: There is
these may detect only a limited number of
no effective treatment. General hygienic
strains of ANV because of its high antigenic
precautions are the only applicable
diversity.

preventive measures.

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AVIAN SPIROCHETOSIS

(Avian borreliosis)

Avian spirochetosis is an acute, febrile,
contains Borrelia. Ingestion of bile-stained septicemic, bacterial disease that affects
fecal droppings containing the spirochete,
a wide variety of birds.

contamination of feed or water, and
cannibalism during spirochetemia. can

Etiology, Epidemiology, and Trans
result in infection. After the bite of an
mission: The causal organism, Borrelia
infected tick, the incubation period is
anserina, is an actively motile spirochete,

-3-12 da.ys.

-0.2-0.3 µm x 8-20 µm, and consists of 5-8
loosely arranged coils. Cultivation in vitro is

Clinical Findings: Signs a.re highly
difficult. Borrelia will grow on Barbourvruia.ble, depending on the vimlence of Stoenner-Kelly medium but loses virulence
the spirochete, and may be absent. Signs
after 12 passages. It can also be propagated
include listlessness, depression, somnoin embryonating duck or chick embryos or lence, moderate to marked shivering, and
in young ducks or chicks.

increased thirst. Ruffled feathers, anemia,

Spirochetosis is found in temperate or
and pale combs can be noticed as well, and
tropical regions, wherever the biologic
inappetence can lead to reduced weight.

vectors are found. The most common vector Young birds are affected more severely than isArgas persicus, the "cosmopolitan" fowl older ones. During the initial stages of the
tick, but other Argas spp transmit the
disease, there is usually a green or yellow
bacteria in different geographic areas. In
diarrhea. with increased ura.tes. The course
the western USA, a highly efficient vector
of the disease is 1-2 wk. Mild strains ru·e
is A sanchezi.

common. However, in many tick-infestecl

Diverse immunologic and serologic types
geographic areas, morbidity can approach
of B anserina have been demonstrated in

100% and mortality may be 33%-77%. Egg
many areas. Recovery from one type
production in layers or breeders may be
confers solid immunity against the
reduced by 5o/o-10%, with a higher number
homologous types for ;:cl yr, but not against
of small eggs.

heterologous strains. Relapses, repo1ted
for some human Borrelia infections, are

Lesions: The spleen is enlarged, with
unknown in B anserina infection of birds.

petechial or ecchyrnotic hemmTha.ges,

Therefore, any reinfection can be attributed
appearing dark or mottled. However, a
to a heterologous type.

contrasting situation may be seen in

Generally, an infected A rgas tick can

Mongolian pheasants, in which the spleen is
transmit the bacteria at every feeding and
reported to be small and pale. Occasionally,
maintains the infection tluoughout larval,
the liver may be swollen and contain focal
nymphal, and adult stages. The ticks also
areas of necrosis. Kidneys may be enlarged
transmit the infection transovarially, ie,
and pale. A green, catarrhal enteritis is
the F
common.

1 larvae are infective. Ticks remain
infected despite feeding on chicks
hyperimmune to B anserina or on chicks

Diagnosis: Diagnosis depends on
with high blood levels of chemotherapeutic
demonstration of Borrelia in the blood,
agents effective againstBorrelia. Other
either as actively motile during dru·kfield
vectors (lice, mosquitoes, some species of
microscopy, as stained spirochetes in
ticks, inanimate objects) can transmit the

Giemsa.-stained blood smears, or by PCR. In
spirochete mechanically to a susceptible
yow1g birds, the Borrelia may reach vast
host whenever the piercing apparatus
mm1bers per oil-in1mersion field and persist
becomes contaminated with blood that
for several days. Older birds usually have

2814

AVIAN SPIROCHETOSIS
low nw11bers of Bo?'l'elia that are detected bloodstream, the sudden liberation of large
only with difficulty, or not at all, and that
quantities of spirochetal degradation
persist for only 1-2 days. Increased
products can result in higher mortality than
numbers of inunatw-e RBCs are noticed due
with no treatment.

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to the anemia. Silver staining can be used to

Control must be directed against the
demonstrate the bacteria in tissues.

biologic vector. Argas ticks are notable for Agar-gel diffusion and various serologic
their long lifespan, ability to survive for
tests have been described but are of
extended periods without a blood meal,
questionable value because of the diverse
efficiency in transmitting the spirochete,
serotypes that exist in some localities.

and ability to remain secw-ely hidden in

Specific agglutinins clump the spirochetes
cracks and crevices often beyond the
in successively larger clumps during the
effective reach of pesticides. Accordingly,
tenninal stages of the disease. Agglutination
control is difficult. A combination of tick
lysis then begins to disintegrate these clwnps, eradication and inunwuzation is the most and spirochetal degradation products are
effective means of control.

liberated, which may result in pyrexia. Death

Inunwuzation can be highly successful
occurs most often 1-3 days after Borrelia
and, next to eradication of the biologic
disappear from tl1e bloodstream. Spirochetal
vector, is the preferred method of control.

antibodies are readily detected in yolks of

Bacterins prepared from local strains of
eggs laid by infected hens.

Bor'relia have been used witl1 success.

Vaccines may be prepared from formalin- or

Treatment and Control: Several antiphenol-inactivated material from lysates of bacterial agents are effective. The most
blood, tissues, embryos, or eggs infected
widely used are penicillin derivatives, but
with B anserina, and may be lyophilized or
streptomycins, tetracyclines, and tylosin
liquid. Whole-egg propagated bacterins are
are also effective. The antibiotics can be
usually given in one or two IM ir\jections.

completely effective if begun when the

Little if any cross-protection is afforded to
number of spirochetes per oil-in1mersion
different serotypes. Birds nonnally have
field is low or moderate; however, if large
protective immwuty after recovering from
numbers of spirochetes are present in the
natural infection.

COLI BACI LLOSIS

(Colisepticemia, Escherichia coli infection) Colibacillosis occurs as an acute'fat.al
full protection against all of the serogroups
septicemia or subacute pericarditis,
that cause infections. Virulence factors
airsacculitis, salpingitis, and peritonitis.

include possession of large virulence

It is a conunon disease of economic imporplasmids and the abilities to r.esist phagotance in poultry and is seen worldwide.

cytosis and serwn killing, acquire iron
in low iron conditions, and adhere to host

Etiology and Pathogenesis: Escheri
structures. APEC are generally nontoxi
chia coli is a gram-negative, rod-shaped
genic and poorly invasive.

bacteriwn normally found in the intestine of

Large nwnbers of E coli are maintained in
poultry and most other aninlals. Although
the poultry house environment through fecal
most serotypes are nonpathogenic, a limited contanlination. Initial exposure to APEC
nun1ber produce extraintestinal infections.

may occur in the hatchery from infected or

Avian pathogenic E coli (APEC) strains are
contaminated eggs. Although mostE coli
commonly of tl1e 01, 02, and 078 seroisolated from colibacillosis are well equipped groups, but many others have also been
with virulence factors that distinguish them
associated witl1 cellulitis and colibacillosis.

from fecal conunensal strains, systemic

There is considerable diversity of seroinfection often involves predisposing groups among clinical isolates, with a
environmental factors or infectious causes.

high percentage of APEC isolates being

Thus, mycoplasmosis, infectious bronchitis,
untypeable. Therefore, no single E coli

Newcastle disease, hemorrhagic enteritis,
serogroup used as a bacte1in can provide
and turkey bordetellosis, or exposure to

DUCK VIRAL HEPATITIS

2815
poor air quality and other environmental
heart blood, liver, or typical visceral lesions
stresses, may precede colibacillosis.

in a fresh carcass indicates primary or

Systemic infection occurs when large
secondary colibacillosis. Consideration
numbers of APEC gain access to the
should be given to predisposing infections

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bloodstream from the respiratory tract
and environmental factors. Pathogenicity of
or intestine. Bacteremia progresses to
isolates is established using multiplex PCR
septicemia and death, or the infection
panels for plasm.id-mediated virulence
extends to serosal surfaces, pericardium,
genes or when parenteral inoculation of
joints, and other organs.

young chicks or poults results in fatal
septicemia or typical lesions within 3 days.

Clinical Findings and Lesions: Signs

Pathogenicity can also be detected by
are nonspecific and vary with age, organs
inoculation of the allantoic sac of 12-day-old
involved, and concmTent disease. Young
chicken embryos. Resulting gross lesions
birds dying of acute septicemia have few
include cranial and skin hemotThages in
lesions except for an enlarged, hyperemic
addition to encephalomalacia in embryos
liver and spleen with increased fluid in body
inoculated with virulent isolates.

cavities. Birds that survive septicemia
develop subacute fibrinopwulent airsac

Treatment and Control: Treatment
culitis, pericarditis, pe1ihepatitis, and
strategies include attempts to control
lymphocytic depletion of the bursa and
predisposing infections or environmental
thymus (unusually pathogenic salmonellae
factors and early use of antibacte1ials
produce sin1ilar lesions in chicks). Although
irnlicated by susceptibility tests. Most
airsacculitis is a classic lesion of colibacilisolates are resistant to tetracyclines, losis, it is unclear whether it results from
streptomycin, and sulfa drugs, although
primary respiratory exposure or from
therapeutic success can sometimes be
extension of serositis. Sporadic lesions
achieved with tetracycline. In fact, 90% of
include pneumonia, arthritis, osteomyelitis,
clinical isolates ai·e resistant to tetracycline,
peritonitis, and salpingitis.

with 600/o of isolates resistant to five or more
antibiotics. Fluoroquinolone use is now

Diagnosis: Unlike pathogenic E coli
barmed in many cow1t1ies, including the
associated with illnesses in other anin1al

USA. Commercial bacterins administered to
species, avian isolates are generally
breeder hens or chicks have provided some
nonhemolytic on sheep (5%) blood agar.

protection against homologous E coli

Isolation of a pure culture of E coli from
serogroups.

DUCK VIRAL HEPATITIS

Duck viral hepatitis is an acute, highly
be confused with duck hepatitis B virus,
contagious, viral disease of young ducklings
a hepadnavirus infection of older ducks.

characterized by a short incubation petiod,
sudden onset, high mortality, and chai·acter

Etiology: The otiginally desctibed, most
istic liver lesions. The disease is of
widespread, and most virulent DHV Type I
economic importance in all duck-raising
has been renamed duck hepatitis A virus
areas of the world. Three distinct types of
type 1 (DHAV-1) and is now classified in the
duck hepatitis virus (DHV) have been
genus Avihepatovirus in the Picomavitidae
isolated from diseased ducklings. A natural
family. It is readily propagated in chicken
outbreak of DHV Type I has been reported
and duck embryos. Two new geno/serotypes,
in mallard ducklings; experin1ental DHV

DHAV-2 and DHAV-3, have been identified in

Type I infections have been produced in

China, Taiwan, and Korea. They do not
goslings, turkey poults, young pheasants,
produce hemagglutinins. Field experience
quail, and guinea fowl. In Muscovy ducks,
with DHA V -1 indicates that egg transmis

DHV Type 1 has been reported to cause
sion does not occur. The disease can be
pancreatitis and encephalitis. The viruses
transmitted experimentally by parenteral
that cause hepatitis in ducklings should not
or oral adn1inistration of infected tissues.

2816

DUCK VIRAL HEPATITIS

Viruses that differ from classic DHAV-1
embryos. The virus can be identified by
have been recognized as causes of hepatitis
neutralization with specific antisera or by
in ducklings. DHV Type II, now classified as
inoculation into both susceptible and
duck astrovirus type 1 (DAstV-1), is difficult
immune ducklings. DHAV-1 can also be
to propagate under laboratory conditions;
identified by reverse transcriptase PCR.

DHV Type III is also now classified as an

DAstV-1 and DAstV-2 are not neutralized

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astrovirus (DAstV-2) and can be propagated by classic DHAV-1 antiserum.

in duck ( but not chicken) embryos. Distinct
serologic variants of DHAV-1, named DHV

Prevention and Treatment: Prevention

Type Ia and N-DHV, have also been
is by strict isolation, particularly during
described.

the first 5 wk of age. Contact with wild
wateifowl should be avoided. Rats have

Clinical Findings: The incubation period
been reported as a reservoir host of the
for DHAV-1 is 18-48 hr. Affected ducklings
vims; therefore, pest control is indicated.

become lethargic, lose balance, paddle

Immunization of breeder ducks with
spasmodically, and die within minutes,
modified-live virus vaccines, using DHA V -1,
typically with opisthotonos. Although adults DAstV-1, and DAstV-2 , provides parenteral may become infected, clinical signs have
in11Uunity that effectively prevents high
not been seen in ducks> 7 wk old. Mortality
losses in young ducklings. The DHAV-1
may be as high as 95% in ducklings.

vaccine is administered SC in the neck to

Practically all deaths occur within 1 wk
breeder ducks at 16, 20, and 24 wk of age
after onset of signs.

and every 12 wk thereafter throughout

The clinical course of DAstV-1 infection is the laying pe1iod. Three immunizations similar to that ofDHAV-1 and can be seen in
are advisable for passive protection of
ducklings immune to DHAV-1 infection.

ducklings.

DAstV-2 infections are seen in ducklings

An inactivated DHAV-1 vaccine for use in
despite inununity to DHAV-1. The clinical
breeder ducks that have been previously
course ofDAstV-2 infection is less severe,
primed with live DHAV-1 has been
and mortality is rarely >30%.

described. A single dose of the inactivated

Lesions: The lesions caused by all three
vaccine, given IM before the birds come
types of DHV are similar. The liver is
into lay, provides passive in11Uunity for a
enlarged and covered with hemorrhagic foci complete laying cycle to progeny ducklings.

up to 1 cm in diameter. The spleen may be

The chick-embryo origin, modified-live
enlarged and mottled. Kidneys may be

DHAV-1 vaccine also can be used for early
swollen and renal blood vessels congested.

vaccination of ducklings susceptible to

DHAV-1 ( progeny of nonirnrnune breeders).

Diagnosis: A presuniptive diagnosis can

This vaccine is administered SC or by foot
be based on the history and lesions. Sudden
web stab in a single dose to day-old
onset, rapid spread, and short course,
ducklings. Vaccinated ducklings rapidly
together with characteristic liver lesions,
develop an active immunity within 3--4 days.

are highly suggestive of duck-viral hepatitis.

Antibody against DHAV-1, prepared from

DHAV-1 may be isolated in duck embryos,
the eggs of hyperirnrnunized chickens and
day-old ducklings, and duck-embryo liver
administered SC in the neck at the time of
cell cultures, or less easily in chicken
initial loss, is an effective flock treatment.

ENTEROCOCCOSIS

Enterococcosis has been reported in a

Etiology and Epidemiology: Enterovariety of avian species worldwide.

cocci are nonmotile, gram-positive,

Enterococcus spp are normal microflora
catalase-negative coccoid bacteria that
found in the intestinal tract of poultry and
appear singly, in pairs, or in sho1t chains on
other bird species; infections are usually
stained smears. Enterococcus spp isolated
secondary to another disease. Enterococcus from birds with clinical disease include infections can result in either an acute or

E avium, E durans, E faecalis, E Jaecium,
subacute/clu-onic form.

and E hirae. E faecal is affects birds of all

ERYSIPELAS

2817
ages, but infection is especially devastating
dium has also been reported along with
for embryos and young chicks. E cec01um
infar·cts throughout the internal organs.

has been associated with artluitis in broiler

Focal granulomas can be found in many
chickens.

tissues as a result of septic emboli.

Transmission is via the oral and/or

Grani-positive bacte1ial colonies are readily
aerosol routes as well as from skin wounds.

seen in tlu·ombosed vessels and within

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Wection may result in septicemia.

ar·eas of necrosis.

Endocarditis can occur when the infection
progresses to a subacute/chronic stage.

Diagnosis: History, clinical signs, lesions, Brain necrosis and encephalomalacia in
and demonstration of enterococci in blood
yotmg chickens have been reported in
or on impression smears are suggestive of
enterococcosis. Although enterococcosis
enterococcosis. Isolation of Enterococcus
has been reported in poultry species, it
spp from lesions will confirm the diagnosis.

should also be noted that some strains of

Enterococci are easily isolated on blood

Enlerococcus have a beneficial effect on
agar. Differential diagnoses includes
growth and feed efficiency and are used as
bacterial septicemic diseases such as
probiotics.

staphylococcosis, streptococcosis,
colibacillosis, pasteurellosis, and erysipelas.

Clinical Findings: In the acute form of
enterococcosis, clinical signs are related to
septicemia and include depression, lethargy, Treatment and Prevention: Antibioruffled featliers, cliarThea, and a decrease in tics, including penicillin, erythromycin,
novobiocin, oxytetracycline, chlortetra.cyegg production. In the subacute/chronic fonn, depression, lanieness, and head
cline, or tetracycline, have been used to
treat acute and subacute infections.

tremors may be noted. If tmtreated, most

Clinically affected birds respond well ear·ly
affected birds die. Egg transmission or fecal
contamination of hatching eggs can often
in the course of the disease, but treatment
efficacy decreases as the disease prolead to late embryo mortality, and an gresses. Antimicrobial susceptibility testing
increased number of hatchli.ngs are unable
to "pip" tlirough the shell at hatch.

should be pe1formed to ensure that the
most efficacious antibiotic is used.

Lesions: Acute enterococcosis lesions

Prevention 3.lld control require preventinclude splenomegaly, hepatomegaly, ing inununosuppressive diseases arid
enlar·ged kidneys, and congestion of
conditions, because enterococcosis often
subcutaneous tissue. Multi.focal, whitish-tan occurs secondary to another disease. In ar·eas of necrosis may be observed on the
addition, ensuring proper cleaning arid
liver and spleen. Omphalitis or enlar·ged
disinfection of tile facilities can reduce
yolk sacs may be seen in infected chicks
environmental sources.

or poults. In tlie subacute/chronic fonn,
lesions include pe1icarditis, perihepa.titis,

Zoonotic Risk: A high percentage of
airsacculi.tis, artliritis and/or tenosynovitis,
ready-to-eat poultry products are contamiosteomyelitis, myocarditis, arid valvular nated with Enterncoccus spp; however,
endocar·ditis. An enlarged, flaccid heart with food poisoning in people has not been pale to hemonhagic ar·eas in the myocar�
reported.

ERYSIPELAS

Erysipelas is a bacterial disease caused
has also been isolated from the surface
by infection witli Erysipelothri.x rhusi
slime on fish (without causing disease),
opathiae. The disease is most often seen as which may serve as a source of infection for
septicemia, but urticaria.I and endocar·dia.I
other species. From an economic standpoint,
fmms exist. E rhusiopalhiae infects a wide
turkeys are the most important poultry
range ofhoth a.vi.an and manunalian hosts.

species affected, but serious outbreaks have

The disease has been reported in domestic
occurred in chickens, ducks, and geese.

fowl, feral avian species, and captive wild

Among affected manuna.ls, swine are the
birds and marnmals. Wection in reptiles arid
most economically in1portant species, but
arnphibiartS has been reported. The organism E i"husiopathiae infection is also a cause of

2818

ERYSIPELAS
polyarthritis in Jambs. (See also ERYSIPEW

Epidemiology: Erysipelas occurs

THRIX RHUSIOPATHIAE INFECTION, p 625.)

sporadically in poultry of all ages. It is

Erysipelas in poultry is seen worldwide
ubiquitous in nature and found where
and, although considered a sporadic
nitrogenous substances decompose.

disease, endemic areas exist.

Turkeys are susceptible regardless of sex

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or age, although under field conditions it

Etiology: E rhusiopalhiae is a facultative, is more common in older birds. Recent
anaerobic bacteriwn. Two additional genoevidence indicates there may be a mic species have been desc1ibed: E lonsil
genetically related resistance in turkeys.

larum, and most recently E inopinala, but The incidence in males is reported to be
neither is considered pathogenic for poultry.

higher, but this is not supported by experi

Morphologically, E tonsilla1um and
mental data. Erysipelas may affect the

E inopinata cannot be distinguished from
fertility of males and may contribute to

E rhusiopathiae. E rhusiopathiae stains
downgrading and processing losses.

gram-positive but tends to decolorize,

Infection results from entrance of the
paiticularly in older cultures. The organism
organisms through breaks in the skin,
is small, non-acid fast, nonmotile, does not
through the mucous membranes such
fom1 spores, and produces no !mown toxins. as during artificial insemination, by There is no flagellwn, but a capsule has been
ingestion of contaminated foodstuffs
demonstrated. The cellular morphology of

(particularly cannibalism of infected

E rhusiopa.thiae is vaiiable. The presence
carcasses), and possibly by mechanical
of virulence factors such as neuranunidase
transmission via biting insects. The
play a role in bacterial attachment and
poultry red mite (seep 2877) can harbor
invasion of host cells. Cells freshly isolated
the organism and may serve as a
from tissues during acute infection or from
mechanical vector. Fighting and cannismooth colonies are straight or slightly balism increase losses.

curved small rods that may occur in short

The organism is shed in feces from
chains. Cells from older cultures or rough
infected animals and contan1inates the soil,
colonies tend to become filamentous and
in which it may swvive for long periods
may be confused with mycelia. The
depending on temperature and pH. Poultry,
filamentous fom1 occurs more frequently
as well as other animals, may be carriers
after repeated passages on aitificial media.

and shed the organism without showing

E rhusiopathiae has tluee colony types
clinical signs of disease. Carriers can
and grows readily on ordinaiy culture media shed from feces, wine, saliva, and nasal containing the blood or sera of various
secretions. Transmission into poultry
animals. Growth is enhanced by reducing
houses via rodents can occur.

the oxygen content or increasing the carbon

In nonvaccinated flocks, morbidity and
dioxide level to 5%--10%. Optimal incubation
mortality rates may reach 40%--500A,, but
temperature is 35° --37°C, and the optimal
mortality is usually< 15%. In vaccinated
pH range is 7.4-7.8.

flocks, some birds may be depressed for

The organism is not readily destroyed
a short period and recover. Mortality in
by the usual laboratory disinfectants. It
vaccinated and nonvaccinated poultry is
is quite resistant to dessication and can
influenced by the virulence of the organism.

swvive smoking and pickling processes.

No correlation has been shown to exist

It may swvive in litter or soil for various
between the serotype, chemical structure,
lengths of time. Infected carriers may shed
or biochemical pattern and the manifesta the organism, seeding the environment and tion of the septicemic, urticarial, or
making disinfection of premises difficult. It
endocardial fom1s of erysipelas.

is inactivated by a 1:1,000 concentration of
bi.chloride of mercury, 0.5% sodium

Clinical Findings: Erysipelas is primarily
hydroxide solution, 3.5% liquid cresol, 5%
an acute infection that results in sudden
solution of phenol, quatemaiy ai11.tnonium,
death. In an affected flock, a few birds may
chlorine, or 0.5% fom1alin as long as it is not
be depressed but easily ai·oused; within
in organic matter.

24 hr, a few birds will be dead. Just before

Although 26 different serotypes of
death, some birds may be very droopy, with

E rhusiopathiae were described based
an W1steady gait. Chronic clinical disease in
on an agar gel diffusion test, some of these
a flock is not usual but does occur; birds
serotypes have been assigned to E tonsil
may have cutaneous lesions and swollen
larum after its confirmation as a separate
hocks. Turkeys with vegetative endocarditis
species. E rhusiopathiae serotypes 1, 2,
usually do not have clinical signs and may
and 5 have been most frequently isolated
die suddenly. Erysipelas should be
from poultry.

suspected in flocks that have been

ERYSIPELAS

2819
artificially inseminated 4-5 days before an
diagnosis is made, penicillin should be
episode of death without clinical signs.

administered IM at 22 ,000 U/kg body wt,

Rainy, cold weather coinciding with the
simultaneously with a full dose of erysipelas
onset of sexual maturity increases risk of
bacterin. Injectable penicillin is warranted
clinical disease. Clinical signs in chickens
for an acute outbreak but may be an

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include general weakness, depression,
extra-label use. In situations in which it is
diarrhea, and sudden death. Most sick birds
impractical to handle every bird, administradie. In laying hens, egg production may drop tion of penicillin in tl1e drinking water at markedly. Decreased egg production and

395,000 VIL for 4-5 days reduces losses.

coajunctival edema can be seen in organic,

Sulfonamides and oral oxytetracycline are
cage-free flocks.

not effective; broad-spectrum antibiotics,

Lesions: At necropsy, a generalized
eg, erytl1romycin, are effective. Antibiotic in
darkening of the skin or various sized areas
feed or water treats only tl10se in the flock
of diffuse darkening is common. The liver
that are still eating and drinking nom1ally
and spleen are usually enlarged and friable
and may not have dramatic results.

and may be mottled. Other gross lesions

Recovered birds have a high degree of
such as pe1itonitis, pericarditis, petechiaresistance. Vaccination with a bacterin tion of the heart, catarrhal exudate in the
helps protect those birds in the flock not yet

GI tract, and degeneration of fat associated
infected. However, bacterin-derived
with the thigh and heart may be noted.

immwuty is not long-lasting and may require

Vascular damage and fibrin thrombi are
two or more injections at intervals of2 -4
common findings on microscopic
wk. Antibiotic therapy or vaccination does
examination.

not elin1inate the cai,ier state. Antibiotic
resistance to tetracycline has been reported.

Vaccination will control erysipelas. Both

Diagnosis: A presumptive diagnosis can
inactivated and live vaccines are available
be based on an impression smear of the liver for use in turkeys; only vaccines approved or spleen or on a smear of cardiac blood or
for use in tw-keys should be used. The use of
bone marrow that shows gran1-positive,
bacterins in flocks used for meat is useful
slender, pleomorphic rods. Bone marrow is
but labor intensive. For breeders, the
the tissue of choice in partially decomposed
bacterin should be given every 4 wk before
specimens. Isolation and identification of
onset of egg production. The use of live

E rhusiopathiae is necessary for definitive vaccines administered in the drinking water
diagnosis. Identification can be made by
does not require hai1dli.ng each bird and,
fluorescent antibody staining and PCR.

therefore, is less stressful. Live vaccines

PCR can distinguish E 1-husiopathiae from
require two doses at intervals of2-3 wk.

E tonsilla1um. A mouse ear scarification

Commercially available swine erysipelas
model has been described and is paiticuvaccine can be used in layers and is given at larly helpful for mixed cultures. An indirect
up to two times the recommended dose for

ELISA is available, but virtually all poultry
swine via iajection. It does not interfere
are exposed, with antibody levels increasing with egg production. Although the swine with age. Caution must be used in attemptvaccine is safe, no challenge studies have ing reisolation, because the organism
been done.

produces pinpoint colonies that may be

There are no specific husbandry
easily overlooked or masked by fasterrecommendations other than sound growi.ng bacteria. Highly selective media
management practices for the control
are available for reisolation.

of erysipelas in poultry, paiticularly in

Infections with Escherichia coli or
endemic areas. After an outbreak,

Pasteurella multocida, as well as
equipment should be thoroughly disinfected
salrnonellosis and peracute Newcastle
and dead birds removed from the premises.

disease, may be confused with the
septicemic fonn of erysipelas. Urticaria and

Zoonotic Risks: E rhusiopathiae can endocarditis may be caused by other miscelinfect people and causes three different laneous bacterial or fungal pathogens.

syndromes: erysipeloid, a generalized

Noninfectious differential diagnoses
cutaneous fom1, and a septicemic form with
include poisoning, stainpede injwies, or
endocai·ditis. The organism usually enters
predators.

through cuts in the skin, and those at risk
include people who handle infected tissues,

Treatment, Control, and Prevention:

such as veterinarians, butchers, and fish

The antibiotic of choice is a rapid-acting
handlers. There have been no reports of
penicillin such as potassium or sodiun1
people becoming infected through the oral
penicillin. As soon as a preswnptive
route.

2820

FATTY LIVER HEMORRHAGIC SYNDROME

FATTY LIVER HEMORRHAGIC SYNDROME

Fatty liver hemorrhagic syndrome (FLHS)

usually based on a scale of 1 -5, in which

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was first described in the 1950s as

1 = no hemorrhage; 2 = 1-5 hemorrhages;
excessive fat in the liver of prolific laying

3 = 6-15 hemorrhages; 4 = 16-25 hemm�
hens, associated with varying degrees of
rhages; and 5 = >25 hemorrhages, as well as
hemorrhage. The condition is almost
a massive, usually fatal, hemorrhage. There
universally confined to caged birds fed
is some evidence that fatty liver disorder
high-energy diets and is most often seen in
also impairs calcium metabolism in the bird,
white-egg layers in warm, summer months.

and hence skeletal integrity and eggshell

The liver is usually enlarged, putty colored,
quality. Layers with FLHS have increased
and very friable, showing varying degrees
blood levels of estrogen, osteocalcin, and
of hemorrhage. The abdominal cavity often
leptin-like protein. There seems to be
contains large amounts of oily, unsaturated
concomitant upregulation in bone turnover,
fat. Affected birds often have pale combs,
which is a very significant occwTence for a
likely as a consequence of reduced egg
laying hen that already relies on significant
production. The ovary is usually active, at
daily flLLX of calcium in and out of the
least in the early stages of FLHS, and the
skeleton.

metabolic and physical stress associated

Attempts have been made to prevent
with oviposition may be factors that induce
or treat the condition through dietary
the final fatal hemorrhage.

modification. Substituting carbohydrate with

Because FLHS seems to occur only when
supplemental fat, while not increasing the
birds are in a positive energy balance, body
energy content of tl1e diet, seems to be
weight monitoring is a good diagnostic tool,
beneficial. Presumably such modification
as is knowledge of daily feed intake and
means that the liver needs to synthesize Jess
environmental temperature. Through
fat for yolk Replacement of com with other
force-feeding techniques, it has been shown
cereals, such as wheat and barley, is often
that FLHS is caused by a surfeit of energy
beneficial. However, this substitution may
rather than an excess of any particular nutriinvolve reducing the dietary energy level or ents such as fat or carbohydrate. The
necessitate using additional fat to maintain
condition can be induced experimentally in
isoenergetic conditions, two factors known
layers and even male birds by administrato influence FLHS. FLHS has reportedly tion of estrogen. This supports the concept
been reduced tlu·ough the use of various
that FLHS occurs more freqt�ently in
byproduct feeds such as distiller's grains, fish
high-producing birds that presumably are
meal, and alfalfa meal. Altl10ugh such mode
producing more estrogen from very active
of action is tmclear, wlintentional supplemenovaries. Injecting immature pullets with tation of selenium may be involved. There are
testosterone also causes increase<lfeed
reports of layers having greater incidence of
intake and liver fat accumulation, although
fatty liver when fed chelated trace minerals
witl10ut any major incidence of fatty liver.

versus conventional inorganic minerals.

FLHS is easy to recognize at necropsy

However, the use of organic minerals in
because of the liver hemorrhage and the fact
layer diets is increasing, and FLHS is not
that the liver is enlarged and engorged with
usually reported. There are also reports of
fat. This makes tl1e liver friable, and it is
association withMycoplasma infection.

difficult to remove each lobe in one piece.

FLHS is best prevented by not allowing an

The pale yellow color of the liver, while
excessive positive energy balance in older
characteristic, is not always specific to
birds. Body weight can be monitored and,

FLHS. N onnal layers that are fed appreciwhen potential problems are seen, remedial able quantities of yellow com or high levels
action taken to limit energy intake through
of xanthophyll pigments will also have a
the use of lower energy diets and/or change
yellow-colored liver but without associated
in feed management. A wide energy:protein
hemorrhages. A number of specific diet
ratio in the diet will aggravate FLHS. When a
ingredients can induce liver hemorrhage
fann has a history of FLHS, the diet should
but without concomitant accumulation of
contain at least 0.3 ppm selenitun, ideally as
excess fat. Likewise, feeding rancid fat can
organic selenium, up to 100 ru vitamin E/kg
cause liver hemorrhage, again without fat
diet, and appropriate levels of an antioxidant
accumulation. In birds witl1 FLHS, the liver
such as etl10xyquin. These vaiious additives
dry matter is characteristically at Jeast40%
collectively help to limit the occUITence of
fat. The degree ofFLHS can be described as
tissue rancidity, and hence hemorrhage of
a poultry liver hemorrhage score, which is
the excess fat in the liver.

SUDDEN DEATH SYNDROME OF BROILER CHICKENS

2821

SUDDEN DEATH SYNDROME

OF BROILER CHICKENS

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(Flip-over disease, Acute death syndrome, Dead in good condition) A syndrome of sudden death has been
help in diagnosis. Dead birds ai·e well
reported in most areas of the world that
fleshed, have an empty or partially filled
raise broilers intensively. Young, healthy,
crop, at1d feed in the gizzard. The abdomen
fast-growing broiler chickens die suddenly
is distended because the bird is fat and the
with a short, terminal, wing-beating
intestines are filled with ingesta, indicating
convulsion. Many affected broilers just "flip
peracute death. The muscles ai·e mottled
over" and die on their backs; 60%---800/o are
red and white as a result of focal congestion,
males. The condition is uncommon or
and the organs ai·e moderately to severely
unrecognized when low-density feed is used. congested. There may be small hemot'

rhages in the liver and kidney. Although the

Etiology and Epidemiology: The
ventricles of the heart ai·e contracted, there
cause is unknown, but it is thought to be a
is no sign of hype1trophy, and the attia ai·e
metabolic disease related to carbohydrate
dilated and blood filled. The lungs are
metabolism, lactic acidosis, loss of cell
congested and frequently edematous;
membrane integrity, and intracellular
however, pulmonary edema increases with
electrolyte imbalance. Recent studies link
time after death and is not prominent in
this disease to cardiac arrhythmias. The
broilers that are examined within a few
modern broiler, which has been selected for
minutes of death. The gallbladder may be
growth rate and feed conversion efficiency,
small or empty, because feed intake is
has a predisposition to cardiac atThythmias.

nom1al up tmtil the time of death.

One study found the prevalence of
atThythmias to be much higher in broilers

Diagnosis: Sudden death syndrome

(27%) than leghorns (1%), but it is not clear
should be suspected in well grown and
whether this predisposition is dietary or
otherwise healthy-looking broilers found
genetic. Stress is the most likely trigger of
dead on their backs, because that position
cardiac atThythmias in broilers, which
is rare in death from other causes except
predisposes the bird to death from
cai·diac tamponade, asphyxia, and ascites
ventricular fibrillation. The prevalence
syndrome (seep 2871). The syndrome is in a rapidly growing healthy broiler flock
also the likely cause when dead birds tl1at
is typically 0.5%---4%.

are otherwise in good condition ai·e found
lying on tl1eir sides or breasts randomly

Clinical Findings: Broilers show no
tlu·oughout the pen. Diagnosis is supported
premonitory signs. They appeai· healthy
by necropsy findings if there is a lack of
and may be feeding, sparring, walking, or
obvious pathology (ie, a digestive tract
resting, but suddenly extend their necks,
filled with ingesta, contracted ventricles,
gasp or squawk, and die rapidly with a shott
dilated and blood-filled atria, lung
period of wing beating and leg movement,
congestion, and edema). The presence
during which they frequently flip onto their
of characteristic microscopic lesions in
backs. They also may be found dead on their cardiomyocytes and subendocai·dial sides or breasts.

Purkinje cells is helpful in confurning the

Sudden death syndrome may occur as
diagnosis. Affected cells have vacuolated
early as day 3 and may continue w1til 10-12
sarcoplasm, cytoplasmic eosinophilia,
wk in roaster flocks. Mortality usually peaks and nuclear pyknosis.

between days 12 at1d 28, although it may

The condition called sudden death
peak as early as day 9. If growth is rest1icted syndrome in Australia in broiler breeders early, it may peak only after day 28.

coming into production is a clifferent

Mortality of 0.25%-0.5% per day can occur
disease; it is rep01ted to be caused by
for 1-3 days.

potassium deficiency. Simi!ai· mortality
caused by a combination of high environ

Lesions: There an� no specific gross
mental temperature and hypophosphatemia
lesions. Recent studies indicate that
or by acute hypocalcemia has been rep01ted
affected birds have characteristic microin North America.

scopic lesions in cardiomyocytes and

Sudden death in turkeys can be caused
subendocardial Purkir\je cells, and this may
by choke, aortic rupture (seep 2787), focal

2822

SUDDEN DEATH SYNDROME OF BROILER CHICKENS

(obstructive) granulomatous pneumonia,
rnized by slowing the growth rate of
or by hypertrophic cardiomyopathy ( see
broilers, particularly during the first 3 wk
p 2790) with lung congestion and edema,
of life. Growth rate can be moderated by
splenomegaJy, and perirenaJ hemorrhage
controlling nutrient intake. This can be

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(seep 2789).

accomplished by reducing the number of
hours of light per day, reducing the energy

Prevention and Control: The incidence
and protein level in the diet, or limiting the
of sudden death syndrome can be mini-
amount of feed provided.

FOWL CHOLERA

Fowl cholera is a contagious, bacterial
diseased birds that contaJ11inate their
disease that affects domestic mid wild birds
environment. In addition, P multocida
worldwide. It usually occurs as a septicemia
survives long enough to be spread by
of sudden onset with high morbidity and
contantinated crates, feed bags, shoes,
mortality, but chronic and asyn1ptomatic
a11d other equipment. The infection does
infections also occur.

not seem to be egg-tra11srnitted.

Etiology and Transmission: Pasleurella
mullocida, the causal agent, is a small,

Clinical Findings: Clinical findings vary
graJ11-negative, nonmotile rod with a
greatly depending on tl1e comse of disease.

capsule that may exhibit pleomorphism

In acute fowl cholera, finding a large
after repeated subculture. P mullocida is
number of dead birds without previous
considered a single species aJtl1ough it
signs is usually the first indication of
includes three subspecies: mullocida,
disease. Mortality often increases rapidly.

Se'f)lica, and gallicida. Subspecies In more protracted cases, depression,
mullocida is the most common cause
anorexia, mucoid discharge from the
of disease, but Se'f)lica a11d gallicida may mouth, ruffled feathers, diarrhea, and
also cause cholera-like disease.

increased respiratory rate are usually seen.

In freshly isolated cultmes or in tissues,

Pneumonia is particularly common in
the bacteria have a bipolar appearance
turkeys.

when stained with Wright's stain. Although

In chronic fowl cholera, signs and lesions

P mullocida may infect a wide variety of
are generally related to localized infections
animals, strains isolated from nonavian
of the sternal bursae, wattles,joi.nts, tendon
hosts generally do not produce fowl
sheaths, and footpads, which often are
cholera. Strains that cause fowl cholera
swollen because of accumulated fibri.nosuprepresent a nwnber of inlrnunotypes ( or purative exudate. There may be exudative
serotypes), which complicates efforts at
coajunctivitis and pharyngitis. Torticollis
widespread prevention using bacterins.

may result when the meninges, ntiddle ear,

The organism is susceptible to ordinary
or cranial bones are infected.

disinfectants, swilight, drying, and heat.

Lesions: Lesions observed in peracute

Turkeys and wate1fowl are more susceptiand acute forms of the disease are primarily ble than chickens, older chickens are more
vascular disturbances. These include
susceptible tha11 young ones, and some
general passive hyperemia aJ1d congestion
breeds of chickens are more susceptible
throughout the carcass, accompanied by
than others.

enlargement of the liver and spleen.

Chronically infected birds a11d asympto

PetechiaJ and ecchymotic hemorrhages are
matic carriers are considered to be major
common, pmticularly in subepicm·diaJ and
sources of infection. Wild birds may
subserosaJ locations. Increased aJ110tmts
introduce the orgmtism into a poultry flock,
of peritoneal a11d pericardia] fluids m·e
but marnmaJs (including rodents, pigs, dogs, frequently seen. In addition, acute aJ1d cats) may also carry tl1e infection.

oophoritis with hyperentic follicles may

However, the role of tl1ese as a rese,voir has be observed. In subacute cases, multiple, not been thoroughly investigated. Dissentismall, necrotic foci may be dissentinated nation of P mullocida within a flock and
throughout the liver and spleen.

between houses is p1imarily by excretions

In ctu·onic fomis of fowl cholera,
from tl1e mouth, nose, and conjunctiva of
suppurative lesions may be widely

FOWL CHOLERA 2823
suppurative lesions of chronic cholera may
be more difficult. At necropsy, bipolar
microorganisms may be demonstrated by the
use of Wright's or Giemsa stain of impression
smears obtained from the liver i.n the case of

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acute cholera. In addition, inummofluorescent microscopy and in situ hybridization have been used to identify P mullocida in
infected tissues and exudates.

PCR has been used for the detection of

P mullocida in pure and mixed cultures
and clinical samples. This method may
help identify carrier animals within flocks.

However, the specificity and sensitivity of
the PCR must be improved. P multocida
can be subgrouped by capsule serogroup
antigens into five capsular types (A, B, D,

E, and F) and into 16 somatic serotypes.

Somatic serotyping is important to choose
the right bacterins for prevention.

However, conventional serotyping suffers
from problems with reproducibility and
reliability, and tl1e metl10ds are quite
laborious. Recently, a multiplex PCR has
been developed that can differentiate
between different somatic serotypes. This
will be of great value as a diagnostic tool
and enable more efficient vaccine
development in the future.

Serologic testing can be done by rapid
whole blood agglutination, scrum plate
agglutination, agar diffusion tests, and

ELISA. Serology may be used to evaluate

Swollen wattles in a broiler breeder male as
vaccine responses but has very limited
the result of a chronic fowl cholera infection.

value for diagnostic purposes.

Courtesy of Dr. Jean Sander.

Several bacterial infections may be
confused with fowl cholera based solely
on the gross lesions. Escherichia coli,
ilistributed, often involving the respiratory

Salmonella enterica, Ornithobacterium
tract, the conjunctiva, and adjacent tissues
rhinotracheale, gran1-positive cocci, and
of the head. Gaseous arthritis and produc

Erysipelolhri.x 1·husiopalhiae (erysipelas)

tive inflammation of the peritoneal cavity
may all produce lesions indistinguishable
and the oviduct are common in chronic
from those caused by P multocida.

infections. A fibrinonecrotic dennatitis
that includes caudal parts of the dorsum,

Prevention: Good management practices,
abdomen, and breast and involves the cu tis,
including a high level of biosecurity, are
subcutis, and underlying muscle has been
essential to prevention. Rodents, wild birds,
observed in turkeys and broilers. Sequespets, and other anin1als that may be carriers tered necrotic lung lesions in poultry should
of P multocida must be excluded from
always raise suspicion of cholera.

poultry houses. Adjuvant bacterins are
widely used and generally effective;

Diagnosis: Altl1ough the history, signs, and autogenous bacterins are recommended
lesions may aid iliagnosis, P mullocida
when polyvalent bacterins are found to be
should be isolated, characterized, and
ineffective. Thus, it is in1portant to know the
identified for confirmation. Primary isolation
most prevalent serotypes within an area to
can be accomplished using media such as
choose the right bacterins. Attenuated live
blood agar, dextrose starch agar, or tryptivaccines are available for administration in case soy agar. Isolation may be improved by
drinking water to turkeys and by wing-web
the addition of 5% heat-inactivated serum.

inoculation to chickens. These live vaccines

P multocida, can be readily isolated from
can effectively induce inununity against
viscera of birds dying from peracute/acute
different serotypes of P multocida. They are fowl cholera, whereas isolation from
recommended for use in healthy flocks only.

2824

FOWL CHOLERA

Treatment: A number of drugs will lower
mortality, as do sulfamethazine and
mortality from fowl cholera; however, deaths sulfadirnethoxine. Sulfas should be used may resume when treatment is discontinued, with caution in breeders because of showing that treatment does not eliminate
potential toxicity. High levels of tetracycline

P multocida from a flock. Eradication of
antibiotics in the feed (0.04%), drinking
infection requires depopulation and cleaning
water, or administered parenterally may

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and disinfection of buildings and equipment.

be useful. N orfloxacin administered via

The premise should then be kept free of
drinking water is also effective against
poultry for a few weeks.

fowl cholera. However, many countries do

Sulfonamides and antibiotics are
not allow the use of quinolones in foodcommonly used; early treatment and producing animals, including poultry,
adequate dosages are important. Sensitivity
because of the risk of development of drug
testing often aids in dmg selection and is
resistance. Penicillin is often effective
important because of the emergence of
for sulfa-resistant infections. In ducks,
multiresistant strains. Sulfaquinoxaline
a combined irtjection of streptomycin and
sodium in feed or water usually controls
dihydrostreptomycin can be effective.

FOWLPOX

FOWLPOX IN CHICKENS AND
to persist for extended periods in multiple

TURKEYS
age poultry complexes because of slow
spread of the vims and availability of

Fowlpox is a slow-spreading viral infection
susceptible birds.

of chickens and turkeys characterized by
proliferative lesions in the skin that

Clinical Findings: The cutaneous form of
progress to thick scabs ( cutaneous form)

fowlpox is characterized by nodular lesions
and by lesions in the upper GI and
on various parts of the unfeathered skin of
respiratory tracts (diphtheritic form).

chickens and on the head and upper neck of

Virulent strains may cause lesions in the
turkeys. Generalized lesions of feathered
internal organs (systemic form). Fowlpox
skin may also be seen. In some cases,
is seen worldwide.

lesions are lintited cltiefly to the feet and
legs. The lesion is initially a raised,

Etiology and Epidemiology: The large
blanched, nodular area that enlarges,

DNA vims (an avipoxvirus in the Poxviridae becomes yellowish, and progresses to a family) is resistant and may survive in the
thick, dark scab. Multiple lesions usually
environment for extended pe1iods in dried
develop and often coalesce. Lesions in
scabs. Photolyase and A -type inclusion
various stages of development may be
body protein genes in the genome of
found on the same bird. Localization around
fowlpox vims appear to protect the vims
the nostrils may cause nasal discharge.

from environmental insults. Field and

Cutaneous lesions on the eyelips may cause
vaccine strains have only minor differences
complete closure of one or both eyes. Only a
in their genomic profiles, although the
few birds develop cutaneous lesions at one
strains can be differentiated to some extent
time. Lesions are prominent in some birds
by restriction endonuclease analysis and
and may sig1tificantly decrease flock
imrnunoblotti.ng. Recently, molecular
performance.

analyses of vaccine and field strains of

In the diphtheritic fom1 of fowlpox,
fowlpox vimses have shown some
lesions develop on the mucous membranes
significant differences. The vims is present
of the mouth, esophagus, pharynx, larynx,
in large numbers in the lesions and is
and trachea ( wetpox or fowl diphtheria).

usually transmitted by contact through

Occasionally, lesions are seen almost
abrasions of the skin. Skin lesions (scabs)

exclusively in one or more of these sites.

shed from recovering birds in poultry

Gaseous patches firmly adherent to the
houses can become a source of aerosol
mucosa of the larynx and mouth or proliferainfection. Mosquitoes and other biting tive masses may develop. Mouth lesions
insects may serve as mechanical vectors.

interfere with feeding. Tracheal lesions

Transmission within flocks is rapid when
cause difficulty in respiration. Laryngeal
mosquitoes are plentiful. The disease tends
and tracheal lesions in chickens must be

FOWLPOX

2825

The genomic profiles of field isolates and
vaccine strains of fowlpox virus can be
compared by restriction fragment length
polymorphism. This method is useful to
compare closely related DNA genomes.

However, because of the large size of the

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genome, minor differences are difficult to
detect by this method. Detailed genetic
analysis reveals differences between
vaccine strains and field strains responsible
for outbreaks of fowlpox in previously
vaccinated chicken flocks. Whereas vaccine
strains of fowlpox virus contain remnants of
long terminal repeats of reticuloendotheliosis virus (REV), most field strains contain Scab-like lesion on the unfeathered portion
of the skin due to fowl pox on a turkey.

full-length REV in their genome.

Courtesy of Dr. Jean Sander.

Nucleic acid probes derived from cloned
genomic fragments of fowlpox virus can
also be used for diagnosis. This procedure is
especially useful for differentiation of the
differentiated from those of infectious
diphtheritic fom1 of fowlpox (involving the
laryngotracheitis (seep 2912), which is
trachea) from infectious laryngotracheitis.

caused by a herpesvirus. In cases of

PCR can be used to amplify genomic DNA
systemic infection caused by virulent
sequences of va.iious sizes using specific
fowlpox virus strains, lesions may be seen in
primers. This procedure is useful when an
internal organs. More than one fonn of the
extremely small a.inount of viral DNA is
disease, ie, cutaneous, diphtheritic, and/or
present in the sample. PCR has been used
systemic, may be seen in a single bird.

effectively to differentiate field and vaccine

Often, the course of the disease in a flock
strains of the virus, whether full-length REV
is protracted. Extensive infection in a layer
is present in those strains that are associated
flock results in decreased egg production.

with outbreaks in vaccinated birds. DNA

Cutaneous infections alone ordinarily cause
isolated from the formalin-fixed tissue
low or moderate mortality, and these flocks
sections of birds that are histologically
generally return to normal production after
positive for fowlpox can be used for PCR
recovery. Mortality is usually high in
amplification of genomic fragments using
diphtheritic or systemic infections.

specific primers. Because most outbreaks of
fowlpox in previously vaccinated chickens

Diagnosis: Cutaneous infections usually
a.i·e caused by strains with a genome that conproduce characteristic gross and microtains full-length REV, use of REV envelope-scopic lesions. When only small cutaneous specific primers to determine the presence
lesions are present, it is often difficult to
of full-length REV is helpful in such cases.

distinguish them from abrasions caused

Two monoclonal antibodies that
by fighting. Microscopic examination of
recognize different fowlpox virus antigens
affected tissues stained with H&E reveals
have been developed. These monoclonal
eosinophilic cytoplasmic inclusion bodies.

antibodies are useful for strain differentia

Cytoplasmic inclusions are also detectable
tion by immunoblotting.

by fluorescent antibody and immunohisto

The complete nucleotide sequence of the
chemical methods ( using antibodies against
fowlpox virus genome has been determined.

fowlpox virus antigens). The elementary

It is useful in comparing the sequences of
bodies in the inclusion bodies can be
selected genes of other avian poxviruses.

detected in smears from lesions stained by
the Gimenez method. Viral particles with

Prevention and Treatment: Where
typical poxvirus morphology can be
fowlpox is prevalent, chickens and turkeys
demonstrated by negative-staining electron
should be vaccinated with a live-embryo or
microscopy as well as in ultrathin sections
cell-culture-propagated virus vaccine. The
of the lesions. The virus can be isolated by
most widely used vaccines are attenuated
inoculating chorioallantoic membrane of
fowlpox virus and pigeonpox virus isolates
developing chicken embryos, susceptible
of high i.m.munogenicity and low pathogenicbirds, or cell cultures of avian origin.

ity. In high-risk a.i·eas, vaccination with an

Chicken embryos (9-12 days old) from an
attenuated vaccine of cell-culture origin in

SPF flock are the preferred and convenient
the first few weeks of life and revaccination
host for virus isolation.

at 12-16 wk is often sufficient. Health of

2826

FOWLPOX
birds, extent of exposure, and type of
genome has been determined. Canarypox
operation determine the timing of vaccinavirus infection is usually severe, and tions. Because the infection spreads slowly,
mortality sometimes approaches 1000/o.

vaccination is often useful in limiting spread

Cutaneous lesions may develop, as may
in affected flocks if administered when <200/o
systemic infection with cytoplasmic

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of the birds have lesions. Passive immunity
inclusion bodies detected in lesions on
may interfere with multiplication of vaccine
histologic exantination. A commercial
virus; progeny from recently vaccinated or
vaccine for canaries is available in the USA.

recently infected flocks should be vaccinated Poxvirus infection in psittacines may also only after passive inummity has declined.

be severe, especially in blue-fronted

Vaccinated birds should be examined 1 wk

Amazon parrots. Poxviruses isolated from
later for swelling and scab formation (''take") psittacines appear to be antigenically at the site of vaccination. Absence of"take"

different from poxviruses of other avian
indicates lack of potency of vaccine, passive
species.

or acquired immunity, or improper

Genomic profiles of canarypox,
vaccination. Revaccination with another
mynal1pox, and quail pox viruses show
serial lot of vaccine may be indicated.

marked differences from fowlpox virus

Naturally infected or vaccinated birds
when their DNA is compai.·ed by restriction
develop hum oral as well as cell-mediated
fragment length polymorphism after
immune responses. Hu.n10ral inunune
restJ.iction endonuclease digestion.

responses can be measured by ELISA

Quail pox virus shows marked antigenic
or virus neutralization tests.

differences from fowlpox virus and,
although some cross-reacting antigens ai.·e

Zoonotic Risk: There is no zoonotic
present, provides limited or no crossrisk associated with fowlpox virus. Avian protection against fowl pox virus. Avianpox
poxviruses cause a productive infection in
virus infection has been considered as a
avian species but a nonproductive infection
population-limiting factor in endangered
in manunalian hosts. Consequently,

Hawaiian forest birds. Avianpox viruses
avianpox viruses have been used as vectors
isolated from Hawaiian crows (Corvus
for expression of genes from mammalian
hawaiiansis ), Hawaiian geese (Branta
pathogens in the development of safe recom
sandvicensis ), Palila (Loxiodes baille-ui), binant vaccines.

and Apapane species (Himatione
sanguinea) are different from each other

POX IN OTHER AVIAN SPECIES
and from fowlpox virus. Similarly, a
poxvirus isolated from an Andean condor

Wectio.ns with avian poxvirus have been

(Vultm· gryphus) at the San Diego Zoo is
seen in a vai.iety of wild and pet birds. Some
antige.nically, genetically, and biologically
isolates are primarily infectious for only
different from fowlpox virus. Like fowlpox
the homologous host, whereas others are
virus, these viruses appear to be suitable
infectious for one or more additional
vectors for expression of foreign genes
species. In the absence of genetic infom1atoward development of genetically modified tion on most of these viruses:classification
virus vaccines for manunalian species.

has usually been based on host pathogenic

Several cai.1arypox virus vectored vaccines
ity or cross-protection studies. The
expressing genes of manunalian pathogens

.nucleotide sequence of canarypox virus
are available commercially .

GOOSE PARVOVIRUS INFECTION

(Derzsy disease, Goose hepatitis, Goose plague)

Goose parvovirus infection is a highly

Muscovy ducks and several hybrid duck
contagious and fatal disease of goslings and
breeds are also susceptible to ai.1other

Muscovy ducklings, often causing as much
pai.vovirus that has been shown to be
as 700/o-1000/o mortality in goslings <4 wk old. antigenically related to goose parvovirus.

Goose pai.vovirus has been reported from

This so-called Muscovy duck pai.vovirus
all the major goose-fai.1.1ting cou.ntJ.ies of
has been isolated from an outbreak ai.nong

Europe and the Far East, where the disease

Muscovy ducks in California. Goose parvois of serious economic significance.

virus has not been detected in the USA.

GOOSE PARVOVIRUS INFECTION

2827

Etiology: Goose parvovirus is a member
diurn. The main microscopic lesions are
of the family Parvoviridae and, based on
pronounced degenerative changes in the
phylogenetic analysis, has been shown to be
myocardial cells and the presence of
related to the dependovirus genus. Apart

CowdJ.y type-A intranuclear inclusion
from the Muscovy duck parvovirus, to which bodies.

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it is closely related, goose parvovirus shows
no similarity to the other avian or man1ma

Diagnosis: A preswnptive diagnosis is
lian parvoviruses. After primary infection,
based on the characteristic clinical course,
the virus replicates in the intestinal wall and,
age incidence, and gross and histologic
after a short viremic phase, reaches the
lesions. Cenfirrnation can be obtained after
heait, liver, and other organs.

isolation of the parvovirus in cell cultures or
embryonated eggs derived from susceptible

Transmission and Epidemiology: The
geese and Muscovy ducks. Presence of the
virus is excreted in large amounts in the
vims can be confirmed by electron
feces of infected birds, resulting in rapid
microscopic examination of infected
spread by direct and indirect means.

cultures and neutralization with specific

Outbreaks are often initiated in susceptible
goose parvovirus antiserwn. Diagnosis can
goslings after transmission of the virus via
also be confinned by direct detection of
eggs laid by infected breeder geese.

antigen or vims in tissues from infected

Evidence suggests that older, subclinically
birds, by immunofluorescence, or by the_ use
infected geese may act as caniers. Infected
of PCR. Serologic tests for goose parvovuus
eggs are often the source of the virus when
include vims neutralization, agar gel
outbreaks of goose parvovims occur in
precipitation, in1.munofluorescence, and
countries or geographic locations formerly

ELISA.

free of the disease. Serologic evidence

Although goose parvovirus causes
suggests that the vims is present in several
disease in both geese and Muscovy ducks,
species of wild geese in Europe. No other

Muscovy ducks ai·e also infected with
avian or biologic vectors have been
another antigenically related parvovi.Jus.

identified.

This virus causes serious disease in

Muscovy ducklings, but not in goslings, and

Clinical Findings:

can be detected and differentiated using

In susceptible goslings

PCR combined with sequencing or
and ducklings, clinical signs vary according
restriction fragment length polymorphism.

to the age of the birds. The course of the

Differential diagnoses should also include
disease in birds < 1 wk old is rapid, with
duck viral enteritis ( duck plague, see
anorexia and death occurring within 2-5
p 2799), which affects all types of waterdays. Mortality can reach 1000/o in birds fowl. Duck viral hepatitis (seep 2815)

infected in the hatchery. In older birds, the
causes a fatal disease in ducklings but fs
disease follows a more protracted course,
not pathogenic for goslings or Muscovy
characterized by ocular and nasal disducklings. Riemerella anatipestifer and chai·ge, a profuse white diarrhea, ai1d

_

Pasteurella multocida may also cause high
weakness. The eyelids and uropygial glands
mortality in goslings and Muscovy ducklings
are red and swollen. Birds that survive the
but can be differentiated by bacterial
acute stage show profound growth
isolation and identification.

retardation, with loss of feathers and
reddening of the skin, particularly on the

Prevention and Treatment: Goslings
back. Birds may stnnd in a "penguin-like"

should be hatched together only from
posture due to accumulation of ascitic fluid
flocks that are known to be free of goose
in the abdomen. In 2- to 4-wk-old birds,
parvovirus; many outbreaks are attributed
mortality can reach 10%, but morbidity
to the practice of custom-hatching eggs
levels may be much higher. No clinical signs
from various sow·ces. Eggs should be
are seen in older birds, although adults will
imported only from countries that can
respond inununologically. An enteric form
guarantee freedom from goose parvovims.

of goose parvovirus infection has been

Geese that have survived an outbreak
docwnented to exist.

should not be used for breeding purposes.

Lesions: Gross lesions include the

Both live, inactivated oil emulsion vaccines
presence of a fibrinous pseudomembrane
and baculovirus expressed VP2 capsidcovering the tongue and oral cavity, peril1epbased recombinant vaccines are available atitis, pericarditis, pulmonary edema, liver
and ai·e widely used in coW1tries where the
dystrophy, and catarrhal enteritis. In acute
disease is endemic. Vaccination of breeding
cases, the heart is characteristically
flocks induces high levels of maternal
rounded at the apex, with a pale myocar-
antibody in the progeny until -2 wk of age.

2828

HELMINTHIASIS

HELMINTHIASIS

(Nematode and cestode infections)

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Approximately 100 wom1 species have been eg, males of Tetrameres spp are elongated recognized in wild and domestic birds in the and slender, whereas gravid females are USA. Nematodes (roundworms) are the
globe-shaped. The size and shape of
most significant in number of species and
nematode species vary widely; ascaricls
in economic impact. Of species found in
are sturdy and long ( up to 4.5 in.

commercial poultry, the common round[116 mm]); capillaricls are more delicate, wonn (Ascaridia go/Ii) is by far the most
slender, and long (2.3 in. [60 mm]); and
common. Field studies show that poultry
other nematodes are much shorter
maintained under free-range conditions

(0.08-0.48 in. (2-12 mm]).

may be heavily parasitized; therefore,

Cestodes (tapeworms) also vary in size.

control measures such as preventing

Raillietina spp may be > 12 in. (30 cm), infections or chemotherapy are likely to
whereas Davainea proglottina often
improve weight gain and egg production. In
is <0.16 in. (4 mm). The proglotticls of
surveys of poultry raised under nonconfrneindividual tapewom1s are hermaphroditic.

ment conditions throughout the world, an

Tapeworms have been recovered in the
incidence of infection >80% is not
thousands from individual chickens and
w1conunon.

turkeys.

Generally, nematodes have separate

See TABLE: 5 for information on common
sexes that have morphologic differences;
nematodes ar1d cestodes of poultry.

iiM·ii COMMON HELMINTHS OF POULTRY

Intermediate

Host or Life

Organ

Parasite

Host

Cycle

Infected

Pathogenicity

NEMATODES

Amidostomum Duck, goose,

Direct

Gizzard

Severe
anseri
pigeon

Ascaridia

Turkey

Direct

Small intestine

Moderate
dissimilis

Ascaridia

Chicken, turkey, Direct

Small intestine Moderate
galli
duck,quail

Capillaria

Chicken, turkey, Earthworms

Small intestine jvloclerate to
caudinj!ata
cluck,garne
severe
birds, pigeon

Capillaria.

Chicken, turkey, None or

Mouth,

Severe
conto1·ta
cluck, game birds earthworms
esophagus, crop

Capillaria

Chicken, turkey, Direct

Small intestine, Severe
obsignata
goose, pigeon,
ceca
quail

Cheilospirura Chicken, turkey, Grasshoppers, Gizzard Moderate
hamulosa
garne birds
beetles

Cyathosloma Turkey, duck

Direct or

Trachea

Severe
bronchial is
earthworm

Cy1nea colini Turkey, game

Cockroaches

Proventriculus Mild
birds

(continued)

HELMINTHIASIS

2829

COMMON HELMINTHS OF POULTRY (continued)

Intermediate

Host or Life

Organ

Parasite

Host

Cycle

Infected

Pathogenicity

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Disphmynx

Chicken, turkey, Sowbugs

Proventriculus Moderate to
nasuta
game birds,
severe
pigeon

Gongylonema Chicken, game

Beetles,

Crdp, esopha-

Mild
ingluvicola
birds
cockroaches
gus, proven-
triculus

Heterakis

Chicken, turkey, Direct

Ceca

Mild, but trans-
gallinorum
duck, game birds
mits agent of
histomoniasis

Heterakis

Quail, duck,

Direct

Ceca

Severe
isolonche
pheasant

Ornithostron-

Pigeon, dove

Direct

Small intestine Severe
gylus qiwdrira-
cliatus

Oxyspirura

Chicken, turkey, Cockroaches

Eye

Moderate
mansoni
guinea fowl,
quail

Strnngyloides Chicken, turkey, Direct

Ceca

Moderate
avium
quail, goose

Subulura

Chicken, turkey, Earwigs,

Ceca

Mild
brumpti
duck, game birds grasshoppers,
beetles,
cockroaches

Syngamus

Chicken, turkey, None or

Trachea

Severe
trachea
pheasant, quail
earthwonn

Tetra meres

Chicken, turkey, Grasshoppers, Proventriculus Moderate to·
americana
duck,game
cockroaches
severe
birds, pigeon

1'richostrongy- Chicken, turkey, Direct

Ceca

Severe
lus tenuis
duck, game
birds, pigeon

CESTODES

Choanotaenia Chicken

House flies

Upper intestine Moderate
infundibulwn

Davainea

Chicken

Slugs, snails

Duodenum

Severe
proglottina

Metroliasthes Turkey

Grasshoppers Intestine

Unknown
lucida

Raillietina

Chicken

Beetles

Duodenum,

Mild
cesticillus
jejunw11

Raillietina

Chicken

Ants

Lower intestine Severe, nodules
echinobothrida

Railliel'ina

Chicken

Ants

Lower intestine Severe
tetragona

2830

HELMINTHIASIS

Transmission: Modem confinement
source of infection when ingested by
rearing of poultry has significantly reduced
poultry. Litter beetles may also serve as
the frequency and variety of endoparasite
a mechanical vector.

infections, which are corrunon in ranged

The life cycle of Capillaria may be direct
birds and in backyard flocks. However,

(C obsignala), .require an intermediate host VetBooks.ir
severe parasitism still may be seen in
such as earthworms (C caudinfiata),
floor-reared layers, breeders, turkeys, or
or be either direct or use eaithwo1ms
pen-reared game birds where management

(C conlorta). Laival development in the egg problems may exist. Contributing factors
takes 8-15 days depending on temperature.

include the use of poorly managed built-up

Worms reach maturity in 20-26 days after
litter (which fosters the propagation of
ingestion by the final host.

intermediate hosts and the accumulation

The ga.pewonn Syngamus trachea
of infective eggs) and resistance of the
inhabits the trachea and lungs of many
parasites to therapeutic drugs. Range
domestic and various wild birds. Wection
infections of nematodes such as H elerakis
may occur directly by ingestion of infective
gallinanim and Syngamus trachea may eggs or laivae; however, severe field
increase because of seasonal or climatic
infection is associated with ingestion of
abundance of specific invertebrate
transport hosts such as earthwonns, snails,
intem1ediate hosts, eg, large numbers of
slugs, ai1d arthropods ( eg, flies). Many
ea.rthwom1s brought to the surface by
ga.pewonn larvae may encyst and survive
spring rains. Some species have been
witl1in a single inve1tebrate for yeai-s.

associated with large nwnbers of darkling

Although ga.pewom1s are not a problem in
beetles, which may act as mechanical
confinement-reai·ed poult1y, they cause
vectors of infective eggs.

serious economic losses in gan1e-farm pens

Nematodes have either a species-specific,
and in rai1ge-reared chickens, pheasants,
direct life cycle with bird-to-bird transmisturkeys, and peacocks. Cyathosloma sion by ingestion of infective eggs or larvae,
bronchialis is the gapewonn of geese
or an indirect cycle that requires an
and ducks.

inte1mediate host ( eg, insects, snails, or

Eggs of Oxyspirura mansoni, Manson
slugs). Eggs of many nematode species
eyeworm, are deposited in tl1e eye, reach
are resistant to low temperatures and
the pharynx via the nasolacrimal duct, are
disinfectants but may be more susceptible
swallowed, passed in the feces, and
to heat and desiccation.

ingested by the Surinam cockroach,

The life cycle of A galli is simple and

Pycnoscelus surina.mensis. Larvae reach
direct. Eggs in the droppings become
the infective stage in the cockroach. When
infective in l 0-12 days under optin1al
infected intem1ediate hosts are eaten,
conditions. The infective eggs a.re ingested
liberated larvae migrate up the esophagus to
and hatch in the provent1iculus, and the
the mouth and then through the nasolacrilarvae live free in the lumen of the mal duct to the eye, where the cycle is
duodenum for the first 9 days. They then
completed. Other insect species may also
penetrate the mucosa, ca.using he1J1on-hages, serve as tl1e inte1mediate host.

return to the lwnen by 17-18 days, and

Cestodes require an intermediate host
reach maturity at 28-30 days. Levels of

( eg, insects, crustaceans, eaithworms, or
infection are often underestimated, because snails). Floor layers, breeders, and broilers early larval stages are barely visible and can
ai·e infected with Raillietina aesticillus by remain for long periods within intestinal
tissues, whereas adult stages in the lwnen
are generally fewer in nun1ber. Maturation
of larval stages can be hampered by adult
wom1 nwnbers, thereby increasing the tin1e
larval stages remain in intestinal tissues and
continue to cause damage.

The life cycle of H gall'inarum is similar
to tl1at of A galli. The greatest production of eggs for each egg ingested occurs in
the 1ing-necked pheasant, followed by the
guinea fowl and chicken. The larvae a.re
closely associated with the cecal tissue, but
a true tissue phase rarely occurs. Most of
the adult wonns are found at the blind end
of the ceca. Ea.rthwonns may ingest the

Heterakis gallinarum in the cecal pouches of a eggs of the cecal wom1 and serve as a
chicken. Courtesy of Dr. Jean Sander.

HELMINTHIASIS

2831
ingestion of the intermediate host, small

Oxyspirura mansoni is a slender
beetles that breed in contaminated litter.

nematode, 12-18 nun long, found beneath

Cage layers in unscreened houses may
the nictitating membrane of chickens and
become infected with Clwanotaenia infun
other fowl in tropical and subtropical
dibiilum by eating its intermediate host, the regions. The parasite causes various

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house fly. Lltter beetles in proximity may
degrees of inf1all1mation, lacrimation,
also serve as intermediate hosts.

corneal opacity, and disturbed vision.

More than 3,000 of the microscopic

Among other nematodes, Amidostomum
tapeworn1 Davainea proglottina have been
anseris attacks the gizzard lining of ducks recovered from a single bird. Several species and geese alld causes dark discoloration, of slugs and snails serve as intennediate
necrosis, alld sloughing at the parasitic loci.

hosts, and > 1,500 infective parasites have

Dispharynx nasuta causes ulceration,
been recovered from a single slug.

thickening, and maceration of the proventriculus; heavily infected birds may die.

Pathogenesis and Clinical Findings:

Tetrameres americana, a b1ight red wonn

Ascaridia, Heterakis, and Capillaria spp discernible tllrough the proventricular wall,
are widely distributed and cause such
causes diaiThea, emaciation, alld wiili heavy
nonspecific signs as general unthriftiness,
infection, death. Trichostrongylus tenuis
inactivity, depressed appetite, and retarded
causes inflan1ed ceca, weight loss, anemia,
growth; in severe cases, death may result. A
alld death, especially in young birds.

mere few ascaiids may depress weight, and

Ornithostmngylus quadriradiatus, a
larger nun1bers may block the intestinal
blood-sucking parasite, causes pigeons to
tract. Ascaiids may migrate up the oviduct
regmgitate bile-stained fluid mixed with

(via the cloaca) to become enshelled later
food; greenish mucoid diarrhea from
within the egg (an aesthetic, but not a public
hemorrhagic intestines, emaciation, alld
health, problem, avoidable by careful
death follow.

egg-candling before the release of eggs to

Most pathogenic tapewonns ai·e found
market). A dissimilis (turkey rom1dworn1)

in the small intestine; the scolex, usually
may also migrate out of the intestine,
buried in the mucosa, generally causes mild
through the portal system, and into the
lesions. Davainea proglottina may cause
liver, causing hepatic granulomas.

weight loss. Raillietina tetragona causes

H gallina1um, a mild pathogen, in large
weight loss and decreased egg production;
nmnbers may cause thickening, inflamma

R echinobothrida produces granulomas at
tion, or nodulation in the cecal walls.

its attachment sites ("nodular disease").

lnfection with H gallinarom has been
associated with cecal and hepatic granulo

Diagnosis: A reliable diagnosis Call be
mas. H eterakis isolonche, highly pathomade only by accurate identification of the genic in pheasants, may cause 500Ai
individually recovered parasites; careful
mortality. H gallina1um carries Histo
and complete necropsy techniques are
monas meleag1idis, the protozoan that
essential. Only by specific recognition of the
causes histomoniasis (seep 2835).

parasite can meallingful recommendations

C contorta in the mucosae of the crop
for flock therapy and mallagement be made.

and esophagus, and C obsignata in the
wall of the small intestine, cause marked

Treatment and Control: Improvement
thickening and inflammation of the organs.

of mallagement alld sanitation in confined

Birds harboring large nmnbers of these
operations will generally lower the parasite
threadlike worms become weak ai1d
levels in tl1e birds. In range birds, the only
emaciated and may die.

option is to move to new pastures, although

Young birds are the most severely
the benefit that may result will be of short
affected by gapeworn1s. Sudden death and
duration. Application of approved
vern1inous pnemnonia characterize early
insecticides to soil alld litter when premises
outbreaks. Signs of gasping, choking,
are unoccupied may interrupt the life cycle
shaking of the head, inanition, emaciation,
of tl1e parasite by destroying its intermediand suffocation may follow. Necropsy ate host. When the premises are restocked,
reveals adult gapeworms obstructing the
groups of birds of different species or ages
lunlina of the trachea, bronchi, and lungs.

should be widely separated to avoid spread

Respiratory inflammation may be present.

of parasites. Migration of litter beetles or

The blood-red, female gapeworm is usually
other insects may infect new or widely
found in copulation with a much smaller,
separated housing.

paler male with its head embedded deep

Approved compounds are very limited in
in the host tissue. The joined pair have a
the USA Because of frequently changing

"¥"-shaped or forked appeai·ance.

regulations, the status of ally medication

2832

HELMINTHIASIS
should be checked before its administranot be ad.ministered dwing molt, because it tion. Approved drugs for the USA are listed
may interfere with feather regrowth.

online in the FD A's Green Book and in the

Hygromycin B given at 8--12 g/ton in feed
commercially available Feed Compendiwn.

is used to control ascarids, cecal worn1s,

Only approved drugs may be used in birds and capillarids in chickens. A withdrawal producing eggs or meat for the commercial
time of 3 days is required. Cownaphos,

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market. Label directions and recommended

0.004% in feed for 10-14 clays for replacedoses should be followed precisely, with ments, or 0.003% in feed for 14 days for
scrupulous adherence to withdrawal times.

layers, has been commonly used against

Piperazine compounds are relatively
capillarids. Chickens <8 wk old should not
nontoxic and have been widely used against
be given this medication, and it should
ascariasis. Because of this, drug resistance
not be used within 10 clays of vaccination
is widespread in many regions of the world.

or other stress. In birds maintained on

Several piperazine salts are available
contaminated litter or exposed to infected
internationally. Because only the piperazine
birds, the medication regimen should be
moiety is efficacious, doses should be
repeated using the same dosages as the first.

calculated based on mg of active piperazine/ There should be at least 3 wk between the bird. Piperazine should be completely
first and second cow·se of treatment.

conswned by birds within a few hours,

I -Iygromycin B is a cholinesterase inhibitor,
because only relatively high concentrations
and treated birds should not be exposed to
of the drug elin1inate worn1s. It may be given other cholinesterase inhibitors ( drugs, to chickens as a single dose, 50 mg/bird
insecticides, pesticides, or chemicals)

( <6 wk old), 100 mg/bird (�6 wk old), in the
within 3 days before or after treatment.

feed at 0.2%-0.4% or in the drinking water at

As a treatment for Manson eyeworm,

0.1%-0.2%; it may be administered to tw·keys a local anesthetic can be applied to the at 100 mg/bird ( <12 wk old) or 200 mg/bird
eye, and the worms in the lacrimal

(� 12 wk old). Some practitioners recomsac exposed by lifting the nictitating mend the addition of molasses to unmedimembrane. A 5% cresol solution (l-2
catecl water after piperazine administration,
drops) placed in the lacrimal sac kills the
so as to induce an osmotic flushing,
worms immediately. The eye should he
theoretically removing any of the remaining
irrigated with sterile water immediately to
worms from the intestinal tract. For severe
wash out the debris and excess solution.

cases, treatment can be repeated after 14

The eyes improve within 48-72 hr and
days. These medications must be withgradually become clear if the destructive drawn 14 clays before slaughter. Piperazine
process caused by the parasite is not too
is not approved in the USA for birds
far advanced.

producing eggs for hwnan consmnption.

The use of diatomaceous eaith supple

Fenbenclazole is approved in the USA
mented at 2% in feed and fed continuously
for use in growing turkeys at the rate of
lowers numbers of Helerakis and Capil

14.5 g/ton of feed (16 ppm), fed continually
laria in chickens. The efficacy of several
as the sole ration for 6 days for the removal
essenlial oils have been measw-ed, with
of Ascaridia cl·issimilis and Helerakis inconsistent results.

gallinarum. No withdrawal tin1e is

Several compounds are reported to be
required. One study indicates a possible
effective against nematode infections but
negative effect on sperm quality by the cl.tug.

are not approved for use in poult1y or other

It has been suggested that an alternative
avian species in the USA. Three such
drug be used for treatment of breeding toms
compounds, tetramisole at 40 mg/kg,
or that the sperm nmnber and frequency
flubendazole at 30 ppm in feed, and
of artificial inseminations be increased.

iver.mectin 1 % at 10 mg/mL in water were

Fenbendazole is not approved for use in
effective in removing A galli, H gallinaium,
other poult1y in the USA but is effective
and Capillaria in chickens. Pyrantel
againstAscai'is when administered once at

Lartrate was more effective then pyrantel

10-50 mg/kg; if needed the treatment can be
pan1oate against the adult stage of A galli, repeated after 10 days. At 10-50 mg/kg,
and it was somewhat effective against Cap
fenbendazole when administered daily over
illai'ia when adtninistered at 15-25 mg/kg.

5 days is effective against Capillai'ia.

Levamisole administered at 25-30 mg/kg

Fenbenclazole is also efffective against
appears to be effective against A dissimilis,
other nematodes when ad.ministered at

H gallinaium, ai1d C obsignata; it can also be 10-50 mg/kg/clay for 3-5 days or as a single
given in the dtinking water at 0.03%-0.06%.

dosage of 20-100 mg/kg, or added to the

Phenothiazine has been used to treat cecal
d1inking water at 125 mg/L for 5 clays or to
wom1s in chickens at 0.5 g/bird and in
the feed at 100 mg/kg. Fenbendazole should
hffkeys at 1 g/bird, given in 1 day. Combined

HEMORRHAGIC ENTERITIS/ MARBLE SPLEEN DISEASE

2833
in drinking water as a 1-day treatment,

125 ppm is effective in tmkey poults.

phenothiazine (0.5%--0.56%) and piperazine

Can1bendazole provided control when given

(0.11%) have been used to treat heterakids
in three treatments of 50 mg/kg for chickens
and ascarids; this drug combination is no
and 20 mg/kg for turkeys. Albendazole
longer approved for poultry in the USA.

administered as a single oral suspension

Methyridine irtjected SC at a dose of 25-45

(5 mg/kg bird weight) was reported effective

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mg/bird is effective in clearing C obsignata.

against A galli, H ga.llinmum, and

In pigeons, a SC irtjection of 1 mL of lOOAi

C obsignala. The drug also has been
methyridine in the pectoral region or leg of
rep01ted effective against cestodes if
pigeons removed Capillaria, but the drug
administered at 20 mg/kg. There are no
must be handled with care because contact
published withdrawal times. Nitarsone
with skin may produce lesions. Coumaphos
at 170 g/ton (0.01875%) of feed has been
removes Capillaria in quail. Haloxon at
repo1ted to reduce A dissimilis fecundity

25 and 50 mg/kg, or at 750 ppm in the feed
and wom1 burden in chickens and turkeys.

for 5--7 days, has good activity against

There have been some repo1ts of

Capillaria in chickens and quail.

experimental drug treatment for other

Fenbendazole at 20 mg/kg for 3--4 days
nematodes. Cambendazole (60 mg/kg),
effectively removes gapeworms in
pyrantel (100 mg/kg), citarin (40 mg/kg),
pheasants. Toxicity has been reported in
mebendazole (10 mg/kg for 3 days), and
pigeons that received fenbendazole at the
fenbendazole have been reported to be
rate of 30 mg/kg for 5 days. Thiabendazole
effective againstAmidostomum anseris.

administered at 0.05% in the feed continu

Trichostrongylus tenuis is controlled by
ally for 2 wk can be used for treatment of
cambendazole (30 mg/kg), pyrantel
gapeworms in pheasants, and when given

(50 mg/kg), thiabendazole (75 mg/kg),
continually for 2!4 days is said to help
mebendazole (10 mg/kg for 3 days), and
prevent and control infections. Withdrawal
citarin ( 40 mg/kg). At recommended levels
of 21 days is required for meat constm1ption; for chickens, mebendazole has some specific precautions should be observed in
rep01ted effect against Dispharynx nasula,
feeds containing bentonite. Tetramisole at
tetramisole against Subulura b1umpli and

3.6 mg/kg for 3 consecutive days in the

Slrongyloides avium, and piperazine
drinking water removes gapeworms.

against Telrameres.

Poultry treated while larvae are migrating in

Poultry producers wanting to treat for
the body develop immunity to gapew01rns,
tapewom1s should be aware that expulsion
even though therapy may abort larval
of the parasite will be a short-term remedy if
migration. Levamisole fed at a level of 0.04%
the scolex is not removed or if the intennefor 2 days or at 2 g/gal. drinking water for diate host is not eliminated as a source of

1 day each month has proved to be an
reinfection. Butynorate in combination with
effective control in game birds. Kiwis are
piperazine and phenothiazine as a feed
reported to be acutely sensitive to levarniadditive or individual tablets has shown sole at doses well within the safe range for
some efficacy. Other promising experidomesticated poultry. Mebendazole fed mental drugs include chlorophene and
prophylactically at 64 ppm or cmatively at
niclosamide. None is approved in the USA.

HEMORRHAGIC ENTERITIS/

MARBLE SPLEEN DISEASE

Hemorrhagic enteritis is an acute GI

Species-specific differences in clinical
disorder affecting yotmg turkeys 2!4 wk old.

response are thought to be related to

In its most severe form, it is characterized
differences in the target organs for
by depression and hemorrhagic droppings.

anaphylaxis ar1d variation in viral patho

Mortality may be increased; however, this is
type. Infection with less virulent pathotypes
rare because of extensive use of vaccines.

in either host often may go undetected until

Marble spleen disease is an acute respirasecondary bacterial infections begin to tory disease of pheasants characterized by
develop as a result of viral-induced
depression, enlarged mottled spleens,
immtmosuppression.

pulrnonar-y congestion, and death. Both

Similar diseases have been seen
diseases are caused by sin1ilar viruses.

sporadically in other species of birds such

2834

HEMORRHAGIC ENTERITIS/MARBLE SPLEEN DISEASE
as chickens (splenomegaly), guinea fowl,
splenomegaly. Concomitant or prior
peafowl, and chukar partridges.

exposure to necrotic enteritis (seep 2802),
coccidiosis (seep 2791), Newcastle disease

Etiology and Epidemiology:

virus (seep 2856), Bordetella avium (see

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The etiologic agent is a nonenveloped,
p 2907), or Mycoplasma gallisepticum and
icosahedral DNA virus, 70-90 nm in

M synoviae (seep 2841) can exacerbate the
diameter. It is a member of the family
problem. Similar multiple agent interactions

Adenoviridae and the genus Siadenovirus.

have been implicated in mortality associ

Based on differences in presentation within
ated with the use of vaccines for hemorhost species, numerous viral pathotypes rhagic enteritis.

appear to exist. These differ slightly at

Marble spleen disease typically affects
the DNA level but are indistinguishable
pheasants 3--8 mo old. Onset is acute, with
serologically.

dyspnea, asphyxiation, and sudden death

Both hemorrhagic enteritis and marble
occurring as a result of pulmonary
spleen disease are geographically widecongestion and edema. Mortality is spread and considered endemic in areas
commonly 2%----3% but can reach 15%.

where turkeys and pheasants are raised

Secondary bacterial infections as a result of
commercially. The usual route of infection
inununosuppression have also been noted.

is oral, and virus is often introduced onto
previously uninfected premises via

Lesions: Necropsy of moribund or dead
personnel or equipment contaminated
birds infected with hemorrhagic enteritis
with infectious feces. Turkey poults and
virus reveals gross congestion and
pheasants 3--4 wk old are resistant to
occasional intralwninal hemorrhage in the
infection because of age-related resistance
proximal small intestine. The spleen is
or, more commonly, the presence of
usually enlarged, f1iable, and mottled white,
maternal antibody. The virus may survive
except in birds that have hemorrhaged
under moist conditions (ie, in litter) well
extensively. Hem01Thage in the intestine is
beyond the refractory period. As infection
not common in field cases. Histopathologic
begins to cycle through a flock, large
changes in the duodenum include congesquantities of virus are shed in the feces, tion, hemorrhage, and necrosis of the
which facilitates rapid spread through
intestinal epithelium. This lesion in
susceptible birds. Morbidity usually
particular is thought to be the result of
approaches 1000/o for both hemorrhagic
a virally induced, cytokine-mediated
ente1itis and marble spleen disease.

anaphylactic reaction, with the GI tract
being considered the target shock organ in

Clinical Findings: In commercial
turkeys. Basophilic intranuclear inclusions
operations, hemorrhagic enteritis typically
can be found in lymphocytes and macaffects turkeys 6-12 wk old but is most rophages in a variety of tissues ( eg,
common between 7-9 wk of age. In
intestine, liver, and lungs) but predomioutbreaks involving highly virulent nantly in the spleen, where lyrnphoreticular
pathotypes, clinical signs can include
hyperplasia and lymphoid necrosis are
depression, pallor, and bloody droppings.

noted. lntranuclear inclusions in the renal

Acute mortality can range from 1 %-600/o,
tubular epithelial cells of the kidneys can be
with an average of 10"/o--15% throughout a
seen in turkeys that have recovered from

2-wk period. Birds that survive the acute
hemorrhagic enteritis.

phase experience a transient inununosuppression related to the lymphotrophic, lyrnphocytopathic nature of the virus.

This often manifests itself in the fonn of
secondary bacterial infections, eg,
colibacillosis (seep 2814) -10-14 days after
exposure to the virus. Thus, a second
peak in mortality, potentially overlapping
the first, may be seen and, in less virulent
outbreaks, may actually dominate the
clinical picture. The second wave of
mortality often lasts 2-4 wk and is
characterized by lesions commonly
associated with bacterial respiratory
disease or septicemia, eg, fibrinopurulent
pnewnonia, airsacculitis, pe1icarditis,

Enlarged, mottled spleen in a turkey with
peritonitis, perihepatitis, hepatomegaly, and
hemorrhagic enteritis. Courtesy of Dr. Jean Sander.

HISTOMONIASIS

2835

On histopathologic evaluation of
parasitic, and toxic enteritides of turkeys.

pheasants with marble spleen disease,

In pheasants with acute respiratory disease,
flooding of the atria and tertiary bronchi
differential diagnoses include Newcastle
with fibrin and RBCs, as well as generalized
disease, avian influenza, and in the case of

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vascular congestion and focal necrosis, are
birds reared in confinement, gaseous toxins.

often seen in the lung. As with hemorrhagic
enteritis, this response may be anaphylactic

Treatment, Control, and Prevention:

in nature, with the lung being considered

Vimlent outbreaks of hemorrhagic enteritis
the target shock organ in the pheasant.

have been successfully treated and

Splenomegaly with lymphoreticular
controlletl by SC injection of exposed birds
hyperplasia and lymphoid necrosis also
with 0.5-1 mL of antiserum obtained from
occur and are the characteristic lesions for
recovered flocks. It is presumed that a
which marble 8pleen disease is named.

similar approach may be effective for

Basophilic or magenta-colored intranuclear
pheasants. In anticipation of secondary
inclusions may be found in a variety of
bacterial complications, antibiotics may be
tissues excluding the GI tract, with the
used, but if possible, an infom1ed choice
highest concentration of virus found in the
should be made based on current antibiotic
spleen.

susceptibility profiles for locally obtained

Escherichia coli isolates. In addition to

Diagnosis: Diagnosis of vimlent
good biosecurity, prevention hinges on the
outbreaks of hemorrhagic enteritis or
use of vaccines administered in the water
marble spleen disease can often be made
at -4-5 wk of age. Commercially available
based on clinical signs and gross lesions.

tissue culture products and crude splenic

Confirmation is by histopathology and the
preparations containing avirulent isolates
presence of seroprecipitating vims in the
produce lifelong protection. Quality control
spleen as determined by agar gel immunoon crude splenic preparations, such as diffusion. PCR techniques to detect
examining them for bacteria, Mycoplasma,
hemorrhagic enteritis viral DNA in tissue
and other viruses, should be done before
have also been described and are in regular
they are prepared. A subunit vaccine to
use in select laboratories. To determine
prevent hemorrhagic enteritis in turkeys
whether hemorrhagic ente1itis or marble
has been described in Europe.

spleen disease is a predisposing factor in

Vaccines intended for use in turkeys
cases of bacterial respirato1y disease or
should not be used in pheasants, and vice
septicemia, or to verify a primary diagnosis,
versa, because the avirulent isolates used
acute and convalescent sera (3 wk apart)

for vaccinating one species are typically
can be tested using either agar gel
virulent in the other. Because of the
immunodiffusion or ELISA. In turkeys,
potential for interaction with other agents,
differential diagnoses include colibacillosis,
including live vaccines, regular disease
pasteurellosis, paratyphoid, and erysipelas.

monitoring and careful integration of

Reticuloendotheliosis or lyrnphoproliferahemorrhagic enteritis and marble spleen tive disease should be considered when
disease vaccines into flock vaccination
lyrnphoreticular hyperplasia is the
protocols is encouraged. Intuitively,
predominant lesion. GI lesions without
vaccines should not be administered to
splenic involvement should evoke
birds exhibiting signs of illness or within
consideration of other viral, bacterial,

2 wk of any other vaccination.

HISTOMONIASIS

(Blackhead, Infectious enterohepatitis)

Histomoniasis is caused by a protozoan

Etiology: The causative agent of
that infects the ceca, and later the liver, of
histomoniasis is the anaerobic, single cell
turkeys, chickens, and occasionally other
protozoan pai·asite Histomonas melea
galliform birds. In turkeys, most infections
gridis that can exist in flagellated (8-15 µm are fatal, whereas in other galliforms
in diaineter) ai1d amoeboid (8-30 µmin
susceptibility vaiies between species and
diameter) forms. Histomonas is most often
breeds.

transmitted in embryonated eggs of the

2836

HISTOMONIASIS
cecal nematode H eterakis gallinarum.

A large percentage of chickens and other
gallinaceous birds harbor this worm, which
serves as a reservoir. Three species of
earthwonns can act as vectors for H gallina1um larvae containingH meleagridis, VetBooks.ir
which are infective to both chickens and
turkeys. H meleagridis survives for long
periods within Heterakis eggs, which are
resistant and may remain viable in the s01!

for yea.rs. Histomonads are released from

H eterakis larvae in the ceca a few days after entry of the nematode and replicate rapidly
in the ceca. The parasites migrate into the
submucosa and muscularis mucosae and

Liver lesions, an enlarged ceca with cores,
cause extensive and severe necrosis.

and inflammation seen in multiple tissues of

Histomonads reach the liver either by the
a turkey with histomoniasis. Courtesy of Dr. Larry vascular system or via the peritoneal cavity,

R. McDougald and Dr. Robert B. Beckstead.

and rounded necrotic lesions quickly
appear on the liver surface. Histomonads
interact with other gut organisms, such as
bacteria and coccidia, and depend on these
the cecal wall, leading to peritonitis and
for full virulence. In turkeys, transmission is
involvement of other organs. The ceca
by direct cloaca! contact with infected birds
contain a yellowish green, caseous exudate
or via fresh droppings, resulting in histoor, in later stages, a dry, cheesy core. Liver_
moniasis quickly spreading throughout
lesions ai·e highly variable in appearance; m
the flock. Infection has not been shown
turkeys, they may be up to 4 cm in diameter
to spread in this manner in chickens.

and involve the entire organ. ln some cases,

Traditionally, histomoniasis has been
the liver will appear green or tan. The liver
thought of as affecting turkeys, while doing
and cecal lesions together are pathognolittle damage to chickens. However, monic. However, the liver lesions must be
outbreaks in chickens may cause high
differentiated from those of tuberculosis,
morbidity, moderate mortality, and
leukosis, avian trichomonosis, and mycosis.

extensive culling. Liver lesions tend to be

Lesions are also seen in other organs, such
less severe in chickens but often involve
as the kidneys, bursa ofFabricius, spleen,
secondary bacterial infections. Morbidity
and pancreas. Studies by PCR show that
can be especially high ip young layer or

Histomonas DNA can be found in the blood
breeder pullets. Layer flocks recover but
and in the tissues of most organs, whether
lack w1.iformity. Experin1ental infections
lesions are present or not. Histopathologic
with Histomonas of 16-wk-old layers have
examination is helpful for differentiation of
demonstrated reduced egg production
diseases.

during infection. Tissue responses to

Histomonads are intercellular, although
infection may resolve in 4 wk, but birds
they may be so closely packed as to appear
may be ca.n·iers for another 6 wk.

intracellular. The nuclei are much smaller
than those of the host cells, and the cyto

Clinical Findings: Signs of histomoniasis
plasm less vacuolated. Scrapings from .

are apparent in turkeys 7-12 days after
the liver lesions or ceca may be placed m
infection and include listlessness, reduced
isotonic saline solution for direct microappetite, drooping wings, unkempt feathers, scopic examination; Histomonas spp and yellow droppings in the later stages
must be differentiated from other cecal
of the disease. The origin of the name
flagellates. Molecular diagnosis is possible

"blackhead" is obscure and misleading, with with published PCR primers.

only a few birds displaying a cyanotic head.

Yow1g birds have a more acute disease and

Prevention and Treatment: Because
die within a few days after signs appear.

healthy chickens and gan1ebirds onen carry

Older birds may be sick for some ti.me and
the ceca.I wom1 vector, any contact between
become emaciated before death.

turkeys and other galliforms should be
avoided and care should be taken to reduce

Lesions: The primaiy lesions of histothe worm population. Worm eggs, from moniasis are in the ceca, which exhibit
contan1inated soil, can be tracked inside by
marked inflamrnat01y changes and
workers, causing infection. Althropods
ulcerations, causing a thickening of the
such as flies may also serve as mecharucal
cecal wall. Occasionally, these ulcers erode
vectors. Because H gallinarum ova can

INFECTIOUS BURSAL DISEASE

2837
survive in soil for many months or years,
using live cultures is not practical. Killed
turkeys should not be put on ground
organisms stimulate some immunity when
contaminated by chickens. Once estabgiven SC or IP but do not offer protection.

lished in a turkey flock, infection spreads

No drugs are cun-ently approved for use
rapidly without a vector through direct
as treatments for histomoniasis. Nitarsone
contact. Dividing a facility into subunits
is available for prophylaxis by feed

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using barriers can contain the outbreaks to
medication. Nitarsone is mixed with the
specific units. Histomonads that are shed
feed at 0.01875% and fed continually. A 5-day
directly into the environment die quickly.

withdrawal period is required for animals

Thus, in a turkey facility, where H eterakis is slaughtered for hwnan conswnption. Under unable to complete its life cycle, decontamimost conditions, nitarso.ne is effective, nation is not required.

although some outbreaks in turkeys on

Immunization has only been partially
medication have been reported. Historically,
successful in controlling histomoniasis, and
nitroirnidazoles such as ronidazole,
reports differ on its effectiveness. The
ipronidazole, and dimetridazole were used
immune response of turkeys to live
for prevention and treatment and were
attenuated Histomona.s requires 4 wk to
highly effective. Some of these products
develop. Vaccination of 18-wk-old pullets
can be used by veterinary presc1iption

5 wk before experimental infection has
in non-food-producing birds. Frequent
been shown to prevent a drop in egg producworming of chickens with benzirnidazole tion. Most workers have concluded that
anthelmintics helps reduce exposure to
inununization of birds against this disease
heterakid wonns that carry tl1e infection.

INFECTIOUS BURSAL DISEASE

(Gumboro disease)

Infectious bursal disease (IBO) is seen
to IBDV have been seen in several wild
in domestic chickens worldwide. It can
avian species. The contribution oflBDV
present as a clinical or subclinical disease,
to disease in these wild birds is unknown.

but irnmunosuppression and related
secondary infections are typically seen.

Clinical Findings: IBD is highly

Severity of tl1e immunosuppression
contagious; results of infection depend on
depends on the virulence of the infecting
age and breed of chicken and virulence of
virus and age of the host.

ilie virus. Infections may be subcliI1ical or
clinical. Infections before 3 wk of age are

Etiology and Transmission: IBD is
usually subcliiucal. Chickens are most
caused by a bimavi..rus (infectious bursal
susceptible to clinical disease at 3-6 wk of
disease virus; IBDV) that is most readily
age when inunature B cells populate the
isolated from the bursa ofFabricius but may bursa and maternal immunity has waned, be isolated from other organs. It is shed in
but severe infections have occurred in
tl1e feces and transferred from house to

Leghorn chickens up to 18 wk of age.

house by fomites. It is very stable and

Early subclinical infections are the most
difficult to eradicate from premises.

important fom1 of the disease because of

Two serotypes of IBDV have been
economic losses. They cause severe,
identified. The serotype 1 viruses cause
long-lasting inununosuppression due to
disease in chickens and, witlun tl1em,
destruction of immature lymphocytes in the
antige11ic variation can exist between
bursa of Fabricius, iliyrnus, and spleen. The
strains. Antigenic drift is largely responsible
hwnoral (B cell) immune response is most
for this antigenic variation, but antigenic
severely affected; the cell-mediated (T cell)

differences can also occw· through genome
i.nunune response is affected to a lesser
homologous recombination. Serotype 2
extent. Chickens inununosuppressed by
strains of the virus infect cluckens and
early IBDV infections do not respond well
turkeys but have not caused cliiucal disease
to vaccination and are predisposed to
or inununosuppression in iliese hosts.

infections with normally nonpatl1ogenic

IBDVs have been identified in otl1er avian
viruses and bacte1ia. Conunon diseases are
species, including penguins, and antibodies
usually exacerbated by IBDV infections.

2838

INFECTIOUS BURSAL DISEASE

Some strains of IBDV can cause subclinical
cloacal bursa without inflan1mation.

infections in older birds (3----6 wk old), which

Chickens that have recovered from IBDV
leads to losses from poor feed efficiency
infections have small, atrophied, cloaca]

and longer times to market. In these cases,
bursas due to the destruction and lack of

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the irnrnunosuppression is usually transient, regeneration of the bursal follicles.

and convalescent birds may recover most
or all of their hw11oral immune function.

Diagnosis: Molecular diagnostic assays

However, secondary infections that occur
are most often used to identify IBDV in
during the transient immunosuppression
diagnostic samples. They use reversecan cause significant economic losses.

transcliptase PCR to identify the viral

In clinical infections, onset of the disease
genome in bursa tissue. Sequence analysis
occurs after an incubation of3-4 days.

of the VP2 coding region has been used to

Chickens may exhibit severe prostration,
further characterize the viruses. Samples
incoordination, watery diarrhea, soiled vent
for molecula.i· diagnostic testing are
feathers, vent picking, and inflammation of
typically collected after maternal antibodies
the cloaca. F1ock morbidity is typically
have waned. IBDV may be isolated in 8- to
lOO"Ai, and mortality can range from 5%-20"Ai. 11-day-old, antibody-free chicken embryos Recovery occurs in d wk, and broiler
with inocula from birds in the early stages of
weight gain is delayed by 3--5 days. The
disease. The cholioallantoic membrane is
presence of maternal antibody will modify
more sensitive to inoculation than is the
the clinical course of the disease.

allantoic sac. Some strains ofIBDV may also

Virulence of field strains of the vi.ms
be isolated in cell cultw-es that include
va.iies considerably. Viruses that range from
chicken embryo fibroblasts, cells from the
naturally attenuated to very virulent (vv)

cloaca! bursa, and established avian and
have been obse1ved. The vvIBDV strains
man1malian cell lines. Cell culture-adapted
that can cause high mortality (>20"Ai) were
strains ofIBDV produce a cytopathic effect
first detected in Europe. They spread
and may be used for quantitative titration of
throughout the Middle East, Asia, and
the vi.ms and vi.ms-neutralization assays.

Africa, were detected in South and Central

Amelica in 1999, and in the USA in 2009.

Control: There is no treatment. Rigorous

Lesions: At necropsy, the lesions seen
disinfection of contaminated fa.i,11s after
will depend on the strain ofIBDV. For
depopulation has achieved limited success.

strains that cause a clinical disease, the

Live vaccines of chicken embryo or
cloaca] bursa is swollen, edematous,
cell-culture oligin and of varying low
yellowish, and occasionally hemorrhagic,
pathogenicity can be administered by eye
especially in birds that died of the disease.

drop, drinking water, or SC routes at 1--21

Strains ofvvIBDV cause similar cloacal
days of age. Replication of these vaccines
bursa lesions, and congestion and
and thus the in1111une response can be
hemorrhage of the pectoral and leg muscles
altered by maternal antibody, although the
can also occur. IBDV strains that cause
more virulent vaccine strains can override
subclinical disease ( sometimes referred to
higher levels of maternal antibody. Vectored
as variant strains) cause atrophy of the
vaccines that express the IBDV VP2 protein
in herpesvirus of turkeys (HVT) can be used
in ovo or at hatch. These HVT-IBD vaccines
are not affected by maternal antibodies.

Vaccines that use live-attenuated viruses
bound to antibodies (in1rnune-complex
vaccines) are also available for in ovo or
at hatch administration.

High levels of maternal antibody during
early brooding of chicks in broiler flocks

(and in some commercial layer operations)

can minimize early infection, subsequent
irnrnunosuppression, or both. Breeder
flocks should be vaccinated one or more
times during the growing period, first with
a live vaccine and again just before egg
production with an oil-adjuvanted,

Enlarged, hemorrhagic bursa of Fabricius
inactivated vaccine. Inactivated vaccines of
in a chicken infected with very virulent
chicken embryo, bursa, or cell-culture origin
infectious bursa I disease virus. Courtesy of
are available. The latter vaccines induce

Dr. Daraf J. Jackwood.

higher, more Wliform, and more persistent

LISTERIOSIS

2839
levels of antibody than do live vaccines. The

The goal of any vaccination program for
immune status of breeder flocks should be

IBD should be to use vaccines that most
monitored pe1iodically with a quantitative
closely match the antigenic profile of the
serologic test such as virus neutralization
field viruses. Diagnostic testing for the

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or ELISA. If antibody levels decrease,
genomic sequences of field strains can
hens should be revaccinated to maintain
be used to select the most appropriate
adequate inmmnity in the progeny.

vaccination program.

LISTERIOSIS

Listeriosis is caused by the bacteriwn
lateral recun1bency, ataxia, torticollis, leg

Listeria monocytogenes. Although many
paddling, opsisthotonos, paresis, and
species of birds, including chickens,
paralysis have been seen.

turkeys, pigeons, ducks, geese, canaries,
and cockatiels, are susceptible to infection,

Lesions: Birds affected with the
clinical disease in birds is rare. Generally,
septicemic fo1m of listeriosis often have
young birds are more susceptible to
extensive degeneration and necrosis of the
infection and more likely to develop clinical
myocardiwn, with splenomegaly, necrotic
disease than older birds. In chickens, the
foci in the liver, and pericarditis. Other
disease occurs sporadically as either
lesions reported in broilers include ascites
septicemia or encephalitis.

and petechial hemorrhages in the myocai�
diwn, liver, kidneys, and spleen. In the
encephalitic forn1, no gross lesions ai·e seen

Etiology, Epidemiology, and
in the brain, but histopathologic lesions ai·e

Pathogenesis: L monocylogenes
remarkable and include disseminated
is a gran1-positive, nonsporeforming,
microabscesses, extensive fibrinous
facultative intracellular, rod-shaped
tlu-ombosis, foci of hemorrhages, necrosis
bacterium. It is widely distributed and

(malacia) of the parenchyrna, perivasculai·
commonly found in the environment. In
cuffs of lyrnphocytes and macrophages, and
temperate zones, the primary habitats of
gliosis. Gran1 stain of tissues reveals typical
the organism are soil and decaying
gram-positive bacteria within the lesions.

vegetation. The organism is common

Lesions are found in the medulla oblongata,
in poorly preserved stored corn silage.

where they are generally most severe, and in

L monocytogenes has been isolated from
t11e optic lobes and cerebellwn.

the intestinal tract of healthy animals,
including different species of mammals,

Diagnosis: In the septicemic fonn, gross
birds, and fish. Transmission occurs via
lesions should arouse suspicion, and
ingestion, inhalation, or wound contamihistopathologic lesions should allow nation. In ruminants, the encephalitic form preliminary diagnosis of bacterial septiceof listeriosis develops after entry of the mia. Diagnosis is confim1ed by i.mmw10hisorganism through minor injuries in the tochemistry to demonstrate L monocy
conjunctiva or oral and nasal mucosa with
logenes in the tissues or by isolation of the subsequent migration along peripheral
organism, usually from the liver and/or
nerves to the brain. It is unknown if this
spleen in the septicemic form and brain in
same route of infection occurs in birds.

the encephalitic form. Direct culture of

Contamination of poultry farms with fecal
affected tissues, especially the brain, may
material from nearby food animal farms
not always be successful because of the low

( eg, cattle or swine farms) is an in1portant
concentration of orgailisms in affected
source of infection, especially after a rain
tissues. Recovery of L monocylogenes
or flooding. Wounds from beak trimming
increases significantly if a portion of the
and vaccine injection are possible sites of
specimen is refrigerated for 4--8 wk and
entry for the organism.

subcultured weekly. Alternatively, tissue
may be macerated or blended with a general

Clinical Findings: In the septicemic fonn
nutrient broth ( eg, trypticase soy broth,
of listeriosis, clinical signs are not specific
brain heait infusion) at a ratio of 1:10. The
and include depression, lethargy, and
broth media is incubated at 35°C (95°F) for
sudden death. In the encephalitic form,

5-7 days and examined daily for growth.

2840

LISTERIOSIS

Differential diagnoses for septicemic
trimethoprim-sulfamethoxazole. Treatlisteriosis include other bacterial septicemias ment of the encephalitic fmm is usually such as colibacillosis, pasteurellosis, and
unsuccessful. Prevention should focus on
erysipelas. For encephalitic liste1iosis,
identifying and eliminating potential sources
differential diagnoses include viral
of infection.

encephalitides, eg, Marek's disease and exotic

Newcastle disease. With the latter, neurologic

Zoonotic Risk: Listeriosis is a serious

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signs (torticollis, opisthotonos) typically
zoonotic disease. L monocylogenes is
follow high mortality in the flock, and lesions
recognized as an important foodborne
of the disease are present in visceral organs.

pathogen in people and is of great concern
to the public and poultry industry.

Treatment and Prevention: Antibio

Outbreaks of listeriosis usually follow
tics may be used successfully to treat the
exposure to raw or uncooked poultry
septicemic fonn of the disease. In vitro,
products but have also occurred after

L monocytogenes is susceptible to penicillin, contaminated ready-to-eat poultry meat tetracycline, erythromycin, gentamicin, and
products were ea.ten.

MALABSORPTION SYNDROME

(Runting-stunting syndrome, Pale bird syndrome)

Malabsorption syndrome is a transmissible

1-3 wk old. It is characterized by uneven
disease characterized by sttmted growtl1 and
growth; temporary stunting; permanent
a lack of skin pign1entation in growing
run ting; lack of pigmentation in the skin,
chickens, most commonly broiler breeds.

feet, or beak; slow feathering; broken or

Turkeys may also be affected; in these birds,
twisted feathers ("helicopter wings");
it resembles poult enteritis mortality
undigested feed in the feces; and poor feed
syndrome. The disease has been identified in
conversion ratios. Diarrhea is common
virtually all cow1tiies in which intensive poulduring the initial phases, and eating feces try production occurs. It has been associated
is seen. Other signs include lan1eness,
with several different enteric viruses and
osteodystrophy, and secondary encephaloappears to be multifactorial, although the mala.cia. Severely affected birds do not
true etiology remains to be identified. Poor
respond inrn1ediately to changes in feed
management may contiibute to the problem.

or management practices and are usually
culled from flocks before processing. The

Etiology and Transmission: The disease
nwnber affected in a flock can vary from a
has been reproduced with ba.cteiia-free
few to 900Ai.

intestinal homogenates, suggesting a viral
origin. Enteroviruses, pa.rvovi.ruses,

Lesions: The severity and type of lesions
astroviruses, calicivintses, a.rena.vin1ses,
resulting from both field and laboratory
toga.viruses, reoviruses, and rotaviruses
infections vary with the particular agents or
have been implicated. Enteroviruses,
combinations of a.gents involved. Lesions
reoviruses, and mycotoxins have been
often include enlarged proventriculi, small
considered tl1e most likely etiologic factors,
gizzards, pancreatic atrophy, and orange
although recent reports suggest an
mucus in the small-intestinal lwnen. No
impmtant role for astroviruses and wmsual
consistent microscopic lesions a.re fow1d,
pa.rvovi.ruses. A problem hampering the
although cystic lesions in the small intestine
understanding of the etiology is the inability
have been described, and sometin1es
to isolate these viruses. Because tl1e disease
changes are present in the bursa and
is seen in very y0tmg chicks, it is likely the
thynms. Encephalomalacia or rickets may
vi.ruses are ve1tically transmitted, although
be seen occasionally, preswna.bly as a result
fecal/oral spread occurs after hatching. The
of mala.bsorption or malassimilation of
involvement of feedborne mycotoxins is not nutrients.

well tmderstood.

Diagnosis: Clinical signs and postmortem

Clinical Findings: The disease is
lesions pern1it a preswnptive diagnosis.

typically recognized in broiler chicks

Because of the complex etiology and the

MYCOPLASMOSIS

2841
presence of enteric viruses in normal flocks,
and sanitation and avoidance of intercui0
laboratory investigations may be diificult to
rent disease are beneficial. No vaccines
interpret, particularly because virus culture
prevent malabsorption syndrome. Some
may be difficult or impossible. Poor early
reovirns vaccines are marketed to prevent
management of flocks ( especially feed and
the stunting and poor feed conversions due
water supply and temperature control) may
to pathogenic reoviruses. Feeds should be

VetBooks.ir
lead to a similar picture in the absence of
analyzed for dietary toxins, and high levels
specific infection.

of toxins should not knowingly be fed to
commercial poultry. Antibiotics and vitamin

Prevention and Control: There is no
supplements can be helpful.

effective treatment for severely affected
birds. Good broiler farm hygiene will reduce Zoonotic Risks: There have been no the burden of challenge caused by multiple
reported zoonotic risks associated with
infectious organisms. Good flock nutrition
malabsorption syndrome.

MYCOPLASMOSIS

Mycoplasmas are bacteria that lack a cell
resistant, although M gallisepticum causes
wall and are the smallest prokaryotes
coajunctivitis in wild house finches (and

(0.2-0.8 µm in dian1eter). They have
some sinillar species) in North An1erica.

complex nutritional requirements but will

M gallise-pticwn is the most pathogenic
grow on specialized artificial mediwn
avian mycoplasma; however, considerable
containing serwn. Growth in broth and
strain variability is manifest in a range of
on agar media is slow (5-21 days), and
host susceptibility, virulence, clinical
the small (0.1-1 mm diameter) colony
presentation, and immunologic response.

morphology typically has a "fried egg"

Integral membrane surface proteins
appearance under low magnification.

( adhesins) that attach to receptors on

Mycoplasmas do not survive for more
host cells, allowing for colonization and
than a few days outside the host and are
infection, are in1po1tant virulence factors
vulnerable to common disinfectants.

involved in antigenic variation and immtme

Several Mycoplasma species have been
evasion.

isolated from avian hosts; M gallise-pticum,

M synoviae, M meleagridis, and M iowae
are the most important. Each has

Epidemiology and Transmission:

distinctive epidemiologic and pathologic

M gallisepticwn is transmitted ve1tically
characteristics.

within some eggs (transovarian) from
infected breeders to progeny, and horizontally via infectious aerosols and through

MYCOPLASMA GALLISEPTICUM
contan1ination of feed, water, and the
environment, and by hwnan activity on

INFECTION
fomites (shoes, equipment, etc). Infection
may be latent in some birds for days to

(Chronic respiratory disease, Infectious
months, but when birds are stressed
sinusitis)

horizontal transmission may occur rapidly

M gallisepticwn is commonly involved in
via aerosols and the respiratory route, alter
the polymicrobial "chronic respiratory
which infection and clinical disease spread
disease" of chickens; in turkeys, it
through the flock. Flock-to-flock transmisfrequently results in swollen infraorbital sion occurs readily by direct or indirect
sinues and is called "infectious sinusitis."

contact from the movement of birds,

These diseases affect chickens and tui·keys
people, or fomites from infected to
worldwide, causing the most significant
susceptible flocks. Some potential
economic losses in large commercial
reservoirs of M gallise-pticum in the USA
operations, and are commonly seen in
are noncommercial (backyard) flocks,
noncommercial flocks. Infection also
multiple-age layer flocks, and some
occurs in pheasants, chukar partridges,
free-ranging songbird species. Good
peafowl, pigeons, quail, ducks, geese, and
management and biosecurity practices are
psittacine birds. Songbirds are generally
necessary to enstu-e thatM gallisepticum

2842

MYCOPLASMOSIS
infections are not introduced to commercial

Uncomplicated M gallisepticum
poultry from these and other sources. In
infections in chickens result in relatively
many outbreaks, the source of infection is
mild catarrhaJ sinusitis, tracheitis, and
unknown. Cold weather, poor air quality or
airsacculitis. E coli infections are often
crowding, concurrent infections, and some
concurrent and result in severe air sac thick

VetBooks.ir
live virus vaccinations may facilitate
ening and turbidity, with exuclative
infection, disease, and transmission.

accun1ulations, adhesive pericarditis, and

Epitheliwn of the conjw1ctiva, nasal
fibrinous perihepatitis. Turkeys develop
passages, sinuses, and trachea are most
severe mucopurulent sinusitis and varying
susceptible to initial colonization and
degrees of tracheitis and airsacculitis.

infection; however, in severe, acute disease,

Microscopically, involved mucous
infection may also involve the bronchi, air
membranes are thickened, hyperplastic,
sacs, and occasionally lungs. Once infected,
necrotic, and infiltrated with inflammatory
birds may remain carriers for life. There is a
cells. The mucosa] lamina propria contains
marked interaction (poly:microbiaJ disease)

focal areas of lymphoid hypoplasia and
between respiratory viruses, Escherichia
genninaJ center formations.

coli, and M gallisepticum in the pathogenesis and severity of chronic respiratory Diagnosis: History, clinical signs, and
disease.

typical gross lesions may be suggestive of

M gallisepticum infection. Serology by

Clinical Findings and Lesions: In
agglutination and ELISA methods are
chickens, infection may be inapparent or
conrn10nly used for stuveillance. Hemaggluresult in varying degrees of respiratory tination-inhibition is used as a confinnatory
distress, with slight to marked raJes,
test, because nonspecific false agglutination
difficulty breathing, coughing, and/or
reactions may occur, especially after
sneezing. Morbidity is high and m01tality low injection of inactivated oil-emulsion in tmcomplicated cases. Nasal discharge and
vaccines or infection with M synoviae.

conjunctivitis with frothiness about the eyes

M gallisepticum should be confirmed by
may be present. The disease is generally
isolation from swab samples of infraorbitaJ
more severe in turkeys than in chickens,
sinuses, nasal turbinates, choa.naJ cleft,
and swelling of the infraorbitaJ sinuses is
trachea, air sacs, lungs, or conjunctiva.

common. Feed efficiency and weight gains

Primary isolation is made in mycoplasma
are reduced. Commercial broiler chickens
mecliwn containing 100/o-15% serum.

and market turkeys may suffer high

Colonies on agar medimn are used for
condemnations at processing clue to
species identification by inrn1unofluoresairsacculitis. In laying flocks, birds may fail cence with species-specific antibodies.

to reach peak egg production, and the overall PCR can also be used for detection of production rate is lower than nonnaJ.

M gallisepticum DNA using swabs taken
directly from infected sites ( choana, sinuses,
trachea, air sacs) or after growth in culture.

Mycoplasma isolates must be identified
by species, because birds may also be
infected with nonpathogenic mycoplasmas.

E coli infection, Newcastle disease, avian
influenza, and other respiratory diseases

( eg, infectious bronchitis in chickens)

should be considered in the differential
diagnosis and can act as inciting or
contributing pathogens.

Treatment, Control, and Prevention:

Most strains of M gallisepticum are
sensitive to a nun1ber of broad-spectrum
antibiotics, including tylosin, tetracyclines,
and others but not to penicillins or those that
act on the cell wall. Tylosin or tetracyclines
have been commonly used to reduce egg
transmission or as prophylactic treatment to
prevent respiratory disease in broilers and

Turkey infected with M gallisepticum has
clear-mucoicl and dried nasal exudate and a
turkeys. Antibiotics may alleviate the clinical
swollen infraorbital sinus. Courtesy of North
signs and lesions but do not elin1inate

Carolina State University Poultry Health Management.

infection. Regulations on the use of

MYCOPLASMOSIS

2843
antibiotics in food animals are rapidly
swine) and nicotinamide adenine dinucleoevolving and should be consulted before use. tide (NAD) are required for growth in Prevention is based largely on obtaining
mycoplasma media.

chicks or poults from M gallisepticum-free

M synoviae isolates vary widely in
breeder flocks. Eradication of M gallisepti
virulence, and suspected virulence factors

VetBooks.ir
cum from chicken and turkey commercial
include acll1esins, sialidase, nitric oxide, cell
breeding stock is well advanced in the USA
invasion, and antigenic variation and
because of control progran1s coordinated
in1mune evasion.

by the National Poultry Improvement Plan.

The most effective control program is to

Epidemiology and Transmission:

establish M gall'isepticum-free breeder

M synoviae is egg transmitted (transovarflocks, managed and maintained under good ian), but the infection rate in breeder hens is biosecurity to prevent introductions, and
low, and some hatches of progeny may be
monitored regularly with serology to
free of infection. Horizontal transmission
continually confirm infection-free status. In
is similar to that of M gallisepticum ( see valuable breeding stock, treatment of eggs
p 2841), primarily via the respiratory tract,
with antibiotics or heat has been used to
with direct and indirect routes.

eliminate egg transmission to progeny.

The incidence of M synoviae infection

Medication is not a good longterm control
in commercial poultry in the USA has
method but has been of value in treating
decreased because of the National Poultry
individual infected flocks.

Improvement Plan control programs

Laying chickens free of M gallisepticum
implemented for chicken and tmkey
are desirable, but infection in commercial
breeders. However, M synoviae infections
multiple-age egg farms where depopulation
of multiple-age layer flocks are common and
is not feasible is a problem. Inactivated,
may contribute to decreased egg production.

oil-emulsion bacterins are available and help
prevent egg production losses but not

Clinical Findings and Lesions: Although
infection. Three live vaccines CF-strain, ts-11,
slight rales may be present in birds with
and 6/85) have been licensed in the USA for

M synoviae respiratory infection, usually
use during the growing phase to provide
no signs are noticed. Birds under stress or
some protection dwing lay and may be used
with concmrent infections are more likely
in some areas with permission of the State
to be clinically affected. The first signs of

Veterinarian. F-strain is of low virulence in
infectious synovitis include pale-bluish
chickens but is fully virulent for turkeys.

head parts and lan1eness in many birds

Vaccinated chickens remain carriers of
with a tendency to sit. The more severely

F -strain, and in1munity lasts through the
affected birds are depressed and found
laying season. Vaccine strains ts-11 and 6/85
resting around feeders and waterers. flocks
are less virulent, offer the advantage of
and footpads are swollen, and sternal
improved safety for nontarget birds, and
bursitis (breast blisters) may be seen.

are widely used in commercial layers. A

Morbidity is usually low to moderate
commercial recombinant fowlpox-M gal
with mortality of 1 % -1 (JOA,. Effects on egg
lisepticum vaccine has been marketed.

production are usually not apparent,

MYCOPLASMA SYNOVIAE

INFECTION

(Infectious synovitis)

M synoviae was first recognized as an acute to chronic infection of chickens and turkeys
that produced an exudative tendinitis and
synovitis (infectious synovitis); it now
occurs most conunonly as a subclinical
infection of the upper respiratory tract,
especially in multi-age layer flocks. M synoviae infection is also a complication of airsacculitis in association with Newcastle
disease or infectious bronchitis. It is
distributed worldwide and is seen primarily
in chickens and turkeys, but ducks, geese,

Swollen foot pad and swollen hock joint in
guinea fowl, parrots, pheasants, and quail
chickens with infectious synovitis (M synoviae
infection).

may also be susceptible. Serun1 (preferably

Courtesy of American Association of Avian

Pathologists.

2844

MYCOPLASMOSIS
but instances of transient egg production

MYCOPLASMA MELEAGRIDIS
drops have occurred in layer flocks.

INFECTION

Respiratory lesions may be absent, or
consist of mild mucoid tracheitis or sinusitis M meleagridis causes an egg-transmitted with airsacculitis when birds are stressed

(transovarian) disease of breeder turkeys
from poor air quality or challenged with
that primarily in1pacts progeny with

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Newcastle disease or infectious bronchitis.

airsacculitis but has also been associated

Early in infectious synovitis, a creamy to
with decreased hatchability from infected
viscous yellow-gray exudate is present
breeder flocks and with poor growth and
in most synovial structures but most
skeletal abnormalities in progeny.

commonly seen in swollen hock and wing

M rneleagridis is strongly host-specific
joints. In chronic cases, this exudate may
for turkeys (not for chickens), and with
become inspissated; livers are enlarged and
successful control programs (National
sometimes green, spleens are enlarged,

Poultry In1provernent Plan in the USA)

kidneys are enlarged and pale, and birds
major turkey prin1ary breeders have
may be weak and thin with breast blisters
eliminated the infection from their stocks,
from sternal recw11bency.

producing eggs and poults free of

M meleagridis.

Diagnosis: Skeletal abnormalities and
trauma must be eliminated as the cause of

Epidemiology and Transmission:

lan1eness. Differential diagnoses include

Before control programs, turkeys
viral tenosynovitis as well as staphylococcal worldwide were commonly infected with and other bacterial joint infections.

M meleag1idis. Infection of progeny

A presW11ptive diagnosis based on clinical occurs primarily through vertical ( egg) signs and gross lesions should be confm11ed
transmission with rates that vary over the
by laboratory tests. Serw11 plate agglutinalaying season. At the hatchery, organisms tion or ELISA are used to detect M synoviae
may be spread horizontally via aerosols
antibodies, but cross-reactions with M galli
from the respiratory tract or to the vent on
septicum and other nonspecific reactions
contaminated hands during vent-sexing.

may occur. These reactors are confumed as

Respiratory tract infection also leads to
seropositive by hemagglutination-inhibition
horizontal transmission among birds
or by culture, isolation, and identification of
within yom1g growing flocks and may be a
the organism. PCR may be used to rapidly
factor in the spread to flocks previously
detectM synoviae DNA from pre- or
free of infection (flock-to-flock transmispostmortem specin1ens. In tmkeys, the sion). In some infected turkeys, organisms
agglutination test for M synoviae may not
localize in the reproductive tract; thus, the
be reliable, especially in birds with
source of vertical transmission in hens is
predominantly respiratory infection.

organisms incorporated in eggs. In toms,
the phallus and adjacent tissues (cloaca)

Treatment, Control, and Prevention:

become infected and contaminate the

The National Poultry Improvement Plan
semen. Artificial insemination of turkey
coordinates control and serology-based
hens with infected semen is an additional
smveillance programs for M synoviae
in1portant method of transmission.

similar to those for M gallisepticum.

Additionally, indirect transmission may

These programs have resulted in eradicaresult from management pra.ctices such tion of the infection in most prin1ary
as vaccination, whereby mycoplasmas
breeder flocks of chickens and turkeys in
are carried manually from infected to
the USA. Chicks and poults should be
noninfected turkeys via contaminated
obtained from M synoviae-free breeders
hands, clothing, and equipment.

and raised with biosecurity to prevent

The marked difference in the pathointroduction. Antibiotics in the feed may genicity of various strains of M melea
be beneficial in prevention of synovitis but
gridis results in variable clinical
are expensive and not very effective in
manifestations, with airsacculitis in
established cases. When M synoviae
poults being the most common. High
involvement in airsacculitis is an anticiprevalence of airsacculitis with low pated problem, preventive antibiotic
mortality in poults suggests a highly
therapy during the time of respiratory
evolved host-parasite relationship.

reaction to Newcastle disease and
infectious bronchitis vaccines may be

Clinical Findings and Lesions: Egg
helpful. A live temperature-sensitive
transmission and embryo infection reduces
vaccine (MS-H) is commercially available
hatchability (due to late embryo mortality),
and permitted in some areas.

po ult quality, and growtl1 rate. Only mild

MYCOPLASMOSIS 2845
respiratory signs may be seen despite high

MYCOPLASMA IOWAE
rates of airsaccuJitis in poults from infected INFECTION
hens. Egg-borne infections may impact
early rapid growth of hockjoints,

M iowae infection of turkey breeder hens
periarticular tissues, cervical vertebrae,
has been most commonly associated with
and adjacent bone, producing skeletal
late embryo mortality and reduced

VetBooks.ir
abnonnalities such as crooked (wry) necks
hatchability and occasionally with a low
or leg deforn1ities. Adult breeders usually
prevalence of leg abnom1alities in their
show no signs of venereal or respiratory
young progeny. M 'iowae requires enriched
infection.

media with cholesterol, similar to those

Hatched poults may have airsacculitis
used for other avian mycoplasmas for
with variable degrees of thickening,
culture and isolation, but is resistant to
turbidity, foamy yellow exudate, and
bile salts.

caseous flecks. These lesions recede with
age. Poults with WIY neck may have cervical Epidemiology and Transmission:

airsacculitis and osteomyelitis of adjacent

M iowae is egg transmitted (transovarian)

vertebrae. The generalized skeletal lesions
in turkeys, and horizontal transmission
that may develop in poults 1-6 wk old are
with slow spread within a flock may occur.

characterized by chondrodystrophy or by

Antigenicity and virulence vary considervarus deforn1ities and perosis.

ably an1ong M iowae strains. Infection

Microscopic lesions in hens consist of
rates in turkey flocks in Europe and N mth
lymphocytic foci in the fimbria, uterus, and

Ame1ica have been reduced by intensive
vagina, with plasma cells and heterophils in
eradication efforts in certain primary
the lamina propria of the reproductive tract.

breeding stocks, butM iowae is not

Infected embryos and young pouJts show
currently included in the National Poultry
inflammatory lesions of pneumonia and

Improvement Plan. It is a relatively
exudative airsacculitis.

uncommon infection of chickens and
has been reported in geese.

Diagnosis: A high prevalence of

Chickens and turkeys experimentally
airsacculitis in day-old poults suggests
inoculated have shown airsacculitis,

M meleagridis infection. Serology by
stunting, poor feathering, and leg lesions.

agglutination (tube or plate) or ELISA can

These effects are rarely recognized in the
demonstrate antibody. Confirn1ation was
field, except for some outbreaks in young
generally by hemagglutination-inhibition
turkeys with skeletal lesions.

serology or by culture, isolation, and
identification of the organism. PCR is now

Clinical Findings and Lesions: Affected
used to detect M meleagridis DNA from
turkey breeder flocks show no clinical signs
pre- or postmortem specimens. M galli
other than reduced hatchability (usually
septicum, other Mycoplasma spp, and mixed infections (polyrnicrobial disease)

must be considered in the differential
diagnosis.

Treatment, Control, and Prevention:

Turkey eggs or pouJts should be obtained
from breeder flocks free of'M meleagridis
and monitored by serology and/or by
exan1ining pipped embryos or cull poults
for airsacculitis. Semen used for insemination must be free of M meleagridis.

Dipping eggs in tylosin or other antibiotic
reduces the incidence of transmission in
infected flocks. However, this practice
has been generally eliminated with the
eradication of M meleagridis from p1imary

Mycoplasma iowae infection, turkeys. (A)

breeder flocks and is only used by

Normal vs chondrodystrophic legs (left) of
multiplier breeders when there is an

28-day-old turkeys; note short, thick shanks
outbreak. Injection of a suitable antibiotic
and toes. (B) Legs of a 42-day-old turkey
at 1 day of age or water medication for the
showing bilateral chondrodystrophy; note
first 5-10 days appeared to reduce infection short, thick legs with enlarged hocks and marked medial bowing of both legs.

and airsacculitis caused by M meleagridis

Courtesy
of North Carolina State University Poultry Health
and in1prove weight gain.

Management.

2846

MYCOPLASMOSIS

2%-5%) due to embryo mortality in the last

Diagnosis: In turkeys, M iowae infection 10 days of incubation. In many flocks, the
should be considered in cases of late
hatchability returns to nonnal after 1-2 mo.

embryo mortality and decreased hatchabil

Dead turkey embryos are edematous,
ity and in young turkeys with leg and
congested, and stunted; they may have
vertebral chondrodystrophy. M meleagridis

VetBooks.ir

"clubbed down." Poul ts experin1entally
and nutrient deficiencies are the top
challenged in ovo or at 1 day of age
differential diagnoses for these conditions,
developed various skeletal defom1ities such respectively.

as rotated tibia, deviated toes, chondrodys

Turkeys develop only a weak antibody
trophy, or erosion of the aiticular cartilage
response to M iowae, and no reliable
of the hock joint. Chicks experimentally
serologic test is available. Diagnosis relies
challenged at 1 day of age developed
on cultme, isolation, and identification of
tenosynovitis and ruptured tendons.

the organism, or on detection of M iowae

Natural infections in several young

DNA byPCR.

commercial turkey flocks were associated
with skeletal lesions consistent with

Treatment, Control, and Prevention:

chondrodystrophy, characterized by leg

The best method of control and prevention
and vertebral deformities. Microscopic
is to establish and maintain turkey breeder
skeletal lesions were characterized by
flocks free of M iowae. Surveillance is
excess cartilage matrix and disorganizachallenging because serology is unreliable, tion of chondrocytes, features of osteobut flock monitming by PCR and strict chondrosis.

biosecwity should help.

MYCOTOXICOSES

A mycotoxicosis is a disease caused by
hatchability. Some effects ai·e directly
a natural toxin produced by a fungus.

attributable to toxins, whereas others

In poultry, this usually results when
are indirect, such as reduced feed intake.

toxin-producing fungi grow in grain and

Susceptibility to aflatoxins vai·ies, but in
feed. Hundreds of mycotoxins have been
general, ducklings, turkeys, and pheasants
identified, and many are pathogenic.

ai·e susceptible, while chickens, Japanese

Mycotoxins may have additive or
quail, ai1d guinea fowl are relatively
synergistic effects with other natural
resistant.

toxins, infectious agents, and nutritional

Clinical signs vary from general
deficiencies. Many are chemically stable
untluiftincss to high morbidity and
and maintain toxicity over tin1e . .(See also
mortality. At necropsy the lesions ai·e found

MYCOTOXICOSES, p 3005.)

mainly in the liver, which can be reddened

The significance of mycotoxin problems
due to necrosis and congestion or yellow
in poultry is probably considerable but yet
due to lipid accumulation. Hemorrhages
insidious. The in1pact on poultry production
may occm in liver and other tissues. In
may be best measured indirectly by the
clu·onic aflatoxicosis, the liver becomes
improvements in weight gain, feed
yellow to gray and atrophied. The aflatoxins
efficiency, pigmentation, egg production,
are carcinogenic, but twnor fom1ation is
and reproductive perfonnance that
rare with the natural disease, probably
accompany effective control programs
because the birds do not live long enough
for mycotoxins.

for this to occm.

Aflatoxicosis: The aflatoxins are toxic

Fusariotoxicosis: The genus Fusarium
and carcinogenic metabolites of Aspergil
produces many mycotoxins iitjurious to
lusjlavus, A para.siticus, and others.

poultry. The trichothecene mycotoxins

Aflatoxicosis in poultry prirnaiily affects
produce caustic and radiomin1etic patterns
the liver but can involve immunologic,
of disease exemplified by T-2 toxin and
digestive, and hematopoietic fLU1ctions.

diacetoxyscirpenol (DAS). Deoxynivalenol

Aflatoxin can adversely affect weight gain,

(vomitoxin, DON) and zearalenone ai·e comfeed intake, feed conversion efficiency, mon trichothecene mycotoxins that are
pigmentation, processing yield, egg
relatively nontoxic for poultry but may
production, male and female fertility, and
cause disease in pigs.

MYCOTOXICOSES

2847

Fusariotoxicosis in poultry caused by
atrophied and disfigured. Vesicles and
the t1ichothecenes results in feed refusal,
ulcers develop on the shanks of the legs and
caustic iajury of the oral mucosa and areas
on the tops and sides of the toes. In laying
of the skin in contact with the mold, acute
hens, feed consun1ption and egg production

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digestive disease, and iajury to the bone
are reduced.

marrow and immune system. Lesions
include necrosis and ulceration of the oral

Citrin in Mycotoxicosis: Citrinin is
mucosa, reddening of the GI mucosa,
produced by Penicillium and Aspergillus mottling of the liver, atrophy of the spleen
and is a natural contaminant of com, rice,
and other lymphoid organs, and visceral
and other cere'al grains. Citrinin causes a
hemorrhages. In laying hens, decreased
diw·esis that results in watery fecal
egg production can be accompanied by
droppings and reductions in weight gain.

depression, recumbency, feed refusal, and

At necropsy, lesions are generally mild
cyanosis evident in the comb and wattles.

and involve the kidney.

Ducks and geese develop necrosis and pseu

Oosporein Mycotoxicosis: Oosporein
domembranous inflammation of the esophais a mycotoxin produced by Chaetornium gus, proventriculus, and gizzard.

spp that causes gout and high mo1tality in

Other Fusmium mycotoxins cause
poultry. Chaetomium are found on feeds
defective growth of long bones. The
and grains, including peanuts, rice, and
fumonisin mycotoxins produced by
com. Oosporein mycotoxicosis is seen

Fverticillioides (fom1erly F moniliforme) as visceral and articular gout related to
in1pair feed conversion without causing
inlpaired renal function and increased
specific lesions. Moniliformin is also
plasma concentrations of uric acid.

produced by F verticillioides and is

Chickens are more sensitive to oosporein
cardiotoxic and nephrotoxic in poultry.

than turkeys. Water conswnption increases

F verticillioides causes ear rot, kernel rot, during intoxication, and fecal droppings
and stalk rot of unharvested com and is
become Wlformed and fluid.

found in stored high-moisture shelled com
and on other grains that appear sound.

Cyclopiazonic Acid: Cyclopiazonic acid
is a metabolite ofAspergillus.fl,avus, which Ochratoxicosis: Ochratoxins are quite
is the predominant producer of aflatoxin in
toxic to poultry. These nephrotoxins are
feeds and grains. In chickens, cyclopiazonic
produced chiefly by Penicillium viridica
acid causes in1paired feed conversion,
tum and Aspergillus ochraceus in grains decreased weight gain, and mortality.

and feed. Ochratoxicosis causes prinlarily

Lesions develop in the proventriculus,
renal disease but also affects the liver,
gizzard, liver, and spleen. The proventricuin1mune system, and bone marrow. Severe lus is dilated, and the mucosa is thickened
intoxication causes reduced spontaneous
and sometinles ulcerated.

activity, huddling, hypothermia, diarrhea,
rapid weight loss, and death. Moderate

Sterigmatocystin: Sterigmatocystin, a
intoxication impairs weight gain, feed
biogenic precursor to aflatoxin, is hepatoconversion, pigmentation, carcass yield, toxic and hepatocarcinogenic but is less
egg production, fertility, and hatchability.

common than aflatoxin.

Ergotism: Toxic ergot alkaloids are

Diagnosis: Mycotoxicosis should be
produced by Claviceps spp, which are fungi
suspected when the history, sigris, and
that attack cereal grains. Rye is especially
lesions are suggestive of feed intoxication,
affected, but also wheat and other leading
and especially when moldy ingredients or
cereal grains. The mycotoxins form in the
feed are evident. Toxin exposw-e associated
sclerotiwn, a visible, hard, dark mass of
with conswnption of a new batch of feed
mycelium that displaces the grain tissue.

may result in subclinical or transient

Within the sclerotiwn are the ergot
disease. Chronic or intennittent exposure
alkaloids, which affect the nervous system,
can occur in regions where grain and feed
causing convulsive and sensory neurologic
ingredients are of poor quality or when
disorders; the vascular system, causing
feed storage is substandard or prolonged.

vasoconstriction and gangrene of the

Impaired production can be a clue to a
extremities; and the endocrine system,
mycotoxin problem, as can improvement
including new-oendocrine control of the
because of correction of feed management
anterior pituitary gland.

deficiencies.

In chicks, the toes become discolored due

Definitive diagnosis involves detection
to vasoconstriction and ischemia. In older
and quantitation of the specific toxin(s).

birds, vasoconstriction affects the comb,

This can be difficult because of the rapid
wattles, face, and eyelids, which become
ai1d high-volwne use of feed ai1d ingredients

2848

MYCOTOXICOSES
in poultry operations. Diagnostic laboratohave a sparing effect but are not practical ries differ in their respective capabilities
for larger production units.

to test for mycotoxins and should be
contacted before sending samples. Feed

Prevention: Prevention of mycotoxicoses
and also birds that are sick or recently dead
should focus on using feed and ingredients
should be submitted for testing. A necropsy
free of mycotoxins and on management

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and related diagnostic tests should
practices that prevent mold growth and
accompany feed analysis if mycotoxicosis
mycotoxin formation during feed transport
is suspected. Concmrent diseases can
and storage. Regular inspection of feed
adversely affect production and should be
storage and feeding systems can identify
considered. Sometimes, a mycotoxicosis
flow problems, which allow residual feed
is suspected but not confirmed by feed
and enhance fungal activity and mycotoxin
analysis. In these situations, a complete
formation. Mycotoxins can form in decayed,
laboratory evaluation can exclude other
crusted feed in feeders, feed mills, and
significant diseases.

storage bins; cleaning and co1Tecting the

Feed and ingredient samples should be
problem can have inunediate benefits.

properly collected and promptly submitted

Temperature extremes cause moisture
for analysis. Mycotoxin fonnation can be
condensation and migration in bins and
localized in a batch of feed or grain. Multiple promote mycotoxin fonnation.

samples taken from different sites increase

Ventilation of poultry houses to avoid
the likelihood of confinning a mycotoxin
high relative hun1idity also decreases the
formation zone (hotspot).

moisture available for fungal growth and

San1ples should be collected at sites of
toxin formation in the feed. Antifungal
ingredient storage, feed manufacture and
agents added to feeds to prevent fungal
transport, feed bins, and feeders. Fungal
growth have no effect on toxin already
activity increases as feed is moved from
formed but may be cost-effective in
the feed mill to the feeder pans. San1Ples
coajunction with other feed management
of 500 g ( l lb) should be collected and
practices. Organic acids (propionic acid,
submitted in separate containers. Clean

500-1,500 ppm [0.5---1.5 g/kg]) are effective
paper bags, properly labeled, are adequate.

inl1ibitors, but the effectiveness may be

Sealed plastic or glass containers are
reduced by the particle size of feed
appropriate only for short-tenn storage and
ingredients and the buffering effect of
transport, because feed and grain rapidly
certain ingredients. Sorbent compounds
dete1iorate in airtight containers.

such as hydrated sodium calcium
alun1inosilicate (HSCAS) effectively bind

Treatment: The toxic feed should be
and prevent absorption of aflatoxin.

removed and replaced witb unadulterated

Esterified glucomannan, derived from the
feed. Concmrent diseases should be treated
cell wall of the yeastSaccharomyces
to alleviate disease interactions, and
cerevisiae, is protective against aflatoxin substandard management practices must

B1 and ochratoxins. It reduces toxicity
be corrected. Some mycotoxins increase
through the binding and reduction in
requirements for vitanuns, trace minerals
bioavailability of fumonisins, zearalenone,

( especially seleniun1), protein, and lipids
and T-2 toxin. Various other fennentation
and can be compensated for by feed
products, algae and plant extracts, and
supplementation and water-based
microbial feed additives have demonstrattreatment. Nonspecific toxicologic ed ability to bind or degrade mycotoxins
therapies using activated charcoal
and may be applicable and appropriate for

( digestive tract adsorption) in the feed
the situation.

NEOPLASMS

Depending on whether the etiologic agent
of poultry: Marek's disease, caused by a
is known, neoplasms of poultry are divided
herpesvirus, and avian leukosis/sarcoma
into two main categories: virus-induced
and reticuloendotheliosis, caused by
neoplasms and neoplasms of unknown
retroviruses. While these neoplastic
etiology. There are three economically
diseases cause economic losses from tumor
important virus-induced neoplastic diseases mortality and poor performance, some of

NEOPLASMS

2849
them have served as highly suitable models
virulent Marek's disease virus strains and is
to study neoplasia.

further divided into pathotypes, designated

A rare neoplastic disease of turkeys
as mild (m), virulent (v), very virulent (vv),
lmown as lymphoproliferative disease that
and very virulent plus (vv+ ). Gallid
has been repo1ted in Europe and Israel is
herpesvirus 3 (MDV-2) and Meleagrid
induced by a retrovirus that is distinct from
herpesvirus 1 (turkey herpesvirus, MDV-3)

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both the leukosis/sarcoma and reticuloenrepresent a virulent virus strains isolated dotheliosis viruses. Although reports
from chickens and turkeys, respectively,
suggest that lymphoproliferative disease
and are commonly used as vaccines against
has recently been detected by PCR in a

Marek's disease.

small number of wild turkeys in the USA,
incidence of the disease has always been

Transmission and Epidemiology:

sporadic and therefore is not discussed in

The clisease is highly contagious and readily
this chapter.

transmitted an1ong chickens. The virus

Neoplasms of w1lmown etiology are
matures into a fully infective, enveloped
classified according to their morphologic
form in the epitheliw11 of the feather follicle,
characteristics; they include a wide variety
from which it is released into the envir·onof benign and malignant neoplasms. Of ment. lt may survive for months in poultiy
these twnors, only dermal squamous cell
house litter or dust. Dust or dai1der from
carcinoma (avian keratoacanthoma),
infected chickens is particulai'ly effective in
multicentric histiocytosis, and adenocai�
transmission. Once the virus is introduced
cinoma are discussed in this chapter.

into a chicken flock, regardless of vaccination status, infection spreads quickly from MAREK'S DISEASE
bird to bird. Infected chickens continue to
be carriers for long periods ai1d act as

Chickens are the most impo1tant natural
sources of infectious virus. Shedding of
host for Marek's disease virus, a highly
infectious virus can be reduced, but not
cell-associated but readily transmitted
prevented, by prior vaccination. Unlike
alphaherpesvirus with lymphotropic
virulent strains of Mai·ek's disease virus,
properties of gainmaherpesviruses. Quail
which ai·e highly contagious, turkey
can be naturally infected, and turkeys can
herpesvirus is not readily ti·ansmissible
be infected experimentally. However,
ainong chickens (although it is easily
severe clinical outbreaks of Mare k's disease
transmitted ainong turkeys, its natural
in commercial turkey flocks, with mortality
host). Attenuated Mai·ek's disease virus
from tumors reaching 400h-800A, between
strains vary greatly in their trai1smissibility

8 and 17 wk of age, were reported in France,
an1ong chickens; the most highly attenuated

Israel, and Germany. In some of these cases,
ai·e not transmitted. Mai·ek's disease virus is
tl1e affected turkey flocks were raised in
not ve1tically transmitted.

proximity to broilers. Turkeys ai·e also
commonly infected with turkey herpesvirus

Pathogenesis: Currently, four phases of

(HVT), an avirulent strain related to Mai·ek's
infection in vivo ai·e recognized: 1) early
disease virus that is commonly used as a
productive-restrictive virus infection

Mai·ek's disease vaccine in chickens. Other
causing ptimarily degenerative chai1ges,
birds and marnmals appeai· to be refractory

2) latent infection, 3) a second phase of
to the disease or infection.

cytolytic, productive-restrictive infection

Mai·ek's disease is one of the most
coincident witl1 pennanent immunosupubiquitous avian infections; it is identified pression, and 4) a proliferative phase
in chicken flocks worldwide. Every flock,
involving nonproductively infected
except for those maintained w1der strict
lymphoid cells that may or may not progress
pathogen-free conditions, is presw11ed to
to the point of lymphoma formation.

be infected. Although clinical disease is

Productive infection may occur transiently
not always appai·ent in infected flocks, a
in B lymphocytes within a few days after
subcli.nical decrease in growth rate and egg
infection with virulent Marek's disease virus
production may be economically importailt.

strains and is characterized by antigen
production, which leads to cell death.

Etiology: Mare k's disease virus is a

Because few if any virions are produced,
member of the genus M ardivirus within the this has also been termed a restrictivesubfainily Alphal1e1pesvirinae. Witllin the productive infection. Productive infection
genusMardivirus ai·e tlu·ee closely related also occurs in the feather follicle epithespecies previously designated as three liwn, in which enveloped virions ai·e
serotypes of Mare k's disease virus. Gallid
produced. Latent infection of activated
herpesvirus 2 (MDV-I) represents all

T cells is responsible for tl1e longterm

2850

NEOPLASMS
carrier state. No antigens are expressed, but
follicles ( conunonly termed skin leukosis)

virus can be recovered from such lymphomay be noted in broilers after defeathering cytes by co-cultivation with susceptible
during processing and are a cause for
cells in tissue cultures. Some T cells,
condemnation. The bursa is only rarely
latently infected with oncogenic Marek's
twnorous and more frequently is atrophic.

disease virus strains, undergo neoplastic

Histologically, the lesions consist of a mixed

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transformation. These transfonnecl cells,
population of small, medium, and large
provided they escape the immune system of
lymphoid cells plus plasma cells and large
the host, may multiply to form characterisanaplastic lymphoblasts. These cell tic lymphoid neoplasms. Cell-mediated
populations undoubtedly include tumor
and hun1oral imrnw1e responses are both
cells and reactive inflan1matory cells. When
directed against viral antigens, with
the bursa is involved, the tun10r cells
cell-mediated inununity probably being
typically appear in interfollicular areas.

the most in1portant.

Diagnosis: For the diagnosis of Marek's

Clinical Findings: The incidence of
disease, it is critical to diagnose the tumors

Mare k's disease is quite variable in
and not the infection because Marek's
commercial flocks and depends on strain
disease is considered ubiquitous within
and dose of virus, age at exposure, maternal
conm1ercial poultry flocks. Usually,
antibody, host gender and genetics, strain
diagnosis is based on enlarged nerves ar1d
and dose of vaccine virus, and several
lyn1phoid tumors in various viscera. The
environmental factors, including stress. In
absence of bursa.I tumors helps distinguish
addition to lymphoid neoplasms, Marek's
this disease from lymphoid leukosis (see
disease virus can also induce other clinically below), although the presence of bursa.I distinct disease syndromes, including
tumors does not exclude Mar·ek's disease.

transient paralysis, early mortality

Mar·ek's disease car1 develop in chickens as
syndrome, cytolytic infection, atheroscleroyoung as 3 wk old, whereas lymphoid sis, and persistent neurologic disease.

leukosis typically is seen in chickens >14 wk

Typically, affected birds show only
old. Reticuloendotl1eliosis, although rare,
depression before death, but a transient
car1 easily be confused witl1 Marek's disease,
paralysis syndrome has been associated
because both diseases feature enlarged
with Marek's disease; chickens become
ne1ves and T-cell lymphomas in visceral
ataxic for periods of several clays and then
organs. A diagnosis based on typical gross
recover. This syndrome is rare in inmmlesions may be confirmed histologically, or nized birds. Death is usually the result of
preferably by demonstration of predomiparalysis, rendering the birds unable to nar1t T -cell populations ar1d Marek's viral
reach food and water.

DNA in lymphomas by histochemistry ar1d

Lesions: Enlarged nerves are one of the

PCR, respectively. There is a quantitative
most consistent gross lesions in affected
association between viral load ar1cl Marek's
birds. Various peripheral nerves, but
disease tun1ors; most tumor-bearing
particularly the vagus, brachial,.and sciatic,
chickens have high viremia titers and ar·e
become enlarged and lose their striations.

usually PCR positive. Thus, the demonstra

Diffuse or nodular lymphoid twnors may be
tion of high quar1tities of virus, viral DNA,
seen in various organs, particularly the liver,
or viral ar1tigens in twnor cells ar1d the
spleen, gonads, heart, lung, kidney, muscle,
exclusion of other relevant tun10r viruses
and proventriculus. Enlar·ged feather
should be sufficient for a specific diagnosis
ofMarek's disease. Furthennore, Marek's
disease lymphomas usually lack evidence of
clonally integrated avian retroviruses or
alteration of the cellular oncogene c-myc.

Control: Vaccination is the central
strategy for the prevention ar1d control of

Mar·ek's disease. The efficacy of vaccines
can be improved, however, by strict
sarutation to reduce or delay exposw·e and
by breeding for genetic resistance. Probably
the most widely used vaccine consists of
turkey herpesvirus (HVT), which has seen

Typical presentation of leg paresis in a
rapidly increased use as a backbone in
chicken with Marek's disease. Courtesy of
recombinar1t vaccines featuring the

Dr. Jean Sander.

insertion of genes from other poultry

NEOPLASMS

2851
viruses, such as Newcastle disease virus

Members of this RNA group of viruses

(seep 2856), infectious bursal disease virus have sinillar physical and molecular

( see p 2837), or infectious laryngotracheitis characteristics and share a common
virus (seep 2912). These recombinant
group-specific antigen. Detection of the
vaccines offer protection against both
major antigen (p27) present in the core of

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Marek's disease virus and the inserted virus.

leukosis/sarcoma viruses fonns the basis of

Bivalent vaccines consisting of HVT and
several diagnostic tests. Lymphoid leukosis
either the SB-1 or 3018/1 strains of Gallid
occurs naturally only in chickens. Experiherpesvirus 3 have been used to provide mentally, some of the viruses of tl1e leukosis/
additional protection against challenge with
sru·coma group can infect and produce
virulent Marek's disease virus isolates. The
tumors in otl1er species of birds or even
most protective commercial vaccine
man11nals. The infection is known to exist in
currently available appears to be CVI988/
viltually all chicken flocks except for some

Rispens, an attenuated Marek's disease

SPF flocks from which it has been eradivirus strain that is also commonly mixed cated. Tumor mortality commonly accounts
with HVT at vaccination. Because vaccines
for -lo/o-2"A, of birds, with occasional losses are administered at hatching and require
of ,c20%. Subclinical infection, to which most

1-2 wk to produce an effective immunity,
flocks are subject, decreases several
exposure of chickens to virus should be
important performance traits, including egg
minimized dUiing the first few days after
production and quality. The frequency of
hatching.

infection has been reduced substantially in

Vaccines are also effective when
the primary breeding stocks of several
administered to embryos at the 18th day
commercial poultry breeding companies,
of incubation. In ovo vaccination is now
particularly egg-type breeders. In recent
performed by automated technology and is
years this control program has expanded,
widely used for vaccination of commercial
and infection has become infrequent or
broiler chickens, mainly because of reduced absent in certain commercial flocks. The labor costs and greater precision of vaccine
frequency of lymphoid leukosis twnors even
administration.

in heavily infected flocks is typically low

Proper handling of vaccine during

( <4%), and disease is often inapparent. As
thawing and reconstitution is crucial to
much as 1.5% excess mmtality per wk has
ensure that adequate doses are adminisbeen reported in commercial broile1°breeder tered. Cell-associated vaccines are generally flocks naturally infected with subgroup more effective than cell-free vaccines,

J avian leukosis virus.

because they are neutralized less by
maternal antibodies. Under typical

Etiology: Lymphoid leukosis is caused by
conditions, vaccine efficacy is usually >909'o.

certain members of the leukosis/sarcoma

Since the advent of vaccination, losses from
group of aviru1 retroviruses. Isolates that can

Mare k's disease have been reduced
induce lymphoid leukosis in chickens are
dramatically in broiler and layer flocks.

con11nonly called avian leukosis viruses and

However, disease may become a serious
are divided into subgroups A, B, C, D, and J,
problem in individual flocks or in selected
on the basis of differences in their viral
geographic areas ( eg, the Delmruva broiler
envelope glycoproteins, which determine
industry). Of the many causes proposed for
antigenicity, viral interference patterns with
tl1ese excessive losses, early exposure to
members of the same and different
very virulent virus strains appears to be
subgroups, and host range. Subgroups A and
among the most important.

B are most prevalent in western countries.

Since the initial isolation of subgroup J avian

LYMPHOID LEUKOSIS
leukosis virus in England, the virus has been
isolated from broile1�breeder stocks that
expe1ience myeloid neoplasms (myelocy

(Avian leukosis)

toma) in many other countries. A sixth

Under natural conditions, lymphoid
subgroup (E) designates nononcogenic
leukosis has been the most common fom1
endogenous viruses produced by viral genes
of tl1e leukosis/sarcoma group of diseases
integrated into the host cell DNA All field
seen in chicken flocks, although in the 1990s strains of avian leukosis virus are oncogenic, myeloid leukosis become prevalent in
although some differences in oncogenicity
meat-type chickens. The International
and replicative ability have been recognized.

Conm1ittee on Taxonomy of Viruses placed

Recently, recombinant avian leukosis
viruses of the avian leukosis/sarcoma group
viruses with the envelope of subgroup B and
in the Alpharetrovirus genus of the fan1ily long terminal repeat of subgroup J have

Retrovi1idae.

been isolated from field cases of myeloid

2852

NEOPLASMS
leukosis in commercial layers. Another

The virus is not highly contagious
recombinant avian leukosis virus with the
compared with other viral agents and
envelope of subgroup A and long terminal
is readily inactivated by disinfectants.

repeat of subgroup E was shown to be a

Transmission can be reduced or eliminated

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contan1inant in commercial Marek's disease
by strict sanitation. After the infection is
vaccines. Thus, recombination between two
eradicated, standard disease control and sanidifferent subgroups of avian leukosis virus tation practices can keep chicken flocks free
can occur in field conditions and cause
of the disease. The role of males in transmiseconomic losses.

sion of avian leukosis virus is unce1tain.

lnJected cocks appru·ently do not influence

Transmission and Epidemiology:

the rate of congenital infection of progeny but

Chickens are the natural hosts for all viruses
act only as virus catTiers and sources of
of the leukosis/sa.rcoma group; these vi.ruses
contact or venereal infection to other birds.

have not been isolated from other avian
species except pheasants, prutlidges, and

Pathogenesis: Lymphoid leukosis is a
quail. Avian leukosis virus is shed by the hen
clonal malignancy of the bursal-dependent
into the albumen or yolk, or both; infection
lymphoid system. Transformation invariably
probably occurs after the onset of incubaoccurs in the intact bursa, often as eru·ly as tion. Congenitally infected chickens fail to

4-8 wk after infection. Tumors are often not
produce neutralizing antibodies and usually
detectable until -14 wk of age. Death rarely
remain viremic for life. Horizontal infection
occurs before 14 wk of age and is more
after hatching is also in1portant, especially
frequent ru·ound the time of sexual matwit.y.

when chicks ru·e exposed i..nm1ediately after

The disease can be prevented, even up to 5
hatching to high doses ofvi.rus, eg, in feces of mo of age, by treatments that destroy the congenitally infected chicks or in contatnibursa. The tumors ru·e composed almost nated vaccines. Holizontally infected
entirely of B lymphocytes that, in many
chickens have a transient viremia followed
instances, have IgM on their surfaces. No
by antibody production. The earlier the
antittm1or immune response has been recoginfection, the more likely it is to lead to nized. Antiboclies are readily induced after
tolerance, persistent viremia, and tumors.

infection, except when tolerance occurs.

Other factors known to increase the

The induction of lymphoid leukosis
susceptibility of chickens to horizontal
tumors can be enhru1ced in chickens
infection include the absence of maternal
coinfected with serotype 2 Marek's disease
antibodies and the presence of endogenous
virus, a common vaccine virus. This
retroviruses, especially those associated
enhancement requires a genetically suswith the late feathering (K) gene. Tumors ceptible chicken and early infection with
ru·e more frequent in congenital than in
lymphoid leukosis virus in addition to
horizontal infections, but many more
serotype 2 Mru·ek's disease vaccination.

chickens ru·e exposed horizontally than

Because most commercial chicken strains
congenitally. Rates of embryo transmission
ru·e resistant, ru1d lymphoid leukosis virus
typically are 1%-lOOAi; virtually all chicks in
infection has been lru·gely eradicated from
an infected flock ru·e exposed by contact.

susceptible stocks, enhancement is not

Congenital and, in some cases, early h01izoncurrently recognized as a field problem.

tal infection can induce pem1anent cruTier

A subclinical disease syndrome characte1°
states charactelized by shedding of virus or
ized by depressed egg production in the
antigen into the environment ru1d into eggs.

absence oftLUnor fonnation is more

Late infection (ie, inoculation at 12-20 wk
importat1t economically than are deaths from
of age) is unlikely to lead to viral shedding.

lyn1phoid leukosis. Chickens with subclinical

Four classes of avian leukosis virus
disease usually shed virus or viral antigen
infection are recognized in mature
into the albwnen of eggs. The pathogenic
chickens: (1) no viremia, no antibody (1/-A-);
mechanisms ru·e poorly w1derstood.

(2) no viremia, with antibody (II-A+); (3)

with viremia, with antibody (1/+A+ ); and

Clinical Findings and Lesions: Chickens

(4) with viremia, no antibody (1/+A-). Birds
with lymphoid leukosis have few typical
in an infection-free flock and genetically
clinical signs. These may include inapperesistant birds in a susceptible flock fall into tence, weakness, dian·hea, dehydration, and
the catego1y V-A-. Genetically susceptible
emaciation. Infected chickens become
birds in ru1 infected flock fall into one of the
depressed before death. Palpation often
other three categories. Most are V-A+, and a
reveals an enlarged bwsa ru1d sometimes
minolit.y, usually <lOOAi, ru·e V+A-. Most
an enlru·ged liver. Infected birds may not

V+A-hens trru1smit the virus to a vru-ying but
necessarily develop tw11ors, but they
relatively high proportion of their progeny.

may lay fewer eggs.

NEOPLASMS

2853

Diffuse or nodular lymphoid tumors are

Diagnosis: Because avian leukosis virus
common in the liver, spleen, and bursa and
is widespread among chickens, virus
are found occasionally in the kidneys,
detection tests, including virus isolation and
gonads, and mesentery. Involvement of

PCR and the demonstration of antigen or

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the bursa has been considered virtually
antibody, have limited or no value in
pathognomonic, although bursal lymphodiagnosing field cases of lymphomas. Gross mas are also known to be induced by
characteristics of diagnostic significance
reticuloendotheliosis vinis. Sometimes the
include the tun1orous involvement of the
bursa! tumors are small and seen only after
liver, spleen, or bursa in the absence of
careful examination of the m ucosal surface
peripl\eral nerve lesions. The tumors are
of the organ. Usually, no enlargement of
found in birds >14 wk old. Histologically,
peripheral nerves is apparent, although such the lymphoid cells are tmiform in character, lesions have been noted after experimental
large, and contain IgM and B-cell markers
inoculation of subgroup J virus. Microscopion their surface. Tumors can be differentically, the tumor cells are unifonn, large ated from those of Marek's disease by
lymphoblasts. Mitotic figures are frequent.

gross and microscopic pathology and by

Outbreaks of neoplasms other than
molecular techniques that demonstrate the
lymphoid leukosis such as myelocytomas,
characteristic clonal integration of proviral
hemangiomas, and renal tumors have also

DNA into the tumor cell genome with the
been noted in meat-type chickens infected
associated disruption of the c-myc
with subgroup J avian leukosis virus.

oncogene. Lymphoid leukosis cannot easily

Myelocytomatosis and skeletal myelocytobe differentiated from B-cell lymphomas mas may cause protuberances on the head,
caused by reticuloendotheliosis virus
thorax, and shanks. Myelocytomas may
except by virologic assays; however, such
occur in the orbit of the eye, causing
tumors probably are extremely rare. Severa.I
hemorrhage and blindness. Hemangiomas

PCR primers specific for detection of the
may occur in the skin, appearing as "blood
most commonly isolated avian leukosis
blisters," which may rupture and bleed.

viruses, particularly subgroups A and J,

Renal tumors may cause paralysis due to
have been developed. Other primers
pressure on the sciatic nerve. Microscopispecific for endogenous, subgroup E avian cally, in cases of myelocytomas induced by
leukosis virus have also been used. PCR has
subgroup J avian leukosis virus, the liver
been used to detect and characte1ize avian
shows a massive intravascular and extraleukosis virus strains contanlinating vascular accumulation of myeloblasts
commercial live virus vaccines of poultry.

characterized by the presence of cytoplas

ELISA kits for detection of antibodies to
mic eosinophilic granules.

avian leukosis virus subgroups A, B, and J

Most strains of leukosis/sarcoma viruses
are available commercially.

also induce nonlymphoid tumors (including
sarcomas), erythroblastosis, myeloblasto

Control: Eradication of avian leukosis
sis, myelocytomas, hemangiomas,
virus from primary breeding stocks is the
nephroblastomas, osteopetrosis, and
most effective means to control avian
related neoplasms. The nature of the tumors leukosis virus infection and lymphoid and their frequency depend on virus strain,
leukosis in chickens. Breeder flocks are
chicken strain, age, dose, and route of
evaluated for vir·a.l shedding by testing for
infection. Occasional outbreaks of
viral antigens in the albumen of eggs with
predominantly one type of tumor are seen in enzyme inununoassays or by biologic assays the field. TI1e Rous sarcoma virus, a member for infectious virus. Eggs from shedder hens of this group, has been widely studied in the
are discarded, so that progeny flocks
laboratory. Each strain usually causes a
typically have reduced levels of infection. lf
predominantly neoplastic disease and can
raised in small groups, infection-free flocks
be distinguished on the basis of pathogeniccan be derived with relative ease. These ity. Some viruses ( eg, Rous sarcoma and
control measures are applied only to
erythroblastosis viruses) contain a viral
primary breeder flocks. Voluntary programs
oncogene that enables the virus to induce
to reduce viral infection have already
neoplasms within a. short incubation period,
reduced mortality from lymphoid leukosis
but such viruses are rare in the field. Others
and improved egg production in most layer
cannot replicate on their own and require a
strains; similar programs were equally
nondefective helper virus. In recent years,
successful in certain meat strains. Some
avian leukosis virus infection has been
breeders favor, and have virtually achieved,
shown to be associated with the so-called
total eradication, while others favor a

"fowl glioma.," characterized by cerebellar reduced level of vir·al infection. Some
hypoplasia. and myoca.rditis.

chickens have specific genetic resistance to

2854

NEOPLASMS
infection with certain subgroups of virus.

prompted the name reticuloendotheliosis

Although genetic cellular resistance is
but is not commonly seen in tl1e field.

unlikely to replace the need for reduction
or eradication of the vims, the cellular

Transmission and Epidemiology:

receptor gene has recently been cloned, and

Horizontal transmission is probably more

VetBooks.ir
quick molecular assays for viral susceptibilimportant than vertical, aliliough botl1 have ity could be developed. Thus far, vaccinabeen docwnented in chickens and turkeys.

tion for tumor prevention has not been

Transmission by mosquitoes and other
promising.

blood-sucking insects is suspected. The
vims has been isolated from litter. A high

RETICULOENDOTHELIOSIS
rate of congenital infection has been
demonstrated in naturally infected turkeys,

Reticuloendotheliosis designates a group
but such flocks are probably rare. The virus
of neoplastic and immunosuppressive
has been transmitted accidentally tJu·ough
syndromes in several avian species caused
use of contanunated vaccines. Most
by reticuloendotl1elio is vims, a member of
commonly, however, flocks seroconvert
the avian retrovirus group. The host range
after 10 wk of age without clinical disease or
of reticuloendotl1eliosis virus is much
vit·al shedding to progeny. Experin1entally,
broader than that of Marek's disease or
contact transmission occurs, but ilie vims is
avian leukosis. Natural infection and
neitl1er highly contagious nor highly stable
disease occurs in chickens, turkeys, ducks,
in the envirorm1ent. Partial or complete
geese, and quail; probably many species of
genomic insertion of reticuloendotl1eliosis
birds can be infected. Mammals appear
vims in the genome of otl1er avian viruses,
refractory, aliliough certain mammalian
namely fowlpox and Marek's disease vimses,
cell cultures are susceptible.

has been desc1ibed. However, the signifi

Reticuloendotheliosis vims is not as
cance of such insertion in transmission of
ubiquitous as Marek's disease and avian
reticuloendotl1eliosis vit'US is not known.

leukosis vimses but is more widely

Although semen from tolerantly infected
distributed than once believed. Many recent
turkeys contains infectious virus, tl1e role of
cases have been attJibuted to accidental
tl1e torn in vertical transmission is not clear.

contamination of live vims poultry vaccines
such as Marek's disease vims and fowl pox

Pathogenesis: The nondefective strains
virus witl1 reticuloendotheliosis virus.

of reticuloendotheliosis virus produce three

Although clinical outbreaks are not
distinct syndromes: non-neoplastic rw1ting,
frequently seen, serologic surveys suggest
acute neoplastic disease, and chronic
that the virus is prevalent in both chicken
neoplastic disease resulting in Band T
and turkey flocks in many cquntiies,
lymphomas. Typically, the rw1ting syndrome
including ilie USA.

is seen4-10 wk after administration of
contanunated vaccines to day-old chicks,

Etiology: Reticuloendotheliosis vims is
which can lead to dramatic economic
immunologically, morphologically, and
losses. Chronic neoplastic disease has
structurally distinct from the leukosis/
been induced experimentally in chickens,
sarcoma group of avian retrovirnses. The
turkeys, and ducks; one type occurs in

International Conunittee on Taxonomy of
chickens after latent periods of >4 mo and

Viruses has classified reticuloendotheliosis
appears identical to lymphoid leukosis. As
viruses witlun the family Retroviridae,
in lyn1phoid leukosis, tl1ese tlll11ors are
subfanuly Orthoretrovitinae, genus
composed ofB cells, are bursal-dependent,

Gammarelrovints. Aliliough all isolates and have IgM on tl1eir surface. Acute neobelong to a single serotype, tluee subtypes plasia, which occurs after a latent period
of reticuloendotheliosis vims have been
of 6-8 wk, also has been seen in chickens,
identified on the basis of neuti·alization tests
turkeys, ducks, and quail. This tun1or in
and differential reactivity with monoclonal
chickens involves T cells and may be
antibodies. Strains can be ftuther classified
confused with Marek's disease.

by their ability to replicate in cell culture.

Most field isolates appear to be nondefective Clinical Findings and Lesions: The for replication in cell cultures and contain
clinical findings for runting syndrome include
no vit·al oncogene. One unique laboratory
weight loss, paleness, occasional paralysis,
sti·ain ( strain T) is defective for replication
and abnormal featl1ering (Nakanuke
in cell cultures and contains a viral
disease). Deatl1 from acute or cl1ronic
oncogene, v-rel, tl1at is responsible for an neoplasia is preceded by depression and
acute reticulwn cell neoplasia in experimenoccasionally by some of tl1e san1e clinical tally inoculated chicks; tl1is neoplasm
changes desc1ibed for tl1e rw1ting syndrome.

NEOPLASMS

2855

The abnormal feather lesion, in which the
and viral antigens, or molecular hybridizabarbules are compressed to the shaft over a tion can be used in the differential diagnosis
small part of its length, may be of diagnostic
of avian viral lymphomas, including
value. Other lesions include bursal and
reticuloendotheliosis.

thymic atrophy, enlarged nerves, and

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anemia. Neoplasms typically involve the

Control: No control measures are
liver, spleen, intestine, and heart. The bursa
currently practiced. An experimental
is involved in the chronic B-cell lymphomas
recombinant fowlpox vims vaccine has
of chickens in a manner similar to that of
been developed. Some breeder companies
lymphoid leukosis. Nonbursal (T-cell)

wish to avoid seroconversion of their
lymphomas with shorter latent periods and
primary breeder stocks to obviate
lesions superficially resembling those of
restrictions on export of progeny to certain

Mare k's disease also are recognized in
countries, but reliable teclmiques to prevent
chickens. In turkeys, prominent lesions
horizontal transmission have not been
include enlarged livers and nodular lesions
developed. Elimination of vertical
on the intestines; the bursa is only rarely
transmission would presun1ably be possible
tumorous. The twnors, regardless of type
by removing potential transmitter hens;
or host species, are usually composed of
rearing progeny under isolated conditions
unifonn, large, lymphoreticular cells.

would prevent horizontal infection. Many
of these principles have successfully been

Diagnosis: Because lesions induced by
applied to the control of avian leukosis vims
reticuloendotheliosis virus are so diverse
in chickens. Such control procedures could
and resemble so closely those of other
be considered if reticuloendotl1eliosis vims
tumors, diagnosis at necropsy is difficult. A
infection becomes endemic in especially
diagnosis of reticuloendotheliosis requires
valuable breeding stock, as was the case
not only the presence of typical gross and
with reticuloendotheliosis virus infection in
microscopic lesions but also the demonstrathe endangered Attwater's prairie chickens.

tion of reticuloendotheliosis virus. Because
reticuloendotheliosis vims is not yet as

NEOPLASMS OF UNKNOWN
ubiquitous as avian leukosis and Marek's
disease vimses, the demonstration of

ETIOLOGY
infectious vims, viral antigens, and pro

Of the nun1erous twnors of unknown
viral DNA in tumor cells has significant
etiology in poultry, dermal squamous cell
diagnostic value. The nerve lesions are
carcinoma (avian keratoacanthoma),
usually less extensive and may contain
multi centric histiocytosis, and adenocarcimore plasma cells than in Marek's disease, nomas are the most common but appear to
but in other cases are difficult to differentibe of limited economic importance.

ate by histology. The run ting syndrome is
easily confused with irnrnunosuppressive

Avian Keratoacanthoma: These
syndromes caused by other viral agents.

neoplasms can occw· at relatively high

The chronic B-cell lyn1phomas induced
frequencies in some broiler flocks.

experimentally in chickens cannot easily

Carcasses with extensive lesions are
be distinguished from those of lymphoid
condenmed at slaughter, while less affected
leukosis except by virus studies, including
birds undergo trim.ming. Condemnations of

PCR. Similarly, the T -cell lymphomas of
whole carcasses represent a significant
chickens cannot easily be distinguished
economic loss. Typically, the lesions are
from Marek's disease except by vims
seen during processing after the skin has
studies. However, both B- and T-cell
been defeathered as crater-like ulcers with
lyn1phomas induced by reticuloendothelioraised margins within feather tracts. In Jive sis virus contain a clonally integrated DNA
chickens, the ulcers usually contain a
provirus usually associated with the c-myc
mixture of keratin, cell deb1is, and bacteria.

oncogene, which can be demonstrated by

Histologically, lesions appear as proliferaappropriate molecular methods. The tive expansion of feather follicle epithelium.

chronic lymphomas that are seen in turkeys

An etiologic agent has not yet been
must be differentiated from lymphoprolifidentified, and the true neoplastic nature erative disease of turkeys based on
of the lesion has not been confirmed.

histology, vims isolation, and character

Transmissibility of tltis tumor has neither
ization of the vims-associated reverse
been demonstrated nor excluded.

transcriptase for activity in the presence of
manganese or magnesium ions. Techniques

Multicentric Histiocytosis: This
based on inununocytochernistry with
condition of young broiler chickens is
monoclonal antibodies to cellular, tumor,
characterized by both splenomegaly and

2856

NEOPLASMS
hepatomegaly. Miliary (0.5-5 mm), white
infected with subgroup J avian leukosis
to yellow nodules can be seen in the
virus.

spleen, liver, and kidneys. Microscopically,
nodules of spindle-shaped cells diffusely

Adenocarcinomas: Adenocarcinomas of
expand periarteriolar lymphoid sheaths.

the ovary or oviduct are relatively common

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These histiocytic cells contain elongated
incidental tumors in mature chickens.

oval, fusiform, or more bizarrely config

These neoplasms often are characterized
ured nuclei. No definitive etiologic agent
by multiple miliary implant tumors on the
has been identified. A somewhat similar
mesentery and other visceral surfaces,
condition with lesions, termed "histiocytic
frequently accompanied by ascites. These
sarcomatosis," has been described in
twnors are not known to be virus-induced
meat-type chickens experimentally
or to be transmissible.

NEWCASTLE DISEASE AND OTHER

PARAMYXOVIRUS INFECTIONS

NEWCASTLE DISEASE
some clifferences may be seen if the NOV
strain is adapted to a particular species.

(Avian pneumoencephalitis, Exotic or
velogenic Newcastle disease)

Epidemiology and Transmission: Viru

Newcastle disease is an infection of
lent NOV strains are endemic in poultry in
domestic poultry and other bird species with most of Asia, Africa, and some coW1tries of virnlent Newcastle disease virns (NOV). It is

North and South Ame1ica. Other coW1tries,
a worldwide problem tliat presents
including the USA and Car1ada, are free of
primarily as an acute respiratory disease,
those strains in poultry and maintain that
but depression, nervous manifestations, or
status with import restrictions and
diarrhea may be the predominant clinical
eradication by destroying infected poultry.

fonn. Severity depends on the virulence of

Cormorants, pigeons, and irnpo1ted
the infecting virus and host susceptibility.

psittacine species are more commonly

OccwTence of the disease is reportable and
infected with vNDV and have also been
may result in trade restrictions.

sources of vNOV infections of poultry. NOV
strains of low virulence are prevalent in

Etiology and Pathogenesis: NOV,
poultry arid wild birds, especially watersynonymous with avian paramyxovirus fowl. Infection of domestic poultry with
serotype 1 (PMV-1), is an RNA vims and tl1e
loNOV contributes to lower productivity.

most important of the 11 known PMV -

Infected birds shed virus in exhaled air,
serotypes as a pathogen for poultry. The
respiratory discharges, and feces. Virus is
original classification of NOV isolates into
shed during incubation, during the clinical
one of three virulence groups by chicken
stage, and for a varying but lirnited period
embryo and chicken inoculation as virulent
during convalescence. Virus may also be

(velogenic), moderately virulent (mesopresent in eggs laid during clinical disease genic ), or of low virulence (lentogenic) has
and in all par·ts of the car·cass during acute
been abbreviated for regulatory purposes.

vNOV infections. Chickens are readily

Velogens and mesogens are now classified
infected by aerosols and by ingesting
as virulent NOV (vNOV), the cause of
contaminated water or food. Infected

Newcastle disease and reportable infection,
chickens and other domestic and wild bir·ds
whereas infections with lentogens, the low
may be sources of NOV. Movement of
virulence NOV (loNOV) widely used as
infected birds and transf Pr of virus,
live vaccines, are not reportable. Clinical
especially in infective feces, by the
manifestations vary from high morbidity
movement of people and contan1inated
and mortality to asyn1ptomatic infections.

equipment or litter ar·e the main methods

Severity of infection depends on virus
of vir1.1s spread between poultry flocks.

virulence and age, inm1W1e status, and
susceptibility of the host species. Chickens

Clinical Findings: Onset is rapid, and signs are the most and waterfowl the least
appear tl1roughout the flock within 2-12 days
susceptible of domestic poultry; however,

(average 5) after aerosol exposure. Spread is

NEWCASTLE DISEASE AND OTHER PARAMYXOVIRUS INFECTIONS

2857
slower if the fecal-oral route is the primary
virus that is inhibited with NDV antiserum
means of transmission, particularly for caged or by detection of NDV RNA by reverse birds. Young birds are the most susceptible.

trai1scriptase PCR. A rise in NDV antibody

Obse1ved signs depend on whether the
titer by hemagglutination-inhibition or
infecting virus has a predilection for

ELISA of paired sernm sainples inilicates

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respiratory, iligestive, or nervous systems.

NDV infection. To confirm iliagnosis,

Respiratory signs of gasping, coughing,
identification of an isolate such as vNDV is
sneezing, and rales predominate in infections established by the rapidity of killing day-old with loNDV. Ne1vous signs of tremors,

SPF chicks inoculated by the intra.cerebral
paralyzed wings and legs, twisted necks,
route, the intra.cerebral pathogenicity index,
circling, clonic spasms, and complete
or by the presence of a specified an1ino acid
paralysis may accompany, but usually follow, motif at the cleavage site of the fusion tl1e respiratory signs in nemotropic
protein (F) precursor (FO). Reference
velogenic disease. Nervous signs with
laboratories use nucleotide sequence
iliarrhea are typical in pigeons, and nervous
analysis to detect genetic differences for
signs are frequently seen in connorants and
comparison of isolates from different
exotic bird species. Respirato1y signs with
outbreaks a11d to identify the somce of those
depression, watery greenish diarrhea, and
infections. The acute fonn of ND should be
swelling of the tissues of tl1e head and neck
differentiated from otl1er diseases !mown to
are typical of the most virulent form of tl1e
cause high mortality, such as highly
ilisease, viscerotropic velogenic Newcastle
pathogenic avian influenza (seep 2902).

disease, although nervous signs are often
seen, especially in vaccinated poultiy.

Prevention: Vaccines are available for

Varying degrees of depression and inappechickens, tmkeys, and pigeons and are tence are seen. Partial or complete cessation
used to induce an antibody response, so
of egg production may occur. Eggs may be
vaccinated bids must be exposed to a lai·ger
abnormal in color, shape, or swiace and
dose of vNDV to be infected. Unfortunately,
have watery albwnen. Mortality is vaiiable

ND vaccines do not provide sterile immunity,
but can be as high as 10001<, with vNDV
ai1d in maiw areas of the world vaccines are
infections. Well-vaccinated birds may not
used to prevent losses from sickness and
show any signs of being infected except for a
death. Live lentogenic vaccines, chiefly B 1
decrease in egg production, but these birds
and La.Sota strains, are widely used and
will shed virus in saliva and feces. Poorly
typically administered to poultry by mass
vaccinated birds may develop torticollis,
application in drinking water or by spray.

ataxia, or body and head tremors 10---14

Mucosa! immunity induced in birds
days after infection and may recover with
vaccinated by live vaccines applied by these
supportive care.

routes decreases the ainount of vNDV the

Lesions: Remarkable gross lesions are
vaccinated birds will shed if infected with
usually seen only witl1 viscerotropic velovNDV, compai·ed with the in1mune response genic Newcastle disease. Petechiae may
induced by an inactivated vaccine. Mass
be seen on the serous membranes; hemorvaccination methods are less labor intensive rhages of the proventricular mucosa and
but if not applied properly may lead to <85%
intestinal serosa are accompanied by
of the flock being immunized, which is
multifocal, necrotic hemorrhagic areas
needed for herd immunity. Alternatively,
on the mucosa! surface of the intestine,
inilividual administration of live vaccines is
especially at lymphoid foci such as cecal
via tl1e nai·es or cor\junctival sac. Healthy
tonsils. Splenic necrosis and hemorrhage and chicks are vaccinated as early as day 1-4 of edema around the thymus may also be seen.

life. However, delaying vaccination until the

In contrast, lesions in birds infected witl1
second or tl1ird week avoids maternal
loNDV strains may be limited to congestion
ai1tibody interference with an active immune
and mucoid exudates seen in the respiratory
response. Mycoplasma, some other
tract with opacity and thickening of the air
bacteria, and other viruses affecting the
sacs. Secondary bacterial infections increase
respiratory ti·act, if present, may act
the severity of respiratory lesions.

synergistically with some vaccines to
aggravate the vaccine reaction after spray
administration.

Diagnosis: NDV can be isolated from

Oil-adjuvanted inactivated vaccines ai·e
oropharyngeal or cloaca! swabs or tissues
also used after live vaccine in breeders ai1d
from infected birds by inoculation of the
layers and may be used alone in situations
allantoic cavity of9- to 11-day-old SPF
where use of live virus may be contrainiliembryonated chicken eggs. Infection is cated (eg, in pigeons). In countries where
confinned by recovery of a hemagglutinating vNDV is endemic, a combination of live

2858

NEWCASTLE DISEASE AND OTHER PARAMYXOVIRUS INFECTIONS
virus and inactivated vaccine can be used;
species. Primary infections in poulby are
or alternatively, if pemtitted by Jaw, a live
believed to be the result of contact with
mesoge11ic strain vaccine may be used in
wild birds. The method of transntission to
older birds. The frequency of revaccination
cltickens or turkeys is unclear. PMV-3 has
to protect chickens throughout life largely
been isolated from in1ported exotic and other

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depends on the 1isk of exposure and
bird species held in captivity. Psittacines
virulence of tl1e field virus challenge.

appear to be the primary host, altllough

Adntini.stering inactivated vaccines is more

PMV-3 will spread among passeri.nes in
labor intensive, because each bird has to be
captivity. There are no reports of isolation
handled individually. Accidental inoculation
of PMV-3 from wild birds. The metllod of
of human tissues with oil-based vaccines
transntission among turkeys is unclear, and
requires prompt medical treatment.

spread witllin a flock is usually slow.

Fowl pox or turkey herpesvirus-vectored

NOV vaccines are commercially available

Clinical Findings: Infections by PMV-2,
for chickens and have the advantage of

-3, -6, and -7 in turkeys have produced mild
being able to be adntini.stered in ovo at tl1e
to severe respiratory disease, drops in egg
hatchery. These vaccines must be reconstiproduction, reduced hatchability and tuted as directed by the manufacturer and,
infertility of eggs, and increased numbers of
because they take 3-4 wk to produce a
white-shelled eggs. Infection witll PMV-2
protective level of immunity, biosecuri.ty is
has produced mild respiratory disease in
even more important. A commercial kit to
chickens, but PMV-2 infection is usually
detect levels of antibodies induced by these
most severe in turkeys, especially breeders.

vaccines is not yet available.

Infection is more severe when accompanied
by secondary pafuogens.

Zoonotic Risk: All NOV strains can
produce a transitory coajunctivitis in

Diagnosis: Most diagnoses are made by
people, but tl1e condition has been lintited
clinical signs and con.finned by serology.

primarily to laborato1y workers and vaccina

PMV-2, -3, -6, and -7 can be isolated from
tion teams exposed to large quantities of
oropharyngeal or cloaca] swabs, or tissue
virus. Before poulby vaccination was widely samples from infected birds by inoculating practiced, coajunctivitis from NOV infection
the allantoic cavity of 8- to I 0-day-old
occurred in crews eviscerating poulby in
embryonating chicken eggs. Confuma-
processing plants. The disease has not been
tion of the virus as PMV can be done by
reported in people who rear poulby or
hemagglutination inhibition tests with
consume poulby products.

specific antiserum to individual serotypes.

However, PMV-1 (Newcastle disease virus)

OTHER AVIAN PARAMYXOVIRUS
and PMV-3 may cross-react in hemagglutina

INFECTIONS
tion inhibition tests (and in oilier serologic
tests such as ELISA), wltich causes

Avian paramyxovirus infections have
interpretation problems in vaccinated birds.

been reported in chickens and turkeys in

Birds vaccinated against Newcastle disease
association with respiratory dis.ease or
show a rise in hemagglutination inJtibition
decreases in egg production.

titers to botll viruses if subsequently
infected with PMV-3.

Etiology and Epidemiology: There are

12 recognized serotypes of avian paramyxo

Prevention and Control: No vaccines
viruses (PMV-1 to PMV-12). Newcastle
are available for PMV-2, -6, and -7. Inactidisease virus (PMV-1, seep 2856) is the vated oil-emulsion vaccines against PMV-3
most important pathogen of tltis group
have been used in turkey breeder flocks.

for poulby, but PMV-2, -3, -6, and -7 are

These are injected twice, 4 wk apart, before
occasionally associated with disease in
tlle birds begin to lay ( usually when 20-24
chickens and turkeys. The most recent
wk old). The risk of introducing PMV-2 and
serotypes (PMV-10, -11, and -12) were
oilier paramyxoviruses from wild birds may
isolated from Rockhopper penguin
be mi11intized by bird-proofing poulby

(Eudypt.es chrysocome) in the Falkland
houses and using good hygiene and

Islands, Common S11ipe (Gallinago
biosecurity practices. Treatment of
gallinago) in France, and Eurasian
secondary bacterial infections with

Widgeon (Anas penelope) in Italy,
antibiotics has had some success. PMV-3
respectively, and were the first new
appears to spread slowly.

serotypes in >30 yr.

PMV-2 has been isolated from wild birds,

Zoonotic Risk: No human infections have
mainly passe1ines, and caged psittacine
been reported for PMV-2 to PMV-12 viruses.

POISONINGS

2859

OMPHALITIS

(Navel ill, "Mushy chick" disease, Yolk sac infection) VetBooks.ir

Omphalitis is a condition characterized by
unabsorbed, infected yolks often produce
infected yolk sacs, often accompanied by
chicks or poults with reduced weight gain.

unhealed navels in young fowl. It is

There is no specific treatment; antibiotic
infectious but noncontagious and is
use is based on the prevalent bacterial type
associated with poor regulation of
involved. Even then, treatment may not
incubation temperatme or humidity and
result in satisfactory outcomes, because
marked contamination of the hatching eggs
severely affected chicks and poults often
or incubator. If young poultry are placed in
die, and unaffected birds are unlikely to be
contan1inated transportation boxes before
aided by antibiotic treatment. The disease
their navels are completely closed, bacteria
is prevented by careful control of temperacan migrate up the patent yolk stalk and tW"e, humidity, and sanitation in the
infect the yolk sac.

incubator. Only clean, uncracked eggs

The navel may be inflamed and fail
should be set. If it is necessary to set dirty
to close, producing a wet spot on the
eggs, they should be segregated from clean
abdomen; a scab may be present. Opportuneggs. Sanitizing detergents must be used istic bacte1ia ( coliforms, staphylococci,
according to directions if eggs are washed.

Pseudomonas spp, and Proteus spp) are Tin1e, temperature, and frequent changes of
often involved, and mixed infections are
water are as critical as the concentration of
common. Proteolytic bacte1ia are prevalent
sanitizer in both wash and rinse water. The
in outbreaks. The yolk sac is not absorbed

1inse should be wai111er than the wash
and often is highly congested or may
water (which should be warmer than the
contain solidified pieces of yolk material;
internal temperatme of the egg) but should
peritonitis may be extensive. Edema of the
not be >60°C.

sternal subcutis may be seen. Affected

The incubator should be cleaned and
chicks or poults usually appear norn1al until
disinfected thoroughly between hatches. If
a few hoW"S before death. They have little
fumigation is to be clone with forn1aldehyde,
interest in food and water and are often
vents should be closed. Thirty mL of 400A,
found severely dehydrated. Depression,
fmmaldehyde/0.6 m3, or pai·afom1aldehyde
drooping of the head, and huddling near the

(in the strength recommended by the
heat somce usually are the only signs.

manufacturer), should be allowed to

Mortality often begins at hatching and
evaporate in the closed incubator or hatcher.

continues to 10-14 days of age, with losses

The machines are readily contan1i.nated after
of as much as 15% in chickens and 500Ai in
fumigation unless the exterior of the
tmkeys. Chilling or overheating dW"ing
machines and the rooms in which they are
shipment may increase losses. Persistent,
located are also cleaned and disinfected.

POISONINGS

See also TOXICOLOGY, p 2948 et seq.

be collected for potential analysis in cases of

When toxicosis in a poultry flock is
suspected toxicosis include dead or recently
suspected based on mortality, on decreased
eutl1anized birds that showed clinical signs,
production/growth, or on other clinical signs 2 lb (1 kg) of the feed available when the such as paralysis, the flock owner or
birds were showing clinical signs, and
veterinarian should maintain and allow

500 mL of drinking water. For tl1e safety
access to historical records. These records
of workers as well as poultry, the grower
include use of disinfectants and rodenticides should have access to material safety data and insecticides on the premises, medicasheets for each chemical used on the tions administered in feed and water, and
premises. Cai·casses should be refrigerated
nutiitional additives to the feed. Sainples to
as soon as possible for exanlination by the

2860

POISONINGS
veterinarian or laboratory diagnostician.

tion can result in rodent bait consmnption

Consultation with a toxicologist or
by poultry with usually acute toxic effects.

laboratory diagnostician before collecting

First-generation anticoagulant rodenticides,
samples is hlghly recommended.

including warfaiin, chlorphacinone,

VetBooks.ir
diphacinone, and COlll11tetralyl, require

Aflatoxin: Aflatoxicosis is one of the most
continual ingestion by rodents to induce
common intoxications in modern poultry
toxic effects. Second-generation or
production systems. Certain species of
single-feed anticoagulants, including

Aspergillus and Penicillimn can produce brodifacolll11, bromadialone, difenacolll11,
aflatoxins in feedstuffs. The production of
and difethialone, can be acutely fatal to
aflatoxins can occur either in the field where rodents. Clinical signs in poultry ai·e related the crops are grown or during storage.

to the anticoagulant effects and usually

Acute aflatoxicosis is characterized by
observed as sudden death with gross
inappetence, ataxia, convulsions, opisthotohemorrhagic lesions in one or more body nos, depression, and death. A gross lesion
sites, pa.iticularly lung, intestine, and
often seen with acute aflatoxicosis is an
peritoneal cavity. These lesions can be
enlarged yellow liver. All poultry are
confused with flight ir\jury (gamebirds)

susceptible to aflatoxicosis; however, ducks
and tralll11a from wild animals a.i1d dogs.

and turkeys are particularly sensitive.

Definitive diagnosis of anticoagulant
toxicosis should be based on gross lesions,

Ammonia (aerosolized): Ammonia gas
history of anticoagulant application, and
is produced by the metabolism of uric acid
anticoagulant screen on liver of dead birds
by bacteria that can thrive in wet poultry lit

(available at several USA veterina.iy
ter. High ammonia levels often occur during diagnostic laboratories).

the winter when ventilation is minimized to
conserve heat and thus hlgh litter moisture

Botulism: Clostridium botulinum
is common. Increased anunonia levels of
bacteria produce several exotoxins that are

25-30 ppm can damage the mucociliary
an10ng the most potent toxins known. In
apparatus of the upper respiratory tract,
ducks and geese, botulism outbreaks
and higher levels (50-75 ppm) can cause
commonly occur in the Sllllliller months in
decreased feed intake as well as caustic
the vicinity of poorly aerated ponds and
burns to the cornea, which can result in
lakes. The waterfowl ingest the toxin by
blindness. These birds will often fail to find
eating dead invertebrates from the margins
adequate food and water, resulting in death.

of these lakes or eating maggots on the
carcasses of ducks that have already

Anticoagulant Rodenticides: Rodentisucclll11bed to the intoxication. In pheasant cides can be safely applied to poultry
and broiler flocks, where the timely removal
houses so that rodent baits are sequestered
of dead birds has not been practiced,
from the flock; however, careless applica-
carcasses can also become a source of
toxin. The classic clinical sign of botulism
intoxication in poultry is paralysis of the
muscles of the neck or "limberneck." The
toxin also causes paralysis affecting the
legs, wings, and eyelids. Diagnosis of
botulism is often based on exclusion of
other possible causes, although intestinal
contents and blood can be collected for
botulism toxin analysis (mouse inoculation
assay), which is available at several USA
diagnostic laboratories.

Calcium: Excessive calcium intake in
broiler chicks results in urolithiasis and
visceral gout (hyperuricemia) with urate
deposits on the abdominal viscera and in
the joints. Tetailic convulsions cai1 also be
seen in chicks consuming excess calcilll11.

Calcilll11 levels >2% will induce these lesions

Pullets ex
in broilers. Feeding calcium in excess of3"Ai
posed to high levels of aerosolized
wet litter developed blindness as
before the onset of egg production will
in
ammonia
a result of corneal ulcers. Courtesy of Dr. Robert induce the same lesions in egg-type or

Porter.

meat-type pullets.

POISONINGS

2861

Carbon Monoxide: This poisoning

Lead: Lead poisoning usually is caused by
commonly arises from exhaust fumes
paint or orchard-spray material. Metallic
when chicks are being transported by
lead in amounts of7.2 mg/kg body wt is
truck or from improper ventilation in
letl1al. Signs are depression, inappetence,

VetBooks.ir
hatchers. Mortality may be high unless
emaciation, tlurst, and weakness. Greenish
fresh air is provided immediately. At
droppings are commonly seen within 36 hr.

necropsy, the beak and face are cyanotic,

As poisoning progresses, the wings may be
and a characteristic bright pink color is
extended downward. Young birds may die
noted throughout the viscera, particuwithin 36 hr after ingestion. Acute lead larly the lungs. Diagnosis can be
poisdning may be diagnosed from tl1e history
confirmed by a spectroscopic analysis
and necropsy findings of a greenish brown
of the blood.

gizzard mucosa, ente1itis, and degeneration
offue liver and kidney. Chronic poisoning

Coffee Weed Seed: Senna obtusifolia
results in emaciation and in atrophy of tl1e
seeds are frequently found in com and
liver and heart. The pericardium is distended
soybeans. When present at �2%, tl1ey reduce
wifu fluid, the gallbladder is thickened and
feed intake and lower body weight, increase
enlarged, and urate deposits a.re usually
feed conversion in broilers, and significantly fotmd in t11e kidneys. Ingestion of lea.d shot depress egg production in laying birds.

often occurs in wild waterfowl on heavily

Necropsy lesions are absent.

gtmned feeding grounds. Retention of only a
few lead pellets in the gizzard can kill a duck.

Copper: Copper sulfate has been used
as a water additive for treatment of crop

Mercury: Poisoning occurs from mercurial
mycosis (Candida overgrowth) or
disinfectants and fungicides, including
nonspecific digestive tract disorders in
mercurous chloride ( calomel) and bi chloride
poultry. Copper sulfate in a single dose of
of mercury (corrosive sublimate). Clinical

> l g is fatal. The signs are watery diarrhea
findings are progressive weakness and
and listlessness. A cata.1Thal gastroenteritis
incoordination. Diarrhea. may occur,
and bums or erosions in the lining of tl1e
depending on the an1otmt ingested. The
gizzard, accompanied by a greenish,
caustic action of fue chemical may produce
seromucous exudate throughout the
gray areas in fue moufu and esophagus,
intestinal tract, are found at necropsy.

which usually ulcerate if t11e bird lives >24 hr.

Ca.tarrhal inflanm1ation offue proventriculus

Crotalaria: Seeds of many species are and intestines may occur; if a large amount of
toxic to chickens. Concentrations >0. 05% in mercury is ingested, extensive hemmThage
the feed produce signs of toxicosis. At 0.2%,
may occur in tl1ese organs. The kidneys are
weight gain is reduced markedly; 0.3%
pale and studded witl1 small, whita foci. The
causes death in 18 days. Lesions consist of
liver shows fatty degeneration.

ascites, swelling or cirrhosis of the liver, and
hemorrhages. Resistance to tl1e toxin

Nicarbazin: This chemical coccidiosta.t
increases witl1 age.

is used in broilers. It should not be fed to
layers, because it can cause discoloration

Diazinon: Diazinon is an organic
and reduced ha.tchability of eggs (alfuough
phosphate and cholinesterase inhibitor
the effect is reversible once the nicarbazin is
commonly used to control a variety of
withdrawn). It also may result in reduced
insects armmd poultry houses. It should not
heat tolerance in birds exposed to high
be used inside poultry houses. Chickens will temperature and humidity.

consume tl1e diazinon crystals, which
results in lacrirnation, diarrhea, dyspnea,

Nitrofurazone: This has been used to
and death. Necropsy lesions include lung
treat several bacterial diseases in poultry,
edema, fatty livers, and severe enteritis. The
but it is no longer approved for use in many
diazinon crystals might be seen in the crop
countries, including fue USA. When fed at
and gizzard contents. Diagnosis can be

0.022%, it causes hyperexcitability manifest
confirmed by testing brain for cholineste1�
by rapid movements, loud squawking, and
ase activity.

frequent falling forward. In turkeys, which
are more sensitive to nitrofurazone than are

Gossypol: Cottonseed meal contains
chickens, it produces cardiac dilatation,
appreciable amounts of gossypol, which
ascites, and when fed at 0.033%, death.

produces severe cardiac edema tl1at results
in dyspnea, weakness, and anorexia. When

3-Nitro-4-hydroxyphenylarsonic Acid:

fed to laying hens, gossypol also causes

When tl1is compound, widely used in feed to
egg-yolk discoloration.

improve weight gain and feed efficiency, is

2862

POISONINGS
improperly mixed or fed at a level 2-3 times

Narasin: This ionophore is often
higher than norn1al, it induces a high-pitched
administered in combination with the
chirp and a "duck-walking" stance. Ataxia, chemical nicarbazone to prevent coccidineck extension, and paralysis can occur in osis in broilers but can be particularly toxic
chickens and turkeys that consume excessive in turkeys ( often noted on product label), VetBooks.ir
amounts. Clinical signs are usually reversible
resulting in flaccid paralysis of the wings
in a few minutes. Chronic exposure may
and legs. Toxic effects have also been
produce intrallepatic cholangitis.

described in broilers sin1ultaneously treated
with tian1ulin or sulfonamides.

Polychlorinated Biphenyls (PCBs):

Residues have been reported in the fatty

Salinomycin: Salinomycin is commonly
tissue of chickens and turkeys in excess of
used as an anticoccidial compound in the
the 5 ppm permitted in edible tissue, and in
broiler industry. It is safe when used at
egg products in excess of the pemtitted

60 gtton of feed. Toxicities occw-when broiler

0.5 ppm. PCBs depress egg production and
feed containing salinomycin is accidentally
hatchability, and levels of 50 ppm result in
fed to naive breeder hens. Clinical signs in
citThosis of the liver and ascites in broilers
these hen flocks include paralysis with the
and a drop in egg production and hatchabillegs extended backward and decreased ity in hens. (See also
feed consumption, egg production, and

PERSISTENT HALOGENATED
hatchability. Levels of salinomycin > 10 gtton

AROMATIC POISONING, p 3056.)

in breeder-hen feed are sufficient to produce

Polyether lonophores: Polyether
these clinical signs. Necropsy lesions are
ionophores facilitate transport of divalent
absent in birds with this clinical picture.

cations across cell membranes to inteliere
with osmoregulation, resulting in cell

Polytetrafluoroethylene (PTFE):

mpture. Toxicosis caused by ionophores is

PTFE is a synthetic fluoropolymer resin
relatively common in poultry, because these
highly resistant to heat and chemically
compounds are commonly administered for
stable with low reactivity. PTFE has been
the prevention and treatment of coccidiosi.s
used as nonstick coating for frying pans
and are subject to overdosing and mixing

(Teflon®) and has been used to coat heat
etTors. Additionally, these ionophores can
lamps and heater filaments that might be
interact with certain medications, such as
used in poultry houses. Although generally
sulfonan1ides, to cause toxicosis signs when heat stable, PTFE heated above 280°C
the ionophore concentration in the feed is

(536°F) can produce aerosolized hydrogen
norn1al. Examples of ionophores used in
fluoride, carbon fluoride, carbon monoxide,
poultry are described below.

and low-molecular-weight fluoropolymers.

PTFE pyrolysis products can cause direct

Lasalocid: Lasalocid is an anticoccidial
caustic damage to the lung, resulting in
compound that has been used in hot
marked pulmonary edema and hemotThage.

smnmer months, because it increases water

Birds are often found dead with no
consumption. When used at other times of
premonitory signs. Diagnosis is based on
the year, the level of salt in the ration is
gross lesions, history of using new heating
reduced to prevent excessive water
lambs or filaments coated with PTFE, and
elimination and wet litter problems. If the
excluding other possible causes of
salt level is reduced too much, it will result
pulmonary hemotThage.

in stunting, increased lan1eness, and a
characteristic clinical picture in broilers
manifested by the bird walking on its toes.

Propane: Propane is commonly used in

This clinical syndrome has been called
poultry facilities as a fuel source to provide
lasalocid toxicity when, in reality, it is due
heat for young poultry. Chicks are often
to low levels of salt in the feed.

surrounded by a cardboard brooder ring to
provide a safe, wann environment during

Monensin: This ionophore coccidiostat
the first week of life. If a defective heater
is widely used in the broiler industry. At
leaks propane into the brooder ring, the
levels > 120 ppm it reduces feed intake and
propane gas will displace the lighter air,
weight gain; in layers, egg production is
resulting in asphyxiation of the chicks. On
reduced. Signs of toxicity include a
necropsy, these chicks have congested,
characte1istic paralysis in which the legs are edematous lungs that sink when placed in extended backward. If naive turkeys are
forn1alin.

switched to a feed that contains monensin,
they become paralyzed with the legs extend

Quaternary Ammonia: Quatemaryed backward and mortality occurs; no anm1onia-based compounds are widely used
lesions are seen at necropsy.

as disinfectants. (See also ANTISEl'l"ICS AND

POISONINGS

2863

DISINf'ECTANTS, p 2738.) 1\u·keys are very
testicle is pathognomonic of salt toxicity in
sensitive; levels of 150 ppm result in substanyoung birds.

tial mortality. Clinical signs include reduced
water intake, nasal and ocular discharge,

Sulfonamides: Sulfonamides are widely
facial swelling, and gasping. Necropsy
used for treatment of several bacterial and

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lesions include caseous ulcers at the base of
protozoa] infections in poultry and are
the tongue and commissmes of the mouth.

usually administered in drinking water.

Sulfaquinoxaline, when fed at 0.25%, results

Selenium: Ingestion of feeds containin severe pancytopenia. Hemorrhages are ing >5 ppm of selenium decreases the
common on t!l.e legs, breast muscle, and in
hatchability of eggs due to deformities of
virtually all abdominal organs. The bone
the embryos, which are unable to emerge
marrow is pale, and the blood is slow to
from the shell because of beak anomalies.

clot. Toxicity is frequently seen in hot

Eyes may be unilaterally hypoplastic or
weather when sulfaquinoxaline is provided
aplastic, and feet and wings may be
in drinking water. Water consun1ption
defonned or underdeveloped. Selenium at
increases rapidly as the temperature

10 ppm, as in seleniferous grains in the
increases, which leads to increased drng
laying ration, usually reduces hatchability
intake. This toxicity usually is responsive
to zero. Young laying hens entering egg
to vitantln K therapy.

production are more susceptible than
older hens.

Sulfur: Elemental sulfur is often used in

Mature birds seem to tolerate more
broiler houses in an attempt to improve
selenium in their feed than do pigs, cattle,
growth rate and feed conversion and to
or horses and do not exhibit signs of
minimize bacterial disease. The compound
poisoning other than poor hatchability of
is applied to the floor after the litter has
their eggs. Starting rations containing
been removed. Elemental sulfur is also used

8 ppm selenium have reduced the growth
in dust baths for treatment of ectoparasites
rate of chicks, but 4 ppm had no noticeable
in adult layers. If the an1ount of new litter
effect. Rations containing as little as
placed in the house is inadequate, young

2.5 ppm have resulted in meat and eggs
chicks will come in contact with the sulfur,
with concentrations of selenium in excess
resulting in conjunctivitis and cutaneous
of the suggested tolerance lin1it in foods.

bums, especially tmder the wings and on

Sodiwn arsenite and some of the organic
the legs. Clinically, the birds appear cold
arsenicals, when administered to laying
and tend to huddle; in many instances,
hens with selenium, have increased
death will occm due to the birds piling up,
hatchability.

causing overheating and suffocation. When
sulfur comes into contact with moisture,

Sodium (salt): The addition of 0.5% salt
sulfuric acid is produced, which results in

(NaCl) to the ration of chickens and
the bums.

turkeys is recommended, but amounts

>2% are usually considered dangerous.

Thiram: Thirarn is used to treat seed

Rations for chicks have contained as much
com. It is toxic to chicks at 40 ppm and to
as 8% without injurious effect, but in
goslings at 150 ppm; it causes leg defonnipoults, rations containing 4% were harmful ties and weight loss. At 10 ppm, it causes
and levels of 6%-8% have resulted in
soft-shelled eggs, and at 40 ppm, egg
mortality. The addition of 2% NaCl to the
production and hatchability are reduced.

feed, or 4,000 ppm in the water, depresses

Tm key poults tolerate up to 200 ppm.

growth in young ducks and lowers the
fertility and hatchability of the eggs in

Toxic Fat: A crystalline halogen has been
breeding stock.

identified as the "toxic fat" factor in some Salt levels high enough to produce
feeds. In young pullets, it reduces growth,
poisoning may be reached when salty
retards sexual development, and increases
protein concentrates ( eg, fish meal) are
mortality. Hatchability is decreased.

added to rations already fortified with salt

Turkeys and ducks are less susceptible than
or when the salt is poorly incorporated in
chickens. Signs of intoxication include
the feed. Sporadic poisoning also has been
mffled feathers, droopiness, and dyspnea.

reported from accidental ingestion of rock

Lesions include ascites and hydropericarsalt or salt provided for other livestock.

diun1, liver necrosis, subepicardial

Necropsy findings are not diagnostic;
hemorrhage, and bile duct hyperplasia.

enteritis and ascites are common. Watery

Altl1ough tl1e an1ount of toxin varies in feeds
droppings and wet litter often are suggesfrom different somces, 0.25o/er0.5% fed for tive of a high salt intake. Edema of the

35-150 days produces typical lesions.

2864

RIEMERELLA ANATIPESTIFER INFECTION

RIEMERELLA ANATIPESTIFER INFECTION

(New duck disease, Infectious serositis, Pasteure//a anatipestifer infection) VetBooks.ir

Infection with Riemerella anatipestifer is
be seen. Mortality is usually 2%-500Ai. A high
a contagious, widely distributed bacterial
proportion of affected birds develop
disease that primaiily affects young ducks
mucopurulent or caseous salpingitis.

and less frequently turkeys and geese. Other Affected breeding stock should be waterfowl, chickens, and pheasants
slaughtered, because mally become blind
occasionally may be affected.

layers.

Affected turkeys, usually 5--15 wk old,

Etiology and Transmission: R anati
often exhibit dyspnea, droopiness, hm1ched
pestifer is grain-negative, nonsporulating, back, laineness, alld a twisted neck.

catalase and oxidase positive, and

Fibrinous pericai·ditis and epicarditis are
non-motile. It grows microaerophilically in
the most pronounced lesions. There may
enriched media. R anatipestifer possesses
also be fibrinous perihepatitis, airsacculitis,
few characteristic phenotypic properties,
alld purulent synovitis. Osteomyelitis,
so isolation and identification procedures
meningitis, alld focal pneun1onia are seen
should be polyphasic. A definitive diagnosis
occasionally. Mortality is 5o/o-600A,, alld
should include genotypic identification
conderrmations are 3o/o-13%.

(PCR an1plification of a partial region of the
rpoB or the 168 rRNA gene with subsequent

Diagnosis: Diagnosis is based on typical
sequencing is recommended). Just like

CNS signs (if present), lesions, and isolation

Pasteurnlla multocida, Rana tipestifer
and identification of the causative orgai1ism
includes a number (>20) of immunotypes

(using traditional biochemical chai·acteriza

( or serotypes). This complicates efforts at
tion). Other diseases, eg, colibacillosis (see
widespread prevention using bacterins,
p 2814), salmonellosis (seep 195), alld
because no cross-protection occurs
chlallwdiosis (seep 2808), may produce
between serotypes. However, cmTently,
similar lesions. Chocolate agar medimn is
much effort is on the seai·ch for crossrecommended for isolation, although blood protective vaccine candidates using ai1
agar is also used, with incubation at 37°C in
immunoproteomics approach.

a calldle jar or under 5% carbon dioxide.

The epidemiology and pathogenesis are

Several PCR-based diagnostic tests have
poorly understood. Ducks are believed to
been described, including assays for the
be infected from the envirorunent by the
ompA gene, 168 rRNA, rpoB gene, alld all respiratory route or when R anatipestifer is ERIC fragment. The published PCR tests are introduced into lesions oftl1e webbed foot.

all able to detectR anatipestifer, but a high Turkeys may be infected by injuries or by
rate of false-positive reactions may occur.

the respiratory route when allother •

Consequently, PCR ainplification of a partial
pathogen disrupts tl1e respiratory epitheregion of the rpoB or the 168 rRNA gene limn. Once the infection is established on
with subsequent sequencing Call be
a farm, it frequently becomes endemic.

recorrunended to confirm identification.

Recently, matrix-assisted laser desorption

Clinical Findings and Lesions: Signs
ionization time-of-flight mass spectrometry
usually develop after all incubation period

(MALDI-TOF MS) has been used successof2-5 days. Affected ducks, usually 1-7 wk fully for identification. The isolate should
old, often have oculai· alld nasal discharges,
be serotyped ( only a few laboratories are
mild coughing alld sneezing, tremors of the
capable), because the infonnation may be
head alld neck, alld incoordination. In
needed for vaccine selection alld epidemiotypical cases, affected ducklings lie on their logic studies. Plate agglutination is rapid
backs, paddling their legs. Stunting may
and convenient for this purpose. However,
occur. Necrotic dermatitis on the lower
unless titrations are carried out, only
back or around the vent may also be seen.

absorbed sera should be used because of

Fibrinous exudate in the pericardia] cavity
the existence of multiple alltigenic factors
alld over tl1e surface of tlle liver is the most
within a single strain. Biochemical
chai·acteristic lesion. Fibrinous airsacculitis
chai·acte1istics can be used to differentiate
is conunon, alld infection of the CNS Call
this orgailism from other bacteria that cause
result in fibrinous meningitis. The spleen
importallt diseases of ducks alld turkeys,
alld liver may be swollen. Pneumonia may
particularly Escherichia coli, P multocida.,

SALMONELLOSES

2865

Salmonella enterica, Coenonia anatine,
common in1munotypes of R anatipestifer,

Avibacterium gallinarum, and Bordetella are available for use in ducks. An autog
avium. Impression smears help to
enous oil-emulsion bacte1in can be used in
determine whether chlamydia is involved.

turkeys. Breeder ducks can be vaccinated

VetBooks.ir
with a bacterin or live vaccine to provide

Prevention and Control: Careful
protection to the ducklings that may last for
management practices are in1portant for
up to 2-3 weeks of age. A combination of
prevention of infection. A high level of
penicillin and streptomycin, or sulfaquinbiosecurity is essential. Cleaning and oxaline can be used for initial treatment,
disinfection between flocks and separation
but an antibiotic sensitivity test should be
of flocks on multiple-age farms are other
peiformed, because multiresistant strains
factors of major importance. Rigid
may develop. Enrofloxacin has also proved
sanitation and depopulation are necessary
highly effective in preventing mortality in
for elimination of the disease on endemiducklings when administered in ilie cally infected farms.

drinking water. However, cuJTent legislation

A bacterin and, more recently, a live
in many countries does not allow the use of
vaccine, which include the three most
quinolones in production animals.

SALMON ELLOSES

Salmonella infections are classified as
once common but has been eradicated from
nonmotile serotypes (S Pullorun1,
most commercial chicken stock in the USA,

S Gallinarun1) and ilie many motile
although it may be seen in other avian
paratyphoid Salmonella. These Salmonella species (eg, guinea.fowl, quail, pheasants,
infections have a worldwide distribution. As sparrows, pa.nots, canaries, and bulla result of the institution of a testing and finches) and in small backyard or hobby
control progran1 in the USA through tl1e
flocks. Infection in manm1a.Js is rare,

USDA-administered National Poultry
although experimental or natural infections

Improvement Plan, tl1e incidence of
have been rep01ted ( chimpanzees, rabbits,

S Pullorurn or S Gallinarun1 has decreased guinea pigs, chinchillas, pigs, kittens, foxes,
dramatically. Historically, S Arizonae was
dogs, swine, mink, cows, and wild rats).

placed in its own category, but it is now

Transmission can be vertical (transovarincluded with the paratyphoid Salmonella.

ian) but also occurs via direct or indirect

S Arizonae is an egg-transmiited disease
contact with infected birds (respiratory or
primarily of young turkeys. In addition
fecal) or contaminated feed, water, or litter.

to ilie above nonmotile salmonellae,

Infection transmitted via egg or hatchery

Salmonella paratyphoid infections in
contamination usually results in death
poultry are relatively common and have
during the first few days of life up to 2-3 wk
public health significance because of
of age. Transmission between farms is due
contaminated poultry product consumpto poor biosecurity.

tion.

S Pullorum and S Gallina.rum are highly Clinical Findings and Lesions: The
host-adapted to chickens and turkeys.

disease may be seen in all age groups, but

There are >2,500 nonhost-adapted species
birds <4 wk old are most commonly

(paratyphoid) tl1at may be transmitted to
affected. Birds may die in tl1e hatchery
almost all animals.

shortly after hatching. Affected birds huddle
near a heat source, are anorectic, appear

PULLORUM DISEASE
weak, and have whitish fecal pasting around
the vent ( diarrhea). Survivors are small in

Etiology and Transmission: Infections
size and frequently become asymptomatic
with Salmonella Pullorum usually cause
carriers with localized infection of the
very high mortality (potentially approaching ovary. Some of ilie eggs laid by such hens lOOOA,) in young chickens and turkeys within
hatch and produce infected progeny.

the first 2-3 wk of age. In adult chickens,

There may be no lesions due to an acute
mmtality may be high but frequently there
septicemia and death. Lesions in young
are no clinical signs. Pullorurn disease was
birds usually include unabsorbed yolk sacs

2866

SALMONELLOSES
and classic gray nodules in the liver, spleen,
foci; enlarged spleen and kidneys; anemia;
lungs, heart, gizzard, and intestine. Fi.rm,
and ente1itis.

cheesy material in the ceca ( cecal cores)

and raised plaques in the mucosa of the

Diagnosis: Diagnosis should be conlower intestine are sometimes seen.

firmed by isolation, identification, and

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Occasionally, synovitis is prominent. Adult
serotyping of S Gallinarurn (National
caniers usually have no gross lesions but

Poultry Improvement Plan testing
may have nodular pericarditis; fibrinous
procedtffe).

peritonitis; or hemorrhagic, atrophic,
regressing ovarian follicles with caseous

Treatment and Control: Treatment and
contents. In mature chickens, chronic
control are as for pullonm1 disease (see
infections produce lesions indistinguishable above). There are no federally licensed from those of fowl typhoid (see below).

vaccines in the USA. In other countries,
vaccines (killed or modified live) made from

Diagnosis: Lesions may be highly
a rough strain of S Gallinanun (9R) had suggestive, but diagnosis should be
vaiiable results in controlling mortality.

confirmed by isolation, identification, and

More recently, vaccines derived from outer
serotyping of S Pullorurn. Infections in membrane proteins, mutant strains, and a
mature birds can be identified by serologic
virulence-plasmid-cured derivative of
tests, followed by necropsy evaluation

S Gallinaium have shown promise in
complemented by microbiologic culture
protecting birds against challenge. The
and typing for confumation. Official testing
standai·d serologic tests for pullorum
recommendations for flocks in the USA are
disease are equally effective in detecting
outlined in the National Poultry Improvefowl typhoid.

ment Plan.

PARATYPHOID INFECTIONS

Treatment and Control: Treatment of
infected flocks to alleviate the perpetuation

Etiology: Paratyphoid infections can
of the carrier state is not recommended.

be caused by any one of the many non

Control is based on routine serologic testing host-adapted salmonellae. These Salmonella of breeding stock to assure freedom from
infect many types of birds, maimnals,
infection. In addition, management and
reptiles, and insects. Paratyphoid infections
biosecurity measures should be taken to
are of public health significance via
reduce the introduction of S Pullonun from contai11ination and mishandling of poultry
feed, water, wild birds, rodents, insects, or
products. S Typhirnurium, S Enteritidis, people. Birds should be purchased from

S Kentucky, S Heidelberg, S Hadar, and sources free of S Pullorwn ..

S Saintpaul are an10ng the most common Salmonella, infections in poultry. Some

FOWL TYPHOID
serotypes are more pathogenic than others.

The prevalence of other species varies

Etiology and Epidemiology: The
widely by geographic location.

causal agent is Salmonella Gallinarurn.

Transmission usually occurs horizon

The incidence of fowl typhoid is low in the
tally from infected birds, contaminated

USA, Canada, and some European countries environments, or infected rodents. Except but is much higher in other countries.

for S Enteritidis and S Arizonae, transmis

Although S Gallinarw11 is egg-transmitted sion of most serotypes to progeny from
and produces lesions in chicks and poults
infected breeders is mainly through fecal
similar to those produced by S Pullorurn,
contai11ination of the eggshell. S Enteritidis there is a much greater tendency to spread
and S Arizonae can infect the inte1ior of the among growing or mature flocks. Mortality
egg through transovarial transmission.

in young birds is similar to that seen in

Infected birds remain caniers.

S Pullorum infection but may be higher
in older birds.

Clinical Findings and Lesions: AIt110ugh not common, clinical signs are Clinical Findings and Lesions: The
sometimes seen in young birds. Mortality is
disease may be acute or chronic. Clinical
most often limited to the first few weeks of
signs and lesions in young birds are similar
age. Depression, poor growth, weakness,
to those seen with S Pullonun infection.

diaiThea, and dehydration are hallmarks of

Older birds may be pale, dehydrated, and
the disease, altl10ugh these clinical signs are
have diarrhea. Lesions in older birds may
not distinctive.

include a swollen, friable and often

Lesions may include an enlarged liver
bile-stained liver, with or without necrotic
with focal necrosis, unabsorbed yolk sac,

STAPHYLOCOCCOSIS

2867
enteritis with necrotic lesions in the
vaccination, and it should be used in
mucosa, and cecal cores. Infections
combination with other control measures
occasionally localize in the eye or synovial
to reduce the incidence of Salmonella
tissues. Conversely, there may be no lesions
infection.

due to acute death caused by septicemia.

S Enteritidis (a paratyphoid Salmonella VetBooks.ir

Isolation, identification, and serotyping of
serotype) is a major food safety concern
the causal agent are essential for diagnosis.

primarily for the egg-laying industry.

Serology is not highly reliable.

Possible sources in commercial layers
include transmission from breeders,

Treatment and Control: General control
contaminatecl environments, infected
measures for the paratyphoid Salmonella
rodents, and contaminated feed. Transmisinclude strict sanitation in the hatchery, sion to progeny from breeders is mainly
fumigation of hatching eggs, pelleting of
through eggshell contamination, although,
feed, cleaning and disinfection of poultry
unlike other paratyphoid Salmonella,
houses, rodent control, and use of
transovarial transmission may also occur.

competitive exclusion products. Mainte

The National Poultry Improvement Plan
nance of poultry in confinement and
includes S Enteritidis control measures
exclusion of all pets, wild birds, and rodents
in breeders, including depopulation of
help prevent introduction of infection. The
infected breeder flocks, cleaning and
use of antibiotics is highly debated. Several
disinfection of pullet and layer houses,
antibacterial agents help prevent mortality
rodent control programs, pest managebut cannot eliminate flock infection and ment, feed management, use of competitive
may lead to drng resistance. Vaccination
exclusion products, vaccination, biosecuwith live or ki.1.led products has been used.

rity, and proper handling and refrigeration

Complete protection is not afforded by
of eggs.

STAPHYLOCOCCOSIS

Staphylococcosis is a bacterial disease that
has been used to distinguish among the
can affect a wide range of avian species,
different strains. Staphylococcus toxins
including poultry, and is seen worldwide.

can enhance the pathogenicity of a strain.

Staphylococcus aureus is most conunon.ly
isolated from staphylococcosis case&, but

Transmission, Epidemiology, and
species such as S hyicus have also been

Pathogenesis: Because Staphylococcus
reported as the causative agent of osteomyis part of the norn1a.l skin and mucosa! flora, elitis in turkey pou.lts. The disease condimany infections are the result of a wound, tions associated with staphylococcosis
mucosa! damage, or both. Infection can
vary with the site and route of inoculation
also occur in the hatchery as a result of
and can involve the bones, joints, tendon
contan1ination of an open navel. Birds that
sheaths, skin, sternal bursa, navel, and yolk
are inrn1unocompromised are also more
sac. Economic losses may resu.lt from
prone to staphylococcal infections. Once in
decreased weight gain, decreased egg
the host, S aureus invades the metaphyseal
production, lameness, mortality, and
area of the nearest joint, which leads to
condemnation at slaughter.

osteomyelitis and localization within that
joint. Alternatively, the bacteria can invade

Etiology: S aureus is a gram-positive, the bloodstrean1 and lead to a systemic
catalase-positive, coccoid bacteria that
infection in mu.ltiple organs.

appears in grape-like clusters on stained
smears. S aureus is the most common

Clinical Findings: Omphalitis, or inisolate recovered from clinical cases. Most fection of the yolk sac, caused by S aureus
pathogenic strains have been coagu.lasehas been reported in young chicks and positive; however, coagu.lase-negative
poults (seep 2859). Its prevalence depends

Staphylococcus, including S hyicus, S epi
on its presence in the breeder flock and
dermidis, and S gallinarum have been the hatchery environment. Navel infections
reported from clinical cases. Phage typing
can occur in young hatchlings if the navel

2868

STAPHYLOCOCCOSIS
becomes infected with Staphylococcus.

Diagnosis: Although some lesions may be

Gangrenous dermatitis can occur after skin
suggestive of a Staphylococcus infection,
tratuna and subsequent contam.ination with
d.iagnosis is confirmed by identifying the

Staphylococcus. lmmunocompromised
organisms from stained smears of the lesion

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birds have a h.igher prevalence of gangreand by culture on blood agar plates.

nous dennatitis. Because Staphylococcus is

Phenotyping and genetic techn.iques have
found on the skin, skin injuries can also lead been used to classify stra.ins of poultry to localized abscesses, such as on the foot

S aureus. Differential d.iagnoses include

(btunblefoot). Finally, Staphylococcus can

E coli and Pasteurella mullocida as well be dispersed systemically and can cause
as other septicem.ic d.iseases of poultry.

arthritis, synovitis, osteomyelitis, and
endocard.itis. MostStaphylococcus

Treatment and Prevention: Staphyloinfections in poultry cause synovitis, with coccosis can be successfully treated with
lameness being the most common clinical
antibiotics, but an antim.icrobial susceptibilpresentation. The bones and associated ity test should be performed because
joints most frequently affected are those of
antibiotic resistance is common. Antibiotics
the leg, especially the stifle and tibiotarsus.

used to treat Staphylococcus infections

In addition, septicemia can result in green
include penicillin, erythromycin, lincomylivers or livers with multifocal necrosis and/
cin, and spectinomycin. Proper management
or granulomas. In acute infections, a sudden to prevent injury and in1munocomprom.ised increase in mortal.ity may be noted.

poultry helps prevent staphylococcosis.

Lesions: Chicks with omphalitis have

Because wounds are the primary route by
navels that are moist and dark, and affected
wh.ich Staphylococcus can enter the body, it birds are often lethargic. Infected yolk sacs
is important to reduce all potential sources
are retained longer than un.infected yolk
of injury to the bird. Wood splinters in litter,
sacs, wh.ich are nom1alJy resorbed by the
protruding wires from cages, and fighting/
developing ch.ick with.in the first week of
cann.ibalism have been associated with skin
life. Wected yolks are abnormal in color
wounds and staphylococcosis. Because

( dark green to brown), have a doughy
beak and toe trimming procedures in young
consistency, and are odorous. Gangrenous
chickens and turkeys could result in a
dennatitis is often reported in in1munocomstaphylococcal septicem.ia, ensuring that prom.ised ch.ickens and is often due to a
equ.ipment is sanitary will help to prevent
combination of S aureus and Clostridium outbreaks. Good litter management is
septicum and/or Escherichia, coli. Affected important in controlling foot-pad injuries to
areas are usually hemorrhagic and crepitant.

prevent bumblefoot. Hatchery san.itation

Lesions associated with septicem.ia are most and good egg management practices are also common. With.in the musculoskeletal
in1portant to reduce navel infections and
system, affected bones often have focal
omphalitis.

yellowish areas of necrosis, wh.ile lesions in
the joints contain purulent exudate. At the

Zoonotic Risk: S aureus can cause food processing plant, green liver has been
poisoning in people. Enterotoxin-producing
reported in turkeys that have had osteostrains are found on clin.icalJy healthy poultry, myelitis and synovitis. Liver spots and
and proper precautions should be taken
granulomas resulting from septicem.ia have
during the handling and.cooking of poultry
been a cause of liver condemnation. In acute products. Meth.icillin-resistant S aureus infections, necrosis and vascular congestion

(MRSA) has been isolated from poultry meat
are seen in the liver, spleen, kidneys, and
in a ntunber of countries, but the prevalence
other internal organs. Vegetations on the
and significance for hun1an health are
heart valves have been reported.

incompletely understood.

STREPTOCOCCOSIS

Streptococcosis has been reported in
form. Flock mortality can be as high as
numerous bird species throughout the

50%. Because streptococci are part of the
world. There are two forms of the disease,
normal flora of the intestinal mucosa of
an acute septicemic form and a chronic
most avian species, infections are often

TUBERCULOSIS

2869
thought to occur secondarily to other
salpingitis, pericarditis, myocarditis, and
diseases.

valvular endocarditis. Lesions on the heatt
valves appear as small yellowish white or

Etiology and Epidemiology: Streptan raised areas on the valvular surface.

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tococci are nonmotile, gram-positive,

Focal granulomas, as a result of septic
catalase-negative coccoid bacte1ia that
emboli, can be found in many tissues.

occur singly, in pairs, or in short chains

Gran1-positive bacterial colonies are readily
when observed on stained smears.

observed in thrombosed vessels and within

Streptococcus spp commonly associated
necro�ic foci microscopically.

with disease in avian species include

S zooepidemicus (S gatlinanim), S bovis,

Diagnosis: History, clinical signs, and

S dysgalactiae, S gallinaceus, and S muta,ns. lesions, along with demonstration of Strep

Streptococci have been associated with
tococcus-like bacteria in blood fihns or
acute septicemia, joint infections, cellulitis,
in1pression smears of affected tissues, allows
osteomyelitis, and endocarditis. Transmisfor a preswnptive diagnosis of streptococsion is via oral or aerosol routes as well as cosis. Isolation of Streptococcus spp from
through skin irtjwies.

lesions confums the diagnosis. Streptococci
can be cultured easily on blood agar.

Clinical Findings: Streptococcal

Differential diagnoses include other
infections can be localized or septicemic.

bacterial septicemic diseases, including

Endocarditis and lan1eness occur during the staphylococcosis, enterococcosis, subacute or chronic stage of the infection.

colibacillosis, pasteurellosis, and erysipelas.

In S zooepidemicus infections

Infectious laryngotracheitis, pasteurellosis

, clinical

,
signs are typical of an acute septicemic
avian influenza, and exotic Newcastle
infection, and lethargic birds are often
disease should be considered as differential
prostrate. In affected layers, egg production
diagnoses when blood is noted coming from
may drop by 15%. In pigeons, S bovis
the mouth.

infection produces acute mortality with
lan1eness, inappetence, diarrhea, and the

Treatment and Control: Antibiotics,
inability to fly. Acute fibrinopurulent
including penicillin, erythromycin,
cortjunctivitis has been noted in infections
novobiocin, oxytetracycline, chlortetracaused by other Streptococcus spp.

cycline, and tetracycline, have been used
to treat acute and subacute infections.

Lesions: Lesions in the acute septicemic

Clinically affected birds respond well
fom1 include splenomegaly, hepatomegaly
early in the course of the infection, but

(with or without reddish tan to white
this response decreases as tl1e disease
multifocal necrotic foci), and enlarged
progresses within a flock. Antimicrobial
kidneys. There may also be serosanguineous susceptibility testing should be performed fluid in the subcutaneous space and in the
to select a suitable antibiotic.

pericardium. Bloodstained feathers around

Because streptococcosis often occurs
the mouth and head due to blood from the
secondary to other diseases, it is irnpmtant
oral cavity have been reported occasionally. to prevent immunosuppressive diseases Cellulitis involving the skin and subcutaneand conditions. In addition, because skin ous tissues has been associated with both
wounds can provide an entry for Strepto

Escherichia coli and S dysgalactiae.

coccus, it is important to reduce this risk Chronic streptococcal infections result in
factor. Proper cleaning and disinfection can
arthritis and/or tenosynovitis, osteomyelitis, reduce environmental sources of infection.

TUBERCULOSIS

Tuberculosis is a slowly spreading,
turkeys. Tuberculosis is more prevalent
chronic, granulomatous bacterial
in captive than in free-living wild birds.

infection characterized by gradual

It is unlikely to be seen in commercial
weight loss. All birds appear to be
poultry because of the short life span
susceptible, although to variable degrees; and husbandry practices used. (See also pheasants seem to be highly susceptible,

TUBERCULOSIS AND OTHER MYC013ACTERIAL
whereas the disease is uncommon in

INFECTIONS,]) 687.)

2870

TUBERCULOSIS

Etiology and Epidemiology: Myco

Live birds may be tested with M avium
bacterium avium ss is the most conunon

PPD tuberculin, although these tests are
cause, although M genavense has been
of limited value in birds that do not have
isolated from some psittacine birds.

wattles (it is often difficult to inject

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Seroagglutination tests of isolates are
tuberculin intradermally because of skin
recommended to differentiate strains of
thickness at other sites). A test conduct

M avium that cause disease in chickens
ed in skin on the underside of the wing
and birds from those that fail to produce
has been used in Japanese quail exposed
disease in these species. M tuberculosis,
to M avium. The injection site is
the cause of tuberculosis in people, has
observed at 24 and 48 hr for induration
infrequently been isolated from parrots and
and swelling. A positive test indicates
canaries. M avium is very resistant; it can exposure to M avium; however, a
survive in soil for ;:,,4 yr, in 3% hydrochloric
negative test is of little or no significance.

acid for ;:,,2 hr, and in 2% sodium hydroxide

Large numbers of acid-fast bacteria in
for;,30min.

smears from lesions provide a tentative

Tuberculosis is found worldwide, most
diagnosis. Mycobacteriologic examinacommonly in small, barnyard flocks and tion is required to confirm a diagnosis.

in zoo aviaries; it is rarely found in young

Isolates can be identified based on
flocks. Wild birds, such as cranes,
biochemical, drug susceptibility, and
spruTows, starlings, and raptors, have
seroagglutination tests and by restriction
been found to be infected. Tuberculosis
length polymorphism analyses.

has been found in emus and other ratites.

The movement of ratites through sales ru1d

Prevention and Control: Addition of
the long life of these animals have made
exotic birds to an exhibit should originate
tuberculosis a major concern for ratite
from a closed collection with no histmy of
producers. Isolation of ratites purchased
tuberculosis, ie, tuberculosis has not been
at sales is essential to prevent the
reported previously or diagnosed on
introduction of tuberculosis into
necropsy during tl1e past 5 yr. If no history is
established flocks.

available, the birds should be quarantined

Infected birds with advanced lesions
or maintained in a separate exhibit away
often excrete the organism in their feces;
from the bird aviruy. Transmission is by
therefore, ingestion of contan1inated feces
ingestion of food or water contan1inated
is the most conunon route of transmission.

with M avium ss, ie, feces from contagious

Carcasses and offal may infect predators
birds. Therefore, it is reconm1ended that
and cannibalistic flock mates. Rabbits, pigs,
endangered and valuable species be housed
nonhuman prin1ates, and mink are readily
in individual exhibits.

infected. Cattle exposed to contaminated

Chemotherapy is ineffective, because
feces may develop granulomatous lesions in
mostM avium complex organisms ru·e
lymph nodes associated with the GI tract
resistant to antituberculosis drugs. In
and respond to M bovis purified protein
commercial poultty flocks, relatively rapid
derivative (PPD) tuberculin and to PPD of
turnover of populations, together with

M aviiim. M avium serovar l is often isolated improved general sanitation, has largely from tuberculous free-living wild birds
elin1inated this once common infection.

and birds in captivity. M avium ss and

Infected poultry should be destroyed, and

M genavense have been isolated from
housing facilities tl10roughly cleaned and
inununocompromised people; however,
disinfected using cresylic compounds.

these organisms only rarely cause disease

Quaternruy runmoniun1 compounds and
in noninrn1unocompromised individuals.

halogens ( eg, chlorine) do not effectively
kill mycobacteria. In exhibits with dirt

Clinical Findings and Diagnosis: Signs
floors, several inches of the floor should be
usually do not develop until late in the
removed and replaced with dirt from a place
infection, when birds become emaciated
where poultry have not been maintained. All
and sluggish and lruneness may be seen.

openings should be screened against wild

In chickens, granulomatous nodules of
birds.

varying size ru·e often found in the liver,

Aviru1 tuberculosis in zoos is difficult to
spleen, bone mruTow, and intestine. Some
eradicate. New additions to the aviruy
exotic species may have lesions in the liver
should be quarantined for ;:,,6 mo. Isolation
and spleen without intestinal or bone
and quru·antine of birds of unknown status
marrow involvement. Small mesenteric
purchased at sales is essential to prevent
nodules may be found. Lesions ru·e not
intt·oduction of tuberculosis into estabmineralized.

lished flocks.

MISCELLANEOUS CONDITIONS OF POULTRY

2871

TURKEY VIRAL HEPATITIS

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Turkey viral hepatitis is an acute, highly
be confluent. Areas of hemmThage or
contagious, frequently subclinical disease
congestion are also present and frequently
of turkey poults 5 wk of age. The disease is
obscure the degenerative changes.

widespread and common in some areas,

Occasionally, the liver is diffusely bilewith morbidity rates of as much as 1009'o.

stained. Liver lesions may resemble those

Mortality has been reported only in poults,
of bacte,ial infections, particularly from
is confined to a 4- to 8-day period, and may

Salmonella spp, PasleureUa. mullocida, or reach25%.

Escherichia coli, and infections caused by

Group 1 and Group 2 avian adenovirus and

Etiology: A picoma-like virus from poults
reovirus. The pancreas frequently exhibits
with typical lesions has been reported, but
relatively large, circular, gray areas of
its etiologic role has not been conclusively
degeneration. In the subclinical fonn, lesions
established. The causal virus has not been
are less extensive, and hepatic hemorrhage
fully classified, but a picomavirus from
or congestion is seldom prominent. Affected
turkeys with typical lesions of turkey viral
tissues return to nom1al in 3---4 wk.

hepatitis has been molecularly characterized and proposed as a new species in the Diagnosis: Salmonella spp and other order Picomavirales. It is isolated without
bacterial infections produce necrotic areas
difficulty from the liver and a variety of
in the liver that can be confused with those
other tissues, including the pancreas,
of viral hepatitis. Bacterial infections must
spleen, and kidney, as well as feces. The
be differentiated by appropriate culturing
virus is isolated less consistently from older
techniques. Liver lesions may resemble
birds. It grows readily in the yolk sac of 5- to
those of histomoniasis, but the absence of

7-day-old chicken or turkey embryos. It is
cecal lesions in turkey viral hepatitis helps
them1ostabile; resistant to ether, phenol,
to differentiate the two diseases. With
and creolin but not fonnalin; and susceptihistomoniasis, histologic examination or ble to high, but not low, pH.

demonstration of the respective etiologic
agents is necessary. Diagnosis is aided by

Clinical Findings: Disease is usually
demonstration of picomavirus by in1munosubclinical and becomes apparent only histochemical or molecular techniques from
when the birds are stressed. Affected birds
poults with typical lesions.

are stunted and unthrifty. Morbidity and
mortality vary according to the severity of

Control: There is no known treatment.

stress. In poults <5 wk old, morbidity may

Secondary bacterial invasion does not
reach lOOOA, and mortality 100/o-25%. Breeder
appear to be important, but if it occurs, it
flocks may exhibit decreased production,
should be treated on the basis of specific
fertility, and hatchability.

etiology. Although recovered birds
demonstrate resistance to infection, neutral

Lesions: Gross lesions are confined to
izing antibodies have not been detected.

the liver and pancreas. In the liver, foci of

Improved sanitation may be of value in
necrosis are 1-3 mm in diameter and may
preventing dissemination of the agent.

MISCELLANEOUS CONDITIONS

OF P OULTRY

ASCITES SYNDROME
fluid, which accwnulates most frequently
in tl1e two ventral hepatic, peritoneal, or

(Pulmonary hypertension syndrome,
pericardial spaces, may contain yellow

Waterbelly)

protein clots. Ascites may result from
increased vascular hydraulic pressure,

Ascites is an accumulation of noninflanunavascular dan1age, increased tissue oncotic tory transudate in one or more of the
pressure, or decreased vascular oncotic
peritoneal cavities or potential spaces. The

(usually colloidal) pressure, but is most

2872

MISCELLANEOUS CONDITIONS OF POULTRY
commonly associated with venous
blood (eg, acidosis, carbon monoxide),
hypertension resulting from right heart
increase blood volume (eg, sodiwn), or
failure in response to increased pulmonary
interfere witil blood flow tllrough tile lung
resistance.

( eg, lung patl10logy that narrows or

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The most common cause of ascites is
occludes capillaties, increased RBC rigidity,
increased vascular hydraulic pressure in the
or polycythemia with increased blood
venous system, which is most commonly
viscosity) may result in flock outbreaks of
caused by right ventricular failure (RVF),
pulmonary hypertension syndrome witil or
also associated witl1 hepatic fibrosis. It is
without ascites.

well documented that most cases are

The incidence of pulmonary hypertension
caused by a genetic predisposition to
syndrome is >2% in some broiler and many
pulmonary hypertension, which progresses
roaster flocks and is occasionally 15%-200/o
to congestive heart failure and terminal
in other roaster flocks. Right ventricular
ascites in many cases.

hypertrophy is the response to an increased

Pulmonary hypertension occurs
workload and eventually leads to RVF if the
frequently in chickens secondary to high
volume or pressure load persists. Hypertroaltitude-associated hypoxia with resultant phy and dilatation of tile tight ventriculai·
polycythemia and increased blood viscosity.

wall is directly related to pulmonary

It also occurs frequently secondary to tl1e
hypertension, and tile ratio of the tight

RBC rigidity of sodium toxicity and less
ventricle to tile total ventricular mass can
frequently from lung patilology. When
be used as a measure of the increased
ascites occurs at low altitudes in meat-type
pressure load on tile right ventricle.

chickens, which have a high metabolic
oxygen requirement, it is usually caused
by primary or spontaneous pulmonary

Clinical Findings: Occasionally, young
hypertension because of insufncient
broilers develop pulmonary hypettension
capacity of the pulmonary capillaries. Cold
syndrome, particularly if increased sodium
stress, even briefly, during the fast 3 wk of
or lung pathology ( eg, aspergillosis) is
life is known to markedly increase
involved, but mortality is greatest after
predisposition to ascites syndrome.

5 wk of age. There are no signs until RVF

In poultry, liver dan1age may be caused by
occurs and ascites develops. Clinically
aflatoxin or by toxins from plants such as
affected broilers are cyanotic, the

Crolalaria. In broiler chickens, obstructive abdominal skin may be red, and peripheral
cholangiohepatitis (caused by Closlridiurn
vessels congested. Because growth stops
perf1ingens infection) is the most corrunon as RVF develops, affected broilers may be
cause of the liver damage, which results in
smaller thai1 their pen mates. However,
ascites. In both meat-type ducks and
rapid growth rate is a known predisposing
breeders, amyloidosis of the liver may also
factor, and sometimes the largest broilers
cause ascites.

are affected, with occurrence in males
more frequent than in females. The ascites

Pathogenesis and Epidemiol gy:

increases the respiratory rate and reduces

Pulmonary hypertension syndrome is caused exercise tolerance. Affected broilers by increased pressure in the pulmonary
frequently die on their backs. Not all
aiteries when tile heait tries to pump more
broilers that die from pulmonary
blood through the lungs to meet tile body's
hypertension syndrome have ascites.

oxygen requirement. The resultant volume

Death may occur suddenly before signs
and pressure overload on the tight ventricle
are seen.

cause dilatation and hypertrophy of tile

Lesions: Most lesions are the result of
right ventricular wall, valvular insufficiency,
increased venous hydraulic pressure

RVF, and ascites.

secondary to RVF. There is a variable

Bird lungs ai·e rigid and fixed in the
an10unt of clear yellow fluid and clots of
thoracic cavity. The capillaties can expand
fibrin in tile hepatoperitoneal spaces. The
very little to accommodate increased blood
liver may be swollen and congested, or fu-m
flow. Lw1g size in propottion to body weight, and irregular witil edema, and have clotted and particularly to muscle mass, decreases
protein adherent to the surface. It may be
as meat-type chickens grow. Increased
nodular or shrunken; it may be white with
blood flow results in prin1ary pulmonary
subcapsular edema and a thickened capsule
hypertension and cor pulmonale with
or have large or small blebs of fluid between
sporadic cases of RVF and ascites in
the capsule ai1d tile visceral peritoneum.

fast-growing broilers. Predisposing factors

Hydropericardium is mild to mai·ked, and
that increase oxygen demand ( eg, cold),
occasionally there is peticarditis witl1
reduce oxygen-carrying capacity of tile
adhesions, usually from secondary

MISCELLANEOUS CONDITIONS OF POULTRY

2873
infections. Right ventricular dilatation and
trauma (Staphylococcus) or as an extension
mild to marked hypertrophy of the right
of a systemic infection.

ventricular wall may be noted. The right
atrium and vena cava are markedly dilated

BREAST BUTTONS

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in most cases. Occasionally, there is
thimling of the left ventricle. The lungs are

Breast buttons develop in a location similar
extremely congested and edematous. The
to that of breast blisters (see above). They intestine may or may not be empty.

have a localized, hard crust on the surface
and a core of c(ead skin and chronic

Diagnosis: Broilers that die from ascites
inflainmation extending into tl1e subcutis.

or suddenly as the result ofRVF or

The cause is not well defined, but a breast
pulmonary hypertension can be identified
button may stait as a chemical burn due to
by the enlarged heait; enlarged, thickened
prolonged contact of poorly featl1ered skin
right ventricle; or fluid in the body cavities
with wet litter containing ai11monia or
and heait sac. If the wall of the tight
toxins. The presence of good quality, dry
ventricle is enlarged or thickened, the
litter is associated with a reduced number
broiler has probably died from pulmonai,7
of affected turkeys.

hypertension syndrome, even if there is no
fluid in the body or heait sac.

CANNIBALISM

Control: Reducing the birds' metabolic

Cannibalism stems from aggressive
oxygen requirement by slowing growth or
behavior of chickens and turkeys that
reducing feed density or availability can
may begin by feather pecking by socially
prevent ascites caused by pulmonary
dominant birds. It may also involve vent
hypertension syndrome. Enviromnental
pecking immediately after oviposition, or
temperature, hwnidity, and air movement
picking at skin on the head, comb, wattles,
should be controlled to prevent excessive
or toes. No single cause has been
loss of body heat, particularly in the early
identified, but crowding, excessive light
neonatal period. Even brief exposure to
intensity, and nutritional imbalances are
cold stress during the first weeks of life
correlated with its occurrence. Additionis known to predispose flocks to this ally, in overweight pullets entering egg
condition. Ascites caused by other factors
production or hens in production, mucosa

( eg, sodium, lung dainage, liver dainage, etc) will protrude from the vent dming and can be prevented by avoiding the etiologic
after egg laying, and this red tissue attracts
agents involved. Altitudes >3,000 ft (900 m)

pecking. Other factors are insufficient
are unsatisfactory for meat-type chickens,
feeder space, mineral and vitain.in
and growth must be slowed to prevent
deficiencies, skin injuries, and failure to
mortality. More care to prevent chilling is
remove any dead birds daily. In addition to
also necessary at higher altitudes. Research
the loss of birds due to pecking trauma,
has demonstrated that broilers cai1 be genetcannibalism often leads to transmission of ically selected for both resistance and
infectious diseases ( eg, e1,7sipelas) and
susceptibility to pulmonary hypertension
botulism.

syndrome and associated ascites.

Control depends on correcting or
reducing the above risk factors. Interven

BREAST BLISTERS
tions include correcting an inadequate diet,
replacing mash feed with pelleted feed,

In chickens and turkeys, a bursa lined with
rearing birds on floor litter rather than slats,
synovial membrane is nonnally present
reducing light intensity, and providing
over the anterior projection of the keel
perches as a refuge for targeted birds.

bone. When this bursa becomes inflan1ed by

Environmental enrichment such as hanging
trawna or infection, fluid accumulates and
white or yellow strings may be beneficial.

appears as a fluid-filled blister 1-3 cm in

Trimming the sharp distal end (tip) of the
dian1eter. Factors in trawna to the bursa
upper beak will decrease skin traU111a from
include poor feathering, hard flooring, and
pecking; th.is may be done at 1 day of age
leg weakness, which is associated with
and repeated between 6 and 12 wk of age in
increased time of sitting on the keel
maturing pullets or turkeys. The tip of the

(sternum). Coarse bedding materials or wet
beak can also be treated by infrared heat on
litter conditions are predisposing factors
the day of hatching, which results in a
and should be corrected when identified.

shortened beak witl1 minimal stress.

Infectious causes of sternal bursitis include

Caute,ization is required to provide

Mycoplasma synoviae, Staphylococcus,
hemostasis dllling beak trimming in older
and Pasteurella spp, either from local
poultry.

2874

MISCELLANEOUS CONDITIONS OF POULTRY

FLUKE INFECTIONS
turkeys. The crop is grossly distended and
contains foul-smelling fluid, feed, and litter.

Modem poultry housed indoors are

Feed utilization is impaired, and severely
essentially free of flukes, because all flukes
affected birds become thin or emaciated.

require a snail as an intermediate host and

Survivors often are condemned or trinuned

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often require a third invertebrate host.

at processing to reduce contamination by

However, these parasites persist in backyard crop contents.

poultry (seep 1815), which may have contact The cause is not known, but a hereditary
with snails or other hosts and wild birds. The predisposition, potentially associated with trend toward free-range rearing of poultry
hyperphagia, has been suggested in turkeys.

may increase the exposure of poultry to this

Incidence may increase with erratic or
type of parasite, but flukes are mainly
excessive feed or water conswnption. Vagus
reported in wild birds with low prevalence.

nerve dan1age has also been postulated as a

Prosthogonimus macrorchis, the
cause in rare cases. There is no known
oviduct fluke of poultry, infects birds after
efficacious treatment.

they conswne infective metacercariae in
larval or mature dragonflies, the secondary
host. The fluke matures in -2 wk in the

URATE DEPOSITION (GOUT)

bursa ofFabricius or, in gallinaceous birds

Avian species excrete nitrogenous wastes
without a functional bursa ( eg, chickens,
as urates bound in colloidal fom1 with
turkeys, pheasants), in the oviduct.

mucus in their urine. Renal dysfunction

Light infections without signs appear in
decreases the clearance of uric acid from
ducks and other birds with a functional
the blood, which results in hyperuricemia
bursa. In gallinaceous birds, heavy infections with precipitation of insoluble products in the oviduct cause inappetence, droopiwithin the kidney itself or other organs, ness, weight loss, calcareous cloaca]

leading to urate deposition or urolithiasis
discharge, depressed egg production, and an

(gout). Urate deposits are white and
increase in soft-shelled eggs. Lesions range
semisolid and must be differentiated from
from mild i.nflanunation to distention or
yellow fib1inous or purulent i.nflan1matory
rupture of the oviduct; death may result.

exudates that are secondary to infectious

Diagnosis by fecal examination is unreliable,
causes, such as synovitis, peritonitis,
because fluke eggs are not consistently
perihepatitis, and pe1icarditis.

present. Adult flukes may appear in the bird's Visceral urate deposition occurs after
eggs or be found in the oviduct on necropsy.

rapidly progressing renal failure, or as a

To prevent fluke transmission, birds must
teffilinal event with acute decompensation
be kept from feeding on dragonflies. There
of chronic renal disease. Deposits develop
is no effective treatment approved for use in most commonly on the pericardiwn, poultry. Carbon tetrachloride, a common
peritoneun1, and liver capsule, and rarely
remedy, is highly toxic to chickens and
on synovial surfaces of joints and tendons.

other birds.

Microscopically, urate deposits are often

Collyiiclumfaba, another common fluke
seen as feathe1y crystals or basophilic
in birds, appear as subcutaneous cysts
spherical masses, usually with little

4-6 nun in diameter (usually containing two
inflammation due to the rapid course.

adults) anywhere on the body but more

Visceral urate deposition may be secondary
frequently near the vent in turkeys,
to urolithiasis, which is common in older
chickens, and other birds. The cysts ooze an
laying chickens. Progressive obstruction
exudate, which attracts flies and predisof the ureters by uroliths causes kidney poses to bacterial infection. Signs in young
atrophy "upstream" of the site of ureteral birds include locomotor difficulty and
obstruction and compensatory hypertrophy
inappetence; heavy infections may cause
by the undamaged portions of the kidney.

death. The parasites can be removed

Distended ureters often contain brittle,
surgically. The life cycle is unknown but
white, staghom calciwn urate calculi or
probably involves snails and insects such
uroliths.

as dragonflies or mayflies. Prevention of

Predisposing factors for visceral urate
infection requires restricting birds from
deposition and urolithiasis in poultry
bodies of water and areas frequented by
include infectious bronchitis virus, avian
aquatic insects.

nephritis virus, and cryptosporidiosis.

Noninfectious causes include dehydration,

PENDULOUS CROP
ingestion of feed containing >3% calcium
by nonlaying chickens, vitamin A

Incidence of pendulous crop is low in flocks
deficiency, and exposure to myotoxins (eg,
of chickens but appears to be increasing in
oosporein). Other avian species commonly

ECTOPARASITES

2875
develop visceral deposits secondary to

Deposits develop on synovial membranes
nephrotoxin exposure, most commonly
in the toes and wing joints and incite a
aminoglycoside antibiotics or heavy
chronic granulomatous reaction to urate
metals.

crystals (tophi). Articular urate deposi

Articular urate deposition is less
tion may be seen in birds that have

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common and occurs after longterm
hereditary defects in uric acid metaboincreases in serum levels of uric acid.

lism or that are fed excessive protein.

ECTOPARASITES

BEDBUGS
and death, particularly in young birds. Bites
around the eyes can cause ulcerations,

Cimex lectularius is a common bloodsuckresulting in blindness.

ing parasite in temperate and subtropical

The Western chicken flea, or black hen
climates that attacks poultry, people, and
flea, Ceratophyllus nige1·, seems to be most other manunals. It is rare in modem
confined to the Pacific coast area of the USA
laying operations, but breeding houses and
and Canada. This flea breeds in droppings
pigeon lofts may become heavily infested.

and feeds on birds only occasionally. The

The life cycle may be completed in 2-6 wk

European chicken flea, C gallinae, is or extend much longer, because nymphs
found worldwide. It breeds in nests and
can withstand fasting for -70 days, and
litter and is on the birds only to feed. In addiadults for as long as 12 mo. Feeding usually tion to chickens, it attacks many other birds
occurs at night. Bedbugs become engorged
as well as people and domestic pets. Heavy
within 10 min, then hide in cracks and
flea infestations cause host emaciation and
crevices. If attacked by large numbers of
reduced egg production.

bedbugs, birds may become irritable and

The most important flea control measures
anemic. Bites are usually followed by
are removing infested litter and dusting the
swelling and itching due to ir\jection of
litter surface with carbaryl, coun1aphos,
saliva into the wound. Signs of infestation
malathion, or pyretlrroids to kill inunature
include bug fecal droppings on eggs and
fleas. Insect growth regulators such as
nest boxes, breast and leg skin lesions,
methoprene are also effective. Sticktightreduced egg production, and increased feed fleas can be controlled by topical applicaconsumption.

tion of pyrethrin.

Control is best accomplished by
thoroughly cleaning the houses, reducing
hiding places for the bedbugs, and

FLIES AND GNATS
fumigating the houses with organophosphates or pyrethroids that remain on Biting Midge
sw·faces providing access to hosts.

Culicoides spp (Ceratopogonidae) feed on

FLEAS
blood and transmit blood parasites to birds.

They are vectors for transmission of

The sticktight flea, Echidnophaga

Haemoproteus to ducks and geese in
gallinacea, is a major poultry pest in the

Canada and turkeys in North America, and
subtropical and tropical New World. It is
of Leucocytozoon to chickens in Southeast
unique among poultry fleas in that the adults Asia and Japan. They also transmit the skin become sessile parasites and usually remain mite Myialges anchora. (Epiderrnoptidae).

attached to the skin of the head or anus for

Bites are reddish and itch for as long as 3
days or weeks. The adult females forcibly
days. Midges feed at twilight or night, and
eject their eggs so that they reach surroundtypical mesh screens do not keep them out.

ing litter. The larvae develop best in sandy,

Pyretlrroid insecticides can provide
well-drained litter. Hosts of the adult flea
temporary control.

include chickens, turkeys, pigeons,
pheasants, quail, people, and many other

Black Fly
man1mals. Fleas cause irritation, restless

Simulium spp (Sirnuliidae ), also known
ness, and blood loss that results in anemia
as buffalo gnats and turkey gnats, are

2876

ECTOPARASITES
bloodsuckers and transmit leucocytozoonotoxemia, and paralysis. Egg production sis (seep 2783) to ducks, turkeys, and other decreases. Red spots can be seen on the
birds. They are most abundant in the north
skin where the ticks have fed. Because the
temperate and subarctic zones, but many
ticks are nocturnal, the birds may show

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species are found in tropical areas. They
some uneasiness when roosting. Death is
often attack in swarms and cause weight
rare, but production may be severely
loss, reduced egg production, anemia, and
depressed.

death of birds either directly or tl1rough

After houses are cleaned, walls, ceilings,
disease transmission. Control is extremely
cracks, imd crevices should be treated
difficult because immature stages are
thoroughly ( using a high-pressure sprayer)

restricted to running water, which is often
with carbaryl, coumaphos, malathion,
some distance from the poultry farm. Larval
permethrin, stirofos, or a mixture of stirofos
control can be achieved with applications of and dichlorvos. Cracks and crevices should Ba,cillus thuringiensis israelensis during
be filled in.

early spring before adults emerge. Chemical
larvicides such as temephos and metl1oxy

LICE
chlor can also be used. Screens of 24 mesh
per in. (2.54 cm) or smaller are required for

Avian lice, which belong to the order
adult control. However, black flies rarely

Mallophaga, have a life cycle of -3 wk and
enter shelters.

nom1ally feed on bits of skin or feather
products. Lice may live for several months

Pigeon Fly
on the host but only remain alive for -1 wk

The pigeon fly, Pseudolynchia cana1iensis
off the host. People and other mammals

(Hippoboscidae), is an important bloodmay harbor avian lice, but only temporarily.

sucking parasite of pigeons in warm or tropi

In intensive poultry systems, the most
cal areas. It can transmit the blood parasites
conm10n and economically important louse

Haemoproteus and 1iypanosoma, the skin to both chickens and turkeys is M enacan
mite Myialges anchora (Epidem1optidae),
thu s stramineus, the chicken body louse,
and pigeon lice (Columbicola columbae). It
which typically is fow1d on t11e breast, vent,
may also cause heavy losses in squabs. The
and thighs. It punctures soft quills near their
pigeon loft should be cleaned every 20 days,
base or gnaws the skin at the base of the
and squabs can be dusted with pennethrin
feathers and feeds on the blood. Chickens
or delta.methrin.

are less commonly infested with Menopon
gallinae ( on feather shafts), Lipeurns
caponis (mainly on the wing feathers),

FOWL TICKS

Cuclotogaster hetet'Ographus (mainly on
tl1e head and neck), Goniocotes gallinae

The fowl tick, Argas persicus, is found

(very small, in the fluff), Goniodes gigas
worldwide in tropical and subtropical

(the large chicken louse), Goniodes
countries and is the vector of B01relia
d:issimil'is (the brown chicken louse),
ansetina (avian spirochetosis, seep 2813) Men.acanthus cornutus (the body louse),
and the rickettsiaAegyptianella pullo1um,

Uchida pallidula (the small body louse), or
which causes fowl disease (aegyptianello

Oxylipeu1us dentatus. Turkeys may also
sis, seep 2780). In tl1e USA, theArgas
be infested with Chelopistes meleag1idis
persicus complex has been divided to

(the large turkey louse), and Oxylipeurus
include A miniatus,A sanchezi, and A
polytrapezius (the slender turkey louse).

rndiatus in addition to A persicus. These Because lice tnmsfer from one bird
ticks are particularly active in poultry
species to another when the hosts ill'e in
houses during warm, dry weatl1er. All stages close contact, other domestic and caged may be found hiding in cracks and crevices
birds may be infested with species of
during the day. Larvae can be found on the

Mallophaga that are usually host-specific.

birds, because they remain attached and

Lice also sometimes reach new bird hosts
feed for 2-7 days. Nymphs and adults feed
by using louse flies (Hippoboscidae) for
at night for 15-30 min. Nymphs feed and
transportation. Some lice of geese and
molt several times before reaching the
swans are vectors of filarial nematodes.

adult stage. Adults feed repeatedly, most

Heavy populations of the chicken body
commonly under tl1e wings, and t11e females louse decrease reproductive potential in lay as many as 500 eggs after each feeding.

males, egg production in females, and

Adult females may live >4 yr witl1out a
weight gain in growing chickens. The skin
blood meal.

irritations are also sites for secondary

Fowl ticks produce anemia (most
bacterial infections. Other species of lice
in1portant), weight loss, depression,
are not highly pathogenic to mature birds

ECTOPARASITES 2877
but may be fatal to chicks. Examination

Eastern, Western, and Venezuelan equine
of birds, particularly around the vent and
encephalitis viruses, fowl poxvirus, and the
under the wings, reveals eggs or moving lice
bacteriaSalmonella Enteritidis, Pasteur
on the skin or feathers.

ella multocida, Coxiella burnetii, and

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Lice are usually introduced to a farm

Borrelia anserina has been demonstrated.

through infested equipment ( eg, crates or

Obtaining mite-free birds and using good
egg flats) or by gallifonn birds. Lice are best
sanitation practices are inlportant to
controlled on caged chickens or turkeys by
prevent a buildup of mite populations. Once
spraying with pyrethroids, carbaryl,
poultry hav� been infested, control may be
coumaphos, malathion, or stirofos. Birds
achieved by spraying or dusting the birds
on the floor are more easily treated by
and litter with amitraz, carbaryl, coumascattering carbaryl, coumaphos, malathion, phos, malathion, stirofos, or a pyrethroid
or stirofos dust on the litter. Eggs are not
compound in areas where the parasites
killed, so insecticide treatment should be
have not developed resistance to these
repeated after 10 days.

chemicals. Miticide spray treatments must
be applied with sufficient force to penetrate

MITES
the feathers in the vent area. Nicotine
sulfate is an effective fumigant for mites but

The most economically important of the
is particularly hazardous. Pyrethrins and
many external parasites of poultry are mites
piperonyl butoxide are initially active but
of the families Dermanyssidae ( chicken
have poor residual killing power. For
mite, northern fowl mite, and tropical fowl
control of chicken mites, in addition to
mite) and Trombiculidae (turkey chigger).

treating the birds, the inside of tl1e house
and all hiding places for the mite (such as

Chicken Mite
roosts, behind nest boxes, and cracks and

(Red mite, Roost mite, Poultry mite)

crevices) must be treated thoroughly using
a high-pressure sprayer. Dinlethoate and

De,manyssus gallinae infests chickens,
fenthion may be used as residual house
turkeys, pigeons, canaries, and various wild
sprays when poultry are not present. Inert
birds worldwide. These bloodsucking mites
dusts such as diatomaceous earth and pure
will also bite people. While rare in modern
syntl1etic an10rphous silicas can be effective,
commercial cage-layer operations, it is
but application rates need to be high when
found in breeder and small farm flocks.

the hwnidity is very high. Systemic control

Chicken mites are nocturnal feeders that
with ivennectin (1.8--5.4 mg/kg) or
hide during the clay under manure, on
moxidectin (8 mg/kg) is effective for short
roosts, and in cracks and crevices of the
petiods, but the high dosages are expensive,
chicken house, where they deposit eggs.

close to toxic levels, and require repeated

Populations develop rapidly during the
use.

warmer months and more slowly in cold
weather; the life cycle may be completed in

Common Chigger
only 1 wk. A house may remain infested for

6 mo after birds are removed.

The common chigger, Trombimla

Transmission of the chicken mite, as well
a{freddugesi, and other chigger species
as the northern fowl mite and the tropical

(harvest mites, red bugs) infest birds as well
fowl mite (see below), is by mite dispersion as people and other mammals, feeding on
or by contact with infested birds, anin1als,
partially digested skin cells and lyn1ph.

or inaninlate objects. In the integrated

Heavily parasitized birds become droopy,
poultry industry, mites are dispersed most
refuse to eat, and may die from starvation
frequently on inanimate objects such as egg
and exhaustion. Larvae may be found either
flats, crates, or coops or by personnel going
singly or in clusters on the ventral portion of
from house to house or farm to farm.

the birds. Control on the range is aided by

Heavy infestations of either chicken
keeping the grass cut short and dusting with
mites or northern fowl mites decrease
sulfur, carbaryl, or malathion.

reproductive potential in males, egg
production in females, and weight gain in

Depluming Mite
young birds; they can also cause anemia and The deplumi.ng mite, Neocnemidocoptes death. Chicken mites may be found in the
gallinae, is found worldwide and burrows
chicken houses during the day, particularly
into the epidennis at the base of feather
in cracks or where roost poles touch
shafts, causing intense irritation and featl1er
supports, or on birds at night. Their role as
pulling and loss in chickens, pheasants,
vectors of other pathogens in nature needs
pigeons, and geese in spring and summer.

study, but experin1ental transmission of

Hyperkeratosis, skin lesions, and digit

2878

ECTOPARASITES
necrosis can result from the burrowing.

usually tunnels into the tissue under the

Affected birds should be isolated and
scales of the legs. It is rare in modem
treated with ivermectin, malathion, or
poultry facilities. When found, it is usually
sevin dust.

on older birds on which the irritation and

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exudation cause the legs to become

Feather Mite
thickened, encmsted, and unsightly. Feet

Most feather mites belong to the families
and leg scales become raised, resulting in

Analgidae, Pterolichidae, and Proctophyllan1eness. Birds stop feeding, and death can lodidae. Surface feather mites feed mainly
result after several months. This mite may
on feather oils, deb1is, fungi, and skin
occasionally attack the comb and wattles.

scales. More than 25 species, including

The entire life cycle is in the skin; transmis

Megninia C'ltbilalis, M ginglymura, and
sion is by contact. lnfections can be latent

Plerolichus obtusus, are found on domestic for long periods tmtil stress triggers a mite poultry, but they are rare on modem poultry
population increase.

ranches. Quill mites (Syringophilidae and

For control, affected birds should be

Gaudoglyphidae) Live in quills and feed on
culled or isolated, and houses cleaned and
quill tissue or fluids obtained by piercing the sprayed frequently as recommended for tl1e calanms wall. Sy1ingophilus bipeclinalus
chicken mite (see above). Individual birds
is found in chicken and turkey feather quills
should be treated with oral or topical
worldwide, and Columbiphilus polonica,
ivermectin or moxidectin (0.2 mg/kg), l()OA,

Derrnoglyphus elongalus, and Gaudogly
sulphur solution, or 0.5% sodium fluoride.

phus minor live in chicken quills in Europe.

Feather mites do Little economic dan1age

Cyst Mite
but may reduce egg production via malnutri

Laminosioptes cyslicola,, the fowl cyst
tion, feather loss, and de1matitis. Affected
mite, is a small cosmopolitan parasite of
birds should be dusted with pyrethrin or
chickens, turkeys, and pigeons that is most
carbaryl powder, or oral or topical
often diagnosed by observing white to
ivem1ectin can be applied.

yellowish caseocalcareous nodules -1-3
mm in diameter in the subcutis, muscle,

Northern Fowl Mite
lungs, and abdominal viscera. Careful
examination of the skin and subcutis of

The northern fowl mite, Ornilhonyssus
sylviarum,
birds under a dissecting microscope
is the most important parasite
frequently reveals the mites. DestI·oying
of caged layers and breeding chickens in
the bird has been the best control for this
the USA and is a serious pest of chickens
parasite, but ivennectin may be effective.

throughout the temperate zone of other
cotmtries. On turkeys, it is second in
importance only to the turkey chigger in

Tropical Fowl Mite
areas where the turkey chigger is found. It

The tropical fowl mite, Ornilhonyssus
has been reported from many species of
bursa, is distributed throughout the wam1er birds and from rats, mice, and people;
regions of the world and has been reported
however, fertile populations are reported
in Hawaii, Texas, Florida, Illinois, Indiana,
only on birds. Northern fowl mites are

Maryland, and New York. It closely
obligate bloodsucking parasites that
resembles the northern fow! mite (see
nom1ally spend their entire life cycle (-1 wk) above) in its biology and habits but lays a on the host. Off the host, mites may Live as
greater proportion of its eggs in the nest.

long as 2 mo, depending on temperature and Hosts include chickens, turkeys, ducks, relative humidity. Northern fowl mites are
pigeons, span-ows, starlings, mynall birds,
found on eggs or by parting feathers in the
and people. Western equine encephalomyvent area, which may have thick, cmsty elitis virus has been recovered from this
skin, severe scabbing, and soiled feathers.

mite, but there is no evidence it transmits

Western equine encephalomyelitis, St.

the virus.

Louis encephalitis, and Newcastle disease

For clinical findings and control, see
vimses, as well as fowlpox vims, have been
above.

isolated from these mites. However, tl1e mites
are not significant vectors oftl1ese vimses.

Turkey Chigger

For clinical findings and control, see above.

The larvae of Neoschongaslia, americana,
the turkey chigger, are parasitic on

Scaly Leg Mite
numerous birds. Across the southern USA,

The scaly leg mite, Knernidocoptes mutans, they are the major pest of turkeys ranged on is a small, spherical, sarcoptic mite that
heavy clay soils in the summer. The chiggers

GANGRENOUS DERMATITIS

2879
feed in groups of as many as 100 mites per

St. Louis encephalitis, fowlpox, and West
lesion for 8-15 days. Turkeys may have

Nile viruses. West Nile virus is transmitted

25-30 lesions each. One lesion, 3 mm in
from infected birds to other birds prin1arily
dian1eter, may cause significant downgradby mosquitoes, particularly Cule.x spp in the ing at market tin1e. To prevent downgrading,

USA, and has been found in >200 species

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turkeys must be protected for at least 4 wk
of birds in America, including chickens,
before marketing.

turkeys, pigeons, budgerigars, cockatiels,

Sprays or dusts of carbaryl, malathion,
ducks, finches, and birds of prey. (See also
or chlorpyrifos on turkey ranges control

WES!' NILE vr�us INFECTION, p 2893.)

chiggers. A preventive measure now used in

Removal of mosquito-breeding habitats
many turkey-growing areas includes a shift
by emptying water-filled containers,
from range to confinement rearing, or use of clearing pool and pond edges of emergent sheds to provide shade.

vegetation, draining swan1py areas, and
filling low areas that collect water are the

MOSQUITOES
best physical control measures. Insecticidal control involves chemicals such as Mosquitoes that feed on poultry blood
malathion, propoxur, permethrin, chlorpyriusually belong to the genera Cu lex, Aedes, fos, or temephos. lnsect growth regulators
or Psorophora. Large numbers can
such as methoprene and cliflubenzuron
decrease egg production or cause death.

are also effective. Microbial control of

Mosquitoes transmitPlasmodiiim gal
mosquito larvae uses Bacillus lhwingienlinacemn ( chicken malaria), P hermani sis israelensis and, against Culex spp, (in turkeys), and other Plasmodium

Bacillus sphaericus. Screening to prevent
species causing avian malaria. They also
mosquito entry, residual wall sprays, and
transmit many viruses, including Eastern
fogging within poultry houses also aid in
and Western equine encephalomyelitis,
control.

GANGRENOUS DERMATITIS

(Necrotic dermatitis, Clostridial dermatitis, Gangrenous cellulitis, Gangrenous dermatomyositis, Gas edema disease)

Gangrenous dennatitis is a disease of
inclusion body hepatitis. Environmental
turkeys and chickens caused by Clost1id
conditions that promote poor litter
ium septicum, C pe1fringens type A, and
conditions may also predispose flocks to

Staphylococc:us aureus, either singly or in gangrenous dernrntitis, especially when
combination. The condition is characterized present in coajtmction with challenges from by rapid onset of acute mortality. Birds
immunosuppressive viruses. Failing to
succun1bing to the infection have necrosis
remove moribund or dead birds may
of the skin and subcutaneous tissue, usually
increase incidence of the disease, because
involving the breast, abdomen, wing, or
such birds serve as a reservoir for the
thigh.

causative agent(s). Management practices

Both clostridia and staphylococci are
that lead to scratching, such as overcrowdubiquitous in the poultry house environing, feed outages, meal time feeding, and ment and in (intestine) or on (skin) tl1e
bi.rd migration in t1.mnel-ventilated houses
birds. The presence of these organisms,
may increase incidence of infection.

however, does not necessarily indicate a

Affected fanns tend to have repeat
disease challenge. Other conbibuting
outbreaks if the environment is not tJ·eated.

factors are tl10ught to play a major role in

Incidence and severity of tl1e disease
development of clinical disease within a
depend on the bacterial strains involved in
flock. For example, gangrenous dermatitis
tl1e infection, their ability to produce toxins,
often is believed to occur as a sequela of
and the specific toxins produced.

other diseases that produce imrnunosuppressive effects such as infectious bursa!

Clinical Findings: The incubation period
disease, chicken infectious anemia,
is relatively short (12-24 hr), with deatl1
reticuloendotheliosis, reovirus, and
occuntng in well-fleshed birds. Otl1er

2880

GANGRENOUS DERMATITIS
mortality and characteristic gross lesions.

Diagnostic confirmation is based on the
presence of lesions and isolation of the
causative agent( s) from affected tissue.

Diagnosis of an underlying etiology is often

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necessary to fully understand the complexity of gangrenous dermatitis, because manifestation of the disease may be
preceded by other inunune-compromising
infectious agents.

Treatment and Control: Total cleanout
and disinfection of affected houses has
reduced or eliminated gangrenous
dem1atitis infection on farms with historical

Necrotic area of the skin with serosanguineproblems. Salting of floors has also reduced ous exudate due to clostridial infection in a
bacterial challenge in subsequent flocks.

chicken with gangrenous dermatitis. Courtesy

Reducing excessive moisture and microbial
of Dr. Jean Sander.

levels in poultry house litter and mininuzing
trauma are useful adjuncts to other
clinical findings are general in nature and
prevention and control measures. Where
include depression, incoordination,
infection is secondary to predisposing viral
inappetence, leg weakness, ataxia, and high
infection, modification of vaccine progran1s
fever.

directed at immunosuppressive agents may
be used to control widespread gangrenous

Lesions: Gross lesions consist of dark
dermatitis.

reddish purple to green, weepy areas of

Gangrenous dennatitis has historically
the skin. Affected areas usually include
been treated effectively with adnunistration
abdomen, breast, wings, or legs. Areas of
of many broad-spectrum and gram-positive
affected demti.s and subcutis are characterantibiotics. Water acidifiers have been used ized by extensive blood-tinged edema, with
in cases to reduce, but not eliminate, mortalor without gas ( crepitus ). Infection may ity where mortality rates are low or
extend into underlying musculature, which
antibiotic efficacy has been poor.

may be discolored and contain edema and
gas. Lesions in turkeys may be seen around

Zoonotic Risk: The zoonotic potential
the tail head, with blisters and tissue edema
and public health significance of gangrepresent around the tail.

nous dermatitis is thought to be minimal,
because nearly all affected birds succumb

Diagnosis: Presumptive diagnosis may be
quickly to infection and do not survive to
assigned based on an acute increase in
processing age.

DISORDERS OF THE SKELETAL SYSTEM

Production characteristics of modem
and downgrading. Bone fractures in spent
poultry lines ( eg, body weight in broiler
hens may be a welfare issue. Before
chickens, egg production in laying hens)

postmortem exan1ination, flocks should
place high demands on the skeletal system,
be assessed; live, lame birds should be
and inadequacies in nutrition or husbandry
exan1ined, and general flock health and
often result in skeletal diseases. Skeletal
management assessed. Serum san1ples may
disorders may be primarily infectious or
be collected for viral and mycoplasmal
noninfectious; both may be seen concurserology and/or biochemistry ( eg, serum rently within a flock. Skeletal disorders
calcium). Gross pathology alone is often
cause lameness from biomecha.nical
insufficient, and histopathology is usually
dysfunction and in broiler chickens result
necessary to reach a diagnosis. Bone ash
in poor growth, culled birds, increased
measurement, feed nutritional analysis, and
mortality ( caused by starvation and
bacteriology are useful complementary
dehydration), and carcass condemnation
investigations.

DISORDERS OF THE SKELETAL SYSTEM

2881

NONINFECTIOUS SKELETAL
tibiotarsus (tibial dyschondroplasia).

DISORDERS IN BROILERS

Dyschondroplasia can develop in other
bones such as the proximal and distal

Rotational (Torsional) and Angular
femur and tarsometatarsus. The lesion in

(Valgus/Varus) Deformities: These
the proximal tibiota.rsus can be associated

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deformities often are seen as distinct flock
with anterior bowing of the tibiotarsus and
problems. The most common abnormalisometimes fractures distal to the plug of ties are seen in the distal limb and involve
cartilage. Factors shown to influence the
lateral or medial deviation and/or external
incidence and severity of dyschondroplasia
rotation. Valgus or varus deviation of the
include genetic!selection, rapid growth,
intertarsaljoint is the most common
calcium:phosphorus ratio in feed,
deformation in broiler chickens. Males are
metabolic acidosis due to excess chlo1ide
more commonly affected. The pathogenin feed, acid/base imbalance, copper-defiesis of the leg deformation is not well cient diet, Fusariuin spp contamination of
defined. Deformity may be a consequence
the feed, and exposure to dithiocarbamate
of rickets at a younger age (see below).

fungicides and certain antibiotics such as

Poor mineralization of the bone, as in
salinomycin. The most common causes in
rickets, increases the potential for
modem broiler flocks may be marginal
deformation and therefore the incidence
inadequacies in dietary calcium or a
and severity of deformities. Bone
calcium:phosphorus imbalance. The
deformities may also be due to chondrodisease is seen in broiler chickens, turkeys, dystrophy secondary to nutritional
and ducks.

deficiencies (eg, choline, biotin, pyridoxine, folic acid). In breeds predisposed to Rickets: Rickets develops in growing
deformities, the incidence may be reduced birds due to deficiency of vitamin D, by slowing the growth rate via feed
calcium, or phosphorus (seep 2930 and
restriction or lighting programs. Rotated
p 2937) or by calcium:phosphorus
tibia has been a major problem in turkeys
imbalance. Inadequate nutrition or
and a minor problem in Leghorns and
intestinal disease with malabsorption can
guinea fowl. Excessive external tibial rotabe the cause of the mineral or vitamin tion occurs during development, but the
deficiency or in1balance. In tickets,
pathogenesis is not well understood.

abnonnal endochondral ossification with

Genetic, nutritional, and management
failure of mineralization leads to defective
factors are thought to be involved. The
bone fonnation, flexible long bones with
lack of bone angulation differentiates
subsequent bone deformities ( eg, va.rus,
rotated tibia from valgus and varus
valgus), and fractures. Lesions are most
deformation.

prominent at sites of rapid growth where
cartilage contributes most significantly to

Spondylopathies: Vertebral deformities
skeletal growth (eg, long bones, ribs).

and/or displacements (spondylopath.ies)

Thick and pliable ribs and/or knobs at the
such as lordosis and kyphosis are common
costochondraljunction (rachitic rosary)

in thoracic vertebrae, particularly at the
due to tllickened and flared metaphyses are
level of the free thoracic vertebra
classic gross lesions. Beaks and claws can

Spondylolisthesis ("kinky back") is a
be soft and pliable. Hypertrophy and
developmental disorder resulting in rotation hyperplasia of tl1e parathyroid glands are of the free thoracic vertebra with ventral
present. Subclinical rickets with only
displacement of the anterior end and
marginal tllickening of the growth plates is
ove1"riding of the posterior end, causing
fairly common and often associated with
spinal cord compression and posterior
poor perfonnance of broiler chickens.

paralysis. Spondylolisthesis is the most

Bone pathology and bone ashing to
common vertebral column deformity, but
estimate calcium and phosphorus content
incidence is low in most broiler flocks.

a.re useful diagnostic tools.

Growth rate and confonnation influence
this developmental disorder.

Degenerative Joint Disease: Degenerative joint disease is seen mainly in the Dyschondroplasia: Dyschondroplastic
coxofemoral, femorotibial, and intertarsal
lesions are masses of avascular cartilage
joints of broilers and male turkeys near
extending from the growth plate into the
market weight. Reluctance to move,
metaphysis and are attributed to the failure
abducted legs, and lameness can be
of chondrocyte differentiation. This results
observed. The pathogenesis is not well
in a focal thickening of the growth plate and defined, but osteochondrosis or cartilage is most commonly seen in the proximal
lesions and genetic factors may be involved.

2882

DISORDERS OF THE SKELETAL SYSTEM

NONINFECTIOUS SKELETAL
feather and egg shell remains) can be

DISORDERS IN BREEDERS
examined to monitor for contamination
with staphylococci.

Osteopenia (Osteoporosis and

Staphylococcal infections in joints and

Osteomalacia): Cage layer fatigue (see
tendons are also seen in breeders. Out

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p 2897) describes a syndrome in which
breaks are often due to bacterial infection
laying hens become paralyzed in their cages
subsequent to an existing tendinitis. A
and have b1ittle bones. Layers 25---50 wk old
history of other diseases such as coccidiosis
are most severely affected. Osteopenia in
is often associated with an increase in
cage layer fatigue is a consequence of
staphylococcal infections in breeders. In
osteoporosis, a deficiency in the quantity of
some instances, reoviruses may also be
nonnal fully mineralized structural bone,
isolated. (See also VTRALARTt-mms, p 2886.) and osteomalacia, a reduction in bone

The virus is vertically transmitted. Vaccines
density. The sternum is often defonned, and
against the condition have been developed.

the ribs infolded at the junctions of the

Escherichia coli is often responsible for
sternal and vertebral portions. Fractures
flock outbreaks of arthritis and osteomyelioccur in the long bones and vertebrae. Bone tis in broiler chickens and turkeys.

cortices are thin, and the medullary bone is

Osteomyelitis and arthritis are sequelae of
osteomalacic. Parathyroid glands are
septicemia, and these outbreaks may be
hypertrophic and hyperplastic. This
associated with enteric or respiratory
syndrome is due in part to a lack of exercise
disease. Infection of bones,joints, and
of hens held in cages and to selection for
periarticular tissues with E coli, Staphylo
high egg production, but poor nutrition,
coccus aureus, or S hyicus is refen-ed to as with inadequate calcium, phosphorus, and/
turkey osteomyelitis complex (TOC) or
or vitamin D, exacerbates the condition.

green-liver osteomyelitis complex. Green

Although prevention of osteopenia in layers
discoloration of the liver is often associated
with nutritional management has not been
with TOC and is mostly observed at the
successful, sources of calciw11 that enable
processing plant but is rare in birds that
the slow release of mineral, such as oyster
died or are euthanized in the field.

shell, appear to give the best results to

Enter·ococcus cecorum is a commensal
reduce development of osteopenia and
enteric bacte1iwn that can cause epidemics
improve eggshell quality.

of osteomyelitis, arthritis, and spondylitis in
broilers and broiler breeders. Enterococcal

Articular Gout: Seep 2874.

spondylitis is a defined clinical syndrome

INFECTIOUS SKELETAL

DISORDERS

Coagulase-positive staphylococci (see also

STAPHYLOCOCCOSIS, p 2867) are frequently
responsible for bacterial in!ections in the
bones and joints of broiler chickens.

Mycoplasma synoviae (seep 2843) may
also play a role in infectious bone disorders.

In broilers, bacterial infections are most
common in the proximal femur and
proxinlal tibiotarsus in birds >22 days old.

In the proximal femur, the condition is also
refen-ed to as femoral head necrosis, which
is reported to be the most common cause of
lameness in broiler chickens. The etiology
appears to be ve1tically transmitted
staphylococci, often in combination with
infection by immunosuppressive viruses

( eg, INFECTIOUS BURSAL DISEASE, seep 2837).

Floor eggs have been shown to be common
can-iers of staphylococci, so their use
should be avoided. A high standard of hatchery hygiene can reduce this risk. Formaldehyde funligation within the hatchers is also likely to help. In addition, hatchery fluff

Osteomyelitis of the tibiotarsus in a 43-daysamples (ie, hatching deb1is such as down old broiler. Courtesy of Dr. H.J. Barnes.

MYOPATHIES

2883
with infection of the free thoracic and

Viral Arthritis: Seep 2886.

adjacent vertebrae, resulting in chronic
osteomyelitis and spinal cord compression.

Osteopetrosis: Osteopetrosis in

Clinical signs of leg paresis often develop in
chickens is due to infection with specific
broilers >35 days old.

strains of avian leukosis virus (seep 2851).

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Other sporadic causes of osteomyelitis

Growth and differentiation of osteoblasts is
and/or arthritis in poultry include Pastew0
altered by the virus, resulting in diaphyseal
ella mullocida, Ornithobacteiium
and/or metaphyseal, periosteal, and
rhinotracheale, Truepei·ella (Arcanobacte
circmnferential accumulation of woven and
rium) pyogenes, Entei-ococcus spp,
lamellar bone. Osteopetrosis is bilaterally

Streptococcus spp, Salmonella spp, symmetrical and involves the long bones,

Streptobacillus moniliformis, and
especially the tibiotarsus and tarsometatar

Aspergillus spp.

sus. Birds 8--12 wk old are most commonly

Osteomyelitis and arthritis are detected
affected. Lymphoid leukosis often occurs
on gross examination by examination of
in chickens with osteopetrosis. Avian
articular surfaces and bone physes.

osteopetrosis differs from man1ma.lian

Detection of subtle lesions requires
osteopetrosis in which a defect in osteohistopathology. Affected joints are often clast function results in abnorrnal bone
swollen with fibrinous or caseous exudate.

resorption and accumulation of primary

Bones have areas of lysis and/or replacespongiosa in the marrow cavity.

ment by caseous exudate, most often within
the physcal region.

Amyloid Arthropathy: Extensive amyloid

Response to treatment with antibiotics
arthropathy is primarily caused by Enlei<J
cmrently approved for use in poultry is
coccus jaecalis or Mycoplasma synoviae.

often poor for bacterial bone and joint

Clinical cases are seen only occasionally and
infections. Antibiotics may be used to
most frequently affect the hock joint. Brown
control tl1e bacteremia contributing to
layer chickens are particularly susceptible.

new cases and to modify the bacterial flora

Some cases have been attributed to
within a flock. When individual birds a.re
contamination of a previously sterile vaccine
of high value, long-term antibiotic therapy
diluent with E jaecalis dming administration may improve some less severe cases.

( eg, Mare k's vaccine in day-old chicks).

Control requires minimizing sources of

Joints may be enlarged by yellow-orange
infection and stock susceptibility.

material in the articular space.

MYOPATHIES

EXERTIONAL MYOPATHY
myopathy after transport of poultry can also
occm and is associated with increased body

Exertional myopathy results from overly
size and weight, increased transport time to
strenuous muscular exercise and can be
processing plant, cool ambient temperaprecipitated by preexisting conditions such tmes, and valgus leg deformities.

as selenium deficiency. Inadequate energy
metabolism and/or mechanical stresses

Deep Pectoral Myopathy
occurring dming contraction are thought to
be the cause of myofiber degeneration. The

(Degenerative myopathy, Green muscle
lesions can be monophasic (resulting from
disease)

a single event, eg, transport, captme, or

Deep pectoral myopatl1y is characterized by
restraint myopathy) or polyphasic (with
degeneration, necrosis, and fibrosis of the
repeated or ongoing events). Early gross
deep pectoral (supra.coracoideus) muscle
lesions include muscle pallor with edema or
in heavy meat birds ( chickens, tmkeys ),
bloodstained transudate. There is swelling,
secondary to excessive muscle activity
degeneration, necrosis, and mineralization

( exertional myopa.thy and compartment
of.muscle fibers, witl1 edema, hemmThage,
syndrome).

and infiltration of heterophils and

The function of the deep pectoral muscle
macrophages. Deep pectoral myopathy and
is to elevate the wing. Although well-develcaptme myopathy are the main examples of oped in modem meat birds, the muscle is
exertional myopathy in birds. Leg muscle
little used. After episodes of prolonged wing

2884

MYOPATHIES
flapping ( eg, handling, when a lame bird
present in peracute cases. Ischemic and
uses its wings to assist an1bulation, or when
myoglobinuric nephrosis may be present in
a bird is placed on its back), deep pectoral
birds that survive for a few days. Prognosis
muscle irtjury and swelling occurs. Because
of symptomatic birds is usually poor, but

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of the tight surrounding fascia, the swollen
treatment of single, valuable birds can be
muscle cannot expand, which results in
attempted and may be successful. Such
collapse of the blood vessles supplying the
treatment may consist of a combination
muscle. The decreased ( or lack of) blood
of corticosteroids, vitan1in E, selenium,
petfusion leads to ischemia, tissue hypoxia,
parenteral fluids, and forced feeding in
and muscle necrosis ( compartment
coajw1ction with physiotherapy. Prevention
syndrome). The lesion can be produced
is best. Well-planned and executed capture
artificially by stimulating the deep pectoral
and restraint that minimizes pursuit time,
muscle to contract and can be prevented
struggling, noise, and visual stinrnJaLion is
by surgically opening the fascia! sheath
key. Sedation or anesthesia can be useful.

covering the muscle before exercise.

The myopathy may be unilateral or

Transport Myopathy of Turkeys
bilateral with the central 1/3-213 of the
muscle most prominently affected. Early,

(Leg edema syndrome)

the involved muscle is pale, swollen, and

Heavy toms are prinlarily affected by
edematous. Later, it acquires a green
transport myopatlly, altl10ugh it also
coloration and becomes drier and sharply
develops in hens. Transport myopathy is
demarcated from adjacent, viable muscle.

associated with increased body size and

Eventually, the necrotic muscle becomes
weight, increased transpott tin1e to
enclosed in a thick, fibrous capsule. The
processing plants, cool ambient temperadefect can be identified by a flattening or tures, and valgus leg defomtities. The
depression of the breast over affected
pathogenesis is unknown but preswned to
muscles, by palpation, or by transilluminabe similar to that of exertional myopathy.

tion of carcasses at slaughter.

Often, only one leg is affected. No evidence

Flock prevalence is usually low, but
of external trauma is seen. Skin over
prevalence as high as 25% has been
edematous subcutaneous tissue is pale,
reported, with few birds developing the
feather follicles are less visible, and the skin
disease before 24 wk of age. Deep pectoral
slips easily over underlying muscle when
myopathy occurs frequently in turkey
moved. Occasionally, there is crepitation.

breeder hens during artificial insemination.

Affected areas are dark when the edema

The disease is usually subclinical, and major tous areas contain blood. Typically, when Joss is from downgrading or condemnation
lesions are cut, tile edematous subcutis is
at processing. Deep pectoral myopathy is
a few to several millin1eters thick and is
not easy to detect at processing when birds
amber, occasionally green, or rarely red.

are marketed as whole carcasses.

Purulent exudate is absent, which

Incidence can be decreased by careful
distinguishes transport myopat.hy from
handling of susceptible t>irds to prevent
cellulitis. If hemorrhage is present, the
excessive wing flapping and, as a longtenn
adductor muscles usually are torn. Removal
method, by selective breeding because
of affected legs at processing results in
the condition has a genetic component.

carcass downgrading. Microscopically,

Supplementing rations with selenium,
acute muJtifocal muscle necrosis is found,
vitanlin E, or methionine has not influenced
primarily in the adductor muscles.

incidence.

Sometimes subacute or chronic lesions
are seen, suggesting earlier episodes of
myopathy. Serum CK increases sharply

Capture Myopathy
between farn1 and processing. This is now a

Capture myopathy ( exertional rhabdomyrare disease because of programs designed olysis) is mainly seen in zoo and wild birds
to improve leg strength and confot11lation,
and is rare in poultry. Long-legged wading
as well as improved handling and transporbirds are particularly susceptible. Capture tation conditions.

myopathy results from exertion, struggle, or
stress occurring during capture, handling,

MECHANICALLY INDUCED
immobilization, or transport. Hyperthermia

MYOPATHY
and metabolic acidosis due to anaerobic
glycolysis are important factors. Pale

Avascular necrosis caused by pressme in
skeletal muscle, especially muscle from the
heavy birds that are down because of
legs, or sometimes cardiac muscle, is seen
lameness or leg defomtity is seen occasiongrossly. However, no gross lesions are ally and occurs most frequently in tile breast

MYOPATHIES

2885
muscle. On gross examination, the tissue
and is covered by a heavy aponeurosis in
is firm and pale. Hi.stologic examination
which the tendon is embedded. Rupture of
reveals swelling, hyalinization, and necrosis
the aponeurosis and muscle occurs as a
of fibers with edema, heterophils, and

1-2 cm horizontal wound on the anterior

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macrophages at the periphery.

and/or lateral surface of the muscle. It
occurs above the middle of the tibiotarsus

Rupture of the Gastrocnemius Tendon at the top of the ossifying tendon where the Rupture of the gastrocnemius tendon is
tendon attaches to the muscle. Rupture
conm1on in meat-type chickens, particularly usually occurs at 10-14 wk, the age at roasters and breeders, and rare in turkeys.

which turkey leg tendons become ossified,

The rupture is due to application of excess
reducing the elasticity of the tissue in that
weight to previously damaged tendons
location.

(most frequently by reoviral or staphylococ

Rupture of the peroneus longus muscle
cal tendinitis), or it can be spontaneous. The is an uncommon muscle lesion. It is most intra- and peritendi.nous fibroplasias that
frequent in females and may affect as much
occur after infectious tendinitis make the
as 5% of the flock. The separation of tl1e
tendon larger but weaker because of
muscle likely occurs slowly, caused by
replacement of normal strong, dense tendon activity such as repeated springing, in collagenous connective tissue with weaker,
turkeys that are becoming heavier and
dense, irregular connective tissue.

maturing earlier. Affected birds are not

Synechi.ae between the tendon and its
lan1e, but the resulting hem01Thage causes a
sheath may also develop, limiting the
red, blue, or green discoloration under the
tendon's range of motion. Application of
skin around and ventral to the rupture site
no1mal or excess weight to these previously

(drun1stick). This results in dowi1grading
daniaged tendons results in partial or
of the carcass at processing. The affected
complete tearing or rupture. In noninfecportion can be trimmed.

tious spontaneous tendon rupture, the
cause of the rupture is uncertain but may

NUTRITIONAL MYOPATHY
be a combination of weaker tendons and
heavier body weight in meat-type chickens.

Nutritional myopathy in chickens, turkeys,

Rupture of the tendon of one leg puts stress
waterfowl, and ostriches is attributed to
on the other tendon, and bilateral rupture is
vitan1i.n E/selenium deficiency. However, as
frequent. Affected birds are lan1e or "dowi1
in rnanunals, seleniwn deficiency is most
on their hocks" ( creepers). Hemon-hage
often the main cause of the myopatl1y.

from the utjury above the hock on the back

Vitamin E deficiency, when accompanied by
of the leg is visible as red, blue, or green
a sulfur amino acid deficiency, causes
discoloration of the tissues, depending on
nutritional myopathy in chicks b.Y. -4 wk
the age of the lesion. No discoloration
of age. Lesions of vitamin E/selenium
may be visible in chronic lesions. Tissue
deficiency have been reported in skeletal
discoloration results in condenmation of

(especially breast muscle), heait, and
the affected part at processing ( red-leg,
smooth muscle (gizzai·d and intestine) of
green-leg). The ruptured tendon can be
clucks, turkeys, and chickens. Arsenic, zinc,
palpated as a hard mass on tl1e back of the
copper, and otl1er metals are antagonistic
leg above tl1e hock. Broiler breeders> 12 wk
to selenium, and exposure to these other
old are most commonly affected, and flock
metals may precipitate outbreaks. Gross
incidence may be as high as
lesions, with pale foci or streaking, are

20%.

similai· to those of nutritional myopathies in
manm1als. Microscopic chai1ges include

Rupture of the Peroneus (Fibularis)

focal or widespread myofiber swelling,

Longus Muscle
edema, hyalinization, mineralization,

The peroneus muscle originates on the
degeneration, and lysis with infiltration of
proximal end of tl1e tibiotarsus and patelJar
macrophages and heterophils. Hypercellutissue, with attachments to other muscles in larity from proliferation of satellite cells
that area. In turkeys, the insertion appears
may be prominent if regeneration is
to be in three places. A small band of tissue
occun-ing. Poultry feeds in many parts
from the medial side of the muscle runs to
of the world contain added selenium at
the lateral tibial condyle. The main muscle

0.1-0.4 ppm to prevent this myopathy.

tendon crosses the lateral side of the hock
and joins other tendons that extend the

TOXIC MYOPATHY
hock and may affect foot and toe movement. The muscle is thin and wide, covering Ionophores ai·e toxic at increased doses.

the anterior and lateral surface of the leg,

Ionophore toxicity causes muscle damage

2886

MYOPATHIES
with incoordination, leg wealrness,
cytic and/or granulomatous inflan1matory
dian-hea, dyspnea, and reduced feed intake
infiltrate is present within the muscle and
and weight. Stw1ting may also occur. Type I
subcutis. The inflammatory infiltrate can

("red muscle" or oxidative) fibers are most extend to the epidural spaces. With
susceptible, and lesions are most prominent
oil-emulsion vaccines, empty spaces

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in the leg musculature. Lesions may also be
representing lipid droplets surrounded by
found in heart and gizzard muscle. Adult
a granulomatous inflanunatory reaction
birds (chickens, turkeys, ratites) and birds
can be seen.

with no previous exposure are more
sensitive to ionophore coccidiostats.

MINIMAL MYOPATHY

Gross and histologic changes are similar to
those of nutritional myopathy (see above).

A minimal myopathy is seen in otherwise

Ionophores promote movement of cations
nonnal meat-type poultry. Affected birds
across the cell membrane, causing
show no clinical signs, and their muscles are
disruption of the ionic equilibrium,
grossly nonnal, but microscopically there is
increased intracytoplasmic concentration
mild myofiber degeneration and fat
of Ca2+, and cell death. The toxic dose of
accumulation between myofibers. Focal or
ionophores is decreased if they are used in
multi.focal scattered myofibers are
cor\junction with tiamulin, erytJiromycin, or
hyalinized and mineralized. More severe
chloramphenicol. Salinomycin at the dose
examples of this lesion contain individual
reconm1ended for chickens (60 g/ton) is
myofiber necrosis, increased fat, and
toxic for turkeys; doses> 15 g/ton are toxic
fibroplasia between fibers. No specific
in turkeys. Monensin (100 g/ton) and
cause has been detennined for these
lasalocid (100 g/ton) at the dose recomminin1al changes, which have been obse,ved mended for chickens are not toxic to
by avian pathologists but are not described
turkeys.

in the literature. Minimal myopathy is not an

Coffee senna (Senna occidentali s)

established name for this condition.

toxicity can produce clinical signs and gross
and histologic changes in muscles sin1ilar to

GENETIC MYOPATHY
those seen in ionophore toxicity.

Type II glycogen storage disease (acid

INJECTION SITE INJURY
maltase deficiency, Pompe disease) has
been reported in Japanese quail. Symptoms
lr\jection of antibiotics and vaccines in any
start between 4 and 6 wk of age, and
location can result in focal inflammatory
affected quail show progressive myopathy
myositis. Cellulitis and myositis in the neck with reduced ability or inability to lift their region causing post1.1ral and/or neurologic
wings, fly, or get back on their feet after
signs can be seen in poultry after improper
being placed on their back (flip test).

administration of vaccines. It is most

Glycogen deposition occurs in skeletal
commonly seen in broiler chicks. Affected
muscle, cardiac muscle, and smooth
birds may show ataxia, twisting of the
muscle, as well as in the brain and spinal
neck, leg paralysis, and rec"umbency. Swellcord. Both red and white muscle is ing of the subcutaneous and muscle tissue
affected, but lesions are more pronounced
in the neck region at the ir\jection site is
in the pectoralis superficial is (white
seen grossly. Microscopically, a lympho-
muscle).

VIRAL ARTHRITIS

(Tenosynovitis, Reoviral arthritis)

Reovirus infections are ubiquitous in
hydropericardium, and occasionally
commercial poultry flocks. They are global
respiratory disease. In many instances, the
in distribution, although the virulence of
association of the reovirus with disease is
viruses appears to differ between regions.

uncertain. An exception to this is viral

Most strains are nonpathogenic and appear
arthritis, or tenosynovitis, because it can be
to survive hannlessly in the intestine,
reproduced experimentally by infecting
whereas others have been associated with
birds with reovirus alone.

several disease conditions, including

Viral arthritis results in severe lameness
malabsorption and other ente1ic disorders,
in heavy broiler breeds of chickens and

VIRALARTHRITIS

2887
occasionally in laying breeds. Although
peak of production or beyond, probably
lameness in turkeys has sometin1es been
because of reactivation of persistent virus at
reported to be associated with avian
sexual maturity. Affected birds walk with
reoviruses, experin1ental evidence in the past a sWted gait or prefer not to move. In the has been unable to confinn that turkeys are
most severe fom1, mpture of the gastrocne

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as susceptible to these viruses as chickens.

mius tendon is conrn1on, although digital

However, recent field evidence from the USA
flexor tendons are sometimes affected and
indicates the presence of novel reoviruses
many cull birds are seen around the feeders
causing arthritis and tendon rupture
and waterers. The most severely affected
clinically identical to that in chickens.

birds do not recover; less severely affected

Reoviruses have been isolated from a range
birds may recover in 4-{j wk. Infection is
of other avian (including wild) species, and
asymptomatic in many birds. Feed efficiency
it is possible that cross-infection occurs,
and rate of weight gain are decreased.

although ducks and geese have reoviruses

Mortality is 2%-10% and morbidity 5%-500Ai.

that differ genetically from those of chickens.

Lesions: An acute, fulminating infection

Etiology and Pathogenesis: Viral
is occasionally seen in young chicks and
arthritis is caused by avian reoviruses, which
embryos with cardiomegaly, hepatomegaly,
are RNA viruses related to but distinct from
and splenomegaly with necrotic foci.

manunalian reoviruses. Strains differ in

Edema around the tendons of the leg is
virulence, ranging from those causing
marked, petechial hemoIThages develop in
arthritis and sometin1es death to those that
the synovial membranes above the hock,
exist harmlessly in the gut. The mechanisms
and fusion and calcification of the tendon
that determine whether a reovirus is
bundles are common. Blood clots and
pathogenic or harmless are poorly
hemoIThages are seen accompanying
understood. Several antigenic types a.re
mpture of the gastrocnemius tendon. In the
known, and although some cross-protection
most severe cases, pitted erosions of the
occurs between types, it is rarely complete.

cartilage of the distal tibiotarsus ar·e seen

Most infections are acquired by ingestion.

with flattening of the condyles. Histologi

After intestinal replication, the virus spreads
cally, the synovial cells are hypertrophied,
via the bloodstrean1 to all parts of the body.

hyperplastic, and infiltrated by lymphocytes

Pathogenic viruses localize in the hock joint,
and macrophages. The synovia contain
where they cause arthritis. Other organs,
lyn1phoid aggregates with heterophils and
such as the liver, may be affected.

macrophages. In the heart, infiltration of
heterophils or lymphocytes between

Transmission and Epidemiology:

myocardial fibers is a consistent finding.

Avian reoviruses can be egg transmitted, so
infected breeder hens pass virus to chicks.

Diagnosis: A presumptive diagnosis can be

Transmission is short-lived, and only a small based on unilateral or bilateral swelling of the nucleus of chicks can-y virus. Infection is
tendons of the shank ar1d tendon bundle
spread locally to hatchmates by the
above the hock and on the inflan1111a.tory
fecal-oral route. The virus is quite resistant
changes in the tendons and synovia.

to inactivation and can persist on farm
described above. However, other ca.uses of
materials for many days or weeks. Fomites
lan1eness such as Mycoplasma synoviae
are important.

or Escherichia coli should be considered.

Serious outbreaks of viral arthritis are

Reovirus can be isolated from affected joints
followed by a decreased incidence in later
in primar-y chick embryo kidney, liver, or lung
hatch groups of birds from the same parent
cell cultures, or via the yolk sac or cho1ioalflock and may be related to decreased egg lantoic membrane of embryona.ted chicken
transmission and development of maternal
eggs. In view of the widespread nature of
immunity. Day-old chicks a.re more susreovirus infections without disease, isolation ceptible than older birds when exposed
from the gut is not significant. In many
by natural means. The younger the chick
laboratories, PCR is used for vims identificawhen infected, the more likely it is that tion and is more rapid and sensitive than
disease will develop.

isolation. Avian reoviruses ar·e now classified
according to their sigma surface proteins,
and the indications ar·e that the novel USA

Clinical Findings: Viral arthritis usually is turkey and European chicken viruses ar·e
seen in broilers 4-8 wk old as unilateral or
different from the conunon ones associated
bilateral swellings of the tendons of the
with viral arthritis. The turkey isolates are
shank and above the hock. It can also be
genetically related to the turkey enteric
found in much older chickens, usually at
reoviruses, but further molecular analysis

2888

VIRAL ARTHRITIS
is awaited. In view of the ability of avian
prevent egg transmission. In view of egg
reoviruses to recombine, it is possible these
transmission and the greater susceptibilnew arthritogenic variants in both species ity of baby chicks, the main objective of
have evolved by this means. ELlSA is the
vaccination is to ensure good immunity in
serologic test of choice, and most birds are
the parent flock. Vaccination programs

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positive early in infection. Virus neutralizashould be directed to the serotype(s) tion tests and challenge of immunized
present in local flocks. Adult birds are less
chickens can be used to identify the specific
susceptible to clinical disease if exposed
serotype. However, serologic results can be
by natural routes. Currently available
difficult to interpret in view of the ubiquity
commercial vaccines against viral
of reovirus infections. Culture procedures
arthritis are not effective against the
should be used to differentiate mycoplasmal
newly encountered chicken viruses
and other bacterial infections.

described in Europe or against those
causing arthritis in turkeys.

Treatment and Control: There is no
treatment. Live and killed vaccines are

Zoonotic Risk: There have been no
available. Maternal antibodies prevent
reported zoonotic risks associated with
early infection in chicks and minimize or
avian reovirus infections.

AVIAN ENCEPHALOMYELITIS

(Epidemic tremor)

Avian encephalomyelitis (AE) is a viral
biphasic mortality pattern. The main clinical
disease of young chickens, turkeys,
signs are ataxia and leg weakness that varies

Japanese quail, pheasants, and pigeons.

from sitting on hocks to paresis that

Turkeys are less susceptible to natural
progresses to paralysis and recumbency.

infection and generally develop a milder

Fine tremors of the head and neck are
clinical disease than chickens. Ducklings
evident in some birds and a.re characteristic
and guinea fowl are susceptible to
of the disease. They are responsible for the
experimental infection. AE is characterized
common name, epidemic tremors. Tremors
by neurologic signs that result from
vary in frequency and severity and are best
infection of the CNS with an RNA virus in
seen after birds are disturbed or excited.

the family Picomaviridae. Infection occurs

This can easily be done by placing the bird
via vertical and horizontal transmission. If a
on its back and letting it right itself. Cupping
breeder flock becomes infected during egg
the bird in one's hands often results in a buzzproduction, the virus is verti..cally transmiting feeling because of rapid, fine tremors.

ted to the offspring and a major outbreak

Severely affected birds lay on their side and
occurs. The disease often appears in a series exhibit intermittent fine tremors of the head, of flocks hatched from the infected breeder
neck, and legs. Horizontally infected chicks
flock. Field strains of the virus are
usually show clinical signs at 2-4 wk of age;
enterotropic and multiply in the intestine.

thus, clinical disease progresses through the

Infected birds shed the virus in their feces
flock for the first few weeks, and the episode
for a few clays to a few weeks, which se1ves
is usually over by the time the flock is -4 wk
to spread the infection to hatchmates. There old. Morbidity and mortality rates vary and is no convincing evidence that the virus
depend on the level of egg transmission and
persists in infected birds. AE virus is
degree of immunity in the flock. In severe
resistant to envirorunental conditions and
outbreaks, both morbidity and mortality may
may remain infectious for long periods.

exceed 500Ai.

After 4 wk of age, chickens are resistant

Clinical Findings: Vertically infected
to disease but not infection. An exception
chicks conm10nly show clinical signs during
occtll'S occasionally in older chickens after
the first week after hatching, although signs
vaccination with egg-embryo-adapted
may be present in a few birds at hatching.

conunercial vaccines. Affected birds exhibit

Clinical signs appear later in hatchmates that typical CNS signs like those seen in younger are horizontally infected by the fecal-oral
chicks.

route. Vertical infection followed by

In laying chickens, there is a.sudden,
horizontal infection causes a characteristic

5%--l()OA, drop in egg production, which

BOTULISM

2889
usually lasts for <2 wk, followed by a return
showing nervous signs, in which case they
to normal production. There is no deteriorawill have CNS lesions similar to those in tion in egg shell quality. Hatchability may
young birds.

drop as much as 5% during the decline in egg
production due to late embryonic m01tality.

Diagnosis: Diagnosis is based on history,

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Infected eggs are laid during the period of
clinical signs, and characteristic histopathoviremia, which usually lasts 1-2 wk.

logic lesions in the brain and spinal cord. The

Lesions: No gross lesions are seen in the
diagnosis is best confirmed by isolation and
brain of infected birds. Gray to white foci
identification of the vi.ms. Tissues collected
may be visible on cut smfaces of the muscle
for virus isolation must include the brain and
of the gizzard. Weeks after infection, opacity duodenum with the pancreas. Demonstraof eye lenses (cataracts) may occur in a tion of AE virus antigen in the brain, spinal
small percentage of chickens that survive
cord, and other tissues by inm1U11ofluoresthe infection. Microscopic lesions in the cent and immU11ohistochemical staining is

CNS are found in the brain ( cerebral
a reliable method of diagnosis. The major
peduncle, cerebellum, brain stem) and
differential diagnosis for neurologic signs in
spinal cord and consist of degeneration and
very yoU11g chicks is bacterial or mycotic
necrosis of neurons, perivascular lymphoencephalitis. Rickets and nutritional cytic cuffing, and gliosis with formation of
encephalomalacia are next in the list of
glial nodules. ln the cerebellun1, there are
differential diagnoses, although the clinical
areas of necrosis or loss of Purkinje cells
manifestations of these diseases differ from
and replacement by glial nodules that
those in AE. ln adults, serologic testing of
extend into the molecular layer of the
acute and convalescent sera to demonstrate
gray matter. Neuronal lesions of central
an increase in antibody titers helps establish
chromatolysis, shrinkage and increased
a diagnosis.

basophilia, satellitosis, and neuronophagia
are best foUlld in neuron clusters (nuclei) in

Prevention: Immunization of breeder
the brain stem, arbor vitae of the cerebelpullets at 10-15 wk of age with a commerlm11, and lateral horn (gray matter) of the cial live vaccine prevents vertical transmisspinal cord. Central chromatolysis of sion of the virus and provides progeny
neurons is characterized by rOlmding of
with maternal immunity. Vaccination of
the cell contour and displacement of Niss!

table-egg flocks is also advisable to prevent
granules to the periphery. Dorsal root
decreases in egg production. AE vaccine is
ganglia have multifocal nodular collections
usually combined with fowlpox vaccine
of lymphocytes.

and given by wing-web inoculation. Also

A common microscopic lesion outside
available is a live fowlpox-vectored
the CNS is diffuse or nodular lymphocytic
infectious laryngotracheitis and AE
infiltrates in the gizzard muscle, muscular
combination vaccine. Affected chicks and
layer of the esophagus and proventriculus,
poults are ordinarily destroyed because
myocardium, and pancreas. Except for
they rarely recover.

cataracts, microscopic lesions generally are

AE virus does not cause disease in people
not foUlld in infected adults U11!ess they are
or other man1mals.

BOTULISM

(Limberneck, Western duck sickness)

Botulism is an intoxication that results
dogs, horses, laboratory rodents, and
from ingestion of preformed exotoxin of
various zoo animals. Intoxications are spo

Clostridium botulinum. The disease
radic in poultry, but massive mortality has
occurs worldwide and has been identified
occurred in waterfowl. Ruminants fed
in at least 117 species of wild birds
poultry manure contaminated with C botu
representing 22 families. There is concern
linum spores have developed the disease.

that endangered avian species may be at
risk of extinction because of the disease.

Etiology: C bol'ulinum is a gram-positive, Mammalian species affected by the toxin
spore-fonning, anaerobic bacteriU111. There
include people, mink, ferrets, cattle, pigs,
are four genotypically distinct groups,

2890

BOTULISM
designated by the Roman numerals I to IV.

farm, often affecting the san1e houses or

All strains of C botulinum can produce
pens. The disease tends to be most severe in
neurotoxins that cause flaccid paralysis.

pen-reared pheasants with mortality up to

Seven immunologically distinct toxins,

1 OOOA,. Often, the source of tl1e toxin in these
designated by the letters A to G, are
outbreaks is difficult to find, leading to

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produced by different strains, which are
speculation that botulism in poultry is a
classified into toxinotypes (A-G) according

"toxico-infection." Toxico-infection, also to the type of toxin produced.

called "gut toxigenesis," results from

Botulin um toxins are the most potent
proliferation of C botulinum in the
naturally occurring toxins. They are
intestine witl1 subsequent production and
neurotoxins with an affinity for motor
absorption of the toxin. It is unclear what
neurons. After absorption, the toxin binds
factors cause C botulinum to proliferate in irreversibly to the presynaptic membrane of
the intestine and produce toxin. Studies
cholinergic ne1ve terminals. It enters the
have shown that healthy broilers do not
cell and blocks release of acetylcholine
harbor C botulinum type C in the ceca, and
across the neuromuscular junctions,

C botulinum was not recovered from the
resulting in flaccid paralysis. Death results
environment of poultry houses that did not
from cardiac and respiratory failure. Outhave a history of botulism. These findings breaks in poultry and waterfowl are presuggest that C botulinum is neither dominantly caused by type C toxin. Type A
frequent nor widespread in broiler
toxin occasionally causes botulism in
populations and that outbreaks result from
domestic chickens. Type E toxin has been
infrequent and sporadic colonization of
the cause of botulism in fish-eating birds
flocks with C botitlinum introduced into
such as gulls.

a poultry house.

C botulinum is ubiquitous, inhabiting
soils and freshwater wetland (lakes,
marshes) sediments. It is commonly found

Clinical Findings: Clinical signs in
in the intestine of wild birds, but its
poultry and wild birds are similar. Leg
presence in the intestine of healthy poultry weakness and paresis that progress to is questionable. Spore germination and
flaccid paralysis of the legs, wings, neck,
cell multiplication with toxin production
and eyelids are characteristic clinical
require an anaerobic environment that
signs. "Limbemeck," the common name
must also provide the necessary subfor botulism in birds, comes from the neck strates and conditions required for
paralysis typically seen in affected birds.

multiplication. For toxinotype C, optimal

Signs in broiler chickens may also include
growth occurs between 25°C and 40°C,
ruffled or quivering feathers, feathers that
which may explain why most outbreaks
are easily pulled out, labored breatl1ing,
of botulism in waterfowl occur during
and sometimes diarrhea with excess
the summer and fall.

urates in loose droppings. Severely
affected birds are in ventral recumbency

Epizootiology: Wetlands are home to
on the floor with their eyes partially or
numerous invertebrates that can accumucompletely closed and neck outstretched.

late high levels of botulin um toxin. Car

They are unable to lift or hold their neck
casses and organic matter provide suitable
up and cannot raise their eyelids because
substrates for multiplication of C botuli
of the flaccid paralysis that develops.

num and toxin production. Invertebrates,

Affected birds may have.their legs
especially fly larvae (maggots), feed on
extended behind them, because they are
carcasses that have died from botulism and unable to pull them into a normal sitting thus consume botulinum toxin. They are
position. Weakness is the earliest sign in
resistant to the toxins and concentrate
waterfowl. Birds are initially reluctant to
them in their bodies. Outbreaks in
fly when approached and have weak
waterfowl and other water birds result
wing-beats and difficulty taking flight. As
from consumption of toxin-laden
the disease progresses, they lose their
invertebrates. Birds that die from botulism
ability to fly and exhibit stumbling gaits
become infested with maggots, which
and eventually paralysis. Birds in water
perpetuates the outbreak in what is known
can drown, because they cannot keep their
as a "carcass-maggot cycle." Evidence
heads above the water. The incubation
suggests that botulism may also result from period and time to onset of clinical signs direct ingestion of decaying organic matter
is determined by the amount of toxin
that contains toxin.

absorbed.

Outbreaks in conunercial poultry are rare

Lesions: C botulinum toxins do not
and generally tend to recur on the san1e
cause lesions in affected birds, but maggots

VIRAL ENCEPHALITIDES

2891
or other invertebrates may be found in
poisoning, and acute, virulent infectious
the crop. Carcasses are usually in good
diseases (fowl cholera, duck viral enteritis,
condition and do not show evidence of
highly pathogenic avian influenza, etc).

a chronic or debilitating disease.

Control and Prevention: Affected birds

Diagnosis: Preliminary diagnosis is
may recover without treatment. Antibiot

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based on clinical signs and absence of
ics effective against clostridia may be
gross or microscopic lesions that can
useful if the disease is toxico-infectious.

explain the neurologic signs. Definitive

Collection and disposal of dead birds is
diagnosis requires demonstration of the
critical to prevent and limit outbreaks,
toxin in serum from sick birds. Liver, crop
especially in pheasant and broiler chicken
contents, gizzard contents, and intestinal
flocks. Fly control may reduce the risk of
washes from moribund or very freshly
toxic maggots in the environment. Some,
dead birds may also be collected for toxin
but not all, recurrent outbreaks in broiler
detection. Samples from dead birds are
flocks may be prevented by cleaning and
unreliable, because C botulinum toxin
disinfecting with products effective
can result from postmortem multiplicaagainst spore-forming bacteria. Disinfection of the organism and toxin production. tion around poultry houses is suggested, It is preferred to collect serum from birds
because spores can be found outside of the
with clinical signs of varying severity. A
houses and be reintroduced. In waterfowl
bioassay test in mice (mouse-protection
outbreaks, ducks should be dispersed from
test) used to be the standard method to
affected areas and water levels stabilized.

detect C botulinum toxins, but molecular

Elimination of large, shallow areas may
tests based on ELISA are now preferred.

prevent conditions favorable for decay of

PCR can be used on a variety of samples
vegetation and die-off of inve1tebrates.

to detect the genes responsible for toxin

Active immunization with inactivated
production and differentiate the different
type C bacterin-toxoids has been successtoxinotypes. Because botulinum toxins ful in pheasant operations but is not
are heat labile and can be destroyed at
cost-effective or feasible in commercial

80°C for �10 min, sera must be refrigerchickens and wild ducks. Treatment with ated or frozen as soon as possible after
type-specific antitoxin is effective but not
collection and shipped with ice packs to
practical.

the testing laboratory.

Leg weakness or paralysis may be the only

Zoonotic Risk: The zoonotic potential of
sign in mild intoxications, which must be
type C botulism is minin1al. Botulism in
differentiated from Marek's disease, drug and people is caused mostly by toxin types A, B, chemical toxicosis ( especially ionophore
and E. Furthennore, pathogenicity of toxin
toxicity), or appendicular skeletal problems.

type C for people is questionable. However,

In waterfowl, botulism must be differentibotulism caused by type C toxin has been ated from chemical toxicosis, especially lead
confinned in several nonhuman primates.

VIRAL ENCEPHALITIDES

Encephalitis in poultry and farm-reared

Eastern Equine Encephalitis:

gan1ebirds may be caused by several

Eastern equine encephalitis (EEE) is most
different arboviruses. These include
commonly a disease of horses ( see p 1291 ); Eastern equine encephalitis (EEE) virus,
however, many outbreaks of EEE in

Western equine encephalitis (WEE) virus,
farm-raised ringnecked pheasants and

Highlands J (HJ) virus, Israel turkey
chukar partridges have been identified. EEE
meningoencephalitis virus, and West Nile
occurs only sporadically in other species of
virus (See also WEST NILE VlRUS INFECTION IN
poultry (turkeys, ducks), gaine birds, and

POULTRY, p 2893). The te,m "arbovirus," an ratites (emus). EEE virus is found primarily
abbreviation of arthropod-borne virus,
in the eastern parts of North America,
is used to describe a virus that replicates
throughout Central America and the
in a hematophagous (bloodsucking)

Caribbean, and in eastern parts of South
aithropod and is transmitted by bite to

America. In the USA, EEE has been
a vertebrate host.

identified in most states east of the

2892

VIRAL ENCEPHALITIDES

Mississippi River, as well as Louisiana. and
consist of edema of spinal cord white matter,

Texas; it is seen most often in Atlantic
lyrnphocytic meningitis, and microgliosis.

sea.boa.rd and Gulf Coast states. Reported

Ra.tites exhibit depression, hemorrhagic
isolations of the virus in Europe and Asia
diarrhea., emesis of bloodstained ingesta,
have not been confirmed.

and high mmta.lity (as much as SOOA,).

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EEE outbreaks genera.lly occur in late

Hemo1Thagic enteritis is tl1e principal lesion
summer and fall as a consequence of
seen on postmortem exrunina.tion.

increasing nw11bers of mosquito vectors.

Microscopic lesions include necrosis of

Culiseta melanitra, the principal mosquito
hepatocytes ru1d intestinal mucosa.

vector, is likely responsible for transmission
to poultry and game birds. Transmission to

Western Equine Encephalitis: Western
mammalian species most likely occms by
equine encephalitis (WEE) virus has many
other mosquitoes such as Aedes and
chru·acteristics in common with EEE virus;

Coquillellidia spp, which feed on birds but however, it is rru·ely associated with disease
also have a propensity to bite mammals. The in a.viru1 species. WEE virus was identified virus has also been identified in a variety of
as the ca.use of encephalitis and high
other mosquitoes. Wild birds, primarily the
mortality in turkeys; affected tmkeys
sma.ller species of Passeriformes, a.re the
exhibited somnolence, tremors, ru1d leg
principal vertebrate hosts of EEE virus.

paralysis. WEE virus also has been

These birds rarely become ill but serve as
identified as a ca.use of decreased egg
maintenance and amplifying hosts for the
production in turkeys.

virus in the transmission cycle.

WEE is seen ma.inly in western pa.tts of

Epornitics ofEEE virus infection in
the USA and Canada, Central America, and
pheasants a.re believed to be initiated by

South America. 1n the USA and Canada, it
mosquito-borne infection of one or more
is transmitted principally by Culisela
birds in a flock, and subsequently spreading
tarsalis, a mosquito vector that is relatively within the flock as a result of feather picking common west of the Mississippi River.

and cannibalism. 1n ra.tites, the virus may be
transmitted by the fecal-oral route.

Highlands J Virus: Highlru1ds J (HJ)

Clinical disease produced by EEE virus in virus is a ca.use of encephalitis in chuka.r poultry and game birds is usually atttibuted
prutridges. Chukru-s exhibit somnolence,
to CNS infection with or without visceral
ruffled fea.tl1ers, and recumbency before
involvement. However, EEE also may
death. HJ virus infection in this species is
produce viscera.I infections with little or
associated with high mortality. Microscopic
no involvement of CNS tissues.

lesions prin1a.rily consist of nonpurulent

Pheasants develop incoordina.tion,
meningoencepha.litis and focal myocardial
depression, leg paralysis, torticollis, and
necrosis. HJ virus can ca.use decreased egg
tremors. Mortality may be as high as SOOA,.

production in tmkeys. The virus has been

Gross lesions a.re not observed; however,
identified only in eastern parts of the USA.

microscopic changes in the CNS consist
of vasculitis, patchy necrosis, new·ona.l

Israel Turkey Meningoencephalitis:

degeneration, and meningeal inflammation.

Israel turkey meningoencepha.litis has been

Chuka.r partridges exhibit clinical signs
repo1ted only in turkeys. It generally occurs
of depression, somnolence, and high
only in birds> 10 wk old. While the specific
mortality (300/o-SOOA,). Pa.le, focal areas
vector has not been identified, the seasonal
genera.lly a.re present on hearts of affected
incidence and sporadic occurrence in flocks
birds, and spleens a.re mottled and enlarged.

on the san1e farms strongly suggest that it is

Microscopic lesions consist of gliosis,
transmitted by insect vectors, most likely
sa.tellitosis, pe1ivascula.r lymphocytic infiltramosquitoes and Culicoides. Turkeys exhibit tion in the bra.in, and myocardial necrosis
neurologic dysftmction characterized by
with lymphocytic infiltration in the herut.

progressive paresis ru1d paralysis, with

Turkeys with EEE virus infection may
variable mortality. Morbidity and mortality
exhibit drowsiness, incoordina.tion,
rates average 15%--3()DA, but may be as high
progressive weakness, pru·a.Iysis of legs and
as SOOAi. In turkey breeder hens, egg
wings, and low mortality ( <5%). 1n turkeys,
production drops severely. Gross lesions in

EEE virus also has been identified as a
affected turkeys include splenomega.ly or
ca.use of decreased egg production.

a.trophy of the spleen, ca.tarrha.l enteritis,

Ducklings infected with EEE virus
and myocarditis. The principal microscopic
develop a pru·a.Iytic disease chru-a.cterized
lesions a.re nonpurulent meningoencepha.liby sudden onset, posterior paresis, and tis characterized by submeningea.l arid
paralysis; mo1ta.lity rates in affected flocks
perivascula.r lyrnphocytic infiltration and
range from 2% to 6()DA,. Microscopic lesions
focal myocardial necrosis.

WEST NILE VIRUS INFECTION IN POULTRY

2893

Diagnosis: Diagnosis of EEE, W EE,

Formalin-inactivated EEE virus vaccines,
and HJ virus infection or Israel turkey
prepared for use in horses, have been used
meningoencephalitis may be confirmed
to protect pheasants against EEE, although
by isolation and identification of the
their efficacy has been questioned.

virus, detection of viral antigens in tis

One-tenth the equine dose of either an

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sues by ELISA, detection of viral RNA in
eastern or bivalent eastern and western
tissues using reverse transcriptase PCR
vaccine is injected into the pectoral muscle,
procedures, and serologic testing. Virus
preferably at 5-6 wk of age or when birds
can be isolated by inoculation of newborn a.re released from the brooder house.

mice, day-old chickens, embryonated

Israel turkey meni.ngoencephalitis also
chicken eggs, or a variety of cell cultures.

can be controlled by vaccination. A live

Brain, spleen, liver, and serum are the
attenuated vaccine has been prepared by
preferred materials for diagnostic
serial passage of virus in Japanese quail
analyses.

kidney cells; this vaccine is highly

Arbovirus infections must be distinguished efficacious and commercially available.

from other causes of neurologic disease in
poultry and game birds such as Newcastle

Zoonotic Risk: EEE and WEE viruses a.re
disease virus (seep 2856,) avian encephalozoonotic agents and potential ca.uses of myelitis virus (seep 2888), botulism ( see significant hwnan disease. These viruses
p 2889), and listeriosis (seep 2839).

result in neurologic disease that may
prog,-ess to paralysis, convulsions, coma, and

Prevention and Control: EEE, WEE,
death. The case fatality rate for EEE vims in
and HJ virus infection and Israel turkey
people is 50%-75%, and survivors often have
meningoencephalitis are best prevented
permanent new·ologic sequela.e. WEE virus
by measures aimed at reducing vector
is Jess severe, with a case-fatality rate of
populations. Such measures include

-3"/er-7"/o; most infections a.re subcli.nical.

reduction of vector habitats by modifying

Hwnan infection usually is acquired by
the environment or by chemical spraying. If
mosquito bite; laboratory and cli.nically
feasible, farms that raise susceptible avian
acquired infections a.re rare. However, ca.re
species should be located away from
should be ta.ken to a.void contact or droplet
swamps and other areas that provide
exposure when handling suspect infected
habitat for vectors.

birds or pe1fonning necropsies.

WEST NILE VIRUS INFECTION IN POULTRY

See also �;QUINE ARBOVIRAL ENCEPHALOMYELITIS, died in tl1e northeast USA, notably in the New
p 1291.

York City area

West Nile virus (WNV), a J:la.vivirus related to
the St. Louis encephalitis/Japanese encephali

Etiology and Epidemiology: WNV is
tis complex, was first isolated from the blood
considered to be endemic in many countries
of a febrile Ugandan woman in 1937. TI1e virus of Africa, Asia, southern Ew·ope, and North was first described as the cause of a West Nile

America. Since 2001, serologic evidence of
fever epidemic in people in Israel in 1951; in a
the spread ofWNV into Latin America, the
later outbreak, severe meni.ngoencephalitis

Ca.iibbean, and South America has been
was seen in elderly patients. The role of
reported. Epidemics appear in the hwnan
mosquitoes in viral transmission was clearly
population at infrequent intervals in some
delineated in a series of field studies in Egypt
of these coW1tries, and there is evidence
in the 1950s. Wild birds were identified as the
of viral transmission between Africa a.11d
reseIVoir of tl1e vi.Ius a.roW1d the same time.

Europe by migrating birds. Most outbreaks

Cases of West Nile fever in horses were
have occtUTed during the sW11mer months
repo1ted several years later. WNV was first
and ca.11 continue W1til cold nights reduce
associated with disease in domestic avian
mosquito vector activity, notably Culex spp.

species in 1997, when flocks of yoW1g geese

Geese a.i·e the only known natural hosts of
in Israel were affected witl1 a neuropa.ralytic

WNV an1ong domestic avian species. Most
disease. In August 1999, the disease appeared
of the flocks affected in the Israel outbreaks
for tl1e first time in the Western hemisphere
were 5-9 wk old, but goslings as yoW1g as
when wild and zoo birds, horses, and people

3 wk and as old as 11 wk were also affected.

2894

WEST NILE VIRUS INFECTION IN POULTRY

Adult breeding flocks were clinically
used on fonnalin-fixed paraffin-embedded
unaffected, but virus-neutralizing antibodtissues, in particular brain and kidney, to ies were found. Mortality of young Muscovy
visualize viral antigens in inJected birds.

ducks but not young chickens or tmkey

Several forms of ELISA have also been
poults was induced experin1entally with a
developed for flaviviruses.

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WNV isolate. While chickens are not killed

Neurologic signs in young geese must
by WNV, they do develop antibodies against
be distinguished from those ca.used by
the disease and have been used as sentinels

Riemerella infections, especially R ana
to monitor WNV presence. Neither chickens tipestif er. Other bacteria. include Strepto
nor turkeys develop high enough levels of
coccus gallolyticus, and Erysipelothrix, viremia to infect mosquitoes or transmit the

Listeria, and Salmonella spp. Neurotropic virus to other animals.

viruses include Newcastle disease, which is
rare in geese, and avian influenza. Iono

Transmission: The principal route of viral phore intoxication can induce paralytic
transmission is by the bite of a mosquito
signs. Aspergillus also causes brain lesions (primarily Ciilex spp ). In the USA during
and caseous nodules in the lungs.

1999 and 2000, most of the viral isolates
were made from C pipiens and C restvans.

Prevention and Control: Mosquito

WNV has been isolated, RNA detected, or
control is a mandatory component of
antibodies found in 62 mosquito species in
any arboviral disease control progran1.

North America. In Africa and the Middle

Unf01tunately, this is difficult to implement

East, the usual vector is C univittatus, and in a rural environment because of the
in Europe, C pipiens and C modestus. WNV
distances that mosquitoes can fly or be
has also been isolated from at least 10 tick carried by prevailing winds. Standing water
species.

and similar insect breeding sites in the
vicinity of densely populated avian farms

Clinical Findings: Affected geese show
should be treated with larvicides. Poultry
various degrees of neurologic involvement
houses should be constructed to be insect
ranging from recun1bency to leg and wing
free. Because many arboviral diseases
paralysis. Affected birds are either reluctant
are zoonoses, much can be achieved by
or unable to move when disturbed. Signs of
cooperation with hun1an disease surveilincoordination are pronounced, and some lance agencies.

birds flip over while attempting to stand.

Control of WNV in geese is confined

Naturally affected geese show t01ticollis
to vaccinating young flocks at risk,
and opisthotonos. Mortality rates of
especially those raised during months

20%--6()0;6 have been reported, probably
when Culex spp a.re most numerous.

due to horizontal spread of the virus.

Because of confounding factors such as
possible horizontal transmission of virus,

Lesions: Pathologic changes include
a.JI birds in the flock should be vaccinated.

splenomegaly, hepatomegaly, and pallor of

Because of the age-related susceptibility
the myocardium and occasionally of the
to the virus, goslings should be immukidneys. The meningeal blood-vessels are nized as young as possible, preferably at
ir\jected. Microscopic brain lesions consist

3 wk old. Currently, WNV vaccines are not
of lymphocytic perivascula.r infiltration and
available commercially in North America,
neuronal degeneration. Small necrotic
although several types have been
foci a.re present in the myocardiw11, but
developed and widely used in domestic
lymphocytic infiltration is minimal.

geese in Israel. Laboratory trials have
been performed with a formalclehyde

Diagnosis: The tissues of choice to isolate ina.ctiva.ted suckling mouse brain-derived the virus from paralytic or dead birds a.re
product. More than 75% of geese
the brain, spleen, and kidneys. Homogenvaccinated with a single close of vaccine ates a.re inoculated into the brain of
at 3 wk of age were protected, and 94%
newborn mice, into embryona.ted eggs
protection was achieved with 2 doses
by the yolk sac route, or into Vero and
given 2 wk apart. Inactivated vaccines
mosquito cell line cultures. Reverse
prepared from chick embryos or Vero
transcriptase PCR with RNA extracted
cells a.re not protective because of their
from either brain material or cell culture
low antigenic mass. Other vaccines either
supernatant can also be pelfom1ed. Gene
approved for use in geese or under study
expression assays/probes for rapid
include poxvirus vector vaccines and
molecular diagnosis of field-collected
subunit vaccines that use WNV compomosquitoes and avian tissues are also nents such as membrane protein or
available. In1111unohistochemistry can be
envelope protein.

ARTIFICIAL INSEMINATION

2895

ARTIFICIAL INSEMINATION

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Attificial insemination (AI) is widely used
be frozen, but reduced fertility linlits
to overcome low fettility in conunercial
usage to special breeding projects. Under
turkeys, which results from unsuccessful
experinlental conditions, fertility levels of
mating as a consequence of large, heavily

900/o have been obtained in hens inseminated
muscled birds being unable to physically
at 3-day intervals with 400-500 million
complete the mating process. This is a
frozen-thawed chicken spermatozoa.

serious and costly problem in the produc

Several commercial semen extenders are
tion of commercial turkey hatching eggs.

available and are routinely used, paiticu

In most conunercial chicken production
lai·ly for turkeys. Extenders enable more
systems in the USA, it has not been
precise control over inseminating dose and
necessary to implement AI programs
facilitate filling of tubes. Results may be
because natural mating results in adequate
comparable to those using undiluted semen
fettility levels, but AI is routinely used in
when product directions ai·e followed.

special breeding work and research.

Dilution should result in an insemination

However, as managing conunercial broiler
dose containing -300 million viable
breeders to maximize fettility becomes
spe1matozoa for turkeys. However, the
more challenging, the use of AI in comrne1�
nun1ber of spermatozoa inseminated will
cial poultry operations outside the USA is
rai1ge from 150-300 million viable cells
becoming more conunon. Certainly, tl1e use
depending on the age of the turkey hens
of AI in chickens, as in turkeys, can improve
inseminated. In chickens, the nwnber of
fertility; however, the cost of inlplementing
diluted semen inseminated will range from

AI on a large scale is often cost prohibitive.

-100-200 million spetm cells per insemina

Collecting semen from a chicken or
tion. Producers usually determine the
turkey is done by stimulating the copulaspermatozoa concentration 3.11d dilute the tory organ (tl1e phallus) to protrude by
semen to obtain the approptiate spem1 cell
massaging the abdomen and the back over
concentration for either the turkey or
the testes. This is followed quickly by
chicken.

pushing the tail forward witl1 one hand

For insemination, when holding the hen
and, at the same time, using the thumb
upright, pressure is applied to the abdomen
and forefinger of the same hand to apply
ai·ound the vent, particularly on the left side.

pressure in the area and to "milk" semen

This causes the cloaca to eve1t 3.11d tl1e
from the ducts of this organ. Semen flow
oviduct to protrude, so that a syringe or
response is quicker and easier to stinlulate
plastic straw can be inserted -1 in. (2.5 cm)

in chickens tl1an in turkeys. The semen may
into the oviduct 3.lld tl1e appropriate amount
be collected with an aspirator (turkeys) or
of semen delivered. As the semen is
in a small tube or any cup-like container. In
expelled by the inseminator, pressure
turkeys, the volume averages -0.35-0.5 mL,
around the vent is released, which assists
with a spermatozoon concentration of 6 to
the hen in retaining spem1 in the vagina or

>8 billion/mL. In chickens, volun1e is 1-2
oviduct. When inseminating undiluted
times that of turkeys, but the concentration
turkey semen, the high sperm cell concenis about one-half. Collected semen is usually tration allows for 0.025 mL ( -2 billion
pooled and diluted with an extender before
spem1atozoa) to be inseminated at regulai·
use.

intervals of 7-10 days, yielding optinlal

Chicken and turkey semen begins to lose
fertility. In chickens, because of the lower
fertilizing ability when stored > 1 hr. Liquid
spermatozoon concentration 3.11d shotter
cold ( 4 °C) storage of turkey and chicken
duration of fertility, 0.05 mL ofw1diluted
semen can be used to transport semen
pooled semen, at intervals of 7 days, is
and maintain spermatozoa! viability for
required. The hen's squatting behavior

-6--12 hr. This short-term storage of semen
indicates receptivity and the time for the
is conunon in turkeys, while not as common
first insemination. For maxinrnl fertility,
in chickens. When using liquid cold storage
inseminations may be started before tl1e
for> 1 hr, turkey semen must be diluted with
initial oviposition in turkeys, whereas this
a semen extender at least 1: 1 and then
is not necessary in chickens. Fertility tends
agitated slowly (150 rpm) to facilitate
to decrease later in tl1e season; therefore,
oxygenation; chicken semen should be
it may be justified to inseminate more
diluted and then cooled-agitation is not
frequently or use more cells per inseminanecessary. Chicken and turkey semen may tion dose as hens age.

2896

DISORDERS OF THE REPRODUCTIVE SYSTEM

DISORDERS OF THE

REPRODUCTIVE SYSTEM

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CYSTIC RIGHT OVIDUCT

EGG-BOUND OR IMPACTED

Fluid accwnulation in the vestigial right

OVIDUCTS
oviduct is a conui1on fmding in hens. The

A fully fonned egg may lodge in the shell
abdominal cyst is filled with clear fluid and
gland or vagina because the egg is too big
is attached to the right side of the cloaca!

( eg, double-yolked) or because of hypocalwall. The cyst may vary in size from barely cernia, calcium tetany, or previous tra.wna
perceptible to 15-20 cm in diameter. An

(usually pecking) to the vent and/or vagina
increased incidence has been seen in flocks
that obstructs oviposition. This condition
after infectious bronchitis virus outbreaks.

may be more prevalent in young hens that

Oviductal cysts are a necropsy fmding that
are brought into production before body
rarely, if ever, affect flock perfo1mance.

development is adequate or in hens that are
overweight or obese. It occurs more often

DEFECTIVE OR ABNORMAL EGGS during spring and swnmer months because of overstimulation of birds by increasing

Most "ridged," "sunbw·st," "slab-sided,"

light intensity and day length, which can be
soft-shelled, or double-shelled eggs are the
compOLmded by rapid increases in the
result of eggs colliding in the shell gland
amount of feed and/or excessive protein
region of the oviduct when an ovwn (yolk)

Qysine ). This is a medical emergency in pet
is released too soon after the previous one.

birds but is usually recognized only during

Necropsy examinations have demonstrated
necropsy in commercial poultry. When
that two full-sized eggs can be found in the
impaction occurs, eggs that continue to
shell gland pouch. As the second egg comes
form create layers of albwnen and yolk
in contact with the first, pressw·e is exerted,
material, and the oviduct becomes very
disrupting the pattern of mineralization. The large. Some eggs are refluxed to the abdomifirst egg acquires a white band and chalky nal cavity (abdominal laying), and affected
appearance, while the second egg is
hens assume a penguin-like posture.

flattened on its contiguous surface (ie,
slab-sided). Pimpled or rough eggs may
have been retained too long in the shell

EGG PERITONITIS
gland. Blood spots result when a follicle
vessel along the stigma ruptures as the

(Egg yolk peritonitis)

ovw11 is being released. Meat spots occur

Egg peritonitis is characterized by fibrin
when a piece of follicle membrane or
or albwnen-like material with a cooked
residual albwnen from the previous day
appearance among the abdominal viscera.

is incorporated into the developing egg.

It is a common cause of sporadic death in

Many abnom1alities appear to have no
layers or breeder hens, but in some flocks
specific cause, but the incidence is much
may become the major cause of death
higher in hens subjected to stressful
before or after reaching peak production
management conditions, rough handling, or
and give the appearance of a contagious
vaccination during production. A significant
disease. It is diagnosed at necropsy.

increase in the number of soft-shelled eggs

Peritonitis follows reverse movement of
is also common as a result of viral diseases
albwnen and Escherichia coli bacteria.

such as infectious bronchitis, egg drop
from the oviduct into the abdomen. If the
syndrome, and Newcastle disease.

incidence is high, culture should be done to

Small eggs with no yolk form a.round
differentiate betweenPasteurella (fowl
a nidus of material (residual albun1en) in the cholera) or Salmonella infection. Antibiotic rna.gnwn of the oviduct. Small eggs with
treatment of peritonitis caused by E coli
reduced albwnen and eggs with defective
infections is usually ineffective. Manageshells may be the result of damage to the ment of body weight and tuillormity,
epitheliwn of tl1e magnw11 or shell gland.

reproductive development ( ovary follicle

Very rarely, foreign material that enters
growth and maturation), and drinking water
the oviduct through the vagina ( eg, a
sanitation are the best preventive strategies.

roundworm) may be incorporated into

When hens have too many large ovarian
an egg.

follicles, a problem described as erratic

DISORDERS OF THE REPRODUCTIVE SYSTEM

2897
oviposition and defective egg syndrome
respond to calcium IV if there are no

(EOOES) is seen in broiler breeders.

fractures of the legs or vertebrae. The use

This condition is accompanied by a high
of large particle size calcium (limestone,
incidence of double-yolked eggs, prolapses
oyster shell) in the diet may be beneficial.

of the oviduct, internal ovulation, and/or

High rates of mortality due to fractures are

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internal laying that often results in egg
common in birds affected with osteoporoperitonitis and mortality. EOOES is sis. This situation is more common in
prevented by avoiding light stimulation
broiler breeder hens in slatted houses due
of underweight pullets too early and by
to the trauma caused by jumping on and off
following guidelines for body weight and
the slats. Ru{>tured egg follicles indicating
unifonnity, and lighting recommendations
trawna can be found during necropsy
for each breeder strain. Overweight hens
examination of these birds.

may also have a higher incidence of erratic

A condition known as hypocalcemia or
ovulations and mortality associated with
calciun1 tetany (paralysis) has been seen in
egg peritonitis.

modern or high-yielding broiler breeder
hens. Signs such as panting, spread wings,

FALSE LAYER
and prostration may be seen in the early
morning hours preceding paralysis and

These hens ovulate normally, but the yolk is
death by asphyxia. Careful postmortem
dropped into the abdominal cavity rather
examination reveals a fully active ovary and
than being collected by the oviduct because
the presence of a partially or fully fanned
of inflammation and resulting obstruction
egg in the shell gland in the absence of other
of the oviduct after infection with Escheri
lesions. This indicates that the hen used all
chia coli or Mycoplasma gaUise'J)licum.

available calcium from the bloodstream in

The yolk is absorbed from the abdominal
an effort to complete the egg shell. The
cavity. The hen looks like a normal layer but
condition is common in flocks with poor
does not produce eggs. Hypoplasia of the
body weight uniformity that are fed
ovary and oviduct has been associated with
high-calciun1 diets in the weeks before the
infectious bronchitis vims infections (see
onset of lay and brought into production
p 2909) at an early age (1-2 wk). Atresia or
by drastic increases in day length and feed
even atrophy of the ovary are caused by
allocation. Hypocalcemia can be prevented
severe stress, chronic infections, insuffiby management practices that promote cient feed intake, inadequate feeder space,
body weight uniformity and avoid
and feed refusal due to mycotoxins in the
excessive/premature allocation of
feed.

high-calcimn diets and light stimulation.

Mortality can be reduced by the administration ("topping of the feed") of 5 g of oyster HYPOCALCEMIA, SUDDEN
shell per hen for 3 consecutive days, and ·

DEATH, OSTEOPOROSIS, OR
addition of vitamin 03 to the drinking water.

CAGE LAYER FATIGUE

This treatment should be suspended for

3 days and then repeated. Severe cases will

Pullets or hens with insufficient dietary
require continual treatment for 2-3 wk
calcium, phosphorns, or vitan1in 03 may

(3 days of treatment followed by 3 days
die suddenly or be found paralyzed from
without). Feeding of recomrnended levels of
hypocalcemia while shelling an egg. This
calciwn, using large-particle-size calciwn,
may be associated with high production and and providing adequate ventilation and withdrawal of calcium from bones for egg
cooling are helpful to prevent or reduce
shell production, in which case the main
the incidence of this condition.

lesion may be osteoporosis. At necropsy,

Mortality and the presence of an egg
there is an egg in the shell gland and the ova
in the shell gland also can be caused by
are active and fully developed. There are no
a condition referred to as sudden death
other lesions, although medullary bone may
syndrome, first reported in Australia This is
be lacking. Paralyzed hens respond to
believed to be caused by marginal levels of
calcium IV, and this response may be useful
potassium and phosphorns in the diet,
in diagnosis.

resulting in cardiomyopathy.

Osteoporosis is a major cause of death
in high-production flocks. Hens with

INTERNAL LAYER
osteoporosis may show similar signs at
necropsy, or the ova may be regressing with

In these hens, partially or fully fanned eggs
no egg in the oviduct. The femur is always
are found in the abdominal cavity. Such eggs
fragile, and medullary bone is always absent reach the cavity by reverse peristalsis of the in osteoporosis. These hens may also
oviduct. If they have no shell, they are often

2898

DISORDERS OF THE REPRODUCTIVE SYSTEM
misshapen because of partial or complete
except when yolk material migrates
absorption of the contents. Frequently, only
through the air sacs to the lung and causes
empty shell membranes are present. No
foreign body pneumonia. Free yolk is seen
control or treatment is known. This
in many cases of acute illness, injury, or
condition is related to en-atic ovulation
forced molt. Regression of the ovary is

VetBooks.ir
and defective egg syndrome (seep 2896).

frequently caused by low body weight,
deliberate reduction of feed, overcrowd

INFERTILITY
ing, or lack of feeder space. Infectious
diseases such as Newcastle disease, fowl

Infertility caused by male management
cholera, pullornm disease, and avian
problems is common. Problems may be
influenza are known to cause this
caused by an inadequate nwnber of healthy
condition. It can also result from severe
males or because males have reduced
stress, which is often accompanied by
sperm production resulting from chronic
feather molt, emaciation, and dehydration.

disease, inadequate feed intake, or
starvation (harsh feed restriction).

PROLAPSE OF THE OVIDUCT

However, obese females may be less
efficient in transporting sperm to the

When an egg is laid, the vagina everts
infundibulwn, resulting in reduced
through the cloaca to deliver the egg. U
fe1tilization of the ovum as it is released
there has been injury to the vagina, such as
from the ovary. The male must be dominant
from a large or double-yolk egg, or if the
to the females, or mating will not occur.

hen is fat, the vagina may not retract

Commercial turkey hens are inseminated
immediately, leaving it exposed for a short
artificially with semen collected from the
time. This may result in cannibalism (see
toms and used the same day (seep 2895).

p 2873). When the protruding organ is

Parthenogenesis is responsible for some
pecked by other hens, the complete
infertility in turkeys. There are host sperm
oviduct and parts of the adjacent intestinal
glands in the oviduct of females, and live
tract may be pulled from the abdominal
sperm can be retained for 3-4 wk. Watercavity ("peckout"). Bleeding from the vent fowl have a rudimentary penis, and
is obse1ved as a result of pecking.

prolapse of the penis is occasionally

Alternatively, the vagina swells, carmot
repmted in drakes. There is no treatment.

retract, and remains prolapsed ("blowout"). The hen dies from shock. Prolapse NEOPLASIA
has been associated with excessive/
premature photostimulation, poor body

The most frequent tumor of the reproducweight uniformity, early laying (inadequate tive system is adenocarcinoma of the
body size), large eggs, double-yolked eggs,
oviduct. Neoplastic cells are shed from
and obesity. Cannibalism may be
tumors in the oviduct into the abdominal
prevented by beak trimming, managing
cavity. They implant on the ovary, pancreas,
light intensity, maintaining appropriate
and other viscera and produce multiple,
stocking density, and avoiding nutritional
hard, yellow nodules. Tkey may block
deficiencies.

lymph return and result in ascites. The
incidence increases with age, and this twnor SALPINGITIS
may be a frequent cause of death after 2 yr.

Affected hens are condemned at processing. Salpingitis is an inflammation of the Leiomyoma of the broad ligament is an
oviduct, which may contain liquid or
estrogen-induced hypertrophy of the
caseous exudate. In young pullets, it is
smooth muscle of the broad ligan1ent. It
often clue to Mycoplasma gallisepticiim,
is benign and is an incidental finding at

Escherichia coli, Salmonella spp, or
necropsy or processing.

Pasteurella multocida (fowl cholera)

A variety of ovarian and testicular
infection and can result in reduced egg
tumors has been described. Marek's
production. It is a frequent lesion in
disease ( see p 2849) is a common cause
female broilers and ducks at processing.

of tw110rs of the ovary.

On gross examination, salpingitis may be
difficult to differentiate from impacted

OOPHORITIS AND OVARY
oviduct in adults. As the oviduct becomes

REGRESSION
nonfunctional, the ovaries a.re usually
atrophied. Unless associated with an

Regression of the ovary may result in
infectious problem, this condition tends to
leakage of free yolk into the abdomen
be found sporadically during necropsy of

(yolk peritonitis); this rarely causes death
cull hens.

EGG DROP SYNDROME '76

2899

SEX REVERSAL

Neoplasia in the adrenal glands or
ovary that result in the production

If the normal left ovary of a hen is
of testosterone could also cause the
destroyed by infection, the vestigial right
development of male secondary sexual
organ may develop as a testicle and the
characteristics (comb and wattles) in

VetBooks.ir
hen may develop male characteristics.

affected females.

EGG DROP SYNDROME '76

Egg drop syndrome '76 (EDS '76) is an
grown in contaminated duck-embryo
atadenovirus-induced disease characterized fibroblasts. The virus became established by Lhe production of pale, soft-shelled, and
in chickens, causing substantial problems
shell-less eggs by apparently healthy laying
with egg shell quality and loss of eggs. All
hens. The disease in laying hens has
ages and breeds of chickens are susceptible
conunonly been called "egg drop synto infection. Disease tends to be most drome," but the full name ( egg drop
severe in heavy broiler-breeders and hens
syndrome '76 [EDS '76]) should be used to
producing brown eggs. Japanese quail
distinguish it from the recently recognized

( Coturnix colurnix japonica) also develop
flaviviral disease of ducks, which has been
disease. There are rare reports that the egg
called "egg drop syndrome in ducks," and
drop syndrome virus (EDSV) has caused

"duck egg drop syndrome," creating
either a drop in egg production or respirapotential for confusion.

to1y tract disease in other species, eg,
turkeys, ducks, geese, and quail.

Etiology: EDS '76 is caused by a

Three patterns of disease are recogdouble-stranded DNA virus, duck adenovinized in chickens: 1) Classical EDS '76
rus l (also known as EDSV), which belongs
occurs when primary breeding stock are
to the genus A ladenovirus. The virus
infected and the virus is transmitted
commonly infects both wild and domestic
vertically through the egg. The virus often
ducks and geese, but evidence of infection
remains latent until the progeny chick
has also been found in coots, grebes,
reaches sexual maturity, at which time
herring gulls, owls, storks, swans, and quail.

the virus is excreted in the eggs and

The adenovirus group antigen cannot be
droppings, infecting susceptible contacts.

demonstrated by conventional means, and

2) Endemic EDS is the result of horizontal

EDSV differs from other avian adenoviruses infection of the flock during lay. It is by strongly agglutinating avian RBCs, a fact
usually seen in commercial egg layers.

that allows use of a hemagglutination

Contaminated egg collection trays are
inhibition test for detection of antibodies to
one of the main vehicles of horizontal
the virus. The virus grows to high titers in
transmission between flocks, and
embryonated duck and goose eggs and in
outbreaks are often associated with a
cell cultures of duck or goose 01igin. It
common egg-packing station. 3) Sporadic
replicates well in chick-embryo liver

EDS '76 has been recognized occasionally
cells, less well in chick kidney cells, and
in flocks. This is due either to direct
comparatively poorly in chick-embryo
contact with domestic ducks or geese
fibroblasts. It does not grow in embryonated or, more often, to use of a water supply chicken eggs or in manunalian cells. The
contan1inated with wildfowl droppings.

virus is resistant to pH range 3-10 and to

Although infection by this route is
heating for 3 hr at 56°C (132.8°F). Infectivity uncommon, there is always a risk that is lost after treatment with 0.5% formaldethese introductions of the virus could hyde or 0.5% glutaraldehyde.

form a starting point for endemic disease.

Only one serotype of EDSV has been

The main method of hmizontal spread is
recognized to date.

through contanlinated eggs or equipment
such as trays, crates, trucks, or personnel.

Epidemiology and Pathogenesis: The

Droppings are also infective. The virus can
natural hosts for EDSV are ducks and geese.

be transmitted by bleeding or vaccination

It is thought tl1at the virus was introduced to needles. Insect transmission may be chickens through a vaccine that had been
possible but has not been proved.

2900

EGG DROP SYNDROME '76

After horizontal infection, the virus grows (so the disease name may be a misnomer), to low titers in the nasal mucosa. This is
the number of useable eggs produced falls
followed by viremia, vi.ms replication in
by 10%--400/o. Egg production by the flock
lymphoid tissue, and then massive
usually returns to normal. In flocks in
replication for -5 days in the pouch shell
which there has been some spread of vi..rus

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gland. Changes in the egg shell coincide
and some of the birds have antibody (usuwi.th vi.ral replication in the shell gland. Both ally 100/er-200/o), the condition is seen as a the exterior and interior of eggs produced
failure to achieve predicted production tarbetween 8 and -18 days after infection gets; careful exan1ination shows that these
contain virus. Exudate and secretions from
flocks experience a series of small group
the oviduct are rich in virus and pass into
episodes of infection and disease. Birds
the droppings, which may become mildly
wi.th antibody slow the spread of vi.ms.

to moderately watery for 2-3 days. Unlike

There is no effect on fertility or hatchabilother fowl adenoviruses, there is little, if ity of those eggs wi.th a shell quality that is
any, virus growth in the epithelial cells of
satisfactory for setting.

the intestine. lnterestingly, the massive vi.ral
replication in the pouch shell gland occurs

Diagnosis: Production of pale, thinafter seroconversion, a fact that is useful shelled and shell-less eggs by a flock that
diagnostically.

appears otherwise healthy should raise

Chicks hatched from infected eggs may
strong suspicion of EDS '76. Transient mild
excrete vi.rus and develop antibody. More
depression and/or mild watery droppings
often, the virus remains latent, and antibody
may be noted. Ridged eggs and poor internal
does not develop until the bird starts to lay,
quality are not features of EDS '76. Poor egg
at which time the vi.ms reactivates and
shell quality at peak production in healthy
grows in the oviduct, repeating the cycle.

hens should also raise strong suspicion of
classical EDS '76. With endemic or sporadic

Clinical Findings: ln flocks without

EDS '76, disease can develop in laying hens
antibody, the first sign of the disease is the
of any age. In cage units, spread can be slow,
production of pale-shelled eggs, quickly
and the signs may be overlooked or
followed by production of soft-shelled
perceived as a small depression (2%--4%)

and shell-less eggs. lntemal quality of eggs
of egg yi.eld.

is w1affected in experimentally induced

Clinically, EDS '76 can be distinguished
disease. Transient dullness may be seen
from Newcastle disease (seep 2856) and
in the days before the shell changes are
influenza vi.rus infections (seep 2902) by the noticed. The thin-shelled and shell-less eggs absence of illness, and from infectious are fragile, and the birds tend to eat them;
bronchitis ( see p 2909) by the absence of
these eggs also may get trampled into litter
respiratory signs, the absence of ridged and
and may be ove'rlooked unless a careful
malformed eggs, and the absence of poor
examination is made. Although it has been
internal egg quality. Coniirmatory laborashown experimentally that eggs usually tory testing is needed for definitive
continue to be produced at a nonnal rate
diagnosis. Searching for evidence of
seroconversion is the easiest diagnostic
approach for nonvaccinated flocks. When
selecting birds for diagnosis, especially in
cage units, it is important to target hens that
have produced affected eggs, because if the
problem is due to EDSV infection, these
hens will already have seroconverted. A
hemagglutination-inhibition test using fowl

RBCs, and ELISA, are the serologic tests of
choice. In addition, the serun1 neutralization
test can be used for coniinnation. The
double immunodiffusion test also has been
used. PCR-based tests and antigen capture

ELISA tests have been used to detect EDSV

DNA and antigen, respectively. Again,

Eggs produced by hens in a flock with
appropriate selection of the hens to be

EDS'76. One normal egg is present (center,
back row). Affected eg
examined is very important. EDSV can be
gs include pale and
thin-shelled eggs and shell-less eggs. The
isolated by inoculating cmbryonated duck
contents of the egg at the bottom right have
or goose eggs or duck- or chick-embryo
been lost, leaving a thick, collapsed shell
liver cell cultures. It is important to select
membrane. Courtesy of Dr. Joan Smyth.

recently infected birds for testing, but these

ASPERGILLOSIS

2901
can be difficult to identify, especially if the
prevented by separating chickens from
birds are on litter. An easier method is to
other birds, especially waterfowl. General
feed affected eggs to antibody-free hens.

sanitary precautions are indicated, and

These hens can then be tested for seroconpotentially contaminated water should be version after the first abnormal eggs are
chlorinated before use.

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produced, or tested for evidence of EDSV

Inactivated vaccines with oil adjuvant

DNA or antigen by PCR or antigen capture
are available and, if properly administered,

ELISA, respectively, or virus isolation can
successfully prevent the disease. They
be attempted from the pouch shell gland
reduce but do not prevent vims shedding.

of these hens.

The�e vaccines are given during the growing
period, usually at 14-18 wk of age, and can

Control: There is no treatment for EDS
be combined with other vaccines, such as

'76. The classic form has been eradicated
those for Newcastle disease. Sentinel
from primary breeders. Use of dedicated
chickens may be placed along with
equipment and egg trays for each fann,
vaccinated chickens and periodically
and/or washing and disinfecting plastic egg
checked for antibodies, which would allow
trays before use, can help to control the
detection of the presence of virus in the
endemic fonn. The sporadic fom1 can be
flock.

AIR SAC MITE

Cytodites nudus is a small cosmopolitan
and two nymphal stages. Infestation
mite occasionally noticed as white spots on
densities vary, and clinical signs range from
the bronchi, lungs, air sacs, and abdominal
none to weakness, weight loss, pneumonia,
organs of chickens, turkeys, pheasants,
peritonitis, pulmonary edema, and death.

pigeons, canaries, and mallards. (See also

Recommended treatments include
p 1906.) These mites are readily transmisivermectin, a nearby dichlorvos pest strip sible between birds through coughing. They

(placed out of reach of the birds), topical
are rarely found in commercial industries.

moxidectin, or a pyrethrin/piperonyl

The 14- to 21-day life cycle involves a larval
butoxide spray.

ASPERGILLOSIS

(Brooder pneumonia, Mycotic pneumonia, Pneumomycosis) Aspergillosis is a disease, usually of the
spores during hatching in contan1inated
respiratory system, of chickens, turkeys,
incubators or when placed on mold-bearing
and less frequently ducklings, pigeons,
litter. In older birds, infection is caused
canaries, geese, and many other wild and
primaiily by inhalation of spore-laden dust
pet birds. In chickens and turkeys, the
from containinated litter or feed or dusty
disease may be endemic on some farms;
rai1gc areas. Morbidity can be underestiin wild birds, it appears to be sporadic, mated in finishing flocks until slaughter
frequently affecting only an individual
inspection reveals pulmonaiy lesions.

bird. Severe outbreaks usually occur in
birds 7-40 days old. (See also ASPERGILLOSIS

Clinical Findings and Lesions: Dyspnea,
in mammals, p 633, and in PET BIRDS, p 1899.) hyperpnea, somllolence at1d other signs of
nervous system involvement, inappetence,

Etiology and Epidemiology: Aspergil
emaciation, at1d increased thirst may be
lusfumiga,tus is a common cause of the
seen. In chicks or poults up to 6 wk old, the
disease. However, several other Aspergillus lungs are most frequently involved. Airsaccuspp may be incrinlinated.

litis is a cause of postmmtem condemllation

High mortality rates are seen in chicks
in young mature turkeys intended for food
and poults that inhale large nun1bers of
supply. Pulmonary lesions are characterized

2902

ASPERGILLOSIS
by white to yellow plaques and nodules a few conosis, zygomycosis), and nutritional mm to several cm in diameter; occasionally,
encephalomalacia.

mycelial masses may be seen within the air
passages on gross examination. The plaques

Treatment and Control: Treatment
and nodules also may be found in the syrinx,
of affected birds is generally ineffective.

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air sacs, liver, intestines, and occasionally

Spontaneous recovery from pulmonary
the brain. The encephalitic form is most
aspergillosis can occur if reexposure to
common in turkeys. An ocular fonn is seen
the mold is prevented. Strict adherence
in chickens and turkeys as mycotic keratitis,
to sanitation procedures in the hatchery
in which large plaques may be expressed
minimizes early outbreaks. Grossly
from the medial can thus.

contan1inated or cracked eggs should not
be set for incubation, because they enable

Diagnosis: The fungus can be clemonbacterial and fungal growth and may strated by culture or by microscopic
explode and disseminate spores throughexan1ination of fresh preparations. One of out the hatching machine. Contaminated
the plaques is teased apart and placed on a
hatchers should be thoroughly cleaned
suitable mediun1, usually resulting in a pure
and fumigated with enilconazole or
culture of the organism. Histopathologic
formaldehyde. Avoiding moldy litter or
examination using a special fungus stain
ranges serves to prevent outbreaks in
reveals granulomas containing mycelia.

older birds. Cleaned pens should be

Differential diagnoses include infectious
sprayed or fumigated with enilconazole
bronchitis, Newcastle disease, infectious
following label directions, and all
laryngotracheitis, mycobacteriosis,
equipment should be cleaned and
colibacillosis, other mycoses ( eg, ochro-
disinfected.

AVIAN INFLUENZA

Avian influenza (Al) viruses infect

Epidemiology and Transmission: LP
domestic poultry as well as pet, zoo, and

Al viruses are distributed worldwide and
wild birds. In domestic poultry, Al viruses
are recovered frequently from clinically
are typically of low pathogenicity (LP),
normal shorebirds and migrating waterfowl.

causing subclinical infections, respiratory

Occasionally, LP viruses are recovered from
disease, or drops in egg production.

imported pet birds and ratites. The viruses

However, a few Al viruses cause severe
may be present in village or backyard flocks
systemic infections with high mortality.

and other birds sold through live-poultry

This highly pathogenic (HP) fom1 of the
markets, but most commercially raised
disease has historically been called fowl
poultry in developed countJ.ies are free of Al
plague. In most wild birds, Al viral
viruses. The HP viruses arise from mutation
infections are subclinical except for the
of some H5 and H7 LP viruses and cause
recent H5N 1 HP Al viruses of Eurasian
devastating epidemics. Stan)ping-out
lineage.

programs are used to quickly eliminate the

HP viruses in developed countries, but

Etiology: Al viruses are type A orthosome developing counb.ies may use myxoviruses characterized by antigenically
vaccines to control HP viruses.

homologous nucleoprotein and matrix

The incubation period is highly variable
internal proteins, which are identified by
and ranges from a few days in individual
serology in agar gel immunodiffusion
birds to 2 wk in t11e flock. Transmission

(AGID) tests. Al viruses are fmther divided
between individual birds is by ingestion or
into 16 hemagglutinin (Hl-16) and 9
inhalation. Naturally and experimentally,
neuraminidase (N 1-9) subtypes based on
cats and dogs have been infected witl1 one
hemagglutinin inhibition and neuran1inistJ.·ain of H5N 1 Eurasian HP Al virus. Experidase inhibition tests, respectively. Most mental infections occurred after respiratory

Al viruses (Hl-16 subtypes) are of low
exposure, ingestion of infected chickens, or
pathogenicity, but some of the H5 and H7 Al
contact exposw·e, but cats were more
viruses are highly pathogenic for chickens,
susceptible than dogs. Potentially, domestic
turkeys, and related gallinaceous domestic
pets could serve as a transmission vector
poultry.

between farms, but the ability of other Al

AVIAN INFLUENZA

2903
vimses, including other H5N l strains, to
oral and nasal discharges. In severely
infect pets is unknown. Other manm1als that affected bit·ds, greenish diarrhea is have been experimentally infected include
conm1on. Birds that survive the peracute
pigs, ferrets, rats, rabbits, guinea pigs, mice,
infection may develop CNS involvement
mink, and nonhw11an p1imates. Transmisevident as torticollis, opisthotonos, VetBooks.ir
sion between farn1s is the result of breaches
incoordination, paralysis, and drooping
in biosecwity practices, principally by
wings. The location and severity of
movement of infected poultry or contamimicroscopic lesions are highly variable and nated feces and respiratory secretions on
may consist of edema, hemorrhage, and
fomites such as equipment or clothing.

necrosis in parenchymal cells of multiple

Airborne dissemination between farms may
visceral organs, skitl, and CNS.

be important over limited distances. Limited
spread by wild birds of the Eurasian H5Nl

Diagnosis: LP and HP AT viruses can be

HP Al virus has been suggested but is not
readily isolated from oropharyngeal and
typical of other HP Al viruses. OU1er HP Al
cloaca! swabs, and HP Al viruses from many
and all LP Al have minimal potential to
internal organs. Al viruses grow well in the
infect dogs and cats.

allantoic sac of9- to 11-day-old embryonating chicken eggs, and U1ey agglutit1ate Clinical Findings and Lesions: Clinical

RBCs. The hemagglutmation is not inhibited
signs, severity of disease, and mmtality
by ewcastle disease or other paramyxovirates vary depending on Al virus strain and ral antiserw11. Al viruses are identified by
host species.

demonstrating the presence of 1) influenza

Low Pathogenicity Avian Influenza

A matrix or nucleoprotein antigens using

Viruses: LP Al viruses typically produce

AGID or other suitable immunoassays, or
respiratory signs such as sneezing, coughing,

2) viral RNA using an influenza A-specific
ocular and nasal discharge, and swollen
reverse transcriptase-PCR test.

infraorbital sinu es in poultry. Sinusitis is

LP Al must be differentiated from other
conm1on in domestic ducks, quail, and
respit·ato1y diseases or causes of decreased
tmkeys. Lesions in the respiratory tract
egg production, mcludmg I) acute to
typically include congestion and inflanimasubacute vit·al diseases such as infectious tion of the trachea and lungs. In layers and
bronchitis, infectious laryngotracheitis, low
breeders, there may be decreased egg
virulent Newcastle disease, and infections
production or fertility, ova ruptme ( evident
by other paramyxovimses; 2) bacterial
as yolk in the abdominal cavity) or
diseases such as mycoplasmosis, infectious
involution, or mucosa! edema and inflanunaco1yza, ornithobacteriosis, turkey coryza, tory exudates in the lwnen of the oviduct. A
and the respit·atory forn1 of fowl cholera;
few layer and breeder chickens may have
and 3) fungal diseases such as aspergillosis.

acute renal failure and visceral urate

HP Al must be differentiated from other
deposition (visceral gout). The morbidity
causes of high mortality such as virulent
and mortality is usually low unless

Newcastle disease, peracute septicemic
accompanied by secondary bactelial or viral
fowl cholera, heat exhaustion, and severe
infections or aggravated by environmental
water deprivation.

stressors. Sporadic infections by any
subtype of LP Al viruses can occur, but H9N2 Prevention and Treatment: Vaccines LP Al is common in poultry in Asia, the
can prevent clinical signs and death. Furthe1�

Middle East, and North Aflica.

High Pathogenicity Avian Influenza

Viruses: Even in the absence of secondary
pathogens, HP Al viruses cause severe,
systemic disease wi.U1 high mortality in
chickens, turkeys, and other gallinaceous
poultry; mo1tality can be as high as 1000;6 in a
few days. In peracute cases, clinical signs or
gross lesions may be lackitlg before death.

However, in acute cases, lesions may
include cyanosis and edema of the head,
comb, wattle, and snood (tmkey); edema
and red discoloration of the shanks and feet
due to subcutaneous ecchyrnotic hemorrhages; petechial hemorrhages on visceral Hemorrhagic skin visible on the feet of a
chicken with avian influenza.

organs and in muscles; and blood-tinged

Courtesy of

Dr. David E. Swayne.

2904

AVIAN INFLUENZA
more, viral replication and shedding from
occurred, usually as isolated, rare,
the respiratory and GI tracts may be reduced
individual cases. Most htm1an cases have
in vaccinated birds. Specific protection is
originated from infection with Eurasian
achieved through autogenous virus vaccines

H5N 1 HP AI vims and, most recently,
or from vaccines prepared from AI virns of

Chinese H7N9 LP AI virus. The total

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the same hemagglutinin subtype. Antibodies
accumulated hwnan cases of H5Nl HP AI
to the homologous viral neura.minidase
virus in Asia and Africa from 2003-2013 is
antigens may provide pa.ttial protection.

648, of which 384 were fatal. The prima.iy

Cun·ently, only inactivated whole AI virus,
risk factor for human infection has been
recombinant fowlpox-AI-H5, and recombidirect contact with live or dead infected nant herpesvir·us-turkey-AI-H5 (rHVf-AI-H5)

poultry, but a few cases have resulted from
vaccines a.re licensed in the USA. The use of
consw11ption of uncooked poultry products,
any licensed AI vaccine requires approval
defeathering of infected wild swans, or
of the State Veterinarian. In addition, use of
close contact with hun1an cases. Respira

H5 and H7 AI vaccines in the USA requires
tory infection has been the most frequent

USDA approval. Treating LP-affected flocks
presentation of human H5Nl cases. For
with broad-spect.1un1 antibiotics to control

H7N9 LP AI, total accw1rnlated hwna.i1 cases
seconda.iy pathogens and increasing house
in China for 2013 is 137, of which 45 were
temperatures may reduce morbidity and
fatal. Most cases had exposure risk to
mortality. Treatlnent with a.i1tivira.l comlive-poult1y markets. Conjunctivitis was the pounds is not approved or recommended.

most frequent symptom in hun1an cases of

Suspected outbreaks should be reported

H7N7 HP AI virus infection in the Neth et'

to appropriate regulatory authorities.

lands during 2003, with 89 confinned cases
and 1 fatality. Other HP AI virnses and all LP

Zoonotic Risk: AI viruses exhibit host

AI vimses have produced very rare or no
adaptation to birds. Hwnan infections have
hwnan infections.

AVIAN METAPNEUMOVIRUS

(Turkey rhinotracheitis, Avian pneumovirus, Swollen head syndrome) Avian metapneun10vitus (a.MPV) causes
people. Experimental studies suggest that
turkey rhinotraclJeitis, an a.cute respiraturkeys also may be susceptible to llMPV.

tory tract infection of turkeys. It is also

Complete genome sequencing confirmed
associated with swollen head syndrome in
that the genomic organization of hMPV is
broilers and broiler breeders, as well as egg
sin1ila.r to tl1at of a.MPV. Overall, little is
production losses in layers. The virus was
known about the cross-species pathogenicfirst detected in turkeys in South Africa in ity of these two vituses.

the late 1970s and has spread to a.II the
major poultry-producing areas in the world
except for Australia. a.MPV has been

Etiology: aMPV is.a member of the
detected not only in chickens and turkeys
fa.t11ily Pa.ranwxoviridae and of subfamily
but also in pheasants, Muscovy ducks,

Pneumovirinae, which consists of the
and guinea fowl. Geese, most other duck
genus Pneumovirus (including the human
species, and possibly pigeons a.re suggested
and bovine respiratory syncytia.l viruses)

to be refractory to disease. Epidemiologic
and the genus Metapneumovirus.

studies provide evidence for the circulation

Currently the genus Metapneumoviius
of a.MPV in wild birds, especially watercomprises a.MPV and hMPV.

associated species. Some outbreaks have

Isolates of a.MPV a.i·e grouped in subtypes
been attributed to vaccine-derived viruses,

A to D. The sequence of the attachment
which may persist for several months in the
glycoprotein (G protein) can be used to
environment. Wection with aMPV is often
subtype different strains. Based on the
complicated by seconda.iy bacteria.I
phylogenetic a.t1alysis of F protein
infections, leading to high economic losses.

sequences, it was suggested that the

In 2001 the first human metapnewnovirus

European subtypes A, B, and D a.re all more

OlMPV) was isolated and classified as a
closely related to each other than to subtype
member of the genusMetapneumoviius,

C. More recently, a.MPV subtype C isolates
which causes respiratory infections in
were also identified in pheasants in Korea

AVIAN METAPNEUMOVIRUS

2905
and water-associated bird species in

The incubation period is 3-7 clays, and

Europe. The latter was shown to be of a
morbidity in birds of all ages may reach
different genetic lineage than the USA

100%. Mortality may be lo/o--30<>A,depending
subtype C isolates. Irrespective of the
on age and constitution of the flock as well

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differences within subtype C, isolates of
as secondary infections. Birds without
this subtype display a hlgher amino acid
secondary infections with good constitution
sequence homology to hMPV than to
may recover within 7 -10 days. However, in

European aMPV subtypes A, B, and D.

birds with secondary infections and under
poo.r management, the disease may be

Transmission and Epidemiology:

prolonged and exacerbated by ai..rsacculitis,

The spread of aMPV appears to depend on
pericar·ditis, pnew11onia, and peri..hepatitis.

the poultry population density, standard of

Infection in chlckens and pheasants is
hygiene, and biosecurity. Within or between
less clearly defined and may not always be
poultry flocks, aMPV may spread rapidly
associated with clinical signs. aMPV is
horizontally by direct contact or by contact
associated with swollen head syndrome in
with contanlinated material. aMPV is
chickens. This condition is characte1ized by
assumed to be highly contagious. The
swelling of the peri- and infraorbital sinuses,
enveloped virus is rapidly destroyed after
frothy eyes, nasal dischar·ge, to1ticollis, and
release from the host to the environment.

opisthotonos due to ear infection. Typically,

Because aMPV affects mainly ciliated

<4% of the flock is affected, although
epithelial cells of the upper respiratory tract, respirato1y signs may be widespread.

transmission is most likely to be airborne,

Mortality is rar·ely >2%. 1n broiler breeders
especially by aerosol. But ciliated cells of
and commercial layers, egg production and
the reproductive tract and possibly macroquality are frequently affected.

phages also may be target cells of aMPV.

Lesions: Macroscopic lesions depend

Metapneumovi.rus subtype C was isolated
on the cowse of infection, especially on
from eggs of experimentally infected SPF
secondary bacterial infections, and ar·e most
turkeys, but it was suggested that the
prominent on days 4-10 after infection.

ve1tical route may be sho1t-lived and may

Gross lesions induced after experin1ental
play only a minor role in viral transmission.

infection are due to rhlnitis, tracheitis,

Birds appear to shed aMPV for only a few
sinusitis, and ai..rsacculitis. Infected birds
days after infection. This short period of
may be free of gross lesions. Serous to
shedding suggests that there is no latency or
turbid mucus may be observed in tl1e nasal
carrier status under experimental condicavity, nasal turbinates, trachea, and in tions. There is evidence that on farms aMPV
infraorbital sinuses. Dming the course of
may persist for longer periods. Reconvalesinfection, the secreted mucus turns from cent flocks may be repeatedly reinfected
clear and serous to turbid and purulent.

with aMPV within one fattening pe1iod.

Nonspecific signs of inflarnmation, such as
swelling and hyperemia of t11e mucosa and

Clinical Findings: aMPV induces an
excessive mucus, can be seen in the upper
acute, highly contagious infection of the
respirato1y tract and in the air sacs. If
upper respiratory tract of turkeys and
secondary bacterial infections are present,
chickens. The disease affects all age groups,
copious inflarnmatory exuclates are found in
although younger birds seem to be more
the respirato1y tract. 1n addition, pneumosusceptible. In fattening turkeys the upper nia, pericarditis, perihepatitis, splenorespiratory tract is predominantly affected, megaly, and hepatomegaly are seen. 1n the
while in laying hens only a mild respiratory
reproductive tract of laying turkeys, lesions
infection with a drop in egg production and
car1 include egg peritonitis, ovary and
egg quality has been seen. Coughing
oviduct regression, folded shell memassociated with lower respiratory tract branes in the oviduct, and misshapen eggs.

involvement may lead to prolapses of the

Microscopic exan1ination of the upper
uterus in laying turkeys.

respiratory tract, including the secondary

Typical respiratory signs in young turkeys bronchi during the first 2 clays after aMPV
include serous, watery nasal and ocular
infection, reveals loss of cilia, increased
discharge; frothy eyes; and conjunctivitis.

glandular activity, congestion, and mild

At later stages, signs include mucopurulent,
mononuclear infiltration of t11e submucosa.

turbid nasal discharge; plugged nostrils;

The most pronounced microscopic lesions
swollen infraorbital sinuses; and snicking,
ar·e found in the mucosa or the nasal
sneezing, coughing, or tracheal rales. These
turbinates, whlch may be the most suitable
respiratory signs are accompanied by
tissue for microscopic evaluation and
depression, anorexia, and ruffled feathers.

diagnosis of aMPV infection. Harclerian

2906

AVIAN METAPNEUMOVIRUS
glands and lacrimal glands may also show
antibodies to both of these subgroups
infiltration of lymphocytes and fonnulation
because of some cross-reactivity, the
of lymphoid follicle-like structures in the
homologous antigen should be used for tl1e
interstitial tissue and around the secondary
efficient detection of subgroup C. The
collecting ducts.

subtype specificity of the applied test may

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result in limited or no detection of other

Diagnosis: Obtaining samples from the
subtypes or new emerging aMPV strains
upper respiratory tract of birds in the early
that do not cross-react.

stages of the disease is extremely important

Paran1yxoviruses (particularly Newcastle
when attempting virus isolation. Especially
disease and paramyxovirus 3 (seep 2856),
in broiler-type chickens, samples should be
infectious bronchitis virus (seep 2909), and taken before the sixth day after infection.

influenza viruses (seep 2902) may cause

Once clinical signs are obvious, the isolation respiratory disease and egg production of replicating aMPV may not be successful.

problems in chickens and tw·keys that

The most suitable san1ples for aMPV
closely resemble aMPV infection. These
detection are tracheal and choanal swabs.

viruses can be differentiated on the basis

Tracheal organ cultures prepared from
of morphology, hemagglutinating and
turkey or chicken embryos, or 1- to
neuran1inidase activity, and molecular

2-day-old chicks, are the most sensitive for
characteristics. A wide range of bacteria
primary isolation of aMPV. Ciliostasis may
and Mycoplasma spp can cause signs very
occur within 7 days of aMPV A and B but not similar to those of aMPV. These agents are subtype C inoculation or after passages. The
frequently present as secondai.y oppo1tu.nisvirus has also been isolated after the tic pathogens and may mask tl1e presence
inoculation of6- to 8-day-old embryonated
of the aMPV.

chicken or turkey eggs via the yolk sac route
and identified by electron microscopy, virus

Prevention and Treatment: Good
neutralization test, or molecular techniques.

management practices can significantly

Cell cultures have not proved successful for
reduce the severity of infection, especially
the primary isolation of the virus. However,
in turkeys; in particular, optimal ventilation,
once the virus has been isolated and
stocking densities, temperature control,
adapted in the systems above, it will grow in
litter quality, and biosecw·ity have a positive
a variety of avian and manm1alian cultures.

influence on the outcome of the disease.

Reverse transcriptase PCR (RT-PCR), as

Some success in reducing disease severity
well as real-time RT-PCR, tests targeting
by controlling secondary bacterial
the F, N, or G gene of aMPV have been
infections with antibiotics has also been
developed and are widely used to detect
reported.

the virus in clinical-material, particularly

Both live and inactivated vaccines are
respirato1y swabs. Some nested RT-PCR
available for inunu.nization of chickens and
tests have been constructed so that the
turkeys and are widely used in countries
subtype as well as the identity of virus can
where the disease is endemic. Maternal
be determined from the clinical san1ple.

antibodies do not provide sufficient

Based on tl1e growing amount of genome
protection against aMPV infection and do
sequence data and access to sequencing
not interfere significantly with vaccination.

techniques, detailed characterization and

Thus, a vaccination prograi.n should plan for
molecular differentiation of isolated aMPV
the first immunization as soon as possible
strains is commonly done. Antigen
after hatching. It is crucial to achieve a
detection tests have also been developed,
homogenous state of inunu.nization per
including inununofluorescence and
flock and farm by application of an adequate
inununoperoxidase assays on botl1 fixed
vaccine dose to all birds.

and unfixed tissues.

Live vaccines, which may be applied

Because of difficulties in isolation and
by spray or drinking water in the field,
identification of aMPV, serologic assays have stimulate both local respiratory and been developed to confirm infection in
systemic inununity, and cross-protection
commercial chickens and turkeys. A number between subtypes may occur. But live of commercial ELlSA kits are available and
vaccines may induce only short-lived
are conrn1only used, but other techniques,
protection, especially for grow-out of
including virus neutralization and indirect
toms, because of the fast decline of local
immunofluorescence tests, have also been
immu.nity. Thus, repeated revaccination
used. Both acute and convalescent serum
of tw·keys is common practice. There is,
san1ples should be submitted for analysis.

however, a risk of reversion of the live

Although ELlSA systems that use either
vaccine stains to more virulent variants.

subgroup A or B strains as antigens detect

Inactivated aMPV vaccines are often used

BORDETELLOSIS

2907
for booster immunization of layer and
vaccines. As experimentally shown, in
breeder flocks after priming with live
ovo vaccination may also be a promising
vaccines. While inactivated vaccines alone
strategy for effective, early induction of an
induce only partial protection against aMPV
immune response. Besides live attenuated

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infection, the most efficient and long-lasting
and classical inactivated vaccines, some
protection is achieved by a combined
genetically engineered viruses, including
prime-boost vaccination progran1. This
recombinant vectored vaccines, have been
program comprises repeated prin1ing with
designed and tested under experin1ental
live attenuated vaccines and booster
conditions. These have induced partial
immunization with inactivated adjuvanted
protection and need further development.

BORDETELLOSIS

(Turkey coryza, Bordetella avium rhinotracheitis) Avian bordetellosis is a highly infectious,
nonpathogenic. When the bacillus is grown
acute upper respirato1y tract disease of
in broth media high in nutrients, filamenturkeys characterized by high morbidity and tous fonns can be observed.

usually low mortality. Other synonyms

The mechanism of pathogenesis involves
previously used for the disease include A/cali
the ability of B avium to destroy ciliated
genes rhinotracheitis, adenovirus-associated
epithelial cells in the trachea. Ce1tain
respiratory disease, acute respiratory disease
strains of the bacteria adhere to the ciliated
syndrome, and turkey rhinotracheitis.

pseudostrati.fied columnar epithelium and

Although the disease primarily affects
produce toxins, some of which appear to be
turkeys, quail a.re also susceptible, and it is an
similar to those from other Bordetella spp.

opportunistic infection in chickens. Damage

Toxins associated with pathogenic strains
to the upper respiratory tract from prior
of B avium include a heat-labile toxin,
exposure to an upper respiratory disease
tracheal cytotoxin, dem10necrotic toxin,
agent or vaccine such as infectious bronchitis and osteotoxin. Adherence factors virus or Newcastle disease vims, or from an
associated with the bacterium include the
environmental irritant such as anunonia, is
hemagglutinin Baal autotransporter protein
necessary to induce signs in chickens.

and possibly pill and componeuts associ

Bordetellosis has been identified in
ated with lipopolysaccharide. Damage to
almost every area of the world where
the tracheal cartilage with distortion and
turkeys are intensively reared. Historically,
discoloration of the tracheal rings is often
it has been severe in focal areas and rare or
observed and thought to be caused by the
nonapparent in other locations. The reasons cytotoxin and/or the osteotoxin. Some for these epidemiologic differences are not
mortality is due to suffocation from
known.

Etiology and Pathogenesis: The
causative agent is Bordetella avium, a
gran1-negative, nonfermentative, motile,
aerobic bacillus. It can be grown using
many different media, including Mac

Conkey agar, Bordet-Gengou agar, veal
infusion broth, trypticase soy broth, blood
agar, and brain-heart infusion broth. Strains
of B avium typically produce small (0.2-1
nun diameter after 24 hr incubation),
compact, translucent, glistening pearl-like
colonies with smooth edges. After serial
passage in the laboratory, a rough colony
type with a dry appearance and a serrated,
irregular edge can be observed for some

Scanning electron microscopy of a trachea
isolates. Rough colonies represent a global
from a poult 3 days after Bordetella avium
infection; note numerous B avium cells
suppression of virulence factors inB avium attached to ciliated columnar epithelial cells.

termed antigenic variation and are

Courtesy of Dr. Mark W. Jackwood.

2908

BORDETELLOSIS
increased mucus production in the trachea
bifurcation. The lining of the trachea may
and tracheal collapse. As with many
have extremely mild hemorrhage in some
bacterial infections, iron acquisition is
cases, and softening of the tracheal rings is
necessary for colonization and spread of
usually felt. In addition, a dorsal/ventral

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B avium in the host. Virulence factor
flattening of the trachea can sometimes be
expression is globally controlled by a
observed. Pnew11onia and airsacculitis
virulence gene locus in response to
ai·e observed only when the disease is
environmental conditions that favor
complicated by another disease agent.

antigenic variation an10ngB a:uium isolates.

Damage to the upper respiratory tract can

Diagnosis: Diagnosis of infection is
lead to secondaiy infections with Escheri
confirmed by isolation of B avium on
chia coli or other agents, which can

MacConkey agar and identification using
significantly increase the severity of the
standard biochemical assays. Nonfermentdisease. In many cases, tuxkeys infected ing, small, slow-growing colonies from
solely with B avium recover within 4---6 wk specin1ens from the anterior trachea are
without serious consequences.

typical. The bacteriwn is best isolated from
the anterior trachea; cultures ta.ken from

Epidemiology and Transmission: Morthe sinuses frequently become overgrown bidity is usually 80%--lOO"A, in young turkeys.

with other, fasteHeplicating bacteria such

Mortality can range from (JOA, in birds with
as Proteus spp.

uncomplicated disease to >400,1, if secondaiy

Serology is also important, and both
invaders ai·e present. Mortality can increase
microagglutination ( detects IgM) and ELISA
and signs can become severe if young

( detects IgG) tests ai·e available. The
turkeys infected with B avium also become
microagglutination test can detect specific
infected with other agents ( eg, E coli,
antiboclies --1 wk after infection. The ELISA

Newcastle disease virus) or when environtest generally detects specific ai1tibodies >2
mental conditions in turkey barns are less
wk after infection and has the added benefit
than optimal. Bordetellosis is a major
of detecting maternal antibody. Monoclonal
initiator of colibacillosis in turkeys. There
antibody-based agglutination and indirect
is an age-related resistance to the disease.

in1munofluorescent tests as well as PCR

'fur keys >4--5 wk old are most often
tests have also been used to identify
refractory to the disease but not infection,

Bavium.

and thus can be a factor in spread of the

Other nonfennenters, B bronchiseptica
bacterium.

and B hinzii, which ai·e for tl1e most part B avium is highly contagious and easily
nonpathogenic, can sometimes be isolated
transmitted from infected turkeys to
from the trachea and must be differentiated
susceptible birds by direct contact. It can
from B avium. Patl1ogenic B avium can be also be transmitted tlu·ough contaminated
clifferentiated by growth and colony morpholdrinking water, feed, and litter, which can ogy on MacConkey agar, no growth on
remain infectious for 1--6 mo.

minin1al essential mediwn, a negative urease
reaction, and hemagglutination of guinea pig

Clinical Findings: Signs of the disease
erythrocytes. B a:uium also agglutinates usually occur 7--10 days after infection
chicken and turkey erytlu·ocytes.

and include sinusitis with a clear nasal
discharge that can be observed when
pressure is applied to the nai·es. Foainy

Treatment: Treatment witl1 antin1icrobial
watery eyes, a snick or cough, mouth
agents by aerosol, injection, or in the water
breathing, dyspnea, tracheal rales, and
has not been effective, even tl1ough B avium
altered vocalization are also characteristic.

may be highly sensitive. The tracheal

Complicated disease can result in more
epitl1elium of the turkey is a clifficult location
exaggerated signs including airsacculitis.

to medicate even though blood levels of tl1e
antimicrobial appeai· to be adequate.

Lesions: Lesions are primarily found in

Resistance to streptomycin, sulfonamides,
the upper respiratory tract and consist of
and tetracycline cai1 be carried on plasmids
nasal and tracheal exudates, collapse of
and has been observed for some strains of
cartilaginous rings, and progressive loss

B auium. Antimicrobial therapy may
of ciliated epithelium. In uncomplicated
be helpful for secondaiy colibacillosis.

disease, the tracheal epithelium can return
to nom1al 4---6 wk after the onset of signs.

Control and Prevention: Vaccination

At necropsy, turkeys with characteristic
with bacterins ai1d a live temperaturebordetellosis have watery eyes and sensitive mutant vaccine have given mixed
extensive mucus in the sinuses and trachea,
results depending on the age of the turkey
which rarely extends below the tracheal
and the method of administration.

INFECTIOUS BRONCHITIS

2909

Typically, turkeys >3 wk old respond
and disinfection after field outbreaks
positively to vaccination with the live
is essential. Most of the commonly
temperature-sensitive vaccine. Vaccinaused disinfectants are effective.

tion is not widely practiced by turkey

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breeders, and the immunity that is passed

Zoonotic Risk: B avium may be a rare to progeny generally comes from natural
opportunistic pathogen in people. In adinfections.

dition, a closely related organism, B hinzii,

B avium is easily carried between farms.

also isolated from poultry, has been

Thus, prevention should include a good
associated with septicemia and bacteremia
biosecw·ity program. Rigorous cleanup
in older or immunocompromised people.

INFECTIOUS BRONCHITIS

Infectious bronchitis is an acute, highly
have tracheal rales for 10-14 days. Concontagious disease of major economic jW1ctivitis and dyspnea may be seen, and
impo1tance in commercial chicken flocks
sometimes facial swelling, particularly with
throughout the world. It is usually
concurrent bacterial infection of the sinuses.

characterized by respiratory signs, although

Chicks may appear depressed and huddle
decreased egg production and poor egg
under heat lamps. Feed conswnption and
quality are sometimes seen in breeders and
weight gain are reduced. Infection with
layers. Some strains of the etiologic agent,
nephropathogenic strains can cause initial
infectious bronchitis virus (IBV), are
respiratory signs, then later depression,
nephropathogenic, causing interstitial
ruffled feathers, wet droppings, greater water
nephritis, particularly in chicks. Associaintake, and death. In layers, egg production tions with myopathy and proventriculitis
may drop by as much as 700Ai, and eggs are
have also been reported.

often misshapen, with thin, soft, rough, and/
or pale shells, and can be smaller and have

Etiology and Epidemiology: IBV is a
watery albW11en. In most cases, egg
coronavirus that only causes disease in
production and egg quality return to 1101°
chickens, although some other birds may be
ma!, but this may take up to 8 wk In most
subclinically infected. Some serotypes are
outbreaks mortality is 5%, although mortality
geographically restricted, but multiple
rates are higher when disease is compli-cated
serotypes commonly cocirculate in one
by concurrent bacterial infection. Nephrogeographic region. In recent years, a novel pathogenic strains can induce interstitial

IBV genotype, the QX sti·ain, has become
nephritis with high mortality ( up to 600A,) in
increasingly common in Asia and Europe.

young chicks. Infection of young chicks may

IBV is shed by infected chickens in respiracause pennanent damage to the oviduct, tory discharges and feces, and it can be
resulting in layers or breeders that never
spread by aerosol, ingestion of contaminated
reach normal levels of production.

feed and water, and contact with contaminated equipment and clothing. Naturally Lesions: In the respiratory tract, the
infected chickens and those vaccinated with
trachea, sinuses, and nasal passages may
live IBV may shed vims inte1mittently for up
contain serous, catarrhal, or caseous
to 20 wk after infection. The incubation
exudates, and the air sacs a foamy exudate
period is generally 24-48 hr, witl1 the peak in
initially, progressing to cloudy thickening. If
excretion of virus from tl1e respiratory tract
complicated by infection with E coli, tl1ere lasting� days after infection. The severity
may be caseous airsacculitis, perihepatitis,
of disease and the body systems involved are
and pericarditis. Birds infected when very
influenced by the strain of tl1e virus; the age,
young may have cystic oviducts, whereas
strain, in1lllune status, and diet of the
those infected while in lay have an oviduct
chickens; and cold sti·ess. In addition,
of reduced weight and length and regrescoinfection with Mycoplasma gallisepticum, sion of the ovaries. Infection with nephro

Mycoplasma synoviae, Escherichia coli,
pathogenic strains results in swollen,
and/or Avibacterium paragallinaium can
pale kidneys, with the tubules and ureters
exacerbate disease.

distended with w·ates; in birds with
urolithiasis, the ureters may be distended

Clinical Findings: Morbidity is commonly
with urates and contain uroliths, and the
close to lOOOA,. Chicks may cough, sneeze, and kidneys may be atrophied.

2910

INFECTIOUS BRONCHITIS

Diagnosis: L aboratory confirmation is
analyzed by nucleotide sequencing, or
required for diagnosis of respiratory fonns
compared with reference strains using
because of similarities to mild fonns of
high-resolution melting curve analysis.

disease caused by agents such as Newcastle

Genotype detem1ination based on the S l
disease virus, avian metapneumovirus,
region can be complemented by analyzing

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infectious laryngotracheitis virus, mycoplasother regions of the viral genome, including mas, A paragallinarum, and Ornithobacte
the nucleocapsid gene and the 5' untrans
rium rhinotracheale. Demonstration of
lated region. These analyses can also aid in
seroconversion or a rise in antibody titer
rapid detection of novel recombinant IBVs.

against IBV by ELISA, or hemagglutination
inhibition or virus neutralization tests can

Control: No medication alters the course
be used for diagnosis when there is a history
ofIBV infection, although antimicrobial
of respiratory disease or reduced egg
therapy may reduce mortalities caused by
production.

complicating bacterial infections. In cold

Definitive diagnosis is generally based on
weather, increasing the ambient temperavirus detection and identification. Virus can ture may reduce mortalities, and reducing
be isolated by inoculation of homogenates
the protein concentrations in feed and
of tracheal, cecal tonsil, and/or kidney tissue providing electrolytes in drinking water into 9- to 11-day--old SPF chicken embryos,
may assist in outbreaks caused by
with growth ofIBV indicated by embryo
nephropathogenic strains.

stunting and curling, and deposition of

The attenuated vaccines used for
urates in the mesonephros, with variable
inununization may produce mild respiratory
mortality. Alternatively, IBV may be isolated
signs. These vaccines are initially given to
in tracheal organ cultures, with growth of

1- to 14-day-old chicks by spray, d1inking
virus indicated by cessation of cilial motility. water, or eye drop, and birds are commonly Several blind passages of the virus may be
revaccinated. Revaccination with a virus
necessary for isolation of some field strains.

from a distinct serotype can induce broader

More rapid diagnosis may be achieved using
protection. Attenuated or adjuvanted
reverse transcriptase-polymerase chain
inactivated vaccines can be used in breeders
reaction (RT-PCR) assays to detect viral
and layers to prevent egg production losses.

RNA in nucleic acid extracts of tracheal,

There are many distinct serotypes ofIBV,
cecal tonsil, or kidney tissue.

and new or variant serotypes, which are not

Typing viruses can help distinguish
fully controlled by existing vaccines, are
vaccine and field strains and may help
identified relatively frequently. Some
diagnose outbreaks caused by serotypes
variants may be derived from recombination
distinct from those of the vaccines used in a
between existing field strains and vaccine
flock. Serotypes have been identified using
strains, whereas others result from point
sera from SPF chickens inoculated with
mutations in existing strains. Selection of
known serotypes in virus neutralization
vaccines should be based on knowledge
tests. However, because this is expensive
of the most prevalent serotype( s) on the
and time consuming, it is not Ieadily
premises. The correlation between serotype
available. A restricted range of serotypeand protection is imperfect, and definition of specific monoclonal antibodies (MAb) have
the most approp1iate vaccine, or combinabeen developed for serotyping, but direct tion of vaccines, may require experin1ental
detection viral antigen using these MAbs
assessment of several combinations of
to inununohistochemically stain tissue
vaccines to identify the most effective
sections from diseased birds is of limited
regimen. The most conunonly used live
value because of the low concentration of
vaccines in the USA contain derivatives
antigen in tissues. The MAbs have been best
of the Massachusetts, C onnecticut, and
used after propagation in chicken embryos,

Arkansas strains, whereas in Australia,
to detect viral antigen in the chorioallantoic
where the most prevalent serotypes are
membranes by inununofluorescence or
distinct from most other countries, vaccines
inununoperoxidase staining, or in the
are based on derivatives of the VicS and
allantoic fluid by ELISA. Analyses of the

Armidale strains. In Europe, vaccines
products ofRT-PCR assays are now
incorporating derivatives of the 4/91 strain
conunonly used to identify the virus
and those derived from QX-like viruses are
serotype and to identify individual strains
available. Vaccination with selected variant
within serotypes. The S l region of the spike
serotypes may be of use when these variants
glycoprotein gene determines the serotype,
are the dominant strain in flocks, although
and R T -PCR products derived from this
regulatory authorities in some countries only
region can be subjected to restriction
pennit use of vaccines derived from the
fragment length polymorphism analysis,

Massachusetts strain.

INFECTIOUS CORY2A

2911

INFECTIOUS CORYZA

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Infectious coryza is an acute respiratory

Commercial fam1s that have multiple-age
disease of chickens characterized by nasal
flocks tend to perpetuate the disease. Egg
discharge, sneezing, and swelling of the face transmission does not occur. Molecular under the eyes. It is found worldwide. The
techniques such as restriction endonuclease
disease is seen only in chickens; reports of
analysis �d ribotyping have been used to
the disease in quail and pheasants probably
trace outbreaks of infectious coryza.

describe a similar disease that is caused by
a different etiologic agent.

In developed countries such as the USA,

Clinical Findings: In the mildest fom1 of
the disease is seen primarily in pullets and
the disease, the only signs may be depreslayers and occasionally in broilers. In the sion, a serous nasal discharge, and occasion

USA, it is most prevalent in commercial
ally slight facial swelling. In the more severe
flocks in California and the southeast,
forn1, there is severe swelling of one or both
although the northeastern USA has
infraorbital sinuses with edema of the
experienced significant outbreaks. In
surrounding tissue, which may close one or
developing countries, the disease often is
both eyes. In adult birds, especially males,
seen in very young chicks, even as young as
the edema may extend to the intermandibu3 wk old. Poor biosecurity, poor environlar space and wattles. The swelling usually ment, and the stress of other diseases are
abates in 10-14 days; however, if secondary
likely reasons why infectious coryza is more infection occurs, swelling can persist for of a problem there. The disease has no
months. There may be varying degrees of
public health significance.

rales depending on the extent of infection.

In Argentina, a septicemic fom1 of the

Etiology: The causative bacterium
disease has been reported, probably due to
is
concun-ent infections. Egg production may

Avibacleriiim paragallinarum, a
gram-negative, pleomorphic, nonmotile,
be delayed in young pullets and severely
catalase-negative, microaerophilic rod that
reduced in producing hens. Birds may have
requires nicotinamide adenine dinucleotide
diarrhea, and feed and water consumption

CV-factor) for in vitro growth. When grown
usually is decreased during acute stages of
on blood agar with a staphylococcal nurse
the disease.

colony that excretes the V-factor, the

Lesions: In acute cases, lesions may be
satellite colonies appear as dewdrops,
limited to the infraorbital sinuses. There
growing adjacent to the nurse colony.

is a copious, tenacious, grayish, semifluid

V -factor-independentAv pa.ragallinarum
exudate. As the disease becomes chronic or
have been recovered in South Africa and
other pathogens become involved, the sinus

Mexico. The most commonly used
exudate may become consolidated and turn
serotyping scheme is the Page scheme,
yellowish. Other lesions may include
which groups Av paragallinarum isolates
conjunctivitis, tracheitis, bronchitis, and
into three serovars (A, B, and C) that
airsacculitis, particularly if other pathogens

COJTelate with inununotype specificity.

are involved. The histopathologic response
of respiratory organs consists of disintegra

Epidemiology and Transmission:

tion and hyperplasia of mucosa! and glandu

Chronically ill or healthy carrier birds are
lar epithelia and edema with infiltration of
the reservoir of infection. Chickens of all
heterophils, macrophages, and mast cells.

ages are susceptible, but susceptibility
increases with age. The incubation period is

Diagnosis: Isolation of a gram-negative,

1-3 days, and the disease duration is usually
satellitic, catalase-negative organism from

2-3 wk Under field conditions, the duration
chickens in a flock with a history of a rapidly
may be longer in the presence of concurrent
spreading coryza is diagnostic. The catalase
diseases, eg, mycoplasmosis.

test is essential, because nonpathogenic

Infected flocks are a constant threat to
hemophilic organisms, which are catalaseuninfected flocks. Transmission is by direct positive, are present in both healthy and
contact, airborne droplets, and contaminadisea5ed chickens. A PCR test that can be tion of drinking water. "All-in/all-out"

used on the live chicken and that has proved
management has essentially eradicated
superior to culture, even in developing
infectious coryza from many commercial
countries, has been developed. A real-time
poultry establishments in the USA.

version of the PCR is also available.

2912

INFECTIOUS CORYZA

Production of typical signs after inoculation

Because serovai-s A, B, and C ai·e not
with nasal exudate from infected into suscepcross-protective, it is essential that bacterins tible chickens is also reliable diagnostically.

contain the serovai-s present in the target

No suitable serologic test exists; a hemagglupopulation. Vaccination should be completed VetBooks.ir
tination-inhibition test is the best of those

-4 wk before infectious coryza usually
available. Swelling of the face and wattles
breaks out on the individual faim. Antibodies
must be differentiated from that seen in fowl
detected by the hemagglutination-inhibition
cholera (seep 2822). Other diseases that
test after bactetin administration do not
must be considered are mycoplasmosis,
necessarily c01Telate with protective
laryngotracheitis, Newcastle disease,
immunity. Cont.rolled exposure to live
infectious bronchitis, avian influenza,
organisms also has been used to immunize
swollen head syndrome ( ornithobacterosis ),
layers in endemic areas.

and vitamin A deficiency.

Because early treatment is important,

While currently found only in South
water medication is recorrunended

Afiica and Mexico, the presence of a
immediately until medicated feed is

V-factor-independentAv paragallinarum
available. Erythromycin and oxytetramust also be considered. The Av paragal
cycline are usually beneficial. Several
linarum PCR is an ideal diagnostic tool in
new-generation antibiotics ( eg, fluoroquin
this situation.

olones, macrolides) are active against
infectious coryza Vaiious sulfonamides,

Control and Treatment: Prevention is
sulfonainide-tri.rnethoprim, and other
the only sound metl10d of control. "All-in/
combinations have been successful.

all-out" faim programs with sound manage

Antibiotic use in chickens is subject to
ment and isolation methods are the best way
national regulations that vary from country
to avoid infectious coryza Replacements
to country, and use and efficacy of the
should be raised on the same farm or
various antibiotics must be reviewed in the
obtained from clean flocks. If replacement
light of the relevant national regulations. In
pullets are to be placed on a fann that has a
more severe outbreaks, although treatment
history of infectious coryza, bacterins ai·e
may result in in1provement, the disease may
available to help prevent and control tl1e
recur when medication is discontinued.

disease. USDA-licensed bacterins are

Preventive medication may be combined
available, and bactetins also ai·e produced
witl1 a vaccination prograin if started pullets within states for intrastate use. Bacterins
are to be reared or housed on infected
also are produced in many other countries.

premises.

INFECTIOUS LARYNGOTRACHEITIS

Infectious laryngotracheitis (ILT) is an
inactive. The moutl1 and beak may be
acute, highly contagious, herpesvirus
bloodstained from the tracheal exudate.

infection of chickens and pheasants

Mortality vaiies but may reach 50% in adults
characterized by severe dyspnea, coughing,
and is usually due to occlusion of the
and rales. It can also be a subacute disease
trachea by hemotThage or exudate. Signs
with nasal and oculai· discharge, tracheitis,
usually subside after -2 wk, although some
conjunctivitis, and mild rales. The disease is
birds may show signs for longer petiods.

caused by Gallid herpesvirus I, commonly

Strains of low virulence produce little or no
known as infectious lai-yn.gotracheitis virus
mortality with mild respiratory signs and a

(ILTV). It has been reported from most
slight decrease in egg production.

areas of the USA in which poultry are

After recovery, birds remain can·iers for
intensively reared, as well as from many
life ai1d become a source of infection for
other countries.

susceptible birds. The latent virus can be
reactivated under stressful conditions.

Clinical Findings: In the acute form,

Infection also may be spread mechanically.

gasping, coughing, rattling, and extension of Several epidemics have been traced to the the neck during inspiration are seen 5--12
transport of birds in containinated crates,
days after natural exposure. Reduced
and the practice of litter spread in pastures
productivity is a varying factor in laying
is believed to be related to epidemics of the
flocks. Affected birds are anorectic and
disease.

QUAIL BRONCHITIS

2913

Diagnosis: The acute disease is characdiphtheiitic form of fowl pox infection that te1ized by the presence of blood, mucus,
produces intracytoplasmic inclusions.

yellow caseous exudates, or a hollow

Field isolates and vaccine strains of
caseous cast in the trachea. Microscopi

ILTV are routinely differentiated by PCR
cally, a desquamative, necrotizing tracheitis
an1plification of single or multiple ILTV

VetBooks.ir
is characteiistic of acute disease. In the
genome areas, followed by sequencing of
subacute fonn, punctifonn hemorrhagic
the PCR products and comparative analysis
areas in the trachea and larynx and mild
of the sequences obtained. More recently,
conjunctivitis with lacrirnation may be
field isolates and vaccines strains have been
detected. A rapid diagnosis can be achieved
differentiated more accurately by full
by detection of intranuclear inclusion
gen\:ime sequencing analysis.

bodies in the tracheal epithelium early in
the cow·se of the disease; results of the
microscopic examination can be rapidly

Control: In endemic areas and on fanns
confinned by detection of viral DNA using
where a specific diagnosis is made, fue
virus-speciilc PCR assays. Isolation and
disease is controlled by implementation
identification of the virus is done in chicken
of biosecuiity measmes and vaccination.

embryos or tissue culture from embryo liver

Vaccination is done with live attenuated
or kidney cells or from kidney cells from
vaccines and viral vector recombinant
adult chickens. Chicken embryos are
vaccines. Live vaccines oiiginated from
preferred for virus isolation. Chorioallanvirulent isolates tl1at were attenuated by toic membrane of developing chicken
consecutive passages in embryos or tissue
embryos (9-12 days old) is inoculated with
culture. These are applied via eye drop or
the specimen. Microscopic examination of
through mass vaccination by water or spray.

the chorioaliantoic membrane lesion shows

Viral vector recombinant vaccines in
intranuclear inclusions. On microscopic
fowlpox and herpesvirns of turkeys have
exan1ination of the trachea, intranuclear
been designed to express ILTV immunogenic
inclusion lesions produced by ILTV
proteins and are administered to individual
infection must be differentiated from the
birds by in ovo, SC, or wing-web vaccination.

QUAIL BRONCHITIS

Quail bronchitis is a naturally occurring,
birds. Conjunctivitis, mild to severe
highly contagious, often fatal respiratory
tracheitis (the trachea may be completely
disease of bobwhite quail, seen both in the
filled with mucus), airsacculitis, hepatitis,
wild and in captivity. The disease is of
and gaseous distention of the intestines may
major economic significance to gamebird
be seen. Multiple pale, pinpoint (3 mm) foci
breeders and has a worldwide distribution.

of necrosis in the liver and mottling and

It is a se1ious disease on certain farms
enlargement of tl1e spleen are common
where quail are pen-raised, and particularly
lesions in infected birds. Mortality may
when quail of different ages are maintained
reach 1000/o in birds <2 wk old but is usually
on the san1e premises.

<25% in birds >4 wk old.

The causative agent, quail bronchitis

The disease is often self-limiting.

vims, is a Group I serotype 1 avian

Expe1imental vaccines have proved
adenovirus that can be readily isolated from
ineffective in preventing quail bronchitis.

the respiratory tract of acutely affected

There is no speciilc treatment, but
birds. The virus is also easily isolated from
increasing the brooder temperature by
fecal samples, intestine, liver, and occasion3°-5°F (l.5°-3°C), preventing "piling up,"

ally the bursa ofFabricius. lt is highly
and avoiding contact between older and
contagious and spreads rapidly furough
younger birds and other avian species are of
multiple-age w1its. Other avian species,
value, as are stiict isolation and sanitation.

particularly chickens, may be carrie1s.

Inunwtity is long lasting, possibly for life,

Clinical signs include respiratory distress, and recovered birds can be retained for coughing, sneezing, rales, and na.sal or
breeders. New birds should not be
ocular discharge. Loose, watery droppings
introduced to premises without a 30-day
are common in some acutely affected older
quarantine.

2914

NUTRITION AND MANAGEMENT: POULTRY

NUTRITION AND MANAGEMENT: POULTRY

VetBooks.ir

NUTRITIONAL REQUIREMENTS poultry and the energy content of feedstuffs are expressed in kilocalories (1 kcal equals

Poultry convert feed into food products

4.1868 kilojoules). Two different measures
quickly, efficiently, and with relatively low
of the bioavailable energy in feedstuffs are
environmental impact compared with other
in use, metabolizable energy (AME,.) and
livestock. The high rate of productivity of
the tme metabolizable energy (TME,.).

poultry results in relatively high nutrient

AME,. is the gross energy of the feed minus
needs. Poultry require the presence of at
tl1e gross energy of the excreta after a
least 38 dietary nutrients in appropriate
correction for the nitrogen retained in
concentrations and balance. The nutrient
the body. Calculations ofTME,. make
requirement figures published in Nutrient
an additional correction to account for

Requirements of Poultry (National
endogenous losses of energy that are not

Research Council, 1994) are the most recent
directly attributable to tl1e feedstuff and are
available and should be viewed as minimal
usually a more useful measure. AME,. and
nutrient needs for poultry. They are derived

TME,. are similar for many ingredients.

from experimentally dete1mined levels after However, the two values differ substantially an extensive review of the published data.

for some ingredients such as feather meal,

Criteria used to detennine the requirement
rice, wheat middlings, and corn distiller's
for a given nutrient include growtl1, feed
grains with solubles.

efficiency, egg production, prevention of

Poultry can adjust their feed intake over a
deficiency symptoms, and quality of poultry
considerable range of feed energy levels to
product. These requirements asswne tl1e
meet their daily energy needs. Energy needs
nutrients are in a highly bioavailable fonn,
and, consequently, feed intake also vary
and they do not include a margin of safety.

considerably with enviromnental tempera

Consequently, adjustments should be made
ture and an1ount of physical activity. A bird's
based on bioavailability of nutrients in
daily need for amino acids, vitan1ins, and
various feedstuffs. A margin of safety
minerals are mostly independent of these
should be added based on the length of
factors. The nutrient requirement values in
time the diet will be stored before feeding,
the following tables are based on typical
changes in rates of feed intake due to
rates of intake of birds in a thermoneutral
environmental tempera.hire or dietary
environrnent consuming a diet that contains
energy content, genetic strain, husbandry
a specific energy content ( eg, 3,200 kcal/kg
conditions ( especially the level of sanitafor broilers). !f a bird conswnes a diet that tion), and the presence of stressors (such
has a higher energy content, it will decrease
as diseases or mycotoxins ).

its feed intake; consequently, tl1at diet must
contain a proportionally higher an1ow1t of

Water: Water is an essential nutrient.

amino acids, vitamins, and minerals. Thus,

Many factors influence water intake,
nutrient density in the ration should be
including envirom11ental temperature,
adjusted to provide appropriate nutrient
relative humidity, salt and protein levels of
intake based on requirements and the actual
the diet, birds' productivity (rate of growth
feed intake.

or egg production), and the individual bird's

Because of the ability of poultJy to adjust
ability to resorb water in the kidney. As a
their feed intake to accommodate a wide
result, precise water requirements are
range of diets with differing energy content,
highly variable. Water dep1ivation for 2'12 hr
tl1e energy values listed in the nutiient
has an adverse effect on growtl1 of young
requirement tables in this section ( see TABLES
poultry and egg production of layers; water

6--15) should be regarded as guidelines ratl1er
deprivation for ;o,36 hr results in a marked
tl1an absolute requirements.

increase in mortality of both young and

Appropriate body weight and fat
mature poultry. Cool, clean water,
deposition are important factors in reaiing
uncontaminated by high levels of minerals
pullets for maximal egg production. Most
or other potential toxic substances, must
strains of White Leghorn chickens have
be available at all times.

relatively low body weights and do not tend,
under norn1al feeding, to become obese.

Energy Requirements and Feed

Feed is normally provided for ad lib intake to

Intake: The energy requirements of
this strain of pullets. For brown-egg stJ·ains

NUTRITION AND MANAGEMENT: POULTRY

2915
of chickens, some degree of restriction is
restriction and dietary nutrient guidelines
often practiced ( -90% of ad lib feeding) to
specific for their strains.

prevent precocial onset of lay. Broiler strains
tend to become obese if fed ab lib; feed

Amino Acid Requirements: Poultry,
restriction is necessary for broiler pullets
like all anin1als, synthesize proteins that
and broiler breeders. When feed restriction

VetBooks.ir
contain 20 L-arnino acids. Birds are w1able
is practiced, the feed levels of amino acids,
to synthesize 9 of these an1ino acids because
vitamins, and minerals must be proportionof the lack of specific enzymes: arginine, ally increased to prevent deficiencies. Most
isoleucine, leucine, lysine, methionine,
large commercial breeders provide feed
phenylalanine, threonine, tryptophan, and
l�ll!l·I NUTRIENT REQUIREMENTS OF GROWING PULLETS•

Age (wk)

0-6

6-12

12-18

18 to lstEgg

WHITE-EGG LAYERS

Body weight (g)b

450

980

1,375

1,475

Protein

18

16

15

17

Arginine

1.0

0.83

0.67

0.75

Lysine

0.85

0.60

0.45

0.52

Methionine

0.30

0.25

0.20

0.22

Methionine + cystine

0.62

0.52

0.42

0.47

Threonine

0.68

0.57

0.37

0.47

Tryptophan

0.17

0.14

0.11

0.12

Calcium

0.90

0.80

0.80

2.00

Phosphorus, available

0.40

0.35

0.30

0.32

BROWN-EGG LAYERS

Body weight (g)b

500

1,100

1,500

1,600

Protein

17

15

14

16

Arginine

0.94

0.78

0.62

0.72

Lysine

0.80

0.56

0.42

0.49

Methionine

0.28

0.23

0.19

0.21

Methionine + cystine

0.59

0.49

0.39

0.44

Threonine

0.64

0.53

0.35

0.44

Tryptophan

0.16

0.13

0.10

0.11

Calcium

0.90

0.80

0.80

1.8

Phosphorus, available

0.40

0.35

0.30

0.35

• Requirements are listed as percentages of diet. Nutrient levels should be adjusted to meet specific strain requirements, level of feed intake, and body weight and skeletal development.

b Average body weight at end of each pe1iod.

2916

NUTRITION AND MANAGEMENT: POULTRY

NUTRIENT REQUIREMENTS OF LAYING HENS AT DIFFERENT FEED

INTAKES•

Pounds (approx.)/100 birds/day

18

20

22

24

26

VetBooks.ir

Grams of feed/bird/day

80

90

100

110

120

WHITE-EGG LAYERS

Protein

18.8

16.7

15.0

13.6

12.5

Arginine

0.88

0.78

0.70

0.64

0.58

Lysine

0.86

0.77

0.69

0.63

0.58

Methionine

0.38

0.33

0.30

0.27

0.25

Methionine + cystine

0.73

0.64

0.58

0.53

0.48

Threonine

0.59

0.52

0.47

0.43

0.39

Tryptophan

0.20

0.18

0.16

0.15

0.13

Calcium

4.12

3.67

3.30

3.00

2.75

Phosphorus, available

0.31

0.28

0.25

0.23

0.21

BROWN-EGG LAYERS

Protein

22.5

20.0

18.0

16.4

15.0

Arginine
l.06

0.94

0.85

0.77

0.71

Lysine
l.05

0.93

0.84

0.76

0.70

Methionine

0.45

0.40

0.36

0.33

0.30

Methionine + cystine

0.89

0.79

0.71

0.65

0.59

Threonine

0.71

0.63

0.57

0.52

0.48

Tryptophan

0.24

0.21

0.19

0.17

0.16

Calcium

5.00

4.44

4.00

3.64

3.33

Phosphorus, available

0.38

0.33

0.30

0.27

0.25

• Requirements are listed as percentages of diet.

valine. Histidine, glycine, and proline can be
added to the diet in pmified form ( eg,
synthesized by birds, but the rate is usually

DL-methionine and L-lysine) to minimize the
insufficient to meet metabolic needs and a
total protein level as well as the cost of the
dietary source is required. These 12 an1ino
diet. This has the added advantage of
acids are referred to as the essential amino
minimizing nitrogen excretion.

acids. Tyrosine and cysteine can be
synthesized from phenylalanine and methio

Vitamins: Requirements for vitamins A, D,
nine, respectively, and are referred to as
and E are expressed in IU. For chickens,
conditionally essential because they must
l IU of vitamin A activity is equivalent to 0.3
be in the diet if phenylalanine or methionine
rncg of pure retinol, 0.344 mcg of retinyl
levels are inadequate. The diet must also
acetate, or 0.6 mcg ofl3-carotene. However,
supply sufficient an10unts of nitrogen to
young chicks use 13-carotene less efficiently.

aUow the synthesis of nonessential amino

One IU of vitamin D is equal to 0.025 mcg of
acids. Essential amino acids are often
cholecalciferol (vitamin D ). Ergocalciferol

3

NUTRITION AND MANAGEMENT: POULTRY

2917
lffl=lll=I NUTRIENT REQUIREMENTS OF BROILERS•

Ageb

0-3wk

3-6wk

6-Swk
kcal AME/kg dietc

3,200

3,200

3,200

VetBooks.ir

Crude protein ct

23.00

20.00

18.00

Arginine

1.25

1.10

1.00

Glycine + serine

1.25

1.14

0.97

Histidine

0.35

0.32

0.27

Isoleucine

0.80

0.73

0.62

Leu cine

1.20

1.09

0.93

Lysinee

1.10

1.00

0.85

Methionine

0.50

0.38

0.32

Methionine + cystine

0.90

0.72

0.60

Phenylalanine

0.72

0.65

0.56

Phenylalanine + tyrosine

1.34

1.22

1.04

Pro line

0.60

0.55

0.46

Threonine

0.80

0.74

0.68

Tryptophan

0.20

0.18

0.16

Valine

0.90

0.82

0.70

" Requirements are listed as percentages of diet.

b The 0- to 3-, 3- to 6-, and 6- to 8-wk intervals for nutrient requirements are based on chronology for which research data were available; however, these nuttient requirements are often implemented at younger age intervals or on a weight-of-feed consumed basis.

c These are typical dietary energy concentrations. Different energy values may be appropriate depending on local ingredient prices and availability.

d Broiler chickens do not have a requirement for crude protein per se. However, there should be sufficient crude protein to ensure an adequate nitrogen supply for synthesis of nonessential amino acids.

Suggested requirements for crude protein are typical of those derived with com-soybean meal diets, and levels can be reduced when synthetic amino acids are used.

c Recent research has shown that higher levels of lysine are needed for maximal growth and efficiency of modem broilers.

(vitamin D2) is used with an efficiency of
widely distributed in practical feedstuffs

<10% of vitamin D3 in poultry.

and can spare the requirement for choline

One IU of vitamin Eis equivalent to 1 mg
but cannot completely replace it in the diet.

of synthetic DL-a-tocopherol acetate.

All vitamins are subject to degradation

Vitamin E requirements vary with type and
over time, and this process is accelerated by
level of fat in the diet, the levels of selenium
moisture, oxygen, trace minerals, heat, and
and trace minerals, and the presence or
light. Stabilized vitamin preparations and
absence of other antioxidants. When diets
generous margins of safety are often applied
high in long-chain highly polyunsaturated
to account for these losses. This is
fatty acids are fed, vitamin E levels should
especially true if diets are pelleted,
be increased considerably.

extruded, or stored for long periods.

Choline is required as an integral pa.J.t
of the body phospholipid, as a pa.it of

Minerals: Much of the phosphorus in
acetylcholine, and as a source of methyl
feedstuffs of plant origin is complexed by
groups. Growing chickens can also use
phytate and is not absorbed efficiently by
betaine as a methylating agent. Betaine is
poultry. Consequently, it is critical that only

2918

NUTRITION AND MANAGEMENT POULTRY

•@=i!#I PROTEIN AND AMINO ACID REQUIREMENTS OF TURKEYS•

Age (wk)

Male:

0-4

4-8

8-12 12-16 16-20 20-24

VetBooks.ir

Breeding

Female:

0-4

4-8

8-11 11-14 14-17 17-20 Holding Hens

Energy base
kcal ME/kg
dietb

2,800 2,900 3,000 3,100 3,200 3,300 2,900

2,900

Protein

28.0

26

22

19

16.5

14

12

14

Arginine

1.6

1.4

1.1

0.9

0.75

0.6

0.5

0.6

Glycine+

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.5
serine

Histidine

0.58

0.5

0.4

0.3

0.25

0.2

0.2

0.3

Isoleucine

1.1

1.0

0.8

0.6

0.5

0.45

0.4

0.5

Leucine

1.9

1.75

1.5

1.25

1.0

0.8

0.5

0.5

Lysine

1.6

1.5

1.3

1.0

0.8

0.65

0.5

0.6

Methionine

0.55

0.45

0.4

0.35

0.25

0.25

0.2

0.2

Methionine+ 1.05

0.95

0.8

0.65

0.55

0.45

0.4

0.4
cystine

Phenylalanine 1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.55

Phenylalanine 1.8

1.6

1.2

1.0

0.9

0.9

0.8

1.0

+ tyrosine

Threonine

1._o

0.95

0.8

0.75

0.6

0.5

0.4

0.45

Tryptophan

0.26

0.24

0.2

0.18

0.15

0.13

0.1

0.13

Valine

1.2

1.1

0.9

0.8

0.7

0.6

0.5

0.58
a Requirements are listed as percentages of diet.

b These ai·e typical ME concentrations for com-soya diets. Different ME values may be appropriate if other ingredients predominate.

Adapted, with permission, from Nut1ient Requirements of Poultry, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

the available phosphorus and not the total
lizable energy and water. Some additional
phosphorus levels be considered. Approprinutrients may be necessary for growth and ate calciun1 nutrition depends on both the
development under certain conditions.

level of calciwn and its ratio to that of

These include vitan1in C, pyrroloquinoline
available phosphorus. For growing poultry,
quinone, and several heavy metals.

this ratio should not deviate substantially

Non-nutrient antioxidants, such as
from 2: 1. The calciwn requirement of laying
ethoxyquin, are usually added to poultry
hens is very high and increases with the rate
diets to protect vitan1ins and unsaturated
of egg production and age oft.he hPn.

fatty acids from oxidation. Antibiotics at
low levels (5-25 mg/kg of feed, depending

Other Nutrients and Additives: The
on the antibiotic) and stufeit copper (150
chick has requirements for 38 nutrients,
ppm) are sometimes included to improve
together with an adequate level of metabo-
growth rate and feed efficiency. Enzymes

NUTRITION AND MANAGEMENT: POULTRY

2919

IBNlll·I NUTRIENT REQUIREMENTS OF PHEASANTS•

Energy base

0-4wk

4--8wk

9-17wk

Breeding
kcal ME/kg dietb

2,800

2,800

2,700

2,800

VetBooks.ir

Protein(%)

28

24

18

15

Glycine + serine (%)

1.8

1.55

0.5

Lysine(%)

1.5

1.40

0.8

0.68

Methionine + cystine (%)

1.0

0.93

0.6

0.6

Linoleic acid (%)

Calcium(%)

1.0

0.85

0.53

2.5

Phosphorus, available(%)

0.55

0.5

0.45

0.40

Sodium(%)

0.15

0.15

0.15

0.15

Chlorine (%)

0.11

0.11

0.11

0.11

Iodine (mg)

0.3

0.3

0.3

0.3

Riboflavin (mg)

3.4

3.4

3.0

4.0

Pantothenic acid (mg)

10

10

10

16

Niacin (mg)

70

70

40

30

Choline (mg)

1,430

1,300

1,000

1,000

• Requirements are listed as percentages or as mg/kg of diet. For values not listed, see requirements of turkeys (TABLE 9 and TABLE 15) as a guide.

b These are typical dietary energy concentrations.

Adapted, with permission, from Nutrient Req1tirements of Poult,y, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

that increase the bioavailabili ty of dietary
considerably because of differences in the
phosphorus, energy, and protein are often
nutrient density of feed, strain or breed of
used in poultry diets when their costs are
bird, amount of feed wasted, and environnot prohibitive. In some cases, phytase ment.al temperature.

enzymes are used to decrease the amount

Most diets used to feed poultry are
of phosphorus in the excreta to meet
nutritionally "complete" and commercially
environment.al regulations.

mixed, ie, prepared by feed manufacturing
companies, most of which employ trained
nutritionists. The formulation and mixing

FEEDING AND
of poultry feeds requires knowledge and

MANAGEMENT PRACTICES
experience in purchasing ingredients,
experin1ent.a1 testing of fom1Ulas, laboratory

Success of the feeding program should be
control of ingredient quality, and computer
measured by how it achieves the breeder's
applications. In1proper mixing can result in
goals for proper weight and development
vitamin and mineral deficiencies, Jack of
specific to each strain. Feed and the length
protection against disease, or drug toxicity.

of time required to attain certain weights in

The physical fom1 of the feed influences
pullets and turkeys are presented in the
the expected results. Most feeds for starting
growth and feed tables elsewhere in thls
and growing birds are pro<lut:e<l as pellets
chapter (seep 2914). The figures in these
or cmmbles. In the pelleting process, the
tables can be used as a guide to estimate
mash is treated with steam and then passed
the amount of feed required but will vary
through a suitably sized die under pressure.

2920 NUTRITION AND MANAGEMENT POULTRY

14N•ili NUTRIENT REQUIREMENTS OF BOBWHITE QUAIL·

Starting

Growing

Breeding

Energy base kcal ME/kg dietb 2,800

2,800

2,800

VetBooks.ir

Protein(%)

26

20

24

Glycine + serine(%)

Lysine(%)

Methionine + cystine (%)

1.0

0.75

0.90

Linoleic acid (%)

Calcium(%)

0.65

0.65

2.4

Phosphorus, available (%)

0.45

0.30

0.7

Sodium(%)

0.15

0.15

0.15

Chlorine (%)

0.11

0.11

0.11

Iodine (mg)

0.3

0.3

0.3

Riboflavin (mg)

3.8

3.0

4.0

Pantothenic acid (mg)

12

9

15

Niacin (mg)

30

30

20

Choline (mg)

1,500

1,500

1,000
a Requirements are listed as percentages or as mg/kg of diet. For values not listed, see REQUIREMENTS

OF LAYING HENS (TABLE 7) and LEGHORN-TYPE CHlCKENS (TABLE 14) as a guide.

b These are typical dietary energy concentrations.

Adapted, with permission, from Nut,rient, Requirements of Poultry, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

The pellets are then cooled quickly and
or the strain's breeder company should be
d1;ed by means of a forced air draft. The
followed with regard to the feeding of extra
conditions under whic]l pelleting occurs
calcium, grit, or whole grain. Fresh, clean

( eg, use of an expander rather than an
water should always be readily available.

extruder, exposure to high temperature, use
of soft pellets) have an important effect on

VACCINATION PROGRAMS
the nutritional quality of the pellets or of the
crumbles produced by crushing the pellets.

See TABLES 16-21 for recommended vaccination programs for broilers, broiler-breeders, FEEDING METHODS
conunercial layers, turkeys, duck breede1s,
and conunercial ducklings.

For newly hatched birds of any species, a

"complete" feed in crumble form is the

MANAGEMENT OF GROWING
progran1 of choice, regardless of other

CHICKENS
considerations. A "complete" feed program
for growing stock, particularly for laying and

Broiler houses generally have specific areas
breeding stock, is also highly recommended.

designated for brooding. These areas could

Advantages of the "complete" feed progran1
be throughout the whole house but with
over the "mash and grain" system include the rings of cardboard ( often referred to as sin1plicity of feeding, accuracy of medicachick guards) used to keep chicks ar0tmd a tion, in1proved balance of dietary nutrients,
heat source; more commonly, an area of the
and superior feed conversion efficiency.

house is curtained off and preheated before

Regardless of the system of feeding,
chick placement. Either way, the brooder
recommendations of the feed manufacturer
area floor temperature should be between

NUTRITION AND MANAGEMENT: POULTRY

2921
lffl:llltl NUTRIENT REQUIREMENTS OF PEKIN DUCKS•

Starting

Growing

Energy base

(0-2wk)

(2-7wk)

Breeding
kcal ME/kg dietb

2,900

3,000

2,900

VetBooks.ir

Protein(%)

22

16

15

Arginine (%)

1.1

1.0

Lysine(%)

0.9

0.65

0.6

Methionine+ cystine (%)

0.7

0.55

0.5

Calcium(%)

0.65

0.6

2.75

Phosphorus, available (%)

0.40

0.30

0.30

Sodium(%)

0.15

0.15

0.15

Chlorine (%)

0.12

0.12

0.12

Magnesium (mg)

500

500

500

Manganese (mg)

50

?

?

Zinc (mg)

60

?

?

Seleniwn (mg)

0.2

?

?

Vitamin A (IU)

2,500

2,500

4,000

Vitamin D (IU)

400

400

900

Vitamin K (mg)

0.5

0.5

0.5

Riboflavin (mg)

4

4

4

Pantothenic acid (mg)

11

11

11

Niacin(mg)

55

55

55

Pyridox.ine (mg)

2.5

2.5

3.0

"Requirements are listed as percentages or as units or mg/kg of diet. For nutrients not listed, see NUTRIENT REQUIREMENTS OF BROILmS (TABLE 8) as a guide.

b These are typical dietary energy concentrations.

Adapted, with permission, from Nutrient Requirements of Poultty, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

85°-90°F (29.4°-32.2°C). As the birds

At least 3 in. (7.5 cm) of suitable litter,
become older, the brooder temperatme is
clean for each brood and spread to an even
lowered 5°F (2.8°C) each week until it is
depth, should be provided at the start. Litter

70°F (21.1 °C). At -1 wk of age, the chick
must be free of mold; it should absorb
guards are removed or the curtains are
moistme without caking, be nontoxic, and
opened, and the chicks have access to the
of large enough particle size to discomage
additional space in the house. In particularly consumption. Chicks are staited with 24 hr large chicken houses, there may be a second of light for several days; thereafter, light is area cmtained off for several days ( up to
reduced. Both length of day and intensity of

10-14 days of age) before the chicks are
light are important. Lighting programs vary
given access to the complete house. Ample
widely, depending on whether housing is
space should be provided for feeders and
windowless or open-sided, and should
waterers, which should be well distributed
comply with recommendations of major
in the house.

breeders in similar situations.

2922

NUTRITION AND MANAGEMENT: POULTRY

IM;i!IFI NUTRIENT REQUIREMENTS OF GEESE·

Starting

Growing

Energy base

(0-4wk)

(after 4 wk)

Breeding
kcal ME/kg dietb

2,900

3,000

2,900

VetBooks.ir

Protein(%)

20

15

15

Lysine(%)

1.0

0.85

0.6

Methionine + cystine (%)

0.6

0.5

0.5

Calcium(%)

0.65

0.6

2.25

Phosphorus, available (%)

0.3

0.3

0.3

Vitamin A (lU)

l ,500

1,500

4,000

Vitamin D (IU)

200

200

200

Riboflavin (mg)

3.8

2.5

4.0

Pantothenic acid (mg)

15

10

10

Niacin(mg)

65

35

20
a Requirements are listed as percentages or as units or mg/kg of diet. For nutrients not listed, see NtrrRIENT HEQUIREMENTS OF BHOILERS (TABLE 8) as a guide.

b These a.re typical dietary energy concentrations.

Adapted, with permission, from Nutrient Requirements of Poult1y, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

When reaiing pullets to be used as
an adult house should also be given at least
commercial egg laying or meat type

1 wk to adjust to their new environment
breeding hens, feeding systems are often
before the stress of egg production begins.

combined with day-length control dwing

Beaks should be retrinm1ed as necessary,
rearing to influence the rate at which birds
aI1d cull birds removed at the time of
matw·e. Under certain conditions, pullets
rehousing.

may be beak trimmed at the hatchery or,

Feeders and waterers should be of the
in rare cases, within the first 7 days after
proper type, size, and height for the stock
hatch. In controlled environment housing,
and management system. Feeders that 3.1·e
day lengths 3.1·e controlled more precisely;
too shallow, too narrow, or lacking a lip or
with dim lights, beak trimming may be
flange on the upper edge may pennit excess
delayed tmtil later in the growing period.

feed waste. Uneven distribution of waterers

Pullets should be treated for ex1:emal and
or lack of water space results in reduced
internal parasites as required. Vaccination
intake and thus-reduced performance.

should be used to control problem diseases
of the geographic area ( see p 2920).

Artificial Lights: Day length should be

Many commercial egg laying type pullets
increased gradually as the pullets come into
arc re3.1·ed in cages. The cage manufacturer
egg production and should reach a 14-to
usually supplies specific instructions

16-hr light periocVday at peak production for
regarding heating, bird density, and feeding
both market-egg and hatching-egg layers. An
space. Most commercial rations are fortified intensity of at least 1 foot-canclle of light with sufficient nutrients to meet the

(10 lux) at the feed trough should be
requirements of cage-reared birds.

provided; this is about equal to one 60-watt
light bulb to each 100 sq ft (-9 sq m), hanging MANAGEMENT OF LAYING

7 ft (2.1 m) above the birds. Production may

CHICKENS
decrease if day length or light intensity is
reduced dilling the laying period. With cage

Most laying pullets are housed in cages
systems of all types, illtU11ination is more

3.11d should be moved to these facilities at
even if smaller wattage bulbs placed closer
least 1 wk before egg production begins.

together 3.1·e used, rather than large bulbs

Breeders moved from a growing house to
suspended over the center of each aisle. With

NUTRITION AND MANAGEMENT POULTRY

2923

LINOLEIC ACID, MINERAL, AND VITAMIN REQUIREMENTS OF

LEGHORN-TYPE CHICKENS•

18wkto

VetBooks.ir

Age

0-6wk

6-18wk lstegg

Layers Breeders

Linoleic acid (%)

LOO

LOO

LOO

LOO

LOO

Potassium(%)

0.25

0.25

0.25

0.15

0.15

Sodium(%)

0.15

0.15

0.15

0.15

0.15

Chlorine (%)

0.15

0.15

0.15

0.13

0.13

Magnesiwn (mg)

600

500

400

500

500

Manganese (mg)

60

30

30

20

20

Zinc(mg)

40

35

35

35

45

Iron (mg)

80

60

60

45

60

Copper(mg)

5

4

4

?

?

Iodine(mg)

0.35

0.35

0.35

0.035

0.01

Selenium (mg)

0.15

0.1

0.1

0.06

0.06

Vitamin A (IU)

1,500

1,500

1,500

3,000

3,000

Vitamin D3 (IU)

200

200

300

300

300

Vitamin E (IU)

10

5

5

5

10

Vitamin K (mg)

0.5

0.5

0.5

0.5

LO

Riboflavin (mg)

3.6

1.8

2.2

2.5

3.6

Pantothenic acid (mg)

10

10

10

2

7

Niacin(mg)

27

10

10

10

10

Vitamin B12 (mg)

0.009

0.003

0.004

0.004

0.08

Choline (mg)

1,300

900

500

1,050

1,050

Biotin (mg)

0.15

0.1

0.1

0.1

0.1

Folacin (mg)

0.55

0.25

0.25

0:25

0.35

Thiamine (mg)

LO

LO

0.8

0.7

0.7

Pyridoxine (mg)

3

3

3

2.5

4.5
a Requirements are listed as percentages or as Lmits or mg/kg of diet. Assumes an average daily intake of 110 g of feed/hen/day.

Adapted, with permission, from Nillrient Requirements qf Poult1y, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

tiered cages, the bulbs are suspended 6-7 in.

flock activities, including hatch date, regular

(15-18 cm) above the level of the top cage.

body weights (to ensure that the pullets will
have reached optimal body weight when

Record Keeping: Successful intensive
they are brought into egg production),
poultry keeping requires good records of all
lighting progran1, house temperatures,

2924

NUTRITION AND MANAGEMENT: POULTRY

LINOLEIC ACID, MINERAL, AND VITAMIN REQUIREMENTS

OF TURKEYS•

Age (wk)

VetBooks.ir

Male:0-4 4-8

8-12 12-16 16-20 20-24

Breeding

Female: 0-4 4-8

8-11 11-14 14-17 17-20 Holding Hens

Energy base
kcal ME/kg
dietb

2,800 2,900 3,000 3,100 3,200 3,300 2,900

2,900

Linoleic acid (%) 1.0

1.0

0.8

0.8

0.8

0.8

0.8

1.1

Calcium(%)

1.2

1.0

0.85

0.75

0.65

0.55

0.5

2.25

Phosphorus,

0.6

0.5

0.42

0.38

0.32

0.28

0.25

0.35
available (%)

Potassium (%)

0.7

0.6

0.5

0.5

0.4

0.4

0.4

0.6

Sodium(%)

0.17

0.15

0.12

0.12

0.12

0.12

0.12

0.12

Chlorine(%)

0.15

0.14

0.14

0.12

0.12

0.12

0.12

0.12

Magnesium (mg) 500

500

500

500

500

500

500

500

Manganese ( mg) 60

60

60

60

60

60

60

60

Zinc (mg)

70

65

50

40

40

40

40

65

Iron (mg)

80

60

60

60

50

50

50

60

Copper (mg)

8

8

6

6

6

6

6

8

Iodine ( mg)

0.4

0.4

0.4

0.4

0.4

0.4

0.4

0.4

Selenium (mg)

0.2

0.2

0.2

0.2

0.2

0.2

0.2

0.2

Vitamin A (IU)

5,000 5,000 5,000 5,000

5,000

5,000 5,000

5,000

Vitan1in De (IC) 1,100 1,100 1,100 1,100

1,100

1,100 1,100

1,100

Vitamin E (IU)

12

12

10

10

10

10

10

25

Vitamin K (mg)

1.75

1.5

1.0

0.75

0.75

0.5

0.5

1.0

Riboflavin ( mg) 4.0

3.6

3.0

3.0

2.5

2.5

2.5

4.0

Pantothenic

10

9

9

9

9

9

9

16
acid (mg)

Niacin (mg)

60

60

50

50

40

40

40

40

Vitamin B12 (mg) 0.003 0.003 0.003 0.003 0.003 0.003 0.003

0.003

Choline (mg)

1,600 1,400 1,100 1,100 950

800

800

1,000

Biotin ( mg)

0.2

0.2

0.125 0.125 0.100 0.100 0.100

0.2

Folacin (mg)

1.0

1.0

0.8

0.8

0.7

0.7

0.7

1.0

Thian1ine (mg)

2

2

2

2

2

2

2

2

Pyridoxine ( mg) 4.5

4.5

3.5

3.5

3.0

3.0

3.0

4.0
a Requirements are listed as percentages or as units or mg/kg of diet.

b These are typical ME concentrations for com-soya diets. Different ME values may be appropriate if other ingredients predominate.

< These concentrations of vitamin D are satisfactory when the dietary concentrations of calcium and available phosphorus confom1 with those in this table.

Adapted, with pem1ission, from Nut,-i.ent Requirements of Poult,y, 1994, National Academy of Sciences, National Academy Press, Washington, DC.

NUTRITION AND MANAGEMENT POULTRY

2925

•d=iiiti VACCINATION PROGRAM FOR BROILERS•

Vaccine

Age

Route

Type

Marek's diseaseb

1 day

SC

Turkey herpesvirus and

VetBooks.ir

SB-1 or Rispens strain for
high-challenge areas

Newcastle disease

1 day or

Coarse spray

Bl

14-21 days

Water or coai;se Bl orLaSota
spray

Infectious bronchitis

1 day or

Coarse spray

Massachusetts

14-21 days

Water or coarse Massachusetts
spray

Infectious bursa!

14-21 days

Water

Inte1mediate
disease

"This is an example of a typical vaccination progran1. Individual programs are highly variable and reflect local conditions, disease prevalence, severity of challenge, and individual preferences.

b Most USA commercial broiler hatcheries use an in ovo vaccination system for Marek's disease at 17-19 days of embryonation. Infectious bursal disease vaccine (mild strain) may be combined with Marek's disease vaccines. Vectored vaccines in which Maxek's and fowl pox vaccines have been safely modified to carry immunizing antigens for laryngotracheitis, Newcastle disease, or infectious bursa] disease are also commonly used in ovo or day-old chicks. Connecticut strain is often combined with Massachusetts. Bronchitis vaccine is usually combined with Newcastle. Other bronchitis strains such as Arkansas 99 and Florida 88 are included in some areas. Vaccinations at 14-21 days are optional. A single drinking water application for Newcastle clisease/bronch.itis is also common.

disease history, medication and vaccina
layers per Cage: Within the guidelines
tion dates, quantity and type of feed given
indicated in TABLE 22 and TABLE 23, most

(important in calculating efficiency of feed
colony cages house 5-10 layers. The ideal
utilization), and mortality.

flock size depends on several factors,
including labor and cost, and is best

Floor Space, Feeding, and Water
determined by the individual poultry

Requirements: Egg-production birds
manager or producer.

usually spend tl1eir entire lives in cages.

Allliough some broiler breeders are

ORGANIC PRODUCTION
sinillarly housed, most are reared on litter

PRACTICES
floors or in pens in which as much as
two-tllirds of the floor is slatted. For

Organic Poultry: According to livestock
egg-strain pullets reared in cages, there is
standards, birds for slaughter designated
little chance of altering fue feeding and
as organic must be raised under organic
watering space available, but periodic
management starting no later than the
checks are necessary to ensure that feed and second day of life. Preventive management water are being continuously supplied. With
practices, including the use of vaccines to
the success of nipple- and cup-waterers and
keep animals healthy, are used; however,
the various types of automatic feeding
antibiotics cannot be used for any reason,
systems, it becomes more difficult to give
and federal regulations prohibit the use of
specific recommendations for feeding and
honnones in all poultry. Organic managewatering space. Decisions must be made ment standards prohibit producers from
about optimal floor space and feeding and
withholding treatment from a sick or injured
watering requirements based on advice
anin1al, but aninlals treated with a prohibited
from equipment manufacturers, primary
medication may not be sold as organic. All
breeders, careful observation, and past
organically raised aninlals must have access
experience as to productivity. See TABLE 22
to the outdoors; fuey may be temporarily
and TABLE 23 for space requirements for
confined only for reasons of health, safety, or
egg-strain and meat-strain birds. Environto protect soil or water quality.

mental housing and various types of

For a product to be labeled with the
ventilation may alter these specifications.

"USDA organic" seal, it must comply with

2926

NUTRITION AND MANAGEMENT POULTRY
ihi=l·ifi VACCINATION PROGRAM FOR BROILER BREEDERS•

Age

Vaccine

Route

'fype

1 day

Marek's disease

SC

Turkey herpesvirus

VetBooks.ir

6-7days

Tenosynovitis

SC

Live (Mild)

14-21 days

Newcastle/infectious

Water

Bl/Mass
bronchitis

14-28days
lnfectious bursa!

Water

Intermediate
disease

4wk

Newcastle/infectious

Water or

Bl/Mass
bronchitis
coarse spray

6---Swk

Tenosynovitis

SC

Live (Mild)

8 -lOwk

Infectious bursaJ

Water or

Live
disease
coarse spray

8---10 wk

Newcastle/infectious

Water or

Bl orLaSota/Mass
bronchitis
coarse spray

10-12 wk

EncephaJornyelitis

Wing web

Live, chick-embryo origin

10-12 wk

Fowlpox

Wing web

Modified live

10-12 wk

Chicken infectious

Wing web

Modified live
anemia

10-12 wk

Laryngotracheitis

Intraocular

Modified live

10-12 wk

Tenosynovitis

Parenteral

Inactivated

10-12 wk

Fowl cholera

Parenteral or Inactivated

Wing web

Live CU, PM-1, or M9

12-14wk

Newcastle/infectious

Water or

Bl or LaSota/Mass
bronchitis
aerosol

14-18wk

Fowl cholera

Parenteral or Inactivated

Wing web

Live CU, PM-1, or M9

16---lSwk

Infectious bursa]

Parenteral

Inactivated.

disease

16---lSwk

Tenosynovitis

Parenteral

Inactivated

16---lSwk

Newcastle/infectious Water or

Bl or LaSota/Mass
bronchitis
aerosol

Every60-90

Newcastle/infectious

Parenteral

Inactivated
days or 18wk
bronchitis

"This is an example of a vaccination program. Individual programs are highly variable and reflect local conditions, disease prevalence, severity of challenge, and individual preferences. SB-1, MDV301, or Rispens strain may be combined with turkey herpesvirus in some areas. Vaccination for fowlpox and laryngotracheitis depends on local requirements. Other strains of infectious bronchitis (Connecticut, Arkansas 99, Florida 88, etc) are included in some areas.

NUTRITION AND MANAGEMENT: POULTRY

2927
itM•li:N VACCINATION PROGRAM FOR COMMERCIAL LAYERS•

Age

Vaccine

Route

'fype

1 day

Marek's disease

SC

1\irkey herpesvirus and

VetBooks.ir

SB-1

14-21 days Newcastle/infectious

Water

Bl/Mass
bronchitis

14-21 days

Infectious bursa! disease Water

Intermediate

5wk

Newcastle/infectious

Water or coarse Bl/Mass
bronchitis
spray

8-10 wk

Newcastle/infectious

Water or coarse Bl or LaSota/Mass
bronchitis
spray

10-12 wk

Encephalomyelitis

Wing web

Live, chick-embryo origin

10-12 wk

Fowl pox

Wing web

Modified live

10--12 wk

Laryngotracheitis

Intraocular

Modified live

10--14 wk

Mycoplasma

Intraocular or

Mild live strain
gallise-pticum b
spray
or 18wk

Parenteral

Inactivated

12-14 wk

Newcastle/infectious

Water or aerosol Bl or LaSota/Mass
bronchitis

16---lSwk

Newcastle/infectious

Water or aerosol Bl or LaSota!Mass
bronchitis

Every60-90 Newcastle/infectious

Parenteral

Inactivated
days or 18
bronchitis
wk

• This is an example of a vaccination program. Individual programs are highly variable and reflect local conditions, disease prevalence, severity of challenge, and individual preferences.

b The use of M gallisepticum vaccine is regulated or prohibited in some states. SB-1 or MDV301 may be combined with turkey herpesvirus in some areas, or Rispens strain may be used in high-chal)enge areas. Vaccination for infectious bursal disease, laryngotracheitis, and fowlpox depends on local requirements. Other strains of infectious bronchitis (Connecticut, Arkansas 99, Florida 88, etc) a.re included in some areas. M gallisepticum and Haemophilus gallinarum (coryza.) are used only on infected, multiage premises in some areas.

USDA National Organic Standards. Con

The first step toward organic certificagress passed the Organic Foods Production tion for a poultry producer is to select a

Act in 1990, and the USDA established
third-party certifier. The USDA keeps
national organic standards in 2002. As of
an actively updated list of accredited

2011, the organic layer flock in t11e USA
certification agencies, all of which follow
was approxinlately 6.5 million hens, and
the san1e USDA National Organic Standthe average number of organic broilers ards. The producer then submits an
processed each week was approxinlately
application and Organic System Plan (OSP)

0.5 million birds. This represents approxito the selected ce1tification agency. In mately 2.3% of the layer population and
livestock production, this plan includes

0.3% of the broiler production. In the years
infonnation on the animal source, feeding
from 2001 to 2011, the organic layer flock
practices, management practices, health
has grown 4000Ai, and broilers processed as
care, recordkeeping, and product labeling.

organic has grown 9000A,. However, it is

The certifier then reviews t11e OSP and, if
important to realize that there are years in
it is deemed adequate, assigns a quali1ied
tl1e past 10 when both layer and broiler
organic inspector to tl1e livestock facility.

organic numbers have shrunk from one year

The inspector conducts a detailed
to the next. Growth of these areas is not a
evaluation of the OSP and the actual farm
straight and predictable line.

practices, provides a written exit interview

2928

NUTRITION AND MANAGEMENT POULTRY

IM:i!iii VACCINATION PROGRAM FOR TURKEYS·

Age (wk)b Market Turkeys Breeder Hens

Breeder Toms

2-3

NDc81-8l<ior

ND, 81-81 or LaSota,

ND, 81-81 or LaSota,

VetBooks.ir

LaSota, owe or

DW or spray

OW or spray
spray

4

Hemorrhagic

Hemorrhagic enteritis,

Hemorrhagic enteritis,
enteritis, DW

DW

DW

6

Fowl cholera/

Fowl cholera, DW (live)

Fowl cholera, DW (live)

DW(live)or SC
or SC (inactivated)

or SC (inactivated)

(inactivated)

9-10

ND, LaSota,

ND, LaSota, DW or spray ND, LaSota, DW or spray

OW or spray

12

Fowl cholera,

Fowl cholera, DW (live)

Fowl cholera, DW (live)

DW(live)or SC
or SC (inactivated)

or SC (inactivated)

(inactivated)

15

ND, LaSota,

ND, LaSota, DW or spray ND, LaSota, DW or spray

OW or spray

18

Fowl cholera, DW (live)

Fowl cholera, DW (live)

or SC (inactivated)

or SC (inactivated)

21

ND, LaSota, DW or spray ND, LaSota, DW or spray

24

Fowl cholera, DW (live)

Fowl cholera, DW (live)

or SC (inactivated)

or SC (inactivated)

26

Erysipelas, DW (live) or

Erysipelas, DW (live) or

SC (inactivated)

SC (inactivated)

Pox, WW•

Pox, WW

28

ND, SC (inactivated)

ND, SC (inactivated)

Fowl cholera, DW (live)

Fowl cholera, DW (live)

or SC (inactivated)

or SC (inactivated)

Encephalomyelitis, DW

Encephalomyelitis, DW

" Recommendations are for production areas where the diseases listed are common. ln addition, other vaccinations may be advisable if previous experience indicates prevalence of certain diseases in the area. These may include turkey bordetellosis eye drop vaccine at l day old and in water or spray at 14 days old, or bacterin; paramyxovirus 3 and influenza A (prevalent hemagglutinin) at 26--28 and 40
wk old; erysipelas-live or killed prodncts might be required for market turkeys, and repeated vaccinations might be required for breeders; and salmonellosis bacte1ins at 24 and 28 wk old.

" Recommended age at vaccination is an approximation.

c ND= Newcastle disease
c1 Spray ND vaccines should not be used for birds suffering from respiratory disease; in such cases and at that age, tl1e mild Bl-Bl strain vaccine could be used in water. Tinting of vaccination depends on maternal antibody levels.

c OW = drinking water; WW= wing web stab
r Live fowl cholera vaccines should be used only in healthy flocks.

of findings to the producer, and prepares a

Animal Production Claims and
report to the certifier. If the farm is found to

"Natural" Claims: The USDA Food
meet all National Organic Program stand

Safety and Inspection Se1vice (FSIS)

ards, an organic certificate may be issued.

pem1its the use of animal production claims

The livestock product must be labeled with
and the term "natural." FSIS pe1mits the
infonnation identifying both the producer
application of "animal production claims"

and certifier ("Certified orga.nk by .. . "). The (ie, truthful statements a.bout the raising of use of the USDA organic seal on packaging
animals from which meat and poultry
is optional. Organic certification requires
products are derived) on the labeling of
annual inspections of the poultry farm.

meat and poultry products. For many yea.rs,

NUTRITION AND MANAGEMENT: POULTRY

2929

VACCINATION PROGRAM FOR DUCK BREEDERS

Age

Vaccine

Route

'fype

1 day old

Riemerella anatipestifer Aerosol

Live vaccine•

VetBooks.ir

10-14days

R anatipestifer

Drinking water

Live vaccine•

3wk

R anatipestijer

SC

Bacterinb

4wk

Duck viral hepatitis

SC

' Live vaccinec (Type 1)

4wk

Duck viral enteritis

SC

Live vaccinec

10and20wkd R anatipestifer

SC

Bacterinb

10and20wk

Duck viral hepatitis

SC

Killed virus vaccine

(Type 1)

a A live, avirulent vaccine consisting of the three major serotypes (1, 2, and 5) of R anatipestifer

"A fonnalin-inactivated cell suspension of the three major serotypes (1, 2, and 5) of R anatipestifer.

Bacterins and killed virus vaccines are administered SC in the neck.

" A modified-live virus vaccine of chick embryo origin.

d White Pekin breeder ducks normally start egg production at 24 wk of age. Egg production can be accelerated or delayed and breeder vaccination should be completed before the onset of egg production to optimize the passage of parental immunity to the progeny.

animal production claims have served as an

The term "natural" may be used when
alternative to the use of the term "organic"

products contain no artificial ingredients
on the labeling of meat and poultry products and are no more than minimally processed in the absence of a mliformly accepted
in accordance with FSIS Policy Memo 05 5.

definition. Thus, producers may wish to

This tem1 may be used in combination with
continue the use of animal production
the claim "certified organic by (a certifying
claims (eg, "Raised Without Added
entity)" when these requirements are met.

Honnones," "Free Range," "No Antibiotics The definition of "naturally raised" is being Ever," "All Vegetarian Diet") on meat and reviewed by the USDA and may result in
poultry labeling. The system FSIS has in
changes to these definitions.

place to evaluate the necessary supporting
docmnentation to ensure the accuracy of
animal production claims, such as producer
affidavits of specific raising protocols or

A nutritional deficiency may be due to a
independent third-party progran1s with
nutrient being omitted from the diet,
audits, will continue to be used whenever
adverse interaction between nutJ.ients in
these types of claims are made.

otherwise apparently well-fmtified diets, or

VACCINATION PROGRAM FOR COMMERCIAL DUCKLINGS

Age

Vaccine

Route

'fype

1 day old

Riemerella anatipestifer Aerosol

Live vaccine•

10-14days R anatipestifer

Drinking water

Live vaccinea

3wk

R anatipestifer

SC

Bacterinb

•A live, avirulent vaccine consisting of the three major serotypes (1, 2, and 5) of R anatipest�{er b A fonnalin-inactivated cell suspension of the three major serotypes (1, 2, and 5) of R anatipestifer is recommended for preventive immunization on farms where the disease is endemic or epidemic. An Eschericlvia coli bacterin can also be used where field challenge warrants. Ducklings should not be vaccinated within 21 days of slaughter.

2930

NUTRITION AND MANAGEMENT: POULTRY
the overriding effect of specific antinutriessential an"li..no acids result in retarded ents. The latter two scenarios are difficult
growtl1 or reduced egg size or egg producto diagnose, because diet analysis suggests tion. If a diet is deficient in protein or certain
a nom1al level of the nutlient(s) under
an"li..no acids, the bird may initially conswne investigation. Micronutlients such as
more feed in an attempt to resolve the

VetBooks.ir
vitan"li..ns and trace n"li..nerals are usually deficiency. After a few days, this transient
added to diets in the fom1 of stand-alone
increase in feed intake shifts to a situation
micro premixes, so it is rare to see classic
of reduced feed intake. Consequently, there
symptoms of deficiency of individual
will be infe1ior feed efficiency, and the birds
nutrients-rather, the effect seen is more
are invariably fatter as a consequence of
commonly a compilation of many individual
overconsun"li..ng energy.

metabolic conditions. In many instances, a

All conunercial breeds of poultry have
correct diagnosis can be made only by
an amazing ability to consLm1e energy Lo
obtaining complete information about diet
requirement regardless of dietary energy
and management, clinical signs in the
concentration, asswning tl1ey can physically
affected living birds, necropsies, and tiseat enough feed in extreme situations. A sue analyses. Unfo1tunately, tissue, and
deficiency of energy can therefore occur only
especially liver and serwn analysis, can be
if the diet is so low in energy concentration
misleading, because relative to the time of
tl1at the bird physically cannot eat a sufficient
initial occurrence of any deficiency, the bi.rd
quantity of feed to normalize energy intake.

often sequesters nutlients in the liver, and

With a deficiency of energy, the bird will grow
so even with deficient diets, liver assays
slowly or stop ovulating. As sources of
show erroneously high values. This latter
energy, protein and amino acids will be
effect is most significant for n"li..nerals such deaminated, and any lipids will W1dergo
as copper.

l3-0xidation. The latter condition can lead to

A diet that, by analysis, appears to
ketosis, which more commonly occurs in
contain just enough of one or more
manunals, yet the classic signs are sinillar.

nutrients may actually be deficient to some
degree in those nutrients. Stress (bacterial,

MINERAL DEFICIENCIES
parasitic, or viral infections; high or low
temperatures; etc) may either interfere
with absorption of a nutrient or increase

Calcium and Phosphorus Imbalances
the quantity required. Thus, a toxin or

A deficiency of either calciW11 or phosphomicroorganism, for example, may destroy rus in the diet of young growing birds
or render unavailable to the bi.rd a particular results in abnom1al bone development, even nutrient that is present in the diet at
when the diet contains adequate vitan"li..n D
apparently adequate levels according to

3

(seep 2937). A deficiency of either calciwn
conventional chemical or physical assay
or phosphorns results in lack of nom1al
procedures.

skeletal calcification. Rickets is seen mainly
in growing birds, whereas calcium

PROTEIN, AMINO ACID, AND
deficiency in laying hens results in reduced

ENERGY DEFICIENCIES
shell quality and subsequently osteoporosis.

This depletion of bone structure causes a

The optimal level of balanced protein intake
disorder commonly referred to as "cage
for growing chicks is -18%-23% of the diet;
layer fatigue." When calcium is mobilized
for growing poults and gallinaceous upland
from bone to overcome a dietary deficiency,
game birds, -26o/<r300/o; and for growing
the cortical bone erodes and is w1able to
ducklings and goslings, -20o/o-22%. If tl1e
support the weight of the hen.

protein and component an"li..no acid content
of the diet is below these levels, birds tend

Rickets: Rickets occms most commonly in
to grow more slowly. Even when a diet
young meat birds; the main characteristic is
contains the reconunended quantities of
inadequate bone mineralization. Calciun1
protein, optimal growth also requires
deficiency at the cellular level is the main
sufficient quantities and proper balance
cause, although feeding a diet deficient or
of all the essential an"li..no acids.

in1balanced in calciwn, phosphorus, or

Few specific signs are associated with
vitan"li..n D
a deficiency of the various an"li..no acids,

3 can also induce this problem.

Young broilers and turkey poults can exhibit
except for a peculiar, cup-shaped appearlan1eness at -10-14 days of age. Their bones ance of the feathers in chickens with
are rubbery, and the rib cage is flattened and
arginine deficiency and loss of pigment in
beaded at the attachment of the vertebrae.

some of the wing feathers in bronze turkeys

Rachitic birds exhibit a disorganized
with lysine deficiency. All deficiencies of
cartilage matrix, with an irregular vascular

NUTRITION AND MANAGEMENT: POULTRY

2931

MINIMUM SPACE REQUIREMENTS FOR WHITE LEGHORN

EGG-STRAIN BIRDS•

Age (wk)

VetBooks.ir

0-6

7-17

18onward

CAGES

Floor area per bird (sq in.)

25

45

60

Straight trough feeder space

2

2.5

3
per bird, not less than (in.)

Waterers

Birds per nipple

15

10

8

Birds per cup

25

15

12

Trough space per bird (in.)

2

LITTER AND SLATS

Floor area-litter only or combined 0.5

1-1.5
with slats (sq ft/bird)

Straight trough feeder space

2

3.5
per bird (in.)

Pans (15 in. [38 cm] diameter)

per 100 birds

Full fed

3

4

5

Restricted

5

Waterers

Birds per fount

100

50

25

Trough space per bird (in.)

2
a Requirements for White Leghorns and brown-egg layers are different.

penetration. There is an indication of
by providing adequate levels and potency
impaired metabolism of collagen precursors
of vitanun 03 supplements, and by ensuring
such as hyaluronic acid and desmosine.

that the diet is formulated to ensure optimal

Rickets is not caused by a failure in the
utilization of all fat-soluble compounds.

initiation of bone mineralization but rather by Young birds have limited ability to digest impairment of the early maturation of this
saturated fats, and these undigested
process. There is often an enlargement of the
compounds can complex with calcium to
ends of the long bones, with a widening of the
fonn insoluble soaps, leading to an induced
epiphyseal plate. A determination of whether
deficiency of calciun1. Again, this situation
rickets is due to deficiencies of calciwn,
cannot be diagnosed through diet assay for
phosphorus, or vitamin 03, or to an excess
calcium but rather through excreta assay
of calciwn ( which induces a phosphorus
of this mineral. Diets must also provide a
deficiency) may require analysis of blood
correct balance of calciwn to available
phosphorus levels and investigation of
phosphorus. For this reason, ingredients
parathyroid activity.

notoriously variable in their content of

In most field cases of rickets, a deficiency
these minerals, such as animal proteins,
of vitamin 03 is suspected. This can be due
should be used with extra caution. In recent
to sin1ple dietary deficiency, inadequate
years, the use of 25(0H)03 has become very
potency of the 03 supplement, or other
popular as a partial replacement for vitamin
factors that reduce the absorption of

03, with reports of greatly reduced
vitamin 03. Rickets can best be prevented
incidence of rickets, especially in poults.

2932

NUTRITION AND MANAGEMENT: POULTRY

SPACE REQUIREMENTS FOR MEAT-STRAIN BIRDS

Cups or Fountsb

Age

Floor Spacea

Feeder Spaceh

(per 1,000 birds)

VetBooks.ir

From day 1

Heated area 5 sq ft

10 trays/1,000 (feed

8
brooder/100 chicks
little and often)

From wk 1

1 sq ft/bird

2 in./bird

20

From wk8

2 sq ft/bird

4 in./bird

30

Mated adults All litter:

4 in./bird

30 (60 in hot weather)

3 sq ft/bird
l'2 to 2/3 slats:

21A sq ft/bird
a Welfare programs in broiler production are relatively proscriptive on space requirements and should be appropriately referenced; the below listings are general guidelines.

b For feeder and drinking trough space, both sides of the trough should be counted. Drinking trough space (all ages) isl in. (2.5 cm) per bird but doubled for adults in hot weather.

This metabolite is similar to that naturally
electrolyte, and particularly high levels of
produced in the liver of birds in the first step
chloride relative to other dietary cations,
of conversion of vitanun D3 to l,25(0H)2D3,
seem to be a major contributor in many field
the active form of the vitanun. The comoutbreaks. More tibial dyschondroplasia is mercial fonn of25(0H)D3 is therefore
also seen when the level of dietary calcium
especially useful if nonnal liver metabolism
is low relative to that of available phosis compromised in any way, such as occurs phorns, or more conunonly when diet
with mycotoxins or other "natural" toxins
phosphorus is high relative to calcium.

in the feed that potentially in1pair liver

Treatment involves dietary acljustment of
metabolism.

the calciun1:phosphorus ratio and by achieving a dietary electrolyte balance of -250

Tibial Dyschondroplasia (Osteochon
mEq/kg. Dietary changes rarely result in
drosis): Tibial dyschondroplasia is charcomplete recovery. Tibial dyschondroplasia acterized by an abnormal cartilage mass
can be prevented by tempe1ing growth
in the proximal head.of the tibiotarsus.

rate; however, programs of light or feed

It has been seen in all fast-growing types of
restriction must be considered in relation to
meat birds but is most common in broiler
economic consequences of reduced growth
chickens. Regardless of diet or enviro1m1enrate. There is evidence that replacement ta1 conditions, fast versus s[ow growth rate
of some of the dietary vitamin D3 with
seems to at least double the incidence of
metabolites such as 1,25(0H)D3 improves
tibial dyschondroplasia. Signs can occur
chondrocyte differentiation and hence
early but more usually are not initially seen
limits occurrence of this skeletal disorder.

until 14-25 days of age. Birds are reluctant
to move, and when forced to walk, do so

Cage Layer Fatigue: High-producing
with a swaying motion or stiff gait. Tibial
laying hens maintained in cages sometimes
dyschondroplasia results from disruption of
show paralysis during and just after the
the no1mal metaphyseal blood supply in the
period of peak egg production due to a
proximal tibiotarsal growth plate, where the fracture of the vertebrae that subsequently disruption in nutrient supply means the
affects the spinal cord. The fracture is
normal process of ossification does not
caused by an impaired calcimn flux related
occur. The abnormal cartilage is composed
to the high output of calcium in the eggshell.

of severely degenerated cells, with

Layers are capable of early egg production
cytoplasm and nuclei appearing shrunken.

exceeding 95% for at least 6 mo, which

Affected cartilage contains less protein and
places even more pressure on maintenance
less DNA.

of adequate calcimn flux between the diet,

The exact cause of tibial dyschondroplathe skeleton, and the oviduct. Because sia is unknown. Incidence can quickly be
rnedullary bone reserves become depleted,
altered tlu·ough genetic selection and is
the bird uses cortical bone as a source of
likely affected by a major sex-linked
calci mn for the eggshell. The condition is
recessive gene. Imbalance of dietary
rarely seen in floor-housed birds, suggesting

NUTRITION AND MANAGEMENT: POULTRY

2933
that reduced activity within the cage is a
potential causes of perosis and chonclropredisposing or associated factor. Affected dystrophy, and also the production of
birds are invariably found on their sides in
thin-shelled eggs and poor hatchability
the back of the cage. At the time of initial
in mature birds (see also CALCIUM AND
paralysis, birds appear healthy and often

PHOSPHORUS IMBALANCES, p 2930).

VetBooks.ir
have a shelled egg in the oviduct and an

The most dramatic classic effect of
active ovary. Death occurs from starvation
manganese deficiency syndrome is perosis,
or dehydration, because the birds simply
characterized by enlargement and
cannot reach feed or water.

malfonnation of the tibiometatarsaljoint,

Affected birds will recover if moved to
twisting and bending of the distal end of the
the floor. A high incidence of cage layer
tibia and the proximal end of the tarsometafatigue can be prevented by ensming the tarsus, thickening and shortening of the leg
normal weight-for-age of pullets at sexual
bones, and slippage of the gastrocnemius
maturity and by giving pullets a hightendon from its condyles. Increased intakes calcium diet (minimun1 4% calcium) for at
of calcium and/or phosphorus will
least 7 days before first oviposition. Older
aggravate the condition because of reduced
caged layers are also susceptible to bone
absorption of manganese via the action of
breakage during removal from the cage and
precipitated calciun1 phosphate in the
transport to processing. It is not known
intestinal tract. In laying hens, reduced egg
whether cage layer fatigue and bone
production, markedly reduced hatchability,
breakage are related. However, bone
and eggshell thinning are often noted.

strength cannot practically be improved

A manganese-deficient breeder diet can
without adverse consequences to other
result in chondrodystrophy in chick embryos.

economically important traits such as

This condition is characte1ized by shortened,
eggshell quality. Cage layer fatigue is
thickened legs and shortened wings. Other
undoubtedly related to high, sustained egg
signs can include a parrot beak brought about
output and associated clutch lengths of
by a disproportionate shortening of the lower

200-230 eggs laid on successive days.

mandible, globular contour of the head due to

Diets must provide adequate quantities of
anterior bulging of the skull, edema occurring
calcim11 and phosphorus to prevent deficien just above the atlas joint of the neck and cies. However, feeding diets that contain
extending posteriorly, and protruding of thP

>2.5% calcium dUiing the immature growing
abdomen due to unassinlilated yolk. Growth
period ( <16 wk) produces a high incidence
is also reduced, and development of down
of nephritis, visceral gout, calcimn urate
and feathers is retarded. A manganese-defideposits in the ureters, and sometimes high cient chick has a characteristic star-gazing
mortality, especially in the presence of infecposture, because the physiology of tl1e inner tious bronchitis virus. Eggshell strength and
ear becomes defective.

bone strength can both be improved by feed

Defonnities cannot be correctect'by
ing -500/o of the dietary calcium supplement
feeding more manganese. Effects of
in the fom1 of coarse limestone, with the
manganese deficiency on egg production
remaining half as fine particle limestone.

are fully corrected by feeding a diet that

Offe1ing the coarse supplement pennits the
contains at least 30-40 mg of manganese/kg,
birds to satisfy their requirements when
provided the diet does not contain excess
they need it most, allowing the coarse
calciun1 and/or phosphorus. There is an
material to be retained in the gizzard where
indication of the need for Fe2+ ions as well
the calcium can be absorbed continually
as manganese to correct the deficiency,
and especially at night-time when the bird is
although most conunercial poultry diets
not feeding. A reacWy available calcium and/
contain a smfeit of iron.

or calciw11 phosphate supplement is often
effective if started very soon after paralysis

Iron and Copper Deficiencies
is first observed. Although these supplements may be advantageous to afflicted Deficiencies of both iron and copper can
layers, they are not ideal for the regular
lead to anemia. Iron deficiency causes a
birds in the flock; therefore, decisions
severe anemia with a reduction in PCV. In
regarding treatment are often influenced
colo1�feathered strains, there is also loss of
by the seve1ity of the condition and the
pigmentation in the feathers. The birds'

proportion of the flock affected.

requirements for RBC synthesis take
precedence over metabolism of feather

Manganese Deficiency
pigments, although if a fortified diet is
introduced, all subsequent feather growth

A deficiency of manganese in the diet of
is nonnal and lines of demarcation on the
inm1ature chickens and turkeys is one of the feathers are part of diagnosis. Iron may

2934

NUTRITION AND MANAGEMENT: POULTRY
be needed not only for the red feather
of abnormally long, lacy feathers. Adminispigments, which are known to contain iron, tration of thyroxine or iodinated casein
but also to function in an enzyme system
reverses the effects on egg production, with
involved in the pigmentation process.

eggshell quality returning to normal. The

Ochratoxin at 4----8 mcg/g diet also causes an
iodine content of an egg is markedly

VetBooks.ir
iron deficiency characterized by hypochroinfluenced by the hen's intake of iodine.

mic microcytic anemia. Aflatoxin also

Eggs from a breeder fed an iodine-deficient
reduces iron absorption.

diet will exhibit reduced hatchability and

Young chicks become lan1e within 2-4 wk
delayed yolk sac absorption. Rapeseed meal
when fed a coppe1°deficient diet. Bones are
and, to a lesser extent, canola meal contain
fragile and easily broken, the epiphyseal
goitrogens that cause thyroid enlargement
cartilage becomes thickened, and vascular
in young birds. Iodine deficiency in poultry
penetration of the thickened cartilage is
can be avoided by supplementing the feed
markedly reduced. These bone lesions
with as little as 0.5 mg of iodine/kg, although
resemble the changes noted in birds with a
a level of 2-3 mg/kg is more conunonly
vitamin A deficiency. Copper is required for
provided to sustain good feathering in
cartilage fom1ation, and certain antinutrifast-growing birds.

ents such as some grain funligants have
been shown to impact skeletal develop

Magnesium Deficiency
ment, likely via interaction with copper
metabolism. Copper-deficient chickens may

Natural feed ingredients are rich in
also display ataxia and spastic paralysis.

magnesiun1; thus, deficiency is rare and

Copper deficiency in birds, and especially
magnesium is never specifically used as a
in turkeys, can lead to rupture of the aorta.

supplement to poultry diets. Newly hatched

The biochemical lesion in the copperchicks fed a diet totally devoid of magnesium deficient aorta is likely related to failure to
live only a few days. They grow slowly, are
synthesize desmosine, the cross-link prelethargic, and often pant and gasp. When cursor of elastin. The lysine content of
disturbed, they exhibit brief convulsions and
copper-deficient elastin is three times that
become comatose, which is sometimes
seen in control birds, suggesting failure to
temporary but often fatal. Mortality is quite
incorporate lysine into the desmosine
high on diets only marginally deficient in
molecule. In field cases of naturally
magnesium, even though growth of survivors
occurring aortic rupture, many birds have
may approach that of control birds.

<10 ppm copper in the liver, compared with

A magnesiun1 deficiency in laying hens

15---30 ppm nonnally seen in birds of
results in a rapid decline in egg production,
comparable age. High levels of sulfate ions,
hypomagnesemia, and a marked withdrawal
molybdenum, and also ascorbic acid can
of magnesium from bones. Egg size, shell
reduce liver copper levels. A high incidence
weight, and the magnesium content of yolk
of aortic rupture has been seen in turkeys
and shell are decreased. Increasing the
fed 4-nitrophenylarsonic acid. The problem
dietaiy calciun1 of laying hens accentuates
can be resolved by feeding higher levels of
these effects. Magnesium seems to play a
copper, suggesting that products such as·
central role in eggshell formation, although

4-nitro may physically complex with copper. it is not clear whether there is a structural need or whether magnesium sin1ply gets

Iodine Deficiency
deposited as a cofactor along with calcium.

Magnesium requirements for most

Iodine deficiency results in a decreased
classes of chickens seem to be -500-600
output of thyroxine from the thyroid gland,
ppm, a level that is usually achieved with
which in turn stimulates the anterior
contributions by natural feed ingredients.

pituitary to produce and release increased
amounts of thyroid stimulating honnone

(TSH). This increased production ofTSH

Potassium, Sodium, and Chloride
results in subsequent enlargement of the

Deficiencies
thyroid gland, usually termed goiter. The

Although requirements for potassiwn,
enlarged gland results from hypertrophy
sodium, and chloride have been clearly
and hyperplasia of the thyroid follicles,
defined, it is also in1portallt to maintain a
which increases the secretory surface of
balance of these and all other electrolytes in
the follicles.

the body. Often termed electrolyte balance

Lack of thyroid activity or inhibition of
or acid-base balance, the effects of
the thyroid by administration of thiouracil
deficiency of any one element are often a
or thiow·ea causes hens to cease laying and
consequence of alteration to this importallt
become obese. It also results in the growth
balance as it affects osmoregulation.

NUTRITION AND MANAGEMENT: POULTRY

2935

Simple Deficiency: A deficiency of
overall balance that is in1portant. Electrochloride causes ataxia with classic signs of lyte balance, also referred to as acid-base
nervousness, often induced by sudden noise balance, is affected by three factors: the or fright. The main sign of hypokalemia is an balance and proportion of these electrolytes overall muscle weakness characterized by
in the diet, endogenous acid production,

VetBooks.ir
weak extremities, poor intestinal tone with
and the rate of renal clearance.

intestinal distention, cardiac weakness, and

In most situations, the body maintains a
weakness and ultimately failure of the
normal balance between cations and anions
respiratory muscles. Hypokalemia is apt to
in the body such that physiologic pH is
occur during severe stress. Plasma protein
maintained. If there is a shift toward acid or
is increased, causing the kidney, under the
base conditions, metabolic processes return
influence of adrenocortical hormone, to
the body to a norn1al pH. Actual electrolyte
discharge potassium into the urine. During
imbalances are rare, because regulatory
adaptation to the stress, blood flow to the
mechanisms must sustain optimal cellular
muscle gradually improves and the muscle
pH and osmolarity. Electrolyte balance can
begins uptake of potassiun1. As liver
therefore more correctly be described as
glycogen is restored, potassium returns
the changes that necessarily occur in the
to the liver.

body processes to achieve norn1al pH. In

Birds fed a diet low in both protein and
extreme situations, such modifications in
potassium or that are starving grow slowly
regulatory mechanisms seem to adversely
but do not show a potassium deficiency.

affect other physiologic systems, and they

Potassium derived from catabolized tissue
produce or accentuate potentially
protein replaces that lost in the urine. The
debilitating conditions.

ratio of potassiun1 to nitrogen in wine is

Electrolyte imbalance causes a number of
relatively constant and is the same as that
metabolic disorders in birds, most notably
found in muscle. Thus, tissue nitrogen and
tibial dyschondroplasia and respiratory
potassium are released together from the
alkalosis in layers. Tibial dyschondroplasia
catabolized tissue.

in young broiler chickens can be affected by

A deficiency of sodiun1 leads to a
the electrolyte balance of the diet. The
lowering of osmotic pressure and a change
unusual development of the cartilage plug at
in acid-base balance in the body. Cardiac
the growth plate of the tibia can be induced
output and blood pressure both decrease,
by a number of factors, although its

PCV increases, elasticity of subcutaneous
incidence can be greatly increased by
tissues decreases, and adrenal fwlction is
metabolic acidosis induced by feeding
impaired. This leads to an increase in blood
products such as NH4Cl. Tibial dyschondrouric acid levels, which can result in shock plasia seems to occur more frequently when
and death. A less severe sodium deficiency
the diet contains an excess of sodium
in chicks can result in retarded growth, soft
relative to potassiun1, along with very high
bones, corneal keratinization, impaired
chloride levels. The latter situation is most
food utilization, and a decrease in plasma
easily remedied by substitution of sodium
volume. In layers, reduced egg production,
bicarbonate for sodium chloride in the diet.

poor growth, and carmibalism may be

Overall electrolyte balance is always
noted. A nun1ber of diseases can result in
important but is most critical when chloride
sodium depletion from the body, such as GI
or sulfur levels are high. With low dietary
losses from diarrhea or urinary losses due
chloride levels, there is often little response
to renal or adrenal damage.

to the manipulation of electrolyte balance;
however, when dietary chloride levels are
high, it is critical to make acljustments to the

Electrolyte Imbalance: Electrolyte
dietary cations to maintain overall balance.

balance is commonly described by the

Alternatively, chloride levels can be reduced,
simple forn1ula of Na+ K- Cl expressed as
altl10ugh chickens have requirements of
mEqlkg of diet. An overall dietary balance

-0.12%-0.15% of tlle diet, and deficiency
of 250-300 mEq/kg is generally considered
signs will develop with dietary levels <0.12%.

optimal for normal physiologic function.

Sodium content of drinking water can have a

The buffering systems in the body ensure
meaningful impact on total sodium intake of
the maintenance of near norn1al physiologic
the bird. When drinking water contains >300
pH, preventing electrolyte in1balance. The
ppm of sodiun1, it may be necessary to
primary role of electrolytes is in maintereduce sodium levels in tile diet. A recent nance of body water and ionic balance.

innovation in poultry nutrition that impacts

Thus, requirements for elements such as
electrolyte balance is the use of phytase
sodium, potassium, and chloride carmot be
enzyme. This commonly used exogenous
considered individually, because it is the
enzyme supplement is intended to reduce

2936

NUTRITION AND MANAGEMENT: POULTRY
dependence on supplemental phosphorus,

Chicks hatched from zinc-deficient hens ai·e
but it has been shown to concomitantly
weak and caimot stand, eat, or d1ink. They
reduce renal excretion of sodium. Diets
have accelerated respiratory rates and
tl1erefore need less supplemental sodium
labored breatlling. If tl1e chicks are

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when tl1ey contain phytase enzyme.

clisturbed, tl1e signs are aggravated and tl1e
chicks often die. Retarded featl1ering and

Selenium Deficiency
frizzled featl1ers are also fotmd. However,

A deficiency of seleniwn in growing
tl1e major defect is grossly impaired skeletal
chickens causes exuclative diathesis. Early
development. Zinc-deficient embryos show
signs of w1thriftiness and ruffled featl1ers
micromelia, curvature of tl1e spine, and
usually occur at 3-6 wk of age, depending
shortened, fused tl1oracic and lwnbai·
on tl1e degree of deficiency. The edema
vertebrae. Toes often are missing and, in
results in weeping of the skin, which is often extreme cases, tl1e embryos have no lower seen on tl1e inner surface of tl1e thighs and
skeleton or limbs. Some embryos ai·e
wings. The birds bruise easily, and large
run1pless, and occasionally the eyes are
scabs often form on old bruises. In laying
absent or not developed.

hens, such tissue damage is unusual, but
egg production, hatchability, and feed

VITAMIN DEFICIENCIES
conversion a.re adversely affected.

The metabolism of seleniun1 is closely

Vitan1in deficiencies are most commonly
linked to tl1at of vitan1in E, and signs of
due to inadvertent omission of a complete
deficiency can sometimes be treated witl1
vitantin premix from tl1e birds' diet. Multiple
eitl1er tl1e mineral or the vitan1irl. Vitamin E
signs ai·e tl1erefore seen, although in
can spare seleniun1 in its role as an
general, signs of B vitamin deficiencies
antioxidant, and so some seleniumappear fu-st. Because there are some stores responsive conditions can also be treated by of fat-soluble vitanlins in tl1e body, it often supplemental vitamin E. In most countries,
takes longer for tl1ese deficiencies to affect
there a.re limits to tl1e quantity of selenium
tl1e bird, and it may take montl1s for
tl1a.t can be added to a diet; the upper limit is vitamin A deficiency to affect adult birds.

usually 0.3 ppm.

Treatment and prevention rely on an

The commonly used forms a.re sodium
adequate dietary supply, usually microenselenite and, more recently, organic capsulated in gelatin or starch along with an
selenium chelates. Feeds grown on
antioxidant. Vitatnin destruction in feeds is
high-selenium soils a.re sometimes
a factor of time, temperature, and hwnidity.

necessaiily used in poultry rations and are

For most feeds, efficacy ofvitanlins is little
good sources of seleniun1. Fish meal and
affected over 2-mo storage witl1irl mixed
dried brewer's yeast are also rich in
feed.

available selenium.

Vitamin A Deficiency

Zinc Deficiency

Dependirlg on liver stores, adult birds could

Zinc requirements and signs of deficiency
be feel a vitatnin A-deficient diet for 2-5 mo
ai·e influenced by dietary ingredients. In
before signs of deficiency develop.

semipurified diets, it is difficult to show a

Eventually, birds become emaciated and
response to zinc levels much above 25-30
weak with ruffled featl1ers. Egg production
mg/kg diet, whereas in practical comdrops markedly, hatchability decreases, and soybean meal cliets, requirement values ai·e
embryonic mo1tality increases. As egg
increased to 60-80 mg/kg. Such vaiia.ble
production declines, tl1ere will likely be only
zinc needs likely relate to phytic acid
small follicles in tl1e ovary, some of wltich
content of the diet, because tl1is ligai1cl is a
show signs of hemorrhage. A watery
potent zinc chelator. lf phytase enzyme is
discharge from tl1e eyes may also be noted.

used in diets, the need for supplemental

As tl1e deficiency continues, milky white,
zinc is reduced by up to 10 mg/kg diet.

cheesy material accumulates in tl1e eyes,

In young chicks, signs of zinc deficiency
making it impossible for birds to see
include retarded growtl1, sho1tening and

(xerophtl1almia). The eye, in mai1y cases,
tl1ickening of leg bones and enlargement of
may be destroyed.

tl1e hock joint, scalirlg of tl1e skin ( especially

The first lesion usually noted in adult
on tl1e feet), very poor fea.tl1e1ing, loss of
birds is in tl1e mucous glands of the upper
appetite, and in severe cases, m01tality.

alimentary tract. The normal epithelium

Although zinc deficiency can reduce egg
is replaced by a stratified squan1ous,
production in aging hens, the most st1iking
keratinized layer. This blocks tl1e ducts of
effects ai·e seen in developing embryos.

the mucous glands, resulting in necrotic

NUTRITION AND MANAGEMENT: POULTRY

2937
secretions. Small, white pustules may
treatment usually results in faster recovery
be found in the nasal passages, mouth,
than supplemtation via the feed.

esophagus, and pharynx, and these may
extend into the crop. Breakdown of the

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mucous membrane usually allows

Vitamin 03 Deficiency
pathogenic microorganisms to invade these

Vitamin D3 is required for the nom1al
tissues and cause secondary infections.

absorption and metabolism of calcium and

Depending on the quantity of vitamin A
phosphorus. A deficiency can result in
passed on from the breeder hen, day-old
rickets in ypung growing chickens or in
chicks reared on a vitamin A-deficient diet
osteoporosis and/or poor eggshell quality
may show signs within 7 days. However,
in laying hens, even though the diet may be
chicks with a good reserve of maternal
well supplied with calcium and phosphorus.

vitamin A may not show signs of a

Abnonnal skeletal development is
deficiency for up to 7 wk. Gross signs in
discussed under calciwn and phosphorus
chicks include anorexia, growth retardaimbalances (seep 2930) and manganese tion, drowsiness, weakness, incoordination,
deficiency (seep 2933).

emaciation, and ruffled feathers. If the

Laying hens fed a vitamin Drdeficient diet
deficiency is severe, the chicks may become
show loss of egg production within 2-3 wk,
ataxic, which is also seen with vitamin E
and depending on the degree of deficiency,
deficiency (see below). The yellow pigment
shell quality deteriorates almost instantly.

in the shanks and beaks is usually Jost, and

Using a com-soybean meal diet with no
the comb and wattles are pale. A cheesy
supplemental vitruni.n D3, shell weight
material may be noted in the eyes, but
decreases dramatically by -150 mg/day
xerophthalmia is seldom seen because
throughout tl1e first 7 days of deficiency.

chicks usually die before the eyes become

The less obvious decline in shell quality with
affected. Secondary infection may play a
suboptimal, rather than deficient, supplerole in many of the deaths noted with acute ments is more difficult to diagnose, especially
vitamin A deficiency.

because it is very difficult to assay vitru11in D3

Yow1g chicks with chronic vitamin A
in complete feeds.

deficiency may also develop pustules in the

There is a significant increase in plasma
mucous membrane of the esophagus that
l,25(0H)2D3 of birds producing good
usually affect the respiratory tract. Kidneys
versus poor eggshells. Feeding purified
may be pale and the tubules distended
l ,25(0H)2D3 in1proves the shell quality of
because of wic acid deposits, and in
these inferior layers, suggesting a potential
extreme cases, the ureters may be plugged
inherent problem with metabolism of
with urates. Blood levels of wic acid can
cholecalciferol.

rise from a nom1al level of -5 mg to as high

Retarded growth and severe leg
as 40 mg/100 mL. Vitamin A deficiency does
weakness are the first signs noted when
not inte1fere with uric acid metabolism but
chicks are deficient in vitru11in D3. Beaks and
does prevent nom1al excretion ofwic acid
claws become soft and pliable. Chicks may
from the kidney. Histologic findings include
have trouble walking and will take a few
atrophy of the cytoplasm and a Joss of the
steps before squatting on their hocks. While
cilia in the columnar, ciliated epitheliun1.

resting, they often sway from side to side,

Although vitanlin A-deficient chicks can
suggesting loss of equilibrium. Feathering is
be ataxic, similar to those with vitamin E
usually poor, and an abnom1al banding of
deficiency, no gross lesions are found in the
feathers may be seen in colored breeds.

brain of vitru11in A-deficient chicks as com

With cluonic vitamin D3 deficiency, marked
pared with degeneration of the Purki.nje cells skeletal disorders are noted. The spinal in the cerebellum of vitru11in E-cleficient
column may bend downward and the
chicks (see below). The livers of ataxic
stemwn may deviate to one side. These
vitamin A-deficient chicks contain little
structural changes reduce tl1e size of the
or no vitamin A.

thorax, with subsequent crowding of the

Because stabilized vitanlin A suppleinternal organs, especially the air sacs. A ments are almost wliversally used in poultry characteristic finding in chicks is a beading diets, it is unlikely that a deficiency will be
of the ribs at the junction of the spinal
encountered. However, if a deficiency does
column along with a downward and
develop because of either inadvertent
posterior bending. Poor calcification can
omission of the vitanlin A supplement or
also be seen at tl1e epiphysis of tl1e tibia and
inadequate feed preparation, up to 2 times
femur. By inunersing the split bone in a
the nom1ally recommended level, should be
silver nitrate solution and allowing it to
fed for -2 wk. Vitamin A can be adminisstand under incandescent light for a few tered through the drinking water, and such
minutes, the calcified areas are easily

2938

NUTRITION AND MANAGEMENT: POULTRY
distinguished from the areas of caiti]age.

disappearance of the Purkinje cells and

Adding synthetic l ,25(0H)2D3 to the diet of
separation of the granular layers of the
susceptible chicks reduces the incidence
cerebellar folia. Because of its inherently
of this condition. Although respon1e is
low level of vitamin E, the cerebellwn is

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variable, results suggest that some leg
particularly susceptible to lipid peroxidaabnormalities may be a consequence of tion. In prevention of encephalomalacia,
inefficient metabolism of cholecal�iferol.

vitainin E functions as a biologic antioxi

In laying hens, signs of gross pathology
dant. The quantitative need for vitai1lin E
are usually confined to the bones atid
for this function depends on the amount
parathyroid glands. Bones are soft and
of linoleic acid and polyunsaturated fatty
easily broken, and the ribs may be�ome
acids in the diet. Over prolonged periods,
beaded. The ribs may also show spontaneantioxidants have been shown to prevent ous fractures in the sternovertebrai region.

encephalomalacia in chicks when added to

Histologic examination shows decteased
diets with very low levels of vitai11in E or in
calcification in the long bones, with excess
chicks fed vitai11in E-depleted purified
of osteoid tissue and parathyroid eh}argediets. Chicks hatched from breeders that ment.

are given additional dietaiy vitainin E seem

Dry, stabilized forms ofvitanlin l)

less susceptible to lipid peroxidation in the

3 are
recommended to treat deficiencies. In cases brain. The fact that antioxidants can help of severe mycotoxicosis, a wateHl1iscible
prevent encephalomalacia, but fail to
forn1 of vitanlin D3 is administered ln the
prevent exudative diathesis or muscular
drinking water to provide the a.mOllnt
dystrophy in chicks, strongly suggests that
nom1ally supplied in the diet. In ca�es of
vitainin E is acting as an antioxidant in this
in1paired liver function, metabolites of
situation. Exudative diathesis results in a
vitai11in D are the usual choice for treatsevere edema caused by a marked increase ment.

in capillary pern1eability. Electrophoretic
patterns of the blood show a decrease in

Vitamin E Deficiency
albunlin levels, whereas exudative fluids
contained a protein pattern sinillar to that

The three main disorders seen in clucks
of normal blood plasma.

deficient in vitainin E are encephalomala

Vitanlin E deficiency accompanied by
cia, exudative diathesis, and mUSCl\lar
sulfur an1ino acid deficiency results in
dystrophy. The occurrence of thes�
severe muscular dystrophy in chicks by
conditions depends on various oth�r dietary -4 wk of age. This condition is characterand envirorm1ental factors.

ized by degeneration of the muscle fibers,

Encephalomalacia is seen in conunercial
usually in the breast but sometimes also in
flocks if diets are very low in vitanl.in E, if
the leg muscles. Histologic examination
an antioxidant is either onl.itted or is not
shows Zenker's degeneration, with
present in sufficient quantities, or it the diet
perivascular infiltration and marked
contains a reasonably high level of an
accun1u.lation of infiltrated eosinophils,
unstable and unsaturated fat..For exudative
lymphocytes, and histocytes. Accwnuladiathesis to occur, the diet must be deficient tion of these cells in dystrophic tissue
in both vitai11in E and seleniun1. Signs of
results in an increase in lysosomal
muscular dystrophy are rare in chi<::ks,
enzymes, which appear to function in the
because the cliet must be deficient in both
breakdown and removal of the products of
sulfur anl.ino acids and vitanlin E. Because
dystrophic degeneration. Initial studies
the sulfur amino acids are necessary for
involving the effects of dietary vitamin
growth, a deficiency severe enough to

E on muscular dystrophy show that the
induce muscular dystrophy is unlikely to
addition of selenium at 1-5 mg/kg diet
occur under commercial condition:;;. Signs
reduced the incidence of muscular
of exudative diathesis and muscular
dystrophy in chicks receiving a vitamin
dystrophy can be reversed in chick:;; by

E-deficient diet that was also low in
supplementing the diet with liberal amounts
methionine and cysteine, but did not
of vitainin E, asswning the deficiency is not
completely prevent the disease. However,
too advanced. Encephalomalacia rt\ay
seleniun1 was completely effective in
respond to vitanlin E supplementation,
preventing muscular dystrophy in chicks
depending on the extent of the damage to
when the diet contained a low level of
the cerebellum.

vitanlin E, which alone had been shown to

The classic sign of encephaloma.lacia is
have no effect on the disease. Throughout
ataxia. The results from hemorrhage and
the past few years, the incidence of
edema within the granular layers ot the

"muscular dystrophy-type" lesions in the
cerebellum, with pyknosis and eve ritual
breast muscle of older (>35 day) broilers

NUTRITION AND MANAGEMENT: POULTRY

2939
has increased. Characteristic parallel
intestine. Chicks are anemic, which may
white striations on the muscle are similar
be due in part to loss of blood but also to
to those seen in chicks with muscular
development of hypoplastic bone marrow.

dystrophy, yet on analysis the diet of these

Although blood-clotting time is a reasonable
birds seems adequate in vitamin E as well
measure of the degree of vitanlin K

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as selenium.

deficiency, a more accurate measure is

Studies with chicks on the interrelationobtained by determining the prothrombin ships between antioxidants, linoleic acid,
time. Prothrnmbin tin1es in severely
selenium, and sulfur amino acids have
deficient chicks may be extended from a
shown that selenium and vitan1in E play
normal o.li.17-20 sec to 5-6 nun or longer.

supportive roles in several processes, one of No major heart lesions are seen in vitanlin which involves cysteine metabolism and its

K-deficient chicks such as those that occur
role in prevention of muscular dystrophy in
in pigs.

chickens. Glutathione peroxidase is soluble

A vitanlin K deficiency in poultry may be
and located in the aqueous portions of the
related to low dietary levels of the vitanlin,
cell, whereas vitanlin Eis located mainly in
low levels in the maternal diet, lack of
the hydrophobic environments of memintestinal synthesis, extent of coprophagy, branes and in adipose tissue and other lipid
or the presence of sulfur drugs and other
storage cells. The overlapping marU1er in
feed additives in the diet. Chicks with
which vitamin E and seleniw11 function in
coccidiosis can have severe damage to their
the cellular antioxidant system suggest that
intestinal wall and can bleed excessively.

they spare one another in prevention of

Antinli.crobial agents can suppress
deficiency signs.

intestinal synthesis of vitan1in K, rendering

Only stabilized fat should be used in
the bird completely dependent on the diet
feeds. Adequate levels of stabilized vitamin
for its supply of the vitanlin. Synthesis of

E should be used in conjunction with a
vitanlin K does occur in the bacteria
commercial antioxidant and at least 0.3 ppm resident in the bird's digestive tract; seleniwn. Signs of exudative diathesis and
however, such vitanlin K remains inside the
muscular dystrophy due to vitamin
bacterial cell, so the only benefit to the bi.rd

E deficiency can be reversed if treatment
arises from the bacterial cell digestion or via
is begtm early by administering vitamin E
coprophagy.

through the feed or drinking water. Oral

The inclusion of menadione at 1--4 mg/ton
administration of a single dose of
of feed is an effective and conunon practice
vitan1in E (300 IU per bi.rd) usually causes
to prevent vitamin K deficiency. If signs of
remission.

deficiency are seen, the level should be
doubled. A nwnber of stress factors ( eg,
coccidiosis and other intestinal parasitic

Vitamin K Deficiency
diseases) increase the requirements fcir

Impairment of blood coagulation is the
vitanlin K. Dicwnarol, sulfaquinoxaline, and
major clinical sign of vitanlin K deficiency.

warfatin are antimetabolites of vitanlin K.

With a severe deficiency, subcutaneous and
internal hemorrhages can prove fatal.

Vitamin K deficiency results in a reduction

Vitamin 812 Deficiency
in prothrombin content of the blood, and in

Vita.nun 812 is an essential part of several
the young chick, plasma levels are as low as
enzyn1e systems, with most reactions

2% of normal. Because the prothrombin
involving the transfer or synthesis of methyl
content of newly hatched chicks is only
groups. Although the most important

-400Ai that of adult birds, young chicks are
function ofvitanlin 812 is in the metabolism of
readily affected by a vitanlin K-deficient
nucleic acids and proteins, it also functions in
diet. A carryover of vitanli.n K from Lhe hen
carbohydrate and fat metabolism.

to eggs, and subsequently to hatched chicks,
ln growing chickens, a deficiency of
has been demonstrated, so breeder diets
vitanli.n 812 results in reduced weight gain
should be well f01tified. Hemorrhagic
and feed intake, along with poor feathering
syndrome in day-old chicks has been
and nervous disorders. Although deficiency
attributed to a deficiency of vitamin K in the
may lead to perosis, this is probably a
diet of tl1e breeder hens. Gross deficiency of
secondary effect due to a dietary deficiency
vitanlin K results in such prolonged blood
of methionine or choline as sources of
clotting that severely deficient chicks may
methyl groups. Vitanlin 812 may alleviate
bleed to death from a slight bruise or other
perosis because of its effect on the synthesis
injury. Borderline deficiencies often cause
of methyl groups. Other signs reported in
small hemorrhagic blenli.shes. Hemorrhages
poultry are anenli.a, gizzard erosion, and
may appear on the breast, legs, wings, in the
fatty infiltration of the heart, liver, and
abdonlinal cavity, and on the swface of the
kidneys. Laying hens initially appear to be

2940

NUTRITION AND MANAGEMENT: POULTRY
able to maintain body weight and egg

Niacin (Nicotinic Acid) Deficiency
production; however, egg size is reduced.

In breeders, hatchability can be markedly

There is considerable evidence that poultry
reduced, although several weeks may be
and even chick and turkey embryos, can '

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needed for signs of deficiency to appear.

synthesize niacin but at a rate too slow for

Changes noted in embryos from 8
optimal growth. It has been claimed that a

1,deficient breeders include a general
marked deficiency of niacin cannot occur
hemorrhagic condition, fatty liver, fewer
in chickens unless there is a concomitant
myelinated fibers in the spinal cord and
deficiency of the amino acid tryptophan,
high incidence of mid-te1m embryo' deaths.

which 1s a niacin precursor.

Deficiency of vitamin 8

Niacin deficiency is characterized by

12 is highly
unlikely, especially for birds grown on litter
severe disorders in the skin and digestive
or where animal-based ingredients are used.

organs. TI1e first signs are usually loss of

Treatment involves feeding up to 20 mcg/g
appetite, retarded growth, general weakness,
feed for 1-2 wk.

and diarrhea. Deficiency produces enlargement of the tibiotarsaljoint, valgus-varus bowmg of the legs, poor feathe1ing, and

Choline Deficiency
dem1atitis on the head and feel

In addition to poor growth, the classic sign

Niacin deficiency in chicks can also result
of choline deficiency in chicks and poults is
in "black tongue." At -2 wk of age, the
perosis. Perosis is first characterized by
tongue, oral cavity, and esophagus become
pmpomt hemorrhages and a slight puffiness
distinctly inflamed. In the niacin-deficient
about the hock joint, followed by an
hen, weight loss, reduced egg production,
apparent flattening of the tibiometatarsal
and a marked decrease in hatchability can
joint caused by a rotation of the metatarsus.

result. Turkeys, ducks, pheasants, and

The metatarsus continues to twist and may
goslings are much more severely affected by
become bent or bowed so that it is out of
ruacm deficiency than are chickens. Their
alignment with the tibia. When this
apparently higher requirements are likely
condition exists, the leg cannot adequately
related to their less efficient conversion of
support the weight of the bird. The articular
tryptophan to niacin. Ducks and turkeys
cartilage is displaced, and the Achilles
with a niacin deficiency show a severe
tendon slips from its condyles. Perosis is
bowing of the legs and an enlargement of
n�t a specific deficiency sign; it appears
the hock joint. The main difference between
with several nutrient deficiencies.

tl1e leg seen in niacin deficiency and perosis

Although choline deficiency readily develas seen in manganese and choline ops in chicks fed diets low in choline a
deficiency is that with niacin deficiency
deficiency in laying hens is not easily'

tl1e Achilles tendon seldom slips from its
produced. Eggs contain -12-13 mg of
conclyles.

choline/g of dried whole egg. A large egg

Niacin deficiency in chickens may be
contams -170 mg of choline, found almost
prevented by feeding a diet that contains
entirely in the phospholipids. Tl\.us, there
niacin at 2:30 mg/kg; however, many
appears to be a considerable need for
nutlitionists recommend 2-2.5 times as
choline
much. An allowance of 55-70 mg/kg of feed

. to produce an egg. In spite of this,
producmg a marked choline deficiency in
appears to be satisfactory for clucks e1eese

0
laying hens has been difficult, even when
and turkeys. Ample niacin should b�
highly purified diets essentially devoid of
provided in poultiy diets so as to spare
choline are provided for a prolonged period.

the utilization of tiyptophan.

Under these conditions, the choline content
of eggs is not reduced, suggesting possible

Pantothenic Acid Deficiency
intestinal synthesis by the bird.

Pant?thenic acid is the prosthetic group

Diets that contain appreciable quantities
within co
of soybean meal, wheat bran, and wheat

.enzyme A, an important coenzyme
mvolved m many reversible acetylation
shorts are unlikely to be deficient in choline. reactions in carbohydrate, fat, and amino Soybean meal is a good source of choline
acid metabolism. Signs of deficiency
and wheat byproducts are good sources �f
therefore relate to general avian metabolism.

betaine, which can perform the methyl

The major lesions of pantothenic acid
donor function of choline. Other good
deficiency involve the nervous system, the
sources of. choline are distiller's grains,
adrenal cortex, and the skin. Deficiency may
fishmeal, liver meal, meat meals, distiller's
result m reduced egg production; however,
solubles, and yeast. A number of commera marked drop in hatchability is usually cial choline supplements are available and
noted before this event. Embryos from hens
supplemental choline is routinely used in
with pantothenic acid deficiency can have
most poultry feeds.

subcutaneous hemorrhages and severe

NUTRITION AND MANAGEMENT: POULTRY

2941
edema, with most mortality showing up
then frequently walk on their hocks with
during the later part of the incubation
the aid of their wings. The leg muscles are
period. In chicks, the first signs are reduced
atrophjed and flabby, and the skin is dry and
growth and feed conswnption, poor
harsh. In advanced stages of deficiency, the

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feathering with feathers becoming ruffled
chicks lie prostrate with tl1eir legs extended,
and brittle, and a rapidly developing
sometimes in opposite directions. The chardermatitis. The comers of the beak and the acteristic sign of riboflavin deficiency is a
area below the beak are usually the worst
marked enlargement of the sciatic and
affected regions for dermatitis, but the
brachia! nerve sheaths; sciatic nerves
condition is also noted on the feet. In severe
usually show the most pronounced effects.

cases, the skin of the feet may cornify, and

Histologic examination of the affected
wart-like lumps occur on the balls of the
nerves shows degenerative changes in the
feet. The foot problem often leads to
myelin sheaths that, when severe, pinch the
bacte1ial infection.

nerve. Thjs produces a permanent stimulus,

Liver concentration of pantothenic acid is which causes the curled-toe paralysis.

reduced during a deficiency, with the liver

Signs of riboflavin deficiency in hens are
becoming atrophied, with a faint dirty
decreased egg production, increased
yellow color developing. Nerve fibers of the
embryonic mortality, and an increase in size
spinal cord may show myelin degeneration.

and fat content of the liver. Hatchability

Pantothenic acid-<leficient chicks show
declines within 2 wk when hens are fed a
lymphoid cell necrosis in the bursa of

1iboflavin-cleficient diet but returns to near

Fabricius and thymus, together with
nonnal when riboflavin is restored. Affected
lyrnphocytic paucity in the spleen. The foot
embryos are dwarfed and show characte1iscondition in chicks and the poor feathering tically defective "clubbed" clown. The
are difficult to differentiate from signs of a
nervous system of these embryos shows
biotin deficiency. In a pantothenic acid
degenerative changes much like tl1ose
deficiency, dermatitis of the feet is usually
described in riboflavin-deficient chicks.

noted first on the toes; in contrast, a biotin

Clubbed down is periodically seen in cases
deficiency primarily affects the foot pads
of poor hatchability, when the "reject"

and is usually more severe. Ducks do not
chicks or dead embryos show this
show the usual signs noted for chickens and
condition, even though the breeder diet is
turkeys, except for retarded growth, but
apparently adequate in riboflavin. Anecdomortality can be qujte high.

tal evidence suggests greater occurrence of

Most poultry diets contain supplements
this clubbed-dow11 condition in fanns that
of calciwn pantothenate. Periodically,
select "floor-eggs" for incubation.

growing chickens fed practical diets

Signs of riboflavin deficiency first appear
develop a scaly condition of the skin,
at 10 days of incubation, when embryos
the exact cause of which is not known.

become hypoglycemic and accw11ulate

Treatment with both calciw11 pantothenate
intem1ediates of fatty acid oxidation.

(2 g) and riboflavin (0.5 g) in the drinking

Although flavin-dependent enzymes are
water (50 gal [190 L]) for a few days has
depressed with riboflavin deficiency, the
been successful in some instances. Diets
main effect seems to be in1paired fatty acid
usually contain supplemental pantothenic
oxidation, which is a critical function in tl1e
acid at 12 mg/kg.

developing embryo. An autosomal recessive
trait blocks tl1e fommtion of the 1iboflavinbinding

Riboflavin Deficiency
protein needed for transpmt of

1iboflavin to the egg. Although the adults

Many tissues may be affected by riboflavin
appear nom1al, tl1eir eggs fail to hatch
deficiency, although the epitheliwn and the
regardless of dietary riboflavin content. As
myelin sheaths of some of the main nerves
eggs become deficient in riboflavin, the egg
are major targets. Changes in the sciatic
albwnen loses its characteristic yellow
nerves produce "curled-toe" paralysis in
color. In fact, albwnen color score has been
growing chickens. Egg production is
used to assess riboflavin status of birds.

affected, and riboflavin-deficient eggs do

Chicks receiving diets only partially
not hatch. When the diet is inadvertently
deficient in riboflavin may recover
devoid of the entire spectrwn of vitamins,
spontaneously, indicating tl1at tl1e
it is signs of riboflavin deficiency that first
requirement rapidly decreases with age.

appear. When chicks are fed a diet deficient

A 100-rncg dose should be sufficient for
in riboflavin, their appetite is fairly good but
treatment of riboflavin-deficient clucks,
they grow slowly, become weak and
followed by incorporation of an adequate
emaciated, and develop diarrhea between
level in the diet. However, when the
tl1e first and second weeks. Deficient chicks
curled-toe deformity is longstanding,
are reluctant to move unless forced and
in-epa.rable damage occurs in the sciatic

2942

NUTRITION AND MANAGEMENT: POULTRY
nerve and the administration of riboflavin
sintilar to that described for pantotheltic
is no l�nger curative.

acid deficiency (seep 2940). Perosis and

Most diets contain up to 10 mg of
footpad dem1atitis are also characteristic
liboflavin/kg. Treatment can be given as two signs. Although signs of classic biotin VetBooks.ir
sequential daily 100-mcg doses for chicks or
deficiency are rare, occurrence of fatty liver
poults, followed by an adequate amount of
and kidney syndrome (FLKS) is importailt
riboflavin in feed.

to commercial poultry producers. FLKS was
first described in Denmark in 1958 but was

Folic Acid (Folacin) Deficiency
not a major concern until the late 1960s,

A folacin deficiency results in a macrocytic
when the condition became more prevalent

(megaloblastic) anemia and leukopenia.

and especially so in Europe and Australia.

Tissues with a rapid turnover, such as

Chicks --3 wk old become lethargic and
epithelial linings, GI tract, epidemtis, and
unable to stand, then die within hours.

bone maiTow, as well as cell growth and

Mortality is usually quite low at 1 % --2% but
tissue regeneration, are principally affected.

can reach 20%--300,1,. Postmortem exaniina

Poultry seem more susceptible to folacin
tion reveals pale liver and kidney with
deficiency than other farm animals.

accumulation of fat.

Deficiency results in poor feathering, slow

The condition as described in the 1960s
growth, an anemic appearance, and
was usually confined to wheat-fed birds and
sometimes perosis. As anemia develops, the
was most problematic in low-fat, high- .

comb becomes a waxy-white color, and pale energy diets. High vitainin supplementatio_n mucous membranes in the mouth are noted.

in general corrected the p�oblem, and _biotin

Increased erythrocyte phosphoribosylpyrowas isolated as the causative agent. It is now phosphate concentration can be used as a
known that biotin in wheat has exceptiondiagnostic tool in folacin-defic1ent chicks.

ally low availability. The tligger of

There may also be daniage to liver
high-energy diets led to investigation of
parenchyrna and depleted glycogen
biotin in carbohydrate metabolism. Chicks
reserves. Although turkey poults show
with FLKS are invariably hypoglycemic,
some of the same signs as chickens,
emphasizing the importailce of biotin in two
mortality is usually higher and the birds
key enzymes, namely pyruvate carboxylase
develop a spastic type of cervical pai·alysis
and acetyl Co-A carboxylase. Acetyl Co-A
that results in the neck becoming stiff and
carboxylase appears to preferentially
extended.

sequester biotin, such that with low biotin

The abnormal feather condition in
availability and need for high de novo fat
chickens leads to weak and brittle shafts,
synthesis (high-energy, low-fat diet),
and depigmentation d!'.velops in colored
pyrnvate carboxylase activity is severely
feathers. Although a folacin deficiency can
compromised. Even with this imbalance,
result in reduced egg production, the main
birds are able to grow. However, with a
sign noted with breeders is a marked
concurrent deplivation in feed intake or
decrease in hatchability associated with an
increased demand for glucose, hypoglyceincrease in embryoltic mortaI.ity, usually mia develops, leading to adipose catabolism
during the last few days of incubation.

and the characteristic accumulation of fat m

Embryos have deforn1ed beaks and bending
both liver and kidneys. Birds with FLKS
of the tibiotai-sus. Birds may exhibit perosis, rarely show signs of classic biotin but the lesions seen differ histologically
deficiency.

from those that develop due to choline or

Plasma biotin levels < 100 ng/100 mL have
manganese deficiency. Abnormal structure
been reported as a sign of deficiency.

of the hyaline cartilage and retardation of

However, recent evidence suggests that
ossification are noted with folacin
plasma biotin levels are quite inse_nsitive to
deficiency. Increasing the protein content
the birds' biotin status, and that biotin levels
of the diet has been shown to increase the
in the liver or kidneys are more useful
severity of perosis in chicks receiving diets
indicators. Plasma pyruvic carboxylase is
low in folic acid, because there is an
positively correlated with dietary biotin
increased folacin demand for uric acid
concentration, at1d levels plateau much
synthesis.

later than does the growth response to

Signs of folic acid deficiency in poultry
supplemental biotin.

can be prevented by ensuring diets contain

Embryos are also sensitive to biotin
supplements of up to 1 mg/kg.

status. Congeltital perosis, ataxia, at1d
characteristic skeletal defomlities may be
seen in embryos and newly hatched chicks

Biotin Deficiency
when hens are fed a deficient diet.

Biotin deficiency results in demiatitis of the

Embryonic deformities include a shortened
feet and the skin around the beak and eyes
tibiotarsus that is bent posteriorly, a much

NUTRITION AND MANAGEMENT: POULTRY

2943
shortened tarsometatarsus, shortening
hatchability. Severe deficiency can cause
of the bones of the wing and skull, and
rapid involution of the ovary, oviduct, comb,
sho1tening and bending of the ante1ior end
and wattles, and of the testis in cockerels.

of the scapula. Syndactyly, which is an

Feed consun1ption in vitamin BG-deficient
extensive webbing between the third and
hens and cockerels declines sharply.

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fourth toes, is seen in biotin-deficient

Although a partial molt is seen in some
embryos. Such embryos are chondrodyshens, nom1al egg production returns within trophic and characterized by reduced size,

2 wk after provision of a normal dietary
parrot beak, crooked tibia, and shortened
level of pY1idoxine.

or twisted tarsometatarsus.

Deficiency can be prevented by adding

A munber of factors increase biotin

PY1'idoxine at 3-4 mg/kg feed.

requirements, including oxidative rancidity
of any feed fat, competition by intestinal

Thiamine Deficiency
microorganisms, and lack of carryover into
the newly hatched chick or poult. It is good

Polynemitis in birds represents the later
practice to add 150 mg biotin/tonne of feed,
stages of a thianune deficiency, probably
especially when significant a.mounts of wheat caused by buildup of the intem1ediates of or wheat byproducts are used in the diet.

carbohydrate metabolism. Because the
brain's inrn1ediate source of energy results

Pyridoxine (Vitamin 8
from the degradation of glucose, it depends

6) Deficiency
on biochemical reactions involving

A vitamin B6 deficiency causes retarded
thiamine. In the initial stages of deficiency,
growth, dennatitis, and anemia. Because
lethargy and head tremors may be noted. A
a major role of the vitamin is in protein
marked decrease in appetite is seen in birds
metabolism, deficiency can result in
fed a thia.nune-deficient diet. Poultry are
reduced nitrogen retention. Dietary proalso susceptible to neuromuscular tein is not well utilized, and thus nitrogen
problems, resulting in impaired digestion,
excretion increases. Increased iron levels
general weakness, star-gazing, and frequent
and decreased copper levels are noted in
convulsions.

the serum, and iron utilization appears to be

Polyneuritis may be seen in mature birds
markedly decreased. The resulting anemia

-3 wk after they are fed a thian1ine-deficient
is likely due to a disturbance in the
diet. As the deficiency progresses, birds may
synthesis of protoporphyrins. Anemia is
sit on flexed legs and draw back their heads
often noted in ducks but is seldom seen in
in a star-gazing position. Retraction of the
chickens and turkeys. Young chicks may
head is due to paralysis of the anterior neck
show nervous movements of the legs when
muscles. Soon after this stage, chickens lose
walking and often undergo spasmodic
the ability to stand or sit upright and topple
convulsions, leading to death. During
to the floor, where they may lie with heads
convulsions, the chicks may run about
still retracted. Thiamine deficiency may also
ain1Iessly, flapping their wings and falling
lead to a decrease in body temperature and
with jerking motions. The greater intensity
respiratory rate. Testicular degeneration
of activity, resulting from vitamin B6
may be noted, and the heart may show slight
deficiency, distinguishes these signs from
a.trophy. Birds consmning a thiaminethose of encephalomalacia. Gizzard erosion deficient diet soon show severe anorexia..

has been noted in vitanun BG-deficient

They lose all interest in feed and will not
chicks. It can be prevented by inclusion of
resume eating U11less given thianune. If a

1 % taurocholic acid in the diet, leading to
severe deficiency has developed, thianune
the speculation that pyridoxine is involved
must be force-fed or injected to induce the
in tamine synthesis and is important for
chickens to resmne eating.

gizzard integrity. In pyridoxine deficiency,

Thiamine deficiency is most common
collagen maturation is incomplete,
when poorly processed fish meals are used,
suggesting that this vita.nun is essential for
because they contain thiaminase enzyme. In
integrity of the connective tissue matrix.

such situations, adding extra thiamine may

A chronic deficiency can result in perosis,
be ineffective. There is no good evidence
with one leg usually being crippled and one
suggesting that, U11like in some man1rnalian
or both middle toes bent inward at the first
species, certainFusarium mycotoxins
joint.

can increase the need for supplemental

In adult birds, pyridoxine deficiency
thianune. In otherwise adequate diets,
results in reduced appetite, leading to
deficiency is prevented by supplements
reduced egg production and a decline in
of thiamine up to 4 mg/kg.

VetBooks.ir

TOXICOLOGY

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TOXICOLOGY INTRODUCTION 2948

Absorption, Distribution, Metabolism, and Excretion 2949

Factors Affecting the Activity of Toxica'(lts 2950

Diagnosis ofToxicosis 2950

Principles of Therapy ofToxicosis 2951

TOXICOLOGIC HAZARDS IN THE WORKPLACE 2952

Carbon Monoxide 2952

Cyanide 2953

Hydrogen Sulfide 2954

Nitrogen Dioxide 2955

Phosphine Gas Sources 2955

Lack of OXYgen 2955

ALGAL POISONING 2956

CYANIDE POISONING 2959

FOOD HAZARDS 2964

Avocado 2964

Bread Dough 2965

Chocolate 2966

Macadamia Nuts 2967

Raisins and Grapes 2968

Xylitol 2968

HERBICIDE POISONING 2969

Inorganic Herbicides and Organic Arsenicals 2994

Organic Herbicides 2996

HOUSEHOLD HAZARDS 3000

Alcohols 3000

Chlorine Bleaches 3001

Corrosives 3001

Alkaline Batteries 3003

Cationic Detergents 3003

Detergents, Soaps, and Shampoos 3004

MYCOTOXICOSES 3005

Managing a Suspected Mycotoxicosis 3010

Mycotoxin Adsorbents 3010

Aflatoxicosis 3011

Ergotism 3012

Estrogenism and Vulvovaginitis 3014

Facial Eczema 3015

Fescue Poisoning 3016

Fescue Lameness 3016

Summer Fescue Toxicosis 3017

2946

TOXICOLOGY

Fumonisin Toxicosis 3017

Mycotoxic Lupinosis 3018

Paspalum Staggers 3019

Slaframine Toxicosis 3019

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Trichothecene Toxicosis 3020

SMOKE INHALATION 3021

TOXICITIES FROM HUMAN DRUGS 3024

Toxicities from Over-the-Counter Drugs 3024

Cold and Cough Medications 3025

Decongestants 3026

Analgesics 3027

Gastrointestinal Drugs 3030

Multivitamins and Iron 3030

Topical Preparations 3031

Herbal Supplements 3032

Toxicities from Prescription Drugs 3032

Cardiovascular Medications 3032

Tranquilizers, Antidepressants, Sleep Aids, and Anticonvulsants 3034

Muscle Relaxants 3036

Topical Agents 3036

Prescription N onsteroidal Anti-inflammatory Drugs 3037

Toxicities from Illicit and Abused Drugs 3038

FEED CONTAMINANTS

IONOPHORE TOXICITY 1175 (Mus)

NONPROTEIN NITROGEN POISONING 3043

INDUSTRIAL TOXICANTS

COAL-TAR PRODUCTS POISONING 3045

ETHYLENE GLYCOL TOXICITY 3046

Propylene Glycol Toxicosis 3048

NITRATE AND NITRITE POISONING 3049

PENTACHLOROPHENOL POISONING 3052

PETROLEUM PRODUCT POISONING 3053

PERSISTENT HALOGENATED AROMATIC POISONING 3056

INSECTICIDES, ACARICIDES, AND MOLLUSCICIDES

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY 3058

Carbamate Insecticides 3059

Chlorinated Hydrocarbon Compounds 3060

Insecticides Derived from Plants 3063

Organophosphates 3064

Delayed N eurotoxicity from Triaryl Phosphates 3069

Pesticide Potentiating Agents 3069

TOXICOLOGY

2947

Solvents and Emulsifiers 3069

Sulfur and Lime-sulfur 3070

METALDEHYDE POISONING 3070

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METALS AND MICRONUTRIENTS

ARSENIC POISONING 3071

Inorganic Arsenicals 3071

Organic Arsenicals 3073

COPPER POISONING 3073

FLUORIDE POISONING 3075

IRON TOXICITY IN NEWBORN PIGS 3077

LEAD POISONING 3078

MERCURY POISONING 3080

MOLYBDENUM POISONING 3081

SALT TOXICITY 3083

SELENIUM TOXICOSIS 3085

Chronic 3086

Subchronic 3087

Acute 3087

ZINC TOXICOSIS 3088

PLANTS AND FUNGI

BRACKEN FERN POISONING 3089

GOSSYPOL POISONING 3092

POISONOUS MUSHROOMS 3095

Toxin Latent Period <3 hr After Ingestion 3098

Toxin Latent Period >6 hr After Ingestion 3100

Toxin Latent Period >24 hr After Ingestion 3101

Miscellaneous Poisonous Mushrooms 3102

POISONOUS PLANTS 3103

Houseplants and Ornamentals 3103

Range Plants of Temperate North America 3103

PYRROLIZIDINE ALKALOIDOSIS 3150

QUERCUS POISONING 3152

RYEGRASS TOXICITY 3153

Annual Ryegrass Staggers 3153

Perennial Ryegrass Staggers 3154

SORGHUM POISONING 3155

SWEET CLOVER POISONING 3156

2948

TOXICOLOGY

POISONOUS AND VENOMOUS ORGANISMS

CANTHARIDIN POISONING 3157

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SNAKEBITE 3159

TOAD POISONING 3161

VENOMOUS ARTHROPODS 3162

Spiders and Scorpions 3162

Hyrnenoptera 3164

RODENTICIDES

RODENTICIDE POISONING 3165

Anticoagulant Rodenticides (Warfarin and Congeners) 3165

Bromethalin 3167

Cholecalciferol 3168

Zinc Phosphide 3169

STRYCHNINE POISONING 3170

TOXICOLOGY INTRODUCTION

For a discussion of common poisonings in

A toxic agent is referred to as a toxicant
poultry, seep 2859.

or poison. The term toxin refers to a poison

Veterimuy toxicology involves the
produced by a biologic source ( eg, venoms,
evaluation of toxicosis and deficiencies,
plant toxins); the redundant term biotoxin
identification and characterization of
is occasionally used. Toxicosis, poisoning,
toxins and determination of their fate in
and intoxication are synonymous terms
the body, and treatment of toxicosis.

for the disease produced by a toxicant.

Toxicology has been receiving even more

Toxicity (sometimes incorrectly used
attention in the general public with the
instead of poisoning) refers to the amOLmt
widespread interest in crime scene
of a toxicant necessary to produce a
investigator (CSI) television shows. The
detrimental effect.

recent worldwide melanline contamination

Acute toxicosis refers to effects during
in pet and swine feed, pet jerky treats
the first 24-hr period. Effects produced by
causing illness and death, and concerns
prolonged exposure (�3 mo) are referred
with use of [3-agonists in food animals
to as chronic toxicosis. Tern1s such as
demonstrates the relevancy of veterinary
subacute and subchronic are used to cover
toxicology to current animal health and
the large gap between acute and chronic.

food safety. Veterinary toxicology can be

All toxic effects are dose dependent. A
challenging because of the low frequency
dose may cause undetectable, therapeutic,
of cases observed in a practice setting.

toxic, or lethal effects. A dose is expressed

When a toxicosis occurs, it often involves
as the an1ount of compound per unit of body
a large number of animals and may also
weight, and toxicant concentration as part
involve litigation. A current veterinary
per million or part per billion. These
toxicology reference book is helpful to
quantitative expressions are also used for
ensure the correct samples are obtained
feedstuffs, water, and air, as well as for
and submitted for diagnosis.

tissue levels.

TOXICOLOGY INTRODUCTION

2949

LD50 is the dose that is lethal to 50% of
metabolized xenobiotic agents are more
a test sample. It is an estimator of lethality
toxic than the original compow1d. This is
and the most common expression used to
ref en-eel to as lethal synthesis. Metabolism
rate the potency of toxicants. Other terms
of many organophosphorous insecticides
used for prediction of illness or lethality
produces metabolites more toxic than the

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include no observed effect level (NOEL),
initial ( or parent) compounds ( eg, parathion
maximum nontoxic dose (MNTD), and
to paroxan).

maximum tolerated dose or minim tun toxic

There are two phases of metabolism.

dose(MTD).

Phase I includes oxidation, reduction, and
hydrolysis mechanisms. These reactions,

ABSORPTION, DISTRIBUTION,
catalyzed by hepatic enzymes, generally

METABOLISM, AND EXCRETION
convert foreign compounds to derivatives
for Phase II reactions. Products of Phase I,

The basis of toxicology involves the
howeve1� may be excreted as such, if polar
absorption, distJ.ibution, metabolism, and
solubility pennits translocation. Phase II
excretion (ADME) of a toxicant. Knowledge
principally involves conjugation or synthesis
of these processes is in1portant to evaluate
reactions. Common conjugates include

1isk of exposure to toxins. (See also
glucuronides, acetylation products, and

DISPOSITION AND FATE or DRUGS, p 2492.) combinations with glycine. Metabolism of
xenobiotic agents seldom follows a single

Absorption: Absorption may occur
pathway. Usually, a fraction is excreted
through the alimentary tract, skin, lungs, via
unchar1ged, ar1d the rest is excreted or stored
the eye, mammary gland, or uterus, as well
as metabolites. Significant differences in
as from sites of injection. Toxic effects may
metabolic mechanisms exist between
be local, but the toxicant must be dissolved
species. For exan1ple, because cats lack
and absorbed to some extent to affect the
fonns of glucuronyl transferase, their ability
cell. Solubility is the primary factor affecting to coajugate compow1ds such as morphine absorption. Insoluble salts and ionized
and phenols is compromised. Increased
compounds are poorly absorbed, whereas
tolerai1ce to subsequent exposures of a
lipid-soluble substances are generally
toxicant, in some instances, is due to enzyme
readily absorbed, even through intact skin.

induction initiated by the previous exposure.

For example, baiium is toxic, but bariun1
sulfate can be used for intestinal contJ.·ast

Excretion: Excretion of most toxicants and
radiography because of low absorption.

their metabolites is by way of the kidneys.

Some excretion occurs in the digestive tract

Distribution: Distribution or transloand some via milk Many polar and highcation of a toxicant is via the bloodstreai11 to molecuJar-weight compounds ar·e excreted
reactive sites, including storage depots. The
into the bile. An enterohepatic cycle occurs
liver receives the portal circulation and is
when these compounds are excreted from
the organ most commonly involved with
the liver via bile, reabsorbed from the
intoxication (and detoxification). The.

intestine, and retmned to the liver. Milk
selective deposit of foreign chemicals in variis also all excretion patl1way for some ous tissues depends on receptor sites. Ease
toxicants. The excretion rate may be of
of chemical distribution depends largely
primary concern, because some toxicants
on its water solubility. Polar or aqueouscan cause violative residues in food-producsoluble agents tend to be excreted by the ing animals. The route of adnlinistration,
kidneys; lipid-soluble chemicals ai·e more
close, and condition of the animal-to name
likely to be excreted via the bile and accumua few factors----<:ar1 have a profound effect late in fat depots. The highest concentration
on excretion rates. Toxicants are removed in
of a toxin within an animal is not necessaiily
the kidney by glomemlar filtration, tubular
found in the organ or tissue on which it
excretion by passive diffusion, and active
exerts its maxin1al effect (the tai·get organ).

tubular secretion. The damage to the kidney

Lead may be found in highest concentrations from the excretion of xenobiotics is specific in bone, which is neither a site for toxic
to the anatomic location where tl1e excretion
effects nor a reliable tissue for toxicologic
occurs. Excretion sites are proximal tubules,
interpretation. Knowledge of the translocaglomeruli, medulJa, papilla, ar1d loop of tion characteristics of toxicants is necessary

Henle. The proximal convoluted tubule is the
for proper selection of organs for analysis.

most common site of toxicat1t-incluced injmy.

The importa!lt Phase I enzymes present in

Metabolism: Metabolism or biotransfot0
the kidney ai·e cytochrome P450, prostaglanmation of toxicants by the body is an din syntl1ase, and prostaglandin red uctase.

"attempt to detoxify." In some instances,

The Phase I enzyn1e cytochrome P450 is

2950

TOXICOLOGY INTRODUCTION
present in the kidney at 100/o of the level of
during the winter cold, and plant nitrate
the liver. Important Phase II enzymes
levels are affected by rainfall amounts.

present in the kidneys are UDP-glucuronosyltransferases (UGT), sulfotransferases, Biologic Factors: Various species and
and glutathione-S-transferase.

strains within species react differently to a

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The medulla and papilla are the target
particular toxicant because of variations
sites for phenylbutazone, the tubules are
in absorption, metabolism, or elimination.

targets for many plant toxins, the loop of

Functional differences in species may also

Henle is the target site for fluoride, and the
affect the likelihood of toxicosis, eg, species
glomeruli for immune complexes.

unable to vomit can be intoxicated with a

The elimination or disappearance (by
lower close of some agents.

metabolic change) of a chemical from an

Age and size of the animal are primary facorgan or the body is expressed in terms of tors in toxicosis. Metabolism and translocahalf-life (t'h), defined as the an1ount of tion of xenobiotic agents are compromised
time required for the disappearance of half
by the unclerclevelopecl microsomal enzyme
of the compound. The rate of elimination
system in young animals. Membrane perusually depends on the concentration of meability and hepatic and renal clearance
the compound. A constant fraction ( eg, 1-2)

capabilities vary with age, species, and
eliminated per unit of time is refeITed to as
health. The amOLmt of to xi cant required to
first-order kinetics. A metabolic reaction may cause pathology is generally coITelatecl to dictate the rate of elimination. A constant
body weight, but with greater body weight,
amount eliminated per unit of time is referred a disproportionate increase in toxicity (per to as zero-order kinetics. Different body
wut body weight) of a compound often
compartments will likely have different elimioccurs. Body swiace area may coITelate nation rates. A two-compartment system
more closely with the toxic close. No
describes elimination that is initially rapid
measurement paran1eter is consistent for

( eg, from the central or plasma component)

every situation.

and subsequently slower from the peripheral

Nutritional and dietary factors, hormonal
component ( eg, liver, kidney, or fat).

and health status, organ pathology, stress,
and sex all affect toxicosis. Nutritional
factors may directly affect the toxicant (ie,

FACTORS AFFECTING THE
by altering absorption) or indirectly affect

ACTIVITY OF TOXICANTS
the metabolic processes or availability of
receptor sites. The copper-molybclenwn

Toxicosis potential is usually dete1T!1ined
sulfate interaction is an example of both.

more by the multitude of related factors
than by actual toxicity of the toxicant.

Chemical Factors: The chemical nature

Exposure-related, biologic; or chemical
of a toxicant cletem1ines solubility, which in
factors regulate absorption, metabolism,
tum influences absorption. Nonpolar or
and elimination, and thus, influence
lipid-soluble substances tend to be more
observed clinical consequences.

readily absorbed than polar or ionized
substances. The vehicle or carrier of the

Factors Related to Exposure: Dose is
toxic compound also affects its availability
the primary concern; however, the exact
for absorption. Isomers, including optical
intake of a toxicant is seldom known.

isomers, vary in toxicity. For exan1ple, the

Duration and frequency of exposure are

-y isomer of hexachlorocyclohexane (linimportant. The route of exposure affects clane) is more toxic than other isomers.

absorption, translocation, and perhaps

Adjuvants are fo1mulation factors used to
metabolic patl1ways. Exposure of a toxialter the toxicologic effect of the active ingrecant relative to periods of stress or food client ( eg, piperonyl butoxide enhances t11e
intake may also be a factor. After ingestion
insecticidal activity of pyretluins). Binding
of some toxicants, emesis may occur if t11e
agents, enteric coating, and sustainedstomach is empty, but if partly filled, the release preparations influence absorption
toxicant is retained and toxicosis can
of the active ingredient. As absorption is
occur. Environmental factors, such as
delayed, toxicity decreases. Flavoring agents
temperature, humidity, and barometric
affect palatability and thus the an1ount
pressure, affect rates of consumption and
ingested.

even the occuITence of some toxic agents.

Many mycotoxins and poisonous plants

DIAGNOSIS
are coJTelatecl with seasonal or climatic
changes. For example, the ischemic effects

Diagnosis of a toxicosis, as with any
of ergot toxicosis are more often seen
disease, is based on history, clinical signs,

TOXICOLOGY INTRODUCTION

2951
lesions, laboratory examinations, and in some Oral emetics include syrup of ipecac cases, analytical procedures. Circumstantial (10-20 mL, PO in dogs) and hydrogen evidence is valuable and should be noted
peroxide (2 mUkg, PO). Apomorphine
but does not replace a thorough clinical and
can be used in dogs parenterally at a
postmortem examination. Histories from
dosage of 0.05-0.l mg/kg.

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animal owners may stress obvious factors

Gastric lavage, using an endotracheal
and omit subtle, in1portant details. "Sudden
tube and the largest bore stomach tube
death" is often actually "tardy observation,"

possible, is done on the unconscious or
or sometimes the animal is simply found
anesthetized animal. The head is lowered to
dead.

a 30° angle, and 10 mL of lavage fluid ( water

Pertinent data and samples should be
or saline) per kg of body weight is gently
submitted to the diagnostic laboratory. A
flushed into the stomach and then removed.

complete history is necessary to develop the

This process is repeated until returned fluid
scheme of laboratory investigation and may
is clear. Cathartics and laxatives may be
be valuable in case of litigation. Infom1ation
indicated in some instances for more rapid
should be detailed. For example, a notation of elimination of the toxicant from the GI CNS signs is insufficient; most animals exhibit tract. A gastrotomy or rumenotomy may be some type of CNS signs before death. Exact
necessary when lavage techniques are
actions and signs should be described.

insufficient ( or too slow in ruminants).

Examples of pertinent information include

When the toxicant cannot be physically
the following: 1) number of animals exposed/ removed, certain agents administered orally sick/dead, age, weight, and a chronology of
can adsorb it and prevent its absorption from
morbidity and mortality; 2) clinical signs and
the alin1entary tract. Activated charcoal
course of the disease; 3) any prior disease

( 1-2 g/kg) effectively adsorbs a wide variety
conditions; 4) lesions seen at necropsy, with
of compounds and usually is tl1e adsorbent
careful exanlination of ingesta; 5) response
and detoxicant of choice when toxicosis is
to treatment ( medication should be listed
suspected. The maxin1um amount of
to avoid analytic confusion); 6) related
a drug adsorbed by activated charcoal is
events, eg, feed change, water source, other

-100-1,000 mg/g of charcoal. Sorbitol is
medications, feed additives, pesticide applicasometimes added to activated charcoal to tions; 7) description of facilities ( a drawing or
increase its palatability (in people) and to
digital photograph may be helpful), access
increase the GI transit time and flush out
to refuse, machinery, etc; and 8) recent past
charcoal-bound toxins more rapidly.

locations and when moved. The diagnostic

Activated charcoal should not be used in
laboratory should be contacted if there are
animals with known hypersensitivity or
questions regarding the appropriate sample,
allergy to the drug. With administration of
amount, or container. (See also COLLECTION
high doses, vomiting, constipation, or

AND SUBMISSION 01' LABORATORY SAMPLES, p 1584,
diarrhea may occur, and feces will appear
and TABLE 1, GUIDELINES FOR SUBMITTING SAMPLES
black

FOR TOXICOLOGIC EXAMINATION, p 1586.)

Supportive Therapy: Supportive therapy

PRINCIPLES OF THERAPY
is often necessary until the toxicant can be
metabolized and eliminated. The type of

At initial examination, certain immediate,
support required depends on the animal's
life-saving measures may be needed. Beyond clinical condition. Supportive efforts may this, treatment for toxicosis includes three
include control of convulsive seizures,
basic principles: 1) prevention of furtlier
maintenance of respiration, treatment for
absorption, 2) supportive/symptomatic
shock, correction of electrolyte in1balance
treatment, and 3) specific antidotes.

and fluid loss, and control of cardiac
dysfunction, as well as alleviation of pain.

Prevention of Further Absorption:

Topically applied toxicants usually can be

Specific Antidotes: Specific antidotes
removed by thorough washing with soap
for various toxicants work by various
and water; clipping of the hair or wool
mechanisms. Some complex with the
may be necessary. Emesis is of value in
toxicant (eg, the oximes bind with
dogs, cats, and pigs if done within a few
organophosphorous insecticides, and
hours of ingestion. Emesis is contraindi

EDTA chelates lead). Others block or comcated when the swallowing reflex is pete for receptor sites ( eg, vitamin K
absent; the animal is convulsing;
competes with the receptor for coumarin
corrosive agents, volatile hydrocarbons,
anticoagulants). A few affect metabolism
or petroleum distillates are involved; or
of the toxicant ( eg, nitrite and thiosulfate
risk of aspiration pneumonia is imminent.

ions release and bind cyanide).

2952

TOXICOLOGIC HAZARDS IN THE WORKPLACE

TOXICOLOGIC HAZARDS IN

VetBooks.ir

THE WORKPLACE

Veterinarians are potentially exposed to

CARBON MONOXIDE
myriad potent pharmaceuticals and other
hazardous materials as part of their work

Carbon monoxide (CO) will most comenvirorunent, and particularly during monly be encountered by veterinarians
patient decontamination procedures
working in enclosed spaces ( eg, intensive

(most notably dennal decontamination).

animal production facilities) being heated

Therefore, knowledge of important
by combustion sources ( eg, gas space
toxicologic workplace hazards and basic
heating). Accordingly, this exposure most
personal protective equipment (PPE) is
commonly occurs during cold weather and
important. It is critical to recognize that
winter. Indeed, epidemics of fatal CO

PPE is the "last line of defense" and not
poisoning notoriously occur during extreme
a panacea for toxicologic hazards. The
winter weather conditions, especially in
overarching principle is to avoid exposure
cortjunction with electrical power failures
if at all possible. Over-reliance on inad

(ie, use of combustion heaters, electrical
equately fitted or inappropriate types of
generators, combustion engines, combus

PPE continues to be a substantial cause of
tion power tools, wood heaters, etc, in
human casualties because of the feeling of
enclosed spaces without adequate
overconfidence these devices can provide.

ventilation). Like cyanide, CO is also a

In particular, respirators should be
component of smoke inhalation poisoning.

selected, fitted, and tested by persons

Inhalation is the main route of exposure to
qualified to do this.

CO. CO poisoning is the most common fom1

The following general PPE principles
of fatal air poisoning in many countries.

apply: The general minimum assumed PPE

CO is colorless and tasteless and has
is Jong pants, a long-sleeved shirt, socks,
no odor, making it especially hazardous
closed footwear, and eye protection.

in occupational settings, particularly

Gloves with appropriate chemical
in enclosed spaces with inadequate
resistance characteristics for a given
ventilation. The use of CO monitors and/
situation should be used; gloves should be
or testing of breathing air with a Drager
changed regularly, and double gloving
tube apparatus or similar test method
clone if necessa1y. If there is any risk of
are strongly recommended before entry
significant inhalation and eye exposure,
into any envirorunent where CO might
a properly fitted full-face respirator and
be present. The use of CO monitors in
appropriate filters/cartridges should be
animal production facilities being heated
used. If there is any doubt 1:egarding air
by combustion sources is strongly
quality, it should be tested before entry
recommended.

into a potentially contaminated space

CO binds to hemoglobin, forming

(particularly if it is a potentially contamicarboxyhemoglobin and disrupting blood nated closed space). Anyone entering into
oxygen transport. The development of
a confined space should be able to be
impaired hemoglobin oxygen transport can
extracted/rescued without others needing
cw11ulatively progress over time because of
to enter the space. If there is any question
the relatively slow reversal of carboxyregarding the safety of the work environhemoglobin to normal hemoglobin. Thus, ment, one should not work alone.

CO poisoning can "creep up tmexpecteclly

Appropriate antidote kits (eg, cyanide
and without being noticed" over time. The
antidote kit) should be readily available if
signs and symptoms of CO poisoning in
relevant to the situation. Relevant human
people are relatively nonspecific. One of
exposure guidelines and limits are set by
the early and important indicators of
local regulatory agencies.

exposure to excessive amounts of CO is

Although this chapter is not meant to be a
development of a severe and persistent
comprehensive discussion of every possible
headache. Other conm1on early clinical
toxicologic workplace hazard faced by
signs include dizziness, weakness, nausea,
veterinarians, some common, imp01tant,
vomiting, chest pain, shortness of breath,
and potentially lethal agents known to have
irritability, and altered mental status. Loss
caused injuries and fatalities to veterinarof consciousness, coma, and death can ians are briefly discussed.

occw·. Other signs and symptoms include

TOXICOLOGIC HAZARDS IN THE WORKPLACE

2953
tachycardia, tachypnea, hypotension,
and warning in relation to exposure. TI1e
various neurologic findings (including
wearing of cyanide detection devices and/or
impaired memory and cognitive and
testing of breathing air with a Drager tube
sensory disturbances), metabolic acidosis,
apparatus or sin1ilar test method is strongly
arrhytlunias, myocardial ischemia or
recommended before entry into any

VetBooks.ir
infarction, and noncardiogenic pulmonary
environment where cyanide might be
edema; any organ system can be involved.

present.

Many survivors of severe CO poisoning

The major potential route of workplace
have hypoxic brain injuries, which can be
exposure in veterinary medicine is by
associated with personality changes,
inllalati@n. Substantial skin absorption can
memory deficits, disturbances in voluntary
occur if the atmospheric concentration is
muscle movements, and the appearance of
high or if the skin comes into contact with
involuntary movements (extrapyramidal
cyanide solutions. High ambient temperasyndromes).

tures and high hwnidity appear to increase

Persons with significant CO poisoning
skin absorption. Skin or clothing contamihave been described as having a "healthy"

nation with cyanide-containing materials
red complexion and mucous membranes
can result in off-gassing of cyanide vapor
because of the presence of high levels of
and inhalation. Exposure by any route can
carboxyhemoglobin. Normal pulse
cause systemic toxicity. Cyanide is also a
oximeters will not detect the presence of
skin and eye irritant. Children are more
carboxyhemoglobin; pulse co-oxirnetry is
susceptible to poisoning because of their
required. Additionally, blood carboxyhemohigher minute ventilation per kg body wt.

globin levels correlate poorly with the

Significant cyanide exposures result in
clinical severity of the poisoning.

death within a few minutes because of the

There is no specific antidote for CO
atTest of mitochond1ial oxidative phospho-
poisoning. Resuscitation combined with

1ylation, histotoxic hypoxia, and severe
oxygen is the only known effective
metabolic acidosis, which results in rapid
approach to treatment. Rescue and
onset CNS, cardiovascular, and respiratory
treatment of individuals with CO poisoning effects. CNS signs at1d symptoms in people is a matter for properly equipped and
develop very quickly and are nonspecific:

trained professionals.

excitement, dizziness, nausea, vomiting,
headache, and weakness, which progresses

CYANIDE
to drowsiness, tetanic spasm, locltjaw,
convulsions, hallucinations, loss of

Important sources of exposure in veteri-
consciousness, and terminal coma.

nary medicine include rumen contents of

Cardiovascular signs include arrhytlm1ias
grazing animals that have consumed or been
and intractable hypotension. Respiratory
poisoned with plant cyanogenic glycosides
signs typically include shortness of breath

( eg, during necropsy/sample collection
and chest tightness, rapid breathing, and
procedures), handling or exposure to cyanide increased depth of respirations progressing vertebrate pesticide agents ( or animals
to agonal respiration. Pulmonary edema and
poisoned by them), and combustion sources
cyanosis of the skin may or may not be

(particularly of nitrogen-containing materials
present. Severe, intractable anion-gap
such as plastics, wool, silk). Aqueous
metabolic acidosis due to lactic acidosis
solutions of cyanide are commonly referred
typically develops rapidly. Cyanide
to as prussic acid, and hydrocyanic acid and
poisoning swvivors usually develop some
formonitrile are commonly used synonyms.

form of hypoxic brain dan1age, and this can

(See also CYANIDE POISONING, p 2959.)

be associated with personality changes,

Solutions of hydrogen cyanide are
memory deficits, disturbances in voluntaiy
colorless or pale-blue liquid at room
muscle movements, and appeai·ance of
temperature. Cyanide is very volatile and
involuntary movements ( extrapyramidal
highly toxic, and flanunable/explosive
syndromes).

concentrations can rapidly develop at

Victin1s exposed only to hydrogen
normal temperatures and pressures,
cyai1ide gas do not pose secondary
especially in enclosed spaces.

contanlination risks to rescuers, but

Hydrogen cyanide gas has a distinctive,
resuscitation without a barrier should not
bitter almond smell; however, the ability
be attempted. Victims whose clothing or
of people to detect the odor is genetically
skin is contatninated with hydrogen cyanide
determined. Anosmic individuals (20%---400A,
liquid or solution can secondarily contamiof the hwnan population) are not able to nate response personnel by direct contact
detect it. Accordingly, odor detection
or through off-gassing vapor. Dermal
cannot be relied on in tem1S of detection
contact with cyanide-contaminated victims

2954

TOXICOLOGIC HAZARDS IN THE WORKPLACE
or with gastric contents of victims who may

Hydrogen sulfide is also a notable mucous
have ingested cyanide-containing materials
membrane and respiratory tract irritant, and
should be avoided.

the acute and/or delayed (up to 72 hr after

Veterinarians poisoned by cyanide
exposure) respiratory distress syndromes
require speedy treatment, rapid adminisare common sequela of prolonged VetBooks.ir
tration of antidotes, and specialist care.

inhalation exposure to nonacutely fatal

Great care should be taken by rescuers
levels of hydrogen sulfide.

who plan to enter a contamination "hot

Hydrogen sulfide acts by inactivating
zone." Many human casualties have
mitochondrial cytochrome oxidase,
occurred because of well-intentioned
resulting in the failure of oxidative
but misguided attempts at rescue from
metabolism, histotoxic hypoxia, and
hydrogen cyanide-contaminated hot
acute anion-gap metabolic acidosis.

zones. Rescue and emergency treatment

Its mode of action resembles that
is best left to those with specialized
of cyanide. Acute exposure to high
training in these areas.

concentrations of hydrogen sulfide will
result in sudden collapse and death due
to central respiratory failure (hydrogen

HYDROGEN SULFIDE
sulfide knock-down effect) caused by its
peracute effects on the brain. Signs and

Vete1inarians are most likely to encow1ter
symptoms of acute exposure include
hydrogen sulfide emanating from conceninitial CNS stimulation, nausea, headtrated decaying organic matter ( eg, septic/
aches, impaired gait, dizziness, disturbed
sewage ponds/manure handling facilities
equilibrium, tremors, convulsions, skin
in intensive animal production facilities,
and eye irritation, coma, respiratory
rotting feed stores, carcass pits, etc).

paralysis, and death. Many survivors

When near sewage ponds, it is particularly
of acute hydrogen sulfide poisoning
in1portant not to disturb the swface of the
have hypoxic brain and cardiac injuries.

pond or to cause mixing of the contents,

Hypoxic brain damage can be associbecause this will trigger degassing of ated with personality changes, memory
dissolved hydrogen sulfide.

deficits, disturbances in voluntary

Hydrogen sulfide is a colorless, flan1mamuscle movements, and appearance of ble, and very rapidly toxic gas. Hydrogen
involuntary movements (extrapyramidal
sulfide is slightly heavier than air, tends to
syndromes).

accwnulate in low-lying, poorly ventilated

Low concentrations of hydrogen sulspaces, and is highly flan1mable and fide ( -50 ppm) rapidly produce upper
explosive. It has a characteristic rotten-egg
respiratory tract irritation, and prolonged
odor that can be sensed at concentrations
exposure can result in pulmonary irritation
as low as 0.5 ppb. However;the sensitivity

( cough, shortness of breath, and bronto hydrogen sulfide odor is genetically chial or lung hemorrhage, bronchitis, and
detennined, and a significant proportion
immediate or delayed pulmonary edema).

of the human population has poor odor

Cyanosis may be present. Hydrogen suldetection ability to this gas; additionally, fide inhalation is associated with cardiac
extended exposure (2-15 min at 100 ppm)

arrhythmias. Nausea and vomiting are
to hydrogen sulfide results in paralysis of
also common.

the olfactory nerve, resulting in a loss of

Chronic, repeated, lower-level hydrogen
ability to detect the gas. Therefore, odor is
sulfide exposure is associated with
not a reliable indicator of the presence of
hypotension, headache, nausea, loss of
hydrogen sulfide and cannot be relied on to
appetite, weight loss, ataxia, conjunctivitis,
provide a warning of hazardous concentrachronic cough, and new·opsychological tions. The use of hydrogen sulfide monitors
disorders.

and/or testing of breathing air with a Drager

Ill-advised and poorly equipped attempts
tube apparatus or similar test method are
at rescuing victims from hydrogen sulfide-strongly recommended before entry into contaminated hot zones have resulted in
any environment where hydrogen sulfide
large nun1bers of hydrogen sulfide-associmight be present.

ated hwnan casualties. There is cwTently

Veterinarians are typically exposed to
no effective antidote for hydrogen sulfide
hydrogen sulfide via inhalation. Children
poisoning. Resuscitation combined
are more susceptible because of their high
with oxygen is tile only known effective
minute volwne to weight ratio and higher
approach to treatment. Rescue and
lung surface area to body weight ratio.

treatment of individuals with hydrogen

Prolonged exposure to hydrogen sulfide
sulfide poisoning is a matter for properly
is notably irtitating to the skin and eyes.

equipped and trained professionals.

TOXICOLOGIC HAZARDS IN THE WORKPLACE

2955

NITROGEN DIOXIDE

PHOSPHINE GAS SOURCES

(Silo filler's disease)

Phosphide salts ( conunonly zinc and
aluminum) release phosphine gas in the

Veterinarians are most likely to encounter
presence of acids and have been extensively
nitrogen dioxide in association with grain

VetBooks.ir
used as vertebrate pesticides. Veterinarians
silos, grain silo chutes in intensive animal
are most conunonly exposed to phosphine
production facilities, silage, silage bags,
via inhalation when attempting to deconand silage pit vents. When a silo or pit is taminate and treat an.i.mals that have been
filled with fresh organic material (grain,
poisoned with �inc or alun1inum phosphide
grass etc), nitrogen dioxide is formed by
rodenticides or during necropsy/sample
anaerobic fennentation. High levels can
collection procedures on anin1als that died
develop at the top of grain in silos or at the
from these poisonings. Phosphine gas is
top of silage pits within hours of their
also used as a fumigant for grain and other
filling. Veterinarians working in or around
agricultural products.

silo chutes and hatches or silage pits or

Phosphine is a colorless, flammable, and
silage bags during the first 10 days or so
explosive gas. Technical grade phosphine
after fill will be exposed to nitrogen

(the type most commonly encow1tered by
dioxide. Silo chutes and other nearby
veterinarians) has an unpleasant, garlic-like,
structures exposed to significant levels of
rotting fish-like smell, due to the presence of
nitrogen dioxide are often stained yellow
substituted phosphine and diphosphane. The
to red by the gas.

human odor threshold for phosphine is below

Nitrogen dioxide is a reddish, waterrelevant exposure Inn.its; the iinplication is insoluble, reactive gas with a characteristic
that persons who can smell phosphine are
pungent odor. Because of its low water
being exposed to a hazardous level.

solubility, it is not scrubbed by the upper

Phosphine is described as a "general
respiratory tract. It penetrates deeply into
protoplasm.ic poison," and it is extremely
the lung, where it is reactive with lung
and acutely toxic after inhalation. Acute
surface fluids and acts as a pulmonary
inhalation exposure to phosphine can result
irritant. When nitrogen dioxide contacts the
in respiratory, neurologic, and GI effects.

Jung surface fluids, it slowly hydrolyzes to

Signs and symptoms may include headnitrous and nitric acid, producing chemical aches, dizziness, fatigue, drowsiness,
pneun10nitis and pulmonary edema.

burning substemal pain, nausea, vomiting,

Acute, high-level exposures to nitrogen

GI distress, cough with fluorescent green
dioxide result in acute respiratory distress
sputum, labored breathing, chest tightness,
syndrome in people, which is characterized
pulmonary irritation, pulmonary edema,
by rapid or delayed onset ( up to 72 hr after
tremors, and convulsions (may occur after
exposure) progressive pulmonary edema
apparent recovery). Skin contact with
and respiratory failure. Nitrogen dioxide
phosphides may result in numbness and
acute respiratory distress syndrome is Jess
paresthesia. Chronic occupational
conunon than other toxic injuries, because
exposure effects include upper respiratory
the pungent odor and other effects of
tract inflanunation, weakness, dizziness,
nitrogen dioxide usually trigger an escape
nausea, jaundice, liver effects, increased
from the source of exposure. This type of
bone density, and symptoms referable to
severe effect is more likely if the affected
the GI, cardiorespiratory, and central
person cannot escape.

nervous systems.

More common acute signs and symptoms

Veterinarians are very strongly encourinclude cough, light-headedness, dyspnea, aged to use respiratory and eye protection
chest tightness, choking, sweating, chest
when dealing with patients poisoned by zinc
pain, and wheezing. Because of nitrogen
or aluminun1 phosph.ide; emergency room
dioxide's low water solubility, mucous
staff casualties have occurred during
membrane and eye irritation are relatively
treatment of hw11an patients poisoned with
uncommon signs.

these agents.

Usually of greater concern is the capacity

There is no antidote for phosphine
of nitrogen dioxide inhalation to induce
poisoning, and emergency treatment
sometimes severe delayed effects, including
requires specialist care.

bronchiolitis obliterans (fever, cough, and
dyspnea), respiratory insufficiency new--0nset LACK OF OXYGEN
asthma, COPD, and hypoxia/cyanosis.

There is no specific antidote for nitrogen

Veterinarians commonly encounter
dioxide poisoning. Treatment requires
low-oxygen environments in enclosed
specialist medical care.

spaces that contain biologically respiring

2956

TOXICOLOGIC HAZARDS IN THE WORKPLACE
materials. Freshly cut plant material will

Entry into low-oxygen envirorunents can
continue to be metabolically active, and
result in rapid loss of consciousness and
thus potentially consume oxygen from the
death. Typical signs and symptoms of
air, for surprisingly long periods of time. If
hypoxia include lightheadedness, fatigue,
such materials ( eg, grains, hays, freshly cut
numbness, tingling of extremities, nausea,

VetBooks.ir
timber, etc) are stored in sealed confined
ataxia, confusion, disorientation, hallucinaspaces ( eg, silos, ship holds, etc) with little tions, behavioral change, severe headaches,
ventilation, a low-oxygen atmosphere will
reduced consciousness, papilledema,
develop. Such circumstances have resulted
breathlessness, pallor, tachycardia, and
in significant human casualties and deaths.

tachypnea, with eventual progression to

Such environments should always be
cyanosis, slow heart rate/cor pulmonale and
treated with suspicion, and their atmoslow blood pressure, and death.

phere tested for the presence of breathable

Ill-considered and poorly equipped
air; testing with a flame is not an adequate
rescue attempts from low-oxygen
method. It is strongly recommended that
environments have resulted in many
individuals do not work alone in such
human casualties. Rescue operations
envirorunents and that a metl10d of safe
under such circumstances are best
extraction of a person entering into such
performed by properly equipped and
environments is immediately available.

trained professionals.

ALGAL POISONING

Algal poisoning is an acute, often fatal

Anabaena, Aphanizomenon, and
condition caused by high concentrations of

Planlctothrix, while saxitoxins (also
toxic blue-green algae (more commonly
called paralytic shellfish toxins) can be
known as cyanobacteria-literally
produced by Anabaena, Aphanizomenon,
blue-green bacteria) in drinking water as
and Lyngbya. Hepatotoxic heptapeptides
well as in water used for agriculture,
called microcystins can be produced by
recreation, and aquaculture. Fatalities and

Anabaena, Microcystis, Nos toe, and
severe illness of livestock, pets, wildlife,

Planklolhrix. The brackish water genus
birds, and fish from heavy growths of cyano

Nodularia produces a hepatotoxic
bacteria waterblooms occur in almost all
pentapeptide related, in both structure
countries of the world. Acute lethal
and function, to microcystins. Cylindro
poisonings have also been documented in
spermopsis, Anabaena, Aphanizomenon,
people. Poisoning usually otcurs during

Raphidiopsis, and Umezakia can produce warm seasons when the waterblooms are
a potent hepatotoxic alkaloid called
more intense and of longer duration. Most
cylindrospermopsin. Some genera,
poisonings occur an1ong aninlals drinking
especially Anabaena, can produce both
cyanobacteria-infested freshwater, but
neuro- and hepatotoxins. If a toxic
aquatic animals, especially maricultured
waterbloom contains both types of toxins,
fish and shrimp, are also affected. The
the neurotoxin signs are seen first, because
toxins of cyanobacteria comprise six
their effects occur much sooner (minutes)

distinct chemical classes collectively called
than those of the hepatotoxins (1 to a
cyanotoxins.

few hours). Other noncyclic peptides and
amino acids produced by cyanobacteria

Etiology, Epidemiology, and Patho
can also have biological activity. One
genesis: Although toxic strains within
recent amino acid with neurologic degspecies ofAnabaena, Aphanizomenon, enerative activity is BMAA (15-methylamino

Cylindrospennopsis, Mici·ocystis,
alanine). BMAA has been implicated as the

Nodularia, Nos toe, Oscillatoria, and
causative agent of amyotrophic lateral

Planlctothrix am responsible for most
sclerosis or parkinsonism dementia.

cases of toxicity, there are >30 species of

Poisoning usually does not occw· unless
cyanobacteria that can be associated with
there is a heavy waterbloom that forms a
toxic waterblooms. Neurotoxic alkaloids
dense surface scum. Factors that contribute

(called anatoxins) can be produced by
to heavy waterblooms are nutrient-rich

ALGAL POISONING

2957
eutrophic to hypereutrophic water and
organophosphate anticholinesterase called
wann, sunny weather. Evidence supports
anatoxin-a( s ). Anabaena, Aphan'izomenon,
the observation that global climate change

Cylinclrospe,mopsis, and Lyngbya can causes earlier, more intense, and longerproduce the potent, presynaptic sodium VetBooks.ir
lasting warm weather that leads to more
channel blockers called saxitoxi..11s.

extensive waterblooms of cyanobacteria.

Agriculture practices ( eg, runoff of

Clinical Findings and Lesions: One of
fertilizers and animal wastes) that promote
the earliest effects (15-30 min) of microcysnut1ient emichment also contribute to and tin poisoning is increased serum concentraintensify waterbloom formation. The tions of bile acids, alkaline phosphatase,
problem is augmented by light winds or

-y-glutan1yltransferase, and AST. The WBC
wind conditions that lead to areas of very
count and clotting times increase. Death
high (scum) concentrations of cyanobactemay occur within a few hours (usually ria, especially leeward shoreline locations
within 4-24 hr), up to a few days. Death
where livestock drink. Experiments with
may be preceded by coma, muscle tremors,
both toxin groups have revealed a steep
paddling, and dyspnea. Watery or bloody
dose-response curve, with as much as 900/o
dian·hea may also be seen. Gross lesions
of the lethal dose being ingested without
include hepatomegaly due mostly to
measurable effect. Animal size and species
intrallepatic hemorrhage. Intact clumps
sensitivity influence the degree of intoxicaof greenish cyanobacteria can be found i..11
tion. Monogastric anin1als are less sensitive
the stomach and GI tract, and there is a
than ruminants and birds. Depencling on
greenish stain on the mouth, nose, legs,
waterbloom densities and toxin content,
and feet. Hepatic necrosis begins centrianimals may need to ingest only a few lobularly and proceeds to the periportal
ounces to be affected. However, if the
regions. Hepatocytes are disassociated and
waterbloom is less dense or cyanotoxin
rounded. After death, debris from disascontent is low, as much as several gallons sociated hepatocytes can be found in the
may be needed to cause acute o.r lethal
pulmonary vessels and kidneys. Clinical
toxicity. Among domestic animals, dogs are
signs of neurotoxicosis progress from
most susceptible to a toxic waterbloom.

muscle fasciculations to decreased

This is due to their preference for swinuning movement, abdominal breathing, cyanosis, and drinking in dense waterblooms and a
convulsions, and death. Signs in bi..l·ds
greater species sensitivity to the cyanotoxare similar but include opisthotonos. In ins, especially the neurotoxins.

smaller ani.nlals, death is often preceded by

Although the species sensitivity and signs
leaping movements. Cattle and horses that
of poisoning can vary depending on the type
survive acute poisoni..11g may have signs of
of exposure, the gross and histopathologic
photosensitization in areas exposed t0 light
lesions are quite similar among species

(nose, ears, and back), followed by hair loss
poisoned by the hepatotoxic peptides and
and sloughing of the skin.

neurotoxic alkaloids. Death from hepatotoxicosis induced by cyclic peptides is Diagnosis: Diagnosis is based prin1aiily
generally accepted as being the result of
on history (recent contact with cyanobacteintrallepatic hemorrhage and hypovolemic ria waterbloom), signs of poisoning, and
shock. This conclusion is based on large
necropsy findings. Samples of the waterincreases in liver weight as well as in hepatic bloom should be taken as soon as possible hemoglobin and iron content that account
for microscopic exainination to confirm the
for blood loss sufficient to induce ilTeverspresence of the toxigenic cyanobacteria ible shock. In animals that live more than a
and for cyanotoxin analysis. Although there
few hours, hyperkalemia or hypoglycemia,
are nontoxic and toxic strains of all the
or both, may lead to death from liver failure
known toxic species, it is not possible to
within a few days to a few weeks.

identify a toxic strain by visual exanli.na

Neurotoxicosis, with death occurring
tion. Cyanobacteria are detected by light
in minutes to a few hours from respiratory
microscopy, identified using morphologic
arrest, may result from ingestion of the
chai·acte1istics, and counted per standard
cyanobacteria that produce neurotoxic
volume of water. Stai1dai·d protocols to
alkaloids. Species and strains of Anabaena,
san1ple and monitor cyanobactelia as well

Aphanizomenon, Oscillal01ia, and
as practical keys for the identification of

Planklolhrix can produce a potent,
toxic species are available.

postsynaptic cholinergic ( nicotinic) agonist

Some laboratories cai1 analyze for the
called anatoxin-a that causes a depolarizi..11g
cyanotoxilis either by chemical or biologic
neuromuscular blockade. Strains of
assay. Animal bioassays (mouse tests) have

Anabaena can produce an irreversible
traditionally been used to detect the

2958

ALGAL POISONING
presence of the entire range of cyanotoxins
other water supply is available, anin1als
based on survival times and signs of
should be allowed to drink only from shore
poisoning. These tests provide a definitive
areas kept free (by prevailing winds) of
indication of toxicity, although they cannot
dense surface scwns of cyanobacteria..

be used for precise quantification of

Some efforts have been made to erect

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compow1ds in water or to determine
surface barriers (logs or floating plastic
compliance with standards for environmenbooms) to keep shore a.r·eas free of surface tal levels. A nwnber of analytic techniques
sewn, but these a.r·e not very successful.

are available to detem1ine microcystins in

Cyanoba.cteria.can be controlled by adding
water. These techniques must provide for
copper sulfate (CuS0
quantitative comparison to the guideline

4) or other copperbased algicidal treatments to the water. The or regulatory value in tem1S of toxicity
usual treatment for CuS0 is 0.2-0.4 ppm,
equivalents. The method most suitable in

4
equivalent to 0.65-1.3 oz/10,000 gal. of water
this regard is high-performance liquid
or 1.4-2.8 lb/a.cre-foot of water. Livestock
chromatography (HPLC) or HPLC coupled

( especially sheep) should not be watered
with mass spectrometry. These methods still
for at least 5 days after the last visible
involve estimation of the concentration and
evidence of the cyanoba.cteria. waterbloom.

therefore provide only an estin1ate of

CuS0 is best used to prevent wa.terbloom
toxicity. This is largely due to the limited

4
fo1ma.tion, and care should be taken to
availability of certified reference standards
avoid water that has dead cyanoba.cteria.

for the cyanotoxins. Commercial reference
cells, either from treatment with algicide or
materials, purified from laboratory cultures
natural aging of the bloom, because most
or waterbloom material, for some microcysttoxin is released in the water only after ins, nodularin, cylindrospennopsin, and saxibreakdown of the intact cyanoba.cteria toxins are available. A synthetic reference
cells. A chemical control method receiving
material for anatoxin-a is also available. No
attention are comp0tmds to bind and
known conrn1ercial reference material is
remove phosphorus from eutrophic waters.

available for anatoxin-a(s). Newer methods

This has the potential to minimize one of the
of inunw10assay, for quantification purposes, more in1portant nutrients responsible for are also available. These include conunercial
cya.noba.cteria wa.terblooms. Common

ELISA kits in hoth laboratory and field
phosphorus treatments include lime,
fom1a.ts for microcystins/nodula.rin,
aluminwn sulfate, ferric chloride, and some
cylindrospennopsin, and saxitoxins. Also
types of clay particles. These treatments
available is a receptor-binding assay
also act as flocculating a.gents and fonn
colorin1etric plate kit for ana.toxin-a
particulates with algae cells and other
debris that settle out and remove the bloom

Treatment:. After removal from the
from the water colwnn. For example, when
contaminated water supply, affected anin1als
alwn (potassiwn alW11inum sulfate) is used
should be placed in a protected area out of
in a water supply, a precipitate (floe) forms
direct swilight. Ample quantities of water and that carries algae cells, dirt, and bacteria. to good quality feed should be ma.de available.

the bottom, but charged items such as

Because the toxins.have a steep dosephosphate and colloids are botmd by the response curve, surviving animals have a
same precipitate through their charges.

good chance for recovery. Although therapies A newer, effective phosphorus-binding for cyanoba.cterial poisonings have not been
compoW1d product available in the USA
investigated in detail, activated charcoal
since 2010 uses a pa.tented phosphorusslurry is likely to be of benefit. In laboratory locking technology containing lanthanW11
studies, an ion-exchange resin such as

(5%), a naturally occurring earth element,
cholestyramine has proved useful to absorb
embedded inside a clay matrix ( -95%).

the toxins from the GI tract, and certain bile

Source water management techniques for
acid transport blockers such as cyclosporin
control of cyanoba.cterial growth include

A, rifampin, and silyma.rin injected before
flow maintenance in regulated rivers,
dosing of microcystin have effectively
water mixing techniques both to eliminate
prevented hepa.totoxicity. No therapeutic
stratification and reduce nut1ient release
antagonist has been foW1d effective against
from sedin1ents in reservoirs, and the
ana.toxin-a, cylindrospermopsin, or the
use of algicides in dedicated water supply
saxitoxins, but atropine and activated
storages. Algicides disrupt cells and liberate
charcoal reduce the muscarinic effects of
intra.cellular toxins. Algicide use should
the anticholinesterase ana.toxin-a.( s ).

be in accordance with local environment
and chemical registration regulations.

Prevention: Removal of animals from

In situations where multiple offtakes a.re
the affected water supply is essential. If no
available, the selective withdrawal of water

CYANIDE POISONING

2959
from different depths can minimize the
ozone, while killing cells, will result in the
intake of high surface accumulations of
release of free cyanotoxin. Therefore, the
cyanobacterial cells.

practice of prechlorination or preozonation

Water treatment techniques can be hlghly
is not recommended without a subsequent
effective to remove both cyanobacterial
step to remove dissolved cyanotoxins.

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cells and cyanotoxins ( especially microcyst

Microcystins are readily oxidized by a
ins) with the appropriate technology. Most
range of oxidants, including ozone and
cyanotoxins remain intracellular, unless the
chlorine. Adequate contact time and pH
cells are lysed or damaged from age or
control are needed to achieve optimal
stress from water conditions or chemical
removal of these compounds, whlch is more
treatment. The one exception is cylindrodifficult in the presence of whole cells.

spermopsin, which is actively secreted from

Microcystins, anatoxin-a, cylindrospermopeven healthy cells. This makes it possible to sin, and some saxitoxins are also adsorbed
remove cells and cyanotoxins ( especially
from solution by both granular activated
microcystins) by coagulation and filtration
carbon and, less efficiently, by powdered
in a conventional treatment plant.

activated carbon. The effectiveness of the

Treatment of water containing cyanobacteprocess should be determined by monitorrial cells with oxidants such as chlorine or ing cyanotoxin in the product water.

CYANIDE POISONING

In acute cyanide poisoning, cyanide ions

Etiology: Various chemical forms of

(CN-) bind to, and inhibit, the ferric (Fe3+)

cyanides are found in plants, fumigants,
heme moeity fom1 of mitochondrial
soil sterilizers, fertilizers (eg, cyanan1ide),
cytochrome c oxidase (synonyms: Ma,
pesticides/rodenticides ( eg, calcium
complex IV, cytochrome A3, EC 1.9.3.1).

cyanomide) and salts used in industrial

This blocks the fourth step in the rnitochonprocesses, such as gold mining, metal d!ial electron transport chain (reduction of
cleaning and electroplating, photographic

02 to H20). resulting in the arrest of aerobic
processes, and others. Hydrogen cyanide
metabolism and death from histotoxic
is also known as prussic acid, and cyanide
a.noxia. Tissues that heavily depend on
salts liberate cyanide gas in the presence
aerobic metabolism such as the heart
of acids ( eg, in the stomach). Cyanide prepaand brain are particularly susceptible rations are still used as vertebrate pest
to these effects. Cyanide also binds to
control agents for control of feral pigs, fox,
other heme-containing enzymes, such as

Australian brush-tailed possums, and other
members of the cytochrome p450 family,
pest or predator species in a .nun1ber of
and to myoglobin. However, these tissue
countries. Cyanide salts are still used as
cyanide "sinks" do not provide sufficient
killing agents in entomology and (illegally)

protection from histotoxic anoxia The
as a method of fishing and/or collection of
acute lethal dosage of hydrogen cyanide
aquarium fish species (ie, cyanide fishing).

(HCN) in most anin1al species is -2 mg/kg.

Combustion of common polyacrylonitriles

Plant materials containing �200 ppm of

(plastics), wool, silk, keratin, polyurethane
cyanogenic glycosides are dangerous.

(insulation/upholstery), melamine resins

There are at least two fom1s of chronic

(household goods), and synthetic rubber
cyanide poisoning in domestic aninlals:

results in the release of cyanide gas. Car

1) hypothyroidism due to disruption of
fires are notorious sources of cyanide
iodide uptake by the follicular thyroid
exposure, and cyanide is also a notable
cell sodium-iodide syn1porter by thiocycomponent of internal combustion engine anate, a metabolite in the detoxification of
exhaust and tobacco smoke. Carbon
cyanide, and 2) chronic cyanide and plant
monoxide poisoning with cyanide gas is
cyanide metabolite ( eg, various glutamyl
thus an extremely common component

[3-cyanoalanines )-associated neuropathy
of smoke inhalation toxidromes.

toxidromes ( eg, equine sorghum cystitis

Toxicity can result from accidental,
ataxia syndrome, cystitis ataxia syndromes
improper, or malicious use or exposure.

in cattle, sheep, and goats).

However, in livestock species, the most

2960

CYANIDE POISONING
frequent cause of acute and chronic
syndrome. Invertebrates such as Burnet
cyanide poisoning is ingestion of plants
moths (Zygaena spp) that feed on bird'sthat either constitutively contain cyanofoot trefoils), as well as certain centipede genic glycosides or are induced to produce
and millipedes, are potentially hazardous
cyanogenic glycosides and cyanolipids as
food sources for exotic pet species.

a protective response to environmental

Plant cyanogenesis in response to

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conditions (plant cyanogenesis). Plant
environmental stressors is an important
cyanogenesis is a common process and has
part of the etiology and risk of acute
been documented in >3,000 different plant
cyanogenic glycoside poisoning. Within
species distributed over -110 different
plants, amino acids that are not used for
families of fems, gymnosperms, and
protein synthesis can be metabolized to
angiosperms. Of these plants, -300 species
o.-hydroxynitriles and then to cyanogenic
are potential causes of acute and chronic
glycosides. Plants are protected from the
cyanogenic glycoside poisoning, and there
potential adverse effects of cyanogenic
are -75 different cyanogenic glycosides (all
glycosides by two features: cyanogenic
of which are 0-!3-glycosidic derivatives of
glycosides are largely found within cell
o.-hydroxynitriles ). Plant species of notable
vacuoles, and the presence of the detoxifyveterinary in1portance include Sorghum ing enzyme !3-cyanoalanine synthase ( which
spp (Johnson grass, Sudan grass, and S
is responsible for production of some of the
bicolor, the common cereal grain crop
cyanide derivatives putatively involved in
referred to as "sorghum" or the synonyms
the chronic cyanide-associated neurologic
durra, jowari, milo ), Acacia grnggii
toxidromes). Even so-called "acyanogenic"

(guajillo ), Amelanchier alnifolia (western
plants can become toxic under appropriate
service berry), Linum spp (linseeds and
environmental circumstances. Environmenflaxes), Smnbucus nigra (elderberry), tal conditions that danrnge relevant plant

Buckley suckleyana (poison suckleya),
species, reduce protein synthesis, enhance

Triglochin maritima and T palustris
the conversion of nitrate to an1ino acids in

(marsh arrow grasses), Manni/wt
the presence of reduced protein synthesis,
esculenlum ( cassava), all members of the
and/or inhibit !3-cyanoalanine synthase

Prunus genus until proved otherwise
potentially increase the risk of cyanogen

(apricot, peach, chokecherry, pincheny,
esis. Relevant envirorunental factors
wild black cherry, ornamental cheny,
include crushing, wilting, freezing, high
peaches, nectarines, apricots, almonds, bird
environmental temperatures, herbicide
cherries, black thorn, cherry law·els
treatment, water stress, cool moist growing

[ conunercial orchard species are often
conditions, nitrate fertilization, high soil
specifically bred for low cyanide content;
nitrogen:phosphorus ratios, soil phosphohowever, ornamental members of this genus rus deficiency, low soil sulfur ( decreases are often highly poisonous]), Nandina
detoxification of cyanogenic glycosides to
domestica (heavenly or sacred bamboo),
thiocyanates within plants), insect attack,

Phaseolus lunatus (lima beans), members
and various plant diseases. Herbicide
of the Vi,cia genus until proved otherwise
treatment of plants is important in that

(vetches; often, pasture species have-been
it may also increase plant palatability.

bred for low cyanogenesis ), Lotus spp

Crushing and/or mastication of potentially

(bird's-foot treefoils; often, pasture species
cyanogenic plants is in1portant in develophave been bred for low cyanogenesis ), ment of the acute toxidrome, because this

Trifolium sp ( clovers; often, pasture
releases cyanogenic glycosides from plant
species have been bred for low cyanide
cell vacuoles and exposes them to
content), Zea mays (corn), Eucalyptus spp catabolism by 13-glucosidase and hyclroxyni

(gum trees), Hydrangea spp (hydrangeas),
trile lyase present in the plant cell cytosol.

Pte1idimn aquilinum (bracken fem),

Yotmg, rapidly growing areas of plants and

Bahia oppositifolia (bal1ia), and Chaenom
areas of regrowth after cutting often have
ales spp (flowering quince) (See also SORGHUM high cyanogenic glycoside content. As a POISONJNG, p 3155). A munber of insect species
rough approximation, rapidly growing
are also able to synthesize hydrogen cyanide Sorghum spp are often hazardous until they and/or sequester hydrogen cyanide that is
reach -60 cm in height; however, this is no
derived from the cyanogenic glycosides of
guarantee of safety, and if there is any doubt
their plant hosts (notably the USA eastern
regarding cyanogenic potential, samples of
tent caterpillar Malacosoma ame,icanum
potential forage should be tested. Plant
that is associated with mare reproductive
seeds and leaves typically have higher
loss syndrome (see also MARE REPRODUCTIVE
cyanogenic potential, while the fleshy parts

LOSS SYNDROME, p 1343); however, cyanide is
of fruits generally have low levels. Drying
not the cause of ma.re reproductive loss
often increases the cyanogenic potential of

CYANIDE POISONING

2961
plants, whereas ensiling may reduce
acid intake) is associated with neuropathy
cyanide content by -50%.

syndromes in horses and ruminants.

[3-glucosidase and hydroxynitrile lyase are

Sorghun1 cystitis ataxia syndrome of
also present in the rumen rnicroflora, and a
horses is associated with diffuse nerve

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rumen pH of -6.5-7 favors conversion of
fiber degeneration in the lateral and ventral
cyanogenic glycosides to cyanide. Rwninants funiculi of the spinal cord and brain stem.

on high-energy grain rations are somewhat

Similar syndromes have been described
less susceptible, because their lower rwnen
in rwninants. Comparisons between
pH ( -4--6) reduces the fom1ation of cyanide.

these syndromes as chronic cyanogenic

Consw11ption of water before grazing on
glycoside--associated hw11an myeloneucyanogenic pastures appears to increase the ropathies such as Konzo and tropical ataxic
risk. Monogastiic animals with low stomach
neuropathy have been made; however, the
pH are also somewhat less susceptible to
precise toxins and modes of action are yet
cyanogenic glycoside poisoning. However,
to be fully defined. All of these toxidromes
these factors do not guarantee immunity
appear to be related to a combination of
from poisoning.

chronic cyanide/cyanogenic glycoside

Under conditions of low-level exposure,
exposure combined with low dietary sulfur
mammals detoxify -80% of ingested cyanide
and/or sulfur amino acid intake and possibly
to thiocyanate via mitochondrial rhodanese.

other nutritional deficiencies. Lathyro

Thiocyanate is then largely excreted in urine. genic plant cyanide metabolites such as Often, the rate of the rhodanese pathway

[3--cyanoalanine have been implicated as
is limited by the availability of thiosulfate;
causative or at least contiibutory agents.

also notably, dogs have lower overall rho

Chronic, low-level cyanogenic glycoside
danese activity than other species. Minor,
exposure (notably from Sorghum spp)

but toxicologically important, pathways
has been associated with musculoskeletal
of detoxification in mammals include the
teratogenesis ( ankyloses or aitlu·ogryposes)

combination of cyanide with hydroxycoand abortion.

bala.min (vitamin B,2.,) to yield cyanocobalamin (vitamin B,2), and the nonenzymatic Clinical Findings: Acute cyanide combination of cyanide with cysteine to
poisoning: Signs generally occur within
form [3 -thiocyanoalanine, which is conve1ted

15-20 n1in to a few hours after animals
to 2-ilninothiazolidine-4-ca.rboxylic acid
consun1e toxic forage, and survival after
and subsequently excreted. Small a.mounts
onset of clinical signs is rarely >2 hr.

of [3-thiocyanoalanine are also excreted in

Excitement can be displayed initially,
saliva Dietary levels of sulfur an1ino acids
accompanied by rapid respiration rate.

( L-cysteine and L-methionine) strongly

Dyspnea follows sho1tly, with tachycai·dia.

influence the rate of detoxification of

The classic "bitter almond" breatl1 smell
cyanide, and low dietary intakes are
may be present; however, the ability to
associated with higher blood cyanide levels,
detect this smell is genetically detem1ined
partiCLLiarly under conditions of chronic,
in people, and anosrnic people ( a significant
low level exposure. Dietary sulfur and sulfur
prop01tion of the population) carmot detect
amino acid intake are known to sti·ongly
it. Salivation, excess lacril11ation, and
affect the neurologic toxidromes associated
voiding of urine and feces may occur.

with chronic cyanide/cyanogenic glycoside

Vomiting may occur, especially in pigs.

exposure in people.

Muscle fasciculation is common and

Chronic low-level cyanide/cyanogenic
progresses to generalized spasms and coma
glycoside exposure is associated with
before death. Animals may stagger and
increased exposure to the cyanide metastruggle before collapse. In other cases, bolite thiocyanate. Under conditions of
sudden unexpected death may ensue.

thiocyanate overload, thiocyanate acts as a

Mucous membranes are bright red but may
competitive inhibitor of thyroid follicular
become cyanotic tem1inally. Venous blood
cell iodine uptake by the sodium/iodide
is classically described as "cherry red"

symporter. This results in reduced iodibecause of the presence of high venous nation of tyrosine, reduced T 3 synthesis,
blood p02; however, this color rapidly
increased blood TSH, goiter, and hypothychanges after death. Serw11 a.nu11onia and roidism. Similar effects occur with some
neutral ai1d aromatic ai11ino acids are
plant glucosinolates (goitrogenic glycotypically increased. Cardiac arrhythmias are sides). Seleniwn deficiency appears to
common due to myocai·dial histotoxic
enhance these effects.

hypoxia. Death occurs during severe

Chronic, low-level cyanide/cyanogenic
asphyxial convulsions. The heart may
glycoside exposure ( often in combination
continue to beat for several minutes after
with low dietary sulfur and/or sulfur a.n1ino
struggling, and breathing stops. The

2962

CYANIDE POISONING
elimination half-life of cyanide in dogs is

Diagnosis: Appropriate history, clinical
reported to be 19 hr, so prognosis of
signs, postmortem findings, and demonstrarecove1y without therapeutic intervention tion ofHCN in J"UI1len (stomach) contents
is grave: it would take more than 4 days to
or other diagnostic specinlens support a
eliminate >95% of the cyanide present.

diagnosis of cyanide poisoning. Vete1inar

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Chronic cyanide poisoning: Chronic
ians should be aware of the possible need
cyanogenic glycoside hypothyroidism
to use approp1;ate personal protective
will present as hypothyroidism with or
equipment, including a respirator, when
without goiter. Cystitis ataxia toxidromes
collecting sainples that may liberate cyanide
are typically associated with posterior
gas ( eg, =en contents and J"UI1len gas
ataxia or incoordination that may progress
cap). A rapid qualitative and presumptive
to in-eversible flaccid paralysis, cystitis
diagnosis can be made by testing represensecondary to urinaiy incontinence, and tative plant samples or stomach contents
hindlimb wine scalding and alopecia. Death,
using the picric acid paper test or by
although uncommon, is often associated
collecting mmen gas cap sainples by
with pyelonephritis. Late-term abortion
trocarization and testing with a Draeger
and musculoskeletal teratogenesis may
cyanide gas detection tube or other cyanide
also occur.

gas detection system. Negative results
with such rapid presumptive tests do not

Lesions: Acute cyanide poisoning:

completely exclude the possibility of

Necropsy personnel may require appropriate
cyanide poisoning. Suitable specinlens
personal protective equipment, including
for more sophisticated testing include the
respirators with suitable cartridges. Venous
suspected food source, mmen/stomach
blood is classically described as being "bright contents, sai11ples of the mmen gas cap, cheny red"; however, this color rapidly fades
heparinized whole blood, liver, and muscle.

after death or if the blood is exposed to the

Antemortem whole blood is preferred; other
atmosphere. Whole blood clotting may be
specimens should be collected as soon as
slow or not occur. Mucous membranes may
possible after death, preferably within 4 hr.

also be pink initially, then become cyanotic

Specinlens should be sealed in an airtight
after respiration ceases. The run1en may be
container, refrigerated or frozen, and
distended witl1 gas; in some cases the odor
submitted to the laboratory without delay.

of"bitter almonds" may be detected after

When cold storage is unavailable, inlmeropening. Rw11en contents may provide a sion of specinlens in l %---3% mercuric
positive sodium picrate paper test ( or
chloride has been satisfacto1y. The rationale
positive results on other rapid cyanide test
for using liver as a diagnostic sample is
strip systems). RWllen gases may provide
that cyanide binds to the Fe3+ form of
positive results in cyanide Draeger tube
cytochrome p450 and other heme-containing
rapid test systems. Agonal hemorrhages
metabolic enzymes. The rationale for using
of the heart may be seen. Liver, serosal
skeletal muscle is that cyanide will bind to
surfaces, tracheal mucosa, and ltmgs may be
the iron moiety in myoglobin.

congested or hemorrhagic; so111e froth may

Where available, measurement of the
be seen in respiratory passages. Cyanide also
urinary metabolite of cyanide, thiocyanate,
binds to iron (both Fe2+ and Fe3+) present in
may reveal increased concentrations after
myoglobin ( although this occurs more
cyanide poisoning.

slowly than the binding to cytochrome c

Hay, green chop, silage, or growing plants
ox:idase and, hence, is not protective); this
containing >220 ppm cyanide as HCN on a
may result in a generalized dark coloration of wet-weight (as is) basis are very dangerous skeletal muscle. Neither gross nor histologic
as aninlal feed. Forage containing <100 ppm
lesions are consistently seen.

HCN, wet weight, is usually safe to pasture.

Multiple foci of degeneration or necrosis

Analyses pe1fom1ed on a dry-weight basis
may be seen in the CNS of dogs chronically
have the following criteria: > 750 ppm HCN
exposed to sub lethal an10unts of cyanide.

is hazardous, 500----750 ppm HCN is doubtful,

These lesions have not been reported in
and <500 ppm HCN is considered safe.

livestock.

Nonnally expected cyanide concentra

Chronic cyan·ide poisoning: Goiter may
tions in blood of most animal species are
be present. Cystitis ataxia toxidromes are
usually <0.5 mcg/mL. Minin1al lethal blood
characterized by opportunistic bacterial
concentrations are ---3 mcg/mL or less.

cystitis with or without pyelonephritis and

Cyanide concentrations in muscle are sinillar
diffuse nerve fiber degeneration in the
to those in blood, but concentrations in liver
lateral and ventral funiculi of the spinal cord are generally lower than those in blood. In and brain stem. Hindlimb urine scalding and dogs, whole blood cyanide concentrations alopecia may be present.

may be 4-5 tinles greater than senun

CYANIDE POISONING

2963
concentrations l1ecause of binding to ferric
preceded by nitrite induction of methemoions and sequesJ.ration in RBCs.

globinemia in cases of confirmed cyanide

Differential d1agnoses include poisonings
poisoning. However, because thiosulfate
by nitrate or nitl'ite, urea, organophosphate,
is generally well tolerated, it is often
carbamate, chlc'rinated hydrocarbon
administered alone in situations when

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pesticides, and loxic gases ( carbon
cyanide exposure is likely but unconfinned
monoxide and l 1ydrogen sulfide), as well as

( eg, smoke inhalation or exposure to fires).

infectious or nohlnfectious diseases and

Hydroxocobalamin (vitamin B12a) is also
other toxidrom''s that cause sudden death.

used as a cyanide antidote. Hydroxocobalamin detoxifies cyanide by binding to it and Treatment, Cclntrol, and Prevention:

forming cyanocobalan1in (ie, another decoy

Immediate treat tnent is necessary. The goal
receptor approach), which is then excreted
of treatment is t1, break the cyanidein urine. It has the adva11tages that it is cytochrome c o 'tidase bond and reestablish
relatively well tolerated, does not comprothe mitochondrial electron transport chain.

mise blood oxygen-carrying capacity, and

One way to accc .1mplish this is by using Fe3+
does not produce hypotension. Hydroxocoin hemoglobin (le, inducing methemobalainin does produce chromaturia ( which globinemia), w11ich then acts as a highmay result in false urinalysis results), as affinity decoy cllemical receptor for cyanide
well as infusion site reactions, GI upset,
and fom1s cyanJl1ethemoglobin. Classically,
pruritus, and dysphagia. The suggested
vaiious nitJites have been used for this
dosage is 70 mg/kg, infused IV over 15 min,
purpose; eg, in111tled amyl nitJite followed
repeated as necessary.

by IV iajection c'f a nitJite salt (typically

Sulfai1egen (as the sodium or triethai10lasodium nitJite) has been used to rapidly mine salt) has been developed for treatment
induce methem' ,globinemia Cyanide bound
of cyanide mass poisoning incidents. This
to rnethemoglollin can then be detoxified
approach has the advantage that sulfanegen
by rhodanese to thiocyanate. Because the
is water soluble a11d ca.11 be administered
rhodanese-med1ated detoxification of

IM. Sulfanegen is a prodrug that generates
cyanide to thiocyanate is usually capacity

3-mercaptopyruvic acid (3-MP), an
and rate limited by the availability of sulfur
intermediate in cysteine metabolism, which
donors, treatm€ht with nitiites is usually
again acts as a decoy receptor for cyanide.

followed up by iltjection of sodium

By itself, the half-life of3-MP is too sh01t to
thiosulfate. oral dosing with sodium
be effective against cyanide poisoning. For
thiosulfate into 1.he rumen and/or stomach
this reason, prodrugs such as sulfanegen
has also been s11 ggested because the reaction have been developed to increase the between thiosulfate and cyanide can also
duration of action of3-MP in vivo.

occur nonenzyl11atically, and this may reduce

Alternative inducers of methemoglobineany ongoing prl' duction of cyanide in the mia such as 4-dimethyl-aininophenol
rumen/stomacl1 environments.

(DMAP; IM at 5 mg/kg) or hydroxylainine

If possible, tl'e contents of one 0.3-rnL vial hydrochlorine (IM at 50 mg/kg) have been of amyl nitrite ehould be inhaled by the
suggested, because they produce methemoanin1al as soon 1JS possible after exposure, globinemia more quickly than the nitrites
followed by an Iv infusion of sodiwn nitrite
currently in use. However, these hemo

(10 g/100 mL of distilled water or isotonic
globin-oxidizing agents are also relatively
saline; 20 mg,'k!\ body wt) over 3-4 min.

toxic to RBCs a11d can induce severe effects

Nitrite treatmel 1t is then followed by a slow
such as hemolysis and renal dan1age. These

IV injection of !'Odium thiosulfate (200A, w/w) "rapid agents" still have the disadvantage of at �500 mg/kg. ,1 'hiosulfate is generally well
reducing blood oxygen-carrying capacity.

tolerated; how•' ver, vomiting and hypoten

Other alternative antidotes in clinical
sion can occur. The thiosulfate iajection can development a11d use worldwide include be repeated if 11'ecessary. Oral administradicobalt-ethylenediaininetetraacetic acid tion of thiosulf11te can also be considered in

(EDTA) and a-ketoglutaric acid. Although
an attempt to c invert any cyanide in the
hydroxycobalainin has been approved by
stomach/rumell into thiocyanate. Sodium
the FDA for use in the USA, none of the
nitrite therapy I nay be carefully repeated at
others is readily available. Dicobalt-EDTA

10 mg/kg, ever,' 2-4 hr or as needed. Ideally,
releases cobalt ions that react with cyanide
decisions regafding repeated treatment
ions; highly stable cyanide-cobalt comwith nitrites sh' )U!d consider the degree plexes are then excreted by the kidneys.

of methemoglobinemia present.

This drug is very potent and has in1rnediate

Notably, thi&ulfate treatment alone has
action but is reported to have nw11erous,
been successfil l in some cases. However,
severe adverse effects in people. The
thiosulfate ti·ef tment should ideally be
investigational antidote a-ketoglutaric acid

2964

CYANIDE POISONING
has a molecular configuration that renders it have acceptable cyruude levels, to reduce amenable to nucleophilic binding of cyanide danger from prnssic acid poisoning. Animals without generation of methemoglobin.

should be fed before first ttuning out to

Pretreatment with this drug reduced lethal
pastw·e; hung1y ruumals may conswne
outcomes and increased efficacy of sodium
forage too rapidly to detoxify HCN released

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thlosulfate, but postexposure efficacy in
in tl1e run1en. Animals should be turned out
animals is unknown.

to new pasttu·e later in the day; potential for

Sodium thiosulfate alone is also an
prnssic acid release is reported to be hlghest
effective antidotal therapy at �500 mg/kg, IV, dw'Lng early morning hours. Free-choice salt plus 30 g/cow, PO, to detoxify any remaining and mineral with added sulfur may help HCN in the rw11en. When available, oxygen
protect against prnssic acid toxicity. Grazing
should be used to supplement nitrite or
should be monitored closely during periods
tluosulfate therapy, especially in small
of environmental stress, eg, drought or frost.

animals. Hyperbatic oxygen tl1erapy

Abundant regrowtl1 of sorghun1 can be

(1000/o oxygen breathed inte1mittently at
dangerous; tl1ese shoots should be frozen
a pressure >l atmosphere absolute) causes
ru1d wilted before grazing.

a.ti above-no1mal pattial pressure of oxygen

Green chop forces livestock to eat both

(P02) in arterial blood and mru·kedly
stems aJ1d leaves, thereby reducing
increases the amount of oxygen dissolved
problems caused by selective grazing.

in plasma Oxygen-dependent cellulai·

Cutting height can be raised to minin1ize
metabolic processes benefit from heightinclusion of regrowth.

en eel oxygen tension in capillaries and

Sorghum hay ru1d silage usually lose ;;,5()%
enhanced oxygen diffusion from capillaries
of prussic acid content during cw'ing aJ1d
to critical tissues. Activated chai·coal does
ensiling processes. Free cyanide is released
not effectively absorb cyanide and thus is
by enzyme activity and escapes as a gas.

not recommended PO for ru1tidotal therapy.

Although a rru·e occurrence, hazardous

Caution is indicated in treatment. All
concentrations of prnssic acid may still
cyruude antidotes are toxic by themselves.

remain in tile final product, especially if the

Many clliucal signs of nitrate and prussic
forage had an extremely !ugh cyanide
acid poismung are similar, and i.r\jecting
content before cutting. Hay has been dried
sodiun1 nitrite induces methernoglobineat oven temperatures for up to 4 days with mia identical to that produced by nitrite
no significaJ1t loss of cyanide potential.

poisoning. lf in doubt of the diagnosis, rnetl1-

These feeds should be aJ1alyzed before
ylene blue, IV, at 4-22 mg/kg, may be used to
use whenever high prussic acid concentrainduce methernoglobin. Because methylene tions ru·e suspected. Potentially toxic feed
blue can serve as both a donor and acceptor
should be diluted or mixed with grain or
of electrons, it can r�duce methemoglobin
forage t11at is low in prussic acid content
in the presence of excess rnethernoglobin
to achieve safe concentrations in tile final
or induce methemoglobin when only
product. At least in theory, the risk of
hemoglobin is present (but sodium nitrate
chronic cyruude poisoning syndromes may
is the more effective treatment for cyanide
be reduced by iodine supplementation in
poisoning if the diagnosis is certain).

the case of hypotllyroiilism and by

The best preventive step is to test suspect
sulfur-contai1ung an1ino acids in the case of
feed and/or pastures before allowing
chronic neurologic toxidromes. Great care
consumption. Pasture and forage sorghums
must be taken when providing supplemen

( eg, Sudan grass and sorghtm1-Sudan grass
tal elemental sulfur sources in run1inru1ts
hybtids) should not be grazed until tl1ey are
because of tl1e possible risk of polioen

>60 cm tall or have been proved by testing to
cephalomalacia (seep 1281).

FOOD HAZARDS

AVOCADO
goats, horses, nuce, rabbits, guinea pigs,
rats, sheep, budgerigms, caJ1aries,

Ingestion of avocado (Persea americana)

cockatiels, ostriches, chlckens, turkeys, and
has been associated witll myocardial
fish ru·e susceptible. Caged birds appear
necrosis in matnmals and birds and with
more sensitive to the effects of avocado,
sterile mastitis in lactating mammals. Cattle, while chlckens and turkeys apperu· more

FOOD HAZARDS

2965
resistant. Although an old case report exists
the abdominal cavity, pericardial sac, and
of two dogs developing myocardial dan1age
thoracic cavity. The heait may contain
after avocado ingestion, dogs appear to be
pale streaks. Histopa.thologic lesions in
relatively resistanl compared with other
the ma.mmaiy gland include degeneration

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species.

and necrosis of secret01y epitheliwn,
with interstitial edema at1d hemoITha.ge.

Etiology: Ingestion of fruit, leaves, stems, Myocai·dial lesions include degeneration
and seeds of avocado has been associated
at1d necrosis of myocai·dial fibers, which are
with toxicosis in animals; leaves are the
most pronounced in ventricular walls and
most toxic patt. The Guatemalan vai·ieties
septtun; interstitial hemorrhage at1d/or
of avocado have been most conunonly
edema may be present. In horses, symmet-
associated with toxicosis.

1ic ischemic myopa.thy of the head muscles

When purified, the toxic p1inciple in
and tongue, as well as ischemic myelomalaavocado, persin, causes mastitis in lactating cia. of the lwnbar spinal cord, have been
mice at 60-100 mg/kg, and dosages > 100
described.

mg/kg result in myocai·dial necrosis. Goats
develop severe mastitis when ingesting

Diagnosis: Diagnosis of avocado toxicosis

20 g of leaves/kg, whereas 30 g of leaves/kg
relies on history of exposure and clinical
results in cai·diac ir\ju1y. Acute cai·diac
signs. There ai·e no readily available specific
failure developed in sheep fed avocado
tests that will confi.nn diagnosis. Differential
leaves at 25 g/kg for 5 days; 5.5 g/kg of leaves diagnoses include other causes of mastitis fed for 21 days or 2.5 g/kg for 32 days caused

( eg, infectious) and other myocai·dial
chronic cardiac insufficiency. Budgerigars
disorders, including ionophore toxicosis,
fed 1 g of avocado fruit developed agitation
yew toxicosis, vitai11in E/seleniwn
at1d feather pulling, while 8. 7 g of mashed
deficiency, gossypol, cai·diac glycoside
avocado fruit resulted in death within 48 hr.

toxicosis ( eg, oleander), cai·diomyopathy,

Myocardial ir\jury, mastitis, and colic have
and infectious myocai·ditis.

been reported in horses ingesting avocado
fruit at1d/or leaves.

Treatment: NSAIDs and analgesics may
benefit animals with mastitis. Treatment

Pathogenesis: Avocado causes necrosis
for congestive heart failure ( eg, diuretics,
and hemorrhage of mammary gland
antiatThytlunic drugs) may be of benefit
epithelium of lactating mammals ai1d myobut may not be economically feasible in cai·dial necrosis in birds and mammals.

livestock.

Persin isolated from avocado leaves has
caused lesions similar to those rep01ted in
natural cases.

BREAD DOUGH

Clinical Findings: In lactating anin1als,

Raw bread dough ma.de with yeast poses
sterile mas ti tis occurs within 24 hr of
mechanical and biochemical hazards when
exposure to avocado, accompanied by a
ingested, including gastric distention,

75%decrease in milk production. Affected
metabolic acidosis, and CNS depression.

matnmary glands are firm, swollen, and

Although any species is susceptible, dogs
produce watery, curdled milk. Lactation
ai·e most conunonly involved because of
may provide a degree of protection against
their indiscriminate ea.ting habits.

myocardial ir\jury when avocado is ingested
at lower doses. In nonlactating manunals, or Pathogenesis: The watm, moist at higher doses, myocai·dial insufficiency
environment of the stoma.ch serves as an
may develop within 24-48 hr of ingestion
efficient incubator for the replication of
and is characterized by lethai·gy, respiratory
yeast within the dough. The expanding
distress, subcutaneous edema, cyanosis,
dough mass ca.uses the stoma.ch to distend,
cough, exercise intolerance, and death.

resulting in vascular compromise to the

Horses may develop edema of the head,
gastric wall similar to that seen in gast1ic
tongue, and brisket. Birds develop lethargy,
dila.tation/volvulus. With sufficient gastric
dyspnea, anorexia, subcutaneous edema of
distention, respiratory compromise occw'S.

the neck and pectoral regions, and may die.

Yeast fem1entation products include
ethanol, which is absorbed into the

Lesions: Mai1m1ary glat1ds are edematous
bloodstream, resulting in inebriation and
and reddened, with wa.te1y, curdled milk. In
metabolic acidosis.

animals with cardiac insufficiency, there is
congestion of lungs at1d liver, often with

Clinical Findings: Early clinical signs
dependent subcutaneous edema. There may may include unproductive attempts at be pulmonaiy edema and free fluid within
emesis, abdominal distention, and

2966

FOOD HAZARDS
depression. As ethanol intoxication
methylxanthines theobromine (3, 7-climethdevelops, the anin1al becomes ataxic and ylxanthine) and caffeine (1,3,7-tJ.imethyldiso1iented. Eventually, profound CNS
xanthine). Although the concentration of
depression, wealrness, recumbency, coma,
theobromine in chocolate is 3-10 times that

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hypothem1ia, or seizures may be seen.

of caffeine, both constituents contribute to

Death is usually due to the effects of the
the clinical syndrome seen in chocolate
alcohol rather than from gastric distention;
toxicosis. The exact amount of methylxanhowever, the potential for dough to trigger thines in chocolate varies because of the
gastric dilatation/volvulus in susceptible
natural variation of cocoa beans and
dog breeds should not be overlooked.

variation within brands of chocolate
products. However, in general, the total

Diagnosis: A presumptive diagnosis can
methylxanthine concentration of d1y
be based on history of exposure and clinical
cocoa powder is -800 mg/oz (28.5 mg/g),
signs. Blood ethanol levels are consistently
unsweetened (baker's) chocolate is
increased in cases of bread dough toxicosis.

-450 mg/oz (16 mg/g), semisweet chocolate

Differential diagnoses include gastric
and sweet dark chocolate is -150-160 mg/oz
dilatation/volvulus, foreign body obstruc

(5.4-5. 7 mg/g), and milk chocolate is
tion, ethylene glycol toxicosis, and ingestion -64 mg/oz (2.3 mg/g). Chocolate bars of other CNS depressants ( eg, benzodiazlabeled as a percentage of cocoa/cacao are epines).

based on unsweetened chocolate, ie, a 65%
cacao bar would contain -293 mg ( 450 mg x

Treatment: With recent ingestions in

0.65) of methylxanthines per oz (10.4 mg/g).

asymptomatic aninlals, emesis may be

White chocolate is an insignificant source of
attempted, although the glutinous nature
methylxanthines. Cocoa bean hulls contain
of bread dough may make removal via

-255 mg/oz (9.1 mg/g) methyl.xanthines.

emesis difficult. In anin1als in which emesis

The LD,,o of both caffeine and theobro

( whether induced or spontaneous) has
mine is reportedly 100-200 mg/kg, but
been unsuccessful, gastric lavage may be
severe signs and deaths may occur at much
attempted. Cold water introduced into
lower dosages, and individual sensitivity to
the stomach may slow the rate of yeast
methyl.xanthines vruies. ln general, mild
fennentation and aid in dough removal. In
signs (vomiting, dirui:hea, polydipsia)

rare cases, surgical removal of the dough
may be seen in dogs ingesting 20 mg/kg,
mass may be required. Animals presenting
cardiotoxic effects may be seen at
with signs of alcohol toxicosis should be

40-50 mg/kg, and seizures may occur at
stabilized and any life-threatening condidosages �60 mg/kg. One ounce of milk tions corrected before attempts to remove
chocolate per pound of body weight is a
the dough are made. Alcohol toxicosis is
potentially lethal dose in dogs.

managed by correcting acid-base abnormalities, managing cardiac arrhythmias Pathogenesis: Theobromine and caffeine
as needed, and maintaining nom1al body
are readily absorbed from the GI tJ.·act and
temperature. Providing fluid diuresis to
widely distributed throughout the body.

enhance alcohol elin1ination may be helpful

They are metabolized in the liver and

Anecdotally, yohimbine (0.1 mg/kg, IV) has
m1dergo enterohepatic recycling. Methylbeen used to stimulate severely comatose xanthines ru·e excreted in the m·ine as
dogs with alcohol toxicosis.

both metabolites and unchanged parent
compounds. The half-lives of theobromine

CHOCOLATE
and caffeine in dogs ru·e 17.5 hr and 4.5 hr,
respectively.

Chocolate toxicosis may result in poten

Theobromine ruid caffeine competitively
tially life-threatening cardiac arrhythmias
inhibit cellular adenosine receptors,
and CNS dysfunction. Chocolate poisoning
resulting in CNS stimulation, diuresis, ruid
occurs most commonly in dogs, although
tachycru·dia. Methylxanthines al o increase
many species are susceptible. ContJ.ibuting
intracellular calcimn levels by increasing
factors include indiscriminate eating habits
cellular calcium entry ruid inhibiting
and readily available sources of chocolate.

intracellular sequestration of calcium by

Deaths have also been reported in livestock
the sarcoplasmic reticulum of striated
fed cocoa by-products and in animals
muscle. The net effect is increased strength
consuming mulch from cocoa-bean hulls.

and contractility of skeletal ruid cardiac
muscle. Methylxanthines may also

Etiology: Chocolate is derived from the
compete for benzodiazepine receptors
roasted seeds of Theobroma cacao. The
within the CNS ruid inhibit phosphodiesterprimary toxic principles in chocolate are the ase, resulting in increased cyclic AMP

FOOD HAZARDS

2967
levels. Methylxanthines may also increase
tion), decontamination should be percirculating levels of epinephrine and formed. Induction of emesis using
norepinephrine.

apomorphine or hydrogen peroxide should
be initiated; in aninlals that have been

Clinical Findings: Clinical signs of

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sedated because of seizure activity, gastric
chocolate toxicosis usually occur within
lavage may be considered. Activated

6--12 hr of ingestion. Initial signs may
charcoal (1-4 g/kg, PO) should be adminisinclude polydipsia, vomiting, dian·hea, tered; because of the enterohepatic
abdominal distention, and restlessness.

recirculation of methylxanthines, repeated

Signs may progress to hyperactivity,
doses should be ad.ministered. every 12 hr in
polyuria, ataxia, rigidity, tremors, and
symptomatic animals for as long as signs
seizures. Tachycardia, premature ventricuare present ( control vomiting with lar contractions, tachypnea, cyanosis,
metoclopramide, 0.2-0.4 mg/kg, SC or IM,
hypertension, hyperthermia, bradycardia,
qid. as needed).

hypotension, or coma may occur. Hypoka

Other treatment for symptomatic animals
lemia may occur late in the course of the
includes maintaining thermo regulation,
toxicosis, contributing to cardiac dysfunccorrecting acid-base and electrolyte tion. Death is generally due to cardiac
abnormalities, monitoring cardiac status
arrhythmias, hyperthem1ia, or respiratory
via electrocardiography, and placing a
failure. The high fat content of chocolate
urinary catheter (methylxanthines and their
products may tiigger pancreatitis in
metabolites can be reabsorbed. across the
susceptible animals.

bladder wall). Clinical signs may persist up

Lesions: No specific lesions may be
to 72 hr in severe cases.

found in animals succumbing to chocolate
toxicosis. Hyperemia, hemorrhages, or

MACADAMIA NUTS
congestion of multiple organs may occur as
agonal changes. Severe arrhythmias may

Ingestion of macadamia nuts by dogs has
result in pulmonary edema or congestion.

been associated. with a nonfatal syndrome

Chocolate or cocoa bean hulls may be
characterized. by vomiting, ataxia, weakpresent in the GI tract at necropsy.

ness, hypertherrnia, and depression. Dogs
are the only species in which signs have

Diagnosis: Diagnosis is based on history
been repo1ted.

of exposure, along with clinical signs.

Amphetamine toxicosis, ma huang/guarana

Etiology: Macadamia nuts are cultivated.

( ephedra/caffeine) toxicosis, pseudoephedfrom Macadamia inlegrifolia in the contirine toxicosis, cocaine toxicosis, and nental USA and M tetraphylla in Hawaii
ingestion of antihistamines, antidepresand Australia. The mechanism of toxicity sants, or other CNS stimulants should be
is not known. Dogs have shown signs after
considered in the differential diagnosis.

ingesting 2.4 g of nuts/kg body weight. Dogs
experin1entally dosed with commercially

Treatment: Stabilization of symptoprepared. macad.an1ia nuts at 20 g/kg matic animals is a priority in treating
developed clinical signs within 12 hr and
chocolate toxicosis. Methocarbamol
were clinically nom1al without treatment

(50-220 mg/kg, slow IV; no more than
within 48 hr.

330 mg/kg/day) or diazepam (0.5-2
mg/kg, slow IV) may be used for tremors

Clinical Findings: Within 12 hr of ingestion, and/or mild seizures; barbiturates may be
dogs develop weakness, depression,
required for severe seizures. Arrhythmias
vomiting, ataxia, tremors, and/or hyperther-
should be treated as needed: propranolol

1nia. 'Iremors may be secondary to muscle

(0.02-0.06 mg/kg, slow IV) or metoprolol
weakness. Macadamia nuts may be identified.

(0.2-0.4 mg/kg, slow IV) for tachyarrhythin vomitus or feces. Mild transient increases mias, atropine (0.01-0.02 mg/kg) for
in sefUill triglycerides, lipases, and alkaline
bradyarrhythmias, and lidocaine (1-2
phosphatase were reported. in some dogs
mg/kg, IV, followed by 25-80 mg/kg/min
experin1entally dosed with macad.arnia nuts;
infusion) for refractory ventricular tachthese values quickly returned to baseline.

yarrhythmias. Fluid diuresis may assist

Signs generally resolve within 12-48 hr.

in stabilizing cardiovascular function
and hastening urinary excretion of

Diagnosis: Diagnosis is based on history
methylxanthines.

of exposure and clinical signs. Differential

Once animals have stabilized, or in
diagnoses include ethylene glycol toxicosis,
animals presenting before clinical signs
ingestion of hypotensive agents, and
have developed ( eg, within 1 hr of inges-
infectious diseases (eg, viral enteritis).

2968

FOOD HAZARDS

Treatment: For asymptomatic dogs with
with 3% hydrogen peroxide (2 rnUkg; no
recent ingestion of more than 1-2 g/kg,
more than 45 mL), followed by activated
emesis should be induced; activated charcoal charcoal. With large ingestions or in cases may be of benefit with large ingestions.

in which vomiting and/or diarrhea has

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Fortunately, most symptomatic dogs recover
spontaneously developed within 12 hr of
without any specific treatment. Severely
ingestion of grapes or raisins, aggressive
affected dogs may be given supportive
fluid diuresis for a minimum of 48 hr is
treatment such as fluids, analgesics, or
recommended. Renal function and fluid
antipyretics.

balance should be monitored during fluid
administration. For oliguric dogs, urine

RAISINS AND GRAPES
production may be stimulated by using
dopamine (0.5-3 mcg/kg/min, IV) and/or

Ingestion of grapes or raisins has resulted
furosemide (2 mg/kg, IV). Anuric dogs are
in development of an uric renal failure in
unlikely to swvive unless peritoneal dialysis
some dogs. Cases reported to date have
or hemodialysis is performed; even then,
been in dogs; anecdotal reports exist of
the prognosis is guarded.

renal failure in cats and ferrets after
ingestion of grapes or raisins. It is not

XYLITOL
known why many dogs can ingest grapes or
raisins with impunity while others develop

Xylitol is a sugar alcohol used to sweeten
renal failw·e after ingestion. The condition
sugar-free products such as gwns, candies,
has not been reproduced experimentally,
and baked goods. Ingestion of xylitol or
although raisin extracts have been shown
xylitol-containing products by dogs has
to cause damage to canine kidney cells in
resulted in development of hypoglycemia
vitro.

and, less commonly, hepatic injwy and/or
failure. Dogs are the only species in which

Pathogenesis: The exact mechanism of
xylitol toxicosis has been reported.

toxicity is unknown, although the primary
injwy appears to be in the proximal renal

Pathogenesis: In most manm1als, xylitol
tubular epitheliwn. Affected dogs develop
has no significant effect on insulin levels,
an uric renal failure within 72 hr of ingestion
but in dogs, xylitol stinlulates a rapid,
of grapes or raisins. A clear dose-response
dose-dependent insulin release that can
relationship has not been determined, but
result in profound hypoglycemia. Dosages
as few as 4-5 grapes were implicated in the
of xylitol over -75-100 mg/kg (34--45 mg/lb)

death of an lS-lb (8.2-kg) dog.

have been associated with hypoglycemia in
dogs. Some dogs ingesting xylitol at dosages

Clinical Finding:;: Most affected dogs

>500 mg/kg (227 mg/lb) may develop severe
develop vomiting and/or diarrhea within
hepatic insufficiency or failure, the

6-12 hr of ingestion of grapes or raisins.

mechanism of which is unknown.

Other signs include lethargy, anorexia,
abdominal pain, weakness, dehydration,

Clinical Findings: Signs of hypoglycemia
polydipsia, and tremors lShivering). Serwn
can develop within 30 min of ingestion or
creatinine levels tend to 1ise early and
may be delayed up to 12-18 hr if the xylitol
disproportionately compared with serwn
is in a substrate that slows its absorption
urea nitrogen levels. Oliguric or an uric

(eg, some gum products). Clinical signs of
renal failure develops within 24-72 lu-
hypoglycemia include vomiting, weakness,
of exposure; once anwic renal failure
ataxia, depression, hypokalemia, seizures,
develops, most dogs die or are euthanized.

and coma. Signs of liver injwy may not

Transient increases in serum glucose, liver
occur until �24-48 hr after ingestion of
enzymes, pancreatic enzymes, serum
xylitol, although increases in liver enzymes
calcium, or serw11 phosphorus develop in
are often detectable within 8-12 hr of
some dogs.

ingestion. Clinical signs of liver injwy
include depression, vomiting, icterus, and

Diagnosis: Diagnosis is based on history
coagulopathy; other findings include
of exposure, along with clinical signs. Other
hyperbilirubinemia, tlu·ombocytopenia, and
causes of renal failure ( eg, ethylene glycol,
hyperphosphatemia. Hyperphosphatemia is
cholecalciferol) should be considered in the
considered a poor prognostic indicator,
differential diagnosis.

because it was present in 4 of 5 dogs that
died of liver failure after xylitol ingestion

Treatment: Prompt decontamination of

(phosphorus was not measured in tl1e fifth
significant ingestion of grapes or raisins
dog). Not all dogs that develop xylitolis recommended. Emesis may be induced induced liver injwy develop hypoglycemia.

HERBICIDE POISONING

2969

Diagnosis: Diagnosis is based on clinical
should be monitored every 1-2 hr for at
findings and history of exposure. Other
least 12 hr, while liver values should be
causes of hypoglycemia include hypoglyceevaluated every 24 hr for at least 72 hr. If mic drugs, juvenile hypoglycemia, hunting
hypoglycemia develops, it should be

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dog hypoglycemia, insulinoma, and
managed with dextrose IV boluses and/or
parenteral insulin overdose. Differential
constant-rate infusions. Hypoglycemia may
diagnoses for liver insufficiency include
persist as long as 24 hr or more, so
infectious ( eg, leptospirosis, viral hepatitis),
treatment should be continued until the dog
enviromnental (eg, heat stroke, trauma),
can maintain a nonnal blood glucose level
and toxic ( eg, iron, acetan1inophen,
without supplemental dextrose. Dextrose
mushroom, blue-green algae, cycad palms)

should be administered to dogs ingesting
causes. Lesions of dogs succumbing to liver
xylitol at >500 mg/kg (227 mg/lb), even
injury have included hepatic necrosis with
though normoglycemic, and hepatoprotecloss of normal hepatic architecture.

tants such as N -acetylcysteine, S-adenosylmethionine, and silymarin should be Treatment: Because of the potential for
considered. Treatment of coagulopathy or
rapid onset of clinical signs of hypoglyceother manifestations of liver insufficiency mia, emesis should ideally be attempted
should be performed as needed. The
only under veterinary supervision and in
prognosis for uncomplicated hypoglycemia
asymptomatic aninlals. Activated charcoal
is good, if prompt treatment is obtained.

does not appreciably bind xylitol and is not

Mild increases in liver enzyme usually
reconunended. If> 75-100 mg/kg (227 mg/lb) resolve within a few days. Severe increases of xylitol has been ingested, a.ninlals should
in liver enzymes and/or signs of liver
be hospitalized and baseline blood glucose
insufficiency indicate a more guarded
values measured; dogs ingesting >500 mg/kg prognosis; in one study, 62.5% of dogs with (227 mg/lb) of xylitol should have baseline
signs of liver injtu)' died or were euthanized
liver values measured. Blood glucose
despite aggressive veterinat)' intervention.

HERBICIDE POISONING

Herbicides are used routinely to control
animals occurs. The tinle recommended
noxious plants. Most of these chemicals,
before treated vegetation is grazed or used
par-ticularly the more recently developed
as animal feed is available for a nwnber of
synthetic organic herbicides, are quite
products.

selective for specific plants and have low

Most health problems in animals result
toxicity for man1mals; other, less-selective
from exposme to excessive quantities of
compounds ( eg, sodium arsenite, arsenic
herbicides because of improper or careless
trioxide, sodium chlorate, anm10nium
use or disposal of containers. When
sulfan1ate, borax, and many others) were
herbicides are used properly, poisoning
fonnerly used on a large scale and are more
problems in veterinary practice are rare.

toxic to animals.

With few exceptions, it is only when animals

Vegetation treated with herbicides at
gain direct access to the product that acute
proper rates normally will not be hazardous
poisoning occurs. Acute signs usually will
to animals, including people. Particularly
not lead to a diagnosis, although acute GI
after the herbicides have dried on the
signs are frequent. All common differential
vegetation, only small amounts can be
diagnoses should be excluded in animals
dislodged. When herbicide applications
showing signs of a sudden onset of disease
have been excessive, dan1age to lawns,
or sudden death. The case history is critical.

crops, or other foliage is often evident.

Sickness after feeding, spraying of pastures

The residue potential for most of these
or crops adjacent to pastures, a change in
agents is low. However, runoff from
housing, or direct exposme may lead to a
agricultmal applications and entrance into
tentative diagnosis of herbicide poisoning.

drinking water carmot be excluded. The

Generally, the nature of exposure is har·d to
possibility of residues should be explored if
identify because of storage of herbicides in
significar1t exposure of food-producing
mis- or unlabeled containers. Unidentified

2970

HERBICIDE POISONING
spillage of liquid from containers or powder
subsumed under the term "biomonitoring."

from tom or damaged bags near a feed

Accurate biomonitoring is an in1portant tool
source, or visual confusion with a dietary
to evaluate htunan or animal exposure to
ingredient or supplement, may cause the
such herbicides by measuring the levels of
exposure. Once a putative chemical source
these chemicals, their metabolites, or altered

VetBooks.ir
has been identified, an anin1al poison
biologic structures or functions in biologic
control center should be contacted for
materials such as urine, blood or blood
information on treatments, laboratory tests, components, exhaled air, hair or nails, and and likely outcome.

tissues. The use of urine is advantageous

Chronic disease caused by herbicides
because of ready availability. As such, urine
is even more difficult to diagnose. It
has been used for biomonitoring of several
may include a history of herbicide use in
herbicides, including 2,4-D, 2,4,5-T, MCPA
proximity to the animals or animal feed or

(2-methyl- 4-chlorophenoxyacetic acid),
water source, or a gradual change in the
atrazine, diuron, alachlor, metolachlor,
animals' perfonnance or behavior over a
paraquat, diquat, in1azapyr, imazapic,
period of weeks, months, or even years.

in1azethapyr, imazan1ox, in1azaquin, and

Occasionally, it involves manufacture or
irnazamethabenz-methyl herbicides, with
storage of herbicides nearby. San1ples of
the objective to assess exposure and health
possible sources (ie, contanunated feed
risk to exposed anin1als.

and water) for residue analysis, as well as

If pois011ing is suspected, the first step
tissues from exposed animals taken at
in management is to halt further exposure.

necropsy, are essential. Months or even

Anin1als should be separated from any
years may be required to successfully
possible source before attempting to
identify a problem of chronic exposure.

stabilize and support them. If there are

To recognize whether an animal has
life-threatening signs, efforts to stabilize
been exposed to herbicides or accidental
animals by general mitigation methods
poisoning, standardized analytical proceshould be started. Specific antidotal dures for diagnostic investigation of biologic
treatments, when available, may help to
mate1ials have become established and are
confirm the diagnosis. As time pennits, a

•ttN•i• HERBICIDE POISONING

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

Acetochlor

2,148--2,950 mg/kg

Dog , lyr

Rabbit 4,1 66 mg/kg

12 mg/kg/day

Acifluorfen

1,300 mg/kg (F)

Rat, 2yr

Rabbit >2,000 mg/kg

18 0ppm

Acrolein

2 9mg/kg

Rat, 13wk

Rabbit 231 mg/kg

150mg/Lin
drinking water

Alachlor

930-1,200 mg/kg

Dog, 90days

Rabbit 1 3,300 mg/kg

<200 mg/kg/day

Ametryn

1,009-1,405 mg/kg

Rat reproduction,

Rabbit 2,020 mg/kg

50ppm
a-Metolachlor

2,675-2,952 mg/kg

Dog, 90days

Rat 2,020 mg/kg

0.01 25 mg/kg/day

HERBICIDE POISONING

2971
more detailed history and investigation
herbicides (see TABLE 1). Comparative toxic should be completed. The owner should be
doses (TD) and lethal doses (LD) of
made aware of the need for full disclosure
selected herbicides in domesticated
of facts to successfully dete1mine the
species, such as monkeys, cattle, sheep,
source of poisoning, eg, unapproved use
pigs, cats, dogs, and chickens, is also

VetBooks.ir
or failure to properly store a chemical.

summarized (see TABLE 2). The infom1ation is only a guideline, because the toxicity of

Toxicity and Management of
herbicides may be altered by the presence
of other ingredients ( eg, impurities,

Poisoning
surfactan'ts, stabilizers, emulsifiers)

There are >200 active ingredients used as
present in the compound. With a few
herbicides; however, some of them are
exceptions, most of the newly developed
believed to be obsolete or no longer in use.

chemicals have a low order of toxicity to

Of these, several have been evaluated for
mammals. However, some herbicides, such
their toxic potential and are discussed
as atrazine, buturon, butiphos, chloridazon,
below. More specific information is
chlorpropham, cynazine, 2,4-D and 2,4,5-T
available on the label and from the
alone or in combination, dichlorprop,
manufacturer, cooperative extension
dinoseb, dinoterb, linuron, mecoprop,
service, or poison control center. Selected
monolinuron, MCPA ( 2-methyl-4-chloroinformation on herbicides, such as the phenoxyacetic acid), prometryn, propaacute oral toxic dose (LD50) in rats, the chlor, nitrofen, silvex, TCDD ( a common
amount an animal can be exposed to
contaminant during manufacturing process
without being affected (no adverse effect
of some herbicides such as 2,4-D and
level), the likelihood of problems caused by

2,4,5-T), and tridiphane, are known to have
dem1al contact in rabbits ( dermal LD50, eye
adverse effects on development of embryos
and skin irritation), deleterious effects on
and reproduction abnonnalities in
avian species, and toxicity to fish in water,
experin1ental anin1als. A list of such
is included for some commonly used
chemicals is sun1rnarized in TABLE 3.

•4H•!• HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

LC50 5 day

LC50 96hr

Skin-mild

Bobwhite quail and Mallard Rainbow trout 0.45 mg/L

Eye-mild
duck 5,620 mg/kg

LC50 8day

LC50 96hr

Skin-moderate

Mallard duck >

Rainbow trout 31 mg/L

Eye-severe

10,000 mg/kg

LD50 (oral)

LC50 24 hr

Skin-severe

Bobwhite quail 19 mg/kg

Bluegill and Rainbow trout Eye-severe

Mallard duck 9. 1 mg/kg

0.0 24 mg/L

Skin-mild

LD50 (oral)

Skin-irritation

Birds >2, 250 mg/kg

Guinea pig-dem1al

LC50 5 day
sensitization

Birds >5,620 ppm

Eye-mild

LC50 8day

LC50 96hr

Skin-slight

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-mild duck >10,000 ppm

3.9-lOppm

C continued)

2972

HERBICIDE POISONING
lrtNIII HERBICIDE POISONING (cont'inued)

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Atrazine

2,000-3,080 mg/kg

Dog, l yr

Rabbit 7,500 mglkg

150 ppm

Rat, 2 yr

IO ppm

Amitrole

4,080 mglkg (M)

Rat, 13wk

Rat >5,000 mglkg

2 mg/kg/day

Ammonium

3,900 mglkg

Rat, 105 days
sulfarnate

10,000 mglkg/day

Bensulfron methyl >5,000 mglkg

Rat, dog, 2 yr

Rat >2,000 mglkg

750 ppm in diet

Bensulidec

271-770 mglkg

Dog,90days

Rabbit 3,950 mg/kg

12.5 mglkg/day

Bentazon
l,lOO mglkg

Rat, 90days

Rat >2,500 mglkg

( cat 500 mglkg)

3.5 mglkg/day

Dog, 90days

7.5 mglkg/day

Bispyribac sodium

Rat, 2 yr

1.1 mglkg/day (M)

1.4 mg/kg/day (F)

Borax

2,000-6,000 mglkg

Bromacil

5,200 mglkg

Rat, clog, 2 yr

Rabbit >5,000 mglkg

250 mglkg/day

Bromoxynil

190-779 mglkg

Rat, 90days

Rabbit >2,000 mglkg

50 mglkg/day

Butachlor"

2,000-3,300 mglkg

Rabbits maternal

Rat> 13.3 glkg
and fetal effects,

50 mglkg/day

Butylatec

>5,431 mglkg (M)

Rat, 2 yr

Rabbit >4,640 mglkg

4,659 mglkg (F)

20 mglkg/day

Dog, 1 yr

25 mglkg/day

Carfentrazone ethyl >5,000 mglkg

Rat, 2 yr

Rat >5,000 mglkg

9 mg/kg/day (M)

3 mglkg/clay (F)

HERBICIDE POISONING

2973

•tM•!• HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

VetBooks.ir

LC60 8day

LC6096hr

Skin-slight

Mallard duck

Rainbow trout 8.8 mg/L

> 10,000 ppm in diet

LD60

Skin-mild

Mallard duck 2,000 mg/kg

Eye-mild

LD,;o

LC60 48hr

Skin-none

Bobwhite quail

Crucian carp 1,000- 2,000

3,000mg/kg
mg/L

LC6096hr

Skin-none

Bluegill and Rainbow

Eye-serious
trout >150 ppm

LD50

LC6096hr

Eye-none

Bobwhite quail 3 wk

Bluegill 1.4 mg/L

50 mg/kg, poor hatchability Rainbow trout 0. 7 mg/L

LD60

LC6096 hr

Slight iITitant

Japanese quail 720 mg/kg

Bluegill 616 mg/L

Mallard duck 2,000 mg/kg

Rainbow trout 1,060 mg/L

LC60

LC5096hr

Skin-minor

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-minor duck >5,620 ppm

>100ppm

LC60 8day

LC60 48hr

Skin-irritating

Bobwhite quail and Mallard Bluegill 71 mg/L

Eye-irritating
duck >10,000 mg/kg

Rainbow trout 56 mg/L

Acute LD60

LC6096hr

Skin-none

Bobwhite quail 100 mg/kg

Rainbow trout 0.05 mg/L

Eye-none

Mallard duck 200 mg/kg

Skin-none

Eye-moderate

Guinea pig-dermal
sensitization

LC50 8day

LC6096hr

Skin-moderate

Bobwhite quail 40,000

Bluegill 6.9 mg/L

Eye-mild
mg/kg

Rainbow trout 4.2 mg/L

Mallard duck 46,400 ppm in
diet

LC60

LC6096 hr

Skin-none to slight

Bobwhite quail and Mallard Bluegill 2 ppm

Eye-minimum
duck >5,620 ppm

Rainbow trout 16 ppm

( continued)

2974

HERBICIDE POISONING
lr�=IIII HERBICIDE POISONING (continued)

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Chloramben

5,620 mg/kg

Rabbit >3,160 mg/kg

Chlorotoluron

>10,000 mg/kg

Chlorpropham

4,100-7,000 mg/kg

Rat , dog, 2 yr

100-350 mg/kg/day

Chlorsulfuron

5,545 mg/kg (M)

Rat,2yr

Rabbit >3,400 mg/kg

6,293 mg/kg (F)

100 ppm in diet

Chlorthal dimethyl

3,000-12,000 mg/kg Rat , 2yr

Rabbit >2,000 mg/kg

<50 mg/kg/day

Clethodim

1,630 mg/kg (M)

Dog, lyr

Rabbit >5,000 mg/kg

1,360 mg/kg (F)

>l mg/kg/day

Clodinafop-

1,392 mg/kg (M)

Dog, 90days

Rabbit >2,000 mg/kg
propargyl

2,271 mg/kg (F)

0.346 mg/kg/day (M)

1.89 mg/kg/day (F)

Clomazone

2,077 mg/kg (M)

Dog, 1 yr

Rabbit >2,000 mg/kg

1,369 mg/kg (F)

<2.5 mg/kg/day

Clopyralid

>4,300 mg/kg

Rat , 2yr

Rabbit >2,000 mg/kg

50 mg/kg/day

Cloransulam-methyl >5,000 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

10 mg/kg/day

Copper chelate

498mgfkg

Rabbit >2,000 mg/kg

Copper sulfate

470mgfkg

Rabbit >8,000 mg/kg

Cyanazined

182-334 mg/kg

Dog, 2yr

Rabbit >2,000 mg/kg

<225 mg/kg/day

Cycloate

2,000--3,190 mg/kg

Dog, 240 mg/kg/day Rabbit >4,640 mg/kg

HERBICIDE POISONING

2975

•tM•f • HERBICIDE POISONING (continued) Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

VetBooks.ir

LC50 8 day

Not toxic to fish

Skin-mild

Mallard duck > 4,640 mg/kg

Eye-mild

LC50 96 hr

Rainbow trout> 100 mg/L

LD50 8day

LC50 48 hr

Skin-moderate

Mallard duck >2,000 mg/kg Bluegill 6.3-6.8 mg/L

Eye-moderate

Rainbow trout3-6 mg/L

LC50 8day

LC50 96 hr

Skin-none

Mallard duck >5,000 mg/kg Rainbow trout >250 mg/L

Eye-mild

LD50 young

Not toxic to fish

Skin-none

Bobwhite quail 5,500 mg/kg

Eye-mild

LC50 8day

LC50

Skin-none

Bobwhite quail 4,270 ppm

Bluegill 13 ppm

Eye-moderate

Mallard duck 3,978 ppm in

Rainbow trout 18 ppm
diet

LC50

LC50

Skin-none

Birds >5,000 ppm

Freshwater fish 0.3 ppm

Eye-slight to severe

LD50 8 day

LC50 96 hr

Skin-mild

Bobwhite quail and Mallard Bluegill 3 4 mg/L

Eye-moderate
duck 5,620 ppm in diet

Rainbow trout 19 mg/L

LC so

LC50 96 hr

Skin-mild

Bobwhite quail and Mallard Bluegill 125 mg/L

Eye-severe
duck > 4,640 ppm in diet

Rainbow trout 103.5 mg/L

LC50 5 day

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill > 15 4 ppm

Eye-slight
duck >5,620 ppm

Rainbow trout >86 ppm

LC50 8 day

LC50 96 hr

Skin-slight

Mallard duck> 1,000 ppm in Bluegill 1.2-7.5 mg/L

Eye-moderate
diet

Rainbow trout <0.2- 4 mg/L

LD50 (oral)

LC5096hr

Skin-moderate

Pheasant 1,000 ppm in diet Bluegill 4.4-7.3 mg/L

Eye-severe

( estimated)

Rainbow trout 0.135 mg/L

LD50

LC50 96hr

Skin-none

Bobwhite quail 400 mg/kg

Bluegill 23 mg/L

Eye-mild

Mallard duck >2,000 mg/kg Rainbow trout 9 mg/L

LC50 7 day

LC50 96hr

Skin-none

Bobwhite quail >56,000

Rainbow trout 5.6 mg/L

Eye-none
mg/kg

(,..,..-1,; ...... ,,,,..,,.1\

2976 HERBICIDE POISONING
l�·HIII HERBICIDE POISONING (continued)

Acute Oral

NOAELa

Compound

LD

VetBooks.ir

50-Rat

(oral)

Acute Dermal LD50

Cyhalofopbutyl

>5,000 mg/kg

Dog

Rat >5,000 mg/kg

46. 7 mg/kg/day (M)

45.9 mg/kg/day (F)

Dalapon

6,600-9,330 mg/kg

Di -allateci

340-460 mg/kg

2,4-D

370-700 mg/kg

Rat, 2yr

Rabbit >2,000 mg/kg

50 mg/kg/day

2,4-D dimethyl-

949-4,650 mg/kg

Dog, l yr

Rabbit >2,000 mg/kg
amin e

1 mg/kg/day

2,4-D isooctyl ester

500-700 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

1 mg/kg/day

Dazomet

551-646 mg/kg (M)

Rat, 2 yr

Rabbit >2,000 mg/kg

335-562 mg/kg (F)

1.6 mg/kg/day

Dicamba
l,707mg/kg

Rat, 2y r

Rabbit >2,000 mg/kg

125 mg/kg/day

Dog, 2yr

50mg/kgday

Dichlob enil

>3,160 mg/kg

Rat, 2y r

Rabbit >1,350 mg/kg

>20 ppm in di et

Pig, 6mo

>50 ppm in di et

Dichlorprop or

700 mg/kg (M)

Rat, 4mg/kg

. Mous e 1,400 mg/kg

2,4-DP

500 mg/kg (F)

Diclosulam

>5,000 mg/kg

Rat, 0.05 mg/kg

Rabbit >2,000 mg/kg

Difenzoquat

617 mg/kg (M)

Dog, lyr

Rabbit >2,000 mg/kg

( methylsulfate)

373 mg/kg (F)

20 mg/kg/day

Diflu fenzopyr

1,600 to

Dog, lyr

Rabbit >5,000 mg/kg

>5,000 mg/kg

28 mg/kg/day (M)

26 mg/kg/day (F)

HERBICIDE POISONING

2977

•i·N•f • HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

VetBooks.ir

LC50 96 hr

Skin-none

Bluegill >99.2 mg!L

Eye-minimal

Rainbow trout >l.65 mg!L

LC50 96hr

Fish 210- 340 mg!L

LC50 96hr

Fish 8.2 mg!L

LC508 day

LC50 96 hr

Skin-none

Mallard duck

Bluegill >300 mg!L

Eye-moderate

>4,640 mg/kg

Rainbow trout 800 mg!L

LC508 day

LC50 96 hr

Skin-minimal

Mallard duck

Bluegill 524 mg!L

Eye-severe

>5,600ppm

Rainbow trout 250 mg!L

As for 2,4-D (above)

Skin-none

Eye-severe

LD50

LC so

Skin-mild

Bobwhite quail

Rainbow trout

Eye-severe

415 ppm in diet

2.4- 16.2 mg!L

LC508 day

LC50 96hr

Skin-moderate

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-extreme duck >4,600 mg/kg

> 1,000 mg!L

LC508day

LC50 96hr

Skin-none

Mallard duck

Bluegill and Rainbow

Eye-mild to moderate

>5,200 ppm in diet
trout 7 mg!L

LCw

LC50

Skin-none

Upland birds , waterfowl

Bluegill 1.1 mg!L

Eye-none

>10,000 ppm in diet

Rainbow trout

100-200 mg!L

LC50

Skin-moderate

Most sensitive aquatic

Eye-moderate
species 10-100 mg!L

LCw8day

LC50 96hr

Skin-mild

Bobwhite quail and Mallard Bluegill 696 mg!L

Eye-mild
duck 4,640 ppm in diet

Rainbow trout 711 mg!L

LC50

LC so

Skin-very slight

Mallard duck >5,620 ppm

Bluegill 135 ppm

Eye-mild to slight

Rainbow trout 106 ppm

(conl'inued)

2978

HERBICIDE POISONING
lr�:1111 HERBICIDE POISONING (contimied)

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Dirnethenamid

429-1,293 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

50-250 ppm in diet

Dinoterb

25mg/kg

Diquat

231-440 mg/kg

Rat reproduction ,

Rabbit >400 mg/kg
l mg/kg/day

Dithiopyr

>5,000 mg/kg

Dog, lyr

Rabbit >5,000 mg/kg

<0.5 mg/kg/day

Diuron

3,400mg/kg

Dog, 2yr

Rat >2,000 mg/kg

25mg/kg

DNOC

25-85mg/kg

Rat , 2yr

Rat 600-2,000 mg/kg

0.59 mg/kg/day

Rabbit 1,000 mg/kg

EPTC (s-ethyldipro- 1,630mg/kg

Dog, 90days

Rabbit 2, 750-
pylthiocarbamate)

20mg/kg

5,000mg/kg

Ethalfluralin

Rat >5,000 mg/kg

Rat , mouse ,

Rabbit >2,000 mg/kg

(dog, cat

90 days

>200mg/kg)

68mg/kg

Ethephon

1,600-4,229 mg/kg

Rat , 2yr

Rabbit >5,000 mg/kg

375 mg/kg/day

Mouse , 78 wk

4.5 mg/kg/day

Fenoxapropd

2,357 mg/kg (M)

Dog, 2yr

Rabbit >1,000 mg/kg

2,500 mg/kg (F)

0.375 mg/kg/day

Fenoxaprop-ethyl"

4,430mg/kg

Dog, 2yr

Rat >5,000 mg/kg

0.9 mg/kg/day

Flamprop-methyl

1,210mg/kg

Dog, 2yr

Rat >294 mg/kg

10 mg/kg/day

HERBICIDE POISONING

2979

•M=i!f • HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

LC

VetBooks.ir
so

LC50

Skin-mild

Bobwhite quail and Mallard Bluegill 6.4 mg/L

Eye-moderate
duck >5,620 ppm in diet

Rainbow trout 2.6 mg/L

LC50

Toxic to fish

Partridges 3-5 ppm in diet

LC50

LC50

Skin-none

Paitridges 270-300

Fish 80-210 mg/L

Eye-mild
ppm in diet

LC50

LC50

Skin-slight

Bobwhite quail and Ma!lai·d Bluegill 0. 7 mg/L

Eye-moderate
duck >5,260 ppm in diet

Rainbow trout 0.5 mg/L

LC50

LC50

Skin-none

Bobwhite quail 1, 730 ppm

Bluegill 7.4 mg/L

Eye-mild

Mallard duck >5,000 ppm in Rainbow trout 4.3 mg/L
diet

LD50

LC50

Skin-erythema and edema

Japanese quail 10-25 mg/kg Fish 0.2-13 mg/L

Eyes-corrosive

Guinea pig--dennal
sensitization

LC50 7 day

LC50

Skin-mild

Bobwhite quail

Bluegill 27 mg/L

Eye-severe

20,000 ppm in diet

Rainbow trout 19 mg/L

LC508day

LC50

Skin-slight to moderate

Bobwhite quail and Mallard Bluegill 0.03-0.1 mg/L

Eye-slight
duck >5,000 ppm

Rainbow trout 0.037-

0.136 mg/L

LC508day

LC50 96 hr

Skin-corrosive

Mallard duck >10,000 ppm Bluegill 222-300 mg/L

Eye-corrosive

Rainbow trout

254-350 mg/L

LD50 Japanese quail

LC50

Skin-slight

>5,000 mg/kg

Bluegill 3.3 mg/L

Eye-serious nonreversible

Rainbow trout 3.4 mg/L
corneal opacity

LC508 day

LC50

Skin-slight

Bobwhite quail ai1d Mallard Bluegill 0.31 mg/L

Eye-moderate
duck 5,620 ppm

Rainbow trout 0.46 mg/L

LD50

LC50 96 hr

Skin-none

Bobwhite quail 4,640 mg/kg Rainbow trout 4. 7 mg/L

Eye-none

Mallard duck >1,000 mg/kg

( continued)

2980

HERBICIDE POISONING
lrl:1111 HERBICIDE POISONING (conl'inued) Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Florasulam

>6,000 mg/kg

Dog, l yr

Rabbit >2,000 mg/kg

5 mg/kg/day

Fluazifop-p-butyl

3,680-

Rat, 90days

Rabbit >2,400 mg/kg

4,096 mg/kg (M)

> 10 mg/kg/day

2,451-

2,721 mg/kg (F)"

Flucarbazone-

>5,000 mg/kg

Dog, l yr

Rat >5,000 mg/kg
sodium

35.9 mg/kg/day

Flufenacet

1,617 mg/kg (M)

Dog, 1 yr

Rat >2,000 mg/kg

589 mg/kg (F)

1.29 mg/kg/day

Flumetsulam

>5,000 mg/kg

Rat >2,000 mg/kg

Flumiclorac

3,200 to

Dog, 1 yr

Rat >2,000 mg/kg

>5,000 mg/kg

100 mg/kg/day

Fluometuron

>8,000 mg/kg

Rat, 103wk

Rat >2 g/kg

125 mg/kg/day

Rabbit 10 g/kg

Fluroxypyr

.>5,000 mg/kg

Dog, 1 yr

Rat >2,000 mg/kg

150 mg/kg/day

Fluthiacet

>5,000 mg/kg

Dog, lyr

Rat >2,000 mg/kg

57.6 mg/kg/day (M)

30.3 mg/kg/day (F)

Foramsulfuron

>3,881 mg/kg

Rat, 2 yr

Rat >5,000 mg/kg

849 mg/kg/day (M)

1,135 mg/kg/day (F)

Fosamine

24,000 mg/kg

Rat, 90days

Rabbit> 1,683 mg/kg
ammonium

1, 000 mg/kg

Glufosinate

1,510-2,030 mg/kg

Dog, lyr

Rat > 1,390 mg/kg

(ammonium salt)

5 mg/kg/day

Glyphosate

4,230-5,600 mg/kg

Dog, 2 yr

Rabbit >5,000 mg/kg

>500 mg/kg/day

HERBICIDE POISONING

2981

•M:i!j• HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

VetBooks.ir

LD 14day

LC 96hr

Skin-none

50

Japanese quail 175 mg/kg

50

Rainbow trout> 100 mg/L

Eye-none

LD 5day

LC

Skin-slight

50

50 96hr

Bobwhite quail >4,659 ppm Bluegill 0.5 mg/L

Eye-mild

Mallard duck >4,321 ppm

Rainbow trout 1.4 mg/L

NOAEC (reproduction)

NOAEL (chronic)

Skin-none

Mallard duck 233 mg/kg/day Rainbow trout 2. 75 mg/L

Eye-minimal

LC 5day

LC

Skin-none

50

Bobwhite quail >5,317 ppm

50

Bluegill 2.26- 2.4 ppm

Eye-minimal

Mallard duck >4,970 ppm

Rainbow trout

3.49- 5.84 ppm

LC

LC,,o

Skin-none

50

Mallard duck >5,620 ppm

Bluegill >300 ppm

Eye-slight

Rainbow trout >293 ppm

LC

LC 96 hr

Skin-severe

50

Mallard duck >5,620 ppm

50

Bluegill 17.4 mg/L

Eye-moderate

Rainbow trout 1.1 mg/L

LC50 96 hr

Bluegill 96 mg/L

Rainbow trout 47 mg/L

Crucian carp 17 mg/L

LC 5day

LC 96hr

Skin-none

50

Mallard duck >5,000 ppm

50

Bluegill 14.3 mg/L

Eye-slight

Rainbow trout

13.4-100 mg/L

LC 5day

LC 96hr

Skin-none

50

Bobwhite quail and Mallard

50

Bluegi\1140 mcg/L

Eye-minimal
duck >5,620 ppm

Rainbow trout 43 rncg/L

LC

Skin-moderate

50

Bobwhite quail and Mallard

Eye-mild
duck >5,000 ppm

10

LC

Skin-none

50

Mallard duck

50

Bluegill 670 mg/L

Eye-moderate to severe

> 10,000 ppm in diet

Rainbow trout 1,000 rng/L

LC 5day

LC 96hr

Skin-slight

50

Japanese quail

50

Bluegill 56-75 mg/L

Eye-moderate to severe

>5,000 mg/kg

Rainbow trout >26. 7 mg/L

LC50 8day

LC 96 hr

Skin-none

Bobwhite quail and Mallard

50

Bluegill 120 mg/L

Eye-slight to moderate
duck 4,500 ppm in diet

Rainbow trout 86 mg/L

( continued)

2982 HERBICIDE POISONING
lfd:1111 HERBICIDE POISONING (contim,ed)

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Hal osulfuron
l,287mg/kg

Dog, 13wk

Rat >5,000 mg/kg

10 mg/kg/day

Hexazin one
l,690mg/kg

Rat, 2yr

Rabbit >5,278 mg/kg

250 mg/kg in diet
lmazamethabenz-

>5,000 mg/kg

Dog, 1 yr

Rabbit >2,000 mg/kg
methyl
l,OOOppm
lmazaquin

>5,000 mg/kg

Dog, 1 yr

Rabbit >2,000 mg/kg
l,OOOppm

Imazamox

>5,000 mg/kg

Dog, 1 yr

Rat >4,000 mg/kg

40,000ppm

Imazapic

>5,000 mg/kg

Dog, 1 yr

Rabbit >2,000 mg/kg

5,000ppm

Imazapyr

>5,000 mg/kg

Dog, 1 yr feeding

Rabbit >2,000 mg/kg
l,OOOppm

Rat 300 mg/kg/day

(teratol ogy)

lmazethapyr

>5,000 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

25 mg/kg/day

Is oproturon

1,800-2,400 mg/kg

Dog, 90days

Rat >3.2 g/kg

Rat, 2yr

3mg/kg/day

Is oxaflutole

>5,000 mg/kg

Dog, lyr

Rat >2,000 mg/kg
l,200ppm

Linuron

1,200-4,000 mg/kg

Dog, 2yr

Rabbit >5,000 mg/kg

6.25 mg/kg/day

( observed anemia)

Maleic hydrazide

>5,000 mg/kg (acid) Dog, 1 yr

Rabbit

>6,950 mg/kg

25mg/kg

>20,000 mg/kg

(Na+ salt)

>3,900 mg/kg

(K+ salt)

MCPA

700-1,160 mg/kg

Rat, 7m o

Rabbit 3,400-

100 mg/kg/day

4,800mg/kg

(l owers wt gain)

HERBICIDE POISONING

2983

•M=i!j• HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

VetBooks.ir

LC50 5 day

LC5()96hr

Skin-slight

Bobwhite quail and Mallard Bluegill> 118 mg/L

Eye-slight
duck >5,620 ppm

Rainbow trout> 131 mg/L

LC50 5-8day

LC5() 96hr

'Skin-none

Bobwhite quail and Mallard Bluegill 370-420 mg/L

Eye-severe but reversible
duck> 10,000 ppm in diet

Rainbow trout

320-420 mg/L

Skin-none

Eye-slight

Skin-slight

LC50

LC5() 96hr

Skin-none

Mallard duck >5,672 ppm

Bluegill >119 ppm

Eye-none

Rainbow trout >122 ppm

Skin-slight

Eye-moderate

LC50 8day

LC5() 96hr

Skin-mild

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-more severe duck >5,000 ppm in diet

>100 mg/L

LD5()

LC5() 96hr

Skin-mild

Bobwhite quail and Mallard Bluegill 420 mg/L

Eye-irritation reversible
duck >2, 150 ppm in diet

Rainbow trout 340 mg/L

LC50 96 hr

Skin-none

Crucian carp 193 mg/L

Eye-none

Rainbow trout 240 mg/L

LC5() 5 day

LC5()96hr

Skin-minimal

Bobwhite quail and Mallard Bluegill >4.5 mg/L

Eye-minimal
duck >4,255 ppm

Rainbow trout > 1. 7 mg/L

LC5() 5-8day

LC0096hr

Skin-mild

Japanese quail >5,000 ppm Bluegill and Rainbow trout Eye-moderate Mallard duck 3,083 ppm in

16mg/L
diet

LD50

LC5() 96hr

Skin-slight

Bobwhite quail and Mallard Bluegill 1,608 mg/L

Eye-severe
duck > 10,000 mg/kg

Rainbow trout 1,435 mg/L

LD50

LC50 96hr

Skin-slight

Bobwhite quail 377 mg/kg

Bluegill and Rainbow trout Eye-moderate

90 mg/L

(continued)

2984

HERBICIDE POISONING

•pj:j•j• HERBICIDE POISONING (continued)

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

MCPB

4,700mg/kg

Rat , 6mo

Rat >2,000 mg/kg

1.6 mg/kg/day

Mecoprop

930-1,2 10 mg/kg

Rat , 90days

Rabbit 900 mg/kg

3.8 mg/kg/day

Dog , 90days

15 mg/kg/day

Mesotrione

>5,050 mg/kg

Rat >5,050 mg/kg

Metam (sodium and 1,800 mg/kg (M)

Rat, 65days

Rabbit
isothiocyanate)

1, 700 mg/kg (F)

(inhalation, in

10,000 mg/kg

97 mg/kg (isothio-
inspired air)

cyanate)

6 hr/day for 5 days/
wk at 0.045 mg/L

Methyl bromide

Acute LC50

Safe threshold for

(inhalation)

people

4.5mg/Lair

0.065 rng/L air

Methyl isothio-

82 mg/kg(M)

Dog, 2 yr

Rabbit
cyanate

10 mg/Lin drinking

2 02 mg/kg (F)

water

145 mg/kg (M)

Metobromuron

2,450-2,500 mg/kg

Rat, 2 yr

Rabbit >2,000 mg/kg

2 50 mg/kg/day

Dog, 100 mg/kg/day

Metolachlor"

800--2, 780 mg/kg

Rat, 90days

Rabbit >5,000 mg/kg

1,000 mg/kg

Rat >10 g/kg

Dog , 90days

500mg/kg

Metosulam

>5,000 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

10 mg/kg/day

Metribuzin

1,090--2,300 mg/kg

Rat, 2 yr

Rat , rabbit

5mg/kg

>2 0,000 mg/kg

Dog, 2 yr

2 .5mg/kg

Napropamide

>5,000 mg/kg

Dog , 13wk

Rabbit >4,640 mg/kg

<100 mg/kg

HERBICIDE POISONING

2985

IHNIII HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

LC50 8day

LC50 96 hr

Skin -moderate

VetBooks.ir

Bobwhite quail and Mallard Bluegill 14 mg/L

Eye-moderate
duck >5,000 ppm in diet

Rainbow trout 4.3 mg/L

LC50

LC50 96hr

Skin-slight

Bobwhite quail and Mallard Bluegill > 100 mg/L

Eye-intense
duck 5,000- 5,500 ppm in

Rainbow trout 124 mg/L
diet

1050

LC50 96hr

Skin-slight

Bobwhite quail

Bluegill and Rainbow

Eye-moderate

>2,000 mg/kg
trout> 120 mg/L

Mallard duck

>5,200 mg/kg

LC50

LC50 96hr

Skin-corrosive

Bobwhite quail > 10,000

Bluegill 0.04 7 mg/L

Eye-corrosive

Mallard duck >5,000 ppm in Rainbow trout 0.029 mg/L
diet

Acute toxicity

Skin-severe

Bluegill 11 mg/L

Eye-severe

LC50 5day

LC50 96hr

Skin-corrosive

Mallard duck

Bluegill 0.13 mg/L

Eye-severe

10,936 mg/kg

Rainbow trout 0.37 mg/L

LC50 8day

LC50 96 hr

Skin-moderate

Bobwhite quail

Bluegill 4 mg/L

Eye-moderate

>20,000ppm

Rainbow trout 3 mg/L

Mallard duck

>4,640 ppm in diet

LC50 5day

LC50 96hr

Skin-none

Bobwhite quail and Mallard Bluegill 15 mg/L

Eye-none
duck> 10,000 ppm in diet

Rainbow trout 3 mg/L

Skin-none

Eye-slight

LC50

LC50 96hr

Skin-none

Bobwhite quail

Bluegill SO mg/L

Eye-none
and Mallard duck

Rainbow trout

>4,000 ppm in diet

64- 76 mg/L

LC50 5day

LC50 96 hr

Skin-none

Bobwhite quail

Bluegill 20- 30 mg/L

Eye-none

>5,600ppm

Rainbow trout 9- 16 mg/L

Mallard duck

7,200 ppm in diet

( continued)

2986

HERBICIDE POISONING
lttHIII HERBICIDE POISONING ( continued)

Acute Oral

NOAELR

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Naptalam

>5,000 mg/kg

Rat , dog, 90 days

Rabbit
l ,770mg/kg
l,OOOmg/kg

>20,000 mg/kg

(Na+ salt)

(Na+ salt)

Nicosulfuron

Mouse >5,000 mg/kg Dog, 1 yr

Rat, rabbit

>5,000ppm

>2,000 mg/kg
in diet(M)

Oxadiazon

>5,000 mg/kg

Rat , dog, 2 yr

Rabbit >2,000 mg/kg
lOOmg/kg

Oxyfluorfen

Rat, dog

Rat, 2yr

Rabbit >5,000 mg/kg

>5,000 mg/kg

2mg/kg

Dog, 2.5 mg/kg

Paraquat

150-283 mg/kg

Rat, 2yr

Rat >2,000 mg/kg

(dichloride)

l.25mg/kg

(finished product)

Dog, 1 yr

0.45mg/kg

Pebulate
l,120mg/kg

Rat , 2yr

Rabbit 4,640 mg/kg

15 ppm in diet

(eye lesions)

Pendimethalin

1,050 to

Dog, 2yr

Rabbit >5,000 mg/kg

>5,000 mg/kg

12.5 mg/kg/day

Phenmedipham

8,000mg/kg

Dog, 2yr

Rat >2,000 mg/kg

>1,000 ppm in diet

Rabbit> 10,000 mg/
kg

Picloram

5,000-8,200 mg/kg

Rat, 2yr

Rabbit >4,000 mg/kg

150 mg/kg/day

Prometlyn

3, 750--5,235 mg/kg

Dog, 90days

Rabbit >2,000 mg/kg

<200 ppm in diet

Propanil

1,080 to

Dog, 2yr

Rabbit >5,000 mg/kg

>2,500 mg/kg

<85 ppm in diet

Propoxycarbazone >5,000 mg/kg

Dog, lyr

Rat >5,000 mg/kg

258 mg/kg (M)

55. 7 mg/kg (F)

HERBICIDE POISONING

2987

•H=i!f• HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECh
in Water

Skin and Eye Irritation

VetBooks.ir

LC50 8 day

LC50 96hr

Skin-mild

Bobwhite quail 5,600 ppm

Bluegill 354 mg/L

Eye-moderate

Mallard duck >10,000 ppm

Rainbow trout 76 mg/L
in diet

'

LC50

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-moderate duck >5,620 ppm in diet

>l,OOOmg/L

LC50

LC50 96 hr

Skin-moderate

Bobwhite quail and Mallard Bluegill 12.5 mg/L

Eye-mild
duck >5,620 ppm in diet

Rainbow trout 2 mg/L

LC50

LC50 96 hr

Skin-none

Bobwhite quail >5,000

Bluegill 0.2 mg/L

Eye-moderate

Mallard duck >4,000 ppm in Rainbow trout 0.41 mg/L
diet

LC50 5 day

LC50 96 hr

Skin-slight

Bobwhite quail 981 ppm

Rainbow trout 26 mg/L

Eye-moderate

Mallard duck 4,048 ppm in
diet

LC50

LC50 96 hr

Skin-slight

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-mild duck >2,400 ppm in diet

7.4 mg/L

LC50 8 day

LC50 96 hr

Skin-none

Bobwhite quail 3,149 ppm

Bluegill 0.199 mg/L

Eye-mild

Mallard duck 10,900 ppm in Rainbow trout 0.138 mg/L
diet

LC50 4day

LC50 96hr

Skin-moderate

Bobwhite quail >2,480 ppm Bluegill 760 mg/L

Eye-severe
in diet

LC50 21 day

Rainbow trout >210 mg/L

LD50 8day

LC50 96hr

Skin-mild

Bobwhite quail >2,500

Bluegill 14.5 mg/L

Eye-moderate

Mallard duck >5,000 mg/kg Rainbow trout 19.3 mg/L

LC50 5--7 day

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill 10 mg/kg

Eye-slight
duck> 10,000 ppm in diet

Rainbow trout 2.5--2.9 mg/L

LC50 8 day

LC50 96 hr

Skin-moderate

Bobwhite quail 2,861 ppm

Bluegill 2.3 mg/L

Eye-serious

Mallard duck 5,627 ppm in

Rainbow trout 4.6 mg/L
diet

Skin-slight

Eye-minimal

( continued)

2988

HERBICIDE POISONING

IHNIII HERBICIDE POISONING (continued)

Acute Oral

NOAELa

Compound

1050-Rat

(oral)

Acute Dermal 1050

VetBooks.ir

Propyzamide

5,620-8,350 mg/kg

Dog, 2 yr

Rabbit 3,160 mg/kg

>7.5 ppm in diet

Pyrazon

3,030-3,600 mg/kg

Dog, 2 yr

Rat >2,000 mg/kg

1,500 ppm in diet

Pyridate

1,285-1,412 mg/kg

Dog, l yr

Rabbit >2,000 mg/kg

30 mg/kg/day

Pyrithiobac-sodium 4,000 mg/kg

Rat (longterm),

Rat >2,000 mg/kg

59 mg/kg

Quinclorac

3,060 mg/kg (M)

Dog, 1 yr

Rat >2,000 mg/kg

2,190 mg/kg (F)

142 mg/kg/day (M)

140 mg/kg/day (F)

Quizalofop-p-ethyl

1,210-

Dog, lyr

Rat, mouse, rabbit

1,670 mg/kg (M)

<10 mg/kg/day

> 10,000 mg/kg

1,182-

1,480 mg/kg (F)

Rimsulfuron

>5,000 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

50 ppm in diet

Sethoxydim

3,200 mg/kg (M)

Dog, lyr

Rat, mouse

2,676 mg/kg (F)

>8.86 mg/kg (M)

>5,000 mg/kg

>9.41 mg/kg (F)

Siduron

>7,500 m�g

Rat,2 yr

Rabbit >5,500 mg/kg

500 ppm in diet

Simazine

>5,000 mg/kg

Rat, 2 yr

Rabbit

>5 mg/kg/day

>10,200 mg/kg

Sodium chlorate

1,200-7,000 mg/kg

Rabbit 500 mg/kg

Sulfentrazone

2,416-3,297 mg/kg

Rat, 10 mg/kg/day

Rat >5,000 mg/kg

( oral developmental
studies)

Sulfosulfuron

>5,000 mg/kg

Mouse, 90 days

Rat >5,000 mg/kg

7,000 mg/kg of diet

HERBICIDE POISONING

2989

•#H•f • HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECb
in Water

Skin and Eye Irritation

VetBooks.ir

LC50 8day

LC50 96 hr

Skin-slight

Bobwhite quail and Mallard Bluegill 100 mg/L

Eye-moderate
duck >10,000 ppm in diet

Rainbow trout 72 mg/L

LC50

Skin-slight

Bluegill 40 mg/L

Eye-slight

LC50 8day

LC50 96 hr

Skin-none

Bobwhite quail >5,000 ppm Rainbow trout >l.2 mg/L

Eye-slight
in diet

LC5()

LC50 96 hr

Skin-mild

Bobwhite quail and Mallard Bluegill 5.8 mg/L

Eye-moderate
duck >6,300 ppm

Rainbow trout 8.2 mg/L

1050

LC50 96 hr

Skin-irritating

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-moderate duck >5,000 mg/kg

>100mg/L

LC50 8day

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill 0.46-2.8 mg/L

Eye-slight
duck >5,000 ppm in diet

Rainbow trout 10. 7 mg/L

LC5() 8day

LC50 96 hr

Skin-mild

Bobwhite quail >5,620 ppm Bluegill 100 mg/L

Eye-mild

Mallard duck >2,510 ppm in Rainbow trout 32 mg/L
diet

LC50 8day

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill and Rainbow trout Eye-moderate duck >5,600 ppm in diet

>1,000mg/L

LC50

LC50 48hr

Skin-slight

Bobwhite quail and Mallard Crucian carp 18 mg/L

Eye-slight
duck> 10,000 mg/kg

LC50 8day

LC50 96 hr

Skin-none

Bobwhite quail >5,260 ppm Bluegill and Rainbow trout Eye-none Mallard duck 10,000 ppm in >100 mg/L
diet

LC50 48hr

Skin-moderate

Fish 10,000 mg/L

Eye-moderate

LD50

LC50 96 hr

Skin-mild

Bobwhite quail and Mallard Bluegill 93.8 mg/L

Eye-moderate
duck >5,620 ppm

Rainbow trout> 130 mg/L

1050

LC50 96hr

Skin-slight

Bobwhite quail and Mallard Rainbow trout >97 mg/L

Eye-slight
duck 5,620 ppm

(continued)

2990 HERBICIDE POISONING

IH=IIII HERBICIDE POISONING ( continued)

Acute Oral

NOAELa

Compound

LD50-Rat

(oral)

Acute Dermal LD50

VetBooks.ir

Tebuthiuron

644mg/kg

Dog, 1 yr

Rabbit >200 mg/kg

>25 mg/kg/day

Thiazopyr

>5,000 mg/kg

Dog, 1 yr

Rat >5,000 mg/kg

0.8 mg/kg/day

Thifensulfuron-

>5,000 mg/kg

Rat , 2yr

Rabbit >2,000 mg/kg
methyl

25 ppm in diet

Tralkoxydim

1,258 mg/kg CM:)

Rat (teratogen),

Rat >2,000 mg/kg

934 mg/kg (F)

30mg/kg

Trial late

800-2,165 mg/kg

Dog, 2yr

Rabbit 8,200 mg/kg

15 mg/kg/day

(highest tested)

Triasulfuron

>5,000 mg/kg

Dog, 1 yr

Rat >2,000 mg/kg

129 mg/kg/day

Tribenuron-methyl

>5,000 mg/kg

Dog, lyr

Rabbit >2,000 mg/kg

875 ppm in diet

Trichloracetic acid

3,200-5,000 mg/kg

Rat >2,000 mg/kg

Triclopyr

630-729 mg/k�

Rat , 2yr

Rabbit >2,000 mg/kg

3mg/kg/day

Tri.fluralin

>5,000 mg/kg

Dog, 2yr

Rabbit >?,000 mg/kg

18. 75 mg/kg/day

Vernolate

1,200-1,900 mg/kg

Dog, 90days

Rabbit >1,955 mg/kg

>38 mg/kg/day

• NOAEL = No obse1vable adverse effect l<;;vel, daily dosage or ppm concentration in the diet b NOAEC = No observable adverse effect Concentration c Liquid
d Obsolete or no active registration
c Technical grade chemical

HERBICIDE POISONING

2991
lrtNIII HERBICIDE POISONING (continued)

Toxicity to Fish

Avian Toxicity/NOAECh
in Water

Skin and Eye Irritation

VetBooks.ir

LD50

LC50 96 hr

Skin-slight

Bobwhite quail and Mallard Bluegill 112 mg!L

Eye-slight
duck >2,500 mg/kg

Rainbow trout 144 mg/L

LD50

LC50

Skin-slight

Bobwhite quail and Mallard Bluegill and Rainbow

Eye-slight
duck 5,328 mg/kg
trout 3. 5 mg/L

LC50 8day

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill and Rainbow

Eye-moderate
duck >5,620 mg/kg
trout 100 mg!L

LD50

LC50 96 hr

Skin-mild

Mallard duck >3,020 mg/kg Bluegill >6.1 mg!L

Eye-mild

Rainbow trout> 7.2 mg!L

LC50 8 day

LC50 96 hr

Skin-moderate

Bobwhite quail and Mallard Bluegill 1.3 mg/L

Eye-slight
duck >5,000 mg/kg

Rainbow trout 1.2 mg!L

LC50 8day

LC50 96 hr

Skin-none

Bobwhite quail and Mallard Bluegill and Rainbow

Eye-none
duck >5,000 ppm
trout > 100 ppm

LC50

LCw96hr

Skin-none

Bobwhite quail and Mallard Bluegill 760 mg/L

Eye-mild to moderate
duck >5,620 ppm

Rainbow trout 730 mg!L

LDw

Not toxic to fish

Skin-severe

Chicken 4,280 mg/kg

Eye-severe

LCw8day

LCw96hr

Skin-none

Bobwhite quail 2,935 ppm

Bluegill 148 mg/L

Eye-slight

Mallard duck >5,401 ppm in Rainbow trout 117 mg/L
diet

LCw8day

LCw96hr

Skin-none

Bobwhite quail and Mallard Bluegill 0.05--0.07 mg!L

Eye-moderate
duck >5,000 ppm in diet

Rainbow trout

0.02- 0.06 mg/L

LCw 7day

LC50 96 hr

Skin-none

Bobwhite quail 12,000 ppm Bluegill 8.4 mg/L

Eye-none
in diet

Rainbow trout 9.6 mg!L

2992

HERBICIDE POISONING

ORAL TOXIC DOSES (TD) AND LETHAL DOSES (LD) OF

HERBICIDES IN DOMESTIC SPECIES

Compound

TD/LD Species

Dosage (mg/kg)

VetBooks.ir

Phenoxy acid derivatives

Phenoxy acid and its

LD50

Chickens

547
sodium salt

Dogs

100-800

LD

Pigs

500

Hens

380-765

TD

Pigs

100

Calves

200

Butyl glycol ester

TD

Cattle

250 for 3 days

Sheep

250 for 2 days

Amine salts

TD

Cattle

250 for 10 days

Sheep

250 for 10 clays
or 500 for 7 days

Bipyridyl compounds or
quaternary ammonium

Paraquat

Dogs

25-50

Cats

35

Monkeys

50-70

Cattle

35-50

Chickens

110-360

LD

Sheep

8-10

Pigs

75

Diquat

Dogs

100-200

Cats

35-50

Cattle

20--40

Chickens

200--400

Ureas and thioureas

Diuron

TD

Cattle

100 for 10 days

Sheep

250 or 100 for 2 clays

Chickens

50 for 10 days

Linuron

TD

Dogs

100-200

Cats

35-50

( continued)

HERBICIDE POISONING

2993

ORAL TOXIC DOSES (TD) AND LETHAL DOSES (LD) OF

HERBICIDES IN DOMESTIC SPECIES (continued) Compound

TD/LD Species

Dosage (mg/kg)

Cattle

20-40

VetBooks.ir

Chickens

200-400

Tebuthiuron

LD50

Cats

>200

TD

Cats

200

Dogs

>500

TD

Dogs

50 /clay for 3 mo8

Chickens,

No deaths were reported at a
quail, or clucks dosage of 500 mg/kg body wt.

Protoporphyrinogen
oxidase inhibitors

Metribuzin

Cats

>500

Anilide, acetamides, or
amide compounds

Propanil

Dogs

1 ,217

Propyzamicle

Dogs

>10 ,000

Dinitrophenolic compounds

DNOC

LD50

Hens

26

Dogs

50

Pigs

50

Goats

100

TD

Cattle

2-50

Sheep

20-50

LD

Sheep

25 for5 days

Dinoseb

LD50

Hens

26

TD

Cattle

25 for8 clays

Sheep

25 for 10 clays

Dinitroaniline

Trifluralin

Dogs

>2 ,000

Bromacil

TD

Cattle

250

Chickens

500 for 10 days

( continued)

2994

HERBICIDE POISONING

ORAL TOXIC DOSES (TD) AND LETHAL DOSES (LD) OF

HERBICIDES IN DOMESTIC SPECIES (continued) Compound

TD/LD Species

Dosage (mg/kg)

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Sheep

50 for 10 days or 250 for 8 days

Carbamates and
thiocarbamate
compounds

Asulan1

LD50

Rabbits

>2,000

Chickens

>2,000

Dogs

>5,000

Di-allate

LD50

Dogs

510

TD

Chickens

150 for 10 days or 250 for 7
days

Cattle

25 for 5 days or 50 for 3 days

Sheep

25 for 5 days or 50 for 3 days

Phenrnediphan1

LD50

Dogs

>4,000

LD50

Chickens

>3,000

Picrolinic acid de1ivative

Picloran1

LD50

Cattle

>750

Sheep

>l,000
a Anorexfa and weight loss reported. No deaths were repoited in dogs at a tebuthiuron dosage of 500 mgtkg body wt.

INORGANIC HERBICIDES AND
recommended. Rwninants (including deer)

ORGANIC ARSENICALS
are apparently attracted to and lick plants
poisoned with arsenite.

Substances such as inorganic arsenicals

The highly soluble organic arsenicals can

(sodium arsenite, arsenic trioxide), organic
concentrate in pools in toxic quantities after
arsenicals (methyl arsonate, methyl arsonic
a rain has washed them from recently
acid), sodium chlorate, an1monium
treated plants. Arsenicals are used as
sulfamate, borax, and many others were
desiccants or defoliants on cotton, and
fonnerly used on a large scale. These older
residues of cotton harvest fed to cattle may
herbicides are nonselective, generally
contain toxic amounts of arsenic. Signs and
cheaper, more toxic, and more likely to
lesions caused by organic arsenical
cause problems than newer compounds.

herbicides resemble tl10se of inorganic

Their use has been mostly curtailed in
arsenical poisoning. Single toxic oral doses
developed countries.

for cattle and sheep are 22-55 mg/kg.

Poisoning may be expected from smaller
doses if consumed on successive days.

Arsenicals: The use of inorganic

Dimercaprol (3 mg/kg for large animals,
arsenicals as herbicides has been reduced
and 2.5-5 mg/kg for small animals, IM, every
greatly because of livestock losses,

4-6 tu') is the reconunended therapy.

environmental persistence, and their

Sodiwn thiosulfate also has been used
carcinogenic potential. These compounds

(20-30 g, PO, in -300 mL of water for cattle;
can be hazardous to anin1als when used as
one-fourth this dose for sheep); however, a

HERBICIDE POISONING

2995

HERBICIDES WITH POTENTIAL TO CAUSE DEVELOPMENTAL

TOXICITY IN EXPERIMENTAL ANIMAL S

Compound

Effects

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Atrizine

Disruption of ovarian cycle and induced repetitive
pseudopregnancy ( rats, at high doses)

Buturon

Cleft palate, increased fet;aJ mortality (mice)

Butiphos

Teratogenic (rabbit)

Chloridazon

Malfmmations

Chlorpropham

Malformations or other developmental toxicity (mice) Cynazine

Malformations such as cyclopia and diaphragmatic hernia (rabbits); skeletal variations in rats

2,4-D• or 2,4,5-T• alone

Malfmmations such as cleft palate, hydronephrosis;
or in combination
teratogenic (mice, rats)

Dichlorprop

Teratogenic (mice); affect postnatal behavior (rats) Dinosebb

Multiple defects (mice, rabbits)

Dinoterb

Skeletal malformations (rats); skeletal,jaw, head, and visceral (rabbits)

Linuron

Malformations (rats)

Mecoprop

Malformations (mice only)

Monolinuron

Cleft palate (mice)

MCPN

Teratogenic and embryotoxic (rats), teratogenic (mice) Prometryn

Head, limbs, and tail defects (rat)

Propachlor

Slightly teratogenic (rats)

Nitrofenb

Malformations (mice, rats, hamsters)

Silvex

Teratogenic (mice)

TCDD•

Malformations/teratogenic (fetotoxicity in chickens, rats, mice, rabbits, guinea pigs, hamsters, and monkeys)

Tridiphane

Malformations such as cleft palate (mice); skeletal variations (rats)

"TCDD is a common contaminant during the manufacturing process of some herbicides such as 2,4-D
and 2,4,5-T.

b Obsolete
c 2-methyl-4-chlorophenoxyacetic acid
rationale for its use is not established, and
sulfamate to some extent and, in some
it may be unrewarding. (See also ARSENIC
studies, exposed animals made better gains

POISONING, p 3071.)

than did control animals. However, sudden
deaths have occurred in cattle and deer that

Ammonium Sulfamate: Ruminants
consumed treated plants. Large doses
apparently can metabolize anunonium

(> 1.5 g/kg) induce ammonia poisoning in

2996

HERBICIDE POISONING
ruminants. Treatment is designed to lower

Tissues can be irritated after contact. For
rumen pH by dilution with copious amounts example, mouth lesions have been seen of water to which weak acetic acid (vinegar) after contact with recently sprayed pastures.

has been added.

Skin irritation and corneal opacity occur on
external exposure to these chemicals, and

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Borax: Borax is toxic to animals if
inhalation is dangerous. Animals, including
consumed in moderate to large doses
people, have died as a result of drinking

(>0.5 g/kg). Poisoning has not been reported from contaminated containers.

when borax was used properly but has

Paraquat and diquat have somewhat
occurred when it was accidentally added to
different mechanisms of action. Diquat
livestock feed and when borax powder was
exerts most of its hamtful effects in the GI
scattered in the open for cockroach control. tract. Animals drinking from an old diquat Principal signs of acute poisoning are
container showed anorexia, gastritis, GI
diarrhea, rapid prostration, and perhaps
distention, and severe loss of water into
convulsions. An effective antidote is not
the lumen of the GI tract. Signs of renal
known. Balanced electrolyte fluid therapy
impaim1ent, CNS excitement, and
with supportive care is indicated.

convulsions occur in severely affected
individuals. Lung lesions are uncommon.

Sodium Chlorate: Many cases of chlorate

Paraquat has a biphasic toxic action
poisoning of livestock have occurred both
after ingestion. Immediate effects include
from ingestion of treated plants and from
excitement, convulsions or depression
accidental consun1ption offeed to which
and incoordination, gastroenteritis with
it was mistakenly added as salt. Cattle someanorexia, and possibly renal involvement times are attracted to foliage treated with
and respiratory difficulty. Eye, nasal, and
sodium chlorate. Considerable quantities
skin irritation can be caused by direct
must be consumed before signs of toxicity
contact, followed within days to 2 wk by
appear. The minin1un1 lethal dose is 1.1 g/kg
pulmonary lesions as a result of lipidfor cattle, 1.54-2.86 g/kg for sheep, and membrane peroxidation and thus destruc5.06 g/kg for poultry. Ingestion results in tion of the type I alveolar pneumocytes.

hemolysis of RBCs and conversion of Hgb to

This is reflected in progressive respiratory
methemoglobin. Treatment with methylene
distress and is evident on necropsy as
blue (10 mg/kg) must be repeated frequently
pulmonary edema, hyaline membrane
because, unlike the nitrites, the chlorate ion
deposition, and alveolar fibrosis.

is not inactivated during conversion ofHgb to

There is no specific treatment. Because
methemoglobin and is capable of producing
these chemicals are absorbed slowly,
an unlimited quantity of methemoglobin
intensive oral administration of adsorbents
as long as it is present in tl1e body. Blood
in large quantities and cathartics is advised.

transfusions may reduce some of the tissue

Bentonite or Fuller's earth is preferred, but
anoxia caused by methemoglobin; IV isotonic activated charcoal will suffice. Toxicity of saline can hasten elimination of the chlorate
paraquat is enhanced by deficiency of
ion. Mineral oil containing 1 % sodium
vitamin E or selenium, oxygen, and low
thiosulfate will inhibit further absorption
tissue activity of glutathione peroxidase.

of chlorate in monogastric anin1als.

Therefore, vitamin E and selenium with
supportive therapy may be useful in early

ORGANIC HERBICIDES
stages of intoxication. Excretion may be
accelerated by forced diuresis induced by

Anilide, Acetamides, or Amide
mannitol and furosemide. Oxygen therapy

Compounds: These herbicides (propanil,
and fluid therapy are contraindicated.

cypromid, clomiprop, bensulide, dimethenarnid) are plant growth regulators, and Carbamate and Thiocarbamate
some members of this group are more toxic

Compounds: These herbicides (terbuthan others. Hemolysis, methemoglobinecarb, asulam, carboxazole, EPTC, pebulate, mia, and immunotoxicity have occurred
triallate, vernolate, butylate, thiobencarb)

after experimental exposure to propanil.

are moderately toxic; however, they are

(For discussion of bensulide, see p 2997.) used at low concentrations, and poisoning
problems would not be expected from

Bipyridyl Compounds or Quaternary
normal use. Massive overdosage, as seen

Ammonium Herbicides: The bipyridyl
witl1 accidental exposure, produces signs
compounds ( diquat, paraquat) produce
similar to those induced by the insecticide
toxic effects in the tissues of exposed
carbamates, with lack of appetite,
animals by development of free radicals.

depression, respiratory difficulty, mouth

HERBICIDE POISONING

2997
watering, diarrhea, weakness, and seizures.

that aid in restoration of liver function are

Thiobencarb has induced toxic neuroparecorrunended.

thies in neonatal and adult laboratory rats.

It appears to increase pem1eability of the

Dinitrophenolic Compounds: Several

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blood-brain barrier. There is no suitable
substituted dinitrophenols alone or as
antidote. Supportive and symptomatic
salts such as dinitrophenol, dinitrocresol,
treatment is recommended.

dinoseb, and binapacryl are highly toxic to
all classes of animals (LD 20-100 mg/kg

50

Aromatic/Benzoic Acid Compounds:

body wt). Poisoning can occur if animals

The herbicides in this group ( chloramben,
are sprayed accidentally or have immedidicamba, and naptalam) have a low order of ate access to forage that has been sprayed,
toxicity to domestic anin1als, and poisoning
because these compounds are readily
after nmmal use has not been reported.

absorbed through skin or lungs. Dinitro

Environmental persistence and toxicity to
phenolic herbicides markedly increase
wildlife is also low. The signs and lesions are oxygen consumption and deplete glycogen similar to those described for the phenoxy
reserves. Clinical signs include fever, dyspacid derivatives (see below). There is no nea, acidosis, tachycardia, and convulsuitable antidote. Supportive and symptosions, followed by coma and death with a matic treatment is recommended.

rapid onset of rigor mortis. Cataracts can
occur in animals with chronic dinitrophenol intoxication. In cattle and other Phenoxy Acid Derivatives: These
ruminants, methemoglobinemia,
acids and their salts and esters (2,4-D
intravascular hemolysis, and hemopro[2-4-dichlorophenoxyacetic acid], teinemia have been seen. Exposure to
dalapon, dichlorprop [2,4-DPJ, 2,4,5-T
these compounds may cause yellow

[2,4,5-trichlorophenoxyacetic acid], 2,4-DB, staining of the skin, conjunctiva, or hair.

MCPA, MCPB, mecoprop, and silvex) are

An effective antidote for dinitrophenol
commonly used to control undesirable
compounds is not known. Affected animals
plants. As a group, they are essentially
should be cooled and sedated to help
nontoxic to animals, except silvex which
control hyperthermia. Use of physical
is unusually very toxic. When large doses
cooling measures ( eg, cool baths or
are fed experimentally, general depression,
sponging and keeping the animal in a
anorexia, weight loss, tenseness, and
shaded area) are recommended. Atropine
muscular weakness (particularly of the
sulfate, aspirin, and antipyretics should not
hindquarters) are noted. Large doses in
be used. Dextrose-saline infusions in
cattle may interfere with rumen function.

combination with diuretics and tranquiliz

Dogs may develop myotonia, ataxia,
ers such as diazepan1 ( not barbiturates) are
posterior weakness, vomiting, diarrhea,
very useful. Phenothiazine tranquilizers are
and metabolic acidosis. The oral LD for
contraindicated. IV administration of large

50

2,4-D and 2,4,5-T in dogs is 100--800 mg/kg.

doses of sodiwn bicarbonate (in carni

Even large doses, up to 2 g/kg, have not
vores), parenteral vitamin A, and oxygen
been shown to leave residues in the fat
therapy may be useful. If the toxin was
of animals. These compounds are plant
ingested and the anin1al is alert, emetics
growth regulators, and treatment may
should be administered; if the anin1al is
result in increased palatability of some
depressed, gastric lavage and treatment
poisonous plants as well as increased
with activated charcoal should be
nitrate and cyanide content.

performed.

The use of 2,4,5-T was curtailed because

In ruminants with methemoglobinemia,
extremely toxic contaminants, collectively
methylene blue solution (2o/o-4%, 10 mg/kg,
called dioxins (TCDD and HCDD), were

IV, tid, during the first 24--48 hr) and
found in technical grade material (see
ascorbic acid (5-10 mg/kg, IV) are useful.

p 3056). TCDD is considered carcinogenic,
mutagenic, teratogenic, and fetotoxic, and

Organophosphate Compounds:

is able to cause reproductive damage and

Organophosphate compounds such as
other toxic effects. Although manufacturing
glyphosate, glufosinate, and bensulide are
methods have reduced the level of the
broad-spectrun1, nonselective systemic
contaminants, use of this herbicide is very
herbicides. Glyphosate and glufosinate exist
limited worldwide.

as free acids, but because of their slow

Treatment is usually symptomatic and
solubility they are marketed as the
supportive. IV fluids should be given to
isopropyl amine or trimethylsulfonium salts
promote diuresis. Adsorbents and drugs
of glyphosate and the ammonium salt of

2998

HERBICIDE POISONING
glufosinate. These are widely used herbicides agents. Altered calcium metabolism and with low toxicity. However, they are toxic to
bone morphology have been seen in
fish. Sprayed forage appears to be preferred
laboratory anin1als. Recovery from diuron
by cattle for 5-7 days after application, but
intoxication is quick (withi11 72 hr), and no

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this causes little or no problem.

signs of skin iITitation or dermal sensitiza

Dogs and cats show eye, skin, and upper
tion have been reported in guinea pigs. After
respiratory tract signs when exposed during
repeated administration, hemoglobin levels
or subsequent to an application to weeds
and RBC counts are significantly reduced,
or grass. Nausea, vomiting, staggering, and
while methemoglobin concentration and
hindleg weakness have been seen in dogs

WBC counts are increased. Increased
and cats exposed to fresh chemical on
pigmentation (hemosiderin) in the spleen is
treated foliage. The signs usually disappear
seen histopathologically. LiJluron in sheep
when exposure ceases, and minimal
causes erytllrocytosis and leukocytosis with
symptomatic treatment is needed. However, hypohemoglobinemia and hypoproteinemia, formulations of these compounds may
hematuria, ataxia, enteritis, degeneration of
lead to hemolysis and GI, cardiovascular,
the liver, and muscular dystrophy. In
and CNS effects due to presence of the
chickens, it leads to weight loss, dyspnea,
surfactant polyoxyethyleneamine.

cyanosis, and diarrhea. It is nontoxic to fish.

Treatment should include washing the

Fluometuron is less toxic t11an diuron. In
chemical off the skin, evacuating the
sheep, depression, salivation, g1inding of
stomach, and tranquilizing the anin1al.

teeth, chewing movements of the jaws,

Massive exposure with acute signs due to
mydriasis, dyspnea, incoordination of
accidental poisoning should be handled as
movements, and drowsiI1ess are conunonly
an organophosphate poisoning (seep 3064).

seen. On histopathology, severe congestion

Bensulide, listed as a plant growth
of the red pulp witil corresponding atrophy
regulator, has an oral LDii() in rats of
of the white pulp of the spleen and depletion

271-770 mg/kg; in dogs, the lethal dose is
of the lymphocyte elements have been

>200 mg/kg. The most prominent clinical
reported. The acute LDii() of isoproturon in
sign is anorexia, but other signs are sinillar
rats is sinillar to that of diuron.

to those caused by 2,4-D poisoning.

Polyurea herbicides have been suspected
to have some mutagenic effects but do not

Triazolopyrimidine Compounds:

have carcinogenic potential. In general,

Triazolopyrinlidine herbicides include
these compounds do not cause developcloransularn-methyl, diclosulan1, florasumental and reproductive toxicity, except for larn-methyl, flumetsularn, and metosularn.

monolinuron, linuron, and buturon, which

The acute oral toxicity is very low. There
are known to cause some teratogenic abnoris no suitable antidote. Supportive and malities in experimental animals. There is
symptomatic treatment is recommended.

no suitable antidote. Supportive and
symptomatic treatment is recommended.

Ureas and Thiourea Compounds:

The ureas and thioureas (polyureas) are

Polycyclic Alkanoic Acids or Aryloxy
available under different names such as
phenoxypropionic Compounds: Memdiuron, fluometuron, isoproturon, linuron, bers of tlus group ( diclofop, fenoxaprop,
buturon, chlorbromuron, chlortoluron,
fenthiaprop, fluazifop, haloxyfop) have
chloroxuron, difenoxuron, fenuron,
moderately low toxicity (acute oral LDii() in
methiuron, metobromuron, metoxuron,
rats 950 mg/kg to >4,000 m�g), except for
monuron, neburon, parafluron, siduron,
haloxyfop-methyl (LDii() -400 mg/kg). These
tebuthiuron, tetrafluron, and thidiazuron.

compounds are more toxic if exposure is

Of these, diw·on and fluometuron are the
dermal. The dem1al LD50 of diclofop in
most commonly used in the USA, whereas
rabbits is only 180 mg/kg. There is no
isoproturon is mostly used in other
suitable antidote. Supportive and symptocountries. In general, these compounds matic treatment is reconunended.

have low acute toxicity and are unlikely to
present any hazard in normal use, except

Triazinylsulfonylurea or Sulfonylurea
tebuthiuron, which may be slightly

Compounds: Toxicity of this group of
hazardous. Cattle are more sensitive to polyherbicides ( chlorsulfuron, sulfometuron, urea herbicides than sheep, cats, and dogs.

etharnetsulfuron, chloremuron) appears to

Signs and lesions are sinillar to those
be quite low. The oral acute LDii() in rats is in
described for the phenoxyacetic herbicides
the range of 4,000-5,000 m�g. The dem1al

( see above). The substituted urea herbicides acute LD50 in rabbits is -2,000 mg/kg. There
induce hepatic microsomal enzymes and
is no suitable antidote. Supportive and
may alter metabolism of other xenobiotic
symptomatic treatment is reconunended.

HERBICIDE POISONING

2999

Triazines and Triazoles: Triazines and
and propachlor. Low doses in rats and dogs
triazoles have been used extensively as
do not produce any adverse effects, but
selective herbicides. These herbicides are
longtern1 exposure in dogs causes liver
inhibitors of photosynthesis and include
toxicity and affects the spleen. Ocular
both the asymmetric and synunetlic
lesions produced by alachlor are considered
triazines. Exan1ples of symmetric triazines
to be unique to the Long-Evans rat, because

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are chlorostriazines ( sinlazine, atrazine,
the response has not been seen in other
propazine, and cyanazine), the thiomethylstrains of rats or in mice or dogs.

s-triazines (ametryn, prometryn, terbutryn),

Compared with other substituted
and methoxy-s-triazine (prometon). The
anilines, propachlor is severely irritating to
commonly used asyn1rnetric triazine is
the eye and slightly irritating to the skin.

metribuzin.

Propachlor produces skin sensitization in

These herbicides have low oral toxicity
guinea pigs. High doses of propachlor
and are unlikely to pose acute hazards in
produce erosion, ulceration, and hyperplanormal use, except arnetryn and metribusia of the mucosa and herniated mucosa!

zin, which may be slightly to moderately
glands in the pylo1ic region of stomach and
hazardous. They do not irritate the skin
hyperti·ophy and necrosis of the liver in rats.

or eyes and are not skin sensitizers. The

In dogs, there is poor diet palatability, which
exceptions are atrazine, which is a skin
results in poor feed consw11ption and
sensitizer, and cyanazine, which is toxic
weight loss. There is no suitable antidote.

by the oral route. Sensitivity of sheep and

Supportive and symptomatic ti·eatment is
cattle to these herbicides is appreciably
recommended.

high. The main signs are anorexia,
hemotoxia, hypothermia, locomotor
lmidazolinones: Imidazolinone
disturbances, irritability, tachypnea, and
herbicides include imazapyr, inlazamethhypersensitivity. Simazine is excreted in abenz-methyl, imazapic, imazethapyr,
milk, so it is of public health concern.

irnazamox, and imazaquin. These are

Atrazine is more toxic to rats but
selective broad-spectrum herbicides.

comparatively less toxic to sheep and

Imidazolinone herbicides caused slight to
cattle than simazine. When cultured
moderate skeletal myopathy and/or slight
human cells are exposed to atrazine,
anemia in dogs during 1-yr dietary toxicity
splenocytes are damaged; bone marrow
studies with three structurally similar
cells are not affected. Atrazine induces
intidazolinones (imazapic, imazaquin, and
liver microsomal enzymes and is
imazethapyr). There is no evidence of any
converted to N-dealkylated derivatives.

adverse effect on reproductive perfor

In contrast to simazine, it is not excreted
mance or of fetal abnormalities in rats
in milk. There is no suitable antitlote.

or rabbits. There is no suitable antidote.

Supportive and symptomatic treatment

Supportive and symptomatic treatlnent is
is recommended.

reconm1ended.

Protoporphyrinogen Oxidase

Other Herbicides: Bromacil and terbacil

Inhibitors: Protox inhibitors may be
are commonly used metl1yluracil comdiphenyl ether (OPE) or non-diphenyl pounds. Toxic doses of bromacil can be
ether (non-OPE) such as nitrofen and
hazardous, especially for sheep, but no field
oxadiazon. In the past few years,
case of toxicity has been reported. The
numerous other non-oxygen-bridged
nitrile herbicides, ioxynil and bromoxynil,
compounds (non-OPE protox inhibitors)

may uncouple and/or inhibit oxidative
with the same site of action (carfentraphosphorylation. Ioxynil, presumably zone, JV 485, and oxadiargyl) have been
because of its iodine content, causes
marketed. Protox inhibitors have little
enlargement of the thyroid gland in rats.

acute toxicity and are unlikely to pose

A number of substances are used as
an acute hazard in normal use. These
defoliants in agriculture. For example,
compounds increase porphyrin levels in
sulfuric acid is used to destroy potato
animals when administered orally; the
haulms and two closely related trialkylphosporphyrin levels return to normal within phorothioates (DEF and merphos) to
a few days. There is no suitable antidote.

defoliate cotton. A notable feature of the

Supportive and symptomatic treatment
latter is that it produces organophosphateis recommended.

induced delayed neuropathy in hens.

Chlomequat is used as a growth regulator

Substituted Anilines: The most comon fruit trees. The signs of toxicity in monly used herbicides of tllis group are
experimental animals indicate that it
alachlor, acetochlor, butachlor, metolachlor, is a partial cholinergic agonist.

3000

HOUSEHOLD HAZARDS

HOUSEHOLD HAZARDS

VetBooks.ir

See also RODENT!CIDE POISONING, p 3165;
primates.) Alcohols are eliminated via the

TOXICITIES FROM HUMAN DRUGS, p 3024; POISONOUS
urine as parent compound as well as

PLANTS, p 3103; and FOOD HAZARDS, p 2964.

metabolites. In dogs, up to 5()0A, of a dose of

Household chemicals (eg, products
methanol may be eliminated unchanged via
containing alcohols, bleaches, or corrothe lungs.

sives) found in the home represent a risk of

Alcohols are GI irritants, and ingestion
toxicosis if companion animals are exposed
may result in vomiting and hypersalivato concentrates or undiluted products, but tion. Alcohols and their metabolites are
casual exposure to areas in which these
potent CNS depressants, affecting a
compounds have been used appropriately
variety of neurotransmitters within the
rarely causes any serious problems.

nervous system. Metabolites such as
acetaldehyde may stimulate the release

ALCOHOLS
of catecholamines, which can affect
myocardial function. Metabolic acidosis

Alcohol toxicosis results in metabolic acidoresults from the formation of acidic sis, hypothermia, and CNS depression. All
intermediates, and both parent comspecies are susceptible.

pounds and metabolites contribute to
increases in osmolal gap. Hypothermia

Etiology: Ethanol, methanol, and
may develop due to peripheral vasodilaisopropanol are the alcohols most tion, CNS depression, and interference
frequently associated with toxicosis in
with thermoregulatory mechanisms.

companion animals. Ethanol is present

Hypoglycemia develops secondary to
in a variety of alcoholic beverages, some
alcohol-induced depletion of pyruvate,
rubbing alcohols, drug elixirs, and
resulting in inhibition of gluconeogenesis.

fermenting bread dough (seep 2965).

Methanol is most commonly found in

Clinical Findings and Diagnosis:

windshield washer fluids (windshield

Signs generally begin within 30-60 min

"antifreeze"). The lethal oral dose of
of ingestion and include vomiting, diarrhea,
methanol in dogs is 4-8 ml/kg, although
ataxia, disorientation (inebriation), depresignificant clinical signs may be seen at ssion, tremors, and dyspnea. Severe cases
lower dosages. Isopropanol is twice as
may progress to coma, hypothennia, seizures,
toxic as ethanol and is found in rubbing
bradycardia, and respiratory depression.

alcohols and in alcohol-based flea sprays

Death is generally due to respiratory failure,
for pets. Oral dosages of isopropanol
hypothermia, hypoglycemia, and/or meta

�0.5 ml/kg may result in significar1t
bolic acidosis. Pneumonia secondary to
clinical signs in dogs.

aspiration of vomitus is possible.

The determination of blood alcohol

Pathogenesis: All alcohols are rapidly
levels may help to confirm the diagnosis
absorbed via the GI tract and most are well
of alcohol intoxication.

absorbed dermally; toxicosis from
overspraying pets with alcohol-based flea

Treatment: Stabilization of severely
sprays is not uncommon. Alcohols reach
symptomatic animals is a priority.

peak plasma levels within 1.5--2 hr and are

Adequate ventilation should be mainwidely distributed throughout the body.

tained, and cardiovascular and acid-

They are metabolized in the liver to
base abnormalities should be corrected.

acetaldehyde (ethanol), formaldehyde

Seizures can be controlled with diazepam

(methanol), and acetone (isopropanol);

(0.5-2 mg/kg, IV) as needed. For asymptothese intermediate metabolites are then matic animals, induction of emesis may
further converted to acetic acid, formic
be of benefit in the first 20-40 min after
acid, and/or carbon dioxide. (In people and
ingestion. Activated charcoal is not thought
some other primates, accumulation of
to appreciably bind small-chain alcohols
formic acid after methanol ingestion results
and is not often recommended. Bathing
in retinal and neuronal damage; nonpriwith mild shampoo is recommended for mates are efficient at eliminating fonnic
significant dermal exposures. Supportive
acid and therefore do not develop the
care, including thermoregulation and fluid
blindness and cerebral necrosis seen in
diuresis to enhance alcohol elimination,

HOUSEHOLD HAZARDS

3001
should be administered. Anecdotally,
immediate coughing, gagging, sneezing,
yohimbine (0.1 mg/kg, IV) has been used to
or retching. In addition to the immediate
stimulate respiration in severely comatose
respiratory signs, animals exposed to
dogs with alcohol toxicosis.

concentrated chlorine fumes may develop

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pulmonary edema 12---24 hr after exposure.

CHLORINE BLEACHES

Ocular exposures may result in epiphora,
blepharospasm, eyelid edema, and/or

Exposure to undiluted chlorine bleaches
corneal ulceration. Dermal exposure
may result in GI, dermal, and ocular
may result in mild dermal irritation and
irritation or ulceration as well as significant;
bleaching of ti'le hair coat. Oral, dermal,
respiratory irritation. All species are
and ocular irritation or ulceration are
susceptible. Because of the countercurrent
possible. Respiratory lesions may include
anatomy and physiology of the avian lung,
tracheitis, bronchitis, alveolitis, and
caged birds are at increased risk of
pulmonary edema.

succumbing to fumes from bleaches and
other cleaning agents.

Treatment: For oral exposures, emesis
and activated charcoal are contraindi

Etiology: Chlorine bleaches are primarily
cated; instead, dilution with milk or water
used as household cleaners and pool
is recommended. Any spontaneous
sanitizers. Household bleaches tend to
vomiting should be managed, and animals
contain sodium hypochlorite at 3%---1 OOA.,
should be monitored for development
and pH of these products may range from
of GI irritation/ulceration (see below). In 9 ( mildly irritating) to > 11 ( corrosive). Pool cases when protracted vomiting causes
treatments may contain lithium, calcium, oc
electrolyte or hydration abnormalities,
sodium hypochlorites at concentrations up
fluid therapy may be of benefit. For
to 700/o-80%, with pH that may range from
respiratory exposures, the animal should
acidic to alkaline. Pets may be exposed
be moved to an area with fresh air and
by chewing on containers of undiluted
monitored for dyspnea. Stabilization
product, drinking from buckets containing
of severely dyspneic animals is a must;
product diluted in water, or swimming in
pulmonary edema should be treated as
recently treated pools.

needed. Bathing with mild shampoo and
thorough rinsing is recommended for

Pathogenesis: The relative hazard of a
significant dermal exposures. Ocular
particular bleach product depends on the
exposures should be treated with 10---20
concentration of hypochlorite, pH, and
min of ocular inigation with physiologic
dilution of the product. In general, levels
saline, followed by fluorescein staining of
of hypochlorite <10% tend to be mild
the cornea to detect corneal injury.

irritants; however, if the product has a
pH> 11 or <3.5, alkaline or acid corrosive

CORROSIVES
injury may occur. Dilution of bleaches
with water per label directions will often

Acid or alkaline corrosives produce
reduce the corrosive potential of these
significant local tissue injury that can result
products and make them little more
in full-thickness burns of skin, cornea, and
than mild GI or ocular irritants. Mixing
the mucosa of the oral cavity, esophagus,
of hypochlorite and ammonia produces
and stomach. All species are susceptible.

highly toxic chloramine gas that can

Heavy coats may provide some protection
cause acute respiratory distress or
from dermal exposure.

delayed onset of pulmonary edema
within 12---24 hr of exposure.

Etiology: Corrosives are divided into
acid and alkaline corrosives. Acidic

Clinical Findings and Lesions: Ingeshousehold products include anti-rust tion of dilute or moderate pH household
compounds, toilet bowl cleaners,
bleach products rarely causes more than
gun-cleaning fluids, automotive batteries,
mild vomiting, hypersalivation, depresswimming pool cleaning agents, and sion, anorexia, and/or diarrhea. Concenetching compounds. Alkaline corrosive trated(> 10%) bleach products or products agents include drain openers, automatic with pH> 11 may cause significant GI
dishwasher detergents, toilet bowl
corrosive injury. Ingestion or inhalation
cleaners, radiator cleaning agents, and
of significant amounts of chlorine bleach
swimming pool algicides and "shock"

occasionally results in hypernatremia,
agents. In general, alkaline products with
hyperchloremia, and/or metabolic
pH > 11 pose risk of significant corrosive
acidosis. Acute inhalation may result in
injury.

3002

HOUSEHOLD HAZARDS

Pathogenesis: Acids produce immedimay develop secondary to perforating ate coagulative necrosis of tissue and
ulcers of esophagus or stomach. Respiraimpart significant pain on contact, which tory lesions may include tracheitis,
may limit exposure. Alkaline agents
bronchitis, pneumonitis, pulmonary

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produce immediate, penetrating liquefacedema, or aspiration pneumonia.

tive necrosis of tissue; the lack of
significant discomfort on contact with

Treatment: Because of the rapid action
alkaline products may result in prolonged
of corrosive agents, much of the damage
exposure. For these reasons, burns from
from exposure occurs before treatment
alkaline products tend to be deeper and
can be started. Stabilization of animals
more extensive than burns from acidic
presenting as dyspneic, in shock, or witl1
agents. Burns from alkaline agents may
severe electrolyte abnormalities is always
take up to 12 hr after exposure to become
a priority. For recent oral exposures,
fully apparent, whereas the extent of acid
immediate dilution witl1 water or milk
burns is usually evident shortly after
should be done. Under no circumstances
contact. Esophageal burns are more
should emesis be attempted because of
common with alkaline agents, and the
the risk of further mucosal exposure to
absence of significant oral burns does not
corrosive material. Likewise, gastric
necessarily indicate that no esophageal
lavage is contraindicated because of the
damage has developed. Full-thickness
risk of perforation of weakened esophaulceration of the esophagus may result in geal/gastric walls and the risk of further
pleuritis or peritonitis due to leakage of
exposure of mucosa to the corrosive
ingesta into body cavities. Esophageal
material as it is removed. Attempts to
burns may result in stricture formation
chemically neutralize an acid with weak
during healing, resulting in dysphagia,
alkali (or alkali with weak acid) are also
megaesophagus, and aspiration pneumocontraindicated because of the production nia. Additionally, although the contents
of exothermic reactions that can result in
of the stomach may serve to buffer and
thermal burns. Activated charcoal is
dilute corrosive agents, gastric ulceration
ineffective in cases involving ingestion of
and possibly perforation may occur with
corrosives, and tl1e presence of charcoal
significant exposures. Respiratory
on damaged mucosa may impede wound
exposure to corrosives ( especially acids)

healing.

may result in respiratory distress, tracheo

After dilution, general supportive care
bronchitis, or pneumonitis. Dermal or
should be instituted, including monitoring
ocular exposures may result in severe
for respiratory difficulty, pain manageulceration of dermis or cornea.

ment, antibiotics (if ulcers are present),
and anti-inflammatories as needed.

Clinical Findings and Lesions: Clinical

Endoscopic evaluation of the esophagus
signs that may occur after ingestion of
and stomach for ulceration should be
corrosive agents include vocalization,
performed -12 hr after exposure; this time
hypersalivation, lethargy, polydipsia,
fran1e will allow the full extent of tissue
vomiting ( with or without blood),
injury to become apparent. The use of
abdominal pain, dysphagia, pharyngeal
corticosteroids in cases witl1 significant
edema, dyspnea, and oral, esophageal,
esophageal mucosal injury is controverand/or gastric ulceration. In severe cases, sial. Corticosteroids decrease inflanunashock may develop rapidly after exposure.

tion and may aid in minimizing stricture

Lesions are initially milky white to gray
formation, but t11ey also suppress the
but gradually tum black as eschar
immune system and may enhance
formation occurs. Necrotic tissue may
susceptibility to secondary infection.

slough within days of exposure. Dyspnea,

In animals with significant oral and/or
cyanosis, and pulmonary edema may
esophageal burns, gastrostomy tubes may
occur secondary to inhaled corrosive
be necessary to provide nutrition while
agents. Dermal exposure may result in
affected tissues heal.

significant burns, with local pain,

Dermal or ocular exposures should
erythema, and tissue sloughing. Ocular
be managed by flushing with copious
exposure may cause blepharospasm,
amounts of water or physiologic saline;
epiphora, eyelid edema, conjunctivitis, or
eyes should be flushed for a minimum of
corneal ulceration. Burns of skin, cornea,

20 min, followed by fluorescein staining.

and GI mucosa range from mild ulceration

Standard topical treatments for dermal
to full-thickness necrosis with extensive
or ocular burns should be instituted as
tissue sloughing. Peritonitis or pleuritis
needed.

HOUSEHOLD HAZARDS

3003

Alkaline Batteries
casing has been punctured. When disk

Ingestion of alkaline batteries poses
batteries have been ingested, 20 mL

. a risk
of GI tract corrosive injury and foreign
boluses of tap water every 15 min will
body obstruction. Dogs are most commonly
decrease the severity and delay the

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involved.

development of current-induced
esophageal ulceration. The decision on
whether to remove a battery from the

Etiology: Alkaline batteries are present
in many household electronic products,
stomach depends on the size of the
including remote controls, hearing aids,
animal,.battery size, and evidence of
toys, watches, computers, and calculators.

battery puncture. Radiography may be

Most alkaline dry cell batteries use
performed to determine the location of
potassiwn hydroxide or sodiwn hydroxide
the battery casing; generally, batteries
to generate currents. Nickel-cadmiwn and
that have passed through the pylorus will
lithium batteties also tend to contain
pass through the intestinal tract
alkaline material.

uneventfully (adding bulk to the diet and
judicious use of cathartics may facilitate
passage). Serial radiography to verify

Pathogenesis: The alkaline gel in
battery location is recommended until
batteties causes liquefactive necrosis of
the battery is expelled. Batteries that do
tissues on contact, resulting in bums that
not pass through the pylorus within 48 hr
can penetrate deeply into tissue. Lithiwn
of ingestion are unlikely to pass on their
disk or "button" batteties may lodge in the own and may require surgical or
esophagus and generate a current against
endoscopic removal. Batteries that have
the esophageal walls, resulting in circular
obviously been punctured should be
ulcers that have the potential to be perremoved surgically to prevent gastric or forating. Some battery casings may contain
intestinal ulceration due to leakage of
metals such as zinc or mercury, posing
alkaline gel. Endoscopic removal is not
hazards of foreign body obstruction and
recommended in cases in which it is
metal toxicosis if they remain in the stomach suspected that the battery casing has for prolonged petiods. Additionally, small
been punctured. Treatment of cases with
batteties ( especially disk batteries) may be
suspected oral, esophageal, or gastric
inhaled and pose a choking hazard.

ulceration is the same as for other
alkaline corrosive injuries (seep 3001).

Clinical Findings and Lesions: For

Dermal or ocular exposures to alkaline
discussion of alkaline burns, see p 3001. Forgels should be managed by copious eign body obstruction may present as vomitrinsing of the area with tap water (skin) ing, anorexia, abdominal discomfort, or
or physiologic saline solution (eyes). The
tenesmus. Respiratory obstruction due to
affected areas should be monitored for
battery inhalation may present with acute
development of ulcers, and topical
onset of dyspnea and cyanosis. Mucosa!

therapy administered as needed.

bums may occur within the oral cavity,
esophagus, and less commonly, stomach.

Perforation of the esophagus may lead to

Cationic Detergents
secondary pyothorax, while gastric

Exposure to cationic detergents may result
perforation may result in acute blood loss
in local corrosive tissue injury as well as
and/or peritonitis.

severe systemic effects. All species are
susceptible. Cats are at increased tisk of

Diagnosis: Radiographs may help to
oral exposure because of grooming habits.

confirm the diagnosis as well as the
location of the battery; however, some disk

Etiology: Cationic detergents are
batteries do not show up well on radiopresent in a variety of algicides, germigraphs. Differential diagnoses include GI cides (including quaternary ammonium
or respiratory foreign bodies and other
compounds), sanitizers, fabric softeners
oral, dermal, or ocular corrosive agents.

(including dryer softener sheets), and
liquid potpourris. Concentrations of

Treatment: For batteries swallowed
cationic detergents �2% have been
intact without any chewing, induction of
associated with oral mucosa! ulcers in
emesis may result in expulsion. Because
cats.

of the risk of leakage of alkaline gel
onto oral and esophageal mucosa during

Pathogenesis: Cationic detergents are
vomiting, emesis should not be induced
locally corrosive agents, causing dennal,
if there is any possibility that the battery
ocular, and mucosa! injury similar to that

3004

HOUSEHOLD HAZARDS
of alkaline corrosive agents. Additionally,
detergents; products included in this group
exposure to cationic detergents may result
include human and pet shan1poos, liquid
in systemic effects ranging from CNS
hand dish washing soaps, bar bath soaps
depression to pulmonary edema. The

( except homemade soaps, which may

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mechanism for these systemic effects is
contain lye), many laundry detergents,
not known.

and many household all-purpose cleaners.

Most are of moderate pH, but agents with

Clinical Findings and Lesions: Signs
pH> 11 ( eg, electric dishwasher detergents)

of oral exposure include oral ulceration,
are alkaline coITosives and should be
stomatitis, pharyngitis, hypersalivation,
treated as such (seep 3001).

swollen tongue, depression, vomiting,
abdominal discomfort, and increased

Pathogenesis: Anionic and nonionic
upper respiratory noises within 6-12 hr
detergents are mild irritants; many have
of ingestion. Affected animals frequently
been pH adjusted to have minirnaJ dermal
have significant fever and increases in
irritation, although ocular and nrncosaJ

WBC counts. Systemic effects include
irritation is possible. There is no apprecimetabolic acidosis, CNS depression, able systemic absorption of these a.gents,
hypotension, coma, seizures, muscular
and toxicity is limited to ocular, oral, or
weakness and fasciculation, collapse,

GI ir1itation, which is usually mild and
and pulmonary edema. Dermal irritation,
self-linliting. Ca.ts exposed to undiluted
erythema, ulceration, and pain are
shampoos or other products containing
possible with dermal contact. Conjuncsodium lauryl sulfate may develop signitivitis, blepharospasm, eyelid edema, ficant respiratory compronlise after
lacrimation, and corneal ulceration may
inhalation during groonling, including
be seen secondary to ocular exposure.

dyspnea, increased bronchial secretions,

Lesions can include GI, ocular, or dermal
and nlild pulmonary edema. Although the
irritation or ulceration.

exact mechanism of this syndrome is not
known, it may relate to interference by the

Treatment: Systemic signs should be
detergent with normal pulmonary
treated symptomatically, eg, diazepam
surfactants.

(0.5-2 mg/kg, slow IV) for seizures, fluid
therapy for hypotension, etc. Because of

Clinical Findings: Nausea, vomiting,
the potential for corrosive mucosa] injury,
and diarrhea are the most common signs.

induction of emesis and administration of

Secondary dehydration and electrolyte
activated charcoal are contraindicated
in1balance may develop in rare instances
with cationic detergents. For recent oral
due to protracted vomiting or diatThea. Mild
exposures, milk or water can be given for
ocular irritation is possible, with lacrimadilution, and the anin1aJ monitored for tion and blepharospasm. No significant
development of oral or esophageal burns.

lesions beyond mild local irritation are seen.

Oral burns should be treated the same

Cats grooming after application of sodium
as other corrosive injuries (seep 3001).

lauryl sulfate-containing products may

Dermal and ocular exposures should be
develop moist respiratory sounds, cyanosis,
managed by thorough flushing of the
and dyspnea within 1-3 hr of exposure.

affected area with tepid water or physiologic saline, followed by monitoring for Treatment: Dilution witl1 milk or water
development of dem1aJ or ocular irritation
may reduce the risk of spontaneous
or ulceration. Topical treatment for dem1al
vomiting. Vonliting is usually self-limiting
or ocular burns should be instituted as
and responds to short periods of food a11d
needed; in severe cases, analgesics may be
water restriction. In severe cases or in
indicated.

aninlals with sensitive stomachs, antiemetics may be required ( eg, metoclopranlide, DETERGENTS, SOAPS, AND

0.2-0.4 mg/kg, PO, SC, or IM, qid). Rarely,

SHAMPOOS
parenteral fluid therapy is required to
correct electrolyte or hydration abnom1ali

Exposures to products containing anionic
ties due to protracted vomiting or diarrhea.

and nonionic detergents generally cause

For ocular exposures, irrigation of eyes
mild GI irritation that responds well to
using tepid water or physiologic saline for
symptomatic care. All animals are

5 min will usually suffice. For cats that have
susceptible.

respiratory compromise, supplemental
oxygen and general supportive care are

Etiology: Mild detergents, soaps, and
recommended; in most cases, signs resolve
shampoos contain anionic and nonionic
within 24 hr.

MYCOTOXICOSES

3005

MYCOTOXICOSES

VetBooks.ir

For discussion of mycotoxicoses in poultry,
suspected, differential diagnoses must be
see p2846.

carefully established by thorough clinical

Acute or chronic toxicoses can result
and historical evaluation, examination of
from exposure to feed or bedding contamiproduction records, and appropriate nated with toxins produced during growth
diagnostic testing.

of various saprophytic or phytopathogenic

Mycotoxicoses are generally not
fungi or molds on cereals, hay, straw,
successfully treated with medical therapy
pastures, or any other fodder. These toxins
after diagnosis. A preventive approach
are not consistently produced by specific
with recognition of risk factors and
molds and are !mown as secondary (not
avoiding or reducing exposure is preessential) metabolites that are fom1ed ferred. Best management practices are
under conditions of stress to the fungus
aimed at prevention of the occurrence
or its plant host.

of mycotoxins, inactivation of the pre

A few principles characterize rnycoformed toxin in grain or feed, and toxic diseases: 1) The cause may not be
adsorption or inactivation of the toxin
immediately identified. 2) They are not
in the GI tract. Testing of suspect grain
transmissible from one animal to another.

at harvest, maintaining clean and dry

3) Treatment with drugs or antibiotics has
storage facilities, using acid additives ( eg,
little effect on the course of the disease.

propionic acid) to control mold growth in

4) Outbreaks are often seasonal, because
storage, ensuring effective air exclusion
particular climatic sequences may favor
in silage storage, and reducing storage
fungal growth and toxin production.

time of prepared feeds are established

5) Study indicates specific association
procedures to prevent mycotoxin formawith a particular feed. 6) Large numbers tion. Acidic additives control mold
of fungi or their spores found on examinagrowth but do not destroy preformed tion of feedstuffs does not necessarily
toxins.

indicate that toxin production has

There are no specific antidotes for
occurred. However, absence of molds
mycotoxins; removal of the source of the
does not exclude mycotoxicosis, because
toxin (ie, the moldy feedstuff) eliminates
feed storage or preparation conditions,
further exposure. The absorption of some
eg, acid treatment or high pelleting, can
mycotoxins (eg, aflatoxin) has been effea
destroy molds while the heat-tolerant
ctively prevented by aluminosilicates.

mycotoxin persists.

If financial circumstances do not allow

Diagnosis of mycotoxic disease requires
for disposal of the moldy feed, it can be
a combination of information. Most veteriblended with unspoiled feed just before nary mycotoxicoses are found in large
feeding to reduce tne toxin concentraaninlal species, but important outbreaks tion. This approach should be monitored
can happen in pets and exotic aninlals.

by follow-up toxin analysis and may not

Especially impo1iant in diagnosis is the
be acceptable to regulatory agencies.

presence of a disease documented to be

Alternatively, feed with known mycocaused by a !mown mycotoxin, combined toxin concentrations can be fed to less
with detection of the mycotoxin in either
susceptible species, remembering that
feedstuffs or animal tissues.

some mycotoxins such as aflatoxin could

Sometimes more than one mycotoxin
result in violative food residues in the
may be present in feedstuffs, and their
absence of illness. When contaminated
different toxicologic properties may cause
feed is blended witn good feed, care must
clinical signs and lesions inconsistent
be taken to prevent further mold growth
with tliose seen when animals are dosed
by the toxigenic contaminants. This may
experimentally with pure, single mycotoxbe accomplished by thorough drying ins. Some mycotoxins are immunosuppresor by addition of organic acids ( eg, sive, which may allow viruses, bacteria, or
propionic acid).

parasites to create a secondary disease that

Important mycotoxic diseases occur
is more obvious than tl1e primary. When
in domestic anin1als worldwide (see
immunosuppression by a mycotoxin is

TABLE 1).

3006

MYCOTOXICOSES
itM•il MYCOTOXICOSES IN DOMESTIC ANIMALS

Toxins

Regions Where

Disease

(When Known)

Fungi or Molds

Reported

VetBooks.ir

Aflatoxicosis

Aflatoxins

Aspergillus.fiavus, Widespread

A parasiticus

( wanner climatic
zones)

Diplodiosis

Unknown

Diplodia zeae

South Africa

Ergotism

Ergot alkaloids

Claviceps piirpurea Widespread

Paspalinine and

Cpaspali,

Widespread
paspalitrems,

C cinerea
tremorgens

Estrogenism and

Zearalenone

Fusarium

Widespread
vulvovaginitis
graminearum

Perfect state:

Gibberella zeae

Facial eczema

Sporidesmins

Pithomyces

Widespread

(Pithomycotoxico-
charlarnm
sis)

Fescue foot

Ergovaline

Neotyphodium

USA, Australia,
coenophialum

New Zealand,

Italy

Fusariotoxicosis,

Nonmacrocyclic

Fusarium

Widespread
vomiting and feed
trichothecenes
sporotrichioides,

(except for
refusal in pigs

(deoxynivalenol, T-2

Fculmorum,
deoxynivalenol,
toxin, diacetoxyscir-

F graminearum,
more likely in
penol [DAS], many

Fnivale; other
temperate to
other trichothecenes)

fungal species
colder climates)

Leukoencephalo-

Fumonisin B,

Fusarium

Egypt, USA,
malacia
verticilloides

South Africa,

Greece

Mycotoxic lupinosis Phomopsins

Phomopsis

Widespread

( as distinct from
leptostromiforrnis
alkaloid poisoning)

MYCOTOXICOSES

3007

•t#:iil• MYCOTOXICOSES IN DOMESTIC ANIMALS (continued) Contaminated

Animals

Signs and

Toxic Foodstuff

Affected

Lesions

VetBooks.ir

Moldy peanuts, soybeans,

All poultry, pigs,

Major effects in all species are
cottonseeds, rice, sorghum,
cattle, sheep, dogs slow growth and hepatotoxicosis.

corn (maize), other cereals

See also AFLATOXICOSIS, p 3011, and

MYCOTOXICOSES IN POULTRY, p 2846.

Moldy corn (maize)

Cattle, sheep

Nervous system disorders, cold
and insensitive limbs. Recovery
usual on removal of source.

Seed heads of many grasses,

Cattle, horses,

Peripheral gangrene, late
grains
pigs, poultry
gestation suppression of lactation
initiation. Seep 3012.

Seed heads of paspalum

Cattle, horses,

Acute tremors and ataxia.

grasses
sheep

See PASPALUM STAGGEllS, p 3019.

Moldy corn (maize) and

Pigs, cattle, sheep, Vulvovaginitis in pigs, anestrus or pelleted cereal feeds, standing poultry
pseudopregnancy in mature sows,
corn, corn silage, other grains
early embryonic death of swine
embryos, estrogenism in cattle
and sheep, reduced egg production in poultry. See also p 3014.

Toxic spores on pasture litter

Sheep, cattle,

See also p 3015.

farmed deer

Tall fescue grass (Lolium

Cattle, horses

Lameness, weight Joss, hyper
arundinacea)

therrnia, heat intolerance, dry
gangrene of extremities,
agalactia, thickened fetal
membranes. See also p 3016.

Cereal crops, moldy roughage Pigs, cattle,

Vomiting and feed refusal
horses, poultry

( deoxynivalenol), loss of appetite
and milk production, diarrhea,
staggers, skin irritation, immunosuppression; recovery (from T-2, DAS) on removal of contaminated
feed. See also p 3020.

Moldy corn (maize)

Horses, other

Depends on degree and specific

Equidae, pigs
site of brain lesion. See also p 3017.

Moldy seed, pods, stubble, and Sheep, occasion

Lassitude, inappetence, stupor,
haulm of several Lupinus spp ally cattle, horses, icterus, marked liver injury.

affected by Phomopsis stem
pigs

Usually fatal. See also p 3018.

blight

( continued)

3008

MYCOTOXICOSES

•4H•J• MYCOTOXICOSES IN DOMESTIC ANIMALS (continued) Toxins

Regions Where

Disease

(When Known)

Fungi or Molds

Reported

VetBooks.ir

Myrotheciotoxico

Macro cyclic

Myrothecium

Southeast
sis, dendrodochiotrichothecenes
verrucaria,

Europe, former
toxicosis

( verrucarins,

M roridum

USSR
roridins, etc)

Macro cyclic

M verrucaria

Brazil
trichothecenes

(baccharinoids)

Ochratoxicosis

Ochratoxin, also

Aspergillus

Widespread
citrinin
ochraceus and
others, Penicillium
viridicatum,

Pcitrinum

Penicillium-associ- Penitrem A

P crustosum,

Widespread
ated tremorgens

P cyclopium,

P commune

Roquefortine

P roqueforti

Perennial ryegrass Lolitrems

Loli um perenne,

Australia, New
staggers

Neotyphodium

Zealand, Europe,
lolii, an endophyte USA
fungus confined to

L perenne

Poultry hem or-

Probably aflatoxins

Probably Aspergil-

USA
rhagic syndrome
and rubratoxins
lusfiavus, A
clavatus, Penicil-
lium purpuroge-
num, Alternaria, sp

Pulmonary edema, 4-lpomeanol

Fusarium solani

USA
emphysema

Porcine pulmonary Fumonisin 81 and

Fusarium

USA,South
edema

Fumonisin 82
verticilloides

Africa

Slobbers syndrome Slaframine (and

Rhizoctonia

USA
swainsonine)

leguminicola

MYCOTOXICOSES

3009

•riN•i• MYCOTOXICOSES IN DOMESTIC ANIMALS (continued) Contaminated

Animals

Signs and

Toxic Foodstuff

Affected

Lesions

VetBooks.ir

Moldy rye stubble, straw

Sheep, cattle,

Acute-dian·hea, respiratory
horses
distress, hemorrhagic gastroenteritis, immunosuppression, death.

Ch�onic-ulceration of GI tract,
unthriftiness, gradual recovery.

See also p 3020.

Plants of Baccharis spp

Cattle, other

Epithelial necrosis of GI tract. See
that contain the toxins
herbivores
also p 3020.

Moldy barley, corn (maize),

Pigs, poultry

Perirenal edema, enlarged pale
wheat
kidneys with cortical cysts, and
tubular degeneration and fibrosis;
immunosuppression, polyuria
and polydipsia.

Cereal grains, cheese, fruit,

Cattle, dogs,

Neurotoxic signs, including
meats, nuts, refrigerated foods; horses, sheep
continual tremors, seizures,
compost
hyperexcitability, ataxia.

Vomiting and CNS signs in dogs.

As above, and in silage

Endophyte-infected ryegrass

Sheep, cattle,

Tremors, incoordination,
pastures
horses, deer
collapse, convulsive spasms. See
also RYEGRASS STAGGERS, p 3153.

Moldy grain and meal

Growing chickens Depression, anorexia, no weight
gain, widespread internal
hemorrhages, sometimes aplastic
anemia, deatl1. See MYCOTOXICOSES

IN POULTRY, p 2846.

Moldy sweet potatoes

Cattle

Acute pulmonary edema, leading
to interstitial pneumonia and
emphysema.

Com

Swine

Acute interlobular pulmonary
edema and hydrotl10rax cause
anoxia and cyanosis. Survivors
may develop icterus and chronic
hepatotoxicosis.

Black patch disease, legumes

Sheep, cattle

Salivation, bloat, diarrhea,

(notably red clover) eaten as
sometimes death. Recovery usual
forage or hay
when removed from clover. See
also SLAFRAMINE TOXICOSIS, p 3019.

(continued)

3010

MYCOTOXICOSES

•#H•i• MYCOTOXICOSES IN DOMESTIC ANIMALS (continued) Toxins

Regions Where

Disease

(When Known)

Fungi or Molds

Reported

Stachybotryo

Macrocyclic

Stachybotrys atra

Former USSR,

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toxicosis
trichothecenes

(S alternans)

southeast Europe

( satratoxin, roridin,
verrucarin)

Sweet clover

Dicumarol

Penicillium spp,

North America
poisoning

Mucorspp,

Aspergillus spp

Tremorgen ataxia

Penitrems, verruculo

Penicillium

USA,South
syndrome
gen, paxilline,
crustosum,

Africa, probably
fumitremorgens,

P puberulum,
worldwide
aflatrems, roquefortine P verruculosum,

P roqueforti,

Aspergillus fiavus,

Afumigatus,A
clavatus, and others

Managing a Suspected
plastic). Dry samples are preferable in a

Mycotoxicosis
paper bag to prevent condensation during
transport and storage. San1ples should be

When mycotoxicosis is suspected, correcdried at l 76°-194°F (S0°-90°C) for -3 hr to tive actions could include the following:

reduce moisture to 12o/er-13%. lf mold stud.ies

1) Change the feed even when a specific
are to be done, dry at l 40°F (60°C) for
mycotoxin is not identified. 2) Thoroughly

6-12 hr to preserve fw1gal activity.

inspect storage bins, mixing equipment, and
feeders for caking, molding, or musty odors.

3) Remove contaminated feed and clean

Mycotoxin Adsorbents
equipment and sanitize with hypochlorite

Adsorption ofrnycotoxins in contaminated

(laundry bleach) to reduce contammating
feeds is an area of active research. A.tlatoxins
fungi. 4) Analyze for lrnown mycotoxins.

are effectively adsorbed by the alun1inosili5) Use spore counts or fungal cultures for cate feed additives ( see below). However, this some indication of potential mycotoxin
group of adsorbents are of little or limited use
production. 6) lf storage conditions or grain
for other mycototoxins. Trichothecene
moisture are adverse, use a mold inhibitor to
rnycotoxins, including deoXYnivalenol, are
reduce or delay mold growth. Remember,
not readily adsorbed by common feed
mold inhibitors do not destroy preformed
add.itives. The alun1inosilicate adsorbents
toxins. 7) Use a mycotoxin adsorbent if
tl1at are effective against afiatoxins have
appropriate for the mycotoxin suspected.

lirn.ited or no benefits against trichothecenes.

8) Save a representative sample of each diet

Sodiwn bentonite is an effective adsorbent
mixed until animals are at 1 mo beyond when for afiatoxins in cattle and poultry but the feed was consumed. 9) Take a represenappears ineffective for trichothecenes and tative sample of suspect feed after rn.illing by
zearalenone. The polymeric glucomannan
passing a cup through a moving auger stream
adsorbents (GM) are useful for poultry
at frequent intervals, mixing samples
growth and feed conswnption with low
thoroughly, and saving a 4.5-kg (10-lb)

natural concentrations of afiatoxin,
san1ple for analysis. Alternatively, use probe
ochratoxin, T -2 toxin, and zearalenone.

sampling of recently blended grain in bins or

When added to Pusarium-contan1inated
trucks at five locations in each structure for
d.iets, GM reduced the nwnber of stillborn
each 6 feet of depth. Freeze or dry samples,
piglets compared witl1 controls. GM
and subm.it for analysis in a paper bag ( not
adsorbent efficacy for ruminants has been

MYCOTOXICOSES

3011

•&N•J• MYCOTOXICOSES IN DOMESTIC ANIMALS (continued) Contaminated

Animals

Signs and

Toxic Foodstuff

Affected

Lesions

Moldy roughage, other

Horses, cattle,

Stomatitis and ulceration,

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contaminated feed
sheep,pigs
anorexia, leukopenia, extensive
hemorrhages in many organs,
inflammation and necrosis in the
gut, inu11unosuppression. See also

TRICHOTHECENE TOXJCOSIS, p 3020.

Sweet clover (Melilotus spp)

Cattle, horses,

Vitamin K antagonism with coagusheep
lopathy and hemorrhage. See also
p 3156.

Moldy feed; high-protein food All species, but

Tremors, polypnea, ataxia,
products, even under
dogs are quite
collapse, convulsive spasms.

reftigeration, eg, cream
susceptible
cheese, walnuts
variable in different studies. Cholestyramine
are susceptible if toxic diets are fed over
has been an effective binder of fumonisins
long periods. Experimentally, all species of
and zea.ralenone in vitro and for fumonisins
animals tested have shown some degree of
in animal experiments, but response in cattle
susceptibility. Dietary levels of aflatoxin (in
is unknown. Although various adsorbents are ppb) generally tolerated are s50 in young allowed for animal feed in various countries,
poultry, slOO in adult poultry, s50 in weaner
none is FDA approved in the USA.

pigs, s200 in finishing pigs, <50 in dogs, <100
in calves, and <300 in cattle. Approximately

AFLATOXICOSIS
two times the tolerable levels stated is likely
to cause clinical disease, including some

Aflatoxins are produced by toxigenic strains mortality. Dietary levels as low as 10-20 ppb of AspergiUus jlavus and A pamsiticus on result in measurable metabolites of aflatoxin
peanuts, soybeans, com (maize), and other

(aflatoxin M1 and M2) being excreted in milk;
cereals either in the field or dtuing storage
feedstuffs that contain aflatoxins should not
when moisture content and temperatures
be fed to dairy cows. Acceptable regulatory
are sufficiently high for mold growth.

values in milk may range from 0.05 ppb to

Usually, this means consistent day and night 0.5 ppb in different countries; individual temperatures > 70°F. The toxic response
state or federal regulatory agencies should
and disease in mammals and poultry varies
be consulted when contamination occurs.

in relation to species, sex, age, nutritional

Aflatoxins are metabolized in the liver to
status, and the duration of intake and level
an epoxide that binds to macromolecules,
of aflatoxins in the ration. Earlier recogespecially nucleic acids and nucleoproteins.

nized disease outbreaks called "moldy

Their toxic effects include mutagenesis
com toxicosis," "poultry hemorrhagic
due to alkylation of nuclear DNA, carcinosyndrome," and ''AspergiUus toxicosis"

genesis, teratogenesis, reduced protein
may have been caused by aflatoxins.

synthesis, and i.mmunosuppression. Reduced

Aflatoxicosis occurs in many parts of
protein synthesis results in reduced producthe world and affects growing poultry tion of essential metabolic enzymes and

( especially ducklings and turkey poults ),
structural proteins for growth. The liver is
young pigs, pregnant sows, calves, and dogs. the principal organ affected. High dosages Adult cattle, sheep, and goats are relatively
of aflatoxins result in hepatocellular
resistant to the acute form of the disease but necrosis; prolonged low dosages result in

3012

MYCOTOXICOSES
reduced growth rate, imrnunosuppression,
examination of the liver should indicate the
and liver enlargement.

nature of the hepatotoxin, but hepatic
changes are somewhat similar in Senecio

Clinical Findings: In acute outbreaks,
poisoning (seep 3150). The presence and
deaths occur after a short period of
levels of aflatoxins in the feed should be

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inappetence; other acute signs include
determined. Acutely affected animals
vomiting, depression, hemmThage, and
have increases in liver enzymes (alkaline
icterus. Subacute outbreaks are more usual,
phosphatase, AST, or ALT), bilirubin, sermn
with unth.riftiness, weakness, anorexia,
bile acids, and protlu·ombin ti.me. Chronic
reduced growth and feed efficiency, and
exposure can cause hypoproteinemia
occasional sudden deaths. Laboratory

(including decrease in both albumin and
changes in most species are related to liver
globulin). Aflatoxin M, (p1incipal metabolite
damage, coagulopathy, and in1paired protein of aflatoxin B,) can be detected in urine, synthesis. Specific laboratory changes
liver, kidney, or milk of lactating animals
include increased AST, ALT, and alkaline
if toxin intakes are high. Aflatoxi.n residues
phosphatase; hypothrombinemia, proin organs and dairy products generally are longed prothrombin and activated partial
eliminated within 1-3 wk after exposure
thromboplastin times, hype.rbilirubinemia,
ends.

hypocholesterolemia, hypoalbuminemia,
and variable thrombocytopenia. Generally,

Control: Contaminated feeds can be
aflatoxin concentrations in feed twice the
avoided by monitoring batches for aflatoxin
tolerable levels given above are associated
content. Local crop conditions (drought,
with acute aflatoxicosis. Recently, acute and
insect infestation) should be monitored as
fatal aflatoxicosis with many of these signs
predictors of aflatoxin formation. Young,
and laboratory changes has been docunewly weaned, pregnant, and lactating mented in dogs. Frequently, there is a high
animals require special protection from
incidence of concmTent infectious disease,
suspected toxic feeds. Dilution with
often respiratory, that responds poorly
noncontaminatecl feedstuffs is one
to the usual dmg therapy. Dairy cattle
possibility, but tl1is may not be acceptable
experience inappetence, and ruminants may on a regulatory basis. Cleaning to remove have decreased n.uninal contractions at high lightweight or broken grains will often concentrations(> 1,000 ppb) of aflatoxins.

substantially reduce mycotoxin concentra

Liver damage can lead to reduced clotting
tion in remaining grain. Anunoniation
factor synthesis with acute to chronic
reduces aflatoxin contanlination in grain
hemorrhage. Subclinical effects are reduced
but is not currently approved by the FDA for
growth rate and feed efficiency, hypoprouse in food animals in the USA because of teinemia, and reduced resistance to some
tmcertainty about by-products produced.

infectious diseases despite vaccination.

Nun1erous products are marketed as

Lesions: In acute cases, there are
anticaking agents to sequester or "bind"

widespread hemonhages and icterus. The
aflatoxins and reduce absorption from the
liver is the major target organ. Microscopi

GI tract. One effective binder for aflatoxins
cally, the liver is enlarged and snows
is hydrated socliwn calciun1 alw11inosilimarked fatty accumulations and massive cates (HSCAS), which reduce the effects of
centrilobular necrosis and hemorrhage. In
aflatoxin when fed to pigs or poultry at 10
subacute cases, the hepatic changes are not
lb/ton (5 kg/tonne). They also provide
so pronounced, but the liver is somewhat
substantial protection against dietaty
enlarged and finner than usual. There may
aflatoxin. HSCAS reduce aflatoxi.n M1 in
be edema of the gallbladder. Microscopimilk by -500A, but do not eliminate residues cally, the liver shows periportal inflanm1aof aflatoxin M, in milk from dairy cows feel tory response and proliferation and fibrosis
aflatoxin 81• Otl1er adsorbents (socliun1
of the bile ductules; the hepatocytes and
bento1lites, polymeric glucomaimans) have
their nuclei (megalocytosis) are enlarged.

shown variable but paitial efficacy in

The GI mucosa may show glandular atrophy reducing low-level aflatoxin residues in and associated inflammation. Rarely, there
poultry ai1cl dairy cattle. To elate, the FDA
may be tubular degeneration and regenerahas not licensed ai1y product for use as a tion in the kidneys. Prolonged feeding of

"mycotoxin binder" in ailirnal feeds.

low concentrations of aflatoxins may result
in diffuse liver fibrosis (cirrhosis) and,

ERGOTISM
rarely, carcinoma of tl1e bile ducts or liver.

Ergotisrn is a worldwide disease of farm

Diagnosis: Disease history, laboratory
animals that results from ingestion of
data, necropsy findings, and microscopic
sclerotia of the parasitic fungus Claviceps

MYCOTOXICOSES

3013
pwpurea, which replaces the grain or seed
sloughed. In a similar way, the tip of the tail
of rye and other small grains or forage
or ears may become necrotic and slough.

plants, such as the bromes, bluegrasses,

Exposed skin areas, such as teats and
rescues, and ryegrasses. The hard, black,
udder, appear unusually pale or anemic.

elongated sclerotia may contain varying

Abo1tion is not seen.

quantities of ergot alkaloids, of which

The most consistent lesions at necropsy

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ergotamine and ergonovine (ergometrine)

are in the skin and subcutaneous parts of
are pharmacologically most imp01tant.

the extremities. The skin is nonnal to the

Cattle, pigs, sheep, and poultry are involved
indented line, but beyond, it is cya.notic and
in sporadic outbreaks, and most other
hardened in advanced cases. Subcutaneous
species are susceptible. Poisoning can come hemoIThage and some edema occur from grazing seed heads or from infected
proximal to tile necrotic area.

grains in concentrate rations.

In pigs, ingestion of ergot-infested
grains may result in reduced feed intake

Etiology: Ergot causes vasoconstriction
and reduced weight gain. Occasionally,
by direct action on the muscles of the
swine may show necrosis of tl1e tips of ears
arterioles, and repeated doses injure the
or tail. If fed to pregnant sows, ergotizecl
vascular endothelium. These actions
grains result in lack of udder development
initially reduce blood flow and eventually
witll agalactia at parturition, and tl1e piglets
lead to complete stasis with ternlinal
born may be smaller than nonnal. Most of
necrosis of the extremities clue to throthe litter die witllin a few days because of mbosis. A cold environment predisposes
starvation. No other clinical signs or lesions
the extremities to gangrene. In addition,
are seen.

ergot also causes stin1ulation of the CNS,

Clinical signs in sheep are sinlilar to
followed by depression. Ergot alkaloids
tllose in cattle. Additionally, tl1e mouth
inhibit pituitary release of prolactin in many
may be ulcerated, and marked intestinal
man1malian species, with failure of both
inflan1mation may be seen at necropsy. A
man1mary development in late gestation
convulsive syndrome has been associated
and delayed initiation of milk secretion,
witl1 ergotism in sheep.

resulting in agalactia at parturition. Ergot
alkaloids have also been associated with

Diagnosis: Diagnosis is based on finding
heat intolerance, clyspnea, and reduced milk tile causative fungus ( ergot sclerotia) in production in dairy cattle, sinlilar to the
grains, hay, or pastures provided to live

"summer syndrome" described for fescue
stock showing signs of ergotism. Ergot
toxicosis.

alkaloids may be extracted and detected in
suspect ground grain meals. At 200-600 ppb,

Clinical Findings and Lesions: Cattle
ergot alkaloids may cause clinical signs and
may be affected by eating ergotized hay or
effects; however, this is influenced by the
grain or occasionally by grazing seeded
relative an1ounts of various ergot alkaloids
pastures infested with ergot. Lameness,
in the grain.

the first sign, may appear 2-6 wk or more

Identical signs and lesions of lameness,
after initial ingestion, depending on the
and sloughing of the hooves and tips of
concentration of alkaloids in the ergot and
ears and tail, are seen in fescue foot in
the quantity of ergot in the feed. Hincllimbs
cattle grazing in winter on tall fescue grass
are affected before forelimbs, but the extent
infected with an endophyte fungus, in which
of involvement of a limb and the number of
the ergot alkaloid ergovaline is considered
limbs affected depends on the daily intake
a major toxic principle. In gilts and sows,
of ergot. Body temperature and pulse and
lactation failure not associated witl1 ergot
respiration rates are increased. Epidemic
alkaloids must be differentiated from
hyperthermia and hypersalivation may
prolactin inhibition due to ergot.

also occur in cattle poisoned with C purpurea (see also mSCUE POISONING, p 3016). Ergot Treatment: In horses, parenteral use of
alkaloids may interfere with embryonic
the dopamine D2 antagonist clomperidone
development in pregnant females.

(1.1 mg/kg, PO, bid for 10-14 clays) is

Associated with the lameness are
effective in prevention of agalactia from
swelling and tenderness of the fetlock
ergot alkaloids in fescue. Use against tile
joint and pastern. Within -1 wk, sensation
same alkaloids produced by C purpurea
is lost in the affected part, an indented
could be medically logical (seep 3016).

line appears at the limit of normal tissue,
and dry gangrene affects the distal part.

Control: Intake of ergot boclies should be

Eventually, one or both claws or any part

<0.1%of tlle total diet, and concentrations
of tl1e limbs up to the hock or knee may be
of ergot alkaloids should be <100 ppm in the

3014

MYCOTOXICOSES
total diet. Ergotism can be controlled by an
compounded for cattle and pigs; in com
immediate change to an ergot-free diet. In
ensiled at the green stage; and very rarely
pregnant sows, however, removal of ergot
m hay. It has been detected occasionally
in late gestation ( <l wk before partrnition)

m samples from pastures in temperate
may not correct the agalactia syndrome,
climates at levels believed sufficient to

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and arumals with clinical peripheral
cause reproductive failure of grazin"

"

gangrene will not likely recover. Under
herbivores.

pasture fee.ding conditions, frequent grazmg or toppmg of pastures prone to ergot infestation during the summer months

Clinical Findings: Clinical effects cannot
reduces flower-head production and helps
be distinguished from excessive estrogen
control the disease. Grain that contains
administration. Physical and behavioral
even small amounts of ergot should not be
signs of estrus are induced in young gilts by
fed to pregnant or lactating sows.

as little as 1 ppm dietary zearalenone. In
pigs, zearalenone primarily affects weaned
and prepubertal gilts, causing hyperemia

ESTROGENISM AND
and enlargement of the vulva (known as

VULVOVAGINITIS
vulvovaginitis). There is hypertrophy of the
mammary glands and uterus, and abdomi

(Fusarium estrogenism)

nal straining results in prolapse of the

Pusarium spp molds are extremely
uterus in severe cases. Removal of affected
common and often contaminate growing
grain results in return to nonnal in -1 wk.

plants and stored feeds. Com (maize),

Zearalenone causes reproductive
wheat, and barley are commonly contamitoxicosis in sexually mature sows by nated. In moderate climates w1der hwnid
inhibiting secretion and release of
weather conditions, F graminearum may
follicle-stimulating hormone (FSH)

produce zearalenone, one of the resorcyclic
resulting in arrest of preovulatory o�arian
acid lactones (RALs ). Zearalenone (formerly follicle maturation. Reproductive effects in called F
sexually mature sows depend on time of

2 toxin) is a potent nonsteroidal
estrogen and is the only known mycotoxin
consumption. Zearalenone fed at 3-10 ppm
with primarily estrogenic effects. Often,
on days 12-14 of the estrous cycle in open
zearalenone is produced concurrently with
gilts results in retention of corpora lutea
deoxynivalenol. Depending on the ratio of
and prolonged anestrus (pseudopregnancy)

these two my co toxins, signs of reduced feed for up to 40-60 days. Zearalenone fed at intake or reproductive dysfw1ction may

�30 ppm in early gestation (7-10 days after
predominate, but presence of deoxynivalebreeding) may prevent implantation and nol may limit exposure to zearalenone, thus
cause early embryonic death. Zearalenone
reducing its practical effect:

metabolites can be excreted in milk of

Zearalenone binds to receptors for
exposed sows, resulting in hyperestrogenic

17!3-estradiol, and this complex binds
effects in their nursing piglets.

to estradiol sites on DNA Specific RNA

In cattle, dietary concentrations > 10 ppm
synthesis leads to signs of estrogehism.

may cause reproductive dysfunction in

Zearalenone is a weak estrogen with
daily heifers, altl10ugh mature cows may
potency 2-4 times less than estradiol. Under
tolerate up to 20 ppm.

controlled administration, zearalanol, a

YoW1g males, both swine and cattle, may
closely related RAL, is widely used in cattle
become infertile, with atrophy·of the testes.

as an anabolic agent.

However, mature boars appear W1affected

Estrogenism due to zearalenone was first
by as much as 200 ppm dietary zearalenone.

clinically recognized as vulvovaginitis in

Ewes may show reduced reproductive
prepubertal gilts fed moldy com (maize),
perfom1ance (reduced ovulation rates and
but zearalenone is occasionally reported as
nwnbers of fertilized ova, and markedly
a suspected disease-causing agent for
increased duration of estrus) and abortion
sporadic outbreaks in dairy cattle, sheep,
or premature live births.

chickens, and turkeys. High dietary

Lesions: Lesions in pigs include ovarian
concentrations (>20-30 ppm) are required
atrophy and follicular atresia, uterine
to produce infertility in cattle and sheep,
edema, cellular hypertrophy in all layers
and extremely high dosages are required to
of the uterus, and a cystic appearance in
affect poultry.

degenerative endometrial glands. The
mammary glanru; show ductal hyperplasia

Etiology: Zearalenone has been detected
and epithelial proliferation. Squamous
in com, oats, barley, wheat, and sorghwn
metaplasia is seen in the cervix and vagina

(both fresh and stored); in rations

Sexually mature sows will have retained

MYCOTOXICOSES

3015
corpora lutea for 40-70 days after exposw-e,

South American countries, and probably
consistent with signs of pseudopregnancy.

North America. Sheep, cattle, and farmed
deer of all ages can contract the disease, but

Diagnosis: Diagnosis is based on
it is most severe in young animals.

reproductive perfom1ance in the herd or

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flock, clinical signs, history of diet-related

Etiology and Pathogenesis:

occurrence, and excluding other known

Sporidesmins are secondary metabolites
causes of infertility. Chemical analysis of
of the saprophytic fungus Pithomyces
suspect feed for zearalenone and careful
clwrtarum, which grows on dead pasture
examination of reproductive organs at
litter. The wann ground temperatw-es and
necropsy are required. As a bioassay, virgin
high humidity required for rapid growth of
prepubertal mice fed diets or extracts of
this fungus restrict disease occurrence to
zearalenone-conta.minated feed demonhot SUI11.l11er anrl autumn periods shortly strate enlarged uteri and vaginal comi.ficaafter wam1 rains. By observing weather tion typical of estrogens.

conditions and estin1ating toxic spore

Differential diagnoses include reproducnumbers on pastures, danger periods tive tract infections and other causes of
can be predicted and fanners alerted.

impaired fertility such as diethylstilbestrol

The sporidesmins are excreted via the
in the diet of housed stock. In grazing
biliary system, in which they produce severe
herbivores, especially sheep, the plant
cholangitis and pericholangitis as a result
estrogens ( eg, isoflavones associated with
of tissue necrosis. Biliary obstruction may
some varieties of subterranean and red
be seen, which restricts excretion of bile
clovers, and cou.mestans in certain fodders
pigments and results in jaundice. Similarly,

[ eg, alfalfa]) should be considered.

failw-e to excrete phylloerythrin in bile leads
to photosensitization.

Control: Unless stock are severely or

Previous ingestion of toxic spores causes
chronically affected, usually reproductive
potentiation; thus, a succession of small
functions recover and signs regress 1-4 wk
intakes of the spores can lead to subsequent
after intake of zearalenone stops. However,
severe outbreaks.

multiparous sows may remain anestrous up
to 8---10 wk.

Clinical Findings, Lesions, and

Management of swine with hyperestro

Diagnosis: Few signs are apparent tmtil
genism should include changing the grain
photosensitization and jaundice appear
immediately. Signs should stop within 1 wk.

-10-14 days after intake of the toxins.

Animals should be treated symptomatically

Anin1als frantically seek shade. Even short
for vaginal or rectal prolapse and physical
exposw-e to the sun rapidly produces the
damage to external genitalia. For sexually
typical erythema and edema of photodennamature sows with anestrus, one 10-mg dose titis in nonpigmented skin. The animals suffer
of prostaglandin F2a, or two 5-mg doses on
considerably, and deaths occur from one to
successive days, has corrected anestrus
several weeks after photodermatitis appears.

caused by retained corpora. Alfalfa and

Characteristic liver and bile duct lesions
alfalfa meal fed to swine at 25% of the ration
are seen in all affected animals whether
may reduce absorption and increase fecal
phot.osensitized or not. In acute cases
excretion of zearalenone, but this is often
showing photodern1atitis, livers are initially
not considered practical. Feeding activated
enlarged, icteric, and have a marked lobular
charcoal, cholestyran1ine, or alfalfa meal
pattern. Later, there is atrophy and marked
may reduce zearalenone absorption and
fibrosis. The shape is distorted, and large
retention, but the high concentrations
nodules of regenerated tissue appear on the
needed generally render this impractical.

surface. In subclinical cases, livers often
develop extensive areas in which the tissue is
depressed and shrunken below the norn1al

FACIAL ECZEMA
cont.ow-, which distorts and roughens the
capsule. Generally, these areas are associated

(Pithomycotoxicosis)

with fibrosis and thickening of corresponding

In this mycotoxic disease of grazing livebile ducts. The bladder mucosa commonly stock, the toxic liver iajury conunonly
shows hemorrhagic or bile pign1ent-stained
results in photodynamic dermatitis. In
ulcerative erosions with circumscribed
sheep, the face is the only site of the body
edema
readily exposed to ultraviolet light, hence

The clinical signs together with characthe common name. The disease is most teristic liver lesions are pathognomonic. In
conu11on in New Zealand but also occurs
live animals, high levels of hepatic enzymes
in Australia, France, South Africa, several
may reflect the extensive iajury to the liver.

3016

MYCOTOXICOSES

Control: To minimize intake of pasture
have been confim1ed in cattle, and sintilar
litter and toxic spores, short grazing should
lesions have been repmted in sheep.

be avoided. Other feedstuffs should be fed

Tall fescue is a cool-season perennial
dwing danger periods; encomaging clover
grass adapted to a wide range of soil and
dominance in pastmes helps to provide a
climatic conditions; it is used in Australia
milieu w1suited to growth and sporulation
and New Zealand for stabilizing the banks of

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of P chartarum on litter.

watercourses. It is the predominant pasture

The application of benzimidazole
grass in the transition zone in the eastern
fungicides to pastw-es considerably restJ.icts and central USA. Fescue lan1eness has been the buildup of P charta1um spores and repo1ted in Kentucky, Tennessee, Florida,
reduces pastw-e toxicity. A pasture area

California, Colorado, and Missomi, as well
calculated at 1 acre (0.45 hectare )/15 cows
as in New Zealand, Australia, and Italy.

or 100 sheep should be sprayed in midsum

The causative toxic substance, ergovamer with a suspension of thiabendazole.

line, has actions similar to those produced

When danger periods of fungal activity are
by sclerotia of Claviceps purpurea.

predicted, animals should be allowed only

However, ergot poisoning (seep 3012) is not on the sprayed areas. The fungicide is
the cause of fescue lan1eness. Ergotism
effective within 4 days after spraying,
is most prevalent in late SLinlmer when
provided that no more than 1 in. (2.5 cm)

the seed heads of grass matw-e. Fescue
of rain falls within 24 hr dming the 4-day
lameness is most conunon in late fall and
period. After this time, heavy rainfall does
winter and has been reproduced in cattle by
little to reduce the effectiveness of spraying, feeding dried fescue free of seed heads and because the thiabendazole becomes
ergot. However, occasionally, ergotized
incorporated within the plants. Pastmes
fescue seed produced in early summer may
will then remain safe for -6 wk, after which
inadve1tently be baled and result in ergot
spraying should be repeated to ensme
toxicosis instead of or in addition to fescue
protection over the entire dangerous
toxicosis.

season.

The endophyte fungusN coenophialum

Sheep and cattle can be protected from
growing within the fescue plant can
the effects of sporidesmin if given adequate
synthesize ergot alkaloids. The ergot
amounts of zinc. Zinc may be administered
alkaloid ergovaline has been detected in
by drenching witl1 zinc oxide slurry, by
toxic fescue and constitutes -900A, of the
spraying pastmes with zinc oxide, or by
ergopeptide alkaloids produced. Ergovaline
adding zinc sulfate to drinking water.

content of infected tall fescue often

Sheep may be selectively bred for natw-al
ranges from 100 to 500 ppb, and >200 ppb
resistance to the toxic effects of sporiis considered a toxic concentration.

desmin. The heritable trait for resistance

Susceptible species from most to least
is high. Ran1 sires are now being selected in
sensitive are horses, cattle, and sheep.

stud and commercial flocks for resistance

Endophyte-infected fescue that does not
either by natmal field challenge or by
produce ergovaline has not caused fescue
low-level, controlled dosage of ran1 lan1bs
toxicosis. In cattle, >900A, of ergovaline
with sporidesmin.

metabolites are found in urine. Removal
of aninrnls from infected fescue pasture

FESCUE POISONING
reduces urinary ergovaline below detectable concenti·ations within 48 hr.

Fescue Lameness

Ergovaline is an agonist for dopamine D2

(Fescue foot)

receptors, which initiate several physiologic
abnonnalities. First, inhibition of prolactin

Fescue lameness, which resembles ergot
secretion causes agalactia in horses and
poisoning, is believed to be caused by ergot
swine and reduced lactation in cattle. The
alkaloids, especially ergovaline, produced
dopan1inergic effect also causes imbalances
by the endophyte fungus Neotyphodium
of progesterone and estJ.·ogen, associated
coenophialum in tall fescue grass (Loli um witl1 early parturition for cattle and
arundinaceurn, fom1erly Festuca
prolonged gestation with oversized fetuses
arundinacea). It begins with lameness in
in mares. Finally, inadequate prolactin
one or both hindfeet and may progress to
disturbs the hypothalamic thennoregulanecrosis of the distal part of the affected tory center, leading to temperature
limb(s). The tail and ears also may be
intolerance when environmental temperaaffected independently of the lan1eness. In tw-e exceeds 31 °C (88°F).

addition to gangrene of these extremities,

Some reports indicate an increased
animals may show loss of body mass, an
incidence of fescue lan1eness as plants age
arched back, and a rough coat. Outbreaks
and after severe droughts. Strains of tall

MYCOTOXICOSES

3017
fescue vary in their toxicity ( eg, Kenenvironmental temperatures ai·e > 75° -80°F
tucky-31 is more toxic than Fawn) because

(24 ° -27°C) and if high nitrogen fertilizer has
of variation in infection level with the
been applied to the grass.

fungus and to high variability within a

Medical treatment for equine agalactia/
strain. ln some Kentucky-31 fescues,
reproductive syndrome is dompe1idone

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infection levels cannot be detected. High
administered at 1.1 mg/kg, PO, bid for 10---14
nitrogen applications appear to enhance
days. For control ai.1d prevention, toxic tall
toxicity. Susceptibility of cattle is subject to
fescue pastures must either be destroyed and
individual vaiiation.

reseeded with seed that does not contain

Low environmental temperature may
endophytic fungus, or infected fields must
exacerbate the lesions of fescue lameness;
be managed to avoid the high 1isk factor.

however, high temperatures increase the

Transfer of the fungus from plant to plant
severity of a toxic problem known as
is primaiily, if not solely, llu-ough infected
epidemic hyperthermia or "summer
seed. Not using pastures drning hot weather,
syndrome," in which a high proportion of a
diluting tall fescue pastures with interseeded
herd of cattle exhibits hypersalivation and
legwnes, clipping or close grazing of pastures
hyperthennia. The toxin appears to be a
to reduce seed fonnation, or offering other
vasoconstrictor acting as an a2-adrenergic
feedstuffs help reduce severity. Removing
agonist on blood vessels; this promotes
pregnant horses or cattle l mo before
hyperthem1ia in hot weather and results
partu1ition will usually prevent parturitionin cold extremities during cold weather.

and lactation-related problems. Specific

Another cause of this is poisoning with
feed additives may provide some protec

C purpurea ( ergot alkaloids).

tion against contaminated hay. Yeast cell

Erythema and swelling of the coronary
delivatives known as glucomatmatlS are
region occur, and cattle are alert but lose
reported to in1prove performance by preventweight and may be seen "paddling" or ing toxin absorption in cattle; a seaweed
weight-shifting. The back is slightly arched,
product is repo1ted to Jessen the inmlunoand knuckling of a hind pastern may be an suppressive effects of toxic tall fescue. (See
initial sign. There is progressive laineness,
a.I.so ABDOMINAL FAT NECROSIS, p 360.) anorexia, depression, and later, dry
gangrene of the distal linlbs (hindlirnbs

FUMONISIN TOXICOSIS
first). Signs usually develop within 10-21
days after turnout into a fescue-contami

Fwnonisins are responsible for two
nated pasture in fall. A pe1iod of frost tends
well-desclibed diseases of livestock, equine
to increase the incidence.

leukoencephalomalacia and porcine

For control, all infected forage should be
pulmonary edema.

removed.

Equine leukoencephalomalacia is a
mycotoxic disease of the CNS that affects
horses, mules, at1d donkeys. It occurs

Summer Fescue Toxicosis
sporadically in North and South An1erica,

Sununer fescue toxicosis is a waim season

South Africa, Europe, and China. It is
condition characterized by reduced feed
associated with the feeding of moldy com
intake and weight gains or milk production.

(maize), usually over a period of several

The toxin(s) affects cattle, sheep, at1d
weeks. Fwnonisins are produced worldhorses during the swnrner when they are wide primarily by F'usarium verticillioides
grazing or being fed tall fescue forage or

(previously Fmonil'if01me Sheldon) at1d
seed contaminated with the endophytic

Fprolijeratum. Conditions favoring
fimgusNeotyphodium coenophialum. The
ftunonisin production appeai· to include a
severity of the condition varies from field to
period of drought during the growing season
field at1d year to year.

with subsequent cool, moist conditions

Signs other than reduced perfonnat1ce,
during pollination and kernel fonnation.

which may appear within 1 -2 wk after

Tlu-ee toxins produced by the fungi have
fescue feeding is staited, include fever,
been classified as fumonisin B, (FB,), B
tachypnea, rough coat, lower serwn

2

(FB
prolactin levels, and excessive salivation.

2), and B3 (FB3). CuITent evidence
suggests that FB, at1d FB

The animals seek wet spots or shade.

2 ai·e of sin1ilar
toxicity, whereas FB

Lowered reproductive pelionnance also

3 is relatively nontoxic.

Com grain may conunonly contain 1-3 ppm
has been reported. Agalactia has been
fumonisins, but occasionally some years as
reported for both horses and cattle.

much as 20---100 ppm. The toxins are

Thickened placentas, delayed parturition,
concentrated prilnai·iJy in molded, damaged,
and birth of weak foals have been reported
or light test weight com. Major health
in horses. The severity increases when
effects are seen in Equidae and swine.

3018

MYCOTOXICOSES

Signs in Equidae include apathy,

No effective treatment is available.

drowsiness, pharyngeal paralysis,

Avoidance of moldy corn is the only
blindness, circling, staggeting, and
prevention, although this is difficult because
recwnbency. The clinical comse is usually
the corn may not be grossly moldy or may

1-2 days but may be as short as several
be contained in a mixed feed. However,

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homs or as long as several weeks. Icterus
most of the toxin is present in broken or
may be present when the liver is involved.

small, poorly fom1ed kernels. Cleaning grain

The characteristic lesion is liquefactive
to remove the screenings markedly reduces
necrosis of the white matter of the
fumonisin concentration. Corn suspected of
cerebrwn; the necrosis is usually unilateral
containing fumonisins should not be given
but may be asymmetrically bilateral. Some
to horses. Binding of fumonisins with
horses may have hepatic necrosis similar
glucose has been demonstrated to alleviate
to that seen in aflatoxicosis. Horses may
or eliminate toxicosis in pigs, but developdevelop leukoencephalomalacia from ment of the process on a commercial scale
prolonged exposure to as little as 8--10
has not yet been accomplished. Advisory
ppm fumonisins in the diet, and onset of
exposure guidelines by the FDA have
nemologic signs almost invariably leads
reco.nm1ended total dieta.ty concentrations
to death.

(ppm) as follows: horses <1, swine <10,

Fumonisins have also been repo1ted
ruminants <30, poultry <50, breeding
to cause acute epidemics of disease in
ruminants and poultiy < 15 ppm.

weanling or adult pigs, characterized by
pulmonary edema and hydrothorax.

MYCOTOXIC LUPINOSIS

Porcine pulmonary edema (PPE) is
usually an acute, fatal disease and appears

Lupines (Lupinus spp) cause two distinct
to be caused by pulmona.r.y hypertension
forms of poisoning in livestock: lupine
with transudation of fluids in the thorax,
poisoning and lupinosis. The fom1er is a
resulting in interstitial pulmona.r.y edema
nervous syndrome caused by alkaloids
and hydrothorax. Acute PPE results after
present in bitter lupines; the latter is a mycoconsumption of fumonisins for 3-6 days at toxic disease characterized by liver injury
dietary concentrations> 100 ppm. Morbidity and jaundice, which results mainly from the within a herd may be >509i,, and mortality
feeding of sweet lupines. Lupinosis is imporamong affected pigs is 500/o--l 000/o. Signs tant in Australia and South Africa and also
include acute onset of dyspnea, cyanosis
has been reported from New Zealand and
of mucous membranes, weakness,

Emope. There is increasing use of sweet
recun1bency, and death, often within 24 Ju·
lupines, either as forage crops or tJu·ough
after the first clinical signs. Affected sows
feeding of their residues after grain harvest,
in late gestation that survive acute PPE may
as sti·ategic feed for sheep in Mediterranean
abort within 2--3 days, presumably as a
climate zones. Sheep, and occasionally
result of fetal anoxia. Prolonged exposure
cattle and horses, are affected, and pigs
of pigs to sublethal concentrations of
are also susceptible.

fumonisins results in hepatotoxicosis
characterized by reduced growth;-icterus;

Etiology and Pathogenesis: The causal
and increased serum levels of cholesterol,
fungus is Phomopsis /,eptostromifonnis,
bilirubin, AST, lactate dehydrogenase, and
which causes Plwmopsis stem-blight,

-y-gluta.tnyltra.tIBferase.

especially in white and yellow lupines; blue

The biochemical mechanism of action for
varieties are resistant. It produces sunken,

PPE or liver toxicosis is believed to be due
linear stem lesions that contain black,
to the ability offumonisins to interrupt
stromatic masses, and it also affects the pods
sphingolipid synthesis in many animal
and seeds. The fungus is also a saprophyte
species, and fatalities result from disturand grows well on dead lupine material bances in cardiopulmonary dynamics

( eg, haulm, pods, stubble) under favorable
leading to acute pulmonary edema.

conditions. It produces phomopsins as

Cattle, sheep, and poultry a.r.·e considersecondary metabolites on infected lupine ably less susceptible to fumonisins than are
material, especially after rain.

horses or swine. Cattle and sheep tolerate
fumonisin concentrations of 100 ppm with

Clinical Findings, Lesions, and
little effect. Dieta.ty concentrations of

Diagnosis: Clinical changes are mainly

150-200 ppm cause inappetence, weight
attributable to toxic hepatocyte injury,
loss, and mild liver da.r.nage. Poultry are
which causes mitotic arrest in metaphase,
affected by concentrations of >200-400
isolated cell necrosis, and hepatic enzyme
ppm and may develop inappetence, weight
leakage, with loss of metabolic and
loss, and skeletal abnormalities.

excretory function.

MYCOTOXICOSES

3019

Early signs in sheep and cattle are
remains good, and anin1als will eat if feed
inappetence and listlessness. Complete
is provided. Affected animals may be
anorexia and jaundice follow, and ketosis is
belligerent and dangerous to approach
common. Cattle may show lac1imation and
or handle. After prolonged exposure,
salivation. Ketosis is a common sequela in
condition is lost and complete paralysis can

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pregnant cattle or recently calved cows.

occur. The time of onset of signs depends

Survivors may develop hepatic cirrhosis.

on the degree of the infestation of seed

Sheep may become photosensitive, and a
heads and the grazing habits of ilie animals.

skeletal muscle myopathy can develop. As

Experimentally, early signs appear in cattle
disease progresses, liver failure may cause
after sclerotia at -100 g/day has been adminhepatoencephalopathy characterized by istered for >2 days. Aliliough the mature
stumbling, disorientation, and recumbency
ergots are toxic, tl1ey are most dangerous
before death. In acute outbreaks, deaths
just when iliey are matwing to tl1e hard,
occur in 2-14 days.

black (sclerotic) stage.

In acute disease, icterus is marked. Livers

Medical treatment is usually not
are enlarged, orange-yellow, and fatty. More
necessary, unless animals have physical
clu·onic cases show bronze- or tan-colored
injuries or are compromised from
livers tl1at are firm, contracted in size, and
dehydration or lack of eating. Recovery
fibrotic. Copious amounts of transudates
follows removal of the anin1als to feed not
may be fow1d in the abdominal and thoracic
contaminated witi1 sclerotia of C paspali.

cavities and in ilie pericardia! sac. Some

Animals are Jess affected if left alone and
anin1als may have spongifom1 lesions in the
provided readily available nutritious
brain.

forages. Care should be taken to prevent

Feeding of moldy lupine material,
accidental access to ponds or rough terrain
togeilier with clinical signs and increased
where accidental trauma or drowning could
levels of serun1 liver enzymes, strongly
occur. 1bpping of the pasture to remove
indicate lupinosis.

affected seed heads has been effective in
control.

Control: Frequent surveillance of sheep
and of lupine fodder material for character

SLAFRAMINE TOXICOSIS
istic black spot fungal infestation, especially
after rains, is advised. The utilization of

Trifolium pratense (red clover) may
lupine cultivars, bred and developed for
become infected with tl1e fungus Rhizocto
resistance to P leptostromiformis, is
nia leguminicola (black patch disease),
advocated. Oral doses of zinc (�0.5 g/day)

especially in wet, cool years. Rarely, other
have protected sheep against liver injury
legwnes (white clover, alsike, alfalfa) may
induced by phomopsins.

be infected. Slaframine is an indolizidine
alkaloid recognized as tl1e toxic principle,

PASPALUM STAGGERS
and it is stable in dried hay and probably
in silage. Horses are highly sensitive to

This incoordination results from eating
slaframine, but clinical cases occur in
paspalun1 grasses (Paspalum spp) infested
cattle as well. Profuse salivation ( salivary
by Claviceps paspali. The life cycle of tlus syndrome) develops within hours after first
fungus is sin1ilar to that of C purpurea ( see conswnption of containinated hay; signs
p 3012). Toxic infestations are most likely
also include mild lacrimation, diarrhea, mild
after humid, wet summers. The yellow-gray
bloat, and frequent urination. Morbidity
sclerotia, which mature in the seed heads in
can be high, but deatl1 is not expected,
autumn, are round, roughened, and 2-4 mm
and removal of contaminated hay allows
in diameter. Ingestion of sclerotia causes
recovery and return of appetite witl1in
nervous signs in cattle most commonly, but

24-48 hr. A related alkaloid, swainsonine,
horses and sheep also are susceptible.

produced by R leguminicola, has caused a

Guinea pigs can be affected experimentally.

lysosomal storage disease from prolonged

The toxicity is not ascribed to ergot
exposure, but its importance in ilie salivary
alkaloids; ilie toxic principles are thought to
syndrome is not confirmed. Diagnosis is
be paspalinine and paspalitrem A and B,
tentatively based on recognition of ilie
tremorgenic compounds from the sclerotia.

characteristic clinical signs and the

A sufficiently large single dose causes
presence of"black patch" on ilie forages.

signs that persist for several days. Animals

Chemical detection of slaframine or
display continuous trembling of the large
swainsonine in forages helps to confirm the
muscle groups; movements are jerky and
diagnosis. There is no specific antidote to
in coordinated. If they attempt to run, iliey
slaframine toxicosis, although atropine may
fall over in awkward positions. Appetite
control at least some of the prominent

3020

MYCOTOXICOSES
salivary and GI signs. Removal of animals
radiomirnetic injury ( damage to dividing
from the contaminated hay is essential.

cells) is expressed as lyn1phopenia or

Prevention of Rhizoctonia infection of
pancytopenia. Eventually, hypotension may
clovers has been difficult. Some clover
lead to deatl1. Many of the severe effects
varieties may be relatively resistant to black
described for expe1irnental trichothecene

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patch disease. Reduced usage of red clover
toxicosis are due to dosing by gavage. From
for forages or dilution with other feeds is
a practical perspective, high concentrations
helpful.

of trichotl1ecenes often cause feed refusal
and therefore are often self-limiting as a

TRICHOTHECENE TOXICOSIS
toxic problem.

Because of tl1e irrununosuppressive

The trichothecene mycotoxins are a group
action of trichothecenes, secondary
of closely related secondary metabolic
bacterial, viral, or parasitic infections may
products of several families of imperfect
mask the primary injwy. The lymphatic
or plant pathogenic fungi. Those of most
organs are smaller than normal and may
importance in much of the world are
be difficult to find on necropsy.

produced species of F'usarium, but also

Refusal to consun1e contaminated
from genera of 'Ihchothecium, Myrothe
feedstuffs is the typical sign, which limits
cium, Cephalosporium, Stachybotrys,
development of otl1er signs. If no other food

'Jhchodesma, Cylindrocarpon, and
is offered, animals may eat reluctantly, but

Verticimonosporium. Trichothecenes are
in some instances, excessive salivation and
classified as nonmacrocyclic ( eg, deoxynivomiting may occur. In tl1e past, the ability valenol [DON] or vomitoxin, T-2 toxin,
to cause vomiting had been ascribed to
diacetoxyscirpenol [DAS], and others)

DON only (hence the common name
or macrocyclic ( eg, satratoxin, roridin,
vomitoxin). However, oilier members of
verrucarin). For livestock, the most
tl1e trichothecene family also can induce
in1portant trichothecene mycotoxin is
vomiting.

DON, which is commonly a contaminant of

In North America and many other pruts
corn, wheat, and other corru11odity grains.

of tl1e world, DON is a substantial concern

Lesser amounts ofT-2 toxin and DAS are
because of its corrunon occurrence in feed
found sporadically in the same somces.

grains and its well-known ability to cause

The trichothecene mycotoxins are highly
feed refusal. Swine appear to be most
toxic at the subcellular, cellular, and organic sensitive to feed refusal, with greater system level. Trichothecenes inhibit protein
tolerance by horses and dogs and even
synthesis by affecting 1ibosomes to
higher acceptance by rwninants.

interfere with protein synthesis and

In swine, reduced feed intake may occur
covalently bond to su[fhydryl groups.

at dietru-y concentrations as low as 1 ppm,

Toxicity of T-2 toxin and DAS is based on
and refusal may be complete at 10 ppm.

direct cytotoxicity and is often referred to

Ruminants generally will readily consume
as a radiomimetic effect ( eg, bone marrow
as much as 10 ppm dietru-y vomitoxin, and
hypoplasia, gastroenteritis, diarrhea,
beef cattle have tolerated 12-20 ppm in
hemorrhages). Direct contact with skin and
some circun1stances. Poultry may tolerate
oral cavity causes irritation and ulceration.

as much as 100 ppm. Horses may accept as

Stomatitis, hyperkeratosis witl1 ulceration
much as 35-45 ppm dietary DON witl1out
of tl1e esophageal portion of tl1e gastric
feed refusal or adverse clinical effects. Dogs
mucosa, and necrosis of the GI tract have
also will refuse foods containing DON,
been seen after ingestion of trichotl1ecenes.

usually at concentrations >5 ppm. Related

Systemic effects ofT-2 and DAS are often
effects of weight loss, hypoproteinemia, and
self-limiting because of oral irritation and
weakness may follow prolonged feed
feed refusal.

refusal. There is little evidence that DON

Given in sublethal toxic doses via any
causes reproductive dysfunction in
route, tl1e trichothecenes are irrunw10supdomestic animals. Experin1ental studies pressive in man1mals; however, longterm
suggest that DON may cause variable
feeding of high levels of T-2 toxin does not
effects of immunosuppression or imrnuseem to activate latent viral or bacterial nostimulation, but research is continuing to
infections. The toxins may affect function
define whetl1er DON has a practical role in
of helper T cells, B cells, or .macrophages,
disease susceptibility in field conditions.

or tl1e interaction among these cells.

Feed refusal caused by DON is a learned

Irritation of tl1e skin and mucous memresponse known as taste aversion. The branes and gastroenteritis are another set
major effect of DON is feed refusal; it is
of signs typical of trichotl1ecene toxicosis.

rarely if ever a cause of the trichotl1ecene

Hemorrhagic diathesis can occur, and the
effects described above. It appears related

SMOKE INHALATION

3021
to brain neurochemical changes in
abortions have been seen. Death may occur
serotonin, dopamine, and 5-hydroxyin 2-12 days.

indoleacetic acid. Feed refusal response to

Myrotheciotoxicosis and dendrodo

DON varies widely an10ng species. DON in
chiotoxicosis have been reported from the
swine causes conditioned taste aversion,
former USSR and New Zealand. The signs

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and swine appear to recognize new flavors
resemble those of stachybotryotoxicosis,

(eg, flavo1ing agents) added to DON-conbut death may occur in 1-5 days.

tain.ing feed and thus develop aversion to
the new taste as well. Once uncontaminated

Diagnosis: Because the clinical signs
feed is provided, animals usually resume
are nonspecific, or masked by secondary
eating within 1-2 days. A less well-known
infections and disease, diagnosis is difficult.

mycotoxin, fusaric acid, appears to interact

Analysis of feed is often costly and tin1e
with DON in the neurochemical response,
conswning but ideally should be attempted.

leading to feed refusal.

lnte1im measures are carefully examining

Confirmation of increased levels of DON
feedstuffs for signs of mold growth or
by analysis in a ration is often used to
caking of feed particles and switching to an
confirm DON-related feed refusal or to
alternative feed supply. Change of feed
judge the fitness of a feed ingredient.

supply often results in improvement and

However, some mycotoxins may be
tlms may provide one more clue that the

"masked" or undetected by routine assay
original feed was contanlinated.

methods. These coajugated mycotoxins
may escape detection and not provide

Control: Symptomatic treatment and
adequate warning of feed refusal levels. Use
feeding of uncontaminated feed are
of binders for DON mycotoxin is currently
recommended. Steroidal antishock and
an active area of research. Currently, the
anti-inflan1matory agents, such as methylalun1inosilicates effective for aflatoxins prednisolone, prednisolone, and dexamethappear not to be useful against DON.

asone, have been used successfully in

Glucomannan yeast-derived adsorbents
experin1entaJ t.tials. Poul tty and cattle are
may have potential to improve some aspects more tolerant of trichothecenes than are of DON feed refusal in swine, but work is
pigs. Pigs exposed to DON often recover
ongoing to clarify use of this catego1y of
appetite promptly when uncontanlinated
detoxicants. DON has been removed from
feed is offered.

barley by an abrasive pearling procedure,

DON-contaminated feed treated with
which removed two-thirds of DON with loss
various adsorbents, including calciun1
of only 15% of the grain mass. This and other aluminosilicates, bentonite, sodium fonns of cleaning grain may prove useful to
bisulfite, and yeast-based glucomarmans
decrease DON when alternative grain is not
have not been helpful to correct feed refusal
available. In addition, diverting grain from
in swine. Addition of 0.2% glucomarmari
swine to the more tolerable runlinants is an
mycotoxin adsorbent to DON-contaminated
alternative as well.

diet for pregnant sows increased percent

Macrocyclic trichothecene-related
age of pigs born live but did not correct
diseases have received a number of specific
reduced feed intake. Physical seed
names. The best known is stachybotryo
treat.tnent ( abrasive pearling procedure) has
toxicosis of horses, cattle, sheep, pigs, and removed two-thirds of DON from barley. In
poultry, first diagnosed in the fonner USSR
general, cleaning and removal of damaged
but occur1ing also in Europe and South
grain (screenings) improves feed quality

Af1ica. Cutaneous and mucocutaneous
and acceptance of mycotoxin-contanlinated
lesions, panleukopenia, nervous signs, and
grains.

SMOKE INHALATION

Smoke inllalation caused by fires is a major
of tl1em1al injwy to the upper airways,
cause of fatalities in anin1als. It usually
oxygen deprivation, and toxicity from
involves inllalation of a complex mixture of
inhaled materials. Smaller animals and in
toxicologic agents and pyrolysis products.

paiticular birds are usually more suscepti

If\iwy typically results from a combination
ble to inhaled toxicants because of their

3022

SMOKE INHALATION
greater respiratory minute volume per unit

Carbon monoxide poisoning is ubiquitous
mass and relatively larger respiratory
after smoke inhalation. Carbon monoxide is
surface area per unit mass.

produced by the incomplete combustion of
any orgai1ic material. Carbon monoxide

Etiology: Important agents involved in
binds to hemoglobin to forrn carboxyhemo

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smoke inhalation include thermal injury,
globin, which cannot carry oxygen and,
soot, carbon monoxide, cyanide gas,
therefore, results in tissue hypoxia. A visible
nitrogen, methane, oxides of nitrogen
flan1e is not necessaiy for carbon monoxide

(NOJ, zinc oxide, phosphorns, sulfur
poisoning, and gas appliances can liberate
trioxide, titanium tetrachloride, oil fog,
large ainounts of it. Epizootics of fatal

Teflon® particles, and Teflon® pyrolysis
cai·bon monoxide poisoning classically
products (polymer fun1e fever). Nitrogen
occur during periods of cold weather,
and methane are not especially toxic;
particularly after an electrical outage.

however, they are important in fires because

NOx have low water solubility, and low
they dilute oxygen in the breathable
concentrations generally cause delayed
atmosphere.

pulmonaiy irritation. Also, compared with

Inhalation thermal injury can occur
other agents, the N02 present in NOx reacts
without obvious external irtjuries and be
relatively slowly with respiratory secrerelatively slow to manifest, so it is often clinitions, forming nitrous (HN02) and nitric cally underestimated. Airway compromise

(HN03) acid. The end result is delayed
generally peaks 12-24 hr after initial irtjury.

chemical pneumonitis and pulrnonaiy

Except for steam inhalation and possibly
edema. These features often result in
inhalation of particles with continuing
delayed clinical recognition of NO, irtjuries.

pyrnlysis, inhalation thermal injuries are

Zinc oxide fumes are a classical cause of
usually confined to the upper aiiways
metal fun1e fever and are formed when zinc
because of their large heat capacitance.

or zinc alloys (eg, galvanized metals, brass)

Bums of the upper ai!way typically induce
ai·e heated. Metal fume fever is a classical
upper aiiway edema. Loss of oncotic
cytokine cascade acute phase-like
pressure and fluid resuscitation can
response. Notably, tolerance to zinc oxide
exacerbate these effects. Inhalation of stean1 fumes develops rapidly but is also quickly typically produces severe lung injuries.

lost.

Carbonaceous soot particles are not

Phosphorous, titanium tetrachloride,
especially toxic in themselves. However,
and sulfur trioxide fun1es ai·e notoriously
they act as carriers of other toxicants
irritating. Titanium tetrachloride releases
adsorbed onto the surfaces of soot particles. hydrochloric acid in contact with water This results in increased toxicant exposure
in respiratory secretions. Inhaled sulfur
and, depending on particle size, deeper
trioxide forms sulfuric acid when it contacts
penetration of toxicants into·the respiratory
respiratory secretions. Smoke machines
system. The degree and site of damage
that atomize mineral oils can produce an oil
depends on paiticle size, particle surface
mist that is mildly in-itating to the respiraarea, solubility, concentration, duration of tory system and may trigger underlying
exposw·e, and rate of particle clear!lllce.

respiratory conditions.

Large, chemically reactive and irritating

Inhalation of PTFE (Teflon®) fumes
particles tend to affect the upper airways
triggers acute malaise, fever, and respiraand are cleared quickly, whereas smaller, tory irritation (polymer fume fever). It can
low-solubility particles tend to affect the
result in severe chemical pneurrionitis and
deeper respiratory structures and are
is notoriously lethal for caged birds. In
cleai·ed more slowly.

addition to overheated cooking wai·e,

Important inhaled blood agents/

Teflon® fume fever has been caused by
asphyxiants that disrupt tissue oxygen
bwning of hair spray, dry lub1icants, and
delivery or utilization include cyanide,
water-proofing sprays.

carbon monoxide, nitrogen, and methane.

Cyanide inhalation is extremely common

Clinical Findings: The most important
with smoke inhalation. Essentially,
aspects of the history ai·e duration of
pyrolysis of most nitrogen-containing
exposure, the circumstances of exposure
materials (eg, nitrocellulose, nylon, wool,

( eg, enclosed versus open spaces), an1ount
silk, asphalt, polyurethane, and many
of smoke inhaled, severity of injury to other
plastics) will liberate cyanide. Cyanide is a
animals, and the sources of the smoke (ie,
rapidly acting histotoxic agent that inhibits
what toxicants are likely to have been
mitochondrial cytoclu·ome c oxidase, resultpresent in the smoke). Unfortunately, this ing in the arrest of aerobic metabolism. (See
type of information is rarely available.

also CYANIDE POISONING, p 2959.)

Exposure to smoke in an enclosed space,

SMOKE INHALATION

3023
prolonged entrapment, carbonaceous

Bronchoscopy and la.iyngoscopy are the
oculonasal discharges, a history of
gold standard methods to diagnose and
resuscitation, evidence of respiratory
assess smoke inhalation. Bronchoscopy is
distress, and altered consciousness all
the single most reliable method to establish
indicate a higher risk of serious lung
the diagnosis and extent/severity of injllly. It

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damage. Preexisting respiratory diseases
is generally superior to and more accmate

( eg, COPD) will likely increase the seve1ity
than other diagnostic methods (including
of injury.

clinical examination). Classic findings

Clinically serious smoke inhalation often
include severe subglottic injury, erythema,
occurs in the absence of obvious external
charring, deposition of soot, edema, and/or
physical injury. However, facial burns,
mucosa] ulceration.

oropharyngeal blistering and/or edema,

Ordinary pulse oximetry (two wavechanged voice, stridor, coughing, upper lengths) is inaccmate when carboxyhemoairway mucosa] lesions, and carbonaceous globin and/or methemoglobin are present.

discharges may be present. Evidence of

Both situations will generate falsely high
lower respiratory tract injury such as
pulse oximetry readings that are not
tachypnea, dyspnea, cough, decreased
reflective of the degree of underlying
breath sounds, wheezing, rales, rhonchi,
disease. Pulse co-oxin1etry (four or five
and retractions may be present. Both upper
wavelengths) is more reliable in these
and lower respiratory injury may be
situations.

relatively slow to develop and may peak

Pa02 is a poor indicator of carbon

12-24 hr or even later after exposure. There
monoxide poisoning and/or cellular
is always a substantial 1isk of delayed
hypoxia, because it reflects the amount of
airway obstruction secondary to upper
oxygen dissolved in blood. This is not
airway edema for at least 24-48 hr after
altered in carbon monoxide poisoning,
initial injury. Lack of apparent injury
because the dissolved oxygen is a small
immediately after smoke inhalation should
fraction of total a.iterial blood oxygen
not reduce the level of clinical suspicion.

content. Because blood gas machines

In general, evidence of asphyxiant
usually calculate oxygen satw-ation based
exposme commonly includes CNS
on Pa02, this measmement will also be
depression, changes in affect, lethargy,
inaccurate.

generalized muscle weakness, and

Blood carboxyhemoglobin measureobtundation. Nemologic injury seconda.iy ments may tmderestimate the actual level of
to hypoxia, often permanent, is common
exposme if oxygen has been administered
under these circun1stances. Coma after
before sample collection. Additionally,
smoke inhalation is most conm1only caused
there is a poor correlation between
by severe carbon monoxide poisoning and
carboxyhemoglobin level and the ultin1ate
the ensuing hypoxia. The prognosis is poor.

neurologic outcome in cases of significant

The onset of zinc oxide fume fever is
poisoning.

typically delayed by 4-8 hr after exposure.

Metabolic acidosis and increased lactate

Common clinical signs include general
is common when hypoxia, carboxyhemomalaise, cough, sternal pain, voice changes, globin, cyanide poisoning, methemoglobine-and fever. 'Iypically, these signs are

1nia, and trauma are present. Very high
self-lin1iting, and recovery is rapid unless
blood lactate levels are typical in acute
high levels of exposure have occurred. In
cyanide poisoning. Given the usually
these cases, there is often an apparent
slow turnaround tin1e associated with
period of recove1y followed by onset of
cyanide measmements, high levels of blood
dyspnea and respiratory distress 24-36 hr
lactate combined with a hist01y of smoke
later.

inhalation provide a strong index of

Polymer (Teflon®) fun1e fever typically
suspicion of cyanide poisoning. Cyanide
presents as general malaise, cough, sternal
measmements are strongly correlated
pain, voice changes, and fever. Severe lung
with exposU1·e and toxicity levels.

injmies are conm1on in birds, and sudden

Clinically significant smoke inhalation is
death is a common outcome.

often associated with declines in hemoglobin and PCV approximately 1 wk after Diagnosis: ln1portant diagnostic
expos me.

techniques include laryngoscopy/bronchos

Pulmonary radiographic changes after
copy, pulse oxin1etry/co-oximetry, arterial
smoke inhalation typically develop 24-36 hr
bloorl gases, carboxyhemoglobin level
after exposme. An initially clear chest radiodetermination, lactate level detennination, graph does not exclude significant lung

CBCs, chest in1aging, electrocardiography,
injury after smoke inhalation. Repeat
and pulmonary function testing.

imaging at 24-36 hr after exposure typically

3024

SMOKE INHALATION
demonstrates radiographic signs consistent
mia is not recommended in cases of smoke
with atelectasis, pulmonary edema, and
inhalation because of the risk of fmther
hyperinflation. Depending on the agents
reducing oxygen-carrying capacity of the
involved, late radiographic changes may
blood in the presence of carboxyhemoreflect fibrosis and bronchiolitis obliterans.

globinernia. Because of its efficacy, ease of

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CT changes typically develop earlier than
administration, and low toxicity, hydroxochest radiographic changes and classically cobalamin administration is currently
consist of peribronchial ground-glass
recommended in cases of smoke inhalation.

opacities and peribronchial consolidations.

Hydroxocobalamin can be combined with

Brain CT findings may demonstrate cerebral thiosulfate administration. Data are limited hypoxia-associated ischemia and injuries
on the effectiveness of thiosulfate alone;
to the globus pallid us, which are nearly
however, it is useful in cyanide poisoning
pathognomonic for carbon monoxide
and will not compromise oxygen-carrying
poisoning.

capacity of the blood (ie, unlikely to cause
harm and may be beneficial).

Treatment, Control, and Prevention:

Methemoglobinemia after smoke

Treatment involves maintenance of the
inhalation is unconunon and can be managed
airway, aggressive management of acute
with methylene blue treatment if required.

respiratory distress, antidote treatment if

Notably, N -acetylcysteine has been
warranted, suppression of inflammation,
effective for the treatment of polymer fume
and prevention of secondary infections
fever. Chest physiotherapy is regarded as
with broad spectrum antibiotics. Severe
being beneficial. Low tidal volmne
carbon monoxide poisoning combined
positive-pressure ventilation (PEEP) and
with significant smoke inhalation is almost
high-frequency percussive ventilation
unifonnly fatal in people; thus, euthanasia

(HFPV) have been demonstrated to
should be considered early in the treatment
increase short-tenn smvival in people but
and assessment processes.

are rarely available in veterinary practice.

Maintenance of the airway either by

Bronchodilation with a 132-agonist ( eg,
endotracheal intubation or tracheostomy
albuterol, terbutaline, epinephrine) is an
is often critical given that severe upper
impo1tant aspect of treatment, because
airway edema may occur. It is often better
smoke induces bronchospasm and
to intubate earlier in the disease progresbronchoconstriction. When combined with sion, because delayed airway edema may
airway edema, these effects contribute to
subsequently make intubation difficult or
airway obstruction.

impossible.

The effectiveness of corticosteroids after

Carbon monoxide poisoning should
smoke inhalation is contentious. Corticoalways be assumed to have occurred in steroids are notably beneficial in cases of
all individuals with s1i1oke inhalation. The
metal fume fever.

mainstay of treatment is oxygen supple

Control and prevention of smoke
mentation.

inhalation involves avoidance of exposure,

Some degree of cyanide poisoning should
adequate ventilation if smoke is likely to be
also be assumed in almost aH cases of smoke present, and use of smoke detection inhalation. Induction of rnethemoglobine-systems.

TOXICITIES FROM HUMAN DRUGS
ship must exist for veterinarians to
recommend extra-label use of these drugs
to their clients. Most are not approved for

Human drugs or nutritional supplements
veterinary use by the FDA, and safety of
available without a prescription are
most OTC drugs has not been determined
known as over-the-counter (OTC)

in animals. Veterinarians should undermedications. Exposures to OTC drugs in stand the potential risks of using OTC
pets can be accidental or intentional. A
medications and communicate these risks
valid client-patient-veterinarian relation-
to their clients.

TOXICITIES FROM HUMAN DRUGS

3025

COLD AND COUGH
etha.nolanline-derivative antihistamines

MEDICATIONS
occur within 1-5 hr; elimination half-lives
vary from 2.4-10 Ju·. A recommended dosage
of dimenhydrinate and diphenhydramine i.n

Antihistamines
cats and dogs is 4---8 mg/kg and 2-4 mg/kg,

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Antihistammes are H1-receptor antagonists
respectively. Hyperactivity or depressiol'.1,
that provide symptomatic relief of allergic
hypersalivation, tachypnea, and tachycarsigns caused by histanline release, including dia are the most common adverse effects pruritus and anaphylactic reactions. They
reported with these antihistamines,
are also used as sedatives and antiemetics.

generally within 1 hr of exposw·e.

Antihistan1ines belong to different classes

Promethazine hydrochloride is an
and are categorized as first- or secondethylanlino derivative ofphenothiazine generation (also called nonsedating)

and first-generation antihistamine used
antihistan1ines. First-generation antihistato manage motion sickness. Promethazi.Jle mines may cause adverse effects because of
is widely distributed in body tissues and
their cholinergic activity and ability to cross
readily crosses the placenta. Overdoses may
the blood-brain banier. Second-generation
result in CNS depression or excitation. CNS
antihistamines are more lipophobic than
depression was reported in a dog 30 min
first-generation antihistamines and are
after ingesting promethazine at 1 mg/kg.

thought to lack CNS and cholinergic effects

Meclizine is a first-generation piperaat therapeutic doses. Antihistan1ines are zine-derivative antiltlstamme conunonly
often found in combination with other
used as an antiemetic. Peak plasma
ingredients ( eg, decongestants, analgesics
concentrations occur within 2--3 hr of oral
like acetaminophen or NSAIDs) in many
administration. Meclizine is prinlarily

OTC cold, sinus, and allergy medications.

excreted as metabolites in urine, with a

Chlorpheniramine is a first-generation
reported serum half-life of 6 Ju·. The
propylarnine-derivative antihistamme. Oral
recommended dose in dogs is 25 mg/day
absorption of chlorpheniramine in dogs is

(per dog). When dogs have received
rapid and complete, reaching peak plasma
meclizine at <33 mg/kg, only mild hyperticconcentrations in 30-60 min. Chlorphetivity or depression has been reported.

nirarnine maleate undergoes substantial

Loratadine is a tricyclic, long-acting
first-pass effect. Chlorphenirarnine and
antihistamine with selective peripheral
its metabolites are primarily excreted in
hista.nline H1-receptor antago1tlst activity.

urine. The recommended dose in cats and

In people, loratadine is well absorbed orally
dogs is 1 -2 mg and 2---8 mg respectively, PO,
and extensively metabolized to an active
bid-tid. Mild clinical signs such as depresmetabolite. Most of the parent drug is sion and GI upset have been reported for
excreted unchanged in the urine. The mean
dosages < 1 mg/kg. Significant clinical signs
elimination half-life in people is 8.4 hr.

such as ataxia, tremors, depression or

Loratadine appears to have a large margin
hyperactivity, hyperthem1ia, and seizures
of safety in aninlals. The suggested dose
may be seen within 6 hr of ingestion of large
in dogs is 5-10 mg, PO, once to twice daily
amounts.

(per dog). No deaths were repo1ted at oral

Clemestine, because of its low oral
dosages up to 5 g/kg in rats and mice. In rats,
bioavailability in dogs (3% vs 20%-- 7()0;(, in
mice, and monkeys, no clinical signs were
people), may have limited effectiveness at
seen at 10 times the maxinmm recomthe recommended dosages of 0.05----0.1 mg/kg, mended hwnan daily oral dose.

PO, bid; 1.34 mg of clemestine fun1erate is

Cetirizine, a major metabolite of
equivalent to 1 mg of clemestine. Common
hydroxyzine, is a piperazine derivative
adverse effects of clemestine may include
nonsedating antihistamme. It selectively
sedation, lethargy, and a.nticholinergic signs
inl1ibits peripheral H1 receptors and does

( dry mouth, tachycardia, agitation,
not have significant a.nticholinergic or
decreased intestinal secretions/motility).

antiserotonergic effects when used at the

Dimenhydrinate and diphenhy
recommended dosage. The reconunended
dramine are first-generation ethanolaminedosage for histamine-mediated pmritic derivative antihistammes. Dimenhydrinate
conditions in dogs is 1 mg/kg, PO, once to
is used for its antiemetic effects and for
twice daily, and 5 mg, PO, bid for cats. The
prevention of motion sickness in dogs and
drug appears to be well tolerated in dogs
cats. Diphenhydramine is well absorbed
and cats. The minimum lethal dosage is
orally in people but undergoes first-pass

237 mg/kg in mice and 562 mg/kg in rats.

metabolism in the liver with only 40%--60%

Adverse reactions include vomiting,
of the drug reaching the systemic circulahypersalivation, sedation, drowsiness, tion. Peak plasma concentrations of
and occasionally hyperactivity.

3026

TOXICITIES FROM HUMAN DRUGS

Treatment: Treatment of antihistamine

Imidazolines are sympathomimetic
toxicosis is primarily symptomatic and
agents, with primary effects on a-adrsupportive. Emesis should only be energic receptors and little if any effect on
considered in asymptomatic patients.

13-adrenergic receptors. Oxymetazoline

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Activated charcoal may be useful for recent
is readily absorbed orally. Effects on
ingestion. Symptomatic patients should be
a-receptors from systemically absorbed
watched for anticholinergic signs (agitation, oxymetazoline hydrochloride may persist mydriasis, tachycardia, decreased intestinal
for up to 7 hr after a single dose. The
motility) and treated as needed. Cardiovaselimination half-life in people is 5-8 hr.

cular functions (heart rate and blood

It is excreted unchanged both by the
pressure) and body temperature should be
kidneys (30%) and in feces (lOOAi).

closely monitored. Propranolol (0.02-0.06
mg/kg, IV) can be helpful to treat consistent

Clinical Findings: In dogs, signs
tachycardia in normotensive patients.

of intoxication may include vomiting,

Diazepam can be used to control seizures
bradycardia, cardiac arrhythmias, poor
or seizure-type activity. Physostigrnine is
capillary refill tin1e, hypotension or
recommended to counteract the CNS
hypertension, panting, increased upper
anticholinergic effects of antihistamine
respiratory sounds, depression, weakness,
overdoses in people, although the risk of
collapse, nervousness, hyperactivity, or
seizures associated with this drng may limit
shaking. These signs usually appear within
its use. IV fluids should be given as needed.

30 min to 4 hr after exposure. In general,
inlidazoline decongestant exposure may
affect the GI, cardiopulmonary, and nervous

Dextromethorphan
systems.

Dextromethorphan is a nonsedating,
nonaddictive, centrally acting opioid

Treatment: Decontan1ination (induccough suppressant. It is available in many tion of emesis and administration of

OTC cold and cough medications. At
activated charcoal) may not be practical
the recommended dosage, it enhances
because of the rapid absorption and onset
the threshold for coughing. It is rapidly
of clinical signs. Heart rate and rhythm
absorbed orally and converts to the active
and blood pressure should be assessed,
metabolite dextrorphan in the liver. Cough
and an ECG obtained if needed. IV fluids
suppressant activity can last 3-12 hr,
should be given, along with atropine at
depending on the formulation. Overdoses

0.02 mg/kg, IV, if bradycardia is present.

can cause CNS and GI effects such as agita

Diazepam (0.25-0.5 mg/kg, IV) can be
tion, hallucination, nervousness, mydriagiven if CNS signs (eg, apprehension, sis, shaking, vomiting, or diarrhea. Some
shaking) are present. Serum electrolytes
clinical signs may be similar to those of

(ie, potassium, sodium, chloride) should
serotonin syndrome (agitation, disorientabe assessed and corrected as needed.

tion, hyperthermia, nervousness, shaking). Yohimbine, a specific a2-adrenergic Treatment is mainly supportive care.

antagonist, can also be used at 0.1 mg/kg,

Diazepam can be used to control some of

IV, and repeated in 2-3 hr if needed. If
the CNS effects. Phenothiazine tranquilizyohimbine is not available, atipamezole ers (acepromazine or chlorpromazine)

can be used at 50 mcglkg, one-fourth IV
or cyproheptadine (1.1 mg/kg, PO or per
and the rest IM; it can be repeated ·in
rectum, for dogs, and 2-4 mg per cat;

30-60 min if there is no improvement.

repeat once in 6-8 hr if needed) can be
given for serotonin syndrome.

Phenylephrine

Phenylephrine is a sympathomin1etic an1ine

DECONGESTANTS
with mainly an a1-adrenergic receptor
lmidazoline Decongestants
agonist effect, available OTC as a decongestant in oral formulations (5-10 mg The imidazoline derivatives, oxymetazotablets), nasal sprays, or eye drops line, xylometazoline, tetrahydrozoline,

(0.25%-1%). It has poor oral bioavailability
and naphazoline, are found in topical

(38%) in people because of a significant
ophthalmic and nasal decongestants
first-pass effect and extensive metabolism
available OTC. They are generally used as
by monoamine oxidases in the GI tract and
topical vasoconstrictors in the nose and
liver. The oral LD
eyes for temporary relief of nasal conges50 in rats and mice is 350 mg/kg and 120 mg/kg, respectively. The
tion due to colds, hay fever or other upper
half-life is 2-3 hr. CNS stimulation, agitation,
respiratory allergies, or sinusitis.

nervousness, and hypertension are possible

TOXICITIES FROM HUMAN DRUGS

3027
but less frequent with phenylephrine than

(3-4 mg/kg, IV), or pentobarbital to effect.

with pseudoephedrine. Treatment is mainly

Diazepam should be avoided, because it can
symptomatic care and is similar to that for
exaggerate hyperactivity. Phenothiazines
pseudoephedrine toxicosis (see below).

should be used with caution because they
can lower the seizure threshold, lower

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Pseudoephedrine and Ephedrine
blood pressure, and cause bizarre behavioral changes. Tachycardia can be con

Pseudoephedrine is a sympathomimetic
trolled with propranolol at 0.02---0.04 mg/kg,
drug found naturally in plants of the genus

IV, repeated if needed, or with esmolol at

Ephedra. Several states in the USA have

0.2---0.5 mg/kg, given.slowly IV or as a
limited the availability and use of pseuconstant-rate infusion at 25---200 mcg/kg/min.

doephedrine as an OTC decongestant

IV fluids should be given. Acidifying the
because of its use as a precursor in illegal
urine with ammonium chloride (50 mg/kg,
amphetamine synthesis. It is being replaced

PO, qid) or ascorbic acid (20-30 mg/kg, IM
with other decongestants such as phenylor IV, tid) may enhance urinary excretion of ephrine.

pseudoephedrine. Acid-base status should

Pseudoephedrine is a stereoisomer
be monitored if ammonium chloride or
of ephedrine and is available as the
ascorbic acid is given. Electrolytes, heart
hydrochloride or sulfate salt. Both
rate and rhytlun, and blood pressure should
ephedrine and pseudoephedrine have
be monitored. Excessive trembling or
a- and 13-adrenergic agonist effects. The
shaking can cause myoglobinuria; if this
pharmacologic effects of the drugs are due
occurs, kidney function should be
to direct stimulation of adrenergic receptors monitored. Significant and persistent and the release of norepinephrine.

hypertherrnia due to severe hyperactivity

In people, pseudoephedrine is rapidly
and CNS excitation could result in
absorbed orally. The onset of action is 15-30 disseminated intravascular coagulation.

min, with peak effects within 30-60 min.

Clinical signs of toxicosis can last 1-4 days.

With extended-release preparations (12-24

The presence of pseudoephedrine in urine
hr), onset of clinical signs can be delayed
can support the diagnosis.

(2-8 hr) and duration of clinical signs can be
longer than with regular preparations. It is
incompletely metabolized in the liver.

ANALGESICS

Approximately 900A, of the drug is elin1inated
through the kidneys. Renal excretion is

Over-the-Counter Nonsteroidal
accelerated in acidic urine. Elimination

Anti-inflammatory Drugs
half-life varies between 2-21 hr, depending

NSAIDs are the most commonly used class
on urinary pH.

of human medications in the world.

Because of their widespread availability and

Clinical Findings: Pseudoephedrine and
use, acute accidental ingestion of human
ephedrine overdose can result in mainly

NSAIDs in dogs and cats is quite common.

sympathon1in1etic effects, including

Ibuprofen, aspirin, and naproxen are some
agitation, hyperactivity, mydriasis,
of the most commonly encountered NSAIDs
tachycardia, hypertension, sinus arrhythin pet anin1als.

mias, anxiety, tremors, hypertherrnia, head

NSAIDs inhibit the enzyme cyclooxygebobbing, hiding, and vomiting. Clinical signs nase (COX; also referred to as prostaglandin can be seen at dosages of 5---6 mg/kg, and
synthetase ), blocking the production of
death may occur at 10--12 mg/kg.

prostaglandins. It is believed that most

NSAIDs act through COX inhibition,

Treatment: Treatment of pseudoephedalthough they may also have other rine toxicosis consists of decontamination,
mechanisms of action. (See also p 2714.)

controlling the CNS and cardiovascular

Ibuprofen, 2-( 4-isobutylphenyl)

effects, and supportive care. Vomiting
propionic acid, is used for its anti-inflanunashould be induced only in asymptomatic tory, antipyretic, and analgesic properties in
patients, followed by administration of
animals and people. It is rapidly absorbed
activated charcoal with a cathartic. If
orally in dogs, with peak plasma concentrathe animal's condition contraindicates tions seen in 30 min to 3 hr. Presence of food
induction of emesis, a gastric lavage with
can delay absorption and the time to reach
a cuffed endotracheal tube should be
peak plasma concentration. The mean elimiperformed. Hyperactivity, nervousness, or nation half-life is -4.6 hr. Ibuprofen is
seizures can be controlled with acepromametabolized in the liver to several metabozine (0.05---1 mg/kg, IM, IV, or SC), chlorlites, which are mainly excreted in the urine promazine (0.5---1 mg/kg, IV), phenobarbital
within 24 hr. The major metabolic pathway

3028

TOXICITIES FROM HUMAN DRUGS
is via coajugation with glucuronic acid,
liver, lungs, and heait. Salicylic acid is
sometimes preceded by oxidation and
eliminated by hepatic coajugation with
hydroxylation.

glucuronide and glycine. Renal clearance is

Ibuprofen has been recommended in
enhai.1ced by an alkaline urinaiy pH. There
dogs at 5 mg/kg. However, prolonged use
are significant differences in the elimination

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at this dosage may cause gastric ulcers and
ai.1d biotransformation of salicylates ainong
perforations. GI irritation or ulceration,
different species. Plasma half-lives vaiy

GI hemorrhage, and renal damage are the
from 1-37.6 hr in animals.

most commonly reported toxic effects of

Aspirin toxicosis is usually characterized
ibuprofen ingestion in dogs. In addition,
by depression, fever, hyperpnea, seizures,

CNS depression, hypotension, ataxia,
respirato1y alkalosis, metabolic acidosis,
cardiac effects, and seizures can be seen.

coma, gastric irritation or ulceration, liver

Ibuprofen has a nai.Tow margin of safety
necrosis, or increased bleeding tin1e.

in dogs. Dogs dosed with ibuprofen at

Seizures may occur as a consequence of

8-16 mg/kg/day, PO for 30 days, showed
severe intoxication, although the exact
gastric ulceration or erosions, along with
cause is unknown.

other clinical signs of GI disturbances. An

Cats ai·e deficient in glucuronyl transacute single ingestion of 100-125 mg/kg ferase and have a prolonged excretion of
can lead to vomiting, diarrhea, nausea,
aspi.J.in (half-life 37.5 hr). No clinical signs
abdominal pain, and ai.10rexia. Renal failure
of toxicosis occurred when cats were given
may follow dosages of 175---300 mg/kg. CNS
aspirin at 25 mg/kg every 48 hr for up to 4 wk.

effects (ie, seizures, ataxia, depression,

Dosages of 5 grains (325 mg), bid, can be
coma) in addition to renal and GI signs can
lethal to cats.

be seen at dosages >400 mg/kg. Dosages

Dogs tolerate aspirin better than cats;

>600 mg/kg ai·e potentially lethal in dogs.

however, prolonged use can lead to

Cats are susceptible to ibuprofen
development of gastric ulcers. Regular
toxicosis at approximately half the dosage
aspirin at dosages of 25 mg/kg, tid, has
required to cause toxicosis in dogs. Cats
caused mucosa! erosions in 50% of dogs
ai·e especially sensitive, because they have
after 2 days. Gastric ulcers were seen by day
limited glucuronyl-coajugating capacity.

30 in 66% of dogs given aspirin at 35 mg/kg,

Ibuprofen toxicity is more severe in ferrets

PO, tid. Sinillai·Jy, 43% of dogs given aspirin
than in dogs that consume sin1ilar dosages.

at 50 mg/kg, PO, bid, showed gastric ulcers

'lypical toxic effects of ibuprofen in ferrets
after 5-6 wk of dosing. Acute ingestion of
involve the CNS, GI, and renal systems.

450-500 mg/kg can cause GI disturbances,

Aspirin (acetylsalicylic acid), the
hyperthermia, panting, seizures, or coma.

salicylate ester of acetic acid, is the

Alkalosis due to sti.J.nulation of the
prototype of salicylate drugs. It is a
respirato1y center can occur early in the
weak acid derived from phenol. The oral
course of intoxication. Metabolic acidosis
bioavailability of aspirin may vaiy because
with an increased anion gap usually
of differences in drng formulation. Aspirin
develops later.

reduces prostaglandin and thromboxane

Naproxen, a propionic acid-derivative
synthesis by COX inhibition. Salic:ylates

NSAID, is available OTC as ai.1 acid or the
also uncouple mitochond1ial oxidative
sodiun1 salt. It is available as tablets or gel
phosphorylation and inhibit specific
caps (200-550 mg) or as a suspension ( 125
dehydrogenases. Platelets are incapable
mg/5 mL). Structurally and pha,rrnacologiof synthesizing new cyclooxgenase, leadcally, naproxen is si.J.nilai· to carprofen and ing to an effect on platelet aggregation.

ibuprofen. In people and dogs, it is used

Aspirin is rapidly absorbed from the
for its anti-inflaTI1matory, analgesic, ai.1d
stomach ai.1d proxin1al small intestine in
antipyretic properties.

monogastric animals. The rate of absorption

Oral absorption of naproxen in dogs is
depends on gastric emptying, tablet
rapid, with peak plasma concentration
disintegration rates, and gast1ic pH. Peak
reached ill 0.5-3 hr. The repo1ted eliminasalicylate levels are reached 0.5---3 hr after tion half-life in dogs is 34-72 hr. Naproxen
ingestion. Topically applied salicylic
is highly proteill bound (>99%). In dogs,
acid can be absorbed systemically.

naproxen is primai·ily elimi.J.1ated through

Aspirin is hydrolyzed to salicylic acid
the bile, whereas ill other species, the
by esterases in the liver and, to a lesser
pri.J.11aiy route of elirnillation is through the
extent, in the GI mucosa, plasma, RBCs,
kidneys. The long half-life of naproxen in
and synovial fluid. Salicylic acid is 50%-70%
dogs appeai-s to be because of its extensive
protein bound, especially to albumin.

enterohepatic recirculation.

Salicylic acid readily distributes to

Several cases of naproxen toxicosis in
extracellular fluids and to the kidneys,
dogs have been reported. Dosages of

TOXICITIES FROM HUMAN DRUGS

3029

5.6-11.1 mg/kg, PO, for3-7 days have ca.used salicylates because of the reduced risk of melena., frequent vomiting, abdominal pain,
gastric ulceration.

perforating duodenal ulcer, weakness,

Acetanlinophen is rapidly absorbed from
stumbling, pale mucous membranes,
the GI tract. Peak plasma concentrations
regenerative anemia, neutrophilia. with a left
are usually seen within an hour but can be

VetBooks.ir
shift, increased BUN and crea.tinine, and
delayed with extended-release fom1uladecreased total protein. Acute toxicity from tions. It is unifonnly distributed into most
a single oral dose of 35 mg/kg has been
body tissues. Protein binding varies from
reported. Ca.ts may be more sensitive to

5%-200/o. The metabolism of acetan1inophen
na.proxen toxicity than dogs because of their
involves two major conjugation pathways in
limited glucuronyl-cortjuga.ting ca.pa.city.

most species. Both involve cytochrome

P450 metabolism, followed by glucuronida.

Treatment: Treatment of NSAID
tion or sulfa.ti.on.

toxicosis consists of early decontamina

Ca.ts are more sensitive to acetanlinophen
tion, protection of the GI tract and
toxicosis, because they are deficient in
kidneys, and supportive ca.re. Vomiting
glucuronyl transferase and therefore have
should be induced in recent exposures,
linuted ca.pa.city to glucuronidate this
followed by administration of activated
drng. In ca.ts, acetaminophen is primarily
charcoal with a cathartic. Activated
metabolized via. sulfation; when this
charcoal can be repeated in 6-8 hr to
pathway is saturated, toxic metabolites are
prevent NSAID reabsorption from
produced. In dogs, signs of acute toxicity
enterohepa.tic recirculation. Use of
are usually not seen wuess the dosage

H,-receptor antagonists (ra.nitidine, famoof a.cetan1inophen exceeds 100 mg/kg.

tidine, cimetidine) may not prevent GI

Clinical signs of methemoglobinemia. have
ulcers but can be useful in treating them.

been rep01ted in 3 of 4 dogs at 200 mg/kg.

Omeprazole, a proton-pump inhibitor

Toxicity can be seen at lower dosages with
used to inhibit gastric acid secretions,
repeated exposures. In ca.ts, toxicity can
can be used instead of an H, blocker at
occur with 10-40 mg/kg.

0.5-1 mg/kg/day, PO, in dogs. Sucralfate

Methemoglobinemia. and hepa.totoxicity

(dogs: 0.5-1 g, PO, bid-tid; ca.ts: 0.25-0.5
characterize a.cetanlinophen toxicosis.

tablet, PO, bid-tid) reacts with hydrochlo

Renal i..njwy is also possible. Acute
ric acid in the stoma.ch and forms a
kera.toconjunctivitis sicca. has been
paste-like complex that binds to the
rep01ted in some dogs after acetaminophen
proteins in ulcers and protects them from
ingestion. Ca.ts primarily develop methemofurther damage. Because sucralfate globinemia. within a few hours, followed by
requires an acidic environment, it should

Heinz body formation. Methemoglobinemia.

be given ;,,30 min before administering H,
makes mucous membranes brown or
antagonists. Misoprostol (dogs: 1-3 mcg/
muddy in color and is usually accompanied
kg, PO, tid) has been shown to prevent GI
by tachycardia., hyperpnea., weakness, and
ulceration when used concomitantly with
lethargy. Other clinical signs of acetaminaspirin and other NSAIDs.

ophen toxicity include depression,
lV fluids should be given at a diuretic rate
weakness, hyperventilation, icterns,
if the potential for renal damage exists.

vomiting, hypothermia, facial or paw

Alkalinization of the urine with sodiwn
edema, cyanosis, dyspnea., hepatic necrosis,
bicarbonate results in ion trapping of
and death. Liver necrosis is more common
salicyla.tes in kidney tubules and can
in dogs than in cats. Liver damage in dogs
increase their excretion. However, ion
is usually seen 24-36 tu· after ingestion.

trapping should be used judiciously and

Centrilobula.r necrosis is the most common
only in cases when the acid-base balance
fonn of hepatic necrosis seen with a.cetan1ican be monitored closely. Baseline renal nophen toxicity.

function should be monitored and
rechecked at 24, 48, and 72 hr. Prognosis

Treatment: The objectives of treating
depends on the dose ingested and how
acetaminophen toxicosis are early
soon the animal receives treatment after
decontamination, prevention or treatexposure.

ment of methemoglobinemia. and hepatic
damage, and provision of supportive

Acetaminophen
ca.re. A Schirmer tear test (to confirm
keratoconjunctivitis) can be used if

Acetaminophen is a synthetic nonopiate
necessary. Induction of emesis is useful
derivative of p-aminophenol widely used in
when performed early. This should be
people for its antipyretic and analgesic
followed by administration of activated
prope1ties. Its use has largely replaced
charcoal with a cathartic. Activated

3030

TOXICITIES FROM HUMAN DRUGS
charcoal may be repeated, because

Ranitidine is widely distiibuted throughout
acetaminophen undergoes some
the body. H2 blockers are primarily
enterohepatic recirculation.

metabolized in the liver. Nizatidine,

Administration of N-acetylcysteine
famotidine, and ranitidine are excreted in

(NAC), a sulfur-containing amino acid,
the urine as metabolites and unchanged

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can reduce the extent of liver injury or
drng, whereas cimetidine is eliminated in
methemoglobinemia. NAC provides
feces. The elin1ination half-life for these
sulfhydryl groups, directly binds with
drngs is short (-2 .2 hr). Because cimetidine
acetaminophen metabolites to enhance
may inhibit the hepatic microsomal enzyme
their elimination, and serves as a glusystem, ingestion of an H2 blocker may tathione precursor. It is available as a lOOA, or
result in reduced metabolism of certain

200Aisolution. The loading dose is 140 mg/kg
drugs, including 13 blockers, calcium
ofa 5%solution IV or PO (diluted in 5%
channel blockers, diazepam, metronidazole,
dextrose or sterile water), followed by
and theophylline.

70 mg/kg, PO, qid for generally seven or

H2 blockers have a wide margin of safety,
more treatments (some authors recomwith acute oral overdoses typically resulting mend up to 17 doses). Vomiting can occur
in minor effects such as vomiting, diarrhea,
with oral NAC. NAC is not labeled for IV
anorexia, and dry mouth. Serious adverse
use; however, it can be administered as a
effects, such as tremors, hypotension, and
slow IV (over 1 5-20 min) with a0 .2-micron
bradycardia, are more likely to occur with IV
bacteriostatic filter. Activated charcoal and

H.-blocker overdoses. The minimum lethal
oral NAC should be administered 2 hr apart,
dose offamotidine in dogs is >2 gfkg, PO, and
because activated charcoal could adsorb

300 mg/kg, IV. Single oral doses of nizatidine

NAC.

at 800 mg/kg in dogs were not lethal. Most

Liver enzymes should be monitored and
exposures require only monitoring for
rechecked at 24 and 48 hr. The animal
development of GI signs and supportive
should also be monitored for methemocare, although massive overdoses may also globinemia, Heinz body anemia, and
warrant decontamination.

hemolysis. Fluids and blood transfusions
should be given as needed. Ascorbic acid

Antacids

(30 mg/kg, PO or injectable, bid-qid) may
further reduce methemoglobin levels.

Antacids come in pill and liquid forms

Cimetidine (5-10 mg/kg, PO, IM, or IV), a
and are frequently used to treat GI
cytochrome P4 50 in.ltibitor, may help reduce upset. Common antacids include calcium formation of toxic metabolites and prevent
carbonate, aluminum hydroxide, and
liver damage in dogs only. Cimetidine
magnesiun1 hydroxide (milk of magnesia).

should not be used in cats. In vitro evidence

These agents are poorly absorbed orally.

indicates that use of cimetidine in cats

Calcium- and aluminum-containing
can produce more toxic metabolites of
antacids generally cause constipation,
acetaminophen. S-Adenosyl methionine has
whereas magnesium-containing antacids
been suggested as an acljunct to manage
tend to cause diarrhea. Some products
acute or chronic hepatic injury at f8 mg/kg,
contain both aluminum and magnesium

PO, for 1-3 mo in dogs and cats.

salts in an attempt to balance their
constipating and laxative effects. Acute
single ingestion of calcium salts may cause

GASTROINTESTINAL DRUGS
transient hypercalcemia but is "unlikely to
be associated with significant systemic

H2-Receptor Antagonists
effects. Induction of emesis within 2-3 hr

Hrreceptor antagonists are strnctural
of exposure may help prevent severe GI
analogues of histamine, commonly used to
upset.

treat GI ulcers, erosive gastritis, esophagitis,
and gastiic reflux. They act at the H2

MULTIVITAMINS AND IRON
receptors of parietal cells to competitively
inhibit histamine, reducing gastiic acid

The common ingredients in multivitamins
secretions during basal conditions and
include ascorbic acid (vitamin C),
when stimulated by food, amino acids,
cyanocobalamin (vitamin B.,), folic acid,
pentagastrin, histamine, or insulin.

thiamine (vitamin B1), riboflavin (vitamin

Cimetidine, famotidine, nizatidine, and

B2), niacin (vitamin 83), biotin, pantothenic
ranitidine are examples of th.is group, also
acid, pyridoxine (vitamin B6), calcium,
commonly referred to as H2 blockers. These
phosphorus, iodine, iron, magnesiwn,
drngs are rapidly absorbed, reaching peak
copper, zinc, and vitan1ins A, D, and E.

plasma concentrations within 1-3 hr.

Among these ingredients, iron and vitamins

TOXICITIES FROM HUMAN DRUGS

3031

A and D may cause significant systemic
nausea, peeling skin, weakness, tremors,
signs. Acute ingestion of other listed
convulsions, paralysis, a11d death.

ingredients in companion anin1als can result

Vitamin Dis included in ma11y calciw11
in self-limiting GI upset ( eg, vomiting,
supplements to aid the absorption of the
diarrhea, anorexia, lethargy). However,
calcium. Most vitamins contain cholecal

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toxicity is typically rare in pets.

ciferol (vitamin 03). After consumption,

Multivitan1in preparations contain varying cholecalciferol is converted into 25-hydroamounts of iron. Unless otherwise listed, xycholecalciferol ( calcifediol) in the liver,
iron should be asstm1ed to be elemental iron.

which is subsequently converted to the

Various iron salts may contain 12o/o-48%
active metabolit� 1,25-dihydroxycholecalelemental iron. Iron has direct caustic or ciferol ( calcitriol) in the kidneys. One IU of
irritant effects on the GI mucosa. It can also
vitainin D,3 is equivalent to 0.025 mcg of
be a direct mitochondrial poison. Once the
cholecalciferol. Even though the oral LD,,o
iron-carrying capacity of serun1 has been
of cholecalciferol in dogs has been reported
exceeded, free iron is deposited in the liver,
as 88 mg/kg, signs have been seen at
where it dan1ages mitochondria and leads to
dosages as low as 0.5 mg/kg. Vomiting,
necrosis of periportal hepatocytes. Signs of
depression, polyuria a11d polydipsia, a11d
iron toxicosis usually develop within 6 hr.

hyperphosphatemia may be seen within 12

Initial vomiting and diarrhea, with or
hr of a significant vitai11in D exposw·e,
without blood, may be followed by
followed by hypercalcemia a11d acute renal
hypovolemic shock, depression, fever,
failure in 24-48 hr. In addition to renal
acidosis, and liver failure 12-24 hr later,
failure, the kidneys, heart, a11d GI tract may
often with a period of apparent recovery in
show signs of necrosis a11d mineralization.

between. Oliguria and anuria secondaiy to

Initial treatment should include decontamishock-induced renal failure may also occur.

nation a11d assessment of baseline calciwn,

Ingestion of elemental iron at >20 mg/kg
phosphorus, BUN, and creatit1ine. Multiple
generally warra11ts decontamination
doses of activated charcoal with a cathartic

(emesis) a11d administration of GI protectshould be administered. If clinical signs of a11ts. Activated charcoal does not bind iron
toxicosis a11d significa11t hypercalcemia/
well. Additional treatment a11d monitoring is
hyperphosphatemia develop, treatment
necessaiy for patients that have ingested
consists of saline diuresis a11d the use of
elemental iron at >60 mg/kg. Milk of
furosemide, corticosteroids, a11d phosphate
magnesia (magnesiun1 hydroxide; 5-30 mL
binders. Specific agents such as (salmon)

once or twice daily, per dog) ca11 complex
calcitonin or painidronate may be needed
with iron to decrease its absorption from
for anitnals that remain hypercalcemic
the GI tract. Serun1 iron levels a11d the total
despite symptomatic treatment. Stabilizaserun1 iron binding capacity should be tion of serum calciun1 may require days of
checked at 3 hr a11d again at 8-10 hr after
treatment because of the long half-life of
exposure. If serun1 iron is >300 mcg/dL
calcifediol (16--30 days).

along with clinical signs such as repeated
vomiting a11d shock, or greater tha11 the total
iron binding capacity, chelation therapy may

TOPICAL PREPARATIONS
be needed. Deferoxai11ine ( 40 mg/kg, IM,
every 4-8 hr) is a specific iron chelator a11d

Zinc Oxide
is most effective within 24 hr of ingestion,

Zinc oxide ointments or creams are
before iron has been distributed from blood
commonly used as topical skin protectto tissues. Other signs should be treated ants, astringents, and bactericidal agents.

symptomatically.

Most ointments contain 10%-40% zinc

Vitamin A toxicity after consumption of
oxide. Acute ingestion of zinc oxidelarge amounts of fish oil or bear's liver has containing products usually results in
been well documented, but it is less likely to
gastric irritation (vomiting) and diarrhea,
occur after acute ingestion of m ultivitainins. without the intravascular hemolysis and The ainount of vitamin A needed to cause
liver and renal damage associated with
toxic effects is 10-1,000 times the dietaiy
ingestion of elemental zinc. Signs are usurequirements for most species. The vitamin ally seen within 2-4 hr of a significant

A requirement for cats is 10,000 IU/kg of
exposure. Vomiting animals should be
diet fed, with levels up to 100,000 IU/kg of
managed symptomatically a11d supportdiet considered to be safe. For dogs, the ively. Some dogs show hypersensitivityrequirement is 3,333 IU/kg of diet fed, with type reactions manifested by facial and
up to 333,300 IU/kg of diet considered to be
ocular edema. Such cases can be treated
safe. Signs associated with acute vitan1in A
with diphenhydrarnine or other antiallertoxicity include general malaise, a11orexia, gic medications.

3032

TOXICITIES FROM HUMAN DRUGS

HERBAl SUPPLEMENT'S

Veterinarians also can prescribe certain
hun1an drugs for anin1als. Safety data for

Ma Huang (Ephedrine) and Guarana
human prescription drugs in ce1tain anin1al

{Caffeine)

species may not be available-most are not

Several herbal supplements, sold with the
approved for veterinary use by the FDA.

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claim of providing weight loss and energy,

A valid client-patient-vete1inarian relationcontain guarana (Paullinia cupana ), a ship must exist for veterinarians to
natural source of caffeine, and ma huang
recommend extra-label use of htm1an

(Ephedra sinica), a natural source of
prescription medications to their clients.

ephedrine. The an1ount of ma huang and
guarana present in herbal products may

CARDIOVASCULAR MEDICATIONS
vary considerably (labels should be read

See also
for amounts). In people, use of herbal

SYSTEMIC PHARMACOTHERAPElITICS OF
supplements containing guarana and ma

THE CARDIOVASCULAR SYSTEM, p 2525.

huang have been linked to acute hepatitis,
nephrolithiasis, hypersensitivity myocardi

Angiotensin-converting Enzyme
tis, and sudden death. In dogs, accidental

(ACE) Inhibitors
ingestion of herbal supplements containing

Several angiotensin-converting enzyme
ma huang and guarana can have synergistic

(ACE) inhibitors ( eg, enalapril, captopril,
effects when ingested together and can
lisinopril, benazepril) are used therapeutilead to severe hyperactivity, tremors, cally to treat congestive heart failure in dogs
seizures, vomiting, tachycardia, hypcrtherand cats. The primary concern in cases of mia, and death within a few hours of
acute ACE inhibitor overdose is usually
exposure. The use of ephedra-containing
marked hypotension. If hypotension is
supplements has been banned by the FDA.

severe, secondary renal damage may

For treatment, seep 3027.

result. Onset occurs within a few hours of
exposure, depending on the agent ( extended

5-Hydroxytryptophan
release fonnulations may have a delayed

Several OTC herbal supplements containonset of action). Other clinical signs of ing 5-hydroxytryptophan (5-HTP) or
overdose may include vomiting, poor

Oriffonia seed extracts claim to treat
mucous membrane color, weakness, and
depression, headaches, insomnia, and
tachycardia or bradycardia. Activated
obesity. Orally, 5-HTP is rapidly absorbed
charcoal is effective in binding the drug from
and constitutively converted to serotonin
the GI tract if administered within 1-2 hr of

(5-hydroxyttypta.mine). In cases of 5-HTP
ingestion. Blood pressure should be
overdose, excessive concentrations of
monitored and IV fluids given at twice the
serotonin at target cells (GI, CNS,
maintenance rate if hypotension develops.

cardiovascular, and respiratory systems)

Renal function should be monitored if
can lead to a serotonin-like syndrome in
severe or persistent hypotension develops.

dogs (eg, seizures, depression, tremors,
ataxia, vomiting, diarrhea, hyperthe1mia,

Calcium Channel Blockers
transient blindness, and death). Clinical

CalcitU11 chaimel blockers ( eg, diltiazem,
signs can develop within 4 hr after
amlodipine, nifedipine, verapa.mil) inhibit
ingestion and last up to 36 hr. Treatment
movement of calcium from extracellular
consists of early decontan1ination, control
sites through cell membrane-based calciwn
of CNS signs (diazepam, barbiturates,
charmels. The most common signs seen
phenothiazines such as acepromazine or
with overdoses of calcium charmel blockers
chlorpromazine ), thennoregulation ( cool
are hypotension, bradycardia, GI upset,
water bath, fans), fluid therapy, and
noncardiogenic pulmonary edema, and
administration of a serotonin antagonist
heart block. Reflex tachycardia may
such as cyproheptadine (1.1 mg/kg, PO or
develop in response to the drop in blood
rectally for dogs, and 2-4 mg per cat, once
pressure.

or twice at an 8-hr interval).

Management of an acute overdose
includes correcting hypo tension and
rhythm disturbances. In general, emesis
is induced within 2 hr of ingestion only if
the animal is showing no clinical signs.

Induction of emesis in animals with signs

Pets commonly ingest prescription
can increase vagal tone and worsen the
medications from counte1tops, pill minders,
bradycardia. Activated charcoal binds
mail-order packages, or other sources.

unabsorbed dmg in the GI tract ai1d is most

TOXICITIES FROM HUMAN DRUGS

3033
useful when administered within the first
bradycardia and hypotension; respirato1y
few hours after ingestion; if a sustaineddepression, coma, seizures, hyperkalemia, release product was ingested, repeat doses
and hypoglycemia may occm. It is also
of activated charcoal every 4-6 hr for a
possible to precipitate congestive heart
total of2-4 doses can provide additional
fail me. Significant clinical signs may arise

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benefit. Specific therapies should be
even at therapeutic (published) doses-no
instituted based on blood pressme, heart
approved veterinary products are on the
rate, ECG, and blood chemistry profiles.

market.

IV fluids are recommended; calcium

Because of rapid absorption, emesis
gluconate (10% solution at 0.5-1.5 mL/kg,
should only be induced in asymptomatic
slow IV) should be added while monitoranimals within 2 hr'of ingestion. Adminising the ECG closely. Atropine (0.02-0.04
tration of activated charcoal should be
mg/kg) can be given for bradycardia;
considered if either multiple tablets or
isoproterenol can be used if the ECG
capsules or sustained-release formulation
indicates atrioventricular block. For
tablets are ingested. Heart rate, blood
persistent hypo tension not corrected by
pressure, and clinical condition should be
administration of IV fluids, synthetic
monitored for several hours, because
colloids (Hetastarch), dopamine (1-20
extended-release pills can lead to delayed
mcg/kg/min), or dobutamine (2-20 mcg/kg/ onset of clinical signs. If clinical signs do min) can be given via continuous IV
develop, blood chemist.ties should also be
infusion. A temporary cardiac pacemaker
measmed. Hypotension should be treated
may be needed in cases of severe cardiac
with IV fluids; atropine can be used for
conduction distmbances unresponsive lo
bradycardia. Glucagon or isoproterenol
medical therapy. Calcium channel blockers can also be used if needed (see above). If may interact with almost any other
hyperkalemia is confirmed, administration
cardioactive medication, resulting in
of insulin, followed by IV glucose, may d1ive
more profound bradycardia, hypotension,
the excess potassitm1 back into the cells.

and depression of cardiac contractility.

Because of the lipophilic nature of calciLun
channel blockers, using IV lipid emulsion

Phenylpropanolamine
solution (IntralipidTM 20% solution) may

Phenylpropanolarnine (PPA) is a sympathohelp sequester calcium channel blockers mimetic amine used p1imarily for t.t·eating
in overdose situations and prevent them
urinaiy incontinence in dogs and cats. PPA
from reaching their site of action. The
is believed to indirectly stimulate both
recommended dose of 20% lipid emulsion
ex- and 13-adrenergic receptors, causing the
solution in dogs is 1.5 mlJkg, IV, as an
release of norepinephrine. It is rapidly
initial bolus followed by 0.25 mL/kg/min
absorbed orally and distributes to various
for 30-60 min. This dose can be repeated in tissues, including the CNS. PPA is mainly 6 hr for a total of three treatments. Serum
excreted through the kidneys as a parent
color and response should be monitored. If drug. Overdose of PPA can result in CNS
serwn color is yellow, repeating the dose
effects ( restlessness, agitation, nervousshould be delayed until it becomes clear.

ness) and cardiovascular signs (hyperten

If no response is seen after three doses,
sion or hypotension, tachycardia or
lipid emulsion should be discontinued.

bradycai·dia, premature ventricular

Hyperlipidemia, infection, intravascular
contractions, cai·diovascular collapse).

hemolysis, lack of efficacy, and embolism

Dogs can also show piloerection, hype1°
are potential adverse effects associated
emia, vomiting, hypertl1ermia or hypotherwith IV lipid emulsion therapy. The use of mia, and mydriasis. Treatment consists of

IV lipid emulsion for the treatment of some
early decontamination ( emesis in asympto

Jipophilic drug overdoses is experimental
matic animals within a couple of hours
and should be considered only if other
of ingestion, followed by acln1inistration
conventional treatment options fail.

of activated chai·coal). CNS effects and

Efficacy and safety of IV lipid emulsion
mild hypertension can be managed with
has not been studied.

acepromazine (0.02 mg/kg, IV or IM,
repeated as needed). A nit.t·oprusside
constant-rate infusion can be tried for

13 Blockers
hypertension not responsive to aceproma

Drugs in this class ( eg, propanolol,
zine. Lidocaine can be considered for
metoprolol, atenolol, tin10lol, esmolol) act
t.t·eating premature ventriculai· contractions.

by competitively inhibiting catecholamine

IV fluids should be given to promote
binding to 13-adrenergic receptor sites. The
excretion. Other signs should be treated
most common signs of overdose are
symptomatically.

3034

TOXICITIES FROM HUMAN DRUGS

Diuretics
closely monitored for responsiveness to

Oral diuretic agents include thiazides ( eg,
stimuli and adequate breathing. IV fluids
chlorothiazide, hydrochlorothiazide), loop
will help suppo1t blood pressure. If the
diuretics such as furosemide, and potasaffected animal is recumbent and severe siwn-sparing agents such as spironolactone
respiratory depression has developed, the

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(an aldosterone antagonist) and trian1-
reversal agent flwnazenil can be given at a
terene. Osmotic diuretics, administered by
dosage of0.01 mg/kg, slow IV, in both cats
ir\jection, include mannitol and w·ea. The
and dogs. Flumazenil has a short half-life,
most common signs of diuretic overdose
so it may need to be repeated. Benzodiazeinclude vomiting, depression, polyi.u'ia and pines should not be used to control CNS
polydipsia, and electrolyte changes.

excitation, because a paradoxical reaction

Electrolytes, especially potassiw11, may
may occur. ln such situations, low doses of
shift subsequent to a large ingestion of a
acepromazine or barbiturates may be useful
diuretic. Management should include
to control initial CNS excitation.

monitoring hydration and electrolytes,
with correction as needed.

Antidepressants

Antidepressants fall into several classes. An

TRANQUILIZERS,
overdose of almost any of them can result

ANTIDEPRESSANTS, SLEEP AIDS,
in development of serotonin syndrome

AND ANTICONVULSANTS

(see below).

See also

Selective Serotonin Reuptake

SY�'TEMIC' Pl IAllMAC'OTIIERAPElrr!CS OF

Inhibitors: Selective serotonin reuptake

TME ERVOUS SYSTEM, p 2590.

inhibitors (SSR!s) include sertraline,

Benzodiazepines
fluoxetine, paroxetine, and fluvoxamine.

They block the activity of serotonin

Benzodiazepines bind -y-aminobutyiic acid
receptors at presynaptic membranes and

(inhibitory neurotransmitter) receptors and
have little effect on other neurotransmitare used for seizure control and as anxiolyters. In veterinary medicine, these SSR!s tics. Whereas diazepam is probably best
are sometimes used to control aggres

!mown in the veterinary field, alprazolam,
sion, obsessive-compulsive disorder,
chlordiazepoxide, clonazepan1, lorazepam,
separation anxiety, pruritus, and
oxazepam, and triazolam are all commonly
inappropriate elimination in dogs and
prescribed medications. In general, all are
cats. Overdosage of SSRis in dogs and
rapicily and fairly completely absorbed,
cats is manifested by vomiting, lethargy,
lipophilic, and highly protein bound.

mydriasis, ataxia, shaking, seizures,

Metabolism is mostly by glucuronidation,
hyperactivity, tachycardia or bradycarso cats may be more sensitive to adverse dia, and vocalization (see below).

effects. Several have active metabolites ( eg,
diazepan1, clorazepate) and consequently

Tricyclic Antidepressants: Tticyclic
have much longer duration of signs.

antidepressants ( eg, amitliptyline, clomi

The most common signs seen, at a wide
pramine, nortliptyline) are commonly used
range of dosages, are CNS depression,
psychoactive agents. They are stt·ucturally
respiratory depression, ataxia, wealrness,
similar to the phenothiazines, with similar
disorientation, nausea, and vomiting. Some
anticholinergic, adrenergic, and ex-blocking
anin1als, especially at high doses, may
properties. After absorption, these agents
show CNS excitation instead of depression
are extensively boW1d to plasma proteins

(paradoxical reaction), which may be
and also bind to tissue and cellular sites,
followed by CNS depression. Otl1er
including the mitochondria Cyclic anticommon signs are hypothennia, hypotendepressants block the anune pwnp and sion, tachycardia, muscle hypotonia, and
stop neuronal reuptake ofnorepinephrine,
meiosis. Some cats develop signs of acute,
serotonin, and dopan1ine. These agents also
potentially fatal hepatic failure after
appear to have a slight cx-adrenergic blocking
repeated oral administration of diazepan1
effect. Tricyclics may exe1t their major toxicfor several days.

ity via a nonspecific membrane-stabilizing

Emesis can be induced if ingestion is
effect, similar to chlorpromazine and the 13
recent and no clinical signs are present.

blockers. Tricyclics also have central and

Gastric lavage, followed by administration
petipheral anticholinPrgic activity, along
of activated charcoal, can be performed
with antihistanlinic effects. Clinical signs of
if the ingested amount is very high. The
toxicosis include CNS stimulation (agitation,
anin1al should be kept warm and quiet and
confusion, pyrexia), cardiac arrhythmias,

TOXICITIES FROM HUMAN DRUGS

3035
hype1tension, myoclonus, nystagmus,
such as acepromazille or chlorpromazine
seizures, metabolic acidosis, winary
also have alltiserotonergic effects alld Call
retention, dry mouth, mydriasis, and
be used to control hyperactivity. Benzocliazconstipation. This may be followed by CNS
epilles such as diazeparn Call be used to
depression (lethargy), ataxia, hypothermia,
control CNS effects. 13 blockers such as

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respiratmy depression, cyanosis, hypotenproprai10lol (0.02-0.04 mg/kg, TV) Cal1
sion, and coma.

be used to control tachycai·dia. Other
treatment measures may illclude induction

Monoamine Oxidase Inhibitors: Monoof emesis ill asymptomatic anin1als within an1ine oxiclase inhibitors are antidepressants 2 hr of exposure, followed by administraused mainly to treat atypical depression in tion of activated charcoal alld IV fluids.

people. In dogs, selegiline, a monoamine_
oxiclase-B inhibitor, is used to treat Cushing

Barbiturates
disease and cognitive clysfw1ction ( canine
dementia). Selegiline is absorbed rapidly

Both long-acting and sho1t-acting barbituorally. Metabolites of selegiline include rates may be encountered. The long-acting_
amphetamine and metharnphetamine. Its
group includes phenobarbital, mephobarb1-
halI-life in clogs is
tal, alld primidone-all commonly used as

-1 hr.

allticonvulsallts or sedatives. The short

Miscellaneous (Atypical) Antidepres
acting (butabarbital, pentobarbital, secobar
sants: These antidepressants have
bital) alld ultra short-acting (thiarnylal alld
nonselective receptor-blocking effects and
thiopental) bai·biturates ai·e used mainly for
are used when SSRis or t1icyclic antidepresinduction of allesthesia ai1d seizure control.

sants have not been effective. Exan1ples

All are readily absorbed from the gut all cl
include bupropion, trazoclone, and
have extensive liver metabolism; metabomiitazapine.

lites are prm1aiily excreted via the kidneys.

The onset of clinical signs vaiies from 15

Treatment: Emesis should be induced in
min to several hours, alld duration Call be up
cases of recent exposure
to several days for the long-acting class. The
if the anin1al is
asymptomatic. This can be followed by
most common signs are sedation, ataxia,
activated charcoal ( even several hours after
respiratory depression, coma, loss of
ingestion) plus a cathaitic
reflexes, h

�uch as sorbitol
ypotension, alld hypotherrrua.

or sodiwn sulfate (magnes1wn sulfate 1s

Management is ain1ed at life support .

contraindicated, because it can add to CNS
while attempting to remove wm1etabohzed
depression). Diazeparn can be given to
drug from the body. Emesis should be

.

control seizures. Serotonin syndrome signs
induced if the exposure is very recent alld
should be managed as needed. Heait rate
the animal is asyn1ptomatic. Gastric lavage
and rhythm should be monitored, and
while protecting the airway Call remove
carcliac arrhythmias treated. Atropine
much of the drug still ill the stomach.

should not be used to control bradycarclia,

Activated charcoal readily adsorbs
because it can aggravate anticholinergic
barbiturates; small doses repeated eve1y
effects of tricyclic antidepressants.

4-6 hr Call further decrease the body
burden even if overdose has resulted from
use of ::.n iI\jectable product. IV fluids Call be

Serotonin Syndrome: This group of
clinical signs usually includes three of the
given to support blood pressure. Respirafollowing features: altered mental status, tory effort alld effectiveness needs to be
agitation, nervousness, myoclonus,
closely monitored; treatment may reqwre

.

h
positive-pressure ventilation or oxygen.

ype1Teflexia, tremors, diaIThea, incoord1-
nation cardiovascular changes (!,ea.it rate

Doxaprarn (1-5 mg/kg, slow IV in dogs,
and bl�od pressure), alld fever.

alld 5-1 O mg/cat) may help to stimulate

It often
occurs because of repeated use or overdose
respiration. Support to maintain body
or ingestion of substai1ces that result in
temperature may be necessary. Comatose
illCreased free levels of serotonin, such as
anin1als should be intubated with a cuffed
alltidepressallts or profound stirnulallts
endotracheal tube, because aspiration is a

(eg, arnphetai11ines). Cyproheptadine is
common complication. Depencling on the
a serotonin antagonist often used for
dose, aggressive supportive treatment may
treatment. It is available only as a tablet but
be necessary for 1-3 days.

call be dissolved ill a small ai11ount of saline
alld admmisterecl per rectwn at 1.1 mg/kg ill

Sleep Aids
dogs or 2 mg/dose in cats. If there is a good Zolpidem, zaleplon, alld eszopiclone
response to the initial dose, it Call be . .

are drugs used as sleep aids and have a
repeated only if signs recur. Phenothiazmes
mechaitlsm of action Silllilar to that of the

3036

TOXICITIES FROM HUMAN DRUGS
benzodiazepines. These agents have a ve1y
shaking, coma, seizLLres, bradyca.rdia,
rapid onset ( usually <30 min) and a similarly hypothem1ia, and blood pressLLre abno1°
short half-life. While the expected result
malities. Cyclobenzaprine, often used in
from ingestion would be marked sedation,
management of acute muscle spasms, is
paradoxical excitement also occLLrs.

almost completely absorbed after an oral

VetBooks.ir

Dosages as low as 0.22 mg/kg have resulted
dose, with peak plasma levels in 3-8 hr.

in sedation and ataxia, and dogs have

It has extensive liver metabolism and
developed tremors, vocalizing, and pacing

W1dergoes enterohepatic recirculation.

at dosages as low as 0.6 mg/kg.

The most common signs seen in dogs and

GI decontamination can be performed if
cats include depression and ataxia.

the ingestion was recent and no signs are

Treatment of muscle relaxant overdose
seen. For mild signs, keeping the pet quiet
consists of symptomatic and supportive
and in a safe place may suffice. U paradoxicare. Vomiting should be induced if the cal excitement develops, symptomatic
exposLLre is recent and no clinical signs are
treatment should be given and will vary witl1 present, followed by administration of tl1e signs and their intensity. Hyperexcitaactivated charcoal. Respiratory support tion may be controlled witl1 low doses of

(ie, ventilator) should be provided if
acepromazine or other phenothiazines. Use
needed. Recumbent or comatose animals
of diazepa.m may aggravate signs of CNS
should be monitored for hypothermia and
depression. Flwnazenil (0.01 mg/kg, IV) can
aspiration. Seizures can be controlled witl1
be used if clinical signs of toxicosis a.re
diazepa.m. Cyprohepta.dine (1.1 mg/kg, PO,
severe.

once or twice every 8 hr) seems to work
well for vocalization in dogs. IV fluids
should be given as needed. Treatment with

Phenothiazine Tranquilizers

IV lipid emulsion solution may be

The most commonly used phenothiazines
beneficial (seep 3032).

in veterinary medicine are acepromazine,
chlorpromazine, and promazine. In domestic
anin1als, tl1ey a.re used as tranquilizers,

TOPICAL AGENTS
preanestl1etic a.gents, a.ntiemetics, and for
treatment of CNS agitation after specific

Pets ingest many topical preparations, often
drng overdoses (amphetamines, cocaine).

resulting in only mild gastroenteritis. For

The most common signs of overdose a.re
example, ingestion of most corticosteroidsedation, weakness, ataxia, collapse, containing crean1s or ointments usually
behavioral changes, hypothermia., hypotenresults in only mild to moderate stomach sion, tachycardia, and bra.dycardia.

upset, polydipsia, and polyphagia.. However,

Treatment consists of symptomatic and
ingestion of certain topical agents in pet
supportive care. Because of the rapid onset
animals, such as 5-fluoroura.cil and ca.lcipotof CNS signs, emesis should only be riene, can be fatal even at low doses.

attempted in a recent exposLLre and should
be followed by administration of activated
charcoal and a cathartic. Repeated doses

5-Fluorouracil
of activated charcoal may be helpful,

5-FluoroLLracil (5-FU) is available as an
especially for large ingestions. Hypotension
ointment (1 % or 5%) or topical solution (1 %,
should be treated with IV fluids. Dopamine

2%, or 5%). It is used in tl1e treatment of skin
may be used if fluid administration does not
cancers and solar kera.toses in people. Most
correct hypo tension. Body temperature,
exposLLres result from accidental ingestion,
heart rate, and blood pressw·e should be
altl1ough occasionally 5-FU is used
monitored and treated symptomatically.

extra-label in pets. Ingestion in dogs and
cats leads to the onset of signs within a few
how·s. In dogs, signs have been seen at

MUSCLE RELAXANTS
dosages as low as 8.6 mg/kg, with the
minimwn lethal dose reported as 20 mg/kg.

The most commonly encow1tered centrally

Initial signs include severe vomiting, which
acting muscle relaxants include ba.clofen,
may progress to bloody vomiting and
ca.iisoprodol, metl1ocarba.mol, tizanidine,
diruThea. Signs often progress to severe
and cyclobenza.prine. Ba.clofen is rapidly
tremors, ataxia, and seizLLres. In cats and
absorbed orally. The onset of clinical signs
dogs, 5-FU may be converted to fluorociof toxicosis may be <30 min to 2 lu- after trate and interfere with fue Kreb's cycle,
ingestion. The most common signs of
which may be one cause of seizures a.11d
toxicosis a.re vocalization, salivation,
ataxia. Generally, 5-FU destroys rapidly
vomiting, ataxia, weakness, tremors,
dividing cells, affecting the GI tract, liver,

TOXICITIES FROM HUMAN DRUGS

3037
kidneys, CNS, and bone marrow. The

Treatment of calcipotriene toxicosis
mortality rate among dogs ingesting 5-FU
involves standard decontan1ination ( emesis
is high.

induction, administration of activated

All 5-FU exposures in pets should be
charcoal and a cathartic) and reduction
treated aggressively. Treatment consists
of serum calcium concentrations by saline

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p1imarily of symptomatic and supportive
diuresis, furosemide, and corticosteroids,
care. Emesis should be induced, and the
with or without salmon calcitonin treatment
animal given activated charcoal and a

(seep 568). Concurrent use of pamidronate
cathartic if it is asymptomatic and the

(1.3-2 mg/kg diluted in saline and given IV
ingestion has occuned within 1 hr.

over 2 hr) in dogs may be a useful adjunctive

Symptomatic animals ( eg, vomiting or
therapy. Calcipotriene toxicosis cases
seizuring) should be stabilized first. The GI
usually require monitoring of serum
tract should be protected with sucralfate
calcium, phosphorus, BUN, and creatinine

(1 gin large dogs, 0.5 g in small dogs, PO,
for several days or even weeks. Signs of
tid) and inhibitors of gastric acid secretion
renal failure are managed with ongoing
such as cimetidine. Diazepam may be used
supportive fluids.

initially to control seizures and tremors, but
in severe cases it is usually not effective,

PRESCRIPTION NONSTEROIDAL
and other anticonvulsants such as
pentobarbital (3-15 mg/kg, IV slowly

ANTI-INFLAMMATORY DRUGS
to effect) or phenobarbital (3-30 mg/kg,

For a general discussion of commonly seen
slowly IV to effect) can be used. Constantadverse effects and treatment of NSAID
raLe infusion using diazepam or barbiturates toxicosis, seep 3027.

has successfully controlled severe seizures.

If this also fails to control CNS signs, gas

Etodolac
anesthetics ( eg, isoflurane) and propofol

( 4-6 mg/kg, IV, or as a continuous drip at 0.6

Etodolac is an indole acetic acid-derivative
mg/kg/min) can be tried. IV fluids should be

NSAID labeled for use in dogs to treat pain
given, and body temperature monitored.

and inflammation associated with

Monitoring electrolytes, serum chemistries
osteoarthritis. It is rapidly absorbed orally,

(liver-specific enzymes and renal function),
with peak sernm concentrations seen 2 hr
and CBC is usually required for -2 wk.

after dosing. It is primarily eliminated

Surviving dogs may show evidence of bone
through the bile. The elimination half-life
manow suppression later. For severe
is 8--12 hr. Etodolac appears to be well
neutropenia in dogs, administration of
tolerated by dogs when used at the labeled
filgrastim or granulocy:te colony-stimulating
dosage (10-15 mg/kg/day, PO) for 1 yr. With
factor at 4-6 mcg/kg, SC, may be useful.

multiple doses, clinical signs of toxicity
such as GI ulcers, vomiting, diarrhea, and
weight loss can be seen at 40 mg/kg. Six of 8

Calcipotriene
dogs died or became moribund because of

Calcipotriene, used to treat psoriasis

GI ulceration at 80 mg/kg.

in people, is available as an ointment or
crean1 (0.005% or 50 mcg,'g). Calcipotriene

Meloxicam
is a novel structural analogue of calcitriol

Meloxican1 is an enolic acid-derivative

(1,25-dihydroxycholecalciferol), the most

NSAID approved for use in dogs and cats
active metabolite of cholecalciferol
for controlling pain and inflammation.

(vitan1in D3). Accidental ingestion of 40--60

Meloxicam is available as a solution
mcg/kg of calcipotriene in dogs has been
for injection (5 mg,'mL) and as an oral
associated with life-threatening hy:percalcesuspension. In cats, it has been approved mia. Clinical signs usually occur within
for use as a single SC injection at 0.3 mg/kg.

24-72 hr of ingestion and include anorexia,

In dogs, the recommended initial dosage
vomiting, diarrhea, polyuria and polydipsia,
is 0.2 mg/kg, followed by 0.1 mg/kg, PO.

depression, and weakness. Serwn calcium

Meloxican1 has a good margin of safety in
is usually increased within 12-24 hr and
dogs. Oral administration at 0.1 mg/kg for
may remain above normal for weeks. This

26 weeks was well tolerated in dogs. Some
is usually accompanied by an increase in
dogs at 0.3 or 0.5 mg/kg, PO, for 42 days
serum phosphorus concentration and
have shown clinical signs consistent with
calcium phosphorus product and soft-tissue

NSAID toxicity (vomiting, dianhea, renal
mineralization. Acute renal failure as
effects). In caL'>, the margin of safi>ty
evidenced by increased BUN and creatinine
appears to be narrow; extra-label dosing
levels, coma, and death occur in severe or
at 0.1-0.2 mg/kg, PO, for a few days has
untreated cases.

caused adverse effects.

3038

TOXICITIES FROM HUMAN DRUGS

Deracoxib

Etodolac is well absorbed orally in dogs,

Deracoxib is a coxib COX--2 inhibitor (in
with peak plasma concentration seen in
vitro) used to treat osteoarthritis in

2 hr. It is primarily excreted through bile,
dogs.

It is not approved for use in cats. The
and the half-life in dogs is 8-12 hr. In dogs,
recommended dosage is 1-2 mg/kg/day or
etodolac at 40 mg/kg/day was associated

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3-4 mg/kg/day as needed for postoperative
with GI ulcers, weight loss, emesis, and
pain, not to exceed 7 days of therapy. Oral
local occult blood Joss. Dosages of
bioavailability in dogs is > 900/o; the time to

80 mg/kg/day caused 6 of 8 dogs to die or
peak serum concentration is -2 hr. In a
become moribund because of GI ulceration.

14--day study of dogs that received 10 mg/kg,
no clinically observable adverse effects

Nabumetone
were seen. Dogs that received 25 mg/kg/day,

Naburnetone differs from other NSAIDs

50 mg/kg/day, or 100 mg/kg/day for 10-11
in that it is neutral as opposed to acidic.

days showed vomiting and melena; no

The risk of GI ulcers from nabw11etone is
hepatic or renal lesions were seen in these
considered less than that of other NSAIDs.

dogs. Dogs ingesting > 100 mg/kg should be

Nabumetone is primarily excreted in the
aggressively decontaminated and treated
wine in most species. However, in dogs,
with IV fluids to prevent renal dan1age.

when nabun1etone was administered at

20 mg/kg, only 27% of the dose was found
in the urine. The reported oral LD

Piroxicam

50 of
nabu.rnetone in rats is >2 glkg. At a dosage

Piroxican1 is an oxicam derivative. It is not
of >300 mg/kg, the lower GI tract and the
approved in dogs and cats but has been used kidneys were affected in rats, mice, rabbits, at 0.3 mg/kg, PO, every other day. Piroxican1
and rhesus monkeys.

in dogs and people has a long half-life ( 40 hr
and 50 hr, respectively) likely due to
extensive enterohepatic recirculation. The
irOXICITIES FROM ILLICIT

LD.50 of piroxicam in dogs is > 700 mg/kg.

ND ABUSED DRUGS

Adverse GI effects were seen in 18% of dogs
given piroxica.rn at 0.3 mg/kg/day, PO, for

Exposmes to illicit or abused drugs in pet
several months.

animals can be accidental, intentional, or
malicious. Occasionally, drug-sniffing dogs
also ingest these substances. Because of the

Diclofenac
illegal nature of illicit or abused drugs,

Diclofenac is a phenylacetic acid derivative
owners may provide inaccmate, incomstructmally related to meclofenamate plete, or misleading exposw·e histories.

sodium and mefenan1ic acid. After a single

Illicit drugs are often adulterated with other
injection of diclofenac sqdiw11 at 1 mg/kg in
pharmacologically active substances,
dogs, 35%--400/o is excreted in the mine. The
making the diagnosis even more difficult.

reported oral LD50 of diclofenac sodiw11 in

In suspected cases of exposure to illicit or
dogs is 500 mg/kg.

abused drugs, an attempt should be made to
gather infom1ation about the animal's
lndomethacin
environment; amount of exposme; and time

Indomethacin is an indole acetic acid
of onset of clinical signs and their type,
derivative available as the base and as
severity, and dmation. These questions will
the sodium trihydrate salt. The drug is
help include or exclude possible exposme
structurally and phan11acologically related
to an illicit or abused drug. Illicit and abused
to another NSAID, sulindac. The reported
drugs are often known by street names that
oral LD
vary from area to area. A call to a local

50 of indomethacin in rats is 12 mg/kg.

Administration of indomethacin to dogs at
police station, or anin1al or human poison

2 mg/kg for 30 days resulted in GI ulcers in
control center, may help identify the illicit

600/o of dogs and perforation in 200/o.

substance if its street name is known. Most
human hospitals, emergency clinics, and
some veterinary diagnostic laboratories

Etodolac
have illicit drug screens available and can

Etodolac, an indole acetic acid derivative,
check for the presence of illicit drugs or
is used for pain relief, osteoarthritis, and
their metabolites in different body fluids.

rhew11atoid arthritis in people. It is

The presence of a parent drug or its
approved in the USA for use in dogs
metabolites in blood or mine may help

(> 12 mo old) to manage pain and inflammaconfim1 exposme in suspect cases. The tion associated with osteoarthritis. The
laboratories should be contacted for
suggested dosage in dogs is 10-15 mg/kg.

information on the types of samples needed

TOXICITIES FROM HUMAN DRUGS

3039
and time required to complete the screens

Clinical Findings and Diagnosis:

or tests.

Clinical signs of ru11pheta.J.11ine and cocaine

Commonly available over-the-counter
toxicosis are similar and difficult to
drug test kits may help exclude a suspected
differentiate clinically. The only difference
case of illicit drug toxicosis. They are
may be U1e longer duration of clinical signs

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designed to detect drug metabolites in
of amphetamine toxicosis because the
the urine and can detect most commonly
half-life of an1phetamine is longer than
available illicit or recreational drugs such as

U1at of cocaine. The most commonly
amphetamines, cocaine, marijuana, opiates,
reported signs a.re hyperactivity, aggression,
and barbitmates. The sensitivities and
hyperthennia, tremors, ataxia, tachycru·dia,
specificities of these test kits may vary. The
hypertension, myd1iasis, circling, head
kits are inexpensive, efficient, and easy to
bobbing, and death.

use, but the instructions provided with each

Diagnosis is as for cocaine (see below)

kit should be followed carefully for best
and relies mostly on owner knowledge of
results.

exposure. Most amphetamines and related
drugs or their metabolites a.re detectable in
the stomach contents and urine. They are

Amphetamines and Related Drugs
difficult to detect in plasma unless large

Amphetamines and their derivatives are
runounts have been ingested.

CNS and cardiovascular system stimulants
commonly used in people for suppression

Treatment: Phenothiazines are preferred
of appetite, na.rcolepsy, attention deficit
to control CNS signs in an1pheta.J.1line
disorder, parkinsonism, and some behavior toxicosis (see below for cocaine toxicosis).

disorders. Some commonly encountered

Other anticonvulsants, such as diazepam,
amphetamines or related drugs a.re benzbarbiturates, or isoflurane, may be used if phetamine, dextroamphetan1ine, lisdexamneeded. Acidifying the urine with ammofetamine, pemoline, methylphenidate, nium chloride (25-50 mg/kg/day, PO, qid) or
phente1mine, diethylpropion, phendimeascorbic acid (20-30 mg/kg, PO, SC, IM, or trazine, methan1phetamine, and phenme

IV) may enhance ru11phetamine elinlination
trazine. Amphetamines sold on the street
in the wine. However, this should be done
have common names such as speed,
only if acid-base status can be monitored.

bennies, or uppers. Commonly used

Cyproheptadine (1.1 mg/kg, PO or per
adulterants are caffeine, ephedrine, or
rectun1) may also be given once or twice
phenylpropanolamine.

(6--8 hr apart) for serotonin syndrome

(disorientation, muscle stiffness, agitation).

Pharmacokinetics and Toxicity:

Heart rate and rhythm ( see p 3040 for using Amphetantlnes a.re rapidly absorbed in U1e

13 blockers to treat tachycardia), body

GI tract, reaching peak plasma concentratemperature, and electrolytes should be tions in 1-2 hr. Sustained-release formulamonitored and treated as needed.

tions have a delayed absorption and
relatively longer half-life. The plasma
half-life of an1phetamines depends on the

Cocaine
urinary pH. With an alkaline pH, the half-life
is 15-30 hr; with an acidic pH, the half-life is

Cocaine (benzoylmethylecgonine) alkaloid

8-10 hr. The acute oral LD
is obtained from the leaves of the coca

50 of amphetamine
in rats and mice is 10---30 mg/kg. ln people,
plant, Erythroxylon coca and E monogym
deaths have been repo1ted after ingestion
num. Some common street names for
of metharnphetamine at 1.3 mg/kg.

cocaine a.re coke, gold dust, stardust, snow,

C, white girl, white lady, baseball, and
speedball (cocaine and heroin). Cocaine

Pathogenesis: Amphetanline stimulates
alkaloid from coca leaves is processed into
the release of n01·epinephrine, affecting
cocaine hydrochloride salt, then reproboth c,- and [3-adrenergic receptor sites.

cessed to form cocaine alkaloid or free base

Amphetamine also stimulates catechola

( a process called free-basing or base
nline release centrally in U1e cerebral
balling), which is colorless, odorless,
c01tex, medullruy respiratory center, and
tra.J.1Spa.rent, and more heat stable.

reticulru· activating system. It increases the

Free-base cocaine is also called crack, rock,
amount of catecholantlne at ne1ve endings
or flake. Cocaine is cut ( diluted) several
by increasing release and inhibiting
times before it reaches the user. Xanthine
reuptake and metabolism. The neurotransalkaloids, local anesthetics, and decongesmitters affected in the CNS a.re norepinephtants a.re some of the most common rine, dopanline, and serotonin.

adulterants.

3040

TOXICITIES FROM HUMAN DRUGS

Cocaine is a schedule II drug approved for clinical signs should be stabilized first before hwnan use. Its medical uses are restricted to attempting decontamination. Emesis can be topical administration as a local anesthetic
induced in a recent exposure if the anin1al is
on mucous membranes of the oral, larynasymptomatic and has tl1e ability to guard its geal, and nasal cavities. However, it is
airway via a gag reflex. This should be
mostly used as a recreational drug.

followed by administration of activated

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charcoal with a cathartic. lithe anin1al's

Pharmacokinetics and Toxicity:

condition contraindicates induction of

Cocaine is absorbed from most routes.

emesis ( eg, presence of CNS signs or

Orally, it is better absorbed in an alkaline
extreme tachycardia), a gastric lavage with a
mediwn (ie, intestine). In people, -200;6 of an cuffed endotracheal tube to reduce the risk oral dose is absorbed. The reported plasma
of aspiration should be perfonned. A dose of
half-life is 0.9-2.8 hr. Cocaine is extensively
activated charcoal with a cathartic should be
metabolized by liver and plasma cholinesleft in the stomach after the lavage.

terases to several inactive metabolites that

Controlling the CNS signs may require use
are p1imarily excreted in the urine. The
of more than one anticonvulsant. Clinical
acute LD5() of cocaine hydrochloride
signs of CNS excitation can be controlled
administered IV in dogs is 13 mg/kg; the
with diazepam; however, the effects of

LD IOo is 12 mg/kg in dogs and 15 mg/kg in
diazepam are short-lived, and repeated
cats. The oral LD5() in dogs is believed to be
administration may be needed. Phenothia2-4 times more than the IV dose.

zine tranquilizers such as acepromazine

(0.05----1 mg/kg, IV, IM, or SC, repeated as

Pathogenesis: Cocaine acts on the
needed) or chlorpromazine (0.5----1 mg/kg, IV
sympathetic division of the autonomic
or IM) also usually work well to control the
nervous system. It blocks the reuptake of

CNS effects. However, phenothiazines
dopamine and norepinephrine in the CNS,
should be used cautiously, because they may
leading to feelings of euphoria, restlessness,
lower the seizLu-e threshold. lf phenothiaand increased motor activity. Cocaine can zines are ineffective, phenobarbital at 3-4
also decrease concentrations of serotonin
mg/kg, IV, or pentobarbital, IV to effect,
or its metabolites. Topical use of cocaine
could be used. lf CNS signs are uncontrolled
causes vasoconstriction of small vessels.

by the preceding measures, a gas anesthetic

Hyperthem1ia in cocaine toxicosis may
such as isoflw·ane may be useful.

develop either due to increased heat

Blood pressure, heart rate and rhythm,
production from muscular activity or due to

ECG, and body temperature should be monidecreased heat loss from vasoconstriction.

tored frequently and treated as needed.

Propranolol at 0.02-0.06 mg/kg, IV, tid-qid,

Clinical Findings and Diagnosis: CNS
or other 13-blocking agents such as esmolol
excitation, hyperactivity, shaking, ataxia,

(0.2-0.5 mg/kg, slow IV over 1 min, or 25----200
panting, agitation, mydriasis, nervousness,
mcg/kg/min as a constant-rate infusion) can
seizures, tachycardia, hype1tension, acidosis, be used to control tachycardia. After CNS
or hyperthem1ia characterize cocaine
and cardiovascular effects have been
toxicosis. CNS depression and coroa may
stabilized, IV fluids should be administered,
follow CNS excitation. Death may be due to
and electrolyte changes and acid-base status
hyperthermia, cardiac arrest, or respiratory
monitored and corrected as needed.

arrest. Some nonspecific chemistry changes

Treatment and monitoring should continue
may include hyperglycemia and increased
until all clinical signs have resolved.

CK and liver-specific enzymes.

Diagnosis is based on a history of
exposure and the presence of characteristic

Ecstasy (MDMA or 3,4-Methylene
clinical signs. Identification of cocaine in
dioxymethamphetamine)

plasma, stomach contents, or urine can

Ecstasy is a semisynthetic psychoactive
confirm exposure. Differential diagnoses
designer drug ( developed by street chemists
include amphetamines, pseudoephedrine,
with minor structural changes in parent
ephedrine, caffeine, chocolate, metaldecompounds) with hallucinogenic and hyde, strychnine, tremorgenic mycotoxins,
an1phetarnine-like properties. Street nan1es
lead, nicotine, perrnethrin (cats) and other
include Adam, XTC, E, Roll, X, or Love Drug.

pesticides, and encephalitis.

A typical dose may be 75----150 mg. MDMA is
believed to cause excessive release of

Treatment: The objectives of treatment
serotonin. It also binds to serotonin
are GI decontamination, stabilization of CNS transporter (a protein), which is responsible and cardiovascular effects, thennoregulafor removing serotonin from the synapse.

tion, and supportive care. Anin1als with

The overall effect is increased serotonin and

TOXICITIES FROM HUMAN DRUGS

3041
serotonergic effects. MDMA also affects
conunon street names. Clinical signs of
dopamine and norepinephrine. Studies in
toxicosis from ingestion of synthetic
rodents indicate that use of MDMA can lead
marijuana in dogs can be more severe
to permanent serotonergic neuronal injury.

and last longer ilian those of THC.

In pets, MDMA toxicosis is not conunon.

It is usually acute and occurs from

Pharmacokinetics and Toxicity: The

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accidental ingestion (powder, pills, or
most conunon route of exposure is oral.

capsules). Clinical signs develop within

After ingestion, THC goes through a

30 min to 2 hr after ingestion and may
substantial first-pass effect. It is metaboconsist of syrnpathomirnetic effects (CNS
lized by liver microsomal hydroxylation
excitation, agitation, hyperactivity, pacing,
and nonmicro oma.l oxidation. In dogs,
hyperthermia, tachycardia, hype1tension,
clinical signs begin within 30-90 min and
seizures LJust like an1phetarnines ]),
can last up to 72 hr. THC is highly lipophilic
sedation, or signs thought to be related to
and readily distributes to the brain and
hallucination ( vocalization, disorientation,
other fatty tissues after absorption. The
muscle rigidity). The half-life in people is
oral LD50 of pure THC is 666 mg/kg in rats

7.6-8. 7 hr. Treatment is similar to that for
and 482 mg/kg in mice. However, clinical
amphetamine toxicosis (seep 3039). For
effects of marijuana are seen at much lower
serotonergic effects (agitation, muscle
doses than this.

rigidity, nervousness), antiserotonergic
drugs such as cyproheptadine can be tried

Pathogenesis: THC is believed to a.ct

(1.1 mg/kg, PO, repeated once in 6-8 hr).

on a unique receptor in the brain that is
selective for canna.binoids and is responsi

Marijuana
ble for the CNS effects. Cannabinoids can
enhance the fo1mation of norepinephrine,

Marijuana refers to a mixture of cut, dried,
dopamine, and serotonin. They can also
and ground flowers, leaves, and sterns of the
stimulate release of dopa.mine and enhance
leafy green hemp plant Cannabis saliva.

-y-aminobutyric acid turnover.

Several cannabinoids are present in the
plant resin, but delta-9-tetra11ydrocannabi

Clinical Findings and Diagnosis: The
nol (THC) is considered the most active and
most conunon signs of marijuana toxicosis
main psychoactive agent. The concentration
arc depression, ataxia, bradycardia, hypoof THC in marijuana varies between lo/o-8"Ai.

the1mia, vocalization, hypersalivation,

Hashish is the resin extracted from the top
vomiting, diarrhea., uiina.ry incontinence,
of the flowering plant and is higher in THC
seizures, and coma.

concentration than marijuana. Street names

Diagnosis is based on a history of
for marijuana include pot, Mary Jane,
exposure and typical clinical signs. THC is
hashish, weed, grass, THC, ganja, bhang, and difficult to detect in body f1uids because of.

charas. Pure THC is available by prescripthe low levels foui1d in ilie plasma. Urine tion under the generic name dronabinol.

testing at human hospitals or using an

A synthetic cannabinoid, nabilone, is also
over-the-counter marijuana. drug test kit
available. Marijuana or hashish sold on the
in the early course of exposure may help
streets may be contaminated with phencyconfirm the diagnosis. Marijuana toxicosis clidine, LSD, or other drugs.

can be confused with ethylene glycol

Marijuana is a schedule I controlled

(antifreeze, seep 3046) or ivennectin
substance mostly used by people as a

Loxicosis; hypoglycemia; benzodia.zepine,
recreational drug. It is also used as an
barbiturate, or opioid overdose; interve1teantiemetic for chemotherapy patients bral disc problems; or head trauma.

and to decrease intra.ocular pressure
in glaucoma patients. Some clinicians

Treatment: Treatment consist.s of
advocate the use of dronabinol as an
supportive ca.re. If the exposure is recent
appetite stimulant, but tl1e dysphoric effects and there are no contraindications, emesis of this drug outweigh any benefit of appetite
should be induced and activated charcoal
stimulation.

administered. Comatose animals should

Synthetic marijuana is a designer drug
be monitored for aspiration pneun10nia.,
in which different herbs or incense or other
given IV f1uids, treated for hypothermia., and
leaJy materials are sprayed with laboratoryrotated frequently to prevent dependent synthesized chemicals. The use of syntl1etic
edema or decubital ulceration. Dia.zepa.m
marijuana produces psychoactive effects
can be given for sedation or to control
similar to those of THC. It is often claimed
seizures. Treatment and monitoring
to be natural, safe, and legal. Spice, K-2,
should continue until all clinical signs have
skunk, and moon rocks are some ofilie
resolved (up to 72 hr in dogs). For cases of

3042

TOXICITIES FROM HUMAN DRUGS
synthetic marijuana toxicosis, in addition to in hLUnan adults is 7-14 mg/kg; in infants, the preceding treatment options, use of IV

2.5 mg of hydrocodone has been letl1al.

lipid emulsion solution may be considered.

Pathogenesis: The effects of opioids

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Opiates
are due to their interaction with opiate
receptors(µ, K, l'i, er, ands) foLU1d in the

The term opiate initially referred to all
limbic system, spinal cord, thalamus,
naturally occLUTing alkaloids obtained from hypothalan1us, striatum, and midbrain.

the sap of the opiLUn poppy (Papave,·

Opioids may be agonists, mixed agonist
somniferum). Opium sap contains
antagonists, or antagonists at these
mo1phine, codeine, and several other
receptors. Agonists bind and activate a
alkaloids. Cun·ently, opioid refers to all
receptor, whereas antagonists bind withdrugs, natural or syntl1etic, tl1at have out causing activation.

morphine-like actions or actions mediated
through opioid receptors. Structurally,

Clinical Findings: The prin1ary effects
opioids can be divided into five classes.

of opioids are on the CNS, respiratory,

Some of the common agents within each
cardiovascular, and GI systems. Conunonly
class are 1) phenanth.renes-morphi.ne,
reported clinical signs of toxicosis include
heroin, hydromorphone, oxymorphone,

CNS depression, drowsiness, ataxia,
hydrocodone codeine and oxycodone·
vomiting, seizmes, miosis, coma, respira2) morphina.n'-butorphanol; 3) diphen�ltory depression, hypotension, constipation/
heptanes-methadone and propoxyphene;
defecation, and death. Some animals-espe4) phenylpiperidi.nes-meperidi.ne, cially cats, horses, cattle, and swine--can
diphenoxyiate, fentanyl, loperan1ide, and
show CNS excitation instead of CNS depresprofadol; and 5) benzomorphans-pentazosion.

cine and buprenorphine. Some of tl1e widely
used opioids in veterinary medicine include

Diagnosis: Diagnosis of opioid toxicosis
trarnadol, buprenorphine, fentanyl,
is based on history of exposme and tl1e
loperan1ide (antidiarrheal), and hydromortypes of clinical signs (CNS and respiratory phone. The use of meperidine is no longer
depression) present. Plasma opioid levels
conunon.

are usually not clinically useful. Urine may

Opioids are used primarily for analbe used to detennine exposme to opioids gesia. In addition, they are used as cough
using some of the over-the-counter illicit
suppressants and to treat diarrhea
drug kits (manufacturer's instructions

Occasionally, opioids are used for sedation
should be followed). Opioid toxicosis
before smgery and as a supplement to
should be differentiated from ethylene
anestl1esia.

glycol, ive1mectin, benzodiazepine,
barbitmate, and marijuana toxicosis, as well

Pharmacokinetics and Toxicity: Opias hypoglycemia-inducing conditions.

oids are generally well absorbed after oral,
rectal, or Parenteral administration. Some

Treatment: Clinical signs can be reversed
more lipophilic opioids are also assorbed
witl1 the opiate antagonist naloxone. The
through nasal, buccal, respiratory (heroin,
dosages in different species are dog and
fentanyl, bu.prenorphine), or transdennal
cat, 0.04-0.16 mg/kg, IV, IM, or SC; rabbit

(fentanyl) routes. For some opioids, there is and rodent, 0.01-0.1 mg/kg, SC or IP; horse, variable reduction in bioavailability because 0.01-0.02 mg/kg, IV. Administration of of a first-Pass effect when given orally.

naloxone should be repeated as needed

Opioids generally undergo hepatic

(hourly), because its duration of action may
metabolis111 with some fom1 of conjugation,
be shorter than tl1at of the opioid toxicity
hydrolysis, oxidation, dealkylation, or
being treated. A.tlin1als should be closely
glucuronidation. Because cats are deficient
monitored for respiratory depression and
in glucuronidase, the half-life of some
ventilatory support provided if.needed.

opioids in cats may be prolonged. After

Other signs should be treated syn1ptomatiabsorption, opioids a.re rapidly cleared from cally. Dysphoric reactions (vocalization, blood and stored in kidney, liver, brain, lung, agitation, restlessness, and excitation) s_pleen, skeletal muscle, and placental
can be treated with diazeparn or otl1er
tissue. Most of the opioid metabolites are
benzodiazepines. For serotonin-like
excreted tl1.rough the kidneys.

syndrome ( disorientation, muscle rigidity,

Toxicity of opioids in anin1als is highly
agitation) induced by some opioids,
variable. In dogs, morphine administered
cyproheptadine (1.1 mg/kg, PO or per
at 100-200 mg/kg, SC or IV, is considered
rectrnn) once or twice (6-8 hr apart) can
lethal. The estimated lethal dose of codeine
be tried.

NON PROTEIN NITROGEN POISONING

3043

NONPROTEIN NITROGEN POISONING

(Ammonia toxicosis)

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P oisoning by ingestion of excess urea
urea/kg body wt may cause adverse effects;
or other sources of nonprotein nitrogen
dosages of 1-1.5 g/kg are usually lethal.

(NPN) is usually acute, rapidly progressive,

Urease activ.ity in the equine cecwn is -25%
and highly fatal. NPN is any source of
that of the rumen, and horses may receive
nitrogen not present in a polypeptide

NPN as a feed additive; however, horses are

(precipitable protein) fonn. Sources ofNPN
more sensitive to urea than other monogashave different toxicities in various species, trics, and dosages ;:,:4 g/kg can be lethal.

but mature ruminants are affected most

Ammoniwn salts at 0.3-0.5 g/kg may be
commonly. After ingestion, NPN undergoes
toxic in all species and ages of fann animals;
hydrolysis and releases excess ammonia
dosages ;:>:1.5 g/kg usually are fatal. P igs and (NH3) into the GI tract, which is absorbed
neonatal calves are generally Wlaffected by
and leads to hyperammonemia.

ingestion of urea except for a transient
diuresis. Wild birds (silver gulls) rep01tedly

Etiology: Ruminants use NPN by conhave been poisoned after consuming water verting it via the nuninal microflora to
contaminated with urea fertilizer spillage.

anm1onia, which is then combined with

Livestock may require days or weeks for
carbohydrate-derived keto acids to fonn
total adaptation before nunen microflora
amino acids. The most conm1on sources
can utilize the gradually increasing amoW1ts
of NPN in feeds are urea, urea phosphate,
of urea or other NPN in the diets; however,
ammonia (anliydrous), and salts such as
adaptation is lost relatively quickly ( 1-3
monoammoniwn and dia.nm1oniw11
days) once NPN is removed from the diet.

phosphate. Because feed-grade urea is

Diets low in energy and high in fiber are

Wlstable, it is formulated (usually pelleted)

more commonly associated with NPN
to prevent degradation to NH3. Biuret, a less
toxicosis, even in acclimated anin1als.

toxic source of NPN, is being used less

Highly palatable supplements (such as
frequently than in the past. Natural protein
liquid molasses or large protein blocks
sources such as rice hulls, beet or citrus
cnunbled by precipitation), range cubes, or
pulp, cottonseed meal, and straw or other
improperly maintained lick tanks may lead
low-{!uality forages may be treated with
to conswnption of lethal amounts ofNPN.

anllydrous an1monia to increase available

A related CNS disorder in cattle fed
nitrogen in supplemented livestock diets.

anlllloniated high-{!uality hay, silage,

Fermentation byproducts from alcohol
molasses, and protein blocks is thought to be

( ethanol) manufacture are a source of NPN
caused by fomiation of 4-methylirnidazole
that comes from incomplete proteins, and

( 4-MI) through the action of NH3 on soluble
these products are conm10.nly used in liquid
carbohydrates (reducing sugars) in these
or feed supplements. Most sources of NPN
feedstuffs. C attle fed dietary components
are provided to nuninants by direct addition
containing 4-MI develop a syndrome known
of dry supplement to a complete mixed or
as the "bovine bonkers syndrome," named
blended diet, by free-choice access to
for the wildly abeJTant behavior exhibited.

NPN-containing range blocks or cubes, or by

Signs relate to CNS effects, with stampeding,
lick tank systems combined w;th molasses
ear twitching, trembling, champing,
as a supplement. Ammonia or NPN
salivating, and convulsions. Because nursing
poisoning is a common sequela of abrupt
calves are affected, the toxic principle apparchange to urea or other NPN in the diet when ently is excreted in milk Ammoniated only natural protein was previously fed;
low-{J_uality forages do not have sufficient
animals have to be gradually acclimated to
concentrations of reducing sugars to form

NPN so that rumen rnicroflora can increase

4-MI, and thus serve as a relatively safe
in nwnbers to use the NH3 produced. Also,
nitrogen sow·ce for acclimated animals.

farm animals sometimes drink liquid

Another related disorder involves
fertilizers or ingest diy granular fertilizers
accidental excessive exposure of ruminants
that contain anlllloniwn salts or urea.

( cattle and sheep) to raw soybeans.

Ruminants are most sensitive, because

Soybeans have high concentrations of both
urease is normally present in the functional
carbohydrates and proteins, as well as
rumen after 50 days of age. Dietary exposure urease. Overconswnption can cause acute of unacclin1ated ruminants to 0.3-0.5 g of
carbohydrate fermentation and excessive

3044

NONPROTEIN NITROGEN POISONING
ammonia release, resulting in ammonia

Diagnosis: Ammonia or NPN poisoning is
toxicosis and lactic acidosis. Affected
suggested by signs, lesions, history of acute
animals have engorged rumens with a gray,
illness, ru1d dietary exposure. Exposure to
amorphous mass inside.

excess NPN may be evaluated through
laboratory analysis for the rum11onia

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Clinical Findings: The period from w·ea
nitrogen (NH3-N) in botl1 ru1temortem and
ingestion to onset of clinical signs is 20-60
postrno1tem specimens and for urea or
min in cattle, 30-90 min in sheep, and longer
other NPN in suspected feeds and other
in horses. Early signs include muscle
dietary sources. Specimens for NI-!3-N
tremors ( especially of face and ears),
ru1alysis include rw11inal-reticular fluid,
exophthalmia, abdominal pain, frothy
semm, whole blood, ru1d urine. All
salivation, polyuria, and bruxism. Tremors
specimens should be frozen immediately
progress to incoordination and weakness.

after collection and thawed only for

Pulmonruy edema leads to mru·ked
analysis; alternatively, ruminal-reticulru·
salivation, dyspnea, and gasping.

fluid may be preserved with a few drops of

Horses may exhibit head pressing; cattle
saturated mercuric chloride solution added
are often agitated, hyperi.rritable, aggressive,
to each 100 mL of specin1en.

and belligerent as toxicosis progresses;

Anin1als dead more than a few hours in
sheep usually appear depressed. An eru"ly
hot runbient temperatures or 12 tu· in
sign in cattle is ruminal atony; as toxicosis
moderate clin1ates probably have tmdergone
progresses, nuninal tympany is usually
too much autolysis to be of diagnostic value.

evident, and violent struggling ru1d

The runount of urea or tl1e equivalent NPN
bellowing, a mru·kedjugular pulse, severe
in biologic specin1ens is meaningless;
twitching, tetanic spasms, and convulsions
however, urea and NPN should be determay be seen. Affected cattle with belligerent mined in representative feeds and other
aberrant behavior may have produced some
dietruy sources. Values for urea and NPN in

4-MI in vivo tlu·ough reaction of excessive
feed pennit calculation of the protein

NH3, released from NPN, with cru·bohydrates
equivalent (1 part protein= 0.36 pru1S urea; 1
and reducing sugars in the mmen. The PCV
part urea= 2.92 parts protein) in feed as well
and serwn concentrations of NI-!3, glucose,
as the total estimated dose of NPN ingested.

lactate, potassitm1, phosphoms, AST, ALT,

NH3-N concentrations of <!2 mg/100 mL in
and BUN usually are significantly increased.

blood, semrn, or vitreous hwnor indicate

As death nears, anin1als become cyanotic,
excess NPN exposure. Clinical signs usually
dyspneic, anuric, and hyperthermic, and
appear at -1 mg/100 rnL. The concentration
blood pH decreases from 7.4 to 7.0.

of NH3-N in runlinal-reticular fluid is >80

Regurgitation may occur, especially in
mg/100 mL in most cases of NPN poisoning
sheep. Death related to excess NPN usually
and may be >200 mg/100 mL. Acclimated
occw·s within 2 hr in cattle, 4 hr in sheep,
rwninants fed diets !ugh in legun1e hay,
ru1d 3-12 hr in horses. Sw-vivors recover in
soybean meal, cottonseed meal, linseed

12-24 hr with no sequelae.

meal, fish meal, or milk byproducts may

Carcasses of animals dying of NPN
have NH
poisoning apperu· to bloat and decompose

3-N concentrations in run1en fluid
approaching 60 mg/100 mL witl1 no appru·ent
rapidly, witl1 no specific chru·acte1istic
toxicity. The pH of ruminal-reticulru· fluid
lesions. Gross brain lesions are not usually
should also be determined; a pH of7.5-8 (at
repo1ted in NPN-induced rumnonia toxicosis, ti.me of death) is indicative of NPN toxicity.

but histopathologic lesions may include

Differential diagnoses include poisonings
neuronal degeneration, spongy degeneration
by nitrate/nitrite, cyru1ide, organophosof the neuropil, and congestion and phate/cru·brunate pesticides, raw soybean
hemonhage in tl1e pia mater. Frequently,
overload, 4-methylirnidazole, lead,
pubnonruy edema, congestion, ru1d petechial
chlorinated hydrocarbon pesticides, and
hemorrhages may be seen. Mild bronchitis
toxic gases ( cru·bon monoxide, hydrogen
and catru-rhal gastroenteritis are often
sulfide, nitrogen dioxide); acute infectious
reported. Regurgitated and inhaled mmen
diseases; and noninfectious diseases such
contents ru·e commonly found in the trachea
as encephalopathies ( eg, Jeukoencephaloand bronchi, especially in sheep. The odor of malacia, hepatic encephalopathy, polioen

NH;, may or may not be appru·ent in ingesta
cephalomalacia), enterotoxemia or run1en
from a freshly opened mrnen or cecwn. A
autoi.ntoxication, protein engorgement,
ruminal or cecal pH <!7.5 from a recently dead
grain engorgement, rwninal tympany, and
ruli.mal is highly suggestive of NPN poisoning. pulmonary adenomatosis. Nutritional ru1d The runlinal pH remains stable for several
metabolic disorders related to hypocalce-
hours after deatl1 tmder most circwnstances

1nia, hypomagnesenlia, and otl1er elemental
but continues to rise in NPN toxicosis.

aberrations should also be considered.

COAL-TAR PRODUCTS POISONING

3045

Treatment: Examination and treatment

Supportive therapy is indicated and
may be difficult because of sudden and
includes IV isotonic sal.ine solutions to
violent behavior. Animals that are recumcorrect dehydration, and IV calciun1
bent and moribund usually do not respond
gluconate and magnesiun1 solutions to
favorably to treatment.

relieve tetanic seizures. Convulsions may

If possible, affected animals should be
also be controlled with sodiwn pentobarbi

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treated by rwninal infusion of 5% acetic acid
tal or other injectable anesthestic agents.

( vinegar, 0.5-2 Lin sheep and goats and 2--8 L
in cattle). Ruminal-reticular fluid specimens

Prevention and Control: Urea should
for analysis should be taken before acetic
not be fed at a rate exceeding 2%-3% of the
acid therapy. Concomitant infusion of iced
concentrate or grain pdrtion of ruminant

(0---4 °C) water ( up to 40 L in adult cattle,
diets and should be limited to �1%of the
proportionally less in sheep and goats) is also total diet. Additionally, NPN should reconm1ended. Acetic acid lowers rumen pH
constitute no more than one-third of the
and prevents further absorption of NH
total nitrogen in the rwninant diet. Once the

3 by
converting tmcharged NH
decision is made to feed NPN, animals must

3 to the charged
anunoniw11 ion (NH
be slowly adapted to, and maintained on, a

4 •); administration may
have to be repeated if affected animals again
consistent dietary NPN content with no
show clinical signs. Acetic acid inactivates
significant deviation; cows fed range cubes
existing NH
with NPN must receive the cubes daily with

3 in the GI tract and rapidly fonns
anunoniwn acetate, which can be used by
no interruptions. Temporary absences of
rwnen microflora but does not release NH

NPN from the diet should be avoided at all

3.

Cold water lowers the rwnen temperatme
costs. Overconsun1ption of palatable liquid
and dilutes the reacting media, which slows
supplements can be controlled by the
mease activity. In severely affected valuable
addition of phosphoric acid; l % phosphorus
animals, removed rw11en contents should be
from phosphoric acid should restrict
replaced with a hay slwTy, and a transfer of
conswnption of liquid supplement to
some rwnen contents from a healthy animal

-2 lb/anirnal/day. Although properly
may serve as an inoculwn to restore nonnal
adapted adult cattle can tolerate urea at a
function. Rwninal tympany should be
rate of up to l g/kg body wt/day, a safer
con-ected if indicated, and a trocar may be
feeding rate is no more than half that
installed to prevent recun·ence.

amow1t.

COAL-TAR PRODUCTS POISONING

A variety of coal-tar de1ivatives induce
hydroxytoluenes, are used in soaps and
acute to chronic disease in animals, with
disirlfectants. Coal-tar and pine-tar pitch are
clinical signs that vary based on the conthe brown to black, amorphous, polynuclear stituents. Clinical effects are acute to
hydrocarbon residues left after coal tar is
chronic hepatic dan1age with signs of
redistilled. Access of animals to coal tars is
icterus, ascites, anemia, and death. Pheoften by direct chewing on or conswnption nolic components may cause renal tubular
of product, rather than inclusion in feed or
damage. Coal tar-related poisoning has
water. Clay pigeons ( older products), tar
been reported in faun animals and pets.

paper, creosote-treated wood, and bitwnenbased flooring are typical sources.

Etiology: The distillation of coal tar yields Phenol is the most important toxicant in
a variety of compounds, three of which are
coal-tar products and is found in antisepnotably toxic: cresols (phenolic compounds), tics, creosote, gem1icides, cleaners, and crude creosote ( composed of cresols, heavy
disinfectants. The approxin1ate oral acute
oils, and anthracene), and pitch. Tars are also

LD5() of phenol for most species is 0.5 g/kg,
produced from crude petrolew11 or wood.

except for cats, which are more susceptible

Creosote contains less volatile liquid and
because of limited ability to fom1 glucuronsolid aromatic hydrocarbons of coal tar and ides and excrete phenols. Phenols are
some phenols. They have been used for
directly corrosive, and ingestion results
restiicted applications as wood prese1vain oral and upper gastroente1ic necrosis.

tives. Cresols, composed mainly of

After oral or dermal absorption, phenols

3046

COAL-TAR PRODUCTS POISONING
accwnulate in the liver and kidneys,
necrosis also can be present. The blood clots
conunonly resulting in liver damage and
slowly or not at all. TI1e car·cass is icteric.

renal tubular necrosis.

Excessive fluid is found in the peritoneal

Cresols are readily absorbed orally and
cavity.

through the skin. The oral lethal dose is

100--200 mg/kg, except in cats, which are

Diagnosis: Differential diagnoses include

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more sensitive. Sows in creosote-treated
toxic plant poisonings (Crolalaria, Senecio,
wooden farTowing crates delivered stillborn
cocklebm), aflatoxicosis, blue-green algae
pigs. Coal tar-s may reduce absorption of
poisoning, fwnonisin toxicosis, gossypol
vitan1in A by sows. Other species are less
toxicosis, yellow phosphorus poisoning,
susceptible ( eg, the leU1al dose of creosote in and vita.ruin E or seleniwn deficiency.

calves is 4 g!kg). Pitch is no longer used as a

Fragments of tar paper or other sow·ces of
binder in clay pigeons, but road asphalt,
coal tars found in the GI tract, or chemical
some insulation, and tar· paper and roofing
detection of coal-tar· products in liver,
compounds may still contain cresols.

kidney, senun, or mine, aid in confuming

Flo01i.ng wiU1 lignite pitch or asphalt can
the diagnosis. Laboratory changes include
reduce growth rate and/or cause liver
hypoglycemia, and increases in serum liver
darnage in pigs.

enzymes, U1ymol tmbidity, chloride, and
phosphorus. Proteinmia, hematw-ia, and

Clinical Findings: The cresols and
w-inary cells and casts reflect kidney
phenols are locally corrosive, causing
dar11age from phenolic fractions of coal tars.

necrosis and scarring of skin, mouth, and

A rapid presumptive test is to mix 1 mL of
esophagus; CNS stimulation, trem01-s,
urine with 0.1 mL of 20"Ai ferric chloride;
and incoordi.nation; ar1d cardiovascular
purple color indicates phenol, but results
depression and shock. Capillary dan1age
should be confurned by a laboratory.

and hepatic or renal damage can occm.

Icterus can result from intravascular·
hemolysis and hepatic darnage. Death can

Treatment: There is no specific antidote
occur from 15 min to several days after
for coal-tar product poisoning. Emetics and
exposme. The fu-st sign of pitch poisoning
gastric lavage are not recommended for
often is several dead animals. Signs may
recent oral exposure, but activated charcoal
progress to weakness, ataxia, sternal
and saline cathartics may reduce absorprecumbency, icterus, coma, ar1d death.

tion. Owners may reduce acute exposure by

Secondary anemia may develop. Other
adn1inistration of egg whites to dilute and
problems have included stillbirths in pigs
bind the phenols. Dermal exposures ar-e
ar1d hyperkeratosis in calves.

mitigated by bathing with glycerol followed
by liquid dish soap. Supportive therapy for

Lesions: Phenols, cresols, and creosote
shock, liver and kidney darnage, respiratory
produce contact initation of sl<in, mouth,
failure, and acidosis are irnport3.11t
and esophagus and nonspecific liver and
supportive measures for individual animals.

kidney lesions. The liver is markedly swollen

N-acetylcysteine (140 mg/kg, IV, loading
with a diffuse, mottled appear·ance. There
dosage, followed by 70 mg/kg, qid for
is centrilobular liver necrosis, with blood
anoU1er 3 days) has been recommended.

replacing the lost cells and filling the center

Oral antibiotics, B vitamins, vitarnin E, and
of the lobule. Renal tubular degeneration and high-quality-protein diets may aid recovery.

ETHYLENE GLYCOL TOXICITY

All anin1als ar-e susceptible to ethylene
availability of antifreeze, its sweet taste and
glycol (EG) toxicity, but it is most common
small minimum lethal dose, and the lack of
in dogs and cats. Most intoxications ar-e
public awareness of the toxicity (ie,
associated with ingestion of ar1tifreeze,
in1proper storage and disposal) contlibute
which is typically 95% EG. These 95%
to the frequency of this intoxication. In
commercial antifreeze preparations are
addition, antifreeze may be ingested by way
diluted -50"Ai with water when used in
of intentional poisoning or because it is the
vehicle cooling systems. The widespread
only available liquid in cold weather. Other

ETHYLENE GLYCOL TOXICITY

3047
sources of EG include some heat-exchange
those caused by wunetabolized EG and
fluids used in solar collectors and ice-rink
those caused by its toxic metabolites. The
freezing equipment and some brake and
onset of clinical signs is almost inm1ediate
transmission fluids. Cutaneous absorption
and resembles alcohol ( ethanol) intoxicafrom topical products that contain EG has tion. Dogs and cats exhibit vomiting due to
been reported to cause toxicity in cats.

GI initation, polydipsia and polyuria, and

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EG intoxication occurs most commonly
neurologic signs (CNS depression, stupor,
in temperate and cold climates, because
ataxia, knuckling, decreased withdrawal
antifreeze is used both to decrease the
and righting reflexes). Polydipsia occurs due
freezing point and to increase the boiling
to osmotic stimulation of tile thirst center,
point of radiator fluid. In colder climates, the and polywia occurs due to an osmotic incidence of EG intoxications is seasonal,
diuresis and decreased production and
with most cases occurring in the fall, winter,
release of anti.diuretic hormone. As CNS
and early sp1ing, when antifreeze is added to
depression increases in seve1ity, dogs and
radiator fluid or when cooling systems are
cats drink less; however, the osmotic
flushed.

diuresis continues and results in dehydra

The minimwn lethal dose of undiluted EG
tion. Dogs may appear to transiently recover
is 1.4 mllkg body wt in cats, 4.4 mllkg in
from these CNS signs -12 hr after ingestion.

dogs, 7-8 mllkg in poultry, and 2-10 mllkg

Oligw·ic acute renal failure usually
in cattle. Yotmger animals may be more
develops between 12 and 24 hr in cats and
susceptible.

between 36 and 72 hr in dogs. Signs include
letl1argy, anorexia, dehydration, vomiting,

Pathogenesis: EG is rapidly absorbed
diarrhea, oral ulcers, salivation, tachypnea,
from the GI tract; in dogs, blood concentraand possibly seizures or coma. The kidneys tions of EG peak within 3 hr of ingestion.

are often swollen and painful on abdominal

Approximately 500/o of ingested EG is
palpation.

excreted unchanged by the kidneys;

Pigs ingesting EG are usually depressed,
however, a series of oxidation reactions
weak, and reluctant to move; knuckling,
in tl1e liver and kidneys metabolize the
posterior ataxia, trembling, collapse,
remaining EG. Toxic metabolites of EG
abdominal distention, pulmonary edema,
cause severe metabolic acidosis and renal
and muffled heait sounds ai·e common
tubular epithelial damage.

sequelae. Poultry may become drowsy,

The first of two rate-limiting biotransforataxic, dyspneic, and recwnbent; torticollis, mation steps is the production of glycoaldemffled feailiers, and wate1y droppings ai·e hyde from EG by the enzyme alcohol
also seen. Cattle may become depressed,
dehydrogenase. Glycolaldehyde is then
tachypneic, and ataxic, and develop
rapidly metabolized to glycolic acid. The
paraparesis or recun1bency. Epistaxis and
oxidation of glycolic acid to glyoxylic acid is hemoglobinuria have also been seen in the second rate-limiting step, which allows
cattle that have ingested Jai·ge doses of EG.

glycolic acid to accun1ulate, resulting in
acidosis and nephrotoxicosis. Glyoxylic

Lesions: Renal tubular epithelial necrosis
acid is rapidly metabolized to formic acid,
with calciwn oxalate crystals in the tubular
carbon dioxide, glycine, serine, and oxalate.

lunlina is the characteristic finding ofEG

Oxalate is not furtl1er metabolized and is
intoxication. Calciwn oxalate crystals appear
cytotoxic to the renal tubular epitheliwn
birefringent when viewed wiili polarized
and exacerbates the metabolic acidosis.

light. Pulmonary edema and hemorrhagic

Glycolic acid and oxalate are the metabogastroenteritis are conunon secondaiy lites thought to be most responsible for
findings in dogs and cats. Pigs and cattle
acute tubular necrosis associated with EG
often develop renal and pe1irenal edema.

ingestion. Oxalate also combines witl1

Pigs may also have pulmonary edema witl1
calciwn to form a soluble complex that is
tan fluid in the pleural and peritoneal cavities.

excreted via glomerular filtration. Calciwn

Poultry usually do not develop gross lesions.

oxalate crystals fmm within the lwnina of
tubules as water is reabsorbed from the

Diagnosis: Diagnosis is often difficult
glomerular filtrate and tl1e pH decreases
because the nonspecific multisystemic signs

(smaller nun1bers of calciwn oxalate
may appear similai· to other types of CNS
crystals may also be observed in the
disease or traunm, gastroente1itis,
adventitia of blood vessel walls tl1roughout
pancreatitis, ketoacidotic diabetes mellitus,
the body).

and acute renal failw·e due to renal ischemia
or other nephrotoxicants. If ingestion of EG
is not witnessed, diagnosis is usually based

Clinical Findings: Clinical signs are doseon a combination of history, physical and time-dependent and can be divided into
examination, and laboratory data.

3048

ETHYLENE GLYCOL TOXICITY

Within 3 hr of ingestion of toxic doses
alcohol dehydrogenase is decreased by
ofEG, dogs and cats develop normochlodirect inactivation or by competitive remic metabolic acidosis with an increased
inhibition. 4-Methylpyrazole (4-MP,
anion gap, minimally concentrated or
fomepizole) effectively inactivates alcohol
isosthenwic urine with an acidic pH, and
dehydrogenase in dogs without the adverse

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marked serU111 hyperosmolality with an
effects of ethanol and is the treatment of
increased osmolal gap. Sel'U111 osmolality can
choice. The dose of 4-MP (5% solution [50
be increased as much as 100 mOsm/kg above
mg/mL]) is 20 mg/kg body wt, IV, initially,
normal (280--310 mOsm/kg) within 3 hr ofEG followed by 15 mg/kg, IV, at 12 and 24 hr, and ingestion. TI1e difference between measured

5 mg/kg, IV, at 36 hr. Commercial fo1mulaand calculated (1.86 [Na•+ K•] + glucose/18
tions of 4-MP ai·e available. lf 4-MP is not

+ BUN/2.8 + 9) osmolality is referred to as the
available, an ethanol reginlen (5.5 mL of 2()0A,
osmolal gap. The gap is caused by the
ethanol/kg body wt, IV, every 4 hr for five
presence of osmotically active particles ( eg,
treatments ai1d then eve1y 6 lu· for four
ethylene glycol) in the sel'U111 that are not
additional treatments) is reconm1ended.

factored into the above equation. Calcium

In cats, 4-MP is ineffective at the canine
oxalate crystalhnia may be observed as early
dosage, and either a higher, extra-label
as 3 and 6 hr after ingestion in cats and dogs,
dosage (125 mg/kg initially, followed by 31.3
respectively. Monohydrate calciU111 oxalate
mg/kg at 12, 24, and 36 hr after the initial
crystals ( clear, 6--sided prisms) are more comdose) or ethanol is used. The recommended mon than dihydrate calciU111 oxalate crystals
dosage is 5 mL of 200A, ethai101/kg body wt

(maltese cross or envelope-shaped). EG
diluted in IV fluids ai1d given as a drip over 6
concentrations in sel'Uln and urine are detectlu- for five treatments, and then over 8 hr for able by 1-2 hr after ingestion. Conunercial
four more treatments.

test kits can detect sefU111 EG concentrations

The metabolic acidosis associated with
of �50 mg/clL. Some antifreeze preparations
metabolism of EG is corrected by adminiscontain fluorescein, which appears b1ight tration of sodium bicarbonate. The formula
yellow-green when viewed U11der a Wood's

0.3 - (0.5 x kg body wt) x (24 - plasma
lamp. Urine fluorescence has been used as a
bicai·bonate) is used to determine the dose,
qualitative adjU11ctive test in suspected EG
in mEq of bicarbonate. One-half of this dose
ingestions in people and may be of value in
should be given IV slowly to prevent
veterinaiy medicine. Hyperphosphaternia
overdose, and plasma bicarbonate
has been seen in dogs within 3 hr of ingestion
concentrations should be monitored every
of commercial antifreeze solutions that

4--6 hr. Additional doses of bicarbonate
contain phosphate rust inhibitors. This
based on the above formula are frequently
hype1phosphatemia resolves before the
necessaiy. Monitoring urine pH may also be
onset of EG-induced acute renal failure and
helpful, with a goal of maintaining the urine
azotemia, then recurs when the animal
pH between 7.0 and 7.5.

becomes azotemic.

In dogs and cats with azotemia or in
oliguric acute renal failure, inhibition of

Treatment: The prognosis vai·ies inversely
alcohol dehydrogenase is of little benefit,
with the ainoU11t of tinle that elapses-between because almost all of the EG has already ingestion and initiation of treatment. Treatbeen metabolized. The prognosis for these ment is ainled at decreasing absorption
animals is guarded to poor. Treatment
of ingested EG, increasing excretion of
should include correction of fluid,
wm1etabolized EG, preventing metabolism
electrolyte, and acid-base disorders and,
of EG, and correcting the metabolic acidosis
if possible, induction of diuresis.

that occurs with EG metabolism. Further
absorption ofEG is prevented by induction

PROPYLENE GLYCOL TOXICOSIS
of emesis or gastric lavage ( or both) within

1-2 hr of ingestion, although the rapidity of

Although less toxic than EG, ingestion of

EG absorption from the GI tract suggests
propylene glycol (PG) may be associated
these procedures may not be beneficial.

with a toxic syndrome similar to the acute

Vomiting should not be induced in a dog or
phase of EG toxicosis. The oral LDu0 of PG
cat exhibiting neurologic signs because of
in dogs is -9 mllkg. In cats, ingestion of a
increased risk of aspiration. Activated
diet containing 6%-12% PG can result in
charcoal is not likely to reduce absorption of

Heinz body formation and decreased RBC

EG from the GI tract. Once absorption has
swvival. Treatment of PG toxicosis is
occurred, excretion of EG is increased by
largely supportive-the use of alcohol
fluid therapy designed to correct dehydradehydrogenase inhibitors is not indicated.

tion and increase urine production. To

Ingestion of PG may result in false-positive
prevent metabolism of EG, the activity of

EG test kit results.

NITRATE AND NITRITE POISONING

3049

NITRATE AND NITRITE POISONING

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Many species are susceptible to nitrate and
excessive nitrate content in livestock diets,
nit1ite poisoning, but cattle are affected
especially when coupled witl1 management
most frequently. Rwninants are especially
errors.

vulnerable because the rwninal flora

Nitrate toxicosis can also result from
reduces nitrate to ammonia, with nitrite
accidental ingestion of fertilizer or other

( -10 times more toxic than nitrate) as an
chemicals. Nitrate concentrations may be
intem1ediate product. Nitrate reduction
hazardous in ponds that receive extensive

(and nitrite production) occurs in the
feedlot or fertilizer rnnoff; these types of
cecwn of equids but not to the same extent
nitrate sources may also contaminate
as in n.uninants. Young pigs also have GI
shallow, poorly cased wells. Although
microflora capable of reducing nitrate to
nitrate concentrations are increasing in
nitrite, but mature monogast1ic animals
groundwater in the USA, well water is rarely

(except equids) are more resistant to nitrate
the sole ca.use of excess nitrate exposure.

toxicosis because this path way is age-

Water with both high nitrate content and

1.imited.

significant colifo1111 contamination has

Acute intoxication is manifested
greater potential to adversely affect health
ptimarily by methemoglobin fonnation
and productivity than does either nitrate or

(nitrite ion in contact with RBCs oxidizes
bacteria. alone. Livestock losses have
ferrous iron in Hgb to the ferric state,
occwTed dming cold weather due to the
fon11ing stable methemoglobin incapable
concentrating effect of freezing, which
of oxygen transpo1t) and resultant anoxia.

increases nitrate content of remaining water

Secondary effects due to vasodilatory
in stock tanks.

action of the nitrite ion on vascular smooth

Crops that readily concentrate nitrate
muscle may occur. The nitrite ion may also
include cereal grasses ( especially oats,
alter metabolic protein enzymes. Ingested
millet, and rye), com (maize), sunflower,
nitrates may directly initate the GI mucosa
and sorghw11s. Weeds that conm10nly have
and produce abdominal pain and diarrhea.

high nitrate concentrations are pigweed,

Although usually a.cute, the effects of
lamb's-quarter, thistle, Jirnson weed,
nitrite or nitrate toxicity may be suba.cute
fireweed (Kochia), smartweed, dock, and
or chronic and are reported to include

Jolmson grass. Anhydrous ammonia and
retarded growth, lowered milk production,
nitrate fertilizers and soils naturally high in
vitamin A deficiency, mi.nor transitory
nitrogen tend to increase nitrate content in
goitrogenic effects, abortions and
forage.

fetotoxicit;y, and increased susceptibility to

Excess nitrate in plants is generally
infection. Clu·onic nitrate toxicosis remains
associated with dan1p weather conditions
a controversial issue and is not as yet well
and cool temperatures (55°F [l3°C]),
characterized, but most current evidence
although high concentrations are also likely
does not support assertions of lowered milk
to develop when growth is rapid during hot,
production in dairy cows due to excessive
humid weather. Drought conditions,
dietary nitrate exposure alone.

particularly if occuning when plants are
i11una.ture, may leave the vegetation witl1

Etiology: Nitrates and nitrites are used in
high nitrate content. Decreased light, cloudy
pickling and curing brines to preserve
weather, and shadillg associated with
meats, and in certain ma.chine oils and
crowdillg conditions can also cause
anti.J.ust tablets, gunpowder and explosives,
i11creased concentrations of nitrates within
and fertilizers. They may also serve as
plants. Well-aerated soil with a low pH, and
therapeutic a.gents for ce1ta.i.n noninfectious
low or deficient an1ounts of molybdenwn,
diseases, eg, cyanide poisoning. Toxicoses
sulfur, or phosphorns in soil tend to
occur in una.cclimated domestic animals,
enhance nitrate uptake, whereas soil
most conunonly from ingestion of plants
deficiencies of copper, cobalt, or mangathat contain excess nitrate, especially by nese tend to have opposing effects.

hungry anin1als engorging themselves and

Allything that stunts growth increases
ta.king in an enom10us body burden of
nitrate a.ccwnula.tion in the lower part of the
nitrate. Confotmding interactions with
plant. Phenoxy acid derivative herbicides
nonprotein nitrogen, rnonensin, and otl1er

(eg, 2,4-D and 2,4,5-T), applied to nitra.tefeed components may exacerbate effects of accumula.ting plants during early stages,

3050

NITRATE AND NITRITE POISONING
cause increased growth and a high nitrate
brown discoloration evident in moribund
residual (10%---30%) in surviving plants,
or recently dead anin1als is not pathognowhich are lush and eaten with apparent monic, and other methemoglobin inducers
relish even though previously avoided.

must be considered. If necropsy is

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Nitrate, which does not selectively
postponed too long, the brown discoloraaccumulate in fruits or grain, is found tion may disappear with conversion of
chiefly in the lower stalk with lesser
methemoglobin back to Hgb.

amounts in the upper stalk and leaves.

Nitrate in plants can be converted to nitrite

Diagnosis: Excess nitrate exposure can
under the proper conditions of moisture,
be assessed by laboratory analysis for
heat, and microbial activity after harvesting.

nitrate in both pre- and postmortem
specin1ens. High nitrate and nitrite values

Clinical Findings: Signs of nitrite
in postmortem specin1ens may be an
poisoning usually appear suddenly because
incidental finding, indicative only of
of tissue hypoxia and low blood pressure as
exposure and not toxicity. Plasma is the
a consequence of vasodilation. Rapid, weak
preferred premortem specimen, because
heartbeat with subnormal body temperasome plasma protein-bound nitrite could ture, muscular tremors, weakness, and
be lost in the clot if sernm was collected.

ataxia are early signs of toxicosis when

Nitrite present in whole blood also
methemoglobinemia reaches 30%---400/o.

continues to react with Hgb in vitro, so

Brown, cyanotic mucous membranes
these specimens must be centrifuged
develop rapidly as methemoglobinemia
immediately and plasma separated to
exceeds 500/o. Dyspnea, tachypnea, anxiety,
prevent erroneous values of both. Addiand frequent urination are common. Some tional postmortem specin1ens from either
monogastric animals, usually because of
toxicoses or abortions include ocular fluids,
excess nitrate exposure from nonplant
fetal pleural or thoracic fluids, fetal stomach
sources, exhibit salivation, vomiting,
contents, and maternal uterine fluid. All
diarrhea, abdominal pain, and gastric
specin1ens should be frozen in clean plastic
hemorrhage. Affected animals may die
or glass containers before submission,
suddenly without appearing ill, in terminal
except when whole blood is collected for
anoxic convulsions within 1 hr, or after a
methemoglobin analysis. Because the
clinical course of 12---24 hr or longer. Acute
an10unt of nitrate in rumen contents is not
lethal toxicoses almost always are due to
representative of concentrations in the
development of 2'800/o methemoglobinernia.

diet, evaluation of rumen contents is not

Under certain conditions, adverse effects
indicated.

may not be apparent until animals have

Bacterial contamination of postmortem
been eating nitrate-containing forages for
specimens, especially ocular fluid, is likely
days to weeks. Some anin1als that develop
to cause conversion of nitrate to nitrite
marked dyspnea recover but then develop
at room temperature or higher; such
interstitial pulmonary emphysema and have
specimens may have abnormally high
continued respiratory distress; most of
nitrite concentrations with reduced to
these recover fully within 10---14 days.

absent nitrate concentrations. Endog

Abortion and stillbirths may be seen in
enous biosynthesis of nitrate and nitrite by
some cattle 5---14 days after excessive
macrophages stimulated by lipopolysacnitrate/nitrite exposure but likely only in charide or other bacterial products may
cows that have survived a 2'500/o methemoalso complicate interpretation of analytical globinemia for 6--12 hr or longer. Prolonged
findings; this should be considered as a
exposure to excess nitrate coupled with
possible maternal or fetal response to an
cold stress and inadequate nutrition may
infection.

lead to the alert downer cow syndrome ( see

Methemoglobin analysis alone is not a
p l l88) in pregnant beef cattle; sudden
reliable indicator of excess nitrate or nitrite
collapse and death can result.

exposure except in acute toxicosis, because

Lesions: Blood that contains methemo500/o of methemoglobin present will be globin usually has a chocolate-brown color,
converted back to Hgb in ---2 hr, and
although dark red hues may also be seen.

alternative forn1s of nonoxygenated Hgb

There may be pinpoint or larger hemorthat may be formed by reaction with nitrite rhages on serosal surfaces. Hydroperitoare not detected by methemoglobin neun1 and ascites have been reported in
analysis. Nitrate and nitrite concentrations
stillborn calves, as well as edema and

>20 mcg NO:fmL and >0.5 mcg NO/mL,
hemorrhage in the ILmgs and digestive
respectively, in maternal and perinatal
system of perinatal calves with excessive
serum, plasma, ocular fluid, and other
maternal nitrate exposure. However, dark
sinillar biologic fluids are usually indicative

NITRATE AND NITRITE POISONING

3051
of excessive nitrate or nitrite exposure in
be used to evaluate nitrate and nitrite
most domestic animal species; nitrate
content in serun1, plasma, ocular fluid, and
concentrations of up to 40 mcg NOJmL
urine.

have been present in the plasma of healthy

Differential diagnoses include poisonings

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calves at birth but are reduced rapidly as
by cyanide, urea, pesticides, toxic gases ( eg,
nom1al neonatal renal function eliminates
carbon monoxide, hydrogen sulfide),
nitrate in the urine. In acutely poisoned
chlorates, aniline dyes, aminophenols, or
ruminant livestock, nitrate and nitrite
drugs (eg, sulfonamides, phenacetin, and
concentrations as high as 300 mcg NOJmL
acetan1inophen), as well as infectious or
and 25-50 mcg NO/mL, respectively, can
noninfectious diseases (eg, grain overload,
be found in plasma or serum, with - 1/3 less
hypocalcemia, hypomagnesemia, pulmoin postmmtem ocular fluid because of nary adenomatosis, or emphysema) and any
diffusion equilibrium delay. However,
other cause of sudden unexplained deaths.

postmortem ocular fluid nitrate concentrations are relatively stable and remain diagnostically significant for up to 60 hr

Treatment: Slow IV iitjection of 1 %
after death. Once collected, plasma, serum,
methylene blue in distilled water or isotonic
and ocular fluid specimens have stable
saline should be given at 4-22 mg/kg or
nitrate concentration for at least l mo
more, depending on severity of exposure.

at -20°C.

Lower dosages may be repeated in 20----30

Nonnally expected nitrate and nitrite
min if the initial response is not satisfactory.

concentrations in similar diagnostic

Lower dosages of methylene blue can be
specimens are usually <10 mcg NOJmL
used in all species, but only nmlinants can
and <0.2 mcg NO/mL, respectively. Nitrate
safely tolerate higher dosages. If additional
and nitiite concentrations > 10 but <20 mcg
exposure or absorption occurs during

NOJmL and >0.2 but <0.5 mcg NO/mL,
therapy, re-treating with methylene blue
respectively, are suspect and indicate nitrate
every 6--8 hr should be considered. Rumen
or nitrite exposure of unknown duration,
lavage with cold water and antibiotics may
extent, or origin. The possible cont1ibution
stop the continuing microbial production of
of endogenous nitrate or nitrite synthesis
nitrite.

by activated macrophages must also be
considered. The biologic half-life of nitrate

Control: Animals may adapt to higher
in beef cattle, sheep, and ponies was
nitrate content in feeds, especially when
detemlined to be 7. 7, 4.2, and 4.8 hr,
grazing sun1mer armuals such as sorghwnrespectively, so it will be at least five biologic Sudan hybrids. Multiple, small feedings help
half-lives (24-36 hr) before increased nitrate
anin1als adapt. Trace nlineral supplements
concentrations from excessive niti·ate
and a balanced diet may help prevent
exposure din1inish to nonnally expected
nutritional or metabolic disorders associvalues, allowing additional time for valid ated with longtenn excess dietary nitrate
premortem specimen collection.

consun1ption. Feeding grain with high

A latent period may exist between
nitrate forages may reduce nitrite producexcessive maternal dietary nitrate exposure tion. However, caution is advised when
and equilibriun1 in perinatal ocular fluids.

cornbi.Jling other feed additives/components,

Aqueous hun1or is actively secreted into the
including nonprotein niti·ogen, ionophores
anterior chan1ber at a rate of -0.1/mUhr,

(such as monensin) and other growth and
and nitrate and nitrite are thought to enter
performance enhancers, with high-niti·ate
the globe of the eye by this mechanism.

diets in runlinants. Proper management,

Equilibrium between aqueous and vitreous
especially regarding acclimation, is critical.

hw11or is by passive diffusion rather than by

Forage nitrate concentrations > 1 % nitrate
active secretion, so niti·ate or nitiite may be
dry-weight basis (10,000 ppm N03) may
present in comparatively lesser concentracause acute toxicoses in unacclimated tions in vitreous humor after acute
animals, and forage nitrate concentrations
exposure.

s5,000 ppm N03 (dry-weight basis) are

Field tests for nitrate are preswnptive and recommended for pregnant beef cows.

should be confirmed by standard analytical

However, even forage concentrations of
methods at a qualified laboratory. The

1,000 ppm N03 dry-weight basis have been
diphenylanline blue test (1% in concenlethal to hung1y cows engorging themselves trated sulfuric acid) is more suitable to
in a single feeding withi.!1 an how·, so !he total
detemline the presence or absence of
dose of nitrate ingested is a deciding factor.

nitrate in suspected forages. Nitrate test

High-nitrate forages may also be
strips (dipsticks) are effective in detemlinharvested and stored as ensilage rather than ing nitrate values in water supplies and can
dried hay or green chop; this may reduce the

3052

NITRATE AND NITRITE POISONING
nitrate content in forages by up to 500/o.

be avoided. Large round bales with excess

Raising cutter heads of machinery during
nitrate are especially dangerous if stored
harvesting operations selectively leaves the
uncovered outside; rain or snow can leach
more hazardous stalk bases in the field.

and subsequently concentrate most of the

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Hay appears to be more hazardous than
total nitrate present into the lower third of
fresh green chop or pasture with similar
these bales.

nitrate content. Heating may assist bacterial

Water transpo1ted in in1properly cleaned
conversion of nitrate to nitrite; feeding
liquid fertilizer tanks may be extremely high
high-nitrate hay, straw, or fodder that has
in nitrate. Yotmg, tmweaned livestock,
been damp or wet for several days, or
especially neonatal pigs, can be more
stockpiled, green-chopped forage should
sensitive to nitrate in water.

PENTACHLOROPHENOL POISONING

(Penta poisoning)

Pentachlorophenol (PCP), commonly
made of lw11ber treated with PCP may
known as penta, has been used as a
salivate and have irritated oral mucosa.

fungicide, molluscicide, insecticide, and

Both penta and its major metabolite,
wood preservative. Its use is now pemtitted tetrachlorohydroquinone (TCHQ), can only for industrial purposes; agricultural
induce epidermal hyperplasia in mice.

and domestic uses are prohibited, because

Poultry have been exposed to sawdust
it is classified as a highly hazardous
and shavings from penta-treated wood.

pesticide.

Associated adverse effects include reduced

The oral LD50 of pen ta in rats is
growth rates, kidney hype1trophy, and

150-210 mg/kg body wt. Common signs
decreased hun1oral inm1une response.

of poisoning include nervousness, rapid

Penta exposure can also result in an
pulse and respiratory rate, weakness,
off-taste to eggs and meat as a result of
fever, muscle tremors, convulsions, loss
degradation of chlorophenols to chloroaniin righting reflexes, and asphyxial spasms sols. Vaporization or leaching of pen ta in
followed by death. Corneal injury may
pens, enclosures, homes, and barns has
result from splashes or vapor overexposure.

caused illness and death.

Chronic poisoning results in emaciation,

Cattle and pigs exposed to wood treated
fatty liver, nephrosis, and weight loss.

with commercial grade penta had increased

The persistence of pen ta in soil and water
mortality, possibly decreased fertility in
and apparent widespread use has resulted
boars, and reduced productivity (milk,
in significant exposure to animals. Young
meat, etc). The leilial dose in cattle and
swine have died after dermal exposure
sheep is -120-140 mg/kg body wt.

to freshly penta-treated wood used in

Commercial lots of technical-grade penta
farrowing crates or farrowing houses. In
contain small but biologically significant
vivo studies in swine demonstrated that
amounts of highly toxic impurities such as
exposure to pen ta-contaminated soil can
chlorinated dioxins and dibenzofurans,
result in significant dermal absorption of the tetrachlorophenols, and hydroxychlorodipesticide. Penta can be absorbed through phenyl ethers; iliese compounds can exert
intact skin and lungs and is an intense
their own effects such as early fetotoxicity.

irritant to the skin and mucous membranes.

Conunercial-grade penta causes hepatic

Penta absorption in skin was greater in
porphyria, increased nticrosomal monooxywater or water-based mixtures than in 100%
genase activity, and increased liver weight.

ethanol. Because animals typically have

Pure penta was not teratogenic in rats.

access to water at all tin1es, this hydrophilic

Penta can cause residues in animal
characteristic of pen ta suggests enhanced
tissues. Also, a significant an1ount of
dern1al absorption.

hexachlorobenzene is metabolized in

When absorbed, penta increases
animal tissues to pen ta. Pentachlorophenol
metabolism by uncoupling cellular
is considered to be a carcinogen and a
phosphorylation. Animals fed in troughs
twnor promoter, although studies have

PETROLEUM PRODUCT POISONING

3053
shown that the pure material does not

There is no known antidote. Tennination
increase the incidence of tumors in rats
of exposure, bathing dermally exposed
and mice. The technical-grade material has
animals, oral administration of activated
also been shown to be inmmnotoxic in
charcoal, and supportive therapy may be
laboratory studies. Penta must be handled
indicated. Bathing should be clone gently

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very carefully and kept away from animal
with cold water and detergent so as not to
contact.

cause vasodilation and increased

Whole blood analysis for pen ta may aid
absorption. Antipyretics, eg, aspirin and
in the diagnosis of poisoning; diagnosis is
acetaminophen, should not be used.

usually made on the basis of the signs and

Treatment involves cooling the animal
the proximity of treated lumber in the
and administering fluids, electrolytes,
animal's environment.

and anticonvulsants.

PETROLEUM PRODUCT POISONING

Ingestion or inhalation of, or skin contact
different from tl10se of other hydrocarbons
witl1, petrolewn, petrolewn condensate,
that make up most oil and gas products.

gasoline, diesel fuel, kerosene, crude oil, or

Benzene is hemotoxic and a known
other hydrocarbon mixtures may cause
carcinogen at high levels of exposure.

illness and occasionally death in domestic

Toluene causes neurologic signs and
and wild animals. Dogs and cats both may
clan1age at high dosages. Central nervous
ingest petroleum products during grooming
signs occur when sufficient petroleum
of contanunatecl fur or directly from open
product is absorbed into the brain or
containers. Inhalation may occur in poorly
peripheral nerves. Toxicosis generally
ventilated areas where these chemicals
occurs rapidly after exposure.

have been used or stored. Ruminants may

Vaiiation in composition of petrolew11
ingest such products in large an10unts
and petroleum-derived hydrocarbon
because they are thirsty, curious, or seeking
mixtures explains some of the differences in
salt or other nutrients, or if food or water is
toxic effects. Mixtures of low viscosity/high.

contaminated.

volatility ( eg, gasoline, naphtha, kerosene,

Small quantities of petrolew11 product
xylene) have a high aspiration hazai·cl and
used as carriers for insecticides have few
irritant activity on pulmonary tissues.

or no harmful effects, but large quantities

Gasoline and naphtha fractions may induce
and prolonged exposure can induce severe
vomiting, which contributes to aspiration
reactions. Pipeline breaks, accidental
hazai·d. Fractions more viscous than
release from storage, tank car accidents,
kerosene (asphalt, nuneral oil, waxes)

and open or leaky containers are potential
ai·e less likely to be inhaled and, even if
sources. Physical properties can affect
aspirated, are somewhat less dainaging to
exposure and toxicity. Volatility increases
lung tissue. Older formulations of lubricatat lower molecular weight and lower ing oils and greases can be particulai·Jy
saturation or aromaticity. Absorption is
hazardous because of toxic additives or
greater with highly volatile, lower molecular contanunants (eg, lead).

weight hydrocarbons (eg, hexane, gasoline)

Compai·ative toxicity of petroleum
as well as aromatic hydrocarbons (benzene,
hydrocarbons can be considered high
toluene) because of greater lipid solubility.

(oral LD50 <10 mUkg, eg, acetone,

Crude petroleum that has lost much of its
benzene, carbon disulfide, diesel fuel,
lighter, more volatile components through
toluene, xylene), moderate (oral LD50
weathering may still be hazardous.

10-20 mUkg, eg, diesel fuel, gasoline,

Crude oil and gasoline contain varying
heating oil, isopropanol, turpentine), or
amounts of aromatic hyclroca.rbons,
limited ( oral LD50 >20 mUkg, eg, motor oil,
including benzene (2%-5%in gasoline),
jet fuel, lighter fluid). Toxicity of crude oil
toluene, ethylbenzene, and xylene. These
depends on the relative content of
compounds ingested or inhaled in sufficient
kerosene, naphtha, and gasoline. Sweet
amounts can have acute and chronic effects
crude oil (high gasoline, naphtha, and

3054

PETROLEUM PRODUCT POISONING
kerosene content) at -50 mIJkg and sour

CNS signs attributable to pulmonary,
crude oil (low fractions of gasoline,
dermal, or GI absorption of hydrocarbons
naphtha, and kerosene) at 75 mIJkg
or cerebral anoxia include excitability
exposure for 1 wk have caused aspiration

(associated with aromatic fractions

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pneumonia.

benzene, toluene, etc), depression (aliphatic
or saturated low-molecular-weight

Clinical Findings: Petroleum hydrocarhydrocarbons), shivering, head tremors, bon toxicity may involve the respiratory,
visual dysfunction (sometimes associated

GI, or integumentary systems or the CNS.

with lead contamination), and incoordina

In most cases of ingestion, no clinical signs
tion. Acute pneumonia and possibly
are seen, but small animals are reported
pleuritis (coughing, tachypnea, shallow
to show oral irritation, salivation, and
respiration, reluctance to move, head held
champing of jaws, followed by coughing,
low, weakness, oily nasal discharge, and
choking, and vomiting. Pneumonia due to
dehydrated appearance) are seen in some
aspiration of hydrocarbons into the lungs
animals that aspirate highly volatile
is usually the most serious consequence
mixtures; deaths usually are seen within
of ingestion of these materials. Aspiration
days. Respiratory signs may be limited to
can occur during vomiting by monogasdyspnea shortly before death in animals trics or eructation of rumen contents.

that aspirate heavier hydrocarbons.

Pulmonary damage can occur from a

Increased PCV, Hgb, ai1d BUN, indicating
combination of volatility, viscosity, and
mild to moderate hemoconcentration,
surface tension. Higher volatility promotes
are associated with development of
access of vapors to the lung and airways
pneumonia. Neutropenia, lymphopenia,
and displaces alveolar oxygen. Risk of
and eosinopenia occur initially and are
pulmonary toxicity is increased by
followed by a relative increase in
products of lower viscosity and surface
neutrophils.

tension, with increased penetration into

There are a few anecdotal reports of
smaller airways and spread of product to
abortion after exposure. Laboratory data in
a larger lung surface area.

rodents support the occurrence of increased

Acute bloat from petroleum products
fetal loss and decreased fetal growth.

in ruminants has been reported after

However, the doses necessary to affect the
consumption of highly volatile hydrocarfetus were also sufficient to profoundly bons such as gasoline or naphtha. CNS
affect maternal health and weight.

signs may be a result of the anesthetic-like
action of low-molecular-weight aliphatic

Lesions: Aspiration pneumonia is the
hydrocarbons and/or cerebral anoxia that
most consistent postmortem finding in
can result from lung damage·or displaceanin1als that do not die of bloat. This may be ment of oxygen by the more volatile
accompanied by tracheitis, pleuritis, and
hydrocarbons. Some compounds when
hydrothorax if highly volatile fractions such
absorbed in high doses may sensitize the
as gasoline or naphtha are involved. Lung
myocardium to endogenous catecholalesions are usually bilateral and found in the mines. Anorexia, decreased rumen
caudoventral apical, cardiac, cranioventral
motility, and mild depression may begin
diaphragmatic, and intermediate lobes.

in -24 hr and last 3-14 days depending on

Affected portions are dark red and
dose and content. Hypoglycemia may be
consolidated and may contain m_ultiple
seen several days after ingestion. These
abscesses. Encapsulated pulmonary
signs and weight loss may be the only
abscesses may be found in cattle surviving
responses seen in animals that do not
up to several months after aspiration. Skin
bloat or aspirate oil. Some animals do not
lesions may be obvious after repeated
reestablish normal rumen function after
topical application or severe exposure and
ingestion and can develop a chronic
include drying, cracking, or blistering.

wasting condition.

After ingestion of oil, the feces may not

Diagnosis: A hydrocarbon odor may be
be affected until several days later, when
detected in lungs, ruminal contents, and
they become dry and formed, in the case of
feces. Even if ingested in large doses,
kerosene or lighter hydrocarbon fractions;
hydrocarbons may not be visible in
in contrast, heavier hydrocarbon mixtures
ruminal contents after -4 days. Adding

(eg, motor oil) tend to he cathaitic. Oil may
warm water to the GI contents may cause
be found in feces and rumen contents as
any oily contents to collect at the surface,
long as 2 wk after ingestion. Regurgitated
but finding oil in the GI tract does not in
or vomited oil may be seen on the muzzle
itself justify a diagnosis of poisoning; most
and lips.

oils have low toxicity if not aspirated. Sam-

PETROLEUM PRODUCT POISONING

3055
pies of GI contents, lung, liver, kidney, and

Anin1als with evidence of bacterial
the suspected source should be collected
respiratory infection may require broadfor chemical analysis to demonstrate spectrum antibiotic treatment. Pathogens
presence of hydrocarbons in tissue
can be introduced into the lungs from

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(particularly lung) and GI contents and to
aspirated run1en or stomach contents mixed
match those found in tissues and ingesta
with the hydrocarbons. However, the use of
with the suspected source. Samples must
steroids in hydrocarbon aspiration may
be carefully protected from cross-contamifurther reduce the chance of recovery and nation during necropsy and transportation
are generally co traindicated. Treatment of
to the laboratory. Instructions from the
aspiration pneumonia ( see p 1417) is rarely receiving diagnostic laboratory should be
effective, and the prognosis is poor.

checked to ensure collection equipment

However, because signs of aspiration may
and transport containers are appropriate
not appear for several days, prognosis
to prevent evaporative loss of impo1tant
based on initial clinical findings may be
components and contamination. Positive
misleading.

chemical findings together with appropri

Most high-molecular-weight compounds
ate clinical and pathologic findings are
pass through the GI tract unchanged. Most
confim1atory. Diagnosis in oil-field
of the petroleum hydrocarbons are highly
situations has histoiically been complilipophilic and will be stored for varying cated by involvement of other toxicants,
times in tissues with high lipid content,
eg, explosives, lead from grease and "pipe
including fat, nervous tissue, and the liver.

dope," arsenicals, organophosphate esters, Some of the absorbed compounds are caustics (acids or alkalis), and saltwater.

metabolized into more toxic by-products

(eg, benzene, toluene, and n-hexane).

Treatment: Bloat pressure should be

Although most of these compounds do not
released by passing a stomach tube if
remain in the body for prolonged pe1iods,
absolutely necessary to save the life of the
little is known about exactly how long
aninlal; using a trocar risks forcing oil into
tissue levels persist in highly exposed
the peritoneal cavity, which results in
aninlals. The potential for tissue residues
pe1itonitis. Passing a stomach tube
must be considered before tl1e slaughter of
dramatically increases the risk of aspiraaninlals intended for human consumption.

tion, and extreme caution is necessary. In

In poisoning or damage due to cutaneous
the absence of bloat, the prime objectives
exposure, the material should be removed
are to prevent aspiration and to mitigate
from the skin with the aid of soap or mild

GI dysfunction. Rumenotomy to remove
detergents and copious an1ounts of cool
ruminal contents and replace them with
water. The skin should not be brushed or
healthy ruminal material is safer. More
abraded. Further treatment depends on the
chronic cases involving primarily hypofuncclinical signs and is largely restricted to tion of the rumen may also respond to this
supportive therapy.

procedure. Cathartics, if used, should be of

Petroleum hydrocarbon poisoning can be
the saline or sorbitol type; however, there is
avoided only by preventing access to these
no evidence that they in1prove prognosis.

materials through proper storage of home

Recent information no longer supports use
and farm chemicals and well-maintained
of oil-based cathartics for petroleum
fencing around high-risk petroleum
ingestion.

facilities.

Activated charcoal has occasionally
been suggested for use in small animals.

Effects of Oil and Gas Fields on Cattle

Although it does not effectively adsorb

Health and Production: Anecdotal
pctroleun1 distillates, it may be given if
reports in the literature have documented
necessary to adsorb additives and other
producer concerns about the effect of oil
contaminants. Gastric lavage is generally
fields on cattle health and production.

contraindicated for petroleum and volatile

Some observational studies have suggested
hydrocarbon ingestions. Care should be
that exposure to emissions from sour gas
taken to avoid inducing vomiting and
processing plants and sour gas flares
aspiration. Small anin1als with acute

( natural gas containing hydrogen sulfide)

respiratory distress may require supplemay be associated witl1 an increased risk mental oxygen and positive-pressure
of certain reproductive losses in cattle.

ventilation, used cautiously because of

Researchers are currently reexamining
existing physical pulmonary damage.

these findings and exploring the inlpact of

Frequent purging of ventilators is necesoil and gas field emissions on the immw1e sary to elinlinate volatile hydrocarbons.

system.

3056

PERSISTENT HALOGENATED AROMATIC POISONING

PERSISTENT HALOGENATED

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AROMATIC POISONING

Persistent halogenated hydrocarbons
to PHAs is generally from ingestion of

(PHAs) are manmade chemicals and can be
rrn11inant products and farmed and wild
products of incomplete combustion. PHAs
fish. Cats, like small children, are also
are a complex mixture of chemicals with
exposed in the indoor environment.

differing molecular composition. Some PHAs

Soil can be contanlinated by industrial
are added to consrnner products to provide
activity and spreading of waste materials on
w.lique properties and have been/are used as
land. For example, spreading sewage sludge
pesticides and disinfection agents. Most
on soil can cause a 50x increase in the soil

PHAs persist in the environment and are
levels of PCDDs. Levels of PBD Es in sewage
classified as persistent organic pollutants.

sludge have been reported as high as 2.3

PHAs cause acute and chronic toxicity. There ppm (dry), and the most consistentPBDE
is evidence that lifetime chronic toxicity can
in sewage sludge is the penta-PDE. The
be expressed differently during life stages
prin1ary source of the PCDD/Fs in forages
from embryogenesis to senility. Exposure at
harvested from contaminated soils is
early life stages may not be expressed until a
incorporated soil. Grass silages generally
later life stage. PHAs can be biomagnified in
contain more PCDD/Fs tl1an com (maize)

body fat and liver, translocated to t11e fetus,
silage. The congener profile in forages can be
and secreted in milk and eggs. Biomagnificaused to chenlically "fingerprint" the sources.

tion is a process wherein PHAs are

Birds and otl1er animals consun1e soil by
concentrated in fat and liver at a factor
geophagy when feeding. Grazing cattle and
higher t11an dietary levels and is a food safety
sheep can consume up to 17% and 300Ai,
issue. Important groups of PHAs include
respectively, of the dry matter intake as soil.

polybrorninated diphenyl etl1ers (PBDEs),

Ruminants and horses can also be exposed
polychlorinated dibenzo-p-dioxins,
to PHAs by direct atmospheric deposition on
dibenzofurans (PCDD/Fs), polychlorinated
vegetation. Atmospheric levels of PHAs
biphenyls (PCBs), DDT, and triclosan.

generally vary with the season.

Companion animals have indoor

Etiology: Exposure to PHAs results from
envirorunental exposures to PHAs,
contanlination of the indoor envirorunent,
especially the PBDEs, and cats are studied
especially house dust, atmospheric
as a model to assess infant/toddler
deposition of PHAs, amending agricultural
exposure. The PBDEs are a chemical
lands with sewage sludge and industrial
nlixture of congeners solubilized in plastics,
wastes, indust1ial incidents, and feed
carpets and other synthetic fabrics and
contamination including byproduct •
foams, and electronic equipment to retard
ingredients. Indoor dust is an important
combustion. They contanlinate indoor air
route of exposure of companion animals to
as a vapor, migrate from carpets and other

PBDE fire retardants. For the other PHAs,
synthetic fibers, and are a component of
diet is generally considered the primary
house dust. PBDEs can also leach"from
route of exposure. Atmospheric PHAs,
products after disposal. The PBDEs with a
dispersed worldwide, tend to have higher
lower brornination number generally are
concentrations in the arctic and antarctic
more environmentally persistent in food
regions. Atmospheric PI-IAs are deposited
webs. The lligher brominated PBDEs can be
on soil and forages. Consun1ption of
debronlinated by biota to lower brorninated
contaminated forage and soil by rnminants

PBDEs. Burning plastics containing PBDEs
is a significant source of PCDD/Fs and other
forms polybronlinated dibenzo-p-dioxins

PHAs in the food web. Animal by-products

(PBD Ds) and dibenzofurans (PBD Fs ). The
containing PHAs, previously biomagnified

PBD D/Fs have toxicity sin1ilar to that of
in fat and liver by other animals in the food
their chlorinated analogues and have been
web, are also an important source of PHAs
measured in adipose tissue. 'Ihclosan, a
in animal diets. Ball clay contaminated with
polychlorinated hydroxydiphenyl ether, is

PCDDs has been incorporated in the diets of widely used as a broad-spectrnm bactericide food-producing animals, and contanlinated
and is an ingredient in many cleaning agents
clay has been used in hrnnan food processand hygiene products. Surfaces of products ing. Exposure assessments must include all
such as cutting boards, food wrappers,
sources of PHAs. Human dietary exposure
refrigerator llilings, and cat litter can be

PERSISTENT HALOGENATED AROMATIC POISONING

3057
impregnated with tliclosan for bacte1icidal
some PCBs and TCDD/Fs congeners. The
action and to reduce odors. PHAs can be
overall immune effect is reduced native
present in feedstuffs fed to dogs and cats.

resistance to infectious disease and a likely

For example, fish oil, which may be used in
increased risk of neoplasia. The best-studied

VetBooks.ir
fommlated diets, generally is 2-fold higher in
in1munotoxic effect of PHAs is on the

PCDD/Fs than in meat and bone meal.

lymphocytes and acquired inununity. An
abnormal increase in occurrences of

Biomagnification, Translocation, and
infectious diseases can be observed in

Food Safety: PH.As are readily absorbed
affected anin1alsi
from the gut, lungs, and through the skin.

PHAs can alter endocrine functions. The

After absorption, they can be biomagnified

US National Toxicology Program Workshop
in body fat and the liver, translocated to

Review concluded there is evidence to
the fetus, and excreted in milk and eggs.

support an association between selected

Food-producing animals can relay PHAs in
exposure to PHAs and type 2 diabetes in
foods and animal by-products. PHAs are in
people. Studies suggest that some PHAs
rendered animal products, including fat,
may act as obesogens. There is growing
bone, and meat meals. After absorption,
general consensus that increased diagnosis
the congener profile can be altered by
of obesity in companion anin1als cannot be
biotransformation, with the congener
fully explained by genetics, lifestyle, and
profile in tissues and edible animal products
nutrition. Cats with lower capacity to
different from the PHAs absorbed. The
metabolize PCBs have increased risk of
congeners translocated to the fetus can be
acromegaly. In cats, an association between
different from the congeners deposited in
diabetes and PH.A exposure has not been
fat. Toxicity can vary with the congener
demonsti·ated in the studies published.

profile. Biomagnification of PHAs has been

Some PHAs are known to have an effect
estin1ated for chickens and pigs. PHAs
on thyroid endocrinology. The PHAs that
analyzed in chicken fat had biomagnificainduce hepatic midine diphospho-glucw·ontion factors ranging from 7 to 35. For pigs, osyltransferase or sulfotransferase
biomagnification factors ranging from <7 to
isozymes increase biliary excretion of

15 were observed. Lactating and egg-laying
conjugated thyroid ho1mones. Some PCBs
females generally have a lower body burden
or their metabolites may interfere with
of PHAs. The PH.A levels in milk generally
binding of thyroid hormones to transporter
are higher during the early part of the first
proteins and the nuclear receptor. Exposure
lactation. In rainbow trout, -300/o of the
in utero to PCBs can increase brain
dietary PCDD/Fs are transferred to fat
deiodinases and may be a compensatory
located in muscle tissue. The biomagnificaresponse to maintain tissue T3 concenti·ation factor generally varies between PHAs, tions due to decreased fetal circulating and
animal species, and food webs.

brain concentrations ofT4• There is an
association between high levels of PBDEs

Toxicology: Studies have shown that
in house dust and hyperthyroidism in
people and domestic and wild animals
cats. Blood levels of PHAs have not been
are exposed to a chemical soup of PHAs
associated with hyperthyroidism in cats.

throughout a lifetime. The possible

The PBDEs have been shown in laborat01y
antagonistic, additive, synergistic, and
studies to disrnpt thyroid function in mice
potentiating interactions of the PHAs in
and Anlerican kestrels. One mechanism
the mixture are not well known.

appears to be competitive displacement of

PH.A groups and individual PHAs are

T from its carrier protein by hydroxylated
potent up- and down-regulators of enzyme

4

PBDE metabolites. Tetrabromobisphenol
systems by interaction with inununotoxic

A has been shown to alter the thyroid
nuclear receptors; some PHAs interact with
honnone receptor. There is evidence
an assortment of endocrine receptors. Cell
that triclosan disrnpts thyroid ftmction.

signaling can also be disn.ipted. Exposure

PH.As can be steroid honnonal agonists
begins during embryo logic development
and antagonists and can disrnpt endocrine
and continues with possible differing toxic
homeostasis. These disrnptions can cause
effects occuning during development,
reproductive dysfunctions. A study on PCBs
maturation, and aging. For some effects,
in cattle tissues showed that the stimulato1y
toxicity occurring at one life stage may not
effects of follicle-stimulating hormone and
be expressed until the next life stage. The
luteinizing honnone on luteal, granulosa,
general toxicology includes disrnption of
and thecal cells were decreased for
the inunune and endoc1ine systems and
secretion of progesterone, esti·adiol, and
associated organs/functions. Immunotoxictestosterone, respectively. Using cattle ity is considered a sensitive paran1eter for
uterine strips, PCBs have been shown to

3058

PERSISTENT HALOGENATED AROMATIC POISONING
increase the force of myometrial contrac

In cats, acromegaly appears to be linked
tions and increase endometrial section
to a decreased ability to metabolize PCB
of prostaglandin F2a. Exposure to PCBs
congeners. Hyperthyroidism in cats is

VetBooks.ir
and brominated biphenyls can delay onset
associated with high levels of PBDEs in
of parturition in cattle.

house dust. Feeding mink or whale blubber,

There is increasing concern that some
naturally contaminated with PHAs and

PHAs can alter horn1onal function in utero.

other pollutants, to sled dogs was shown

Exposure to PHAs in utero may alter body
to increase occurrences of diffuse
mass index and sexual functions later in life.

thickening of the glomerular capillary wall

Pre-and postnatal exposure to PHAs,
and Bowman's basement membranes.

through endocrine disruption mechanisms,

Tubular hyalinization-degeneration and
may alter manunary gland development and
increased chronic interstitial nephritis
function and increase the 1isk of manunary
were also noted.

diseases. Goats exposed to PCBs in utero had

Blood, plasma, serum, body fat, and liver
altered adenyl function that varied with age
can be assayed for PHAs. These levels can
and sex. The goats had lower basal cortisol
be linked to exposure and clinical and
levels during prepubertal development, and
pathologic findings to establish a putative
this effect persisted during their fust breeding diagnosis.

season. Male goats at 9 mo of age had a
greater and prolonged rise in plasma cortisol

Treatment and Control: There is
levels when subjected to moderate stress.

no known treatment for intoxication by

PHAs can up-regulate the activities of

PHAs. Supportive care is recommended.

cytochrome CYP (P450) and other enzymes.

Attention should be given to the indoor

Changes in drug metabolism can occur.

environment, the use of nonplastic feeding

Changes in CYP activity can increase the
and watering utensils, and feed sources to
formation of the ultimate toxicant of a
prevent exposures to PBDEs. Avoiding
variety of toxic substances. PHAs can also
contact with materials impregnated with
be promoters of carcinogens.

PBDEs reduces the percutaneous
exposure of companion animals. Avoiding

Clinical Findings, Lesions, and
household furnishings and plastics that

Diagnosis: In chickens, acute exposure
contain PBDEs generally reduces the
to PHAs may cause a sudden drop in egg
levels of PBDEs in the indoor environproduction followed by reduced egg ment. Allowing a companion animal more
hatchability. Ascites and edema may be
access to the outdoors reduces the indoor
seen, together with ataxia. Lesions include
exposure to PBDEs. The PHAs in body
degenerative changes in skeletal and
fat are excreted in milk fat and contribute
cardiac muscle. Altered thyroid function is
to the body burden of the neonate. The
associated with anomalous development in
levels in milk are higher in the first
birds and mammals.

lactation.

INSECTICIDE AND ACARICIDE

(ORGANIC) TOXICITY

Insecticides are any substance or a mixture
poisoning is often due to inadvertent or
of substances intended to prevent, destroy,
accidental use, whereas in small animals
repel, or mitigate insects. Similarly, acari

(particularly dogs) poisoning is often due to
cides are substances that can destroy mites.

malicious intent.

A chemical can exert both insecticidal and

Pesticide labels must carry warnings
acaricidal effects. Based on their properties, against use on unapproved species or these chemicals can be classified into four
under untested circumstances. These
groups: 1) organophosphates, 2) carbawarnings may pertain to acute or chronic mates, 3) organochlorines, and 4) pyrethrins toxicity, or to residues in meat, milk, or and pyrethroids. Because of worldwide use,
other animal products. Because labels
these chemicals pose health risks to
change to meet current government
non target species, including people,
regulations, it is important to always read
domestic and companion animals, wildlife,
and follow all label directions accompanyand aquatic species. In large animals, ing the product.

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY

3059

Each exposure, no matter how brief or

Chenlical synthesis rarely yields 1000/o of
small, results in some of the compound being the product of interest, and nonnally there absorbed and perhaps stored. Repeated
are, in variable prop01tions, structurally

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short exposures may eventually result in
related compounds that have biologic
intoxication because of cw11ulative effect.

effects clifferent from those of the compow1d

Eve1y precaution should be taken to
sougllt. A prime exan1ple is dichlorodiphe.nylmininlize hw11an exposure. This may include ethane (DDD): the p,p' -isomer is an effective
frequent changes of clothing with bathing at
insecticide of low toxicity for most
each change, or if .necessary, the use of
mainmals; the o,p' -isomer causes .necrosis of
respirators, rain gear, and gloves impe1vious
the adrenal glands of people and dogs and is
to pesticides. Respirators must have filters
used to treat certain adrenal malfunctions.

approved for the type of insecticide being

In general, products stored under
used ( eg, ordinary dust filters will not protect
temperature extremes or held in paitially
the operator from organophosphorus insectiemptied containers for long periods may cide fumes). Such measures are generally
deteriorate. But during storage, malathion
sufficient to guard against intoxication.

produces isomalathio.n, which is many times

Overexposure to chlorinated hydrocarbon
more toxic than malathion. In addition to
insecticides is difficult to measure except by
isomalathion, two other tectulical in1purities
the occurrence of overt signs of poisoning.

of malatllio.n (malaoxon and trinlethyl

Organophosphate and carban1ate insectiphosphorodithioate) can be formed and cides produce their toxicity by inactivation of
can potentiate the toxicity of malathion
acetylcholinesterase (AChE) enzyme at the
by several fold. Similar inlpurities can be
synapses in nervous tissue and .neuromuscuformed and pote.ntiate the toxicity of another lar junctions, and in RBCs. Therefore, the
organophosphate insecticide, phenthoate.

cholinesterase-inhibiting property of

Storing a chenlical in anything but the
organophosphates or carban1ates may be
original container is hazai·dous, because in
used to indicate degree of exposure if the
time its identity may be forgotten. Accidental
activity of the blood/RBC-AChE is detercontact witl1 anin1als or people may then

.nlined during an early pe1iod of exposure.

have clisastrous consequences. Consumet"

Organic pesticides are known to exert
mixed and unapproved combinations can be
deleterious effects on fish and wildlife as
very dangerous and should never be used.

well as on domestic species. In no event

For exan1ple, sinlulta.neous administration
should amounts greater than those
of two organophosphate insecticides can
specifically recommended be used, and
result in potentiation of malathion toxicity
maximal precautions should be taken to
by a hundredfold.

prevent drift or drainage to acljoining fields,

A number of cholinesterase-inhibiting.

pastures, ponds, streams, or other prenlises
carbamate and organophosphate insectioutside the treatment area.

cides (eg, carbaryl, dichlorvos, methiocarb,

The safety and exposure level of these
carbofuran, paraoxo.n, mevinophos,
compounds in target species has been
aldicarb, and mo.nocrotophos) are also
carefully established, and application
immunotoxic. Impaired macrophage
recommendations and regulations must be
signaling tJu·ough interleukins 1 and 2
followed. Individuals, including veterinarappears to be involved, and the insecticide ians, have been prosecuted for failure to
levels tl1at cause this effect are very low.

follow label directions or to heed label

This can lead to subtle but dainaging
warnings and for failure to warn animal
influences on the health of exposed animals.

owners of the necessaiy precautions.

An ideal insecticide or acaricide should

CARBAMATE INSECTICIDES
be efficacious without risk to livestock
or persons making the application and

The carbamates are esters of carbarnic acid.

without leaving residues in tissues, eggs,

Unlike organophosphates, carbamates are not
or milk Only a few compounds may meet
structurally complex. Presently, tl1e volun1e of
all these requirements.

carbamates used exceeds that of organophos

Poisoning by organic insecticides and
phates, because carbamates are considered to
acaricides may be caused by direct
be safer than organophosphates.

application, by ingestion of contaminated
feed or forage treated for control of plant

Aldicarb: The oral LD5() in rats is 0.9 mg/
parasites, or by accidental exposw·e.

kg, and the dennal LD5() in rabbits is 5 mg/kg.

This discussion is limited to only those

Dogs are frequently poisoned with malicious
insecticides or acaricides most frequently
intent.

hazardous to livestock or likely to leave resi

Carbary!: The oral LD5() in rats is
dues in anin1al products.

307 mg/kg, and the dermal LD5() in rabbits

3060

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY
is 2,000 mg/kg. A 2% spray is nontoxic to
in RBCs or whole blood (live animals), or in
calves; 4% is nontoxic to mature cattle when brain cortex (dead animals). Enzyme applied dermally.

activity that is significat1tly inhibited (>50%)

Carbofuran: The oral 10
is confirmatory. Signs of hypercholinergic

00 in rats, dogs,

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chickens, ducks, pheasants, quails, and wild
activity are usually seen with AChE
birds is 8, 19, 6.3, 0.415, 4.2, 5, and 0.42 mg/kg,
inhibition> 700/o. Screening GI contents for
respectively. Dogs are commonly poisoned
cai·ban1ate insecticides by gas chromatograwith malicious intent by tainting food. The phy coupled with mass spectrometry is
minimum toxic dose in cattle and sheep is
helpful in identification, confirmation, and

4.5 mg/kg, becoming lethal at 18 and 9 mg/kg,
quantitation of a patticular carbainate ai1d
respectively. Cattle and other domestic
aids in differential diagnosis if an organoanimals are often poisoned by accidental phosphate insecticide is also involved.

exposure. Pigs have been poisoned after
drinking water contanlinated by this

Treatment: Treatment of carban1ate poisoncompound. In Africa, wildlife populations ing is similar to that of organophosphate

(including deer, lions, and birds) are declining poisoning in that atropine sulfate i.r\jections because of malicious use of carbofuran. The
readily reverse the effects. Recommended
dermal LD
dosages for atropine ai·e as follows: dogs and

00 in rabbits is 2,550 mg/kg.

cats-dosed to effect (repeated as needed),

Methomyl: The oral LD00 in rats is 17 mg/
usually 0.2-2 mg/kg, parenterally, one-fourtll
kg, and the dermal LD00 in rabbits is >2,000
of the dose given IV and the remainder given
mg/kg. Dogs have been commonly poisoned

SC ( cats should be dosed at the lower end of
with malicious intent by tainting food. Cattle
the ra11ge); cattle and sheep-0.6-1 mg/kg,
have been reported to be poisoned after
one-fou1th of the dose IV and the remainder
consun1ption of forage inadvertently sprayed SC, repeated as needed; horses and with methomyl.

pigs-0.1-0.2 mg/kg, IV, repeated as needed.

Propoxur: The oral LD

Pralidoxime (2-PAM) should not be used

00 is 95 mg/kg in
rats and >800 mg/kg in goats. The dermal
to treat carbainate poisoning. 2-PAM can be

LD
beneficial if poisoning is caused by a mixture

00 in rabbits is> 1,000 mg/kg.

of organophosphates at1d cai·banmtes. Signs
of excessive cholinergic activity may watTant

Clinical Findings: The carbanmte
its use, in case the cause is organophosphate
insecticides act similarly to the organophosexposure. 2-PAM can be fatal if given too phates (seep 3064) in that they inhibit acetyrapidly; it must be administered slowly lcholinesterase (AChE) at nerve synapses

(ie, in 5% saline over a 10-min pe1iod). See
and neuromuscular junctions. This inhibition
also
is reversible because the inhibiting bond is

ORGANOPHOSPHATES, p 3064. Also, 2-PAM
solution should be prepared freshly, because
much less durable; thus, the inhibition of
old solutions are known to produce cyanide.

blood AChE frequently is not evident at tl1e

Use of morphine or barbiturates is contrainlaboratory. Signs include hypersalivation, GI dicated.

hypem1otility, abdominal cramping, vomiting,
diatThea, sweating, dyspnea, cyanosis,
miosis, muscle fasciculations (in extreme

CHLORINATED HYDROCARBON
cases, tetany followed by weakness and

COMPOUNDS
paralysis), and convulsions. In brief, the
acronym SLUD (salivation, lacrimation,

Because of persistent tissue residues and
urination, and diatThea) describes the overall
chronic toxicity, use of chlo1inated hydroclinical features of carbanmte poisoning.

cai'bon compounds has been drastically

Deatl1 usually results from respiratory failure
ctutailed. Only lindane and methoxychlor
at1d hypoxia due to bronchoconstriction
are approved for use on or ai·ound livestock.

leading to tracheobronchial secretion and

Detectable residues of some chlorinated
pulmonary edema.

hydrocarbon insecticides, including BHC,
heptachlor, heptachlor epoxide, lindane, and

Diagnosis: Diagnosis of carbainate
oxychlordat1e, can be found in fatty tissue
poisoning usually depends on history of
after acute or chronic exposure.

exposure to a particular carbainate and

Aldrin: Aldrin is a potent insecticide
response to atropine therapy. However,
sinlilar to dieldrin with the san1e order of
when a history of carbarnate poisoning is
toxicit;y (see below). !tis no longer registered not provided, but cholinergic signs and a
in the USA but was used for tennite control.

clear positive response to atropine suggest

The oral LD00 in rats is 39 mg/kg, and the
carbatnate or organophosphate poisoning,
dermal LD00 in rabbits is 65 mg/kg. In fann

AChE activity levels should be deternlined
aninlals, the toxic dose is -15-30 mg/kg.

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY 3061

Benzene Hexachloride (BHC, HCH,

4.4 mg/kg, whereas adult cattle tolerate 8.8

Hexachlorocyclohexane): Benzene
mg/kg and are poisoned by 22 mg/kg. Pigs
hexachloride (BHC) is composed of 12%---45%
tolerate 22 mg/kg and are poisoned by 44

'I isomer. BHC was a useful insecticide for
mg/kg. Horses are poisoned by 22 mg/kg.

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large animals and dogs but is highly toxic to

Because of its effectiveness against insect
cats in the concentrations necessary for
pests on crops and pasture and the low
parasite control. Only the 'I isomer ( '{-BHC,
dosage per acre, dieldrin is not likely to
lindane) is a useful insecticidal agent; the
poison livestock grazing the treated areas.

other isomers are stored for excessively long

Diets containing 25 ppm of dieldrin have been
periods in body tissues. Lindane, which
fed to cattle and sheep for 16 wk witl10ut
contains >99"/o of the 'I isomer, should be used harmful effects other than residues in fat, in preference to the technical grade ofBHC,
which a.re slow to disappear. Great ca.re must
which contains several isomers. The oral LDw be exercised in marketing animals that have of lindane in rats is 76 mg/kg, and the dermal
grazed treated areas or consumed products

LDw in rabbits is 500 mg/kg. Presently, BHC is
from previously treated areas. There is a zero
not sold in the USA
tolerance level for residues in edible tissues.

Cattle in good condition have tolerated

Statements pertaining to dield..Iin also

0.2% lindane applications, but stressed,
apply, in general, to endrin, the most toxic
emaciated cattle have been poisoned from
of the three chlorinated cyclodiene
spraying or dipping in 0.075% lindane. Horses insecticides.

and pigs appear to tolerate 0.2%-0.5%, and
sheep and goats ordinarily tolerate 0.5%

Endosulfan: Endosulfa.n is widely used
applications. Emaciation and lactation
to control insect and mite pests on a
increase tl1e susceptibility of anin1als to
variety of crops and orchards. It is heavily
poisoning by lindane; such animals should
used on tobacco. Endosulfan is very toxic
be treated with extreme caution. Young
to mammalian species. The oral LDw in rats
calves a.re very susceptible to lindane and are is 18 mg/kg, and the dermal LDw in rabbits poisoned by a single oral dose of 4.4 mg/kg.

is 74 mg/kg. The LD50 of endosulfan in dogs

Mild signs appear in sheep given 22 mg/kg,
is 77 mg/kg. Its lethal dose in cattle is 8 g.

and death occurs at 100 mg/kg. Adult cattle

Generally, cattle a.re poisoned by accidenhave tolerated 13 mg/kg without signs. BHC
tal exposure, and dogs are poisoned by
is stored in body fat and excreted in milk.

malicious intent. Exposure of cattle to
endosulfan produces residues in the liver,

Chlordane: Chlordane is no longer
kidneys, muscle, and milk.

registered as an insecticide in the USA

Exposure occurs when livestock consume

Heptachlor: Heptachlor is not currently
treated plants or when they come in direct
registered in the USA and is not recomcontact through carelessness and accidents. mended for use on livestock in the USA.

The lethal dose of chlordane for most

Among its few agricultural applications,
species is in the range of 200-300 mg/kg.

heptachlor is used for residual control of

Very young calves have been killed by doses
subterranean temtites. The oral LDw in rats
of 44 mg/kg, and the minimum toxic dose
is 40 mg/kg, and the dennal LDw in rabbits
for cattle is -88 mg/kg. Cattle fed chlordane
is 119 mg/kg. Because it is very effective
at 25 ppm of their diet for 56 days showed
against certain plant-feeding insects, it is

19 ppm in their fat at the end of the feeding.

encoW1tered from time to time in some

Topical emulsions and suspensions have
geographic areas grazed by livestock. YoW1g
been used safely on dogs at concentrations
dairy calves tolerate dosages as high as 13
up to 0.25%, provided freshly diluted
mg/kg but are poisoned by 22 mg/kg. Sheep
materials were used; dry powders up to 5%
tolerate 22 mg/kg but a.re poisoned by 40 mg/
have been safe. The no-effect level in dogs
kg. Diets containing 60 ppm of heptachlor
in a 2-yr feeding study was 3 mg/kg. Pigeons
have been fed to cattle for 16 wk without
and Leghorn cockerels and pullets suffered
harmful effects other than residues in fat.

no effects after 1-2 mo exposure to vapors

Heptachlor is converted to heptachlor
emanating from chlordane-treated surfaces.

epoxide by animals and stored in body fat.

The oral LDw in rats is 283 mg/kg, and the

For this reason, a specific analysis pe1fonned
dern1al LDw in rabbits is 580 mg/kg.

for heptachlor usually yields negative results,
while that for epoxide is positive.

Dieldrin: Dieldrin is not a registered
pesticide in the USA Residues limit its

Methoxychlor: Methoxychlor is one
application, and it is one of the most toxic
of the safest chlolinated hydrocarbon
chlorinated hydrocarbon insecticides. The
insecticides and one of the few with active
oral LDw in rats is 40 mg/kg, and the dennal
registration in the USA The oral LO"° in

LDw in rabbits is 65 mg/kg. YoW1g dairy calves rats is 5,000 mg/kg, and tl1e dermal LDw in are poisoned by 8.8 mg/kg, PO, but tolerate
rabbits is 2,820 mg/kg. YoW1g dairy calves

3062

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY
tolerate 265 mg/kg; 500 mg/kg is mildly
amount was elinunated 2 mo after the
toxic. While 1 g/kg produces rather severe
toxaphene was discontinued).

poisoning in young calves, sheep are not
affected. One dog was given 990 mg/kg/day
for 30 days without showing signs. Six

Clinical Findings: The chlorinated

VetBooks.ir
applications to cattle of a 0.5% spray at 3-wk
hydrocarbon insecticides are general CNS
intervals produced fat residues of 2.4 ppm;
stimulants. They produce a great variety of

-0.4 ppm of methoxychlor is found in milk
signs-the most obvious are neuromuscular

1 day after spraying a cow with a 0.5%
tremors and convulsions--and there may be
concentration. Methoxychlor sprays are not
obvious behavioral changes common to
approved for use on animals producing milk
other poisonings and CNS infections. Body
for human consumption. Cattle and sheep
temperature may be very high. Affected
store essentially no methoxychlor when
animals are generally first noted to be more
fed 25 ppm in the total diet for 112 days. If
alert or apprehensive. Muscle fasciculation
methoxychlor is used as recommended,
occurs, becoming visible in the facial region
the established tolerance in fat will not
and extending backward w1til the whole
be exceeded. Commercial products are
body is involved. Large doses of DDT, DOD,
available for garden, orchard, and field
endosulfan, lindane, and methoxychlor cause
crops, and for horses and ponies.

progressive involvement leading to trembling

N un1erous reports suggest that methoxyor shivering, followed by convulsions and chlor has negative reproductive effects in
death. With the other chlorinated hydrocarlaboratory animal experiments, but this has bons, muscular twitching is followed by
not been seen in the field.

convulsions, usually without the intermediate trembling. Convulsions may be clonic or Toxaphene:Toxaphene is no longer
tonic lasting from a few minutes to several
under active registration in the USA. It
hours, or intermittent and leading to the
has been used with reasonable safety if
animal becoming comatose. High fever may
recommendations were followed, but it can
accompany convulsions, particularly in
cause poisoning when applied or ingested in warm environments.

excessive quantities. The oral LD50 in rats is

Behavioral changes such as abnormal

40 mg/kg, and the dermal LD50 in rabbits is
postures (eg, resting the sternum on the

600 mg/kg. Dogs and cats are particularly
ground while remaining upright in the
susceptible. Young calves have been poirear, keeping the head down between the soned by 1% toxaphene sprays, while all
forelegs, "head pressing" against a wall or other fan11 animals except poultry can
fence, or continual chewing movements)

withstand 1 % or more as sprays or dips.

may be seen. Occasionally, an affected

Chickens have been poisoned bY. dipping in
animal becomes belligerent and attacks

0.1 % emulsions, and turkeys have been
other animals, people, or moving objects.

poisoned by spraying with 0.5% matetial.

Vocalization is common. Some animals

Toxaphene is primarily an acute toxicant
are depressed, almost oblivious to their
and does not persist long in the tissues.

surroundings, and do not eat or drink;

Adult cattle have been mildly intoxicated by
they may last longer than those showing

4% sprays and severely affected by 8%. Adult more violent symptoms. Usually, there is cattle have been poisoned from being
a copious flow of thick saliva and urinary
clipped in emulsions that contained only
incontinence. In certain cases, the.clinical

0.5% toxaphene ( an amount ordinarily safe)

signs alternate, with the animal first being
because the emulsions had begun to break
extremely excited, then severely
down, allowing the fine droplets to coalesce
depressed.

into larger droplets that readily adllere to

The sevetity of the signs seen at a given
the hair of cattle. The resultant dosage
time is not a sure prognostic index. Some
becomes equivalent to that obtained by
animals have only a single convulsion and
spray treatments of much higher concentradie, whereas others suffer innumerable tions. Toxaphene is lethal to young calves
convulsions but subsequently recover.

at 8.8 mg/kg but not at 4.4 mg/kg. The

Animals showing acute excitability often
minin1un1 toxic dose for cattle is -33 mg/kg,
have a fever > 106°F ( 41 °C). The signs of
and for sheep between 22 and 33 mg/kg.

poisoning by these insecticides are highly

Spraying Hereford cattle 12 times at 2-wk
suggestive but not diagnostic; other poisons
intervals with 0.5% toxaphene produced a
and encephalitis or meningitis must be
maximum residue of 8 ppm in fat. Cattle
considered.

fed 10 ppm of toxaphene in the diet for 30

Signs of acute intoxication by chlordane
days had no detectable toxaphene tissue
in birds are nervous chirping, excitability,
residues, whereas steers fed 100 ppm for
collapse on hocks or side, and mucous ex11-

112 days stored only 40 ppm in their fat (this
dates in the nasal passages. Signs of subacute

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY

3063
and chronic intoxication are molting,
dehydration, therapy should be directed
dehydration and cyanosis of the comb,
toward rehydration and nomishment either
weight loss, and cessation of egg production.

IV or by stomach tube. Residues in exposed

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Lesions: If death has occurred suddenly,
animals may be reduced by giving a slmry of
there may be nothing more than cyanosis.

activated charcoal or providing charcoal in

More definite lesions occur as the duration
feed. Feeding phenobarbital, 5 g/day, may
of intoxication increases. Usually, there is
hasten residue removal.

congestion of various organs (particularly
the lungs, liver, and kidneys) and a blanched
appearance of all organs if the body

INSECTICIDES DERIVED FROM
temperature was high before death. The

PLANTS
heart generally stops in systole, and there
may be many hemorrhages of varying size

Most insecticides derived from plants ( eg,
on the epicardiwn. The appearance of the
rotenone from Denis and pyrethrins from
heart and lungs may suggest a peracute

Chrysanthemum or Pyreth1um) have
pnewnonia and, if the animal was affected
traditionally been considered safe for use on
for more than a few homs, there may be
anin1als. Nicotine in the form of nicotine
pulmonary edema. The trachea and bronchi
sulfate is an exception. Unless it is carefully
may contain a blood-tinged froth. In many
used, poisoning may result. Pets are exposed
cases, the CSF volume is excessive, and the
to tobacco by ingesting commercial tobacco
brain and spinal cord frequently are
products ( eg, cigarettes or chewing tobacco),
congested and edematous.

whereas livestock may consun1e discarded
tobacco stalks or hay contaminated with

Diagnosis: Chemical analysis of brain,
tobacco plant drippings in the barn. The
liver, kidney, fat, and stomach or rumen
minin1wn lethal dose of nicotine is 1 g in
contents is necessary to confinn chlorinated
cattle, 0.2----0.3 gin horses, 0.1--0.2 g in sheep,
hydrocarbon compound poisoning. The
and 0.02--0.1 g in dogs and cats. Affected
suspected somce, if identified, should also
anin1als show tremors, incoordination,
be analyzed. Brain levels of the insecticide
nausea, disturbed respiration, muscle
are the most useful. Whole blood, serum,
paralysis, and finally coma and death.

and wine from live animals may be analyzed

Nicotine and related alkaloids from tobacco
to evaluate exposme in the rest of the
can cross the placenta and produce teratoherd or flock In food animal poisoning, if genic effects. Recovery from sublethal doses
exposme is more than just the anin1als
is usually complete within 3 hr. Death occurs
visibly affected, fat biopsies from smvivors
within a matter of homs from paralysis of
may be necessary to estin1ate the potential
thoracic respiratory muscles and cardiac
residue. Identification, confirmation, and
arrest. Necropsy may reveal parts of tobacco
quantitation of organochlo1ine insecticides
leaves or stalks in the rumen contents.

are usually done by gas chromatography

Lesions include pale mucous membranes,
coupled with mass spectrometry.

dark blood, hemorrhages on the heart and
in the lungs, and congestion of the brain.

Treatment: There are no lmown specific

Treatment consists of removing the material
antidotes to chlorinated hydrocarbon
by washing or by gastric lavage with tannic
compound poisoning. When exposure is by
acid, adnlinistering activated charcoal,
spraying, dipping, or dusting, a thorough
providing artificial respiration, and treating
bathing without irritating the skin (no
for cardiac arrest and shock
brushes), using detergents and copious

Pyrethrins: Pyrethrins are insecticides
quantities of cool water, is recommended. If
obtained from the flowers of C cinerariae
exposme is by ingestion, gastric lavage and
folium and have been used as insecticides
saline pmgatives are indicated. The use of
for many years. Pyrethrins and pyrethroids
digestible oils such as com oil is contraindiproduce toxicity affecting primarily the cated; however, heavy-grade mineral oil plus
sodiwn channel, but also chloride and
a pmgative hastens the removal of the
calciwn channels of nerve cells. These
chemical from the intestine. Activated
insecticides also interact with nicotinic
charcoal appears to be useful in preventing
acetylcholine receptors. Synergists, such
absorption from the GI tract. When signs are
as piperonyl butoxide, sesamex, piperonyl
excitatory, a sedative anticonvulsant such as
cyclonene, etc, are added to increase
a barbitmate or diazepa.m is indicated.

stability and effectiveness. This is accom

Anything in the environment that stresses
plished by inhibiting mixed function
the animal ( eg, noise, handling) should be
oxidases, enzymes that detoxify pyrethrins
reduced or removed if possible. If the animal
and pyrethroids; wuortunately, this also
shows marked depression, anorexia, and
potentiates manunalian toxicity.

3064

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY

Pyrethroids: Pyrethroids are synthetic
increasing tl1e concentration 5-10 fold in
derivatives of natural pyrethrins. There are
sprays or dips increases the seve1ity of toxic
two types of pyrethroids. Type I compounds
signs, which include hypersalivation, muscle
that lack an a-cyano substituent include
tremors, ataxia, and mild to severe hypother

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pyrethrin I, allethrin, tetramethrin, kadethrin,
mia. The inclusion ofpiperonyl butoxide
resmethrin, phenothrin, and perrnethrin.

in tl1e f omutlation potentiates the toxicity in

Type II compounds that contain a stabilizing
cats. Allergies have also been repo1ted in
a-cyano-3-phenoxybenzyl component include people in contact with o-lirnonene, and it cyfluthrin, cypem1ethrin, fenpropanthrin,
appears to increase de1ma.I absorption of
deltamethrin, cyphenothrin, fenva.Ierate,
some chemicals. When orally administered to
and fluva.Iinate. Type I pyrethroids produce
dogs, o-limonene causes vomiting (meclian
a neurologic syndrome through their effects
effective dose 1.6 mllkg). No antidote is
on both the central and peripheral nervous
available.

systems, with signs including tremors,
incoordination, prostration, seizures, and

ORGANOPHOSPHATES
death. Type II pyTethroids work primarily by

CNS mechanisms to exert the choreoatheto

The organophosphates (0 Ps) are derivatives
sis/salivation syndrome, characterized by
of phosphoric or phosphon.ic acid. OPs
hyperactivity, hunched back, salivation,
have replaced the banned organochJorine
tremors, and incoordination progressing
compounds and are a major cause of anin1a.I
to sinuous writhing movements.

poisoning. They vary greatly in toxicity,

Diagnosis ofpyrethrin/pyrethroid poisonresidue levels, and excretion. Many have been ing is based on clinical signs, history of
developed for plant and aninla.I protection,
exposure, and determination of insecticide
and in genera.I, tl1ey offer a distinct advantage
residue in body tissues and fluids. These
by producing little tissue and environmental
insecticides do not produce characteristic
residue. Some of the OPs developed initially
pathologic lesions.

as pesticides are also used as antl1elrnintics.

Generally, syn1ptomatic and supportive

Five such compounds include dichlorvos,
treatment is required after ingestion of a
trichlo1fon, ha.Ioxon, naphtlla.Iophos, and
dilute pyrethrin or pyretlu·oid preparation.

crufomate. The first two are prin1aiily used

Toxicity may also be due to the solvent.

against parasitic infestations in horses, dogs,

Induction of emesis may be contraindicated.

and pigs; the latter three are used against

A slurry of activated charcoal at 2--8 g/kg
pai·asites in runlinai1ts.

may be administered, followed by a saline

Many of the OPs now used as pesticides
cathartic (magnesium or sodium sulfate [lQOA, ( eg, chlorpyrifos, diazinon, fenitrotllion, solution] at 0.5 mg/kg). Vegetable oils and
ma.Iatllion, paratllion, etc) are not potent
fats, which promote the· intestinal absorption
inhibitors of cholinesterase until activated in
ofpyretlmun, should be avoided. If denna.I
the liver by nlicrosoma.I oxidation enzyn1es;
exposure occurs, tl1e aninla.I should be
they are generally less toxic, and intoxication
bathed with a mild detergent and cool water.

occurs more slowly. Certain OP preparations

The area should be washed very gently so as
are nlicroencapsulated, and tl1e active
not to stimulate the circulation and enhance
compound is released slowly; tllis increases
skin absorption. Initial assessment of the
the duration ofactivity and reduces toxicity,
animal's respiratory and cardiovascular
but the toxic properties ai·e still present.

integrity is important. Further treatment
involves continuing syn1ptomatic and

Organophosphate Insecticides
supportive care. Seizures should be
controlled with eitl1er diazepan1 (adnlinis

Azinphos-methyl (or -ethyl): The maxitered to effect at 0.2-2 mg/kg, IV) or methomum nontoxic oral dose is 0.44 mg/kg f or carban1ol (55-220 mg/kg, IV, not exceeding
ca.Ives, 2.2 mg/kg for cattle and goats, and

200 mg/min). Phenobarbital or pentobarbital

4.8 mg/kg for sheep. The oral LD50 in rats is

(IV), to effect, can be used if diazepam or

5 mg/kg, and the denna.I LD50 in rabbits is
methocarbamol are too short-acting.

220 mg/kg.

Carbophenothion: Carbophenotllion
o-limonene: o-Limonene is the major
has been used as a spray for fiuit trees and
component of the oil extracted from citrus
as a dip or spray for sheep blowfly, keels,
rind. It is used for tile control of fleas on
and lice. Dairy ca.Ives <2 wk old sprayed
cats and for other insect pests. Adult fleas
with water0based fonnuJations showed
and eggs appear to be most sensitive to
poisoning at concentrations �0.05%, and
o-limonene, which is more effective if comadult cattle were poisoned by spraying with bined witll the synergist piperonyl butoxide.

1 %. Sheep ai1d goats have been poisoned by

At recommended dosages, the solution

22 mg/kg, PO, but not by 8 mg/kg. In sheep,
containing o-lirnonene appears to be safe, but 0.1% as a dip produces no signs of poison-

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY

3065
ing. The LD50 for rats is -31 mg/kg; a daily
highly toxic to mat11111als. The oral LD50 is 8
dosage of 2.2 mg/kg for 90 days produced
mg/kg in goats and 2 mg/kg in rats; the dem1al
poisoning. Dogs tolerated a diet containing

LD50 in rats and rabbits is 8 mg/kg. Demeton32 ppm for 90 days. A single application of a O poisoning developed in several hrn1dred

VetBooks.ir
powder containing 1 % of carbophenothion
cattle grazing near cotton treated with this
is lethal to cats.

insecticide. The con-espondi.ng analogues of

Chlorfenvinphos: Adult cattle were
demeton ( demeton-0-methyl at1d demeton-Spoisoned by 5% or higher sprays, whereas methyl) ai·e also used for similai· purposes
young calves were poisoned at concentrabut ai·e les,s toxic than demeton.

tions of 2%. The minimum oral toxic dose

Diazinon: Young calves appear to tolerate
appears to be -22 mg/kg for cattle of all ages. 0.05% spray but are poisoned by 0.1 % concen

The acute oral LD50 for rats is 12 mg/kg, and
trations. Adult cattle may be sprayed at
the dennal LD,,o in rabbits is 3,200 mg/kg.

weekly intervals with 0.1 % concentrations

Chlorpyrifos: The oral LD
without inducing poisoning. Yorn1g calves

50 is 500 mg/kg
in goats and 941 mg/kg in rats. In compatitolerate 0.44 mg/kg, PO, but are poisoned by son with calves, steers, and cows, bulls

0.88 mg/kg. Cattle tolerate 8.8 mg/kg, PO, but

(paiticulai·ly of the exotic breeds) are highly
are poisoned by 22 mg/kg. Sheep tolerate
susceptible to a single dose of chlorpyrifos.

17.6 mg/kg but are poisoned by 26 mg/kg.

The maximum tolerated dose of chlorpyrifos

TI1e oral LD50 in rats is 300 mg/kg, at1d the
in sheep is 750 mg/kg. Sheep given 850 mg/kg
dermal LD50 in rabbits is 379 mg/kg.

died 5 days after dosing, those given 900 mg/

Dichlorvos: Dichlorvos has ma11y uses
kg died on the third day, ai1d a dose of 1,000
on both plants and animals. It is rapidly
mg/kg was lethal within 30 hours. Onset of
metabolized and excreted, and residues
poisoning signs is usually delayed compared
in meat and milk ai·e not a problem if label
with that of many other commonly used
directions are followed. It is of moderate
organophosphates because of the conversion
toxicity, with a minin1rn11 toxic dose of
of chlorpY1ifos to the active cholinesterase

10 mg/kg in yorn1g calves at1d 25 mg/kg in
inhibitor chlorpyrifos-oxon. Chlorpyrifos
horses and sheep. The oral LD,,o in rats is 25
produces reproductive and developmental
mg/kg, PO, and the dermal LD
toxicity.

50 in rabbits is

59 mg/kg. A 1 % dust was not toxic to cattle.

Coumaphos: Coumaphos is used against

Flea collars containing dichlorvos may cause
cattle grubs and a nwnber of other ectoparaskin reactions in some pets. Cats wearing sites and for treatment of premises. The
dichlorvos-impregnated collars ca11 develop
maximum concentration that may be safely
signs of ataxia-depression SY11drome,
used on adult cattle, horses, and pigs is 0.5%. followed by death.

Yorn1g calves and all ages of sheep and goats
must not be sprayed with concentrations

Dimethoate: Dimethoate is used

>0.25%; 0.5% concentrations may be lethal.

extensively in horticulture as a systemic

Adult cattle may show mild toxicity at 1 %
insecticide, but it also kills insects by contact.

concentrations. The minimum lethal dose

When administered PO, the minin1Um toxic
for calves appears to be between 10 and
dose for yorn1g dairy calves was -48 mg/kg,

40 mg/kg. A dose of 25 mg/kg is usually fatal
while 22 mg/kg was lethal for cattle 1 Y1' old.

in sheep. The oral LD

Daily doses of 10 mg/kg for 5 days in adult

50 in rats is 13 mg/kg.

cattle lowered blood cholinesterase activity

Crotoxyphos: Crotoxyphos is used as a
to 20"Ai of normal but did not produce
spray or powder for the control of ectoparapoisoning. Horses have been poisoned by sites on cattle and pigs. Crotoxyphos is of
doses of 60--80 mg/kg, PO. When applied
rather low toxicity; however, Bral1man
topically, 1 % sprays have been tolerated by
cattle are markedly more susceptible than
calves, cattle, and adult sheep. The oral LD5()

European breeds. Cattle ( except as above),
in rats is 215 mg/kg, and the dermal LD50 in
sheep, goats, and pigs all tolerate sprays
rabbits is 400 mg/kg.

containing crotoxyphos at 0.5% levels or
higher. Crotoxyphos is safe at a level of 1 %,

Dioxathion: Dioxathion is a nonsystemic
although skin lesions have been found in
acaricide a11d insecticide for the control of
pigs. Toxic doses appears to be in the 2%
ticks. Dioxathion is a mixture of cis-ai1d
range, except for in Bralunan cattle, in
trat1S-isomers, usually in the ratio of 1:2. The
which 0.144o/o-0.3% may be toxic.

cis-isomer is more toxic than the trat1Sisomer. Used on both plants and ai1irnals, it is Demeton: Demeton is used as a systemic
rapidly metabolized and not likely to produce
insecticide against sucking insects and mites. residues in meat greater than the 1 ppm Demeton is used mainly as a foliage spray
official tolera11ce. Concentrations of <'.0.15%
and has a relatively long residual life. It is a
are generally used on anin1als. The minin1um
mixture of demeton-0 a11d demeton-S at1d is
toxic dose in calves is 5 mg/kg. Sprays of 0.5%

3066

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY
in cattle and sheep or 0.25% in goats and pigs
cattle and fleas in dogs. The rninin1un1 toxic
are nontoxic. Sprays at concentrations up to
dose, PO, is 25 mg/kg for cattle; 50 mg/kg

0.1 % are usually safe for calves and lambs.

is lethal to sheep. The oral LD5() in rats is

Twice thls concentration may produce signs

255 mg/kg, and the dermal 105() in rabbits

VetBooks.ir
of poisoning. Dioxathion at 8.8 mg/kg, PO,
is 330 mg/kg.

has killed young calves, and it produced
intoxication at 4.4 mg/kg. Emaciated cattle

Malathion: Malathion is one of the safest
with severe tick infestation are more
organophosphates because of its selective
frequently poisoned tl1an healthy aninlals.

toxicity; it is highly toxic to insects but

Maximwn residues of dioxatllion in adipose
much less toxic to mammalian species. The
tissue of cattle occm 2-4 days after dipping.

oral LD5() in rats is 885 mg/kg, and tl1e de1mal

The elinlination half-life, after obtaining

105() in rabbits is 4,000 mg/kg. The oral acute
maximwn concentrations, is -16 clays.

toxic close in calves is 10-20 mg/kg and in
adult cattle and sheep is 50-100 mg/kg. In a

Disulfoton: The maxin1w11 nontoxic oral
chronic study in buffalo calves (6-9 mo old),
dose is 0.88 mg/kg for yatmg calves, 2.2 mg/
daily oral administration of malathion at 0.5
kg for cattle and goats, and 4.8 mg/kg for
mg/kg for 1 yr produced no biochelnical or
sheep. Poisoning has occurred in cattle after
clinical effects. Dosages > 1 mg/kg inhibited
consunling harvested forages previously
blood acetylcholinesterase (AChE) activity
sprayed with this insecticide. The oral LD5()

and increased liver enzymes (ALT and AST).

in rats is 2 mg/kg, and fue dennal 105() in

A 20 mg/kg dose produced clinical signs
rabbits is 6 mg/kg. Chronic exposme to
after 10 clays. The acute oral LD
disulfoton may result in tolerance to toxicity.

5() in buffalo
calves is 53 mg/kg. Dennal application by

Ethyl 4-Nitrophenyl Phenylphosphono
spray containing 0.5%or 1% of malatllion
thioate (EPN): EPN is a nonsystemic
had no apparent effect on calves, but 5%
insecticide and acaricide structmally
spray caused death within 75 hr. Malatllion
related to parathlon. The acute oral 10
at 0.5% or 1 % should not be sprayed on

5()

in rats is 8--36 mg/kg. EPN at a dosage of
calves for more than 3 consecutive days.

10 mg/kg was found to be nontoxic to adult

Malathlon is excreted in cow's nlilk.

cattle and sheep. The minimwn oral toxic

Methyl Parathion: Methyl parathion is
close of EPN is 2.5 mg/kg in calves and 25
less toxic than parathion (diethyl parathion).

mg/kg in sheep and yearling cattle. Sprays

The 10
containing 0.025%----0.05% EPN are toxic to

5() in rats from a single oral dose is

9 -25 mg/kg, and the clem1al 10
young calves, and 0.25% EPN is lethal. Dogs

5() in rabbits is

63 mg/kg. Methyl paratllion at 2.5 mg/kg had
were not poisoned at dosages > 100 mg/kg.

no ill effect, but 10 mg/kg daily quickly led to

Famphur: The oral 10
toxic signs. The lethal close in cattle is 100

5() in rats is 35 mg/kg,
and tl1e dennal 10
mg/kg. Methyl parathion is excreted in cow's

5() in rabbits is 2, 730 mg/kg.

The maxi.Jnun1 nontoxic dose is 10 mg/kg in
nlilk. Methyl parathion produces reproduccalves and 50 mg/kg in cattle, sheep, and tive and developmental toxicity.

horses. ln general, Bralm1an cattle are

Mevinphos: The 10
especially susceptible to fa.mphur toxicity.

5() in rats is 3 mg/kg,
and the dermal 10

This compound is effective against warbles

5() in rabbits is 16 mg/kg.

Mevinphos has been commonly used to
in cattle, but ( as for all grubicides) directions
control the population of birds, and thereby
must be followed as to time of application;
caused poisoning in nontarget species. Mevinlarvae killed wllile nligrating and t11e phos at 200 ppm in fue diet is leilial in dogs.

resultant local reaction can cause serious
problems. ln several instances, famphm

Na led: Naled is essentially a dibromipoisoning occun-ed in birds (mainly magpies nated dichlorvos, wllich has the ability to
and robins) shortly after cattle had been
act as a contact insecticide. It has a broad
treated with a pom-on preparation conta.itling spectrum of insecticidal action. Because it famphm.

has a short residual life, it poses relatively

Fenitrothion: Fenitrothlon, also known
little hazard to fish and wildlife. The oral
as sunlithlon, is used as a contact insecticide

105() in rats is 191 mg/kg, and the dem1al
in agriculture and horticultme. The oral 10

105() in rabbits is 390 mg/kg.

5()

in rats is 250 mg/kg, and tl1e de1mal 105() in

Oxydemeton-methyl: The maximun1
rabbits is 1,300 mg/kg. When applied to
nontoxic oral dose is 0.88 mg/kg for young
cattle, its metabolites are excreted at low
calves, 2.2 mg/kg for cattle, and 4.8 mg/kg
levels in nlilk and mine. Fenitrothlon
for sheep and goats.

produces reproductive and developmental
toxicity in chickens.

Parathion: Parathion (diethyl pa.ratllion)

is widely used for control of plant pests

Fenthion: Fenthion is commonly applied
and is approximately one-half as toxic as
topically to control warble infestation in
tetraethyl pyrophosphate (see below). The

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY

3067
oral LD50 in rats is 3 mg/kg, and the dermal

The residues may be removed by giving the

LD50 in rabbits is 6.8 mg/kg. It is used as a dip
animal activated charcoal for several days.

and spray for cattle in some countries (not
in the USA). Most cases of occupational

Ruelene: Ruelene is active both as a

VetBooks.ir
insecticide poisonings in people have been
systemic ar1d contact insecticide in livestock,
attributed to parathion or its degradation
has some ar1thelrn.intic activity, and has
products. The minimwn toxic dose in calves
rather low toxicity. Dairy calves have been
is 0.25-0.5 mg/kg and in cattle is 25--50 mg/kg. poisoned by 44 mg/kg, PO, while adult cattle The mini.Imun oral lethal dose in sheep is
require 88 mg/kg for the sar11e effect. Sheep

20 mg/kg and in goats is 50 mg/kg. The LD
are moderately intoxicated by 176 mg/kg;

50
in dogs

Angora goats are about twice as sensitive.

is 23--35 mg/kg and in cats is 15 mg/kg.

Dem1al sprays containing 0.02%, 1%, and

Pigs have been poisoned by 11 mg/kg and

1 % of parathion are lethal to calves, sheep,
horses by 44 mg/kg. Most livestock tolerate
and goats, respectively. Parathion is used
a 2% topical spray.

extensively to control mosquitoes and

Temephos: Temephos is used as an
insects in orchards and on market garden
insecticide against mosquitoes and midges.

crops. Nonnally, because so little is used per

It is of low toxicity to marmnal.ian species.

acre, it presents no hazard to livestock. How

The oral LD50 for rats is 1 g (or more)/kg,
ever, because of the potency of parathion,
while the dermal LD50 is >4 g/kg. Daily
care should be taken to prevent accidental
exposure of cattle for 1 yr at 1-1.5 mg/kg
exposure. Parathion does not produce
is known to produce clinical signs of poisonsignificant residues in animal tissues.

ing and affect fertility in heife1-s.

Pho rate: Phorate is closely related to

Terbufos: This soil insecticide is used to
demeton (see above). It is a systemic
control com rootworms. The oral LD
insecticide and miticide. The oral LD

50 in

50 in
rats is 1.6 mg/kg. The mini.Jnun1 oral toxic
rats is 1.6 mg/kg, and the dermal LD50 in
dose is -1.5 mg/kg for sheep and cattle.

rabbits is 2.5 mg/kg. The min.imwn toxic

Cases of intoxication i.J1 cattle have occWTed.

dose PO is 0.25 mg/kg in calves, 0. 75 mg/kg

Ingestion of 7.5 mg/kg was lethal to heifel"S.

in sheep, and 1 mg/kg in cattle.

Tetrachlorvinphos: Tetrach101vinphos

Phosmet: Phosmet is a nonsystem.ic
has low toxicity in dogs; chronic feedi.J1g
acaricide and insecticide. The m.ininuun
studies indicate the lowest effect level was
oral toxic dose is 25 mg/kg in cattle and

50 mg/kg/day, and the no observed effect
calves and 50 mg/kg in sheep. Spraying with
level (NOEL) was 3.13 mg/kg/day. The
a 0.5% solution has no toxic effect, but a 1%
minimwn toxic dose in pigs is 100 mg/kg.

solution of phosmet produces intoxication
in cattle. Phosmet is not excreted in milk.

Tetraethylpyrophosphate (TEPP):

Tetraethyl pyrophosphate (TEPP) is one

Ronnel (Fenchlorphos): Ronne! is an
of the most acutely toxic insecticides.

excellent oral systemic insecticide. It is

Although not used on arumals, accidental
effective against many ecto- and endoparaexposure occUl"S occasionally. One herd of sitic arthropods, including cattle giubs,

29 cattle (including calves and adults) was
screw wom1s, and sucking lice. Ronne! is
accidentally sprayed with 0.33% TEPP
also used as a residual spray insecticide to
emulsion; all died with.in 40 min.

control flies, fleas, and cockroaches. The oral

LD

Trichlorfon: Trichlorfon is used as a

50 in rats is 1,250 mg/kg, and the dem1al

LD
systemic insecticide a11d a11thelmintic in

50 in rabbits is 2,000 mg/kg. Ronne!

produces mild signs of poisoning in cattle at
domestic an.in1als. It is also used as a11

132 mg/kg, but severe signs do not appear
acaricide in sheep at the dose rate of 80
until the dosage is >400 mg/kg. The m.inimwn mg/kg at weekly intervals for not more thar1
toxic dose in sheep is 400 mg/kg. Concentra4 wk. The oral LD50 in rats is 630 mg/kg, a11d tions as high as 2.5% in sprays have failed to
the dermal LD50 in rabbits is >2,000 mg/kg.

produce poisoning of cattle, young dairy

As a spray, trichlorfon at a 1 % concentration
calves, or sheep. Poisoning usually occw-s in
is tolerated by adult cattle; given PO, it is
two stages. The anin1al first becomes weak
tolerated by young dairy calves at 4.4 mg/kg
and, although able to move about nom1ally,
but produces poisoning at 8.8 mg/kg. Adult
may be placid. DiarThea, often flecked with
cattle, sheep, and hoIBes appear to tolerate
blood, may also be seen. Salivation and

44 mg/kg, while 88 mg/kg produces
dyspnea then appear if the dose was high
poisoning. Dogs were unaffected when fed
enough. Blood cholinesterase activity

1,000 ppm of trichlorfon for 4 mo. Adminisdeclines slowly over 5--7 days. Ronne!

tration of trichlorfon at 75 mg/kg, PO,
produces residues in meat and milk; strict
produces adverse clinical signs in dogs.

adherence to label restrictions is essential.

Tlichlorfon is metabolized rapidly.

3068

INSECTICIDE ANO ACARICIDE (ORGANIC) TOXICITY

Clinical Findings: In general, OP pesticides edema and congestion, hem01Thages, and
have a narrow margin of safety, and the doseedema of U1e bowel and other organs may response curve is quite steep. Signs of OP
be foWld. Anin1als swviving > l day may
poisoning are those of cholinergic overstirnubecome emaciated and dehydrated.

VetBooks.ir
lation, which can be grouped into U1ree
categories: muscarinic, nicotinic, and central.

Treatment: Tl1ree categmies of drugs are

Muscarinic signs, which are usually flfst to
used to treat OP poisoning: 1) musca.iinic
appear, include hypersalivation, miosis,
receptor- blocking agents, 2) cholinesterase
frequent wination, dia.iThea, vomiting, colic,
reactivators, and 3) emetics, catha.itics, and
and dyspnea due to increased bronchial
adsorbents to decrease further absorption.

secretions and bronchoconstriction.

Atropine sulfate blocks the central and

Nicotinic effects include muscle fasciculaperipheral musca.iirtic receptor-associated tions and weakness. The central effects
effects of OPs; it is administered to effect
include nervousness, ataxia, apprehension,
in dogs and cats, usually at a dosage of 0.2-2
and seizures. Cattle and sheep commonly
mgtkg ( cats at tile lower end of tile range),
show severe depression. CNS stimulation
eve1y 3-6 hr or as often as clinical signs
in dogs and cats usually progresses to
indicate. For horses and pigs, U1e dosage is
convulsions. Some OPs ( eg, a.inidothioates)

0.1--0.2 mgtkg, IV, repeated every 10 min as
do not enter the bra.in easily, so that CNS
needed; for cattle and sheep, U1e dosage is
signs are mild. Onset of signs after exposure

0.6-1 mgtkg, one-Ulird given IV, the remainder
is usually within minutes to hours but may be

IM or SC, and repeated as neeclecl. Atropinizadelayed for >2 days in some cases. Severity tion is adequate when tile pupils are dilated,
and course of intoxication is influenced
salivation ceases, and U1e animal appears
principally by the dosage and route of
more alert. Artimals initially respond well
exposure. In acute poisoning, the primary
to atropine sulfate; however, U1e response
clinical signs may be respiratory distress and
dinlirtishes after repeated treatments.

collapse followed by death due to respiratory Overtreatment witl1 atropine should be muscle pa.i·alysis. In addition to brain and
a.voided. Atropine does not alleviate tile
skeletal muscles, OPs are known to adversely nicotinic cholinergic effects, such as muscle affect other organ systems, including the
fasciculations and muscle paralysis, so dea.U1
cardiovascular, respirat01y, hepatic,
from massive overdoses ofOPs can still
reproductive and developmental, and
occur. Including cliazepan1 in U1e treatment
immune systems.

reduced the incidence of seizures and
increased survival of nonhwnan primates

Diagnosis: An important diagnostic aid
expe1imentally.

for OP poisoning is the detemtination of

An improved treatment combines atropine
acetylcholinesterase ( AChE) activity in blood witl1 the cholinesterase-reactivating oxime, a.i1d brain. Unfortunately, the depression of

2-pyridine aldoxime metilochloride (2-PAM,
blood cholinesterase does not necessarily
pralidoxime chloride). The dosage of2-PAM
correlate with the seve1ity of poisoning;
is 20--50 mgtkg, given as a 5% solution IM
signs are seen when brain AChE aetivity is
or by slow IV ( over 5--10 min), repeated at
inhibited > 7rP/o, and the enzyme in blood
half tile dose as needed. IV 2-PAM must be
reflects, only in a general way, the levels in
given very slowly to a.void rnusculoskeletal
ne1vous tissue. The key factors appear to be
pa.i·alysis a.i1d respiratory arres(;. Response to
the degree and rate at which the enzyme
cholinesterase reactivators decreases with
activity is reduced. Analyses perfom1ed after
time after exposure; therefore, treatment
exposure may be negative, because OPs do
witl1 oximes must be instituted as soon as
not remain long in tissues as U1e parent
possible ( within 24-48 hr). The rate at which
compounds. Chlo1i.nated OP comp0tmds
the enzyme/organophosphate complex
have greater potential for tissue residue.

becomes unresponsive to reactivators

Frozen stomach and rnmen contents should

( due to ageing phenomenon) varies with
be a.i1alyzed for the pesticide, using GC-MS
lhe pa.iticula.i· pesticide.

for identification, conflfmation, and quanti

Removal of the poison from U1e a.ilin1al
tation. Blood/sernm and urine can also be
also should be attempted. lf exposure was
analyzed for residue of OPs or their metadermal, the animal should be washed with bolites. More than 7(1'/o of OPs produce one or detergent and water ( a.bout room temperamore of the six dialkylphosphates ( din1ethyl ture) but without scrnbbing and irritating
phosphate, dietliyl phosphate, dimethyl

U1e skin. Emesis should be induced if oral
thiophosphate, diethyl thiophosphate,
exposure occurred <2 hr previously; emesis
clin1etliyl dithiophosphate, and diethyl
is contraindicated if the animal is depressed.

clithiophosphate ).

Oral administration of nlineral oil decreases

Lesions: Animals with acute OP poisoning
absorption of pesticide from tile GI tract.

have nonspecific or no lesions. Pulmonary

Activated cha.i·coa.J (1-2 gtkg as a water

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY

3069
sltmy) adsorbs OPs and helps elirnination in
cause OPIDN, and field cases have been
the feces. This is pruticularly recommended
seen. The lesions associated with delayed
in cattle. Continued absorption of OPs from
new·otoxicity include demyelination of
the large runow1t of ingesta in the rnmen has
pelipheral and spinal motor tracts due to loss

VetBooks.ir
caused prolonged toxicosis in cattle.

of neurotoxic esterase fwlction. Clinical

Artificial respiration or administration of
signs associated with delayed neurotoxicity
oxygen may be required. Phenothiazine
include muscle weakness and ataxia that
tranquilizers, bru·biturates, and morphine
progresses to flaccid pru·alysis. Signs are
are contraindicated.

usually not manifest until 10-14 days after
exposure to a neurotoxic tliruyl phosphate.

Intermediate Syndrome

There ru·e no specific antidotes.

Organophosphate-induced intcnnediate
syndrome (IMS) has been seen in people

PESTICIDE POTENTIATING
ru1d animals (particularly dogs and cats)

AGENTS
acutely poisoned with a massive dose of an

OP insecticide. OPs lrnown to cause IMS

Piperonyl butoxide is used as a potentiator
include bromophos, chlorpyrifos, cliazinon,
or synergist in many pesticide formulations,
dicrotophos, dirnethoate, disulfoton,
including carban1ates, organophosphates,
fenthion, malathion, merphos, methamiorganochlorines, pyrethrins, pyTethroids, and dophos, methyl parathion, monocrotophos,
o-lin1onene. It decreases breakdown of these
omcthoate, parathion, phosrnet, and
pesticides in the animal or insect's body by
trichlorfon. Clinically, IMS is chru·actelized
inhibiting mixed function oxidase enzymes
by acute paralysis and weakness in the
and makes the pesticide more toxic to the
areas of several cranial motor nerves, neck
insect-and the host. Aninlals that are
flexors, and facial, extraocular, palatal,
debilitated or have decreased drug-metabonuchal, proximal limb, ru1d respiratory lizing capability become more susceptible
muscles 24-96 hr after poisoning. IMS is a
to the pesticide. However, toxins that must
separate clinical entity from acute toxicity
be activated in the body to a toxic fonn
and delayed neuropathy. Generalized
are frequently less toxic when piperonyl
weakness, depressed deep tendon reflexes,
butoxide exposure occurs at the sanie time.

ptosis, and diplopia are also evident. These

This potentiating or synergistic effect has
syn1ptoms may last for several days or
been seen in mru1y species, including cats,
weeks depending on the OP involved.

dogs, rats, and people. Cin1etidine, a drug that

Although the exact mechartisrn of action
reduces stomach acid secretion by blocking
involved in IMS in unclear, the defect occurs gasttic H2 receptors, and the ru1tibiotic at the neuromuscular junction ( decreased
chlorrunphenicol have the sanie effect.

AChE activity and expression of nicotinic
receptors). Despite AChE inhibition, muscle SOLVENTS AND EMULSIFIERS
fasciculations and hypersecretory activities
are absent. There is no specific treatment;

Solvents and emulsifiers are required in
therapy relies on atropine sulfate and 2-PAM most liquid insecticide preparations. Usually and should be continued for weeks.

tl1ey have low toxicity, but like tl1e petroleum
products (which many ru·e), they must be

DELAYED NEUROTOXICITY FROM considered as possible causes of poisoning.

TRIARYL PHOSPHATES

In direct treatlnent witl1 pesticides, emulsification must be thorough, with an average For some time, compow1ds lrnown as triaryl
droplet size of 5 microns (preferably
phosphates ( eg, tliorthocresyl phosphate)

smaller), or excessive an1ounts may stick to
have been used as flru11e retardants,
treated animals. Treatment should be as for
plasticizers, lubricating oils, ru1d hydraulic
petrolew11 product poisoning ( see p 3053).

fluids. They are weak cholinesterase

Acetone: GI initation, nru·cosis, and
inhibitors but do inhibit "neurotoxic
kidney and liver damage are tl1e main signs
esterase" (NTE) present in the brain and
of acetone poisoning. Treatll1ent consists of
spinal cord. A fo1m of delayed neurotoxicity
gastric lavage, oxygen, and a low-fat diet.

results from the inhibition and aging of NTE,

Additional supportive treat111ent to alleviate
often refe1Ted to as OP-induced delayed
clinical signs may be given.

neuropathy (OPIDN). Triru-yl phosphates
have caused accidental poisonings in people
lsopropyl Alcohol: lsopropyl alcohol
and other species ( mostly cattle). Some other poisoning signs are GI pain, cramps, OPs, including EPN, leptophos, pru-athion,
vomiting, diatThea, and CNS depression
haloxon, cliisopropylphosphorofluoridate,

( dizziness, stupor, coma, aJ.ld death from
and tetraethyl pyrophosphate, are lrnown to
respiratory paralysis). The liver aJ.ld kidneys

3070

INSECTICIDE AND ACARICIDE (ORGANIC) TOXICITY
are reversibly affected. Dehydration and
alka.linization is the mainstay of treatment.

pneumonia may occur. Treatment consists

Ethanol retards the oxidation of methanol
of emetics, ga5tric lavage, milk, oxygen, and
and may be given as an adjunct therapy.

artificial respiration.

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Methanol: Typical signs of methanol

SULFUR AND LIME-SULFUR
poisoning include nausea, vomiting, gastric

Sulfur ai1d lime-sulfur ai·e two of the oldest
pain, reflex hyperexcitability, opisthotonos,
insecticides. Elemental sulfur is practically
convulsions, fixed pupils, and acute
devoid of toxicity, although poisoning has
peripheral neuritis. Large overdoses can
occuned occasionally when large amounts
lead to blindness. Toxic effects are due in
were mixed in cattle feed. Specific toxic
pait to the alcohol itself, and in part to
dosages are not known but probably exceed
fonnic acid produced by its oxidation.

4 g/kg. Lime-sulfur, which is a complex of

Treatment should include emetics
sulfides, may ca.use initation, discomfort,

(apomorphine) followed by gastric lavage
or blistering but rarely causes death.

with 4% sodium bicarbonate, saline laxative, Treatment consists of removing residual oxygen therapy, sodium bicarbonate
mate1ial and applying blai1d protective
solution IV, and analgesics; however, the
ointments, plus any supportive measures
prognosis is poor. Intensive and prolonged
that may be indicated.

METALDEHYDE POISONING

Metaldehyde, a cyclic polymer of a.cetaldemetabolized. Enterohepa.tic circulation may hyde, is the active component in mollusciprolong retention of metaldehyde in the cides used to control slugs and snails. Tt
animal, but ultin1a.tely, both metaldehyde
is commonly used in wet coastal areas
and a.cetaldehyde are excreted in the urine.

worldwide. This neurotoxicant has been

Clinical manifestations are attributed
associated with poisoning in a vaiiety of
ptimaiily to metaldehyde, although
domestic and wildlife species, although
acetaldehyde does play a role in the clinical
most poisonings have been repmted in dogs syndrome. Metaldehyde exposw·e alters and a.re related to careless pla.c.ement of
a vaiiety of neurotransmitter concentrabait. Metaldehyde may be combined with tions and enzyme activities. Metaldehyde
other agents such as carbamate insecticides reduces concentrations of -y-aminobutyric to enhance efficacy. It is not considered to
acid, an inhibitory neurotransmitt.er that
be a persistent chemical. Under typical
ca.uses CNS excitation. Reduced concenapplication circumstances, metaldehyde trations of brain serotonin (5-hydroxymay remain effective for as long as 10 days.

tryptanline) and norepinephrine decrease
the threshold for convulsions. Monoamine

Etiology and Pathogenesis: Metaldeoxidase activity is increased after metaldehyde may be purchased in liquid, dust, hyde exposure. Increased muscle a.ctivit-y
granular, or pelleted fom1Ula.tions. The
and the production of acidic metaldehyde
active ingredient may vary from l.5o/<>-5% in
metabolites ca.use severe electrolyte
the formulation. The bait is highly palatable
disturbances and metabolic acidosis.

and potentially addictive, which often
results in consumption of large quantities.

Clinical Signs and Lesions: The clinical

Most avian and mai11ma.lian species are
syndrome is sinillar in most species. Neurosusceptible. The lethal oral dose ranges logic manifestations, which predominate,
from -100-600 mg/kg in vaiious species.

develop within 1--3 hr after ingestion. Severe

After ingestion, metaldehyde tmdergoes
muscle tremors, anxiety, hyperesthesia,
partial hydrolysis in the stomach to produce ataxia, tachycardia, a11d hyperthemlia. may a.cetaldehyde. Both metaldehyde and
be evident initially. As the acidosis becomes
acetaldehyde are readily absorbed from
more severe, depression and hype1pnea. may
the GI tract. The na.tw·e of the stoma.ch
become more evident. As the syndrome
contents and the rate of gastric emptying
progresses, opisthotonos and continuous
influence the rate of absorption and the
tonic convulsions that are =esponsive
onset of the clinical syndrome. After
to external stimuli (in contrast to those
absorption, metaldehyde is rapidly
in strychnine poisoning) are typical

ARSENIC POISONING

3071
manifestations. Emesis, diarrhea, hypersalihypocalcemia also may resemble vation, colic, cyanosis, sweating (horses),
metaldehyde poisoning.

mydriasis, and nystagmus (cats) are often
repmted.

Treatment: There is no specific treatment

VetBooks.ir

No consistent pathognomonic gross or
for metaldehyde poisoning, although
histologic lesions are seen with metaldehyde
aggressive symptomatic treatment during
poisoning. Hepatic, renal, and pulmonary
the first 24 hr will enable most affected
congestion and intestinal ecchyrnotic and
animals to make a full recovery within 2-3
petechial hemorrhages, which may be
days. Activated charcoal and cathartics may
associated with prolonged hyperthemtia, a.re be administered to assist in decontamination conunon. Neuronal degeneration in the brain and to reduce enterohepatic cycling of and hepatic degeneration with cellular
metaldehyde. Diazepa.m (2-5 mg/kg, IV, to
swelling are often present histologically.

effect) may be used to control neurologic
manifestations. Barbiturate treatment should

Diagnosis: A history of exposure plus
be considered with caution, because
the presence of typical clinical disease is
barbiturates compete with acetaldehyde
suggestive of metaldehyde poisoning.

metabolism and induce cytochrome P450

Stomach contents often have a distinctive
enzymes involved in metaldehyde
acetaldehyde or apple cider-like odor.

metabolism. Gas anesthesia may also be

Rapid analysis of stomach contents
a useful alternative. Administration of IV
submitted frozen for metaldehyde and
fluids containing sodium lactate or sodium
acetaldehyde may be useful to confirm the
bicarbonate is essential to correct the
diagnosis. Analysis of urine, blood, or liver
metabolic acidosis and electrolyte
may be useful but is often unreliable.

imbalance. Cold water to correct the

Neurologic, GI, and pulmonary disease
hyperthermia, methocarbamol (150 mg/kg,
caused by other agents may be confused

IV) to produce muscle relaxation, and
with metaldehyde poisoning. Potential
dextrose (IV) or calcium borogluconate (IV)

differential diagnoses include poisonings
to minintize liver damage may be helpful.

by strychnine, roquefortine, sodium

Xylazine is an effective treatment in horses to
fluoroacetate, zinc phosphide, bromethareduce neurologic manifestations. Treatment lin, organophosphate, carban1ate,
options, dosages, and duration of treatment
organochlorine or pyrethroid insecticides,
vary considerably from species to species.

cyanide, blue-green algae, or compost

Metaldehyde and acetaldehyde are

(tremorgonic mycotoxins). Nontoxic
rapidly elin1inated. Consequently, tissue
conditions such as epilepsy, various
residues in food-producing anin1als are not
encephalitic infections, lysosomal storage
a major concern. Withdrawal times, if
diseases, or metabolic diseases such as
established, will be relatively short.

ARSENIC POISONING

The ubiquitous element arsenic (As) is
solubility, species of anin1al involved, and
a nonmetal or metalloid in group V on the
duration of exposure. Therefore, the toxic
periodic cha.rt. It is often referred to as
effects produced by phenylarsonic feed
arsenic metal and for toxicologic purposes
additives and other inorganic and organic
is classified as a metal. It exists in several
compounds must be distinguished. (See also
fonns and has a long history of various uses,

HERBICIDE POISONING, p 2969.)

including insecticides for animals, wood
preservatives, herbicides, and even some

INORGANIC ARSENICALS
medicinal uses. It is responsible for many
poisonings in people and anin1a.ls.

Trivalent arsenicals, or arsenites, are more

Arsenic poisoning is caused by several
soluble and therefore more toxic than the
different forms of tl1e element; the form may
pentavalent, or arsenate, compounds. These
detemtine tl1e toxicity. Arsenic is found as
include arsenic trioxide, arsenic pentoxide,
inorganic and organic forms with valences of sodium and potassium arsenate, sodimn

+3 and +5. Arsenite (As+3) is more toxic than
and potassiun1 arsenite, and lead or calcimn
arsenate (As+5). Toxicity varies with factors
arsenate. The lethal oral dose of sodimn
such as oxidation state of tl1e arse11ic,
arsenite in most species is from 1-25 mg/kg.

3072

ARSENIC POISONING

Cats may be more sensitive. In livestock,
mucosa may be hyperemic. Necrosis may
arsenates are 5-10 times less toxic than
progress to perforation of the gastric or
arsenites. Decreased use of these comintestinal wall. GI contents are often fluid, pounds as pesticides, ant baits, and wood
foul smelling, and blood tinged; tl1ey may

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preservatives has made poisonings less
contain shreds of epithelial tissue. There is
frequent. Arsenites were used to some
diffuse inflan1mation of the liver, kidneys,
extent as dips for tick control. Lead
and other visceral organs. The liver may
arsenate was sometimes used as a
have fatty degeneration and necrosis, and
taeniacide in sheep. Many of these
the kidneys have tubular clan1age. In cases
compounds are no longer used in the USA
of cutaneous exposure, the skin may exhibit
but may still be available in other cOLmtries.

necrosis and be dry or leathery.

Toxicokinetics and Mechanism of

Diagnosis: Chemical detemlination of

Action: Soluble forms of arsenic comarsenic in tissues (liver or kidney) or stomach pounds are well absorbed orally. After
contents provides confinnation. Liver and
absorption, most of the arsenic is bound to
kidneys of healtl1y animals rarely contain >0.1

RBCs; it distributes to several tissues, with
ppm arsenic ( wet wt); toxicity is associated
the highest levels found in liver, kidneys,
witll tissue concentrations >3 ppm (wet wt).

heart, and lungs. In subchronic or chronic

The determination of arsenic in stomach
exposures, arsenic accunmlates in skin,
contents is of value usually witllin the first
nails, hooves, sweat glands, and hair. Most of 24-48 hr after ingestion. The concentration of the absorbed arsenic is excreted in tl1e wine
arsenic in urine can be high for several days
as inorganic arsenic or in methylated fom1.

after ingestion. Drinking water containing

The mechanism of action of arsenic

>0.25 ppm arsenic is considered potentially
toxicosis varies with the type of arsenical
toxic, especially for large animals.

compound. Generally, tissues rich in
oxidative enzymes, such as tl1e GI tract,

Treatment: In animals with recent
liver, kidneys, lungs, endotheliw11, and
exposure and no clinical signs, emesis should
epiden11is, are considered more vulnerable
be induced (in capable species), followed by
to arsenic damage. Trivalent inorganic and
activated charcoal witll a catllartic ( efficacy
aliphatic organic arsenic compotmds exert
of charcoal in arsenic toxicosis remains to be
their toxicity by interacting with sulfhydryl
detemlined) and then oral adnlinistration of
enzymes, resulting in disruption of cellular

GI protectants (small animals, 1-2 hr after
metabolism. Arsenate can uncouple
charcoal) such as kaolin-pectin, and fluid
oxidative phosphorylation.

tl1erapy as needed. In animals already
showing clinical signs, aggressive fluid

Clinical Findings: Poisoning is usually
tl1erapy, blood transfusion (if needed), and
acute, with major effects on the GI tract and
administration of dimercaprol (British
cardiovascular system. Arsenic has a direct
anti-lewisite, 4-7 mg/kg, IM, tic! for 2-3 days
effect on the capillaries, causing damage to
or until recovery) is recommended. In large
microvascuJar integrity, transudation·of
animals, thioctic acid (lipoic acid or ac-lipoic
plasma, loss of blood, and hypovolemic
acid) may be used alone (50 mg/kg, IM, tid,
shock. Profuse watery diarrhea, sometimes
as a2CJOA, solution) or in combination with
tinged with dark blood, is characteristic, as
dirnercaprol (3 mg/kg, IM, every 4 hr for tl1e
are severe colic, dehydration, weakness,
first 2 days, qid for the third clay, ancl bid for
depression, weak pulse, and cardiovascular
tlle next 10 days or until recove1y). In large
collapse. Onset is rapid, and signs are
animals, the efficacy of dimercaprol alone is
usually seen within a few hours ( or up to
questionable. Sodium thiosulfate has also

24 hr). The course may run from hours to
been used, PO, at20- 30 g in 300 rnLof water
several days, depending on tl1e quantity
in horses and cattle, one-fowth tllis dose in
ingested. In peracute poisoning, most
sheep and goats, and 0. 5-3 g in small animals
animals may sinlply be found dead, and a
or as a 20% solution, IV, at 30-40 mg/kg,
few will be f0tmd dead witl1out any lesions.

bid-ti cl for 3-4 days or until recovery. The water-soluble analogues of dimercaprol,

Lesions: In peracute toxicosis, there

2,3--dimercaptopropane-l-sulfonate (DMPS)

are usually some lesions in the GI tract.

and dimercaptosuccinic acid (DMSA), are

Inflammation and reddening of GI mucosa
considered to be Jess toxic and more

Oocal or diffuse) may be seen, followed
effective and could be given orally.

by edema, rupture of blood vessels, and

D-Penicillarnine is reporteclJy an effective
necrosis of epithelial and subepithelial
arse11ic chelator in people. It has a wide
tissue. In ruminants, hyperemic "paintmargin of safety and could be used in animals brnsh" lesions may be seen on the serosal
at 10-50 mg/kg, PO, tid-qid for 3-4 clays.

surface of the omasun1, and the abomasal

Supportive therapy may be of even greater

COPPER POISONING

3073
value, particularly when cardiovascular
poultry diets. Severity and rapidity of onset
collapse is imminent, and should involve IV
a.re dose-dependent. Signs may be delayed
fluids to restore blood volume and correct
for weeks after incorporation of 2-3 times
dehydration. Kidney and liver function
the recommended (100 ppm) levels or may

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should be monitored during treatment.

occur within days when the excess is > 10
times the recommended levels. Chickens

ORGANIC ARSENICALS
are tolerant of arsanilic acid; however,
roxa.rsone can produce toxicosis in turkeys

Phenylarsonic organic arsenicals a.re
at only twice the recommended dose (50
relatively less toxic than inorganic
ppm). In pigs, roxarsone also has a higher
compounds or aliphatic and other aromatic
toxicity than other phenyla.rsonics.

organic compounds.

Aliphatic organic arsenicals include
cacodylic acid and acetarsonic acid. These

Clinical Findings and Diagnosis: The
were historically used as stinmlants in large
earliest sign in pigs may be reduced weight
animals, but their use is now unconunon.

gain, followed by incoordina.tion, poste1ior

Some aliphatic a.rsenicals such as monoparalysis, and eventually quadriplegia.

sodiwn methanearsonate (MSMA) and

Animals remain alert and maintain good
disodiurn methanearsonate (DSMA) are
appetite. Blindness is characteristic of
occasionally used as herbicides or grassbwT
arsanilic acid intoxication but not of other
and crabgrass killers. Ruminants, especially
organic arsenicals. In nuninants, phenylarcattle, a.re very sensitive to MSMA and sonic toxicosis is similar to inorganic arsenic

DSMA. Clinical signs, lesions, and treatment
poisoning. There a.re usually no specific
of aliphatic organic arsenicals are similar to
lesions present in phenyla.rsonic poisoning.

those of inorganic arsenicals, except that

Demyelina.tion and gliosis of peripheral
nm1inants may have necrosis of the mucosa
nerves, the optic tract, and optic ne1ves a.re
of the rumen and omaswn and gelatinous
usually seen on histopa.thology. Analyses
serosal edema of the omastm1 and abomaswn.

of feed for the presence of high levels of

Aromatic organic arsenicals include
phenylarsonics confirm the diagnosis.

trivalent phenyl organics, such as thiacetar

Phenylarsonic poisoning in pigs should be
sa.rnide and arsphenarnine for the treatment
differentiated from salt poisoning, insectiof adult hea.rtwom1s in dogs, and pentavacide poisoning, and pseudorabies. In cattle, lent compounds such as phenyla.rsonic
arsenic poisoning should be differentiated
acids and their salts. Thia.cetarsa.rnide and
from other heavy metal poisoning,
a.rsphena.rnine are no longer used cominsecticide poisoning, and infectious monly, especially since the introduction of
diseases such as bovine viral dianhea..

melarsornine di.hydrochloride (see also

IIEARTWORM DISEASE, p 127).

Treatment and Prognosis: There is

Phenylarsonic compounds were widely
no specific treatment, but the neurotoxic
used as feed a.clditives to improve production
effects are usually reversible if the offending
in swine and poultry rations and to treat
feed is withdrawn witllin 2-3 days of onset
dysentery in pigs. The three major compounds of ataxia. Once paralysis occurs, the ne1ve in this class a.re arsanilic acid, roxa.rsone
damage is irreversible. Blindness is usually

( 4-hydroxy-3-nitrophenyla.rsonic acid), and
irreversible, but animals retain their
nitarsone ( 4-nitro-phenyla.rsonic acid).

appetite, and weight gain is good if
competition for food is elli1lina.ted. Recovery

Etiology: Toxicosis results from an excess may be doubtful when the exposure is long of arsenic-containing additives in pig or
and the onset of intoxication slow.

COPPER POISONING

Acute or chronic copper poisoning is
ton Te1Tiers, an inherited sensitivity to
encountered in most pa.its of the world.

copper toxicosis similar to Wilson disease in

Sheep are affected most often, although
people has been identified. Chronic copper
other species a.i·e also susceptible. In
poisoning has been reported in otl1er breeds
various breeds of dogs, especially Bedling-
of dogs, including Labrador Retrievers, West

3074

COPPER POISONING

Highland White Terriers, Skye Terriers,
copper plumbing; cattle and goats are more

Keeshonds, Ame,ican Cocker Spaniels, and
resistant to copper poisoning than sheep and

Dobe1man Pinschers. A.cute poisoning is
thus are not affected in these instances.

usually seen after accidental administration

Species-specific diets with respect to copper VetBooks.ir
of excessive amounts of soluble copper
are reconunended to minimize the occw0
salts, which may be present in anthelmintic
rence of chronic copper poisoning. Breed
drenches, mineral mixes, or improperly
differences related to the suceptibility to
fom1Ulated rations.

chronic copper poisoning have been repmted

Many factors that alter copper metaboin sheep and goats. Young calves or sheep lism influence chronic copper poisoning by
irtjected with soluble fomis of copper may
enhancing the absorption or retention of
develop acute clinical signs of toxicity
copper. Low levels of molybdenun1 or sulfate
without evidence of a hemolytic crisis.

in the diet are in1portant examples. Primary Copper is used as a feed additive for pigs at
chronic poisoning is seen most commonly

125-250 ppm; levels >250 ppm are dange,0
in sheep when excessive amounts of copper
ous--although as for sheep, other factors
are ingested over a prolonged period. The
may be protective, eg, high levels of protein,
toxicosis remains subclinical until the copper zinc, or iron. Chronic copper toxicosis is that is stored in the liver is released in
more likely to occur with low dietary intake
massive an1ounts. Increased liver enzymes
of molybdenum and sulfur. Reduced
may provide an early warning of the pending
fonnation of copper molybdate or copper
c1isis. Blood copper concentrations increase
sulfide complexes in tissues in1pairs the
suddenly, causing lipid peroxidation and
excretion of copper in wine or feces.

intra.vascular hemolysis. The hemolytic
crisis may be precipitated by many factors,
including transportation, handling, weather

Clinical Findings: A.cute copper poisoning
conditions, pregnancy, lactation, strenuous
causes severe gastroente,itis characte1ized
exercise, or a deteriorating plane of nutrition.

by abdominal pain, diarrhea, anorexia,

Phytogenous and hepatogenous factors
dehydration, and shock. Hemolysis and
influence secondary chronic copper
hemoglobinwia may develop after 3 days
poisoning. Phytogenous chronic poisoning
if the aninlal survives the GI distw-bances.

is seen after ingestion of plants, such as

The sudden onset of clinical signs in chronic
subterranean clover (Trifolium suble1Ta
copper poisoning is associated with the
neum ), that produce a mineral imbalance
hemolytic crisis. The time of onset is
and result in excessive copper retention.

influenced by the concentration of copper in

The plants that are not hepatotoxic contain
the diet. Signs in affected aninlals include nonnal an1ounts of copper and low levels of
depression, lethargy, weakness, recumbency,
molybdenum. The ingestion of plants such
rumen stasis, anorexia, thirst, dyspnea, pale
as Heliotropium europaeum or Senecio spp mucous membranes, hemoglobinuria, and

(seep 3150) for several months may cause
jaundice. Several days or weeks before the
hepatogenous chronic copper poisoning.

hemolytic crisis, liver enzymes, including

These plants contain hepatotoxic alkaloids,

ALT and AST, are usually increased. During
which result in retention of excessive
the hemolytic crisis, methemoglobinemia,
copper in the liver. In dogs with liver
hemoglobinemia, and decreases in PCV
diseases such as chronic active hepatitis
and blood glutathione are usually seen. In

(CAH), the primary clinical signs may
camelid species such as alpacas or llan1as,
resemble those of chronic copper poisoning, no hemolytic crisis is seen, although which can be attributed to the liver damage
extensive liver necrosis remains a consistent
and subsequent retention of excessive
manifestation. Morbid aninlals often rue
copper; however, it is not clear whether CAH within 1-2 days. Herd morbidity is often <5%, causes the accumulation of copper in the
although usually > 75% of affected anin1als
liver or is the result of accumulation.

rue. Losses may continue for several months

A.cute poisoning may follow intakes of
after the ilietaiy problem has been rectified.

20-100 mg of copper/kg in sheep and young

Severe hepatic insufficiency is responsible
calves and of 200-800 mg/kg in matw-e cattle.

for early deaths. A.nin1als that survive the

Chronic poisoning of sheep may occw- with
acute episode may rue of subsequent renal
daily intakes of 3.5 mg of copper/kg when
failw·e. Photosensitization may occur in
grazing pastw-es that contain 15-20 ppm
association with chronic copper poisoning,

( dry matter) of copper and low levels of
reflecting the hepatotoxicity conunon to
molybdenum. Clinical disease may occur in
both syndromes. Cirrhosis of the liver is also
sheep or camelid species that ingest cattle
associated witl1 the syndrome in dogs.

rations, which n01mally contain higher levels

Lesions: A.cute copper poisoning produces
of copper, or when their water is supplied via
severe gastroenteritis with erosions and

FLUORIDE POISONING

3075
ulcerations in the abomasum of ruminants.

oxidative damage to RBCs dwing the

Icterus develops in animals that sUIVive
hemolytic crisis. Ammoniwn tetrathio

>24 hr. Tissues discolored by icterns and
molybdate (1. 7 mg/kg, IV, every other day
methemoglobin are characteristic of chronic
for 6 days) is effective for the treatment
poisoning. Swollen, gurnnetal-colored
and prevention of copper poisoning. This

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kidneys, port-wine-colored urine, and an
treatment, which reduces copper absorption
enlarged spleen with dark broW11-black
and enhances copper elinlination, should be
parenchyma are manifestations of the
used conservatively. A withdrawal period
hemolytic crisis. The liver is enlarged and
of -10 days is required for this medication.

friable. Histologically, there is centrilobular

Daily oral administration of ammonium
hepatic and renal tubular necrosis.

molybdate (100 mg) and sodiw11 thiosulfate

(1 g) for 3 wk reduces losses in affected

Diagnosis: Evidence of blue-green ingesta
lambs. Dietary supplementation with zinc
and increased fecal (8,000-10,000 ppm) and
acetate (250 ppm) may be useful to reduce
kidney (>15 ppm, wet wt) copper levels are
the absorption of copper. Plant eradication
considered significant in acute copper
or reducing access to plants that cause
poisoning. 1n chronic poisoning, blood and
phytogenous or hepatogenous copper
liver copper concentrations are increased
poisoning is desirable. Primary chronic or
dwing the hemolytic period. Blood
phytogenous poiso1ling may be prevented by
concentrations often rise to 5--20 mcg/mL,
top-<lressing pastures with 1 oz of molybdeas compared with nonnal levels of -1 mcg/
nwn per acre (70 g/hectare) in the form
mL. Liver concentrations >150 ppm (wet wt) of molybdenized superphosphate or by are significant in sheep. The concentration
molybdenwn supplementation or resttiction
of copper in the tissue must be determined
of copper intake. I -ligh-risk flocks of sheep
to eliminate other causes of hemolytic
may be supplemented with sodiw11
disease. Molybdenwn tissue concentrations
thiosulfate in the diet to prevent or contt·ol
should be evaluated to detemline whether
chronic copper poisoning. ln dogs, genetic
the syndrome is due to primary or secondtesting is available to identify earners of the ary chronic copper poisoning.

autosomal recessive gene associated with
abnormal copper accwnulation, although the

Treatment and Control: Often, treatment
mode of inheritance is not knoW11 for all
is not successful. The prognosis is poor in all
susceptible breeds. Periodic liver biopsies,
species. GI sedatives and symptomatic
tissue copper detemlination, and liver
treatment for shock may be useful in acute
enzyme assessment may also be useful
toxicity. Penicillamine (50 mg/kg/day, PO, for
to evaluate disease status. In addition to

6 days) or calciwn versenate may be useful if
previously described treatments, zinc suppleadministered in the early stages of disease to mentation and prednisone or prednisolone
enhance copper excretion. Vitanlin C (500
administration enllance copper excretion
mg/day/sheep, SC) has been shoW11 to reduce and linlit development of liver disease.

FLUORIDE POISONING

(Fluorosis)

Fluo1ide exposure from the environment
range from -20-50 mg/kg ( dry weight) in
has been associated with natural contamimost species. In poultry, as much as 200
nation of rock, soil, and water or from
mg/kg can be tolerated. These tolerances
industtial waste or smelting processes.

may vary depending on age, duration of

Fluo1ide compounds have been added to
exposure, and nutritional status. Aninlals
hwnan water supplies at concentrations
with a long, productive life span such as
of -1 mg/kg to reduce dental caries. Tllis
dairy cattle are more susceptible.

recommendation is not universally
accepted. Both acute and chronic toxico

Etiology and Pathogenesis: Fluorides
ses are reported with fluoride ingestion.

are found naturally in rock phosphates and

Maxirnwn tolerance levels in anin1al feeds
limestone. Industrial wastes associated with

3076

FLUORIDE POISONING
fertilizer and mineral supplement progastroenteritis, salivation, restlessness, duction are frequent sources of fluoride
sweating, anorexia, muscle weakness,
exposure. Metal ores associated with steel
stiffness, dyspnea, ventricular tachycm·clia,
and aluminum processing are common
mid clonic convulsions followed by
industrial sources. Fluoride dusts disdepression and death are typically seen.

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persed downwind from these sources

Chronic fluorosis is chm·acterized by
may contaminate forage crops for many
unthri.fty animals with skeletal a.Ild dental
kilometers. Forage crops grown on
abnmmalities. Reduced feed and water
contaminated soil may contain increased
intake accompm1ied by poor weight gain
concentrations of fluoride associated with
mid milk production reflect dental lesions
physical contamination with soil particumid impaired mastication. Mottled, chalky, lates. There is minimal direct uptake of
pitted a.Ild stained enan1el, and w1even and
fluoride by the plant. With the potential of
excessive wem· on the teeth are frequently
fluoride contan1ination in many feed and
seen. Dental pain manifested by lapping of
water sources, it is recommended that
drinking water may be appm·ent. Skeletal
feed-grade phosphates contain <1% fluoride. abnormalities associated with increased Acute fluoride exposure at high concentrabone resorption and remodeling produces tions will cause corrosive damage to tissues. severe la.Jlleness, stiffness, abnom1al hoof In contrast, chronic exposure, which is seen
growtl1, and exostoses. In later stages of the
more frequently, causes delayed or in1paired syndrome, severely affected cattle may be mineralization of bones and teeth. The
forced to move on tl1eir knees because of
solubility of fluoride correlates generally
spm1ing and b1idging of joints. Periosteal
with the degree of toxicity. Fluoride is
hyperostosis is seen on ribs. Metabolically
known to interact with vmious elements,
active and growing bones of young animals
including aluminum, calcium, phosphorus,
are more severely affected. Anemia and
and iodine. Fluoride is a cellular poison that
hypothyrnidism manifested by reduced T�
interferes with t11e metabolism of essential
and T levels plus reduced serw11 calciw11
metals such as magnesium, manganese,

4
concentrations are often present.

iron, copper, and zinc. Because bacterial
metabolism may be affected in a similar

Lesions: Severe GI inflanimation and
ma.Jlller, this attribute accounts for the use
degenerative changes in otl1er orgailS such
of fluoride in dental hygiene products.

as the liver, kidney, and lungs reflect the

Soluble fluoride is rapidly absorbed; -500A,
cytotoxic effects of acute fluorosis. After
is excreted by glomerular filtration. More
clu·onic exposure during pregnancy,
thIDl 95% of the fluoride tl1at is retained is
offspring are more severely affected. Bilateral
deposited in tl1e bones mid teeth, forming
a.Ild syn1metrical skeletal abnormalities m·e
hydroxyapatite after the interference with
present. 'Die bones m·e chalky white with
calcium metabolism mid replacement of
disrupted osteogenesis, accelerated bone
hydroxyl ions. At low levels of fluoride
remodeling, IDld resorption in association
exposure, the solubility of the enmnel is
witl1 production of abnormal bone osteoid
reduced, resulting in protection. t,.t higher
that results in exostoses, sclerosis, and
levels of exposure, the enm11el becomes
osteoporosis. The mandible, ribs, metacm0
dense and brittle. If exposure occurs dming
pals, and metatm-sals are most often affected.

pregnancy, developing bones mid teeth

Exostoses m·e most evident in the long bones.

are severely affected. Faulty, irregular

In addition to tl1e mottled, chalky, stained
mineralization of the matrix associated
teeth exhibiting w1even wem·, eruption of
with altered mneloblastic, odontoblastic,
pern1ID1ent incisor teeth may be delayed.

or osteoblastic activity ultimately results in
poor ena.Jllel fonnation, exostosis, sclerosis,

Diagnosis: A diagnosis of acute fluoride
and osteoporosis.

poisoning should be based on a histmy of
exposure and typical clinical or pathologic

Clinical Findings: Acute poisoning
mmlifestations. Confirmation with urine or
associated with massive ingestion of
serum measurements should be interpreted
ascaricides (sodium fluoride), rodenticides
witll caution, because rapid, tin1e-dependent

(sodium fluorosilicate), or oral dental
elimination of fluoride occUI"S. The measmeproducts will produce clinical disease ment of serun1 calciLm1 and magnesiun1 conwithin 2 hr. The fatal dosage of sodium centrations may provide supportive evidence.

fluoride is -5-10 mg/kg. Toxic ma.Jlifesta

Chronic fluorosis may require many montlls
tions may be evident after consun1ption of
to develop. Fluoride concentrations in

-1 mg/kg. Serum calciun1 and magnesium
tissues must be considered in association
concentrations decline rapidly after the
with history, clinical disease, and necropsy
onset of the clinical syndrome. Severe
finclings. Animals exhibiting skeletal and

IRON TOXICITY IN NEWBORN PIGS

3077
dental abno1malities manifested by

Concentrations ranging from 6,000-13,000
lameness, osteoporosis, anorexia, or
mg/kg and 7,500-11,000 mg/kg, respectively,
reduced productivity should be evaluated for are consistent with a diagnosis of chronic chronic fluorosis. Other disease syndromes
fluorosis ill livestock. Plasma concentrations
such as arthritis; calcium, phosphorous, or
may rise substantially once the skeletal

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vitamin D deficiency; metal toxicities such
concentrations of fluoride approach
as molybdenum, selenium, or arsenic; and
saturation.

ergotism may be confused with chronic
poisoning. In addition to tissue analysis,

Treatment arid Control: Animals
racliographs and histologic evaluation may
developillg acute poisoning may be
provide useful illforn1ation. In livestock,
administered calcium gluconate (IV) and
normal fluoride concentrations ill the cliet
magnesium hydroxide or milk orally to
range from -20-50 mg/kg. Depending on the
mininlize fluoride absorption, although tl1e
duration of exposure and species susceptiprognosis may remam poor if massive bility, concentrations ill the diet rangillg
an10W1ts of fluoride were ingested. Once
from 100-300 mg/kg may produce chronic
manifestations of chronic fluorosis develop,
poisoning. Water concentrations >30 mg,'L
treatment is illeffective. The primary
are considered toxic. In yow1g dairy cattle
objective should be directed toward
with a lengthy lifetilne production potential,
prevention. In many instances, it may be
tolerance levels should be reduced by at
difficult or ilnpractical to remove livestock
least 2 -fold. Because flu01ide does not
from contanunated areas. Supplementation
accumulate i11 soft tissue, analysis of liver
with calcium carbonate, aluminum salts,
and kidney has llinited usefulness. In
magnesium metasilicate, or boron will
livestock, nonnal plasma concentrations
reduce absorption or enhance excretion. It
are <0.2 mg,'L, whereas concentrations
is recommended tl1at livestock consume
ranging from 0.7-1.9 mg/La.re consistent
supplements and nu.neral nuxes containing
with poisoning. Corresponding urmary

< 1 % fiuo1ide content. If it is impractical to
concentrations <0.5 mg,'L are normal. Toxic
lliltit fluoride exposure, raising species with
concentrations based on recent exposure
a relatively short production life, such as
range from 14--120 mg,'L. Fluoride concentrapoultry, pigs, or sheep, should be considtions in bones and teeth may reach levels ered. Reducillg fluoride exposw·e of yoW1g
as high as 1,500 mg/kg and 1,000 mg/kg,
or pregnant animals may linut the developrespectively, without adverse effects.

ment of clu·onic fluorosis.

IRON TOXICITY IN NEWBORN PIGS

Reports of toxicity after SC or IM injection
is edema and a brownish black discoloration
of iron preparations ill newborn piglets are
at the injection site. Waxy degeneration of
sporadic, and the risk is not high; however,
skeletal and heart muscle may be seen; there
toxicity does occur occasionally. In some
may be hem01Thages in the heait and
litters, death occurs quickly, from 30 nun to
necrosis of the liver and kidneys.

6 hr after irtjection; ill others, death is

In the second, less acute form of toxicity,
delayed for 2-4 days. (See au;o NONREGENERA

U1e excess iron appears to block the body's

TIVE ANEMIAS, p 12.)

defense mechanisms by overwhelming the

Toxicity may be seen in three forms. In
phagocytic cells, which illcreases the
the fu-st form, dan1age to the muscles aroW1d Ii kelillood of infection. Death occurs ill U1e injection site causes potassium, among

-2-4 days. In yoW1g piglets, the most likely
other substances, to be released; the blood

Wection is an Escherichia coli enteritis
potassiwn level rises and illterferes with
and, although some of the chru1ges seen
cardiac function. Usually, U1e whole litter
ill the first fonn may be seen at necropsy,
is affected. Piglets may appear anemic,
they ai·e less obvious, and the enteritis
become weak, cannot stand, ru1d have
contributes markedly to deatl1.

muscle tremors followed by convulsions.

The most important precipitating factor

Respiratory distress may be seen. There is
of iron toxicosis ill pigs is a low vitanu.n E or
swelling at the injection site. On necropsy,
selenium status of the sow. If either nutrient
skin and muscles may appear pale, and there is low ill the sow, pigs will either be born

3078

IRON TOXICITY IN NEWBORN PIGS
deficient in vitamin E or selenium or the

A third, more rare forn1 of toxicity is
colostrnrn will not be able to provide
associated with calciphylaxis, the massivE
adequate amounts of these nutrients to meet
mobilization of calciun1 after irtjection of
the antioxidant needs of nursing piglets.

iron preparations, both in the presence and

Supplementing the sow's ruet with 50 ru of
absence of supplementary vitamin D. It

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vitamin E/kg and 0.15 mg of seleniunvkg will
occurs within several days of iron injection
in1prove the status of the sow and prevent
and is associated with development of hard
iron toxicity in the piglets. Ir\jections of
swellings at injection sites. Death may
vitamin E/selen.ium during late gestation
occur, and calcification in other parts of
may also help prevent iron toxicity in piglets. the body may be seen at necropsy.

LEAD POISONING

Lead poisoning in anin1als and people is a
has a profound effect on sulfhydrylmajor concern worldwide. Poisoning in containing enzymes, the thlol content of
animal populations may serve as a sentinel
erythrocytes, antioxidant defenses, and
to assess the extent of environmental
tissues rich in mitochondria, which is
contan1ination and human health problems
reflected in the clinical syndrome. In
related to lead. In veterinary medicine, lead
addition to the cerebellar hemorrhage and
poisoning is most common in dogs and
edema associated with capillary dan1age,
cattle. Lead poisoning in other species is
lead is also irritating, irnmunosuppressive,
lintited by reduced accessibility, more
gametotoxic, teratogenic, nephrotoxic, and
selective eating habits, or lower susceptibiltoxic to the hematopoietic system.

ity. In cattle, many cases are associated with
seerung and harvesting activities when used

Clinical Findings: Acute lead poisoning
oil and battery disposal from machinery is
is more common in young anin1als. The
handled in1properly. With the elimination
prominent clinical signs are associated with
of tetraethyl lead from gasoline in many
the GI and nervous systems. In cattle, signs
countries, the number of lead poisoning
that appear within 24-48 hr of exposure
cases attributed to oil consumption has
include ataxia, blindness, salivation, spastic
cleclin.ecl. Other sources ofleacl include
twitching of eyelids, jaw champing,
paint, linoleum, grease, lead weights, lead
brnx.ism, muscle tremors, and convulsions.

shot, and contaminated foliage growing near

Subacute lead poisoning, usually seen in
smelters or along roadsides. To prevent
sheep or older cattle, is characterized by
future occurrences of lead poisoning, it is
anorexia, rumen stasis, colic, dullness, and
crncial to identify the source. Lead poisoning transient constipation, frequently followed is also encountered in urban environments
by diarrhea, blindness, head pressing,
and during the renovation of old houses
brux.ism, hyperesthesia, and incoordination.

that have been painted with lead-based

Chronic lead poisoning, occasionally
paint, learung to exposure of small anin1als
seen in cattle, may produce a syndrome that
and children. The consumption, through
has many features in conunon with acute or
grooming, of dust containing lead has been
subacute lead poisoning. lmpainnent of the
reported in cats. Improper disposal of
swallowing reflexes frequently contributes
lead-poisoned aninlal carcasses may result
to development of aspiration pneumonia.

in toxicoses in nontarget scavenger aninlals.

Embryotoxicity and poor semen quality

Scavenging by endangered species such as
may contribute to infertility.

the condor raises unique concerns.

GI abnmmalities, including anorexia,
colic, emesis, and cliaIThea or constipation

18.

Pathogenesis: Absorbed lead enters
are predon1inant manifestations in clogs.

the blood and soft tissues and eventually

Anxiety, hysterical barking, jaw champing,
ed
redistributes to the bone. The degree of
salivation, blindness, ataxia, muscle
absorption and retention is influenced by
spasms, opisthotonos, and convulsions may
ruetary factors such as calcium or iron
develop. CNS depression rather than CNS
levels. In run1inants, particulate lead lodged
excitation may be evident in some dogs. In
in the reticulum slowly dissolves and
horses, lead poisoning usually produces a
releases significant quantities of lead. Lead
chronic syndrome characterized by weight

LEAD POISONING

3079
loss, depression, weakness, colic, diruThea,

Treatment: lftissue drunage is extensive,
laryngeal or pharyngeal pru·alysis ( roaring),
pruticulru·ly to tile nervous system, treatment
and dysphagia that frequently results in
may not be successful. In livestock, calciwn
aspiration pneumonia
disodiw11 edetate (Ca-EDT.A) is given IV or

In birds, anorexia, ataxia, loss of

SC (110 mg/kg/day) divided bid for 3 days;

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condition, wing ru1d leg weakness, and
this treab11ent should be repeated 2 days
anemia are tile most notable signs.

later. In dogs, a similar dose divided qid is

Lesions: Animals tl1at die from acute lead
administered SC in 5% dextrose for 2-5 days.

poisoning may have few observable gross

After a 1-wk rest pe1iod, an additional 5-day
lesions. Oil or flakes of paint or battery may
treab11ent may be required if clinical signs
be evident in tl1e GI tract. The caustic action
persist. No approved vete1inary product
of lead salts causes gasb·oenteritis. In tile
containing Ca-EDT.A is cun-ently con1111ernervous system, edema, congestion of tile cially available.

cerebral c01tex, a11d flattening of tile c011ical

Thirunine (2-4 mg/kg/day, SC) alleviates
gyri ru·e present. Histologically, endotllelial
clinical ma.Ilifestations and reduces tissue
swelling, lruninar cortical necrosis, and
deposition of lead. Combined Ca-EDT.A and
edema of tile white matter may be evident.

thianline treabnent appears to produce the

Tubulru· necrosis and degeneration and
most beneficial response.

intrrurnclear acid-fast inclusion bodies may
o-Penicillamine can be administered PO
be seen in tile kidneys. Osteoporosis has been to dogs (110 mg/kg/clay) for 2 wk. However, described in lrunbs. Placentitis and accwnulaundesirable adverse effects such as emesis tion oflead in the fetus may result in abortion.

and a11orexia have been associated witll this
treatment. o-Penicillamine is not recom

Diagnosis: Lead concentrations in vruious
mended for livestock. Succimer (meso
tissues may be useful to evaluate excessive

2,3-dimercaptosuccinic acid [OMS.Al) is
accumulation and to reflect tile level or
a chelating agent tlrnt has proved to be
duration of exposW'e, severity, and prognosis effective in dogs (10 mg/kg, PO, tid for and tile success oftreabnent. Concentrations

10 days) and is also useful in birds. Fewer
of lead in tile blood at 0.35 ppm, liver at
adverse effects have been associated witll

10 ppm, or kidney cortex at 10 ppm are

OMS.A tllan witll Ca-EDTA.

consistent witll a diagnosis oflead poisoning

Catllrutics such as magnesiun1 sulfate
in most species. Many counbies have deemed ( 400 mg/kg, PO) or a mmenotomy may be blood lead concentrations >0.05-0.10 ppm
useful to remove lead from tile GI tract. In
to be a notifiable disease in food-producing
cattle, surge1-y to remove pruticulate lead
aninlals. lnspection or clearance by a
mate1ial from tile reticulw11 after tile
regulatory veterinary officer or biosecurity
ingestion of batteries is rarely successful.

inspector is mandatory before shipment for

Barbiturates or tranquilizers may be indicated
food consun1ption is pennitted.

to control convulsions. Chelation therapy, in

Hematologic abnormalities, which may
combination witll antioxidant treabnent, may
be indicative but not confirmatory of lead
limit oxidative drunage associated witll acute
poisoning, include ane1nia, rutlsocytosis,
lead poisoning. Antioxidants such as
poikilocytosis, polychromasia, basophilic

N-acetylcysteine (50 mg/kg/day, PO) have
stippling, metru-ubricytosis, and hypochrobeen used in combination witll DMSA.

mia. Blood or urinru-y 6-runinolevulinic acid

Mobilization of lead at parturition,
and free erytlu·ocyte protoporphY1in levels
excretion of lead into milk, and lengtlly
are sensitive indicators of lead exposure
withdrawal times in food-producing
but may not be reliable indicators of clinical
animals raise considerable controversy
disease. Radiologic examination may be
regarding the rationale for treatment
useful to determine tile magnitude oflead
from both public health and animal
exposure.

management perspectives. The half-

Lead poisoning may be confused with
life of lead in the blood of cattle ingestotller diseases tllat cause nervous or GI ing particulate lead is usually >9 wk.

abnormalities. In cattle, such diseases may

Withdrawal times, which may be > 1 yr,
include polioencephalomalacia, nervous
should be estimated by periodic
coccidiosis, tetanus, hypovitan1inosis A,
monitoring of blood lead concentrations.

hypomagnesemic tetru1y, nervous acetone

In a herd of cattle with confirmed cases
mia, organochl01ine insecticide poisoning,
of lead poisoning, all potentially exposed
arsenic or mercury poisoning, brain abscess
cattle should be evaluated. A small but
or neoplasia, rabies, listeriosis, and
significant portion of the asymptomatic

Haemophilus infections.

cattle may have concentrations of lead

In dogs, rabies, distemper, and hepatitis
in tissues that exceed recognized food
may appear similar to lead poisoning.

safety standards.

3080

MERCURY POISONING

MERCURY POISONING

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Historically, mercury poisoning was a
interstitial pneumonia. All fonns of mercmy
common occurrence in both htm1an and
cross the placenta. Inorganic forms of
aninlal populations. The replacement of
mercmy bind to sulfhyd1yl groups in
mercury products used for medicinal,
enzymes and other thiol-containing
agricultural, or industrial purposes has
molecules such as cysteine and glutathione.

resulted in a decline in acute and chronic

Tissues 1ich in these components, such as
poisoning, although many wildlife species
the renal cortex, accm1mlate significant
remain at risk. Predator species considered
concentrations of mercury. Inorganic
to be near the top of the food chain, such as
forms of mercury are cytotoxic and highly
fish, seals, polar bears, and various bird
corrosive. Consequently, these fom1s of
species, bioaccmnulate significant quantities mercury cause severe infla.inmation, ulcers, of mercury from dietary sources. Commerand direct tissue necrosis in the GI tract.

cial fish products such as tw1a have been

Pale, swollen kidneys marLifested histologiassociated with chronic poisoning in htm1an cally by tubular necrosis and interstitial
and animal (cats) populations. Mercury
nephiitis are consistent findings.

exists in a va.iiety of chemical fo1ms,
including elemental mercury ( eg, them1om

Clinical Findings· The inhalation of
eters, light bulbs), inorganic mercurial
corrosive elemental mercury vapors that

(mercuric or mercurous) salts ( eg, batteries,
produces severe dyspnea and compromised
latex paints), and organic mercury (a.iyl,
respiratory fm1ction is usually fatal at high
methyl, or ethyl). Fossil fuels represent a.ii
levels of exposure. Nem·ologic ma.ilifestaimportant environmental source of mercwy.

tions may eventually develop if exposure is

In the environment, inorganic fmms of
not excessive. Inorganic mercury, related to
mercmy are conve1ted to methylmercury
its corrosive nature, produces prima.i·i]y GI
m1der anaerobic conditions in the sediment
ma.i1i.festations, including colic, anorexia,
of most water bodies. Sin1ilar conversions
stomatitis, pharyngitis, vomiting, diarrhea,
may also occur in the body.

shock, dyspnea, and dehydration. Death
often occurs within hours at high levels of

Pathogenesis. The physical, chemical,
exposure. Animals that survive may exhibit
and kinetic prope1ties of the various fonns
eczema, skin keratini.zation, anuria,
of mercury play an i.mpo1ta.i1t role influencpolydypsia, hematuria, or melena.

ing the clinical marLifestations, the extent

Neurologic marLifestations, including CNS
and nature of lesions, and the tissue
depression or excitation sinular to that
distribution of mercury. The organic fom1s
which occurs in orga.i1ic mercmy poisoning,
of mercury, prima.i·i!y ruethylmercury, are
may develop after clu-onic exposm·e.

lipid soluble and well absorbed orally.

Depending on the level of exposure to

Consequently, bioaccmnulation is extensive
organic mercury compom1ds such as
in tissues such as the brain, kidney, and
methylmercury, clinical marLifestations may
fetus. Methylmercury interferes with
require days to develop. Because these
metabolic activity, resulting in degeneration
compollllds are not corrosive, GI signs are
and necrosis in ma.i1y tissues, although the
not seen. Neurologic marLifestations tl1at
brain and fetus are more susceptible. In the
predominate include blindness, ataxia,
brain, histologically, neuronal degeneration
incoordination, tremors, abnormal
a.i1d perivascuJa.i· cuffing is evident in the
behavior, hypem1etria, nystagmus (cats),
cerebrocortical grey matter. Cerebellar
and tonic-clonic convulsions. Advanced
atrophy or hypoplasia a.i1d Purkinje cell
stages may be cha.i·acterized by depression,
degeneration are seen. Encephalomalacia,
anorexia, proprioceptive defects, total
the loss of myelin, a.i1d necrosis of axons
blindness, paralysis, and high mortality.

may also be evident. Methylmercmy is

The nervous system of yollllg, developing
rnutagenic, carcinogenic, embryotoxic, and
animals is particula.i·Jy susceptible to
highly teratogenic. The inorganic forms of
organic mercury exposure, which is
mercury, including elemental mercury, are
frequently marLifested by cerebella.i· ataxia
poorly absorbed after de1mal exposure.

a.i1d death.

Elemental mercury vapors are inhaled and
rapidly absorbed. This highly toxic fonn of

Diagnosis: The considerable va.iiation
mercury produces corrosive bronchitis and
associated with tl1e clinical marLifestations

MOLYBDENUM POISONING

3081
related to the form of mercury and the
renal disease, or nemologic dysfunction
dmation of exposure accentuates the need
rnrulifested by tremors, ataxia, or convulfor multiple tissue analyses. Because sions. Metals such as lead, ru-senic, thallium,
inorganic forms of mercruy are excreted in
or cadn1iun1; insecticides, including
the mine, urina1y mercury concentrations
organophosphate, carbrunate, or organo

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are the most reliable indicator of exposure.

chlorine compounds; oxalates; vitrunin D;

In contrast, organic mercmy compounds,
or mycotoxins such as T-2 toxin should be
which bioaccumulate in soft tissues, are
considered. Infectious diseases, including
most approp1iately assessed in the liver,
hog cholera, erysipelas, and feline parvovikidney, or brain tissues. In most species, ms, may resemble mercury poisoning.

blood, kidney, brain, and feed concentrations of mercury <0.1 mg,'kg ( wet weight) Treatment and Control: Because the
are considered nom1al. In poisoned species,
neurologic and renal damage is iITeversible,
concentrations >6 mg,'kg (blood), 10 mg,'kg
treatment alternatives may be ineffective.

(kidney), 0.5 mg,'kg (brain), and 4 mg,'kg

Consequently, the prognosis for a complete

(feed, dry weight) are consistent with a
recovery is ve1y poor. In food-producing
diagnosis of mercury poisoning. Generally,
ru1imals, significant rnercmy accm11ulation
the kidney is considered to be the most
in edible tissues and profound effects on
useful tissue diagnostically. Concentrations
reproduction limit treatment options.

in all tissues may be substantially higher

Euthanasia and disposal, in consultation
after chronic exposme. Marine man1mals
with regulatory officials, is recommended.

and fish often contain substantially

Oral administration of activated chru'coal
increased concentrations of mercury that

( 1-3 g,'kg) and sodium thiosulfate (0.5-1 g,'kg)

may not be associated with clinical disease
will bind mercruy ru1d limit absorption.

(as such concentrations would be associ

Vitan1in E and selenium, which are
ated in traditional livestock or companion
antioxidants, may limit oxidative danmge.

animal species), but they may be a potential

Chelation therapy may be useful if treatsource of exposure for more susceptible ment is struted soon after exposure before
species, pruticularly the fetus or younger
nephrotoxic effects become severe. The
animals. Other measurements, including the
lipid-soluble chelator dimercaprol (3 mg,'kg
presence of proteinruia, azoternia, or a
body wt, IM, every 4 hr for 2 days, followed
nonregenerative anemia, may provide useful by qid treatment on day 3 and bid treatment evidence to support a diagnosis of mercmy
for 10 days) may be beneficial. For organic
poisoning. The diagnosis may be made on
mercury poisoning, 2.3-dimercaptosuccinic
the basis of tissue analysis in association
acid (10 mg,'kg, PO, tid for 10 days) has
with appropriate histopathology, clinical
been useful in dogs. If the GI tract has been
pathology, clinical mariifestations, and
decontanlinated for mercury, adntinistration
history. Differential diagnoses may include
of penicillrunine (50-100 mg,'kglday, PO, for
conditions that produce GI disturbances,

2 wk) may reduce clinical signs.

MOLYBDENUM POISONING

Molybdenum is an essential element
metabolism related to the utilization,
associated with a vru'iety of metalloenzymes bioavailability, and kinetics of copper are ru1d corresponding metabolic functions.

runong the most biologically significant

Excessive dietary intake of molybdenum
interrelationships in vete1inruy medicine.

induces a secondary copper deficiency.

The complexity of the interactions is not

The syndrome, predominately reported in
fully understood. In ruminru1ts, vruious
rurninru1ts (ve1-sus nonrun1inru1t species)

molybdates react with sulfides to produce
is seen worldwide. Cattle ru1d sheep are
thiomolybdate compounds, which react

-10-fold more susceptible thru1 other
with copper to form ill1 insoluble complex
species. Acute toxicity associated with
that is poorly absorbed. The reduced copper
massive doses is rarely encom1tered.

absorption in1pairs copper utilization ru1d
the synthesis of a variety of copper-depend

Etiology: The interactions associated
ent proteins. The reduced bioavailability of
with copper, molybdenum, ru1d sulfate
copper ultimately induces secondary

3082

MOLYBDENUM POISONING
copper deficiency. Excessive molybdenum
evident in black anin1als associated with
intake also enhances the excretion of
impaired tyrosinase activity and reduced
copper. Based on this observation, the
melanin synthesis. Pica, unthriftiness,
administration of tetrath.iomolybdates may
microcytic hypochromic anemia, emaciabe a useful treatment for chronic copper tion, joint pain characterized by lan1eness,

VetBooks.ir
poisoning (seep 3073). The limited bacterial and osteoporosis often manifested by bone fonnation of thiomolybdates in monogastric fractures ar·e seen. Molybdenw11 competes animals is primarily responsible for the
with phosphorus utilization, resulting in
tolerance to molybdenum encountered in
reduced mineralization of bone. In heifers,
these species. Excessive molybdenwn
fertility is reduced. Delayed puberty, poor
exposure may also impair a variety of
conception rates, decreased weight at
enzymes involved in collagen and elastin
puberty, and decreased milk production are
maintenance and stability, which has been
common. Reduced libido has been reported
associated with cardiovascular disorders.

in bulls. In sheep, particularly in lan1bs <30

Molybdenum exposure may reduce
days old, the animals exhibit stiffness of the
phospholipid synthesis in nervous tissue,
back and legs and have difficulty rising. The
resulting in demyelination and neurologic
syndrome in sheep is known as enzootic
disorders clinically.

ataxia, or swayback. Abnormal develop

The susceptibility to molybdenum toxicity
ment of cormective tissue and growth plates
in runlinants depends on a nun1ber of factors, are apparent in affected animals. Manifestaincluding 1) ruetary copper content-susceptions appear within 1 -2 wk if molybdemm1
tibility increases as the copper content
levels are excessive.

decreases; 2) dietary sulfate content-sus

Occasionally, acute toxicity may be
ceptibility increases with high sulfate levels
encoW1tered in cattle or sheep. Anorexia
by impairing copper utilization, whereas low
and lethargy may be evident within 3 days.

sulfate content enhances susceptibility by

Deaths begin within 1 wk and may continue
reducing molybdenwn excretion; 3) the
for many months. Neonates frequently
chemical fom1 of molybdenun1-waterexhibit llind.lirnb ataxia that often prosoluble fonns foWld in fresh feed are more gresses to the forelimbs. Salivation and
toxic; 4) sulfur-containing 3Jllino acids may
scant mucoid feces are common.

alter copper utilization or molybdenum

At necropsy, hemosiderosis, periacinar to
excretion; 5) anin1al species-cattle are more
severe hepatic necrosis, ar1d nephrosis are
susceptible; 6) age-young animals are more
evident. In affected sheep, neuronal
susceptible, and excretion of molybdenw11
degeneration, demyelination, and lysis of
into milk may produce toxicoses in nursing
white matter are seen in nervous tissue.

calves; 7) season of year-molybdenwn
concentrations in plants increase in the fall;

Diagnosis: Distinguishing between

8) plant species-legumes bioaccumulate
primar'Y copper deficiency and seconda!'}'

more molybdenun1; and 9) breed differcopper deficiency related to excessive ences-seen in sheep and goats.

molybdenwn exposure is important. Often

Molybdenw11 toxicity has been encounwith molybdenum toxicity. there is a poor tered in regions of the world containing
correlation between tissue concentrations
peat, muck, or shale soil types that are
of copper and clinical clisease. Clinical
naturally contaminated with molybdenW11.

improvement after copper sulfate adminis

Industrial contamination associated with
tration provides valuable support for the
mining or metal production or areas using
diagnosis. Analysis of the ration for copper
molybdenwn-contarninated fertilizers result and molybdenwn concentrations is in enhanced uptake of molybdenum by
recommended. In cattle rations, a
plants used as a feed source.

copper:molybdenwn ratio of6:l is optimal.

If the ratio is less than 2: 1, molybdenum

Clinical Findings: The manifestations of
toxicity will occur. Ratios exceeding 15:l
molybdenum toxicity are related primarily
may cause chronic copper poisoning.

to impaired copper metabolism and

Absolute molybdenw11 concentrations in
utilization, resulting in secondar'Y copper
the diet > 10 mg/kg will cause poisoning
deficiency. 'Iypically, the syndrome is a herd
independent of copper consumption.

problem, with morbidity as high as 8CJOA,.

Massive molybdenwn exposure in the

In cattle, clinical disease is char·acterized
ration >2,000 mg/kg will result in death.

by severe, persistent diarrhea with the

Analysis of the liver and plasma for
presence of green, liquid feces containing
molybdenum provides useful insight to
gas bubbles, often referred to as peat or
confirm the diagnosis, but the concentrateart scours. Depigmentation, resulting in tions must be interpreted in association
fading achromotrichia of the hair coat, is
with the comparable tissue concentrations

SALTTOXICITY

3083
of copper. In cattle, liver concentrations >2
molybdenwn is rapidly eliminated and food
ppm ( wet weight) and plasma concentraproducts are safe for consumption within a tions >0.1 ppm are consistent with a
relatively sho1t time. If the dietary exposure
diagnosis of molybdenwn poisoning in the
carmot be reduced, elimination of molybdepresence of a low copper status. Other nwn in the milk may produce toxicosis in

VetBooks.ir
disease syndromes characterized by
nursing calves. Dietary supplementation
emaciation or unthriftiness (parasite
with copper sulfate will reduce the
infections, selenosis, fluorosis, ergotism),
bioavailability of molybdenwn in the GI
diarrhea (metal poisonings, GI infections),
tract, ultimately reducing absorption and
and lameness or bone abn01malities
enhan ing excretion. ln feed containing

(fluorosis, selenosis, ergotism, lead
molybdenwn at >5 mg/kg, supplementation
poisoning) may resemble molybdenwn
with 1 % copper sulfate in salt will control
poisoning and should be investigated as
development of the syndrome. In recovered
possible etiologies.

mining areas, the supplementation may
need to be increased to as much as 5%

Treatment and Prevention: Most
copper sulfate in the salt. When the
treatment options are associated with the
conswnption of mineral supplements is
biological interactions associated with
impractical, the treatment may be
copper, molybdenwn, and sulfate. Under
administered as a weekly drench. Ir\jectable
circwnstances in which dietary exposure is
products such as copper glycinate or copper
difficult to eliminate, simple treatment with
edetate (Cu-EDTA) may be given at a dose
copper products may be futile. If the source
of 120 mg/cow. These products are
of molybdenun1 can be removed, excess
approved only in some jurisdictions.

SALT TOXICITY

Excessive salt (sodiun1 chloride, NaCl)

significantly or abolished completely by
intake can lead to the condition known as salt appropriate management of factors such as poisoning, salt toxicity, hypematremia, or
mechanical failure of waterers, overcrowdwater deprivation-sodiwn ion intoxication.

ing, unpalatable medicated water, new

The last term is the most descriptive, giving
surroundings, or frozen water sourees. Both
the result (sodiwn ion intoxication) as well
swine and poultry on normal diets can be
as the most common predisposing factor
severely affected when water intake is

( water deprivation.) Salt poisoning is unlikely completely restricted or when conswning to occur as long as sodiwn-regulating
high-salt diets with moderate water
mechanisms are intact and fresh drinking
restiiction. Increased water requirements
water is available.

increase the susceptibility of lactating cows

Salt poisoning has been repo1ted in
and sows to salt poisoning, especially in
virtually all species of animals all over
response to sudden restrictions in water.

the world. Although salt poisoning has

High concentrations of salt in the diet ( up
historically been more common in swine
to 13%) have been used to limit feed intake

(the most sensitive species), cattle, and
of cattle. Salt-deprived animals or those not
poultry, there are increasing reports of
acclimated to high-salt diets can overconadverse effects in dogs from acute excess swne these feeds, making the animals prone
salt conswnption. The acute oral lethal
to salt poisoning. Improperly formulated or
dose of salt in swine, horses, and cattle is
mixed feed can be sources of excess salt.

-2.2 g/kg; in dogs, it is -4 g/kg. Sheep appear

The use of whey as a feed or as a component
to be the most resistant species, with an
of wet mash can add to sodiwn intake.

acute oral lethal dose of 6 g/kg.

Additional sources of excess sodiwn can
include high-saline ground water, brine, or

Etiology: ln general, animals can tolerate
seawater.

high concentrations of salt or sodium in the

Chickens can tolerate up to 0.25% salt in
diet if they have continuous access to fresh
drinking water but are susceptible to salt
water. Salt poisoning is often directly related poisoning when water intake is restricted.

to water consumption and can be reduced

Wet mash containing 2% salt has caused salt

3084

SALT TOXICITY
poisoning in ducklings. High salt content in
inflammation of the meninges. During the
wet mash is more likely to cause poisoning
first 48 hr, swine develop eosinopenia,
than in dry feed, probably because birds eat
eosinophilic cuffs around vessels in the
more wet mash.

cerebral c01tex and adjacent meninges, and

Sheep can tolerate 1% salt in clrinl<lng
cerebral edema or necrosis. After 3-4 days,

VetBooks.ir
water; however, 1.5% may be toxic. It is
eosinophilic cuffs are usually no longer
generally recommended that drinking water present. Cattle do not develop eosinophilic contain <0.5% total salt for all species of
cuffs but can have edema of the skeletal
livestock.

muscles as well as hydropericardiLUn.

Companion animal expos mes to excess

Chickens can also have hydroperica.rdiLUn.

salt have included the use of salt as an

In a.cute cases, no gross lesions may be
emetic (no longer reconm1endecl) and
present in any species.

the ingestion of various salt-containing
materials including rock salt and dough-salt

Diagnosis: Serum and CSF concentramixtures. Dogs have been reported to tions of sodilll11 > 160 mEq/L, especially
develop hypematremia after swin1ming/
when CSF has a greater sodiLU11 concentraplaying in the ocean (which contains 3.5%
tion than senun, indicate salt poisoning.

soditm1) without having access to fresh

Brain sodiun1 concentrations >2,000 ppm
water. Horses appear to be rarely affected

( wet weight) are considered diagnostic in
with classic salt poisoning but can develop
cattle and swine. There is a lack of data on
it under conditions of increased salt intake
normal brain sodiLUn concentrations in
and sudden water restriction.

other common domestic species, making
interpretations of brain sodiLUn concentra

Clinical Findings: In pigs, early signs
tions difficult. Characteristic history and

(rarely seen) may be increased thirst,
clinical signs, along with clinical pathology,
pruritus, and constipation. Affected pigs
postmo1tem findings, and analyses of feed
may be blind, deaf, and oblivious to their
or water for socliLUn content are essential
sw-roundings; they will not eat, drink, or
for establishing a diagnosis.

respond to external stimuli. They may

In swine, differential diagnoses include
wander aimlessly, bLU11p into objects, circle,
insecticide poisoning ( organochlorine,
or pivot around a single limb. After 1-5 clays
organophosphorus, and carbamate),
of limited water intake, intermittent seizures phenyla.rsonic poisoning, and pseudorabies.

occw-with the pig sitting on its haunches,

In cattle, differential diagnoses include
jerl<lng its head backward and upward, and
insecticide and lead poisoning, polioenfinally falling on its side in clonic-tonic cephalomala.cia., hypomagnesemic tetany,
seizures and opisthotonos. Terminally, pigs
and the nervous fonn of ketosis.

may lie on their sides, paddling in a coma,
and die within a few to 48 tu·.

In cattle, signs of acute salt poisoning

Treatment: There is no specific treatment
involve the GI tract and CNS. Salivation,
for salt poisoning. Inunedia.te removal of
increased thirst, vomiting (regurgitation),
offending feed or water is imperative. Fresh
abdominal pain, and diarrhea are followed
water must be provided to all animals,
by ataxia, circling, blindness, seizures, and
initially in small amounts at frequent intervals
partial paralysis. Cattle sometimes manifest
to a.void exacerbation of clinical signs. On a
belligerent and aggressive behavior. A
herd basis with large animals, water intake
sequela of salt poisoning in cattle is dragging should be linlited to 0.5% of body w�ight at of hindfeet while walking or, in more severe
hourly intervals until normal hydration is
cases, knuckling of the fetlockjoint.

accomplished, usually taking several days.

In poultry and other birds, clinical signs

Severely affected animals can be given water
include increased thirst, dyspnea, fluid
via stomach tube. The rno1tality rate may be
discharge from the beak, weakness, diarrhea,

>500Ai in affected animals regardless of
and leg paralysis.

treatment. In small animals before the onset

Excess salt intake in dogs results in
of clinical signs, the a.cute ingestion of salt
vomiting within several hours of ingestion.

can best be treated by allowing the animal

The clinical signs can progress to weakness,
access to water and closely obseiving it for
diarrhea., muscle tremors, and seizures.

several hours. Emetics may be used in dogs if
known ingestions occur and the dog is not

Lesions: Postmortem examination may
yet showing clinical signs.

reveal some degree of gastric ir1ita.tion,

For all affected animals, the treatment
including ulceration and hemorrhages. The
should slowly retLUn the anin1al to normal
content of the GI tract may be a.bnonnally
water and electrolyte balance over 2-3 days.

dry. Histopa.thologic lesions may be limited

Quickly lowe1ing the serum sodilll11
to the brain and include cerebral edema and
concentration will increase tl1e osmotic

SELENIUM TOXICOSIS

3085
gradient between the senun and the brain,

IV fluids can be made to approximate the
with water following the gradient into the
senun sodiwn concentration of the animal, or
brain and increasing the likelihood of severe a solution containing sodiwn at 170 mEq/L
cerebral edema.

can be used initially, with the concentration

Monitoring semm sodium concentration
decreased as clinical signs in1prove. 1n dogs,
is the first step in treating individual animals. a series of warm water enemas given at VetBooks.ir

Serum sodium levels should be lowered at a
intervals of several hours has helped reduce
rate of 0.5---1 mEqll)hr. The use of slightly
acutely increased sodiwn levels. 1f brain
hypertonic IV fluids has been recommended
edema is suspected, mannitol, dexamethato reduce the likelihood of cerebral edema.

sone, or DMSO may.be helpful.

SELENIUM TOXICOSIS

Selenium is an essential element that has a
are replaced with selenomethionine and
narrow margin of safety, witl1 tl1e difference
selenocysteine, respectively. Replacement
between adequate and potentially toxic
of these amino acids with seleniw11-containconcentrations in tile diet being awroxiing amino acids also affects cell division and mately 10- to 20-fold. Feed supplements,
growth. Especially susceptible are the cells
resulting in final seleniwn content of 0.2-0.3
that form keratin (keratinocytes) and the
ppm, are added to diets to prevent deficiency sulfttr-containing keratin molecule.

and resultant diseases such as white muscle

Selenium tllerefore weakens tl1e hooves and
disease in cattle and sheep, exe1tional
hair, which tend to fracture when subjected
myopathy in horses, hepatosis dietetica in
to mechanical stress.

pigs, and exudative diathesis in chickens.

The maximwn tolerable concentrations for

Etiology: All animal species are
seleniwn in most livestock feed is considsusceptible to scleniwn toxicosis. However, ered to be 2-5 ppm, altl10ugh some believe
poisoning is more common in forage-eating

4-5 ppm can inhibit growth.

animals such as cattle, sheep, horses, and

Seleniwn is an essential component of
other herbivores that may graze seleniwn

>25 selenoenzymes and selenoproteins. The
containing plants. Plants may accumulate
most recognized of these are tl1e glutathione seleniwn when the element is follild at high peroxidase enzymes that act as antioxidants
concentrations in the soil, but pH and
in the body. 1n excess, seleniwn potentially
moisture content of tile soil play roles in the
has three general toxic effects: the direct
relative bioavailability of seleniwn to plants.

inhibition of cellular oxidation/reduction

Generally, selenium is most bioavailable to
reactions by depleting glutathione and
plants when tlley grow on more alkaline

S-adenosylrnethionine reserves, the
soils with low rainfall ( <50 cm). The
production of free radicals that cause
alkalinity and low moistllfe content of tl1e
oxidative tissue damage, and tl1e replacesoil tend to allow more of tl1e seleniW11 to be ment of sulfur/sulfur-containing amino
retained as the oxidized fom1 of selenate,
acids in tl1e body with seleniurn/selenowhich is tile most readily available for plant arnino acids. The inhibition of nwnerous
uptake. Because low moistw·e in the soil
cellular ftmctions by high concentrations
decreases the anaerobic environments to
of seleniwn results in acute generalized
greater depths, drought conditions could
cytotoxicity. The replacement of sulfurallow for more/deeper seleniW11 in tile soil containing anlino acids witll seleno-amino
to be oxidized into plant-available forms,
acids leads to altered stmctw·e and ftmction
resulting in year-to-year variability in
of cellular components and enzymes due to
available seleniW11 for plant uptake.

loss of the disulfide bonds that commonly

Seleniwn-accwnulating plants have been
occur between sulfur-containing anlino
categorized based on tlleir relative
acids. Loss of these disulfide bonds can alter
requirements and ability to accwnulate
the three-dimensional configuration of
seleniW11. Obligate indicator plants require
proteins, potentially resulting in loss of or
large a.rnoW1ts of seleniW11 for growth and
diminished enzyme activity. The most
contain high seleniwn concentrations ( often
co nun only altered sulftu�containing amino

>1,000 to 10,000 ppm). Obligate indicators
acids are methionine and cysteine, which
include species ofAstragalus, Stanle-ya,

3086

SELENIUM TOXICOSIS

Machaeranthera, Oonopsis, andXylorhiza.

available for uptake by plants and would

Facultative indicator plants absorb and
not result in high exposure potential.

tolerate higher concentrations of soil

Tissue seleniwn content is the basis for
selenimn, with accumulations ranging from
diagnosing seleniwn poisoning in aninlals.

trace amounts to a few thousand ppm, but

Organic chemical fonns of seleniw11 have

VetBooks.ir
they do not require seleniw11 for growth.

greater bioavailability and are retained in the

Facultative indicators include species of
tissues for much longer pe1iods. Thus, timing

Aster, Castillfc!ja, Grindel:ia, A triplex,
of the exposure in relation to the collection

Gatierreaia, and Comandra. Nonaccwnulaof tissue, blood, or serum, as well as the tor plants, such as most grasses, passively
chemical fom1 of the seleniwn exposure,
absorb much lower amounts of seleniwn
must be taken into account when interpretfrom the soil, resulting in trace an1ounts to ing the seleniwn content. In addition, some
a few hundred ppm.

species vaiiability in regard to concentra

Nwnerous organic and inorganic
tions also occurs. In acute tox:icosis, the
chemical forms of selenium are potentially
blood and serum selenim11 concentrations
present in plants. Nonaccumulator plants
are generally >3-4 ppm, and in chronic
primarily contain selenomethionine, while
tox:icosis, it is generally > 1-2 ppm. Liver
indicator plants contain more selenate and
generally contains >3-5 ppm seleniwn in
methylselenocysteine. In comparison, most
acute cases, whereas in chronic cases it
supplemental dietary sources are in the
should be > 1.5 ppm. Kidney of seleniwnform of selenite, but selenomethionine poisoned animals generally contains > 1-5
supplements are becoming more commonly
ppm. Hair and hoof wall may have > 1.5-5
used in marketed products.

ppm seleniw11 in chronic poisoning. A

Poisoning may also occur in swine,

"garlicky" odor on the animal's breath may poultry, and other species consuming
be noted; this finding is more prominent with
grain raised on seleniferous soils or, more
acute poisoning but can be seen with clu·onic
commonly, due to errors in feed formulapoisoning as well. The odor is due to tion. Selenium toxicosis after ingestion
elimination pathways producing methylated
of selenium-containing shampoos or
seleniun1 metabolites that are volatile and
selenium supplement tablets is rare in
expired but may last for only 1-2 days after
small animal pets but can occur. Several
an acute poisoning incident.

factors are known to alter selenium
toxicity; however, in general, a single

CHRONIC SELENIUM TOXICOSIS
acute oral dose of selenium in the range of

1-10 mg/kg may be lethal in most animals.

(Alkali disease)

Parenteral selenium products are also

Chronic seleniwn poisoning usually
quite toxic, especially to young anin1als,
develops when livestock consmne
and have caused cteaths in piglets, calves,
seleniferous forages and grains containing
lambs, and dogs at dosages as low as 1

5-50 ppm of seleniw11 for many weeks or
mg/kg. Younger animals tend to be more
months, although chronic exposure to high
susceptible to selenium poi:;oning, and
concentrations of inorganic seleniwn can
the chemical forms can l'esult in some
also produce chronic selenosis. Naturally
differences in relative toxicity.

occurring seleno-amino acids in plants are
readily absorbed and inse1ted into proteins

Diagnosis: Severity of clinical signs of
in place of their corresponding sulfur-conseleniwn tox:icosis depends on the quantity taining amino acids (ie, selenomethionine in
and duration of exposure. Poisoning in
place of methionine or selenocysteine in
anin1als is characterized as acute, subchronic, place of cysteine ). Until recently, two types or chronic. Diagnosis is based on clinical
of chronic seleni Lllll poisoning were
signs, necropsy findings, and laboratmy
discussed in the literature: alkali disease
confirmation of the presence of high seleniwn and blind staggers. Blind staggers is no content in an aninlal's diet (feed, forage,
longer believed to be caused by seleniwn
grains, or water), serum, blood, or tissues ( eg,
but by sulfate toxicity due to conswnption
kidney, liver). Selenium in the diet at >5 ppm
of high-sulfate alkali water and/or high
may produce mild clinical effects after
sulfur-containing forages. Excess sulfate
prolonged exposure of �30 days. Concentra

(> 1% of diet) leads to polioencephalomalations of 10-25 ppm would be expected to cia and the classical signs of blind staggers.

produce severe clinical signs with prolonged

Animals consun1ing milk vetch (Astragalus
exposure. Environmental exposure potential
bisulcatus) have demonstrated clinical
should be based on forage, feed, or water
signs similar to those of blind staggers.

content, not on soil seleniwn content,

Although milk vetch contains high levels of
because some chemical forms in soil are not
seleniun1, evidence now indicates that the

SELENIUM TOXICOSIS

3087
alkaloid swainsonine in milk vetch is
reproductive perfmmance associated with
responsible for locoism and produces the
seleniwn poisoning can be decreased by
neurologic clinical signs.

copper supplementation. Addition of
arsenic salt at 0.00375% to enhance biliary

Clinical Findings: Alkali disease has
excretion of seleniw11 or a high-protein diet

VetBooks.ir
been reported in cattle, sheep, and horses.

to bind free seleniwn has historically been

Affected animals are inactive, weak,
used to reduce incidence of seleniwn
anorexic, lame, emaciated, anemic, and lack poisoning in cattle. However, this has vitality. In addition, the most distinctive
minin1al to poor overall efficacy. Chronilesions are those produced by damage of cally seleniun1-poisoned animals are less
the keratin of the hair and hooves. For
likely to thrive than herdmates, even after
horses, the predominant clinical manifestaexposure has been stopped.

tion is lameness due to founder. The animal

Forages should be tested regularly in
has a rough hair coat, and the long hairs of
high-seleniun1 areas to evaluate year-tothe mane and tail brPak off, giving a "bob"

year risk
tail and "roached" mane appearance.

Abnormal growth and structure of horns
and hooves result in circular ridges and

SUBCHRONIC SELENIUM
cracking of the hoof wall at the coronary

TOXICOSIS
band. Extremely long, deforn1ed hooves
that turn upward at the ends also may be

Pigs fed a diet supplemented witl1 seleniw11
seen. Subsequent lameness is compounded

>20-50 ppm for >3 days develop a
by degeneration of joint cartilage and
subchronic selenium toxicosis characterbone. Reduced fertility and reproductive ized by neurologic abnormalities. Animals
perforn1ance occurs, especially in sheep
are initially ataxic and uncoordinated,
and cattle. Reproductive pe1fonnance may
followed by anterior paresis, then
be impaired with a dietary seleniwn content
quadriplegia. Even though new·ologic
lower than that required to produce tl1e
in1pairn1ent is occurring, the pigs continue
other typical signs of alkali disease. Other
to eat, which would indicate nemologic
lesions may include liver cirrhosis, ascites,
damage that is not centrally mediated. The
and myocardial necrosis/scarring.

hooves show breaks and impaired growth

Birds also may be affected with chronic
similar to those seen in cattle. Alopecia
seleniwn toxicosis. Eggs with >2.5 ppm
may also be seen. In sows, conception rate
seleniwn from birds in high seleniun1 areas
decreases and the nwnber of stillborn pigs
have low hatchability and embryos tliat are
increases. Lesions of subchronic toxicosis
usually deformed. Teratologic effects include include focal synrn1etric poliomyelomalaunderdeveloped feet and legs, malfonned cia, which is most prominent in the cervical
eyes, crooked beaks, and ropy feathers.

and thoracic spinal cord. Death may result

This has been a problem witl1 waterfowl in
from complications of permanent paralysis.

southern California, where selenium was

Hoof and hair dan1age is similar to but in
concentrated in lakes by runoff.

most cases less severe than that seen in

1n seleniwn-poisoned animals, so.me
chronic seleniwn toxicosis. Treatment is
alterations in blood chemistries occur. These similar to that for chronic toxicosis, but changes include decreased prothrombin
spinal lesions are usually pernianent.

activity, fibrinogen, and glutathione, as well
as increased serum alkaline phosphatase,

ACUTE SELENIUM TOXICOSIS

ALT, AST, and succinic dehydrogenase.

Acute oral selenium poisoning due to

Treatment and Control: There is no
consumption of plants or mis-mixed diets
specific treatment for seleniwn toxicosis.

with concentrations >50 ppm ( dosages

Eliminating the source and exposure, as

1-10 mg/kg or greater, depending on the
well as symptomatic and supportive care
species, age, and chemical fonn of selenium)

of the animal, should be started as soon
is not common but has caused large losses in
as possible. Addition of substances that
cattle, sheep, and pigs. Anin1als usually avoid
antagonize or inhibit the toxic effects of
plants with high seleniW11 content because
seleniwn in the diet may help reduce the
of their offensive odor; however, when
risk of seleniun1 toxicosis. A high-protein
pastme is limited, accwnulator plants may
diet, linseed oil meal, sulfur, arsenic, silver,
be tl1e only food available. In some cases,
copper, cadmiun1, and mercwy have
plants may not have the profound offensivP
reduced seleniun1 toxicity in laboratory
odor. Young animals are most susceptible to
animals, but their use under field conditions
acute parenteral seleniw11 toxicosis with
is limited. However, some of the poor
dosages of 0.2-0.5 mg/kg. Clinical signs are

3088

SELENIUM TOXICOSIS
different from those of chronic selenosis and
consumption or i.rtjection of selenium.

are characterized by abnormal behavior,

The major lesions are pulmonary edema,
respiratory difficulty, GI upset, and sudden
pulmonary congestion, pulmonary
death. Abnom1al posture and depression,
hemorrhage, hepatic necrosis, myocardial
anorexia, unsteady gait, diarrhea, colic,
necrosis, myocardial hemorrhage, and

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increased pulse and respiration rates, frothy
potentially renal necrosis.

nasal discharge, moist rales, and cyanosis

Blood or serum selenium concentration
may be noted. Sheep usually show these
in acute poisoning is often higher than in
signs to a much lesser degree or just become
chronic poisoning. Treatment consists of
depressed and die suddenly.

symptomatic and supportive care.

Most deaths usually follow within a few

Acetylcysteine to boost systemic glutahours to 2 days after an acutely toxic thione concentrations may be beneficial.

ZINC TOXICOSIS

Zinc is an essential trace metal that plays

Clinical Findings and Lesions: Clinical
an in1portant role in many of the body's
signs vary based on the duration and degree
enzymatic processes. It is ubiquitous in
of exposure. Signs progress from anorexia,
nature and exists in many fonns. The
vomiting, diarrhea, and lethargy to more
ingestion of some fonns of zinc causes the
advanced signs such as intravascular
creation of toxic zinc salts in the acidic
hemolysis, icterus, hemoglobinuria, cardiac
environment of the stomach. Zinc toxicity
arrhythmias, and seizures. Large anin1als
has been documented in people as well as
often show decreases in weight gain and milk
in a wide range of la.rge, small, exotic, and
production, and lameness has been reported
wild anin1als. Exposure typically sterns from
in foals secondary to epiphyseal swelling.

dietary indiscretion. Household sources

Major histopathologic frndings include
of zinc include paint, batteries, automotive
hepatocellula.r centrilobular necrosis with
parts, zinc oxide creams, vitamin and mineral
hemosiderosis and va.cuola.r degeneration,
supplements, zipper pulls, board-gan1e
renal tubular necrosis with hemoglobin
pieces, pet carrier screws and nuts, and
casts, and pancreatic duct necrosis with
the coating on certain types of pipes and
fibrosis of the interlobular fat.

cookware. One of the rnostwell-lmown
sources of zinc that causes toxicity after

Diagnosis: Radiodense foreign bodies are
ingestion is the USA Lincoln penny. Some
easily seen on ra.diographs of the GI tract
pennies minted dUiing 1983, and all pennies
and should raise suspicion of potential zinc
minted since, are 97.5% zinc by w�ight
toxicosis in animals with correlating clinical

(-2,440 mg of elemental zinc per coin).

signs. Changes in the CBC, chemistry profile,
urinalysis, and coagulation profile reflect the

Pathogenesis: The low pH in the
degree of toxicity to various organ systems.

stomach causes the release of free zinc,

The hemograrn can reveal anemia characterwhich then fonns soluble, caustic zinc ized by changes in erythrocyte morphology
salts. These salts are absorbed from the
such as spherocytosis and Heinz body
duodenum and rapidly distributed to the
formation. (It has been suggested that
liver, kidneys, prostate, muscles, bones,
zinc's interference with enzymes such as
and pancreas. Zinc salts have direct irritant
glutathione reductase leads to erytlu·ocyte
and corrosive effects on tissue, interfere
fragility due to oxidative damage.) The
with the metabolism of other ions such
leukogran1 often shows a mature neutroas copper, calcium, and iron, and inl1ibit philic leukocytosis secondary to stress,
erythrocyte production and function. The
pancreatitis, and a regenerative response by
mechanisms by which zinc exe1ts these
the bone marrow. Serum chemistry changes
toxic effects are not completely tmderstood.

that a.re seen secondary to hepatic da.n1age

The LD50 of zinc salts in cases of acute
include increases in bilirubin, the transamitoxicity has been reported to be -100 mg/kg.

nases, and alkaline phosphatase.

Also, diets containing high levels of zinc

As zinc a.ccun1ulates in the pancreas,

(>2,000 ppm) have been rep01ted to cause
increases in amylase and lipase can be seen
chronic zinc toxicosis in large anin1als.

following pancreatitis and pancreatic

BRACKEN FERN POISONING

3089
necrosis. Glomerular damage and renal
tried within the first hour or two of
tubular epithelial necrosis result in
exposure but may not be rewarding in
increases in BUN, creatinine, amylase,
advanced cases because zinc objects can
and urine protein. Hemoglobinwia can
adhere to the gastric mucosa.

be differentiated from hematwia during

Proton pwnp inhibitors and Hrblockers
urinalysis; the wine color will not clear after can be used to decrease the formation of zinc VetBooks.ir
centrifugation in the presence of hemoglosalts in the stomach before removal of the binuria. Prolongation of prothrombin time
source of zinc, and gastroprotectant therapy
and activated partial thromboplastin time
with sucra.lfate can later be considered to
can also result from toxic effects on the
help address gastric ulceration.

synthesis or function of coagulation factors

Diuresis with a balanced crysta.lloid
and the loss of clotting proteins through the
solution is indicated to promote renal
glomerulus of the kidneys.

excretion of zinc and prevent hemoglobinu

The hematologic and clinical findings
ric nephrosis.

in anin1als with zinc toxicosis are sin1ila.r

There is debate rega.i·ding the necessity of
to the changes in a.tlinlals with in1munechelation therapy in cases of zinc toxicosis.

mediated hemolytic anemia (IMHA). Zinc

Animals often recover from zinc intoxication
toxicosis can ca.use the direct antiglobulin
after only supportive ca.i·e and removal of the
test ( direct Coombs' test) to be positive
source. Chelation therapy can enhance elimiin the absence of a primary autoimmune nation of zinc and thus accelerate recovery,
disorder, so the direct Coombs' test is not
but there is some concern that chelation
a reliable method to differentiate zinc
treatment may actua.lly increase zinc
intoxication from IMHA.

absorption from the intestines. Chelation

Zinc levels can be measured in blood to
can be achieved through the use of specific
confirm toxicosis, although this is usually
compounds. Ca-EDTA chelates zinc when
wmecessary to diagnose zinc poisoning in
given at 100 mg/kg/day, IV or SC, for 3 days
the clinical setting. In dogs and cats, the

( diluted and divided into fom doses) but may
normal serum zinc level is 0 .7-2 mcg/mL.

exacerbate zinc-induced nephrotoxicity.

Reference laboratories usua.lly request

Although they have been used to treat
that samples be submitted in green-top
animals with zinc toxicity, o-penicillamine
heparinized tubes, royal blue-top trace
a.t1d dimercaprol (British anti-lewisite) have
element tubes, or purple-top EDTA tubes.

not been specifica.lly validated for this

Methods to quantify zinc levels from
purpose. Reported dosages are 110 mg/kg/
saliva and hair have not been validated in
day for 7 -1 4 days for o-penicilla.tnine, and
domestic animals, and measuring zinc in

3-6 mg/kg, tid, for 3-5 days for dirnercaprol.

urine is llllfeliable because elimination of

Chelation therapy with any of these agents
zinc through the kidneys is variable.

should be performed only after careful
consideration and should be monitored with

Treatment and Prevention: After
serial serum zinc levels to help detem1ine the
stabilizing the animal with fhtids, oxygen,
appropriate duration of treatment.

a.t1d blood products as necessary, removal

With early diagnosis and treatment, the
of the source of zinc as early as possible
outcome is usually favorable for animals
is para.tnount. This often requires surgery
with zinc toxicosis. Eliminating exposme
or endoscopy. Inducing emesis to remove
to zinc in the environment is essential to
chronic gastric zinc foreign bodies may be
prevent recurrence.

BRACKEN FERN POISONING

Bracken fern (Pteridium aquilinum) is
killed by frost or drought. It spreads
found throughout the world and is among
primarily through dense rhizome
the five most numerous vascular plants.

networks and can dominate plant

The species includes numerous subspecommunities, especially those burned or cies and varieties, and plant size varies
disturbed. Bracken fern may be found in
with frond lengths of0 .5-4.5 m. Bracken
a diversity of sites but is most common in
fern is perennial, with erect deciduous
semishaded, well-drained, open woodfronds that remain green until they are lands.

3090

BRACKEN FERN POISONING
primary cause of enzootic hematuria has
been attributed to norsesquiterpene
glycosides (ptaquiloside, ptesculentoside,
ai1d caudatoside). Ptaquiloside is a potent
radionlinletic that initially dainages the bone

VetBooks.ir
marrow aild later is carcinogenic (producing
urinaiy tract neoplasia in rruninaI1ts ). Both
the hemorrhagic syndrome llild uroepithelial neoplasms have been reproduced experimentally with bracken fern llild
ptaquiloside. Although less well characte,�
ized, the other norsesquiterpene glycosides,
which predominate in some bracken fem
populations, probably have sinlilar toxicity

Bracken fern (Pteridium aquilinum), growing ai1d cai·cinogenicity.

from large dense woody rhizomes, forms
deciduous, stipitate, erect to spreading

Acute Brackenism (Hemorrhagic
fronds with nonanastomosing veins. The

Disease): Acute bracken.ism occurs when
pinnae are stalked, opposite or subopposite
aI1in1als ingest high doses over relatively

(inset). Courtesy of Dr. Bryan Stegelmeier.

short durations of weeks or months. It is
characterized by bleeding. This toxicity is

Syndromes: A variety of syndromes
have been associated with bracken fern
attributed to ptaquiloside's radionlinletic
poisoning. TI1ese syndromes are largely
dainage to proliferating bone marrow stem
determined by the dose and duration, and
cells. This is seen as depletion of bone
also by the species of the poisoned ai1in1al.

maiTow megakaryocytes followed by
panhypoplasia. The leukogran1 often shows

Enzootic Hematuria: Enzootic
a mixed response. In the initial phases,
hematuria is the most common result of
monocytosis may be pronounced aild
bracken fern poisoning. It prinlaiily affects
followed by graI1ulocytopenia and
cattle and, less frequently, sheep. It is charthrombocytopenia. Final phases include acterized by intennittent hematuria and
mai·ked thrombocytopenia with ai1emia,
anemia Poisoning most often occurs druing
leukopen.ia, ai1d hypergainmaglobulinemia.

late sUI11mer when other feed is scarce, or

U1inalysis generally shows hematruia aild
when animals ai·e fed hay containing
proteinuria. Affected animals have both an
bracken fern. Poisoning requires prolonged
increased susceptibility to infection and a
exposures; affected livestock must ingest
tendency for sponta!leous hemorrhage.

bracken fern for several weeks to yeai·s

Lower doses of bracken fem for longer
before disease develops.

duration ai·e more likely to be carcinogenic.

Affected cattle ai·e weak, rapidly lose

The effects seem cumulative, as animals are
weight, and develop pyrexia (106° -l l0°F
exposed repeatedly for years. Often the

[41 ° -43°C]) once clinical effects manifest.

onset of clinical disease Call be delayed for

Calves often have difficulty breathing, with
weeks, or even months, after animals have
pale mucous membranes. Hemorrhages vary
been removed from bracken fem-infested
from minor mucosa! petechia to effusive
ranges aild pastures. The carcinogenic
bleeding, and at times large blood clots fo1rn
potential of bracken fern aild ptaquiloside
that may be passed in the feces. Coagulation
has been confinne.d not only in livestock but
is prolonged, and bleeding may be proalso in rats, mice, guinea pigs, quail, aild nounced and excessive even at small wounds Egyptian toads.

such as small insect bites or minor scratches.

Ptaquiloside is excreted in the urine aild

Once anin1als develop clinical disease,
milk, and small aI11ounts have also been
poisoning is almost always fatal. Postmoridentified in skeletal muscle aild liver of tem exaininations usually reveal multiple
poisoned ailinlals even after a 15-day
hemorrhages or bruises throughout the
withdrawal period. Containinated milk
carcass. Necrotic ulcers in the GI tract
retains toxicity; it has been shown to
may be noted. The bladder mucosa often
produce GI neoplasms in rats. Several
contains small hemorrhages; dilated vessels; investigators have suggested ptaquiloside or vascular, fibrous, or epithelial neoplasms.

neoplastic traI1sfo1rnation may be promoted

Other neoplasms in the upper GI tract of
or enhaI1ced by bovine papillomavirns
cattle and other species have also been
infection. However, this may be a secondary
rcpmted . In most cases, mixtures of hemochai1ge due to bracken fern-associated rrhagic and neoplastic lesions ai·e found.

myelodysplasia aild subsequent inllTiuno

Although not all bracken fem toxins
suppression that ai·e likely to promote
have been completely characterized, the
papillomavi.rus infection.

BRACKEN FERN POISONING

3091

Bright Blindness: A less common
mortality is usually >900;6. Measurement of
manifestation of ptaquiloside toxicity is
the platelet cow1t is recommended, because
called bright blindness. It is seen clinically
it is the best prognostic indicator for
as tapetal hypen-eflectivity that is most
poisoned animals.

commonly reported in sheep in parts of

Treatment of thiamine deficiency in

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England and Wales. Affected sheep are
horses is highly effective if diagnosis is
pe1manently blind and adopt a characterisma.de early. Injection of a thiamine solution tic alert attitude. The pupils respond poorly
at 5 mg/kg is suggested, given initially IV
to light, and ophthalmoscopic examination
every 3 hr, then IM for several days. Oral
of sheep with advanced disease reveals
supplementation may be required for an
narrowing of arteries and veins and a pale
additional 1---2 wk, although SC injection
tapetum nigrum with fine cracks and spots
of 100---200 mg/day for 6 days has been
of gray. Histologically, the lesion is seen as
successful in some cases. Thian1ine
severe atrophy of the retinal rods, cones,
treatment should also include animals
and outer nuclear layer that is most
sinillarly exposed but not yet showing
pronounced in the tapetal portion of the
clinical disease, because signs can develop
retina. Affected animals often have many of
days or weeks after removal from the
the other bracken fem-associated lesions
source of bracken.

such as bone marrow suppression,

Antibiotics may be useful to prevent
hemorrhage, in1munosuppression, and
secondary infections. Blood or even platelet
urinary tract neoplasia.

transfusions may be appropriate but require

Bracken Staggers: Bracken fem
large volun1es (2---4 L blood) to effectively
poisoning in monogastric animals was first
treat cattle. Though untested, treatment
recognized as a neurologic disease when
with granulocyte-ma.cropha.ge colony-stimhorses consun1ed contaminated hay.

ulating factor ( used to treat a.plastic anemia

Ingestion at a rate of 20%---25% bracken fem
in people) may also be considered.

for <!3 mo may result in bracken staggers.

Clinical signs in horses include anorexia,

Prevention: Poisoning, a.part from
weigllt loss, incoordination, and a crouching
thiamine deficiency, is essentially untreatstance while arching the back and neck with able; however, it is most easily controlled
the feet placed wide apart. When the horse
by preventing exposure. Bracken fem is
is forced to move, trembling muscles are
usually grazed for want of alternative
noted. In severe cases, tachycardia and
forages. Most commonly, animals are forced
an-hytlunias a.re present; death ( usually 2---10
to eat bracken fem when other forage is
days after onset) is preceded by convulsions,
exhausted in late sunui1er, although some
clonic spasms, and opisthotonos. These
animals may develop a taste for the yow1g
changes are due to bracken fem thianlinases.

tender shoots and leaves. Poisoning can be

The resulting disease is similar to vitanlin
a.voided by improving pasture management

B
to increase production of alternative forage.

1 deficiency, and therefore most animals
respond to thianrine therapy. Horses seem to

It has been suggested that alternating
be particularly susceptible, whereas disease
bracken fem--contan1ina.ted and nonconin pigs is rare. In pigs, the signs of thiamine tarnina.ted pastures at 3-wk intervals can
deficiency are less distinct and may resemble minimize poisoning.

heart failure. Affected pigs become anorectic

Bracken fem growth can be retarded
and lose weigllt. Dea.th can occur suddenly
by close grazing or trampling in alternative
after recumbency and dyspnea.. Th..ian1ine
grazing pasture systems. Bracken fem
deficiency is generally not a problem in
density can be reduced by regular cutting of
ruminants, because the vitanlin is synthethe mature plant or, if the land is suitable, by sized in the rumen; however, polioencepha.deep plowing. Herbicide treatment using lomala.cia. (seep 1281) associated with
asulam or glyphosa.te can be an effective
in1pa.ired thia.nline metabolism in sheep has
method of control, especially if combined
been attributed to consumption of bracken
with cutting before treatment. Some
fem and rock or mulga. fem ( Cheilanthes
bracken fem populations contain very low
sieberi) in Australia.

or no ptaquiloside. More work is needed to
identify these populations, detennine why
they are not toxic, and use this information

Treatment: Initial treatment for all
to predict or reduce toxicity.

species is to discontinue exposure to
bracken fem; however, disease can appear

Human Poisoning: Initial epidemiologic
weeks after livestock are removed from the
studies suggest that consumption of milk
fem-infested area. In a.cutely affected cattle,
from cattle with access to bracken

3092

BRACKEN FERN POISONING
increases risk of human esophageal or
have shown an association between
gastric cancer. Certainly the greater risk to
consumption of bracken crozier and
people is direct consumption of bracken
esophageal cancer. Additionally, ptaquilofem. Rhizomes have been used to make side has been found as an environmental
flour, and the young shoots or croziers are
contaminant in soil and water, and air-borne
considered a delicacy in many parts of the
spores may also present a tisk of human

VetBooks.ir
world. Although preparing and cooking lessexposure. Human exposure through any ens the toxicity of ptaquiloside, it has been
means should be of concern, because
identified in these foods. Japanese scientists ptaquiloside is a proven carcinogen.

GOSSYPOL POISONING

Gossypol poisoning, usually chronic,
cottonseed as both protein-bound and free
cumulative, and sometimes insidious,
fonns; only the free form is toxic. Gossypol
follows consumption of cottonseed or
content of cottonseeds vai·ies from a trace
cottonseed products that contain excess
to >6%and is affected by plant species and
free gossypol. It is of most concern in
variety and by environmental factors such
domestic livestock, especially prerurni.nants
as climate, soil type, and fertilization.

or immature ruminants and pigs; mature

Gossypol is a natural component of all but
rnrninants are more resistant to gossypol's
the rarely produced "glandless" vatiety of toxic effects. However, gossypol toxicosis
cotton.

can affect high-producing dairy cows with

Cottonseed is processed into edible
high feed intake, dairy goats, and other
oil, meal, !inters (short fibers), and hulls.

mature rumi.nants fed excess gossypol for

Cottonseed meal is marketed with 500/o-90%
long petiods. It has also been reported i.n
protein, depending on intended use.

dogs fed cottonseed meal in diets or housed

Cottonseed and cottonseed meal are widely
on cottonseed bedding.

used as protein supplements in animal
feed. Cottonseed oil soapstock (foots) is

Etiology: Gossypol, the predominant
the ptincipal by-product of cottonseed oil
pigment and probably the major toxic
refining. Cottonseed soapstocks are being
ingredient in the cotton plant (Gossypium
increasingly used as animal feed additives;
spp ), and other polyphenolic pigments are
cottonseed hulls are used as a source of
contained withi.n small, cliscret.e strnctmes
additional fiber in animal feeds and contain
called pigment glands foung in vaiious paits
much lower gossypol concentrations thai1
of the cotton plant. Gossypol is found in
do whole cottonseeds.

Lipid-soluble gossypol is readily
absorbed from the GI tract. It is highly
protein-bound to amino-acids, especially
lysine, and to dietary iron. The precise
mechanism of action is not known, but
gossypol renders mai1y aini.no acids unavailable by the fonnation of a Schiff's base-type derivative as well as additional protein/
gossypol interactions. Gossypol also affects
enzymatic reactions critical for many
biologic processes, including the ability
of cells to respond to oxidative stress and
i.nhibition of oxygen release from hemoglobin. Cortjugation, metabolism, and winaiy excretion of gossypol is limited;
most is eliminated in the feces.

All ailirnals ai·e susceptible, but monogas

Gossypium spp (cotton plant), young plant.

trics, prerunlinants, immature run1inants,

Courtesy of Dr. Cecil Brownie.

and poultry appear to be affected most

GOSSYPOL POISONING

3093
frequently. Adult nuninants are able to
nonrnminant species are secondaiy to the
detoxify gossypol by fom1ation of stable
more toxic effects, particulai·Jy in females.

complexes with soluble proteins in the

Signs of prolonged excess gossypol
nun en, thus preventing absorption,
exposure in mai1y animals are reduced
something Jacking in swine, preruminants,
growtl1 rate, weight Joss, weakness, anorexia,

VetBooks.ir
and young 11.Ullinants with only a partially
and increased susceptibility to stress. Young
functioning nunen. Pigs, guinea pigs, and
lan1bs, goats, and calves may suffer cai-cliorabbits are reported to be sensitive. Dogs myopatlly ai1d sudden death; if the course
and cats appear to have intermediate
is more chronic, they may be depressed,
sensitivity. Goats may be more sensitive to
anorectic, and have pronounced dyspnea.

gossypol than are cattle. Horses appear

Adult dairy cattle may show weakness,
relatively resistant but caution is still
depression, anorexia, edema of the brisket,
advised. Toxic effects usually occm only
and dyspnea, and also have gastroenteritis,
after longterm exposme to gossypoI, often
hemoglobinuria, and reproductive problems.

weeks to rnontl1s.

In monogastric animals, acute exposure may
result in sudden circulatory failure, whereas

Clinical Findings: Signs may relate
subacute exposure may result in pulmonary
to effects on the cardiac, hepatic, renal,
edema secondary to congestive heart failure;
reproductive, or other systems. Prolonged
anemia may be another conunon sequela.

exposure can cause acute heart fail me

Violent dyspnea ("thumping") is the outstandresulting from cardiac necrosis. Also, a form ing clinical sign in pigs. In dogs, gossypol of cardiac conduction failure similar to
poisoning is prinlaiily reflected by cardiohyperkalemic heart fail me can result in toxic effects; condition dete1iorates progresudden death. Pulmonary effects, labored ssively, and ascites may be marked. Affected
breathing, and chronic clyspnea are most
dogs may show polydipsia and have serum

Ii kely secondary to cardiotoxicity from
electrolyte inlbalances, most notably
congestive heart fail me.

hyperkalemia, with pronOLmced ECG

Hepatotoxicity can be a prinlary effect
abnormalities.

from direct damage to hepatocytes or
metabolism of phenolic compounds to

Lesions: An enlarged, flabby, pale,
reactive intermediates, or liver necrosis may
streaked, and mottled heart witll pale
be secondary to congestive heart failme.

myocardial streaking, enlai·ged and dilated

Gossypol inhibits glutathione-S-transferase,
ventricles, ai1d valvular edema may be
inlpairing the liver's ability to metabolize
evident. Skeletal muscles may also be
xenobiotic compounds. Hematologic effects
pale. A froth-filled trachea and edematous,
include anemia with reduced munbers of
congested lungs are conunon, witll inte

RBCs and increased RBC fragility, decreased rstitial pulmonaiy edema and markedly oxygen release from oxyhemoglobin, and
edematous interlobular septa. Generali.zed
reduced oxygen-carrying capacity of blood
icterus and an enlarged, congested, mottled
witl1 lowerecl Hgb and PCV values clue to
or golden, friable "nutmeg" liver with
complexing of iron by gossypol.

distinct lobulai· patterns may be seen. The

Reproductive effects include reduced
kidneys, spleen, and other splanchnic organs
libido with decreased spermatogenesis and
may be congested, possibly with petechiae;
spenn motility, as well as spem1 abnonnalimild renal tubular nephrosis may be present.

ties (which are reversible) resulting from

Hemoglobinuria and edema and hyperenzyme inhibition of steroid synthesis in emia of the visceral mucosa may develop.

testicular Leydig cells. Specific mitochon

Cardiomyopathy in affected dogs has been
drial damage in spermatozoa appears to
characterized as focal or general, granular
cause immobility and depressed spenn
myocardial degeneration witll edema
counts. Extensive damage to genninal
between and within myofibers; severe
epitheliwn in botl1 ran1s and bulls fed
abnormalities in contractility have resulted
excessive gossypol may be responsible
in right-side congestive heait failure without
for depressed spem1atogenesis. Effects
pronounced dilatation, and pulmonary or
in females may include irregular cycling,
hepatic chai1ges cai1 be minimal.

luteolytic disruption of pregnancy, and
direct embryotoxicity; probable mecha

Diagnosis: Diagnosis is based on the
nisms include an endocrine effect on the
following: 1) a history of dietary exposure
ovary as well as a direct cytotoxic effect on
to cottonseed meal or cottonseed products
tl1e uterus or embryo. Green discoloration
over a relatively long period; 2) signs,
of egg yolks and decreased egg hatchability
especially sudden death or chronic dyspnea,
have been repmtecl in poultry. However,
affecting multiple animals within a group;
anti.fertility and reproductive effects in many 3) lesions consistent with the reported

3094

GOSSYPOL POISONING
syndrome and associated cardiomyopathy spp), oleander (Neriitrn oleander), yellow and hepatopathy, with increased amounts
oleander or yellow-be-still tree (Thevetia
of fluids in various body cavities; 4) no
pe1uviana), purple foxglove (Digitalis
response to antibiotic therapy; and 5) the
purpurea), lily-of-the-valley (Convallaria presence of significant concentrations of
rnajalis), dogbane (Apocynurn spp), VetBooks.ir
free gossypol in the diet. Analyses of
coffee senna (Senna occidentalis ),
dietary components for free gossypol
bracken fern (Pteridiurn aquilinurn),
must be correlated with history, clinical
white snakeroot (Eupatoriurn rugosurn),
signs, and postmortem findings. However,
death ca.mas (Zygadenus spp), lantana
as with many feecl-inclucecl toxicoses, the

(Lantana carnara), monkshood
responsible feed may be already com

(Aconiturn napellurn), and milkweed
pletely consumed and not available for

(Asclepias spp ).

analysis. Free gossypol at > l 00 mg/kg ( l 00
ppm) of feed in the diet of pigs or young
ruminants <4 mo old supports a presump

Prevention, Treatment, and
tive diagnosis. Adult ruminants can

Control: There is no effective treatment
detoxify higher concentrations of
for gossypol poisoning. Adsorbents such
gossypol, but intake should still be <1,000
as activated charcoal and saline cathaitics
ppm in the diet. Gossypol toxicosis
are of little value because of the chronic
developed in mature dairy goats each fed
exposure and cumulative nature of
an estimated 350-400 mg gossypol/day for
gossypol. If gossypol toxicity is suspected,

3 mo in a diet containing -400 ppm free
all cottonseed products should be removed
gossypol. Adverse effects on semen
from the diet immediately. However,
quality (decreased sperm motility and
severely affected animals may still die up
morphologic abnormalities) occurred in
to 4 wk after withdrawal of gossypol from
young bulls fed a concentrate containing
the diet. Recovery depends primai·ily on

1,500 ppm free gossypol (providing 8.2 g
the extent of toxic cardiopathy. Because
free gossypol/head/day). Cottonseed meal
exposure is usually chronic, and lifecontaining 26.6% (266,000 ppm) total threatening lesions may be advanced
gossypol and 0.175% (1,750 ppm) free
before a diagnosis is made, a favorable
gossypol was toxic when fed to adult
prognosis for complete recovery may be
dogs for an unspecified length of time;
unrealistic. Mild to moderate myocardial
however, the equivalent oral dosage of
lesions may be reversible with time if
free gossypol fed was <6 mg/kg/clay.

stress is minimized and animals ai·e

Gossypol can gradually accumulate in
carefully handled. However, poor weight
the kidneys and liver, which are additional
gains in affected livestock and increased
specimens for postmortem analyses. In
susceptibility to stress may persist for
sheep, gossypol concentrations (free or
several weeks after cottonseed products
bound) > 10 ppm in the kidneys and >20
are removed from the diet. A high-quality
ppm in the liver suggest excess gossypol
diet supplemented with lysine, methionine,
exposme. However, background and
and fat-soluble vitamins should be
significantly increased tisime gossypol
included in suppo1tive therapy. Seleniun1
concentrations have not been determined
or copper deficiencies may potentiate
in all anin1al species, so tissue analyses may gossypol toxicosis.

be of limited diagnostic value.

A high intake of protein, calciun1

Differential diagnoses include poisonhydroxide, or iron salts appears to be ings by cardiotoxic ionophoric antibiotics
protective in cattle. MatLtre cattle should

(eg, monensin, lasalocid, salinomycin,
also be given ;?4()0A, of dry-matter intake
narasin) and ammonia, nutritional or
from a forage source, and dietary gossypol
metabolic disorders (eg, seleniun1, vitaconcentrations should be limited to �1,000
min E, or copper deficiency), infectious
ppm, because 1,500 ppm may cause
diseases, noninfectious diseases (eg,
anemia, poor growth, or decreased milk
pulmonary adenomatosis, emphysema),
production. Swine and yow1g ruminants
mycotoxicoses caused by Fusariurn
ai·e affected by dietary gossypol concentracontaminated grain, and toxicoses caused tions> 100 ppm. Added iron of up to 400
by plants with cardiotoxic and other
ppm in swine diets and up to 600 ppm in
effects. Cardiotoxic plants (seep 3103),
poultry diets was reported to be effective in
which may cause confusing or similar
preventing signs and tissue residues of
clinical signs and postmortem lesions,
dietai-y gossypol exposure when used in
include English yew (Taxus baccata),
ratios of 1:1 to 4:1 of iron to free gossypol.

Japanese yew (Tcuspidata), laurel

Poult1-y are affected by dietai-y gossypol

(Kalrnia spp), azalea (Rhododendron
concentrations >200 ppm.

POISONOUS MUSHROOMS

3095

POISONOUS MUSHROOMS

VetBooks.ir

Mushrooms are the fruiting bodies of
a variety of fleshy fungi that are found
worldwide. They typically appear suddenly
from growing vegetative (myceliurn)

portions, and they contain spores as
reproductive mlits. Fungi lack chlorophyll;
their nutritional requirements are met by
utilizing organic mate1ial from a saprophytic,
parasitic, and/or mycorrhizal life cycle.

Exposure is by ingestion. Although most
muslu·ooms are edible and safe, a few
contain diverse secondary metabolites

( cyclopeptides, monomethylhydrazine,
orelli.ne/orellanin, muscari.ne, ibotenic acid
and musci.mol, psilocybin, and unknowns)

that on ingestion/absorption result in mild to
severe illness and even death. The mushroom
species most frequently implicated in hwnan/
animal muslu·oom fatalities globally is

Amanila phalto'ides. MostAmanila species
are typically identified by their physical
characteristics: veil ( universal/partial), cap or
pile us ( with scales-remnants of universal
veil), la.mellae (gill-like, spore-bearing
structure under surface of pile us), spores

(reproductive structure-white to black and
other shades of color), stipe/stalk ( cap

Amanita
support), annulus or ring (remnant of partial
phalloides. Courtesy of Dr. Cecil Brownie.

veil on stipe below pileus ), volva ( renmant of
universal veil at base of bulb), and myceliun1.

Other characteristics helpful in the identisigns in exposed animals largely dictates the fication of some poisonous mushrooms are
prognosis. A long delay time is synonymous
listed in TABLE 5.

with fatality (TABLE 6). However, sho1t latent The time lapse (latent period) between
periods do not always indicate smvival,
mushroom ingestion and observed clinical
because the anin1al may have ingested a

PHYSICAL CHARACTERISTICS OF COMMON POISONOUS

MUSHROOMS

Genus
and

Color of Cap/

Species

Spores

Habitat

Season

Range

Amanita

Red-tan to yellow/ Ground-pine,

Autumn/winter: Widespread,
muscaria
orange/ white
spruce, birch,

June-Nov
common in
poplar, and oak

East and
trees

California

A pantherina

White with

Ground under Autunm/winter: Rocky
whitish patches;
conifers

June, Sept-Oct, Mountains/
dark to yellow-

(Douglas fir)

Nov-Feb

West coast;
brown/white at

(California)

rare in East
margin

( continued)

3096

POISONOUS MUSHROOMS

PHYSICAL CHARACTERISTICS OF COMMON POISONOUS

MUSHROOMS (continued)

Genus
and

Color of Cap/

Species

Spores

Habitat

Season

Range

VetBooks.ir

A phalloides Yellow/green or

Ground under Autumn: late

Massachusetts
green/white
conifers,

Sept-Nov,
to Virginia west
hardwoods;

Nov-Jan
to Ohio; Pacific
junipers and
northwest to
oaks

California

Avirosa

White/white

Ground; mixed Autumn: late

North America
woods; grass,

June-early Nov
near trees

Chlorophyl-

White/green or

Lawn,

Summer:

Florida to
tum
grayish white
pastures,

Aug-Sept

California,
molybdites
meadows,
common in
fairy rings

Denver, reported
in New York and

New Jersey

Clitocybe spp White/white

Ground

Perennial

Widespread in
orth America

Cortinarius Orange/brown

Ground under July-Aug; Sept- Widespread in
orellanus
conifers

Oct(Rocky

North America

Mountains)

Gale'lina spp Brown-orange/

Ground-wood, Autumn/spring: Throughout
rust-brown
well-decayed

Oct-Nov,

North America
conifers and

May-June
logs

Gyromitra

Brown-rusU

Ground under Spring:

Throughout
esculenta
yellow to buff
conifers

April-early June North America

Inocybespp

Brown/bright

Ground

Autmnn:

Widespread in
rusUorange-

May-Nov

No1th America
brown or dull
gray-brown

Lepiotaspp

White with

Ground

July-Oct

Throughout
brownish scales/ conifers, grass, (Michigan,

North America
white
leaf litter, oak

Ohio); July-Nov
and mixed

(Florida);
woods

Nov-Feb

(California)

Paxillits

Brown/sienna

Ground: single/ July-Nov

Widespread in
involutus

(clay-brown)

numerous on

North America
wood in mixed
woods

Psilocybe

Brown/lilac

Ground/wood/ Year round

Gulf Coast
cubensis
brown to dark
dung ( cattle,
purple brown
horses)

Ritssula

Reddish/white to Single/group;

July-Sept

Widespread in
emetica
yellowish white/
on sphagnun1

North America
whitish
moss, rarely on
very rotten
wood, conifers,
or mixed woods

POISONOUS MUSHROOMS

3097

POISONOUS MUSHROOMS: ONSET OF ACTION AND ORGANS

TARGETED

Mushrooms

Toxin

Onset'Ilme

Organ/System

VetBooks.ir

LATENT PERIOD >6 HR AFTER INGESTION; LIFE-THREATENING

Arnanita

Cyclopeptides, a

6-24 hr, rarely

Primarily liver,
phallo'ides;
and 13 amanitins,

>24 hr
kidney secondary

Avirosa
phallotoxins,
virotoxins

Conocybe.frla:ris
a and 13 amanitins

6---14 hr, rarely

Primarily liver

>24hr

Co1'1inarius

Orellanin, orelline

3-14days

Primarily renal"

gentil'is

(days/weeks)

Caterina auturnna- a and 13 amanitins

6---14 hr, rarely

Primarily liver
tis; G venenata

>24hr

Gyrornit1·a

Monomethyl-

6---24 hr

CNS
escutenta
hydrazine

Lepiotaspp
a and 13 amanitins

6---14 hr, rarely

Primarily liver

>24 hr

LATENT PERIOD :,3 HR AFTER INGESTION; NOT LIFE-THREATENING

Arnanita rnuscaria; Isoxazoles: ibotenic 30 min-2 hr; CNS

A pantherina
acid muscimol
recovery 4-24 hr

Chtorophyllurn

Unknown

30min-3hr;

GI
rnotybdiles
recovery 1-2 days

Ctitocybe deatbata; Muscarine

30min-2 hr;

Autonomic ne1vous

Ctitocybe spp;
recovery 6---24 hr
system

Inocybespp

Paxillus invotutus Unknown

1-3 hr; recovery

Immune system

2-4days

Psitocybe spp;

Psilocybin and

30-60 min;

CNS

Conocybe smithii;
psilocin
rarely6 hr

Gyrnnopitus specta-
b'ilis; Panaeotus
siibbalteatus

Russula ernetica

Unknown

30min-3hr;

GI
recovery 1-2 days

" No reported veterinary cases

3098

POISONOUS MUSHROOMS
combination of non-lethal/lethal mushroom

Clinical Findings: Within 30-120 min
species growing in the same location
of ingestion, there is mild to excessive

( dilution effect, or dose determines
cholinergic stimulation-ataxia, vomiting,
toxicity). In mushroom species with clinical
abdominal pain, salivation, lac1imation,
signs that appear <3 hr after ingestion,
watery diarrhea, miosis, bronchoconstric

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effects are generally self-limiting and not
tion, bradyca.i·dia, arrhythmias, hypotenlife-threatening. Those with clinical signs sion/hypertension, and shock.

that appear >6 hr after ingestion are
life-threatening.

Diagnosis: Diagnosis may be based on a

The sudden appearance of mushrooms
history of mushroom ingestion, identificaand their short lifespan within the tion of suspected mushroom and consistent
environment, coupled with the indiscrimiclinical signs, response to supportive care, nate eating habits of many animals, creates
a.t1d atropine therapy. Tests used to evaluate
diagnostic challenges. History and time
fluid and electrolyte status in severe
after ingestion at which clinical signs are
gastroenteritis cases, together with a liver
seen determine the treatment approach
profile, may be useful.

and prognosis. Establishing the tin1e of
ingestion may be difficult to in1possible.

Treatment: Other than offering support

With no proven antidotes to treat mushive ca.i·e (fluid and electrolyte replacement), room poisonings, treatment is prima.tily
treatment is wmecessa.iy in most cases. In
directed at deconta.tnination, mushroom
life-threatening cases, atropine therapy
identification when possible, and intensive

(0.2-2 mg/kg, a pmtion of the calculated
supportive care.

dose given IV and the remaining portion

IM or SC), repeated as necessary, is the

TOXIN LATENT PERIOD <3 HR
treatment of choice. Efficacy of treatment

AFTER INGESTION
should be based on lack of respiratory
difficulties and respirato1y secretions and

Clitocybe dealbata, C dilatata, and not on mydriasis. Excessive atropine

/nocybespp
therapy can lead to anticholinergic effects

( eg, tachycardia, GI stasis, behavioral

Clitocybe are fleshy, small mushrooms with
changes, a.t1d hype1thermia); therefore,
white-tan-grey caps, gills that are attached
a.t1in1als should be monitored.

and that descend the stalk, and white spore
print. They are widely distributed and
usually grow on the ground in open woods,

Amanita muscaria and A pantherina
parks, and lawns. Inocybe a.i·e small, brown A manila muscaria have an orange-red cap
muslu·ooms that grow on conifers or
with distinctive white to yellow warts, gills
broad-leaf ea trees and oak woods
that are somewhat attached, white spore

(mycorrhizal). They have a cap with a knob,
print, ring stalk, and bulbous base (cup).

ringless stalk, veil covered immature gills,

A pantherina have a tan to yellow-brown/
no remnant of universal veil, and a spore
dark brown cap with white patches, a ringed
print that is brightrustJorange-brown or
stalk with basal bulb, and white spore print.

gray-brown.

Both of these mushrooms a.i·e foW1d in

The toxin in these mushrooms is
coniferous and deciduous forests of the
muscarine, a quaternary anunonium

Pacific northwest.

compow1d that is poorly absorbed orally

The toxins in these mushrooms are
and does not cross the blood-brain baffier.

isoxazole derivatives: ibotenic acid, which

Its cholinergic effects a.i·e therefore
is strncturally sin1ilar to the stimulatory
peripheral. The absorbed portion is quickly
neurotransmitter glutamic acid, and its
distributed throughout the body and
decarboxylated metabolite muscimol,

W1dergoes urinary excretion. Musca.tine
which is stereochemically similar to the
is structurally sin1i!a.i· to acetylcholine, a
inhibitory neurotransmitter -y-an1inobutyric
cholinergic neurotra.t1smitter. Whereas the
acid (GABA). They both cross the bloodacetylcholine-muscarine receptor complex brain barrier and effect fW1ctional changes
is susceptible to acetycholinesterase
within the CNS. The toxic dose of ibotenic
inactivation, the musca.i·ine-muscarine
acid is reported to be 30-60 mg, and that of
receptor complex is not. Muscarine
musci.rnol is 6 mg (ingestion of more than
competes with acetylcholine at cholinergic
two mushrooms).

receptor binding sites, leading to excessive

Ibotenic acid undergoes spontaneous
stin1ulation of postganglionic cholinergic
decarboxylation (stomach, liver, and brain),
fibers and the subsequent observed clinical
forming muscimol, which is a GABAsigns ( cholinergic excess).

receptor agonist. Both a.i·e analogues of

POISONOUS MUSHROOMS

3099

-y-aminobutyric acid and act as weak,
weight proteins found throughout the
noncompetitive inhibitors of GABA
mushroom.

(inhibits neuronal and glial GABA uptake).

This reduces the inhibitory effect of the

Clinical Findings: Within minutes to

Purkinje cells in the cerebellum, increases
hours (0.5-3 hr) after exposure, clinical

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brain serotonin, and decreases catecholasigns become evident. These include mine levels.

vomiting, bloody diarrhea, abdominal pain,
muscle cramps, liver injury, and circulatory

Clinical Findings: Both compounds are
disturbances that are self-limiting. Although
rapidly absorbed from the GI tract. The
recove1y generally occws within 6-24 hr,
onset of clinical signs (tachycardia,
it could be prolonged or become life
hypotension, ataxia, seizures, hyperthermia, threatening (rare) in cases ofhypovolemic vomiting, muscle fasciculation, mydriasis,
shock, oliguria, and/or transient increased
incoordination, hyperactivity [paddling,

BUN secondary to dehydration. Death is
chewing movements], opisthotonos,
rare.

respiratory depression, coma, and death)

are reportedly seen within 30-120 min after

Diagnosis: A tentative diagnosis may be
ingestion. Duration of signs is -24 hr.

based on history and early onset of reported
clinical signs (gastroenteritis-vomiting

Diagnosis: Diagnosis is based on a history and bloody diarrhea). Except for dehydraof ingestion, clinical presentation, and tion, there are no systemic signs. If the
response to treatment (symptomatic,
mushroom is available, the gills (light green)

suppmtive, and specific drugs, eg,
and spore print (green) color may be used
benzodiazepine ).

to distinguish C molybdites, the most
common GI irritant mushroom species,
from others.

Treatment: Symptomatic and supportive
treatment includes maintaining hydration

Treatment: There are no specific

(IV fluids), keeping airways free of
antidotes. Dehydration and electrolyte
respiratory secretions, and frequent
imbalance should be addressed. Gastric
positional changes. Seizures may be
lavage and activated charcoal therapy may
controlled with diazeparn (0.5 mg/kg, IV to
be considered. Analgesics are useful in
effect; repeated as needed), phenobarbital
some cases, but caution should be

(6 mg/kg, IV), or pentobarbital (5-15 mg/kg,
exercised in administering acetaminophen

IV). Benzodiazepines and barbiturates are

(inherently hepatotoxic) to hepatic insult

GABA-receptor agonists and may potentiate cases. Phenothiazines interact adversely CNS and respiratory depression. Muscarine
with toxins to induce CNS and/or GI effects.

concentrations in A muscaria are very low,

Fluids and vasopressors should be
and peripheral effects are more anticholinad.ministered in hypovolemic shock cases.

ergic than cholinergic. Therefore, atropine

Liver and kidney functions should be
therapy is contraindicated.

monitored.

Chlorophyllum molybdites and

Psilocybe cubensis, Conocybe

Russula emetica
cyanopus, Gymnopilus spectabilis,

Chlorophylliim molybdites mushrooms
and Panaeolus subbalteatus
have caps that are large, white to brown,

Psilocybe cubensis are small, brown,
egg-shaped, convex knobbed to flat, with
slender-stalked mushrooms. They
numerous cinnamon or buff scales. They
commonly grow in piles of dung and
have unattached white gills, green or
fertilized grasses in moist areas throughout
grayish-olive spores, and a 1ing on the stalk.

the USA, especially in the southeastern and

They are common in the southern and
northwest regions. The mushrooms develop
central USA. Russula emetica mushrooms
a blue-green color in handled and injured
have a reddish, slin1y cap with shmt whitish
areas. They have yellowish, sticky to moist
stalk and gills; no veils; and a white to
caps with brown gills; a persistent ring on
yellowish-white spore print. They grow
the stalk; and a purple-brown spore print.

singly or in a group and are found through

Conocybe cyanopus are small and fragile,
out the USA. The toxins in these mushwith brown caps, brown gills, and a large rooms are varied and unknown GI irlitants
ring midway down the long, thin stalk. The
that are thought to be high-molecular-
spore print is cinnamon brown. They are

3100

POISONOUS MUSHROOMS
widely distributed in North America.

TOXIN LATENT PERIOD >6 HR

Gymnopilus spectabilis are large

AFTER INGESTION
yellow-orange mushrooms with an orange
to rust orange spore print. They are found in

Amanita phalloides, A virosa,
clusters on wood, stw11ps, or on the grow1d

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over bw·ied wood. Panaeolus siibbaltealus

Lepiota helveo/a, Galerina
have broadly cortical to flat caps with a dark
autumna/is, G venenata, and
belt around margin, brown gills, hairy

Conocybe filaris
reddish stalks, and a blackish spore print.

These mushroom species account for >95%

They are widely distributed in North
of the reported mushroom-induced deaths.

America.

They are common tl1roughout No1th

These hallucinogert.ic mushrooms contain America and a.i·e associated with oaks and psilocybin and psilocin, which a.re indole
birch trees.

alkaloids simila.r to lysergic acid diethyl

A manila phalloicles and A virnsa have arnide (LSD). Psilocybin undergoes rapid
olive to green caps with veil patches, gills
dephosphorylation (plasma, kidneys, and
that a.i·e unattached to the stalk, a white
liver), forming psilocin, which is structu.rally spore print, and stalks with a ring ( often but sin1ilar to serotort.in (stimulatory to
not always) and a cup (volva) or remnants
serotort.in receptors in the central and
at the base. The features of Lepiota helveola
peripheral nervous systems). Metabolites
are simila.i· to those of Amani/,a spp but
cross the blood-brain barrier and concenwithout volva; they have scaly caps with trate in bra.in tissue. Growth conditions,
a knob in the center and stalks with
geographic location, storage conditions, and a. movable ring. Galerina aittumnalis mushroom species a.re factors that influence (a.utwnn galerina.), G venenata, and toxin concentrations. Ingestion of five or six

Conocybefua1is have brownish, tacky caps
dried mushroom caps is reported to be
with yellowish gills becoming rust and a
toxic.

ring on tlleir brownish stalks. They have
no volva, a.i1d their spore print is brown to

Clinical Findings: Clinical signs occwrust-brown. These species are abundant on within 0.5-1 hr; they are rarely delayed as
well-decayed coniJerous and deciduous logs
long as 3 hr after ingestion. Signs include
throughout North America.

vocalization, aggression, nystagmus, ataxia,

Toxin present in these mushrooms
tachycardia, vomiting, urinary incontiinclude cyclopeptide aniatoxins (bicyclic nence, dyspnea, mydriasis, weakness,
octapeptides), phallotoxins, and virotoxins
hyperthennia., mild methemoglobinemia.,

(bicyclic heptapeptides). Amatoxins (o. and
and hallucination, with recove1y within 6 lu·

13 an1aniti.n derivatives) are the most potent;
of observed clinical signs.

tl1ey are not found in all Amanita spp. An
estimated reported letllal dose is 0.1 mg/kg

Diagnosis: A history of mushroom

( equivalent to the concentrations in one cap
ingestion, identification of suspected
of A phalloicles) across animal species.

mushroom(s), consistent clinical presenta

Whereas tile a.inatoxins are repmted to be
tion, and response to supportive and
well absorbed orally, phallotoxins and
symptomatic care are critical for diagnosis.

virotoxins are not. Amanitins a.i·e not

With isoxa.zole-induced toxicity, coma is
protein bound and a.i·p excreted in urine
distinctly expressed; however, the opposite

(800/o--900!.i), feces, and bile (7%). A.ma.toxins
is true in psilocin-induced toxicity. Tests
bind to nuclea.i· RNA polymerase-11
detecting psilocin and its glucuronide

(transcription phase), thus preventing the
metabolite in urine, serum, and blood,
fo1ma.tion of phosphodiesterase bonds
altllough confirmatory, are not widely
and subsequent RNA, DNA, and protein
available clirt.ically.

synthesis. High-protein synthesis cells a.i·e
most sensitive. Amatoxins a.i·e prilna.i·ily

Treatment: Treatment is primarily
liver toxins, but they also affect many organ
symptomatic and supportive. Dia.zepa.rn
systems, resulting in hypoglycemia, blood

(0.5-1 mg/kg, IV, with incremental dose
clotting defects, thyrnid/parathyroid
increase of 5-10 mg to effect) or phenoba.i0
functional anomalies, renal failure, and
bital (6 mg/kg to effect) may be given. Body
intestinal da.inage ( enterohepatic recirculatemperatu.re should be rnort.itored. In some tion of the toxin).

cases, leaving the art.imal untreated in a
quiet, dark environment might be all that is

Clinical Findings: Signs can be cha.i·acternecessary.

ized in four phases: 1) latent (6-12 hr after

POISONOUS MUSHROOMS

3101
ingestion), in which the anin1al shows no

Gyromitra esculenta
clinical signs; 2) GI signs (as long as 24 hr
after ingestion); 3) remission (as long as 72

These mushrooms have a non-gilled, yellowlu· after ingestion), in which the animal brown to dark-red, deeply Wiinkled,
appears to have recovered; and 4) hepatid
honeycomb (unlike true morels that are

VetBooks.ir
renal (3-6 days after ingestion), leading to
hallowed and not chambered), saddlerecovery or death tlu·oughout the next 7-14
shaped cap on a short stalk. They are found
days. The reported long latent phase is of
on the ground under conifers throughout
diagnostic importance. The GI phase,

North America. The toxin involved is the
indicated by vomiting, abdominal discomhydrazone gyromitrin, which on ingestion is fort, hepatitis, and pancreatitis
hydrolyzed to'N-methyl-N-formylhydrazine
follows and
signals initial hepatic, hematologic,

( depletes hepatic cytochrome P-450) and
cardiovascular, endocrine, CNS, and renal
monomethylliydrazine (inl1ibitor of
changes. The remission phase follows, only
the coenzyme pyridoxal phosphate and
to enter a fulminant hepatidrenal phase,

-y-aminobutyric acid in tl1e CNS 6--12 hr after
indicated by icterus, hypoglycemia, and
ingestion. The concentration of gyromitrin
coma, 3--4 days after ingestion. Recovery or
varies witl1 enviromnental conditions.

death (>500A,) from hepatic and/or renal
failure occurs 7-14 days after muslu-oom

Clinical Findings: Vomiting, watery
ingestion.

diarThea, abdon1inal discomfo1t, convulsions and coma may be noted 6--24 hr after Diagnosis: Mushroom id
ingestion of a toxic dose. Methemoglobine

.ent.ification
characteristics, coupled with consistent
mia and hemolytic anemia, hepatitis,
clinical signs as stated above, is diagnostic.

jaundice, neplmtis, and death develop some

Meixner test results (time taken, and
time later. Deatl1 appears to be due to
color intensity of suspected mushroom
hepatorenal failure.

specimen-fresh, vomited fragments)

would be diagnostic. During the GI phase,

Treatment: Activated charcoal (1 g/kg)

animals should be monitored for decreased may be helpful if given early after ingestion.

serum thyroxine levels, hypoglycemia,

IV fluids should be given as needed. IV
and/or increased insulin, calcitonin, and
pyTidoxine controls neurologic signs, and
parathyroid levels. Routine blood and
methylene blue can be given in cyanotic and
serum chemistry profiles are unremarkable methemoglobin cases. PyTidoxine-induced until liver/kidney damage. Because the
peripheral neuropathy from adn1inistering
toxin is primarily hepatotoxic, changes in
high doses should be avoided. For the

.

clotting factor V, fibrinogen, and kidney
induced hepatic encephalopathy, supp01t1ve
and liver profiles would also be helpful.

tl1erapy is essential. In addition to monitor

Amanitins can be detected in urine from
ing methemoglobin levels, hepatic and renal
animals not showing clinical signs. They
functions should also be monitored.

are also detectable in liver and kidney
specimens as Jong as 22 days after

TOXIN LATENT PERIOD >24 HR
ingestion.

AFTER INGESTION

Treatment: There are no specific antidotes.

Cortinarius orellanus and C rainierensis Silibinin (not FDA approved), penicillin G

TI1ese mushrooms have a colorful but

(high levels), combined silibinin/penicillin,
mostly brownish cap, stalk, and young gills;
cimetidine, N-acetylcysteine, or vitan1in C
the matured gills are orange-rust in color.

therapies have been used with some success

The spore print is bright rust/orange-brown/
in people and could tl1erefore be tJ.ied,
gray-brown but not purple-brown. Stalks
altl1ough animal study data are not readily
may or may not have a ring-like zone.

available. Hypoglycemia remains an adverse

The toxins involved are orelline and
effect witl1 or witl1out treatJ.nent. Suppmtive
orellanine, which are chemically related to
care (IV fluids, dextJ.·ose, and antibiotics)

the herbicide diquat (bipY)idyl derivatives).

counters the effects of severe liver and

Thin-layer chromatography can detect
kidney damage. Early institution oftJ.·eatment orellanine in renal biopsy material long after is essential to save the animal; tl1e prognosis
clinical exposure but not in urine and/or
is poor after hepatidrenal patl1ology.

blood during clinically active states.

Activated charcoal (1 g/kg witl1 catl1artic)

Ingestion of tlu-ee to ten caps is reported to
during the first 24 hr after ingestion absorbs
be lethal. There have been no reported
amanitin undergoing enterohepatic
cases from ingestion of species grown in
recirculation and tl1us may be helpful.

North America.

3102

POISONOUS MUSHROOMS

Clinical Findings: The onset of clinical
interfere with sulfur-containing amino acid
signs is delayed (17 days after ingestion).

incorporation. Drying decreases toxicity.

Signs include anorexia, vomiting, diarrhea/
constipation, gastritis, thirst, and polyuria

Clinical Findings: Signs may appear as
progressing to oligUiic renal failure in 3-14
early as 3 days but as long as 6 days after

VetBooks.ir
days after initial clinical signs. The kidney
exposure and include anorexia, diarrhea,
seems to be the target organ; lesions include salivation, hypertherrnia, depression, interstitial nephritis, tubular damage, and
hyperemic coronary band, hemorrhage
fibrosis. Hepatic damage is infrequently

(anterior chamber of eyes), oral ulceration,
reported. In most cases, marked improvealtered keratinization (hair/hoof loss, ment over an extended period (6 mo) is
similar to selenitm1 poisoning), and
seen; however, chronic renal failure occurs
recumbency. Death or recovery may be
in some cases.

expected in 3-15 days.

Diagnosis: Urinalysis indicates concen

Diagnosis: These mushrooms grow
trated urine, hematuria, protein, and RBC
exclusively among eucalyptus plants, so
casts early in the latent period, followed by
history of exposure to eucalyptus is key.

diluted urine with protein and few casts

Selenium exposure and toxicity causes similater. It therefore becomes necessary to lar signs. The duration and outcome of the
monitor renal function. Renal pathology
clinical expression helps to confirm
without hepatic involvement after a Jong
diagnosis.

latent period (days) has been reported in
people. Blood, urinalysis, and kidney profile Treatment: Treatment involves removing testing would be supportive. Mushroom
the affected animal from fue source and
identification can differentiate Cortinarius
offering supportive care. Recovery requires
spp from Paxillus involutus, a mushroom
time.

reported to cause hypersensitivity leading
to renal failure.

Paxillus involutus

Treatment: Treatment should be focused

Paxillus involutus has a dry or slimy,
on decontan1ination, mushroom identificabrownish cap with an in-rolled margin and tion ( often difficult), and intensive
yellowish gills descending a short distance
supportive care. Hemodialysis should be
on the brown, smooth stalk. The spore print
instituted until nonnal kidney function
is clay-brown. P involutus is widely
retUins. Pentobarbital and/or furosemide
distributed in North America. It may appear
usage should be avoided or lin1ited, because
singly or in groups of several, near or on
tl1ese drugs increase toxicity.

wood in mixed woods in the spring/autumn.

The toxin is unknown, but it may cause
hypersensitivity over time, leading to kidney

MISCELLANEOUS POISONOUS
failure.

MUSHROOMS

Clinical Findings: Vomiting, diarrhea,
cardiovascular irregularity, and RBC

Ramaria flavo-brunnescens
destruction may be noted 1-3 hr after

Ramariaflavo-brunnescens is found
ingestion. Recovery generally takes 2-4
exclusively in eucalyptus woods in North
days but could be longer. Acquired

America, Australia, Brazil, and Uruguay, and
sensitivity develops over time.

is easily identified from fue spore print color
of pale buff to brownish yellow. It is

Diagnosis and Treatment: A diagnosis
reported to be poisonous to rUininants
can be made based on mushroom identifica

( cattle and sheep). The toxin is an unknown, tion, consistent clinical signs, and response volatile compound or compounds found
to supportive care. Treatment involves
throughout the plant that is reported to
symptomatic and supportive measures.

POISONOUS PLANTS

3103

POISONOUS PLANTS

VetBooks.ir

HOUSEPLANTS AND
which fom1 part of the normal range plant

ORNAMENTALS
conununity. Poisonous plants can be found
in most plant communities and should be

Plants are an important part of the decor of
considered in most grazing situations.

homes; pets having access to these plants

Livestock poisoning by plants often can
often chew on or ingest them, with toxicity a
be traced to problems of management or
possible outcome (see TABLE 7). Inquiries to range condition, rather than sin1ply to the
poison control centers on plants ingested by
presence of poisonous plants. Usually,
children <5 yr old are estimated at 5%--l()OA, of animals are poisoned because hunger or
all in qui.ties. Similar estimates ( although not
other conditions cause them to graze
documented) could be made for pets.

abnormally. Overgrazing, trucking, trailing,

Little research has been done on the
conalling, or introducing animals onto a
toxicity of houseplants. Most are hybrids,
new range tend to induce hunger or change
and selecting for growth outside their
behavior, and poisoning may occur.

natural environment could affect their

Not all poisonous plants are unpalatable,
degree of toxicity. Age of the pet, boredom,
and they are not restricted to overgrazed
and changes in the sunoundings are factors
ranges and pastures. Furthermore,
that may affect the incidence of poisoning.

poisonous plants do not al ways kill or

Puppies and kittens are very inquisitive, and
otherwise hann animals when conswned;
mouth or chew almost any and everything.

the dose detem1ines toxicity. Many plants

Pets ( especially single household pets) of all can be either useful forage or toxic. For ages may become bored or restless if left
exan1ple, plants such as lupine and
alone or confined for too long at any one
greasewood may be part of an anin1al's diet,
tin1e, and chewing on objects for relief is
and the animal is poisoned only when it
common. Pets of all ages also explore
consumes too much of the plant too fast.

changes in their environment ( eg, pets

To prevent poisoning, it is important to
collUl10nly chew the leaves or ripe berries
understand the factors involved when a
of potentially poisonous plants placed in
useful forage becomes a poisonous plant.

the home during holidays).

Definitive diagnosis of suspect plant
poisonings is difficult. It is important to be
fan1iliar with the poisonous plants growing

RANGE PLANTS OF TEMPERATE
in the specific area and the conditions under

NORTH AMERICA
which livestock may be poisoned. A
tentative diagnosis is possible if the

Poisonous plants are among the important
following information is available: 1) any
causes of economic loss to the livestock
local soil deficiencies or excesses ( which
industry and should be considered when
may complicate plant toxicities or sin1ply
evaluating illness and decreased productivconfuse as to cause of a syndrome), 2) the ity (see TABLE 8). Poisonous plants can affect syndromes associated with each of the
anin1als in many ways, including death,
poisonous plants in the area, 3) the time of
chronic illness and debilitation, decreased
year during which each is most likely to
weight gain, abortion, birth defects,
cause problems, 4) the detailed history of the
increased parturition interval, and
animal( s) over the last 6--8 mo, and 5) any
photosensitization. In addition to these
change of management or envirorunental
more obvious losses, other considerations
condition that may cause an animal to
include loss of forage, additional fencing,
change its diet or grazing habits (in some
increased labor and management costs,
cases, eg, locoism, this may be all that is
and frequently interference with proper
required in addition to identification of the
harvesting of forage.

plant involved). Identification of the plant is

Most poisonous range plants fall into
important, whatever its stage of growth, and
two general categories: those that are
is especially useful if it can be identified in
indigenous to a range and increase with
the stomach contents of the poisoned
heavy grazing, and those that invade after
animal. Chemical analysis of to xi cants often
overgrazing or disturbance of the land.

is not useful. Metabolic profiles are useful for

Among those not in these categories are
some toxicities, and in some, the necropsy
certain locoweeds and larkspurs, both of
lesions are distinctive ( see TABLE 8).

3104

POISONOUS PLANTS

•@�1111 POISONOUS HOUSEPLANTS AND ORNAMENTALS•

Scientific Name

(Family)

Common Name

Important Characteristics

Ab1us precalorius Rosary pea, Precatory

Climbing/twining vine on other objects

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(Fabaceae)

bean, Prayer beads,
as substratwn. Compound leaves/light

Crab's eye
sensitive, pale reddish purple flowers,
pea-shaped pods with 3 -5 red seeds with
black spots. Jewelry handicrafts as
souvenir gifts in homes.

Adenium obesum Desert rose, Mock

Succulent shrubs or small trees.

(Apocynaceae)

azalea, Desert azalea

Perennials, milky viscous sap with fleshy
swollen sterns. Simple, fleshy to leathery,
lanceolate, dark leaves. Showy flower
clusters-red petals with pink or white
centers at tip of branch. Fruits-follicles
with many seeds. Houseplant grown
outside in dry, hot locations.

Agapanlhus

African blue lily,

Grows to a height of -2 ft in large

01ienlal'is

Blue African lily
containers. Perennial herbs with simple,

(Liliaceae)

herut-shaped, thin, highlighted veins,
variegated leaves; yellow-green spathe;
grown from rhizomes.

Agave ammicana Century plant,

Clumps of thick, long strap-shaped blue/

(Agavaceae)

American aloe
green leaves with hook (margin) and
pointed spines (tip). Central flower stalk
with small tubular flowers in clusters.

Aglaonema

Chinese evergreen,

Central stem with solid medium green or
modes tum

Painted drop tongue
splotched gray/green leaves; small

(Araceae)

greenish flowers.

Allamanda

Allamanda, Yellow

Ornamental, sprawling, woody climbing
calhartica
allan'landa
shrub with large yellow flowers: opposite

( Apocynaceae)

lance-shaped leaves: fruitless.

Alocasia spp

Elephant's ear

Erect perennials from rwming rhizomes;

(Araceae)

single, long-stemmed, spear-headed
varicolored leaves; prominent veins.

Aloe barbadensis Barbados aloe, Cw-acao Succulent herb with cluster of narrow (Liliaceae)

aloe
fleshy, spinous or coarsely serrated
margin leaves, with hook spines on leaf
margin. Dense spiked tubular yellow
flowers at end of single stalk.

POISONOUS PLANTS

3105

POISONOUS HOUSEPLANTS AND ORNAMENTALS• (contin,,ed) Comments and Toxic Principles and Effects

Treatment

Abrin, a plant lectin (taxalburnin) related to ricin Ingested whole intact seeds

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in hard seed coat, released when chewed on or
nontoxic in most cases. GI
otherwise broken. Toxin inhibits celluar protein
clinical signs; assess dehydration
synthesis.

and electrolyte status. Electrolyte
replacement therapy in severe
cases.

Cardioactive steroids and cardiac glycosides

Syn1ptomatic
throughout entire plant. Na+/K+ ATPase inhibition,
increased intracellular Ca2+ leading to myocardial
excitation, bradycardia, ventricular tachycardia/
fibrillation and heart block, hyperkalemia,
abdominal distress, vomiting, anorexia, and
inactivity.

Unknown toxin(s) but thought to be a sticky, acrid, Symptomatic irritant latex rather than allergens. Calcium oxalate crystals and unknowns found in all parts, especially rhizomes. Ingestion causes immediate intense pain,
local irritation to mucous membranes, excess
salivation, swollen tongue and pharynx, diarrhea,
and dyspnea. Pets' access to plant associated with
rhizomes brought indoors for winter storage.

Sap contains calcium oxalate crystals; saponins and Symptomatic acrid volatile oil in leaves and seeds. On ingestion, causes dermal and oral mucosa! irritation and
edema.

The entire plant contains calcium oxalate crystals.

Symptomatic

On ingestion, causes oral mucosa! irritation and
edema.

Contains plumericin, a GI irritant found in the bark, Based on exposure dose (abdominal leaves, fruit, seeds, and sap.

discomfort, diarrhea, dehydration,
and electrolyte inlbalance).

Symptomatic therapy (rehydration
and electrolyte replacement) in
severe cases.

Water-insoluble calcitun oxalate and possible

Burning/painful/inflammatory
proteinaceous toxins (raphides) in leaves, stems,
reaction in mouth on ingestion.

and tubers.

Analgesics and/or demulcents may
be indicated. Systemic reaction to
insoluble calcium oxalate not
reported.

Contains anthraquinone glycosides (barbaloin,

Symptomatic; control diaremodin) and chrysophanic acid in the latex of the rhea and fluid loss.

leaves; higher concentrations in younger leaves. On
ingestion, causes abrupt, severe diarrhea and/or
hypoglycemia, with vomiting in some cases.

(contin1led)

3106

POISONOUS PLANTS

•M=iiD POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Scientific Name

(Family)

Common Name

Important Characteristics

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Anlhurium spp

Antl1w·iwn, Flamingo

Dark green or shiny broad heait-shaped,

(Araceae)

lily, Flamingo flower,
lealliery leaves; a persistent white/

Tail flower
scat-let/green spike; flowering, colorful
berries.

Arumspp

Italian arwn, Black

Stemless plant with large ovate leaves

(Araceae)

calla, Starch root,
and tuberous roots; showy flower, purple

Cuckoopint
enclosing a spike having red fruits;
conm10n houseplant of Europe/Near

East origin.

Aucubajaponica Japanese aucuba,

Cultivated as an omai11ental and house

(Cornaceae)

Japanese laurel,
plant (large bush) witl1 coaisely toollied,

Spotted laurel
large opposite leaves; purple flowers in
panicle at end of branches; scarlet berry,
single seed fruit; ma.tmes in eai·ly winter.

Brurifei,sia

Yesterday-today-and

Evergreen shrubs to small trees willi
paucijlora
tomorrow, Lady-of-llie alternate, undivided, tootltless, lliick, fioribunda
night
ra.llier lea.lliery, lustrous leaves. Winter

(Solanaceae)

blooming; large showy sometimes
fragrant flowers, clustered or solitary at
the branch ends, willi 5-lobed tubular
calyx, 5 petals, and funnel-shaped corolla.

Fruits berry-like capsules.

Caladium spp

Caladiwn, Fancy leaf

Perennial herbs willi simple, heatt

(Araceae)

caladiurn, Angel wings
shaped, lliin, highlighted veins, variegated leaves; yellow-green spa.llie; grown from rhizomes.

Cannabis saliva !Vlary Jane, Marijuana.,

Annual herb, grown from seeds, ;:,6 ft tall.

(Cannabaceae)

Grass, Pot, Hashish,

Leaves opposite or alternate, palma.tely

Indian hemp, Reefer,
compound willi 5-7 linea.r, coatSely

Weed
dentate leaflets; small green flowers at tip

(male) or along entire lenglli (female) of
branch; fruits achenes. Grown for its
fiber; legally cultivated under federal
license only in most states.

Capsicum

Cherry pepper, Chili

Annual shrub; brat1ched, erect stem;
annuu1n
pepper, Ornamental
dark, glossy, ovate, entire margin leaves;

(Solanaceae)

pepper, Capsicwn
white flowers. Fruits a.re shiny berries of
vai·ious colors, shapes, sizes.

POISONOUS PLANTS

3107

•tJ:iiD POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Comments and Toxic Principles and Effects

Treatment

Native to tropical America (co nun on houseplant);

On ingestion, painful/burning

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raphides (water-insoluble calcium oxalate and
sensation and inflanm1ation of oral
proteinaceous toxins) in leaves and stems.

cavity. Remove from source;
symptomatic treatment helpful, but
clinical signs subside over time.

Entire plant contains yet to be identified GI toxin

Analgesics for oral mucosa!

( once thought to be calcium oxalate); dose-dependirritation and pain, rehydration, ent mucous membrane irritation, ulcerations,
antiemetics, and electrolyte
abdominal discomfort, vomiting, diarrhea, and
replacement as needed.

dehydration.

Aucubin (acid labile glycoside) found throughout

None in small dose exposure
the plant ( concentrated in fruit, which is colorful cases. Rehydration, antiemetics,
and to which pets are attracted). Large exposure
and electrolyte replacement may
dose required for toxicity (GI discomfort).

be necessary in severely affected
cases.

Alkaloid components (atropine, scopolamine,

In severely depressed animals,
hyoscyamine) found in the flowers, leaves, bark,
stimulants (respiratory and
and roots. On ingestion, animals show tachycardiac), along with supportive cardia, dry mouth, dilated pupils, ataxia, tremors,
therapy recommended.

depression, urinary retention, and sometimes coma

(deep sedation). Not reported to cause death.

Calciwn oxalate crystals and unknowns found in

Symptomatic
all parts, especially rhizomes. Ingestion causes
immediate intense pain, local irritation to mucous
membranes, excess salivation, swollen tongue and
pharynx, diarrhea, and dyspnea. Pets' access to
plant associated with rhizomes brought indoors
for winter storage.

Leaves, stems, and flower buds of mature plants

Remove animal from source.

contain tetrahydrocannabi.nol (THC) and related

Effectiveness of emetics limited
compounds. THC concentrations vary with plant
by antiemetic effect of THC. Oral
variety (1 o/<Hl%), parts (female flowers have highest tannic acid, activated charcoal,
concentrations), processing ( extracts have as much followed by saline cathartics have as 28"!6), sex, and growing conditions. Lethal dose for been recommended. Stimulants dogs >3 g/kg body wt. Pets' exposure usually from ( cardiac and respiratory) along
accidental access to this plant being used for
with supportive therapy essential
in-home treatment of cancer patient or for illegal
in severely depressed animals.

(in most states) recreational uses by owner. Pets

Recovery slow at best. See also

( dogs primarily) show ataxia, vomiting, mydriasis,
p 3041.

prolonged depression, tachycardia or bradycardia,
salivation, hyperexcitability, tremors, and hypothermia. Death results when vital CNS regulatory centers are severely depressed.

Capsaicinoids (capsaicin) in the mature frnits,

Symptomatic; irritation reliefsolanine and scopoletin in foliage; irritating to the cool water irrigation, topical or

GI tract, with vomiting and diarrhea. Not likely to
oral mineral or vegetable oil.

be lethal.

Rarely topical anesthetics.

(continued)

3108

POISONOUS PLANTS

POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Scientific Name

(Family)

Common Name

Important Characteristics

CaUwranthus

Madagascar periwinkle, Perennial herb with milky sap; erect VetBooks.ir
reseus

Bigleafperiwinkle,
stems with glossy green opposite leaves;

( Apocynaceae)

Vinca, Large periwinkle solitary rose-pink to white flowers.

Cultivated as an ornamental.

Chlorophytwn

Spider plant, St.

Rhizomatous herbs with leaves slightly
spp (Liliaceae)

Bernard's lily,
glossy, succulent, narrow, strap-like,

Airplane plant
green-some with a broad, yellow, or
white band down the middle; long,
cream, hanging stems with small, white
flowers developing into plantlets. Often
grown in hanging baskets.

Colchicwn

Autumn crocus, Crocus, Popular house or yard plant, perennial autwnnale

Fall crocus, Meadow
herb, ovoid w1derground corm covered

(Liliaceae,
saffron, Wonder bulb
with brown membrane or scales. Leaves

Colchicaceae)

large, lanceolate, basal, ovate, smooth,
ribbed, appear in spring and die back
before flowering. Flowers tubular,
solitary, pale purple or white appearing in
fall; fruit a 3-celled ovoid capsule with
numerous seeds.

Convalla1ia

Lily-of-the-valley,

Herbaceous perennial from slender
majalis

Conval lily, Mayflower
running rhizome; stern leafless, bearing

(Liliaceae)

a 1-sided raceme of nodding white,
aromatic, bell-shaped flowers; leaves 2 or

3, basal to 1 ft long. Fruit a red berry but
seldom formed.

Cyclamen spp

Cycfamen, Snowbread, Herbaceous plants, grown from rhizomes (Primulaceae)

Shooting star
or tubers. Petioled, heart-shaped, deep
green intermixed with lighter green
coloration (san1e leaf), serrated leaves;
stems upright, with a terminal pink or
white butterfly-like flower.

Dieffen/Jachia spp Dumbcane

Fairly tall, erect, rmbranched, fleshy

(Araceae)

plant; stem girdled with leaf scars; leaves
large, thickly veined, sheath-like petioles,
white or yellow spots on blade.

POISONOUS PLANTS

3109

•M9f H POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Comments and Toxic Principles and Effects

Treatment

Vin ca alkaloids (vincristine/vinblastine) throughout Aggressive supportive and VetBooks.ir
the plant inhibit microtubule formation. Toxic
symptomatic therapy essential,
exposures lead to pharyngeal pain, GI signs
with extended monitoring.

(abdominal pain, severe diarrhea), dehydration,
peripheral nerve damage, bone marrow suppression/depression, and cardiovascular damage.

More commonly grown for its filtering ability. Pets

Symptomatic

(especially cats) reach these plants either by
climbing or when plantlets fall from mature stems.

Unknown toxin(s) found in leaves and plantlets.

Vomiting, salivation, retching, and transient
anorexia seen in cats within hours of ingestion.

Deaths and diarrhea not reported.

Colchicine and related alkaloids found throughout Prolonged course due to slow plant. These alkaloids are heat stable and not
excretion of colchicine. Gastric
affected by drying. Colchicine is used experimenlavage; supportive care for tally in genetic investigations, and medically in the dehydration and electrolyte losses treatment of gout in people. It is cun1Ulative and

(fluid therapy); CNS, circulatory,
slowly excreted. Milk of lactating animals is a major and respiratory disturbances.

excretory pathway. Clinical signs include thirst,

Analgesics and atropine recomdifficult swallowing, abdominal pain, profuse mended for abdominal pain and
vomiting and diarrhea, weakness, and shock within diarrhea.

hours of ingestion. Death from respiratory failure.

Cardiac glycosides (convallarin, convallamarin,

Aimed at gut decontamination
convallatoxin), irritant saponins found in leaves,

(gastric lavage) and at correcting
flowers, rhizome, and water in which flowers have
bradycardia (atropine), conducbeen kept. Variable latent period depending on tion defects (phenytoin), and
dose. GI signs (vomiting, trembling, abdominal
electrolyte imbalance such as
pain, diarrhea), progressive cardiac irregularities
hyperkalemia (IV electrolytes).

(irregular heart beats, AV block), and death.

Electrocardiographic and serum

Hyperkalemia in acute cases. Gastroenteritis,
potassiwn monitoring necessary.

petechial hemorrhages throughout.

Triterpinoid saponins found in tuberous rhizomes

Symptomatic
cause GI irritation, thereby increasing systemic
absorption and severe toxicity. Anorexia, diarrhea,
convulsions, and paralysis are observed clinical
signs. Pets have greater access to these plants over winter months (both pets and plants are indoors).

Calcium oxalate crystals and unknown toxic

Symptomatic
proteins (possibly asparagine or protoanemonin) in
all parts, including sap. On ingestion, immediate
intense pain, burning, and inflanunation of mouth
and throat, anorexia, vomiting, and possibly
diarrhea, with tongue extended, head shaking,
excessive salivation, and dyspnea. Immediate pain
limits amount consun1ed. Death infrequent.

(continued)

3110

POISONOUS PLANTS

•&H•D POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Scientific Name

(Family)

Common Name

Important Characteristics

Digitalis

Foxglove

Erect biennial with simple, petioled (long

VetBooks.ir
piupurea
on lower, short or sessile on upper),

(Scrophulariac)

alternate, toothed, hairy, ovate to
lanceolate leaves. Purple, pink, red,
white, or yellow tubular flowers (with
spots) in terminal racemes; fruit is a
capsule with many seeds.

Dracaena spp

Dragon tree

Robust, palm-like houseplant with

(Agavaceae)

lance-shaped, thin, variegated, alternate,
non-petioled leaves. Yellow, red, or green
stripes along leaf margins in some
species. Lower leaves are lost, leaf scars
remain and clearly demarcated, tern1inal
leaves retained as plant matures.

Epipremnum

Golden pathos, Hunter's Climbing vine with large heart-shaped aureum
robe, Taro vine,
yellow streaked leaves. Outdoor plants in

(Araceae)

Amarillo
the tropics, indoor potted plant (leaves
are much smaller).

Euphorbia

Poinsettia, Christ

Perennial shrub with milky, whlte sap
pulcherrima
mas flower, Christmas
throughout. Leaves alternate, petioled,

(Euphorbiaceae) star
distinctly veined, entire or lobed, and
conspicuously bright red, pink, or whlte

(terminal leaves), lower leaves remain
green. Flowers small and inconspicuous.

Ficusspp

Weeping fig, Rubber

Numerous species (trees/shrubs/ vines)

(Moraceae)

tree, Climbing fig
within the family. Milky sap (leaves,
stems) in all. Commonly cultivated as
potted and/or indoor landscape
houseplants.

Hederaspp

Canary ivy, English ivy, Climbing vine (wall cover); leaves with (Araliaceae)

Common ivy

5 lobes on young and root-free stems;
non-lobed leaves (mature sections and
root-free stems). Fruits are black berries
when mature. Plant escapes cultivation;
common houseplants.

Hyacinthus spp

Hyacinths

Garden ornan1entals that grow from

(Liliaceae)

bulbs (close resemblance to onion bulbs)

and flower in early spring. Bulbs harvested and stored in fall for replanting in spring.

flex aquifolium

English holly, Euro

Evergreen shrub with leaves leathery,

(Aquifoliaceae)

pean holly
glossy upper surface, spiny toothed,
alternate, and petioled; fruits red to
yellow berries with many seeds and
aromatic taste.

POISONOUS PLANTS

3111

•0:i!fi POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Comments and Toxic Principles and Effects

Treatment

Cardiac glycosides ( digitoxin, digitalin, digoxin,

Symptomatic

VetBooks.ir
and others), saponins, and alkaloids found
throughout plant. Potency not affected by d1ying.

Generally, acute abdominal pain, vomiting, bloody
diarrhea, frequent urination, irregular slow pulse,
tremors, convulsions, and rarely death.

Alkaloids, saponins, and resin found in leaves.

Symptomatic, to correct fluid and

Vomiting and severe diarrhea indicative of GI
electrolyte imbalance.

irritation expected. Clinical cases have not been
reported.

Entire plant is poisonous. Contains water-insoluble Oral pain resolves slowly without calcium oxalate raphides and unknown proteinatreatment. ln severe cases, ceous toxins throughout. Causes immediate intense demulcents and analgesics may be pain (oral cavity) on chewing any portion of plant.

indicated. Systemic involvement,
if any, is not associated with
raphide chewing and release of
insoluble calciw11 oxalate.

Milky sap contains unknown toxic principle(s);

Symptomatic; gastric lavage,
irritates mucous membranes and causes excessive activated charcoal, and saline salivation and vomiting but not death. Toxicity
cathartics should be considered.

(hybrid species) not supported experimentally.

Toxic diterpenes (ingenol derivatives) found in
other Euphorbia spp have not been found in this species.

Furocownarins, psoralens, ficin, sesquiterpinoid

Symptomatic and supportive ca.re
glycoside, and triterpines are found in sap and
as needed.

implicated (although not clear) in dermatologic
toxicity ( contact dermatitis) in pets/people.

Hederin, a saponin found in berries and leaves.

Concerns GI-associated problems

Toxin poorly absorbed on ingestion; therefore,

( dehydration, vomiting, and
limited toxic effects observed. Large exposure
electrolyte disturbances). Correct
dose results in GI effects (abdominal discomfort,
dehydration; antiemetics and
diarrhea). Allergic sensitization conunon in people electrolyte supplementation.

( contact dermatitis).

Calciun1 oxalate c1ystals and alkaloids (toxic poten Symptomatic tial yet to be defined) fow1d in bulbs. After ingestion of toxic dose (bulbs), vomiting, diarrhea, and rare
deaths reported. Bulbs in storage may be accessible
to pets.

Saponins; an alkaloid (theobromine ), triterpene

Symptomatic (at best)

compounds, and unknown compounds with digitalislike cardiotonic activity have been found in leaves, fruits, and seeds. Abdominal pain, vomiting, and
diarrhea seen after ingestion of �2 berries. Death rare.

(continued)

3112

POISONOUS PLANTS

•M:J!D POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Scientific Name

(Family)

Common Name

Important Characteristics

Kalanchoe spp

Kalanchoe, Air plant,

Winter flowering, herbaceous, succulent,

VetBooks.ir

(Crassulaceae)

Cathedral bells
nonhardy annuals or perennials. Fleshy,
serrate or crenate, opposite, petioled
leaves. Bright red, orange, or pink
flowers in umbel. Stems become woody
and untidy with age.

Lilium longijlo

Easter lily, Tnunpet lily Plants grown from bulbs; leaves alternate rum, L tigrinum
or whorled, sessile, linear or lanceolate

(Liliaceae)

blades; large showy funnel-form flowers.

Fruits capsules with numerous, flat
seeds.

Narcissus spp

Daffodils,

Plant grown from bulb with leaves

(Amaryllidaceae) Amaryllis,
arising from ground. Flower(s) white or

Naked lady lily
yellow arising from stalk. Plant grows
from bulb ( extends partially above
ground). Flowers of various colors, red,
pink, and white most common.

Persea americana Avocado pear, Alligator Trees or shrubs with long branches (Lauraceae)

pear
arising from tenninal buds, widely
cultivated for its fruits. Three commonly
cultivated races (Mexican, Guatemalan,
and West Indies). Leaves ovate-elliptical,
entire, alternate, veined, dark-green
above and paler below, papery to the feel.

Flowers inconspicuous, yellow-green in
axillary or terminal panicles; fruit berry,
ovoid to pyriform in shape with thick,
leathery, glossy dark green skin over
lime-green to yellow flesh and a smooth,
ovoid, solitary seed.

Ph'ilodendron spp Philodendron

Climbing vines with aerial roots; leaves

(Araceae)

(major attraction as a houseplant) are
large, unlobed or µinnately lobed and
heart-shaped; rarely flowering.

Phoradendron

Mistletoe

Perennial parasitic shrub that grows
jlavescens
on deciduous trees. Evergreen, ovoid,

(Viscaceae)

opposite leaves on round, highly
branched, green stem. White berries with
single seed. Brought into homes during

Cluistmas season.

Rhododendron

Azalea, Rhododendron Evergreen or deciduous shrub with spp (Ericaceae)

simple, alternate, entire leaves; funnelshaped flowers in terminal umbel-like clusters or solitary and of various colors;
fruits are capsules with many seeds.

POISONOUS PLANTS

3113

•@=iifl POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Comments and Toxic Principles and Effects

Treatment

VetBooks.ir

Cardiac glycosides found in leaves. Within hours of Symptomatic; atropine has been ingesting toxic dose, depression, rapid breathing,
effective in rabbits.

teeth grinding, ataxia, paralysis, opisthotonos

(rabbit), and death (rat).

Unknown toxin found throughout plants. Renal

Emetics, activated charcoal,
failure in cats 2-4 days after ingestion. Not reported saline cathaitic, and nursing toxic to other species. Vomiting, depression, loss of care-as for renal failure-within appetite within 12 hr after ingestion. Increased
hours of ingestion. Delayed
creatinine, BUN, phosphorus, and potassium
treatment is associated with poor
indicate toxicity.

prognosis.

Bulbs are poisonous; contain lycorine and related

Most exposures result in limited
phenanthridine alkaloids. If small dose ingested,
toxic responses and resolve
few or no clinical signs; if large-dose exposure,
without treatment. In large-dose
vomiting, abdominal discomfort, diarrhea,
exposure, symptomatic treatment
dehydration, and electrolyte imbalance.

with rehydration, antiemetics,
electrolyte replacement.

All above-ground parts (leaves in particular)

Primarily symptomatic and
reported toxic to cattle, horses, goats, rabbits,
supportive (seep 2964).

canaries, ostriches, and fish. Responsible toxin a
monoglyceride. Oil found in fruits used for cosmetic purposes. Toxicity associated with noninfectious
agalactia ( cattle, rabbits, goats), pulmonary
congestion, cardiac arrhythmia, submandibular
edema, acute death (rabbits, caged birds, goats),
respiratory distress, generalized congestion,
subcutaneous edema, and hydrope1icardiurn

(suggestive of cardiac failure [ caged birds]). In caged birds, clinical signs may be seen within 24 hr ( usually after �12 hr), with death 1-2 days after exposure.

Calcium oxalate crystals and unidentified proteins Symptomatic throughout entire plant. On ingestion, immediate
pain, local irritation to mucous membranes,
excessive salivation, edematous tongue and
pharynx, dyspnea, and renal failure. Excitability,
nervous spasms, convulsions, and occasional
encephalitis repmted in cats.

Amines ([3-phenylethylamine, acetylcholine,

Symptomatic
choline, and tyramine), toxic proteins (viscotoxins), and unknowns in all parts. Vomiting, profuse diarrhea, dilated pupils, rapid labored breathing,
shock, and death from cardiovascular collapse
within hours of ingesting toxic dose.

Andromedotoxins (grayanotoxins) fotu1d in all

Symptomatic; gastric lavage,
pa.its, including pollen ai1d nectar. Within hours
activated charcoal, saline
of ingestion of toxic dose (1 glkg), salivation,
cathartics, calcium injection, and
lacrimation, vomiting, diai-:rhea, dyspnea, muscle
antibiotics to control possible
weakness, convulsions, coma, and death. Signs
pnelUllonia suggested.

may last several days, but toxin is not cumulative.

( continued)

3114

POISONOUS PLANTS

•tM•fl POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Scientific Name

(Family)

Common Name

Important Characteristics

VetBooks.ir

Sansevieria spp

Sansevieria, Snake

Hardy, succulent houseplant. Leaves

(Agavaceae)

plant, Mother-in-law's
erect, elongate, lanceolate, and flat or
tongue
cylindrical, dark green with or without
a yellow stripe along the margins, and
horizontal gray bands throughout; many
yellow star-like flowers on tall central
raceme or spike.

Schejfiera spp

Schefflera, Umbrella

Fast-growing evergreen with glossy,

(Araliaceae)

tree
palmately compound leaves that hang
and spread, appearing like an umbrella.

Depending on the species, leaflets
increase with plant maturity and become
more compact; veins pronounced;
margins entire to slightly crenate.

Solanum

Jerusalem cherry

Shrub with simple, lanceolate, entire
pseudocapsicum
or slightly serrated leaves. Small, star

(Solanaceae)

shaped white flowers. Ripe fmits are red,
shiny berries with many white seeds.

Taxusspp

Yew

Evergreen tree or small erect shmb with

(Taxaceae)

alternate, needle-like, glossy (upper
surface), dull (lower surface) leaves.

Seeds (generally one per fruit) blackbrown or green, nearly enclosed in a cup-shaped, fleshy, red covering (aril).

Zamia pumila

Coontie, Florida

Palm-like plant with thick underground

(Zamiaceae)

arrowroot, Seminole
fleshy, tuberous stem from which grow
bread, Cycad
few pinnately compound, palm-like
leaves -2 ft long; cones containing
inch-long, shiny, orange-red seeds.

a Images for many of the plants described here, as well as for plants of Australia, the Catibbean, and South Africa, ai·e available online at www.merckvetmanual.com.

POISONOUS PLANTS

3115

•MiiM POISONOUS HOUSEPLANTS AND ORNAMENTALS• (continued) Comments and Toxic Principles and Effects

Treatment

VetBooks.ir

Hemolytic saponin and organic acids found in

Symptomatic; fluids and electroleaves and flowers. Vomiting, salivation, diarrhea, lytes may be necessary.

and hemolysis related to GI activity of these
compounds.

Oxalate found in the leaves. Mucous membrane

Symptomatic
irritation, salivation, anorexia, vomiting, and if
severe enough, diarrhea.

Solanocapsine and related alkaloids found in leaves Symptomatic; gastric lavage, and fruits. Anorexia, abdominal pain, vomiting,
activated charcoal, electrolytes
hemo1Thagic diarrhea, salivation, progressive
and fluids, and anticonvulsants
weakness or paralysis, dyspnea, bradycardia,
suggested.

circulatory collapse, dilated pupils, and convulsions reported.

The alkaloids (taxines and ephedrine), cyanide, and Symptomatic at best; usually futile volatile oils found throughout plant except the
once clinical signs appear.

fleshy aril. Nervousness, trembling, ataxia, dyspnea, Atropine may be helpful.

collapse; bradycardia progressing to cardiac
standstill and death without struggle. Empty right
side of heart; dark, tarry blood in left side of heart; limited nonspecific postmortem lesions.

The glucoside cycasin and its aglycone methyl

No specific therapy; IV fluids and
azoxyrnethanol (a colon-specific carcinogen in
symptomatic care recommended.

mice) found in leaves, seeds, and stem. Ingestion
associated with hepatic and GI disturbances and
ataxia. Clinical signs are persistent vomiting,
diarrhea, abdominal pain, depression, and muscular
paralysis. A nemologic condition characterized by
hindleg paralysis (hyperextension followed by
incomplete extension) has been reported in cattle.

3116

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA•

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGER OUS SEASON: SPRING AND FALL

Allarnanda cathartica, Native to tropical America (2

Sheep, cattle, and goats

A blanchetti
cultivated taxa in North America);

(Apocynaceae)

indoors and as ornamentals.

Allamanda, Yellow
allamanda, Golden
trumpet, Purple
allamanda

Cicutaspp

Open, moist to wet environments;

All

Water hemlock
throughout North America

Hyrnenoxys odorata

Roadways, lakebeds, flooded areas, Sheep, rarely cattle Bitterweed
overgrazed range; southwest

Hyrnenoxys

Arid foothills (6,000-8,000 ft

Sheep, cattle, goats
richardsonii

[l,800-2,400 ml); western

Pingue, Colorado
rubber weed

Oxalisspp,

Herb/ornamentals found as weeds,

Sheep, rarely cattle

O corniculata
growing from rhizomes/bulbs in

(Oxalidaceae)

fields and/or grazing pasture;

Wood sorrel, Creeping worldwide
lady's sorrel, Creeping
yellow wood sorrel

POISONOUS PLANTS

3117

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (conti,wed)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SPRING AND FALL

Perennial, evergreen

The entire plant contains alkylir_i

Supportive, antidiarshrub, climbing; leaves doid-type terpinoids (allamandin, rheals
simple, whorled;
qallamandin, allamandacin), iridioids
leathery, margins
plumericin and plumieride, and little
entire, axillary glands cardiotoxin. GI irritants in all parts at base; large showy,

(highest concentrations in the sap
yellow or purple petal and roots). On ingestion, causes flowers; fruit is spiny
excess salivation, ruminal atony,
capsule with numerabdominal cramps, diarrhea,
ous winged seeds.

dehydration, and electrolyte
imbalance. Little cardiotoxic effects
and no deaths. Lethal dose (fresh
foliage) in cattle is 30 g/kg body wt.

White flower, umbels. Resinoids (cicutoxin, cicutol) in Sedatives to control

Veins of leaflets ending roots, stem base, young leaves.

spasm and heait action.

at notches. Stems

Toxicity retained when dry, except in Prognosis good if alive hollow except at
hay. Rapid onset of clinical signs,

2 hr after ingestion.

nodes. Tuberous roots with death in 15-30 min. Salivation, from chambered
muscular twitching, dilated pupils.

rootstock.

Violent convulsions, coma, death.

Poisoning in people common.

Multibranched annual Sesquiterpene lactone (hymeno

Toxin cumulative.

or perennial up to 2 ft vin) in fresh or dry plant. Salivation, Avoid overgrazing.

high. Yellow flower
vomiting, green nasal discharge,

Remove from pasture.

head. Leaves divided
depression, anorexia, abdominal
into narrow glandupain. Lesions include inflan1mation lar segments.

of GI tract, foreign body pneumonia,
renal degeneration.

Perennial herb. Leaves San1e as for H odorala (above).

Same as for H odorata.

bright green, divided
into narrow glandular
segments.

Annual/perennial with High oxalate contents throughParenteral calcium
palmately compound
out. Acute, subacute, or chronic
solution. Supportive
leaves with 3 leaflets
manifestation after chronic
care to allow for
on erect or ascending ingestion. Clinical signs-progrestubular regeneration.

stem. Inflorescence
sion from depression, weakness,
cymes or umbel or
labored respiration to prostration,
solitary flower; fruits
coma, and death in 1-2 days in
are capsules with
acute cases. Chronic cases-weight
many seeds and basal loss, anorexia, polyuria, edema, ariels.

increased BUN and creatinine
levels, failure to concentrate urine,
presence of oxalate crystals in
urine sediments, and renal failure.

(continued)

3118

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: SPRING AND FALL (continued)

Zephyranlhes

Ornamental, commonly grows from Horses, cattle, and alamasco
bulbs in low woods and wet
indoor pets (cats)

(Amaryllidaceae)

meadow areas.

Atamasco lily, Rain lily,

Zephyr lily, Easter lily

DANGEROUS SEASON: SPRING

Baplisia spp (Papilio

Open woods in Eastern North

Horses, cattle, goats
noideae, Leguminosae, America on clay, loam, and sandy Fabaceae)

soils

False indigo, Wild
indigo, Rattle weed,

Yellow indigo, Indigo
weed

Caesalpinia spp

Grown in the tropics in dry, open

Cattle, sheep, prob

(Leguminosae)

shrub or lowland rain forest. Found ably horses

Nikals, Grey nicker
in southwestern USA. Ornamentals
bean
cultivated in warmer areas.

Nolina lexana

Open areas on rolling hills and

Cattle, sheep, goats

Sacahuista, Beargrass
slopes; southwest USA and Mexico

POISONOUS PLANTS

3119

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SPRING AND FALL (continued)

Basal leaves with

Phenanthridine (lycorine, tazet-

Prompt resolution of
star-shaped white
tine) and other alkaloids primarily in dermatologic signs with flowers turning pink
the bulbs but also in the leaves and
discontinued exposure.

on fading.

flowers. Anticholinergic-type effects Supportive care

(inhibitor of protein synthesis,
antiemetics, antidiardecreases heart rate, and cardiac ab rheals, and electrolyte normalities) in cats. Vomiting, excess replacement. Rarely salivation, bloody diarrhea ( dehydra lethal.

tion and electrolyte imbalance),
seizures, cardiac function changes,
and dennatitis.

DANGEROUS SEASON: SPRING

Herbaceous perenni

Contains quinolizidine alkaloid

Remove anin1als from
als, branched solitary cystisine, pyridine alkaloids plant source.Syn1ptostem, palmately
anagyrine and baptifoline, and other matic and supportcompound sessile/
related nicotine-like alkaloids.

ive care.

short petiole, 3-leaflet Interact with nicotinic, muscarinic, leaves; terminal or
and acetylcholinergic receptors. On
axillary raceme
ingestion, causes severe diarrhea in
inflorescence. Flowers cattle, decreased appetite, excess with variably colored
salivation, incoordination, and
petals; legumes
tremors. Fetal anomalies can be
stipitate with one to
produced.

many seeds. Plants
black-gray or silvery
gray when dry in the
field or as hay.

Perennial tree,shrub, Gallotannins (30%---50%), phyto

Supportive care-IV
or herb armed with
hemagglutinins in fruit and flowers
fluids, electrolytes,
thorns, erect or
and diterpenoids pulcherralpin and
antiemetics, and
climbing stem, 2
caesalpin in the leaves. Within a few antidiarrheals.

pinnately compound
hours of ingestion, animals show
leaves, terminal
vomiting, ± bloody diarrhea,
racemes, showy
abdominal discomfort, and
yellow to orange or red dehydration. Not reported to cause flowers, legumes ovate death.

with 2 to many seeds.

Perennial with many

Unidentified hepatotoxin (buds,

Remove animals from
clustered, long narrow flowers, fruit). Photosensitization, area where plant grows
leaves. Stem mostly
anorexia, icterus, prostration. Dark
during blooming
underground. Several urine, yellowish discharge from eyes, season. Oral daily zinc flower stems with
nostrils. Lesions include hepatic and oxide (not zinc sulfate) many small, white
renal degeneration, GI inflammation. supplementation at 30
flowers in clusters.

mg/kg body wt appears
promising. (See also

PHOTOSENSITIZATION,
p 976).

(continued)

3120

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: SPRING (continued)

Peganum harmala

Arid to semiarid ranges; western

Cattle, sheep, probably

African rue

USA
horses and camels

Phytolacca ameiicana Distmbed rich soils such as recent Pigs, cattle, sheep,

Pokeweed, Poke
clearings, pastures, waste areas;
horses, people
eastern half of USA

Quercus spp

Most deciduous woods; throughout All grazing animals, Oaks

North America
mostly cattle

Sarcobatus

Alkaline or saline bottom soils, not Sheep, cattle
veimiculatus
in higher mow1tains; arid west.

Greasewood, Black

Dangerous season spring; may be
grease wood
year-row1d.

X an lhimn spp

Fields, waste places, exposed

All animals, more

Cocklebur
shores of ponds or rivers; throughcommon in pigs
out North America. Dangerous
season spring and occasionally fall.

POISONOUS PLANTS

3121

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

'Ireatment

DANGEROUS SEASON: SPRING (continued)

Multibranched, leafy,

Related 13-ca.rboline indole alkaloids

Unpalatable. Eaten
perennial, bright

(seeds, leaves, stems; seeds more
only under drought
green, succulent herb. toxic). Anorexia, hindleg weakness, conditions. General

Leaves divided.

knuckling of fetlock, listlessness,
supportive care most

Flowers white, single. excess salivation, subnonnal helpful.

temperature, pollakiuria. Lesions
include gastroente1itis, with
hemotThages on heart and under
liver capsule.

Tall (to 9 ft), glabrous, Oxalic acid, a saponin (phytolacca

No specific remedy for
green, red-purple,
toxin ), and an alkaloid (phytolaccin) intoxication. Supportperennial herbs.

in a.II parts; roots most toxic.

ive and symptomatic

Berries black-purple,

Vomiting, abdominal pain, bloody
care helpful. Monitor
staining, in drooping
diarrhea, hemolytic anemia, drop in
for hypotension and
racemes.

production (dairy cattle). Terminal
other cardiac effects.

convulsions, death from respiratory Oils and protectants (GI failure. Lesions include ulcerative
tract). Dilute acetic
gastritis, mucosal hemorrhage, dark acid PO, stimulants.

liver.

Blood transfusion

(hemolytic anemia).

Mostly deciduous

Gallotannin thought to be the toxin

Diet must consist of >500/o
trees, rarely shrubs,

(young leaves and swollen or
oak buds and young
with 2-4 leaves
sprouting acorn). Anorexia, rumen
leaves for a period of
clustered at tips of all
stasis, constipation, followed by dark tin1e. Increased BUN with twigs. Diverse leaf
tarry diarrhea, dry muzzle, frequent
diet history diagnostic.

shape. Acorn fruiting
urination, rapid weak pulse, death.

Treatment symptomatic.

body.

Lesions include pe1irenal edema,

Oral runlinatorics helpful.

nephrosis, gastroenteritis.

See also p 3152.

Large deciduous shrub Oxalates ( sodium and potassium) Toxic when large
with spiny stems.

1 O"/e>--15% dry weight Oeaves primarily, quantity consumed in Fleshy, alternate,
less so in stems and fruits). Dyspnea, short time. Do not allow round in cross-section. weakness, depression, some
hungry animals to graze

Flowers inconspicusalivation, atony of GI tract, coma, plant. Parenteral
ous.

death (neurologic effects and renal
calciun1 solution offers
failure). Hyperkalemia, hypocalcetemporary relief but mia, increased BUN. Lesions include relapses.

hemorrhage and edema of rumen
wall, ascites, swollen kidneys (renal
tubular necrosis and dilation).

Coarse annual herb.

Carboxyatractyloside (seeds and

Seedlings or grain

Fruit covered with
young seedlings). Anorexia,
contaminated with
spines, 2-beaked, with depression, nausea, vomiting, seeds. Oils and fats PO

2 compartments.

weakness, rapid weak pulse,
may be beneficial;
dyspnea, muscle spasms, convulparenteral glucose and sions. Lesions include GI inflammabicarbonate are
tion, acute hepatitis, nephritis.

reported helpful;
warmth, stimulants IM.

(contim,ed)

3122

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORiH

AMERICA• (cont.inued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: SPRING (continued)

Zygadenusspp

Foothill grazing lands, occasionally Sheep, cattle, horses Death camas, Meadow boggy grasslands, low open woods; death camas, Grassy
throughout North and Central
death camas

America

DANGEROUS SEASON: SPRING AND SUMMER

Aesculus spp

Woods and thickets; eastern USA

All grazing animals

Buckeye
and California

Amianthium

Open woods, fields, and acid bogs;

All grazing animals
muscaetoxicum
eastern USA

Fly poison, Staggergrass, Crow poison,

Gray fly poison

Delphinium spp

Either cultivated or wild, usually in All grazing animals, Larkspurs
open foothills or meadows and
mostly cattle; sheep are
among aspen; mostly western USA. somewhat resistant.

Dangerous season spring and

.

summer, also seeds in fall.

Descurainia pinnata

Dense stands especially in wet

Cattle

Tansy mustard
years; arid southwest

POISONOUS PLANTS

3123

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SPRING (continued)

Perennial, bulbous,

Cevanine-type veratrurn azasteroid

Seeds most toxic.

unbranched herbs
alkaloids, steroidal alkaloids,

Leaves and sterns lose
with basal, flat,
glycoalkaloids, and ester alkaloids
toxicity as plant
grass-like leaves.

(all parts). Salivation, vomiting,
matures. Atropine

Flowers greenish,
muscle weakness, ataxia or
sulfate and picrotoxin
yellow, or pink; in
prostration, fast weak pulse, coma,

SC.

racemes or panideath ( central respiratory deprescles. No onion odor.

sion). No distinctive lesions.

DANGEROUS SEASON: SPRING AND SUMMER

Trees or shrubs.

Glycoside, aesculin; also alkaloids

Young shoots and seeds

Leaves opposite and
and saponins in all parts, especially
especially poisonous.

palmately compound. seeds and leaves. Depression,

Treatment only in

Seeds large, glossy
incoordination, twitching, paralysis, severe cases. Stimubrown, with large inflanunation of mucous membranes. lants and purgatives.

white scar.

Prevent access to toxic
plant. Recovery in days.

Rarely fatal.

Bulbous perennial

Unidentified alkaloid, similar

No practical treatment.

herb. Leaves basal,
to those with Zygadenus (all parts).

Especially dangerous
linear. White flowers in Salivation, vomiting, rapid and for animals new to
a compact raceme, the irregular respiration, weakness, pasture. Keep animals
pedicels subtended by death from respiratory failure.

well fed.

short, brownish
bracts.

Annual or perennial

Polycyclic diterpenoid alkaloids

Young plants and seeds
erect herbs. Flowers

( eg, delphinine) in all parts, fresh or more toxic. Toxicity each with 1 spur, in
dry. Straddled stance, arched back,
decreases with
racemes. Perennial
repeated falling, forelegs first.

maturity. Antidote
with tuberous roots.

Constipation, bloat, salivation,
physostigrnine rather

Leaves palmately
vomiting. Death from respiratory
than atropine.

lobed or divided.

and cardiac failure. Most often no
lesions.

Annual to 2 ft tall, stem Toxic principle unknown; must be Administer 2-3 gal.

and leaves covered
grazed over relatively long period.

(8-12 L) water bid with
with fine pubescence. Partial or complete blindness, stomach tube. Include

Leaves alternate,
inability to use tongue or swallow,
nomishment if animal
deeply pinnately

"paralyzed tongue," "blind staggers," weak. Prognosis good if dissected. Infloreswandering, head pressing, emaciatreatment started early.

cence on elongated
tion, death if not treated.

Possibly mustards
raceme. Flower small
cause same condition.

with 4 spreading
yellow to yellow-green
petals. Fruit is copula
with 2 carpels and Jong
waxy seeds in 2 rows.

(continued)

3124

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: SPRING AND SUMMER (continued)

Lantanaspp

Ornamentals and wild; in lower

All grazing anin1als

Lantana
coastal plain of southeast USA, and except horses
southern California

Senna obtusifolia

Found in cultivated (corn, soybean, All grazing animals, Coffeepod, Sicklepod
or sorghum) and abandoned fields, mostly cattle, and along fences, roadsides; naturalized poultry (seep 2861) in eastern USA

Senna occidentalis

Common along roadsides, waste

Cattle, horses,

Coffee senna, Coffee
areas and pastures; naturalized in
chickens, goats, sheep,
weed, Styptic weed,
eastern USA
rabbits

Wild coffee

Tetradymia spp

Arid foothills and higher desert and Sheep

Horse brush
sagebrush ranges, dense stands
along trails; western USA

POISONOUS PLANTS

3125

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SPRING AND SUMMER (continued)

Shrubs. Young sterns

Triterpenes (lantadene A and B) and Remove plants from 4-angled. Leaves
tmknowns in all parts, especially
pasture (herbicide
opposite. Flowers in
leaves and green berries. Anorexia,

2,4-D susceptible).

flat-topped clusters,
jaundice, watery feces, photosensiti Keep animals out of yellow, pink, orange,
zation. Lesions include degenerative light sources after or red. Berries black.

changes in liver and kidneys. Deatll
eating plant.

clue to liver insufficiency, renal
failure, myocardial damage.

Annual sluub frequently Toxic principles tllought to be same Treatment ineffective found in san1e fields as as in S occidentalis. Clinical signs, in down animals;

S occidentaiis.

although sinlilar, less severe with
salvaging most

Distinguishing features S obtusifolia.

economic. Heat labile
include leaflets fewer
toxins not known to
in number and more
persist as residue. Meat
rounded. Seed pods
from affected animals
long, round to 4-sided
should be safe for
and more curved. Seeds
hw11a.n consumption.

shiny, brown, and
rhomboid.

Annual herb >3 ft tall, Anthraquinones ( emodinglycosides No specific treatment
witl1 glandular,
and oxyrnethylanthraquinone ),
known. Symptomatic
alternate pinnately
chrysarobin and lectin (toxalbuniins), and supportive care compound leaves
and alkaloids are associated with GI
essential. Although

(8-12 ovate to
dysfunction and myodegeneration.

gross lesions similar to
lanceolate leaflets,

Afebrile, ataxic, with ciian·hea and
those of vitamin E/
terminal pair largest). coffee-color urine, recw11bent but eat selenium deficiency, Flowers are yellow,
and are alert shmtly before deatl1.

this therapy is
axillary, solitary, or in Increased semrn CK and isocitric contraindicated.

short racemes. Long,
dehydrogenase activities; hyper

Mineraloco1ticoid
flat, straight to slightly kalemia and myoglobinwia frequent. therapy may facilitate curved pods with

Lesions include cardiac and skeletal
potassium excretion.

clearly outlined seed
muscle degeneration. Congestion,

Remove animals from
contents. Of the pods, fatty degeneration, and centrilobular source. Salvaging for seeds, and wilted
necrosis (liver) in addition to tubular economic reasons (see foliage, seeds are most degeneration (kidneys) also repo1ted. Senna obtusifolia, toxic.

Deatl1 probably due to hyperkalernic above).

heart failure.

Shrubs witll yellow

Furanoeremophilanes (tetradymol

Photosensitization
flowers in spring, not
and others). Photosensitization,
seen witl1 conctm·ent
later. Leaves spiny,

"bighead," loss of hair and wool, skin ingestion of otl1er green silvery white. Early
ulcerations, blindness, secondary
forages. Remove aninlals
deciduous.

infections. Lesions include dermal
from plant source and
necrosis and edema, hepatic and
sunlight. Antihistamines,
renal degeneration. Abmtions may
topical antibiotics, and
occur.

parenteral corticosteroids beneficial.

Recovery slow and
possibly incomplete.

(continued)

3126

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: SPRING AND SUMMER (continued)

Veratrum spp

Low, moist woods and pastures, and Sheep, cattle

False hellebore,
high mountain valleys; western USA

Skunk cabbage

DANGEROUS SEASON: SUMMER AND FALL

Acer rubrzim

Moist land and swamps; eastern

Horses

Red maple

Apocynum spp

Open woods, roadsides, fields;

All

Dogbanes
throughout North America

Centaurea 1·e-pens

Waste areas, roadsides, railroads,

Horses

Russian knapweed
and overgrazed rangeland; not
common in cultivated or irrigated
pastures; mostly western and upper
midwestern USA

POISONOUS PLANTS

3127

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (contin,,ed)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SPRING AND SUMMER (continued)

Erect herbs.Leafy

Steroidal alkaloids. Vomiting, ex

Respiratory and heart
throughout, leaves
cess salivation, cardiac arrhythmia,
stimulants.

large and plaited.

bradycardia, dyspnea, muscle

Flowers small and
weakness and paralysis, coma,
white or greenish.

congenital cyclops in lambs from
ewes exposed to V californicum.

DANGEROUS SEASON: SUMMER AND FALL

A large tree at

Unknown toxic principle(s) in wilted Not common.

maturity. Leaves
leaves. Methemoglobinemia, Heinz

Methemoglobinemia a
opposite, 2-6 in.

body anemia, and intravascular
prognostic indicator.

across, palmately 3- or hemolysis; weakness, polypnea, Isotonic fluids, oxygen,

5-lobed each, roughly tachycardia, depression, icterus, and blood transfusion
triangular, and
cyanosis, brownish discoloration
can be helpful.

coarsely toothed. Red of blood and urine.

Methylene blue therapy
to yellow polygamous
not rewarding. Early
flowers. Fruit, a pair of
ascorbic acid treatment

I-seeded winged units
essential for recovery.

connected at base.

Erect, branching,

A resinoid and glucoside with some

Symptomatic ( cardioperennial herb with
cardioactivity found in leaves and
toxin) IV fluids and
milky sap arising from stems of green or dry plants.

gastric protectants
creeping underground Increased temperature and pulse, suggested.

root stock. Leaves
dilated pupils, anorexia, discolored
opposite. Flowers
mucous membranes, cold extremiwhite to greenish white ties, death.

in terminal clusters.

Fruit long, slender,
paired, with silkyhaired seeds.

Perennial weed with

Unidentified alkaloid in fresh or

More toxic than C
slender rhizomes.

dried plant. Chronic exposure, acute solstitialis (below) but Stems erect and well
onset of signs. Inability to eat or
with similar pathology
branched.Leaves
drink, facial dystonia, chewing,
and prognosis. Some
pinnately lobed to
yawning, standing with head down,
relief with massive
entire, not spiny,
severe facial edema, gait nonnal,
doses of atropine but
narrowed basally but
head pressing, aimless walking or
not an effective
not petioled and of
excitement most severe the first 2
treatment. Euthanasia
decreasing length up
days, become static thereafter. Death recommended.

the plant. Thinly
from starvation, dehydration,
pubescent or glabrous. aspiration pneumonia.

Blue, pink, or white
flowers. One-seeded
fruit with whitish,
slightly ridged
attachment scar.

( contin1led)

3128

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: SUMMER AND FALL (continued)

Centaiirea so ls titialis Waste areas, roadsides, pastures; Horses

Yellow star thistle,
mostly western

Yellow knapweed

Eupatorium rugosum Woods, cleared areas, waste places, Sheep,cattle,horses White snakeroot
usually the moister and richer soils;
eastern USA

Hypochaeris radicata Native to the Mediterranean and Horses

Flatweed, Cat's-ear,

South America; widely distributed

Gosmore
in the USA-Pacific states, eastern/
southeastern USA

Oxyt enia acerosa,

Arid, alkaline soils in foothills,

Cattle, sheep

Ivaacerosa
sagebrush plains; western USA

Copperweed

Perilla f1 ·utes cens

Ornamental originally from India,

Cattle primarily, horses

Perilla mint, Beefsteak escaped to moist pastures, fields, and other livestock
plant
roadsides, and waste places;
susceptible
southeastern USA

POISONOUS PLANTS

3129

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SUMMER AND FALL (continued)

Annual weed. Leaves

Unidentified alkaloid. Involuntary

Horses graze because
densely covered with
chewing movements, twitching of
of lack of other forage.

cottony hair. Terminal lips, flicking of tongue. Mouth Extended pe1iod of
spreading cluster of
commonly held open. Unable to eat; consumption essential bright yellow flowers
death from ciehyclration, starvation,
for toxicity. Liquefactive
with spines below.

aspiration pneumonia.

necrosis of substantia

Branches winged.

nigra and globus pallidus

(brain) pathognomonic.

No treatment. Euthanasia recommended.

Erect perennial herb.

Complex benzyl alcohol (tremetol in "Milk sickness" or Tremetol leaves,
leaves and st.ems). Excreted via milk; "trembles." Treatment opposite, simple,
cumulative. Weight loss, weakness,
nonspecific and
serrated. Flowers
trembling (muzzle and legs)

symptomatic. Heart and
small, white, and
prominent after exercise, constiparespiratory stimulants many. Often grows
tion, acetone odor, fatty degeneraand laxative may be in large patches.

tion of liver, partial paralysis of
necessary. Remove
throat, death in 1-3 days.

animal from access to
plant, discard milk

(hazardous to people).

Perennial herb with

Unknown; associated with but not

Tranquilizers, sedatives,
viscid sap, stemless.

proven cause of a neurologic
mephenesin, and

Simple, serrated to
condition in horses-stringhalt
thiamine ( questionable
lobed, basal, alternate (hypermetria/hyperflexion of pelvic effectiveness); longterm leaves. One to several limb) in dry years. Sudden onset phenytoin therapy seems
bright yellow flowers
of abnormal gait; flexion/delayed
helpful .. Treatment with
per plant.

extension of hocks, knuckling of
baclofen also repo1ted
carpal joints, laryngeal hemiplasia;
helpful. Surgery (pelvic
spontaneous recovery possible, but
tenotomy of the lateral
condition could be permanent.

digital extensors)

reported helpful.

Tall, annual/perennial Unknown (pseudoguaianolide

No specific treatment.

herb with narrow
sesquiterpene lactones found in

Supplement diet or
leaflets. Flowers in
species-consistent clinical signs
change pasture.

many heads resemwith these toxins); all above-ground bling goldenrod.

parts, green or dry. Metabolic
disease, anorexia, marked depression, weakness, coma; death without struggle within 1-3 days.

Annual, freely

Green or dry, 3-substituted furans

Treatment ineffective
branched, squared

(perilla ketone, egomaketone,
once clinical signs
stems. Opposite,
isoegomaketone). Signs 2-10 clays
severe. Parenteral
purple or green,
after exposure include dyspnea
steroids, antihistamines,
coarsely serrated

(especially on exhaling), open-mouth and antibiotics may help.

leaves. White to purple breathing, lowered head, reluctance Handle gently (prevents flowers. Strong
to move, death on exertion. Lesions exertion and death).

pungent odor when
include pulmonary emphysema and Avoid/lin1it grazing crushed.

edema.

during flowering and
fruiting period.

(continued)

3130

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (cont,inued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: SUMMER AND FALL (continued)

Prosopis glandulosa

Dry ranges, washes, draws;

Primarily cattle, also

Mesquite
southwest
goats; sheep resistant

Robinia pseudoacacia Open woods, roadsides, pin elands, All grazing animals, Black locust, False
on clay soils preferably; eastern
mostly horses
acacia, Locust tree

USA

Rumex crispus

Commonly found on acid or

Cattle, sheep

Curly dock, Dock,
sterile, graveled, seasonally moist

Sorrel
soils of waste places, pastures, and
fields throughout USA

Solanumspp

Fence rows, waste areas, grain and All

Nightshades, Jerusalem hay fields; throughout No1th cherry, Potato, Horse

America
nettle, Buffalo bur

POISONOUS PLANTS

3131

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: SUMMER AND FALL (continued)

Perennials, deciduous Unknown principle in the beans.

High sucrose content
shrub or small tree

Chronic wasting with rumen atony,
of beans alters rumen
with smooth or
excess salivation, continual chewing. microflora, inhibiting furrowed gray bark,

Partial paralysis of tongue, facial
cellulose digestion and
paired spines. Leaves
muscle tremor, submandibular

B vitamin synthesis if
divided. Legume pod
edema, anemia. Lesions include
grazed for extended
long, constricted
emaciation, small fu'm kidneys and
period.

between seeds.

liver, gastroenteritis, filled rumen.

Tree or shrub.

The glycoside robitin, a lectin

Laxatives and stinrn

Deciduous, alternate, (hernagglutinin), and the phytotoxins lants suggested. Treatpinnately compound robin and phasin found throughout
ment symptomatic.

(>10 elliptic to ovate
plant, although flowers have been
leaflets) leaves. Pair of suggested as the toxic principles.

spines at base of each Diarrhea, anorexia, weakness, leaf. Flowers in loose, posterior paralysis, depression, fragrant, white to
mydriasis, cold extremities;
cream, drooping
frequently lan1initis and weak pulse.

racemes. Flattened,

Deat11 infrequent; recovery period
brown pods containextensive. Postmortem lesions
ing 4-8 seeds.

restricted to GI tract.

Perennial herb with

Oxalic acid and soluble oxalate in

In acute cases, death
erect sterns, 3-4 ft tall. leaves, stem, and seeds. Acute is too rapid for any

Leaves alternate,
course (hypocalcernia, labored
treatment. Symptolanceolate to elliptic,
breathing, anorexia, depression,
matic and supportive
finely crisped margins, muscle fasciculation, tremor, care can be helpful.

base obtuse to
weakness, teeth grinding, pulmonary Remove animals from cuneate, petioles form edema, tetany, seizure, recurnbency, source. Calcium IV to sheath around stern.

and prostration); subacute (hypocal correct hypocalcernia is Flowers small,
cemia, altered kidney function) or
ineffective. Give lime
numerous, greenish, in chronic course (renal fibrosis, renal water to precipitate long terminal panicles; insufficiency, and urolithiasis ).

oxalate and prevent
fruit an achene, papery Hemorrhage, edema (rumen and absorption. Allow

3-winged, with
abomasal walls), and ascites
animals to develop
lustrous brown seeds.

(intestinal mucosa) seen in toxic
tolerance to oxalate
cases. Death resulting from shock
by exposure to small
and hemorrhagic rumenitis.

amounts over time. Do
not allow animals to
graze pasture or offer
hay highly contan1inated with oxalateproducing plants.

Fruits small; yellow,

Glycoalkaloid solanine (leaves,

Pilocarpine, physostigred, or black when
shoots, unripe berries). Acute
rnine, GI protectants.

ripe; structurally like
hemorrhagic gastroenteritis,

Seeds may contanunate
tomatoes; clustered on weakness, excess salivation, grain.

stalk arising from stern dyspnea, trembling, progressive between leaves.

paralysis, prostration, death.

(co11tim,ed)

3132

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (con1.in11ed)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: FALL AND WINTER

AlliU?n cepa,

Cultivated and grown on rich soils

Cattle, horses, sheep,

A canadense
throughout USA
clogs

Onions ( cultivated
and wild)

Astrolepis sinuata

Dry rocky slopes and crevices,

Sheep, goats, cattle
coch'isensis
chiefly limestone areas; southwest

Jimmy fern, Cloak fern

Daubentonia puriicea Cultivated and escaped, in waste All

Rattlebox, Purple

• places; southeastern USA coastal
sesbane
plain

Glottidium vesicarium Mostly open, low ground, aban-All

Bladderpod, Rattlebox, doned cultivated fields; southeast-Sesbane, Coffeebean
em USA coastal plain

POISONOUS PLANTS

3133

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: FALL AND WINTER

Biennials and

N -propyl disulfide, an oxidant, in all Clinical signs sin1ilar perennials, bulb
parts. Anemia develops within days
to toxicity induced by
plants, onion odor.

of exposure. Toxicosis in cattle

S-metl1ylcysteine

Leaves basal, green,
associated with prolonged ingestion sulfoxide (a rare toxic hollow, cylindrical (A of large amounts of onions. N-propyl an1ino acid in Brassica cepa), lustrous green, disulfide inhibits RBC glucose-spp) in livestock.

flat (A canadense);

6-phosphate dehydrogenase, leading Susceptibility to onion flowers on hollow
to hemolysis and formation of Heinz poisoning varies across flowering stalks, termi bodies. Clinical signs are hemoglobi animal species: cattle nal umbels of many
nuria, diarrhea, loss of appetite,
more susceptible than
small blooms; fruits
jaundice, ataxia, collapse, and
horses and dogs, which

3-celled capsules with possible death if untreated.

are more susceptible
many seeds.

Hemolytic anemia reported in
than sheep and goats.

livestock ingesting wild onions.

Remove animals from

Heinz body anemia; swollen, pale,
source and prevent
necrotic liver; hemosiderin in liver,
future access to cull
kidneys, and spleen are reported
onions. Symptomatic
pathologic lesions.

and supportive care
essential.

Evergreen from

Unknown (excreted in milk).

No specific treatment.

rhizomes, perennial,

Nervous syndrome, incoordination,

Supportive and general
erect fem with divided arched back, trembling, increased nursing care helps.

leaves, folding when
respiratory rate and pulse. Death

Avoid driving during
dry. Leaflets about as
when not allowed to rest.

danger period. Provide
wide as long, scaly on
ample watering, placed
back
to avoid long walks.

Allow rest if sign.s
occur.

Annuals or perennials, S punicea most toxic species (0.1 %

Symptomatic treatshrub. Leaves
body wt toxic to sheep and cattle).

ment; specific cause
pinnately compound

Toxin(s) not fully characterized, but unknown. Seeds with <!20 leaflets.

saponins are primary suspects; 12-24 poisonous. Remove Flowers orange-red,
hr delay in clinical signs after
animal from source.

rose, or purple.

ingestion. Rapid pulse, weak

Fluids and electrolytes

Legwne pods (<!5
respiration, diarrhea, death.

for dehydration.

seeds) longitudinally

4-winged.

Tall annual. Legume

Unknown (green plant and seeds). In Green seeds are more pods flat, tapered at
ruminants, hemorrhagic diarrhea,
toxic. Remove aninlal
both ends, 2-seeded.

shallow rapid respiration, fast
from source immedi

Leaves pinnate,
irregular pulse, coma, death. Lesions ately. Syn1ptornatic, divided. Flowers
include hemorrhages in abomaswn
general supportive
yellow.

and intestines, dark tarry blood.

treatment-saline
purgatives, rumen
stinrnlants, IV fluids.

(continued)

3134

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: FALL AND WINTER (continued)

H alogelon glomeratus Deserts, overgrazed areas, winter Sheep, cattle

Halogeton
ranges, alkaline soils; western USA
lsocoma plurifl,ora

Dry plains, grasslands, open

Cattle, sheep, horses

(H aplopappus
woodlands, and along irrigation
heterophyllus)

canals; alkaline soils; southwestern

Ray less goldenrod,

USA and northern Mexico

Burroweed, Jimmyweed

Juglans nigr a

Native to eastern USA; now

Horses

Black walnut
from eastern seacoast, west to

Michigan and most of the Midwest,
south to Georgia and Texas

Melilotus ojf1Cinalis

Commonly found on alkaline soils, ·Most commonly cattle, andMalba
fields, roadsides, and waste places; also horses and sheep Sweet clover, White
forage crop in southern and
sweet clover
northern USA

Sophora secundijlora

Hills and canyons, lin1estone soils;

Cattle, sheep, goats

Mescal bean, Coral
southwestern Texas into Mexico
bean, Sophora,

Frijolito, Texas
mountain laurel

POISONOUS PLANTS

3135

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA" (cont'inued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: FALL AND WINTER (continued)

Annual herb. Leaves

Oxalic acid, oxalate. A@ute course.

Toxic dose constuned
fleshy, round in cross

Rapid labored respiration, depresover short period.

section, tip with stiff
sion, weakness, coma, death. Lesions Increase water constunphair. Axillary flowers include hemorrhages and edema of
tion. Standard therapy IV
inconspicuous.

rumen wall, swollen kidneys, oxalate calcitun borogluconate Fruits bracted and
crystals in kidneys and rumen wall.

(helpful in cattle, delay
conspicuous.

deaths in sheep). Calcitun
supplement (83"/o alfalfa,

15% calciun1 carbonate,

2% molasses) in feed
before grazing. Halogeton
forage can be helpful.

Herbicide 2,4-D control.

Bushy perennial 2-4 ft Complex benzyl alcohol (trem

"Milk sickness." Similar
tall, with many yellow etol); resin acid; prinrnrily nursing treatment to E rugosum
flowerheads.Leaves
young and nonlactating animals.

intoxication. Prevent
alternate, linear,

Reluctance to move, trembling,
access to plants (growing
sticky.

weakness, vomiting, dyspnea,
season). Remove young
constipation, prostration, coma,
and discard milk
death.

(hazardous to people).

Tree with deciduous,

Juglone, phenolic derivative of

Nonfatal; lanlinitis and
alternate, pinnately
naphthoquinone. Shavings with as
edema of lower limbs.

compound leaves
little as 20"A, black walnut toxic

Remove shavings

( munerous lanceolate
within 24 hr of exposure. Reluctance promptly ( relief signs).

leaflets with serrated
to move; depression; increased

Treat for limb edema
margins); leaflets in
temperature, pulse, respiration rate, and lanl.initis. Improvemiddle are largest. Male abdominal sounds, digital pulse, hoof ment in 24-48 hr with no and female flowers on
temperature; distal limb edema;
sequelae. NSAIDs are
same tree but different lan1eness. Severe laminitis with mainstay; prazosin,
inflorescences.Thick
continued exposure.

nifedipine are promishusked nut does not
ing. Avoid corticosteopen when ripe. Twigs
roids (worsen existing
have chambered pith.

vasoconstriction).

Annual or biennial

See S\VEET CLOVER POISONING, p 3156.

Seep 3156.

herb 3-6 ft tall. Leaves
alternate, pinnately
compound with

3 obovate leaflets,
serrated margins.

Yellow or white
flowers on racemes.

Small I-seeded pods.

Evergreen shrub or

Quinolizidine alkaloid (seeds and

Symptomatic. Toxic
small tree. Leaves
probably leaves). Violent trembling, effect not cwnulative, alternate, divided, and stiff gait, falling on exercise, recumconsume large amounts leathery. Flowers
bent for a few minutes, becoming
quickly. Seeds more
violet-blue, fragrant.

alert and eating.

dangerous when

Seeds large and bright
crushed.

red with hard seed
coat, in legume pod.

3136

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: FALL, WINTER, AND SPRING

Melia azedarach

Fence rows, brush, waste places;

Pigs and sheep, others

Chinaberry
southern USA

(dogs) less susceptible

DANGEROUS SEASON: ALL SEASONS

Acacia berlandieri

Semiarid rangelands; southwest

Sheep, goats

Guajillo, Catclaw,
ern Texas into Mexico

Blackbrush, Acacia

Agave lechuguilla

Low limestone hills, dry valleys, and Sheep, goats, cat

Lechuguilla
canyons; southwest. Dangerous all
tle, usually durseasons, especially spring.

ing drought

Agrostemma githago

Weed, grainfields, and waste areas; All

Corn cockle
throughout North Ame1ica

Asclepias spp

Dry areas, usually waste places,

Air

Milkweeds
roadsides, streambeds, western

USA

Astragalus spp,

Mostly western

All grazing animals

0.xytropis spp (certain
species only)

Locoweed

POISONOUS PLANTS

3137

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA•1 (contim,ed)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: FALL, WINTER, AND SPRING

Small to medium

Several alkaloids and a saponin (all

Gastroenteritis usual.

deciduous tree. Fruit
parts), fluit most toxic. Restlessness, Recovery may be cream or yellow with
vomiting, constipation, cyanosis,
spontaneous. Laxatives
a furrowed globose
rapid pulse, dyspnea, death within
and GI protectants
stone, persisting on

24hr.

suggested.

tree through winter.

Large amount required
for intoxication.

DANGEROUS SEASON: ALL SEASONS

Deciduous shrub

Amine, N-methyl-!3-phenyl

Dominates vegetation in
or small tree. Leaf
ethylamine. Chronic course. Ataxia
some areas. Valuable to
divided. Flowers white of hindquarters (limberleg), marked sheep industry due to to yellowish in dense
excitation, prostration, remain alert, high nutritive value and heads. Fruit a legume death from starvation.

dominance. Supplement
with margins
dtuing drought to reduce
thickened.

possibility of poisoning.

Perennial, stemless,

Unidentified hepatotoxin (caus-

Remove animals
with thick, fleshy,
ing photosensitivity) and a toxic
from range and
tapered leaves having saponin (abortifacient action).

provide shade. See
sharply serrated

Subacute course. Listlessness,

PHOTOSENSITIZATJON,
margins. Flowers
anorexia, icterus, yellow discharge
p976.

infrequently with tall
from eyes and nostrils, photosensititerminal panicle.

zation, coma, death.

Green winter annual

Saponin (githagenin) in seeds. Acute Maintain hydration (fluids with silky-white hairs, course. Profuse watery diarrhea, and electrolytes) and
opposite leaves,
vomiting, dullness, general weakcontrol diarrhea Oils and purple flowers, black
ness, tachypnea, hemoglobinuria,

GI protectants. Neutralize
seeds.

death.

toxin ( dilute acetic acid

PO). Blood transfusions
may be necessary.

Perennial erect herbs,

Steroid glycosides and toxic resinous Sedatives, laxatives, shrubs, vines, or small
substances (all parts), green or dry.

and IV fluids suggested.

trees with milky sap.

Staggering, tetanic convulsions,

Prevent plant consump

Leaves simple,
bloating, dyspnea, dilated pupils,
tion. Do not feed
opposite/whorled with rapid and weak pulse, coma, death.

milkweed-contaminatentire margins. Seeds
ed hay.

silky-hairy from
elongated pods.

Stemmed or stemless Swainsonine. Depression, emacia

Avoid grazing of source.

perennial herbs.

tion, incoordination, dry luste1°

Both green and dry

Leaves alternate and
less hair. Abortions. Neurovisceral
plants toxic.

pinnately compound.

cytoplasmic vacuolation, congestive

Flowers leguminous.

right heart failure in cattle grazing at

Chronic intoxication.

high altitudes.

(continued)

3138

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Aslragalus spp ( certain Nearly all

All grazing animals
species only)

Milk vetch, etc (many
common names)

Aslragalus spp ( certain Seleniferous areas, mostly western All grazing animals species only- selenium and midwestern
accumulators)

Many common names

Baccharis spp

Open areas, often moist; southeast

Cattle

Silverling, Baccha.ris,
ern and southwestern USA

Yerba-de-pasmo

Brassica spp,

Fields, waste areas, hay meadows,

Cattle, horses, pigs

Raphanus spp,
roadsides; throughout North

Descurainia spp,

America

Berteroa incana

Mustards, Crucifers,

Cress; and for B
incana, Hoary alyssum,

Hoary false alyssum

Cesl1um diurnum,

Open woods and fields; Gulf

Cattle, horses, and dogs

Cnoclurnum

Coast states (Florida, Texas)

(ingesting cholecalcif

Day-blooming
and California
erol-based rodentijessarnine and
cides)

night-blooming
jessarnine, respectively

POISONOUS PLANTS

3139

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

As above.

Miserotoxin, other aliphatic nitro

Avoid grazing of
compounds. Posterior paralysis,
preflower stage.

goose-stepping, depression, rough
coat, pulmonary emphysema, acute
death, cord demyelination.

As above.

Selemum (chrome). Slow growth,

Avoid grazing seleniferreproductive failure, loss of hair, ous plants for extended
sore feet, acute death.

periods. See SELENIUM

TOXICOSIS, p 3085.

Shrubs. Numerous

Unidentified. Acute course. Rumen

Most dangerous in early
small, whitish flowers. stasis, bloat, anorexia, excess growing stage. Toxin

Leaves resin-dotted
salivation, diarrhea, staggering,
concentrated in leaves
and persistent
trembling, restlessness, polypnea,
and flowers. No specific
southward.

tachycardia, death.

treatment. Treatment
toward relief of
diarrhea is best.

Annuals/biennials

Glucosinolates (isothiocyanate,

No specific treatment
herbaceous weeds
thiocyanates, nitiites) in seeds and

(B incana disease in
with temlinal clusters vegetative parts, fresh or dry. Acute/ horses). Phenylbutaof yellowish flowers chronic course. Anorexia, severe
zone, flunixin,
and slender, elongated gastroenteritis, salivation, diarrhea, furosemide or other
seed pods.

paralysis, photosensitization,
diuretics helpful in
hemoglobinuria. Unknown toxin(s)

relieving pain,
in B incana cause rapid onset of
inflammation, and
transient distal limb edema, lanlinitis edema. Remove from (horses), and severe GI disturbances source. Administer GI with continued exposure. Late
protectants (mineral
abortions and/or weak, premature
oil).

foals at birth.

Evergreen shrubs or tall Atropine-like alkaloids (fruit), Prevent fu1ther access
bush; leaves alternate,
saponins (fruit and sap), and
of animals to plants. In
ovate smooth-edged;
glycosides of 1,25-dihydroxycholeearly stages, treatment flowers white, tubular, calciferol Oeaves primarily, stem, might be effective and
small clusters, fragrant fruits, and roots) are found.

cost-effective. Correct
by day; fruit, a

Gastroenteritis develops on
fluid and electrolyte
greenish-white to
ingestion of fruits. Vomiting,
imbalances in cases
lavender (inunature ),
depression, anorexia, chrome weight with persistent becoming dark purple
loss with normal appetite, choppy
vomiting or diarrhea.

to black (mature),
stiff gait, increased pulse, persistent Reduce or prevent fleshy berry, with
hypercalcemia and hyperphoshypercalcemia
several small, black,
phatemia, calcinosis (aorta, carotid

( calciuresis, diuretics,
oblong seeds, dispersed and pulmonary arteries, tendons, steroids, calcitortin).

by birds in droppings.

ligaments, and kidneys). Parathyroid Maintenance therapy of Leaves longer, mght
atrophy, thyroid (C-ccll) hypertrodiuretics and steroids fragrant flowers, white phy, and osteopetrosis reported with may be necessary.

fiuits at matruity
chronic ingestion of leaves.

( C nocturnum ).

(continued)

3140

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Conium macula tum

Roadside ditches, damp waste

All

Poison hemlock
areas; throughout North America

Crotalaria spp

Fields and roadsides; eastern and

All

Crotalaria, Rattlebox
central USA

Cynoglossum o.fficinale Common in waste places, roadsides, Cattle, sheep, horses Hound's tongue
and pasturnd areas throughout USA

Datura stramonium

Fields, barn lots, trampled pastures, All

Jimson weed, Thorn
and waste places on rich bottom
apple
soils; throughout North America

POISONOUS PLANTS

3141

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Purple-spotted hollow Piperidine alkaloids (coniine and Coniine excreted via
stem. Leaves resemble others) in vegetative parts. Acute lungs and kidneys,
parsley, parsnip odor
course. Dilated pupils; weakness;
mousy odor of breath
when crushed.

staggering gait; slow pulse,
and urine diagnostic.

Taproot. Flowers
progressing to rapid and thready.

Administer saline
white, in umbels.

Slow, irregular breathing; death from cathartics; neutralize respiratory failure. Teratogenic in
alkaloids with tannic
cattle.

acid, together with
stimulants.

Annual or perennial

Pyrrolizidine alkaloid (monocrota

Cwnulative, fresh or
legume. Yellow
line) and other unidentified alkaloids dry. No treatment.

flowers in racemes,

(all parts, especially seeds). Chronic
pods inflated. Bracts
course. Chickens-diarrhea, pale
at base of pedicels of
comb, ruffled feathers; horses-unflowers and fruits
thriftiness, ataxic, walking in circles,
persistent. Leaves
icterus; cattle-bloody diarrhea,
sin1ple or divided.

icterus, rough coat, edema,

Seeds in harvested
weakness. Death may occur from a
grain.

few weeks to months after ingestion.

Annual or biennial

Pyrrolizidine alkaloids (0.6%-2.1 % of Know source and herbaceous plant,
dry matter) including heliosupine
quality of hay.

rough hairy stem and
and echinatine in the foliage.

Treatment symptomatic
foliage, 3-4 ft tall.

Unpleasant odor discourages
and supportive at best.

Leaves alternate,
conswnption when fresh, becomes

Affected animals
oblanceolate,
palatable in hay and is readily
seldom recover.

narrowed to petiole
consumed. Toxic insult primarily

(lower), lanceolate,
hepatic and chronic in nature.

sessile, clasping

Pyrrolizidine alkaloids (inactive)

(upper). Flowers
undergo hepatic metabolization to
numerous in coiled
active intermediates-pyrroles
racemes, without

(alkylating agent), which are toxic.

bracts, blue, purple, or Clinical signs are anorexia, white blooms. Fruit,
depression, rough hair coat,
burr-like from 4
hemorrhage, tenesmus, bloody feces,
outlets, thickly
ataxia,jaundice, death. Hepatic
covered with hooked
lesions of necrosis, edema,
prickles.

megalocytosis, bile duct hyperplasia,
and cytoplasmic vacuolation
reported.

Leaves wavy. Flower

Tropane alkaloids (atropine,

All parts, mainly in hay
large (4 in.), white,
scopolarnine, hyoscyanune) in all
or silage. Urine from
tubular. Fruit a spiny
parts, seeds in particular. Acute
anin1al dilates pupils
pod, 2 in. (5 cm) Jong. course. Weak rapid pulse and of laboratmy animals
heartbeat, dilated pupils, dry mouth, (diagnostic). Treatment incoordination, convulsions, coma.

nonspecific; cardiac
and respiratory
stimulants (physostigmine, pilocarpine,
arecoline).

( continued)

3142

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICAa (continued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Diymaria pachyphylla Heavy alkaline clay soil in low areas Cattle, sheep, goats Inkweed, Thickleaf
or dry, overgrazed pastures;
dryrnary
southwestern USA

Festuca arundinacea

A coarse, hardy, drought-resistant

Mostly cattle and

Tall fescue
grass; Pacific Northwest, Missomi,
horses

Oklahoma, and Kentucky; major
pasture grass in southeastern USA

Gelsemium semper

Open woods, thickets, swamps, low All
virens, G rankinii
areas, and open fields; southeastern

Yellow jessamine,

USA

Evening trumpet
flower, Carolina
jessamine

Gutimrezia

Widespread over dry range and

Cattle, sheep, goats,
microcephala
desert; primarily southwestern USA pigs

Threadleaf, Snakeweed, Small-head
matchweed, Sticky
snake weed

Helenium hoopesii

Moist slopes and well-drained

Sheep, rarely cattle

Orange sneezeweed
mom1tain meadows; abundant in
overgrazed areas; western USA

Helenium

Moist ground; southern USA

Cattle, sheep, goats
microcephalum

Small head sneezeweed

POISONOUS PLANTS

3143

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

VetBooks.ir

Characteristics

Toxic Principle and Effects

Treatment

DANGEROUS SEASON: ALL SEASONS (continued)

Multibranched,

Problem in heavily overgrazed:areas. Dangerous during succulent, prostrate

Unknown toxin. Sudden onset of
drought, after rain, or at
annual. Opposite or
diarrhea, restlessness, depression,
night. Avoid overstockwhorled appearing
coma, death. Lesions include
ing to improve range. In
leaves. Small white
gastroenteritis with congestion of
well-fed and watered
flowers.

liver, kidneys, spleen. Petechial
animals, little or no
hemorrhages on heart.

problem observed. Poor
response to treatment.

Coarse, deeply rooted

See FESCUE POISONING, p 3016.

Seep 3016.

perennial grass. Broad,
dark-green, ribbed,
rough upper surface, and
smooth sheathed leaves.

Grows in clumps.

Climbing or trailing

Potent neurotoxic alkaloids

No specific treatment.

vines. Evergreen,

(gelsemine and others, related to

Relaxants and sedatives
entire, opposite
strychnine) in all parts. Gelsemine
suggested. PO adminisleaves. Yellow tubular the most toxic. Acute course.

tration of strong teal
flowers, very fragrant. Weakness, incoorclination, clilated coffee or poison
pupils, convulsions, coma, death
hemlock suggested on
within 48 hr. Llrnberneck in fowl.

early exposure (before

Clinical signs indicative of a poor
observation of clinical
prognosis.

signs) seems helpful in
reducing further toxin
absorption (more basic
stomach pH).

Multibranched,

Unknown. Steroidal effect of

No specific treatment.

perennial (toxicologisaponins, mono- and cliterpene acids. Supplementing diet will cally significant),

Acute poisoning, anorexia, listlesshelp but not entirely resinous shrub. Simple ness, hematuria, diarrhea followed prevent abortion in
leaves, alternate;
by constipation. In cattle, abortions
cattle.

yellow-flowered
with retained placenta, stillbirths, or
heads.

premature and weak calves.

Annuals, biennials,

Sesquiterpene lactones (helenalin,

Cumulative. Aspiration
perennial herb. Orange hyrnenoxin). Subacute course (spew pneumonia frequent.

sunflower-like heads
ing sickness). Depression, weakness, Remove from access to or yellow flowers.

restlessness, stiff gait, salivation,
plant. Graze sneezeweed

Leaves alternate.

pronounced vomiting, emaciation,
areas for only short
eventual death.

periods of time. Can
graze intermittently with
some success.

Annual, erect herb,

Sesquiterpene lactone (helenalin)

Cumulative. Remove
simple-stemmed below, in flowering stage. Depression, from pasture. Catharbushy above. Stem
weakness, restlessness, stiff gait,
tics may help.

winged. Narrow leaves salivation, vomiting.

throughout. Flowers in
small heads; disk pale
red-brown, rays yellow.

( continued)

3144

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

VetBooks.ir

Common Names

Habitat and Distribution

Affected Animals

DANGEROUS SEASON: ALL SEASONS (continued)

Hypericum

Dry soil, roadsides, pastures,

Sheep, cattle, horses,
perforatum
ranges; throughout North America
goats

St. John's-wo1t,

Goatweed, Klamath
weed

Kalmiaspp

Rich moist woods, meadows, or

All, often sheep

Laurel, Ivybush,
acid bogs; eastern and northwest

Lambkill
ern. Dangerous all seasons,
especially winter and spring.

Kochia scoparia

Throughout North America

Cattle, sheep

Kochia, Burning bush,

Fireball, Fireweed,

Poor man's alfalfa

Ligustrum spp

An ornamental; common as hedge;

All livestock

Privet, Ligustrurn,
found at abandoned farn1 home

Hedge plant
sites, along fences, and in bottomlands; eastern USA Lupinus spp

Dry to moist soils, roadsides, fields, Sheep, cattle, goats, Lupines, Silky lupine,
and mow1tains; throughout, but
horses, pigs

Sink lupine, Bluebonnet poisoning mostly western USA

POISONOUS PLANTS

3145

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (conl'inued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Perennial herb or

Photodynamic pigment (hypericin). Remove animals from woody below. Leaves

Subacute course. Photosensitization, source and sunlight.

simple, opposite or
pruritus and erythema, blindness,

Corticosteroids
whorled, dotted.

convulsions, diarrhea, hypersensitiv parenterally, topical Flowers many, yellow, ity to cold water contact, death.

broad-spectrum
with many stamens.

antibiotics.

Woody shrub.

Resinoid (andromedotoxin) and a

Undigested rumen

Evergreen, glossy
glucoside (arbutin) in vegetative
contents and ingesta
leaves. Flowers pink
parts. Acute course. Incoordination, in lungs at necropsy.

to rose, showy.

excess salivation, vomiting, bloat,

Laxatives, demulcents,
weakness, muscular spasms, coma,
nerve stimulants,
death.

atropine.

Annual to 5 ft tall.

An alkaloid has been suggested. This Haivested foliage is Many branched stems plant may also accumulate nitrate source of toxin. Protect
give bushy appearand oxalate. Disease syndromes:

from sun in case of
ance. Leaves petiolate, photosensitization, weight loss, and photosensitization; lanceolate, thin, and
polioencephalomalacia, which
treat polioencephaloflat; alternate. Fruit
seems intensified by slow growth
malacia with vitamin B.

has 5 wedge-shaped
and sulfates.

Supplement with
wings.

copper (preventive
against polioencephalomalacia).

Shrubs up to 15 ft tall. Ligust1in, ligustron, syringin, Treatment symptomatic

Simple, opposite,
syringopicrin, and other unknown
and supportive; correct
short-petioled,
compounds in leaves and fruit.

dehydration.

evergreen or

Primarily GI irritants. Diarrhea,
deciduous leaves.

abdominal pain, incoordination,

Numerous small,
paresis, weak pulse, hypothermia,
white flowers in
convulsions, sometimes death.

panicles. Fruit is 1- to

2-seeded, black or
dark blue berry that
persists throughout
winter.

Perennials. Leaves

Quinolizidine alkaloids (20 known)

Do not disturb sick
simple or palmately
concentrated in seeds (fresh and
animals; remove from
divided. Flowers blue, dry); some piperidine alkaloids.

source as they begin to
white, red, or yellow in Acute course. Inappetence, dyspnea, recover. No effective terminal raceme.

struggle, convulsions, death from
treatment, but
respiratory paralysis. Lupinosis
survivors recover

(hepatotoxicosis) not a reported
completely. See also
problem in the USA. Some species
p 3018.

teratogenic in cattle ( crooked calf
disease, weak and deformed calves,
stillbirths).

(cont-inued)

3146

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Nandina domeslica

Common ornamental in southern

All grazing animals,

Nandina, Heavenly

USA
especially ruminants
bamboo, Chinese
sacred ban1boo

Neiium oleandei·

Common ornamental in southern

All

Oleander, Laurel rosa,
regions

Laurel blanco

Photiniafrasei·i,

Common ornamental (hedge or

All grazing animals,

P sei--i-ulala, P glabra
screen) in southern USA
mostly ruminants

Fraser's photinia,

Chinese photinia, Red

Ieaf photinia, Red tip
photinia

Pinus pondei·osa

Coniferous forests of Rocky

Cattle. Sheep and deer

Ponderosa pine,

Mountains at moderate elevations;
seem not to be affected.

Western yellow pine
western USA. Dangerous all
seasons, especially winter.

Prumts caroliniana

Woods, fence rows, and often

All grazing animals

Laurel cherry, Cherry
escaped from cultivation; southern
laurel, Mock orange
regions. Dangerous all seasons,
especially winter and spring.

POISONOUS PLANTS

3147

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Upright, tmbranched,

Cyanogenic glycosides in foliage and Acute outcome
and multistenuned,
fruits, hydrolyzed in GI tract to free
precludes effective
evergreen sluub, 3-7 ft cyanide, thereby affecting cellular treatment for most; IV
tall. Alternate, bi- to
respiration. See CYANIDE POISONING,
sodium nitrite/sodium
tripinnately compound p 2959. Prognosis good if animal thiosulfate treatment
leaves; leaflets
survives for 1 hr after signs begin.

of choice. Pi crate test
subsessile, ellipticindicates toxic
lanceolate, half as wide
potential of the plant.

as long, entire, leathery,

See CYANIDE POISONING,
metallic bluish-green
p2959.

becoming purple in fall.

Small, white flowers;

2 -seeded, bright red
berries in large pan.ides
persist tlu·oughout fall
and winter.

Evergreen shrub or

Digitoxin-type glycosides (oleandro No specific treatment.

tree. Leaves whorled
side, nerioside, and others) in all

Atropine in conjunction
and prominently,
parts, fresh or dry. Acute course.

with propranolol
finely, pinnately veined Severe gastroenteritis, vomiting, reported helpful.

beneath. Flowers
diarrhea, increased pulse rate,
showy, white to deep
weakness, death.

pink.

Evergreen shrubs,

Same as for N domestica (above).

Sa.me as for

10-15 ft tall. Alternate,

N domestica.

oblong-ovate sen-ated
leaves, copper-red

(when young)tuming
dark green in 2-4 wk.

Prominent, whitish
flowers in spring; showy,
red berries in fall.

Evergreen tree,

Unknown toxin ( diterpene esters of Pine-needle ingestion 150-180 ft. Leaves
isocupressic acid are suspected).

during last half of
in groups of 3,

Chronic comse. Abortions in late
gestation-may abort
yellowish green, 7 -11
gestation, stillbirths or weak calves, after single exposme.

in. long. Small soft
depressed, edema.of vulva.and

Supportive care,
cones, seeds mature in udder, retained placenta.

remove retained

2-3 yr. Bark platy,
placenta, treat metritis,
reddish orange.

provide good nutrition.

Keep pregnant cows
away from source.

Leaves evergreen,

Hydrocyanic acid (wilted leaves,

See CYANIDE POISONING,
shiny, leathery. Broken bark, and twigs). Pera.cute course.

p2959.

twigs with strong

Difficult breathing, bloat, staggering,
cherry bark odor. Fruit convulsions, followed by prostration black.

and death. Mucous membranes and
blood bright red.

(continued)

3148

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (cont,inued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Pnm1tsspp

Waste areas, fence rows, woods,

All grazing animals,

Chokecherries, Wild
orchards, prairies, dry slopes
mostly cattle and sheep
cherries, Peaches

Psilostrophe spp

Open range lands and pastures;

Sheep primarily; cattle

Paperflowers
southwestern USA
and goats less
susceptible and less
likely to eat the plant.

Pleridium aquilinum Dry poor soil, open woods, sandy All grazing animals

Bracken fern, Bracken, ridges, throughout No1th America Brake fern

Ricinus communis

Cultivated in southern regions

All

Castor bean

Seneciospp

Grassland areas; mostly western

Cattle, horses, sheep to

Groundsel, Senecio

USA
a limited extent in USA

Sorghum halepense

Weed of open fields and waste

All grazing animals

Johnson grass
places; southern and scattered
north to New York and Iowa

Sorghum vulgare

Forage crops and escapes;

All

Sorghum, Sudan grass, throughout North America

Kafir, Durra, Milo,

Broomcorn, Schrock,
etc

POISONOUS PLANTS

3149

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

VetBooks.ir

DANGEROUS SEASON: ALL SEASONS (continued)

Large shrubs or trees. Glycoside-yielding cyanide (rumen Mucous membranes,

Flowers white or pink. hydrolysis). Excitement lea.ding to bright pink color;

Cherries or peaches.

depression, clyspnea., incoordina.tion, blood, bright red color.

Crushed twigs with
convulsions, prostration. Death may See CYANIDE POISONING, strong odor.

occur in 15 min from asphyxiation.

p2959.

Perennial composite.

Sesquiterpene la.ctone. Depression,

Antimicrobial actions

Erect, woolly stems
incoordination, anorexia, weakness, of sesquiterpene branching from base.

trembling, rapid irregular pulse and
lactone in rumen affect

Leaves simple,
respiration, coughing, vomiting,
metabolism. Supplealternate, petioled.

aspiration pneumonia, death.

ment diet with sodium

Many small heads of
sulfate and high
yellow flowers.

protein.

Leaves firm, leathery,

See BRACKEN FERN POISONING, p 3089.

Seep 3089.

3-pinna.te.

Large, palrna.tely lobed Phytotoxin-ricin in all parts ( seeds Diagnosis based on leaves. Seeds
especially toxic). Acute to chronic
presence of seeds, RBC
resembling engorged
course (death or recovery). Violent
agglutination, precipitin
ticks, usually 3 in
purgation, straining with bloody
test. Specific antiserwn,
somewhat spiny pod.

diarrhea, weakness, salivation,
ideal antidote;
trembling, incoordina.tion.

sedatives, a.recoline
hydrobromide,
followed by saline
cathartics suggested.

Perennial or annual

Pyrrolizidine alkaloids, volatile oils, Effects a.re cumulative.

herbs. Heads of yellow and nitrogen oxides (fresh or dry).

Liver biopsy diagnostic
flowers with whorl of Acute poisoning not common.

in early stages. Liver
bracts below.

Dullness, ain1less walking, increased ftmction test of value pulse, rapid respiration, weakness,
for subclinica.l
colic, delayed death ( clays to
condition in cattle.

months). In cattle, prolapsed rectum No general treatment.

from persistent straining. In horses,

See also p 3150.

nervous signs evident in later stages.

Coarse grass with

Sa.me as for S vulgarn (below).

Sa.me as for S vulgare.

large rhizomes and
white midvein on leaf.

Topped by large, open
panicle.

Coarse grasses with

Hydrocyanic acid ( drought,

Hay safe for cyanide
terminal flower
trampling, frost, second growth) and (volatile), not safe for cluster. Some to 8 ft
nitrate (heavy in vegetative parts).

nitrate (analyze). See
ta.II.

Acute course. Difficult breathing,

CYANIDE POISONING,
bloat, staggering, convulsions, death. p 2959, and NITRATE AND

Blood bright red (cyanide) or

NITRITE POISOINING,
chocolate brown (nitrate).

p3049.

(continued)

3150

POISONOUS PLANTS

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (conl,inued)

Scientific and

Common Names

Habitat and Distribution

Affected Animals

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DANGEROUS SEASON: ALL SEASONS (continued)

Ta.xus spp

Most of North America; Japanese

All except deer

Yew
and English yew common ornamen-
tals

Tri.glochin spp

Salt marshes, wet alkaline soils,

Sheep, cattle

Arrow grass
lake shores; dangerous all seasons,
especially dry season; northern half
of N 01th America

" lmages for many of the plants described here, as well as for plants of Australia, the Caribbean, and South Africa, are available online at www.merckvetmanual.com.

PYRROLIZI DINE ALKALOI DOSIS

(Seneciosis, Senecio poisoning, Ragwort toxicity) Typically, pyrrolizidine alkaloidosis is a

Etiology and Pathogenesis: More
chronic poisoning that results in hepatic
than 300 toxic factors (alkaloids with a
failure. It is caused by many toxic plants,
pyrrolizidine base) have been found in
most commonly of the generaSenecio,
plants, with some plants containing a

Crotalaria, Heliotropium, Ams'inckia,
mixture of several different pyrrolizidine

Echium, Cynoglossum, and
alkaloid toxins. Sjacobea containsjacobine; Trichodesma. These plants grow mainly
retrorsine, seneciphylline, and monocrotain temperate climates, but some (eg, line are other pyrrolizidine alkaloids

Crotalaria spp) require tropical or
frequently incriminated in toxicities.

subtropical climates. The plants most

These plants, which under normal
often implicated include ragwort
conditions are avoided by grazing animals,

(Sjacobea), groundsel (Sriddellii,
may be eaten dwing drought conditions.

S longilobus), rattleweed (Crotalaria

Some animals may eat these plants
retusa), and seeds of yellow tarweed
preferentially as roughage when tl1ey are

(A interrnedia).

available on extremely lush pasture.

Cattle, horses, farmed deer, and pigs are

Animals are also poisoned by eating tl1e
most susceptible; sheep and goats require
plant material in hay, silage, or pellets.

-20 times more plant mate1ial than cattle.

Seeds from Crotala1'ia, A msinckia, and
lndjvidual susceptibility varies greatly

Heliotropiiim spp, which have been
within species; young growing animals are
harvested with grain, have caused disease
most susceptible.

in horses, cattle, pigs, and poultry.

PYRROLIZIDINE ALKALOIDOSIS

3151

POISONOUS RANGE PLANTS OF TEMPERATE NORTH

AMERICA• (continued)

Important

Comments and

Characteristics

Toxic Principle and Effects

Treatment

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DANGEROUS SEASON: ALL SEASONS (continued)

Evergreen perennial

Toxic alkaloids in bark, leaves,

Poisoning usually
tree or shrub. Bark
seeds. Gaseous distress, diarrhea,
results when branches
reddish brown then
vomiting, tremors, dyspnea, dilated
and trimmings fed to
flaking in scales. Leaves pupils, respiratory difficulty, livestock
lineai; 0.5-1 in. (1.5-2.5 weakness, fatigue, collapse, coma, cm) long, 2-ranked on
convulsions, bradycardia, circulatwig, upper smface
tory failure, death. Death may be
dark green, lower
rapid.

yellow-green, midribs
prominent. Flowers
unisexual, inconspicuous. Fruit single stony
seed. Bright scai·let
color.

Grasslike, except

Hydrocyanic acid in leaves.

Often, animals found
leaves are thick Heads Salivation, dyspnea, excitement dead. See CYANIDE
of fruits globular on
followed by depression, incoorclina

POISONING, p 2959.

erect raceme.

tion, prostration, convulsions

Flowers inconspicuous. followed by death from anoxia.

The alkaloids are metabolized in the liver
plant may even have ceased months earlier.

to highly reactive pyrroles, which produce

The ongoing hepatic dai11age in these
cytotoxic effects on target sites, most
instat1ces is suspected to be due to the
commonly the nuclei of hepatocytes. Other
recycling of toxic pynoles as they ai·e
tat·get sites may include the epithelial and
released from one dying cell and taken up by
vascular tissues of the kidneys and lungs.

at10ther. Clinical progression may also be

These toxic pyrroles cross-link DNA strands altered by concUJ.Tent hepatic pathology; and also unite DNA with nucleoproteins
a hemolytic crisis may be precipitated in
such as act.in. These moleculai· alterations
sheep with excessive hepatic copper stores
ai·e presumed to create the cytotoxic,

(seep 3073).

ai1timitotic, and megalocytic effects
ln horses and cattle, signs include loss
characteristic of pyrrolizidine alkalosis.

of condition, ai10rexia, dullness, and constipation or diarrhea Tenesmus and passing of bloodstained feces may be followed by rectal

Clinical Findings: Hepatic pathology
prolapse, especially in cattle. Ascites and
with associated clinical signs is the most
icterus may be present, and cattle and sheep
common manifestation of pyrrolizidine
sometimes show intemuttent photosensitizaalkalosis in domestic anin1al species. Acute ti.on (seep 976). Some anin1als become
intoxication is chai·acterized by sudden
progressively weaker and reluctant to move.

death from hemorrhagic hepatic necrosis

Others exlubit signs of hepatic encephalopaand visceral hemorrhages. This is a rare thy such as head-pressing, yawning, aim.less
event, because the poor palatability of these
wandering, or even frenzied and aggressive
plants makes rapid ingestion of lai·ge
behavior. Pica may be seen. Death may occur
quantities of the toxins uncommon. More
suddenly or after prolonged recmnbency with
chronic exposure is typical, and the liver
hepatic coma and high levels of anm1onia in
reflects the cmnulative ai1d progressive
the blood.

effects of repeated ingestion of small doses

Less common clinical signs that have
of toxin. Clinical signs may not be seen for
been described with pyrrolizidine toxicoses
several weeks or months after initial
include inspiratory dyspnea in ponies due to
exposure. Consw11ption of the offending
laryngeal and pharyngeal paralysis, dyspnea

3152

PYRROLIZIDINE ALKALOIDOSIS
due to interstitial pnewnonia in horses, and
been described but is not widely available.

renal disease in pigs.

More commonly, a presumptive diagnosis

Lesions: In acute cases, the liver may
is ma.de based on clinical signs, compatible
be enlarged, hemorrhagic, and icteric. In
changes in biochemical para.meters,
clu·onic cases, it is atrophied, fibrous, finely
and a history of exposure. When hepatic

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nodular, and usually pale with a glistening
cirrhosis is extensive, hypoalbuminemia.

swface due to fibrous thickening of the
and hyperglobulinemia. develop. Serum
capsule. Other livers are markedly icteric.

levels of fibrinogen, bilirubin, -y-gluta.myl

The gallbladder is often edematous and
transfera.se, and glutan1a.te dehydrogenase
grossly distended with thick, mucoid bile.

may be increased, but it should be

Edema of the aboma.sum and segments
recognized that the insidious nature of
of the bowel, mesentery, and associated
this disease can result in smprisingly
lymph nodes is common, and there may
mild serum biochemical changes. Hepa.tic
be a.scites. In some cases, nw11erous small
biopsy is often useful, especially if
hemorrhages are present in the abdominal
megalocytic change is seen. Other
serous membranes. The lw1gs of some
hepa.totoxins, such as copper or a.fla.toxin,
severely affected horses may be emphyseas well as infections such as chronic fa.sciomatous and fail to collapse (often due to liasis, must be considered before ma.king
ingestion of Crotalaria spp ).

the diagnosis. At necropsy the diagnosis

Characteristic histologic changes occw-in
can often be ma.de based on gross findings,
the liver. Irreversible enlargement of
together with characteristic histologic
individual hepatocytes (megalocytosis) is
changes in hepatic, pulmonary, and/or
often seen; it is conspicuous in horses and
renal tissues. Hepatic assay for pyrrolic
sheep but less pronounced in cattle. In cattle, metabolites can also be performed.

marked perivenous fibrosis of sublobula.r
veins is usually present, but this is not a

Treatment and Control: Fwther intake
consistent finding in horses and sheep. In all
of toxic plant material must be prevented.

species, increases in connective tissue, both

Animals showing signs rarely recover, and
within and around the lobules, are marked.

lesions present in a.symptomatic animals

Bile duct hyperplasia is variable but may be
may progress and result in further losses
the most striking microscopic change seen
over several months. Because high proin some livers. Pulmonary changes seen in tein intake may precipitate clinical signs,
horses exposed to some Crntalaria spp may
rations high in carbohydrates a.re indicated.

include hyperplasia. of bronchoalveolar

Suppo1tive treatment for dehydration and
epitheliun1, congestion, septa! fibrosis, and
photosensitiza.tion may be needed.

emphysema.. Renal tubular lining cells and

Preventing further outbreaks by reducing
glomerula.r epithelial c�lls also may be
exposure should be stressed.

individually enlarged in pigs.

Sheep a.re conunonly used for grazing
control of these plants, but this practice
carries risks unless sheep destined for early

Diagnosis: Chemical analysis of whole
slaughter a.re used. Biologic control of
blood for toxic metabolites oon confirm
plants with predator moths, flea beetles, and
recent exposw-e but depends on the
seed flies has met with variable success.

half-life of RBCs to which these pyrroles

Senecio and related toxic species in
a.re bound. An ELISA that recognizes
pastures have been controlled satisfactorily
riddelliine and closely related pyrrolizidine
by annual herbicide applications, preferably
alkaloids present in whole blood has also
in spring before hay or silage conservation.

OUERCUS POISONING

(Oak bud poisoning, Acorn poisoning)

Most animals a.re susceptible to Quercus
occur 3-7 days a.f'ter consumption of large
poisoning, although cattle and sheep are
quantities of young oak leaves in the spring
affected most often. Most species of oak
or green a.corns in the fall. Fallen trees

(Quercus spp) found in Europe and North
associated with a recent stmrn a.re often

America a.re considered toxic. Clinical signs
repo1ted with outbreaks. Feed restriction

RYEGRASS TOXICITY

3153
before exposure plays a crucial role
of hepatotoxicity characterized by increased
enhancing susceptibility. Mortality as high
liver enzymes may also be present.

as 7{)0A, may be seen. Malformed calves and

Diagnosis is based on clinical findings,
abmtions have been reported in darns
necropsy, history, and histopathologic
conswning acorns dwing the second
examination of the kidney (ie, nephrosis).

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trimester of pregnancy. The toxic principle,

Other common diseases that resemble oak
which appears to be pyrogallol, gallotanpoisoning include pigweed (Amara.nthus nins, polyhydroxyphenolic compounds, or
spp) poisoning, an1inoglycoside antibiotic
their metabolites produced by microbial
poisoning, oxalate poisoning, and ochrahydrolysis in the rumen, binds and toxicosis.

precipitates proteins, which results in

Consumption of a pelleted ration

GI and renal dysfunction.

supplement (1 kg/head/day) containing

Signs include anorexia, depression,

10%--15% calcium hydroxide plus access
emaciation, brisket edema, dehydration,
to more palatable feeds may be used as a
rumen stasis, tenesmus, smell of ammonia on
preventive measure if exposure to acorns
the breath, serous ocular or nasal discharge,
or oak leaves cannot be avoided. Calcium
polydipsia, polywia, hematuria, icterus,
hydroxide, activated charcoal, ruminatoand constipation followed by mucoid to rics, and purgatives (such as mineral oil [l
hemoffhagic diaffhea Renal insufficiency,

1/500 kg], sodium sulfate [l kg/400 kg], or
which is evident 4---6 days after exposure,
magnesiwn sulfate [450 g/400 kg]) may be
may be characterized by increased BUN and
effective antidotes if administered early in
creatinine, proteinwia, glucoswia, hyperbilithe course of disease. Polyethylene glycol rubinuria, hyperphosphatemia, hypocalce

(1 gtkgtday) administered in the feed or
mia, and urine with a low specific gravity. Pale water will bind tannins and reduce tissue swollen kidneys characte1ized by coagulative
damage. Fluid therapy to correct dehydranecrosis of the proxin1al convoluted tubular tion and acidosis and transplantation of
cells, perirenal edema, subcutaneous edema,
ruminal microflora may be beneficial.

ascites, and hydrothorax are common

Clinical recovery usually occurs within
necropsy findings. Edema and subserosal

60 days but is rare if renal dysfunction is
petechial or ecchymotic hemmrhage of
severe. Improved range management to
intestinal mucosa and ulceration of the
limit grazing in immature oak stands will
esophagus and runien may be seen. Evidence
prevent development of the syndrome.

RYEGRASS TOXICITY

ANNUALRYEGRASS STAGGERS
colonized by R toxicus. These bacteriainfected galls are present in infected annual This often fatal neurotoxic disease occurs in
ryegrass pastures from early spring onward,
livestock of any age that graze pastures in
but they are most toxic when the plants
which armual ryegrass (Loliiim rigidum) is
senesce. Hence, animals show no sign of
present and in the seedhead stage of growth. toxicity until late spring and sunimer. Spread It is seen in western and southern Australia
of bacteria-infested nematodes to adjacent
and in South Africa from November to
healthy armual ryegrass pastures is slow.

March. Hay of Festuca 1ubra commutata

The corynetoxins are highly toxic

(Chewing's fescue) with Rathayibacter
glycolipids that inhibit specific glycosylation
lox'icus-infected seedhead galls has caused
enzyn1es and therefore deplete or reduce
a similar disease in cattle and horses in
activity of essential glycoproteins. Experi

Oregon. Outbreaks of ergot alkaloid toxicity
mentally, the corynetoxins deplete
in cattle on L i'igidum have been repmted in fibronectins and cause failure of the hepatic South Africa and should not be confused
reticuloendothelial system. Cardiovascular
with armual ryegrass staggers.

function and vascular integrity are conse

In Australia, the responsible corynetoxins
quently impaired, and peripheral circulation

(members of the tunicaniinyluracil group)

and oxygen distJibution is compromised.

are produced in seedhead galls induced by

Twlica.mycin irreversibly downregulates the
the nematodeAnguinajunesta and
expression of specific -y-aniinobutyric acid

3154

RYEGRASS TOXICITY
receptors and causes cell death in cultured
south Australia the bacterium in emerging
brain neurons. Hence, the clinical expression seedheads is detected and quantified by of the disorder is nervous.

ELISA. Early detection of toxic fields enables

Outbreaks occur 2-6 days after animals
farwers to mow the heads off grass or to
graze a pasture that contains annual
allow grazing before the grass becomes too

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ryegrass infected at a toxic level. Deaths
toxic. Grazing of hay aftennatl1 from toxic
occur within hours, or as long as l wk after
pastmes should be avoided. Burning annual
onset of signs. Characteristic neurologic
ryegrass pastures in the fall destroys most of
signs a.re similar to those of perennial
the galls colonized by bacteria and minimizes
ryegrass staggers (seep 3154). However,
the lisk of toxicity in the following season.

mmtality from annual 1yegrass toxicity is
commonly 4()0/c,--500/o and occasionally

PERENNIAL RYEGRASS
higher. The lesions include congestion,

STAGGERS
edema, hemorrhage of the brain and lungs,
and degeneration of the liver and kidneys.

TI1is neurotoxic condition of grazing

Diagnosis is based on the characteristic
livestock of all ages occurs only in late
neurologic signs of tremors, incoordination,
spring, swnmer, and fall and only in pastures
rigidity, and collapse when stressed, with
in which perennial ryegrass (Lolium
animals often becoming apparently nonnal
perenne) or hyblid rye grass are the major
again when left undistmbed. When animals
components. Sheep, cattle, horses, farmed
a.re severely affected, nervous spasms
deer, and llamas a.re susceptible. In New
supervene, and convulsions could be

Zealand, a high incidence most year;; causes
precipitated by either forced exercise or high
considerable loss ar1d seriously disrupts
ambient temperatures. A thorough history
management procedures and stock
and evaluation of tl1e pastures will assist in
movement. Perennial ryegrass staggers
differentiation of staggers caused by other
occurs sporadically in parts of North and
grasses such as perennial ryegrass, phalaris,

South America, Europe, and Australia
and the ergots of paspalum and other grasses.

The tremorgenic neurotoxins responsible

Polioencephalomalacia and enterotoxemia
ar·e lolitrems, mainly lolitrem B. These
a.re other differential diagnoses.

indole diterpene alkaloids a.re produced in

Clinical signs identical to tl10se of annual
perennial and hybrid ryegrasses infected
ryegrass toxicity have been described in
with the endophytic fungus Neotyphodium

Australia in animals grazingAgrostis
lolii. The an10unts of fungal hyphae and
avenacea ( annual blown grass), Polypogon lolitrem Bin infected plants increase to
monspeliensis (annual beard grass), or
toxic levels as tl1e temperature rises in late

Ehrha1"la longijlora (annual veldtgrass) spring and decrease again to safe levels in
infected with nematode galls containing
the cooler seasons. Mycelia of the fungus

R toxicus. These diseases have been called
ar·e present in all above-ground parts of
flood plain staggers, Stewart range
infected plants but a.re especially concensyndrome, and veldtgrass staggers, trated in leaf sheaths, flower stalks, and
respectively. Although the same bacterium
seed. Infected plants exhibit no signs, and
is responsible for all the diseases, the
the fungus is spread only through infected

Anguina nematode vectors ofR toxicus for seed. Viability of the endophyte gradually these three grasses a.re different species
declines when infected seed is stored at
than theAfunesta associated witl1 annual
ambient temperatures and moderate to high
ryegrass toxicity. Whereas the infloreshmnidity, so that few seeds cantain viable cences of a.rmual ryegrass infected witl1 A
endophyte after 2 yr. Lolitrem B acts as a

Junes ta usually appear· nom1al, nematodepotent large conductarlce calcium-activated infested inflorescences of tl1ese other
potassimn (BK) channel inhibitor. It is
grasses show distinctive signs.

thought that the incoordination observed

A significar1t increase in survival of sheep
when animals a.re exposed to lolitrem Bis
experimentally poisoned with tunican1ycin
caused by interference with neuronal
was observed after treatment witl1
transmission in the cerebellwn; no specific
derivatives of 13-cyclodextrin. TI1e promising
histologic lesion is recognized. N lolii also result with this toxin-binding agent offers
produces the ergopeptine alkaloid
hope for treatment of animals once tl1ey have ergovaline, which is the alkaloid responsibecome affected with annual ryegrass ble for fescue toxicosis. Ergovaline raises
staggers. Losses from tl1e disorder can be
the temperature of animals in the warmer
minimized by early recognition of signs and
months of the year, inducing heat stress. It
removal to safe grazing or by reducing
also depresses prolactin levels, and reduced
grazing pressure. Gall identification is
milk yield in cows has been recorded in
difficult in a.rmual ryegrass pastures, and in

New Zealand and Australia.

SORGHUM POISONING

3155

Signs develop gradually over a few days.

is spontaneous in 1-2 wk if animals are

Fine tremors of the head and nodding
moved to nontoxic pastures or crops.

movements are the first signs noted in

Because the endophyte and the lolitrems
animals approached quietly and watched
and ergovaline are not uniforn1ly distributed
carefully. Noise, sudden exercise, or fright
within ryegrass plants, control by grazing

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elicits more severe signs of head nodding
management can help reduce or prevent t11e
with jerky movements and incoordination
disease. Lolitrems and ergovaline are
when first moved. Running movements are
concentrated in the leaf sheath and
stiff and bounding with marked incoordinainflorescences. If pastures are not tion and often result in collapse in lateral
overgrazed do"711 into the leaf sheath zone
recumbency with opisthotonos, nystagmus,
or grazed when the plants are flowering,
and flailing of stiffly extended limbs. In Jess
then animals should be relatively safe even
severe cases, the attack soon subsides, and
when a high propo1tion of the ryegrass
the animal regains its feet within minutes.

plants are infected with endophytes.

If the anin1al is again forced to run, the

Encouragement of growth of other grass
episode is repeated. Signs are most severe
species and legumes in established swards
when the animal is heat stressed.

also reduces the intake of toxic grass.

Within flocks and herds, individual

Safe new pastures can be established
susceptibility varies greatly, and this trait is
using ryegrass seed with little or no
heritable. In outbreaks, morbidity may reach
endophyte infection. Alternatively, seed that

800h-90%, but mortality is low (0-5%). Deaths
has been stored at ambient temperatures for
are usually accidental, often by drowning

18---24 mo probably contains few viable
when drinking from ponds or streams, or due endophytes and would produce nontoxic to the inability to forage for food and water.

pastures. However, the presence of

The strict seasonal occurrence of
endophyte in grasses makes the plants
characteristic tremors, incoordination, and
resistant to attack from many insects; thus,
collapse in several or many animals grazing
infected pastures are more persistent than
predominantly perennial ryegrass pastures
endophyte-free pastures. Cul ti vars of
strongly implicates this disease. Reference
ryegrass artificially infected with a strain of
to the botanical composition of the pastures endophyte that does not produce lolitrem B
will exclude annual ryegrass toxicity (see
or ergovaline are available in New Zealand.

p 3153) and paspalum staggers (seep 3019),

Signs of ryegrass staggers have not been
which have similar clinical signs and
seen in animals grazing these grasses. A
seasonality. Microscopic examination of
strain of Neolyphodium that produces
the leaf sheatl1s of the ryegrass sward will
compounds known as epoxy janthetrems
reveal the extent of endophyte infection.

has been developed that offers an extended

Because movement and handling of
range of pasture insect resistance with the
animals exacerbates signs, individual
trade-off of sporadic occmTence of
treatment is generally impractical. Recovery low-level staggers.

SORGHUM POISONING

(Sudan grass poisoning)

Sorghun1 species are drought-tolerant
have grazed hybrid Sudan pastures for
plants that may produce neuropathic and
weeks to months and produces axonal
teratogenic manifestations. Sorghum
degeneration and myelomalacia in the
poisoning has been seen primaiily in the
spinal cord and cerebellum. (See also
southwestern USA and Australia. The

CYANIDE POISONING, p 2959.) Consun1ption of
syndrome is reported almost exclusively in
the seed will not produce the syndrome.

horses, although a sin1ilar disease has been

Sorghm11 poisoning is characterized by
reported in sheep and cattle. Lathyrogenic
posterior ataxia or incoordination, cystitis,
nitriles such as [3-cyanoalanine, cyanogenic
urinary incontinence (which predisposes
glycosides, and nitrates have been
both male and female horses to cystitis),
suggested as causative agents. The
and alopecia on the hindlegs due to urine
syndrome develops in horses after they
scald. The loss of urinary bladder function

3156

SORGHUM POISONING
is related to degeneration of spinal cord
the primary concern. Consumption of
neurons. The incoordination may progress
sorghum hybrids with low cyanogenic
to irreversible flaccid paralysis. Defonnities
potential or restriction of access to sorghum
of the fetal musculoskeletal system
grasses may limit the incidence. Dietaiy

(ankylosis or arthrogryposis) and abortion
supplementation with sulfur may be

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may occur during late pregnancy. The
beneficial. Affected horses often die from
diagnosis is based on the analysis of urine
pyelonephritis. Treatment with antibiotics
for evidence of cystitis, characterization of
may be helpful, but a full recove1y is rare
spinal cord lesions, and analysis of forage
if ataxia has developed. Consw11ption of
for cyanide. Although fatal poisoning is
pastures containing sorghwn plant species
infrequent, the impact on reproduction is
is not recommended for horses.

SWEET CLOVER POISONING

Sweet clover poisoning, an insidious
content of tl1e particular sweet clover
hemorrhagic disease, is seen in anin1als that
variety being fed, age of the animals, and
consume toxic quantities of spoiled sweet
an10W1t of feed conswned. If the dicumarol
clover (Melilotus ojficinalis and M alba) content of the ration is low or variable,
hay or silage.

anin1als may conswne it for montl1s before
signs of disease appear.

Etiology: During the process of spoiling,

The first indication of d.icwnarol
the cotm1arins in sweet clover are converted poisoning may be the death of one or more to toxic d.icwnarol, a potent vita.111in K
animals. In affected animals, tl1e first signs
antagonist and anticoagulant. Any method
may be stiffness and lameness, due to
of hay storage that allows molding of sweet
bleeding into tl1e muscles and joints.

clover promotes the likelihood of fom1ation

Hematomas, epistaxis, or GI bleeding may
of d.icumarol in the hay. Weathered, large
also be seen. Death is generally caused by
round bales, particularly the outer po1tions,
massive hemorrhage or bleeding after il\iwy,
usually contain the highest concentrations
surge1y, or parturition. Neonatal deaths
of dictm1arol. When toxic hay or silage is
rarely occw- witl10ut signs in tl1e dam.

conswned for several weeks, dicwnarol
alters proenzymes required for synthesis of

Diagnosis: Poisoning occurs when sweet
prothrombin, resulting in hypoprothromclover hay or silage is conswned continually binemia (by preventing fom1ation of the.

for relatively long periods. Diagnosis is
active enzyme). It probably also interferes
made by identifying compatible signs and
with synthesis of factor VII and other
lesions and markedly prolonged blood
vitainin K-dependent coagulation factors
clotting tin1e or demonstration of reduced

(seep 44). Dicwnarol concentrations of
plasma prothrombin concentrations. '.!'he

20-30 mg/kg of hay ingested throughout
nature of the coagulopathy can be
several weeks are usually required to cause
confirmed in the laboratory when tl1e
poisoning in cattle. The toxic agent crosses
prothrombin time is prolonged. Sweet
the placenta in pregnant animals, and
clover poisoning is normally a herd
newborn animals may be affected at birth.

problem, making conditions that affect

All species of animals studied are susceptiindividual anirnals,such as blackleg, ble, but instances of poisoning involve cattle
pasteurellosis, bracken fern poisoning,
and, to a lin1ited extent, sheep, pigs, and
and aplastic anemia, less likely causes.

horses.

Rodenticide poisoning (seep 3165) is the
primary differential diagnosis in which such

Clinical Findings and Lesions: Clinical
large hemorrhages are also likely to occur.

signs are referable to hemorrhages that

Congenital or inherited diseases affecting
result from faulty blood coagulation. The
coagulation factors or blood platelets ( eg,
time between consumption of toxic sweet
hemophilia A) may produce similar large
clover and appearance of clinical disease
hemorrhages but with largely different
varies greatly and depends on the d.icumarol
morbidity.

CANTHARIDIN POISONING

3157

Treatment: The hypoprothrombinemia,
transfusion is sufficient to cotTect mild cases
hemotThages, and anemia can be immediif additional exposure is stopped.

ately cotTected, to a degree, by IV admirtistration of whole blood. This may be difficult in Prevention: Cultivars of sweet clover low
large animals, because effective dosages
in cmunarin and safe to feed ( eg, Polara)

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range from 2--10 L of fresh blood per 1,000 lb
have been developed. If one of these is not

( 450 kg) body wt. Care should be taken to
available, the only certain method of
ensure that donor animals are not receiving
prevention is to avoid feeding sweet clover
sweet clover feed. All clinically affected
hay or silage. Although well-cured sweet
animals should receive a transfusion, which
clover is not dangerous, the absence of
can be repeated if necessary. In addition, all
visible spoilage is insufficient evidence of
severely affected animals should receive
safety.

parenteral admirtistration of synthetic

Alternating sweet clover hay suspected of
vitamin K, (phytonadione). SC or IM ir\jection containing dicumarol with other roughage is recommended to avoid the substantial risk
such as alfalfa or a grass-legume hay
of anaphylaxis; SC vitanlin K, may not be as
mixture can be used to avoid severe
effective as IM treatment. The usual dosage
poisoning. A 7- to l 0-day period on the sweet
recommended for cattle isl mg/kg, bid-tid for clover hay, followed by an equal time on the 2 days. Although it is more costly, vitanlin K,
alternative hay, can prevent poisoning, but it
is more effective tl1an K3 (menadione).

will not completely prevent prolonged

Because reversal of the dicumarol by
bleeding tinles. Because some animals have
vitamin K, requires synthesis of coagulation
higher 1isks of serious hemotThage (surgical
proteins, several hours are required for
candidates or pending paiturition), they
significant improvement in homeostasis, and
should not receive sweet clover hay for a

>24 lu· is required to completely restore
minimw11 of2-3 wk, and preferably �4 wk,
coagulation. Either vitanlin K, or a blood
before surgery or paitwition.

CANTHARIDIN POISONING

(Blister beetle poisoning)

In natme, cantharidin is found in beetles
various orgai1ic solvents but only slightly
belonging to the Meloidae fanlily. More tl1an
soluble in water. It is highly irritating and

200 species of these beetles ai·e found
causes acantholysis and vesicle formation
throughout tl1e continental USA, but
when in contact with skin or mucous
members of the genus Epicauta are most
membranes. After ingestion, it is absorbed
frequently associated with toxicosis in
from tl1e GI tract and rapidly excreted by the
horses. TI1e striped blister beetles (E occi
kidneys. The minimun1 lethal oral dose
dentalis, E temexia, andEvittata) are
in horses has not been established, but it
paiticularly troublesome in the southwestern appears to be < l mg/kg body wt. As little USA. The black blister beetle, E pennsyl
as 4--6 g of dried beetles may be fatal to a
vanica, has caused toxicosis in horses in
horse. The toxicity of cantharidin does not

Illinois. Cantharidin is the sole toxin, but its
decrease in stored hay, and cantharidin is
concentration in beetles varies widely.

also toxic to people, cattle, sheep, goats,

Blister beetles usually feed on various
dogs, cats, rabbits, and rats.

weeds and occasionally move into alfalfa
fields in large swairns. These insects ai·e
gregaiious and may be fowid in hay in lai·ge

Clinical Findings: The severity of clirtical nun1 bers when it is baled. One flake of alfalfa signs associated with cantharidin toxicosis may contain several hundred beetles, but a
varies according to dose. Signs may range
flake from tl1e other end of the saine bale
from nlild depression or discomfort to severe
may have none. Animals ai·e usually exposed pain, shock, and death. Typical signs are by eating alfalfa hay or alfalfa products that
related to GI and winary tract irritation,
have been contai11inated witll blister beetles. endotoxemia and shock, hypocalcemia, and myocardial dysfunction. The onset and

Pathogenesis: Cantharidin is an odorduration of signs can vary from homs to days.

less, colorless compound that is soluble in

TI1e signs seen most frequently include

3158

CANTHARIDIN POISONING
varying degrees of abdominal pain, deprescan be positively identified if from one of sion, anorexia, and frequent attempts to drink
the three striped species.

small amounts of water or submerge the

Certain laboratory findings are particumuzzle in water. Some horses show only signs larly helpful in differentiating cantharidin of depression or make frequent attempts to
toxicosis from other causes of acute abdom

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urinate. Urine may be blood-tinged or contain
inal crisis. Serun1 calcium concentration is
blood clots but frequently appears nom1al.

usually markedly decreased and may

A striking feature is that affected horses
remain low for a prolonged tinle. Serum
invariably have dark, congested mucous
magnesium concentration is also typically
membranes, even if otl1er systemic signs of
low, and concentration of senm1 CK usually
toxicosis are minin1al. Sweating, delayed
increases markedly within 24 hr of onset. In
capillary refill tinle, increased heart and
acutely affected horses, urinalysis typically
respiratory rates, and increased rectal
reveals markedly decreased specific gravity
temperature are other conunon signs.

(usually <1.010) and varying degrees of

Less frequent signs include oral erosions;
hema.turia.. Peritoneal fluid usually contains
salivation; synchronous diaphragmatic
increased protein (>4 g/dL) but nom1al
flutter, a stiff, shmt-strided gait; and diarrhea
numbers of WBCs and nom1al fibrinogen
that may contain blood. Horses that ingest a
concentration. Other laboratory a.bnom1alimassive amount of toxin may show signs of ties may include mild increases of senmi
severe shock and die within homs.

urea nitrogen and crea.tinine and development of hypoproteinemia.. Acutely affected Diagnosis: Both high-performance liquid
horses a.re almost al ways hyperglycemic.

clu·omatography and gas clu·omatography
or mass spectrometry analyses are

Treatment: There is no specific antidote
sensitive, reliable methods of detecting
for cantharidin poisoning, but prompt,
cantharidin in gastric contents or in urine.

vigorous symptomatic therapy is necessary

The concentration of cantharidin in urine
for a good outcome. Oral administration of
becomes negligible in 3-4 days, so urine
mineral oil aids in evacuation of the GI tract,
should be collected early in the course of
and repeated dosing may be indicated.

disease if it is to be analyzed. Microscopic

Activated charcoal, PO, may be helpful
evaluation of stomach contents (and often
if given early. Other oral adsorbents
cecal contents) of fatally poisoned horses
containing ditriocta11ed.ral smectite might
may reveal fragments of the insect, which
be helpful as well, but their efficacy has not
been evaluated. Calcium and magnesium
supplementation for prolonged periods is
almost always indicated. Other syn1ptoma.tic therapy includes administration of fluids, analgesics, and diuretics and
maintenance of normal blood pH and serw11
electrolyte concentrations. The prognosis
for affected horses inlproves daily if no
complications occur.

Prevention: Prevention is by feeding
beetle-free hay. The hay field must be
scouted before it is cut a.rid dming baling,
because the insects can be crnshed in the
cutting and crimping process as well as
during baling. Areas of the field that contain
swa.nns of beetles must be avoided for a few
days because most of the insects will leave.

Once the beetles have left, these areas can
be harvested.

First-cutting hay is almost always free
of blister beetles, because the insects
overwinter as suba.dults and usually do
not emerge until late May or June in the
southwestern USA. Likewise, the last
cutting of hay is often safe, because it is

Epicauta pardalis blister beetle. Courtesy
usually harvested after the adult insects are
of Dr. D. G. Schmitz.

no longer active.

SNAKEBITE

3159

SNAKEBITE

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Venomous snakes of North America are
cattle seldom die as a direct result of
members of either of two families: 1) the
snakebite, but deaths may follow bites on the

Elapidae or coral snakes (Mie1urus spp ); or muzzle, head, or neck when dyspnea results 2) the Crotalidae, or pit vipers (rattlesnakes
from excessive swelling. Serious secondary

[ Crolalus spp], cottonmouth moccasin
dan1age son'tetimes occurs; livestock bitten

[Agkislrodon piscivorus], and copperhead
neru· the coronary band may slough a hoof.

[A cortotri.1::]). Elapids are generally

Snakebite with envenomation is a true
restricted to southern edges of the USA,
emergency. Rapid exan1ination and appropriwhereas crotalids are dispersed across the ate treatment are parru11otmt. Owners should
continent. Because of their wider distribunot spend time on first aid other than to keep tion and less secluded natmes, bites by
the anin1al quiet and limit its activity. The
crotalids are much more common than
following conm10nly touted measures are
elapid bites. Rattlesnakes account for most
ineffective and can be potentially harmful:

snakebite-related deaths in people and
use of ice, cold packs, or sprays; incision ru1d
domestic anin1als in the USA. Although
suction; tourniquets; electJ.ic shock; hot

Australia is home to a large number of
packs; and delay in presentation for medical
venomous snakes from the families
trcatJ.11cnt ( waiting w1til problems develop).

Colubridae, Hydrophiidae, and Elapidae,
the most clinically significant venomous

Diagnosis: ln many instances, the bite
species are elapids, pruticularly the black
has been witnessed, ru1d diagnosis is not

(Pseudechis), brown (Pseudonaja textilis), a problem. However, fractmes, abscesses,

Taipan (Oxyuranus sp), and tiger (Notechis spider envenomations (seep 3162), or
scutatus) snakes.

allergic reactions to insect bites or stings

Crotalids have long, hinged, tubular fangs
could all potentially be confused with a
with which they strike, inject venom (a
snakebite by the inexperienced eye. When
voluntary action), and withdraw. Many
possible, the dead snake should be brought
bites by vipers reportedly do not result in
along with the bitten anin1al; mutilation of
injection of substantial quantities of venom
the snake's head should be avoided, because
and ru·e therefore tern1ed "dry bites."

this may hinder proper identification. Some

Crotalid venom is typically hemotoxic,
bites do not result in envenomation or have
necrotizing, ru1d anticoagulant, although a
been made by nonvenomous snakes. IJ1
nemotoxic component is present in the

Australia, venom detection test kits have.

venom of some species, eg, the Mojave
been developed to detect the various snake
rattlesnake (C scutulatus sculitlatus).

venoms and detemtine the appropriate

North American elapids have short fangs
antivenom to use, but these appear to be
that deliver a nemotoxic venom that
infrequently used for veterinary patients.

pru·alyzes the respiratory center. Except for

Typical crotalid bites are characterized by
death adders (Acanlhophis spp ), the venom severe local tissue damage that spreads from delivery system of which resembles that of
the bite site. The tissue becomes markedly
crotalids, Australian elapids tend to have
discolored within a few minutes, and dark,
relatively short, grooved to tubular fangs.

bloody fluid may ooze from tl1e fru1g wounds

TI1e venoms of Australian elapids may have
if not prevented by swelling. The epidermis
neurotoxic, myotoxic, procoagulant,
may slough when tl1e overlying hair is
anticoagulant, and/or hemolytic properties;
clipped or pruted. Hair may hide the typical
pronounced cardiovascular abnonnalities
fang marks. Sometimes, only one fang mark
have been associated with envenomation by or multiple punctmes are present. Nemotiger ru1d brown snakes.

logic signs, including muscle fasciculations,

Fatal snakebites are more conm1on in
are possible if nemotoxic crotalid venom is
dogs than in other domestic anin1als.

involved. ln elapid snakebites, pain and

Because of the relatively small size of some
swelling are minin1al, ru1d systemic
dogs in proportion to the amount of venom
nemologic signs predominate. Signs of coral
injected, the bite of even a small snake may
snake envenornation include tetraparesis,
be fatal. ln dogs and cats, mortality is
ptyalism, tachypnea, shallow/abdon1inal
generally higher in bites to the thorax or
breathing, depressed gag reflex, ataxia,
abdomen than bites to the head or extremimuscle fasciculation, decreased spinal ties. Because of their lru·ger sizes, horses and
reflexes, ru1d quiet mentation. Australian

3160

SNAKEBITE
elapid bite victims may show collapse,
drai11ine, should be administered SC. In
vomiting, ptyalism, tremors, tachypnea,
severe envenomations, multiple vials of
urinary ancVor fecal incontinence, tetrapareantivenom/a.ntivenin may be required, sis, hemolysis, coagulopathy, rhabdomyolyalfuough fuis is frequently cost-prohibitive VetBooks.ir
sis, swelling at the bite site, renal failure,
in veterinaiy patients.

ancVor delayed immune-mediated hemolytic

Antivenin generally helps significantly
anemia (red-bellied black snake).

in mairnging fue pain of a crotalid bite, but
opioid ai1algesics may be used as needed for

Treatment: Intensive therapy should be
residual pain. lf coagulopathy (U1rombocytoinstituted as soon as possible, because penia, disseminated intravascular coagulai.1Teversible effects of venom begin inunedition, etc) occurs, appropriate treatment, ately after envenomation. The bite site(s)

including blood replacement products and
should be shaved, and the wounds cleansed
heparin sodiwn (in mini dose at 5-10 U/kg!lu·
thoroughly with gennicidal soap. For animals
or low dose at 50-100 U/kg, SC, tid), should
bitten by crotalids, the leading edge of tissue
be administered. Hemoglobin glutainer-200
swelling should be marked on the skin with a

(bovine) or hetastai·ch may be helpful to
magic marker at frequent inte1vals to monitor manage hypovolemia; however, colloids the spread of tissue injwy. All snakebite
should be used witl1 caution because of tl1eir
victims should be monitored closely for a
potential to leak out of dainaged vessels and
minirnwn of24 ( crotalid) to 48 ( elapid) hr
pull fluids into tissue beds.

for the development of clinical signs.

Several potential pathogens, including

Treatment for crotalid envenomation

Pseudomonas aeruginosa, Clostridium
should be directed toward preventing or
spp, C01ynebacteriwn spp, ai1d staphylocontrolling shock, neutralizing venom, cocci have been isolated from the mouth of
preventing or controlling coagulopathy, minirattlesnakes. However, llie incidence of mizing necrosis, and preventing secondaiy
wound infection after snake bites is low,
infection. Any dog or cat presented wiU1in 24
and many cliniciai1s use antibiotics only
hr of a snakebite showing signs of crotalid
when significant tissue necrosis is present.

envenomation requires intensive treatment,

Broad-spectrum antibiotics such as
starting with IV c1ystalloids to combat
ai11oxicillin/clavula11ate or cephalosporins
hypotension. Rapid-acting corticosteroids
are preferred.

may be of benefit in the first 24 lu· to help

Tetanus a11titoxin also should be
control shock, protect against tissue
considered, especially in horses, and other
damage, and minimize U1e likelli1ood of
supportive treatment should be adminisallergic reactions to ai1tivenin; however, tered as needed ( eg, blood or plasma
prolonged use of corticosteroids is not
trai1sfusions in the case of hemolytic or
recommended. Monitoring for the developanticoagulant venoms). In most cases, smgiment of echinocytes or coaguJopathy is cal excision of tissue is in1practical or
reconunended, because U1ese are often eai·ly
unwarranted. Antihistainines have been
signs of severe envenornation.

rep01ted to be contraindicated, but

Antivenom is the only direct and specific
diphenhydrainine hydrochloride (10-50 mg,
means of neutralizing snake v�nom.

SC or IV) has been shown to be helpful to

Antivenorns available against No1th
manage fractious patients a11d may possibly

An1erican pit vipers include equine-derived
assist in minimizing ,;sk of allergic
polyvalent antivenin, ovine-origin polyreactions to antivenin.

valent F( ab) fragment antivenin, and

Animals bitten by elapids may be treated
equine-origin polyvalent F( ab )2 fragment
willi supportive care as needed (IV fluids,
antivenin. The F(ab) antivenins use the
ventilatory support, anticonvulsants, etc)

F(ab) components of the inu11W1oglobulin
and antivenom/ai1tivenin, if available.

molecule, resulting in an antivenin fuat has

Ventilatory support is frequently required for
lower risk of allergic reaction, faster

6-8 hr in anin1als experiencing Australian
reconstitution, and potency sirnilai· to fuat
elapid envenomation; additional vials of
offue polyvalent immunoglobulin.

ai1tivenom can reduce ventilator tin1e.

Antivenin is most effective if administered

Anti venom against coral snake venoms is
in the fu-st 6 lu· after fue bite, although
no longer being manufactured in the USA,
improvement in clinical condition may be
altl10ugh some practitioners have received
seen after antivenin administered �24 hr
special permission to import coral snake
after fue bite. In U1e unlikely event of an
antivenom from Mexico. In Australia,
ai1aphylactic reaction to fue antivenin,
several a11tivenoms/antivenins ai·e available

0.5-1 mL of 1: 1,000 epinephrine, with or
for use in veterinaiy patients. A polyvalent
without antihistamines such as diphenhy-
antivenin is available for use when U1e

TOAD POISONING

3161
identity of the snake cannot be ascertained,

Prognosis: The prognosis of snakebite
and many clinicians prefer to use the
depends on the type and species of snake,
polyvalent antivenin for all envenomations.

location of the bite, size of the victim,

Additionally, animals bitten by Australian
degree of envenomation, and the time
elapicls should be monitored for developinterval between the bite and the institution VetBooks.ir
ment of coagulopathy, hemolysis, renal
of treatment. Animals that smvive elapid
i[\jmy, cardiovascular abnonnalities, or
bites generally make full recoveries, but
rhabclomyolysis; appropriate treatment
crotalid bites can result in longterm
should be instituted as needed. As with
sequelae clue to tissue necrosis (amputacrotalicl bites, broacl-spectrwn antibiotics tion, loss of function, etc), depending on the
may be indicated if there is risk of infection
severity of the bite and the promptness and
of the bite wound.

aggressiveness of treatment instituted.

TOAD POISONING

Dogs and, less frequently, ca.ts may be
convulsions and death. Severity depends on
poisoned by oral exposme to many types of
host factors, extent of exposure, length of
toads. Severity varies greatly, depending on
time since exposme, and species of toad.

extent of contact and type of toad. Toxins

Local effects (profuse, sometimes frothy
are produced by all toads, but potency
salivation, accompanied by vigorous head
varies with species and apparently between
shaking, pawing at the mouth, and retching)

geographic locations within individual
are in1mediate, probably because the toxin
species. Toad toxin, a defensive mechanism, is extremely irritating. Vomiting is not is secreted by large glands located dorsal
unusual, especially in severe cases, and
and posterior to the eyes and by smaller
although it may persist for several hours, no
glands distributed throughout the skin. The
further signs may develop in poisoning by
toxin, a thick, creamy white, highly irritating common indigenous toads. With more substance, can be expelled quickly by the
severe intoxication, as from R marina or
contraction of periglandular muscles in the

I alvarius, cardiac arrhythmias, dyspnea,
skin. Its many components include
cyanosis, and seizmes are characteristic.

bufagenins, which have digitalis-like effects, Cardiac and CNS involvement can be and bufotoxins, which block soclillll1
life-threatening.

channels in nerves similar to the actions
of local anesthetics, catecholan1ines, and

Treatment: A specific antidote for toad
serotonin. The most toxic species in the
toxins is not available. Therapy is directed

USA is the giant or marine toad, Rhinella
at minimizing toxin absorption and
marina (formerly Bufo marinus), an
controlling associated clinical signs.

introduced species that is established in

Minimal treatment may be required after

Florida, Hawaii, and Texas. R marina is
exposure to toxins in areas where less
also known as the cane toad in Australia,
toxic toads are found. The mouth should
where its range extends across the
be inunediately and thoroughly flushed
northeastern half of the continent. Mortality
with copious amounts of water. Affected
ranges from 20%--1000/o in untreated cases,
animals should be prevented from inhaling
depending on exposure circmnsta.nces. The
aerosols of saliva or water that contain

Colorado River toad, Incillus (f01merly
toad toxin. Atropine may reduce the

Bufo) alvarius, found in the southwestern
volume of saliva and the risk of aspiration

USA and northern Mexico, is another toad
but should not be used until cardiovascuof sufficient size to have potentially lethal lar status is assessed. More severely
levels of toxins in its skin secretions.

affected animals require more extensive
therapy. Cardiac arrhythmias should be

Clinical Findings and Diagnosis:

identified and controlled u;;ing standard

Encounters with toads are most common in
treatment protocols (see also ARR1-1YT11�nAS, warm or mild weather. Signs of poisoning
p 90). If bradyarrhythmias exist,
are variable and range from local effects to
atropine or dopa.mine should be considered;

3162

TOAD POISONING
tachyarrhythmias should be treated with
azepines, barbiturates, or a combination
lidocaine, phenytoin, propranolol, or
of the two. Anesthetics that predispose to
procainamide hydrochloride. Digoxinventricular fibrillation ( eg, halothane) specific Fab may be considered in cases of should be avoided. Supplemental oxygen severe arrhythmias refractory to standard
and mechanical ventilation may also be

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antiarrhythmic therapy. CNS excitation, if
needed if cyanosis and dyspnea are
present, should be controlled by benzodi-
prominent.

VENOMOUS ARTHROPODS

Envenomation of animals by poisonous
acetylcholine at synaptic junctions, which
arthropods is relatively unconunon and
continues until neurotransmitters are
difficult to recognize. It may be suspected
depleted. The resulting severe, painful
relative to presenting clinical signs, but
cramping of all large muscle groups
confim1atory evidence is rare because of
accounts for most of the clinical signs
the inability to capture the offending
attributed to envenomation.

arthropod.

Unless there is visual confirmation of a
widow spider bite, diagnosis must be based

SPIDERS AND SCORPIONS
on clinical signs, which include restlessness
with apparent anxiety or apprehension;

Spiders of medical importance in the USA
rapid, shallow, irregular respiration; shock;
do not inflict particularly painful bites, so it
abdominal rigidity or tenderness; and
is unusual for a spider bite to be suspected
painful muscle rigidity, sometimes
until clinical signs appear. It is also unlikely
accompanied by intennittent relaxation
that the spider will remain in close

(which may progress to clonus and
proxinuty to the victim for the time required
eventually to respiratory paralysis). Partial
for signs to develop (30 min to 6 hr). Abnost
paresis also has been desclibed.

all spiders are venomous, but few possess

An antivenin ( equine origin) is comm et'

the attributes necessary to cause clinical
dally available but is usually reserved for
envenomation-in manm1als-mouth parts
confirmed bites of high-risk individuals
of sufficient size to allow penetration of

(very young or very old). Symptomatic
the skin and toxin of sufficient quantity
treatment is usually sufficient but may
or potency to result in morbidity.

require a combination of therapeutic agents.

The spiders in the lJSA that are capable

Calciwn gluconate IV (10 mL of a 100/o
of causing clinical envenomation belong to
solution is the usual hwnan dose) is
two groups: widow spiders (Latrodectus
reportedly helpful. Meperidine hydrochlospp) and brown spiders (mostly Loxosceles ride or morphine, also given IV, provides
spp).

relief from pain and produces muscle
relaxation. Muscle relaxants and diazepa.i11

Widow Spiders: Widow spiders usually
are also beneficial. Tetanus antitoxin also
bite only when accidental skin contact
should be administered. Recovery may be
occurs. The most conm1on species is the
prolonged; wealrness and even partial
black widow spider, Latrodeclus mac tans,
paralysis may persist for several days.

characterized by a red hourglass shape on
its ventral abdomen. In the western USA,

Brown Recluse Spiders: There are
the western black widow, L hesperus,
at least 10 species of Loxosceles spiders
predominates, while the brown widow,
in the USA, but the brown recluse spider,

L bishop'i, is found in the south, and the red L reclusa, is the most conunon, and
widow, L geomet1icus, is found in Florida.

envenomation by it is typical for the genus.

Venom from these spiders is one of the

These spiders have a violin-shaped marking
most potent biologic toxins. The most

( or "fiddleback") on the spider's dorswn, the important of its five or six components is
cephalothorax, although it may be indistinct
a neurotoxin that causes release of the
or absent in some species. In the northwestneurotransmitters norepinephrine and ern USA, the wu·elated spider Tegenaria

VENOMOUS ARTHROPODS

3163
agrestis reportedly causes a clinically
recluse spider bites. In people, it is adminindistinguishable den11onecrosis in people istered at 100 mg, bid, for 14-25 days.

and presumably in domesticated animals.

Broad-spectrum antibiotics are useful in

Brown recluse spider venom has vasoconpreventing secondary infection, and tetanus strictive, thrombotic, hemolytic, and
immunoprophylaxis should be considered.

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necrotizing properties. It contains several
enzymes, including a phospholipase

Tarantulas: Tarantulas (many assorted

(sphingomylinase D) that attacks cell
genera and species) are common throughmembranes. Pathogenetic mechanisms out the USA and South America. They are
of the characteristic dermal necrosis are
increasingly being kept as household pets
poorly understood, but activation of
throughout the world. Along with many
complement, chemotaxis, and accumulaother exotic arthropods, they a.re frequently tions of neutrophils affect ( or amplify) the
sold in exotic pet stores.

process.

Tarantulas should not be mixed with or

A history of a bite by a brown recluse
allowed contact with other domesticated
spider is useful but rare. A presumptive
pets. Fine hairs (setae), present over much
diagnosis may be based on the presence of
of the tarantula's abdomen, may be
a discrete, erythematous, intensely pruritic
discharged ( or cast off) by the tarantula as a
skin lesion that may have irregular
defense mechanism against larger
ecchymoses. Within 4---8 hr, a vesicle
creatures. If these fine hairs make contact
develops at the bite wound, and sometimes
with unprotected skin, they can produce
a blanched zone surrounds the erythemacontact allergic reactions. Care must be tous area, producing a "bull's-eye"

taken to keep these fine hairs from entering
appearance to the lesion. The central area
the eye, particularly the cornea, because
sometin1es appears pale or cyanotic. The
they can be quite difficult to remove. In
vesicle may degenerate to an ulcer that,
addition, the bite of the tarantula can be
unless treated in a timely manner, may
fatal to dogs or cats, which are ve1y
enlarge and extend to underlying tissues,
susceptible to tarantula venom. Safety of
including muscle. Sometimes, a pustule
the tarantula is another reason to keep these
follows the vesicle and, on its breakdown, a
spiders separated from other pets, because
black eschar remains. The final tissue defect a dog or cat can easily injure or kill a pet may be extensive and indolent and require
tarantula.

months to heal. However, medical
authorities claim that not all brown recluse

Scorpions: Most of the scorpions found
spider bites result in severe, localized
throughout the USA possess posterior
dermal necrosis.

abdominal stingers that connect to venom

Systemic signs sometimes accompany
glands. The stinger and its associated
brown recluse spider envenomation and
venom can be used both as mechanisms of
may not appear for 3-4 days after the bite.

self-defense and of predation. For the most

Hemolysis, thrombocytopenia, and
part, the stings of these scorpions are
disseminated intravascular coagulation are
considered to be innocuous in most
more likely to occur in cases with severe
domesticated mammalian species, because
den11al necrosis. Fever, vomiting, edema,
the a.mount of venom is too minute or the
hemoglobinuria, hemolytic anemia, renal
venom has very little pha.n11acologic
failure, and shock may result from systemic
potency. The sting of these arthropods is
loxoscelism.

analogous to an insect sting/bite, with pain

In known spider bites, early treatment can
and swelling at the site of the injury.

be successful, but unfortunately, many cases

Relative to pha.m1acologically potent
are not recognized until cutaneous necrosis
scorpion stings in domesticated animals,
has become extensive; treatment at that
there are two geographic scenarios of veteristage is less rewarding but is still of value.

nary clinical importance. The first involves
lnlmediate application of cold packs is

Centruroides sculpturatus, commonly
beneficial, and if administered early, corticoknown as the Arizona bark scorpion. This steroids protect against cutaneous necrosis
venomous arthropod can be found in all
by stabilizing cell membranes and suppress counties of Arizona, into western New ing chemotaxis. Corticosteroids also tend to

Mexico, southern Utall, southern Nevada to
protect against systemic involvement.

the Las Vegas vicinity, California along the

Radical excision has been advocated, but its

Colorado River (where it is rare), and down
value is questionable. Dapsone, an inhibitor
to the area of the state of Sonora, Mexico. It
of leukocyte function, which is frequently
has been reported to produce envenomation
used in the treatment of leprosy, is currently
in dogs; however, its sting is similar to that
considered the drug of choice for brown
of the venomous hymenopterans, producing

3164

VENOMOUS ARTHROPODS
local pain and swelling with the possibility
with vigila.i1t monitoring of heaJt rate, heart
of associated hypertension. Most animals
rhythm, 311d blood pressure. IV fluids are
recover without a problem, but more severe
indicated to prevent vascular collapse.

reactions are possible.

Anlihistan1ines and corticosteroids should

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The second scenario involves myriad
also be given. The animal may require
geographic locales ( eg, desert-like and
intubation to provide supplemental oxygen.

jungle ecosystems) throughout the world
where many venomous scorpions abound.

People with penchants for hiking the world

Africanized Honeybees ("Killer
should be warned to be wary of visits to

Bees"): The conui1on honeybees in
these areas, and traveling with canine

America were brought to the New World by
companions in such scenarios should be

Europea.11 settlers; as a result, the European
strongly discouraged.

varieties of honeybees established
themselves throughout orth and South

America. In the 1950s, African colonies of

HYMENOPTERA
bees were crossed with the docile European
varieties of honeybees in laboratories in

Honey Bees, Wasps, Hornets, and

Brazil, but their offspring m311aged to escape

Yellow Jackets: There are many
from the laboratory environment. These
venomous hymenopterans (eg, honey bees,
hybridized offsp1ing were characterized by
wasps, hornet, yellow jackets), in which the
excitability, aggressive defense of the hive,
female drone possesses a barbed ovipositor
aJ1d frequent swaJming activity. Since their
on the tip of the abdomen that connects to
escape in 1957, these "killer bees" have
paired venom glands. Bees possess a barbed spread throughout most of South America, stinging apparatus; after stinging the victin1,
ttu·ough Central America aJ1d Mexico, 311d
bees die because the stinger and its
into the southern regions of the USA; their
associated venom sac are pulled out of the
raJ1ge is expected to exp311d n01thw31·d.

abdomen. Wasps, hornets, and yellow

Afric311ized bees are difficult to distinjackets possess a stinging apparatus that is guish morphologically from their European
not barbed; they are capable of stinging
counterpaits. Their stinging behavior is
multiple times. The venom glands of
prin131·ily defensive, eg, in response to a
honeybees contain a hydrolyzing protein,
perceived threat to the colony. These bees
mast cell degranulating peptides, a
habitually sting en masse. Once initiated,
phospholipase, hyaluronidase, vasoactive
stinging recrnitment within the colony C311
a.inines, and a netu·otoxin apanlin.

result in hundreds or thousands of stings;

A single bee sting will produce pain,
bees may pursue their victim for as far as
swelling, erythema, eqema, and local

1 km. Hives are generally found in exposed
induration, which can be followed by
locations such as on tree braJ1ches or in old
pruritus at the injection site. The incidence
tires or boxes where domesticated animals
of anaphylactic reactions is not known in
may come in contact with them. Stings
companion animals-if a severe systemic
occur generally in the vicinity of the hive.

reaction has not occurred within 30 min, it

Smaller pets are particularly susceptible to
is not likely to occur. In dogs, bee and wasp
the effects of multiple stings, because they
stings cause only local redness, erythema,
receive a larger dose of venom/kg body wt.

and transient pain. Dogs may vocalize when

It is the cumulative dose of venom that
sttmg and may rub their mouth and eyes on
becomes fatal.

the ground. Usually cutaneous reactions

Animals that receive massive envenomaappear quickly a.i1d regress spontaneously.

tions are visibly depressed a.i1d usually

With repeated stings, anaphylaxis, with
febrile. They may exhibit facial paralysis,
salivation, vomiting, diarrhea, circulato1y
ataxia, seizures, aJ1d neurologic signs. The
collapse, pallor, or cyanosis, may result
urine may be dark brown or red, 311d the

(seep 823).

feces are bloody. Bloody or dark brown

The stinger/ovipositor (if present) with
vomitus may be seen. Leukocytosis may be
accompanying venom glands should be
present. The aJ1imal may be thrombocytoremoved, if it can be located. In severe cases penic; disseminated intravascular coagulawith urticaria, epineplu'ine should be given tion may be imminent. Urinalysis may reveal

IM. In cases of anaphylaxis, epinephrine
gra.imlar casts due to renal tubular daJ11age.

should be in1mediately administered, SC, at

The 311irnal may develop acute renal failure
adusage of 1:1,000 (0.1-0.5 mL) for dogs or
caused by acute tubul31· necrosis or direct
cats. This dosage can be repeated every
toxic effect of massive envenomation. Dogs

10-20 min. When given IV, it must be diluted
may develop a secondary intmune-mediated
to l: 10,000, and 0.5-1 mL is ad.ministered
hemolytic 311emia.

RODENTICIDE POISONING

3165

Access to cardiac monitoring, suppleimmediately. A papule will forn1 at the sting mental oxygen, "crash cart" drugs, and
site and develop into a sterile pustule. These
airway intubation must be readily available.

pustules are pruritic and may become

Any animal that receives massive, multiple
secondarily infected due to self-inflicted

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stings must be hospitalized, treated
traun1a. Regional reactions can occur and
aggressively, and hospitalized for 24 hr
may be erythematous, indurated, and quite
after cessation of clinical signs.

pmritic. Regional edema may be severe
enough to impede blood flow to a limb.

Fire Ants: Fire ants (red imported fire

Systemic or anaphylactic reactions can
ants and black imported fire ants) are not
produce clinical signs removed from the
native to North An1erica but were introsite of the initial sting, including urticaria, duced into the USA in the early years of the
cutaneous edema, laryngeal edema,

20'11 century. Since their introduction, red
bronchospasrn, vascular collapse, and
imported fire ants (Solenopsis invicta)

death. Deaths due to systemic anaphylaxis
have colonized more than 310 million acres
occur within minutes of the sting, whereas
in 12 southern states, whereas black
deaths due to venom toxicity occur >24 hr
imported fire ants (S richteri) have been
after the sting.

contained in a small area in Alabama and

There are no treatments to prevent or

Mississippi. Fire ants attack domestic
resolve localized reactions to fire ant
animals and native wildlife. The ant anchors
stings; however, symptomatic therapy
onto its victin1 with its prominent mandimight be beneficial. Local reactions may bles, tucks its abdomen under its body, and
be treated with antihistanlines, topical
stings with its non barbed stinger, a modified cmticosteroids, water or alcohol ovipositor with an associated venom gland.

compresses, ice, and topical treatment

It retracts its stinger, rotates its body to the
with menthol and camphor. Warm baths
side, and stings again. This act is repeated in
may provide some relief for dogs. Regional
a circular pattern. Unlike bees, wasps, and
reactions occur less frequently and should
hornets, fire ants inject their venom slowly.

be treated with antihistamines, corticos

Each ant can deliver 0.11 µL with a total of
teroids, analgesics, and fluid therapy.

20 consecutive stings before the venom

Antibiotics are indicated for secondary
gland is depleted.

infections. Anaphylactic reactions to fire

The typical reaction to a fire ant sting is
ant stings are treated simila.rly to those
a wheal and flare, which usually resolves
from honeybees, wasps, and yellow
within an hour. Pain and inflanunation begin jackets (see above).

RODENTICIDE POISONING

Many poisons have been used against
questions to determine the day and time of
rodent pests. If baits are not well secw·ed,
exposure, brand name and manufacturer
they may be ingested directly by nontarget
of rodenticide, active ingredients and their
animal species (farm anin1als, pets, and
concentration, package size, and the
wildlife). Sometimes, nonta.rget species
potential amount missing. The Environmay ingest recently poisoned rodent pests mental Protection Agency (EPA) registraand develop relay or secondary poisoning.

tion nwnber is the most accurate way to

Occasionally, baits may be used maliconfirm identity of an active ingredient.

ciously or intentionally to kill either domes

There is no way to identify differing class
tic animals or wildlife. This chapter
by color, shape, or size of a bait.

discusses only the most commonly used
rodenticides currently available in the

ANTICOAGULANT RODENTICIDES
market: anticoagulants, bromethalin,
cholecalciferol, and zinc phosphide.

(WARFARIN AND CONGENERS)

Strychnine poisoning (seep 3170) is

Anticoagulant rodenticides inhibit the
discussed separately.

enzyme vitamin K epoxide reductase, which

Whenever a rodenticide exposure is
norn1ally reactivates vitamin K, a cmcial
suspected, owners should be asked history
component in a number of normal clotting

3166

RODENTICIDE POISONING
factors, after those factors are consumed in
bromadiolone is 6 days, with maxin1un1
normal maintenance. Potentially dangerous
effects estimated at 12-15 days. Brodifacoum
to all mammals and birds, anticoagulant
may continue to be detectable in serum for
rodenticides are a common cause of
up to 24 days. All of these may be detected in
poisoning in pets and wildlife. Intoxications
liver even after serum levels drop.

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in domestic animals have resulted from

Clinical signs generally reflect some
contamination of feed with anticoagulant
manifestation of hemorrhage, including
concentrate, malicious use of these
anemia, hematomas, melena, hemothorax,
chemicals, and feed mixed in equipment
hyphema, epistaxis, hemoptysis, and
used to prepare rodent bait.

hematuria, any of which may lead to

All anticoagulants have the basic
weakness, ataxia, colic, polypnea, etc.

coumarin or indanedione nucleus. The

Petechiae rarely develop until after

"fast-generation" anticoagulants (warfarin, repeated small bleeds have consumed too
pindone, coumafuryl, coumachlor,
many platelets. Depression and anorexia
isovaleryl indanedione, and others less
may be seen in all species even before
frequently used) require multiple feedings
bleeding occurs. Typically, the onset of
to result in toxicity. The "intermediate"

clinical signs is delayed ( due to consumpanticoagulants (chlorophacinone and in tion of vitamin K-dependent clotting
particular diphacinone) require fewer
factors) for 3-7 days after exposure ( can be
feedings than "first-generation" chemicals, a little earlier with a fairly large dose). Dogs
and thus are more toxic to nontarget
can also show nonspecific clinical signs,
species. The "second-generation" anticosuch as limping or swollen joints (due to agulants (brodifacoum, bromadiolone,
hemorrhage in thejoints), coughing or
difethiolone) are highly toxic to nontarget
wheezing (bleeding in the lungs), bulging of
species ( dogs, cats, livestock, or wildlife)

eyes (retrobulbar hemorrhages), and pale
after a single feeding. Secondary poisoning
mucous membrane color. Sudden death
in nontarget animal species from anticoaguwith no obvious clinical signs is also lants has also been documented. The
possible.

concentration of brodifacoum and

Anticoagulant rodenticide toxicosis may
bromadiolone in the bait available as pellets
be diagnosed based on history of availabilor blocks is usually 0.005% and that of ity of the bait in the animal's environment
difethiolone 0.0025%.

and evidence of exposure (missing or

Anticoagulants antagonize vitamin K,
chewed up package/bait, passing of
which interferes with the nom1al synthesis of
greenish blue feces [color of the bait]) but
coagulation proteins (factors I, II, VIl, IX, and
cannot be discounted if there is no known

X) in the liver; thus, adequate an1ounts are
history of exposure. Differential diagnoses
not available to convert prothrombin into
when hemorrhage is encountered include
tl1rombin. A latent period, dependent on
disseminated intravascular coagulation,
species, dose, and activity, is required, during
congenital factor deficiencies, von
which clotting factors already present are

Willebrand disease, platelet deficiencies,
used up. New products have.a longer biologic and canine ehrlichiosis. A prolonged half-life and therefore prolonged effects
prothrombin time (PT), activated partial

( which require prolonged treatment). For
thromboplastin time (APTT), or thrombin
exan1ple, the half-life in canine plasma of
time in the presence of normal fibrinogen,
warfarin is 15 hr, diphacinone is 5 days, and
fibrin degradation products, and platelet
counts is strongly suggestive of anticoagulant rodenticide toxicosis, as is a positive therapeutic response to vitamin K1•

Stomach contents, serum, or plasma can be
analyzed for the presence of anticoagulant
to confirm a diagnosis. Most veterinary
diagnostic laboratories have an "anticoagulant screen" to detect most of the anticoagulants available in the market in the serum, plasma, liver, or kidney.

Vitamin K1 is antidotal. Because the vast
majority of exposures are to the secondgeneration agents, recommended dosages are generally 3-5 mg/kg/day, PO, for 3-4
wk. Treating for an extra week will not be

Anticoagulant rodenticide poisoning, thorax
harmful, whereas discontinuing treatment
hemorrhage. Courtesy of Dr. Frederick W. Oehme.

too soon can be lethal. The best way to

RODENTICIDE POISONING

3167
lrnow when to stop vitamin K1 treatment is
than anticoagulants (bromethalin,
by checking the PT time 72 hr after the last
cholecalciferol) are allowed for sale in
dose of vitamin K1 has been given. If PT
retail stores for use by consumers. 3) All
at that point is normal, treatment with
outdoor, above-ground use must be in a
vitamin K1 can be stopped; if it is still
bait station intended to be resistant to

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prolonged, treatment with vitan1in K for 1
children and pets. 4) Loose poison baits

1
more week is warranted. The doses should

(pellets, meals) are prohibited. 5) All
be administered with small amow1ts of
outdoor products are to be placed with.in
fatty food (milk, meat, or cheese), because

50 feet of a building. 6) Professional use
fat will enhance vitamin K1 absorption.

products are available in quantities of at

Administering half of the daily dose every
least 8 or 16 pounds (second-generation

12 hr will provide more constant levels of
anticoagulants) or at least 4 pounds
vitamin K1• In animals exhibiting clinical

(first-generation anticoagulants); they are
signs when coagulation factors are
to be placed in bait stations. 7) Professional
abnonnal, it is probably safer to avoid
class anticoagulants (second-generation)

injections (unless the animal is unable to
are not to be marketed in "consumer"

take vita.min K1 orally) because of the risk
stores (grocery, hardware, or club stores).

of bleeding and hematoma formation at the

The possible unintended end result of
injection site. Also, the possibility of
these new EPA regulations is likely to be a
anaphylactoid reaction cannot be excluded
higher incidence of exposure to rodent baits
when vitamin K injection is administered
that contain either bromethalin or

1
parentally.

cholecalciferol (vitamin D3).

Fresh or frozen plasma (9 mUkg)

or whole blood (20 mUkg) IV may be

BROMETHALIN
indicated to replace needed clotting factors
and RBCs immediately if bleeding is

Bromethalin, a nonanticoagulant,
present. Administration of oxygen may be
single-dose rodenticide, is a neurotoxin
very useful. Activity should be limited as
available as bars (blocks), pellets, seed,
much as possible during the first week of
and worm. Mole baits are sold as worm
therapy to minimize bleeds due to trauma
containing 0.025% bromethalin, whereas
to tissues. Oral vitamin K alone (3-5 mg/kg,
rat and mouse baits contain 0.01%

1

PO) can be used to prevent coagulopathy
brornethalin. Bromethalin and its main
after a lrnown exposure to an anticoagumetabolite desmobromethalin are strong lant.

uncouplers of oxidative phosphorylation.

If a coagulopathy has developed, recheck

This results in intra-myelin fluid accumuing the PT and APTT every 24 hr until lation, leading to long nerve demyelinanormalized should be considered. At the tion and intra-myelin cerebral edema. The
end of a course of vitanlin K supplementanet result is cerebral and spinal edema 1
tion, a coagulation profile is needed -48--72
and increased CSF pressure, leading to
hr after the last dose to confirm that no
neurologic dysfunction. In toxicity trials,
indication of coagulopathy remains.

the oral toxic dose of bromethalin when

Vitamin K3 given as a feed supplement is
used as part of bait appears to be much
ineffective in treatment of anticoagulant
lower than the dose administered as a
rodenticide toxicosis. Administration of
technical grade agent. For example, in
vitanlin K3 by injection in horses has been
dogs, an average lethal dose of technical
associated with acute renal failure and is
grade bromethalin is reported to be 4. 7
never an appropriate treatment.

mg/kg but 2.38 mg/kg in bait. Young dogs

To increase protection to nontarget

( < 1 yr old) appear more sensitive; death
animal species and children, the US
has been reported at dosages of -1 mg/kg

EPA has promulgated new rules on
in bait. Dogs are more commonly
packaging and availability of anticoinvolved. Cats are 2-3 times more agulants. Some of the highlights of
sensitive than dogs.

these new rules include the following:

Bromethalin can cause either an acute or

1) Consumer products available in retail,
a subacute/chronic syndrome, depending on
hardware, grocery, or convenient stores
the dose ingested. At doses equivalent to or
with under a pound of bait can no longer
more than the average lethal dose, dogs may
contain second-generation anticoagulants
develop an acute convulsant ( or high-dose)

(brodifacoum, difethlalone, bromadiolone,
syndrome resulting in clinical signs within
or difenacoum). 2) Only first-generation

4---36 hr of exposure; such signs include
anticoagulants (warfarin, diphacinone,
hyperexcitability, muscle tremors, grand
chlorophacinone) or rodenticides other
mal seizures, hindlimb hypen-eflexia, CNS

3168

RODENTICIDE POISONING
depression, hyperthennia, and death. The
fluid shift into the gut. The clinical signs of
paralytic ( subacute or chronic) syndrome is
acute hypernatremia may mimic those seen
seen at lower doses, and clinical signs may
with bromethalin toxicosis.

not appear for several days ( up to 7 days)

At a bromethalin dosage of 0.5-0. 75

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after exposure. Initial signs may include
mg/kg in dogs, or 0.1-0.3 mg/kg in cats, an
depression, hindlimb wealrness or paresis,
initial dose of activated chai·coal at 1-2 g/kg
decreased propioception, ataxia, and posbody wt should be considered. A repeat sible tremors. Muscle wealrness often prodose at half the original dose at 8-hr gresses from posterior to anterior muscles.

intervals for a total of three doses can be

Cats typically develop paralytic syndrome
administered, again being awai·e of and
irrespective of dose of bromethalin.

monitoring for possible hypernatremia.

Presumptive diagnosis ofbromethalin

At a bromethalin dosage of �O. 75 mg/kg in
toxicosis is made based on known or
dogs, or �0.3 mg/kg in cats, administration
suspected history of exposure to the bait,
of six doses of activated chai·coal over 48 hr
followed by development of neurologic

(repeat every 8 hr) can be considered to
signs within 1-7 days of exposure.

reduce the body burden by interrupting

Diagnosis can be confirmed by detecting
enterohepatic recirculation.

the presence of bromethalin or its major

Use of mannitol and corticosteroids has
metabolite in liver, kidney, brain, or fat; this been suggested to treat clinical signs, analysis is available only in some veteribecause they may help manage cerebral nary diagnostic laboratories in the USA.

edema due to other causes. However, this

Based on the history of exposure,
has not been shown to be very helpful, likely
bromethalin toxicosis should be considered
because of the presence of intra-myelin
when there is moderate to acute onset of
edema. Diazepain, barbiturates, and other
weakness, hindlirnb paralysis, tremors, and
anticonvulsant medications should be used
seizures. Some other toxicologic and
to control seizures and other CNS signs. Full
nontoxicologic differential diagnoses
recove1y may require days to weeks of
should include ethylene glycol toxicosis,
treatment.

marijuana ingestion, 2,4-D and other
phenoxyacetic acid herbicide toxicosis,

CHOLECALCIFEROL
copper head snake envenomation (cats),
intervertebral disc problems, spinal cord

Cholecalciferol ( vitainin D3) is used both as
and CNS trauma, and tick paralysis.

a dietary supplement and a rodenticide. It

Treatment of bromethalin toxicosis is
appears to be toxic at a much lower dose
aimed at early decontamination (induction
when consumed in a bait forn1 than when
of emesis and administration of activated
ingested as a technical grade agent. Most
charcoal) in an asymptomatic animal
rodenticide baits contain 0.075% cholecalcifand controlling CNS signs (seizures) and erol. Incidence of vitanun D3 toxicosis in
providing supportive care in a symptoanimals is relatively less than that of matic animal. Emesis using 3% hydrogen
anticoagulant and bromethalin toxicosis.

peroxide solution or apomorphine in

Relay toxicosis from vitainin D:i has not been
dogs and xylazine in cats within 4 hr of
documented. One international unit (1 IU) of
ingestion may remove some bait from the
vitainin D3 in nutritional supplement is
gut. Depending on the ingested dose of
equivalent to 0.025 mcg of cholecalciferol.

bromethalin, administration of activated

Cholecalciferol toxicosis is characterized
charcoal is considered an effective method
by hyperphosphatemia and hypercalcemia,
to prevent toxicosis. Bromethalin underleading to renal failure, cardiac abnormaligoes enterohepatic recirculation, so ties, hypertension, CNS depression,
administration of repeated doses of
anorexia, vomiting, diarrhea, and lethargy.

activated charcoal may be helpful.

The increased calcium and phosphorus can

The following can be used as a guideline to lead to calcification of soft tissue, notably treat bromethalin exposure in dogs and cats:

the highly vascular ai·eas of kidneys and

At a bromethalin dosage of 0.1-0.49
lungs, as well as within the walls of the great
mg/kg in dogs, or 0.05-0.1 mg/kg in cats,
blood vessels.

emesis alone within 4 hr of exposure may

Clinical signs generally develop within
be adequate. If emesis is not successful, or

18-36 hr of ingestion; initial signs can
if> 4 hr have elapsed since ingestion, a
include depression, anorexia, polyuria, and
single dose of activated charcoal at
polydipsia. The serum phosphorus more

1-2 g/kg body wt is indicated. Whenever
commonly rises first, at -12-24 hr after
administering activated charcoal, the
ingestion, with serum calcium levels rising
clinician must remain aware of the risk of
within another 12-24 hr. Nausea, vomiting,
aspiration or hypernatremia secondaiy to
hematemesis, and depression are common

RODENTICIDE POISONING

3169
as the clinical signs progress. It is important
hr) has been suggested to decrease calciw11
to obtain a baseline biochemistry profile as
and phosphorus levels, but this treatment is
early as possible after the expos me, so that
no longer used conunonly. The two major
each animal can be monitored based on
disadvantages a.re that some anin1als may
individual values.

become refractory to calcitonin, and that

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Ingestion of vitan1in 0,1 at >0.1 mg/kg may
once this therapy is instituted the use of
require decontamination (induction of
panliclronate is not helpful.

emesis and administration of activated

Calcium and phosphorus levels should
charcoal) and monitoring of sel"LUl1 calciwn,
be monitored and treated W1til they retw·n
phosphorus, and renal values. Emesis can '

to baseline. Treatment may have to be
be induced within 2 hr of exposure with 3%
continued for days or weeks because of
hydrogen peroxide or apomorphine in dogs
the lipophilic natme of vitamin 03. Renal
and xylazine in cats. Activated charcoal at
function should be monitored, and other

1-2 g/kg is an appropriate initial close for
clinical signs treated as needed.

decontamination, and a second half close
after -6--8 hr may be helpful. In addition, use

ZINC PHOSPHIDE
of cholestyramine, a bile acid sequestrant,
may be useful to decrease the body btuclen

Zinc phosphide is a component in a number
of vitamin 03 that undergoes enterohepatic
of mole, gopher, ground squirrel, and vole
recirculation with bile acids. However, the
baits intended for outdoor use only. It is a
efficacy of cholestyramine to reduce vitamin dark gray powder, not soluble in water, and 0,3 levels in dogs has not been determined.

is conunonly sold in 2%-5% bait pellets,

The recommended dosage is 0.3--0.5 g/kg,
paste, or tracking powder. In the past
dissolved in liquid and administered orally
several years, an oat-based bait labeled for
every 6--8 hr for 3 -5 clays, depending on the
killing prairie voles has been marketed.

initial close of cholecalciferol ingested.

There is evidently no way to identify this

Prematme initiation of calcimesis (see
grain mixture, and bait ingestion has
below) may disrupt normal calciwnresulted in letl1al exposure to a mm1ber of phosphorus metabolism, triggering
horses. The clinical effects of alun1inw11
osteoclasts to move additional calciwn into
phosphide, used as a grain fun1igator, are
the blood strean1, artificially increasing
similar to those of zinc phosphide.

serun1 calciwn and phosphorus levels and

Lethal closes of zinc phosphide vary
mimicking vitamin 03 toxicosis.

markedly between species and are much

Once the biochemical values begin to
more toxic to species w1able to vomit. The
increase, there a.re two approaches to
phosphide salts are w1stable in an acid
management. The first is to promote
envirorunent. At gastric pH, they degrade
calcimesis by administering normal (0.9%)

rapidly to form phosphine gas. Presence
saline at 2-3 times nom1al rates. Furosemicle
of food in the stoma.ch, which will trigger
at 2.5-4.5 mg/kg, PO, every 6--8 hr promotes
release of gastric acid, increases the rate
calciw11 excretion but can also increase
of this transition. Phosphine gas, when
fl uicl loss ( so hydration status should be
inhaled, results in acute noncarcliogenic
monitored). Prednisolone at 1-3 mg/kg, PO,
pulmonary edema. Vomiting, often
bicl-ticl, can reduce bone resorption as well
hemorrhagic, is a conunon presenting sign
as decrease calciwn absorption from the
in animals capable of vomiting. Tachypnea,
intestine. Treatment with a phosphate
ataxia, weakness, trembling, collapse,
binder (alwninwn hydroxide 30--90 mg/kg,
seizmes, and cleatl1 may ensue.

PO, in divided closes) to decrease phospho

If there is no food in tl1e stomach,
rus absorption and feeding a diet low in
w1clegraclecl zinc phosphide can be
calcitm1 should also be considered.

absorbed systemically. An anin1al surviving

The preferred treatment for persistent
for 48 hr can then have liver and/or renal
significant hypercalcemia is pamidronate,
fa.ilme within 5-14 clays clue to absorption
an injectable bisphosphonate that inhibits
of intact zinc phosphide. Zinc phosphide is
osteoclastic bone resorption. It is administhought to block cytochrome C oxiclase, tered at 1.3-2 mg/kg via slow IV infusion in
leading to fonnation of highly reactive
saline over 2 hr. After administration, as the
oxygen compounds, which ca.use most of
calcium and phosphorus levels start to
the tissue injmy; the most severe clan1a.ge is
decrease, supportive therapies (fw·osemicle, in tissues with the highest oxygen demand, preclnisolone) should be tapered. A repeat
ie, brain, lungs, liver, and kidney.

close may be required if significant

Phosphine gas is a public health hazard.

hypercalcemia redevelops.

Animal owners and veterinary staff
ln the past, use of salmon calcitonin
members must be cautious while inducing

( administered at 4-6 ill/kg, SC, every 2-3
emesis, because tl1ey can be exposed to

3170

RODENTICIDE POISONING
phosphine gas from the presence of zinc
charcoal, the larger zinc phosphide
phosphide bait in the stomach contents
molecule may be. If vomiting is ongoing,
after vomiting. The gas is reported to have a
administration of activated charcoal should
garlic-like or fishy odor.

be avoided because of the aspiration risk.

Management of zinc phosphide ingestion

Obtaining a baseline biochemical profile,

VetBooks.ir
relies on effective decontamination. If the
with repeat evaluation of liver and renal
animal has not already vomited, emesis can
values at 24, 48, and possibly 72 hr, is
be induced by use of apomorphine.

recommended. Use of N-acetylcysteine

Decreasing gastric acid may be beneficial,
may be beneficial, with a loading dose of
via oral magnesium hydroxide antacid or

140 mg/kg, followed by 70 mg/kg every 6
using famotidine at 1 mg/kg, SC. IV fluid
hr for six total doses. Administration of
support is recommended while the animal

S-adenosyl methionine (SAM-e) may also
is under observation. Use of activated
be beneficial. Seizmes should be controlled
charcoal may be considered; although
with diazepan1 or barbitmates, and other
metals are poorly bound by activated
signs treated symptomatically.

STRYCHNINE POISONING

Strychnine is an indole alkaloid obtained
most of the toxic dose is eliminated within
from the seeds of the lndian tree St1ych1ws

24--48 hr.

nu.x-vomica. Strychnine-containing baits are Strychnine inhibits competitively and
cwTently labelled for below-ground use and
reversibly the inhibitory nemotransmitter
are intended for the control of pocket
glycine at postsynaptic neuronal sites in
gophers. Their use as indoor pesticides has
the spinal cord and medulla. This results
been elinlinated since 1989. ln the past,
in unchecked reflex stin1ulation of motor
strychnine has been used as a pesticide to
nemons affecting all the striated muscles.

control rats, moles, gophers, and coyotes.

Because the extensor muscles are relatively

Strychnine is highly toxic to most domestic
more powerful than the flexor muscles, they
anin1als. Its oral LD50 in dogs, cattle, horses,
predominate to produce generalized 1igidity
and pigs is 0.5--1 mg/kg, and in cats is 2 mg/kg. and tonic-clonic seizures. Death results Strychnine is considered a restricted-use
from anoxia and exhaustion.

pesticide. Its sale is forbidden in a number
of states. Grain-laced or pelleted commer

Clinical Findings: The onset of strychcial baits (usually <0.5%) are· often dyed red nine poisoning is fast. After oral exposure, or green. Malicious or accidental strychclinical signs may appear within 30-60 min.

nine poisoning, although not very common

Presence of food in the stomach can delay
in the USA, occurs mainly in small animals,
onset. Early signs, which.may often be
especially dogs and occasionally cats, and
overlooked, consist of apprehension,
rarely in livestock. Most poisonings occur
nervousness, tenseness, and stiffness.

when non target species consume

Vomiting is possible but uncommon.

commercial baits. Young and large-breed,

Severe tetanic seizures may appear
intact male dogs are more likely to be
spontaneously or may be initiated by
involved. Most poisonings are reported
stimuli such as touch, SOWld, or a sudden
from the western USA.

bright light. An extreme and overpowering
extensor rigidity causes tl1e animal to

Pathogenesis: Strychnine is ionized in an assume a "sawhorse" stance. Hyperthermia acidic pH and then rapidly and completely

(104°-l0 6 °F (40°-41 °C]) due to stiffness
absorbed in the small intestine. It is metaboand seizures is often present in dogs. The lized in the liver by microsomal enzymes.

tetanic convulsions may last from a few

The highest concentrations of strychnine
seconds to -1 min. Respiration may stop
are foWld in the blood, liver, and kidneys.

momentarily. Intennittent periods of

Strychnine and its metabolites are excreted
relaxation are seen dming convulsions but
in the urine. Depending on the quantity
become less frequent as the clinical course
ingested and treatment measmes taken,
progresses. The mucous membranes

STRYCHNINE POISONING

3171
become cyanotic and the pupils dilated.

bait in the GI tract with activated charcoal.

Frequency of the seizures increases, and

Because of the rapid onset of clinical signs,
death eventually occurs from exhaustion
emesis may be of lin1itecl value in most
or asphyxiation during seizures. If
cases. If exposure is recent and no clinical
untreated, the entire syndrome may last
signs are present, emesis should be

VetBooks.ir
only 1-2 hr. There are no characteristic
induced with 3% hydrogen peroxide (small
necropsy lesions. Sometimes, because
animals and pigs) at 1-2 ml/kg, PO,
of prolonged convulsions before death,
maximWll 3 tbsp, repeated once after 30
agonal hemorrhages of heart and lungs and
min if vomiting has not occurred;
cyanotic congestion from anoxia may be
apomorphine (dogs only) at 0.03 mg/kg, IV,
seen. Animals dying from strychnine
or 0.04 mg/kg, IM; or xylazine (dogs or cats)

poisoning have rapid rigor mortis.

at 0.5-1 mg/kg, IV or IM. If emesis cannot
be induced, gastric lavage should be

Diagnosis: Tentative diagnosis of
perfom1ed with tepid water. Animals
strychnine poisoning is usually based
already seizuring should be anesthetized
on history of exposure and clinical signs.

first ( with pentobarbital), and an en do tra

Recovery of strychnine alkaloid from the
cheal tube passed before gastric lavage.

stomach contents, vomitus, liver, kidneys,

After emesis or gastric lavage, activated
or urine should be considered diagnostic.

charcoal should be administered at 2 -3 g/kg

Sometimes, urine may not have a detectin small animals and 0.5-1 g/kg in large able an1ow1t of strychnine present if
animals with a cathaitic such as magneanalyzed 1-2 days after exposure; siWTI sulfate at 250 mg/kg, PO, or sorbitol
therefore, multiple san1ples should be
at 1-3 ml/kg, PO.

collected and analyzed. Occasionally,

Seizures should be controlled in small
poisoned animals may show presence
animals with pentobarbital, IV to effect,
of undigested grain-laced red or green
repeated as necessary. Muscle relaxants
strychnine bait in the stomach.

such as methocai·bainol at 100-200 mg/kg,

Strychnine poisoning can be confused

IV, also work well; they should be repeated
with poisonings by several other seizurias needed with a maxin1al close of 330
genic substances such as metaldehyde;
mg/kg/clay. ln large aninlals, chloral hydrate
tremorgenic mycotoxins (penitrem a);
or xylazine can be used to control seizures.

organochlorine, organophosphate, or

Other medications such as glyceryl
carbamate insecticides; fluoroacetate
guaiacolate (5%, 110 mg/kg), diazepan1, and

(1080); zinc phosphide; nicotine; 4-aminoxylazine have been used in dogs to control pyridine; caffeine; or human medications
seizures with vaiiable success. Propofol

(tricyclic antidepressants, 5-fluorouracil,

(3-6mg/kg, IV, or 0.1-0.6 mg/kg/min as a
metronidazole, isoniazid). Acute, massive
constant-rate IV infusion) can also be tried
hepatic necrosis (hepatic encephalopathy)

to control seizures in dogs or cats.

can also produce clinical signs that

Isoflurane inhalation anesthesia can be used
resemble those of strychnine poisoning.

in small animals if preceding measures to
control seizures do not work.

Severely affected dogs should be

Treatment: Strychnine poisoning is an
intubated, and aitificial respiration provided.

emergency, and treatment should be

Acidification of urine with anm1oniwn
instituted quickly. Treatment should be aimed chloride (100 mg/kg, bid, PO) may be useful at decontamination, control of seizures,
for ion trapping and urinary excretion of the
prevention of asphyxiation, and supportive
alkaloid. IV fluids should be administered to
care. Seizures should be controlled, and
force diuresis and maintain normal kidney
symptomatic animals stabilized before
function. Hyperthennia treatment (fans, cool
decontamination is attempted.

bath) should be given if necessary. Acid-base

Decontan1ination consists of removal
balance should be monitored and co1rected
of gastric contents by inducing emesis or
as needed. Most clinical cases may require
gast1ic lavage, and binding of remaining

1-3 clays of treatment.

VetBooks.ir

REFERENCE GUIDES

VetBooks.ir

NORMAL RECTAL TEMPERATURE RANGES 3173

RESTING HEART RATES 3174

RESTING RESPIRATORY RATES 3174

URINE VOLUME AND SPECIFIC GRAVITY 3175

BLOOD-GAS REFERENCE RANGES 3175

HEMATOLOGIC REFERENCE RANGES 3176

SERUM BIOCHEMICAL REFERENCE RANGES 3178

CLINICAL CHEMISTRY SI CONVERSION FACTORS 3180

WEIGHT TO BODY SURFACE AREA CONVERSION 3182

TEMPERATURE EQUIVALENTS AND CONVERSIONS 3183

METRIC SYSTEM PREFIXES AND SYMBOLS 3183

WEIGHTS AND MEASURES EQUIVALENTS AND CONVERSIONS 3184

PERCENTAGE, PPM, AND PPB CONVERSIONS 3184

MILLIGRAM-MILLI EQUIVALENT CONVERSIONS AND ATOMIC

WEIGHTS 3185

IH=IIII NORMAL RECTAL TEMPERATURE RANGES

Species
oc
op

Cattle

Beef cow

36.7-39.1

98.0-102.4

Dairy cow

38.0-39.3

100.4-102.8

Cat

38.1-39.2

100.5-102.5

Chicken (daylight)

40.6-43.0

105.0-109.4

Dog

37.9-39.9

100.2-103.8

Goat

38.5-39.7

101.3-103.5

Horse

Mare

37.3-38.2

99.1-100.8

Stallion

37.2-38.1

99.0-100.6

Pig

38.7-39.8

101.6-103.6

Rabbit

38.6-40.1

101.5-104.2

Sheep

38.3-39.9

100.9-103.8

Adapted from Robertshaw D. Temperature Regulation and Thermal Environment, in Dukes' Physiology of Dornestic Anirnals, 12th ed., Reece WO, Ed. Copyright 2004 by Cornell University.

3174

REFERENCE GUIDES

IH=i!ii RESTING HEART RATES

Species
bpm(range)

Cat

120-140

VetBooks.ir

Chick

350-450

Chicken (adult)

250-300

Dairy cow

48-84

Dog

70-120

Elephant

25-35

Goat

70-80

Guinea Pig

200-300

Hamster

300-600

Horse

28-40

Mouse

450-750

Ox

36---60

Pig

70-120

Rabbit

180-350

Rat

250-400

Rhesus monkey (anesthetized)

160-330

Sheep

70-80

Adapted from Detweiler DK and E1ickson HH, Regulation of the Heait, in Dukes' Physiology of Domestic Animals, 12th ed., Reece WO, Ed. Copy1ight 2004 by Cornell University.

itM•il RESTING RESPIRATORY RATES

Species

Breaths/min (range)

Cat

16-40

Dairy cow

26---50

Dog

18-34

Horse

10-14

Pig

32-58

Sheep

16---34

Adapted from Reece WO, Respiration in Mammals, in Dukes' Physiology of Domestic Animals, 12th ed., Reece WO, Ed. Copyright 2004 by Cornell University.

REFERENCE GUIDES

3175

IM;l!ii URINE VOLUME AND SPECIFIC GRAVITY

Volume

Species

(mUkg body wt/day)

Specific Gravity (range)

VetBooks.ir

Cat

10-20

1.020-1.040

Cow

17-45
l. 030-1. 045

Dog

20-100

1.016---1.060

Goat

10-40

1.015-1.045

Horse

3-18

1. 025-1. 060

Pig

5-30

1.010-1.050

Sheep

10-40

1.015-1.045

Adapted from Reece WO, Kidney Function in Mammals, in Dukes' Physiology of Domestic An;mals, 12th eel., Reece WO, Eel. Copyright 2004 by ComeU University.

ith•ii BLOOD-GAS REFERENCE RANGES

Measure

Units

Dog

Cat

Cow

Horse

IN CONVENTIONAL (USA) UNITS
pH

7.31-7.42

7.24-7.40

7.35-7.50

7.32-7.44

HC03
mEq/L

17-24

17-24

20-30

24-30
pC02
mmHg

29-42

29-42

35-44

36-46
p0
mmHg

85-95

85-95

92

94

2

IN SI UNITS

HC0
µrnol/L

17-24

3

17-24

20-30

24-30
pC02
kPa

3.86---5.60

3.86---5.60

2.67-3.99

4.67-6.13
p0
kPa

11.3-12.66

11.3-12.66

12.26

12.53

2

3176

REFERENCE GUIDES

IH=i!ii HEMATOLOGIC REFERENCE RANGES

Conventional

VetBooks.ir

(USA) Units

SI Units Dog

Cat

Cow

PCV

%
x 10- 2 IJL 35-57

30-45

24-46

Hgb
g/dL
x 10 g/L

11.9-18.9 9.8-15.4 8-15

RB Cs
x I06/µL

X 10 12/L

4.95-7.87 5.0-10.0 5.0-10.0

Reticulocytes

%

%

0-1.0

0-0.6

Absolute
x I03/µL

X 109/L

<80

<60
reticulocyte count

MCV
fL
fL

66-77

39-55

40-60

MCH
pg
pg

21.0-26.2 13-17

11-17

MCHC
g/dL
x IO g/L

32.0-36.3 30-36

30-36

Platelets
x 103/µL
x 109/L

211-621

300-800 100-800

MPV
fL
fL

6.1-10.l

12-18

3.5-6.5

WBCs
x I03/pL

X 109/L

5.0-14.l

5.5-19.5 4.0-12.0

Neutrophils

%

%

58-85

45-64

15-33

(segmented)

x I03/µL

X 109/L

2.9-12.0

2.5-12.5 0.6-4.0

Neutrophils

%

%

0 -

3

0-2

0-2

(band)

x I03/µL
x 109/L

0-0.45

0-0.3

0-0.1

Lymphocytes

%

%

8-21

27-36

62-63
x 103/µL

X 109/L

0.4-2.9

1.5-7.0

2.5-7.5

Monocytes

%

%

2-10

0-5

0-8
x I03/µL

X 109/L

0.1-1.4

0-0.9

0-0.9

Eosinophils

%

%

0 -

9

0-4

0-20
x 103/µL
x 109/L

0-1.3

0 -

0.8

0-2.4

Basophils

%

%

0-1

0-1

0-2
x 103/µL
x 109/L

0-0.14

0-0.2

0-0.2

M:E

0.75-2.5

0.6-3.9

0.3-1.8

Plasma proteins
g/dL

IOg/L

6.0-7.5

6.0-7.5

6.0-8.0

Plasma fibrinogen
mg/dL
g/L

150-300

150-300 100-600

REFERENCE GUIDES

3177

HEMATOLOGIC REFERENCE RANGES (continued) Vietnamese

Potbellied

VetBooks.ir

Horse

Pig

Sheep

Goat

Rabbit Llama

Pig

Ostrich

27-43

36-43

27-45

22-38

33-50

29-39

22-50

32

10.1-16.1 10-16

9-15

8-12

10-17

12.8-17.7 7.8-16.2

12.2

6.0-10.4

5-8

9-15

8-18

5-8

11.3-17.7 3.6-7.8

1. 7

0-0.1

37-49

50-68

28-40

16-25

58-67

20.9-28

55-71

174

13.7-18.2 17-21

8-12

5.2-8

18-24

61

35.3-39.3 30-34

31-34

30-36

29-37

43.1-46.6 31-36

33

117-256

200-500 800-1,100 300-600

250-650

204-518

4.0-6.0

5.6-12.l

11-22

4-8

4-13

5.2-12.5 7.5-21.5 5.2-17.9

5.5

52-70

28-47

10-50

30-48

20-75

60-74

0-63

63"

2.9-8.5

2-15

0.7-6.0

1.0-7.2

1-9.4

4.6-16

0-11.4

3.4

0-1

0-4

0
rare

0-1

0-1

0-0.1

0 -0.8

0-0.35

0-0.19

21-42

39-62

40-55

50-70

30-85

13-35

15-55

34

1.2-5.1

3.8-16.5 2-9

2-9

1.6-10.6 1-7.5

0.8-9.8

1.87

0-6

2-10

0-6

0-4

1-4

1-4

0-13

2.8

0-0.7

0-1

0-0.75

0-0.55

0.05-0.5 0.05-0.8 0-0.67

0.15

0-7

0.5-11

0-10

1-8

1-4

0-15

0-12

0.3

0-0.8

0-1.5

0-1

0.05-0.65 0.05-0.5 0-3.3

0-0.73

0.02

0-2

0-2

0-3

0-1

1-7

0-2

0

0.2

0-0.3

0-0.5

0-0.3

0-0.12

0.05-0.9 0-0.4

0-0.61

O.Ql

0.5-1.5

1.2-2.2

0.77-1.7

0.7-1.0

6.0-8.5

6 -8

6-7.5

6-7.5

5.4-8.3

5.4-7.5

100-500

200-400 100-500

100-400

200-400 100-400

100-400

Data on vruious species compiled and adapted in pa.it from multiple sources, including Latimer KS, Duncan & Prasse's Veterinary Laboralo1y Medicine: Clinical Palhology, 5th eel., Wiley-Blackwell, 2011; and Weiss DJ, Wardrop KJ, Schal,n's Vele,-ina,y Hematology, 61.h Ed., Wiley-Blackwell, 2010. Reference ranges vary between laboratories. Values provided by the reference laborato,y should be used.

MCV = mean corpusculru· volume

MCH = mean corpuscu]ru· hemoglobin

MCHC = meru1 corpusculm hemoglobin concentration

MPV = mean platelet volwne

M:E = myeloicl:e1yth.roicl ratio

"J-leterophil

3178

REFERENCE GUIDES
ld=i!D SERUM BIOCHEMICAL REFERENCE RANGES

Measure

Units

Dog

Cat

Cow

Horse

VetBooks.ir

IN CONVENTIONAL (USA) UNITS

ALT

U/L

10-109

25-97

Amylase

U/L

226-1,063 550-1,458

Alk phosa

U/L

1-114

0-45

AST

U/L

13-15

7-38

60-125

160-412

CK

U/L

52-368

69-214

0-350

60-330

GGTa

U/L

6-17.4

6-32

LDH

U/L

0-236

58-120

112-456

SD Ha

U/L

4.3-15.3 1-8

Bicarbonate
mEq/L

17-24

17-24

20-30

24-30

Bilirubin
mg/dL

0---0.3

0---0.1

0-1.6

0--3.2

Calcium
mg/dL

9.1-11.7

8.7-11.7

8.0-11.4 10.2-13.4

Chloride
mEq/L

110-124

115-130

99-107

98-109

Cholesterol
mg/dL

135-278

71-156

Creatinine
mg/dL

0.5-1.7

0.9-2.2

0.5-2.2

0.4-2.2

Glucose
mg/dL

76-119

60-120

40--100

62-134

Magnesium
mg/dL

1.6-2.4

1.7-2.6

1.5-2.9

1.4-2.3

Phosphorus
mg/dL

2.9-5.3

3.0-6.1

5.6-8.0

1.5-4.7

Potassium
mEq/L

3.9-5.l

3. 7---6.1

3.6-4.9

2.9-4.6

Protein
g/dL

5.4-7.5

6.0-7.9

6.7-7.5

5.6-7.6

Albumin
g/dL

2.3-3.l

2.8-3.9

2.5-3.8

2.6-4.1

Globulin
g/dL

2.7-4.4

2.6-5.1

3.0-3.5

2.6-4.0

Sodium
m�q/L

142-152

146-156

136-144 128-142

Urea nitrogen
mg/dL

8-28

19-34

10-25

11-27

IN SI UNITS

Bicarbonate
mmol/L

17-24

17-24

20--30

24-30

Bilirubin
µmol/L

0-5.1

0-1.7

0 -27.4

0 -54.7

Calcium
mmol/L

2.3-2.9

2.2-2.9

2.0-2.8

2.5-3.3

Chloride
mmol/L

110-124

115-130

99-107

98-109

Cholesterol
mmol/L

3.5-7.2

1.8-4.0

Creatinine
µmol/L

44-150

80-194

44-194

35-194

Glucose
mmol/L

4.2-6.6

3.3-6.7

2.2-5.6

3.4-7.4

REFERENCE GUIDES

3179

IH=IIH SERUM BIOCHEMICAL REFERENCE RANGES (continued) Vietnamese

Potbellied

Pig

Sheep

Goat

Rabbit

Llama

Pig

Ostrich

VetBooks.ir

IN CONVENTIONAL (USA) UNITS

31-58

26---34

6---19

45-80

6---14

10.9-95.l

200-400

118-395

68-387

93-387

12-96

41-92

27-160

32-84

60-280

167-513

35-130

216---378

16---64

252-401

2.4-22.5

8.1-12.9

0.8-8.9

140-372

17-101

212.5-2,851.5 1,655-4,246

10--60

20-52

20-56

0-7

7-29

14.5-56.2

0-1

380-634

238-440

123-392

88-487

869-2,047

1.0-5.8

5.8-27.9

14.0-23.6

1-17

18-27

20-25

0-10.0

0.1-0.5

0-0.1

0-0.7

0-0.l

0.2-0.45

7.1-11.6

11.5-12.8 8.9-11.7

11-14

8.0-10.3

10.0-18.4

94-106

95-103

99-110.3

102-109

106---113

94-105

36---54

52-76

80-130

10-80

35-113

1.0-2.7

1.2-1.9

1.0-1.8

0.5-2.5

1.1-2.5

1.0-2.3

85-150

50-80

50-75

75-155

103-160

59.8-175.2

187-247

2.7-3.7

2.2-2.8

2.8-3.6

1.82-3.77

5.3-9.6

5.0-7.3

4.2-9.1

4.0--6.5

3.1-10.8

4.0-6.8

4.4-6.7

3.9-5.4

3.5-6.7

3.5-6.9

4.6---7.l

3.7-5.0

4.5-5.9

7.9-8.9

6.0-7.9

6.4-7.0

5.4-7.5

5.8-7.5

6.6---8.9

4-5.4

1.9-3.9

2.4-3.0

2.7-3.9

2.7-5.0

3.6-4.8

3.6---5.0

5.3-6.4

3.5-5.7

2.7-4.1

1.5-2.7

1.6---2.9

135-150

139-152

142-155

138-150

148-155

139-148.8

147-157

10-30

8-20

10-20

20-45

12-34

4.2-15.1

1.4-2.2

IN SI UNITS

18-27

20-25

0-17.1

1.71-8.55 0 -1.71

0-12

0-17.l

3.4-7.7

1.78-2.9

2.88-3.2

2.23-2.93 2.7-3.5

2.2-2.58

2.5-4.6

94-106

95-103

99-110.3

102-109

106---113

94-105

0.93-1.40 1.35-1.97 2.07-3.37 0.3-2.1

0.91-2.93

141-239

106---168

88.4-159

44.2-221 97.2-221

88.4-203.3

4.72-8.33 2.78-4.44 2.78-4.16 4.1-8.6

5.72-8.89 3.3-9.9

10.4-13.7

3180

REFERENCE GUIDES

SERUM BIOCHEMICAL REFERENCE RANGES (continued) Measure

Units

Dog

Cat

Cow

Horse

VetBooks.ir

Magnesium
mmol/L

0.7-1.0

0.7-1.1

0.6---1.2

0.6---0.9

Phosphorus
mmol/L

0.9-1.7

1.0-2.0

1.8-2.6

0.5-1.5

Potassium
mmol/L

3.9-5.1

3.7-6.1

3.6---4.9

2.9-4.6

Protein
g/L

54-75

60-79

67-75

56---76

Albumin
g/L

23-31

28-39

25-38

26---41

Globulin
g/L

27-44

26---51

30-35

26---40

Sodium
mmol/L

142-152

146---156

136---144 128-142

Urea nitrogen
nunol urea/L 2.9-10.0

6.8-12.1

3.6---8.9

3.9-9.6

1ti:111:1 CLINICAL CHEMISTRY SI CONVERSION FACTORS

Conventional

Conversion

Measure

(USA)Units

Factor (x)

SI Units

Alkaline phosphatase

IU/L

1.0

U/L

ALT

U/L

1.0

U/L

Albumin
g/dL

10.0
g/L

Ammonia (NH4)

mcg/dL

0.5872
µmol/L

Amylase

Somogyi units

1.85

U/L

AST

U/L

1.0

U/L

Bilirubin
mg/clL

17.10
µmol/L

Calcium
mg/dL

0.25
nm101/L

Carbon dioxide
mEq/L

1.0
mmol/L

Chloride
mEq/L

1.0
mmol/L

Cholesterol
mg/clL

0.026
mmol/L

Copper
mcg/dL

0.16
µmol/L

Cortisol
mcg/dL

27.6
nmol/L

CK

IU/L

1.0

U/L

Creatinine
mg/clL

88.40

�1mol/L

Fibrinogen
mg/dL

0.01
g/L

Glucose
mg/dL

0.055
mmol/L

Iron, binding
mcg/dL

0.179
µmol/L

Iron, total
mcg/dL

0.179

�111101/L

REFERENCE GUIDES

3181

SERUM BIOCHEMICAL REFERENCE RANGES (continued) Vietnamese

Potbellied

Pig

Sheep

Goat

Rabbit

Llama

Pig

Ostrich

VetBooks.ir
l.11-1.52 0.9-1.31

0.31-1.48

0.75-1.55
l.71-3.10 l.62-2.36
l.4-2.9
l.3-2.l
l.0-3.49

1.3-2.2

4.4-6.7

3.9-5.4

3.5-6.7

3.5-6.9

4.6;--7.l

3.7-5.0

4.5-5.9

79-89

60-79

64-70

54-75

58-75

66--89

40-54

19-39

24-30

27-39

27-50

36--48

36-50

53-64

35-57

27--41

15-27

16--29

135-150

139-152

142-155

138-150

148-155

139-148.8

147-157

3.6-10.7

2.8--7.1

3.6--7.1

7.1-16.l

4.3-12.1
l.5-5.4

0.5-0.8

Data on various species compiled and adapted in pa,t from multiple sources, including Latimer KS, Duncan & Prasse's Veterinmy Laborato1y Medicine: Clinical Pathology, 5th Eel., Wiley-Blackwell, 201 l; and Kaneko JJ, Harvey JW, Bruss ML, Clinical Biochemist,y qf Domestic Animals, 6th Ed., Academic Press, 2008. RPference ranges vary between laboratories. Values provided by the reference laboratory should be used.

"Alk phos = alkaline phosphatase; GGT = gamma glutamyltransfcrase; SDI-I = sorbitol clehydrogenase CLINICAL CHEMISTRY SI CONVERSION FACTORS (continued) Conventional

Conversion

Measure

(USA) Units

Factor(x)

SI Units

Lipase

IU/L

1

U/L

Cherry-Crandall U

278

U/L

Magnesium
mEq/L

0.5
mmol/L

Osmolality

Osm/kg

1.0
mmol/L

Phosphorus
rng/dL

0.323
mmol/L

Potassium
rnEq/L

1.0
mmol/L

Protein, total
g/dL

10.0
g/L

Sodium
mEq/L

1.0
mmol/L

Triglycerides
mg/dL

0.011
mmol/L

Triiodothyronine (T3)

mcg/dL

15.6
nmol/L

Thyroxine (T4)

mcg/dL

12.87
nrnol/L

Urea nitrogen
mg/dL

0.357
mmol/L

Uric acid
rng/dL

0.059
mmol/L

Urine protein/creatinine
gig

0.113
g/mmol
ratio

Xylose absorption
mg/dL

0.067
mmol/L

Adapted from Veterina,y Laborat01y Medicine: lnte1prelation and Diagnosis, Meyer DH, Harvey JW, 3rd ed., Copyright 2004, with permission from Elsevier.

3182

REFERENCE GUIDES

•&Nill WEIGHT TO BODY SURFACE AREA CONVERSION

Dogs

Cats

Body

BSA

Body

BSA

Body

BSA

VetBooks.ir
wt (kg)

(rn2)

wt(kg)

(rn2)

wt(kg)

(rn2)

0.5

0.064

26

0.886

0.5

0.063

1.0

0.101

27

0.909

1.0

0.100

1.5

0.132

28

0.931

1.5

0.131

2.0

0.160

29

0.953

2.0

0.159

2.5

0.186

30

0.975

2.5

0.184

3.0

0.210

31

0.997

3.0

0.208

3.5

0.233

32

1.018

3.5

0.231

4.0

0.255

33

1.039

4.0

0.252

4.5

0.275

34

1.060

4.5

0.273

5

0.295

35

1.081

5.0

0.292

6

0.333

36

1.101

5.5

0.312

7

0.370

37

1.121

6.0

0.330

8

0.404

38

1.142

6.5

0.348

9

0.437

39

1.162

7.0

0.366

10

0.469

40

1.181

7.5

0.383

11

0.500

41

1.201

8.0

0.400

12

0.529

42

1.220

8.5

0.416

13

0.558

43

1.240

9.0

0.433

14

0.587

44

1.259

9.5

0.449

15

0.614

45

1.278

10.0

0.464

16

0.641

46

1.297

17

0.668

47

1.315

18

0.694

48

1.334

19

0.719

49

1.352

20

0.744

50

1.371

21

0.769

51

1.389

22

0.793

52

1.407

23

0.817

53

1.425

24

0.840

54

1.443

25

0.864

55

1.461

Note: body surface area (BSA) in square meters = K x (body wt in gramsV:3) x 10-< K = constant ( 10.1 for dogs and 10.0 for cats)

REFERENCE GUIDES

3183
lrti=IIIH TEMPERATURE EQUIVALENTS AND CONVERSIONS

�C = (°F-32) x 5/9

Celsius (°C)

°F = (°C x 9/5) +32

Fahrenheit (°F)

VetBooks.ir

0

Freezing

32

36.0

96.8

36.5

97.7

37.0

98.6

37.5

99.5

38.0

100.4

38.5

101.3

39.0

102.2

39.5

103.1

40.0

104.0

40.5

104.9

41.0

105.8

41.5

106.7

42.0

107.6

100

Boiling

212
ltM•lil METRIC SYSTEM PREFIXES AND SYMBOLS

Factor

Prefix

Symbol

Factor

Prefix

Symbol

101s
exa

E

10-1
deci
d
lQl5
peta
p

10-2
centi
c

1012
tera

T

10-3
milli
m
lQ9
giga

G
lQ-6
micro
µ

106
mega

M

10-9
nano
n

103
kilo
k

10-12
pico
p

102
hecto
h

10-15
fem to
f

10
deka
da

10-18
atto
a

3184

REFERENCE GUIDES

14H!itl WEIGHTS AND MEASURES EQUIVALENTS AND CONVERSIONS

Length

1 m = 39.37 in.

1 ft= 30.48 cm

1 yd= 91.44 cm

1 in. = 2.54 cm

VetBooks.ir

Weight3

1 kg = 2.205 lb
l lb = 0.454 kg

1 g = 0.035 oz

1 oz= 28.35 g

1 mg= 0.015 grain

1 grain = 64.8 mg

1 ton = 2,000 lb

1 metric ton = 1,000 kg= 2,205 lb

Capacity
linperial system:

1 gal. = 3. 785 L

1 gal. = 4.55 L

1 quart= 0.946 L

1 quart= 1.136 L

1 pint= 473.2 mL

1 pint = 568.26 mL

1 oz= 29.57 mL

1 tablespoon= 15 mL

1 teaspoon = 5 mL

'Avoirdupois (used in the USA as the common system of measuring weight) unless otherwise specified ltM!iFI PERCENTAGE, PPM, AND PPB CONVERSIONS
ppm
ppb

Percentage

0.001

1

0.0000001

0.01

10

0.000001

0.1

100

0.00001

1,000

0.0001

10

0.001

100
o.oi

1,000

0.1

10,000

Other useful conversions: 1 mg/kg= l ppm; 1 g/ton = l.l ppm; JOO g/ton = 110 ppm

REFERENCE GUIDES

3185

MILLIGRAM-MILLIEQUIVALENT CONVERSIONS AND ATOMIC

WEIGHTS

Ion

Atomic Weight

Valence

VetBooks.ir

Hydrogen (H)

1

Carbon(C)

12

4

Nitrogen (N)

14

3

Oxygen(O)

16

2

Sodium(Na)

23

1

Magnesium (Mg)

24

2

Phosphate (P)"

31

3,5

Chlorine (Cl)

35.5

Potassium (K)

39

1

Calcium (Ca)

40

2

Note: The milliequivalent (mEq) is the unit of measure often used for electrolytes. It indicates the chemical activity, or combining power, of an element relative to the activity of 1 mg of hydrogen.

Thus, 1 mEq is represented by 1 mg of hydrogen (1 mole) or 23 mg of Na+, 39 mg of K+, etc.

(mg/L) x valence
mEq/L = molecular weight

(mEq/1) x molecular weight
mg/L =
valence
a As phosphorus, inorganic

VetBooks.ir

INDEX

Page numbers in bold type indicate principal references.

VetBooks.ir

A
heel, sheep 1170
hepatic 341

Aardvarks, nutrition 2297
jowl, swine 734

Abamectin 2647
liver

Abattoir sanitation 1646
cattle 352

Abdominal
large animals 340
distention 155
muscle, horses 1181
large animals 24 7
nocardial 666
fat necrosis 360
pancreatic 412
pain 157
rabbits 1946
ping 156
reptiles 1991
trauma 1669
spinal, pigs 1163

Abdominocentesis, horses 1711
subsolar, horses 1114

Abducent nerve 1216
toe, sheep 1171

Aberrant parasites 1311

Absidia 1335

Abnom1al

Absolute erythrocytosis 43
behavior 1534

Absorption, distribution, metabolism, and
fetal development, calves 2177
excretion 2949
repetitive behaviors 1535

Absorption of drugs 2493
teeth

Abuse, animal 1579
eruption, large animals 177

Acacia
number 164
berlandieri 3136
position, shape, and direction 164
greggii 2960

Abomasum

Acanthamoeba spp 1264
diseases 221, 238

Acanthocephala
displaced 238
marine man1mals 1865
emptying defect, sheep 168
small anin1als 421
impaction, dietary 244

Acantllocephaliasis 2462
right torsion of 238

Acanthocheilonema
ulcers 241
odendhali 1866
volvulus 238
reconditum 914

Abortion
spirocauda 1866
bovine, epizootic 1336
spp 1866
camelids 1346

Acantholysis 827
cattle 1333, 2177
fan1ilial 850
contagious 1348

Acantlloma
mycotic 1335
infundibular keratinizing 944
enzootic
papillary 524
ewes 1338

Acanthomatous
goats 1340
an1eloblastoma 366
footllill 1336
epulis 366
goats 1340

Acanthophis 3159
chlan1ydial 1340

Acanthosis nigricans 970
horses 1343, 2195

Acariasis 2462
bacterial 1345
cutaneous 914
viral 1444
hedgehogs 1831
large animals 1332
marine man1mals 1865
ovine enzootic 599
pulmonary, nonhuman primates
pigs 1341

1880
sheep 1337

Acaricide (organic) toxicity 3058
small animals 2226

Accelerated idioventricular rhytllm 96

Abrus precato?ius 3104

Accessory

Abscesses
carpal bone fracture, horses 1125
cervical, swine 734
pathways 95
corneal, stromal 494
tilyroid tissue 552
foot, sheep 1170

3187

3188

INDEX

ACE inhibitors 75, 107, 2533

Actinobacillus
toxicity 3032
actinoides 590

Acepromazine 1544, 2548, 2600, 2604
actinomycetemcomitans 179

Acer
arthritidis 589
negundo 1186
equuli 158, 159, 197, 340, 349, 589, 1263,

VetBooks.ir
pseudopla,ta,nus 1186

1443,2092,2191,2196
rubium3126
lignieresii 158, 589, 668, 1368
spp 1186
pleuropneumoniae 589, 724, 1465,

Acetamides poisoning 2996

1469, 1470, 1936

Acetaminophen 2111, 2602, 2717
seminis 1063, 2217
toxicity 452, 3029
spp 121,289,589, 1345, 1449,2089

Acetic acid 2739
suis 589, 627, 721, 727, 733, 1500, 1157

Acetochlor 2970
ureae 590
poisoning 2999

Actinobacter spp 2659

Acetone toxicity 3069

Actinobaculum suis 1500

Acetonemia, cattle 1024

Actinomyces

Achalasia
actinoides 591
cricopharyngeal 166
bovis 228, 590, 668, 1368, 2418, 2655,
esophageal sphincter 166

2665

Achilles tendon
hordeovulneris 591
contraction, large animals 1231
israelii 591
disruption, small animals 1203
naeslundii 591

Acholeplasma oculi 513
spp 177, 482, 590, 668, 1094, 1263, 1834,

Achyla 641

1861,2418,2571,2676,2696,2704

Acid-base balance 1686
suis 591

Acid rebound 2552
viscosus 591

Acidifying agents

Actinomycetes 2571
ruminoreticular 2563
marine mammals 1861
urinary 2625

Actinomycin D 2729, 2733

Acidine dyes 2744

Actinomycosis 590, 2418

Acidosis

Action potential 1209
ruminal 225

Activated
sheep 2167
charcoal 2553

Acifluorfen 2970
clotting time 49

Acinetobacter spp 864, 2191, 2665
partial thromboplastin time 44

Acinonyx jubatus 2060

Active

Acitretin 2737
immunization 2767

Acne udder 1386
surveillance 2398

Aconitum napellum 3094

Activity, vacuum 1537

Acorn poisoning 3152

Acupuncture 2079

Acquired

Acute
anestrus, small animals 2230
bovine pulmonary emphysema and
aurotrichia, dogs 849
edema 1439
coagulation protein disorders 53
brackenism 3090
laryngeal paralysis 1238
bronchointerstitial pneumonia, foals 1452
platelet function disorders 50
death syndrome, poultry 2821
thrombocytopenia 47
enteritis, in salmonellosis 197
vascular disorders 51
equine respiratory syndrome 707

Acremonium
hepatic
coenoph'ialum 360
disease, horses 338
spp 640
necrosis, cattle 339

Acriflavine 2744
hepatitis, large animals 338

Acrochordons 955
idiopathic polyradiculoneuritis 1240

Acrodermatitis, lethal, dogs 852
intermittent porphyria, feline 987

Acrolein 2726, 2970
intestinal obstructions, large animals

Acromegaly, feline 551

245

Actinic
multiglandular mastitis, sows 1374
dermatitis, cats 525
necrotizing ulcerative gingivitis, dogs
keratosis 945

364

Actinobacillosis 589
respiratory distress syndrome, feedlot
sheep 2168
cattle 1442

INDEX

3189

Acute (continued)

receptor agonists 2610
selenium poisoning 3087

Adrenocorticotropic hormone 542
toxicosis 2948

Adult
uniglandular mastitis, sows 1375
onset panhypopituitarism 548

VetBooks.ir

Acycloguanosine 2745
rickets 1052

Acyclovir 2745, 2746

Advanced cardiac life support 1671

Adaptive

Advancement flaps 1705
immunity 814

Adverse food reactions, small animals
deficiencies 819

855,2379
responses, excessive 823

Aedes

Addison disease 574
aegypti 888
hypercalcemia in 565
albopictus 888
marine mammals 1860
spp 127, 521, 888, 1295, 2467, 2469, 2471,

Adenitis

2473,2479,2481,2483,2784,2879,
granulomatous sebaceous 848

2892
sebaceous 523
vexans 730, 888

Adeniwn obesum 3104

Aegyptianella

Adenocarcinoma
pullorum 926, 938, 2780, 2876
anal sac 564
spp 2780
apocrine gland 950

Aegyptianellosis, birds 2780
biliary, small animals 470

Aelw·ostrongylus
ceruminous gland 535
abstrusus 1421, 1483, 1490
hepatoid gland 952
spp 1486
poultry 2856

Aerobactei·
pulmonary, sheep and goats 1477
aerogenes 580, 1878, 2695
sebaceous gland 951
hydrophila 1878

Adenohypophysis 542

Aeromonas

Adenoma
hydrophila 289, 1746, 1757, 1779, 1996
apoc1ine
salrnonicida 1749, 1757, 1784, 1809
ct uctular 950
spp 281, 287, 1735, 1737, 1757, 1787,
gland 949

1809, 1810, 1813, 1896, 1984, 1991,

C-cell 577

1992,2191
ceruminous gland 535

Aerophagia, horses 1547
hepatocellular, small animals 470

Aesculus spp 3122
hepatoid gland 951

Afghan Hound myelopathy 1229
pars intermedia 547

Afibrinogenemia, congenital 51
pituitary 547, 549

Aflatoxicosis 3006, 3011
sebaceous gland 951
poultry 2860
thyroid 559

Afoxolaner 2755

Adenomatosis

African
porcine intestinal 299
blue lily 3104
pulmonary, sheep 1477
hedgehogs 1828

Adenovirus
horse sickness 696
avian ( quail) 2913
rue 3120
marine mammals 1867
sleeping sickness 892, 2444
reptiles 1994
swine fever 711

Adhesions, intr a -abdominal, horses 259
tick bite fever 2434

Adipose tissue tumors 958
tumbu fly 902

Aditoprim 2674

Agalactia

Acljuvants 2768
bovine 1387
depot 2768
goats 1367
immunostimulatory 2768
large a11imals 1358

Adnexal dysplasia 955
small animals 2229

Adrenal
syndrome, sows 1373
cortex 573

Agapanthus orientalis 3104
glands 573

Agapornis sp 1908
medulla 575

Agave
hyperplasia 577
americana 3104
tumors 576
lechuguilla 344, 977, 3136

Adrenalitis, autoimmune 831

Age estimation, by examination of teeth

13-Adrenergic

171
agonists 2764

Agenesis, renal 1497
dosages (table) 2610

3190

INDEX

Aggression 1535

Algal poisoning 2956
bulls 1552

Aliivibrio salmonicida 1809
cats 1573

Aliphatic organic arsenicals 3073
cattle 1552

Alkali disease 3086

VetBooks.ir
chickens 1557

Alkaline
dogs 1561
battery poisoning 3003
horses 1546
phosphatase 1591
reptiles 1999

Alkaloidosis, pyrrolizidine 3150
swine 1554

Alkhurma virus 2466

Aggressive fibromatosis 956

Alkyl sulfonates 2726

Aging, dogs 1569

Alkylating agents, antineoplastic 2726

Agkistrodon

Allamanda 3104, 3116
cortot1ix 3159
blanchetti 3116
piscivorus 3159
cathartica 3104, 3116

Aglaonema modestum 3104

Allergen-specific immunotherapy 854
a2-Agonists 2110

Allergic
i3rAgonists 2614
alveolitis, extrinsic 1441

Agonists, 13-adrenergic 2764
asthma 825

Agonists (drugs) 2503
breakthrough 825

Agranulocytes 1612
bronchiolitis 825

Agrostemma gitlwgo 3136
bronchitis

Agrostis avenacea 3154
cats 1490

Aino virus 622
chronic 825

Air
bronchopulmonary aspergillosis 2438
bladder, fish 1784
colitis 825
plant 3112
contact hypersensitivity 831
quality 2116
dermatitis, flea 882
sac mite, birds 1906, 2901
enteritis 825

Airplane plant 3108
gastritis 825

Airway
pneumonitis, small animals 1478
inflammatory disease
rhinitis 824
horses 1456
cattle 1429
species approach 2609

Allergy
systemic therapy 2610
food 825, 855, 2379
inhalation therapy 2613
intestinal 825
emergency 1662
milk 824

Akabane virus 620

Allethrin 2756

Alachlor 2970

Alligator pear 3112
poisoning 2999

Alli um

Alanine aminotransferase 1591
canadense 3132

Alaria
cepa3l32
alata426

Alloglugea 1740
canis 426

Alloherpesviruses, fish 1762
spp 426

Alloimrnune

Albendazole 2645
hemolysis 11

Albinism 848
thrombocytopenia, fetal and

Albumin 1590
neonatal 47

Albuterol 2610, 2614

Allylamines 2705

Alcaligenes sp 864, 2191, 2907

Alocasia spp 3104

Alcelaphine herpesvirus 759

Aloe American 3104

Alcohol 2739

Aloe barbadensis 3104
isopropyl, toxicity 3069

Aloe Barbados 3104
poisoning 3000

Aloe Curacao 3104

Alcuroniun12587,2588

Alopecia 841

Aldactazide 75
associated with melanoderma 523

Aldicarb toxicity 3059
hereditary 846

Aldosterone 573
pinna] 522

Aldrin 2749
progressive 851
toxicity 3060

Alpaca fever 1852

Alendronate 569

Alpacas 1844

Aleutian disease, fen-ets 1825
anesthesia 184 7

Algae intoxication 343
clinical pathology 1847

INDEX

3191

Alpacas (continued)

spp 35, 751,806,928, 1314,2437
congenital and inherited anomalies 1851
variegatum 751, 761, 929, 2435
dental development and care 1850

Amblyopia, Irish Setters 1235
diseases 1851

Ambystoma

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drug use 1847, 1845 (table)

mexicanum 1743, 1841
handling 1846
tigrinum 1741, 1743
herd health 1850

AMDUCA 2520
management 1844

Arnebiasis 202
neonatal care 1850

Ameiva sp 1996
nutrition 1846

Amelanchier alnifolia 2960
parasite control 1850

American
reproduction 1848
aloe 3104
vaccination 1850
dog tick 930

Alprazolam 1544, 2604
trypanosorniasis 2442

Altemaria spp 643, 1264

Ametryn 2970

Alternative veterinary medicine 2078
poisoning 2999

Alwninum phosphide poisoning 3169

Amianlhium muscaetoxicum 3122

Alveolar

Amide poisoning 2996
emphysema 1428

Amidostomiim anseris 2831, 2833
hyclatid tapeworm 422

Amikacin 2663, 2666

Alveoli 1411

Amiloride 2624

Alveoli tis

Aminacrine 2744
allergic extrinsic 1441

Amino acid
diffuse fibrosing 1442
deficiencies

A manila
poultry 2930
muscaria 3095, 3098
hom10nes 540
pantherina 3095, 3098
requirement
phalloides 3095, 3096, 3100
horses 2316
spp 3095
pigs 2335
virosa 3096, 3100
poultry 2915

Amantadine 2111, 2746

Arninocyclitols 2662

Amaranthus spp 3153
antibiotics, miscellaneous 2669

Amarillo 3110

Arninoglycosides 2662

Amaryllis 3112
adverse effects and toxicity 2667

Amazona spp 1924
antimicrobial activity 2663

Ambiphyra spp 1754, 1755, 1779, 1801
bacterial resistance 2664

Amblyomma
classes 2662
americanum 23, 693, 803, 928, 940,
dose rates/dosages (table) 2666

1315,2421,2433
effects on laboratory tests 2668
astrion 929
elimination, distribution, clearance 2666
aureolatum 2437
general properties 2663
auricularium 929
interactions 2668
cajennense 928, 2437
in renal failure, dosage 2667
cohaerens 929
milk discard times (table) 2669
dissimile 930
mode of action 2662
gemma929
pharmacokinetic features 2665
hebraeum 929, 940, 2435
special clinical concerns 2667
imitator 929
therapeutic indications 2666
incisum 930
withdrawal times (table) 2669
integrum 929

Aminopenicillins 2655
latepunctatum 930

Aminopentan1ide 2548
lepidum 929 , 2435

Aminosidine 2663
maculatum 29, 520, 928, 1315, 2437

Aminotransferases 431
mudlairi 929

Arniodarone 76, 2539
naponense 930

Amiota spp 512
neumanni 929

Amitraz 2751, 2755
oblongoguttalum 930

Amitriptyline 1544, 2605, 3034
ovale 29, 929

Arnitrole 2972
parvum 929

Amlodipine 109, 2534, 2540, 3032
pomposum 929

Armni
pseudoconcolor 929
majus977
scalpturatwn 930
visnaga977

3192

INDEX

Ammonia

Analgesia, local and regional 2111
and liver disease 334, 436

Analgesic poisoning 3027
toxicity 3043

Analgesics 2107, 2600
poultry 2860
dosages (table) 2602

VetBooks.ir

Ammonium
used in emergency practice (table) 1694
chloride 2625

Anaphylactic
sulfamate 2972
reactions, localized 824
poisoning 2995
shock 824

Arnorolfine 2706

Anaphylaxis 823

Amoxicillin 2618, 2655, 2657, 2658, 2659
pneumonia, cattle 1441

Amoxicillin-clavulanic acid 2619, 2658
systemic 824

Amphetamine toxicity 3039

Anaplasma

Amphibians 1734
associated rhabdomyolysis 1180
anesthesia 1737
bovis 18
as laborato1y animals 1743
caudatum 18
bacterial diseases 1737
centrale 18
chlamydiosis 1738
marginale 18, 910, 930, 933, 934, 936,
clinical techniques 1735

938
emergency care 1742
mesaetenim 931
environment and husbandry 1734
ovis 18, 930
fungal diseases 1738
phagocytophilum 18, 48, 120, 283, 660,
infectious diseases 1737

697, 772, 774,803,934, 1180, 1263,
mycobacteriosis 1738

1299,2434
neoplasia 1741
platys 18, 48, 803
noninfectious disorders 1741
pullorum 926
nutritional diseases 1741
spp 10, 18, 753, 803, 925, 931, 933, 936
parasites 1740

Anaplasmosis 18
preferred optimal temperature zone

Anaplastic sarcomas 961

1734

Anas penelope 2858
trauma 1741

Anatid herpes 2799
viral diseases 17 41

Anconeal process, ununited, dogs 1196

Amphibiocystidium 1739

Ancylostorna

Amphibiolhecum 1739
braziliense 137, 416, 2458

Amphimerus pseudofelineus 407,
caninurn 416, 1264, 2458

485,2448
ceylanicum 417, 2458

Amphiprion spp 1779
spp 396, 2651

Amphistomes 328
tubaeforme 137, 416

Arnphotericin B 2574, 2575, 2698, 2700

Andes virus 2470

Arnpicillin 2618, 2655, 2657, 2658, 2659

Androgen 573

Arnprolium 2795

Anemia 7, 1611

Amputation neuromas 958
acute hemolytic 1611

Amrinone 2532
acute hemorrhagic 1611

Amsinckia 3150
and renal disease 13
intermedia, 3150
aplastic 13, 1612

Amycolatopsis spp 1345
aplastic hemorrhagic, poultry 2785'

O'.-Amylase 1592
autoimmune hemolytic 1612

Amylase, serum 1593
blood loss 9

Arnyloid arthropathy, poultry 2883
bone marrow, primary 13

Arnyloidoses 592
chicken infectious 2785
hepatic 350
chronic

Arnyloidosis
hemolytic 1612
cutaneous nodular 961
hemorrhagic 1612
hepatic 472
of chronic disease 13
large animals 350
congenital 851
small animals 1518
copper deficiency 12

Amyloodinium spp 1746, 1754, 1795, 1802
dennatitis syndrome, poultry 2785

Anabaena 2956
dogs and cats, nutrition in 2380

Anabolic steroids 2541, 2545, 2590
equine infectious 699, 1250

Anagen 838
feline infectious 28

Anal sac
hemolytic 10
adenocarcinoma 564
immune-mediated 10
disease 187
heritable causes 12

INDEX

3193

Anemia (continued)

welfare 1579, 1644
hypoplastic 1612
downer cow 1192
immune-mediated hemolytic 826
in feedlots 2134
infectious 10

Animal Welfare Act 1836, 2052

VetBooks.ir
salmon 1764

Anionic surfactants 2743
iron deficiency 12

Anisakiasis 2456
nonregenerative 12

Anisakis spp 2456
nutritional 12

Anisocytosis 1611
regenerative 9

Anisognathia 177
virus infection, avian or chicken 2785

Ankyloglossia 163
vitamin B deficiency 13

Ankylosing spondylosis, cattle 1086

Anencephaly, large animals 1222

Annelids, zoonotic diseases 2462

Anesthesia

Annual ryegrass staggers 3153
amphibians 1737

Annulocyte 1611
distal digital, cattle 1068

Anodontia 164
llamas and alpacas 184 7

Anomalies
marine mammals 1857
bladder 1498
regional, horses 1101
congenital and inherited 613
zoo animals 2050
cardiovascular system 76

Anesthetic myopathies, horses 1186
digestive system 162

An estrus
integumentary system 845
acquired, small animals 2230
mouth, large animals 176
bitches 2222
musculoskeletal system 1042
cows 2173
nervous system 1222
cytology 1608
reproductive system 1329
prolonged, small animals 2230
urinary system 1496

Aneurysm 141
renal 1496

Angel wings 3106
ureteral 1498

Angioedernatous plaques 824

Anomalohimalaya spp 930

Angioendotheliorna 960

Anopheles 127, 888

Angiokeratomas 959
quadrimacu/,atus 888

Angiolipomas 958

Anoplocephala

Angiornatosis 959
magna319

Angioneurotic edema 857
pe1:foliala 259, 260, 262, 319, 2647, 2650

Angiopathy, hypertensive, turkeys 2789

Anoplotaenia dasyuri 2045

Angiosarcornas 960

Anorchism 1331

Angiostrongyliasis 2454

Anorectal strictures 189

Angiostrongylus

Anorexia
cantonensis 1264, 1313, 2456
as behavioral manifestation, horses 1550
cosla1icensis 2454
dogs and cats, nutrition in 2381
vasorum 1421

Anoxia 1412

Angiotensin-converting enzyme inhibitors

Antacids 2551

107,2533
poisoning 3030
toxicity 3032
ruminoreticular 2562

Anguilla spp 1765

Antagonists (drugs) 2503

Anguina 3154

Anterior

Junesta 3153
enteritis, horses 260

Angular limb deformity
lens luxation 1699
dogs 1203
uvea 495
foals 1046
uveitis 496, 830, 1699

Anhinga anhinga 1313

Anthelmintics 304, 2637

Anilide poisoning 2996
mechanisms of action 2637

Animal
miscellaneous 2651
abuse 1579
pharmacokinetics 2639
adjusting 2081
resistance 2644
assisted therapy, activities, and
safety 2642
education 1578
withholding periods 2642
chiropractic 2081

Anthrax 593, 2418
human bond 1575
human infection 596

Medicinal Drug Use Clarification Act

Anlhurium spp 3106

(AMDUCA) 2491, 2520

Antiarrhythmics 98, 2535

3194

INDEX

Antibacterial
for urinary tract infection 2617
agents 2652, 2744
virulence and resistance 2630
for skin infections 2571

Antineoplastic
used in pet birds (table) 1897
agents 2722

VetBooks.ir
growth promoters 2765
classification 2726

Antibiotic-responsive diarrhea 401
miscellaneous 2734

Antibiotics
patterns of toxicity 2724
antineoplastic 2733
resistance 2723
antistaphylococcal, dosages 2572
antibiotics 2733
ionophore 2765
chemotherapeutic agents, handling 2725
nonionophore 2766
chemotherapy, principles 2723
phosphoglycolipid 2766

Anting (hedgehogs) 1828
toxicity, rabbits 1938

Antiparasitics, skin 2576
use in backyard poultry 1823

Antipsychotics 2604

Antibodies 815

Antiseptics 2738
monoclonal 2773

Antistaphylococcal antibiotics, dosage

Antibody-mediated cytotoxic reactions 826
rates 2572

Anticholinergic drugs 2553, 2612

Antithrombotic drugs 2544

Anticoagulant rodenticide poisoning 3165

Antitussive drugs 2608
in poultry 2860
dosages (table) 2609

Anticoagulants 2542

Antiulcerative drugs (table) 2550
disorders 54

Antiviral agents 2744
oral 2543
dose rates (table) 2746

Anticonvulsants 2590
miscellaneous 2748
toxicity 3034

Anus

Antidepressants 2605
diseases 187
toxicity 3034
evaluation 1218

Antidiarrheal drugs (table) 2552

Anxiety 1535

Antidiuretic hormone 543, 550

Anxiolytics 2601

Antiernetic drugs 2548, 2549 (table)

Aortic

Antiepileptic drugs 2590, 2596
body tumors 578
for status epilepticus (table) 2591
regurgitation 71
types and dosages (table) 2592
rupture, turkeys 2787

Antifoaming agents 2562
stenosis 71, 78

Antifreeze poisoning 3046

Aotus trivirgatus 1876

Antifungal agents 2697

Apgar score, equine neonates (table) 1724
dosage rates 2574

Aphanizomenon 2956
pet birds (table) 1901

Aphanomyces 1761
skin 2573
invadans 1803
topical 2706
spp 1803

Antihistamines 2548, 2709

Apiosoma spp 1754, 1755, 1779, 1801
dosages 2578

Aplasia cutis 846
integumentary system 2577

A.plastic anemia 13, 1612
toxicity 3025
hemorrhagic, poult1y 2785

Anti-inflammatory agents 2707

Apnea

Antilocapra americana 738
foals 1725

Antimetabolites, antineoplastics 2731

Apocrine

Antimicrobial
adenomas 949
adverse effects and toxicity 2629
cystomatosis 949
agents, miscellaneous 2692
ductular adenomas 950
combination therapy 2636
gland
dosing regimens 2634
adenocarcinomas 564, 950
drug disposition 2629
adenomas 949
feed additives 2765
cyst 949
mechanism of action 2628
cystic dilations or hyperplasia 949
resistance 2134, 2630, 2631
tumors 949, 950
susceptibility testing 2635

Apocynum spp 3094, 3126
therapy

Apodia 1049
combination 2636

Apomorphine 2547
in diarrhea 2552

Aponomma spp 930
requirements for success 2635

Apophallus donicum 427
respiratory system 2613

Apparent volume of distribution 2499

INDEX

3195

Appendageal system 838

Araraquara virus 24 70

Appetite, drugs affecting 2544

Ara.tinga spp 1909, 1924

Apramycin 2669

Arboviral encephalomyelitis, equine

Aprinomectin 2754

1291

VetBooks.ir

Aquaculture 17 43-See also Aquarium

Arcanobacterium
fishes, Aquatic systems
animalium 1861
bacterial diseases 175 7
phocae 1861
drugs used in USA (table) 1750
pyogenes-See 'I'rueJ)erella pyogenes
health certification 1747
spp 1861
infectious diseases 1753

Arcobacter
mycotic diseases 1761
butzleri 191, 193, 2420
necropsy and diagnostic techniques
cibarious 193

1746

C1yaerophilus 191, 193, 2420
parasitic diseases 1755
skin·owii 191, 193, 2420
production medicine and biosecmity
thereius 191, 193

1745
trophiarum 193
production methods 1744
spp 191, 2420
reportable diseases and regulatory

ArctoceJ)halus
concerns 1747
forsteri 1863
systems
gazella 1864
recirculating 1754
tropicalis 1863
drugs for use in (table) 1790

Argas
therapeutic considerations 1748
africolumbae 938
viral diseases 1761
arboreus 938

Aquarium fishes 1779-See also
miniatus 938, 2876

Aquacultme, Aquatic systems
persicus 938, 940, 1315, 2813, 2876
bacterial diseases 1809
radiatus 1315, 2876
common parasitic diseases (table) 1780
sanchezi 938, 2813, 2876
common viral diseases (table) 1782
spp 19, 925, 938, 1314, 2780, 2785, 2813
diseases of regulatory concern in the
walkerae 1315

USA (table) 1786

Argasid ticks 925, 938

FDA-approved drugs (table) 1790

Argentinean hemorrhagic fever 2476
fish families 1781

Argulus spp 1740, 1748, 1757, 1795, 1808
management 1784

Arildone 2748
metazoan parasites (table) 1802

Arizona bark scorpion 3163
mycotic diseases 1811

Armillifer spp 2464
neoplasia 1814

Amold-Chiari malfom1ation, large animals
nutritional diseases 1798

1225
parasitic disease 1799

Aromatic
protistan parasites (table) 1798
amide 2650

Aquatic Animal Health Plan, National 1747
organic arsenicals 3073

Aquatic systems 1766-See also

Arrested development, larval 304

Aquaculture, Aquarium fishes

Arrhythmias 90, 1673
analysis 1768
broilers 2821
dissolved gases 1771
cardiac 71, 90, 1673
environmental diseases 1769, 1772
respiratory sinus 68

(table)

Arrhythmogenic rigiht ventricular
environmental history 1769
cardiomyopathy 117
equipment for system and water

Arrowgrass 3150
analysis 1768

Arsenic
infectious diseases, fish 1778
inorganic compounds 3071
life support components 1767
organic compounds 3073
toxicants 1770
poisoning 1254, 2994, 3071
types 1766
trioxide poisoning 2994
water analysis 1768

Artelial
reference ranges (table) 1770
dilators 2534, 2535

AraA 2745
pedicle grafts 1705

Arabian fading syndrome 849
thromboembolism 126

Arachnoid

Arteriovenous malformation 450
cysts, small animals 1230

Alteritis, equine viral 701, 1448
diverticuli, small animals 1230
and abortion 1344
pseudocysts, small animals 1230

Arteliviridae 701

3196

INDEX

Atthritis

Ascaridia
degenerative, small animals 1197
dissimilis 2831
and encephalitis, caprine 747, 1093
galli 2828

Erysipelas, sheep 2168
spp 2831
immune-mediated, small animals 1198

Ascarids

VetBooks.ir
infectious
cattle 311
large animals 1062
causing CNS disease 1312
pigs 1158
impaction, horses 259
potbellied pigs 1935
reptiles 1997
small animals 1197

Asca1is
infective, large animals 1062
lumbricoides 321
large animals 1060
spp 321, 324, 2647, 2832
mycoplasma infection 1352
suum 298, 316, 320, 2456, 2646, 2647
neoplastic, small animals 1198

Ascarops 322
pet birds 1912
strongylina 322
pigs 1158, 1160

Ascites 91, 445
reoviral, poultry 2886
syndrome, poultry 2871
rheumatoid, canine 822

Asclepias spp 3094, 3136
septic

Aseptic
distal interphalangeal joint, cattle
meningitis, dogs 1229

1088
necrosis of femoral head, dogs 1194
large animals 1062

Asian taeniasis 2454
small animals 1197

Asparaginase 2730
traumatic, large animals 1060

Aspartate aminotransferase 1591
viral, poultry 2886

Aspergillosis 633, 2438

Atthrocentesis, cattle 1070
allergic bronchopulmonar'Y 2438

Arthrode1ma be1ihamiae 1832, 1835
backyard poultry 1823

Atthrogryposis 621, 1044
marine marnmals 1864
cattle 1045
pet birds 1901
multiplex 614
poultry 2901

Arthropathies

Aspergillus
large animals 1060
defiectus 634
small animals 1194
felis 633

Atthropathy
fiavus 633, 1901, 2846, 2847, 3011
amyloid, poultry 2883
fumigatus 158, 270, 633, 1901, 2701,
degenerative, cattle 1086

2901

Atthropods
nidulans 633
causing CNS disease 1310, 1314
niger 633, 1901
nonhuman primates 1880
ochraceus 2847
ratites 1965
parasiticus 2846, 3011
venomous 3162
spp 158, 494, 505, 633, 640, 1205, 1249,
zoonotic diseases 2462, 2464, 2466

1251, 1264, 1335, 1346, 1425, 1463,

Atthroscopy, in lameness

1489, 1761, 1899, 1902, 1993,2052,
cattle 1070

2177,2196,2438,2575,2701,2703,
horses 1101

2705,2706,2739,2S47,2860,2883,
small animals 1193

2894,2901,3010,3011

Atticular
le?TeUS 633
gout, poultry 2882
toxicosis 3011
process-synovial intervertebral
viridinutans 633
articulation processes, horses 1147 Asphyxia

Attificial insemination
foals 1725
cattle 2175
syndrome, perinatal 2094
dogs 2224

Aspicularis tetrapte1·a 2029
goats 2184

Aspiration
horses 2201
fine-needle 1598
pigs 2209
pneumonia 1417
poultry 2895
reflex 1488
sheep 2218

Aspirin 2602, 2717

Arum spp 3106
toxicity 3028

Arvicathus abysinicus nubilans 760

Assistance dogs 1578

Aryloxyphenoxypropionic poisoning 2998

Assisted reproductive technologies 1329

Ascariasis 2456

Association (epidemiology) 2403

INDEX

3197

Asler3086

A triplex 3086

Asthenia, cutaneous 50, 849

Atrophic

Asthma
gastritis 388
allergic 825
rhinitis
feline bronchial 1490
pigs 1465

VetBooks.ir

Astragalus
potbellied pigs 1936
bisulcatus 3086

Atrophy, ilis 496
spp 126, 138, 985, 1333, 3085, 3086, 3136, Atropine 2553, 2612

3138

Attack rate 2398

Astrakhan spotted fever 2434

Attention defieit disorder, dogs 1567

Astringents 2542

Atypical

Astrocytomas 1270
histiocytomas 952, 961

Astrolepis sinuata cochisensis 3132
interstitial pneumonia, bovine 1439

Astronotus ocellatus 1810
myoglobinuria, horses 1186

Astrovirus, mink 1874

Aucubajaponica 3106

Asularn poisoning 2996

Attjeszky disease 1300, 1342

Asystole 1673
mink 1874

Atamasco lily 3118

Aural plaques, equine 524

Ataxia

Auranofin 2583
enzootic 1093, 1225, 1253

Aurantiactinomyxon ictalw-i 1756
progressive, Charolais cattle 1227

Awicular-See also Ear
terriers 1228
chondritis 526

Atelerix 1835
dermatitis, necrotic, swine 524
albiventris 1828
rupture, turkeys 2787

Atenolol 76, 2538, 3033

Aurothiomalate 2583

Atherosclerosis, pet birds 1914

Aurotrichia, acquired, dogs 849

Athesmia 2041

Australian

Atlantoaxial subluxation, small animals
bat lyssavirus 24 78

1230
itch, sheep 918

Atopic

Austrobilharzia spp 2450
dermatitis 825, 853

Autoimmune
canine 853
adrenalitis 831
feline 855
skin disorders 827
disease 823
thyroiditis 831

Atopic-like dermatitis 853

Automatic exposure control, radiography

Atopy 853

1627

Atoxoplasma spp 1904, 2780, 2781

Autotorny 1976

Atoxoplasmosis, birds 1905, 2781

AV conduction disturbances 93

Atracurium 2587, 2588

Avascular necrosis, poultry 2884

Atrazine 2972

Averrnectins 2638, 2647, 2750
poisoning 2999

Aversive conditioning 1540

Atresia

Avian-See also Birds, Pet birds, Poultry
ani 169
adenovirus ( quail) 2913
llamas and alpacas 1851
anemia virus infection 2785
choanal, horses 1462

Aspergillus infection, zoo animals 2052
coli 169, 620
bornavirus 1909
llamas and alpacas 1851
borreliosis 2813
ilei 169

Campylobacter infection 2806
jejunae 169
chlamydiosis 599, 2808
rectal 169
encephalomyelitis 2888
vulvi 1332
backyard poultry 1822

Atrial
flu 2472
fibrillation 72, 95
gastric yeast 1903
lone 95
influenza 1911, 2902
primary 95
highly pathogenic, zoo birds 2054
flutter 95
ratites 1965
kick 68
keratoacanthorna 2855
premature complexes 94
leukosis 2851
septa! defects 72, 82
mycobacte1iosis 1898
standstill 93
zoo animals 2053
persistent 120
nephritis viral infections 2812

Atrioventricular block 93
paramyxovirus 24 76, 2858

3198

INDEX

Avian (continued)

Baccharis spp 3138
pneumoencephalitis 2856

Bacillary hemoglobinuria 341, 601
pneumovirus 2904

Bacillus
polyomavirns 1907
aneurinolyticus 1281
vibrionic hepatitis 2806
anthracis 593, 2418, 2655

VetBooks.ir

Avibacterium
cereus 2177
gallina,rum 2865
piliformis 340
paragallinarum 2909, 2911
sphaericus 2879

Avipoxvirus, poultry 2824
spp 864, 1897, 2571

Avocado
thiaminolyticus 1281
pear 3112
thuringiensis 2753
poisoning 2964
israelensis 886, 2876, 2879

Axial pattern flaps 1705

Bacitracins 2693

Axon 1209

Back

Axonopathy, progressive, Boxer dogs 1229
broken, rabbits 1954

Axonostenosis 1261
disorders, horses 1146

Axonotmesis 1243, 1261

Backgrounding, calves 2131

Azalea 3112

Backyard poultry 1815

Azaperone 2600
diseases 1819, 1821

Azathioprine 2556, 2582
laying and reproduction 1818

Azidothymidine 2747
management 1816

Azinphos-ethyl toxicity 3064
physical examination 1815

Azinphos-methyl toxicity 3064
vaccination 1819

Azithromycin 2687

Baclofen 2589, 3036

Azlocillin 2655

Bacteria

Azo dyes 2744
antimicrobial resistant, feedlots 2134

Azoospennia, dogs 2239
antin1icrobial susceptibility 1597

Azotemia, small animals 1512
culture identification 1596

Azoturia, horses 1178
in urine 1618

Aztreonam 2656

Bacterial

B
abortion, horses 1345
coldwater disease 1759

B cells 57
diseases

B vitamins, as appetite stimulants 2546
amphibians 1737

Babesia
ferrets 1824
bovis 20, 21, 23, 931, 936, 1264, 2440
llamas and alpacas 1851
bigemina 20, 21, 23, 936
marine mammals 1861, 1863
caballi 23, 930, 933
mink 1871
canis 23, 407, 931, 936
nonhuman primates 1878
conradae 22
pet birds 1896
divergens 22, 23, 934, 2440
rabbits 1944
duncani 22, 2440
reptiles 1991
equi 23, 35, 931, 933, 936
spinal column and cord 1249
felis 23
zoonotic 2418, 2420, 2422, 2424, 2426,
gibsoni 23, 932

2428,2430,2432
major 23, 931
gill disease 1759, 1778
microti 22, 934, 2440
kidney disease, fish 1759
molasi 23, 931
pneumonia
ovata 932
cattle 1436
ovis 23
rats 2028
perroncitoi 23
prostatitis 2622
rossi 23

Bactericidal agents 2637
shortti 2785

Bacteriostatic agents 2637
spp 9, 10, 18, 21, 23, 33, 435, 826, 925, 931, Bacteroides 934,936,941, 1003,2441,2780,2785
fragilis 178, 289, 2655, 2664, 2684, 2688,
trautmanni 23

2691,2696
venatorum 22
melaninogenicus 1081, 2696
vogeli 23
intermedius 365

Babesiosis 21, 2440
splanchn'icus 178
birds 2785
spp 352, 482, 1263, 1449, 1943, 2093,

Babinski reflex 1218

2571,2655,2686,2691

Baby chick nephropathy 2812
ureolyticus 193

INDEX

3199

Bahia oppositifolia 2960

Bayou virus 24 70

Balaena mysticetus 1867

Beak

Balaenoptera borealis 1867
and feather disease, psittacine 1908

Balamuthia mand1illaris 1264
anomalies, reptiles 1999

Balanitis, venereal, equine 1357
trimming, pet birds 1888

VetBooks.ir

Balanoposthitis

Bean castor 3148
enzootic 1372

Beard grass, annual 3154
small animals 1401

Beargrass 3118
venereal, sheep 872

Bedbugs, poultry 2875

Balantidiasis 2442

Bedding, laf>oratory animals 1840

Balantidium

Bee stings 3164
coli 158, 2442

Beef
spp 1878, 2047
cattle-See also Cattle

Baldy calf syndrome 850
health-management interaction

Baleanoptera musculus 1860

2119

Bambermycins 2765
management 2119

Bamboo
nutrition 2248

Chinese sacred 3146
reproduction, management of
heavenly 3146

2171

Bandages 1705
feedlots, management 2126

Bandera syndrome 1226
quality assurance 2133

Bandicota spp 2456
safety programs 2133

Bang's disease 1335, 1348
tapeworm disease 2454

Baptisia spp 3118

Beefsteak plant 3128

Barbados aloe 3104

Behavior

Barbering, mice 2031
abnormal 1534

Barber's pole worm, cattle 308
changes in pain 2105

Barbiturate toxicity 3035
medicine, introduction 1533

Barker 2094
modification 1540

Barking pig syndrome 721
problems 1545

Barmah Forest virus 2466
cats 1571

Barn itch, cattle 916
cattle 1551

Barns, ventilation 2118
chickens 1557

Bartonella
diagnosis 1537
clarridgeiae 2422
dogs 1559
henselae 28, 362, 1481, 2399, 2422
goats 1556
recurrentis 909
horses 1546
spp 28, 121, 362, 881, 1017, 2032, 2171,
pet birds 1920

2422
prognosis 1539

Basal cell
sheep 1556
epitheliomas 944
swine 1554
tumors 944
treatment 1539

Basaliomas 944
resources 1535

Basement membrane zone 837
social 1545

Basenji enteropathy 168
cats 1570

Basic cardiac life support 1671
cattle 1551

Basidiobolomycosis 645
chickens 1557

Basidiobolus
dogs 1557
ranarum645
goats 1556
spp 645, 1739, 1993
horses 1545

Basophilia 62
sheep 1555

Basophils 5, 57, 1613
swine 1553

Basosquamous cell carcinomas 944
therapy 1539

Bastard strangles, horses 1454
drugs, cats and dogs (table) 1544

Bat nutrition 2294
principles 1543

Batrachochytrium dendrobatidis 1738
training, zoo animals 2049

Battery, alkaline, poisoning 3003

Benazepril 2533, 3032

Baylisascaris

Beneckea chitinovora 1991
procyonis 416, 1252, 1312, 1953, 2007,

Benedenia spp 1756, 1807

2042,2103,2460

Benign
spp 1312, 1954, 1965,2048,2052,2460
fibroblastic tumors 955
tasmaniensis 2045
footrot, sheep 1167

3200

INDEX

Benign (continued)

Biliary
nonvirus-associated papillomatous
adenocarcinomas, small animals 470
lesions 943
atresia, large animals 349
prostatic hyperplasia 1406
cirrhosis 459

VetBooks.ir
tumors, oral, small animals 366
cystadenoma 4 78

Bensulfron methyl 2972
cysts, small animals 477

Bensulide 2972
tree rupture 480
poisoning 2996, 2997

Bilirubin 1592, 1595

Bent leg, goats 1093
deconjugation 439

Bentazon 2972
in urine 1617

Benzathine cephapirin 2663

Binapacryl poisoning 2997

Benzene hexachloride 2749

Bioallethrin 2750
toxicity 3061

Bioavailability of drugs 2495

Benzimidazoles 2639, 2645, 2748

Biochemistry, clinical 1590

Benzodiazepines 2545, 2589, 2594, 2601

Biocontainment 2069, 2073
toxicity 3034

Bioexclusion 2069, 2071

Benzoic acid 2739

Biologic response modifiers in cancer

Benzoyl peroxide 2740
therapy 2735

Benzoylphenyl ureas 2752

Biomarkers, cardiac 101

Benzphetamine 3039

Biosecurity 2068

Benzylpenicillin 2654
in aquaculture 1745

Bermejo virus 2470
home aquarium 1797

Berteroa incana 704

Biotin deficiency

Bertiella stude,i 1881, 2450
mink 1875

Bertielliasis 2450
pigs 2345

Besnoitia
poultry 2942
bennetti 597

Biotoxin 2948
besnoiti 597

Bipolaris sp 643, 1264
caprae 597

Bipyridine compounds 106
darlingi 597

Bipyridyl poisoning 2996
jellisorri 597

Bird tongue, in dogs 163
oryctofelisi 597

Birds-See also Avian, Pet birds, Poultry
sauriana 597
nutrition 2288
spp 158, 208, 597
pet 1885
tarandi 597
antifungals used in (table) 1901
wallacei 597
antimicrobials used in (table) 1897

Besnoitiosis 597
bacterial diseases 1896

Betamethasone 2607, 2712
cage size recommendations (table)

Betanodaviruses, fish 1765

1885

Bethanechol chloride 2627
clinical pathology 1889

Bezzi's blow fly 900
feather destructive behavior 1927

Bias 2399, 2402
drugs used in (table) 1928

Bibersteinia trehalosi 765, 1474
geriatric diseases 1912

Bicarbonate 1592
hematologic values (table) 1890

Biceps brachii tendon, tenosynovitis, small
management 1885
animals 1202
mycotic diseases 1899

Bicipital bursitis, horses 1129
neoplasms 1915

Bijidobacillus 444
nutritional diseases 1917

Bijidobacte,iurn spp 2370, 2696
parasites 1904

Big
pediatric diseases 1892
brisket 137
psychotropic medications for feather
head
plucking 1928
horses 1052
regurgitation differential diagnoses
rabbits 1950

(table) 1900
rams 602, 2168
reproductive diseases 1920
liver disease 343
drugs used in (table) 1923

Bigleaf periwinkle 3108
toxicities 1924

Biguanides 2739
trauma 1925

Bile
viral diseases 1907
acids 332, 436, 1592
zoo, prevention of flight 2053
duct obstruction 478

Bisacodyl 2559
pathologic changes, small animals 439

Bisga.ard ta.xon 589
pe1itonitis 480

Bishop's weed 977

INDEX

3201

Bismuth subsalicylate 2553

Blood

Bison bonasiis 738
chemist1y analysis 1590

Bisphosphonale 569, 2737
crossmatching 16

Bispyribac sodium 2972
cysts, valvular 115

Bile wounds 1707
flow, hindrance 70

VetBooks.ir

Bithionol 2650
gas reference ranges (table) 3175

Bilhynict sp 428
groups 15

Biting
loss anemia 9
housefly 890
parasites 18
lice 908
products 1681
midges 887
sample preparation and evaluation 1613
poultry 2875
substitutes 18

Bitterweed 3116
transfusions 15, 17

Black
typing 16
calla 3106
volume replacement 17, 1666

Creek Canal virus 2470
worms, horses 316
disease 325, 341, 603, 2168

Blooclborne organisms, birds 2780
flies 886

Bloodsucking lice 908
poultry 2875

Bloody
greasewood 3120
milk 1389
hen flea 2875
scours, pigs 301
locust 3130

Blow fly, Bezzi's 900
patch disease 3019

Blue
spot disease, birds 2781

African lily 3104
tongue, poultry 2940
bag, rabbits 1949
walnut 3134
breasts, rabbits 1949

Blackbrush 3136
eye 799

Blackhead, poultry 2835
wing disease 2785

Blackleg 602, 1171, 2168

Bluebonnet 3144

Blacktail, fish 1755, 1807

Bluecomb, turkeys 2797

Bladder

Bluetongue, 619, 738, 1337, 1339
anomalies 1498
abortion 1337
tumor antigen test 1619

Boar

Bladderpod 3132
effect 2203

Blaslomyces
management 2203
de,malilidis 634, 1205, 1251, 1264,
spermiogram values 2207

1425, 1826,2438,2697,2699,2701,
usage guidelines 2210

2705,2706

Body
spp 505,638,830,2574,2575
cavity fluids 1605

Blastomycosis 634, 2438
condition scores

Bleach, chlorine, poisoning 3001
cattle, breeding 2121, 2263

Bleeder, horses 1457
clogs and cats (tables) 2354, 2355

Bleeding-See also Hemorrhage
horses (table) 2316
back syndrome, potbellied pigs 1934
louse (poult1y) 2876
diatheses 46
surface area weight conversion (table)

disorders 44

3182

Bleomycin 2729, 2733, 2734
temperature regulation, 1015

Blepharitis 490

Bog spavin

Blighia spp 618
cattle 1088

Blind
horses 1135
quarters, udder 1387

Bohle iridovirus 1741
staggers 3086

Bolbophoius

Blister
coi�fusus 1757
beetle poisoning 3157
damnijicus 1754
disease, reptiles 1991

Bolbosoma spp 1865

Blisters, breast, poult1y 2873

Bolivian hemorrhagic fever 2476

Bloat

Bombina 01·ien/,alis 1743
ruminants 227

Bonding, human-animal 1575
small animals 384

Bone

Block vertebrae, small animals 1229
marrow, anemia, primary 13

13-Blockers 76
remodeling, horses 1120
toxicity 3033
spavin, horses 1133

3202

INDEX

Bone (continued)

hydrosawi 930
trauma, small animals 1205
oudemansi 930
tumors, small animals 1205
spp 928, 930

Bonkers syndrome, bovine 3043

Bots

Bont tick 929
horses 315

VetBooks.ir

Boophil'US
rabbit 901
microplus 935, 940, 2576, 2752
rodent 901
spp 19, 21, 927, 935

Bottle jaw, cattle 309, 310

Borax 2972

Botulism 601, 605, 1242
poisoning 2996
birds 2860, 2889

Border disease 622
forage 606
abortion, sheep 1338
horses 2159

Bordelella
mink 1871
avivm 1896, 2834, 2865, 2907
poultry 2860, 2889
rhinotracheitis, turkeys 2907
toxicoinfectious 606
bronchiseptica 453, 1443, 1465, 1469,

Boutonneuse fever 2434

1478, 1488, 1492, 1835, 1879, 1945,

Bovicola 2751

2016,2420,2608,2908
bovis 910, 2576
hinzii 2908
caprae 912
parapertussis 765
equi 912
pertussis 2768
limbata 912
spp 2688, 2692, 2772, 2907
ovis 911

Bordetellosis 2420

Bovine-See also Cattle
turkeys 2907
abortion, epizootic 1336

Boric acid 2739
atypical interstitial pneW11onia 1439

Bomavirus, avian 1909
bonkers syndrome 3043

B01Telia
coronavirus 271
afzelii 659, 2420
cystitis and pyelonephritis 1499
anserina 926, 938, 1821, 2813, 2876,
demodicosis 916

2877
ephemeral fever 741
ba,1Jmiensis 659
genital campylobacteriosis 1347
burgdorj'eri 119, 120, 505, 659, 934,
herpesvirus 1385, 1392, 1434

1263, 1511, 1622,2415,2420,2768
and abortion 1334
crocidurae 2420
vaccination, exotic manimals 2055
duttoni 939, 2420
high-moW1tain disease 137
garinii 659, 2420
imrnw1odeficiency-like virus 822
hermsii 2420
leukemia virus 743
hispanica 939, 2420
leukocyte adhesion deficiency 60
japonica 2420
leukosis 743
lonestmi 928
lyrnphosarcoma 743
miyamotoi 659
papillomavirus 1386
persica 939, 2420
petechial fever 7 45
recurrentis 909, 2420
pleuropneurnonia, contagious 1438
spielmanii 2420
progressive degenerative
spp 2032, 2781, 2813
myeloencephalopathy 1227
suilla, 1165, 2571
pulmonary emphysema and edema,
theile1i 93 7
acute 1439
turicatae 926, 2420
pyelonephritis 1499
vincenti 364
respiratory

BotTeliosis 659, 2420
disease complex 1431
avian 2785, 2813
disease, Mannheimia haemolytica

Bos
associated 1436
giunniens gninniens 738
syncytial virus 1433
indicus 19, 21, 515, 752, 941, 1377, 2246
rhinotracheitis virus, infectious 1434
taW1kS 19, 21, 515, 752, 759, 937, 941,
secondary recumbency 1188

1377,2246
spongifonn encephalopathy 1284, 2482

Bot fly
teats, diseases 1385
equine 2464
thrombopathia 50
human 2464
ulcerative mammillitis 1385

Bothriocroton
viral diarrhea 267, 621, 1436
m1kginans 930
and abortion 1334
concolor 930
warts 1386

INDEX

3203

Bowed tendon, horses 1121
progran1, heifer replacements and cows

Bowel

2172
disease, inflammatory
soundness 2230
horses 291
boars 2237
small animals 397
bulls 2231

VetBooks.ir
edema 716
dogs (male) 2237

Bowen disease, feline 947
examination 2183

Brachia! plexus
male 2230
avulsion 1244
mare 2189
injury 1261
small animals 2219

Brachiaria brizantha 977
goats 2183, 2234

Brachycephalic dwarfs 1043
rams 2233

Brachygnathia 162
stallions 2200, 2234

Brachyspira
timing, dogs 2224
hampsonii 301

Bright blindness 3091
hyodysenteria.e 158, 197, 297, 301, 2694

Brisket disease 137
inte1media 297, 301

Brodifacoum poisoning 3166
murdochi 297

Broilers, nutrition (table) 2917
pilosicoli 297

Broken
spp 158, 2669
back, rabbits 1954
suanatina 301
heads 895

Brachytherapy 1654
mouth, sheep 177

Bracken fern 3148

Bromacil 2972
poisoning 3090
poisoning 2999
staggers 3091

Bromadiolone poisoning 3166

Brackenism, acute 3090

Bromethalin poisoning 3167

Bradybaena spp 328

Bromide

Bradykinin 2707
toxicity 2597

Brain

Bromocryptine 2607
stem disorders 1222, 1226

Bromoxynil 2972
tumors 1270
poisoning 2999
hematogenous metastatic 1272

Bronchial asthma, feline 1490

Brake fern 3148

Bronchiectasis 1414

Bran disease 1052, 2325

Bronchiolitis

Branchial
allergic 825
arch, fourth, defect, horses 1461
obliterans 1414
cyst 165

Bronchitis 1413

Branta sandvicensis 2826
allergic, cats 1490

Brassica
chronic allergic 825
napus 977
infectious
spp 977, 1003,2168,2347,3133,3138
backyard poultry 1822

Braxy 605
poultry 2909

Brazilian hemorrhagic fever 2476
quail 2913

Bread dough, poisoning 2965
venninous 1421

Breast blisters, poultry 2873

Bronchoalveolar lavage 1605

Breast buttons, poultry 2873

Bronchodilators 111

Breathing, emergency 1663
methylxanthine, dosages 2611

Breeding-See also Parturition,

Bronchoesophageal fistula, small animals

Reproduction

373
aggression, horses 1547

Bronchointerstitial pneumonia, acute,
cattle 2175
foals 1452
evaluation 2120

Bronchopneumopathy, eosinophilic 825,
goats 2184

1479
horses 2201

Bronchopulmonary aspergillosis, allergic
management

2438
cats 2224

Brooder pneumonia 2901
dogs 2221

Brooklynella spp 1801
pigs 2207

Broomcorn 3148
problems

Brotianide 2650
cattle 1551

Brown
swine 1555
atrophy, cattle 1045

3204

INDEX

Brown (continued)

sheep 1170
blood disease, fish 1775
zoo animals 2052
chicken louse 2876

Bunarnicline 2651
dog tick 936

Bunclibugyo ebolavirus 2470
ear tick 937

Bunos/omum

VetBooks.ir
recluse spiders 3162
phlebotorniirn 310, 2458
stomach worm, cattle 308
spp 303, 310, 313, 2638

Broxyquinoline 2697
tiigonoce'J)halurn 312, 313

Brucella

Bwwaviriclae 761
abortus 1064, 1091, 1335, 1339, 1340,

Buphagiis spp 941

1346, 1348, 1350, 1402,2420

Buphthalrnia, rabbits 1959
canis 505, 1205, 1249, 1400, 1402, 1623,

Buprenorphine 2602, 3042

2219,2224,2229,2237,2239,2422

Bupropion 3035
ceti 1861

Burial 1640
melilensis 1339, 1340, 1346, 1348, 1350,

Burkholdeiia 2426

1351, 1402,2183,2420
rnallei 706, 2424
ovis 1339, 1351, 2166, 2215, 2217, 2234
oklahorneiisis 2426
pinnipedialis 1861, 2422
pseuclornallei 661, 1863, 2426
spp 692, 931, 1064, 1337, 1339, 1348,

Burn shock 1719

1861,2125,2423,2665,2671

Burning
suis 1341, 1343, 1348, 1350, 1402, 2420
bush 3144

Brucellosis 1348, 2420
carcasses 1640
and abortion 1335

Burns
cattle 1348
clogs and cats, nutrition in 2384
dogs 1402, 2229
horses 1719
goats 1350
mouth, small animals 365
and abortion 1340
reptiles 2000
horses 1350

Burroweecl 3134
marine mammals 1861

Bursa] disease, infectious, poultry 2837
pigs 1350

Bursatti 904
and abortion 1343

Bursitis
sheep 1351
large animals 1064
and abmtion 1339
suppu:rative, horses 1350

Brugia

Bursoscopy, horses, lan1eness 1101
malayi 2458

Buspirone 1544, 2601, 2604
paha,ngi 2458

Buss disease 1308
spp 2458

Busulfan 2731

Bruised sole and corns, horses 1107

Butabarbital 3035

Bruit de canon 94

Butachlor 2972

Brwifelsia pauciflorajl.oribunda 3106
poisoning 2999

Buboes 677

Butorphanol 2549, 2602, 2609, 3042

Bucked shins, horses 1123, 1131

Butterfly ve1tebrae, small animals 1229

Buckeye 3122

Buttress foot, horses 1115

Budesonide 2556

Buturon poisoning 2998

Budgerigar fledgling disease 1907

Butylate 2972

Buffalo
poisoning 2996
bur 3130

Bypass tracts 95
flies 892
gnats 886

Buffalopox virus 2466
c

Buja 930

Cabergoline 2607
alvarius 3161

Caca/ua, spp 1889, 1904, 1908, 1909
mminus 1743, 3161

Cache Valley virus 619, 622

Bulbar necrosis, infective, sheep 1170
abortion, sheep 1338

Bull reproductive management 2174

Cachexia, nutrition in, clogs and cats 2381

Buller steer 1552

Caesalpinia spp 3118

Buller syndrome 2763

Caffeine toxicity 3032

Bulling 1354

Cage layer fatigue 1820, 2882, 2897, 2930,

Bullnose 1468

2932

Bullous pemphigoid 828

Calaclium spp 3106

Bumblefoot 1170, 2868

Calcaneal bursitis, horses 1139
pet birds 1913

Calcifying epitheliomas of Malherbe 949

INDEX

3205

Calcimimetics 570
enteritis 191, 2422

Calciphylaxis 3078
fetus 191, 1337, 1347, 2665, 2696

Calcipotriene toxicity 3037
fetus 1336, 1337, 1346, 1347, 2217

Calcitonin 562, 570
testudinum 193, 2422

Calcitriol 572
venerealis 1336, 1347, 2232, 2422

VetBooks.ir

Calcium 1592
helveticus 191
carbonate crystals 1618
hyointestinalis 191
channel blockers 2534
infection, avian 2806
toxicity 3032
insulaenigrae 193
deficiency 1050
jejuni 158, 191, 273, 276, 403, 459, 1336,
pet birds 1919

1337, 1878, 1964,2217,2422,2554,
pigs 2344

2806
poultry 2930
jejuni 192, 194, 1337
hydroxide 2739
lmi 1337, 2806
metabolism disorders 561, 987
mucosalis 191
oral supplementation 572
peloridis 193
oxalate crystals or stones 1618
spp 191, 300, 374, 378, 380, 396, 399, 403,
parenteral treatment 572

623, 1075, 1336, 1337, 1340, 1347,
phosphate deposition, Great Danes 1229

1872, 1879,2125,2166,2170,2174,
regulating hormones 561

2376,2554,2806
requirement
sputoium 191
laying hens 2918
subantai·cticus 193
pigs 2336
upsaliensis 191, 403
sheep 2346
ureolyticus 193
toxicity, poultry 2860
voluciis 193

Calculi

Campylobacteriosis
prostatic 1408
bovine genital 134 7
urinary-See Urolithiasis
cows, and abortion 1336

Calf
enteric 191
cow pair management 2181

Canary ivy 3110
dairy, feeding 2280

Canarypox 1910
diphtheria 1429

Cancer-See also Neoplasia, Tumors
immunoglobulin 1625
eye, cattle 515
management 2122, 2178
pain 2113
nutrition 2124
therapy, biologic response modifiers

Calicivirus infections

2735
feline 453, 1481

Candida
maiine mammals 1867
albicans 159, 364, 636, 671, 1720, 1832,
rabbits 1951

1894, 1899,2703,2791

Calicophoron 328
fumata 636

California
glabrala 1899
encephalitis virus 2466
kntsei 341
hare coltivirus 2468
pampsilosis 1899
serogroup infections 2466
spp 158, 218, 494, 636, 1264, 1346, 1425,

Calliphorn

1508, 1835, 1880, 1899, 1900, 1993,
spp 895, 897

1994,2039,2414,2574,2575,2617,
stygia 897

2622,2662,2697,2698,2699,2701,

Callilhri.x spp 1876

2703,2706,2739,2861

Callorhinus ursinus 1856
trnpicalis 1899

Calodium hepaticum 2456

Candidatus 26

Caloric requirements, dogs and cats

Mycoplasma

Calving
haemaloparvum 26
mai1agernent 2178
haemola.mae 26, 28
paralysis 1244
haemominulum 26, 28

Can1elids-See Llan1as, Alpacas
tuiicensis 26, 28

Camelpox 2468

Cai1didiasis 636

Cmnpylobacler
mai·ine mammals 1864
abortion, sheep 1337
pet birds 1899
avium 193
poultry 2791
cana.densis 193

Canine-See also Dogs
coli 191,2422,2806
adenovirus 798
cryaerophilus 191
vaccination, exotic manm1als 2058

3206

INOtX

Canine (continued)

Cannibalism
aggression 1561
backyard poultry 1820
atopic dermatitis 853
pigs 1554
benign familial chronic pemphigus 850
poultry 2873
cholangiohepatitis 459
rabbits 1954

VetBooks.ir
chronic

Cannon
axonal degeneration 1238
bone fracture. horses 1124
hepatitis 460
waves 94
cyclic neutropenia 61

Cantharidin poisoning 3157
demodicosis 922

Caparinia spp 1832
distemper 777

Capillm·ia
encephalomyelitis 1250
aerophila 1484, 1490, 2456
serology 1622
caudiriflata 2830
vaccination, exotic mammals 2055
contorta 2830
virus, ferrets 1825
felis 1618
dysautonomia 1256
cati 1511
ehrlichiosis 803
hepatica 2456
serology 1622
obsignata 2830
eosinophilic furunculosis 972
philippinensis 2456
extramedul!ary plasmacytomas 961
plica 1511, 1618
fibrous histiocytoma 957
spp 1808, 2830
flu 1479

Capillariasis 2456
herpesvirus 51, 453, 779

Ca.pnocytophaga
immune-mediated disease, eye, therapy
canimorsus 2422

2569
cynodegmi 2422
infectious hepatitis 453, 798

Capped elbow and hock 1064, 1140
influenza 1479

CaprinNee also Goats
vaccination, exotic man1rnals 2058
arthritis and encephalitis 747, 1093,
interdigital palmar and plantar

1250,2151
comedones and follicular cysts 862
demodicosis 918
juvenile cellulitis 526
herpesvirus 759, 1341
lymphoma40
myotonia 1175
treatment 2737
pleuropneun1onia, contagious 1474
malignant fibrous histiocytoma 959
posthitis and vulvitis 1372
mammary tumors 1404

Capsicum 3106
mucous membrane papil!omatosis 953

Capsicum annuum 3106
multiple system degeneration 1227

Captopril 3032
nasal mites 1480

Capture myopathy, poultry 2884
neurofibrosarcoma 959

Carassius auratus 1806
parvovirus 373

Carbamates 2749, 2754
serology 1622
insecticides 2750, 3059
vaccination, exotic man1mals 2057
toxicity 2992, 2996, 3059
perineuroma 959

Carban1azepine 1545, 2599
rheumatoid arthritis 822

Carbapenems 2656
scabies 920

Carbaryl 2750,2754
spindle-cell sarcoma 959
toxicity 3059
sterile nodular granulomatous

Carbenicillin 2655
dennatitis of the pinna 527

Carbimazole 560
stomatitis 363

Carbofuran toxicity 3060
thrombopathia 50

Carbohydrate
transmissible venereal tumor 1408, 2045
engorgement 222
urolithiasis 1527
requirement
vacuola.r hepatopathy 467
dairy cattle 2265
warty dyskeratomas 944
dogs and cats 2369

X-linked muscular dystrophy 616

Carbolic acid 2742

Canis latrans 1303

Carbon monoxide

Canker 1905
toxicity, poultry 2861
birds 2804
workplace exposure 2952
horses 1108

Carbonic anhydrase inhibitors 2624

Cannabis
use in glaucoma 2570
poisoning 3041

Carbophenothion toxicity 3064
saliva 3041, 3106

Carboplatin 2730, 2735

INDEX

3207

Carboxazole poisoning 2996
denmarki 938

Carboxyatractyloside 343
kelleyi 926, 938

Carboxypenicillins 2655
puertoricensi s 926

Carcasses
spp 925, 926, 938
condemnations 1645
talaje926
disposal 1639
vespertilionis 938

VetBooks.ir

Carchesium spp 1802

Carisoprodol 3036

Carcinoids 576

Carrnustine 2731

Carcinoma

Carnitine metabolism, inherited disorders
basal cell 944

1233
basosquamous cell 944

Carnivores
epidermoid 945
parasites of 1310
hepatocellular, small animals 469
zoo, nutrition 2296
matrical 949

Carolinajessan1ine 3142
pet birds 1916

Carotid body tumors 578
prickle cell 945

Carp edema virus 1814
squamous cell cutaneous 945

Carp pox 1812
thyroid 559

Carpal

C-cell 577
bones, fracture, horses 1125
trabecular 952
breakdown, small animals 1199

Cardiac-See also Heart
disorders, horses 1121, 1125
an·hythmias 71, 90, 1673
hygroma, cattle 1091
broilers 2821
slab fracture, horses 1125
biomarkers 101
subchondral bone disease, horses 1126
catheterization 99

Carprofen 2602, 2718
conduction disturbances 93

Cartilaginous exostoses 1229
defects, llamas and alpacas 1851

Carvedilol 76, 2538
disease 112

Case-control studies 2401
compensation 100

Case fatality rate 2398
pet birds 1914

Caseous lymphadenitis, sheep and goats
glycosides 2529

63,2167
neoplasia 123

Castanospcnnine toxicities 1043
output 70

Castelo dos Sonhos virus 2470
shunts 79, 83

Castilleja 3086
tamponade 122

Castor

Cardiomyopathy 115
bean 3148
arrhythmogenic right ventricular 117
oil 2559
dilated 115

Castration, calves 2123
ferrets 1828

Casts (urine) 1618

Duchenne 121

Cat-See also Cats
hypertrophic 117
flea typhus 2434
restrictive/unclassified 119
foods 2373
turkeys, spontaneous 2790
liver fluke 2448

Cardiopulmonary resuscitation 1670
scratch disease 2422
drugs used in (table) 1672

Catagen 838
open 1673
cysts, isthmus 947

Cardiovascular

Cataplexy, small animals 1225
disease

Cataracts 499
diagnosis 73
birds 1912
medication toxicity 3032
diabetes mellitus, dogs 581
system
inherited (table) 500
abnormalities 70

Catarrhal
congenital and inherited anomalies 76
bovine vaginitis 1392
introduction 67
fever 758
pharmacotherapeutics 2525
gastroenteritis, epizootic, mink 1874
principles of therapy 74

Catastrophic pleural space disease 1664

Cardioversion 96

Catclaw 3136

Care and grooming, small animals 2169

Catharanthus reseus 3108

Carfentrazone ethyl 2972

Cathartics 2559

Carias
dose rates (table) 2559
amblus 938

Cathedral-bells 3112
capensis 926, 938

Catheterization, cardiac 99

3208

INDEX

Cationic
pasture 2280
detergent poisoning 3003
productivity 2136
surfactants 2743
protein requirements 2271

Cats-See also Cat, Feline, Small animals
quality control programs 2142
aggression 1573
rations 2278
breeding management 2224
record keeping 2144

VetBooks.ir
nutrient requirements (table) 2357
replacement 2138
nutrition 2354
reproduction, management of 2137,
pregnancy determination 2225

2171
respiratory diseases 1478
respiratory diseases 1429

Cat's-ear plant 3128
vitamin requirements 2277

Cattle-See also Bovine, Beef cattle, Dairy
water requirement 2273
cattle
feedlot
beef
disease ejpidemics 2129
energy requirement 2249
nutrition 2129
feeding 2263
processing procedures 2132
breeding herd 2263
record keeping 2128
finishing cattle 2264
gastrointestinal parasites 308
stocker cattle 2263
grubs 876
health-management interaction 2119
health-management interaction 2119,
management 2119

2135
mineral requirements 2262
immunization programs 2178
nutrient requirements (tables) 2254,
lameness 1066

2256
bones and joint disorders 1086
nutrition 2248
horn capsule and corium disorders
performance modifiers 2264

1082
protein requirement 2249
soft tissue disorders causing 1091
reproduction, management of
management beef feedlots 2126

2171
neurologic disorders with lameness, grut
vitan1in requirement 2258
abnormalities 1088
water requirement 2249
open herds 2126
breeding 2175
plague 771
body condition score 2121
pregnancy testing 2120
evaluation 2120
purchase for feedlot 2131
health and production management
replacement heifers 2125

2122
reproduction, management of 2120,
nutrition 2121

2171
program, heifer replacements and
respiratory diseases 1429
cows 2172
transpo1tation 2130
vaccinations 2122
welfare 1192, 1579, 2134
closed herds 2126

Cauda equina neuritis 1241
dairy

Caudal
culling 2138
cervical spondylomeylopatlly, small
disease and productivity 2139
animals 1230
dry cow management 2139
occipital malformation syndrome 1226
energy requirements 2269
stomatitis, cats 362
fat requirement 2271

Causality (epidemiology) 2403
feed additives 2284

Gavia porcelliis 1838
feeding 2278

Cayenne tick 928
guidelines (table) 2266

Cebus 1883
health and production 2139
albij1·ons 1876
healtll-management interaction

Cecal impaction, horses 262

2135

Cefachlor 2659
health management program 2140

Cefadroxil 2619, 2659, 2661, 2662
herd size 2138

Cefamandole 2659
lan1eness 1066

Cefazolin 2659, 2661, 2662
management 2135

Cefepime 2660
mineral requirements 2274

Cefoperazone 2659
neurologic disorders with lan1eness

Ceforanide 2659
or gait abnormalities 1088

Cefotaxime 2659, 2661
nutrition 2136

Cefotiam 2659

INDEX

3209

Cefovecin 2619, 2660, 2661, 2662

Cerebrospinal fluid

Cefoxitin 2659
analysis 1219

Cefpodoxime 2619, 2660, 2661, 2662
cytology 1608

Cefsulodin 2659

Ceroid lipofuscinosis 1234, 1236

Ceftiofur 2619, 2659, 2660, 2661, 2662,

Ceruminous gland tmnors 535

VetBooks.ir

2663

Cervical

Ceftriaxone 2659
abscess, swine 734

Cefuroxime 2659
lesion (tooth), small animals 181

Cell-mediated
mucocele, small animals 368
immune reactions 830
prolapse 1390 ,
immunity 816
spondylomyelopathy, small animals 1230
deficiencies 820
stenotic myelopathy, large animals 1228

Cellulitis
vertebral malformation-malarticulation
canine juvenile 526

1245
gangrenous, poult1y 2879

Cervix, double external os 1331
tarsal, cattle 1092

Cervus spp 1313

Cenchrus spp 2321

Cestodes-See also Tapewonns

Central
ca.using CNS disease 1311
core myopathy 1233
marine mammals 1866

European tickborne encephalitis 2480
nonhuman primates 1881
nervous system 1209
pet birds 1906
helminths and arthropods of 1310
poultry 2828
progressive retinal atrophy 503
public health importance (table) 428

Centrocestusformosanus 1754, 1757
small animals 421, 422 (table), 428

Centronuclear myopathy 1200

(table)

Centruroides sculpturatus 3163
zoonotic infections 2450, 2452, 2454,

Centmy plant 3104

2482

Cephalexin 2619, 2659, 2661, 2662

Cestnim

Cephalorhynchus hectori 1869
diitmum 566, 570, 1053, 3138

Cephaloridine 2659
nocturnum 3138

Cephalosporins and cephan1ycins 2659

Cetirizine 3025
adverse effects and toxicity 2662

Chabertia
bacterial resistance 2660
ovina 311, 312
dose rates 2661, 2662 (table)

spp 304, 311, 314
effects on laboratory tests 2662

Chaenomales spp 2960
interactions 2662

Chaetoclon
milk discard tin1es (table) 2663
miliaris 1814
pharmacokinetic features 2660
multicinclus 1814
therapeutic indications 2661

Chaetomium spp 2847
withdrawal times (table) 2663

Chagas' disease 38, 2442

Cephalosporiiim 3020

Chalazion 490

Cephalothin 2659

Chameleo spp 1969

Cephamycins 2659

Champing, pigs 1554

Cephapirin 2659, 2662

Chancres 36

Cephradine 2659

Chancllerella quiscali 1965, 2782

Ceratophyllus

Charmel catfish virus disease 1762
gallinae 2875

Chapare virus 24 76
niger 2875

Charbon 593

Cercarial dermatitis 2450

Chastek paralysis, mink 1874

Cercopithecine herpesvirus 2472

Chediak-Higashi syndrome 59

Cerebellar

Cheilanthes siebeii 1282, 3091
abiotrophies

Cheilitis, small animals 364
large animals 1225

Cheilospirura hamulosa 2828
small animals 1226

Chelating a.gents, hypocalcemia 572
disorders 1222, 1225

Chelopistes meleagriclis 2876
herniation 1277

Chelydra spp 1971
hypoplasia

Chemical residues, food and fiber 2518
large animals 1225

Chemodectomas 578
small animals 1226

Chemoreceptor organs, tumors 578

Cerebral disorders, congenital 1222

Chemosis 492

Cerebrocortical necrosis 1281

Chemotherapeutics 2627

3210

INDEX

Chemotherapy
felis 506, 599, 1481, 2060, 2422, 2566
agents, safe handling 2725
gallinacea 599
canine lymphoma 2738
mmidarum 599
pet birds 1917
pecomm 506, 513, 599, 753, 1262, 1308
tw11or response 2722
pneumoniae 506, 599, 1473, 1738

VetBooks.ir

Chenopod'ium spp 1282
psitlaci 492, 506, 599, 1063, 1065, 1481,

Cherry

1738, 1836, 1897,2186,2428,2808
eye 490
serotypes and types of birds (table)

laurel 3146

2809
pepper 3106
spp 505,507,513,598,623, 1333, 1337,
wild 3148

1346, 1383, 1438, 1738, 1897, 1912,

Chewing

2052,2177,2568,2654,2669,2671,
lesions, small animals 365

2676,2684,2688,2808
lice 908
suis 506, 599, 1738

Cheyletiella
trachomatis 506, 599, 2810
blakei 922, 2576

Chlan1ydial
parasitovorax 922, 1953
cor\junctivitis 506
spp 843,855, 1953,2462,2576
encephalomyelitis 1308
yasgmi 922, 2576
infections 598

Cheyletiellosis 922
pnew11onia, cattle 1438

Chick nephropathy 2812
polyarthritis-serositis 1065

Chicken

Chlan1ydiosis 598, 2422
anemia virus infection 2785
abortion, cows 1336
infectious anemia 2785
amphibians 1738
mite 2877
avian 599, 2808
nutrition 2915

C psittaci serotypes and types of
broilers (table) 2917
birds (table) 2809
leghorn (table) 2923
ovine 599

Chigger borne rickettsiosis 2438
pet birds 1897

Chiggers 924

Chlamydophila-See Chlamydia
common, poultry 2877

Chlornequat poisoning 2999
horses 919

Chloramben 2974
turkey 2878
poisoning 2997

Chikungunya virus 2468

Chlorambucil 789, 2555, 2582, 2727, 2731

Chili pepper 3106

Chloramine-T, in aquaculture 1752

Chilling, mink 1876

Chloranline toxicity, fish 1770

Chilodonella spp 1801

Chloran1phenicol 2619, 2683

Chinaberry 3136
dosages (table) 2687

Chinchillas 2003
elin1ination and distribution 2686
biology 2003

Chlorbromuron poisoning 2998
husbandry 2004

Chlordane 2749
iatrogenic disorders 2010
toxicity 3061
infectious diseases 2005

Chlordiazepoxide 3034
metabolic and nutritional disorders

Chlorernuron poisoning 2998

2007

Chlorfenvinphos 2754
neoplasia 2010
toxicity 3065
parasites 2006

Chlorhexidine 2739
physical exan1ination 2005

Chloride 1592
reproductive disorders 2010
deficiency, poultry 2934
traumatic injuries 2009
inorganic 2741

Chinese
organic 2741
evergreen 3104

Chlorinated
photinia 3146
hydrocarbon toxicity 3060
sacred bamboo 3146
mink 1875

Chip fractures, horses 1118
naphthalene toxicity 974

Chirodiscoides caviae 2017

Chlorine 2741

Chiropractic manipulations 2081
bleach poisoning 3001

Chlamydia
toxicity, fish 1770
abortu:; 599, 1336, 1338, 1340, 1346,

Chlorocebus aethiops 1876

1738,2217,2422

Chloronicotines 2754
avium599

Chloronicotinyls 2754
caviae 506, 599, 2017

INDEX

3211

Chlorophacinone poisoning 3166
ovis 917

Chlorophyllum molybdites 3096, 3099
spp 843,914,916,919, 1854

Chlornphytum spp 3108
texanus 916

Chlorothiazide 2624, 3034

Chorioptic mange

Chlorotoluron 2974
cattle 916

VetBooks.ir

Chloroxuron poisoning 2998
horses 919

Chloroxylenols 2742
sheep and goats 917

Chlorpheniramine 3025

Chorioretinitis 503

Chlorpromazine 2548, 2600, 2604, 3036

Choroid plexus papillomas 1271

Chlorpropham 2974

Christmas

Chlorpyrifos 2750, 2754
flower 3110
toxicity 3065
star 3110

Chlorsulfuron 2974

Chromatolytic neuronal degeneration,
poisoning 2998
multisystemic 1234

Chlortetracycline 2679, 2684

Chromium requirement, pigs 2338

Chlorthal dimethyl 2974

Chromodacryorrhea, rats 2032

Chlortoluron poisoning 2998

Chromomycosis, an1phibians 1739

Choanal atresia

Clll'omosomal abnormalities 614, 1329,
birds 1896

1330
horses 1462

Chronic
llamas and alpacas 1851
active hepatitis, large animals 345

Choanotaenia irifundibu,lum 2831
allergic bronchitis 825

Choclo virus 2470
axonal degeneration, canine 1238

Chocolate poisoning 2966
colitis, drug therapy 2555

Choke
degenerative radiculomyelopathy 1246
horses 1720, 1721
egg laying, pet birds 1920
large animals 215
hepatitis

Chokecherries 3148
canine 460

Cholangiohepatitis 344

Doberman Pinschers 464
canine 459

Labrador Retrievers 464
large animals 340

Skye Terriers 465

Cholangitis/cholangiohepatitis syndrome,

West Highland White Terriers 462
feline 481
indigestion, ruminants 233

Cholangitis, large aninrnls 349
inflammatory demyelinating

Cholecalciferol-See Vitamin D
polyneuropathy 1240

Cholecystitis
mastitis, sows 1375
emphysematous 475
obstructive pulmonary disease, horses
small animals 4 73

1455,2152

Cholecystocentesis 438
pain management 2112

Choledochitis, emphysematous 475
relapsing idiopathic

Choledocholithiasis, large animals 344
polyradiculoneuritis 1240

Cholelithiasis
respiratory disease
small animals 479
birds 1823, 2841
large animals 344
rats 2028

Cholera, fowl 2822
ruminal acidosis 225

Cholesterol 1592
selenium poisoning 3086

Choline deficiency
toxicosis 2948
pigs 2345
ulcerative paradental syndrome 363
poultry 2940
wasting

Chondritis, auricular 526
disease 1286

Chondrodysplasia 163
goats 2151
hereditary, lambs 1048

Ch1ysanthemum 2750, 3063

Chondrolipomas 958
cinera1-iaefolium 3063

Chondromalacia, horses 1143

Ch1yseobacterium meningosepticum

Chondroprotective agents 2721

1263

Chondrosarcomas, ferrets 1826

Ch1ysomya bezziana 834, 892, 898, 899,

Chordomas, ferrets 1826

900,929,2462

Choriomeningitis, lymphocytic 831,

Ch1ysops

2474
discalis 693

Chorioptes
spp 889
bovis 916, 917, 919, 2576

Ch1ysosporium 1993
equi 919

Chuzan virus 619, 622

3212

INDEX

Chylothorax 1414
backyard poultry 1820

Chytridiomycosis, amphibians 1738
pet birds 1922

Cicer ai-ietinum 1458

Cloacitis, infectious, reptiles 1993

Cicuta, spp 3116

Cloak fern 3132

Cilia abnormalities 490

Clodinafop propargyl 2974

VetBooks.ir

Cimetidine 2551, 3030

Clomazone 2974

Cimex lect,ulariiis 2875

Clomiprarnine 1544, 2605, 3034

Cinacalcet 570

Clomiprop poisoning 2996

Cingulate gyrus herniation 1277

Clonazepa.m 1544, 2592, 2595, 2599

Cionella lubrica 327

Clonidine 1544

Ciprofloxacin 2670

Cloning, domestic animals 2075

Circling disease 656

Clonorchiasis 2446

Circovirus diseases, porcine 723, 1342

Clonorchis sinensis 428, 2446

Circulation, emergency 1665

Clopidol 2796

Circumanal gland tumors 951

Clopyralid 2974

Cirsiiim arvense 1282

Cloransulan1-methyl 2974

Cisapride 2557
poisoning 2998

Cisplatin 2730, 2734, 2735

Clorazepate 1544, 2592, 2599, 2604

Citrobacter

Clorsulon 2638, 2651
ji·eundii 1991, 1992

Closantel 2650
spp 1374, 1737, 1896, 1984, 1993, 2191,

Clostridia-associated enterocolitis,

2655,2660
horses 285, 607

Citrullinemia 616

Clostridial
large animals 1223
dermatitis, poultry 2879

Cladophialophorn 643
diseases 601, 2422, 2424

Cladosporium
vaccination, exotic man1mals 2059
spp 643, 1739, 1993, 2703
myonecrosis 1171
trichoides 1264
myositis

Clarithromycin 2558
horses 1181

Classical swine fever 713
marine mammals 1861
and abortion 1342
vaccines 613

Claviceps

Clostridium
paspali 3019
botulinum 605, 898, 1242, 1257, 1585,
pwpiirea 3012, 3016, 3019

1824,2159,2301,2860,2889
spp 2847
carnis 1171

Claw
chauvoei 602, 604, 613, 1171, 1181, 1850,
examination, cattle 10�7

1962,2060,2133
trimming, cattle 1074
colinum 1964, 2803, 2805

Clear-eyed blindness 904
difficile 158, 197, 281, 285, 287, 289, 293, Clearance, of drugs 2500, 2520

607,608,609, 1452,2013,2020,2023,

Cleft lip 162

2153,2422,2631,2691,2692,2693

Cleft palate 162
swine 293

Clemestine 3025
haemolyticwn 10, 341, 601, 613, 2060,

Clenbuterol 2607, 2611

2133

Clethodirn 2974
novyi 325, 341, 602, 603, 604, 613, 1171,

Climbing fig 3110

1850,2060,2133,2168

Clindamycin 2690, 2692
type B 604

Clinical
pe1j'ringens 10, 158, 197, 270, 273, 276,
biochemistry 1590

281,285,289,293,295,378,396,
samples 1594

603,604,607,608,609,613,998,
hematology 1610

1171, 1181, 1585, 1850, 1851, 1883,
microbiology 1595

1884, 1964,2060,2068,2123,2133,

Clinostomum 1740

2150,2153,2167,2187,2311,2353,

Clioquinol 2697

2424,2664,2696,2773,2802,2805,

Clioxanide 2650

2872,2879

Clitocybe
type A 608, 609, 1181, 2879
dealbata 3097, 3098
type C 609, 613, 2167
dilatata 3098
type D 610, 2167
spp 3096 (table), 3098
pilifonne 159, 200, 340, 454, 1948, 2013,

Cloaca!

2023
papillomatosis, pet birds 1909
septicum 603, 604, 613, 1171, 1181, 1850,
prolapse

2060,2133,2868,2879

INDEX

3213

Clostridium (continued)

Coffee weed seed poisoning, poultry 2861
sordellii 602, 603, 604, 613, 1171, 1850,

Coffeebean 3132

2060

Coffeepod 3124
spiroforme 1943, 1947

Coggins test 700
sporogenes 1181, 1281

Cognitive dysfunction, clogs 1569

VetBooks.ir
spp 10, 119, 158, 287, 329, 340, 350, 374,

Coho1t studies 2400

378,391,396,475,482,682, 1176,

Coital exanthema, equine 1357, 1392

1449, 1861, 1897, 1947, 1951,2041,

Colchicii-m

2042,2089,2091,2093,2554,2655,
autumnale 3108

2676,2696,2792,2805,3160
spp 618
tetani, 611, 1254, 1883, 2060, 2133, 2157,

Cold

2168,2187,2773
agglutinin disease 827

Clot strength, poor, Greyhounds 53
and cough medications, poisoning 3025

Clot1imazole 2701

Coldwater disease 1759

Clotting factors, lyophilized concentrates

Colesiota conjunctivae 513

2542

Colibacillosis

Cloxacillin 2656, 2658
backyard poultry 1823

Club foot, horses 1150
enteric, pigs 296

Onemidocoptes pilae 1906
potbellied pigs 1933

Coagulation
poultry 2814
disorders 44, 46, 51
rabbits 1948
screening tests 45
septicemic 7 49

Coal-tar products poisoning 3045

Colic, horses 248

Coarctation, aorta 79

Coliforms and mastitis 1362

Cobalt requirement, sheep 2347

Colinus virginianus 2805

Cocaine toxicity 3039

Colisepticemia 749

Cocal virus 2480
poultry 2814

Coccid'ioides

Colistimethate 2692
immitis 637, 638, 1205, 1251, 1264,

Colistin 2692

1425, 1826, 1880,2438,2697,2699,

Colitis

2701
allergic 825
spp 505, 830
chronic 2555

Coccidioidomycosis 455, 637, 2438
drugs for (table) 2555

Coccidiosis 203, 2168
equine ehrlichial 283
calves 273
granulomatous 169
cats 208
idiopathic, horses 607
cattle 205
right dorsal, horses 265
dogs 208
small animals 377
ferrets 1826

Colitis-X, horses 286
goats 207, 2150

Collagenolytic granuloma, horses 972
marine mammals 1867

Collagenosis, progressive dermal, pigs 852
mink 1876

Collagenous nevi 955
pet birds 1905

Collar galls 979
pigs 208

Collateral ligament injury, horses 1131, 1141
poultry 2791

Collection of laboratory samples 1584
rabbits 1952

Collie
sheep 206, 274
eye anomaly 502

Cochliomyia
granuloma 957
hominivorax 898, 899, 928, 2462, 2753
nose 975
macellaria 897

Collimators 1627

Cockle 893

Colloids 1679

Cocklebur 3120
synthetic (table) 1680
toxicosis 343

Collyriclumfaba 2874

Codeine 2608, 3042

Colobornas, iris 496

Coenonia ana line 2865

Colon, horse

Coenuriasis 2450, 2452
foreign body obstruction 266

Coenurosis 1311
impaction 262, 266

Coenurus cerebralis 1310, 1311, 1314
infiltrative disease 288

Coenzyme Q10 111
left dorsal displacement 264

Coffee bean toxicity, poultry 2886
motility pattern 250

Coffee senna 3124
right dorsal displacement 265

Coffee weed 3124
volvulus 265

3214

INDEX

Colony monitoring, laboratory animals 1841
articular rigidity 1044

Color dilution alopecia 847
coagulation protein disorders 51

Colorado
deafness 519, 1236
rubber weed 3116
and developmental anomalies, mouth,
tick fever 2468

Iar·ge animals 176

VetBooks.ir

Columbicola columbae 2876
disorders

Colurnbiformes, nutrition 2290
bovine udder 1387

Columbiphilus polonica 2878
molecular basis (table) 617

Columnaris disease, fish 1759, 1810
erythropoietic porphyria 986

Comandra 3086
hepatic fibrosis, large animals 350

Combination
hypogan1maglobulinemia 819
antimicrobial therapy 2636
hypomyelination, small animals 1226
vaccines 2771
hypothyroidism 553

Comedones (palmar and plantar) and
foals 559
follicular cysts, canine interdigital 862
and inherited anomalies 613

Common
car·diovascular system 76
bot, horses 315
digestive system 162
cattle grub 876
integumentary system 845
chigger, poultry 2877
musculoskeletal system 1042
digital extensor tendon, rupture, horses
nervous system 1222

1127
reproductive system 1329
ivy 3110
urinary system 1496
liver fluke 324
laryngeal paralysis 1231

Community veterinary practice 1575
lordosis, foals 104 7

Compartment syndrome 1188
megaesophagus 166, 1233

Competitive nondepolarizing agents 2586
muscular dystonia, cattle 1175
dosages 2588
myasthenia gravis 1232

Complement 813
myoclonus 1234
deficiencies 819

Labrador Retrievers 1232

Complement-derived peptides 2707
myopathies, horses 1187

Complementary ar1d alternative veterinary
neoplasms, integumentary system 852
medicine 2078
papillomas, foals 943

Complex vertebral malforn1ation 616
photosensitization, sheep 978

Compounded drugs/preparations 2490,
platelet function disorders 49

2491
portosystemic shunts, large animals 351

Compression test, positive 1199
pseudomyotonia, cattle 1176

Compulsive disorders 1535.

scoliosis, foals 104 7
canine 1561
thrombocytopenia 4 7
feline 1574
vascular disorders 50

Computed
ve1tebral malfonnations, small animals
radiography 1628

1229
tomography 1635
vestibular disease 1226

Computerized recording, digital lesions,

Congestive heart failure 73
cattle 1068
bovine 137

Concrete hock, cattle 1092
dogs and cats, nutrition in 2382

Condenmations, carcasses 1645

Conical flukes 328

Conditioning

Conidiobolomycosis 645
classical 1540

Conidiobolus 645
operant 1540
coronatus 645

Conduction
incongruus 645
deafness 519
lamprauges 645
disturbances, cardiac 93

Conium maculatum 162, 618, 3140

Conflict 1536

Conjunctiva 492
aggression, dogs 1563
edema 492
related elimination, dogs 1569
grarmloma 957

Conformational

Conjunctivitis 492
abnorn1alities, eyelids 489
chlamydia! 506

Confounding 2402
feline chlamydia!, therapy 2566

Congenital
feline herpesvirus, therapy 2566
afibrinogenemia 51
inclusion, guinea pig 507
anemia 851
rabbits 1945
anomalies, llarnas and alpacas 1851

Connective tissue tumors 836, 955

INDEX

3215

Conocephalus spp 328

Copperweed 3128

Conocybe

Coprophagia
cyanopus 3099
dogs 1568
filaris 3097, 3100
horses 1550
smilhii 3097

Coquillettidia spp 2471, 2892

VetBooks.ir

Constipation

Cor triatriatum sinister and dexter 86
dogs and cats, nutrition in 2382

Coral
potbellied pigs 1933
bean 3134
small animals 380
disease, fish 1802

Constricted toe syndrome, birds 1896

Cording up, horses 1178

Contact hypersensitivity 831

Cordylobia

Contagious
anthropophaga 902, 2462
abortion, cattle 1348
rodhaini 2462
agalactia 1352

Corkscrew claw, cattle 1086
bovine

Corn cockle 3136
pleuropneurnonia 1438

Cornea 493
pyelonephritis 1499
dystrophies 495
caprine pleuropneumonia 1474
edema, marine mammals 1857
ecthyrna, sheep and goats 866, 2150,
foreign bodies 1697

2468
lacerations 1698
equine metritis 1371
sequestration and keratitis 494
footrot, sheep 1167
stromal abscesses 494
pustular dermatitis 866
ulcers

Continuous murmurs 89
deep stromal 1697

Contracaecum spp 1866, 2456
marine mammals 1857

Contracted tendons 1042
rabbits 1957
horses 1150

Cornifying epitheliomas
kids 1093
cystic intracutaneous 947

Contraction of Achilles tendon, large
intracutaneous 944
animals 1231

Corns

Contrast procedures, radiography
cattle 1082

1632
horses 1107

Controlled trials 2402

Coronary sinus, horses 1115

Conure bleeding syndrome 1889

Corona viral

Conval lily 3108
encephalomyelitis 728

Convallaria majalis 3094, 3108
enteritis, turkeys 2797

Coonhow1d paralysis 1240

Coronavirus 298

Coontie 3114
calves 276

Cooperia
cattle 271, 272
curticei 312
equine intestinal disease 287
oncophora 310, 2648
feline enteric 383
pectinata 310
lan1bs 273
punctata 310

Corpus
spp 304, 310, 2644, 2648, 2649
hemorrhagicwn 2173

Copper
luteum 2173
associated hepatopathy 170, 460

Corrosives, household, injuries 3001
chelate 2974

Corticosteroid-induced leukogram 59
deficiency 1225, 1253

Corticosteroids 2110, 2710--See also
anemia 12

Glucocorticoids, Steroids
goats 1093
administration 2713
horses 2327
adverse effects 2713
llamas and alpacas 1855
mode of action 2711
pigs 2344
pharmacokinetics 2713
poultry 2933
pharmacologic effects 2711
poisoning 3073
physiologic effects 2711
large animals 342
potencies (table) 2712
poultry 2861
therapeutic uses 2714
requirement

Cortinarius
pigs 2337
gentilis 3097
sheep 2347
orellanus 3096, 3101
sulfate 2974
rainierensis 3101
in aquaculture 1752
spp 3102

3216

INDEX

Cortisol 2712

Coxofemoral luxation
excess 573
cattle 1087

Corvus
horses 1145
brachyninchus 1911

Crab's eye 3104
hawaiiansis 2826

Cranial

VetBooks.ir

Corydoras spp 1 783, 1799
and caudal ligament if\jmies, horses 1141

Co1ynebacle1ium
cruciate ligament rupture, small animals
bovis 1359

1198
cystitidis 1499
nerve block 1214
diphlheroides 1249
nerves 1214
eqii-i 679

Craniomandibular osteopathy, dogs 1203
kulscheii 2028

Craniopharyngioma 549
pa.rvum947

Cranium bifida 1222
pilosiim 1499

Orassicauda spp 1866
pseudotubei-culosis 63, 66, 341, 1181,

Creatine kinase 1591

1473, 1852,2148,2151,2166,2167,

Creatinine 1591

2183,2424,2518,2571

Creep ration, lambs (table) 2350
infection, horses and cattle 66

Creeping
ovis 2148, 2151
lady's sorrel 3116
pyogeiies 1499
yellow wood sorrel 3116
reiiale 1372, 1392, 1499, 2217, 2617

Crenosoma vulpis 1421, 1490
spp 666, 671, 679, 864, 1063, 1094, 1499,

Creosote poisoning 3045

1854, 1896,2571,3160

Cresol 2742
ulcei·ans 2424
poisoning 3045

C01ynosoma

Cress 3138
eiihydm 1865

Cresylic acid 2742
spp 1865

Cribbing, horses 1547

Coryza

Cricopharyngeal achalasia 166, 370
gangrenous 758

Crimean-Congo hemorrhagic fever 751,
infectious, chickens 2911

761, 2470
turkey 2907

Critical care, monitoring 1685

Cosmiomnia

Crocodilians, nutrition 2306
hippopolameiisis 930

Crocus 3108
sp 928, 930

Cromolyn sodium 2615

Co-trimazine 2674

Crooked calf disease 618

Co-trimoxazole 2674

Crop

Co-trimoxine 2674
burns 1894

Cotton undetfur, mink 1875
feeding 1891

Colurnix colwnix japon'ica 2805, 2899
mycosis, poultry 2791

Colylophoron 328
pendulous, poultry 2874

Cough, one-mile, pigs 722
stasis 1894

Coumachlor poisoning 3166

Cross-fostering

Coumafuryl poisoning 3166
calves 1552

Coumaphos 2638, 2651, 2750
lambs 1556
toxicity 3065

Crossed extensor reflex 1218.

Counterconditioning 1540

Crnssiella equi 1345

Cow-calf pair management 2181

Crossmatching, blood 16

Cowd1ia ruminantium 752, 925, 928,

Crolalaria

936
poisoning, poultry 2861

Cowdriosis 751
retusa 3150

Cowpox 868, 2468
spp 2872, 3046, 3140, 3150
virus infection, cats and other species
o,·olalus

870
scululalus scululatus 3159

Coxiella 1333
spp 3159
burnetii 623, 770, 933, 934, 938, 1338,

Crotoxyphos toxicity 3065

1339, 1340, 1346, 1836,2032,2217,

Crow poison 3122

2434,2877

Cruciate ligament rupture, small animals
abortion, goats 1340

1198
sp 928, 1333, 1340

Crucifers 3138

Coxiellosis 623

Cruetzfeldt-Jakob disease, variant 2482

INDEX

3217

Crufornate 2651
pipiens-quinqiiefasciatus 24 79

Crushing piglets 1554
restvans 2894

Crutching 898
spp 127, 521, 888, 1293, 2479, 2481, 2483,

Ciyptobia

2784,2879,2893
iubila ns 1783, 1755, 1806
tarsalis 888, 1293, 1294, 2479, 2483

VetBooks.ir
spp 1803, 1808
tritaeniorhynchus 24 73

Ciyplocaryon
tiiteniD'lynchiis 24 79
initcms 1754, 1800
univillatus 2894
spp 1794

Culicoid hypersensitivity 887

Cryptococcosis 637, 2438

Culicoides

Cryptococcus
brevii,arsis 739
bacillisporus 1826
crepusculaiis 1965
gallii 638
iinicola 696, 739
neoformans 637, 1205, 1251, 1264, 1346,
insignis 739

1425, 1489, 1826, 1864, 1904,2438,
obsoletus-deumlji 739

2574,2575,2699,2701,2703,2705
oxystoma 622
var grubii 1826
sonorenS'is 739
spp 505, 638, 1489, 1904, 2574, 2575,
spp 521, 620, 696, 738, 741, 826, 887, 905,

2697

1295, 1337, 1339,2753,2782,2783,

C1yptocotyle lingua 427

2875,2892

Cryptophthalrnia, birds 1896
vaiipennis 1295

Cryptorchidism 1330, 2220

Cul is eta

Cryptosporidiosis 209, 2442
errat'icus 1293
calves 278
melanura 1293, 2471, 2892
horses 287
spp 888, 1295, 2479, 2784
pet birds 1905
tarsalis 2892
poultJy 2798

Culling, cattle
reptiles 1999
breeding 2120

C1yptosporidium
dairy 2138
andersoni 209
feedlot 2134
bovis 209

Curacao aloe 3104
canis 2442

Curb, horses 1138

Jelis 2442

Curled-toe paralysis, poultry 2941
hominis 209

Curly dock 3130
meleagridis 2442

Curvulciiia spp 640, 643
inuiis 2442

Cushing disease/syndrome 543, 573
parllUm 209, 275, 276, 280, 1853, 1881,
ferrets 1827

2442
peripheral, horses 1006
ryanae 209
treatment 545
saiirophilum 1999

Cutaneous
serpentes 1999
acariasis 914
spp 158, 209, 278, 287, 291, 298, 1619,
apocrine gland tumors 949

1806, 1905, 1965, 1971,2007,2170,
asthenia 50, 849

2798
cysts, keratinized 947
viatorum 2442
derrnatophilosis, marine mammals 1863

Cryptostegia grandijlora 119
habronemiasis 904

Crysotherapy 2583
histiocytomas 966

Crystalloids 1677
histiocytosis 966

Crystalluria 1618
hypoplasia, focal, swine 846

Crystals (urine) 1618
ichthyoses 847

Ctenocephalides
inverted papillomas, dogs 953
canis 880, 1953, 2435
larva migrans 417, 2458

Jelis 880, 1953, 2435
leishmaniosis 2442
spp 677, 2577
lymphosarcoma 852, 961

Cuckoopint 3106
epitheliotropic 962

Cucloloyasler heterographus 2876
nonepitheliotropic 962

Cul ex
manifestations of multisystemic and
annulirostris 2467, 2477, 2479
metabolic defects 850
cedecci 1293
mast cell twnors 963
modestiis 2894
ferrets 1826
nig1ipalpus 2479
mucinosis 850
pipiens 1294, 2894
myiasis, twtles 1996

3218

INDEX

Cutaneous (continiied)

follicles 1354
neuroendocrine tumors 961
intra.cutaneous comifying epithelioma
nodular amyloidosis 961

947
papillomas, dogs 953
lesions, subchondral 1062
poxvirus infection, marine mammals 1869
ovary disease

VetBooks.ir
smooth muscle tumors 961
as a herd problem 1357
streptothrichosis 858
cattle 1354
tags 955
gerbils 2014
trunci reflex 1218
mares 1357
twnors 942
pet birds 1922
ulcerative disease, septicemic, turtles
right oviduct, poultry 2896

1991

Cysticercosis 1311, 2452, 2454

Cuterebm

Cysticercus cellulosae 1311
infestation, small animals 879

Cystine-binding agents 2625
spp 897, 901, 1996, 1252, 1264, 1311,

Cystine stones, dogs 1530

1314, 1489, 1833,2464

Cystinuria, dogs 1530

Cyanazine 2974

Cystitis
poisoning 2999
bacterial, small animals 1508

Cyanide
bovine 1499
poisoning 2959
feline
workplace exposme 2953
idiopathic 2383

Cyanobacteria, poisoning 2956
interstitial 1532

Cyanocobalamin-See Vitamin 812
sterile 1532

Cyathomostomiasis, horses 287
pigs 1500

Cyathostoma bronchialis 2830
potbellied pigs 1936

Cyathostominosis, larval, horses 317

Cystoisospora

Cycad 3114
delphini 1867

Cycadales spp 618
spp 203

Cyclamen spp 3108

Cystomatosis, apocrine 949

Cyclic hematopoiesis in gray Collies 47, 61

Cystophora C'listata 1869

Cycloate 2974

Cysts

Cyclobenzaprine 3036
apocrine gland 949

Cyclooxygenase 2714
arachnoid, small animals 1230

Cyclophosphamide 789, 2582, 2726, 2727,
biliary, small animals 477

2737, 2738
branchial 165

Cyclopia, large animals 1223
choledochal 478

Cyclopiazonic acid 2847
dentigerous 165

Cyclops spp 904, 1808
derrnoid 846, 948

Cyclosporine 2583
epidermal inclusion 947

13-Cyfluthrin 2750, 2756
epidem10id 947, 1230

Cyhalofopbutyl 2976
esophageal duplication 165

Cylindrocarpon 3020
feather 1927

Cylindrospennopsis 2956
follicular 846, 1354

Cylindruria 1618
canine interdigital 862

Cymopterus watsonii 977
small animals 1395

Cyniclomyces guttulatus 1952, 1953, 2009
head and neck 165

Cynodon dactylon 976, 977
hepatic

Cynoglossum
congenital 170
officinale 3140
small animals 4 77
spp 977, 3150
hybrid 948

Cypennethrin 2750, 2756
infundibular follicular 947

Cypionate 2606
interdigital 862

Cyproheptadine 2546, 2613
intra.cranial intra-araclrnoid 1272

Cypromid poisoning 2996
intran1UraJ inclusion 165

Cyrnea colini 2828
iridic 496

Cyromazine 2752, 2756
isthmus catagen 947

Cyst mite poultry 2878
keratinized cutaneous 947

Cystadenoma, biliary 478
lateral cervical 165

Cystic
matrix 947
apocrine gland
panfollicular 948
dilations 949
paraprostatic 1407
hyperplasia 949
pedal bone, horses 1107

INDEX

3219

Cysts (continued)

Damalinia
pilar 947
bovis 910
prostatic 1407
breviceps 1854
renal 1497
caprae 912
sebaceous 947
crassipes 912

VetBooks.ir
sinus, horses 1463
equi 912
subepiglottic, horses 1460
limbata 912
thyroglossal duct 165
ovis 911
trichilemmal 94 7

Dancing Doberman disease 1238
valvular blood 115

Dandruff, walking 922

Cytarabine 2728, 2732

Dandy-Walker syndrome 1226

Cytaitxzoon

Danofloxacin 2670
felis 23

Dantrolene 2589
spp 10, 23

Daphnia spp 1808

Cytauxzoonosis 23

Dapsone 2583

Cythioate 2577, 2754

Dark nose syndrome, llamas and alpacas

Cytodites nudus 2901

1855

Cytokines 817

Datura stramonium 3140
and inflammation 2708

Daubentonia pimicea 3132

Cytology 1597

Daunorubicin 2733
fluid san1ples 1599

Davainea proglottina 2828, 2831
results 1602

Day-bloomingjessamine 3138
san1ples 1589

Dazomet 2976
interpretation 1599

2,4-DB poisoning 2997
specific sites 1604

DDD 2749

Cytoplasmic

DDE 2749
granules in cells 1603

DDT 2749, 3056
vacuoles in cells 1604

Dead in good condition, poultry 2821

Cytosine arabinoside 2732

Deafness 518

Cytotoxic reactions, antibody-mediated
congenital 519, 1236

826

Death camas 3122

Debridement, wounds 1703

D

Decamethonium 2587

Deciduomata 2225

2,4-D 2976

Deciduous teeth, persistent 182
poisoning 2997

Decongestants 2616

2,4-D-dimethlyamine 2976
poisoning 3026
o-Limonene toxicity 3064

Decoquinate 2796

Dacarbazine 2727, 2731

Decubital ulcers 1708

Dacryocystitis 491

Deep pectoral myopathy, poultry 2883
rabbits 1945

Deer flies 889

Dactinomycin 2729, 2733

DEET2756

Dactylogyrus sp 1754

DEF poisoning 2999

Daffodils 3112

Deficiencies

Dairy
amino acids, poultry 2930
calf pnewnonia 1431
biotin
cattle-See also Cattle
mink 1875
culling and replacement 2138
poultry 2942
disease and productivity 2139
calciwn 1050
dry cow management 2139
pet birds 1918, 1919
health-management interaction 2135
pigs 2344
macromineral requirements 2276
poultry 2930
management 2135
chloride, poultry 2934
nutrition 2136, 2265
choline
productivity 2136
pigs 2345
quality control programs 2142
poultry 2940
record keeping 2144
copperl225
reproduction, management of 2137,
goats 1093

2171
horses 2327

Dalapon 2976
llan1as and alpacas 1855
poisoning 2997
pigs 2344

Dalmatian leukodystrophy 1234
poultry 2933

3220

INDEX

Deficiencies (continued)

horses 2327
energy
marine mammals 1860
horses 2324
mink 1874
poultry 2930
poultry 2943
fat, pigs 2343
small animals 442, 2355, 2371

VetBooks.ir
folacin, poultry 2942
vita.min A 1223, 1234
folic acid, poultry 2942
horses 2327
glycogen branching enzyme 1046
pet birds 1918
iodine 558
poultry 2936
pet birds 1918
rabbits 1959
pigs 2344
vitamin B6 1212
poultry 2934
poultry 2943
iron
vitamin B,2
horses 2327
horses 2328
pigs 2344
poultry 2939
poultry 2933
vitamin C
magnesium
guinea pigs 2018
horses 2327
nonhuman primates 1883
poultry 2934
vitamin D 1050, 1094
manganese, poultry 2933
horses 2327
minerals
nonhuman primates 1883
horses 2325
pet birds 1918
poultry 2930
poultry 2937
monophosphate synthase 616
reptiles 2001
niacin
vitamin E 1174, 1228, 1247
pigs 2344
horses 2327
poultry 2940
marine mammals 2298
nicotinic acid, poultry 2940
mink 1874
pantothenic acid, 1242
pigs 2344
pigs 2345
poultry 2938
poultry 2940
vitamin K, poultry 2939
phosphorus 1050
vitamins
horses 2326
horses 2327
pet birds 1918
pigs 2344
pigs 2344
poultry 2936
poultry 2930
zinc 2585
potassium
hereditary 851
horses 2326
horses 2327
poultry 2821, 2934
pigs 2344
protein
poultry 2936
horses 2325

Deformities, skeletal, poultry 2881
pigs 2343

Degeneration of motor neurons 1248
poultry 2930

Degenerative
pyridoxine, poultry 2943
a.rthropa.thy, cattle 1086
riboflavin 1341
arthritis, small animals 1197.

horses 2320, 2328
diseases
pigs 2344
peripheral nerve 1238
poultry 1242, 2941
spinal column and cord 1245
salt
encephalomyelopathy, equine 1228
horses 2326
joint disease
marine mammals 1860
large animals 1063
poultry 2935
pigs 1164
selenium 1174
poultry 2881
horses 2327
small animals 1197
pigs 2344
left shift 58
poultry 2936
lumbosacral stenosis 1246
sodium chloride
myeloencephalopa.thy
marine mammals 2298
bovine progressive 1227
pigs 2344
equine 1246
poultry 2934, 2935
myelopathy 1246, 1229
taurine 110
myopathy, poultry 2883
thiamine 1212, 1253, 1281
radiculomyelopathy, chronic 1246
amphibians 1741
valve disease 112

INDEX

3221

Degloving injuries 1707

Dentistry 175-See also Dental, Teeth

Dehorning calves 2123
large animals 175

Dehydration, horses, estimation 1709
small animals 178

Delayed
zoo animals 2053
neurotoxicily from triaryl phosphates

Dentofacial trauma, small animals 185

3069

Dentostomella translilcida 2013

VetBooks.ir
organophosphate intoxication 1254

Deoxyacyclovir 2745
patella release, horses 1142

Deoxynivalenol 3014

Delphinapterus leucas 1860, 1865

Deplwning mite 2877

Delphinium spp 3122

Depolarizing age11ts 2587

Delphinus

Deracoxib 3038
capensis 1869

Dermacento1·
delphis 1860
albipictus 927, 930, 933, 1315

Deltamethrin 2750
andersoni 51, 693, 806, 930, 1243, 1293,

Dembrexine 2616

1315,2437,2466,2469,2477

Demethylchlo1tetracycline 2679
dissimilis 930

Demeton toxicity 3065
halli 931

Demodectic mange-See also Mange
hunteii 931
canine 922

Latus 931
cattle 916
marginatus 931, 2437
feline 923
necrosis-erythema-lyn1phadenopathy
horses 919

2436
marine mammals 1865
nigrolineatus 930
pigs 920
nitms 927, 930
sheep and goats 918
nuttalli 2437

Demodex
occidmtalis 930
aurati 2023
parumaptei,ls 931
bovis 916
reticularis 23
caballi 919
reticulatus 931, 2437
canis 490, 863, 865, 922, 2576
silvanlm 931
caprae 918
spp 19, 23, 806, 928, 930, 1314, 2437,
cati 490, 505, 923

2471, 2477
e1iceti 2023
variabilis 51, 137, 693, 806, 930, 1243,
equi 919

1315,2437,2466,2577
gatoi 490, 505, 923

Dennal
ghanensis 916
collagenosis, progressive, pigs 852
ovis 918
squamous cell carcinoma, poultry 2855
phylloides 919, 920

Dermanyssus
spp 528, 529, 843, 855, 862, 863, 914, 916,
gallinae 1821, 1906, 2014, 2877

1392, 1621, 1854,2023,2045,2576
spp 2462

Demodicosis-See Demodectic mange

Dem1atitis 838

Demyelinating
actinic, cats 525
disorders 1236
and nephropathy syndrome, porcine
polyneuropathy, chronic inflammatory

723

1240
a.topic 825, 853

Demyelination of Miniature Poodles 1228
a.topic-like 853

Dendrites 1209
auricular, swine 524

Dendrodochiotoxicosis 3008, 3021
cercarial 2450

Dental-See also Dentistry, Teeth
clostridial, poultry 2879
care
contact ear 522
horses 2155
contagious pustular 866
potbellied pigs 1931
digital, cattle 1075
caries
filarial, cattle 907
large animals 178
flea allergy 880, 882
small animals 185
gangrenous, poultry 2879
development 171
insect bite 521
llan1as and alpacas 1850
interdigital, cattle 1080
disease, rabbits 1954
lip fold, small animals 364
formulas (table) 172
moist, rabbits 1957
malocclusion, rabbits 1955
mycotic 858
star 171
nasal, gerbils 2012

Dentigerous cysts 165
nasal solar, dogs 975

3222

INDEX

Dem1atitis (contimied)

Dermoglyphus elongatus 2878
necrotic

Dermographism 857
poultry 2879

Dermoid cysts/sinuses 846, 948, 1230
udder 1387

Dermospori.dium 1739

Pelodera 907

Der·o digilata 1754, 1756

VetBooks.ir
photodynamic 3015

Derquantel 2639
pinna 520

Derris 3063
canine sterile nodular

Derry disease 1235
pyogramulomatous 527

Derzsy disease 2826
porcine juvenile pustular psoriasiform

DES 2761

979

Descemetocele 1697
rhabditic 907

Descurainia
solar, feline 525
pinnala 3122
summer 888
spp 3138
superficial necrolytic, small animals

Desensitization 1540

468,974

Dese1t
udder 1386
azalea 3104
verrucosa, horses 1116
rose 3104
water 427

Des mi tis

Dermatobia hominis 876, 878, 879, 889,
inferior check ligan1ent, horses 1123

1314,2464
suspensory, horses 1122

Dermatofibromas 955

Desmoid

Dem1atofibrosarcomas 957
extra-abdominal 956

Dermatofibrosis, generalized nodular, dogs
tumors 956

852,955,974

Desmopathies, horses 1146

Dermatomyositis

Desmopressin 2542, 2625

Collies and Shetland Sheepdogs 1233

Destructive behaviors, dogs 1568
fan1ilial, dogs 851

Detergents, poisoning 3004
gangrenous, poultry 2879
cationic 3003

Dermatopathy, zinc-responsive, familial 852

Detomidine 2602

Dennatophilosis 858, 2424

Development, canine 1558
cutaneous, marine mammals 1863

Developmental
sheep 2167
abnormalities, teeth, small animals

Der·matophilus

182
congolensis 858, 866, 869, 1863, 1880,
orthopedic disease, horses 1148

2424, 2571
osteopathies, small aninlals 1203
spp 67, 1992

Devil facial tumor disease 576, 2044

Dermatophytosis 872, 2440-See also

Devon Rex, hereditary myopathy 1233

Ringworm

Dew poisoning 343
cattle 874

Dewlap, wet, rabbits 1957
dogs and cats 874

Dexamethasone 2607, 2712, 2734
horses 875

Dextrans 1679
marine mammals 1864

Dextroamphetan1ine 3039
pigs 875

Dextrocardia 86
rabbits 1949

Dextromethorphan 2609, 3026
reptiles 1993

Di-allate 2976
sheep and goats 875

Diabetes

Dennatoses
insipidus 550, 2625
nasal, dogs 975
mellitus 579
systemic, miscellaneous 973
dogs and cats, nutrition in 2383
zinc-responsive 974
nonhuman primates 1883

Dermatosis
pet birds 1925
diabetic 974
reptiles 2001
filarial 904, 2576

Diabetic
hereditary lupoid, dogs 851
dermatosis 974
psoriasiform-lichenoid, dogs 848
ketoacidosis 581
solar 945
neuropathy 1241
ulcerative, sheep 872, 1392

Diabolicoptes sarcophilus 2045
vegetans, pigs 848

Diagnostic
zinc-responsive, llamas and alpacas 1855
imaging 1626

Dermatosparaxis 849
procedures, private practice laboratory

Dennis 837

1590

INDEX

3221

Diamfenetide 2650

Dictyocaulus

Diaminopyrimidines 2674, 2796
arnjieldi 1421

Diamond skin disease 626
eckerti 1421
marine manunals 1862
jUa1ia 1421, 1473

Diamphenethide 2650
spp 1421, 1473

VetBooks.ir

Diapause 304
viviparns 1421, 2133, 2646, 2648, 265t

Diaphragmatic

Dicumarol poisoning 3156
flutter, synchronous, horses 1183

Dicyclanil 2752
hernia 1418

Didelphis 39

Diarrhea
albiventris 1060
antimicrobial therapy 2552
virginiana 1060, 1309
bovine viral 1436

Diejfenbachia spp 362, 3108
dogs and cats, nutrition in 2381

Dieldrin 2749
drug therapy 2552
toxicity 3061
foals 289, 290

Diesel fuel poisoning 3053
gray mink 1876

Di estrus
horses 281
bitches 2222
miscellaneous causes 288
cytology 1394, 1607
nutrition in 2329

Dietary
recurrent 288
abomasal impaction 244
large intestinal 157
indigestion, ruminal 221
neonatal ruminants 275
supplements 2086
osmotic 156
magnesium, equine 998
pigs 293, 298

Diethylcarbamazine 2651
age distribution (table) 294

Diethylpropion 3039
ratites 1964

Diethylstilbestrol 2607, 2626, 2761
small intestinal 157
poisoning, mink 1875

Diastolic

Difenoxuron poisoning 2998
dysfunction 100

Difenzoquat (methylsulfate) 2976
function, reduced 71

Difethiolone poisoning 3166
munnurs 89

Diffuse

Diaveridine 2796
fibrosing alveolitis 1442

Diazeparn 1544, 2545, 2589 2598 2594
idiopathic skeletal hyperostosis 1241

2600,2601,2604,2627 3034
lipomatosis 958

Diazinon 2750, 2754

'

pneumonia 1413
toxicity 3065

Difloxacin 2670, 2673
poultry 2861

Diflubenzw-on 2752, 2756

Dibenzofurans 3056
in aquaculture 1753

Dibothriocephalus talus 2452

Diflufenzopyr 2976

Dicamba 2976

Digestive system-See also Gastric,
poisoning 2997

Gastrointestinal, Intestinal

Diceros bicomis 2060
congenital and inherited

Dichelobacter nodosus 1075 1080 1081
anomalies 162

1166, 1167

'

'

'

function 154

Dichlobenil 2976
introduction 154

Dichlorometaxylenol 2742
pathophysiology 155

Dichlorprop 2976
pharmacotherapeutics 2544
poisoning 2997
monogastric 2544

Dichlorvos 2651, 2750, 2754
ruminant 2561
toxicity 2997, 3065
principles of therapy 161

Diclazuril 2797

Digit malfom1ation 1046

Diclofenac 3038

Digital

Diclofop poisoning 2998
dermatitis, cattle 1075

Diclosulam 2976
radiography, direct 1628
poisoning 2998
sheath tenosynovitis 1121

Dicloxacillin 2656

Digitalis glycosides 75, 107

Dicofol 2749

Digitalis purpurea 3094, 3110

Dicrocoeliasis 2446

Digitmia decumbens 2321

D·icrocoelium

Digoxin 107, 2529
dendriticum 324, 327, 671, 2446

Dihydrostreptomycin 2662
hospes 327, 2446
toxicity, gerbils 2013

3224

INDEX

Dihydrotachsterol 572

DiroJilaria 505

Diiodohydroxyquin 2697
immit'is 127, 888, 921, 1264, 1312, 1421,

Dilatation

1618, 1619, 1826, 1866, 1867,2456,
esophagus, small animals 370

2576,2649,2680
and volvulus, gastric, small
repens 2458

VetBooks.ir
animals 384
lenuis 2458

Dilated

Dirofilariasis 127, 2456
cardiomyopathy 115

Dirofilarosis 127
ferrets 1828

Disc disease, intervertebral 124 7
pores of Winer 948

Discospondylitis 1249

Diltiazem 76, 2539, 3032

Disease outbreaks, handling 2074

Dimenhydrinate 3025

DISHA 1569

Dimethenarnid 2978

Disinfectants 2738
poisoning 2996
vapor-phase 2744

Dimethoate toxicity 3065

Disinfection of premises 1639

Dimethyl sulfoxide 2624

Dislocation of fetlock, cattle 1087

Dimethyltubocurarine 2587

Disophenol 2650

Dimetridazo\e 2696

Dispha1ynx nasuta 2831

Dinitolmide 2797

Displacement

Dinitrocresol poisoning 2997
abomasal 238

Dinoseb poisoning 2997
behavior 1536

Dinotefuran 2754
of colon, horses 264

Dinoterb 2978

Disposal of carcasses 1639

Dioclophyma renale 1511, 1618, 2456

Dissecting aneurysm, turkeys 2787

Dioctophymosis 2456

Disseminated

Dioxathion toxicity 3065
intravascular coagulation 1689

Dioxin poisoning 2997
hemangiomas 959

Dipetalonema 1881

Distal
reconditum 882, 914, 1619
denervating disease 1239

Diphacinone poisoning 3166
phalanx fracture, horses 1108

Diphenhydrarnine 3025
polyneuropathy, Rottweilers 1239

Diphenoxylate 2554, 3042

Distemper

Diphenylhydantoin 2600
canine 777

Diphtheria
viral serology 1622
calf 1429
dry land 66
fowl 2824
encephalitis encephalomyelitis, canine

Diphyllobothriasis 2452

777, 1250

DiphyUobolhrium
ferrets 1825
dendriticum 2452
horses 1453
lanceolatum 1866
mink 1873
lalum 426, 2452

Distention
nihonkaiense 2452
abdominal 156
pac'i,fi,cum 1866, 2452
large animals 24 7
spp 426, 428, 2452
small intestinal, large animals 24 7

Diplodiosis 3006

Distichia 490

Diplogonopoius tetraplerous 1866

Distribution of drugs 2495

Dippity pig syndrome, potbellied pigs 1934

Disulfoton toxicity 3066

Diptera 505, 2752

Ditch fever 283

Dipterans

Dithiopyr 2978
biting 885

Diuretics 103, 2623
myiasis 897
dosages 2623
nonbiting 894
in glaucoma 2570

Dipylidiasis 2452
in heart failure 103, 2525

Dipyl'idium 2651
in hypercalcemia 568
caninum 422, 423, 426, 882, 914, 2452,
osmotic 2570, 2624

2650
potassium-spaiing 2624

Dipyrone 2602
thiazide 2624

Diquat 2978
toxicity 3034
in aquaculturP 1753

Diuron 2978
poisoning 2996
poisoning 2998

Direct digital radiography 1628

Diverticula, esophageal 166, 373

Dirlotapide 2544

Diverticuli, arachnoid, small animals 1230

INDEX

3225

DL-Methionine 2625

Dressings, wounds 1704

DMNA poisoning, mink 1875

Drnmaius novaehollandiae 1960

DMS02624

Dronabinol 3041

ONOC2978

Dropped hock, small anjmals 1203

Dobrava virus 2470

Drugs

VetBooks.ir

Dobutamine 106 , 2532
absorption 2493

Docetaxel 2733
action 2502

Dock 3130
administration, zoo anin1als 2050

Docusate 2560

Animal Medicinal Drug Use Clarification

Dog foods 2373

Act2520

Dogbane 3126
bioavailability 2495

Dogs-See also Canine, Small animals
clearance 2500
behavior 1557
concentration 2503
problems 1559
disposition and fate 2492
breeding management 2221
distribution 2495
nutrient requirements 2356 , 2357
dosage forms 2508
nutrition 2354
close and response 2505
pregnancy determination 2225
efficacy 2506
respiratory diseases 1478
excretion 2498
tapeworm infection 2452
htunan, poisoning 3024

Dolasetron 2549
illicit, toxjcity 3038

Oolichocephalic dwarfs 1043
maximum residue limits 2519

Dolphin pseudopox 1863
median inhibito1y concentration 2506

Dominance 1536
metabolism 2496

Domperidone 2558
ove1�the-counter, poisoning 3024

Dopamine 2532 , 2625
parenteral dosage forms 2511
antagonists 2607
potency 2505

Dopan1inergic agents 2607
receptor affinity 2506

Doppler
residues
echocardiography 98
in animal fibers 2521
ultrasound 1634
in foodstuffs 2519

Doran1ectin 2647
routes of administration 2508

Dorsal
selectivity 2506
displacement, soft palate, horses 1459
signal transduction 2504
nasal alopecia, llamas and alpacas 1855
specificity 2506

Dose-response cmves 2505
steady state 2502

Double
structure-activity relationships 2504
muscling, cattle 1045
therapeutic index 2506
pored dog tapeworm 422

D1y
sole, cattle 1084
land distemper 66

Dourine 38 , 1392
sow mastitis 1375

Doves, nutrition 2290

Drymmia pachyphylla 3142

Downer cow syndrome 1188

DryopterisfUix 506

Doxapram 2616

Dubin-Johnson syndrome, sheep 351

Doxepin 1544 , 2585

Duchenne cardiomyopathy 121

Doxorubicin 2728 , 2733 , 2737

Duck
induced myocardial failure 120
egg drop syndrome 2899

Doxycycline 2679, 2683

Pekin, nutrition (table) 2921
o-Penicillamine 2625
plague 2799

Dmcaena spp 3110
viral

Dracunculiasis 2456
enteritis 2799

Dracunculus
hepatitis 2815
insignis 904

Dugbe virus 761
medinensis 904 , 2456

Dugong dugong 1856
spp 1997

Dumb rabies 1304

Dragon tree 3110

Dumbcane 3108

Drains, wound 1704

Dummy2094

Draschia

Duodenitis, horses 218
megastorna 315 , 505

Duocle1utis-jejunitis, horses 260
sp 511

Durra3148

Drawer sign 1198

Ouvenhage virus 2478

3226

INDEX

Dwarf
mites 521
brachycephalic 1043
ferrets 1826
dolichocephalic 1043
rabbits 1953
pituitary 549
necrosis, swine 524
tapeworm 2452
papillomas 524

VetBooks.ir

Dwarfism 1046
pinna, diseases 522

Dyes (antibacterial) 2744
plaques, equine 524

Dysautonomia 1255
teeth, horses 165
canine 1256
tick 939
equine 1257

East Coast fever 34
feline 1255

Easter lily 3112, 3118
leporine 1257

Eastern equine encephalitis/
wild hares 1257
encephalomyelitis 1291, 2470

Dyschondroplasia 1042, 1044
in birds 1965, 2891
horses 1148

Eating disorder
pigs 1164
dogs 1568
poultry 2881
horses 1550
tibial, poultry 2932

Ebola hemorrhagic fever 24 70

Dysecdysis, reptiles 1974, 2000

Ebolavirus 2470

Dysentery

Ebstein's anomaly 84
swine 301

Eccrine gland tumors 950
winter, cattle 271

Ecdysis 1968

Dysfibrinogenemia 51

Echidnophaga gallinacea, 880, 2875

Dysgalactia syndrome, sows 1373

Echinochasmus japonicus 2446

Dyshormonogenetic goiter, familial 559

Echinococcosis 1311, 2452

Dyskeratomas, canine warty 944

Echinococcus

Dyskeratosis 851
granulosits 422, 1311, 2452. 2650

Dysmaturity, foals 559, 1726
multilocularis 422, 1312, 2452

Dysmyelination 1236
oligm·thrns 2452

Dysplasia
spp 2650, 2651
growth plate, horses 1149
vogeli 2452
hepatoportal microvascular 170

Echinophlhirius horridus 1866
radial and ulnar, dogs 1203

Echinostoma

Dyspnea 1413
hortense 2446

Dysraphism, spinal, small animals 1230
ilocanum 2446

Dysrhythmia 90
revolutum 2446

Dystocia
spp 2446

COWS 2180

Echinostomiasis 2446
foals 1724

Echium spp 977, 3150
mares 2198

Echocardiography 98, 1634
pet birds 1921

Eclampsia 571
reptiles 2001
horses 987
small animals 1395, 2227
small animals 992

Dystonia, muscular, cattle 1175

Eclectus spp 1896, 1906, 1908, 1924

Dystrophies

Ecologic studies 2400
associated with calcium, phosphorus,

Econazole 2701
and vitan1in D 1050

Ecstasy, toxicosis 3040
muscular 1043, 1231

Ecthyma, contagious 866, 2468

X-linked 1233

Ectoparasites
neuraxonal
chemotherapeutic agents 2749
large animals 1227
examination for 1620
small animals 1229
poultry 2875

Dystrophy-like myopathies 1043
rabbits 1953
reptiles 1996

E

Ectoparasiticides 2748

Ear-See also Auricular
large animals 2748
canal tumors 534
small animals 2754
folded, cats 525

Ectopic
hematoma 524
rhythm 90
infections, turtles 1993
thyroid tissue 552
mange, sheep and goats 918
ureter 1498

INDEX

3227

Ectrodactyly syndrome 1050
adenoides 2792

Ectropion 489
alabamensis 205

Eczema, facial 3006, 3015
arloingi 207

Edema
aub'U1nensis 205
angioneurotic 857
bovis 205

VetBooks.ir
bowel 716
brunelli 2792, 2803
conjunctiva 492
chinchilla 2007
corneal, marine mammals 1857
christenseni 207
disease, pigs 296, 716
colchici 2791, 2793
gut 716
coloni 2793
hereditary neuraxial 1234
crandallis 207
laryngeal 1419
debliecki 208
malignant 604
dispersa 2792, 2793
porcine pulmonaiy 3018
duodenalis 2793
pulmonaiy 1414, 3008
flavescens 1952
tracheal, feeder cattle 1430
ga.llopa,vonis 2792

Edentates, nutrition 2297
hagani 2792

Edrophoniurn 2588
innocua 2792

Edwardsiella
inteslinalis 1952
ictaluri 1749, 1754, 1757, 1782, 1809
in-esidua 1952
piscicida 175 7
kofoidi 2791, 2793
spp 1993
legionensis 2791, 2793
tarda 1757
lettyae 2791, 2793

Eendenpest 2799
macusaniensis 355, 359, 1846, 1853

Egg
magna 1952
abnormal, poultry 2896
maxima 2792, 2802
binding
media 1952
backyard poultry 1821
meleag1idis 2792
pet birds 1921
meleag1imitis 2792
bound, poultry 2896
mitis 2792
defective, poultry 2896
mivati 2792
drop syndrome '76 2899
necatrix 2791
laying, excessive, pet birds 1920
neodebliecki 208
peritonitis, poultry 2896
ninakohlyakimovae 207
yolk coelomitis, pet birds 1922
nodulosa 1867

Ehlers-Danlos syndrome 50, 849
ovina 207

Ehrharta longijlora 3154
ovinoidalis 207

Ehrlichia
pacijica 2793
bovis 18, 937
perforans 1952
canis 48, 803, 936, 1250, 1622, 2434
phasiani 2791, 2793
serology 1622
phocae 1867
chaffeensis 803, 928, 931, 2432
praecox 2792
equi 18,697, 772,803,2434
scabra 208
ewingii 803, 928, 931, 2432
southwelli 1806
muris 803, 934, 2434
spinosa208
ondi?i 746
spp 158, 203, 205, 206, 207, 208, 298,
phagocytophila 18, 772

1740, 1806, 1853, 1952, 1998,2696,
platys 18

2791,2793,2796,2798,2802
risticii 2554
stiedae 1952
ruminanti'U'ln 752, 925, 928, 936,
subrotunda 2792

1996,
tenella 2791, 2792
sennetsii 283
tetartooimia 2793
spp 9, 10, 283, 803, 2567
trichechi 1867

Ehrlichial colitis, equine 283
lruncala 2793

Elu·lichiosis 2432
zuernii 205
canine 803, 1250

Eisenmenger syndrome 81
equine monocytic 283

Elacatiniis spp 1779
granulocytic, equine 697

Elaeophora schneideri 904, 1312

Scnnetsu 808

Elaeuphorosis 904

Eimeria

Elaphas maa:irnus 2054
acervulina 2792, 2802

Elaphostrongylus cervi 1313

3228

INDEX

Elbow

Eastern equine, in poultry 2891
dysplasia, dogs 1196
equine viral 1291
fractures, horses 1131

Japanese B 1342, 2472

Electrical alternans 124

Lacross 2468

Electrocardiogran1 68

Murray Valley 2476

VetBooks.ir

Electrocardiography 92
old dog 777, 831

Electrocution 655

Powassan virus 24 76

Electroencephalogram 1220

Pug 1224

Electrolyte imbalance, poultry 2934, 2935

Russian spring-summer 2480

Electromechanical dissociation 68

St. Louis 2478

Electromyogram 1220
tickborne 2480

Elephant endotheliotropic herpesvirus

Western equine, in poult1y 2892
infection 2054

Ence'J)halitozoon

Elephant's ear 3104
cuniC'ltli 1264, 1346, 1945, 1953, 1954,

Elimination

1958,2444
behavior problems, dogs 1568
hellem 2444
half-life 2501
intestinalis 2444
inappropriate, cats 1573

Encephalitozoonosis, rabbits 1954

Elizabelhkingia meningose'J)ticiim 1263

Encephalocoele 1222

Elokomin fluke fever 808

Encephalomalacia

Elso heel, cattle 1091, 1231
poultry 2938

Embolism 141

Encephalornyelitis 1262-See also
fibrocartilagenous 1255

Encephalitis

Embolus 141
avian 2888

Embryo transfer 2239
backyard poultry 1822

Embryonal nephroma 1522
bovine, sporadic 1308

Embryonic death, cattle 2177
canine distemper 1250

Emergencies, ophthalmic 1696
caprine aitlu·itis 1250

Emergency
chlai11ydial 1308
care, amphibians 1742
coronaviral 728
evaluation and initial treatment 1660
equine, arboviral 1291
medicine 1658
horses 1250
equine 1708
ovine 2474
foals 1723
pigs 1251
monitoring 1674
porcine enteroviral 1307
primaiy survey 1660
sheep 1250, 1299
seconda1y smvey 1667
sporadic bovine 1308
specific diagnostics at1d therapy 1668

Teschovirus 1307
thoracotomy 1673
virus, porcine hemagglutinating 1251

Emetic drugs (table) 2548

Encephalornyelopathy

Emodepside 2638
degenerative, equine 1228

Emodin 2559
equine herpesvirus 1250, 1251

Emotional health, veterinai·ia11s 1580

Simmental, large animals 1227

Emphasematous putrifactive disease of

Encephalomyocai·ditis virus infection 718,
catfish 1758

2470

Emphysema

Encephalopathy
alveolai· 1428
bovine spongiform 1284
and edema, acute bovine pulmonaiy 1439
hepatic 443
interstitial 1428
lai·ge animals 336
pulrnonaiy 1428, 3008
small animals 443, 1224

Emphysematous cholecystitis/
hypoxic ischemic 2094
choledochitis 475
foals 1728

Empyema 1414
neonatal 1224, 2094
guttural pouch, horses 1463
foals 1728

Emulsifiers, toxicity 3069
transmissible

Emus 1960
mink 1874

Enalapril 2533, 2625, 3032
spongiform 1286

Enamel lesions, teeth 164

Endemic (epidemiology) 2397

Encephalitides, viral, poult1y 2891

Em.lucanlial

Encephalitis 1262-See also
cushion defects 86

Encephalomyelitis
fibroelastosis 120
distemper 777

Endocarcliosis 112

INDEX

3229

Endocarditis, infective 121

Clostridiurn perfri,ngens, pigs 295

Endocrine
corona.viral, turkeys 2797
disease
eosinophilic 825
ferrets 1827
granulomatous, horses 291
pathogenesis 541
hemorrhagic, poultry 2833

VetBooks.ir
principles of therapy 542
horses 251
reptiles 2000
infectious, feline 796
system
jejunitis, horses 260
introduction 538
mucoid, rabbits 1947
regulation 540
necrotic, poultry 2802

Endocrinopathy-associated erythrocytosis
parvoviral, feline 796

43
proliferative, porcine 299

Endodontic disease, small animals 180
rota.viral, pigs 30 l

Endogenous steroids 2759
transmissible, turkeys 2797

Endometrial
ulcerative, poult1y 2805
biopsy, mares 2192
viral
swab, mares 2191
duck 2799

Endometritis, large animals 1369
mink 1873

Endoparasites, diagnosis

Enterobacte1'

large animals 1620
aerogenes 1368
small animals 1619
agglornerans 1345

Endrin 2749
spp 476, 671, 1374, 1896, 1993, 2089, 2191,
toxicity 3061

2655,2659,2660,2665,2671,2692

Energy

Enterococcosis, birds 2816
deficiency

Enterococcus
horses 2324
aviurn 2816
poultry 2930
cecoiurn 2816, 2882
requirement
durans 731, 735, 2816
beef cattle 2249
faecalis 2671, 2816, 2883
dairy cattle 2269
faeciurn 731, 735, 2622, 2671, 2690, 2816
dogs and cats 2365
hirae 731, 735, 2816
goats 2308
spp 476, 731, 1263, 1508, 1810, 1897,
horses 2313

2093,2617,2816,2883
pigs 2333

Enterocolitis
poultry 2914
clostridia-associated, horses 285, 607
sheep 2345
potbellied pigs 1933

English

Enterocolopathy, sand, horses 287
holly 3110

Enterocytozoon bieneusi 2444
ivy 3110

Enterohemorrhagic E coli 2424

Enhydra lutris 1856

Enterohepatitis, infectious, poult1y 2835

Enilconazole 2702

Enterolithiasis, horses 264

Enrotloxacin 2619, 2670

Enteropathy

Entarnoeba

Basenji 168
dispar202
equine proliferative 289
histolytica 158, 202, 1881
gluten-sensitive 168
invadens 202, 1998
proliferative hemorrhagic, pigs 299
spp 1878, 2699
protein-losing 168

Entan1oebiasis, reptiles 1998

Enterotoxemia 601, 609

Entenpest 2799

Clostridiurn peifringens 609, 610

Enteque

Escherichia coli 716
ossificans 1052
pigs 296
seco 1052
goats 2311

Enteric
necrotic enteritis, poultry 2802
campylobacteriosis 191
rabbits 1947
colibacillosis, pigs 296
sheep 2167
corona.virus, feline 383

Entornophthora spp 1865
duplication 169

Entomophthoromycosis 645
septicemia, catfish 1758

Entropion 488

Enteritis

Envirorm1ental
acute
diseases
in salmonellosis 197
fish 1769, 1772 (table)

allergic 825
marine manunals 1857
anterior, horses 260
reptiles 1999

3230

INDEX

Environmental (continued)

hai11aitomas 943
enrichment, nonhuman primates 1884
inclusion cysts 947

Enzootic

Epidermis 837
abortion

Epidermitis, exuuative, pigs 860
goats 1340

Epidermoid

VetBooks.ir
ovine 599, 1338
carcinomas 945
ataxia, large animals 1093, 1225, 1253
cysts 94 7, 1230
balanoposthitis 1372

Epidern1olysis bullosa syndromes 850
bovine leukosis 743

Epide1-rnophyton spp 872, 2573, 2575,
calcinosis 1052

2699,2704
hematuria 3090

Epididymis, abnormalities 1330
nasal

Epididyrnitis, small animals 1400
granuloma 1429

Epiglottic entrapment, horses 1460
tumor, sheep 1472

Epilepsy
pneumonia
fan1ilial, large animals 1223
calves 1431
idiopathic
pigs 1467
large animals 1223
posthitis and vulvitis 1372
small a.ninlals 1224

Eosinophilia 62
temporal lobe 1224

Eosinophilic

Epinephrine 575, 2532, 2542, 2610
bronchopneurnopathy 825, 1479

Epiphysitis
enteritis 825
goats 1093
funmculosis, canine 972
horses 1149
gastritis 388

Epiploic forainen 261
granuloma complex 971

Epipodophyllotoxins 2735
granulomatous syndrome, pulmonary

Epipremnum aureum 3110
nodular 1479

Epirubicin 2734
keratitis, feline, therapy 2570

Episcleritis 2569
myositis, dogs 1201

Episclerokeratitis, nodular granuloma.tous
plaque, cats 972

957
ulcer, cats 971

Epista.xis 1412

Eosinophils 5, 57, 1600, 1606, 1612

Epistylis spp 1754, 1779, 1801

Ependyrnomas 1271

Epithelial cells 1601

Epe1ythrozoon 26
in urine 1617
ovis 26

Epitheliocystis, fish 1810
parnum 26, 913

Epitheliogenesis imperfecta. 163, 846
suis 26, 913

Epitheliomas
wenyonii 26
basal cell 944

Ephedra 3027
cystic intra.cutaneous cornifying 947
sinica 3032
intra.cutaneous cornifying 944

Ephedrine 2626
of Malherbe, calcifying 949
poisoning 3027, 3032
sebaceous gland 951

Ephemeral fever, bovine 741

Epitheliotropic cutaneous

Epicauta 3157
lyn1phosarcomas 962
occidenlalis 3157

Epiva.g 1392
pennsylvanica 3157

Epizootic
temexia 3157
bovine abortion 1336
vittata 3157
cataiTha.l enteritis, ferrets 1825

Epidemic
cellulitis-pinkeye 701
curve 2405
hema.topoietic necrosis 1763
diarrhea, porcine 298
hemorrhagic disease 619
in epidemiology 2397
lyn1phangitis 639
hype1thermia 3013, 3017

EPN toxicity 3066
polyaithritis 2466, 2478

Epoetin a.lfa 2541
tremor, poultry 2888

Epostaiie 2607

Epidemiology

Eprinomectin 2647
analytical 2399

Epsiprantel 2650
basic principles 2397

EPTC 2978
descriptive 2399
poisoning 2996
terms and concepts 2397

Epulis

Epidermal
fibroma.tous 366
and hair follicle twnors 943
ossifying 366

INDEX

3231

Equine-See also Horses

Ergotainine 3013
abortion, virus 1444, 1457

Ergotism 3006, 3012
arboviral encephalomyelitis 1291
poultry 2847
aural plaques 524

E1istalis tenax 903
bot fly 2464

Erodium977

VetBooks.ir
chorionic gonadotropin 2606

Erratic
coital exanthema 1357, 1392
oviposition and defective egg syndrome
degenerative encephalomyelopathy/

2896
myeloencephalopathy 1228
parasites 1311
demodicosis 919

Error (epidemiology) 2403
dysautonomia 1257

Eruption of teeth (table) 173
ehrlichial colitis 283

Erysipelas 625
emergency medicine 1708
arthritis, sheep 2168
encephalomyelitis
marine mammals 1862
arboviral 1291
pigs, 626, 1160

Eastern 24 70
potbellied pigs 1934
vaccination, exotic mammals 2057
poultry 2817

Venezuelan 2480
vaccination, exotic mainmals 2058

Western 2482

Erysipeloid 625, 2424, 2819
eosinophilic granuloma 972

Erysipelolhrix
gastric ulcer syndrome 218
inopinata 626, 2818
granulocytic ehrlichiosis 697
insidiosa 1063
grass sickness 1257
rhusiopathiae 341, 625, 626, 628, 629, 721, herpesvirus 341, 1392

733, 1066, 1094, 1155, 1157, 1158,
and abottion 1344

1160, 1343, 1353, 1810, 1862, 1934,
encephalomyelopathy 1250

2058,2163,2424,2655,2817,2823
infection 1444, 1446
spp 1063, 1166, 1992, 2894
vaccination, exotic mammals 2057
tonsillarum 626, 2818
infectious anemia 699, 1250

Erythema, necrolytic migratory 468
influenza 1447

Erythrocytosis 43
leukoencephalomalacia 3017

Erythromycin 2558, 2687, 2690, 2691
metabolic syndrome 548, 1006

Erythropoiesis 4
metritis, contagious 1371

Erythropoietic porphyria 852
monocytic ehrlichiosis 283
congenital 986
morbillivirus 707, 1448

Erythropoietin 4
motor neuron disease 1248

Erythroxylon
multinodular pulmonary fibrosis 1446
coca 3039
mycotic placentitis 1346
monogymnum 3039
proliferative enteropathy 289

Escape rhythm, ventricular 97
protozoa! myeloencephalitis 1251, 1309

Escherichia
recurrent uveitis 508, 830
coli 121, 155, 158, 169, 197, 210, 273, 275, respiratory syndrome, a<:ute 707

289,296,301,329,340,341,355,
rhabdomyolysis syndrome 1048

377,396,402,403,475,476,482,
rhinopneumonitis 341

529,580,671,682, 716, 721, 730,
and abortion 1344

733, 749,864, 1063, 1066, 1081,
sarcoid 954

1157, 1166, 1190, 1204, 1249, 1263,
ocular 516

1343, 1345, 1346, 1353, 1367, 1368,
syndrome X 1006

1369, 1374, 1383, 1396, 1397, 1398,
typhoid 701

1406, 1442, 1443, 1449, 1490, 1492,
uveitis 508

1499, 1500, 1508, 1510, 1720, 1823,
therapy 2567

1825, 1853, 1871, 1872, 1878, 1896,
venereal balanitis 1357

1913, 1922, 1932, 1933, 1935, 1948,
viral

1951, 1962, 1964, 1965, 1992, 1993,
aiteritis 701, 1448

2007,2008,2020, 2021,2042,2043,
and abortion 1344

2089,2092,2098, 2123,2130,2135,
encephalitis 1291

2162,2164,2168, 2191,2196,2210,
rhinopnewnonitis 1444

2376,2417,2424, 2553,2554,2571,

Ergasilus spp 1808

2617,2653,2659, 2676,2680,2692,

Ergocalciferul 572

2693,2695,2734, 2739,2766,2768,

Ergometrine 3013

2800,2814,2842,2864,2868,2882,

Ergonovine 3013

2887,2896,2897, 2898,2908,2929,

Ergot poisoning 974

3077

3232

INDEX

Escherichia (continued)

Ethalfluralin 2978
enterohemorrhagic infections 2424

Ethametsulfuron poisoning 2998
enterotoxemia, pigs 296, 716

Ethanol 2739
infection, poultry 814

Ethephon 2978
spp 2654, 2655

Ethmoid hematoma, horses 1462

VetBooks.ir

Esc1ichtius robustus 1860

Ethopabate 2795, 2796

Esmolol 76, 3033

Ethyl alcohol 2739

Esophageal and pharyngeal trauma, pet

Ethylene
birds, 1894
glycol toxicity 3046

Esophagitis, small animals 372
oxide 2744

Esophagus

Ethylenea.mines 2726
congenital anomalies 166

Etodolac 2719, 3037, 3038
lower sphincter, achalasia 166

Etofenprox 2756
dilatation, small animals 370

Etoposide 2734, 2735
diseases

Etretinate 2737
large animals 215

Eubaclel'ium spp 1263, 1500, 2696
small animals 370

Eucalyptus spp 2960
diverticula 166, 373

Eucoleus aerophilus 1421, 2456
duplication cysts 165

Eudyptes chrysoco'Yne 2858
dysmotility, small animals 371

Eugenol 1753
foreign bodies, small animals 372

Euhyalomma glabrwrn lruncatum 933
groove reflex, 2564

Eumetopias jubatus 1864
neoplasia, large animals 217

Eupalorium nigosum 119, 1175, 1186,
obstruction

3094,3128
drugs for 2561

Euphorbia pulcherrima 3110
horses 1720

European 2478
large animals 215
bat lyssavirus 24 78
stenosis, small animals 371
chick flea 2875
strictures
holly 3110
large animals 217

Ewylr-ema
small animals 371
coelomaticwn 328
worm, small animals 412
ovis 328

Espichacao 1052
pancreaticum 328

Espichamento 1052
procyonis 429, 485

Essential fatty acids, for pruritus 844, 2578
spp 324, 328

Estate ketosis 1022

Eustrongyhdes ignotus 1314

Estimation of age by examination of teeth

Euthanasia 1641

171
methods by species (table) 1642

Estradiol 2759, 2760
of pets and emotions 1580
esters 2606
rabbits 1941

Estrogen 573

Eutrombicula aljreddugesi 924
dogs 2223

Evening trumpet flower 3142

Estrogenism

Evisceration, postcastration, horses 1722

Fusarium 3014

Exanthema, equine coital 1357
and vulvovaginitis 3006, 3014

Excitement urination, dogs 1569

Estrogen, synthetic nonsteroidal 2761

Excretion of drugs 2498

Estrus-See also Heat

Exencephaly, large animals 1222
cows, irregularities 2173

Exercise and fatigue 1008
cytology 1607

Exertion al
dogs 1393, 2222
myopathies
goats 2182
dogs 1202
hormonal control 2244
horses 1178
horses 2189
poultry 2883
induction
rhabdomyolysis 1048
goats 2184
chronic 1178
sheep 2212, 2213
sporadic 1178
manipulation, small animals 2225
poultry 2884
prolonged, small animals 2230

Exhausted horse syndrome 1011
psychic, horses 1550

Exocrine
sows and gilts 2207
pancreas, small animals 407
synchronization 1329
pancreatic insufficiency 168, 401, 409, 1593

Eszopiclone 3035

Ex·ophiala 643

INDEX

3233

Exostoses

Factor I deficiency 51
cartilaginous 1229

Factor II disorders 51
metacarpal bones, horses 1123

Factor VII deficiency 51
metatarsal bones, horses 1132

Factor VIII deficiency 51
multiple cartilaginous, small animals 1204 Factor VIII related antigen 49

VetBooks.ir
supracarpal, horses 1126

Factor IX deficiency 52

Exotic animals

Factor X deficiency 52
nutrition 2287

Factor XI deficiency 52
vaccination 2054

Factor XII deficiency 52

Expectorants 2616

Facultative

Extensor process fracture, horses 1115
myiasis 897

External parasiticides 2748
parasites 1311

Extinction behavior 1542

Fading kitten syndrome 793

Extra-abdominal desmoicls 956

Fagopyi·wn esculentuin 977

Extra-label drug use 2490

Failure

Extradural tumors 1275
heart 73

Extrahepatic
of milk letdown 1387
bacterial infections, small animals 455
of omasal transport 233
bile duct obstruction 478
of passive transfer 2088
biliaiy system, small animals 473
to thrive, pet birds 1895

Extrai11eclullary plasmacytomas 952, 961

False

Extraskeletal giant cell tumors 957
acacia 3130

Extrinsic allergic alveolitis 1441
blackleg 1171

Exudate, characteristics 1605
gid 1314

Exudative
hellebore 3126
diathesis, poultry 2936, 2938
indigo 3118
epidermitis, pigs 860
layer 2897

Eye-See also Ocular, Ophthalmology
negative 2403
and systemic diseases 505
positive 2403
flies 896
pregnancy, small animals 1395
gnats 896
thoroughpin, horses 1138
local anesthetics 2566

Famciclovir 2745
neoplasia 515

Fainilial
cats 518
acantholysis 850
cattle 515
ainaurotic idiocy 1235
dogs 516
dermatomyositis, dogs 851
horses 516
dyshormonogenetic goiter 559
pharmacotherapeutics (systemic) 2565
epilepsy, large animals 1223
penetrating trauma 2568
footpad hyperkeratosis 848
physical exainination 488
reflex myoclonus 1232
principles of therapy 542
vasculopathy, clogs 851
prolapse 504
zinc-responsive clern1atopathy 852

Eyelid 488

Famotidine 2551, 3030
atresia, birds 1896

Fainphur toxicity 3066
conformational abnormalities 489

Fan belt injuries 1707
inflainmation 490

Fanconi syndrome 1520
lacerations 1696

Fannia spp 512, 895

Eyeworms 510, 2460

Fai· eastern tickborne encephalitis 2480
large animals 510

Fai-cy 706
small animals 512

Farmer's lung disease 1441

Fasciola
giganlica

F

33, 324, 326, 2446
hepatica 324, 328, 602, 1620, 1850, 1853,

Face flies 894

2168,2446,2638,2641,2646

Facial
spp 1881, 2641
eczema 3006, 3015

Fascioliasis 2446
gerbils 2012

Fascioloides inagna 324, 326, 327
nerve 1216

Fasciolopsiasis 2446
trauma 1244

Fasciolopsis buski 2446
paralysis 1258

Fat
idiopathic 1239
deficiency, pigs 2343
tumor disease, Tasmanian devils 576, 2044
necrosis, abdominal 360

3234

INDEX

Fat (continued)

poult1y 2919
requirement
sheep 2348
dairy cattle 2271
pregnant ewes 2348, 2349
small animals 2367
sheep 2348

Fatigue
sows and litters 2342
and exercise 1008

Feedlot

VetBooks.ir
prevention IO 12
beef management 2126

Fatty
bloat 230
acids
cattle purchase 2131
essential 2578
control and prevention of disease 2130
for heart failure 110
records 2128
liver

Felban1ate 2599
backyard poultry 1820

Felicola subrostratus 913
disease, cattle 1018

Feline-See also Cats
and kidney syndrome, poultry 2942
acquired symmetic alopecia 842
hemorrhagic syndrome, poultry
acromegaly 551

2820
acute intermittent porphyria 987
syndrome, poultry 2820
atopic dermatitis 855

Faucitis, small animals 361

Bowen disease 947

Favus, backyard poultry 1823
bronchial asthma 1490

Fazadinium 2587
calicivirus 453, 1481

Fear 1536
vaccination, exotic man1mals 2058
cats 1574
chlamydia! conjuntivitis, therapy 2566
dogs 1560, 1562
cholangitis/cholangiohepatitis
horses 1549
syndrome 481

Feather
democlicosis 923
cysts 1927
clysautonomia 1255
destructive behavior 1927
endocrine alopecia 842
mites 2878
enteric coronavirus 383
pecking or plucking, chickens 1557,
eosinophilic keratitis, therapy 2570

1927
hepatic lipiclosis 456, 2385

Febantel 2645
herpesvirus

Fecal softeners 2560
conjw1ctivitis, tllerapy 2566

Feed
rhinotracheitis vaccination, exotic
additives
man1mals 2058
antimicrobial 2765
hypertensive retinopatl1y, therapy
dairy cattle 2284

2570
concentrates, horses 2326
hypokalemic polymyopathy 1201
intake, poultiy 2914
idiopathic cystitis 2383
nutrient content, beef cattle
immunodeficiency virus 821

(table) 2250
serology 1621

Feeding-See also Nutrition
infectious
beef cattle 2263
anemia 28
breeding herd 2263
enteritis 796
finishing 2264
peritonitis 453, 780, 1251
stocker cattle 2263
interstitial cystitis 1532
clai1y calves 2280
leukemia virus 790, 821
dairy cattle 2278
associated enteritis 793
horses
serology 1621
aged 2329
lower urinaiy tract disease 1531
sick 2328
nutrition in 2383
laboratory animals 1840
lyn1phocytic portal hepatitis 482
llamas and alpacas 1846
lymphoma ai1cl leukemia 790
methods, poultry 2920
lyn1phosarcoma-leukemia complex,
orphan foal 2329
ocular 518
pigs, weanlings 2342
mairnnary
potbellied pigs 1932
hypertrophy 1396, 1404
practices
tw11ors 1404
clogs and cats 2376
multicentric squamous cell carcinuma
horses 2321
in situ 947
pigs 2340
myelopathy 1251

INDEX

3235

Feline (continued)

tall 3142
nonsuppurative
toxicity 360
meningoencephalomyelitis 1252

Festuca
odontoclastic resorption lesion 181
arundinacea 3016, 3142
panleukopenia 796
rubra commulala 3153
vaccination, exotic mammals 2057

Fetal

VetBooks.ir
panleukopenia-like syndrome 793
anasarca 620
parvoviral enteritis 796
alloimmune thrombocytopenia 4 7
pneumonitis 506, 1481
development, calves, abnormal 2177
polioencephalomyelitis 1252
membranes, retained, large animals
proliferative and necrotizing otitis

1381
externa 525

Fetlock
respiratory disease complex 1481
dislocation, cattle 1087
scabies 921
disorders, horses 1118
solar dermatitis 525

Fetus, effect of reproductive therapy on
sterile cystitis 1532

2608
stomatitis 362

Fever
symmetic alopecia, acquired 842

African swine 711
toxoplasmosis, ocular therapy 2566

African tick 2434
urolithaisis 1531

Argentinean hemorrhagic 2476
urologic syndrome 1531, 1608

Astrakhan spotted 2434
viral rhinotracheitis 1481

Bolivian hemorrhagic 2476

Femoral

Boutonneuse 2434
head, aseptic necrosis, dogs 1194
bovine ephemeral 741
nerve, injuries 1244
bovine petechial 7 45
paralysis, cattle 1089

Brazilian hemorrhagic 2476

Fenbendazole 2645
cat scratch 2422

Fenchlorphos toxicity 3067
catarrhal 758

Fenitrothion toxicity 3066

Colorado tick 2468

Fenoxaprop 2978

Crimean-Congo hemorrhagic 751, 761,
ethyl 2978

2470
poisoning 2998
dogs and cats, nutrition in 2384

Fenoxycarb 2755

East Coast 34

Fentanyl 3042

Elokomin fluke 808

Fenthiaprop poisoning 2998
fleaborne spotted 2434

Fenthion 2754

Israeli spotted 2434
toxicity 3066
lassa 2474

Fenuron poisoning 2998
malignant catarrhal 758

Fenvalerate 2750

Mediterranean spotted 2434

Ferguson reflex 2197
milk

Fern
cattle 988
bracken 3148
sheep and goats 991
brake 3148

Omsk hemorrhagic 2476
cloak 3132
pasture 772

Jimmy 3132

Q or query 623, 2434

Ferrets 1824
rat bite 2428
distemper 1825
relapsing 2420
endocrine disorders 1827

Rift Valley 2478
fungal diseases 1826

Rocky Mountain spotted 806, 2436
infectious diseases 1824, 1825

Ross River 2478
management 1824
sennetsu 2434
neoplasia 1826
spotted 2434
noninfectious diseases 1828
swine 713
parasites 1826

Tal1yna 2468
vaccinations 1824
tick 20, 806

Fertility, male, preservation 2231
tick bite 2434

Fescue
tickborne 772
foot 3006, 3016
undulant 1348
grass toxicusis, horses, and abortion
unkown origin 1015

1344

Venezuelan hemorrhagic 2476
lan1eness 3016

Wesselsbron 2480
poisoning 3016

West Nile 2480

3236

INDEX

Fiber requirements, dogs and cats 2369
diseases of regulatory concern (table)

Fibrillation, ventricular 97, 1673

1786

Fibrinoid leukodystrophy 1234
families 1781

Fibrinolytic agents 2543
management 1784

Fibroadenoma complex, cats 1396
medications 1790

VetBooks.ir

Fibroblasts 1601
metazoan parasites 1802

Fibrocartilagenous embolism 1255
rnycotic diseases 1811

Fibrohistiocytic tumors 957
nutrition 2307

Fibrolipomas 958
nutritional diseases 1798

Fibroma 955
parasites 1 799
durom 955
protistan (table) 1798
interdigital, sheep 1170
pox 1812
molle 955
tapeworm infection 2452
odontogenic 366
viral diseases 1782 (table),1812
soft 955

Fissures of the claw, cattle 1085
virus, rabbits 1950

Fistulas

Fibromatosis 956
oronasal 162
epulis 366
perianal 187

Fibropapillomatosis 852
rectourethral 169
reptiles 1995
rectovaginal 169, 1499

Fibrosarcomas 957
urethrorectal 1499
low-grade 956

Fistulous withers 905, 1064, 1350
oral 367

Fixation of patella, horses 1142
pet birds 1916

Flamingo

Fibrosing alveolitis, diffuse 1442
flower 3106

Fibrosis
lily 3106
hepatic, congenital 170

Flamprop-methyl 2978
pulmonary, equine nodular 1446, 1457

Flatulent colic 251
small intestinal, horses 293

Fla.tweed 3128

Fibrotic myopathy

Flaviviruses 1294
clogs 1200

Flavobacte1iurn
horses 1187
brnnchioph'i!'U1n 1749, 1759

Fibrous
colurnnarn 1749, 1759, 1782, 1786,
histiocytornas, canine 955, 957, 959

1810
osteodystrophy 1054
psychrophilurn 1749, 1759

Fibrovascular papillomas 955
spp 1752, 1759, 1778

Fibularis

Flavophospholipol 2766
longus muscle rupture, turkeys 2885

Flea
tertuis rupture, horses 1137
allergy dermatitis 880, 882

Ficus spp 3110
bite hypersensitivity 882

Fila.rial dermatitis, cattle 907, 2576
borne typhus 2436

Fila.rial clermatosis 904

•

Fleas 880

Filariasis 2456
poultry 2875
birds 2782
rabbits 1953

Malayan 2458
sand 2466

Filaricls, causing CNS disease 1312

Flesh flies, gray 901

Filarnides

Flexion deformities, horses 1150
hirthi 1484

Flexor
spp 1486, 1881
reflex 1218
fllth-breecling flies 895
tendons, contracted 1042

Finastericle 2607

Flies 885

Fine-needle aspiration 1598

African tumbu 902

Fipronil 2756
biting 885

Fire ants 3165
black 886

Fireball 3144
buffalo 892

Fireweecl 3144
deer 889

Firocoxib 2720
eye 896

First aid
face 894
equine 1713
filth-breeding 895
and transport 1659
gray flesh 901

Fish 1779
head 895
bacterial diseases 1809
hippoboscid 894

INDEX

3237

Flies (continued)

Fluke fever, Elokomin 808
horn 891

Flukes-See also Trematodes
horse 889
conical 328
louse 894
infections, poultry 2874
mango 902
intestinal, small animals 426

VetBooks.ir
moth 887
lancet 327, 2466
myiasis-producing 897, 899
liver
new forest 893
cat 2448
nonbiting 894
common 324

Oriental 900
giant 326, 327
plantation 895
large Americai1 327
poultry 2875
lesser 327
sand 887
small 2448
skin maggot 902
small animals 427, 484
spider 893
lW1g 2448
stable 890
small animals 1483
synanthropic 896, 897
mai'ine mammals 1866
tsetse 892
pancreatic 328

Flight prevention, zoo birds 2053
rumen 328

Flip-over disease, poultry 2821
ruminants 324

Floating, teeth 176, 177
salmon poisoning 426

Flood plain staggers 3154
small anin1als 426, 484

Florasulan1 poisoning 2980
zoonotic 2446, 2448, 2450

Florasulam methyl poisoning 2998

Flumazenil 3034

Flo1fenicol 2684

Flumequine 2669
dosages (table) 2687

Flumethasone 2607, 2712
elimination and distribution 2686

Flumethrin 2750

Florida arrowroot 3114

Flumetsulan1 2980

Flu
poisoning 2998
canine 1479

Flumiclorac 2980
pig 1470

Flunidazole 2696

Fluazifop-p-butyl poisoning 2998

Flunixin meglumine 2602

Fluazifop poisoning 2998
ai1d acute anterior uveitis 509

Fluazuron 2752

Fluometuron 2980

Flubendazole 2645
poisoning 2998

Flucarbazone-sodium 2980

Fluoride poisoning 3075

Flucloxacillin 2656

5-Fluorocytosine 2703

Fluconazole 2575, 2622, 2701, 2702

Fluoroquinolones 2669

Flucytosine 2575, 2703

Fluorosis 3075
adverse events and toxicity 2704
cattle and sheep 177
antifungal activity 2703

5-Fluorouracil 2728, 2732
dose rates 2703
toxicity 3036
effects on laboratory tests 2704

Fluoxetine 1544, 2605
fungal resistance 2703

Fluphenazine 2604
interactions 2704

Fluralaner 2755
mode of action 2703

Fluroxypyr 2980
therapeutic indications 2703

Flutamide 2607

Fludrocortisone 2712

Fluthiacet 2980

Flufenacet 2980

Fluvoxainine 1544

Flufenoxuron 2752

Fly

Flufenprox 2756
poison 3122

Fluid
strike 897
analysis, samples 1589

Foal
body cavity, cytology 1605
cai·e 2159
compaitments 1675
diarrhea 289
deficit 1676
dysmaturity, hypothyroidism 559
dynainics 1675
emergencies 1723
resuscitation 1676
heat diaiThea 289
selection 1676, 1681
immunoglobulin 1625
therapy 1675
intensive care 1723
equine, emergency 1708
orphan, feeding 2329
in hypercalcemia 568
rejection 1550

3238

INDEX

Foal (continued)

Forarnsulfw-on 2980
uroperitoneum 1506

Forebrain disorders 1222

Focal

Foreign bodies
adnexal dysplasia 955
colon obstruction, horses 266
cutaneous hypoplasia, swine 846
corneal 1697

VetBooks.ir
pnewnonia 1413
esophagus, small animals 372

Focused feeding, goats 2182
marine mammals 1858

Fog fever 1439
pet birds 1894

Folacin deficiency, poultry 2942
pnewnonia 1417

Folic acid 2540
sole, cattle 1084
analogues 2732

Forelimb, angular defonnity, dogs 1203
antagonists 2796

Forestomach, ruminant, diseases 221
deficiency, poultry 2942

Formaldehyde 2742, 2744

Follicle

Formalin 2743
dysplasia 847
in aquaculture 1750, 1790
stimulating hom1one 542, 2606

Formamidines 2751, 2755

Follicles, vestibular ly:mphocytic 1392

Formicafusca 327

Follicular

Fosamine anunonium 2980
cystic ovary disease 1354

Fosfomycin 2693
cysts 846, 1354

Foul in the foot, cattle 1081
canine interdigital 862

Founder-See Laminitis
infundibular 947

Fourth branchial arch defect, horses 1461
small animals 1395

Fowl
mange, cattle 916
cholera 2822
parakeratosis, hereditary congenital 847
diphtheria 2824

Fonsecaea spp 643, 1739
plague 2902

Food
ticks 2876
adverse reactions, small animals 855
typhoid 2866
allergy 825, 855, 2379

Fowlpox 2824
dog and cat 2373
backyard poultry 1822
hazards 2964

Foxglove 3110
intolerance, small animals 2379

Fractures-See also Lan1eness
reactions, adverse 855
cattle 1088
safety 2406
horses
regulation 2410
cannon bone 1124
throwing, cattle 1553
carpal bone 1125

Foodborne
distal phalanx 1108
diseases 2408
emergency care 1713
pathogens 2409
metacarpal bones 1124

Foot
metatarsal bones 1124
abscess, sheep 1170
navicular bone 1108
and-mouth disease 629, 2470
os pedis l l08
and tail mange, cattle 916
patella 1142
care, horses 2155
pelvic 1145
disorders
phalanges ll08, l l l8
horses 1107
saucer l l23
pigs 1157, 1162
sesarnoids l l 19
scald 1167
splint bones l l24
goats 1094
potbellied pigs 1935
sheep 1167
reptiles 1999

Footbaths, cattle 1073
small animals, joint 1199

Foothill abortion 1336
zoo animals 2053

Footpad hyperkeratosis, familial 848

Fragmentation

Footrot
medial coronoid process ll96
cattle 1081
patella, horses ll42
eradication 169

Fran1ycetin 2663
goats 1094

Francisella
sheep 1167
noatunensi,S 1 760
strawberry 866
novicida 693

Forage
spp 624, 1761
botulism 606
tularensis 692, 928, 1950, 1950, 2032,
mite, horses 919

2048,2415

INDEX

3239

Francisella tularensis (continued)

Fiisobacteriurn
holarct'ica 693, 2430
necrophorurn 64, 158, 341, 352, 1081,
rnediasiatica 2430

1165, 1166, 1167, 1170, 1171, 1368,
novicida 2430

1369, 1419, 1429, 1442, 1468
tularensis 693, 2430
spp 364, 1263, 1449, 1472, 2571, 2696

VetBooks.ir

Francisellosis, fish 1760

Fraser's photinia 3146

F'ree-gas bloat 228

G

Freemartinism 1330

Gabapentin 1545, 2111, 2599

Frenkel'ia spp 2007

Gad flies 876

Frijolito 3134

Gadding 877

Fringed tapewonn, sheep 314

Gaigeria

Frostbite
pachyscelis 313
ears 526
spp 313
teat 1386

Gait evaluation 1217

Frothy bloat 227

Caterina

Frounce 1905, 2804
auturnnalis 3097, 3100

5-F'U toxicity 3036
spp 3096
fucosidosis, English Springer Spaniels
venenata 3097, 3100

1235

Gall sickness 18

F'uel poisoning 3053

Gallan1ine 2587, 2588
fulminant hepatic failure 442

Gallbladder

Fume fever, polymer 3022
disorders, small animals 477

Furnonisin toxicosis 3017
and extrabiliary system 473
functional
mucocele, dogs 475
claw trimming 1074
rupture, small animals 474
islet cell tun10rs 582

Gallinaceous birds, nutrition 2292
fundus, ocular 501

Gallinago gallinago 2858
fungal infections 632-See also Mycotic

Gallop rhythms/heart sound 88
amphibians 1738

Galls 979
ferrets 1826

Gallus
spinal column and cord 1251
dornesticus 1815
zoonotic 2438, 2440
gallus 1815

Fungus, in urine 1618

Galvayne's groove 172
fur

Gamithromycin 2687, 2690,
clipping, mlnk 1875

2691
slip, chinchillas 2005

Gammopathies 832

F'uraltadone 2696
monoclonal 832
furazolidone 2696
polyclonal 832
furious rabies 1304

Ganciclovir 2745, 2746
furosemide 75, 2527, 2623, 3034

Gangliocytomas 1271

F'urunculoid myiasis 903

Ganglioneuritis, sensory 1241

F'urunculosis

Gangliosidosis 1234, 1235
eosinophilic, canine 972

Gangrene 1171
interdigital 862

Gangrenous
salmonids 1809
cellulitis, poultry 2879

F'usariotoxicosis 3006
coryza 758
poultry 2846
dermatitis, poultry 2879

Fuswiurn
dermatomyositis, poultry 2879
estrogenism 3014
pneumonia 1417
grarninewwn 3014

Ganjam virus 761
rnonilijO'lme 2847, 3017

Gapeworm, birds 2830
proliferaturn 3017

Gas
solani 1442, 1769, 1778, 1811, 3008
bladder, fish 1784
spp 495, 640, 1864, 1993, 2761, 2846,
bloat 228

2881,2943,3010,3014,3020,
bubble disease, fish 1773

3094
edema disease, poultry 2879
verticillioides 284 7, 3017
fields, effects on cattle 3055
fused vertebrae, small
gangrene 601, 1171, 2425
animals 1229
toxic, and interstitial pneumonia, cattle

Fusiformis nodosus 2655

1442
fusion beats 97

Gasoline poisoning 3053

3240

INDEX

Gasterophilus
small anin1als 393
haemorrhoidalis 315
tl1erapy 2550
intestinalis 315

Gatierreaia 3086
nasalis 315

Gaucher disease 1235
spp 315, 897, 2464, 2649

Gaudoglyphus minor 2878

VetBooks.ir

Gastric-See also Digestive,

Gavage feeding, birds 1891

Gastrointestinal, Intestinal

Geese, nutrition (table) 2922
dilatation

Geldings, stallion-like behavior 1550
horses 258

Gelsemiimi
nonhuman primates 1883
mnkinii 3142
and volvulus, small animals 384
sempervii'ens 3142
nutrition in 2384

Gemcitabine 2728, 2732
foreign bodies, ferrets 1828

Generalized
impaction, horses 258
glycogenosis, large animals 1228
rnpture 258
metabolic disorders, nervous system
stasis, rabbits 1956

1234
ulcers
nodular dermatofibrosis, dogs 852, 955,
horses 218

974
mink 1876

Genetic
pigs 219
analysis, laboratory 1589
yeast, avian 1903
myopathies

Gastrin-secreting islet cell tumors 583
large animals 1175

Gastrinomas 576, 583
poultry 2886

Gastritis

Genital
allergic 825
abnormalities
small animals 386
female 1331
traumatic, ruminants 230
male 1330

Gastrocnemi us
camplyobacteriosis, bovine 134 7
muscle rupture, cattle 1091
horsepox 1357
tendinitis, horses 1139
infections, rabbits 1946

Gastrodiscoides hominis 2446
tract 1323

Gastrodiscoidiasis 2446
female 1326

Gastroenteritis
male 1327
epizootic catarrhal, mink 1874

Gentamicin 2620, 2663, 2666
hemorrhagic, dogs 396

Geomyces 640
transmissible, pigs 302

Geophagia, horses 1548

Gastrointestinal-See also Digestive,

Geosmithia 640

Gastric, Intestinai

Geotiichum
diseases
ccmdidum 1264
nonhuman primates 1878
spp 640, 1993
llamas and alpacas 1852

Gerbils 2011
drug poisoning 3030
biology 2011
neoplasia
dihydrostreptomycin toxicity 2013
horses 291
husband1y 2012
small animals 388
iatrogenic conditions 20lq
obstruction, small anin1als 390
infectious diseases 2012
parasites
metabolic and nutritional disorders
cattle 308

2013
goats 312
neoplasia 2014
horses 287, 315
physical examination 2012
pigs 298, 320
traumatic injuries 2013
rnminants 303
zoonotic risk 2014
sheep 312

Geriatric-onset laryngeal paralysis
small animals 412
polyneuropathy 1238
prokinetic drugs 2556

Germ cell tumors 1271
tract

Gestation-See also Pregnancy
infectious disease 158
periods (table) 1324
noninfectious diseases 161
prolonged
pathogens 158, 159
associated with fetal death 1379
ulcers
associated with fetal deformity
large animals 218

1379
marine manunals 1858
cattle and sheep 1377

INDEX

3241

Giant

Glucagonoma 576
cell tumors 957
syndrome 468
kidney worm infection 1511, 2456

Glucocerebrosidosis 1235
liver fluke 326, 327

Glucocorticoids 568, 573, 844, 2545, 2546,

Giardia

2556,2578,2582,2607,2612,2615,

VetBooks.ir
agilis 211

27l�ee a.lso Corticosteroids,
ardeae 211

Steroids
duodena.tis 211, 276, 2006, 2442
as appetite stimulants 2546
intes tinalis 211
in hypercalcemia 568
lamblia 211, 2006, 2442
in neoplasia 2734
microti 211
for pruritus 844
muris 211, 2029
systemic use in integumentary system
psillaci 211

2579
spp 158, 205, 211, 287, 374, 378, 398, 402, Glucose 1592, 1595

403,665, 1619, 1853, 1877, 1881,
in urine 1616

1905, 1965,2006,2011,2012,2047,

Glucosuria, renal, small animals 1521

2060,2555,2695,2697

Glufosinate 2980

Giardiasis 211, 2442
poisoning 2997
horses 287

Glugea spp 1812
malabsorption, treatment 406

Glutamate dehydrogenase 1591
pet birds 1904

-y-Glutamyl transferase 1590

Giardosis 211

Glutaral 2743

Gid 1311

Glutaraldehyde 2742
false 1314

Gluten-sensitive enteropathy 168

Giganlobilharzia spp 2450

Glycerol 2624

Gilbert syndrome, sheep 351

Glyceryl guaiacolate 2589, 2616

Gilt and sow management 2202

Glycogen branching enzyme deficiency 1046

Gingivitis
horses 1187
acute necrotizing ulcerative, dogs 364

Glycogen storage disease 1043, 1233
small animals 178, 361
small animals 472

Gingivostomatitis, cats 362

Glycogenosis 1043, 1236

Ginkgo biloba 1570
generalized, large ai1imals 1228

Cirella nigricans 1868

Glycolysis 5

Girth itch 875

Glycopeptides 2693

Glanders 706, 2424

Glycopyrrolate 2612

Glandular mammary hypertrophy, cats

Glycosides, cardiac 2529

1396

Glyphosate 2980

Glanzmaim thrombasthenia 50
poisoning 2997

Glasser's disease 720

GM, gangliosidosis 1234, 1235

Glaucoma 497, 1698

GM
drug therapy 2570

2 gangliosidosis 1234, 1235

Gnathostoma
infantile, rabbits 1959
binucleatum 2458

Glioblastoma multiforme 1271
doloi-esi 2458

Glipizide 581
hispidum 2458

Gli1icola porcelli 2017
spinigerum 1314, 2458

Globidiosis 597
spp 322, 2458

Globoid cell leukodystrophy 1234, 1235

Gnathostomiasis 2458

Glomerular disease 2625

Gnats 887
small animals 1517
buffalo 886

Glomerulonephritis
eye 896
membranoproliferative 829
poultry 2875
small animals 1511, 1518

Goatpox 869

Glossina

Goats-See also Caprine
fusca 36
common diseases 2150
morsitans 36
gastrointestinal parasites 312
palpalis 36
health-management interaction 2147
spp 36, 892, 2753
lameness 1092

Glossitis, small animals 361, 365
management 2147

Glossopharyngeal nerve 1216
nutrition 2149, 2308

Glossoplegia, large animals 214
nutritional diseases 2311

Glollidium vesica,riiim 3132
parturition 2186

Glucagon 579
perinatal management 2149

3242

INDEX

Goats (continued)

diseases, hypercalcemia 567
pregnancy 2186
enteritis, horses 291
pseudopregnancy 1381
episclerokeratitis, nodular 957
reproduction, management of 2182
meningoencephalomyelitis, dogs 1252,
respiratory diseases 1471

1264

VetBooks.ir

Goatweed 3144
reactions 830

Goiter 558
sebaceous adenitis 848
fan1ilial dyshormonogenetic 559

Granulopoiesis 56

Goitrogenic substances 559

Grapes, poisoning 2968

Gold-dust, fish 1802

Grass

Gold salts 2583
sickness, equine 1257

Golden
staggers 996
pathos 3110
tetany 996
trumpet 3116

Gray

Goldfish ulcer disease 1809
diarrhea, mink 1876

Gonadotropin-releasing hormone 2606
flesh flies 901

Gonads 1323
fly poison 3122

Gongylonema
patch disease, turtles 1995
ingluvicola 2829
underfur, mink 1875
pulchrum 2458

Grazing, sheep 2164

Gongylonemiasis 2458

Greasewood 3120

Goniocoles gallinae 2876

Greasy

Goniodes
heel 919
dissim'ilis 2876
horses 1116
gigas 2876
pig disease 860

Gonitis, horses 1143

Great Dane myopathy 1200

Goose

Green
hepatitis 2826
liver osteomyelitis complex 2882
parvovirus infection 2826
muscle disease, poultry 2883
plague 2826

Grey nicker bean 3118

Gopher ears, llamas 1851

Grief and pet loss 1580

Gorging, dogs 1568

Griffonia 3032

Gosrnore 3128

Grindelia 3086

Gossypium spp 3092

Griseofulvin 2704

Gossypol poisoning 3092
adverse effects and toxcity 2705
poultry 2861
antifungal activity 2704

Gotch ear 520
dose rates (table) 2705

Goussia spp 1806
effects on laboratory tests 2705

Gout
fungal resistance 2704
backyard poultry 1818
interactions 2705
pet birds 1926
pharmacokinetic features 2704
poultry 2874
therapeutic indications 2705
articular 2882

Grooming, small animals 2169
reptiles 2000, 2304

Groundsel 3148, 3150

Graaff-Reinet disease 1475

Growth

Grafts, skin 1706
honuone 542, 2581, 2764

Grain overload 222, 352
nutrition

(}rampus griseus 1867
cats 2378

Granisetron 2549
dogs 2378

Granular
plate dysplasia, horses 1149
venereal disease 1392
promotants 2758
vulvitis 1392
antibacterial 2765
vulvovaginitis 1392
steroid hom1ones 2759

Granulocytes 5, 56, 1612
synthetic steroid hormones

Granulocytic ehrlichiosis 2432

2761
equine 697
stimulants, pigs 2342

Granuloma

Grubs, cattle 876
collagenolytic, horses 972

Guaifenesin 2589, 2616
cnzootic nasal 1429

Guajillo 3136
eosinophilic,cats 972

Guanarito virus 2476

Granulomatous

Guanidine 2748
colitis 169, 377

Guarana 3032

INDEX

3243

Guinea

Haematobia
pigs 2014
in'ilans 891, 908, 1360, 2753
antibiotic dosages (table) 2020
exig1ia 892
biology 2014
spp 907, 2751, 2752
husbandry 2015

Haemalopinus

VetBooks.ir
iatrogenic disorders 2019
asini 912
inclusion conjunctivitis 507
euiyslernus 910
infectious diseases 2016
quadi'ipertuses 910
metabolic disorders 2018
spp 2751
miscellaneous disorders 2020
suis 870, 913
neoplasia 2019

H aemobarlonella
nutritional disorders 2018
felis 28
physical exan1ination 2015
spp 10, 26
reproductive disorders 2019

Haemonchus
zoonotic risk 2021
contortus 305, 312, 322, 2150, 2640,
wom1 infection 904, 2456

2644,2648,2649,2651

Gulf coast tick 928
placei 308, 311

Gumboro disease, poultry 2837
spp 9, 303, 312, 2638, 2651

Gunshot injuries 1708

Haenwphilus

(}urlita paralysans 1313
aclinomycetemcomilans 179

Gut edema 716
agni 1263

Guttierrezia micracephala 1833, 3142
ga/linarum 2927

Guttural pouch disease, horses 1463
injluenzae 1879

Gymnopilus spectabilis 3097, 3099
pamhaemolyticus 1469

Gyrodaclylus
pamsuis 627, 670, 671, 720, 724, 730, 733,
salaris 1756

1158, 1163, 1263, 1465, 1470, 1935
spp 1807
spp 197, 1063, 1157, 1372, 1430, 2028,

Gyromilm esC'Ulenta 3096, 3101

2174,2177,2654,2655,2688,3079

Gyropus ovalis 2017
suis 715

Haemoprateus

H
infection, birds 2782

Hz-receptor antagonist poisoning 3030
lophortyx 2782

Habituation 1542
meleagridis 2783

Habronema
spp 894, 1904,2780,2782,2875,2876
microstoma 315, 505

Hageman deficiency 52
muscae 315, 505, 890

Hair
spp 315, 511, 904, 1264
chewing, rabbits 1956

Habronemiasis, cutaneous 904
follicle tumors 943, 948

Haemagogus spp 2482
growth 838

Haemaphysalis
loss 841
aciculifer 932
matrix tumors 949
anamala 932

Hairballs, rabbits 1956
bispinosa 932

Hairworm, horses 319
concinna 931

Hairy
fiava 2435
shaker disease 622, 1225, 1338
inermis 932
warts, cattle 1075
kopelda.ghicus 932

Half-life 2501, 2520, 2950
leachi 23, 932

Halicephalobus
longicornis 932
deleti'ix 1252, 1311, 1313
moschis1iga 932
gingivalis 1264, 1297
paimala 932

Halichoeius grypus 1864
parva 931

Halocei·ciis lagenorhynchi 1865
pospelovashlromae 932

Halofuginone hydrobromide 2796
punctala 23, 931

Halogenated aromatics poisoning 3056
iugosa 932

Halogens and halogen-containing
silacea 932
compounds 2741
spinigera 932, 24 73

Halogeton glamei·atus 3134
spp 23, 35, 928, 931, 1314

Haloperidol 2604
sulcala 931

Halosulfmon 2982
libetensis 932

Haloxon 2651
xinjiangensis 932
toxicity 1254

3244

INDEX

Haloxyfop poisoning 2998
rate 68

Hamartomas 846, 852, 942, 1271
rates, resting (table) 3174
epidermal 943
sounds 88
sebaceous gland 950

I-lea.rtwa.ter 751
vascular 852

Heartw01m disease 72, 127

VetBooks.ir

I-lan1burger gill disease 1755, 1807
a11tigen testing 130

Hammondia
ferrets 1826
heydorni 665
marine mainmals 1866
sp 158, 208
treatment

Hamsters 2021
ca.ts 136
biology 2022
dogs 132
husbandry 2022
ferrets 136
infectious diseases 2023

I-iea.t-See also Estrus
miscellaneous ilisorders 2024
exhaustion, rabbits 1957
neoplasia 2023
silent, cows 2173
physical examination 2022

Heavenly bainboo 3146
zoonotic risk 2024

Heaves, horses 1443, 1455

Hansenula spp 1899

Heavy metals toxicity, fish 1771

I-lantaan virus 2470

Hedern spp 3110

Han ta viral

Hedge plant 3144
iliseases 24 70

Hedgehogs 1828
pulmonary syndrome 2470
diseases 1831

I-la.ntavirus 2028, 2032, 24 70
management 1829

Haplopappus helerophyllus 3134
physiologic data (table) 1829

Haplorchis spp 2446
zoonoses 1835

Hard

Heel
ticks 925
abscess, sheep 11 70
udder, goats 747
erosion, cattle 1079
udder syndrome, sows 1373
flies 876

Hardware disease 230
sheared, horses 1117

Harelip 162

Heifer replacement 2125

I-laivest mites 924

Helenium
horses 919
hoopesii 3142

Hashish 3106
microcephalum 3142
poisoning 3041

Helicobacler

Hawthorne effect 2402
bizzozeronii 395

Head
canis 396, 2424
evaluation 1214

Jelis 395
flies 895
heilmannii 395
injuries, horses 1718
infection, small a11ima.ls 394
shaking, horses 1549
mustelae 1824
tilt, rabbits 1945
pull01um 2424
trauma, dogs a11d cats, nutrition in 2384
pylori 395, 2013

Healing by second intention 1704
spp 218, 220, 387, 388, 389, 393, 394,

Health benefit (hmna11) of pet ownership

1824, 1843, 1878,2013,2550,2688

1577

Heliosoma spp 1757

I-lealth-ma11agement interaction-See also

Heliotropiiim

Ma11agement
europaeum 3074
beef cattle 2119
spp 977, 3150
dairy cattle 2135

Helisoma spp 426
goats 2147

Hellebore, false 3126
horses 2151

I-lelminthiasis
pigs 2160
goats 2150
sheep 2164
poultry 2828
small aiumals 2169
sheep 274

I-lea.rt-See also Cardiac

I-lelminths-See also Parasites, Worms
disease 87, 120
causing CNS disease 1310
endpoints 73
intestinal, drug treatment, small animals
failure 73, 87, 99

418,419
ma11a.gement 103
nonhumai1 primates 1881
murmurs 88, 89
reptiles 1997
innocent 77
skin 904

INDEX

3245

He!oderma spp 1967

Venezuelan 2476

I-Iemagglutinating encephalomyelitis virus,
with renal syndrome 2470
porcine 1251
gastroenteritis, clogs 396

I-Iemangiomas 959
rnyelopathy, postanesthetic, horses 1255
disseminated 959
pneumonia, mink 1871

VetBooks.ir

Hemangiopericytomas 958, 959
pulmonary, exercise-induced, horses 1457

Hemangiosarcomas 960
purpura, horses 830, 1182

Hematinics 2540
septicemia 756

I-Iematogenous metastatic brain tumors 1272
fish 1809

Hematologic reference ranges (table) 3176
sole, cattle 1079

Hematology 1610
syndrome, poultry 3008, 3011

Hematoma

Hernorrhagica, purpura, horses 830, 1182
auricular 524

Hemostasis 44
ethmoid, horses 1462

Hemostatic disorders 44
valvular 115

Hemostatics 2542

Hematopoiesis, cyclic in gray Collies 47, 61 Hemothorax 1414

Hematopoietic
horses 1717
cell

Hemotropic mycoplasmas 26
leukemia 62

Hemp, Indian 3106
neoplasia 62

Henclra virus infection 707, 1448, 2472
system, introduction 4

Henipcwiius 707, 721, 1448, 2472

Hematuria, enzootic, 3090

Henneguua

Hemivertebrae, small animals 1229
ictaluri 1754

Hemlock
spp 1807
poison 3140

Hens, laying, nutrition (table) 2916
water 3116

Heparin 2542

Hemobartonellosis 28

Hepatic-See also Liver

Hemochromatosis, large animals 349
abscesses 341

Hemoglobin 4
amyloidosis 350, 472
concentration 1610
arteriovenous malformation 450

Hemoglobinuria
capillariasis 2456
bacillary 341, 601
coccicliosis, rabbits 1952
postparturient 1002
cysts

Hemolysis
congenital 170
alloimmune 11
small animals 477
metabolic causes 12
disease
rnicroangiopathic 12
idiopathic acute, horses 338

Hemolytic anemia 10
laboratory analyses 430
immune-mediated 10, 826
large animals 329

Hemophilia 51, 52
llamas and alpacas 1853

Hemoplasmas 26
small animals 429

Hemoplasmosis 28
nutrition in 439, 2385

Hemoptysis 1413
encephalopathy

Hemorrhage-See also Bleeding
large animals 336
pulmonary, exercise-induced, horses
small animals 443, 1224

1457
failure

Hemorrhagic
foals 349
aplastic anemia, poultry 2785
large animals 336
bowel syndrome
small animals 442
cattle 270
fibropolycyslic disorders 477
pigs 296
fibrosis
disease, 3090
congenital 170
viral, rabbits 1951
large animals 350
enteritis, poultry 2833
flukes
enteropathy, proliferative, pigs 299
ruminants 324
fever
small animal 427

Brazilian 24 76
function tests, small animals 436

Crimean-Congo 751, 761, 2470
lipidosis

Ebola 2470
birds 1895

Marburg 2474
feline 456, 2385

New World 2476
large animals 346, 1018

Omsk 2476
mink 1876

3246

INDEX

Hepatic (contimwd)

Hepatozoon 505, 2780, 2785
lobe atrophy, horses 350
americanum 29
lobe torsion 350
canis 29, 60
necrosis, acute, cattle 339

Hepatozoonosis
neoplasia

American canine 29

VetBooks.ir
large animals 348

Old World 29
small animals 469

Heptachlor toxicity 3061
nutrition in, dogs and cats 2385

Herbage and browse, goats 2310
vein, outflow obstruction 451

Herbal

Hepatitis
medicine 2084
acute, large animals 338
supplement poisoning 3032
avian vibrionic 2806

Herbicide poisoning 2969
chronic 462
inorganic 2994
active, large animals 345
organic 2996
canine 460

Hereditary-See also Inherited

Cocker Spaniels 464
alopecia and hypotrichosis 846

Doberman Pinschers 464
chonclroclysplasia, lambs 1048

Labrador Retreivers 464
deafness 518

Skye Terriers 465
diseases, mink 1876

West Highland White Terriers 462
hyperchylomicronemia, neuropathy
goose 2826

1232
hydroperic:arclium, poultry 2788
lupoicl clennatosis, clogs 851
idiopathic 462
macrothrombocytopenia, Cavalier King
inclusion body, poultry 2788

Charles Spaniels 47
infectious
myopathies, horses 1187
canine 453, 798
neoplasms, integumentary system 852
large animals 340
neuraxial edema 1234
necrotic 341, 603
quadriplegia, Irish Setters 1235
lobular dissecting, small animals
zinc deficiency syndromes 851

466

Hem1aphroclitism 1329
lymphocytic portal, feline 482

He1metia illucens 895
postvaccinal, horses 338

Hernias 166, 1047
serum, horses 338
diaphragmatic 1418
viral
hiatal 167
duck 2815
inguinal 167
turkeys 2871
horses 262

Hepatitis A virus, nonhuman primates
perinea] 188

1882
peritoneopericarclial 167

Hepatitis E 24 72
peritoneopericardial diaphragmatic 86

Hepatocellular
pleuroperitoneal 167
adenomas, small animals
scrotal 167

470
umbilical 167
carcinomas, small animals 469

Herniation, brain 1277

Hepatochlor 2749

Heroin 3042

Hepatocutaneous syndrome, small animals Herpes anatid 2799

452,468, 974

Herpes B virus 2472

Hepatogenous photosensitization 977

Herpesviral hematopoietic necrosis,

Hepatoid gland tumors 951
goldfish 1813

Hepatolithiasis, large animals 344

Herpesvirus

Hepatopathy
angelfish 1813

Cocker Spaniel 464
bovine 1392, 1434
copper-associated 170, 460
and abo1tion 1334

Maltese dogs 466
canine 51, 453, 779
toxic, large animals 342
caprine 1341
vacuolar, canine 467
elephant endotheliotropic 2054

Hepatoportal microvascular dysplasia
encephalomyelopathy, horses 1250,

170

1251

Hepatosis dietetica, pigs 117 4
equine 341, 1392, 1444

Hepatotoxic plants 343
and abortion 1344

Hepatotoxins
fish 1762, 1812
large anin1als 341
marine mammals 1868
small animals 451
nonhw11an primates 1882

INDEX

3247

Herpesvirus (continued)

Histiocytoma 1604

Pacheco's 1908
atypical 952, 961
pigs, and abortion 1342
canine malignant fibrous 959
reptiles 1995
cutaneous 966

HES 1679
fibrous, canine 957

VetBooks.ir

Hetacillin 2655
malignant fibrous 957

Heterakis

Histiocytosis
gallinarum 2830, 2832, 2836
of Bernese Mountain Dogs 967
isolonche 2831
cutaneous 966
spp 2831
malignant 1272

Heterobilharzia americana 427, 484
mulicentric, poultry 2855

Heterodox-us spiniger 913

Histomonas

Heterophils 1612
rneleagridis 2831, 2835

Heterophyes
spp 2696
heterophyes 427

Histomoniasis, poultry 2835
spp 2446

Histophilosis 754

Heterophyiasis 2446

Histophilus 1283, 1372

Heteropolaria spp 1754, 1779
meningoencephalitis 2129

Heterotopic polyodontia 165
ovis 1373

Hexachlorocyclohexane toxicity 3061
somni 533, 754, 1262, 1337, 1432, 1436,

Hexachlorophene 2650, 2742

2131,2133,2217,2689

Hexamita

Histoplasma
meleagridis 2801
capsulatum 157, 159, 378, 639, 1205,
spp 1965, 1998

1251, 1264, 1346, 1425,2007,2697,

Hexan1itiasis, poultry 2801

2699,2701,2705,2706

Hexazinone 2982
var capsulatum 2440

Hexestrol 2761
var duboisii 2440

Hiatal hernia 167
farciminosum 639

High
spp 402,404,505,830,2052,2574,2575
altitude disease, bovine 137

Histoplasmosis 455, 639, 2440
cis-cypermethrin 2750
treatment 406
mountain disease, bovine 137

Hitra disease 1809
palmar nerve block, horse 1104

Hives 824, 857
plantar nerve block, horse 1106

Hobby poult1y 1815

4-point block, horse 1104

Hock, dropped, small animals 1203

Highlands J virus 1291

Hog-See also Pigs, Porcine, Swine
poultry 2892
cholera 713

Highly pathogenic avian influenza 2472
and abortion 1342
zoo birds 2054
flu 1470

Himatione sanguinea 2826

Hollow wall, horses 1116

Hip

Holly 3110
disorders, horses 1144

Holocalyx glaziovii 977
dysplasia

Holokartikos crassipes 921
cattle 1087

Homeopathy 2087
dogs 1196

Homosexuality, sheep 1556
luxation, small animals 1199

Hoof trin1, zoo animals 2053

Hippelates

Hookworms-See also Nematodes
pallipes 896
marine mammals 1866
spp 896
sheep and goats 313

Hippobosca equina 893
small animals 416

Hippoboscid flies 894

Hoose 1421

Hippocarnpus spp 1779

Hordeum spp 591

Hirstiella spp 1996

Horizontal fissures, cattle 1085

Hirsutism 54 7

Hormonal

Hirudiniasis 2462
agents, antineoplastic 2734

Histamine
control of estrus 2244
and inflammation 2708
therapy, integumentary system
receptor antagonists 2551

2578
toxicity, marine mammals 1860

Hormones 538

Histiocytic
amino acid, modified 540
sarcomas 1272
antidiuretic 550
sarcomatosis, poultry 2856
calcium-regulating 561
tumors 836, 961
deficiency 541

3248

INDEX

Hormones (continued)

Household chemicals/products, poisoning
measurement 540

3000
overproduction 541

Houseplants
parathyroid 561
and hypercalcemia 566
protein/polypeptide 538
poisonous 3103

VetBooks.ir
steroid 539, 2758

HousesoiHng
as growth promoters 2759, 2761
cats 1572
thyroid 553
clogs 1568
thyroid-stimulating 553

Housing

Horn
barns and types 2117
capsule and corium disorders, cattle
laboratory animals 1839

1082

Houttuynia stnithionis 1965
flies 891

5-HTP poisoning 3032

Horner syndrome 531, 1210, 1258, 1260

Huarizo 1844

Hornet stings 3164

Human

Horse
ailimal bond 1575
flies 889
bot fly 2464
nettle 3130
chorionic gonadotropin 2606
tick 930
drug toxicities 3024

Horsebrush 3124
ewingii ehrlichiosis 2432

Horsepox, genital 1357
granulocytic

Horses-See also Equine
anaplasmosis 2434
abortion 2195
ehrlichiosis 2434
aged, feeding 2329
health, benefits of pet ownership 1577
artificial insemination 2201
influenza virus, ferrets 1825
body condition scores 2316
rnonocytic ehrlichiosis 2432
breeding 2201

Humoral
soundness 2189, 2200
immunity 815
colic 248
immunodeficiencies 819
dental care 2155

Hungry-bone syndrome 1056
emergency medicine 1708

Hunter's robe 3110
estrus detection 2189

Himlerellus hookeii 937
exhausted syndrome 1011

Husk 1421
feeding 2321, 2326

Hutch burn, rabbits 1957
foot care 2155

Hyacinths 3110
gastrointestinal

Hyacinthus spp 3110
parasites 315

Hyalohyphomycosis 640
tract 248

Hyalornma
health-management interaction 2151
albiparmaturn 933
housing 2152
anatolicurn
lameness 1096
anatolicurn 932
management 2151
excava tum 933
neonatal
asiaticuin
emergencies 1723
asiaticurn 933
intensive care 1723
caucasicuin 933
nutrition 2153, 2312
kozlovi 933
nutritional diseases 2323
clet.ritwn 933
parasite control 2156
clrornedaiii 696, 933
during pregnancy 2195
e1 y thmeum 933
paiturition 2196

.finnchinii 933
pasture 2152
glabrum trunca tum 933
perinatal cai·e 2159

Hyalornrna (subgenus) 932
pregnancy determination 2194
anatolicurn
prepurchase examination 1647
cmatol'icurn 932
reproduction, management of 2187
e:1:cavaticrn 933
respiratory diseases 1443
asiaticum 933
sick, feeding 2328
asiaticurn 933
urolithiasis 1505
caucasicurn 933
vaccinations 2157
kozlovi 933
broodmares 2195
del1'itum 933

How1cl's tongue plant 3140
clromedmii 933

House fly, biting 890

Jranchinii 933

INDEX

3249

Hyalomma Hyalomma (continued)

Hydromyelia, small animals 1230
impellatum 933

Hydronephrosis 1521
lusitanicum 933

Hydropericardium syndrome, poultry 2788
m01:ginalum 933

Hyclrntaea
isaaci 933
initans 895, 1365

VetBooks.ir
maigirwtmn 933
spp 895
iujipes 933

Hydrothorax 1414
turanicum 933

Hydroureter 1521
sclmlzei 933

[3-Hydroxybutyrate 1592
scupense 933

Hydroxyethyl stru·ch 1679

Hyalomasta (subgenus) 932

Hydroxyquinolines 2697
aegyptium 932

5-Hydroxytryptophan poisoning 3032

Hyalommina (subgenus) 932

Hydroxyurea 2731, 2734, 2735
arabica 932

Hygroma973
brevipunctata 932
carpal, cattle 1091
hussaini 932
horses 1127
kumari 932

Hymenochirus boettgeii 1743
punt 932

Hymenolepiasis 2452
rhipicephaloides 932

Hymeiiolepis
impeltatum 933
diminuta 2013, 2454
impressiim 933
nana 2013, 2454
m01ginalum isaaci 933

Hyn1enoptera stings 3164
maiginatum iujipes 933

Hymenoxys
mai:gina,tum turanicum 933
odorata 3116
nilidum 933
iichardsonii 3116
schulzei 933

Hyoscine butylbromide 2553
scupense 927, 933

Hyostrongylus
spp 19, 23, 35, 751, 928, 932, 940, 2467,
rubidiis 298, 322

2471
spp 322
lruncatum 684, 933

Hyperactivity, dogs 1567

Hyalommasta 932, 940

Hyperadrenocorticism 543, 573
aegyptium 932
ferrets 1827

Hyalommina
peripheral, horses 1006
arabica 932
treatment 545
brevipunctata 932

Hyper3lllmonemia
hussaini 932

Morgan foals 351
kumari 932
primary, horses 350
punt 932

Hyperbilirubinemia syndromes, large
rhipicephaloides 932
animals 351

Hybomitra 904

Hypercalcemia 566

Hybrid
cats, idiopathic 565
cysts 948
diagnostic tests 567
sinus beat 97
dogs and cats 562

Hydatid tapeworm 422
horses 570

Hydralazine 108, 2534
hyperparathyroidism 564

Hydranencephaly 621
hype1vitaJninosis D 566
large animals 1223
laboratory abnormalities 569
small animals 1224
of malignancy 563

Hydrangea spp 2960
osteolytic lesions 566

Hydrocephalus
renal failure 565

Bull Mastiffs 1234
treatment 568
large animals 1223

Hypercalciuria, dogs 1528
rabbits 1959

Hypercholesterolemia, dogs 170
small animals 1224

Hyperchylomicronernia

Hydrochlorothiazide 2624, 3034
dogs and cats 171

Hydrocodone 2609, 3042
hereditary neuropathy 1232

Hydrogen

Hypercoagulable states 46
peroxide 2548, 2740

Hyperdontia 164
sulfide

Hypereosinophilic syndrome 57, 62
toxicity, fish 1771

Hyperesthesia, cats 1574
workplace exposure 2954

Hypeiicum 288

Hydromorphone 3042
pe1fora,tum 977, 3144

3250

INDEX

Hyperkalemia 1004, 1005
osteopathy

Hyperkalemic periodic paralysis, horses
dogs 1205

1047, 1184, 1231
reptiles 200 l

Hyperkeratosis

Hyperuricemia, reptiles 2000

VetBooks.ir
footpad, familial 848

Hypervitaminosis A 1253
idiopathic, llamas and alpacas 1855

Hypervitaminosis D, in hypercalcemia 566
teat end 1386

Hyphema 497

Hyperkeratotic dern1atosis, idiopathic

Hypoadrenoco1ticism 574
nasal or perioral, llamas and
hypercalcemia in 565
alpacas 1855

Hypobiosis 304

Hyperketonemia 1025

Hypocalcemia

Hyperlipemia, large animals 346
chelating agents 572

Hyperlipidemia 170, 1232, 2385
cows 988
dogs, nutrition in 2385
dogs and cats 570

Hypermagnesemia 996
goats 991

Hyperostosis, skeletal, diffuse idiopathic
hens 2897

1247
horses 572, 1183

Hyperoxaluria, primary 1232
and hypoparathyroidism 570

Hyperparathyroidism
and hypoproteinemia 571
primary 564, 1054
and pancreatitis 571
renal secondary 1056
periparturient, small animals 992

Hyperphosphatemia 1002
and phosphate enema toxicity 571

Hyperpigmentation postinflammatory 970
in puerperal tetany 571

Hyperplasia
puerperal, small animals 992
hepatoid gland 951
in renal disease 571
sebaceous gland 950
sheep 991, 2167
vaginal, small animals 1399
small animals 995

Hyperplastic and seborrheic syndromes
tetany, horses 987

847
treatment 572

Hyperpnea 1413

Hypochaeris radicata 3128

Hypersecretion, intestinal 155

Hypochromasia 1611

Hypersensitivity

Hypoderma
contact 831
bovis 876, 1252, 1311, 1314, 2464, 2576
culicoid 887
linea,tum 876, 2464, 2576
flea bite 882
spp 876,879,902, 1264, 1314,2464,2576
pneumonitis 829
tarandi 876
cattle 1441

Hypodermosis, cattle 876
pet birds 1929

Hypodontia 164

Hypersialosis, small animals 367

Hypofibrinogenemia 51

Hypersomatotropism 551

Hypogalactia syndrome, periparturient,

Hypertension
sows 1373
pulmonary 125

Hypogammaglobulinemia 819
syndrome, pulmonary, poultry 2871
congenital 819
systemic 125
transient 820
in chronic kidney disease 1512

Hypoglossal nerve 1217

Hype1tensive

Hypoglycemia 582
angiopathy, turkeys 2789
agents, oral 581
retinopathy, feline, therapy 2570
puppy 1225

Hyperthermia 1015

Hypokalemia 1004
epidemic 3013, 3017
adult cattle 1004
malignant 1027, 1231

Hypokalemic
horses 1179
myopathy
small animals 1201

Burmese cats 1232

Hyperthyroidism 559
dairy cattle 1173
treatment 559
polymyopathy, feline 1201

Hype1trichosis 547

Hypomagnesemia

Hypertriglyceridemia, dogs 170
sheep 2167

Hypertrophic
subclinical, critically ill animals
cardiomyopathy 117

998
gastropathy 388

Hypomagnesemic tetany
neuropathy, Tibetan Mastiff dogs 1231
calves 997
osteodystrophy, dogs 1204
cattle and sheep 996

INDEX

3251

Hypomyelination 1236
ldioventricular rhythm 96
congenital, small animals 1226

Idoxuridine 2745, 2746

Hypomyelinogenesis 1225

Ifosfamide 2726, 2727
congenita, large animals 1225

Heal impaction, horses 258

Hyponatremia, marine mammals 1860

Ileitis pigs 299

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Hypoparathyroidism 1057

Ileocolonic agangliosis 169

.dogs and cats 570
flex aquifolium 3110
idiopathic 1057

Iliopsoas muscle trauma, dogs 1203

Hypophosphatemia 562, 1000

Illicit drug toxicity 3038

Hypophysis 542

Imaging

'

Hypoplastic anemia 1612
diagnostic 1626

Hypoproteinemia
equine lameness 1098
horses 291
liver disease, small animals 437
and hypocaJcemia 571

Imazamethabenz-methyl poisoning 2982,

HypoptyaJism 369

2999

Hypospadias 1331

Imazamox 2982

Hypothyroid neuropathy 1241
poisoning 2999

Hypothyroidism 553

Imazapic 2982
congenital 553
poisoning 2999
dysmaturity in foals 559

Imazapyr 2982
horses 1006
poisoning 2999
juvenile-onset 553

Imazaquin 2982
treatment 557
poisoning 2999

Hypotrichosis, hereditary 846

Imazethapyr 2982

Hypovolemic shock 1665
poisoning 2999

Hypoxia 1412

Imepenem 2656, 2658
workplace exposure 2955

Imidacloprid 2751, 2754

Hypoxic ischemic encephalopathy 2094
lmidazoles 2701
foals 1728
adverse events and toxicity 2702
antifungaJ activity 2701
antimicrobial spectra 2701
dose rates (table) 2702

Ibuprofen 3027
effects on laboratory tests 2703
lchthyobodo spp 1740, 1802
fungal resistance 2701

Ichthyophonus 1739
interactions 2703
lchthyophthirius multijiliis 1754, 1800
mode of action 2701

Ichthyoses, cutaneous 847
pharmacokinetic features 2701

Icterohemoglobinuria 341
therapeutic indications 2702

Idarubicin 2734
lmidazoline decongestant poisoning 3026

Idiopathic

Tmidazolinone poisoning 2999
acute hepatic disease, horses 338

Imidazothiazoles 2638, 2640, 2646
atrophy, thyroid gland 553

Imipramine 1544, 2605
chronic hepatitis 462

Immersion foot, llan1as and alpacas 1854
colitis, horses 607

Immune
cystitis, feline 2383
complex disease 828
facial paralysis 1239
function, excessive 822
focal eosinophilic enterocolitis, horses 291
globulins 2773
hypercaJcemia of cats 565
mediated
hyperkeratosis, llamas and alpacas 1855
arthritis, small animals 1198
hypoparathyroidism 1057
disease, canine, eye, therapy 2569
inflammatory diseases, spinal column
hemolytic anemia 10, 826
and cord 1252
meningitis 823
nasal or perioraJ hyperkeratotic
myopathies horses 1182
dermatosis, llamas and alpacas
polymyositis, horses 1182

1855
thrombocytopenia 4 7, 827
polyradiculoneuritis
reactions, cell-mediated 830
acute 1240
system 8ll
chronic relapsing 1240
memory 817
skeletal hyperostosis, diffuse 124 7
tumors 831
thrombocytopenia 4 7
vasculitis 525
thrombocytopenic pupura 4 7

Immunity
trigeminal neuropathy 1241
adaptive 814

3252

INDEX

Immunity (continued)

mink 1876
cell-mediated 816
small animals 1524
humoral 815

Incontinentia lactis 1389
innate 812

Incubation periods (table) 1325
defects 818

Indian tick typhus 2434

VetBooks.ir

Immunization

Indigestion
active 2767
chronic, run1inants 233
passive 2773
of late gestation 234
program
simple, ruminal 221
breeding cattle (table) 2178
syndrome, vagal, ruminants 233
broodmares (table) 2196

Indigo
neonatal calves (table) 2179
false 3118

Immunodeficiencies
weed 3118
primary 818
wild 3118
secondary 821
yellow 3118
selective 820

Indomethacin 3038
virus-induced 821

Incloxacarb 2577, 2755

Immunodeficiency diseases 818

Inermicapsifer spp infection 2454
combined 820

Infantile glaucoma, rabbits 1959

Immunoglobulins 6

Infarctive hemorrhagic purpura, horses
calf 1625

1182
foal 1625

Infected oil gland, sheep 1170
lmmw1ologic diseases 817

Infectious

Immunology
anemia
type I reactions 823
chicken 2785
type II reactions 826
equine 1250
type III reactions 828
feline 28
type IV reactions 830
arthritis

Immunomodulators, integumentary
large animals 1062
system 2581
pigs 1158

Immunoreactive trypsin 1592
potbellied pigs 1935

Immunostimulants 2581
small animals 1197
lmmunosuppressants 2582
bovine rhinotracheitis virus 1434

Imrnunosuppressive disease, nonhwnan
and abortion 1334
primates 1882
bronchitis, poultry 2909

Immunotherapy 2767
bursal disease, poultry 2837
allergen-specific 854
canine hepatitis 798
in atopic dermatitis 854
vaccination, exotic mammals 2058
nonspecific 277 4
cloacitis, reptiles 1993

Impacted
coryza, chickens 2911
oil gland, sheep 1170
diseases
oviduct, birds 1921, 2896
fish 1778

Impaction, cecun1 and large intestine,
rati tes 1964
horses 262
spinal colum.n and cord 1249

Impedance, vascular 70
urinary system

Im perforate lacrirnal puncta 491
large animals 1499

Impetigo,udderl386
small animals 1508

Impression smears, cytology 1599
enteritis, feline 796

Impulse control aggression, dogs
enterohepatitis, poultry 2835

1563
hematopoietic necrosis, fish 1762

Inborn errors of metabolism 984
hepatitis

Incarceration, internal, horses 261
canine 453

Incidence/incidence rate 2398
large animals 340

Incidental parasites 1311
necrotic 341
lncillus alva1ius 3161
keratocoajunctivitis 512, 2568

Inclusion
laryngotracheitis, poultry 2912
body disease, boid snakes 1994
myopathies, horses 1180
body hepatitis, poultry 2788
necrotic hepatitis 603
coajunctivitis, guinea pig 507
ophthalmia 512
cysts, epidermal 94 7
pancreatic necrosis, fish 1765

Incontinence, urinary
peritonitis, feline 453, 780, 1251
drug therapy 2626
pododermatitis, zoo animals 2052

INDEX

3253

Infectious (continued)

integumentary system 845
polyarthritis, swine 720
llan1as and alpacas 1851
pustular vulvovaginitis 1392, 1434
musculoskeletal system 1042
salmon anemia 1764
nervous system 1222
serositis, birds 2864
urinary system 1496

VetBooks.ir
sinusitis, birds 2841
reproductive system 1329
spleen and kidney necrosis vims, fish 1814
diseases, mink 1876
stomatitis, reptiles 1992
disorders, carnitine metabolism 1233
synovitis, birds 2843
polyneuropathy, Leonberger clogs 1232
tracheobronchitis, clogs 1491
retinopathies 502

Infective

Inkweed 3142
arthritis, large animals 1062

Innate immunity 812
bulbar necrosis, sheep 1170

Innocent heart murmurs 77
endocarditis 121
fnocybe spp 3096, 3097, 3098

Inferior check ligament, horses, desmitis

Inodilators 2531
or sprain 1123

Inorganic arsenicals 3071

Infertility 1328

Inotropes 105, 2529
poultry 2898

Insect
small animals 2229
bite dermatitis 521

Infiltrative
growth regulators 2751, 2755
colonic disease, horses 288
repellents 2753
lipomas 958

Insecticides 2753

Inflammation 2707
toxicity 3058
chemical mediators 2707, 2708 (table)

mink 1875
oral, small animals 361

Insectivores, nutrition 2297
pathophysiology 2707

Inspection

Inflammatory
meat 1644
airway disease
postmortem 1644
horses 1443, 1456
premortem 1644
species approach 2609

Inspissated bile syndrome 439
systemic therapy 2610

Insulin 579
bowel disease
dysregulation syndrome, horses 1006
horses 291

Insulinomas 576, 582
small animals 397
ferrets 1827
cells 1600
lntegumentary system-See also Skin
diseases, spinal column and cord
congenital and inherited anomalies 845

1249
defects of structural integrity 849
disorders, peripheral nerve 1239
introduction 837
liver disease, small animals 481
neoplasms, congenital and hereditary
reticulosis 1252

852

Influenza 2472
pharmacotherapeutics (systemic) 2571
avian 1911, 2902
principles of therapy, topical 844
canine 1479

Intercligital
equine 1447
cysts 862
ferrets 1825
dermatitis
marine mammals 1868
cattle 1080
mink 1873
sheep 1167
swine 1470
fibroma, sheep 1170

Infraspinatus contracture, small animals 1202
furunculosis 862

Infundibular
hyperplasia, cattle 1082
follicular cysts 94 7
palmar and plantar comeclones and
keratinizing acanthoma 944
follicular cysts, canine 862

Inguinal hernias 167
phlegmon, cattle 1081
horses 262

Interferon 2708, 2746

Inhalational

Interleukins 2708
anthrax 593

Intermediate syndrome 3069
pneumonia 1417

Internal
therapy, airway disease 2613
hemorrhage, turkeys 2787

Inhetitccl-See also Hereditary
incarceration, horses 261
anomalies 613
layer 2897
cardiovascular system 76
papillomatosis, pet birds 1908
digestive system 162

Intersex conditions 1329

3254

INDEX

Interstitial
poultry 2934
cystitis, feline 1532
radioactive 559
emphysema 1428
requirement
keratitis 493
pigs 2337
nephritis, small animals 1511
sheep 2347

VetBooks.ir
pneumonia 1413
systemic 2576
atypical bovine 1439
toxicity 558
cattle 1439
lodochlorhydroxyquin 2697
lntersuckling, calves 1552

Iodophores 2741

Interventional

Iodoquinol 2697
radiology 1655
lohexol clearance test 1496
studies 2402

Ionophores 2694, 2796

Inte1vertebral disc disease 124 7
antibiotics 2765

Intestinal-See also Digestive, Gastric,
toxicity 1175, 1242

Gastrointestinal
horses 1186
adenocarcinoma, nonhuman primates
poultry 2862, 2885

1884
loxynil poisoning 2999
adenomatosis, porcine 299

4-Ipomeanol toxicity 1442
allergies 825

!pomoea batatus 1442
capillariasis 2456

Jpratropium bromide 2615
coccidiosis, rabbits 1952

Ipronidazole 2696
diseru:;es

Iridic cysts 49G
horses and foals 281

Iridocyclitis 496, 1699
llamas and alpacas 1853
lridoviruses
pigs 293
fish 1763, 1814
rabbits 194 7
reptiles 1996
ruminants 266

Iris
flukes, small animals 426
atrophy 496
hypersecretion 155
colobomas 496
obstruction, large animals 245
prolapse 1697
salmonellosis, pigs 296

Iron 2540
spirochetosis, pigs 297
deficiency
threadworm 298
anemia 12
trichostrongylosis, sheep and goats 313
horses 2327
viruses, pigs 303
poultry 2933

Intolerance, food, small animals 2379
pigs 2344

Intoxication 2948
requirement, pigs 2337
algal 343
storage disease, pet birds 1919

Intra-abdominal adhesions, horses 259
toxicity 3030

Intra-arachnoid cysts, intracranial 1272
large animals 342

Intracranial intra-arachnoid cyst.s 1272
newborn pigs 3077
lntracutaneous cornifying epitheliomas

Irregular wear, teeth, large animals 177

944

Irritable aggression, dogs 1563
cystic 947

Ischemic
lntradural-extramedullary tumors 1275
necrosis, reptiles 1999

Jntrahepatic bacterial infections, small
neuromyopathy 1244
animals 455

Ischiatic paralysis, cattle 1089
lntramedullary tumors 1276

Islet cell tumors

Intramural inrlusion cysts lfi5
functional 582

In traoc ular
gastrin-secreting 583
inflammation, drug therapy 2568

Islets of Langerhans 579
iajudes, penetrating 1697

!socoma
pressure, tonometry 498
plmijlom 3134

Intubation, nasogastric, horses 1710
wrighlii 1175, 1186
lntussusception, horses 260

Isoflupredone 2712

Inverted papillomas, cutaneous, dogs 953

2,4-D isooctyl ester 2976

Iodides 2706
lsopropanol 2739
poisoning 974

Isopropyl alcohol 2739

Iodine 2741
toxicity 3069
deficiency 558

Isoproterenol 2532, 2610
pet birds 1918
lsoproturon 2982
pigs 2344
poisoning 2998

INDEX

3255

Isosorbide 2624

Japanese
lsospora
aucuba 3106
bitrTOWSi 208
encephalitis 1342, 2472
canis 208
laurel 3106
felis 208

Jejuna] hemorrhage syndrome 270

VetBooks.ir
neorivolta 208

Jerusalem cherry 3114, 3130
ohioensis 208

Jessamine 3138, 3142
iivolta 208

Jiggers 2466
spp 158, 203, 208, 1740, 1998, 2780, 2781, Jimmy fern 3132

2785,2798

Jimmyweed 3134
suis 158, 295, 298, 301

Jimson weed 3140

Isosporiasis, birds 2781

Johne's disease 762

Isosporosis, birds 2781

Johnson grass 3148

Isotretinoin 2585

Joint

Isovaleryl indanedione poisoning 3166
contracture, congenital 620

Isoxaflutole 2982
disease, degenerative

Isoxazolines 2755
large animals 1063

Isoxazolyl penicillins 2656
poultry 2881

Israel turkey meningoencephalitis 2892
small animals 1197

Israeli spotted fever 2434
fractures, small animals 1199

Isthmus catagen cysts 947
ill

Italian arum 3106
foals 589

Itch mite
goats 1094
cattle 917
pigs 1156
sheep 918
trauma, small animals 1198

Itching 843

Josamycin 2687

Itraconazole 2574, 2701, 2702

Jowl abscess, swine 734

Iva aceTosa 3128

Joyeuxiella pasqualei 422

Ivermectin 2576, 2647, 2648

Jug a

Ivory Coast ebolavirus 2470
plicifera 808

Ivybush 3144
silicula 808
lxodes

Juglans nigra 3134
affi,nus 934

Juin virus 2476
cavipalpus 934

Juquitiba virus 2470
cornuatus 1315

Juvenile
drakenbergensis 934
honnone analogues 2752
gibbosus 934
onset panhypopituitarism 549, 553
hirslii 1315
pustular psoriasifonn dermatitis, pigs 979
holocyclus 935, 1243, 1315, 2437
jellisoni 934
kashmiricus 934

K
kazakstani 934

Kadam virus 937
lewisi 934

Ka.fir 3148
minor934

Kalaazar 2442
muris 934

Kalanchoe spp 3112
neotomae 934

Kalicephalus spp 1997
pacijicus 659, 698, 803, 934

Kalmia spp 3094, 3144
pavlovskyi 934

Kanamycin 2663, 2666
persulcatus 659, 934, 2435

Kaolin-pectin formulations 2553
ricinus 23, 659, 772, 774, 934, 1299,

Kasen 887

2441,2475,2481

Keds, sheep 893
rubicundus 934, 940, 1243, 1315

Kennel
scapularis 659, 698, 803, 934, 1315
cough 1491
sinensis 934
tick 936
spp 19, 659, 698, 803, 927, 928, 934, 1314, Keraphyllocele, horses 1109

2421,2435,2437,2441,2477,2785

Keratinized cutaneous cysts 947
tasmani 2437

Keratinizing acanthoma, infundibular 944

Ixodid ticks 926, 928

Keratitis

J
and corneal sequestration 494
feline herpesvirus, therapy 2566

Jaagsiekte 1477
interstitial 493

Jack sores 904
sicca 831

3256

INDEX

Keratitis (continued)

1964, 1984, 1992,2006,2041,2089,
superficial 493

2092,2098,2192,2617,2631,2654,
ulcerative 494

2655,2659,2665,2669,2671,2676,

Keratoacanthoma 944

2680,2684,2692
avian 2855

Kleingrass toxicosis 343

VetBooks.ir

Keratoconjunctivitis

Klossiella 1998
infectious 512, 2568

Knap weed
mycoplasma infection 1352

Russian 3126
proliferative 957
yellow 3128
sicca 492

Knernidocopl es

Keratomas 948
rnutans 2878
horses 1109
p'ilae 1906

Kcratosis

Knobrot 1373
actinic 945

Knuckling, horses 1150
senile 945

Kochia 3049
solar 945
scop0,1i0, 977, 1282, 3144

Kerion reaction, clogs 874

Kogia breviceps 1864

Kerosene poisoning 3053

Koi

Ketan1ine 2110
herpesvirus 1812

Ketoaciclosis, in diabetes 581
sleepy disease 1814

Ketoconazole 2701, 2702, 2573

Koilocytic atypia 952

Ketonemia, cattle 1024

Koilocytosis 952

Ketones 1595

Krabbe disease 1235
in urine 1617

Kunkers 642

Ketoprofen 2604, 2719

Kyasanur Forest virus 932, 2466, 2472

Ketosis
cattle 1024

L
estate 1022

L-Glyceric acicluria 1232
pregnancy, ewes and does 1021

La bouhite 1475
rabbits 1957

La Fora disease 1236

Kicking

Labels, pet foods 2373
cattle 1552

Laboratory
horses 1548
animals 1836

Kidney-See also Renal
amphibians 1743
acidosis, small animals 1520
bedding 1840
cytology 1610
colony monitoring 1841
disease
feeding 1840
chronic, small animals 1512
housing 1839
stages 1512
management 1839
failure, small animals 1512
mice and rats 2032
injury, acute, small animals 1516
physiologic data (table) 1842
polycystic 1497
regulatory requirements 1836
tubular defects, small animals 1520
sanitation 1841
tumors, small animals 1522
used in research 1838
worm infection
water 1840
giant 2456
private practice, diagnostic procedures
mink, clog 1511

1590
swine 1502
rodents, infectious agents (table) 2033

Killer bees 3164
samples, collection and submission 1584

Kilovoltage potential 1626

Labrador Retriever myopathy 1200, 1233

Kinky back, poultry 2881

Lacazia loboi 1864

Kissing

Lacerations 1707
lesions (teeth) 363
horses 1716
spines 1146

Lacrimal
ulcers (teeth) 363
apparatus 490

Klamath weed 3144
puncta, imperforate 491

Klebsiella
sac inflammation 491
pneurnoniae 1263, 1345, 1370, 1374,

LaCross encephalitis 2468

1492, 18�5. 1879, 1945,2191,2196,

13-Lactam antibiotics 2652

2200,2235,2663,2671
antimicrobial activity 2652
spp 121, 671, 1263, 1353, 1359, 1362,
bacterial resistance 2653

1368, 1374, 1449, 1508, 1872, 1896,
mode of action 2652

INDEX

3257

Lactate dehydrogenase 1592
intestine

Lactation tetany, horses 987
congenital anomalies 168

Lactic
diarrhea 157
acid 2739
impaction, horses 262
acidosis 222
mouth bowel worm, cattle 311

VetBooks.ir

Lactobacillus
periwinkle 3108
acidophilus 2343
stomach worm, cattle 308
spp 444, 1083, 1896, 2291, 2370,
strongyles, horses 316

2408
turkey louse 2876

Laclococcus spp 1810

Largemouth bass virus 1764

Lactulose 2560

Larkspur 3122

Lady-of-the-night 3106

Larva migrans

Laegenoi·hynchus
cutaneous 417, 2458
aculus 1864
neural 416
albiroslris 1869
ocular 415, 1312
obliqitidens 1863
visceral 415, 2457, 2460

Lagenidiosis 641

Larval

Lagenidium spp 641
cyathostominosis, horses 317

Lagomorphs, nutrition 2300
inhibition 304

Lagophthalmos 489
worm infection, rabbits 1953

Laguna Negra virus 2470

Laryngeal

Lamb
chondropathy 1419
rejection 1556
disorders 1419
stealing 1556
edema 1419
feeding 2349
hemiplegia, horses 1458
formulas 2350
necrobacillosis 1429

Lambda-cyhalotlu·in 2750
paralysis 1420

Lambing management 2168
acquired 1238

Larnbkill 3144
congenital 1231

Larnbliasis 211
polyneuropathy, geriatric-onset,

Lambliosis 211

1238

Lamellar suppuration, sheep
tumors, small animals 1485

1171

Laryngitis 1413, 1419

Lan1eness-See also Fractures
necrotic 1429
cattle 1066

Laryngotracheitis, infectious, poultry 2912
risk factors 1070

Lasalocid 2765, 2796
exan1ination, horses I 097

Laser therapy 2083
fescue 3016

Lasionycleris noclivaga,ns 1303
goats 1092

L-Asparaginase 2730, 2734
horses 1096

Lassa fever 2474
pigs 1151

Lateral
breeding 1070, 1162
ce1vical cyst 165
potbellied pigs 1934
palmar nerve block, horse 1105
sheep 1166

Lates calcarifei· 1764
postdipping 629

Lathyrus
small animals 1192
odoratus 2787

Laminitis
spp 1458
cattle 1082

Lalrodectiis
horses 1109
bishopi 3162
goats 1095
geometricus 3162
septic, sheep 1171
heperns 3162

Laminosioples cysticola 2878
mactans 3162

Lan1ziekte 605
spp 3162

Lancet fluke 327, 2246

Laurel 3144

Langerhans cells 1604
blanco 3146

Lankesterellosis, birds 2781
cherry 3146

Lantana
rosa 3146
cainara 344, 977, 3094

Lavage, wounds 1703
spp 330, 3124

Lawsonia inlmcellulaiis 158, 197, 220,

Large

289,296,300,354,355,359, 1824,

American liver fluke 327

1878, 1948,2023,2161
chicken louse 2876
infection, foals 289

3258

INDEX

Laxatives 2559

Leporine dysautonomia 1257

Layer

Leprosy 692, 2426
false 2897

Leptomeningeal cysts 1230
internal 2897

Leptospira

Laying

Autumnalis 650, 1862

VetBooks.ir
backyard poultry 1818
bijlexa 646
hens, nuttition (table) 2916
borgpetersenii 646, 654

L-Carnitine 110

Bratislava 647, 650, 652, 653, 654, 1343

LD50 2949

Canicola 650, 653, 654, 1334, 1862, 2058,

Lead poisoning 1458, 3078

2133,2655
gerbils 2012

Grippotyphosa 453, 646, 650, 652, 653,
mink 1875

654, 1334, 1340, 1345,2059,2133
pet birds 1924

Hardjo 646, 652, 653, 654, 1334, 1345,
poultry 2861

2059,2133

Leakers, teat 1389
hardo-prajitno 646, 1345

Lechiguana 879

Icterohaemorrhagiae 647, 650, 652, 653,

Lechuguilla 3136

654, 1334, 1346, 1862,2058,2133

Leeches
interrogans 10, 453, 508, 646, 650, 652,
reptiles 1996

653,654, 1334, 1340, 1343, 1345,
zoonotic diseases 2462

1346, 1508, 1511,2058

Left
kirschneri 646, 652, 654
displaced abomasum 238

Pomona 349, 453, 508, 647, 650, 652, 653,
dorsal displacement of colon, horses 264

654, 1334, 1340, 1343, 1345, 1862,
heart failure 101

2059,2133
laryngeal hemiplegia 1458
type kennewicki 652, 1345
shift 58
spp 362, 508, 646, 830, 1333, 1340, 1341,

Leg

1343, 1345, 1836, 1850, 1862,2048,
banding, birds 1889

2052,2058,2125,2133,2152,2163,
deformity, birds 1895

2415,2665,2676
edema syndrome, turkeys 2884

Leptosplrosis 646, 2426
mange
cattle 653
cattle 916
and abortion 1334
horses 919
dogs 453, 650
pet birds 1906
goats 653
weakness syndrome, pigs 1164
and abortion 1340

Legg-Calve-Perthes disease 1194
horses 652

Legionella 624
marine mammals 1862

Leiomyomas 961
people 647

Leiomyosarcomas 961
pigs 654

Leishmania
and abortion 1343
braziliensis 800, 2442
ruminants 653
chagasi 800
vaccination, exotic man1mals 2058
donova,ni 1511

Lepus 1937, 1950
infantum 800

Lernaea spp 1740, 1748, 1757, 1795,
mexicana 937, 2442

1808
peruviana 2442

Lesser liver fluke 327
spp 39, 407, 456, 505, 800, 887, 1881,

Letdown failure, milk 1387

2574,2577,2699

Lethal acrodermatitis, dogs 852
tropica 2442

Leucocytozoon

Leishmaniosis 456, 800, 2442
andrewsi 2783
visceral 800
caulle1yi 2783

Lemur calla 1876
sabrazesi 2783

Lens 499
schoutedeni 2783
displacement 501
simondi 2783
luxation, anterior 1699
smithi 2783

Lentigo 849
spp 886, 1904, 2780, 2783, 2875

Lepeophtheirus

Leucocytozoonosis, birds 2783
salmonis 1764, 1808

Leuconostoc 1679
spp 1757

Leukemia

Lepiota
bovine 743
helveota 3100
feline 790
spp 3096
primary 14

INDEX

3259

Leukemoid response 58

Lime-sulfur toxicity 3070

Leukocyte

Limnatis nilolica 2462
adhesion deficiency 819, 852

Limonene toxicity 3064
disorders 56

Limping syndrome 1481

Leukocytosis 57

Lincomycin 2690, 2692

VetBooks.ir

Leukodystrophy

Lincosa.inides 2690

Dalmatian 1234
adverse effects and toxicity 2692
fibrinoid 1234
antimicrobial activity 2690
globoid cell 1234, 1235
bacterial resistance 2690

Leukoencephalomalacia 3006
dosages (table) 2692
equine 3017
effects on laboratory tests 2692

Leukoencephalomyelopathy, Rottweilers
interactions 2692

1229
mode of action 2690

Leukogran1 abnormalities 57
pharmacokinetic features 2691

Leukopenia 57
therapeutic indications 2692

Leukosis, bovine 7 43
withdrawal times 2692
enzootic 743

Lindane 2749, 2754
lymphoid, poultry 2851
toxicity 3060
skin, poultry 2850

Lingua dissecta 365

Leukotrienes 2709

Linguatula se1Ta,la 2466

Levamisole 2646

Linognathus 2751

Levetiracetam 1545, 2598
africanus 911

Libido, poor
ovillus 911
cattle 1552
pedalis 911
stallions 1550
setosus 913
swine 1555
stenopsis 912

Libostrongylus douglassii 1965
vituli 910, 2576

Lice 908

Linseed oil, raw 2556, 2559
fish 1808

Linum spp 2960
llamas and alpacas 1854

Linuron 2982
ma.iine mammals 1865
poisoning 2998
nonhuman primates 1881

Lip
poultry 2876
bot, horses 315

Lidocaine 2537, 2615
fold dermatitis, small animals
intravenous 2558

364

Life support 1671
lacerations, large animals 213

Ligan1ent
and leg ulceration, sheep 872
cranial cruciate, rupture 1198
tight, Shar-Pei 163
injury, collateral, horses 1131

Lipase 1592
medial palmar intercarpal, horses 1126
serum 1593

Lightning stroke and electrocution 655

Lipeurus caponis 2876

Lignophagia, horses 1548

Lipidosis, hepatic

Ligustrum spp 3144
birds 1895

Lilium
feline 456
longijf,orum 3112
large animals 346, 1018
tig1inum 3112
mink 1876

Lily

Lipofuscinosis 1045

African blue 3104
ceroid 1234, 1236

Atamasco 3118

Lipomas 958
conval 3108
infiltrative 958

Easter 3112, 3118
pedunculated, horses 261
flamingo 3106
pet birds 1915
of-the-valley 3108

Lipomatosis 360
rain 3118
diffuse 958

St. Bernard's 3108

Liponyssoides sanguineus 2436,
trumpet 3112

2462
zephyr 3118

Lipoptena depressa 893

Limb

Liposarcomas 959
defonnities, foals 1046
pet birds 1916
paralysis 1259

Lippia rehmanni 977

Limber leg, cattle 1045

Lisdexamfetamine 3039

Limbemeck, poultry 2889

Lisinopril 3032

3260

INDEX

Lissencephaly, small animals 1224

Lobar pneumonia 1413

Listerellosis 656

Lobomycosis, marine mammals 1864

Listeria

Lobular
ivanovii 2426
dissecting hepatitis 466

VetBooks.ir
monocytogenes 513, 656, 658, 1158,
pneumonia 1413

1263, 1336, 1339, 1340, 1343, 1346,

Local anesthetic

1935, 1947,2006,2426,2839
eye 2566
spp 329, 657, 1337, 2048, 2177, 2376,
techniques 2111

2655,2894

Localized anaphylactic reactions 824

Listeriosis 656, 2426

Lochia 2228
abortion

Lockjaw 611, 1255
cows 1336
pet birds 1896
goats 1340

Locomotion scoring, cattle 1068
sheep 1339

Locoweed 3136
poultry 2839
toxicity 59, 138
rabbits 194 7

Locust tree 3130

Listonella spp 1809

Loin disease, cattle 606

Lislrophorus gibbus 1953

Loli um

Lithium 2605
arundinacemn 3016

Lilomosoides carinii 2030
perenne 3154

Liver-See also Hepatic
rigidum 3153
abscesses

Lomustine 2727, 2731
cattle 352

Lone atrial fibrillation 95
large animals 340

Lone-star tick 928
biopsy 438

Longus capitis muscle, rupture, horses
congenital anomalies 169

1464
cytology 438

Loop diuretics 103
disease

Loperamide 2554, 3042
horses, nutrition in 2329

Loratadine 3025
inflammatory, small animals 481

Lorazepam 1544, 3034
pet birds 1915

Lordosis, congenital, foals 1047
large animals 329

Lotus spp 2960
small animals 429

Louping ill 1299, 2474
fluke

Louse flies 894
cat 2448

Low
common 324
grade fibrosarcomas 956
giant 326, 327

4-point block, horse 1104
large American 327

Lower
lesser 327
esophageal sphincter achalasia 166
small 2448
motor neurons 1210
small animals 427, 484
respiratory tract inflammation, horses
hemorrhage score, poultry 2820

1456
syndrome, fatty, poultry 2820

Loxiodes bailleui 2826

Lizard poisoning syndrome, cats 429

Loxosceles

Lizards 1975
reclusci 3162
nutrition 2307
spp 3162

Llamas and alpacas 1844

Lucilia
anesthesia 1847
caesar 898
abortion 1346
cuprina 897, 898, 2753
clinical pathology 1847
illuslris 897
congenital and inherited anomalies 1851
seJ"icala 897
dental development and care 1850
spp 895, 897
diseases 1851

Lufenuron 2577, 2756
drugs used in (table) 1845

Lumbosacral
handling 1846
junction abnormalities, horses
herd health 1850

1147
management 1844
stenosis, degenerative 1246
neonatal care 1850

Lumpy
nutrition 1846
jaw 590
parasite control 1850
zoo animals 2053
reproduction 1848
skin disease 868
vaccinations 1850
wool 858

INDEX

3261

Lung
leukosis, poultry 2851
eye-trachea disease, turtles 1995
tun10rs of the skin 961
fluke disease 2448

Lymphoma
flukes, small animals 1483
associated with hypercalcemia 564
mites, marine mammals 1865
canine 40, 2737

VetBooks.ir
nematodes, small animals 1483
feline 790
parenchymal disease 1664
ferrets 1826
tumors, small animals 1485, 1486
hepatic, small animals 4 71

Lungworm
malignant, bovine 7 43
infection 1421
pet birds 1917 '

marine mammals 1865

Lymphopenia 61
treatments (table) 1425

Lymphoproliferative disease, turkeys 2849

Lupines 3144

Lymphosarcoma
poisoning 3018
associated witl1 hypercalcemia 564

Lupinosis, mycotoxic 343, 3006, 3018
bovine 743

Lupinus
cutaneous 852, 961
caudatus 162, 618
feline 790

Joimosus 618
lymphohistiocytic 963
la.xifl,orus 618
nodular 963
nootkatensis 618
pet birds 1917
sericeus 162, 618
sporadic bovine 743
spp 1044, 3018, 3144
subcutaneous 963

Lupoid demiatosis, hereditary, dogs 851

Lynchia spp 894

Luteal cystic ovary disease 1356

Lyngbya 2956

Luteinizing hormone 542

Lynx rufus 23
small animals 1624, 2223

Lynxacariasis 924

Lutzoniyia spp 887, 2442

Lynxacarns rndovskyi 924

Luxations

Lyophilized
coxofemoral,cattle 1087
canine albumin 1681
patellar,cattle 1087
concentrates of clotting factors 2542
horses, emergency care 1713

Lyperosia 2751

Lyme disease 120, 659, 2420

Lysosomal storage disorders 1234, 1235
serology 1622
large animals 1223

Lymecycline 2679
small anin1als 1225

Lyninaea spp 604

Lyssaviruses 24 78

Lymph nodes, cytology 1604

Lymphadenitis 63
caseous, sheep and goats 63, 2167

M
streptococcal 734

Ma huang poisoning 3032

Lymphadenopathy, tickbome 931

Macaca 2472

Lymphangiectasia 168

Jascicularis 1876
treatment 406
niulalla 1876

Lyrnphangioma 959
nemestrina 1876

Lymphangiosarcomas 960

Macadaniia

Lymphangitis 63
integrifolia 2967
epizootic 639

/,elmphylla 2967
ulcerative, horses 66

Macadamia nuts, toxicity 2967

Lymphocystis disease, fish 1814

Macaw wasting disease 1909

Lymphocytes 6, 57, 58, 1600, 1607, 1613

Macdonaldius oscheri 1996

Lymphocytic

Machaeranlhera 3086
choriomeningitis 831, 2474

Machupo virus 2476
plasmacytic

Mackerel poisoning 1860
enterocolitis, horses 291

Macracanthorhynchosis 2462
gastritis 388

Maci·acanthorhynchus
stomatitis, cats 362
hirudinaceus 321, 2462
portal hepatitis feline 482
ingens 421
thyroiditis 553
spp 321, 421
tumors 836, 961

Macrocyclic lactones 2640, 2647, 2750,

Lymphocytosis 61

2754

Lymphohistiocytic lymphosarcoma 963
environmental effects 2647

Lymphoid
in cattle 2648
hyperplasia, pharyngeal, horses 1459
in clogs and cats 2649

3262

INDEX

Macrocyclic lactones (continued)

Malassimilation syndromes, large
in horses 2649
animals 353
in small ruminants 2649

Malathion 2750, 2754
in swine 2649
toxicity 3066

Macrocytes 1611

Malayan fiJaiiasis 2458

VetBooks.ir

Macrocytosis 8

Maldigestion 168

Macroglossia 163
dogs, nutrition in 2385

Macrolide antibiotics 2558, 2687

Male fertility, preservation 2231
adverse effects and toxicity 2689

Maleic hydrazide 2982
antimicrobial activity 2688

Malfo1mation
bacterial resistance 2688
of digits 1046
classes 2687
tumors
dose rates/dosages 2689, 2690 (table)

brain 1272
general properties 2687
spinal cord 1276
interactions 2689

Malignancy, hypercalcemia of 563
milk discard times (table) 2691

Malignant
mode of action 2688
cataiThal fever 758
therapeutic indications 2689
edema 604, 1171, 2168
withdrawal times (table) 2691
fibrous histiocytomas 957, 959

Macrophages 5, 1600, 1603, 1605, 1607
hair matrix tumor 949

Macrorhabdosis 1903
head catarrh 758

Macrorhabdus 1899
histiocytosis 1272
ornithogaster 1903
hyperthermia 1027, 1231

Macrothrombocytopenia, hereditary,
horses 1179

Cavalier King Charles Spaniels 47
pigs 1176

Mad
small animals 1201
dog syndrome 1304
lyn1phoma, bovine 743
itch 1300
melanoma, oral 367

Madagascar pe1iwinkle 3108
melanomas, dogs 968

Maduramicin 2796
pilomatricomas 949

Madurella spp 640, 2701
trichoepitheliomas 948

Maedi 1250, 1475

Malocclusion 177-See also Dental,

Mafenide 2675

Dentistry, Teeth

Maggots 897
chinchillas 2008
rat-tailed 903
guinea pigs 2021

Magnesiwn 1592
potbellied pigs 1931
deficiency
rabbits 1955
horses 2327
small animals 184
poultry 2934

Mainmalian tuberculosis, zoo animals
equine dietary supplement 998

2053
metabolism disorders 995

Mainmals (zoo), nutrition 2293
requirement, pigs 2337

Manunary
salts 2560
cytology 1610

Magnetic resonance imaging 1636
development, precocious, in heifers 1387

Magnolia officinali,s 1543, 1567
edema, sows 1373

Maintenance fluids 1684
fibroadenomatosis, cats 1396

Malabsorption 156, 168
hypertrophy, feline 1396, 1404
dogs, nutrition in 2385
tumors 1403
idiopathic intestinal, treatment 406

Mammillitis
mechanisms (table) 401
bovine herpes 1385
small intestine, treatment 405
bovine ulcerative 1385
syndrome, poultry 2840

Management 2066
syndromes, small animals 400
backyard poultry 1816

Malacosoma americanum 1344, 2960
beef cattle 2119

Malaria
calves 2122
nonhuman primates 2444
calving 21 78
pigeon 2783
chickens

Malassezia
growing 2920
pachyderrrwtis 529, 856, 2574
laying 2922
spp 529, 533, 844, 852, 853, 855, 863,
dairy cattle 2135

864,970,974,980, 1904,2440,2575,
fish 1784

2702,2739
goats 2147

INDEX

3263

Management (conliniied)

Maple
horSPS 2151
red 3126
laboratory animals 1839
syrup w·ine disease 1234
lambing 2168

Marble spleen disease, birds 2833

VetBooks.ir
llan1as and alpacas 1844

Marbofloxacin 2619, 2670, 2673
marine man1mals 1856

Marburg hemorrhagic fever 2474
mink 1870

Mare reproductive loss syndrome 1343
neonate 2087

Marek's disease 2849
pain 2104
backyard poultry 1822
pigs 2160

Mares
potbellied pigs 1929
abortion 2195
poultry 2919
breeding soundness 2189
rabbits 1937
partmition 2196
ratites 1960
postpartum 2200
reproduction
pregnancy determination 2194
cattle 2171
vaccination schedule 2196
goats 2182

Marey reflex 68
horses 2187

Margaropus
pigs 2201
reidi 935
potbellied pigs 1931
spp 928, 935
sheep 2212
wileyi 935
small animals 2219
winlhemi 935
reptiles 1968

Marijuana 3106
sheep 2164
toxicity 3041
small animals 2169

Marine man1mals 1856
zoo animals 2046
anesthesia 1857

Manchester wasting disease 1052
bacterial diseases 1861

Mandibular
envirorunental diseases 1857
osteomyelitis, zoo animals 2053
management 1856
prognathism, birds 1895
mycotic diseases 1863

Manganese
neoplastic diseases 1870
deficiency, poultry 2933
nut:tition and nutlitional diseases 1859, 2297
requirement, pigs 2337
parasitic diseases 1865

Mange 914, 2462
restraint 1856
cattle 914
viral diseases 1867
dogs and cats 920

Marking behavior
horses 918
cats 1572
llamas and alpacas 1854
clogs 1569
marine mammals 1865

Mmmola monax 928
nonhuman primates 1881

Maropitant 2549
pet birds 1906

Marrow aspiration and biopsy 14
pigs 919

Marsilea drummondii 1281
potbellied pigs 1934

Marsupials, nutrition 2298
sheep and goats 917

Massage 2081

Mango fly 902

Mast cells 1603

Mannheimia
sarcomas 963
granulomatis 879
tumors, cutaneous 963
haemolytica 341, 533, 765, 1263, 1367,

Masticatory myositis, dogs 1201

1412, 1431, 1432, 1436, 1438, 1469,

Mastitis

1472, 1474, 1863,2059,2131,2660,

COWS 1358, 1362

2688,2767,2769,2771
ewes 1367
associated bovine respiratory disease
goats 1367

1436
large animals 1358
spp 765, 2124, 2164
mares 1368
pneumonia, sheep and goats 1474
mink 1872

Mannihol esculentum 2960
nocardial 666

Mannitol 2560, 2624
rabbits 1949
cx-Mannosidosis 984, 1234, 1235
small animals 1396

J3-Mannosidosis 984, 1093, 1234
sows 1368, 1373

Mansonia spp 889, 2458

Mastocytomas 963

Manson's eyewom1, poultry 2830

Mastocytosis 852

Manual therapy 2081

Masturbation, bulls 1551

3264

INDEX

Maternal aggression, dogs 1565

Melanocytic tumors 967

Matrical carcinoma 949

Melanocytomas 967

Matrix cysts 94 7

Melanocytosis 852

Mature fat cells 1602

Melanoderma 523

Mavacoxib 2720

Melanoides tuberculata 1754, 1757

VetBooks.ir

Maximum residue limits, drugs 2519

Melanomas 967, 1603

May-Grunwald Giemsa stain 1598
malignant, oral 367

Mayflower 3108
pigs 852

Mazama930
potbellied pigs 1934

MCPA 2982

Melanophages 1603
poisoning 2997

Melatonin 2581, 2607

MCPB2984

Melena 156
poisoning 2997

Melengestrol acetate 2760

MDMA toxicosis 3040

Melia azedarach 3136

Meadow saffron 3108

Melilotus

Measles
alba 3134, 3156
mumps, and rubella vaccination, exotic
ojficinalis 3134, 3156
mammals 2059

Melioiclosis 661, 2426
nonhuman primates 1882

Melophagus ovinus 893, 894

Meat

Meloxicam 2716, 2720, 3037
inspection 1644

Melphalan 2727, 2731
unwholesome, detection 1646

Membranoproliferative glomerulonephritis

Mebendazole 2645

829

Mechanically induced myopathy, poultry

Menacanthus

2884
cornutus 2876

Mechanobullous diseases 850
stramineus 2876

Mechlorethamine hydrochloride 2726

Menangle virus 2474

Mecillinam 2655

Menichlopholan 2650

Mecistocirrus digitatus 308, 312

Meningeal

Meclizine 3025
cysts 1230

Meclofcnan1ic acid 2604, 2718
sarcomatosis 1273

Meconium impaction 2096

Meningioangiomatosis 1272

Mecoprop 2984

Meningiomas 1273
poisoning 2997

Meningitis 1262

Mecletomidine 2602
aiteritis, steroid responsive 1229

Medial
aseptic, dogs 1229
coronoid process, fragmented,
immune-mediated 823
dogs 1196

Meningocele 1222
humeral condyle, osteochonclrosis,

Meningoencephalitis 1262
dogs 1196

Israel turkey 2892
palmar intercarpal ligament, hcu-ses 1126

Meningoencephalocele 1222

Medicago

Meningoencephalomyelitis
saliva 977
feline nonsuppurative 1252
spp 976, 977
granulomatous, clogs 1252, 1264

Medical causes of aggression, dogs 1565
pyogranulomatous 1264

Medium stomach worm, cattle 308

Meniscus injuries, horses 1141

Medroxyprogesterone acetate 2581

Menopon gallinae 2876

Medulloblastomas 1272

Mental health, ofveterinariai1s 1580

Megabacteria 1903

Meperidine 2602, 3042

Megaesophagus

Mephenytoin 2600
congenital 166, 1233

Mephobai·bital 3035
dogs 370

Merbromin 2741
llamas and alpacas 1853

6-Mercaptopurine 2732

Megalocytiviruses, fish 1764

Mercuric bichloride 2741

Megasphaem elsdenii 226

Mercury poisoning 974, 3080

Megestrol acetate 2225, 2546, 2225, 2581
poultry 2861

Megninia

Meriones
cubitalis 2878
spp 2011, 2013
ginglymura 2878
unguiculates 2011

Meiacanthus spp 1779

Merkel cell tumors 952

Melanoconion spp 1293

Meropenem 2658

Melanocyte-stimulating hormone 542

Merphos poisoning 2999

INDEX

3265

MERS2474

Methanol toxicity 3070

Mesalamine 2555

Methicillin 2656

Mescal bean 3134
resistant Staphylococcus aurnus

Mesenchymal cells 1601
infections 2426, 2573

Mesenteric

Methimazole 560

VetBooks.ir
rents 261

DL-Methionine 2625
torsion, small intesHne, pigs 296

Methiuron poisoning 2998

Mesna 2726

Methocarbamol 2589, 3036

Mesocricetus aura/us 2021

Methomyl toxicity 3060

Mesomycetozoans, amphibians 1739

Methoprene 2755

Mesotrione 2984

Methoprim 2674

Mesquite 3130

Methotrexate 2728, 2732

Metabolic

Mcthoxychlor 2749, 2754, 3060
body weight 2367
toxicity 3061
bone disease

Methyl bromide 2984
amphibians 1741

Methyl isothiocyanate 2984
pet birds 1919

Methyl parathion toxicity 3066
reptiles 2001

Methylbenzoquate 2796
disorders 984

Methylphenidate 3039
affecting liver, small animals 468

Methylprednisolone 2712
generalized, nervous system 1234

Methylxanthine bronchodilators
large animals 1223

2531, 2611
peripheral nerve 1241
dosages (table) 2611
production-related 985

Metobromuron 2984
osteodystrophies 1054
poisoning 2998
storage disorders, spinal cord 1249

Metoclopramide 2549, 2556
syndrome, equine 548, 1006

Metocurine 2587

Metabolism of drugs 2496

Metolachlor 2970, 2984

Metabolizable energy 2365
poisoning 2999

Metacarpal disorders, horses 1121

Metomidate 1753

Metagonimiasis 2446

Metoprolol 76, 3033

Metagonimus

Metorchiasis 2448
miyatai 2446

Meto1'chis
spp 2446
albidus 429
takahashii 2446
conjunctus 429, 485, 2448
yokogawai 427, 2446
spp 429

Metaldehyde poisoning 3070

Metosulam 2984

Metam (sodium and isothiocya.nate) 2984
poisoning 2998

Metaphyseal osteopathy, small

Metoxuron poisoning 2998
animals 1204

Metribuzin 2984

Metapneumovirus, avian 2904

Metric system prefixes and symbols

Melarhizium 1993

(table) 3183
anisopliae 2753

Metritis

Metarubricytosis 62
acute puerperal 1368

Metastatic
contagious equine 1371
brain tumors, hematogenous 1272
large animals 1368
pneumonia, cattle 1442
small animals 1397
tumors

Metrnliasthes lucida 2829
liver, small animals 4 71

Metronidazole 2555, 2696
lung, small animals 1486

Mevinphos toxicity 3066
skin 969

Mexiletine 76, 2537

Metastrongyles causing CNS disease 1313

Mezlocillin 2655

Met,astrongylus

Miamiensis spp 1801
ap1i 1421

Mibolerone 2607
pudenclotectus 1421

Mice 2025-See also Rodents
salmi 1421
as laboratory animals, management
spp 1422, 1425

2032

Metatarsal bone fractures, horses 1124
as pets, diseases of 2028

Metatarsus disorders, horses 1131
biology 2025

Methacycline 2679
husbandry 2025

Methadone 3042
neoplasia 2030

Methan1phetamine 3039
physical examination 2027

3266

INDEX

Mice (continued)

Mineral
respiratory mycoplasmosis 2028
deficiencies
tapeworm 2454
horses 2325
typhus 2436
pigs 2344
zoonotic risk 2032
poultry 2930

Miconazole 2701
mixtures, sheep 2353

VetBooks.ir

Microangiopathic hemolysis 12
requirements

Microbiology
beef cattle 2552, 2262
in-house 1595
dairy cattle 227 4
san1ples 1585
dogs and cats 2372
specimen selection and processing 1596
goats 2309

Microchipping, pet birds 1889
horses 2317

Micrococcus spp 476, 864, 1896, 1991
pigs 2336

Microcystis spp 977, 2956
poultry 2917

Microcytes 1611
sheep 2346

Microfilariae, birds 2782

Mineralocmticoids 573

Microfilaricide treatment for heartworrn

Minimal
disease 135
inhibitory concentration 2634

Microglossia 163
myopathy, poultry 2886

Micropolysporafaeni 1441, 1442

Mink 1870

Microptems salmoides 1764
bacterial diseases 1871

Microsporidia, fish 1811
distemper 1873

Microsporidiosis 2444
encephalopathy, transmissible 1874

Microsporidium 1740
management 1870

Microspo1wn
nutritional diseases 1874
audouinii 873
poisonings 1875
canis 873, 874, 875, 876, 1826, 1864,
prion disease 1874

1949,2007,2574
viral diseases 1872
gallinae 1823
viral enteritis 1873
gypseum 872, 874, 875, 876, 2007

Minocycline 2679, 2682
nanum 873, 874, 875, 1826, 2574

Mirounga angustirost1is 1864
spp 872, 1832, 1835, 1880, 1904, 2440,

Mirtazapine 2546, 3035

2573,2575,2699,2704

Misoprostol 2552

Microlhoracius cameli 1854

Mistletoe 3112

Microvascuiar dysplasia 446

Mites

Micrnrns spp 3159
air sac 1906, 2901

Micturition disorders, small animals 1524
feather 1906, 2878

Midazolarn 2600
infestation 914

Middle East respiratory syndrome 2474
marine mammals 1865

Midges
nasal, canine 1480
biting 887
pet birds 1906
owl 887
poultry 2877

Mifepristone 2607
psoroptic 521

Milbemycins 2638, 2647, 2750
rabbits 1953

Milia 947
reptiles 1996

Milk
sarcoptic 521
allergy 824
scaly face or leg mite 1906
bloody 1389

Mithrarnycin 569, 2733
ejection (letdown) failure 1387

Mitochondrial myopathy 1233
fever

Mitomycin 2733
cows 988

Mitotane 545, 2580, 2730, 2734, 2735
sheep and goats 991

Mitotic inhibitors, antineoplastic 2732
spots 321

Mitoxantrone 2729, 2733, 2734
thistle 2561

Mitral
vetch 3138
regurgitation 70

Milker's nodes or nodules 868, 2474
stenosis 85

Milking parlors, reluctance to enter 1553
valve dysplasia 84

Milkweed 3136

Mobitz type II block 94

Miller's disease 1052

Mock

Milo 3148
azalea 3104

Milrinone 2532
orange 3146

Milzbrand 593

Modulators, ruminoreticular 2563

INDEX

3267

Moist dermatitis, rabbits 1957
diseases

Mokola virus 2478
large animals 213

Moldy
small animals 361
corn toxicosis 3011

Moxalactam 2659
sweet potato toxicity 1442

Moxidectin 2576, 2640, 2647, 2754

VetBooks.ir

Molybdenum poisoning 3081

Moxostoma spp 1784

Monachus monachus 1869

MRSA infections 2426

Monday morning disease 1202

MTI 800 2756

Monensin 2694, 2765, 2796

Mucinosis, cutaileous 850
poisoning, poultry 2862

Mucocele,

Monepantel 2638, 2641
gallbladder, dogs 475

Moniezia
salivary, small animals 368
benedeni 312

Mucocutaneous leishmaniosis 2442
e.rpansa 312, 314

Mucoid
spp 305, 319, 2646, 2650
enteritis, rabbits 194 7

Moniliella 643
enteropathy, rabbits 1948

Monitoring

Mucolytic drugs 2616
critically ill animals 1685

Mucopolysaccharicloses 59, 1235
in emergency medicine 1674

Muco1· spp 1335, 1346, 1739, 1865, 1901,

Monkeypox 867, 1882, 2474

1935, 1993,2177, 2196,3010

Monoclonal

Mucosa! disease complex, cattle 267, 268
antibodies 2773

Mucous membrai1e papiUomatosis, canine
gan1111opathies 832

953

Monocytes 5, 57, 1613

Mud fever, turkeys 2797

Monocytic ehrlichiosis, equine 283

Muellerius capillaris 1421, 1473

Monodon monoceros 1870

Mugil cephalus 1764

Monogastric digestive system,

Mulbeny heart disease, pigs 1174
pharmacotherapeutics 2544

Mule foot 1045

Mononuclear phagocytes 5

Mules operation 898

Monoplegia 1259

Mulga fern poisoning 3091

Monuron poisoning 2998

Multicentric

Mood-stabilizing drugs 2605
histiocytosis, poultry 2855

Moon
squai11ous cell cai-cinoma in situ,
blindness 508
feline 947
eye, rabbits 1959

Multifocal disorders, congenital, nervous

Moose tick 930
system 1222, 1234

Moraxella

Multiglandulai· mastitis sows 1374
bovis 512, 894, 897, 2568

Multinoclulai· pulrnonai-y fibrosis,
bovociili 512
equine 1446
ovis 513

Multinucleated cells 1601

Morbidity (epidemiology) 2308

Multiple

Morbillivirus
cartilaginous exostoses 1204, 1229
equine 707, 1448
myeloma 564
maiine mai11mals 1869
system degeneration, canine 1227

Morganella mO'lgan'ii 1992, 1993

Multisystemic

Marone
chromatolytic neuronal degeneration
ch1ysops 1764

1234
saxatilis 1764
eosinophilic epitheliotropic disease,

Morphine 2602, 2608, 3042
horses 291

Mortality (epidemiology) 2398
neuronal degeneration 1234

Mosquitoes 522, 888

Multivitamin poisoning 3030
of poultry 2879

Mummification, fetal 1379

Moth flies 887

Munge, llan1as and alpacas 1855

Mother-in-law's tongue 3114

Murine-See also Mice

Motility-modifying drugs 2553
respiratory mycoplasmosis 2028

Motion sickness 1267
typhus 2436

Motor neuron disease, equine 1248

Murmurs, heart 88, 89

Mouse tapeworm 2454

Murray Valley encephalitis 1294, 2476

Mouth

Mus muse1ilus 1838, 2024
burns and trauma, small animals 365

Musca
congenital ai10malies 162
aiitmnnalis 510, 514, 894, 906
large animals 176
clomestica 730, 873, 890, 895, 897

3268

INDEX

Musca (continued)

paratuberculosis 355, 688,
lusoria906

692, 762,2428
spp 512, 906
bovis 687, 689, 690, 691, 692, 1825, 1863,
vitripennis 906

1898,2053,2870

:ranlhomelas 906
canellii 687

VetBooks.ir

Musc'ina spp 895
caprne 687

Muscle
chelona.e 692, 1738, 1810, 1863, 1993
atrophy, horses 1177
chitae 1863
cramping, horses 1182
fcl1'cinogenes 667
crush syndrome, cattle 1175
jlavescens 692
fasciculations, horses 1177

Jortuitmn 690, 692, 1366, 1738,
relaxants 2588

1810, 1863
dosages 2589
gast1·i 692
toxicity 3036
genavense 687, 1898, 2870
strain, horses 1147
goi·donae 692
tumors, small animals 1203
haemophilum 1993

Muscular
intmce/lulare 687, 692, 1898
dystonia, congenital, cattle 1175
kcmsasii 688, 692
dystrophy 1043, 1231
leprae 692
poultry 2938
leprnemurium 690, 692

X-linked 1233
marinum 692, 1738, 1810, 1836, 1863,
fatigue 1008

1993
steatosis 1043
microti 687, 690
system, pha1macotherapeutics 2586
mungi 687
trauma, small animals 1202
nonchromogenicwn 692

Musculoskeletal-See also Skeletal
parnlubercu/osis 158, 762, 1853
defecls, llamas and alpacas 1851
phlei 692, 1366
disorders, ratites 1966
pinnipedii 687, 691, 1863
system 1039
sc1·qjitlaceum 692
congenital and inherited anomalies
senegalense 667

1042
simiae 2428
introduction 1039
smegmatis 692, 1366, 1863
phannacotherapeutics 2586
spp 158, 454, 666, 670, 679, 687, 1366,

Mushrooms, poisonous 3095

1778, 1786, 1810, 1825, 1897, 1964,

Mushy chick disease 2859

1971,2041,2688

Musladin-Lueke syndrome 1232
szulga i 1738

Mustards 3138
te1rne 692

Mustela
t1iviale 692
putoiius furo 1824
lnberculosis 454, 687, 689, 690, 691,
vison 1870

1825, 1863, 1898,2053,2665,2870

Myastl1enia gravis 828
ulcemns 1993, 2428
acquired 1239
vaccae 692, 1366
congenital 1232
xenopi 692, 1738

Mycetomas 640

Mycoplasma

Mycobacterial infections 687, 2426, 2428
agalactiae 1352
amphibians 1738
arginini 1353
other than tuberculosis 692
bovigenitalium 1353, 1365, 1383
reptiles 1993
bovis 1263, 1353, 1365, 1387, 1431,

Mycobacteriosis

2140
avian, zoo animals 2053
bo voculi 512
birds 1898
calffornicuin 1365
marine manm1als 1863
canadense 1365
reptiles 1993
capricolwn 1367

Mycobacterium
capricolum 1352
abscessus 1738
cap1ipne111noniae 1474
af1icanum 687
conjunctivae 513, 1353
avium 454, 687, 689, 690, 691, 692, 1738,
edwm·dii 1263

1825, 1898,2870

Jelis 1263, 1449, 1481
avimn 687, 688, 690, 2870
gallisepticum 1263, 1823, 2834, 2841,
complex 687, 690, 691, 692, 2426

2843,2845,2897,2898,2909,2927
hominissuis 687, 690
infection, birds 2841
intracellulare 1836
haerrwfelis 25, 27

INDEX

3269

Mycoplasma, (cont.inued)

Mycotoxins, fish 1761, 1811
haemolamae 1852

Myelitis, verminous 1252
hemotropic 26

Myelodysplasia 14
hyopnewnoniae 724, 730, 1936, 2163
small animals 1230
hyo1·hinis 671, 721, 733, 1158, 1160,

Myeloencephalilis, equine protozoa]

1163, 1467, 1935

1251, 1309

VetBooks.ir
hyosynoviae 627, 1153, 1160, 1163, 1465, Myeloencephalopathy, degenerative, 1467, 1470, 1935
equine 1246
iowae 2841

Myelofibrosis 14
infection, birds 2845

Myelolipomas, small animals 471
meleagridis 2841, 2846

Myelopathy
infection, birds 2844

Afghan Hound 1229
mycoides 1063, 1263, 1367
ce1vical stenotic, large animals 1228
cap1i 1352, 1474
degenerative, dogs 1229, 1246
mycoides 1095, 1352, 1438, 1474
feline leukemia virus 1251
ovipneumoniae 765, 1473, 1474
postanesthetic hemorrhagic,
ovis 27
horses 1255
parvwn 26
progressive, Murray Grey cattle
pulmonis 2028, 1263

1227
putrefaciens 1352, 1367

Myialges anclwra 2875, 2876
spp 10, 18, 26, 435, 492, 505, 512, 671,

Myiasis 885, 897, 899, 1314, 2462

748, 1063, 1092, 1095, 1096, 1358,
cutaneous, turtles 1996

1365, 1367, 1392, 1406, 1430, 1472,
facultative 897

1481, 1492, 1508, 1863, 1897, 1912,
furunculoid 903

2028,2029, 1263,2219,2568,2654,
mink 1876

2669,2671,2688,2820,2835,2845,
obligatmy 897

2857,2906
producing flies 897, 899
synoviae 1823, 2834, 2841, 2873, 2882,

Mynal1s, nutrition 2293

2883,2887,2909

Myobia musculi 2029
infection, birds 2843

Myocardial
wenyonii 27
disease 71

Mycoplasmal pneumonia
failure 120
cattle 1438
doxorubicin-induced 120
pigs 1467

Myocarditis 119

Mycoplasmas, hemotropic 26

Chagas' 120

Mycoplasmosis
tickborne 120
goats 1095

Myocardium, oxygen consumption 69
poulb.y 2841

Myoclonus, congenital 1234

Mycoses 632

Labrador Retrievers 1232

Mycosis

Myocoptes musculinus 2029
fungoides 962

Myofibrillar hypoplasia, piglets 1049
guttural pouch 1463

MyoglobinU1ia, horses 1048

Mycotic-See also Fungal
atypical 1186
abortion, cows 1335

Myonecrosis, clostridial 1171
dermatitis 858

Myopathies
diseases
associated with congenital articular
fish 1761
rigidity 1044
marine mammals 1863
dysti·ophy-like 1043
nonhuman primates 1880
exe1tional
pet birds 1899
dogs 1202
rabbits 1944
horses 1177
reptiles 1993
fibrotic dogs 1200
infections 632

Great Dane 1200, 1233
lupinosis 3006, 3018
hereditary, Devon Rex 1233
placentitis, equine 1346
horses 1176, 1177
pneumonia 1425, 2438
hypokalemic Bmmese cats 1232
poultry 2901

Labrador Retriever 1233
stomatitis, small animals 364
mitochondrial 1233

Mycotoxic lupinosis 343, 3018
ncmalinc rod 1233

Mycotoxicoses 342, 3005
nutritional
large animals (table) 3006
large animals 1172
poultry 2846
pigs 1162

3270

INDEX

Myopathies (contimied)

Nasal
pigs 1171
alopecia, llamas and alpacas 1855
poultry 2883
bot, sheep 1473
ruminants 1171
catarrh, rabbits 1945

VetBooks.ir
small animals 1200
cavity, flush 1607

Myoporum laetum 977
dermatitis, gerbils 2012

Myo itis
dermatoses, dogs 975
eosinophilic, dogs 1201
discharge 1412
extraocular muscles 2569
mites
immune-mediated, horses 1182
canine 1480
masticatory, dogs 1201
marine mammals 1865
mink 1874
passage diseases, horses 1461
ossificans, dogs 1201
polyps, horses 1461

Myotonia congenita 1175, 1184, 1231, 1233
schistosomiasis 32
or dystrophica, horses 1184
septum, horses 1461

Myotonic disorders, horses 1184
solar demiatitis, dogs 975

Myrotheciotoxicosis 3008, 3021
tumors

Myrolhecium 3020
enzootic, sheep 1472

Myxedema 554
small animals 1484
coma 555

Nasitrerna spp 1866

Myxobolus cerebralis 1755, 1807

Nasogastric intubation, horses 1710

Myxofibrosarcomas 957

Nasolacrimal

Myxomatosis, rabbits 1950
and lacrimal apparatus 490

Myxomatous AV valve degeneration 112
duct

Myxosarcomas 957
atresia 491
multiple openings 491

N

Nasopharyngeal polyps 535

Natan1ycin 2698

N-Acetylcysteine 2616

National Aquatic Animal Health Plan 1747

Naalehu disease 1052

Navel ill

Nabumetone 3038
poultry 2859

Naegleria fowle1ia 1264
sheep 2168

Nafcillin 2656

Navicular

Naftifine 2705
bone fracture, horses 1108

Nagana 892
disease, horses 1112

Nail t1imming

N-Butylscopolammonium bromide
llan1as and alpacas _1851

2612
pet birds 1888

Neburon poisoning 2998
zoo anin1als 2053

Neck

Nairobi sheep disease 760
evaluation 1217

Nairovirus 751, 761
lesion (tooth), small animals 181

Nakanuke disease, poultry 2854

Necrobacillosis, laryngeal 1429

Naked lady Wy 3112

Necrolytic

Nalbuphine 2602
dermatitis, superficial 468, 974

Naled toxicity 3066
migratory erythema 452, 468

Nalidixic acid 2669, 2673

Necropsy, zoo animals 2048

Nandina domestica 2960, 3146

Necrosis, proliferative tlu·ombovascular,

Nannizziopsis miesii 1993
pinnae, dogs 526

Nanophyetiasis 2448

Necrotic

Nanophyetus salmincola 426, 808, 2448
dermatitis

Nanotechnology 2522
poultry 2879

Naphazoline 3026
reptiles 1991

Naphthalophos 2638, 2651
udder 1387

Napropamide 2984
ear syndrome, swine 524

Naproxen 3028
entelitis, poultry 2802

Naptalam 2986
hepatitis, infectious 341, 603
poisoning 2997
laryngitis 1429

Narasin 2796
rhinitis, pigs 1468
poisoning, poultry 2862

Necrotizing

Narcissus spp 3112
polyarteri tis 830

Narcolepsy, 1223, 1225
sialometaplasia, dogs 369

Nartheciurn ossifmgum 977
ulcerative stomatitis, dogs 364

INDEX

3271

Nectunts maculosus 1743
mouth, large animals 214

Nedocromil 2615
nervous system 1267

Negative
pain 2113
predictive value 2404
pancreatic 411
punishment 1541
peripheral nerve 1242

VetBooks.ir
reinforcement 1541
pet birds 1915

Neisseria spp 533, 2655, 2688, 2692
poultry, reproductive system 2898

Nemaline rod myopathy 1233
rabbits 1959

Nematodes-See also Roundworms,
rectal 189

Hookworms, Whipworms
reptiles 2002
causing CNS disease 1312, 1314
respiratory system, small animals
lung, small animals 1483

1484
marine mammals 1866
skin and soft tissues 942
poultry 2828
spinal column and cord 1252
ratites 1965
minary system, small animals 1522
reptiles 1997

Neoplasms-See Neoplasia, Tumors
zoonotic infections 2454, 2456, 2458,

Neoplastic

2460,2462
arthritis, small animals 1198

Nematodirus
reticulosis 1252
battus 306, 310, 313

Neorickettsia
helvetianus 310, 313
elokominica 808
spalhiger 310
helminthoeca 158, 283, 808
spp 303, 310, 312, 313, 2649, 2651
risticii 158, 281, 283, 290, 808, 2153,

Neobeneclenia spp 1754, 1755, 1756, 1807

2158,2554

Neocnemiclocoptes gallinae 2877
sennetsu 808, 2434

Neolipoptenaferrisi 893
spp 803, 808

Neomycin 2663, 2666

Neoschongastia americana 2878

Neon tetra disease 1811

Neospora

Necnatal
and abortion in cattle 1333
alloimmune thrombocytopenia 47
caninum 663, 671, 686, 1241, 1252, 1264,
encephalopathy 1224, 2094

1333, 1339, 1346
foals 1728
hitghesi 663, 1264, 1291, 1309
isoerythrolysis 11
spp 158, 505
malacljustment syndrome 2094

Neosporosis 663, 1252
management 2087

Neostigmine 2588
large animals 2087

Neotoma spp 677
small animals 2096

Neotrombicula autwnnalis 924
polyarthritis, pigs 1156

Neotyphodium 3155
uveitis 2093
coenophialum 360, 618, 1344, 3006,

Neonate, effect of reproductive

3016,3017
therapy on 2608
lolii 3154

Neonicotinoids 2754

Nephritis

Neonicotinyls 2754
interstitial, small animals 1511

Neon tetra disease 1811
viral infections, avian 2812

Neoplwna spp 1911

Nephroblastomas 1522

Neophoca cinerea 1863

Nephroliths 1525

Neoplasia-See also Cancer, Tumors

Nephroma, embryonal 1522
amphibians 1742

Nephropathy
congenital and hereditary 852
baby chick 2812
cytology 1601
protein-losing 168
esophagus, large animals 217

Nephrotic syndrome 1518
eye and associated structures

Nerium oleander 3094, 3146

515

Nerve
ferrets 1826
blocks, horses 1101
fish 1814
peripheral diseases 1238
gastrointestinal
sheath tumors 958, 1242
horses 291

Nervous system
small animals 388
clinical pathology 1219
hepatic
congenital and inherited
small animals 469
anomalies 1222
large animals 348
disease mechanisms 1212
marine mammals 1870
evaluation 1213

3272

INDEX

Nervous system (continued)

Neutrophils 5
helminths and arthropods of 1310
cytology 1600
imaging 1220
hematology 1612
introduction 1209

Nevus/nevi 846, 942
lesions 1210
collagenous 955

VetBooks.ir
neoplasia 1267
epidermal 943
para.neoplastic disorders 1280

New
pharmacotherapeutics 2590
animal drng 2490
principles of therapy 1220
duck disease 2864
toxicities 1212
forest flies 893
tumors, dogs and cats (table) 1268, 1269
tank syndrome, fish 1775, 1797

Netilmicin 2663, 2666

World

Netobimin 2645
hemorrhagic fever 2476

Nettle rash 857
sand flies 887

Neurapraxia 1261
screwworm 899

Neuraxial edema, hereditary 1234

Newcastle disease 2476, 2856

Neuraxonal dystrophy
backyard poultry 1822
large animals 1227
pet birds 1910
small animals 1229

Niacin deficiency

Neurilemmomas 958, 1242
pigs 2344

Neuritis
poultry 2940
cauda equina 1241

Niacinamide 2584
ttigeminal 1241

Nicarbazin 2797

Neurocysticercosis 2454
poisoning, poultry 2861

Neuroendocrine tumors 576

Niclofolan 2650
cutaneous 961

Niclosamide 2650
primary cutaneous 952

Nicosulfuron 2986

Neurofibromas 958, 1242

Nicotiana

Neurofibrosarcomas 958, 959
glauca 618

Neurohypophysis 543
tabacum 618

Neurologic

Nicotine sulfate toxicity 3063
disorders, cattle, and lameness 1088

Nicotinic acid deficiency, poultry 2940
evaluation 1213

Nictitating membrane, hypertrophy and

Neuromas
prolapse 490
amputation 958

Niemann-Pick disease 1235
traumatic 958

Nierembe1gia veitchii 1053

Neuromuscular

Nifedipine 3032
blocking agents 2586

Nifuraldezone 2696
disorders 1231

Nifurprazine 2696
congenital 1222

Night-blooming jessan1ine 3138
junction diseases 1238

Nightshades 3130

Neuromyopathy, ischemic 1244

Nikals 3118

Neuronal degeneration, multisystemic

Nimorazole 2696

1234

Nipal1 virns 721, 2476

Neuropathy

Nitenpyram 2754
diabetic 1241

Nitrates 108
of hereditary hyperchylomicronemia
organic 2535

1232
poisoning 3049
hypertrophic, Tibetan Mastiffs 1231

Nitric oxide 2709
hypothyroid 1241

Nitrites
para.neoplastic 1242
organic 2535
sensory
poisoning 3049

Border Collies 1232

3-Nitro-4-hydroxyphenylarsonic acid

Dachshunds 1232
poisoning, poultry 2861

Pointers 1232

Nitrobenzamides 2797
trigeminal idiopathic 1241

Nitrofurans 2695

Neuropraxia 1243

Nitrofurantoin 2620, 2695

Neurothekomas 958

Nitrofurazone 2695

Neurotmesis 1243, 1261
poisoning, poultry 2861

Neurotransmitters 1209

Nitrogen

Neurotropic affinity 1311
dioxide, workplace exposure 2955

Neutrophilic vasculitis 851
mustards 2726

INDEX

3273

Nitroglycerin 108, 2535

Nongovernmental organizations 2391

Nitroimidazoles 2696

Nonhuman primates 1876

Nitromersol 2741
bacterial diseases 1878

Nitroprusside 108, 2535
enrichment 1884

Nitroquanidines 2754
mycotic diseases 1880

VetBooks.ir

Nitroscanate 2651
nutrition 2299

Nitrosoureas 2726
nutritional diseases 1883

Nitroxynil 2650
parasitic diseases 1880

Nits 908
psychological well-being and

Nizatidine 2558, 3030
environmental enrichment 1884

No-see-ums 887
therapeutics (table) 1877

Nocai'dia
viral diseases 1882
abscessus 668

Nonionophore antibiotics 2766
aj,icana 667, 668

Non-neoplastic enlargement of the thyroid
arlhrilidis 667
gland 558
asteroides 666, 1366, 2688

Nonprotein nitrogen poisoning 3043
brn siliensis 666

Nonrandomized trials 2402
cyriacige01yica 667

Nonregenerative anemias 12
elegans 668

Nonspecific immunotherapy 2774
fai'C'inica 666

Nonsteroiclal anti-inflammatory drugs
nova 666

2110, 2544, 2714
otitidisraviarum 666
administration 2715
pseudobrasiliensis 666
adverse effects 2716
puris 667
pharrnacokinetics 2715
spp 666, 670, 679, 1249, 1263, 1345, 1861,
pharmacologic effects 2715

2655,2671,2676,2704
poisoning 3027, 3037
tenerifens·is 668
horses 292
transvalensis 666

Nonstrangulating infarction, horses 251
veterana 667

Nonsuppurative

Nocarcliofom1 placentitis, mares 1345
rneningoencephalomyelitis, feline 1252

Nocarcliosis 666
polyarthritis, lan1bs 628
marine mammals 1861

Norepinephrine 575, 2542

N-Octyl bicycloheptene dicarboxamide

Norfloxacin 2670

2757

Northern

Nodal premature complexes 94
cattle grub 876

Nodular
fowl mite 2878
amyloiclosis, cutaneous 961

No1triptyline 3034
clermatofibrosis, dogs 852, 955, 974

Nosomma sp 928, 935
disease, birds 2831

Nose
eosinophilic granulomatous syndrome,
bot
pulmonary 1479
horses 315
fasciitis 956, 957
sheep 1473
granulomatous episclerokeratitis
tumors, small animals 1484

957,2569

Nostoc 2956
hyperplasia, hepatic, small animals 469

Notechis scutatus 3159
lymphosarcoma 963

Notoedres
necrobiosis of collagen, horses 972
cati 505, 521, 921, 1834, 1953,
worm

2462
cattle 311
spp 855, 1832
sheep 313

Notoedric mange, cats 921

Nodularia 2956

Novobiocin sodium 2694

Nolina

NSAIDs-See Nonsteroidal anti-
spp 977
inflammatory drugs
texana344

Nuclear

Nondepolarizing agents,
medicine imaging 1638
competitive 2586
sclerosis 499
dosages 2588
scintigraphy 1638

Nonepitheliotropic cutaneous

Null hypothesis 2400
lymphosarcoma 962

Nursing

Nonfunctional
disease, mink 1875
pituitary tumors 547, 548
refusal, piglets 1555
quarters, udder 1387

Nutraceuticals 2086

3274

INDEX

Nutrient
sheep 2345
concentrations, horses (table) 2324
small animals 2170, 2354
requirements
in disease management, 2379
cats 2357, 2358
snakes 2306
cattle 2248
subungulates 2301

VetBooks.ir
dogs 2356
tortoises 2307
horses and ponies (table) 2314
toucans 2293
pigs 2329, 2330, 2333 (tables)

turkeys (table) 2918, 2924
sheep 2345
turtles 2306
small animals 2366
ungulates 2301

Nutrition 2066-See ai,so Feeding
waterfowl 2292
aardvarks 2297
zoo ai1in1als 2287, 2293
backyard poultry 1817

Nutritional
bats 2294
deficiencies
beef cattle 2248
poultry 2929
birds 2288
diseases
columbifonnes 2290
an1phibians 1741
gallinaceous 2292
dogs and cats 2354
passerines 2290
fish 1798
piscivores 2291
goats 2311
psittacines 2288
horses 2323
raptors 2291
marine mai11ma1s 1859
calves 2124
mink 1874
carnivores (zoo) 2296
nonhuman primates 1883
cats 2354
pet birds 1917
cattle 2171
pigs 2343
breeding 2121
sheep 2353
beef2248
disorders
dairy 2265
peripheral nerve 1242
feedlot 2129
spinal cohunn and cord 1253
chickens
muscular dystrophy 1172
broilers (table) 2917
myodegeneration, 1urninai1ts 1172
growing pullets (table) 2915
myopathies
laying hens (table) �916
horses 1185
crocodilians 2306
pigs 1174
dairy cattle 2265
poultry 2885
dogs 2354
ruminants 1172
ducks, Pekin (table) 2!!21
osteodystrophies 1051
edentates 2297
osteopathies, small animals 1205
exotic animals 2287
panniculitis 1200
fish 2307
requirements
geese (table) 2922
beef cattle 2248
goats 2149, 2308
dogs and cats 2354
horses 2153, 2312
goats 2308
insectivores 2297
horses 2313
lagomorphs 2300
pigs 2329
lizards 2307
poultry 2914
llan1as and alpacas 184 (j
sheep 2345
marine man1mals 1859. 2297
secondary hyperparathyroidism
marsupials 2298
horses 2325
mynahs 2293
pet birds 1919
pheasants (table) 2919
steatitis 1200
pigeons and doves 2290
supplements, zoo animals 2288
pigs 2329

Nymphomania
potbellied pigs 1932
cattle 1551
poultry 2914
horses 1550
primates 2299

Nystagrnus, pendular 1236
quail (table) 2920

Nystatin 2698, 2700
rabbits 1943
rati tes 2292
reptiles 2302

0
rodents 2300

Oak bud poisoning 3152

INDEX

3275

Oaks 3120

Old

Obesity
dog encephalitis 777, 831
dogs and cats 2386
tank syndrome, fish 1775, 1797
horses 1550

World
pet birds 1918
sand flies 887

VetBooks.ir
treatment of 2544
screwwonn 900

Obligato1-y myiasis 897

Oleander 3146

Observation bias 2399
yellow3094

Observer bias 2402

Oleandomycin 2687

Obsessive-compulsive disorders 1535

Olfacto1-y nerve 1214
dogs 1561

Oligodendrogliomas 1273

Obstipation, small animals 380

Oligodontia 164

Obstruction

Ollulanus
acute intestinal, large animals 245
sp 387, 413
colon, horses 266
tricuspis 413
esophageal, horses 1720

Omasal transpo1t, failure 233
gastrointestinal, small animals 390

Omeprazole 2551

Obstructive

Omphalitis 2092
pulmonary disease, chronic,
poultt-y 2859
horses 1455

Omphalophlebitis 2092
mopathy, small animals 1521

Omsk hemorrhagic fever 2476

Obturator paralysis, cattle 1089

Onchocerca

Occipital
cervicalis 888, 905, 2460, 2576
lobe herniation 1277
dewitteijapunica 2460
malformation syndrome 1226
gutturosa 905, 908, 2460

Occipitoatlantoaxial malformation, large
jakutensis 2460
animals 1228
lienalis 905, 908

Occlusal anomalies 162

Lupi 2460

Ochlerotatus spp 2482
rnticulata 2460

Ochotona princeps 1937
spp 511, 886, 905

Ochragaster lunifer 1344
volvulus 886, 2644

Ochratoxicosis 3008

Onchocerciasis 905
poultry 2847

Onchocercosis 2460

Ochroconis spp 1739

Oncicola

Oclacitinib 2583
canis 421

Octenidine dihydrochloride 2743
spp 421

Ocular-See also Eye, Ophthalmology

Oncorhynchus spp 1762
fundus 501

Ondansetron 2549
injuries, horses 1718

Ondiri disease 745
larva migrans 415

One Health 2390
mycoses, tl1erapy 2567

One-mile cough, pigs 722
squamous cell carcinoma

Onion poisoning 3132
cattle 515

Onychomycosis, horses 1116
horses 516

Oomycosis 641

Oculomotor nerve 1215

Oonopsis 3086

Odds ratio 2401

Oophoritis, poultry 2898

Odobenus rosmarus 1860

Oosporein mycotoxicosis, poultry 2847

Odocoileus virginianus 738
o,p'DDD 2734

Odontogenic fibromas 366

Ophionyssus natric·is 1974, 1996

Oecanlhus spp 328

Ophthalrnia

Oesophagostomiasis 2460
infectious 512

Oesophagoslomum
periodic 508
columbianum 312, 313

Ophthalmic
denta,tum 322, 2644
emergencies 1696
quadrispinulatum 322
manifestations of systemic disease
radiatum 311

505
spp 298, 304, 311, 313, 322, 1881, 2460,

Ophthalmology 488-See also Eye, Ocular

2647
rabbits 1957

Oestrus ovis 897, 1314, 1471, 1473, 2464

Opiates 2553

Oil
poisoning 3042
fields, effects on cattle 3055

Opioids 2107
gland, impacted/infected, sheep 1170

Opisthorchiasis 2448

3276

INDEX

Opislhorchis
biirsa 2878
felineus 427, 2448
spp 2462
spp 428
sylviarum 1821, 2014, 2878
viverrini 427, 2448

Ornithosis 599, 2428

Optic
pet birds 1897

VetBooks.ir
atrophy 504
poultry 2808
nerve 504, 1214

Ornilhostrongylus quaclriradiatus 2831
hypoplasia 504

Oronasal fistulas 162
neuritis 1701

Orphan
therapy 2569
birds and man1mals 2100

Oral
foal, feeding 2329
anticoagulants 2543

Orthopedic disease, developmental, horses
dosage forms of drugs 2508

1148
hypoglycemia agents 581

Orthophthaldehyde 2743
inflammatory and ulcerative disease,

Orthopoxvirus 867
small animals 361

01tolani sign 1197

Orange sneezeweed 3142

Oiyctolagus 1951, 1952

Orbifloxacin 2619, 2670, 2673
cuniculus 1937

Orbital cellulitis 504

Os pedis fracture, horses 1108

Orchiepididymitis, chronic, small

Oscilla toria spp 977, 2956, 2957
animals 1401

Oseltamivir 2748

Orchitis, small animals 1400

Oslerus osleri 1421, 1484, 1490

Orf 866, 2468

Osmotic

Organic
diarrhea 156
arsenicals 3073
diuretics 2570, 2624
nitrates and nitrites 2535
use in glaucoma 2570
poultry 2925

Osselets 1120

Organochlorines 2749, 3058

Ossifying epu!is 366

Organophosphates 2651, 2749, 2754

Osteitis, pedal, horses 1114
intermediate syndrome 3069

Osteoaithritis
toxicity 1243, 2997, 3064
horses 1119, 1143, 1145, 1126
delayed 1254
large animals 1063

Orgling 1848
pain 2113

Orgotein 2722
small ai1imals 1197

Oriental fly 900

Osteoarthrosis, pigs 1161

Orient'ia tsiitsugamushi 2438

Osteoblastic cells 1603

Onnetoprim 2674, 2796

Osteochondral disease, horses 1118

OnnetoprimlsulfadimethoXine 2679

Osteochondritis clissecans

Oman1ental
horses 1128, 1148
pepper 3106
large animals 1061
plants, poisonous 3103

Osteochonclroma

Ornithobacterimn rhino/racheale
distal radius, horses 1126

2823,2883,2910

Osteochonclromatosis, small animals 1204

Ornithodorns

Osteochondrosis 1044
braziliensis 939
dogs 1195, 1196
coriaceus 926, 939, 1337
horses 1148
crossi 939
humeral condyle, dogs 1196
dugesi 939
pigs 1161, 1164
ermticus 711
poultry 2932
jU'/1.1,COSUS 939
stifle, horses 1140
gurneyi 939

Osteodystrophies 1050
lahorensis 939
bulls 1053
moubata 711, 939
fibrous 1054
papUlipes 939
hype1trophic, clogs 1204
porcinus 939
metabolic 1054
rostratiis 939
nutritional 1051
savignyi 939

Scottish Fold 1204
spp 711,925,939,2421,2467

Osteogenesis imperfecta 1044
lholoza:ni 939

Ostcohemochromatosis 986
turicata 939

Osteolytic lesions, hypercalcemia 566

Ornithonyssus

Osteomalacia 1052
bacotil832,2013,2023,2030,2032
nonhuman primates 1883

INDEX

3277

Osteomalacia (continued)

Ovine-See also Sheep
pigs 1163
chlamydiosis 599
poultry 2882
demodicosis 918

Osteomyelitis
encephalomyelitis 1299, 2474
mandibular, zoo animals 2053
enzootic abo,tion 599
pigs 1161, 1163
herpesvirus 759

VetBooks.ir
small animals 1204
posthitis and vulvitis 1372, 2168
spinal, reptiles 1993
progressive pneumonia 1475
vertebral 1249
pulmonary adenocarcinoma 1477

Osteopathies

Ovipleislophora ovariae 1811
small animals 1203

Ovis canaclensis 738
spinal, reptiles 1993

Ovulation, small animals 1393, 1624

Osteopenia, poultry 2882

Owl midges 887

Osteopetrosis l 044

Ox warbles 876
chickens 2883

Oxacillin 2656

Osteoporosis

Oxadiazines 2755
backyard poultry 1820

Oxadiazon 2986
pigs 1163

Oxalis
poultry 2882, 2897
corniculala 3116

Ostei'tagia
spp 3116
ci'rcumcincla 312

Oxantel 264 7
oslerlagi 304, 308, 322, 2644, 2646, 2648

Oxazepam 1544, 2546, 2604
spp 303, 312, 2645

Oxfendazole 2645
lrijiircala 312

Oxibendazole 2645

Ostertagiosis, cattle 309

Oxidizing agents 2740

Ostriches 1960

Oxolinic acid 2669

Otaria byronia 1869

Oxpeckers 941

Otitis

Oxyclozanide 2650
externa 527

Oxycodone 3042
feline proliferative and necrotizing

Oxydemeton-methyl toxicity 3066

525

Oxyfluorfen 2986
interna 531

Oxygen lack, workplace exposure 2955
rabbits 1945

Oxyglobin 1681
media531

Oxylipeurus
rabbits 1945
clenla/,us 2876
reptiles 1993
polylrnpezius 2876

Oto bi us

Oxymetazoline 3026
lagophilus 940

Oxyrnorphone 2602, 3042
megnini 520, 926, 939, 1177, 1183, 1315

Oxyspirura mansoni 2830, 2831
spp 925, 938, 939, 1314

Oxylenia acernsa 3128

Otocinclus 1783

Oxytctracycline 2679, 2682, 2683, 2684

Otoclecles 855, 2576

Oxytocin 543, 2607
cynotis 137, 529, 921, 1826, 2576, 2577

Oxytrema silicula 426

Otodectic mange 921

Oxytmpis spp 126, 138, 985, 1333, 3136

Otostrnngylus circumlil1ts 1865

Oxyurnnus sp 3159

Outbreak investigation 2404

OxyU1is

Ovarian
equi 316, 2646
abnormalities 1331

Sp 316
activity, pigs (table) 2208
dysgenesis 1331
p
hereditary hypoplasia 1331

?value 2403
regression, poultry 2898

Pacheco's disease 1908
remnant syndrome, small animals 1397

Paclitaxel 2730, 2733

Ovaries 1325

Paecilomyces

Overeating disease 610
spp 640, 1993

Overlearning 1542
variotii 1264

Overtraining syndrome 1012

Pagetoid reticulosis 962

Oviduct

Pagophilus gmenlanclicus 1864
cystic, poultry 2896

Pain
fluke, poultry 2874
alleviation 2106
impacted 1921, 2986
assessment 2104, 2105
prolapse, poultry 2898
behavioral changes 2105

3278

INDEX

Pain (continued)

Papaver somniferum 3042
cancer 2113

Papaveraceae spp 618
chronic, management 2112

Paperflowers 3148
induced aggression, dogs 1565

Papillar stomatitis, large animals 215
management 1193, 2104

Papillary acanthoma 524

VetBooks.ir
osteoarthritis 2113

Pap ill edema 504
perception 2104

Papillitis 1701
recognition and assessment 2105

Papillomas 952

Painted drop tongue 3104
congenital, foals 943

Palatitis, small animals 361
cutaneous, dogs 953

Palatopharyngeal arch, rostral
inverted 953
displacement, horses 1461
ear 524

Pale bird syndrome 2840
fibrovascular 955

Palisade worms, horses 316
mouth, dogs 366

Palmar
rep ti! es 1996
and plantar comedones and follicular

Papillomatosis 952
cysts, canine interdigital 862
cloaca!, pet birds 1909
carpal breakdown, small animals 1199
pet birds 1908
digital nerve block, horses 1104
rabbits 1951
nerve block, horses 1104

Papillomatosis, canine mucous membrane

Palpebral reflex 1216

953

PAM 3068

Papillomatous lesions, nonvirus-

Pamidronate 569, 3169
associated 943

Pan troglodytes 1882

Papillomavirus, bovine 1386

Panaeolus subbalteatus 3097, 3099

Papio spp 1876

Panaque

Papovavirus, birds 1907
spp 1783

Paracapillaria philippinensis 2456
suttoni 1806

Parachlamydia acanlha,moebae 506

Pancrealipase 2560

Parachlorometaxylenol 2742

Pancreas 579

Paracoccidioides brasiliensis 2701
disease, fish 1765

Parafilmia
exocrine, small animals 407
bovicola 894, 906

Pancreatic
multipapillosa 907
abscesses 412

ParajUaroides dec01us 1865
fluke 328

Parafluron poisoning 2998
insufficiency, exocrine 168, 401, 409

Paragonimiasis 1312, 2448
lipase inrnrnnoreactivity 1593

Paragonimus
neoplasms 411
afiicanus 2448
pseudocyst 412
heterotremus 2448
tests 1593
kellicotti 1312, 1483

Pancreatitis
me.:r:icanus 2448
l>ypocalcemia 571
spp 1487
small animals 407
westermani 1312, 1483, 2448

Pancuroniurn 2587, 2588

Parainfl uenza 3

Pandemic (epidemiology) 2397
virus 1433

Panfollicular cysts 948
vaccination, exotic manrn1als

Panhypopituitarism

2059
adult-onset 548

Parakeratosis 975
juvenile-onset 549
ruminal 237

Pan'icum

Paralysis
coloratum 343, 2321
calving 1244
spp 977, 2321
cattle 1088

Panleukopenia, feline 796
femoral 1089

Panniculitis, nutritional 1200
ischiatic 1089

Panniculus 838
obturator 1089
reflex 1218
peroneal 1090

Pannus 493
radial 1089

Panosteitis, dogs 1204
suprascapular 1088

Pansteatitis, cats 2388
tibial 1090

Panstrongylus 39

Coonhound 1240

Pantothenic acid deficiency 1242
curled-toe, poultry 2941
pigs 2345
facial 1258
poultry 2940
idiopathic 1239

INDEX

3279

Paralysis (continued)

internal, diagnosis
hyperkalemic periodic 1047, 1231
l3.1·ge a.J1imals 1620
laryngeal 1420
small animals 1619
limb 1259

Jl3.111as a.J1d alpacas 1850, 1854
pha.Jyngeal 186
marine ma.J11mals 1865

VetBooks.ir
range, poultry 1822
neurotropic affinity 1311

Stocka.J'd 1228
nonhLtn13.11 primates 1880
tick 1243, 1314, 2466
pet birds 1904
tongue, large a.J1imals 214
potbellied pigs 1930, 1934
transient, poultry, Marek's disease 2850
rabbits 1952

Paralytic rabies 1304
rep ti! es 1996

Para.Jnesonephric duct, segmental aplasia
ratites 1965

1331
small a.J1imals 2170

Para.Jnphistomes 328
spinal column a.J1d cord 1252

Paramphistomum spp, 328, 1620
zoo a.J1imals 204 7
p3.1·3.111yxovirus infections
zoonotic 2440, 2442, 2444
avia.J1 2856, 2858

Parasiticides
ca.J1ine distemper 777
application methods 2516
reptiles 1995
external 2748
p3.1·3.11asal sinuses

Parastrongyloides 2041
horses 1462

Parastrongylus
tumors, small a.J1imals 1484
cantonensis 2456

P3.1·3.11eoplastic
cos tmicensis 2454
disorders, nervous system 1280

Parathion toxicity 3066
neuropathy 1242
p3.1·athyroid

Paranoplocephala mamillana 319
gla.J1ds 561
p3.1·aphimosis, small a.J1imals 1401
hormone 561

Pa.J·apoxvirus 2446

Paratuberculosis 762

Paraprostatic cysts 1407
goats 2151

Pa.J·aquat (dichloride) 2986
p3.1·atyphoid infections, poultry 2866
poisoning 2996

Paraustrostrongylus 2041

Parascaris

Paravaccinia 868
equorum 259, 291, 316, 682, 2156, 2644,

Paregoric 2554

2649

Parelaphostrongylus tenuis 1252, 1264,
sp 316

1311, 1313

Parasites-See also Flukes, Helminths,

Parenteral route of administration, drugs

Worms

2511
aberra.J1t 1311

Paresis
a.Jnphibi3.11S 1740
facial 1258
aquaculture 1755
parturient
backyard poultry 1821
goats 991
blood 18
sheep 991
calves 2124
progressive, Angora goats 1228
carnivores 1310
spastic 1231
chinchillas 2006
cattle 1091
control in pregna.J1t m3.1·es 2195

Paromomycin 2663
erratic 1311

Paronchocerca helicina 1313
external, exa.J11ination for 1620

Paroxetine 1544, 2605, 3034
facultative 1311

Parrot
ferrets 1826
fever 2808
fish 1799
mouth (horses) 162, 176
fish f3.111ilies (table) 1780

Pa.J'S intermedia adenomas 547
gastrointestinal 159

Parturient paresis
cattle 307, 308
cows 988
goats 312
goats 991
horses 287, 315
sheep 991
pigs 298, 320

Parturition-See also Breeding,
rumina.J1ts 303

Reproduction
sheep 308, 312
goats 2186
smaJl 3.11imals 412
mares 2196
horses 2156
pigs 2210
incidental 1311
small a.J1imals 2227

3280

INDEX

Parulis 362

Pattern baldness 523

Parvoviral enteritis, feline 796

Pcmllin·ia cupana 3032

Parvovirus 796

Pavo spp 2292
canine 373

Pawing, horses 1549
nutrition in 2387

Paxillus involutus 3096, 3102

VetBooks.ir
feline 796

Peaches 3148
goose 2826

Peat scours 3082
mink 1825

Pebulate 2986
porcine, and abo1tion 1342
poisoning 2996

Paspalum

Pedal
spp 3019
bone cyst, horses 1107
staggers 3019
osteitis, horses 1114

Passalurus arnlriguus 1954

Pedicinus oblusus 1881

Passerines, nutrition 2290

Pediculosis-See Lice

Passive

Peduncle disease 1759
immunization 2773

Pedunculated lipomas, horses 261
surveillance 2398

Peestersiekte 1373

Pastern disorders, horses 1118

Peganum hcn·mala 3120

Pas leiirella

Pegaspargase 2735
anatipestifer infection, birds 2864

Pelger-Huet anomaly 59
haemolytica 765

Pelodem
mullocida 64, 533, 724, 756, 765, 926,
dermatitis D07

1157, 1263, 1343, 1413, 1431, 1432,
slmngyloides 907, 908

1436, 1465, 1466, 1469, 1472, 1474,

Pelvic

1478, 1863, 1936, 1944, 1945, 1946,
fracture, horses 1145

1954,2041,2131,2177,2428,2571,
limbs, evaluation 1218

2660,2668,2689,2769,2800,2819,

Pemoline 3039

2822,2827,2864,2868,2871,2877,

Pemphigoid, bullous 828

2883,2898

Pemphigus
gallicida 2822
canine benign familial chronic 850
mullocida 2822
erythematosus 525
septica, 2822
foliaceus 525, SD
pneumonia
vulgaris 828
marine mammals 1870

Penciclovir 2745
sheep and goats 1474

Pendimethalin 2986
pneiimotropica 2032

Pendular nystagmus 1236
spp 340, 750, 765, 1205, 1430, 1443,1449, Pendulous crop, poultry 2874

1465, 1469, 1472, 1474; 1478, 1508,

Penicillins 2654

1835, 1896, 1936, 1945,2191,2654,
adverse events and toxicity 2658

2655,2661,2665,2676,2688,2692,
classes 2654

2873,2896
dose rates/dosages 2657, 2658 (table)

trnhalosi 765, 1474
effects on laboratory tests 2658

Pasteurellosis 2428
elimination, distribution, clearance 2657
pigs 1469
interactions 2658
rabbits 1944
milk discard times 2659, 2659 (table)

sheep and goats 765
pharmacokinetics 2656

Pasture
structure-activity relationships 2656
bloat 229
therapeutic indications 2657
dairy cattle 2280
withdrawal times (table) 2659
fever 772

Penicilliosis 643
horses 2152

Penicillium
myopathy 1186
associated tremorgens 3008

Patellar
citrinmn 3008
ligan1ent injuries, horses 1143
commune 3008
luxation
crnslocum 3008
catlle 1087
cycloµiwn 3008
horses 1142
griseoj'ulvum 643
small animals 1194
mamejfei 643

Patent
roquefu rti 3008
ductus arteriosus 72, 79
spp 640, 643, 1489, 1901, 1993, 2701,
urachus 2092

2847,2860

Pathologic thrombosis 54
viriclicatwn 2847, 3008

INDEX

3281

Penile frenulum, persistent 1331

Peri renal

Penis, short, congenital 1331
hemorrhage syndrome, turkeys 2789

Pennisetum spp 2321
pseudocysts 1497

Penta poisoning 3052

Peritoneal fluid, characteristics 674

Pentachlorophenol poisoning 3052

Peritoneopericardial hernia 86, 167

Pentastomid infections 2464

Peritonitis 670

VetBooks.ir
reptiles 1998
bile, small animals 480

Pentazocine 2602, 3042
cattle 673

Pentobarbit.al 3035
dogs and cats 673

Pentosan polysulfate sodium 2721
egg, poultry 2896

Pentoxifylline 2584
feline infectious 453, 780, 1251

Peptococcus spp 2696
horses, 251, 673

Peptos treptococcus

New World camelids 673
anaerobius 1263
pigs 673
spp 178, 731, 1449, 1991, 2696
small ruminants 673

Peracetic acid 2740

Periwinkle 3108

Perennial ryegrass staggers 3008, 3154

Permethrin 2750, 2756, 2757

Perfom1ance modifiers, beef cattle 2264

Peroneal

Peri anal
paralysis, cattle 1090
fistula 187
nerve injuries 1244
gland tumors 951

Peroneus
tumors 188
longus muscle rupture, turkeys 2885

Periarteritis nodosa 830
tertius rupture

Pericardia!

cattle 1091
disease 122
horses 1137
effusion 123

Perosis, poult1y 2933, 2939, 2940, 2942,

Pe1icarditis, septic 123

2943

Perilla

Perosomus elumbis 620, 1045
frutescens 1442

Per·sea americana 2964, 3112
ketone toxicity 1442

Persistent
mint 3128
atrial standstill 120

Perimyotis subjlmms 1303
halogenated aromatics poisoning 3056

Perinatal
penile frenulum
asphyxia syndrome 2094
large animals 1331
management
small animals 2220
goats 2149
pupillary membranes 496
horses 2159
right aortic arch 85

Perinea! hernia 188

Personal protective equipment 2952

Perineuromas 958, 959

Peste

Periodic
des petits ruminants 766
ophthalmia 508
du canard 2799
paralysis, hyperkalemic 1047, 1231

Pesticide
pinna! alopecia 522
potentiating agents 3069

Periodontal disease
residue, animal fibers 2521
large animals 177

Pet
small animals 178
birds 1885-See also Avian, Birds,

Periodontitis, small animals 178, 361

Poult1y

Periparturient
food
hypocalcemia, small animals 992
labels 2373
hypogalactia syndrome, sows 1373
types 2374
problems, small animals 2228

Petaurus

Peripheral
breviceps 2035

Cushing disease, horses 1006
gracilis 2042
neTVe and muscle disorders, congenital

Petechial fever, bovine 7 45

1222

Pethia conchonius 1810
neTVe

Petroleum product poisoning 3053
diseases 1238

Phacochoerus aethiopicus 711
injuries 1244

Phacoclastic uveitis, rabbits 1958
sheath tumors 958

Phaenicia
trauma 1243
sericata 898
tumors 1242, 1276
spp 895, 897
neTVous system 1209

Phaeohyphomycosis 643

3282

INDEX

Phagocytes 5

Phenylephrine 2626

Phagocytosis 818
poisoning 3026
deficiencies in 818

Phenylimidazoles 2701

Phalangeal fractures, horses 1108, 1118

Phenylmercmic nitrate 2741

Phantom moose disease 930

Phenylpropanolamine 2626

VetBooks.ir

Pharn1acodynamics (general) 2502
toxicity 3033

Pharmacokinetics (general) 2499

Phenylpyrazoles 2756

Pharmacology 2490

Phenytoin 2537, 2589, 2600

Pharmacotherapeutics-See also Principles

Pheochromocytomas 548, 575, 576
of therapy

Phialophora spp 643, 1739, 2703
cardiovascular system 2525

Phialosimplex 640
digestive system 2544

Philodendron spp 3112
eye 2565

Philometra sp 1808
integumentary system 2571

Phimosis, small animals 1402
muscular system 2586

Phlebotomus spp 887
nervous system 2590

Phobias 1536
reproductive system 2606
dogs 1560
respiratory system 2608
horses 1549
urinary system 2617

Phoca

Pharyngeal
hispida 1870
lymphoid hyperplasia, horses
sibirica 1856

1427, 1459
vitulina 1859
mucocele 068

Phocoena
paralysis 186
phocoena 1860
trauma 1427
spinipinnis 1869

Pharyngitis 1426

Phodopus
horses 1459
roborovskii 2021
small animals 361
sungonts 2021

Phaseolus limatus 2960

Phomopsis leptostromiforrnis 343, 3018

Pheasants, nutrition (table) 2919

Phoradendron.fl,avescens 3112

Pheidole megacephala 941

Phorate toxicity 3067

Phellodendron amurense 1543, 1567

Phorrnia

Phenazopyridine hydrochloride 2744
regina 897

Phendimetrazine 3039
spp 895, 897

Phenethicillin 2654

Phortica vmiegala 512

Phenicols 2683

Phosmet 2750, 2754
adverse events and toxicity 2686
toxicity 3067
antimicrobial activity.2684

Phosphate 1592
bacterial resistance 2684
enema toxicity 571
effects on laboratory tests 2687

Phosphine workplace exposure 2955
interactions 2687

Phosphodiesterase inhibitors 109, 2531
mild discard times 2687

Phosphoglycolipid antibiotics 2766
mode of action 2684

Phosphonoacetic acid 2748
pharmacokinetic features 2684

Phosphorus
therapeutic indications 2686
deficiency 1000, 1050
withdrawal times 2687
goats 2309

Phenmedipham 2986
horses 2326

Phenmetrazine 3039
pet birds 1918

Phenobarbital 1220, 1545, 2592, 2595, 2596,
pigs 2344

1545
poultry 2930

Phenols
metabolism disorders 999
and related compounds 2742
requirement
substituted 2638, 2650
pigs 2336

Phenothiazine tranquilizers 2548
sheep 2346
toxicity 3036

Phosphorylase deficiency, Charolais cattle

Phenothrin 2750

1175

Phenoxy acid derivatives poisoning 2997

Photonia

Phenoxybenzamine 2627
fmseri 3146

Phenoxyrnethyl-penicillin 2654
glabra 3146

Phentermine 3039
sm7ulata 3146

Phenylarsonic compounds 3073

Pholobactmium spp 1809

Phenylbutazone 2604, 2717

Photodynamic dermatitis 3015

INDEX

3283

Photosensitization 976

Ping, abdominal 156
congenital, sheep 978

Pingue 3116
hepatogenous 977

Pink tooth 986
primary 976

Pinkeye 512
secondary 977

Pinky syndrome 849

VetBooks.ir
type IV 977

Pinna-See also Ear

Phthalylsulfathiazole 2674
alopecia 522

Phlhirus pubis 913
dermatitis, arthropod bite 520

PhyUanthus abnormis 344
diseases 520

Phylloerythrin 977

Pinus ponderosa 3146

Physaloptera spp 387, 413, 1997

Pin worms

Physeal dysplasia, horses 1149
horses 316

Physiologic data
rabbits 1954
common domestic animals (tables) 3173 Pioniis spp 1886
laboratory animals (table) 1842

Piperacillin 2655

Physitis, horses 1149

Piperazine 2638, 2639, 2651

Physocephalus 322
penicillins 2655
sexalatus 322

Piperonyl butoxide 2752, 2757, 3069

Phytolacca americana 3120

Piping, fish 1771

PI-3 1433

Pirimiphos 2750

Pica

Piroxicam 3038
dogs 1568

Piscinoodinium spp 1740, 1802
horses 1548

Piscirickellsia salmonis 1760

Picloram 2986

Piscivorous birds, nutrition 2291

PIE syndrome 825, 1479

Pitch poisoning 3045

Pietrain creeper syndrome 1043

Pillwmyces chartanun 340, 3015

Pigeon

Pithomycotoxicosis 3006, 3015
fever 66

Pituitary
fly 2876
adenomas 547, 549
malaria 2783
pet birds 1916
nutrition 2290
dwarfism 549

Pigeonpox 1910
gland 542

Pigment
tumors 1274
abnormalities, skin 848
nonfunctional 547, 548
metabolism, aberrant 977

Pityriasis rosea, pigs 848, 979

Pigs-See also Porcine, Swine

Pityrosporum spp 2705
boar management 2203

Pivampicillin 2655
breeding 2207

Pizzle
feeding 2340
disease 1373
flu (swine influenza) 1470
rot 1372
gastrointestinal parasites 320
sheep 2168
health-management interaction 2160

Placenta, retained, large animals 1381
lameness 1151

Placental sites, subinvolution, small
management 2160
animals 1399
nutrition 2329

Placentitis, mycotic, equine 1346
nutritional diseases 2343

Plague 677, 2428
parturition 2210
cattle 771
potbellied 1929
duck 2799
pregnancy tests 2211
fowl 2902
respiratory diseases 1464
goose 2826
reproduction, management of 2201

Planktothrix 2956
teacup 1929

Plantation flies 895

Pilar cysts 94 7

Plants, poisonous 3103

Pilomatricomas 949

Plaques, aural, equine 524

Pilonidal sinus, small animals 1230

Plasma biochemistry analysis 1590

Pimaricin 2698, 2700

Plasmacytic-lyrnphocytic synovitis 822

Pirnobendan 75, 105, 2531

Plasmacytomas 1604

Pindone poisoning 3166
extran1edullary 952, 961

Pine

Plasmacytosis, mink 1872

Ponderosa 3146

Plasmodium
tar 2742
durae 2784

Western yellow 3146
cynomolgi 2444

3284

INDEX

Plasmoclium (contimiecl)

nonhuman primates 1879
gallinaceum 2784, 2879

Pasteurella, sheep and goats 1474
heimani 2784, 2879
potbellied pigs 1936
infection, birds 2784
progressive, sheep and goats 1475
juxtanucleare 2784
rabbits 1945

VetBooks.ir
knowlesi 2444
reptiles 1992
relictum 2784

Rhoclococcus equi 1451
spp 888, 1881, 1904, 1905, 2444, 2780,
shipping fever 1431, 1432

2784,2879
small animals 1486

Platelets 7, 1613
summer, beef calves 1431
evaluation 1615
vern1inous 1421
disorders 46, 49, 50
viral, calves 1431

Platynosomum concinnum 428, 484

Pneumonitis

Play aggression, dogs 1563
allergic, small animals 1478

Pleistophora
feline 506, 1481
hyphessob'lyconis 1811
hypersensitivity 829
spp 1740, 1782
cattle 1441

Pleocytosis 1608
pet birds 1929

Plesiomonas shigelloicles 1863

Pneumonysso·icles ca,ninum 974, 1480

Pleural space disease 1664

Pnmimonyssus

Pleurisy 1414
caninum 974, 1480
horses 1449
spp 1880

Pleuritis 1414

Pneumothorax 1414
horses 1449
horses 1717

Pleuroperitoneal hernia 167
tension 1664

Pleuropneumonia

Pneumovirus, avian 2904
contagious

Pododermatitis
bovine 1438
circwnscripta, cattle 1076
caprine 1474
infectious, zoo animals 2052
horses 1449
pet birds 1913
pigs 1469
ulcerative, rabbits 1958

Plum bladders, mink 1871

Podophyllotoxin 2735

Pneumocystis 821

Podotrochlitis, horses 1112
jiroveci 1425, 1452, 1487

Podotrochlosis, horses 1112

Pneumoencephalitis, avian 2856

Poinsettia 3110

Pnewnomycosis 2438

4-Point block, horse 1104
poultry 2901

Point-of-care tests 1594

Pneumonia 1413

Poison hemlock 3140
acute bronchointerstitial, foals 1452

Poisonings 2948--See also Toxicities,
aspiration 1417

To xi coses
bacterial, cattle 1436

ACE inhibitors 3032
bovine atypical interstitial 11139
acetan1ides 2996
brooder 2901
acetan1inophen 3029
chlamydia!, cattle 1438
acetochlor 2999
dairy calf 1431
acorns 3152
enzootic
alachlor 2999
calves 1431
alcohol 3000
pigs 1467
algae 2956
foreign body 1417
alkaline battery 3003
gangrenous 1417
aluminum phosphide 3169
hemorrhagic, mink 1817
amet1yn 2999
inhalation 1417
an1ides 2996

Mannheimia, sheep and goats 1474
an1monium sulfarnate 2995
marine mammals 1861
arnphetan1ines 3039
metastatic, cattle 1442
analgesics 3027
morbillivirus, equine 707
angiotensin-converting enzyme
mycoplasmal
inhibitors 3032
cattle 1438, 1439
anilide 2996
pigs 1467
annual ryegrass 3153
mycotic 1425
antacid 3030
poultry 2901
anticoagulant rodenticides 3165
nocardial 666
anticonvulsants 3034

INDEX

3285

Poisonings (continiied)

cresol 3045
antidepressants 3034

Crntalaria, poultry 2861
antifreeze 3046
cyanazine 2999
antihistamine 3025
cyanide 2959
arsenic 1254, 2994, 3071
cyanobacteria 2956

VetBooks.ir
arsenic trioxide 2994
cypromid 2996
aryloxyphenoxypropionics 2998

2,4-D 2997
asulam 2996
dalapon 2997
atrazine 2999

2,4-DB 2997
avocado 2964
decongestant 3026
barbiturates 3035

DEF 2999
battery, alkaline 3003
demethenamid 2996
bensulide 2D96, 2997
detergents 3004
benzodiazepines 3034
cationic 3003
binapacryl 2997
dew343
bipyridyl compotmds 2996
diagnosis 2950
bleach, chlorine 3001
diazinon, poultry 2861
blister beetle 3157
dicamba 2997

13-blockers 3033
dichlorprop 2997
borax 2996
diclofop 2998
bracken fem 3090
diclosula.m 2998
bread dough 2965
dicumarol 3156
brodifacoum 3166
diesel fuel 3053
bromacil 2999
diethylstilbestrol, mink 1875
bromadiolone 3166
difenoxmon 2998
bromethalin 3167
difethiolone 3166
bromoxynil 2999
dinitrocresol 2997
butachlor 2999
dinitrophenol 2997
buturon 2998
dinoseb 2997
butylate 2996
dioxin 2997
caff Pine 3032
diquat 2996
calcipotriene 3037
diuretics 3034
calcium channel blockers 3032
diw·on 2998

Cannabis 3041

DMNA, mink 1875
cantharidin 3157
drugs (human) cardiovascular 3032
carbamate 2992, 2996, 3059
drugs (human) gastrointestinal 3030
carbon monoxide, poultry 2861
drugs (human) ove1°the-collllter 3024
carboxazole 2996
drugs (hw11an) prescription 3032
cationic detergents 3003

Ecstasy 3040
chlomequat 2999
ephedrine 3027, 3032
chloramben 2997

EPTC 2996
chlorbromuron 2998
ergot 974
chlorenmron 2998
ethametsulfuron 2998
chlorinated hydrocarbon, mink 1875
fenoxaprop 2998
chlorine bleach 3001
fenthiaprop 2998
chlorophacinone 3166
fenuron 2998
chloroxuron 2998
fescue 3016
chlorsulfuron 2998
florasulam-methyl 2998
chlo1toluron 2998
fluazifop 2998
chocolate 2966
flumetsulam 2998
cholecalciferol 3168
fluometuron 2998
clomiprop 2996
fluoride 3075
cloransulan1-methyl 2998

5-f1uorouracil 3036
coal-tar products 3045

5-FU 3036
cocaine 3039
fuel 3053
coffee weed seed, poultry 2861
fumonisin 3017
cold and cough medications 3025
gasoline 3053
copper3073
gl tLfosinate 2997
poultry 2861
glyphosate 2997
coumachlor 3166
gossypol 3092
coumafuryl 3166
poultry 2861
creosote 3045
grapes 2968

3286

INDEX

Poisonings (continued)

nitrate 3049
guarana 3032
nitrite 3049

Hz-receptor antagonists 3030
nitrofurazone, poultry 2861
haloxyfop 2998

3-nitro-4-hydroxyphenylarsonic acid,
hashish 3041
poultry 2861

VetBooks.ir
herbal supplements 3032
nonprotein nitrogen 3043
herbicides 2969
nonsteroidal anti-inflammatory drugs
household chemicals/products 3000

3027, 3037
houseplants 3103

NSAIDs 3027, 3037

5-HTP 3032
oak bud 3152
human drugs 3024
opiates 3042

5-hydroxytryptophan 3032
organophosphate 1243, 2997, 3064
illicit drugs 3038
ornamental plants 3103
imazamethabenz-methyl 2999
parafluron 2998
imazamox 2999
paraquat 2996
imazapic 2999
pebulate 2996
imazapyr 2999
pent.a3052
imazaquin 2999
pentachlorophenol 3052
imazethapyr 2999
perennial ryegrass 3008, 3154
imidazoline 3026
petroleum products 3053
imidazolinones 2999
phenothiazine tranquilizers 3036
insecticide, mink 1875
phPnoxy acid derivatives 2997
iodides 974
phenylephrine 3026
ioxynil 2999
phenylpropanolamine 3033
iron 3030
pindone 3166
isoproturon 2998
pitch 3045
isovaleryl indanedione 3166
plants 3103
kerosene 3053
polybrominated biphenyls,
lasalocid, poultry 2862
mink 1875
lead 3078
polychlorinated biphenyls
mink 1875
mink 1875
poultry 2861
poultry 2862
linuron 2998
polycyclic alkanoic acids 2998
lupines 3018
polyether ionophore poultry 2862
ma huang 3032
polytetrafluoroethylene, poultry 2862
mackerel, marine mammals 1860
polyureas 2998
marijuana 3041
poultry 2859

MCPA2997
prescription drugs 3032

MCPB2997
prometon 2999

MDMA3040
prometryn 2999
mecoprop 2997
propachlor 2999
mercury 974, 3080
propane, poultry 2862
poultry 2861
propanil 2996
merphos 2999
propazine 2999
metaJdehyde 3070
propylene glycol 3048
methiuron 2998
pseudoephedrine 3027
metobromuron 2998
ptaquiloside 3090
metolachlor 2999
quaternary ammonia, poultry 2862
metosulam 2998

Quercus 3152
metoxuron 2998
raisins 2968
mink 1875
range plants of temperate No1th
molybdenum 3081

America 3103
monensin, poultry 2863
relay 3165
monoamine oxidase inhibitors 3035
rock fern 3091
monuron 2998
rodenticide 3165
mulga fern 3091
ryegrass 3153
multivitamin 3030
salinomycin, poultry 2862
muscle relaxants 3036
salt, poultry 2863
mushrooms 3095
secondary 3165
naptalam 2997
selective serotonin reuptake inhibitors
narasin, poultry 2862

3034
neburon 2998
selenium 3085
nicarbazin, poultry 2861
poultry 2863

INDEX

3287

Poisonings (continued)

Poisonous plants 3103

Senecio 3150

Poke 3120
scombroid, marine mammals 1860

Pokeweed 3120
shampoo 3004

Polioencephalomalacia 1281
siduron 2998
goats 2311

VetBooks.ir
silvex 2997

Polioencephalomyelitis
simazine 2999
feline 1252
slaframine 3019
porcine 1251, 1307
sleep aids 3034, 3035

Poliomyelitis, vaccination, exotic
soap 3004
mammals 2059
sodiw11

Poll evil 1064, 1350
arsenite 2994

Polled intersex goat 615
chlorate 2996

Poloxan1er-iocline 2741
chloride 3083

Polyarteritis nodosa 830
sorghum 3155

Polyarthritis

SSRis 3034
epidemic 2466, 2478
street drugs 3038
idiopathic 822
streptomycin, mink 1875
infectious, swine 720
strychnine 3170
nonsuppurative, lambs 628
sudan grass 3155
pigs 720, 1156
sulfaquinoxaline
serositis, chlan1yclial, large animals
mink 1875

1065
poultry 2863
small animals 1198
sulfometuron 2998

Polybrominated
sulfonamides, poultry 2863
biphenyl poisoning 3056
sulfonylureas 2998
mink 1875
sulfur, poultry 2863
poultry 2862
sweet clover 3010, 3156
diphenyl ethers 3056

2,4,5-T 2997

Polychlorinatecl
tebuthiuron 2998
biphenyl poisoning 3056
terbacil 2999
mink 1875
terbucarb 2996
poultry 2862
terbutryn 2999
dibenzo-p-dioxins 3056
tetrail uron 2998

Polychromasia 1611
thallium sulfate 974

Polyclonal gammopathies 832
therapy 2951

Polycyclic alkanoic poisoning 2998
thidiazuron 2998

Polycystic kidneys 1497
thiobencarb 2996

Polycythemia 43, 1611
thiocarbamate 2996

Polycythemia vera 43
thioureas 2998

Polydactyly 1045, 1050
thiran1, poultry 2863

Polydipsia
triallate 2996
clogs 1568
triazines 2999
horses 1548
triazinylsulfonylureas 2998
potbellied pigs 1937
triazoles 2999

Polyene macrolide antibiotics 2698
triazolopyrimides 2998
adverse effects and toxicity 2700
tricyclic antidepressants 3034
antifungal spectra 2698
toad 3161
dose rates 2699, 2700 (table)

topical agents/drugs 3031, 3036
effects on laboratory tests 2701
toxic fat, poultry 2863
fungal resistance 2698
tranquilizers 3034
interactions 2700
phenothiazine 3036
mode of action 2698
treatment 2951
pharmacokinetic features 2699
ureas 2998
therapeutic indications 2699
vernolate 2996

Polyether ionophore poisoning, poultry
vitamin 3030, 3031

2862
warfarin and congeners 3165

Polyethylene glycol 2560
wood preservatives, mink 1875

Polygonum 977
xylitol 2968

Polymer fume fever 3022
zinc 3088

Polymicrogyria 1224
oxide 3031

Polymyopathy, hypokalemic, feline
phosphide 3169

1201

3288

INDEX

Polymyositis

Pores of Winer, dilated 948
dogs 1201

Pork tapeworm disease 2454
immune-mediated, horses 1182

Porphyria 4, 852

Polymyxins 2692
congenital e1ytlu·opoietic 986

Polyneuritis equi 1241
etythropoietic 852

VetBooks.ir

Polyneuropathy
feline acute intermittent 987

Alaskan Malamute 1231

Porphyrinuria 986
demyelinating, clu·onic inflammato1y

Porphyrnmonas

1240
denlicanis 178
distal, Rottweilers 1239
gulae 178
inherited, Leonberger dogs 1232
levii 1392

Polyodontia 164, 177
salivosa 178
heterotopic 165

Portal

Polyomavirus, avian 1907
hepatitis, lyn1phocytic, feline 482

Polyphagia, dogs 1568
hypertension 445

Polypogon monspeliensis 3154

Portosystemic

Polyps
shunts 169
nasal, horses 1461
acquired 450
nasopharyngeal 535
congenital
rectal 189
lai·ge animals 351

Polyradiculonemitis
small animals 430
idiopathic
vasculai·
acute 1240
anomalies 447
chronic relapsing 1240
malformations 446
protozoa! 1241

Posaconazole 2701

Polysaccharide storage myopathy 1048,

Positive

1179
compression test 1199

Polyserositis, porcine 720
inotropes 2529

Polysulfated glycosaminoglycan 2721
predictive value 2404

Polytetrafluoroethylene poisoning
punislunent 1541
pet birds 1924
reinforcement 1541
poultry 2862

Positron emission tomography 1639

Polyurea poisoning 2998

Possessive aggression, dogs 1563

Polyuria, potbellied pigs 1937

Postanesthetic hemorrhagic myelopathy,

Ponderosa pine 3146
horses 1255

Poor man's alfalfa 3144

Postanesthetic myopathy, horses 1186

Population at risk 2397

Postcastration evi ceration, horses 1722

Porcine-See also Pigs, Swine

Postdipping lameness, sheep 629
circovirus disease 723, 1342

Posthitis, sheep and goats 1372, 2168
cystitis-pyelonephritis 1500

Postinftai1m1atory hyperpigmentation 970
dermatitis and nephropathy syndrome

Postmaturity, foals 1726

723

Postmortem inspection 1644
enteroviral encephalomyelitis 1307

Postpaitum
epidemic diarrhea 298
care, small animals 2228
hemagglutinating encephalomyelitis
dysgalactia syndrome, sows 1373

728, 1251
hypocalcemia, small animals 992
herpesvirus 1342
period, mares 2200
intestinal adenomatosis 299

Postpaiturient hemoglobinuria 1002
juvenile pustular psoriasiform

Postresuscitation care 1674
dem1atitis 979

Postvaccinal hepatitis, horses 338
malignant hyperthennia 1176

Postweai1ing
paivovirns 1342
mastitis, sows 1375
polioencephalomyelitis 1251, 1307
multisystemic wasting syndrome, swine
polyserositis 720

723
proliferative enteritis 299

Polmnochoerus porcus 711
pulmonai·y edema 3008, 3018

Potassium 1591
reproductive and respiratoty syndrome
bromide 1545

729, 1341
citrate 2625
respiratory and neurologic syndrome
clavulanate, ainoxicillin 2658

721
deficiency

RN(-) glycogen storage disease 1176
horses 2326
stress syndrome 1027, 1231
poultry 2821, 2934

INDEX

3289

Potassium (continued)

cows 2120, 2176
iodide 2706
clogs and cats 2225
metabolism disorders 1003
goats 2185
permanganate 2741
rnar·es 2194

VetBooks.ir
in aquaculture 1752
pigs (table) 2211
peroxymonosulfate 2740
sheep 2216
requirement, pigs 2337
false, small animals 1395
sparing diuretics 104, 2529, 2624
goats 2186

Potato (plant) 3130
ketosis, ewes and does 1021

Potbellied pigs 1929
pigs 2186
dental care 1931
prevention, small animals 2226
diseases 1933
tem1ination, small ar1imals 2226
feeding and nutrition 1932
toxemia
gastrointestinal diseases 1933
cows 1020
integw11entary system problems 1934
ewes and does 1021, 2167, 2312
management 1929
primary 1022
musculoskeletal disorders 1934
rabbits 1957
nervous system disorders 1935
secondar-y 1022
reproduction 1931

Preirnmunization, feeder calves 2131
respirato1y problems 1936

Prekallikrein deficiency 53
urinary system problems 1936

Prelar11initic syndrome, horses 1006
vaccinations 1930

Premack principle 1542

Potentiated sulfonamides 2674

Premature ventricular contractions 72

Potentiating agents, pesticides 3069

Prematurity, foals 1726

Potomac horse fever 283, 808, 1346

Premises disinfection 1639

Poult enteritis mortality syndrome 2840

Premortem inspection 1644

Poultry-See also Aviar1, Birds

Prepuce
artificial insemination 2895
abnormalities 1311
backyar·d 1815
prolapse, bulls 1331
hemorrhagic syndrome 3008, 3011

Prepurchase exar11ination
hobby 1815
horses 1647
mite 2877
ruminants and swine 1649
nutrition 2914

Presbycusis 519
orgar1ic production 2925

Prescription drug toxicities 3032
vaccination 2920

Pressure wounds 1708

Povidone-iodine 2741

Presystolic gallop heart sound 88

Powassan virus encephalitis 2476

Prevalence 2398

Pox

Prevention of flight, zoo birds 2053
birds 2824, 2826

Preventive health care, small animals
diseases 867

2169
nonhwnan primates 1882

Prevolella
pet birds 1910

·intennedia 178
rickettsial 2436
melaninogenica 1368

Poxvirus
spp 1075
marine marrn11als 1869

Preweaning mortality, pigs 2211
ratites 1965

Priapism, small animals 1402

Poxviruses, vaccinia-related 2480

Prickle cell carcinomas 945

Pradofloxacin 2619, 2670, 2673

Prima1-y

Pralidoxime chloride 3068
atrial fibrillation 95

Prallethrin 2750
cutaneous neuroenclocrine tumors 952

Prayer beads 3104
erythrocytosis 43

Praziquantel 2650
hyperarm11onemia, horses 350

Prazosin 2535
hyperoxaluria 1232

Precatory bean 3104
hyperpar·athyroidism 564, 1054

Precocious mar11rnar-y development,
immune-mediated thrombocytopenia 47
heifers 1387

Jung tll111ors, small animals 1485

Preconditioning, feeder calves 2131
photosensitization 976

Predato1-y aggression, dogs 1565
pregnancy toxemia 1022

Preclnisolone 2712, 2734
ruminal tyrnpany 227

Prednisone 2712, 2731, 2734, 2737
screwworm 899

Pregnancy-See also Gestation
skeletal tumors 1274
determination
visceral gout, reptiles 2000

3290

INDEX

Primates (nonhuman)-See Nonhuman
gill disease 1755, 1807
primates
hemorrhagic enteropathy, pigs 299

Primidone 2598, 3035
keratoconjunctivitis 957

Principles or therapy-See also
kidney disease, fish 1755, 1807

Pharmacotherapeutics
and necrotizing otitis externa, feline 525

VetBooks.ir
cardiovascular system 74
thrombovascular necrosis, pinnae, clogs
digestive system 161

526
endocrine system 542

Prolonged gestation, cattle and sheep
integumentary system, topical 844

1377
nervous system 1220

Promazine 2600, 3036
poisoning 2951

Promethazine 3025
reproductive system 1328

Prometon poisoning 2999
respiratory system 1416

Prometryn 2986
urinary systeml496
poisoning 2999

Prion diseases 2482

Propachlor poisoning 2999

Privet 3144

Propane poisoning, poultry 2862

Probenecid 2658

Propanil 2986

Probenzirnidazoles 2638, 2639
poisoning 2996

Probiotics 2766

Propanolol 3033

Procainamide 2536

Propazine poisoning 2999

Procarbazine 2731, 2734, 2735

Propentofylline 1545

Prochlorperazine 2548, 2604

Propionate 2606

Procoagulant disorders 54

P1·opionibacte1iiim

Production
acnes 787, 955, 2582, 2768
enliancers 2758
spp 1263, 2696
related metabolic disorders 985

Propofol 2595

Proestrus bitches 2222

Propoxur 2750, 2754

Profaclol 3042
toxicity 3060

ProjUicollis spp 1865

Propoxycarbazone 2986

Proflavine 2744

Propoxyphene 3042

Progesterone 573, 2581, 2607, 2759, 2760

Propranolol 76, 1544, 2538
assay 1394

Proptosis
canine 1624, 2223
eye 504

Progestins, synthetic 2607
trmui1atic 1696

Prognathia 163

Propylene

Progressive
glycol toxicosis 3048
alopecia 851
oxide 2744
ataxia, Charolais cattle 1227

Propylthiouracil 560
axonopathy, Boxer dogs 1229

Propyzamide 2988
degenerative myeloencephalopathy,

Prosopis glandulosa 3130
bovine 1227

Prospective cohort study 2400
dermal collagenosis, pigs 852

Prostaglandin F,0 2607
myelopathy, Murray Grey cattle 1227

Prostatic
paresis, Angora goats 1228
calculi 1408
pnewnonia, sheep and goats 1475
cysts 1407
retinal atrophy 502
diseases 1405

Proinsulin 579
hyperplasia, benign 1406

Prokinetic drugs, gastrointestinal 2556,
neoplasms 1407

2557 (table)

Prostatitis 1406

Prolactin 542
bacterial 2622

Prolapse

Prosthenorchis 1881
eye 504

Proslhogonimus macrorchis
oviduct, poultry 2898

2874
prepuce 1331

Protective aggression, dogs 1564
rectal 189

Protein
uterine 1389
deficiency
vaginal and cervical 1390, 1399
horses 2325

Proliferative
pigs 2343
enteritis, porcine 299
poultry 2930
enteropathy
losing
equine 289
enteropathy 155, 168
rabbits 1948
nephropathy 168

INDEX

3291

Protein (continued)

Pseudochromis spp 1779
requirement

Pseudocowpox 868, 2474
beef cattle 2249
teat skin 1386
dairy cattle 2271

Pseudocyesis, dogs 1395
dogs and cats 2366

Pseudocysts

VetBooks.ir
goats 2309
arachnoid, small animals 1230
horses 2316
perirenal 1497
pigs 2335

Pseucloephedrine 2626
sheep 2346
poisoning 3027
in urine 1616

Pseucloglanders 661, 2426

Proteus

Pseuclohermaphroditism 1330
mirabilis 528, 864, 2622

Pseuclohypoparathyroidism 1057
spp 341, 580, 671, 1204, 1249, 1383, 1397, Pse-udoloma 1508, 1527, 1720, 1737, 1825, 1872,
new'Ophilia 1811

1896, 1913, 1984, 1992, 1993,2191,
spp 1782

2571,2617,2619,2620,2622,2654,

Pseitclolynchici 894

2655,2659,2660,2665,2669,2671,
canariensis 894, 2876

2676,2680,2684,2692,2695,2859,

Pseiulomonas

2908
ae-ruginosa 528, 530, 1345, 1359, 1365,
vulga1is 2660

1369, 1374, 1383, 1443, 1452, 1871,

Prothrombin

1878,2005,2007,2177,2191,2196,
disorders 51

2200,2235,2630,2653,2655,2659,
time 44

2662,2663,2664,2670,2671,2680,

Protistan parasites, fish (table) 1798

2684,2688,2695,2739,3160

Protists 1 755

Jtuoresce-ns 1779

Protodiastolic gallop heart sound 88
spp 340, 530, 533, 671, 856, 864, 898,

Proloopalina spp 1784

1205, 1397, 1492, 1508, 1720, 1735,

Prolophormia le17·aenovae 897

1737, 1809, 1871, 1873, 1896, 1935,

Protoporphyria 852

1945, 1946, 1957, 1964, 1971, 1984,

Proloslrongylus rufescens 1421, 1473

1991, 1992, 1993,2000,2006,2089,

Prototheca

2191,2235,2571,2617,2619,2654,
wickm·hamii 1264

2655,2660,2676,2692,2739,
spp 158, 505, 1362, 1366

2859
zopfii 1264, 1367

Pseudomyiasis 903

Protozoa

Pseudomyotonia, cattle 1176
in avian blood (table) 2781

Pseilclonaja textilis 3159
nonhwnan primates 1881

Pseudoneoplastic skin conditions, pet
pet birds 1904
birds 1915
ratites 1965

Pseuclophylliclean tapeworms
reptiles 1998

2454
zoonotic 2440, 2442, 2444

Pseuclopox, dolphins 1863

Protozoa!

Pseudopregnancy
diseases
clogs 1395
liver, small animals 455
goats 1381
spinal column and cord 1251

Pseudopterygiurn, rabbits 1958
myeloencephalitis, equine 1251, 1309

Pseudoptyalism 367
polyradiculoneuritis 1241

Pseudorabies

Proventricular dilatation disease, pet birds
mink 1874

1909
pigs 1300, 1342

Proximal
virus, and abortion 1333
enteritis-jejunitis, horses 260

Pseuclote11-anova spp 2456
suspensory desmitis, horses 1122

Psilocybe

P1unus
cubensis 3096, 3099
caroliniana 3146
spp 3097
spp 2960, 3148

Psilostrophe spp 3148

Pruritus 843

Psittacine

Pseudalleschmia 640
beak and feather disease 1908
boydii 640
nutrition 2288

Pseudechis 3159
pediatric diseases 1892

Pseudo-lumpy skin disease 869
polyomavirus 1907

Pseudocapillaroides 1740
proventricular dilatation disease 1909
xenopi 1740

Psittacosis 599, 2428, 2808
pet birds 1897

3292

INDEX

Psorerga I es

Pullets, nutrition (table) 2915
bos 917

Pullorum disease, poultry 2865
ovis 918

Pulmonary
spp 914, 1881
abscessation, cattle 1437

Psorergatic mange
acariasis, nonhuman primates 1880

VetBooks.ir
cattle 917
adenocarcinoma, sheep and goats 1477
sheep 918
aclenomatosis, sheep 1477

Psoriasiform
capillariasis 2456
dermatitis, juvenile pustular, pigs 979
disease, chronic obstructive, horses
lichenoid clermatosis, clogs 848

1443, 1455

Psornbia
edema 1414, 3008
bos 917
porcine 3008, 3018
ovis 918, 2576
emphysema 1428, 3008
spp 914
and edema, bovine 1439

Psornplw1-a
fibrosis, equine multinoclular 1446
colwnbiae 888
hemorrhage, exercise-induced, horses
spp 888, 889, 2879

1457

Pso1-optes
hypersensitivity syndrome, macaws
cuniculi 527, 915, 918, 1953

1889
eqiii 918
hypertension 125
ovis 915, 917, 918, 2751
pet birds 1914
spp 843, 914, 918, 1854, 2576
syndrome, poultry 2871

Psoroptic mange
hype1tensive hea1t disease, bovine 137
cattle 915
infiltration with eosinophilia 825, 1479
horses 918
noclulru· eosinophilic granulomatous
sheep 918
syndrome 1479

Psychic estrus, horses 1550
syndrome, hantaviral 24 70

Psychogenic water consumption,
thromboernbolism, small ru1imals 1487
potbellied pigs 1937

Pulmonic stenosis 71, 78

Psychological well-being, nonhuman

Pulpitis, small animals 180
primates 1884

Pulpy kidney disease 610

Psychotropic agents 2601

Pulse deficits 90
for feather plucking pet birds (table) 1928 Pulseless electrical activity 1673
for skin disorders 2584

Pulses, types 90

Ptaquilosicle poisoning 3090

Pulsion cliverticula, small animals 373

Pte1·idium

Pulsus
aquilinum 506, 1282, 2960, 3089, 3094,
al ternans 90

3148
bigeminus 90
spp 273
paracloxus 90

Pternlichus obtusus 2878
pru-vus et tru·d us 90

Pternphyllwn scalare 1814

Puncture wounds, foot, horses 1114

Pternp11 s spp 708, 721

Punishment

Ptyalism, small animals 367
negative 1541

Public health 2390
positive 1541
agencies 2390

Punkies 887
essential fw1ctions 2396

Punlignis tetrazona 1810
foci of prevention 2396

Pupillru-y
law 2411
light reflex 1215
national indicators 2395
membranes, persistent 496
roles of veterinarians 2391

Puppy hypoglycemia 1225
significant achievements 2393

Pure reel cell aplasia 13, 827
surveillance 2398

Purine

Puerperal
analogues 2732
hypocalcemia, small animals 571, 992
nucleosicles 2745
mastitis, sows 1373

Purple
metritis, acute 1368
allamancla 3116
tetany, small animals 571, 992
mint toxicity 1442

Puffy hock, cattle 1088
sesbane 3132

Pug encephalitis 1224

Purpura hemorrhagica, horses 830, 1182

Pu lex

Pustular
iiritans 1953
psoriasiform dermatitis, pigs 979
simulans 880
vulvovaginitis, infectious 1392, 1434

INDEX

3293

Puumala virus 2470

Quinclorac 2988

Pycnoscelus sw-inmnensis 2830

Quinidine 2536

Pyelonephritis

Quinolines 2796
cattle 1499

Quinolones 2669
pigs 1500
adverse effects and toxicity 2673

VetBooks.ir
small animals 1510
antimicrobial activity 2670

Pyloric stenosis 167
bacterial resistance 2671

Pyode1111a 863
classes 2669

Pyogranulomatous meningoencephalitis
dosages (table) 2673

1264
effects on laboratory tests 2674

Pyometra
general properties 2670
large animals 1370
interactions 2674
small animals 1397
mode of action 2670
stump 1397
pharmacokinetic features 2671

Pyramidal disease, horses 1115
therapeutic indications 2672

Pyrantel 264 7

Quiscalus quiscua 1313

Pyrazon 2988

Quittor, horses 1115

Pyrethrins 2750, 2756

Quizalofop-p-ethyl 2988
toxicity 3058, 3063

Pyrethroids 2750, 2756
toxicity 3058, 3064

R

Pyrethrum 3063

Rabbitpox 1951

Pyridate 2988

Rabbits 1937

Pyridostigmine 2588
bacterial diseases 1944

Pyridoxine deficiency, poultry 2943
bots 901

Pyrimetharnine 2674, 2796
calicivirus disease 1951

Pyrimidines
dental disease 1954, 1955
analogues 2732
dysautonomia 1257
nucleosides 2745
euthanasia 1941

Pyriprole 2756
fibroma virus 1950

Pyriproxyfen 2752, 2755
heritable diseases 1959

Pyrithiobac-sodium 2988
housing 1941

Pyrrolizidine alkaloidosis 3150
intestinal diseases 194 7

Pythiosis 641
management 1937

Pylhium
mycotic diseases 1944
insidiosum 378, 641
neoplasia 1959
spp 402, 2698
noninfectious diseases 1954
nutrient requirements (table) 1944
nutrition 1943

Q
orphaned kits 1939

Q fever 623, 2434
parasites 1952

Quadriceps
restraint 1938
contracture, small animals 1202

Shope fibroma virus 1950
tie-down, dogs 1202
therapeutics 1938

Quadriplegia, hereditary, Irish Setters 1235
viral diseases 1950

Quail

Rabies 1251, 1302, 2478
bronchitis 2913
f1.ufous form 1304
disease 2805
management 1306
nutrition (table) 2920
paralytic or dumb form 1304

Quarantine, zoo animals 2047
ringed seal 1870

Quarter crack, horses 1116
vaccination, exotic mammals 2059

Quaternary ammonia poisoning, poultry
zoonotic risk 1306

2862

Rachycentron canadum 1764

Queening 2227

Radfo1·d'ia

Queensland
affinis 2029
itch 887
ensifera 2030
tick typhus 2436

Radial

Qu,ercus
and ulnar dysplasia, dogs 1203
poisoning 3152
paralysis, cattle 1089
spp 3120, 3152

Radiation

Que1y fever 623, 2434
safety 1630

Quillaja saponaria 2768
scatter 1627

3294

INDEX

Radiation (continued)

Ratites 1960
therapy 1651
chick management 1964
pet birds 1917
digestive system disorders 1965

Radiculomyelopathy, chronic degenerative
infectious diseases 1964

1246
management 1960

VetBooks.ir

Radiography 1626
musculoskeletal disorders 1966
contrast procedures 1632, 1635
nutrition 2292
direct digital 1628
parasites 1965
interpretation 1631
reproduction 1962
patient restraint 1629
toxicities 1966
processing 1628
trauma 1966
safety 1630

Rats 2025-See also Rodents
thoracic 91
as laboratory animals, management 2032

Radiology, interventional 1655
as pets, diseases of 2028

Rafoxanide 2650
biology 2025

Ragwort 3150
husbandry 2025
toxicity 3150
neoplasia 2030

Raillietina
physical examination 2027
celebensis 2454
zoonotic risk 2032
ces ticillus 2830

Rattle
demeraiiensis 2454
belly, lambs 274
echinobolhrida 2831
weed 3118
infection 2454

Rattlebox 3132, 3140
spp 2454, 2828

Rattus
tetragona 2831
no1'Vegicus 1838, 2030, 2470

Railroad disease/siclmess 1030
rattus 2030, 2470

Rain lily 3118
spp 2456

Raisins, poisoning 2968

Rayless goldenrod 3134

Ramaiiaflavo-brunnescens 3102

Reactive aitway disease, horses 1443

Ramichlo1idiwn 643

Recall bias 2401, 2402

Ramphas/os spp 2293

Recirculating aquaculture systems 1754

Rams

Recording, digital lesions, cattle 1068
feeding 2351

Rectal
reproductive management 2217
atresia 169

Ram.a
diseases 187
catesbeiana 1738, 1743
neoplasms 189
pipiens 1741, 1743
polyps 189

Randomized controlled trials 2402
prolapse 189

Range
potbellied pigs 1934
paralysis, poultry 1822
strictures 189
plants, poisonous 3103
pigs 300
supplements, sheep (table) 2352°
tears 190

Rangifer spp 1313
horses 1721

Ranitidine 2551, 2558, 3030
temperature ranges (table) 3173

Ranula, small animals 368

Rectourethral fistula 169

Ranunculus

Rectovaginal
bulbosus 977
constriction 1332
spp 977
fistula 169, 1499

Raphanus spp 3138

Recurnbency, bovine secondary 1188

Raphidiopsis 2956

Recurrent

Raptors, nutrition 2291
aitway obstruction, horses 1455, 2152

Rash illness, Southern tick-associated
diarrhea, horses 288

2420
uveitis, equine 508

Rat

Red
bite fever 2428
bag delivery 2094
tail syndrome 615
blood cell(s) 4
tailed maggot 903
count 1610
tapeworm 2454
evaluation 1614

Rathayibacter toxicus 3153
indices/measurements 8, 1610

Rations
in urine 1617
dairy cattle 2278
cell aplasia, pure 827
goats 2311
eye 1699

INDEX

3295

Red (continued)

Repetitive behaviors 1535
leaf photinia 3146
canine 1561
leg syndrome, amphibians 1737

Replacement
maple 3126
breeding progran1, cattle 2172
mites 2877
heifers 2125

VetBooks.ir
pet birds 1906

Reproduction-See also Breeding,
nose, cattle 1434

Partmition
sea bream iridovirus 1814
backyard poultry 1818
stomach worm, pigs 322
hormonal control 2244
tears, rats 2032
llamas and alpacas 1848
tip photinia 3146
management
water disease 341, 601
cattle 2120, 2171, 2174
worm disease, fish 1808
goats 2182
worms, horses 316
horses 2187

Redirected
pigs 2201
aggression, dogs 1563
potbellied pigs 1931
behavior 1537
sheep 2212

Regenerative anemias 9
small animals 2219

Regional anesthesia
nutrition in, small animals 2378
cattle 1068
phannacologic control 1329
horses llOl
rabbits 1939

Regurgitation, pet birds (table) 1900
ratites 19G2

Reinforcement
zoo animals 2046
negative 1541

Reproductive
positive 1541
cycle, features 1326, 1327

Reinforcers, second-order 1541
diseases

Rejection of lambs 1556
female small animals 1393

Relapsing fever 2420
male small animals 1400

Relative
pet birds 1920
erythrocytosis 43
poultry 2896
risk 2401
reptiles 2001

Relaxants, skeletal muscle 2588
indices, swine 2202

Relaxin 1624
and respiratory syndrome, porcine 729

Relay poisoning 3165
system

Renal-See also Kidney
congenital and inherited anomalies
agenesis 1497

1329
anomalies 1496, 1497
introduction 1323
cysts 1497
phannacotherapeutics 2606
disease
principles of therapy 1328
anemia in 13
technologies 1329
ferrets 1828
therapy, effect on fetus or neonate
goldfish 1806

2608
horses, nutiition in 2329

Reptiles 1967
hypocalcemia 571
anestl1esia and analgesia 1977, 1978 (table)

pet birds 1913
antimicrobial drugs used in (table) 1985
dropsy, goldfish 1806
bacterial diseases 1991
dysfunction
drug used in (table) 1989
diagnostic tests 1496
endocrine diseases 2000
small animals 1512
environmental diseases 1999
dysplasia 1496
food composition (tables) 1972
failure, hypercalcemia 565
husbandry requirements (table) 1970
glucosuria, small animals 1521
management 1968
hypoplasia 1496
metabolic diseases 2000
lipidosis, mink 1876
mycotic diseases 1993
secondary hyperparathyroidism 1056
neoplastic diseases 2002
tubular
nutrition 1969, 2302
acidosis, horses 1507
parasites 1996
defects, small animals 1520
parasiticides used in (table) 1987

Rendering 1640
physical examination 1971

Renibacteriiim salmoninarum 1759
pneumonia 1992

Reoviral infection, poultry 2886
protozoa! diseases 1998

Reoviridae 696
reproductive diseases 2001

3296

INDEX

Reptiles (continued)

Reticuloendotheliosis, poultry 2854
respiratory infections 1992

Reticulopericarditis, tratm1atic 123
restraint 1971

Reticuloperitonitis, traumatic 230
space requirements (table) 1968

Reticulosis
traumatic injuries 1999
inflarnmato1y 1252

VetBooks.ir
viral diseases 1994
neoplastic 1252

Residues
pagetoid 962
chemical, food and fiber 2518

Reticulum cell sarcomas 961
in foodstuffs 2519

Retinal

Resistance
atrophy 503
anthelmintics 2644
degeneration 1701
antifungals 2697, 2698, 2701, 2703, 2704
detachment 503, 1701
antimicrobials 2622, 2630, 2631, 2633,
dysplasia 502

2653,2660,2664,2671, 2676,2680,
pigment epithelial dystrophy 503

2684,2688,2690

Retinoids 2737
antineoplastic agents 2723

Retinopathies, inherited 502

Resorptive lesion (tooth), small animals

Retractor penis muscle, short 1331

181

Retrobulbar hemorrhage, traumatic 1696

Resource guarding, dogs 1563

Retrospective cohort study 2400

Respiratory

Reverse
diseases
sneeze 1488
cattle 1429

T, 553
control 1415

Rhctbclias spp 1736, 1740, 1997
horses 1443

Rhabditic dermatitis 907
llamas and alpacas 1854

Rhabditorids causing CNS disease 1313
pigs 1464

Rhabdomyolysis
reptiles 1992
horses 1176
sheep and goats 1471
small animals 1202
small animals 1478
syndrome, horses 1048
nutrition in 2384

Rhect
distress syndrome, acute, feedlot cattle
americanct 1960

1442
pennala 1960
and neurologic syndrome, porcine 721

Rheas 1960
rates, resting (table) 3174

Rheumatoid arthritis, canine 822
severe acute syndrome 2478

Rhinella marina 3161
sinus arrhythmia 68

Rhinitis 1413
sounds 90
allergic 824
stimulants 2616
cattle 1429
syncytial virus, bovine 1433
atrophic, pigs 1465
system
necrotic, pigs 1468
introduction 1411
rabbits 1945
neoplasia, small animals 1484
small animals 1488
pharmacotherapeutics 2608

Rhinoclaclosporium spp 1739
principles of therapy 1416

Rhinoeslius pwpiinms 2464
tract

Rhinopneumonitis, equine 34.1
inflammation, horses 1456
viral 1344, 1444
viral infections, cattle 1433, 1436

Rhinoplem bonasus 1806

Response substitution 1542

Rhinosporidiosis 644, 2444

Reston ebolavirus 2470

Rhinospoi·icliwn

Restraint
seeberi 644, 2444
marine mammals 1856
spp 2697
zoo animals 2049

Rhinotracheitis

Restrictive cardiomyopathy 119
feline viral 1481

Resuscitation
infectious bovine 1434
cardiopulmonary 1670
and abortion 1334
endpoints (table) 1683
vaccination of exotic
foals 1724
mammals 2055

Retained
turkey 2904, 2907
fetal membranes, large animals 1381

Rhipicentoi·
placenta, large animals 1381
bicornis 935
spectacles, reptiles 1974
nullctll'i 935
ulnar cartilage cores, dogs 1204
spp 928, 935

INDEX

3297

Rhipicephalus

1ubropei·tinctus 1345
annulatus 936, 2441
spp 666, 671, 679, 2689
cippendiculatus 34, 761, 937, 940, 2435

Rhoclocleiidrnn spp 3094, 3112
bergeoni 938

Rhodotomla

Boophilus (subgenus) 935
mucilaginos'is 1904

VetBooks.ir
bursa 23, 935
spp 2699
camicasi 938

Ribavirin 2745, 2746
capensis 938

Ribeirnla 1740
compositus 938

Riboflavin deficiency
decolorntus 936, 2435
horses 2328
duttoni 937, 939
pigs 2344
evertsi 935, 937
poultry 1242, 2941
evei·tsi 937, 1315

Ricinus communis 3148
mimeticus 937, 1315

Rickets 1051
gertrudae 938
adult 1052
gla brnscutatiirn 935 , 937
mink 1875
guilhoni 938
nonhuman primates 1883
haeinaphysalo·ides 936
pigs 1161, 1163
hurti 938
poultry 2881, 2930
jeanelli 938

Rickettsia 624
kochi (neavi) 937
aeschlimannii 933, 2436
longus 938
a.fi'icae 929, 2434
liinulatus 938
akari 2032, 2436
micrnplus 935, 940, 941, 2441, 2576,
amblyomnii 928, 2436

2752
australis 2436
moiicheti 938
con01ii 933, 936, 2434
muhleiisi 938
felis 807, 882
nitens 937
heilongjiangensis 931, 2436
occulatus 937
helvetica 2436
pilans 936
honei 930, 2436
praetextal.us 938
japonica 2436
prnvus 937
massiliae 937, 2436
pseudolongus 938
monaceiisi 2436
pulchellus 937
moosei·i 2436
piimilio 936, 2437
parkeri 520, 806, 929, 2436
punctatus 937, 1315
prowazekii 909, 2348
pusillus 936
moult ii 931, 2436

Rhipicephalus (subgenus) 936

1·hipicephali 937
rossicus 936
ricketts'ii. 51, 803, 806, 928, 929, 930,
sanguineus 23, 29, 803, 806, 935, 936,

937, 1250

941, 1315,2435,2437
salmonis 1760
sanguineus 696
sibirica 931, 2436
schulzei 936
slovaca 931, 2436
seiiegaleiisis 938
spp 520, 623, 911, 928, 1760, 1971, 2032,
simus 938

2416,2567,2684,2688
seiisu stricto 938
typhi 807, 882
spp 19, 21, 23, 761, 803, 927, 928, 935,

Rickettsial

941, 1314,2435,2471
diseases
sulcatus 938
fish 1760
supert1·itus 938
small animals 803
tricuspis 938
spinal column and cord 1250
turanicus 936, 938
thrombocytopenia 48
zambeziensis 937
zoonotic 2432, 2434, 2436, 2438

Rh'izoctonia legmninicola 214, 3019
pox 2436

Rhizopus spp 1335, 1739, 1901

Rickettsiosis, chigge r -borne 2438

Rhodnius 39

Rieinernlla 2894

Rhodococcosis 679
anal'ipest�fe1· 2800, 2827, 2894, 2929

Rhodococcus
infection, birds 2864
equi 67, 158, 289, 316, 341, 354, 359, 505, Rifamide 2694

679, 1263, 1443, 1451, 1452, 1709,

Rifampicin 2694

2153,2196,2688,2694

Rifampin 2694
pnemnonia 1451

Rifan1ycins 2694, 2748

3298

INDEX

Rift Valley fever 768, 2478

Round cells 1602

Right
tw11ors, differentiation 1604
displaced abomasum 238

Rowid heart disease, turkeys 2790
dorsal colitis, horses 265

Roundworms-See also Nematodes
dorsal displacement of colon, horses 264
birds 1905

VetBooks.ir
heart failure 103
pigs 320
hepatic lobe atrophy, horses 350
raccoon 416
torsion, abomasum 238
small animals 415
ventricular cardiomyopathy,
turkey 2831
arrhythmogenic 117
zoonotic infections 2454, 2456, 2458,

Rirnantadine 2746, 2747

2460,2462

Rirnsulfuron 2988

Roup, birds 2804

Rindcrpcst 771

Roxarsone 2797

Ringbone 1119

Rubber

Ringtail, rats 2031
jaw syndrome 1054, 1057, 1205

Ringworm 872, 2440-See also
puppy disease 50

Dermatophytosis
tree 3110
backyard poultry 1823
vine 119
nonhw11an primates 1880

Rubeola infection, nonhuman primates
rabbits 1949

1882

Risperidone 2604

Ruelene toxicity 3067

Risus sardonicus 1255

Rule of 20 1685

Roachback 1047

Rumen

Roaring, horses 1458
impaction 222

Robenacoxib 2720
flukes 328

Robenidine 2797

Rwnenitis 222

Robinia pseudoacacia 3130

Rumex crispus 3130

Rock fern poisoning 3091

Ruminal

Rocky Mountain
acidosis 225
spotted fever 51, 806, 926, 1250, 2436
drinking 236
wood tick 930
fluid transfer 2562

Rodenticides, anticoagulant
parakeratosis 237
ingestion 53
tynlpany 227
poisoning 3165

Rw11inant
poultry 2860
digestive system, pharmacotherapeutics

Rodenlolepis nana 2013

2561

Rodents 2002--See also Mice, Rats
forestomach, diseases 221
biologic data (table) 2003
prepmchase examination 1649
bots 901
urolithiasis 1502
nutrition 2300

Ruminoreticular

Rolitetracycline 2679
acidifying agents 2563

Romanowsky stains 1598
antacids 2562

Ronidazole 2696
motility modifiers 2563

Ronne! toxicity 3067

Ruminoreticulum, drug disposition 2564

Roost mite 2877

Ruminotorics 2562

Rosary pea 3104

Rwiting-stunting syndrome, chickens

Ross River fever 2478

2840

Rostral

Rupture
cerebellar vermis herniation 1277
cranial cruciate ligament, small animals
displacement of palatopharyngeal arch,

1198
horses 1461
fibularis longus muscle, turkeys 2885

Rotational defonnities, birds 1895, 2881
gastrocnemius muscle/tendon

Rota virus
cattle 1091
birds 2803
poultry 2885
cattle 272
longus capitis muscle, horses 1464
enteritis, pigs 301
peroneus
foals 144, 290
longus muscle, turkeys 2885
lan1bs 273
tertius, cattle 1091
rabbits 1951

Russian
ruminants 276
knapweed 3126

Rotenone 3063
spring-summer encephalitis 2480

Rotlaufseuche 701

Russula emelica 3096, 3099

INDEX

3299

Rust, fish 1802

Gallinarum 195, 199, 1815, 1822, 2865,

Rye grass

2866
staggers

Hadar 2866
annual 3153

Heidelberg 297, 1822, 2866
perennial 3008, 3154

Infantis 297

VetBooks.ir
toxicity 3153

Kentucky 1822, 2866
s

Montevideo 195

Muenchen 282

Saaremaa virus 2470

Newport 195, 282, 1825

Sabelhes spp 2482

Paratyphi 195

Sabia virus 2476

Pullorum 195, 1815, 1822, 2865, 2866

Sacahuista 3118

SaintpauJ 2866

Saccharomyces
spp 119, 158, 195, 272, 275, 281, 287, 288,
boulardii 286

289,300,325,329,340,354,374,
cernvisiae 2343, 2848

378,396,399,403,459,623,671,

Sacchm·omycopsis guttulat.a 2009

682, 749, 1263, 1337, 1343, 1473,

Saccharopolyspora Spinosa 2756

1711, 1823, 1830, 1832, 1835, 1853,

Sacrocaudal dysgenesis 1230

1863, 1878, 1897, 1933, 1962, 1964,

Sacroiliac joint abormalities, horses 1147

1971, 1991, 1993,2006,2016,2045,

Saddle sores 979

2048,2052,2068,2089,2092,2123,

S-Adenosylmethionine 2561

2130,2135,2170,2376,2394,2406,

Sagenomella 640

2410,2414,2654,2655,2659,2665,

Saguinus spp 1876

2671,2684,2692,2695,2696,2766,

Saimiri sciureus 1876

2798,2805,2865,2866,2871,2883,

Saint

2894,2896,2898

Bernard's lily 3108

TiJene 1835

John's wort 3144

Typhi 195

Louis encephalitis 2478
lyphimurium 195, 199, 275, 280, 281,

Salbutamol 2610, 2614

297,300, 1339, 1822, 1825, 1835,

Salicyclic acid 2739

1933,2866

Salicylanilides 2638, 2641, 2650

Typhisuis 297

Salicylazosulfapyridine 2674
vaccines 199

Salinomycin 2765, 2796

W01thington 297
poisoning, poultry 2862

Salmonellosis 195, 2430

Salivary
backyard poultry 1822
disorders, small animals 367
cattle and sheep 196
fistula, small anin1als 368
dogs and cats 197
gland
horses 196, 281
infarction 369
pigs 196
necrosis 369
intestinal 296
tumors, small animals 368
poultry 2865
mucocele, small animals 368
sheep 274

Salmeterol 2614
and abortion 1339

Salmo spp 1762

Salmon poisoning

Salmon
disease 808
anemia, infectious 1764
fluke 426
poisoning disease 808

Salmonid alphaviruses 1765
poisoning fluke 426

Salpingitis, poultry 2898

River virus 2468

Salsola, luberculali}'<nmis

Salmonella

1380

Abortusovis 195, 1339, 2217

Salt

Agona 281
deficiency

Anaturn 195
horses 2326

Arizonae 1993, 2865, 2866
marine mammals 1860

Choleraesuis 195, 199, 297, 627, 671,
poultry 2935

721, 730, 733, 1825, 1933, 1935
requirement, sheep 2346
kunzendorf 297
toxicity 3083

Derby 297
mink 1875

Dublin 195, 199, 275, 1339
poultry 2863
enlerica 195, 281, 2420, 2823, 2865
potbellied pigs 1936

Enteritidis 195, 199, 1823, 1835, 2191,

Salvelinus spp 1762

2866,2877

Sambucus nigra 2960

3300

INDEX

SAMe 2561

Sarcoptes

Sample collection and submission 1584
scabiei 521, 1826, 1881, 1953,2576,2577

Samples for clinical biochemistry 1594
var bovis 914, 917

San Miguel sea lion virus 738, 1867
var canis 920

Sand
var caprae 917

VetBooks.ir
enterocolopathy, horses 287
var equ i 918
fleas 2466
var ovis 917
flies 887
var suis 2162
tampan 939
spp 843, 855, 914, 917, 1387, 1621, 1854,

Sand crack

2576
cattle 1085

Sarcoptic mange-See also Mange
horses 1116
cattle 914

Sanitation
dogs 920
abattoir 1646
horses 918
laboratory animals 1841
pigs 919

Sansevie,ia spp 3114
potbellied pigs 1934

Saprnlegnia
sheep 917
diclina 641

Sarcosporidiosis 2444
spp 641, 1761, 1778, 1803, 1811

SARS 2478

Saprolegniasis, amphibians 1739

Saucer fractures, horses 1123

Sarcobatus vermiculal11s 3120

Scab, sheep 918

Sarcocystis

Scabies
auchenfoe 1059, 1346
canine 920
calcha si 1059
cattle 914

CClp1'0CCllliS 1059, 1172
feline 921
crnzi 10, 1059, 1172, 1346

Seal ct, cattle 1080

.fayeri 1059, I 060

Scale rot 1991

.fus�f'cmn is 2444

Scaly
gigantea 1059
face mite, pet birds 1906
hirciccrn is 1059
leg mite, poultry 2878
hii'suta 1059, 1172

Scapulohumeral dysplasia, miniatme
hominis 1059, 1172, 2444
horses, 1128
marine mammals 1867

Scarlet red 2744
medusi.formis 1059

Scatter radiation 1627
meischaiana 1059, 2444

Scedospoiiwn 640
moule'i 1059
apiospe1mum 640, 1901
nesbilli 2444

Schejfiem spp 3114
neurnna 663, 1060, 1251," 1264, 1291,

Schiff-Sherrington phenomenon 1219, 1254

1309, 1867, 1907,2152

Schislosoma
ovicanis 1172
bovis 31
porcUelis 1059
curnssoni 31
sinensis 1059
guineensis 2450
spp 158, 208, 686, 1058, 1172, 1309, 1867,
haematobiwn 31

2444,2785,2798
incognilum 31
suihominis 1059
indicwn 31
tenella 1059
inte,·calalwn 2450

Sarcocystosis 1058, 2444
japonicwn 31
pet birds 1906
mansoni 2450
horses 1180
mmgrnbow'iei 2450
ruminants 1172
mallheei 31

Sarcoids, equine 954
mekongi 2450
periocular 516
nasale31

Sarcomas
spi ncla le 31
anaplastic 961
spp 31, 1881, 2650
histiocytic 1272

Schistosomiasis 31, 1312, 2448
mast cell 963
nasal 32
reticulum cell 961
urinary 2450
soft tissue 955
visceral 32
spindle-c-ell, canine 959

Schistosom us reflex us 620
undifferentiated 961

Schmallenberg virus 622

Sa.rcomatosis, histiocytic, poult1y 2856

Schrock 3148

Sm'COphaga spp 895, 897

Schwannomas 958, 1242

INDEX

3301

Sciaenops ocellatus 1 764

Select agents 2393

Sciatic

Selection bias 2399, 2402
nerve injuries 1244

Selective serotonin reuptake inhibitors
paralysis, cattle 1089

2605

VetBooks.ir

Scissor beak, birds 1896
toxicity 3034

Sclerostomes, horses 316

Selegiline 1545

Scolecobasidiwn 643

Selenium

Scoliosis, congenital, foals 1047
deficiency 1174

Scombroid poisoning, marine mammals
horses 2327

1860
pigs 2344'

Scorpion bites 3162
poultry 2936

Scorpions 3162
poisoning 3085

Scottish Fold osteodystrophy 1204
poultry 2863

Scotty cramp 1232
requirement

Scours 275
pigs 2347
bloody, pigs 301
sheep 2353

Scrapie 1288

Selenomonas ruminantium 226

Scratches, horses 1116

Self

Screwworm 2462
anointing, hedgehogs 1828

New World 899
care, veterinarians 1580

Old World 900
mutilation, horses 1549
primary 899
suckling, goats 1557

Scrotal

Semduramicin 2796
hernias 167

Semen
mange, rams 917
collection

Scrub typhus 2438
boars 2204

SCUD, tmtles 1991
bucks 2183

Scmvy, nonhumai1 primates 1883
bulls 2175, 2232

Sebaceomas 950
cats 2221

Sebaceous
dogs 2238
adenitis 523
horses 2235
granulomatous 848
rams 2217
cysts 947
evaluation
glands 838
boars 2205
sheep 1170
bucks 2183
tumors 950
bulls 2232
hyperplasias, senile 950
cats 2221

Seborrhea 980
dogs 2221, 2238
ear margin 523
horses 2235

Seborrheic syndromes 847
rams 2218

Secobai·bital 3035

Semi-ring block at the pastern, horse 1104

Secondary

Seminal vesiculitis, bulls 1383
erythrocytosis 43

Seminole bread 3114
hyperparathyrnidism, renal 1056

Senecio
nutritional hyperparathyroidism;
jacobea 3150
reptiles 2001
longilobus 3150
photosensitization 977
poisoning 3150
poisoning 3165

1·iddellii 3150
pregnai1cy toxemia 1022
spp 618, 977, 3012, 3046, 3074, 3148,
recumbency, bovine 1188

3150
renal hyperparathyroidism; reptiles 2001

Seneciosis 3150
ruminal tyn1pany 228

Senile
visceral gout, reptiles 2000
keratosis 945

Second-intention healing 1704
sebaceous hyperplasias 950

Sedatives 2600

Senna 2559

Segmental aplasia
coffee 2886, 3094, 3124
mesonephric duct structures 1331
obtusij'olia 1175, 2861, 3124
of the rectum 169
occiclentalis 1186, 2886, 3094, 3124

Seizures

Sennetsu
control 1220
ehrlichiosis 808
potbellied pigs 1936
fever 2434

Selan1ectin 2576, 2647, 2754

Sensitivity 2403

3302

INDEX

Sensitization (behavior) 1542

Sethoxydim 2988

Sensorineural deafness 519

Severe acute respiratory syndrome 2478

Sensory

Sex
ganglioneuritis 1241
honnones 573, 2581
neuropathy
reversal, poultry 2899

VetBooks.ir

Border Collies 1232

Sezary syndrome 962

Dachshtmds 1232

Shaker

Pointers 1232
calf syndrome 1234

Seoul virus 2470
foal syndrome 606

Separation anxiety, canine 1560

Shaky mink syndrome 1874

Sepsis

Shampoo 845
clinical manifestations 2092
poisoning 3004
foals 1728, 2089

Shaping behavior 1542
small animals 455

Shar-Pei fever 473

Septic arthritis

Shasta River crud 283
distal interphalangeal joint, cattle 1088

Sheared heels, horses 1117
lan1initis, sheep 1171

Sheath rot 1372
large animals 1062

Shedding
small animals 1197
of the teeth 164

Septicemia
skin, reptiles 2000
hemorrhagic 756

Sheep-See also Ovine
in salmonellosis 197
extensive grazing 2164

Septicemic
gastrointestinal parasites 312
colibacillosis 749
health-management interaction 2164
cutaneous ulcerative disease, turtles
keds 893

1991
lameness 1166
disease 749
management 2164

Serologic test kits 1621
nose bot 1473

Serology san1ples 1587
nutrition 2345

Serositis
nutritional diseases 2353
infectious, birds 2864
organic production 2166
transmissible 1308
pregnancy determination 2216
large animals 1065
pulmonary adenomatosis 1477

Serotonin
reproduction, management of 2212
and inflammation 2708
respiratory diseases 1471
syndrome 3035
scab 918

Serous tarsitis, cattle 1088
tick 934

Se17alia

Sheeppox 869
marcescens 1359, 1896

Shigella spp 158, 1878, 2655, 2659, 2692,
spp 1366, 1991, 2680

2696

Sertraline 1544, 2605

Shigellosis, nonhuman primates 1879
toxicity 3034

Shins

Serum
bucked, horses 1123
amylase 1593
sore, horses 1123
biochemical reference ranges (table)

Shipping fever pneurn�mia 1431, 1432, 2130

3178

Shivers, horses 1183
biochemistry analysis 1590

Shock 1675
hepatitis, horses 338
anaphylactic 824
lipase 1593
hypovolemic 1665
trypsin-like irnmw1oreactivity 1593,

Shooting star 3108

1594

Shope fibrorna, rabbits 1950

Service dogs 1578

Short retractor penis muscle 1331

Sesamoid

Shoulder fractures, horses 1128
fractures, horses 1119

Shunts
nerve block, horses 1104
cardiac 79, 83

Sesan1oiditis, horses 1120
portosystemic 169

Sesbane 3132
acquired, small animals 450

Setaria

Shuttle progran1, poultry 2794
ce1·vi 1313

SI conversion factors (table) 3180
digitata 1312

Sialadenitis, small anin1als 369
spp 671, 906, 908, 1252, 1264, 1297, 1313, Sialadenosis, dogs 369

2321

Sialocele, small animals 368

INDEX

3303

Sialornetaplasia, necrotizing, dogs 369

Sinusitis

Siberian ulcer 593
cattle 1429

Sick sinus syndrome 72, 93
horses 1462

Sicklepod 3124
infectious, birds 2841

SI conversion factors (table) 3180, 3181
small animals 1488

VetBooks.ir

Sidebone, horses 1117

Sisomicin 2663

Siduron 2988

Sit-fasts 869
poisoning 2998

Situs inversus 86

Sildenafil 2535

Skeletal -See also Musculoskeletal

Silent heat
disorders, poultry 2880
cows 1551, 2173
hyperostosis, diffuse idiopathic 1247
horses 1549
muscle relaxants 2588

Silica stones, dogs 1531
dosages 2589

Silky lupine 3144

Skin 837-See also Integumentary system

Silo filler's disease 1442, 2955
autoimmune djsorders 827

Silver
congenital anomalies 846
compounds 2741
diseases
sulfadiazine 2675
diagnosis 839

Silverling 3138
history 839

Silvex poisoning 2997
laboratory procedures 840

Simazine 2988
llamas and alpacas 1854
poisoning 2999
physical examination 840

Simian
fragility syndrome 974
immunodeficiency virus 821, 1882
grafts 1706
type D retrovirus 821
helminths 904

Sin1mental encephalomyelopathy 1227
leukosis, poultry 2850

Simondsia 322
maggot fly 902

Simons'iella 1606
photosensitization 976

Simple
pigment abnormalities 848
indigestion, ruminal 221
shedding, reptiles 2000
renal cysts 1497
tw110rs 942

Sin Nombre virus 2470

Skijab'ingylus

Simulium
chitwoodmum 1313
callidum 886
nasicola 1313
damnosum 886

Skunk cabbage 3126
exiguum886

Slaframine toxkosis 214, 3019
metallicum 886

Slavers or slavery mouth, lan1bs 27.4
neavei 886

Sled-runner hooves, goats 1092
ochraceum 886

Sleep aid toxicity 3034, 3035
spp 521,524,886,905,2783,2875

Sleeping

Sindbis virus 1292, 2478
disease, fish 1765

Single photon emission computed
sickness, African 2444
tomography 1639

Sleepy foal disease 589

Sink lupine 3144

Slender turkey louse 2876

Sinoatrial

Slipper foot, cattle 1086
arrest 93

Slobbers
block 93
chinchillas 2008

Sinus
rabbits 1954, 1957
arrest 93
syndrome 3008
arrhythmia 93

Slurry heel, cattle 1079, 1080
respiratory 68

Smacking, horses 1546
beat, hybrid 97

Small
bradycardia 92, 1673
airway inflanunatory disease, horses
cysts, horses 1463

1456
node abnonnalities 92
animals-See also Cats, Dogs
pause 93
breeding soundness 2219
rhythm 92
care and grooming 2169
tachycardia 93
diseases of the mouth 361

Sinuses
estrus manipulation 2225
dermoid 846
health-management interaction 2169
head and neck 165
lameness 1192
paranasal, horses 1462
management 2169

3304

INDEX

Small (continued)

cephapirin 2663
nutrition 2170, 2354
chlorate 2988
parasite control 2170
poisoning 2996
preventive health care 2169
chloride
reproduction, management of 2219
deficiency 2344

VetBooks.ir
respiratory diseases 1478
poultry 2935
traveling 2170
poisoning 3083
vaccinations 2169
deficiency
body louse (poultry) 2876
marine mammals 1860, 2298
head matchweecl 3142
poultry 2934
head sneezeweecl 3142
hydroxide 2739
intestine
iodide 2706
congenital anomalies 168
µentobarbital 2595
diarrhea 157
perborate 2740
distention, large animals 247
requirement, pigs deficiency
fibrosis, horses 293
restriction, for heart failure llO
mesenteric torsion, pigs 296
salts 2560
volvulus, horses, 260
stibogluonate 2577
liver fluke 2448

Soft
stomach worm, cattle 308
fibromas 955
strongyles, horses 317
palate dorsal displacement, horses 1459

Smears 900
tissue
impression 1599
clisorclers, cattle, and lameness 1091

S-Methoprene 2752
sarcomas 955

Smoke inhalation 3021

Solanurn

Smooth muscle tumors, cutaneous 961
esuriale 1053

Snake
rnala,coxiJlon 566, 570, 1053
mite 1974, 1996
pseudocapsicurn 3114
plant 3114
soclornaeurn 570

Snakebite 3159
spp 3130

Snakeroot, white 3128
torvwn 1053

Snakes

Solar
bacterial diseases 1991
dermatitis
clysecclysis 2000
feline 525
envirorm1ental disease 1999
nasal, clogs 975
inclusion body disease 1994
clermatosis 945
management 1968
keratosis 945
mycotic diseases 1993

Sole
nutrition 2306
bruised, horses 1107
parasites 1996
double, cattle 1084
traumatic injuries 1999, 2000
foreign bodies, cattle 1084
viral diseases 1994
hemorrhage, cattle 1079

Snakeweecl 3142
thin, cattle 1079

Snapping, horses 1546
ulcer, cattle 1076

Sneezeweecl 3142

Solenopotes capilla,tus 910, 2576

Snotsiekte 758

Solenopsis

Snowbreacl 3108

'invicta 3165

Snuffles, rabbits 1945

1ichteri 3165

Soap poisoning 3004

Solvents, toxicity 3069

Social behavior 1545

Somatostatin 579
cats 1570

Somatotropin 542, 2581
cattle 1551

Sophom secundijlom 3134
chickens 1557

Sorbitol 2560
clogs 1557
clehyclrogenase 1592
goats 1556

Sore
horses 1545
hocks, rabbits 1958
sheep 1555
mouth, sheep and goats 866,
swine 1553

2150

Socia lye 2739
muzzle, sheep 739

Sodium 1591
nose, gerbils 2012
arsenite poisoning 2994
shins, horses 1123
carbenicillin 2658

Sorehead 904

INDEX

3305

Sorghum

Spindle cells 1603
bicolor 2960

Spindle-cell sarcoma, canine 959
halepense 2321, 3148

Spinetoram 2756
poisoning 1254, 3155

Spinosad 2577, 2751
spp 1254, 2960

Spinosyns 2751, 2756

VetBooks.ir
sudcinense 618, 2321

Spinous ear, tick 520
vulgcire 618, 3148

Spiramycin 2687

Sorrel 3130

Spirillum minus 2428

Creeping lady's 3116

Spirocerca lupi 371, 372, 412, 419
wood 3116

Spirochetosis
yellow wood 3116
avian 2813

Sotaliafluvialilis 1864
intestinal, pigs 297

Sotalol 76, 2538
rabbits 1949

Sour crop, poultry 2791

Spiroindoles 2638

Soiiroubea 1543, 1567

Spirometra

South African paralysis tick 934
mansonoicles 423

Southern tick-associated rash illness 2420
spp 426, 1997, 2454

Sow management 2202

Spironolactone 75, 2624, 3034

Space requirements

Spironucleus
egg-strain birds (table) 2931
colwrnbae 2801
meat-strain birds (table) 2932
meleagridis 2801

Sparganosis 2454
mm·is 2029

Spasmolytics 2588
spp 1755, 1783, 2801

Spastic

Spirurid worms, reptiles 1997
paresis, cattle 1091, 1231

Splayleg
syndrome, cattle 1090
birds 1895

Specific gravity, urine 1615
piglets 1049, 1157

Specificity 2403
rabbits 1959

Spectacles, retained, reptiles 1974

Splendidqfi.laria quiscula 1313

Spectinomycin 2663, 2669

Splenic fever 593

Specular reflector 2194

Splenomegaly, ferrets 1827

Spem1atogonial stem cells 2231

Splints, horses 1123, 1124, 1132

Spermiogram values, boars 2207

Spondylomyelopathy, cervical, small

Spennophilus spp 677
animals 1230

Sphaerospora auralus 1806

Spondylopathies, poult1y 2881

Spilopsyllus cuniculi 521

Spondylosis

Spider
ankylosing, cattle 1086
bites 3162
deformans 1249
flies 893

Spongiforrn
lan1b syndrome 1048
degenerative conditions 1235
plant 3108
encephalopathy, bovine 1284

Spina bifida 1228, 1230

Spontaneous

Spinal
cardiomyopathy, turkeys 2790
abscesses, pigs 1163
recovery (behavior) 1542
accessory nerve 1217

Sporadic
column and cord diseases 1245
bovine encephalomyelitis 1308
cord
exertional rhabdornyolysis 1178
acute injmy 1221
lyrnphosarcoma, bovine 743
disorders 1222, 1227

Sporidesmins 3015
tumors 1275

Sporolhri:;;
defects
schenckii 644, 1863, 2415, 2440, 2576,
cattle 1046

2697,2703,2705,2706
foals 1047
spp 2574
dysraphism, small animals 1230

Sporotrichosis 644, 2440
muscular atrophy 1248

Spotted
large animals 1227
fever 2434, 2436
small animals 1228
laurel 3106
osteomyelitis, reptiles 1993

Spraddleleg, piglets 1049, 1157
osteopathy, reptiles 1993

Spraying (mine), cats 1570, 1572
processes, horses 1146

Spring
reflexes 1218, 1219
summer encephalitis, Russian 2480
trauma 1254
viremia of carp 1813

3306

INDEX

Squamous cell carcinoma

Slegasles parlilus 1814
cutaneous 945

Stem cells spermatogonial 2231
in situ, feline multicentric 947

Stenella coe11tleoalba 1867
ocular

Stenosis
cats 518
cardiac valves 71

VetBooks.ir
cattle 515
esophageal, small animals 371
horses 516
pyloric 167
oral 367
teat 1388
pet birds 1916

Step mouth 177
poultry 2855

Slephanofilaria

SSRI toxicity 3034
slilesi 891, 907

Stable
zahee1i 908
files 800

Stephanofilariasis 907
footrot, cattle 1080

Stephanurns

Stachybotryotoxicosis 3010, 3021
denlalus 321, 1252, 1314, 1502, 1618

Stachybolrys 3010, 3020
sp 1502, 2649

Staggergrass 3122

Stereotypic behaviors 1537

Staggering disease 1252
cats 1574

Staggers 1030, 1311
dogs 1561
grass 996
goats 1557

Stall walking, horses 1548
horses 1547

Stanleya 3085
sheep 1556

Staphage lysate 2582
swine 1555

Staphylectomy, horses 1460

Sterigmatocystin 2847

Staphylococcosis, poultry 2867

Sterile cystitis, feline 1532

Staphylococcus

Steinoslorna lrncheacoliirn 1906
aureus 64, 67, 341, 668, 774, 1063, 1081,

Steroids 2758-See also Co1ticosteroids,

1181, 1359, 1449, 1490, 1720, 1825,

Glucocorticoids

1863, 1897, 1945,2012,2017,2029,
anabolic 2541, 2545, 2590

2032,2089,2140,2177,2196,2571,
complications 2763

2654,2655,2660,2664,2679,2739
endogenous 539, 2759
chromogenes 920
as growth promoters 2759
epide1midis 341, 1063, 1359, 1374, 1896,
synthetic 2760

2654,2656,2867

Stewart range syndrome 3154
gallinarnrn 2867

Sticktight flea 2875
horninis 920

Sticky snakeweed 3142
hyicus 525, 860, 979, 1359, 1370, 2571,

Stiff

2867,2882
lamb disease 1172
inlerrnedius 530,1359, 1897, 2571, 2661
stifle disease, dogs 1202
pseudinlermedius 856, 863, 981, 2571,

Stifle

2622,2654,2660
disorders, horses 1140
schleiferi 981, 2571
fractures, horses 1143
sirnulans 1833

Stilbene estrogens 2761
spp 121, 178, 476, 671, 724, 844, 864, 981, Slilesia 2650

1157, 1204, 1249, 1263, 1374, 1406,

Stings, Hyn1enoptera (bees, wasps, ants)

1500, 1508, 1527, 1596, 1897, 1913,

3164

1922, 1935, 1964, 1992,2009,2010,

Stockard paralysis 1228

2191,2229,2617,2654,2655,2661,

Stomach

2671,2676,2873
atony, llamas and alpacas 1853
xylosus 1359, 2012
congenital anomalies 167

Starch root 3106
wom1s

Starvation, mink 1876
cattle 308

Status epilepticus 1220, 2591
horses 315
drug treatment (table) 2591
pigs 322

Steady state plasma concentration, drugs
reptiles 1997

2502
small animals 413

Steatitis

Stomatitis
cats, nutrition in 2388
cats 362
marine mammals 1860
dogs 363
mink 1874
large anin1als 215
nutritional 1200
papillar 215

Steatosis, muscular 1043
mycotic, small animals 364

INDEX

3307

Stomatitis (continued)

Streptodornase 2543
small animals 361

Streptogran1ins 2690
vesicular 694, 2480

Streptokinase 2543

StomOX'lJS calcitrans 521, 890, 894

Streptomyces

Storage disorders 984
avermitilis 2576, 2750

VetBooks.ir

Straelensia cynotis 924
cattleya 2656

Straelensiosis 924
cyanogriseus 2750

Straight hock, large animals 1231
derived antibiotics 2733

Strangles, horses 1453
fradiae 2693
bastard 1454
hygroscopicus 2576

Strangulating obstruction, horse 251
nodosus 2575, 2698

Straw itch mite, horses 919
spp 668, 264 7

Strawberry footrot 858, 866

Streptomycin 2662

Stray voltage in animal housing 2113
toxicity

Street drug toxicity 3038
gerbils 2013

Streptobacilliis moniliformis 2027, 2028,
mink 1875

2428,2883

Streptomycin/dihydrostreptomycin 2666

Streptococcal infections 2430

Streptothrichosis
pigs 731
cutaneous 858

Streptococcosis, birds 2868
marine man1rnals 1863

Streptococcus

Streptozotocin 2727, 2731
agalactiae 1359, 1367, 1368, 2140

Stress leukogram 59
bovis 222, 226, 1083, 2177, 2869

Strictures, rectal and anorectal 189
canis 2430

Strike 897
dysgalactiae 1359, 2869

Stringhalt, horses 1137, 1239
dysgalactiae 734

Strobilocephalus triangularis 1866
equisimilis 731, 734, 1158

Stroma-free hemoglobin 1681
equi 505, 682, 826, 830, 1176, 1181, 1182, Stromal abscesses, cornea 494

1368,2152,2157,2159

Strongyles
equi 341, 1180, 1263, 1443, 1453
large, horses 316
zooepidemicus 341, 671, 1345, 1346,
small, horses 317

1443, 1449,2016,2430

Strongyloides
equisimilis 1368, 2191
avium2833
faecalis 2655, 2664, 2695
fuelleborni 2460

Jaecium 2343
papillosus 310, 312
gallinaceus 2869
ransomi 298, 323
gallinarum 2869
spp 303, 310, 314, 319, 323, 414, 1740,
gallolyticus 2894

1878, 1881, 1997, 2458
iniae 1810, 2430
stercoralis 414, 1314
moniliformis 2032
westeri 291, 319, 354, 682, 2156, 2195,
mutans 2869

2646
plurextonim sp nov 735

Strongyloidiasis 2460
pneumoniae 1456, 1879, 2016, 2028,

Strongylus

2766
edentatus 316
porci sp nov 735
equinus 316
porcinus 731, 734
spp 1264
pseudoporcinus sp nov 735
vulgaris 142, 249, 256, 316, 317,
pyogenes 2032, 2431, 2695

354,1252, 1297, 1314
spp 67, 119, 121, 178, 337, 340, 341, 476,

Strnthio camelus 1960

482,671, 724, 731, 750, 1204, 1249,

Struthioliperurus strulhionis 1965

1263, 1358, 1397, 1406, 1463, 1500,

Struvite stones

1508, 1596, 1746, 1754, 1757, 1810,
cats 1532

1854, 1896, 1897, 1898, 1935, 1945,
dogs 1527

1964, 1992, 1993,2089,2092,2617,

Strychnine poisoning 3170

2655,2671,2869,2883

Strychnos nux-vomica 3170
suis 627, 671, 721, 730, 731, 1157, 1158,

Stump pyometra 1397

1263, 1935

Sturdy 1311
uberis 1359

Stye 490
vi1idans 1368

Styptic weed 3124
zooepidemicus 1368, 1369, 1825,

Subacute rurninal acidosis 225

1852, 2016, 2191, 2196, 2200,

Subao1tic stenosis 71

2613, 2869

Subarachnoid cysts 1230

3308

INDEX

Subchondral

Sulfan1ethazine 2674, 2678, 2679
bone cyst, horses 1127

Sulfamethoxypyridazine 2674
bone disease, carpus, horses 1126

Sulfapyridine 2674, 2678
cystic lesions 1062, 1140

Sulfaquinoxaline 2796

Subchronic selenium poisoning 3087
poisoning

VetBooks.ir

Subclinical
mink 1875
ketosis 1027
poultry 2863
ruminal acidosis 225

Sulfasalazine 2555, 2674

Subconjunctival hemorrhage 492

Sulfasomidine 2674

Subcutaneous

Sulfathiazole 2674, 2678
hypoplasia, swine 846

Sulfentrazone 2988
lymphosarcoma 963

Sulfisoxazole 2674

Subepiglottic cyst, horses 1460

Sulfometuron poisoning 2998

Subinvolution of placental sites, smalJ

Sulfonan1ides 2674, 2796
animals 1399
adverse effects and toxicity 2677

S11,blima oclono 429
antimicrobial activity 2675

Sublingual mucocele 368
bacterial resistance 2676

Subluxation, atlantoaxial, smalJ animals
dosages (table) 2678

1230
effects on laboratory tests 2678

Submission of laboratory samples 1584
interactions 2678

Submissive urination, dogs 1569
milk discanl times 2678, 2679 (table)

Subsolar abscess, horses 1114
mode of action 2675

Substituted phenols 2638, 2641, 2650
pharmacokinetic features 2676

Subulurn b?'umpti 2833
poisoning, poult1y 2863

Subungulates, nutrition 2301
potentiated 2674

Succinylcholine 2587
milk discard times 2680

Succinylsulfathiazole 2674, 2678
withdrawal times 2680

Succussion 240
regulatory considerations 2678

Sucking lice 908
therapeutic indications 2677
marine mammals 1865
topical 2674

Suck/ey suck/eyc,nc, 2960
withdrawal times 2678, 2679 (table)

Sucralfate 2551

Sulfones 2583

Sudan

Sulfonylurea poisoning 2998
ebolavirus 2470

Sulfosulfuron 2988
grass 3148

Sulfur
poisoning 3155
dioxide 2743

Sudden
poisoning, poultry 2863
acquired reti11al degenE!ration 1701
requirement, pigs 2337
death
toxicity 1282, 2863
poultry 2897

Sulpiride 2607
syndrome

Sumithion toxicity 3066
broilers 2821

Summation gallop heart sound 88
turkeys 2789

Swnmer

Sugar gliders 2035
bleeding 907
commonly used drugs (table) 2039
colds, horses 316
diseases and syndromes 2041
dermatitis 888
hematologic and sennn biochemistry
fescue toxicosis 3017
values (table) 2037
pasture-associated pulmonary disease,
physiologic data (table) 2036
horses 1455

Suicide, veterinarians 1580
pneumonia, beef calves 1431

Sulfabromethazine 2679
sores 904

Sulfabromomethazine 2674
syndrome 3017

Sulfacetamide 2674

Sunburn, potbellied pigs 1934

SulfachlorpyTidazine 2674

Superficial

Sulfadiazine 2674, 2678
keratitis 493

Sulfadirnethoxicline 2679
necrolytic dermatitis 468, 974

Sulfadimethoxine 2674, 2678

Supernumerary

Sulfadimidine 2674
teats 1388

Sulfaetho:,,.'YJ}yridazine 2674, 2678
teeth 164, 177

Sulfafurazole 2674

Superovi1lation 1329

Sulfaguanidine 2674

Supplements, herbal, poisoning 3032

Sulfamerazine 2674

Suppurative bursitis, horses 1350

INDEX

3309

Supracarpal exostosis, horses 1126

Syncytial virus, bovine respiratory 1433

Suprascapular

Syndactyly 1045, 1050
paralysis, cattle 1088

Synergists, used with insecticides 2757
nerve injmies 1244

Syndrome X, horses 1006
neuropathy, horses 1129

Syngam11s lrnchea 2830

VetBooks.ir

Supravent1icular

Synostosis 104 7
premature complexes 94

Synovial fluid, cytology 1606
tachycardia 95

Synovitis

Surface-active compounds 2743
chronic proliferative 1120

Surfactants 2743
infectious, birds 2843
anionic 2743
plasmacytic-lymphocytic 822
cationic 2743
villonoclular 1120

Surra 38

Synthetic

Surveillance 2069, 2073
nonsteroiclal estrogens 2761
public health 2398
steroids 2760

Suspensory

Syphacia obvelata 1997, 2013, 2029
clesmilis, horses 1122

Syphilis, rabbits 1949
ligaments, udder, breakdown 1388

SyTinghydromyelia 1230

Suxarnethoniw11 2587

Syringomyelia

Swainsonine 3019
clogs 1226

Swayback 1047, 1225, 1253, 3082
small animals 1230
goats 1093

Syrin,qophilus bipeclinalus 2878

Sweat

Symwlicus spp 2292
glands 838

Syrnp of ipecac 2548
itch 887

Systemic

Sweating sickness 684
anaphylaxis 824

Sweeney, horses 1129, 1244
dermatoses, miscellaneous 973

Sweet
hemostatics 2542
clover 3134
iniian1mato1y response syndrome 823
poisoning 3010, 3156
iodine 2576
itch 826, 887
lupus erythematosus 829

Swim bladder, fish 1784
pasteurellosis, sheep and goats 765

Swimmer's itch 2450
pharmacotherapeutics

Swine-See also Pigs, Porcine
cardiovascular system 2525
cholera 713
digestive system 2544
clemodicosis 920
eye 2565
dysentery 301
integumentary system 2571
erysipelas 626
muscular system 2586
fever 713
nervous system 2590

African 711
reproductive system 2606
classical, and abortion 1342
respiratory system 2608
flu 1470
urinary system 2617
gastrointestinal parasites 320

Systolic
influenza 1470, 2472
clicks 88
potbellied pigs 1936
dysfunction 99
kidney worm infection 1502
murmurs 89
prepurchase examination 1649
reproductive indices 2202
vesicular disease 735

T

Swinepox 870

2,4,5-T poisoning 2997

Swollen head 602

Ti553
syndrome, poultry 2904

T, 553, 557

Sylvilagus 1937, 1950, 1951

T cells 57
bachmani 1950

Tabaims spp 36, 889, 904

Symbiotic mange, cattle 916

Tachya.rrhytl1m ias 94

Syn1pathomimetic amines 106

Tachycardia

Symphysodon spp 1810
supraventricular 95

Synantllropic flies 896, 897
ventricular 96

Syncerus coffer 34

Taenia

Synchronizatfon of estrus 1329
asia/'ica 2454

Synchronous diaphragmatic flutter 91,
b1mmi 2452

1183
coenurus 2007

3310

INDEX

Taenia (continued)

Taylorella equigenitalis 1371, 2192, 2201,
crassiceps 423, 2452

2235
multiceps 423, 2450

Teacup pigs 1929
multiceps 1310, 1311

Teart scours 3082
pisiformis 423, 1953

Teat-See also Udder

VetBooks.ir
saginata 428, 2454
diseases, bovine 1385
serialis 423, 1953, 2450
encl, hyperkeratosis 1386
soliwn 428, 1311, 2452, 2454
frostbite 1386
spp 423, 905, 1264, 2650, 2651
obstruction 1388
laeniaeform'is 422, 423
sphincter, inadequate 1389
taiwanensis 2454
stenosis 1388

Taeniasis 2454
supernumerary 1388

Asian 2454

Tebuthiuron 2990

Tagging 898
poisoning 2998

Tags, cutaneous 955

Teeth-See also Dental, Dentistry

Tahyna fever 2468
abnormal

Taiga tick 934
eruption 177

Tail
number 164
biting
position, shape, and direction 164
mink 1875
clapping, horses 1546
swine 1554
congenital abnormalities 164
defects, llamas and alpacas 1851
development 171
evaluation 1218
abnom1al, small animals 182
flower 3106
enamel lesions 164

Talampicillin 2655
eruption (table) 173

Talfan disease 1251, 1307
abnormal, large animals 177

Tall fescue 3142
estimation of age by examination 171

Tamoxifen 2607
irregular

Tanapox 2478
shedding 163

Tansy mustard 3122
wear, large animals 177

Tapewonns--See also Cestodes
malocclusion
beef 2454
rabbits 1955
cattle 312
small animals 184
clog 2452
malformed, small anin1als 183
clwarf 2452
supernumerary 177
fish 2452
uneruptecl, small animals 183
horses 319

Tege1iaiia agrestis 3162
larval, rabbits 1953

Teladorsagia
marine mammals 1866
circumcincta 312, 2644, 2648, 2649,
mouse 2454

2651
pork 2454
spp 2644
poultry 2828

Telogen 838
pseudophylliclean 2454

Temephos toxicity 3067
rat 2454

Temocillin 2656
reptiles 1997

Temozolomicle 2731
sheep 314

Temperature
small animals 421
body, regulation 1015
zoonotic infections 2450, 2452, 2454
equivalents and conversions (table)

Tapirus le1Testris 930

3183

Tarantulas 3163

Temporal lobe

Taro vine 3110
epilepsy 1224

Tarsal cellulitis, cattle 1092
herniation 1277

Tarsus disorders, horses 1133

Tenacibaculum maiitimum 1759

Tasmanian devils 2043

Tendinitis, large animals 1121
facial tumor disease 576, 2044

Tenclinous winclpuffs 1066

Tassel foot 1906

Tendon

Taurine deficiency 110
conunon digital extensor, rnpture,

Taxanes 2733
horses 1127

Ta:rus
contracted
baccata 3094
horses 1150
cuspida ta 3094
kids 1093
spp 3114, 3150
flexor, contracted 1042

INDEX

3311

Tenesmus 156
pharmacokinetic features 2680

Teniposide 2735
therapeutic indications 2681

Tenoscopy, horses, lameness 1101
withdrawal times 2683

Tenosynovi tis

Tetraclymia spp 977, 3124
digital sheath, horses 1121

Tetraethyl pyrophosphate toxicity 3067

VetBooks.ir
biceps brachii tendon, small animals

Tetrafluron poisoning 2998

1202

Tetrahydropyrimidines 2638, 2640, 2647
large animals 1066

Tetrahydrozoline 3026
poultry 2886

Tetrahymena

Tension pneumothorax 1664
corlissi 1801

Tepoxalin 2721
spp 1740, 1754, 1801

TEPP toxicity 3067

Tetralogy of Fallot 72, 83

Teratogens 614

Tetra meres

Terbacil poisoning 2999
mneiicana, 2831

Terbinafine 2705
spp 2828, 2833

Terbucarb poisoning 2996

Tetramethrin 2750

Terbufos toxicity 3067

Tetramisole 2646

Terbutaline 2610

Tetrapetaloneina 1881

Terbutryn poisoning 2999

Texas mountain laurel 3134

Ternidens deminulus 2460

Thallium sulfate poisoning 974

Ternidensiasis 2460

Thamnophis sp 2304

Terrapins 1976

Theiler disease 329, 338

Territorial aggression, dogs 1564

Thei Leri a 1003

Teschen disease 1251, 1307
annulata 33, 35, 933

Teschovirus encephalomyelitis 1251, 1307
b'UJ[eh 35

Testes 1325
equi 23, 35
abnormalities 1330
hirci 35
hereditary hypoplasia 1331
lestoquarcli 33, 35

Testosterone 2590, 2607, 2626, 2759, 2760
luweiishuni 33, 35

Tetanus 601, 611, 1254
mulans35
nonhuman primates 1883

01-ientalis 35
potbellied pigs 1935
ovis 35, 931
sheep 2168
parva 33, 34, 35, 936, 1264
vaccination, exotic mammals 2059
lawrencei 34

Tetany
pai-va 942
grass 996
sergenti 35
hypocalcemic, horses 987
spp 10, 23, 33, 34, 35, 925, 931, 933, 936,
hypomagnesemic

937, 1003
calves 997
la,urotragi 35
cattle and sheep 996
uilenbeigi 33, 35
lactation, horses 987
velifei·a 35
puerperal 571

Theileriases 33
small animals 992

Thelazia
transport
cal�f'orniensis 512, 2460
horses 987
callipaeda 512
ruminants 1030
gulosa 510

Tetrabolhiiumforsteri 1866
laciymalis 510

Tetracapsuloides bryosalmonae 1756
rhodesii 510

Tetrachlo1vinphos 2750
skijabini 510
toxicity 3067
spp 510, 513, 894

Tetracyclines 2584, 2620, 2679, 2683

Thelaziasis 510, 2460
adverse effects and toxicity 2682

Theobroma cacao 2966
antimicrobial activity 2680

Theophylline 2531, 2612
bacterial resistance 2680

Therapy, animal-assisted 1578
classes 2679

Thermal injuries, horses 1719
dosages (table) 2683

Thermography, horses, lameness 1100
effects on laboratory tests 2683

Thevetia peiuviana 3094
elimination, distribution, clearance 2682 Thiabendazole 2645, 2701, 2702
general properties 2679

Thiamine deficiency 1212, 1253, 1281
interactions 2683
amphibians 1741
milk discard times (table) 2684
horses 2327
mode of action 2680
marine mammals 1860

3312

INDEX

Thiamine deficiency (conlimied)

Thrombopathia
mink 1874
bovine 50
poultry 2943
car1ine 50

Thiamphenicol 2684

Lhrumbasthenic 50

Thiamylal 2594, 3035

Thromboplastin time, activated partial 44

VetBooks.ir

Thiazide diuretics 75, 104, 2528,

Thrombopoietin 7

2625,3034

Tlu-ombosis

Thiazopyr 2990
embolism and aneurysm 141

Thickleaf drymary 3142
pathologic 46, 54

Thidiazuron poisoning 2998
vena cava, cattle 1442

Thifensulfuron-methyl 2990

Thrombus 141

Thimerosal 2741

Thrush

Thin
horses 1117
ewe syndrome 64
poultry 2791
sole, cattle 1079

Thumping, pigs 3093

Thiobencarb poisoning 2996

Thumps

Thiocarbamate poisoning 2996
horses 1183

6-Thioguanine 2732
pigs 321, 1469

Thiopental 3035

Thymic aplasia 820

Thiophanate 2645

Thyroglossal duct cyst 165

Thioridazine hydrochloride 2604

Thyroid

Thiosemicarbazones 2748
adenoma 559

Thiotepa 2731
car·cinoma 559

Thiothixene 2604

C-cell tumors 577

Thiourea poisoning 2998
cells 1603

Thira.m poisoning, poult1y 2863
gland 552

Thistle, yellow star 3128
idiopathic atrophy 553

Thlaspi arvense 977
non-neoplastic enlargement 558

Thoracic
hormones 553, 2579
limbs, evaluation 1217
removal 560
trauma 1668
stimulating hormone 542, 553

Thoracotomy, emergency 1673
tissue, ectopic 552

Thorn apple 3140

Thyroidectomy 560

Thorny-headed worms

Thyroictitis
fish 1757
autoimmune 831
pigs 321
lymphocytic 553
small animals 421

Thyrotropic hormone 542

Thoroughpin, horses 1066, 1138

Thyrotropin 553
false 1138

Thyroxine 553, 557, 1624

Threadleaf 3142

Thysanosoma actinioides 305, 314

Thread worm

Tianmlin fumarate 2694
intestinal, cattle 310

Tibial
pigs 323
dyschondroplasia, poultry 2932

Three-day sickness 741
hemimelia 615

Throat bot, horses 315
ne1ve

Thrombasthe.nia, Glanzmann 50
block, horse 1107

Thrombasthenic thrombopathia 50
injuries 1244

Thrombin time 51
paralysis, cattle 1090

Thrombocytopathy 7

Ticarcillin 2655, 2657, 2658

Thrombocytopenia 7, 1613

Tick
acquired 47
bite fever 2434
congenital 4 7
fever 20, 806
drug-induced 48

Colorado 2468
fetal and neonatal alloimmune 47
paralysis 1243, 1314, 2466
idiopathic 47
pyemia 774
immune-mediated 47, 827

Southern, rash illness 2420
vaccine-induced 48
spinous ear· 520

Thrombocytopenic purpura, idiopathic 47
typhus, Queensland 2436

Thrombocytosis 7, 1613

Tickborne

Thromboelastography 46
encephalitis 2480

Thromboembolism
fever 772
arterial 126
lymphadenopathy 931
pulmonary, small ar1imals 1487
relapsing fever 2420

INDEX

3313

Ticks 925

Toxic
argasid 925, 938
epidermal necrolysis 525
control 940
disorders
fowl 2876
peripheral nerve 1242

VetBooks.ir
ixodid 926, 928
spinal column and cord 1254
removal 940
fat poisoning, poultry 2863
reptiles 1996
gases and interstitial pnetunonia, cattle
vaccines 941

1442

Tigecycline 2679
hepatopathy, large animals 342

Tight-lip syndrome, Shai0Pei 163
myopathies

Tilmicosin 2687, 2690, 2691
horses 1186

Timolol 3033
pigs 1175

Tinidazole 2696
poultry 2885

Tiopronin 2625
ruminants 1.175

Tissue

Toxicant 2948
oxygen content 69

Toxicities-See also Poisonings, Toxicoses
type plasminogen activator 2543
acaricide (organic) 3058

Tizanidine 3036
acetaminophen 452

Toad poisoning 3161
acetone 3069

Tobacco toxicosis, pet birds 1924
affecting nervous system 1212

Tobramycin 2663
aflatoxin, poultry 2860

Tocainide 2537
aldicarb 3059

Toe
aldrin 3060
abscess, sheep 1171
ammonia (aerosolized) poultry 2860
malposition, birds 1896
anticoagulant rodenticide, poultry 2860
necrosis syndrome, cattle 1078
antineoplastic agents 2724

Tolfenamic acid 2718
a1thropods 3162

Tolnaftate 2705
azinphos-ethyl 3064

Toltrazuril 2797
azinphos-methyl 3064

Tomography, computed 1635
benzene hexachloride 3061

Tongue
botulism, poultry 2860
anomalies 163
bromide 2597
paralysis, large animals 214
calcium, poultry 2860
rolling, cattle 1553
carbamate insecticides 3059
worms 2464
carbaryl 3059

Tonometry (table) 498
carbofuran 3060

Tonsillitis, small animals 361, 1490
carbophenothion 3064

Tooth resorption, small animals 181
castanospermine 1043

Tophi, poultry 2875
chlordane 3061

Topical
chlorfenvinphos 3065
agents (human drugs), toxicity 3031,
chlorinated hydrocarbons 3060

3036
chlo1inated naphthalene 974
antifungal agents 2706
chlorpyrifos 3065
dosage fonns, drugs 2514
coffee senna, poultry 2886

Topiramate 2594, 2600
coumaphos 3065

Torsalo 878
crotoxyphos 3065

Torsemide 75, 2527
o-limonene 3064

Torsional deformities, poultry
demeton 3065

2881
diazinon 3065

Tortoises, nutrition 2307
dichlorvos 2997, 3065

Torulopsis glabrnla 2703
dieldrin 3061

Total
dihydrostreptomycin, gerbils 2013
protein 1590, 1594
dimethoate 3065
serum bile acids 436
dioxathion 3065

Toucans, nutlition 2293
disulfoton 3066

Toxaphene 2749
emulsifiers 3069
toxicity 3062
endosulfan 3061

Toxascaris 2651
endrin 3061
leonina415

EPN 3066

Toxemia, pregnancy
ethylene glycol 3046
cows 1020
famphur 3066
ewes and does 1021
fenchlorphos 3067

3314

INDEX

Toxicities (continued)

terbufos 3067
fenitrothion 3066
tetrachlorvinphos 3067
fenthion 3066
tetraethyl pyrnphosphate 3067
fescue 360
tobacco, pet birds 1924

VetBooks.ir
haloxon 1254
toxaphene 3062
heptachlor 3061
t1iaryl phosphate 3069
hexachlorocyclohexane 3061
trichlorfon 3067
histan1ine, marine mammals 1860
vitamin A 3031
insecticides 3058
rabbits 1959
insecticides derived from plants 3063
vitamin D, pet birds 1919
iodine 558
zinc 3088
ionophore 1175, 1186, 1242
fish 1771
poultry 2862, 2885
pet birds 1924

4-ipomeanol 1442

Toxicity 2948
iron, newborn pigs 3077

Toxicoinfectious botulism 606
isopropyl alcohol 3069

Toxicologic hazards, workplace 2952
lead 1458

Toxicology
gerbils 2012
introduction 2948
pet birds 1924
samples 1586
lime-sulfur 3070

Toxicoses-See also Poisonings, Toxicities
o-Limonene 3064
acute 2948
lindane 3060
aflatoxins 3011
locoweed 59

AJsike clover 343
macadan1ia nuts 2967

Aspergillus 3011
malathion 3066
ammonia 3043
methanol 3070
chronic 2948
methomyl 3060
cocklebur 343
methoxychlor 3061
copper, large animals 342
methyl parathion 3066
ergot 3012
mevinphos 3066
fumonisin 3017
moldy sweet potato 1442
fungi 3005
mushrooms 3095
iron, large animals 342
naled 3066
kleingrass 343
nicotine sulfate 3063
molds3005
organophosphates 3064
moldy corn 3011
delayed 1254

NSAID, horses 292
oxydemeton-methyl 3066
slaframine 214, 3019
parathion 3066
summer fescue 3017

Perilla ketone 1442
trichothecene 3020
pet birds 1924

Xanthium 343
phorate 3067

Toxicosis 2948-See Poisonings, Toxicities,
phosmet 3067

Toxicoses
phosphate enema 571

Toxin 2948
polytetrafluorethylene, pet birds 1924

Toxocara
propoxur 3060
canis 321, 415, 1264, 1312, 2460, 2647
pyrethrins 3058, 3063
cati 137, 415, 2460
pyrethroids 3058, 3064
spp 311,415,505, 1312,2415,2650,2651
purple mint 1442
vitulontm 311
ragwort 3150

Toxoplasma
rati tes 1966
gondii 407, 455, 623, 685, 1241, 1252,
ronnel 3067

1264, 1338, 1339, 1346, 1487, 1836,
ruelene 3067

1867, 1882,2007,2170,2186,2217,
salt3083

2376,2416,2566
mink 1875
spp 159, 208, 505, 687, 821, 830, 1337,
potbellied pigs 1936

1619, 1867, 1965,2676,2785,2798
snakebite 3159

Toxoplasmosis 455, 685, 1252, 1338, 1340,
solvents 3069

2444,2566
streptomycin, gerbils 2013
abortion
sulfur 1282, 2863
goats 1340
sumition 3066
small ruminants 1338
temephos 3067
feline, therapy, ocular 2566

TEPP 3067
marine rnan1mals 1867

INDEX

3315

Trabecular carcinomas 952
spinal cord 1254

Tracheal
thoracic 1668
collapse 1478

Traumatic
edema syndrome of feeder cattle 1430
arthritis, large animals 1060
lavage, cytology 1605
gastritis, ruminants 230

VetBooks.ir
tumors, small animals 1485
injuries, reptiles 2000

Tracheitis 1413
rnyopathies

Tracheobronchitis
horses 1186
infectious, dogs 1491
cattle 1175
small animals 1490
neuromas 958

Tracheostomy, horses 1713
proptosis 1696

Traction diverticula, small animals 373
reticulopericarditis 123

Tragopan spp 2292
reticuloperitonitis 230

Trailer-related problems, horses 1549

Traveling with pets 2170

Tralkoxydim 2990

Trazodone 1545

Tramadol 2111

Trematodes-See also Flukes

Tranquilizers 2600
causing CNS disease 1312
phenothiazine 3036
marine mammals 1866
and sedatives without analgesic effects
reptiles 1997

(table) 2600
zoonotic infections 2446, 2448, 2450
toxicity 3034

Tremorgen ataxia syndrome 3010

Transfaunation 161

Tremorgens 3008

Transfusions, blood 15, 17

Trenbolone acetate 2758, 2760, 2761

Transient
and estradiol benzoate 2761
asystole 102

Trench mouth, dogs 364
hypogammaglobulinemia 820

'I'l·eponem.a

Transitional vertebrae, small animals
denticola 1075

1229
pallidum 1949

Transmissible
paraluiscuniculi 1946, 1949, 1957
enteritis, turkeys 2797
phagedenis 1075
gastroenteritis, pigs 302
spp 178, 525
mink encephalopathy 1874
vincentii 1075
serositis 1308

Treponematosis, rabbits 1949
large animals 1065

Triage 1659, 1660
spongifom1 encephalopathy 1286
parameters (table) 1661
venereal tumors 967, 1604

Triallate 2990
canine 1408
poisoning 2996

Transport

Triamcinolone 2712
myopathy, turkeys 2884

Triamterene 2624, 3034
tetany

Triaryl phosphate toxicity 3069
horses 987

Triasulfuron 2990
ruminants 1030

'I'liatoma39

Transportation

T:riazine 2752
of injured horses 1716
derivatives 2726
of injured small animals 1659
poisoning 2999

Transudates, characteristics 1605

Triazine/pyrimidine 2752

Trauma 1668

T:riazinylsulfonylurea poisoning 2998
abdominal 1669

Triazolan1 3034
amphibians 1742

Triazole poisoning 2099
backyard poultry 1820

Triazolopyrimidine poisoning 2998
bone, small animals 1205

Tribenuron-methyl 2990
equine 1713

'I'libulis terrestris 977
facial nerve 1244

'I'licaine methanesulfonate 1753
joint, small animals 1198

'I'lichechus
and lameness, goats 1095
inunguis 1867
marine mammals 1858
manatus latirostris 1856
muscular, small animals 1202

T:tichilemmal cysts 94 7
nonhuman primates 1884

Trfr:hinella
peripheral nerve 1243
britovi 737, 2460
pet birds 1925
murrelli 737
rati tes 1966
nativa 737, 2460
reptiles 1999
nelsoni 737, 2460

3316

INDEX

'lhchinella (continued)

Tiichotheciwn 3020
papuae 737

Trichuriasis 2462
patagoniensis 737

'Ji·ichwis
pseuclospiralis 737, 2045, 2460
ovis 312

VetBooks.ir
spiralis 736, 1314, 2460
spp 303,312,314,323,421, 1881,2651
spp 736
suis 298, 320, 323, 324, 2462, 2647,
zimbabwensis 737, 2460

2649

Trichinellosis 736, 2460
t1ichiuro 2462

Trichinosis 736, 2460
vulpis 378, 396, 421, 2462

Trichloracetic acid 2990

Triclabendazole 2645

Trichlorfon 2651, 2750

Tr·iclopyr 2990
toxicity 3067

Triclosan 3056

1hchobilharzia spp 2450

Tri cuspid

Trichoblastomas 944
regurgitation 70

Tri choclecles
valve dysplasia 84
canis 882, 913

Tr'icyclic antidepressants 2605
equi 912
toxicity 3034
paiwnpilosus 912

Tr·iethylenethiophosphoramide 2731

Tiichoclesma 3020, 3150

Trifluoperazine hydrochloride 2604

Tiichodina spp 1746, 1754, 1779, 1801

Triflupromazine 2600

Ti'ichodinella spp 1801

Triiluralin 2990

Trichoepitheliomas 948

Triiluridine 2745, 2746

Trichofolliculomas 948

Tr·ifobiasis 343

Tiichogaster

Ti'ifoliwn

/eeri 1814
hyb1iclum 343, 977, 2321
lrichoplerus 1814
prnlense 977, 3019

Tricholemmomas 948
spp 977, 2960

'Ji·ichomonas
sublermnewn 1337, 1391, 3074
gallinae 1905, 804

Trigeminal
spp 1965, 2047, 2125, 2699
nerve 1215
slable1i 2804
neuritis 1241

Trichomoniasis
neuropathy, idiopathic 1241
cattle 1384

Tiiglochin
and abo1tion 1335
ma1itima 2960
pet birds 1905
pa.lus tris 2960

Trichomonosis, birds 2804
spp 3150

Tiichophyton

Triglycerides 1595
equinum 873, 874, 875, 2574

Triiodothyronine 553
e1ina.cei 1832

1):ilosta.ne 2580
mentagrophytes 873, 874, 875, 1826,

Tr·imethoprim 2674

1832, 1949,2007,2018,2030,2574

Trimethoprirn/sulfa.diazine 2679, 2680
e1inacei 1835

Trimethoprim/sulfa.doxine 2680
menlagrnphytes 2018

Trirnethoprim/sulfona.mides 2620

1ubrwn 873

Tiioclontopho11ts
spp 872, 1864, 1880, 1904, 2440, 2573,
spp 316, 317

2575,2699,2704
tenuicollis 31 7
terrestre 872

Ti'ipa.rtiella spp 1754, 1801

Ve'/1UCOSU'm 873, 874, 875, 876, 2574

Ti'iselumjlavescens 566, 570, 1053

1'richosporon 1993

Ti·i tri.chomonas

Trichostrongyliasis 2462
foetus 378, 1335, 1346, 1384, 2232

Tr'ichostrongylosis, intestinal, sheep and
spp 158, 403
goats 313

Ti'ixacarus ca.viae 2017, 2462

'lhchostrongylus

Troca.rization, horses 1712
a.xei308,312,319

Tr·ochlea.r nerve 1215
colub1'iformis 313, 314, 2644

'Ji·oglotrema

1·ugatus 313
acutwn 1312
spp 303, 312, 319, 1881, 2644, 2651
salmincola 2448
tenuis 2831

Troglotremiasis 1312
vilriniis 313

Trolcandornycin 2687

Trichothecene

Timnb-icula. a(fmddugesi 2877
mycotoxins, poultry 2846

Tr·ombiculidiasis, horses 919
toxicosis 3020

Tr·ombiculosis 924

INDEX

3317

Tropical

Tubocurarine 2587, 2588
fowl mite 2878

Tubular genital tract 1323
warbles 876, 878

Tularemia 692, 2430

'I'rueperella
rabbits 1950

VetBooks.ir
pyogenes 64, 122, 341, 352, 533, 775, 895, Tulatllromycin 2690, 2691

897, 1081, 1157, 1161, 1164, 1165,

Tumblers 888

1166, 1170, 1171, 1335, 1343, 1359,

Tumbu fly 2462

1365, 1367, 1368, 1369, 1373, 1383,

Tumor necrosis factor 2708

1419, 1436, 1442, 1475, 1499, 1500,

Tumors--See also Cancer, Neoplasia

2151,2177,2655,2883
adipose tissue 958
abortion in cows 1335
adrenal medulla 576
spp 1472, 2655, 2680
aortic body 578

Trumpet
apocrine gland
flower, evening 3142
anal sac origin 950
lily 3112
cutaneous 949

Trunk evaluation 1218
basal cell 944

1'iypanosorna
benign fibroblastic 955
brucei 892
bone, small animals 1205
bnlcei 35
brain 1270
gambiense 35, 2444
carotid body 578
rhodesiense 35, 2444
ceruminous gland 535
congo/ense 35
chemoreceptor organs 578

C?UZi 38, 120, 802, 1835, 2032, 2442
circumanal gland 951
eqiiiperdiirn 38
connective tissue 836, 955
evansi 38
cutaneous 942
rnelophagiwn 40, 893
apocrine gland 949
simiae35
mast cell 963
spp 10, 35, 802, 933, 1264, 1803, 1808,
smooth muscle 961

1881,2574,2699,2780,2876
cytology, evaluation 1602
theileri 40, 923, 937
desmoid 956
lheodori 40
ear canal 534
vivax 35, 936
eccrine gland 950

Trypanosomes
epidermal 943
birds 2785
extraskeletal giant cell 957
nonpathogenic 40
fibroblastic, benign 955
tsetse-transmitted (table) 36
fibrohistiocytic 957

Trypanosomiasis 35, 2444
giant cell

American 2442
extraskeletal 957
drug treatment 37
of soft parts 957

Trypsin-like immunoreactivity 1592, 1593,
growth, response to chemotherapy 2722

1594
hair

Tsetse flies 36, 892
follicle 943, 948

Tuberculosis 687, 2430
matrix 949
birds 2869
hepatoid gland 951
carcass condemnation 1646
histiocytic 836, 961
cats 690
with histiocytic differentiation 966
cattle 689
immune system 831
deer 689
islet cell 583
dogs 690
kidney, small animals 1522
elephants 690
larynx and trachea, small animals 1485
elk 689
lower urinary tract, small animals 1523
free-ranging and captive hoofed animals
lung, small animals 1485

691
lymphocytic 836, 961
goats 689
lymphoid, of t11e skin 961
guinea pigs 691
mammaiy 1403
horses 690
mast cell, cutaneous 963
marine man1mals 691, 1863
melanocytic 967
nonhuman primates 691, 1879

Merkel cell 952
pigs 690
metastatic, skin 969
rabbits 690
muscle, small animals 1203
sheep 689
ne1ve sheatll 958, 1242
zoo animals 2053
ne1vous system, dogs and cats (table) 1268

3318

INDEX

Tumors (continued)

Typhoid
neuroendocrine 576
equme 701
cutaneous 961
fowl 2866
primary cutaneous 952

Typhus 2438
nose and para.nasal sinuses, small
cat fl ea 2434

VetBooks.ir
animals 1484
flea.borne 2436
oral, small animals 366, 367
lndian tick 2434
pain 2113
murine 2436
perianal gland 951

Queensland tick 2436
peripheral nerve 1276
scrub 2438
sheath 958

Tyrosinemia 852
pituitary 1274

Tyzzer disease 199
nonfunctional 547, 548
large aiumals 340
poultry 2848
rabbits 1948
salivary gland, small anin1als 368
small aiumals 454
sebaceous gland 950

1'lJZzeria
skin and soft tissues 942
pemiciosa 2793
skin, metastatic 969
spp 2793
smooth muscle, cutaneous 961
spinal cord 1275
u
thyroid C-cell 577
transmissible venereal 967

Uberreiter rusease 493
urinary tract, lower, small aninlals

Uchida pallidula 2876

1523

Udder-See also Teat
vascular 959
abscess 1389

Tunga
acne 1386
infections 2466
congenital disorders 1387
penelrans 2466
diseases 1385

Tupaia glis 1882
edema, bovine 1387

Turkey
hematoma 1388
cardjomyopathy, spontaneous 2790
in1petigo 1386
chigger 2878
physiologic rusorders 1387
corona.viral enteritis 2797
sores 1387
coryza.2907
structural disorders 1388
fowlpox 2824
support breakdown 1388
nutlition 2918, 2924 (table)

syndrome, sows 1373
osteomyelitis complex 2882
tramna 1388
rhinotracheitis 2904

Ulcer
rota.viral infection 2803
eosinophilic, cats 971
viral hepatitis 2871
sole, cattle 1076

Turkish slipper hooves, goats 1092

Ulceration, lip and leg, sheep 872

Tursiops spp 1860 •

Ulcerative

Turtles, nutrition 2306
balanoposthitis and vulvitis 1373

Twin lamb disease 1021
dermatitis, reptiles 1991

Twinnmg, horses 1343
clermatosis, sheep 872 , 1392

Twitch muscle 838
disease

Tying-up
oral, small animals 361
horses 1048, 1178
septicemic cutaneous, turtles 1991
small animals 1202
enteritis, poultry 2805

Tylosin 2555, 2687, 2690, 2691
keratitis 494

Tympany
lymphangitis, horses 66
guttural pouch 1464
manunillitis, bovine 1385
ruminal 227, 228
pododermatitis, rabbits 1958

Type D enterotoxemia 610
stomatitis, reptiles 2304

Type 1 polysaccharide storage myopathy

Ulceromembranous stomatitis, clogs 364

1179

Ulcers

Type 2 polysaccharide storage myopathy
abomasal 241

1179
corneal, marine mainmals 1857

Type 1 reactions 823
decubital 1708

Type II reactions 826
gastric/gastrointestinal

Type III reactions 828
horses 218

Type IV reactions 830
large animals 218

INDEX

3319

Ulcers, gastrointestinal (continued)

system
llamas and alpacas 1853
congenital anomalies 1496
marine mammals 1858
infectious diseases
mink 1876
large animals 1499
pigs 219
small animals 1508

VetBooks.ir
small animals 393
introduction 1494
therapy 2550
noninfectious diseases

Ulnar cartilage cores, retained, dogs 1204
large animals 1502

Ultrasonography 1632
small animals 1512
contrast agents 1635
pharmacotherapeutics 2617

Doppler 1634
principles of therapy 1496
horses, lameness 1099
tract

Umbilical hernia 167
disease, feline 1531
llamas and alpacas 1851
nutrition in 2383

Umbrella tree 3114
infections

Umezakia 2956
bacterial 261 7

Uncinaria
fungal 2622
spp 396, 1866, 2651
treatment, small animals 2618
stenocephala 417

Urination

Unclassified cardiomyopathy 119
excitement, dogs 1569

Underfur
submissive, clogs 1569
cotton, mink 1875

Urine
gray, mink 1875
bacte1ial culture 1495

Undifferentiated sarcomas 961
bilirubin 1617

Undulant fever 1348
burn, rabbits 1957

Ungulates, nutrition 2301
chemistries 1615

Uniglandular mastitis, acute, sows 1375
clarity 1615

Un united anconeal process, dogs 1196
collection methods 1495

Unwholesome meat, detection 1646
color 1615

Upper motor neurons 1209
crystals 1618

Urachal remnants 1498
cytology 1608

Urate
glucose 1616
deposits, birds 2874
ketones 1617
stones, dogs 1529
marking, cats 1572

Urea 1591, 1595, 2624
odor 1615
poisoning 2998
pH 1616

Ureaplasma
controlling 2625
diversum 1336
protein 1616
cows and abortion 1336
reagent strips 1616
spp 1372
sediment 1617
ureolyticum 1392
specific gravity 1615

Ureido-penicillins 2655
urobilinogen 1617

Ureteral anomalies 1498
voltune and specific gravity (table) 3175

Ureteroliths 1525

Urobilinogen, in urine 1617

Urethral

Urocystoliths 1525
anomalies 1498

Urogenital defects, llan1as and alpacas 1851
defects, horses 1507

Urolithiasis
obstruction, small animals 1521,
canine 1525, 1527

1526
nutrition in 2388

Urethroliths 1525
chickens 2874

U rethrorectal fistulas 1499
equine 1505

Urinalysis 1494, 1615
feline 1525, 1531

Urinary
large animals 1502
acidifiers 2625
mink 1871
calculi, goats 2312
potbellied pigs 1936
incontinence 2626
rabbits 1959
drug therapy 2626
ruminants 1502
mink 1876

Uroliths 1525, 1526
small animals 1524

Uronenia spp 1754, 1801
infections, mink 1871

Uropathy, obstructive, small animals 1521
retention 2627

Uroperitoneum, foals 1506
stones-See Urolithiasis

Uropsylla tasmanica 2045

3320

INDEX

Ursodeoxycholic acid 2561
gene deleted 2769

Ursodiol 2561
killed 2768

Ui·sus rnaiitirnus 1856
live 2767

Urticaria 857
polynucleotide 2770

VetBooks.ir

U rticarial reactions 824
prime boost 2772

Usutu virus 2480
production 2773

Uterine
subunit 2768
prolapse and eversion 1389
tick 941
subinvolution, small animals 2229
types 2768

Uterus
virus-vectored 2769
didelphys 1332

Vaccinia
unicornis 1331
like viruses 2480

Uvea
related poxviruses 2480
anterior 495
virus 2466, 2480

Uveitis 1699

Vacuolar hepatopathy, canine 467
anterior 496, 830

Vacuum activity 1537
equine

Vagal indigestion syndrome, ruminants 233
recurrent 508, 830

Vagmal
therapy 2569
cytology 1394, 1607
neonatal 2093
hyperplasia, small animals 1399
phacoclastic, rabbits 1958
prolapse 1390
rickettsial, therapy 2567
small animals 1399
v
stricture 1332

Vaginitis

Vaccination
catarrhal bovine 1392
backyard poultry 1819
large animals 1391
broiler breeders (table) 2926
small animals 1399
broilers (table) 2925

Vagococcus spp 1810
broodmares 2195

Vagus nerve 1216
schedule (table) 2196

Valacyclovir 2745
calves 2124

Valerate 2606
cattle

Valgus
breeding 2122
deformity, poultry 2881
feedlot 2129
deviation, foals 1046
commercial layers (table) 2927

Valley fever 637
ducklings, commercial 2929

Valproic acid 2599, 2605
ducks, breeders 2929

Valve disease, degenerative 112
exotic mammals 2054, 2056 (table)

Valvular
ferrets 1824
blood cysts 115
horses 2157
disease 70
llamas and alpacas 1850 •
hematoma 115
potbellied pigs 1930

Vancomycin 2693
poultry 2920

Vapor-phase disinfectants 2744
ratites 1962

Variant Cruetzfeldt-Jakob Disease 2482
replacement heifers 2125

Varus deformity, poultry 2881
schedules 2771

Vascular
broodmares (table) 2196
diseases/disorders 50 72
small animals 2169
malformations 1275
turkeys (table) 2928
peripheral nerve 1244
zoo animals 2048, 2054
spinal cord 1255

Vaccine-induced thrombocytopenia 48
resistance 70

Vaccines 2767
ring anomalies 85 166
administration 2770
tumors 959
adverse reactions 2772

Vasculitis 526, 830
attenuated 2769
neutrophilic 851
canine melanoma 2736
small animals 1511
clostridial 613

Vasculopathy familial, dogs 851
combination 2771

Vasoactive drugs 2534

DNA 2770

Vasodilators 2534
failures 2772
in heait failure 108
gene cloning 2768

Vasopressin 543

Vci.uchornia spp 1801

INDEX

3321

Vecuronium 2587
malformations, congenital, small

Vedaprofen 2719
animals 1229

Veldtgrass staggers 3154
osteomyelitis 1249

Velvet, fish 1802

Vertical fissures, cattle 1085

VetBooks.ir

Vena cava thrombosis, cattle 1442

Verticimonosporium 3020

Venereal

Vesicular
balanitis, equine 1357
disease, swine 735
balanoposthitis and vulvitis, sheep 872
exanthema, swine 738
disease, granular 1392
stomatitis 694, 2480
tumors, transmissible canine 1408

Vesiculovirus 694
vulvitis, sheep 872

Vestibular lymphocytic follicles 1392

Venezuelan

Vestibulocochlear nerve 1216
equine encephalitis/encephalomyelitis

Vestibulovaginal hypoplasia 1332

1291,2480

Veterinary
hemorrhagic fever 2476

Feed Directive 1749, 2634

Venomous arthropods 3162
practice, community/family

Venous dilators 2535

1575

Vent

Vibrio
blow-out, backyard poultry 1820
choleme 1809, 2432
disease, rabbits 1949
paraha,emolyticus 2430
prolapse, reptiles 2002
spp 1757, 1779, 1809, 1863

Ventilation 2116
vulnijicus 2432
dilution effect 2117

Vibrionic hepatitis, avian 2806
in cold weather 2117

Vibriosis 2430, 2432
in warm weather 2119
fish 1809
mismanaged 2118
sheep, and abortion 1337

Ventricular

Vicia spp 2960
contraction force 69

Vidarabine 2745, 2746
escape rhythm 97

Vinblastine 2729, 2732
fibrillation 97, 1673

Vinca
flutter 1673
alkaloids 2732
premature
spp 618, 3108
complexes 96

Vincent stomatitis, dogs 364
depolarizations 72

Vincristine 2729, 2732, 2737
septa! defects 72, 81

Vinorelbine 2730
tachycardia 96

Viral

Ver du Cayor 902
aiteritis, equine 701

Verapamil 3032
and abortion 1344

Vern ti um
arthritis, poultry 2883, 2886
album 1380
diarrhea, bovine 1436
californicum 162, 618, 1223, 1337, 1380,
diseases

3127
amphibians 1741
spp 3126
ferrets 1825

Vermin control, in laboratory animal
fish 1761
environments 1841
llan1as and alpacas 1852

Vem1inous
marine mammals 1867, 1870
bronchitis 1421
mink 1872
myelitis 1252
nonhumai1 primates 1882
pneumonia 1421
pet birds 1907

Vernolate 2990
rabbits 1950
poisoning 2996
reptiles 1994

Veronaea botiyosa, 1761
spinal column and cord 1250

Verruca
zoonotic 2466
planum 953
encephalitides, poultry 2891
vulgaris 952
encephalopathy and retinopathy, fish

Vertebral

1765
bodies, horses 1147
enteritis
deformities
duck 2799
pigs 1160
mink 1873
poultry 2881
erythrocytic necrosis, fish 1763
malformation-malarticulation, cervical
hemorrhagic

1245
disease, rabbits 1951

3322

INDEX

Viral (continued)

Vitamin E deficiency 1174, 1228, 1247
hepatitis
horses 2327
duck 2815
marine mammals 1860, 2298
turkeys 2871
mink 1874
respiratory tract infections, cattle 1433,
pigs 2344

VetBooks.ir

1436
poultry 2938
rhinopneumonitis, equine 1444, 1448

Vitamin K 2542
rhinotracheitis, feline 1481
antagonists 2543

Virginiamycin 2690, 2765
deficiency, poultry 2939

Virulent footrot, sheep 1167

Vitamins and minerals, for skin disorders

Virus highlands J, poultry 2892

2584

Visceral

Vitiligo 849
gout, reptiles 2000

Volume of distribution 2499, 2521

Jarva migrans 415, 2460

Volvulus
leishmaniosis 800, 2442
abomasal 238
schistosomiasis 32
colon, horses 265

Viscerotropic velogenic Newcastle disease
dogs 384
pet birds 1910
large animals 247

Vision Joss, acute 1699
small intestinal, horses 260

Visna 1476

Vomiting

Vitamin
and wasting disease 728
deficiencies
drugs used to control or stimulate
horses 2327

2547
poultry 2936
pet birds (table) 1900
req uirem en ts
von Willebrand disease 49
beef cattle 2257

Voriconazole 2701
dairy cattle 2277

Vorticella spp 1802
dogs and cats 2370

Vultur g1yphus 2826
goats 2310

Vulvar atresia or hypoplasia 1332
horses 2319

Vulvitis
pigs 2238
goats 1372
poultry 2916
granular 1392
sheep 2347
large animals 1391
toxicity 3030
sheep 1372

Vitan1in A
venereal, sheep 872
deficiency 1223, 1234

Vulvovaginitis 3006
horses 2327
and estrogenism 3014
pet birds 1918
granular 1392
poultry 2936
infectious pustular 1392, 1434
rabbits 1959
toxicity 3031
rabbits 1959
w

Vitan1in B deficiency

Walking dandruff 922
anemia 13
rabbits 1953
horses 2328

Walnut, black 3134
poultry 2939

Wanderer 2094

Vitamin B6 (pyTidoxine) deficiency 1212

Wa,ngiella spp 1739
poultry 2943

Warbles

Vitamin B,2 (cyanocobalanlin) 2540
cattle 876
deficiency, poultry 2939
small animals 901

Vitan1in C deficiency
tropical 876, 878
guinea pigs 2018

Warfarin 2543
nonhuman primates 1883
and congeners, poisoning 3165

Vitanlin D 562, 572
toxicity 2543
deficiency 1050, 1094

Warts 952
horses 2327
bovine, teats 1316
nonhuman prin1ates 1883
hairy, cattle l 075
pet birds 1919

Warty dyskeratomas, canine 944
pigs 2344

Wasp stings 3164
poultry 2937, 3168

Wasting
requirement, reptiles 2001, 2305
chronic, goats 2151
toxicity 1054, 3031, 3168
syndrome, postweaning multisystemic,
pet birds 1919
swine 723

INDEX

3323

Water

Whirling disease 1755, 1807
analysis, aquatic systems 1768

White
dermatitis 427
bile syndrome 439
hemlock 3116
blood cells 5, 1612
problems, home aquarium 1797
evaluation 1615

VetBooks.ir
requirement
in urine 1617
beef cattle 2249
comb, backyard poultry 1823
dairy cattle 2273
fat disease, marine mammals 1860
dogs and cats 2366
line disease
exotic and zoo animals 2288
cattle 1077
goats 2308
horses 1116
horses 2313
muscle disease 1172, 2286
laboratory animals 1840
goats 1095, 2312
pigs 2332
pigs 1162
poultry 2914
sheep 2353

Waterbelly
snakeroot 3128
poultry 2871
sweet clover 3134
small ruminants 2312

Whitmore disease 661

Waterfowl, nutrition 2292

Widow spiders 3162

Watery mouth disease, lambs 274

Wild

Wave mouth 177
cherries 3148

Weaning, calves 2124
coffee 3124

Weaver syndrome 1227
indigo 3118

Weaving, horses 1548

Wilms' tumor 1522

Weeping fig 3110

Windpuffs 1066, 1121

Weepy eye, rabbits 1945

Windsucking, horses 1547

Weidekrankheit 1052

Windswept, goats 1093

Weight

Wing clipping, pet birds 1888
loss, horses 291

Winter
to body surface area conversion (table)

dysentery, cattle 271

3182
tick 930

Weights and measures equivalents and

Wire worm, cattle 308
conversions (table) 3184

Withdrawal

Welfare
reflex 1218
animal 1579, 1644
time 2520
downer cow 1192

Withholding periods, anthelmentics
in feedlots 2134

2642

Wenckebach phenomenon 94

Wobbler syndrome 1245

Wenyonella spp 2793
dogs 1230

Werneckiella equi 912
horses 1228

Wesselsbron disease 775, 2480

Wobbly hedgehog syndrome 1834

West Nile virus 1294, 2480

Wohlfahrtia
pet birds 1911
magnijica 2464
poultry 2893
spp 1876, 2464
reptiles 1996
vigil 901, 2464
zoo animals 2054

Wolbachia 73, 76, 128, 2680

Western
pipiens 128
chicken flea 2875

Wolves (warbles), small animals 901
duck sickness 2889

Wonder bulb 3108
equine encephalitis/encephalomyelitis

Wood

1291, 2482
chewing, horses 1548
in poultry 2892
preservative poisoning, mink 1875
yellow pine 3146
sorrel 3116

Wet

Wooden tongue 589
belly disease, mink 1876

Woolsorter's disease 593
dewlap, rabbits 1957

Working dogs 1578
tail, han1sters 2023

Workplace toxicologic hazards 2952

Wetpox, birds 2824

Worms-See also Cestodes, Nematodes

Whelping 2227
of Cayor 902

Whipworms 298--See also Nematodes
intestinal, drug treatment, small animals
infection 2462

418, 419
sheep 314
small animals 421

3324

INDEX

Wounds

Yerba-de-pasmo 3138
closure 1703

Yei·sinia
debridement 1702, 1703
enlerocolilica 158, 273, 274, 276, 2006,
drains 1704

2432
dressings 1704
peslis 677, 1836, 2032

VetBooks.ir
healing
pseudoluberculosis 198, 274, 1836, 1853,
general principles 1702

2006,2432
poor 1706
ruckeri 1758
horses 1716
spp 396, 1878
penetrating abdominal 1717

Yersiniosis 2432
inflammation 1702
fish 1758
lavage 1703

Yesterday-today-and-tomorrow 3106
management 1701

Yew 3114, 3150
initial 1702

Yolk sac infection
open, management 1704
poultry 2859
proliferation in healing 1702
and retention, ostrich chicks 1964
remodeling 1702
surgical repair 1705
udder and teats 1388
z

Wrigglers 888

Zaire ebolavirus 2470

Wright stain 1598

Zaleplon 3035

Wry

Zalophotrerna hepalicurn 1867
face, llan1as and alpacas 1851

Zalophus califoinianus 1860
neck, rabbits 1945

Zarnia purnila 3114
x

Zea mays 2960

Zearalanol 3014

X-linked muscular dystrophies 1233

Zearalenone 2761, 3014

X-rays 1626

Zephymnlhes alarnasco 3118

Xanlhiurn

Zephyr lily 3118
spp 3120

Zeranol 2761,2762
slrurnariurn 343

Zidovudine 2746, 2747
toxicosis 343

Zinc

Xanthomas, pet birds 1915
bacitracin 2765

Xanthosis 1045
deficiency 2585

Xenopus
hereditary 851
laevis 1738, 1743, 1841
horses 2327

/,ropicalis 1743, 1841
pigs 2344

Xerostomia, small animals 369
poultry 2936

Xylazine 2548, 2602, 2607
oxide poisoning 3031

Xylitol poisoning 2968
phosphide poisoning 3169

Xylohypha 643
requirement

Xylometazoline 3026
pigs 2337

Xylorhiza 3086
sheep 2347
responsive dermatopathy, familial, dogs
y

852
responsive dermatoses 974

Yeast
toxicity 3088
avian gastric 1903
fish 1771
in urine 1618
pet birds 1924

Yellow

Zollinger-Ellison syndrome 583
allamanda 3104, 3116

Zolpidem 3035
buttons, birds 2804

Zonisamide 2598
fat disease 1200

Zoo
cats 2388
animals 2046
mink 1874
anesthesia 2050
fever 2482
behavioral training 2049
indigo 3118
clinical care programs 2048
jacket stings 3164
common
jessan1ine 3142
dtsorders 2052
knapweed 3128
procedures 2052
star thistle 3128
diagnostic techniques 2049
wood 3116
drug administration 2050

INDEX

3325

Zoo (continued)

Zooeyia 2413
geriatric 2054

Zoonoses 2414
husbandry 2046
diseases 2170
management 2046
emergence and reemergence
nutrition 2048, 2287

2416

VetBooks.ir
parasite control 2047
prevention 2417
pest control 2048
role of immunosuppression
preventive medicine 2047

2415
quarantine 2047
transmission 2414
regulato1y issues 2052
treatment 2417
reproduction 2046
zoo animals 2052
restraint 2049

Zwoegersiekte 1475
vaccination 2048

Zygadenus spp 3094, 3122
zoonoses 2052

Zygaena spp 2960
mammals

Zygomatic mucocele 368
diets (table) 2295

Zygornycetoses, marine mammals 1864
handrearing 2293

Zygomycosis 645
nutrition 2293
an1phibians 1739

VetBooks.ir

Document Outline

- Cover
- Title Page
- Dedication
- Copyright
- Previous and Foreign Language Editions
- Other Merck Books
- Foreword
- Guide for Readers
- Contents
- Abbreviations and Symbols
- Editorial Board
- Contributors
- Circulatory System
- Eye and Ear
- Endocrine System
- Generalized Conditions
- Immune System
- lntegumentary System
- Metabolic Disorders
- Musculoskeletal System
- Nervous System
- Reproductive System
- Respiratory System
- Urinary System
- Behavior
- Clinical Pathology and Procedures
- Emergency Medicine and Critical Care
- Exotic and Laboratory Animals
- Management and Nutrition
- Public Health
- Pharmacology
- Poultry
- Toxicology
- Reference Guides
- Index

Table of Contents

- Cover
- Title Page
- Dedication
- Copyright
- Previous and Foreign Language Editions
- Other Merck Books
- Foreword
- Guide for Readers
- Contents
- Abbreviations and Symbols
- Editorial Board
- Contributors
- Circulatory System
- Eye and Ear
- Endocrine System
- Generalized Conditions
- Immune System
- lntegumentary System
- Metabolic Disorders
- Musculoskeletal System
- Nervous System
- Reproductive System
- Respiratory System
- Urinary System
- Behavior
- Clinical Pathology and Procedures
- Emergency Medicine and Critical Care
- Exotic and Laboratory Animals
- Management and Nutrition
- Public Health
- Pharmacology
- Poultry
- Toxicology
- Reference Guides
- Index